5

Domestic Water Consumption

IN THE LATE NINETEENTH AND early twentieth centuries, industrial wastes contaminated many rivers and streams (Tarr, 1985). These waterways often supplied drinking water for urban populations, so gross contamination of many sources of drinking water became widespread. This eventually led to laws initially passed by state legislatures and later Congress (such as the Federal Water Pollution Control Act of 1948), that required intervention by the U.S. Public Health Service and subsequently by the U.S. Environmental Protection Agency (EPA) to ensure the safety of the nation's water supply. In general, water supplies are now safe bacteriologically, and usually free of gross contamination or obvious chemical pollution. However, drinking water can still be a source of harm to human health, particularly in areas where there are chemical dumps and where aquifers have been contaminated (Ram and Schwartz, 1987). Runoff from fields after nitrate and pesticide use for agricultural purposes also can contaminate drinking water, as can aromatic and aliphatic compounds that leak from underground gasoline storage tanks. Moreover, exposure is not limited to ingestion, but occurs through outgassing or volatilization in other uses of domestic water, as discussed in Chapter 3.

Marsh and Caplan (1987) point out that the existence of abandoned hazardous-waste sites largely stems from the strong sanctions that



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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 5 Domestic Water Consumption IN THE LATE NINETEENTH AND early twentieth centuries, industrial wastes contaminated many rivers and streams (Tarr, 1985). These waterways often supplied drinking water for urban populations, so gross contamination of many sources of drinking water became widespread. This eventually led to laws initially passed by state legislatures and later Congress (such as the Federal Water Pollution Control Act of 1948), that required intervention by the U.S. Public Health Service and subsequently by the U.S. Environmental Protection Agency (EPA) to ensure the safety of the nation's water supply. In general, water supplies are now safe bacteriologically, and usually free of gross contamination or obvious chemical pollution. However, drinking water can still be a source of harm to human health, particularly in areas where there are chemical dumps and where aquifers have been contaminated (Ram and Schwartz, 1987). Runoff from fields after nitrate and pesticide use for agricultural purposes also can contaminate drinking water, as can aromatic and aliphatic compounds that leak from underground gasoline storage tanks. Moreover, exposure is not limited to ingestion, but occurs through outgassing or volatilization in other uses of domestic water, as discussed in Chapter 3. Marsh and Caplan (1987) point out that the existence of abandoned hazardous-waste sites largely stems from the strong sanctions that

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 were enacted between 1952 and 1977 to control air and water pollution. Because of the Federal Water Pollution Control Act (1952), the Clean Air Act (1963), and the Clean Water Act (1977) surface water and ambient air were no longer considered acceptable outlets for the disposal of wastes. Consequently, industries and municipalities turned increasingly to the land for waste disposal. Contamination of groundwater and aquifers occurred where the waste dumps were poorly constructed or managed, or where wastes were disposed of improperly. This chapter reviews evidence about some compounds commonly found at hazardous-waste sites that have been shown to cause adverse effects in humans exposed to these materials from consumption of domestic water. First it discusses studies of cancer risk posed by trihalomethanes (THMs) as an indicator of the sort of effects that can be anticipated from contamination of drinking water by such compounds. Then it assesses the relatively scanty literature on adverse effects that can be linked to the contamination of drinking water from toxic dump sites, including congenital anomalies, cancer, and other chronic diseases. As the importance of lead in drinking water is currently the subject of extensive analysis and regulatory attention, this chapter does not review this topic. Epidemiologic evidence on the risk to health from contaminated water from hazardous-waste sites or other sources of contamination, such as pesticide runoff, has largely been derived from ecologic or descriptive studies, and therefore is seldom conclusive as to cause. The ecologic studies involving broad-scale comparisons of available data are unable to control for important confounding variables, such as smoking or other relevant exposures. Recent literature on the contamination of drinking water include a number of ecologic and case-control studies that evaluate the cancer risk of by-products of chlorination on human health (Jolley et al., 1990). Some chlorination by-products, particularly halogenated hydrocarbons or THMs, occur in greater quantities in drinking water if large amounts of organic matter are present (Burke et al., 1983). Two of these, chloroform and carbon tetrachloride, have been commonly found in the chemical mixtures at some toxic dump sites. Chloroform tends to be readily identified because it is more easily measured. Whether or not they, or other chemicals also present, increase the risk of cancer for exposed residents is unclear (Crump and Guess, 1982). Several case-control studies based on examinations of death certificates have found an increased risk for cancers of the colon, rectum, bladder, breast, brain, and lung in persons who have consumed chlorinated drinking water (Velema, 1987). However the results have not always been consistent and causality cannot reliably be inferred.

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 THMs AND OTHER WATER QUALITY VARIABLES Several hypothesis-generating ecologic studies have been based on cancer incidence data provided by the Iowa cancer registry for 1969 to 1978. The data were taken from municipalities that had populations of at least 1000 and public water supplied by a single source that had remained stable for a minimum of 14 years. Rates for cancers of the lung and rectum among males and females were higher for municipalities using chlorinated surface water compared to those with groundwater sources (Bean et al., 1982a). Subsequently Isacson et al. (1985) studied cancer incidence data for the years 1969-1981 from the Iowa cancer registry for towns with a public water supply from a single stable ground source and the levels of volatile organic compounds and metals found in the finished drinking water of these towns in 1979. This study lessened one of the problems common to ecologic investigations, namely, misclassification of exposure. Early studies of cancer and drinking water associated consumption of water and rates of cancer by comparing the proportion of county or parish residents supplied by surface water sources with overall cancer mortality rates for the total area. In these early studies, the lack of data on individual consumption patterns hampered interpretation of the results. Isacson et al. (1985) used cancer incidence by municipality, along with a survey on drinking water habits, in order to reduce misclassification of exposure. Associations between 1,2dichloroethane and the incidence of cancers of the colon and rectum and between nickel and cancers of the bladder and lung were most clearly seen in males. Although nickel, 1,2-dichloroethane and trichloroethane are known to be carcinogens, the levels of these materials found in this study were well below the nondetectable-response level estimated from the experimental literature on these compounds. The researchers concluded that one plausible explanation of their result is that the mere presence of these industrial effluents in groundwater indicates that exposures have occurred from anthropogenic sources. Thus, the measured substances do not necessarily account for the increased rate of cancer, but rather indicate the presence of other materials. In an earlier report from the Iowa cancer registry, Bean et al. (1982b) considered the contribution of waterborne radioactivity to differences in cancer incidence. They found that incidence rates of cancers of the lung and bladder among males and of cancers of the breast and lung among females were higher in towns where the water supply contained more than 5.0 picocuries per liter of radium-226. A gradient of increasing incidence associated with rising radioactivity levels for

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 three periods also was seen for lung cancer among males. These findings were not explained by smoking patterns or water treatment methods. A nationwide ecologic study examined cancer mortality from 1950 to 1969 and organic contamination of drinking water, using the data on carbon chloroform extract (CCE) and carbon alcohol extract (CAE), available through monitoring for varying periods between 1957 and 1972 at 129 stations throughout the U.S. (Clark et al., 1986). The researchers found strong associations of CCE and CAE with total cancer mortality and mortality from grouped gastrointestinal and urinary tract cancers (Clark et al., 1986). However, scattergrams reveal that much of the associations result from a small number of outliers where mortality rates or pollution levels were unusually high. Although the regression coefficients are statistically significant, they might not represent causal associations, given these outliers. A similar study in Canada evaluated mortality rates in 66 cities between 1973 and 1979 and selected drinking-water characteristics with adjustment for socioeconomic factors (Wigle et al., 1986). Water source, chlorine dose, and the concentrations of asbestos, chloroform, total THMs except chloroform, and total THMs were not significantly correlated with any of the disease categories examined, which comprised all causes of death, all cancers, various cancer sites, and coronary heart disease mortality. When dose of total organic carbon was substituted for chlorine dose in a multivariate analysis, there was a significant association with large intestine cancer among males. One possible reason for the findings could be that in the total data age-standardized mortality rates for overall mortality (males), all cancers combined (males), and stomach cancer (both sexes) had a strong correlation with lower average level of education. The analysis was adjusted for low education in the examination for possible associations with the water variables, as lower education and socioeconomic status are strongly associated with increased cancer risk. In Houston, Texas, an opportunity arose to assess the effect of changing from a lightly chlorinated drinking water source to one that was heavily chlorinated after the construction in 1954 of Lake Houston, which became the source of drinking water for a sizable portion of the city's population (Cech et al., 1987). The concentrations of THMs ranged from below detectable limits to more than 200 micrograms per liter (twice the level allowed by U.S. drinking water standards) in treated lake water. These exposures were described by census tract, and the trends in mortality from urinary tract cancer from 1940 through 1974 were compared with the trends for three other causes of death —respiratory cancer, bronchitis and emphysema, and homicide. Al-

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 though an increase in urinary tract mortality in white females was noted for those exposed to treated lake water by 1970-1974, no increase was noted in white males or in the nonwhite population. It was concluded that a detrimental effect of the switch to chlorinated surface water had not been demonstrated. The largest individual- and population-based case-control study of cancer with evaluations of exposure to by-products of chlorination in drinking water was performed in 1978 in 10 areas of the U.S. (Cantor et al., 1987). These by-products include THMs generated by chlorination, as well as chloroform. A group of 2982 persons with bladder cancer and 5782 control subjects were interviewed in the original study and individual year-by-year profiles of water source and treatment were developed by linking lifetime residential information with historical water utility data from an ancillary survey of 2805 cases and 5258 controls. Risk of bladder cancer increased with intake of beverages made with tap water. The odds ratio for the highest versus the lowest quintile of tap water consumption was 1.43 (95 percent CI 1.23-1.67). The increased risk was largely restricted to persons with at least a 40-year exposure to chlorinated surface water and was not found among long-term users of nonchlorinated ground-water. There was no evidence of confounding by other causes of bladder cancer, including smoking. In particular, women and non-smokers of both sexes, who consumed chlorinated surface water at rates above the median for 60 or more years, had rates of bladder cancer that were more than three times the rates of those who had not consumed treated surface water. In an analysis of the Iowa portion of a national bladder case-control study on bladder cancer, the effect of misclassification on estimates of years of exposure to chlorinated drinking water was investigated (Lynch et al., 1989). It was shown that only with detailed information of the type used by Cantor et al. (1987) would it be possible to derive a significant association of duration of consumption of chlorinated surface water with bladder cancer, while taking account of potential confounders. A case-control study of colon cancer (366 cases, 785 cancer controls, and 654 population controls) in Wisconsin did not find an increased risk associated with an index of THM exposure (Young et al., 1987). Only a small risk of marginal significance was found for exposure to chlorinated water for 0-10 years before diagnosis. The authors noted that the majority of water supplies in Wisconsin contain low levels of THMs and that it is unlikely that a small risk, if present, could have been detected. A case-control study that used interviews with informants of 614

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 individuals who had died of bladder cancer and 1074 individuals who had died of other causes found that the rate of death from bladder cancer among individuals who resided only in communities supplied with chlorine-disinfected drinking water relative to those who resided only in communities supplied with chloramine-disinfected drinking water was 1.6 (95 percent CI 1.2-2.1) (Zierler et al., 1988a). Chloramination of drinking water is a process that results in lower amounts of THMs than result from chlorine disinfection. The effect of contamination of drinking water with arsenic has been investigated in an area of Taiwan with endemic blackfoot disease, a peripheral vascular disease related to continuous exposure to arsenic in artesian well water. Elevated mortality from cancers of the bladder, kidney, skin, lung, liver, and colon was found in association with such exposure (Chen et al., 1985). A subsequent study related arsenic levels in well water in 1964-1966 to age-adjusted mortality rates for 1973-1986 (Wu et al., 1989). A significant dose-response relationship was found for cancers of the bladder, kidney, skin, and lung in both sexes and for cancers of the prostate and liver in males. Another study examined ecologic correlations between arsenic content in well water and mortality from various neoplasms in 314 precincts and townships of Taiwan as a whole (Chen and Wang, 1990). A significant association with the arsenic level in well water was observed for cancers of the liver, nasal cavity, lung, skin, bladder, and kidney in males and females and for prostate cancer in males. Although arsenic is regarded as a cause of blackfoot disease, there has been speculation that other factors in artesian well water, such as humic acid, are involved in what is probably a multistage, multifactorial disease that results from chronic progressive arteriosclerosis (Chen and Wang, 1990). The relationship between chlorinated water and serum cholesterol (SC) levels has also been investigated (Zeighami et al., 1990). Significantly higher SC levels were found in females from chlorinated communities. TOXIC DUMP SITE EXPOSURES CANCER AS THE END POINT Love Canal, New York, is perhaps the best known of toxic dump sites. Human exposure there to chemicals was through contaminated water, although not strictly through drinking water. Rather, contaminated water seeped into the basements of homes and subsequently exposure was largely through inhalation; contaminated soil also played

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 a role. The possibility that Love Canal residents could develop cancer was raised because benzene and γ-hexachlorobenzene, both carcinogens, were found in the wastes at the site. Janerich et al. (1981) published a report that compared cancer incidence for census tracts in the Love Canal area with cancer incidence throughout the state except for New York City. No significant elevation of rates was found among Love Canal residents for any cancer, including those selected a priori for special attention—liver cancer, lymphoma, and leukemia— though the numbers of cancers in the Love Canal census tracts were very small. Thus the standardized incidence ratio for liver cancer was 2.0 in males and 2.9 in females, but this was based on only two observed cases for each sex and was not significant. A further difficulty relates to the fact that numerous other hazardous-waste sites exist in the state. Comparing Love Canal to this area may have produced some dilution of effect, as both populations have incurred exposures from hazardous waste sites. New Jersey also has a large number of toxic dump sites. Najem et al. (1983, 1985) conducted ecologic studies that related cancer mortality at the county and municipal level to environmental variables, including the location of chemical toxic-waste-disposal sites. At the county level they found associations with most gastrointestinal cancers (Najem et al., 1983). In addition, an analysis of age-adjusted female reproductive organ and breast cancer mortality showed significant positive associations between breast cancer mortality and proximity to toxic disposal sites among whites in 21 New Jersey counties (Najem and Greer, 1985). At the municipal level, statistically significant positive associations were found for 8 of 12 cancers considered, with stomach, colon, and rectal cancer clusters being particularly noted (Najem et al., 1985). The clusters of excess cancer mortality were confined for the most part to the highly urban and industrial north-eastern part of the state, and air pollution and lack of information on other possible confounders complicated interpretation of the results. In a reinvestigation of health effects potentially arising from two contiguous wells supplying part of the drinking water for Woburn, Massachusetts, Lagakos et al. (1986) found positive associations between access to domestic water from two contaminated wells and the incidence of childhood leukemia. The wells were contaminated with trichloroethylene, tetrachloroethylene, and chloroform. Large pits of buried animal hides, solvents, and other chemical wastes were discovered as was an abandoned lagoon that was heavily contaminated with lead, arsenic, and other metals. However, Woburn has been an industrial site for more than 130 years, and at the time of this study, EPA had not yet determined the precise sources of the contamina-

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 tion. The wells were closed in 1979, and the leukemia cases studied were diagnosed between 1964—the year the wells began pumping—and 1983. It had previously been determined that 12 cases diagnosed between 1969 and 1979 were in excess—only 5.3 were expected—and these 12 were included in the 20 evaluated by Lagakos et al. (1986). The authors confirm that the 20 cases were significantly higher than the 9.1 expected from national rates. They used two different methods for estimating exposure. A cumulative estimate of exposure from the two wells from birth until age t; and a binary indicator of whether there had been any exposure by age t. Each of these exposure metrics was associated with the incidence of childhood leukemia. The cumulative metric statistically explained about four cases, while the “ever-never” metric explained about six cases. This leaves an excess of five or six cases for which no explanation may be inferred from the reconstructions of well water exposure. Four of the recent leukemia cases occurred in West Woburn, where exposures to contaminated water did not occur, confounding the determination of causality. Analyses of time trends since the wells were closed suggests that the rate of leukemia has fallen significantly, strengthening the inference of a causal association with past exposures. However, this finding does not rule out the possibility that other unrecognized factors may also have been involved in explaining the leukemia cluster, or the possibility that the cluster was a random event. In a commentary, MacMahon (1986) noted that a more complex exposure metric (which might have been expected to more precisely measure exposure than an “ever-never” comparison) in fact led to a lesser degree of association with leukemia. Perhaps the major difficulty with this study is that it was unable to overcome problems in exposure assessment already discussed in Chapter 3. Nevertheless, because the exploration of the incidence of leukemia followed the identification of the contamination of the wells, this study avoids the pitfalls that can arise when many of the cases of leukemia are first identified as part of an original “index” set. Therefore, the same cases did not contribute to the derivation but only to the testing of the hypothesis. The New Jersey Department of Health (Fagliano et al., 1987, 1990) conducted an ecologic study to determine whether there was a relationship between incidence of leukemia and contamination of public drinking-water supplies with volatile organic compounds (trichloroethylene, tetrachloroethylene, 1,1,1-trichloroethane, and related chlorinated solvents) known to have been derived from improper disposal. These compounds are used in metal degreasing, dry cleaning, and in some household products. An excess of leukemia among females, but not among males, was found in towns in the highest of

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 three exposure categories in the study years 1979-1984. The standardized incidence ratio for females was 1.53 (95 percent CI 1.02-2.21); for males it was 1.00. The authors were unable to explain this gender difference, but it would seem to weaken the argument that the leukemia was caused by exposure to the toxins. However, for males other exposures, such as those in the workplace, could be more important determinants of leukemia than environmental exposures. A nationwide ecologic study was conducted by Griffith et al. (1989) using the National Priorities Listing (NPL) of hazardous-waste sites developed by EPA and cancer mortality data for 13 major cancer sites by county for 1970-1979. The NPL identified 593 waste sites in 339 U.S. counties in 49 states with analytical evidence of contamination in groundwater that provided a sole source of potable water supply. Significant associations between excess deaths and all counties with hazardous-waste sites were shown for cancers of the lung, bladder, esophagus, stomach, large intestine, and rectum for white males and for cancers of the lung, breast, bladder, stomach, large intestine, and rectum for white females, when compared with the counties that did not have hazardous-waste sites. No adjustment was possible for the effect of industrialization or other confounders at the individual level, such as factors related to lifestyle, including cigarette smoking. Many of the associations were strong and of a similar order in both sexes; there were odds ratios of 5.9 in males and 4.3 in females for cancer of the large intestine. The odds ratio for lung cancer was higher in females (5.2) than it was in males (2.0). These associations could have resulted from factors not considered in the analysis or from other problems with the method of the studies. For example, Greenland (1990) has shown that ecologic estimates can be more sensitive to misspecification and misclassification than are individual-level estimates, primarily because ecologic estimates are based on assumptions and inferences rather than on direct measurements. Wong et al. (1989) conducted ecologic and case-control analyses to evaluate the possibility that contamination of drinking water in Fresno County, California, with dibromochloropropane (DBCP) increased mortality from gastric cancer and leukemia. The study was conducted because a previous ecologic analysis by the California Department of Health Services for 1970 to 1979 found such an association. Mortality data for 1960-1983 were included in the ecologic analyses, and deaths for the period 1975 to mid-1984 were used in the case-control studies; nongastric cancer or leukemia deaths served as controls. The only positive association was an increased risk of leukemia for farm workers. No relationship was found for gastric cancer or leukemia with DBCP contamination of drinking water.

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 Evaluation of the cancer maps by county produced by the National Cancer Institute for 1950 through 1979 reveals areas of high mortality from bladder cancer in several northwestern Illinois counties. This led to an incidence study of bladder cancer cases diagnosed between 1978 and 1985 in those counties (Mallin, 1990). A cluster in males and females was identified by zip code within Winnebago County, a county that had been known in advance of the study to be at risk of groundwater contamination because of the dumping of solid and liquid waste in water supply zones over the last 100 years. It was found that one of four public water wells had been closed due to contamination; two wells were within a half-mile of a landfill site that had ceased to operate in 1970. Tests of these two wells revealed traces of trichloroethylene, tetrachloroethylene, and other solvents. Concern by residents led to the evaluation of another cancer cluster in North Carolina (Osborne et al., 1990). Comparison of cancer deaths for the rural community of Bynum with those expected for the state as a whole showed no increase in the proportion of deaths due to cancer between 1947 and 1964 (range, 9-14 percent), but thereafter there was a steady increase to 58 percent in 1980-1985. Standardized proportionate mortality ratios for cancer for 1957 to 1985 were 2.4 to 2.6 times greater than expected. The number of cancer deaths was small, and the cancers were diverse. The hypothesized cause was the consumption of raw river water by a majority of residents from 1947 to 1976. The river was contaminated with pollutants, including known carcinogens, from industrial and agricultural contamination upstream of the town. Cancer clusters like those investigated by Mallin (1990) and Osborne et al. (1990) often are reported under circumstances that are difficult to evaluate, and it seems likely that few with negative outcomes are reported in the literature. One exception is a study by Day et al. (1989). The investigation was prompted by public concern in Randolph, Massachusetts, that led to a survey of households, with data on cancer supplemented by records from the town, the state, and the Massachusetts cancer registry. Although a cancer cluster was confirmed, overall cancer incidence and mortality in the neighborhood were not elevated. No unusual feature of the cancer data was identified and no environmental hazard was suspected. From 1980 through 1982, 183 patients with esophageal cancer, or 17 percent of all such cases referred to the King Faisal Specialist Research Center, came from the Gassim region of Saudi Arabia, compared with 5 percent of the total cancer patient referrals from this region (Amer et al., 1990). This observation prompted a case-control study of cases diagnosed between 1983 and 1987. The regional dis-

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 parity in referrals persisted, and the only differences noted with referrals from other regions were for sources of drinking water. Traces of petroleum oil were found in five of six water samples from the Gassim region during 1983, compared with 3 of 49 from other areas. Mutagenicity tests on 12 water samples from Gassim showed significant activity in two-thirds of the samples, with up to a 26-fold increase in mutagenic activity in the TA98 bacterial system. The authors also note that aromatic hydrocarbons can occur at higher levels in groundwater than in surface water, due to the lack of evaporation. They point to corroborating evidence on the importance of petroleum and petrochemical exposures. Gottlieb and Carr (1981) report that workers in these industries have more than three times the average rate of esophageal cancer. The authors suggest that contamination of drinking water combined with malnutrition could promote esophageal cancer in the Gassim region. Although this is a reasonable inference from the data presented, it is unclear whether other differences between the regions can explain the differences seen. There are marked variations in esophageal cancer incidence in many areas, some of which could be attributable to differences in nutrition or use of opium. Few data were collected in the study on nutrition, and no data were reported on opium use. ADVERSE PREGNANCY OUTCOMES Following the identification of a cluster of central nervous system defects in the Mount Gambier area of South Australia, a case-control study was performed of 218 pairs from the period 1951-1979 (Dorsch et al, 1984). Compared with women who drank only rainwater, women who consumed principally groundwater had an increase in the risk of bearing a malformed child (RR=2.8, 95 percent CI 1.6-4.4). The malformations in excess of expected rates were of the musculoskeletal central nervous systems. An even stronger association was found after reanalysis for estimated water nitrate concentration (a fourfold increase in risk for those consuming >15 parts per million nitrate). It was recognized that other, as-yet-undetected chemicals could have been responsible for the excess. These might include brominated phenols, which occasionally have been detected in one of the groundwater sources, believed to have resulted from aerial contamination from nearby timber preservation plants. In the investigation of health effects associated with the two wells that supplied part of the drinking water for Woburn, Massachusetts, Lagakos et al. (1986) found positive associations between access to water from the contaminated wells and perinatal deaths, two of five

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 followed discovery of a leak of toxic chemicals in November 1981. The point source was an underground waste solvent storage tank at a semiconductor plant, 0.7 kilometers from a well that supplied drinking water to nearby industrial and residential areas (Swan et al., 1989). The well was removed from service in December 1981 after contamination with solvents (predominantly 1,1,1-trichloroethane or methyl chloroform) was discovered. Because of the concern of residents, the California Department of Health Services conducted two studies. In one, there was an increased prevalence of major cardiac anomalies in children born to persons who lived in the service area of the water company that operated the contaminated well (Swan et al., 1989). A relative risk of 2.2 (95 percent CI 1.2-4.0) was determined for the contaminated area in comparison with the remainder of the county. No excess was observed for the period between September 1982 and December 1983. However, on the assumption that the greatest degree of chemical contamination of drinking water occurred in the three-month period before the leak was discovered, it was expected that the excess cases would be found in children born between May and August 1982. Cases were not found in excess of the expected rate. Therefore, it seemed that the chemical contamination of the drinking water could not explain the excess of cardiac anomalies in children. This conclusion was reinforced by a follow-up telephone interview of 145 mothers of children born with severe cardiac anomalies and 176 mothers of children without such anomalies (Shaw et al., 1990). However, longer-term analyses were not conducted. Although there was a positive association between a mother's consumption of tap water during the first trimester of pregnancy and cardiac anomalies in her infant for the year 1981 that was not present for 1982 or 1983, this appeared unrelated to the source of water and to the incident of contamination. Chlorination by-products should be considered further, given recent studies of TCE and cardiac anomalies discussed below. Consumption of bottled water appeared protective, however. The data could not be used to distinguish between a potential causal agent in the water and differential reporting of exposure by study subjects. In the second study, a cluster of adverse pregnancy outcomes, including spontaneous abortions, low birth weight, and congenital malformations, was identified (Deane et al., 1989). An odds ratio of 2.3 for spontaneous abortion was found in comparison to a census tract free of contaminated water, while the odds ratio for congenital malformations was 3.1. In a subsequent study, Wrensch et al. (1990a) also investigated adverse pregnancy outcomes during 1980-1985 in two communities where solvents had leaked from the underground

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 storage tank to contaminate local drinking water. Two demographically similar unexposed communities also were studied. The period 1980-1981 was considered as that of exposure; 1982-1985 was the post-contamination period. The study did not produce internally consistent results. Thus, the odds ratio (OR) for the original study area of those exposed versus those unexposed for 1980-1981 was 3.5. This may have been due to a low rate of spontaneous abortions in the unexposed community for 1982-1985. This rate for 1982-1985 was substantially below the rate in the same community and that in the exposed community for the same period (the OR for 1982-1985 was 1.0). The rate for spontaneous abortions in 1980-1981 in the exposed community was only marginally higher than that in the same community for 1982-1985. Similarly, the OR for 1980-1981 in the new study area for exposed versus unexposed persons was 0.3, due to a low rate of spontaneous abortions in the new exposed study area. Further, exposure estimates based on hydrogeologic modeling and contaminant distribution within the exposed areas (Wrensch et al., 1990b) also indicate that the leak was not likely to have caused the observed excesses of adverse pregnancy outcomes in the originally studied area. The adverse pregnancy outcomes occurred in areas with lower exposure levels, as opposed to those with higher exposure levels; causes remain unknown. An association has been reported between congenital heart disease and contamination of groundwater in the Tucson valley of Arizona (Goldberg et al., 1990). It had been noted that approximately one-third of patients with congenital heart disease lived in a small area of the Tucson valley in 1973. In 1981, groundwater for a nearly identical area was found to be contaminated with trichloroethylene and to a lesser extent with dichloroethylene and chromium. It was believed that contamination began in the 1950s, and the affected wells were closed after the contamination was discovered. Interviews with parents of 707 children with congenital heart disease, who between 1969 and 1987 had conceived the children in and resided in the Tucson valley for the first trimester of pregnancy, revealed that 35 percent had work or residential contact with the contaminated water. Two random telephone surveys showed that 10.5 percent of the Tucson valley population had such contact. The OR for children with congenital heart disease born to parents where there was active water contamination was 3 compared to those without contact with contaminated water; the ratio decreased to near unity for those who arrived in the contaminated water area after the wells closed. A recent report from the Centers for Disease Control Birth Defects Monitoring Program indicates that cardiac defects made up almost half

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 the malformations that showed increasing trends from 1979 to 1987 (Edmonds and James, 1990). Recorded time trends for such anomalies are likely to include artifacts, such as improved case finding and other improvements in diagnosis, but merit further study. Although causality cannot be assumed from a single study, a study that used a rat model identified a variety of cardiac defects caused by the administration of trichloroethylene and dichloroethylene in solutions delivered through a catheter into the gravid uterus from an intraperitoneal osmotic pump (Dawson et al., 1990). There was a dose-response relationship: 9 percent and 12.5 percent of congenital cardiac anomalies were found in the lower-dose trichloroethylene and dichloroethylene groups; 14 percent and 21 percent, respectively, were found in the higher-dose groups compared with 3 percent in the control group. Experimental studies have also found that TCE applied through a catheter directly into the gravid uterus during the period of heart development induces cardiac anomalies in both chicks (Loeber et al., 1988) and rats (Dawson et al., 1990). Dichloroacetic acid (DCA) and trichloroacetic acid (TCA) are both by-products of chlorine disinfection of water containing natural organic material; TCA is a metabolite of TCE. DCA or TCA exposure of pregnant Long-Evans rats by oral intubation produced dose-related cardiac malformations in fetuses (Smith et al., 1989a,b). Taken together the preceding evidence strengthens the empirical basis for concluding that TCE induces cardiac anomalies in humans. The grounds for this inference include evidence that the relationship is biologically plausible, in that exposure to TCE or its metabolites experimentally induces cardiac teratogenesis in exposed animals (Loeber et al., 1988; Dawson et al., 1990). Moreover, these same effects have been significantly detected in exposed humans, with some evidence of a dose-response relationship in the animal studies. In addition, markers of exposure to TCE have been detected in humans and animals, and the findings are statistically significant. Thus, a chain of evidence links TCE to cardiac anomalies, although additional studies need to be conducted to confirm the association. In addition, extensive studies in animals demonstrate a range of other effects of TCE from reproductive impairment to effects on DNA (ATSDR, 1989), for which corroborating human data do not exist. One cross-sectional study of health problems compared rates of morbidity and mortality from 1980-1985 for a number of chronic diseases, including heart disease, anemia, skin cancer, hypertension, stroke, and chronic kidney disease, in residents of three towns surrounding an abandoned Superfund site in Galena, Kansas, with those of residents in two control towns (Neuberger et al., 1990). Environmental

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 exposures to lead and cadmium and other mine wastes occurred chiefly through domestic water use. Some surface soils may also have provided airborne exposure. Significant elevations in rates of a number of causes of death and disease were evident in persons over age 44. Among residents of the three towns who had lived there at least five years, there was either a statistically significant or borderline excess in women for chronic kidney disease (aged 65), heart disease (aged 45 and older), and anemia (aged 45 and above). This sex difference may reflect the fact that factors such as smoking, work, and drinking are more important determinants of some of these diseases in men than women. A significant excess of mortality also occurred from ischemic heart disease in males and females (aged 65 and older). The authors conclude that environmental agents in Galena City may have contributed to the causation of several chronic diseases in residents. OTHER HEALTH END POINTS An environmental health survey of residents who had consumed drinking water contaminated with leachate from a waste dump where a pesticide plant had deposited large amounts of liquid and solid waste between 1964 and 1972 was conducted in Hardeman County, Tennessee (Clark et al., 1982). Twelve chlorinated organic compounds were found in wells that served individuals living near the dump site. Carbon tetrachloride was the most abundant, and residents had complained of a number of symptoms, including eye and skin irritation; upper respiratory infection; and gastrointestinal symptoms including nausea, diarrhea, and abdominal cramping. The survey used a health questionnaire, a clinical examination, and biochemical screening for liver and kidney dysfunction. Results of the physical examination of 118 individuals found six of 48 individuals in the exposed group had slight hepatomegaly (enlargement of the liver), compared to one of 24 in an intermediate exposed group and none in the 46-member group of unexposed control subjects. The difference between the groups was significant (p=.034) with the Pearson chi-square test. Elevated concentrations of alkaline phosphatase and serum glutamic oxaloacetic transaminase, measures of liver function, were found more often in the exposed group than in the controls. The concentrations fell significantly in follow-up testing two months after use of the contaminated water had ceased. The authors conclude that the clinical and biochemical observations were consistent with transitory liver injury. In a subsequent independent study, Rhamy (1982, cited by Harris et al., 1984) collected health histories and conducted physical examinations on 112 persons who then lived or had formerly

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 lived within three miles of the site. Analyses were restricted to 102 persons who claimed to be exposed. A large number of symptoms was reported, as were liver, eye, and neurological abnormalities on examination. The Rhamy study is almost impossible to interpret because there was no control group, questions on symptoms were asked repeatedly during examinations, and the study was conducted after the contamination had been widely publicized. Thus, recall bias may well explain much of the reported symptomatology. However, after a comprehensive evaluation of this same exposed population, Meyer (1983) reported evidence of hepatomegaly and elevated liver function tests (alkaline phosphatase and serum glutamic oxaloacetic transaminase (SGOT) were elevated at levels of 0.016 and 0.010, respectively, when compared to the control population; albumin and total bilirubin levels were significantly lower) that he attributed to ingestion of organic chemicals, including hepatotoxins. The second larger and more comprehensive study, performed three months after the wells had been closed, showed no difference between the control, intermediate, and exposed groups. Rothenberg (1981) reported on a cross-sectional health survey of residents near a Hyde Park, New York, landfill. The landfill was inactive, but exposure through groundwater to diverse chemicals, including chlorinated hydrocarbons, was suspected. Nine positive associations were found among the 180 variables assessed. With multiple comparisons, such results may chiefly be due to chance variations. It was noted above that the exposures that caused concern in the Love Canal area were not derived from drinking water per se, which came from an uncontaminated municipal source, but from contaminated groundwater from the site that seeped into the basements of homes and led to exposure through sump pumps, soil, and air inside the homes. To evaluate general health effects from such exposures Paigen et al. (1985) conducted a general health survey with inter-viewers inquiring about physician-diagnosed complaints of the parents of 523 Love Canal and 440 control children. An excess of seizures, learning problems, hyperactivity, eye irritation, skin rashes, abdominal pain, and incontinence was found in Love Canal children. It was not possible to eliminate the effects of respondent bias, recall bias, or stress in this study, although the authors believe that the true differences had been under- rather than overestimated. The same group reported on factors related to growth in 493 Love Canal and 428 control children (Paigen et al., 1987), using technicians (who were unaware of the children's place of residence) to conduct the measurements. Of the Love Canal children, the 172 born there who had spent at least 75 percent of their lives in the Love Canal area were significantly shorter for age percentile than were the control children. Mean

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 weight for age percentile also was less in the Love Canal group. These differences could not be accounted for by various potential confounders. Some of the chemicals that contaminate drinking water, such as trichloroethylene (TCE), are known to have neurotoxic effects, although specific neuropsychological testing of potentially exposed subjects has rarely been performed. Feldman et al. (1988) administered a questionnaire and performed clinical testing, nerve-conduction studies, and neuropsychological testing on 28 members of 8 families who had alleged chronic exposure to industrial chemicals as a result of contamination of two public drinking-water wells in Woburn, Massachusetts. Electrophysiological measurement of the blink reflex was used to quantify damage to two cranial nerves known to be affected by TCE exposure. Of the 28 potentially exposed subjects, 4 were not tested because they were too young. The results for three of the subjects were not used because of potential confounders (diabetes, working with TCE, and treatment for leukemia). The results from the remaining 21 were compared with those from 27 laboratory controls. There was a highly significant difference in the conduction latency means of the blink reflex, or the speed with which nerves responded, between the test subjects and the controls, suggesting a subclinical alteration of cranial nerve function due to exposure to TCE. Substantial environmental contamination with chemicals in drinking water has occurred in a number of places in Eastern Europe and in developing countries. One study of pesticide contamination was done in a village in Nicaragua, where children from a community in the path of rainwater runoff from a large crop-dusting airport were tested for cholinesterase levels in comparison with children from an unexposed community (McConnell et al., 1990). Six of 17 children from the exposed community had low cholinesterase levels, the mean level for the 17 being 0.5 international units/milliliter/minute lower (95 percent CI 0.24-0.76) than that for 43 children from the unexposed community. A sample of water from a well in the exposed community showed contamination with toxaphene and chlordimeform at levels above the U.S. Food and Drug Administration's Recommended Acceptable Daily Intake. However, the children also were exposed because they played barefoot in grossly contaminated rainwater runoff from the airport, and the authors believe this was the more important source of exposure. CONCLUSIONS We have commented elsewhere in this report that complete accounts of investigations of cancer and other risks in relation to hu-

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 man exposure to hazardous-waste sites are not generally available because of legal restrictions. Hence, the available literature on the epidemiology of drinking-water contamination and adverse health outcomes is scanty and not conclusive. Nevertheless, several factors lead us to conclude that drinking-water contamination with a number of chemicals is injurious to human health, although the magnitude of the risk cannot be determined. Perhaps the most persuasive evidence now derives from studies of drinking-water contamination with trihalomethanes linked to increased risk of bladder cancer (Cantor et al., 1987). Bladder cancer also has been associated in a large ecologic study with exposure to contaminated drinking water from hazardous-waste sites (Griffith et al., 1989). Bladder cancer is well recognized as chemically induced, and the fact that individual studies have not found an increased incidence of bladder cancer in persons exposed to toxic-waste sites could result from the long latency period generally anticipated for this cancer, and the fact that multiple causes are likely to be involved. Continued surveillance of exposed populations for this sentinel cancer are well justified. Osborne et al. (1990) found a cancer cluster for all cancers with an exceptionally high rate; moreover, the period of the excess corresponded to the estimated time of peak exposure to contaminated domestic water, taking into account the normal latency for cancer. Where increased risk might be anticipated after solvent contamination of drinking water, leukemia and lymphoma are of obvious concern. Unfortunately, the rarity of these diseases and the greater likelihood that a rare cancer will come to notice if clusters occur have resulted in a dearth of studies with sufficient power to detect an increase in risk. Neutra (1990) advocates restricting studies of clusters to those where very high risks are anticipated. However, the number of heavily exposed individuals that might be expected to show an increase in risk of fivefold or more is generally so small that with a cancer as rare as leukemia or lymphoma such risks would be difficult to detect. Meta-analysis might overcome the limitations resulting from the small numbers. This will be discussed in the next report of the committee. A limited number of reports in the peer-reviewed scientific literature have linked spontaneous abortion, low birth weight, and birth defects to drinking-water contamination. The studies in Santa Clara County have been inconclusive as to the cause of the cluster observed. Indeed, it seems likely that the study population was too small to prevent chance variation in frequency of events (as appears to have occurred) from obfuscating the issue. In Love Canal, low birth weight was clearly linked to exposures from the hazardous wastes,

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 although the extent of the time during which it continued is unclear. Such outcomes should continue to be monitored because there is far less difficulty with the latency period for reproductive effects than for cancer. Concerning other health effects, there is evidence that neurologic, hepatic, and immunologic function can be damaged by exposure to drinking water contaminated with toxic chemicals. The long-term consequences of the abnormalities detected, however, are largely unknown and must be the subject of further research, on which the committee will comment in more detail in its next report. REFERENCES Amer, M.H., A. El-Yazigi, M.A. Hannan, and M.E. Mohamed. 1990. Water contamination and esophageal cancer at Gassim region, Saudi Arabia. Gastroenterology 98: 1141-1147 ATSDR (U.S. Public Health Service, Agency for Toxic Substances and Disease Registry). 1989. Toxicological Profile for Trichloroethylene. ATSDR/TP-88/24. Atlanta: Agency for Toxic Substances and Disease Registry. Bean, J.A., P. Isacson, W.J. Hausler, and J. Kohler. 1982a. Drinking water and cancer incidence in Iowa. I. Trends and incidence by source of drinking water and size of municipality Am. J. Epidemiol. 116: 912-923 Bean, J.A., P. Isacson, R.M.A. Hahne, and J. Kohler. 1982b. Drinking water and cancer incidence in Iowa. II. Radioactivity in drinking water Am. J. Epidemiol. 116: 924-932 Burke, T.A., J. Amsel, and K.P. Cantor. 1983. Trihalomethane variation in public drinking water supplies. Pp. 1343-1351 in Water Chlorination: Environmental Impact and Health Effects, Vol. 4. Book 2: Environment, Health, and Risk, R.L. Jolley et al., eds. Ann Arbor, Mich.: Ann Arbor Science. Cantor, K.P., R. Hoover, P. Hartge, T.J. Mason, D.T. Silverman, R. Altman, D.F. Austin, M.A. Child, C.R. Key, L.D. Marrett, M.H. Myers, A.S. Narayana, L.I. Levin, J.W. Sullivan, G.M. Swanson, D.B. Thomas, and D.W. West. 1987. Bladder cancer, drinking water source, and tap water consumption: A case-control study. J. Natl. Cancer Instit. 79: 1269-1279 Cech, I., A.H. Holguin, A.S. Littel, J.P. Henry, and J. O'Connell. 1987. Health significance of chlorination byproducts in drinking water: The Houston experience. Int. J. Epidemiol. 16: 198-207 Chen, C.-J. 1990. Blackfoot disease [letter]. Lancet 336(8712): 442 Chen, C.-J., and C.-.J Wang. 1990. Ecological correlation between arsenic level in well water and age-adjusted mortality from malignant neoplasms Cancer Res. 50: 5470-5474 Chen, C.-J., Y.-C. Chuang, T.-M. Lin, and H.-Y. Wu. 1985. Malignant neoplasms among residents of a blackfoot disease-endemic area in Taiwan: High-arsenic artesian well water and cancers Cancer Res. 45: 5895-5899 Clark, C.S., C.R. Meyer, P.S. Gartside, V.A. Majeti, B. Specker, W.F. Balisteri, and V.J. Elia. 1982. An environmental health survey of drinking water contamination by leachate from a pesticide waste dump in Hardeman County, Tennessee Arch. Environ. Health 37: 9-18

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 Clark, R.M., J.A. Goodrich, and R.A. Deininger. 1986. Drinking water and cancer mortality. Sci. Total Environ. 53: 153-172 Crump, K.S., and H.A. Guess. 1982. Drinking water and cancer: Review of recent epidemiological findings and assessments of risk Ann. Rev. Public Health 3: 339-357 Dawson, B.V., P.D. Johnson, S.J. Goldberg, and J.B. Ulreich. 1990. Cardiac teratogenesis of trichloroethylene and dichloroethylene in a mammalian model J. Am. Coll. Cardiol. 16: 1304-1309 Day, R., J.H. Ware, D. Wartenberg, and M. Zelen. 1989. An investigation of a reported cancer cluster in Randolph, Massachusetts J. Clin. Epidemiol. 42: 137-150 Deane, M., S.H. Swan, J.A. Harris, D.M. Epstein, and R.R. Neutra. 1989. Adverse pregnancy outcomes in relation to water contamination, Santa Clara County, California, 1980-1981 Am. J. Epidemiol. 129: 894-904 Dorsch, M.M., R.K.R. Scragg, A.J. McMichael, P.A. Baghurst, and K.F. Dyer. 1984. Congenital malformations and maternal drinking water supply in rural South Australia: A case-control study Am. J. Epidemiol. 119: 473-486 Edmonds, L.D., and L.M. James. 1990. Temporal trends in the prevalence of congenital malformations at birth based on the Birth Defects Monitoring Program, United States, 1979-1987 Morbid. Mortal. Week. Rep. 39(SS-4): 19-23 Fagliano, J., M. Berry, F. Bove, and T. Burke. 1987. Drinking Water Contamination and the Incidence of Leukemia: An Ecologic Study New Jersey Department of Health, Division of Occupational and Environmental Health. Fagliano, J., M. Berry, F. Bove, and T. Burke. 1990. Drinking water contamination and the incidence of leukemia: An ecologic study Am. J. Public Health 80: 1209-1212 Feldman, R.G., J. Chirico-Post, and S.P. Proctor. 1988. Blink reflex latency after exposure to trichloroethylene in well water Arch. Environ. Health 43: 143-148 Goldberg, S.J., M.D. Lebowitz, E.J. Graver, and S. Hicks. 1990. An association of human congenital cardiac malformations and drinking water contaminants J. Am. Coll. Cardiol. 16: 155-164 Goldman, L.R., B. Paigen, M.M. Magnant, and J.H. Highland. 1985. Low birth weight, prematurity, and birth defects in children living near the hazardous waste site, Love Canal Haz. Waste Haz. Materials 2: 209-223 Gottlieb, M.S., and J.K. Carr. 1981. Mortality studies on lung, pancreas, esophageal and other cancers in Louisiana Pp. 195-204 in R. Peto and M. Schneiderman, eds. Banbury Report 9, Quantification of Occupational Cancer, Cold Spring Harbor Laboratory. Greenland, S. 1990. Divergent Biases in Ecologic and Individual-Level Studies. Invited paper for the Second Annual Meeting of the International Society for Environmental Epidemiology, August 12-15, 1990 University of California, Berkeley. Griffith, J., R.C. Duncan, W.B. Riggan, and A.C. Pellom. 1989. Cancer mortality in U.S. counties with hazardous waste sites and ground water pollution. Arch. Environ. Health 44: 69-74 Harris, R.H., J.H. Highland, J.V. Rodricks, and S.S. Papadopulos. 1984. Adverse effects at a Tennessee hazardous waste disposal site Hazardous Waste 1: 183-204 Isacson, P., J.A. Bean, R. Splinter, D.B. Olson, and J. Kohler. 1985. Drinking water and cancer incidence in Iowa. III. Association of cancer with indices of contamination Am. J. Epidemiol. 121: 856-869 Janerich, D.T., W.S. Burnett, G. Feck, M. Hoff, P. Nasca, A.P. Polednak, P. Greenwald, and N. Vianna. 1981. Cancer incidence in the Love Canal area. Science 212: 1404-1407 Jolley, R.L., L.W. Condie, J.D. Johnson, S. Katz, R.A. Minear, J.S. Mattice, and V.A. Jacobs, eds. 1990. Water Chlorination:Chemistry, Environmental Impact and Health Effects, Vol. 6. Chelsea, Mich.: Lewis.

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 Lagakos, S.W., B.J. Wessen, and M. Zelen. 1986. An analysis of contaminated well water and health effects in Woburn, Massachusetts J. Am. Stat. Assoc. 81: 583-596 Loeber, C.P., M.J.C. Hendrix, S. Diez de Pinos, and S.J. Goldberg. 1988. Trichloroethylene: A cardiac teratogen in developing chick embryos Pediatr. Res. 24: 740-744 Lynch, C.F., R.F. Woolson, T. O'Gorman, and K.P. Cantor. 1989. Chlorinated drinking water and bladder cancer: Effect of misclassification on risk estimates Arch. Environ. Health 44: 252-259 MacMahon, B. 1986. Comment. J. Am. Stat. Assoc. 81: 597-599 Mallin, K. 1990. Investigation of a bladder cancer cluster in northwestern Illinois Am. J. Epidemiol. 132: S96-S106 Marsh, G.M., and R.J. Caplan. 1987. Evaluating health effects of exposure at hazardous waste sites: A review of the state-of-the-art, with recommendations for future research Pp. 3-80 in Health Effects from Hazardous Waste Sites, J.B. Andelman and D.W. Underhill, eds. Chelsea, Mich.: Lewis. McConnell, R., F. Pacheco, K. Wahlberg, W. Klein, O. Malespin, R. Magnotti, M. Akeblom, and D. Murray. 1990. Health effects of environmental pesticide contamination in a third world setting: Cholinesterase depression in children In preparation. Meyer, C.R. 1983. Liver dysfunction in residents exposed to leachate from a toxic waste dump Environ. Health Perspect. 48: 9-13 Najem, G.R., and T.W. Greer. 1985. Female reproductive organs and breast cancer mortality in New Jersey counties and the relationship with certain environmental variables Prev. Med. 14: 620-635 Najem, G.R., D.B. Louria, M.A. Lavenhar, and M. Feuerman. 1985. Clusters of cancer mortality in New Jersey municipalities: With special reference to chemical toxic waste disposal sites and per capita income Int. J. Epidemiol. 14: 528-537 Najem, G.R., I.S. Thind, M.A. Lavenhar, and D.B. Louria. 1983. Gastrointestinal cancer mortality in New Jersey counties, and the relationship with environmental variables Int. J. Epidemiol. 12: 276-289 Neuberger, J.S., M. Mulhall, M.C. Pomatto, J. Sheverbush, and R.S. Hassanein. 1990. Health problems in Galena, Kansas (USA): A heavy metal mining Superfund site. Sci. Total Environ. 94: 261-272 Neutra, R.R. 1990. Counterpoint from a cluster buster. Am. J. Epidemiol. 132: 1-8 NRC (National Research Council). 1986. Data on humans: Clinical and epidemiological studies Pp. 226-249 in Drinking Water and Health, Vol. 6. Washington, D.C.: National Academy Press. Osborne, J.S., III, C.M. Shy, and B.H. Kaplan. 1990. Epidemiologic analysis of a reported cancer cluster in a small rural population Am. J. Epidemiol. 132(Suppl. 1): S87-S95 Paigen, B., and L.R. Goldman. 1987. Lessons from Love Canal, New York, U.S.A.: The role of the public and the use of birth weights, growth, and indigenous wildlife to evaluate health risk Pp. 177-192 in Health Effects from Hazardous Waste Sites, J. B. Andelman and D.W. Underhill, eds. Chelsea, Mich.: Lewis. Paigen, B., L.R. Goldman, J.H. Highland, M.M. Magnant, and A.T. Steegman. 1985. Prevalence of health problems in children living near Love Canal. Haz. Wastes Haz. Materials 2: 23-43 Paigen, B., L.R. Goldman, M.M. Magnant, J.H. Highland, and A.T. Steegman. 1987. Growth of children living near the hazardous waste site Love Canal, New York, USA Hum. Biol. 59: 489-508 Ram, B.J., and H.E. Schwartz. 1987. Bedford, Massachusetts case study. Pp. 341-367 in Planning for Groundwater Protection, G.W. Page, ed. Orlando, Fla.: Academic Press.

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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 Rhamy, R. 1982. Testimony in the United States District Court for the Western District of Tennessee, Eastern Division, Woodrow Sterling et al. vs. Velsicol Chemical Corporation, Transcript of Evidence, September 29 pp. 2976-3092 Rothenberg, R. 1981. Morbidity study at a chemical dump - New York. Morbid. Mortal. Weekly Rep. 30: 293-294 Shaw, G.M., S.H. Swan, J.A. Harris, and L.H. Malcoe. 1990. Maternal water consumption during pregnancy and congenital cardiac anomalies Epidemiology 1: 206-211 Smith, M.K., J.L. Randall, E.J. Read, J.A. Stober, and R.G. York. 1989a. Developmental effects of dichloroacetic acid in Long-Evans rats Teratrology 39: 482 Smith, M.K., J.L. Randall, E.J. Read, and J.A. Stober. 1989b. Teratogenic activity of trichloroacetic acid in the rat. Teratology 40: 445-451 Swan, S.H., G. Shaw, J.A. Harris, and R.R. Neutra. 1989. Congenital cardiac anomalies in relation to water contamination, Santa Clara County, California, 1981-1983 Am. J. Epidemiol. 129: 885-893 Tarr, J.A. 1985. Industrial wastes and public health: Some historical notes, Part I, 1876-1932 Am. J. Public Health 75: 1059-1067 Velema, J.P. 1987. Contaminated drinking water as a potential cause of cancer in humans Envir. Carcino. Revs. (J. Environ. Sci. Health) C5: 1-28 Vianna, N.J., and A.K. Polan. 1984. Incidence of low birth weight among Love Canal residents. Science 226: 1217-1219 Wigle, D.T., Y. Mao, R. Semenciw, M.H. Smith, and P. Toft. 1986. Contaminants in drinking water and cancer risks in Canadian cities Can. J. Public Health 77: 335-342 Wong, O., M.D. Whorton, N. Gordon, and R.W. Morgan. 1988. An epidemiologic investigation of the relationship between DBCP contamination in drinking water and birth rates in Fresno County, California Am. J. Public Health 78: 43-46 Wong, O., R.W. Morgan, M.D. Whorton, N. Gordon, and L. Kheifets. 1989. Ecological analyses and case-control studies of gastric cancer and leukemia in relation to DBCP in drinking water in Fresno County, California Br. J. Ind. Med. 46: 521-528 Wrensch, M., S. Swan, J. Lipscomb, D. Epstein, L. Fenster, K. Claxton, P.J. Murphy, D. Shusterman, and R. Neutra. 1990a. Pregnancy outcomes in women potentially exposed to solvent-contaminated drinking water in San Jose, California Am. J. Epidemiol. 131: 283-300 Wrensch, M., S. Swan, P.J. Murphy, J. Lipscomb, K. Claxton, D. Epstein, and R. Neutra. 1990b. Hydrogeologic assessment of exposure to solvent-contaminated drinking water: Pregnancy outcomes in relation to exposure Arch. Environ. Health 45: 210-216 Wu, M.-M., T.-L. Kuo, Y.-H. Hwang, and C.-J. Chen. 1989. Dose-response relation between arsenic concentration in well water and mortality from cancers and vascular diseases Am. J. Epidemiol. 130: 1123-32 Young, T.B., D.A. Wolf, and M.S. Kanarek. 1987. Case-control study of colon cancer and drinking water trihalomethanes in Wisconsin Int. J. Epidemiol. 16: 190-197 Zeighami, E.A., A.P. Watson, and G.F. Craun. 1990. Chlorination, water hardness, and serum chlolesterol in forty-six Wisconsin communities. Int. J. Epidemiol. 19: 49-58 Zierler, S., L. Feingold, R.A. Danley, and G. Craun. 1988a. Bladder cancer in Massachusetts related to chlorinated and chloraminated drinking water: A case-control study Arch. Environ. Health 43: 195-200 Zierler, S., M. Theodore, A. Cohen, and K.J. Rothman. 1988b. Chemical quality of maternal drinking water and congenital heart disease Int. J. Epidemiol. 17: 589-594