Exposure to elevated concentrations of PM pollution is associated with increased mortality and exacerbation of cardiopulmonary disease. Recent studies have demonstrated evidence of enhanced PM toxicity during periods of increased photochemistry, characterised by high NO or O; suggesting that seasonality may enhance PM toxicity. Therefore, it has been hypothesised that summer constituents of PM would increase the oxidative potential of ambient PM and consequently, their capacity to activate the adaptive immune system, by promoting dendritic cell maturation.
The PM OP of PM and PM selected from winter [high NO] and summer [high O] periods reflecting whole London collections, pooling samples from roadside and background sites was assessed by quantifying their capacity to oxidise AA and GSH per μg of PM. PM characterization included the determination of transition metals. The cytotoxicity associated to PM (0-20 μg/mL) was assessed after exposure to MDDCs from healthy donors (n=6) following a 24-hour incubation. Cell maturation and human inflammatory cytokines were assessed by examining the expression of CD83, CD86, MHC class I and MHC class II; and IL-8, IL-6, IL-10, IL-23 and IL-12p70 (Th2/Th17) by flow-cytometry.
OP/μg was increased in PM samples collected during the summer period after chelator treatment. Metal concentrations were higher in the summer PM sample, with increased Fe concentrations. PM exposures (10 μg/mL) were associated with a decrease in MHC Class I expression. In contrast, PM collected during the summer period induced a significantly increased expression of MHC Class II (p<0.01), CD83 (p<0.05) and CD86 (p<0.01); and enhanced levels of IL-8, IL-6, IL-23 and IL10 measured in MDDCs after 24 h exposure.
The data presented here using contemporary urban PM showed evidence of elevated OP/μg in the summer PM fraction, reflecting their enrichment with oxidant components. PM is more stimulatory than PM for inducing the maturation of MDDCs in culture. The capacity of PM to promote pro-inflammatory cytokines such as IL-8 and IL-23, likely to promote a Th2 profile, suggests these effects might be linked to worsening of chronic respiratory disease as these mediators are linked to asthma.

Copyright © 2020. Published by Elsevier Inc.