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Ambient air pollution and risk of pregnancy loss among women undergoing assisted reproduction.

ABSTRACT: Accumulating evidence suggests that air pollution increases pregnancy loss; however, most previous studies have focused on case identification from medical records, which may underrepresent early pregnancy losses. Our objective was to investigate the association between acute and chronic exposure to ambient air pollution and time to pregnancy loss among women undergoing assisted reproductive technologies (ART) who are closely followed throughout early pregnancy. We included 275 women (345 human chorionic gonadotropin (hCG)-confirmed pregnancies) undergoing ART at a New England academic fertility center. We estimated daily nitrogen dioxide (NO₂), ozone (O₃), fine particulate matter <2.5 μm (PM_2.5), and black carbon (BC) exposures using validated spatiotemporal models estimated from first positive hCG test until day of failure or live birth. Air pollution exposures were averaged over the past week and the whole pregnancy. Multivariable Cox proportional hazards models were used to estimate the hazards ratio (HR) for pregnancy loss for an interquartile range (IQR) increase in pollutant exposure. We tested for violation of proportional hazards by considering an interaction between time (in days) since positive hCG (<30 days vs. ≥30 days) and air pollution. The incidence of pregnancy loss was 29 per 100 confirmed pregnancies (n = 99). Among pregnancies not resulting in live birth, the median (IQR) time to loss was 21 (11, 30) days following positive hCG. Average past week exposures to NO₂, O₃, PM_2.5, and BC were not associated with time to pregnancy loss. Exposure throughout pregnancy to NO₂ was not associated with pregnancy loss; however, there was a statistically significant interaction with time (p-for-interaction<0.001). Specifically, an IQR increase in exposure to NO₂ was positively associated with pregnancy loss after 30 days (HR = 1.34, 95% CI: 1.13, 1.58), but not in the first 30 days after positive hCG (HR = 0.83, 95% CI: 0.57, 1.20). Overall pregnancy exposure to O₃, PM_2.5, and BC were not associated with pregnancy loss regardless of timing. Models evaluating joint effects of all pollutants yielded similar findings. In conclusion, acute and chronic exposure to NO₂, O₃, PM_2.5, and BC were not associated with risk of pregnancy loss; however, higher exposure to NO₂ throughout pregnancy was associated with increased risk of loss 30 days after positive hCG. In this cohort, later pregnancy losses appeared more susceptible to the detrimental effects of air pollution exposure.

SUBMITTER: Gaskins AJ

PROVIDER: S-EPMC7658021 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundAir pollution exposure has been linked with diminished fertility. Identifying the metabolic changes induced by periconception air pollution exposure among women could enhance our understanding of the potential biological pathways underlying air pollution's reproductive toxicity.ObjectiveTo identify serum metabolites associated with periconception air pollution exposure and evaluate the extent to which these metabolites mediate the association between air pollution and live birth.MethodsWe included 200 women undergoing a fresh assisted reproductive technology (ART) cycle at Massachusetts General Hospital Fertility Center (2005-2015). A serum sample was collected during stimulation, and untargeted metabolic profiling was conducted using liquid chromatography with ultra-high-resolution mass spectrometry. Exposure to nitrogen dioxide (NO2), ozone (O3), fine particulate matter <2.5 µm (PM2.5), and black carbon (BC) was estimated using validated spatiotemporal models. Multivariable linear regression models were used to evaluate the associations between the air pollutants, live birth, and metabolic feature intensities. A meet in the middle approach was used to identify overlapping features and metabolic pathways.ResultsFrom the C18 and HILIC chromatography columns, 10,803 and 12,968 metabolic features were extracted. There were 190 metabolic features and 18 pathways that were significantly associated with both air pollution and live birth (P < 0.05) across chromatography columns. Eight features were confirmed metabolites implicated in amino acid and nutrient metabolism with downstream effects on oxidative stress and inflammation. Six confirmed metabolites fell into two intuitive clusters - "antioxidants" and "oxidants"- which could potentially mediate some of the association between air pollution and lower odds of live birth. Tryptophan and vitamin B3 metabolism were common pathways linking air pollution exposure to decreased probability of live birth.ConclusionHigher periconception air pollution exposure was associated with metabolites and biologic pathways involved in inflammation and oxidative stress that may mediate the observed associations with lower probability of live birth following ART.

Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

Project description:BackgroundEmerging evidence suggests a potential association between ambient air pollution and risk of gestational diabetes mellitus (GDM), but results have been inconsistent. Accordingly, we assessed the associations between ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) levels with risk of GDM.MethodsUsing linked data from birth certificates, hospital discharge diagnoses, and air pollution estimates informed by the New York City Community Air Survey, we fit conditional logistic regression models to evaluate the association between residential levels of PM2.5 and NO2 with risk of GDM among 256,372 singleton live births of non-smoking mothers in New York City born 2008-2010, adjusting for sociodemographic factors and stratified on zip code of maternal address.ResultsGDM was identified in 17,065 women, yielding a risk of GDM in the study sample of 67 per 1000 deliveries. In single pollutant models, 1st and 2nd trimester PM2.5 was associated with a lower and higher risk of GDM, respectively. In models mutually adjusting for PM2.5 levels in both trimesters, GDM was associated with PM2.5 levels in the 2nd trimester (OR: 1.06, 95% CI: 1.02, 1.10 per interquartile range increase in PM2.5), but not the 1st trimester (OR: 0.99, 95% CI: 0.96, 1.02). Conversely, GDM was associated with NO2 during the 1st trimester (OR: 1.05, 95% CI: 1.01, 1.09), but not the 2nd trimester (OR: 1.02, 95% CI: 0.98, 1.06). The positive associations between pollutants and GDM were robust to different model specifications. PM2.5 in the 2nd trimester was more strongly associated with GDM among mothers who were aged <35 years and not Medicaid recipients. NO2 in the 1st trimester was more strongly associated with GDM among overweight and parous women.ConclusionsIn this large cohort of singleton births in New York City, NO2 in the 1st trimester and PM2.5 in the 2nd trimester were associated with higher odds of GDM, while 1st trimester PM2.5 was weakly and inconsistently associated with lower odds of GDM.

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Ambient air pollution and risk of pregnancy loss among women undergoing assisted reproduction.

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