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      Ambient Fine Particulate Matter and Preterm Birth in California: Identification of Critical Exposure Windows

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          Abstract

          Exposure to ambient fine particulate matter (particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5)) during pregnancy is associated with preterm birth (PTB), a leading cause of infant morbidity and mortality. Results from studies attempting to identify etiologically relevant exposure periods of vulnerability have been inconsistent, possibly because of failure to consider the time-to-event nature of the outcome and lagged exposure effects of PM2.5. In this study, we aimed to identify critical exposure windows for weekly PM2.5 exposure and PTB in California using California birth cohort data from 2005–2010. Associations were assessed using distributed-lag Cox proportional hazards models. We assessed effect-measure modification by race/ethnicity by calculating the weekly relative excess risk due to interaction. For a 10-μg/m3 increase in PM2.5 exposure over the entire period of gestation, PTB risk increased by 11% (hazard ratio = 1.11, 95% confidence interval: 1.09, 1.14). Gestational weeks 17–24 and 36 were associated with increased vulnerability to PM2.5 exposure. We find that non-Hispanic black mothers may be more susceptible to effects of PM2.5 exposure than non-Hispanic white mothers, particularly at the end of pregnancy. These findings extend our knowledge about the existence of specific exposure periods during pregnancy that have the greatest impact on preterm birth.

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          Ambient air pollution, birth weight and preterm birth: a systematic review and meta-analysis.

          Low birth weight and preterm birth have a substantial public health impact. Studies examining their association with outdoor air pollution were identified using searches of bibliographic databases and reference lists of relevant papers. Pooled estimates of effect were calculated, heterogeneity was quantified, meta-regression was conducted and publication bias was examined. Sixty-two studies met the inclusion criteria. The majority of studies reported reduced birth weight and increased odds of low birth weight in relation to exposure to carbon monoxide (CO), nitrogen dioxide (NO(2)) and particulate matter less than 10 and 2.5 microns (PM(10) and PM(2.5)). Effect estimates based on entire pregnancy exposure were generally largest. Pooled estimates of decrease in birth weight ranged from 11.4 g (95% confidence interval -6.9-29.7) per 1 ppm CO to 28.1g (11.5-44.8) per 20 ppb NO(2), and pooled odds ratios for low birth weight ranged from 1.05 (0.99-1.12) per 10 μg/m(3) PM(2.5) to 1.10 (1.05-1.15) per 20 μg/m(3) PM(10) based on entire pregnancy exposure. Fewer effect estimates were available for preterm birth and results were mixed. Pooled odds ratios based on 3rd trimester exposures were generally most precise, ranging from 1.04 (1.02-1.06) per 1 ppm CO to 1.06 (1.03-1.11) per 20 μg/m(3) PM(10). Results were less consistent for ozone and sulfur dioxide for all outcomes. Heterogeneity between studies varied widely between pollutants and outcomes, and meta-regression suggested that heterogeneity could be partially explained by methodological differences between studies. While there is a large evidence base which is indicative of associations between CO, NO(2), PM and pregnancy outcome, variation in effects by exposure period and sources of heterogeneity between studies should be further explored. Crown Copyright © 2012. Published by Elsevier Inc. All rights reserved.
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            Estimating measures of interaction on an additive scale for preventive exposures

            Measures of interaction on an additive scale (relative excess risk due to interaction [RERI], attributable proportion [AP], synergy index [S]), were developed for risk factors rather than preventive factors. It has been suggested that preventive factors should be recoded to risk factors before calculating these measures. We aimed to show that these measures are problematic with preventive factors prior to recoding, and to clarify the recoding method to be used to circumvent these problems. Recoding of preventive factors should be done such that the stratum with the lowest risk becomes the reference category when both factors are considered jointly (rather than one at a time). We used data from a case-control study on the interaction between ACE inhibitors and the ACE gene on incident diabetes. Use of ACE inhibitors was a preventive factor and DD ACE genotype was a risk factor. Before recoding, the RERI, AP and S showed inconsistent results (RERI = 0.26 [95%CI: −0.30; 0.82], AP = 0.30 [95%CI: −0.28; 0.88], S = 0.35 [95%CI: 0.02; 7.38]), with the first two measures suggesting positive interaction and the third negative interaction. After recoding the use of ACE inhibitors, they showed consistent results (RERI = −0.37 [95%CI: −1.23; 0.49], AP = −0.29 [95%CI: −0.98; 0.40], S = 0.43 [95%CI: 0.07; 2.60]), all indicating negative interaction. Preventive factors should not be used to calculate measures of interaction on an additive scale without recoding.
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              A Cohort Study of Traffic-Related Air Pollution Impacts on Birth Outcomes

              Background Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts. Objectives We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics. Methods With linked administrative data, we identified 70,249 singleton births (1999–2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) μm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth. Results Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI), 1.07–1.49] and an 11% (95% CI, 1.01–1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00–1.04; IDW: OR = 1.05; 95% CI, 1.03–1.08 per 10-μg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance. Conclusion Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.
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                Author and article information

                Journal
                American Journal of Epidemiology
                Oxford University Press (OUP)
                0002-9262
                1476-6256
                September 2019
                September 01 2019
                May 20 2019
                September 2019
                September 01 2019
                May 20 2019
                : 188
                : 9
                : 1608-1615
                Affiliations
                [1 ]Department of Family Medicine and Public Health, School of Medicine, University of California, San Diego, San Diego, California
                [2 ]Division of Epidemiology and Biostatistics, School of Public Health, San Diego State University, San Diego, California
                [3 ]Department of Public Health and Planning, Policy and Design, University of California, Irvine, Irvine, California
                [4 ]School of Medicine, Yale University, New Haven, Connecticut
                [5 ]Air Toxicology and Epidemiology Branch, California Office of Environmental Health Hazard Assessment, Sacramento, California
                [6 ]Scripps Institute of Oceanography, University of California, San Diego, San Diego, California
                Article
                10.1093/aje/kwz120
                31107509
                e1f8db49-6a68-4a26-afe9-0dbd6675bf40
                © 2019

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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