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Prenatal air pollution exposure associates with offspring immune deviation

Published: September 5, 2022

Ambient air pollution exposure is an established risk factor for asthma, allergic rhinitis, and other chronic inflammatory disorders. However, little is known about how long-term exposure to ambient air pollution in early life affects inflammatory mechanisms in the blood and upper airways of children.

In the most recent issue of The Journal of Allergy and Clinical Immunology (JACI), Pedersen & Bønnelykke et al. report on potential mechanisms leading to later risk of asthma and allergy induced by pre- and postnatal exposure to air pollution in 700 children from the Danish Copenhagen Prospective Studies of Asthma in Childhood 2010 cohort. Ambient air pollution concentration to particulate matter (PM2.5 and PM10) and nitrogen dioxide (NO2) was modelled at individual home addresses. Immune mediators in the upper airways were assessed at age four weeks and inflammatory markers in blood at age 6 months. Nasal epithelial DNA methylation and gene expression were assessed at age 6 years. Detailed information on children’s health and covariates was obtained from questionnaires and registers. Associations between early life exposures and changes in airway immunology, systemic inflammation, airway methylation and gene expression, and the odds for asthma and allergy-related outcomes at age 6 years were evaluated.

Higher exposure to ambient air pollution with PM2.5, PM10 and NO2  was found to be associated with an altered airway immune profile at 4 weeks of age, including higher levels of IL-4, a known pro-inflammatory cytokine involved in Type 2 asthma and lower levels of CCL22 and CCL26 which have been shown to be involved in a healthy Type 2 response. This cytokine profile was associated with increased risk of developing allergic sensitization and rhinitis at age 6 years. Prenatal exposure to ambient air pollution was also associated with changes in pro-inflammatory cytokines measured in blood obtained from the children at 6 months of age, particularly increased levels of CXCL8 and decreased levels of IL-1ß. This systemic cytokine profile was associated with an increased risk of asthma development before age 6. No robust association between early life exposure to ambient air pollution and airway DNA methylation or gene expression were found.

In conclusion, the authors show that prenatal exposure to NO2, PM2.5 and PM10 was associated with a perturbed airway immune profile at age 4 weeks and blood inflammatory profile at age 6 months, conferring an increased risk of developing allergic rhinitis and asthma. The findings suggest potential mechanisms mediating long-term risk from prenatal air pollution exposure and indicate an independent detrimental effect of air pollution exposure during pregnancy on offspring health. These findings support the new WHO air quality guidelines as the children were exposed to relative low concentrations, below the current US and EU regulatory guideline levels.

The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.

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