Multi-cohort study demonstrates higher adiposity and cardiovascular risk in never-smoking adults, highlighting secondhand smoke reduction as a key obesity prevention target.
Passive smoking remains a common environmental exposure, yet its contribution to obesity in adults is poorly understood. We analysed data from three nationally representative cohorts—the Korean National Health and Nutrition Examination Survey, the US National Health and Nutrition Examination Survey, and the UK Biobank—comprising 321,903 never smokers. Passive smoking was assessed using cohort-specific questionnaires and serum cotinine where available. In a subset of UK Biobank participants with repeated measurements, clinically relevant weight gain was defined as an increase of ≥ 0·5 standard deviation in baseline body-mass index (BMI). Multivariable regression models, random-effects meta-analyses, and mediation analyses were applied. Passive smoking was associated with higher overall and central adiposity across all cohorts, with a pooled 20% higher odds of overweight or obesity (odds ratio 1·20, 95% CI 1·00–1·40). Dose–response patterns were observed across exposure intensity and serum cotinine levels. During follow-up, passive smoking was consistently associated with clinically relevant weight gain, with adjusted odds ratios of 1·46 (1·15–1·84) within < 5 years, 1·30 (1·14–1·49) within 5–10 years, and 1·46 (1·26–1·70) after ≥ 10 years. Passive smoking was also associated with increased risk of major adverse cardiovascular events, of which approximately 33·5% was accounted for by differences in BMI. Among never-smoking adults, passive smoking was associated with higher adiposity, sustained weight gain, and increased cardiovascular risk, supporting the integration of secondhand smoke prevention into population-level obesity prevention strategies.
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