Jun Liu, Jihong Zhang, Zhou Guo, Zhipeng Wang, Song Zhou, Junming Huang
Higher urinary NNAL was associated with an increased likelihood of OA, with more prominent effects observed in middle-aged adults. Given the cross-sectional design, temporality and causality cannot be established, and the potential association requires confirmation in longitudinal and mechanistic studies.
INTRODUCTION: Osteoarthritis (OA) is the most prevalent degenerative joint disorder globally, yet the impact of smoking on its development remains contentious. The compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a principal metabolite of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is a well-recognized biomarker for smoking exposure. This study aimed to use urinary NNAL as a biomarker to evaluate the association between tobacco exposure and OA.
METHODS: This study was a secondary cross-sectional analysis of pooled data from the 2007-2012 cycles of the National Health and Nutrition Examination Survey (NHANES), including 10848 adults. OA was assessed using self-reported physician diagnosis and radiographic examination, with a Kellgren-Lawrence grade ≥2 indicating radiographic OA; urinary NNAL concentration was used as the biomarker of tobacco exposure. Survey-weighted multivariable logistic regression analysis and subgroup analyses were performed after adjusting for confounding factors.
RESULTS: Elevated urinary NNAL concentrations were positively associated with greater odds of OA. In the fully adjusted model, urinary NNAL concentrations >0.077925 ng/mL were associated with greater odds of OA (adjusted odds ratio, AOR=1.55; 95% CI: 1.36-1.76). Evidence of interaction was observed for age (p for interaction <0.001), but not for sex (p=0.231) or BMI (p=0.127). Among adults aged <60 years, the AOR for the highest versus lowest NNAL category was 1.69 (95% CI: 1.46-1.95), whereas the corresponding AOR was 0.98 (95% CI: 0.82-1.17) among adults aged ≥60 years.
CONCLUSIONS: Higher urinary NNAL was associated with an increased likelihood of OA, with more prominent effects observed in middle-aged adults. Given the cross-sectional design, temporality and causality cannot be established, and the potential association requires confirmation in longitudinal and mechanistic studies.