”MW/ll W J I 133 809 THS 7.51;st “HIllllllilllllllll‘lllllllllHilllllllllllllllllllllllllllll 3 1293 01771 ILHBFUAFU! i Michigan State . University This is to certify that the thesis entitled A Case-Control Study of Colon Cancer and Occupation Among African American Men and Women - A Population-Based Examination presented by Erik Helms has been accepted towards fulfillment of the requirements for Master's aggreeinEpidemiology 6%” M! or professor Daeuygij9¥ 0-7639 MS U is an Affirmative Action/Equal Opportunity Institution PLACE IN RETURN BOX to remove this checkout from your record. To AVOID FINES return on or before date due. MAY BE RECALLED with earlier due date if requested. DATE DUE DATE DUE DATE DUE :19; 35- 2’ 9‘ Eol ma ciClRCanflS-p.“ A CASE-CONTROL STUDY OF COLON CANCER AND OCCUPATION AMONG AFRICAN AMERICAN MEN AND WOMEN - A POPULATION-BASED EXAMINATION BY Erik D. Helms A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Department of Epidemiology 1998 ABSTRACT A CASE-CONTROL STUDY OF COLON CANCER AND OCCUPATION AMONG AFRICAN AMERICAN MEN AND WOMEN - A POPULATION-BASED EXAMINATION BY Erik D. Helms Information obtained on Blacks and Whites from the Occupational Cancer Incidence Surveillance Study (OCISS), a case-referent study investigating workplace risk factors, was analyzed to identify explanatory factors for racial differences in colon cancer risk. A case-control analysis was utilized to test the hypothesis of an increased risk of colon cancer among Blacks. All analyses were adjusted for the potential confounding effects of age, gender, occupation and tobacco use history. No conclusion could be drawn from the data presented that the risk of colon cancer is consistently greater among a majority of occupational groupings for Blacks than for Whites. Sociodemographic or smoking-related characteristics do not appear to be associated with an increased risk of colon cancer, which was consistent among men and women across races. However, the findings of an age-related increase in risk of colon cancer among both races are consistent with SEER incidence data. Although these data cannot address all underlying reasons for observed differences in occupational risks among Blacks and Whites, it underscores the need for further study of the relationship between colon cancer, occupation, and race. ACKNOWLEDGMENTS This study was supported by NIOSH grant #: ROl-OH02067 and SEER grant #: NOl-CNOSZZS. I am most grateful to Dr. G. Marie Swanson for her continued support and guidance throughout my Master's program. I would also like to thank my wife, Michelle, for her patience and encouragement, and my parents and sister for their dedication and support. iii LIST OF TABLES INTRODUCTION BACKGROUND . STAGE/SITE . DIET . . . . SMOKING . . . OCCUPATION . MATERIALS AND RESULTS . . . DISCUSSION . LIST OF REFERENCES METHODS TABLE OF CONTENTS iv LIST OF TABLES Page Table 1: Characteristics of Colon Cancer Cases and Population Controls . . . . . . . . . . . . 23 Table 2: Smoking History, Age, and Work Status of Colon Cancer Cases and Population Controls Among Blacks and Whites . . . . . . . . . . . . 26 Table 3: Colon Cancer Risk Among White and Black Subjects for Selected Usual Industries and Occupations . . . . . . . . . . . . . . . . . . 27 Table 4: Colon Cancer Risk Among Male and Female Subjects for Selected Usual Industries and Occupations . . . . . . . . . . . . . . . . . . 28 Table 5: Logistic Regression Results: Risk of Colon Cancer Among Study Subjects by Age, Race, Gender, Tobacco Use History, and Usual Occupation/Industry . . . . . . . . . . . . . . 31 INTRODUCTION Cancer of the large bowel is second only to lung cancer as a cause of death among men and women due to malignancies in the United States (Potter et al., 1993), and is the fourth most common incident cancer (after breast, lung, and prostate). It has been estimated by the American Cancer Society that there were approximately 94,500 incident cases of colon cancer diagnosed in 1997, and an estimated 46,400 deaths in 1997. The incidence rates show a wide divergence by racial/ethnic group, while within each racial/ethnic group, incidence rates for cancer of the colon among women are slightly lower than those among men (Ries et al., 1994). While incidence rates have seen a general upward trend since 1973, the age-adjusted mortality rates for all races combined have actually fallen 31% for women and 9% for men over the past 30 years (American Cancer Society, 1996). From 1950 to 1991, the five-year relative survival rates have increased from 41% to 60.9%. The overall median age of diagnosis for colon cancer is 72, with the median age of death being 74 years of age (Ries et al., 1994). Colon cancer is essentially the only cancer that occurs with approximately equal frequency in men and women. The lifetime risk of being diagnosed with colon cancer is approximately 6.14% for males and 5.92% for females. Lifetime risk of dying of cancer of the colon is 2.60% for males and 2.65% for females (Ries et al., 1994). Although cancers of the colon are currently the second and third most 1 frequently diagnosed malignancy among men and women respectively, and have increased in incidence during the past two decades, the all-race and all-age incidence had decreased slightly (by 1.3%) between 1988 and 1992 (Ries et al., 1994). However, when this decrease was stratified by race, there was actually an increased incidence among Blacks (.9%). Although incidence rates of colon cancer are not as divergent for Blacks and Whites as are other common malignancies (lung and prostate), the difference is still important to examine due to the higher levels of mortality experienced among the Black population from colon cancer. From the period between 1988 through 1992, the age-adjusted incidence rate of colon cancer among Blacks was 40.4 per 100,000, and 35.5 per 100,000 among Non-Hispanic Whites (Miller et al., 1996). Data indicate that greater numbers of Black males and females are diagnosed with colon cancer at an earlier age than their age-adjusted White counterparts. For Black males, rates per 100,000 begin to differ drastically from Whites in the 35-39 year age group (18.1 vs. 11.2 per 100,000) (Miller et al., 1996), and continue to be diagnosed at higher rates until age 74. The numbers and the extent of disparity between Blacks and Whites are similar for women. In addition, mortality rates from cancer of the colon and rectum combined were generally higher for Blacks (23.4 per 100,000) compared to Non- Hispanic Whites (18.4 per 100,000) (Miller et al., 1996). Cancer of the colon is a highly treatable and often curable disease when localized to the bowel. It is also the second most common cause of cancer death” inore than 90% of cancers of the colon are adenocarcinomas. Very little is known about the etiology of colonic lymphomas and carcinoids which compromise almost all of the remaining histologic types. Little is also known about the relationship between specific histologic subtypes of adenocarcinoma to the environmental risk factors, physiologic processes, and molecular changes? (Potter et al., 1993). Therefore, because of the frequency of this disease, lack of knowledge regarding its specific etiology, and its substantial public health impact in terms of both mortality and morbidity (recurrence is commonly the ultimate cause of death and is associated with the greatest cost), the identification and follow-up of high-risk groups for early stage diagnosis should be a priority for certain subsets of the population. Indeed, the impact of stage severity and comorbidity increases the costs of colon cancer, both in terms of resource use and patient suffering. Taplin et al. (1995) found that the age-adjusted costs of initial care for a patient diagnosed with carcinoma in situ of the colon was $13,848 for local, $15,398 for regional, and $17,223 for distant sites. Additionally, stage and comorbidity were found to be more predictive of cost than age, indicating the need for increased early detection among at-risk populations. Based upon the statistics presented by SEER since 1971, it appears that Blacks fall into this high-risk 3 category. The improvements in survival rates (49% in 1973 to 62% in 1991) and decreased mortality that have been seen in the White population have fallen short of those levels in the Black population (52% in 1991). The all race and age five year relative survival rate for the total population from 1986-1991 was 61%. The rate for Whites over the same period of time was 61.8%, while for Blacks, five-year relative survival rates were 52.4%. Blacks also have a greater likelihood of dying at a younger age than Whites (115/100,000 vs. 81/100,000) between 55 and 64 years of age (Ries et al., 1994). Because of the documented differences in colon cancer incidence and mortality between Blacks and Whites, as well as the overall impact of this disease upon public health, it is important to obtain a better understanding of factors which may contribute to differential rates. The objective of this study is to determine the possible explanatory factors for racial differences in colon cancer risk. Further, this study will examine the association between the occurrence of colon cancer among Black and White males and females and the usual occupations and industries in which they were ever employed, as well as the tobacco use histories of the study subjects. This research utilizes one of the largest population-based samples available to conduct an examination of race, colon cancer, and occupation. BACKGROUND The need to evaluate race and the differential rates in cancer incidence, morbidity, mortality, and survival has 4 been recognized for several decades. However, the difficulty in establishing the determinants of these differences has also been evident. Current state-of-the-art literature concerned with colon cancer has focused mainly upon dietary patterns, exercise habits, family history, and to some extent, stage at diagnosis or tumor site. Much of this research has been limited to samples containing only White males or very small sample sizes. Additionally, very limited smoking histories have been available from population-based studies, and occupational exposures were traditionally obtained from death certificate data, which have been shown to misclassify usual occupation and industry by as much as 30 to 50 percent (Swanson Final Performance Report, National Institute of Occupational Safety and Health, 1995). To the large extent that cancer of the colon is described by heredity and diet, these factors do not fully ascertain causation, nor do they completely describe the disproportionate levels of morbidity and mortality among the Black population. STAGE/SITE Determinants of Black/White differences are often postulated to be a direct result of more advanced disease at diagnosis and socioeconomic differences between Blacks and Whites. Data show that survival rate differences may be due, in part, to the different stage distributions at diagnosis. For White males and females, 38% of all cases were diagnosed as having localized tumors, 37% as regional, 19% as distant, and 6% unstaged. Only 32% of Blacks were 5 diagnosed as localized, while 35% were regional, 25% distant, and 8% unstaged. Overall, relative survival rates vary only slightly by age at diagnosis for both racial groups, although rates are lower for Blacks throughout all age groups than survival rates for Whites (Ries et al., 1994). However, according to Mayberry et a1. (1995), the few studies that have investigated stage differences have been limited by the modest number and type of explanatory factors that were considered. They attempted to determine what characteristics might contribute to the racial differences in colon cancer survival and if a survival disparity remained between Blacks and Whites after adjustment was made for these characteristics. Several investigators have studied the possible relationship between stage and site with respect to Black/White colon cancer survival differences. Mayberry et al. (1996), in a prospective NCI Black/White cancer survival study of 454 Blacks and 521 Whites, found that, after age and gender adjustment, mortality hazard ratios for Blacks were 50% higher than for Whites. Further adjustment for stage reduced the excess mortality to 20% (RR=1.2, CI =1.0- 1.5). Adjustment for poverty and other sociodemographic conditions did not further explain the survival disadvantage among Blacks. It was concluded that stage at diagnosis accounted for more than half of the excess colon cancer mortality experienced among Blacks. An additional study by Coates et a1. (1995) explored specific anatomic site distribution within the colon by race and other colon cancer 6 risk factors to determine whether or not this may contribute to survival differences. Among 1,045 patients from Atlanta, New Orleans, and San Francisco/Oakland, it was found that site was related to stage, grade, and histologic type, and possibly smoking, however, it was not related to race, suggesting that site differences are unlikely to contribute to poorer survival among Blacks/Whites. DIET While as many as 25% of patients with colon cancer have a family history of the disease (Potter et al., 1993), the vast majority of cases of colon cancer appear to be related to environmental factors. A substantial body of research exists on the relationship between mortality from colon cancer and per capita consumption of calories, with special emphasis placed upon examining dietary fat, meat proteins, fiber, cruciferous vegetables, and calcium and other micronutrients (Potter et al., 1993). In general, it appears that a large portion of the colon cancer incidence may be attributed to a diet with high fat and low fiber/vegetable intake. Migrant data have shown that the disease is particularly sensitive to changes in the environment and diet, with incidence rates reaching those of the host country within one to two generations (Potter et al., 1993). Internationally, colon cancer rates are the highest in more developed countries of the Western world, including Europe, Australia, the U.S., and Canada, with incidence rates in the range of 25-35/100,000 during the 1980's. These rates are vastly different from some of the 7 lesser developed nations, where in India for example, incidence rates are 1-3/100,000 and 3.4/100,000 in Nigeria (Potter et al., 1993). Several ecologic and case-control studies demonstrate positive associations between the risk for colon cancer and dietary fat (Willett et al., 1990; Giovannuci et al., 1992; Grahm et al., 1988). Others have found positive associations with the consumption of meat (Willett et al., 1990; Bostick, 1994; Manousos et al., 1983). Separating the independent effects of dietary fats and meats proved to be difficult in these studies. Many etiologic hypotheses related to colon cancer have evolved from the examination of dietary patterns and alcohol consumption upon rate differences between Blacks and Whites. Findings have indicated some geographic differences based upon food frequency questionnaire methodologies. Blacks have been found in general to consume higher fat, lower fiber diets. Finally, as with diet, an association between alcohol and colon cancer has generally been found to be inconsistent (Miller et al., 1983; Ferraroni et al., 1989; Murata et al., 1996; Potter et al., 1993). The topic of diet and its relationship to colon cancer has been explored in detail (Swanson et al., 1993; Dales et al., 1978; Potter et al., 1993; National Academy Press, 1989) and will not be discussed further in this paper. Very little data have been provided to determine the impact of additional exposures and risk factors, such as cigarette smoking and occupational exposures upon colon cancer. Less emphasis has been placed upon these variables in explaining 8 the disproportionate levels of colon cancer morbidity and mortality by race. It is important to recognize that the data on diet remain inconsistent and inconclusive due to population differences and issues related to the validity of measurement instruments. The ascertainment of past and present cigarette smoking habits is much easier to obtain and is generally more reliable. SMOKING There is little debate over the impact and contribution that cigarettes have had upon cancer among the general U.S. population. The first official statement on smoking and health by the U.S. government was contained in the Report of the Advisory Committee to the Surgeon General of the U.S. Public Health Service in 1964 (U.S. Department of Health, Education, and Welfare). Cigarette smoking has been implicated in cancer of the lung, larynx, oral cavity, esophagus, urinary bladder, kidney, and pancreas. Although cigarette smoking has been shown to be positively related to the risk of adenomatous polyp development, a direct causal relationship between cigarettes and colon cancer has not been firmly established. While some studies were unable to definitively establish an increase in risk of colon cancer due to smoking, (Ferraroni et al., 1989; Nyr'en et al., 1996) several other investigators have provided some inferential evidence of a relationship. A recent study by Slattery et a1. (1997), utilizing a population-based case-control study conducted in Northern California, Utah and Minnesota, observed a 50% increase in 9 colon cancer risk from smoking over a pack of cigarettes per day among both men and women. The investigators also found that those who smoked over 20 cigarettes per day and had a larger body mass index were at greater risk than participants who smoked the same amount but were smaller. Chyou et al. (1996) observed 330 incident cases of colon cancer among Hawaii Japanese men from a population of 7,945, and noted that the risk of cancer increased with age, alcohol intake, and pack-years of cigarette smoking. Giovannucci et al. (1994), in a prospective study of cigarette smoking U.S. women, found that although Relative Risk is not significantly increased among women smokers in general, it approaches 2.00 (CI=1.14-3.39) for those who have smoked 10 cigarettes or more for 45 years. The authors also note that, due to the lengthy induction period for colon cancer (35 years), the number or cases related to smoking may continue to increase due to the apparent increase in smoking among younger women in the 1960's and 70's and again in the early 1990's. Finally, in what is probably the largest population studied to date that has been analyzed for the impact of cigarettes and colon cancer, Heineman et al. (1995) followed 248,046 American veterans for 26 years to clarify the relationship between tobacco and colon cancer. Findings indicated, that when controlling for social class and occupational activity, there was a Relative Risk of 1.6 (CI=1.2-2.0) for colon cancer for those that smoked an average of two packs per day or more, and a Relative Risk of 1.4 (CI=1.2-1.8) for those who began 10 smoking by the age of 15, with the authors contending that the issues critical to this study were the length of follow- up and their choice of controls (veterans never using tobacco). Trends of consumption may also affect incidence of colon cancer among Blacks. “Between 1960 and 1987 the age- adjusted colon cancer mortality rate of Black men has increased more per 100,000 than that of White men, from 196.3 to 269.2 in Black vs. 186.6 to 213.4 in White men” (Wynder et al., 1994). In large part, this can be attributed to increases in lung cancer, but the trend differentials of smoking between Blacks and Whites may also have impact upon colon cancer incidence. Wynder (1994) notes that “The percentages of adult African-American men who smoke cigarettes (54.6% in 1974 and 40.6% in 1985) differ significantly from those of smokers among adult White American men (42.3% in 1974 and 32.1% in 1985), reflecting a lower percentage of ex-smokers among the African-American male ever-smokers than among their White American Counterparts". Sorenesen et al. (1986) provide some insight into the smoking habits of individuals based upon occupation. In a sample of 3085 Minneapolis employees, smoking prevalence was the highest among blue collar workers (45.7%) and lowest among professionals (22.9%). What is even more revealing is that blue collar workers were more likely to fail to quit in work-sponsored cessation plans, and were more likely to have smoked for a longer period of time based upon recent quit 11 rates. Data regarding this role of smoking in the etiology of colon cancer, combined with data describing the role of alcohol consumption, may point to the need for improved methods for ascertaining accurate smoking and drinking histories to explore the synergistic effects of the two exposures. OCCUPATION In addition to examining cigarette smoking exposure to investigate the increased risk of colon cancer, the relationship between occupation and colon cancer has been explored by various investigators, and although it is generally not considered an occupational disease, excess incidence of colon cancer has been reported in several occupational classifications, with some emphasis placed upon ethnic differences (Chow et al., 1994; Swanson et al., 1985; Swanson et al., 1995; Lindsay et al., 1993; Courtney et al., 1996; Garabrant et al., 1984; Lynge et al., 1988). However, few investigators have explored the risk differential between Blacks and Whites with respect to occupation and colon cancer. In addition, there are few sources from which these data may be obtained to perform this analysis. According to Swanson and Burns (1995), the study of occupation and its relationship to cancer incidence has often been restricted to men, and more often than not, White men. Again, this may have been due, in part, to the lack of available data, but also may be attributed to the fact that most large U.S. and international cancer registries established linkages to Census occupational information from 12 the 1960's and 1970's, which included a smaller percentage of women and Blacks in the U.S. and Europe. Examples of these demographic limitations can be found in several large population-based occupational cancer studies including The Canadian Labour Force Ten Percent Sample Study (Lindsay et al., 1993), the Cancer Environment Registry of Sweden (Chow et al., 1994), and Data for the Danish National System (Lynge et al., 1988), all of which utilized White males only in their analyses. Associations with colon cancer among occupational subsets of the population have been difficult to establish and often resulted in findings of relatively small increases in risk. Sensitivity in measuring increased risk depends upon several factors, all of which may be considered suspect when discussing studies involving occupational exposures. These factors include population size, the number of years of accumulation of cases, the number of controls per case, incidence of the tumor, the proportion of the population exposed to the carcinogen, accuracy in attributing exposure and disease status, and Type I and II errors (Siemiatycki et al., 1981). Limitations in establishing causality of a disease due to occupational exposures are frequent and are a direct result of the data resources available to researchers for analysis. Typically, a variety of data sources have been used to monitor trends of occupational illness and injury. These include: employer reports, death certificates, birth certificates, Worker's Compensation records, clinical 13 laboratory data, medical examiner reports, hospital discharge records, and national health surveys (Baker et al., 1989). Typically, these forms of data are collected for reasons other than surveillance, and not likely to be representative of the population at risk, and suffer from temporal as well as data validity shortcomings. A study evaluating the quality of death certificate data on occupation (Turner et al., 1987), concluded that the occupations and industries listed on death certificates were accurate for only 54% of the individuals studied. Additionally, other difficulties arise with regard to attributing risk to an increased incidence of colon cancer based upon occupation. Several issues that have been difficult to control for include temporality, recall bias, dose-response relationships, measurements of physical activity, shortcomings of the instruments utilized to measure dietary patterns, and finally, the myriad exposures that occur outside of the workplace. The study of the relationship between colon cancer and occupation has generally focused upon the comparisons between occupational groupings or categories, such as White collar vs. blue collar, industrial vs. service, etc. There has been little exploration into the differences between races and gender within occupational categories. In addition, those studies that have studied occupational risk factors among women have been mortality studies, which are limited by single death certificate entries regarding occupation and lack information on other critical risk 14 factors such as smoking (Swanson et al., 1995). A literature review by Burns et a1. (1991) revealed that between 1984 and 1987, only 14 of 116 articles provided information on non-Whites, and none of them evaluated potential confounders. Siemiatycki et al. (1981) indicate that few occupational exposures are responsible for significant proportions of any given type of cancer simply because it is unusual for a large proportion of a population to be occupationally exposed to any single substance. In addition, these authors indicate that, apart from age and sex, important cofactors such as socioeconomic status, tobacco, and ethnic group are often not included in occupational studies. The OCISS data utilized for this study, however, is unique in that, for each subject, it does include age, sex, ethnic group, and tobacco use history, as well as detailed lifetime work histories. Despite these limitations in studying the relationship between colon cancer and occupation, several established and probable carcinogens that are often encountered in the workplace have been associated with elevated colon cancer risk. Asbestos (Fredriksson et al., 1989; Selikoff et al., 1979) has been shown to elevate cancer risk by two-fold in some studies, while it has not been shown to elevate colon cancer risk in others (Burns et al., 1994; Garabrant et al., 1992). Additionally, synthetic fibers, grains, and wood dust (Siemiatycki et al., 1986) have been implicated in increased colon cancer risk. 15 Occupations that have demonstrated an increased incidence of colon cancer include coke oven workers (Chan et al., 1993), professional and technical workers, administrative, executive and managerial workers, clerical workers, sales personnel (Chow et al., 1994), chemical processing and petroleum production workers, model makers and patternmakers in the automobile manufacturing industry (SMR=487) (Swanson et al., 1985) and construction workers (Demers et al., 1994). Dubrow and Wegman (1983) undertook an analysis of 12 major occupational disease surveillance studies, utilizing only studies for which the association was significant, the association was consistent across the studies, and then the aggregate observed-to-expected ratio was obtained by combining the results of the individual studies. Findings indicated that across studies by occupation, about 33% of these studies had significant associations at the .05 level, indicating the difficulty of finding a relationship in all but the largest studies. Women were observed to have elevated risk when employed in fabricated metals manufacturing, (OR=2.4, CI .7-8.0) and rubber plastics manufacturing industries (OR=3.3, CI .6- 17.1), as were those working in utilities (OR=4.1, CI .8- 20.6). Mortality studies of relationship between occupation and colon cancer have not produced definitive results. A study of 88,289 male and female chemical plant workers revealed a slight increase in mortality from cancer of the large intestine (Teta et al., 1990). A large Canadian study 16 (Lindsay et al., 1993) found increased mortality ratios for colon cancer for individuals employed in clerical occupations, coke oven workers exposed to polycyclic aromatic hydrocarbons, and for locomotive engineers. The Lindsay study suffered from several shortcomings. The authors had no information on smoking or drinking, and industry groupings were based upon incomplete data. The Lindsay study did observe an association among workers employed in occupations characterized by low levels of physical activity and colon cancer (clerical workers). In several studies, occupational exposures were not the focus of the analysis, but rather the occupational physical activity levels (Vena et al., 1985; Sandler et al., 1995; Longnecker et al., 1995; Garabrant et al., 1984). Several investigators have looked into the hypothesis of increased incidence of colon cancer resulting from job-related stress, with equivocal findings (Courtney, et al., 1993; Courtney et al., 1996). While no study can completely control for the large number of difficulties in assessing occupational exposure and increased risk of any cancer, the Occupational Cancer Incidence Surveillance Study (OCISS) provides a unique opportunity to combine population-based cancer registry data with complete occupational and smoking histories, allowing for the assessment of the differences in risk of colon cancer experienced by the Black and White populations. 17 MATERIALS AND METHODS The data file used in this study was constructed from the 1984-1991 Occupational Cancer Incidence Surveillance Study (OCISS), which is a population-based, case-referent investigation of occupational risk factors for 11 cancer sites diagnosed in Detroit Metropolitan area residents. This study includes newly diagnosed cases, who were identified through the Metropolitan Detroit Cancer Surveillance System (MDCSS), a population-based cancer reporting system for Wayne, Oakland, and Macomb counties (Burns & Swanson, 1991). The MDCSS is a founding participant in the National Cancer Institute's SEER Program (Swanson & Brennan, 1981), and selects cases through the MDCSS rapid reporting system, enabling investigators to enroll participants into studies within 2 to 6 weeks after diagnosis (Burns & Swanson, 1991). Incident cancers occurring among Metropolitan Detroit residents enrolled in the study include White and Black cancer cases ages 40-84. This case-control analysis of occupational risks is restricted to newly diagnosed patients with cancer of the colon (ICD-9 CM 153), who were diagnosed between November 1, 1984 and June 30, 1987. Overall, approximately 20,000 interviews (each lasting approximately fifteen minutes) were completed as part of the OCISS, with cases or their spouse or other first degree relative being interviewed by telephone within eight months of their cancer diagnosis. The interviews captured smoking histories, adult medical history, demographic information, residential 18 history, and a complete lifetime occupational history. Racial background was self-reported for both cases and controls. Potential population controls were contacted using lists of randomly generated telephone numbers. Interviewers then obtained a working residential number and recorded the age, race, and gender of all eligible adults in the household, with one member of the household selected at random to be interviewed (Swanson & Burns, 1995). Controls were frequency-matched by age (within 5 years), gender and area of residence (Macomb county, Oakland county, city of Detroit, and Wayne county other than Detroit) (Burns & Swanson, 1991). Individuals who reported ever having a diagnosis of cancer were excluded. The occupational history portion of the interview instrument includes the occupational and industrial titles of all jobs ever held, a description of the duties performed on a daily basis, the duration of the position, and whether the positions were full- or part-time. Occupational coding was performed by a trained coder utilizing key words in the descriptions of the positions held rather than by the job title, thus enabling a more detailed level of coding. Occupation and industry data obtained by the telephone interview are coded according to the three-digit codes of the 1980 Census Bureau classification. Completed interviews underwent a final review by the supervisor of the interviewing unit (Swanson Final Performance Report, National Institute of Occupational Safety and Health, 1995). 19 This analysis focuses upon usual occupation and industry, utilizing grouped codes, which are derived from the 1980 Census Bureau codes. These codes were created by combining appropriate 3-digit codes for occupations or industries with probable similarities in work exposures, and were created by the investigators including consultation with an industrial hygienist, to increase the number of cases included in each industrial and occupational groups (Burns & Swanson, 1991). Occupational and industrial histories were summed into two usual occupations and two usual industries for each respondent. These are defined by summing the total number of months for which a person indicated employment in industries or occupations over their entire work histories. The greatest number of months of exposure was then chosen as the usual occupation or industry for that respondent. All industrial and occupational codes, which were categorized as either exposed or unexposed based upon their potential exposure to known carcinogenic agents, were utilized in this analysis. This analysis reports the association between the occurrence of colon cancer among Black and White males and females and (1) the usual occupations and industries in which they were ever employed, and (2) the cigarette, pipe, and cigar smoking histories of both the cases and controls. The Mantel-Haenszel chi-square test was utilized to evaluate risk differences between cases and controls and between Whites and Blacks based upon work history. These analyses included adjustment for the potential confounding effects of 20 age, gender, and pack-years of smoking. Work history data represent usual industries or occupations that occurred among at least 10 respondents and with odds ratios that were elevated to a level of at least 1.5 among any of the demographic subsets examined (i.e. males/females, Blacks/Whites). A multiple logistic regression model was used to determine the maximum likelihood estimates of the odds ratio (OR) for independent variables. The outcome (dependent) variable in the model was case-control status. The main explanatory variables of interest were binary indicators of occupations and industries with adjustment for race and pack-years of smoking history. Blacks, females, and persons with zero pack-years of smoking were used as the referent groups. Other factors may influence a diagnosis with colon cancer and were included in the model as additional explanatory variables. These factors included several patient demographic variables (age and gender). Indicator variables were created for approximately 30 of the usual occupations or industries that exhibited increased odds ratios based upon the Mantel-Haenszel chi-square tests. The initial logistic models included all main effects and first- order interaction terms, and a combination of backward and forward elimination selection methods were utilized to determine which explanatory variables remained significant. The significance level of the maximum likelihood estimate statistic for variables to be retained in the model was set at 0.05, and ninety-five percent confidence intervals were 21 calculated for each odds ratio. Potential confounders, pack-years of smoking and age, were controlled for in the models. The SAS package v 6.12 (SAS Institute, Cary, North Carolina, USA) was used to construct the datasets and perform the chi-square tests and the logistic regression analysis. RESULTS This study population includes 6,619 Black and White subjects and is comprised of 2,879 colon cancer cases and 3,740 population controls. Interviews conducted with the cases and population controls were carried out either with the patient or a proxy. Among cases, 2129 (73.95%) of the interviews were carried out with the patient, while 368 (12.78%) were proxy interviews of a living subject and 383 (13.27%) were proxy interviews of a deceased subject. Population control interviews were carried out with the actual study subject for 3,459 (92.49%) individuals, while only 7.51% (281) were proxy interviews. The overall response rate for the colon cancer cases was 95%, while the response rate for eligible controls was 97.3%. Demographic characteristics of the study population are presented by race, gender, age, smoking status and history, marital status, and educational history in Table 1. Educational history categories include Elementary (grades K- 6), Jr. High (grades 7 & 8), High School (grades 9-12), College or Technical (12+ years), and Graduate (16+ years). As a result of the frequency-matched design of this study, there are a greater number of controls than cases in this 22 Table l. W Variable Cases (N82879, 43.5%) Controls (N83740, 56.5%) No. (%) lb. (‘) Race 8 Gender White Males 1103 38.3 1423 38.1 Black Males 278 9.7 371 9.9 White Females 1203 41.8 1529 40.9 Black Females 295 10.2 417 11.1 Total 2879 100% 3740 100 Age at Diagnosis 40-49 101 3.5 n/a n/a 50-59 451 15.7 n/a n/a 60-69 981 34.1 n/a n/a 70-79 966 33.6 n/a n/a 80-84 380 13.2 n/a n/a Total 2879 100% n/a n/a Smoking Status Ever 1469 51.0 2103 56.2 Never 1410 49.0 1637 43.8 Tbtal 2879 100% 3740 100% Pack Years of Smoking Nonsmoker 1410 49.0 1637 43.8 1-20 427 14.8 685 18.3 21-40 408 14.2 591 15.8 41-60 310 11.0 432 11.6 61-80 118 4.0 160 4.2 23 Table 1 (cont.) variable Cases (NI2879, 43.5%) Controls (W83740, 56.5%) no. (%) no. (9) 81-100 92 3.0 99 2.6 101-120+ 86 3.0 98 2.6 Missing 28 1.0 38 1.1 Total 2879 100% 3740 100% Marital Status Never 141 5.0 170 4.5 Married 1628 56.5 2048 54.8 Divorced or Separated 249 8.5 418 11.2 Widowed 848 29.5 1093 29.2 N/A Missing 13 .5 11 .3 Total 2879 100% 3740 100% Educational History Elementary 220 7.6 223 6.0 Jr. High 360 12.5 363 9.7 High School 1447 50.3 1976 52.8 College or Technical 610 21.2 878 23.5 Graduate School 161 5.6 239 6.4 Missing 81 2.8 61 1.6 Total 2879 100% 3740 100% 24 sample. Distributions of gender, cigarette/pipe/cigar smoking status, educational history, and marital status among both Black and White cases and controls are similar. Whites constitute 80.1% of the cases and 79% of controls. Table 2 presents a comparison of the two independent variables of interest in this study, age and smoking history, as well as the employment status, among the White and Black populations. As a group, Blacks tended to have higher rates of cancer at earlier ages, (age groupings 40- 49, 50-59, and 60-69) until approximately 70 years of age and older, at which point the White population has a higher percentage of respondents with cancer of the colon. These distributions are consistent with national cancer registry data (Ries et al., 1998). Pack years of cigarette/pipe/ cigar smoking appear to be similar between the case and control groups, as well as both the Black and White populations. Among both Blacks and Whites, a greater percentage of controls than cases were employed at the time of their interview. A slightly greater proportion of cases than controls within both races tended to be homemakers. Unemployment, retirement, and disability rates appear similar between cases and controls, as well as between Blacks and Whites. Odds ratios indicating the colon cancer risk associated with usual occupational and industrial exposures are presented in Tables 3 and 4. Mantel-Haenszel Chi—square 25 Ao¢0nudonn Aaoodfionh AaOOnunhn flwocuuanun Aoocuunmau arcanuccnn H.908 xvowcesu .amdcuea .anacmna 1ammcmomn .ooucmam .«omocmo noxqeusom .am.oaa Aumcmo Aamcme Aamcmoa .ancmm .aecno ooanuuaa .omvcsoo .amcvnmn Aaeecemu .aoocomow .asncomofl Awevcoaofl consume .avcom .avcam .om.mu 1a~.mm .aucov .ascsn oososdsucs xaumcoon .aeuccmn .aom.vfla .aomcnona .pomcaom .oancume cascadsu soapusuun no case an nan-um anon .oooucnona Aaooncaos .oooucnsm .aooucamum .aooucwnan .ooeucuonu Hanna .aa.ma .mu.¢a .oH.e .aacme .aflcew xaavvn oceans: .aa.sa .aaco .oacm .wn.soa .ancom Aoncss +o~HIHoH .aacma .aHCHH .aacm .amcasa .ancmm .ovcco ooHuHm Aoucun .an.o~ .a~.- .amcoem .amvoefl .amvoofi condo .ao«.~nfl .aoflcom .am.~m .amscoao .omaenmn Awascmmw amuse Aymavaflu .aoavmma Apmflcmm Asmacmms Aaoacome .mva.-m oenan aoucwsu .aumcssfl .wsavmm .aoscovm .asacoom Aaencmmm onus .amvcooo .amccmmm .eemcsom .amecsmmm xanccemma .amevmofia noxosucoz “w mnquIm usmqo\emwm\euveusmwu no anus» xusm xaooacuonu .aooncoes .aooucnsm .aooacamum .aooacuman Aaoonvoonn «nuns Anacuna Iascoo .aaacao .aaflcmmm Amocosm .aeflcnmm venom .amucomn .ammcmaw .sflnvmsa .awm.smo~ .aomcflmm .«mncoms msuos .asnvmom .amncmon Aamncoom .aemcomsa .ammvamoa .anncmms mouoo xvoacamm .amd.¢¢a .wmacmoa Assacflom .amacmcm .amflcwmn mmuom .aocsm 1amoao .aecom .wocamu Auscmnu Aancos melee sedbueunn us out flflOOHOh IQ“ dOHOQOO COCO “ECONOE 30“ Havana .010 .«unuusc nan-«n .omnmuzc nouns: .‘a e. r c .4. e. . of .«s. .«e «a s‘. e . . . < . e e: e .i . 04< e . e;- ’ e u o . . e. .N CHAIR mo.vme «season one .mndxoaa mo eueehlxuem .3OH>ueucH us on. now ocuusflua . oo.v qu.o mm.o n m mo.H .ms.o HH.H am no mococh -.o .om.o Hm.H s s om.H .mn.o mm.o oH AH noxuoz Hnuuom Hm.v .uo.o sw.H HH m mH.H .oe.o om.o «a on noucHam om.“ .ms.o v¢.H pm ea No.0 .mn.o mm.o on we um>Hun H~.H .un.o «o.o oH on mn.~ .mo.H om.Ho om me uounuono ocHsuar ~¢.H .uo.o «8.0 we mo on.~ .no.H om.Ho am no souHcau Hm.» .mm.o mm.H m m om.¢ .nH.o Ho.o w v ocHoHoz He.mmH .v~.o an.o H o m¢.c .sm.o oo.~ AH «H umucHum nu.o .mo.o Ho.o H m no.~ .vo.o on.H mH mH ouauuo Hume mm.“ .sH.o sm.o v m m~.m .Ho.H on.~o oH HH Hues HuHoom mzoueemnooo om.o .Hu.o mH.H n m mm.o .mm.o mm.H s m monum>om ~m.¢ .sH.o om.o m m an.H .n¢.o ss.o mH on «Hum: a~.m .v~.o Hm.H m m Hm.~ .nm.o mv.H es en mcHuuoHunam Hand: o~.m .v¢.o mm.H s m se.~ .so.o m~.H AH mH nuance mm.m .me.o os.H s o o~.H .sn.o so.o oH en sumuHHHz no.8 .mo.o hm." MH 8 me.H .so.o mo.o >4 mm nououm unusuuodmn ms.H .mo.o mm.o m m ms.m .am.o mo.~ m m uoOH>umm HuHoom mm.on .mo.o mv.v m o on.m .mm.o so.~ m v .6“: .oqu on.o .-.o mH.H a m ms.m .cm.o ms.H s m unsHo Hm.n .no.o s~.o H n nn.m .Nm.o mo.~ «H m coHuHHom ms.Hnm .oo.o oo.m H o ~¢.n .mo.o mm.H NH HH mcHuHuuo>o¢ us.¢s .so.o oH.m c H o«.~ .mm.o mH.H pH oH Hosanna mm.vm .s~.H oo.HHo m H o~.n .om.o as.H mm oH uoHum uuo mo.sH .oH.o um.H m m vs.~ .mm.o mm.H ow Hm uoHuHHHua Hu.n .«s.o 84.8 H n em.n .nv.H mn.~o we on ocHucHum ou.vH .nn.o mH.u n n «m.H .mm.o Hn.H on on uuchHnuux Ho «mm so some Houucoo Ho amm so some Houucoo .HonHuav «scene Hanna's. unsung seasonan .n CHACH 27 mo.vmo «Hoodoo one .oconan no nusohrxusm .3OH>uousH us one nan counsnoc « so.v .sm.o Ho.~ 4H m He.H 486.0 ~m.o o4 em oucach mo.H .eo.o o~.o H m nm.m .om.o no.H 6H mH uoxuoz Haumom Hm.m .mo.o mm.o H m m¢.H .sm.o ~m.o an «e umuchm -.~H .nm.o so.H m N Ho.H .Hm.o ms.o om ooH um>Huo mm.n .ss.o mo.H mH MH so.H .ms.o mH.H Hm mm uouaumdo mcHnomz m~.~ .mm.o ~¢.H an mm m¢.H .ns.o mo.H Ho as nouHcan m~.nH .No.o mm.o o H mm.¢ .mm.o oo.H oH m mcHuHoz oH.n .eo.o en.o H e um.» .mm.H sH.no pH 8 noucHum mo.m .ms.o «o.~ HH 5 H~.~ .vn.o sm.o m nH muauum Home m~.n .nm.o Nn.H m oH v~.¢ .mo.o no.H HH m xuo: HmHuom moneamaooo oo.mH .so.o mH.H H H o~.¢ .sm.o mm.H o m amouo>am om.H .on.o co.o 0H NH AH.~ .He.o «8.0 oH nH «Hum: He.e .eo.o so.H m s nm.~ .mm.o m¢.H em mm ocHuouHunam Huumz om.m .mo.o oo.n m e mm.H .me.o sm.o mH mH umnnsm c~.m~ .mH.o SH.~ N H mm.H .mo.o ms.o Hw on suuuHHHz ms.H .os.o mH.H me we om.~ .mm.o -.H pH pH umuoum unassuudon sn.~ .nn.o «8.6 m «H sm.Hm.ss.o mm.m m H umoH>umm HuHuom sH.~n .om.o m~.m v H me.~H.mm.o -.m m n .uux .ouH: -.mH .mm.o mm.u e N ~¢.n .m~.o mm.o m o unsHo H¢.v .ne.o om.H m m -.m .sc.o sm.H m m conHHom Hs.HH .mn.o vo.~ m m os.n .mo.o Hm.H HH a mcHuHuum>o¢ ms.n .ss.o mo.H mH NH mm.u .mm.o Ho.H m s Hosanna Hm.m~ .m~.o mm.~ m H mv.n .mo.H ma.Ho on mH aoHam uao s~.oH .mo.H mn.¢o s a Hv.~ .ns.o mn.H em Ha uoHuHHHua oH.m .om.o mH.~ «H a os.n .-.H «H.~o on om mcHueHum mm.H .HH.o on.o e «H mo.~ .so.H me.Ho as He auuHcHsoaz Ho amm mo mono Houucoo Ho amm so mono Houucoo .vvenun. annexes .nanua. anger seasonan 28 statistics were calculated between Black and White males and females for all usual occupations and usual industries collected in the study, however, the results of only 16 industry and 12 occupational groups are presented here. These industries or occupations were chosen based upon each grouping having a minimum of 10 observations or an odds ratio of at least 1.50 among either Blacks or Whites. Table 3 presents an analysis of usual occupations for both cases and controls among Blacks and Whites separately, and adjusts for age, pack years of smoking, and gender, in an effort to examine the potential influence of race on case-control status. Among Whites, the odds ratio for those working in the printing industry was significantly elevated, as was the odds ratio for social workers. Also in Table 3, a number of usual occupations and industries were also elevated for Whites, but not significant, including printing occupations, and usual industries of religion, miscellaneous manufacturers, and social services. For Blacks listed in Table 3, several usual occupations and industries exhibited elevated odds ratios including machinists, apparel industry workers, advertisers, miscellaneous manufacturers, and printers, however, they were not significant. Blacks in car sales and department store industries showed significantly elevated levels of risk. A similar comparison for industry and occupation groups was done comparing males and females, controlling for race, age at interview and pack-years of smoking in Table 4. The highest odds ratios for usual industry for males are found 29 among individuals employed in printing, miscellaneous manufacturing, and social services, as well as those with a usual occupation of printers. Printing is the only industry and occupation significantly elevated for males. Elevations in the odds ratios are also seen among females in Table 4 in the usual industries of printing, utilities, car sales, advertising, clubs, miscellaneous manufacturing, and rubber manufacturing. Usual occupations for females showed excess risk in real estate and finance. The only usual occupation or industry that was significantly elevated for women was utilities. However, it is important to recognize, that in this sample that contains 3,444 females, over 77% (2,676) indicated having a usual occupation of housewife and at the time of interview, 1,776 females had a current work status of homemaker (Table 2), thus, creating difficulties with small cell sizes for most of the usual groupings for the female population. Table 5 displays the results of the multivariate logistic regression analysis. Univariate analyses were run on all variables thought to exhibit an increased risk of colon cancer and are not presented. Variables were selected for the model based upon their level of significance comparing backward and forward elimination techniques. Usual occupations or industries were selected for univariate analyses based upon those presented in Tables 3 and 4. Usual occupations or industries that remained in the model met the minimum 0.05 level of significance and are presented in Table 5. No interactions or higher order terms were 30 Table 5. - 8 8 95% Variable Parameter Standard Odds Ratio Confidence Estimate Error Intervals Intercept -.9557 .1323 Age 2 40 1.00 Age 2 50 .5822 .1315 *1.790 1.383, 2.316 Age 2 60 .6514 .1249 *1.918 1.502, 2.450 Age 2 70 .8430 .1256 *2.323 1.816, 2.972 Age 2 80 1.0888 .1403 *2.971 2.256, 3.911 Black Race 1.00 White Race .0175 .0628 1.018 0.900, 1.151 Female 1.00 Male .0324 .0539 1.033 0.929, 1.148 0 pack years 1.00 1-20 pack years -.2390 .0736 *0.787 0.682, 0.910 21-40 pack years '-.1520 .0765 90.859 0.739, 0.998 41-60 pack years '-.1681 .0855 90.845 0.715, 0.999 61-80 pack years -.1415 .1299 90.868 0.673, 1.120 81-100 peck years .0610 .1529 1.063 0.788, 1.434 101-120 pack years .0047 .1553 0.995 0.734, 1.350 Machine Industry .3015 .1608 1.352 0.987, 1.853 Printing Industry .7819 .2445 *2.186 1.354, 3.529 Utility Industry .5796 .2789 91.785 1.033, 3.084 Car Sales Industry .7851 .2946 *2.193 1.231, 3.906 Miscellaneous Manufacturing 1.3807 .5871 93.978 1.259,12.571 Metal Fabricators .3970 .2244 1.487 0.958, 2.309 *p<.05, 4<.10 31 necessary given the fit yielded from this more parsimonious model. The overall model fit the data with a P < 0.0001. After controlling for other observable variables through the logistic regression analysis, including patients demographics, smoking patterns, and work history, the results show that the odds of increased cancer risk based upon race, gender, and smoking, are equivocal and are not significantly different from 1.00. Both race and gender were forced into the model despite nonsignificant P-values from log-likelihood ratio tests due to the fact that they were main variables of interest. Additionally, no increased risk is seen for any duration of smoking history, relative to those who indicated no history of cigarette, pipe, or cigar smoking. However, some individual coefficients are worthy of note, with positive and significant odds ratios for increasing age beyond age 50, and several occupations and industries. As expected, age group independent variables consistently yielded positive parameter estimates, increasing for each group relative to the study referent group (age 40-49), so that by age 80, individuals are at nearly three times the risk of colon cancer as are those 40- 49 years of age. Other factors besides age may have also influenced cancer incidence among this population. Occupational or industrial exposures in this multiple regression indicated that the odds of having a usual industry of miscellaneous manufacturing carried nearly four times the risk as those not employed in these types of 32 industries. Examples of occupations that fell into this category included Census Bureau classifications 391 (miscellaneous manufacturing industries) and 392 (not specified manufacturing industries). Other industries that exhibited positive and significant parameter estimates included those employed in the printing industry, the car sales industry, and the utilities industry. Other usual occupations or industries that remained in the logistic model were not associated with case status. DISCUSSION This case-control study was designed to test the hypothesis of a potential association of Black race with an increased risk of colon cancer, controlling for known or suspected risk factors, including pack-years of tobacco use, occupational exposures, age, and gender. The literature provides sparse information about the combination of these relationships. Past studies on this subject have been limited by the use of death certificate data to establish occupation, small sample sizes, samples containing only White males, and limited smoking histories. This paper presents the results of this study, which highlight some of the difficulties in examining colon cancer risk, race, occupational risk factors, and the impact of tobacco use. The study utilizes OCISS data, which contains outcome information provided from hospital abstracts of incident cancer cases, along with a lifetime history of occupational information, complete lifetime tobacco use histories obtained by interview. Furthermore, the sample is a large, 33 population based, racially diverse, representative group of subjects from which logical inferences could be made with respect to the goals of this paper. This paper emphasizes three findings. First, the risk of colon cancer increased steadily with age, and this age- related increase in risk occurred for each age-group, controlling for race, gender, pack-years of smoking, and occupational history. Age-related increases in incidence and mortality, as well as colon cancer risk, are well documented. The Surveillance, Epidemiology, and End Results (SEER) Program, indicates a rate of 7.9 cases per 100,000 for those ages 40-44, which increases by over a factor of 4 (33.3 per 100,000) by age 50, to over 214 (214.1 per 100,000) for individuals between 70 to 74 years of age (Ries et al., 1994). In this study, a higher percentage of Blacks were diagnosed with colon cancer at earlier ages than Whites at corresponding ages, until the age of 70, when the percentage of Whites with colon cancer was higher than for Blacks. This information is supported by prior findings. Cooper et al. (1994), found in a database of 75,266 1987 U.S. Medicare patients, that risk levels between Blacks and Whites were similar until 69 years of age, but beyond age 70, risk levels of Whites were greater than those of Blacks. Second, although this study does present some interesting leads for future investigation into the association between race and certain occupational exposures, one cannot conclude from the data presented that the risk of colon cancer is consistently greater in any one usual 34 industrial or occupational grouping for Blacks than for Whites. In actuality, a greater number of usual industries and occupations had significant or elevated but not significant, increases in risk for Whites than for Blacks. It does appear that for certain usual occupations and industries, there is a consistent increase in risk of colon cancer, regardless of race, gender, or smoking histories. There is some evidence for an association between colon cancer and specific industries, such as printing, miscellaneous manufacturing, and utilities. Alternatively, observed risk levels among occupational subgroups among Blacks and Whites may be explained by the inability of these data to measure certain confounders, such as dietary or physical activity patterns, in relation to the main exposures of interest. Third, consistent with earlier research (Potter et al., 1993; Heineman et al., 1995; Giovannucci et al., 1994), the results of this study do not support the association between colon cancer due to smoking for either Blacks or Whites, regardless of pack-year histories. This was consistent in men and women and in Blacks and Whites. Although interview data are commonly used in cancer research, these data have several relevant limitations. Reliance upon survey data limits the ability to accurately assess specific exposures to known carcinogenic agents. Although these data do contain complete lifetime occupational and smoking histories, the levels of physical activity or intensity of exposures to known risk factors 35 cannot be measured. Additionally, these data cannot account for activity levels not related to the respondent's occupations, further limiting the assessment of any relationship between occupation, physical activity, and colon cancer. While a large number of industrial and occupational categories are available for analysis from these data, this may also be considered a limitation. A large number of comparisons across occupational and industrial groups, especially among the Black population, were limited by small numbers within cells. This problem was more common among female subjects. The ability to accurately assess an increase in risk of colon cancer in females compared to males, or between women across various occupations, is severely limited in this study due to the fact that over three-fourths (77%) of the colon cancer cases and controls combined had a usual occupation of housewife. Another difficulty in attempting to attribute an increased risk in colon cancer to a specific occupation or industry is the limited data available on potential confounding variables. No data was collected on diet, alcohol consumption, or family history, all of which have been positively associated with increases in colon cancer risk (Potter et al., 1993). Other variables that were unavailable include income, physical activity, and body mass index. In terms of public health significance, the range of occupational and industrial exposures in this study may be seen as a strength. The relatively large sample size allows 36 for comparisons of many occupational risks. This study represents an investigation of occupational exposures through interview, and provides a complete lifetime occupational assessment, rather than single entry from death certificates. Analyses that utilized OCISS data were performed by Schade and Swanson (1988), and showed a 30-50% error rate for death certificate employment data compared to interview data. Also, one study indicates that the death certificate occupation is the least likely to be the most recent occupation, is somewhat more likely to be usual occupation, and even more likely to be occupation in the last 15 years (Turner et al., 1987). This points to the validity of using data from interview respondents to determine usual occupation and industry, and to using usual occupation as the baseline for the analysis of occupational exposures in this study, rather than most recent occupation. Additionally, because this population-based sample is obtained from hospital abstracts of incident cancer cases, these data can be considered highly accurate regarding the cancer diagnosis, and also fairly representative of the working pepulation in this region of the country. The high overall response rate among cases (95%) and controls (97.3%), as well as a minimal reliance upon proxy interview (15.6%) of all cases and controls, increases the reliability of the occupational data. Because this study is not restricted to White males, as many occupational assessments have been in the past (Lindsay et al., 1993; Lynge et al., 1988), a comparison between the White and Black population 37 is possible, and allows for the testing of differences between these two racial groups, improving the generalizability of the findings. Finally, complete lifetime tobacco use histories are obtained for all OCISS subjects. As a result, the occupational risks take into account the cigarette smoking history of the subjects and its potential confounding effects (Burns & Swanson, 1991). The overall results of this case-control study do not indicate that Blacks have a significantly higher risk of colon cancer than Whites when controlling for occupational exposures, gender, age, and tobacco histories. While there were increases in occupational risk among Blacks (machinists, car sales, department stores) and Whites (printing, social work), the analysis across multiple specific usual occupational and industrial groupings show different workplace risks for Blacks and Whites. Since a greater number of usual industries and occupations were limited by small sample sizes for Blacks, a larger sample of Blacks may have elucidated clearer results with regards to risk of colon cancer associated with certain industries and occupations. Consistent with earlier research, the exposure to any level of cigarette smoking did not appear to increase the risk of colon cancer, however, it was very important to have this variable available to control for its potential confounding effects, especially because of the possibility of the synergistic effects that smoking may have with certain occupational exposures such as asbestos. This study 38 also would have benefitted from more precise measures of other potential carcinogens and biologic agents, as well as diet and physical activity. The implications of these findings are three-fold. First, although these data do not necessarily support an increased risk of colon cancer among Blacks, the population- based incidence and mortality data indicate that certain segments of the Black population, especially those approaching 50 years of age, need to be more aggressively targeted for colorectal cancer screening. Based upon the 1997 Clinical Guidelines and Rationale by the American Gastroenterological Association, ‘Screening for colorectal cancer and adenomatous polyps should be offered to all men and women without risk factors, beginning at age 50' (American Gastroenterological Association, 1997). This is especially relevant for the Black population, given the fact that their incidence rate by age 50 is 50.2 per 100,000 compared to 28.4 per 100,000 for Whites, and also, their rate of mortality due to colon cancer is higher in every single age category than that of Whites (Ries et al., 1998). Second, the results of this paper support the lack of a relationship between tobacco use and colon cancer. This finding was consistent across age, race, and gender, and increased levels of exposure did not exhibit any dose- response relationship. Finally, these data continue to support the need for continued study of the Black population, utilizing larger sample sizes. Even with the high quality of data obtained 39 through a case-referent methodology, this study was limited in its ability to detect increases in risk in many occupations among the Black population due to small cell sizes and points to the need for continued aggressive surveillance of this population. 40 LI ST OF REFERENCES LIST 0? REFERENCES American Cancer Society (1996). Cancer Facts and Figures Amer1can_Cancer_Soc1et¥1_Inci American Gastroenterological Association (1997). Colorectal cancer screening: Clinical guidelines and rationale. Gatroenterolos¥1_112. 594-642. Baker, E. L. , Honchar, P. A. & Fine, L. J. (1989). Surveillance in occupational illness and injury: Concepts and content Amer1can_Journal_of_2ublic_Healthi_12. 9-11 Bostick, R.M., Potter, J.D., Kushi, L.H., Sellers, T.A., Steinmetz, K.A., McKenzie, D.R., Gapstur, S.M., & Folsom, A.R. (1994). Sugar, meat, and fat intake, and nondietary risk factors for colon cancer incidence in Iowa women. Cancer_Causes_and_Controli_5. 38-52. Burns, P.B., & Swanson, G.M. (1991). The occupational incidence surveillance study (OCISS): Risk of lung cancer by usual occupation and industry in the Detroit Metropolitan area. Amer1can_Journal_of_Industr1al_Med1c1nei_12. 655- 671 Chau, N., Bertrand, J.P., Mur, J.M., Figeredo, A., Patris, A., Moulin, J. J. & Pham, Q.T. (1993). Mortality in retired coke oven plant workers. British_fl9urnal_gfi_ Industrial_Medicinei_Efl 127- 135 Chow, W.H., Malker, H.S.R., Hsing, A.W., McLaughlin, .K., Weiner, J. A. Stone, B. J. Ericsson, J. L. E. & Blot, J (1994) Occupational risks for colon cancer in Sweden. Journal_of_0ccunaLional_Med1cinei_36(6). 647-651. Chyou, P. H. Nomura, A. M. & Stemmermann, G. N. (1996). A prospective study of colon and rectal cancer among Hawaii Japanese men Annals_of_Enidem1olog¥1_6(4) 276- 82. Coates, R.J., Greenberg, R.S., May-Ting-Liu, Correa, P., Harlan, L.C., Reynolds, P., Fenoglio-Preiser, C.M., Haynes, M.A., Hankey, B.F., Hunter, C.P., & Edwards, B.K. (1995). Anatomic site distribution of colon cancer by race and other colon cancer risk factors. Diseases_gfi_the_gglgn and_Bectum. Committee on Diet and Health, Food, and Nutrition Board, Commission on Life Sciences. (1989). Die;_and National Academy Press: Washington, D.C. Cooper, G.S., Yuan, Z., Landefeld, S., Johanson, J.P., & Rimm, A.A. (1995). A national population-based study of 41 incidence of colorectal cancer and age: Implications for screening in older Americans. CancerL_15(3). Courtney, J.G., Longnecker, M.P. Theorell, T. & Gerhardsson de Verdier, M. (1993). Stressful life events and the risk of colorectal cancer. Epidemiology‘_§_, 407- 414. Courtney, J. G. Longnecker, M. P. & Peters, R. K. (1996). Psychosocial aspects of work and the risk of colon cancer. Epidem1olos¥1_1(2), 175-180. Dales, L.G., Friedman, G.D., Ury, H.K., Grossman, S., & Williams, S. R. (1978). A case- -control study of relationships of diet and other traits to colorectal cancer in American Blacks Amer1can_Journal_of_En1demiologxi 192(2), 132- 144. Demers, R.Y., Burns, P.B., & Swanson, G.M. (1994). Construction occupations, asbestos exposure, and cancer of the colon and rectum. Q9nInal—9f—QQQHDBLiQnal_Medicin§L 15(9). Dubrow, R., & Wegman, D.H. (1983). Setting priorities for occupational cancer research and control: Synthesis of the results of occupational disease surveillance studies. Journal_Qf_the_Nat1onal_Cancer_Inst1tutei_11(6). FerrarOni, M., Negri, E., La Vecchia, C., D'Avanzo, B., & Franceschi, S. (1989). Socioeconomic indicators, tobacco and alcohol in the aetiology of digestive tract neoplasms. Internat1onal_1ournal_of_En1demiolog¥1_18(3) 556- 561. Fredriksson, M., Bengtsson, N.O., & Hardell, L. (1989). Colon cancer, physical activity, and occupational exposures. Sangeri_fll. 1838-42. Garabrant, D. H. Peters, J. M. Mack, T. M. & Bernstein, L. (1984). Job activity and colon cancer risk. American Journal_of_Enidemiolog¥i_112(6). Garabrant, D. H. Peters, R. K. & Homa, D. M. (1992). Asbestos and colon cancer: Lack of association in a large case- -control study Amer1can_Journal_of_Enidemiologxi_135. 843— 853. Giovannucci, E., Colditz, G.A., Stampfer, M.J., Hunter, D., Rosner, B.A., Willett, W.C., Speizer, & F.E. (1994). A prospective study of cigarette smoking and risk of colorectal adenoma and colorectal cancer in U. S. women. Journal_of_the_Nat1onal_Cancer_Inst1tutei_86(3). Giovannucci, E., Stampfer, M.J., Colditz, G., Rimm, E.B., & Willett, W.C. (1992) Relation of diet to the risk 42 of colorectal adenoma in men. Journal_gfi_§he_flag1gnal Cancer_1nst1tutei_15, 75. Grahm, 8., Marshall, J., Haughey, B., Mittelman, A., Swanson, M., Zielney, M., Byers, T., Wilkinson, G., & West, D. (1988). Dietary epidemiology of cancer of the colon in Western New York. Amer1can_Journal_of_Epidemiclosxi_128. 490- 503. Heineman, B.F., Zahm, S.H., McLaughlin, J.K., & Vaught, J. (1995). Increased risk of colorectal cancer among smokers: Results of a 26- -year follow- up of U. S. veterans and a review. Internat1onal.19urnal_of_sanceri_52 728- 738 Lindsay, J. P. Stavraky, K. M. & Howe, G. R. (1993). The Canadian labor force ten percent sample study: Cancer mortality among men, 1965- 1979. Journal_gf_Qccupat1gnal Med1cinei_35(4). ~ Longnecker, M.P., De Verdier, M.G., Frumkin, H., & Carpenter, C. (1995). A case- -control study of physical activity in relation to risk of cancer of the right colon and rectum in men Internat1onal_Journal_of_Enidem1ologxi 24(1). Lynge, E., & Thygesen, L. (1988). Use of surveillance systems for occupational cancer: Data from the Danish national System Internat1onal_Journal_of_Enidem1olos¥1 11(3), 493 499. Manousos, 0., Day, N.E., Trichopoulos, D., Gerovassilis, P., & Tzonou, A., (1983). Polychronopoulou. Diet and colorectal cancer: A case control study in Greece. Internat1onal.19urnal_of_9ancer1_32. 1- 5. Mayberry, R.M., Coates, R.J., Wesley, M.N., Click, L.A., Chen, V.W., Austin, D.F., Redmond, C.K., Fenoglio- Preiser, C.M., Hunter, C.P., Haynes, M.A., Muss, H.B., Wesley, M. N. ,Greenberg, R. S. & Edwards, B. K. (1995). A determinants of black/white differences in colon cancer survival Journal_of_the_National.§ancer11nst1tute Miller, A.B., Howe, G.R., Jain, M., Craib, K.J.P., & Harrison, L. (1983). Food items and food groups as risk factors in a case- -control study of diet and colo- rectal cancer Internat1onal.19urnal_of_Canceri_32. 155-161. Miller, B.A., Kolonel, L.N., Bernstein, L., Young, Jr. J.L., Swanson, G.M., West, D., Key, C. R. Liff, J. M. Glover, C. S. Alexander, G. A. et al. (1996). Rag1aiLELhn19 '. ‘ 0‘ 0 ‘ o 9‘ r ‘0 , a ‘= '33- °' 14 .004 Cancer_1nst1tute. NIH Pub. No. 96-4104. Bethesda, MD. Murata, M., Takayama, K., Choi, B.C., & Pak, A.W. (1996). A ested case-control study on alcohol drinking, 43 tobacco smoking, and cancer. Canch_ne;egt1gn_and WM), 557-65. Nyr'en, 0., Bergstrom, R., Nystrom, L., Engholm, G., Ekbom, A., Adami, H.O., Knutsson, A., & Stjernberg, N. (1996). Smoking and colorectal cancer: A 20—year follow-up study of Swedish construction workers. Journal_gf_;he WW. 1302- 7 Potter, J.D., Slattery, M.L., Bostick, R.M., & Gapstur, S.M. (1993). Colon cancer: A review of the epidemiology. E .3 . J . E . . Ries, L. A. G., Kosary, C.L., Hankey, B.F., Miller, B.A & Edwards, B K.(1998).SEEE_Cancer_Stet19_t1c_s_Renien. WW Bethesda. MD. ' I Ries, L.A.G., Miller, B.A., Kosary, C.L., Harras, A., & Ewards, 5.x. (1994). W W NIH Pub. No. 94-2789. Bethesda, MD. Sandler, R. S. Pritchard, M. L. & Bangdiwala, S. I. (1995). Physical activity and the risk of colorectal adenomas. Ep1dem1glggy1_§(6). SAS Institute, Inc. (1990). SAS Procedures Guide, Version 6, Third Edition, Cary, NC: SAS Institute Inc. Selikoff, I.J., Hammond, B.C., & Seidman, H. (1979). Mortality experience of insulation workers in the United States and Canada. 1943-1976. Ann_NX_Acad1_Sc111_110, 91- 116 . Siemiatycki, J., Day, N.E., Fabry, J., & Cooper, J.A. (1981). Discovering carcinogens in the occupational environment: A ovel epidemiologic approach. Journal_gf_the Wire). Siemiatycki, J., Richardson, L., & Gerin, M. (1986). Associations between several sites of cancer and nine organic dusts: Results from an hypothesis— generating case- control study in Montreal 1979- 1983. Amer1gan_gguznal_gfi Epidemielesx1_123 235-249 Slattery, M.L., Potter, J.D., Friedman, G.D., Ma, K.N & Edwards, S. (1997). Tobacco use and colon cancer. WW9), 259-64. ° I Sorensen, G., & Pechacek, T. (1986). Occupational and sex differences in smoking and smoking cessation. Journal WW6). 44 Swanson, G.A., Gridley, G., Greenberg, R.S., Schoenberg, J.B., Swanson, G.M., Brown, L. M. , Hayes, R., Silverman, D., & Pottern, L. (1993). A comparison of blacks and whites in three areas of the United States. Nutx111gn and_Caneeri_ZQ. 153- 165. Swanson, G.M. (1988). Cancer prevention in the workplace and natural environment: A review of the etiology, research design, and methods of risk reduction. Cancer1 52(8). Swanson, G. M. (1995). Occupational cancer surveillance: New approaches. Einel_2erformanee_8enert1 \. '09. 9‘ . r o ,-, o O 9. or. e f 2.. 9‘. 9 5-ROl-OHOZO67. Swanson, G.M., Belle, S.H., & Burrows, R.W. (1985). Colon cancer incidence among modelmakers and patternmakers in the automobile manufacturing industry. Journal_gf Qeeunetional_Med1cinei_21(8) Swanson, G.M., Belle, S.H., & Satariano, W.A. (1985). Marital Status and Cancer Incidence: Differences in the Black and White Populations. Cancer_Researgh1_15, 5883- 5889. Swanson, G.M., & Burns, P.B. (1995). Cancer incidence among women in the workplace: A study of the association between occupation and industry and 11 cancer sites. Jeurnal_ef_Qeeupet1enal_end_Enr1renmental_Med1e1nei_31(3) Taplin, S.H., Barlow, W., Urban, N., Mandelson, M.T., Timlin, D.J., Ichikawa, L., & Nefcy, P. (1995). Stage, age, comorbidity, and direct costs of colon, prostate, and breast cancer care. Jeurnal_ef_theINatienal_Cancer_Inst1tutei &1(6). Teta, M.J., Schnatter, A.R., Ott, M.G., & Pell, S. (1990). Mortality surveillance in a large chemical company: The union carbide corporation experience, 1974- 1993. Amer1ean_Jeurnal_of_Industr1al_Med1e1ne._11 435- 447. Turner, D. W. Schumaker, M. C. & West, D. W. (1987). Comparison of occupational interview data to death certificate data in Utah Amer1ean_leurnal_ef_1ndustr1el Med1e1ne1_12. 145- 151 U. S. Department of Health, Education, and Welfare. Public Health Service, Office of the Assistant Secretary for Health. Office on Smoking and Health. Smgk1ng_and_flealth1_a Renert_ef_the_Surgeen_Seneral. 45 Vena, J.B., Grahm, S., Zielezny, M., Swanson, M.K., Barnes, R. E. & Nolan, J. (1985). Lifetime occupational exercise and colon cancer. American_lgurnal_gf En1dem1olos¥+_122(3) Willett, W.C., Stampfer, M.J., Colditz, G.A., Rosner, B. A. & Spiezer, F. E. (1990). Relation of meat, fat, and fibre intake to the risk of colon cancer in a prospective study among women Neu_England_Journal_of_Medicine1_lzl. 1664- 1672. Wynder, E.L., & Hoffman, D. (1994). Smoking and lung cancer: Scientific challenges and opportunities. Cancer Research1_fifi. 5284-5295. 46 MICHIGAN STATE UNIV. LIBRARIES 1111111111111NWWI“111WllllWlllHWl 31293017718374