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Air pollution and pulmonary function in asthmatic children: effects of prenatal and lifetime exposures
Kathleen Mortimer1, Romain Neugebauer, Frederick Lurmann
1Divisions of aEpidemiology, School of Public Health, University of California, Berkeley, CA 4720-7370, USA. kmort@berkeley.edu
Insights
Prenatal exposure to air pollutants like carbon monoxide (CO), particulate matter (PM10), and nitrogen dioxide (NO2) can negatively impact lung function in children with asthma, especially in vulnerable subgroups.
Area of Science:
- Environmental Health
- Pediatric Pulmonology
- Toxicology
Background:
- Prenatal and early life are critical periods for lung development, susceptible to oxidant pollutant-induced remodeling.
- Asthma management is complex, with environmental factors playing a significant role in disease progression.
Purpose of the Study:
- To investigate the association between prenatal and lifetime air pollutant exposures and pulmonary function in children with asthma.
- To identify specific air pollutants and exposure windows impacting lung function in this cohort.
Main Methods:
- Reconstructed prenatal and lifetime air pollutant exposures (Ozone, CO, NO2, PM10) for 232 asthmatic children.
- Utilized geocoding of residences and developed predictive models for 8 pulmonary function measures.
- Employed a novel Deletion/Substitution/Addition algorithm for model selection.
Main Results:
- Second-trimester NO2 exposure linked to reduced FVC and FEV1; first-trimester PM10 linked to reduced PEF.
- Early-life CO exposure negatively affected FEV1/FVC and FEF25-75/FVC.
- Effects were more pronounced in subgroups: African American children, those diagnosed before age 2, and those with prenatal maternal smoking exposure.
Conclusions:
- Prenatal and early-life exposure to CO, PM10, and NO2 adversely affects pulmonary function in specific subgroups of asthmatic children.
- Highlights the importance of early life environmental exposures in pediatric asthma management and prevention strategies.
Background:
Prenatal and early life periods represent critical windows for oxidant pollutant-induced lung remodeling. The objective of this study was to examine the association of prenatal and lifetime exposures to air pollutants with pulmonary function in a cohort of children with asthma.
Methods:
Prenatal and lifetime exposure to several air pollutants was reconstructed for 232 children with asthma from the San Joaquin Valley of California, USA. Prenatal and lifetime residences were geocoded. We obtained data on monthly average ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), and particulate matter with a median aerodynamic diameter <10 microm (PM10) concentrations. Metrics were created for key developmental periods. Predictive models were developed for 8 pulmonary function measures. A newly-developed stepwise model selection procedure-the Deletion/Substitution/Addition algorithm-was implemented and results were compared with those obtained using traditional stepwise methods.
Results:
Second-trimester exposure to NO2 negatively affected forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1), and first trimester exposure to PM10 negatively affected peak expiratory flow (PEF) rate. Exposure to CO in early years of life also had a negative effect on FEV1/FVC and forced expiratory flow between 25% and 75% of FVC (FEF25-75)/FVC. Second trimester exposure to PM10 and exposure to CO in the first 6 years of life had negative effects on forced expiratory flow at 25% of FVC. Prenatal, but not trimester-specific, exposure to CO was negatively associated with FEF25-75. Effects were limited to subgroups, such as children who were African American, those diagnosed with asthma before the age of 2 years, and those exposed to maternal smoking during pregnancy.
Conclusion:
Prenatal and early-life exposures to CO, PM10, and NO2 have a negative effect on pulmonary function in subgroups of asthmatic children.
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