Journal o f Behavioral Medicine, Vol. 13, No. 5, 1990

Cardiovascular Responses to a Quantified Dose of Nicotine as a Function of Personality and Nicotine Tolerance C a r m e n L. M a s s o n I and D a v i d G. Gilbert 1,2

Accepted for publication: January 8, 1990

Correlations between cardiovascular effects o f a quantified dose o f nicotine and personality measures previously shown to predict coronary heart disease were obtained. Thirty male smokers s m o k e d a popular brand o f a regular strength cigarette (1.0 mg FTC-estimated nicotine delivery) on one occasion and a nicotine-free cigarette on another occasion by means o f a quantified smoke delivery system. Partial correlations controlling f o r effects o f body weight, questionnaire-assessed nicotine tolerance, and cardiovascular responses to the nico tin e-free con trol cigarette sh o wed Jenkins A ctivit), Survey Type A scores to correlate positively with nicotine-induced increase in diastolic blood pressure but negatively with nicotine-induced increase in systolic blood pressure. Partial correlations indicated that trait anxiety and depression were significantly associated with nicotine-induced heart rate increases but not with nicotine-induced blood pressure responses. KEY WORDS: anger; anxiety; blood pressure; depression; heart rate; hostility; nicotine; smoking.

INTRODUCTION P e r s o n a l i t y traits o f h o s t i l i t y , d e p r e s s i o n , a n x i e t y , a n d r e l a t e d n e g a t i v e e m o t i o n a l states a p p e a r to be risk f a c t o r s f o r a w i d e v a r i e t y o f diseases, This work was supported by a grant from the Office of Research and Development Administration of Southern Illinois University at Carbondale. This article is based on the first author's thesis, which was supervised by the second author. ~Southern Illinois University at Carbondale, Carbondale, Illinois 62901. 2To whom correspondence should be addressed. 505 0160-7715/90/1000-0505506.00/0 9 1990 Plenum Publishing Corporation

506

Masson and Gilbert

including extent and severity of coronary heart disease (CHD) (reviewed by Booth-Kewley and Friedman, 1987; Williams and Barefoot, 1988). Smokers exhibit an increased incidence of CHD and other health problems, as well as negative- affect-related personality traits similar to those that predict disease independent of smoking (Spielberger, 1986). These personality characteristics exist prior to, as well as subsequent to, taking up smoking (Seltzer and Oechsli, 1985; Spielberger, 1986). Thus, it has been suggested that smokers smoke, in part, as a means of self-medication to reduce states of negative affect associated with neurotic personality traits (Eysenck, 1973; Warburton et al., 1983). Consistent with this self-medication hypothesis, smokers tend to smoke more when they experience anger or other negative emotional states than at other times (Rose et al., 1983; Spielberger, 1986). However, contrary to what one might predict, nicotine has the paradoxical effect of elevating sympathetic nervous system arousal, including heart rate and blood pressure, while simultaneously reducing subjective and behavioral indices of negative affect in many circumstances (Gilbert et al., 1989; Gilbert and Welser, 1989). Since emotional traits (Eysenck, 1967; Navateur and Baque, 1987) and Type A behavior (Harbin, 1989; Houston, 1986) are associated with hyperresponsivity of the sympathetic nervous system (SNS), one could reasonably hypothesize that smoking and nicotine produce relatively larger SNS responses in individuals scoring high in negative emotional traits than in those scoring low in such traits. That is, Type A and highly emotional individuals may be overly reactive not only to psychological/environmental stimuli, but to pharmacological stimuli as well. Thus, heightened activity of the SNS, or underactivity of the parasympathetic nervous system (Muranaka et al., 1988) may be a common biological pathway mediating the relationship between personality and CHD. Individual differences in cardiovascular responsivity to various pharmacological agents have received some attention recently. Individual differences in cardiovascular response to drugs, including isoproterenol (a beta agonist) (Muranaka et al., 1988), caffeine (Li-Neng et al., 1983), and smoking (Cinciripini et al., 1989; Herning et al., 1983) have been reported. While the effects of smoking on cardiovascular function are well documented (Epstein and Jennings, 1986), few studies have assessed individual differences in cardiovascular responses to nicotine as a function of personality differences. The studies that have assessed these associations have been methodologically flawed. Consistent with the view that a basic SNS-related biological mechanism is responsible for the hyperresponsivity of sympathetic end organs observed in Type A individuals, Cinciripini et al. (1989) found Type A's to exhibit larger smoking-related phasic increases in heart rate, relative to Type

Personality Smoking Cardiovascular Response

507

B's. However, Cinciripini and co-workers' findings are confounded due to their failure to monitor or control for individual differences in nicotine intake resulting from individual differences in puff size. In addition, their study did not control for effects associated with the motor act of smoking or for estimated nicotine tolerance. Magnitude of cardiovascular and other acute physiological responses to smoking are a function of amount of nicotine, but not "tar," intake (Epstein and Jennings, 1986). Furthermore, intravenously and otherwise administered nicotine produces, for the most part, the same pattern of physiological response as does smoking (USDHEW, 1988). Thus, the cardiovascular effects of tobacco smoke in experimental investigations, including the present one, are generally referred to as nicotine's effects. In order to control for individual differences in nicotine dose, the present investigation used a previously validated (Gilbert et al., 1988), quantified smoke delivery system (QSDS) to deliver the same, reproducible dose of nicotine to all subjects. In a series of studies in our laboratory the QSDS used in the present study has been found to result in the delivery of reliable doses of nicotine, as assessed by plasma nicotine concentrations and filter pad nicotine assays (Gilbert et al., 1988, 1990). The use of devices such as the QSDS is necessary in investigations of individual differences in response to nicotine via the smoking route since individuals differ greatly in the manner in which they smoke (Wakeham, 1972). These differences in smoking behavior produce large between-subject differences in plasma nicotine concentrations (Herning et al., 1983). Thus, individual differences in cardiovascular responses to normal ad libitum smoking are a function of differences in the actual dose of nicotine obtained as well as differences in responsivity to nicotine. The use of a QSDS allowed us to assess cardiovascular responses to a standard dose of nicotine. Correlations between individual differences in nicotineinduced cardiovascular reactivity and personality variables previously shown to relate to psychologically induced cardiovascular reactivity were determined. There is increasing empirical evidence that nicotine dependence plays a significant role in the maintenance of smoking (USDHEW, 1988). It has also been determined that cardiovascular responses to normal smoking are a function of nicotine dosage (Epstein and Jennings, 1986) as well as to individual differences in responsivity to nicotine (Gilbert and McArthur, 1988). Therefore, the Fagerstrom Tolerance Questionnaire (FTQ), a behavioral estimate of nicotine dependence, was used to control for individual differences in cardiovascular responsivity to nicotine. Studies show that the FTQ correlates with expired CO, plasma nicotine, and nicotine levels (Fagerstrom and Schneider, 1989), measures that reflect daily nicotine intake. In addition, consistent with the view that the FTQ correlates with tolerance to the cardiovascular activating effects of nicotine, Fagerstrom (1978) found a negative

508

Masson and Gilbert

correlation between acute heart rate increases associated with smoking and FTQ scores. These results suggest that smokers who are more physically tolerant, as defined by the FTQ, experience attenuated physiological responses to nicotine compared with less physically tolerant smokers. This is not surprising since physiological tolerance is defined as a reduced physiological responsivity to a substance. However, in contrast to Fagerstrom's results and contrary to this prediction, Lombardo et al. (1988) found that FTQ scores correlated positively with magnitude of heart-rate increase in response to smoking a quantified dose of nicotine. While the experimental design used by Lombardo and associates was superior to that used by Fagerstrom in that it controlled for amount of nicotine intake, it failed to control for nonnicotine-specific activity, including cardiac-somatic coupling, associated with the motor act of smoking. Nonspecific, smoking-related changes in cardiovascular activity due to motoric activity were controlled for in the present study by partialing out cardiovascular responses to the smoking of a tobacco/nicotine-free cigarette. The limited number of studies, their mixed results, and the lack of controls for motor and other activities make it uncertain as to whether or not the FTQ predicts cardiovascular tolerance to nicotine. In addition to the possibility that traits of negative affect may be based on generalized SNS hyperresponsivity, evidence suggests that the physiological pattern of responses associated with anger, fear, and depression differ in important ways (Delp and Sackeim, 1987; Henry, 1986; Schwartz et al., 1981). Thus, the present investigation tested the hypothesis that the pattern of nicotine-induced cardiovascular changes in heart rate and diastolic and systolic blood pressure differ as a function of different emotional traits, Type A behavior pattern, and nicotine tolerance.

METHOD Subjects Thirty male Caucasian students enrolled in introductory psychology courses at a major midwestern university received course credit for their participation in the study. Participants were habitual smokers of 10 or more cigarettes (with a minimum of .7 FTC estimated nicotine delivery) per day for the past year (mean = 17.5; S D = 5.7), and ranged in age from 18 to 35 years (mean = 19.6 years; S D = 2.2 years). Individuals who were current users of any form of psychoactive drug or medication were excluded from the study.

Personality Smoking Cardiovascular Response

509

Apparatus A quantified smoke delivery system similar to the one described in detail by Gilbert et al. (1988) was used to administer quantified doses of cigarette smoke to subjects. Consistent with Federal Trade Commission (FTC) standards for estimating nicotine and "tar" deliveries by machine smoking, the system takes 35-cm 3 2-sec-duration, sinusoidal-shaped puffs at 60-sec intervals. These puffs were drawn by a 60-ml polyethylene syringe with a .25-in.diameter opening. The plunger of the syringe was moved by a mechanical linkage attached to a 15-rpm motor. The cigarette was connected to a twoway valve with a 2.5-cm piece of Penrose drain tubing (5/16-in. diameter). The filter end of the cigarette was placed 8 mm into one end of the drain tubing; the other end was connected to the valve. The remaining opening of the valve was connected to a disposable mouthpiece (a 5-cm-long segment of plastic soda straw) by means of a 2.5-cm length of 5/16-in. Penrose drain tubing. Once the smoke entered the syringe, the two-way valve was turned, allowing the smoke to travel from the syringe to a plastic mouthpiece. The subject then leaned forward and inhaled a puff of smoke from the mouthpiece and held it in his lungs for 5 sec with his mouth open so the experimenter could visually assure that all of the puff was inhaled. Other equipment included a Norelco digital blood pressure device (Model HC-300-1), a Grass Model-AC amplifier (595E) for the measurement of the EKG, and a Catalyst Research carbon monoxide monitor (Model 1000). Subjects were electrically isolated from the EKG channel of the polygraph by an Analog Devices isolation amplifier (Model 292A).

Self-Report Measures Jenkins Activity Survey-Student Version (JAS) (Glass, 1977). The Student version of the JAS was modeled after the original adult version of the JAS (Jenkins et al., 1968), except that items measuring job involvement were modified or deleted (Glass, 1977). This measure is reliable (Yarnold et al., 1986) and validity studies have shown it to correlate with self-esteem, feelings of interpersonal dominance (.40), self-confidence (.24), activity (.52), and need achievement (.17)(Glass, 1977). Buss Durkee Hostility Inventory (BDHI) (Buss and Durkee, 1957). The BDHI is a 75-item scale with reported high (.82) test-retest reliability obtained from a college sample over a 5-week period (Biaggio et al., 1981). This scale has been validated in numerous studies (Biaggio et al., 1981; Ramanaiah et al., 1987; Velicer et al., 1985).

510

Masson and Gilbert

Cook and Medley Hostility Scale (110) (Cook and Medley, 1954). This scale consists of 50 items selected from the MMPI. High test-retest reliability was demonstrated in a sample of physicians after 1 year of testing (.85) (Barefoot et al., 1983). Three independent studies have shown HO to predict CHD incidence and severity (Barefoot et al., 1983; Shekelle et al., 1983; Williams et al., 1980). Profile o f Mood States (POMS) (McNair et al., 1981). The POMS is a 65-item inventory that provides subjective data of feeling, affect, and mood. This instrument contains six oblique factors of which this study used three (Tension-Anxiety, Depression-Dejection, and Anger-Hostility). Validation studies demonstrate an association between POMS scores and emotioninducing conditions and measures of distress (McNair et al., 1981). The present investigation used the trait form of the POMS, in which subjects were asked to indicate how they usually feel. Fagerstrom Tolerance Questionnaire (FTQ) (Fagerstrom and Bates, 1981). This scale was developed to assess degree of physical dependence to nicotine through questions which indirectly assess nicotine intake (number of cigarettes per day and FTC nicotine delivery of habitual cigarette) and questions about the urge to smoke in different situations. The FTQ has been found to predict relapse to smoking after quitting, indices of nicotine intake (blood nicotine and cotinine concentrations and exhaled carbon monoxide levels), and a smoking withdrawal response (body temperature change) and a tolerance response (magnitude of heart rate response to smoking) (reviewed by Fagerstrom, 1978; Fagerstrom and Schneider, 1988). Procedure

Each subject participated in an orientation session and two experimental sessions. During the orientation session the goals of the study were explained, an informed consent form was signed, exhaled breath carbon monoxide concentration was measured, and subjects practiced smoking a cigarette via a quantified smoke delivery system (QSDS). In addition, each subject was required to complete the self-report measures noted above. The day prior to each experimental session, subjects were instructed to abstain from smoking and the use of other drugs (e.g., coffee, alcohol, medications) from midnight of the evening before the upcoming experimental session. Carbon monoxide concentration was obtained at the onset of both experimental sessions to ensure that subjects complied with instructions to refrain from smoking on the morning of the study. During separate experimental sessions subjects smoked a nicotine-free (Free) and a moderatenicotine delivery (1.0-mg) cigarette (Camel Filter) by means of the QSDS. Half of the subjects smoked the nicotine-free cigarette in the first session

Personality Smoking Cardiovascular Response

511

and the tobacco cigarette during the second session; the other half smoked the cigarettes in the reverse order. When smoking from the QSDS, subjects inhaled cigarette smoke at 60-sec intervals. Approximately eight inhalations were required to smoke the cigarette to a point where the char line was 3 mm from the filter overwrap. Smoke from each puff was held in the lungs for 5 sec. Since the QSDS puffs cigarettes at the same rate and volume as estimated by the FTC to be typical of normal smoking behavior, the amount of "tar" and nicotine delivered by this system is proportional to and approximately the same as the FTC machine-estimated "tar" and nicotine delivery of the cigarette. EKG electrodes were attached to the right wrist and left ankle, and a blood pressure cuff was placed around the left arm. Baseline physiological measurements were obtained for 2 min following a 13-min adaptation period.

RESULTS Effects of Nicotine

Effects of nicotine on heart rate (HR) and blood pressure (BP) were assessed with a repeated measures analysis of variance in which the repeated factors were time (baseline, min 4-6 postsmoking, min 19-21 postsmoking) and nicotine dose (0.0 and 1.0 mg). Following the recommendations of Vasey and Thayer (1987), statistical significance of repeated measures effects was based on Geiser-Greenhouse conservative adjustments to the degrees of freedom and Bonferonni multiple-comparisons procedures were used for followup comparisons. Smoking the tobacco cigarette relative to the nicotine-free cigarette was associated with an increase in H R and diastolic blood pressure (DBP) above baseline (see Table I). However, there was no significant effect of nicotine on systolic blood pressure (SBP). Nicotine's effect on H R was demonstrated by a significant nicotine x time interaction [F(2/58) = 45.81, p < .001]. Analyses of simple main effects for H R showed no differences between the nicotine conditions at baseline [F(1/29) = .53]; however, at min 4-6 postsmoking, H R in the nicotine condition was significantly higher than in the nicotine-free condition [F(1/29) = 28.15, p < .001]. Minutes 19-21 postsmoking showed no significant differences between the nicotine and the nicotine-free conditions IF(1/29) = 2.80]. In the nicotine-free condition there was no simple main effect for time, indicating that H R did not differ across time [F(2/58) -- .68]. However, H R changes appeared in the nicotine condition across time [F(2/58) -- 77.02, p < .001]. Bonferonni comparisons of H R in the nicotine condition showed a higher mean H R in min 4-6 as

Nicotine

70.0 (7.6) 84.7 (9.2) 76.1 (8.3)

Free 71.7 (12.3) 72.6 (12.6) 72.5 (10.7)

Nicotine 62.8 (5.8) 69.3 (7.8) 66.5 (7.1)

DBP Free 63.9 (7.8) 63.9 (7.7) 65.8 (6.3)

Nicotine 110.5 (9.0) 114.6 (9.7) 112.0 (12.5)

SBP Free 110.1 (11.7) 112.5 (12.3) 111.0 (10.6)

"The time periods are labeled as follows: T1, baseline; T2, min 4-6 postsmoking; T3, min 19-21 postsmoking.

T1 T2 T3

HR

g (SD)

Table I. Mean Heart Rate and Blood Pressure Across Time for the Nicotine and Nicotine-Free Conditions"

Personality Smoking Cardiovascular Response

513

compared with baseline [F(1/29) = 152.77, p < .001], for min 4-6 versus min 19-21 [F(1/29) = 52.27, p < .001], and for baseline versus min 19-21 [F(1/29) = 26.32, p < .001]. For DBP there was a significant nicotine x time interaction [F(2/58) = 7.36, p < .01]. Simple main effects of nicotine for each of the three time periods for DBP showed no significant differences at baseline between the nicotine and the nicotine-free conditions [F(1/29) = .72]. However, in the nicotine condition at rain 4-6 postsmoking, DBP was significantly higher than in the nicotine-free condition [F(1/29) = 11.76, p < .01]. During rain 19-21 there were no longer any DBP differences between the two nicotine conditions [/7(1/29) = .27]. There was no simple main effect of time within the nicotine-free condition [F(2/58) = 2.34], but DBP did vary with time in the nicotine condition [F(2/58) = 10.96, p < .001]. Bonferonni comparisons in the nicotine condition showed a significant difference between baseline and min 4-6 postsmoking [F(1/29) = 21.90, p < .001] and between baseline and rain 19-21 [F(1/29) = 7.08, p < .05] but no significance between min 4-6 and rain 19-21 [F(1/29) = 4.04, p < .05]. The nicotine x time interaction and nicotine main effect were not significant for SBP [F(2/59) = .49 and F(1/29) = .48, respectively]. However, there were SBP changes across time for both smoking conditions as demonstrated by a significant main effect for time [F(2/58) = 4.83, p < .05].

Correlations Among Cardiovascular, Personality and Tolerance Measures Correlations between F T Q scores and personality measures were obtained in order to assess the degree of association a m o n g self-reported nicotine tolerance, Type A behavior, and negative emotional traits. A measure of indirect expression of hostility and mood-trait measures of anxiety, depression, and anger was derived f r o m the B D H I and the POMS, respectively. Tolerance correlated positively with measures of hostility ( B D H I and H O , r = .47, p < .01, and r = .43, p < .01, respectively), a subscale of the B D H I assessing indirect expression o f hostility (BDHI-Indirect, r -- .53, p < .001), Type A behavior (JAS, r = .31, p < .05), and mood-trait measures of depression and anger (POMS-Depression and POMS-Anger, r = .37, p < .05, and r = .35, p < .05, respectively). Change in DBP was negatively associated with F T Q score (r = - .42, p < .05). This negative correlation was also significant when simultaneously controlling for b o d y weight and DBP change scores occurring during the nicotine-flee condition (r = - . 3 6 , p < .05). Weight was partialed on because drug potency is a function of body weight. Physiological change scores during the nicotine-free condition were partialed out in order to control for

514

Masson and Gilbert

individual differences in reactivity associated with motoric and other nonnicotine-specific processes occurring during smoking. FTQ score did not correlate significantly with HR or SBP change scores. In order to determine how closely personality measures assessing Type A behavior, hostility, and mood-traits were associated with physiological change scores in the nicotine condition, partial correlations (one set controlling for body weight and the nicotine-free condition and a second set controlling for FTQ score as well as body weight and nicotine-free condition) were computed (see Table II). Nicotine-induced HR increases correlated positively with mood-trait measures of depression and anxiety. These correlations remained significant after controlling for body weight, nicotine-free conditions, and FTQ score. Further, nicotine-induced HR changes (partialing on body weight, nicotine-free condition, and FTQ score) failed to correlate with Type A behavior r = .29, p = .07). Nicotine-induced change in DBP correlated negatively with the BDHI (r = - . 4 0 , p < .05) when controlling for body weight and DBP change in the nicotine-free condition; however, this significant association was not sustained when controlling for FTQ score, as well as body weight and nicotinefree response. These results suggest that a behavioral estimate of nicotine dependence is an important variable contributing to the relationship between nicotine-induced cardiovascular reactivity and hostility. DBP results also revealed a positive association between Type A behavior and nicotine-induced change when controlling for body weight, nicotine-free condition, and FTQ score (r = .39, p < .05). In contrast, SBP correlated negatively with Type A when controlling for body weight, nicotine-free condition, and FTQ score (r = - . 3 5 , p < .05).

Correlations Among Cardiovascular Measures In order to assess the degree to which nicotine induced similar changes across the three physiological measures, change scores from baseline were calculated. Change scores were obtained by subtracting baseline values from those of min 4-6 of the postsmoking period in the nicotine condition, resulting in separate change score values for HR, DBP, and SBP. HR change and DBP change were positively correlated (r = .33, p < .05), but HR and SBP change scores were not (r -- .00). Further, the relationship of SBP and DBP change scores was not significant (r = -.16). Table II shows that DBP at baseline correlated positively with nicotine-induced changes in SBP after correcting for body weight, physiological response to the nicotine-free cigarette, and FTQ score. Other response measures did not correlate with baseline cardiovascular variables.

.07 - .01 .07 .28 .29 .47** .36* - .27 .04 - .08

.04 - .07 .04 .29 .29 .49** .35* - .26 .03 - .08

Wt/free/TQ -- .40* - . 19 - .31 .28 - .24 - .18 - . 18 .21 - . 19 - .03

Wt/free - .27 .04 - .21 .39* - . 13 - .05 - . 12 .14 - . 18 - .04

Wt/free/TQ

DBP change

.05 10 .20 .39* .04 .08 .17 - .05 .42* - .28

-. -

Wt/free

.06 .03 - . 14 - .35* .12 .18 .23 - . 11 .47** - .31

Wt/free/TQ

SBP c h a n g e

a W t / f r e e c o l u m n v a l u e s a r e p a r t i a l c o r r e l a t i o n s c o n t r o l l i n g f o r b o d y w e i g h t a n d p h y s i o l o g i c a l c h a n g e scores to the n i c o t i n e - f r e e c o n d i t i o n . W t / f r e e / T Q c o l u m n v a l u e s a r e p a r t i a l c o r r e l a t i o n s c o n t r o l l i n g for weight, n i c o t i n e - f r e e p h y s i o l o g i c a l c h a n g e s , a n d T o l e r a n c e Q u e s t i o n n a i r e score. *p < .05. **p < .01.

BDHI BDHI-IN HO JAS POMS-ANG POMS-DEP POMS-ANX HR-base DBP-base SBP-base

Wt/free

HR change

T a b l e I I . P a r t i a l C o r r e l a t i o n s o f H e a r t R a t e a n d B l o o d P r e s s u r e C h a n g e Scores w i t h P e r s o n a l i t y V a r i a b l e s a n d Baseline C a r d i o v a s c u l a r M e a s u r e s "

=..

O

,7

516

Masson and Gilbert

DISCUSSION As predicted, nicotine increased heart rate and diastolic blood pressure, and the magnitude of these effects was dependent on personality. The Fagerstrom behavioral estimate of nicotine dependence correlated only with DBP. The size of these mean changes (12-bpm HR and 5-ram Hg DBP) is comparable to previous findings using cigarettes with typical FTC nicotine deliveries (0.8 to 1.3 mg) (reviewed by Dembroski, 1986; Epstein and Jennings, 1986). However, contrary to the present findings, most previous studies (Dembroski, 1986; Epstein and Jennings, 1986) report significant, though small, nicotine-induced changes for SBP. Our results failed to show a significant difference in mean SBP increases in the nicotine (4.1 mm Hg) relative to the non-nicotine condition (2.4 mm Hg). Type A behavior (Student-JAS) correlated positively with nicotineinduced changes in DBP. However, contrary to predictions, Type A behavior correlated negatively with nicotine-induced changes in SBP. One cannot account for these two correlations in terms of a behavioral estimate of nicotine dependence, body weight, or generalized responsivity, since these effects were controlled for by partial correlational analyses. Therefore, the association between the Type A dimension and blood pressure responsivity appears to be the result of nicotine-specific influences that are differentially involved in the regulation of diastolic and systolic blood pressures. Since nicotineinduced heart rate and diastolic pressure changes were correlated, it is not surprising that HR also tended to correlate with Type A behavior. This correlation of Type A behavior with nicotine-induced HR changes is consistent with predictions and with previous research showing HR hyper-reactivity to smoking in Type A individuals (Cinciripini et al., 1989). The present results for HR and DBP change support the hypothesis that individuals scoring higher on Type A behavior are more cardiovascularly reactive because of some basic biological hyperreactivity of the sympathetic nervous system. However, the reduced SBP response to nicotine seen in Type A individuals in the present study are contrary to this view. The effects on SBP are especially interesting given that previous studies have shown that Type A's are hyperreactive in SBP to psychologically mediated environmental stressors (Myrtek and Greenlee, 1984). It may be that Type A individuals are characterized by a downregulation of the number of cardiac beta-adrenergic receptors because of excessive and frequent activation of this system as they repeatedly try to cope with daily challenges via Type A behavioral patterns. Studies have shown decreases in beta-adrenergic receptors to be a function of the concentration and duration of exposure to agonists (Watanabe et al., 1982). Given the possibility of such down-regulation in Type A individuals, one might expect that pharmacologic challenge by nicotine would be associated with a diminished beta-adrenergic-mediated SBP response.

Personality Smoking Cardiovascular Response

517

Depression and anxiety correlated with nicotine-induced physiological changes in a similar pattern that differed from that observed for Type A behavior. Depression and anxiety correlated positively with nicotine-induced increases in heart rate, but not with blood pressure responses. This similarity in correlational pattern is consistent with the fact that state and trait measures of anxiety and depression tend to be highly correlated (Carson, 1986) and with evidence suggesting that anxiety and depression tend to be more similar to each other than to anger and Type A behavior in terms of their physiological correlates and associated coping styles (passive versus active) (Henry, 1986). Contrary to predictions, the only trait measure of hostility to correlate with cardiovascular responsivity was the Buss-Durkee scale. Previous research has demonstrated a positive association between the acute experience of anger and increased DBP (Ax, 1953; Roberts and Weerts, 1982). In contrast, the present study found a significant negative correlation for Buss-hostility trait and nicotine-induced DBP changes. However, this correlation was no longer significant when controlling for Fagerstrom Tolerance Questionnaire score. Thus, it appears that a greater degree of self-reported nicotine dependence in individuals with high Buss-Durkee hostility was responsible for the negative association between diastolic response to nicotine and Buss-Durkee hostility. The highly significant correlation between Buss-hostility and FTQ score is consistent with this view. Further evidence of a hostility-tolerance link is provided by the observation that FTQ score, like Buss-Durkee hostility, correlated negatively with DBP changes. Based on the observation that smokers who experience depression, anxiety, or irritability more frequently habitually consume more cigarettes than more emotionally stable individuals (Spielberger, 1986), one would expect individuals high in negative emotional traits to score high on the FTQ. Consistent with this expectation, FTQ score was significantly positively correlated with Type A behavior, hostility (BDHI, BDHI-Indirect, and HO) and mood-trait measures (POMS-Depression and POMS-Anger). Since nicotine reduces negative affect in some conditions (Gilbert, 1979; Gilbert and Welser, t989), it may be that persons who experience high degrees of negative affect attempt to alleviate discomfort by self-medicating with smoking (Warburton et al., 1973). Our results support the view that the FTQ is, to a limited extent, a measure of tolerance to nicotine's cardiovascular activating effects. FTQ score correlated in the predicted negative direction with DBP response to nicotine challenge, although it failed to do so with HR or SBP responses. Evidence consistent with the view that high FTQ scores are associated with lower cardiovascular responses to nicotine was provided by Fagerstrom (1978), who found a significant negative association between FTQ scores and nicotineinduced HR changes. However, his findings for the validity of the FTQ as

518

Masson and Gilbert

a measure of HR tolerance to nicotine were not supported by the present results, or by a previous investigation assessing the validity of the FTQ (Lombardo et al., 1988). The observed differences across studies may be attributable to the failure of Fagerstrom's study to control for nicotine dose, body weight, and non-nicotine-specific responsivity to smoking. Although plasma nicotine concentrations were not assessed in the present investigation, there is reason to believe that reliable, standardized doses of nicotine were in fact administered. Previous studies in our laboratory found the use of the QSDS in the manner applied in the present study to result in reliable nicotine filter pad deliveries and plasma concentrations (Gilbert et al., 1988, 1990). These studies have shown the variances in plasma nicotine across subjects associated with QSDS smoking to be much smaller than with ad libitum smoking. Since smokers' plasma nicotine concentrations vary with intravenously administered standard doses of nicotine to about the same degree as in our previous QSDS studies (Feyerabend et al., 1985), the small variances in plasma nicotine observed in our previous QSDS studies were most likely due primarily to slight unreliabilities in plasma nicotine assays and to individual differences in pharmacokinetics of nicotine, rather than differences in nicotine dose of the inhaled smoke. Nonetheless, in the present study it is impossible to rule out the theoretical possibility that the correlations of cardiovascular responses with FTQ and personality are a result of slight differences in plasma nicotine. The ideal study would assess plasma nicotine changes associated with QSDS smoking. It is important to note that the FTQ may be a valid measure of certain very important aspects of nicotine tolerance and dependence without correlating negatively with any or all cardiovascular responses to quantified doses of nicotine. For example, it may be that the FTQ adequately assesses individual differences in the degree to which individuals develop noncardiovascular (e.g., electrocortical, subjective, or behavioral) tolerance to and dependence upon nicotine. It is unlikely that all physiological and behavioral response systems respond equally to nicotine challenges and have equal tendencies to develop tolerance to nicotine. In summary, the present findings showed that nicotine-induced changes in cardiovascular measures tend to be associated with personality variables and FTQ score. Consistent with predictions that different personality traits are associated with differential patterns of cardiovascular responsivity, Type A behavior and Buss-Durkee hostility differed from trait depression and anxiety. Type A behavior was negatively associated with nicotine-associated changes in SBP, while DBP and HR were correlated in the expected direction. However, for Buss-Durkee hostility the association was in a negative direction and disappeared when controlling for a behavioral measure of nicotine dependence. In contrast, measures of emotionality (depression and anxiety) correlated positively only with HR changes. The differential pattern of

Personality Smoking Cardiovascular Response

519

c o r r e l a t i o n s b e t w e e n p e r s o n a l i t y v a r i a b l e s a n d c a r d i o v a s c u l a r m e a s u r e s suggests t h a t d i f f e r e n t p e r s o n a l i t y traits a r e a s s o c i a t e d w i t h d i f f e r e n t u n d e r l y ing b i o l o g i c a l m e c h a n i s m s . F i n a l l y , t h e p r e s e n t s t u d y p r o v i d e s s u p p o r t f o r t h e use o f q u a n t i f i e d s m o k e d e l i v e r y in t h e a s s e s s m e n t o f i n d i v i d u a l d i f f e r ences in r e s p o n s e t o n i c o t i n e .

REFERENCES

Ax, A. F. (1953). The physiological differentiation between anger and fear in humans. Psychosom. Med. 15: 433-442. Barefoot, J. C., Dahlstrom, W. G., and Williams, R. B., Jr. (1983). Hostility, CHD incidence, and total mortality: A 25-year follow-up study of 255 physicians. Psychosom. Med. 45: 59-63. Biaggio, M. K., Supplee, K., and Curtis, N. (1981). Reliability and validity of four anger scales. J. Person. Assess. 45: 639-648. Booth-Kewley, S., and Friedman, H. S., (1987). Psychological predictors of heart disease: A quantitative review. Psyehol. Bull 101: 343-362. Buss, A. H., and Durkee, A. (1957). An inventory for assessing different kinds of hostility. J, Consult. PsychoL 21: 343-349. Carson, T. P. (1986). Assessment of depression. In Ciminero, A. R., Calhoun, K. S., and Adams, H. E. (eds.), Handbook o f Behavioral Assessment, John Wiley, New York. Cinciripini, P. M., Nezami, E., and Mace, R. M. (1989). Cardiovascular reactivity and smoking in coronary prone (Type A) and non-coronary prone (Type B) subjects. Addict. Behay. 14: 83-90. Cook, W. W., and Medley, D. M. (1954). Proposed hostility and phasic-virtue scales for the MMP1. J. Appl. Psyehol. 38: 414-418. Delp, M. J., and Sackeim, H. A. (1987). Effects of mood on lacrimal flow: Sex differences and asymmetry. Psyehophysiology 24: 550-556. Dembroski, T. M. (1986). Overview of classic and stress-related risk factors: Relationship to substance effects on reactivity. In Matthews, K. A., Weiss, T. M., Falkner, B., Manuck, S. B., and Williams, R. B., Jr. (eds.), Handbook o f Stress, Reactivity, and Cardiovascular Disease, John Wiley and Sons, New York, pp. 275-291. Epstein, L. H., and Jennings, J. R. (1986). Smoking, stress, cardiovascular reactivity, and coronary heart disease. In Matthews, K. A., Weiss, S. M., Dembroski, T. M., Falkner, B., Manuck, S. B., and Williams, R. B., Jr. (eds.), Handbook o f Stress, Reactivity, and Cardiovascular Disease, John Wiley and Sons, New York, pp. 291-309. Eysenck, H. J. (1967). The Biological Basis o f Personality, Charles C Thomas, Springfield, Ill. Eysenck, H. J. (1973). Personality and the maintenance of the smoking habit. In Dunn, W. L., Jr. (ed.), Smoking Behavior: Motives and Incentives, Winston, Washington, D.C. Fagerstrom, K.-O. (1978). Measuring degree of physical dependence to tobacco smoking with reference to individualization of treatment. Addict. Behav. 3: 235-241. Fagerstrom, K.-O., and Bates, S. (1981). Compensation and effective smoking by different nicotine dependent smokers. Addict. Behav. 6: 331-336. Fagerstrom, K.-O., and Schneider, N. G. (1989). Measuring nicotine dependence: A review of the Fagerstrom Tolerance Questionnaire. J. Behav. Med. 12: 159-182. Feyerabend, C., Ings, R. M. J., and Russell, M. A. H. (1985). Nicotine pharmacokinetics and its application to intake from smoking. Br. J. Clin. Pharm. I9: 239-247. Gilbert, D. G. (1979). Paradoxical tranquilizing and emotion-reducing effects of nicotine. Psychol. Bull. 86: 643-661. Gilbert, D. G., and McArthur, S. F. (1988). Heart rate responses to quantified doses of nicotine as a function of anger expression, Type A behavior, and nicotine tolerance. Psychophysiology 25:450 (abstract).

520

Masson and Gilbert

Gilbert, D. G., Jensen, R. A., and Meliska, C. J. (1988). A system for administering quantified doses of tobacco smoke to human subjects: Plasma nicotine and filter pad validation. Pharmacol. Biochem. Behav. 31: 905-908. Gilbert, D. G., Meliska, C. J., and Jensen, R. A. (1990). Subjective correlates of smokinginduced elevations of plasma beta-endorphin and cortisol (submitted for publication). Gilbert, D. G., Robinson, J. H., Chamberlin, C. L., and Speilberger, C. D. (1989). Effects of smoking/nicotine on anxiety, heart rate, and lateralization of EEG during a stressful movie. Psychophysiology 26:311-320. Gilbert, D. G., and Welser, R. (1989). Emotion, anxiety, and smoking. In Ney, T., and Gale, A. (eds.), Smoking and Human Behavior, Wiley, Chichester, pp. 171-196. Glass, D. C. (1977). Behavior patterns, stress, and coronary disease. In Festinger, L., and Schacter, S. (eds.), Complex Human Behavior, John Wiley and Sons, New York, pp. 177-189. Harbin, T. J. (1989). The relationship of Type A behavior pattern and physiological responsivity: A quantitative review. Psychophysiology 26:110-119. Henry, J. P. (1986). Neuroendocrine patterns of emotional response. In Plutchik, R., and Kellerman, H. (eds.), Emotion: Theory, Research, and Experience, Fol. 3, Academic Press, Orlando, Fla., pp. 37-60. Herning, R. I., Jones, R. T., Benowitz, N. L., and Mines, A. H. (1983). How a cigarette is smoked determines blood nicotine levels. Clin. Pharmacol. Ther. 33: 84-90. Houston, B. K. (1986). Psychological variables and cardiovascular and neuroendocrine reactivity. In Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Faulkner, B., Manuck, S. B., and Williams, R. B., Jr. (eds.), Handbook of Stress Reactivity and Cardiovascular Disease, John Wiley and Sons, New York, pp. 207-230. Jenkins, C. D., Rosenman, R. H., and Zyzanski, S. J. (1968). Failure to support the validity of the Fagerstrom Tolerance Questionnaire as a measure of physiological tolerance to nicotine. Addict. Behav. 13: 87-90. Manuck, S. B., and Krantz, D. S. (1968). Psychophysiologic reactivity in coronary heart disease and essential hypertension. In Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Faulkner, B., Manuck, S. B., and Williams, R. B., Jr. (eds.), Handbook of Stress, Reactivity and Cardiovascular Disease, John Wiley and Sons, New York, pp. 11-34. McNair, D. M., Lorr, M., and Droppleman, L. F. (1981). Profile of Mood States, Educational and Industrial Testing Service, San Diego, pp. 1-29. Muranaka, M., Monou, H., Suzuki, J., Lane, J. D., Anderson, N. B., Kuhn, C. M., Schanberg, S. M., McCown, N., and Williams, R. B. (1988). Physiological responses to catecholamine infusions in Type A and Type B men. Health Psychol. 7: 145-163. Myrtek, M., and Greenlee, M. W. (1984). Psychophysiology of Type A behavior pattern: A critical analysis. J. Psychosom. Res. 28: 455-466. Naveteur, J., and Baque, E. F. (1987). Individual differences in electrodermal activity as a function of subjects' anxiety. Person. Individ. Diff. 8: 615-626. Ramanaiah, N. V., Conn, S. R., and Schill, T. (1987). On the content saturation of the BussDurkee Hostility Inventory scales. Psychol. Rep. 61: 591-594. Roberts, R. J., and Weerts, T. C. (1982). Cardiovascular responding during anger and fear imagery. Psychol. Rep. 50: 219-230. Rose, J. E., Ananda, S., and Jarvik, M. E. (1983). Cigarette smoking during anxiety-provoking and monotonous tasks. Addict. Behav. 8: 353-359. Rosenman, R. H., Brand, R. J., Jenkins, C. D., Friedman, M., Straus, R., and Wurm, M. (1975). Coronary heart disease in the Western Collaborative Group Study: Final followup experience of 8 89 years. JAMA 233: 872-877. Schwartz, G. E., Weinberger, D. A., and Singer, J. A. (1981). Cardiovascular differentiation of happiness, sadness, anger, and fear following imagery and exercise. Psychosom. Med. 43: 343-364. Seltzer, C. C., and Oechsli, F. W. (1985). Psychosocial characteristics of adolescent smokers before they started smoking: Evidence of self-selection. J. Chron. Dis. 38: 17-26. Shekelle, R. B., Gale, M., Ostfield, A. M., and Paul, O. (1983). Hostility, risk of coronary heart disease, and mortality. Psychosom. Med. 45:109-114.

Personality Smoking Cardiovascular Response

521

Spielberger, C. D. (1986). Psychological determinants of smoking behavior. In Tollison, R. D. (ed.), Smoking and Society: Toward a More Balanced Assessment, Heath, Lexington, Mass., pp. 89-134. United States Department of Health, Education and Welfare (1988). TheHealth Consequences of Smoking: NicotineAddiction. A Report of the Surgeon General, U.S. Government Printing Office, Washington, D.C. Vasey, M. W., and Thayer, J. F. (1987). The continuing problem of false positives in repeated measures ANOVA in psychophysiology: A multivariate solution. Psychophysiology 24: 479-486. Velicer, W. F., Govia, J. M., Cherico, N. P., and Corriveau, D. P. (1985). Item format and structure of the Buss-Durkee Hostility Inventory. Aggress. Behav. 11: 65-82. Wakeham, H. (1972). Recent trends in tobacco and tobacco smoke research. In Schmeltz, I. (ed.), The Chemistry of Tobacco and Tobacco Smoke, Plenum Press, New York. Warburton, D. M., Wesnes, K., and Revell, A. (1983). Personality factors in self-medication by smoking. In Janke, W. (ed.), Response Variability to Psychotropic Drugs, Pergamon Press, New York, pp. 167-181. Watanabe, A. M., Jones, L. R., Manalin, A. S., and Besch, H. R. (1982). Cardiac autonomic receptors: Recent concepts from radiolabeled ligand-binding studies. Circ. Res. 50: 161-174. Williams, R. B., Jr., and Barefoot, J. C. (1988). Coronary-prone behavior: The emerging role of the hostility complex. In Houston, B. K., and Snyder, C. R. (eds.), Type A Behavior Pattern: Research, Theory, and Intervention, John Wiley and Sons, New York, pp. 212-253. Williams, R. B., Haney, T. L., Lee, K. L., Kong, Y., Blumenthal, J. A., and Whalen, R. E. (1980). Type A behavior, hostility, and coronary atherosclerosis. Psychosom. Med. 42: 538-548. Yarnold, P. R., Mueser, K. T., Grau, B. W., and Grimm, L. G. (1986). The reliability of the student version of the Jenkins Activity Survey. J. Behav. Med. 9: 410-414.