DNA damage has long been known to play an essential role in tumorigenesis induced by chemical carcinogen exposure. The preponderance of data generated during the past approximately 50 years of cancer research indicates that DNA damage and DNA adduct formation are necessary but not sufficient for tumor induction by chemical carcinogenesis. This is true for all of the species studied, including experimental animals, some animals in the wild, and humans. Cetaceans, which include whales, dolphins and porpoises, are a challenge to evaluate because tissues are difficult to obtain, and cancer rates, with a single exception, are low (0.7-2.0 %). However, both non-specific (chromosomal aberrations, DNA strand breaks, 8-hydroxy-2'-deoxyguanosine, mitochondrial DNA damage), and chemical-specific (aromatic DNA adducts, and carcinogenic polycyclic aromatic hydrocarbon [PAH]-DNA adducts) DNA damage have been found in cetaceans. For some types of DNA damage, cetaceans may carry a burden similar to that seen in many other species, including humans, but linking DNA damage to cancer rates in cetaceans has been largely impossible. The one exception is a population of beluga whales in the St. Lawrence Estuary (SLE) in Quebec, Canada, where correlations have been found between long-term PAH exposure, PAH-DNA adducts in small intestinal crypt cells, and a high rate (7%) of gastrointestinal cancers. Taken together, the current literature demonstrates that cetaceans may carry a burden of many types of DNA damage and, given the example of the SLE beluga, cetaceans may sustain a potential susceptibility to pollution-induced tumorigenesis. Knowledge of DNA damage and cancer rates in whales is critically important for understanding and predicting the health of marine life, human life, and the aquatic environment of our planet.
Keywords: Clastogenicity; DNA adduct; Dolphin; Genotoxicity; Porpoise; Whale.
Published by Elsevier B.V.