CLINICAL STUDY: ENDOTHELIAL FUNCTION
The impact of heavy passive smoking on arterial endothelial function in modernized Chinese
Kam S. Woo, MD, FRACP, FACC*,
Ping Chook, MD*,
Hok C. Leong, MD ,
Xin S. Huang, MD and
David S. Celermajer, PhD, FRACP
* Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, People's Republic of China
Department of Medicine, Kiang Wu Hospital, Macau, People's Republic of China
Department of Medicine, University of Sydney, Sydney, Australia
Manuscript received December 30, 1999;
revised manuscript received March 30, 2000,
accepted June 2, 2000.
Reprint requests and correspondence: Prof. K. S. Woo, c/o Department of Medicine and Therapeutics, Prince of Wales Hospital, Shatin, Hong Kong, Peoples Republic of China kamsangwoo{at}cuhk.edu.hk
OBJECTIVES
The study evaluated whether heavy exposure to environmental tobacco smoke (passive smoking) might damage arterial function in modernized Chinese.
BACKGROUND
Heavy passive smoking is associated with arterial endothelial dysfunction in Caucasian, but not rural Chinese, subjects.
METHODS
We studied 20 young (mean age 36.6 ± 7.0 years) nonsmoking asymptomatic casino workers (9 men) in Macau who were exposed to environmental tobacco smoke for over 8 h/day for at least two years and 20 normal subjects (control subjects). These two groups were carefully matched for age, gender, body mass index (BMI), blood pressure, vessel diameter, cholesterol and glucose levels. Brachial artery diameter was measured by high-resolution B-mode ultrasound at rest, after flow increase (causing flow-mediated endothelium-dependent dilation) and after sublingual nitroglycerin (an endothelium-independent dilator).
RESULTS
Flow-mediated dilation (mean ± SD% of diameter changes) was significantly lower in passive smokers (6.6 ± 3.4%) compared with the controls (10.6 ± 2.3%) (p < 0.0001). Nitroglycerin-induced dilation of the two groups were similar. Upon multivariate analysis, passive smoking exposure was the strongest independent predictor (ß = 0.59; p = 0.0001) for impaired flow-mediated endothelium-dependent dilation (model R2 = 0.75, F value = 6.1, p = 0.0001).
CONCLUSIONS
In modernized Chinese, as in Caucasians, exposure to heavy environmental tobacco smoke causes arterial endothelial dysfunction, a key early event in atherosclerosis. This may have serious implications for cardiovascular health in China, currently in a process of rapid modernization.
|
Abbreviations and Acronyms
| | BMI | = body mass index | | BP | = blood pressure | | FMD | = flow-mediated dilation | | HC | = total plasma fasting homocyst(e)ine | | HDL-C | = high-density lipoprotein cholesterol | | LDL-C | = low-density lipoprotein cholesterol | | NO | = nitric oxide | | NTG | = nitroglycerin-induced dilation | | TC | = total cholesterol | | TG | = triglyceride |
|
This article has been cited by other articles:

|
 |

|
 |
 
K. Kallio, E. Jokinen, O. T. Raitakari, M. Hamalainen, M. Siltala, I. Volanen, T. Kaitosaari, J. Viikari, T. Ronnemaa, and O. Simell
Tobacco Smoke Exposure Is Associated With Attenuated Endothelial Function in 11-Year-Old Healthy Children
Circulation,
June 26, 2007;
115(25):
3205 - 3212.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. G. Maresh, H. Xu, N. Jiang, C. G. Gairola, and R. V. Shohet
Tobacco smoke dysregulates endothelial vasoregulatory transcripts in vivo
Physiol Genomics,
May 11, 2005;
21(3):
308 - 313.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. L. Bots, J. Westerink, T. J. Rabelink, and E. J.P. de Koning
Assessment of flow-mediated vasodilatation (FMD) of the brachial artery: effects of technical aspects of the FMD measurement on the FMD response
Eur. Heart J.,
February 2, 2005;
26(4):
363 - 368.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
X. Zhang, X. O. Shu, G. Yang, H. L. Li, Y. B. Xiang, Y.-T. Gao, Q. Li, and W. Zheng
Association of Passive Smoking by Husbands with Prevalence of Stroke among Chinese Women Nonsmokers
Am. J. Epidemiol.,
February 1, 2005;
161(3):
213 - 218.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. D. Brook, B. Franklin, W. Cascio, Y. Hong, G. Howard, M. Lipsett, R. Luepker, M. Mittleman, J. Samet, S. C. Smith Jr, et al.
Air Pollution and Cardiovascular Disease: A Statement for Healthcare Professionals From the Expert Panel on Population and Prevention Science of the American Heart Association
Circulation,
June 1, 2004;
109(21):
2655 - 2671.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. S. Barua, J. A. Ambrose, L.-J. Eales-Reynolds, M. C. DeVoe, J. G. Zervas, and D. C. Saha
Heavy and light cigarette smokers have similar dysfunction of endothelial vasoregulatory activity: An in vivo and in vitro correlation
J. Am. Coll. Cardiol.,
June 5, 2002;
39(11):
1758 - 1763.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
B.-q. Zhu, R. E Sievers, A. E. Browne, R. T Hillman, K. Chair, R. J Lee, K. Chatterjee, S. A Glantz, and W. W Parmley
The renin-angiotensin system does not contribute to the endothelial dysfunction and increased infarct size in rats exposed to second hand smoke
Journal of Renin-Angiotensin-Aldosterone System,
March 1, 2002;
3(1):
54 - 60.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Zitzmann, M. Brune, B. Kornmann, J. Gromoll, S. von Eckardstein, A. von Eckardstein, and E. Nieschlag
The CAG Repeat Polymorphism in the AR Gene Affects High Density Lipoprotein Cholesterol and Arterial Vasoreactivity
J. Clin. Endocrinol. Metab.,
October 1, 2001;
86(10):
4867 - 4873.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|