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Epidemiology of Cancer by Tobacco Products and the Significance of TSNA
Published in Roger O. McClellan, Critical Reviews in Toxicology, 2017
Prakash C. Gupta, P. R. Murti, R. B. Bhonsle
As stated earlier, there was considerable confusion in the literature, with often quoted statements such as “the high incidence of oral cancer in India is due to betel nut chewing.” The question of carcinogenecity of chewing areca nut without tobacco was addressed in an epidemiological review,29 and it was shown that chewing betel quid without tobacco carried either an “insignificant” or a “significantly lower risk” for oral cancer compared with chewing tobacco containing quids. A dissenting note has come from South Africa, where women of Indian origin chew areca nut without tobacco and are not exposed to other risk factors such as smoking or alcohol, but show a high risk for oral cancer (RR of 43.9).76
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Areca nut contains several alkaloids and tannins. Arecoline is the most common alkaloid in areca nut, which also contains a variety of amines that are nitrosated in saliva during quid chewing. All these substances contribute to carcinogenicity. Aqueous extracts of areca nut produce a variety of cellular effects including: DNA strand-breaks, sister chromatid exchange, micronucleus formation, gene mutations, chromosomal aberrations and increased cellular proliferation. These were found in both in vivo animal tests and in vitro experiments with mammalian cells. Similar effects were noted in tests with areca-nut alkaloids. Arecoline inhibited TP53 expression in human epithelial cells. Irritation of oral tissues from the quid, combined with the generation of ROS, produce indirect DNA damage.