Arsenic Concentrations In Drinking Water Research Articles

Arsenic exposure and measures of glucose tolerance in Bangladeshi adults: A cross-sectional study.

Arsenic has been associated with diabetes and impaired glucose tolerance in many studies, although some reports have shown null findings. We conducted a cross-sectional study among 300 adults in Bangladesh. Participants were randomly selected from a roster of 1800 people who previously participated in studies of arsenic and skin lesions. We measured fasting glucose and insulin levels. We assessed drinking water arsenic concentration using graphite furnace atomic absorption spectrophotometry (GF-AAS) and toenail arsenic concentration using inductively coupled mass spectrometry (ICP-MS). We ran covariant-adjusted, linear regression and spline models to examine associations of arsenic concentrations with the homeostatic model assessment of insulin resistance (HOMA-IR), a marker of insulin resistance, and HOMA of beta-cell function (HOMA-β), a marker of beta-cell function. Among 285 participants with complete data, the median (IQR) arsenic concentration was 4.0 (6.9) μg/g in toenails and 39.0 (188.5) μg/L in drinking water. Arsenic concentrations were not associated with insulin resistance or beta-cell function. HOMA-IR was 0.67% lower and HOMA-β was 0.28% lower per µg/g increment in toenail arsenic, but these effect estimates were small, and confidence intervals crossed the null value. Although arsenic exposure has been associated with diabetes, we found no evidence of an adverse effect on insulin resistance or beta-cell function.

Relations between personal exposure to elevated concentrations of arsenic in water and soil and blood arsenic levels amongst people living in rural areas in Limpopo, South Africa

Exposure to arsenic even at low levels can lead to adverse health outcomes, however, there is a paucity of research from South Africa in relation to human exposure to arsenic. We investigated long-term exposure of residents in Limpopo province, South Africa, in a cross-sectional study by analysing water, soil and blood arsenic concentrations from two arsenic-exposed (high and medium–low exposure) villages and one non-exposed (control) village. There were statistically significant differences in the distribution of arsenic in water, soil and blood amongst the three sites. The median drinking water arsenic concentration in the high-exposure village was 1.75 µg/L (range = 0.02 to 81.30 µg/L), 0.45 µg/L (range = 0.100 to 6.00 µg/L) in the medium- / low-exposure village and 0.15 µg/L (range = < limit of detection (LOD) to 29.30 µg/L) in the control site. The median soil arsenic concentration in the high-exposure village was 23.91 mg/kg (range = < LOD to 92.10 mg/kg) whilst arsenic concentrations were below the limit of detection in all soil samples collected from the medium-/low-exposure and control villages. In the high-exposure village, the median blood arsenic concentration was 1.6 µg/L (range = 0.7 to 4.2 µg/L); 0.90 µg/L (range = < LOD to 2.5 µg/L) in the medium-/low-exposure village and 0.6 µg/L (range = < LOD to 3.3 µg/L) in the control village. Significant percentages of drinking water, soil and blood samples from the exposed sites were above the internationally recommended guidelines (namely, 10 µg/L, 20 mg/kg and 1 µg/L, respectively). Majority of participants (86%) relied on borehole water for drinking and there was a significant positive correlation between arsenic in blood and borehole water (p-value = 0.031). There was also a statistically significant correlation between arsenic concentrations in participants’ blood and soil samples collected from gardens (p-value = 0.051). Univariate quantile regression found that blood arsenic concentrations increased by 0.034 µg/L (95% CI = 0.02–0.05) for each one unit increase in water arsenic concentrations (p < 0.001). After adjusting for age, water source and homegrown vegetable consumption in multivariate quantile regression, participants from the high-exposure site had significantly higher blood concentrations than those in the control site (coefficient: 1.00; 95% CI = 0.25–1.74; p-value = 0.009) demonstrating that blood arsenic is a good biomarker of arsenic exposure. Our findings also provide new evidence for South Africa on the association between drinking water and arsenic exposure, emphasising the need for the provision of potable water for human consumption in areas with high environmental arsenic concentrations.

The impact of prenatal and early-life arsenic exposure on epigenetic age acceleration among adults in Northern Chile.

Exposure to arsenic affects millions of people globally. Changes in the epigenome may be involved in pathways linking arsenic to health or serve as biomarkers of exposure. This study investigated associations between prenatal and early-life arsenic exposure and epigenetic age acceleration (EAA) in adults, a biomarker of morbidity and mortality. DNA methylation was measured in peripheral blood mononuclear cells (PBMCs) and buccal cells from 40 adults (median age = 49 years) in Chile with and without high prenatal and early-life arsenic exposure. EAA was calculated using the Horvath, Hannum, PhenoAge, skin and blood, GrimAge, and DNA methylation telomere length clocks. We evaluated associations between arsenic exposure and EAA using robust linear models. Participants classified as with and without arsenic exposure had a median drinking water arsenic concentration at birth of 555 and 2 μg/l, respectively. In PBMCs, adjusting for sex and smoking, exposure was associated with a 6-year PhenoAge acceleration [B (95% CI) = 6.01 (2.60, 9.42)]. After adjusting for cell-type composition, we found positive associations with Hannum EAA [B (95% CI) = 3.11 (0.13, 6.10)], skin and blood EAA [B (95% CI) = 1.77 (0.51, 3.03)], and extrinsic EAA [B (95% CI) = 4.90 (1.22, 8.57)]. The association with PhenoAge acceleration in buccal cells was positive but not statistically significant [B (95% CI) = 4.88 (−1.60, 11.36)]. Arsenic exposure limited to early-life stages may be associated with biological aging in adulthood. Future research may provide information on how EAA programmed in early life is related to health.

Ambient UVR and Environmental Arsenic Exposure in Relation to Cutaneous Melanoma in Iowa.

Intermittent sun exposure is the major environmental risk factor for cutaneous melanoma (CM). Cumulative sun exposure and other environmental agents, such as environmental arsenic exposure, have not shown consistent associations. Ambient ultraviolet radiation (UVR) was used to measure individual total sun exposure as this is thought to be less prone to misclassification and recall bias. Data were analyzed from 1096 CM cases and 1033 controls in the Iowa Study of Skin Cancer and Its Causes, a population-based, case-control study. Self-reported residential histories were linked to satellite-derived ambient UVR, spatially derived environmental soil arsenic concentration, and drinking water arsenic concentrations. In men and women, ambient UVR during childhood and adolescence was not associated with CM but was positively associated during adulthood. Lifetime ambient UVR was positively associated with CM in men (OR for highest vs. lowest quartile: 6.09, 95% confidence interval (CI) 2.21–16.8), but this association was not as strong among women (OR for highest vs. lowest quartile: 2.15, 95% CI 0.84–5.54). No association was detected for environmental soil or drinking water arsenic concentrations and CM. Our findings suggest that lifetime and adulthood sun exposures may be important risk factors for CM.

Arsenic Secondary Methylation Capacity Is Inversely Associated with Arsenic Exposure-Related Muscle Mass Reduction.

Skeletal muscle mass reduction has been implicated in insulin resistance (IR) that promotes cardiometabolic diseases. We have previously reported that arsenic exposure increases IR concomitantly with the reduction of skeletal muscle mass among individuals exposed to arsenic. The arsenic methylation capacity is linked to the susceptibility to some arsenic exposure-related diseases. However, it remains unknown whether the arsenic methylation capacity affects the arsenic-induced reduction of muscle mass and elevation of IR. Therefore, this study examined the associations between the arsenic methylation status and skeletal muscle mass measures with regard to IR by recruiting 437 participants from low- and high-arsenic exposure areas in Bangladesh. The subjects’ skeletal muscle mass was estimated by their lean body mass (LBM) and serum creatinine levels. Subjects’ drinking water arsenic concentrations were positively associated with total urinary arsenic concentrations and the percentages of MMA, as well as inversely associated with the percentages of DMA and the secondary methylation index (SMI). Subjects’ LBM and serum creatinine levels were positively associated with the percentage of DMA and SMI, as well as inversely associated with the percentage of MMA. HOMA-IR showed an inverse association with SMI, with a confounding effect of sex. Our results suggest that reduced secondary methylation capacity is involved in the arsenic-induced skeletal muscle loss that may be implicated in arsenic-induced IR and cardiometabolic diseases.

Chlorination by-products in drinking water and risk of bladder cancer – a population-based cohort study

BACKGROUND AND AIM: Exposure to chlorination by-products has been consistently associated with an increased risk of bladder cancer in case-control studies, but confirmation from large-scale cohort studies are lacking. We assessed the association of drinking water trihalomethanes (THM), a surrogate for chlorination by-products, with risk of bladder cancer in 58,672 men and women in two population-based cohorts. METHODS: We used data, including questionnaire information, from the Swedish Infrastructure for Medical Population-Based Life-Course and Environmental Research (SIMPLER). Individual exposure to THM was assessed by combining residential information from register with municipal THM monitoring data. Participants were categorized into no chlorination, low (15 µg/L) or high (15 µg/L) THM exposure dependent on their area of residence. Incident bladder cancer cases were ascertained from 1998 through 2019 via register linkage. Associations were examined using multivariable-adjusted Cox proportional hazards regression models, including information on smoking habits and drinking water arsenic concentrations. RESULTS:The mean THM concentration was 6.6 ± 2.2 µg/L and 17.1 ± 2.1 µg/L in the low and the high exposure category, respectively. During a mean follow-up of 16 years (965,590 person-years), 831 bladder cancer cases were ascertained. We observed no overall association of THM with risk of bladder cancer. The hazard ratio was 0.90 (95% confidence interval: 0.73 – 1.11) when comparing the highest exposed group with those in the non-chlorinated areas. The null association remained after restricting the analysis to long-term residents and across strata of smoking status and cancer stage. CONCLUSIONS:Our results suggest that at THM concentrations below 20 µg/L, which is representative of chlorinated drinking waters in most European countries, chlorination by-product exposure is not associated with risk of bladder cancer. KEYWORDS: Chlorination by-products, Disinfection by-products, Trihalomethanes, Bladder cancer, Water quality, Drinking water

Arsenic in US correctional facility drinking water, 2006-2011

Background: Very little is known about the quality of drinking water in US correctional facilities (e.g. detention centers, prisons, jails, etc.), which disproportionately detain people of color. The current Environmental Protection Agency’s maximum contaminant level (MCL) for arsenic in public drinking water is 10 µg/L. We estimated drinking water arsenic concentrations in US correctional facilities to determine if incarcerated persons remain at risk for chronic, elevated water arsenic exposure relative to the non-incarcerated US population.Methods: We obtained 230,158 arsenic monitoring records for 37,098 community water systems (CWSs) from the Environmental Protection Agency’s Third Six Year Review of Contaminant Occurrence dataset (covering 2006-2011). We compared six-year average arsenic concentrations in all CWSs versus CWSs exclusively serving correctional facilities. We separately evaluated the Southwestern US (where groundwater arsenic concentrations are relatively high) versus non-Southwestern US.Results: Average six-year water arsenic concentrations were higher for CWSs exclusively serving correctional facilities in the Southwest (6.41 µg/L, 95% CI 3.48, 9.34) compared to all other Southwestern CWSs (3.11 µg/L, 95% CI 2.97, 3.24) and to other CWSs across the rest of the US (1.39 µg/L, 95% CI 1.35, 1.42). Compared to other US CWSs and to other Southwestern CWSs, correctional facility CWSs in the Southwest were more likely to report six-year arsenic averages exceeding 10 µg/L (1.6%, 5.8%, and 26.1% of systems, respectively).Conclusions: CWSs exclusively serving correctional facilities in the Southwestern US reported average water arsenic concentrations twice as high as those reported by all other CWSs in the Southwest, and more than a quarter reported six-year averages exceeding the EPA’s regulatory MCL. Strict enforcement of the EPA’s drinking water regulations and a comprehensive review of other drinking water contaminants in CWSs serving correctional facilities is necessary to protect the health and human rights of all incarcerated persons in the US.

Arsenic and Immune Response to Influenza Vaccination in Pregnant Women and Newborns

Background/AimsThere is a gap in understanding of whether arsenic exposure during pregnancy alters the maternal immune response and antibody transfer to the infant. We aimed to establish a birth cohort in a region with low-moderate drinking water arsenic concentrations to investigate the relationship between arsenic exposure and immunogenicity of a seasonal quadrivalent inactivated influenza vaccine (IIV) in pregnant women and infants.MethodsWe established a birth cohort (NCT03930017) at the JiVitA Maternal and Child Health and Nutrition Research Project site, which covers ~650,000 people over 500 km2 in rural northern Bangladesh. We planned to enroll 850 pregnancies to achieve a desired sample size of 400 mother-infant pairs at three-months postpartum, based on minimum detectable differences in geometric mean hemagglutination inhibition antibody titers for seasonal quadrivalent IIV antigens when comparing the highest and lowest quartiles of arsenic exposure. From July 2018 to June 2019, we screened women of reproductive age to identify incident pregnancies. Multiparous pregnant women were enrolled in gestational weeks (GW) 13-16. At enrollment, we collected drinking water, urine, blood, and saliva, and administered IIV.ResultsWe screened 52,000 women to identify 2,623 incident pregnancies in multiparous women. Of these, 1,338 were identified prior to GW 16, 846 consented, and 784 enrolled. We followed 567 mother-infant pairs to three-months postpartum. At enrollment, all participants contributed drinking water, urine, blood (processed as plasma, serum, and peripheral blood mononuclear cells), and saliva. An analysis of 40 drinking water samples selected at random found that arsenic concentrations were comparable to arsenic-endemic regions of the U.S. (geometric mean: 3.03 µg/L, geometric standard deviation: 9.54 µg/L, range: 0.05 to 96.83 µg/L).ConclusionsThe number of pregnancies enrolled in our cohort yielded the sample size needed to investigate prespecified aims related to low-moderate arsenic exposure and altered maternal and child immune response.

Determinants of arsenic methylation efficiency and urinary arsenic level in pregnant women in Bangladesh

BackgroundPrenatal inorganic arsenic (iAs) exposure is associated with pregnancy outcomes. Maternal capabilities of arsenic biotransformation and elimination may influence the susceptibility of arsenic toxicity. Therefore, we examined the determinants of arsenic metabolism of pregnant women in Bangladesh who are exposed to high levels of arsenic.MethodsIn a prospective birth cohort, we followed 1613 pregnant women in Bangladesh and collected urine samples at two prenatal visits: one at 4–16 weeks, and the second at 21–37 weeks of pregnancy. We measured major arsenic species in urine, including iAs (iAs%) and methylated forms. The proportions of each species over the sum of all arsenic species were used as biomarkers of arsenic methylation efficiency. We examined the difference in arsenic methylation using a paired t-test between first and second visits. Using linear regression, we examined determinants of arsenic metabolism, including age, BMI at enrollment, education, financial provider income, arsenic exposure level, and dietary folate and protein intake, adjusted for daily energy intake.ResultsComparing visit 2 to visit 1, iAs% decreased 1.1% (p < 0.01), and creatinine-adjusted urinary arsenic level (U-As) increased 21% (95% CI: 15, 26%; p < 0.01). Drinking water arsenic concentration was positively associated with iAs% at both visits. When restricted to participants with higher adjusted urinary arsenic levels (adjusted U-As > 50 μg/g-creatinine) gestational age at measurement was strongly associated with DMA% (β = 0.38, p < 0.01) only at visit 1. Additionally, DMA% was negatively associated with daily protein intake (β = − 0.02, p < 0.01) at visit 1, adjusting for total energy intake and other covariates.ConclusionsOur findings indicate that arsenic metabolism and adjusted U-As level increase during pregnancy. We have identified determinants of arsenic methylation efficiency at visit 1.

Arsenic exposure and serum antibody concentrations to diphtheria and tetanus toxoid in children at age 5: A prospective birth cohort in Bangladesh

BackgroundArsenic can impair immune function. Timing of exposure can influence potential immunotoxicity of arsenic exposure. We examined the association between drinking water arsenic concentrations (W-As) measured repeatedly during different exposure windows in early life and serum concentrations of IgG antibodies against diphtheria and tetanus toxoids (diphtheria and tetanus antibody). MethodsA prospective cohort of pregnant women was recruited in Bangladesh (2008–2011). Averaged W-As levels were calculated for: pregnancy (W-Aspregnancy): ≤16 weeks gestation and <1 month; toddlerhood (W-Astoddlerhood): 12 and 20–40 months; and early childhood (W-Aschildhood): 4–5 years. Serum was collected from 502 vaccinated children at age 5 and concentrations of diphtheria and tetanus toxoid IgG (i.e. antibody) were quantified. Antibody concentrations >0.1 IU/mL were considered clinically sufficient for protection. Associations were estimated using linear and logistic regression models. ResultsInverse associations were observed between W-Aspregnancy and serum diphtheria antibody levels, while null associations were observed between W-As and tetanus antibody. Children within the highest versus lowest tertile of W-Aspregnancy had 91% greater odds of having clinically insufficient concentrations of diphtheria antibody (Odds ratio:1.91, 95% confidence interval (CI): 1.03, 3.56). Among females, a doubling in W-Aspregnancy was associated with 12.3% (95%CI: −20.1%, −4.5%) lower median concentrations of diphtheria antibody. Tetanus antibody was only associated with W-Aspregnancy among females (percent change in median: −9.5%, 95%CI: −17.6%, −1.3%). Among children who were stunted or underweight, a doubling in W-Aspregnancy was associated with decreased diphtheria antibody of 19.8% (95%CI: −32%, −7.5%) and 14.3% (95%CI: −26.7%, −2%), respectively. ConclusionsAmong vaccinated children, W-As measured during pregnancy was associated with decreased diphtheria antibody levels, but not tetanus antibody. However, W-As measured during toddlerhood and early childhood were not associated with either antibody outcome. Children's sex and malnutrition status were important effect modifiers of W-As for both diphtheria and tetanus antibody levels, highlighting the importance of these factors and the timing of the exposure when evaluating the effect of arsenic on humoral immunity.

Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

BackgroundMore than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW).Participants and methodsA cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW.ResultsResidents with ACDW ≥ 10 parts per billion (ppb) had experienced a “feeling of weakness” and “chronic numbness or pain” significantly more often than those with ACDW < 10 ppb. Residents with ACDW ≥ 50 ppb had three types of sensory disturbances significantly more often than those with ACDW < 50 ppb. In children, there was no significant association between symptoms or signs and ACDW.ConclusionSubjective symptoms, probably due to peripheral neuropathy, occurred at very low ACDW (around 10 ppb). Objective peripheral nerve disturbances of both small and large fibers occurred at low ACDW (> 50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health.

Arsenic exposure through drinking Water and oxidative stress Status: A cross-sectional study in the Ayeyarwady region, Myanmar

Arsenic is a well-known toxic heavy metal that is naturally dispersed in groundwater. Whereas arsenic is widely accepted to be involved in oxidative stress damage, little is known about arsenic-induced oxidative damage in relationship to contaminated drinking water as a source. The aim of this study was to determine the association between arsenic exposure through drinking water and oxidative stress status by measuring levels of urinary 8-hydroxydeoxyguanosine (8−OHdG) as a biomarker of oxidative stress damage in a Myanmar population. A questionnaire-based survey and drinking water and urine sampling (n = 198) were performed to assess the association between arsenic exposure and urinary 8−OHdG concentration in the Ayeyarwady Region, Myanmar. Urinary arsenic concentrations were significantly correlated with drinking water arsenic concentrations (Spearman’s rho = 0.32, p < 0.001). Multivariate linear regression analysis showed that higher urinary arsenic concentrations were significantly associated with higher 8−OHdG concentrations (coefficient = 0.09, 95% confidence interval, 0.03 – 0.15; p = 0.002). The present study identified that exposure to arsenic through drinking water could induce an increase in the urinary 8−OHdG concentration, reflecting increased oxidative DNA damage. These findings provide evidence that may explain the role of arsenic-induced oxidative stress in the pathophysiology of arsenic-induced diseases including cancers.

A Prospective Cohort Study Examining the Associations of Maternal Arsenic Exposure With Fetal Loss and Neonatal Mortality.

Arsenic crosses the placenta, possibly increasing the risk of adverse reproductive outcomes. We aimed to examine the association between maternal arsenic exposure and fetal/neonatal survival using data from a prospective cohort study of 1,616 maternal-infant pairs recruited at a gestational age of ≤16 weeks in Bangladesh (2008-2011). Arsenic concentration in maternal drinking water was measured at enrollment. Extended Cox regression (both time-dependent coefficients and step functions) was used to estimate the time-varying association between maternal arsenic exposure and fetal/neonatal death (all mortality between enrollment and 1 month after birth). In a sensitivity analysis, we assessed gestational arsenic exposure using maternal urine samples taken at enrollment. We observed 203 fetal losses and 20 neonatal deaths. Higher arsenic exposure was associated with a slightly decreased mortality rate up to the middle of the second trimester, and then the mortality rate switched directions around 20 weeks' gestation. In the step function model, the hazard ratios for combined mortality (fetal loss and neonatal death) per unit increase in the natural log of drinking water arsenic concentration (μg/L) ranged from 1.35 (95% CI: 1.08, 1.69) in weeks 25-28 to 0.81 (95% CI: 0.65, 1.02) in weeks 9-12. This nonlinear association suggests that arsenic may exert survival pressure on developing fetuses, potentially contributing to survival bias, and may also indicate that arsenic toxicity differs by fetal developmental stage.

Association between Serum Anti-Diphtheria Toxoid Antibodies and Drinking Water Arsenic Exposure in a Prospective Birth Cohort in Rural Bangladesh

Background. There is evidence that arsenic exposure in early life modulates humoral immunity.Objective. We examined the association between drinking water arsenic concentrations to diphtheria vaccine-antibody concentrations measured at age 5.Methods. A prospective cohort of pregnant women was recruited in Bangladesh (2008-2011). Drinking water arsenic was measured at &amp;#8804;16 weeks gestation, &amp;lt;1 month birth, between ages 20 to 40 months, and between ages 4 to 5 years, in a total of 510 children. Serum was collected from children at age 5. Concentrations of anti-diphtheria toxoid IgG antibody were quantified using enzyme linked immunosorbent assays. Antibody concentrations below 0.1 IU/mL were considered insufficient for long-term clinical protection. Linear and logistic regression models assessed the association between vaccine antibody and arsenic concentrations.Results. We found negative associations between arsenic exposure and concentrations of vaccine antibodies. The largest effects occurred with exposures measured during the in utero and neonatal periods. A 1-unit increase in natural log maternal water arsenic at &amp;#8804;16 weeks gestation was associated with 9.9% greater odds of insufficient clinical titers of anti-diphtheria antibody compared to being clinically protected (Odds Ratio(OR): 1.10, 95% confidence interval(CI): 1.00, 1.21). After adjusting for paternal income, maternal education, breastfeeding duration, birth type, sex, child age, and BMI at blood draw, this association was attenuated where a 1-unit increase in natural log maternal drinking water arsenic at &amp;#8804;16 weeks gestation was associated with a 4.3% greater odds of insufficient clinical titers of diphtheria antibody compared to being clinically protected (OR: 1.04, CI: 0.93, 1.17).Conclusion. This study provides preliminary evidence early life arsenic exposure is associated with a decreased likelihood of clinically protective levels of serum antibody to diphtheria, despite appropriate immunization.

Early Life Arsenic Exposure and Non-Malignant Respiratory Illnesses among Adolescents in Rural Bangladesh

Background/Aim: Evidence suggests that exposure to arsenic through drinking water increases the risk of non-malignant respiratory illnesses including impairment of lung function in adults. However, early life arsenic exposure and subsequent respiratory system effects in adolescents have not been reported so far. Methods: The study was conducted in rural Bangladesh, Matlab. A cohort of 200 children now aged 11-22 years were enrolled of which 107 had in utero and early childhood (first five years) exposure to drinking water arsenic concentration over 400µg/L (exposed group) and 93 had less than 10 µg/L (unexposed group). Histories of respiratory symptoms were collected through a validated structured questionnaire (ISAAC). Lung function (FEV1, FVC) was tested by EasyOne spirometry following the standard American Thoracic Society criteria. Water arsenic concentrations were measured by hydride generation atomic absorption spectrophotometry. Results: The mean age was 15 years. Chronic respiratory symptoms were evident in male participants in the exposed group. In an adjusted model, boys with in early life arsenic exposure (&gt;400 µg/L) were more likely to report wheezing attacks 1-3 times/week (Prevalence Odds Ratio (POR): 4.99, 95% Confidence Interval (CI): 1.00-24.9), wheezing after exercise (POR: 4.14, 95% CI: 1.05-16.4) and waking up with chest tightness (POR: 5.01, 95% CI: 1.00-25.0). Decrease in FEV1 (-117.3 ml, CI: -246.5, 11.8) and FVC (-135.2 ml, CI: -269.9, -0.37) were observed in male respondents in the exposed group compared to the unexposed. No respiratory impairment was observed among exposed girls. Conclusions: High exposure to arsenic in utero and early childhood may result in increased risk of chronic respiratory symptoms and decrements in lung function in adolescent males. We plan to follow this unique cohort further to see if early life arsenic exposure respiratory effects persist in males as they grow older, and remain absent in females.

Assessment of Nutritional Status of Infants Living in Arsenic-Contaminated Areas in Bangladesh and Its Association with Arsenic Exposure.

Data is scarce on early life exposure to arsenic and its association with malnutrition during infancy. This study followed the nutritional status of a cohort of 120 infants from birth to 9 months of age in an arsenic contaminated area in Bangladesh. Anthropometric data was collected at 3, 6 and 9 months of the infant’s age for nutritional assessment whereas arsenic exposure level was assessed via tube well drinking water arsenic concentration at the initiation of the study. Weight and height measurements were converted to Z-scores of weight for age (WAZ-underweight), height for age (HAZ-stunting), weight for height (WHZ-wasting) for children by comparing with WHO growth standard. Arsenic exposure levels were categorized as <50 μg/L and ≥50 μg/L. Stunting rates (<−2 SD) were 10% at 3 months and 44% at both 6 and 9 months. Wasting rates (<−2 SD) were 23.3% at 3 months and underweight rates (<−2 SD) were 25% and 10% at 3 and 6 months of age, respectively. There was a significant association of stunting with household drinking water arsenic exposure ≥50 μg/L at age of 9 months (p = 0.009). Except for stunting at 9 months of age, we did not find any significant changes in other nutritional indices over time or with levels of household arsenic exposure in this study. Our study suggests no association between household arsenic exposure and under-nutrition during infancy; with limiting factors being small sample size and short follow-up. Difference in stunting at 9 months by arsenic exposure at ≥50 μg/L might be a statistical incongruity. Further longitudinal studies are warranted to establish any association.

Quantitative drinking water arsenic concentrations in field environments using mobile phone photometry of field kits

Arsenic (As) groundwater contamination is common yet spatially heterogeneous within most environments. It is therefore necessary to measure As concentrations to determine whether a water source is safe to drink. Measurement of As in the field involves using a test strip that changes color in the presence of As. These tests are relatively inexpensive, but results are subjective and provide binned categorical data rather than exact determinations of As concentration. The goal of this work was to determine if photos of field kit test strips taken on mobile phone cameras could be used to extract more precise, continuous As concentrations. As concentrations for 376 wells sampled from Araihazar, Bangladesh were analyzed using ICP-MS, field kit and the new mobile phone photo method. Results from the field and lab indicate that normalized RGB color data extracted from images were able to accurately predict As concentrations as measured by ICP-MS, achieving detection limits of 9.2μg/L, and 21.9μg/L for the lab and field respectively. Data analysis is most consistent in the laboratory, but can successfully be carried out offline following image analysis, or on the mobile phone using basic image analysis software. The accuracy of the field method was limited by variability in image saturation, and variation in the illumination spectrum (lighting) and camera response. This work indicates that mobile phone cameras can be used as an analytical tool for quantitative measures of As and could change how water samples are analyzed in the field more widely, and that modest improvements in the consistency of photographic image collection and processing could yield measurements that are both accurate and precise.

Benchmark Dose Modeling Estimates of the Concentrations of Inorganic Arsenic That Induce Changes to the Neonatal Transcriptome, Proteome, and Epigenome in a Pregnancy Cohort.

Prenatal inorganic arsenic (iAs) exposure influences the expression of critical genes and proteins associated with adverse outcomes in newborns, in part through epigenetic mediators. The doses at which these genomic and epigenomic changes occur have yet to be evaluated in the context of dose-response modeling. The goal of the present study was to estimate iAs doses that correspond to changes in transcriptomic, proteomic, epigenomic, and integrated multi-omic signatures in human cord blood through benchmark dose (BMD) modeling. Genome-wide DNA methylation, microRNA expression, mRNA expression, and protein expression levels in cord blood were modeled against total urinary arsenic (U-tAs) levels from pregnant women exposed to varying levels of iAs. Dose-response relationships were modeled in BMDExpress, and BMDs representing 10% response levels were estimated. Overall, DNA methylation changes were estimated to occur at lower exposure concentrations in comparison to other molecular endpoints. Multi-omic module eigengenes were derived through weighted gene co-expression network analysis, representing co-modulated signatures across transcriptomic, proteomic, and epigenomic profiles. One module eigengene was associated with decreased gestational age occurring alongside increased iAs exposure. Genes/proteins within this module eigengene showed enrichment for organismal development, including potassium voltage-gated channel subfamily Q member 1 (KCNQ1), an imprinted gene showing differential methylation and expression in response to iAs. Modeling of this prioritized multi-omic module eigengene resulted in a BMD(BMDL) of 58(45) μg/L U-tAs, which was estimated to correspond to drinking water arsenic concentrations of 51(40) μg/L. Results are in line with epidemiological evidence supporting effects of prenatal iAs occurring at levels <100 μg As/L urine. Together, findings present a variety of BMD measures to estimate doses at which prenatal iAs exposure influences neonatal outcome-relevant transcriptomic, proteomic, and epigenomic profiles.

Low-level arsenic exposure via drinking water consumption and female fecundity - A preliminary investigation

High level arsenic exposure is associated with reproductive toxicity in experimental and observational studies; however, few data exist to assess risks at low levels. Even less data are available to evaluate the impact of low level arsenic exposure on human fecundity. Our aim in this pilot study was a preliminary evaluation of associations between low level drinking water arsenic contamination and female fecundity. This retrospective study was conducted among women previously recruited to a hospital-based case-control study of spontaneous pregnancy loss in Timiṣ County, Romania. Women (n=94) with planned pregnancies of 5–20 weeks gestation completed a comprehensive physician-administered study questionnaire and reported the number of menstrual cycles attempting to conceive as the time to pregnancy (TTP). Drinking water samples were collected from residential drinking water sources and we determined arsenic levels using hydride generation-atomic absorption spectrometry (HG-AAS). Multivariable Cox-proportional hazards regression with Efron approximation was employed to evaluate TTP as a function of drinking water arsenic concentrations among planned pregnancies, adjusted for covariates. There was no main effect for drinking water arsenic exposure, yet the conditional probability for pregnancy was modestly lower among arsenic exposed women with longer TTPs, relative to women with shorter TTPs, and relative to unexposed women. For example, 1µg/L average drinking water arsenic conferred 5%, 8%, and 10% lower likelihoods for pregnancy in the 6th, 9th, and 12th cycles, respectively (P=0.01). While preliminary, our results suggest that low level arsenic contamination in residential drinking water sources may further impair fecundity among women with longer waiting times; however, this hypothesis requires confirmation by a future, more definitive study.

Characteristic features of studies attributing chronic disease to low concentrations of arsenic in drinking water

Introduction: Arsenic in drinking water can cause multiple health effects, including cancer, cardiovascular disease and chronic respiratory disease. The epidemiological evidence comes from populations with prolonged exposure above 100µg/L of inorganic arsenic in water. However, many recent publications claim to find health effects from drinking water containing less than 50µg/L of arsenic. This paper looks to see if they have characteristic validity-related features. Methods: We identified published studies conducted in populations where drinking water arsenic concentrations had been less than 50µg/L. We scored studies based on the following points, with 1 for good quality on each point and 0 if not. We totaled the scores for each study with a possible range of 0-7. 1. Did the authors discuss scientific plausibility of their findings at such low water concentrations? 2. Did the authors present their findings in a manner that made their implausibility apparent? 3. Was there evidence of increased risks in some simple stratified analyses? 4. Were key results from analyses confined to complex non-transparent statistical modeling? 5. Did exposure data span at least 20 years of measured drinking water concentrations? 6. Was exposure data confined to one point in time? 7. Was arsenic in water measured with sufficient latency before the outcomes? Results: 21 publications attributed chronic disease to arsenic in drinking water below 50µg/L. The average score was 1.5. Only one study scored above 3, and it had serious study design problems separate from the criteria addressed in our scoring. Conclusions: The studies claiming health effects of arsenic in populations whose drinking water contained less than 50µg/L have serious flaws. Greater rigor is needed in peer review of proposed studies and of publications involving low arsenic water concentrations. Regulatory agencies need to be very cautious about using these studies for risk assessment.