Arsenic In Drinking Water Research Articles

Arsenic in Drinking Water and Lung Cancer Mortality in the United States: An Analysis Based on US Counties and 30 Years of Observation (1950–1979)

Background. To examine whether the US EPA (2010) lung cancer risk estimate derived from the high arsenic exposures (10–934 µg/L) in southwest Taiwan accurately predicts the US experience from low arsenic exposures (3–59 µg/L). Methods. Analyses have been limited to US counties solely dependent on underground sources for their drinking water supply with median arsenic levels of ≥3 µg/L. Results. Cancer risks (slopes) were found to be indistinguishable from zero for males and females. The addition of arsenic level did not significantly increase the explanatory power of the models. Stratified, or categorical, analysis yielded relative risks that hover about 1.00. The unit risk estimates were nonpositive and not significantly different from zero, and the maximum (95% UCL) unit risk estimates for lung cancer were lower than those in US EPA (2010). Conclusions. These data do not demonstrate an increased risk of lung cancer associated with median drinking water arsenic levels in the range of 3–59 µg/L. The upper-bound estimates of the risks are lower than the risks predicted from the SW Taiwan data and do not support those predictions. These results are consistent with a recent metaregression that indicated no increased lung cancer risk for arsenic exposures below 100–150 µg/L.

Elevated childhood exposure to arsenic despite reduced drinking water concentrations — A longitudinal cohort study in rural Bangladesh

ObjectivesThe aim of this study was to evaluate the massive efforts to lower water arsenic concentrations in Bangladesh. MethodsIn our large mother–child cohort in rural Matlab, we measured the arsenic concentrations (and other elements) in drinking water and evaluated the actual exposure (urinary arsenic), from early gestation to 10years of age (n=1017). ResultsMedian drinking water arsenic decreased from 23 (2002–2003) to <2μg/L (2013), and the fraction of wells exceeding the national standard (50μg/L) decreased from 58 to 27%. Still, some children had higher water arsenic at 10years than earlier. Installation of deeper wells (>50m) explained much of the lower water arsenic concentrations, but increased the manganese concentrations. The highest manganese concentrations (~900μg/L) appeared in 50–100m wells. Low arsenic and manganese concentrations (17% of the children) occurred mainly in >100m wells. The decrease in urinary arsenic concentrations over time was less apparent, from 82 to 58μg/L, indicating remaining sources of exposure, probably through food (mean 133μg/kg in rice). ConclusionDespite decreased water arsenic concentrations in rural Bangladesh, the children still have elevated exposure, largely from food. Considering the known risks of severe health effects in children, additional mitigation strategies are needed.

A pilot study of low-moderate drinking water arsenic contamination and chronic diseases among reproductive age women in Timiş County, Romania.

We conducted a pilot study of associations between drinking water contaminated by inorganic arsenic (iAs), mostly <10 μg/L, and self-reported chronic diseases in 297 pregnant women. Adjusted for confounding variables, we identified a positive association between iAs and heart disease (OR = 1.63, 95%CI 0.81-3.04, p = 0.094), which was stronger for women living at their current residence ≥ 10 years (OR = 2.47, 95%CI 0.87-10.43, p = 0.058). Confounder-adjusted associations were also suggested for iAs with kidney disease (OR = 1.32, 95%CI 0.77-2.21, p = 0.265) and with high blood pressure (OR = 1.36, 95%CI 0.68-2.39, p = 0.300). A post hoc power analysis indicated the need for a larger study with more statistical power.

Consumption of arsenic-contaminated drinking water and anemia among pregnant and non-pregnant women in northwestern Romania

Anemia is a global health problem. To evaluate the impact of low-moderate water arsenic exposure (mostly <10µg/L) on anemia, we conducted a cross-sectional study of 217 Romanian women. The adjusted prevalences for ‘any’ anemia (prevalence proportion ratio (PPR)=1.71, 95% CI 0.75–3.88) and pregnancy anemia (PPR=2.87, 95% CI 0.62–13.26) were higher among drinking water arsenic exposed women than among unexposed women. These preliminary data underscore the need for a more definitive study in this area.

Placental arsenic concentrations in relation to both maternal and infant biomarkers of exposure in a US cohort.

Arsenic crosses the placenta and may have adverse consequences in utero and later in life. At present, little is known about arsenic concentrations in placenta and their relation to maternal and infant exposures particularly at common levels of exposure. We measured placenta arsenic in a US cohort potentially exposed via drinking water from private wells, and evaluated the relationships between placenta and maternal and infant biomarker arsenic concentrations. We measured total arsenic concentrations in placental samples from women enrolled in the New Hampshire Birth Cohort Study (N=766). We compared these data to maternal urinary arsenic (total arsenic and individual species) collected at approximately 24-28 week gestation, along with maternal post-partum toenails and infant toenails using non-parametric multivariate analysis of log10-transformed data. We also examined the association between placental arsenic and household drinking water arsenic. Placenta arsenic concentrations were related to arsenic concentrations in maternal urine (β 0.55, P value <0.0001), maternal (β 0.30, P value 0.0196) and infant toenails (β 0.40, P value 0.0293) and household drinking water (β 0.09, P value <0.0001). Thus, our data suggest that placenta arsenic concentrations reflect both maternal and infant exposures.

Sustainable Management for Arsenic (As) Free Safe Drinking Water in Bangladesh: A Review

Sustainable Management for Arsenic (As) Free Safe Drinking Water in Bangladesh: A Review

Sustainable Management for Arsenic (As) Free Safe Drinking Water in Bangladesh: A Review

The presence of elevated levels of naturally occurring arsenic in groundwater of Bangladesh has severely impaired the decade long effort of providing safe water to its population. Most of the recognized stages of arsenic poisoning have been identified in Bangladesh and the risk of arsenic poisoning in the population is increasing every day. The severity of arsenic contamination is demanding extensive research in this field. Many studies have been carried out in Bangladesh, West Bengal in India and other countries as well, but the situation is still out of sound control. In order to minimize arsenic exposure, a work to provide various alternate safe drinking water options to the exposed population has been initiated. This article implies to look at the sustainable management for safe drinking water in Bangladesh by reviewing different measures to remedy the arsenic contamination in groundwater.

Arsenicosis Case Identification, Diagnosis and Management Protocol for Early Patient Medicare Administration and Treatment

Many countries in the world, especially South Asia e.g., Bangladesh, India, Nepal, Vietnam, China and Myanmar are facing ground water arsenic contamination problems and it has been recognized as an emerging threat and challenge to public health (Ahmad et al, 2004). Pakistan, following the arsenic crisis in Bangladesh and in other neighboring countries, has recognized the need of assessing drinking water quality for arsenic contamination in late nineties (PCRWR 2002). Ground water arsenic contamination has emerged as a serious socio-economic and human health concerns all over the world, including Pakistan. Likewise , around 25-36 % population of two provinces in Pakistan is exposed to drinking water arsenic contamination over 10 ppb. It may be reasonable to disregard the presence of some arsenic in the water, but beyond 50 ppb is considered dangerous (NAPAM 2005). Keeping in view the adverse impacts of arsenic contamination on human health, various initiatives by different governmental and non-governmental departments and organizations were taken, without resource integration and prudent coordination mechanisms amongst the various stakeholders (IUCN, 2007). These practices resulted in wastages of scarce resources, rather than pooling up all the resources and getting maximum. During this process some experiences have been gained related to planning, implementation, monitoring and management of arsenic mitigation. As arsenic contamination causes serious health issues, therefore, the timely identification and diagnosis of arsenicosis patients remained a major problem due to absence of standard operating procedures / protocols . The arsenicosis patients identification was being observed and realized after the appearance of arsenicosis symptoms, like skin pigmentation etc, on the body parts of the effected persons. Over and above, there was no set procedures to administer the treatment and case management of such arsenicosis patients. Therefore, well designed protocols or standard operating procedures have been documented which may assist while carrying out identification of suspected arsenicosis patients. This paper will provide road map for arsenicosis diagnostic procedures, treatment administration , case management and behavioral change communication by creating awareness amongst such affected communities, prior getting prey of arsenicosis victim.

Monitoring and Impact Evaluation System for Arsenic Mitigation Interventions - Arsenic Contamination Areas of Pakistan

Drinking water arsenic contamination has emerged as a big nuisance to public health and approximately 137 million people around the world consume arsenic contaminated water, exceeding the WHO threshold of 10 μg/L. In Pakistan context, various arsenic mitigation initiatives were undertaken by different NGOs and government departments which were confined to one time measure and resultantly turned to be un-sustainable. Continuous surveillance of drinking water sources is crucial for the well being of humans for which systemised procedures for regular monitoring of the arsenic contaminated water sources has been evolved. Identifications of contaminated water sources for random and blanket arsenic testing surveys will make the monitoring & evaluation process more reliable and prudent. Grid system approach for taking water samples has been discussed and evolved which yield meaningful results. For field test validation, 10% of water samples are recommended to be tested in the laboratory by using atomic absorption spectrometer (ASS). Well thought out institutional arrangements / linkages have been evolved for achieving government buying which is necessary to make the monitoring and evaluation process sustainable. Though, the donors and NGOs have played an important role in addressing the arsenic contamination issues in many countries, including in Pakistan, yet the ultimate ownership for the success of interventions lies with the government and its line departments.

Lung Cancer in Younger Adults Following Childhood Exposure to Low Concentrations of Arsenic in Water

Background: Arsenic drinking water concentrations &gt;100 µg/L are a known cause of cancer, but the risks at lower concentrations are unknown and controversial. With its unusual geology and good information on past exposure, northern Chile is one of the best places in the world to investigate the long-term impacts of arsenic. Methods: We performed a lung cancer case-control study in areas in northern Chile with a wide range of drinking water arsenic concentrations. Previously we reported evidence of high lung cancer odds ratios (OR) for arsenic concentrations &gt;100 µg/L. In this analysis, we calculated lung cancer ORs, adjusted for age, sex, and smoking, for those 92 cases and 288 population-based controls who had no known exposure above 100 µg/L at any point in their lives. Results: For exposures =40 years ago, lung cancer odds ratios (ORs) adjusted for age, sex, and smoking for increasing tertiles of arsenic exposure were 1.00, 1.43 (90% confidence interval, 0.82- 2.52), and 2.01 (1.14-3.52) (p-trend=0.02). Median arsenic water concentrations by tertile were 6.5, 23.0, and 58.6 µg/L. For subjects under age 65, corresponding ORs for exposures before age 25 were even higher. Adjustments for occupation, diet, and socioeconomic status had little impact on results. Conclusion: These findings provide rare new evidence that drinking water arsenic concentrations below 100 µg/L are associated with increased risks of lung cancer. These results also suggest that early-life exposure may cause marked increases in lung cancer in younger adults at arsenic water concentrations approaching those commonly found in the United States.

Prenatal arsenic exposure and the epigenome: identifying sites of 5-methylcytosine alterations that predict functional changes in gene expression in newborn cord blood and subsequent birth outcomes.

Prenatal exposure to inorganic arsenic (iAs) is detrimental to the health of newborns and increases the risk of disease development later in life. Here we examined a subset of newborn cord blood leukocyte samples collected from subjects enrolled in the Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Gómez Palacio, Mexico, who were exposed to a range of drinking water arsenic concentrations (0.456-236 µg/l). Changes in iAs-associated DNA 5-methylcytosine methylation were assessed across 424,935 CpG sites representing 18,761 genes and compared with corresponding mRNA expression levels and birth outcomes. In the context of arsenic exposure, a total of 2919 genes were identified with iAs-associated differences in DNA methylation. Site-specific analyses identified DNA methylation changes that were most predictive of gene expression levels where CpG methylation within CpG islands positioned within the first exon, the 5' untranslated region and 200 bp upstream of the transcription start site yielded the most significant association with gene expression levels. A set of 16 genes was identified with correlated iAs-associated changes in DNA methylation and mRNA expression and all were highly enriched for binding sites of the early growth response (EGR) and CCCTC-binding factor (CTCF) transcription factors. Furthermore, DNA methylation levels of 7 of these genes were associated with differences in birth outcomes including gestational age and head circumference.These data highlight the complex interplay between DNA methylation, functional changes in gene expression and health outcomes and underscore the need for functional analyses coupled to epigenetic assessments.

Differential susceptibility of human peripheral blood T cells to suppression by environmental levels of sodium arsenite and monomethylarsonous acid.

Human exposure to arsenic in drinking water is known to contribute to many different health outcomes such as cancer, diabetes, and cardiopulmonary disease. Several epidemiological studies suggest that T cell function is also altered by drinking water arsenic exposure. However, it is unclear how individual responses differ to various levels of exposure to arsenic. Our laboratory has recently identified differential responses of human peripheral blood mononuclear cell (HPMBC) T cells as measured by polyclonal T cell activation by mitogens during sodium arsenite exposure. T cells from certain healthy individuals exposed to various concentrations (1–100 nM) of arsenite in vitro showed a dose-dependent suppression at these extremely low concentrations (∼0.1–10 ppb) of arsenite, whereas other individuals were not suppressed at low concentrations. In a series of more than 30 normal donors, two individuals were found to be sensitive to low concentration (10 nM equivalent ∼1 ppb drinking water exposure) to sodium arsenite-induced inhibition of T cell proliferation produced by phytohemagglutinin (PHA) and anti-CD3/anti-CD28. In an arsenite-susceptible individual, arsenite suppressed the activation of Th1 (Tbet) cells, and decreased the percentage of cells in the double positive Th17 (RORγt) and Treg (FoxP3) population. While the majority of normal blood donors tested were not susceptible to inhibition of proliferation at the 1–100 nM concentrations of As+3, it was found that all donors were sensitive to suppression by 100 nM monomethylarsonous acid (MMA+3), a key metabolite of arsenite. Thus, our studies demonstrate for the first time that low ppb-equivalent concentrations of As+3 are immunosuppressive to HPBMC T cells in some individuals, but that most donor HPBMC are sensitive to suppression by MMA+3 at environmentally relevant exposure levels.

Increased lung and bladder cancer incidence in adults after in utero and early-life arsenic exposure.

From 1958 to 1970, >100,000 people in northern Chile were exposed to a well-documented, distinct period of high drinking water arsenic concentrations. We previously reported ecological evidence suggesting that early-life exposure in this population resulted in increased mortality in adults from several outcomes, including lung and bladder cancer. We have now completed the first study ever assessing incident cancer cases after early-life arsenic exposure, and the first study on this topic with individual participant exposure and confounding factor data. Subjects included 221 lung and 160 bladder cancer cases diagnosed in northern Chile from 2007 to 2010, and 508 age and gender-matched controls. ORs adjusted for age, sex, and smoking in those only exposed in early life to arsenic water concentrations of ≤110, 110 to 800, and >800 μg/L were 1.00, 1.88 [95% confidence interval (CI), 0.96-3.71], and 5.24 (3.05-9.00; P(trend) < 0.001) for lung cancer, and 1.00, 2.94 (1.29-6.70), and 8.11 (4.31-15.25; P(trend) < 0.001) for bladder cancer. ORs were lower in those not exposed until adulthood. The highest category (>800 μg/L) involved exposures that started 49 to 52 years before, and ended 37 to 40 years before the cancer cases were diagnosed. Lung and bladder cancer incidence in adults was markedly increased following exposure to arsenic in early life, even up to 40 years after high exposures ceased. Such findings have not been identified before for any environmental exposure, and suggest that humans are extraordinarily susceptible to early-life arsenic exposure. Policies aimed at reducing early-life exposure may help reduce the long-term risks of arsenic-related disease.

Arsenic in drinking water and urinary tract cancers: a systematic review of 30years of epidemiological evidence.

BackgroundArsenic in drinking water is a public health issue affecting hundreds of millions of people worldwide. This review summarizes 30 years of epidemiological studies on arsenic exposure in drinking water and the risk of bladder or kidney cancer, quantifying these risks using a meta-analytical framework.MethodsForty studies met the selection criteria. Seventeen provided point estimates of arsenic concentrations in drinking water and were used in a meta-analysis of bladder cancer incidence (7 studies) and mortality (10 studies) and kidney cancer mortality (2 studies). Risk estimates for incidence and mortality were analyzed separately using Generalized Linear Models. Predicted risks for bladder cancer incidence were estimated at 10, 50 and 150 μg/L arsenic in drinking water. Bootstrap randomizations were used to assess robustness of effect size.ResultsTwenty-eight studies observed an association between arsenic in drinking water and bladder cancer. Ten studies showed an association with kidney cancer, although of lower magnitude than that for bladder cancer. The meta-analyses showed the predicted risks for bladder cancer incidence were 2.7 [1.2–4.1]; 4.2 [2.1–6.3] and; 5.8 [2.9–8.7] for drinking water arsenic levels of 10, 50, and 150 μg/L, respectively. Bootstrapped randomizations confirmed this increased risk, but, lowering the effect size to 1.4 [0.35–4.0], 2.3 [0.59–6.4], and 3.1 [0.80–8.9]. The latter suggests that with exposures to 50 μg/L, there was an 83% probability for elevated incidence of bladder cancer; and a 74% probability for elevated mortality. For both bladder and kidney cancers, mortality rates at 150 ug/L were about 30% greater than those at 10 μg/L.ConclusionArsenic in drinking water is associated with an increased risk of bladder and kidney cancers, although at lower levels (<150 μg/L), there is uncertainty due to the increased likelihood of exposure misclassification at the lower end of the exposure curve. Meta-analyses suggest exposure to 10 μg/L of arsenic in drinking water may double the risk of bladder cancer, or at the very least, increase it by about 40%. With the large number of people exposed to these arsenic concentrations worldwide the public health consequences of arsenic in drinking water are substantial.

A prospective cohort study of the association between drinking water arsenic exposure and self-reported maternal health symptoms during pregnancy in Bangladesh.

BackgroundArsenic, a common groundwater pollutant, is associated with adverse reproductive health but few studies have examined its effect on maternal health.MethodsA prospective cohort was recruited in Bangladesh from 2008–2011 (N = 1,458). At enrollment (<16 weeks gestational age [WGA]), arsenic was measured in personal drinking water using inductively-coupled plasma mass spectrometry. Questionnaires collected health data at enrollment, at 28 WGA, and within one month of delivery. Adjusted odds ratios (aORs) and 95% confidence intervals (95% CI) for self-reported health symptoms were estimated for each arsenic quartile using logistic regression.ResultsOverall, the mean concentration of arsenic was 38 μg/L (Standard deviation, 92.7 μg/L). A total of 795 women reported one or more of the following symptoms during pregnancy (cold/flu/infection, nausea/vomiting, abdominal cramping, headache, vaginal bleeding, or swollen ankles). Compared to participants exposed to the lowest quartile of arsenic (≤0.9 μg/L), the aOR for reporting any symptom during pregnancy was 0.62 (95% CI = 0.44-0.88) in the second quartile, 1.83 (95% CI = 1.25-2.69) in the third quartile, and 2.11 (95% CI = 1.42-3.13) in the fourth quartile where the mean arsenic concentration in each quartile was 1.5 μg/L, 12.0 μg/L and 144.7 μg/L, respectively. Upon examining individual symptoms, only nausea/vomiting and abdominal cramping showed consistent associations with arsenic exposure. The odds of self-reported nausea/vomiting was 0.98 (95% CI: 0.68, 1.41), 1.52 (95% CI: 1.05, 2.18), and 1.81 (95% CI: 1.26, 2.60) in the second, third and fourth quartile of arsenic relative to the lowest quartile after adjusting for age, body mass index, second-hand tobacco smoke exposure, educational status, parity, anemia, ferritin, medication usage, type of sanitation at home, and household income. A positive trend was also observed for abdominal cramping (P for trend <0.0001). A marginal negative association was observed between arsenic quartiles and odds of self-reported cold/flu/infection (P for trend = 0.08). No association was observed between arsenic and self-reported headache (P for trend = 0.19).ConclusionModerate exposure to arsenic contaminated drinking water early in pregnancy was associated with increased odds of experiencing nausea/vomiting and abdominal cramping. Preventing exposure to arsenic contaminated drinking water during pregnancy could improve maternal health.

What is the role of obesity in the aetiology of arsenic-related disease?

Consumption of arsenic contaminated drinking water causes a large variety of adverse health outcomes. Body mass index (BMI), which is linked to diet, is positively associated with arsenic methylation capacity. We investigated the association between an obesity-related diet and arsenic body burden from exposure to naturally contaminated drinking water among Nova Scotia residents. We collected home drinking water and toenail clipping samples among 960 men and women aged 35 to 69years in Nova Scotia, Canada from 2009 through 2010. We measured body composition and arsenic concentrations in drinking water and toenails clipping samples and collected socio-demographic, behavioural, and dietary information via standardized questionnaires. We derived an obesity-related dietary pattern score using reduced rank regression. Across quartiles of the obesity-related dietary pattern score there were no significant differences in drinking water arsenic concentrations, but there was an inverse trend in arsenic concentrations in toenails across the dietary pattern score (P=0.01). Compared with individuals in the first quartile of the dietary pattern score, those in the second through fourth quartiles had decreased likelihoods of high toenail arsenic (≥85 percentile). The corresponding odds ratios (95% confidence intervals [CI]) were 0.81 (95% CI, 0.49, 1.36), 0.57 (95% CI, 0.33, 0.99), and 0.55 (95% CI, 0.31, 0.98), respectively (P for trend=0.02). We conclude that given similar levels of naturally occurring arsenic exposure via drinking water, an obesity-related dietary pattern was associated with significantly lower arsenic concentrations in toenails. Further studies to investigate the underlining mechanisms are warranted.

Effect of prenatal arsenic exposure on DNA methylation and leukocyte subpopulations in cord blood

Prenatal arsenic exposure is associated with increased risk of disease in adulthood. This has led to considerable interest in arsenic’s ability to disrupt fetal programming. Many studies report that arsenic exposure alters DNA methylation in whole blood but these studies did not adjust for cell mixture. In this study, we examined the relationship between arsenic in maternal drinking water collected ≤ 16 weeks gestational age and DNA methylation in cord blood (n = 44) adjusting for leukocyte-tagged differentially methylated regions. DNA methylation was quantified using the Infinium HumanMethylation 450 BeadChip array. Recursively partitioned mixture modeling examined the relationship between arsenic and methylation at 473,844 CpG sites. Median arsenic concentration in water was 12 µg/L (range < 1- 510 µg/L). Log10 arsenic was associated with altered DNA methylation across the epigenome (P = 0.002); however, adjusting for leukocyte distributions attenuated this association (P = 0.013). We also observed that arsenic had a strong effect on the distribution of leukocytes in cord blood. In adjusted models, every log10 increase in maternal drinking water arsenic exposure was estimated to increase CD8+ T cells by 7.4% (P = 0.0004) and decrease in CD4+ T cells by 9.2% (P = 0.0002). These results show that prenatal exposure to arsenic had an exposure-dependent effect on specific T cell subpopulations in cord blood and altered DNA methylation in cord blood. Future research is needed to determine if these small changes in DNA methylation alter gene expression or are associated with adverse health effects.

Environmental arsenic exposure and microbiota in induced sputum.

Arsenic exposure from drinking water is associated with adverse respiratory outcomes, but it is unknown whether arsenic affects pulmonary microbiota. This exploratory study assessed the effect of exposure to arsenic in drinking water on bacterial diversity in the respiratory tract of non-smokers. Induced sputum was collected from 10 subjects with moderate mean household water arsenic concentration (21.1 ± 6.4 ppb) and 10 subjects with low household water arsenic (2.4 ± 0.8 ppb). To assess microbiota in sputum, the V6 hypervariable region amplicons of bacterial 16s rRNA genes were sequenced using the Ion Torrent Personal Genome Machine. Microbial community differences between arsenic exposure groups were evaluated using QIIME and Metastats. A total of 3,920,441 sequence reads, ranging from 37,935 to 508,787 per sample for 316 chips after QIIME quality filtering, were taxonomically classified into 142 individual genera and five phyla. Firmicutes (22%), Proteobacteria (17%) and Bacteriodetes (12%) were the main phyla in all samples, with Neisseriaceae (15%), Prevotellaceae (12%) and Veillonellacea (7%) being most common at the genus level. Some genera, including Gemella, Lactobacillales, Streptococcus, Neisseria and Pasteurellaceae were elevated in the moderate arsenic exposure group, while Rothia, Prevotella, Prevotellaceae Fusobacterium and Neisseriaceae were decreased, although none of these differences was statistically significant. Future studies with more participants and a greater range of arsenic exposure are needed to further elucidate the effects of drinking water arsenic consumption on respiratory microbiota.

Relationship between drinking water and toenail arsenic concentrations among a cohort of Nova Scotians

Consumption of arsenic-contaminated drinking water is associated with increased cancer risk. The relationship between arsenic body burden, such as concentrations in human toenails, and arsenic in drinking water is not fully understood. We evaluated the relationship between arsenic concentrations in drinking water and toenail clippings among a cohort of Nova Scotians. A total of 960 men and women aged 35 to 69 years provided home drinking water and toenail clipping samples. Information on water source and treatment use and covariables was collected through questionnaires. Arsenic concentrations in drinking water and toenail clippings and anthropometric indices were measured. Private drilled water wells had higher arsenic concentrations compared with other dug wells and municipal drinking water sources (P<0.001). Among participants with drinking water arsenic levels ≥1 μg/l, there was a significant relationship between drinking water and toenail arsenic concentrations (r=0.46, P<0.0001). Given similar levels of arsenic exposure from drinking water, obese individuals had significantly lower concentrations of arsenic in toenails compared with those with a normal weight. Private drilled water wells were an important source of arsenic exposure in the study population. Body weight modifies the relationship between drinking water arsenic exposure and toenail arsenic concentrations.

Arsenic methylation and lung and bladder cancer in a case-control study in northern Chile

In humans, ingested inorganic arsenic is metabolized to monomethylarsenic (MMA) then to dimethylarsenic (DMA), although this process is not complete in most people. The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases. To date, however, relatively little is known about its role in lung cancer, the most common cause of arsenic-related death, or about its impacts on people drinking water with lower arsenic concentrations (e.g., <200μg/L). In this study, urinary arsenic metabolites were measured in 94 lung and 117 bladder cancer cases and 347 population-based controls from areas in northern Chile with a wide range of drinking water arsenic concentrations. Lung cancer odds ratios adjusted for age, sex, and smoking by increasing tertiles of %MMA were 1.00, 1.91 (95% confidence interval (CI), 0.99–3.67), and 3.26 (1.76–6.04) (p-trend <0.001). Corresponding odds ratios for bladder cancer were 1.00, 1.81 (1.06–3.11), and 2.02 (1.15–3.54) (p-trend <0.001). In analyses confined to subjects only with arsenic water concentrations <200μg/L (median=60μg/L), lung and bladder cancer odds ratios for subjects in the upper tertile of %MMA compared to subjects in the lower two tertiles were 2.48 (1.08–5.68) and 2.37 (1.01–5.57), respectively. Overall, these findings provide evidence that inter-individual differences in arsenic metabolism may be an important risk factor for arsenic-related lung cancer, and may play a role in cancer risks among people exposed to relatively low arsenic water concentrations.