Smoking is associated with increased plasma
homocysteine levels, and both are associated with an increased risk of
cardiovascular disease. However, little information is available on the effects of
passive smoking on the level of
homocysteine in nonsmokers. We analyzed the data of self-reported never-smokers (aged > or = 20 years, n = 3,232), who were from the Third National Health and Nutrition Examination Survey. We quantified the passive
nicotine exposure by dividing the never-smokers into quartiles as based on the serum
cotinine values. Multiple linear and logistic regression models were used to determine any independent relationships between serum
cotinine concentration and levels of
homocysteine,
vitamin B12, and
folate. An elevated
homocysteine level was defined as a concentration greater than the 80th percentile. A reduced
folate or
vitamin B12 level was defined as a concentration less than the 20th percentile.After adjusting for age, gender, body mass index, race,
folate and
vitamin B12 levels, increased
cotinine levels (quartile III and IV) were found to be associated with
hyperhomocysteinemia. There was a strong nonlinear increase in the serum
homocysteine levels across the quartiles of
cotinine. Multivariate analysis showed that age, male gender, non-Caucasian, low levels of
folate and
vitamin B12, and increased serum
cotinine (quartile II-IV) were independently associated with elevated
homocysteine levels. In conclusion, these findings indicate that passive
smoke exposure in never-smokers is positively and independently associated with plasma
homocysteine levels in a dose-dependent manner. These findings may help further determine the link between
passive smoking and cardiovascular events.