[Show abstract][Hide abstract] ABSTRACT: Background. During the conduct of a cohort study intended to study the associations between mixed metal exposures and child health outcomes, we found that 78% of 309 children aged 20–40 months evaluated in the Munshiganj District of Bangladesh had blood lead concentrations ≥5 íµí¼g/dL and 27% had concentrations ≥10 íµí¼g/dL. Hypothesis. Environmental sources such as spices (e.g., turmeric, which has already faced recalls in Bangladesh due to high lead levels) may be a potential route of lead exposure. Methods. We conducted visits to the homes of 28 children randomly selected from among high and low blood lead concentration groups. During the visits, we administered a structured questionnaire and obtained soil, dust, rice, and spice samples. We obtained water samples from community water sources, as well as environmental samples from neighborhood businesses. Results. Lead concentrations in many turmeric samples were elevated, with lead concentrations as high as 483 ppm. Analyses showed high bioaccessibility of lead. Conclusions. Contamination of turmeric powder is a potentially important source of lead exposure in this population.
Journal of Environmental and Public Health 08/2014; 2014(730636).
[Show abstract][Hide abstract] ABSTRACT: Prenatal arsenic exposure is associated with increased risk of disease in adulthood. This has led to considerable interest in arsenic's ability to disrupt fetal programming. Many studies report that arsenic exposure alters DNA methylation in whole blood but these studies did not adjust for cell mixture. In this study, we examined the relationship between arsenic in maternal drinking water collected ≤ 16 weeks gestational age and DNA methylation in cord blood (n = 44) adjusting for leukocyte-tagged differentially methylated regions. DNA methylation was quantified using the Infinium HumanMethylation 450 BeadChip array. Recursively partitioned mixture modeling examined the relationship between arsenic and methylation at 473,844 CpG sites. Median arsenic concentration in water was 12 µg/L (range<1- 510 µg/L). Log 10 arsenic was associated with altered DNA methylation across the epigenome (P = 0.002); however, adjusting for leukocyte distributions attenuated this association (P = 0.013). We also observed that arsenic had a strong effect on the distribution of leukocytes in cord blood. In adjusted models, every log 10 increase in maternal drinking water arsenic exposure was estimated to increase CD8+ T cells by 7.4% (P = 0.0004) and decrease in CD4+ T cells by 9.2% (P = 0.0002). These results show that prenatal exposure to arsenic had an exposure-dependent effect on specific T cell subpopulations in cord blood and altered DNA methylation in cord blood. Future research is needed to determine if these small changes in DNA methylation alter gene expression or are associated with adverse health effects.
Epigenetics: official journal of the DNA Methylation Society 02/2014; 9(5). · 5.11 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Chronic exposure to high levels of arsenic in drinking water is associated with increased risk of type 2 diabetes mellitus (T2DM), but the association between lower levels of arsenic and T2DM is more controversial. Therefore, this study evaluated the association between low to moderate arsenic exposure and T2DM. In 2009-2011, we conducted a study of 957 Bangladeshi adults who participated in a case-control study of skin lesions in 2001-2003. The odds ratio of T2DM was evaluated in relationship to arsenic exposure measured in drinking water and in subjects' toenails (in 2001-2003) prior to the diagnosis of T2DM (in 2009-2011). Compared with those exposed to the lowest quartile of arsenic in water (≤1.7 µg/L), the adjusted odds ratio for T2DM was 1.92 (95% confidence interval (CI): 0.82, 4.35) for those in the second quartile, 3.07 (95% CI: 1.38, 6.85) for those in the third quartile, and 4.51 (95% CI: 2.01, 10.09) for those in the fourth quartile. The relative excess risk of T2DM was 4.78 for individuals who smoked and 8.93 for people who had a body mass index (weight (kg)/height (m)(2)) greater than 25. These findings suggest that exposure to modest levels of arsenic in drinking water was associated with increased risk of T2DM in Bangladesh. Being overweight or smoking was also associated with increased risk of T2DM.
American journal of epidemiology 09/2013; · 4.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Chronic exposure to arsenic in drinking water is associated with increased risk of type 2 diabetes mellitus (T2DM) but the underlying molecular mechanism remains unclear.
This study evaluated the interaction between single nucleotide polymorphisms (SNPs) in genes associated with diabetes and arsenic exposure in drinking water on the risk of developing T2DM.
In 2009-2011, we conducted a follow up study of 957 Bangladeshi adults who participated in a case-control study of arsenic-induced skin lesions in 2001-2003. Logistic regression models were used to evaluate the association between 38 SNPs in 18 genes and risk of T2DM measured at follow up. T2DM was defined as having a blood hemoglobin A1C level greater than or equal to 6.5% at follow-up. Arsenic exposure was characterized by drinking water samples collected from participants' tubewells. False discovery rates were applied in the analysis to control for multiple comparisons.
Median arsenic levels in 2001-2003 were higher among diabetic participants compared with non-diabetic ones (71.6 µg/L vs. 12.5 µg/L, p-value <0.001). Three SNPs in ADAMTS9 were nominally associated with increased risk of T2DM (rs17070905, Odds Ratio (OR) = 2.30, 95% confidence interval (CI) 1.17-4.50; rs17070967, OR = 2.02, 95%CI 1.00-4.06; rs6766801, OR = 2.33, 95%CI 1.18-4.60), but these associations did not reach the statistical significance after adjusting for multiple comparisons. A significant interaction between arsenic and NOTCH2 (rs699780) was observed which significantly increased the risk of T2DM (p for interaction = 0.003; q-value = 0.021). Further restricted analysis among participants exposed to water arsenic of less than 148 µg/L showed consistent results for interaction between the NOTCH2 variant and arsenic exposure on T2DM (p for interaction = 0.048; q-value = 0.004).
These findings suggest that genetic variation in NOTCH2 increased susceptibility to T2DM among people exposed to inorganic arsenic. Additionally, genetic variants in ADAMTS9 may increase the risk of T2DM.
PLoS ONE 08/2013; 8(8):e70792. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A repeated measures study was conducted in Pabna, Bangladesh to investigate factors that influence biomarkers of arsenic exposure. Drinking water arsenic concentrations were measured by inductively-coupled plasma mass spectrometry (ICP-MS) and urinary arsenic species [arsenite (As3), arsenate (As5), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA)] were detected using High Performance Liquid Chromatography (HPLC) and Hydride Generated Atomic Absorption Spectrometry (HGAAS). Linear mixed effects models with random intercepts were used to evaluate the effects of arsenic contaminated drinking water, genetic polymorphisms in glutathione-S-transferase (GSTT1 and GSTM1) on total urinary arsenic, primary methylation index [MMA/(As3+As5)], secondary methylation index (DMA/MMA), and total methylation index [(MMA+DMA)/(As3+As5)]. Drinking water arsenic concentrations were positively associated with total urinary arsenic concentrations and total methylation index. A significant gene-environment interaction was observed between urinary arsenic exposure in drinking water GSTT1 but not GSTM1 where GSTT1 null individuals had a slightly higher excretion rate of arsenic compared to GSTT1 wildtypes after adjusting for other factors. Additionally, individuals with GSTT1 null genotypes had a higher primary methylation index and lower secondary methylation index compared to GSTT1 wildtype after adjusting for other factors. This data suggests that GSTT1 contributes to the observed variability in arsenic metabolism. Since individuals with a higher primary methylation index and lower secondary methylation index are more susceptible to arsenic related disease, these results suggest that GSTT1 null individuals may be more susceptible to arsenic-related toxicity. No significant associations were observed between GSTM1 and any of the arsenic methylation indices.
Journal of Indian Society of Periodontology 05/2013; 67(2):197-207.
[Show abstract][Hide abstract] ABSTRACT: Background: Chronic exposure to arsenic is associated with skin lesions. However, it is not known whether reducing arsenic exposure will improve skin lesions. Objectives: To evaluate the association between reduced arsenic exposures and skin lesion recovery over time. Methods: A follow-up study of 550 individuals was conducted in 2009-2011 on a baseline population of skin lesion cases (N=900) previously enrolled in Bangladesh in 2001-2003. Arsenic in drinking water and toenails, and skin lesion status and severity were ascertained at baseline and follow-up. Logistic regression and generalized estimating equation (GEE) models were used to evaluate the association between log10-transformed arsenic exposure and skin lesion persistence and severity. Results: Water arsenic concentrations decreased in this population by 41% overall, and 65 individuals who had skin lesions at baseline had no identifiable lesions at follow-up. Every log10 decrease in water and toenail arsenic was associated with 22% (odds ratio (OR) = 1.22; 95% CI: 0.85, 1.78) and 4.5 times (OR = 4.49; 95% CI: 1.94, 11.1) relative increase in skin lesion recovery in adjusted models, respectively. Additionally, lower baseline arsenic levels were significantly associated with increased odds of recovery. A log10 decrease in toenail arsenic from baseline to follow-up was also significantly associated with reduced skin lesion severity in cases over time (mean score change = -5.22 units; 95% CI: -8.61, -1.82). Conclusions: Reducing arsenic exposure increased the odds that individual with skin lesions would recover or show less severe lesions within ten years. Reducing arsenic exposure must remain a public health priority in Bangladesh and in other regions affected by arsenic contaminated water.
Environmental Health Perspectives 10/2012; · 7.26 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Arsenic is an epigenetic toxicant and could influence fetal developmental programming.
We evaluated the association between arsenic exposure and DNA methylation in maternal and umbilical cord leukocytes.
Drinking-water and urine samples were collected when women were at ≤ 28 weeks gestation; the samples were analyzed for arsenic using inductively coupled plasma mass spectrometry. DNA methylation at CpG sites in p16 (n = 7) and p53 (n = 4), and in LINE-1 and Alu repetitive elements (3 CpG sites in each), was quantified using pyrosequencing in 113 pairs of maternal and umbilical blood samples. We used general linear models to evaluate the relationship between DNA methylation and tertiles of arsenic exposure.
Mean (± SD) drinking-water arsenic concentration was 14.8 ± 36.2 μg/L (range: < 1-230 μg/L). Methylation in LINE-1 increased by 1.36% [95% confidence interval (CI): 0.52, 2.21%] and 1.08% (95% CI: 0.07, 2.10%) in umbilical cord and maternal leukocytes, respectively, in association with the highest versus lowest tertile of total urinary arsenic per gram creatinine. Arsenic exposure was also associated with higher methylation of some of the tested CpG sites in the promoter region of p16 in umbilical cord and maternal leukocytes. No associations were observed for Alu or p53 methylation.
Exposure to higher levels of arsenic was positively associated with DNA methylation in LINE-1 repeated elements, and to a lesser degree at CpG sites within the promoter region of the tumor suppressor gene p16. Associations were observed in both maternal and fetal leukocytes. Future research is needed to confirm these results and determine if these small increases in methylation are associated with any health effects.
Environmental Health Perspectives 03/2012; 120(7):1061-6. · 7.26 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We determined whether single nucleotide polymorphisms (SNPs) in the glutathione S-transferase omega (GSTO) and arsenic(III)methyltransferase (AS3MT) genes were associated with concentrations of urinary arsenic metabolites among 900 individuals without skin lesions in Bangladesh. Four SNPs were assessed in these genes. A pathway analysis evaluated the association between urinary arsenic metabolites and SNPs. GSTO1 rs4925 homozygous wild type was significantly associated with higher monomethylarsonic acid (MMA) and dimethylarsinic acid urinary concentrations, whereas wild-type AS3MT rs11191439 had significantly lower levels of As(III) and MMA. Genetic polymorphisms GSTO and As3MT modify arsenic metabolism as evidenced by altered urinary arsenic excretion.
[Show abstract][Hide abstract] ABSTRACT: Inorganic arsenic is metabolized to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). Limited evidence suggests that the ability to fully metabolize arsenic into DMA influences susceptibility to disease. To determine whether percentage of MMA was predictive of disease, the authors used data from a case-control study conducted in Bangladesh (2001-2003). Persons who were diagnosed with keratosis, melanosis, Bowen's disease, or squamous cell carcinoma were matched on age, sex, and village to persons without these conditions. This analysis was restricted to persons who had no missing data on covariates (859 cases, 868 controls). A path analysis was used to evaluate simultaneously the association between the percentage of all urinary arsenic metabolites and the odds of skin lesions using PROC CALIS in SAS, version 9.1 (SAS Institute, Inc., Cary, North Carolina) and Mplus, version 6.1 (Muthén & Muthén, Los Angeles, California). The odds of skin lesions were significantly associated with log(10) percentage of MMA (adjusted odds ratio (OR(adj)) = 1.56, 95% confidence interval (CI): 1.15, 2.12) but not log(10) percentage of inorganic arsenic (OR(adj) = 1.06, 95% CI: 0.75, 1.50) or log(10) percentage of DMA (OR(adj) = 1.07, 95% CI: 0.33, 3.46). This novel analysis confirmed that persons who excrete a higher proportion of MMA have a greater risk of skin lesions after data are adequately controlled for urinary arsenic metabolites, current arsenic exposure, and other risk factors.
American journal of epidemiology 03/2011; 173(7):778-86. · 4.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Since 1996, 52,202 water samples from hand tubewells were analyzed for arsenic (As) by flow injection hydride generation atomic absorption spectrometry (FI-HG-AAS) from all 64 districts of Bangladesh; 27.2% and 42.1% of the tubewells had As above 50 and 10 μg/l, respectively; 7.5% contained As above 300 μg/l, the concentration predicting overt arsenical skin lesions. The groundwater of 50 districts contained As above the Bangladesh standard for As in drinking water (50 μg/l), and 59 districts had As above the WHO guideline value (10 μg/l). Water analyses from the four principal geomorphological regions of Bangladesh showed that hand tubewells of the Tableland and Hill tract regions are primarily free from As contamination, while the Flood plain and Deltaic region, including the Coastal region, are highly As-contaminated. Arsenic concentration was usually observed to decrease with increasing tubewell depth; however, 16% of tubewells deeper than 100 m, which is often considered to be a safe depth, contained As above 50 μg/l. In tubewells deeper than 350 m, As >50 μg/l has not been found. The estimated number of tubewells in 50 As-affected districts was 4.3 million. Based on the analysis of 52,202 hand tubewell water samples during the last 14 years, we estimate that around 36 million and 22 million people could be drinking As-contaminated water above 10 and 50 μg/l, respectively. However for roughly the last 5 years due to mitigation efforts by the government, non-governmental organizations and international aid agencies, many individuals living in these contaminated areas have been drinking As-safe water. From 50 contaminated districts with tubewell As concentrations >50 μg/l, 52% of sampled hand tubewells contained As <10 μg/l, and these tubewells could be utilized immediately as a source of safe water in these affected regions provided regular monitoring for temporal variation in As concentration. Even in the As-affected Flood plain, sampled tubewells from 22 thanas in 4 districts were almost entirely As-safe. In Bangladesh and West Bengal, India the crisis is not having too little water to satisfy our needs, it is the challenge of managing available water resources. The development of community-specific safe water sources coupled with local participation and education are required to slow the current effects of widespread As poisoning and to prevent this disaster from continuing to plague individuals in the future.
Water Research 11/2010; 44(19):5789-802. · 5.32 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Urinary arsenic metabolites (UAs) are used as biomarkers of exposure and metabolism.
To characterize inter- and intraindividual variability in UAs in healthy individuals.
In a longitudinal study conducted in Bangladesh, we collected water and spot urine samples from 196 participants every 3 months for 2 years. Water arsenic (As) was measured by inductively coupled plasma-mass spectrometry and urinary As [arsenite, arsenate, monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA)] were detected using high-performance liquid chromatography-hydride-generated atomic absorption spectrometry. We used linear mixed-effects models to compute variance components and evaluate the association between UAs and selected factors.
The concentrations of UAs were fairly reproducible within individuals, with intraclass correlation coefficients (ICCs) of 0.41, 0.35, 0.47, and 0.49 for inorganic As (InAs), MMA, DMA, and total urinary As (TUA). However, when expressed as a ratio, the percent InAs (%InAs), %MMA, and %DMA were poorly reproducible within individuals, with ICCs of 0.16, 0.16, and 0.17, respectively. Arsenic metabolism was significantly associated with sex, exposure, age, smoking, chewing betel nut, urinary creatinine, and season. Specificity and sensitivity analyses showed that a single urine sample adequately classified a participant's urinary As profile as high or low, but TUA had only moderate specificity for correctly classifying drinking water exposures.
Epidemiologic studies should use both urinary As concentrations and the relative proportion of UAs to minimize measurement error and to facilitate interpretation of factors that influence As metabolism.
Environmental Health Perspectives 04/2009; 117(3):455-60. · 7.26 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To characterize the effects of maternal arsenic exposure on birth weight.
Hair, toenail, and drinking water samples were collected from pregnant women (n = 52) at multiple time points during pregnancy and from their newborns after birth. Total arsenic was measured using inductively coupled plasma-mass spectrometry. The association between arsenic and birth weight was investigated using linear and logistic regression models.
Maternal hair arsenic measured early in pregnancy was associated with decreased birth weight (beta = -193.5 +/- 90.0 g, P = 0.04). Maternal hair and drinking water arsenic levels measured at first prenatal visit were significantly correlated with newborn hair arsenic level (rho = 0.32, P = 0.04 and rho = 0.31, P = 0.04).
Results suggest that maternal arsenic exposure early in pregnancy negatively affects newborn birth weight and that maternal hair provides the best integrated measure of arsenic exposure.
Journal of Occupational and Environmental Medicine 11/2007; 49(10):1097-104. · 1.80 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The association between arsenic exposure from drinking water and toenail arsenic concentrations appears to be non-linear at low exposure levels. To investigate whether this observation is a result exposure misclassification, a dietary exposure assessment was conducted in a cohort of 47 women concurrently enrolled in a prospective longitudinal biomonitoring study in Pabna, Bangladesh. Arsenic intake was evaluated using a duplicate diet study design which collected food and water samples for a total of 6 days. Total inorganic arsenic was measured in 24-hour composite food samples (N=282) using inductively coupled plasma-mass spectrometry coupled with a dynamic reaction cell (ICP-DRC-MS). Average annual tubewell arsenic concentrations and toenail arsenic concentrations were computed for each participant using biomonitoring data from the prospective study. Separate multivariate regression models evaluated the association between drinking water, total dietary intake, and total dietary dose with toenail arsenic, a biomarker of internal dose. In these models, dietary intakes were adjusted using the residual method to provide estimate that was independent of water arsenic concentrations. Median daily arsenic intake from food and drinking water was 48.3 microg/day and 4.2 microg/day. Taking into consideration participant's body weight, the median daily arsenic dose was 1.0 microg/kg-day from food and 0.1 microg/kg-day from drinking water although drinking water exposure was highly skewed and was the dominant exposure route for the upper 25th percentile of the distribution. The regression model that used total daily arsenic intake from food (beta=0.46; 95%CI: 0.18-0.73) and drinking water (95%CI: 0.26-0.38) explained the most variability in toenail arsenic concentrations (R(2)(a)=0.71). The effect estimates for food and drinking water are similar suggesting that both sources have a similar contribution to internal dose.
Journal of Environmental Science and Health Part A 11/2007; 42(12):1827-34. · 1.14 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Single-nucleotide polymorphisms in genes related to DNA repair capacity and ultraviolet exposure have not been well investigated in relation to skin lesions associated with arsenic exposure. This population based case-control study, of 600 cases and 600 controls, frequency matched on age and gender in Pabna, Bangladesh, in 2001-2002, investigated the association and potential effect modification between polymorphisms in Xeroderma Pigmentosum complementation group D (XPD) (Lys751Gln and Asp312Asn) genes, tendency to sunburn and arsenic-related skin lesions.
Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).
No significant association was observed between skin lesions and the XPD 312 Asp/Asn (adjusted OR = 0.87, 95% CI = 0.65-1.15) Asn/Asn (adjusted OR = 0.76, 95% CI = 0.50-1.15) (referent Asp/Asp); XPD 751 Lys/Gln (adjusted OR = 0.92, 95% CI = 0.69-1.23) Gln/Gln (adjusted OR = 0.98, 95% CI = 0.66-1.45) (referent Lys/Lys). While we did not observe any evidence of effect modification of these polymorphisms on the association between well arsenic concentration and skin lesions, we did observe effect modification between these polymorphisms and sunburn tendency and arsenic-related skin lesions. Individuals with the heterozygote or homozygote variant forms (Asp/Asn or Asn/Asn) had half the risk of skin lesions (OR = 0.45, 95% CI = 0.29-0.68) compared with those with the wild-type XPDAsp312Asn genotype (Asp/Asp) and individuals with heterozygote or homozygote variant forms (Lys/Gln or Gln/Gln) had half the risk of skin lesions (OR = 0.47, 95% CI = 0.31-0.72) compared with those with the wild-type XPDLys751Gln genotype (Lys/Lys), within the least sensitive strata of sunburn severity. We observed effect modification on the multiplicative scale for XPD 751 and XPD 312.
XPD polymorphisms modified the relationship between tendency to sunburn and skin lesions in an arsenic exposed population. Further study is necessary to explore the effect of XPD polymorphisms and sun exposure on risk of arsenic-related skin lesions.
[Show abstract][Hide abstract] ABSTRACT: Genetic polymorphisms in the base excision DNA repair pathway may influence individual susceptibility to arsenic and the development of arsenic-induced skin lesions. Data from a case-control study of 792 cases and 792 matched controls conducted in Bangladesh from 2001 to 2003 were analyzed using conditional logistic regression to assess the associations between four common base excision repair (BER) genetic polymorphisms X-ray repair cross-complementing group 1 (XRCC1) Arg399Gln, XRCC1 Arg194Trp, human 8-oxoguanine DNA glycosylase (hOGG1) Ser326Cys and apurinic/apyrimidinic endonuclease (APE1) Asp148Glu and arsenic-induced skin lesions including melanosis and keratosis. Adjusted for toenail arsenic, body mass index, education, smoking and betel nut use, individuals with the APE1 148Glu/Glu polymorphism had a 2-fold increased odds of skin lesions compared with individuals with the 148Asp/Asp genotype (1.93; 95% confidence interval 1.15, 3.19). Gene-environment interactions between toenail arsenic and XRCC1 Arg194Trp and APE1 Asp148Glu were observed. Within the lowest arsenic tertile, APE1 148Glu/Glu had 2.5 times the odds ratio compared with wild-type, whereas within the highest tertile of arsenic the odds ratios for skin lesions did not differ. In contrast, at low arsenic levels, the odds ratios for skin lesions did not differ much by XRCC1 Arg194Trp genotype. However, at the highest tertile of arsenic, the XRCC1 194Arg/Arg polymorphism conferred a 3-fold larger odds ratio for skin lesions compared with XRCC1 194Trp/Trp. Individuals may have different odds for developing skin lesions based in part on their genetic profile for BER and their arsenic exposure history. Future research on arsenic-induced skin lesions should consider the impact of genetic variation to individual susceptibility to arsenic toxicity.
[Show abstract][Hide abstract] ABSTRACT: 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.
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.
Median daily total As intake was 48 microg As/day [interquartile range (IQR), 33-67) from food and 4 microg 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 microg As/kg-day. Two of the 33 women who used a well with < 50 microg As/L exceeded this recommendation.
When drinking water concentrations exceeded the Bangladesh drinking water standard of 50 microg 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 microg As/L.
Environmental Health Perspectives 06/2007; 115(6):889-93. · 7.03 Impact Factor