Particulate Air Pollution Exposure and C-reactive Protein During Early Pregnancy

Lee, Pei‐Chen; Talbott, Evelyn O.; Roberts, James M.; Catov, Janet M.; Sharma, Ravi; Ritz, Beate

doi:10.1097/ede.0b013e31821c6c58

Cited by 102 publications

(102 citation statements)

References 40 publications

(63 reference statements)

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“…Furthermore, inflammation and oxidative stress in the early of pregnancy or toward the end of pregnancy are also related to the onset of parturition. We have previously reported air pollution exposure to be associated with increased C-reactive protein concentrations (>8 μg/ml) in early pregnancy (Lee et al 2011) and a Dutch cohort study recently confirmed these observations (van den Hooven et al 2012a). …”

Section: Introductionmentioning

confidence: 67%

Prenatal air pollution exposure and ultrasound measures of fetal growth in Los Angeles, California

Ritz

Qiu²,

Lee

et al. 2014

Environmental Research

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Background Few previous studies examined the impact of prenatal air pollution exposures on fetal development based on ultrasound measures during pregnancy. Methods In a prospective birth cohort of more than 500 women followed during 1993-1996 in Los Angeles, California, we examined how air pollution impacts fetal growth during pregnancy. Exposure to traffic related air pollution was estimated using CALINE4 air dispersion modeling for nitrogen oxides (NOx) and a land use regression (LUR) model for nitrogen monoxide (NO), nitrogen dioxide (NO2) and NOx. Exposures to carbon monoxide (CO), NO2, ozone (O3) and particles <10 μm in aerodynamic diameter (PM10) were estimated using government monitoring data. We employed a linear mixed effects model to estimate changes in fetal size at approximately 19, 29 and 37 weeks gestation based on ultrasound. Results Exposure to traffic-derived air pollution during 29 to 37 weeks was negatively associated with biparietal diameter at 37 weeks gestation. For each interquartile range (IQR) increase in LUR-based estimates of NO, NO2 and NOx, or freeway CALINE4 NOx we estimated a reduction in biparietal diameter of 0.2-0.3 mm. For women residing within 5 km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0 mm per IQR increase in CO and NO2. Effect estimates were robust to adjustment for a number of potential confounders. We did not observe consistent patterns for other growth endpoints we examined. Conclusions Prenatal exposure to traffic-derived pollution was negatively associated with fetal head size measured as biparietal diameter in late pregnancy.

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Section: Introductionmentioning

confidence: 67%

Prenatal air pollution exposure and ultrasound measures of fetal growth in Los Angeles, California

Ritz

Qiu²,

Lee

et al. 2014

Environmental Research

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“…Animal studies provide support for this mechanism by demonstrating air pollution exposure can lead to inflammation in the lung (Tamagawa et al 2008) that disrupts insulin action by inducing inflammation in adipose (Sun et al 2009; Xu et al 2011) and vascular tissue (Sun et al 2005; Tamagawa et al 2008). Recently, studies in human populations have also linked air pollution with elevated levels of C-reactive protein (CRP), a marker of systemic inflammation, in healthy young adults (Rich et al 2012), a diabetic population (Khafaie et al 2013) and in pregnant women (van den Hooven et al 2012; Lee et al 2011). CRP levels, in turn, are associated with increased risk of type 2 diabetes (Wang et al 2013) and gestational glucose intolerance (Lowe et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Preconception and early pregnancy air pollution exposures and risk of gestational diabetes mellitus

Robledo

Mendola

Yeung

et al. 2015

Environmental Research

171

124

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Background: Air pollution has been linked to gestational diabetes mellitus (GDM) but no studies have evaluated impact of preconception and early pregnancy air pollution exposures on GDM risk. Methods: Electronic medical records provided data on 219,952 singleton deliveries to mothers with (n=11,334) and without GDM (n=208,618). Average maternal exposures to particulate matter (PM) <2.5 microns (PM2.5) and PM2.5 constituents, PM <10 microns (PM10), nitrogen oxides (NOx), carbon monoxide, sulfur dioxide (SO2) and ozone (O3) were estimated for the 3-month preconception window, first trimester, and gestational weeks 1-24 based on modified Community Multiscale Air Quality models for delivery hospital referral regions. Binary regression models with robust standard errors estimated relative risks (RR) for GDM per interquartile range (IQR) increase in pollutant concentrations adjusted for study site, maternal age and race/ethnicity. Results: Preconception maternal exposure to NOX (RR=1.09, 95% CI: 1.04, 1.13) and SO2 (RR=1.05, 1.01, 1.09) were associated with increased risk of subsequent GDM and risk estimates remained elevated for first trimester exposure. Preconception O3 was associated with lower risk of subsequent GDM (RR=0.93, 0.90, 0.96) but risks increased later in pregnancy. Conclusion: Maternal exposures to NOX and SO2 preconception and during the first few weeks of pregnancy were associated with increased GDM risk. O3 appeared to increase GDM risk in association with mid-pregnancy exposure but not in earlier time windows. These common exposures merit further investigation.

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“…An impaired placental function could be caused by oxidative stress, inflammation, coagulation, impaired endothelial function or haemodynamic responses 3435 Women who were exposed to ambient air particles and ozone during early pregnancy are more likely to have elevated levels of C reactive protein levels, systematic inflammation driven by air pollution exposure being an underlying mechanism behind adverse birth outcomes 35. Trophoblastic invasion during formation of the placenta might be disrupted by proinflammatory cytokines 36…”

Section: Discussionmentioning

confidence: 99%

“…34 35 Women who were exposed to ambient air particles and ozone during early pregnancy are more likely to have elevated levels of C reactive protein levels, systematic inflammation driven by air pollution exposure being an underlying mechanism behind adverse birth outcomes. 35 Trophoblastic invasion during formation of the placenta might be disrupted by proinflammatory cytokines. 36 37 Air pollution in early pregnancy (first trimester) is of particular interest because this is the period when pollutants would be expected to interfere with maternal vascular remodelling processes.…”

Section: Discussionmentioning

confidence: 99%

Traffic pollution at the home address and pregnancy outcomes in Stockholm, Sweden

Olsson

Mogren

Eneroth³

et al. 2015

BMJ Open

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BackgroundFor the past two decades, several studies have reported associations between elevated levels of ambient air pollution and adverse pregnancy outcomes, although with varying conclusions.ObjectivesTo examine possible associations between the traffic pollution situation at the home address, for women who did not change address during pregnancy, and three types of pregnancy outcomes: spontaneous preterm delivery, children born small for gestational age (SGA) and pregnancy-induced hypertensive disorders.MethodsWe used data for the Greater Stockholm Area from the Swedish Medical Birth Register to construct a cohort based on all pregnancies conceived between July 1997 and March 2006, n=100 190. The pregnancy average nitrogen oxide, NOx, levels and annual mean daily vehicles at the home address were used as exposure variables. Mixed-model logistic regression was performed to assess any associations between exposure and outcome.ResultsThere was an association between elevated traffic pollution exposure during pregnancy and pregnancy-induced hypertensive disorders. A 10 µg/m3 increase in the pregnancy average NOx level at the home address resulted in an OR of 1.17 (95% CI 1.10 to 1.26). The 2nd to 4th quartiles of NOx were all associated with an increased risk of SGA, but there was no difference in the risk estimate among the higher quartiles. There was a tendency of a higher risk of spontaneous preterm delivery in relation to higher levels of NOx. There was no evidence of an association between vehicle flow, the cruder indicator of traffic pollution, and the studied outcomes in this study.ConclusionsIn this large cohort, there was a fairly strong association between vehicle exhaust levels at the home address and pregnancy-induced hypertensive disorders, after adjustment for important risk factors.

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Particulate Air Pollution Exposure and C-reactive Protein During Early Pregnancy

Cited by 102 publications

References 40 publications

Prenatal air pollution exposure and ultrasound measures of fetal growth in Los Angeles, California

Prenatal air pollution exposure and ultrasound measures of fetal growth in Los Angeles, California

Preconception and early pregnancy air pollution exposures and risk of gestational diabetes mellitus

Traffic pollution at the home address and pregnancy outcomes in Stockholm, Sweden

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