No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Respiratory effects and arsenic contaminated well water in Bangladesh
Abstract
Arsenic in drinking water causes a widespread concern in Bangladesh, where a major proportion of tube wells is contaminated. Arsenic ingestion causes skin lesions, which is considered as definite exposure. A prevalence comparison study of respiratory effects among subjects with and without arsenic exposure through drinking water was conducted in Bangladesh. Exposed participants were recruited through health awareness campaign programs. Unexposed participants were randomly selected, where tubewells were not contaminated with arsenic. A total of 169 individuals participated (44 exposed individuals exhibiting skin lesions; 125 unexposed individuals). The arsenic concentrations ranged from 136 to 1000 micro g l(-1). The information regarding respiratory system signs and symptoms were also collected and the analyses were confined to nonsmokers. The crude prevalence ratio for chronic bronchitis and chronic cough amounted to 2.1 (95% CI 0.7-6.1). The prevalence ratios for chronic bronchitis increased with increasing exposure, i.e., 1.0, 1.6, 2.7 and 2.6 using unexposed as the reference. The prevalence ratios for chronic cough were 1.0, 1.6, 2.7 and 2.6 for the exposure categories, using the same unexposed as the reference. The dose-response trend was the same (P < 0.1) for both conditions. These results add to evidence that long-term ingestion of arsenic exposure can cause respiratory effects.
... Heavy metals cause oxidative stress in aerobic cells by increasing reactive oxygen species (ROS). It has been linked to changes in the nervous system, cognitive impairment, infertility, foetal harm, preterm birth, cardiovascular disease, bronchitis, and coughing [13]. Cancers of the lung and bladder are the most common sites where it's carcinogenic effects manifest [14,15]. ...
... In addition, chronic consumption may result in neurobehavioral and neuropathic changes, memory loss, a decrease in intellectual level, infertility disorder, foetal injury, premature delivery, cardiovascular diseases, chronic cough, and chronic bronchitis [13]. In most cases, its carcinogenic effects manifest as lung and bladder cancer [14,27]. ...
Heavy metals are inherently non-biodegradable elements of the earth's crust that collect and remain in the ecosystem in perpetuity due to both human and natural activity. Their contamination in seasonings remains a public health concern because of the frequency of use. Prolonged exposure to these heavy metals is a severe health risk worldwide. This study evaluated the potential health risk of heavy metal exposure from consuming commercially produced food seasonings in Enugu, Nigeria. Thirty (30) commercially produced food seasonings were selected by simple random sampling and grouped into five (5) according to different batches. Atomic absorption spectroscopy was used to analyze arsenic, cadmium, lead and nickel. The level of arsenic in group SA(1.28±0.21mg/kg), SB(1.73±0.31mg/kg), SC(1.13±0.17mg/kg), SD (2.11±0.20mg/kg) were observed to be above (1.00mg/kg), the WHO maximum permissible limit. Cadmium levels in SA (0.36±0.01mg/kg) were observed to be above (0.30 mg/kg), the WHO maximum permissible limit. The estimated daily intake, hazard quotient and hazard index of the metals were within the normal range. The presence of heavy metals above WHO permissible limits in commercially produced food seasonings should be a public health concern. To protect the population's health, producers, retailers, and vendors of seasonings should be informed of the hazards of exposing their products to heavy metal contamination. Continuous surveillance of commercially produced food seasonings for heavy metal contamination is recommended.
... Non-cancerous health effects like Blackfoot disease, diabetes, hypertension and chronic obstructive pulmonary disease have been reported from many As affected areas [7,23,[31][32][33][34]. ...
... To our knowledge there are no earlier epidemiological studies on prenatal As exposure and lower respiratory tract infection and diarrhoea in infancy of the offspring. Some studies have reported As related respiratory symptoms and signs such as chronic cough, bronchitis and bronchiectasis, in relation to drinking water with high As levels [31,127,128]. ...
... Heavy metals cause serious carcinogenic and noncarcinogeneic effects in body i.e. at low level ingestion of arsenic may cause noncarcinogenic effects like sore throat and irritated lungs, nausea, vomaiting, darkening of skin lesions and warts 216)). Furthermore, its chronic intake may lead to neurobehavioral and neuropathic alterations, loss of memory, lowering of intellectual level, infertility disorder, fetal damage, premature delivery, cardiovasclar dieases, chronic cough and chronic bronchitis (Milton and Rahman, 2002). While, its carcnogenic effecs may be shown in the form of lung and bladder cancer usually (Cohen et al., 2015;Sanyal et al., 2020). ...
Carcinogenic and health hazard causing heavy metals have been increasing in our dietary stuffs due to large amount of industrial effluents being dumped in water bodies that are ultimately used for irrigation purposes. The study was aimed to assess and compare the mean concentrations of heavy metals (Cd, As and Pb) in soil and vegetables irrigated with four different sources (Ground water, river water, domestic sewage water and industrial untreated effluents and domestic waste water receiving drains) for the estimation of carcinogenic and non-carcinogenic health risk associated with them. Prepared samples were analyzed by through ICP-OES. Statistical analysis revealed that domestic sewage water and drains water usage for irrigation purposes leads to high values of Estimated Daily Intake (EDI) of metals through vegetation. To assess the carcinogenic effects values daily intakes, Total hazard quotients (THQs) and Health indexes (HI), while for carcinogenic effects, Total cancer risks (TCR) were determined. The results of present study revealed that the daily intakes of these metals are far less than that of permissible levels but their bio-accumulating behavior produce high risks to human health. The HI values revealed that waste water usage is producing the vegetables of high health risks. In adults, the HI of Phaseolus vulgaris, Spinacia oleracea, Brassica compestris, Raphnus sativus, Daucus carota and Solanum tuberosum assessed as 0.81, 1.52, 1.26, 0.12, 0.22, and 0.15 (ground water irrigation), 0.046, 0.75, 0.51, 0.68, 0.90 0.064 (River Ravi water irrigation), 1.23, 3.34, 4.81, 4.23, 1.41 and 3.43 (domestic sewage irrigation) and 3.04, 5.50, 6.08, 2.50, 5.34 and 5.13 (Drain waste water irrigation), respectively. It was observed that cancer risks of As exceeded the threshold (1 Â 10 À4) in all i.e. ground river, domestic sewage and drain water grown vegetables, while, Cd and Pb were in permissible range.
... Arsenic exposure will cause inflammation, while long-term exposure to arsenic can cause chronic inflammation [30,31]. Ingested arsenic is associated with non-malignant pulmonary diseases such as bronchitis, asthma, and pneumonia [32][33][34]. Increased levels of serum Immunoglobin E and reduced lung function parameters have been reported in populations exposed to arsenic [5,35]. Several studies have also suggested that arsenic exposure in utero and in childhood is associated with an increased risk of respiratory effects [36][37][38]. ...
Arsenic is an environmental factor associated with epithelial–mesenchymal transition (EMT). Since macrophages play a crucial role in regulating EMT, we studied the effects of arsenic on macrophage polarization. We first determined the arsenic concentrations to be used by cell viability assays in conjunction with previous studies. In our results, arsenic treatment increased the alternatively activated (M2) macrophage markers, including arginase 1 (ARG-1) gene expression, chemokine (C-C motif) ligand 16 (CCL16), transforming growth factor-β1 (TGF-β1), and the cluster of differentiation 206 (CD206) surface marker. Arsenic-treated macrophages promoted A549 lung epithelial cell invasion and migration in a cell co-culture model and a 3D gel cell co-culture model, confirming that arsenic treatment promoted EMT in lung epithelial cells. We confirmed that arsenic induced autophagy/mitophagy by microtubule-associated protein 1 light-chain 3-II (LC3 II) and phosphor-Parkin (p-Parkin) protein markers. The autophagy inhibitor chloroquine (CQ) recovered the expression of the inducible nitric oxide synthase (iNOS) gene in arsenic-treated M1 macrophages, which represents a confirmation that arsenic indeed induced the repolarization of classically activated (M1) macrophage to M2 macrophages through the autophagy/mitophagy pathway. Next, we verified that arsenic increased M2 cell markers in mouse blood and lungs. This study suggests that mitophagy is involved in the arsenic-induced M1 macrophage switch to an M2-like phenotype.
... Heavy metals cause serious carcinogenic and noncarcinogeneic effects in body i.e. at low level ingestion of arsenic may cause noncarcinogenic effects like sore throat and irritated lungs, nausea, vomaiting, darkening of skin lesions and warts 216)). Furthermore, its chronic intake may lead to neurobehavioral and neuropathic alterations, loss of memory, lowering of intellectual level, infertility disorder, fetal damage, premature delivery, cardiovasclar dieases, chronic cough and chronic bronchitis (Milton and Rahman, 2002). While, its carcnogenic effecs may be shown in the form of lung and bladder cancer usually (Cohen et al., 2015;Sanyal et al., 2020). ...
Carcinogenic and health hazard causing heavy metals have been increasing in our dietary stuffs due to large amount of industrial effluents being dumped in water bodies that are ultimately used for irrigation purposes. The study was aimed to assess and compare the mean concentrations of heavy metals (Cd, As and Pb) in soil and vegetables irrigated with four different sources (Ground water, river water, domestic sewage water and industrial untreated effluents and domestic waste water receiving drains) for the estimation of carcinogenic and non-carcinogenic health risk associated with them. Prepared samples were analyzed by through ICP-OES. Statistical analysis revealed that domestic sewage water and drains water usage for irrigation purposes leads to high values of Estimated Daily Intake (EDI) of metals through vegetation. To assess the carcinogenic effects values daily intakes, Total hazard quotients (THQs) and Health indexes (HI), while for carcinogenic effects, Total cancer risks (TCR) were determined. The results of present study revealed that the daily intakes of these metals are far less than that of permissible levels but their bio-accumulating behavior produce high risks to human health. The HI values revealed that waste water usage is producing the vegetables of high health risks. In adults, the HI of Phaseolus vulgaris, Spinacia oleracea, Brassica compestris, Raphnus sativus, Daucus carota and Solanum tuberosum assessed as 0.81, 1.52, 1.26, .12, 0.22, and 0.15 (ground water irrigation), .046, 0.75, 0.51, 0.68, 0.90 .064 (River Ravi water irrigation), 1.23, 3.34, 4.81, 4.23, 1.41 and 3.43(domestic sewage irrigation) and 3.04, 5.50, 6.08, 2.50, 5.34 and 5.13 (Drain waste water irrigation), respectively. It was observed that cancer risks of As exceeded the threshold (1x10⁻⁴) in all i.e. ground river, domestic sewage and drain water grown vegetables, while, Cd and Pb were in permissible range.
... However, Bangladesh continues to follow the previous WHO guideline value of 50 µg arsenic/L in drinking water as an acceptable level (WHO 1984). Studies have reported associations between arsenic exposure and increased risk of a wide range of diseases and conditions, including skin lesions , cardiovascular (Moon et al. 2012;Rahman 2002) and respiratory diseases (Milton and Rahman 2002) and lung function (von Ehrenstein et al. 2005), type-2 diabetes (Navas-Acien et al. 2006), and malignancies of skin and internal organs (International Agency for Research on Cancer 2004). ...
Background: Millions of individuals worldwide, particularly in Bangladesh, are exposed to arsenic, mainly through drinking water from tube wells. Arsenic is a reproductive toxicant, but there is limited knowledge of whether it influences pubertal development. Objectives: We evaluated the association between prenatal arsenic exposure and age at menarche. Methods: This prospective study was based on data from two studies conducted in Matlab, Bangladesh—the Maternal and Infant Nutrition Interventions in Matlab (MINIMat) trial and the Health Consequences of Arsenic in Matlab (AsMat) study. We included 809 MINIMat girls who participated in assessing age at menarche from July 2016 to June 2017 and had prenatal arsenic exposure data through the AsMat study via measurements in tube well water used by the mothers during pregnancy. The exposure was categorized into
... Rahman et al. (2011) found that arsenic exposure during pregnancy was linked with increased morbidity in infectious diseases during infancy. Some studies have reported a higher prevalence of chronic bronchitis and cough in residents from Bangladesh exposed to high arsenic levels compared with unexposed residents, and this rate increased when the concentrations of arsenic in water increased as well (Milton et al. 2001;Milton and Rahman 2002). Positive association between high arsenic exposure via drinking water and respiratory symptoms such as dyspnea, asthma, eye irritation, headache, sore throat, dry cough, and cough with phlegm as well as others was found in adults from India (Das et al. 2014). ...
Environmental arsenic exposure in adults and children has been associated with a reduction in the expression of club cell secretory protein (CC16) and an increase in the expression of matrix metalloproteinase-9 (MMP-9), both biomarkers of lung inflammation and negative respiratory outcomes. The objectives of this study were to determine if the levels of serum CC16 and MMP-9 and subsequent respiratory infections in children are associated with the ingestion of arsenic by drinking water. This cross-sectional study included 216 children from three Yaqui villages, Potam, Vicam, and Cocorit, with levels of arsenic in their ground water of 70.01 ± 21.85, 23.3 ± 9.99, and 11.8 ± 4.42 μg/L respectively. Total arsenic in water and urine samples was determined by inductively coupled plasma/optical emission spectrometry. Serum was analyzed for CC16 and MMP-9 using ELISA. The children had an average urinary arsenic of 79.39 μg/L and 46.8 % had levels above of the national concern value of 50 μg/L. Increased arsenic concentrations in drinking water and average daily arsenic intake by water were associated with decreased serum CC16 levels (β = − 0.12, 95% CI − 0.20, − 0.04 and β = − 0.10, 95% CI − 0.18, − 0.03), and increased serum MMP-9 levels (β = 0.35, 95% CI 0.22, 0.48 and β = 0.29, 95% CI 0.18, 0.40) at significant levels (P < 0.05). However, no association was found between levels of these serum biomarkers and urinary arsenic concentrations. In these children, reduced serum CC16 levels were significantly associated with increased risk of respiratory infections (OR = 0.34, 95% CI 0.13, 0.90). In conclusion, altered levels of serum CC16 and MMP-9 in the children may be due to the toxic effects of arsenic exposure through drinking water.
... N200 million people in over 70 countries have been estimated to expose to drinking water As beyond the WHO's provisional guideline value of 10 μg·L −1 (Naujokas et al., 2013). Chronic iAs exposure via drinking water can result in skin lesions (Ahsan et al., 2000), respiratory system diseases (Calderon et al., 2001;Milton and Rahman, 2002), cardiovascular disease (Lee et al., 2002;Rahman et al., 2015), nervous effects (Tsai et al., 2003), and carcinogenic disease, such as skin cancer (Luster and Simeonova, 2004), lung cancer (Ferreccio et al., 2000;Smith et al., 1998) and bladder cancer (Morales et al., 2000;Steinmaus et al., 2003). Health effects of chronic exposure to iAs through drinking water has been observed in America (Welch et al., 2000), Argentina (Tapia et al., 2019), Bangladesh (Horneman et al., 2004), Chile (Smith et al., 1998), China (He and Charlet, 2013). ...
The health effects of drinking water exposure to inorganic arsenic are well known but are less well defined for dietary exposure. The rising concerns of arsenic risks from diet motivated this study of arsenic concentrations in highland barley, vegetables, meat, and dairy products to evaluate arsenic exposure source and to assess health risks among rural residents of Ngari area, western Tibet. Total arsenic and arsenic speciation were measured by inductively coupled plasma mass spectrometry (ICP-MS) and high-performance liquid chromatography combined with ICP-MS (HPLC-ICP-MS) respectively. Average total arsenic concentrations of 0.18 ± 0.21 (n = 45, median: 0.07 mg·kg⁻¹), 0.40 ± 0.57 (n = 17, median: 0.15 mg·kg⁻¹), 0.21 ± 0.16 (n = 12, median: 0.17 mg·kg⁻¹), and 0.18 ± 0.08 (n = 11, median: 0.22 mg·kg⁻¹) were observed in highland barley, vegetables, meat, and dairy products, respectively. Inorganic arsenic was determined to be the main species of arsenic in highland barley, accounting for about 64.4 to 99.3% (average 83.3%) of total arsenic. Nearly half (44.4%) of the local residents had ingested >3.0 × 10⁻⁴ mg·kg⁻¹·d⁻¹ daily dose of arsenic from highland barley alone, above the maximum oral reference dose recommended by the United States Environmental Protection Agency (USEPA). The inorganic arsenic daily intake from highland barley was 3.6 × 10⁻⁴ mg·kg⁻¹·d⁻¹. Dietary exposure to inorganic arsenic alone increased the cancer risk probability to 5.4 in 10,000, assuming that the inorganic arsenic in highland barley has the same carcinogenic effects as that in water.
... Several studies in adults have suggested an increased risk of respiratory symptoms and diseases including impairment of lung function following chronic exposure to inorganic arsenic. [1][2][3][4][5][6] Long-term exposure to inorganic arsenic has been found to be associated with increased risk of respiratory symptoms such as chronic cough, dyspnea and breathlessness and the relationships were dose-dependent. [7][8][9][10] A cross-sectional study in Bangladesh found a greater risk of chronic bronchitis with added sounds in chest among people having arsenic-induced skin lesions compared with people without these lesions. ...
Background:
We previously reported chronic respiratory effects in children who were then 7-17 years of age in Matlab, Bangladesh. One group of children had been exposed to high concentrations of arsenic in drinking water in utero and early childhood (average 436 µg/L), and the other group of children were never known to have been exposed to >10 µg/L. The exposed children, both males and females, had marked increases in chronic respiratory symptoms.
Methods:
The current study involves a further follow-up of these children now 14-26 years of age with 463 located and agreeing to participate. They were interviewed for respiratory symptoms and lung function was measured. Data were collected on smoking, body mass index (BMI), and number of rooms in the house as a measure of socioeconomic status.
Results:
Respiratory effects were still present in males but not females. In the high exposure group (>400 µg/L in early life) the odds ratio (OR) among male participants for dry cough in the last 12 months was 2.36 (95% confidence interval [CI] = 1.21, 4.63, P = 0.006) and for asthma OR = 2.51 (95% CI = 1.19, 5.29, P = 0.008). Forced vital capacity (FVC) was reduced in males in the early life high-exposure group compared with those never exposed (-95ml, P = 0.04), but not in female participants.
Conclusions:
By the age range 14-26, there was little remaining evidence of chronic respiratory effects in females but pronounced effects persisted in males. Mechanisms for the marked male female differences warrant further investigation along with further follow-up to see if respiratory effects continue in males.
... Four studies have examined arsenic and chronic bronchitis; three found a greater odds [28][29][30] and one found reduced odds [6]. Despite epidemiologic evidence, little is known regarding arsenic-induced effects on airway physiology [31,32]. ...
Background:
Arsenic exposure through drinking water is an established lung carcinogen. Evidence on non-malignant lung outcomes is less conclusive and suggests arsenic is associated with lower lung function. Studies examining low-moderate arsenic (< 50 μg/L), the level relevant for most populations, are limited. We evaluated the association of arsenic exposure with respiratory health in American Indians from the Northern Plains, the Southern Plains and the Southwest United States, communities with environmental exposure to inorganic arsenic through drinking water.
Methods:
The Strong Heart Study is a prospective study of American Indian adults. This analysis used urinary arsenic measurements at baseline (1989-1991) and spirometry at Visit 2 (1993-1995) from 2132 participants to evaluate associations of arsenic exposure with airflow obstruction, restrictive pattern, self-reported respiratory disease, and symptoms.
Results:
Airflow obstruction was present in 21.5% and restrictive pattern was present in 14.4%. The odds ratio (95% confidence interval) for obstruction and restrictive patterns, based on the fixed ratio definition, comparing the 75th to 25th percentile of arsenic, was 1.17 (0.99, 1.38) and 1.27 (1.01, 1.60), respectively, after adjustments, and 1.28 (1.02, 1.60) and 1.33 (0.90, 1.50), respectively, based on the lower limit of normal definition. Arsenic was associated with lower percent predicted FEV1 and FVC, self-reported emphysema and stopping for breath.
Conclusion:
Low-moderate arsenic exposure was positively associated with restrictive pattern, airflow obstruction, lower lung function, self-reported emphysema and stopping for breath, independent of smoking and other lung disease risk factors. Findings suggest that low-moderate arsenic exposure may contribute to restrictive lung disease.
... This arsenic is believed to result from arsenic-rich iron oxides in sediments being dissolved and released into the groundwater aquifer [2,3]. There is a growing body of literature linking arsenic exposure to adverse respiratory outcomes including reduced lung function [4][5][6], cough [7][8][9][10][11][12][13], and less conclusively lower respiratory tract infections [14], bronchitis [12,15,16], and pulmonary tuberculosis mortality [17]. However, most studies have been conducted in adult populations, and there have been no studies to date evaluating the association between arsenic and pneumonia in pediatric populations. ...
... This is also true in humans . For example, in the lung, there is increasing evidence that chronic bronchitis and bronchiectasis are associated with increasing exposures to inorganic arsenic (Mazumder et al., 2000;Mazumder, 2007;Milton and Rahman, 2002;Parvez et al., 2008Parvez et al., , 2010von Ehrenstein et al., 2005). These disorders involve toxicity, inflammation and regenerative proliferation. ...
Inorganic arsenic (iA) in the drinking water is a human carcinogen (bladder, lung, and skin). The mode of action involves metabolism to trivalent arsenicals that react with sulfhydryl groups in critical proteins, leading to cytotoxicity with regenerative proliferation, involving a threshold at in vitro concentrations >0.1 μM. Adverse biologic effects at such tissue concentrations in rodents occur with ≥10 ppm of iAs in diet or drinking water. On the basis of mode of action, in vitro, and in vivo studies, anticipated drinking water exposures of 50–150 μg/L exceed a tissue concentration of >0.1 μM in humans. Epidemiologic investigations evaluating populations exposed at levels <150 μg/L iAs in drinking water are consistent with such a threshold for cancer.
... Chronic arsenic toxicity, which is due to low-concentration exposure over a long period of time, impairs the same organs and tissues as acute toxicity, although in cases of higher exposure levels, skin and nervous system disturbances are usually more pronounced (Lagerkvist and Zetterlund 1994;Ahsan et al. 2006;Naujokas et al. 2013). Chronic arsenic intoxication has been caused not only by drinking contaminated groundwater (Mazumder et al. 1998;Milton and Rahman 2002;Chakraborti et al. 2003;Otto et al. 2006;Chen 2014;Del Rio et al. 2017;Rehman et al. 2018) but also by occupational exposures, such as mining (Ishinishi et al. 1977;Kawasaki et al. 2002;Eisler 2004) and work with copper smelters (Feldman et al. 1979;Lubin et al. 2008;Halatek et al. 2009;Sinczuk-Walczak et al. 2010). ...
Chronic arsenic intoxication is known to cause multisystem impairment and is still a major threat to public health in many countries. In Toroku, a small village in Japan, arsenic mines operated from 1920 to 1962, and residents suffered serious sequelae of arsenic intoxication. We have performed annual medical examinations of these residents since 1974, allowing us to characterize participants’ long-term health following their last exposure to arsenic. The participants could not be described as having “chronic arsenic intoxication,” because their blood arsenic levels were not measured. In this study, we defined them as having “probable arsenic intoxication.” Symptoms frequently involved the sensory nervous system, skin, and upper respiratory system (89.1–97.8%). In an analysis of neurological findings, sensory neuropathy was common, and more than half of the participants complained of hearing impairment. Longitudinal assessment with neurological examinations and nerve conduction studies revealed that sensory dysfunction gradually worsened, even after exposure cessation. However, we could not conclude that arsenic caused the long-term decline of sensory function due to a lack of comparisons with age-matched healthy controls. This is the first study to characterize the longitudinal sequelae after probable arsenic exposure. Our study will be helpful to assess the prognosis of patients worldwide who still suffer from chronic arsenic intoxication.
... For example, compared to individuals from the less exposed city of Arica, those from Antofagasta with high early life exposure reported more breathlessness, had a 12.2% lower forced vital capacity and 11.5% lower forced expiratory volume in one second. Impaired lung function has also been associated with arsenic exposure in other areas of the world such as West Bengal (De et al. 2004) and Bangladesh (Milton and Rahman 2002). ...
Abbreviations:
ALT: alanine aminotransferase; AMI: acute myocardial infarction; AST: aspartate aminotransferase; ATSDR: Agency for Toxic Substances and Disease Registry; CVD: cardiovascular disease; DMA: dimethylarsinate; DOHaD: Developmental Origins of Health and Disease; EPA: U.S. Environmental Protection Agency; ER-α: estrogen receptor alpha; HDL: high-density lipoprotein; HOMA-IR: homeostatic model assessment of insulin resistance; iAs: inorganic arsenic; LDL: low-density lipoprotein; MetS: metabolic syndrome; MMA: monomethylarsonate; NAFLD: non-alcoholic fatty liver disease; PND: postnatal day; ppb: parts per billion; ppm: parts per million; SAM: S-adenosylmethionine; USFDA: United States Food and Drug Administration.
... In addition, exposure to arsenic in drinking water has been associated with respiratory, neurological, and diabetic mellitus. It has been reported that chronic respiratory inflammation are caused by arsenic-induced respiratory diseases [3], and peripheral neuropathy, encephalopathy, and polyneuropathy are caused by nervous system diseases [4]. An epidemiologic report on the risk of miscarriage and preterm birth in chronic exposure to arsenic during pregnancy [5], and the report of congenital anomalies [6] suggest that exposure to arsenic may cause reproductive and developmental abnormalities [7]. ...
Recent epidemiological studies have reported adverse health effects, including skin cancer, due to low concentrations of arsenic via drinking water. We conducted a study to assess whether low arsenic contaminated ground water affected health of the residents who consumed it. For precise biomonitoring results, the inorganic (trivalent arsenite (As III) and pentavalent arsenate (As V)) and organic forms (monomethylarsonate (MMA) and dimethylarsinate (DMA)) of arsenic were separately quantified by combining high-performance liquid chromatography and inductively coupled plasma mass spectroscopy from urine samples. In conclusion, urinary As III, As V, MMA, and hair arsenic concentrations were significantly higher in residents who consumed arsenic contaminated ground water than control participants who consumed tap water. But, most health screening results did not show a statistically significant difference between exposed and control subjects. We presume that the elevated arsenic concentrations may not be sufficient to cause detectable health effects. Consumption of arsenic contaminated ground water could result in elevated urinary organic and inorganic arsenic concentrations. We recommend immediate discontinuation of ground water supply in this area for the safety of the residents.
... Epidemiological studies have reported an association between arsenic exposure and increased risks of various cancers and non-cancerous diseases. These include skin lesions (Rahman et al. 1999a;Tondel et al. 1999), hypertension (Rahman et al. 1999b), cardiovascular and respiratory diseases (Milton and Rahman 2002;Moon et al. 2013), diabetes mellitus (Navas-Acien et al. 2008), and malignancies of skin and internal organs (IARC 2004). Arsenic can easily pass through the placenta and poses a threat to early human development (Vahter 2009) ...
Epidemiological studies have suggested a negative association between early life arsenic exposure and fetal size at birth, and subsequently with child morbidity and growth. However, our understanding of the relationship between arsenic exposure and morbidity and growth is limited. This paper aims to systematically review original human studies with an analytical epidemiological study design that have assessed arsenic exposure in fetal life or early childhood and evaluated the association with one or several of the following outcomes: fetal growth, birth weight or other birth anthropometry, infant and child growth, infectious disease morbidity in infancy and early childhood. A literature search was conducted in PubMed, TOXLINE, Web of Science, SciFinder and Scopus databases filtered for human studies. Based on the predefined eligibility criteria, two authors independently evaluated the studies. A total of 707 studies with morbidity outcomes were identified, of which six studies were eligible and included in this review. For the growth outcomes, a total of 2959 studies were found and nine fulfilled the criteria and were included in the review. A majority of the papers (10/15) emanated from Bangladesh, three from the USA, one from Romania and one from Canada. All included studies on arsenic exposure and morbidity showed an increased risk of respiratory tract infections and diarrhea. The findings in the studies of arsenic exposure and fetal, infant, and child growth were heterogeneous. Arsenic exposure was not associated with fetal growth. There was limited evidence of negative associations between arsenic exposures and birth weight and growth during early childhood. More studies from arsenic-affected low- and middle-income countries are needed to support the generalizability of study findings.
... There is strong evidence of a general association between inorganic arsenic and non-malignant respiratory illness, including lung function impairment, chronic cough, chronic bronchitis and acute respiratory tract infections, pulmonary nodule, diffuse interstitial lung disease and chronic obstructive pulmonary disease, bronchiectasis, bullousemphysema, as well as non-malignant lung disease mortality (Ergün et al., 2017;Milton & Rahman, 2002;Smith et al., 2011). Some reports and studies have documented marked pulmonary as well as other negative health effects of early life arsenic exposure (i.e., in utero and/or early childhood) throughout the lifespan (Ragib et al., 2009;Sanchez, Perzanowski, & Graziano, 2016;Smith et al., 2006;Srivastava, D'Souza, Sen, & States, 2007;Steinmaus et al., 2016;Vahter, 2008). ...
Arsenic and its compounds are well-established, potent, environmentally widespread and persistent toxicants with metabolic, genotoxic, mutagenic, teratogenic, epigenetic and carcinogenic effects. Arsenic occurs naturally in the Earth's crust, but anthropogenic arsenic emissions have surmounted the emissions from important natural sources such as volcanism. Inorganic arsenicals exhibit acute and chronic toxicities in virtually all cell types and tissues, and hence arsenic intoxication affects multiple systems. Whereas acute arsenic intoxication is rare and relatively easy to diagnose, chronic arsenic intoxication (CAsI) is common but goes often misdiagnosed. Based on a review of the literature as well as our own clinical experience, we propose a chronic arsenic intoxication diagnostic score (CAsIDS). A distinctive feature of CAsIDS is the use of bone arsenic load as an essential criterion for the individual risk assessment of chronic arsenic intoxication, combined with a systemic clinical assessment. We present clinical examples where CAsIDS is applied for the diagnosis of CAsI, review the main topics of the toxicity of arsenic in different cell and organ systems and discuss the therapy and prevention of disease caused or aggravated by chronic arsenic intoxication. CAsIDS can help physicians establish the diagnosis of CAsI and associated conditions.
... Arsenic in trivalent form is considered to be more toxic than Asia China, Taiwan, India, Bangladesh, Thailand, Japan, Vietnam Chen et al. 1994, Mandal et al. 1996, Chatterjee et al. Nepal, Pakistan, Myanmar, Cambodia, Sri Lanka, Philippines, Iran 1993, Dhar et al. 1997, Nickson et al. 2000 Laos, Korea Williams et al. 1996, Kondo et al. 1999, Berg et al. 2001, Agusa et al. 2006, Hoang et al. 2010, Luu et al. 2009, Wijesekara & Marambe 2011, Fonseka et al. 2012Europe Romania, Hungary, England, Germany, Greece, Spain, Poland, Cardiovascular Acrocyanosis and Raynaud's Phenomenon, Heart attack, cardiac arrhythmias, thickening of blood vessels, loss of circu lation leading to gangrene of extremities, hypertension, (Barringer & Reilly 2013) Dermal Hyperpigmentation, basal cell carcinoma and squamous cell carcinoma, abnormal skin thickening, Symmetric hyperk eratosis of palms and soles (palmoplantar), melanosis or depigmentation, bowen's disease, facial edema, Desquamation Gastrointestinal Esophagitis, Colitis, anorexia, weight loss, Heartburn, nausea, abdominal pain, Liver Cancer (Robert & Anna 2008) Hematological Anemia, low white-blood-cell count (leucopenia), Megalobastosis Neurological Brain malfunction, hallucinations, memory loss, seizures, coma, peripheral neuropathy, hearing loss, encephalopathy Pulmonary, Respiratory Chronic cough, restrictive lung disease, cancer, Lung Cancer, Laryngitis, tracheal bronchitis, rhinitis, pharyngitis, short ness of breath, perforation of nasal Septum (Abul & Mahfuzar 2002) Renal Hematuria, proteinuria, shock, dehydration, cortical necrosis, cancer of kidneys and bladder, Nephrosis and Nephritis (Yu et al. 2009) Reproductive Spontaneous abortions, still-births, congenital malformations of fetus, low birth weight, prostate cancer (Yang et al. 2008, Rahman et al. 2013) pentavalent form. According to the present review, it is evident that major source of arsenic in groundwater is geogenic in nature. ...
Arsenic is present in earth’s crust and occurs in more than 200 natural minerals. Under favourable environmental conditions, arsenic enters into the groundwater. Groundwater has been the major source of arsenic exposure to human population around the world. The incidence of arsenic in drinking water, above the standard limit (0.05mg/L as per IS: 10500) has emerged as a major public health problem. Water constituting arsenic above 10µg/L is a major concern. Arsenic has reference dose or reference value of 3E-4 mg.kg-1.d-1 as an estimate of a daily exposure to the human population that is likely to be without an appreciable risk of deleterious effects during a lifetime. Lesions manifest at exposure levels of about 0.002-0.02 mg As kg-1.d-1. The trivalent form of arsenic is considered to be 60 times more toxic than pentavalent form. This communication contemplates on presenting the sources of arsenic, and the influencing factors that facilitate arsenic to groundwater, health implications and present regulation on drinking water standards. From the review, it is clear that the consumption of arsenic contaminated water can cause a wide range of acute and chronic diseases in humans. The source of arsenic for groundwater is mainly geogenic in nature. Therefore, if the groundwater is selected as the source of water, routine monitoring for arsenic becomes a vital step before it is conveyed to the end users for drinking or irrigation or industrial purposes.
... This is also true in humans . For example, in the lung, there is increasing evidence that chronic bronchitis and bronchiectasis are associated with increasing exposures to inorganic arsenic (Mazumder et al., 2000;Mazumder, 2007;Milton and Rahman, 2002;Parvez et al., 2008Parvez et al., , 2010von Ehrenstein et al., 2005). These disorders involve toxicity, inflammation and regenerative proliferation. ...
Inorganic arsenic induces a variety of toxicities including cancer. The mode of action for cancer and non-cancer effects involves the metabolic generation of trivalent arsenicals and their reaction with sulfhydryl groups within critical proteins in various cell types which leads to the biological response. In epithelial cells, the response is cell death with consequent regenerative proliferation. If this continues for a long period of time, it can result in an increased risk of cancer. Arsenicals do not react with DNA. There is evidence for indirect genotoxicity in various in vitro and in vivo systems, but these involve exposures at cytotoxic concentrations and are not the basis for cancer development. The resulting markers of genotoxicity could readily be due to the cytotoxicity rather than an effect on the DNA itself. Evidence for genotoxicity in humans has involved detection of chromosomal aberrations, sister chromatid exchanges in lymphocytes and micronucleus formation in lymphocytes, buccal mucosal cells, and exfoliated urothelial cells in the urine. Numerous difficulties have been identified in the interpretation of such results, including inadequate assessment of exposure to arsenic, measurement of micronuclei, and potential confounding factors such as tobacco exposure, folate deficiency, and others. Overall, the data strongly supports a non-linear dose response for the effects of inorganic arsenic. In various in vitro and in vivo models and in human epidemiology studies there appears to be a threshold for biological responses, including cancer.
... 3. Lung inflammation (NIOX MINO®)study participants exhale into a machine which detects exhaled nitric oxide, a marker for eosinophilic airway inflammation [30]. Previous reports showed an association of arsenic exposure with respiratory effects and inflammatory response of airway cells [31,32]. ...
Background:
Millions of people worldwide are exposed to dangerous levels of arsenic (above the WHO water standard of 10 ppb) in drinking water and food. Lack of nutritious foods exacerbates the adverse health effects of arsenic poisoning. The micronutrient selenium is a known antagonist to arsenic, promoting the excretion of arsenic from the body. Studies are in progress examining the potential of using selenium supplement pills to counteract arsenic toxicity. We are planning a clinical trial to test whether high-selenium lentils, as a whole food solution, can improve the health of arsenic-exposed Bangladeshi villagers.
Methods/design:
A total of 400 participants (about 80 families) will be divided into two groups via computer-generated block randomization. Eligibility criteria are age (≥14) years) and arsenic concentration in the household tube well (≥100 ppb). In this double-blind study, one group will eat high-selenium lentils grown in western Canada; the other will consume low-selenium lentils grown in Idaho, USA. Each participant will consume 65 g of lentils each day for 6 months. At the onset, midterm, and end of the trial, blood, urine and stool, plus hair (day 1 and at 6 months only) samples will be collected and a health examination conducted including assessment of acute lung inflammation, body mass and height, and blood pressure. The major outcome will be arsenic excretion in urine and feces, as well as arsenic deposition in hair and morbidity outcomes as assessed by a biweekly questionnaire. Secondary outcomes include antioxidant status, lipid profile, lung inflammation status, and blood pressure.
Discussion:
Selenium pills as a treatment for arsenic exposure are costly and inconvenient, whereas a whole food approach to lower the toxic burden of arsenic may be a practical remedy for Bangladeshi people while efforts to provide safe drinking water are continuing. If high-selenium lentils prove to be effective in counteracting arsenic toxicity, agronomic partnerships between Canada and Bangladesh will work to improve the selenium content of the Bangladeshi-grown lentil crops. Results will be presented to the community to promote informed food choices, which may include increasing selenium in their diet.
Trial registration:
ClinicalTrials.gov NCT02429921.
... This arsenic is believed to result from arsenic-rich iron oxides in sediments being dissolved and released into the groundwater aquifer [2,3]. There is a growing body of literature linking arsenic exposure to adverse respiratory outcomes including reduced lung function [4][5][6], cough [7][8][9][10][11][12][13], and less conclusively lower respiratory tract infections [14], bronchitis [12,15,16], and pulmonary tuberculosis mortality [17]. However, most studies have been conducted in adult populations, and there have been no studies to date evaluating the association between arsenic and pneumonia in pediatric populations. ...
Background:
Pneumonia is the leading cause of death for children under 5 years of age globally, making research on modifiable risk factors for childhood pneumonia important for reducing this disease burden. Millions of children globally are exposed to elevated levels of arsenic in drinking water. However, there is limited data on the association between arsenic exposure and respiratory infections, particularly among pediatric populations.
Methods:
This case control study of 153 pneumonia cases and 296 controls 28 days to 59 months of age in rural Bangladesh is the first to assess whether arsenic exposure is a risk factor for pneumonia in a pediatric population. Cases had physician diagnosed World Health Organization defined severe or very severe pneumonia. Urine collected during hospitalization (hospital admission time point) and 30 days later (convalescent time point) from cases and a single specimen from community controls was tested for urinary arsenic by graphite furnace atomic absorption.
Results:
The odds for pneumonia was nearly double for children with urinary arsenic concentrations higher than the first quartile (≥6 μg/L) at the hospital admission time point (Odd Ratio (OR):1.88 (95 % Confidence Interval (CI): 1.01, 3.53)), after adjustment for urinary creatinine, weight for height, breastfeeding, paternal education, age, and number of people in the household. This was consistent with findings at the convalescent time point where the adjusted OR for children with urinary arsenic concentrations greater than the first quartile (≥6 μg/L) was 2.32 (95 % CI: 1.33, 4.02).
Conclusion:
We observed a nearly two times higher odds of pneumonia for children with creatinine adjusted urinary arsenic concentrations greater than the first quartile (≥6 μg/L) at the hospital admission time point. This novel finding suggests that low to moderate arsenic exposure may be a risk factor for pneumonia in children under 5 years of age.
... In animal models, transplacental arsenic exposure affects lung development, by altering pulmonary structure and function Ramsey et al. 2013b), changing expression of lung morphogenesis and structurally important extracellular matrix genes (Petrick et al. 2009;Ramsey et al. 2013b), and increasing susceptibility to infection (Ramsey et al. 2013a). Studies from Bangladesh and West Bengal described increased incidence of respiratory disorders, chronic bronchitis, decreased lung function, and bronchiectasis among arsenicexposed individuals, compared with unexposed adults (Mazumder et al. 2000Milton et al. 2001;Milton and Rahman 2002;von Ehrenstein et al. 2005). In Antofogasta, Chile, where public water arsenic levels reached nearly 900 μg/L from 1958 to 1971, residents experienced increased rates of mortality from pulmonary tuberculosis (Smith et al. 2011), and those exposed to high arsenic levels in utero or during early life had higher mortality from lung cancer, bronchiectasis, and chronic lung disease, than residents of a nonexposed region ). ...
Background:
Arsenic has been linked to disrupted immune function and greater infection susceptibility in highly exposed populations. Well arsenic levels above the EPA limit occur in our U.S. study area and are of particular concern for pregnant women and infants.
Objectives:
We investigated whether in utero arsenic exposure affects the risk of infections and respiratory symptoms over the first year of life.
Methods:
We prospectively obtained information on infant infections and symptoms, including their duration and treatment (n = 412) at 4, 8 and 12 months using a parental telephone survey. Using generalized estimating equation models adjusted for potential confounders, we evaluated the association between maternal pregnancy urinary arsenic and infant infections and symptoms over the first year.
Results:
Each doubling of maternal urinary arsenic was related to increases in the total number of infections requiring prescription medication in the first year (RR = 1.1; 95% CI: 1.0, 1.2). Urinary arsenic was related specifically to respiratory symptoms (difficulty breathing, wheezing and cough) lasting ≥ 2 days or requiring prescription medication (RR = 1.1; 95% CI: 1.0, 1.2; RR = 1.2; 95% CI: 1.0, 1.5, respectively), and wheezing lasting ≥2 days, resulting in a doctor visit or prescription medication treatment (RR = 1.3; 95% CI: 1.0, 1.7; RR = 1.3; 95% CI: 1.0, 1.8, and RR = 1.5; 95% CI: 1.0, 2.2). Associations also were observed with diarrhea (RR = 1.4; 95% CI: 1.1, 1.9) and fever resulting in a doctor visit (RR = 1.2; 95% CI: 1.0, 1.5).
Conclusions:
In utero arsenic exposure was associated with a higher risk of infection during the first year of life in our study population, particularly infections requiring medical treatment, and with diarrhea and respiratory symptoms.
... In view of the suspected human carcinogenicity of arsenite, the United States Environmental Protection Agency (USEPA) has set a human health criterion for total dissolved arsenic in sea water (0.0175 g/L) for the consumption of fish products [8]. Millions of people worldwide are at risk due to long-term arsenic-contaminated groundwater consumption [9], which has become a global public health problem. Inorganic arsenite has been classified by the International Agency for Research on Cancer as a human carcinogen [8]. ...
Arsenic is a ubiquitous heavy metal in the marine environment and has a complex biogeochemistry that has significant implications for its toxicity to marine organisms and their consumers. The average concentration of total arsenic in uncontaminated sea water ranges from 1 to 2. μg/L and in marine sediments from 5 to 15. μg/g dry weight (near-shore and estuaries sediments), and average concentration is about 40. μg/g (deep sea sediments). The dominant form of arsenic in sea water is inorganic arsenate. The most toxic and potential carcinogen, inorganic arsenite, is rarely found in oxic sea water and marine sediments. Marine organisms such as phytoplankton, bacteria, and algae accumulate arsenate from surrounding sea water and reduce it to arsenite, and subsequent methylation leads to the synthesis of organoarsenicals, which are ultimately released/excreted in the sea water. Marine animals have limited ability to accumulate inorganic arsenic from sea water, whereas they largely accumulate organic forms of arsenic consumed from their food chain. Arsenic-containing seafood is the main route of arsenic access to the human body. Arsenobetaine, the major organic form of arsenic in seafood, is non-toxic and/or non-carcinogenic to humans. The majority of organoarsenicals present in the seafood are rapidly excreted, little of which is accumulated by human beings. However, recently a few forms of methylated arsenicals have been reported to exert their toxic effects in in vitro studies.
... Chronic As poisoning occurs usually upon repeated or continuous exposure to small amount of As (Ratnaike 2013). The chronic effects of inorganic As exposure via drinking water include skin lesions, such as hyperpigmentation, and respiratory symptoms, such as cough and bronchitis and reproductive disorders Ahsan et al., 2000;Milton andRahman 2002, Sen andChaudhuri 2008). The cardiovascular, gastrointestinal, neurological and urinary systems are some of the other systems most affected in humans (Lee et al., 2002;Mukherjee et al., 2003). ...
Arsenic (As) is a naturally occurring toxic metalloid which is introduced into the environment through natural geochemical processes and several anthropogenic actions. Since it is a carcinogen, there is an urgent need to efficiently remove As from contaminated soil and water. This review elaborates the chemistry and environmental distribution of As along with several bioremediation approaches to alleviate As pollution. Highlight
... Exposure to As may result in neurobehavioral and neuropathic effects in adolescence, 31 effects on memory and intellectual function, 32 reproductive effects with increased fetal loss and premature delivery, 27,33 steatosis, 34 cardiovascular diseases, 35 ischemic heart diseases, 36 carotid atherosclerosis, and respiratory system effects such as chronic cough and chronic bronchitis. 37 Even at concentrations as low as 0.4 µg L -1 , iAs has been reported to behave as an endocrine disruptor that is able to alter gene transcription. 38 Despite the number of in vivo and in vitro studies trying to elucidate the role of As in the development of diabetes in humans, the current available evidences are not adequate to establish a causal role. ...
Sandra Munera-Picazo,1 Marina Cano-Lamadrid,1 María Concepción Castaño-Iglesias,2 Francisco Burló,1 Ángel A Carbonell-Barrachina11Food Quality and Safety Group, Department of Agro-Food Technology, Universidad Miguel Hernández, Orihuela, 2Servicio de Pediatría, Hospital Universitario San Juan de Alicante, Alicante, SpainAbstract: Rice is a staple food for over half of the world population, but there is some concern about the occurrence of arsenic (As) in this cereal and the possible overexposure to this metalloid. Recently, the Codex Alimentarius Commission established a maximum limit of 200 µg kg–1 for inorganic arsenic (iAs) in rice. Because the maximum content of As in water has been reduced to 10 µg L–1, intoxication through rice and rice-based products can be considered an important source of As poisoning. The chronic effects of this iAs exposure can be lung and bladder cancer, skin lesions, or other noncarcinogenic diseases. There is clear evidence of high levels of iAs in rice and rice-based products. Different solutions for the reduction of As intake are proposed at different levels: 1) during the plant-growing process through agronomic practices, 2) pretreatment of rice before its use in the food industry, 3) optimization of the conditions of unit operations during processing, and 4) by cooking.Keywords: arsenic speciation, food safety, dietary exposure, Oryza sativa
... A recent study conducted within highly contaminated areas had found that 17-35% of the populations examined have skin lesions and up to 3.4% of them have gangrene and ulcers [6]. Skin lesions were the most common and prime manifestation of arsenic toxicity that had been considered as definite exposure [25]- [27]. ...
Arsenic, an occurring element can be found in geological formations, across the globe. In some countries it has been pinpointed as a contributor to groundwater contamination. Threats to health, economy, and social well-being are present, especially in remote regions and countries that are developing. This document offers an overview of arsenic's chemistry the factors influencing its forms and its environmental impact upon exposure. It also delves into an examination of groundwater pollution caused by arsenic. The effects on agriculture, social welfare, economy, and health are clarified through a case analysis dealing with groundwater contamination in Bangladesh. The document further discusses established methods for removing arsenic that are often used for remediation purposes. It explores how the presence of compounds like iron and phosphate in groundwater can impact the efficiency of arsenic removal processes. It also provides illustrations of projected filtration systems intended to remove arsenic from residential groundwater in order to provide rural communities access to pure drinking water. The last part provides suggestions for enhancing the efficiency and usefulness of these filtering devices for home usage.
While Arsenate [As (V)] is the predominant species under aerobic conditions (Xu et al., Environ Sci Technol 42:5574–5579, 2008; Li et al., Environ Sci Technol 43:3778–3783, 2009b); in soil solutions, it may be as high as 5–20% (Khan et al., Environ Sci Technol 44:8515–8521, 2010), under typical flood conditions. Arsenic contamination of groundwater is a geogenic process. Oxidation of arsenopyrites or reduction of ferric oxyhydroxide or both forms an important pathway for As release in the groundwater. Iron and arsenic-bearing minerals formed in situ or brought along by rivers, combined with sulphur and form arsenopyrite (FeAsS).
Arsenic (As), a toxic metalloid, primarily originates from both natural and anthropogenic activities. Reports suggested that millions of people globally exposed to high levels of naturally occurring As compounds via inhalation and ingestion. There is evidence that As is a well-known lung carcinogen. However, there has been relatively little evidence suggesting its non-malignant lung effects. This review comprehensively summarises current experimental and clinical studies implicating the association of As exposure and the development of several non-malignant lung diseases. Experimental studies provided evidence that As exposure induces redox imbalance, apoptosis, inflammatory response, epithelial-to-mesenchymal transition (EMT), and affected normal lung development through alteration of the components of intracellular signaling cascades. In addition, we also discuss the sources and possible mechanisms of As influx and efflux in the lung. Finally, current experimental studies on treatment strategies using phytochemicals and our perspective on future research with As are also discussed.
Arsenic (As), a naturally occurring metalloid, has been a major concern to the environment due to its adverse effects on the plants and human. Arsenic uptake and accumulation in plants has not only impaired the plant processes leading to loss in growth and crop yield but also resulted in toxicity in human due to biomagnification. With decades of research on the effects of arsenic accumulation on plant growth and development and its consequences in human health, we briefly discuss the effects of As on plants and humans. In the first part of the review the principles of uptake of As by plant from soil are discussed. In the second part, the primary mechanism through which the As accumulation affect plant productivity are discussed. The last part describes the effect As has on different human organs. Our mini-review serves to guide the ongoing and future research on the effects As contamination.
Arsenic is a ubiquitous environmental toxicant, found in high concentrations worldwide. Although abundant research has dealt with arsenic-induced cancers, studies on mechanisms of non-malignant lung diseases have not been complete. In addition, decades of research have mostly concentrated on high-dose arsenic exposure, which has very limited use in modeling the biological effects of today's low-dose exposures. Indeed, accumulated evidence has shown that low-dose arsenic exposure (i.e. ≤100 ppb) may also alter lung homeostasis by causing host susceptibility to viral infection. However, the underlying mechanism of this alteration is unknown. In this study, we found that low-dose sodium arsenite (As (III)) repressed major airway mucins-MUC5AC and MUC5B at both mRNA and protein levels. We further demonstrated that this repression was not caused by cellular toxicity or mediated by the reduction of a common mucin-inducing pathway-EGFR. Other established mucin activators- dsRNA, IL1β or IL17 were not able to override As (III)-induced mucin repression. Interestingly, the suppressing effect of As (III) appeared to be partially reversible, and supplementation of all trans retinoic acid (t-RA) doses dependently restored mucin gene expression. Further analyses indicated that As (III) treatment significantly reduced the protein level of retinoic acid receptors (RARα, γ and RXRα) as well as RARE promoter reporter activity. Therefore, our study fills in an important knowledge gap in the field of low-dose arsenic exposure. The interference of RA signaling, and mucin gene expression may be important pathogenic factors in low-dose arsenic induced lung toxicity.
The arsenic concentration is an important issue in compost production. The main inputs of a compost factory, including kerbsides, green wastes, food industry wastes, and river weeds are investigated in this study. Also, this study investigated how treated timbers, ashes, and other contamination can impact arsenic concentration in compost production. The results showed that most treated timbers and all ashes of treated and untreated timbers contained significant amounts of arsenic. These results revealed that the presence of a small amount of treated timber ashes can significantly increase the arsenic concentration in composts. The results of the study show the arsenic concentration in compost increase during cold months, and it dropped during summer, which would be mostly because of high arsenic concentration in ashes of log burners. This study shows ashes of burning timbers can impact arsenic contamination mostly because of using Copper-Chrome-Arsenic wood preservatives (CCA). Also, the lab results show the arsenic level even in ashes of untreated timber is around 96 ppm. The ashes of H3, H4, and H5 treated timbers contain approximately 133,000, 155,000, and 179,000 ppm of arsenic, which one kg of them can increase arsenic concentration around 10 ppm in 13.3, 15.5 and 17.9 tons of dry compost products. The main problem is many people look at ashes and treated timber as organic materials; however, ashes of treated and untreated timbers contained high concentrations of arsenic. Therefore, it was necessary to warn people about the dangers of putting any ashes in organic waste bins.
The life style and child raising environment in Asia are quite different compared with Western countries. Besides, the children's environmental threats and difficulties in conducting studies could be different. To address children's environmental health in Asia area, the Birth Cohort Consortium of Asia (BiCCA) was co-established in 2011. We reviewed the mercury, polychlorinated biphenyls, perfluoroalkyl substances, phthalates, and environmental tobacco smoke in pervious based on birth cohort studies in Asia. The aim of this study was to summarize the traditional environmental pollution and the target subjects were also based on the birth cohort in Asia area. Environmental pollutants included air pollutants, pesticides focusing on organochlorine pesticides, diakylphosphates, and pyrethroid, and heavy metals including lead, arsenic, cadmium, manganese, vanadium, and thallium. Fetal growth and pregnancy outcomes, childhood growth and obesity, neurodevelopment and behavioral problems, and allergic disease and immune function were classified to elucidate the children's health effects. In total, 106 studies were selected in this study. The evidences showed air pollution or pesticides may affect growth during infancy or childhood, and associated with neurodevelopmental or behavioral problems. Prenatal exposure to lead or manganese was associated with neurodevelopmental or behavioral problems, while exposure to arsenic or cadmium may influence fetal growth. In addition to the harmonization and international collaboration of birth cohorts in Asia; however, understand the whole picture of exposure scenario and consider more discipline in the research are necessary.
This study seeks to identify the spatial risk pattern of households (HHs) exposed to arsenic contamination in Bangladesh by adjusting potential socio-economic, demographic factors. Data from Bangladesh Multiple Indicator Cluster Survey 2012–13 are used where hierarchical Bayesian spatial ordered logit model is implemented. The analysis shows that 25% of HH water samples were arsenic contaminated, although the majority (95%) of HHs used improved water sources. Arsenic contamination risk in the HH water was significantly associated with water source type and location, place of residence and districts. The model-based spatial prediction reveals that the north-east and south-west parts of Bangladesh have a high risk of contamination. To ensure the quality of HH water, our findings suggest that chemical test should be promoted considering the spatial risk of arsenic contaminations variations among HHs of Bangladesh. Furthermore, the study findings can effectively contribute in the planning of future interventions and programs.
Arsenic is a naturally occurring toxic metalloid within the Earth’s crust. It is found primarily in drinking water and food. Chronic exposure to high levels of arsenic is associated with a wide range of human diseases including typical skin lesions (hyperpigmentation, hypopigmentation, and keratosis), cancer, diabetes, cardiovascular disease (CVD), neurocognitive outcomes, etc. In this chapter, we will introduce the evidence indicating association between arsenic exposure and increased risks of the lifestyle-related diseases [cancer, type 2 diabetes (T2D), and CVD], including epidemiological studies and animal studies. Current understanding of the mechanisms underlying these diseases and arsenic exposure will also be reviewed.
Man interacts with the biosphere, atmosphere, hydrosphere and the lithosphere for sustaining himself on earth. This interaction ranges from the level of regional pattern of climate, geography and geology to different elements in rock, soil and water. In the universe, lighter elements are more frequently encountered than the heavier ones. In the Periodic Table of elements, the first 26 elements comprise, by weight, 99% of the continental crust. Again out of these 26, the first 20 make up more than 99% by weight of the human body. The living tissue of both animals and plants comprise 11 elements such as sodium, magnesium, potassium, calcium, hydrogen, carbon, oxygen, phosphorus, sulphur, nitrogen and chlorine. Iron is present in those species that have haemoglobin. Besides these 11 elements, the living tissue also requires certain other elements for functioning properly. These elements, available in traces, constitute the substances that help to regulate the different processes of life. Trace elements, necessary for nutrition, include fluorine, chromium, manganese, iron, cobalt, copper, zinc, selenium, molybdenum and iodine. Nickel, aluminum, arsenic and barium are observed to concentrate in human tissues with age. Concentration of trace elements generally is found to increase from rock to soil to water to plants to animals. Many trace elements, beyond certain levels of concentration, often cause serious health problems, when the human body is exposed to them (Keller 1985). Arsenic and fluoride have precipitated health issues of grave concern (Mathur 2004).
Arsenic is a Class I carcinogen causing cancer of the skin, lungs, bladder, liver, kidney, and probably prostate and ovary. Exposure can be by ingestion of contaminated drinking water or food, or by inhalation of fumes from burning coal. Arsenic does not induce point mutations like a classic DNA-damaging mutagen. The carcinogenic mechanism is unclear, but evidence exists supporting DNA repair inhibition, stem cell expansion, reactive oxygen generation, aneuploidy, and epigenetic dysregulation. The lack of UV signature mutation spectra in arsenic-induced skin cancers argues against DNA repair inhibition as a mechanism. Recent studies on epigenetic dysregulation point toward differential gene expression consistent with a role in arsenic carcinogenesis. Limited animal models for arsenic carcinogenesis and limited studies conducted in human cancers caused by arsenic exposure limit the ability to elucidate mechanisms. Research focused on tumors from people suffering from arsenicosis is needed for a clearer understanding of molecular events underlying arsenic-induced carcinogenesis.
While exposure to arsenic can occur through a number of routes, including ingestion in water, foods, and soil, early work focused on the ability of arsenic to increase the risk of lung cancer through inhalation, especially in occupational settings. This chapter focuses on the role of arsenic in airway remodeling and how that relationship might lead to both carcinogenic and noncarcinogenic lung diseases. It outlines lung cancer and noncancer adverse health outcomes following arsenic exposures that have been reported in human populations and/or animal studies. Those adverse outcomes suggest that the extracellular matrix (ECM) and aberrant cell motility and wound repair are targets of arsenic, leading to the chronic lung disease phenotypes seen in populations exposed to high levels of arsenic. Aberrant wound repair and signaling mechanisms involved in cellular migration, as well as changes in airway epithelial barrier structure and function, have been demonstrated following arsenic exposure as well.
Background:
Arsenic in drinking water has been associated with increases in lung disease, but information on the long-term impacts of early-life exposure or moderate exposure levels are limited.
Methods:
We investigated pulmonary disease and lung function in 795 subjects from three socio-demographically similar areas in northern Chile: Antofagasta, which had a well-described period of high arsenic water concentrations (860μg/L) from 1958 to 1970; Iquique, which had long-term arsenic water concentrations near 60μg/L; and Arica, with long-term water concentrations ≤10μg/L.
Results:
Compared to adults never exposed >10μg/L, adults born in Antofagasta during the high exposure period had elevated odds ratios (OR) of respiratory symptoms (e.g., OR for shortness of breath=5.56, 90% confidence interval (CI): 2.68-11.5), and decreases in pulmonary function (e.g., 224ml decrease in forced vital capacity in nonsmokers, 90% CI: 97-351ml). Subjects with long-term exposure to arsenic water concentrations near 60μg/L also had increases in some pulmonary symptoms and reduced lung function.
Conclusions:
Overall, these findings provide new evidence that in utero or childhood arsenic exposure is associated with non-malignant pulmonary disease in adults. They also provide preliminary new evidence that long-term exposures to moderate levels of arsenic may be associated with lung toxicity, although the magnitude of these latter findings were greater than expected and should be confirmed.
Arsenic, which is ubiquitous in the environment, has become a worldwide public health problem. It has become evident that increasing use of arsenic-containing insecticides, herbicides, fungicides, pesticides, and wood preservatives, and through the mining and burning of coal has modified the global cycle of arsenic. Arsenic enters to biosphere primarily by leaching from geological formations. Its ubiquity in the environment has led to the evolution of arsenic defense mechanisms in every organism studied, from Escherichia coli to humans. Arsenic ranks 20th in natural abundance, consisting about 0.00005% of the earth's crust, 14th in seawater, and 12th in the human body. The relative ubiquity of arsenic operon and the processes involved in arsenic detoxification and resistance, indicate that there have been important selective factors in microbial evolution. These taxonomically diverse and metabolically versatile microorganisms have evolved a number of mechanisms to gain energy for their growth from this toxic element in their environment, and developed detoxification mechanisms including oxidation, reduction, and methylation for increased tolerance and resistance to high levels of arsenic in their environment. Through a variety of detoxification and respiratory mechanisms, microorganisms have the ability to greatly influence the speciation of arsenic within the environment, and thus play a significant role in the arsenic cycle and impact of arsenic toxicity.
An alarmingly large population of developing world specially India and Bangladeshis exposed to arsenic poisoning due to continuous usage of arsenic-contaminated groundwater. Experts believe this to be the greatest case of mass poisoning in the history of theworld. The domestic and international response to address this crisis, unfortunately, hasbeen slow and somewhat discouraging. Even though handling the arsenic crisis is anenormous task, nevertheless, it needs to be addressed.Arsenic contamination of groundwater especially in Bangladesh, India, Nepal andPakistan has mainly occurred due to natural reasons. As per the most plausible theory, inthe Late Pleistocene to the recent times, iron and arsenic-bearing sulphidic minerals inupper reaches of the Ganges river belt may have undergone oxidation due to exposure toatmosphere during erosion, resulting in subsequent mobilization of arsenic and irondownstream.Besides, the same problem, but to a lesser extent, has also been observed in otherparts of the world as well, such as China, Taiwan, Inner Mangolia, Obuasi Ghana,Corodoba Argentina, Antofagasta, Chile Mexico, Britain and more recently in UnitedStates. Considering the rate at which this poison is spreading its web to the most interiorparts all over the world, there is an urgent need to develop ways to mitigate this problemby reducing the level of arsenic in drinking water to tolerable limits through easy andinexpensive means.There has been considerable advancement in water treatment technologiesworldwide since the discovery of the arsenic contamination in West Bengal, India,Bangladesh and elsewhere. This chapter, therefore, looks at remedial measures withspecial emphasis on cost and feasibility for third world nations such as India, Bangladesh,Nepal and Pakistan to provide arsenic free water. This chapter also examines use of otheralternative water resources, such as surface water and rainwater harvesting for the thirdworld nations to aid policy makers and managers who may oversee and advise long-termsolutions for this acute poisoning of ground water.
A prospective study of respiratory symptoms
associated with chronic arsenic exposure in
Bangladesh: findings from the Health Effects of
Arsenic Longitudinal Study (HEALS)
The objective of this study was to assess whether arsenic exposure is a risk factor for diabetes mellitus as indicated in a few earlier studies. Arsenic in drinking water is known to occur in western Bangladesh, and in 1996, two of the authors conducted a survey of the prevalence of diabetes mellitus among 163 subjects with keratosis taken as exposed to arsenic and 854 unexposed individuals. Diabetes mellitus was determined by history of symptoms, previously diagnosed diabetes, glucosuria, and blood sugar level after glucose intake. The crude prevalence ratio for diabetes mellitus among keratotic subjects exposed to arsenic was 4.4 (95% confidence interval 2.5-7.7) and increased to 5.2 (95% confidence interval 2.5-10.5) after adjustment for age, sex, and body mass index. On the basis of a few earlier measurements of arsenic concentrations in drinking water by the authorities in Bangladesh and another 20 new ad hoc analyses, approximate time-weighted exposure levels to arsenic in drinking water could be estimated for each subject. Three time-weighted average exposure categories were created, i.e., less than 0.5, 0.5-1.0, and more than 1.0 mg/liter. For the unexposed subjects, the corresponding prevalence ratios were 1.0, 2.6, 3.9, and 8.8, representing a significant trend in risk (p < 0.001). The result corroborates earlier studies and suggests that arsenic exposure is a risk factor for diabetes mellitus.
-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.
Exposure to arsenic causes keratosis, hyperpigmentation, and hypopigmentation and seemingly also diabetes mellitus, at least in subjects with skin lesions. Here we evaluate the relations of arsenical skin lesions and glucosuria as a proxy for diabetes mellitus.
Through existing measurements of arsenic in drinking water in Bangladesh, wells with and without arsenic contamination were identified. Based on a questionnaire, 1595 subjects > or = 30 years of age were interviewed; 1481 had a history of drinking water contaminated with arsenic whereas 114 had not. Time weighted mean arsenic concentrations and mg-years/l of exposure to arsenic were estimated based on the history of consumption of well water and current arsenic concentrations. Urine samples from the study subjects were tested by means of a glucometric strip. People with positive tests were considered to be cases of glucosuria.
A total of 430 (29%) of the exposed people were found to have skin lesions. Corresponding to drinking water with < 0.5, 0.5-1.0, and > 1.0 mg/l of arsenic, and with the 114 unexposed subjects as the reference, the prevalence ratios for glucosuria, as adjusted for age and sex, were 0.8, 1.4, and 1.4 for those without skin lesions, and 1.1, 2.2, and 2.6 for those with skin lesions. Taking exposure as < 1.0, 1.0-5.0, > 5.0-10.0 and > 10.0 mg-years/l of exposure to arsenic the prevalence ratios, similarly adjusted, were 0.4, 0.9, 1.2, and 1.7 for those without and 0.8, 1.7, 2.1, and 2.9 for those with skin lesions. All series of risk estimates were significant for trend, (p < 0.01).
The results suggest that skin lesions and diabetes mellitus, as here indicated by glucosuria, are largely independent effects of exposure to arsenic although glucosuria had some tendency to be associated with skin lesions. Importantly, however, glucosuria (diabetes mellitus) may occur independently of skin lesions.
Nine districts in West Bengal, India, and 42 districts in Bangladesh have arsenic levels in groundwater above the World Health Organization maximum permissible limit of 50 microg/L. The area and population of the 42 districts in Bangladesh and the 9 districts in West Bengal are 92,106 km(2) and 79.9 million and 38,865 km(2) and 42.7 million, respectively. In our preliminary study, we have identified 985 arsenic-affected villages in 69 police stations/blocks of nine arsenic-affected districts in West Bengal. In Bangladesh, we have identified 492 affected villages in 141 police stations/blocks of 42 affected districts. To date, we have collected 10,991 water samples from 42 arsenic-affected districts in Bangladesh for analysis, 58,166 water samples from nine arsenic-affected districts in West Bengal. Of the water samples that we analyzed, 59 and 34%, respectively, contained arsenic levels above 50 microg/L. Thousands of hair, nail, and urine samples from people living in arsenic-affected villages have been analyzed to date; Bangladesh and West Bengal, 93 and 77% samples, on an average, contained arsenic above the normal/toxic level. We surveyed 27 of 42 districts in Bangladesh for arsenic patients; we identified patients with arsenical skin lesions in 25 districts. In West Bengal, we identified patients with lesions in seven of nine districts. We examined people from the affected villages at random for arsenical dermatologic features (11,180 and 29,035 from Bangladesh and West Bengal, respectively); 24.47 and 15.02% of those examined, respectively, had skin lesions. After 10 years of study in West Bengal and 5 in Bangladesh, we feel that we have seen only the tip of iceberg.
Images
Figure 1
Figure 2
Figure 3
Figure 4
The contamination of groundwater by arsenic in Bangladesh is the largest poisoning of a population in history, with millions of people exposed. This paper describes the history of the discovery of arsenic in drinking-water in Bangladesh and recommends intervention strategies. Tube-wells were installed to provide "pure water" to prevent morbidity and mortality from gastrointestinal disease. The water from the millions of tube-wells that were installed was not tested for arsenic contamination. Studies in other countries where the population has had long-term exposure to arsenic in groundwater indicate that 1 in 10 people who drink water containing 500 micrograms of arsenic per litre may ultimately die from cancers caused by arsenic, including lung, bladder and skin cancers. The rapid allocation of funding and prompt expansion of current interventions to address this contamination should be facilitated. The fundamental intervention is the identification and provision of arsenic-free drinking water. Arsenic is rapidly excreted in urine, and for early or mild cases, no specific treatment is required. Community education and participation are essential to ensure that interventions are successful; these should be coupled with follow-up monitoring to confirm that exposure has ended. Taken together with the discovery of arsenic in groundwater in other countries, the experience in Bangladesh shows that groundwater sources throughout the world that are used for drinking-water should be tested for arsenic.
A large population in West Bengal, India has been exposed to naturally occurring inorganic arsenic through their drinking water. A cross-sectional survey involving 7683 participants of all ages was conducted in an arsenic-affected region between April 1995 and March 1996. The main focus of the study was skin keratoses and pigmentation alterations, two characteristic signs of ingested inorganic arsenic. Strong exposure-response gradients were found for these skin lesions. The study also collected limited information concerning respiratory system signs and symptoms, which we report here because increasing evidence suggests that arsenic ingestion also causes pulmonary effects.
Participants were clinically examined and interviewed, and the arsenic content in their current primary drinking water source was measured. There were few smokers and analyses were confined to non-smokers (N = 6864 participants).
Among both males and females, the prevalence of cough, shortness of breath, and chest sounds (crepitations and/or rhonchi) in the lungs rose with increasing arsenic concentrations in drinking water. These respiratory effects were most pronounced in individuals with high arsenic water concentrations who also had skin lesions. Prevalence odds ratio (POR) estimates were markedly increased for participants with arsenic-induced skin lesions who also had high levels of arsenic in their current drinking water source (> or = 500 microg/l) compared with individuals who had normal skin and were exposed to low levels of arsenic (<50 microg/l). In participants with skin lesions, the age-adjusted POR estimates for cough were 7.8 for females (95% CI : 3.1-19.5) and 5.0 for males (95% CI : 2.6-9.9); for chest sounds POR for females was 9.6 (95% CI : 4.0-22.9) and for males 6.9 (95% CI : 3.1-15.0). The POR for shortness of breath in females was 23.2 (95% CI : 5.8-92.8) and in males 3.7 (95% CI : 1.3-10.6).
These results add to evidence that long-term ingestion of inorganic arsenic can cause respiratory effects.
Concentrations of 23 elements in lung, liver and kidney from deceased smelter workers are compared with those from rural and urban controls. The analyses were made by neutron activation analysis and atomic absorption spectrophotometry. Significantly higher levels of antimony, arsenic, cadmium, chromium, cobalt, lanthanum, lead and selenium were found in the smelter workers lungs (n = 85) compared with the rural controls (n = 15). Significantly higher concentrations of antimony, arsenic and lead were observed among all smelter workers compared with urban controls (n = 10). The highest increase, about 11-fold, was found for antimony in smelter workers compared with non-exposed controls. A six-fold increase was noted for arsenic. Workers who died from lung cancer (n = 7) had the lowest lung selenium content relative to concentrations of other metals, both compared with other disease categories among the workers (GI-cancer, other cancers, cardiovascular diseases, cerebrovascular diseases, other causes) and with the two control groups. The low lung selenium concentrations may have influenced the development of lung cancer. The highest lung tissue levels of cadmium were found in the lung cancer group. Smokers and ex-smokers were over-represented in this group and tobacco is a known cadmium source. The highest, or one of the highest, lung values for some of the other metals (antimony, arsenic, cadmium, lanthanum and lead) were observed in one or several of the lung cancer cases. Metal concentrations in liver (metabolism) and kidney (excretion) reflect the systemic distribution. The highest cadmium levels in the liver and the lowest selenium content in the kidney were found among the lung cancer cases. A multifactorial genesis for the development of lung cancer is concluded from this study, which visualizes the need for systematic health surveillance and follow-ups both in active and retired workers.
Investigations on the arsenic contamination of human environment in the northern provinces of Tarapaca, Antofagasta, and Coquimbo, as well as clinical studies on endemic chronic arsenic poisoning, were made. In Tarapaca Province, the total number of exposed nitrate workers since 1890 was about 30,000. But in Antofagasta and Coquimbo Provinces (1970), the number of exposed persons was 265,000 and 142,000 respectively. In Antofagasta Province, some population groups have been exposed to dietary arsenic for periods up to 41 years. The safety standard of arsenic in drinking water in the Federal Republic of Germany and in the U.S.A. is 0.05 ppm. The Hojalar, Toconce, Loa and Siloli Rivers exhibited a mean of 0.992, 0.940, 0.337 and 0.104 ppm, respectively. Soil samples from Antofagasta Commune exhibited a mean of 4.374 ppm. The mean arsenic levels found in fresh vegetables were partly high: lettuce 0.062, cauliflower 0.070, celery 0.104, and radish 0.100 mg/100 g. In other food items: fresh cow's milk 0.083 ppm, fresh human milk 0.216, vanilla ice cream 0.156, orange juice 0.120, pineapple juice 0.390, spaghetti 0.014 mg/100, and canned mackerel 0.025 mg/100g. The mean levels (ppm) in soft drinks and beer were high in Pepsi Cola (0.265), Ginger-ale (0.275), Bilz (0.275), Fanta (0.250), Coca Cola (0.204), Seltz water (0.291), Pilsner beer (0.553), Escudo (0.388), and Malta (0.484). Almost all the signs and symptoms of chronic arsenic poisoning observed in children at Antofagasta Commune in the 1968-69 period markedly decreased their prevalence in 1972, because of the decrease in the arsenic level of drinking water. The weighted mean arsenic concentration in drinking water at Antofagasta Commune for 1955-1970 (up to 30th April) was 0.5980 ppm. The corresponding level (weighted mean) from 1st June, 1970 to 30th March, 1972 was 0.815 ppm. In May 1970, a Water Filtration Plant went into operation at Salar del Carmen, near Antofagasta. A similar Filtration Plant in July 1978 started operating at Cerro Topater, near Calama. Based on mean age (years) and mean value of arsenic dose (mg/kg body weight/day), a weighted non linear regression model was developed. The non linear regression equation was C = 0.0303 exp (- 0.0257 t) + 0.0720 exp (- 0.2636 t), where C is arsenic concentration expressed as mean dose and t is time expressed as mean age.
Studies in Taiwan and Argentina suggest that ingestion of inorganic arsenic from drinking water results in increased risks of internal cancers, particularly bladder and lung cancer. The authors investigated cancer mortality in a population of around 400,000 people in a region of Northern Chile (Region II) exposed to high arsenic levels in drinking water in past years. Arsenic concentrations from 1950 to the present were obtained. Population-weighted average arsenic levels reached 570 microg/liter between 1955 to 1969, and decreased to less than 100 microg/liter by 1980. Standardized mortality ratios (SMRs) were calculated for the years 1989 to 1993. Increased mortality was found for bladder, lung, kidney, and skin cancer. Bladder cancer mortality was markedly elevated (men, SMR = 6.0 (95% confidence interval (CI) 4.8-7.4); women, SMR = 8.2 (95% CI 6.3-10.5)) as was lung cancer mortality (men, SMR = 3.8 (95% CI 3.5-4.1); women, SMR = 3.1 (95% CI 2.7-3.7)). Smoking survey data and mortality rates from chronic obstructive pulmonary disease provided evidence that smoking did not contribute to the increased mortality from these cancers. The findings provide additional evidence that ingestion of inorganic arsenic in drinking water is indeed a cause of bladder and lung cancer. It was estimated that arsenic might account for 7% of all deaths among those aged 30 years and over. If so, the impact of arsenic on the population mortality in Region II of Chile is greater than that reported anywhere to date from environmental exposure to a carcinogen in a major population.