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LIBRARY
Michigan State
University

 

 

 

This is to certify that the
dissertation entitled

ES IN PESTICIDE USE AND DIETARY RISK IN THE

SINCE THE PASSAGE OF THE FOOD QUALITY
PROTECTION ACT (FQPA) IN 1996

presented by

FAYE REGINA AQUINO VI RAY

has been accepted towards fulfillment
of the requirements for the

degree in Resource Development-
Environmental Toxicology

 

 

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gig/{115% /C'; .5156 ‘2
Date

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5/08 K:IProj/Aoc&PrelelRC/DateDue.indd

CHANGES IN PESTICIDE USE AND DIETARY RISK IN THE USA SINCE THE
PASSAGE OF THE FOOD QUALITY PROTECTION ACT (FQPA) IN 1996
By

Faye Regina Aquino Viray

A DISSERTATION

Submitted to
Michigan State University
in partial fiJlfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY
Resource Development-Environmental Toxicology

2009

ABSTRACT

CHANGES IN PESTICIDE USE AND DIETARY RISKIN THE USA SINCE THE
PASSAGE OF THE FOOD QUALITY PROTECTION ACT IN 1996

By
Faye Regina Aquino Viray

The enactment of the Food Quality Protection Act (FQPA) in 1996 resulted in
major changes in the registration of pesticides. These included increased safety for
infants and children, the reregistration of older pesticides including the use of aggregate
and cumulative exposure assessments, and the expedited registration of reduced-risk
(RR) pesticides. Special regulatory focus has been on three groups of pesticides: the
neurotoxic organophosphate (OP) and carbamate (NMC) insecticides, and the BZ
carcinogenic fungicides. Despite the pressure to substitute RR pesticides for these older,
toxicologically suspect compounds, there has been little public analysis of changes in the
pesticide use and residue levels or of changes in dietary risk resulting from FQPA. This
study aims to assess these changes. The data were obtained from publicly-available
databases, i.e. the USDA’s Pesticide Data Program, the California Department of
Pesticide Regulation, the CropLife Foundation, and the FDA’S Total Diet Study.

The use and food residue detects of individual OPS showed a strong declining
trend with an approximately 50% overall decline for the group from 1994 to 2006. The
use of NMCs also declined approximately 70% fiom 1994 to 2006, but their residue
detection trends were variable and did not clearly correspond to the decline in use. The
use of the BZ fungicides declined less (10-20%) and there was no overall decrease in
residue detects for most of these compounds. The R insecticides and fiingicides showed

a steady increase over this time such that they are now central in pest management

programs for fruits and vegetables but the residue data are too limited to establish a trend.
It was estimated that approximately 50% (33—60%) of the RR pesticides were registered
by USDA’s IR-4 program. In some cases, residue detections were unexpectedly high and
greater than those for the older compounds. Since the RR pesticides are applied at much
lower rates than the older compounds, their adoption has resulted in lower levels of
chemical use in fruit and vegetable production. This decreased environmental load,
coupled with the improved toxicological profiles of the RR compounds, implies an
increase in environmental and worker safety as well as a reduction in dietary risk.

The replacement of the B2 carcinogenic fungicide, iprodione, by the IR-4
registered RR compound, fludioxonil for use on stone fruits, was selected as a case study
to illustrate changes in dietary risk after FQPA. Both the DEEM and Lifeline exposure
assessment programs were used. The exposures were compared to the reference doses
(Rfl)s). The percentage of the Rst estimated for fludioxonil were lower than those for
iprodione in both acute and chronic exposures, and the iprodione risks declined
significantly after the passage of F QPA. These risks were highest for the 1-2 year old age
group and declined rapidly thereafter with age. However, the largest contribution to food
safety was through the reduction in carcinogenic risk due to reduced levels of exposure to
iprodione and the lack of carcinogenicity of fludioxonil. A comparison of these risks at
different tiers of analysis showed that both the acute and chronic dietary risks generally
decreased from the lower to higher tiers (tier 1>tier 2>tier 3) which is expected Since the
input parameters become more realistic at higher tiers of analysis. Finally, a comparison
of the DEEM and LifeLine programs in these analyses revealed comparable results

despite considerable differences in their approaches to estimating dietary exposures.

ACKNOWLEDGEMENTS

I would like to express my deepest gratitude to those who helped me get through
my PhD journey...To Dr. Dan Bronstein, my advisor, and Dr. Bob Hollingworth, my
research advisor, for their academic guidance and the time, patience and effort they
devoted to help me finish my degree; to Dr. Karen Chou and Dr. Mike Hamm, my
committee members, for their very valuable suggestions and comments; to the IR-4 for
the financial assistance and to Dr. Jerry Baron, Dr. Dan Kunkel, Dr. Dave Thompson and
Ms. Diane Infante for their recommendations and for providing much needed IR-4 data;
to David Hrdy, David Miller, Sheila Piper and Dr. Jeff Hemdon of the EPA for the
opportunity and the training experience during my volunteer study at EPA, for reviewing
my dietary analysis data and for the numerous consultations; to Karl Schnelle, Bruce
Young and Beth Julien of CARES, to Steve Petersen and Dr. Barbara Petersen of DEEM,
to Dr. Christine Chaisson and Kerry Diskin of LifeLine and to Jack Zabic of Dow for
their assistance in using the computer models; to Nathan Reigner and Leonard Gianessi
of the CLF and to Roger Fry of the PDP for providing the databases; to Cheryl Drefs,
John Stutz, Mary Votaw, and Terry Schmer of the CA-DPR for their help in gaining
access to the CA-DPR databases; to Dr. John Wise and Dr. Larry Olsen for their inputs
and suggestions; and to the RD and the BITS faculty, staff and friends for their
assistance.

To my CIPS friends-Lee Duynslager, David Mota-Sanchez, Chris Vandervoort
Jeff and Jan for all their help with my dissertation, for the company, fi'iendship,

encouragement and for making my stay at Room 206 enjoyable and memorable; to

iv

Desmi, Dozie and to all my MSU fi'iends; to my friend, Jowel for the prayers,
encouragement and spiritual nourishment; to my cousin Kuya Cary and my Aunt Aning
who made the beginning of my PhD journey possible;

To my parents, Tatay & Inay, for their love, guidance and encouragement, and to
my in-laws for their support;

To my husband, Manny, for his unwavering love, support, patience,
understanding, encouragement, and trust;

And lastly I thank the Lord for giving me the strength to overcome the hurdles

throughout this journey especially during those times when I was at my wit’s end.

.. Faye

TABLE OF CONTENTS

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

LIST OF TABLES .......................................................... . ................................................... x
LIST OF FIGURES ........................................................................................................... xi
LIST OF ABBREVIATIONS .......................................................................................... xiv
CHAPTER 1 ....................................................................................................................... 1
INTRODUCTION .................................................................................. 1
1.1 Pesticide Regulation Before the Food Quality Protection Act (FQPA) ........................ 1
1.2 Driving Forces for the Enactment of the FQPA in 1996 - -- .. ....... 3
1.3 Major Regulatory Changes Imposed by the FQPA ...................................................... 5
1.4 EPA’s Response to the FQPA- - - 7
1.5 The IR-4 Project ......... 10
1.6 Need for Evaluation of Changes and Impacts Since the Passage of the FQPA .......... 12
BIBLIOGRAPHY ............................................................................................................. 19
CHAPTER 2 - ............................................................................................. 22
PESTICIDE USE TRENDS .............................................. 22
2.1 Pesticide Use Databases .............................. 25
2.1.1 California Department of Pesticide Regulation (CA-DPR) .. 26
2.1.2 CropLife Foundation (CLF) - 27
2.1.3 National Agricultural Statistics Service (NASS) ........... 28
2.1.4 Doane AgroTralc - - ......................................... 29
2.1.5 Buckley Report ................................................................................................. 29

2.2 The IR-4 Program ....................................................................................................... 30
2.3 Objectives - .......................................................................................... 30
2.4 Methods ................................................................................................................... 31
2. 4. 1 Selection of Pesticides . - . . 31

2. 4. 2 Pesticide Toxicity ............................................................. 31

2. 4. 3 Survey and Evaluation of Pesticide Use Databases ......................................... 36

2. 4 .4 Pesticide Groups Use Trend Analysis .............................................................. 37
2.4.5 Individual Pesticide Use Trend Analysis . ........................ 37
2.4.6 Environmental Load and Application Rate ...................................................... 37

2.5 Results and Discussion - - -- . ................. 39
2.5.1 Pesticide Groups .............................................................................................. 39
2.5.2 Individual Pesticides ............................................................. 42
2.5.2.1 B2 Carcinogenic Fungicides ..................................................................... 42
Iprodione - ...................................................................... 42
Mancozeb........................... ............................................................................... 43

vi

Maneb ................................................................................................................ 45

Captan ............................................................................................................... 45
Chlorothalonil ................................................................................................... 46
2.5.2.2 N-methylcarbamates ................................................................................. 47
Aldicarb ............................................................................................................. 47
Carbaryl ............................................................................................................. 48
Carbofuran ........................................................................................................ 50
Methomyl .......................................................................................................... 51
Oxamyl .............................................................................................................. 52
2.5.2.3 Organophosphates ..................................................................................... 52
Azinphos-methyl (AZM) .................................................................................. 52
Chlorpyrifos ...................................................................................................... 54
Diazinon ............................................................................................................ 55
Dirnethoate ........................................................................................................ 56
Disulfoton. ......................................................................................................... 57
Fonofos .............................................................................................................. 58
Methamidophos ................................................................................................. 59
Methyl parathion ............................................................................................... 60
Acephate ............................................................................................................ 61

F enamiphos ....................................................................................................... 62
Methidathion ..................................................................................................... 62
2.5.2.4 Reduced-risk Fungicides ........................................................................... 63
Azoxystrobin ..................................................................................................... 63
Cyprodinil ......................................................................................................... 64
Fenhexamid ....................................................................................................... 65
Fludioxonil ........................................................................................................ 66
Mefenoxam ....................................................................................................... 67
Trifloxystrobin .................................................................................................. 68
2.5.2.5 Reduced-risk Insecticides ......................................................................... 68
Acetarniprid ....................................................................................................... 69
Buprofezin ......................................................................................................... 70
Imidacloprid ...................................................................................................... 71
Pyriproxyfen ...................................................................................................... 73
Spinosad ............................................................................................................ 73
Bifenazate .......................................................................................................... 75
Indoxacarb ......................................................................................................... 75
Methoxyfenozide .............................................................................................. 75
Pymetrozine ...................................................................................................... 76
Tebufenozide ..................................................................................................... 77
Thiarnethoxarn .................................................................................................. 77
2.5.3 IR-4’s Role in Registering Reduced-risk Pesticides ........................................ 78
2.5.4 Decrease in Application Rates with Reduced-risk Compounds ...................... 79
2.6 Conclusion .................................................................................................................. 84
BIBLIOGRAPHY ............................................................................................................. 87

vii

CHAPTER 3 ........................................................................................ 96

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

PESTICIDE RESIDUE TRENDS ............................ -- 96
3.1 Pesticide Residue Databases ....................................................................................... 96
3.1.1 US. Department of Agriculture Pesticide Data Program (U SDA—PDP) ......... 97
3.1.2 California Department of Pesticide Regulation (CA-DPR) ............................. 99
3.1.3 Food and Drug Administration (FDA) ........................................................... 100
3. 2 Objectives ............................ 102
3. 3 Methods -- .............................. 102
3. 3. 1 Survey and Evaluation of Pesticide Residue Databases ................................ 102
3. 3. 2 Pesticide Residue Trends ............................................................................... 103
3.3.2.1 Individual Pesticide Residue Trends ....................................................... 103
3.3.2.2 Individual Pesticide Residue Trends with High Percent Detects ............ 103
3.3.2.3 Residue Trends for Pesticide Groups 104
3.3.2.4 Pesticide Residue Detection Frequency in the FDA Total Diet Study
(TDS) ................... - ..... 104
3 .4 Results and Discussion ....... 105
3 ..4 1 Overall Residue Trends of Pesticide Groups. 105
3 ..4 2 Individual Pesticides with High Percent Detects and/or Distinct Trends in
Residue Detection - 108
3.4.2.1 Azinphos—methyl ..................................................................................... 110
3.4.2.2 Chlorpyrifos ............................................................................................ 111
3.4.2.3 Dimethoate .............................................................................................. 1 12
3.4.2.4 Methamidophos ....................................................................................... 113
3.4.2.5 Methyl parathion.. ............................................................ 114
3.4.3 Unexpected Residue Trends ..... ............ 115
3.4.4 Pesticide Residue Databases and Trend Analysis .......................................... 118
3.5 Conclusion . - ...................................... 121
BIBLIOGRAPHY ........................................................................................................... 124
CHAPTER 4 ................................................................................................................... 127
IMPLICATIONS OF THE FQPA FOR DIETARY RISK: A CASE STUDY .............. 127
4.1 Pesticide Risk Assessment ........................................................................................ 127
4.2 Dietary Risk Assessment Computer Models ............................................................ 130
4. 2. 1 Dietary Exposure Evaluation Model (DEEM) ............................................... 131
4. 2. 2 LifeLine ........................................................ 133
4. 2. 3 Cumulative Aggregate Risk Evaluation System (CARES) ........................... 134
4. 2. 4 Comparison of the DEEM, LifeLine and CARES Programs ......................... 135
4.2.4.1 Reference Population .............................................................................. 136
4.2.4.2 Binning Methodology ............................................................................. 136
4. 2. 4. 3 Reference Population Bodyweights ........................................................ 137
3. 2. 4. 4 Model Weights" -- ............................................. 137
4. 3 Dietary Risk Assessment Using Tiered Analysis ..................................................... 138
4. 4 Objectives - . ...................................................................................... 138
4.5 Methods ................................................................................................................. 139

viii

4.5.] Selection of a Pesticide-Crop Combination for the Case Study .................... 139

 

 

 

 

 

 

 

 

4.5.2 Dietary Risk Exposure Assessment Scenario .. ............... 141
4.6 Results and Discussion .............................................................................................. 146
4.6.1 Variation in the Dietary Exposure at Different Tier Levels ........................... 148
4.6.2 Comparison of Estimated Exposures from the DEEM and LifeLine
Assessment Models - ......... 154
4.6.3 Dietary Risk Before and After the FQPA . 155
4.6.4 Dietary Risks of Iprodione Compared to Fludioxonil .................................... 157
4.6.5 Generalizability of the Iprodione-Fludioxonil Case Study ............................ 158
4.7 Conclusion ................................................................................................................ 164
BIBLIOGRAPHY ........................................................................................................... 167
CHAPTER 5 SUMMARY, CONCLUSIONS AND RECOMMENDATIONS ............ 171
APPENDICES -- - - ........................................................... 177
APPENDIX A Preliminary Selected Pesticides .............................................................. 178
APPENDIX B Pesticide Toxicity Properties ...................................... 180
APPENDIX C Individual Pesticide Use Charts ........................ 199
APPENDD( D Individual Pesticide Residue Detects Charts ....... 208
APPENDIX E Acute and Chronic Exposure and Risk Estimates for Iprodione ........... 221
APPENDD( F Acute and Chronic Exposure and Risk Estimates for F ludioxonil ........ 230

ix

Table 2.1

Table 2.2

Table 2.3

Table 2.4

Table 4.1

Table 4.2

Table 4.3

Table 4.4

Table 4.5

LIST OF TABLES

Selected pesticides for use and residue trend analyses ....................

Percent change in the use of the B2 carcinogen, OP and NMC

 

pesticide groups.-- - - ........................................

Level of reduced-risk fungicides acreage based on the

CA-DPR 2006 data - ..............................................

 

Level of reduced-risk insecticides acreage based on the
CA-DPR 2006 data

......... 32

......... 39

........ 63

........ 69

 

The EPA’s tiered approach for exposure analysis ........

.129

 

Differences between DEEM, LifeLine and CARES ........................

Dietary exposure assessment input parameters for iprodione
and fludioxonil ....................

....... 136

- 144

 

 

Toxicity parameters used in the dietary exposure assessment for
iprodione and fludioxonil .............................. -

145

 

Carcinogenic “clusters” based on the 1986, 1996 and 2005 cancer
classification guidelines - . . - - -

159

 

Figure 1.1

Figure 2.1

Figure 2.2

Figure 2.3
Figure 2.4
Figure 2.5
Figure 2.6
Figure 2.7
Figure 2.8
Figure 2.9
Figure 2.10
Figure 2.11
Figure 2.12
Figure 2.13
Figure 2.14
Figure 2.15
Figure 2.16
Figure 2.17

Figure 2.18

LIST OF FIGURES

“Images in this dissertation are gresented in color.”

Registration of active ingredients considered to be safer chemicals ........ 16

Acreage treated and pounds applied of the OPS, NMCs and

 

reduced-risk insecticide groups ................................................................ 41
Acreage treated and pounds applied of the B2 carcinogenic and the

reduced—risk fungicide groups ............... 42
Use of iprodione based on the CA-DPR and the CLF data ...................... 43
Use of mancozeb based on the CA-DPR and the CLF data ...................... 44
Use of maneb based on the CLF and the CA-DPR data ........................... 45
Use of aldicarb based on the CA-DPR and the CLF data. ....................... 48
Use of carbaryl based on the CA-DPR and the CLF data ......................... 49
Use of carbofuran based on the CA-DPR and CLF data .......................... 50
Use of methomyl based on the CA-DPR and CLF data ........................... 51
Use of azinphos-methyl based on the CA-DPR and the CLF data ........... 54
Use of Chlorpyrifos based on the CA-DPR and CLF data ........................ 55
Use of diazinon based on the CA—DPR and the CLF data ........................ 56
Use of dirnethoate based on the CA-DPR and CLF data .......................... 57
Use of disulfoton based on the CA-DPR and CLF data ........................... 58
Use of fonofos based on the CA-DPR and CLF data ............................... 59
Use of methamidophos based on the CA-DPR and CLF data .................. 60
Use of methyl parathion based on the CA-DPR and CLF data ................ 61
Use of azoxystrobin based on the CA-DPR and CLF data ....................... 64

xi

Figure 2.19
Figure 2.20
Figure 2.21
Figure 2.22
Figure 2.23
Figure 2.24
Figure 2.25
Figure 2.26
Figure 2.27

Figure 2.28

Figure 2.29

Figure 2.30
Figure 2.31

Figure 3.1

Figure 3.2

Figure 3.3

Figure 3.4

Figure 3.5
Figure 3.6
Figure 3.7

Figure 3.8

Use of cyprodinil based on the CA-DPR and CLF data ........................... 65
Use of fenhexamid based on the CA-DPR and CLF data ......................... 66
Use of fludioxonil based on the CA-DPR and CLF data .......................... 67
Use of mefenoxam based on the CA-DPR and CLF data ......................... 68
Use of acetamiprid based on the CA-DPR and CLF data ......................... 70
Use of buprofezin based on the CA-DPR and the CLF data .................... 71
Use of imidacloprid based on the CA-DPR and the CLF data ................. 72
Use of pyriproxyfen based on the CA-DPR and the CLF data ................. 73
Use of spinosad based on the CA-DPR and the CLF data ........................ 74

Environmental load of the anticholinesterase and the reduced-risk
insecticide groups ...................................................................................... 80

Environmental load of the B2 carcinogenic and the reduced-risk
fungicide groups ........................................................................................ 81

Overall environmental load of the insecticide and the fungicide groups. 82

Application rates of the insecticides and the fungicides groups ............... 83
Residue detections for the OP, NMC and BZ pesticide groups
based on the PDP residue data ................................................................ 106
Residue detections for the OP, NMC and B2 pesticide groups
based on the CA-DPR residue data ......................................................... 106
Frequency of pesticide occurrence in adult foods ................................... 107

Frequency of pesticide occurrence in selected infant

and toddler foods ..................................................................................... 108
Percent detects for azinphos-methyl ....................................................... 11 1
Percent detects for Chlorpyrifos .............................................................. 1 12
Percent detects for dimethoate ................................................................ 1 13
Percent detects for methamidophos ........................................................ 1 14

xii

Figure 3.9
Figure 3.10
Figure 3.11
Figure 3.12
Figure 4.1
Figure 4.2
Figure 4.3
Figure 4.4a
Figure 4.4b
Figure 4.5
Figure 4.6
Figure 4.7

Figure 4.8

Figure 4.9

Percent detects for methyl parathion ....................................................... 1 15
Percent detects for carbaryl ..................................................................... 1 16
Percent detects for imidacloprid ............................................................. I. 18
Percent detects for acetamiprid ............................................................... 1.18
The risk assessment process .................................................................... 128
Iprodione acute risk estimates for peaches (Tiers l and 2) .................... 148
Iprodione acute risk estimates for peaches (Tier 3) ............................... 149
Iprodione chronic risk estimates for peaches (DEEM) ........................... 149
Iprodione chronic risk estimates for peaches (LifeLine) ........................ 150
Fludioxonil acute risk estimates for peaches .......................................... 150
Fludioxonil chronic risk estimates for peaches ....................................... 151
Iprodione cancer risk for peaches ........................................................... 153

Dietary acute toxicity categories of the old and new insecticides
and fungicides ......................................................................................... 160

Carcinogenic “clusters” of the old and new insecticides
and fimgicides ......................................................................................... 161

xiii

aPAD

AMS

BEAD

CA-DPR

CAG

CARES

CLF

CMG

cRfl)

CSFII

CSREES

DEEM

DRI

EBDC

EDSP

EDSTAC

EPA

ETU

FDA

FEPCA

LIST OF ABBREVIATIONS

Acute Population Adjusted Dose

Acute Reference Dose

Agricultural Marketing Service

Azinphos-methyl

Biological and Economic Analysis Division
California Department of Pesticide Regulation
Cumulative Assessment Group

Cumulative and Aggregate Risk Evaluation System
CropLife Foundation

Common Mechanism Group

Chronic Reference Dose

Continuing Surveys of Food Intake by Individuals
Cooperative State Research, Education, Extension Service
Dietary Exposure and Evaluation Model

Dietary Risk Index

ethylenebisdithiocarbamate

Endocrine Disruption Screening Program
Endocrine Disruptor Screening and Testing Committee
Environmental Protection Agency

ethylthiourea

Food and Drug Administration

Federal Environment Pesticide Control Act

xiv

FF DCA
FIF RA
FQPA
FT
GAO

HCB

ILSI
IR-4
IRED
IRIS
LOAEL

LOD

MOE

NAPIAP
NAS
NASS
NCF AP
NCHS
NDs

NHANES

Federal Food, Drug and Cosmetic Act

Federal Insecticide, F ungicide and Rodenticide Act
Food Quality Protection Act

Field Trial

General Accounting Office

hexachlorobenzene

Highest Field Trial

International Life Sciences Institute

Interregional Research Project No. 4

Interim Reregistration Eligibility Decision
Integrated Risk Information System

Lowest Observed Adverse Effect Level

Limit of Detection

Modifying Factor

Margin of Exposure

Multiresidue method

National Agricultural Pesticide Impact Assessment Program
National Academy of Sciences

National Agricultural Statistics Services
National Center for Food and Agricultural Policy
National Center for Health Statistics

Non-detects

National Health and Nutrition Examination Surveys

XV

NMCS
NOAEL
NOEL
NRC
OIG
OP(s)
OPP
PCT
PDP

ppm
PUMS

RPF
SAES
SAP
SDWA
TDS
UF
USDA

WPS

N-methylcarbamates

No Observed Adverse Effect Level
No Observed Adverse Effect Level
National Research Council

Office of Inspector General
Organophosphate(s)

Office of Pesticide Program
Percent Crop Treated

Pesticide Data Program

Parts per million

Public Use Micro Data Sample
Raw Agricultural Commodity
Reregistration Eligibility Decision
Reference Dose

Relative Potency Factor

State Agricultural Experiment Stations
Scientific Advisory Panel

Safe Drinking Water Act

Total Diet Study

Uncertainty Factor

United States Department of Agriculture

Worker Protection Standard

xvi

CHAPTER 1
INTRODUCTION

1.1 Pesticide Regulation Before the Food Quality Protection Act (FQPA)

Pesticides in the United States are regulated under the Federal Insecticide,
F ungicide and Rodenticide Act (F IFRA) and the Federal Food, Drug and Cosmetic Act
(F F DCA). The Environmental Protection Agency (EPA) registers pesticide uses under
the FIFRA and sets pesticide tolerances in food under the F F DCA. The Food and Drug
Administration (FDA) enforces the tolerances for most foods, and the tolerances for
meat, poultry and some egg products are implemented by the US. Department of
Agriculture (USDA). Regulation dates back to 1910 when the Federal Insecticide Act
was passed “to ensure the quality of pesticide chemicals purchased by consumers” in
response “to concerns from the US. Department of Agriculture (USDA) and farm groups
about the sale of fraudulent or substandard ‘ pesticide products, which was common at that
time” (T oth 1996). In 1947 the FIFRA was enacted and extended the coverage to include
herbicides and rodenticides. Under the FIF RA, tolerances were set for pesticide residues
in food. It required registration of all pesticide products with the USDA before they were
sold within or outside the US. The standards for labeling the products were set and
labeling was also required. The EPA was created in 1970 and was charged to administer
the FIFRA. The FIFRA was amended in 1959 and in 1964 but the most significant
changes took effect in 1972 under the Federal Environmental Pesticide Control Act
(F EPCA). The changes included (T oth 1996):

1. Requirement that all pesticides (including those sold interstate) be

registered with EPA and classified by the agency for general or

restricted use.

2. Certification was required for persons applying restricted use
pesticides.
3. Set a new registration standard for pesticides, allowing the registration
of a pesticide only if it could be determined that the pesticide would
not cause unreasonable adverse eflects.
With this law, the emphasis on pesticide regulation in the US. moved fiom quality
assurance and adequate labeling of pesticide products to the protection of public health
and the environment from their potential hazards (T oth 1996). The FIFRA was further
revised and amended from 1975 to 1981 to improve the registration process of pesticides
and “provide for consideration of the agricultural benefits of pesticides in regulatory
decision made by the EP ” according to Toth (1996), and the pesticides registered before
August 1975 were reviewed as a consequence of the amendments. In 1988, FIFRA was
further amended “to establish a 9-year schedule for completion of the reregistration of
pesticide active ingredients registered before November 1984 and to impose substantial
fees on registrants to cover much of the costs of the registration”. This led to voluntary
cancellations of thousands of registrations by registrants due to obsolescence, costs and
data requirements; only a few were suspended or canceled by the EPA. Worker safety
also became a concern and led to the revision of the Worker Protection Standard (WPS)
for agricultural pesticides which took effect in 1992. It required modification of labels to
include the use of personal protective equipment, restriction of re-entry intervals of
workers to pesticide-treated areas, and notification of workers about treated areas.
The Federal Food and Drugs Act, or Pure Food Law, enacted in 1906 was

intended for public protection from adulterated or misbranded food but it did not include

pesticide residues. The Food and Drug Administration (FDA) was authorized to enforce
the tolerances for chemicals to protect public health when the FFDCA was passed in
1938. The Miller Amendment to the FFDCA required tolerances be set for all pesticides
and further required any raw agricultural commodity to be condemned as adulterated if it
contained a pesticide residue above the tolerance level established by the FDA (Toth
1996). Food additives were also covered in the 1958 amendment through the Food
Additives Amendment. This implied that processed foods containing pesticide residues
that exceeded tolerance levels were considered “adulterated and subject to seizure similar
to raw agricultural commodities” according to Toth (1996). The amendment also
included the Delaney Clause which called for a zero tolerance for any food additive
(including pesticides) that might cause cancer.
1.2 Driving Forces for the Enactment of the FQPA in 1996

The Food Quality Protection Act (F QPA) amended both the F IFRA and the
FF DCA, and one of the major driving forces of the enactment of the F QPA was the huge
backlog at the EPA when it started the review of pesticide registrations in 1975. During
the period of 1976 to 1988, the EPA’S review or reregistration of older pesticides was
proceeding at a much slower pace than originally anticipated by the EPA or Congress
(Toth 1996). This underlined the need to have a more rapid reregistration process.
Conoems about the risk and safety of farm workers and applicators were also major
drivers for the changes in the pesticide regulation. The Delaney Clause was highly
criticized in some quarters and was also a reason for the F QPA. Its concept of zero
carcinogenic risk inhibits the flexibility of a regulatory agency to make tolerance
decisions based on the latest risk models because it means that even the most trivial risk

cannot be allowed and it also “creates a false expectation that a processed food will not
3

have any cancer-causing substances in it” (Vogt 1995). Vogt (1995) further commented
that since the Delaney Clause sets a standard only for carcinogenic residues that
concentrate in processed foods, the same pesticide chemical must meet inconsistent
requirements (zero-risk versus risk-benefit balancing) depending on whether it is found
in/on processed or raw food. This is often referred to as the “Delaney Paradox”. The
Delaney Clause also limited the introduction of lower-risk pesticides that could replace
older and potentially more hazardous compounds also according to Vogt (1996). The
National Academy of Sciences (NAS) was tasked by the EPA to “review the conflicting
standards and basis for tolerance setting” in 1984. In the 1987 analysis report, Regulating
Pesticides in Food: The Delaney Paradox by the NAS/National Research Council (NRC)
it was concluded that pregnant women, infants and children faced unique risks from
pesticide exposure, and that existing EPA risk assessment procedures were not taking
these unique risks into account (Landrigan and Benbrook 2006). The increased emphasis
on protecting the health of infants and children led to the creation and refinement of the
US. Department of Agriculture’s Pesticide Data Program (PDP) and to major EPA
research initiatives.

Endocrine disruption became a critical focus and was also a contributor to the
passage of the FQPA. It has led to the development of the Endocrine Disruptor Screening
Program (EDSP) by the EPA, when the FQPA and the Safe Drinking Water Act (SDWA)
were amended in 1996. The program required the EPA to “develop a screening program,
using appropriate validated test systems and other scientifically relevant information to

determine whether certain substances may have an effect in humans that is similar to an

effect produced by a naturally occurring estrogen or other endocrine effect as the EPA
may designate” (U .S.EPA 2007b).
1.3 Major Regulatory Changes Imposed by the FQPA

The passage of the FQPA was a turning point in the regulation of pesticides and
led to several major changes:

I Amendments to the FFDCA provided special provision for the more sensitive
population, i.e. infants and children (FQPA 1996) and an additional lO-fold safety factor
when establishing acceptable levels of exposure was required “to fmther protect infants
and children unless reliable information in the database indicates that it can be reduced or
removed” (U .S.EPA 2007c).

I The focus of regulating pesticides switched from balancing risks and benefits
to a greater emphasis on public health and the environment. The Delaney Clause was
removed when the FF DCA was amended and the FQPA enacted in 1996. The F QPA
eliminated the distinction between raw-food and processed-food tolerances so that all
pesticide residues are regulated under an amended FFDCA section 408 that requires all
tolerances be “safe”, ensuring a “reasonable certainty of no harm” fiom pesticides (NRC
2000) and established a single health-based standard. Although the switch has been
significant, in practice benefit considerations are still important.

I Tolerances were required for the issuance of emergency exemptions. Section
18 of the FIFRA authorizes EPA to permit state and federal agencies to allow the
unregistered use of a pesticide for a limited time if EPA determines that emergency pest
conditions exist and no registered pesticide would be effective (NRC 2000) and
tolerances were now required for pesticides under the emergency exemption. This is a

very significant aspect of the FQPA and the NRC (2000) noted that this “had the most
5

profound effect on the ability of the agency to meet its deadlines, and it is responsible in
part for the reduced number of new uses and new active ingredients”.

I Tolerance reassessment and reregistration of pesticides were required by the
F QPA. Under the FQPA, there was increased provision for the assessment and
quantification of the risks from pesticides. The F QPA required reevaluation of all
tolerances set before August 1996 within ten years. Pesticides containing any active
ingredient registered before November 1, 1984 were required to be reregistered and a
periodical review every 15 years was also mandated for the reregistered pesticides.

I Aggregate exposure assessment was developed by the EPA as part of the
reregistration process. It considers all routes such as dietary, drinking water, and non-
occupational exposures to a single chemical for risk assessment purposes.

I Cumulative exposure assessment was also developed by the EPA. It requires
assessing the cumulative risk from exposure to pesticides and other substances that have
of a “common mechanism of toxicity” (EPA, 2002). The F QPA also requires
consideration of endocrine disruption effects for tolerance reassessment and risk
evaluation (U .S.EPA 2007c). An environmental endocrine disruptor is defined as an
exogenous agent that interferes with the synthesis, secretion, transport, binding, action, or
elimination of natural hormones in the body that are responsible for the maintenance of
homeostasis, reproduction, development, and/or behavior (U .S.EPA 1997). This called
for the EPA to develop the Endocrine Disruptor Screening Program (EDSP) that is
responsible for testing and screening for possible endocrine disruptors. As of late 2008,

the EDSP program had yet to be finalized by EPA.

I FQPA required the development of a minor use program in the EPA and
provided that special considerations be afforded to minor use actions (U .S.EPA, 2007b).

I FQPA mandated and required EPA to expedite the approval of reduced-risk
pesticides.

1.4 EPA’s Response to the FQPA

The main requirement of the FQPA since its enactment in 1996 is to accomplish
the review and reassessment of tolerances of pesticides within ten years according to the
new standards. By August 2006, EPA had completed over 99% of the 9,721 tolerance
reassessments required by F QPA. Three thousand two hundred tolerances were
recommended for revocation and 1,200 tolerances were modified and the safety of 5,237
tolerances was confirmed. Nearly 4,400 out of 17,592 individual pesticide end-use
product registrations have been cancelled (U .S.EPA 2006a). Also, the addition of the
extra ten-fold factor for children’s safety is now a standard in dietary risk assessment.
Another outcome of the FQPA is the impact assessment fiom aggregate exposure from
food, residential and non-residential sources that EPA requires for reregistration of
pesticides and the introduction of cumulative risk assessments for pesticides having a
common mechanism of toxicity. The EPA completed the cumulative risk assessments of
the organophosphate and the carbamate pesticide groups in 2006 and 2007, respectively.

The primary issue dealt with during the development of the cumulative exposure
assessment method was the consideration of what constitutes a common mechanism of
toxicity. A common mechanism of toxicity group consists of chemicals for which
scientifically reliable data demonstrate that the same toxic effect occurs in or at the same
organ or tissue by essentially the same sequence of major biochemical events (U .S.EPA

2007a). The EPA worked with the International Life Sciences Institute (ILSI) and
7

participated in workshops to discuss this issue in relation to the organophosphates.
Consequently, the common mechanism of toxicity of the carbamates, chloracetanilides,
thiocarbamates and dithiocarbarnates was also considered. A series of consultation and
deliberations in developing the method included hazard and dose-response assessment,
endpoint selection, and probabilistic approach issues and the use of advanced computer
risk assessment models such as LifeLine and the Dietary Exposure and Evaluation Model
(DEEM). Probabilistic analysis involves the use of a statistical technique (e. g. Monte
Carlo analysis) to quantify both the distribution of exposures to pesticide residues and the
probability or chance of exposure to any particular residue level (U.S.EPA 2000).

Worker safety and exposure also became a concern and led to the establishment
of guidelines specifically addressing worker exposure by the EPA. The Worker
Protection Standard (WPS) is a federal regulation designed to protect agricultural
workers (people involved in the production of agricultural plants) and pesticide handlers
(people mixing, loading, or applying pesticides, or doing other tasks involving direct
contact with pesticides) (U .S.EPA 2005). The 2005 WPS contains “requirements for
pesticide safety training, notification of pesticide applications, use of personal protective
equipment, restricted reentry intervals following pesticide application, decontamination
of supplies, and emergency medical assistance”.

The Endocrine Disruptor Screening Program (EDSP) was created by the EPA in
1998 due to increasing concerns and evidence that some chemicals affect the endocrine
system. In June 2007 EPA published the EDSP draft list of initial active ingredients and
pesticide inerts to be considered for screening. The inadequacy of conventional testing

methods to determine if a substance would interact with a specific component of the

endocrine system and whether additional testing is needed by the EPA to firlly assess and
characterize the effects on both humans and animals were some of the issues considered
by the EPA in the creation of the EDSP (U .S.EPA-EDSP 2000). It went through series of
consultations and deliberations and started with the formation of the Endocrine Disruptor
Screening and Testing Committee (EDSTAC) in 1996 “to provide advice and counsel to
EPA on a strategy to screen and test chemicals and pesticides that may be the cause of
endocrine disruption in humans, fish and wildlife” (U .S.EPA 1996). The issues that were
discussed included developing a selection and prioritization process for chemicals and
pesticides for screening; development of a process for identifying new and existing
screening tests and mechanisms for validation; the availability of validated screening
tests for early application; and processes and criteria for deciding when additional tests,
beyond screening tests, are needed and how many of these additional tests will be
validated (U .S.EPA 1996). A tiered method for screening and testing for chemicals that
might have hormonal effects was also deliberated on and was included in the EDPS’s
report to Congress in 2000. The tier 1 screening included identification of substances
which have the potential to interact with the endocrine system and tier 2 would confirm
that potential and characterize the effects (U .S.EPA-EDSP 2000).

The reassessment and reregistration process of older pesticides paved the way for
exploring the use of safer, reduced-risk compounds as replacements for the older
pesticides such as organophosphates (OPS), carbamates and BZ (probable human)
carcinogens thought to be particularly likely to cause harmful effects. The Office of
Pesticide Program (OPP) of the EPA initiated the Conventional Reduced-Risk Program

to “expedite the review and regulatory decision-making process of conventional

pesticides that pose less risk to human health and the environment than existing
conventional alternatives” (U .S.EPA 2006b). The program’s goal is to rapidly register .
commercially viable alternatives to riskier conventional pesticides such as neurotoxins,
carcinogens, reproductive and developmental toxicants, and groundwater contaminants
(U .S.EPA 2006b). The EPA (2006b) considers a pesticide use as reduced-risk if it meets
some or all of the following criteria:

I Low impact on human health

I Low toxicity to non-target organisms (birds, fish and plants)

I Low potential for groundwater contamination

I Lower use rates

I Low pest resistance potential, and

I Compatibility with Integrated Pest Management
However, reduced-risk pesticides do not necessarily lack all potential to cause harm.
They are defined relative to a specific existing compound. The EPA’s decision on the
reduced—risk pesticides is made at the use level for a pesticide/use combination and “is
based on comparison between the proposed use of the pesticide and existing alternative
currently registered on that use site” (U .S.EPA 2006b).

1.5 The [R-4 Project

Minor (specialty) crops generally do not give enough incentive to manufacturers
to support the costs of the registration of pesticides. Consequently, the State Agricultural
Experiment Stations (SAES) established the Interregional Research Project No. 4 (IR-4)
in 1963 “to facilitate regulatory clearances for crop protection chemicals on specialty or
minor food crops as well as minor uses on major crops (corn, soybean, cotton, small

grains, etc.) with funding from USDA” (IR-4 2006a). These minor or specialty crops
10

include many fruits and vegetables, nuts, herbs, spices, and ornamental and nursery
plants. They are planted in low acreage but are high value crops and account for more
than $43 billion in annual production and occupy 12 million acres of farmland although
they are grown on low acreage farms (Miller 2007) from which twenty-six states across
the US. derive more than 50% of their agricultural crop sales (IR-4 2006b).

The IR-4 conducts controlled field trials with application of pesticides to crops of
interest followed by analysis of the residues. Petitions with a requested tolerance or other
clearance are then submitted to the EPA and when approved, the new use is added to the
pesticide label and the use becomes legal. The minor use program of the EPA was
created as mandated by the FQPA and required the EPA to address minor use
registrations, reregistrations and policy issues. The US. EPA (U .S.EPA Undated),
defines “minor use” as the use of a pesticide on an animal, on a commercial agricultural
crop or site, or for the protection of public health where—

(1) the total United States acreage of the crop is less than 300,000 acres,

as determined by the Secretary of Agriculture; or
(2) the Administrator, in consultation with the Secretary of Agriculture,
determines that, based on information provided by an applicant for
registration or a registrant, the use does not provide sufficient
economic incentive to support the initial registration or continuing
registration of a pesticide for use and—
a. there are insufficient efficacious alternative registered

pesticides available for use; or

11

b. the alternatives to the pesticide use pose greater risk to the
environment or human health; or

c. the minor use pesticide plays or will play a significant part in
managing pest resistance; or

d. the minor use pesticide plays or will play a significant part in
an integrated pest management program.

The IR-4 program has been very active in promoting the registration of reduced-
risk pesticide uses after the F QPA in collaboration with EPA’S Conventional Reduced-
Risk Program. Since the IR-4 was established, it has achieved more than 10,000 pest
control clearances on food crops (including biopesticide uses) and more than 10,000
clearances on ornamental crops (Miller 2007). Since 2000, over 80% of IR-4’s research
effort has involved new pest management technologies with biopesticides and lower risk
chemistries (IR-4 2005).

1.6 Need for Evaluation of Changes and Impacts Since the Passage of the FQPA

So far there has been little publicly-available analysis of the changes in pesticide
usage after the F QPA or of the effects this may have had on pesticide residues in the US.
diet and the attendant changes in dietary risk. In 2006 the EPA issued a report on its
accomplishments since the enactment of the F QPA. Among the achievements claimed by
the EPA were (U .S.EPA 2006a): the establishment of the extra ten-fold children’s safety
factor, timely reassessments (at that time they had completed 99% of the reregistration
requirements), refinement of the pesticide risk assessment process, development of the
aggregate and cumulative exposure assessment methods, more collaboration with the
public for exchange of information, creation of advisory committees to ensure

stakeholder consultation, establishment of a public participation process, and a pesticide
12

web site to enhance the transparency of the public process. In spite of the tremendous
achievements by the EPA, there was no evaluation and measurement of how pesticide use
and the dietary risks have changed since the F QPA was passed.

The US. EPA-Office of the Inspector General (OIG) reviewed and evaluated the
activities of the EPA related to the implementation of the F QPA and released their report
in 2006. The primary goal of the OIG was “to evaluate the effectiveness of EPA’s Office
of Pesticide Programs (OPP) in measuring the overall impact of FQPA implementation
activities” (U .S.EPA-OIG 2006a). The evaluation included reviews of internal documents
and reports, inputs from internal program staffs and internal and external stakeholders,
“other research on potential human health indicators related to pesticide exposures,
dietary risk and reductions in risk due to EPA action” and “analysis of publicly available
toxicological and residue data supporting EPA dietary risk assessments to assess the
impact of F QPA on dietary pesticide risks from 1994 through 2003” (U .S.EPA-OIG
2006a). According to the report, the EPA-OIG “found that OPP has primarily measured
its success and the impact of F QPA by adherence to its reregistration schedule rather than
by reductions in risk to children’s health”. They concluded that the “EPA can measure
the impact of FQPA on children’s health more efficiently through the examination of
pesticide exposure data, and changes in usage patterns, substitutions and import trends”
(U .S.EPA-OIG 20063). The OIG further recommended that “OPP work to move away
fiom primarily using outputs as performance measures, and implement a suite of output
and outcome measures to assess the human health and environmental impacts of its
works”. The OIG, through a contractor, developed and recommended a novel approach,

the Dietary Risk Index (DRI), to measure the impact of FQPA. This is a basic unit of

13

measure proposed for use in tracking pesticide dietary risk (U .S.EPA-OIG 2006b). In
response, the OPP questioned the validity of the index because “it makes no distinction
among the potential adverse effects prevented by OPP action” which cannot be simply
summed to develop an overall risk estimate, and has to be further reviewed more
thoroughly (U .S.EPA-OIG 2006a). It is not clear that OPP has pursued this approach
further.

California through its Department of Pesticide Regulation (CA-DPR) became the
first and only state to initiate the requirement for full reporting of all pesticide use in
agriculture in 1990. It required growers and commercial pest control operators to report
monthly pesticide use. The records are collected, processed and stored in the CA-DPR
use database and are made available to the public. The database is beneficial for assessing
pesticide use in the areas of risk assessment, worker health and safety, water quality and
pest management among others. The CA-DPR annually publishes the Statewide
Summary of Pesticide Use Report Data which includes a brief narrative overview and a
breakdown of the pounds and acreage of pesticide use. One volume is indexed by
chemical and the second indexed by commodity. Data are studied and analyzed and the
agency issues annual analyses of pesticide use trends. The CA-DPR on-line report for
2006 showed a continued decline in pounds of organophosphate and carbamates used
with approximately 17M pounds in 1995 declining to 7M pounds in 2006 (CA-DPR
2006, 2007b). However, the use of chemicals known to cause cancer varied but remained
almost unchanged overall from 1995 to 2006. The noticeable decrease in use of the

organophosphates and carbamates shows the impact of the FQPA. California also collects

14

and maintains an extensive pesticide residue database for produce in California that is
available and accessible to the public.

The registration and adoption of newer and safer pesticides have increased as a
result of the FQPA. The NRC (2000) cited current patterns of use of modern pesticides
that are considered reduced-risk chemicals based on the biennial report of the EPA Office
of Pesticide Programs (U .S.EPA 1999). The report showed that the proportion of
pesticide active ingredients that are considered to be safer than conventional pesticides,
i.e. biological chemicals and reduced-risk conventional chemicals, has steadily increased
from 1994 to 1999 as shown in Figure 1.1. The CA-DPR reported that pesticide use
statistics in 2006 showed continued progress toward safer, less toxic pest management
and an overall decline in the use of pesticides by nearly six million pounds fiom 2005 to
2006 (CA—DPR 2007a). The use of lower risk pesticides increased fiom 2004 to 2005
with 630,000 pounds applied (60% increase) and 2.4 million acres treated (39%
increase).

There has only been very limited analysis of changes in pesticide residue levels in
foods since the passage of the FQPA. An analysis of selected organophosphate pesticide
residues in produce using data fiom the USDA-PDP fi'om 1994 through 2004 was
conducted by Punzi (Punzi 2005) and was presented during the Florida Pesticide Residue
Workshop and Foodbome Pathogen Analysis Workshop in 2005. A simple graphical
method was used “to allow examination of the relatively large amount of data without the

use of statistical tools so that, at a glance (i.e., using eyeball statistics), a trend could be

15

 

NUMBER OF PESTICIDE REGISTRATIONS BY CATEGORY

 

 

 

 

 

 

 

 

I] BIOLOGICALS I REDUCED-RISK fl CONVENTIONAL
CONVENTIONAL CHEMICALS
CHEMICALS
40
35 l—
30
g 25 ~—
.:
2
,_ 20
‘2
0
Lu
cc

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

     

 

 

Figure 1.]. Registration of active ingredients considered to be safer chemicals
(U.S.EPA 1999).

immediately apparent even to those unaccustomed to examining residue testing data”
(Punzi 2005). Several pesticide-commodity pairs were studied for residue trends. The
Chlorpyrifos residues in apples showed decreased percent detections from 25% in 1999 to
less than 1% in 2002. This is consistent with the regulatory action of the EPA in 2000
when it started phasing out uses of Chlorpyrifos on fi'uits and only pro-bloom application
was allowed in apples (Punzi 2005). In the same study, clear trends for the increase in the
detection rates of phosmet was reported and was correlated to the decrease in detection

l6

 

rate of methyl parathion “presumably due to the cancellation of the latter” according to
Punzi (2005). In a summary report on the residue data collected by the USDA—PDP,
Punzi et al. (2005) showed a slight decrease in detection rates with time although the
annual rates varied fiem 71% in 1993 to 42% in 2003. From 1997 to 2003 (except for
1999 and 2002), the detection rates were steady at 55i2% which was “noteworthy
considering that different groups of commodities are analyzed each year and not all the
same pesticides are measured on each commodity” (Punzi et al. 2005). Punzi (2005)
concluded that “the percentage of samples with detections was remarkably similar
for several commodities over, in some cases, nearly a lO-year period”. These results
indicate that differences in the limits of detection and variations in crops sampled and
pesticides analyzed each year make analysis and establishing of trends difficult This
shows that the PDP database is not set up for trend analysis but is very useful for other
purposes such as exposure assessment at given times.

Although there are some limited reports on the changes in the use and residue
levels of pesticides since the enactment of the FQPA, the dietary risks have not been
investigated, except for the EPA-OIG report (U .S.EPA-OIG 2006a, b) which used a
novel and questionable method. Measming the dietary risks of the old pesticides and
evaluating how it has changed are means to assess the effectiveness of the FQPA and,
given adequate data sources, can be undertaken by using computer programs developed
to handle risk assessments under the F QPA, such as the Cumulative and Aggregate Risk
Evaluation System (CARES), Dietary Exposure and Evaluation Model (DEEM) and
LifeLine computer programs. These programs use the probabilistic approach wherein the

entire range of consumption and residue values is used “to estimate the distribution of

17

exposure for the population of concern and the probability of exposure at any particular
level and allows for a more realistic estimate of exposure” (U .S.EPA 2000). The
development of these programs resulted from the new requirements of the FQPA which
presented many technical challenges to EPA. The competing programs all address these
challenges but in somewhat different ways and all are used by regulators.

From the above review, it is apparent that surprisingly little has been published on
the impact of the manifold changes in pesticide regulation implemented by the FQPA on
pesticide use patterns, the adoption of reduced—risk pesticides, the levels of pesticide
residues in the diet, and on changes in dietary risk with particular reference to infants and
children. It is equally clear that there is a need for additional studies on these topics. A
further area worthy of study is to assess how the IR-4 program has contributed to these
changes in minor crop production, pesticide uSe, and dietary risk, particularly in the
registration of reduced-risk pesticides. These pesticides have become increasingly
important since the restrictions and cancellation of uses of a number of the old

compounds as a result of the FQPA.

l8

BIBLIOGRAPHY

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20

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Minor Uses of Pesticides. US. Environmental Protection Agency. Report.
http://wvxw.epa.g0v/pesticides/minoruse/minor use mtpdf

 

Vogt DU. 1995. The Delaney Clause Effects on Pesticide Policy. Washington, DC:
National Council for Science and the Environment. Report
http://wwwcnieorg/NLE/CRSreports/Pesticides/pest-1.Cfm

 

21

CHAPTER 2
PESTICIDE USE TRENDS

In 1996 the FQPA set in motion major regulatory changes on the registration and
use of pesticides. The initial focus was on the more toxic older compounds such as the
insecticidal organophosphates (OPS) and the N—methylcarbamates (NMCS).
Reregistration was required for all pesticides containing any active ingredient that was
first registered before November 1984 (F IF RA 2004). The FQPA also requires aggregate
and cumulative risk assessments as part of the reregistration process. Aggregate risk
assessment is associated with the combination of all pathways and exposures to a single
chemical while the cumulative risk assessment combines exposures to different chemicals
having a common mechanism of toxicity. The cumulative risk assessments of the OPS
and the NMCS, which are the most widely used groups of insecticides, were completed in
2006 and 2007, respectively (OP preliminary cumulative risk assessment released in
2001 ). The cumulative risk assessments used the relative potency factor (RPF) approach
which is a method for determining the combined risk associated with exposure to the OPS
or the NMCS and is calculated as the “ratio of the toxic potency of a given chemical to
that of the index chemical” (U .S.EPA 2006d, 2007 g). Brain cholinesterase inhibition was
selected as the toxicity endpoint with methamidophos and oxamyl as the index chemicals
used for the cumulative risk assessments of the OPS and the NMCS, respectively. After a
number of regulatory actions to reduce uses and restrict exposure, the EPA concluded
that “the results of the OP cumulative risk assessment support a reasonable certainty of
no harm finding as required by the FQPA” (U .S.EPA 2006d) and the “cumulative risks

from food, water, and residential exposure to NMCS do not exceed the Agency’s level of

22

concern” (U .S.EPA 2007g). The regulatory consequences of the FQPA are additional
restrictions and cancellations of uses and tolerances set for many important pesticides
found to have the potential for unacceptable detrimental effects to humans.

The B2 carcinogenic fungicides (the B25, classified as probable human
carcinogens) were also among the priority pesticides to be evaluated under the FQPA.
Chlorothalonil, captan, maneb, iprodione and mancozeb are some of these 32 fimgicides
that are very important in disease management (Ragsdale 2000). The EPA is also
focusing on evaluating available data for the pyrethroid pesticides to determine if this
group calls for a cumulative assessment. The EPA will employ various measurements
and modeling tools, studies and data analysis “to identify and quantify critical routes and
pathways of exposure for the pyrethroids pesticides and to assess population estimates of
aggregate and cumulative pyrethroids exposure” (U .S.EPA 2007c).

Subsequent to the passage of FQPA, in 1997 the EPA established a priority
system for reviews of “new chemicals, new uses, experimental use permits and
registration amendments, requiring the review of scientific data” as follows (Tinsworth
2000):

I Methyl bromide alternatives

I Reduced-risk candidates

I US. Department of Agriculture-EPA identified potentially vulnerable
crops

I Minor use priorities

I Non-minor use priorities; and

I Pesticides that addressed trade irritants.

23

The OP replacements were placed next to methyl bromide alternatives in 1998 when the
EPA revised the list. This was due to the EPA’s risk concerns presented by OP products
that were on the market at that time both for individual OP compounds and as a group of
compounds that may have a common mechanism of toxicity (Tinsworth 2000).

Despite the extensive regulatory actions intended to change use patterns and
reduce pesticide risk since 1997, few studies have been published to show the effect of
the regulatory actions on the use of pesticides and virtually none are available in the
refereed literature. The California Department of Pesticide Regulation (CA-DPR)
releases annual reports containing comprehensive data on the pounds of individual active
ingredients (ai.) applied for agricultural and non-agricultural uses, and the total aores
treated with pesticides by commodity. Composite data are provided for several classes of
compounds, e. g. usage of reproductive toxins, carcinogens, organophosphates,
carbamates, groundwater and toxic air contaminants, oils, biopesticides and fumigants.
The CA-DPR also reports the general use trends of these pesticides. In a study conducted
by Epstein and Bassein (2003), California Pesticide Use Reports were utilized to study
the use of pesticides for the production of fi'uits, vegetables and nuts in California form
1993 to 2000. The study showed “no trend towards decreased or increased usage of the
pesticides on “risk” lists that are used to control vegetable and fruit diseases in the field”
(Epstein and Bassein 2003). On the other hand, the report by the US General
Accounting Office (GAO) (U .S.GAO 2001) indicated that the “riskiest subset of
pesticides” including organophosphates, carbamates and possible carcinogens decreased
by 14% from 455M pounds of active ingredient in 1992 to about 390M pounds in 2000.

The CA-DPR 2006 report (CA-DPR 2007a) shows continued decline of the

24

anticholinesterases (OPs and NMCS) from 1997 to 2006 for both agricultural and non-
agricultural applications.

National usage reports have also been released by Gianessi and Silvers (2000)
and Gianessi and Reigner (2006a., b). Gianessi and Silvers (2000) compared pesticide
usage based on the data collected by the National Center for Food and Agricultural Policy
(NCFAP) from 1992 to 1997. The NCFAP trend study focused on active ingredients that
have undergone noticeable changes in the usage patterns between 1992 and 1997 at the
national aggregate level, as estimated in the NCF AP national pesticide use database
(Gianessi and Silvers 2000). The NCF AP pesticide use report released in 2006 showed an
aggregate decrease in fimgicide use by 17M pounds and a reduction of 61 M pounds in
herbicide use between 1997 and 2002 (Gianessi and Reigner 2006b). This study
complements the limited information available on how the use of pesticides has changed
over time. There are virtually no publications on this topic in the refereed scientific
literature.

2.1 Pesticide Use Databases

Several pesticide usage databases are publicly and electronically available.
Among the agencies that maintain pesticide use databases are the USDA National
Agricultural Statistics Services (NASS), the CropLife Foundation (CLF) and the
California Department of Pesticide Regulation (CA-DPR). In addition, proprietary
databases are produced, most notably the Doane AgroTrak and the Buckley Reports.
However, there is no comprehensive publicly available national database on pesticide
usage. These databases vary in a number of ways and have different advantages and

disadvantages for use analysis. The CA-DPR use database has a comprehensive

25

collection of data and has annual use data available while the CLF and NASS both cover
national use of pesticides. Although the CA-DPR database represents California only, the
state is “the largest and most diverse agricultural producer in the United States and
produces more than half of the country’s fruits, vegetables and nuts and uses
approximately 22% of the total agricultural pesticides in the nation” (U .S.GAO 2001).
The CLF has a collection of data fiom various sources including NASS, individual state
reports, USDA crop profiles and the CA-DPR annual reports. However, the CLF reports
are released only every five years and the use data are not specific for any particular year.
The Doane AgroTrak and the Buckley Report may have the most complete and
comprehensive national statistics of pesticide use but the major disadvantage is their
proprietary nature and very expensive acquisition cost.

2.1.1 Calg'fomia Department of Pesticide Regulation (CA-DPR)

California is the only state that requires full reporting of all pesticide use. The
pesticide use reporting program is internationally recognized as the most comprehensive
of its kind in which more than 2.5 million records of chemical applications are annually
collected and processed by the CA-DPR. The pesticide use reporting process starts before
the pru'chase and use of a pesticide with the property owners (or pesticide applicators)
obtaining an identification number fi'om the county where any pest control work is to be
performed Site identification numbers are obtained by growers fi'om the County
Agricultural Commissioner for each location and crop/commodity where pest control
activities are to be undertaken. The identification number is recorded on the restricted
material permit or other approved form. Geographic information, operator identification

or permit number, name and address and field location are among the information

26

required for agricultural application reports. Non-agricultural applications require less
information which includes pesticide product name and manufacturer product registration
number, and amount used among others. The staff at the County Agricultural
Commissioner’s office reviews the reports for accuracy and they are entered into a
county database and transferred monthly to the CA-DPR. The CA-DPR uses the data for
risk assessment, for safety and protection of the health of workers, protection of
endangered species, and air and water and assessments of pest management alternatives.
2.1.2 CropLife Foundation (CLF)

The CLF releases national pesticide use reports every five years and there have
been three national summary reports issued dated 1992, 1997 and 2002. The pesticide use
database is not specific for any particular year. The first report was released in 1995 by
the National Center for Food and Agricultmal Policy (N CFAP) compiled from state-level
usage database that quantified the use of each active ingredient by crop and state
(Gianessi and Reigner 2006a). The report on pesticide usage was based on crop acreage
for 1992 and usage patterns for 1990-1993 and the 1995 NCFAP report is referred to as
the 1992 report; the 1997 report represents 1995-1998 usage patterns and crop acreage
data for 2007; and the 2002 report represents 2002 acreage data and use surveys from
1999 through 2004. State and crop pesticide use data from publicly available reports are
organized into a national database of pesticide use in US. crop production. The CLF use
database is a collection of usage data fiorn various sources. Gianessi and Reigner (2006b)
listed the following sources of information:

I Surveys conducted by the National Agricultural Statistics Service (NASS)

27

Reports for individual states and selected crop by USDA’s Cooperative
State Research, Education and Extension Service (CSREES) and national
pesticide benefit assessments conducted by USDA’s National Agricultural
Pesticide Impact Assessment Program (NAPIAP)

USDA Crop Profile reports

State of California Department of Pesticide Regulation Annual Reports
Assignments. In cases where usage profiles for a crop in a state were not
available fi'orn the above sources, usage estimates were assigned by
assuming that a state’s pesticide use profile for an active ingredient/crop
combination is similar to that of a nearby state. Use coefficients (% acres
treated and average annual rate) from known states were applied to the
corresponding crop acreage based upon Census of Agriculture acreage

planted figures in the unknown states.

A survey of extension service specialists for pesticide use profile information is

conducted by CLF for states and crops not covered completely by the available surveys

and reports.

2.1.3 National Agricultural Statistics Service (NASS)

The NASS publishes reports on agricultural chemical use every year, covering

selected vegetables and fruits in alternate years, starting in 1990 for vegetables and 1991
for fi'uits. Use data are fi'om surveys funded by the US. Department of Agriculture
Pesticide Data Program (U SDA-PDP). Chemical use information on targeted vegetable
and fi'uit crops fiom various states is collected by NASS to support the evaluation of food

safety and water quality issues by USDA-PDP. NASS provides online access to the

28

Agricultural Chemical Use Database from which a variety of useful information can be
obtained. This information includes acreage of commodity planted, percent acres treated,
active ingredient (a.i.)/acre/treatment/, average number of treatments, a.i./acre and total
a.i. used. The database contain vast amount of pesticide use data, but the parameters
reported are limited with only the data for the minimum, maximum and average uses
accessible. The actual data are not reported which make trend data reporting less
accurate. There are also limitations due to discontinuities in the crop coverage with time.
2.1.4 Doane AgroTrak

Doane AgroTrak provides data on agrochemical use and is the major source of
information for the US. EPA Biological and Economic Analysis Division (BEAD), but it
is not a publicly available database and can only be used internally by the subsciber.
Doane is proprietary to a purchaser at a cost of $500,000 per year (Holm 2005). The
report covers 58 crops with 40 variables in principal states and it maintains
confidentiality of the sample size to the paying clients.
2.1.5 Buckley Report

The Buckley report covers 31 crops and is also available only to clients on a
proprietary basis. It develops its surveys through 72 field/crop consultants who collect
data fiom growers, agriculture consultants, extension agents, dealers, co-op advisors and
food processors. The Buckley Report summarizes data on the state level for the following
variables: active ingredient, brand name, formulation, cost, acres treated, volume used,
target pests and the product group markets. The Buckley cotton insecticide report costs
$36,500 while the specialty crop report is $75,000. The EPA has purchased the Buckley

Report in the past but does not do so currently (Holm 2005).

29

2.2 The IR-4 Program

The IR-4 program is fimded by the USDA to develop pesticide registrations and
clearance for use on minor and specialty crops. These crops include many fi'uit, vegetable
and nut crops. Minor crops are defined by EPA as those being grown on less than
300,000 acres nationally. Approximately half the registration petitions submitted
annually to EPA originate with IR-4. Since the passage of FQPA the program has
focused most of its attention on facilitating the registration of reduced-risk and GP
replacement pesticides and since 2000, 70-80% of its studies have been on these new
compounds (IR-4 2006). However the extent to which this program has contributed to
the availability and use of these safer materials has not been evaluated.
2.3 Objectives

The objectives of this section of the study are to assess the following in the US.
since the enactment of the FQPA in 1996:

1. Changes in the use levels of selected higher risk pesticides (anticholinesterase
insecticides and B2 carcinogenic fungicides) in fi'uit, vegetable and nut
production.

2. Changes in the use of safer (reduced-risk) compounds as replacements in
these aspects of agriculture.

3. The contributions of the IR-4 program to the enhanced availability of reduced-

risk pesticides for rrrinor and specialty crop uses.

30

2.4 Methods
2.4.] Selection of Pesticides

The preliminary selection of the conventional pesticides and pesticide groups was
conducted based on human health concerns and toxicological endpoints. These groups
were the organophosphates (OPS) and N-methylcarbamates (NMCS) (anticholinesterases),
and the B2 carcinogens (Appendix A) that have been the major focus of regulatory
attention by the EPA following the passage of the FQPA. Fungicides and insecticides that
have been classified as reduced-risk were selected as well and were mostly those that
have been registered since the passage of the F QPA. These have been the primary focus
of efforts for registration for specialty crops, including many fruits, vegetable and nut
crops, by IR-4.

The selection of pesticides fi'om each group was narrowed down to those listed in
Table 2.1. The selection was based on high usage and major health concerns. The use
(pounds applied and acres treated) for these pesticides were plotted and the trends were
analyzed.
2.4.2 Pesticide Toxicity

The toxicological properties including the F QPA factor (additional safety factor)
for the CPS, NMCS, B2 carcinogens, and the reduced-risk pesticides were compiled and
shown in Appendix B. The reduced-risk pesticides and the B2 fungicides have low acute
oral toxicities but the B23 have some developmental and neurotoxicity concerns. The OPs
(except for acephate and diazinon) and the NMCS are of high acute oral toxicity.
However, there is some level of toxicity to aquatic and/or terrestrial organisms for both

the conventional and reduced-risk pesticides. Azinphos-methyl, Chlorpyrifos,

31

Table 2.1. Selected pesticides for use and residue trends analyses

 

 

 

 

 

 

 

B2 OPs NMCs Reduced-risk Reduced-risk
Carcinogens Fungicides Insecticides
l.captan 1. acephate l. aldicarb l. azoxystrobin 1. acetamiprid
2.chloro- 2. azinphos— 2. carbofuran 2. cyprodinil 2. bifenazate

thalonil methyl 3. carbaryl 3. fenhexamid 3. buprofezin
3.iprodione 3. chlorpy- 4. methomyl 4. fludioxonil 4. imida-
4.mancozeb rifos 5. oxamyl 5. mefenoxam cloprid
5.maneb 4. diazinon 6. trifloxy— 5. indoxacarb
5. dimethoate strobin 6. methoxy-
6. disulfoton fenozide
7. fenamiphos 7. pymet—
8. fonofos rozine
9. methamid- 8. pyriproxi-
ophos fen
10. methida- 9. spinosad
thion 10. tebufen-
ll. methyl ozide
parathion ll. thiameth—
oxam

 

disulfoton and methamidophos have been reported to cause worker exposure concerns.

The FQPA factors used for the reassessment of the pesticides ranged fi'om 1X to 5X

except for methyl parathion and Chlorpyrifos with 10X. Some of the pesticides are

included in the Endocrine Disruptor Screening Program (EDSP) draft list which “presents

the draft list of the first group of chemicals that will be screened for the EPA’s EDSP”

(U .S.EPA 2007c). These pesticides include B23 (captan, cholorothalonil and iprodione),

the OPS (acephate, azinphos-methyl, Chlorpyrifos, diazinon, dimethoate, disulfoton,

methamidophos, methidathion, methyl parathion) and the NMCS (aldicarb, carbaryl,

carbofirran, methomyl and oxamyl), and the reduced-risk insecticide imidacloprid. Based

on the toxicological properties of the various pesticides, the reduced-risk pesticides have

significantly fewer toxicity concerns, either acute or chronic, compared to the

conventional pesticides.

32

 

The organophosphate (OP) group was the EPA’s first priority group reviewed
under the Food Quality Protection Act (U .S.EPA 2007b). The OPs are of great concern
due to their potential neurotoxicity caused by the inhibition of cholinesterase in both the
central and peripheral nervous systems (Mileson et al., 1998 cited by (U .S.EPA 2006d)).
The toxicological properties of the individual OP pesticides are shown in Appendix B.

The N-methylcarbamate (NMC) pesticides are also cholinesterase inhibitors, but
are classified as a separate group from the CPS. The NMCS were concluded to have a
common mechanism of toxicity in 2001 by the US. EPA. The Common Mechanism
Group (CMG) was established “based on the shared structural characteristics and
similarity and their shared ability to inhibit acetylcholinesterase (AChE)” (U .S.EPA
2005a). In 2004 the EPA assigned ten carbamate pesticides as members of the
Cumulative Assessment Group (CAG) that included aldicarb, carbaryl, carbofirran,
oxamyl and methomyl. Appendix B shows the toxicological properties of these
pesticides.

Carcinogenic chemicals have been classified in several different ways by EPA.
The 1986 classification consisted of the following categories (U .S.EPA 2007a):

I Category A: Human carcinogen

I Category B: Probable human carcinogen

- Bl: agents for which there is limited evidence of carcinogenicity
from epidemiologic studies

- B2: agents for which there is sufficient evidence from animal
studies and for which there is inadequate evidence or no data fiom

epidemiologic studies

33

I Group C: Possible human carcinogen
I Group D: Not classifiable as to human carcinogenicity
I Group E: Evidence of non-carcinogenicity for humans
In 1996 the “Proposed Guidelines for Carcinogenic Risk Assessment” was released by
the EPA and provided the following revision of the carcinogenicity classification
(U .S.EPA 2007a):
I Known/Likely: available tumor data effects and other key data are adequate to
convincingly demonstrate carcinogenic potentials for humans.
I Cannot be determined: data are not adequate to convincingly demonstrate
carcinogenic potentials for humans.
I Not likely: no basis for human hazard concern
The most recent carcinogenic classification of chemicals is fiom the 2005 Guidelines for
Carcinogen Risk Assessment. They are referred to as descriptors and consist of the
following categories (U.S.EPA 2007a):
I Carcinogenic to humans
I Likely to be carcinogenic to humans
I Suggestive of evidence of carcinogenic potential
I Inadequate information to assess carcinogenic potential
I Not likely to be carcinogenic to humans
I Multiple descriptors: more than one descriptor can be used when an agent’s
effects differ by dose or exposure route.
In this study, the carcinogenic fimgicides considered were based on the 1986

classification and thus are referred to as the BZ carcinogens or the B25 (agents for which

34

there is sufficient evidence from animal studies and for which there is inadequate
evidence or no data from epidemiologic studies). These ftmgicides include captan,
chlorothalonil, iprodione, mancozeb and maneb and the toxicological properties are
shown in Appendix B.

Captan is a member of the N-trihalomethylthio group of compounds and
metabolizes to the highly reactive species thiophosgene that causes much of its observed
toxicity (U .S.EPA 199%). The irritant properties of captan can be attributed to
thiophosgene and “may be responsible for the intestinal tumors in mice, although the
exact mode if action is unclear”. The US. EPA has established dietary, occupational and
residential acute and chronic toxicological endpoints for captan.

Chlorothalonil has been classified by the EPA as “likely” to be a human
carcinogen. It contains an impurity, hexacholorbenzene (HCB), which has also been
classified by the EPA as B2 carcinogen based on data that show significant increases in
tumor incidences in hamsters and rats (U .S.EPA l999d). The acute and chronic NOEL
and the Rfl) were established for chlorothalonil and HCB.

Iprodione was classified as a B2 carcinogen by EPA based on evidence of tumors
in both sexes of mice (liver) and in the male rat (Leydig cell). A No Observed Effect
Level (NOEL) and Reference Dose (RflD) were established based on combined chronic
toxicity and carcinogenicity in rats. Iprodione is also associated with endocrine disruption
according to the EPA but “the extent of these effects and the mode of action are not yet
fully understood” (U .S.EPA 1998c). Neurodevelopmental studies are also lacking for this

compound.

35

Mancozeb, a dithiocarbamate firngicide, targets the thyroid organ through its
metabolite, ethylenethiourea (BTU). Thyroid toxicity was manifested as alterations in
thyroid hormones, increased thyroid weight, and microscopic thyroid lesions and thyroid
tumors (U .S.EPA 2005b). Neurotoxicity is also a concern for mancozeb exposure due to
the developmental effects observed after dosing with mancozeb or ETU. The No
Observed Adverse Effect Levels (N OAELs) and the Lowest Observed Adverse Effect
Levels (LOAELs) have been established for mancozeb to address these concerns. There
have also been concerns regarding endocrine effects of mancozeb based on available
human health and ecological effects data according to the EPA (U .S.EPA 2005b).

The carcinogenic potential of the related dithiocarbamate fungicide, maneb, is
also considered to be due to its B2 carcinogen metabolite, ETU. The cancer risk of maneb
has been assessed “by estimating exposure to maneb—derived ETU and using the ETU
potency factor” and in 1999 the EPA concluded that cancer risk for maneb and the other
EBDC fungicides should continue to be evaluated this way (U .S.EPA 20050). Maneb
also showed possible thyroid effects which may “indicate potential endocrine disruption”
based on ecological and human health effects data (U .S.EPA 2005c).

2.4.3 Survey and Evaluation of Pesticide Use Databases

The pesticide use databases were surveyed and evaluated for comprehensiveness
and continuity of data from 1992 to 2006. The databases evaluated were the CA-DPR, the
NASS and the CLF. Doane AgroTrak and the Buckley Report were also considered but
their expensive purchase cost was the limiting factor preventing their use. The CA-DPR
has the most complete and comprehensive use data and reports and the CLF database has

a nationwide coverage of pesticide use and thus both were selected as the main sources of

36

use data for trend analysis. The NASS database does not have the actual usage data
publicly available (i.e. only the minimum, maximum and average data are reported) and
these are not accurate to use in trend analysis.
2.4.4 Pesticide Groups Use Trend Analysis

The overall use trends for conventional pesticide groups (OPS, NMCS, and B2
carcinogens) were compared based on the cumulative acres treated and pounds applied
for fruits, vegetables and nut crops. The total acres treated and pounds applied, and
percent change in use were calculated and compared for the years 1994 and 2006 based
on the CA-DPR data and for 1992 and 2002 based on the CLF data.
2.4.5 Individual Pesticide Use Trend Analysis

The total pounds applied and total acres treated data fiom 1992 to 2006 for fi'uits,
vegetables and nut crops for the individual OP, NMC, and BZ carcinogenic pesticides
were compiled from the CA-DPR and the CLF pesticide use databases. The reduced-risk
pesticides were classified as to low, medium or high use (acres treated) based on the 2006
CA-DPR data. Changes in use trends were analyzed and were correlated with the
regulatory history of the pesticides. The reason for the changes in use was assessed based
on the regulatory history and the expert opinion of people knowledgeable in the pesticide
selected.
2.4.6 Environmental Load and Application Rate

The environmental load (lbs/acre) was calculated fi'orn the ratio of the total
pounds applied and the total acres treated. The application rate is the ratio of the total

pounds of the pesticides applied and the total number of applications per year. Both were

37

calculated for the insecticides (OPS, NMCS and reduced-risk) and the fungicides (B23 and

reduced-risk) based on the CA-DPR pesticide use data from 1992 to 2006.

38

2.5 Results and Discussion
2.5.1 Pesticide Groups

The percent change in acres treated and pounds applied of the B2, OP and NMC
pesticide groups based on the CA-DPR (California) and the CLF (national) data are
shown in Table 2.2. The two databases provide reasonably similar results. The NMCS had
the most significant decrease in use (74% (CA-DPR) and 72% (CLF) in pounds applied
and 60% (CA-DPR) and 65% (CLF) in acres treated), but a considerable decrease in
acreage and application amounts of the CPS was also evident. The B2 frmgicides showed
much less change with 21% and 11% decreases in pounds applied. The CA-DPR data
Show a decrease of 17% in acres treated for this group, but the acreage treated with B25
increased by 29% based on the CLF data. This is not necessarily surprising since the two
databases differ in geographical range and in the timeframes for data collection. Concerns
about the neurotoxic effects of the NMCS have led to several reassessments and
additional risk assessments of these compounds and were included in the carbamate
cumulative risk assessment. According to the CA-DPR the pounds of carbamates applied
“continued to decline as they have for nearly every year since 1995” (CA-DPR 2005).

Table 2.2. Percent change in the use of the B2 carcinogen, OP and NMC pesticide
groups

 

 

 

 

 

 

 

 

Percent change
Pesticide CA—DPR (1994-2006) CLF(1992—2002)
Groups Pounds Acres Pounds Acres
applied treated applied treated
Oganophosphate -47.6 -46.9 -57.4 -76.9
N-methylcarbamate -74.0 -60.1 -71.5 -65.0
B2 Carcincfin -21.2 -17.1 -1 1.2 29.3

 

 

 

 

 

The use of the OPS decreased by 48% in pounds applied and 47% in acres treated

based on the CA-DPR data while the CLF data showed 57% and 77% decline in pounds

39

applied and in acres treated, respectively. This is due to the major regulatory changes

brought about by the enactment of the F QPA that required reassessments of old

pesticides and additional requirements for aggregate and cumulative risk assessments.

Worker exposure and occupational concerns were also major contributing factors to the

decline in use of the OPS. Although regulatory activity has been a primary reason for

decreased use of the anticholinesterases and increased use of the reduced-risk pesticides,

pesticide use decisions are complex and additional reasons for this switch in individual

situations could be because:

some older pesticides were discontinued because of business decisions by
the chemical pesticide industry

there were changes in cropping systems and pest pressures

some older pesticides became less competitive because of the improved
properties and convenience of replacement compounds e. g. improved
systemic properties and increased use as seed treatments rather than foliar
sprays, as well as greater compatibility with pest management programs
some older pesticides became less effective as the target pests developed
resistance

the alternating use of different pesticide classes has increased as a

resistance management strategy

Trends in use of the CPS, NMCS, and the reduced-risk insecticide groups are

shown in Figure 2.1. Based on the CA-DPR data, there is an apparent continuously

increasing trend in both acres treated and pounds applied with the reduced-risk

insecticides while the CPS and the NMCS declined quite regularly from 1996 to 2006.

40

The reduced-risk insecticides acres treated started to exceed that of the NMCS in 1997
and the OPS in 2002 and the pounds applied almost equaled that of the NMCS in 2006.
The trend in acres treated and pounds applied with the B2 firngicides is not as clear as for
the insecticides (Figure 2.2). The acres treated increased fi'om ~lM in 1992 to ~3.5M in
2000 but then declined to a constant level fiom 2001 with ~1.7 M in 2006. The increase
in the acres treated (~3.6M) for the B23 in 2000 is mostly fi'om iprodione. The pounds
applied increased fiom ~1M in 1992 to ~5M in 1998 but declined to ~2.5M in 2006. On
the other hand, the use of the reduced-risk fungicides continuously increased fi'om <0.5M
acres in 1997 to ~1.5M acres in 2006 and almost equaled the acres treated with the B23.

The pounds applied increased from ~50,000 pounds in 1992 to ~350,000 pounds in 2006.

 

 

Anticholinesterase and RR Insecticide Groups Use Trend

 

 

 

 

 

 

 

 

 

 

 

 

 

4,000,000
3,000,000 -
2,000,000
1,000,000
if“; L, "‘5‘"?
0 . W . . .
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
—+—OPs (lbs) - e - OPS (acres)
+ Carbamates (lbs) - as - Carbamates (acres)
—e— RR Insecticides (lbs) - <3 — RR Insecticides (acres)

 

 

 

 

 

 

Figure 2.1. Acreage treated and pounds applied of the OPS, NMCs and reduced-
risk insecticide groups.

41

 

32 and RR Fungicide Groups Use Trend

 

 

5,000,000
4.000.000
3,000,000 , ,
2,000,000 f “ ” " #7 7 ’ ,
' "i r’w 7” :; P:;;}£'}i; R
1,000,000 ” "
0 a~ a ~ 1"}: ”*9?
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
823 (lbs) — c: — 323 (acres)
—I—- RR Fungicides (Ibs) - E — RR Fungicides (acres)

 

 

 

 

Figure 2.2. Acreage treated and pounds applied of the B2 carcinogenic and the
reduced-risk fungicide groups.

A regular increase in the use of reduced-risk pesticides from their first use in 1995
to 1.7 million pounds in 2005 is also evident fi'om a summary graph for all reduced-risk
compounds and uses combined that was developed by CA-DPR (CA-DPR 2006).
Similarly, summary data documenting the continued decline in total anticholinesterase
insecticide use, with an overall decrease of about 50% from 1994 through 2006, were
recently provided by CA-DPR (CA-DPR 2007a).

2.5.2 Individual Pesticides

2.5.2.1 BZ Carcinogenic Fungicides

Iprodione

Iprodione was first registered as a fungicide in the US. in 1979 with major uses
on agricultural crops, omamentals, turfgrass and for residential ornamental applications.
In 1998 the use of iprodione for postharvest pathogen control on Stone fruits was
cancelled (Adaskaveg et al. 2005), preharvest uses were restricted, and the removal of all

42

residential uses followed due to cancer and occupational risk concerns (U .S.EPA 1998d).
Figure 2.3 shows the trend in the CA-DPR and the CLF use data for iprodione. Among
the B23 considered in this study, the CLF use data are greater than that of the CA-DPR
except for iprodione. This implies that most of the agricultural uses of iprodione could
have come from California. However, the CA-DPR data Show an unexpected peak of
increased acres treated for iprodione in 2000 due mostly to uses on nectarines (~500,000
acres), peaches (~550,000 acres) and plums (~500,000 acres). Apart fiom this peak, after

the 1998 use restrictions, use fell by about 50%.

 

 

 

 

 

 

 

 

 

 

Iprodione
2,500,000
2,000,000 f\
1,500,000 / X
1,000,000
a I
500,000 - L
0 I I I I I I I T
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied + CLF Acres treated

 

 

 

 

 

 

Figure 2.3. Use of iprodione based on the CA-DPR and the CLF data.

Mancozeb

Mancozeb was first registered in 1948 for use on food and ornamental crops to
prevent harvested crops fiom deterioration in storage and transport (U .S.EPA 2005b).
Other uses include seed treatments and horticultural applications. Registration standards
were issued in April 1987 but a Special Review of mancozeb and other

ethylenebisdithiocarbarnates (EBDCS) identified the pesticide group and its metabolite as
43

a developmental toxicant and a probable human carcinogen. The EPA canceled all uses
of mancozeb and other EBDC products on several crops including nectarines, peaches,
and spinach in 1992 because “the dietary risks of EBDCS exceeded the benefits for the
canceled food/feed uses” (U .S.EPA 2005b). Requirements for personal protective
equipment for workers using EBDCS were also established by the EPA. The CLF and the
CA-DPR data Show similar use trends for mancozeb (Figure 2.4). Based on the CA-
DPR data there has been relatively constant pounds applied and acres heated fiom
1994 to 1997 but this has been variable and has decreased since then. There were
significant increases in 1998 and 2006. Increased acres treated and pounds applied in
1998 were due to the increased use on grapes (~138K lbs), onions (>100K lbs) and

potatoes (>100K lbs) and in 2006 the major increased uses were on onions and on grapes.

 

 

 

 

 

Mancozeb
10,000,000 800.000
' A L 700,000
8.000.000 . Z \ 0 . 600000
. 500,000

 

 

 

 

 

 

 

6,000,000
'51 NM / _ 400,000 9
4,000,000 ‘ . 300000 ‘5
N W . s
I r 200,000
2,000,000 - K
' L 100,000
0 r r T r T r r T 0
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.4.Use of mancozeb based on the CA-DPR and the CLF data.

Maneb

Maneb was first registered in the U.S. in 1962 for food and ornamental crop uses
and belongs to the EBDC pesticide group. In 1987 the EPA expressed health concerns for
its metabolite, ethylenethiourea (BTU), including carcinogenic, developmental, and
thyroid effects. In 1992, the EPA cancelled various maneb uses when the EPA
“concluded that the dietary risks of EBDCS exceed the benefits” for some feed/food uses
(U.S.EPA 2005c). In 2005, the EPA (U.S.EPA 2005c) reported that uses of maneb on
sweet corn, grapes, apples and fig were not eligible for reregistration and these were
voluntarily canceled by the registrants. National use (Figure 2.5) data Show an overall

decline in the use of maneb but the CA-DPR data does not Show any significant decrease.

 

_— .a

 

 

 

 

 

 

 

 

 

 

Maneb
4.000.000 1,800,000
0 r 1,600,000
3,000,000 A A l’ig'é’fi
“- 4
6 2000000 NV\ M “1'°°°'°°° 5,3
' ' Pf - 800,000 ,0,
- 600,000 ’°
1,000,000 a a _ - 400,000
I - 200,000
0 I r I I I I I I O
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied —-m— CLF Acres treated

 

 

+CA—DPR Tot lbs applied —x—-CA-DPR Tot acres treated

 

 

 

 

Figure 2.5.Use of maneb based on the CLF and the CA-DPR data.

Captan
In 1951, captan was first registered for the control of fungal diseases in fi'uit

crops. It is registered for use on terrestrial and greenhouse food crops, seed treatments

45

and ornamental sites as well as non-food indoor uses but various uses of captan were
cancelled and several tolerances were revoked in 1993 and 1999. The Reregistration
Eligibility Decision (RED) for captan was issued in 1999 and it retained its previous
classification as a B2 carcinogen (U .S.EPA 2004a). In 2004, a re-evaluation of the cancer
risk assessment for captan was requested by the Captan Task Force and it was concluded
that captan is not “likely to be a human carcinogen nor pose cancer risks of concern when
used in accordance with approved product labels” (U .S.EPA 2004a) based on the weight-
of-evidence approach. However, as a compound with a probable threshold for
carcinogenic action, it is likely to cause cancer in humans following prolonged, high
level-oral exposures (Wilkinson et al. 2004). No significant change in the overall use
trend of captan is evident based on the CA-DPR and the CLF data (Appendix C) but there
was a noticeable increase in pounds applied in 1998 based on the CA-DPR data due to
high usage on almonds (~1.1M lbs) in that year. The cancer reclassification of captan is a
probable explanation for the continued use of captan as well as its low susceptibility to
resistance due to its multiple modes of action and broad spectrum control of fungi, and its
low cost.

Chlorothalonil

Chlorothalonil was first registered for food use on potatoes in 1970 and is used
mainly on food crops and for outdoor residential applications. In 1987, the EPA classified
chlorothalonil as a B2 carcinogen. It contains an impurity, hexachlorobenzene (HCB) that
is also classified as a B2 carcinogen based on data that Show significant increases in
tumor incidences in hamsters and rats (U .S.EPA l999d). In 1997, evaluation of the

weight-of-evidence was conducted by the EPA with reference to the carcinogenic

46

potential of chlorothalonil and supported a classification of chlorothalonil as ‘likely’ to be
a human carcinogen by all routes of exposure (U .S.EPA 1999d). Tolerances have been
established for combined residues of chlorothalonil and its impurity. Acute and chronic
NOELS and Rfl)s have also been set for chlorothalonil, HCB and its metabolite. The use
of chlorothalonil has been comparatively constant with a slow decline Since 1997 as
shown in Appendix C. The decline may be attributed to its continued classification as a
B2 carcinogen even after its reevaluation but clorothalonil too has advantages of cost,
low resistance potential and broad spectrum efficacy that help to maintain its use.

2.5.2.2 N-methylcarbamates

Aldicarb

The first use of aldicarb was registered in 1970 and is currently registered for use
on many agricultural crops. In 1981 aldicarb was classified as a restricted use pesticide
and subjected to Special Review in 1984. The sale and use of aldicarb on potatoes was
voluntarily suspended in 1990 due to detection of tolerance-exceeding residues in
individual potatoes (Angier et al. 2006). Consequently, the registrant agreed to cancel
other uses to reduce dietary risks but these were later reinstated in Florida, Idaho,
Washington and Oregon after new application methods demonstrated significantly lower
residues in potatoes (U .S.EPA 2007f). However, the EPA (2007f) still has aldicarb under
the Special Review process “because of risks of ground water contamination”. Aldicarb
shows a decreasing trend in use from 1992 to 2006 as shown in Figure 2.6. Total pounds
applied decreased by 66% based on the CLF data (1992-2002) and 91% based on the CA-
DPR data between 1994 and 2006. Aldicarb has a very high acute toxicity and a record of

causing human poisoning, and the EPA noted that there are “human health risks of

47

concern associated with the current registered uses of aldicarb from drinking water
exposure, and potential environmental risks of concern to birds, mammals and fish”
(U.S.EPA 2007f) which account for the decline in the use of aldicarb. In 2007 the EPA
determined that products containing aldicarb “unless labeled and used as specified (in the

aldicarb reregistration eligibility document), would present risks inconsistent with FIFRA

 

 

 

 

 

 

 

 

 

and FFDCA” (U.S.EPA 20071).
Aldicarb
2,000,000 . 25,000
1,600,000 . 20,000
1,200,000 VXK 15,0009
5 6:
° 800,000 VA 10,0003
400,000 W 5,000
0 , , , , , , , , -
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied + CLF Acres treated
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.6.Use of aldicarb based on the CA-DPR and the CLF data.

Carbaryl

Carbaryl was first registered in 1959 for use on cotton but its applications have
increased to include many food uses. Its use came under scrutiny in the 19803 when
health risks became a concern. In 1988, the Registration Standard issued in 1984 was
revised and included terms and conditions for its continued registration (U .S.EPA
2003b). In 2001, the EPA identified a common mechanism of toxicity for the N-
methylcarbarnates (NMCS) that included carbaryl. The Interim Reregistration Eligibility

Decision (IRED) for carbaryl was released in 2003 which addressed potential health and
48

ecological risks and included rate reductions and revocations of tolerances for several
uses including stone fi'uits and citrus (U .S.EPA 2003b, 2007g). Data Call-Ins were issued
by the EPA in 2005 that required submission of more data on toxicology, worker
exposure monitoring and environmental fate for carbaryl. This resulted in voluntary
cancellations of the products by many of the registrants. According to the EPA
“approximately 80% of all of the carbaryl end-use products registered at the time of the
2003 [RED have since been canceled through this process or other voluntary
cancellations” (U .S.EPA 2008a). Carbaryl shows an overall decline in use trend as Shown
in Figure 2.7 except for a spike in 1995 when the elevated use was due to increased use
of carbaryl on oranges based on the CA-DPR data. These use trends clearly correspond to

the regulation of the use of carbaryl.

Carbaryl

 

 

 

 

 

 

 

 

 

 

 

 

 

 

3,500,000 1,600,000
3,000,000 1.400.000
2.500,000 L 1,200,000
— 1,000,000
1.1. 2,000,000
5| ~ 800,000 9
1,500,000 _ 600,000 .0
‘0
1,000,000 r- 400’000 a
500,000 — 200,000
- L 0
1992 1994 1996 1998 2000 2002 2004 2006
Year
-O-CLF lbs applied '-I-—CLF Acres treated
+CA—DPR Tot lbs applied —x—CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.7.Use of carbaryl based on the CA—DPR and the CLF data.

49

Carbofuran

Carbofuran was first registered in the U.S. in 1969 to control soil and foliar pest
on different field, fruit and vegetable crops. In the 19903, changes were made in the
labels of carbofuran (e.g. reduced application rates) by the registrants due to ecological
and drinking water risks. Since 1994 the sales of granular carbofuran were limited to
2,500 lbs per year in the U.S., for use only on certain crops (U.S.EPA 2006b). Based on
the ecological and human health risk assessments related to carbofuran uses, the EPA
“had determined that all uses of carbofirran do not meet the standard for continued
registration under FIFRA” (U.S.EPA 2006b). In keeping with this regulatory activity,
Figure 2.8 shows use trends from the CLF where the pounds applied decreased by 81%
from about 3.3M pounds in 1992 to 625,000 pounds 2002, and from the CA-DPR

database showing a 93% decline from 96,000 pounds in 1994 to only 6,700 pounds in

 

 

 

 

 

 

 

 

2006.
Carbofuran
4,000,000
~ 100,000
3,000,000 " ‘ — 80,000
: 2.000.000 H 8 - 60.0005;
u o
L 40,000;
1,000,000 1“ 3’
- 20,000
0 I I 1 I T T I I o
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied -x--CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.8.Use of carbofuran based on the CA-DPR and CLF data.

50

Methomyl

Methomyl was first used as an insecticide in commercial plantings of
chrysanthemurns and was registered by E. I. Dupont de Nemours and Co. in 1968. Its
current registered uses include agricultural, industrial and commercial applications. In
1978 it was classified as restricted use pesticide, and a registration standard, modified
tolerances and labels were issued in 1989. Greenhouse and ornamental uses were
voluntarily cancelled in 1998. The EPA maintained the restricted use classification based
on its acute toxicity and use patterns (U.S.EPA 19981). Between 1994 and 2006, the
pounds of methomyl applied decreased by 75% and acres treated by 71% based on the
CLF data; and by 55% and 49% in pounds applied and acres treated, respectively, based
on the CA-DPR data (Figme 2.9). A significant decrease in the use of methomyl is
evident after the enactment of the F QPA as a result of the voluntary cancellations and its

classification as a restricted use compound.

 

 

 

 

 

 

 

 

 

 

 

 

Methomyl
2,500,000
2,000,000 3
I
1,500,000 .
1,000,000
0 r I I I T If I F
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied +CLF Acres treated

 

 

 

 

 

 

Figure 2.9.Use of methomyl based on the CA-DPR and CLF data.

51

Oxamyl

E.I. DuPont de Nemours, Inc. first used oxamyl on omamentals, tobacco, and on
non-bearing fruit in 1974 and more uses have been added since then (U .S.EPA 2000d).
Oxamyl is registered for use on terrestrial food and feed crops. The first Registration
Standard was issued in 1987 and was updated in 1991. In 2002, the EPA revoked several
oxamyl uses because they were no longer considered as feed items (U .S.EPA 2002a). The
EPA concluded that minimal risks were associated with oxamyl except for dietary intake
by children 1-6 years old which EPA believed was “due to an overestimation of exposure
and consequently risk because of the rapid reversibility of oxamyl induced cholinesterase
inhibition was not accounted for” (U .S.EPA 2000d). The use of oxamyl shows a
moderate overall decreasing trend as shown in Appendix C. However, the CLF data
shows an increase in pounds applied in 2002 compared to 1992. Based on the CA-DPR
data, usage decreased by 43% in pounds applied and 56% in acres treated from 1994
compared to 2006. The USDA reports that growers are using lower rates (0.46 to 0.62 lb
ai/A) and applying the pesticide less frequently (about twice per year compared with the
allowable 12 times) (U .S.EPA 2000d).

2.5.2.3 Orgammhosphates

Azinphos-methyl (AZM)

Azinphos-methyl was first registered as an insecticide in the U.S. in 1959. The
major uses of AZM include applications on fruits and vegetables and on nursery plants.
The Worker Risk Strategy, 8 process which looked at over 80 chemicals that had any
reported worker incidents in California was initiated by the EPA in 1992 and AZM was

ranked 5"I among the 28 chemicals required for the development of additional incident

52

data. In 1993 the use of AZM on sugarcane was limited to prescriptive use only in
Louisiana and required prior approval of the state for all applications due to large fish
kills (U.S.EPA 2001b). This use was subsequently cancelled voluntarily by all AZM
registrants in 1999. In 1998, the California Department of Pesticide Regulation (CA-
DPR) and the EPA took actions to protect agricultural workers. The CA-DPR issued a
120-day emergency regulation to protect workers exposed to AZM use on grapes and on
most tree crops. The EPA took this action to the national level and worked with the CA-
DPR to establish interim mitigation measures that were firlly implemented for the 1999
growing season. Further, the EPA granted use cancellations requested by the registrants
of AZM (U .S.EPA 2000b) and in 2000, the EPA revoked and modified some tolerances
for AZM in and on various crops (U .S.EPA 2000a). More cancellations of AZM uses
were implemented in 2005 and in November 2006, the EPA issued a final decision to
phase out all remaining uses of AZM by September 30, 2012 (U.S.EPA 2006a). The use
of AZM follows this regulatory activity closely and has continuously declined fiom 1996
to 2006 as shown in Figure 2.10. The CLF data show about a 47% decrease in pounds
applied and 50% in acres treated while there is a 91% decrease for both based on the CA-

DPR data.

53

 

 

 

 

 

 

 

 

 

 

Azinphos-methyl
500.000
~ 400.000
- 300,000 n
P
. 200,000 a
w
r 100,000
0 I I I I I I I T o
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied + CLF Acres treated
+CA-DPR Tot lbs applied —x—CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.10.Use of azinphos-methyl based on the CA-DPR and the CLF data.

Chlorpyrifos

Chlorpyrifos was first registered in 1965 for use on foliage and soil-home insect
pests on food and feed crops. In 1996 tolerances were revised for residues of chlorpyrifos
in or on several raw agricultural commodities by establishing time-limited tolerances as
permanent tolerances (U .S.EPA 1996a). Various indoor uses of chlorpyrifos were
eliminated in 1997 to reduce indoor exposure of children and other sensitive groups. In
2000, nearly all residential uses were phased out following an agreement between the
registrants and the EPA (U .S.EPA 2002d). In July 2002 several tolerances for
chlorpyrifos were revoked because they were no longer needed or were associated with
food uses that were no longer registered in the U.S. (U.S.EPA 2002a). Figure 2.11 shows
the decline in the use of chlorpyrifos over time based on the CLF data. This amounted to
56% fewer pounds applied and 88% fewer acres treated, which was probably due to the
preliminary risk assessment by the EPA that “showed acute dietary risks from food

exceeded the acute population adjusted dose (aPAD) for infants, all children, and nursing
54

females of child-bearing age (13-50 years old) (U .S.EPA 2002d). The EPA also recorded
the registrants’ agreement to eliminate use on tomatoes and restrict use on apples to
address excessive risks. On the other hand, the CA-DPR data Show a different pattern
where use decreased from 1997 to 2003 but has increased again Since then. This is
primarily due to a large increase in use on almonds but increased use on walnuts and

oranges also contributed to this late rise.

 

 

 

 

 

 

 

 

 

Chlorpyrifos
16,000,000 1,600,000
12,000,000 fiflkf 1.200.000
0
I A g
5 8,000,000 I i ”\‘x 800,000 6::
4,000,000 1 400,000
I
o T T I I I I I I 0
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.11.Use of chlorpyrifos based on the CA-DPR and CLF data.

Diazinon

Diazinon was first registered in the U.S. in 1956 as an insecticide, acaricide and
nematicide for fi'uits, vegetables, and forage and feed crops. In 2001 EPA approved
requested product cancellations and amendments to terminate all indoor uses after
negotiations with the technical registrants due to the findings of the EPA that diazinon, as
currently registered, was an exposure risk, especially to children (U .S.EPA 2001a). Other
agricultural uses were also cancelled in 2001 except for spinach, strawberries and

tomatoes due to a nationwide need for the application of diazinon on these crops

55

(U .S.EPA 2001a). More cancellations of agricultural uses followed fiom 2001 to 2003.
The EPA’s Interim Reregistration Eligibility Decision (IRED) human health risk
assessment for diazinon in 2004 indicated residential and occupational risk concerns but,
acute and chronic food risks were below the level of concern (U .S.EPA 2004c).
Generally, diazinon shows a moderate but regular decreasing use trend since 1994
(Figure 2.12) based on the CA-DPR data. The CLF data showed the same trend from

1992 to 1997 but with a slight increase in pounds applied in 2002.

2_ ,,_A, H. H ._h Eh __ -_. _- i i a_ _1

 

 

 

 

 

 

 

 

 

 

 

1,200,000
1,000,000
800,000
600,000 -
400,000
200,000
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied -x—CA-DPR Tot acres treated
—e—cu= lbs applied —- CLF Acres treated

 

 

 

 

 

 

Figure 2.12.Use of diazinon based on the CA—DPR and the CLF data.

Dimethoate

Dirnethoate was first registered and used in the U.S. in 1962. It has been used on
both food and non-food products as well as in a variety of non-agricultural applications.
In 2000 all non-agricultural and residential uses of dimethoate were cancelled (U .S.EPA
2006c) and more use cancellations on various crops followed in 2004 (U .S.EPA 2004b).

Further uses were cancelled in 2005 including those on seven crops (apples, broccoli

56

raab, cabbage, collards, grapes, head lettuce, and spinach) that were identified as
significant dietary risk contributors along with four crops for which there were no field
trial data to support tolerances (fennel, lespedeza, tomatillo, and trefoil) (U.S.EPA
2006c). Since its peak in the early 19903, it appears that the use of dimethoate has
declined regularly with an overall decline of greater than 50% by 2006 based on both

databases (Figure 2.13).

 

 

1,600,000 Dimethoate 800,000

1,200,000 {A 600,000
800,000 MXPW 400,000
400,000

W 200,000

 

 

 

 

 

 

 

 

O I I I T l I I i T o
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

+CLF lbs applied +CLF Acres treated

+CA-DPR Tot lbs applied -x—CA-DPR Tot acres treated
Figure 2.13. Use of dimethoate based on the CA-DPR and the CLF data.

 

 

 

 

 

 

Disulfoton

The initial registration of disulfoton as an insecticide occurred in 1961. It is used
on food, feed and non-food crops and in residential applications as well. During the
reregistration process several changes to disulfoton registrations were proposed by Bayer
Corporation, the technical registrant of disulfoton, that were later accepted by the EPA as
interim risk mitigation measures (U .S.EPA 2002c). In 2002, Bayer “elected to voluntarily
cancel certain product and/or delete product uses fi'om their product labels rather than

develop the data necessary to support reregistration” (U .S.EPA 2002c). Other changes

57

included application rate reductions and voluntary cancellations and deletions of uses no
longer supported by Bayer. The use of disulfoton significantly decreased as shown in
Figure 2.14 from 757,000 lbs in 1992 to 111,000 lbs (85%) in 2002, based on the CLF

data, and flour 114,000 lbs in 1994 to 19,000 lbs in 2006 (83%) based on the CA-DPR

 

 

 

 

 

 

 

 

data.
Disulfoton
800.000 . 200,000
600,000 L 150,000
\ . Q
5, 400,000 a 100,000 a
U B
200,000 50,000
0 I I I I I I I I 0
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied -I~— CLF Acres treated
+CA-DPR Tot lbs applied ->(-CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.14.Use of disulfoton based on the CA-DPR and CLF data.

F onofos

Staufi‘er Chemical Company developed and initially marketed fonofos in 1967.
F onofos was used on fi'uit and vegetable crops as a soil insecticide. Environmental risk
assessment revealed a very high toxicity of fonofos to birds and to fi'eshwater and salt
water organisms according to the EPA (U .S.EPA 199%). In December 1997 Zeneca Ag
Products requested voluntarily cancellations of fonofos registrations and all other
remaining fonofos products were cancelled by November 2, 1998 (U .S.EPA 1999b). This
accounts for the 100% decline in the use of fonofos from 1992 to 2004 as Shown in

Figure 2.15.
58

 

Fonofos
8,000,000 50,000

 

6,000,000 ” 40900

,u- m ,, 30'm0
5 4,000,000 ‘
O )\\/\ . 20,000
2,000,000 r

”XE r10,000
0 u I I . I I ‘0

1990 1992 1994 1996 1998 2000 2002 2004 2006

Year
+CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied —x—CA-DPR Tot acres treated

 

 

HdG'VD

 

 

 

 

 

 

 

 

 

 

 

Figure 2.15.Use of fonofos based on the CA-DPR and CLF data.

Methamidophos

Methamidophos was first registered in the U.S. in 1972 to control a broad
spectrum of insects on potatoes, cotton and cole crops. The EPA reported risks to
agriculttual workers resulting from exposure to methamidophos. According to the EPA,
the risks to workers of acute exposure exceeded the EPA’s level of concern and
California human incident data showed acute worker exposure incidents associated with
methamidophos use (U .S.EPA 1997c). Bayer Corporation, the technical registrant of
methamidophos, voluntarily cancelled all uses in 1997 except for use on cotton, potatoes,
tomatoes and alfalfa. In December 1999 the registrant had also voluntarily phased-in
closed mixing and loading systems for all remaining uses to address potential worker
exposures (U.S.EPA 2002g). Figure 2.16 shows the continuous decline in the use of
methamidophos since 1994. The CLF data Show that total pounds used has declined

fi'om 800,000 lbs in 1992 to only 287,000 lbs in 2002 (64%) while CA-DPR Shows a

59

99% decrease from 154,000 lbs in 1994 to 1,700 lbs in 2006. This continuous decline in

use is attributable to the cancellations of most of the uses of methamidophos.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

r -_ - _ - .1 , ,
Methamidophos
1,000,000
:5 600,000 I Q
U '0
400,000 3
200,000
0 I I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
—e—CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied —x—CA-DPR Tot acres treated

 

 

 

 

 

 

Figure 2.16.Use of methamidophos based on the CA—DPR and CLF data.

Methyl parathion

Methyl parathion was first used in 1954 as an insecticide/acaricide on many
terrestrial foods and feed crops. In 1986 label registrations were changed to enhance
worker safety. In 1996, the EPA and the registrants of methyl parathion products agreed
to change the packaging, formulation and labeling of their products to prevent illegal
diversion in indoor use (U.S.EPA 1997g). The EPA and the registrants subsequently
agreed to voluntarily cancel a number of crop uses to address dietary concerns and
commited to conducting studies to refine potential occupational risk concerns (U .S.EPA
2003a). The cancelations included uses on fruits and vegetables commonly eaten by
children. In 2001, tolerances for various fruits and vegetable crops were revoked due to
dietary risk concerns and more revocations followed in 2002. Figure 2.17 Shows

increased use fiom 1992 to 1997/1998 but it has decreased considerably Since then due to
60

the voluntary cancellations of uses. The pounds applied increased by 61% (CA-DPR)
from 1992 to 1999 but decreased by 64% from 1999 to 2002. The use has actually
increased since 2002 probably due to its effectiveness and low cost in its remaining uses

which rrrinimize food residues.

r’“ — u.‘ 7*. 7* 2, -— ‘ __ , _—r v~ -. .fii v 7, . ._k ——__—.. — .~_

Methyl parathion
1 ,600,000 150,000

m I l 125,000
1,200,000

_ N \ — 100,000

a 800,000 Wm . / 75.000

\W r 50,000

W ~ 25,000

0 I I I I I I I I O
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

+CLF lbs applied —1I—CLF Acres treated
+CA-DPR Tot lbs applied -x—CA-DPR Tot acres treated

 

 

 

UdCl‘VD

 

400,000

 

 

 

 

 

 

 

 

 

 

Figure 2.17. Use of methyl parathion based on the CA-DPR and CLF data.

Acephate

Acephate was first registered for ornamental use in the U.S. in 1973 and first used
on food in 1974. Uses of acephate include application on food crops, and at residential,
public health and other non-food Sites. In 1987, a Registration Standard was issued that
imposed several interim measures to reduce dietary, occupational, and domestic exposure
from the registered uses of acephate (U.S.EPA 20010). Human health concerns have
been reported by the EPA concerning risks to workers who load, mix and/or apply
acephate to agricultural sites, golf courses and home lawns, in and around residential,
commercial, institutional and industrial buildings and recreational areas (U .S.EPA

20010). In April 2002 the EPA approved the voluntary cancellations of acephate uses by
61

various product registrants. Acephate exhibits a downward use trend as shown by the
CA-DPR and the CLF data (Appendix C). The use decreased by 25% (CLF) and 59%
(CA-DPR) in pounds applied from 1994 to 2006 due mainly to the need to reduce worker
exposure risks.

F enamiphos

Chemagro Corporation first registered fenanriphos in 1972. Food uses of
fenamiphos included fruits and vegetables and non-food uses included commercial and
industrial sites and ornamental crops. The Registration Standard and data call-in were
issued by the EPA in 1987 to better understand the risks associated with using
fenarrriphos (U .S.EPA 20020. In 1994, the registrants made voluntary risk mitigation
measures including use restrictions and reductions in response to the preliminary health
and ecological risk assessments provided by the EPA (U .S.EPA 2002f). In 2002 the EPA
approved use deletions on cotton and pineapple. Since 1997, the use of fenamiphos
follows a strongly decreasing trend that is attributable to the regulatory actions taken. in
1994 (Appendix C).

Methidathion

Methidathion was first used as a broad spectrum insecticide in 1972. Food crop
uses of methidathion include fi'uits and vegetables while non-food uses consist of
commercial and industrial applications. In 1983 a Registration Standard was issued for
methidathion and was revised and reissued in 1988. Risk assessment was conducted in
1999 to address occupational exposure to pesticide handlers and workers. Results from
the risk assessment conducted by the EPA Showed five of the 18 agricultural scenarios

exceeded the level of concern (U .S.EPA 2002b). The use of methidathion declined

62

rapidly from 1994 to 2002 and has remained low since then as shown by the CA-DPR
data (Appendix C). The EPA reported occupational risks and acute and chronic risk to
birds, mammals and aquatic Species of concern (U .S.EPA 2002h) which are probable
explanations for the downward trend in its use.

2.5.2.4 Reduced-risk Fungicides

The registration and use of the reduced-risk fungicides have increased regularly
following the passage of the FQPA as previously shown in Figures 2.1 and 2.2.
However, apart fiom the data fiom CA-DPR, use data on these recent compounds that
could be used to assess trends is very limited. In order to simplify the analysis, the
acreage use of the reduced-risk firngicides were classified as low, medium or high based
on the 2006 CA-DPR data shown in Table 2.3. Among the fimgicides, fludioxonil and
fenhexamid belonged to the low acreage classification whereas mefenoxam,
trifloxystrobin, azoxystrobin and cyprodinil were classified as medium in acreage treated.
No reduced-risk fungicides exceeded 500,000 acres in use.

Table 2.3. Level of reduced-risk fungicides acreage
based on the CA-DPR 2006 data.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Reduced-risk Acres Treated
Fungicides (CA-DPR f2006)

Fludioxonil 29,241 0 - 199,999 acres Low

F enhexamid 161,025 200,000-499,999 acres Medium
Mefenoxam 263,961 500,000-999,999 acres High
Trifloxystrobin 386,030

Azoxystrobin 390,552

Cyprodinil 420,155

Azoxystrobin

Azoxystrobin was first registered for use on non-residential turf in 1997. Food use

registrations followed in the same year for crops such as grape, peach, tomato and peanut.

63

More use registrations on crops such as cucurbit, potato and stone fruit were approved in
1999, and on onion, citrus, soybean, leafy, root and tuber vegetables in 2000.
Registrations for mostly vegetables and some fruits were also approved in 2001 and
2002. The registrations of azoxystrobin for use on artichoke, asparagus, and the brassica
group in 2003 and on herbs, spices, safflower and sunflower in 2006 were obtained by
the R4 program. Azoxystobin is not classified as a carcinogen and has low acute and
chronic toxicity to humans, birds, mammals and bees, but it is highly toxic to some
freshwater, marine and estuarine fish and invertebrates” (U.S.EPA 1997a). Figure 2.18
shows the use of azoxystrobin increased rapidly fiom 1996 to about 2000 and has

consistently been used since then based on the CA-DPR and CLF data.

a- a N-“ a- _-__...__-_, --_- ~ ,.__ ___ l

 

 

 

 

 

 

Azoxystrobin
2,000,000 _ 500,000
1,600,000 A ., 400,000
3 1,200,000 f/ m/ 300,000 5
800,000 200,000 3
400,000 W 100,000
0 . r . a r . . o

 

 

1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

+CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied -—X—CA-DPR Tot acres treated

 

 

 

 

 

 

 

Figure 2.18.Use of azoxystrobin based on the CA-DPR and CLF data.

Cyprodinil

Cyprodinil was first registered for use on stone fruits in 1998 followed by uses on
onions and strawberries in 2001. Other uses include foliage applications on almonds,

grapes and stone fi'uits. The EPA (U.S.EPA 1998a) reported no mutagenic,
64

developmental and reproductive effects and it is classified as a “not likely”. (E)
carcinogen based on the lack of oncogenic effects on all tested species. In 2003 the IR-4
program registered cyprodinil for use on bushberry, caneberry, pistachio, watercress,
brassica leafy vegetables, herbs and lychee fruits. Cyprodinil is of low risk (Appendix B)
and appears to pose relatively little human toxicity risk due to low use rate, low risk to
groundwater, low dietary risk and low worker exposure (U .S.EPA 1998a) which helps to
explain the continuously increasing use with ~183,000 acres treated in 1999 and

~420,000 acres treated in 2006 based on the CA-DPR data (Figure 2.19).

 

 

 

 

 

 

 

 

 

 

Cyprodinil
500,000
I
300,000 /&y
200,000 1
100,000 ”41’ ‘ “It" ‘
o I I I I I I I
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied +CLF Acres treated

 

 

 

 

 

 

Figure 2.19. Use of cyprodinil based on the CA—DPR and CLF data.

F enhexamid

Fenhexamid was first registered in 1999 for use on strawberries, grapes and
omamentals followed by uses on almond and stone fi'uits in 2000. Fenhexamid is
classified by the EPA as a “not likely” human carcinogen based on the lack of evidence
of carcinogenicity in male and female rats and mice (U .S.EPA 1999a) and no evidence of

genotoxicity and mutagenicity has been found. The IR-4 program obtained several
65

registrations for fenhexamid in 2003 (cucumber, fruiting vegetables, leafy greens and
stone fruit), and in 2006 (ginseng, pear, cilantro, pepper and pomegranate). Figure 2.20
shows the continuously increasing use in the pounds applied and acres treated of

fenhexamid (12,000 lbs in 1999 and 66,000 lbs in 2006 based on the CA-DPR data).

 

 

 

 

 

 

 

 

Fenhexamid
200.000
150,000 /)‘
100,000 flkv
50,000 W
O I I I I I I I
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied -x—CA-DPR Tot acres treated
+CLF lbs applied +CLF Acres treated

 

 

 

 

 

Figure 2.20.Use of fenhexamid based on the CA-DPR and CLF data.

Fludioxonil

The first registration of fludioxonil was in 1995 for use on corn followed by its
use on potato and seed treatments for several nuts and vegetables in 1997. In 1998 more
tolerances for vegetables such as brassica leafy vegetables, legumes, leaves of root and
tuber vegetables, and bulb vegetables were established. The EPA reported no concern for
acute dietary risk for fludioxonil and it has been classified as “not classifiable as to
human carcinogenicity or Group D, that is, the evidence is inadequate and cannot be
interpreted as showing either the presence or absence of a carcinogenic effect” (U .S.EPA
1998b). More uses of fludioxonil were later approved for use on strawberries and bulb

vegetables in 2000, for turf in 2001 and caneberry, pistachio, stone fruit and watercress in
66

 

2002. Many of these registrations were obtained by the IR-4, i.e. the pome group (e.g.
apples and pears), asparagus, beets, the melon subgroup (e. g. cantaloupes and
watermelons), carrots, the stone fiuit group (cherry, peach, plum and nectarine), citrus,
cucumbers, garlic, spinach, squash, tomatoes, sweet potatoes, and yarns. The increasing

use trend of fludioxonil is shown in Figure 2.21.

 

 

 

 

 

 

 

 

Fludioxonil
30,000
25,000 ' /I\\//
20,000
15,000 1
.0... f.
5,000 / L— 1"

 

 

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

 

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied -—I— CLF Acres treated

 

 

 

 

 

Figure 2.21. Use of fludioxonil based on the CA-DPR and CLF data.

Mefenoxam

Mefenoxam is the active form in the isomer mixture of the fungicide metalaxyl. It
was registered in 1996 to replace all previous uses of metalaxyl (U .S.EPA 1996b). Ciba
Crop Protection voluntarily cancelled all of the registrations of metalaxyl to allow for the
full environmental benefit provided by the registration of end-use products containing
mefenoxam” (U .S.EPA 1996b). Mefenoxam has shown a consistent medium level of use
in California in replacing metalaxyl since its registration as shown in Figure 2.22 and the

CLF data show a clear increase fi'om 1997 to 2002.

67

 

 

Mefenoxam
600,000 I
500,000
400,000

300,000 . W
200.000

0
100,000 g
0 I I I I I

1992 1994 1996 1998 2000 2002 2004 2006 2008

 

 

 

 

 

 

 

 

 

 

Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied — III—CLF Acres treated

 

 

 

 

 

 

 

Figure 2.22.Use of mefenoxam based on the CA-DPR and CLF data.

T rifloxystrobin

The first registration of trifloxystrobin, obtained in 1999, was for use on porne
fruit, grapes, cucurbits, peanuts, bananas, turf and omamentals. Further registrations
followed in 2000 and 2002 for use on more fruits and vegetables including almonds,
citrus, pecans and stone fiuit. The IR-4 program obtained registrations in 2003 for the
leafy petiole and root vegetable subgroups and barley and oats in 2006. Trifloxystrobin is
classified as a “not likely human carcinogen” and exhibited no mutagenic properties
(U .S.EPA 199%). However, kidney and liver toxicity at high doses were noted from
subchronic and chronic toxicity studies. Trifloxystrobin has been continuously used at a
medium level since its initial registration (Appendix C). In the CA-DPR data there was
no clear increase in the pounds applied but the acres treated increased from 2000 to 2006.

2.5.2.5 Reduced-risk Insecticides

 

The levels of acreage treated with the reduced-risk insecticides based on the CA-

DPR 2006 data are shown in Table 2.4 and are classified as low, medium or high in the
68

same way as the reduced-risk fungicides. Among the reduced-risk insecticides,
imidacloprid, methoxyfenozide and Spinosad were classified as having a high (>500,000)
level of acres treated. Tebufenozide had the lowest acres treated (15,517) while its
relative, methoxyfenozide, has the second highest acreage treated (840,464).
Methoxyfenozide is an analog of tebufenozide which is now preferred since it is active at
lower dose and against a broader range of pests than tebufenozide, and shows a high
degree of safety to nontarget insects (Borchert et al. 2004). This explains the huge
difference in the level of usage between the two analogous insecticides.

Table 2.4. Level of reduced-risk insecticides
acreagg based on the CA-DPR 2006 data.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Reduced-risk Acres Treated
Insecticides" (CA-DPR/2006)
TCbllfCHOZide 15,517 0 _ 199,999 acres LOW
“methoxam 27,034 200000499999 acres Medium
Pymetrozine 53.5 80 500,000-999,999 acres High
Buprofezin 68,682
Bifenazate 153,356
Pyriproxifen 1 66,208
Acetarniprid 207,705
Indoxacarb 242,607
Imidacloprid 623,030
Methoxyfenozide 840,464
Spinosad 863,977

 

*Listed as 0P alternatives by the EPA (U.S. EPA 2008b).

Acetarniprid

Registrations for the use of the neonicotinoid insecticide, acetamiprid, on cotton,
porne fi'uit, citrus, grapes, and brassica crops, among others, were completed in 2002 and
this was followed by its registration for the use on potatoes in 2005. It has been classified
as an “unlikely” human carcinogen and showed generalized non-specific toxicity and did
not appear to have specific target organ toxicity (U .S.EPA 2002b). The EPA also
reported low mammalian acute and chronic toxicity, and no positive evidence was found

69

[0.

[0

‘6

l\(

all

to indicate carcinogenicity, neurotoxicity, mutagenicity or endocrine disruption. Figure
2.23 shows that use of acetamiprid has been increasing from 2002 (~39,000 acres treated)

to 2006 (~208,000 acres treated) based on the CA-DPR data.

 

 

Acetarniprid

 

250,000
200,000 x
150,000 //
100,000 I /

 

 

 

 

 

 

 

 

5...... ,/
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied -x—CA-DPR Tot acres treated
+CLF lbs applied + CLF Acres treated

 

 

 

 

 

 

Figure 2.23. Use of acetamiprid based on the CA-DPR and CLF data.

Buprofezin

Buprofezin is an insect growth regulator with very low vertebrate toxicity. In
1997, an emergency exemption for use of buprofezin on cotton was requested but at that
time buprofezin was an unregistered material and its proposed use was as a “new
chemical” (U .S.EPA 1997d). Requests for pesticide tolerances for emergency exemptions
for the use of buprofezin on cucurbits and tomatoes were also made and approved in
1998 and expired in 1999. In 2000 buprofezin was registered for use on cucurbit
vegetables and head lettuce, followed by use registration on almonds, citrus, cotton,
grapes and tomatoes in 2001. The IR-4 program completed its registration on beans,
lychees and pistachios in 2003. In 2005 additional use registrations were completed for

avocado, guava, peach, porne fruit, and sugar apple. The EPA identified no concerns for
70

cancer risks for buprofezin (U .S.EPA 1997b). The use of buprofezin increased ficm
1997 but declined to zero in 2000 (Figure 2.24) due to the expiration of the emergency

registration. It rose rapidly again from 2001 as the registered uses expanded.

Buprofezin
80,000

/
60,000
..,... //

' 2:7
20,000 A

 

 

 

 

 

 

 

 

 

O I I v I I I I
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
—e— CLF lbs applied + CLF Acres treated

 

 

 

 

 

 

Figure 2.24.Use of buprofezin based on the CA-DPR and the CLF data.

Imidacloprid

Inridacloprid is a systemic insecticide in the neonicotinoid group used to control
a wide range of sucking chewing insects that was first registered for use in the U.S. in
1994 and was the first insecticide in its chemical class to be developed for commercial
use (Cox 2001). It is now one of the most commonly used insecticides worldwide. Cox
(2001) reported its uses on cotton, fi'uits, vegetables, turfgrass and ornamental plants
among others. In 1995, tolerance for irnidaloprid residues in or on the raw agricultural
commodity dried hops was set as requested by IR-4. Tolerances for sugar beets, sweet
corn, safflower and the legume vegetables crop group among others were approved in
1998. In 2001 imidacloprid was registered for use on leaf petiole vegetables and citrus.

In 2003 tolerances were established for stone fi'uits, strawberries, gooseberry and other
71

berries and for blueberries in 2004. (U.S.EPA 1998c). Imidacloprid was formd to cause
neurotoxicity in rats following a single high oral dose, and caused alterations in brain
weight in rats based on a 2-year carcinogenicity study, but it has been classified under
Group E, no evidence of carcinogenicity for humans (U .S.EPA 1998c). Studies have also
shown that imidacloprid is non-mutagenic (U .S.EPA 19980). The use of imidacloprid has
increased rapidly and to a high level since its initial registration as shown in Figure 2.25
although most of the increases occurred between 1994 and 1996. It is of low risk, highly
effective as an OP replacement and has uses on numerous crops which explain its
increasing use trend. Concerns have been expressed about its toxicity to honey bees and
possible role in colony collapse disorder. These concerns have yet to be substantiated,

although its use has been limited in some countries for this reason (Oldroyd 2007).

 

Imidacloprid
2,500,000 800,000

I
1,500,000 .

~ 400.000

 

 

 

F
\

 

HdCI'VD

3 1,000,000 1/
~ 200,000

500,000
0 W 0

1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

+CLF lbs applied + CLF Acres treated

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

 

 

 

 

 

 

 

 

 

Figure 2.25.Use of imidacloprid based on the CA-DPR and the CLF data.

72

Pyriproxyfen

Pyriproxyfen, another insect growth regulator, was first registered in 1998 for use
on cotton. Walnut, porne fruit, citrus, fiuiting vegetables and tree nut uses were approved
in 1999. In 2001 use on pistachios was registered; on stone fi'uits, blueberry, lychee and
guava in 2002; and brassicas and cucurbit vegetables, olives, avocados, figs, okra, and
sugar apple fruits in 2003. Some of the use registrations in 2002 and 2003 were by IR-4.
Pyriproxyfen is a Group E carcinogen which indicates evidence of non-carcinogenicity in
humans and it has been found by the EPA to cause no concern for acute dietary exposure
to its residues (U.S.EPA 1997c). Figure 2.26 Shows a consistent increase in use of
pyriproxyfen with an increase in acres treated and pounds applied based fi'om the CA-

DPR data from 1997 (50,000 acres treated) to 2006 (166,000 acres treated).

 

____.. -_~ —_ —__.__ _ . _

Pyriproxifen

175,000
150,000
125,000
100,000
75,000
50,000
25,000

0

1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

+CA-DPR Tot lbs applied -—*—CA-DPR Tot acres treated
+CLF lbs applied —-I~ CLF Acres treated

 

 

 

 

 

 

Figure 2.26.Use of pyriproxyfen based on the CA-DPR and the CLF data.
Spinosad
Spinosad is an insect-specific nemotoxic natural product produced by microbial

fermentation which is highly effective against chewing insects but shows little, if any,
73

vertebrate toxicity. The first food uses of spinosad (almonds, apple, citrus, and brassica,
fi'uiting and leafy vegetables) were registered in 1998. More use registrations for fiuits
and vegetables followed such as: cucurbit vegetables, stone fiuit, and legumes in 1999;
cilantro, apples, pistachios, tropical fiuits, among others in 2000; asparagus, cranberries,
porne fiuit, strawberries and others in 2001; the berry group, grapes, herbs, peanuts, root
and tuber vegetables in 2002; and mint and onions in 2006. The 2002 and 2006
registrations were by the IR-4. No carcinogenic, mutagenic or developmental toxicity
effects were observed for spinosad (U .S.EPA Undated-a) and no neurotoxic effects were
observed in rats in acute, chronic or subchronic studies. The high efficacy, particularly
against chewing insects and very low risk of using spinosad contributes to its high and
increasing use (Figure 2.27). Spinosad is also marketed for organic use since it is a

natural compomrd which is an additional explanation for the increasing use.

 

1,200,000
300.000 /
#1

 

 

 

 

 

 

 

 

 

 

L r 9 . - i,
0 e i T T 3' ' ' .
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied -x—CA-DPR Tot acres treated
+CLF lbs applied —-I-— CLF Acres treated

 

 

 

 

 

 

Figure 2.27. Use of spinosad based on the CA-DPR and the CLF data.

74

Bifenazate

Primarily an acaricide, bifenazate was first used on omamentals in 1999. In 2002
the EPA classified bifenazate as “not likely” to be a human carcinogen and food use
registrations including stone fi'uits were completed in the same year. The IR-4 registered
the uses of bifenazate on cucurbits, fruiting vegetables, mint, pistachio, tomatoes and tree
nuts in 2003 and registered it in collaboration with Uniroyal in 2006 for stone fi'uit, pea,
and tuberous and com vegetables. The continuously increasing use of bifenazate since
1999 is shown in Appendix C.

Indoxacarb

The initial registrations of indoxacarb in 2000 were on cotton, fruiting vegetable,
leafy vegetables, lettuce, sweet corn and porne fruit; and on peanut, potato and soybean in
2002. According to the EPA, indoxacarb has moderate to low acute and chronic toxicity
and does not cause mutagenic, carcinogenic, developmental and reproductive effects
(U .S.EPA 20000). Although neurotoxicity was observed in some studies, it was only at
fatal doses (U .S.EPA 20000). In 2007, the EPA approved more tolerances of indoxacarb
on various groups of fi'uits and vegetables as requested by EJ. du Pont de Nemours and
IR—4 (U .S.EPA 2007d). Indoxacarb use increased sharply after its introduction in 2000
and has remained about constant since then (Appendix C) which is presumably due to its
effectiveness as an OP replacement against chewing insects and its relatively low
toxicity.

Methoxyfenozide

Methoxyfenozide is an insect growth regulator and was registered in 2000 for use

on pears, apples and other porne fi'uits (U .S.EPA Undated-b). In 2002, tolerances were

75

established for methoxyfenozide and its metabolites for residues on various agricultural
food commodities as requested by IR-4 and Rohm and Haas Company. More tolerances
requested by IR-4 and Dow AgroSciences for residues on various fiuits and vegetables
were established in 2004 (U .S.EPA 2004d). Requested tolerances on soybeans and their
byproducts were set in 2006. Methoxyfenozide exhibit effectiveness at lower dose against
a broader range of pests and little effect on non-target organisms (Borchert et al. 2004;
Carlson et al. 2001) than an earlier analog, tebufenozide. This explains the increasing use
of methoxyfenozide both in pounds applied and acres treated fi'om 2005 to 2006
(Appendix C).

Pymetrozine

Pymetrozine is primarily a systemic insecticide acting against sucking insects. It
was first registered in 1999 for use on tuberous and com vegetables, omamentals, and
tobacco. More registrations followed on cucurbits and fruiting vegetables in 2000, and
on leafy and brassica vegetables and pecans in 2001. In 2005 the IR—4 was responsible for
its registration for use on asparagus. It is non-mutagenic and is of low acute toxicity to
humans, birds, aquatic organisms, mammals and bees. However, it has been classified by
the EPA as a “likely” human carcinogen because of tumor occurrence in some of the
Species tested, and mechanistic arguments have been advanced to explain the
carcinogenicity (U .S.EPA 2000c). However, the EPA concluded that due to “limited
sites, low use rates, and low exposure, the carcinogenic risk to humans is below the level
of concern (U.S.EPA 2000c). Pymetrozine has been used continuously since 2000 as

shown in Appendix C but in relatively small amounts.

76

T ebufenozide

The first completed registration of the insect growth regulator tebufenozide was in
1995 for use on walnuts. In 1998 use registration was approved for pecans; in 1999 for
leafy, brassica and fruiting vegetables, cranberries, the berry group and mint, pome fi'uit,
sugarcane, turnips, and canola; for tree nuts in 2000; and for citrus, grapes, and tuberous
and corm vegetables in 2004. Several of the use registrations completed in 1999 and 2004
were by IR-4. Several tolerances for emergency exemptions for the use of tebufenozide
have been approved by the EPA for various crops such as cranberries, peppers, peanuts
and non-brassica leafy vegetables since its first use was registered. Tebufenozide has
been classified as a Group E carcinogen, with no evidence of carcinogenicity based on a
2-year carcinogenicity study in rats and an 18-month study in mouse (U .S.EPA 1997f).
Its use increased until 2003 but decreased rapidly since then as shown in Appendix C due
to its substantial replacement by methoxyfenozide.

Thiamethoxam

Thiamethoxam, another member of the neonicotinoid group, was registered in
2000 for use on barley, canola, cotton, sorghum and wheat for seed treatments. Approved
registrations for fruits and vegetables including cucurbits, fi'uiting vegetables, tuberous
and corm vegetables, and porne fruit followed in 2001; for beans, stone fiuit and
sunflowers in 2003; and for mint in 2004. Thiamethoxam is considered as slightly acutely
toxic via the oral route and of low toxicity via the dermal and inhalation routes of
exposure and did not Show evidence of reproductive, developmental or mutagenic
toxicities (Antunes-Kenyon 2001). Thiamethoxam has been used continuously since its

initial registration as shown in Appendix C.

77

2.5.3 IR-4 ’s Role in Registering Reduced-risk Pesticida

Numerous reduced-risk fungicides and insecticides have been registered by the
IR-4 for use on fiuit, vegetable and nut crops. Among the fungicides are azoxystrobin,
cyprodinil, fenhexamid, fludioxinil, and trifloxystrobin, and the insecticides include
bifenazate, buprofezin, indoxacarb, methoxyfenozide, pymetrozine, pyriproxyfen,
spinosad, tebufenozide and tlriarnethoxam. All of these insecticides are listed by the EPA
as OP alternatives (U .S.EPA 2006c, 2008b). The overall use of these lR-4 registered
reduced-risk pesticides has increased noticeably since the inception of the F QPA (as
previously discussed and shown in Figtn'es 2.1 and 2.2). Gianessi and Silvers (2000)
reported that the use of older pesticides decreased by 3.0 M pounds due to “newly
registered, more cost-effective fungicides” such as azoxystrobin. Azoxystrobin is among
the several newly—introduced broad-spectrum reduced-risk fungicides adopted on a broad
range of crops between 1997 and 2002 and it has significantly reduced the use of older
active ingredients such as chlorothalonil (Gianessi and Reigner 2006a). Azoxystrobin is
also very effective against fungal diseases not controlled by chlorothalonil and many
growers alternate azoxystrobin with chlorothalonil for a more effective control against
fungal diseases (NSF-CIPM 1999). It was ranked 41” among the top 100 pesticides used
in California in 2006 judged by acres treated (CA-DPR 2007a). The IR-4 obtained
registrations on 34 (47%) of the 72 crops with reported uses of azoxystrobin.

Spinosad and imidacloprid are among the reduced-risk insecticides that have been
widely and increasingly used since their initial registration. Spinosad was rank 23rd out of
the top 100 pesticides by cumulative acres treated (901,535 acres) in California (CA-DPR

2007b). Spinosad was used on 110 fruits and vegetables based on the 2006 Summary

78

Report by the CA-DPR and 36 of these uses were registered by IR-4 (33%).
Inridacloprid was ranked 31St by the CA-DPR among the top 100 pesticides by acres
heated in 2006 (765,752 acres) (CA-DPR 2007b). Imidacloprid uses were on 79 fi'uits
and vegetables and 47 (60%) of these were registered by IR-4. Imidacloprid is sold under
the hade names Admire and Provado, the main chemical used on Colorado potato beetle,
and is very effective at low dosages. Admire has largely replaced oxamyl as the
insecticide in soil-applied drenches whereas Provado has replaced many of the standard
foliar insecticides (NSF-CIPM 1999). Also according to NSF-CIPM (1999), there have
been essentially no chemicals that can serve as effective alternatives to imidacloprid.
From these examples it would be reasonable to conclude that IR-4 has been responsible
for roughly 50% of the registrations of reduced-risk pesticide currently in major use on
fiuit vegetables and nut crops in California. 1

A further example of the impact of the IR-4 registration of reduced-risk products
is found in the post-harvest heahnent of stone fiuits such as peaches, nectarines and
plums. The common use of iprodione, a B2 carcinogen, for this purpose was canceled by
EPA in 1998 because of the high residues left at consumption. As described ftuther in
Chapter 4 iprodione has been entirely replaced in this use by the reduced-risk fungicide,
fludioxonil with concurrent improvements in consumer safety. The fiudioxonil
regish'ation for the entire stone fruit group was obtained by IR-4.
2.5.4 Decrease in Application Rates with Reduced-risk Compounds

The reduced-risk pesticides are generally used at significantly lower application
rates than the conventional compounds they are replacing which have the effect of

decreasing the amount of chemical applied to the environment (environmental load). The

79

data in Figure 2.28 Show the environmental loads (calculated as the ratio of the total lbs
of pesticide applied and the total acres treated based on the CA-DPR data) of the
anticholinesterase and the reduced-risk insecticides, and Figure 2.29 shows the same data
for the B2 carcinogenic and the reduced-risk fungicide groups. The 0P3 show a constant
environmental load (~1.2 lbs/acre) over the years from 1992-2006, while the NMCS were
used at 1.32 lbs/acre in 1992 and this decreased to 0.84 lb/acre in 2006. The
environmental load for the reduced-risk insecticides is 5 to 12-fold lower than for the
anticholinesterase group with an environmental load of 0.08 to 0.25 lb/acre fi'om 1992 to
2006. The environmental loads of the reduced-risk fungicides Show a slight increase from
0.12 lb/acre in 1997 to 0.21 lb/acre in 2006 but these are still considerably lower than the

environmental load of the B2 ftmgicides which stayed constant in the range of 1.0 to 1.5

 

 

 

 

 

 

 

 

 

 

lbs/acre.
Environmental load
2.00
1.60 l
2 1.20 - ——
8
3 0.80
0.40
‘\"a\
.i . . +. Weir—kw
0.00 7 I r f f I I I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+Carbamates +0Ps —+— RR Insecticides

 

 

 

 

 

 

Figure 2.28. Environmental load of the anticholinesterase and the reduced-risk
insecticide groups.

80

 

 

 

 

 

 

 

 

 

 

 

Environmental load
2.00
. ”a"-
1.50 _,.-- “2% I... v i ‘ If”;
it art a —-e-—x,/’
g 100 ‘
g - Is-
2
0.50
W
Cam I I I I I I I I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
“e—BZs +RR Fungicides

 

 

 

 

 

 

Figure 2.29. Environmental load of the BZ carcinogenic and the reduced-risk
fungicide groups.

Figure 2.30 shows the combined environmental loads of the new and the old
pesticides grouped into insecticides and fungicides. This demonshates the impact of the
increasing use of the reduced-risk compounds on the overall environmental loads of the
insecticide and fungicide groups. The reduced-risk pesticides have substantially
decreased the overall loads in these groups fiom 1994 to 2006 by 45% for the insecticides
and by 54% for the fimgicides. These results lead to the conclusion that the use of the
reduced-risk pesticides is likely to lead to a lower impact on the environment compared
to the conventional pesticides because of both their lower use rates and their decreased

level of toxicity in many cases.

81

 

Environmental load

 

 

 

 

 

 

1.80
a, 1.20
g RSV \
a 0.90
9 8%
0.60 {3 2 Q
0.30
0.00 i r

 

 

 

1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

-B-Lbslacre (0P3, Carbamates & RR insecticides)

+Lbs/acre (32 Carcinogenic and RR fungicides)

 

 

 

 

 

 

 

Figure 2.30. Overall environmental load of the insecticide and the fungicide groups.
Trends in the amount (lbs) of pesticide used in an application (application rate)
for the insecticide and fungicide groups are shown in Figure 2.31. These application
amounts also follow a declining trend for both groups from 1994 to 2006 with an
approximately 50% decline in the amount of fungicides and a 60% decrease in the
quantity of insecticides used in each application. This is another indicator of the positive
effect that reduced-risk compounds (at lower application rates) have replaced the

conventional chemicals.

82

 

Application Rate

 

50.0

 

 

 

 

 

 

 

 

 

g 40.0 ‘—.¢\
.0.
*8" 30.0 Mk
E 200 m
C
3 10.0
0.0 r r e . . . .
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
—e—Lbslapplieation -e—Lbslapplication
(0P3, Carbamates & RR Insecticides) (82 & RR fungicides)

 

 

 

 

 

 

Figure 2.31. Application rates of the insecticides and the fungicides groups.

83

2.6 Conclusion

Based on the data available from CA-DPR and CLF, the use of the OP and NMC
anticholinesterase insecticides has decreased substantially over the years from 1992 to
2006, especially since the enachnent of the FQPA in 1996. As a class, the OPS have
declined by approximately 50% in pounds applied and the NMCS even more by 70-75%.
The use of many of the most important members of these classes has declined by over
80%, e.g. the decline in pounds applied based on the 1992 and 2002 CLF data were
carbofuran (81%), disulfoton (85%), fonofos (100%) and methidathion (81%). Based on
the 1994 and 2006 CA-DPR data the OPS and the NMCS that had the most significant
decrease in pounds applied were carbofiuan (93%), aldicarb (91%), carbaryl (84%),
azinphos—methyl (91%), fonofos (100%), and methamidophos (99%). These two groups
were the initial focus of regulatory attention after F QPA and much of the corresponding
decrease in use is due to the cancellation and reshiction of uses and lowering of
tolerances. However, the decreased use is not uniform for all OPS and NMCS, e.g. the use
of chlorpyrifos remains high based on the CA-DPR data and the decline in use of
acephate has been relatively modest. Similarly oxamyl use has declined less than that for
the rest of the NMCS.

In parallel with the decreased use of the anticholinesterase insecticides, the
reduced-risk insecticides, many of them specifically classified as OP replacements, have
increased regularly in use so that now they play a central role in the management of
arthropod pests. This hansition is likely to continue as additional regulatory actions
remove anticholinesterase uses and pest management shategies further increase their

emphasis on safer chemistries with lower environmental impacts.

84

In conhast to the anticholinesterases, the B2 flmgicides have undergone only a
limited decline in use of 10-20% since the FQPA was passed. Individual members of the
group such as iprodione have been the target of specific actions because of elevated risk
and thus have undergone larger decrease in use, but generally it appears that, despite their
classification as probable human carcinogens, these compounds have not been found in
the diet at levels that cause regulatory concern for the EPA. These B2 compormds have
strong advantages for pathogen conh'ol including low cost, low resistance potential and
broad spechurn activity. However, there has also been a regular increase in use of the
reduced-risk fungicides since F QPA. This can be athibuted to the need to replace specific
B2 uses lost to the limited regulatory activity such as the elimination of iprodione for
postharvest use, but also because many newer compounds have distinct advantages
including very high efficacy, broad spech'um, and systemic activity that allows more
limited curative heahnents for pathogens rather than being reshicted to preventative uses
as with the older B2 compounds.

Finally, most of the reduced-risk pesticides are used at significantly (5 tolO-fold)
lower application rates than the older compounds evaluated in this study. The decreasing
use of the OPS and the NMCS and the increasing use of the reduced-risk insecticides and
ftmgicides have therefore led to an appreciable overall decrease in the amounts of
chemical pesticides being applied in the production of fruit, vegetable and nut crops.
Taken in conjunction with the greatly improved toxicological properties of many of the
reduced-risk compounds, this decrease in application rates is likely to lead to a lower
environmental impact in addition to the Significant improvements in worker safety and

lowered dietary risks that have resulted from the passage of the F QPA.

85

Overall, the available pesticide use databases are not well set up for trend
analyses. There is a lack of continuous and comprehensive collection of national
pesticide use data. They are not well integrated and do not allow for cross-database
analysis. Each of the databases follows a different protocol in the monitoring procedures.
The sampling procedure, as well as the commodities sampled and the pesticides analyzed
each year, varies for each database which make the data discontinuous and inconsistent.
Pesticide use databases that are possibly more complete and comprehensive such as the
Doane AgroTrak and the Buckley Report are available but at a very high acquisition cost.
Due to their proprietary nature, their accuracy and sampling methods cannot be compared
to publicly-accessible and widely-used databases. The deficiencies of the databases
maintained by government agencies have been recognized and an Advisory Committee
was recently appointed by the U.S.DA-NASS to assess whether there was support to
expand and improve them including the development of an integrated national system for
pesticide use data collection and distribution. It was concluded that the current data
collection approach was currently regarded as “adequate” and that there was a lack of
sufficient interest in developing more comprehensive and continuous databases to justify
an increased budget request. In particular, the proprietary Doane Report system currently
satisfies the needs of both EPA and the agrochemical industry (Gianessi and Mitenbuler
2006). However, the fact remains that no comprehensive data collection system exists
that allows ready public access, and that there are significant gaps and discontinuities in

those databases to which the public does have access.

86

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http://www.epa.gov/pesticides/cumulative/common_mechigroups.htm

 

U.S.EPA. 2007c. Draft List of Initial Pesticide Active Ingredients and Pesticide Inerts to
be Considered for Screening under the Federal Food, Drug, and Cosmetic Act.
U.S. Environmental Protection Agency. Report. Federal Register / Vol. 72, No.
116. Notice.

U.S.EPA. 2007d. Indoxacarb; Pesticide Tolerance. Environmental Protection Agency.
Report. Federal Register/ Vol. 72, No. 132. Final Rule.

U.S.EPA. 2007e. ORD Pyrethroids Project. U.S. Environmental Protection Agency.
September 2007. http://epa.gov/heasd/regulatory/proiccts/dlc pyrethroidshtm

U.S.EPA. 2007f. Reregistration Eligibility Decision (RED)-Aldicarb. Washington, D.C.:
U.S. Environmental Protection Agency. Report.

94

U.S.EPA. 2007g. Revised N-methylcarbamate Cumulative Risk Assessment.
Washington, D.C.: U.S. Environmental Protection Agency. Report.

U.S.EPA. 2008a. Amended Reregistration Eligibility Decision (RED)«Carbaryl.
Washington, D.D.: U.S. Environmental Protection Agency. Report.
http://wwwepa. gov/oppsrrd l / RE Ds/carbaryl-red-amended. pdf

 

U.S.EPA. 2008b. Reduced Risk/Organophosphate Alternative Decisions for
Conventional Pesticides. Updated 2/12/08. U.S. Environmental Protection
Agency. Report. http://\nuv.epa.gov/opprdOO l /workplan/complctionsportrait.pdf

 

U.S.EPA. Undated-a. Spinosad-Pesticide Fact Sheet. Washington, D.C.: U.S.
Environmental Protection Agency. Report.

U.S.EPA. Undated-b. The United States Environmental Protection Agency Report on
Minor Uses of Pesticides. U.S. Environmental Protection Agency. Report.
http://www.epa.gov/pesticides/minoruse/minor use rpjpdf

U.S.GAO. 2001. Agricultural Pesticides: Management Improvements Needed to Further
Promote Integrated Pest Management. U.S. General Accounting Office. Report.
http://umw;g,ao.gov/new.items/d0l 815de

 

Wilkinson CF, Arce G, Gordon EB. 2004. Scientific Analysis of the Data Relating to the
Reclassification of Captan Under EPA's New Guidelines for Carcinogen Risk
Assessment. Report. CTF 0104.
http://www.tera.org/pcer/CAPTAN/(‘aptanRevDoc.pdf

95

CHAPTER 3
PESTICIDE RESIDUE TRENDS

As EPA administered the FQPA, the use of some older pesticides, particularly the
organophosphates (OPS) and the N-methylcarbamates (NMCS), and to a lesser extent
some B2 carcinogenic fungicides, has declined, as demonstrated in Chapter 2. This
should have decreased the frequency of occurrence and levels of their residue in the food
supply and thus have led to an increase in food safety to meet the ultimate objective of
these regulatory actions. In this section, changes in these key pesticide residues since the
passage ofthe FQPA are examined to determine to what extent such reductions can be
documented and the degree to which residues of the newer, lower risk replacements can
now be found in the diet.

3.1 Pesticide Residue Databases

Federal or state agencies that maintain substantial pesticide residue databases
include the U.S. Department of Agriculture Pesticide Data Program (USDA-PDP), the
Food and Drug Administration (FDA), and the California Department of Pesticide
Regulation (CA-DPR). The residue databases are developed for different purposes often
based on specific regulatory priorities, vary in important ways, and have advantages and
disadvantages for other specific purposes such as trend analysis. The FDA mainly
samples surveillance type commodities which are those of which it has “no prior
knowledge or evidence that a specific food shipment contains illegal pesticide residues”
(U .S.FDA 2000b) but also for many years FDA has run an annual market basket survey
of chemical residues in samples of foodstuffs collected in several cities across the U.S.

and converted into cooked meals. The PDP residue database is comprehensive in national

96

coverage but has limited continuity of data over the years. The CA-DPR also maintains a
comprehensive and relatively continuous state level residue database. The downside of
both the PDP and the CA-DPR databases for trend analysis is the variability in the crop
samples analyzed and sampling procedures and fiequency, and changes in the limits of
detection in the sample analyses with time.

3.1.1 U.S. Department of Agriculture Pesticide Data Program (USDA-PDP)

The Pesticide Data Program (PDP) was initiated in 1991 by the U.S. Department
of Agriculture to collect pesticide residue data in flesh and processed foods. It is
“administered within the Agricultural Marketing Service (AMS) which employs
specialists that provide standardization, grading and market news services for many
major commodities vital to U.S. agriculture (cotton, dairy, fiuit and vegetable, livestock
and poultry)” (Pimzi et al. 2005). The PDP data are used by the FDA, the U.S.DA
Economic Research Service and Foreign Agricultural Service, and by the U.S.
Environmental Protection Agency (EPA) as a primary source for dietary risk assessment.
Italsoprovidesdataonminorcropsandonfoodsconsumedmostlybyinfantsand
children to meet specific regulatory requirements. It is intended to provide a statistically
valid sampling of human dietary intakes across the U.S.

Several states (California, Colorado, Florida, Maryland, Michigan, Minnesota,
Montana, New York, Ohio, Texas, Washington and Wisconsin) participate in the
sampling and testing programs of the PDP. The collection of commodities depends on the
production volume and population fiom where the samples are taken. Foods analyzed
since the program started represent foods which are consumed in relatively high amounts,

often by children and with the exception of meats and frozen commodities, can be eaten

97

raw (Punzi et al. 2005). Samples are collected from terminal markets and chain store
distribution centers. Sampling at these locations allows for residue measurements that
include pesticides applied during crop production and those applied after harvest (such as
fimgicides and growth regulators) and takes into account residue degradation while food
commodities are in storage (U .S.DA-PDP 2006a). Both imported and domestic
commodities are represented in the commodities sampled by PDP, but almost all of the
samples are of domestic origin However, several commodities are grown domestically
for some part of the year and imported for the remaining part. The choice of crops, and
to some extent the pesticides, is governed by priorities set by the EPA based on flieir data
needs and on information about the types and amormts of food consumed by infants and
children (U.S.DA-PDP 2006b). As a dietary risk assessment support program, PDP
focuses its pesticide testing on registered uses for the commodities in the program rather
than screening for all potential illegal uses (U .S.DA-PDP 2006a). More extensive
residue data are required for pesticides with current registered uses and for compounds
that show a need for more extensive residue data based on toxicity data and preliminary
estimates of dietary exposure. Other pesticides monitored by the PDP are those for which
EPA has instituted modified use directions as part of risk mitigation requirements. Thus,
the data collected vary from year to year so that continuous records of the residues in
specific crops are generally not available, and, not unreasonably, the results are focused
on commodities that play a major role in the U.S. diet and PDP rarely if ever assesses
residues in more minor dietary components such as apricots, blueberries or cauliflowers.
Multiresidue methods (MRMs) are used to analyze for pesticide residues in the

participating laboratories and allow for detection of numerous compounds in a single

98

analysis. However, some pesticides, such as the dithiocarbamate fimgicides, are not
amenable to this MRM methodology. After residue analysis, the data are stored in the
electronic database and include sample collection and product information, residue
findings, and process control recoveries for each sample analyzed as well as the fortified
recoveries for each set of samples. Summary reports are published annually and the data
are available on the USDA website.

3.1.2 California anrtnrart of Pesticide Regulation (CA-DPR)

The California Department of Pesticide Regulation (CA-DPR) analyzes pesticide
residues to enforce the tolerances set by the U.S. EPA. Samples are collected from
channels of trade such as points of entry (seaports and state border stations), packing
sites, and the wholesale and retail markets. The commodities are collected from
individual lots of domestic and imported foods. The CA-DPR only samples fiesh produce
and analyzes them as the rmwashed, whole (rmpeeled), raw commodity. Arormd 8,000
samples are collected annually covering about 150 different commodities. Eighty percent
of the samples are of approximately 75 commodities important in the diets of infants and
children, or in the population overall. Multiresidue screens are then used in the amlysis
of the samples. Selected samples receive specific analysis for non-screenable pesticides
of enforcement concern (CA-DPR 2001).

The CA-DPR classifies domestic and imported food samples as either
“surveillance” or “compliance”. Surveillance samples are those with no prior knowledge
Or evidence that a specific food shipment contains illegal pesticide residues; and

compliance samples are those that follow up to the finding of an illegal residue or when

99

other evidence suggests that a pesticide residue problem may exist as defined by CA-
DPR. Most of the samples collected are the surveillance type.

According to the CA-DPR the “data collected under regulatory monitoring are
extensive but are not statistically representative of the overall residue situation for a
particular pesticide, commodity, or place of origin” (CA-DPR 2001). This may be due to
biases incurred by focusing on factors such as commodities or places of origin with a
history of violation, or with large volume of production or significant levels of
importation. The number of commodities sampled and analyzed for a particular pesticide
each year may not be sufficient to represent the overall residues for a commodity in
commerce (CA-DPR 2001).

The CA-DPR coordimtes with other agencies in the conduct of pesticide residue
analysis. The U.S. FDA is one of the agencies the CA-DPR works closely with to plan
sampling strategies so as to avoid duplication of samples collected and analyzed Results
are shared between the two agencies and they also cooperate on necessary investigations
of potential violations. California is also part of USDA’s Pesticide Data Program (PDP)
wherein data are provided for dietary exposure assessments.

3.1.3 Food and DrugAdrniuistr-otion (FDA)

The Food and Drug Administration (FDA) pesticide monitoring program has two
components: regulatory and incidence level monitoring, and the Total Diet Study (TDS).
Regulatory monitoring includes sampling of domestic and international flesh and
processed produce. Factors considered by the FDA in plarming the types and numbers of
samples to collect include review of recently generated state and FDA residue data,

regional intelligence on pesticide use, the dietary importance of the food, information on

100

the amomt of domestic food and imported food that enters interstate commerce, the
chemical characteristics and toxicity of the pesticide, and the production volume and
pesticide usage patterns. Domestic produce, mostly raw agricultural produce, are sampled
as close as possible to the distribution system; import samples are collected at the point of
entry into U.S. commerce and analyzed as the unwashed, whole (unpeeled), raw
commodity (U .S.F DA 2000b). Sampled commodities are mostly “surveillance” types
which according to U.S. FDA (2000b) mean “there is no prior knowledge or evidence
that a specific food shipment contains illegal pesticide residues”. In instances when an
illegal residue is found or if there are otha pesticide residue problems, follow-up or
compliance samples are collected. Multiresidue methods (MRMs) are used to analyze for
pesticide residues.

Incidence/level monitoring is used by the FDA, complementary to regulatory
monitoring, “to increase FDA’s knowledge about particular pesticide/commodity
combinations by analyzing certain foods to determine the presence and levels of selected
pesticides” (U.S.FDA 2000b). The FDA uses statistically based monitoring surveys to
assess whether the data fiom regulatory monitoring are representative of the overall
residue situation for a particular pesticide, commodity or place of origin.

The market basket survey is carried out by the FDA for the Total Diet Study
(TDS), a major constituent of its pesticide and chemical contaminant monitoring
program. In conducting the TDS, foods from the supermarkets or grocery stores are
sampled four times a year, once from each of the four geographic regions of the country.
The four market baskets (each market basket a composite of like foods purchased in three

cities in a given region) is comprised of 285 foods that are representative of over 3,500

101

 

differ

13bit

different foods reported in the USDA food consumption surveys. Food is prepared to be
table-ready and then analyzed for pesticide residues by multi-residue methods. The levels
of pesticides found are used in conjunction with the USDA food consumption data to
estimate the dietary intakes of the pesticide residues (U.S.FDA 2000b, 2003). The
program is not established to develop a statistically valid cross-section of food
consumption in the U.S. and many of the newer reduced-risk pesticides are not yet
included in the analytical methodology.
3.2 Objectives

The objective of this section of the study is to assess the changes in the incidence
of residue detections of selected higher risk pesticides (anticholinesterase insecticides and
B2 carcinogenic fungicides) and their safer replacements in finit, vegetable and nut crops
since the enactment of the F QPA in 1996.
3.3 Methods
3.3.1 Survey and Emluation ofPa'ticide Raidue Databasa

The available pesticide residue databases were surveyed for comprehensiveness
and continuity of data over time. The PDP and the CA-DPR databases have the most
complete and comprehensive residue data over the time period of interest and were
selected for the analysis of the residue trends. The FDA ongoing market basket surveys
also provided additional useful confirmatory data.

Although assessing actual residue levels would be the most direct measure of
changing exposure and risk, there are difliculties in developing a single summary
measure for the varying residues detected in multiple samples. The residue levels do not

show a normal distribution, the median value is typically zero, and the mean is often

102

driven by one or more high values which are outliers and do not accurately represent the
dataset For this reason, the frequency of detections, expressed as the percentage of the
samples analyzed that contained the pesticide at or above the level of detection (LOD),
was calculated as the major indicator for trends in the occurrence of residues.

3.3.2 Pesticide Residue Trends

3.3.2.1 Individual Pesticide Residue Trends_

The annual CA-DPR residue databases from 1994 to 2006 were downloaded fi'om
the CA—DPR website (CA-DPR 2009). The PDP residue data were fiom the PDP Search
Utility containing searclmble data for pesticides and commodities for each year from
1993-2006 and was obtained fiom Roger Fry (USDA Agricultural Marketing Service,
Manassas, VA). The number of times a given pesticide was detected (reached the LOD)
was determined for each of the fresh fruits, vegetables and nuts in the survey. Grains,
meats, and processed foods were not included. The value for percent detects was
calculated based on the total number of detects and the total number of samples analyzed.
The annual PDP and CA-DPR percent detects were plotted for each pesticide for each
year fiom 1994 to 2006 and the trends analyzed and correlated to pesticide use and
regulatory history. The commodities sampled and analyzed each year vary for both the
databases, whichmeanthatacommodityanalyzedinone yearmay notbeanalyzedinthe
following year.

3 .3.2.2 Individual Pesticide Residue Trends with High Percent Detects

The pesticides (both conventional and reduced-risk) with %detects Z 10% and
with % detects Z 5% but < 10% at any point from 1994 to 2006 were identified and

were the focus for trend analysis. The percentage detects classifications were based on

103

the percentile ranking of all the compounds showing detects based on the PDP data.
Approximately 10% of the pesticides in the PDP database have exceeded the 10% detects
level at some time during the study period, and 20% have been within the 5% to 10%
detects range.

3.3.2.3 Resiere Trends for Pesticide Gm

The sum of all the percent detects for each group of the older pesticides (OPs,
NMCS, and the 323) was calculated for each year fi'om 1994 to 2006 both for the PDP
and the CA-DPR data. The overall percent detects were plotted and the trends analyzed.

3.3.2.4 Pesticide ResidzLe Detection FLegltemy in the FDA Tog] Diet SM (TDS)

The U.S. FDA publishes annual reports on the Total Diet Study (TDS) that
contain summary data for the frequency of occurrence of detectable pesticide residues
which are found in at least 2% of the food samples in the study. These data are collected
both for the diets of infants and toddlers, and for the rest of the U.S. population (termed
here “adults”). The results fiom 1995 to 2006 were evaluated for pesticides that have at
least five years of residue occurrence at the 2% or greater level. The trend in percent
occurrence for these pesticides were plotted, and analyzed for trends in comparison to

results fiorn the other databases.

104

3.4 Results and Discussion
3.4.1 Overall Residue Trends of Pesticide Groups

The occurrence of detectable residues for all pesticide groups (OPS, NMCS, B23
and reduced-risk compounds) vary considerably in the data taken from PDP (Figure 3.1).
This makes any trend analysis somewhat speculative. Considering the most recent results
fi'om 1999 to 2006, all three groups of older compounds do show a downward trend in
detections, but this conclusion depends heavily on the low level of detects observed in
2006. Additional data for more years would be needed to confirm these trends. A strong
downward trend would be expected for the anticholinesterases in view of the 50%
decrease in use of OPS and 70% decrease in use of NMCS found in Chapter 2. On the
other hand, only a modest decrease in residue detections would be predicted for the B2
fimgicides based on changes in use.

Surprisingly, the CA-DPR data do not confirm any decrease in residue detections
for these groups (Figure 3.2). No clear trend is evident in the data for either OPS or
NMCS fi'om 1994 to 2006, and there is a Slight increase in residue detection for the B23.
Also, the incidence of residue detections fiom the CA-DPR data is less than that fi'om
PDP by about 50%. The reduced-risk compounds have percent detection records fiom
only a few recent years and distinct residue trends cannot be determined although the
results again tend to be very variable and the percent detects for some individual
compounds are high, such as acetamiprid and imidacloprid where the detection rates are

as high as 20% to 25%.

105

lz,z.____ l - ,_ . _ n m___ a- _

Overall percent detects (PDP data)

 

 

35.0 ‘

 

30.0

 

 

25.0

20.0 +OPS

 

15.0

 

—O— 825
10.0 ,

 

5.0

 

 

 

 

0.0

 

s99“ «.999 996 «.991 99% 3999 1°°° 10°” 10$ 1°65 10°“ 1‘96

 

Figure 3.1. Residue detections for the OP, NMC and BZ pesticide groups based on

the PDP residue data.

 

Overall percent detects (CA-DPR data)

 

13.0
16.0 a, I ride—*4

As I / \
14.0 \ 1‘ ‘ . a-

12.0 — s- ‘x
10.0 ’4 2’ e—

I
8.0 ’ \ ’ ‘ev .0

 

 

 

 

 

 

—a— UPS

 

 

 

 

 

5.0 r—‘~

4.0 Tim—"Tr ‘
2.0 Y I-

0.0 i .1
S99“ 3996 «.996 «.991 «99% 3999 1‘90 '9‘)" 1°01 1°03 19°“ 196’

‘ jun?"- 3‘ - .- 32s

 

 

 

‘l"
.1
.4
T.
.l
.4

 

Figure 3.2. Residue detections for the OP, NMC and BZ pesticide groups based on

the CA-DPR residue data.

from the FDA’s annual Total Diet Studies (TDS) from 1995 to 2006 as provided in

A third source of information on trends in residue detection fi'equencies come

106

+Carmabates

 

/ .. I 6 “l -I- Carmabates

 

annual FDA reports (U.S.FDA 1995, 1996, 1997, 1998, 1999, 2000a, 2001, 2002, 2003,
2004, 2005, 2006). The trends in incidence of detects for selected pesticides is shown in
Figure 3.3 for the “adult” diets, and in Figure 3.4 for infant and toddler diets. The results
are for individual compounds that appear at least five times in the FDA data over this
time period. Clear post-FQPA trends for the adult diets are not clear except that iprodione
falls below the FDA’S 2% detects reporting limit after 2001 in keeping with the
regulatory history described for this compormd in Chapter 2. The data are clearer for the
infant and toddler diets where most compounds have downward trend over the post—
FQPA period with the exception of the NMC, carbaryl. Iprodione, methyl parathion and
dimethoate residue detects all decrease considerably, in keeping with their much reduced

use.

Frequency of Occurrence of Pesticide Residue in TDS Foods Other
‘ than Infant and Toddler Foods‘ (U.S. FDA)

 

-e—Acephate

+ Dimethoate

-I-Chlorpyrifos I
-,~— Methamidophos }

—,Ir—Iprodione

 

+Carbaryl

 

I 1995 1997 1999 7.001 1003 1005

*Pest icides with detections for 2 5 years

 

 

Figure 3.3. Frequency of pesticide occurrence in adult foods.

107

 

 

 
   

Frequency of Occurrence of Pesticide Residue in TDS Foods in Selected
Infant and Toddler Foods“ (U.S. FDA)
35 i
-I—Chlorpyrifos
30 ~ -
25 " ' +Dimethoate
20 - —
%
15 . _ -)t-Methyl
parathion
| 10 ., —
g 5 _ -~—Iprodione

i +Carba ryl
1995 1997 1999 200‘ 1003 1005

l

1 ‘Pesticides with detection frequencies of at least 2% for 2 5 years
Figure 3.4. Frequency of pesticide occurrence in selected infant and toddler foods.

 

Carbaryl and chlorpyrifos residues are still regularly formd even in 2006. The use
of these two compounds, although reduced, has not been eliminated and large amounts
are still applied in the U.S. based on the CLF data (Figures 2.7 and 2.11), so the regular
occurrence of measurable residues is not unexpected. The clear decline in residue
occurrences in the infant and toddler diet fits with one of the primary goals of FQPA to
specifically reduce exposure and risk in this group. However, it is interesting to note that
the fiequency of pesticide occurrences in the infant and toddler foods is still
‘ approximately twice that in the adult foods.

3.4.2 Individual Pesa'cides with High Percent Detects and/or Distinct Trends in
Residue Detection '

The percent detects for the individual pesticides (both conventional and reduced-

risk) have a wide range of values (0.0] to 26%) based on the PDP and the CA-DPR data.

The pesticides with percent detects Z 10%, and percent detects Z 5% but < 10% at any

108

 

point from 1994 to 2006 were identified as the greatest contributors to food residues and
were the main focus for trend analysis (Figures 3.5 through 3.6).

Individual pesticides fiom all the groups, except NMCS, are formd in the highest
percent detects category (%detects 2 10% at any point). The OPS in this highest
occurrence class include azinphos-methyl (Figure 3.5), chlorpyrifos (Figure 3.6) and
methamidophos (Figure 3.8), and the B23 include captan and iprodione (Appendix D).
Rather surprisingly in view of their low use rates, several reduced-risk compounds also
showed high residue detects. This includes imidacloprid (Figure 3.11), acetamiprid
(Figure 3.12); and cyprodinil, fenhexamid, and tebufenozide (Appendix D). The
pesticides that had percent detection between 5% and 10% include the OPS-acephate
(Appendix D), dimethoate (Figure 3.7) and methamidophos (Figure 3.8); B2-
chlorothalonil (Appendix D); NMCS-carbaryl (Figure 3.10), methomyl and oxamyl
(Appendix D); and the reduced-risk pesticides-azoxystrobin, methoxyfenozide and
spinosad Shown in Appendix D. The 5% detections for these pesticides were all from
periods after the FQPA was enacted except for dimethoate that had approximately 5%
detects only in 1994 and has not exceeded this level since then.

The high percent detects (>10%) for the conventional pesticides are often variable
and occurred in different years between 1994 and 2006. The detections for azinphos-
methyl, chlorpyrifos in the years pre-FQPA were consistent with the high usage of these
pesticides at that time. Methamidophos on the other hand, showed >5% detects despite
the steep decline in use due to cancellation of most if its uses in 1997. The higher levels
of residue detects for the 323 were fiom years both before and after FQPA and are

consistent with the relatively constant use of many of the B25.

109

Individual OPS showed the most distinct decline in residue detects compared to
other pesticides. Among these OPS are azinphos-methyl, methyl parathion, dimethoate,
methamidophos and methidathion. These pesticides were also among those with >5%
and >10% detects (at any point) except for methidathion.

3.4.2.1 Azithos-methgl

The percent detects for azinphos-methyl (AZM) Showed an increasing trend fiom
1994 to 1997 but this decreased fiom 16% in 1997 to 1% in 2003 based on the PDP data.
The CA-DPR residue data shows much lower percent detects values than that of the PDP
and no obvious trend with time (Figure 3.5). However, it is interesting to note that
azinphos-methyl is not among the FDA report on the frequency of occurrence of
pesticide residues although it is analyzed in the FDA total diet study. This means that the
residue occurrence is below the 2% limit set by the FDA and this low level of azinphos-
methyl residue is due to the different sample preparation used in the total diet study in
which food is prepared table-ready and then analyzed for residues. The decline in the
PDP residue detections corresponds well with the overall decreasing use trend based on
both national (CLF) and California (CA-DPR) data as previously shown in Figures 2.10.
The decline in the detection is attributed to clmnges in the use patterns and safety issues
of AZM. Worker safety and ecological effects were concerns in some parts of the U.S. in
the early 19905 and in 1999 the EPA took mitigation measures to address these concerns.
Cancellations and terminations of uses of AZM started in 1999 and final decision to
phase out all remaining uses of AZM by September 2012 are consistent with the

continuous decline in the detection of AZM residues.

110

 

Azinphos-methyl
18.0

15.0 1‘

iii: \

gen V W A

3 3.0 \ / X
W

 

 

 

 

 

 

 

 

 

 

32
0.0 T l I I I I I I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+PDP % detects +CA-DPR % detects

 

 

 

 

 

 

Figure 3.5. Percent detects for azinphos-methyl.

3.4.2.2 Chlorpyrifos

In the PDP national residue data, chlorpyrifos Shows a Slow decline in residues
since FQPA (Figure 3.6) from a transient peak at ~12% in 1996 to ~3% in 2006. This
corresponds reasonably closely to FDA Total Diet Study (TDS) results in Figures 3.3 and
3.4. These residue detection results also parallel the decreasing use trend for chlorpyifos
nationally as shown in the CLF use data (Figure 2.11). However, the CA-DPR residue
results are differnet. They show a Slight but steady increase in detects with time. This too
fits with the use data which did not Show the same decline in California that was seen
nationally (Figure 2.11). The national decline figures are attributable to the revision of
tolerances for several raw agricultural commodities in 1996 and the revocation of
tolerances for a number of uses in 2002 (U .S.EPA 2002a). There were also excessive
acute dietary risks for infants and children and nursing females from EPA studies, and
registrants agreed to eliminate use on tomatoes and restrict use on apples to address the

risk (U .S.EPA 2002b). Punzi (2005) presented data in a poster which has not been

111

published that tracked the changes in percent detects in the PDP program fiom 1994 to
2004 for chlorpyrifos on several individual crops. On apples, the percentage detects fell,
they were fairly constant on peppers and lettuce, and rose on peaches. This illustrates the
complexity of trend analysis over a variety of crops and agricultural production systems.
The decline in apple detects was steep from 25% in 1999 to <1% in 2002 and was
attributed to the restriction of chlorpyrifos applications to the prebloom period by EPA in

2000.

14.0
12.0 ‘
10.0
8.0
6.0
4.0
2.0

0.0 I I I I I T I I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

 

 

 

 

 

 

% detects

 

 

 

 

 

 

 

Year
+PDP % detects +CA-DPR % detects

 

 

 

 

 

 

 

Figure 3.6. Percent detects for chlorpyrifos.

3.4.2.3 Dimethoate

Dimethoate shows a decrease in residue detection from 4.7% in 1994 to 1.4% in
2006 based on the PDP data as Shown in Figure 3.7. This is parallel to the decline in use
based on both the CLF and the CA-DPR data (Figure 2.13). As the result of a
developmental neurotoxicity study that led to revised risk assesments, seven crops

(apples, broccoli raab, cabbage, collards, grapes, head lettuce, and spinach) were

112

identified as significant dietary risk contributors and these uses were cancelled in 2005

(U .S.EPA 2006), so a further decrease in dimethoate residues is to be expected in future

 

 

 

 

 

 

data.
Dimethoate
5.0
\
a W /\
g 3.0
s /
as 2.0
00 r i i i

 

 

 

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year
+PDP % detects +CA-DPR % detects

 

 

 

 

 

 

 

Figure 3.7. Percent detects for dimethoate.

3.4.2.4 Methamidoghos

The decline in residue detection of methamidophos (Figure 3.8) since 1999 is
attributed to the cancellation of almost all its uses on food crops, especially in 1997 when
Bayer Corporation, its technical registrant, voluntarily canceled all its uses except for
cotton, tomatoes (special local need only) and potatoes. This is also consistent with the
strong decrease in use as shown and discussed in Chapter 2. However, it is notable that
the slight decline in residue detects in the California data does not correlate well with the
extremely steep drop in its use over the same time period and very limited use on food
crops since 1999 (Figure 2.16). The reasons for this are unclear. These residues
presumably were fiom the few remaining uses of methamidophos (eg. potatoes and

tomatoes).

113

 

Methamidophos

 

15.0

.:. /\/ \—/‘\
2:3 Wee

' h I l r I T

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

 

 

 

% detects

 

 

 

 

Year
+PDP % detects +CA-DPR % detects

 

 

 

 

 

 

 

Figure 3.8. Percent detects for methamidophos.

3.4.2.5 Methyl parcdhdon

The decline in the percent detections of methyl parathion is the most Significant
and continuous among the other pesticides (F igrne 3.9). Although the residue detects
were never very high, the PDP percent detects in 1996 were ~3% and fell to zero by
2004. Dietary concerns and occupational risks were the main driving forces in the
voluntary cancellations of many of its uses that started in 1997 as described previously in
Chapter 2. The use trends for methyl parathion do not follow the same track to zero as the
residue detects (Figure 2.17) because the cancellations focused on those uses that left the
highest residues in finits and vegetables and those uses with low levels of dietary residue

levels were left intact. Thus there is continued use but much lower dietary residues.

114

 

Methyl parathion
4.00

3.00 V’\ A
2.00

1.00 \7

000 RM M

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

+PDP % detects +CA-DPR % detects

 

 

 

% detects

 

 

 

 

 

 

 

 

 

 

 

Figure 3.9. Percent detects for methyl parathion.
3.4.3 Unexpected Residue Trends

The F QPA and other regulatory actions mostly address the conventional
pesticides that are of the greatest human health and ecological concern. These pesticides
are expected to decline both in the use and the detected residues. This in fact is true for
most of the pesticides considered in this study but unexpected trends were also observed
in some of the OPS, the NMCS and the reduced-risk compounds. Among the OPS, the
CA-DPR percent detects for chlorpyrifos Show a slight increase over the years contrary to
the declining trend based on the PDP data. The NMCS in general do not Show distinct
downward residue trends, e.g. carbaryl as shown in Figure 3.10, despite Showing the
highest declines in use. The reasons for this are unclear and merit further study. The OPS
were the first focus of the EPA following the enactment of the F QPA and attention only
turned to the carbamates later, so many of the regulatory actions for the carbamates have

been quite recent. Although the EPA identified a common mechanism of toxicity for the

115

 

Carbaryl

 

 

60 A /\
° J
g: . 1M

0.0 T I I T I I I
1990 1992 1994 1996 1998 2000 2002 2004 2006

 

 

 

 

 

Year

 

-e— PDP % detects +CA-DPR % detects

 

 

 

 

 

 

Figure 3.10. Percent detects for carbaryl.

carbamates in 2001, the preliminary cumulative risk assessment was published in 2005
and the revised cumulative risk assessment for the carbamates, taking into account recent
regulatory changes, was issued for comment late in 2007. Many uses of carbaryl,
carbofuran and methomyl were only canceled or modified in the period fiom 2005 to
2007. Further reductions in use and residues may Show up in the future, but the
cumulative risk assessments indicate that as a group the carbamates are now not of
dietary concern if these cancelations and use changes are included. The dietary risks for
the individual carbamates generally were below the EPA’S level of concern and this
conclusion was in part based on the rapid reversibility of inhibition of cholinesterase by
carbamates compared to the CPS. Also, fewer carbamates than OPS are included in the
cumulative risk assessment, and there are fewer individual chemicals to fill the carbamate

cumulative risk cup. However, despite the later focus on the carbamates the data from

116

Chapter 2 (e.g. Figure 2.1 and data for individual compounds), Show that the use of
NMCS has been declining steadily since the mid-19908, before the passage of F QPA.
Several of the reduced-risk pesticides have high level of percent detects (>10%)
and in some case >20% as shown in Figure 3.11 for imidacloprid and in Figure 3.12 for
acetamiprid, which is unexpected since the use rates of these chemicals is generally
much lower than that of the OPS, NMCS and B2 fungicides (Figures 2.28 and 2.29). In
keeping with this observation, Punzi (2005) noted that imidacloprid was detectable in
almost 80% of the samples of peppers analyzed in the PDP program in 2003 and 2004.
These high rates of reduced-risk compound detection may be attributable to several
factors. Many of the reduced-risk compounds are now widely used on fruits and
vegetables because of their low dietary risks. For the same reason, legal applications can
be made close to, or even alter, harvest potentially leading to higher residues. Some of
these pesticides are also systemic (e.g. the neonicotinoid inseticides such as imidacloprid
and the strobilurin fungicides) and Spread through the plant tissues unlike other pesticides
that stay on or near the surface and would be removed if samples are washed and peeled
prior to analysis as in the PDP methodology (Punzi et al. 2005). The systemic reduced-
risk compounds therefore tend to leave higher residues at harvest which are not removed
before analysis. One factor that is probably not involved is the possibility that the LODs
are lower for these newer compounds than the older conventional ones. An examination
of the LODs in the PDP analytical program did not reveal any obvious trends in this

direction.

117

 

Imidacloprid

30.0
25.0 N

20.0 /

15.0

 

 

 

 

 

% detects, PDP

10.0

 

5.0
0.0 . r”

Y I I I

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

 

 

 

 

Figure 3.1 1. Percent detects for imidacloprid.

 

Acetarniprid

25.0

 

 

n. 20.0
D

a. \

£150 \

i 10.0

.2 \
5.0

0.0 I I I I I I I r
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

 

 

 

 

 

 

Year

 

 

 

Figure 3.12. Percent detects for acetamiprid.

3.4.4 Pesticide Residue Databases and T rend Analysis
Despite the trends with selected OPS described above, overall the PDP percent

detects do not Show distinct residue detection trends for most of the pesticides and are

118

1 /_

 

quite variable fiom year to year in many cases. This could be due to differences in
sampling methods, changes in the use patterns for the pesticides, and changing LODS in
residue analysis. The variability in the residue detects trend is consistent with Punzi’s
study on the percent detects of chlorpyrifos on apples and dimethoate on spinach using
the PDP residue data that showed variation in the residues with different LODS (Punzi
2005). In another study by Punzi et a] (Punzi et al. 2005), where the overall percent of
samples with detects (65% of which were fiuits and vegetables) decreased fiom 1993 to
2003 based on the PDP residue data, noted that varying groups of commodities are
analyzed every year and different pesticides measured on each commodity. On the other
hand, the trend in the residue detects based on the CA—DPR data are more consistent,
which implies more uniform monitoring and perhaps sampling methods but with
relatively very low detects. Both the PDP and the CA-DPR databases residue data are
useful for the purposes for which they were established and have been of tremendous use
especially in dietary risk assessments. However, these databases are not set up for trend
analysis, hence the variabilities and inconsistencies of residue data over the years.

The sampling procedures vary for each residue database. The PDP randomly
samples commodities using a statistical design to obtain a statistical representation of the
U.S. food supply. The CA-DPR also employs random sampling of surveillance
commodities. The FDA samples individual lots of domestic and imported foods;
imported samples are collected at the point of entry while the domestic samples are
collected as close to the point of production in the distribution system (U .S.FDA 2003).
Although statistical random sampling is done, the commodity or crops sampled at

different times still vary depending on factors such as production volume, dietary

119

importance, and pesticide toxicity among others as well as the information/data priorities
set by EPA as in the case of the PDP. These lead to inconsistencies in the commodities
sampled each year and thus they do not Show continuity over time.

The differences in the limits of detection (LODS) fi'om the use of different and
increasingly sensitive analytical instruments are another factor that contributes to the
variability in residue detections. The PDP, the CA-DPR and the FDA use various
methods to analyze for pesticide residues in food, e.g. multi-residue and single residue
methods. These methods vary in their sample preparation and the analytical instruments
used in the residue analyses and have different LODS. The EPA defines LOD as “the
lowest concentration that can be determined to be statistically different fiom a blank
(negative control sample)” and assigns “non-detects” (NDS) to samples that “do not bear
at or above the LOD” (U .S.EPA 1998). Continuous testing of new technologies and
development of new techniques are being done by program scientists to improve the level
of detection according to PDP (U .S.DA-PDP 2006b). More advanced instruments have
lower LODS and are capable of detecting very small residue concentrations, thus
resulting in more residues detected. Although this is certainly likely to be a factor over
time, its actual impact on the percent detects is less clear. A study by Punzi (2005)
indicated that variations in the LODS as high as 10-fold for the same compound between
different laboratories conducting residue studies for PDP often did not greatly change the

percent detects that were obtained, with an estimated maximum 2-fold increase.

120

3.5 Conclusion

The OPS showed an overall decrease in residue detection fiequency in accord with
their declining use as intended by regulations instituted under F QPA although the data
were often quite variable. The downward trend in residues was particularly clear with
some individual compounds such as azinphos-methyl and methyl parathion that have
been subjected to the most rigorous regulation. The residue detection frequency was also
variable for the B2 frmgicides and they did not generally Show a strong decline in either
the use or residue trends. The NMCS Showed considerable variability in the residue
detections but no clear downward trend. This does not correspond to their rapid decline in
use. It is unclear why this should be. The record for residue detections with the reduced-
risk pesticides is brief, and for several the detection rates were low and variable. This
made establishing a trend difficult. Some of these pesticides, however, showed
unexpectedly high percent detects, e. g. imidacloprid, acetamiprid, tebufenozide,
cyprodinil and fenhexamid. These detections could be due, at least in part, to the systemic
properties of some of these pesticides particularly those with considerable use on fruits
and vegetables, and to applications that are made close to harvest.

Limited data from the FDA’S Total Diet Study suggest that residue reductions in
the diets of infants and toddlers for pesticides with the most fiequent detection patterns
were greater than those in the diets of older children and adults, and this would be in
agreement with one of the primary goals of F QPA.

The residue databases are set up according to the requirements and needs ofthe
regulatory agencies and these apparently do not include a primary focus on trend

analysis. Establishing pesticide residue trends is therefore diffith because of the

121

variability in sampling procedures and the types of commodities sampled each year.
Innovations in instrumentation have led to considerably higher sensitivity in residue
determinations and the consequent lowering of LODS over time potentially increases the
number of detections which would tend to confound trend analysis based on the
percentage of samples containing a residue above the LOD. With fairly modest
modifications, these databases, particularly that of the PDP, could be utilized for
purposes other than those for which they are established at present. To allow residue
trends, and therefore dietary risk trends, to be assessed over time, more consistent and
continuous sampling of selected important dietary commodities would be required. This
expansion would require an increased budget but it would greatly enhance the current
usability and Significance of these databases. With more consistent sample analysis and a
more comprehensive and consistent residue databases, dietary risk trend analysis could be
accurately determined. Most important, this would allow the direct assessment of the
impact of major regulatory actions such as those initiated under the FQPA and would
allow adjustments to be made, if necessary, to assrne that their goals of risk management
are being achieved. In a recent review by the EPA’s Office of the Inspector General of
the EPA Office of Pesticide Program’s implementation of FQPA, criticisms were made
of the lack of measurement of direct impacts and outcomes. In response EPA-OPP stated
that “OPP is in agreement that a scientifically—sound, risk-based measure would provide a
more accurate and effective indicator” but that “despite considerable effort, OPP has been
unable to develop a scientifically sound measure that uses available data and can be

implemented efficiently” (U .S. EPA, 2006f). This clearly underlines the current difficulty

122

in establishing reliable data and approaches to conduct comprehensive risk assessments

on pesticide residues in the U.S. diet.

123

BIBLIOGRAPHY

CA-DPR. 2001. Regulating Pesticides: The California Story. A Guide to Pesticide
Regulation in California 2001. California Department of Pesticide Regulation.
Report. www.cdprca.gmi/docs/pressrls/dprguide/dprguidepdf

CA—DPRResidue Monitoring Program. Annual Residue Data. California Department of
Pesticide Regulation.
http:Huuwcdpnca.f.10\'.v"docs“en forceI’rcsiduer’rsmonmnu.htm

Punzi J. 2005. Residues of Organophosphate Pesticides from the U.S. Department of
Agriculture’s Pesticide Data Program 1994-2003 [Poster]. St. Petersburg Beach.

Punzi J, Lamont M, Haynes D, Epstein RL. 2005. USDA Pesticide Data Program:
Pesticide Residues on Fresh and Processed Fruit and Vegetables, Grains, Meat,
Milk and Drinking Water. Outlooks on Pest Managementzl3 1-137.

U.S.DA—PDP. 2006a. Pesticide Data Program Annual Summary Calendar Year 2004.
Washington, D.C.: United States Department of Agriculture-Pesticide Data
Program. Report. vwnvams.usda.gov/science/pdp/Summary'ZOOdif

U.S.DA-PDP. 2006b. Pesticide Data Program Annual Summary, Calendar Year 2006.
Washington, D.C.: U.S. Department of Agriculture Pesticide Data Program.
Report. http://wwwams.usda.g0v/science/pdp/Summarv2006.pdf

U.S.EPA. 1998. Assigning Values to Nondetected/Nonquantified Pesticide Residues in
Human Health Dietary Exposure Assessments (1 1/30/98 Draft). U.S.
Environmental Protection Agency. Report. http://wwwepagov/EPA-
PEST/1998/December/Day-04/6025.pdf

U.S.EPA. 2002a. Acephate, Anritraz, Carbaryl, Chlorpyrifos, Cryolite, et al.; Tolerance
Revocations. U.S. Environmental Protection Agency. Report. Federal Register/
Vol. 67, No. 147. Rules and Regulations.

U.S.EPA. 2002b. Interim Reregistration Eligibility Decision (IRED)-Chlorpyrifos.
Washington, D.C.: U.S. Environmental Protection Agency. Report.
http://www.epagovflresticides/reregistration/REDs/chlorpyrifos iredpdf

124

U.S.EPA. 2006. Interim Reregistration Eligibility Decision (IRED)—Dimethoate.
Washington, D.C.: U.S. Environmental Protection Agency. Report.
http://vmw.epagoxz/oppsrrd l r’REDs/di methoate_ired.pdf

 

U.S.FDA. 1995. Food and Drug Administration Pesticide Program: Residue Monitoring
1995. U.S. Food and Drug Administration. Report.
http://wwwcfsan.'fda.gov/~acrobat/pes95respdf

 

U.S.FDA. 1996. Food and Drug Administration Pesticide Program: Residue Monitoring
1996. U.S. Food and Drug Administration. Report.
http://wv~w.cfsan.fda.gov/~acrobat/pes96rep.pdf

 

U.S.FDA. 1997. Food and Drug Administration Pesticide Program: Residue Monitoring
1997. U.S. Food and Drug Administration. Report.
http://wmvcfsan.fda.gov/~acrobat/pes97rep.pdf

 

U.S.FDA. 1998. Food and Drug Administration Pesticide Program: Residue Monitoring
1998. U.S. Food and Drug Administration. Report.
http://vmw.cfsan.fda.gov/~acrobat/pes98reppdf

U.S.F DA. 1999. Food and Drug Administration Pesticide Program: Residue Monitoring
1999. U.S. Food and Drug Administration. Report.
http://wwwcfsan.fda.gov/~acrobatLpes99rep.pdf

U.S.FDA. 2000a. Food and Drug Administration Pesticide Program: Residue Monitoring
2000. U.S. Food and Drug Administration. Report.
http://wuwcfsan.fda.gov/~acrobat/pesOOrcp.pdf

U.S.F DA. 2000b. U.S. Food and Drug Administration Pesticide Monitoring Database
User's Manual. U.S. Food and Drug Administration. Center for Food Safety and
Applied Nutrition. Nov 2005.
http://uwwcfsan.fda.gov/~dms/pcs99usr.html#Background

U.S.FDA. 2001. Food and Drug Administration Pesticide Program: Residue Monitoring
2001. U.S. Food and Drug Administration. Report.
http://wwwcfsanfda. gov/~ac robat/pcsOl reppdf

U.S.F DA. 2002. Food and Drug Administration Pesticide Program: Residue Monitoring
2002. U.S. Food and Drug Administration. Report.

http://wwwcfsan.fda.gov/~dms/pesO2rep.html

 

125

U.S.F DA. 2003. Food and Drug Administration Pesticide Program Residue Monitoring
2003. Food and Drug Administration. Report.
http://vtwwcfsan.fda.go\!/~acrobat«/pes03reppdf

U.S.FDA. 2004. Food and Drug Administration Pesticide Program: Residue Monitoring
2004. U.S. Food and Drug Administration. Report.
http://uuwvcfsan.fda.goxl'/~dms/pcso4rep.html

U.S.FDA. 2005. Food and Drug Administration Pesticide Program: Residue Monitoring
2005. U.S. Food and Drug Administration. Report.
http://wwnvcfsan.fdagov/«dms/pesOSrep.html

 

U.S.FDA. 2006. Food and Drug Administration Pesticide Program: Residue Monitoring
2006. U.S. Food and Drug Administration. Report.
http://wuwcfsan.fda.gov/~dmsfigcs06rep.html

 

126

CHAPTER 4
IMPLICATIONS OF THE FQPA FOR DIETARY RISK: A CASE STUDY

4.1 Pesticide Risk Assessment

The U.S. Environmental Protection Agency (EPA) conducts pesticide risk
assessment as required by the FQPA. The process involves four major steps: hazard
identification, dose-response assessment, exposure assessment and hazard
characterization (Figure 4.1). Hazard identification involves review of toxicological
information to determine the harmful effects a chemical might cause. In the dose-
response assessment step, the dose level at which the effects occurred, and the population
group in which the effects are most likely to be exhibited are identified. The exposure
assessment step evaluates the amount of pesticide to which an individual is exposed from
oral, dermal, and inhalation routes of exposme. The final step in the process is the
characterization of risk. This is the process of combining hazard, dose-response, and
exposure information to describe the overall magnitude of the public health impact,
reviewing the assessment for quality and consistency and finally, setting acceptable levels
of risk (U .S.EPA 1999).

The dietary exposure assessment of pesticides is an integral part of and is equally
important as the other components of the risk assessment process wherein both acute
(contact with a substance over a short period of time) and chronic (contact over a long
period of time) exposmes are assessed. Major inputs in conducting the dietary exposure
assessment are pesticide residue levels and food consumption data, corrections for the

percent of the crop treated with the given compound, residue modifications during

127

 

 

Hazard Identification
What health effects can be

caused by the pesticide?

 

 

 

 

  
  
 

 

  

t v
Exposure Dose-Response
Assessment Assessment
How much of the pesticide What are the health effects
are people exposed to at different exposure levels?
through food, drinking
water, and various non—

 

 

 

1

Risk Characterization
What is the extra risk of health
problems likely to result from
a pesticide in the exposed
population?

 

   

 

 

 

Figure 4.1. The risk assessment process (U .S.EPA 1999).
food processing (processing factors), and other data that might influence residue levels.
The EPA uses a tiered approach consisting of four tier levels to obtain increasingly more
realistic exposure assessment values (Table 4.1). The initial screening of pesticides is
done at the first tier level. This is the worst case scenario and uses the pesticide tolerance
as the assumed residue level and a conservative assumption of 100% crop treated. A
considerable overestimation of actual pesticide residue is expected fi'om these very

conservative assumptions because, according to Suhre (2000), they reflect the maximum

128

Table 4.1. The EPA’s tiered approach for exposure analysisl

 

 

 

 

 

 

 

 

 

Tier Acute Exposure Chronic Exposure Result

Tier 1 - Tolerance-level residues - Tolerance-level - Tolerance value used in
- Assume 100% crop residues risk assessment
treated - Assume 100% crop

treated

Tier 2 - Tolerance-level residues - Tolerance-level - For acute assessment,
(or highest residue found residues tolerance or field trial
in a field trial) for items - Incorporate % crop value used in risk
consumed as single- treated information assessment
servings - For chronic assessment,
- Average field trial multiply residue level by
residues for blended % crop treated (e.g., 10
commodities (e.g., wheat) ppm x 20%CT=2ppm)
- Assume 100% crop
treated

Tier 3 - Use probabilistic - Use average of - For acute assessments,
techniques crop field trial use a distribution of
- Use distribution of crop residues or residues, incorporating %
field trial residues for monitoring data for crop treated data (e.g., if
items consumed as single blended 20% of the crop is
servings commodities treated, there will be an
- Use average of crop field - Use crop treated 80% chance of choosing
trial residues or 95th information zero residue)
percentile from - Use processing - For chronic
monitoring data for factors assessments, multiply the
blended commodities - Use refined field trial or monitoring
- Use % crop treated livestock dietary residue value by the %
information (as part of burdens for meat, crop treated (e.g., 8 ppm
probabilistic techniques) milk, poultry, and x 20%CT=1.6 ppm)
- Use processing factors eggs residue values

Tier 4 - Market basket survey - Special studies - Allows additional
(single-serving-sized (market basket refinement; produces
samples) surveys, consumer more realistic exposure
- Use processing factors processing studies, estimates
or other studies residue degradation

studies, etc.)

 

I EPA ’s Risk Assessment Process for Tolerance Reassessment. U.S. Environmental Protection

Agency. Stafl Paper #44. October 8, I 999

application rate and shortest pie—harvest interval. If the risks calculated from the initial

screening are acceptable, no further analysis is required, but if the tier 1 results are

unacceptably high, more refined data would be used and higher tiers of analysis would be

129

 

employed. The level of resources and data needed to refine exposure estimates increase
with each tier (U.S.EPA 2000a). In tier 2 acute analysis, field trial residues are used
with the tolerance level retained for chronic exposure but a correction for percent crop
treated is included. Tier 3 involves the use of probabilistic techniques (Monte Carlo
analysis) and residue distributions for acute exposme. Even more refined data such as
market basket sm'vey data and special residue studies are used in the tier 4 analysis.
4.2 Dietary R'uk Assessment Computer Models

Requirements by the F QPA to conduct cumulative risk assessment (in which risks
from all compounds having a common mode of action are summed) and aggregate risk
assessment (where exposure from all sources (dietary, water and residential) are summed)
presented many technical challenges to the EPA and resulted in the development of three
software programs for conducting such complex assessments, i.e. Dietary Exposure
Evaluation Model (DEEM), LifeLine, and Cumulative Aggregate Risk Evaluation
System (CARES). These competing programs all address these challenges but in
somewhat different ways and all are used by regulators. These programs use probabilistic
methods of amlysis which give distributions for population exposure and for food
consumption and thus provide more realistic results. The deterministic (single value)
approach is the traditional method of conducting risk assessment. It is based on average
diets and ‘worst case’ single estimates of potential exposure and provides no
quantification of the proportion of the population at risk (Petersen 2000). Deterministic
methods are now being supplemented with probabilistic models to better inform
quantitative risk management decisions (Harris et al. 2001). A probabilistic method of

analysis is defined as an analysis in which frequency (01' probability) distributions are

130

assigned to represent variability in quantities having a distribution as the form of output,
making it possible to estimate the proportion of the population at risk (Cullen and Frey
1999; Kempton 2001). It employs the Monte Carlo simulation approach which is used for
generating representative distribution of values for each of the inputs (residue levels and
dietary intakes) in a generic exposure (or dose) equation to derive an output distribution
of exposure (or doses) in the population (Cullen and Frey 1999; U.S.EPA 1997).

4.2.1 Dietary Exposure Evaluation Model (DEEM)

The Dietary Exposure Evaluation Model (DEEM) was developed by Novigen
Sciences, Inc. (now Exponent, Inc.) as a model for conducting Monte Carlo dietary risk
assessments. It contains food consumption data fiom the USDA 1989-1992 and 1994-
1996 Continuing Surveys of Food Intake by Individuals (CSFII) translated into food
ingredients using the model’s translation database. The consumption surveys were
conducted by personal interviews of statistically selected individuals who were asked to
recall everything they ate and drank in the previous 24 hours. DEEM is composed of
four modules: the main DEEM module, the Acute and the Chronic analysis modules and
the RDF gen module. The dietary exposme assessment models based on the CSFII are
provided by the Acute and the Chronic modules. The RDFgen module automates single
analyte and cumulative residue distribution adjusfinents and the creation of summary
statistics and Residue Distribution Files based on the USDA Pesticide Data Program
(PDP) monitoring data or user-provided residue data. The main DEEM module is used to
create and edit residue files for specific chemical or cumulative applications and to
launch the Acute, Chronic and RDFgen modules (Kidwell et al. 2000). DEEM uses the

distribution of the daily consmnption data to calculate acute dietary exposures. A simple

131

distribution approach is used for non-Monte Carlo application, and the probabilistic
method is provided by Monte Carlo applications. Chronic exposures “are typically
derived as point estimates using average consumption and residue estimates” (Barraj et
al. 2000). The mean food consumption files are fixed data sets included in DEEM and are
unalterable (Kidwell et al. 2000). They are pie-calculated on a per capita basis for each
raw agricultural commodity (RAC) and food/form reported in the CSFII surveys (Barraj
et al. 2000). DEEM’s chronic exposure is expressed either as percent reference dose
(%Rfl)), margin of exposure (MOE), or as a cancer risk estimate, depending on the
toxicological information provided by the user. The reference dose (RtD) is “an estimate
(with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the
human population (including sensitive subgroups) that is likely to be without an
appreciable risk of deleterious effects during a lifetime” and is determined by using the

equation (Barnes and Dourson 1988; U.S.EPA 1993):

NOAEL =No Observed Adverse Eflect Level
RjD = NOAEL / (UF x MF); UF= Uncertainty Factor
MF=Modijinng Factor

The MOE is the raio of the highest dose that is fiee of toxicity to animals (e.g. NOAEL)
and the human dietary exposure level (U .S.EPA 2000a) and is expressed as:

MOE = NOAEL /dietary exposure
The MOE in effect is the margin between human exposure and the safe dose for animals
and represents a “safety” factor. The user has the option of specifying which of the
measures to use. The chronic module uses a “data base of pre-calculated per-capita means
of food consumption data (g/kg—bw-day) for each raw agricultural commodity (RAC) and

food form reported in the CSFII surveys” (Barraj et al. 2000) to calculate the chronic

132

exposures. The per capita daily mean exposures are calculated for each of the standard
populations and the per capita exposure for all the standard population groups are
reported directly, along with the risk estimates based on the user-specified endpoint.
DEEM is the default program used by the EPA to assess pesticide dietary risks since
approximately 1998.
4.2.2 LifeLine

The LifeLine model was developed by the Hampshire Research Group (now
managed by The LifeLine Group) under a cooperative agreement with the EPA and the
USDA “to develop publicly accessible risk assessment software for a wide range of
anticipated users” (U .S.EPA 2004). LifeLine uses a probabilistic model for the
characterization of pesticide risk from dietary, residential and drinking water related
sources as well as population-based aggregate and cumulative exposure. It provides a
powerful tool to understand the relative contributions of these sources and how they vary
across the individuals’ lives, and it estimates the history of each individual’s exposures to
a pesticide from all sources; the patterns of exposure for a population over time; the
distribution ofexposure across a population at any age and season; and the corresponding
risks for non-cancer toxic effects associated with those exposures, as well as the lifetime
cancer risk (LifeLine 2002a, 2007). The software models exposure for each day of an
individual’s life from a simulated population (140,000) across their lifetime (0 to 85
years). LifeLine generates exposure files for each simulated individual, fiorn which
exposure estimates are extracted for the age and gender based subpoprrlations. Exposure
assessmentfiompssficidesmclrflesmemeofmsiduedmmocessmgfacmmmd

probability of use that are integrated to generate a complete set of potential residues. This

133

set of residues is then used to generate residues for the food as consumed. The dietary
exposure calculation uses a recipe file or a translation file that “provides on a
proportional basis, the ingredients (specific food forms of commodities) in a food that
was reported to be eaten in the dietary consumption survey” (LifeLine 2002b). It
identifies the mass contribution of the food’s ingredients, and the distribution of residues
from the food as consumed is calculated using the residue distributions fiom the
ingredients. LifeLine is also used by EPA in conducting dietary risk assessment of
pesticides.

4.2.3 Cumulative Aggregate Risk Evaluation System (CARES)

The Cumulative Aggregate Risk Evaluation System (CARES) is a program that
accommodates both aggregate and cumulative risk assessment analyses and can model
exposure from various sources such as dietary, residential and drinking water. It uses the
deterministic approach to calculate risks for tier 1 analysis and employs the probabilistic
method using Monte Carlo simulation for higher tiered analysis. CARES randomly
generates a reference population (100,000 individuals) based on the 5 million individuals
from the 1990 U.S. Census Public Use Micro Data Sample (PUMS) dataset and a 365-
day exposme profile is created for each individual. The reference population is then
“matched” with other databases (e.g. CSFII) to obtain other variables needed in the
exposure assessment. The unique feature of CARES is the ability to identify and
statistically describe specific exposure contributions across the matrices of source, route,
and population sub-group and this includes conducting a comprehensive suite of
contribution, sensitivity and other data analysis (ILSI 2003). CARES is now maintained

by the International Life Sciences Institute (ILSI) but was originally funded and

134

developed by member agrochemical companies of CropLife America to conduct complex
exposure assessments and to address FQPA mandates for short-term, intermediate
duration, and lifetime food, drinking water and residential and aggregate and cumulative
exposure and risk calculations (U .S.EPA 2004). There is no final version of CARES yet
but there have been several evaluation versions released. Computer bugs and glitches
have been discovered in previous versions of CARES; hence it is continuously
undergoing development. The development of CARES temporarily ceased after its
transfer to ILSI due to lack of funding. The EPA lists CARES among the models “in
common use in EPA’s Office of Pesticide Program” (U .S.EPA 2007b) in addition to
DEEM and LifeLine.
4.2.4 Comparison of due DEEM, LifeLine and CARES Program

The EPA Scientific Advisory Panel (SAP) (U .S.EPA 2004) compared the three
risk assessment models using a common data set for a hypothetical pesticide and
identified various factors through which the models differ from one another. Differences
between the results from the three programs were relatively minor. Design assumptions,
data sources and databases were identified as the variations associated with the dietary
modules which may lead to differences in estimated exposures (U .S.EPA 2004). These
factors are shown in Table 4.2 followed by individual discussion of the factors based on

the SAP report.

135

Table 4.2. Differences between DEEM, LifeLine and CARES (U .S.EPA 2004).

 

 

 

 

 

 

 

 

 

 

Factor DEEM LifeLine CARES
Reference Population CSFII Survey Natality (NCHS) Census (PUMS)
Binning Random (2 Day Random (Age, Gower
Methodology Diaries) Season) Dissimilarity

Index
Reference Population CSFII Normalized LifeLine (N HANES) CSFII
Bodyweight Normalized
Model Weight CSF II Survey Equal Weights CARES
(Random) (Stratified)
Modeled Population US Population US Population US Population
(N atality, Mortality)

 

 

4.2.4.1 Reference Population

LifeLine models the “starting population” when individuals are “born” based on
natality data fiom the National Center for Health Statistics (NCHS). The modeled
individuals then grow, move to new areas, age and die. According to the EPA, “LifeLine
tracks each day in each individual’s life and develops an internally consistent exposure
history based on cross-linked databases such as the U.S. Census Bureau’s American
Housing History, National Home and Garden Pesticide Use Survey, etc.” (U .S.EPA
2004). DEEM uses all individuals in the CSFII in its exposure calculations. CARES on
the other hand uses a reference p0pulation (100,000 individuals) fiom a 5% Public Use
Microdata Sample (PUMS) file from the U.S. Census.

4.2.4.2 Blning Methogology

LifeLine groups individuals into “bins” by age and season. According the SAP
report (2004), “to generate a series of diets for an individual over that individual’s
lifetime, LifeLine matches (and draws from) only those individuals which have similar
ages and only fiom those consumption diaries that arose fiom the specific season of

interest”. CARES uses sinrilar binning method with some additional criteria and the

136

GOWER dissimilarity index is used to create the matches. DEEM uses the CSFII food
diaries for individuals with reported two days of consumption.

4.2.4.3 Reference Population Bodyweights

In LifeLine, bodyweiglrt is determined through correlation of the individual’s
height and age. This allows for the body weight and the surface areas of an individual to
be “kept internally consistent across an individual’s entire life” (LifeLine 2002b).
LifeLine obtains the amount of food consumed from the CSFII. DEEM and CARES
calculate exposure from the product of consumption (based on the CSFII) and the
pesticide residue concentration in that food.

3.2.4.4 Model Weights

DEEM uses the CSFH weights directly to reflect the U.S. population. In CARES
the reference population is weighted to produce a population similar to that of the U.S.
population (U .S.EPA 2004). The LifeLine model is “self-weighting in the sense that
individuals are “born” on the basis of (and in direct proportion to) natality data from the
National Center for Health Statistics (NCHS) National Health and Nutrition Examination
Surveys (NHANES) and DEEM uses CSFH sampling weights directly which, in turn,

reflect the U.S. population” (U.S.EPA 2004).

Other than this EPA model study, there appears to be nothing published regarding

the results provided by the different exposure and risk assessment programs that were

developed in response to F QPA.

137

4.3 Dietary Risk Assessment Using Tiered Analysis
Although the results of the EPA dietary risk assessments have often been the
subject of public discussion, little has been published that examines the effects of the tier
analysis system or of different risk assessment models on risk estimates. In one of the few
published studies on the tiered system of dietary exposure analysis, Wright et al. (2002)
showed that estimated exposrnes to the OP insecticide, chlorpyrifos, from the highest tier
level were much lower than from the tier 1 (tolerance level) exposure assessment. Oliver
et al. (2000) reported a significant decrease in the estimated acute and aggregate dietary
risks of chlorpyrifos using typical refinements at higher tiers of analysis (Oliver et al.
2000)
4.4 Objectives
The risk assessment process has increased in complexity and improved in realism
tremendously in the past decade and has evolved fiom the use of the deterministic
approach to probabilistic methods of analysis. The probabilistic approach is widely used
in the U.S. and Europe and has been employed in various studies to determine exposures
to pesticides. However, little has been published that shows the impact of the F QPA on
pesticide exposure and dietary risk, or the variability in risk estimates that arise from the
different assumptions involved in the EPA’s tiered approach to risk assessment, or from
the use of different risk analysis programs. This study therefore aims to:
1. Assess the clmnge in dietary exposures and risks through replacing an
older, higher risk pesticide with a safer replacement compound registered
by IR-4 on selected crops as a typical example of such changes made in

response to FQPA.

138

2. Evaluate and compare the dietary exposure estimates at the different tier
levels using standard risk assessment models.
3. Evaluate and compare the dietary exposures using different dietary risk
assessment models.
4.5 Methods
4.5.1 Selection of a Pesticide-Crop Combination for the Case Study
The selection of the pesticides and the crop for the dietary exposure assessment
was based on the following criteria:

1. Crop was frequently treated with anticholinesterases or 823 in its
production.

2. The pesticide(s) have a reasonably continuous record of use and residues
in databases from before the passage of F QPA to present;

3. Altermrtive apparently safer pesticide(s) were registered by IR-4 and
were used to directly replace the older compound(s);

4. Crop makes a measurable contribution to the diet and the risk can be
assessed using newer risk assessment programs, with a focus on infant-
child diets and other sensitive populations.

After extensive analysis, which revealed very few situations that met all these criteria, the
use of the fungicides iprodione (BZ carcinogen) and fludioxonil on peaches and other
stone fruit satisfied the criteria and was selected as the case study for the dietary exposure
assessment. One of the major uses of iprodione was as a postharvest dip or spray on
peaches, nectarines and other stone fruits to prevent rotting during storage and transport

with an application rate of 50,000 to 65,000 pounds per year (U .S.EPA 1998b). Peaches

139

are among the EPA’s list of 10 commodities significant in the diets of children (U .S.FDA
2002). In 1998 the use of iprodione for postharvest treatments was canceled by EPA and
fludioxonil was used very widely as a replacement (Thompson 2008). Various uses of
fludioxonil have been registered by IR-4, including its use on stone fi'uits, and it has
“replaced iprodione completely (100%)” since 1999 for post-harvest uses on peaches,
plums and nectarines (Adaskaveg 2008). It was identified as having a spectrum of
activity and efficacy comparable to the canceled iprodione based on a study on reduced-
risk fimgicide effectiveness on stone fruits (Adaskaveg et al. 2005). F ludioxonil also has
had 70-80% usage as an iprodione replacement on peaches in Georgia since 1997 when
most uses of iprodione was removed from commerce (Brannen 2008). Several studies
have also identified the potential .of fludioxonil as a replacement for iprodione. The study
conducted by Northover and Zhou (2002) showed the activity of fludioxonil against
rhizopus rot on peaches. F ludioxonil at 25 pg/mL concentration caused a 95% reduction
in infection comparable to iprodione at a higher concentration (250 ug/mL) with a 77-
95% reduction. In another study on the control of brown rot and gray mold on peaches
and nectarines, fludioxonil applications resulted “in very high levels of decay control,
similar to that of the former industry standard, iprodione” (Forster et al. 2007). The pre-
harvest use of iprodione was also restricted around the same time as the post-harvest uses
were cancelled to further wrease iprodione residues, i.e. through an increased pre-
harvest interval to more than seven days and reduced application rates (U .S.EPA 1998b).
The reduction in iprodione residues alter 1997 thus could originate fiom these changes in

both me and post-harvest uses on stone fruits.

140

4.5.2 Dietary Risk Exposure Assessment Scenario

Tiered dietary exposure assessments (tiers 1, 2 and 3) were conducted for
iprodione and fludioxonil on peaches alone and on the entire stone fruits group (EPA
crop group 12 including apricots, peaches, nectarines, plums and cherries), using DEEM
and LifeLine for different population age groups. Several preliminary trial runs were
done using CARES but computer bugs and crashes were encountered (and reported to the
software developers). Since CARES is still being developed and evaluated, it was not
used further in the dietary assessment. Acute and chronic exposure levels at the different
tier levels were determined using the corresponding parameters for each tier shown in
Table 4.3. Residue values reported as zeroes or non-detects (N Ds) from the PDP residue
database were assigned one-half of the limit of detection (LOD) according to the EPA
default policy (U .S.EPA 1998a). The percent crop treated data for iprodione were derived
fromtheratioofthetotalareatreatedandthetotalareaplanted foreachcropbasedon
the National Center for Food and Agricultural Policy/CropLife Foundation (NCFAP/
CLF) 1992, 1997 and 2002 data. The percent crop treated used for the fludioxonil dietary
risk assessments were those used by the EPA for the tolerance establishments of
fludioxonil on stone fruits (U.S.EPA 2002). The processing factors used were the default
factors published in the DEEM manual (Kidwell et a1. 2000).

The toxicity values used in the analyses were compiled fi'om published documents
(Table 4.4) and are those used by the EPA in the dietary risk assessments of iprodione
and fludioxonil. Other studies considered by the EPA were also looked at and based on
the review of these studies, the toxicity values selected are reasonable. The %RfD was

used as an estimate of risk and calculated based on the NOAEL and the uncertainty

141

factors. The Rfl) approach is based on assumptions that a threshold exists and lies
between the NOAEL and the LOAEL but there is no way of knowing the “true” threshold
fi'om these data. Another assumption is that the errors fiom the NOAEL and LOAEL
studies are minimal. However, this approach involves uncertainties and limitations.
Uncertainties come fi'om various sources: a) uncertainty (errors) from the “distance” of
the NOAEL to the true threshold; b) uncertainty fiom the doses used in determining the
NOAEL; and c) rmcertainty factors used in calculating the RfD. A limitation of the Rfl)
approach is that it can only be used to compare across compounds having the same
mechanism of toxicity. The “net result is that exposures resulting in the same RfD do not
imply the same level of risk for all chemicals, and that exposures above the RfD do not
represent the same increase in risk for all chemicals” (Beck et al. 2001). The comparison
of iprodione and fludioxonil is difficult because of the differences in the mechanisms of
toxicity. However, assessment of the changes in risk for individual compound using the
RH) approach is possible and although it has limitations, it is a reasonable and accepted
method. It also incorporates the different uncertainty factors set by the EPA for different
compounds.

The acute and chronic exposures fiom tiers 1, 2 and 3 were compared for the
stone fruit group as a whole and for peaches alone. The changes in the dietary risks
before and after the F QPA were assessed using the tier 3 acute exposure analysis. At this
tier level, the 1995, 2000 and 2006 PDP residue data and corresponding 1992, 1997 and
2002 NCFAP/CLF calculated percent crop treated were used to estimate the exposure

levels and represent the risks before and after the enactment of the FQPA. The exposure

142

values from using DEEM and LifeLine models were also evaluated to determine how the
two compare.

The license for DEEM was purchased from Exponent (1150 Connecticut, Ave.
NW, Suite 1100 Washington, DC 20036). The copy of LifeLine was obtained fiom The

LifeLine Group, Inc. (4610 Quarter Charge Drive, Annandale, VA 22003) and the

 

CARES model was downloaded from the ILSI website (http://cares.ilsi.org/). Both

LifeLine and CARES are available with no license fees.

143

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144

Table 4.4. Toxicity parameters used in the dietary exposure assessment for
i rodione and f'ludioxonil

 

 

 

 

 

 

 

 

 

gngr'rtzters Iprodionel Fludioxonil 2’3
Acute NOEL=20 mg/kg/day NOAEL=100 mg/kg/day
LOEL=120 mg/kg/day LOAEL=1000 mg/kg/day
Based on decreased anogenital Based on increase in the fetal
distance (AGD) in male pups fiom incidence and litter incidence of
a prenatal developmental toxicity dilated reml pelvis and dilated
study in rats. ureter from a prenatal
F QPA Factor=3X (females 13+ developmental toxicity study in
years old) rats.
UF=100 FQPA Factor=lX
aRfl)=0.2 mg/kg/day UF=100
aRfl)=1.0 mg/kg/day
Chronic NOEL=6.1 mg/kg/day NOAEL=3.3 mg/kg/day
LOEL=12.4 mg/kg/day LOAEL = 35.5
Based on histopathological lesions mg/kg/day (F)
in the male reproductive system and Based upon decreased weight
efl'ects in adrenal glands from a gain (F) and decreased body
combined chronic weight, reduction in
toxicity/carcinogenicity study in hematological parameters
rats. (platelets), increase in
FQPA Factor=3X cholesterol and alkaline
UF=100 phosphatase, and increased
cRfl)=0.02033 mg/kg/day relative liver weight (M) from
chronic toxicity study in dogs.
F QPA Factor=1X
UF=100
cRfl)=0.033 mg/kg/daL
Q“ 4.39 x 10'2 NA
’ (U.S.EPA I998b)
2 (U.S. EPA 2002)
3(U. 5. EPA 2000c)

145

4.6 Results and Discussion

The exposure levels (mg/kg/day) and the percent of the acute or chronic reference
doses (%RfD) calculated by both the DEEM and LifeLine models were used in assessing
the exposure of various population groups to iprodione and fludioxonil residues on
peaches and on the stone fi'uits group. The EPA reference doses (Rfl)s) are exposures
that are likely to be without an appreciable risk of adverse effects to the human
population (including susceptible subgroups). The chronic reference dose (cRfl)) is an
estimate of a daily oral exposure for a chronic duration (up to a lifetime), and the acute
reference dose (aRfD) is an estimate of a daily oral exposure for an acute duration (24
hours or less) (U .S.EPA-IRIS 2008). Exposure estimates that are less than 100 percent of
the Rfl)s are generally regarded as “not likely to be associated with adverse health
effects, and are therefore less likely to be of regulatory concern” (U.S.EPA 1993).
However, “it should not be categorically concluded that all doses below the Rfl) are
‘acceptable’ (or will be risk-free), and that all in excess of the Rfl) are ‘unacceptable’ (or
will result in adverse effects)” according to the EPA (1993). The EPA employs the 95th
percentile of exposure for the less refined exposure assessments (tiers l and 2) and the
99.9th percentile when probabilistic assessment techniques are used (tiers 3 and 4)
(U .S.EPA 2000b). According to the EPA Office of Pesticide Programs (OPP), “with
probabilistic assessments, the use of the 99.9‘“ percentile generally produces reasonable
high-end exposure such that if that exposrne does not exceed the safe level, OPP can
conclude there is a reasonable certainty of no harm to the general population and all

significant population groups” (U.S.EPA 2000b). In this study the tier 1 and tier 2

146

exposures were assessed at the 95th percentile of the population and the tier 3 exposures
at the 99.9th percentile.

The carcinogenicity of a chemical is expressed in terms of the cancer potency
factor (Q*). A higher Q“ value indicates a higher potency of a chemical as a carcinogen
judged from animal studies (U .S.EPA 20003). The measure of cancer risk is expressed as

a probability, e. g. 1x10'6, which means that “for every one million exposed persons, one

would expect, at the most (upper boundary), one more cancer than would otherwise
occur, and the increased incidence may be less” (U .S.EPA 20003). This has generally
been regarded as an “acceptable” carcinogenic risk by the EPA.

While the use of a tiered approach in risk assessment and regulation is logical to
focus activity on those situations where additional attention is needed to assess whether
risk is acceptable, it should be kept in mind that tier 1 acute and chronic exposures and
cancerrisksareupperestimatesanddonotrepresentestimatesofreal risk. It is important
to note this to avoid common misunderstandings of the level of risk when these are

communicated to the public. The cancer risk value of 1x10'6is an upper bound estimate

which is unlikely to be exceeded and often will considerably overestimate cancer risk.
Again, if communicated to the public as actuarial predictions of cancer cases, the use of
these ‘Vvorst case” cancer risk estimates can lead to misunderstandings and undue public
concern. A disadvantage of quantitative cancer risk assessment is that it is subject to
considerable uncertainties and it is difficult to communicate the results concisely and

accurately to the public.

147

4.6.1 Variation in the Dietary Exposure at Different Tier Levels

The iprodione and fludioxonil acute and chronic exposure estimates and the
cancer risks fiom iprodione for peaches are shown in Figures 4.2 to 4.6 (%Rst are
shown on separate y-axes). The raw data for peaches and the stone fruits group are given
in Appendix E for iprodione and in Appendix F for fludioxonil. The results for these two
commodities were generally very similar. The estimated iprodione and fludioxonil acute
and chronic exposures were highest at tier 1 and, as expected, decreased substantially at

higher tier analysis in most cases.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

I r di n A x r , Pe h
p o o e cuteE posu e ac es Tierl(PCT=100%,
3.0 . .
40.0 _. Tolerance,ereLrne)
%RfD, Acute
36-0 2.5
32.0
A 28.0 2.0 as —e—'lier1(PCT=100%,
': 24 0 g. Tolerance, DEEM)
.93 ' A %RfD, Acute
l; 20 0 1.5 d
e ' 2
0‘ 16.0 1‘3
33 .- 1.0 g
12.0 : -o- 'lier2(PCT=100%,
: HFT Residue,
8.0 0.5 LifeLine) %RfD,
4.0 n Acute
0.0 e 0.0
05 3‘) 81' 3:»9 0,59 - ." Tier 2 (RCT=100%,
vi“ at? ”fies 359’ 6.39 9;," “355°" HFT Resrdue,
Nb t>$ is crewman),
Acute

 

 

Figure 4.2. Iprodione acute risk estimates for peaches (Tiers l and 2).

148

 

16.0

14.0

12.0

10.0

96 RfD
oo
0

4.0

2.0

0.0

 

\

Figure-“4

50.0
45.0
F3401:
025
H 351:
3
.2 30.(
L:
302 25.!
33 ZOJ
15.1
10.

Iprodione Acute Exposure, Peaches _ A- “er 3 (1992 PG, 1995
PDP Residue, DEEM)
%RfD, Acute

 

 

"Er-- Tier3 (1997 PCT, 2000
PDP Residue, DEEM)
%RfD, Acute

 

—re - Tier 3 (2002 PCT, 2006
PDP Residue, DEEM)
%RfD, Acute

—t—Tier 3 (1992 PCT, 1995
PDP Residue, LifeLine)
%RfD, Acute

+Tier 3 (1997 PCT, 2000
PDP Residue,LifeLine)
%RfD, Acute

 

+Tier 3 (ZWZ PCT, 2006
PDP Residue,LifeLine)
%RfD, Acute

 

Figure 4.3. Iprodione acute risk estimates for peaches (Tier 3).

Iprodione Chronic Exposure, Peaches (DEEM) —e—Tier 1

 

 

   
   

 

 

 

 

 

 

 

(pcr=100%,
I 50.0 1————~ , l 3.0 DEEM)%RfD,
450 it _ fl 4 Chronic
3400 J L 2-5 +Tler2(1992
a, ' PCI',DEEM)
H35.o 7 _ 2.0 as %RfD,
E 30.0 — 3; Chronic
3250 , ? -EI- ner2(2ooz
E G. PCF,DEEM)
3220-0 V %RfD'
150 _ Chronic
10.0 i —9|(-—Tier3(1992
PCT, DEEM)
5.0 — %RfD,
0.0 ~ Chronic
es sti .55 61,1 359 0,9 50" --)<- “83 (2002
SW” “9" 9.99" P99" >995" “Pa" “,6" :CJfBDEEM)

Chronic

 

Figure 4.4a. IpToIiione chronic risk estimates for peaches (DEEM—y

149

?

 

J

I
1

 

,- , 7 c.-. . 7, . r. .A]

Iprodione Chronic Exposure, Peaches (LifeLine)

 

 
 
        
  

 

 

     

—O—Tier 1
55-0 4-0 (PCT=100%,
50.0 3 5 LifeLine) %RfD,
45-0 ' Chronic
l A 40.0 3.0 +Tier2 l
3 as (PCT=1992 PCT,
H 35.0 2.5 I, LifeLine)%RfD,
2 30.0 1L“ . '6 Chronic }
g 250 _ > 2'0 g -€-i- TierZ
.9 20° _ , 1.5 a (Pcr=2ooz PCT,
a: - 3 v LifeLine)%RfD,
39 15,0 ——‘ \\ 1.0 Chronic
1 10.0 —— ’ " \q < ' “9'3
5.0 _ I _ g _ : ~‘\ » 0.5 (PCT=1992 PCT,‘
Ll ‘ -. . .g§:~~ .. -- LifeLine)%RfD,
‘ 0.0 —, , : - . , ‘— ' ' - _'- " 0-0 Chronic
es :L 5: «,1 5,9 9 0:: ~ ~ -. Tier 3 (2002
‘ WW “$53 “$53 “956’ 9,55% 9510) P3958 PCT, LifeLine)
‘9’ %RfD, Chronic \

[

Figure 4.41). Iprodione chronic risk estimates for peaches (LifeLine).

!

i

\

Fludioxonil Acute Exposure, Peaches _ ,_ fie, 1(PCT=100%,

Tolerance, DEEM)
" %RfD, Acute

"0" Tier 2 (PCT=100%, HFT
- Residue, DEEM) %RfD,
Acute l

 

- —* - Tier 3 (2006 PDP
Residue, DEEM) %RfD,‘
Acute .

-0—Tier 1 (PCT=100%,
Tolerance,LifeLine)
%RfD, Acute

-0— Tier 2 (PCT=100%, HFT
‘ Residue, LifeLine)

 

 

s :1. .6 ’1. 9 %RfD, Acute
\V”e cf} e53 6A 33A ’1. 580* ‘
p) p9, P3 e5 s s P
P" pat” use P‘" --—ruer 3 (2006 PDP
Residue, LifeLine)
%RfD, Acute

Figure 4.5. Fludioxonil acute risk estimates for peaches.

150

 

 

 

 

 

 

1 Fludioxonil Chronic Exposure, Peaches .. .. her 1 (PCT=100%,
9.0 r 4.00 Tolerance, DEEM)
' I %RfD, Chronic
8.0 3.50
| 1 - - .- - Tier 2 (Tolerance,
37.0 1 3.00 PCT, D-EEM) %RfD,
a6 0 + 1‘ 2 50 3? Chronic
25.0 -- ' 3 -o—Tuer 1 (PCT=100%,
g . 2.00:. Tolerance,LifeLine
34.0 E )%RfD, Chronic
323") -- , — '4 +T‘Ier2 (Tolerance,
2 0 __ _ 1_oo PCT, LifeLine)
’ ' O %RfD, Chronic
1.0 -‘ ~— 0.50
E —e - Tier 3 (Ave. FT,
0.0 , —.— r 0.00 PCT, DEEM) %RfD,
Chronic
s :L .5 {L «,9 9 ox
fie 55 53 6’ ’5' 0) ‘5
v~\‘ 9!? pa?“ ‘4?" pi?" e51 as? —9— Tier 3 (Ave. FT,
PCT, LifeLine) ‘

I %RfD, Chronic

Figure 4.6. Fludioxonil chronic risk estimates for peaches.

In the one exception to the tier 1> tier 2 > tier 3 trend found in all the other
examples, the estimated acute risk fiom tier 1 to tier 2 with iprodione (Figure 4.2) shows
an unusually large drop due to the great difference between the exposure calculated using
the tolerance level (tier 1) and from using actual field trial residue data (tier 2). The
estimated risk then rises again at tier 3. The iprodione residue level used at tier 1 was
very high (tolerance = 20 ppm) and this remained as the tolerance level although it had
been proposed to be lowered by the EPA in 2004; in 2007 the EPA did not take any
action on the iprodione tolerances and it remains at 20 ppm (U.S.EPA 2007a). Usually
there is a much closer relationship between the highest field trial residues and the
tolerance level that is derived from them. The calculated risk rises again in tier 3 since at
this level the exposure is calculated for the 99.9“ percentile of the population and not the

95m percentile (for tiers 1 and 2). The iprodione estimated risks (%Rfl)) for ages 1-2 for

151

tier 1 and tier 2 are 34% and 1.1%, respectively; for tier 3 the risks are 15.0%, 9.2% and
6.3% for 1992, 1997 and 2002, respectively based on assessments using DEEM. In most
other studies conducted as part of this work, risk typically falls in the order tierl > tier 2
> tier 3, as expected. However there is considerable variation in the degree of decrease in
risk calculated under these scenarios, e.g. for acute exposure at ages1-2 to fludioxonil, the
ratio of the tier 1 estimate to that for tier 3 is only 2.0, whereas for fludioxonil chronic
exposure the ratio is 15 based on DEEM results; for iprodione chronic exposure it is
approximately 120 (using 2002 PCT at tier 3) and 68 (using 1992 PCT (at tier 3), and for
iprodione’s cancer risk it is approximately 135 (using 2002 PCT at tier 3) and 68 (using
1992 PCT at tier 3). The iprodione acute risk tier 1 and tier 3 ratio for 1-2 y.o. is 2.3
(1992 PCT at tier 3) and 5.5 (2002 PCT at tier 3).

The chronic exposure estimates for iprodione on peaches shown in F igm'es 4.4a
and 4.4b declined significantly from tier 1 to tier 3 in these analyses. From tier 1 to tier 2
the %RfD decreased from ~48-54%Rfl) to ~29-33%Rfl) (using higher percent crop
treated from 1992) and ~l4—17%RfD (using the lower percent crop treated) and declined
further to <1% at tier 3 for ages 1-2. Within the tier 2 and tier 3 levels, the exposure
levels varied due to the percent crop treated values used in the analyses. Higher exposure
estimates were derived using the 1992 PCT (with higher percent crop treated) compared
to using the 2002 PCT (with lower percent crop treated).

The carcinogenic property of iprodione is the major concern for dietary risk,
although risk from its endocrine efiects has yet to be fully evaluated. Figure 4.7 shows
the cancer risks for iprodione on peaches and these follow the same declining trend with

tier level as the acute and chronic exposures. At tier 1, the cancer risk for peaches is

152

lxlO'4 which is considerably greater than the 1x10'6 guideline and would cause cancer
risk concerns at this level of analysis. The cancer risks decrease, as expected as the tier
level inputs become more refined. At tier 3 the cancer risk is significantly lower and
ranged fiom 1.4x10'6 to 7.5x10'7 and is less than the 1x10"S guideline for level of
concern. This indicates that the several regulatory actions taken to reduce exposure to
acceptable levels were successful. But it should be noted that additional exposure and risk
can come from dietary residues of iprodione fiem additional food uses, e.g. grapes and

almonds and a number of other fi'uits and vegetables.

I Iprodione Cancer Risk, Peaches j

 

I 1.045-04 71. ,, , , , ,, I

   

9.115-05 17*
1 7.81E-05 L»

 

 

6.51E-05 f
5215-05 1

 

I DEEM

 

Cancer risk

3.91505 1 7 ~

 

l 2.61E-05 If I LifeLine
1

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‘ \Q

 

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s
wfi I
|_ _ . __ _ , ________1
Figure 4.7. Iprodione cancer risk for peaches.

The effect of the exposure refinements underlying the increasing tier levels seen
here were generally consistent with the results from the study on the comparison of
exposures to chlorpyrifos at different levels of refinements of exposure that included

tolerance levels, highest field trials residues, residue monitoring data and percent crop

153

treated conducted by Wright et al. (2002) and Oliver et al. (2000). Results from the study
by Wright et al. (2002) showed an approximately 55% reduction in exposure estimates by
using tolerance value compared to using the highest field trial value, and inclusion of the
percent crop treated “fm'ther decreased the exposme estimates” (Wright et al. 2002). The
inclusion of food residue measurements fiom a specially designed market basket study,
govemment-sponsored residue monitoring data, probabilistic methodologies, market
share information and food processing data were identified by Wright et al. (2002) as
contributing factors to the significant reduction in the estimated exposures at higher tier
levels. A study of the effect of higher tiered analysis on the acute dietary risk of
chlorpyrifos using DEEM showed a 26—fold decrease in estimated risk from tier 2 to tier
4 at the 99.5'" percentile and a 7-fold decrease from tier 3 to tier 4 at the 99.9th percentile
for children 1 to 6 years old (Oliver et al. 2000). These trends are also consistent with the
results from this study although, as noted, the degree of change between tiers varies from
study to study.
4.6.2 Cam-iron of W Exposures firm: the DEEM and LifeLine Assessment
Models

The DEEM and Lifeline programs use quite different approaches in modeling
dietary exposure and would not be expected to give exactly the same results. Despite
these differences, this study shows that the exposure estimates fi'om DEEM and from
LifeLine are closely comparable with a difference of only ~5% in most cases. This is
consistent with the findings of the EPA Scientific Advisory Panel (SAP) on the
comparison of the dietary risk assessment models which, using a hypothetical data set,

showed “close agreement between DEEM and LifeLine estimated exposures” and “little

154

substantive difference” between exposures predicted by the two computer sofiwares
(U.S.EPA 2004). In a few cases, differences > 5% were seen e.g. DEEM tends to give
higher exposure estimates for the 50+ years old age group than LifeLine (e.g. Figures 4.2
and 4.5) but this was not the case in all comparisons. Differences in %Rfl) of >5%
between the two models were only found for iprodione on stone fi'uits (ages 1-2) at tier 1,
with differences in %Rfl) of 11% and 14% for acute and chronic exposures (Appendix
B), respectively; 9% at tier 2 (1992 PCT) chronic exposures on stone fruits and 6% at the
tier 1 chronic analysis on peaches for the same age group. However, the cancer risk
estimates for iprodione on peaches using DEEM and LifeLine were almost exactly the
same as shown in Figure 4.7. The fact that the results from the two programs are
remarkably similar despite their different methodologies tends to give confidence that the
risk estimates are realistic.
4.6.3 Dietary Risk More and Afler the F QPA

The dietary risk comparison and trend analysis from before and after the FQPA
were based on the tier 3 acute analysis (Figure 4.3). The acute risk levels from using the
1995 PDP residue level (representing pre-FQPA) were highest (15%Rfl) for ages 1-2)
and follow an overall decline afier the FQPA, i.e. 9 to 11%Rfl) (2000 PDP residue level)
and 6 to 7%Rfl) (2006 PDP residue level) for the same age group, even though these
exposures were not at the level of concern even before the FQPA. A similar drop in risk
is seen with the chronic exposure to iprodione in 2002 compared to 1992 (Figures 4.4a
and 4.4b). This is due to lower percent crop treated values in 2002 (30%) compared to
that in 1992 (60%). Both the acute and chronic data reveal that the estimated risks are

highest for children from ages 1 to 2 and this is followed by the risk fi'om ages 3 to 5.

155

Risks to other age groups and the population in general tend to be much lower. This
arises fiom the high consumption of peaches and other stone fruit by infants and young
children and rmderlines the importance of giving special consideration to these age
groups in assessing and reducing risk. This distinction would be lost in simpler risk
assessments that utilize average consumption data for the population as a whole. Overall,
the yormger age groups tend to have higher exposure estimates than the other
subpopulations.

One source of uncertainty in these estimates lies in the substitution of l/zLOD for
the non-detects in samples from treated crops, as typically practiced by EPA. In 1995,
2000 and 2006, the VzLODs for iprodione on peaches were 30%, 37% and 57%,
respectively of the total non-zero values used in the assessment The assumption of
‘/2LOD could have driven most of the exposure estimates especially in 2006 when more
thanhalfoftheresiduevaluesusedintheassessmentwere VzLODs,andthismighttend
to overestimate actual residue levels and risk. Also, Monte Carlo techniques were used at
this level of amlysis and different results are likely for each nnr since different sets of
variables (e.g. consumption) are sampled each time the amlysis is done. Such variability
in results was observed in this study from repeated analyses using the same input
parameters, especially for LifeLine, but the variability between runs was 5% or less.

A similar decrease in trend in the dietary exposure and risk estimates of iprodione
before and after the F QPA for stone fruits is shown in Appendix E. However, the acute
exposure at tier 3 (using the 1995 PDP residue for iprodione) is mrderestimated since the
only available stone fruit residue data for that year was for peaches, thus the exposure

estimates (~15%Rfl)) are the same for peaches and for the stone fruits group. This again

156

illustrates the problems in obtaining residue data that are recorded on a consistent basis
from year to year.

The decline in the risk estimates from before and after the FQPA in this study is
consistent with results of the OIG study using the dietary risk index (DRI) approach to
measure the impact of the FQPA (U .S.EPA-OIG 2006a), e.g. the DRI for chlorpyrifos on
apples show a large decrease in exposure, and thus in risk. The DRI decreased by 98% in
1996 to 4% in 2002 due to strong regulatory actions specifically intended to reduce
chlorpyrifos residues on apples. Although the DRI approach is questionable in assessing
overall risk fiorn multiple compounds or residues in multiple crops because the additivity
of the risks cannot be assumed, it is a more reasonable approach to assessing changing
risk from single pesticides on a single crop.

4.6.4 Dietary Risks of Iprodione Compared to Fludioxonil

The fludioxonil acute and chronic exposure estimates for peaches are shown in
Figures 4.5 and 4.6 and in Figures 4.2 to 4.4 for iprodione. None of these three tier
estimates for either compomd would give cause for regulatory concern. However, the
mechanisms of toxicity for iprodione and fludioxonil are different and the uncertainty
factors used were also different (i.e. chronic F QPA factor=3X for iprodione) and do not
allow for a direct comparison of the acute and chronic risk estimates of the two
pesticides. But the most significant risk reduction is that the cancer and endocrine
disruptor effects are eliminated where fludioxonil has replaced iprodione. Although
regulatory actions were taken after FQPA to reduce the cancer risk estimates to less than

1 x 10'6 for iprodione, as illustrated in Figure 4.7, this involved the cancellation of its

157

uses on stone fruit for all postharvest uses, and the modification of its uses for preharvest
applications.
4.6.5 Generalizabilitv of the Iprodione-Fludioxonil Case Study

The significant impact of the replacement of several iprodione uses with
fludioxonil is the lack of iprodione’s potentially serious carcinogenic (and possibly its
endocrine-disrupting) properties. To what degree is this conclusion generalizable in
assessing the impact of the FQPA? Each case is different in detail, and the extent to
which the use of older compounds have been reduced and replaced in specific uses by the
reduced-risk chemicals is often partial, complex, and difficult to analyze. However there
is reason to believe that on a broader level the case study developed here is a reasonably
typical representation of the contribution of the FQPA to food safety.

To enable a broad comparison, the toxicological properties of typical FQPA target
compounds and meir reduced-risk replacements were collected in Appendix B and are
shown graphically in Figures 4.8 and 4.9. Figure 4.8 shows the dietary acute categories
and Figme 4.9 shows the cancer classifications of the compormds. The cancer
classification guidelines have rmdergone several revisions and changes since they were
first introduced in 1986. There have been three sets of guidelines used by the EPA for
classifying carcinogenic potential (the 1986, 1996 and 2005 guidelines). As a result of the
revisions, chemicals have been given cancer classifications depending on the year they
were evaluated and which classification guidelines were being used at that time. The
different pesticides considered in this study have classifications based on all the three
guidelines, which makes direct comparisons difficult According to the EPA, the

different designations “cannot be directly compared” and “the designation for any

158

substance must be considered in the context of the system under which it was review ”
(U.S.EPA 2006). For the purpose of this study (that is to show and compare the overall
carcinogenic properties of the old compounds and the newer pesticides) the cancer
classifieations for the pesticides were simplified to lessen the number of categories. The
carcinogenic classifications that are as reasonably close as possible in their descriptions
were combined and grouped into five “clusters”. However, these “clusters” do not imply
that the classifications across the three carcinogenic guidelines are equivalent.

Table 4.5. Carcinogenic “clusters” based on the 1986, 1996 and 2005 cancer
classification guidelines.

 

 

 

 

 

 

 

 

 

Cluster Cancer Classification Guidelines
1986 1996 2005
[1] Known A-human carcinogen Known/Likely Carcinogenic to
humans
[2] Probable/Likely B (Bl & B2)— Likely to be
probably human carcinogenic to
carcinogen humans
[3] Possible/ C-possible human Suggestive
Suggestive carcinogen evidence of
carcinogenic
potential
[4] Unclassifiable D-not classifiable as Cannot be Inadequate
to human determined information to
carcinogenicity assess carcinogenic
tential
[5] Not likely to be E-evidence of non- Not likely Not likely to be
carcinogenic carcinogenicity for carcinogenic to
humans humans

 

 

 

 

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161

Appendix B shows the differences in the toxicity properties of the old and the
reduced-risk insecticides and fungicides. The OPS are generally cholinesterase inhibitors
and exhibit neurological and, sometimes, developmental effects. They are all on the
Endocrine Disruptor Screening Program (EDSP) drafi list except for fenamiphos and
fonofos, but most are not likely to be carcinogens. The NMCS are
neurotoxic/cholinesterase inhibitors and are also included in the EDSP drafi list but are
not likely to be carcinogenic. Besides causing carcinogenic and developmental effects,
the B2 fungicides captan, chlorothalonil and iprodione are also in the EDSP drafi list but
are not classified as cholinesterase inhibitors and tend to have low acute toxicities. By
comparison, the reduced-risk insecticides raise fewer and less intense toxicological
concerns compared to the conventional pesticides, ofien offering a much higher level of
safety in standard animal tests. These insecticides are not cholinesterase inhibitors and
are classified as OP alternatives by the EPA, most are “not likely” to be carcinogens, and
they do not exhibit developmental or serious neurological toxicity. The reduced-risk
fungicides have low acute toxicities, are non-cholinesterase inhibitors, non-carcinogenic
and no evidence of developmental effects were shown fi'om studies for most of them.

Figure 4.8 shows more specifically the dietary acute toxicity categories of the DP
and NMC, and the reduced-risk insecticides, and the B2 carcinogenic and the reduced-
risk fungicides. The majority of the CPS and the NMCS are classified as highly acutely
toxic/category l (73%) while 64% of the reduced-risk insecticides belong to category IV
(not acutely toxic). 0n the other hand, the B2 carcinogenic and the reduced-risk
fungicides are mostly not acutely toxic (category IV) (80% and 83%, respectively). The

carcinogenic classification of the old and the new pesticides are shown in Figure 4.9.

162

Most of the OPS and NMCS (75%) and the reduced-risk insecticides (82%) and all the
reduced-risk frmgicides belong to the “not likely to be carcinogenic” cluster.

From these comparisons it can be concluded that the difl‘erences between the
toxicological properties of iprodione and fludioxonil are quite typical of the B2
carcinogenic fimgicides and their replacements (Figures 4.8 and 4.9). The risks fiom the
OPs and the NMCS are more closely related to their high acute toxicities and neurotoxic
effects. However, the reduced-risk replacement compounds are much more selective in
their toxicity to insects and very much safer to vertebrates (Appendix B). Although they
are not entirely lacking in hazard, particularly environmentally, the decrease in acute
toxicity is of such a magnitude and their residue levels low enough, that, in practice, they
appear to present no realistic dietary risk. As the use of many of the most toxic OPs and
NMCS has been eliminated or greatly reduced, and their residues in the food supply have
declined, risk has declined accordingly as shown by the data on the reduction in risk fi‘om
specific OPS in the diet presented in the EPA-OIG report using the DRI approach. At the
same time, the use of the reduced-risk insecticides has con'espondingly increased without
introducing significant dietary risks, and, although the quantitative assessment of this
trend would be very difficult if not impossible on a comprehensive basis, it is inevitable

that these responses to FQPA have enhanced the safety of the U.S. food supply.

163

4.7 Conclusion

Establishing dietary risk trends requires comprehensive, consistent and
continuous residue data. The publicly-available PDP database has national residue
coverage while the CA-DPR database covers mostly California-based commodity residue
dataonly. Bothdatabasesareusedforseveralpmposesbuttheyarenotprimailysetup
for use in dietary risk trend analysis. There is lack of continuity in the commodities
sampled because they vary each year, and the analytical sensitivity changes with time,
which makes establishing both residue and dietary risk trends difficult. This probably is a
factor leading to the conclusion of EPA-OPP (U .S.EPA—OIG 2006a, b) that despite
considerable effort, they have been unable to develop a scientifically sound method that
uses available data to assess the public health impacts of their regulatory program. A
database designed to serve this purpose is needed and would be very useful to analyze
and determine how the dietary risks fiom pesticides have changed over the years and to
provide a gauge on how the implementation of regulations such as FQPA has succeeded
in its primary goal of changing dietary exposure, particularly for infants and children.

The tiered analysis of exposure is an integral part of the EPA’s pesticide
regulatory methodology. In this study, the exposure estimates at the different tier levels,
both for acute and chronic assessments, vary and tend to decrease as the tier level gets
higher wherein the input parameters become more realistic (i.e. residue monitoring data
and adjustment factors). However the degree of decrease is very variable from case to
case. Where the decrease in estimated risk is considerable as the tier level increases, the

initial estimates provided by lower tier analysis, while clearly useful for the initial

164

evaluation of the need for regulation, do not accurately represent me actual risk and can
be seriously misleading if presented publicly without further explanation.

The use of actual residue monitoring data and percent crop treated values from
various years at the tier 3 level allowed for a comparison of the dietary risk estimates
before and after the FQPA. The decrease in the acute risk estimates for iprodione at the
tier 3 level before and after the FQPA, even though they were not at the level of concern
even before the FQPA, denotes regulatory consequence of the FQPA. This is an
indication of lower residues detected and regulatory actions to decrease the use of
iprodione over time.

There were differences in the exposure estimates derived from the DEEM and
LifeLine programs, but overall the results were closely comparable and it is unlikely that
they would provide results that differ enough to create a regulatory dilemma. The
differences were due to the significant variations in how these programs model exposure.
In those situations where these programs utilize Monte Carlo methodology, the variability
inherent in dris method approaches that typically seen between the DEEM and Lifeline
estimates.

The differences in the mechanism of toxicity of iprodione and fludioxonil did not
allow comparison in the risk estimates between the two compounds. Although iprodione
presents little realistic acute toxic risk, it is both a carcinogen that can present
unacceptable levels of risk and has endocrine disruptor properties that have not yet been
fully evaluated. These risks are eliminated through its replacement by fludioxonil.
Fludioxonil is virtually devoid of acute toxic risk and the regulatory endpoint for its

chronic toxicity is failure to gain weight without distinct pathology. Further, the actual

l. 65

residue levels of fludioxonil in stone fruits are well below those calculated to be safe for
lifetime consumption. These contrasting toxicological profiles are quite typical of the
older and the reduced-risk replacement compounds, and in this respect, the case study
here may have broader applicability. This analysis suggests that, although the results will
not be numerically identical with other crops and chemicals, the general results obtained
here with iprodione and fludioxonil may reasonably represent the kind of decrease in
dietary risk associated with the broader replacement of the B2 carcinogens and
anticholinesterases with other reduced-risk pesticides. This example illustrates the
contribution that FQPA has made to enhancing the safer use of pesticides and to the
significant role of the IR-4 program in ensuring that these reduced-risk materials are

broadly available to the growers of many fi'uit, vegetable and nut crops.

166

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Tolerance Actions. U.S. Environmental Protection Agency. Report. Federal
Register/ Vol. 72, No. 147. Final Rule.

U.S.EPA. 2007b. Cumulative Risk Assessment Methods and Tools. U.S. Environmental
Protection Agency. September 6, 2007.
http://www.epa.gov/opp0000l/cumulati\'c/nrctlrods_toolshtm

U.S.FDA. 2002. Food and Drug Administration Pesticide Program: Residue Monitoring
2002. U.S. Food and Drug Administration. Report.
http://www.cfsan.fda.gov/~dms/pCSOZrephtml

Wright JP, Shaw MC, Keeler LC. 2002. Refinements in Acute Dietary Exposure
Assessments for Chlorpyrifos. J. Agric. Food Chem. 50:235-241.

170

CHAPTER 5
SUMMARY, CONCLUSIONS AND RECOMMENDATIONS

The passage of FQPA resulted in major regulatory changes for pesticides. Some
of these changes include added requirements to reregister pesticides (with focus on older
compounds-OPS, NMCS and B2s), requirement of aggregate and cumulative risk
assessments, an additional safety factor for the protection of infants and children, and the
expedited registration of uses of reduced-risk and OP replacement pesticides. These
requirements effected significant changes in the use of both traditional and reduced-risk
pesticides but only a few studies have been published to show these changes. In this
study, the trends in use of these pesticides were assessed since the F QPA was passed in
1996 using data fi'om the California Department of Pesticide (CA-DPR) and the CropLife
Foundation (CLF) databases. These sourees showed an overall substantial decrease in the
use of the anticholinesterases, OPs (50%) and the NMCS (70-75%), the two pesticide
groups that were the initial focus of regulatory action, over the years fiom 1992 to 2006.
However, the use of some of the individual pesticides in these classes (eg. chlorpyrifos
and oxamyl) remained high or showed less decline. Conversely, the reduced-risk
insecticides showed a consistent increasing trend in use and are now a central part of pest
management in fruit and vegetable production. This trend fits well with the declining use
of the CPS in view of the fact that most of the reduced-risk insecticides are OP
replacements. On the other hand, the use of the BZ fungicides declined by only 10-20%
since the enactment of the FQPA. Despite their carcinogenic potential, their use and
residues in most cases have not been found to be at levels of regulatory concern by the

EPA. They also have the advantages of low cost, low resistance potential and broad

171

spectrum activity against pathogens. The reduced-risk fungicides have also shown a
regular increase in use since the FQPA that can be attributed to very high efficacy
compared to the older B2 pesticides and in some case their systemic action and more
desirable spectrum of activity. I

The application rates (lbs/application) of the reduced-risk pesticides were found to
be significantly lower (5 to lO-fold) than the older pesticides. These lower application
rates combined with the substantial decline in use of the anticholinesterases and, to a
lesser degree, the 82 fungicides, have led to an overall decrease in the amount of
pesticides applied in the production of fi'uits, vegetables and nut crops. In combination
with the improved toxicological profiles of the reduced-risk compounds, this is likely to
lead to lower environmental impacts. It was concluded that the USDA IR-4 minor use
pest management program was responsible for obtaining approximately 50% of these
reduced-risk registrations.

The changes in the residue detection since the passage of the FQPA were also
examined for both the traditional and newer pesticides using the USDA Pesticide Data
Program (PDP) and the California Department of Pesticide Regulation (CA-DPR)
databases. The residue data for the CPS, NMCS and the B2s showed considerable year-
to-year variability which tended to obscure trend analysis. The OPs, however, still
showed an overall decline in residue detection fiequency with individual OPs such as
azinphos-methyl and methyl parathion having a more distinct downward trend since they
have been subject to the most rigorous regulatory actions. The lack of an overall decline
in the residue detection trend for the B2 fungicides corresponds to their modest decline in

use. However, the lack of an obvious decrease in residue detections for the NMCS does

172

not correspond to the steep decline in their use. The reason for this is not clear. Some of
the individual reduced-risk pesticides such as imidacloprid, acetamiprid and tebufenozide
showed unexpectedly high pereent detects. These higher detections can be due to
applications tlmt are made close to harvest, and in part, to the systemic properties of some
of these pesticides, particularly those with substantial use on fi'uits and vegetables.
However, the record for residue detections for the reduced-risk compounds is brief and
several of the detection rates were low and variable, which make establishing a trend
difficult.

Little Ins been published that examines the impact of the F QPA on pesticide
exposure and dietary risks. The risk assessment process has evolved fiom the use of
deterministic to probabilistic methods of analysis. The newer processes are more complex
but are more realistic, give information regarding the distributions of exposures and risks,
and now are widely employed. The following study used two probabilistic risk
assessment programs, DEEM and Lifeline. The EPA’s tiered approach in assessing
dietary risk was employed to determine changes in a dietary risk from iprodione and
fludioxonil on stone fiuits using residue data from 1995 to 2006. The risks tend to be
lower as the tier level gets higher because of more refined and realistic input parameters.
Inthis study,theresultsfiomtheuseofthetieredapproachshowedthatthedietaryrisk
varies at different tier levels and proved that the use of more realistic inputs (i.e. residue
monitoring data and residue adjustment factors) tend to result in lower risk estimates. For
thisreason,thetier l riskestimatesshouldnotbetakenasactualriskestimates,butthey

are useful for initial regulatory evaluation. The dietary risk assessments were conducted

173

using the DEEM and LifeLine programs. The results using these different models for
assessing exposure and risk were comparable with less than 5% difference in most cases.
The fludioxonil-iprodione case study was used to assess the changes in the dietary
risk from replacing an older compound with an lR-4-registered pesticide and how risk
has changed since the F QPA was enacted. Fludioxonil has replaced iprodione in its
postharvest uses on the stone fi'uits group and for peaches as an individual crop, and the
use of iprodione for preharvest treatment has also been restricted. The reference dose
(RfD) was used as a gauge for the potential effects of pesticides at other doses but, as the
EPA noted, it should not be “categorically concluded that all doses below the RH) are
‘acceptable’ or will be risk-free, and that all in excess of the Rfl) are ‘unacceptable’ or
will result in adverse effects”. Although limited, this is a reasonable and useful approach
for now. However, the differences in the mechanism of toxicity between fludioxonil and
iprodione do not allow for comparison of the risk estimates of these two compounds. But
the significant contribution to food safety is the elimination of cancer risk fiom the
replacement of iprodione with fludioxonil (which was registered by IR-4 for use on stone
fiuits group) for post harvest uses. The acute dietary risk estimates from iprodione have
been shown to decrease after the passage of FQPA (15% ofthe Rfl) and 7% ofthe Rfl),
using 1995 and 2006 PDP residue data, respectively) even though they were not at the
level of EPA concern even before the F QPA. The reduction in the dietary risk results
from the post-FQPA decrease in use of iprodione which lowered residues. It is also
representative of the kind of decreased dietary risk that comes fi'om the use of reduced-

risk pesticides as replacement for older compounds.

174

This study utilized the publicly-available databases such as the PDP, CA-DPR

and the CLF databases for the use, residue and dietary risk trend analyses. Each of the

databases follows a different protocol in their monitoring methods and thus, does not

allow for cross-database analysis. Overall, these databases are not set up for trend

analysis. There is a lack of continuous and comprehensive national use and residue data.

The type and quantity of crops sampled vary each year and make the data discontinuous.

These factors make establishing trends in use, residue and dietary risk difficult.

This study is a preliminary attempt at analyzing the changes in pesticide use, residue

detection and dietary risk as a result of the enactment of the F QPA. However, the

findings in this study can be further expanded through the following recommendations:

1.

There is a need for a more comprehensive database for pesticide use with a national
coverage that can be used for trend analysis. This would require use data to be
gathered annually on a defined series of key food crops. The sampling method
should be developed to give reasonable coverage of all significant growing areas in
the U.S. For example, the expansion of the use data collection of the National
Agricultural Statistics Service (NASS) database would be a significant source of
data for assessing and establishing pesticide use trends and the resultant changes
brought about by regulatory changes. In addition, the data provided by NASS is
publicly-available compared with privately-owned databases such as the very
expensive Doane Survey. Unfortunately previous attempts to expand the NASS
database in this way have not been strongly supported by potential users.

There is also a need for residue databases with more consistent sampling size and

more uniform types of crops sampled every year to parallel the more comprehensive

175

use data. The PDP database has a national coverage and maintains annual residue
reports for various crops, but lacks consistency in the type and size of crops sampled
each year that makes establishing trends difficult. Identifying the key crops grown in
different parts of the U.S. and the consistent sampling of these commodities would
greatly enhance the residue database and this could be utilized to more accurately
assess the status of and changes in dietary risk with time and as a result of specific
regulatory actions.

It is impossible to develop a single index to indicate the overall level of risk posed
by dietary pesticide residues, and how this changes with time, because there are
many different toxicological endpoints for these compounds so that estimated risks
cannot be combined together to provide a single value. However, it should be
possible to conduct such a continuing study for groups of compounds with a
common mechanism of toxicity and to follow these compounds as a group using the
relative potency factor approach to allow normalization of the data from different
compormds. This approach is illustrated by the cumulative risk assessment for
organophosphates conducted by EPA (2002) (Organophosphate Pesticides: Revised
Cumulative Risk Assessment http://www.epa.gov/opp00001/cumulative/rra—opl). In
the simplest case, this cumulative assessment would require an assumption of
additivity for the normalized exposures to the several compounds, which may well
be an approximation, but overall, this analysis conducted consistently and at regular
intervals, would provide a better insight into the direction and magnitude of changes

in dietary risk than any we now have available.

176

APPENDICES

177

APPENDIX A
Preliminary Selected Pesticides

178

List of Preliminary Selected Pesticides

 

 

 

 

 

 

 

B2 OPs NMCs Reduced-risk Reduced-risk
Carcinoggns Fungicides Insecticides
1. captan 1. acephate 1. aldicarb 1. azoxy- l. acetamiprid
2. chloro- 2. azinphos 2. bendio- strobin 2. bifenazate

thalonil methyl carb 2. cyprodinil 3. buprofezin
3. folpet 3. chlorpy- 3. carbaryl 3. fenhexamid 4. cinnam-
4. iprodione rifos 4. carbofuran 4. fludioxonil aldehyde
5. mancozeb 4. coumaphos 5. formet- 5. mefenoxam 5. fipronil
6. maneb 5. DDVP anate HCl 6. trifloxy- 6. hexaflum-
(dichlor— 6. methio— strobin uron
vos) carb 7. imida-
6. demeton 7. methomyl cloprid
7. diazinon 8. oxamyl 8. indoxacarb
8. dicroto-phos 9. propoxur 9. novaluron
9. dimethoate 10. thioben- 10. methoxy-
10. disulfoton carb fenozide
11. ethion 11. thiodicarb ll. pymet-
12. ethoprop rozine
l3. fenamiphos l2. pyripro-
14. fenthion xifen
15. fonofos 13. spinosad
16. malathion 14. tebufen-
17. metham- ozide
idophos 15. thiameth-
18. methida- oxam
thion
19. methyl
parathion
20. naled
21 . oxydem-
eton methyl
22. parathion
23. phorate
24. phosalone
25. phosmet
26. profenofos
27. sulfotep
28. sulprofos
29. tetrachlor-
vinphos
30. trichlorfon

 

179

 

APPENDIX B
Pesticide Toxicity Properties

180

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28302 8%.... 02088 .25.“

3x8 £858 gonna .omxS DEE—mug .omxou £05888": .3on 333"“ £35 Saar

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

WE: ma
£3.55 £38m 98V mx
5%. a. 033 :2 =2 :2. 33% @588
32 .maam 2? .E .Ez 38389: :32 A23 39...
mm xm .moEfiafim ma . oz .0 853m 82 oz E -fifiom .m
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came 23 388%
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a:
93 mg
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moEomwm—E gum—633.9. 2: a: 83.8.3.3 >335; .md amen—25¢.

192

 

:& 82

 

 

 

 

 

 

 

 

 

 

 

 

moans Huh—50:8 PE
£30m £988? 32 8 :2 bmomxo: 93
.39an mEmewuo Savage—got $2 mémm
:28 2a 033 23:3 mo baa A33 use;
:3 V: 59% 8E 383 oz 8:8me oz 82 02 ”a %an6
:3
ca .6
whoaomdsm 938
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£820 £85.? b8:— AaQA 888
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mafia wx
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£0283 £0980 SEEQBgou $2 2 ASQA
.ommomu§~ MO @5330 x33 €98
:fl 5 ,mofifiafim oz 8523 oz 82 02 £6 2 Augie

 

 

.P.=8...m.m 55%?

193

10.

ll.

12.

BIBLIOGRAPHY

U.S.EPA, Reregistration Eligibility Decision-Acephate. 2001, U.S.
Environmental Protection Agency: Washington, DC.

2007. http://pcsticideiMoog/”Search Chemicalsjsp

 

U.S.EPA, Reregistration Eligibility Decision-Azinphos-methyl. 2001, U.S.
Environmental Protection Agency: Washington, DC.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Chlorpyrifos. 2002,
U.S. Environmental Protection Agency: Washington, DC.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Diazinon. 2004,
U.S. Environmental Protection Agency: Washington, DC.

U.S.EPA. Organophosphate Pesticides in F ood-A Primer on Reassessment of
Residue Limits. 2006 October 11, 2005 [cited 2006 March 30]; Available from:

http://wvwv.epagov/Qesticides/op/primer.htm.

 

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Disulfoton. 2002,
U.S. Environmental Protection Agency: Washington, DC.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Fenamiphos. 2002,
U.S. Environmental Protection Agency: Washington, DC.

Extoxnet F onofos. 2008.

U.S.EPA, R. E.D F acts-O-Ethyl S-phetolletlgllphosphonodithiolate (F onofos).
1999, U.S. Environmental Protection Agency: Washington, DC.

U.S.EPA, Interim Reregistration Eligibility Decision for Methamidophos. 2002,
U.S. Environmental Protection Agency: Washington, DC.

Extoxnet Methidathion. 2008.

194

13.

14.

15.

16.

17.

18.

19.

20.

21.

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23.

24.

25.

U.S.EPA, Interim Reregistration Eligibility Decision for Methidathion. 2002,
U.S. Environmental Protection Agency: Washington, D.C.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Methyl Parathion.
2003, U.S. Environmental Protection Agency: Washington, D.C.

Extoxnet Aldicarb. 2008.

U.S.EPA, Reregistration Eligibility Decision (RED)-Aldicarb. 2007, U.S.
Environmental Protection Agency: Washington, D.C.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Carbaryl. 2004,
U.S. Environmental Protection Agency: Washington, D.C.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)- Carbofia-an. 2006,
U.S. Environmetal Protection Agency: Washington, D.C.

U.S.EPA, Reregistration Eligibility Decision (RED)-Methomyl. 1998, U.S.
Environmental Protection Agency: Washington, D.C.

Extoxnet Oxamyl. 2008.

U.S.EPA, Interim Reregistration Eligibility Decision (IRED)-Oxamyl. 2000, U.S.
Environmental Protection Agency: Washington, D.C.

U.S.EPA, Reregistration Eligibility Decision (RED)-Captan. 1999, U.S.
Environmental Protection Agency: Washington, D.C.

U.S.EPA, Reregistration Eligibility Decision (RED)—Chlorothalonil. 1999, U.S.
Environmental Protection Agency: Washington, D.C.

U.S.EPA, Reregistration Eligibility Decision-Iprodione. 1998, U.S.
Environmental Protection Agency: Washington, D.C.

U.S.EPA, Reregistration Eligibility Decision-Mancozeb. 2005, U.S.
Environmental Protection Agency: Washington, D.C.

195

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

U.S.EPA, Reregistration Eligibility Decision-Maneb. 2005, U.S. Environmental
Protection Agency: Washington, D.C.

U.S.EPA, Acetarniprid-Pesticide Fact Sheet. 2002, U.S. Environmental Protection
Agency: Washington, D.C.

U.S.EPA, Bifenazate-Pesticide Fact Sheet. 1999, U.S. Environmental Protection
Agency: Washington, D.C.

Bifenazate; Pesticide Tolerance. 2002, U.S. Environmental Protection Agency.

Nichino America, I. Buprofezin (Applaud 70DF) Material Safety Data Sheet.
2003 [cited 2008; Available from: http://www.cdms.net/LDat/mp6UHOO1.pdf.

 

Buprofezin; Pesticide Tolerance. 2006, U.S. Environmental Protection Agency.
Buprofezin; Pesticide Tolerance. 2003, U.S. Environmental Protection Agency.

Imidacloprid; Pesticide Tolerances. 1998, U.S. Environmental Protection
Agency.

Imidacloprid; Pesticide Tolerance. 2004, U.S. Environmental Protection Agency.

Cox, C., Imidacloprid-Insecticide Fact Sheet. Journal of Pesticide Forum, 2001.
21(1): p. 15-21.

Imidacloprid; Pesticide Tolerances. 2006, U.S. Environmental Protection
Agency.

U.S.EPA, Indoxacarb-Pesticide Fact Sheet. 2000, U.S. Environmental Protection
Agency: Washington, D.D.

CA—DPR, Methoxyfenozide Public Report 2003-3. 2003, California Department of
Pesticide Regulation.

Methoxyfenozide; Pesticide Tolerance. 2006.

196

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

U.S.EPA, Pymetrozine-Pesticide Fact Sheet. 2000, U.S. Environmental Protection
Agency: Washington, D.D.

Fuj irnori, K., Pyriproxyfen-Toxicological Evaluations. 1999, FAO, “’HO and
International Program on Chemical Safety (IPCS): Rome.

Pyriproxyfen; Pesticide Tolerance. 2007, U.S. Environmental Protection Agency.

U.S.EPA, Spinosad-Pesticide Fact Sheet. Undated, U.S. Environmental
Protection Agency: Washington, D.C.

Spinosad; Pesticide Tolerances. 2002, U.S. Environmental Protection Agency.

U.S.EPA. EPA 's Risk Assessment Process for Tolerance Reassessment. 1999;
Available fi’om: www.cpagov/opp feadl /traclpap_er44.pdf.

 

Tebufenozide; Pesticide Tolerance. 2004, U.S. Environmental Protection Agency.

Syngenta Crop Protection, 1. Thiamethoxam (Optigard) Material Safety Data
Sheet. 2008.

Thiamethoxam; Pesticide Tolerance. 2007, U.S. Environmental Protection
Agency.

U.S.EPA, Azowstrobin-Fact Sheet. 1997, U.S. Environmental Protection Agency.

U.S.EPA, Azoxystrobin-Pesticide Tolerance. 2003, U.S. Environmental
Protection Agency.

U.S.EPA, Cyprodinil-Pesticide Fact Sheet. 1998, U.S. Environmental Protection
Agency: Washington, D.C.

U.S.EPA, F enhexamid-Pesticide Fact Sheet. 1999, U.S. Environmental Protection
Agency: Washington, D.C.

Syngenta Crop Protection, I. (2001) F ludioxonil (Maxim) Material Safety Data
Sheet. 2008.

197

54.

55.

56.

57.

58.

U.S.EPA, F ludioxonil; Pesticide Tolerance. 2002, U.S. Environmental Protection
Agency.

Syngenta Crop Protection, 1. Mefenoxam (Subdue Marx) Material Safety Data
Sheet. 2008.

U.S.EPA, Mefenoxam; Pesticide Tolerance. 2001, U.S. Environmental Protection
Agency.

U.S.EPA, Trifloxystrobin-Pesticide Fact Sheet. 1999, U.S. Environmental
Protection Agency: Washington, D.C.

U.S.EPA, T rifloxystrobin; Pesticide Tolerance. 2003, U.S. Environmental
Protection Agency.

198

APPENDIX C
Individual Pesticide Use Charts

199

B2 carcinogenic fungicides

 

 

 

 

 

 

 

 

 

 

Captan
5,000,000 1,750,000
4,000,000 a A i 1'500'000
/ \ l 1,250,000
3.000.000 .- . _ 1,000,000?
C32,000,000 N \ ”59°00 8
~ 500,000 ’°
1’000'000 “ . ~ 250,000
0 r r I l I I r I O
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied +CLF Acres treated

 

+CA-DPR Tot lbs applied --)<--CA-DPR Tot acres treated

 

 

 

 

 

16,000,000

12,000,000

CLF

8,000,000

4,000,000

 

 

 

 

 

 

 

 

 

 

Chlorothalonil
1,000,000
, ~ 800,000
~ 600,000 n
3?
0
~ 400,000 3
~ 200,000
0 l I l T I l l l 0
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied +CLF Acres treated

+CA-DPR Tot lbs gaplied +CA-DPR Tot acres treated

 

 

 

200

 

N-mcthylcarbamate insecticides

 

 

u.
._l
U

 

 

Oxamyl
400,000 120,000
I O r 100,000
300,000 - 0
~ 80,000

 

 

 

200,000 A YA I 60,000
’/\ / \x—x—x/x r 40,000
100,000 X W

 

 

 

. 20,000
0 T I I I I I I I 0
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CLF lbs applied +CLF Acres treated

 

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

UdO-VD

 

201

 

Organophosphate insecticides

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Acephate
800,000
600,000 . I
I
9 a
400,000
200,000
0 I T l T l l i I
1990 1992 1994 1996 998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied +CLF Acres treated
Fenamiphos
400,000
0
300.000
200,000
100,000
0 I I I T T I T I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
+CLF lbs applied --I-CLF Acres treated

 

 

 

 

202

 

 

 

Methidathion

 

400,000

 

300,000 /
I

 

 

200,000 /

 

100,000

 

0 T I

 

 

T

l T U T I

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

+CLF lbs applied

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

+CLF Acres treated

 

 

203

 

Reduced-risk fungicide

 

 

400,000
300,000
200,000
100,000

0

Trifloxystrobin

 

 

 

 

 

 

 

I I

1992 1994 1996

1998 2000 2002 2004 2006 2008
Year

 

 

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

+CLF lbs applied

 

+CLF Acres treated

 

 

204

 

Reduced-risk insecticides

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Bifenazate
200,000
150,000 //x
100,000 I
50,000 ”/i
0 I I I I T T
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied —x-CA-DPR Tot acres treated
—e—CLF lbs applied —~I— CLF Acres treated
Indoxacarb

 

 

 

 

 

 

 

 

 

 

 

 

 

300,000 I
250,000
200,000 Xv/
150,000 .2/
100,000 /
50,000 /
0 s T 1 . I .
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
+CA-DPR Tot lbs applied -><—CA-DPR Tot acres treated
-e—CLF lbs applied --!—- CLF Acres treated

 

 

 

205

 

 

 

Pymetrozine

 

 

 

 

 

 

 

120,000
100,000 . /
l 80,000 7’
5 60,000
40,000
20,000 /

 

 

 

60,000
50,000
40,000
30,000
20,000
10,000
0

1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

+ CLF lbs applied

 

+ CLF Acres treated
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

Eda-VD

 

 

 

 

 

 

 

 

 

Methoxyfenozide
1,000,000
300,000 X
400,000
200,000 ‘A
0 I I r T .

 

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

 

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

 

206

 

 

 

Tebufenozide

1,200,000 300,000

900,000

//\" \ r 200,000
600,000 "

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

(1
>
L‘- c':
.. / \, 400,000 .1.
300,000
w 0 \
o " I I I O
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
—e—CLF lbs applied +CLF Acres treated
+CA-DPR Tot lbs applied +CA-DPR Tot acres treated
Thiamethoxam
300,000 40,000
/\\ r 30,000
200,000 ..
5 ~ 20,000 a;
u a
100,000 3
~ 10,000
M
0 I T I 1 T T I 0
1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
—e—CLF lbs applied -+I— CLF Acres treated

 

 

+CA-DPR Tot lbs applied +CA-DPR Tot acres treated

 

 

207

 

 

APPENDIX D
Individual Pesticide Residue Detects Charts

208

B2 carcinogenic fungicides

 

% detects

 

 

 

owhmoo

 

 

 

 

 

 

 

l

l

 

 

1.

 

l

%detects
O—th-bolmflm
! l ';

 

 

 

 

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
l Year

———~—-.-~————~ ‘H

l

 

 

 

l + PDP—",6 detects _ i 4— CA—DPR % detects

 

 

209

 

8

0

3
o
1:

Iprodione

 

25.0

 

20.0 A
15.0

 

/ \

A
/\

 

 

*5, If}. \ /
MW

 

 

0.0 fl . r

 

I I r I I

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

+PDP % detects

+CA-DPR % detects

 

210

 

 

 

 

Carbamate insecticides

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Aldicarb
0.02
I

8 0.015 I *Wv A- - W
8
t; 0.01 W *W—v- W W ~W
'U
a!

0.005 W WWW , -A, 32‘ ___,,,

0 I H—Q—O—Q—O—V—O—Q—HWe
1990 1992 1994 1996 1998 2000 2002 2004 2006

f _ __ %, Year _ _

+ PDP % detects —-—— CA-DPR % detects f_

Methomyl

10
s l
1:
.\°

0 l l I T I I 7 l

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
s -._‘~___.__ __ _ _!9€L_ s
r a fillifisfiti A, A l _. +9§EEPL®E9 W- ,

 

211

 

 

 

 

 

 

 

 

 

 

l a-
l
i 8 6

'U
. g 2 it

0 I . M I . T T l

l 1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
,n___ ____, :32L________ Us a
l l, :BDP %ietefis s __ A l. :—£P:£1’1%33t69_ ,

 

212

Organophosphate insecticides

l Acephate

 

% detects

 

 

 

 

owe-moo
I:
l
l

 

I Year

 

 

 

 

 

 

 

 

 

 

 

 

213

 

 

 

. 0 Y .
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
l ——— A.
. *WPDP%detects +CA-DPR°/gdetects l
Fenamiphos
0.04
EODSWW W
0.02 Th' W
O
=2 0.01 W WW—
0 w.
1990 1992 1994 1996 1998 2000 2002 2004 2006
Year
7 75W)" EB? @9667 7:77EWWCADPR % detesss- 1
Fonofos
0.03
0.025WWW W ,L W W W WW W W W—
£0.02WWW W W W W W W W W WWWWWWWW-W
I
80.015WWW WWW W W WWWWWWW
°\. 0.01W~WWWWWWWWWWWWWWWWW
0.005WWWWWWWW-6WWWWWWWW —W
0 , , e e e c e WW ¢
19901992199419961998 2000 2002 2004 2006
Year
riPEFE/oEéEcE 7 f W7CEEEB7§¥§§7 7

 

Disulfoton

 

0.04

 

0.03 _,

 

 

0.02
0.01 —~

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Reduced-risk fungicides

 

 

 

 

 

Azoxystrobin

10-
25 8 — A T —
a.

- 6.2 _ v 7,; i _
3., %%%%% 77-- s 7,
‘D
32 2 s i »_ ,_ ‘_ -‘-

0 v I l I ' I I T

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

 

 

 

 

Cyprodinil
14 7
12 ~ W 4 — * ~ W
3
a 10 ~— * a a
Q 8 AW‘ + A v 7
g.-
'0 4 ,s____‘_nm,,mfi_i_,nfl ,
32
2, _-,w_‘ *-_i**-____._‘
O I I I I I l
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

215

 

Fenhexamid

 

35
30_ - _______I _II, 7 ”Av,” ,_44,-.
25

20 w~ w — ~v~s mi
15 ea 7! -i ,f... f --
10 — in rt—w __, I- —»—
5 7* * *____ ____, _i 7‘ _
0 - . . . . T ,
1990 1992 1994 1996 1998 2000 2002 2004 2006

Year

% detects, PDP

 

 

 

 

 

 

 

 

 

% detects, PDP
N w A

—l

  

 

 

      

 

I I 7 j I

1990 1992 1994 1996 1998 2000 002 2004 2006 2008

1 Year 1

 

 

216

°/o detects, PDP

 

% detects, PDP

 

Reduced-risk insecticides

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

If i it Bifenazate _ w A
2
1.5 W~WW .— _ . ‘\\
1 _ _ v i ,7 i A *_ I
0.5 «» _, WW——* . - ., _ ,_ ___,
0 Y , . , T . , r
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year i
I I ”I 73%;.{77 7 77 7 I
0.12
0.09 - --W .W W ‘______._.7-,
0% W w..i W W W722222 7 -4..-, _ ,
0.03W-WWW—W WA-*__,__
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

 

217

 

 

 

 

  

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

2 Indoxacarb
l 25
3 20W W W WW W W
a.
- 15 _. _ A A _ _ m
g. -2 . -- 2 l 2 -
'0
:gesm _____¥___- m
l o 7 Y " T » I7 r
l 1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
1 Year
Methoxyfenozide
30.0
25.0
a.
220.0
515.0
.3.
010.0
'0 O
a! 5.0
0.0 I I I I I I I I
1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year
_ __ DIME s __.h _‘ __ _,__l w,
Pymetrozine
1 l
30.8WW—W~
a.
-0.6WWWWWWWWWWWWW—~
s.- I
° 1
320.2«— WWWW WWWWWWWW W—
E o I . I I I T T l
l 1990 1992 1994 1996 1998 2000 2002 2004 2006 zooalI
Year I
,l

218

 

 

 

 

 

 

 

 

 

1990 1992 1994 19% 1998 2000 2002 2004 2006 2008
Year

Spinosad

 

 

 

 

%detecta,PDP
O N -b O) 00
l
l
l
l
l
l
l

A__-.‘ .I/

I v ' I - T

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
Year

 

+ Spinosad ' I sanzamfaeci; 7. I

l l
l

 

219

 

% detects, PDP
O 00 O) (O
* I
l
I
l
l
l
l

 

 

 

 

I I I

1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

Year

 

 

 

 

 

0 T I I t
l 1990 1992 1994 1996 1998 2000 2002 2004 2006 2008

I Year

 

T I I I

 

220

APPENDIX E
Acute and Chronic Exposure and Risk Estimates for Iprodione

221

60:28.23. s0.00 83:53 95300 0 $0
00:20.23 50.0 0.2553» 2:80.08 m 35» W 2&5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

80 00080.0 med 00080.0 $5.” 03080 000 8080.0 002 0038.0 85005
92 8080.0 8.0 8080.0 9.0 0380.0 30.0 8800.0 0?? 0088.0 Emma +0m 80¢.
00." 03000.0 m0.N 0880.0 N0.N 0380.0 mm.0 8800.0 8.00 8008.0 0:50.05
N00 34:00.0 2.10 3800.0 m0; 3080.0 2.0 03000.0 :0 0208.0 Emma 0v-0m mow<
3; 0980.0 0m; 0380.0 00.0 000800 E .0 3008.0 SN 8080.0 85005
m0; 000N000 mm; $800.0 NmN 3080.0 8.0 8880 Sue 8800.0 2me 072 mow<
mm.m 0880.0 Gd 0 8000.0 006 00: 00.0 00.0 0038.0 0000 0088.0 0:50.“:
Ed 0980.0 Sum 3300.0 m0.v 8008.0 00.0 8300.0 000.8 00020.0 Emma N70 mom<
00+ 00800.0 00.m 0808.0 5.0 8008.0 em; 00800.0 0m.Nm 00080.0 0:50.05
05m 00218.0 80 3800.0 50.0 8030.0 0m; $300.0 0N.0m 288.0 2me Wm mow<
mm .0 0808.0 02. 8030.0 8.2 0088.0 m0; 00080.0 00.0w 0003 0.0 0:50.05
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Sim 8080.0 28 0880.0 mmé 0038.0 3.0 8008.0 0v.mfi 00080.0 850.05
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8.x. 8:8me 8.x. 2:8me ease oBmomxm 8.x. 830me 8.x. 8309mm

2.28m .50 0:230 090 3:230 090 82 $533M 90:828.
80m .0100 NO0N 000m Hum 002 .900 N00HHHOA Hum 080000.000 .8000uhomv 0:585 98.5

m 5E. N 5E. 0 BE. .8 Emma 583000

 

 

 

 

 

 

 

83.... one: .8.“ 32358 95333 83: 2.28.5— .E— 505004

222

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

   

 

00.0 080000 00.0 030000 000 0000000 3.0 0000000 00.00 000000 +00 8 <
00.0 050000 00.0 030000 00.0 0000000 00.0 000800 00.3 0000000 0v-00 mom<
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8:03@ .56 83:58 0.5893 06.3.50 0:369:16 6.66 $656.3.

225

 

 

 

 

 

 

 

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36.—6.6 0:36 6:3 8.6326 .86 8608630 06666.. .5053 0.866565 .md— N66509:.

226

Appendix E-6- Iprodionsasutg riskewtimlatwkfozgtoae fruit: ([imLamB) _

i

 

 

Anpendix E7gelnr91iqyeec2tgisk @tingfl 9199211793 (Iigr_3L__ ___

% RfD

 

 

16.0

14.0

12.0

10.0

4.0

2.0

0.0

Iprodione Acute Exposure, Stone fruits

 

 

 

 

 

 

 

 

 

- 0- Tier 1
4 0 (PCT=100%,
' Tolerance,
3,5 DEEM) %RfD,
Acute
3’0 —-0—Tler 1
2.5 32 (PCT =100%,
2?. Tolerance,LifeLi
2-0 g ne) %RfD, Acute
1.5 E
5 - - O - Tier 2
1.0 (PCT=100%, HFT
0 5 Residue, DEEM)
' %RfD, Acute
0.0
—O—Tier 2
(PCI'=100%, HFT
Residue,
LifeLine) %RfD,
Acute

Iprodione Acute Exposure, Stone fruits - ,5- 119; 3 (1992 PCT, 1995

E PDP Residue, DEEM)
%RfD, Acute

 

 

 

-- {3}" Tier 3 (1997 PCT, 2000
PDP Residue, DEEM)
%RfD, Acute

 

 

-¥é - Tier 3 (2002 PCT, 2006

' PDP Residue, DEEM)
a %RfD, Acute

-t—Tier 3 (1992 PCT, 1995

 

 

 

 

 

 

 

 

 

f— A-——--—*—- 7,7 . ~ - PDP Residue, LifeLine)
l {S ‘ %RfD, Acute
i / " . +Tler 3 (1997
i . 1 ~. 6 . T . PCBZOOOPDP, LifeLine)
5 IL 5, ’L 9 %RfD, Acute
\\We 9395 P995 t’fi'q’A 5‘ A $10) 969*
9.9; P, e “,6 >9: —-+é—Tier 3 (2002 PCT, zoos
PDP Residue,LifeLine)
%RfD, Acute

227

 

 

Appendix E,-8- , Iprodione shrank wiggling? I01 §t93e_fr,uitsv!9ingD@Mi

—0—Tler 1
‘ iprodione Chronic Exposure, Stone fruits (DEEM) (pa-flows,

DEEM) %RfD,

I 70.0 +— , , ' fl 5-0 Chronic

+Tier 2 (1992
40 PCT ,DEEM)
%RfD, Chronic

  

*3.

-El- Tier 2 (2002 T
PCT, DEEM)
%RfD, Chronic

o
96

 

N
(2 193) am

+Tier 3 (1992 t
PCT, DEEM) %
%RfD, Chronic 1

es :1 .‘a {L ’ 9 9 02¢ - ->(- Tier 3 (2002 ‘

l \xfi' 62‘ 62°" as” 9" '9" ea" PCT, DEEM) ,
P pt NI, W “as we," Nb .

1 %RfD, Chronic J

Iprodione Chronic Exposure, Stone fruits (LifeLine) ‘

 

 

 

 

’ . —0-Tier 1 '
80.0 1 (PCT=100%, 1
I I I 5'00 LifeLine) %RfD, '
L: 70. 0 } Chronic
' L 4 oo —l—Tler 2 (1992
3 .
HBO' '0 ' ! PCT, LifeLine)
In x .
E 50.0 __ _ 3.00 a %RfD, Chronic
V o
| 940.0 ~ — q - a- Tier 2 (2002
1 n: 2.00 LI; PCT, Lifeline)
3330- 0 g %RfD, Chronic
20. o H:rfi ’
f 1.00 ,_ _ Tier 3 (1992
10. o — I — ., ~ PCT, LifeLine)
1 if; %RfD, Chronic
) 0.0 “' Ii 0.“)
.6 ’L 9 9 — -- TierB (2002
«:13 s A 69"
wfie" “95 figs ”956’ ”253% s’LO) “$25 PCT, LifeLine)
%RfD, Chronic
i ,

 

228

Appegdixj: 10; Iprodione cancer risk estimates for stone fruits

Cancer risk

 

1.3504 1
1.6504 #7
1.4504
1.2504 ‘
1.0504 .
8.0505 ;
6.0E-05 . »
4.0505 1 ,
2.0505 ‘
1.0E-08 ‘

Iprodione Cancer Risk, Stone fruits

 

 

 

 

 

 

 

 

 

I DEEM
lLiftene
' 140506 I 9.81E-07
I I 1 01E-06
(.0
1" d5"?
(50

 

229

 

APPENDIX F
Acute and Chronic Exposure and Risk Estimates for Fludioxonil

230

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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33.: 2.3... .8.“ 83338 0.5235 353 ___—03.2....— AH fiuaomm<

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233

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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692.289 ..8 83:58 0.5893 2.8.39 _Ecxcmcafi .vum Mme—$97..

234

{Appendix IE. Findigqniljcgte r111; afimatcs 19! Stgpeefteits

 

3.0

Fludioxonil Acute Exposure, Stone fruits

 

2.5

2.0

1.5

% RfD

 

 

- 0- Tier iTPCT=iOO%,fi
- - 0 - Tier 2 (PCT=100%,
—t - Tier 3 (2006 PDP

i_ —o— Tier 1 (PCT=100%,
W ‘ +Tier 2 (PCT=100%,

Acute
- i- Tier 3 (2006 PDP

Tolerance, DEEM)
%RfD, Acute

HFT Residue,
DEEM) %RfD,
Acute

Residue, DEEM)
%RfD, Acute

Tolerance,LifeLine)
%RfD, Acute

HFI' Residue,
LifeLine) %RfD,

Residue, LifeLine)
%RfD, Acute

 

 

TEAppendix F,6. Fludioxonil chronic risk estimates for stone fruits

l

_ 96 RfD (Tiers 1 & 2)

H
.N
O

Fludioxonil Chronic Exposure, Stone fruits

5.0

 

H
P
D

 

 

235

P
c

S”
o

N
o

2"
o

‘- 0.0

(s 13!.L) am %

—0— Her 1 (PCT =100%,
Tolerance, DEEM)
%RfD, Acute

—-l— Tier 2 (Tolerance,
PCT, DEEM) %RfD,
Acute

—+—Tier 1 (PCT=100%,
Tolerance,LifeLine),
%RfD, Acute

—l— Tier 2 (Tolerance,
PCT, LifeLine)
%RfD, Acute

- {-3- Tier 3 (Ave. FT,
PCT, DEEM) %RfD,
Acute

- @- Tler 3 (Ave. FT,
PCT, LifeLine)
%RfD, Acute