Cancer incidence and high environmental arsenic concentrations in rural populations: Results of an ecological study

A number of ecological studies have suggested associations between arsenic in drinking water and increased rates of some cancers. To investigate associations in areas with high environmental arsenic concentrations, geographical areas with surface soil inorganic arsenic concentrations of >100 mg/kg and/ or drinking water arsenic concentrations >0.01 mg/l were selected and the relationship with cancer incidence explored. Standardised incidence rates (SIRs) for cancer were generated for 22 areas between 1982 and 1991 using Victorian Cancer Registry data and Victorian cancer rates as a baseline. SIRs were also generated for combined areas according to environmental exposure type, i.e. whether an area had high soil and/or high water arsenic concentrations. The SIRs for both males and females for the combined 22 areas were increased for all cancers 1.06 (95% confidence interval, CI; 1.03-1.09), prostate cancer 1.14 (1.05-1.23), kidney cancer 1.16 (0.98-1.37), melanoma 1.36 (1.24-1.48), chronic myeloid leukemia 1.54 (1.13-2.10) and breast cancer in females 1.10 (1.03-1.18). When stratifying into exposure categories, the SIR for prostate cancer was significant at 1.20 (1.06-1.36) for the high soil/high water category only. No significant dose- response relationship between drinking water and individual cancers was observed. Of the a priori cancers associated with environmental arsenic exposure, only prostate cancer incidence was significantly elevated in this study. This result was likely confounded by a number of factors and was limited by low power and exposure misclassification.     

The association of drinking water source and chlorination by-products with cancer incidence among postmenopausal women in Iowa: a prospective cohort study.

OBJECTIVES: This study assessed the association of drinking water source and chlorination by-product exposure with cancer incidence. METHODS: A cohort of 28,237 Iowa women reported their drinking water source. Exposure to chlorination by-products was determined from statewide water quality data. RESULTS: In comparison with women who used municipal ground-water sources, women with municipal surface water sources were at an increased risk of colon cancer and all cancers combined. A clear dose-response relation was observed between four categories of increasing chloroform levels in finished drinking water and the risk of colon cancer and all cancers combined. The relative risks were 1.00, 1.06, 1.39, and 1.68 for colon cancer and 1.00, 1.04, 1.24, and 1.25 for total cancers. No consistent association with either water source or chloroform concentration was observed for other cancer sites. CONCLUSIONS: These results suggest that exposure to chlorination by-products in drinking water is associated with increased risk of colon cancer.     

Chlorinated drinking water and pancreatic cancer: A population-based case-control study

In order to examine the potential association between chlorinateddrinking water and the incidence of pancreatic cancer, a population-basedcase-control study was performed on data obtained from the Turkuarea in Finland. The study base was approximately 220,000 persons.All 183 pancreatic cancer cases, diagnosed during 1989–1991,were included in the study. Each case had 2 randomly selectedcontrols. The criterion for the exposure to chlorination by-products(CBPs) was that the subject had had chlorinated drinking waterfrom a surface source available at home. Residential addresseswith chlorinated or non-chlorinated water were obtained forup to the previous 20 years prior to diagnosis. The odds ratios(OR) varied between 0.20 and 0.66 depending on the length ofthe cumulative exposure time. This indicates that those exposedto chlorinated drinking water had a lower risk of contractingpancreatic cancer than the unexposed. The result is in grossagreement with earlier investigations which have mainly shownnegative or inadequate associations. The side-effects of drinkingwater disinfection are unproven, because the published researchresults are inconsistent. The benefits of chlorination, however,are undeniable. Continuous water disinfection is needed in orderto avoid waterborne epidemics and chlorination is the only availablemethod in many countries.     

不同饮水类型与结直肠癌发病率的流行病学研究

目的 探索不同饮水类型与结直肠癌发病率之间的关系。方法 随机抽取了浙江省海宁市的８个乡镇为研究区,应用回顾前瞻性研究方法,分别对不同饮水类型的结肠、直肠癌发病率进行分析并作相对危险度（ＲＲ）估计。结果 饮用井水、自来水、河水和池塘水者的结直肠癌发病率男性分别为３．１９／１０万、７．９９／１０万、４５．０６／１０万和１２６．０４／１０万;女性分别为３．０６／１０万、５．１７／１０万、６３．４３／１０     

Arsenic in drinking water and lung cancer: a systematic review

Exposure to inorganic arsenic via drinking water is a growing public health concern. We conducted a systematic review of the literature examining the association between arsenic in drinking water and the risk of lung cancer in humans. Towards this aim, we searched electronic databases for articles published through April 2006. Nine ecological studies, two case-control studies, and six cohort studies were identified. The majority of the studies were conducted in areas of high arsenic exposure (100 μg/L) such as southwestern Taiwan, the Niigata Prefecture, Japan, and Northern Chile. Most of the studies reported markedly higher risks of lung cancer mortality or incidence in high arsenic areas compared to the general population or a low arsenic exposed reference group. The quality assessment showed that, among the studies identified, only four assessed arsenic exposure at the individual level. Further, only one of the ecological studies presented results adjusted for potential confounders other than age; of the cohort and case-control studies, only one-half adjusted for cigarette smoking status in the analysis. Despite these methodologic limitations, the consistent observation of strong, statistically significant associations from different study designs carried out in different regions provide support for a causal association between ingesting drinking water with high concentrations of arsenic and lung cancer. The lung cancer risk at lower exposure concentrations remains uncertain.     

Industrial risk factors for colorectal cancer

Colorectal cancer is the second most common malignancy in the United States, and its incidence rates have sharply increased recently, especially in males. Industrial exposures, both occupational and environmental, are important colorectal cancer risk factors that are generally unrecognized by clinicians. Migration studies have documented that colorectal cancer is strongly associated with environmental risk factors. The causal role of occupational exposures is evidenced by a substantial literature associating specific work practices with increased colorectal cancer risks. Industrially related environmental exposures, including polluted drinking water and ionizing radiation, have also been associated with excess risks. Currently, there is a tendency to attribute colorectal cancer, largely or exclusively, to dietary and other lifestyle factors, thus neglecting these industrially related effects. Concerted efforts are needed to recognize the causal role of industrial risk factors and to encourage government and industry to reduce carcinogenic exposures. Furthermore, cost-effective screening programs for high-risk population groups are critically needed to further reduce deaths from colorectal cancer.     

Drinking water and cancer incidence in Iowa. III. Association of cancer with indices of contamination

With data from the Iowa Cancer Registry, age-adjusted sex-specific cancer incidence rates for the years 1969-1981 were determined for towns with a population of 1,000-10,000 and a public water supply from a single stable ground source. These rates were related to levels of volatile organic compounds and metals found in the finished drinking water of these towns in the spring of 1979. Results showed association between 1,2 dichloroethane and cancers of the colon and rectum and between nickel and cancers of the bladder and lung. The effects were most clearly seen in males. These associations were independent of other water quality and treatment variables and were not explained by occupational or other sociodemographic features including smoking. Because of the low levels of the metals and organics, the authors suggest that they are not causal factors, but rather indicators of possible anthropogenic contamination of other types. The data suggest that water quality variables other than chlorination and trihalomethanes deserve further consideration as to their role in the development of human cancer.     

饮用水源中的微囊藻毒素与大肠癌发病的关系

目的：研究不同类型饮用水源中的微囊藻毒素与大肠癌发病的关系。方法 在浙江省海宁市的８个乡镇,对近２０年的共４０８例大肠癌患进行一生中饮水情况的调查,并分别采集井水、自来水、池塘水及河浜水的水样,用间接竞争酶联免疫方法测定微囊藻毒素的含量。结果：饮用池塘水及河浜水的大肠癌发病率均明显高于饮用水和自来水的发病率,经与饮用井水相比,饮用自来水,河浜水及池塘水的相对危险度分别为１．８８、７．９４和７．７     

Health significance of chlorination byproducts in drinking water: the Houston experience

In 1954, following the construction of Lake Houston, a change from lightly chlorinated ground sources to a heavily chlorinated surface source of drinking water took place for a sizable part of the population in the city of Houston, Texas. This has provided the opportunity to compare the incidence of urinary tract cancer mortality in populations exposed to heavily chlorinated and lightly chlorinated drinking water. The spatial, diurnal, and seasonal concentrations of chlorination byproducts (trihalomethanes) in Houston water were assessed. The range of concentrations varied from below the limits of detection in treated ground water, to more than 200 mg/l (twice the level allowed by US drinking water standards) in treated lake water. The mortality experience by gender, by race, and by age cohorts for the period 1940 to 1970 from urinary tract cancers and three comparison causes was determined for 56 of Houston's census tracts classified by the duration of exposure to the surface water. By the 1970's 20 years following the switch to surface water, an increase was detected in urinary cancer mortality rates for white females without a corresponding increase observed for white males. No clear-cut trends were found for the non-white population. On balance, a detrimental urinary cancer effect associated with a switch to chlorinated surface water has not been demonstrated yet.     

结肠癌和直肠癌危险因素的巢式病例对照研究

目的：探讨结肠癌和直肠癌的危险因素。方法：应用巢式病例对照研究方法,对一个6万余人队列随访10年队列中196例新发结、直肠癌病例作为病例组;从该队列中随机抽取980名正常人作为对照组,对有关暴露因素进行单因素分析和多因素非条件logistic回归分析,结果：年龄在病例组和对照之间差异有显著性,病例组年龄高于对照组,且结肠癌的发病年龄高于直肠癌。多因素分析表明,除年龄外,粘液血便中、肠息肉史与结肠癌关系密切,OR值分别为：2．961（95％CI：1．202－7．298）和8．941（95％CI：1．820－43．926）,饮用混合水与直肠癌的OR值为1．823（95％CI:1．024－3．247）。结论：结、直肠癌的危险因素不尽相同。除年龄是结、直肠癌发病的一个共同重要因素外,肠息肉史和粘液血便史与结肠癌有关联,而饮用混合水则与直肠癌关系密切。     

The rate of gastroenteritis in a large city before and after chlorination

There is conflicting evidence about the contribution of drinking water to endemic community gastroenteritis in water supplies which meet conventional microbiological standards with some studies reporting associations between drinking water and endemic disease and others finding no evidence that water is implicated in disease. This study reports the results of an ecological study investigating the effect on community gastroenteritis of chlorinating a city of over 3 million people in the mid 1970s. Prior to chlorination faecal coliforms were regularly identified in the water. Admissions for gastroenteritis and attendances to the Emergency Department of the Royal Children's Hospital, Melbourne's major children's hospital, were measured between 1974 and 1980 inclusive and the influence of chlorination on rates of gastroenteritis was examined. No statistically significant difference was found in the number of admissions or emergency department visits before and after chlorination of the water supply. The study highlights the need for caution when interpreting the relationships between drinking water and gastroenteritis. The result suggests that water was not a dominant contributor to the burden of gastrointestinal disease in the community despite faecal coliforms being present in the water supply. It indicates the need for caution when attributing significant illness to drinking water when there have been only small changes in water quality without first stringently reviewing the studies methodology and understanding their limitations.     

Bladder cancer and exposure to water disinfection by-products through ingestion, bathing, showering, and swimming in pools

Bladder cancer has been associated with exposure to chlorination by-products in drinking water, and experimental evidence suggests that exposure also occurs through inhalation and dermal absorption. The authors examined whether bladder cancer risk was associated with exposure to trihalomethanes (THMs) through ingestion of water and through inhalation and dermal absorption during showering, bathing, and swimming in pools. Lifetime personal information on water consumption and water-related habits was collected for 1,219 cases and 1,271 controls in a 1998-2001 case-control study in Spain and was linked with THM levels in geographic study areas. Long-term THM exposure was associated with a twofold bladder cancer risk, with an odds ratio of 2.10 (95% confidence interval: 1.09, 4.02) for average household THM levels of >49 versus < or =8 micro g/liter. Compared with subjects not drinking chlorinated water, subjects with THM exposure of >35 micro g/day through ingestion had an odds ratio of 1.35 (95% confidence interval: 0.92, 1.99). The odds ratio for duration of shower or bath weighted by residential THM level was 1.83 (95% confidence interval: 1.17, 2.87) for the highest compared with the lowest quartile. Swimming in pools was associated with an odds ratio of 1.57 (95% confidence interval: 1.18, 2.09). Bladder cancer risk was associated with long-term exposure to THMs in chlorinated water at levels regularly occurring in industrialized countries.     

Does ozonation of drinking water reduce the risk of bladder cancer?

BACKGROUND: Epidemiologic studies of drinking water disinfection byproducts have focused primarily on the carcinogenic potential of chlorination byproducts. Because drinking water has been ozonated in France for decades, we were able to assess the carcinogenic risk of the disinfection byproducts generated by both ozonation and chlorination. METHODS: We used data from a case-control study of bladder cancer conducted between 1985 and 1987 in 7 French hospitals. We compared 281 cases and 272 controls for whom we could reconstruct at least 70% of the residential exposure to drinking water contaminants over a 30-year period. RESULTS: When we took potential confounders and exposure to chlorination byproducts into account, the risk of bladder cancer decreased as duration of exposure to ozonated water increased (OR = 0.60 [95% CI = 0.3-1.3] for 1-9 years; OR = 0.31 [0.1-0.7] for 10 years or more). Simultaneously, the risk of bladder cancer increased with duration of exposure to chlorinated surface water and with the estimated trihalomethane content of the water. Our data suggest that ozonation reduces the risk associated with the chlorination of surface water and that ozonation alone could have an independent beneficial effect on bladder cancer risk. CONCLUSIONS: Our results are consistent with experimental evidence that ozonation in combination with chlorination decreases the concentration of trihalomethane in treated water and eliminates some of the mutagenicity of raw water.     

Associations between stomach cancer incidence and drinking water contamination with atrazine and nitrate in Ontario (Canada) agroecosystems, 1987-1991

BACKGROUND: Nitrate and atrazine are two chemicals that are heavily used in certain sectors of agriculture. They are suspected to be associated with the development of certain types of tumours. METHODS: Existing data were obtained on the incidence of specific types of cancers, contamination of drinking water with atrazine and nitrate, and related agricultural practices for the 40 ecodistricts in the province of Ontario. The data were merged into a georelational database for geographical and statistical analyses. Weighted (by population size) least squares regression analyses were conducted while controlling for confounding socioeconomic and lifestyle factors. Maximum likelihood spatial error models were estimated when least square regression error terms were found to be spatially autocorrelated using the Moran's I statistic. RESULTS: Atrazine contamination levels (range 50-649 ng/l, maximum acceptable concentration [MAC] = 60000 ng/l) were positively associated (P < 0.05) with stomach cancer incidence and negatively associated with colon cancer incidence. Nitrate levels, (range 0-91 mg/l, MAC = 10 mg/l) were negatively associated with stomach cancer incidence. CONCLUSION: The associations found at the ecodistrict level, both positive and negative, if confirmed by other studies, raise serious questions about maximum allowable limits for atrazine, as well as possibilities of complex trade-offs among disease outcomes, and interactions of biophysical and social mechanisms which might explain them. Although the negative associations appear to have no direct biological explanations, such counter-intuitive outcomes may occur in complex systems where social and biological variables interact.     

An ecologic study of nitrate in municipal drinking water and cancer incidence in Trnava District,Slovakia

Contamination of drinking water by nitrate is an evolving public health concern since nitrate can undergo endogenous reduction to nitrite, and nitrosation of nitrites can form N-nitroso compounds, which are potent carcinogens. We conducted an ecologic study to determine whether nitrate levels in drinking water were correlated with non-Hodgkin lymphoma and cancers of the digestive and urinary tracts in an agricultural district (Trnava District; population 237,000) of the Slovak Republic. Routinely collected nitrate data (1975-1995) for villages using public water supplies were computerized, and each village was categorized into low (0-10 mg/L), medium (10.1-20 mg/L), or high (20.1-50 mg/L) average levels of total nitrate in drinking water. Observed cases of cancer in each of these villages were ascertained through the district cancer registry for the time period 1986-1995. Standardized incidence ratios (SIRs) and 95% confidence intervals (CI) for all cancer and selected cancer sites were calculated by indirect standardization using age- and sex-specific incidence rates from the entire district. For all cancer in women, SIRs increased from villages with low (SIR=0.87; 95% CI 0.72-0.95) to medium (SIR=1.07; 95% CI 1.00-1.13) to high (SIR=1.14; 1.06-1.22) levels of nitrate (P for trend <0.001); there was a similar trend for all cancer in men from low (SIR=0.90; 95% CI 0.81-0.99) to medium (SIR=1.08, 95% CI 1.02-1.16), but not for high (SIR=0.94; 0.88-1.02), nitrate levels (P for trend <0.001). This pattern in the SIRs (from low to high nitrate level) was also seen for stomach cancer in women (0.81, 0.94, 1.24; P for trend=0.10), colorectal cancer in women (0.64, 1.11, 1.29; P for trend <0.001) and men (0.77, 0.99, 1.07; P for trend=0.051), and non-Hodgkin lymphoma in women (0.45, 0.90, 1.35; P for trend=0.13) and men (0.25, 1.66, and 1.09; P for trend=0.017). There were no associations for kidney or bladder cancer. These ecologic data support the hypothesis that there is a positive association between nitrate in drinking water and non-Hodgkin lymphoma and colorectal cancer.     

Nitrogen-nitrate exposure from drinking water and colorectal cancer risk for rural women in Wisconsin, USA

One unintentional result of widespread adoption of nitrogen application to croplands over the past 50 years has been nitrate contamination of drinking water with few studies evaluating the risk of colorectal cancer. In our population-based case-control study of 475 women age 20–74 years with colorectal cancer and 1447 community controls living in rural Wisconsin, drinking water nitrate exposure were interpolated to subjects residences based on measurements which had been taken as part of a separate water quality survey in 1994. Individual level risk factor data was gathered in 1990–1992 and 1999–2001. Logistic regression models estimated the risk of colorectal cancer for the study period, separately and pooled. In the pooled analyses, an overall colorectal cancer risk was not observed for exposure to nitrate-nitrogen in the highest category (10 ppm) compared to the lowest category (<0.5 ppm). However, a 2.9 fold increase risk was observed for proximal colon cancer cases in the highest compared to the lowest category. Statistically significant increased distal colon or rectal cancer risk was not observed. These results suggest that if an association exists with nitrate-nitrogen exposure from residential drinking water consumption, it may be limited to proximal colon cancer.     

Municipal drinking water nitrate level and cancer risk in older women: the Iowa Women's Health Study

Nitrate contamination of drinking water may increase cancer risk, because nitrate is endogenously reduced to nitrite and subsequent nitrosation reactions give rise to N-nitroso compounds; these compounds are highly carcinogenic and can act systemically. We analyzed cancer incidence in a cohort of 21,977 Iowa women who were 55-69 years of age at baseline in 1986 and had used the same water supply more than 10 years (87% > 20 years); 16,541 of these women were on a municipal supply, and the remainder used a private well. We assessed nitrate exposure from 1955 through 1988 using public databases for municipal water supplies in Iowa (quartile cutpoints: 0.36, 1.01, and 2.46 mg per liter nitrate-nitrogen). As no individual water consumption data were available, we assigned each woman an average level of exposure calculated on a community basis; no nitrate data were available for women using private wells. Cancer incidence (N = 3,150 cases) from 1986 through 1998 was determined by linkage to the Iowa Cancer Registry. For all cancers, there was no association with increasing nitrate in drinking water, nor were there clear and consistent associations for non-Hodgkin lymphoma; leukemia; melanoma; or cancers of the colon, breast, lung, pancreas, or kidney. There were positive associations for bladder cancer [relative risks (RRs) across nitrate quartiles = 1, 1.69, 1.10, and 2.83] and ovarian cancer (RR = 1, 1.52, 1.81, and 1.84), and inverse associations for uterine cancer (RR = 1, 0.86, 0.86, and 0.55) and rectal cancer (RR = 1, 0.72, 0.95, and 0.47) after adjustment for a variety of cancer risk/protective factors, agents that affect nitrosation (smoking, vitamin C, and vitamin E intake), dietary nitrate, and water source. Similar results were obtained when analyses were restricted to nitrate level in drinking water from 1955 through 1964. The positive association for bladder cancer is consistent with some previous data; the associations for ovarian, uterine, and rectal cancer were unexpected.     

Chlorinated drinking water and bladder cancer: effect of misclassification on risk estimates

Data are presented from the Iowa portion of the National Bladder Cancer Case-Control Study demonstrating the effect of misclassification on depressing odds ratio estimates for years of exposure to chlorinated drinking water and bladder cancer. Four methods (METHODS 1 through 4) of quantifying chlorination exposure with sequentially decreasing degrees of misclassification are presented for the 268 bladder cancer cases and 658 population-based controls fulfilling criteria for inclusion in this study. Twenty-eight other risk factors for bladder cancer were considered along with chlorinated drinking water exposure estimated by METHOD 4. Stepwise regression models included as significant factors cigarette smoking (p less than .001), chlorination exposure (p = .038), and irradiation to the pelvic area (p = .040). Replacement of chlorinated drinking water exposure estimated by METHOD 4 with any of the remaining three methods resulted in models that included cigarette smoking and irradiation to the pelvic area, but not chlorination exposure. Thus, misclassification of chlorination exposure signified the difference between observing and not observing an association with bladder cancer.     

Health impacts of long-term exposure to disinfection by-products in drinking water in Europe: HIWATE

There appears to be very good epidemiological evidence for a relationship between chlorination by-products, as measured by trihalomethanes (THMs), in drinking water and bladder cancer, but the evidence for other cancers, including colorectal cancer appears to be inconclusive and inconsistent. There appears to be some evidence for a relationship between chlorination by-products, as measured by THMs, and small for gestational age (SGA)/intrauterine growth retardation (IUGR) and preterm delivery, but evidence for other outcomes such as low birth weight (LBW), stillbirth, congenital anomalies and semen quality appears to be inconclusive and inconsistent.     

Chlorination, chlorination by-products, and cancer: a meta-analysis.

OBJECTIVES. Individual epidemiological investigations into the association between chlorination by-products in drinking water and cancer have been suggestive but inconclusive. Enough studies exist to provide the basis for a meaningful meta-analysis. METHODS. An extensive literature search was performed to identify pertinent case-control studies and cohort studies. Consumption of chlorinated water, surface water, or water with high levels of chloroform was used as a surrogate for exposure to chlorination by-products. Relative risk estimates were abstracted from the individual studies and pooled. RESULTS. A simple meta-analysis of all cancer sites yielded a relative risk estimate for exposure to chlorination by-products of 1.15 (95% CI: 1.09, 1.20). Pooled relative risk estimates for organ-specific neoplasms were 1.21 (95% CI: 1.09, 1.34) for bladder cancer and 1.38 (95% CI: 1.01, 1.87) for rectal cancer. When studies that adjusted for potential confounders were pooled separately, estimates of relative risks did not change substantially. CONCLUSIONS. The results of this meta-analysis suggest a positive association between consumption of chlorination by-products in drinking water and bladder and rectal cancer in humans.