Health effects of tobacco

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The health effects of tobacco can be significant, depending on the way the tobacco is used (smoked, snuffed or chewed) and the amount. Major health effects of smoking, the most common use of tobacco, include an increased risk in lung cancer and cardiovascular disease.

Contents

Epidemiology

Prevalence

Percentage of females smoking any tobacco product
  no data   0.3–9.9   10–24.9   25–53.3
Percentage of males smoking any tobacco product. Note the difference between the two scales.[1]
  no data   5.8–29.9   30–49.9   50–70.2

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".[2] Smoking has therefore been studied more extensively than any other form of tobacco.[3]

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 some 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.[4]

Smoking is generally five times higher among men than women,[4] however, the gender gap begins decline with younger age.[5][6] For example, 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.[7] In developed countries smoking rates for men have peaked and have begun to decline, however for women they continue to climb.[8]

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—roughly half of which live in Asia. Evidence shows that around half of those who begin smoking in adolescent years go on to smoke for 15 to 20 years.[7]

The WHO states that "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. For example, while up to 30% of men are former smokers in developed countries, only 2% of men in China have quit, and 10% in Vietnam.[9] 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.[10] In the developing world, however, tobacco consumption is rising by 3.4% per year as of 2002.[7]

The WHO in 2004 projected 58.8 million deaths to occur globally[11] from which 5.4 million are tobacco-attributed,[12] and 4.9 million as of 2007.[13] As of 2002, 70% of the deaths are in developing countries.[13]

Vectors

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Cigarette smoking 
Cigarette smoking is the most common method of tobacco consumption, it is generally inhaled as to Cigar smoking.
Cigar smoking 
Cigar smoking is generally not inhales as to cigarette smoking, because alkalinity and poor amount of nicotine can quickly become irritating.[14][15] 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. The NIH study concerned those who smoked at least one cigar per day, and stated "The health risks associated with less than daily smoking (occasional smokers) are not known."[16] 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.
Pipe smoking 
Pipe smoking is the usage of tobacco from which the tobacco leaves are ground and placed into a pipe for inhalation.
Secondhand smoke 
Second hand smoke also called passive smoking, it is a involuntary inhalation from the end of cigarette, cigar, pipe, or otherwise.
Chewing tobacco 
Chewing tobacco is one of the oldest ways of consuming tobacco leaves.[citation needed] The leaves are gently compacted against the lip. This stimulates the salivary glands, which leads to the development of a spittoon.

Studies

See also: Tobacco litigation

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."[17] 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.[18]

The health effects of tobacco have been significant for the development of the science of epidemiology. As the mechanism of carcinogenity 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 individial cases, on the causal link in the stochastic expression of the toxicity as actual disease.[19]

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.

Effects

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Tobacco use leads most commonly 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[20] to 10[21] years fewer than nonsmokers.[20] About half of male smokers will die of illness due to smoking.[22] Of specific diseases, the association with lung cancer is strongest both in the public perception and etiologically, with people who have smoked tobacco at some point having a lifetime risk of developing lung cancer of around one in ten[23]. If one looks at men who continue to smoke tobacco, the risk increases to one in six[24]. 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[25][26].

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[27], and the reduction in their lung function will stop.

Cardiovascular

Since establishing causation through experimental trials was not possible due to ethical restrictions, a lengthy study was conducted in order to establish the strong association necessary to allow for legislative action against tobacco consumption.

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 cardiovascular 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.[28]

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.[29]

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.[citation needed]

There is no credible evidence that "Low Tar," "Light," or "Ultra Light" cigarettes are safer than regular cigarettes.[30] 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.

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.[31][32] 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."[16]

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. 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 highly toxic, yet the company suppressed the finding during the next two decades.[33] 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.[34]

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."[16] Pipe smoking involves significant health risks,[35][36] particularly oral cancer.[37][38] 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.[39] Smoking has been proven to be an important factor in the staining of teeth.[40][41] Halitosis or bad breath is common among tobacco smokers. Tooth loss has been shown to be 2[42] to 3 times[43] higher in smokers than in non-smokers.[44] 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.[citation needed]

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,[45][46] and being a current smoker has been linked to a fourfold increase in the risk of invasive pneumococcal disease.[47] 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.[48] The usage of tobacco also increases rates of infection: common cold and bronchitis, chronic obstructive pulmonary disease, emphysema and chronic bronchitis in particular.[citation needed]

Smoking reduces the risk of Kaposi's sarcoma in people without HIV infection.[49]

Psychological

Smokers report a variety of physical and psychological effects from smoking tobacco. Those new to smoking will 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)[50] of Alzheimer's disease and decline in cognitive abilities[51], reduced memory and cognitive abilities in adolescent smokers[52], brain shrinkage (cerebral atrophy)[53][54]

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.[55] 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.[56] Longer abstinence may lead to insomnia and even mild depression. The onset of these symptoms is very fast, nicotine's half-life being only 1 hour. 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,[citation needed] 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.[57]

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.[50]

Former and current smokers have a lower incidence of Parkinson's disease compared to people who have never smoked,[58][59] 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.[60]

A very large percentage of schizophrenics smoke tobacco as a form of self medication.[61][62][63][64] 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.[65] 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.[66] Some studies suggest that a link exists between smoking and mental illness, citing the high incidence of smoking amongst those suffering from schizophrenia[67] and the possibility that smoking may alleviate some of the symptoms of mental illness,[68] but these have not been conclusive.

Reproductive

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.[69] 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."[70] Miscarriages are not included in WHO estimates of deaths attributable to smoking.

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.[71] 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.[72]

There is increasing evidence that the harmful products of tobacco smoking kill sperm cells.[73][74] 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.[75]

Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers,[76] and it is a key cause of erectile dysfunction (ED).[77][78][76] Smoking causes impotence because it promotes arterial narrowing.[79]

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.[80] There is some evidence for decreased rates of endometriosis in infertile smoking women,[81] although other studies have found that smoking increases the risk in infertile women.[82] 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,[83] but overall the evidence is unconvincing.[84]

There is limited evidence that smoking reduces the incidence of pregnancy-induced hypertension,[85] but not when the pregnancy is with more than one baby (i.e. it has no effect on twins etc.).[86] 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.[87]

Other areas

The primary risks of tobacco usage include many forms of cancer, particularly lung cancer,[88] cancer of the kidney,[89] cancer of the larynx and head and neck, breast cancer,[90][91] bladder,[92] esophagus, pancreas,[93] and stomach.[94] 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).[95]

Factors

See also: List of additives in cigarettes

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 raditation, sunlight exposure, workplace exposure, and socioeconomic factors that affect exposures and susceptibility—may be a major contributor to the development of cancer.[96] Other factors that play a major role in cancer development are infectious diseases, aging, and individual susceptibility such as genetic predisposition.[97] 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.[98]

Chemical carcinogens

Chemical structure of the carcinogen benzopyrene diol epoxide
Benzopyrene, a major mutagen in tobacco smoke, in an adduct to DNA.[99]

There are over 19 known carcinogens in cigarettes.[100] The following are some of the most potent carcinogens:

Radioactive carcinogens

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. 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 pCi 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),[106] 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.[107]

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.[citation needed] 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.[108][109]

Nicotine addiction

Nicotine molecule

Nicotine that is contained in cigarettes or cigarette substitute (may or may not contain nicotine [110], e.g.: ruyan, etc) 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[citation needed] and/or psychological[citation needed] 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.[27] 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.[111]

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,[112] 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.

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%.[113]

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.[114] 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.[115]

Indirect effects

An indirect public health problem posed by cigarettes is that of accidental fires, usually linked with consumption of alcohol. Numerous cigarette designs have been proposed, some by tobacco companies themselves, which would extinguish a cigarette left unattended for more than a minute or two, thereby reducing the risk of fire. Among American tobacco companies, some have resisted this idea, while others have embraced it. RJR Reynolds was a leader in making prototypes of these cigarettes in 1983[116] and will make all of their U.S. market cigarettes to be fire-safe by 2010.[117] Phillip Morris is not in active support of it.[118] Lorillard, the nation's third largest tobacco company, seems to be ambivalent.[118]

See also

References

Notes

  1. ^ WHO REPORT on the global TOBACCO epidemic 2008, pp.267–288.
  2. ^ "Prevalence of current tobacco use among adults aged ≥ 15 years (percentage)". World Health Organization. Retrieved on 2009-01-02.
  3. ^ "Mayo report on addressing the worldwide tobacco epidemic through effective, evidence-based treatment" 2. World Health Organization. Retrieved on 2009-01-02.
  4. ^ a b "Guindon & Boisclair" 2004, pp. 13-16.
  5. ^ Women and the Tobacco Epidemic: Challenges for the 21st Century 2001, pp.5-6.
  6. ^ Surgeon General's Report—Women and Smoking 2001, p.47.
  7. ^ a b c "WHO/WPRO-Smoking Statistics". World Health Organization Regional Office for the Western Pacific (2002-05-28). Retrieved on 2009-01-01.
  8. ^ Mortality from Smoking in Developed Countries 1950-2000: indirect estimates from national vital statistics 2006, p.9.
  9. ^ "WHO/WPRO-Tobacco". World Health Organization Regional Office for the Western Pacific (2005). Retrieved on 2009-01-01.
  10. ^ VJ Rock, MPH, A Malarcher, PhD, JW Kahende, PhD, K Asman, MSPH, C Husten, MD, R Caraballo, PhD (2007-11-09). "Cigarette Smoking Among Adults --- United States, 2006". United States Centers for Disease Control and Prevention. Retrieved on 2009-01-01. "[...]In 2006, an estimated 20.8% (45.3 million) of U.S. adults[...]"
  11. ^ The Global Burden of Disease 2004 Update 2008, p.8.
  12. ^ The Global Burden of Disease 2004 Update 2008, p.23.
  13. ^ a b "WHO/WPRO-Tobacco Fact sheet". World Health Organization Regional Office for the Western Pacific (2007-05-29). Retrieved on 2009-01-01.
  14. ^ http://www.neptunecigar.com/co/faq-how_to_smoke_a_cigar.aspx
  15. ^ [1]
  16. ^ a b c National Institutes of Health (1998-04-10). "Background on Cigar Monograph: Cigars: Health Effects and Trends". Retrieved on 2008-01-04.
  17. ^ Richard Doll, Richard Peto, Jillian Boreham, Isabelle Sutherland (June 2004). "Mortality in relation to smoking: 50 years' observations on male British doctors". BMJ 328 (1519): 1519. doi:10.1136/bmj.38142.554479.AE. PMID 15213107. http://bmj.bmjjournals.com/cgi/content/abstract/328/7455/1519. 
  18. ^ Pell JP, Haw S, Cobbe S, et al (July 2008). "Smoke-free legislation and hospitalizations for acute coronary syndrome". N. Engl. J. Med. 359 (5): 482–91. doi:10.1056/NEJMsa0706740. PMID 18669427. 
  19. ^ Review (Helsingin Sanomat 30.3.2008, [2]) on Allan M. Brandt: The Cigarette Century. Basic Books. ISBN 978-0465070473. http://www.cigarettecentury.com/
  20. ^ a b Ferrucci L, Izmirlian G, Leveille S, et al (1999). "Smoking, physical activity, and active life expectancy". Am. J. Epidemiol. 149 (7): 645–53. PMID 10192312. 
  21. ^ Doll R, Peto R, Boreham J, Sutherland I (2004). "Mortality in relation to smoking: 50 years' observations on male British doctors". BMJ 328 (7455): 1519. doi:10.1136/bmj.38142.554479.AE. PMID 15213107. 
  22. ^ Doll R, Peto R, Wheatley K, Gray R, Sutherland I (1994). "Mortality in relation to smoking: 40 years' observations on male British doctors". BMJ 309 (6959): 901–11. PMID 7755693. 
  23. ^ David C. Christiani. "Lung Cancer Suscepitibility and Outcomes study". Harvard School of Public Health. Retrieved on 2009-01-03.
  24. ^ Villeneuve PJ, Mao Y (1994). "Lifetime probability of developing lung cancer, by smoking status, Canada". Canadian journal of public health. Revue canadienne de santé publique 85 (6): 385–8. PMID 7895211. 
  25. ^ Witschi H (November 2001). "A short history of lung cancer". Toxicol. Sci. 64 (1): 4–6. PMID 11606795. http://toxsci.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=11606795. 
  26. ^ Adler I. Primary malignant growths of the lungs and bronchi. New York: Longmans, Green, and Company; 1912., cited in Spiro SG, Silvestri GA (September 2005). "One hundred years of lung cancer". Am. J. Respir. Crit. Care Med. 172 (5): 523–9. doi:10.1164/rccm.200504-531OE. PMID 15961694. 
  27. ^ a b Quitting Smoking: Why To Quit and How To Get Help - National Cancer Institute
  28. ^ a b Facchinetti et al. α,β-Unsaturated Aldehydes in Cigarette Smoke Release Inflammatory Mediators from Human Macrophages. American Journal of Respiratory Cell and Molecular Biology. Vol. 37, pp. 617-623, 2007. DOI: 10.1165/rcmb.2007-0130OC
  29. ^ "Health : Young smokers' heart attack risk", BBC. Retrieved on 18 December 2005. 
  30. ^ U.S. District Judge Gladys Kessler's Final Opinion, p.740
  31. ^ David M. Burns, M.D. (February 1998). "Cigars: Health Effects and Trends".
  32. ^ Symm B, Morgan MV, Blackshear Y, Tinsley S (2005). "Cigar smoking: an ignored public health threat". J Prim Prev 26 (4): 363–75. doi:10.1007/s10935-005-5389-z. PMID 15995804. 
  33. ^ "Secondhand Smoke Fact Sheet", American Lung Association June 2007.
  34. ^ "Tobacco-Free Florida", Centers for Disease Control & Prevention Fact Sheets
  35. ^ American Cancer Society. "Questions About Smoking, Tobacco, and Health". Retrieved on 2008-01-04.
  36. ^ Henley SJ, Thun MJ, Chao A, Calle EE (June 2004). "Association between exclusive pipe smoking and mortality from cancer and other diseases". J. Natl. Cancer Inst. 96 (11): 853–61. PMID 15173269. http://jnci.oxfordjournals.org/cgi/content/full/96/11/853. 
  37. ^ Loren Stein. "Pipe Smoking". A Healthy Me!. Retrieved on 2008-01-04.
  38. ^ Commission on Life Sciences. "Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects (1986)". Retrieved on 2008-01-04.
  39. ^ Johnson GK, Slach NA (2001). "Impact of tobacco use on periodontal status" (PDF). J Dent Educ 65 (4): 313–21. PMID 11336116. http://www.jdentaled.org/cgi/reprint/65/4/313.pdf. 
  40. ^ Reibel J (2003). "Tobacco and oral diseases. Update on the evidence, with recommendations". Med Princ Pract 12 Suppl 1: 22–32. doi:10.1159/000069845. PMID 12707498. 
  41. ^ Ness L, Rosekrans Dde L, Welford JF (January 1977). "An epidemiologic study of factors affecting extrinsic staining of teeth in an English population". Community Dent Oral Epidemiol 5 (1): 55–60. PMID 264419. 
  42. ^ Albandar JM, Streckfus CF, Adesanya MR, Winn DM (December 2000). "Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss". J. Periodontol. 71 (12): 1874–81. PMID 11156044. 
  43. ^ Dietrich T, Maserejian NN, Joshipura KJ, Krall EA, Garcia RI (April 2007). "Tobacco use and incidence of tooth loss among US male health professionals". J. Dent. Res. 86 (4): 373–7. PMID 17384035. http://jdr.iadrjournals.org/cgi/pmidlookup?view=long&pmid=17384035. 
  44. ^ Al-Bayaty FH, Wahid NA, Bulgiba AM (February 2008). "Tooth mortality in smokers and nonsmokers in a selected population in Sana'a, Yemen". J. Periodont. Res. 43 (1): 9–13. doi:10.1111/j.1600-0765.2007.00988.x. PMID 18230101. 
  45. ^ Davies PDO, Yew WW, Ganguly D, et al. (2006). "Smoking and tuberculosis: the epidemiological association and pathogenesis". Trans R Soc Trop Med Hyg 100: 291–8. doi:10.1016/j.trstmh.2005.06.034. PMID 16325875. 
  46. ^ Jha P, Jacob B, Gajalakshmi V, et al. (2008). "A nationally representative case–control study of smoking and death in India". N Engl J Med 358 (11): 1137–1147. doi:10.1056/NEJMsa0707719. PMID 18272886. http://content.nejm.org/cgi/content/full/358/11/1137?query=TOC. 
  47. ^ Nuorti JP, Butler JC, Farley MM, et al (2000). "Cigarette smoking and invasive pneumococcal disease.". N Engl J Med 342: 681–9. doi:10.1056/NEJM200003093421002. PMID 10706897. http://content.nejm.org/cgi/content/abstract/342/10/681. 
  48. ^ Arcavi L, Benowitz NL (2004). Cigarette smoking and infection. 164. pp. 2206–16. doi:10.1001/archinte.164.20.2206. PMID 15534156. http://archinte.ama-assn.org/cgi/content/full/164/20/2206. 
  49. ^ Goedert JJ, Vitale F, Lauria C, et al (November 2002). "Risk factors for classical Kaposi's sarcoma". J. Natl. Cancer Inst. 94 (22): 1712–8. PMID 12441327. http://jnci.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12441327. 
  50. ^ a b Osvaldo P. Almeida, Gary K. Hulse, David Lawrence, and Leon Flicker (January 2002). "