Zastanawiasz się, jak wydać pracę doktorską, habilitacyjną lub monografie? Chcesz dokonać zmian w stylistyce i interpunkcji tekstu naukowego? Nic prostszego! Zaufaj Wydawnictwu Borgis - wydawcy renomowanych książek i czasopism medycznych. Zapewniamy przede wszystkim profesjonalne wsparcie w przygotowaniu pracy, opracowanie dokumentacji oraz druk pracy doktorskiej, magisterskiej, habilitacyjnej. Dzięki nam nie będziesz musiał zajmować się projektowaniem okładki oraz typografią książki.

© Borgis - Medycyna Rodzinna 2/2018, s. 177-184 | DOI: 10.25121/MR.2018.21.2.177
Andrzej Sobczak1, 2
Does switching to electronic cigarettes reduce the harm caused to the cardiovascular system by tobacco smoking?
Czy przejście na elektroniczne papierosy redukuje szkody w układzie sercowo-naczyniowym wywołane paleniem tytoniu?
1Zakład Chemii Ogólnej i Nieorganicznej, Wydział Farmaceutyczny z Oddziałem Medycyny Laboratoryjnej, Śląski Uniwersytet Medyczny w Katowicach
2Zakład Szkodliwości Chemicznych i Toksykologii Genetycznej, Instytut Medycyny Pracy i Zdrowia Środowiskowego w Sosnowcu
Streszczenie
Największa liczba przedwczesnych zgonów w wyniku palenia czynnego i palenia biernego następuje w wyniku chorób sercowo-naczyniowych. Wprowadzenie w ostatniej dekadzie na rynek konsumencki alternatywnych form dostarczania nikotyny wywołało ożywioną dyskusję dotyczącą szkodliwości tych wyrobów. W prezentowanej pracy poglądowej porównano mechanizmy negatywnego wpływu dymu tytoniowego i aerozolu generowanego z elektronicznych papierosów na układ sercowo-naczyniowy. Przytoczono opinie autorytetów z dziedziny kardiologii oraz prestiżowych organizacji i instytucji, dotyczące tego zagadnienia. Dokonano oceny redukcji szkód w układzie sercowo-naczyniowym po zastąpieniu przez palacza papierosów konwencjonalnych papierosami elektronicznymi. Dostępne wyniki badań wskazują, że główną przyczyną negatywnego wpływu aerozolu z elektronicznych papierosów na układ sercowo-naczyniowy jest nikotyna. Brak procesu spalania w elektronicznych papierosach powoduje, że ogromna ilość związków z dymu tytoniowego nie występuje w aerozolu. Oznacza to znacznie słabsze oddziaływanie tej grupy związków na układ sercowo-naczyniowy. W konsekwencji zastąpienie palenia tytoniu elektronicznymi papierosami lub innymi bezdymnymi formami przyjmowania nikotyny powinno prowadzić do zmniejszenia ryzyka powstania chorób sercowo-naczyniowych, jednakże go nie eliminując.
Summary
The largest number of premature deaths associated with active and passive smoking are due to cardiovascular diseases. The introduction of alternative nicotine delivery devices to the consumer market over the last decade has inspired a vivid debate on the harmfulness of these products. This review compares the mechanisms of the negative influence of tobacco smoke and the aerosol generated from electronic cigarettes on the cardiovascular system. The opinions of authorities in cardiology, as well as those of prestigious organisations and institutions on the matter, are quoted in the paper. Harm reduction following the replacement of conventional cigarettes with electronic ones has been assessed. Available research shows that the main cause of the negative effects of the aerosol from electronic cigarettes to the cardiovascular system is nicotine. No combustion process in electronic cigarettes results in the lack of a vast amount of smoke compounds normally found in cigarette smoke. This results in a smaller influence of these compounds on cardiovascular system. As a consequence, substituting cigarette smoking with electronic cigarettes or other smokeless tobacco products should lead to a reduction in the risk of cardiovascular diseases, however, not to eliminating the risk.
Introduction
The number of deaths due to smoking illustrates the enormously negative effect of tobacco smoke on health. It is estimated that between 1964 and 2014 nearly 21 million USA residents died prematurely as a result of smoking. Cardiovascular and metabolic diseases accounted for the premature death of 7.8 million Americans, cancer for 6.58 million and respiratory diseases for 3.8 million Americans. Cases of premature death also included 2.5 million passive smokers, 108,000 children and 86,000 victims of fire caused by cigarette butts (1). It is estimated that every year 480,000 individuals die in the United States as a result of smoking-related diseases. In the European Union tobacco consumption is responsible for 700,000 deaths every year and it is estimated that smokers live 14 years shorter than they could (2).
Smokers most commonly associate tobacco smoking with lung cancer. However, it is cardiovascular diseases (CVD) that account for the largest proportion of smoking-related deaths (fig. 1).
Fig. 1. Proportion of deaths due to diseases caused by active and passive exposure to tobacco smoke in 1965 – 2015; based on (1)
The reason for the negative impact of tobacco smoke on the cardiovascular system is the substantial amount of toxic compounds inhaled by the smoker. In 2012 the U.S. Food and Drug Administration (FDA) published a list of 93 harmful and potentially harmful constituents (HPHCs) present in tobacco smoke and tobacco (3). Each of them was assessed for carcinogenicity, addictive properties as well as respiratory, reproductive or developmental and cardiovascular toxicity. In the case of cardiovascular toxicity 12 substances were selected which include 4 compounds from the polycyclic aromatic hydrocarbon (PAH) group. Their presence in tobacco smoke is the result of chemical transformations which occur during the smoking of tobacco products.
Smoking-related mechanisms which lead to cardiovascular diseases
The toxic components of tobacco smoke affect the smoker’s body in multiple ways. This multiplicity of effects is associated with the fact that tobacco smoke includes an enormous number of chemical substances of various types which contain various reactive chemical groups (hydroxyl, carboxyl, amine, aldehyde, thiol) and a large group of free radicals. Many of them can have a direct effect on the haemodynamics of circulation, affect the lipid balance, disrupt homeostasis systems and cause lesions in the vascular endothelium. It is important since vascular endothelial dysfunction is treated by many authors as the fundamental component of cardiovascular disease pathogenesis. Vascular endothelial dysfunction has even been described as ‘the risk of the risk factors’, which shows that it is of fundamental importance for the future development of vascular lesions leading to the formation of atherosclerotic plaque (4). The basic mechanisms mediating the effects of tobacco smoke on the cardiovascular system include (5):
– vascular endothelial damage and dysfunction,
– change in the concentration of atherogenic plasma lipoprotein fractions,
– haemodynamic stress,
– oxidative stress,
– activation of neutrophils,
– increase in blood coagulability,
– increase in fibrinogen concentration and blood viscosity.
According to a report of the Surgeon General of the United States (1), the whole mechanism through which tobacco smoking affects the cardiovascular system is very complex but well-documented (fig. 2a). New research indicating a cause-and-effect relationship between smoking and CVD which has been conducted in recent years does not challenge this mechanism (6-8).
Fig. 2a, b. Comprehensive mechanism mediating the effects of tobacco smoke (a) and e-cigarette aerosol (b) on cardiovascular function; based on (1,17)
Three pathways of tobacco smoke influence on the human body have been identified. The first one involves the products of tobacco combustion (PAH, oxidising compounds, respirable particles). They cause vascular endothelial dysfunction and platelet activation. The second pathway is initiated by carbon monoxide. It reacts with haemoglobin to form carboxyhaemoglobin, which is not able to carry oxygen. The third mechanism mediating the negative effect of tobacco smoke on the cardiovascular system is associated with nicotine inhalation. Nicotine causes sympathetic nervous system activation and the release of catecholamines: adrenaline and noradrenaline, which increase cardiac output and oxygen demand through a rapid increase in blood pressure, heart rate and vasoconstriction. All three pathways are interrelated, but the strength of their negative effects on the cardiovascular system is different. The highest importance is attributed to the first group of compounds, while the strength of the negative effects of nicotine is still a controversial matter. This is due to epidemiological data and clinical trials of nicotine patches which suggest that it is not nicotine but other substances contained in tobacco smoke that increase the risk of death as a result of myocardial infarction and stroke to the highest extent (1). The lack of consensus regarding the role of nicotine in CVD is clearly seen in the opinions of authorities in cardiology. Benowitz and Fraiman (9) believes that the impact of nicotine on CVD is small, while Bhatnagar (10) considers nicotine to pose a significant threat to the cardiovascular system.
The former opinion is supported by the HPHC list. It includes both carbon monoxide and nicotine, however, they are attributed only reproductive and developmental toxicity and, in the case of nicotine, addictive properties as well.
Smoking-related harm reduction following a switch to electronic cigarettes
The most important difference between tobacco smoking and electronic cigarette (e-cigarette) use is the lack of the process of combustion in e-cigarettes. In e-cigarettes a nicotine fluid (called e-liquid) is used instead of tobacco. It contains nicotine, base substances (glycerine, propylene glycol) and flavouring. However, in the process of aerosol generation in e-cigarettes new compounds are formed as a result of high temperature. There are between about a dozen to several dozen such compounds and their number depends on the type of e-cigarette and the parameters of aerosol generation. However, their number is extremely small compared to the number of substances contained in tobacco smoke, which is estimated to include nearly 6 thousand substances (11).
Tayyarah and Long (12) concluded that the main stream of tobacco smoke from a cigarette contains 1,500 times more compounds from the HPHCs list than e-cigarette aerosol. Only five compounds from this group were found in the aerosol generated from the majority of commercially available nicotine liquids at amounts which might be a potential threat to the user’s health. These include acetaldehyde, acetone, acrolein, formaldehyde and nicotine. One of the most commonly cited multicentre studies demonstrated that the quantities of compounds contained in the aerosol are 9 to 450 times smaller than in tobacco smoke (13). Reports by prestigious institutions and organisations confirm the lower quantities of toxic compounds in the aerosol compared to tobacco smoke (14-18).
When we use the assessment criteria proposed for tobacco smoke (fig. 2a) to evaluate the impact of the aerosol on the cardiovascular system we can see a significant difference in the number of pathways and the strength of their influence (fig. 2b). There is no pathway associated with the presence of carbon monoxide, which binds to haemoglobin and causes chronic myocardial ischaemia in smokers. The strength of the pathway initiated by the products of combustion is much weaker due to the lack of PAH and a lower amount of oxidising compounds. The comparison of solid particles present in tobacco smoke and the aerosol remains a controversial issue. The composition and characteristics of solid particles in the aerosol are significantly different from those of tobacco smoke. At the same time, there are no sufficient data to determine their cardiovascular toxicity (17).
A smoker who stops using tobacco products and switches to e-cigarettes reduces the inhalation of the products of tobacco combustion to a large extent. Consequently, the negative influence of the aerosol on vascular endothelial function should be lower than that of tobacco smoke. This is corroborated by an extensive analysis by Knura et al. (19). The authors conclude that current data show vascular endothelium to be damaged by the aerosol, but to a smaller extent than by tobacco smoke. A recent study published in the prestigious journal „Circulation” demonstrates that oxidative stress caused by oxidising agents following the use of an e-cigarette increases to a smaller extent than in the case of a conventional cigarette (20).
A report by the United States Academies of Sciences concludes that there is limited evidence that the use of e-cigarettes is associated with a short-term increase in systolic blood pressure, oxidative stress, arterial rigidity and vascular endothelial dysfunction (17).
Based on clinical trials conducted to date Professor Benowitz and Burbank conclude that the general acute circulatory failure associated with e-cigarettes is consistent with the effect of nicotine use (21). In addition, the authors believe that the cardiovascular risk associated with nicotine inhaled from e-cigarettes is small in individuals with no symptoms of cardiovascular disease. Individuals with a diagnosed CVD are indeed at risk, but to a lesser extent than smokers. If conventional cigarettes are completely replaced with electronic ones, the harm will be significantly reduced, benefiting the cardiovascular system.
According to the recommendations for clinical guidance by the American Heart Association (AHA): „If a patient has failed initial treatment, has been intolerant to or refuses to use conventional smoking cessation medication, and wishes to use e-cigarettes to aid quitting, it is reasonable to support the attempt” (22).
Conclusions
The analysis of available data indicates that the replacement of tobacco smoking with smoke-free nicotine delivery systems leads to a decrease in CVD risk, but does not eliminate it completely. This could be expected considering the significantly lower amount of toxic substances contained in e-cigarette aerosol compared to tobacco smoke. Therefore, e-cigarettes constitute a classic substitution therapy used as part of the harm reduction strategy (23).
The fact that the use of smoke-free nicotine delivery systems is a less harmful form of nicotine addiction was known earlier. Since 1970 in Sweden there has been a growing interest in snus, a tobacco-based product which is placed behind the upper or lower lip, from where nicotine is absorbed. Currently, this product has practically ousted tobacco smoking in men in this country. Consequently, according to WHO data, CVD mortality in Sweden is the lowest in Europe and 2.4 times lower than the European average (24). Smokers should bear that in mind when reading media reports discussing single publications regarding e-cigarette aerosol toxicity. These publications are often based exclusively on studies conducted on cells without comparison to an equivalent amount of tobacco smoke in identical experimental conditions. They should also primarily remember that every form of nicotine delivery is harmful and it is only complete quitting of the habit that will bring actual health benefits.
Piśmiennictwo
1. U.S. Department of Health and Human Services: The Health Consequences of Smoking – 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health 2014.
2. Special Eurobarometer 458 „Attitudes of Europeans towards tobacco and electronic cigarettes” Report. European Union, 2017; http://ec.europa.eu/COMMFrontOffice/PublicOpinion.
3. Food and Drug Administration: Harmful and potentially Harmful Constituents in Tobacco Products and Tobacco Smoke. Established List. Federal Register 2012; 77(64): 20034-20037.
4. Bonetti PO, Lerman LO, Lerman A: Endothelial dysfunction: a marker of atherosclerotic risk. Arterioscler Thromb Vasc Biol 2003; 23: 168-175.
5. Benowitz NL: Cigarette smoking and cardiovascular disease: pathophysiology and implications for treatment. Prog Cardiovasc Dis 2003; 46(1): 91-111.
6. Csordas A, Bernhard D: The biology behind the atherothrombotic effects of cigarette smoke. Nat Rev Cardiol 2013; 10(4): 219-230.
7. Aune D, Schlesinger S, Norat T, Riboli E: Tobacco smoking and the risk of atrial fibrillation: A systematic review and meta-analysis of prospective studies. Eur J Prev Cardiol 2018. DOI: 10.1177/2047487318780435.
8. Aune D, Schlesinger S, Norat T, Riboli E: Tobacco smoking and the risk of sudden cardiac death: a systematic review and meta-analysis of prospective studies. Eur J Epidemiol 2018; 33(6): 509-521.
9. Benowitz NL, Fraiman JB: Cardiovascular effects of electronic cigarettes. Nat Rev Cardiol 2017; 14(8): 447-456.
10. Bhatnagar A: E-Cigarettes and Cardiovascular Disease Risk: Evaluation of Evidence, Policy Implications, and Recommendations. Curr Cardiovasc Risk Rep 2016; 10: 24.
11. Perfetti TA, Rodgman A: The complexity of tobacco and tobacco smoke. Beitr Tabakforsch Int 2011; 24: 215-232.
12. Tayyarah R, Long GA: Comparison of select analytes in aerosol from e-cigarettes with smoke from conventional cigarettes and with ambient air. Regul Toxicol Pharmacol 2014; 70(3): 704-710.
13. Goniewicz ML, Knysak J, Gawron M et al.: Levels of selected carcinogens and toxicants in vapour from electronic cigarettes. Tob Control 2014; 23(2): 133-139.
14. Public Health England: E-cigarettes: an evidence update A report commissioned by Public Health England. 2015.
15. Royal College of Physicians: Nicotine without smoke. 2016.
16. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. E-Cigarette Use Among Youth and Young Adults. A Report of the Surgeon General, 2016.
17. National Academies of Sciences, Engineering, and Medicine: Public health consequences of e-cigarettes. DC: The National Academies Press, Washington 2018.
18. McNeill A, Brose LS, Calder R et al.: Evidence review of e-cigarettes and heated tobacco products 2018. A report commissioned by Public Health England. London: Public Health England.
19. Knura M, Dragon J, Łabuzek K, Okopień B: Wpływ używania papierosów elektronicznych na funkcje śródbłonka naczyniowego. Pol Merkur Lekarski 2018; 44(259): 26-30.
20. Ikonomidis I, Vlastos D, Kourea K et al.: Electronic cigarette smoking increases arterial stiffness and oxidative stress to a lesser extent than a single conventional cigarette: an acute and chronic study. Circulation 2018; 137(3): 303-306.
21. Benowitz NL, Burbank AD: Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends Cardiovasc Med 2016; 26(6): 515-523.
22. Bhatnagar A, Whitsel LP, Ribisl KM et al.: American Heart Association Advocacy Coordinating Committee, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Quality of Care and Outcomes Research. Electronic cigarettes: a policy statement from the American Heart Association. Circulation 2014; 130(16): 1418-1436.
23. Prokopowicz A: Redukcja szkód związana z przyjmowaniem substancji psychoaktywnych. Med Rodz 2018; 21(1): 73-79.
24. Ramström L, Wikmans T: Mortality attributable to tobacco among men in Sweden and other European countries: an analysis of data in a WHO report. Tob Induc Dis 2014; 12(1): 14.
otrzymano: 2018-05-10
zaakceptowano do druku: 2018-05-31

Adres do korespondencji:
Andrzej Sobczak
Zakład Chemii Ogólnej i Nieorganicznej Wydział Farmaceutyczny z Oddziałem Medycyny Laboratoryjnej Śląski Uniwersytet Medyczny w Katowicach
ul. Jagiellońska 4, 41-200 Sosnowiec
tel.: +48 607-755-688, +48 (32) 293-23-56
asobczak@sum.edu.pl

Medycyna Rodzinna 2/2018
Strona internetowa czasopisma Medycyna Rodzinna

Pozostałe artykuły z numeru 2/2018: