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Chronic Sidestream Cigarette Smoke Exposure Causes Lung Injury in Rabbits

Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Patricia M. Joseph

Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

R. Clark Lantz

Arizona Health Sciences Center, Tucson, Ariz., USA

David S. Lazarus

Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Walter K. Jung

Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Charles A. Hales

Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

The effects of sidestream cigarette smoke (SSCS) (a 15-min exposure per day for 20 days) were determined on markers of lung injury in New Zealand white rabbits (n = 9) and a control group (n = 6). The SSCS consisted of air and smoke which were aspirated by syringe from a funnel inverted over a lit ciga rette. The rabbits were placed in an environmental chamber into which 3 liters of SSCS were injected over a 15-min period each day. Chronic SSCS caused an increase (p < 0.05) in pulmonary epithelial clearance (k) of technetium labeled diethylenetriamine pentaacetate (^99mTcDTPA); k = 0.83 (±0.07) for the SSCS-exposed group and 0.66 (± 0.02) for the control group. This increase in lung permeability was accompanied by an increase in bronchoalveolar lavage (BAL) white cell count; SSCS = 83,353 ( ± 11,954) cells/mm3 BAL fluid versus control = 16,450 (± 6,683) cells/mm3 BAL fluid and an increase in BAL leukotriene E4; SSCS = 742 (± 285) pg/ml BAL fluid compared with 76 (± 2) pg/ml BAL fluid for controls. Cultured SSCS alveolar macrophages (AMs) produced more superoxide (O₂); 2.4 (± 0.8) nmol O₂/10⁶ AMs versus 0.4 (± 0.2) nmol O₂/10⁶ AMs for controls after incubation for 18 h with 10 µg/ml lipopolysaccharide. Electron microscopy demonstrated that the airway mu cosa of SSCS rabbits was infiltrated by eosinophils, and light microscopy showed focal clusters of neutrophils in perivascular and capillary spaces. It is concluded that SSCS exposure can induce lung injury.

Indoor and Built Environment, Vol. 1, No. 6, 341-347 (1992)
DOI: 10.1177/1420326X9200100605


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