Nasal cavity carcinogens: Possible routes of metabolic activation

Stephen S. Hecht, Andre Castonguay, Dietrich Hoffmann

Research output: Chapter in Book/Report/Conference proceedingChapter

4 Scopus citations


A variety of chemicals induce nasal cavity cancer in experimental animals. Many of these compounds also give tumors in other organs, depending on the species and route of administration. In almost every case, studies on the metabolic conversion of these compounds to reactive intermediates that can covalently bind to cellular macromolecules (metabolic activation) have been carried out in tissues other than the nasal cavity. Thus, the mechanisms of metabolic activation of nasal cavity carcinogens are really not known. In this chapter, some of the major metabolic pathways that could possibly be involved in carcinogenesis by a representative group of nasal cavity carcinogens will be outlined. This includes various nitrosamines, industrial solvents, alkylating agents, haloalkanes and haloalkenes, and miscellaneous substances such as p-cresidine, phenacetin, nickel, formaldehyde, and isopropyl oils. These compounds were chosen because of their structural diversity and, in many cases, their environmental importance.

Original languageEnglish (US)
Title of host publicationNasal Tumors in Animals and Man Volume III
Subtitle of host publicationExperimental Nasal Carcinogenesis
PublisherCRC Press
Number of pages32
ISBN (Electronic)9781351359887
ISBN (Print)9781138550599
StatePublished - Jan 1 2017


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