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Updated: Jun 26, 2026
11:38
High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents (HPHC)
Published on: May 10, 2016
Carcinogenicity of hexavalent chromium
A L Holmes1, S S Wise, J P Wise
1Wise Laboratory of Environmental & Genetic Toxicology, Maine Center for Toxicology & Environmental Health, University of Southern Maine, 96 Falmouth St., Portland, ME 04104, USA.
The Indian Journal of Medical Research
|December 25, 2008
Summary
Hexavalent chromium (Cr(VI)) causes lung cancer, with insoluble compounds being more potent. Genomic instability appears to be the primary driver of chromate carcinogenesis, according to recent studies.
Area of Science:
- Toxicology
- Carcinogenesis
- Environmental Health
Background:
- Hexavalent chromium (Cr(VI)) is an industrial metal and a known human lung carcinogen.
- Particulate, water-insoluble Cr(VI) compounds are suspected to be more potent carcinogens.
- The precise carcinogenic mechanism of Cr(VI) remains incompletely understood.
Purpose of the Study:
- To review and synthesize recent findings on Cr(VI)-induced carcinogenesis.
- To investigate the underlying mechanisms of Cr(VI) carcinogenicity.
- To propose a mechanistic model for chromate-induced lung cancer.
Main Methods:
- Review of human epidemiological data.
- Analysis of animal study findings.
- Examination of in vitro and cell culture experimental results.
- Integration of data within established carcinogenesis paradigms.
Main Results:
- Cr(VI) exposure is linked to human lung tumors.
- In vivo and in vitro studies provide evidence for Cr(VI)'s carcinogenic effects.
- Genomic instability emerges as a key factor in Cr(VI) carcinogenesis.
- Epigenetic modifications and multistage carcinogenesis are considered but appear secondary.
Conclusions:
- The carcinogenic mechanism of hexavalent chromium is primarily driven by genomic instability.
- Understanding this mechanism can inform risk assessment and prevention strategies for Cr(VI) exposure.
- Further research is warranted to fully elucidate the role of genomic instability in chromate carcinogenesis.
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