Description

Background: Given the increasing prevalence of wildfires worldwide, understanding the effects of wildfire air pollutants on human health, in specific, immunological pathways, is crucial. Exposure to air pollutants is associated with cardiorespiratory disease, however, immune, and epithelial barrier alterations require further investigation.

Objective: Determine the impact of wildfire smoke exposure on the immune system and epithelial barriers, using proteomics and immune cell phenotyping.

Methods: A San Francisco Bay area cohort (n=15; age:30±10y) provided blood samples before (October2019-March2020; AQI=37) and during a major wildfire (August 2020; AQI=80). The exposure samples were collected 11 days (range:10-12days) following continuous exposure to wildfire smoke. We determined alterations in 506 proteins, including zonulin family peptide (ZFP), immune cell phenotypes by mass cytometry (CyTOF), and their interrelationship using a correlation matrix.

Results: Targeted proteomic analyses (n=15) revealed a decrease of Spondin-2 and an increase of Granzyme A, B, and H, KIR3DL1, IL-16, Nibrin, PARP-1, C1QTNF-1, FGF-19, and vWF following 11 days in average continuous exposure to smoke from a large wildfire (p<0.05). We also observed a large correlation cluster between immune regulation pathways (IL-16, GZMA, GZMB, GZMH, KIR3DL1), DNA repair (PARP-1, NBN), and NK cells. We did not observe changes in ZFP levels suggesting a change in epithelial barriers. However, ZFP was associated with immune cell phenotypes (Naive CD4+, Th2 cells).

Conclusion: We observed functional changes in critical immune cells and their proteins during wildfire smoke exposure. Future studies in larger cohorts or firefighters exposed to wildfire smoke should further study immune changes and targets for interventions.