Abstract
Several cancer risk factors (exposure to ultraviolet-B, pollution, toxins and pathogens) have been identified for wildlife, to form a “cancer risk landscape.” However, information remains limited on how the spatiotemporal variability of these factors impacts the prevalence of cancer in wildlife. Here, we evaluated the cancer risk landscape at 49 foraging sites of the globally distributed green turtle (Chelonia mydas), a species affected by fibropapillomatosis, by integrating data from a global meta-analysis of 31 publications (1994–2019). Evaluated risk factors included ultraviolet light exposure, eutrophication, toxic phytoplanktonic blooms, sea surface temperature, and the presence of mechanical vectors (parasites and symbiotic species). Prevalence was highest in areas where nutrient concentrations facilitated the emergence of toxic phytoplankton blooms. In contrast, ultraviolet light exposure and the presence of parasitic and/or symbiotic species did not appear to impact disease prevalence. Our results indicate that, to counter outbreaks of fibropapillomatosis, management actions that reduce eutrophication in foraging areas should be implemented.
Highlights
Cancers are a group of diseases that emerge in multicellular organism hosts when cells stop collaborating with surrounding cells, and obtain the ability to proliferate in an uncontrolled manner [1,2]
To define the cancer risk landscape of green turtles, we identified potential risk factors associated with fibropapillomatosis from the published literature [23]
There was no evidence that fibropapillomatosis prevalence in green turtles at a global scale was impacted by: exposure to ultraviolet radiation (OR: 1.00, 95% confidence intervals (95% CI): 1.00–1.00 for mean annual Ultraviolet light (UV) exposure), seabed depth (OR: 0.99, 95% CI: 0.84–1.17 for mean depth), phosphate concentration (OR: 0.44, 95% CI: 0.03–6.75 for mean phosphate concentration), or sea turtle status
Summary
Cancers are a group of diseases that emerge in multicellular organism hosts when cells stop collaborating with surrounding cells, and obtain the ability to proliferate in an uncontrolled manner [1,2]. The emergence of cancers mirrors speciation events, in which new parasitic species emerge and consume the resources of hosts, reducing overall fitness [3,4,5]. One transmissible cancer depleted > 80% of Tasmanian devils, a keystone predator, from the ecosystem of the island of Tasmania (Australia) [16]. This catastrophic event caused the complete reorganization of the trophic chain, releasing meso-predators from competition with Tasmanian devils, and allowing invasive species, such as feral cats (Felis catus), to proliferate [11,12]
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