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, People’s Republic of China
kamsangwoo{at}cuhk.edu.hk
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Abstract
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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.
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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 |
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Cigarette smoking is an important risk factor for development of atherosclerosis, including coronary artery disease (1,2). This detrimental effect is not limited to active smoking. Exposure to environmental tobacco smoke (passive smoking) is also associated with increased cardiovascular risk in reports from Western countries (3,4). Furthermore, in healthy young Caucasian adults, prolonged passive smoke exposure is associated with arterial endothelial dysfunction, a key early event in atherogenesis (5).
We have previously reported that in healthy young adults in rural China compared with Caucasians (6), cigarette smoking may be associated with lesser effects on arterial endothelial function. Whereas active smokers in China develop arterial endothelial dysfunction, albeit to a less extent when compared with modernized Caucasians, passive smoking exposure has a minimal impact on arterial endothelial function. This suggests the possibility of relative protection in rural Chinese, in terms of cigarette-related arterial endothelial dysfunction (7). Many regions of China, however, including Hong Kong, Macau, Shanghai, and Beijing, are now rapidly undergoing modernization of diet and lifestyle. Because passive smoking is widespread in mainland China, it will be important to establish the effects of passive smoke on vascular disease in such "modernized," as opposed to rural, Chinese subjects. The present study has therefore evaluated the impact of exposure to heavy passive smoking on arterial endothelial function in modernized Chinese living in Macau, the "Monte Carlo of the Orient."
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Subjects and methods
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Subjects.
We studied 20 nonsmoking healthy young casino workers in Macau who were exposed to environmental tobacco smoke at their workplace for over 8 h per day six days a week for at least two years (passive smokers). Twenty age- and gender-matched nonsmoking (both active and passive) subjects in other wide varieties of employment from manual laborers to sedentary executives served as controls; these had been enrolled in an ongoing community atherosclerosis study performed in healthy volunteers attending Macau’s Kiang Wu Hospital. This is part of the multicenter community atherosclerosis study in aged and young Chinese carried out in mainland China, Hong Kong, Sydney, and San Francisco, as described previously (7–9). None of these subjects had diabetes mellitus or any history of hyperlipidemia, hypertension, or family history of premature vascular disease. All were clinically well and taking no regular cardiovascular medications. All subjects gave informed consent in their native language. The study was approved by the institutional committee on ethical practice.
Study design.
Each subject made a visit to the Kiang Wu Hospital in Macau, during which a medical history was taken, supine blood pressure (BP) measured, height and weight were recorded, and vascular reactivity of brachial artery was studied. Body mass index (BMI) was calculated as weight (kg) divided by height (m2). In every case, venous blood was sampled after >12 h of fasting for analysis of lipid levels; it was done on the same day or within one week of the vascular reactivity study.
Fasting serum cholesterol (TC) and triglycerides (TGs) were assayed enzymatically by using the Boehringer Mannheim Hitachi 911 analyzer at the Prince of Wales Hospital in Hong Kong. High-density lipoprotein cholesterol (HDL-C) was measured after precipitation with phosphotungstate-magnesium. Low-density lipoprotein cholesterol (LDL-C) was calculated by means of the Friedewald formula as described previously (10). The core laboratory at the Prince of Wales Hospital is currently accredited, with intra-assay imprecision of cholesterol measurement <3% and accuracy standardized by the Center for Disease Control, National Heart, Lung, and Blood Institute (U.S.) program.
Vascular reactivity studies.
All scans were performed by the same operator (X.S.H.). The ultrasound method for measuring vascular reactivity (endothelium-dependent and endothelium-independent arterial dilation) has been described in detail previously (5–8). In brief, the diameter of the brachial artery was measured on B-mode ultrasound images, using Advanced Technology Laboratory HDI system (Bothell, Washington), with a L10 5-MHz (mid-frequency of 7.5 MHz) linear-array transducer. In all studies, longitudinal scans of the brachial artery were obtained at rest, then during reactive hyperemia produced by inflation of a pneumatic tourniquet placed on the forearm to a pressure of 250 mm Hg for 4 min, followed by release (with increased flow-producing endothelium-dependent dilation) and finally after 400 µg sublingual nitroglycerin (an endothelium-independent dilator). Doppler-derived arterial flow was measured at rest and during hyperemia as described previously (5–8). The accuracy, reproducibility, and low inter-observer error for such measurement of arterial physiology have all been demonstrated previously (11). Endothelium-dependent dilation of the brachial artery is mainly due to nitric oxide (NO) release by the endothelium (12) and correlates well with coronary endothelial function in the same subjects (13).
Data analysis.
In every case, the diameter of the artery was measured by an independent observer (P.C.), who was blinded to the identities of the subjects and the stage of the experiment. Endothelium-dependent and nitroglycerin-induced dilation NTG (expressed as percent change in vessel diameter) were calculated, as described elsewhere (5,6,8,14). Reactive hyperemia was calculated as the maximal flow recorded in the first 15 s after cuff deflation, divided by rest flow (5).
Statistical analysis.
Descriptive data are expressed as mean value ± SD, unless otherwise stated. The baseline characteristics and vascular physiological responses of the two groups were compared by independent sample t tests. The prospectively defined primary end point of this study was endothelium-dependent flow-mediated dilation (FMD), and all other comparisons were adjusted for multiple tests by use of Hochberg’s modification of the Bonferroni procedure (15). The determinants of endothelium-dependent dilation and NTG were assessed by multiple linear regression analysis, with age, passive smoking (yes/no), duration of exposure to environmental tobacco smoke, gender, BP, TC, HDL-C or LDL-C, BMI, degree of hyperemia, and vessel size entered as independent variables. Statistical significance was inferred at a two-tailed p value of <0.05.
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Results
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Baseline characteristics.
Of the 20 passive smokers, 9 were men and 11 were women. Their mean age was 36.6 ± 7.0 years. They were exposed to environmental tobacco smoke for >8 h a day, six days a week, for 9.2 ± 6.1 years (range 2 to 24 years). Their total, HDL and LDL cholesterol levels, were all within the normal range for southern Chinese (16,17). The two groups were well matched for age, gender, BMI, BP, fasting blood lipids, glucose, folate, total plasma homocyst(e)ine (HC) levels, and vessel size (Table 1).
Vascular reactivity.
Mean brachial artery diameters were similar. Reactive hyperemia after cuff release was >600% in each group studied. In response to this, the FMD was 10.6 ± 2.3% in the controls and 6.6 ± 3.4% in the passive smokers (mean difference: 4%; 95% confidence interval [CI]: 3–5.4%) (p < 0.001) (Table 2) (Fig. 1). It was impaired in both the male (p < 0.001) and female passive smokers (p < 0.001) compared with controls. By contrast, nitroglycerin-induced responses were similar in the two groups (Table 2) (Fig. 1). No correlation was seen between the duration of environmental passive smoking and the impaired FMD (r = 0.1, p = 0.63). Upon multivariate analysis, passive smoking was the strongest predictor of impaired FMD (ß = –0.59, p = 0.001), independent of the effects of age, gender, and the other variables measured (model R2 = 0.75; F value = 6.1; p = 0.0001). When such analysis was performed with nitroglycerin-induced response as the dependent variable, neither passive smoking nor any of the other measured variables was significantly related to this parameter.
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Figure 1 Flow-mediated endothelium-dependent dilation (FMD) and nitroglycerin-induced dilation (NTG) in control and passive smoking subjects (PS). The FMD in the passive smokers was significantly lower (p < 0.0001) than in the controls, but NTG responses of the two groups were similar (p = 0.2). In each box plot, the bottom and top of the box represent the 25th percentile and the 75th percentile, respectively. The line across each box represents the median value, and the vertical lines encompass the entire range of values for each group of the participants.
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Discussion
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Dose-related arterial endothelial dysfunction in passive smoke–exposed young adults has been documented in Caucasian subjects, the extent of which may be equivalent to the vascular abnormality found in age-matched active smokers (5). Such detrimental effects of environmental tobacco smoke (85% sidestream and 15% inhaled smoke) have been related to carbon monoxide, benzopyrene, or other toxic substances in both sidestream and inhaled smoke, some of which may be found in higher concentration in sidestream than in inhaled smoke owing to incomplete combustion (3,4). These toxic substances may be injurious to arterial wall, causing endothelial dysfunction (5) and accelerating atherosclerosis in animal experiments (18–20). In humans, impaired endothelial production and bioavailability of NO (21), enhanced platelet aggregation (22), coronary artery spasm (23), and adverse effects on lipid profiles have been associated with passive smoking (24). By contrast, rural Chinese seem to be relatively protected from the effects of environmental tobacco smoke on arterial endothelial function (6).
The present study suggests that heavy environmental tobacco smoke exposure is associated with vascular dysfunction in modernized as opposed to rural young adult Chinese. Greater intensity of exposure to environmental tobacco smoke (>8 h a day) and a closer proximity to multiple active smokers in a more enclosed environment in the casino may contribute to this observed difference. Equally plausible, however, is that some environmental aspect(s) of the modernization process may enhance the susceptibility of these subjects to the deleterious effects of environmental tobacco smoke. A genetic difference is unlikely, as the majority of subjects studied in Macau originate from southern China, and Pun Yu village (where we studied the rural Chinese) is only 50 miles away. Consistent with the potentially harmful vascular effects of modernization in the Chinese population, we have recently demonstrated a higher incidence of subclinical atherosclerosis (carotid intima-media thickening) among modernized Chinese in Sydney, Australia, and Hong Kong, compared with rural Chinese in southern mainland China (9). Potentially pro-atherogenic change of lifestyles and dietary habits were observed in modernized Chinese, with consumption of more meat, deep-fried food, and dairy products, but less flavonoid-containing plant protein, green vegetables, and tea (25).
Apart from passive smoking, the two study groups had no traditional atherosclerosis risk factors. Their lipid profiles were similar to the levels we reported previously in urban southern Chinese (16,17). Likewise, their HC levels, reported to be higher in cigarette smokers (26), were similar and within normal physiological range in the two groups. For the elucidation of the nature of possibly protective environmental factors, perhaps other emerging risk factors should be explored in rural and modernized Chinese, including plasma phytoestrogen, LDL-C oxidizability, and particle size (27–29).
Significance and implications.
Cigarette smoking remains highly prevalent (70% of men, 10% of women) in most parts of mainland China (30), and passive exposure to environmental tobacco smoke is common and often unavoidable. The present findings that passive smoking impairs arterial endothelial function (a key marker of early atherosclerosis) in asymptomatic modernized Chinese may have an important public health and medical–legal implications in China, now in a rapid and widespread process of modernization. Large numbers of subjects in mainland China may therefore be vulnerable to the hazards related to passive smoking in the future, with potentially serious consequences. Similar interactions among risk factors, ethnicity, and atherogenesis may also exist for other environmental and risk factors, such as diabetes mellitus, hypercholesterolemia, and hypertension. These are also becoming more prevalent in China, and further prospective study of these issues is warranted.
Arterial endothelial dysfunction is not only relevant to primary prevention of atherosclerotic diseases; it has been recently reported that among patients with angina pectoris, impaired FMD of brachial artery may be independently predictive of cardiac events over the next five-year period (31).
Study limitations.
Except for passive smoking, the two groups of subjects were identical in their prevalence of traditional or emerging (plasma folate or homocyst[e]ine) risk factors. It is possible, however, that unmeasured differences existed between the groups. Difference in psychological stress factor is unlikely to be prevalent, as the casino employee (passive smokers) should have been well adapted to their routine work in the casino. There has been difficulty in quantifying the "dose" of passive smoking with certainty, as the intensity of exposure depends on a large number of variables, such as hours of exposure per day, the proximity to active smokers, the numbers of active smokers in the room, and the size and ventilation of the rooms where passive smoking occurs (5). In the present study, passive smoking was identified and assessed by self-reporting of a structured questionnaire, which we have previously shown to be reliable (5). As a better alternative, air levels of nicotine, carbon monoxide, and other particulates in the exposure room of the casino, or plasma cotinin levels in the studied subjects, can be measured. All the passive smokers have been exposed to heavy environmental tobacco smoke, for >8 h each day at work 6 days a week and for >2 years. They were probably maximally affected by such heavy exposure, the effect of which could reach a plateau. Therefore, no dose-dependent relationship could be established between duration of passive smoking and endothelium-dependent dilation.
Our previous work has documented that endothelial function is unimpaired in rural Chinese passive smokers compared with nonsmoking controls, by contrast to Caucasian counterparts. Thus, a rural Chinese group was not specifically included in this study.
Vascular reactivity may vary with phases of menstrual cycle (32). In the present study, an accurate assessment of menstrual phase was not specifically obtained from the premenopausal women. This should not have confounded our result, as all subjects have been screened at random in relation to their menstrual phase in both groups, and the differences in vascular reactivity between the two groups were seen in both men and women. Similarly, the two groups were gender matched, and differential analyses according to gender are probably not worthwhile in view of the small numbers of subjects studied.
Conclusions.
Though passive smokers in rural China may be protected from developing early arterial damage, exposure to heavy environmental tobacco smoke in more modernized Chinese subjects is associated with significant impairment of endothelial function, independent of age, gender, and traditional risk parameters. This may have adverse implications for cardiovascular risk in modernizing Oriental populations.
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Acknowledgments
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We wish to thank Alice Cheung, research nurse at the Department of Medicine and Therapeutics, The Chinese University of Hong Kong, for assistance with the design of the figure and drafting of the article.
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Footnotes
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This work was supported by a grant from the Hong Kong Heart Foundation Ltd. and the Cardiac Research Fund of the Chinese University of Hong Kong, and the Chinese Atherosclerosis Trust. Dr. Celermajer is supported by the Medical Foundation, University of Sydney.
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Abstract
Subjects and methods