Influence of cigarette smoking on cardio-inflammatory biomarkers among healthy individuals or cardiopulmonary disorder patients: systematic review and meta-analysis.
Cigarette smoking is linked to increased levels of several inflammatory biomarkers, with more pronounced effects observed in current smokers and males. The findings underscore the importance of smoking cessation programs.
Where it sits
this study against the rest of the elamipretide corpusSummary and findings
This meta-analysis investigated the effects of cigarette smoking on cardio-inflammatory biomarkers in healthy individuals and patients with cardiopulmonary disorders. A total of 55 studies with 116,147 participants were included, measuring biomarkers such as CK-MB, hsCRP, and NT-proBNP. The analysis found significant increases in multiple biomarkers associated with smoking.
Abstract
<h4>Background</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusion</h4>These findings provide a mechanistic link for smoking-related cardiopulmonary risk and reinforce the importance of cessation programs.
Background
Cigarette smoking is recognized as a significant contributor to cardiopulmonary diseases through mechanisms involving chronic inflammation. Previous studies examining the relationship between smoking and cardio-inflammatory biomarkers have produced inconsistent results, necessitating a comprehensive analysis. This meta-analysis aims to clarify the effects of smoking on specific biomarkers associated with inflammation and heart damage.
Methods
A systematic search was conducted across multiple databases, including PubMed, Scopus, Web of Science, and MagIran, up to April 22, 2026. The analysis included case-control studies that measured the effects of smoking on various blood biomarkers, with a total of 55 studies and 116,147 participants. Data were analyzed using a random effects model to calculate unstandardized mean differences, with subgroup analyses performed by smoking status, gender, and health status.
Results
The meta-analysis found significant increases in several biomarkers associated with smoking. Current smokers exhibited widespread elevations in biomarkers, while former smokers showed significant changes only in hsCRP and P-selectin. The analysis indicated that smoking elevated six biomarkers in healthy individuals, whereas only ICAM-1 and hsCRP were elevated in those with cardiopulmonary disease.
Interpretation
The findings support the notion that smoking contributes to a pro-inflammatory state and subclinical heart damage, aligning with previous literature on smoking's detrimental effects. While the statistical significance of the findings is clear, the clinical significance may vary based on individual health status and smoking history. Limitations include potential confounding factors and variability across studies, which may affect the robustness of the conclusions drawn.
Key findings
- Significant increases in CK-MB levels, E-selectin, ICAM-1, NT-proBNP, hsCRP, P-selectin, TnI, and TnT associated with smoking.
- Current smokers showed widespread biomarker elevations; former smokers had significant changes only in hsCRP and P-selectin.
- In healthy individuals, smoking elevated six biomarkers; in those with cardiopulmonary disease, only ICAM-1 and hsCRP were elevated.
Limitations
- Potential confounding factors not accounted for.
- Variability in individual studies may affect results.
- Inconclusive results for VCAM-1 due to wide confidence intervals.