Health effects of tobacco (Вплив (шкідливий) тютюну (куріння) на здоровя) + комп. переклад + ілюстрації - Мої файли - Каталог файлів

Tobacco is the single greatest cause of preventable death in the United States and worldwide. Tobacco use leads most commonly to diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, strokes, chronic obstructive pulmonary disease (COPD), emphysema, and cancer (particularly lung cancer, cancers of the larynx and mouth, and pancreatic cancer). It also causes peripheral vascular disease and hypertension, all developed due to the exposure time and the level of dosage of tobacco. Furthermore, the earlier and the higher level of tar content in the tobacco filled cigarettes causes the greater risk of these diseases. Cigarettes sold in developing nations tend to have higher tar content, and are less likely to be filtered, potentially increasing vulnerability to tobacco-related disease in these regions.

The World Health Organization (WHO) estimates that tobacco caused 5.4 million deaths in 2004 and 100 million deaths over the course of the 20th century. Similarly, the United States Centers for Disease Control and Prevention describes tobacco use as "the single most important preventable risk to human health in developed countries and an important cause of premature death worldwide."

Smoke contains several carcinogenic pyrolytic products that bind to DNA and cause many genetic mutations. There are over 19 known chemical carcinogens in cigarette smoke. Tobacco also contains nicotine, which is a highly addictive psychoactive chemical. When tobacco is smoked, nicotine causes physical and psychological dependency. Tobacco use is a significant factor in miscarriages among pregnant smokers, it contributes to a number of other threats to the health of the fetus such as premature births and low birth weight and increases by 1.4 to 3 times the chance for Sudden Infant Death Syndrome (SIDS). The result of scientific studies done in neonatal rats seems to indicate that exposure to cigarette smoke in the womb may reduce the fetal brain's ability to recognize hypoxicconditions, thus increasing the chance of accidental asphyxiation. Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers, and is a key factor causing erectile dysfunction (ED).

Smoke, or any partially burnt organic matter, contains carcinogens (cancer-causing agents). The potential effects of smoking, such as lung cancer, can take up to 20 years to manifest themselves. Historically, women began smoking en masse later than men, so an increased death rate caused by smoking amongst women did not appear until later. The male lung cancer death rate decreased in 1975 — roughly 20 years after the initial decline in cigarette consumption in men. A fall in consumption in women also began in 1975 but by 1991 had not manifested in a decrease in lung cancer related mortalities amongst women.

Smoke contains several carcinogenic pyrolytic products that bind to DNA and cause genetic mutations. Particularly potent carcinogens are polynuclear aromatic hydrocarbons (PAH), which are toxicated to mutagenic epoxides. The first PAH to be identified as a carcinogen in tobacco smoke was benzopyrene, which has been shown to toxicate into an epoxide that irreversibly attaches to a cell's nuclear DNA, which may either kill the cell or cause a genetic mutation. If the mutation inhibits programmed cell death, the cell can survive to become a cancer cell. Similarly, acrolein, which is abundant in tobacco smoke, also irreversibly binds to DNA, causes mutations and thus also cancer. However, it needs no activation to become carcinogenic.

* Polynuclear aromatic hydrocarbons are tar components produced by pyrolysis in smoldering organic matter and emitted into smoke. Many of them are highly carcinogenic and mutagenic, because they are toxicated to mutagenic epoxides, which areelectrophilic alkylating agents. The first PAH to be identified as a carcinogen in tobacco smoke was benzopyrene, which been shown to toxicate into a diol epoxide and then permanently attach to nuclear DNA, which may either kill the cell or cause agenetic mutation. The DNA contains the information on how the cell function; in practice, it contains the recipes for protein synthesis. If the mutation inhibits programmed cell death, the cell can survive to become a cancer cell, a cell that does not function like a normal cell. The carcinogenity is radiomimetic, i.e. similar to that produced by ionizing nuclear radiation. Tobacco manufacturers have experimented with combustionless vaporizer technology to allow cigarettes to be consumed without the formation of carcinogenic benzopyrenes. However, such products have not become popular.

* Acrolein is a pyrolysis product that is abundant in cigarette smoke. It gives smoke an acrid smell and an irritating, lachromatory effect and is a major contributor to its carcinogenity. Like PAH metabolites, acrolein is also an electrophilic alkylating agent and permanently binds to the DNA base guanine, by a conjugate addition followed by cyclization into a hemiaminal. The acrolein-guanine adduct induces mutations during DNA copying and thus causes cancers in a manner similar to PAHs. However, acrolein is 1000 times more abundant than PAHs in cigarette smoke, and is able to react as is, without metabolic activation. Acrolein has been shown to be a mutagen and carcinogen in human cells. The carcinogenity of acrolein has been difficult to study by animal experimentation, because it has such a toxicity that it tends to kill the animals before they develop cancer. Generally, compounds able to react by conjugate addition as electrophiles (so-called Michael acceptors after Michael reaction) are toxic and carcinogenic, because they can permanently alkylate DNA, similarly to mustard gas or aflatoxin. Acrolein is only one of them present in cigarette smoke; for example, crotonaldehyde has been found in cigarette smoke. Michael acceptors also contribute to the chronic inflammation present in tobacco disease.

* Nitrosamines are a group of carcinogenic compounds found in cigarette smoke but not in uncured tobacco leaves. Nitrosamines form on flue-cured tobacco leaves during the curing process through a chemical reaction between nicotine and other compounds contained in the uncured leaf and various oxides of nitrogen found in all combustion gases. Switching to Indirect fire curing has been shown to reduce nitrosamine levels to less than 0.1 parts per million.

In addition to chemical, nonradioactive carcinogens, tobacco and tobacco smoke contain small amounts of lead-210 (210Pb) and polonium-210 (210Po) both of which are radioactive carcinogens. The presence of polonium-210 in mainstream cigarette smoke has been experimentally measured at levels of 0.0263–0.036 pCi (0.97–1.33 mBq), which is equivalent to about 0.1 pCi per milligram of smoke (4 mBq/mg); or about 0.81 pCi of lead 210 per gram of dry condensed smoke (30 Bq/kg).

Research by NCAR radiochemist Ed Martell determined that radioactive compounds in cigarette smoke are deposited in "hot spots" where bronchial tubes branch. Since tar from cigarette smoke is resistant to dissolving in lung fluid, the radioactive compounds have a great deal of time to undergo radioactive decay before being cleared by natural processes. Indoors, these radioactive compounds linger in secondhand smoke, and therefore greater exposure occurs when these radioactive compounds are inhaled during normal breathing, which is deeper and longer than when inhaling cigarettes. Damage to the protective epithelial tissue from smoking only increases the prolonged retention of insoluble polonium 210 compounds produced from burning tobacco. Martell estimated that a carcinogenic radiation dose of 80–100 rads is delivered to the lung tissue of most smokers who die of lung cancer.

Nicotine that is contained in cigarettes and other smoked tobacco products is a stimulant and is one of the main factors leading to continued tobacco smoking. Although the amount of nicotine inhaled with tobacco smoke is quite small (most of the substance is destroyed by the heat) it is still sufficient to cause physical and/or psychological dependence. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. Despite the design of various cigarettes advertised and even tested on machines to deliver less of the toxic tar, studies show that when smoked by humans instead of machines, they deliver the same net amount of smoke. Ingesting a compound by smoking is one of the most rapid and efficient methods of introducing it into the bloodstream, second only to injection, which allows for the rapid feedback which supports the smokers' ability to titrate their dosage. On average it takes about ten seconds for the substance to reach the brain. As a result of the efficiency of this delivery system, many smokers feel as though they are unable to cease. Of those who attempt cessation and last three months without succumbing to nicotine, most are able to remain smoke free for the rest of their lives.[48] There exists a possibility of depression in some who attempt cessation, as with other psychoactive substances. Depression is also common in teenage smokers; teens who smoke are four times as likely to develop depressive symptoms as their nonsmoking peers.

Although nicotine does play a role in acute episodes of some diseases (including stroke, impotence, and heart disease) by its stimulation of adrenaline release, which raises blood pressure, heart rate, and free fatty acids, the most serious longer term effects are more the result of the products of the smouldering combustion process. This has enabled development of various nicotine delivery systems, such as the nicotine patch or nicotine gum, that can satisfy the addictive craving by delivering nicotine without the harmful combustion by-products. This can help the heavily dependent smoker to quit gradually, while discontinuing further damage to health.

Nicotine is a highly addictive psychoactive chemical. When tobacco is smoked, most of the nicotine is pyrolyzed; a dose sufficient to cause mild somatic dependency and mild to strong psychological dependency remains. There is also a formation ofharmane (a MAO inhibitor) from the acetaldehyde in cigarette smoke, which seems to play an important role in nicotine addiction probably by facilitating dopamine release in the nucleus accumbens in response to nicotine stimuli. According to studies by Henningfield and Benowitz, nicotine is more addictive than cannabis, caffeine, ethanol, cocaine, and heroin when considering both somatic and psychological dependence. However, due to the stronger withdrawal effects of ethanol, cocaine and heroin, nicotine may have a lower potential for somatic dependence than these substances. About half of Canadians who currently smoke have tried to quit. McGill University health professor Jennifer O'Loughlin stated that nicotine addiction can occur as soon as five months after the start of smoking.[55]

Recent evidence has shown that smoking tobacco increases the release of dopamine in the brain, specifically in the mesolimbic pathway, the same neuro-reward circuit activated by drugs of abuse such as heroin and cocaine. This suggests nicotine use has a pleasurable effect that triggers positive reinforcement. One study found that smokers exhibit better reaction-time and memory performance compared to non-smokers, which is consistent with increased activation of dopamine receptors. Neurologically, rodent studies have found that nicotine self-administration causes lowering of reward thresholds—a finding opposite that of most other drugs of abuse (e.g. cocaine and heroin). This increase in reward circuit sensitivity persisted months after the self-administration ended, suggesting that nicotine's alteration of brain reward function is either long lasting or permanent. Furthermore, it has been found that nicotine can activate long term potentiation in vivo and in vitro. These studies suggest nicotine’s "trace memory" may contribute to difficulties in nicotine abstinence.

Genetic markers of more than 35,000 people (mostly smokers and ex-smokers) were surveyed by scientists in three separate studies, and all three found lung cancer to be associated with similar sets of genetic differences. The genetic variations of note encode nicotine receptors on cells and were identified on a region of chromosome 15. Possessing a single copy of the mutation raises an individual's risk of lung cancer by approximately 30%; for two copies the increase is about 80%. The gene was found to be attributable to 14% of lung cancer cases, and it was found to confer similar lung cancer risks irrespective of smoking status or quantity smoked.

Another study related to genetic changes in smokers was conducted by Wan L Lam and Stephen Lam from the BC Cancer Agency, in 2007. The study revealed that cigarette smoke can turn on or off some of the genes, which otherwise would remain inactive. Some changes on genetic level could be reversed after the smoking was quit, yet others could not. Examples of reversible genes involved the so-called xenofobic functions, nucleotide metabolism and mucus secretion. Smoking turns off some DNA repair genes that cannot be reversed. It also switches off some genes responsible from protection from cancer growth in the body.

A person's increased risk of contracting disease is directly proportional to the length of time that a person continues to smoke as well as the amount smoked. However, if someone stops smoking, then these chances gradually decrease as the damage to their body is repaired. A year after quitting, the risk of contracting heart disease is half that of a continuing smoker. The health risks of smoking are not uniform across all smokers. Risks vary according to amount of tobacco smoked, with those who smoke more at greater risk. Light smoking is still a health risk. Likewise, smoking "light" cigarettes does not reduce the risks.

Tobacco use most commonly leads to diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, Chronic Obstructive Pulmonary Disease (COPD), emphysema, and cancer, particularly lung cancer, cancers of thelarynx and mouth, and pancreatic cancer. Overall life expectancy is also reduced in regular smokers, with estimates ranging from 10 to 17.9 years fewer than nonsmokers. About two thirds of male smokers will die of illness due to smoking.The association of smoking with lung cancer is strongest, both in the public perception and etiologically. People who have smoked tobacco at some point have about a one in ten chance of developing lung cancer during their lifetime. If one looks at men who continue to smoke tobacco, the risk increases to one in six. Historically, lung cancer was considered to be a rare disease prior to World War I and was perceived as something most physicians would never see during their career. With the postwar rise in popularity of cigarette smoking came a virtual epidemic of lung cancer.

Secondhand smoke is a mixture of smoke from the burning end of a cigarette, pipe or cigar and the smoke exhaled from the lungs of smokers. It is involuntarily inhaled, lingers in the air hours after cigarettes have been extinguished, and can cause a wide range of adverse health effects, including cancer, respiratory infections and asthma. Nonsmokers who are exposed to secondhand smoke at home or work increase their heart disease risk by 25–30% and their lung cancer risk by 20–30%. Secondhand smoke has been estimated to cause 38,000 deaths per year, of which 3,400 are deaths from lung cancer in non-smokers.It should be noted here that although these studies present these facts and figures, there is no mention of how much second hand smoke was fed to those participating in the studies.

Smoking also increases the chance of heart disease, stroke, atherosclerosis, and peripheral vascular disease. Several ingredients of tobacco lead to the narrowing of blood vessels, increasing the likelihood of a blockage, and thus aheart attack or stroke. According to a study by an international team of researchers, people under 40 are five times more likely to have a heart attack if they smoke.[93]

The current Surgeon General’s Report concluded that there is no risk-free level of exposure to secondhand smoke. Even short exposures to secondhand smoke can cause blood platelets to become stickier, damage the lining of blood vessels, decrease coronary flow velocity reserves, and reduce heart rate variability, potentially increasing the risk of heart attack. New research indicates that private research conducted by cigarette company Philip Morris in the 1980s showed that secondhand smoke was toxic, yet the company suppressed the finding during the next two decades.

Although cigarette smoking causes a greater increase of the risk of cancer than cigar smoking, cigar smokers still have an increased risk for many health problems, including cancer, when compared to non-smokers. As for Environmental Tobacco Smoke (ETS, or "Second-hand Smoking"), the NIH study points to the large amount of smoke generated by one cigar, saying "cigars can contribute substantial amounts of tobacco smoke to the indoor environment; and, when large numbers of cigar smokers congregate together in a cigar smoking event, the amount of ETS produced is sufficient to be a health concern for those regularly required to work in those environments."

Smoking tends to increase blood cholesterol levels. Furthermore, the ratio of high-density lipoprotein (the "good" cholesterol) to low-density lipoprotein (the "bad" cholesterol) tends to be lower in smokers compared to non-smokers. Smoking also raises the levels of fibrinogen and increases platelet production (both involved in blood clotting) which makes the blood viscous. Carbon monoxide binds to haemoglobin (the oxygen-carrying component in red blood cells), resulting in a much stabler complex than haemoglobin bound with oxygen or carbon dioxide—the result is permanent loss of blood cell functionality. Blood cells are naturally recycled after a certain period of time, allowing for the creation of new, functional erythrocytes. However, if carbon monoxide exposure reaches a certain point before they can be recycled, hypoxia (and later death) occurs. All these factors make smokers more at risk of developing various forms of arteriosclerosis. As the arteriosclerosis progresses, blood flows less easily through rigid and narrowed blood vessels, making the blood more likely to form a thrombosis (clot). Sudden blockage of a blood vessel may lead to an infarction (stroke). However, it is also worth noting that the effects of smoking on the heart may be more subtle. These conditions may develop gradually given the smoking-healing cycle (the human body heals itself between periods of smoking), and therefore a smoker may develop less significant disorders such as worsening or maintenance of unpleasant dermatological conditions, e.g. eczema, due to reduced blood supply. Smoking also increases blood pressure and weakens blood vessels.

A study of an outbreak of A(H1N1) influenza in an Israeli military unit of 336 healthy young men to determine the relation of cigarette smoking to the incidence of clinically apparent influenza, revealed that, of 168 smokers, 68.5 percent had influenza, as compared with 47.2 percent of nonsmokers. Influenza was also more severe in the smokers; 50.6 percent of the smokers lost work days or required bed rest, or both, as compared with 30.1 percent of the nonsmokers.

Perhaps the most serious oral condition that can arise is that of oral cancer. However, smoking also increases the risk for various other oral diseases, some almost completely exclusive to tobacco users. The National Institutes of Health, through the National Cancer Institute, determined in 1998 that "cigar smoking causes a variety of cancers including cancers of the oral cavity (lip, tongue, mouth, throat), esophagus, larynx, and lung." Pipe smoking involves significant health risks, particularly oral cancer. Roughly half of periodontitis or inflammation around the teeth cases are attributed to current or former smoking. Smokeless tobacco causes gingival recession and white mucosal lesions. Up to 90% of periodontitis patients who are not helped by common modes of treatment are smokers. Smokers have significantly greater loss of bone height than nonsmokers, and the trend can be extended to pipe smokers to have more bone loss than nonsmokers. Smoking has been proven to be an important factor in the staining of teeth. Halitosis or bad breath is common among tobacco smokers. Tooth loss has been shown to be 2 to 3 times higher in smokers than in non-smokers. In addition, complications may further include leukoplakia, the adherent white plaques or patches on the mucous membranes of the oral cavity, including the tongue, and a loss of taste sensation or salivary changes.

Tobacco is also linked to susceptibility to infectious diseases, particularly in the lungs. Smoking more than 20 cigarettes a day increases the risk of tuberculosis by two to four times, and being a current smoker has been linked to a fourfold increase in the risk of invasive pneumococcal disease. It is believed that smoking increases the risk of these and other pulmonary and respiratory tract infections both through structural damage and through effects on the immune system. The effects on the immune system include an increase in CD4+ cell production attributable to nicotine, which has tentatively been linked to increased HIV susceptibility. The usage of tobacco also increases rates of infection: common cold and bronchitis, chronic obstructive pulmonary disease, emphysema and chronic bronchitis in particular.

In a study of men aged 24 to 36 seeking treatment for infertility, Panayiotis Zavos, Ph.D., confirmed the results of earlier studies demonstrating that smoking harms sperm quality in every way, from longevity to motility. But Zavos also found that smoking affected sexual behavior. The smokers had sex an average of 5.7 times per month, while the nonsmokers reported an average of 11.6 encounters. And on a scale of 1 to 10, the smokers rated the quality of sex at a lackluster 5.2, compared to 8.7 for nonsmokers."

Smokers often report that cigarettes help relieve feelings of stress. However, the stress levels of adult smokers are slightly higher than those of nonsmokers, adolescent smokers report increasing levels of stress as they develop regular patterns of smoking, and smoking cessation leads to reduced stress. Far from acting as an aid for mood control, nicotine dependency seems to exacerbate stress. This is confirmed in the daily mood patterns described by smokers, with normal moods during smoking and worsening moods between cigarettes. Thus, the apparent relaxant effect of smoking only reflects the reversal of the tension and irritability that develop during nicotine depletion. Dependent smokers need nicotine to remain feeling normal.

Most smokers, when denied access to nicotine, exhibit symptoms such as irritability, jitteriness, dry mouth, and rapid heart beat. The onset of these symptoms is very fast, nicotine's half-life being only 2 hours. Withdrawal symptoms can appear even if the smoker's consumption is very limited or irregular, appearing after only 4–5 cigarettes in most adolescents. An ex-smoker's chemical dependence to nicotine will cease after approximately ten to twenty days, although the brain's number of nicotine receptors is permanently altered, and the psychological dependence may linger for months or even many years. Unlike some recreational drugs, nicotine does not measurably alter a smoker's motor skills, judgement, or language abilities while under the influence of the drug. Tobacco withdrawal has been shown to cause clinically significant distress.

Most notably, some studies have found that patients with Alzheimer's disease are more likely not to have smoked than the general population, which has been interpreted to suggest that smoking offers some protection against Alzheimer's. However, the research in this area is limited and the results are conflicting; some studies show that smoking increases the risk of Alzheimer's disease. A recent review of the available scientific literature concluded that the apparent decrease in Alzheimer risk may be simply because smokers tend to die before reaching the age at which Alzheimer normally occurs. "Differential mortality is always likely to be a problem where there is a need to investigate the effects of smoking in a disorder with very low incidence rates before age 75 years, which is the case of Alzheimer's disease," it stated, noting that smokers are only half as likely as non-smokers to survive to the age of 80.

Former and current smokers have a lower incidence of Parkinson's disease compared to people who have never smoked, although the authors stated that it was more likely that the movement disorders which are part of Parkinson's disease prevented people from being able to smoke than that smoking itself was protective. Another study considered a possible role of nicotine in reducing Parkinson's risk: nicotine stimulates the dopaminergic system of the brain, which is damaged in Parkinson's disease, while other compounds in tobacco smoke inhibit MAO-B, an enzyme which produces oxidative radicals by breaking down dopamine.

A very large percentage of schizophrenics smoke tobacco as a form of self medication. The high rate of tobacco use by the mentally ill is a major factor in their decreased life expectancy, which is about 25 years shorter than the general population. Following the observation that smoking improves condition of people with schizophrenia, in particular working memory deficit, nicotine patches had been proposed as a way to treat schizophrenia. Some studies suggest that a link exists between smoking and mental illness, citing the high incidence of smoking amongst those suffering from schizophrenia and the possibility that smoking may alleviate some of the symptoms of mental illness, but these have not been conclusive.

Data from multiple studies suggest that anxiety disorders and depression play a role in cigarette smoking. A history of regular smoking was observed more frequently among individuals who had experienced a major depressive disorder at some time in their lives than among individuals who had never experienced major depression or among individuals with no psychiatric diagnosis. People with major depression are also much less likely to quit due to the increased risk of experiencing mild to severe states of depression, including a major depressive episode. Depressed smokers appear to experience more withdrawal symptoms on quitting, are less likely to be successful at quitting, and are more likely to relapse.

Evidence suggests that non-smokers are up to twice as likely as smokers to develop Parkinson's disease or Alzheimer's disease. A plausible explanation for these cases may be the effect of nicotine, a cholinergic stimulant, decreasing the levels of acetylcholine in the smoker's brain; Parkinson's disease occurs when the effect of dopamine is less than that of acetylcholine. In addition, nicotine stimulates the mesolimbic dopamine pathway (as do other drugs of abuse), causing an effective increase in dopamine levels. Opponents counter by noting that consumption of pure nicotine may be as beneficial as smoking without the risks associated with smoking, although this is unlikely due to the importance of the MAO-B inhibitor compounds of tobacco in preventing neurodegenerative diseases.

Studies suggest that smoking decreases appetite, but did not conclude that overweight people should smoke or that their health would improve by smoking. This is also a cause of heart diseases. However due to some new processes of treating tobacco, especially in the case of cigarette, heavy smokers tend to become overweight as the processing involves large quantities of starch.This effect is not seen in occasional smokers. Smoking also decreases weight by overexpressing the gene AZGP1 which stimulates lipolysis.

Although there is a protective effect of current smoking against ulcerative colitis, smoking increases the risk of Crohn's disease, the other form of inflammatory bowel disease. There is some evidence for decreased rates of endometriosis in infertile smoking women, although other studies have found that smoking increases the risk in infertile women. There is little or no evidence of a protective effect in fertile women. Some preliminary data from 1996 suggested a reduced incidence of uterine fibroids, but overall the evidence is unconvincing.

Вплив тютюну на здоров'я є обставини, механізми та чинники споживання тютюну на здоров'я людини. Епідеміологічні дослідження були зосереджені головним чином на куріння тютюну, яка була вивчена більш широко, ніж будь-які інші форми споживання.

Тютюн є єдиною причиною предотвратимой смертності в Сполучених Штатах [3] і у всьому світі. [4] Вживання тютюну призводить найчастіше до хвороб, що впливають на серце і легені, з курінням, будучи основним фактором ризику розвитку інфарктів, інсультів, хронічної обструктивної хвороба легень (ХОЗЛ), емфізема та рак (особливо рак легенів, рак гортані і рота, і раком підшлункової залози). Він також викликає захворювання периферичних судин і гіпертонією, все розроблено у зв'язку з часом експозиції і рівня дози тютюну. Крім того, раніше й більш високий рівень вмісту смол в тютюнових заповнені сигарет викликає більший ризик цих захворювань. Сигарети продаються в країнах, що розвиваються, як правило, мають більш високий вміст смол, і мають менше шансів бути відфільтровані, що потенційно підвищує їх вразливість для пов'язаних з тютюном хвороб у цих регіонах.

Всесвітня організація охорони здоров'я (ВООЗ) вважає, що тютюн викликало смерті 5,4 мільйона чоловік в 2004 році і 100 мільйонів випадків смерті протягом 20-го століття. Аналогічним чином, Центрами США з контролю і профілактиці захворювань описує тютюн використання в якості "найбільш важливим запобігти ризику для здоров'я людини в розвинених країнах і важливою причиною передчасної смерті в усьому світі."

Дим містить канцерогенні кілька піролітичних продуктів, які зв'язуються з ДНК і викликають багато генетичних мутацій. Є понад 19 відомих хімічних канцерогенів у сигаретному димі. Тютюн також містить нікотин, який є сильне звикання психоактивних хімічних речовин. Коли тютюн курили, нікотин викликає фізичну та психологічну залежність. Вживання тютюну є важливим чинником у викиднів серед вагітних курців, вона вносить свій внесок до ряду інших загроз для здоров'я плоду, таких як передчасні пологи і низька вага при народженні і збільшується від 1,4 до 3 разів шанс для синдром раптової дитячої смерті (SIDS ). Результаті наукових досліджень, проведених у новонароджених щурів, здається, показують, що дія сигаретного диму в утробі матері може зменшити здатність мозку плоду визнати hypoxicconditions, тим самим збільшуючи ймовірність випадкового задухи.Захворюваність імпотенції становить близько 85 відсотків вище, в чоловіків, які палять в порівнянні з некурящими, [11] і є ключовим чинником, що викликає еректильної дисфункції (ЕД).

		П`ятниця, 26.04.2024
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