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additional studies that may help explain how exposure to BCE affects human nerve cell development and how it might relate to neurological disorders. "We can clearly state that we found an increase in a component of PKA, and PKA is known to be involved in neural development. The BCE mixture is capable of altering neural development, and alterations in neural development are thought to be a cause of autism," says Jill Kreiling, first author of the paper and a member of Reinisch's lab. But Kreiling cautions, "We cannot say at this time if the alteration we see in clam embryos is the same alteration that causes autism. That will require future research." In fact, Reinisch and Kreiling have already begun the next phase of their work. They are currently examining the origins of BCE toxicity at the single-neuron level to learn what genes are turned on and off by the exposure to the chemical mixture. The research is focused on a family of genes known as P53, which helps to regulate the cell cycle. They have also moved their studies to a new model system: the zebrafish, a vertebrate with more similarities to humans. Reinisch's work on BCE is funded by a STAR grant from the United States Environmental Protection Agency. Science supported by the STAR program is rigorously peer reviewed. Study Background and Research Methods When MBL researcher Carol Reinisch first heard news stories about Brick Township, New Jersey--a town that was the center of an ATSDR* study in the year 2000 that documented a higher than usual rate of autism spectrum disorder and explored its link to bromoform, chloroform, and tetrachloroethylene in Brick's water supply--it got her thinking. "My hypothesis was this: While it had been proven that individually the chemicals don't impact nerve cell development, the combination of all three might pose increased risks," she says. So Reinisch decided to test the chemical cocktail, in similar proportions to those found in Brick, on a species of surf clam readily
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