Is Systemic Inflammation Associated with Passive Smoke Exposure? A Population-Based Observational Study.
10.4070/kcj.2006.36.7.510
- Author:
Hee Yeol KIM
1
;
Sang Hyun IHM
;
Eun Ju CHO
;
Doo Soo JEON
;
Sang Hong BAEK
;
Ho Joong YOUN
;
Man Young LEE
;
Wook Sung CHUNG
;
Chong Jin KIM
;
Ki Bae SEUNG
;
Tai Ho RHO
;
Jae Hyung KIM
;
Kyu Bo CHOI
;
Soon Jo HONG
Author Information
1. Department of Cardiology, College of Medicine, The Catholic University of Korea, Seoul, Korea. cumckhy@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Smoking passive;
Inflammation;
Cotinine;
Epidemiology
- MeSH:
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
- From:Korean Circulation Journal
2006;36(7):510-515
- CountryRepublic of Korea
- Language:English
-
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.
