Prenatal, Early-Life, and Childhood Exposure to Air Pollution and Lung Function: The ALSPAC Cohort.
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ABSTRACT:
SUBMITTER: Cai Y
PROVIDER: S-EPMC7328307 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Prenatal exposure to traffic pollution has been associated with faster infant weight gain, but implications for cardiometabolic health in later childhood are unknown.Among 1418 children in Project Viva, a Boston-area pre-birth cohort, we assessed anthropometric and biochemical parameters of cardiometabolic health in early (median age 3.3?years) and mid- (median age 7.7?years) childhood. We used spatiotemporal models to estimate prenatal and early life residential PM2.5 and black carbon exposure as well as traffic density and roadway proximity. We performed linear regression analyses adjusted for sociodemographics.Children whose mothers lived close to a major roadway at the time of delivery had higher markers of adverse cardiometabolic risk in early and mid-childhood. For example, total fat mass was 2.1?kg (95%CI: 0.8, 3.5) higher in mid-childhood for children of mothers who lived?<50?m vs. ?200?m from a major roadway. Black carbon exposure and traffic density were generally not associated with cardiometabolic parameters, and PM2.5 exposure during the year prior was paradoxically associated with improved cardiometabolic profile.Infants whose mothers lived close to a major roadway at the time of delivery may be at later risk for adverse cardiometabolic health.
| S-EPMC4974151 | biostudies-other
Project description:Exposure to air pollution during pregnancy has been linked to the risk of childhood cancer, but the evidence remains inconclusive. In the present study, we used land use regression modeling to estimate prenatal exposures to traffic exhaust and evaluate the associations with cancer risk in very young children. Participants in the Air Pollution and Childhood Cancers Study who were 5 years of age or younger and diagnosed with cancer between 1988 and 2008 were had their records linked to California birth certificates, and controls were selected from birth certificates. Land use regression-based estimates of exposures to nitric oxide, nitrogen dioxide, and nitrogen oxides were assigned based on birthplace residence and temporally adjusted using routine monitoring station data to evaluate air pollution exposures during specific pregnancy periods. Logistic regression models were adjusted for maternal age, race/ethnicity, educational level, parity, insurance type, and Census-based socioeconomic status, as well as child's sex and birth year. The odds of acute lymphoblastic leukemia increased by 9%, 23%, and 8% for each 25-ppb increase in average nitric oxide, nitrogen dioxide, and nitrogen oxide levels, respectively, over the entire pregnancy. Second- and third-trimester exposures increased the odds of bilateral retinoblastoma. No associations were found for annual average exposures without temporal components or for any other cancer type. These results lend support to a link between prenatal exposure to traffic exhaust and the risk of acute lymphoblastic leukemia and bilateral retinoblastoma.
| S-EPMC3792733 | biostudies-literature
Project description:BackgroundEvidence in the literature suggests that air pollution exposures experienced prenatally and early in life can be detrimental to normal lung development, however the specific timing of critical windows during development is not fully understood.ObjectivesWe evaluated air pollution exposures during the prenatal and early-life period in association with lung function at ages 6-9, in an effort to identify potentially influential windows of exposure for lung development.MethodsOur study population consisted of 222 children aged 6-9 from the Fresno-Clovis metro area in California with spirometry data collected between May 2015 and May 2017. We used distributed-lag non-linear models to flexibly model the exposure-lag-response for monthly average exposure to fine particulate matter (PM2.5) and ozone (O3) during the prenatal months and first three years of life in association with forced vital capacity (FVC), and forced expiratory volume in the first second (FEV1), adjusted for covariates.ResultsPM2.5 exposure during the prenatal period and the first 3-years of life was associated with lower FVC and FEV1 assessed at ages 6-9. Specifically, an increase from the 5th percentile of the observed monthly average exposure (7.55 μg/m3) to the median observed exposure (12.69 μg/m3) for the duration of the window was associated with 0.42 L lower FVC (95% confidence interval (CI): -0.82, -0.03) and 0.38 L lower FEV1 (95% CI: -0.75, -0.02). The shape of the lag-response indicated that the second half of pregnancy may be a particularly influential window of exposure. Associations for ozone were not as strong and typically CIs included the null.ConclusionsOur findings indicate that prenatal and early-life exposures to PM2.5 are associated with decreased lung function later in childhood. Exposures during the latter months of pregnancy may be especially influential.
| S-EPMC9974878 | biostudies-literature
Project description:BackgroundTraffic-related air pollution exposure may influence brain development and function and thus be related to neurobehavioral problems in children, but little is known about windows of susceptibility.AimsExamine associations of gestational and childhood exposure to traffic-related pollution with executive function and behavior problems in children.MethodsWe studied associations of pre- and postnatal pollution exposures with neurobehavioral outcomes in 1212 children in the Project Viva pre-birth cohort followed to mid-childhood (median age 7.7years). Parents and classroom teachers completed the Behavior Rating Inventory of Executive Function (BRIEF) and the Strengths and Difficulties Questionnaire (SDQ). Using validated spatiotemporal models, we estimated exposure to black carbon (BC) and fine particulate matter (PM2.5) in the third trimester of pregnancy, from birth to 3years, from birth to 6years, and in the year before behavioral ratings. We also measured residential distance to major roadways and near-residence traffic density at birth and in mid-childhood. We estimated associations of BC, PM2.5, and other traffic exposure measures with BRIEF and SDQ scores, adjusted for potential confounders.ResultsHigher childhood BC exposure was associated with higher teacher-rated BRIEF Behavioral Regulation Index (BRI) scores, indicating greater problems: 1.0 points (95% confidence interval (CI): 0.0, 2.1) per interquartile range (IQR) increase in birth-age 6BC, and 1.7 points (95% CI: 0.6, 2.8) for BC in the year prior to behavioral ratings. Mid-childhood residential traffic density was also associated with BRI score (0.6, 95% CI: 0.1, 1.1). Birth-age 3BC was not associated with BRIEF or SDQ scores. Third trimester BC exposure was not associated with teacher-rated BRI scores (-0.2, 95% CI: -1.1, 0.8), and predicted lower scores (fewer problems) on the BRIEF Metacognition Index (-1.2, 95% CI: -2.2, -0.2) and SDQ total difficulties (-0.9, 95% CI: -1.4, -0.4). PM2.5 exposure was associated with teacher-rated BRIEF and SDQ scores in minimally adjusted models but associations attenuated with covariate adjustment. None of the parent-rated outcomes suggested adverse effects of greater pollution exposure at any time point.ConclusionsChildren with higher mid-childhood exposure to BC and greater near-residence traffic density in mid-childhood had greater problems with behavioral regulation as assessed by classroom teachers, but not as assessed by parents. Prenatal and early childhood exposure to traffic-related pollution did not predict greater executive function or behavior problems; third trimester BC was associated with lower scores (representing fewer problems) on measures of metacognition and behavioral problems.
| S-EPMC5056808 | biostudies-literature
Project description:BACKGROUND:Early-life exposure to traffic-related air pollution exacerbates childhood asthma, but it is unclear what role it plays in asthma development. METHODS:The association between exposure to primary mobile source pollutants during pregnancy and during infancy and asthma incidence by ages 2 through 6 was examined in the Kaiser Air Pollution and Pediatric Asthma Study, a racially diverse birth cohort of 24,608 children born between 2000 and 2010 and insured by Kaiser Permanente Georgia. We estimated concentrations of mobile source fine particulate matter (PM2.5, µg/m), nitrogen oxides (NOX, ppb), and carbon monoxide (CO, ppm) at the maternal and child residence using a Research LINE source dispersion model for near-surface releases. Asthma was defined using diagnoses and medication dispensings from medical records. We used binomial generalized linear regression to model the impact of exposure continuously and by quintiles on asthma risk. RESULTS:Controlling for covariates and modeling log-transformed exposure, a 2.7-fold increase in first year of life PM2.5 was associated with an absolute 4.1% (95% confidence interval, 1.6%, 6.6%) increase in risk of asthma by age 5. Quintile analysis showed an increase in risk from the first to second quintile, but similar risk across quintiles 2-5. Risk differences increased with follow-up age. Results were similar for NOX and CO and for exposure during pregnancy and the first year of life owing to high correlation. CONCLUSIONS:Results provide limited evidence for an association of early-life mobile source air pollution with childhood asthma incidence with a steeper concentration-response relationship observed at lower levels of exposure.
| S-EPMC5718963 | biostudies-literature
Project description:BackgroundThe association between prenatal household air pollution (HAP) exposure and childhood blood pressure (BP) is unknown.ObjectiveWithin the Ghana Randomized Air Pollution and Health Study (GRAPHS) we examined time-varying associations between a) maternal prenatal and b) first-year-of-life HAP exposure with BP at 4 years of age and, separately, whether a stove intervention delivered prenatally and continued through the first year of life could improve BP at 4 years of age.MethodsGRAPHS was a cluster-randomized cookstove intervention trial wherein n=1,414 pregnant women were randomized to one of two stove interventions: a) a liquefied petroleum gas (LPG) stove or improved biomass stove, or b) control (open fire cooking). Maternal HAP exposure over pregnancy and child HAP exposure over the first year of life was quantified by repeated carbon monoxide (CO) measurements; a subset of women (n=368) also performed one prenatal and one postnatal personal fine particulate matter (PM2.5) measurement. Systolic and diastolic BP (SBP and DBP) were measured in n=667 4-y-old children along with their PM2.5 exposure (n=692). We examined the effect of the intervention on resting BP z-scores. We also employed reverse distributed lag models to examine time-varying associations between a) maternal prenatal and b) first-year-of-life HAP exposure and resting BP z-scores. Among those with PM2.5 measures, we examined associations between PM2.5 and resting BP z-scores. Sex-specific effects were considered.ResultsIntention-to-treat analyses identified that DBP z-score at 4 years of age was lower among children born in the LPG arm (LPG β=-0.20; 95% CI: -0.36, -0.03) as compared with those in the control arm, and females were most susceptible to the intervention. Higher CO exposure in late gestation was associated with higher SBP and DBP z-score at 4 years of age, whereas higher late-first-year-of-life CO exposure was associated with higher DBP z-score. In the subset with PM2.5 measurements, higher maternal postnatal PM2.5 exposure was associated with higher SBP z-scores.DiscussionThese findings suggest that prenatal and first-year-of-life HAP exposure are associated with child BP and support the need for reductions in exposure to HAP, with interventions such as cleaner cooking beginning in pregnancy. https://doi.org/10.1289/EHP13225.
| S-EPMC10953816 | biostudies-literature
Project description:BackgroundBecause fine particulate matter [PM, with aerodynamic diameter ≤2.5μm (PM2.5)] is a ubiquitous environmental exposure, small changes in cognition associated with PM2.5 exposure could have great societal costs. Prior studies have demonstrated a relationship between in utero PM2.5 exposure and cognitive development in urban populations, but it is not known whether these effects are similar in rural populations and whether they persist into late childhood.ObjectivesIn this study, we tested for associations between prenatal PM2.5 exposure and both full-scale and subscale measures of IQ among a longitudinal cohort at age 10.5 y.MethodsThis analysis used data from 568 children enrolled in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort study in California's agricultural Salinas Valley. Exposures were estimated at residential addresses during pregnancy using state of the art, modeled PM2.5 surfaces. IQ testing was performed by bilingual psychometricians in the dominant language of the child.ResultsA 3-μg/m3 higher average PM2.5 over pregnancy was associated with -1.79 full-scale IQ points [95% confidence interval (CI): -2.98, -0.58], with decrements specifically in Working Memory IQ (WMIQ) and Processing Speed IQ (PSIQ) subscales [WMIQ -1.72 (95% CI: -2.98, -0.45) and PSIQ -1.19 (95% CI: -2.54, 0.16)]. Flexible modeling over the course of pregnancy illustrated mid-to-late pregnancy (months 5-7) as particularly susceptible times, with sex differences in the timing of susceptible windows and in which subscales were most affected [Verbal Comprehension IQ (VCIQ) and WMIQ in males; and PSIQ in females].DiscussionWe found that small increases in outdoor PM2.5 exposure in utero were associated with slightly lower IQ in late childhood, robust to many sensitivity analyses. In this cohort there was a larger effect of PM2.5 on childhood IQ than has previously been observed, perhaps due to differences in PM composition or because developmental disruption could alter the cognitive trajectory and thus appear more pronounced as children get older. https://doi.org/10.1289/EHP10812.
| S-EPMC10010399 | biostudies-literature
Project description:Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007-2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency's Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM10 and PM2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM2.5 was associated with CAS indices, including a 5% increase (? = 1.05, 95% CI 1.00-1.10) in carotid stiffness index beta, a 5% increase (? = 1.05, 95% CI 1.01-1.10) in Young's elastic modulus and a 5% decrease (? = 0.95, 95% CI 0.91-0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.
| S-EPMC4780745 | biostudies-literature
Project description:BACKGROUND:Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5??m (PM2.5) and ozone (O3) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES:We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM2.5 and O3 increase the risk of early developmental delays. STUDY DESIGN:Prospective cohort. SETTINGS:New York State excluding New York City. PARTICIPANTS:4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES:Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM2.5 and O3 estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES:Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM2.5 and O3, and for those living <1000?m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS:Compared to those >1000?m away from a major roadway, those resided 50-100?m [RR: 2.12 (1.00-4.52)] and 100-500?m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10??g/m3 increase in PM2.5 and 0.7%-1.7% for a 10?ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM2.5 exposures. CONCLUSIONS:In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 and O3 were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.
| S-EPMC6541527 | biostudies-literature
Project description:Ambient air pollution is a well-known risk factor of various asthma-related outcomes, however, past research has often focused on acute exacerbations rather than asthma development. This study draws on a population-based, multigenerational panel dataset from the United States to assess the association of childhood asthma risk with census block-level, annual-average air pollution exposure measured during the prenatal and early postnatal periods, as well as effect modification by neighborhood poverty. Findings suggest that early-life exposures to nitrogen dioxide (NO₂), a marker of traffic-related pollution, and fine particulate matter (PM2.5), a mixture of industrial and other pollutants, are positively associated with subsequent childhood asthma diagnosis (OR = 1.25, 95% CI = 1.10⁻1.41 and OR = 1.25, 95% CI = 1.06⁻1.46, respectively, per interquartile range (IQR) increase in each pollutant (NO₂ IQR = 8.51 ppb and PM2.5 IQR = 4.43 µ/m³)). These effects are modified by early-life neighborhood poverty exposure, with no or weaker effects in moderate- and low- (versus high-) poverty areas. This work underscores the importance of a holistic, developmental approach to elucidating the interplay of social and environmental contexts that may create conditions for racial-ethnic and socioeconomic disparities in childhood asthma risk.
| S-EPMC6025399 | biostudies-literature