Tobacco cancer

Chronic use of snuff has caused oropharyngeal cancer. Tobacco and alcohol ambylopia is seen in chronic smokers who are malnourished and alcoholic. Green tobacco sickness occurs in young workers who do not smoke but work with wet, uncured tobacco. Withdrawal symptoms can occur when use of a tobacco product is stopped. 

A large number of polycyclic aromatic hydrocarbons are known Many have been synthesized m the laboratory and several of the others are products of com bustion Benzo[a]pyrene for example is present m tobacco smoke contaminates food cooked on barbecue grills and collects m the soot of chimneys Benzo[a]pyrene is a carcinogen (a cancer causing substance) It is converted m the liver to an epoxy diol that can induce mutations leading to the uncontrolled growth of certain cells... 

Aromatic Hydrocarbons. These are the most toxic of the hydrocarbons and inhalation of the vapor can cause acute intoxication. Benzene is particularly toxic and long-term exposure can cause anemia and leukopenia, even with concentrations too low for detection by odor or simple instmments. The currendy acceptable average vapor concentration for benzene is no more than 1 ppm. PolycycHc aromatics are not sufftcientiy volatile to present a threat by inhalation (except from pyrolysis of tobacco), but it is known that certain industrial products, such as coal tar, are rich in polycycHc aromatics and continued exposure of human skin to these products results in cancer. 

There is insufficient evidence to unequivocally link nitrosamine exposure to elevated risk for human cancer (159). There are, however, a number of specific cases, especially with respect to the tobacco-related nitrosamines, in which exposure to V/-nitroso compounds is of concern. The strongest evidence in this context is probably that relating to oral cancer rates among habitual users of smokeless tobacco (snuff). Oral cancer rates among this group are significantly elevated over those of nonusers, and /V-nitrosonornicotine, and 4-(methylnitrosamino)-l-(3-pyridinyl)-l-butanone [64091 -91 both of... 

I. K. O Neill, J. Chen, and H. Bartsch, eds.. Relevance to Human Cancer of N-Nitroso Compounds, Tobacco Smoke andMjcotoxins, lARC Scientific Pubhcation No. 105, International Agency for Research on Cancer, Lyon, Prance, 1991. 

Effects of indoor air pollutants on humans are essentially the same as those described in Chapter 7. However, there can be some additional pollutant exposures in the indoor environment that are not common in the ambient setting. From the listing in Table 23-1, radon exposures indoors present a radiation hazard for the development of lung cancer. Environmental tobacco smoke has been found to cause lung cancer and other respiratory diseases. Biological agents such as molds and other toxins may be a more likely exposure hazard indoors than outside. 

Chronic Pulmonary Toxicity Chronic damage to the lungs may be due to several subsequent exposures or due to one large dose that markedly exceeds the capacity of pulmonary defense, clearance, and repair mechanisms. Chronic pulmonary toxicity includes emphysema, chronic bronchitis, asthma, lung fibrosis, and lung cancer. The single most important reason for chronic pulmonary toxicity is tobacco smoke, which induces all types of chronic pulmonary toxicity, with the exception of fibrosis. 

Environmental tobacco smoke mid gasoline vapors both contain mixtures of trace luiiounts of many of the individual compounds regulated as Air Toxics under Title 111, section 112 of the 1990 Clean Air Act Amendnmts. Much of the general public is more likely to be exposed to these mixtures during the course of their lives tlian to specific compounds on the air toxics list. Hence, estimation of the cancer risk resulting from exposure to these mixtures is a useful and relevant exercise. 

True. Tobacco smoke is considered in most countries to be the most common cause of lung diseases such as cancer and emphysema. 

There is no conclusive evidence that moderate, long-term use of cannabis causes lasting damage to physical or mental health. However, it is probable that frequent inhalation of cannabis smoke over a period of years will contribute towards bronchitis and other respiratory disorders and possible cancers of the lung and parts of the digestive system. Risks are greater if cannabis is smoked with tobacco. 

The involvement of tobacco smoke carcinogens in the aetiology of lung cancer is conclusively established, but the role of specific chemical carcinogens as inducers of colorectal cancer is much less clear. Mutagenic pyrolysis products derived from cooked food have come under suspicion as possible... 

CHUNG F L (1999) The prevention of lung cancer induced by a tobacco-specific carcinogen in rodents by green and black tea , Proc Soc Exp Biol Med, 220 (4), 244-8. 

N-Nitrosamines are formed during processing and smoking of tobacco products. Proteins, agricultural chemicals and alkaloids in tobacco products serve as major precursors for volatile, nonvolatile, and tobacco-specific nitrosamines (Figure 1). In this review we will summarize the progress achieved in respect to tobacco nitrosamines since the last ACS symposium in Boston in June of 1978 (J ). Additional papers will review the metabolism of cyclic N-nitrosamines, including that of N -nitrosonornicotine 1) and the correlation between tobacco and alcohol consumption and cancer of the upper alimentary tract (J ). 

Table I lists the concentrations of nitrosodimethylamine (NDMA) and nitrosodiethylamine (NDEA) in some of the tobacco products which had greater than 0.5% nitrate content. Tobacco with less than 0.5% nitrate content, such as Bright tobaccos, yielded NDMA, NDEA and nitrosopyrrolidine (NPYR) generally below 5 ppb. The relatively high concentrations of NDMA in fine cut tobaccos and in snuff are possibly of significance in the increased risk for oral cancer among snuff dippers who use these tobacco types repeatedly each day by placing a pinch of the product directly into the gingival buccal fold (6,7).

Wang, X.D. et al., Retinoid signaling and activator protein-1 expression in ferrets given beta-carotene supplements and exposed to tobacco smoke, J. Natl. Cancer Inst., 91, 60, 1999. 

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