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(Hypertension. 1997;30:436.)
© 1997 American Heart Association, Inc.
Articles |
Seasonal Change in 24-Hour Blood Pressure and Heart Rate Is Greater Among Smokers Than Nonsmokers
From the Occupational Health & Rehabilitation Institute (E.K.-B., G.H.), Raanana, Israel; Israel Center for Disease Control (M.S.G.); and Sackler Faculty of Medicine, Tel Aviv University (M.S.G.), Israel.
Correspondence to Dr E. Kristal-Boneh, Occupational Health & Rehabilitation Institute, POB 3, Raanana 43100, Israel.
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Abstract |
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Abstract In general, blood pressure is higher in winter than in summer, and this factor may be partly responsible for the higher mortality from cardiovascular disease in winter. Cigarette smoking causes an acute pressor response that may interact with this cardiovascular response to cold exposure. We sought to determine whether the seasonal variation in blood pressure and heart rate differs between cigarette smokers and nonsmokers. We evaluated 24-hour ambulatory systolic blood pressure (SBP), ambulatory diastolic blood pressure (DBP), and ambulatory heart rate of 97 healthy men (73 nonsmokers and 24 smokers), 28 to 63 years of age, during the summer and winter, taking indoor temperatures into consideration. Smokers and nonsmokers both had higher daytime ambulatory SBPs and DBPs in winter than in summer (after adjustment for potential confounders). However, the winter increase seen in the smokers was significantly higher for mean daytime SBP (7.3 versus 2.7 mm Hg, P<.01), for mean daytime DBP (4.4 versus 3.1 mm Hg, P=.051), and for ambulatory heart rate (3.9 versus -1.7 beats/min, P<.001). The double product increased from summer to winter (daytime) by 10.53 for smokers and by only 0.11 for nonsmokers (P<.01). There was an independent interaction between season and smoking status that affected SBP (standardized ß=0.66, P<.0001) and DBP (standardized ß=0.32, P<.0001). Smokers have a greater seasonal variation in blood pressure and heart rate than nonsmokers and show a larger increase in the cardiovascular load in winter. Smoking apparently potentiates the cardiovascular response to various climatic conditions. Season should be taken into account in studies of blood pressure and in the diagnosis and treatment of hypertension, particularly among cigarette smokers.
Key Words: smoking • blood pressure • season • temperature
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Introduction |
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The general tendency of blood pressure (casual and ambulatory measures) to be higher in winter than in summer1 2 3 4 5 6 7 8 9 10 11 12 13 may be one of the mechanisms underlying the higher cardiovascular mortality observed in winter.14 The reasons for the seasonal variation in blood pressure are apparently complex, involving both long-term regulatory factors and acute responses to environmental temperatures.12 13 The increase in daytime blood pressure from summer to winter is independently and inversely associated with indoor temperature,1 13 15 probably at least in part because of the increase in peripheral resistance at lower environmental temperatures.13 16 17
In 1991, Lloyd18 suggested that since some of the known effects of smoking on the body are similar to the effects of cold exposure, it is conceivable that cold-exposed subjects who also smoke are at higher risk of ischemic heart disease. One of these effects is almost certainly elevated blood pressure, since exposure to cold and smoking both acutely stimulate sympathoadrenal activity, which induces peripheral vasoconstriction.16 17 19 20 21 22 23
Epidemiological studies on casual measurements suggest that blood pressure in chronic cigarette smokers is the same as or lower than that in nonsmokers, even after accounting for the lower BMI of smokers.24 25 26 However, when the ambulatory blood pressures of normotensive subjects and hypertensive patients were compared, the habitual smokers showed higher values during daytime hours.27 28 29 To the best of our knowledge, none of these studies has addressed the possible effect of season of the year or environmental temperature on the relationship between smoking and blood pressure. In a previous analysis of our data we found that cigarette smoking interferes with the physiological seasonal responses in blood cell parameters and plasma volume,30 supporting the theory that there is a difference between smokers and nonsmokers in blood pressure response to seasonal changes.
In the present study we hypothesized that there is a positive association between the increase in blood pressure from summer to winter and cigarette smoking. To test this hypothesis, we evaluated the 24-hour ambulatory SBP and DBP and HR of healthy male smokers and nonsmokers during the summer and winter, taking indoor temperatures into consideration.
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Methods |
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The study population comprised 97 male blue-collar employees in Israeli industries, aged 28 to 63 years, all engaged in similar work (fitting and turning). Working conditions and recruitment criteria were detailed in a previous article.12 Essentially there were no differences in the type of job and physical activity between smokers and nonsmokers. The data for this study were collected before workplace restrictions on smoking were adopted in Israel. Therefore, smokers were not required to go outside to smoke. None of the subjects was under treatment for hypertension or taking any medication that could affect the cardiovascular system. The study was approved by the local Research on Human Subjects Committee. All participants signed an informed consent form, and they were able to withdraw from the study at any time they wished.
The study was carried out on-site, on regular working days, in two identical stages (summer and winter). On each occasion subjects were interviewed about health-related habits peculiar to the time of the year of the examination. Smoking habits were determined by the replies to a comprehensive questionnaire, which has been validated against creatinine-adjusted urinary cotinine concentrations.31 Alcohol intake was estimated as the average amount of alcohol (in milliliters) consumed per month.
Field tests included an examination of the environmental conditions in the workplace and physiological tests. A meteorological system (model M-1/B, YM Electronic Industries, Ltd), containing sensors and a data-logger to detect and record surrounding dry temperature, was set up as closely as possible to the worker before he arrived at work and was operated continuously until the end of the workday. The sensors are accurate to 0.1°C, with a 0.1°C error of measurement (I-128 Pt 100 RTD, Rotronic). Hourly information about the daytime environmental temperature outside the plants was obtained from the meteorological services at Bet Dagan and at Ben-Gurion Airports.
Participants were examined between 6 and 9 AM, before the beginning of the workday, in a temperature-controlled room, in the presence of a trained technician only. Height and weight were measured without shoes, and with the subject wearing only lightweight industrial clothes. Body weight was measured using the Seca (Seca alpha, model 770) electronic scale, accurate to 100 g. Quetelet’s index [weight (kg)/height (m)2] was used as a measure of BMI.
Portable devices for measuring blood pressure were then fitted. To ensure that they were in working order and had been properly installed, blood pressure was measured simultaneously with the ambulatory device and the mercury manometer (sphygmomanometer). Two simultaneous measurements were carried out at 1-minute intervals while the subject was seated.
Ambulatory blood pressure was monitored by the Accutraker II (Stech Medical Instruments), which has been previously evaluated with satisfactory results.32 The device weighs only 300 g and is therefore not uncomfortable to wear. It was programmed to measure blood pressure every 15 minutes during the day and every half hour during the night. While awake, the subjects were asked to lower their arms and to remain inactive during the test. The records were revised to eliminate all measurements that the device had detected as abnormal from a technical point of view. Those records in which at least 80% of the possible readings were acceptable were included in the analysis. Averages were calculated for all readings per hour, for the 24-hour period, and for daytime, nighttime, and working time. The daytime and nighttime periods were defined by the subjects in their journals. Daytime began when the subject rose and continued until he went to bed; the typical daytime period was from 6 AM to 10 PM. (At the beginning of the nighttime period, the subjects were not necessarily asleep.)
Statistical Analysis
Data analyses were carried out using SAS software (SAS
Institute).33 Differences between means were tested using
Student’s t test, and multiple regression analysis
was used to test for seasonal differences in blood pressure and HR
between smokers and nonsmokers after controlling for potential
confounding variables. Results were considered to be statistically
significant at the level of 5%.
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Results |
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The characteristics of the study groups are shown in Table 1. Smokers and nonsmokers were similar in age and leisure-time physical activity. There were no statistically significant differences between groups in weight or BMI, although the smokers were slightly leaner than the nonsmokers. In both groups, alcohol consumption was lower in summer than in winter. There were no differences between the groups in outdoor temperatures on the days of data collection (data not shown). In summer, indoor temperature exposure was similar, and in winter the nonsmokers’ working environment was hotter by 1.6°C than that of the smokers (of no statistical significance). All variables in Table 1 were considered possible confounders and were included in the multivariate analyses.
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The 24-hour blood pressure and HR (crude hourly means) patterns are shown in Figs 1 through 3, and the mean crude values of SBP, DBP, and HR at different periods of the day in summer and in winter are given in Table 2. In general, the results show a much greater winter increase in waking SBP in smokers than in nonsmokers. For DBP, the trend was similar for both groups. Smokers had a significantly higher HR than nonsmokers in both seasons and showed a seasonal pattern that was not seen in nonsmokers. These trends remained statistically significant after controlling for potential confounders.
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Seasonal differences in ambulatory blood pressure and HR adjusted for age, BMI, and alcohol intake for nonsmokers and smokers are shown in Table 3. Both groups had higher daytime ambulatory SBPs and DBPs in winter. The winter increase was significantly greater for smokers for mean daytime SBP (7.3 versus 2.7 mm Hg, P<.01), mean daytime DBP (4.4 versus 3.1 mm Hg, P=.051), and ambulatory HR (3.9 versus -1.7 beats/min, P<.001 ). The double product of SBP and HR increased from summer to winter (daytime) by 10.53 for smokers but only by 0.11 for nonsmokers (P<.01).
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) in Daytime
and Nighttime Means of Ambulatory Blood Pressure and HR in Nonsmokers
and SmokersBecause of the high correlation between season and outdoor temperature, it was not possible to examine their possible effects on ambulatory blood pressure and HR separately. During work-time (7 AM to 4 PM) indoor temperatures were recorded, and we included this variable in multiple regression analyses of the effects of season on blood pressure. A possible interaction between season and smoking status affecting blood pressure was analyzed in a multiple regression model. After adjustment for age, BMI, sports activities, and alcohol consumption, SBP during work hours was independently associated with indoor temperature (P<.0001), with smoking status (P<.0001), and with season (P<.0001). There was an independent interaction between season and smoking status that affected SBP (standardized ß=0.66, P<.0001). Similarly, statistically significant associations were found for DBP. For the interaction between season and smoking status, the standardized ß was 0.32 (P<.0001).
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Discussion |
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The principal, novel finding of this prospective follow-up study is that seasonal variations in both blood pressure and HR are substantially greater among smokers than nonsmokers. The cardiovascular load, expressed by the double product of SBP and HR, showed a much greater increase among smokers in winter. These findings are compatible with our hypothesis that there is a positive association between the summer-to-winter increase in blood pressure and cigarette smoking. Consistent with previous studies of smoking and ambulatory measures of blood pressure in normotensive and hypertensive subjects,28 29 34 35 36 our results indicate that healthy smokers are characterized by greater daytime blood pressures than nonsmokers and that these elevations are much more pronounced in winter than in summer.
Although the increase in blood pressure in cold temperatures in winter has been reported by others,1 2 3 4 5 6 7 8 9 10 11 12 13 the influence of smoking on this relationship has not yet been described, to the best of our knowledge. The present study is the first to report an increase in the seasonal variation in ambulatory blood pressure and HR among smokers. The increase in blood pressure at reduced environmental temperatures is generally attributed to skin vasoconstriction, one of the thermoregulatory responses to cooling, which results in an increased venous return and hence an increased stroke volume. Thus, the fact that smoking results in peripheral vasoconstriction may explain in part the exaggerated daytime blood pressure response in winter among smokers. In contrast, this phenomenon may be viewed from the aspect of the decline in blood pressure in summer because of increased vasodilatation at higher temperatures, with consequent reduced peripheral resistance. As such, it could be argued that cigarette smoking interferes with the normal vasodilatory effect of increased temperatures, inhibiting the expected drop in blood pressure. However, in the latter case, we would expect the nocturnal drop in blood pressure (when subjects keep warm in bed) to be attenuated in smokers; this is not true according to our data. The failure to find evidence of impaired vasodilation among smokers could suggest that heat is such a powerful stimulus to vasodilation that it overcomes the adrenergic stimulus of smoking. Nevertheless, from our data it seems unlikely that impaired vasodilatation is the mechanism underlying exaggerated seasonal changes in blood pressure in smokers. In both seasons, the nocturnal drop in blood pressure was greater in smokers than in nonsmokers, replicating the results reported by Purtak et al.28 Additional studies are warranted to clarify this mechanism.
HR was higher among smokers in both seasons and during the entire day. One explanation may be the known effects of carbon monoxide37 and nicotine on HR.38 The elevated HR of smokers at night may be caused not only by the residual effects of nicotine and carbon monoxide but also by changes in vagal control of the heart, which has been found to be reduced in heavy smokers.39 Hayano et al39 observed a blunted postural response in autonomic cardiac regulation, which may also partly explain why the lower average blood pressure values in smokers are found mainly when blood pressure is measured with the subject seated and at rest. Among smokers, daytime HR was higher in winter than in summer, whereas for nonsmokers there were no seasonal differences. The lack of seasonal changes in HR of nonsmokers suggests that seasonal changes in blood pressure are primarily caused by increased stroke volume in winter. Since smoking and exposure to cold both result in increased sympathetic nervous system activity, as reflected in increased catecholamine release and reduced peripheral circulation,16 17 19 23 40 41 the above findings may suggest that smoking has a modifying (potentiating) effect on the cold temperature–induced elevation in HR, similar to the conjugated effect of smoking and physical activity.38 This is supported by studies reporting that smoking produces a reduction in blood flow to the skin.42
Epidemiological studies have found a lower blood pressure in smokers than in nonsmokers. This may be attributable to nicotine withdrawal (abstinence of smoking) before blood pressure measurements34 43 44 or to relative hypovolemia that occurs because of the vasoconstrictor effects of nicotine during prior smoking. It has also been proposed that in the absence of acute smoking, blood pressure reductions in smokers may be a consequence of the unmasked effects of cotinine-producing relaxation of vascular smooth muscle and dilation of peripheral blood vessels.45 The present results indicate that seasonality, a factor not previously addressed in studies of smoking and blood pressure, may also contribute to the discrepancies between studies on ambulatory measures and casual measures and may explain some of the equivocal findings.
Cigarette smoking is inversely related to body weight; smokers weigh less than nonsmokers.46 47 Since there is no consistent evidence that smokers consume fewer calories or are more physically active than nonsmokers,46 48 it has been suggested that it is the effect of smoking on the metabolic rate that accounts for this difference.49 An inverse association has been reported between seasonal changes in blood pressure and BMI,50 implying that the lower body mass of smokers may be responsible for their increased blood pressure response to environmental temperatures. However, in the present study, the increased seasonal differences in blood pressure and HR were found in smokers after adjustment for BMI. Thus, smoking has an effect on the seasonal variation in blood pressure and HR independent of BMI.
Higher mortality from ischemic heart disease has been observed in winter,14 and it has been suggested that this may be caused in part by the adverse changes in risk factors for heart disease during cold weather. While the actual change in blood pressure may not be sufficient to explain all of the seasonal differences in mortality, it could explain some of them.
We conclude that seasonal changes in blood pressure and cardiovascular load are greater in smokers than in nonsmokers. Thus, both season and smoking status should be taken into account when blood pressure values are interpreted. Only healthy male working subjects were included in the present study, and the results may not necessarily be extrapolated to patients with various disorders or to the general population.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by the Committee for Preventive Action and Research in Occupational Health, The Ministry of Labor and Social Affairs, Jerusalem, Israel.
Received October 18, 1996; first decision November 26, 1996; accepted January 30, 1997.
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