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PubMedDate not supplied

Monitoring of low level arsenic exposure during maintenance of ion implanters.

To delineate potential exposure in ion implanter maintenance, the authors recruited 21 maintenance engineers (exposed group) and 10 computer programmers (controls) at three semiconductor manufacturing facilities. Samples of air, wipes, and urine; used cleaning cloths; and used gloves were collected for the characterization of arsenic exposure. Arsenic levels were very low in environmental samples, but high arsenic levels were found in some wipe samples, used cleaning cloths, and gloves. The average baseline content of urinary arsenic measured for maintenance engineers was 3.6 microg/g creatinine. Maintenance engineers experienced an increase of 1.0-7.8 microg/g creatinine in urinary arsenic levels during ion implanter maintenance. Results of a mixed-model analysis indicated that urinary arsenic levels were associated significantly with time series (p = .0001), and the extent of association was different among the three facilities (p = .0226). The results of this study indicate that arsenic intake via ingestion, rather than through inhalation, might play a significant role in the elevation of urinary arsenic levels. However, a series of urine samples with self-reference continue to be a good approach for the monitoring of low-level arsenic exposure.

Adult↗
PubMedDate not supplied

Arsenic exposure, smoking, and respiratory cancer in copper smelter workers.

A report by Lee and Fraumeni in 1969 linked exposure to arsenic and other contaminants to a threefold excess of respiratory cancer among 8,047 employees at the Anaconda copper smelter. We established vital status through December 1977 for a sample of 1,800 men from the original cohort. Average arsenic concentrations were estimated for each smelter department based on industrial hygiene measurements made from 1943 to 1965. Departments with similar concentrations were combined into four categories of exposure: 1) low (less than 100 micrograms/m3), 2) medium (100-499 micrograms/m3), 3) high (500-4,999 micrograms/m3) and 4) very high (greater than or equal to 5,000 micrograms/m3). Three indices of individual arsenic exposure were developed: time-weighted average, 30-day ceiling, and cumulative. Exposures to sulfur dioxide and asbestos were also examined. Smoking habits were obtained by questionnaire. Mortality was compared to that of men in the State of Montana using the modified lifetable method. A clear dose-response relationship between arsenic exposure and respiratory cancer was demonstrated. Men in the highest exposure category had a sevenfold excess. Those in the low and medium categories had a risk close to that expected. Ceiling arsenic exposure appeared to be more important than did time-weighted average exposure. Sulfur dioxide and asbestos did not appear to be important in the excess of respiratory cancer, although sulfur dioxide and arsenic exposures could not be separated completely. Smoking did not appear to be as important as arsenic exposure. Our findings suggest that had men worked only in departments with low or medium arsenic exposures (i.e., less than 500 micrograms/m3) there would have been little excess respiratory cancer. Since the estimates of arsenic exposure were based on department averages rather than on concentrations for individual jobs, these results must be interpreted with caution.

Aged↗
PubMed2004

Capacity of Lemna gibba L. (duckweed) for uranium and arsenic phytoremediation in mine tailing waters.

The potential of Lemna gibba L. to clean uranium and arsenic contamination from mine surface waters was investigated in wetlands of two former uranium mines in eastern Germany and in laboratory hydroponic culture. Water and plants were sampled and L gibba growth and yield were monitored in tailing ponds from the field study sites. Contaminant accumulation, growth and yield experiments were conducted in the laboratory using synthetic tailing water. Mean background concentrations of the surface waters were 186.0+/-81.2 microg l(-1) uranium and 47.0+/-21.3 microg l(-1) arsenic in Site one and 293.7+/-121.3 microg l(-1) uranium and 41.37+/-24.7 microg l(-1) arsenic in Site two. The initial concentration of both uranium and arsenic in the culture solutions was 100 microg l(-1). The plant samples were either not leached, leached with deionized H2O or ethylenediaminetetracetic (EDTA). The results revealed high bioaccumulation coefficients for both uranium and arsenic. Uranium and arsenic content of L gibba dry biomass of the field samples were as follows: nonleached samples > deionized H2O leached (insignificant ANOVA p = 0.05) > EDTA leached. The difference in both arsenic and uranium enrichment were significantly high between the nonleached and the other two lead samples tested at ANOVA p > 0.001. Estimated mean L gibba density in surface water was 85,344.8+/-1843.4 fronds m(-2) (approximately 1319.7 g m(-2)). The maximum specific growth rate was 0.47+/-0.2 d(-1), which exceeded reported specific growth rates for L gibba in the literature. Average yield was estimated at 20.2+/-6.7 g m(-2) d(-1), giving approximately 73.6+/-21.4 t ha(-1) y(-1) as the annual yield. The highest accumulations observed were 896.9+/-203.8 mg kg(-1) uranium and 1021.7+/-250.8 mg kg(-1) arsenic dry biomass for a 21-d test period in the laboratory steady-state experiments. The potential extractions from surface waters with L gibba L. were estimated to be 662.7 kg uranium ha(-1) yr(-1) and 751.9 kg arsenic ha(-1) yr(-1) under the above conditions.

Araceae↗
PubMed2003

A study on arsenic removal from household drinking water.

Arsenic removal from household drinking water has been receiving considerable attention in the field of water supply engineering. To develop the optimal coagulation protocol, the effectiveness of several operation options such as coagulants, coagulant aids and additives, as well as flocs separation systems were investigated in this study through the use of orthogonal array experiment based on Taguchi method. Arsenic removal mechanism during household coagulation (via manual mixing) was also discussed. The results showed that the addition of kaoline and powder activated carbon (PAC) did not enhance arsenic removal efficiency of ferric sulfate or aluminum sulfate. Similarly, mixture of ferric sulfate and aluminum sulfate (MFA) as well as polymeric ferric silicate sulfate (PFSiS) was also unable to improve the overall arsenic removal efficiency. The mechanism of arsenic removal during coagulation was somewhat different from those experienced in conventional processes. Coprecipitation appeared to be the crucial mechanism for arsenic removal. It is noted from this study that arsenic adsorption isotherm under household operation condition could be described by Langmuir equation. An efficient flocs separation system subsequent to coagulation was essential to achieve the effectiveness of overall arsenic removal. The results obtained from field experiment demonstrated that the method of ferric sulfate coagulation/sand filtration for arsenic removal from household drinking water was acceptable and affordable.

Alum Compounds↗
PubMedDate not supplied

Induction of endogenous Nrf2/small maf heterodimers by arsenic-mediated stress in placental choriocarcinoma cells.

Exposure to inorganic arsenic has been associated with various forms of cancer, nervous system pathogenesis, and vascular diseases, as well as reproductive and developmental toxicity. Here, the effect of inorganic arsenic on placental JAR choriocarcinoma cells was assessed. The nuclear protein levels of the CNC transcription factor Nrf2 were strongly induced in the presence of arsenic. Dosage response experiments showed that 0.5 microM of arsenic is sufficient to augment Nrf2 levels. The expression of the Nrf2 dimerization partners MafG and MafK appeared not to be modulated by arsenic, whereas MafF protein levels were slightly increased. Arsenic also induced the binding of endogenous Nrf2/small Maf DNA-binding complexes to a stress response element (StRE) recognition site. In addition, arsenic caused oxidative stress in the choriocarcinoma cell model as evidenced by an increase in intracellular H2O2 levels. Expression of the enzyme heme oxygenase-1 (HO-1), a known Nrf2 target gene, was upregulated by exposure of JAR cells to arsenic. These results suggest that Nrf2/small Maf heterodimers may play an important role in the response to arsenic-mediated stress in placental cells.

Arsenic↗
PubMed1998

Arsenic levels in drinking water and the prevalence of skin lesions in West Bengal, India.

BACKGROUND: A cross-sectional survey was conducted between April 1995 and March 1996 to investigate arsenic-associated skin lesions of keratosis and hyperpigmentation in West Bengal, India, and to determine their relationship to arsenic water levels. METHODS: In all, 7683 participants were examined and interviewed, and the arsenic levels in their drinking water measured. RESULTS: Although water concentrations ranged up to 3400 microg/l of arsenic, over 80% of participants were consuming water containing <500 microg/l. The age-adjusted prevalence of keratosis was strongly related to water arsenic levels, rising from zero in the lowest exposure level (<50 microg/l) to 8.3 per 100 for females drinking water containing >800 microg/l, and increasing from 0.2 per 100 in the lowest exposure category to 10.7 per 100 for males in the highest exposure level (> or =800 microg/l). However, 12 cases with keratosis (2 females and 10 males) were drinking water containing <100 microg/l of arsenic. Findings were similar for hyperpigmentation, with strong dose-response relationships. Among those with hyperpigmentation, 29 cases were exposed to drinking water containing <100 microg/l. Calculation by dose per body weight showed that men had roughly two to three times the prevalence of both keratosis and hyperpigmentation compared to women apparently ingesting the same dose of arsenic from drinking water. Subjects who were below 80% of the standard body weight for their age and sex had a 1.6 fold increase in the prevalence of keratoses, suggesting that malnutrition may play a small role in increasing susceptibility. CONCLUSION: The surprising finding of cases who had arsenic-associated skin lesions with apparently low exposure to arsenic in drinking water needs to be confirmed in studies with more detailed exposure assessment. Further research is also needed concerning susceptibility factors which might be present in the exposed population.

Adolescent↗
PubMed2005

Arsenic ingestion and increased microvascular disease risk: observations from the south-western arseniasis-endemic area in Taiwan.

BACKGROUND: We established the association between arsenic ingestion and increased risk of vascular diseases associated with diabetes. However, the specific microvascular diseases in relation to arsenic exposure level have not been well reported. METHODS: The study population was obtained through national health database linkage. A total of 28 499 subjects living in the study area were successfully linked with their medical records from the National Health Insurance database in 1999-2000. The arsenic concentrations of artesian well water in the villages of the study area were utilized as indices of previous ingestion level. Both stratified analysis and unconditional logistic regression were used to examine mainly neurological and renal disease in relation to the arsenic exposure taking into account diabetes status. RESULTS: The age-adjusted and gender-adjusted prevalence of microvascular diseases was 7.51% [95% confidence interval (CI) 7.50-7.51] for arsenic level of <0.1 mg/litre, and then increased from 6.59% (6.59-6.60) for the arsenic concentrations of 0.1-0.29 mg/litre to 8.02% (8.02-8.03) and 11.82% (11.81-11.83) for those of 0.3-0.59 mg/litre and > or =0.6 mg/litre in non-diabetic subjects. For diabetic patients, the prevalence was 16.41% (95% CI 16.37-16.45), 15.85% (15.8-15.9), 21.69% (21.6-21.8), and 28.31% (28.2-28.4) for arsenic levels <0.1, 0.1-0.29, 0.3-0.59, and > or =0.6 mg/litre, respectively. The prevalence of microvascular diseases increased significantly with arsenic exposure, especially at higher levels, and the relationship is stronger in diabetics than in non-diabetic subjects. The results for neurological disease are very similar, and the patterns are the same for renal disease. CONCLUSIONS: The increased prevalence of microvascular diseases, including neurological and renal disorders, is associated with arsenic ingestion. This excess risk was further elevated in diabetic subjects. Further studies are necessary to verify the hypotheses of threshold or dose-response relationships.

Adult↗
PubMedDate not supplied

An improved wet digestion procedure for the analysis of total arsenic in biological samples by direct hydride atomic absorption spectrophotometry.

The presence of dimethylarsinic acid (DMAA) in biological samples can cause an underestimation of total arsenic content when analyzed relative to an inorganic arsenic standard by direct hydride flame atomic absorption spectrophotometry. An acid digestion procedure is described that quantitatively recovers DMAA as well as monomethylarsonic acid, inorganic arsenic(III), and arsenic(V) from aqueous and biological samples. Methylated arsenicals are converted to inorganic arsenic by wet digestion with HNO3, H2SO4, and K2Cr2O7 and subsequently reduced to arsenic(III) with Nal. Arsine is generated with NaBH4 and converted to atomic arsenic following immediate introduction into a nitrogen-entrained air-hydrogen flame. This method produces a linear relationship to absorbance within a mass range of 50 to 300 ng arsenic/arsine reaction. A sensitivity of 2 ng arsenic and a detection limit of 7 ng arsenic/arsine reaction were also obtained. Recovery of DMAA from water, urine, feces, or whole blood ranged from 92 to 105% with a coefficient of variation of 5 to 10%.

Animals↗
PubMed1989

A comparison of several measures of exposure to arsenic. Matched case-control study of copper smelter employees.

To explore the relation between respiratory cancer mortality and exposure to airborne arsenic, methods of conditional logistic regression analysis are applied to a matched case-control study of copper smelter employees in Montana. With follow-up data for the period 1938-1977, several measures of arsenic exposure are compared. For men first employed prior to 1925, three measures--the category of maximum arsenic exposure, cumulative arsenic exposure, and time-weighted average arsenic exposure--are good predictors of respiratory cancer mortality. Within this group, there was a significantly elevated relative risk of respiratory cancer mortality associated with medium and heavy exposure to arsenic. For men first employed during 1925-1947, time-weighted average exposure to arsenic (adjusted for age at first employment) is the best predictor. In this group, men with heavy arsenic exposure and initially employed at 16.9 years had a relative risk of 6.0 in comparison to the baseline group with only light exposure to arsenic and initially employed at 31.9 years. No particular advantage is found in lagging exposures 10 years prior to death of the case in each matched set.

Adult↗
PubMed2003

Toxicogenomic analysis of aberrant gene expression in liver tumors and nontumorous livers of adult mice exposed in utero to inorganic arsenic.

Arsenic is a known human carcinogen. We have reported that brief exposure of pregnant C3H mice to arsenite in their drinking water during gestation induced hepatocellular carcinoma (HCC) in male offspring after they became adults. Tumor formation is typically associated with multiple gene expression changes, and this study examined aberrant gene expression associated with transplacental arsenic hepatocarcinogenesis. Liver tumors and nontumorous liver samples were taken at necropsy from adult male mice exposed in utero to either 42.5 or 85 ppm arsenic as sodium arsenite or unaltered water from day 8 to 18 of gestation. Total RNA was extracted and subjected to microarray analysis. Among 600 genes, arsenic-induced HCC showed a higher rate of aberrant gene expression (>2-fold and p < 0.05, 14%) than spontaneous tumors (7.8%). Overexpression of alpha-fetoprotein, c-myc, cyclin D1, proliferation-associated protein PAG, and cytokeratin-18 were more dramatic in arsenic-induced HCC than spontaneous tumors. In nontumorous liver samples of arsenic-exposed animals, 60 genes (10%) were differentially expressed, including the increased expression of alpha-fetoprotein, c-myc, insulin-like growth factor binding protein-1, superoxide dismutase, glutathione S-transferases, and CYP2A4, and the depressed expression of CYP7B1. Real-time RT-PCR analysis largely confirmed these findings. This toxicogenomic analysis revealed several aberrant gene expression changes associated with transplacental arsenic carcinogenesis. It is indeed remarkable that expression changes occurred in adulthood even though arsenic exposure ended during gestation. Some of these aberrantly expressed genes could play a role in the development of arsenic-induced tumors, at least in the liver.

Animals↗
PubMed2003

Arsenic in drinking water and skin lesions: dose-response data from West Bengal, India.

BACKGROUND: Over 6 million people live in areas of West Bengal, India, where groundwater sources are contaminated with naturally occurring arsenic. The key objective of this nested case-control study was to characterize the dose-response relation between low arsenic concentrations in drinking water and arsenic-induced skin keratoses and hyperpigmentation. METHODS: We selected cases (persons with arsenic-induced skin lesions) and age- and sex-matched controls from participants in a 1995-1996 cross-sectional survey in West Bengal. We used a detailed assessment of arsenic exposure that covered at least 20 years. Participants were reexamined between 1998 and 2000. Consensus agreement by four physicians reviewing the skin lesion photographs confirmed the diagnosis in 87% of cases clinically diagnosed in the field. RESULTS: The average peak arsenic concentration in drinking water was 325 microg/liter for cases and 180 microg/liter for controls. The average latency for skin lesions was 23 years from first exposure. We found strong dose-response gradients with both peak and average arsenic water concentrations. CONCLUSIONS: The lowest peak arsenic ingested by a confirmed case was 115 microg/liter. Confirmation of case diagnosis and intensive longitudinal exposure assessment provide the basis for a detailed dose-response evaluation of arsenic-caused skin lesions.

Adolescent↗
PubMed2002

Atmospheric emissions, depositions, and transformations of arsenic in natural ecosystem in Finland.

For the last 2 decades, special attention has been paid to arsenic due to its high concentration in groundwater in many regions of the globe. There are not very many reports on arsenic concentration in the Finnish ecosystem, although the metal has been known to be highly toxic since ancient times. For the majority of people in Finland, the leading exposure route to arsenic is through food consumption. In this study, it has been observed that atmospheric emissions of arsenic from anthropogenic sources have decreased by 90%, which is due to better control technology and strict regulation. Aquatic discharge also was attenuated from 7.1 metric tons (t) in 1990 to 0.7 t in 1999. The concentration of arsenic aerosols in the atmosphere in Finland varies between 0.46 to 0.75 ng m(-3). Its use in pesticides and insecticides also has been phased out in Finland. There is no information available regarding arsenic species in the Finnish environment. Elevated concentrations of arsenic in groundwater has been reported for many countries. In Finland two hot spots are reported--one in the south of Finland and the second in Lapland. In these areas, arsenic concentration in well water is greater than 10 microg l(-1) (WHO recommended value: <10 microg l(-1)). It is believed that the release of arsenic into the Finnish groundwater is geogenic.

Air Pollutants↗
PubMed2000

Reduction and coordination of arsenic in Indian mustard.

The bioaccumulation of arsenic by plants may provide a means of removing this element from contaminated soils and waters. However, to optimize this process it is important to understand the biological mechanisms involved. Using a combination of techniques, including x-ray absorption spectroscopy, we have established the biochemical fate of arsenic taken up by Indian mustard (Brassica juncea). After arsenate uptake by the roots, possibly via the phosphate transport mechanism, a small fraction is exported to the shoot via the xylem as the oxyanions arsenate and arsenite. Once in the shoot, the arsenic is stored as an As(III)-tris-thiolate complex. The majority of the arsenic remains in the roots as an As(III)-tris-thiolate complex, which is indistinguishable from that found in the shoots and from As(III)-tris-glutathione. The thiolate donors are thus probably either glutathione or phytochelatins. The addition of the dithiol arsenic chelator dimercaptosuccinate to the hydroponic culture medium caused a 5-fold-increased arsenic level in the leaves, although the total arsenic accumulation was only marginally increased. This suggests that the addition of dimercaptosuccinate to arsenic-contaminated soils may provide a way to promote arsenic bioaccumulation in plant shoots, a process that will be essential for the development of an efficient phytoremediation strategy for this element.

Arsenic↗
PubMedDate not supplied

Arsenic in glacial drift aquifers and the implication for drinking water--lower Illinois River Basin.

The lower Illinois River Basin (LIRB) covers 47,000 km2 of central and western Illinois. In the LIRB, 90% of the ground water supplies are from the deep and shallow glacial drift aquifers. The deep glacial drift aquifer (DGDA) is below 152 m altitude, a sand and gravel deposit that fills the Mahomet Buried Bedrock Valley, and overlain by more than 30.5 m of clayey till. The LIRB is part of the USGS National Water Quality Assessment program, which has an objective to describe the status and trends of surface and ground water quality. In the DGDA, 55% of the wells used for public drinking-water supply and 43% of the wells used for domestic drinking water supply have arsenic concentrations above 10 micrograms/L (a new U.S. EPA drinking water standard). Arsenic concentrations greater than 25 micrograms/L in ground water are mostly in the form of arsenite (AsIII). The proportion of arsenate (AsV) to arsenite does not change along the flowpath of the DGDA. Because of the limited number of arsenic species analyses, no clear relations between species and other trace elements, major ions, or physical parameters could be established. Arsenic and barium concentrations increase from east to west in the DGDA and are positively correlated. Chloride and arsenic are positively correlated and provide evidence that arsenic may be derived locally from underlying bedrock. Solid phase geochemical analysis of the till, sand and gravel, and bedrock show the highest presence of arsenic in the underlying organic-rich carbonate bedrock. The black shale or coal within the organic-rich carbonate bedrock is a potential source of arsenic. Most high arsenic concentrations found in the DGDA are west and downgradient of the bedrock structural features. Geologic structures in the bedrock are potential pathways for recharge to the DGDA from surrounding bedrock.

Arsenates↗
PubMed2005

Intraindividual variability in arsenic methylation in a U.S. population.

Several recent investigations have reported associations between a reduced capacity to fully methylate inorganic arsenic and increased susceptibility to arsenic-caused cancer. In these studies, methylation patterns were based on a single assessment of urinary arsenic metabolites collected at the time of cancer diagnosis. However, the latency of arsenic-caused cancer may be several decades, and the extent to which a recent measurement can be used to estimate a person's past methylation pattern is unknown. In this investigation, the distribution of urinary inorganic arsenic, monomethylarsonate, and dimethylarsinate was used to assess intraindividual variation in methylation capacity in 81 subjects with low to moderate arsenic exposures. Multiple urine samples were collected from each subject over a 1-year period. Duplicate analyses done on 27 samples were used to assess laboratory measurement imprecision. The intraclass correlation coefficients (ICC) for the proportion of urinary arsenic as inorganic arsenic, monomethylarsonate, and dimethylarsinate in samples taken an average of 258 days apart, were 0.45 [95% confidence interval (95% CI), 0.23-0.63] 0.46 (95% CI, 0.24-0.64), and 0.49 (95% CI, 0.28-0.66). In analyses of duplicate samples, ICCs for the concentration of arsenic species ranged from 0.87 to 0.93, whereas ICCs for species proportions ranged from 0.63 to 0.76. These data suggest that individual methylation patterns remain fairly stable over time, although variability due to measurement imprecision or intraindividual changes over time does occur. This variability could lead to misclassification of methylation patterns and could bias relative risk estimates in studies of methylation and cancer towards the null.

Aged↗
PubMed2004

Chromosomal aberrations in arsenic-exposed human populations: a review with special reference to a comprehensive study in West Bengal, India.

For centuries arsenic has played an important role in science, technology, and medicine. Arsenic for its environmental pervasiveness has gained unexpected entrance to the human body through food, water and air, thereby posing a great threat to public health due to its toxic effect and carcinogenicity. Thus, in modern scenario arsenic is synonymous with "toxic" and is documented as a paradoxical human carcinogen, although its mechanism of induction of neoplasia remains elusive. To assess the risk from environmental and occupational exposure of arsenic, in vivo cytogenetic assays have been conducted in arseniasis-endemic areas of the world using chromosomal aberrations (CA) and sister chromatid exchanges (SCE) as biomarkers in peripheral blood lymphocytes. The primary aim of this report is to critically review and update the existing in vivo cytogenetic studies performed on arsenic-exposed populations around the world and compare the results on CA and SCE from our own study, conducted in arsenic-endemic villages of North 24 Parganas (district) of West Bengal, India from 1999 to 2003. Based on a structured questionnaire, 165 symptomatic (having arsenic induced skin lesions) subjects were selected as the exposed cases consuming water having a mean arsenic content of 214.96 microg/l. For comparison 155 age-sex matched control subjects from an unaffected district (Midnapur) of West Bengal were recruited. Similar to other arsenic exposed populations our population also showed a significant difference (P < 0.01) in the frequencies of CA and SCE between the cases and control group. Presence of substantial chromosome damage in lymphocytes in the exposed population predicts an increased future carcinogenic risk by this metalloid.

Adult↗
PubMed2002

Biological gradient between long-term arsenic exposure and carotid atherosclerosis.

BACKGROUND: Long-term exposure to ingested arsenic has been documented to induce peripheral vascular disease, ischemic heart disease, and cerebral infarction in a dose-response relationship. This study further examined the biological gradient between ingested inorganic arsenic and carotid atherosclerosis. METHODS AND RESULTS: We studied 199 male and 264 female adult residents from the southwestern area of endemic arseniasis in Taiwan. The extent of carotid atherosclerosis was assessed by duplex ultrasonography. Diabetes mellitus was determined by oral glucose tolerance test, hypertension by mercury sphygmomanometers, and serum lipid profiles by autoanalyzers. Information regarding the consumption of high-arsenic artesian well water, cigarette smoking, and alcohol consumption was obtained through standardized questionnaire interviews. Logistic regression analysis was used to estimate the odds ratio and its 95% CI of carotid atherosclerosis for various risk factors. Three indices of long-term exposure to ingested arsenic, including the duration of consuming artesian well water, the average arsenic concentration in consumed artesian well water, and cumulative arsenic exposure, were all significantly associated with prevalence of carotid atherosclerosis in a dose-response relationship. The biological gradient remained significant after adjustment for age, sex, hypertension, diabetes mellitus, cigarette smoking, alcohol consumption, waist-to-hip ratio, and serum levels of total cholesterol and LDL cholesterol. The multivariate-adjusted odds ratio was 3.1 (95% CI 1.3 to 7.4) for those who had a cumulative arsenic exposure of > or =20 mg/L-years compared with those without exposure to arsenic from drinking artesian well water. CONCLUSIONS: Carotid atherosclerosis is associated with ingested inorganic arsenic, showing a significant biological gradient.

Age Factors↗
PubMed1999

Hypertension and arsenic exposure in Bangladesh.

-A prevalence comparison of hypertension among subjects with and those without arsenic exposure through drinking water was conducted in Bangladesh to confirm or refute an earlier observation of a relation in this respect. Wells with and without present arsenic contamination were identified, and we interviewed and examined 1595 subjects who were depending on drinking water from these wells for living, all >/=30 years of age. The interview was based on a questionnaire, and arsenic exposure was estimated from the history of well-water consumption and current arsenic levels. Of the 1595 subjects studied, 1481 had a history of arsenic-contaminated drinking water, whereas 114 had not. Time-weighted mean arsenic levels (in milligrams per liter) and milligram-years per liter of arsenic exposure were estimated for each subject. Exposure categories were assessed as <0.5 mg/L, 0.5 to 1.0 mg/L, and >1.0 mg/L and alternatively as <1.0 mg-y/L, 1.0 to 5.0 mg-y/L, >5.0 but </=10.0 mg-y/L, and >10.0 mg-y/L, respectively. Hypertension was defined as a systolic blood pressure of >/=140 mm Hg in combination with a diastolic blood pressure of >/=90 mm Hg. Corresponding to the exposure categories, and using "unexposed" as the reference, the prevalence ratios for hypertension adjusted for age, sex, and body mass index were 1.2, 2.2, 2.5 and 0.8, 1.5, 2.2, 3.0, in relation to arsenic exposure in milligrams per liter and milligram-years per liter, respectively. The indicated dose-response relationships were significant (P<<0.001) for both series of risk estimates. These results suggest that arsenic exposure may induce hypertension in humans.

Adult↗