Background: Wildfires are increasingly common with wildfire smoke affecting millions globally, yet its impact on immune responses is poorly understood.
Objective: This real-world study, conducted on participants in the Pfizer BNT162b2 COVID-19 vaccine trial, studied the effects of wildfire smoke exposure on long-term vaccine immunity.
Methods: We recruited 52 healthy, non-smoking individuals (ages 26-83) who were either vaccinated (Group 1, n=28) or placebo injected (Group 2, n=24) during heavy wildfire smoke conditions. Group 2 subjects received vaccination several months later, outside of wildfire season. Blood was taken before and 1 month after vaccine or placebo injections, and 6 months after vaccination. We analyzed intracellular cytokines, B and NK cell markers by flow cytometry, and serum immunoglobulin levels against common coronaviruses using multiplex assays.
Results: A robust spike receptor-binding domain (S-RBD)-specific IgG response observed 1 month post booster, declined variably 6 months later. Wildfire smoke acutely increased IL-13 expression by CD56 NK cells at the time of vaccination, that negatively correlated with anti-S-RBD IgG (r=-0.41, p<0.05). Total IgG levels positively correlated with the air quality index (AQI) measured during vaccination (r=0.96, p<0.01). Similarly to age (but not sex, BMI or race/ethnicity), the two-week AQI averages during vaccination showed a significant negative correlation with anti-S-RBD IgG levels 6 months later (r=-0.41, p<0.05).
Conclusion: Wildfire smoke may lead to inappropriate immunoglobulin production and diminished vaccine immunity. We highlight a previously unrecognized pathway involving NK-cell derived IL-13 and non-specific B-cell activation and underscore the significance of environmental exposures in shaping immunity.
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