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Arsenic exposure form drinking water and birth weight
... Several studies have examined the association between prenatal arsenic exposure and birth anthropometric outcomes (Claus Henn et al., 2016;Gilbert-Diamond et al., 2016;Hopenhayn et al., 2003;Kwok et al., 2006;Laine et al., 2015;Myers et al., 2010;Rahman et al., 2009;Yang et al., 2003). While most of these studies were conducted in populations with high average levels of inorganic arsenic in drinking water (e.g., > 50 μg/L) (Hopenhayn et al., 2003;Kwok et al., 2006;Laine et al., 2015;Myers et al., 2010;Rahman et al., 2009;Yang et al., 2003); Claus Henn et al. (2016), and our group examined how prenatal arsenic exposure related to anthropometry at birth in U.S. populations with predominately lower levels of inorganic arsenic in drinking water (e.g., < 10 μg/L). ...
... Several studies have examined the association between prenatal arsenic exposure and birth anthropometric outcomes (Claus Henn et al., 2016;Gilbert-Diamond et al., 2016;Hopenhayn et al., 2003;Kwok et al., 2006;Laine et al., 2015;Myers et al., 2010;Rahman et al., 2009;Yang et al., 2003). While most of these studies were conducted in populations with high average levels of inorganic arsenic in drinking water (e.g., > 50 μg/L) (Hopenhayn et al., 2003;Kwok et al., 2006;Laine et al., 2015;Myers et al., 2010;Rahman et al., 2009;Yang et al., 2003); Claus Henn et al. (2016), and our group examined how prenatal arsenic exposure related to anthropometry at birth in U.S. populations with predominately lower levels of inorganic arsenic in drinking water (e.g., < 10 μg/L). In both of these studies, prenatal arsenic exposure was related to smaller head circumference at birth. ...
Background:
We have previously reported that in utero arsenic exposure is associated with increased length and other anthropometric outcomes at birth in a U.S. cohort. However, it is unknown whether these anthropometric differences persist through early life.
Objectives:
We assessed in utero arsenic exposure in relation to attained anthropometry and growth trajectories through the first year of life.
Methods:
Among 760 mother-infant pairs from the New Hampshire Birth Cohort Study, we assessed in utero arsenic exposure using maternal second trimester urinary arsenic and assessed infant growth from medical records.
Results:
Median maternal second trimester total urinary arsenic (tAs; inorganic arsenic + monomethylarsonic acid + dimethylarsinic acid) was 3.96 μg/L (IQR: 2.02, 6.72). In adjusted linear mixed effects models, each doubling of maternal urinary tAs was associated with a 0.05 increase in length WHO Z score (95% CI: 0, 0.09) over the first year of life which corresponds to an approximately 0.12 cm increase in males and 0.13 cm increase in females at 12 months. No associations were observed between urinary tAs and attained weight, weight-for-length, or head circumference. In adjusted piecewise linear mixed effects models, each doubling of urinary tAs was associated with a 0.07 (95% CI: 0.02, 0.12) cm per month decreased length growth rate through 3.5 months with no evidence of an association thereafter. No associations were observed between urinary tAs and infant weight gain or change in weight-for-length and head circumference through one year.
Conclusions:
On average, infants exposed to higher in utero arsenic attained modestly longer length during the first year, despite having slower linear growth in the first 3.5 months of life. This suggests that the previously demonstrated arsenic-associated longer length among study infants at birth persists through the first year of life. No other anthropometric associations with in utero arsenic exposure were observed across the full study population.
... (R. Loch-Caruso). preterm birth and lower birth weight4567 . In Ahmad's crosssectioned study in Bangladesh [4], pregnancy outcomes in women exposed to high levels of arsenic through drinking water (>50 g/L) were compared with those of women who were exposed to arsenic at levels <20 g/L in drinking water. ...
... Moreover, maternal oral exposure to arsenic during gestation leads to irreversible cellular transformation and a carcinogenic response in the offspring in mice212223, providing further support that arsenic is readily transferred across the placenta with access to the fetus and the trophoblast cells of the placenta and fetal membranes. Therefore, the results of this study may have relevance for epidemiologic studies that found associations between arsenic-contaminated drinking water and adverse pregnancy outcomes4567. Extravillous trophoblast cells are invasive because of their ability to secret proteases that degrade ECM and their ability to subsequent migrate through the matrix defects [25]. Of the secreted proteases, the MMPs are a family of zinc-dependent ECM-degrading enzymes. ...
This study used a first-trimester human extravillous trophoblast (EVT) cell line, HTR-8/SVneo, to investigate whether sodium arsenite (AsNaO(2)) reduces human EVT migration and invasion. Treatments with 2.5 microM AsNaO(2) or less (< or =187.3 microg/L), concentrations that are relevant to human exposures in drinking water, were sublethal to HTR-8/SVneo cells. A 72-h exposure to sodium arsenite inhibited cell migration in a concentration-dependent manner at 0.625, 1.25 and 2.5 microM. Significant changes in cell proliferation were not observed under these treatment conditions. Moreover, inhibition of cell migration was unrelated to phosphorylation of focal adhesion kinase Tyr397. In contrast to cell migration, 72-h exposures to AsNaO(2) (0.3125-2.5 microM) had no significant effects on cell invasion, nor on the activities and protein expression of matrix metalloproteinase (MMP) 2 and MMP9. Because trophoblast migration is important for placentation, these results suggest an effect that could contribute to insufficiency of placental development and adverse pregnancy outcomes.
... Arsenic can readily cross the placenta, and thereby pose a risk to the developing fetus ( Concha et al., 1998;Rudge et al., 2009). Several studies have reported that higher prenatal arsenic exposure is associated with increased risk of adverse birth outcomes including spontaneous abortion ( Milton et al., 2005), stillbirth ( Milton et al., 2005;von Ehrenstein et al., 2006), low birth weight ( Hopenhayn et al., 2003;Kile et al., 2015;M. L. Rahman et al., 2017), neonatal mortality ( Hopenhayn-Rich et al., 2000;A. ...
Background:
Preterm birth is a disease of multifactorial etiologies that has environmental, social, and maternal health components. Individual studies have shown that exposure to arsenic contaminated drinking water, child marriage, and low maternal weight gain during pregnancy contribute to preterm birth. These factors are highly prevalent and often co-exist in Bangladesh, a country in South Asia with one of the world's highest prevalences of preterm birth.
Objective:
To evaluate the individual and interactive effects of prenatal arsenic exposure, child marriage, and pregnancy weight gain on preterm birth in a prospective birth cohort in Bangladesh.
Methods:
During 2008-2011, we recruited 1613 pregnant women aged ≥18years at ≤16weeks of gestation and followed them until 1-month post-partum. We measured total arsenic in drinking water (n=1184) and in maternal toenails (n=1115) collected at enrollment and ≤1-month post-partum, respectively using inductively coupled plasma mass spectrometry. Child marriage (<18years old) was defined using self-report, and 2nd and 3rd trimester pregnancy weight gain was calculated using monthly records. Gestational age was determined at enrollment by ultrasound.
Results:
In multivariate adjusted Poisson regression models, the risk ratios (RR) for preterm birth were 1.12 (95% CI: 1.07-1.18) for a unit change in natural log water arsenic exposure, 2.28 (95% CI: 1.76-2.95) for child marriage, and 0.64 (95% CI: 0.42-0.97) for a pound per week increase in maternal weight during the 2nd and 3rd trimesters. In stratified analysis by child marriage, pregnancy weight gain was inversely associated with preterm birth among women with a history of child marriage (RR=0.58; 95% CI: 0.37-0.92), but not among women with no history of child marriage (RR=86; 95% CI: 0.37-2.01). Mediation analysis revealed that both arsenic exposure and child marriage had small but significant associations with preterm birth via lowering pregnancy weight gain. Similar associations were observed when arsenic exposure was assessed using maternal toenail arsenic concentrations.
Conclusions:
Reducing arsenic exposure and ending child marriage could reduce the risk of preterm birth in Bangladesh. Furthermore, enhancing nutritional support to ensure adequate weight gain during pregnancy may provide additional benefits especially for women with a history of child marriage.
... Of these, one supports an increasing risk with greater exposure while two did not observe a statistically significant association. A prospective cohort study conducted in two Chilean cities with contrasting drinking water arsenic levels, Antofagasta (40 ppb) and Valparaiso (<1 ppb), found that moderate arsenic exposure from drinking water (<50 ppb) during pregnancy was associated with low birth weight[36]. A study from Dalian, China, suggests that maternal exposure to arsenic is associated with impaired fetal growth. ...
Exposure to arsenic has a number of known detrimental health effects but impact on pregnancy outcomes is not as widely recognized. This narrative review examines existing epidemiological evidence investigating the association between arsenic exposure via drinking water and adverse pregnancy outcomes. We reviewed published epidemiological studies from around the world on impact of chronic arsenic exposure on spontaneous abortion, stillbirth, neonatal death, post neonatal death, low birth weight and preterm baby. Plausible mechanisms of arsenic toxicity causing adverse pregnancy outcomes were also determined through literature review. There is convincing evidence to support the association between high inorganic arsenic exposure (>50 ppb) and spontaneous abortion, stillbirth and low birth weight. Limitations of certain studies include study design, small sample size, recall constraints and exposure assessment. There needs to be further research investigating the dose metered impact of arsenic exposure on pregnancy outcomes. Further research on impact of low-moderate arsenic concentration exposure on pregnancy outcomes will allow for appropriate public health policy recommendations.
... This exposure to several heavy metals during pregnancy has been shown to be harmful to the developing fetus, for example, lower birth weight is a documented adverse effect of lead exposure during pregnancy [18]. Similarly, gestational cadmium exposure has been associated with low birth weight (2500g) [19] as was moderate arsenic exposures from drinking water (<50 micro g/L) during pregnancy [20]. Postnatal exposure can also occur via breast milk and ingestion of leaded paint, soil contaminated with lead and water carried in lead pipes. ...
Objectives
Severe acute malnutrition (SAM) is an important risk factor for illness and death globally, contributing to more than half of deaths in children worldwide. We hypothesized that SAM is positively correlated to poverty, low educational attainment, major crime and higher mean soil concentrations of lead, cadmium and arsenic.
Methods
We reviewed admission records of infants admitted with a diagnosis of SAM over 14 years (2000–2013) in Jamaica. Poverty index, educational attainment, major crime and environmental heavy metal exposure were represented in a Geographic Information System (GIS). Cases of SAM were grouped by community and the number of cases per community/year correlated to socioeconomic variables and geochemistry data for the relevant year.
Results
375 cases of SAM were mapped across 204 urban and rural communities in Jamaica. The mean age at admission was 9 months (range 1–45 months) and 57% were male. SAM had a positive correlation with major crime (r = 0.53; P < 0.001), but not with educational attainment or the poverty index. For every one unit increase in the number of crimes reported, the rate of occurrence of SAM cases increased by 1.01% [Incidence rate ratio (IRR) = 1.01 (95% CI = 1.006–1.014); P P<0.001]. The geochemistry data yielded no correlation between levels of heavy metals and the prevalence of malnutrition.
Conclusion
Major crime has an independent positive association with severe acute malnutrition in Jamaican infants. This could suggest that SAM and major crime might have similar sociological origins or that criminality at the community level may be indicative of reduced income opportunities with the attendant increase in poor nutrition in the home.
... The genotoxicitiy, DNA damage and oxidative stress induced by exposure to arsenic are well established (Ostrosky-Wegman et al., 1991;Lerda, 1994;Moore et al., 2002;Martínez et al., 2004;Salazar et al., 2004;Andrew et al., 2006). Arsenic is also teratogenic, able to cross the placental barrier and interfere with foetal development (Nordstr€ om et al., 1979;Hopenhayn-Rich et al., 2000;Ahmad et al., 2001;Centeno et al., 2002;Hopenhayn et al., 2003;Milton et al., 2005). Studies of endemic arsenic areas indicate up to 20% of all deaths among exposed populations can be attributed to the effects of arsenic toxicity (Smith et al., 1998;Argos et al., 2010). ...
... Many exposures during pregnancy have been associated with the outcome of LBW including maternal substance use, including tobacco, and maternal illnesses (e.g., infections, hypertension). Fetal exposure to lead (Pb), mercury (Hg), and arsenic (As) have been associated with other adverse child outcomes (Shirai et al. 2010; Lin et al. 1998; Ahmad et al. 2001; Hopenhayn et al. 2003; Yang et al. 2003). In the research regarding chemical exposures, maternal blood levels, samples from the umbilical cord, infant blood, or maternal urine during pregnancy are used to measure concentrations. ...
Low birth weight (LBW) is associated with a number of maternal environmental exposures during pregnancy. This study explored the association between soil metal concentrations around the home where the mother lived during pregnancy and the outcome of LBW. We used a retrospective cohort of 9,920 mother-child pairs who were insured by Medicaid during pregnancy and lived in ten residential areas, where we conducted soil sampling. We used a grid that overlaid the residential areas and collected soil samples at the grid intersections. The soil was analyzed for the concentration of eight metals [arsenic (As), barium (Ba), chromium (Cr), copper (Cu), lead (Pb), manganese (Mn), nickel (Ni), and mercury (Hg)], and we then used Bayesian Kriging to estimate the concentration at the actual maternal addresses, since we had the GIS coordinates of the homes. We used generalized additive modeling, because the metal concentrations had nonlinear associations with LBW, to develop the best fitting multivariable model for estimating the risk of LBW. The final model showed significant associations for female infants, maternal smoking during pregnancy, non-white mothers, Cu, and As with LBW. The As variable was nonlinear in relation to LBW, and the association between higher concentrations of As with LBW was strong (p = 0.002). We identified a statistically significant association between soil concentrations of arsenic around the home of pregnant women and an increased risk of LBW for her infant.
... Women exposed to As were found to show significant levels of As in umbilical cord and placenta; for example, Concha et al. (1998) reported the presence of As in the cord blood and placenta in women exposed to 200 lg/l of arsenic in their study in Argentina. In a study from northern Chile, high perinatal and neonatal mortality, and reduction in birth weight were reported with drinking water contaminated in the range 90–860 lg/l (Hopen- Rich et al. 2000Rich et al. , 2003). Yang et al. (2003) reported a slightly high rate of preterm birth in an exposed population of Taiwan. ...
Worldwide chronic arsenic (As) toxicity has become a human health threat. Arsenic exposure to humans mainly occurs from the ingestion of As contaminated water and food. This communication presents a review of current research conducted on the adverse health effects on humans exposed to As-contaminated water. Chronic exposure of As via drinking water causes various types of skin lesions such as melanosis, leucomelanosis, and keratosis. Other manifestations include neurological effects, obstetric problems, high blood pressure, diabetes mellitus, diseases of the respiratory system and of blood vessels including cardiovascular, and cancers typically involving the skin, lung, and bladder. The skin seems to be quite susceptible to the effects of As. Arsenic-induced skin lesions seem to be the most common and initial symptoms of arsenicosis. More systematic studies are needed to determine the link between As exposure and its related cancer and noncancer end points.
Arsenic is a public health concern because of its widespread distribution and high toxicity, even when doses are small. Low birth weight (LBW) occurrence, birth weights less than 2500 g, may be associated with prenatal exposure of arsenic from environmental factors and consuming contaminated drinking water and food. The objective of this study was to examine whether mothers living in areas of Escambia and Santa Rosa counties with varying levels of background arsenic in surface soil and water were associated with the occurrence of LBW. Inverse distance weight in ArcGIS was used to interpolate arsenic concentrations from environmental samples and estimate arsenic concentrations by census tracts in the two counties. After excluding multiple births and displaced geocoding addresses, birth data were obtained for the years of 2005 (n = 5845), 2010 (n = 5569), and 2015 (n = 5770) from the Bureau of Vital Statistics at the Florida Department of Health to assess temporal differences. Generalized linear models were used to analyze and compare the association between child and maternal demographic information, socioeconomic characteristics, and the environmental estimates of arsenic with LBW. No significant association was found between environmental arsenic concentration and LBW, suggesting that environmental contamination of the pregnant mother’s census tract may not be a useful proxy in assessing risk for LBW.
Background:
The relationship between arsenic and birth weight is not well understood. The objective was to evaluate the causal relationship between prenatal arsenic exposure and birth weight considering the potential mediation effects of gestational age and maternal weight gain during pregnancy using structural equation models.
Methods:
A prospectively enrolled cohort of pregnant women was recruited in Bangladesh from 2008 to 2011. Arsenic was measured in personal drinking water at the time of enrollment (gestational age <16 weeks, N = 1,140) and in toenails collected ≤1 month postpartum (N = 624) using inductively coupled plasma mass spectrometry. Structural equation models estimated the direct and indirect effects of arsenic on birth weight with gestational age and maternal weight gain considered as mediating variables.
Results:
Every unit increase in natural log water arsenic was indirectly associated with decreased birth weight (β = -19.17 g, 95% confidence interval [CI]: -24.64, -13.69) after adjusting for other risk factors. This association was mediated entirely through gestational age (β = -17.37 g, 95% CI: -22.77, -11.98) and maternal weight gain during pregnancy (β = -1.80 g, 95% CI: -3.72, 0.13). When exposure was modeled using toenail arsenic concentrations, similar results were observed. Every increase in natural log toenail arsenic was indirectly associated with decreased birth weight (β = -15.72 g, 95% CI: -24.52, -6.91) which was mediated through gestational age (β = -13.59 g, 95% CI: -22.10, -5.07) and maternal weight gain during pregnancy (β = -2.13 g, 95% CI: -5.24, 0.96).
Conclusion:
Arsenic exposure during pregnancy was associated with lower birth weight. The effect of arsenic on birth weight appears to be mediated mainly through decreasing gestational age and to a lesser extent by lower maternal weight gain during pregnancy.
This chapter describes the risks of environmental agents as the sum total of all the substances capable of producing an effect, whether physical, chemical or biological, which make up the surroundings and influence the development of an individual. In this context, the chapter discusses occupational, industrial, and environmental agents. Environmental pollutants are usually industrial chemicals released as pollutants into the environment during production, use, recycling, and combustion processes, or into air, water or soil from naturally high sources. These include solvent exposure, which includes exposure to organic solvents such as acetone, carbon disulfide, carbon tetrachloride, chloroform, dichloroethane, dichloromethane, methylethylketone, tetrachloroethylene, and toluene; hydrocarbons such as formaldehyde and formalin, chloroprene, cyanide, photographic/printing chemicals, and pesticides; and metals such as arsenic, cadmium, lead, mercury. Waste disposal sites are also a potential hazard to health, and so are radiations associated with nuclear industry, video display terminals (VTDs), mobile phones, electromagnetic radiation, and electric shocks. In accordance with the maternal protection laws in many countries, pregnant women should not be exposed to toxic, infectious, ionizing or carcinogenic substances. However, in practice many workplaces require pregnant women to handle potentially toxic compounds and do not take into account the possibility that workers might already be pregnant. In addition, non-specific symptoms have to be considered when discussing the tolerability of a certain workplace or household contaminant. If pregnant women complain of repeated symptoms in the workplace-such as headaches, emesis, vertigo-this should be taken seriously.
Background Chronic exposure to toxic metals such as arsenic and cadmium has been implicated in the development of kidney and cardiovascular diseases but few studies have directly measured exposure during inutero and early child development.
Methods We investigated the impact of exposure to arsenic (mainly in drinking water) and cadmium (mainly in rice) during pregnancy on blood pressure and kidney function at 4.5 years of age in rural Bangladesh. The effect of arsenic exposure in infancy was also assessed.
Results Within a cohort of 1887 children recruited into the MINIMat study, exposure to arsenic (maternal urinary arsenic, U-As), but not cadmium, during in utero development was associated with a minimal increase in blood pressure at 4.5 years. Each 1 mg/l increase in pregnancy U-As was associated with 3.69 mmHg (95% CI: 0.74, 6.63; P: 0.01) increase in child systolic and a 2.91 mmHg (95% CI: 0.41, 5.42; P: 0.02) increase in child diastolic blood pressure. Similarly, a 1 mg/l increase in child U-As at 18 months of age was associated with a 8.25 mmHg (95% CI: 1.37, 15.1; P: 0.02) increase in systolic blood pressure at 4.5 years. There was also a marginal inverse association between infancy U-As and glomerular filtration rate at 4.5 years (−33.4 ml/min/1.72 m2; 95% CI: −70.2, 3.34; P: 0.08). No association was observed between early arsenic or cadmium exposure and kidney volume at 4.5 years assessed by ultrasound.
Conclusions These modest effect sizes provide some evidence that arsenic exposure in early life has long-term consequences for blood pressure and maybe kidney function.
Contamination of the environment with arsenic (As) from both anthropogenic and natural sources has occurred in many parts of the world and is recognized as a global problem. Principal anthropogenic sources of As include base metal smelters, gold mines, power plants that burn As-rich coals or treated lumber, disposal sites for wastes from As-processing plants, as well as industrial and municipal dump sites. In many areas, the levels of As in the environment have become one of concern and epidemiological studies have documented various adverse health effects on local populations. Arsenic poisoning episodes from exposure to industrial sources have been reported all over the world; for instance, in Japan, where cases have been associated with pollution around As mines and pollution of groundwater around As-using industries and industrial waste burial sites. Other examples of contaminated environments with increased risk for As poisoning include agricultural lands treated with arsenical pesticides, urban areas, war zones defoliated or sprayed with As compounds, and the superfund sites in the United States and other countries. Although a lot of people get exposed, most often, however, it is not possible to associate the exposure to elevated As levels with adverse human health effects. Nevertheless, long-term cumulative exposure to As in these contaminated environments should be a matter of public health concern and scientific interest.
Arsenic in drinking water causes increased mortality from several cancers, ischemic heart disease, bronchiectasis, and other diseases. This paper presents the first evidence relating arsenic exposure to pulmonary tuberculosis, by estimating mortality rate ratios for Region II of Chile compared with Region V for the years 1958-2000. The authors compared mortality rate ratios with time patterns of arsenic exposure, which increased abruptly in 1958 in Region II and then declined starting in 1971. Tuberculosis mortality rate ratios in men started increasing in 1968, 10 years after high arsenic exposure commenced. The peak male 5-year mortality rate ratio occurred during 1982-1986 (rate ratio = 2.1, 95% confidence interval: 1.7, 2.6; P < 0.001) and subsequently declined. Mortality rates in women were also elevated but with fewer excess pulmonary tuberculosis deaths (359 among men and 95 among women). The clear rise and fall of tuberculosis mortality rate ratios in men following high arsenic exposure are consistent with a causal relation. The findings are biologically plausible in view of evidence that arsenic is an immunosuppressant and also a cause of chronic lung disease. Finding weaker associations in women is unsurprising, because this is true of most arsenic-caused health effects. Confirmatory evidence is needed from other arsenic-exposed populations.
Millions of people worldwide are drinking water with elevated arsenic concentrations. Epidemiologic studies, mainly cross-sectional in design, have suggested that arsenic in drinking water may affect pregnancy outcome and infant health. We assessed the association of arsenic exposure with adverse pregnancy outcomes and infant mortality in a prospective cohort study of pregnant women.
A population-based, prospective cohort study of 2924 pregnant women was carried out during 2002-2004 in Matlab, Bangladesh. Spontaneous abortion was evaluated in relation to urinary arsenic concentrations at gestational week 8. Stillbirth and infant mortality were evaluated in relation to the average of urinary arsenic concentrations measured at gestational weeks 8 and 30.
: The odds ratio of spontaneous abortion was 1.4 (95% confidence interval [CI] = 0.96-2.2) among women with urine arsenic concentrations in the fifth quintile (249-1253 μg/L; median = 382 μg/L), compared with women in the first quintile (<33 μg/L). There was no clear evidence of increased rates of stillbirth. The rate of infant mortality increased with increasing arsenic exposure: the hazard ratio was 5.0 (95% CI = 1.4-18) in the fifth quintile of maternal urinary arsenic concentrations (268-2019 μg/L; median = 390 μg/L), compared with the first quintile (<38 μg/L).
We found evidence of increased risk of infant mortality with increasing arsenic exposure during pregnancy, with less evidence of associations with spontaneous abortion or stillbirth risk.
Arsenic in drinking water is associated with kidney cancer. Beginning in 1958, a region of Chile experienced a rapid onset of high arsenic exposure in drinking water, followed by sharp declines when water treatment plants were installed in 1971.
For the years 1950-1970, we obtained mortality data from death certificates for an exposed region and an unexposed region in Chile. We obtained computerized mortality data for all of Chile for 1971-2000.
Kidney cancer risks for the exposed region compared with the unexposed started to increase about 10 years after high arsenic exposures began in 1958. The peak kidney cancer mortality rate ratio (RR) was 3.4 (95% confidence interval = 2.2-5.1) for men in 1981-1985, with subsequent declines to 1.6 (1.2-2.1) by 1996-2000. Mortality RRs among women were 2.9 (1.8-4.7) in 1981-1985 but remained high longer than for men, increasing further to a RR of 4.4 (3.0-6.4) in 1991-1995. Early-life exposure resulted in an increased RR of 7.1 (3.1-14) for young adults aged 30-39 years, born just before or during the high exposure period.
This study shows a latency pattern of increased mortality from kidney cancer, continuing for at least 25 years after the high exposures began to decline. Early life exposure resulted in markedly higher kidney cancer mortality in young adults.
The aim of this work is to determine whether consuming tap water containing arsenic (20 microg/L) alters oxidative stress levels in female rats and changes vascular response. Whereas nitric oxide produces complete relaxation, arsenic (7 months of exposure) impairs the acetylcholine-induced endothelial relaxation in the rat aorta compared with control rats. Arsenic exposure results in a marked elevation in reactive oxygen species in blood, and delta-aminolevulinic acid dehydratase activity, which is a sensitive biomarker for arsenic toxicity and oxidative stress, is significantly decreased in erythrocytes from 7-month-old rats. Diastolic blood pressure increases significantly in 7-month-old arsenic-treated versus control rats. The percentage of change in peripheral resistance increases. The results indicate that chronic environmental exposure to low levels of arsenic alters the release of vasoactive substances, causes changes in oxidative stress, and increases blood pressure in female rats.
One of the most persistent disparities in American health status is the pronounced difference in birth outcomes between non-Hispanic
black and non-Hispanic white women. Poor pregnancy outcomes have a substantial impact on mortality, morbidity, and health
care costs. Increasing evidence indicates that environmental exposures are associated with poor birth outcomes. This paper
reviews the latest research on how environmental exposures affect pregnancy outcomes and then discusses how these exposures
may be embedded within a context of significant social and host factor stress. The analysis suggests that environmental, social,
and host factors are cumulatively stressing non-Hispanic black women and that this cumulative stress may be a cause of the
persistent disparities in pregnancy outcomes.
Bayingnormen is a region located in western Inner Mongolia China, with a population that is exposed to a wide range of drinking water arsenic concentrations. The relationship between maternal drinking water arsenic exposure and perinatal endpoints (term birth weight, preterm birth, stillbirth and neonatal death) in this region was evaluated in this study.
An analysis was conducted of all singleton deliveries in a defined geographical area of Inner Mongolia from December 1996 to December 1999 (n=9890). Outcome and covariate data were abstracted from prenatal care records. Exposure was based on well-water measures for the maternal subvillage. Mean birth weight at term was compared across four arsenic categories using analysis of covariance. ORs for stillbirth, preterm birth and neonatal death were estimated by logistic regression with arsenic exposure dichotomised at 50 microg/l.
Term birth weight was 0.05 kg higher (95% CI 0.02 to 0.08) in the highest exposure category (>100 microg/l) compared to the reference (below limit of detection to 20 microg/l). Arsenic >50 microg/l was associated with an increased risk of neonatal death (OR 2.01, 95% CI 1.12 to 3.59). No relationship was found between maternal arsenic exposure and preterm or stillbirth delivery.
At the levels observed in our study, arsenic does not appear to contribute to adverse birth outcomes. Exposure may play a role in neonatal death; however, the neonatal death rate in this population was low and this potential association merits further research.
The authors evaluated the association of prenatal arsenic exposure with size at birth (birth weight, birth length, head and chest circumferences). This prospective cohort study, based on 1,578 mother-infant pairs, was conducted in Matlab, Bangladesh, in 2002-2003. Arsenic exposure was assessed by analysis of arsenic in urine collected at around gestational weeks 8 and 30. The association of arsenic exposure with size at birth was assessed by linear regression analyses. In analysis over the full range of exposure (6-978 microg/L), no dose-effect association was found with birth size. However, significant negative dose effects were found with birth weight and head and chest circumferences at a low level of arsenic exposure (<100 microg/L in urine). In this range of exposure, birth weight decreased by 1.68 (standard error (SE), 0.62) g for each 1-microg/L increase of arsenic in urine. For head and chest circumferences, the corresponding reductions were 0.05 (SE, 0.03) mm and 0.14 (SE, 0.03) mm per 1 microg/L, respectively. No further negative effects were shown at higher levels of arsenic exposure. The indicated negative effect on birth size at a low level of arsenic exposure warrants further investigation.
To understand the severity of related health effects of chronic arsenic exposure in West Bengal, a detailed 3-year study was carried out in Murshidabad, one of the nine arsenic-affected districts in West Bengal.
We screened 25,274 people from 139 arsenic-affected villages in Murshidabad to identify patients suffering from chronic arsenic toxicity for evidence of multisystemic features and collected biological samples such as head hair, nail, and spot urine from the patients along with the tubewell water they were consuming.
Out of 25,274 people screened, 4813 (19%) were registered with arsenical skin lesions. A case series involving arsenical skin lesions resulting in cancer and gangrene were noted during this study. Representative histopathological pictures of skin biopsy of different types of lesions were also presented. Out of 2595 children we examined for arsenical skin lesions, 122 (4%) were registered with arsenical skin lesions, melanosis with or without keratosis. Different clinical and electrophysiological neurological features were noticed among the arsenic-affected villagers. Both the arsenic content in the drinking water and duration of exposure may be responsible in increasing the susceptibility of pregnant women to spontaneous abortions, stillbirths, preterm births, low birth weights, and neonatal deaths. Some additional multisystemic features such as weakness and lethargy, chronic respiratory problems, gastrointestinal symptoms, and anemia were also recorded in the affected population.
The findings from this survey on different health effects of arsenic exposure were compared to those from previous studies carried out on arsenic-affected populations in India and Bangladesh as well as other affected countries.
Multisystemic disorders, including dermal effects, neurological complications, and adverse obstetric outcomes, were observed to be associated with chronic arsenic exposure in the study population in Murshidabad, West Bengal. The magnitude of severity was related to the concentration of arsenic in water as well as duration of the exposure.
Between 2001 and 2003, the authors studied pregnancy outcomes and infant mortality among 202 married women in West Bengal, India. Reproductive histories were ascertained using structured interviews. Arsenic exposure during each pregnancy, including all water sources used, was assessed; this involved measurements from 409 wells. Odds ratios for spontaneous abortion, stillbirth, neonatal mortality, and infant mortality were estimated with logistic regression based on the method of generalized estimating equations. Exposure to high concentrations of arsenic (> or =200 microg/liter) during pregnancy was associated with a sixfold increased risk of stillbirth after adjustment for potential confounders (odds ratio (OR) = 6.07, 95% confidence interval (CI): 1.54, 24.0; p = 0.01). Arsenic-related skin lesions were found in 12 women who had a substantially increased risk of stillbirth (OR = 13.1, 95% CI: 3.17, 54.0; p = 0.002). The odds ratio for neonatal death was 2.81 (95% CI: 0.73, 10.8). No association was found between arsenic exposure and spontaneous abortion (OR = 1.01, 95% CI: 0.38, 2.70) or overall infant mortality (OR = 1.33, 95% CI: 0.43, 4.04). This study adds to the limited evidence that exposure to high concentrations of arsenic during pregnancy increases the risk of stillbirth. However, there was no indication of the increased rates of spontaneous abortion and overall infant mortality that have been reported in some studies.
The authors evaluated the effect of arsenic exposure on fetal and infant survival in a cohort of 29,134 pregnancies identified
by the health and demographic surveillance system in Matlab, Bangladesh, in 1991–2000. Arsenic exposure, reflected by drinking
water history and analysis of arsenic concentrations in tube-well water used by women during pregnancy, was assessed in a
separate survey conducted in 2002–2003. Data on vital events, including pregnancy outcome and infant mortality, were collected
by monthly surveillance at the household level. The risk of fetal loss and infant death in relation to arsenic exposure was
estimated by a Cox proportional hazards model. Drinking tube-well water with more than 50 μg of arsenic per liter during pregnancy
significantly increased the risks of fetal loss (relative risk = 1.14, 95% confidence interval: 1.04, 1.25) and infant death
(relative risk = 1.17, 95% confidence interval: 1.03, 1.32). There was a significant dose response of arsenic exposure to
risk of infant death (p = 0.02). Women of reproductive age should urgently be prioritized for mitigation activities where drinking water is contaminated
by arsenic.
Arsenic in drinking water is known to be a cause of lung, bladder, and skin cancer, and some studies report cardiovascular
disease effects. The authors investigated mortality from 1950 to 2000 in the arsenic-exposed region II of Chile (population:
477,000 in 2000) in comparison with the unexposed region V. Increased risks were found for acute myocardial infarction (AMI),
with mortality rate ratios of 1.48 for men (95% confidence interval (CI): 1.37, 1.59; p < 0.001) and 1.26 for women (95% CI: 1.14, 1.40; p < 0.001) during the high-exposure period in region II from 1958 to 1970. The highest rate ratios were for young adult men
aged 30–49 years who were born during the high-exposure period with probable exposure in utero and in early childhood (rate
ratio = 3.23, 95% CI: 2.79, 3.75; p < 0.001). Compared with lung and bladder cancer, AMI mortality was the predominant cause of excess deaths during and immediately
after the high-exposure period. Ten years after reduction of exposures, AMI mortality had decreased, and longer latency excess
deaths from lung and bladder cancer predominated. With these three causes of death combined, increased mortality peaked in
1991–1995, with estimated excess deaths related to arsenic exposure constituting 10.9% of all deaths among men and 4.0% among
women.
Inorganic arsenic is a potent human carcinogen and general toxicant. More than one hundred million people are exposed to elevated concentrations, mainly via drinking water, but also via industrial emissions. Arsenic is metabolized via methylation and reduction reactions, methylarsonic acid and dimethylarsinic acid being the main metabolites excreted in urine. Both inorganic arsenic and its methylated metabolites easily pass the placenta and both experimental and human studies have shown increased risk of impaired foetal growth and increased foetal loss. Recent studies indicate that prenatal arsenic exposure also increases the risk of adverse effects during early childhood. There is a growing body of evidence that the intrauterine or early childhood exposure to arsenic also induces changes that will become apparent much later in life. One epidemiological study indicated that exposure to arsenic in drinking water during early childhood or in utero was associated with an increased mortality in young adults from both malignant and non-malignant lung disease. Furthermore, a series of experimental animal studies provide strong support for late effects of arsenic, including various forms of cancer, following intrauterine arsenic exposure. The involved modes of action include epigenetic effects, mainly via DNA hypomethylation, endocrine effects (most classes of steroid hormones), immune suppression, neurotoxicity, and interaction with enzymes critical for foetal development and programming.
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