Oil pollution toxicity to marine fish has been observed from oil spills such as the Exxon Valdez disaster, and from nonpoint sources, such as surface runoff, which is the largest source of oil pollution in marine waters. Crude oil entering waterways from spills or runoff contain polycyclic aromatic hydrocarbons (PAHs), the most toxic components of oil. The route of PAH uptake into fish depends on many environmental factors and the properties of the PAH. The common routes are ingestion, ventilation of the gills, and dermal uptake. Fish exposed to these PAHs exhibit an array of toxic effects including genetic damage, morphological deformities, altered growth and development, decreased body size, inhibited swimming abilities and mortality. The morphological deformities of PAH exposure, such as fin and jaw malformations, result in significantly reduced survival in fish due to the reduction of swimming and feeding abilities. While the exact mechanism of PAH toxicity is unknown, there are four proposed mechanisms. The difficulty in finding a specific toxic mechanism is largely due to the wide variety of PAH compounds with differing properties.
History
Research on the environmental impact of the petroleum industry began in earnest, during the mid to late 20th century, as the oil industry developed and expanded. Large scale transport of crude oil increased as a result of the increasing worldwide demand for oil, subsequently increasing the number of oil spills. Oil spills provided perfect opportunities for scientists to examine the in situ effects of crude oil exposure to marine ecosystems, and collaborative efforts between the National Oceanic and Atmospheric Administration (NOAA) and the United States Coast Guard resulted in improved response efforts and detailed research on oil pollution's effects. The Exxon Valdez oil spill in 1989, and the Deepwater Horizon oil spill in 2010, both resulted in increased scientific knowledge on the specific effects of oil pollution toxicity to marine fish.
Exxon Valdez oil spill Focused research on oil pollution toxicity to fish began in earnest in 1989, after the Exxon Valdez tanker struck a reef in Prince William Sound, Alaska and spilled approximately 11 million gallons of crude oil into the surrounding water. At the time, the Exxon Valdez oil spill was the largest in the history of the United States. There were many adverse ecological impacts of the spill including the loss of the loss of billions of Pacific herring and pink salmon eggs. Pacific herring were just beginning to spawn in late March when the spill occurred, resulting in nearly half of the population's eggs being exposed to crude oil. Pacific herring spawn in the intertidal and subtidal zones, making the vulnerable eggs easily exposed to pollution.
Deepwater Horizon oil spill After April 20, 2010, when an explosion on the Deepwater Horizon Macondo oil drilling platform triggered the largest oil spill in US history, another opportunity for oil toxicity research was presented. Approximately 171 million gallons of crude oil flowed from the seafloor into the Gulf of Mexico, exposing the majority of the surrounding biota. The Deepwater Horizon oil spill also coincided directly with spawning window of various ecologically and commercially important fish species, including yellowfin and Atlantic bluefin tuna. The oil spill directly affected Atlantic bluefin tuna, as approximately 12% of larval tuna were located in oil-contaminated waters, and Gulf of Mexico is the only known spawning grounds for the western population of bluefin tuna.
Exposure to oil Oil spills, as well as daily oil runoff from urbanized areas, can lead to polycyclic aromatic hydrocarbon (PAHs) entering marine ecosystems. Once PAHs enter the marine environment, fish can be exposed to them via ingestion, ventilation of the gills, and dermal uptake. The major route of uptake will depend on the behavior of the species of fish and the physicochemical properties of the PAH of concern. Habitat can be a major deciding factor for the route of exposure. For example, demersal fish or fish that consume demersal fish are highly likely to ingest PAHs that have sorbed to the sediment, whereas fish that swim at the surface are at a higher risk for dermal exposure. Upon coming in contact with a PAH, bioavailability will affect how readily the PAH is taken up. The EPA identifies 16 major PAHs of concern and each of these PAHs has a different degree of bioavailability. For instance, PAHs with lower molecular weight are more bioavailable because they dissolve more readily in water and are therefore more bioavailable for fish within the water column. Similarly, hydrophilic PAHs are more bioavailable for uptake by fish. For this reason, usage of oil dispersants, like Corexit, to treat oil spills can increase the uptake of PAHs by increasing their solubility in water and making them more available for uptake via the gills. Once a PAH is taken up, the fish's metabolism can affect the duration and intensity of the exposure to target tissues. Fish are able to readily metabolize 99% of PAHs to a more hydrophilic metabolite through their hepato-biliary system. This allows for the excretion of PAHs. The rate of metabolism of PAHs will depend on the sex and size of the species. The ability to metabolize PAHs into a more hydrophilic form can prevent bioaccumulation and halt PAHs from being passed on to organisms further up the food web. Because oil can persist in the environment long after oil spills via sedimentation, demersal fish are likely to be continually exposed to PAHs many years after oil spills. This has been proven by looking at the biliary PAH metabolites of bottom-dwelling fish. For instance, bottom-dwelling fish still showed elevated levels of low molecular weight PAH metabolites 10 years after Exxon Valdez oil spill.
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