Several studies support the finding of increased IL-17 signaling in PM2.5 exposure [51–53], specifically involving enhanced Th17 cell differentiation and increased IL-17 secretion through activation of the aryl hydrocarbon receptor by polycyclic aromatic hydrocarbons (PAHs) present in PM2.5, leading to an inflammatory response and potential exacerbation of lung diseases [53]. This evidence concerns the gene IL17A and lung disorder.