The study cohort consisted of the remaining 2, WAER participants. Table 2 shows the exclusions and follow-up status for the WAER. Fifty-nine individuals in the study cohort were lost to follow-up prior to , moved out of state, and 1, remained in NYS. Table 3 summarizes the gender, age, and race distribution of the cohort along with data on smoking and alcohol use among cohort members 18 years and older at registration.
Race was not included on the questionnaire at the start of enrollment, resulting in a high number of missing observations for that variable.
The person who completed the questionnaire will be referred to as the primary respondent. Unknown values for smoking and alcohol use most often occurred for individuals who were not primary respondents. Unknown responses were recorded more than five times more frequently for individuals for whom information was provided by a family member or friend, compared to primary respondents. Among those for whom relationship to the respondent was known, information was provided by the participant himself or herself for Exclusions based on age, interview date, and missing values reduced the Woodstock population to 1, and 1, for the smoking and alcohol use comparisons, respectively.
Although the stratified estimates are based on small numbers for both the WAER and BRFSS populations and are therefore fairly unstable, the proportion of ever smokers and chronic drinkers was not consistently higher or lower among men and women in the Woodstock cohort compared to the BRFSS estimate.
Routine use of tap water for drinking and cooking was reported for A clothes dryer vented indoors was reported for 6. Small numbers prohibited comparison of cancer incidence by water use patterns. Table 5 presents observed numbers of cancers and SIRs for the unlagged analysis based on residency on the water supply between and among NYS residents.
The SIRs for total, gastrointestinal, and respiratory cancer groupings are all approximately 1. For the gastrointestinal subsites, the SIR for pancreatic cancer was marginally statistically significant at 2. The SIR for esophageal cancer was also elevated among men. However, the increase was not statistically significant and was based on a small number of cases.
With one exception, all respiratory cancers were cancers of the lung and bronchus.
Therefore respiratory cancers are not listed by subsite. Duration of residence on the Woodstock water supply is examined in Table 6. No discernable patterns are observed in the incidence of gastrointestinal cancers across the three categories of length of residency.
Confidence intervals for all duration categories overlapped and none excluded unity. The results of the lagged analyses are shown in Table 7. Increasing lag periods resulted in small decreases in the SIRs for gastrointestinal cancer among both men and women and small increases in the SIRs for respiratory cancer among women. The confidence intervals for the different lag periods overlapped and none excluded unity with the exception of a reduced risk of gastrointestinal cancer among women associated with a minimum of 10 years following first exposure.
The numbers of observations were too small to analyze individual gastrointestinal sites by latency.
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Although the number of individual gastrointestinal subsite cases was too small to permit formal analysis of latency and duration, duration and latency were examined for pancreatic cases to see if the length and timing of residence on the water supply were consistent with an influence of asbestos exposure on cancer risk.
The analyses reported above were repeated using as the date of first exposure. The results for total, gastrointestinal, and respiratory cancer incidence Table 8 are generally similar to those assuming exposure started in Table 5. Duration and latency analyses were also performed using the exposure start date. Again, the results were similar to those presented in Tables 6 and 7 which assumed exposure started in data not shown.
Analysis of cancer incidence for the whole cohort including residents who moved out of state , based on exposure from through , is summarized in Table 9. The incidence of gastrointestinal cancer, respiratory cancer, and all cancers combined was very similar to that observed for the NYS residents cohort Table 5. This prospective cohort study, with a retrospective component for the years , did not demonstrate an increased incidence of total gastrointestinal cancer, total respiratory cancer, or all cancers combined among individuals living on a water supply contaminated with asbestos.
When individual gastrointestinal cancers were examined, only pancreatic cancer was significantly elevated and the excess occurred primarily among males.
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In previous epidemiologic studies, an association has been observed between asbestos fibers in drinking water and incidence of stomach cancer and other gastrointestinal or respiratory cancers Meigs et al. Our study does not confirm the increased risk of stomach cancer noted in some prior studies. The observation of an excess stomach cancer risk in these other studies was limited to men, suggesting that occupation or lifestyle characteristics that differ by gender may play a role in the findings.
Sigurdson noted that stomach cancer mortality had been elevated in the Duluth population prior to the start of asbestos exposure, possibly due to ethnic dietary practices. In the Duluth population, stomach cancer mortality was also elevated among females but the difference was not statistically significant.
Norwegian lighthouse keepers exposed to asbestos-contaminated drinking water also experienced higher than expected rates of stomach cancer. Andersen et al. Although we observed a statistically significant excess of pancreatic cancer among males, the incidence of other individual gastrointestinal cancer sites, respiratory cancer, and all cancers combined, was not elevated and most SIRs were less than 1. Of the studies summarized in Table 1 , a significant association between asbestos exposure and pancreatic cancer was observed in studies by Meigs et al.
Meigs et al.
The regression coefficient for the estimated concentration of asbestos fibers in the water supply was statistically significant for pancreatic cancer among males for the study period only. Since little AC pipe was reported to have been in place in Connecticut water supplies prior to , a stronger association would instead have been expected for the interval if pancreatic cancer was causally related to asbestos exposure Meigs et al.
In the study by Conforti et al. The authors noted that the fit of the regression model was poor and suggested that the "regression data must be viewed with caution. Also a nonsignificant excess of pancreatic cancers among females and a nonsignificant deficit of pancreatic cancers among males were observed in the case-control study by Polissar et al. Although a positive association between exposure to asbestos in drinking water and pancreatic cancer was noted in an early investigation of some of the other study populations cited in Table 1 Masson et al.
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Several explanations other than a causal relation might account for the observed excess of pancreatic cancer among males in our study. Cigarette smoking is the risk factor most consistently associated with pancreatic cancer. In our study, a history of cigarette smoking was available for eight of nine pancreatic cancer cases. Seven of the eight cases were current or former smokers.
Secondly, the observation of an increase in pancreatic cancer primarily among men, but not women, suggests the influence of occupational or lifestyle risk factors. If environmental exposure to asbestos via drinking water was responsible, elevations in pancreatic cancer among both males and females might be expected. Also, due to the anatomic location of the pancreas and the usually poor prognosis at the time of diagnosis, the proportion of pancreatic cancers confirmed histologically is less than that for any other major cancer Anderson et al.
Problems with ascertainment and misclassification are therefore a concern in epidemiologic studies of pancreatic cancer. Lastly, a chance positive finding is possible, particularly when examining 14 sex-specific estimates. Duration of residence on the water supply was used as a surrogate for cumulative exposure to asbestos in the current study in an effort to assess dose-response.
Cancer incidence did not significantly increase with longer duration of residence. Uncertainty about timing of first exposure as well as small numbers of observations by category of duration limited our ability to more accurately and precisely examine the influence of duration of residence on the water supply. Since the latency period for asbestos-related cancers can be years or more Mossman and Gee, , cancers observed in the early years following exposure to asbestos in drinking water might not be attributable to this exposure.
A lagged analysis was conducted, in which individuals were not considered at risk and were not counted in the follow-up for an interval following first exposure. When a causal relationship exists and an appropriate lag period is used, a higher cancer incidence rate would be expected in lagged analyses since the estimated rates would not be diluted by observation time for individuals not yet at risk of exposure-related cancer.
After allowing for latency, significantly higher cancer rates were not observed in the current study for gastrointestinal cancers, respiratory cancers, or all cancer sites combined. Uncertainty about timing of first exposure restricts our interpretation of lagged analyses. The longest interval between first exposure and the end of follow-up in was 39 years based on exposure starting in but would be only 23 years if exposure started in In addition, the small number of WAER participants with long latency limited statistical power of estimates stratified by latency.
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Although the number of individual gastrointestinal subsite cases was too small to permit formal analysis of duration and latency, pancreatic cases were examined in more detail to see if duration and latency were consistent with exposure to asbestos in the water supply. It is unlikely that cancers diagnosed within ten years of first exposure would be related to asbestos exposure. An important limitation of this study is the lack of historical exposure data needed to establish when leaching of asbestos into the water supply first produced measurable exposure.
The AC pipes were installed in the mid- to lates, but asbestos contamination was first detected in A year-old water sample that was tested in contained higher-than-normal levels of asbestos. This indicates that leaching had begun by The use of as the starting time of exposure produced similar results to the analysis based on a start date.
Other than the one water sample believed to have been collected in , we have no evidence regarding the extent of the asbestos contamination in the Woodstock water supply prior to , nor can we estimate changes in exposure over time or by location on the water supply. The water sampling that was performed in November occurred after the water mains were flushed an attempt to remedy the water pressure problem. Deterioration of the pipe was probably aggravated by the forceful flow of water, both from turning the water on after it was turned off for repairs and from flushing the water mains.
The asbestos levels measured may not have represented usual concentrations. Gradual leaching of asbestos may have resulted in generally low concentrations of asbestos. Due to limited information on the actual levels of exposure, this study's findings regarding risk associated with asbestos exposure cannot be generalized to other exposure experiences.
The exposures experienced by the WAER cohort do not appear to have led to a detectable increased risk of cancer. We could not directly control for potential confounding due to risk factors such as smoking, alcohol use, and socioeconomic status in our SIR estimates. Education and income information were not available through the registry so census data were used to assess socioeconomic status. Based on U. Stomach and lung cancer are associated with low socioeconomic status and colorectal cancer is associated with high socioeconomic status Nomura, , Blot and Fraumeni, , Schottenfeld and Winawer, The greater proportion of residents with advanced education, indicative of higher socioeconomic status, could explain the somewhat lower than expected incidence of respiratory cancer among males in the study cohort.
We did not have information on other risk factors for stomach and colon cancers such as diet, physical activity, and body mass Nomura, ; Tomeo et al.
Selection bias in cohort studies most often results from low and differential follow-up of the study population. This is unlikely in the current study, since only 2. Selection bias due to differential participation at the beginning of the study is less of a concern when participant recruitment precedes disease diagnosis, as was the case for most registrants. It nevertheless is possible that individuals in the WAER differed from all eligible residents who lived on the Woodstock water supply. If registrants were generally more "health conscious" than non-participants, our estimates may be biased, possibly explaining the somewhat low incidence of gastrointestinal and respiratory cancers compared to NYS excluding NYC.
The study power for the cancer categories of interest was adequate to detect a modest increase in cancer risk. However, the study power for certain gastrointestinal subsites was relatively low. For example, power to identify an SMR of 2. Strengths of this study are that individual information was obtained from personal interviews of the participants or members of their household. The follow-up rate was high, with 59 persons lost to follow-up from 2, persons in the study cohort 2.