Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults
David S. Celermajer, Ph.D., Mark R. Adams, M.B., B.S., Peter Clarkson, M.B., B.S., Jacqui Robinson, R.N., Robyn McCredie, B.Sc., Ann Donald, and John E. Deanfield, M.B., Ch.B.
Background Passive smoking has been linked to an increased riskof dying from atherosclerotic heart disease. Since endothelialdysfunction is an early feature of atherogenesis and occursin young adults who actively smoke cigarettes, we hypothesizedthat passive smoking might also be associated with endothelialdamage in healthy young-adult nonsmokers.
Methods We studied 78 healthy subjects (39 male and 39 female)15 to 30 years of age (mean ±SD, 22±4): 26 controlsubjects who had never smoked or had regular exposure to environmentaltobacco smoke, 26 who had never smoked but had been exposedto environmental tobacco smoke for at least one hour daily forthree or more years, and 26 active smokers. Using ultrasonography,we measured the brachial-artery diameter under base-line conditions,during reactive hyperemia (with flow increase causing endothelium-dependentdilatation), and after sublingual administration of nitroglycerin(an endothelium-independent dilator).
Results Flow-mediated dilatation was observed in all controlsubjects (8.2±3.1 percent; range, 2.1 to 16.7) but wassignificantly impaired in the passive smokers (3.1±2.7percent; range, 0 to 9; P<0.001 for the comparison with thecontrols) and in the active smokers (4.4±3.1 percent;range, 0 to 10; P<0.001 for the comparison with the controls;P = 0.48 for the comparison with the passive smokers). In thepassive smokers, there was an inverse relation between the intensityof exposure to tobacco smoke and flow-mediated dilatation (r= -0.67, P<0.001). In contrast, dilatation induced by nitroglycerinwas similar in all groups.
Conclusions Passive smoking is associated with dose-relatedimpairment of endothelium-dependent dilatation in healthy youngadults, suggesting early arterial damage.
Passive smoking, which includes exposure to both sidestreamsmoke from burning cigarettes and exhaled mainstream smoke,has been associated with increased respiratory symptoms in children1and excess deaths from lung cancer in adults.2 However, thegreatest morbidity and mortality related to passive smokinghave been attributed to atherosclerotic heart disease in middleand old age; this factor may account for up to 20,000 deathsannually in nonsmokers in the United States alone.3-6
Studies in laboratory animals have shown that passive smokingmay increase atherosclerosis in cholesterol-fed rabbits7 andin cockerels,8,9 but few studies have assessed the effects ofpassive smoking on the arterial wall in humans. Since endothelialdysfunction is an early feature of atherogenesis in vitro,10in laboratory animals,11 and in humans,12,13 it may representan important marker of early vascular damage. We therefore studiedendothelial function in the arteries of healthy teenagers andyoung adults (mean age, 22 years) who had no known risk factorsfor atherosclerosis other than prolonged exposure to environmentaltobacco smoke.
Methods
Subjects
We studied 78 subjects 15 to 30 years of age; all had normalblood pressure, did not have diabetes, and had no history ofhyperlipidemia or family history of premature vascular disease.They were clinically well and taking no regular cardiovascularmedications. Subjects were recruited from among friends, families,hospital staff, and other community volunteers. All subjectsgave informed consent, and the study was approved by the institutionalcommittees on ethical practice.
The control subjects were 26 lifelong nonsmokers who had neverbeen regularly exposed to environmental tobacco smoke at home(both parents or any other cohabitants or both had been nonsmokerswhile the subjects had been living with them) or in the workplace.The passive-smoking group consisted of 26 lifelong nonsmokerswith self-reported histories of exposure to environmental tobaccosmoke at home or at work or both for at least one hour per dayfor at least three years, and the active-smoking group consistedof 26 subjects who were active smokers, with self-reported smokinghistories of at least two pack-years. One pack-year was definedas 20 cigarettes per day for one year, or the equivalent. Inthe passive-smoking group, the average intensity of exposureto environmental tobacco smoke was assessed by questionnaireas light (one to three hours per day), moderate (four to sixhours per day), or heavy (more than six hours per day).
Study Design
Each subject made one visit to the study hospital, during whicha medical history was taken, the supine resting blood pressurewas measured, saliva was collected for later analysis of thecotinine concentration by rapid gas–liquid chromatography,14and the vascular reactivity of the brachial artery was analyzed.Except in the control subjects, the amount of time since thelast exposure to active or passive smoke was less than 24 hoursin every case. Total cholesterol was measured in 70 of 78 subjects(the other 8 had not consented to venesection) at the same timeas or within 12 months of the arterial studies, with the useof a Hitachi 747 AutoAnalyzer. In cases in which fasting sampleswere available, triglycerides were measured with the AutoAnalyzer,high-density lipoprotein was measured after precipitation withdextran sulfate magnesium, and low-density lipoprotein was calculatedby means of the Friedewald formula.15
The ultrasound method for measuring endothelium-dependent andendothelium-independent arterial dilatation has been describedpreviously.13,16 The brachial-artery diameter was measured onB-mode ultrasound images, with the use of a 7.0-MHz linear-arraytransducer and a standard Acuson 128XP/10 system (Mountain View,Calif.). In all studies, scans were obtained with the subjectat rest, during reactive hyperemia, again with the subject atrest, and after sublingual administration of nitroglycerin.The subjects lay quietly for at least 10 minutes before thefirst scan. The brachial artery was scanned in longitudinalsection 2 to 15 cm above the elbow, and the center of the arterywas identified when the clearest picture of the anterior andposterior intimal layers was obtained. The transmit (focus)zone was set to the depth of the near wall, because of the greaterdifficulty of evaluating the "m" line (the interface betweenmedia and adventitia) of the near wall as compared with thatof the far wall.17 Depth and gain settings were set to optimizeimages of the interface between the lumen and the arterial wall,images were magnified with the use of a resolution box function(leading to a video line width of approximately 0.065 mm), andmachine-operating settings were not changed during any study.
When a satisfactory transducer position was found, the skinwas marked and the arm remained in the same position throughoutthe study. A resting scan was obtained, and the velocity ofarterial flow was measured with a pulsed-Doppler signal at a70-degree angle to the vessel, with the range gate (1.5 mm)in the center of the artery. Increased flow was then inducedby the inflation of a pneumatic tourniquet placed around theforearm (distal to the scanned part of the artery) to a pressureof 250 mm Hg for 4.5 minutes, followed by release. A secondscan was performed continuously for 30 seconds before and 90seconds after deflation of the cuff, including a repeated recordingof flow velocity for the first 15 seconds after the cuff wasreleased. Thereafter, 10 to 15 minutes was allowed for recoveryof the vessel, after which an additional resting scan was performed.Sublingual nitroglycerin spray (400 µg) was then administered,and three to four minutes later the last scan was performed.
Data Analysis
The diameter of the vessel was measured in every case by twoindependent observers who were unaware of the results of thequestionnaire, the smoking status of each subject, and the stageof the experiment. Flow-mediated dilatation and nitroglycerin-induceddilatation were calculated by each observer, and the averageresults of the two observations were recorded. We have previouslyshown that this method is accurate and reproducible for measuringsmall changes in arterial diameter,18 with low rates of interobservererror in measuring flow-mediated dilatation.13,16
The arterial diameter was measured at a fixed distance froman anatomical marker (such as a fascial plane or a vein seenin cross section) with the use of ultrasonic calipers. Measurementswere taken from the anterior to the posterior "m" line at end-diastole,coincidently with the R wave on a continuously recorded electrocardiogram.For the reactive-hyperemia scan, measurements of diameter weretaken 50 to 60 seconds after deflation of the cuff. Four cardiaccycles were analyzed for each scan, and the measurements foreach observer were averaged. The vessel diameter in scans obtainedafter reactive hyperemia and the administration of nitroglycerinwas expressed as a percentage of the average diameter of theartery in the two resting (or control) scans (considered as100 percent). Volume flow was calculated by multiplying thevelocity–time integral of the Doppler flow signal (correctedfor angle) by the heart rate and the cross-sectional area ofthe vessel ( x r2). The flow velocity used in our calculationwas measured in the center of the artery; absolute flow maytherefore be overestimated, but relative flow values beforeand after cuff inflation are accurate.19 Reactive hyperemiawas calculated as the maximal flow recorded in the first 15seconds after cuff deflation divided by the flow during thefirst resting (base-line) scan.
Statistical Analysis
Descriptive data are expressed as means ±SD. An analysisof variance for the three groups was performed, followed byScheffé's test for multiple comparisons, to allow pairwisetesting for significant differences between the groups.20 Inthe control subjects and passive smokers, the relation betweenflow-mediated dilatation and intensity of exposure to environmentaltobacco smoke (0 = none, 1 = light, 2 = moderate, and 3 = heavy,as defined above) was assessed by one-way analysis of variance.The determinants of flow-mediated dilatation were then assessedby multiple linear regression analysis, with flow-mediated dilatationas the dependent variable and age, sex, blood pressure, totalcholesterol concentration, vessel size, and intensity of exposureto environmental tobacco smoke as the independent variables.Similar analyses were also performed with nitroglycerin-induceddilatation as the dependent variable. Statistical significancewas inferred at a two-tailed P value of less than 0.05.
Results
Base-Line Characteristics
The subjects had an average age of 22±4 years (range,15 to 30), with similar ages in the three groups studied (Table 1).There were 13 male subjects and 13 female subjects in eachof the control, passive-smoking, and active-smoking groups.Other important base-line characteristics — such as bloodpressure; total, low-density lipoprotein, and high-density lipoproteincholesterol levels; and vessel size and flow at rest —were also similar in all three groups.
Table 1. Base-Line Characteristics of 26 Control Subjects, 26 Passive Smokers, and 26 Active Smokers.
Among the passive smokers, exposure to environmental tobaccosmoke was light for nine subjects, moderate for nine, and heavyfor eight. The duration of passive smoking was 16±8 years(range, 3 to 28); 17 of 26 subjects (65 percent) had been exposedto environmental tobacco smoke throughout childhood. For theactive smokers, cigarette consumption was 7±4 pack-years(range, 2 to 19), and the intensity of exposure was 19±8cigarettes per day (range, 8 to 35).
Vascular-Study Results
The degree of reactive hyperemia produced by cuff inflationand release was similar in the three groups studied (Table 2).In response to this increase in flow, arterial dilatation was8.2±3.1 percent (range, 2.1 to 16.7) in the controls.
Table 2. Vascular-Study Results for 26 Control Subjects, 26 Passive Smokers, and 26 Active Smokers.
In the passive smokers, flow-mediated dilatation was significantlyreduced (3.1±2.7 percent; range, 0 to 9; P<0.001 forthe comparison with the controls) (Figure 1A). Flow-mediateddilatation was impaired in both the male passive smokers (3.2±2.5percent, vs. 7.3±1.9 percent in the controls; P<0.001)and the female passive smokers (3.0±2.9 percent, vs.9.1±3.9 percent in the controls; P<0.001). Flow-mediateddilatation was 4.1±3.3 percent in the subjects with lightexposure to environmental tobacco smoke, 3.1±2.2 percentin those with moderate exposure, and 1.8±2.0 percentin those with heavy exposure (Figure 2).
Figure 1. Comparison of Flow-Mediated Dilatation (Panel A) and Nitroglycerin-Induced Dilatation (Panel B) in 26 Controls, 26 Passive Smokers, and 26 Active Smokers.
Horizontal lines represent the mean values for each group. Flow-mediated dilatation was significantly impaired in the passive and active smokers as compared with the control subjects, whereas nitroglycerin-induced dilatation was similar in all three groups.
Figure 2. Relation between the Intensity of Exposure to Passive Smoking (None, Light, Moderate, or Heavy) and Flow-Mediated Dilatation in 52 Healthy Nonsmoking Teenagers and Young Adults.
For each category of intensity of exposure to environmental tobacco smoke, the box represents the interquartile range (between the 25th and 75th percentiles), with the mean shown as a horizontal bar within each box. The bars outside each box show the range of 95 percent of all values.
In the group of 52 nonsmokers, flow-mediated dilatation wasinversely related to the intensity of exposure to environmentaltobacco smoke on both univariate regression analysis (r = -0.67,P<0.001) and multiple regression analysis (partial r = -0.72,P<0.001). Even in the group of passive smokers only, flow-mediateddilatation was inversely related to the intensity of exposureto environmental tobacco smoke (r = -0.39, P = 0.04). Salivarycotinine levels were not significantly correlated with flow-mediateddilatation on either univariate or multivariate analysis.
In the active smokers, flow-mediated dilatation was 4.4±3.1percent (range, 0 to 10), which was significantly less thanthat in the controls (P<0.001) but similar to the value inpassive smokers (P = 0.48). If the group of passive smokerswas excluded, there was an inverse correlation between flow-mediateddilatation and the number of cigarettes smoked daily (r = -0.57,P<0.001).
In the controls, nitroglycerin-induced dilatation was 18.5±5.2percent (range, 9.5 to 31.8). This response was not impairedin the passive smokers, at 16.4±5.1 percent (range, 8.1to 26.5), or in the active smokers, at 17.2±5.4 percent(range, 8 to 28; P = 0.33) (Figure 1B and Table 2). On multivariateanalysis of the group as a whole, nitroglycerin-induced dilatationwas inversely related to vessel size (P<0.001) but was notsignificantly related to age, sex, blood pressure, or totalcholesterol level.
Discussion
Active cigarette smoking has long been known to predispose peopleto atherosclerotic vascular disease,21 but it has recently becomeevident that exposure to environmental tobacco smoke may alsohave deleterious cardiovascular effects, with enormous publichealth implications.3-6 This study shows that endothelial dysfunction,an important early feature of the atherogenic process, may occurin the systemic arteries of healthy teenagers and young adultsas a result of passive smoking. The impairment of endothelium-dependentdilatation is dose-related and may be equivalent to the degreeof vascular abnormality found in age-matched active smokers.
Environmental tobacco smoke consists of approximately 85 percentsidestream smoke (from the burning ends of cigarettes) and 15percent exhaled mainstream smoke.5 Since cigarettes burn athigher temperatures during inhalation, combustion is more complete,and some toxic components of tobacco smoke are broken down orfiltered out before inhalation. Consequently, many toxic constituents,such as carbon monoxide and benzopyrene, are found in higherconcentrations in sidestream than in inhaled smoke,4 and morethan 4000 chemicals are contained in environmental tobacco smoke.5One or more of these compounds may be injurious to the arterialwall; in laboratory animals, exposure to environmental tobaccosmoke is associated with endothelial dysfunction and with acceleratedatherosclerosis.7-9 Environmental tobacco smoke in both lowand high doses increases the percentage of the aorta coveredby atheroma in cholesterol-fed rabbits,7 and exposing cockerelsto levels of environmental tobacco smoke routinely encounteredby people in smoke-filled environments is associated with anincrease in the size of aortic atheroma plaques.8,9 Sun et al.22have shown that dietary supplementation with l-arginine (theprecursor of nitric oxide, or endothelium-derived relaxing factor)protects cholesterol-fed rabbits from the endothelial dysfunctionassociated with exposure to environmental tobacco smoke, suggestingthat impaired endothelial production of nitric oxide may bepathogenetically important in this animal model of atherosclerosisrelated to environmental tobacco smoke.
We have previously reported impaired endothelium-dependent dilatationin young cigarette smokers.16 In humans, however, there havebeen few data to associate passive smoking with damage to thearterial wall. Short-term exposure to environmental tobaccosmoke is associated with an increase in circulating damagedendothelial cells and also with a tendency toward enhanced plateletaggregation.23-26 It may also be associated with mild coronary-arteryvasoconstriction in nonsmoking adults.27 Passive smoking mayhave adverse effects on lipid profiles,28,29 but in this studythe impairment of vascular reactivity observed in the passivesmokers was not related to the lipid levels, which were similarto those of the control subjects. Passive smoking may also beassociated with an increased thickness of the intima–medialayer of the common carotid artery,30 by an unknown mechanism.
In this study, we have shown that passive smokers have significantlyimpaired arterial endothelial function. Impaired bioavailabilityof nitric oxide, the endothelium-derived relaxing factor, maybe particularly important, since nitric oxide acts to inhibitplatelet aggregation, the adhesion of monocytes to the arterialwall, and proliferation of smooth-muscle cells.31 Dilatationmediated by brachial-artery flow is endothelium-dependent32and is mediated in large part by the release of nitric oxide.33Therefore, our results suggest that the activity of endothelialnitric oxide may be impaired in young passive smokers as wellas in active smokers. In vitro work has also suggested thatdecreased nitric oxide bioactivity might be implicated in smoke-relatedendothelial dysfunction.34 The actual mechanism responsiblefor this arterial damage is not known but may be related tothe effects of tobacco smoke on interactions between plateletsand the vessel wall or on oxidation products or lipid componentsthat change with long-term exposure to smoke.26,29,35,36 Thetoxic substance or substances involved appear to be presentin both environmental and inhaled cigarette smoke.
All the passive smokers in this study were exposed to environmentaltobacco smoke for at least one hour daily. The intensity ofexposure to environmental tobacco smoke depends on a large numberof variables, such as the number of hours of exposure per day,the proximity to the active smoker (or smokers), the numberof active smokers in the home or the workplace, and the sizeand ventilation of the rooms where passive smoking occurs. Therelation between the extent of exposure to environmental tobaccosmoke and endothelial physiology was assessed by structuredquestionnaire rather than by salivary cotinine levels. The latterproved useful in indicating that there were probably no activesmokers in the passive-smoking group and helped substantiateexposure to environmental tobacco smoke in these subjects. Thevalues reflect only recent exposure over a short time (two tofour days) to only one component of smoke, however, and arethus of limited value in quantifying overall exposure to environmentaltobacco smoke. There was, nevertheless, an inverse relationbetween an intensity score for passive smoking, based on thenumber of hours of exposure per day, and endothelium-dependentarterial dilatation. This dose-dependent relation between passivesmoking and endothelial dysfunction is similar to that betweenactive smoking and arterial injury16 and is consistent with(but does not prove) a causative role for environmental tobaccosmoke in the early stages of atherogenesis.
We deliberately studied passive smokers with a heavy environmentalexposure, and the active smokers were young, with light-to-moderatesmoking histories. In this study, the degree of impairment ofendothelium-dependent responses was similar in the active andthe passive smokers. This clearly does not imply equivalentexposure to smoking-related products, however, nor does it allowcomparison of the susceptibility of the arterial wall to damagefrom active smoking with that from passive smoking.
We have previously described this noninvasive method for thein vivo assessment of endothelium-dependent and endothelium-independentarterial dilatation in children and young adults and have foundthe method to be accurate and reproducible.13,16,18 Becausewe studied healthy young adults without known atherogenic riskfactors, such as diabetes or hypertension, which have been shownto cause impaired vascular reactivity,37,38 we were able toinvestigate the effects of passive and active smoking themselveson endothelial physiology. Although it is possible that someunidentified risk factor was present in the passive or activesmokers but not in the controls, the frequency of the majorknown atherogenic risk factors was similar in all three groups.Although only superficial systemic arteries can be studied withthis ultrasound-based method, endothelial dysfunction in thebrachial artery appears to be well correlated with both coronaryendothelial physiology39 and coronary atherosclerosis.40
Large-scale epidemiologic studies have consistently linked passivesmoking to an excess risk of atherosclerotic heart disease,and some authors have suggested that tens of thousands of prematuredeaths in nonsmokers may be related to passive smoking, withthe large majority due to cardiac ischemia.3,4,5,6 We have nowshown that passive smoking is associated, in a dose-dependentmanner, with significant endothelial dysfunction, a key earlyevent in atherogenesis, in healthy teenagers and young adults.
Supported by grants from the National Health and Medical ResearchCouncil of Australia (to Dr. Celermajer), the National HeartFoundation of Australia (to Dr. Adams), the Royal AustralasianCollege of Physicians, the British Heart Foundation (to Dr.Deanfield and Dr. Clarkson), and the Coronary Artery DiseaseResearch Association (to Ms. Donald).
We are indebted to Robyn Richmond and Abilio de Almeida Netofor assistance with the recruitment of subjects for this study.
Source Information
From the Department of Cardiology, Royal Prince Alfred Hospital (D.S.C., M.R.A., J.R., R.M.), and the Heart Research Institute (D.S.C., J.R., R.M.), Sydney, Australia; and the Cardiothoracic Unit, Hospital for Sick Children, London (P.C., A.D., J.E.D.).
Address reprint requests to Dr. Celermajer at the Department of Cardiology, Royal Prince Alfred Hospital, Missenden Rd., Camperdown 2050, Sydney, Australia.
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x r2). The flow velocity used in our calculation was measured in the center of the artery; absolute flow may therefore be overestimated, but relative flow values before and after cuff inflation are accurate.19 Reactive hyperemia was calculated as the maximal flow recorded in the first 15 seconds after cuff deflation divided by the flow during the first resting (base-line) scan. 
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