Local- and regional-scale air pollution modelling (PM10) and exposure assessment for pregnancy trimesters, infancy, and childhood to age 15?years: Avon Longitudinal Study of Parents And Children (ALSPAC).
ABSTRACT: We established air pollution modelling to study particle (PM10) exposures during pregnancy and infancy (1990-1993) through childhood and adolescence up to age ~15?years (1991-2008) for the Avon Longitudinal Study of Parents And Children (ALSPAC) birth cohort. For pregnancy trimesters and infancy (birth to 6?months; 7 to 12?months) we used local (ADMS-Urban) and regional/long-range (NAME-III) air pollution models, with a model constant for local, non-anthropogenic sources. For longer exposure periods (annually and the average of birth to age ~8 and to age ~15?years to coincide with relevant follow-up clinics) we assessed spatial contrasts in local sources of PM10 with a yearly-varying concentration for all background sources. We modelled PM10 (?g/m3) for 36,986 address locations over 19?years and then accounted for changes in address in calculating exposures for different periods: trimesters/infancy (n?=?11,929); each year of life to age ~15 (n?=?10,383). Intra-subject exposure contrasts were largest between pregnancy trimesters (5th to 95th centile: 24.4-37.3??g/m3) and mostly related to temporal variability in regional/long-range PM10. PM10 exposures fell on average by 11.6??g/m3 from first year of life (mean concentration?=?31.2??g/m3) to age ~15 (mean?=?19.6??g/m3), and 5.4??g/m3 between follow-up clinics (age ~8 to age ~15). Spatial contrasts in 8-year average PM10 exposures (5th to 95th centile) were relatively low: 25.4-30.0??g/m3 to age ~8?years and 20.7-23.9??g/m3 from age ~8 to age ~15?years. The contribution of local sources to total PM10 was 18.5%-19.5% during pregnancy and infancy, and 14.4%-17.0% for periods leading up to follow-up clinics. Main roads within the study area contributed on average ~3.0% to total PM10 exposures in all periods; 9.5% of address locations were within 50?m of a main road. Exposure estimates will be used in a number of planned epidemiological studies.
Project description:BACKGROUND:We have developed an open-source ALgorithm for Generating Address Exposures (ALGAE) that cleans residential address records to construct address histories and assign spatially-determined exposures to cohort participants. The first application of this algorithm was to construct prenatal and early life air pollution exposure for individuals of the Avon Longitudinal Study of Parents and Children (ALSPAC) in the South West of England, using previously estimated particulate matter ?10? µm (PM10) concentrations. METHODS:ALSPAC recruited 14 541 pregnant women between 1991 and 1992. We assigned trimester-specific estimated PM10 exposures for 12 752 pregnancies, and first year of life exposures for 12 525 births, based on maternal residence and residential mobility. RESULTS:Average PM10 exposure was 32.6 ?µg/m3 [standard deviation (S.D.) 3.0 ?µg/m3] during pregnancy and 31.4 µg/m3 (S.D. 2.6 ?µg/m3) during the first year of life; 6.7% of women changed address during pregnancy, and 18.0% moved during first year of life of their infant. Exposure differences ranged from -5.3 ?µg/m3 to 12.4 ?µg/m3 (up to 26% difference) during pregnancy and -7.22 ?µg/m3 to 7.64 ?µg/m3 (up to 27% difference) in the first year of life, when comparing estimated exposure using the address at birth and that assessed using the complete cleaned address history. For the majority of individuals exposure changed by <5%, but some relatively large changes were seen both in pregnancy and in infancy. CONCLUSIONS:ALGAE provides a generic and adaptable, open-source solution to clean addresses stored in a cohort contact database and assign life stage-specific exposure estimates with the potential to reduce exposure misclassification.
Project description:Air pollution exposure during pregnancy might affect placental growth and function, perhaps leading to pregnancy complications.We prospectively evaluated the associations of maternal air pollution exposure with markers of placental growth and function among 7,801 pregnant women in the Netherlands.We estimated levels of particulate matter ? 10 µm in aerodynamic diameter (PM10) and nitrogen dioxide (NO2) at the home address for different periods during pregnancy using dispersion modeling techniques. Pro- and anti-angiogenic factors [placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1), respectively] were measured in first- and second-trimester maternal blood and in fetal cord blood samples at delivery. Pulsatility index of the uterine and umbilical arteries was measured by Doppler ultrasound in second and third trimester, and notching was assessed in third trimester. Placenta weight and birth weight were obtained from medical records.Higher PM10 and NO2 exposure levels were associated with lower second-trimester maternal sFlt-1 and PlGF levels. PM10 and NO2 exposures averaged over total pregnancy were associated with higher sFlt-1 and lower PlGF levels in fetal cord blood, consistent with an anti-angiogenic state. PM10 and NO2 exposures were not consistently associated with second- or third-trimester placental resistance indices. NO2 exposure was associated with third-trimester notching (odds ratio 1.33; 95% CI: 0.99, 1.78 per 10-µg/m3 increase in the prior 2 months). PM10 and NO2 exposures were associated with lower placenta weight (-11.8 g; 95% CI: -20.9, -2.7, and -10.7 g; 95% CI: -19.0, -2.4, respectively, per 10-µg/m3 increase in the prior 2 months), but not with placenta to birth weight ratio.Our results suggest that maternal air pollution exposure may influence markers of placental growth and function. Future studies are needed to confirm these findings and explore the maternal and fetal consequences.
Project description:Congenital heart defects are the most prevalent type of birth defects. The association of air pollution with congenital heart defects is not well understood. We investigated a cohort of 8,969 singleton live births in Lanzhou, China during 2010-2012. Using inverse distance weighting, maternal exposures to particulate matter with diameter ?10?m (PM10), nitrogen dioxide (NO2), and sulfur dioxide (SO2) were estimated as a combination of monitoring station levels for the time spent at home and the work location. We used logistic regression to estimate the associations, adjusting for maternal age, education, income, BMI, disease, folic acid intake and therapeutic drug use, and smoking; season of conception; fuels for cooking; and temperature. We found significant positive associations of Patent Ductus Arteriosus (PDA) with PM10 during the 1st trimester, 2nd trimester and the entire pregnancy (OR 1st trimester=3.96, 95% Confidence Interval (CI): 1.36, 11.53; OR 2nd trimester=3.59, 95% Confidence Interval (CI): 1.57, 8.22; OR entire pregnancy=2.09, 95% CI: 1.21, 3.62, per interquartile range (IQR) increment for PM10 (IQR=71.2, 61.6, and 27.4 ?g/m3 respectively)), and associations with NO2 during 2nd trimester and entire pregnancy (OR 2nd trimester= 1.92, 95% CI: 1.11, 3.34; OR entire pregnancy=2.32, 95% Cl: 1.14, 4.71, per IQR increment for NO2 (IQR=13.4 and 10.9 ?g/m3 respectively)). The associations for congenital malformations of the great arteries and pooled cases showed consistent patterns. We also found positive associations for congenital malformations of cardiac septa with PM10 exposures in the 2nd trimester and the entire pregnancy, and SO2 exposures in the entire pregnancy. Results indicate a health burden from maternal exposures to air pollution, with increased risk of congenital heart defects.
Project description:Exposures to ambient air pollutants have been associated with adverse birth outcomes. We investigated the effects of air pollutants on birth weight mediated by reduced fetal growth among term infants who were born in California during 1975-1987 and who participated in the Children's Health Study. Birth certificates provided maternal reproductive history and residence location at birth. Sociodemographic factors and maternal smoking during pregnancy were collected by questionnaire. Monthly average air pollutant levels were interpolated from monitors to the ZIP code of maternal residence at childbirth. Results from linear mixed-effects regression models showed that a 12-ppb increase in 24-hr ozone averaged over the entire pregnancy was associated with 47.2 g lower birth weight [95% confidence interval (CI), 27.4-67.0 g], and this association was most robust for exposures during the second and third trimesters. A 1.4-ppm difference in first-trimester carbon monoxide exposure was associated with 21.7 g lower birth weight (95% CI, 1.1-42.3 g) and 20% increased risk of intrauterine growth retardation (95% CI, 1.0-1.4). First-trimester CO and third-trimester O3 exposures were associated with 20% increased risk of intrauterine growth retardation. A 20-microg/m3 difference in levels of particulate matter < or = 10 microm in aerodynamic diameter (PM10) during the third trimester was associated with a 21.7-g lower birth weight (95% CI, 1.1-42.2 g), but this association was reduced and not significant after adjusting for O3. In summary, O3 exposure during the second and third trimesters and CO exposure during the first trimester were associated with reduced birth weight.
Project description:Background:Previous autism spectrum disorder (ASD) and air pollution studies focused on pregnancy exposures, but another vulnerable period is immediate postnatally. Here, we examined early life exposures to air pollution from the pre- to the postnatal period and ASD/ASD subtypes in the Danish population. Methods:With Danish registers, we conducted a nationwide case-control study of 15,387 children with ASD born 1989-2013 and 68,139 population controls matched by birth year and sex identified from the birth registry. We generated air dispersion model (AirGIS) estimates for NO2, SO2, PM2.5 and PM10 at mothers' home from 9 months before to 9 months after pregnancy and calculated odds ratios (OR) and 95% confidence intervals (CI), adjusting for parental age, neighborhood socio-economic indicators, and maternal smoking using conditional logistic regression. Results:In models that included all exposure periods, we estimated adjusted ORs for ASD per interquartile range (IQR) increase for 9 month after pregnancy with NO2 of 1.08 (95% CI: 1.01, 1.15) and with PM2.5 of 1.06 (95% CI: 1.01, 1.11); associations were smaller for PM10 (1.04; 95% CI: 1.00, 1.09) and strongest for SO2 (1.21; 95% CI: 1.13, 1.29). Also, associations for pollutants were stronger in more recent years (2000-2013) and in larger cities compared with provincial towns/rural counties. For particles and NO2, associations were only specific to autism and Asperger diagnoses. Conclusion:Our data suggest that air pollutant exposure in early infancy but not during pregnancy increases the risk of being diagnosed with autism and Asperger among children born in Denmark.
Project description:The ashes and dust resulting from the 2011 eruptions of the Puyehue volcano in Chile more than doubled monthly averages of PM10 concentrations in Montevideo, Uruguay. Few studies have taken advantage of natural experiments to assess the relationship between ambient air pollutant concentrations and birth outcomes.In this study we explored the effect of particulate matter with diameter of ? 10 ?m (PM10) on perinatal outcomes in Uruguay, a middle-income country in South America with levels of PM10 that in general do not exceed the recommended thresholds. The analyzed outcomes are preterm birth, term birth weight, and term low birth weight.We took advantage of the sharp variation in PM10 concentrations due to the Puyehue eruptions to estimate the associations between mother's exposure to PM10 in each trimester of pregnancy and perinatal outcomes. We use birth registries for 2010-2013 and control for covariates, including maternal and pregnancy characteristics, weather, co-pollutants, and calendar quarter and hospital indicators.A 10-?g/m3 increase in exposure to PM10 during the third trimester was associated with a higher likelihood of a preterm birth [odds ratio (OR) = 1.10; 95% CI: 1.03, 1.19]. The association was robust to different model specifications, and increased with categorical exposure levels (OR for third-trimester PM10 ? 70 vs. < 30 ?g/m3 = 5.24; 95% CI: 3.40, 8.08). Exposures were not consistently associated with birth weight or low birth weight among term births, though second-trimester exposures were associated with higher birth weight, contrary to expectations.Taking advantage of a natural experiment, we found evidence that exposure to high levels of PM10 during the third trimester of pregnancy may have increased preterm births among women in Montevideo, Uruguay. Citation: Balsa AI, Caffera M, Bloomfield J. 2016. Exposures to particulate matter from the eruptions of the Puyehue Volcano and birth outcomes in Montevideo, Uruguay. Environ Health Perspect 124:1816-1822;?http://dx.doi.org/10.1289/EHP235.
Project description:Importance:Thyroid hormones are critical for fetal growth and development. Prenatal particulate matter (PM) air pollution exposure has been associated with altered newborn thyroid function, but other air pollutants have not been evaluated, and critical windows of exposure are unknown. Objectives:To investigate the association of prenatal exposure to ambient and traffic-related air pollutants with newborn thyroid function and identify critical windows of exposure. Design, Setting, and Participants:This cohort study used data from 2050 participants in the Children's Health Study. Statistical analyses were conducted from 2017 to 2018 using pregnancy and birth data from 1994 to 1997 for a subset of participants recruited from schools in 13 southern California communities in 2002 to 2003 when participants were 5 to 7 years of age. Participants were included in statistical analyses if they could be linked to their newborn blood spot and had complete monthly exposure measures for at least 1 air pollutant across pregnancy. Exposures:Prenatal monthly averages of ambient (PM diameter <2.5 ?m [PM2.5] or <10 ?m [PM10], nitrogen dioxide, and ozone) and traffic-related (freeway, nonfreeway, and total nitrogen oxides) air pollutant exposures were determined using inverse distance-squared weighting of central monitoring data and the California Line Source Dispersion model, respectively. Main Outcomes and Measures:Newborn heel-stick blood spot total thyroxine (TT4) measures were acquired retrospectively from the California Department of Public Health. Results:Participants included 2050 newborns (50.5% male), with a median (interquartile range) age of 20 (15-29) hours. The majority of newborns were Hispanic white (1202 [58.6%]) or non-Hispanic white (638 [31.1%]). Sixty-six (3.2%) were black and 144 (7.0%) were from other racial/ethnic groups. The mean (SD) newborn TT4 measure was 16.2 (4.3) ?g/dL. A 2-SD increase in prenatal PM2.5 (16.3 ?g/m3) and PM10 (22.2 ?g/m3) was associated with a 1.2-?g/dL (95% CI, 0.5-1.8 ?g/dL) and 1.5-?g/dL (95% CI, 0.9-2.1 ?g/dL) higher TT4 measure, respectively, in covariate-adjusted linear regression models. Other pollutants were not consistently associated with newborn TT4. Distributed lag models revealed that PM2.5 exposure during months 3 to 7 of pregnancy and PM10 exposure during months 1 to 8 of pregnancy were associated with significantly higher newborn TT4 concentrations (P?<?.05). Conclusions and Relevance:Prenatal PM exposure, particularly in early pregnancy and midpregnancy, is associated with higher newborn TT4 concentrations. Future studies should assess the health implications of PM-associated differences in newborn TT4 concentrations.
Project description:BACKGROUND: The prevalence of asthma in children is a significant phenomenon in the Caribbean. Among the etiologic factors aggravating asthma in children, environmental pollution is one of the main causes. In Guadeloupe, pollution is primarily transported by Saharan dust including inhalable particles. METHODS: This study assesses, over one year (2011), the short-term effects of pollutants referred to as PM10 (PM10: particulate matter <10 µm) and PM2.5-10 (PM2.5-10: particulate matter >2.5 µm and <10 µm) contained in Saharan dust, on the visits of children aged between 5 and 15 years for asthma in the health emergency department of the main medical facility of the archipelago of Guadeloupe. A time-stratified case-crossover model was applied and the data were analysed by a conditional logistic regression for all of the children but also for sub-groups corresponding to different age classes and genders. RESULTS: The visits for asthma concerned 836 children including 514 boys and 322 girls. The Saharan dust has affected 15% of the days of the study (337 days) and involved an increase in the average daily concentrations of PM10 (49.7 µg/m3 vs. 19.2 µg/m3) and PM 2.5-10 (36.2 µg/m3 vs. 10.3 µg/m3) compared to days without dust. The excess risk percentages (IR%) for visits related to asthma in children aged between 5 and 15 years on days with dust compared to days without dust were, for PM10, ((IR %: 9.1% (CI95%, 7.1%-11.1%) versus 1.1%(CI95%, -5.9%-4.6%)) and for PM2.5-10 (IR%: 4.5%(CI95%, 2.5%-6.5%) versus 1.6% (CI95%, -1.1%-3.4%). There was no statistical difference in the IR% for periods with Saharan dust among different age group of children and between boys and girls for PM10 and PM2.5-10. CONCLUSION: The PM10 and PM2.5-10 pollutants contained in the Saharan dust increased the risk of visiting the health emergency department for children with asthma in Guadeloupe during the study period.
Project description:Long-term exposure to ambient air pollution can lead to adverse health effects in children; however, underlying biological mechanisms are not fully understood.We evaluated the effect of air pollution exposure during different time periods on mRNA expression as well as circulating levels of inflammatory cytokines in children.We measured a panel of 10 inflammatory markers in peripheral blood samples from 670 8-y-old children in the Barn/Child, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) birth cohort. Outdoor concentrations of nitrogen dioxide (NO2) and particulate matter (PM) with aerodynamic diameter <10 ?m (PM10) from road traffic were estimated for residential, daycare, and school addresses using dispersion modeling. Time-weighted average exposures during infancy and at biosampling were linked to serum cytokine levels using linear regression analysis. Furthermore, gene expression data from 16-year-olds in BAMSE (n=238) were used to evaluate links between air pollution exposure and expression of genes coding for the studied inflammatory markers.A 10??g/m3 increase of NO2 exposure during infancy was associated with a 13.6% (95% confidence interval (CI): 0.8; 28.1%) increase in interleukin-6 (IL-6) levels, as well as with a 27.8% (95% CI: 4.6, 56.2%) increase in IL-10 levels, the latter limited to children with asthma. However, no clear associations were observed for current exposure. Results were similar using PM10, which showed a high correlation with NO2. The functional analysis identified several differentially expressed genes in response to air pollution exposure during infancy, including IL10, IL13, and TNF;.Our results indicate alterations in systemic inflammatory markers in 8-y-old children in relation to early-life exposure to traffic-related air pollution. https://doi.org/10.1289/EHP460.
Project description:Limited information is available regarding long-term effects of air pollution on blood pressure (BP) and hypertension.We studied whether 1-year exposures to particulate matter (PM) and nitrogen oxides (NOx) were correlated with BP and hypertension in the elderly.We analyzed cross-sectional data from 27,752 Taipei City residents > 65 years of age who participated in a health examination program in 2009. Land-use regression models were used to estimate participants' 1-year exposures to particulate matter with aerodynamic diameter ? 10 ?m (PM10), coarse particles (PM2.5-10), fine particles (? 2.5 ?m; PM2.5), PM2.5 absorbance, NOx, and nitrogen dioxide (NO2). Generalized linear regressions and logistic regressions were used to examine the association between air pollution and BP and hypertension, respectively.Diastolic BP was associated with 1-year exposures to air pollution, with estimates of 0.73 [95% confidence interval (CI): 0.44, 1.03], 0.46 (95% CI: 0.30, 0.63), 0.62 (95% CI: 0.24, 0.99), 0.34 (95% CI: 0.19, 0.50), and 0.65 (95% CI: 0.44, 0.85) mmHg for PM10 (10 ?g/m3), PM2.5-10 (5 ?g/m3), PM2.5 absorbance (10-5/m), NOx (20 ?g/m3), and NO2 (10 ?g/m3), respectively. PM2.5 was not associated with diastolic BP, and none of the air pollutants was associated with systolic BP. Associations of diastolic BP with PM10 and PM2.5 absorbance were stronger among participants with hypertension, diabetes, or a body mass index ? 25 kg/m2 than among participants without these conditions. One-year air pollution exposures were not associated with hypertension.One-year exposures to PM10, PM2.5-10, PM2.5 absorbance, and NOx were associated with higher diastolic BP in elderly residents of Taipei.