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(e.g. cigarette smoking) occur (Reszka and Wasowicz 2001). Individuals with decreased rate of detoxification, with high risk glutathione S-

t r a n s f e r a s e g e n o t y p e s h a v e a s l i g h t l y h i g h e r l e v e


of carcinogen-DNA adducts and more cytoge- netic damages.


Recent attention is focused on understanding the genetic and environmental basis for individual susceptibility to the development of chronic respiratory diseases. Indeed, gene- environment interactions are thought to be critical for several respiratory diseases such as COPD and lung cancer. These disorders are the result of multiple gene-environment interactions occurring over several decades. Further, more emphasis is being concentrated on establishing an association between inheritance of polymorphic chemical metabolizing genes and development of environmental cancer (e.g., lung cancer among cigarette smokers).AATD- related emphysema is caused by an inherited lack of a protective protein called alpha1-antitrypsin (AAT). Several of the GST genes are polymorphic in humans and are currently being investigated as possible cancer-risk modifiers. Moreover, understanding the fundamental gene- environmental interactions in the development of respiratory disorders such as asthma should lead to earlier identification of susceptible individuals and more effective approaches for disease prevention.


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