Discussion
PDDE, lung inflammation
LUNG INFLAMMATION, SECONDARY, RECRUITMENT
Due to the world’s continued reliance on diesel engines and particulate-filtering technology in the transportation sector, co-exposure to DE or PDDE and an environmental allergen is commonplace. This post-hoc study provided an interesting opportunity to provide insight on potential mechanisms by which individual genotypes may be influencing exposure-response phenotypes. However, our present work is a secondary analysis not outlined in our primary design. Therefore, our report is exploratory and hypothesis-generating. Accordingly, we did not perform multiplicity adjustments. Our group has previously demonstrated that co-exposure to allergen and DE or PDDE increases AHR in individuals The GRS was derived from risk alleles in Activated macrophages produce IL-1α High GRS participants showed no significant change in AHR or immune cell recruitment in the DE and allergen co-exposure. The exposure-induced production of the immune mediators IL-1α, MCP-1, IL-6, and TNFα was also reduced with increasing GRS in the DE-A condition. This is contrasted by a previous study that determined that DE and allergen co-exposure causes lung inflammation and DE exposure alone increases non-allergic inflammatory markers and MCP-1The current study has several limitations. Firstly, different allergens in varying concentrations were used to challenge the participants. There may be allergen-specific immune reactions that could complicate this study’s findings. Likewise, the BAL was performed at 48 h post-exposure, thereby limiting our ability to analyze more immediate changes in immune cell recruitment. The modest sample size in our study as well as interindividual variability may also be limiting. To assess potential outlier effects, we performed an analysis that removed the participant with the highest GRS score (Table 