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Gestational diabetes mellitus, prenatal air pollution exposure, and autism spectrum disorder.
ABSTRACT: BACKGROUND:Ambient air pollution and maternal diabetes may affect common biological pathways underlying adverse neurodevelopmental effects. However, joint effects of maternal diabetes and air pollution on autism spectrum disorder (ASD) have not been studied. OBJECTIVE:We evaluated whether prenatal and early-life air pollution exposure interacts with maternal diabetes status to affect ASD risk. METHODS:This retrospective cohort study included 246,420 singleton children born in Kaiser Permanente Southern California hospitals in 1999-2009. Children were followed from birth until age 5, during which 2471 ASD cases were diagnosed. Ozone (O3), particulate matter?
Project description: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?m (PM2.5) and PM2.5 constituents, PM ? 10?m (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.
Project description:BACKGROUND:Studies of effects of air pollution on gestational diabetes mellitus (GDM) have not been consistent, and there has been little investigation of effects of exposure preceding pregnancy. In previous studies, the temporal relationship between exposure and GDM onset has been difficult to establish. METHODS:Data were obtained for 239,574 pregnancies between 1999 and 2009 in a population-based health care system with comprehensive electronic medical records. Concentrations of ambient nitrogen dioxide (NO2), particulate matter (PM) ?2.5??m in aerodynamic diameter (PM2.5) and ?10??m (PM10), and ozone (O3) during preconception and the first trimester of pregnancy at the residential birth address were estimated from regulatory air monitoring stations. Odds ratios (ORs) of GDM diagnosed in the second and third trimesters in association with pollutant exposure were estimated using generalized estimating equation models adjusted for birth year, medical center service areas, maternal age, race/ethnicity, education, census-tract household income, and parity. RESULTS:In single-pollutant models, preconception NO2 was associated with increased risk of GDM (OR?=?1.10 per 10.4?ppb, 95% confidence interval [CI]: 1.07, 1.13). First trimester NO2 was weakly associated with GDM, and this was not statistically significant (OR?=?1.02 per 10.4?ppb, 95% CI: 0.99, 1.05). Preconception NO2 associations were robust in multi-pollutant models adjusted for first trimester NO2 with another co-pollutant from both exposure windows. In single-pollutant models, preconception PM2.5 and PM10 associations were associated with increased risk of GDM (OR?=?1.04 per 6.5??g/m3, 95% CI: 1.01, 1.06; OR?=?1.03 per 16.1??g/m3, 95% CI: 1.00, 1.06, respectively), but these effect estimates were not robust to adjustment for other pollutants. In single-pollutant models, preconception and first trimester O3 were associated with reduced risk of GDM (OR?=?0.94 per 15.7?ppb, 95% CI: 0.92, 0.95; OR?=?0.95 per 15.7?ppb, 95% CI: 0.94, 0.97), associations that were robust to adjustment for co-pollutants. CONCLUSIONS:Maternal exposure to NO2 during the preconception trimester may increase risk of GDM.
Project description:Ambient air pollution has been linked to the development of gestational diabetes mellitus (GDM). However, evidence of the association is very limited, and no study has estimated the effects of ozone.Our aim was to determine the association of prenatal exposures to particulate matter ? 2.5 ?m (PM2.5) and ozone (O3) with GDM.We used Florida birth vital statistics records to investigate the association between the risk of GDM and two air pollutants (PM2.5 and O3) among 410,267 women who gave birth in Florida between 2004 and 2005. Individual air pollution exposure was assessed at the woman's home address at time of delivery using the hierarchical Bayesian space-time statistical model. We further estimated associations between air pollution exposures during different trimesters and GDM.After controlling for nine covariates, we observed increased odds of GDM with per 5-?g/m3 increase in PM2.5 (ORTrimester1 = 1.16; 95% CI: 1.11, 1.21; ORTrimester2 = 1.15; 95% CI: 1.10, 1.20; ORPregnancy = 1.20; 95% CI: 1.13, 1.26) and per 5-ppb increase in O3 (ORTrimester1 = 1.09; 95% CI: 1.07, 1.11; ORTrimester2 = 1.12; 95% CI: 1.10, 1.14; ORPregnancy = 1.18; 95% CI: 1.15, 1.21) during both the first trimester and second trimester as well as the full pregnancy in single-pollutant models. Compared with the single-pollutant model, the ORs for O3 were almost identical in the co-pollutant model. However, the ORs for PM2.5 during the first trimester and the full pregnancy were attenuated, and no association was observed for PM2.5 during the second trimester in the co-pollutant model (OR = 1.02; 95% CI: 0.98, 1.07).This population-based study suggests that exposure to air pollution during pregnancy is associated with increased risk of GDM in Florida, USA.Hu H, Ha S, Henderson BH, Warner TD, Roth J, Kan H, Xu X. 2015. Association of atmospheric particulate matter and ozone with gestational diabetes mellitus. Environ Health Perspect 123:853-859; http://dx.doi.org/10.1289/ehp.1408456.
Project description:BACKGROUND:Emerging 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. METHODS:Using 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. RESULTS:GDM 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. CONCLUSIONS:In 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.
Project description:Prenatal exposure to air pollution has been associated with autism spectrum disorder (ASD) risk but no study has examined associations with ASD severity or functioning. Cognitive ability, adaptive functioning, and ASD severity were assessed in 327 children with ASD from the Childhood Autism Risks from Genetics and the Environment study using the Mullen Scales of Early Learning (MSEL), the Vineland Adaptive Behavior Scales (VABS), and the Autism Diagnostic Observation Schedule calibrated severity score. Estimates of nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), ozone, and near-roadway air pollution were assigned to each trimester of pregnancy and first year of life. Increasing prenatal and first year NO2 exposures were associated with decreased MSEL and VABS scores. Increasing PM10 exposure in the third trimester was paradoxically associated with improved performance on the VABS. ASD severity was not associated with air pollution exposure.
Project description:Previous studies have explored the association between air pollution levels and adverse birth outcomes such as lower birth weight. Existing literature suggests an association, although results across studies are not consistent. Additional research is needed to confirm the effect, investigate the exposure window of importance, and distinguish which pollutants cause harm. We assessed the association between ambient pollutant concentrations and term birth weight for 1,548,904 births in TX from 1998 to 2004. Assignment of prenatal exposure to air pollutants was based on maternal county of residence at the time of delivery. Pollutants examined included particulate matter with aerodynamic diameter < or = 10 and < or = 2.5 microm (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). We applied a linear model with birth weight as a continuous variable. The model was adjusted for known risk factors and region. We assessed pollutant effects by trimester to identify biological exposure window of concern, and explored interaction due to race/ethnicity. An interquartile increase in ambient pollutant concentrations of SO2 and O3 was associated with a 4.99-g (95% confidence interval [CI], 1.87-8.11) and 2. 72-g (95% CI, 1.11-4.33) decrease in birth weight, respectively. Lower birth weight was associated with exposure to O3 in the first and second trimester; whereas results were not significant for other pollutants by trimester A positive association was exhibited for PM2.5 in the first trimester. Effects estimates for PM10 and PM2.5 were inconsistent across race/ethnic groups. Current ambient air pollution levels may be increasing the risk of lower birth weight for some pollutants. These risks may be increased for certain racial/ethnic groups. Additional research including consideration of improved methodology is needed to investigate these findings. Future studies should examine the influence of residual confounding.
Project description:Although ambient air pollution may increase hypertension risk through endothelial damage and oxidative stress, evidence is inconsistent regarding its effect on hypertension in pregnancy. Prior research has evaluated a limited scope of pollution species and often not differentiated preeclampsia, which may have a placental origin, from gestational hypertension. Among 49?607 women with at least 2 singleton deliveries in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Consecutive Pregnancies Study (2002-2010), we estimated criteria pollutant and volatile organic compound levels during pregnancy using Community Multiscale Air Quality models and abstracted gestational hypertension and preeclampsia diagnoses from medical records. Generalized estimating equations accounted for repeat pregnancies and adjusted for ambient temperature and maternal age, race/ethnicity, body mass index, smoking, alcohol, parity, insurance, marital status, and asthma. Air pollution levels were low to moderate (eg, median 41.6 ppb [interquartile range, 38.9-43.7 ppb] for ozone and 35.1 ppb [28.9-40.3 ppb] for nitrogen oxides). Higher levels of most criteria pollutants during preconception and the first trimester were associated with lower preeclampsia risk, while higher second-trimester levels were associated with greater gestational hypertension risk. For example, an interquartile increase in first-trimester carbon monoxide was associated with a relative risk of 0.88 (95% CI, 0.81-0.95) for preeclampsia and second-trimester carbon monoxide a relative risk of 1.14 (95% CI, 1.07-1.22) for gestational hypertension. Volatile organic compounds, conversely, were not associated with gestational hypertension but consistently associated with higher preeclampsia risk. These findings further suggest air pollution may affect the development of hypertension in pregnancy, although differing causes of preeclampsia and gestational hypertension may alter these relationships.
Project description:Opioid use during pregnancy is associated with suboptimal pregnancy outcomes. Little is known about child neurodevelopmental outcomes. We examined associations between maternal opioid prescriptions preconception to delivery (peri-pregnancy) and child's risk of ASD, developmental delay/disorder (DD) with no ASD features, or ASD/DD with autism features in the Study to Explore Early Development, a case-control study of neurodevelopment. Preconception opioid prescription was associated with 2.43 times the odds of ASD [95% confidence interval (CI) 0.99, 6.02] and 2.64 times the odds of ASD/DD with autism features (95% CI 1.10, 6.31) compared to mothers without prescriptions. Odds for ASD and ASD/DD were non-significantly elevated for first trimester prescriptions. Work exploring mechanisms and timing between peri-pregnancy opioid use and child neurodevelopment is needed.
Project description:BACKGROUND:Exposures to extreme ambient temperature and air pollution are linked to adverse birth outcomes, but the associations with small for gestational age (SGA) and term low birthweight (tLBW) are unclear. We aimed to investigate exposures to site-specific temperature extremes and selected criteria air pollutants in relation to SGA and tLBW. METHODS:We linked medical records of 220,572 singleton births (2002-2008) from 12 US sites to local temperature estimated by the Weather Research and Forecasting model, and air pollution estimated by modified Community Multiscale Air Quality models. Exposures to hot (>95th percentile) and cold (<5th percentile) were defined using site-specific distributions of daily temperature over three-month preconception, each trimester, and whole-pregnancy. Average concentrations of five criteria air pollutants and six fine particulate matter constituents were also calculated for these pregnancy windows. Poisson regression with generalized estimating equations calculated the relative risks (RR) and 95% confidence intervals for SGA (weight <10th percentile conditional on gestational age and sex) and tLBW (?37 weeks and <2500g) associated with an interquartile range increment of air pollutants, and cold or hot compared to mild (5-95th percentile) temperature. Models were adjusted for maternal demographics, lifestyle, and clinical factors, season, and site. RESULTS:Compared to mild temperature, cold exposure during trimester 2 [RR: 1.21 (1.05-1.38)], trimester 3 [RR: 1.18 (1.03-1.36)], and whole-pregnancy [RR: 2.57 (2.27-2.91)]; and hot exposure during trimester 3 [RR: 1.31 (1.15-1.50)] and whole-pregnancy [RR: 2.49 (2.20-2.83)] increased tLBW risk. No consistent association was observed between temperature and SGA. Air pollutant analyses were generally null but preconception elemental carbon was associated with a 4% increase in SGA while dust particles increased tLBW by 10%. Particulate matter ?10µm in the second trimester and whole pregnancy also appeared related to tLBW. CONCLUSIONS:Our findings suggest prenatal exposures to extreme ambient temperature relative to usual environment may increase tLBW risk. Given concerns related to climate change, these findings merit further investigation.