Roles of smoke exposure and inflammatory biomarkers in cognitive function among older adults: Findings from two prospective cohort studies.

BackgroundMany studies have established associations between smoke exposure and both accelerated cognitive decline and systemic inflammation. However, their interrelationship remains unclear.ObjectiveThis study aims to provide novel insights into the tripartite relationships linking smoke exposure, inflammatory biomarkers, and cognitive function among older adults.MethodsThis study analyzed data from 2503 participants in the National Health and Nutrition Examination Survey (NHANES, 2011-2014) and 3263 participants in the China Health and Retirement Longitudinal Study (CHARLS, 2011-2012). Serum cotinine was mainly used to assess smoke exposure in NHANES, while self-reported smoking status was used in CHARLS. Cognitive function was assessed using standard cognitive tests in NHANES and CHARLS. Inflammatory biomarkers included NLR, SII, leukocyte, neutrophil and lymphocyte in NHANES and leukocyte in CHARLS. Linear regression, nonlinear threshold effect models, and mediation analysis examined associations and mediating effects.ResultsHigher cotinine was associated with lower cognitive scores in NHANES (β = -0.219, p < 0.001). In CHARLS, current smokers exhibited lower cognitive scores than never-smokers (β = -0.090, p = 0.004). Neutrophil and leukocyte showed linear relationship with cognitive function in NHANES, while other inflammatory indicators showed significant nonlinear threshold effects. Mediation analysis revealed that neutrophil and leukocyte partially mediated 7.39% and 9.75% of the smoke-cognitive decline association.ConclusionsSmoking is related to cognitive decline in older adults from two national cohorts, with neutrophil and leukocyte partly mediating this link in the U.S. cohort. Interventions for smoking cessation and inflammation reduction may help mitigate cognitive decline.