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Arsenic exposure has been linked to poor pulmonary function, and inefficient arsenic metabolizers may be at increased risk. Dietary rice has recently been identified as a possible substantial route of exposure to arsenic, and it remains unknown whether it can provide a sufficient level of exposure to affect pulmonary function in inefficient metabolizers. Within 12,609 participants of HCHS/SOL, asthma diagnoses and spirometry-based measures of pulmonary function were assessed, and rice consumption was inferred from grain intake via a food frequency questionnaire. After stratifying by smoking history, the relationship between arsenic metabolism efficiency [percentages of inorganic arsenic (%iAs), monomethylarsenate (%MMA), and dimethylarsinate (%DMA) species in urine] and the measures of pulmonary function were estimated in a two-sample Mendelian randomization approach (genotype information from an Illumina HumanOmni2.5-8v1-1 array), focusing on participants with high inferred rice consumption. Among never-smoking high inferred consumers of rice (n = 1395), inefficient metabolism was associated with past asthma diagnosis and forced vital capacity below the lower limit of normal (LLN) (OR 1.40, p = 0.0212 and OR 1.42, p = 0.0072, respectively, for each percentage-point increase in %iAs; OR 1.26, p = 0.0240 and OR 1.24, p = 0.0193 for %MMA; OR 0.87, p = 0.0209 and OR 0.87, p = 0.0123 for the marker of efficient metabolism, %DMA). Among ever-smoking high inferred consumers of rice (n = 1127), inefficient metabolism was associated with peak expiratory flow below LLN (OR 1.54, p = 0.0108/percentage-point increase in %iAs, OR 1.37, p = 0.0097 for %MMA, and OR 0.83, p = 0.0093 for %DMA). Less efficient arsenic metabolism was associated with indicators of pulmonary dysfunction among those with high inferred rice consumption, suggesting that reductions in dietary arsenic could improve respiratory health.

This study investigated the effects of dietary arsenic supplementation on laying performance, egg quality, hepatic and renal histopathology, and oxidative stress in the livers and kidneys of laying hens. Furthermore, the nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway was explored to reveal the molecular mechanism of the stress. Five hundred and twelve 40-week-old Hyline White laying hens were randomly allocated to 4 groups with 8 pens per group and 16 hens per pen. The doses of arsenic administered to the 4 groups were 0.95, 20.78, 40.67, and 60.25 mg/kg. The results revealed that dietary arsenic supplementation significantly reduced hen-day egg production (P

The present study aims to estimate geochemical arsenic toxicity in the domestic livestock and possible risk for human and environment caused by them. Daily dietary arsenic intake of an exposed adult cow or bull is nearly 4.56 times higher than control populace and about 3.65 times higher than exposed goats. Arsenic toxicity is well exhibited in all the biomarkers through different statistical interpretations. Arsenic bioconcentration is faster through water compared to paddy straw and mostly manifested in faeces and tail hair in cattle. Cow dung and tail hair are the most pronounced pathways of arsenic biotransformation into environment. A considerable amount of arsenic has been observed in animal proteins such as cow milk, boiled egg yolk, albumen, liver and meat from the exposed livestock. Cow milk arsenic is mostly accumulated in casein (83%) due to the presence of phosphoserine units. SAMOE–risk thermometer, calculated for the most regularly consumed foodstuffs in the area, shows the human health risk in a distinct order: drinking water > rice grain > cow milk > chicken > egg > mutton ranging from class 5 to 1. USEPA health risk assessment model reveals more risk in adults than in children, subsisting severe cancer risk from the foodstuffs where the edible animal proteins cannot be ignored. Therefore, the domestic livestock should be urgently treated with surface water, while provision of both arsenic-free drinking water and nutritional supplements is mandatory for the affected human population to overcome the severe arsenic crisis situation.

Dietary rice consumption can assume a significant pathway of the carcinogenic arsenic (As) in the human system. In search of a viable mitigation strategy, a field experiment was conducted with rice (cv. IET-4786) at geogenically arsenic-contaminated areas (West Bengal, India) for two consecutive years. The research aimed to explore irrigation management (saturation and alternate wetting and drying), and organic amendments (vermicompost, farmyard manure, and mustard cake) efficiencies in reducing As load in the whole soil-plant system. A thrice replicated strip plot design was employed and As content in the soil, plant parts, and the associated soil physicochemical properties were determined through a standard protocol. Results revealed that the most negligible As accumulation in the edible grains was accomplished by vermicompost amendment along with alternate wetting and drying (0.318 mg kg−1) over farmer’s practice of continuous submergence with no manure situation (0.895 mg kg−1). Interestingly, an increase in the grain yield by 25% was also observed. The risk of dietary exposure to As through rice was assessed by target cancer risk (TCR) and severity adjusted margin of exposure (SAMOE) mediated risk thermometer. The adopted strategy made all the risk factors somewhat benign to ensure a better standard of health. The Machine Learning algorithm revealed that Random Forest performed better in predicting grain As concentration than k-Nearest Neighbour and Generalized Regression Model. Hence, if properly calibrated and validated, the former can represent an effective tool for predicting grain As concentration in rice.

The interactive effects of different doses of dietary selenium [as selenomethionine; 1.8 μg g−1 (control), 10 μg g−1 and 40 μg g−1 diet] on the toxicity of dietary arsenic [as arsenite (As3+); 80 μg As per g diet] were investigated in rainbow trout over an exposure period of 30 days. Fish fed with As3+ alone showed an increased hepatic lipid peroxidation (LPO) and a concomitant decline in cellular redox potential (determined as GSH:GSSG) in the liver tissue relative to the control fish. Interestingly, fish fed with low (10 μg g−1) or high (40 μg g−1) concentration of dietary selenomethionine in combination with As3+ showed an even higher degree of hepatic LPO and a further decrease in GSH : GSSG molar ratio relative to the fish treated with As3+ alone. Our study also revealed that exposure to dietary selenomethionine (both at low and high levels) resulted in significantly higher levels of arsenic in target tissues (liver, kidney, and muscle) relative to fish treated with As3+ alone. Similarly, the synchrotron-based X-ray fluorescence imaging analysis also suggested a dose-dependent increase in the co-localization of arsenic and selenium in the brain of fish co-treated with dietary As3+ and selenomethionine. These observations suggested that selenomethionine facilitated arsenic deposition in the brain and likely in other tissues, possibly via bio-complexation. Overall, our findings indicated that elevated dietary selenomethionine can increase the tissue-specific accumulation and toxicity of As3+ in fish during chronic dietary exposure.

Arsenic occurs in both organic and inorganic forms and is contributed by natural as well as anthropogenic sources. Inorganic arsenic, due to its high toxicity, is very critical for toxicological risk assessments from dietary exposure. It had been reported that when water has under low-arsenic concentration, food becomes the primary contributor to arsenic exposure in general population. Arsenic has been found in many food varieties such as rice, wheat, vegetables, fruits, beverages fishes, seafoods, etc. throughout the world, in different forms. Of all, rice plays a dominant role in contributing to the overall dietary exposure to inorganic in most parts, particularly where rice is a staple dietary source. In terms of the vulnerability, younger population is found to have more dietary exposure, which may be attributed to high food consumption on body weight basis and less variation in diet, mostly rice-based products. Although this high food consumption does not reflect a greater risk of adverse effects in them as most of the health effects of arsenic are a result of chronic exposure and only a few have been associated with acute arsenic exposure. Epidemiologic studies have linked chronic or acute dietary arsenic exposures with various adverse health effects such as cancer and many non-malignant manifestations like cardiovascular disease, type II diabetes, skin lesions, respiratory, haematological, immune, reproductive, endocrine, and neurological disorders. The risks associate with the dietary arsenic exposures have become a public health concern and it call for effective intervention to lower the exposure, especially to vulnerable populations.

Arsenic (As) is a common contaminant in the earth's crust and widely distributed in food and drinking water. As exposures have been associated with human disease, including cancer, diabetes, lung and cardiovascular disorders, and there is accumulating evidence that early life exposures are important in the etiology. Mode-of-action analysis includes a critical role for metabolic activation of As species to reactive trivalent intermediates that disrupt cellular regulatory systems by covalent binding to thiol groups. The central role of glutathione (GSH) in the chemical reactions of metabolism and disposition of arsenic species was investigated here. The chemical kinetics were measured for reactions in which GSH is a ligand for trivalent As complex formation, a reductant for pentavalent As species, and a participant in ligand exchange reactions with other biological As-thiol complexes. The diverse reactions of GSH with As species demonstrate prominent roles in: (1) metabolic activation via reduction; (2) transport from tissues that are the primary sources of reactive trivalent As intermediates following ingestion (intestine and liver) to downstream target organs (e.g., lung, kidney, and bladder); and (3) oxidation to the terminal metabolite, dimethylarsinic acid (DMAV), which is excreted. Studies of As metabolism and disposition emphasize the link between metabolic activation vs. excretion of As (i.e., internal dosimetry of reactive species) and the disruption of critical cellular thiol-based regulatory processes that define the dose-response characteristics of disease in human epidemiological studies and animal models and underpin risk assessment.

Health exposure and perception of risk assessment have been evaluated on the populations exposed to different arsenic levels in drinking water (615, 301, 48, 20 µg/l), rice grain (792, 487, 588, 569 µg/kg) and vegetables (283, 187, 238, 300 µg/kg) from four villages in arsenic endemic Gaighata block, West Bengal. Dietary arsenic intake rates for the studied populations from extremely highly, highly, moderately, and mild arsenic-exposed areas were 56.03, 28.73, 11.30, and 9.13 μg/kg bw/day, respectively. Acute and chronic effects of arsenic toxicity were observed in ascending order from mild to extremely highly exposed populations. Statistical interpretation using ‘ANOVA’ proves a significant relationship between drinking water and biomarkers, whereas “two-tailed paired t test” justifies that the consumption of arsenic-contaminated dietary intakes is the considerable pathway of health risk exposure. According to the risk thermometer (SAMOE), drinking water belongs to risk class 5 (extremely highly and highly exposed area) and 4 (moderately and mild exposed area) category, whereas rice grain and vegetables belong to risk class 5 and 4, respectively, for all the differently exposed populations. The carcinogenic (ILCR) and non-carcinogenic risks (HQ) through dietary intakes for adults were much higher than the recommended threshold level, compared to the children. Supplementation of arsenic-safe drinking water and nutritional food is strictly recommended to overcome the severe arsenic crisis.

This study was funded by grants from Spanish Institute of Health Carlos III-Ministry of Economy and Competitiveness (INMA Network G03/176, CB06/02/0041, and FIS-FEDER: PI03/1615, PI04/1436, PI08/1151, PI04/2018, PI04/1509, PI04/1112, PI04/1931, PI05/1079, PI05/1052, PI06/1213, PI06/0867, PI07/0314, PI09/02647, PS09/00090, PI09/02311, MS11/0178, PI13/1944, PI13/2032, PI14/00891, PI16/1288, and PI17/00663). Miguel Servet-FEDER: MSII16/ 00051, CP14/00108 & PI16/00261 (Co-funded by European Regional Development Fund “A way to make Europe”), FEDER funds, MS13/00054. Generalitat de Catalunya-CIRIT 1999SGR 00241, JCI2011–09771–MICINN, Generalitat Valenciana (Conselleria de Sanitat048/2010 and 060/2010 and FISABIO-UGP 15-230, 15-244, and 15-249). Generalitat de Catalunya-CIRIT 1999SGR 00241, and Fundació La Marató de TV3 (090430). Alicia Koplowitz Foundation (2017). Universidad de Oviedo. FISS-PI13/2429. Fundación CajasturLiberbank. Department of Health of the Basque Government (2005111093 and 2009111069). The Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001). The Fundación Roger Torné. ISGlobal is a member of the CERCA Programme, Generalitat de Catalunya. Mònica Guxens is funded by a Miguel Servet fellowship (MS13/00054) awarded by the Spanish Institute of Health Carlos III (Ministry of Economy and Competitiveness). Antonio J. Signes-Pastor and Margaret R. Karagas are funded by the following projects P01ES022832, RD 83544201, R25CA134286 and P42ES007373., Signes-Pastor, A.J., Vioque, J., Navarrete-Muñoz, E.M., Carey, M., García-Villarino, M., Fernández-Somoano, A., Tardón, A., Santa-Marina, L., Irizar, A., Casas, M., Guxens, M., Llop, S., Soler-Blasco, R., García-de-la-Hera, M., Karagas, M.R., Meharg, A.A.

Evaluating the extent of an individual's exposure to arsenic, (potentially) indicative of proximity to smelting activities, poisoning, or dietary history, has proven difficult in archaeological contexts due to uncertainties surrounding how arsenic biogenically accumulates in the tissues commonly found at archaeological sites such as bone and tooth, in addition to issues of diagenesis. In this study, teeth of modern sheep naturally exposed to high amounts of arsenic by means of seaweed in their diet are compared to the teeth of a less exposed ‘control group’ of modern sheep consuming predominantly grass. Through analysis of total arsenic and other element concentrations in samples of enamel, cementum and dentine by hydride generation atomic fluorescence spectrometry (HG-AFS), as well as by bioimaging of radial tooth sections of sheep molars by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS), this research demonstrates that in teeth of sheep exposed to dietary arsenic, arsenic predominantly accumulates in the infundibulum and occlusal dentine. The major route of uptake of arsenic in these teeth is therefore likely not by ingestion and metabolisation during growth of the tooth, as is thought to be the case for lead and barium, but rather due to direct surface contact, potentially even occurring during mastication. The implications of this type of in vivo chemical alteration of teeth for archaeological trace element studies are explored.

Early-life exposure to inorganic arsenic (i-As) may cause long-lasting health effects, but as yet, little is known about exposure among weaning infants. We assessed exposure before and during weaning and investigated the association between solid food intake and infants’ urinary arsenic species concentrations. Following the recording of a comprehensive 3 day food diary, paired urine samples (pre- and post-weaning) were collected and analyzed for arsenic speciation from 15 infants participating in the New Hampshire Birth Cohort Study. Infants had higher urinary i-As (p-value = 0.04), monomethylarsonic acid (MMA) (p-value = 0.002), dimethylarsinic acid (DMA) (p-value = 0.01), and sum of arsenic species (i-As + MMA + DMA, p-value = 0.01) during weaning than while exclusively fed on a liquid diet (i.e., breast milk, formula, or a mixture of both). Among weaning infants, increased sum of urinary arsenic species was pairwise-associated with intake of rice cereal (Spearman’s ρ = 0.90, p-value = 0.03), fruit (ρ = 0.70, p-value = 0.03), and vegetables (ρ = 0.86, p-value = 0.01). Our observed increases in urinary arsenic concentrations likely indicate increased exposure to i-As during the transition to solid foods, suggests the need to minimize exposure during this critical period of development.

Inorganic arsenic is a carcinogen and consumption in low dose may lead to cancer. We estimated the cancer risk of the participants from arsenic endemic regions of West Bengal, India. The probable cancer risk was estimated following the assessment of daily inorganic arsenic intake through drinking water and diets of 20 participants for three consecutive years who had been using low arsenic water in the Indian context (median arsenic concentration in the study Years-I, II and III were 22, 16, 13 µg/l respectively). Probable cancer risk of the population was 2.80 × 10−4, 2.94 × 10−4, 3.12 × 10−4 in the three respective study years (Year-I, II and III); just higher than the US EPA risk level of concern. The arsenic species content of the paired raw, cooked rice and urine was estimated in the as is taken basis. The major diet component, rice contained 72–86% inorganic arsenic whereas urine contains 70% organic arsenic on an average. The cancer risk assessment has been proposed to be modified by inclusion of urine arsenic release, considering the fact of arsenic release through urine. The risk became 1.28 × 10−5, 1.13 × 10−5, 1.01 × 10−5 in the study Year-I, II and III respectively, considering urinary arsenic release, attributed the consideration of urine arsenic release into probable cancer risk estimation.

Rice (Oryza sativa L.), a staple crop for over 50% of the world's population, is also a source of dietary arsenic (As) because of it's efficiencyat accumulating As. Lead–arsenate pesticide was used...

Background The heavy metal arsenic is widely distributed in nature and posses a serious threat to organism’s health. However, little is known about the arsenic-induced inflammatory response in the brain tissues of birds and the relationship and mechanism of the inflammatory response. The purpose of this study was to explore the effects of dietary arsenic on the expression of inflammatory cytokines in the brains of Gallus gallus. Results Seventy-two 1-day-old male Hy-line chickens were divided into a control group, a low arsenic trioxide (As2O3)-treated (7.5 mg/kg) group, a middle As2O3-treated (15 mg/kg) group, and a high As2O3-treated (30 mg/kg) group. Arsenic exposure caused obvious ultrastructural changes. The mRNA levels of the transcription factor nuclear factor-κB (NF-κB) and of pro-inflammatory cytokines, including inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E synthase (PTGEs), in chicken brain tissues (cerebrum, cerebellum, thalamus, brainstem and myelencephalon) on days 30, 60 and 90, respectively, were measured by real-time PCR. The protein expression of iNOS was detected by western blot. The results showed that after being treated with As2O3, the levels of inflammatory-related factor NF-κB and pro-inflammatory cytokines in chicken brain tissues increased (P

The most consumed food samples of cereals (rice, maize and wheat), vegetables (lentil, brinjal, carrot, bean, potato, tomato, onion and chili), fruits (banana, mango and jackfruit), fish (taki, rui, pangas and tilapia), egg (chicken and duck), milk (cow) and meat (chicken, duck, beef and mutton) were collected from some markets of Bogra district northern part of Bangladesh to evaluate the levels of arsenic (As) and associated health risk to the adult’s and child inhabitants. Arsenic is a highly toxic element, and its presence in food composites is a matter of concern to the world scientists. Target hazard quotients (THQs) and target carcinogenic risk were calculated to evaluate the non-carcinogenic and carcinogenic health risk from ingested arsenic. The highest and the lowest mean concentrations of arsenic were noted in the Tilapia fish [(0.94 mg/kg, wet weight (ww)] and beef (0.012 mg/kg, ww). The daily intakes of arsenic via foodstuffs were 1.92 and 3.30 µg/kg-bw/day for rural adults and children and 1.69 and 3.04 µg/kg-bw/day for urban adults and children, respectively. The result shows the highest THQs of arsenic in cereals and vegetables for both the rural and urban inhabitants which exceed the safe limit (>1) indicating that cereals and vegetables are the main food items contributing to the potential health risk. The estimated target cancer risks from ingesting dietary arsenic all exceeded 10−6, indicating increased risk of cancer for adults and children in the study area.

Inorganic arsenic (iAs) is a well-characterized carcinogen, and recent epidemiologic studies have linked chronic exposures to non-cancer health outcomes, including cardiovascular disease, diabetes, skin lesions and respiratory disorders. Greater vulnerability has been demonstrated with early life exposure for health effects including lung and bladder cancer, immunotoxicity and neurodevelopment. Despite its well-known toxicity, there are important gaps in the regulatory oversight of iAs in food and in risk communication. This paper focuses on the US regulatory framework in relation to iAs in food and beverages. The state of existing regulatory agency toxicological assessments, monitoring efforts, standard setting, intervention policies and risk communication are explored. Regarding the approach for standard setting, risk-based evaluations of iAs in particular foods can be informative but are insufficient to create a numeric criterion, given current uncertainties in iAs toxicology and the degree to which traditional risk targets can be exceeded by dietary exposures. We describe a process for prioritizing dietary exposures for different lifestages and recommend a relative source contribution-based approach to setting criteria for arsenic in prioritized foods. Intervention strategies begin with an appropriately set criterion and a monitoring program that documents the degree to which this target is met for a particular food. This approach will promote improvements in food production to lower iAs contamination for those foods which initially do not meet the criterion. Risk communication improvements are recommended to ensure that the public has reliable information regarding sources and alternative dietary choices. A key recommendation is the consideration of meal frequency advice similar to what is currently done for contaminants in fish. Recent action level determinations by FDA for apple juice and infant rice cereal are evaluated and used as illustrations of how our recommended approach can further the goal of exposure mitigation from key sources of dietary iAs in the US.

In the Bengal deltaic region, the shallow groundwater laced with arsenic is used for irrigation frequently and has elevated the soil arsenic in agricultural soil. However, the areas with seasonal flooding reduce arsenic in top layers of the soils. Study shows arsenic accumulation in the deeper soil layers with time in the contaminated agricultural soil (19.40±0.38mg/kg in 0-5cm, 27.17±0.44mg/kg in 5-10cm and 41.24±0.48mg/kg in 10-15cm) in 2013 whereas depletion in 2014 and its buildup in different parts of monsoon rice plant in Nadia, India. Principal Component Analysis and Cluster Analysis were performed, and Enrichment Factor was calculated to identify the sources of arsenic in the soil. Potential Ecological Risk was also calculated to estimate the extent of risk posed by arsenic in soil, along with the potential risk of dietary arsenic exposure. Remarkably, the concentration of arsenic detected in the rice grain showed average value of 1.4mg/kg in 2013 which has increased to 1.6 in 2014, both being above the permissible limit (1mg/kg). These results indicate that monsoon flooding enhances the infiltration of arsenic in the deeper soil layer, which lead to further contamination of shallow groundwater.

The human health risk associated with arsenic in food in Southeast Brazil was quantified. Based on the most commonly consumed food types in the Brazilian diet, the maximum inorganic As (iAs) daily intake from food (0.255 μg kg−1 body weight per day) is approximately 9% of the Benchmark Dose Lower Limit (BMDL0.5) of 3 μg kg−1 body weight per day set by the World Health Organization (WHO) and Food and Agriculture Organization (FAO) Joint Expert Committee in Food Additives (JECFA). When water is included, the contribution of food to the total intake varies from 96.9% to 39.7%. Rice and beans, the main Brazilian staple food, contribute between 67 and 90% of the total As intake from food (46–79% from rice and 11–23% from beans). The substantial contribution of beans to total As food intake is reported for the first time. The broad range of As concentrations in rice and beans highlights the variable and potentially large contribution of both to As food intake in places where diet consists largely of these two food categories.

BACKGROUND: Arsenic is associated with several adverse health outcomes, including some birth defects. Although diet is the predominant route of arsenic exposure in the United States (U.S.), limited data exist regarding pre-pregnancy dietary arsenic consumption among U.S. women. METHODS: Using data collected in the National Birth Defects Prevention Study (NBDPS), we estimated daily dietary arsenic consumption during the year before pregnancy for 10,886 mothers of nonmalformed control children delivered from 1997–2011. Responses to the NBDPS dietary assessment and food item estimates of total and inorganic arsenic were used to estimate consumption. Associations between total and inorganic arsenic consumption and selected maternal characteristics were estimated using multinomial logistic regression. RESULTS: Estimates of mean maternal total and inorganic dietary arsenic consumption were 14.9 and 5.2 μg/day, respectively. Several positive and inverse associations with confidence intervals that excluded the null were observed. Comparing mothers in the middle or high total arsenic consumption tertiles to those in the low tertile, we observed positive associations (odds ratios = 1.3–3.8) for maternal age (≥30 years), lower (0–8 years) or higher (>12 years) education, race/ethnicity (non-Hispanic Black, Hispanic, other), and early pregnancy drinking with no binge episodes, and inverse associations (odds ratios = 0.4–0.8) for age (

Climate change is expected to increase growing temperatures in rice cultivating regions worldwide. Recent research demonstrates that elevated temperature can increase arsenic concentrations in rice tissue, exacerbating an existing threat to rice quality and human health. However, the specific temperature-induced changes in the plant-soil system responsible for increased arsenic concentrations remain unclear and such knowledge is necessary to manage human dietary arsenic exposure in a warmer future. To elucidate these changes, we established four temperature treatments in climate-controlled growth chambers and grew rice plants (Oryza sativa cv. M206) in pots filled with Californian paddy soil with arsenic concentrations of 7.7 mg kg−1. The four chosen temperatures mimicked IPCC forecasting for Northern California, with a roughly 2.5 °C increase between treatments (nighttime temperatures ~2 °C cooler). We observed that arsenic concentrations in porewater, root iron plaque, and plant tissue increased in response to elevated temperature. There was a positive linear relationship between temperature and rice grain arsenic, almost all of which was present as inorganic As (III). Above-ground allocation patterns were consistent across treatments. We found no upregulation in the gene encoding the OsABCC1 transporter, believed to be important for arsenic sequestration in vacuoles and thereby preventing arsenic transfer to grain. Rice plants grown at higher temperatures had more adsorbed arsenic per unit of iron plaque (measured as [As]/[Fe]), indicating temperature may impact arsenic sorption to root plaque. We present evidence that increased soil mobilization of arsenic was the driving factor responsible for increased arsenic uptake into rice grain. Transpiration, which can increase arsenic transport to roots, was also heightened with elevated temperature but appeared to play a secondary role. Our system had low soil arsenic concentrations typical for California. Our findings highlight that elevated growing temperatures may increase the risk of dietary arsenic exposure in rice systems that were previously considered low risk.

Dietary arsenic exposure and chronic health outcomes are of interest, due in part to increased awareness and data available on inorganic arsenic levels in some foods. Recent concerns regarding levels of inorganic arsenic, the primary form of arsenic of human health concern, in foods are based on extrapolation from adverse health effects observed at high levels of inorganic arsenic exposure; the potential for the occurrence of these health effects from lower levels of dietary inorganic arsenic exposure has not been established. In this review, longitudinal cohort studies are evaluated for their utility in estimating dietary inorganic arsenic exposure and quantifying statistically reliable associations with health outcomes. The primary limiting factor in longitudinal studies is incomplete data on inorganic arsenic levels in foods combined with the aggregation of consumption of foods with varying arsenic levels into a single category, resulting in exposure misclassification. Longitudinal cohort studies could provide some evidence to evaluate associations of dietary patterns related to inorganic arsenic exposure with risk of arsenic-related diseases. However, currently available data from longitudinal cohort studies limit causal analyses regarding the association between inorganic arsenic exposure and health outcomes. Any conclusions should therefore be viewed with knowledge of the analytical and methodological limitations.

Summary: The diet is emerging as the dominant source of arsenic exposure for most of the U.S. population. Despite this, limited regulatory efforts have been aimed at mitigating exposure, and the role of diet in arsenic exposure and disease processes remains understudied. In this brief, we discuss the evidence linking dietary arsenic intake to human disease and discuss challenges associated with exposure characterization and efforts to quantify risks. In light of these challenges, and in recognition of the potential longer-term process of establishing regulation, we introduce a framework for shorter-term interventions that employs a field-to-plate food supply chain model to identify monitoring, intervention, and communication opportunities as part of a multisector, multiagency, science-informed, public health systems approach to mitigation of dietary arsenic exposure. Such an approach is dependent on coordination across commodity producers, the food industry, nongovernmental organizations, health professionals, researchers, and the regulatory community. https://doi.org/10.1289/EHP3997

Background Arsenic is widely distributed in the environment in both inorganic and organic forms. Evidence from animal studies suggests that maternal inorganic arsenic may lead to the development of orofacial clefts (OFC)s in offspring. This evidence, together with the limited epidemiologic data available, supports the need for a comprehensive examination of major sources of arsenic exposure and OFCs in humans. Methods Using interview data collected in the National Birth Defects Prevention Study, public and well water arsenic sampling data, and dietary arsenic estimates, we compared expert-rater assessed occupational arsenic exposure, individual-level exposure to arsenic through drinking water, and dietary arsenic exposure between mothers of OFC cases (N = 435) and unaffected controls (N = 1267). Associations for each source of exposure were estimated for cleft lip ± palate (CL/P) and cleft palate (CP) using unconditional logistic regression analyses. Results Associations for maternal drinking water arsenic exposure and CL/P were near or below unity, whereas those for dietary arsenic exposure tended to be positive. For CP, positive associations were observed for maternal occupational arsenic and inorganic arsenic exposures, with confidence intervals that excluded the null value, whereas those for drinking water or dietary arsenic exposures tended to be near or below unity. Conclusions Positive associations were observed for maternal occupational arsenic exposure and CP and for maternal dietary arsenic exposure and CL/P; the remainder of associations estimated tended to be near or below unity. Given the exploratory nature of our study, the results should be interpreted cautiously, and continued research using improved exposure assessment methodologies is recommended.

Arsenic (As) is a ubiquitous metalloid classified as one of the most hazardous substances, but information about its exposure and effects in free-living passerines is lacking. The aim of this study is to elucidate the effect of an As manipulation experiment on survival, growth and physiology of great tits (Parus major). Wild P. major nestlings inhabiting an unpolluted area were dosed with water, 0.2 or 1 μg g−1 d−1 of sodium arsenite (Control, Low and High As groups), whereas those living in a metal-polluted area were dosed with water (Smelter group). Birds accumulated As in tissues (liver, bone and feathers) in a dose-dependent way. Nestlings exposed to 1 μg g−1 d−1 of sodium arsenite showed reduced number of fledglings per successful nest, and those exposed to 0.2 μg g−1 d−1 had reduced wing growth, which could have post-fledging consequences such as increased predation risk. These results suggest that the LOAEL for effects on nestling survival and development in great tits is likely equal to or below 1 μg g−1 d−1. However, limited effects on the biochemical parameters evaluated were found. It has been shown that As may produce oxidative stress and tissue damage, so further research exploring this issue will be carried out in a future study.

The release of a toxicant from a food matrix during the gastrointestinal digestion is a crucial determinant of the toxicant's oral bioavailability. We present a modified setup of the human simulator of the gut microbial ecosystem (SHIME), with four sequential gastrointestinal reactors (oral, stomach, small intestine, and colon), including the salivary and colonic microbiomes. Naturally arsenic-containing rice, mussels, and nori seaweed were digested in the presence of microorganisms and in vitro oral bioaccessibility, bioavailability, and metabolism of arsenic species were evaluated following analysis by using HPLC/mass spectrometry. When food matrices were digested with salivary bacteria, the soluble arsenic in the gastric digestion stage increased for mussel and nori samples, but no coincidence impact was found in the small intestinal and colonic digestion stages. However, the simulated small intestinal absorption of arsenic was increased in all food matrices (1.2-2.7 fold higher) following digestion with salivary microorganisms. No significant transformation of the arsenic species occurred except for the arsenosugars present in mussels and nori. In those samples, conversions between the oxo arsenosugars were observed in the small intestinal digestion stage whereupon the thioxo analogs became major metabolites. These results expand our knowledge on the likely metabolism and oral bioavailabiltiy of arsenic during human digestion, and provide valuable information for future risk assessments of dietary arsenic.

Rice is a major source of dietary arsenic (As). The effects of paddy water management, straw incorporation, the applications of nitrogen fertilizer or organic manure, and the additions of biochar on arsenic accumulation and speciation in rice grain were investigated under field conditions over four cropping seasons in Hunan, China. Treatments that promoted anaerobic conditions in the soil, including continuous flooding and straw incorporation, significantly increased the concentration of As, especially methylated As species, in rice grain, whereas N application rate and biochar additions had little or inconsistent effect. Continuous flooding and straw incorporation also increased the abundance of the arsenite methyltransferase gene arsM in the soil, potentially enhancing As methylation in the soil and the uptake of methylated As by rice plants. Intermittent flooding was an effective method to decrease As accumulation in rice grain.

Exposure to arsenic in arsenic endemic areas is most remarkable environmental health challenges. Although effects of arsenic contamination are well established, reports are unavailable on probable seasonal variation due to changes of food habit depending on winter and summer seasons, especially for endemic regions of Nadia district, West Bengal. Complete 24-h diets, drinking-cooking water, first morning voided urine samples, and diet history were analyzed on 25 volunteers in arsenic endemic Chakdah block of Nadia district, once in summer followed by once in winter from the same participants. Results depicted no seasonal variation of body weight and body mass index. Arsenic concentration of source drinking and cooking water decreased (p = 0.04) from 26 μg L(-1) in summer to 6 μg L(-1) in winter season. We recorded a seasonal decrease of water intake in male (3.8 and 2.5 L day (-1)) and female (2.6 and 1.2 L day(-1)) participants from summer to winter. Arsenic intake through drinking water decreased (p = 0.04) in winter (29 μg day(-1)) than in summer (100 μg day(-1)), and urinary arsenic concentration decreased (p = 0.018) in winter (41 μg L(-1)) than in summer (69 μg L(-1)). Dietary arsenic intake remained unchanged (p = 0.24) over the seasons. Hence, we can infer that human health risk assessment from arsenic needs an insight over temporal scale.

The arsenicosis endemic area in the region of Kuitun and Chepaizi, Dzungaria district, Xinjiang, People Republic of China was the first identified arsenic endemic area in China where arsenic concentration of up to 850. μg/L in the groundwater was reported. An intervention was put in place in 1985 by government to provide an alternative water source at a centralized community level. Sixteen years on since the intervention, we evaluated the health status of 178 villagers from endemic and 179 villagers from control sites. Biomarkers in their urine, included arsenic, porphyrins and malondialdehyde (MDA) were measured and the prevalence of skin lesions was also assessed. The average urinary arsenic (117. ±. 8.3. μg/g of creatinine) from the endemic-villages was significantly higher (p

The relative contribution of dietary arsenic (As) to aggregate daily exposure has not been well-characterized, especially in relation to the current EPA maximum contaminant level (MCL) of 10 p.p.b. for As in drinking water. Our objectives were to: (1) model exposure to inorganic and total As among non-seafood eaters using subject-specific data, (2) compare the contribution of food, drinking and cooking water to estimated aggregate exposure in households with variable background tap water As levels, and (3) describe the upper distribution of potential dose at different thresholds of tap water As. Dietary As intake was modeled in regional study populations and NHANES 2003–2004 using dietary records in conjunction with published food As residue data. Water As was measured in the regional studies. Among subjects exposed to tap water As >10 p.p.b., aggregate inorganic exposure was 24.5–26.1 μg/day, with approximately 30% of intake from food. Among subjects living in homes with tap water As ≤10, 5 or 3 p.p.b., aggregate inorganic As exposure was 8.6–11.8 μg/day, with 54–85% of intake from food. Median inorganic As potential dose was 0.42–0.50 μg/kg BW/day in subjects exposed to tap water As >10 p.p.b. and less than half that among subjects exposed to tap water As ≤10 p.p.b. The majority of inorganic and total As exposure is attributable to diet in subjects with tap water As

Purpose Arsenic is a known human carcinogen and has been linked to adverse health outcomes, including cancer. However, the effects of arsenic exposure from food on health are still unknown. We researched to examine the association between arsenic exposure from food and incidence of cancer in a Japanese population. Methods We conducted a population-based prospective study in 90,378 Japanese men and women aged 45–74 years. Participants responded to a validated questionnaire that included 138 food items. We estimated dietary arsenic intake from 12 food groups (75 items) based on the questionnaire data. During 11 years of follow-up, 7,002 cancer cases were identified. Hazard ratios (HRs) and 95 % confidence intervals (CIs) for cancer were calculated by Cox proportional hazards modeling. Results Total arsenic and inorganic arsenic showed no association with the risk of total cancer in both men and women. Total arsenic and inorganic arsenic intake tended to be associated with an increased risk of lung cancer in men. In particular, these positive associations were strengthened in currently smoking men, with HRs (95 % CI) in the highest categories of arsenic and inorganic arsenic intake compared with the lowest of 1.29 (95 % CI = 1.03–1.61) and 1.36 (95 % CI = 1.09–1.70), respectively. We also detected an interaction between arsenic and inorganic arsenic intake and smoking status in men (pinteraction

Plant science research may help to reduce the potential exposure of people to environmental arsenic pollution. In particular, arsenic phytoremediation and development of low arsenic accumulating plants are two main research foci that hold much promise in helping to tackle the arsenic pollution problem. Plant tissue culture has been useful to aid arsenic toxicity and resistance studies in the laboratory which could better inform phytoremediation studies, for example, involving the arsenic hyperaccumulating Pteris vittata (Chinese brake fern). Transfer of arsenic metabolism-related glutaredoxin genes, for example, has been shown to reduce arsenic accumulation in transgenic plants. In vitro plant cell selection may be, however, an attractive alternative to generation of transgenic plants to yield low arsenic accumulating crop plants (somaclonal variants) aiming to lower dietary arsenic intake.

Chronic exposure to arsenic (As) in food and water is a significant public health problem. Person-specific aggregate exposure is difficult to collect and modeling based on limited food As residue databases is of uncertain reliability. Two cross-sectional population exposure studies, the National Human Exposure Assessment Survey-Arizona and Arizona Border Survey, had a combined total of 252 subjects with diet, water, and urinary As data. Total As was measured in 24-h duplicate diet samples and modeled using 24-h diet diaries in conjunction with several published food surveys of As. Two-stage regression was used to assess the effects of dietary As on urinary total As (uAs): (1) generalized linear mixed models of uAs above versus below the limit of detection (LOD); and (2) restricted models limited to those subjects with uAs>LOD, using bootstrap sampling and mixed models adjusted for age, sex, body mass index, ethnicity, current smoking, and As intake from drinking and cooking water. In restricted models, measured and modeled estimates were significant predictors of uAs. Modeled dietary As based on Total Diet Study mean residues greatly underestimated the dietary intake. In households with tap water As ≤10 p.p.b., over 93% of total arsenic exposure was attributable to diet.

Although “market basket” studies have revealed the presence of arsenic in packaged chicken, 1 , 2 little is known about the concentrations of individual arsenic species found in these birds and how they are metabolized. In this issue of EHP, researchers determined the levels of arsenic metabolites present in chicken breast after feeding the birds an arsenic-based animal drug called roxarsone. 3 There are many different species (chemical forms) of arsenic, some more toxic than others. Exposure to inorganic species has been associated with cancer and other adverse health effects in humans. 4 “We wanted to measure the presence of each arsenic species and describe the elimination kinetics of roxarsone metabolites. Our findings can help guide human exposure assessments,” says senior author X. Chris Le, an environmental chemist at the University of Alberta in Canada. Although roxarsone and other organoarsenic animal drugs are no longer approved for use in U.S. poultry production, some other countries still use them. Roxarsone has been used in poultry feed for nearly 60 years to fight parasites and promote growth. 5 Recent studies have raised concerns over potential human exposure to inorganic arsenic in the livers 6 and meat 2 of chicken fed roxarsone. These studies suggested that roxarsone may be partially transformed to inorganic arsenic inside the chicken body as the drug is metabolized. The U.S. Food and Drug Administration (FDA) has since withdrawn approval for any organoarsenic animal drugs to be used in the United States. 7 However, some countries still allow their use. 8 Le and colleagues conducted a large feeding trial of 1,600 chickens. For the first month, 800 chickens ate feed supplemented with a dose of roxarsone commonly used in poultry production, while 800 chickens ate a control diet without roxarsone. In the final week of the study, all the chickens received a roxarsone-free diet so that the researchers could see how quickly the drug and its metabolites were eliminated from chicken breast meat once exposure stopped. They collected breast meat samples from chickens at several points over the course of the study, then analyzed the arsenic content. Concentrations of unmetabolized roxarsone, arsenite (a highly toxic form of inorganic arsenic), and a previously unidentified arsenic species were all significantly higher in chickens fed roxarsone than chickens on the control diet. During the clearance period, when all the chickens were fed a roxarsone-free diet, levels of most arsenic species declined rapidly. However, levels of roxarsone, arsenite, and the unknown arsenic species remained significantly higher in the roxarsone group even 7 days after exposure ceased. 3 Breast meat from roxarsone-fed chickens had a residual arsenite concentration of 3.1 μg/kg at the end of the study, compared with 0.41 μg/kg in meat from the control chickens. Le and colleagues estimated human daily intake of summed arsenic species from roxarsone-fed chicken would be 0.01 μg/day/kg body weight for a 70-kg adult who ate about 3.5 oz of chicken per day. 3 That’s much lower, the authors point out, than the World Health Organization provisional tolerable daily intake value for inorganic arsenic of 3 μg/day/kg body weight. 9 While the findings suggest that meat from organoarsenic-treated chickens may be a relatively minor source of arsenic exposure, there is ongoing debate over what constitutes safe or tolerable levels of arsenic exposure. 10 “Arsenic appears to be a non-threshold carcinogen, which suggests that any level of exposure corresponds to some level of risk,” says Keeve Nachman, director of the Johns Hopkins Center for a Livable Future Food Production and Public Health Program. “This is a small exposure that is one hundred percent preventable,” he says. Nachman was not involved in the current study. One of the research team’s next steps will be to investigate arsenic species in poultry waste and track how those forms are taken up and metabolized by plants grown in fields fertilized with the waste. They’ll also look for more detailed mechanistic clues about how a chicken’s body metabolizes arsenic. Le says such clues could provide insights into how the human body metabolizes dietary arsenic.

This study assessed the impacts of dietary arsenic trioxide (As2O3) on 26 mineral element contents in the liver and kidney of chicken. A total of 100 male Hy-line cocks were randomly divided into 2 groups (50 chickens in each group), including an arsenic-treated group (basic diet supplemented with As2O3 at 30 mg/kg) and a control group (basal diet). The feeding experiment lasted for 90 days and the experimental animals were given free access to feed and water. We determined 26 mineral elements in the liver and kidney by inductively coupled plasma mass spectrometry (ICP-MS). The results showed that nine element levels (Al, Mn, Co, Cu, Zn, Se, Cd, Ba, and Pb) were significantly decreased (P

Background Dietary exposure from food to toxic inorganic arsenic (iAs) in the general U.S. population has not been well studied. Objectives The goal of this research was to quantify dietary As exposure and analyze the major contributors to total As (tAs) and iAs. Another objective was to compare model predictions with observed data. Methods Probabilistic exposure modeling for dietary As was conducted with the Stochastic Human Exposure and Dose Simulation–Dietary (SHEDS-Dietary) model, based on data from the National Health and Nutrition Examination Survey. The dose modeling was conducted by combining the SHEDS-Dietary model with the MENTOR-3P (Modeling ENvironment for TOtal Risk with Physiologically Based Pharmacokinetic Modeling for Populations) system. Model evaluation was conducted via comparing exposure and dose-modeling predictions against duplicate diet data and biomarker measurements, respectively, for the same individuals. Results The mean modeled tAs exposure from food is 0.38 μg/kg/day, which is approximately 14 times higher than the mean As exposures from the drinking water. The mean iAs exposure from food is 0.05 μg/kg/day (1.96 μg/day), which is approximately two times higher than the mean iAs exposures from the drinking water. The modeled exposure and dose estimates matched well with the duplicate diet data and measured As biomarkers. The major food contributors to iAs exposure were the following: vegetables (24%); fruit juices and fruits (18%); rice (17%); beer and wine (12%); and flour, corn, and wheat (11%). Approximately 10% of tAs exposure from foods is the toxic iAs form. Conclusions The general U.S. population may be exposed to tAs and iAs more from eating some foods than from drinking water. In addition, this model evaluation effort provides more confidence in the exposure assessment tools used.

Run-off from mine tailings ponds constitutes the main anthropogenic release of arsenic in Canada. As a potential consequence, wildlife not normally exposed to arsenic under other circumstances may receive toxicologically relevant concentrations of arsenic compounds in their food and water. To test this hypothesis, and to determine if arsenic is being transported through trophic levels, the arsenic concentrations in members of a short food chain (soil-plant-meadow vole) were measured. Arsenic concentrations were higher in exposed organisms compared with those from a reference location. However, elevated concentrations of arsenic do not necessarily indicate impact, and consequently a biomonitoring study was undertaken to determine if there were sub-cellular effects of exposure in meadow voles (Microtus pennsylvanicus) as a consequence of arsenic exposure. In this work, adenosine triphosphate (ATP) and liver glutathione (GSH) levels were used as biomarkers of exposure and the frequency of red blood cell micronuclei (mono- and polychromatic) was used as a biomarker of effect. ATP results were not conclusive but there was a statistically significant relationship between a reduction of GSH in vole livers and increased liver arsenic concentrations. A statistically significant relationship was also observed between increased micronucleated monochromatic red blood cells in voles from arsenic contaminated sites compared to a background location. The results of the GSH and monochromatic red blood cell investigations suggest that there are possible sub-cellular effects on these voles as a consequence of dietary arsenic exposure. This is the first field study in which such effects have been observed in voles living near mine tailings.

The accurate assessment of dietary intake patterns is important for the determination of total dietary arsenic (As) exposure in As-contaminated regions of Bangladesh. Food intake questionnaires are a common means of assessing food intake. A food frequency questionnaire (FFQ) was designed to assess the daily intake of frequently consumed food items and was successfully implemented to assess dietary patterns and intake of the rural populations in 18 villages from three Districts of Bangladesh (Comilla, Manikganj Sadar, and Munshiganj). The FFQ presented in this paper comprises a complete set of tools which allowed not only collection of information on dietary patterns but also information on the spatial characteristics of the landscape, socio-demographic indicators, and geographic locations of the identified environmental media of the contaminants, which resulted in As exposure to humans. The FFQ was designed in three sections: (1) general household information, (2) household water and rice information, and (3) individual dietary intake of other foods. The dietary intake of other food was then further subdivided into five different food subgroups: (i) grain intake, (ii) protein intake, (iii) fruit intake (iv), vegetable intake, and (v) dal (pulse) intake. During the design and development of the FFQ, emphasis was given to the source of food, the frequency (day/week/month) of consumption, and the daily amount of food consumed by each adult male, adult female, and child to accurately determine the dietary pattern and intake of arsenic in the rural population of Bangladesh. Refereed/Peer-reviewed

Background Millions of people in Bangladesh are at risk of chronic arsenic toxicity from drinking contaminated groundwater, but little is known about diet as an additional source of As exposure. Methods We employed a duplicate diet survey to quantify daily As intake in 47 women residing in Pabna, Bangladesh. All samples were analyzed for total As, and a subset of 35 samples were measured for inorganic arsenic (iAs) using inductively coupled plasma mass spectrometry equipped with a dynamic reaction cell. Results Median daily total As intake was 48 μg As/day [interquartile range (IQR), 33–67) from food and 4 μg As/day (IQR, 2–152) from drinking water. On average, iAs comprised 82% of the total As detected in dietary samples. After adjusting for the estimated inorganic fraction, 34% [95% confidence interval (CI), 21–49%] of all participants exceeded the World Health Organization’s provisional tolerable daily intake (PTDI) of 2.1 μg As/kg-day. Two of the 33 women who used a well with < 50 μg As/L exceeded this recommendation. Conclusions When drinking water concentrations exceeded the Bangladesh drinking water standard of 50 μg As/L, ingested water was the dominant source of exposure. However, as drinking water As concentrations decrease, the relative contribution of dietary As sources becomes more important to ingested dose. The combined intake from both diet and drinking water can cause some individuals to exceed the PTDI in spite of using a tube well that contains < 50 μg As/L.

Cell culture studies have suggested that arsenic exposure results in decreased S-adenosylmethionine (SAM), causing DNA hypomethylation. Previously, we have shown that hepatic SAM is decreased and/or S-adenosylhomocysteine increased in arsenic-deprived rats; these rats tended to have hypomethylated DNA. To determine the effect of dietary arsenic on dimethylhydrazine (DMH)-induced aberrant crypt formation in the colon, Fisher 344 weanling male rats were fed diets containing 0, 0.5, or 50 microg As (as NaAsO2)/g. After 12 wk, dietary arsenic affected the number of aberrant crypts (p

Health risk associated with dietary arsenic intake may be different for infants and adults. Seafood is the main contributor to arsenic intake for adults while terrestrial-based food is the primary source for infants. Processed infant food products such as rice-based cereals, mixed rice/formula cereals, milk-based infant formula, applesauce and purée of peaches, pears, carrots, sweet potatoes, green beans, and squash were evaluated for total and speciated arsenic content. Arsenic concentrations found in rice-based cereals (63–320 ng/g dry weight) were similar to those reported for raw rice. Results for the analysis of powdered infant formula by inductively coupled plasma-mass spectrometry (ICP-MS) indicated a narrow and low arsenic concentration range (12 to 17 ng/g). Arsenic content in purée infant food products, including rice cereals, fruits, and vegetables, varies from

The total arsenic content of 150 paddy rice samples collected from Barisal, Comilla, Dinajpur, Kaunia, and Rajshahi districts, and from the BRRI experimental station at Rajshahi city in the boro and aman seasons of 2000 was determined by hydride generation-inductively coupled plasma emission spectroscopy (ICP). Arsenic concentrations varied from 10 to 420 microg/kg at 14% moisture content. Rice yields and grain arsenic concentrations were 1.5 times higher in the boro (winter) than the summer (monsoon) season, consistent with the much greater use of groundwater for irrigation in the boro season. Mean values for the boro and aman season rices were 183 and 117 microg/kg, respectively. The variation in arsenic concentrations in rice was only partially consistent with the pattern of arsenic concentrations in drinking water tube wells. There was no evidence from yield or panicle sterility data of arsenic toxicity to rice. Processing of rice (parboiling and milling) reduced arsenic concentrations in rice by an average of 19% in 21 samples collected from households. Human exposure to arsenic through rice would be equivalent to half of that in water containing 50 microg/kg for 14% of the paddy rice samples at rice and water intake levels of 400 g and 4 L/cap/day, respectively.

Adult lake whitefish were fed As contaminated diets at nominal concentrations of 0, 1, 10, and 100 microg As/g food (dry weight) for 10, 30, and 64 days. Reduced feed consumption was observed in lake whitefish fed the 100 microg As/g food, beginning on day 45 of exposure. The accumulation and distribution of As in these fish are described in the previous manuscript [Pedlar, R.M., Klaverkamp, J.F., 2001. The accumulation and distribution of dietary arsenic in lake whitefish (Coregonus clupeaformis). Aquat. Toxicol., in press]. At the molecular level of organization, metallothionein (MT) induction occurred in lake whitefish fed the 100 microg As/g food after 10 and 30 days, and in fish fed the 1 and 10 microg As/g diets for 64 days. Dietary As exposure did not have a significant effect on plasma lipid peroxide (LPO) concentrations. At the tissue and organ level, mean liver somatic index decreased significantly in lake whitefish fed the 100 microg As/g food for 64 days. Blood parameters (hematocrit, hemoglobin concentration, red blood cell count, mean cell volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration) were not affected by exposure to As contaminated diets. Liver and gallbladder histopathologies were observed in lake whitefish fed all As contaminated diets after each duration of exposure. Histopathology observed in liver included nuclear, architectural and structural alterations, areas of inflammation, and focal necrosis. Sloughing of the epithelium, dilation of vascular elements, inflammation, edema, fibrosis, and increased width of the submucosa were some of the alterations observed in gallbladders of lake whitefish fed As contaminated diets. Both organs were sensitive to As exposure, as damage occurred with exposure to dietary concentrations of As as low as 1 microg/g. Whole organism parameters were unaltered by dietary As exposure. Based on the results of this study, histopathological alterations in liver and gallbladder, and hepatic MT induction may be useful indicators of As toxicity in environmental monitoring programs that also measure As concentrations in those tissues.

Arsenic is a carcinogen that can also affect the cardiac, respiratory, neurological and immune systems. Children have higher dietary arsenic exposure than adults due to their more restricted diets and greater intake per unit body mass. We evaluated the potential contributions of breast milk and formula to arsenic exposure throughout the first year of life for 356 infants in the prospective New Hampshire Birth Cohort Study (NHBCS) using infant diets reported by telephone at 4, 8 and 12 months of age; measured household water arsenic concentrations; and literature data. Based on our central-tendency models, population-wide geometric mean (GM) estimated arsenic exposures in the NHBCS were relatively low, decreasing from 0.1 μg kg−1 d−1 at 4 months of age to 0.07 μg kg−1 d−1 at 12 months of age. At all three time points, exclusively formula-fed infants had GM arsenic exposures ~8 times higher than exclusively breastfed infants due to arsenic in both tap water and formula powder. Estimated maximum exposures reached 9 μg kg−1 d−1 among exclusively formula-fed infants in households with high tap water arsenic (80 μg/L). Overall, modeled arsenic exposures via breast milk and formula were low throughout the first year of life, unless formula was prepared with arsenic-contaminated tap water.

The non-carcinogenic and carcinogenic risk of arsenic and lead to adults and children via daily dietary intake of food composites in Bangladesh was estimated. The target hazard quotients (THQs), hazard index (HI) and target carcinogenic risk (TR) were calculated to evaluate the non-carcinogenic and carcinogenic health risk from arsenic and lead. Most of the individual food composites contain a considerable amount of arsenic and lead. The highest mean concentrations of arsenic were found in cereals (0.254 mg kg⁻¹ fw) and vegetables (0.250 mg kg⁻¹ fw), and lead in vegetables (0.714 mg kg⁻¹ fw) and fish (0.326 mg kg⁻¹ fw). The results showed the highest THQs of arsenic in cereals and lead in vegetables for both adults and children which exceeded the safe limit (> 1) indicating that cereals and vegetables are the main food items contributing to the potential health risk. The estimated TR from ingesting dietary arsenic and lead from most of the foods exceeded 10⁻⁶, indicating carcinogenic risks for all adult people of the study area.

Background: Young children are estimated to have higher dietary arsenic exposure than adults. Potential dietary sources of exposure include drinking water, infant formula and early foods such as ri...