يعرض 1 - 10 نتائج من 83 نتيجة بحث عن '"ARSENIC EXPOSURE"', وقت الاستعلام: 1.23s تنقيح النتائج
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    المصدر: Public Health Rep

    الوصف: Objectives Chronic exposure to arsenic has been reported as a risk factor for nonmelanoma skin cancer, notably squamous cell carcinoma. However, current knowledge is limited about the association between arsenic exposure and melanoma. Our objectives were to (1) measure the association between total urinary arsenic levels and melanoma compared with nonmelanoma skin cancer and no cancer and (2) analyze the association between water source and melanoma and nonmelanoma skin cancer. Methods We collected cross-sectional data from the 2003-2016 cycles of the National Health and Nutrition Examination Survey. We conducted univariate and multivariate logistic regressions. To evaluate the possible association of skin cancer with source of tap water, we calculated odds ratios for participants with melanoma and nonmelanoma skin cancer, compared with participants with no cancer. Results White race, higher education, higher socioeconomic status, and smoking history were associated with melanoma and nonmelanoma skin cancer in the full study population. After adjusting for age and race/ethnicity, the adjusted odds ratio of participants with >50 μg/L of total urinary arsenic for melanoma or nonmelanoma skin cancer was 1.87 (95% CI, 0.58-6.05) and 2.23 (95% CI, 1.12-4.45) times higher compared with no cancer, respectively. Participants with nonmelanoma skin cancer had 2.06 increased odds of reporting a nonmunicipal water source compared with participants without cancer. Conclusions We did not find a relationship between the incidence of melanoma and exposure to arsenic among US adults. Nonmunicipal water sources were associated with nonmelanoma skin cancer and should be further investigated.

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    المصدر: J Nutr

    الوصف: BACKGROUND: Detoxification of inorganic arsenic (iAs) occurs when it methylates to form monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). Lower proportions of urinary iAs and MMA, and higher proportions of DMA indicate efficient methylation. The role of B-vitamins in iAs methylation in children with low-level arsenic exposure is understudied. OBJECTIVES: Our study objective was to assess the association between B-vitamin intake and iAs methylation in children with low-level arsenic exposure (

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    المؤلفون: Devinder K. Dhawan, Payal Bhardwaj

    المصدر: Toxicology and Industrial Health. 35:593-603

    الوصف: The aim of this study was to understand the effects of zinc supplementation on antioxidant defense systems, hematological indices, and erythrocyte morphology in conditions of chronic arsenic toxicity. Male Wistar rats were segregated into four groups: control, arsenic treated, zinc supplemented, and arsenic + zinc treated. The animals in the arsenic-treated group were given arsenic orally in drinking water in the form of sodium arsenite at a dose level of 100 mg L−1, and zinc was administered to zinc-treated animals in the form of zinc sulfate orally in drinking water at a dose level of 227 mg L−1. The animals were subjected to different treatments for a period of 12 weeks, and various investigations were undertaken that included serum zinc content, activity of antioxidant enzymes, and hematological indices. Further, scanning electron microscopic (SEM) studies were performed to assess morphological changes in erythrocytes. Arsenic treatment significantly reduced serum zinc concentrations, which, however, were restored to near-normal levels upon zinc supplementation. The activities of enzymes involved in antioxidant defense systems were altered in the erythrocyte lysates of arsenic-treated rats, which interestingly revealed a significant improvement upon simultaneous zinc supplementation. A significant reduction in the counts of total leukocytes, neutrophils, and lymphocytes was observed following arsenic intoxication, which came back to near control levels following zinc supplementation. Also, protective effects of zinc were evident from SEM that revealed maintenance of topographical appearances of erythrocytes in conditions of arsenic toxicity. Thus, this study clearly shows the protection afforded by zinc on erythrocytes during arsenic-induced toxicity.

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    المصدر: Heliyon, Vol 7, Iss 3, Pp e06409-(2021)
    Heliyon

    الوصف: Background Based on the cross-sectional and cohort studies, exposure to As via drinking water can cause hypertension. Methods We searched PubMed, ISI WOS, and Scopus for relevant studies up to 1 January 2018 using related keywords. The meta-analysis was done on 10 studies (n = 28255) that report Odds Ratio for hypertension. The extracted ORs between As concentration and hypertension were pooled using random effect models. Study heterogeneity was analyzed using I2. Results The estimated adjusted OR for association between As and hypertension was 1.44 (95% CI: 1.12, 1.84) with I2 = 71%. Dose-Response analysis showed a linear relationship between As and hypertension (OR = 1.0008 95% CI: 1.0003, 1.001). In general, by increase of each unit in arsenic concentration, odds of the hypertension would increase as 0.08%. Conclusion There was a significant relationship between As exposure and hypertension.
    Arsenic, Meta-analysis, Health risk, Chronic exposure, Drinking water

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    المصدر: Carcinogenesis. 40:715-723

    الوصف: Telomere length per se a heritable trait has been reported to be associated with different diseases including cancers. In this study based on arsenic exposed 528 cases with basal cell carcinoma of skin (BCC) and 533 healthy controls, we observed a statistically significant association between decreased telomere length and increased BCC risk (OR = 5.92, 95% CI = 3.92-9.01, P1.32 µg/L) was statistically significantly associated with decreased telomere length (β = −0.026, 95% CI = − 0.05-0.003, P = 0.02). The interaction between arsenic exposure and telomere length on BCC risk was statistically significant (P = 0.02). Within each tertile based on arsenic exposure, the individuals with shorter telomeres were at an increased risk of BCC, with highest risk being in the highest exposed group (OR = 16.13, 95% CI = 6.71-40.00, PP P = 0.0002). The combined effect of highest arsenic exposure and shortest telomeres on the risk of BCC (OR = 10.56, 95% CI = 5.14-21.70) showed a statistically significant departure from additivity (interaction constant ratio 6.56, P = 0.03). Our results show that in the presence of arsenic exposure, decreased telomere length predisposes individuals to increased risk of BCC, with the effect being synergistic in individuals with highest arsenic exposure and shortest telomeres.

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    المصدر: Toxicol Res (Camb)

    الوصف: It is estimated that around 140 million people are drinking highly contaminated water with arsenic (As) as a natural earth’s crust component. On the other hand, the prevalence of neurodegenerative disorders, especially Alzheimer’s disease, is constantly increasing. The aim of the present study was to investigate the correlation between oral arsenic trioxide exposure and its impact on tau protein phosphorylation at Ser262. Fifty-four male mice were randomly divided into three groups and were freely accessed to food and contaminated water of 1 and 10 ppm arsenic trioxide for 3 months, except for control subjects. At the end of each month, As concentration and tau phosphorylation were checked with graphite furnace atomic absorption spectrometer and western blot analysis, respectively. Surprisingly, it was observed that the amount of measured brain arsenic in 10 ppm-exposed subjects was significantly increased after 3 months (P-value ˂ 0.0001). The significant changes in tau phosphorylation were not seen in the 1 ppm-exposed subjects, and it was observed that Ser262 phosphorylation significantly increased after 2 and 3 months in the 10 ppm group (P-value < 0.05). Our results demonstrated that arsenic accumulated in the brain time-dependently and increased Ser262 tau phosphorylation, which is very important in several tauopathies. In conclusion, it could be inferred that environmental arsenic exposure even at very low concentrations could be considered as a reason for increasing the risk of developing neurodegenerative disease.

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    المؤلفون: Lindsey Konkel

    المصدر: Environmental Health Perspectives

    الوصف: Background: The prevalence of type 2 diabetes (T2D) has more than doubled since 1980. Poor nutrition, sedentary lifestyle, and obesity are among the primary risk factors. While an estimated 70% of cases are attributed to excess adiposity, there is an increased interest in understanding the contribution of environmental agents to diabetes causation and severity. Arsenic is one of these environmental chemicals, with multiple epidemiology studies supporting its association with T2D. Despite extensive research, the molecular mechanism by which arsenic exerts its diabetogenic effects remains unclear. Objectives: We conducted a literature search focused on arsenite exposure in vivo and in vitro, using relevant end points to elucidate potential mechanisms of oral arsenic exposure and diabetes development. Methods: We explored experimental results for potential mechanisms and elucidated the distinct effects that occur at high vs. low exposure. We also performed network analyses relying on publicly available data, which supported our key findings. Results: While several mechanisms may be involved, our findings support that arsenite has effects on whole-body glucose homeostasis, insulin-stimulated glucose uptake, glucose-stimulated insulin secretion, hepatic glucose metabolism, and both adipose and pancreatic β-cell dysfunction. Discussion: This review applies state-of-the-science approaches to identify the current knowledge gaps in our understanding of arsenite on diabetes development. https://doi.org/10.1289/EHP4517Test

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    المصدر: Chemosphere. 252

    الوصف: The present study aimed to identify the effects of arsenic on behaviors in Caenorhabditis elegans (C. elegans) and the transgenerational effects. The synchronized C. elegans (P generation) were exposed to 0, 0.2, 1.0, and 5.0 mM NaAsO2 and the subsequent generations (F1 and F2) were maintained on fresh nematode growth medium (NGM). The behaviors and growth were recorded at 0, 12, 24, 36, 48, 60, and 72 h post synchronization. The results demonstrated that arsenic affected various indicators regarding the behavior (head thrash, body bend, movement speed, wavelength, amplitude and so on) and in general the effects started to accumulate from 24 h and lasted throughout the exposure. The behavior impairments were transgenerational with varying patterns, amongst the head thrash and body bend responded most sensitively though the responses gradually declined across generations. Arsenic exposure inhibited the growth (body length, body width, and body area) in P C. elegans from 24 h to 60 h, however there was no difference between treatments groups and the control at 72 h. Arsenic led to a dose-dependent degeneration of dopaminergic neurons in C. elegans, and inhibition of BAS-1 and CAT-2 expressions. The expressions of GCS-1, GSS-1, and SKN-1 were induced by arsenic exposure. Overall, chronic arsenic exposure impaired the behaviors and there were transgenerational effects. The head thrash and body bend responded most sensitively. Arsenic induced behavioral disorders might be attributed to degeneration of dopaminergic neurons which was associated with oxidative stress.