Where there's smoke there might be hypertension

No doubt smoke is harmful for those who actively smoke and continue their tobacco smoking habits. It is nicely illustrated by the long list of smoking-attributable mortality and morbidity conditions. Mortality among current smokers is estimated to be two to three times as high as that among persons who never smoked [1]. There is ample evidence that smoking is the leading preventable cause of death from lung cancer and that smoking causes malignant neoplasms in several other organs of the body. Next to cancer, smoking may cause, precipitate, or aggravate many other clinical conditions including respiratory diseases (e.g. bronchitis, asthma, or chronic obstructive pulmonary disease) and the whole range of cardiovascular diseases from cerebrovascular, ischemic heart to lower limb peripheral artery disease. More than one in every 10 cardiovascular deaths in the world in the year 2000 was attributable to smoking [1,2]. Does this disastrous scenario also apply to so-called ‘passive smoking’, sometimes also termed second-hand smoke (SHS) or environmental tobacco smoke (ETS)? A few decades ago, indirect exposure to the toxic substances of tobacco smoke was anticipated as a widespread and potentially harmful condition but less severe by an order of magnitude than for active smokers. Now there are sound arguments to update that historical paradigm and attribute a more considerable risk to passive smoking than originally assumed. The exposure to SHS was estimated to have caused 379 000 deaths from ischemic heart disease, 165 000 from lower respiratory infections, 36 900 from asthma, and 21 400 from lung cancer in 2004 (nearly 1% of worldwide mortality) [3]. In a meta-analysis that included 29 studies, SHS increased the risk of ischemic heart disease by 31% in never-smokers relative to the risk in those who were not exposed to SHS. The authors estimated effects of SHS between 68 and 86% of the risk of light smoking depending on the level of SHS exposure [4]. From preventive medicine point of view, it should be realized that health consequences raised by passive tobacco smoking are secondary to a clear failure to ban tobacco smoking. Therefore, campaigns aiming at reducing or ban active smoking are needed and if successful, there is a high likelihood it will be translated in a reduced burden of passive tobacco smoking. Moreover, passive smoking may endanger secondary prevention programs. In the recent EUROASPIRE III survey [5] in patients with coronary heart disease, a noteworthy portion of nonsmokers were exposed to ETS and detrimental effects of passive smoking may even have jeopardized part of the beneficial effects of smoking cessation. In recent literature, much attention has been paid to the situation in China. China counts several hundred million smokers and it is assumed that over a million Chinese people die from smoking-related illnesses every year. The burden of passive smoking is huge because of the high number of smokers in connection with some sociological conditions of the Chinese society. Recently, Cai et al.[6] calculated that smoking and exposure to SHS produced substantial economic burden as well as considerable public health impact in rural southwest China. The unfavorable balance might be applicable for the whole country. Although there is a paucity of epidemiological data supporting a close and causal relationship between current smoking and incident hypertension, there is a strong belief that tobacco smoking is a risk for the development of hypertension. How strong is the evidence? The effect of active/chronic smoking on blood pressure progression and incidence of hypertension is a complex and controversial issue. In a cross-sectional analysis of Chinese current smokers, smoking quantity was positively associated with hypertension (probably mediated by inflammation) [7]. This editorial commentary will not deal with the claimed mechanisms by which acute and chronic tobacco smoking, respectively, may lead to transient or prolonged changes in blood pressure responses. However, the association between hypertension and tobacco smoking might not be as straightforward as thought as there are also reports that habitual smokers may show significantly lower blood pressure values than their counterparts. One of the explanations suggested in literature is confounding by lower BMI (leaner smokers) and another one by smokers showing less stress responses. As might be expected, the number of epidemiological studies providing sound evidence for a positive and significant association between hypertension and long-term exposure to ETS is limited. No surprise that the effects of passive smoking on blood pressure and incident hypertension might be more controversial and show a higher degree of complexity than those for current smoking. Makris et al.[8] observed different characteristics for passive smokers: younger with less healthy habits (a less healthy diet, more alcohol consumption) and more masked hypertension. More precisely, masked hypertension was associated with passive smoking in a dose-related manner, and low physical activity, increased heart rate, and postural hemodynamic reaction represent potential accelerators of that phenomenon [8]. Thus, the association between passive smoking and blood pressure might be more difficult to unmask (masked hypertension). From mechanistic point of view, passive smoking evokes complex processes involving, among others, arterial stiffening, altered arterial pulse wave reflection, disturbed microvascular reactivity, and endothelial dysfunction, probably dependent to a large extent on increases in plasma nicotine and sympathetic excitation [9]. All of these mechanisms are candidates to contribute to the development of hypertension. On the contrary, there are only a few studies that investigated the relationship between SHS exposure and high blood pressure among never-smokers. In the National Health and Nutrition Examination Survey 2005–2008, in never-smoker adults, higher SHS exposure objectively measured by serum cotinine levels was found to be associated with SBP and hypertension independent of age, sex, ethnicity, education, alcohol drinking, BMI, glycohemoglobin, total cholesterol, and other confounders [10]. The unfavorable effect of passive smoking starts already at young age. In healthy preschool children, parental smoking was an independent risk of higher blood pressure, adding up to other familial and environmental risks including BMI, parental hypertension, or birth weight [11]. Also for China, there is a paucity of data on the contribution of SHS to incident hypertension and even cross-sectional data on the prevalence of SHS-related hypertension are scarce. In this issue of the Journal of Hypertension, Li et al.[12] studied the effects of passive smoking on hypertension in rural China. They enrolled 392 nonsmoking women from Shanxi province and concluded that in rural areas of China, passive smoking in the home indeed is prevalent and that frequent exposure to SHS is a risk of hypertension. After adjustments for age, BMI, education, occupation, drinking status, physical activity, and menopause, passive smoking conferred a two-fold risk increase of hypertension. The strengths of the study are the design in a rural area of China (high degree of exposure, exposure mostly at home, somewhat less air-polluted area, homogeneous population living closely together) and the appropriate adjustment for some relevant confounders. Although passive smoking was associated with prevalent hypertension, the association could not be confirmed for absolute blood pressure values. Among the study weaknesses, we should mention potential misclassification of the exposure level (no cotinine concentrations were available) and the lack of follow-up data (no data on incidence of hypertension). Data for nonsmoking men would have been a valuable addition as well. In 2010, in the Journal of Hypertension, Jennings and Parati [13] wrote an editorial commentary that accompanied an article from the Ohasama Study reporting a positive association between home blood pressure levels and ETS exposure in nonsmoking women without antihypertensive medication whereas not in the treated patients [14]. They critically reviewed the state of the art at that time and had to conclude that the effect of SHS on blood pressure progression was still a controversial item and, as they called it the ‘killer’ piece of experimental evidence, was not available. It was the feeling of the editorialists that a possible association between blood pressure and passive smoking should be interpreted in a broader context. The message, albeit valuable in its own right, essentially would constitute another argument adding up to an already long list to ban smoking (whether active or passive) from planet Earth [13]. Since its publication, only a few studies have been published on the risk of becoming hypertensive by passive smoking. Thus, the intellectual content of the commentary essentially remains valid for the time being. However, in recent years, the focus moved also somewhat to risks attributed to nontobacco-related smoke. Passive tobacco smoking is by far not the only environmental factor theoretically likely to contribute to incident hypertension. Recent literature identified a long list of widely encountered traffic and industrial smoke-related pollutants that may play a causal role in pathways leading to hypertension and cardiovascular disease. To set the scene, few examples are smoke from traditional household cooking, black carbon emissions from diesel vehicles, coarse particulate matter (PM10) from smoke and industrial pollution, fine particles (PM2.5), and other toxic gases and substances (nitrogen oxides, sulfur oxides, metal dusts). Other incriminated environmental factors include ozone and noise. Indeed recently, several studies positively associated toxic smoke-related agents/pollutants with hypertension. For instance, in a Canadian cohort (Ontario), an increase of 10 μg/m3 of PM2.5 significantly increased the incidence of hypertension (adjusted hazard ratio 1.13) [15]. In Chinese adults from the northeastern cities, not only PM10 but also long-term ambient air pollution with certain pollutants (sulfur dioxide, and ozone but not nitrogen dioxide) was associated with hypertension at least in men [16]. Controlled acute diesel exhaust inhalation was associated with a rapid, measurable increase in SBP not DBP in young nonsmokers, independent of perception of exposure [17]. Even short-term exposure to low levels of air pollution (PM10) in the Swiss Bus Santé and CoLaus population-based studies induced a significant increase of systolic and pulse pressure [18]. Of interest, higher outdoor temperature strengthened the association. An in-depth discussion on the role of noise, ozone, or nontobacco smoke-related pollutants (independent, causal, mediator, a bystander) in the processes leading to hypertension is out of the scope of this editorial commentary. However, when reviewing studies on the associations between traffic or industrial smoke and hypertension, one should bear in mind that noise may cosegregate with traffic and industrial smoke and individual contributions of noise versus pollutants are sometimes difficult to disentangle. Anyhow more research in that particular field is definitely needed. Some words of caution are needed. First, passive tobacco smoking is difficult to quantify. Self-reported exposure to SHS is prone to misclassification. Assaying cotinine (a principal metabolite of nicotine with plasma half-life 19–24 h) in serum is effectively used as a biomarker molecule for exposure to both active smoke and SHS. It could be particularly effective when integrated in routine clinical consultation and with knowledge of smoking dynamics (intensity and duration) [19]. Second, it is still unclear whether the dose–response relationship between cumulatively inhaled smoke and blood pressure progression is linear. Definitely, more experimental studies are needed. Third, the association between passive smoking and endpoints (or incidence of hypertension) might be confounded by healthy lifestyle or there might be an interaction. Do some of the nonsmokers showing an otherwise more healthy risk profile more actively avoid exposure to SHS at home or in the workplace, and does it translate into less blood pressure increase and smoke-related morbidity/mortality? Nonsmokers better adhering to other healthy lifestyle measures may take more advantage of current advice: do not allow guests or passengers to smoke in your home or in your vehicle, insist that smoking restrictions be enforced at work, choose smoke-free care facilities, and patronize businesses with no-smoking policies (advice given by the Mayo Clinic). Fourth, finally but not unimportant, a close association between exposure to airborne particles and incident hypertension remains a controversial issue as population-based large-scale epidemiological studies are scarce. There is still a long way to go to make smoking and thus passive smoking a historical quirk. Moreover, we should realize that banning tobacco smoking will not fully eradicate exposure to smoke. Particularly, in (but certainly not limited to) developing countries, continuous efforts will be needed in the field of traditional home cooking, control on traffic and industrial smoke, and control of smoke exposure at the workplace in order to reduce the burden of smoke-related morbidity/mortality as well as the incidence of smoke-related hypertension. For some of these problems, confounding or interaction with exposure to noise should be kept in mind. Returning to China, the country is now tackling the pandemic of tobacco use. Smoking bans already existed in China, but have largely failed to crack down on the habit. Nonetheless, public awareness of the health hazards of active smoking and SHS is growing. The problem is huge as millions nonsmokers are still exposed to SHS in schools, healthcare facilities, public transportation systems, workplaces, restaurants, and government buildings [20]. Since 2014, nationwide legislation was further adapted to protect people from SHS and ban all forms of tobacco advertising, promotion, and sponsorship [20]. For instance, the city of Beijing implemented China's toughest smoking ban starting from June 1, 2015, prohibiting smoking in all indoor public places, in workplaces, and on public transportation. The legislation is supported by large-scale health education campaigns aiming at increasing awareness and changing smoking habits. One of the remaining problems will be ‘indoor smoking’. Pessimists claim it would be unrealistic to absolutely abolish ‘indoor smoking’ (difficult especially in rural areas because of traditional/sociological factors) as too many people will be unwilling to change their smoking habits. Li et al.[12] added a piece to the puzzling question – ‘Is there hypertension where there's smoke?’ As many crucial pieces of the puzzle are still missing, there is a strong need for well designed epidemiological surveys to further address the association between SHS and incident hypertension. Finally, one should disentangle the effects of passive smoking of tobacco (at home or wherever) from the contribution of smoke that is unrelated to tobacco use (e.g., smoke from traffic, workplaces, and industrial air pollution). Conflicts of interest There are no conflicts of interest.

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