Korean Circ J.  2006 Jul;36(7):510-515. 10.4070/kcj.2006.36.7.510.

Is Systemic Inflammation Associated with Passive Smoke Exposure? A Population-Based Observational Study

• Kim HY
• Ihm SH
• Cho EJ
• Jeon DS
• Baek SH
• Youn HJ
• Lee MY
• Chung WS
• Kim CJ
• Seung KB
• Rho TH
• Kim JH
• Choi KB
• Hong SJ

• KMID: 2227099
• DOI: http://doi.org/10.4070/kcj.2006.36.7.510

Abstract

BACKGROUND AND OBJECTIVES: Passive smoking increases the risk of cardiovascular disease, but the factors responsible for this association remain largely unknown. We sought to determine whether passive smoke exposure is associated with systemic inflammation in a dose-dependent fashion, which is a known risk factor for cardiovascular events.
SUBJECTS AND METHODS
We analyzed the data of self-reported non-smokers, > or =40 years of age, who were from the Third National Health and Nutrition Examination Survey (n=6,595). We quantified the passive nicotine exposure by dividing the non-smokers into quartiles, as based on the serum cotinine values. We used multiple linear and logistic regression models to determine the independent relationship between serum cotinine and the levels of C-reactive protein, fibrinogen and leukocytes, and the platelet expression.
RESULTS
After adjustments were done for age, gender, body mass index and race, the participants in the highest serum cotinine quartile (quartile 4) had circulating platelet, fibrinogen and homocysteine levels that were 6,893/microliter higher (95% confidence interval [CI]: 1,886 to 11,900/microliter, p=0.007), 8.74 mg/dL (95% CI: 2.63 to 14.84 mg/dL, p=0.005) and 0.90 micromol/L (95% CI: 0.36 to 1.43 (micromol/L, p=0.001), respectively, than in those in the lowest quartile of serum cotinine (quartile 1). There was a dose-dependent increase in the circulating fibrinogen, homocysteine and platelet levels across the quartiles of cotinine.
CONCLUSION
These findings indicate that even among nonsmokers, elevated serum cotinine is an independent risk factor for systemic inflammation. This suggests that passive smoke exposure promotes systemic inflammatory response in a dose-dependent fashion. These observations may explain why passive smoking is a risk factor for atherosclerosis and cardiovascular events.

Keyword

Smoking passive; Inflammation; Cotinine; Epidemiology

MeSH Terms

Atherosclerosis
Blood Platelets
Body Mass Index
C-Reactive Protein
Cardiovascular Diseases
Continental Population Groups
Cotinine
Epidemiology
Fibrinogen
Homocysteine
Humans
Inflammation*
Leukocytes
Logistic Models
Nicotine
Nutrition Surveys
Observational Study*
Risk Factors
Smoke*
Tobacco Smoke Pollution
C-Reactive Protein
Cotinine
Fibrinogen
Homocysteine
Nicotine
Smoke
Tobacco Smoke Pollution