UC Merced Professor Receives Prop. 99 Grant Money to Study Tobacco Effects
MERCED - In 1988, California voters approved Proposition 99, an initiative specifying that five percent of cigarette tax revenue be appropriated for research on tobacco-related disease. UC Merced professor Henry Jay Forman is now bringing $420,000 of that money to Merced to study how human bronchial epithelial cells try to protect against the toxins found in cigarette smoke.
"The California Tobacco-related Disease Research Program funds have a reputation for being pretty tough to get, particularly on the first try," says Forman, whose experience researching related topics spans 25 years. "We overcame the odds to bring this research funding to Merced, and that's a good thing as this is a challenging time to obtain research money."
His research group participated in a competitive grant-application process to win the funding in the same way that scientists often compete for grants from organizations like the National Science Foundation or National Institutes of Health. The grant will be awarded over three years.
"Professor Forman's new research project is an example of how his stellar basic research to understand the response of cells to damage is now being applied to work on a problem that affects the lives of many individuals in our community," says Dean Maria Pallavicini of the UC Merced School of Natural Sciences.
Forman will use the new funding to investigate byproducts from smoking-related oxidation of cell membranes that trigger changes in the DNA of bronchial epithelial cells and how those DNA changes increase protective enzymes that shield cells from further damage.
So far it has been generally assumed that the genes in the DNA that regulate production of a group of protective enzymes in the lung, all work in the same way. Forman's hypothesis is that there are important differences among the group that will help him understand how the protective enzymes are made.
The protective enzymes made by cells in response to smoking-related toxins do not provide a sufficient shield against cell damage. If research discovered a way to increase those enzymes, it could be useful for those already addicted to smoking or suffering from smoking-related diseases. Still, Forman emphasizes that even in larger quantities the enzymes would not provide an absolute barrier to smoking-related injury and would not provide a license for smoking.
Forman will conduct the research funded by his new grant in his laboratory at UC Merced's Castle facility until they move to the new campus next year. He describes the project as cell-culture work performed on established bronchial epithelial cell lines as well as cells obtained form autopsy.
Forman arrived at UC Merced in 2003 as one of the original faculty members. He was previously chairman of the Department of Environmental Health Sciences in the School of Public Health at the University of Alabama, Birmingham.