The molecular epidemiology of asbestos and tobacco in lung cancer

Heather H. Nelson; Karl T. Kelsey

doi:10.1038/sj.onc.1205804

The molecular epidemiology of asbestos and tobacco in lung cancer

Heather H. Nelson, Karl T. Kelsey

Epidemiology

Research output: Contribution to journal › Article › peer-review

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Abstract

Asbestos is a well-known toxin and lung carcinogen. Epidemiologic studies have established tobacco smoke and asbestos exposures synergistically interact to enhance lung cancer risk. The biologic mechanism responsible for this interaction has been the subject of considerable debate. Studies have suggested that asbestos may act as a carcinogen by generating free radical and reactive oxygen species, by inducing tissue injury and subsequent cellular growth, via large-scale chromosome loss and by enhancing delivery of tobacco carcinogens to the respiratory epithelium. Recent molecular epidemiologic approaches further suggest that asbestos enhances the mutagenicity of tobacco carcinogens and that it acts, at least in part, independent of the tissue damage responsible for fibrosis.

Original language	English (US)
Pages (from-to)	7284-7288
Number of pages	5
Journal	Oncogene
Volume	21
Issue number	48 REV. ISS. 6
DOIs	https://doi.org/10.1038/sj.onc.1205804
State	Published - Oct 21 2002

Bibliographical note

Funding Information:
This study was supported by NIH grants P42ES5947, ES0002, P42ES07373, CA82354 and CA57494.

Keywords

Asbestos
Lung cancer
Tobacco

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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The molecular epidemiology of asbestos and tobacco in lung cancer

Abstract

Bibliographical note

Keywords

UN SDGs

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