Ludzkie koronawirusy - autor: Krzysztof Pyrć z Zakładu Mikrobiologii, Wydział Biochemii, Biofizyki i Biotechnologii, Uniwersytet Jagielloński, Kraków

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© 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.

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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.
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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.
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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

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