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These particles also induce the release of IL-5 and IL-13, which play an important role in allergic airway diseases such as asthma, while stimulating type 2 ILCs to produce excess IL-5 and IL-13, leading to airway hyperresponsiveness ( 2.50.2 ) and coarse (PM 102.5 ) particulates could induce the production of nitric oxide (NO), IL-6, and tumor necrosis factor (TNF)- from mouse macrophages, and that the insoluble fractions of PM were more potent than the soluble PM fractions, suggesting that components adsorbed on PM play a role in their toxicity ( Studies of asthmatic murine models demonstrated that PM exposure exacerbated the allergic response by unbalancing T cell response causing airway hyperreactivity together with increased levels of immune cells such as eosinophils, macrophages, and of inflammatory mediators including IgE, IL-4, IL-5, IL-13 and decreases in IFN- ( In a rat model of COPD, PM 2.5 exposure led to a decline in lung function and histopathological changes

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