While smoking is a known risk factor for fractures, its precise mechanisms among older women, particularly involving physical function, bone density, and bone microarchitecture, remain incompletely understood. This prospective cohort study included 3,024 community-dwelling Swedish women aged 75-80 years, followed for a median of 7.3 years. Participants were categorized as current smokers (n = 157), former smokers (n = 1,343), and never smokers (n = 1,524). Radiographically verified fractures and all-cause mortality were assessed. Cox proportional hazards models, mediation analyses, and competing risk models evaluated associations between smoking status, fracture risk, and potential mediators, including walking speed and total volumetric bone mineral density (vBMD). Current smokers had significantly increased risks of any fracture (HR 1.35, 95% CI 1.04-1.75) and hip fracture (HR 2.23, 95% CI 1.43-3.49) compared to never smokers. Former smokers exhibited intermediate risks. Women who had ceased smoking for 5-10 years had substantially lower fracture risk than current smokers. Each year since cessation conferred an ~1% relative reduction in fracture and mortality risk. Mediation analyses revealed significant indirect effects via slower walking speed (18-28%) and lower total vBMD, suggesting these factors are key contributors to fracture risk. Importantly, competing risk models confirmed elevated fracture risk in smokers even after accounting for increased mortality. These findings demonstrate that smoking is associated with increased fracture risk in older women, partly through impairments in physical function and vBMD. Smoking cessation appears to confer meaningful skeletal benefits, indicating a need for integrated strategies targeting both behaviour change and physical function to reduce fracture burden in aging populations.
Zoulakis et al. (Tue,) studied this question.