Objectives: Air pollution is strongly associated with asthma, but has not been determined to induce new-onset asthma development in children with atopic dermatitis (AD).
Working hypothesis: To assess whether prenatal/postnatal exposure to air pollutants triggers new-onset asthma development in children with AD.
Study design: Retrospective cohort study.
Patient-subject selection: Data of patients <age 18 years diagnosed with eczema or AD between 2009 and 2019 were extracted from the multicenter Kaohsiung Medical University Hospital Research Database. Patients diagnosed with new-onset asthma were in the asthma group and patients without asthma history were in the non-asthma group.
Methodology: The monthly average concentration of air pollutants for 1, 3, and 5 years before the index date, and 3, 6, and 9 months prenatally were analyzed and further stratified by age, immunoglobulin (Ig) E, and the percentage of eosinophil and eosinophil cationic protein (ECP).
Results: Postnatal exposure to airborne particulate matter (PM2.5 , PM10 ), sulfur dioxide (SO2 ), ozone (O3 ), carbon monoxide (CO), nitric oxide (NO), nitric dioxide (NO2 ), and NOx , and prenatal exposure to PM2.5 , PM10 , SO2 , NO, and NOx were significantly higher in the asthma group than in the non-asthma group. Patients having IgE above 100 IU/ml and ECP less than 24 ng/ml were significantly influenced by postnatal exposure to PM2.5 and PM10 , especially CO, to develop asthma, and those having an eosinophil count >3% were significantly influenced by prenatal exposure to PM2.5 , especially SO2 , NO, and NO2 .
Conclusions: Prenatal and postnatal exposure to air pollution have an association with asthma development in AD patients.
Keywords: allergy; asthma; atopic dermatitis; children; pollutants; prenatal/postnatal exposure.
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