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Increased neutrophil elastase activity in cigarette smokers.
J I Weitz1, K A Crowley, S L Landman
1Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Annals of Internal Medicine
|November 1, 1987
Summary
Cigarette smoking significantly elevates plasma levels of fibrinopeptide A-alpha-1-21, a marker of neutrophil elastase activity. This suggests smoking disrupts the enzyme balance, potentially leading to lung disease.
Area of Science:
- Biochemistry
- Pulmonology
- Toxicology
Background:
- Neutrophil elastase plays a role in lung tissue degradation.
- Cigarette smoking is a known risk factor for various lung diseases.
- The elastase-antielastase balance is crucial for maintaining lung health.
Purpose of the Study:
- To compare plasma levels of neutrophil elastase-derived fibrinopeptide A-alpha-1-21 in smokers and nonsmokers.
- To investigate the acute effects of cigarette smoking on this enzyme activity.
Main Methods:
- Plasma concentrations of fibrinopeptide A-alpha-1-21 were measured.
- Comparison between healthy cigarette smokers and nonsmokers.
- Assessment of enzyme levels before and after smoking three cigarettes in a separate group of smokers.
Main Results:
- Smokers had fivefold higher A-alpha-1-21 levels than nonsmokers (2.0 vs 0.4 nmol/L).
- Acute smoking increased A-alpha-1-21 levels twofold (1.8 to 4.1 nmol/L).
- Elevated levels persisted even after a 12-hour smoking abstinence period.
Conclusions:
- Cigarette smoking significantly perturbs the in-vivo elastase-antielastase balance.
- This imbalance may be a mechanism through which smoking causes lung disease.
- Fibrinopeptide A-alpha-1-21 serves as a biomarker for smoking-induced elastase activity.
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