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PubMed2000

Basal cell carcinoma in chronic arsenicism occurring in Queensland, Australia, after ingestion of an asthma medication.

BACKGROUND: Ingestion of trivalent inorganic arsenic has long been recognized as a cause of basal cell carcinomas (BCCs) and has been reported most often in Taiwan and Singapore. OBJECTIVE: Our purpose was to study the clinical and histologic characteristics of BCCs occurring in Australian Caucasians as a consequence of chronic arsenicism due to ingestion of an arsenic-containing medication. METHODS: Self-referred persons with a history of ingestion of Bell's Asthma Medication were interviewed, and skin examinations were performed. Local age- and sex-matched patients with BCCs were used to compare the distribution and histologic subtypes of BCCs in arsenic-exposed and sporadic cases. RESULTS: Thirty-six persons (21 male, 15 female; mean age, 57 years) participated, all of whom had been exposed to the asthma medication early in life (mean age, 13 years) for a mean duration of 5 years. Each person had at least one cutaneous sign of chronic arsenicism, either self-reported or on examination, and all except one had a history of either BCC or squamous cell carcinoma of the skin, with self-reports of 20 to 2000 skin lesions removed per person. The mean age at first presentation with a BCC was 33 years, but neither latency nor number of skin lesions appeared to be related to duration of exposure to arsenic. BCCs in persons exposed to arsenic occurred more often on sun-protected sites compared with BCCs in age- and sex-matched sporadic cases (P <.001), but the distribution and histologic subtypes between these two groups were similar. CONCLUSION: We have described BCCs in arsenic-exposed Australians and shown that they occur predominantly in sun-protected locations. Although the reported number of skin lesions is very high, the latency and number do not appear to be related to the duration of arsenic exposure. The histologic types of the BCCs occurring in arsenic-exposed persons are not different from sporadic BCCs.

Adult↗
PubMed2004

The role of thiol species in the hypertolerance of Aspergillus sp. P37 to arsenic.

Aspergillus sp. P37 is an arsenate-hypertolerant fungus isolated from a river in Spain with a long history of contamination with metals. This strain is able to grow in the presence of 0.2 M arsenate, i.e. 20-fold higher than the reference strain, Aspergillus nidulans TS1. Although Aspergillus sp. P37 reduces As(V) to As(III), which is slowly pumped out of the cell, the measured efflux of oxyanions is insufficient to explain the high tolerance levels of this strain. To gain an insight into this paradox, the accumulation of acid-soluble thiol species in Aspergillus sp. P37 when exposed to arsenic was compared with that of the arsenic-sensitive A. nidulans TS1 strain. Increasing levels of arsenic in the medium did not diminish the intracellular pool of reduced glutathione in Aspergillus sp. P37, in sharp contrast with the decline of glutathione in A. nidulans under the same conditions. Furthermore, concentrations of arsenic that were inhibitory for the sensitive A. nidulans strain (e.g. 50 mM and above) provoked a massive formation of vacuoles filled with thiol species. Because the major fraction of the cellular arsenic was present as the glutathione conjugate As(GS)3, it is plausible that the arsenic-hypertolerant phenotype of Aspergillus sp. P37 is in part due to an enhanced capacity to maintain a large intracellular glutathione pool under conditions of arsenic exposure and to sequester As(GS)3 in vacuoles. High pressure liquid chromatography analysis of cell extracts revealed that the contact of Aspergillus sp. P37 (but not A. nidulans) with high arsenic concentrations (> or =150 mM) induced the production of small quantities of a distinct thiol species indistinguishable from plant phytochelatin-2. Yet, we argue that phytochelatins do not explain arsenic resistance in Aspergillus, and we advocate the role of As(GS)3 complexes in arsenic detoxification.

Anions↗
PubMed2005

Therapeutic value of Hippophae rhamnoides L. against subchronic arsenic toxicity in mice.

The present study was planned to investigate the therapeutic efficacy of Hippophae rhamnoides L. against the toxic effects of arsenic in mice. H. rhamnoides L. is used as an herbal remedy for gastric ulcers, burns, and some skin and allergic diseases. Twenty-five Swiss albino mice were exposed to arsenic (25 ppm) in drinking water for 3 months. After 3 months different fruit extracts of H. rhamnoides L. (500 mg/kg for 10 days) were administered, the animals were sacrificed, and blood and tissues were assayed for various biochemical indicators of oxidative stress and whether arsenic was removed from tissues. Treatment with different fruit extracts of H. rhamnoides L. showed significant protection from arsenic inhibition of blood delta-aminolevulinic acid dehydratase activity and restored blood reduced glutathione levels. Other hematologic variables like white blood cell counts, hemoglobin, and hematocrit were partially protected by supplementation with a water extract of H. rhamnoides L. (HF-WRT). Significant protection was also observed in altered hepatic, renal, and brain reduced/ oxidized glutathione ratio and thiobarbituric acid-reactive substances levels. The aqueous extract of H. rhamnoides L. (HF-WRT) also provided protection against parameters indicative of liver injury such as aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities. There was also no effect on blood and tissue arsenic concentrations observed except some moderate depletion of blood arsenic concentrations, suggesting that the drug has no ability to chelate intracellular arsenic. It can be concluded from these results that post-treatment with an aqueous extract of H. rhamnoides L. (HF-WRT) significantly protects against arsenic-induced oxidative stress but does not chelate arsenic, suggesting it may have a beneficial role as a supplementing agent during chelation of arsenic by other means.

Animals↗
PubMed2006

Applying a health behavior theory to explore the influence of information and experience on arsenic risk representations, policy beliefs, and protective behavior.

The common sense model (CSM) shows how people process information to construct representations, or mental models, that guide responses to health threats. We applied the CSM to understand how people responded to information about arsenic-contaminated well water. Constructs included external information (arsenic level and information use), experience (perceived water quality and arsenic-related health effects), representations, safety judgments, opinions about policies to mitigate environmental arsenic, and protective behavior. Of 649 surveys mailed to private well users with arsenic levels exceeding the maximum contaminant level, 545 (84%) were analyzed. Structural equation modeling quantified CSM relationships. Both external information and experience had substantial effects on behavior. Participants who identified a water problem were more likely to reduce exposure to arsenic. However, about 60% perceived good water quality and 60% safe water. Participants with higher arsenic levels selected higher personal safety thresholds and 20% reported a lower arsenic level than indicated by their well test. These beliefs would support judgments of safe water. A variety of psychological and contextual factors may explain judgments of safe water when information suggested otherwise. Information use had an indirect effect on policy beliefs through understanding environmental causes of arsenic. People need concrete information about environmental risk at both personal and environmental-systems levels to promote a comprehensive understanding and response. The CSM explained responses to arsenic information and may have application to other environmental risks.

Arsenic↗
PubMed2006

Transcriptome kinetics of arsenic-induced adaptive response in zebrafish liver.

Arsenic is a prominent environmental toxicant and carcinogen; however, its molecular mechanism of toxicity and carcinogenicity remains poorly understood. In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 15 parts/million (ppm) arsenic [As(V)] for 8-96 h to identify global transcriptional changes and biological networks involved in arsenic-induced adaptive responses in vivo. We found that there was an increase of transcriptional activity associated with metabolism, especially for biosyntheses, membrane transporter activities, cytoplasm, and endoplasmic reticulum in the 96 h of arsenic treatment, while transcriptional programs for proteins in catabolism, energy derivation, and stress response remained active throughout the arsenic treatment. Many differentially expressed genes encoding proteins involved in heat shock proteins, DNA damage/repair, antioxidant activity, hypoxia induction, iron homeostasis, arsenic metabolism, and ubiquitin-dependent protein degradation were identified, suggesting strongly that DNA and protein damage as a result of arsenic metabolism and oxidative stress caused major cellular injury. These findings were comparable with those reported in mammalian systems, suggesting that the zebrafish liver coupled with the available microarray technology present an excellent in vivo toxicogenomic model for investigating arsenic toxicity. We proposed an in vivo, acute arsenic-induced adaptive response model of the zebrafish liver illustrating the relevance of many transcriptional activities that provide both global and specific information of a coordinated adaptive response to arsenic in the liver.

Adaptation, Physiological↗
PubMed2006

Arsenic inhibits CFTR-mediated chloride secretion by killifish (Fundulus heteroclitus) opercular membrane.

Killifish are euryhaline teleosts that normally experience rapid changes in the salinity of the swim water. Acclimation to seawater is mediated by cortisol, which by activating glucocorticoid receptors, upregulates CFTR mediated Cl- secretion in the gill and operculum. Arsenic, a toxic metalloid that naturally occurs in the aquatic environment, has been shown to disrupt glucocorticoid hormone-mediated regulation of genes. Because little is known about the effects of environmentally relevant levels of arsenic on ion channels and salt homeostasis, studies were conducted to examine the effects of arsenic on the ability of killifish to acclimate to increased salinity. Arsenic in the swim water or administered by intraperitoneal injection prevented acclimation. To determine if arsenic blocked acclimation by inhibiting CFTR mediated Cl- secretion (Isc), opercular membranes were isolated and mounted in Ussing chambers and the effects of arsenic on Isc were measured. Arsenic (24 hr exposure) reduced Isc in opercular membranes isolated from salt water acclimated killifish. In addition, arsenic acutely (5-10 minutes) and reversibly inhibited Isc with an IC50 = 4.1 microM (305 ppb) when applied to the apical (seawater) side of the operculum, but not when added to the basolateral side of the operculum. Arsenic (4 microM for 60 minutes) also reduced mitochondrial respiration. Thus, environmentally relevant levels of arsenic block acclimation to seawater in killifish by reversibly inhibiting CFTR-mediated Cl- secretion by the opercular membrane, in part by inhibiting mitochondrial respiration.

Acclimatization↗
PubMed2005

Arsenic suppresses gene expression in promyelocytic leukemia cells partly through Sp1 oxidation.

The mechanism by which arsenic dramatically affects gene expression remains poorly understood. Here we report that prolonged exposure of acute promyelocytic leukemia NB4 cells to low levels of arsenic trioxide increased the expression of a set of genes responsible for reactive oxygen species (ROS) production. We hypothesize that arsenic-induced ROS in turn contribute partially to altered gene expression. To identify genes responsive to arsenic-induced ROS, we used microarray gene expression analysis and identified genes that responded to arsenic and hydrogen peroxide but whose response to arsenic was reversed by an ROS scavenger, N-acetyl-L-cysteine. We found that 26% of the genes significantly responsive to arsenic might have been directly altered by ROS. We further explored the mechanisms by which ROS affects gene regulation and found that the Sp1 transcription factor was oxidized by arsenic treatment, with a corresponding decrease in its in situ binding on the promoters of 3 genes, hTERT, C17, and c-Myc, whose expressions were significantly suppressed. We conclude that ROS contributed partly to arsenic-mediated gene regulation and that Sp1 oxidation contributed to gene suppression by arsenic-induced ROS.

Antineoplastic Agents↗
PubMed2002

Evidence for induction of oxidative stress caused by chronic exposure of Chinese residents to arsenic contained in drinking water.

Exposure of experimental animals or cultured cells to arsenic induces oxidative stress, but, to date, no examination of this phenomenon in humans has been reported. In this study we conducted a cross-sectional study in Wuyuan, Inner Mongolia, China, to explore the relationship between chronic arsenic exposure from drinking water and oxidative stress in humans. Thirty-three inhabitants who had been drinking tube-well water with high concentrations of inorganic arsenic (mean value = 0.41 mg/L) for about 18 years constituted the high-exposure group, and 10 residents who lived nearby but were exposed to much lower concentrations of arsenic in their drinking water (mean value = 0.02 mg/L) were selected as the low-exposure comparison group. Results of the present study indicated that although the activity for superoxide dismutase (SOD) in blood did not differ significantly between the two groups, the mean serum level of lipid peroxides (LPO) was significantly higher among the high-exposed compared with the low-exposed group. Elevated serum LPO concentrations were correlated with blood levels of inorganic arsenic and its methylated metabolites. In addition, they showed an inverse correlation with nonprotein sulfhydryl (NPSH) levels in whole blood. The subjects in the high-arsenic-exposure group had mean blood NPSH levels 57.6% lower than those in the low-exposure group. Blood NPSH levels were inversely correlated with the concentrations of inorganic arsenic and its methylated metabolites in blood and with the ratio of monomethylarsenic to inorganic arsenic. These results provide evidence that chronic exposure to arsenic from drinking water in humans results in induction of oxidative stress, as indicated by the reduction in NPSH and the increase in LPO. Some possible mechanisms for the arsenic-induced oxidative stress are discussed.

Adolescent↗
PubMed2004

Mean total arsenic concentrations in chicken 1989-2000 and estimated exposures for consumers of chicken.

The purpose of this study was to estimate mean concentrations of total arsenic in chicken liver tissue and then estimate total and inorganic arsenic ingested by humans through chicken consumption. We used national monitoring data from the Food Safety and Inspection Service National Residue Program to estimate mean arsenic concentrations for 1994-2000. Incorporating assumptions about the concentrations of arsenic in liver and muscle tissues as well as the proportions of inorganic and organic arsenic, we then applied the estimates to national chicken consumption data to calculate inorganic, organic, and total arsenic ingested by eating chicken. The mean concentration of total arsenic in young chickens was 0.39 ppm, 3- to 4-fold higher than in other poultry and meat. At mean levels of chicken consumption (60 g/person/day), people may ingest 1.38-5.24 microg/day of inorganic arsenic from chicken alone. At the 99th percentile of chicken consumption (350 g chicken/day), people may ingest 21.13-30.59 microg inorganic arsenic/day and 32.50-47.07 microg total arsenic/day from chicken. These concentrations are higher than previously recognized in chicken, which may necessitate adjustments to estimates of arsenic ingested through diet and may need to be considered when estimating overall exposure to arsenic.

Age Factors↗
PubMed2005

Evaluation of exposure to arsenic in residential soil.

In response to concerns regarding arsenic in soil from a pesticide manufacturing plant, we conducted a biomonitoring study on children younger than 7 years of age, the age category of children most exposed to soil. Urine samples from 77 children (47% participation rate) were analyzed for total arsenic and arsenic species related to ingestion of inorganic arsenic. Older individuals also provided urine (n = 362) and toenail (n = 67) samples. Speciated urinary arsenic levels were similar between children (geometric mean, geometric SD, and range: 4.0, 2.2, and 0.89-17.7 microg/L, respectively) and older participants (3.8, 1.9, 0.91-19.9 microg/L) and consistent with unexposed populations. Toenail samples were < 1 mg/kg. Correlations between speciated urinary arsenic and arsenic in soil (r = 0.137, p = 0.39; n = 41) or house dust (r = 0.049, p = 0.73; n = 52) were not significant for children. Similarly, questionnaire responses indicating soil exposure were not associated with increased urinary arsenic levels. Relatively low soil arsenic exposure likely precluded quantification of arsenic exposure above background.

Adolescent↗
PubMed2005

Significance of private water supply wells in a rural Nevada area as a route of exposure to aqueous arsenic.

In many rural areas domestic drinking water needs are met by a mixture of public water supplies and private water supplies. Private supplies are not subject to the regulations and management requirements of the Safe Drinking Water Act (SDWA). Amendments to the SDWA recently lowered the standard for arsenic from 50 to 10 ppb in public water supplies (effective in 2006). Churchill County, Nevada, has approximately 25,000 residents. Slightly more than half (13,500) rely on private domestic wells for water supply. Ample data and media publicity about high arsenic concentrations in water supplies and a federally led investigation of a leukaemia cluster suggested that residents of the county would be aware that arsenic concentrations in private wells were highly likely to exceed the 10 ppb standard. A survey carried out in 2002 showed that a majority of respondents (72%) consumed water from private wells and among them a minority (38%) applied treatment. Maximum, median and minimum concentrations of arsenic from all samples (n = 351) were 2,100, 26 and < 3 ppb, respectively. Seventy-four per cent of all samples exceeded 10 ppb. A majority (87%) of those who applied treatment consumed tap water. The relatively low rate of application of treatment suggested that these rural residents did not recognize that consumption could have associated health risks. However, those who applied treatment were approximately 0.3 times as likely to be consuming water with > 10 ppb arsenic than those who consumed water that was not treated. In areas where concentrations of arsenic have been demonstrated to be high, it may be important to conduct a focused educational effort for private well owners to ensure that they take the steps needed to assess and reduce risks associated with contaminants found in tap water, including arsenic. An educational effort could include promoting sampling efforts to determine the magnitude of arsenic concentrations, explaining the risk associated with arsenic consumption and providing information about choices for home treatment systems that are likely to be effective in removing arsenic. This may be especially important in rural areas where adverse health effects are not evident to local populations.

Adolescent↗
PubMed2003

Occurrence of several arsenic compounds in the liver of birds, cetaceans, pinnipeds, and sea turtles.

Concentrations of total arsenic and individual arsenic compounds were determined in livers of birds, cetaceans, pinnipeds, and sea turtles by using hydride generation-atomic absorption spectrometry and high-performance liquid chromatography/inductively coupled plasma-mass spectrometry. Hepatic arsenic concentrations in loggerhead turtles (11.2 +/- 3.0 microg/g dry wt) and black-footed albatrosses (12.2 +/- 10.8 microg/g dry wt) were extremely high among the species examined, and the values were comparable with those of lower trophic marine animals such as fishes, cephalopods, crustaceans, and shellfishes. In all the species, arsenobetaine was the predominant arsenic compound in the livers. Especially, for black-footed albatrosses and black-tailed gull, the mean percentage of arsenobetaine was as high as 97.1 and 87.5, respectively, of extractable arsenic. The present study is among the first on arsenic speciation in avian species. Total arsenic concentration was strongly correlated with the concentration of arsenobetaine, while no significant relationship was observed between total arsenic concentration and other arsenic compounds in these animals. Because arsenobetaine is known to be rapidly excreted into the urine in humans and experimental animals, the observed results suggest that higher trophic marine animals might have a unique metabolism of arsenobetaine and that arsenobetaine plays an important role in the accumulation of arsenic in these animals.

Animals↗
PubMed2003

Bladder cancer and arsenic exposure: differences in the two populations enrolled in a study in southwest Taiwan.

OBJECTIVE: Analyses of bladder cancer mortality in the Black Foot Disease (BFD) endemic area of southwest Taiwan conducted by Morales et al. showed a discontinuity in risk at 400 microg/L arsenic in the drinking water in a stratified analysis and no discontinuity in a continuous analysis. As the continuous analysis presentation had been used by both the NRC and the EPA to assess the carcinogenic risk from arsenic ingestion, an explanation of the discontinuity was sought. METHODS: Review of 40 years of published health studies of the BFD-endemic area of SW Taiwan showed that earlier publications had limited their cancer associations with arsenic levels in artesian well waters and that the reports of Morales et al., NRC, and EPA failed to do so. Underlying data for the Morales et al. study were obtained from the appendix to the NRC report. Bladder cancer mortality rates were calculated from case counts and person-years of observation for each study village. Villages were categorized by water source according to the descriptions from the underlying study. Graphic and regression analyses were conducted of the bladder cancer mortality rates using exposure as a continuous variable and simultaneously stratifying by water source. RESULTS: The median village well arsenic levels ranged from 350 to 934 microg/L for villages solely dependent on artesian well water and from 10 to 717 microg/L for villages not solely dependent on artesian well water. Bladder cancer mortality rates were found to be dependent upon the arsenic level only for those villages that were solely dependent on artesian well water for their water source. Bladder cancer mortality rates were found to be independent of arsenic level for villages with non-artesian well water sources. CONCLUSIONS: The data indicate that arsenic exposure levels do not explain the bladder cancer mortality risk in SW Taiwan among villages not dependent upon artesian well water. The association for villages dependent upon artesian well water may be explained either by arsenic acting as a high-dose carcinogen or in artesian well water as a co-carcinogen with some other aspect of artesian well water (possibly humic acid). Arsenic exposure level alone appears to be an insufficient exposure measure to describe the risk of bladder cancer mortality in the BFD-endemic area. Risk analyses that fail to take water source into account are likely to misrepresent the risk characterization, particularly at low arsenic levels.

Adolescent↗
PubMedDate not supplied

Arsenic burden survey among refuse incinerator workers.

BACKGROUND: Incinerator workers are not considered to have arsenic overexposure although they have the risk of overexposure to other heavy metals. AIM: To examine the relationship between arsenic burden and risk of occupational exposure in employees working at a municipal refuse incinerator by determining the concentrations of arsenic in the blood and urine. SETTINGS AND DESIGN: The workers were divided into three groups based on their probability of contact with combustion-generated residues, namely Group 1: indirect contact, Group 2: direct contact and Group 3: no contact. Healthy age- and sex-matched residents living in the vicinity were enrolled as the control group. MATERIALS AND METHODS: Heavy metal concentrations were measured by atomic absorption spectrophotometer. Downstream rivers and drinking water of the residents were examined for environmental arsenic pollution. A questionnaire survey concerning the contact history of arsenic was simultaneously conducted. STATISTICAL ANALYSIS: Non-parametric tests, cross-tabulation and multinomial logistic regression. RESULTS: This study recruited 122 incinerator workers. The urine and blood arsenic concentrations as well as incidences of overexposure were significantly higher in the workers than in control subjects. The workers who had indirect or no contact with combustion-generated residues had significantly higher blood arsenic level. Arsenic contact history could not explain the difference. Airborne and waterborne arsenic pollution were not detected. CONCLUSION: Incinerator workers run the risk of being exposed to arsenic pollution, especially those who have incomplete protection in the workplace even though they only have indirect or no contact with combustion-generated pollutants.

Adult↗
PubMed1992

Arsenic in induced hair of the rat and its relation to the content in various organs during chronic exposure.

The behaviour of the rate of transfer of arsenic to hair induced at various times during a long-term exposure experiment was examined in rats supplied with 3 mg arsenic per litre of drinking water in the form of chloride. The arsenic was supplied during a period of 560 days. At the beginning a sharp increase was seen in the rate of transfer of arsenic to induced hair, as well as in the content of arsenic in the various organs. Subsequently, the rate of transfer to hair increased slowly but steadily up to the end of the experiment. During that time the level of arsenic in the liver and in the kidneys remained constant, whereas that in the brain and in some other organs increased slowly and irregularly. The correlation between the arsenic in the induced hair and that in the organs was statistically significant in all comparisons. Correlation coefficients greater than 0.7 were found in the comparisons of the content in the induced hair with those in the heart, the pancreas and the forebrain. The findings suggest that the rate of transfer of endogenous arsenic depends on two factors, one being the level of body intake of arsenic during the period of hair growth, the other the degree to which the element had accumulated in the body during the time which elapsed between the onset of arsenic supply and the start of hair growth.

Animals↗
PubMed2007

Genetic and epigenetic changes induced by chronic low dose exposure to arsenic of mouse testicular Leydig cells.

Arsenic is an important environmental carcinogen that affects millions of people worldwide through contaminated water supplies. Genotoxicity of arsenic has been a topic of controversy. Both genetic alterations (mutations) and epigenetic changes (methylation) have been shown to play a crucial role in environmental carcinogenesis. Chronic exposure to arsenic has been shown to induce malignant transformation of mammalian cells. However, the genetic aberrations induced by arsenic in this process are unclear. The purpose of this study was to determine if both lower (1 pg/ml) and higher concentrations (100 ng/ml) of arsenic induces either mutations or methylation changes that could lead to the development of genomic instability in TM3 cells, immortalized Leydig cells derived from normal mouse testis. Two independent exposure times were used in this study which resulted in cells of 33 and 100 generations in age. Arsenic-induced genetic and epigenetic changes were screened at a genome-wide level by random amplified polymorphic DNA (RAPD), also known as AP-PCR method with undigested DNA as well as DNA digested by the methylation sensitive isosizomeric restriction enzymes MSPI and HpaII and untreated controls. Changes in the DNA fingerprint of both, the restriction enzyme digested DNA (indicating methylation changes) as well as undigested DNA (indicating mutations) from arsenic-treated (low as well as high dose) samples were observed as compared to their controls. Thus, this study provides the first evidence at DNA sequence level for mutagenic potential of arsenic. Further characterization of these altered genomic regions is underway. The understanding of these genetic and epigenetic changes in arsenic-induced carcinogenesis will provide a basis for better interventional approaches in both the treatment and prevention of arsenic-induced cancer.

Animals↗
PubMed1980

A morbid condition involving cardio-vascular, broncho-pulmonary, digestive and neural lesions in children and young adults after dietary arsenic exposure.

An investigation on the relationship between dietary arsenic exposure and cardiovascular diseases was made. In Antofagasta Commune, northern Chile, since 1955 arsenic has polluted public drinking water. This environmental contamination is of geological origin. The concentration of arsenic in drinking water for the 1955-1970 period was 0.5980 ppm (weighted mean). In the period June 1970-March 1972, the concentration decreased to 0.0815 ppm (weighted mean), due to a Water Filtration Plant which started operating in May 1970. Greater Santiago showed 0.00 ppm of arsenic in drinking water. Amongst 10 autopsied patients (age range: 1 year 7 months to 18 years) with chronic arsenical dermatosis from Antofagasta Commune, 9 showed marked fibrous intimal thickening of the arterial wall and/or restricted lumen of the left coronary artery, 2 of these 9 also exhibiting myocardial infarction. Of the 10 patients, 7 developed cardiomegaly, which was related to chronic exposure to dietary arsenic. Two series of patients with myocardial infarction under 40 years of age, one from Antofagasta Commune (exposed to arsenic), the other from Greater Santiago (not exposed to arsenic) were compared. The Yates' corrected chi 2 value (1 d.f.) being 11.7776. The difference was statistically highly significant (P approximately equal to 0.0006018). Furthermore, in Antofagasta Commune, the number of cases (< 40 yr) which had myocardial infarction with chronic arsenical dermatosis were compared with the cases (< 40 yr) which showed myocardial infarction without chronic arsenical dermatosis. The Yates' corrected chi 2 value (1 d.f.) was 13.0395. A highly significant difference was detected (P approximately equal to 0.0003044). Children (0-15 yr)from the two cities were also compared.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Micronuclei in exfoliated bladder cells among individuals chronically exposed to arsenic in drinking water.

Inorganic arsenic is an established cause of lung and skin cancer. Epidemiological evidence from Taiwan suggests that arsenic causes more fatal internal cancers, with the highest relative risks reported for bladder cancer. We conducted a cross-sectional biomarker study in a Chilean male population chronically exposed to high (70 subjects) and low (55 subjects) arsenic levels in their drinking water (average concentrations, 600 and 15 micrograms As/liter, respectively). A fluorescent version of the exfoliated bladder cell micronucleus (MN) assay was used employing fluorescence in situ hybridization with a centromeric probe to identify the presence (MN+) or absence (MN-) of whole chromosomes within micronuclei, thereby determining the mechanism of arsenic-induced genotoxicity in vivo. We divided the study population into quintiles by urinary arsenic levels and found an exposure-dependent increase in micronucleated cell prevalence in quintiles 2-4 (urinary arsenic, 54-729 micrograms/liter). The largest increase appeared when quintile 4 was compared to quintile 1 [prevalence ratio, 3.0; 95% confidence interval (CI), 1.9-4.6]. The prevalence of MN+ increased to 3.1-fold in quintile 4 (95% CI, 1.4-6.6), and the prevalence of MN-increased to 7.5-fold in quintile 3 (95% CI, 2.8-20.3), suggesting that chromosome breakage was the major cause of MN formation. Prevalences of total MN, MN+, and MN- returned to baseline levels in quintile 5 (urinary arsenic, 729-1894 micrograms/liter), perhaps due to cytostasis or cytotoxicity. These results add additional weight to the hypothesis that ingesting arsenic-contaminated water enhances bladder cancer risk and suggest that arsenic induces genetic damage to bladder cells at drinking water levels close to the current United States Maximum Contaminant Level of 50 micrograms/liter for arsenic.

Adult↗