Padula, AM; Mortimer, KM; Tager, I
Rationale: Given recent evidence of an association between prenatal air pollution and children’s pulmonary function, application of causal inference methods to this question assumes greater importance. The Fresno Asthmatic Children’s Environment Study (FACES) – Lifetime Exposure (LiTE) examines the influence of prenatal exposure to a number of ambient air pollutants on pulmonary function in asthmatic children aged 6-13 years.
Methods: We geocoded residences during pregnancy with Tele-Atlas. Pollutant concentrations were obtained from the Aerometric Information Retrieval System. Summaries of the entire pregnancy and each trimester were calculated from 24-hour averages of each pollutant. Spirometry was performed by trained staff as part of the FACES Study. We used targeted maximum likelihood estimation (TMLE), a recently developed method for causal inference, to examine the effects of prenatal air pollution exposure on repeated measures of pulmonary function. We calculated the difference in mean pulmonary function (i.e., FVC, FEV1, FEF25-75, FEV1/FVC, FEF25-75/FVC, FEF75) had all children been exposed to “above the median concentration” versus “below the median concentration” of each pollutant (ozone (O3), nitrogen dioxide (NO2), particle matter <10 micro-grams/m3 (PM10), carbon monoxide (CO)). We stratified the data into three age groups (6-8, 9-10, and 11-13 years old) to examine separately the effect across ages.
Results: Our analysis included 162 children with a total of 947 observations over the years of 2000-2005. In general, higher exposure to NO2 during the first and second trimesters had a negative effect on most pulmonary function tests (PFTs). For example, among the 9-10 year olds, higher exposure to NO2 during the 2nd trimester resulted in a population-level decrease in FEF25-75 of 0.148 L/sec (~7.5% decrease). Similarly, higher exposure to CO during each trimester had a negative impact on most PFTs across all age groups, with especially strong effects for the second trimester exposures. Results for PM10 and O3 were less consistent.
Conclusion: We found that prenatal exposures to NO2 and CO, particularly during the second trimester, adversely affect most metrics of pulmonary function among asthmatic children. The use of TMLE provides for a more causal interpretation than traditional regression methods. This recent analysis adds to the evidence that maternal exposure to ambient traffic-related air pollutants can have persistent effects on lung function development in children with asthma.
