Public Release:  Stanford, NOAA scientists discover mechanism of crude oil heart toxicity

Stanford University


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The research, published in the Feb. 14 issue of Science, is part of the ongoing Natural Resource Damage Assessment of the April 2010 Deepwater Horizon oil spill.


Crude oil is a complex mixture of chemicals, some of which are known to be toxic to marine animals. Past research has focused in particular on "polycyclic aromatic hydrocarbons" (PAHs), which can also be found in coal tar, creosote, air pollution and stormwater runoff from land. In the aftermath of an oil spill, PAHs can persist for many years in marine habitats and cause a variety of adverse environmental effects.

The researchers report that oil interferes with cardiac cell excitability, contraction and relaxation - vital processes for normal beat-to-beat contraction and pacing of the heart.

Their tests revealed that very low concentrations of crude oil disrupt the specialized ion channel pores - where molecules flow in and out of the heart cells - that control heart rate and contraction in the cardiac muscle cell.



"The ability of a heart cell to beat," explained Barbara Block, a professor of marine sciences at Stanford, "depends on its capacity to move essential ions like potassium and calcium into and out of the cells quickly. This dynamic process, which is common to all vertebrates, is called 'excitation-contraction coupling.' We have discovered that crude oil interferes with this vital signaling process essential for our heart cells to function properly."

"We've known from NOAA research over the past two decades that crude oil is toxic to the developing hearts of fish embryos and larvae, but haven't understood precisely why," said coauthor Nat Scholz, leader of the Ecotoxicology Program at NOAA's Northwest Fisheries Science Center in Seattle. "These new findings more clearly define petroleum-derived chemical threats to fish and other species in coastal and ocean habitats, with implications that extend beyond oil spills to other sources of pollution such as land-based urban stormwater runoff."


"When we see these kinds of acute effects at the cardiac cell level," Block said, "it is not surprising that chronic exposure to oil from spills such as the Deepwater Horizon can lead to long-term problems in fish hearts, as our NOAA colleagues have observed in studies of larval fish development.

"The protein ion channels we observe in the tuna heart cells are similar to what we would find in any vertebrate heart and provide evidence as to how petroleum products may be negatively impacting cardiac function in a wide variety of animals," she said. "This raises the possibility that exposure to environmental PAHs in many animals - including humans - could lead to cardiac arrhythmias and bradycardia, or slowing of the heart."






They measured the heart cells' response using a combination of sophisticated electro-physiological techniques - including "patch clamping" and "confocal microscopy" - to record how ions flowed into and out of the heart cells, and to identify the specific proteins in the excitation-contraction pathway that were affected by crude oil chemical components.

"We can examine the function of healthy heart cells in vitro and actually measure in the microscope how they respond to the presence of crude oil in real time," said Fabien Brette, a research associate in Block's lab and lead author on the study.

"The normal sequence and synchronous contraction of the heart requires rapid activation in a coordinated way of the heart cells," Block said. "Like detectives, we dissected this process using laboratory physiological techniques to ask where oil was impacting this vital mechanism."



