Toxins released by oil spills send fish hearts into cardiac arrest
Scientists have cracked a cellular biology mystery underlying a harmful effect oil spills have on fish: irregular heartbeats that can lead to cardiac arrest.
In studying the effects of the 2010 Deepwater Horizon oil spill on bluefin tuna spawning in the Gulf of Mexico, the research team discovered that polycyclic aromatic hydrocarbons, or PAHs, block “signaling pathways” that allow potassium and calcium ions to flow in and out of cardiac cell membranes and sustain normal heart rates.
Even very low concentrations of crude oil can disrupt these signaling pathways, slowing the pace of heartbeats, the researchers reported Thursday in the journal Science.
Their study also suggests that PAH cardiotoxicity was potentially a common form of injury among a broad range of species in the vicinity of the oil spilled into one of the most productive ocean ecosystems in the world.
“Until now, PAH’s toxic properties were better known for their cancer-causing effects,” said study coauthor Nathaniel Scholz, manager of the ecotoxicology program for the National Oceanic and Atmospheric Administration’s Northwest Fisheries Science Center in Seattle. “But our work is showing they also have properties that are cardiotoxic, particularly among early life stages of fish.”
“At relatively higher concentrations, the effects on a developing fish heart are severe in that the heart muscle cannot do its job, or becomes deformed -- those fish will die,” he said. “As for exposure to lower concentrations, these fish will survive in clean water. But when we look at them later in life, we find they have changes in the shapes of their hearts, with corresponding impacts on their ability to swim.”
Study leader Barbara Block, a professor of marine sciences at Stanford University, said future research should be extended to include mammals and humans because the signaling pathways of their cardiac cells are similar to those of tuna, and PAHs are found in coal tar, creosote, air pollution and urban runoff.
“This raises the possiblity that exposure to environmental PAHs in many animals -- including humans -- could lead to cardiac arrhythmias and bradycardia, or slowing of the heart,” Block said.
The Deepwater Horizon oil rig explosion was the largest offshore oil spill in U.S. history. It killed 11 workers and unleashed 4 million barrels of crude oil into the environment during the spawning months for Atlantic bluefin tuna.
Electronic-tagging data confirmed that bluefin tuna as well as other pelagic fish including yellowfin tuna, dolphin fish, blue marlin and swordfish in the vicinity of the spill were likely exposed to PAHs, according to the study.
The gulf’s bluefin tuna, which can grow to 12 feet in length, weigh 1,400 pounds and live for 35 years, were already at the mercy of fishing fleets. The gulf population has declined to a shadow of its original abundance since the early 1950s, when industrial harvesting of these animals began.
The researchers studied the effects of Deepwater Horizon oil samples on in vitro preparations of living cardiac cells taken from the hearts of bluefin tuna and yellowfin tuna, many of them caught at sea and held captive at the Tuna Research Conservation Center in Pacific Grove, Calif., and at the nearby Monterey Bay Aquarium.
They bathed those cells in low-dose crude oil concentrations similar to what fish in early life stages may have encountered in the surface waters after the oil spill. A combination of sophisticated electro-physiological techniques were used to record disruptions in signaling pathways due to PAHs.
[Updated 1:30 p.m. PST Feb. 13: BP took issue with the study’s suggestion that the blowout of its deep-water Macondo well may have harmed marine life.
“The paper provides no evidence to suggest a population-level impact on tuna or other fish species in the Gulf of Mexico,” said BP spokesman Jason Ryan. “Bathing isolated heart cells with oil concentrations is simply not comparable to the real-world conditions and exposures that existed in the gulf for whole fish.”]
The research was funded by NOAA, Stanford and the Monterey Bay Aquarium.
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