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Dietary fat and ETS effects on lung epithelial biology

Institution: University of California, Davis
Investigator(s): Laura Van Winkle, Ph.D.
Award Cycle: 2003 (Cycle 12) Grant #: 12IT-0191 Award: $99,827
Subject Area: Pulmonary Disease
Award Type: Inno Dev & Exp Awards (IDEAS)

Initial Award Abstract
Exposure to the air pollutant, environmental tobacco smoke (ETS) is causally associated with lung cancer in both men and women. ETS is a complex mixture that contains over 4000 different chemicals, many of which are well-known human carcinogens and that also injure cells. Lung diseases have increased in prevalence in the latter half of the 20th century. This may be due to several factors in combination such as consumption of a diet high in saturated fat and exposure to the carcinogens and toxins in air pollutants. Lung cancer risk is increased by exposure to ETS. Lung cancer risk may also be increased by a high dietary intake of saturated fat. The most obvious impact of a high fat diet is weight gain. The National Institute of Diabetes, Digestive and Kidney diseases estimates that one-third of Americans, about 58 million people, are overweight. Weight gain has been shown to accelerate loss of lung function (the ability to breath) as people age. Little is known about the effects of a high fat diet on lung cells. Even less is known about how diet affects the lung’s ability to withstand toxins found in ETS. There are sex-based differences in how the lung responds to ETS. The risk for cancers of the peripheral lung is higher in women than in men exposed to tobacco smoke. Epidemiologic studies also suggest that women with altered expression of certain genes and enzymes have an increased risk of cancer. These genes and enzymes interact with tobacco smoke to cause formation of tumors as well as acute toxicity to epithelial cells in the lung. Our hypothesis is that a high fat diet will enhance the toxicity of ETS in the lung. We further hypothesize that these responses will differ by gender. We will try to define the mechanism for the enhanced toxicity. Our long term goal is to define the mechanisms by which an unhealthy lifestyle, such as consumption of a high fat diet, impairs the lung’s ability to resist injury by ETS and thus leads to lung diseases such as cancer, asthma and bronchitis. This research has potential impact for both men and women who smoke or are exposed to ETS and consume a diet high in saturated fat. We expect that these studies will benefit the general population by defining the mechanisms that make a high fat diet and ETS exposure both risk factors for loss of lung function and lung cancer. These studies are highly relevant to TRDRP research priorities regarding the effects of environmental tobacco smoke on human health.

Estrous cycle and estrogen receptor expression in the female mouse lung.
Periodical: Molecular Biology of the Cell Index Medicus:
Authors: Van Winkle LS, Baker GL, Stelck RL, Shimizu JA, Brown CD, Plopper CG ABS
Yr: 0 Vol: Nbr: Abs: A657 Pg:

Estrous cycle alters pulmonary metabolism of naphthalene (NA)
Periodical: Toxicologist Index Medicus:
Authors: Van Winkle LS, Baker GL, Stelck RL, Brown CD, Plopper CG, Buckpitt AR ABS
Yr: 2004 Vol: 78 Nbr: S-1 Abs: 705 Pg: 145