ArticleJournal of lipid and atherosclerosis2026
Association of Smoking Status and Urinary Cotinine Levels With Lipoprotein(a) in Korean Adults.
Article in Journal of lipid and atherosclerosis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Lipoprotein(a) (LP(a)) is a genetically regulated lipoprotein associated with cardiovascular disease. Although primarily heritable, the impact of modifiable factors such as smoking on LP(a) remains unclear, particularly when assessed using objective biomarkers like urinary cotinine. This study examined the association between smoking status-based on both self-reported and cotinine-verified measures-and LP(a) concentrations in Korean adults. Methods: We analyzed 146,129 participants (mean age, 37.1 years; 59.2% men) from the Kangbuk Samsung Health Study from 2011 to 2013. Smoking was defined by self-report (never, former, current) and urinary cotinine ≥50 ng/mL. Serum LP(a) was measured using an immunoturbidimetric assay, with high LP(a) defined as ≥50 mg/dL. Multivariable regression analyses adjusted for relevant covariates. Results: The median LP(a) level was 23.3 mg/dL (interquartile range, 13.4-39.2), and 16.0% of participants had high LP(a). Both cotinine-verified and self-reported current smokers had significantly lower LP(a) levels compared with non-smokers ( Conclusion: Both self-reported and cotinine-verified smoking status were inversely associated with serum LP(a) levels. Although causality cannot be established due to the cross-sectional design, these findings suggest a possible interaction between tobacco exposure and genetically determined LP(a) concentrations, highlighting the need for future longitudinal investigations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.