Modifiable exposures to air pollutants related to asthma phenotypes in the first year of life in children of the EDEN mother-child cohort study
1 Université Pierre et Marie Curie, Paris 6, Sorbonne Universités, UMR S 707: EPAR (Epidémiologie des maladies allergiques et respiratoires), Medical School Saint-Antoine, Paris, France
2 INSERM U 707: EPAR, Paris, France
3 School of Public Health, Peking University, Beijing, China
Citation and License
BMC Public Health 2013, 13:506 doi:10.1186/1471-2458-13-506Published: 24 May 2013
Studies have shown diverse strength of evidence for the associations between air pollutants and childhood asthma, but these associations have scarcely been documented in the early life. The purpose of this study was to evaluate the impacts of various air pollutants on the development of asthma phenotypes in the first year of life.
Adjusted odds ratios were estimated to assess the relationships between exposures to air pollutants and single and multi-dimensional asthma phenotypes in the first year of life in children of the EDEN mother-child cohort study (n = 1,765 mother-child pairs). The Generalized Estimating Equation (GEE) model was used to determine the associations between prenatal maternal smoking and in utero exposure to traffic-related air pollution and asthma phenotypes (data were collected when children were at birth, and at 4, 8 and 12 months of age). Adjusted Population Attributable Risk (aPAR) was estimated to measure the impacts of air pollutants on health outcomes.
In the first year of life, both single and multi-dimensional asthma phenotypes were positively related to heavy parental smoking, traffic-related air pollution and dampness, but negatively associated with contact with cats and domestic wood heating. Adjusted odds ratios (aORs) for traffic-related air pollution were the highest [1.71 (95% Confidence Interval (CI): 1.08-2.72) for ever doctor-diagnosed asthma, 1.44 (95% CI: 1.05-1.99) for bronchiolitis with wheezing, 2.01 (95% CI: 1.23-3.30) for doctor-diagnosed asthma with a history of bronchiolitis]. The aPARs based on these aORs were 13.52%, 9.39%, and 17.78%, respectively. Results persisted for prenatal maternal smoking and in utero exposure to traffic-related air pollution, although statistically significant associations were observed only with the asthma phenotype of ever bronchiolitis.
After adjusting for potential confounders, traffic-related air pollution in utero life and in the first year of life, had a greater impact on the development of asthma phenotypes compared to other factors.