Blood pressure up in a puff of smoke

We should begin by stating that it may not matter whether smoking tobacco products, either directly inhaling or indirectly from the environment, increases blood pressure (BP). Proof that it does will only add to a litany of other reasons why smoking is bad for vascular health and these are already sufficient to support major public health campaigns that are reaping huge benefits around the world [1–3]. Direct or active smoking has been tried, convicted and sentenced as a major cause of death and disability from cardiovascular and other diseases. The effects on BP are not simple, however. Blowing tobacco smoke in the face or the respiratory tract of an experimental animal is a sure way of eliciting an acute stress response [4]. The neural pathways are well established and this technique has contributed much to our knowledge of the pathophysiology of stress. Habitual smokers, however, are reported to have slightly lower BP than nonsmokers, perhaps because they tend to be lean, although a cigarette will elicit a transient pressor response [2,5]. Indeed, different conclusions on the BP effects of smoking have been derived from epidemiological surveys as compared with experimental studies. Experimental evidence is available that cigarette smoking induces an acute rise in BP and in plasma catecholamine levels [6–12]. The increase in BP seems to persist during repeated smoking. In a study by Groppelli et al.[10,11], carried out in 10 normotensive smokers asked to smoke one cigarette every 15 min for 1 h, BP and heart rate were continuously monitored during the smoking period and during the preceding nonsmoking hour through a Finapres device (TNO, Amsterdam, The Netherlands). In six other normotensive smokers asked to smoke two cigarettes per hour throughout the day, BP and heart rate were monitored noninvasively in ambulatory conditions for 8 h during daytime. BP monitoring was repeated during a nonsmoking day. Ambulatory BP and heart rate were measured once every 10 min to study the BP effects of repeated cigarette smoking in details. In resting conditions, the first cigarette caused an immediate and marked increase in BP and heart rate, and the peak BP and heart rate achieved were similar for the remaining three cigarettes. In each instance, the hemodynamic effects were so prolonged that throughout the smoking hour, BP and heart rate were persistently higher than during the nonsmoking hour [11]. The SDs of SBP and DBP and heart rate were also higher during the smoking hour, indicating an increase in BP and heart rate variability. In the six ambulant smokers, daytime BP and heart rate were also persistently higher during smoking than during nonsmoking. The authors concluded [11] that heavy smoking is associated with a persistent rise in BP and also with an increase in BP variability and that these effects (which may escape recognition during an office visit as office BP measurements are performed during nonsmoking) may account for some of the smoking-related cardiovascular risk. Few years later, these findings were confirmed by Verdecchia et al.[13], who found that, although clinic BP was nearly identical in smokers and nonsmokers (158/99 versus 158/98 mmHg), daytime ambulatory BP was significantly higher in the smokers than in the nonsmokers (150/97 versus 143/93 mmHg), whereas night-time BP did not differ between the two groups (129/79 versus 126/78 mmHg). Smokers had a higher heart rate over 24 hours, but not at the time of clinic visits. On the contrary, in many epidemiological studies, BP was reported to be comparable or even lower in smokers than in nonsmokers [14–16]. Such a discrepancy between the results of experimental studies on the direct effect of smoking on BP and the BP data derived from epidemiological observations in smokers might be explained not only by the fact that in the latter case at the time of BP measurement participants were required to stop smoking for a period ranging from at least 30 min to hours, but also by the lower body weight usually found in smokers as compared with nonsmokers, which, in turn, is associated with lower BP levels. Controversial data are available also on the effects of passive smoking on BP. To say that passive, second hand, environmental or indirect smoking (the terms will be used interchangeably) is under a cloud is both a poor pun and an understatement [17]. The circumstantial case is very strong for vascular damage through a broad range of pathways. Nevertheless, the ‘killer’ piece of experimental evidence is lacking. Passive smoking is difficult to quantify outside of the laboratory and the influences are likely to be different if exposure occurs at critical times of development, at differing intensity, frequency and proximity. We do not know the shape, threshold or linearity dose–response relationship in free-living humans; these are likely to vary according to the biological response in question. Passive smoking is easily considered as a lighter form of exposure to the toxic effects of tobacco smoking. Like so-called ‘light’ cigarettes; however, this is misleading and indeed there is a case that passive smoking may be more harmful based on the relative exposure to main stream and side stream smoke [18]. Main stream smoke is what the smoker inhales and exhales and makes up about 15% of the smoke exposure of a passive smoker. The remainder is produced at the tip of the cigarette and contains a higher concentration, in some cases, an order of magnitude more of many of the toxins associated with cigarette smoke. As mentioned above, the dose–effect relationship for indirect smoking is difficult to establish in humans and it has been proposed that the threshold is such that even minimal amounts of exposure produce maximal vascular damage [17,19]. Estimates of the excess risk of coronary disease in passive smokers as a proportion of the excess in active smokers vary from almost 40 to almost 100%. Passive smokers at home have about one-third greater risk of cardiovascular death than those living in smoke-free homes. The mechanisms may include reprogramming in infancy [20], impairment of endothelial function [21], platelet function changes favouring aggregation [22], reduction in circulating endothelial progenitor cells number and/or function [18] and sympathetic overactivity [23], a possibility supported also by the evidence that cigarette smoking is associated with a reduced arterial baroreflex sensitivity [24]. All of these effects have been observed in passive smokers, at least after acute exposure and in most cases in the chronic situation. The adverse effects seem to be present in both the indolent stages of atherosclerosis progression and the acute stage associated with plaque disruption and sudden cardiac death. What about the effects of indirect smoking on BP? Stroke rates are consistently higher in those exposed regularly, often an indicator of an effect on BP [25]. Maternal smoking has been reported to increase cardiovascular reactivity in general in infants, including BP responses to environmental stimuli suggesting some programming changes in reflex centres involved in BP control [20]. In fact, the evidence for enhanced sympathetic nervous responses is perhaps better for passive than for direct smoke inhalation. Makris et al. [26] have reported ambulatory BP measurements in a subgroup of hypertension clinic patients who were found to have normal clinic BP on presentation. Those who were passive smokers had a number of characteristics that differed from those not generally exposed to tobacco smoke. They were younger, dietary assessment suggested a less healthy diet, they consumed more alcohol and more of them had hypertension on ambulatory BP measurement. This raises two possibilities. First, passive smoking may be no more than a marker of a less healthy environment and personal habits. The finding of normal clinic BP and high BP during daily activities, termed masked hypertension, in this group also raises the possibility that the short or perhaps long wait for an appointment in a smoke-free clinic environment was sufficient for the effects of passive smoking on BP to wear off, as suggested for the effects of active smoking. More detailed ambulatory BP studies in controlled environments with measurement of cotinine or other markers would help resolve this question. In the present issue, Seki et al. [27] provide another piece of the jigsaw from the well conducted Ohasama study. A self-administered questionnaire was used to classify participants into those with no exposure, exposure at home, exposure in the workplace and exposure in both the workplace and at home. Self-administered questionnaires of smoking exposure have known limitations, and it would have been wise to combine these with biomarker measurements if anything more than a qualitative assessment is sought. The main finding was a consistent association between exposure to environmental tobacco smoke and SBP, when this occurred at home or both at home and at work. It was not seen in those taking antihypertensive therapy and was also not evident in those exposed only at work or elsewhere, a curious finding that demands further examination. Although some of the measurements at different times of the day were not significantly different between those exposed or not exposed to environmental smoke, there seemed to be about 3 mmHg difference in SBP. This is a novel study in the use of home BP, whereas much of the previous literature has been based on occasional clinic measurements. Some selection occurred and not surprisingly the groups were not well matched in some variables. Particularly, the only group of similar age to the control nonexposed group were those exposed at home. There was also a large difference in the proportion of those taking alcohol between the control and the other groups. The relationship to BP persisted when these differences were taken into account in the statistical analysis. The other variable related to the level of exposure is its intensity. There may be a great difference in response between someone who is exposed to a workmate who has one cigarette per day, compared with another worker who is surrounded by chain smokers, even though both would have been categorized as having exposure every day. In conclusion, if we needed yet another reason to pursue the elimination of tobacco smoking in the community, we may have one in a possible effect not only of active but also of passive smoking on BP. We can be comforted that if exposure cannot be eliminated, the results of the study by Seki et al. suggest that antihypertensive therapy eliminates the difference in BP in hypertensive individuals. However, the public health consequences of the small rise in BP are potentially much greater in the normotensive community and the quest must continue to make smoking a historical quirk without contemporary relevance.