RE: Elevated Bladder Cancer in Northern New England: The Role of Drinking Water and Arsenic.
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ABSTRACT:
SUBMITTER: Koutros S
PROVIDER: S-EPMC6235686 | biostudies-literature | 2018 Nov
REPOSITORIES: biostudies-literature
Publications
RE: Elevated Bladder Cancer in Northern New England: The Role of Drinking Water and Arsenic.
Koutros Stella S Lenz Petra P Hewitt Stephen M SM Kida Masatoshi M Jones Michael M Schned Alan R AR Baris Dalsu D Pfeiffer Ruth R Schwenn Molly M Johnson Alison A Karagas Margaret R MR Garcia-Closas Montserrat M Rothman Nathaniel N Moore Lee E LE Silverman Debra T DT
Journal of the National Cancer Institute 20181101 11
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Project description:Bladder cancer mortality rates have been elevated in northern New England for at least five decades. Incidence rates in Maine, New Hampshire, and Vermont are about 20% higher than the United States overall. We explored reasons for this excess, focusing on arsenic in drinking water from private wells, which are particularly prevalent in the region. In a population-based case-control study in these three states, 1213 bladder cancer case patients and 1418 control subjects provided information on suspected risk factors. Log transformed arsenic concentrations were estimated by linear regression based on measurements in water samples from current and past homes. All statistical tests were two-sided. Bladder cancer risk increased with increasing water intake (Ptrend = .003). This trend was statistically significant among participants with a history of private well use (Ptrend = .01). Among private well users, this trend was apparent if well water was derived exclusively from shallow dug wells (which are vulnerable to contamination from manmade sources, Ptrend = .002) but not if well water was supplied only by deeper drilled wells (Ptrend = .48). If dug wells were used pre-1960, when arsenical pesticides were widely used in the region, heavier water consumers (>2.2 L/day) had double the risk of light users (<1.1 L/day, Ptrend = .01). Among all participants, cumulative arsenic exposure from all water sources, lagged 40 years, yielded a positive risk gradient (Ptrend = .004); among the highest-exposed participants (97.5th percentile), risk was twice that of the lowest-exposure quartile (odds ratio = 2.24, 95% confidence interval = 1.29 to 3.89). Our findings support an association between low-to-moderate levels of arsenic in drinking water and bladder cancer risk in New England. In addition, historical consumption of water from private wells, particularly dug wells in an era when arsenical pesticides were widely used, was associated with increased bladder cancer risk and may have contributed to the New England excess.
| S-EPMC5939854 | biostudies-literature
Project description:BackgroundIngestion of inorganic arsenic in drinking water is recognized as a cause of bladder cancer when levels are relatively high (? 150 µg/L). The epidemiologic evidence is less clear at the low-to-moderate concentrations typically observed in the United States. Accurate retrospective exposure assessment over a long time period is a major challenge in conducting epidemiologic studies of environmental factors and diseases with long latency, such as cancer.ObjectiveWe estimated arsenic concentrations in the water supplies of 2,611 participants in a population-based case-control study in northern New England.MethodsEstimates covered the lifetimes of most study participants and were based on a combination of arsenic measurements at the homes of the participants and statistical modeling of arsenic concentrations in the water supply of both past and current homes. We assigned a residential water supply arsenic concentration for 165,138 (95%) of the total 173,361 lifetime exposure years (EYs) and a workplace water supply arsenic level for 85,195 EYs (86% of reported occupational years).ResultsThree methods accounted for 93% of the residential estimates of arsenic concentration: direct measurement of water samples (27%; median, 0.3 µg/L; range, 0.1-11.5), statistical models of water utility measurement data (49%; median, 0.4 µg/L; range, 0.3-3.3), and statistical models of arsenic concentrations in wells using aquifers in New England (17%; median, 1.6 µg/L; range, 0.6-22.4).ConclusionsWe used a different validation procedure for each of the three methods, and found our estimated levels to be comparable with available measured concentrations. This methodology allowed us to calculate potential drinking water exposure over long periods.
| S-EPMC3230387 | biostudies-literature
Project description:BackgroundA growing number of studies have identified an association between exposure to inorganic arsenic and hypertension. However, results have not been consistent across studies. Additional studies are warranted, given the global prevalence of both arsenic exposure and morbidity attributable to hypertension.MethodsWe analyzed data collected from October 2007-December 2010 for a population-based cancer case-control study in northern Chile. Data included lifetime individual arsenic exposure estimates and information on potential confounders for a total of 1266 subjects. Those self-reporting either a physician diagnosis of hypertension or use of an anti-hypertensive medication were classified as having hypertension (n=612). The association between hypertension and drinking water arsenic exposure was analyzed using logistic regression models.ResultsCompared to those in the lowest category for lifetime highest 5-year average arsenic exposure (<60µg/L), those in the middle (60-623μg/L) and upper (>623μg/L) exposure categories had adjusted hypertension ORs of 1.49 (95% CI: 1.09, 2.05) and 1.65 (95% CI: 1.18, 2.32), respectively. Similar results were observed in analyses of lifetime cumulative exposures and analyses restricted to exposures from the distant past.ConclusionsWe identified evidence of increased odds of hypertension with exposure to arsenic in drinking water among study participants. Our findings add to the growing body of research supporting this association, which could have important public health implications.
| S-EPMC5534354 | biostudies-literature
Project description:The etiology of bladder cancer among never smokers without occupational or environmental exposure to established urothelial carcinogens remains unclear. Urinary mutagenicity is an integrative measure that reflects recent exposure to genotoxic agents. Here, we investigated its potential association with bladder cancer in rural northern New England. We analyzed 156 bladder cancer cases and 247 cancer-free controls from a large population-based case-control study conducted in Maine, New Hampshire, and Vermont. Overnight urine samples were deconjugated enzymatically and the extracted organics were assessed for mutagenicity using the plate-incorporation Ames assay with the Salmonella frameshift strain YG1041 + S9. Logistic regression was used to estimate the odds ratios (OR) and 95% confidence intervals (CI) of bladder cancer in relation to having mutagenic versus nonmutagenic urine, adjusted for age, sex, and state, and stratified by smoking status (never, former, and current). We found evidence for an association between having mutagenic urine and increased bladder cancer risk among never smokers (OR = 3.8, 95% CI: 1.3-11.2) but not among former or current smokers. Risk could not be estimated among current smokers because nearly all cases and controls had mutagenic urine. Urinary mutagenicity among never-smoking controls could not be explained by recent exposure to established occupational and environmental mutagenic bladder carcinogens evaluated in our study. Our findings suggest that among never smokers, urinary mutagenicity potentially reflects genotoxic exposure profiles relevant to bladder carcinogenesis. Future studies are needed to replicate our findings and identify compounds and their sources that influence bladder cancer risk.
| S-EPMC11089907 | biostudies-literature
Project description:Millions of people worldwide are exposed to arsenic-contaminated water. In the largest city in northern Chile (Antofagasta), more than 250,000 people were exposed to high arsenic drinking water concentrations from 1958 until 1970 when a water treatment plant was installed. Because of its unique geology, limited water sources, and good historical records, lifetime exposure and long-term latency patterns can be assessed in this area with better accuracy than in other arsenic-exposed areas worldwide.We conducted a population-based case-control study in northern Chile from October 2007 to December 2010 involving 232 bladder and 306 lung cancer cases and 640 age- and gender-matched controls, with detailed information on past exposure and potential confounders, including smoking and occupation.Bladder cancer ORs for quartiles of average arsenic concentrations in water before 1971 (<11, 11-90, 91-335, and >335 ?g/L) were 1.00, 1.36 [95% confidence interval (CI), 0.78-2.37], 3.87 (2.25-6.64), and 6.50 (3.69-11.43), respectively. Corresponding lung cancer ORs were 1.00, 1.27 (0.81-1.98), 2.00 (1.24-3.24), and 4.32 (2.60-7.17). Bladder and lung cancer ORs in those highly exposed in Antofagasta during 1958 to 1970 but not thereafter were 6.88 (3.84-12.32) and 4.35 (2.57-7.36), respectively.The lung and bladder cancer risks that we found up to 40 years after high exposures have ended are very high.Our findings suggest that prevention, treatment, and other mortality reduction efforts in arsenic-exposed countries will be needed for decades after exposure cessation.
| S-EPMC3848421 | biostudies-literature
Project description:BackgroundN-nitroso compounds are hypothesized human bladder carcinogens. We investigated ingestion of N-nitroso compound precursors nitrate and nitrite from drinking water and diet and bladder cancer in the New England Bladder Cancer Study.MethodsUsing historical nitrate measurements for public water supplies and measured and modeled values for private wells, as well as self-reported water intake, we estimated average nitrate concentrations (mg/L NO3-N) and average daily nitrate intake (mg/d) from 1970 to diagnosis/reference date (987 cases and 1,180 controls). We estimated overall and source-specific dietary nitrate and nitrite intakes using a food frequency questionnaire (1,037 cases and 1,225 controls). We used unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI). We evaluated interactions with factors that may affect N-nitroso compound formation (i.e., red meat, vitamin C, smoking), and with water intake.ResultsAverage drinking water nitrate concentration above the 95th percentile (>2.07 mg/L) compared with the lowest quartile (≤0.21 mg/L) was associated with bladder cancer (OR = 1.5, 95% CI = 0.97, 2.3; P trend = 0.01); the association was similar for average daily drinking water nitrate intake. We observed positive associations for dietary nitrate and nitrite intakes from processed meat (highest versus lowest quintile OR for nitrate = 1.4, 95% CI = 1.0, 2.0; P trend = 0.04; OR for nitrite = 1.5, 95% CI = 1.0, 2.1; P trend = 0.04, respectively), but not other dietary sources. We observed positive interactions between drinking water nitrate and red meat (P-interaction 0.05) and processed red meat (0.07).ConclusionsOur results suggest the importance of both drinking water and dietary nitrate sources as risk factors for bladder cancer.
| S-EPMC6927574 | biostudies-literature
Project description:Millions of people worldwide are exposed to arsenic in drinking water. The International Agency for Research on Cancer has concluded that ingested arsenic causes lung, bladder, and skin cancer. However, a similar conclusion was not made for kidney cancer because of a lack of research with individual data on exposure and dose-response. With its unusual geology, high exposures, and good information on past arsenic water concentrations, northern Chile is one of the best places in the world to investigate the carcinogenicity of arsenic. We performed a case-control study in 2007-2010 of 122 kidney cancer cases and 640 population-based controls with individual data on exposure and potential confounders. Cases included 76 renal cell, 24 transitional cell renal pelvis and ureter, and 22 other kidney cancers. For renal pelvis and ureter cancers, the adjusted odds ratios by average arsenic intakes of <400, 400-1,000, and >1,000 µg/day (median water concentrations of 60, 300, and 860 µg/L) were 1.00, 5.71 (95% confidence interval: 1.65, 19.82), and 11.09 (95% confidence interval: 3.60, 34.16) (Ptrend < 0.001), respectively. Odds ratios were not elevated for renal cell cancer. With these new findings, including evidence of dose-response, we believe there is now sufficient evidence in humans that drinking-water arsenic causes renal pelvis and ureter cancer.
| S-EPMC3817454 | biostudies-literature
Project description:The reported ability of cysteine and cystine to bind typical arsenic oxy-ions in water is used as a basis for a study of the potential for using a surfactant with a cysteine head-group for selective arsenic binding and removal in an ion flotation process. Several different head-group attachment methods are studied with cysteine and cystine and with single- and double-chain surfactants. A comparison of the properties of these surfactants with some other surface-active compounds, with groups like those on cysteine, suggest that few compounds have suitable characteristics for the efficient removal of low levels of arsenic from drinking water. An amino-acid-based single-chain surfactant is synthesized by reacting cysteine with octanoyl chloride to obtain octanoyl cysteine, which is then used in a study of selective ion flotation for the removal of low levels of arsenic from drinking water. This compound has high water solubility and causes extensive foaming in a typical flotation chamber and removed 99.4-99.9% of the 5 mg L-1 arsenic present in the contaminated water in a simple, single-stage ion flotation process, using either air or nitrogen gas. These laboratory results indicate that these surfactants can be useful in the large-scale treatment of low-level arsenic-contaminated water.
| S-EPMC6436586 | biostudies-literature
Project description:New England Bladder Cancer Study (NEBCS)
| PRJNA686154 | ENA
Project description:Naturally occurring arsenic can adversely affect water quality in geologically diverse aquifers throughout the world. Chronic exposure to arsenic via drinking water is a human health concern due to risks for certain cancers, skin abnormalities, peripheral neuropathy, and other negative health effects. Statewide in Minnesota, USA, 11% of samples from new drinking water wells have arsenic concentrations exceeding 10 μg/L; in certain counties more than 35% of tested samples exceed 10 μg/L arsenic. Since 2008, Minnesota well code has required testing water from new wells for arsenic. Sample collection protocols are not specified in the well code, so among 180 well drillers there is variability in sampling methods, including sample collection point and sample collection timing. This study examines the effect of arsenic sample collection protocols on the variability of measured arsenic concentrations in water from new domestic water supply wells. Study wells were drilled between 2014 and 2016 in three regions of Minnesota that commonly have elevated arsenic concentrations in groundwater. Variability in measured arsenic concentration at a well was reduced when samples were (1) filtered, (2) collected from household plumbing instead of from the drill rig pump, or (3) collected several months after well construction (instead of within 4 weeks of well installation). Particulates and fine aquifer sediments entrained in groundwater samples, or other artifacts of drilling disturbance, can cause undesirable variability in measurements. Establishing regulatory protocols requiring sample filtration and/or collection from household plumbing could improve the reliability of information provided to well owners and to secondary data users.
| S-EPMC6282803 | biostudies-literature