Kim Dong-Bin, Oh Yong-Seog, Yoo Ki-Dong, Lee Jong-Min, Park Chan Seok, Ihm Sang-Hyun, Jang Sung Won, Shim Byung Ju, Kim Hee-Yeol, Seung Ki Bae, Rho Tai-Ho, Kim Jae-Hyung
Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Int Heart J. 2010 May;51(3):183-7. doi: 10.1536/ihj.51.183.
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.
吸烟与血浆同型半胱氨酸水平升高有关，而两者均与心血管疾病风险增加相关。然而，关于被动吸烟对非吸烟者同型半胱氨酸水平影响的信息却很少。我们分析了来自第三次全国健康与营养检查调查中自我报告从不吸烟的人群（年龄≥20岁，n = 3232）的数据。我们根据血清可替宁值将从不吸烟者分为四分位数来量化被动尼古丁暴露。使用多元线性和逻辑回归模型来确定血清可替宁浓度与同型半胱氨酸、维生素B12和叶酸水平之间的任何独立关系。同型半胱氨酸水平升高定义为浓度大于第80百分位数。叶酸或维生素B12水平降低定义为浓度小于第20百分位数。在调整年龄、性别、体重指数、种族、叶酸和维生素B12水平后，发现可替宁水平升高（四分位数III和IV）与高同型半胱氨酸血症相关。血清同型半胱氨酸水平在可替宁四分位数间呈强烈的非线性增加。多变量分析表明，年龄、男性、非白种人、叶酸和维生素B12水平低以及血清可替宁升高（四分位数II-IV）与同型半胱氨酸水平升高独立相关。总之，这些发现表明，从不吸烟者中的被动吸烟暴露与血浆同型半胱氨酸水平呈正相关且独立相关，且存在剂量依赖性。这些发现可能有助于进一步确定被动吸烟与心血管事件之间的联系。
