Association of air pollutions and systemic inflammation with early cardiovascular-kidney-metabolic syndrome among middle-aged and elderly adults: a cross-sectional study from CHARLS

Ambient air pollution and systemic inflammation are recognized as risk factors for cardiovascular-kidney-metabolic (CKM) syndrome. However, the joint effect on middle-aged and elderly people in China remains unclear. This research aimed to explore the association between the long-term effects of air pollution/C-reactive protein (CRP) and early CKM syndrome. This cross-sectional cohort involved 9293 participants from the China Health and Retirement Longitudinal Study (CHARLS) in 2015 (Wave 3). The concentrations of air pollutants, including fine particulate matter (PM_2.5), inhalable particles (PM₁₀), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), ozone (O₃) and carbonic oxide (CO), were obtained from the ChinaHighAirPollutants (CHAP), which contains estimates of the concentrations of these air pollutants in residences at the city level. CKM syndrome was diagnosed according to the American Heart Association (AHA) definition, and stages 1 and 2 were defined as early stages in this study. Generalized linear model (GLM) was employed to assess the relationship between air pollutants and CKM syndrome, while the interactions between CRP and air pollutants were also included to evaluate the modified impacts of CRP on the air pollution-CKM association. GLM results revealed that per-SD increases in the concentrations of PM_2.5, PM₁₀, SO₂, NO₂, O₃ and CO were corresponded to elevated CKM prevalence, with ORs (95% CI) of 1.209 (1.085-1.346), 1.263 (1.134-1.406), 1.227 (1.098-1.372), 1.182 (1.060-1.317), 1.135 (1.019-1.265) and 1.160 (1.041-1.292), respectively. Stronger correlations were seen among individuals aged ≤ 65 years, males, urban residents and non-smokers. Moreover, CRP was significantly linked to a greater risk of CKM (OR = 1.207, 95% CI 1.126-1.295). Higher concentrations of air pollutants progressively amplified the risk of CKM syndrome associated with elevated CRP. And the adverse effects of air pollutants were most prominent among individuals with moderate, rather than minimal or severe levels of inflammation. Prolonged exposure to air pollutants has been linked to a greater risk of early CKM syndrome, potentially mediated by inflammatory responses. Particularly, CRP modified the air pollutant-CKM relationship in a complex manner, whereas air pollutants showed a more evident modification of the CRP-CKM association. Considering the ageing population and the health burden posed by CKM, interventions should aim to improve air quality and alleviate systemic inflammatory conditions.