Fine Particulate Matter and Risk of Preterm Birth in Connecticut in 2000-2006: A Longitudinal Study

American journal of epidemiology (Impact Factor: 5.23). 09/2013; 179(1). DOI: 10.1093/aje/kwt216
Source: PubMed


Several studies have examined associations between particulate matter with aerodynamic diameter of 2.5 µm or less (PM2.5) and preterm birth, but it is uncertain whether results were affected by individual predispositions (e.g., genetic factors,
social conditions) that might vary considerably between women. We tested the hypothesis that a woman is at greater risk of
preterm delivery when she has had elevated exposure to ambient PM2.5 during a pregnancy than when she has not by comparing pregnancies in the same woman. From 271,204 births, we selected 29,175
women who had vaginal singleton livebirths at least twice in Connecticut in 2000–2006 (n = 61,688 births). Analyses matched pregnancies to the same woman. Adjusted odds ratios per interquartile range (2.33-µg/m3) increase in PM2.5 in the first trimester, second trimester, third trimester, and whole pregnancy were 1.07 (95% confidence interval (CI): 1.00,
1.15), 0.96 (95% CI: 0.90, 1.03), 1.03 (95% CI: 0.97, 1.08), and 1.13 (95% CI: 1.01, 1.28), respectively. Among Hispanic women,
the odds ratio per interquartile range increase in whole-pregnancy exposure was 1.31 (95% CI: 1.00, 1.73). Pregnancies with
elevated PM2.5 exposure were more likely to result in preterm birth than were other pregnancies to the same woman at lower exposure. Associations
were most pronounced in the first trimester and among Hispanic women.

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    • "e l s e v i e r . c o m / l o c a t e / t o x l e t and prematurity in humans (Bobak, 2000; Leem et al., 2006; Liu et al., 2003; Pereira et al., 2014; Ritz et al., 2007; Sagiv et al., 2005; Suh et al., 2009) and human and mice litters with a high proportion of females (Lichtenfels et al., 2007; Miraglia et al., 2013). A decrease in the number of viable fetuses and an increase in implantation failure were observed in female mice exposed to air pollution from the 10th day of life (Mohallem et al., 2005). "
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    ABSTRACT: This study aimed to verify the development of placental and systemic inflammation in rats exposed to fine particulate matter before or during pregnancy. Wistar rats were exposed to filtered air (control) or to a load of 600μg/m(3) of fine particles in the air. The gene expression of IL-1β, IL-4, IL-6, IL-10, INF-γ, TNF-α and Toll-like receptor 4 in the placenta was evaluated. The serum and placental concentrations of IL-1β, IL-4, IL-6, IL-10, INF-γ and TNF-α were measured. The total and differential blood leukocyte and blood platelet count was assessed. Compared to control animals, IL-4 content was elevated in the fetal portion of the placenta in rats exposed to air pollution before and during pregnancy. Increased IL-4 suggests that a placental inflammatory reaction may have occurred in response to exposure to fine particulate matter and that this cytokine was responsible, among possibly others factors, for resolution of the inflammatory reaction. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Toxicology Letters 12/2014; 232(2). DOI:10.1016/j.toxlet.2014.12.001 · 3.26 Impact Factor
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    • "Future studies might benefit from exposure estimates less reliant on ground monitors, such as land-use or satellite-derived PM 2.5 . In this cohort , 41% of variation in gestational length was attributable to variation between pregnancies to the same woman, compared to 34% in the Connecticut study (Pereira et al., 2014), which might be explained by differences in health inequality. Studies with greater total variation in gestational length plus higher proportions of within-women variation in gestational length are better positioned for studies that adopt our longitudinal design. "
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    ABSTRACT: Objective A recent longitudinal study reported an association between fine particulate (PM2.5) exposure and preterm birth (PTB) in a US cohort. We applied the same design to an Australian cohort to investigate associations with PTB and pre-labor rupture of membranes (PROM). Methods From 287,680 births, we selected 39,189 women who had singleton births at least twice in Western Australia in 1997–2007 (n = 86,844 births). Analyses matched pregnancies to the same women with conditional logistic regression. Results For PROM adjusted odds ratios (ORs) for a 1 μg/m3 increase in PM2.5 in the first trimester, second trimester, third trimester, and whole pregnancy were 1.00 (95% confidence interval (CI): 0.97, 1.03), 1.03 (95% CI: 1.00, 1.06), 1.02 (95% CI: 1.00, 1.05), and 1.02 (95% CI: 0.99, 1.05) respectively. For PTB, corresponding ORs were 1.00 (95% CI: 0.96, 1.04), 1.00 (95% CI: 0.96, 1.04), 0.98 (95% CI: 0.94, 1.02), and 0.99 (95% CI: 0.95, 1.04) respectively. Conclusion Risk of PROM was greater for pregnancies with elevated PM2.5 exposure in the second trimester than were other pregnancies to the same Australian women at lower exposure. There was insufficient evidence for an association with PTB, indicating that a longer time period might be needed to observe an association if a causal effect exists.
    Environment International 12/2014; 73:143–149. DOI:10.1016/j.envint.2014.07.014 · 5.56 Impact Factor
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    • "Only exposure estimates to week 36 were included in third trimester and whole pregnancy. Given previously observed associations between preterm birth and PM 2.5 mass concentration, we assigned exposure estimates to each woman based on the closest monitor within 40 km of the women's residence at time of birth (Pereira et al. 2014). "
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    ABSTRACT: Background: Previous studies have examined fine particulate matter (≤ 2.5 μm; PM2.5) and preterm birth, but there is a dearth of longitudinal studies on this topic and a paucity of studies that have investigated specific sources of this exposure. Objectives: Our aim was to assess whether anthropogenic sources are associated with risk of preterm birth, comparing successive pregnancies to the same woman. Methods: Birth certificates were used to select women who had vaginal singleton live births at least twice in Connecticut during 2000-2006 (n = 23,123 women, n = 48,208 births). We procured 4,085 daily samples of PM2.5 on Teflon filters from the Connecticut Department of Environmental Protection for six cities in Connecticut. Filters were analyzed for chemical composition, and Positive Matrix Factorization was used to determine contributions of PM2.5 sources. Risk estimates were calculated with conditional logistic regression, matching pregnancies to the same women. Results: Odds ratios of preterm birth per interquartile range increase in whole pregnancy exposure to dust, motor vehicle emissions, oil combustion, and regional sulfur PM2.5 sources were 1.01 (95% CI: 0.93, 1.09), 1.01 (95% CI: 0.92, 1.10), 1.00 (95% CI: 0.89, 1.12), and 1.09 (95% CI: 0.97, 1.22), respectively. Conclusion: This was the first study of PM2.5 sources and preterm birth, and the first matched analysis, that better addresses individual-level confounding potentially inherent in all past studies. There was insufficient evidence to suggest that sources were statistically significantly associated with preterm birth. However, elevated central estimates and previously observed associations with mass concentration motivate the need for further research. Future studies would benefit from high source exposure settings and longitudinal study designs, such as that adopted in this study.
    Environmental Health Perspectives 10/2014; 122(10):117. DOI:10.1289/ehp.1307741 · 7.98 Impact Factor
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