Article

Chen Y, Graziano JH, Parvez F, et al. Arsenic exposure from drinking water and mortality from cardiovascular disease in Bangladesh: prospective cohort study. BMJ. 342:d2431

Department of Environmental Medicine, New York University School of Medicine, New York, NY 10016, USA.
BMJ (online) (Impact Factor: 17.45). 05/2011; 342(may05 2):d2431. DOI: 10.1136/bmj.d2431
Source: PubMed

ABSTRACT

To evaluate the association between arsenic exposure and mortality from cardiovascular disease and to assess whether cigarette smoking influences the association.
Prospective cohort study with arsenic exposure measured in drinking water from wells and urine.
General population in Araihazar, Bangladesh.
11,746 men and women who provided urine samples in 2000 and were followed up for an average of 6.6 years.
Death from cardiovascular disease.
198 people died from diseases of circulatory system, accounting for 43% of total mortality in the population. The mortality rate for cardiovascular disease was 214.3 per 100,000 person years in people drinking water containing <12.0 µg/L arsenic, compared with 271.1 per 100,000 person years in people drinking water with ≥ 12.0 µg/L arsenic. There was a dose-response relation between exposure to arsenic in well water assessed at baseline and mortality from ischaemic heart disease and other heart disease; the hazard ratios in increasing quarters of arsenic concentration in well water (0.1-12.0, 12.1-62.0, 62.1-148.0, and 148.1-864.0 µg/L) were 1.00 (reference), 1.22 (0.65 to 2.32), 1.35 (0.71 to 2.57), and 1.92 (1.07 to 3.43) (P = 0.0019 for trend), respectively, after adjustment for potential confounders including age, sex, smoking status, educational attainment, body mass index (BMI), and changes in urinary arsenic concentration since baseline. Similar associations were observed when baseline total urinary arsenic was used as the exposure variable and for mortality from ischaemic heart disease specifically. The data indicate a significant synergistic interaction between arsenic exposure and cigarette smoking in mortality from ischaemic heart disease and other heart disease. In particular, the hazard ratio for the joint effect of a moderate level of arsenic exposure (middle third of well arsenic concentration 25.3-114.0 µg/L, mean 63.5 µg/L) and cigarette smoking on mortality from heart disease was greater than the sum of the hazard ratios associated with their individual effect (relative excess risk for interaction 1.56, 0.05 to 3.14; P = 0.010).
Exposure to arsenic in drinking water is adversely associated with mortality from heart disease, especially among smokers.

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    • "Further, As exposure through drinking water can be more detrimental to lung function than smoking (von Ehrenstein et al., 2005). Prolonged As exposure from drinking water also increases mortality from cardiovascular disease, especially among smokers (Argos et al., 2010; Chen et al., 2011). "
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    ABSTRACT: Millions of people in the deltaic regions of S/SE Asia regularly consume As contaminated groundwater. Arsenic persists within these groundwaters despite being flushed by several pore volumes of recharge, indicative of an in situ solid phase source. Despite the importance of this solid phase source, the identity and reactivity of the minerals hosting and releasing As in the deltaic aquifers remain poorly constrained. Here we seek to define the chemistry and reactivity of As and its host minerals in aquifer sediments recharged by both seasonally saturated and permanent wetlands in the Mekong Delta of Cambodia.Sediment cores were retrieved to depths of up to 30 m. Selective extractions on near-surface sediments (to depths of 4-6 m) indicate that more than a third (27-50%) of the Fe in the profile is "reducible" (citrate-bicarbonate-dithionite-extractable) - nominally consisting of Fe(III) oxides. The Fe(III) oxide fraction was approximately the same under seasonal wetlands (mean = 39%) compared with sediments from beneath permanent wetlands (mean = 37%). Correspondingly, Fe K-edge extended X-ray absorption fine structure (EXAFS) spectra analysis indicates that the Fe mineral phases are predominantly goethite and hematite (30-50%).Analysis of solid phase As speciation by X-ray absorption near edge structure (XANES) spectroscopy showed arsenate in the shallowest sediments (upper 1 and 4 m of seasonal and permanent wetlands), and arsenite and/or As sulfides as the dominant phases in the deeper sediments. The reducible As fraction ranged from 17% to 42% of the total As at both sites. The exception was found in a peat layer at 6 m beneath the seasonal wetland, in which only 1% of the total As was reducible. Arsenian pyrite was the predominant form of As in the peat. Thus, a pool of As hosted by reducible mineral phases persists in sediments below both the seasonal and permanently saturated wetland sites.
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    • "Using such drinking water that does not meet quality standards can lead to serious health threats such as cancer and other diseases. Chen et al. (2010) and (2011) and Smith, Lingas, and Rahman (2000) have investigated the contamination of drinking water with arsenic, and observed an increase in cancer risks, cardiovascular disease, and neuropathy. High nitrate levels in domestic well water cause health concerns for infants and pregnant women due to the in vivo conversion of nitrates to nitrites. "
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    • "Arsenic contamination in groundwater has been reported in several countries, including India, Bangladesh, Taiwan, Chile, Argentina and the USA [1] [2]. The chronic poisoning caused by high levels of arsenic in well waters led to public health emergency in Bangladesh [3] [4]. "
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    ABSTRACT: The groundwater pollutant arsenic can cause various cardiovascular disorders. Angiotensin II, a potent vasoconstrictor, plays an important role in vascular dysfunction by promoting changes in endothelial function, vascular reactivity, tissue remodeling and oxidative stress. We investigated whether modulation of angiotensin II signaling and redox homeostasis could be a mechanism contributing to arsenic-induced vascular disorder. Rats were exposed to arsenic at 25, 50 and 100ppm of sodium arsenite through drinking water consecutively for 90days. Blood pressure was recorded weekly. On the 91st day, the rats were sacrificed for blood collection and isolation of thoracic aorta. Angiotensin converting enzyme and angiotensin II levels were assessed in plasma. Aortic reactivity to angiotensin II was assessed in organ-bath system. Western blot of AT1 receptors and G protein (Gαq/11), ELISA of signal transducers of MAP kinase pathway and reactive oxygen species (ROS) generation were assessed in aorta. Arsenic caused concentration-dependent increase in systolic, diastolic and mean arterial blood pressure from the 10th, 8th and 7th week onwards, respectively. Arsenic caused concentration-dependent enhancement of the angiotensin II-induced aortic contractile response. Arsenic also caused concentration-dependent increase in the plasma levels of angiotensin II and angiotensin converting enzyme and the expression of aortic AT1 receptor and Gαq/11 proteins. Arsenic increased aortic protein kinase C activity and the concentrations of protein tyrosine kinase, extracellular signal-regulated kinase-1/2 and vascular endothelial growth factor. Further, arsenic increased aortic mRNA expression of Nox2, Nox4 and p22phox, NADPH oxidase activity and ROS generation. The results suggest that arsenic-mediated enhancement of angiotensin II signaling could be an important mechanism in the arsenic-induced vascular disorder, where ROS could augment the angiotensin II signaling through activation of MAP kinase pathway. Copyright © 2015. Published by Elsevier Ireland Ltd.
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