63 research outputs found

    Creatinine, diet, micronutrients, and arsenic methylation in West Bengal, India.

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    BackgroundIngested inorganic arsenic (InAs) is methylated to monomethylated (MMA) and dimethylated metabolites (DMA). Methylation may have an important role in arsenic toxicity, because the monomethylated trivalent metabolite [MMA(III)] is highly toxic.ObjectivesWe assessed the relationship of creatinine and nutrition--using dietary intake and blood concentrations of micronutrients--with arsenic metabolism, as reflected in the proportions of InAS, MMA, and DMA in urine, in the first study that incorporated both dietary and micronutrient data.MethodsWe studied methylation patterns and nutritional factors in 405 persons who were selected from a cross-sectional survey of 7,638 people in an arsenic-exposed population in West Bengal, India. We assessed associations of urine creatinine and nutritional factors (19 dietary intake variables and 16 blood micronutrients) with arsenic metabolites in urine.ResultsUrinary creatinine had the strongest relationship with overall arsenic methylation to DMA. Those with the highest urinary creatinine concentrations had 7.2% more arsenic as DMA compared with those with low creatinine (p < 0.001). Animal fat intake had the strongest relationship with MMA% (highest tertile animal fat intake had 2.3% more arsenic as MMA, p < 0.001). Low serum selenium and low folate were also associated with increased MMA%.ConclusionsUrine creatinine concentration was the strongest biological marker of arsenic methylation efficiency, and therefore should not be used to adjust for urine concentration in arsenic studies. The new finding that animal fat intake has a positive relationship with MMA% warrants further assessment in other studies. Increased MMA% was also associated, to a lesser extent, with low serum selenium and folate

    Nutritional Factors and Susceptibility to Arsenic-Caused Skin Lesions in West Bengal, India

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    There has been widespread speculation about whether nutritional deficiencies increase the susceptibility to arsenic health effects. This is the first study to investigate whether dietary micronutrient and macronutrient intake modulates the well-established human risk of arsenic-induced skin lesions, including alterations in skin pigmentation and keratoses. The study was conducted in West Bengal, India, which along with Bangladesh constitutes the largest population in the world exposed to arsenic from drinking water. In this case–control study design, cases were patients with arsenic-induced skin lesions and had < 500 ÎŒg/L arsenic in their drinking water. For each case, an age- and sex-matched control was selected from participants of a 1995–1996 cross-sectional survey, whose drinking water at that time also contained < 500 ÎŒg/L arsenic. Nutritional assessment was based on a 24-hr recall for major dietary constituents and a 1-week recall for less common constituents. Modest increases in risk were related to being in the lowest quintiles of intake of animal protein [odds ratio (OR) = 1.94; 95% confidence interval (CI), 1.05–3.59], calcium (OR = 1.89; 95% CI, 1.04–3.43), fiber (OR = 2.20; 95% CI, 1.15–4.21), and folate (OR = 1.67; 95% CI, 0.87–3.2). Conditional logistic regression suggested that the strongest associations were with low calcium, low animal protein, low folate, and low fiber intake. Nutrient intake was not related to arsenic exposure. We conclude that low intake of calcium, animal protein, folate, and fiber may increase susceptibility to arsenic-caused skin lesions. However, in light of the small magnitude of increased risks related to these dietary deficiencies, prevention should focus on reducing exposure to arsenic

    Adverse Childhood Experiences and Use of Cigarettes and Smokeless Tobacco Products

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    Adverse childhood experiences (ACEs) have been linked to increased use of tobacco products&nbsp;later in life. However, studies to date&nbsp;have ignored smokeless tobacco products. To address this, data from the 2011 Behavioral Risk Factor Surveillance System, which interviewed adults 18&nbsp;years and over (N&nbsp;=&nbsp;102,716) were analyzed. Logistic regression models were fit to estimate odds ratios&nbsp;of ever smoking, current smoking and current smokeless tobacco use in relation to ACEs. Results showed that less than 4&nbsp;% of respondents currently used smokeless tobacco products, while 44.95 and 18.57&nbsp;% reported ever and current smoking, respectively. Physical abuse (OR 1.40; 95&nbsp;% CI 1.14, 1.72), emotional abuse (OR 1.41; 95&nbsp;% CI 1.19, 1.67), sexual abuse (OR 0.70; 95&nbsp;% CI 0.51, 0.95), living with a drug user (OR 1.50; 95&nbsp;% CI 1.17, 1.93), living with someone who was jailed (OR 1.50; 95&nbsp;% CI 1.11, 2.02) and having parents who were separated or divorced (OR 1.31; 95&nbsp;% CI 1.09, 1.57) were associated with smokeless tobacco use in unadjusted models. After accounting for confounders, physical abuse (OR 1.43; 95&nbsp;% CI 1.16, 1.78), emotional abuse (OR 1.32; 95&nbsp;% CI 1.10, 1.57), living with a problem drinker (OR 1.30; 95&nbsp;% CI 1.08, 1.58), living with a drug user (OR 1.31; 95&nbsp;% CI 1.00, 1.72) and living with adults who treated each other violently (OR 1.30; 95&nbsp;% CI 1.05, 1.62) were associated with smokeless tobacco use. Living with someone who was mentally ill (OR 0.70; 95&nbsp;% CI 0.53, 0.92) was associated with smokeless tobacco use after accounting for confounders and all ACEs. Results indicated that some childhood adversities are associated with use of smokeless tobacco products. Special attention is needed to prevent tobacco use&nbsp;of different types among those experiencing ACEs

    Prenatal exposure to ambient air pollutants and congenital heart defects: An umbrella review

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    Background: Prenatal exposure to ambient air pollutants has been linked to congenital heart defects (CHD), but findings of existing systematic reviews have been mixed. Objective: To assess the epidemiological evidence on associations between prenatal exposure to ambient air pollutants and CHD subtypes, based on a systematic overview of reviews (“umbrella review”). Methods: We conducted a systematic search for reviews assessing associations between prenatal exposure to criteria air pollutants and CHD. The risk of bias was evaluated using the Risk of Bias in Systematic Reviews (ROBIS) tool. The certainty of the systematic review findings was graded using the Navigation Guide methodology. Results: We identified eleven systematic reviews, including eight with meta-analyses, assessing in total 35 primary studies of prenatal exposure to criteria air pollutants and various CHD subtypes. The certainty of the findings of four meta-analyses indicating an increased risk for coarctation of the aorta associated with nitrogen dioxide exposure was rated as moderate. The certainty of findings indicating positive, inverse, or null associations for other pollutant-subtype combinations was rated as very low to low, based on low precision and high statistical heterogeneity of summary odds ratios (SOR), substantial inconsistencies between review findings, and methodological limitations of the systematic reviews. Discussion: The inconsistent findings and high statistical heterogeneity of many SOR of the included systematic reviews may partly be traced to differences in methodological approaches, and the risk of bias across included reviews (e.g., inclusion criteria, systematic search strategies, synthesis methods) and primary studies (e.g., exposure assessment, diagnostic criteria). Adherence to appropriate systematic review guidelines for environmental health research, as well as rigorous evaluation of risk of bias in primary studies, are essential for future risk assessments and policy-making. Still, our findings suggest that prenatal exposure to ambient air pollutants may increase risks for at least some CHD subtypes

    WHO Regional Office for Europe

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    Children’s health and environment: A review of evidenc
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