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Preconception and early pregnancy air pollution exposures and risk of gestational diabetes mellitus.
ABSTRACT: 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:Ambient air pollutants may increase preterm birth (PTB) risk, but critical exposure windows are uncertain. The interaction of asthma and pollutant exposure is rarely studied. OBJECTIVE:We sought to assess the interaction of maternal asthma and air pollutant exposures in relation to PTB risk. METHODS:Electronic medical records for 223,502 US deliveries were linked with modified Community Multiscale Air Quality model outputs. Logistic regression with generalized estimating equations estimated the odds ratio and 95% CIs for PTB on the basis of the interaction of maternal asthma and particulate matter with aerodynamic diameter of less than 2.5 microns and particulate matter with aerodynamic diameter of less than 10 microns, ozone (O3), nitrogen oxides (NOx), sulfur dioxide (SO2), and carbon monoxide (CO) per interquartile range. For each gestational week 23 to 36, exposures among women who delivered were compared with those remaining pregnant. Three-month preconception, whole pregnancy, weeks 1 to 28, and the last 6 weeks of gestation averages were also evaluated. RESULTS:On assessing PTB by gestational week, we found that significant asthma interactions were sporadic before 30 weeks but more common during weeks 34 to 36, with higher risk among mothers with asthma for NOx, CO, and SO2 exposure and an inverse association with O3 in week 34. Odds of PTB were significantly higher among women with asthma for CO and NOx exposure preconception and early in pregnancy. In the last 6 weeks of pregnancy, PTB risk associated with particulate matter with aerodynamic diameter of less than 10 microns was higher among women with asthma. CONCLUSIONS:Mothers with asthma may experience a higher risk for PTB after exposure to traffic-related pollutants such as CO and NOx, particularly for exposures 3-months preconception and in the early weeks of pregnancy.
Project description: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?<?2.5??m (PM2.5) and <10??m in aerodynamic diameter, and nitrogen dioxide measured at regulatory air monitoring stations were interpolated to estimate exposures during preconception and each pregnancy trimester, and first year of life at each child's birth address. Hazard ratios (HRs) for ASD were estimated adjusting for birth year, KPSC service areas, and relevant maternal and child characteristics. For each exposure window, interactions were tested between pollutants and a 4-category maternal diabetes variable (none, GDM???24 and <24?weeks' gestation, and pre-existing type 2 diabetes). For an exposure window with statistically significant global interaction between pollutant and diabetes (p?<?0.05), pollutant-associated HRs were estimated separately for each category of maternal diabetes. RESULTS:There were associations of ASD with preconception, first and third trimesters, and first year of life PM2.5, but not with other pollutants. There were, however, interactions of maternal diabetes with first trimester and first year of life O3. Increased ASD risk was associated with first trimester O3 among mothers with GDM?<?24?weeks' gestation [adjusted HR 1.50 per 15.7?ppb O3 (95% CI: 1.08-2.09)]. No O3 associations with ASD were observed in other categories of maternal diabetes. CONCLUSIONS:GDM onset early in pregnancy may increase children's susceptibility to prenatal O3-associated ASD risk. These novel findings merit further investigation.
Project description:Maternal asthma and air pollutants have been independently associated with preeclampsia but rarely studied together. Our objective was to comprehensively evaluate preeclampsia risk based on the interaction of maternal asthma and air pollutants. Preeclampsia and asthma diagnoses, demographic and clinical data came from electronic medical records for 210,508 singleton deliveries. Modified Community Multiscale Air Quality models estimated preconception, first and second trimester and whole pregnancy exposure to: particulate matter (PM)<2.5 and <10µm, ozone, nitrogen oxides (NOx), sulfur dioxide (SO2) and carbon monoxide (CO); PM2.5 constituents; volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs). Asthma-pollutant interaction adjusted relative risks (RR) and 95% confidence intervals (CI) for preeclampsia were calculated by interquartile range for criteria pollutants and high exposure (?75th percentile) for PAHs and VOCs. Asthmatics had higher risk associated with first trimester NOx and SO2 and whole pregnancy elemental carbon (EC) exposure than non-asthmatics, but only EC significantly increased risk (RR=1.11, CI:1.03-1.21). Asthmatics also had a 10% increased risk associated with second trimester CO. Significant interactions were observed for nearly all VOCs and asthmatics had higher risk during all time windows for benzene, ethylbenzene, m-xylene, o-xylene, p-xylene and toluene while most PAHs did not increase risk.
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:BACKGROUND:Maternal air pollution exposure has been related to orofacial clefts but the literature is equivocal. Potential chronic preconception effects have not been studied. OBJECTIVES:Criteria air pollutant exposure during three months preconception and gestational weeks 3-8 was studied in relation to orofacial defects. METHODS:Among 188,102 live births and fetal deaths from the Consortium on Safe Labor (2002-2008), 63 had isolated cleft palate (CP) and 159 had isolated cleft lip with or without cleft palate (CL ±CP). Exposures were estimated using a modified Community Multiscale Air Quality model. Logistic regression with generalized estimating equations adjusted for site/region and maternal demographic, lifestyle and clinical factors calculated the odds ratio (OR) and 95% CI per interquartile increase in each pollutant. RESULTS:Preconception, carbon monoxide (CO; OR=2.24; CI: 1.21, 4.16) and particulate matter (PM) ?10 µm (OR=1.72; CI: 1.12, 2.66) were significantly associated with CP, while sulfur dioxide (SO2) was associated with CL ±CP (OR=1.93; CI: 1.16, 3.21). During gestational weeks 3-8, CO remained a significant risk for CP (OR=2.74; CI: 1.62, 4.62) and nitrogen oxides (NOx; OR=3.64; CI: 1.73, 7.66) and PM ?2.5 µm (PM2.5; OR=1.74; CI: 1.15, 2.64) were also related to the risk. Analyses by individual week revealed that positive associations of NOx and PM2.5 with CP were most prominent from weeks 3-6 and 3-5, respectively. CONCLUSIONS:Exposure to several criteria air pollutants preconception and during early gestation was associated with elevated odds for CP, while CL ±CP was only associated with preconception SO2 exposure.
Project description:Being overweight is an important risk factor for Gestational Diabetes Mellitus (GDM), but the underlying mechanisms are not understood. Weight change between pregnancies has been suggested to be an independent mechanism behind GDM. We assessed the risk for GDM in second pregnancy by change in Body Mass Index (BMI) from first to second pregnancy and whether BMI and gestational weight gain modified the risk.In this observational cohort, we included 24,198 mothers and their 2 first pregnancies in data from the Medical Birth Registry of Norway (2006-2014). Weight change, defined as prepregnant BMI in second pregnancy minus prepregnant BMI in first pregnancy, was divided into 6 categories by units BMI (kilo/square meter). Relative risk (RR) estimates were obtained by general linear models for the binary family and adjusted for maternal age at second delivery, country of birth, education, smoking in pregnancy, interpregnancy interval, and year of second birth. Analyses were stratified by BMI (first pregnancy) and gestational weight gain (second pregnancy). Compared to women with stable BMI (-1 to 1), women who gained weight between pregnancies had higher risk of GDM-gaining 1 to 2 units: adjusted RR 2.0 (95% CI 1.5 to 2.7), 2 to 4 units: RR 2.6 (2.0 to 3.5), and ?4 units: RR 5.4 (4.0 to 7.4). Risk increased significantly both for women with BMI below and above 25 at first pregnancy, although it increased more for the former group. A limitation in our study was the limited data on BMI in 2 pregnancies.The risk of GDM increased with increasing weight gain from first to second pregnancy, and more strongly among women with BMI < 25 in first pregnancy. Our results suggest weight change as a metabolic mechanism behind the increased risk of GDM, thus weight change should be acknowledged as an independent factor for screening GDM in clinical guidelines. Promoting healthy weight from preconception through the postpartum period should be a target.
Project description:Objective:Obesity has become a major, worldwide public health issue and is associated with a greater risk of adverse pregnancy outcomes. Leptin, a hormone produced by adipocytes, is elevated in individuals with obesity and may mediate the association between obesity and pregnancy outcomes. Though leptin levels during pregnancy have been associated with pregnancy outcomes, less is understood regarding preconception levels. Therefore, the objective of this study was to evaluate associations between preconception leptin levels and adverse pregnancy outcomes. Methods:This was a prospective cohort study nested within a large randomized controlled trial conducted at four medical centres in the United States. A total of 1078 women completed the parent study; this analysis involved women who became pregnant during that study (n = 776). Patients were healthy women, ages 18 to 40, attempting to conceive, with 1 to 2 prior pregnancy losses. Participants were followed for less than or equal to 6 cycles while trying to conceive and throughout pregnancy if they conceived. Preconception leptin concentrations were measured in serum collected at baseline then categorized by tertiles (using the lowest as reference group). Weighted log-binomial regression estimated risk ratios (RR) and 95% confidence intervals (CIs) for pregnancy loss, preterm delivery (PTD), gestational diabetes (GDM), and hypertensive disorders in pregnancy, adjusting for age, waist-to-hip ratio (WHR), and body mass index (BMI). Results:The mean (SD) BMI in this cohort was 25.4 ± 6.0. GDM (RR 18.37; 95% CI, 2.39-141.55) and hypertensive disorders of pregnancy (RR 2.35; 95% CI, 1.20-4.61) risks were higher among women in the high tertile after adjusting for age and WHR. The associated risk persisted when adjusting for BMI for GDM but was attenuated for hypertensive disorders in pregnancy. Leptin levels were not associated with risk of pregnancy loss or PTD. Conclusions:Women with higher baseline preconception leptin levels had a higher likelihood of experiencing some adverse pregnancy outcomes including GDM and hypertensive disorders of pregnancy. These findings warrant further evaluation, especially in light of the association between leptin and obesity.
Project description:BACKGROUND:Ambient air pollution may affect fetal growth restriction (FGR) through several mechanisms. However, prior studies of air pollution and small-for-gestational age (SGA), a common proxy for FGR, have reported inconsistent findings. OBJECTIVE:We assessed air pollution in relation to physician-diagnosed FGR and population-based SGA in the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Consecutive Pregnancy Study (2002-2010). METHODS:Among 50,005 women (112,203 singleton births), FGR was captured from medical records and ICD-9 codes, and SGA determined by population standards for birthweight <10th, <5th and <3rd percentile. Community Multiscale Air Quality models estimated ambient levels of seven criteria pollutants for whole pregnancy, 3-months preconception, and 1st, 2nd and 3rd trimesters. Generalized estimating equations with robust standard errors accounted for interdependency of pregnancies within participant. Models adjusted for maternal age, race/ethnicity, pre-pregnancy body mass index, smoking, alcohol, parity, insurance, marital status, asthma and temperature. RESULTS:FGR was diagnosed in 1.5% of infants, and 6.7% were <10th, 2.7% <5th and 1.5% <3rd percentile for SGA. Positive associations of SO2, NO2 and PM10 and negative associations of O3 with FGR were observed throughout preconception and pregnancy. For example, an interquartile increase in whole pregnancy SO2 was associated with 16% (95% CI 8%, 25%) increased FGR risk, 17% for NO2 (95% CI 9%, 26%) and 12% for PM10 (95% CI 6%, 19%). Associations with SGA were less clear. CONCLUSIONS:Chronic exposure to air pollution may be associated with FGR but not SGA in this low-risk population.
Project description:Importance:Although phthalate exposure during pregnancy has been associated with preterm birth, the association of preconception exposure in either parent with preterm birth constitutes a knowledge gap. Objective:To examine the association of paternal and maternal preconception urinary concentrations of biomarkers of phthalates and phthalate substitutes with singleton preterm birth. Design, Setting, and Participants:This study, conducted at an academic fertility center in Boston, Massachusetts, included a prospective preconception cohort of subfertile couples comprising 419 mothers and 229 fathers and their 420 live-born singleton offspring born between January 1, 2005, and December 31, 2018. Statistical analysis was performed from August 1 to October 31, 2019. Exposures:Urinary concentrations of metabolites of phthalates and phthalate substitutes obtained before conception. Main Outcomes and Measures:Gestational age was abstracted from delivery records and validated using the American College of Obstetricians and Gynecologists guidelines for births after medically assisted reproduction. The risk ratio (RR) of preterm birth (live birth before 37 completed weeks' gestation) was estimated in association with urinary concentrations of 11 individual phthalate metabolites, the molar sum of 4 di-(2-ethylhexyl) phthalate (?DEHP) metabolites, and 2 metabolites of 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH, a nonphthalate plasticizer substitute) using modified Poisson regression models adjusted for covariates. Results:The mean (SD) age of the 419 mothers was 34.7 (4.0) years, the mean (SD) age of the 229 fathers was 36.0 (4.5) years, and the mean (SD) gestational age of the 420 singleton children (217 boys) was 39.3 (1.7) weeks, with 34 (8%) born preterm. In adjusted models, maternal preconception ?DEHP concentrations (RR, 1.50; 95% CI, 1.09-2.06; P?=?.01) and cyclohexane-1,2-dicarboxylic acid monohydroxy isononyl ester (MHiNCH, a metabolite of DINCH) concentrations (RR, 1.70; 95% CI, 0.89-3.24; P?=?.11) were associated with an increased risk of preterm birth. After additional adjustment for prenatal ?DEHP or MHiNCH concentrations, the association of maternal preconception exposure to ?DEHP and preterm birth remained robust (RR, 1.69; 95% CI, 1.17-2.44; P?=?.006), while the association of maternal preconception exposure to MHiNCH and preterm birth was attenuated (RR, 1.17; 95% CI, 0.49-2.81; P?=?.72). The remaining urinary metabolites examined in either parent showed no association with preterm birth. Conclusions and Relevance:In this prospective cohort of subfertile couples, maternal preconception exposure to ?DEHP metabolites was associated with an increased risk of preterm birth. The results suggest that female exposure to select phthalate plasticizers during the preconception period may be a potential risk factor for adverse pregnancy outcomes, which may need to be considered in preconception care strategies.
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.