Key result
Cotinine-verified smoking linked to ~5% lower odds of high Lp(a) versus non-smoking.
Why the study?
Although lipoprotein(a) is primarily genetically regulated, the impact of modifiable factors like smoking on its concentrations remains unclear, particularly when assessed using objective biomarkers like urinary cotinine.
Is smoking status associated with serum Lipoprotein(a) concentrations in Korean adults?
Population
146,129 participants from the Kangbuk Samsung Health Study
Comparison
Smoking status by self-report and urinary cotinine levels
Design
Cross-sectional study
Authors
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No clinical action warranted from smoking-Lp(a) link; leaves causality and CV relevance open for prospective study.
Cross-Sectional (n=146,129)
No
Is smoking status associated with serum Lipoprotein(a) concentrations in Korean adults?
Effect estimate: OR 0.946 (95% CI 0.910-0.982)
Absolute Event Rate: 13.9% vs 16.7%
p-value: p=0.005
Smoking status, verified by both self-report and urinary cotinine, is inversely associated with serum Lipoprotein(a) levels in Korean adults.
Kim et al. (2026) conducted a cross-sectional in General population (n=146,129). Cotinine-verified smoking vs. Cotinine-verified non-smoking was evaluated on High Lipoprotein(a) (≥50 mg/dL) (OR 0.946, 95% CI 0.910-0.982, p=0.005). Cotinine-verified smoking was significantly associated with reduced odds of high lipoprotein(a) levels compared to non-smoking (OR 0.946).