Key result
Cigarette smoking is linked to elevated cardio-inflammatory biomarkers, including a ~0.05 mg/L increase in hsCRP.
Why the study?
Cigarette smoking causes cardiopulmonary disease via chronic inflammation, but individual studies evaluating its effects on cardio-inflammatory biomarkers have yielded inconsistent results.
Does cigarette smoking increase cardio-inflammatory biomarkers in healthy individuals and cardiopulmonary disorder patients?
Meta-Analysis (n=116,147)
Does cigarette smoking increase cardio-inflammatory biomarkers in healthy individuals and cardiopulmonary disorder patients?
Mean Difference: 0.05 (95% CI 0.04–0.06)
p-value: p=<0.001
Cigarette smoking is associated with significant elevations in multiple cardio-inflammatory biomarkers, indicating subclinical myocardial injury and systemic inflammation that is most severe in current smokers and males.
Supports smoking cessation counseling; leaves open whether biomarker changes mediate cardiovascular outcomes.
Background Cigarette smoking is a leading cause of cardiopulmonary disease through chronic inflammation, but individual studies on its effects on cardio-inflammatory biomarkers have yielded inconsistent results. This meta-analysis synthesizes evidences of smoking on cardio-inflammatory biomarkers. Methods A systematic search was conducted across PubMed, Scopus, Web of Science, and MagIran up to April 22, 2026. Case-control studies measuring the effect of smoking on specific blood biomarkers (CK-MB, E-selectin, P-selectin, TnI, TnT, hsCRP, ICAM-1, VCAM-1, NT-proBNP) were included. Data were analyzed using a random effects model to calculate unstandardized mean differences. Subgroup analyses were performed by smoking status, gender, and health status. A total of 55 studies comprising 116,147 participants were included. Results Meta-analysis revealed that smoking was associated with significant increases in CK-MB levels, E-selectin, ICAM-1, NT-proBNP, hsCRP, P-selectin, TnI, and TnT. For VCAM-1, the analysis was inconclusive due to wide confidence intervals. Subgroup analysis showed that current smokers had widespread biomarker elevations, whereas former smokers showed significant changes only in hsCRP and P-selectin. Gender-specific analyses indicated more pronounced biomarker elevations in males. By health status, smoking elevated six biomarkers in healthy individuals but only ICAM-1 and hsCRP in those with cardiopulmonary disease. This study confirms that smoking promotes a pro-inflammatory state and subclinical heart damage, as shown by a distinct biomarker profile. The impact varies by exposure and sex, being most severe in current smokers and males, with lingering effects after cessation. Conclusion These findings provide a mechanistic link for smoking-related cardiopulmonary risk and reinforce the importance of cessation programs.
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Hassanpour et al. (2026) conducted a meta-analysis in Healthy individuals or cardiopulmonary disorder patients (n=116,147). Cigarette smoking vs. Non-smokers was evaluated on hsCRP levels (MD 0.05, 95% CI 0.04-0.06, p=<0.001). Cigarette smoking was associated with significant increases in multiple cardio-inflammatory biomarkers, including hsCRP (MD 0.05 mg/L), indicating a pro-inflammatory state and subclinical heart damage.
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