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BACKGROUND: Xenobiotic metabolites are widely present in human urine and can indicate recent exposure to environmental chemicals. Proper inference of which chemicals contribute to these metabolites can inform human exposure and risk. Furthermore, longitudinal biomonitoring studies provide insight into how chemical exposures change over time. OBJECTIVES: We constructed an exposure landscape for as many human-exposure relevant chemicals over as large a time span as possible to characterize exposure trends across demographic groups and chemical types. METHODS: We analyzed urine data of nine 2-y cohorts (1999–2016) from the National Health and Nutrition Examination Survey (NHANES). Chemical daily intake rates (in milligrams per kilogram bodyweight per day) were inferred, using the R package bayesmarker, from metabolite concentrations in each cohort individually to identify exposure trends. Trends for metabolites and parents were clustered to find chemicals with similar exposure patterns. Exposure variation by age, gender, and body mass index were also assessed. RESULTS: Intake rates for 179 parent chemicals were inferred from 151 metabolites (96 measured in five or more cohorts). Seventeen metabolites and 44 parent chemicals exhibited fold-changes ≥10 between any two cohorts (deltamethrin, di-n-octyl phthalate, and di-isononyl phthalate had the greatest exposure increases). Di-2-ethylhexyl phthalate intake began decreasing in 2007, whereas both di-isobutyl and di-isononyl phthalate began increasing shortly before. Intake for four parabens was markedly higher in females, especially reproductive-age females, compared with males and children. Cadmium and arsenobetaine exhibited higher exposure for individuals >65 years of age and lower for individuals <20 years of age. DISCUSSION: With appropriate analysis, NHANES indicates trends in chemical exposures over the past two decades. Decreases in exposure are observable as the result of regulatory action, with some being accompanied by increases in replacement chemicals. Age- and gender-specific variations in exposure were observed for multiple chemicals. Continued estimation of demographic-specific exposures is needed to both monitor and identify potential vulnerable populations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Several epidemiological investigations demonstrated that maternal arsenic (As) exposure elevated risk of fetal growth restriction (FGR), but the mechanism remains unclear. OBJECTIVES: This study aimed to investigate the effects of gestational As exposure on placental and fetal development and its underlying mechanism. METHODS: Dams were exposed to 0.15, 1.5, and 15 mg/L NaAsO2 throughout pregnancy via drinking water. Sizes of fetuses and placentas, placental histopathology, and glycogen content were measured. Placental RNA sequencing was conducted. Human trophoblasts were exposed to NaAsO2 (2 μM) to establish an in vitro model of As exposure. The mRNA stability and protein level of genes identified through RNA sequencing were measured. 푁6-Methyladenosine (m6A) modification was detected by methylated RNA immunoprecipitation–quantitative real-time polymerase chain reason (qPCR). The binding ability of insulin-like growth factor 2 binding protein 2 to the gene of interest was detected by RNA-binding protein immunoprecipitation-qPCR. Intracellular S-adenosylmethionine (SAM) and methyltransferase activity were determined by liquid chromatography– tandem mass spectrometry (LC-MS/MS) and colorimetry, respectively. In vitro As+3 methyltransferase (As3MT) knockdown or SAM supplementation and in vivo folic acid (FA) supplementation were used to evaluate the protective effect. A case–control study verified the findings. RESULTS: Sizes of fetuses (exposed to 1.5 and 15 mg/L NaAsO2) and placentas (exposed to 15 mg/L NaAsO2) were lower in As-exposed mice. More glycogen+ trophoblasts accumulated and the expression of markers of interstitial invasion was lower in the 15 mg/L NaAsO2-exposed mouse group in comparison with control. Placental RNA sequencing identified cysteine-rich angiogenic inducer 61 (Cyr61) as a candidate gene of interest. Mechanistically, mice and cells exposed to As had lower protein expression of CYR61, and this was attributed to a lower incidence of Cyr61 m6A. Furthermore, cells exposed to As had lower methyltransferase activity, suggesting that this could be the mechanism by which Cyr61 m6A was affected. Depletion of intracellular SAM, a cofactor for m6A methyltransferase catalytic domain, partially contributed to As-induced methyltransferase activity reduction. Either As3MT knockdown or SAM supplementation attenuated As-induced Cyr61 m6A down-regulation. In mice, FA supplementation rescued As-induced defective trophoblastic invasion and FGR. In humans, a negative correlation between maternal urinary As and plasma CYR61 was observed in infants who were small for gestational age. DISCUSSION: Using in vitro and in vivo models, we found that intracellular SAM depletion–mediated Cyr61 m6A down-regulation partially contributed to As-induced defective trophoblastic invasion and FGR. [ABSTRACT FROM AUTHOR]

BACKGROUND: Two of the most important causes of global disease fall in the realm of environmental health: household air pollution (HAP) and poor water, sanitation, and hygiene (WASH) conditions. Interventions, such as clean cookstoves, household water treatment, and improved sanitation facilities, have great potential to yield reductions in disease burden. However, in recent trials and implementation efforts, interventions to improve HAP and WASH conditions have shown few of the desired health gains, raising fundamental questions about current approaches. OBJECTIVES: We describe how the failure to consider the complex systems that characterize diverse real-world conditions may doom promising new approaches prematurely. We provide examples of the application of systems approaches, including system dynamics, network analysis, and agent-based modeling, to the global environmental health priorities of HAP and WASH research and programs. Finally, we offer suggestions on how to approach systems science. METHODS: Systems science applied to environmental health can address major challenges by a) enhancing understanding of existing system structures and behaviors that accelerate or impede aims; b) developing understanding and agreement on a problem among stakeholders; and c) guiding intervention and policy formulation. When employed in participatory processes that engage study populations, policy makers, and implementers, systems science helps ensure that research is responsive to local priorities and reflect real-world conditions. Systems approaches also help interpret unexpected outcomes by revealing emergent properties of the system due to interactions among variables, yielding complex behaviors and sometimes counterintuitive results. DISCUSSION: Systems science offers powerful and underused tools to accelerate our ability to identify barriers and facilitators to success in environmental health interventions. This approach is especially useful in the context of implementation research because it explicitly accounts for the interaction of processes occurring at multiple scales, across social and environmental dimensions, with a particular emphasis on linkages and feedback among these processes. [ABSTRACT FROM AUTHOR]

BACKGROUND: The prevalence of type 2 diabetes (T2D) has more than doubled since 1980. Poor nutrition, sedentary lifestyle, and obesity are among the primary risk factors. While an estimated 70% of cases are attributed to excess adiposity, there is an increased interest in understanding the contribution of environmental agents to diabetes causation and severity. Arsenic is one of these environmental chemicals, with multiple epidemiology studies supporting its association with T2D. Despite extensive research, the molecular mechanism by which arsenic exerts its diabetogenic effects remains unclear. OBJECTIVES: We conducted a literature search focused on arsenite exposure in vivo and in vitro, using relevant end points to elucidate potential mechanisms of oral arsenic exposure and diabetes development. METHODS: We explored experimental results for potential mechanisms and elucidated the distinct effects that occur at high vs. low exposure. We also performed network analyses relying on publicly available data, which supported our key findings. RESULTS: While several mechanisms may be involved, our findings support that arsenite has effects on whole-body glucose homeostasis, insulinstimulated glucose uptake, glucose-stimulated insulin secretion, hepatic glucose metabolism, and both adipose and pancreatic b-cell dysfunction. DISCUSSION: This review applies state-of-the-science approaches to identify the current knowledge gaps in our understanding of arsenite on diabetes development. [ABSTRACT FROM AUTHOR]

The article discusses research which investigated the effect of proximity to a Superfund metal site on the health of African American and White women. The study quantified arsenic, cadmium, lead and antimony in toenail clippings of non-Hispanic African American and White women. It attributes the greater susceptibility of African American women to metal exposure to residential segregation and environmental racism.

BACKGROUND: Arsenic is metabolized through a series of oxidative methylation reactions by arsenic (3) methyltransferase (As3MT) to yield methylated intermediates. Although arsenic exposure is known to increase the risk of atherosclerosis, the contribution of arsenic methylation and As3MT remains undefined. OBJECTIVES: Our objective was to define whether methylated arsenic intermediates were proatherogenic and whether arsenic biotransformation by As3MT was required for arsenic-enhanced atherosclerosis. METHODS: We utilized the apoE-/- mouse model to compare atherosclerotic plaque size and composition after inorganic arsenic, methylated arsenical, or arsenobetaine exposure in drinking water. We also generated apoE-/- =As3mt-/- double knockout mice to test whether As3MT-mediated biotransformation was required for the proatherogenic effects of inorganic arsenite. Furthermore, As3MT expression and function were assessed in in vitro cultures of plaque-resident cells. Finally, bone marrow transplantation studies were performed to define the contribution of As3MT-mediated methylation in different cell types to the development of atherosclerosis after inorganic arsenic exposure. RESULTS: We found that methylated arsenicals, but not arsenobetaine, are proatherogenic and that As3MT is required for arsenic to induce reactive oxygen species and promote atherosclerosis. Importantly, As3MT was expressed and functional in multiple plaque-resident cell types, and transplant studies indicated that As3MT is required in extrahepatic tissues to promote atherosclerosis. CONCLUSION: Taken together, our findings indicate that As3MT acts to promote cardiovascular toxicity of arsenic and suggest that human AS3MT SNPs that correlate with enzyme function could predict those most at risk to develop atherosclerosis among the millions that are exposed to arsenic. [ABSTRACT FROM AUTHOR]

BACKGROUND: Arsenicals (roxarsone and nitarsone) used in poultry production likely increase inorganic arsenic (iAs), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and roxarsone or nitarsone concentrations in poultry meat. However, the association between poultry intake and exposure to these arsenic species, as reflected in elevated urinary arsenic concentrations, is unknown. OBJECTIVES: Our aim was to evaluate the association between 24-hr dietary recall of poultry consumption and arsenic exposure in the U.S. population. We hypothesized first, that poultry intake would be associated with higher urine arsenic concentrations and second, that the association between turkey intake and increased urine arsenic concentrations would be modified by season, reflecting seasonal use of nitarsone. METHODS: We evaluated 3,329 participants > 6 years old from the 2003-2010 National Health and Nutrition Examination Survey (NHANES) with urine arsenic available and undetectable urine arsenobetaine levels. Geometric mean ratios (GMR) of urine total arsenic and DMA were compared across increasing levels of poultry intake. RESULTS: After adjustment, participants in the highest quartile of poultry consumption had urine total arsenic 1.12 (95% CI: 1.04, 1.22) and DMA 1.13 (95% CI: 1.06, 1.20) times higher than nonconsumers. During the fall/winter, participants in the highest quartile of turkey intake had urine total arsenic and DMA 1.17 (95% CI: 0.99, 1.39; p-trend = 0.02) and 1.13 (95% CI: 0.99, 1.30; p-trend = 0.03) times higher, respectively, than nonconsumers. Consumption of turkey during the past 24 hr was not associated with total arsenic or DMA during the spring/summer. CONCLUSIONS: Poultry intake was associated with increased urine total arsenic and DMA in NHANES 2003 -- 2010, reflecting arsenic exposure. Seasonally stratified analyses by poultry type provide strong suggestive evidence that the historical use of arsenic-based poultry drugs contributed to arsenic exposure in the U.S. population. CITATION: Nigra AE, Nachman KE, Love DC, Grau-Perez M, Navas-Acien A. 2017. Poultry consumption and arsenic exposure in the U.S. population. Environ Health Perspect 125:370 -- 377; http://dx.doi.org/10.1289/EHP351 [ABSTRACT FROM AUTHOR]

BACKGROUND: Use of nitarsone, an arsenic-based poultry drug, may result in dietary exposures to inorganic arsenic (iAs) and other arsenic species. Nitarsone was withdrawn from the U.S. market in 2015, but its use in other countries may continue. OBJECTIVES: We characterized the impact of nitarsone use on arsenic species in turkey meat and arsenic exposures among turkey consumers, and we estimated cancer risk increases from consuming turkey treated with nitarsone before its 2015 U.S. withdrawal. METHODS: Turkey from three cities was analyzed for total arsenic, iAs, methylarsonate (MA), dimethylarsinate, and nitarsone, which were compared across label type and month of purchase. Turkey consumption was estimated from NHANES data to estimate daily arsenic exposures for adults and children 4-30 months of age and cancer risks among adult consumers. RESULTS: Turkey meat from conventional producers not prohibiting nitarsone use showed increased mean levels of iAs (0.64 μg/kg) and MA (5.27 μg/kg) compared with antibiotic-free and organic meat (0.39 μg/kg and 1.54 μg/kg, respectively) and meat from conventional producers prohibiting nitarsone use (0.33 μg/kg and 0.28 μg/kg, respectively). Samples with measurable nitarsone had the highest mean iAs and MA (0.92 μg/kg and 10.96 μg/kg, respectively). Nitarsone was higher in October samples than in March samples, possibly resulting from increased summer use. Based on mean iAs concentrations in samples from conventional producers with no known policy versus policies prohibiting nitarsone, estimated lifetime daily consumption by an 80-kg adult, and a recently proposed cancer slope factor, we estimated that use of nitarsone by all turkey producers would result in 3.1 additional cases of bladder or lung cancer per 1,000,000 consumers. CONCLUSIONS: Nitarsone use can expose turkey consumers to iAs and MA. The results of our study support the U.S. Food and Drug Administration's removal of nitarsone from the U.S. market and further support its removal from the global marketplace. CITATION: Nachman KE, Love DC, Baron PA, Nigra AE, Murko M, Raber G, Francesconi KA, Navas-Acien A. 2017. Nitarsone, inorganic arsenic, and other arsenic species in turkey meat: exposure and risk assessment based on a 2014 U.S. market basket sample. Environ Health Perspect 125:363-369; http://dx.doi.org/10.1289/EHP225 [ABSTRACT FROM AUTHOR]

BACKGROUND: We have recently shown that biomarker levels of selected metals are higher in Asians than in other U.S. ethnic groups, with important differences within selected Asian subgroups. Much of this difference may be dietary in origin; however, this is not well established. OBJECTIVE: We evaluated dietary intake of toxic metals as a source of increased biomarker levels of metals among U.S. Asians. METHODS: We estimated daily food consumption and dietary intake of arsenic, cadmium, lead, and mercury by combining 24-hr dietary intake recall data from the 2011-2012 National Health and Nutrition Examination Survey (NHANES) with data from the USDA Food Composition Intake Database and FDA Total Dietary Study. We analyzed associations between dietary metal intake and biomarker levels of the metals using linear regression. Further, estimated food consumption and metal intake levels were compared between Asians and other racial/ethnic groups (white, black, Mexican American, and other Hispanic) and within three Asian subgroups (Chinese, Indian Asian, and other Asians). RESULTS: Significant associations (p < 0.05) were found between biomarker levels and estimated dietary metal intake for total and inorganic arsenic and mercury among Asians. Asians had the highest daily fish and rice consumption across the racial/ethnic groups. Fish was the major contributor to dietary mercury and total arsenic intake, whereas rice was the major contributor to inorganic arsenic dietary intake. Fish consumption across the Asian subgroups varied, with Asian Indians having lower fish consumption than the other Asian subgroups. Rice consumption was similar across the Asian subgroups. CONCLUSIONS: We confirmed that estimated dietary intake of arsenic (total and inorganic) and mercury is significantly associated with their corresponding biomarkers in U.S. Asians, using nationally representative data. In contrast, estimated dietary intake of cadmium and lead were not significantly associated with their corresponding biomarker levels in U.S. Asians. CITATION: Awata H, Linder S, Mitchell LE, Delclos GL. 2017. Association of dietary intake and biomarker levels of arsenic, cadmium, lead, and mercury among Asian populations in the United States: NHANES 2011-2012. Environ Health Perspect 125:314-323; http://dx.doi. org/10.1289/EHP28 [ABSTRACT FROM AUTHOR]

INTRODUCTION: The Centers for Disease Control and Prevention (CDC) recently found that Asians have considerably higher biomarker levels of cadmium, lead, mercury, and arsenic than whites, blacks, Mexican Americans, and other Hispanics in the United States. OBJECTIVE: Our goal was to further evaluate the higher metal biomarker levels among Asians. METHODS: Biomarker data (blood cadmium, blood lead, blood mercury, urinary total arsenic, and urinary dimethylarsinic acic) from individuals ≥ 6 years of age were obtained from the 2011-2012 National Health and Nutrition Examination Survey (NHANES). We compared geometric mean levels of these five metal biomarkers in Asians with those of four other NHANES race/ethnic groups (white, black, Mexican American, and other Hispanic), and across three Asian subgroups (Chinese, Asian Indian, and other Asian). We also evaluated associations between biomarker levels and sociodemographic, physical, dietary, and behavioral covariates across the Asian subgroups. RESULTS: Asians had significantly higher levels of all five metal biomarkers than other race/ethnic groups (p < 0.05), regardless of sociodemographic, physical, dietary, behavioral, or geographic characteristics. We also found variations in biomarker levels across the Asian subgroups. In general, Asian Indians had lower levels than the other two Asian subgroups, except for blood lead. The following characteristics were found to be significant predictors of several biomarker levels: sex, age, education, birthplace, smoking, and fish consumption. CONCLUSIONS: Overall, the Asian group had the highest geometric mean biomarker levels for all of the five metal variables. Furthermore, we provided evidence that significant variations in the biomarker levels are present across the Asian subgroups in the United States. CITATION: Awata H, Linder S, Mitchell LE, Delclos GL. 2017. Biomarker levels of toxic metals among Asian populations in the United States: NHANES 2011-2012. Environ Health Perspect 125:306-313; http://dx.doi.org/10.1289/EHP27 [ABSTRACT FROM AUTHOR]

BACKGROUND: Chronic exposure to arsenicals at various life stages and across a range of exposures has been implicated in cardiometabolic and liver disease, but disease predisposition from developmental exposures remains unclear. OBJECTIVES: In utero and post-weaning exposure to trivalent arsenic (AsIII) was examined on the background of a Western-style diet to determine whether AsIII exposure affects metabolic disease. METHODS: Male Swiss Webster mice were exposed to 100 ppb AsIII in utero, after weaning, or both. Ad libitum access to a Western-style diet was provided after weaning, and the plasma metabolome, liver histopathology, liver enzyme activity, and gene expression were analyzed. RESULTS: Hepatic lipid composition and histopathology revealed that developmental AsIII exposure exacerbated Western-style diet--induced fatty liver disease. Continuous AsIII exposure increased cardiometabolic risk factors including increased body weight, insulin resistance, hyperglycemia, and plasma triglycerides. AsIII exposure produced a decrease in the intermediates of glycolysis and the TCA cycle while increasing ketones. Hepatic isocitrate dehydrogenase activity was also decreased, which confirmed disruption of the TCA cycle. Developmental AsIII exposure increased the expression of genes involved in fatty acid synthesis, lipogenesis, inflammation, and packaging of triglycerides, suggesting an increased acetyl coenzyme A (acetyl-CoA) load. CONCLUSIONS: In utero and continuous early-life exposure to AsIII disrupted normal metabolism and elevated the risk for fatty liver disease in mice maintained on a high-fat diet. Our findings suggest that individuals exposed to AsIII during key developmental periods and who remain exposed to AsIII on the background of a Western-style diet may be at increased risk for metabolic disease later in life. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to arsenic (As) concentrations in drinking water > 150 μg/L has been associated with risk of diabetes and cardiovascular disease, but little is known about the effects of lower exposures. OBJECTIVE: This study aimed to examine whether moderate As exposure, or indicators of individual As metabolism at these levels of exposure, are associated with cardiometabolic risk. METHODS: We analyzed cross-sectional associations between arsenic exposure and multiple markers of cardiometabolic risk using drinking-water As measurements and urinary As species data obtained from 1,160 adults in Chihuahua, Mexico, who were recruited in 2008-2013. Fasting blood glucose and lipid levels, the results of an oral glucose tolerance test, and blood pressure were used to characterize cardiometabolic risk. Multivariable logistic, multinomial, and linear regression were used to assess associations between cardiometabolic outcomes and water As or the sum of inorganic and methylated As species in urine. RESULTS: After multivariable adjustment, concentrations in the second quartile of water As (25.5 to < 47.9 μg/L) and concentrations of total speciated urinary As (< 55.8 μg/L) below the median were significantly associated with elevated triglycerides, high total cholesterol, and diabetes. However, moderate water and urinary As levels were also positively associated with HDL cholesterol. Associations between arsenic exposure and both dysglycemia and triglyceridemia were higher among individuals with higher proportions of dimethylarsenic in urine. CONCLUSIONS: Moderate exposure to As may increase cardiometabolic risk, particularly in individuals with high proportions of urinary dimethylarsenic. In this cohort, As exposure was associated with several markers of increased cardiometabolic risk (diabetes, triglyceridemia, and cholesterolemia), but exposure was also associated with higher rather than lower HDL cholesterol. [ABSTRACT FROM AUTHOR]

Background: In humans, inorganic arsenic is metabolized to methylated metabolites mainly by arsenic (+3 oxidation state) methyltransferase (AS3MT). AS3MT polymorphisms are associated with arsenic metabolism efficiency. Recently, a putative N-6-adenine-specific DNA methyltransferase 1 (N6AMT1) was found to methylate arsenic in vitro. Objective: We evaluated the role of N6AMT1 polymorphisms in arsenic methylation efficiency in humans. Methods: We assessed arsenic methylation efficiency in 188 women exposed to arsenic via drinking water (~ 200 µg/L) in the Argentinean Andes by measuring the relative concentrations of arsenic metabolites in urine [inorganic arsenic, methylarsonic acid (MMA), and dimethylarsinic acid] by high-performance liquid chromatography coupled with hydride generation and inductively coupled plasma mass spectrometry. We performed genotyping for N6AMT1 and AS3MT polymorphisms by Taqman assays, and gene expression (in blood; n = 63) with Illumina HumanHT-12 v4.0. Results: Five N6AMT1 single nucleotide polymorphisms (SNPs; rs1997605, rs2205449, rs2705671, rs16983411, and rs1048546) and two N6AMT1 haplotypes were significantly associated with the percentage of MMA (%MMA) in urine, even after adjusting for AS3MT haplotype. %MMA increased monotonically according to the number of alleles for each SNP (e.g., for rs1048546, mean %MMA was 7.5% for GG, 8.8% for GT, and 9.7% for TT carriers). Three SNPs were in linkage disequilibrium (R2 > 0.8). Estimated associations for joint effects of N6AMT1 (haplotype 1) and AS3MT (haplotype 2) were generally consistent with expectations for additive effects of each haplotype on %MMA. Carriers of N6AMT1 genotypes associated with lower %MMA showed the lowest N6AMT1 expression, but associations were monotonic according to copy number for only one genotype and one haplotype. Conclusions: N6AMT1 polymorphisms were associated with arsenic methylation in Andean women, independent of AS3MT. N6AMT1 polymorphisms may be susceptibility markers for arsenic-related toxic effects. [ABSTRACT FROM AUTHOR]

Background: Few prospective studies have evaluated the influence of arsenic methylation capacity on cardiovascular disease (CVD) risk. Objective: We evaluated the association of arsenic exposure from drinking water and arsenic methylation capacity with CVD risk. Method: We conducted a case-cohort study of 369 incident fatal and nonfatal cases of CVD, including 211 cases of heart disease and 148 cases of stroke, and a subcohort of 1,109 subjects randomly selected from the 11,224 participants in the Health Effects of Arsenic Longitudinal Study (HEALS). Results: The adjusted hazard ratios (aHRs) for all CVD, heart disease, and stroke in association with a 1-SD increase in baseline well-water arsenic (112 µg/L) were 1.15 (95% CI: 1.01, 1.30), 1.20 (95% CI: 1.04, 1.38), and 1.08 (95% CI: 0.90, 1.30), respectively. aHRs for the second and third tertiles of percentage urinary monomethylarsonic acid (MMA%) relative to the lowest tertile, respectively, were 1.27 (95% CI: 0.85, 1.90) and 1.55 (95% CI: 1.08, 2.23) for all CVD, and 1.65 (95% CI: 1.05, 2.60) and 1.61 (95% CI: 1.04, 2.49) for heart disease specifically. The highest versus lowest ratio of urinary dimethylarsinic acid (DMA) to MMA was associated with a significantly decreased risk of CVD (aHR = 0.54; 95% CI: 0.34, 0.85) and heart disease (aHR = 0.54; 95% CI: 0.33, 0.88). There was no significant association between arsenic metabolite indices and stroke risk. The effects of incomplete arsenic methylation capacity--indicated by higher urinary MMA% or lower urinary DMA%-- with higher levels of well-water arsenic on heart disease risk were additive. There was some evidence of a synergy of incomplete methylation capacity with older age and cigarette smoking. Conclusions: Arsenic exposure from drinking water and the incomplete methylation capacity of arsenic were adversely associated with heart disease risk. [ABSTRACT FROM AUTHOR]

BACKGROUND: Arsenite (iAsIII) can promote mutagenicity and carcinogenicity of other carcinogens. Considerable attention has focused on interference with DNA repair by inorganic arsenic, especially the nucleotide excision repair (NER) pathway, whereas less is known about the effect of arsenic on the induction of DNA damage by other agents. OBJECTIVES: We examined how arsenic modulates DNA damage by other chemicals. METHODS: We used an NER-deficient cell line to dissect DNA damage induction from DNA repair and to examine the effects of iAsIII on the formation of benzo[a]pyrene diol epoxide (BPDE)-DNA adducts. RESULTS: We found that pretreatment with iAsIII at subtoxic concentrations (10 µM) led to enhanced formation of BPDE-DNA adducts. Reduced glutathione levels, glutathione S-transferase activity and chromatin accessibility were also measured after iAsIII treatment, but none of these factors appeared to account for the enhanced formation of DNA adducts. However, we found that pretreatment with iAsIII increased the cellular uptake of BPDE in a dose-dependent manner. CONCLUSIONS: Our results suggest that iAsIII enhanced the formation of BPDE-DNA adducts by increasing the cellular uptake of BPDE. Therefore, the ability of arsenic to increase the bioavailability of other carcinogens may contribute to arsenic co-carcinogenicity. [ABSTRACT FROM AUTHOR]

Increasing concerns over the use of wood treated with chromated copper arsenate (CCA) in playground structures arise from potential exposure to arsenic of children playing in these play- grounds. Limited data from previous studies analyzing arsenic levels in sand samples collected from CCA playgrounds are inconsistent and cannot be directly translated to the amount of children's exposure to arsenic. The objective of this study was to determine the quantitative amounts of arsenic on the hands of children in contact with CCA-treated wood structures or sand in playgrounds. We compared arsenic levels on the hands of 66 children playing in eight CCA playgrounds with levels of arsenic found on the hands of 64 children playing in another eight playgrounds not constructed with CCA-treated wood. The children's age and duration of playtime were recorded at each playground. After play, children's hands were washed in a bag containing 150 mL of deionized water. Arsenic levels in the hand-washing water were quantified by inductively coupled plasma mass spectrometry. Our results show that the ages of the children sampled and the duration of play in the playgrounds were similar between the groups of CCA and non- CCA playgrounds. The mean amount of water-soluble arsenic on children's hands from CCA playgrounds was 0.50 μg (range, 0.0078-3.5 μg). This was significantly higher (p c 0.001) than the mean amount of water-soluble arsenic on children's hands from non-CCA playgrounds, which was 0.095 μg (range, 0.011-0.41 μg). There was no significant difference in the amount of sand on the children's hands and the concentration of arsenic in the sand between the CCA and non- CCA groups. The higher values of arsenic on the hands of children playing in the CCA playgrounds are probably due to direct contact with CCA-treated wood. Washing hands after play would reduce the levels of potential exposure because most of the arsenic on children's hands was washed off with water. The maximum amount of arsenic on children's hands from the entire group of study participants was < 4 μg, which is lower than the average daily intake of arsenic from water and food. [ABSTRACT FROM AUTHOR]

Six arsenic species [arsenate, arsenite, arsenocholine, arsenobetaine, monomethyl arsonic acid, and dimethyl arsinic acid] present in human urine were determined using ion-exchange chromatography combined with inductively coupled plasma mass spectrometry (IC-ICP-MS). Baseline separation was achieved for all six species as well as for the internal standard (potassium hexahydroxy antimonate V) in a single chromatographic run of less than 30 min, using an ammonium carbonate buffer gradient (between 10 and 50 mM) at ambient temperature, in conjunction with cation- and anion-exchange columns in series. The performance of the method was evaluated with respect to linearity, precision, accuracy, and detection limits. This method was applied to determine the concentration of these six arsenic species in human urine samples (n = 251) collected from a population-based exposure assessment survey. Method precision was demonstrated by the analysis of duplicate samples that were prepared over a 2-year analysis period. Total arsenic was also determined for the urine samples using flow injection analysis coupled to ICP-MS. The summed concentration of the arsenic species was compared with the measured arsenic total to demonstrate mass balance. [ABSTRACT FROM AUTHOR]

The article presents the response by A. H. Smith AH to the comments made by M. Hall, and M. Gamble on his article related to the association between urinary creatinine and arsenic methylation. He mentions that his team highlights the strength of the relationship between urinary creatinine and urinary dimethylarsinic acid (DMA) percent. Further he concludes that nutritional status has influenced on the metabolism of arsenic in expected mother.

Reports on the study about the risk associated with arsenic contaminates exposure to children's health in Bangladesh. Impact of the contaminates on children's learning and memory; Effect of the consumption of water contaminated by arsenic on reduced intellectual function; Rate of the association between arsenic and intellectual function.

The article focuses on a study that hypothesized that that sulfur-reducing bacteria play significant role in the conversion of monomethylarsonic acid (MMA) to a thiolated form, and states that the study tested their hypothesis using a Simulator of the Human Intestinal Microbial Ecosystem (SHIME), a device that mimics the digestive processes. Topics discussed include arsenic biotransformation in colon, arsenic thiolation in the gut and integral role of microbiome in human health.

The article reports that Maryland has banned use of the drug roxarsone in chicken production. The drug which is produced by Alpharma LLC prevents infections caused by parasites called coccidians and helps chickens to grow faster. The ban followed a study conducted by the U.S. Food and Drug Administration (FDA) which showed that levels of arsenic in livers of roxarsone-treated broiler chickens were more as compared to untreated ones.