TL;DR: Several lines of evidence strongly indicate that tobacco-specific nitrosamines have a major role, especially in the causation of oral cancer in snuff-dippers, and should be ideal markers for assessing human exposure to, and metabolic activation of, tobacco smoke carcinogens.
Abstract: Tobacco-specific nitrosamines are a group of carcinogens that are present in tobacco and tobacco smoke. They are formed from nicotine and related tobacco alkaloids. Two of the nicotine-derived nitrosamines, NNK and NNN, are strong carcinogens in laboratory animals. They can induce tumors both locally and systemically. The induction of oral cavity tumors by a mixture of NNK and NNN, and the organospecificity of NNK for the lung are particularly noteworthy. The amounts of NNK and NNN in tobacco and tobacco smoke are high enough that their total estimated doses to long-term snuff-dippers or smokers are similar in magnitude to the total doses required to produce cancer in laboratory animals. These exposures thus represent an unacceptable risk to tobacco consumers, and possibly to non-smokers exposed for years to environmental tobacco smoke. The permission of such high levels of carcinogens in consumer products used by millions of people represents a major legislative failure. Indeed, the levels of tobacco-specific nitrosamines in tobacco are thousands of times higher than the amounts of other nitrosamines in consumer products that are regulated by government authorities. Although the role of tobacco-specific nitrosamines as causative factors in tobacco-related human cancers cannot be assessed with certainty because of the complexity of tobacco and tobacco smoke, several lines of evidence strongly indicate that they have a major role, especially in the causation of oral cancer in snuff-dippers. Epidemiologic studies have demonstrated that snuff-dipping causes oral cancer. NNK and NNN are quantitatively the most prevalent known carcinogens in snuff, and they induce oral tumors when applied to the rat oral cavity. A role for NNK in the induction of lung cancer by tobacco smoke is likely because of its organospecificity for the lung. Tobacco-specific nitrosamines may also be involved in the etiology of tobacco-related cancers of the esophagus, nasal cavity, and pancreas. Because they are derived from nicotine, and therefore should be associated only with tobacco, tobacco smoke and other nicotine-containing products, tobacco-specific nitrosamines as well as their metabolites and macromolecular adducts should be ideal markers for assessing human exposure to, and metabolic activation of, tobacco smoke carcinogens. Ongoing research has demonstrated the formation of globin and DNA adducts of NNK and NNN in experimental animals. Sensitive methods for the detection and quantitation of these adducts in humans would provide an approach to assessing individual risk for tobacco-related cancers.(ABSTRACT TRUNCATED AT 400 WORDS)
TL;DR: Overall nicotine exposure was twice as large after single exposures to smokeless tobacco compared with cigarette smoking, and relatively low levels of nicotine and lesser cardiovascular responses were observed with use of nicotine gum.
Abstract: Because of recent resurgence in its consumption, the effects and health consequences of smokeless tobacco are of considerable public health interest. We studied the extent and time course of absorption of nicotine and cardiovascular effects of smokeless tobacco (oral snuff and chewing tobacco) and compared it with smoking cigarettes and chewing nicotine gum in 10 healthy volunteers. Maximum levels of nicotine were similar but, because of prolonged absorption, overall nicotine exposure was twice as large after single exposures to smokeless tobacco compared with cigarette smoking. All tobacco use increased heart rate and blood pressure, with a tendency toward a greater overall cardiovascular effect despite evidence of development of some tolerance to effects of nicotine with use of smokeless tobacco. Relatively low levels of nicotine and lesser cardiovascular responses were observed with use of nicotine gum. Adverse health consequences of smoking that are nicotine related would be expected to present a similar hazard with the use of smokeless tobacco.
TL;DR: The carcinogenic hazard of oral snuff is of special concern in view of the recent upswing in consumption of smokeless tobacco in the United States.
Abstract: A case–control study in North Carolina involving 255 women with oral and pharyngeal cancer and 502 controls revealed that the exceptionally high mortality from this cancer among white women in the South is primarily related to chronic use of snuff. The relative risk associated with snuff dipping among white nonsmokers was 4.2 (95 per cent confidence limits, 2.6 to 6.7), and among chronic users the risk approached 50-fold for cancers of the gum and buccal mucosa — tissues that come in direct contact with the tobacco powder. In the absence of snuff dipping, oral and pharyngeal cancer resulted mainly from the combined effects of cigarette smoking and alcohol consumption. The carcinogenic hazard of oral snuff is of special concern in view of the recent upswing in consumption of smokeless tobacco in the United States. (N Engl J Med. 1981; 304: 745–9.)
TL;DR: In this article, the role of tobacco smoking, alcohol intake, use of moist oral snuff, dietary factors, occupational exposures, and oral hygiene in the etiology of head and neck cancer was investigated.
TL;DR: All forms of tobacco represent risk factors for oral cancer, but on present evidence, snuff habits as they exist in Scandinavia and probably in the United States carry lower risks of serious health hazards, including oral cancer.
Abstract: For both genders, cancer of the mouth and pharynx ranks sixth overall in the world; it is also the third most common site among males in developing countries. In industrialized countries, men are affected two to three times as often as women, largely due to higher use of alcohol and tobacco. Ethnicity strongly influences prevalence due to social and cultural practices, as well as socioeconomic differences. In population terms, survival rates around the world show little improvement. In terms of etiology, the effects of tobacco use, heavy alcohol consumption, and poor diet together explain over 90 percent of cases of head and neck cancer. All forms of tobacco represent risk factors for oral cancer, but on present evidence, snuff habits as they exist in Scandinavia and probably in the United States carry lower risks of serious health hazards, including oral cancer. Alcohol synergizes with tobacco as a risk factor for all upper aerodigestive tract SCC: this is super-multiplicative for the mouth, additive for the larynx, and between additive and multiplicative for the esophagus. The increase in oral cancer in the Western world has been related to rising alcohol use.