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The health effects of tobacco are the circumstances, mechanisms, and factors of tobacco consumption on human health. Epidemiological research have been focused primarily on tobacco smoking, which has been studied more extensively than any other form of consumption. As of 2000, smoking is practiced by some 1.22 billion people, of which men are more likely to smoke than women, however the gender gap declines with age, poor more likely than rich, and people of developing countries than those of developed countries.

Fresh tobacco, processed tobacco, and tobacco smoke contain carcinogens. The current view on cancer is that carcinogenicity is a stochastic effect, where various environmental factors trigger the development of cancer. While exposure to a carcinogen increases the probability of cancer, the process remains random. For example, smoking tobacco is known to cause cancer in humans, but not all people who smoke necessarily develop smoking-related cancer. In studies on humans, the large number of confounding variables makes it challenging to statistically distinguish their effects.

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.

Epidemiology

Prevalence

While a more general measure of the usage of tobacco (both smoked and smokeless) would be more ideal, the World Health Organization (WHO) reports "data limitations restrict the present indicator to smoked tobacco". Smoking has therefore been studied more extensively than any other form of consumption.

As of 2000, smoking is practiced by 1.22 billion people. Assuming no change in prevalence it is predicted that 1.45 billion people will smoke in 2010 and 1.5 to 1.9 billion in 2025. Assuming that prevalence will decrease at 1% a year and that there will be a modest increase of income of 2%, it is predicted the number of smokers will stand at 1.3 billion in 2010 and 2025.

Smoking is generally five times higher among men than women, however the gender gap begins decline with younger age. As of 2002 in China 67% of men smoke as to 4% of women, however among teens the gap closes to 33% among men as to 8% with women. In developed countries smoking rates for men have peaked and have begun to decline, however for women they continue to climb.

As of 2002, about twenty percent of young teens (13–15) smoke worldwide. From which 80,000 to 100,000 children begin smoking every day, of which roughly half of which live in Asia. Half of those who begin smoking in adolescent years go on to smoke for 15 to 20 years.

"Much of the disease burden and premature mortality attributable to tobacco use disproportionately affect the poor." Of the 1.22 billion smokers, 1 billion of them live in developing or transitional economies. Rates of smoking have leveled off or declined in the developed world, from which the United States have dropped by half from 1965 to 2006 falling from 42% to 20.8% in adults. However, up to 30% of men are former smokers in developed countries, only 2% of men in China have quit, and 10% in Vietnam. In the developing world, however, tobacco consumption is rising by 3.4% per year as of 2002.

The WHO in 2004 projected 58.8 million deaths to occur globally, from which 5.4 million are tobacco-attributed, and 4.9 million as of 2007. As of 2002, 70% of the deaths are in developing countries.

Vectors

• Chewing tobacco is one of the oldest ways of consuming tobacco leaves. The leaves are gently compacted against the lip. This stimulates the salivary glands, which creates sputum.
• Gutka is a preparation of crushed betel nut, tobacco, catechu, lime, and flavorings. It is manufactured, exported, and consumed in India. Social custom does not permit children in India to smoke cigarettes, it has therefore become increasingly popular.
• Smoking encompasses Beedi, Cigarette, Cigar, Hookah, Kreteks, and Pipe.
  • Beedis, similar to cigarettes, are becoming increasingly popular in India and other South-East Asia. It produces three times more carbon monoxide and nicotine and five times more tar than regular cigarettes.
  • Cigarette smoking is the most common method of tobacco consumption. There is no credible evidence that "Low Tar," "Light," or "Ultra Light" cigarettes are safer than regular cigarettes. Most of these terms refer to the type of filter that is used, and can vary depending on the brand. In some countries, advertising cigarettes as being "Light" has been banned. Smoking cigarettes increases mortality rates by 40% in those who smoke less than 10 cigarettes a day, by 70% in those who smoke 10–19 a day, by 90% in those who smoke 20–39 a day, and by 120% in those smoking two packs a day or more.
  • Cigar smoking is generally not inhaled as is cigarette smoke, because the high alkalinity of the smoke can quickly become irritating to the trachea and lungs. The relative risk for cigar-only smokers of all-cause mortality is 1.02 for 1-2 cigars/day, 1.08 for 3-4 cigars/day, and 1.17 for 5+ cigars/day. A NIH study done concerning those who smoked at least one cigar per day, found that "The health risks associated with less than daily smoking (occasional smokers) are not known." Though most cigar smokers do not inhale, those that do have risks of lung cancer similar to cigarette smokers. Increased risk for heart attack is less for cigar smokers, but still present.
  • Hookah, also referred to as Shishas, are smoked in Eastern Mediterranean region. Some studies suggest that hookah smoking is safer than other forms of smoking. However, water is not effective for removing all relevant toxic substances. For instance, the carcinogenic aromatic hydrocarbons are not water-soluble. Several negative health effects are linked to hookah smoking and studies indicate that it is likely to be more harmful than cigarettes, due in part to the volume of smoke inhaled.
  • Kreteks are clove and tobacco cigarettes most commonly smoked in Indonesia.
  • Pipe smoking are the usage of tobacco from which the tobacco leaves are ground and placed into a pipe for inhalation. Pipe smoking has also been researched and found to increase the risk of various cancers by 33%. In addition to the cancer risk, there is some risk of infectious disease resulting from pipe sharing, and other risks associated with the common addition of other psychoactive drugs to the tobacco.
• Secondhand smoke, also called passive smoking, it is a involuntary inhalation from the end of cigarette, cigar, pipe, or otherwise.
• Snuff is a smokeless tobacco inhaled through the nose.
• Snus, also with the variation of dipping tobacco, are placed between the upper lip and teeth, where nicotine is absorbed into the bloodstream through the mucous membrane.

Studies

A team of British scientists headed by Richard Doll carried out a longitudinal study of 34,439 medical specialists from 1951 to 2001, generally called the "British doctors study." The study demonstrated that smoking decreased life expectancy by up to 10 years and that almost half of the smokers died from diseases possibly caused by smoking (cancer, heart disease, and stroke).

After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17 percent reduction in hospital admissions for acute coronary syndrome. 67% of the decrease occurred in non-smokers.

The health effects of tobacco have been significant for the development of the science of epidemiology. As the mechanism of carcinogenicity is radiomimetic or radiological, the effects are stochastic. Definite statements may be made only on probabilities of contracting disease. When considered philosophically and theoretically, it is — in principle — impossible to prove a direct causative link between exposure to a radiomimetic poison such as tobacco smoke and the cancer that follows. Tobacco companies have capitalized on this philosophical objection and exploited the doubts of clinicians, who consider only individual cases, on the causal link in the stochastic expression of the toxicity as actual disease.

There have been multiple court cases on the issue that tobacco companies have researched the health effects of tobacco, but suppressed the findings or formatted them to imply lessened or no hazard.

A study published in the journal Pediatrics refers to the danger posed by what the authors call "third-hand smoke" — toxic substances that remain in areas where smoking has recently occurred. The study was reviewed in an story broadcast by the Voice of America.

Mechanism

Chemical carcinogens

Smoke, or any partially burnt organic matter, is carcinogenic (cancer-causing). The damage a continuing smoker does to their lungs can take up to 20 years before its physical manifestation in lung cancer. Women began smoking later than men, so the rise in death rate amongst women did not appear until later. The male lung cancer death rate decreased in 1975 — roughly 20 years after the fall 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.

There are over 19 known carcinogens in cigarette smoke. The following are some of the most potent carcinogens:

• 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 are electrophilic 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 a genetic 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.

Radioactive carcinogens

In addition to chemical, nonradioactive carcinogens, tobacco and tobacco smoke contain small amounts of lead-210 (Pb) and polonium-210 (Po) both of which are radioactive carcinogens. Lead 210 is a product of the decay of radium-226 and, in turn, its decay product, radon-222; lead 210 then decays to bismuth-210 and then to polonium 210, emitting beta particles in both steps. Tarry particles containing these elements lodge in the smokers' lungs where airflow is disturbed; the concentration found where bronchioles bifurcate is 100 times higher than that in the lungs overall. This gives smokers much more intense exposure than would otherwise be encountered. Polonium 210, for instance, emits high energy alpha particles which, because of their large mass, are considered to be incapable of penetrating the skin more than 40 micrometres deep, but do considerable damage (estimated at 100 times as much chromosome damage as a corresponding amount of other radiation) when a process such as smoking causes them to be emitted within the body, where all their energy is absorbed by surrounding tissue. (Lead 210 also emits gamma rays).

The radioactive elements in tobacco are accumulated from the minerals in the soil, as with any plant, but are also captured on the sticky surface of the tobacco leaves in excess of what would be seen with plants not having this property. As might be expected, the radioactivity measured in tobacco varies widely depending on where and how it is grown. One study found that tobacco grown in India averaged only 0.09 pico-Curies per gram (3.3 Bq/kg) of polonium-210, whereas tobacco grown in the United States averaged 0.516 pCi per gram (19.1 Bq/kg). Another study of Indian tobacco, however, measured an average of 0.4 pCi (15 mBq) of polonium 210 per cigarette, which also would be approximately a gram of tobacco. One factor in the difference between India and the United States may be the extensive use of apatite as fertilizer for tobacco in the United States, because it starves the plant for nitrogen, thereby producing more flavorful tobacco; apatite is known to contain radium, lead 210, and polonium 210. This would also account for increased concentration of these elements compared to other crops, which do not use this mineral as fertilizer.

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). The amount of polonium 210 inhaled from a pack of 20 cigarettes is therefore about 0.72 pCi (27 mBq). This seems to be independent of any form of filtering or 'low tar' cigarette. This concentration results in a highly significant increase in the body burden of these compounds. Compared to nonsmokers, heavy smokers have four times greater radioisotope density throughout their lungs. The polonium 210 content of blood in smokers averages 1.72 pCi per kilogram (64 mBq/kg), compared to 0.76 pCi per kilogram (28 mBq/kg) in nonsmokers. Higher concentrations of polonium 210 are also found in the livers of smokers than nonsmokers. Polonium 210 is also known to be incorporated into bone tissue, where the continued irradiation of bone marrow may be a cause of leukemia, although this has not been proved as yet.

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 the lung tissue of most smokers who die of lung cancer.

In other experiments, the alpha particle dosage from polonium 210 received by smokers of two packs a day was measured at 82.5 millirads (0.825 mGy) per day, which would total 750 rads (7.5 Gy) per 25 years, 150 times higher than the approximately 5 rem (50 mSv) received from natural background radiation over 25 years. Other estimates of the dosage absorbed over 25 years of heavy smoking range from 165 to 1,000 rem (1.65 to 10 Sv), all significantly higher than natural background. In the case of the less radioactive Indian tobacco referred to above, the dosage received from polonium 210 is about 24 millirads (0.24 mGy) a day , totalling 219 rads (2.19 Gy) over 25 years or still about 40 times the natural background radiation exposure. In fact, all these numbers of total body burden are misleadingly low, because the dosage rate in the immediate vicinity of the deposited polonium 210 in the lungs can be from 100 to 10,000 times greater than natural background radiation. Lung cancer is seen in laboratory animals exposed to approximately one fifth of this total dosage of polonium 210.

Whether the quantities of these elements are sufficient to cause cancer is still a matter of debate. Most studies of carcinogenicity of tobacco smoke involve painting tar condensed from smoke onto the skin of mice and monitoring for development of tumors of the skin, a relatively simple process. However, the specific properties of polonium 210 and lead 210 and the model for their action, as described above, do not permit such a simple assay and require more difficult studies, requiring dosage of the mice in a manner mimicking smoking behavior of humans and monitoring for lung cancer, more difficult to observe as it is internal to the mouse.

Some researchers suggest that the degree of carcinogenicity of these radioactive elements is sufficient to account for most, if not all, cases of lung cancer related to smoking. In support of this hypothetical link between radioactive elements in tobacco and cancer is the observation that bladder cancer incidence is also proportional to the amount of tobacco smoked, even though nonradioactive carcinogens have not been detected in the urine of even heavy smokers; however, urine of smokers contains about six times more polonium 210 than that of nonsmokers, suggesting strongly that the polonium 210 is the cause of the bladder carcinogenicity, and would be expected to act similarly in the lungs and other tissue. Furthermore, many of the lung cancers contracted by cigarette smokers are adenocarcinomas, which are characteristic of the type of damage produced by alpha particle radiation such as that of polonium 210. It has also been suggested that the radioactive and chemical carcinogens in tobacco smoke act synergistically to cause a higher incidence of cancer than each alone.

However, the view that polonium 210 is responsible for many cases of cancer in tobacco smokers is disputed by at least one researcher.

Nicotine

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. 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 of harmane (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, overall 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. A study by Perrine concludes that nicotine's potential for psychological dependency exceeds all other studied drugs - even ethanol, an extremely physically addictive substance with severe withdrawal symptoms that can be fatal. 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.

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 suggests nicotine’s "trace memory" may contribute to difficulties in nicotine abstinence.

The carcinogenity of tobacco smoke is not explained by nicotine per se, which is not carcinogenic or mutagenic. However, it inhibits apoptosis, therefore accelerating existing cancers. Also, NNK, a nicotine derivative converted from nicotine, can be carcinogenic.

Genetic

According to three separate studies commissioned by governments in the US and Europe, scientists have identified a genetic link that makes people more likely to become addicted to tobacco. This genetic variation causes individuals to smoke more cigarettes, makes it harder for them to quit and increases their likelihood of developing lung cancer by up to 80%.

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 permanently some genes responsible from protection from cancer growth in the body.

Prognosis

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Most scientists involved in cancer research believe that the environmental factors, which include anything the people interact with such as lifestyle choices, their diet, natural and medical radiation, sunlight exposure, workplace exposure, and socioeconomic factors that affect exposures and susceptibility—may be a major contributor to the development of cancer. Other factors that play a major role in cancer development are infectious diseases, aging, and individual susceptibility such as genetic predisposition. Because of these confounding variables, it is difficult to distinguish which factor or condition contributes to the development of cancer. For example, smoking tobacco is known to cause cancer in humans, but not all people who smoke develop smoking-related cancer; however, with some substances or exposure circumstances, cancer may develop after even brief exposure.

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 the larynx and mouth, and pancreatic cancer. Overall life expectancy is also reduced in regular smokers, with estimates ranging from 2.5 to 10 years fewer than nonsmokers. About half 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.

A person's increased risk of contracting disease is directly proportional to the length of time that a person smokes, as well as to the amount smoked, and doctors use the approximation "pack years" in assessing the likelihood of smoking-related illness. However, if someone stops smoking, then their risk declines over time, and the reduction in their lung function will stop.

Pulmonary

In smoking, long term exposure to compounds found in the smoke such as carbon monoxide, cyanide, and so forth—, are believed to be responsible for pulmonary damage and for loss of elasticity in the alveoli, leading to emphysema and COPD. The carcinogen acrolein and its derivatives also contribute to the chronic inflammation present in COPD.

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.

Cardiovascular

Chronic obstructive pulmonary disease (COPD) caused by smoking, known as tobacco disease, is a permanent, incurable reduction of pulmonary capacity characterized by shortness of breath, wheezing, persistent cough with sputum, and damage to the lungs, including emphysema and chronic bronchitis.

Inhalation of tobacco smoke causes several immediate responses within the heart and blood vessels. Within one minute the heart rate begins to rise, increasing by as much as 30 percent during the first 10 minutes of smoking. Carbon monoxide in tobacco smoke exerts its negative effects by reducing the blood’s ability to carry oxygen.

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 a heart 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.

Latest research of the American biologists have determined that cigarette smoke also influences the process of cell division in the cardiac muscle and changes heart's shape.

The usage of tobacco has also been linked to Buerger's disease (thromboangiitis obliterans) the acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet.

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 (e.g. 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.

Oral

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 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 extend 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.

Infection

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.

Smoking reduces the risk of Kaposi's sarcoma in people without HIV infection.

Psychological

Smokers report a variety of physical and psychological effects from smoking tobacco. Those new to smoking may experience nausea, dizziness, and rapid heart beat. The unpleasant symptoms will eventually vanish over time, with repeated use, as the body builds a tolerance to the chemicals in the cigarettes, such as nicotine. The usage of tobacco also creates cognitive dysfunction, which include: increased risk (or decrease) of Alzheimer's disease and decline in cognitive abilities, reduced memory and cognitive abilities in adolescent smokers, brain shrinkage (cerebral atrophy)

In many respects, nicotine acts on the nervous system in a similar way to caffeine. Some writings have stated that smoking can also increase mental concentration; one study documents a significantly better IQ on the normed Advanced Raven Progressive Matrices test after smoking. Most smokers say they enjoy smoking, which is part of the reason why many continue to do so even though they are aware of the health risks. Taste, smell, and visual enjoyment are also major contributions to the enjoyment of smoking, in addition to camaraderie with other smokers. Ironically, chronic exposure to tobacco smoke may inhibit one's sense of taste and smell, rendering him or her less able to enjoy these aspects of tobacco smoking.

Most smokers, when denied access to nicotine, exhibit symptoms such as irritability, jitteriness, dry mouth, and rapid heart beat. Longer abstinence may lead to insomnia and even mild depression. 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, but nicotine withdrawal symptoms such as irritability and incapacity to concentrate can have an influence on these aspects. 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 due to the fact that 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.

Recent studies have linked smoking to anxiety disorders, suggesting the correlation (and possibly mechanism) may be related to the broad class of anxiety disorders, and not limited to just depression. Current ongoing research are attempting to explore the addiction-anxiety relationship.

Data from multiple studies suggest that anxiety disorders such as 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.

Reproductive

It has been suggested that this section be split out into another article titled Effects of smoking during pregnancy. (Discuss) (April 2009)

A number of studies have shown that tobacco use is a significant factor in miscarriages among pregnant smokers, and that it contributes to a number of other threats to the health of the fetus. Second-hand smoke appears to present an equal danger to the fetus, as one study noted that "heavy paternal smoking increased the risk of early pregnancy loss."

Secondhand smoke is connected to sudden infant death syndrome (SIDS). Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their lungs than those who die from other causes. While smoking during pregnancy increases the risk of SIDS, infants exposed to secondhand smoke after birth are also at a greater risk of Sudden Infant Death Syndrome whether or not the parent(s) smoked during pregnancy. The nicotine obtained from smoking travels through a woman into her breast milk, thus giving nicotine to her child. Second hand smoke has been associated that between 150,000 and 300,000 lower respiratory tract infections in infants and children under 18 months of age, resulting in between 7,500 and 15,000 hospitalizations each year. It is associated with 430 SIDS deaths in the United States annually.

Secondhand smoke is known to harm children, infants and reproductive health through acute lower respiratory tract illness, asthma induction and exacerbation, chronic respiratory symptoms, middle ear infection, lower birth weight babies, and Sudden Infant Death Syndrome, or SIDS. In a study published on August 25, 2004 smoke-free policies were linked to a short-term reduction in admissions for acute myocardial infarction. In a study released on February 12, 2006 warning signs for cardiovascular disease are higher in people exposed to secondhand tobacco smoke, adding to the link between "passive smoke" and heart disease. "Our study provides further evidence to suggest low-level exposure to secondhand smoke has a clinically important effect on susceptibility to cardiovascular disease," said Dr. Andrea Venn of University of Nottingham in Britain, lead author of the study.

According to the U.S. Surgeon General’s Report (Chapter 5; pages 180–194), secondhand smoke is connected to SIDS. Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their lungs than those who die from other causes. Infants exposed to secondhand smoke after birth are also at a greater risk of SIDS.

According to earlier studies the smoking ban led to significant improvements regarding respiratory symptoms and lung function in people visiting bars and restaurants. Previously scientists stated that environmental tobacco smoke leads to coronary heart disease, lung cancer and premature death.

The case is available in the February edition of the American Journal of Industrial Medicine.

There is increasing evidence that the harmful products of tobacco smoking kill sperm cells. Therefore, some governments require manufacturers to put warnings on packets. Smoking tobacco increases intake of cadmium, because the tobacco plant absorbs the metal. Cadmium, being chemically similar to zinc, may replace zinc in the DNA polymerase, which plays a critical role in sperm production. Zinc replaced by cadmium in DNA polymerase can be particularly damaging to the testes.

Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers, and it is a key cause of erectile dysfunction (ED). Smoking causes impotence because it promotes arterial narrowing.

There is limited evidence that smoking reduces the incidence of pregnancy-induced hypertension, but not when the pregnancy is with more than one baby (i.e. it has no effect on twins etc.). Smoking does, however, increase the likelihood of almost every other pregnancy-related health risk to both mother and child, and is the single most preventable cause of illness and death among mothers and infants in the developed world.

Other

Studies suggest that smoking decreases appetite, but did not conclude that overweight people should smoke or that their health would improve by smoking. Smoking also decreases weight by overexpressing the gene AZGP1 which stimulates lipolysis.

The primary risks of tobacco usage include many forms of cancer, particularly lung cancer, cancer of the kidney, cancer of the larynx and head and neck, breast cancer, bladder, esophagus, pancreas, and stomach. There is some evidence suggesting an increased risk of myeloid leukemia, squamous cell sinonasal cancer, liver cancer, cervical cancer, colorectal cancer after an extended latency, childhood cancers and cancers of the gall bladder, adrenal gland and small intestine.

Preliminary reports suggest that smoking can decrease the incidence of acne prophylactically. This was seen by a decreased percentage ratio of patients needing acne medication versus the percentage of entire population of smokers. (A smaller percentage of patients who smoked needed medication than found in the population as a whole).

A protective effect of current smoking against ulcerative colitis, although 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.

A new research has found that women who smoke are at significantly increased risk of developing an abdominal aortic aneurysm, a condition in which a weak area of the abdominal aorta expands or bulges.

Several types of "Smoker’s Paradoxes", (cases where smoking appears to have specific beneficial effects), have been observed; often the actual mechanism remains undetermined. Risk of ulcerative colitis has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking. Smoking appears to interfere with development of Kaposi's sarcoma, breast cancer among women carrying the very high risk BRCA gene, preeclampsia, and atopic disorders such as allergic asthma. A plausible mechanism of action in these cases may be the nicotine in tobacco smoke acting as an anti-inflammatory agent and interfering with the disease process.

History

The late-19th century invention of automated cigarette-making machinery in the American South made possible mass production of cigarettes at low cost, and cigarettes became elegant and fashionable among society men as the Victorian era gave way to the Edwardian. In 1912, American Dr. Isaac Adler was the first to strongly suggest that lung cancer is related to smoking. In 1929, Fritz Lickint of Dresden, Germany, published a formal statistical evidence of a lung cancer–tobacco link, based on a study showing that lung cancer sufferers were likely to be smokers. Lickint also argued that tobacco use was the best way to explain the fact that lung cancer struck men four or five times more often than women (since women smoked much less).

Prior to World War I, lung cancer was considered to be a rare disease, which most physicians would never see during their career. With the postwar rise in popularity of cigarette smoking, however, came an epidemic of lung cancer.

In 1950, Richard Doll published research in the British Medical Journal showing a close link between smoking and lung cancer. Four years later, in 1954 the British Doctors Study, a study of some 40 thousand doctors over 20 years, confirmed the suggestion, based on which the government issued advice that smoking and lung cancer rates were related. The British Doctors Study lasted till 2001, with result published every ten years and final results published in 2004 by Doll and Richard Peto. Much early research was also done by Dr. Ochsner. Reader's Digest magazine for many years published frequent anti-smoking articles. In 1964 the United States Surgeon General's Report on Smoking and Health (referenced below), led millions of American smokers to quit, the banning of certain advertising, and the requirement of warning labels on tobacco products.

The Canadian province of British Columbia has the Tobacco Damages and Health Care Costs Recovery Act.

External links

• Effect of smoking on life expectancy

References

Notes

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