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      Ambient Air Pollution and Risk of Congenital Anomalies: A Systematic Review and Meta-analysis

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          Abstract

          Objective

          We systematically reviewed epidemiologic studies on ambient air pollution and congenital anomalies and conducted meta-analyses for a number of air pollutant–anomaly combinations.

          Data sources and extraction

          From bibliographic searches we extracted 10 original epidemiologic studies that examined the association between congenital anomaly risk and concentrations of air pollutants. Meta-analyses were conducted if at least four studies published risk estimates for the same pollutant and anomaly group. Summary risk estimates were calculated for a) risk at high versus low exposure level in each study and b) risk per unit increase in continuous pollutant concentration.

          Data synthesis

          Each individual study reported statistically significantly increased risks for some combinations of air pollutants and congenital anomalies, among many combinations tested. In meta-analyses, nitrogen dioxide (NO 2) and sulfur dioxide (SO 2) exposures were related to increases in risk of coarctation of the aorta [odds ratio (OR) per 10 ppb NO 2 = 1.17; 95% confidence interval (CI), 1.00–1.36; OR per 1 ppb SO 2 = 1.07; 95% CI, 1.01–1.13] and tetralogy of Fallot (OR per 10 ppb NO 2 = 1.20; 95% CI, 1.02–1.42; OR per 1 ppb SO 2 = 1.03; 95% CI, 1.01–1.05), and PM 10 (particulate matter ≤ 10 μm) exposure was related to an increased risk of atrial septal defects (OR per 10 μg/m 3 = 1.14; 95% CI, 1.01–1.28). Meta-analyses found no statistically significant increase in risk of other cardiac anomalies and oral clefts.

          Conclusions

          We found some evidence for an effect of ambient air pollutants on congenital cardiac anomaly risk. Improvements in the areas of exposure assessment, outcome harmonization, assessment of other congenital anomalies, and mechanistic knowledge are needed to advance this field.

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          Most cited references58

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          Ambient Air Pollution and Pregnancy Outcomes: A Review of the Literature

          Over the last decade or so, a large number of studies have investigated the possible adverse effects of ambient air pollution on birth outcomes. We reviewed these studies, which were identified by a systematic search of the main scientific databases. Virtually all reviewed studies were population based, with information on exposure to air pollution derived from routine monitoring sources. Overall, there is evidence implicating air pollution in adverse effects on different birth outcomes, but the strength of the evidence differs between outcomes. The evidence is sufficient to infer a causal relationship between particulate air pollution and respiratory deaths in the postneonatal period. For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants. For preterm births and intrauterine growth retardation (IUGR) the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies. Molecular epidemiologic studies suggest possible biologic mechanisms for the effect on birth weight, premature birth, and IUGR and support the view that the relation between pollution and these birth outcomes is genuine. For birth defects, the evidence base so far is insufficient to draw conclusions. In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.
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            Effects of transplacental exposure to environmental pollutants on birth outcomes in a multiethnic population.

            Inner-city, minority populations are high-risk groups for adverse birth outcomes and also are more likely to be exposed to environmental contaminants, including environmental tobacco smoke (ETS), polycyclic aromatic hydrocarbons (PAHs), and pesticides. In a sample of 263 nonsmoking African-American and Dominican women, we evaluated the effects on birth outcomes of prenatal exposure to airborne PAHs monitored during pregnancy by personal air sampling, along with ETS estimated by plasma cotinine, and an organophosphate pesticide (OP) estimated by plasma chlorpyrifos (CPF). Plasma CPF was used as a covariate because it was the most often detected in plasma and was highly correlated with other pesticides frequently detected in plasma. Among African Americans, high prenatal exposure to PAHs was associated with lower birth weight (p = 0.003) and smaller head circumference (p = 0.01) after adjusting for potential confounders. CPF was associated with decreased birth weight and birth length overall (p = 0.01 and p = 0.003, respectively) and with lower birth weight among African Americans (p = 0.04) and reduced birth length in Dominicans (p < 0.001), and was therefore included as a covariate in the model with PAH. After controlling for CPF, relationships between PAHs and birth outcomes were essentially unchanged. In this analysis, PAHs and CPF appear to be significant independent determinants of birth outcomes. Further analyses of pesticides will be carried out. Possible explanations of the failure to find a significant effect of PAHs in the Hispanic subsample are discussed. This study provides evidence that environmental pollutants at levels currently encountered in New York City adversely affect fetal development.
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              Exposures to Airborne Particulate Matter and Adverse Perinatal Outcomes: A Biologically Plausible Mechanistic Framework for Exploring Potential Effect Modification by Nutrition

              Objectives The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. Methods We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. Conclusions Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                May 2011
                03 December 2010
                : 119
                : 5
                : 598-606
                Affiliations
                [1 ]Center for Research in Environmental Epidemiology, Barcelona, Spain
                [2 ]Hospital del Mar Research Institute (IMIM), Barcelona, Spain
                [3 ]CIBER Epidemiología y Salud Pública, Spain
                [4 ]Educational Unit of Preventive Medicine and Public Health, Hospital del Mar–Pompeu Fabra University–Agencia de Salut Pública, Barcelona, Spain
                [5 ]Institute of Health and Society, Newcastle University, Newcastle upon Tyne, United Kingdom
                Author notes
                Address correspondence to M. Vrijheid, Centre for Research in Environmental Epidemiology, Barcelona Biomedical Research Park, Doctor Aiguader 88, 08003 Barcelona, Spain. Telephone: 34 932 147 346. Fax: 34 932 147 301. E-mail: mvrijheid@ 123456creal.cat

                The authors declare they have no actual or potential competing financial interests.

                Article
                ehp-119-598
                10.1289/ehp.1002946
                3094408
                21131253
                0b3537f7-a67a-4a0a-8d39-e88dadff1c9a
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 07 September 2010
                : 03 December 2010
                Categories
                Review

                Public health
                congenital abnormalities,air pollution,pregnancy
                Public health
                congenital abnormalities, air pollution, pregnancy

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