Prenatal exposure to air pollution appears to disrupt immune development in the offspring’s early life, in turn increasing the risk of allergic rhinitis and asthma, a recent study has found.
Researchers assessed long-term residence-level air pollution exposure in 700 Danish children who were followed for the development of asthma and allergy. The study focused on three main pollutants: nitrogen dioxide (NO2) and particulate matter with diameter ≤2.5 µm (PM2.5) and ≤10 µm (PM10). Surveillance period ran from conception to 6 years of age.
At 4 weeks and 6 years, the children underwent assessment for nasal mucosal immune mediators. The same analysis for blood inflammatory markers was conducted at 6 months of age, while quantification of nasal epithelial DNA methylation and gene expression was performed at 6 years.
Multivariate logistic regression analysis found that prenatal exposure to NO2, PM2.5, and PM10 strongly altered the children’s nasal immune profile at 4 weeks, which in turn aggravated the odds of allergic sensitization by more than twofold at 6 years (odds ratio [OR], 2.68, 95 percent confidence interval [CI], 1.58–4.62).
A similar effect was reported for allergic rhinitis at 6 years (OR, 2.63, 95 percent CI, 1.18–5.81).
Moreover, prenatal air pollution exposure also altered blood immune profile at 6 months of age, resulting in a higher likelihood of asthma at 6 years (OR, 1.80, 95 percent CI, 1.18–2.76).
In contrast, no such effects were reported for DNA methylation and gene expression in nasal cells at 6 years.