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      Birth Outcomes and Prenatal Exposure to Ozone, Carbon Monoxide, and Particulate Matter: Results from the Children’s Health Study


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          Exposures to ambient air pollutants have been associated with adverse birth outcomes. We investigated the effects of air pollutants on birth weight mediated by reduced fetal growth among term infants who were born in California during 1975–1987 and who participated in the Children’s Health Study. Birth certificates provided maternal reproductive history and residence location at birth. Sociodemographic factors and maternal smoking during pregnancy were collected by questionnaire. Monthly average air pollutant levels were interpolated from monitors to the ZIP code of maternal residence at childbirth. Results from linear mixed-effects regression models showed that a 12-ppb increase in 24-hr ozone averaged over the entire pregnancy was associated with 47.2 g lower birth weight [95% confidence interval (CI), 27.4–67.0 g], and this association was most robust for exposures during the second and third trimesters. A 1.4-ppm difference in first-trimester carbon monoxide exposure was associated with 21.7 g lower birth weight (95% CI, 1.1–42.3 g) and 20% increased risk of intrauterine growth retardation (95% CI, 1.0–1.4). First-trimester CO and third-trimester O 3 exposures were associated with 20% increased risk of intrauterine growth retardation. A 20-μg/m 3 difference in levels of particulate matter ≤ 10 μm in aerodynamic diameter (PM 10) during the third trimester was associated with a 21.7-g lower birth weight (95% CI, 1.1–42.2 g), but this association was reduced and not significant after adjusting for O 3. In summary, O 3 exposure during the second and third trimesters and CO exposure during the first trimester were associated with reduced birth weight.

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          Most cited references34

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          Exposure measurement error in time-series studies of air pollution: concepts and consequences.

          Misclassification of exposure is a well-recognized inherent limitation of epidemiologic studies of disease and the environment. For many agents of interest, exposures take place over time and in multiple locations; accurately estimating the relevant exposures for an individual participant in epidemiologic studies is often daunting, particularly within the limits set by feasibility, participant burden, and cost. Researchers have taken steps to deal with the consequences of measurement error by limiting the degree of error through a study's design, estimating the degree of error using a nested validation study, and by adjusting for measurement error in statistical analyses. In this paper, we address measurement error in observational studies of air pollution and health. Because measurement error may have substantial implications for interpreting epidemiologic studies on air pollution, particularly the time-series analyses, we developed a systematic conceptual formulation of the problem of measurement error in epidemiologic studies of air pollution and then considered the consequences within this formulation. When possible, we used available relevant data to make simple estimates of measurement error effects. This paper provides an overview of measurement errors in linear regression, distinguishing two extremes of a continuum-Berkson from classical type errors, and the univariate from the multivariate predictor case. We then propose one conceptual framework for the evaluation of measurement errors in the log-linear regression used for time-series studies of particulate air pollution and mortality and identify three main components of error. We present new simple analyses of data on exposures of particulate matter < 10 microm in aerodynamic diameter from the Particle Total Exposure Assessment Methodology Study. Finally, we summarize open questions regarding measurement error and suggest the kind of additional data necessary to address them. Images Figure 1 Figure 2 Figure 3
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            Socio-economic disparities in pregnancy outcome: why do the poor fare so poorly?

            In this paper, we review the evidence bearing on socio-economic disparities in pregnancy outcome, focusing on aetiological factors mediating the disparities in intrauterine growth restriction (IUGR) and preterm birth. We first summarise what is known about the attributable determinants of IUGR and preterm birth, emphasising their quantitative contributions (aetiological fractions) from a public health perspective. We then review studies relating these determinants to socio-economic status and, combined with the evidence about their aetiological fractions, reach some tentative conclusions about their roles as mediators of the socio-economic disparities. Cigarette smoking during pregnancy appears to be the most important mediating factor for IUGR, with low gestational weight gain and short stature also playing substantial roles. For preterm birth, socio-economic gradients in bacterial vaginosis and cigarette smoking appear to explain some of the socio-economic disparities; psychosocial factors may prove even more important, but their aetiological links with preterm birth require further clarification. Research that identifies and quantifies the causal pathways and mechanisms whereby social disadvantage leads to higher risks of IUGR and preterm birth may eventually help to reduce current disparities and improve pregnancy outcome across the entire socio-economic spectrum.
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              Outdoor air pollution, low birth weight, and prematurity.

              M Bobak (2000)
              This study tested the hypothesis, suggested by several recent reports, that air pollution may increase the risk of adverse birth outcomes. This study analyzed all singleton live births registered by the Czech national birth register in 1991 in 67 districts where at least one pollutant was monitored in 1990-1991 (n = 108,173). Maternal exposures to sulfur dioxide (SO(2)), total suspended particles (TSP), and nitrous oxides (NO(x)) in each trimester of pregnancy were estimated as the arithmetic means of all daily measurements taken by all monitors in the district of birth of each infant. Odds ratios of low birth weight (< 2,500 g), prematurity (< 37 weeks of gestation), and intrauterine growth retardation (IUGR; < 10th percentile of birth weight for gestational age and sex) were estimated by robust logistic regression. The median (and 25th and 75th percentile) trimester exposures were 32 (18, 56) microg/m(3) for SO(2); 72 (55, 87) microg/m(3) for TSP; and 38 (23, 59) microg/m(3) for NO(x). Low birth weight (prevalence 5.2%) and prematurity (prevalence 4.8%) were associated with SO(2) and somewhat less strongly with TSP. IUGR was not associated with any pollutant. The effects on low birth weight and prematurity were marginally stronger for exposures in the first trimester, and were not attenuated at all by adjustment for socioeconomic factors or the month of birth. Adjusted odds ratios of low birth weight were 1.20 [95% confidence interval (CI), 1.11-1.30] and 1.15 (CI, 1.07-1.24) for a 50 microg/m(3) increase in SO(2) and TSP, respectively, in the first trimester; adjusted odds ratios of prematurity were 1.27 (CI, 1.16-1.39) and 1.18 (CI, 1.05-1.31) for a 50 microg/m(3) increase in SO(2) and TSP, respectively, in the first trimester. Low gestational age accounted for the association between SO(2) and low birth weight. These findings provide further support for the hypothesis that air pollution can affect the outcome of pregnancy.

                Author and article information

                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                November 2005
                18 July 2005
                : 113
                : 11
                : 1638-1644
                [1 ]Department of Preventive Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA
                [2 ]Sonoma Technology Inc., Petaluma, California, USA
                [3 ]Air Resources Board, State of California, Sacramento, California, USA
                Author notes
                Address correspondence to F.D. Gilliland, Department of Preventive Medicine, USC Keck School of Medicine, 1540 Alcazar St., CHP 236, Los Angeles, CA 90033 USA. Telephone: (323) 442-1096. Fax: (323) 442-3272. E-mail: gillilan@usc.edu

                The authors declare they have no competing financial interests.

                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.
                : 9 March 2005
                : 18 July 2005
                Children's Health

                Public health
                nitrogen dioxide,particulate matter,intrauterine growth retardation,air pollution,birth weight,carbon monoxide,maternal exposure,ozone


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