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      International Journal of COPD (submit here)

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      The health burden of pollution: the impact of prenatal exposure to air pollutants

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          Abstract

          Exposure to atmospheric pollutants in both open and closed environments is a major cause of morbidity and mortality that may be both controlled and minimized. Despite growing evidence, several controversies and disagreements exist among the studies that have analyzed the effects of prenatal pollutant exposure. This review article aims to analyze primary scientific evidence of the effects of air pollution during pregnancy and the impact of these effects on the fetus, infant health, and in particular, the respiratory system. We performed a review of articles from the PubMed and Web of Science databases that were published in English within the past 5 years, particularly those related to birth cohorts that began in pregnancy with follow-up until the first years of life. The largest reported effects are associated with prenatal exposure to particulate matter, nitrogen dioxide, and tobacco smoke. The primary effects affect birth weight and other parameters of fetal biometry. There is strong evidence regarding the impact of pollutants on morbidity secondary to respiratory problems. Growing evidence links maternal smoking to childhood asthma and wheezing. The role of passive maternal smoking is less clear. Great heterogeneity exists among studies. There is a need for additional studies on birth cohorts to monitor the relationship between the exposure of pregnant women to pollutants and their children’s progress during the first years of life.

          Most cited references64

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          The Lancet, 380(9859), 2224-2260
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            Prenatal and passive smoke exposure and incidence of asthma and wheeze: systematic review and meta-analysis.

            Exposure to passive smoke is a common and avoidable risk factor for wheeze and asthma in children. Substantial growth in the prospective cohort study evidence base provides an opportunity to generate new and more detailed estimates of the magnitude of the effect. A systematic review and meta-analysis was conducted to provide estimates of the prospective effect of smoking by parents or household members on the risk of wheeze and asthma at different stages of childhood. We systematically searched Medline, Embase, and conference abstracts to identify cohort studies of the incidence of asthma or wheeze in relation to exposure to prenatal or postnatal maternal, paternal, or household smoking in subjects aged up to 18 years old. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated by using random effects model. We identified 79 prospective studies. Exposure to pre- or postnatal passive smoke exposure was associated with a 30% to 70% increased risk of incident wheezing (strongest effect from postnatal maternal smoking on wheeze in children aged ≤2 years, OR = 1.70, 95% CI = 1.24-2.35, 4 studies) and a 21% to 85% increase in incident asthma (strongest effect from prenatal maternal smoking on asthma in children aged ≤2 years, OR = 1.85, 95% CI = 1.35-2.53, 5 studies). Building upon previous findings, exposure to passive smoking increases the incidence of wheeze and asthma in children and young people by at least 20%. Preventing parental smoking is crucially important to the prevention of asthma.
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              Ambient air pollution and low birthweight: a European cohort study (ESCAPE).

              Ambient air pollution has been associated with restricted fetal growth, which is linked with adverse respiratory health in childhood. We assessed the effect of maternal exposure to low concentrations of ambient air pollution on birthweight. We pooled data from 14 population-based mother-child cohort studies in 12 European countries. Overall, the study population included 74 178 women who had singleton deliveries between Feb 11, 1994, and June 2, 2011, and for whom information about infant birthweight, gestational age, and sex was available. The primary outcome of interest was low birthweight at term (weight <2500 g at birth after 37 weeks of gestation). Mean concentrations of particulate matter with an aerodynamic diameter of less than 2·5 μm (PM2·5), less than 10 μm (PM10), and between 2·5 μm and 10 μm during pregnancy were estimated at maternal home addresses with temporally adjusted land-use regression models, as was PM2·5 absorbance and concentrations of nitrogen dioxide (NO2) and nitrogen oxides. We also investigated traffic density on the nearest road and total traffic load. We calculated pooled effect estimates with random-effects models. A 5 μg/m(3) increase in concentration of PM2·5 during pregnancy was associated with an increased risk of low birthweight at term (adjusted odds ratio [OR] 1·18, 95% CI 1·06-1·33). An increased risk was also recorded for pregnancy concentrations lower than the present European Union annual PM2·5 limit of 25 μg/m(3) (OR for 5 μg/m(3) increase in participants exposed to concentrations of less than 20 μg/m(3) 1·41, 95% CI 1·20-1·65). PM10 (OR for 10 μg/m(3) increase 1·16, 95% CI 1·00-1·35), NO2 (OR for 10 μg/m(3) increase 1·09, 1·00-1·19), and traffic density on nearest street (OR for increase of 5000 vehicles per day 1·06, 1·01-1·11) were also associated with increased risk of low birthweight at term. The population attributable risk estimated for a reduction in PM2·5 concentration to 10 μg/m(3) during pregnancy corresponded to a decrease of 22% (95% CI 8-33%) in cases of low birthweight at term. Exposure to ambient air pollutants and traffic during pregnancy is associated with restricted fetal growth. A substantial proportion of cases of low birthweight at term could be prevented in Europe if urban air pollution was reduced. The European Union. Copyright © 2013 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2015
                10 June 2015
                : 10
                : 1111-1121
                Affiliations
                Pediatrics Department, Medical School, University of São Paulo, São Paulo, Brazil
                Author notes
                Correspondence: Sandra E Vieira, Pediatrics Department, Medical School, University of São Paulo, Av Dr Eneas de Carvalho Aguiar, 647, 05403-000, São Paulo, Brazil, Email sandra@ 123456hu.usp.br
                Article
                copd-10-1111
                10.2147/COPD.S40214
                4468952
                26089661
                c4e39362-15bd-4b01-9c4a-e74c095fb52a
                © 2015 Vieira. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Review

                Respiratory medicine
                air pollutants,pregnancy,birth weight,lung disease,tobacco,fetal development
                Respiratory medicine
                air pollutants, pregnancy, birth weight, lung disease, tobacco, fetal development

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