This review provides a comprehensive overview of how heavy metals (arsenic, cadmium, chromium, lead, mercury, nickel) cause cancer through genetic mutations and epigenetic dysregulation. IARC classifies arsenic, cadmium, nickel, and hexavalent chromium as Group 1 human carcinogens. The review covers genotoxicity, mutagenesis, epigenetic modifications (DNA methylation, histone modification, chromatin remodeling, and non-coding RNAs), and cancer-related signaling pathways.
Key numbers
For arsenic:
- IARC Group 1 human carcinogen; established carcinogenicity in lung, skin, bladder, kidney cancers.
- Arsenic induces dose-dependent hypomethylation that persists after exposure, correlating with prolonged carcinogenic potential (citing references 1, 12-14 in the source paper).
- Arsenic raises genome methylation levels, correlating with heterochromatinization and inhibition of tumor suppressor genes MAP2K3 and DKK1.
- The review identifies three key mechanism categories: (1) DNA damage and genomic instability; (2) alteration of gene expression and signal transduction; (3) interference with essential cellular homeostasis.
- Arsenic promotes carcinogenesis through oxidative stress, epigenetic changes, anti-apoptotic and proliferative signaling pathways (citing mechanistic studies in the source).
- For overall lung cancer: arsenic, cadmium, nickel, hexavalent chromium, and lead are five metals identified among the eight most dangerous occupational lung carcinogens.
Methods (brief)
Narrative review of mechanistic and epidemiological literature; no systematic search strategy reported. Focus on genetic mutations and epigenetic modifications in metal-induced carcinogenesis. Sources cover in vitro, animal, and human studies.
Evidence fitness
Supports: mechanistic context for arsenic-induced carcinogenesis in the lung and other organs, particularly via epigenetic dysregulation and DNA damage pathways. Provides context for IARC classification of arsenic and other metal carcinogens. Not a source for food arsenic concentrations or dietary exposure estimates.
Limitations
Narrative (not systematic) review; mechanism emphasis; most evidence from in vitro and animal models; epidemiological studies cited are discussed qualitatively rather than quantitatively synthesized.
Related evidence
Update history
No substantive edit history is available in this build. The full commit record is available in git.