Impact of PM_2.5 components on lung function deterioration and the modifying effects of systemic inflammation in chronic lung disease patients

Background: Previous studies have demonstrated the detrimental effects of PM_2.5 on lung function; however, the specific contributions of its toxic components remain inadequately characterized. The potential synergistic effects of PM_2.5 and systemic inflammation on pulmonary function have not been thoroughly explored. Methods: This national cross-sectional study in China examined the association between long-term PM_2.5 exposure and its constituents (SO₄²⁻, NO₃⁻, NH₄⁺, BC, and OM) with lung function decline in 1182 patients with chronic lung disease, aged 45–89 years. Weighted quantile sum (WQS) analysis identified key toxic components and their combined effects on peak expiratory flow (PEF). Interaction analysis assessed the modifying role of C-reactive protein (CRP). Results: Each interquartile range (IQR) increase in PM_2.5, SO₄²⁻, NO₃⁻, NH₄⁺, BC, and OM exposure was associated with PEF changes of −5.12 % (95 % CI: −9.62 %, −0.40 %), −5.86 % (95 % CI: −10.86 %, −0.57 %), −5.03 % (95 % CI: −9.53 %, −0.31 %), −5.67 % (95 % CI: −10.34 %, −0.77 %), −5.76 % (95 % CI: −10.35 %, −0.93 %), and −4.90 % (95 % CI: −9.27 %, −0.32 %), respectively. BC and SO₄²⁻ were identified as crucial components, with WQS weights of 0.780 and 0.206. Each IQR increase in CRP was associated with a −1.11 % (95 % CI: −1.88 %, −0.345 %) decrease in PEF, indicating that elevated CRP exacerbates the association between PM_2.5 constituents and PEF. Conclusion: Exposure to PM_2.5 and its key components, particularly BC and SO₄²⁻, significantly impairs lung function in chronic lung disease patients, especially with elevated CRP levels. Targeted mitigation of these emissions and anti-inflammatory strategies are essential for high-risk populations.