Prenatal Exposure to Locally Emitted Air Pollutants Is Associated with Birth Weight: An Administrative Cohort Study from Southern Sweden.
Ontology highlight
ABSTRACT:
SUBMITTER: Balidemaj F
PROVIDER: S-EPMC9318414 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Ocean-going ships supply products from one region to another and contribute to the world's economy. Ship exhaust contains many air pollutants and results in significant changes in marine atmospheric composition. The role of reactive halogen species (RHS) in the troposphere has received increasing recognition and oceans are the largest contributors to their atmospheric burden. However, the impact of shipping emissions on RHS and that of RHS on ship-originated air pollutants have not been studied in detail. Here, an updated Weather Research Forecasting coupled with Chemistry model is utilized to explore the chemical interactions between ship emissions and oceanic RHS over the East Asia seas in summer. The emissions and resulting chemical transformations from shipping activities increase the level of NO and NO2 at the surface, increase O3 in the South China Sea, but decrease O3 in the East China Sea. Such changes in pollutants result in remarkable changes in the levels of RHS (>200% increase of chlorine; ∼30% and ∼5% decrease of bromine and iodine, respectively) as well as in their partitioning. The abundant RHS, in turn, reshape the loadings of air pollutants (∼20% decrease of NO and NO2; ∼15% decrease of O3) and those of the oxidants (>10% reduction of OH and HO2; ∼40% decrease of NO3) with marked patterns along the ship tracks. We, therefore, suggest that these important chemical interactions of ship-originated emissions with RHS should be considered in the environmental policy assessments of the role of shipping emissions in air quality and climate.
| S-EPMC8008258 | biostudies-literature
Project description:BackgroundPrior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence. However, few studies have assessed changes in infant body composition or multiple pollutant exposures. Therefore, the objective of this study was to examine relationships between prenatal residential AAP exposure with infant growth and adiposity.MethodsResidential exposure to AAP (particulate matter < 2.5 and 10 microns in aerodynamic diameter [PM2.5, PM10]; nitrogen dioxide [NO2]; ozone [O3]; oxidative capacity [Oxwt: redox-weighted oxidative potential of O3 and NO2]) was modeled by spatial interpolation of monitoring stations via an inverse distance-squared weighting (IDW2) algorithm for 123 participants from the longitudinal Mother's Milk Study, an ongoing cohort of Hispanic mother-infant dyads from Southern California. Outcomes included changes in infant growth (weight, length), total subcutaneous fat (TSF; calculated via infant skinfold thickness measures) and fat distribution (umbilical circumference, central to total subcutaneous fat [CTSF]) and were calculated by subtracting 1-month measures from 6-month measures. Multivariable linear regression was performed to examine relationships between prenatal AAP exposure and infant outcomes. Models adjusted for maternal age, pre-pregnancy body mass index, socioeconomic status, infant age, sex, and breastfeeding frequency. Sex interactions were tested, and effects are reported for each standard deviation increase in exposure.ResultsNO2 was associated with greater infant weight gain (β = 0.14, p = 0.02) and TSF (β = 1.69, p = 0.02). PM10 and PM2.5 were associated with change in umbilical circumference (β = 0.73, p = 0.003) and TSF (β = 1.53, p = 0.04), respectively. Associations of Oxwt (pinteractions < 0.10) with infant length change, umbilical circumference, and CTSF were modified by infant sex. Oxwt was associated with attenuated infant length change among males (β = -0.60, p = 0.01), but not females (β = 0.16, p = 0.49); umbilical circumference among females (β = 0.92, p = 0.009), but not males (β = -0.00, p = 0.99); and CTSF among males (β = 0.01, p = 0.03), but not females (β = 0.00, p = 0.51).ConclusionPrenatal AAP exposure was associated with increased weight gain and anthropometric measures from 1-to-6 months of life among Hispanic infants. Sex-specific associations suggest differential consequences of in utero oxidative stress. These results indicate that prenatal AAP exposure may alter infant growth, which has potential to increase childhood obesity risk.
| S-EPMC8180163 | biostudies-literature
Project description:Mitochondria are sensitive to environmental toxicants due to their lack of repair capacity. Changes in mitochondrial DNA (mtDNA) content may represent a biologically relevant intermediate outcome in mechanisms linking air pollution and fetal growth restriction.We investigated whether placental mtDNA content is a possible mediator of the association between prenatal nitrogen dioxide (NO2) exposure and birth weight.We used data from two independent European cohorts: INMA (n = 376; Spain) and ENVIRONAGE (n = 550; Belgium). Relative placental mtDNA content was determined as the ratio of two mitochondrial genes (MT-ND1 and MTF3212/R3319) to two control genes (RPLP0 and ACTB). Effect estimates for individual cohorts and the pooled data set were calculated using multiple linear regression and mixed models. We also performed a mediation analysis.Pooled estimates indicated that a 10-?g/m3 increment in average NO2 exposure during pregnancy was associated with a 4.9% decrease in placental mtDNA content (95% CI: -9.3, -0.3%) and a 48-g decrease (95% CI: -87, -9 g) in birth weight. However, the association with birth weight was significant for INMA (-66 g; 95% CI: -111, -23 g) but not for ENVIRONAGE (-20 g; 95% CI: -101, 62 g). Placental mtDNA content was associated with significantly higher mean birth weight (pooled analysis, interquartile range increase: 140 g; 95% CI: 43, 237 g). Mediation analysis estimates, which were derived for the INMA cohort only, suggested that 10% (95% CI: 6.6, 13.0 g) of the association between prenatal NO2 and birth weight was mediated by changes in placental mtDNA content.Our results suggest that mtDNA content can be one of the potential mediators of the association between prenatal air pollution exposure and birth weight.Clemente DB, Casas M, Vilahur N, Begiristain H, Bustamante M, Carsin AE, Fernández MF, Fierens F, Gyselaers W, Iñiguez C, Janssen BG, Lefebvre W, Llop S, Olea N, Pedersen M, Pieters N, Santa Marina L, Souto A, Tardón A, Vanpoucke C, Vrijheid M, Sunyer J, Nawrot TS. 2016. Prenatal ambient air pollution, placental mitochondrial DNA content, and birth weight in the INMA (Spain) and ENVIRONAGE (Belgium) birth cohorts. Environ Health Perspect 124:659-665;?http://dx.doi.org/10.1289/ehp.1408981.
| S-EPMC4858384 | biostudies-literature
Project description:This study examined the emissions of nanoparticles and hazardous air pollutants (HAPs) by 3D printer operations and evaluated nanoparticle deposition behavior using a prediction model. Nanoparticles and HAPs were sampled at the Inha University 3D printing center with five fused filament fabrication (FFF)-type 3D printers. The number size distribution of the nanoparticles exhibited a bimodal distribution with dominant peaks over a large size range between 70 and 100 nm and a smaller size range between 10 and 20 nm. With increasing 3D printer operation, the number concentration of 10 nm particles increased, and the final number concentration was 3.6 times higher than that of the background concentration. Nanoparticle formation and agglomeration were characterized by transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Model calculations revealed that a large number of nanoparticles between 10 and 30 nm in size are deposited in the lower human respiratory tract (generation number: 16-22). A total of 14 HAPs species were detected, among which hexane, acrylonitrile, and benzene concentrations were the highest.
| S-EPMC9065366 | biostudies-literature
Project description:High concentrations of air pollutants on roadways, relative to ambient concentrations, contribute significantly to total personal exposure. Estimation of these exposures requires measurements or prediction of roadway concentrations. Our study develops, compares, and evaluates linear regression and nonlinear generalized additive models (GAMs) to estimate on-road concentrations of four key air pollutants, particle-bound polycyclic aromatic hydrocarbons (PB-PAH), particle number count (PNC), nitrogen oxides (NOx), and particulate matter with diameter <2.5 ?m (PM2.5) using traffic, meteorology, and elevation variables. Critical predictors included wind speed and direction for all the pollutants, traffic-related variables for PB-PAH, PNC, and NOx, and air temperatures and relative humidity for PM2.5. GAMs explained 50%, 55%, 46%, and 71% of the variance for log or square-root transformed concentrations of PB-PAH, PNC, NOx, and PM2.5, respectively, an improvement of 5% to over 15% over the linear models. Accounting for temporal autocorrelation in the GAMs further improved the prediction, explaining 57-89% of the variance. We concluded that traffic and meteorological data are good predictors in estimating on-road traffic-related air pollutant concentrations and GAMs perform better for nonlinear variables, such as meteorological parameters.
| S-EPMC4048198 | biostudies-literature
Project description:BackgroundPrenatal household air pollution impairs birth weight and increases pneumonia risk however time-varying associations have not been elucidated and may have implications for the timing of public health interventions.MethodsThe Ghana Randomized Air Pollution and Health Study (GRAPHS) enrolled 1,414 pregnant women from Kintampo, Ghana and measured personal carbon monoxide (CO) exposure four times over pregnancy. Birth weight was measured within 72-hours of birth. Fieldworkers performed weekly pneumonia surveillance and referred sick children to study physicians. The primary pneumonia outcome was one or more physician-diagnosed severe pneumonia episode in the first year of life. We employed reverse distributed lag models to examine time-varying associations between prenatal CO exposure and birth weight and infant pneumonia risk.ResultsAnalyses included n = 1,196 mother-infant pairs. In models adjusting for child sex; maternal age, body mass index (BMI), ethnicity and parity at enrollment; household wealth index; number of antenatal visits; and evidence of placental malaria, prenatal CO exposures from 15 to 20 weeks gestation were inversely associated with birth weight. Sex-stratified models identified a similar sensitive window in males and a window at 10-weeks gestation in females. In models adjusting for child sex, maternal age, BMI and ethnicity, household wealth index, gestational age at delivery and average postnatal child CO exposure, CO exposure during 34-39 weeks gestation were positively associated with severe pneumonia risk, especially in females.ConclusionsHousehold air pollution exposures in mid- and late- gestation are associated with lower birth weight and higher pneumonia risk, respectively. These findings support the urgent need for deployment of clean fuel stove interventions beginning in early pregnancy.
| S-EPMC10911234 | biostudies-literature
Project description:BackgroundImpaired in utero fetal growth trajectory may have long term health consequences of the newborns and increase risk of adulthood metabolic diseases. Prenatal exposure to air pollution has been linked to fetal development restriction; however, the impact of exposure to ambient air pollutants on the entire course of intrauterine fetal development has not been comprehensively investigated.MethodsDuring 2015-2018, two cohorts of mother-infant dyads (N = 678 and 227) were recruited in Shanghai China, from which three categories of data were systematically collected: (1) daily exposure to six air pollutants during pregnancy, (2) fetal biometry in the 2nd (gestational week 24, [GW24]) and 3rd trimester (GW36), and (3) neonatal outcomes at birth. We investigated the impact of prenatal exposure to air pollutant mixture on the trajectory of fetal development during the course of gestation, adjusting for a broad set of potential confounds.ResultsPrenatal exposure to PM2.5, PM10, SO2 and O3 significantly reduced fetal biometry at GW24, where SO2 had the most potent effect. For every 10 μg/m3 increment increase of daily SO2 exposure during the 1st trimester shortened femur length by 2.20 mm (p = 6.7E-21) translating to 5.3% reduction from the average of the study cohort. Prenatal air pollution exposure also decreased fetal biometry at GW36 with attenuated effect size. Comparing to the lowest exposed quartile, fetus in the highest exposed quartile had 6.3% (p = 3.5E-5) and 2.1% (p = 2.4E-3) lower estimated intrauterine weight in GW24 and GW36, respectively; however, no difference in birth weight was observed, indicating a rapid catch-up growth in the 3rd trimester.ConclusionsTo our knowledge, for the first time, we demonstrated the impact of prenatal exposure to ambient air pollutants on the course of intrauterine fetal development. The altered growth trajectory and rapid catch-up growth in associated with high prenatal exposure may lead to long-term predisposition for adulthood metabolic disorders.
| S-EPMC7363555 | biostudies-literature
Project description:Epidemiologic evidence provides some support for a causal association between maternal secondhand smoke (SHS) exposure during pregnancy and reduction in infant birth weight. The purpose of this cross-sectional study is to examine the magnitude of this association in China, where both prevalence and dose of SHS exposure are thought to be higher than in U.S. populations. Women who gave birth in Beijing and Changchun September 2000-November 2001 were interviewed to quantify self-reported prenatal SHS exposure. Their medical records were reviewed for data on pregnancy complications and birth outcomes. Non-smoking women who delivered term babies (?37 weeks gestation) were included in the study (N = 2,770). Nearly a quarter of the women (24%) reported daily SHS exposure, 47% reported no prenatal exposure, and 75% denied any SHS exposure from the husband smoking at home. Overall, no deficit in mean birth weight was observed with exposure from all sources of SHS combined (+11 grams, 95% CI: +2, +21). Infants had higher mean birth weights among the exposed than the unexposed for all measures of SHS exposure. Future studies on SHS exposure and infant birth weight in China should emphasize more objective measures of exposure to quantify and account for any exposure misclassification.
| S-EPMC3509463 | biostudies-other
Project description:In late October 2003, a series of wildfires exposed urban populations in Southern California to elevated levels of air pollution over several weeks. Previous research suggests that short-term hospital admissions for respiratory outcomes increased specifically as a result of these fires.We assessed the impact of a wildfire event during pregnancy on birth weight among term infants.Using records for singleton term births delivered to mothers residing in California's South Coast Air Basin (SoCAB) during 2001-2005 (n = 886,034), we compared birth weights from pregnancies that took place entirely before or after the wildfire event (n = 747,590) with those where wildfires occurred during the first (n = 60,270), second (n = 39,435), or third (n = 38,739) trimester. The trimester-specific effects of wildfire exposure were estimated using a fixed-effects regression model with several maternal characteristics included as covariates.Compared with pregnancies before and after the wildfires, mean birth weight was estimated to be 7.0 g lower [95% confidence interval (CI): -11.8, -2.2] when the wildfire occurred during the third trimester, 9.7 g lower when it occurred during the second trimester (95% CI: -14.5, -4.8), and 3.3 g lower when it occurred during the first trimester (95% CI: -7.2, 0.6).Pregnancy during the 2003 Southern California wildfires was associated with slightly reduced average birth weight among infants exposed in utero. The extent and increasing frequency of wildfire events may have implications for infant health and development.
| S-EPMC3440113 | biostudies-other
Project description:Animal experiments and cross-sectional human studies have linked particulate matter (PM) with increased behavioral problems. We conducted a longitudinal study to examine whether the trajectories of delinquent behavior are affected by PM2.5 (PM with aerodynamic diameter???2.5 ?m) exposures before and during adolescence. We used the parent-reported Child Behavior Checklist at age 9-18 with repeated measures every ~2-3 years (up to 4 behavioral assessments) on 682 children from the Risk Factors for Antisocial Behavior Study conducted in a multi-ethnic cohort of twins born in 1990-1995. Based on prospectively-collected residential addresses and a spatiotemporal model of ambient air concentrations in Southern California, monthly PM2.5 estimates were aggregated to represent long-term (1-, 2-, 3-year average) exposures preceding baseline and cumulative average exposure until the last assessment. Multilevel mixed-effects models were used to examine the association between PM2.5 exposure and individual trajectories of delinquent behavior, adjusting for within-family/within-individual correlations and potential confounders. We also examined whether psychosocial factors modified this association. The results s?ggest that PM2.5 exposure at baseline and cumulative exposure during follow-up was significantly associated (p?<?0.05) with increased delinquent behavior. The estimated effect sizes (per interquartile increase of PM2.5 by 3.12-5.18 ?g/m3) were equivalent to the difference in delinquency scores between adolescents who are 3.5-4 years apart in age. The adverse effect was stronger in families with unfavorable parent-to-child relationships, increased parental stress or maternal depressive symptoms. Overall, these findings s?ggest long-term PM2.5 exposure may increase delinquent behavior of urban-dwelling adolescents, with the resulting neurotoxic effect aggravated by psychosocial adversities.
| S-EPMC5999535 | biostudies-literature