(2' ‘ ' “JUL ‘uf-EI 'l n ' ' ;‘. ' ..| . 3'2“: 35“. 2,. Huang; 0w}? 5%???" " ”3"73‘1; "-4‘11“ M; 115% q: PM” a? ' I. «A h‘o V . mil"! #1!ng ' "95 w “(I M 9&3 '] Wm, II I III/II II IIIIIIIIIIII rHE5i5 3 1293 1_O744 2596 This is to certify that the thesis entitled RESEARCH PAPERS 0N GEOGRAPHIC ASPECTS OF DISEASE PART A: GEOGRAPHIC ASPECTS OF THE CONTROL OF MEASLES: WITH SPECIAL REFERENCE TO MICHIGAN PART B: GEOGRAPHIC ASPECTS OF HYPERTENSION presented by DEBBIE L . BORCHERS has been accepted towards fulfillment of the requirements for M.A. Geography degree in y Major professor Date MA? ‘7’) (3 $0 0-7639 (we ._. _ Em“ ';.. .-- we *1 III Y i Mlchlgan'" 1"; I Univcrn ./ J3} ovsnous FINES: 25¢ per day 90" it“ [#th - RETURNING LIBRARY MATERIALS: _ . Place In book return to remove 5 ’ (“7’55” charge from circulation records W »'c!~;",. 200 A 301+ RESEARCH PAPERS ON GEOGRAPHIC ASPECTS OF DISEASE PART A: GEOGRAPHIC ASPECTS OF THE CONTROL OF MEASLES: WITH SPECIAL REFERENCE TO MICHIGAN PART B: GEOGRAPHIC ASPECTS OF HYPERTENSION By DEBBIE L. BORCHERS A THESIS Submitted to Michigan State University in partial fulfillments of the requirements for the degree of MASTER OF ARTS Department of Geography I980 GEOGRAPHIC ASPECTS OF THE CONTROL OF MEASLES: WITH SPECIAL REFERENCE TO MICHIGAN By Debbie L. Borchers A RESEARCH PAPER Submitted to Michigan State University in partial fulfiIIment of the requirements for the degree of MASTER OF ARTS Department of Geography 1980 ABSTRACT RESEARCH PAPERS ON GEOGRAPHIC ASPECTS OF DISEASE PART A: GEOGRAPHIC ASPECTS OF THE CONTROL OF MEASLES: WITH SPECIAL REFERENCE TO MICHIGAN PART B: GEOGRAPHIC ASPECTS OF HYPERTENSION By Debbie L. Borchers Two diseases, measles and hypertension, are examined from a geographic perspective. Although officially a "preventable“ disease, measles has yet to be brought fully under control in the United States, particularly in Michigan. Geographic approaches to the control of measles, such as planar graph analysis, diffusion modelling and multiple- scale target area approaches are recommended. Epidemiologic and etiologic aspects of hypertension are also discussed. Multiple-scale spatial analysis and interdisciplinary approaches to disease modelling are suggested as ways to improve the identification of high-risk populations and high-risk environmentable variables. ABSTRACT GEOGRAPHIC ASPECTS OF THE CONTROL OF MEASLES: WITH SPECIAL REFERENCE TO MICHIGAN By Debbie L. Borchers The history and current status of measles and its control strategies in the United States and in Michigan in particular reveal that, although officially a "preventable" disease, it has not yet been brought fully under control, despite the availability of an effective vaccine. Epidemiologic studies reveal that attack rates of measles are highest among blacks, persons of lower socio-economic status, inner city residents, and the most densely populated areas. Regionally, the highest rates are found in the East North Central states. Michigan, which had the largest absolute number of cases in I978, and the second highest rate in the country, is examined in this paper. Spatial analysis shows that Michigan's susceptibility rates steadily increased from l976 to I979, and that clustered high- risk populations created a situation favorable for the rapid diffu- sion of measles. Different geographic approaches to disease control and compliance problems, such as planar graph analysis, diffusion modelling and multiple-scale target area approaches, are recommended. ACKNOWLEDGMENTS Special thanks are in order for the many people who helped out with this project: Dr. John Hunter, for his inspiration and advice from start to finish; Dr. Stanley Brunn, for his thorough editing of the manuscript; William Simonsen, Michigan Department of Public Health, Immunization Division, for his suggestions; and Bill Corcoran, whose patience and perseverance made the computer maps possible. ii TABLE OF CONTENTS LIST OF TABLES . LIST OF FIGURES Section I. II. Michigan . III. EPIDEMIOLOGIC ASPECTS OF MEASLES Clinical Characteristics The Diffusion Process . . The Current Status of Measles in the United States. The Status of Measles in Michigan . Spatial Aspects of Measles in Michigan IV. PREVENTION AND CONTROL PROGRAMS Cost-Effectiveness of Immunization Programs . Examples of Successful Approaches to Immunization in the United States . . . . . Approaches to Immunization in Michigan V. SUGGESTIONS FOR IMPROVING THE CONTROL OF MEASLES . Geographic Approaches to Disease Control . Characteristics of Non- Compliers . Suggested Approaches for Improving Compliance VI. SUMMARY AND CONCLUSIONS BIBLIOGRAPHY INTRODUCTION . THE HISTORICAL DEVELOPMENT OF IMMUNIZATION AND ITS EFFECT ON INFECTIOUS CHILDHOOD DISEASES. . . The Development of Immunization Procedures in the United States . . The Development of Immunization Campaigns in iii Page iv Table 10. LIST OF TABLES Mortality Rates for Specified Diseases in the United States, 1850- 1870 . . . . . . . Deaths from Specified Diseases in the United States, 1880-1900 . . . Important Dates in Immunization Development Immunizations Administered by County, District and City Health Departments in Michigan, 1941-1943 Recommended Schedule fbr Active Immunization of Normal Infants and Children . . . . . . . Number of Measles Cases and Case Rates in Michigan, 1900-1978 . . . . . Cases of Measles by Geographic Area in the United States, 1978 . . . . . Measles Cases in Selected Locations, 1976-1978 Vaccination Status of Sampled Measles Cases by Area . School Enterers l976-77 Immune Levels Before and After a School Immunization Enforcement Policy in Detroit iv Page 10 15 19 38 39 41 44 66 Figure 6a. 6b. 7a. 7b. 8a. 8b. LIST OF FIGURES Number of reported cases of measles and measles encephalitis in the United States, 1962-1976 Reported cases of measles by 4-week period USA, epidemiologic year 1969- 70 compared with 1966- 67, 1967- 68, and 1968-69 . . . . States showing increase or decrease of measles cases for epidemiologic year 1969-70 over the epidemio- logic year 1968-69 . Changing measles incidence among age groups in San Francisco, 1964-1975 . . . . . . . Measles antibody response and persistence after natural infection and immunization: a 15-year follow-up . Percentage of susceptible school entrants by county, 1976-1977 . . . . . . . . . Quartile distribution of susceptible school entrants, l976-1977 . . . . . . . . . . Percentage of susceptible school entrants by county, 1977-1978 . . . . . . . . . . . Quartile distribution of susceptible school entrants, 1977-1978 . Percentage of susceptible school entrants by county, - 1978-1979 . . . . . . . . . . . Quartile distribution of susceptible school entrants, 1978-1979 . . . . . . . . . . . Annual benefits and costs of immunization against measles, United States, 1963-1972 . . Page 26 27 29 32 33 47 48 49 50 51 52 58 Figure Page 10. Cases of measles, Texarkana, Texas - Arkansas, June 1970 to January 1971 . . . . . . . . . . . 59 ll. Hypothetical diffusion of information about an immunization program and decisions to receive an immunization in a target population . . . . . . 79 vi I. INTRODUCTION Although measles is an infectious disease easily preventable by vaccination, epidemic outbreaks continue to occur throughout the United States. Reported cases of measles dropped 95 percent between 1963, when the first measles vaccine was licensed, and 1968, leading many public health authorities to believe that eradication of the disease was possible (Riley, 1976). Increasing rates of measles and other vaccine-preventable diseases since the early 19705, how- ever, have diminished hopes of eradication. Studies of epidemic outbreaks have revealed a non-random spatial pattern of measles in the United States. Higher incidence of measles occurs in black populations (Landrigan and Conrad, 1971; Currier et al., 1972; Pyle, 1973) and in areas of lower socioeconomic status (Landrigan and Conrad, 1971; Schiff et al., 1975; Pyle, 1973). In addition, attack rates vary between urban, rural and suburban areas (Landrigan and Conrad, 1971; Cherry et al., 1972). Regional concentrations of measles cases on a national scale are also evident. In the late 1970s, the East North Central states reported the largest numbers of cases and the largest percentage increases in measles incidence (Halpin et al., 1977). Since the development of an effective medical control measure, that is, the vaccine, has failed to bring measles under control, other approaches are needed to stop further unnecessary outbreaks. Evi- dence of spatial variations in measles incidence suggests that the degree to which the disease is controlled varies according to dif- ferent segments of the population and different geographic areas. This paper therefore presents a geographic approach to the problem of the control of measles, with special emphasis on the control problem in Michigan. Michigan was selected as an area of interest because of its particularly poor record of measles control; approxi- mately one-third of the nation's entire measles cases in 1978 occurred in Michigan (Center for Disease Control, 1979). The literature review of historical and epidemiological studies and the data presented in this paper are the result of an attempt to investigate the spatial distribution of measles in the United States and to examine the effectiveness of various disease control strategies. Section 11 provides the historical background of the development of immunization procedures and public health campaigns that paved the way for the possible eradication of many infectious diseases, including measles. The development of specific public health campaigns in Michigan is included in order to place the current control problem in perspective for that state. Section III consists of a description of the clinical significance of measles, a discussion of the diffusion process of epidemics and a literature review of current epidemiologic studies of measles in the United States. The epidemiology of measles in Michigan is also examined in the third section, with an emphasis on the 1978 epidemic and the levels of immunity and susceptibility in the population from 1976 to 1979. Various approaches to the prevention and control of measles in the United States and Michigan are examined in Section IV, including a cost-benefit analysis of immunization programs in general. Section V includes a discussion of selected geographic approaches to the improvement of disease control and compliance behavior. Spatial analytical techniques and diffusion models are suggested as methods that can be used to bring a disease such as measles under control and prevent future outbreaks. Finally, Section VI presents a summary of the previous sections and a dis- cussion of final conclusions. II. THE HISTORICAL DEVELOPMENT OF IMMUNIZATION AND ITS EFFECT ON INFECTIOUS CHILDHOOD DISEASES The Development of Immunization Procedures in the United States Most people today have never seen a case of smallpox or remember a child dying from measles. Yet the infectious diseases of childhood which are now preventable with vaccines contributed greatly to morbidity and mortality rates in the past. The develop- ment of specific vaccines has lessened the dangers associated with many of these diseases and has apparently eliminated one altogether, namely, smallpox. It is perhaps partly due to this lack of visi- bility of certain diseases in society that has led people to become complacent about fulfilling immunization requirements. The history of childhood diseases shows, however, that they were at one time both prevalent and lethal. Smallpox, measles, diphtheria and whooping cough (pertussis) had particularly high mortality rates in the United States in the nineteenth century (Table l). The number of deaths from these diseases remained high through the end of the nineteenth century and on into the mid-19005, except for smallpox which showed quite a dramatic decrease in deaths between 1870 and 1880 (Table 2). Death rates were not available for these years, but the large dif- ference in the number of deaths from smallpox between 1870 and 1880 TABLE 1.--Mortality Rates for Specified Diseases in the United States, 1850-1870. 1850 1860 1879 No. of Death No. of Death No. of Death Disease Deaths Rate* Deaths Rate* Deaths Rate* Smallpox 2,352 10.1 1,271 4.0 4,507 11.7 Measles 2,983 12.9 3,899 12.4 9,237 23.9 Diphtheria N.A. N.A. 1,663 5.3 6,303 16.3 Whooping Cough 5,280 22.8 8,408 26.7 9,008 23.4 SOURCE: Ninth Census of the United States, Reports - Vital Statistics, 1870. *Number of deaths per 100,000 population. TABLE 2.--Deaths from Specified Diseases in the United States, 1880-1900. Disease 1880a 1890b 1900C Smallpox 871 N.A. 3,484 Measles 8,072 9,256 12,866 Diphtheria 38,143 41,677 16,475 whooping Cough 11,064 3,432 9,958 aTenth Census of the United States, Mortality and Vital Statistics, Part I, 1880. bEleventh Census of the United States, Mortality Statistics, Part II, 1890. cTwelfth Census of the United States, Vital Statistics, Part II, 1900. SOURCES: is probably due to the introduction and acceptance of the smallpox vaccine. Some of the decrease may also be attributed to changes in the methods of disease reporting during the 1870-1880 decade. Measles, currently considered a rather mild childhood disease by most people, claimed nearly 13,000 lives at the turn of the century. The distribution of these diseases among the population remained essentially the same until the process of immunization was developed. This process involves "conferring increased resistance (or decreased susceptibility) to infections" and can be either pas- sive or active (Parish and Cannon, 1962, p. 5). Passive immunization consists of preparing immune sera (which contain ready-made anti- bodies) to help cure infectious disease. Reactions within an infected person take place rapidly, even though protection is often temporary. Active immunization, on the other hand, involves the administration of toxins, toxoids and vaccines which help to produce antibodies and prevent a specific disease from occurring. This par- ticular process takes more time to develop than passive immunization and is also capable of conferring protection for longer periods of time (Parish and Cannon, 1962). The idea of conferring protection against infectious dis- eases actually goes back hundreds of years. The Chinese placed dried crusts from the skin of smallpox patients into the nostrils of healthy persons so that they would develop a weakened form of the disease, thereby conferring lifelong immunity (Reidman, 1974). This Chinese practice had gone on fbr centuries but was made popular in the western world by Lady Mary Nortley Montague of England. While living in Turkey in the early 17005, she noticed the women grafting smallpox matter from the end of a needle onto the patient's skin. This particular method, like the Chinese method, is known as variolation or inoculation and produces a milder form of the disease than would occur if one were infected naturally. This method grad- ually led to a decline in the mortality rate from smallpox (Reidman, 1974). The first form of vaccination was introduced into the United States in 1796 by Edward Jenner. The word vaccination was used at this time to distinguish Jenner's method from the previously used term, inoculation, associated with smallpox matter. Jenner injected a young man with pustule matter from a cowpox patient, then later inoculated the same individual with some smallpox fluid. After a series of experiments, Jenner was able to prove that people with cowpox were immune to smallpox and by administering a certain amount of cowpox matter, people could be protected from smallpox (Reidman, 1974). Nearly a century passed before another vaccine was developed. Loeffler discovered the diphtheria bacillus in the 18805 and shortly thereafter Roux and Yersin discovered the diphtheria toxin (Reidman, 1974). The firstdiphtheria antitoxin was administered in Berlin in 1891. Another important breakthrough‘finrdiphtheria occurred with the development of the Schick test (Reidman, 1974). Bela Schick found that people who had recovered fromdiphtheria retained anti- bodies in their serum for life. A test was therefore developed that could detect the susceptible population and thus prevent diphtheria by shots of toxin. Other major events in the development of vaccines and immunization are listed in Table 3. As the knowledge of bacteria, viruses and vaccines prolif- erated, the morbidity and mortality rates of common childhood dis- eases declined. Advances in medical technology alone, however, proved insufficient to combat these diseases. Fear and ignorance hindered many people from accepting vaccination as a way to prevent disease. A group of "anti-vaccinationists" was formed in the early part of the nineteenth century, fearing that vaccines were unpure and would be more harmful than the disease itself (Reidman, 1974). Thus, although Jenner's first successful vaccination occurred in 1796, many states had problems enforcing vaccination requirements well into the nineteenth century. An examination of immunization campaigns in one state, Michigan reveals some of the challenges that have confronted public health workers during the vaccine era. The Development of Immunization Campaigns in Michigan Michigan established a set of rules in 1875 recommending smallpox vaccination for every child under two years of age and for all other persons once every five years. Vaccinations were required for all new employees of incorporated manufacturing companies and for all children entering school. Nevertheless, compliance with these rules was often ignored and led one doctor to complain that . . the very great extent by which the sickness and death rate is reduced in this country through vaccination can hardly be appreciated by our people who have never seen the fearful ravages of smallpox. . . . Some persons do not seem TABLE 3.--Important Dates in Immunization Development. Year Deve10pment 1721 - Lady Montague introduced variolation into England from Turkey. 1709 - Jenner published work on vaccination. 1880 - Existence of diphtheria toxin proved at Pasteur Institute by Roux and Yersin. 1890 - Behring and Kitasato discovered diphtheria antitoxin. 1890 - Behring and Kitasato proved animals could be immunized by repeated doses of tetanus toxin. 1904 - Tetanus antitoxin began to be used pr0phy1actically to treat wounds in the United States. 1906 - Calmette and Guerin of the Pasteur Institute advocated BCG for tuberculosis. 1908 - Mantoux described diagnostic test for tuberculosis in France. 1913 - Schick introduced diagnostic test for diphtheria. 1925 - Serum prophylaxis for measles introduced into Great Britain by Copeman. 1927 - Tetanus toxoid used for human immunization (Paris). 1940 - Pertussis vaccine distributed in Michigan. 1942 - National immunization campaign for diphtheria. 1944 - Human immune serum globulin for measles introduced into the United States by Cohn. 1947 - Gamma globulin being used with success in the United States. 1948 - Compulsory smallpox vaccination of infants ended in Great Britain. 1953 - Salk prepared polio vaccine. 1954 - National Foundation for Infantile Paralysis, Inc. introduced nationwide trial of Salk vaccine. 1956 - Pertussis vaccine became first bacterial vaccine to be inter- nationally standardized. 1962 - World Health Organization initiated worldwide smallpox eradication scheme. 1963 - Measles vaccine licensed in the United States. 1967 - National eradication campaign for measles started. SOURCE: Adapted from H. J. Parish and D. A. Cannon, Antisera, Toxoids, Vaccines and Tuberculins in Prophylaxis and Treat- ment, E. & S. Livingstone Ltd., Edinburgh, 1962, pp. 274-302. 10 capable of grasping the problem, and of appreciating the overwhelming evidence of the utility and comparative safety of the operation (Michigan State Board of Health, 1875, p. xxiv). Prior to the existence of a state vaccination law in Michigan, various vaccination campaigns were carried out. As early as 1837 a severe smallpox epidemic in Detroit prompted a local physician to begin a general vaccination campaign in the city. He further extended his services to the neighboring Indian tribes; 600 Saginaw Indians were vaccinated in 2 days (Michigan State Board of Health, 1875). Another campaign in Detroit during the summer of 1877 resulted in the vaccination of 16,000 persons by the Public Health Department at a cost of $4,015. Private physicians reportedly had vaccinated just as many people during the same period (Michigan State Board of Health, 1877). After much debate concerning a compulsory immunization law, the Michigan State Board of Health passed a law in 1879 stating that physicians must gffgr_vaccinations every year, without cost to persons vaccinated, at the general expense of the locality (Michigan State Board of Health, 1879). Some people felt that a stronger law requiring people to be vaccinated would impinge on personal rights of self-determination and control. Others felt the 1879 law was too weak and further measures were warranted. One suggestion was to establish a "vaccine farm"--a vaccine- producing operation to be maintained by Michigan Agricultural College (now Michigan State University) and to provide for the delivery of public vaccination to every house once a year 11 (Michigan State Board of Health, 1877). In 1894, the Secretary of the State Board of Health stated that sending physicians out to families to offer free vaccinations was "the best way to induce people to be vaccinated" (Michigan State Board of Health, 1894, p. 356). One physician suggested making parents who refused vac- cination for their children subject to a fine of not less than five dollars or ten days in jail for each offense (Michigan State Board of Health, 1894). Beginning in 1875 all children were required to be vaccinated before entering school, but reports of enforcement were rare. One report states that a rigidly enforced exclusion-from—school program in Detroit resulted in the absence of smallpox among the 12,000 school children in the city of 1882 (Michigan State Board of Health, 1882). For the most part, campaigns at this time consisted of the distribution of pamphlets and leaflets on the prevention of smallpox. These were usually sent out to areas where outbreaks occurred or where they were expected to occur, including lumbering camps throughout the state which had new crews of workers every fall (Michigan State Board of Health, 1885). Organized immunization efforts at the state level were not effective until the Bureau of Epidemiology was created after the turn of the century. Free vac- cination clinics were held in a number of places throughout the state. During the summer of 1924 a total of 47,536 persons were vaccinated by State Health Department members (Michigan State Board of Health, 1925-26). Local private physicians also reportedly vaccinated thousands of individuals at this time. Thus, 70 percent 12 of the population of Lansing and its vicinity (91,845 persons) were vaccinated from June 1 to June 20, 1924 (Michigan State Board of Health, 1925-26). The Michigan Department of Public Health began a statewide campaign for protection against diphtheria in January of 1925 (Michigan State Board of Health, 1925-26). Toxin-antitoxin was administered free of charge at scheduled immunization clinics throughout the state. In 4 counties alone, 11,506 children and adults were immunized. Additional diphtheria projects were carried out in 7 counties and 25 cities and towns in other counties. The success of this statewide campaign was demonstrated by a 227 percent increase in the distribution of toxin-antitoxin from 1924 to 1925 (Michigan State Board of Health, 1925-26). Immunization efforts by the State Health Department con- tinued into the 19305. The activities were diverse and included (1) advising local health officers about prevalence and control of communicable disease, (2) providing advice regarding immunization campaigns and furnishing forms and literature, (3) distributing biologic products and (4) conducting research in biologic immuni- zation (Michigan State Board of Health, 1936). In spite of these efforts, questions still remained as to why outbreaks of smallpox and diphtheria continued throughout the state. The Commissioner's Report in 1938 revealed this concern: It is not that our people are unconvinced of the value of protecting themselves against communicable disease. Men and women and children stand in line to be vaccinated, 13 when there is a smallpox outbreak. The health problem is, how can such lineups be made obsolete and unnecessary? The feeling of some health workers is that our most diffi- cult problems lie ahead, in bringing people to act as effectively in their own interest because of understanding and prudence as they do when they are afraid (Michigan State Board of Health, 1939, p. 12). After 44 months of testing, a pertussis vaccine developed in Grand Rapids, Michigan was distributed to physicians through- out the state in 1940 (Michigan State Board of Health, 1940). Dissemination of immunization information was also emphasized during the year, including the distribution of a recommended immunization schedule agreed upon by the medical profession. In addition, immunization record cards accompanied by the recommended immuniza- tion schedules were given to the parents of newborn children along with birth certificates (Michigan State Board of Health, 1940). In 1942 a number of special immunization programs were developed. First, an intense smallpox vaccination program was sponsored by the State Health Department. Its goal was 100 percent protection for infants 6-12 months: however, no results were reported on the success of this program (Michigan State Board of Health, 1942). The second major campaign involved an immunization program for Mexican migrants. Since these migratory workers were known to have a high incidenceirfdiphtheria and low levels of pro- tection against smallpox and diphtheria, the Michigan Medical Society together with county medical societies arranged an immunization schedule for children of these workers. It was noted that clinics were "strategically placed" in the sugar beet areas where the 14 Mexican migrants worked: approximately 5,000 individuals were vaccinated (Michigan State Board of Health, 1942). A third immunization program was instituted nationwide by President Roosevelt in 1942. On February 6, a proclamation was issued recommending that all children should be immunized against diphtheria and smallpox by May 1, "as part of the national plan for defense" (Michigan State Board of Health, 1942, p. 227). The child welfare committee of the Michigan State Medical Society organized statewide programs through local medical societies and health departments. Instead of paying local physicians, token payments from federal funds were made to local medical societies participat- ing in the program. An evaluation of this particular program is impossible due to the lack of data. A comment in the Annual Report of 1942 states that, "Progress reports indicate varying responses in the counties. An interesting outcome of the program has been the discovery of the high percentage of children in many areas who already had received the protective treatments" (Michigan State Board of Health, 1942, p. 227). The number of immunizations administered by county, district and city health departments in the state generally increased during the 19405. Between 1942 and 1943, however, there was a decrease in the number of smallpox, diphtheria and typhoid immunizations given for most age groups (Table 4). Attendance at public lectures and talks reportedly decreased as well. No explanation was provided but it is conjectured that World War 11 may have attracted attention 15 TABLE 4.--Immunizations Administered by County, District and City Health Departments in Michigan, 1941-1943. 1941a 1942 1943° Smallpox - under 1 year 2,373 2,619 3,264 Smallpox - 1-4 years 8,838 13,625 12,026 Smallpox - 5 years and over 35,587 62,293 59,848 TOTAL 46,798 78,537 75,138 Diphtheria - under 1 year 2,748 3,819 4,102 Diphtheria - 1-4 years 9,917 16,597 13,337 Diphtheria - 5 years and over 17,450 37,039 31,657 TOTAL 30,115 57,455 49,096 Typhoid - complete immunization 742 1,761 701 Public lectures and talks 497 677 406 Attendance 14,908 19,160 14,457 SOURCES: aMichigan State Board of Health, Seventieth Annual Report, 1942, p. 212. b Repor , 1943, p. 116. Michigan State Board of Health, Seventy-First Annual cMichigan State Board of Health, Seventy-Second Annual Report, 1944, p. 84. 16 away from immunization concerns and also may have disrupted the production and distribution of vaccines. The importance of immunizations in Michigan was pointed out in terms of dramatic decreases in deaths from diphtheria. The state dropped from 954 deaths in 1921 to 12 deaths in 1951 (Michigan Depart- ment of Public Health, 1952). The need for continuing annual cam- paigns was noted, however, with an emphasis on immunizing children entering school for the first time. Although plans for immunization differed among communities, final responsibility was placed with the parents of each child. By 1951, vaccines existed for diphtheria, whooping cough tetanus and smallpox (Michigan Department of Public Health, 1952). In addition, gamma globulin was available for the prevention and modification of measles (Michigan Department of Public Health, 1952). (It was first supplied by the American Red Cross in 1945-46.) The Michigan Department of Public Health urged parents to immunize their children as early as possible; three months was the recommended age for beginning immunizations. The use of the triple vaccine, DPT (Diphtheria-Pertussia-Tetanus), was encouraged as it was the most convenient method for both parents and physicians. The need for booster shots was also strongly emphasized as a means of acquiring lasting immunity (Michigan Department of Public Health, 1952). The polio vaccine did not come into use until 1954. Polio has never been a particularly prevalent disease in the United States compared to smallpox, measles, and diphtheria. Approximately 1 out of every 1,000 persons in the population was struck with polio but 17 the paralysis caused by the disease made it one of the most feared (Reidman, 1974). The Salk vaccine underwent a massive public trial in April of 1954. Over 1.5 million children participated in the trial, along with 20,000 physicians and health officers, 40,000 nurses, thousands of teachers and a quarter of a million other volunteers. The results of the experiment showed that paralysis occurred six times more frequently in the unvaccinated children and that the vaccine was safe in 80-90 percent of the children (Reidman, 1974). Once the Salk vaccine was formally announced as "safe, potent, and effective," millions of doses were distributed through- out Michigan. It was later learned, however, that several lots of vaccine accidentally contained the live virus, leaving over 200 people with polio and 11 people dead. Following this report, addi- tional precautions were taken in the testing, mixing, and storage of the vaccine in order to restore the confidence of the public. It is not clear what effect this deadly mix-up had on the attitudes of the American public towards immunization, but in the summer of that same year (1954), millions of polio vaccinations continued to be administered across the country. By 1971, the number of polio cases in the United States had dropped from 18,304 in 1954 to only 17 (Reidman, 1974). In spite of fewer reports of the childhood diseases dis- cussed above, state health records indicate that there was continued concern among public health officials regarding the immunization status of residents throughout the 19605. As the decade began, 18 citizens were reminded that 1,011 people in Michigan died and 42,465 persons became ill from 4 preventable diseases--polio, whooping cough, tetanus, and diphtheria (Michigan Department of Public Health, 1960). A national immunization survey carried out in the mid-19605 revealed some startling facts. Of children ages one to four, one- third had not completed the series of three DPT shots and 60 percent had not received the minimal four doses of polio vaccine (Table 5). In addition, one-third of adults between 20-29 years of age had not received even one dose of polio vaccine (Michigan Department of Public Health, 1964). Further analysis of survey results indicated that immunization status was lowest in lower socio-economic areas of cities. This finding prompted the flow of federal funds to finance several local immunization programs (Michigan Department of Public Health, 1965). In this way, funds were finally obtained (in 1967) to purchase measles vaccine for distribution to local health depart- ments in Michigan. Prior to this action, most local health depart- ments had insufficient funds to offer the live virus vaccine licensed in 1963. A "Head Start" program in 1965 had provided some vaccine to children in low income groups but this program did not extend pro- tection to most children throughout the state. In 1967, therefore, the school "Check Point" law became effective, thereby providing funds to buy enough vaccine to protect all children entering Michigan schools (Michigan Department of Public Health, 1967). Most of the funds were connected with the national campaign whose goal was the complete eradication of measles in the United States 19 TABLE 5.--Recommended Schedule for Active Immunization of Normal Infants and Children. Age Vaccine 2 months DPTa, TOPVb 4 months DPT, TOPV 6 months DPT, TOPVC 15 months Measles, mumps, rubella, tuberculin test 18 months DTP, TOPV 4- 6 years DTP, TOPV 14-16 years Tdd; Repeat every 10 years SOURCE: S. Krugman and S. L. Katz, "Childhood Immunization Pro- cedures," JAMA, Vol. 237, No. 121 (1977), p. 2229. aDiphtheria and tetanus toxoids combined with pertussis vaccine. bTrivalent oral poliovirus vaccine. cThis dose is optional if polio is not endemic in the area. dTetanus and diphtheria toxoids (adult type) for those more than 6 years of age. 20 by the end of 1967. This national program established four essen- tial concerns for success: (1) the routine immunization of all infants at the age of one, (2) immunization of all remaining sus- ceptible children before entering public schools, (3) improved disease surveillance at all levels, and (4) immediate epidemic control at the first sign of an outbreak (Conrad et al., 1971). Reasons for the failure of the above program have been proposed by Conrad et a1. (1971) and by Riley (1976). Conrad et a1. contend that the requirements established in the national program were simply not met with any degree of success. For example, the routine immunization of all one year olds, a key point of the program, failed to receive adequate funding. Just as various programs and campaigns for measles were starting, a national cam- paign for rubella was initiated; the measles program lost its priority as a federally funded project (Conrad et al., 1971). As a result, the 26,000 reported cases in 1969 jumped to 75,000 cases in 1971, directly attributable to the declining availability of the measles vaccine (Riley, 1976). A result of this national interest was that the states were' expected to use their revenue sharing funds for immunization pro- grams. Most states, however, failed to use these funds for such purposes. A survey of state revenue sharing appropriations revealed that almost 11 percent of these funds was spent on road repairs, with approximately only 1 percent allocated for all_health services (Riley, 1976). 21 The nation as a whole also failed to meet the other three requirements of the four-point program outlined above. Only 40 percent of all states and territories required measles immunizations for school entry as of 1970. Improvements in disease surveillance and reporting were also noticed in few areas, pointing to the need for better age-specific, epidemiologic data on all measles cases. Furthermore, numerous emergency requests for vaccines suggested that measles cases were not being adequately brought under control soon enough to prevent major outbreaks from occurring in schools and public institutions (Conrad et al., 1971). In these ways, the development of immunization programs in the United States and in Michigan has expanded from the meager efforts of local physicians to massive state and national public campaigns. A reduction in disease case rates following the intro- duction of effective vaccines was a consistent and long-lasting trend for smallpox anddiphtheria. The development of the measles vaccine, however, resulted in only temporary decreases in case rates of measles. An epidemiologic assessment of measles in the United States and in Michigan follows. ‘ III. EPIDEMIOLOGIC ASPECTS OF MEASLES Clinical Characteristics Measles is an extremely contagious viral disease, trans- mitted by direct person-to-person contact or close physical proxi- mity. It is endemic in all areas of the world except the most isolated populations. Measles is both a seasonal disease, usually occurring in late winter and early spring, and a periodic disease, recurring in two to three year epidemic cycles. Attack rates are usually highest among young children, peaking at six years of age in developed countries and two to three years of age in developing countries (Beeson and McDermott, 1971). Symptoms of measles begin to appear after an ll-day (average) incubation period and consist of high fever, malaise, myalgia, headache, photophobia and conjunctivitis. Inflammation of the respiratory tract follows and laryngeal complications may also follow. The appearance of Koplik's spots on the buccal mucosa is a significant diagnostic feature as they often precede or overlap the development of a rash. The rash, which begins behind the ears or on the face, may spread downward to the trunk and extremities: it then fades approximately five days after onset (Beeson and McDermott, 1971). Complications from measles usually stem from secondary bacterial infections. Otitis media (middle ear infection) and 22 23 pneumonia are the most common sequelae: however, the severity of complications is also greatly increased by conditions of overcrowd- ing, malnutrition, and the prevalence of bacterial pathogens in the general population. Other complications may appear, including severe laryngitis, electrocardiographic abnormality, gastrointestinal problems, encephalomyelitis and giant-cell pneumonia. In addition, unfavorably modified measles, characterized by an atypical rash, may result from the administration of inactivated measles vaccine (Beeson and McDermott, 1971). Mortality occurs in 1 out of every 10,000 cases in the United States. Encephalitis, creating the potential for brain damage and mental retardation, develops in.l of every 1,000 cases. Roughly 1 out of every 100 cases results in pneumonia (Halpin et al., 1977). No specific treatment for measles currently exists but immunity can be acquired in a number of ways. An attack of natural measles is considered the most effective way to achieve lifelong immunity. All infants up to six months of age, however, receive transient immunity by placentally transferred maternal antibodies. Immunization can also occur with the administration of gamma globulin (temporary), live virus vaccine with standardized immune globulin, or live further attenuated virus vaccine (Beeson and McDermott, 1971). 24 The Diffusion Process The balance of immune and susceptible persons in the popula- tion is very crucial to the spread of measles. The exact proportion of susceptibles needed to sustain an epidemic has been subject to debate, however. Studies during the early part of the 1900s found that urban areas were protected from epidemics when the level of immunity in the population was greater than 55 percent (Sencer et al., 1967). Thus, the concept of herd immunity was developed. Epidemic outbreaks of measles in the 19705, however, have been reported in populations with immunity levels as high as 85 percent (Schiff et al., 1975) and 89 percent (Wyll and Witte, 1971). Dittman et a1. (1976) found that measles could be eradicated in a community only when 90 percent of the susceptible population was immunized. Cherry et a1. (1972) suggest that the spread of the virus depends not only on the number of susceptibles in a population but also on their opportunities for contact. Modes of spread can be measured in a number of ways. One method involves the use of planar graph techniques which can be used to analyze different spatial processes at different stages of an epidemic (Haggett, 1976). In a study of 2 epidemic waves over a 222-week period, Haggett plotted measles cases in 28 administrative areas. The join-count measure of spatial autocorrelation was used to determine degrees of clustering or separation present during various stages of the epidemics. Patterns of spatial contagion were analyzed by viewing planar graphs based on seven different models of disease diffusion: (1) regional, (2) urban-rural, 25 (3) local contagion, (4) wave contagion, (5) journey-to-work, (6) population size, and (7) population density. Analysis of the graphs showed that (1) during endemic periods infections persisted in larger population clusters and moved slowly through low density rural areas in a sporadic manner, (2) during the advanced phase of the epidemic the influence of population size on spread decreased and the wave effect became much more important, and (3) at the peak of the epidemic wave local contagion was an important factor in the spread of the virus. In addition, the impact of successful vaccina- tion programs could be determined by the lack of distinct advance and retreat phases usually displayed by a classic epidemic wave. In this way, various geographic methodologies can thus be used to predict the spread of epidemic diseases and can also be used to evaluate the impact of immunization programs on the spread of those diseases. More specific suggestions for applying geographic method- ologies to disease control problems are discussed in Section V. The Current Status of Measles in the United States Vaccine licensure has had a profoUnd effect on the epi- demiology of measles in the United States. The number of measles cases dropped over 90 percent from 1963 to 1968, followed by a corresponding decrease in cases of post measles encephalitis (Figure 1). Since 1969, as mentioned above, a resurgence of measles has been evident (Figure 2). An investigation of measles morbidity from epidemologic year 1968-69 to 1969-70, revealed increases in 26 Voccme 500 /ocensed I500 3 "’0’ % 7/ «so 2 c / c £400} % I// g «00 g E 35m % ¢ / «350 g '5 300’ I? g ’i 4 300 0 E2501?“ 4250: t? 200‘ Z 2 e “'1. Encephalitis . 200 2 ; ”OI éégéggg é; /// -Iuo § E 'OOL Z Z Z a g .1 100 i 5 50 / / :1 7 ’// 71”” 4 g. 2% Z??? 172% égaa %Z§Z égi% 2% mzzzlzlgso 1952 ea 54 as so 5: so 59 7o 7. 72 73 74 75 76 SOURCE: Saul Krugman, "Present Status of Measles and Rubella Immunization in the United States: A Medical Progress Report," Journal of Pediatrics, Vol. 90, No. 1 (1977), p. 2’(reprintéd’with permission). Figure l.--Number of reported cases of measles and measles encephalitis in the United States, 1962-1976. 27 12,000 1 10,000-1 1966- 67 8.000 a U! U in ENC i d U I 4.000 ’F—"-\ .969‘7. - ------- ‘ h ”/ ‘~\\ 1557-55 ,-’ . ‘s - 2,000 < u . - j/ssass \\ '- .... .‘.'—:—o—/ “\: ./ .- / ....... O T I V Y 1' 1 1' 1' V 1 44 43 SJ 4 8 12 16 20 24 28 32 36 4O 4-WEEK PERIOD ENDING SOURCE: J. L. Conrad et al., "The Epidemiologic Rationale for the Failure to Eradicate Measles in the United States," American Journal of Public Health, Vol. 61, No. 11 (1971), p. 2306 (reprinted with permission). Figure 2.--Reported cases of measles by 4-week period USA, epidemiologic year 1969-70 compared with 1966-67, 1967-68, and 1968-69. 28 41 states, decreases in 9 states and New York City, and no change in only 1 state (Vermont) (Figure 3). A total of 21,210 new cases were reported for the epidemiologic year 1969-70, with an average increase of 90 percent, for all 50 states over the previous year (Conrad et al., 1971). One particular concern associated with this recent resurg- ence has been the occurrence of measles in previously vaccinated children. The most prominent reason given for this phenomenon seems to be related to the age at which vaccinations are adminis- tered. For instance, Cherry et a1. (1972) found that the average attack rate for children vaccinated under age one was 6.2 percent, compared to an average attack rate of 1.7 percent for those vacci- nated during or after their first birthday. Cherry et al. also discovered that 50 percent of the vaccine failures reported occurred in children vaccinated before the age of one. Another study from Birmingham, Alabama (Currier et al., 1972) revealed even more startling results. Of a total of 37 measles cases reported during an epidemic, 25, or 68 percent, of the children had received live further attenuated virus vaccine. Further investigation of the victims revealed that the attack rate for those immunized at less than 12 months of age was 17.6 percent while those immunized after 12 months of age had an attack rate of 1.9 percent. This difference was significant at p < .01. In this study, the occurrence of measles in vaccinated children was attributed to possible over- dosages of measles immune globulin during immunization and to the 29 - 99 D etc-nus: SOURCE: J. L. Conrad et al., “The Epidemiologic Rationale for the Failure to Eradicate Measles in the United States," American Journal of Public Health, Vol. 61, No. 11 (1971), p. 2308 (reprinted with permission). Figure 3.--States showing increase or decrease of measles cases for epidemiologic year 1969-70 over the epidemiologic year 1968-69. 3O presence of maternal antibodies in children vaccinated under 12 months of age. Several other explanations for the rise in measles cases have been suggested as well. One concerns the seroconversion failure rate which occurs in 3 to 5 percent of those who receive the live attenuated vaccine (Wyll and Witte, 1971). Other reasons include the administration of killed measles virus vaccine by itself and passive immunization with immune serum globulin, techniques which are noted for their inability to confer permanent immunity. Improper handling and storage of vaccines and defective batches of vaccines are cited as additional possibilities (Weiner et al., 1977). A major problem associated with the phenomenon of unsucces- ful immunization is that many people who think they are adequately immunized are actually at risk to contracting measles. This condi- tion has resulted in outbreaks among large numbers of adolescents and young adults throughout the United States. For example, an outbreak in New York involved 12-19 year old students in junior and senior high schools, an unusual departure from past epidemio- logic trends (Weiner et al., 1977). Similarly, an investigation of an epidemic in Ohio revealed that the majority of measles cases occurred in children 10-14 years of age (Halpin et al., 1977). A study of the changing distribution of measles among dif- ferent age groups was conducted in California by Rand et a1. (1976). This study revealed a definite decrease over time in the percentage of cases among the five to nine year old age group and a consequent 31 increase in the lO-14 and 15-19 year old age groups (Figure 4). A comparison of the total number of measles cases and age-specific case rates from 1964 to 1975 in the San Francisco Bay area revealed a declining attack rate for all previously vaccinated age groups except the 10-14 and 15-19 year old age groups. Rand et al. suggest that the lack of a statewide immunization policy until 1964 and the lack of uniform standards and regimens may be responsible for a large population of inadequately vaccinated adolescents and young adults. In general immunity induced by live further attenuated vaccine is apparently long-lasting. Prospective studies of children immunized in four different ways indicate that antibody responses continue to be similar following natural infection and vaccination after 15 years (Krugman, 1977). Geometric mean titers of antibody response were found to be highest after natural infection or Edmonston B vaccine, intermediate following gamma globulin (GG) with Edmonston B vaccine and lowest after immunization with further attenuated measles-virus vaccine, Schwartz strain (Figure 5). Age is considered an important factor in vaccine failures. It has been suggested that measles immunization be delayed until 15 months of age (Krugman, 1977). Reimmunization of those who experienced initial vaccine failures is also recommended. Krugman (1977) contends that no evidence has been found to support the idea that subacute sclerosing panencephalitis is associated with the vaccination of immune persons. Furthermore, the risk of central nervous system complication is much greater following natural 32 l 1 j r 1 T 1 1 Four Bay Area Cunlies 1964 ' ------- 1971 -I o----o 1972 o——o 1975 l 1 z-hg. , ,_ __4 15-19 25-34 I 45-54 + 1 4 10-14 20-24 3544 55+ SOURCE: K. H. Rand et al., "Measles in Adults: An Unforeseen Consequence of Immunization?" JAMA, Vol. 236, No. 9 (1976), p. 1030 (reprinted with permission). Copyright 1970, American Medical Association; Figure 4.--Changing measles incidence among age groups in San Francisco, 1964-1975. 33 Measles Voccme Enders Edmonslon .§ '5: l l ‘3 {>in hafnium (666 _5,2 :9 256* " ~256 ‘5 Natural Measles 4 . - E l28 ---a---~6~."" l- 123 1-... ,, 54- --. » 54 II ~~ - . ' ..... g 32‘1 o- 'c‘s“ - °- .. 32 ’ Measles Vaccine ‘s‘ °\. 3 'GJ Sch-art Straln/ “§ ‘ L '6 o Sch-0 3 8" " 8 8 .5 “ i ‘ 8 (4‘4 l- (4 m 1 1 7Jf‘r fir W 1 j ‘7; 1 1 O h; I 2 3 4 5 IO 15 Years After Natural Infection or Immunization SOURCE: Saul Krugman, “Present Status of Measles and Rubella Immunization in the United States: A Medical Progress Report," Journal of Pediatrics, Vol. 90, No. l (1977), p.3 (reprinted with permission). . Figure 5.--Measles antibody response and persistence after natural infection and immunization: a 15-year follow-up. 34 infection than following vaccination. Even though vaccine failure is a factor in the changing epidemiology of measles within the last decade, most measles cases have occurred in unimmunized children. A susceptible population of five million (children and adolescents) still exists and this is a large enough reservoir to sustain periodic outbreaks of measles (Krugman, 1977). Although measles can be found in all societies, its inci- dence is not evenly distributed throughout the United States. The more frequent occurrence of measles among lower socio-economic groups has been noted in numerous studies. In Landrigan and Conrad's study (1971), 87 percent of measles patients in Los Angeles County were from lower and lower-middle socio-economic groups. Schiff et a1. (1975) noted during their investigation of rubella and measles that Indian children of low socio-economic status showed a lower sus- ceptibility rate of measles than middle class children: this finding suggests that lower income populations are more likely to develop immunity at an earlier age by natural infection. Pyle's (1973) investigation of a measles epidemic in Akron, Ohio revealed that socio-economic status affected the spread of measles through the city. Using cartographic analysis techniques to examine the distri- bution and spread of measles cases, he found that the poorest areas in the city experienced the most severe and most long-lasting epidemic waves. A correlation analysis of 12 socio-economic variables revealed that income and education had the highest negative correlation with measles, -O.643 and -O.606, respectively. 35 The distribution of measles cases also varies among ethnic groups in the United States. A survey of measles in Dallas County, Texas, in which 17 percent of the total population was black, revealed that a disproportionate number, over 50 percent, of the measles patients were black (Landrigan and Conrad, 1971). Simi- larly, during an epidemic in Birmingham, Alabama, 76 percent of the cases occurred in black children: the disease was distributed in four lower socio-economic areas of the city which were predominantly black (Currier et al., 1972). Pyle (1973) also found that areas in Akron with proportionately large black populations, usually located in the inner city, reported the highest attack rates. He reported a value of 0.583 for the correlation of "percent negro" with measles (Pyle, 1973). Although this correlation is not as strong as that of income and measles, these two variables are strongly interrelated. The higher rates among the black population are no doubt a reflection of income and socio-economic status. Contrasts in the characteristics of measles between urban and rural areas have also been noted. Landrigan and Conrad (1971) found that in urban outbreaks most cases (53 percent) occurred among preschoolers (ages one to four), whereas the suburban and rural areas reported the majority of cases (61 percent) among children five to nine years old. This difference was attributed to the earlier age of mingling in nursery schools and day care centers in cities. Similar findings were reported by Cherry et a1. (1972) in their study of measles in St. Louis City and St. Louis County. Attack rates for children up to four years old within the city limits were nearly 36 double those of the five to nine year olds. Within that county, however, attack rates for children five to nine years old was more than four times that of children four years old and under. In addition to urban-rural differences, other regional variations are evident throughout the United States. The existence of a regional concentration of measles cases was first reported by Landrigan and Conrad (1971) who noted that the greatest concentra- tion was in the East North Central states. Although major increases have been reported throughout the country since the early 19705, the East North Central states have reported the largest percentage increase in cases of measles in the latter part of the decade. For example, from 1975 to 1976 Ohio reported a 584 percent rise in measles incidence, compared to a 64 percent increase for the nation as a whole (Halpin et al., 1977). As of March 1977, nationwide reporting was running twice as high as in 1976 and the East North Central states were once again showing the highest increases (Halpin et al., 1977). The most noteworthy increase in this region was reported in Michigan which reported approximately one-third of the nation's total measles cases (over 8,000) in 1978 (Center for Disease Control, 1979). Since Michigan is representative of a high-risk area for measles within the United States, epidemiologic aspects of measles in this state are examined next. The Status of Measles in Michigan Michigan's experience with measles since the turn of the century parallels that of the nation as a whole. In general, case 37 rates have been quite high and the two to three year epidemic cycle has been evident until 1966 (Table 6). Between 1935 and 1942, exceptionally high case rates were reported in 1935, 1938, and 1941 compared to 1936, 1937, 1939, 1940 and 1942; this pattern indicates that epidemics were occurring every three years. Alternating two and three year epidemic waves of measles occurred up until 1966 when the measles vaccine became available to Michigan residents. A sharp decrease in case rates occurred after 1966, dropping from 183.4 per 1000.000 in 1966 to 12.2 per 100,000 in 1965 (Michigan Department of Public Health, Office of Vital and Health Statistics, 1978). Measles incidence continued to decline until 1969, when a slight increase in the number of cases was first reported. A major change occurred in 1970 when the number of cases increased over 400 percent from the previous year. From 1970 through 1978, the two to three year epidemic cycle has become further evident, indicating that a large susceptible population still exists in Michigan (Michigan Department of Public Health, 1978). The sharp increase in the number of cases reported for 1978 is not only high compared to previous years within Michigan but is also approximately three times higher than the number of cases reported by any other state in the country (Table 7). The East North Central states accounted for nearly half of all the measles cases in 1978. Furthermore, 70 percent of those cases in East North Central states occurred in Michigan (Center for Disease Control, 1979). 38 TABLE 6.--Number of Measles Cases and Case Rates in Michigan, 1900- 1978. Number Case Rates Number Case Rates Year of Cases per 100,000 Year of Cases per 100,000 1900 20,356 840.8 1940 20,206 384.4 1901 4,629 188.2 1941 70,748 1,301.1 1902 11,978 479.3 1942 8,569 154.7 1903 8,941 352.3 1943 51,764 962.6 1904 10,386 403.1 1944 26,711 496.7 1905 6,061 ‘231.7 1945 6,328 116.4 1906 7,403 278.9 1946 42,261 740.3 1907 12,139 450.7 1947 9,574 157.8 1908 4,775 174.8 1948 42,952 693.3 1909 9,047 326.5 1949 20,279 319.3 1910 13,934 495.8 1950 38,245 600.2 1911 9,639 332.8 1951 15,227 232.7 1912 2,834 95.0 1952 32,941 491.1 1913 9,185 299.4 1953 23,334 340.5 1914 11,356 360.1 1954 40,725 579.8 1915 4,438 137.0 1955 23,882 330.0 1916 12,143 365.2 1956 41,966 558.4 1917 14,472 424.3 1957 19,070 244.4 1918 6,726 192.4 1958 41.448 526.9 1919 8,885 248.0 1959 12,234 153.7 1920 22,364 609.6 1960 36,161 462.2 1921 3,043 80.4 1961 29,391 371.9 1922 12,107 310.2 1962 25,303 318.7 1923 30,041 747.2 1963 48,752 607.1 1924 18,290 442.0 1964 30,897 381.4 1925 10,332 242.8 1965 28,132 343.1 1926 39,946 913.5 *1966 15,251 183.4 1927 8,303 184.9 1967 1,048 12.2 1928 27,039 586.9 1968 353 4.1 1929 18,040 381.8 1969, 401 4.6 1930 28,129 580.9 1970 1,834 20.7 1931 6,212 127.2 1971 2,659 29.6 1932 42,129 855.4 1972 2,353 26.1 1933 21,654 436.0 1973 4,552 50.2 1934 6,528 130.4 1974 2,365 26.0 1935 79,061 1,565.8 1975 3,253 35.5 1936 2,453 48.2 1976 6,139 67.4 1937 6,154 119.9 1977 1,392 15.2 1938 79,400 1,534.8 1978 8,006 87.7 1939 12,948 248.3 SOURCE: Michigan Department of Public Health, Vital and Health Statistics, 1978 Michigan Health Statistics. *Measles vaccine distributed in Michigan. TABLE 7.--Cases of Measles by Geographic Area in the United States, 1978. Reporting Area No. of Cases Reporting Area No. of Cases UNITED STATES 26,795 EAST SOUTH CENTRAL 1,440 . Kentucky 122 NEW ENGLAND 2’057 Tennessee 966 Maine 1’319 Alabama 102 New Hampshire 86 M‘ . . i 250 Vermont 53 1551551pp "6553c““sett5 253 NEST SOUTH CENTRAL 1,453 Rhode Island 8 Connecticut 328 Arkansas 16 Louisiana 385 MID-ATLANTIC 2,281 Oklahoma 19 Upstate New York 1,438 Texas 1,033 New York City 405 New Jersey 75 MOUNTAIN 266 Pennsylvania 363 Montana 107 EAST NORTH CENTRAL 11.587 fidah9 ‘ . yoming - Ohio 497 . Colorado 37 Indiana 234 . . . New Mex1co - IllTnOTs 1,335 Arizona 57 *Michigan 8,006 Utah 44 WisconSTn 1,515 Nevada 20 WEST NORTH CENTRAL 602 Minnesota 43 PACIFIC 1,624 Iowa 76 Washington 438 Missouri 173 Oregon 529 North Dakota 211 California 654 South Dakota --- Alaska 1 Nebraska 5 Hawaii 12 Kansas 94 Guam 25 sogTH ATLANTIC 5,485 Puerto Rico 315 elaware 7 . . Virgin Islands 6 "aPY‘and 5‘ Pacific Trust District ofColumbia 2 Territories 650 Virginia 2,836 Nest Virginia 1,068 North Carolina 125 South Carolina 199 Georgia 36 Florida 1,161 SOURCE: Center for Disease Control, "Cases of Specified Notifiable Diseases: United States," Morbidity and Mortality Weekly Report, January 5, 1979, p. 532. 40 Within Michigan in 1978, Wayne County reported the highest incidence (1,000 cases) but a fairly low crude morbidity rate (41 per 1000,000 population) compared to the rest of the state (Michigan Department of Public Health, 1978). Ingham County, on the other hand, reported nearly as many cases as Wayne County; the county's crude morbidity rate was 309 per 100,000. The drastic increase in cases reported in Ingham County from 1977 to 1978 compared to those from Wayne County and the city of Detroit are shown in Table 8. The city of Detroit surprisingly shows, according to Table 8, a decrease in cases between 1976 and 1977 and only a slight increase from 1977 to 1978. Since previous studies have indicated that higher attack rates occur among black populations and those of lower socio-economic status, one would expect much higher disease rates than those reported for Detroit, which has a large black population and a large population in the lower socio-economic classes. A school immunization law which went into effect in Detroit in 1976 is no doubt a reflection of its enforcement and the low incidence for 1978 (see Section IV). Two major groups in Michigan were affected by the measles epidemic in 1978. One was children in the upper grades, ages 10-15 years; this group accounted for most of the measles morbidity during the epidemic season. Morbidity was believed to be attributed to ineffective immunization among these children, either because of inactivated vaccines received or vaccines administered before age one (Simonsen, 1978). The second major group affected was 41 TABLE 8.--Measles Cases in Selected Locations, 1976-1978. Number of Cases Location 1976 1977 1978 Ingham County 10 4 840 Wayne County 264 97 _1,000 Detroit 526 417 465 SOURCE: Michigan Department of Public Health, Bureau of Disease Control and Laboratory Services, Division of Epidemiology, Weekly Surveillance Report, 52nd Week, 1976, 1977, 1978. 42 preschoolers. Measles among this segment of the population is con- sidered important because hospitalization rates among two year olds are much higher than among those ten years of age (Simonsen, 1978). One investigation which began in November 1978 attempted to examine certain epidemiologic features of measles cases in Michigan from the 1977-78 epidemic season (Bernier et al., 1978). For example, 1 death from a case of atypical measles was uncovered, in addition to 1 case of encephalitis, 50 hospitalizations and 13 cases of pneumonia. One useful finding evolved from an investiga- tion into the cases reported as measles. A sample of 225 cases from Michigan and 160 cases from Detroit were analyzed fOr whether or not they met the standard Center for Disease Control case defi- nition of measles. A case was designated "measles" if it met three criteria: '(1) fever 3_101° F., or “high"; plus (2) rash duration 3.3 days; plus (3) cough, coryza, or conjunctivitis. Of the sample cases counted as measles, 20 percent of Michigan's cases and 9 percent of Detroit's cases failed to meet the standard case defini- tion; that is, there was apparently a significant amount of over- reporting. This overreporting was supposedly due to a variety of different case report forms used throughout the state and the lack of a standard by which to define and judge measles cases (Bernier et al., 1978). Another significant finding of this Michigan investigation was that most of the cases occurred in children ages 15 months to 18 years with undocumented, unknown, or no vaccination history, and not among adequately vaccinated persons as had been thought. 43 Twenty-five percent of the cases in Michigan and 36 percent of the cases in Detroit occurred among those with a documented vaccination history; that is, defined as having at least the month and year of vaccination recorded or having a written vaccination record examined by an investigator (Table 9). Still, 69 percent of Michigan's cases were considered preventable. The conclusion of Bernier et a1. (1978, p. 18) was that, "Identification and vaccination of those children (including revaccination of those who cannot document a previous vaccination) should have prevented their illness." A statewide study of measles reporting systems was also conducted in 1978 (Bernier et al., 1978). A survey of 43 counties in the state plus Detroit revealed that 3 of the counties had no school reporting system, 8 counties reported no verification system and 4 counties reported neither a school reporting system nor a case verification system. Based on previous experience, school systems with no verification system are accurate in only one out of every two or three cases reported. By applying this estimate of verification to counties with no case verification system, a corrected estimate of measles cases for the state was reduced to 76.4 percent of the original estimate. Furthermore, a corrected measles incidence for Michigan was changed from 297 cases per 100,000 population under 18 years old (as of week 47 in 1978) to 227. Even with the corrected incidence, the state still ranked second highest (behind Maine) in the nation's rate of measles cases (Bernier et al., 1978). Bernier et a1. (1978, p. 26) concluded that even though 24 percent of the measles cases reported in Michigan were false 44 .mmpmmms AFanmoq umgmuwmcou omega can cowapcremu ammo mg» acmumms omega muzpucw mmmmu« .mp .a ..m~m_ .F zaasmumo-N~ anemsoz .camwgowz "ucoamm apgk= ..Pm um gmvcgmm camom “mumaom Ao.¢mv em Am.¢~V mm coepacwuua> oz Am._ev mm Ao.mmv mm Ammconmmm Fangm>v umpcmssuoucs Am.¢mv mm Aw.mmv we Atacama cmpupczv cavemanooo R .02 a .oz magnum cowumcwoum> mm_ u z emP u z mFQEMm macaw cmmwsowz mpasmm “moguwo .mog< zn amommo mmpmmmz uw_asmm co maumpm comumcwuom>uu.m m4m
. 6.35 6.25 5.21 E19423
SOURCE: G. Rose, "The Distribution of Mortality from Hyper-
tension Hithin the United States," Journal of Chronic
Diseases, Vol. 15 (1962), p. 1018.
Figure l.--Age-adjusted death rates for hypertension, designated
by quartiles, for the white population of the United
States, both sexes, ages 40-64, 1949-1951.
25
24.55 - 19.4 -
281.__'_J 235
Deaths per 10,000 ->28.1
,__..<19.4
SOURCE: G. Rose, "The Distribution of Mortality from Hyper-
tension Nithin.the United States," Journal of Chronic
Diseases, Vol. 15 (1962), p. 1021.
Figure 2.--Age-adjusted death rates for hypertension designated by
quartiles, for the non-white population of the United
States, both sexes, ages 40-64, 1949-1951 (excludin
states with rates based on fewer than twenty deaths).
26
mortality rates; therefore their rates were combined. All rates
were age—adjusted to the 1950 population by race.
For the white population, the highest mortality rates were
concentrated in a belt extending from Louisiana to New York. The
lowest mortality rates were located in the Great Plains and Rocky
Mountain states. South Dakota reported the lowest mortality rate
(3.2 per 10,000) and Maryland reported the highest rate (9.5 per
10,000).
A similar regional pattern existed for the non-white popula-
tion except that the rates and magnitude of the variation were much
higher. For example, Arizona reported a mortality rate of 7.4 per
10,000 compared to 44.5 per 10,000 reported in South Carolina. The
lack of data for non-whites in many of the Western states, however,
made further analysis for this population impossible (Rose, 1962).
Mortality rates for hypertensive heart disease showed simi-
lar patterns among the 1960 population (Morton et al., 1975). Peak
mortality rates were reported in the Southeastern states and Hawaii
while the lowest rates occurred in the Great Plains, Southwest and
Rocky Mountain regions and Alaska (Table 7). The 1959-61 mean
mortality rates for hypertension and hypertensive heart disease
also showed that the increased risk of death from hypertension in
the Southeast was greater for blacks than for whites. The peak
hypertension mortality rate for white females occurred in the
mid-Atlantic states of New Jersey, New York and Pennsylvania.
The general pattern for morbidity from hypertensive heart
disease was also consistent for deaths from cerebrovascular
27
TABLE 7.--States with Highest and Lowest Mortality Rates per
100,000 for Hypertensive Heart Disease, 1960.
State
Rate per 100,000*
11 HIGHEST:
South Carolina
Hawaii
District of Columbia
Maryland
Alabama
North Carolina
Louisiana
Delaware
Mississippi
Georgia
Virginia
United States
11 LOWEST:
Arizona
Wyoming
Idaho
Nebraska
Montana
Iowa
Colorado
New Mexico
North Dakota
South Dakota
Alaska
D
co
N mOwa-DGU'INOOO
._a
05
moommoommxsoo
SOURCE:
W. E. Morton, et al., "Distribution of Hypertension
and Renal Disease in Oregon," Public Health Reports,
Vol. 90, No. 1 (1975). p. 35.
*
All rates are age-adjusted.
28
accidents (stroke), often associated with hypertension (Borhani,
1965). The highest mortality rates for 1960 occurred in the
South Central and South Atlantic states while the lowest occurred
in the Southwest and Mountain states. For example, among white
males, age-adjusted death rates ranged from 34.3 per 100,000 in
Wyoming to 90.3 per 100,000 in South Carolina.
Borhani (1965) attempted further analysis of this geo-
graphic clustering by using the Geary contiguity ratio. This ratio
represents the degree of difference from a totally random distri-
bution. In other words, it is a measure of the degree of clustering.
A perfectly random distribution has a contiguity ratio of 1.0. The
values of the contiguity ratio for males and females in 1950 and
1960 differed from unity and that clustering was more pronounced
among males than females (Table 8). These differences were all
statistically significant at p < 0.01.
This clustering pattern observed in the Southeastern United
States has since become known as the "stroke belt" (Hames, 1974,
p. 120). When death rates for stroke in Savannah, Georgia, fOr
example, were compared to those of the United States as a whole,
rates in Savannah were 1.5 to three times higher (Table 9).
In another investigation of deaths from stroke, death
certificates of veterans from Georgia and from five selected
Western states were examined. Of the death certificates that
reported stroke as the underlying cause, 26.3 percent of the death
certificates from Georgia had a record of hypertension while only
9.1 percent of those from the five Western states contained an
29
TABLE 8.--Contiguity Ratio for Age-Adjusted Death Rates from
Cerebrovascular Diseases, by Sex for Coterminous United
States, White Population, 1949-51 and 1959-61.
Year Sex Value of Contiguity Ratio
1950 Male 0.31
Female 0.55
1960 Male 0.33
Female 0.64
SOURCE: N. Borhani, "Changes and Geographic Distribution of
Mortality from Cerebrovascular Disease," American Journal
of Public Health, Vol. 55, No. 5 (1965), p. 677.
TABLE 9.-—Death Rates per 100,000 Persons for Stroke in Savannah,
Georgia and the United States, 1959-61.
Race and Sex Savannah United States
While male 206.1 114.5
White female 130.2 89.0
Black male 545.5 266.0
Black female 886.5 270.0
SOURCE: C. G. Hames, "Natural History of Essential Hypertension
in Evans County, Georgia," Postgraduate Medicine, Vol. 56,
No. 6 (1974), p. 121.
30
entry of hypertension. Furthermore, 85 percent of the deaths in
Georgia in which stroke was named as the cause were natives of
Southern states (Acheson et al., 1973).
The Health and Nutrition Examination Survey of 1971-74
compared blood pressure levels of four main regions in the United
States--Northeast, Midwest, South and West (National Center for
Health Statistics, 1977). For persons 7-74 years old, average
age-adjusted systolic blood pressures in the South were signifi-
cantly higher than those in the Northeast (by 3.3 mm Hg) and in
the West (by 4.3 mm Hg) and were slightly higher than those in
the Midwest (by 2.3 mm Hg). Mean diastolic blood pressures,
however, were similar in all four regions.
In addition to regional patterns such as those described
above, hypertension is more prevalent among persons with certain
levels of income and education. In general, mean blood pressure
levels are inversely related to both family income and educational
levels (National Center for Health Statistics, 1977). Examina-
tions of rural residents in north central Mississippi showed that
those living at the most extreme level of poverty had the most
severe form of hypertension (Pollner and Parrish, 1976). Persons
with the least education also show 47-70 percent more hypertension
than those with the most education (Dyer et al., 1976). Standardi-
zation of age, weight and education distributions results in lower
adjusted hypertension prevalence rates in male and female blacks,
but even when these factors were controlled, hypertension rates
in blacks (approximately 33 percent) remained almost twice as high
31
as in whites (approximately 18 percent) (Hypertension Detection and
Follow-Up Program Cooperative Group, 1977).
Urban-rural differences in hypertension prevalence have also
been observed. Although most studies have shown hypertension to be
more prevalent in urban areas, findings have not been consistent.
In fact, several studies have reported higher prevalence rates in
rural areas (Tyroler, 1977; Eckenfels et al., 1977; National Center
for Health Statistics, 1977). Blacks in rural settings in Jamaica
and Mississippi have shown higher mean blood pressures and higher
prevalence rates of hypertension than their socio-economically
comparable peers in urban places (Tyroler, 1977). In Holmes County,
Mississippi, definite hypertension was recorded in 43.5 percent of
black males and 39.5 percent of black females and it is considered
an endemic chronic disease of this rural community (Eckenfels
et al., 1977). Consistent with these findings, the Health and
Nutrition Examination Survey found systolic blood pressures of
those 7-74 years old to be inversely related to population density
(National Center for Health Statistics, 1977).
As indicated previously, however, the majority of epidemio-
logic studies have reported higher rates of hypertension in urban
areas. A prevalence survey of black residents in the city of
Baltimore, for example, suggests that "hypertension is a particular
problem of metropolitan areas" (Apostolides, 1974, p. 105). Age-
and sex-adjusted prevalence rates in Baltimore ranged from 8.2 per-
cent to 48.8 percent and “distinct ecological differences" within
the target area were noticeable. The highest prevalence rates were
32
found in the most centrally located census tracts and gradually
decreased towards the periphery of the study area (Figure 3).
Selected variables were correlated with age- and sex-
adjusted rates of elevated diastolic blood pressure. The only
variable significantly correlated with hypertension was vacancy
rates of urban dwellings (r = 0.6013, p < 0.01). Correlations with
median income (r = -0.3737) and median education (r = -O.3904) were
in the expected direction but were not strongly significant (p <
0.10). Although there were no significant correlations with popu-
lation decreases among different age groups, the trend was con-
sidered to be consistent with the concept that urban decay involves
the selective out-migration of healthy young adults, leaving the
non-mobile, elderly poor behind. In this way,
the implication of these observations for health planners
is a concentration of individuals eligible for high blood
pressure management living in decayed central city loca-
tions where there is a notorious lack of community-based
primary medical care services (Apostolides, 1974, p. 111).
Studies from Africa also indicate that hypertension is more
prevalent in urban areas than rural areas. Scotch et a1. (1961)
reported that a group of South African urban Zulu adults showed a
significantly higher incidence of hypertension and significantly
higher blood pressure values than a similar group of Zulu adults
living in a rural native reserve. When mean blood pressure levels
of Zulu were compared with those of blacks and whites from Georgia,
Georgia blacks showed the highest mean blood pressure, fbllowed by
urban Zulu, Georgia whites and rural Zulu. In Ghana, hypertension
has been found to be twice as prevalent in urban areas (8.9 percent)
33
3:3, 1155 1111111 25 new”
25-34 PERCINT
35-41 renc£u1
45 PERCENT M10 OVER
*f\\
PROVIDENT
HOSPITAL
UNIVERSITY OF MARYLAND
HOSPHAL \
SOURCE: A. Apostolides et al., ”High Blood Pressure: Its Care and
Consequences in Urban Health Centers," International
Journal of Epidemiolqu, Vol. 3, No. 2 (1974), p. 110
(reprinted with permission).
Figure 3.--Age and sex adjusted prevalence rates of hypertension
among black residents in selected census tracts,
Baltimore, Maryland, 1972.
34
than rural areas (4.5 percent) (Pobee et al., 1977). Analysis of
social variables, such as church membership, family structure, and
marital status, among urban Zulu indicated that those who maintained
traditional cultural practices were more likely to be hypertensive
(Scotch, 1963). In this way, Scotch (1963) suggests that the
development of hypertension is related to an inability to adapt to
the demands of urban living.
Higher rates of hypertension observed in an urban area of
Iran compared to coastal and mountain villages support the theory
that some aspect of city life is related to hypertension (Nadim
et al., 1978). A comparison of blood pressures in three sample
populations showed that mean differences in blood pressures between
mountain villages, coastal villages and Pahlavi City were statis-
tically significant from p < 0.05 to p < 0.01 (Table 10). Hyper-
tension rates were also higher in the city (30.5 percent) than in
the coastal villages (19.8 percent) or mountain\villages (6.6 per-
cent). The average weight of city residents was significantly
higher, but even when weight was controlled for, differences between
mountain villages and the city were statistically significant from
p < 0.01 to p < 0.05 in each age-sex group. Thus, despite the fact
that these population samples contained residents of the same ethnic
origin (Guilan) living less than 100 kilometers apart, considerable
rural-urban differences in the prevalence of hypertension were found.
Nadim et al. (1978) suggest that such differences may be due to the
isolation of mountain villages from city life and/or differences in
diet and exercise in urban and rural areas.
35
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36
In summary, distinct regional patterns of hypertension exist
in the United States and in other areas of the world. The findings
presented here suggest that a number of environmental variables, in
addition to genetic factors, may contribute to the development of
hypertension. Preliminary epidemiologic studies such as those dis-
cussed above have created a wide range of possible etiologies,
implicating, among others, physical environment, lifestyle, diet,
stress and modernization as possible causes of hypertension. A
discussion of these factors follows.
IV. ETIOLOGIES OF HYPERTENSION
A causal relationship between hypertension and some factor
or factors has yet to be firmly substantiated. Results from preva-
lence studies such as those discussed in Section III have generated
numerous hypotheses concerning the probable cause or causes of
hypertension. A variety of genetic and environmental etiologies
have been proposed and there now seems to be some general agreement
that both factors may contribute to the development of hypertension.
This section includes a review of genetic and environmental vari-
ables associated with hypertension. Selected genetic studies are
presented first and are followed by selected studies of environ-
mental factors.
Genetic Etiologies
A family history of hypertension is a strong indication
that an individual will develop hypertension. The exact mechanisms
of heredity's involvement in hypertension is unclear but familial
aggregation of blood pressure in children and adults has been demon-
strated in many studies. For example, blood pressures of natural
children are more similar to those of their families than blood
pressures of adopted children are to their families (Smith, 1977).
Studies have also shown higher correlations of blood pressures
37
38
among monozygotic twins than with other relatives, implicating
genetic determinants of familial aggregation (Smith, 1977).
Ethnic differences in blood pressure values have been
attributed to physiological correlates of ethnicity such as skin
color. The high prevalence of hypertension in the American black
population compared to the American white population led to an
investigation of such a relationship. In Charleston County, South
Carolina, the reflectance of skin color among a black population was
measured in order to estimate the degree of skin pigmentation (Boyle
et al., 1967). Significant differences in the age-adjusted blood
pressures of blacks by skin color were reported. For men, age-
adjusted mean systolic blood pressure increased 3.1 mm Hg and mean'
diastolic blood pressure increased 1.3 mm Hg with each five unit
decrease in skin reflectance. In other words, higher blood pres-
sures were positively associated with darker skin color. For
females, each five unit decrease of skin reflectance showed an
increase of 1.2 mm Hg mean systolic pressure and 0.5 mm Hg mean
diastolic pressure. These differences were highly significant in
both sexes (Boyle et al., 1967). There was also a very significant
difference in mean ages between the darker one-third and the lighter
one-third of the black population. The mean age of the darker one-
third of the population was 45 years for males and 48 years for
females; the mean age of the lighter one-third was 52 years of age
for both males and females. Boyle et al. speculated that the age
differences could be the result of a higher survival rate for blacks
39
with lighter skin or a physiological decrease in skin pigmentation
with age.
The association of hypertension with skin color may be
phychosocial rather than physiological, however, as skin color is
related to opportunities for employment, education, mobility and
social status in general (Keil et al., 1977). A ten-year follow-up
study of black males in Charleston County, South Carolina found that
when social class was examined as a controlling factor, the associa-
tion of hypertension and skin color was greatly reduced (Keil et al.,
1977). Age-adjusted incidence of hypertension was 3.8 times higher
in lower than upper social class blacks and the difference in inci—
dence rates between dark-skinned and light-skinned blacks was not
statistically significant.
The relationships between skin color, blood pressure, socio-
economic level and stress were further examined among white and
black populations in Detroit (Harburg et al., 1978, I and II). Nurse
interviewers rated skin color on a four-point scale and subjects were
grouped according to their ethnic background. Samples were chosen
from designated high and low stress areas, based on measures of
economic deprivation, residential instability, family instability,
crime and density. Partial correlations of nine variables, in addi—
tion to skin color, were determined by the least squares regression
method.
Darker skin color in black males was significantly related
to diastolic pressure (r = 0.25, p < 0.01) and to systolic pressure
at a weaker level (r = 0.14, p < 0.05). This linear relationship
40
was shown to be independent of the nine control variables (age,
height, weight, smoking status, parental hypertension, educational
level, family income, season of the year, and respondent tension)
and stressor areas (Harburg et al., 1978, I). For females the
relationship was linear but not significant. With age and weight
controlled for, residence in high stress areas was related with
borderline significance to blood pressure levels in males 25-39
years of age, regardless of skin color. For males 40-59 years of
age, however, darker skin color was significantly related to blood
pressure, regardless of stress area. The authors suggest that high
blood pressure in older blacks with darker skin color may be attri-
buted to suppressed hostilities and their inability to adapt to
their social-cultural environment regardless of residential area.
Gene admixtures may also be responsible for blood pressure levels,
especially when combined with "socially induced stress" (Harburg
et al., 1978, I).
Among whites, lighter skin color was associated with higher
blood pressure but the magnitude of the association was not signif-
icant (Harburg et al., 1978, 11). European ethnic background, cate-
,gorized by a skin color cline in Europe from Northern areas to the
Mediterranean, was significantly associated with skin color. Sub—
jects of Mediterranean ethnic origins, with darker skin color, had
the lowest blood pressures, and those with Northern European back-
grounds, and lighter skin color, had the highest blood pressures,
independent of age, weight, height, smoking status, parental hyper-
tension, education, income, season, rated tension, and high and low
41
stress areas. The authors suggest that cultural differences in
response to stress may be manifested physiologically in the fbrm
of blood pressure regulation. Specific genetic differences in
physiological mechanisms among various ethnic groups may also
explain blood pressure variations. The fact that older age and
colder season were significantly related to high blood pressures
for Northern Europeans but not for Mediterraneans suggests that
thermo-regulatory mechanisms may be involved (Harburg et al., 1978,
II).
A theory recently proposed by researchers at the University
of Indiana suggests that differences in hypertension rates between
American blacks and whites may be explained by physiological differ—
ences in salt-retention capabilities (Citizens for the Treatment of
High Blood Pressure, 1979). According to this theory, black
Africans, subsisting on low-salt or salt-free diets, developed a
kidney system that could process salt slowly enough to balance the
loss of salt through perspiration and thus cope with chronic sodium
deficiency. The high-salt intake of the average American diet
results in increased blood volume and arterial pressure levels
which help the kidneys process sodium more efficiently; persons
with a reduced capacity to process sodium may therefore be more
susceptible to hypertension (Tobian, 1978). In this way, American
blacks may have inherited a physical adaptation that enabled their
African ancestors to survive in tropical climates but which is
maladaptive for blacks living on a high-salt diet in the United
States.
42
The underlying causes of ethnic differences in blood pres-
sure are open to a variety of interpretations. Eyer (1975) has
stated that although the influence of heredity on blood pressure
values has been demonstrated, only 20 percent of the variation in
phenotypes in a population can be accounted for by heredity of some
sort. This heritability estimate was reportedly derived from quan-
titative examinations of relatives of hypertensives, including
identical and fraternal twins. In addition, a review of inter-
national epidemiological studies has confirmed that "even with the
inclusion of many significant factors correlated with BP, less than
20% of the variation of casual BP in the population can be explained"
(Kesteloot and Joossens, 1978, p. 69). Hypotheses involving numerous
environmental influences on blood pressure have therefore been pro-
posed.
Environmental Etiologies
Environmental variables implicated in the development of
hypertension are diverse and include components of geophysical
environments, socio-cultural environments and personal environments.
Lifestyle
Although socio-cultural context often influences personal
lifestyles, variables associated with individual habits or practiceS'
are considered separately. The environmental factors discussed in
this category include those that can be changed by individual deci-
sions and actions.
43
A factor that shows some of the strongest and most consistent
associations with hypertension is obesity. Studies show that obese
subjects with normal blood pressures are more likely to develop hyper-
tension than normal or underweight normotensives (Smith, 1977). In
addition, hypertensive subjects are at a greater risk of becoming
overweight compared to normotensive subjects. Experimental evidence
has also demonstrated that a weight loss of 20 pounds is capable of
reducing diastolic blood pressure 4 mm Hg (Smith, 1977). In a
nationwide screening of one million people, prevalence rates of
hypertension were 50 percent to 300 percent higher in the group
classified as overweight than in the other normal and underweight
groups (Stamler et al., 1978). Furthermore, the relative frequency
of hypertension with overweight was larger with each higher degree
of blood pressure elevation.
These findings suggest that weight is an important factor in
hypertension, possibly even causative in nature. If this assumption
is correct, "a sizeable potential exists for lowering the prevalence
of hypertension in the population and decreasing its serious conse-
quences through prevention and control of overweight" (Stamler et al.,
1978, p. 1610).
Particular dietary patterns are also associated with hyper-
tension. A study of nomadic pastoralists in Kenya, whose diets con-
sisted mainly of milk, meat and blood, exhibited blood pressure
levels similar to Europeans up to the age of 40 but thereafter
showed no increase with age (Shaper, 1967). Upon entering the army,
a group of nomadic warriors changed from a carbohydrate—free diet
44
to one in which half of their total caloric intake was from carbo-
hydrates. Examinations of the warriors two to three years after
living in this "altered environment” showed a rise in blood pressure
(Shaper, 1967).
Increasing prevalence rates of hypertension among Papago
Indians in Arizona have also suggested that diet is a factor (Strotz
and Shorr, 1973). Before World War II, hypertension was not a
noticeable health problem among this population. The Papago diet
at this time was mostly meat (from hunting or cattle-raising), beans
and some desert plants. After World War II, however, a cash economy
developed on the reservation and the diet changed to a high carbo-
hydrate diet of beans, wheat flour, potatoes and corn, with liberal
use of salt and lard. Simultaneously, the amount of physical labor
decreased as hunting and cattle-raising activities decreased. Strotz
and Shorr (1973) suggest that these factors may have contributed to
the high prevalence of hypertension, some 20 percent, recently
observed among Papago Indians living in Arizona.
Salt is one dietary component which has demonstrated con-
sistent associations with hypertension. Studies of populations with
low and high salt intakes show marked differences in blood pressure
levels with age (Table 11). Although these studies are not adjusted
for weight or age, they do suggest that a relationship exists. The
relationship between salt and hypertension in laboratory animals
has been shown to be direct and unequivocal (Weinsier, 1976).
Experimental studies have established that: (l) the amount of salt
intake is directly proportional to the severity of hypertension;
45
TABLE 11.--Sa1t Intake and Blood Pressure Elevation in Different
Populations, by Age.
SBP* (mm Hg)
20-29 40-49 60-69
Population years years years Dietary Salt
Brazil 107 100 109 No salt, use lyes
(Carajas) of vegetable ash
(K salts)
New Guinea 126 126 123 0.6 g
(Murapins) (24-hour urine)
Botswana 119 116 122 2.0 9
(Kung bushmen) (24-hour urine)
Cook Islands 113 116 125 2.9-4.1 g
(Pukapukas) (24-hour urine)
United States 119 130 149 :10 g/24 hours
Portugal 126 134 155 not measured
Sweden 125 138 159 not measures
Belgium 132 143 163 4 to 20 g
(24-hour urine)
Cook Islands 124 151 165 7.0 to 8.2 g
(Rarotongas) (24-hour urine)
Norway 130 141 167 not measured
Wales 120 138 169 3.0 g
(24-hour urine)
Bahama Islands 129 154 176 15 to 30 g
(Negroes)
(24-hour urine)
SOURCE: J. V. Joossens, "Salt and Hypertension, Water Hardness
and Cardiovascular Death Rate," Triangle, Vol. 12, No. 1
(1973). p. 10.
*58P = Systolic Blood Pressure
46
(2) the younger the age at which a high salt diet is introduced
results in a greater sensitivity Undevelopment of rapid hypertension;
and (3) transient exposure (two to six weeks) to high salt intake in
early life can produce permanently elevated blood pressure.
Although a normal person requires only 0.5 9 salt or less
per day, salt consumption in the United States ranges from 3 g to
30 g, with the majority consuming 7 to 15 g (Weinsier, 1976). Much
of this intake is in the form of canned and frozen foods which many
people are not aware of. Baby foods, which are heavily salted,
expose infants to many times their nutritional requirement. Since
the taste for salt is acquired over time, it would seem prudent to
avoid such foods whenever possible. If salt is indeed a causative
agent of hypertension, it would be possible to reduce the morbidity
and mortality in a relatively simple and economical manner (Joossens,
1973).
Other variables of personal lifestyles associated with
hypertension include cigarette smoking and alcohol consumption. Data
comparing blood pressures of alcohol drinkers and non-drinkers sug-
gest that three or more alcoholic drinks per day is a risk factor
for hypertension (Klatsky et al., 1977). The mean difference of men
consuming three or more drinks per day and non-drinkers was 10.86
'24). In women the mean difference of those consuming
-5).
mm Hg (p < 10
six or more drinks per day and non-drinkers was 5.39 mm Hg (p < 10
However, blood pressures of men taking two or fewer drinks per day
were similar to those of non-drinkers. For women, two or fewer
drinks per day resulted in slightly lower pressures than non-drinkers.
47
Hypertension was much more prevalent among persons having six or
more drinks per day than among non-drinkers (Table 12). All associa-
tions of blood pressure existed independently of age, race, smoking,
coffee use, former heavy drinking, education and obesity (Klatsky
et al., 1977).
Smoking, which is a risk factor for several other diseases,
seems to have an inhibitive effect on blood pressure. Lower mean
blood pressures and body weight values were found in cigarette
smokers compared with non-smokers or former smokers (Seltzer et al.,
1974). Follow-up after a five-year period showed that those who had
quit smoking experienced sharp rises in blood pressure--even those
who lost considerable weight. 0n the other hand, diastolic blood
pressures of smokers failed to increase--even in those who gained
weight. These associations were controlled for age and body weight.
In summary, these aspects of lifestyle are related to the
development of hypertension in individuals. Of course, personal
habits are usually influenced by the larger social and cultural
context in which they exist. These broader types of environmental
influences are examined next.
Socio-Cultural Variables
It is hypothesized that hypertension's association with
socio-cultural variables operates through stress mechanisms.
Numerous studies have shown increases in blood pressure and preva-
lence rates of hypertension in populations subjected to stressful
situations, whether real or perceived.
48
TABLE 12.--Prevalence of Hypertension in Heavy Drinkers and Non-
Drinkers, by Race and Sex.
Prevalence of Hypertension
White Black
Male Female Male Female
Heavy Drinkers 11.21% 11.27% 15.14% 24.18%
(6 or more drinks)
Non-Drinkers 4.61% 6.30% 10.18% 14.71%
SOURCE: Klatsky et al., "Alcohol Consumption and Blood Pressure,"
New England Journal of Medicine, Vol. 296, No. 21 (1977),
p. 1196.
49
According to Smith and Sing (1977), data suggest that life
crises which generate stress may affect blood pressure levels of
persons genetically predisposed to hypertension. Thus, unfamiliarity,
discomfort, or any kind of change in the cultural, social or economic
milieu may precipitate stress which is manifested in a biological
manner--in the form of elevated blood pressure.
Comparative population studies of "primitive" and "modern"
societies suggest that urbanization and the development of Western
lifestyles influence blood pressure levels and the development of
hypertension. For example, death rates for diseases associated with
hypertension, particularly coronary heart disease, are generally two
to three times lower in underdeveloped countries than in developed
countries (Eyer, 1975). Cerebrovascular death rates in Canada and
Ireland are similar to those of American whites but Japan, a highly
urbanized country, has higher rates and Mexico, a less developed
country, has lower rates than the United States (Nefzger et al.,
1973).
Lovell (1967) compared the mean blood pressures of various
ethnic groups, including New Guinea Highlanders, Kalahari bushmen,
Pacific Islanders, South American Indians, Australian aborigines, and
African nomadic tribesmen. Many of the Pacific Island populations
showed lower mean blood pressures than Westerners and the rise of
blood pressure with age that occurs in Europeans was absent in these
populations. In some population samples in New Guinea, mean blood
pressure values actually decreased with age.
50
One explanation for these variations is that when popula-
tions experience some kind of environmental change, mean blood
pressure levels rise and at some critical level of acculturation
the blood pressure starts to rise with age (Seftel, 1978). In this
regard, diet is often implicated in the development of hypertension.
Serum cholesterol levels, which influence arterial pressures, are
low in most underdeveloped countries but the acceptance of Western
lifestyles is associated with an increase in serum cholesterol con-
centrations. Thus, although Eskimos are known for their low serum
cholesterol values, despite a very high-fat diet, most Eskimos in
Alaska and Canadian Eskimos living in Montreal have serum cholesterol
values at least as high as the white population (Shepard, 1974).
Increasing urbanization in Alaskan settlements is also associated
with an average 6 to 12 mm increase in skinfold thickness among
Eskimos (Shepard, 1974).
Other aspects of modernization may also be involved. The
dissolution of the nuclear family, mass unemployment, migration,
and the rapid rate of technological and organizational change are
generally considered stress-producing experiences (Eyer, 1975).
Studies of migrant populations have shown that cultural, social and
economic mobility are associated with elevation of blood pressure
(Smith and Sing, 1977). In this way, stress is attributed to prob-
lems encountered while adapting to unfamiliar environmental
situations.
A study of persons who migrated to the city of Teheran from
rural parts of Iran (Azarbaijan) showed significantly elevated
51
blood pressures (Nadim et al., 1978). The prevalence of hyperten-
sion in rural areas was much lower compared to migrants and non-
migrants living in Teheran and the difference was statistically
significant (p < 0.05). There was no significant difference in
blood pressure levels of migrants and non-migrants living in the
city. Body build was associated with hypertension but even when
ponderal index, a measure of obesity, was controlled for, differ-
ences were not due to obesity alone (Table 13).
A study of migrants living in New Zealand tested the hypoth-
esis that migrants who experience incongruity between their personal
values and interaction with a new society will experience greater
elevations in blood pressure than migrants who experience no such
incongruity (Beaglehole et al., 1977). Migrants from Tokelau, a
culturally and geographically isolated island with a subsistence
economy, had two blood pressure measurements taken and were assigned
a social interaction index derived from five main variables:
(1) ethnic affiliation of co-workers, (2) ethnic affiliation of
friends with whom leisure time was spent, (3) club and association
memberships, (4) degree of participation in Tokelauan community
functions and (5) religious affiliation. In this way, social
interaction was viewed as the extent to which the migrants reacted
with others outside the Tokelauan migrant community. Age-adjusted,
sex-specific blood pressures of Tokelauan adults showed a signifi-
cant positive association between elevated blood pressure and the
degree of social interaction.
52
TABLE 13.--Hypertension by Age, Sex, and Ponderal Index in Samples
Studied in East Azarbaijan and Teheran City.
Ponderal Index
Obese Normal/Thin All
No. % No. % No. %
Sex/Age Sample Studied Ob. Hyp. 0b. Hyp. 0b. Hyp.
Male Rural 28 7.1 85 7.0 113 7.1
40-49 Migrant A2 63 12.7 45 13.3 108 13.0
Urban non-migrants 32 21.9 18 0.0 50 14.0
Migrant Other 21 38.1 15 6.7 36 25.0
Male Rural 23 13.0 40 5.0 63 7.9
50-59 Migrant A2 48 29.2 46 13.3 94 22.3
Urban non-migrants 42 35.7 25 16.0 67 28.4
Migrant Other 27 37.0 13 15.4 40 30.0
Female Rural 57 17.5 72 15.3 129 16.2
40-49 Migrant A2 94 26.6 18 0.0 112 22.3
Urban non-migrants 116 25.9 18 5.6 134 23.1
Migrant Other 107 33.6 26 7.7 133 28.6
Female Rural 27 29.6 47 8.5 74 16.2
50-59 Migrant A2 78 47.4 11 9.1 89 42.7
Urban non-migrants 90 33.3 16 12.5 106 30.2
Migrant Other 62 48.4 18 22.2 80 42.5
All Rural 135 17.0 244 9.4 379 12.1
Migrant A2 283 29.7 120 10.9 403 24.3
Urban non-migrants 280 29.3 77 9.1 357 24 9
Migrant Other 217 38.7 ._zg 12.5 .289 32.2
TOTAL 915 29.8 513 10.1 1428 22.7
SOURCE: A. Nadim et al., "Blood Pressure and Rural-Urban
Migration in Iran," International Journal of Epidemiology,
Vol. 7, No. 2 (1978), p. 138.
53
Increased social interaction with the New Zealand society
was able to explain 1.4-2.3 percent of the total variance in blood
pressure; body mass and length of stay in New Zealand accounted for
7.1-11.0 percent of the variance (Table 14). Although increasing
levels of interaction with a new society may change lifestyles and
result in increased levels of blood pressure, a causal relationship
between hypertension and social interaction was not established.
The decision to emigrate might indicate that an individual has
problems adapting to the social-cultural environment in which he/she
lives (Smith and Sing, 1977). Therefore, those who migrate may have
a high risk for developing hypertension even before they interact
with another society.
Stress is also produced by various types of social and
economic deprivation. In many instances, the distribution of blood
pressure values among different ethnic groups is associated with
such socio-economic variables. For example, although mean blood
pressures are generally lower in underdeveloped countries, some
populations living in underdeveloped societies that evolved under
oppressive conditions (such as the Caribbean) have high average
blood pressures (Eyer, 1975). Blacks living in the United States
and in the West Indies have higher blood pressures than blacks
living in Liberia, historically a principle source of black migra-
tion to the Western hemisphere (Dawber et al., 1967). Also, blood
pressures of migrant Zulu adults living in urban areas of South
Africa under apartheid policy are higher than blood pressures of
Zulu living in rural areas (Scotch, 1963).
‘54
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55
The association of residence in stressful areas with hyper-
tension was examined among blacks and whites living in Detroit
(Harburg et al., 1973). Census tracts were assigned high and low
stressor scores based on socio-economic status indicators and
instability scores derived from variables of economic deprivation,
residential instability, family instability, crime and density.
Predominantly white and predominantly black high and low stress
areas provided the sample population (Figure 4). Measurements of
blood pressure revealed that males in the high stress/black areas
had significantly higher proportions of borderline and definite
hypertension (38 percent) than males living in low stress/black
areas (19 percent), p < 0.01. There was no significant difference
between whites living in high and low stress areas. When the
results were controlled for age, overweight, ponderal index, time
of day, hours since last meal and rated tension at time of readings,
the differences between high and low stress areas were reduced.
Mean blood pressures of black males from high and low stress areas
were still significantly different. White females from high stress
areas also showed significantly higher systolic pressures than those
from low stress areas. Furthermore, blacks in low stress areas did
not differ in levels of blood pressure from whites in low stress
areas. The results of this study are debatable, however, as signif-
icant correlates of blood pressure, such as income, education, diet
and familial hypertension, were not controlled on an individual
basis. The effects of residential stress on hypertension, there-
fore, have yet to be clearly demonstrated.
56
Low mess/block
Highland Park W "mu-Me
Homlromck
High mess/block
High 01'050/whi19
SOURCE: E. Harburg et al., "Sociological Stressor Areas and Black-
White Blood Pressure: Detroit," Journal of Chronic
Diseases, Vol. 26 (1973), p. 598 (reprinted with permission).
Figure 4.--Black and white stressor areas in Detroit.
57
Stress created in the work environment is also associated
with elevations in blood pressure. Noise is one such occupational
hazard. A study of textile mill workers in Iran exposed to an
average noise level of 96 decibels, showed that the weavers had a
significantly greater risk of developing hypertension when compared
to a group of weavers matched for similar socio-economic conditions
who were working in light industries without exposure to an intensive
noise level (Parvizpoor, 1976). Among 821 weavers, 8.5 percent had
definite hypertension and 12.4 percent had borderline hypertension.
Of 412 control subjects, 2.4 percent had hypertension and 4.6 per-
cent were borderline hypertensives. The difference was significant
at p < 0.01. Higher prevalence rates in the weavers appeared at
relatively young ages (30-39 years) and increased with length of
employment in the mill.
Similar findings were reported among 200 male industrial
workers in Sweden tested for hearing loss (Jonsson and Hansson,
1977). Average blood pressures were significantly higher in sub-
jects with noise-induced hearing losses than in subjects with normal
hearing; however, no control variables were considered in this study.
The investigators stated that, although a causal relationship between
noise and blood pressure was not proven, repeated elevations of blood
pressure due to noise stress may cause a permanent rise in blood
pressure due to structural adaptation of the heart and resistance
vessels. A fOllow-up of the preliminary findings, with more detailed
examinations, has been planned. It is hoped that control subjects
58
will be matched for variables such as age, weight, sex, race and
heriditary characteristics.
Exposure to high temperatures is another variable which
may be associated with hypertension. An investigation of the work-
ing conditions of foundry workers in Brazil showed that continued
exposure to high levels of heat was signicantly associated with
higher prevalence rates of hypertension (Kloetzel et al., 1973).
No conclusions can be drawn from this study, however, since there
was no matched group of controls and little quantitative analysis
of the data.
Although the effects of stress on physiologic changes in
blood pressure have been demonstrated in numerous ways, there is
much debate on the precise nature of hypertension's association
with stress (Marx, 1977). For those who view stress as a result
of modernization, "major social changes are necessary to prevent
modern hypertension" (Eyer, 1975, p. 550). Others view stress in
terms of the "interaction between a particular external environment
and a particular kind of person" (Marx, 1977, p. 907). This kind
of genetic-environmental viewpoint supports hypertension control
measures aimed at identification of "individuals of high and low
environmental and biological risk" (Smith and Sing, 1977, p. 789).
Environmental risk factors in the geophysical environment that
have been associated with hypertension are examined next.
59
The Geophysical Environment
The geophysical environment refers to those geologic,
hydrologic and chemical components that exist within defined areas.
Three kinds of variables from the physical surroundings have demon-
strated relationships with hypertension--altitude, water hardness
and trace metals.
High elevations of altitude seem to have a protective effect
against hypertension. A comparison of five small communities in
Peru revealed that the age-adjusted prevalence of systolic hyper-
tension in males was twelve times higher in the two communities at
sea level than in the three villages at altitudes above 13,000 feet
(Ruiz and Penaloza, 1977). The difference was significant at p <
0.001. Diastolic pressures were also higher at sea level but at a
lower level of significance (p < 0.05 to 0.001).
Further analysis showed that:
1. blood pressures of natives living at high altitudes
increased after prolonged residence at sea level
and tended to resemble the pressures of persons
living at sea level.
2. retrospective observation of 100 white males
originally from sea level residences showed that
their blood pressure values decreased after living
from 2 to 15 years at an altitude of 12,400 feet.
3. at sea level, hypertension is more frequent in
females and systolic hypertension is more common
than diastolic hypertension whereas at high
altitudes, hypertension is more frequent in men
and diastolic is the more common type of hyper-
tension.
The diet of populations living at high altitudes such as the Andes
Mountains is suggested as one possible explanation for these
6O
differences. The Andean diet is high in carbohydrates and vege-
table proteins and is noted for its high mineral content, especially
zinc and other trace elements (Ruiz and Penaloza, l977). Physio-
logical differences have also been observed in mountainous areas.
Hypoxia, which determines functional and structural vascular changes,
is a chronic condition at high altitudes and it is hypothesized that
this may improve the supply of blood oxygen to tissues (Ruiz and
Penaloza, 1977). In this way, some kind of biological-environmental
interaction may be responsible for blood pressure variations at
different altitudes.
An examination of changing hypertension rates in different
regions of Colorado has also suggested that altitude may be a factor.
Mean annual rates of hypertension and hypertensive heart disease for
1949-51 and 1959-61 decreased by one-half to one-third in all regions
of Colorado except one-~a band of counties on the high plains lying
at an altitude of 3,500-4,000 feet (Morton, 1970). There were no
known differences in the socio-economic status or the availability
of medical resources among these areas which could be attributed
to the differences in hypertension prevalence.
A survey taken among selective service registrants in
Colorado showed that rates of hypertension were highest in the
lowest altitude stratum and that there was an inverse relationship
between altitude and hypertension rates (Table 15). These rates
should be viewed with caution, however, since the number of hyper-
tensives at high altitudes was very small. The differences could
not be explained by different ethnic compositions of the regions
61
TABLE 15.-—Prevalence of Hypertension Among Colorado Selective
Service System Registrants.
Registrants Listed Hypertension
Mean Population (% with Rate/
Elevation (ft) Total Known BP) Number 1,000
8,000 - 10,152 468 (34.2) 2 4.3
7,000 - 7,999 1,939 (34.2) 7 3.6
6,000 - 6,999 4,423 (30.2) 25 5.7
5,000 - 5,999 18,025 (32.4) 135 7.5
4,000 - 4,999 7,167 (34.5) 81 11.3
3,489 - 3,999 1,142 36.5 ‘_25 .21;2
TOTAL 33,484 (32.9) 275 8.2
SOURCE: W. E. Morton, "Geographic Pattern of Hypertension in
Colorado," Archieves of Environmental Health, Vol. 20
(1970). p. 693.
62
but levels of education, income, occupation and urbanization which
differed in parts of Colorado, may account for some of the altitude
effects (Morton, 1970).
Numerous other studies have established a relationship
between water quality and hypertension morbidity and mortality.
In 1950, death rates from hypertensive heart disease in the United
States were found to be inversely proportional to water hardness
(r = -0.57, p < 0.01), based on the total calcium and magnesium
concentrations in parts per million (Perry and Perry, 1974).
Although a study of hard water towns and soft water towns in Great
Britain reported a correlation of -0.22 for water hardness and
death rates from hypertensive heart disease in 1951, the correlation
coefficient for all cardiovascular diseases was -0.54 in 1951 and
-0.65 in 1961 (Perry, 1972).
Analysis of changes in the water supply in England and
Wales between 1925 and 1955 showed that in towns where the water
supply became softer, mortality from cardiovascular disease
increased 20 percent, compared with an 8.5 percent increase in
cardiovascular deaths in towns where the water supply became harder
(Table 16). In towns where no change in water supply occurred,
cardiovascular death rates increased 11 percent (Perry, 1972).
Areas in Japan with greater acidity in river water were
associated with higher mortality rates from stroke (r = 0.63) and
higher rates of heart disease (r = 0.67) (Schroeder and Kraemer,
1974). In the United States, alpha-radioactivity was used as a
measure of water quality in two hard-water river basins and two
63
TABLE 16.--Mean Percentage Changes in Death Rate from 1951-1961 as
Function of Change in Water Hardness.*
Hardness of Drinking Water
Increased No Change Decreased
Causes of Death (5 towns) (72 towns) (6 towns)
Cardiovascular 8.5 11.2 20.2
Other -10.8 -13.0 -12.4
SOURCE: H. M. Perry, Jr., "Hypertension and the Geochemical
Environment," Annals of the New York Academy of Sciences,
Vol. 199 (1972), p. 211.
*Values are percent changes in death rates in England and
Wales over a lO-year period for males 45-64 years of age. Similar
trends are seen for women and for older men.
64
soft water river basins (Perry, 1972). Death rates from hyper-
tension and ischemic heart disease among 7.5 million people living
in 140 counties along the Ohio, Columbia, Missouri and Colorado
rivers were compared. As Table 17 shows, death rates, except those
from non-cardiovascular disease, decreased as alpha-radioactivity
increased. Comparing the Colorado and Ohio river basins, death
rates from hypertensive heart disease and ischemic heart diseases
were 41 percent and 25 percent lower, respectively, along the
Colorado River, which contains the hardest water.
The substance in hard water that appears to protect against
cardiovascular deaths has yet to be determined. Analysis of 36
components of municipal water supplies failed to disclose any single
element or quality that might influence vascular death rates
(Schroeder and Kraemer, 1974). Water considered to be partially
protective contains alkali metals (lithium, sodium, potassium and
rubidium), alkali earths (magnesium, calcium, strontium and barium)
and essential trace metals vanadium and molybdenum, along with
uranium, boron, silicon and chloride, sulfate and bicarbonate anions
(Schroeder and Kraemer, 1974). This study suggests that it may be
more beneficial to investigate the corrosiveness of soft water
(which dissolves elements such as copper, cadmium, zinc, lead and
antimony from water pipes) than water hardness as an influence of
hypertension morbidity and mortality.
One trace element that has recently aroused suspicions of
involvement in hypertension is cadmium. Experimental results have
shown that rats chronically fed small doses of cadmium will develop
65
TABLE l7.--Death Rates and River Water Radioactivity (Hardness).
Annual Death Rates
Per 100,000 Population
Alpha
Radioactivity a b c
River Basin (c/l) HHD IHD NCVD
Ohio 0.25 40 303 455
Columbia 0.40 33 303 448
Missouri 3.01 28 276 460
Colorado 6.00 23 228 440
SOURCE: H. M. Perry, Jr., "Hypertension and the Geochemical
Environment," Annals of the New York Academy of Sciences,
Vol. 199 (19721, p. 210.
aHypertensive Heart Disease
bIschemic Heart Disease
cNoncardiovascular Disease
66
hypertension (Perry and Perry, 1974). The relationship between
cadmium concentrations and hypertension in humans, however, is less
definitive (Perry and Perry, 1974; Ostergaard, 1977). Renal
cadmium concentration and prevalence of hypertension show similar
geographic distributions in some instances. For example, non-
industrialized areas of Africa are associated with low rates of
hypertension and low levels of renal cadmium while industrialized
areas of Japan show high prevalence rates of hypertension and high
renal cadmium concentrations (Perry and Perry, 1974). On the other
hand, Ostergaard (1977) found higher renal cadmium concentrations
in normotensives than in hypertensive subjects. He suggests that
other studies have not always controlled for confounding variables
such as age and smoking which may influence results. The quality
of drinking water should also be considered in cadmium studies,
since hypertension could be influenced by enhanced cadmium uptake
in soft water supplies.
In these ways, then, factors of the geophysical environment
must be considered as potential contributors to the development of
hypertension. Demonstration of causal relationships has been diffi-
cult because of the interrelated nature of the variables discussed
in this section. For example, higher rates of hypertension found
in persons living in urban areas may be the result of high-salt
diets, sedentary lifestyles, or an inability to cope with the
stresses of modern urban life. Although each variable in itself may
not have a strong effect on the development of hypertension, the
67
synthesis of genetic, dietary and environmental factors may pro-
duce an effect capable of raising blood pressure levels. Inter-
disciplinary research on hypertension, therefore, seems warranted.
V. CONCLUSIONS
Numerous strategies for the prevention and control of hyper-
tension exist. The most common strategy currently in use consists
of hypertension screening programs aimed at identification of hyper-
tensive individuals. Aggressive follow-up programs are also being
tried in order to improve patient compliance once treatment is
initiated. Programs such as those developed by Erfurt and Foote
(l976) involve contacting hypertensive individuals and their physi-
cians by phone, mail or visit in order to chart the patient's
progress in blood pressure reduction over time.
Some believe that hypertension can only be conquered by a
major upheaval in the social structure which will alleviate the
stress created by the modern, urbanized world in which we live.
Behavioral modification, aimed at changing personal habits and
lifestyles, is promoted by others as a way to prevent hypertension.
Still another strategy involves environmental modification. This
entails making living areas more pleasant (and less stressful) by
reducing levels of poverty, crime and crowding and by providing
safeguards against harmful chemical agents in food and water
supplies.
The complex interaction of physiological, psychological
and environmental variables complicates any analysis of hypertension.
68
69
Nevertheless, the endemic nature of hypertension in contemporary
society makes its analysis necessary. Although hypertensive
patients can be told what their chances are of dying from stroke,
congestive heart failure or myocardial infarction, physicians are
unable to explain in certain terms why certain individuals develop
hypertension and others do not. In this paper, various aspects of
hypertension are studied with the hope that some cause of the dis-
ease may be illuminated and future cases may be prevented.
The current state of the literature on hypertension is
quite inadequate. The lack of a standard definition in epidemio-
logical studies is a major problem. Data comparison among hyper-
tension studies, particularly on an international scale, is
extremely difficult due to differences in terminology, methods of
blood pressure measurement and diagnostic criteria. It is hoped
that researchers in the future will make an effort to standardize
these aspects of their investigations.
Future studies should also control for the many confounding
variables that exist in investigations of hypertension. Many of
the earlier studies that fail to control for age, weight, race,
socio-economic status and family history should be viewed with
caution as their results may be biased.
This paper has demonstrated the many ways in which a
geographic perspective can be useful in the study of hypertension.
Since the distribution of hypertension has already been quite well-
defined on an international level and on a national level in the
United States, spatial analyses of hypertension at smaller scales
70
would provide useful results for health planners. In a time of
scarce medical resources, identification of high-risk populations
could be greatly aided by geographers. A wholistic approach to
the study of human-environmental interactions may unravel some of
the etiologic mysteries surrounding hypertension. Integrative
models which synthesize hypertension findings from the behavioral
and social sciences can be used to facilitate interdisciplinary
research of the disease (Stahl et al., 1975). Once high-risk
areas and etiologic factors have been adequately identified,
strategies to improve health care delivery programs and compliance
to treatment regimens can be formulated in a rational and efficient
manner.
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71
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