Title : Association between serum hydroxy cotinine and inflammatory risk among U.S. adults: A weighted multivariable analysis
Abstract:
Background: C-reactive protein (CRP) is a key biomarker of systemic inflammation and a predictor of cardiovascular disease. Environmental exposure to second-hand smoke, measured via serum hydroxy cotinine levels, may elevate CRP levels and increase inflammatory risk. This study examines the association between second-hand smoke exposure and CRP-defined inflammatory risk among U.S. adults, adjusting for sociodemographic and health-related factors.
Methods: A cross-sectional analysis was conducted using 2015–2018 data from the National Health and Nutrition Examination Survey (NHANES). A weighted cumulative logistic regression model was used to evaluate the association between hydroxy cotinine-defined second-hand smoke exposure and CRP categories (low, intermediate, high risk). Survey design elements, including strata, clusters, and sample weights, were applied. Adjusted models controlled for age, gender, race/ethnicity, income, smoking status, BMI category, and diabetes status.
Results: Of 9,254 adults surveyed, 4,669 met the inclusion criteria for complete-case analysis. In unadjusted models, second-hand smoke exposure was significantly associated with higher inflammatory risk (OR=1.38, 95% CI: 1.09–1.73, p=0.0096). In the fully adjusted model (Model 3), the association weakened and lost statistical significance (OR=1.28, 95% CI: 0.95–1.72, p=0.0969). Independent predictors of elevated CRP included female gender (OR=1.74, 95% CI: 1.41–2.14), higher BMI (OR=0.25 for normal vs. overweight/obese, p<0.0001), and diabetes status (OR=0.38 for normal vs. diabetic, p=0.0001). Never smokers were less likely to have elevated CRP (OR=0.80, 95% CI: 0.66–0.95, p=0.0173).
Conclusion: Second-hand smoke exposure shows a marginal association with elevated CRP levels after controlling for key covariates. Obesity, diabetes, and gender are stronger predictors of systemic inflammation. These findings underscore the multifactorial nature of inflammatory risk and support continued public health efforts to reduce environmental tobacco exposure.
