What is the role of environmental exposures in the etiology of alpha1-antitrypsin deficiency (AATD)?

Updated: Sep 11, 2020
  • Author: Dora E Izaguirre Anariba, MD, MPH; Chief Editor: John J Oppenheimer, MD  more...
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Answer

Cigarette smoking accelerates the onset of symptomatic disease by approximately 10 years, by producing an increase in the number of neutrophils (and neutrophil elastase) in the alveolus and inactivating the remaining small amounts of antiprotease. [1] Other factors that can accelerate the onset or worsen symptoms of disease include infections and exposures to dust and fumes, which can also cause the recruitment of neutrophils to the alveoli.

Other than cigarette smoking, the role of environmental exposures on spirometric decline in patients with alpha1-antitrypsin deficiency has been uncertain. Banauch et al investigated the possible interaction of alpha1-antitrypsin deficiency and short-term massive pollution in New York City Fire Department (FDNY) rescue workers responding to the World Trade Center (WTC) collapse. In the first 4 years after the event, they found significant accelerated declines in spirometry and increased respiratory symptoms. Declines were related to the degree of exposure at the disaster site and to the degree of AATD. [8] These results support the theory that environmental factors other than cigarette smoke may play a role in the progression of lung disease in alpha1-antitrypsin-deficient patients. However, the size of the study was very small, and care should be taken in generalizing this theory given the unique nature of the WTC disaster. Further studies are needed.


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