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ORIGINAL ARTICLES |
From the Department of Epidemiology, Harvard School of Public Health, Boston, MA (E.E.M.); Department of Medicine, Harvard Medical School, Boston, MA (G.K.A.); Department of Health Care Policy, Harvard Medical School, Boston, MA (R.C.K.); Department of Psychiatry, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL (L.F.F.); Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA (K.A.M.); Department of Medicine, Baylor College of Medicine, Houston, TX (J.A.H.); and Program on Human and Community Development, The John D. and Catherine T. MacArthur Foundation, Chicago, IL (R.M.R.).
Address correspondence and reprint requests to Robert M. Rose, MD, Mind Brain Body and Health Initiative, 2.210 Ashbel Smith Building, Institute for the Medical Humanities, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1311. E-mail: brose{at}urbancom.net
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ABSTRACT |
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METHODS: Assessments in 1974 to 1978 included physical examinations and recordings (every 20 minutes for 5 hours) of both workload (planes within controller airspace) and blood pressure reactivity. Individual differences in reactivity were used to predict 1994 self-report of ever having been told by a physician to take antihypertensive medication, assessed in a telephone survey of 218 respondents who were normotensive or stage 1 hypertensive in 1974 to 1978.
RESULTS: Each SD increase in baseline systolic reactivity was associated with a 1.7 (p < .019) increase in the relative-odds of 1994 hypertension, after controlling for age, body mass index, and clinic systolic and diastolic blood pressure at clinical examination, with effects comparable for baseline normotensives and stage 1 hypertensives.
CONCLUSION: A 20-year follow-up of originally normotensive and stage I hypertensive workers suggests that increased systolic blood pressure reactivity to work stress is associated with long-term risk of hypertension.
Key Words: cardiovascular reactivity, • epidemiology, • hypertension, • prevention, • screening.
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INTRODUCTION |
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10 years) follow-up periods than the cold pressor studies. Importantly, cold pressor studies with similarly short follow-up periods have not found significant associations between blood pressure reactivity and hypertension (12–14). Second, the subjects in some of these studies are young, so that they are not in the age range of high hypertension risk at follow-up; thus, they only assess increases in resting blood pressure rather than development of hypertension. None of these studies has yet provided a definitive evaluation of the cardiovascular reactivity hypothesis. Such an evaluation would require a long follow-up period, a sample in the age range of risk for hypertension at follow-up, and a naturalistic stressful stimulus. The 1974 to 1978 Air Traffic Controller Health Change Study, originally reported in Psychosomatic Medicine in 1978 (16), and its 1994 follow-up provided a singular opportunity to carry out such a study. The baseline study included a unique measure of psychosocial stress: volume of air traffic in the air space of each controller recorded every 20 minutes for 5 hours during each of 5 typical workdays. Blood pressure, heart rate, and behavioral indicators of stress were measured at the end of each of these 75 observation periods. Subjects were recontacted in 1994, 2 decades after the first baseline assessment, and their health outcomes were assessed by self-report. The baseline sample had an average age of 36, putting respondents well into the age range for risk of hypertension at follow-up. The hypothesis that elevated cardiovascular reactivity to workload in 1974 to 1978 predicted onset of hypertension by 1994 was evaluated in the subsample of subjects who were either normotensive or who had untreated stage 1 hypertension at baseline.
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METHODS |
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160 mm Hg or diastolic blood pressure 100 mm Hg) during at least two of the five clinical examinations (or once if there was only one examination). Two hundred eighteen of the 311 subjects who were not classified as having stage 2 or 3 hypertension at baseline were traced and interviewed by telephone in 1994. Of the 93 1994 nonparticipants, 26 were known to be dead, 29 refused to participate in the follow-up, and 38 were lost to follow-up. The 218 survey participants represent 76.5% of the baseline respondents who did not have 1974 to 1978 hypertension, exclusive of those known to be dead as of 1994. Among the participants, 170 completed all 5 physical exams, and 93 completed all 5 workday assessments in 1974 to 1978. The Institutional Review Board of Boston University School of Medicine approved the baseline study, with all subjects giving written informed consent before participation. The Human Investigation Committee of Rush-Presbyterian-St. Luke’s Medical Center approved the follow-up, with all subjects giving verbal informed consent before participation. The funders of the study had no role in study design, data collection, analysis, interpretation of the data, or the decision to publish this report.
Stress Reactivity
Each of the 1974 to 1978 workday assessments consisted of observations by a trained medical technician of workload and behavioral manifestations of arousal every 20 minutes for 5 hours (15 observations). "Workload" was defined as the number of planes on the air traffic control screen that were transitioning (ie, climbing or descending) within a controller’s airspace. This measure was selected because it accounted for a substantial part of the variance in ratings of how busy, pressed, or pushed the subject appeared in previous work (15,18,19). Interobserver reliability for this measure was greater than 0.9 for each rater (16). Because only 6.2% of observations were at five or more planes, all observations of more than five were given a value of 5. Behavioral manifestations of arousal were operationalized in a 7-point rating scale based on eight dimensions of observable activity and distress: overt appearance, conversational orientation, attention, physical movements, joking/swearing, voice quality, receiving assistance, and coping with hand-offs and pilot requests. Preliminary reliability studies yielded a mean interrater correlation of 0.91 for behavior ratings (15). Because only 0.1% of observations had a rating of 6 or 7, indicating extreme agitation, all ratings of more than 5 were given a value of 5. Simultaneous with workload and behavior observations, systolic and diastolic blood pressure and heart rate were recorded on magnetic tapes using portable automatic recording sphygmomanometers (15).
Outcome Measures
The 1994 telephone interview used structured questions based on the Cardiovascular Health Study (20) to assess each subject’s medical history. A subject was considered to have a history of hypertension if he reported that a physician had ever treated him with antihypertensive medications. Using this definition, 16.5% of respondents, including 12.4% (n = 14) of 1974 to 1978 normotensives and 21.0% (n = 22) of 1974 to 1978 untreated stage 1 hypertensives, were defined as having developed a history of hypertension by 1994.
Other Covariates
In the prediction equations, we controlled for average systolic and diastolic blood pressures obtained over all five 1974 to 1978 medical examinations. Each of these examinations included at least two mercury sphygmomanometer measurements of blood pressure while the subject was seated. One hundred five of the 218 subjects were classified as having baseline untreated stage 1 hypertension using National Heart, Lung and Blood Institute criteria (17) (systolic blood pressure 140 to 159 mm Hg or diastolic blood pressure 90 to 99 mm Hg) during at least two of the five clinical examinations (or once if there was only one examination) in 1974 to 1978, whereas the other 113 were classified as normotensive.
A control was also introduced to account for those individuals who have an exaggerated rise in blood pressure in the physician’s office. This "white-coat hyperreactivity" was defined as having systolic or diastolic blood pressure higher than the mean of the measurements obtained during the subset of times when the subject was on break at work during at least two of the five clinical examinations (or once if there was only one examination). The concern that motivated the use of this control was that cardiovascular reactivity at the doctor’s office could lead to a diagnosis of hypertension by 1994 independently of work stress hyperreactivity.
A number of other factors hypothesized in previous studies to predict hypertension were considered. Age, education, and body mass index were assessed in 1974. Body mass index (weight (kg)/height (m)2) (BMI) was categorized to examine the functional form of the variable; most of the association with the outcome was accounted for by a single dichotomy at 25 kg/m2, indicating being overweight according to the National Heart, Lung, and Blood Institute’s Clinical Guidelines on overweight and obesity (21). Summary measures of smoking and alcohol consumption, which were assessed at multiple examinations during 1974 to 1978, were computed by coding the maximum cigarettes per day and the average frequency of alcohol use reported across assessments. Parental history of cardiovascular disease was defined as positive if a subject reported at any point in the study that either natural parent had ever had any cardiovascular disease or high blood pressure. Participation in the Professional Air Traffic Controllers Organization strike of 1981 was assessed in the 1994 interview.
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ANALYSIS |
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The reactivity variable (E[Yi]) represents systolic blood pressure, diastolic blood pressure, heart rate, or behavior rating. Intercepts and slopes were estimated for the total study sample (ß0 and ß1) as well as for each subject (ß0+b0i and ß1+b1i). The within-subject estimates were based on the sample of between 15 (for respondents who were observed at work on only 1 occasion) and 75 (for respondents who were observed at work on all 5 occasions) subject-specific measures of work stress and reactivity. Missing data were assumed to be missing at random. All reactivity estimates were standardized in the sample as a whole to a mean of 0 and SD of 1 for ease of interpretation. Equations to predict the onset of hypertension as of 1994 were then estimated with a logistic link function using the individual-level 1974 to 1978 stress reactivity measures as predictors. These equations were estimated both with and without taking into account control variables. Control variables were selected based on stepwise selection (p < 0.2) and Akaike’s Information Criterion. All analyses were carried out using the SAS/STAT software package, version 8 (22).
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RESULTS |
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A revised version of the model that relaxes the assumption of linearity in the relationship between systolic reactivity and hypertension (Part II of Table 2) shows that risk of hypertension increases with each quartile of systolic reactivity (p < .02), suggesting that this association is not due to outliers. Respondents having the highest quartile of reactivity are 3.5 times as likely as those in the lowest quartile to develop hypertension over the intervening years (p < .085) in the total sample, after adjusting for confounders. Although this odds-ratio is larger among 1974 to 1978 normotensives (OR = 11.3, p < .06) than among 1974 to 1978 untreated stage 1 hypertensives (OR = 2.1, p < .5), these subsample odds-ratios do not differ significantly from each other (p < .3). The risk for hypertension attributable to increased reactivity may be particularly important in stage 1 hypertension, because nearly 40% in the top quartile of systolic reactivity developed hypertension (20% for normotensives in the top quartile). Reactivity to workload based on diastolic blood pressure, heart rate, or behavior ratings did not predict the development of hypertension.
An additional set of analyses used the outcome variable of ever having been told by a physician to have hypertension. Among the 113 1974 to 1978 normotensives, 22 indicated that they were told they had hypertension, including the 14 who had been prescribed antihypertensive medication; among the 105 1974 to 1978 untreated stage 1 hypertensives, 39 indicated that they were told they had hypertension, including the 22 who had been prescribed antihypertensive medication. Similar to the results shown in Table 2, the analysis using this broader criterion also showed that increased reactivity to workload is a significant predictor of hypertension (OR = 1.8, p < .05 for 1974–1978 normotensives; OR = 1.6, p < .05 for 1974–1978 untreated stage 1 hypertensives), and that risk of developing hypertension increases with each quartile of systolic reactivity (p < .06 for 1974–1978 normotensives, p < .02 for 1974–1978 untreated stage 1 hypertensives).
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DISCUSSION |
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As noted in the introduction, previous studies of cardiovascular reactivity to stressors have been inconclusive, due, at least in part, to a combination of inadequate length of follow-up, young age of the baseline study population, and varying laboratory stress tests. The present study had advantages in all these areas. The follow-up period was 2 decades from the first baseline assessment, respondents were in the age range where hypertension becomes common, and the stressor had potential life or death consequences. Another difference between the current study and previous studies of cardiovascular reactivity to psychosocial stress is that blood pressure reactivity was assessed on 15 occasions on each of up to 5 separate days rather than in a single session on a single day. Increases in blood pressure found in this way are not trivial, considering that the men presumably experienced these surges in blood pressure on a frequent and daily basis.
The finding that only systolic reactivity predicted hypertension suggests that some reactivity measures are more relevant predictors of hypertension than others. Consistent with this possibility, other studies also found that systolic and diastolic reactivity differentially predict hypertension or increased resting blood pressure (2,9). Furthermore, different stressful stimuli may be better suited to cardiovascular reactivity studies. For example, Markovitz et al. (7) found that increased cardiovascular reactivity to a video game was associated with an increase in resting blood pressure over a 5-year follow-up period, whereas reactivity to star tracing was not. Therefore, caution is needed not to interpret the results of the current study too broadly.
The workload measure used here is a unique one. It is not clear whether or how one would design equivalent measures in samples of other occupations. It would be useful for future research to study the associations among reactivities to a wide range of different stressors both in targeted samples and in general population samples in an effort to discover the common denominator among stressful stimuli and stress responses that predict long-term health problems.
Another caution is that the study sample consisted entirely of relatively healthy white males of a single profession who were both self-selected and employer-selected for ability to cope with high-stress work. This occupation is known to be associated with high incidence and prevalence of hypertension (24). Other measures of naturalistic or laboratory psychosocial stress assessed in a different population might not yield comparable evidence of hypertension risk. The results of the study might also have been influenced by the fact that the outcome measure was based on self-report of being treated pharmacologically for hypertension by a physician, and that complete ascertainment was not possible because of death, refusal, and incomplete tracing. That a relatively small proportion of subjects with 1974 to 1978 stage 1 hypertension developed the outcome may be related to the very mild level of blood pressure elevation at baseline (mean clinic blood pressure of 132.3/90.6 mm Hg) and to treatment guidelines of the time suggesting that it may be appropriate to use nonpharmacological treatments for patients with diastolic blood pressures of 90 to 94 mm Hg (25,26).
Despite the specificity of the sample, it should be recognized that air traffic controllers are of considerable importance in their own right in that air traffic control is a critical job in an increasingly complex world. The work performed by air traffic controllers is extremely demanding and challenging, as indicated by the fact that the vast majority of controllers end their careers before the age of retirement with stress-related work disabilities (27). Sustained high vigilance is required for successful air traffic control work. The consequences of errors in judgment, although very uncommon, can be disastrous. It is not surprising, in light of these considerations, that air traffic controllers have a high risk of hypertension.
Studies of this sort could be useful in advancing our understanding of prehypertensive mechanisms of action. It is important to appreciate in this regard that the current study did not assess the role of workload or stress in predicting hypertension, but rather the role of reactivity. An important unresolved issue is whether systolic blood pressure reactivity is a marker of hypertension risk regardless of exposure to stress or is part of the pathogenesis of hypertension that is exacerbated by stress (28). Increased systolic reactivity without changes in diastolic or heart rate reactivity could reflect a state of increased cardiac ionotropy and/or arterial stiffness. Increased arterial stiffness has been described in the adult offspring of families with essential hypertension (29) and in normotensive children of hypertensive parents (30). Our observations are consistent with these studies and the hypothesis that abnormalities in large artery function may be an early finding in individuals who develop hypertension. If high systolic reactivity to workload reflects a genetic trait, and if it leads to hypertension independent of work stress, interventions to transfer air traffic controllers with high systolic reactivity to less stressful jobs may not significantly reduce their elevated risk of hypertension.
Alternatively, if the mechanism of action involves frequent systolic blood pressure surges, presumably damaging to the endothelium, leading to decreased arterial compliance and its consequences, then, for example, we would expect that a job transfer intervention would reduce risk of hypertension. Resolution of these uncertainties, especially if they are accompanied with parallel assessments of more broadly generalizable reactivity measures (eg, ambulatory blood pressure assessments with simultaneous diary measures of stress (31) and evaluation of potential mediating biological processes), could lead to better tests for predicting risk of hypertension and have important implications for counseling and preventive intervention.
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ACKNOWLEDGMENTS |
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The authors thank C. David Jenkins for contributing to the design and implementation of the 1974–1978 baseline study, Michael Hurst for designing the baseline workload measures, Michael Greenberg for coding the follow-up health report data, Garrett Fitzmaurice for providing consultation on statistical analysis, and Lisa Berkman and Deborah Blacker for providing helpful comments on an earlier draft of the paper.
Received for publication August 12, 2003.
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