Genetic susceptibility in pneumoconiosis.
A large number of cellular mediators such as cytokines, antioxidants and growth factors have been implicated in the pathogenesis of chronic inflammatory and fibrotic diseases. Common functional polymorphisms in these genes have been shown to influence individual susceptibility to these diseases. Silicosis, coal worker pneumoconiosis, progressive massive fibrosis and berylliosis are examples of fibrotic pneumoconiosis and are characterized by irreversible fibrotic lesions in the lung resulting from chronic dust inhalation. Although the materials are the major contributory factors of the disease pathogenesis, not all individuals exposed to similar levels develop disease. This suggests that there is a genetic predisposition to their development. Therefore, an understanding of genetic variability and the interaction between genetic and environmental factors is crucial to the identification of high-risk individuals and prevention and treatment of these diseases.
Yucesoy
Berran
B
Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA. yab7@cdc.gov
Luster
Michael I
MI
D000395:Air Pollutants, Occupational / Q000633:toxicity; D020022:Genetic Predisposition to Disease; D006801:Humans; D009784:Occupational Diseases / Q000235:genetics*; D016273:Occupational Exposure / Q000009:adverse effects; D011009:Pneumoconiosis / Q000235:genetics*; D011658:Pulmonary Fibrosis / Q000235:genetics*
D000395:Air Pollutants, Occupational