Abstract
Recently, the President’s Cancer Panel [2008-2009] protested that preventive action is not taken when uncertainty exists about potential harm from a chemical, because the US regulatory approach demands that a hazard be incontrovertibly demonstrated. It is now incontrovertible that formaldehyde increases risks for leukemias. Evidence is also strong that formaldehyde causes some types of DNA damage in humans that are known to require repairs mediated by BRCA1/2 containing pathways. Homologous recombination repairs require BRCA1/2, Fanconi and ATM proteins in these pathways. Biallelic BRCA2 mutations interfere with these repairs and are clearly associated with leukemias, especially myeloid leukemias. Fanconi anemia homozygotes have very high risks for acute myeloid leukemias. Disabling BRCA1/2 related DNA repair processes prevents repair of formaldehyde related DNA damage in laboratory cells. DNA-protein cross links result in the accumulation of DNA double strand breaks in homologous recombination-deficient but not homologous recombination -proficient cells. ATM heterozygotes have increased risks for some leukemias that have been linked to formaldehyde in normal individuals. Weaker evidence suggests increased risk for rare nasopharyngeal or sinonasal cancers in heterozygous BRCA1/2 mutation carriers and in ATM mutation carriers.Formaldehyde is a pervasive environmental carcinogen that is theoretically more likely to cause malignancy in carriers of mutations that disable protective repair pathways. Because of this potential for harm, it is prudent for mutation carriers to immediately avoid formaldehyde, especially high level exposure. The EPA recommends four basic “Steps to Reduce Exposure” for everyone.
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Friedenson, B. Mutations in pathways depending on BRCA1 and BRCA2 may increase cancer risks from an environmental carcinogen. Nat Prec (2011). https://doi.org/10.1038/npre.2011.5669.1
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DOI: https://doi.org/10.1038/npre.2011.5669.1
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