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PubMed2005

Fractionation of sedimentary arsenic from Port Kembla Harbour, NSW, Australia.

The binding of arsenic in sediments of the heavily industrialised Port Kembla Harbour, NSW, Australia, has been investigated. Both dredge and core samples have been used to develop a sieving/sequential extraction (SE) procedure. Dredge samples included oxic surficial and deeper anoxic sediment. The main core sample analysed was 18 cm deep, sliced at 2 cm intervals. Sediment was sieved to three size ranges (<63 microm, 63-250 microm, >250 microm) and each of these was then subjected to a four step SE, sequentially solubilizing arsenic as ion exchangeable, 1 M HCl soluble, NH(2)OH.HCl soluble, and strong oxidising acid soluble. Concentrations of 50-500 mg As kg(-1) were found, elevated well above local background values. The core sample showed elevated concentrations of arsenic within the top 6-8 cm (300-500 mg As kg(-1)), relative to the deeper sediment (100-200 mg As kg(-1)). Substantial portions of the total arsenic present in the 0-8 cm sediments of core and dredge samples, were found to be soluble in 1 M pH 5 phosphate buffer or 1 M HCl. Arsenic in the lower 8-18 cm of the core displayed different solubility, the fourth stage SE strong acid digestion being required to solubilize >90% of the deep sediment arsenic. It appears that diagenesis had resulted in remobilisation of weakly bound arsenic with subsequent diffusion and deposition in surficial layers. Strong acid soluble arsenic present in deeper sediments has two possible origins: sedimented as strongly bound remaining untouched by diagenetic events, or subjected to diagenetic reactions such as pyritization, which lead to more stable crystalline forms of minerals.

Arsenic↗
PubMed2005

Urinary 8-hydroxy-2'-deoxyguanosine in inhabitants chronically exposed to arsenic in groundwater in Cambodia.

Arsenic concentrations in hair and urine, and urinary levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage, were examined for inhabitants of the Mekong Basin in Kratie Province, Cambodia. Also, the arsenic levels of tube-well water were determined. Total arsenic concentrations in tube-well water ranged from <1 to 886 microg L(-1), and 44.8% of these exceeded the WHO drinking water guideline of 10 microg L(-1). Elevated levels of arsenic were observed in the human hair and urine, and also a significant positive correlation was observed between the concentrations in hair and urine. These results suggest that the inhabitants are chronically exposed to arsenic through drinking the tube-well water. Levels of urinary 8-OHdG were higher for the subjects with higher arsenic levels in hair and urine, suggesting that induction of oxidative DNA damage was caused by chronic exposure to arsenic in tube-well water for the inhabitants in Kratie Province. To our knowledge, this is the first report on the oxidative DNA damage caused by chronic exposure to arsenic in groundwater for the inhabitants in Cambodia.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2004

Role of NADPH oxidase in arsenic-induced reactive oxygen species formation and cytotoxicity in myeloid leukemia cells.

Arsenic has played a key medicinal role against a variety of ailments for several millennia, but during the past century its prominence has been displaced by modern therapeutics. Recently, attention has been drawn to arsenic by its dramatic clinical efficacy against acute promyelocytic leukemia. Although toxic reactive oxygen species (ROS) induced in cancer cells exposed to arsenic could mediate cancer cell death, how arsenic induces ROS remains undefined. Through the use of gene expression profiling, interference RNA, and genetically engineered cells, we report here that NADPH oxidase, an enzyme complex required for the normal antibacterial function of white blood cells, is the main target of arsenic-induced ROS production. Because NADPH oxidase enzyme activity can also be stimulated by phorbol myristate acetate, a synergism between arsenic and the clinically used phorbol myristate acetate analog, bryostatin 1, through enhanced ROS production can be expected. We show that this synergism exists, and that the use of very low doses of both arsenic and bryostatin 1 can effectively kill leukemic cells. Our findings pinpoint the arsenic target of ROS production and provide a conceptual basis for an anticancer regimen.

Antineoplastic Agents↗
PubMed1996

Role of arsenic as a reproductive toxin with particular attention to neural tube defects.

Arsenic has been recognized as a human toxicant for over 2000 years. More recently it has been readily accepted as a human carcinogen. Animal research has demonstrated arsenic's ability to have profound detrimental effects on the developing embryo in avian and mammalian species. This article comprehensively reviews the human and animal literature on the subject of the reproductive toxicity of arsenic. A variety of endpoints are considered, including spontaneous abortion, cardiovascular defects, and arsenic's role in the causation of neural tube defects (NTDs). A summary of the literature that has examined the various postulated mechanisms by which arsenic may produce NTDs is also considered. In addition, a discussion of literature relative to the presence of arsenic in the general environment and in the workplace is presented. This article reaches the conclusion that while further research is clearly needed, particularly on the potential toxicity of organic arsenical compounds, the current literature suggests it may be prudent and appropriate to treat inorganic arsenic as a probable human reproductive toxin.

Animals↗
PubMed2003

Determination of total arsenic levels by hydride generation atomic absorption spectrometry in foods from south-east Spain: estimation of daily dietary intake.

The total concentration of arsenic in different foods from south-east Spain was determined by hydride generation atomic absorption spectrometry. Mineralization was carried out with an HNO(3)-HClO(4) mixture in a thermostated sand bath. Arsenic determination was performed by the standard addition method. Analyses of NIST and CBR-CEC reference materials demonstrated the reliability and accuracy of the technique. The highest arsenic levels were found in seafood, cereals, meat and meat by-products. In meat and meat by-products, the total arsenic measured in meat was significantly higher than that in sausages (p<0.05). In cereals, arsenic concentrations in corn and white rice samples were significantly higher (p<0.01) than those measured in wheat by-products. Mean arsenic concentrations in cheese were statistically lower than those in other dairy products (p<0.01). New data have been provided on the total arsenic content of a variety of foods in Spain, which is important for making exposure estimates. The estimated daily intake of total arsenic in the Spanish diet was 221 microg As day(-1).

Arsenic↗
PubMed2002

Removal of arsenic from groundwater using point-of-use reverse osmosis and distilling devices.

Ground water in both the northeastern and southwestern coast areas of Taiwan may contain high concentrations of arsenic. Since no central water supply system is available in some of those areas, point-of-use (POU) water purification devices are considered as an option for providing safe drinking water. In this study, removal of arsenic, using two types of POU purification devices, reverse osmosis (RO) systems and distillers, was investigated. Three commercially available RO systems and two distillers were selected to test their removal efficiency of arsenic from synthetic and real ground water. Experimental results of the three RO systems using synthetic ground water showed that only one system had good removal efficiency for arsenic. In subsequent experiments using real ground water with 0.7 mg l(-1) arsenic, only one RO system was able to meet the drinking water standard after producing about 1,000 l of treated water. For the distilling systems, 99% of the arsenic was removed from both synthetic and real groundwater. The arsenic concentrations in the finished water of both distillers were all below the standard for drinking water. Although systems with higher arsenic removal efficiency seemed to have better removal of total dissolved solids (TDS), no correlation could be found after analysis.

Arsenic↗
PubMed2001

A sustainable community-based arsenic mitigation pilot project in Bangladesh.

A sustainable community-based arsenic mitigation pilot project has been successfully operating for 22 months in the Chapainawabganj arsenic hot spot (Bangladesh) where safe treated drinking and cooking water derived from tubewells is being supplied below the Bangladesh maximum permissible limit (0.05 ppm total arsenic). There has been close community involvement in all stages and the arsenic removal mechanism used adapted from the simple process of adsorption by natural ferric oxyhydroxide. Supplemented ferric oxyhydroxide produces daily de-contaminated water batches until replaced at the end of the cycle. A regional renewal/recycling centre supplies new, and safely stores used, ferric oxyhydroxide. Recycling is beginning where adsorbed arsenic can be separated prior to ferric oxyhydroxide reuse. The mechanism is flexible regarding water volumes, cycle lengths, pre and post-treatment arsenic concentrations, tubewell chemistries and is cost-effective. Pilot project parameters were set at 60 l per day ( < 0.05 ppm total arsenic) and 16 day cycles per tank for each of the four selected families with pretreatment concentrations up to 1.1 ppm. A maximum of ~ 24 g of arsenic is produced from the approximately 900 g (dry) of ferric oxyhydroxide used per tank per year. Anecdotal evidence possibly suggests positive health effects within a few months and villagers report an improved water taste. The project should contribute to coping with such arsenicosis crises and expansion is planned.

Arsenic↗
PubMed1995

Arsenic levels in hair of workers in a semiconductor fabrication facility.

This study examined the relationship between total arsenic levels in hair of employees in a semiconductor fabrication facility and job responsibility, a surrogate variable for arsenic exposure potential. Maintenance personnel who regularly worked in equipment cleaning areas were assumed to have higher potential for occupational exposure than other employees. Occipital scalp hair samples were collected from 30 maintenance personnel, supervisors, and equipment engineers with high, medium, and low potential for exposure and from 26 administrative employees. Total arsenic in hair was measured by atomic absorption spectroscopy with hydride generation. Workplace air and wipe samples were analyzed to verify differing exposure potential in fabrication and administrative areas. Subjects completed written questionnaires to identify possible nonoccupational sources of arsenic. Mean hair arsenic in two of the three groups working in or near fabrication areas was slightly higher but not statistically different from that of administrative controls. Eliminating smokers, only the maintenance group regularly assigned to fabrication areas was higher than administrative controls but still not statistically different. A regression analysis of all factors indicated that sex, tapwater consumption, and dietary habits were significant contributors to arsenic in hair. Trends among these groups were consistent with expected exposure potential, although not dramatically different from controls. Main study conclusions were that (1) nonoccupational sources of arsenic can be expected to contribute more to hair levels in employees than that observed in this particular semiconductor work environment, where safe work practices were believed to be followed; and (2) monitoring should be considered in this industry to identify employees experiencing chronic, low-level arsenic exposures only if the facility also examines nonoccupational sources of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Arsenic↗
PubMed2005

Phytoextraction: simulating uptake and translocation of arsenic in a soil-plant system.

The uptake, transport, and accumulation of metals by plants are functions central to successful phytoextraction. This study investigates the uptake and translocation of arsenic from a contaminated sandy soil by a mature Chinese brake fern (Pteris vittata L.). An existing mathematical model for the coupled transport of water, heat, and solutes in the soil-plant-atmosphere continuum (CTSPAC) was modified to examine the flow of water as well as the uptake and translocation of total arsenic in the xylem of the fern. This model was calibrated using greenhouse measurements before its application. Simulation results showed that about 20% of the soil arsenic was removed by the fern in 10 d, of which about 90% of the arsenic was stored in the fronds and 10% in the roots. Although arsenic mass in the plant tissues increased consecutively with time, arsenic concentration in the xylem sap of the root tips has a typical diurnal distribution pattern: increasing during the day and decreasing at night, resulting from daily variations of frond surface water transpiration. The largest difference in simulated arsenic concentration in the root tips between the day and night was about 5%. This study also suggests that the use of transpiration stream concentration factor (TSCF), which is defined as the ratio of chemical concentration in the xylem sap to that in the external solution, to evaluate the translocation efficiency of arsenic for the hyperaccumulator Chinese brake fern (Pteris vittata L.) could be limited.

Arsenic↗
PubMed2003

The spatial pattern of risk from arsenic poisoning: a Bangladesh case study.

Arsenic poisoning in Bangladesh has been one of the biggest environmental health and social disasters of recent times. About seventy million people in Bangladesh are exposed to toxic levels of arsenic (0.05 mg/L) in drinking water. It is ironic that so many tubewells have been installed in recent times to provide drinking water that is safe from water-borne diseases but that the water pumped is contaminated with toxic levels of arsenic. Along with the clinical manifestations, some social problems have also emerged due to arsenic toxicity. Analysing the spatial risk pattern of arsenic in groundwater is the main objective of this paper. Establishing the extent of arsenic exposure to the people will facilitate an understanding of the health effects and estimating the population risk over the area. This paper seeks to explore the spatial pattern of arsenic concentrations in groundwater for analyzing and mapping 'problem regions' or 'risk zones' for composite arsenic hazard information by using GIS-based data processing and spatial analysis along with state-of-the-art decision-making techniques. Quantitative data along with spatial information were employed and analyzed for this paper.

Arsenic Poisoning↗
PubMed2003

Food chain aspects of arsenic contamination in Bangladesh: effects on quality and productivity of rice.

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.

Arsenic↗
PubMed2002

Acquisition of apoptotic resistance in arsenic-induced malignant transformation: role of the JNK signal transduction pathway.

This study examined the role of signal transduction and apoptosis in malignant transformation induced by arsenic. Prior study showed that chronic arsenite exposure (500 nM, > or =18 weeks) induced malignant transformation in rat liver TRL 1215 cells. In the present work, these transformed cells were compared with passage-matched control cells. In addition, TRL 1215 cells were treated subchronically (up to 6 weeks) with arsenic (termed pre-transformed cells) to define events occurring prior to arsenic-induced transformation. Flow cytometry using annexin/FITC revealed that arsenic-induced apoptosis in transformed cells was markedly suppressed in comparison to control or pre-transformed cells. Ro318220, a strong activator of JNK, enhanced arsenite-induced apoptosis in transformed cells. Densitometric analysis of western blots revealed that the ratios of both Bcl-x(L)/Bax and Bcl-2/Bax were significantly increased (>2.5-fold) in arsenic-transformed cells. Transformed, pre-transformed and control cells were treated with arsenic and levels of phosphorylated extracellular signal-regulated kinases, ERK1/2, JNK1/2 and p38 were determined by western blot analysis. The three mitogen-activated protein kinases (MAPKs) were phosphorylated in a dose-dependent fashion in all cell types. However, the levels of phosphorylated JNK1/2 were markedly decreased in the arsenic-transformed cells, whereas in pre-transformed cells the levels of phosphorylated MAPKs remained the same as in control cells. JNK kinase activity was suppressed in transformed cells whereas Ro318220 enhanced this activity. Thus, during arsenic-induced malignant transformation resistance to apoptosis develops, possibly due to perturbation of the JNK pathway.

Animals↗
PubMed2003

P53 alterations in bladder tumors from arsenic and tobacco exposed patients.

Previous studies demonstrated that tobacco and arsenic exposure are risk factors for bladder cancer. A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure. Information on residential history and lifestyle factors was collected. The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure. Smokers were grouped as ever/never smokers and by pack years of exposure (0, 1-20, >20). Patients were also grouped into four arsenic exposure categories based on the average of the five highest years arsenic concentration in their drinking water: group 1, non-detectable to <10 microg/l (n = 50); group 2, 10-99 microg/l (n = 31); group 3, 100-299 microg/l (n = 35); group 4, >300 microg/l (n = 30). The proportion of tumor samples with p53 mutations and P53 immunopositivity increased strongly with both stage and grade, but not with arsenic exposure or smoking. The prevalence of tumors containing mutational transitions increased markedly with tumor stage (from 14 to 52%, P(trend) = 0.005) and grade (from 11 to 48%, P(trend) = 0.004) and was higher in smokers than in non-smokers (34 versus 18%, respectively, P = 0.10). An increasing trend was observed with pack years of smoking (P = 0.09). The majority of mutations in tumors from both smokers and non-smokers were G-->A transitions, however, in smokers a preference for G-->A transitions at CpG sites was observed (P = 0.07, two-tailed) and a positive trend was observed with pack years of exposure (P = 0.04). A hotspot was found at codon 273 in 12% of the tumors from smokers but was not observed in never smokers (P = 0.05) and a positive trend was observed with pack years of tobacco exposure (P = 0.001). Neither stage nor grade demonstrated a preference for CpG site mutation, suggesting that these changes may be early exposure-related events in carcinogenesis and are not related to tumor progression. Arsenic exposure was not associated with an increased prevalence of p53 mutation or P53 immunopositivity and there was no evidence of interaction between arsenic and smoking with these outcome variables.

Aged↗
PubMed2000

Biliary and urinary excretion of inorganic arsenic: monomethylarsonous acid as a major biliary metabolite in rats.

In rats exposed to arsenite (AsIII) or arsenate (AsV), the biliary excretion of arsenic depends completely on availability of hepatic glutathione, suggesting that both AsIII and AsV are transported into bile in thiol-reactive trivalent forms (Gyurasics et al. [1991], Biochem. Pharmacol. 42, 465-468). To test this hypothesis, the bile and urine of bile duct-cannulated rats injected with AsIII or AsV (50 micromol/kg, iv) were collected periodically for 2 h and analyzed for arsenic metabolites by HPLC-hydride generation-atomic fluorescence spectrometry. Arsenic was excreted predominantly into bile in AsIII-injected rats, but the urine was the main route of excretion in AsV-exposed rats. Injected AsIII was excreted in urine practically unchanged, whereas both AsV and AsIII appeared in urine after administration of AsV. Irrespective of the arsenical administered, the bile contained 2 main arsenic species, namely AsIII and a hitherto unidentified metabolite. Formation of this metabolite could be prevented by pretreatment of the rats with the methylation inhibitor periodate-oxidized adenosine, indicating that it is a methylated arsenic compound. This metabolite could be converted in vitro into monomethylarsonic acid (MMAsV) by oxidation, whereas synthetic MMAsV could be converted into the unknown metabolite by reduction. Consequently, this biliary metabolite of both AsIII and AsV is monomethylarsonous acid (MMAsIII), a long-hypothesized, but never identified, intermediate in the biotransformation of AsIII and AsV. Although MMAsIII is thought to be formed from an oxidized precursor, rats injected with MMAsV did not excrete MMAsIII. In summary, the inorganic arsenicals investigated are transported into bile exclusively in trivalent forms, namely as AsIII and MMAsIII, but are excreted in urine in both tri- and pentavalent forms. Identification of MMAsIII is signified by the fact that this metabolite is more toxic than AsIII and AsV and thus formation of MMAsIII represents toxification of inorganic arsenic.

Animals↗
PubMed2001

Quantitative relationship between arsenic exposure and AP-1 activity in mouse urinary bladder epithelium.

Because of the potential of arsenic for causing cancer in humans, and of the fact of widespread environmental and occupational exposure, deriving acceptable human-limit values has been of major concern to industry as well as to regulatory agencies. Based upon epidemiological evidence and mechanistic studies, it has been argued that a non-linear dose-response model at low-level exposures is more appropriate for calculating risk than the more commonly employed linear-response models. In the present studies, dose-response relationships and recovery studies employing a cancer precursor marker, i.e., activating protein (AP)-1 DNA-binding activity, were examined in bladders of mice exposed to arsenic in drinking water and compared to histopathological changes and arsenic tissue levels in the same tissue. While AP-1 is a functionally pleomorphic transcription factor regulating diverse gene activities, numerous studies have indicated that activation of the MAP kinase pathway and subsequently increased AP-1 binding activities, is a precursor for arsenic-induced cancers of internal organs as well as the skin. We observed previously that within 8 weeks of exposure AP-1 activation occurs in urinary bladder tissue of mice exposed to arsenic in the drinking water. In the present studies, C57BL/6 mice were exposed to sodium arsenite at various concentrations in the drinking water for 8 consecutive weeks. Minimal but observable AP-1 activity occurred in bladder tissue at exposure levels below which histopathological changes or arsenic tissue accumulation was detected. Marked AP-1 DNA-binding activity only occurred at exposure levels of sodium arsenite above 20 microg/ml, where histopathological changes and accumulation of arsenic in the urinary bladder epithelium occurred. Although the experimental design did not allow statistical modeling of the entire dose-response curve, the general shape of the dose-response curve is not inconsistent with the previously proposed hypothesis that arsenic-induced cancer follows a non-linear dose-response model.

Animals↗
PubMedDate not supplied

Effects of water use on arsenic release to well water in a confined aquifer.

Field-based experiments were designed to investigate the release of naturally occurring, low to moderate (< 50 microg/L) arsenic concentrations to well water in a confined sandstone aquifer in northeastern Wisconsin. Geologic, geochemical, and hydrogeologic data collected from a 115 m2 site demonstrate that arsenic concentrations in ground water are heterogeneous at the scale of the field site, and that the distribution of arsenic in ground water correlates to solid-phase arsenic in aquifer materials. Arsenic concentrations in a test well varied from 1.8 to 22 microg/L during experiments conducted under no, low, and high pumping rates. The quality of ground water consumed from wells under typical domestic water use patterns differs from that of ground water in the aquifer because of reactions that occur within the well. Redox conditions in the well can change rapidly in response to ground water withdrawals. The well borehole is an environment conducive to microbiological growth, and biogeochemical reactions also affect borehole chemistry. While oxidation of sulfide minerals appears to release arsenic to ground water in zones within the aquifer, reduction of arsenic-bearing iron (hydr)oxides is a likely mechanism of arsenic release to water having a long residence time in the well borehole.

Arsenic↗
PubMed1976

Inorganic arsenic--ambient level approach to the control of occupational cancerigenic exposures.

In 1820 the first malignancies ascribed as due to occupational arsenic exposure were reported as scrotal cancers among smelters. A century later the causal relationship between chronic occupational, environmental or medical arsenical exposure and skin carcinogenesis was firmly established. From 1948 to 1975, nine out of eleven epidemiological studies have shown, initially or upon review, significant excess mortality from respiratory cancer among diverse occupations exposed to various inorganic arsenicals. Two of the nine studies have shown concommitant, significant excess mortality from lymphatic cancer, and another, from skin cancer. Additionally, two such studies have revealed a dose-response relationship between arsenical exposure and lung carcinogenesis. In the first, reported in 1969, the relationship was semi-quantitative, with a possible interactive role by sulfur dioxide or other contaminants. The other demonstrated a dose-response which was quantitative for arsenic per se. Upon our reinterpretation, this dose-response also demonstrated an increased lung cancer mortality risk apparently at arsenic concentrations above 1 mug/M3, calculated as the 8-hour TWA daily exposure over a 40-year working life. However, these and related data do not reveal a definite no-effect exposure level. Thus, in the absence of data documenting a cancerigenically safe level of occupational exposure and because of the environmental ubiquity of arsenic, the conclusion is drawn that the arsenic body burden of workers should not be occupationally increased above that produced by the ambient level.

Arsenic↗
PubMed2006

Prevalence of arsenic exposure and skin lesions. A population based survey in Matlab, Bangladesh.

STUDY OBJECTIVE: To assess prevalence of arsenic exposure through drinking water and skin lesions, and their variation by geographical area, age, sex, and socioeconomic conditions. DESIGN, SETTING, AND PARTICIPANTS: Skin lesion cases were identified by screening the entire population above 4 years of age (n = 166,934) living in Matlab, a rural area in Bangladesh, during January 2002 and August 2003. The process of case identification involved initial skin examinations in the field, followed by verification by physicians in a clinic, and final confirmation by two independent experts reviewing photographs. The tubewell water arsenic concentrations (n = 13,286) were analysed by atomic absorption spectrometry. Drinking water history since 1970 was obtained for each person. Exposure information was constructed using drinking water histories and data on water arsenic concentrations. MAIN RESULTS: The arsenic concentrations ranged from <1 to 3644 microg/l, and more than 70% of functioning tubewells exceeded the World Health Organisation guideline of 10 microg/l. Arsenic exposure had increased steadily from 1970s to the late 1990s, afterwards a decrease could be noted. In total, 504 skin lesions cases were identified, and the overall crude prevalence was 3/1000. Women had significantly higher cumulative exposure to arsenic, while men had significantly higher prevalence of skin lesions (SMR 158, 95% CI 133 to 188). The highest prevalence occurred in 35-44 age groups for both sexes. Arsenic exposure and skin lesions had a positive association with socioeconomic groups and achieved educational level. CONCLUSIONS: The result showed sex, age, and socioeconomic differentials in both exposure and skin lesions. Findings clearly showed the urgency of effective arsenic mitigation activities.

Adolescent↗