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Laboratory of Environmental Lung Disease (ELD)Stylized alveoli sharing a circle with the outline of a man & women.  A double helix with a mouse climbing over the top overlaps a little.

David Schwartz, M.D.

Our group investigates the genetic and biological determinants of environmental and occupational lung disease. Our research has provided new insights into the pathophysiology and biology of asbestos induced lung disease, interstitial lung disease, environmental airway disease, and innate immunity. We have identified endotoxin or lipopolysaccharide as an important cause of airway disease among those exposed to organic dusts, and that a specific mutation in the Toll-4 gene is associated with a diminished airway response to inhaled LPS in humans.

Recent work is focusing on the:

  • genes that regulate the innate immune response in C. elegans, mice and humans
  • genes involved in the fibroproliferative response in the lung
  • genetic regulation of environmental asthma

The ELD group uses environmental genomics/genetics to understand the etiology and pathogenesis of asthma, pulmonary fibrosis, and diseases influenced by innate immunity.

Specifically, the group studies the biology and genetics of environmental lung disease and host defense. Previous research has provided insight into the pathophysiology, biology, and genetics of environmental airway disease, pulmonary fibrosis, and innate immunity. The Schwartz lab has identified a polymorphism--variation in the normal sequence of a gene--in TLR4, the receptor for endotoxin or lipopolysaccharide (LPS). This discovery is important because the polymorphism in TLR4 results in a blunted response to inhaled LPS, an enhanced risk of Gram- negative sepsis, and a decreased risk of atherogenesis in humans. The group’s current work focuses on identifying other genes that regulate the innate immune response, genes involved in the fibroproliferative response in the lung, and the genetic regulation of specific forms of environmental asthma.

Major areas of research:

  • Genes that regulate the innate immune response in Caenorhabditis elegans, mice and humans
  • Genes involved in the fibroproliferative response in the lung
  • Genetic regulation of environmental asthma
  • Epigenetics of environmental lung disease

Current projects:

  • To use comparative genomics (in vitro, C. elegans, and mice) and high throughput screening to identify genes involved in the innate immune response to PAMPs and live organisms that may be relevant to human host defense.
  • To use linkage and association studies in humans with idiopathic interstitial pneumonia and animal models of pulmonary fibrosis to identify critical genes involved in fibroproliferation.
  • To use genomic expression and epigenetic approaches to identify key regulatory genes in the development of environmental airway disease.

David A. Schwartz, M.D. is the Director of National Institute of Environmental Health Sciences, Director of the National Toxicology Program, and head of the Environmental Lung Disease group. Schwartz, a nationally recognized physician-scientist specializing in environmental lung disease, has authored more than 150 peer-reviewed research papers, 38 book chapters, and a textbook. Schwartz earned his BA in biology from the University of Rochester in 1975, and a medical degree from the University of California, San Diego in 1979.

Indexing terms: environmental lung diseases, innate immunity, lipolysaccharides/endotoxin, pulmonary fibrosis, environmental airway disease, environmental genetics/genomics, and comparative genomics.



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Department of Health and Human Services National Institutes of Health National Heart, Lung, and Blood Institute