Smoking-induced lung cancer

NT028 Witschi, H., and I. Espiritu. Development of tobacco smoke-induced lung tumors in mice fed Bowman-Birk protease inhibitor concentrate (BBIC). Cancer Lett 2002 183(2) 141-146. 

Maybe there was a gene that tended to make the bearer more likely to choose to smoke and also induced lung cancer. 

Smoke of cigarettes is acidic (pH 5.3) and nicotine is relatively ionised and insoluble in lipids. Desired amounts are absorbed only if nicotine is taken into the lungs, where the enormous surface area for absorption compensates for the lower lipid solubility. Cigarette smokers therefore inhale (and have a high rate of death from tar-induced lung cancer). The amoimt of nicotine absorbed from tobacco smoke varies from 90% in those who inhale to 10% in those who do not. 

During the 1960s the Sundermans reported that they had found Ni in MSS (3837). They speculated that Ni could possible react with CO in MSS to form nickel carbonyl. The Sundermans did not successfully induce lung cancer in rats exposed to tobacco smoke although much furor was raised as to their allegations (3837, 3838). 

NO is a mutagenic compound that can cause mutations in Salmonella typhimurium bacteria (Arroyo et al., 1992) as well as induce mutations and chromosomal aberrations in rat primary lung cells exposed to doses of NO below 100 ppm for a few hours (Isomura et al., 1984). Some of this effect might be due to the formation of NO2 in the exposure chamber. Cigarette smoking causes lung cancer, and chronic inhalation exposure to the oxides of nitrogen may contribute to this effect. 

Nitric oxide may interact with the surface of mineral fibres. Cigarette smoke which increases the risk of asbestos-induced lung cancer contains up to 600 [ig NO per cigarette (lARC 1985) raised the fibre-bound NO from 34 to 85 pg NO/g fibre (Leanderson et al. 1997). NO was found in different amounts on chrysotile B, crocidolite, amosite and siUcon carbide whiskers. There was a strong correlation between the amount of NO and the specific surface area of these fibres (r = 0.98). NO could not be demonstrate on rockwool fibres, manmade vitreous fibres MMV21 and MMV22 or silicon nitride whiskers. 

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. 

Polycyclic aromatic hydrocarbons have been classified as human carcinogens because they induce cancers in experimental animals and because smoking and exposure to mixtures of chemicals containing polycyclic aromatic hydrocarbons in the workplace increase the risk of lung cancer in exposed individuals. In experimental animals, benzo(a)pyrene induces cancer in different organs depending on the route of administration.Furthermore, exposure to polycyclic aromatic hydrocarbons commonly occurs in occupations related to traffic (use of diesel engines in transportation and railways). 

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... 

A somewhat related situation can be used to explain the well-publicized lung-cancer inducing effects of P-carotene in heavy smokers. This subpopulation will have low vitamin C levels and hence damage due to smoke components, such as N02 can produce P-CAR which will reach the lung and initiate damage. In nonsmokers, the vitamin C (or other water-soluble antioxidant) is likely to be present in sufficient concentration to preclude this damaging process. Indeed, this speculation has been promoted by the American Chemical Society as the subject of a press release in 1997 (Bohm et al. 1997). 

Liu, C., F. Lian, D. E. Smith, R. M. Russell, and X. D. Wang. 2003. Lycopene supplementation inhibits lung squamous metaplasia and induces apoptosis via up-regulating insulin-like growth factor-binding protein 3 in cigarette smoke-exposed ferrets. Cancer Res 63(12) 3138-3144. 

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