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Air pollution reportedly contributes to the development and exacerbation of atopic dermatitis (AD). However, the exact mechanism underlying this remains unclear. To examine the relationship between air pollution and AD, a clinical, histological, and genetic analysis was performed on particulate matter (PM)-exposed mice. Five-week-old BALB/c mice were randomly divided into four groups (control group, ovalbumin (OVA) group, PM group, OVA + PM group; n = 6) and treated with OVA or PM 10, alone or together. Cutaneous exposure to OVA and PM 10 alone resulted in a significant increase in skin severity scores, trans-epidermal water loss (TEWL) and epidermal thickness compared to the control group at Week 6. The findings were further accentuated in the OVA + PM group showing statistical significance over the OVA group. A total of 635, 501, and 2149 genes were found to be differentially expressed following OVA, PM 10 , and OVA + PM 10 exposure, respectively. Strongly upregulated genes included RNASE2A , S100A9 , SPRR2D , THRSP , SPRR2A1 (OVA vs. control), SPRR2D , S100A9 , STFA3 , CHIL1 , DBP , IL1B (PM vs. control) and S100A9 , SPRR2D , SPRR2B , S100A8 , SPRR2A3 (OVA + PM vs. control). In comparing the groups OVA + PM with OVA, 818 genes were differentially expressed with S100A9 , SPRR2B , SAA3 , S100A8 , SPRR2D being the most highly upregulated in the OVA + PM group. Taken together, our study demonstrates that PM 10 exposure induces/aggravates skin inflammation via the differential expression of genes controlling skin barrier integrity and immune response. We provide evidence on the importance of public awareness in PM-associated skin inflammation. Vigilant attention should be paid to all individuals, especially to those with AD.

Air Pollution and Atopic Dermatitis (AD): The Impact of Particulate Matter (PM10) on an AD Mouse-Model