(June 10, 2003) Bethesda, MD Environmental particles the size of those emanating from cigarette smoke and toxic aerosols interact with our pulmonary surfaces and may lead to lung disease. The location of such cancerous lesions in the bronchial airway may not be a random process, however. Instead, they may be related to a regional pattern of toxic material deposited in selected areas of the lungs. A new study suggests that a specific site the ridge separating the two halves of the bronchial airway -- may be a key factor in developing lung cancer.

Background

Earlier studies of cell dynamics indicate that benign and cancerous lesions alike predominate at the division between the central airways. One study has assessed the likelihood of finding cancer based on the site within the bronchi as ten percent for the main surface and 30 percent each for the lobar, segmental and subsegmental regions. Later research suggests that the accumulation of carcinogenic particles and particles with absorbed carcinogens from cigarette smoke at the airway's carinas -- the ridge separating the openings of the right and left main bronchi at their junction with the trachea -- is a potentially important mechanism for human pulmonary carcinogenesis. Animal studies indicate that clearing particles is much slower in the airway carinas than in the tubular airway segments.

The methods currently used to calculate exposure to particles do not take into consideration the inhomogeneity of either the deposition of the toxin or the clearance patterns of the site. The reported locations of cancer manifestation are therefore at odds with the calculated dose patterns among human bronchial airways. Accordingly, the enhanced deposition along the carinal ridges has been thought to be a more relevant deposition quantity for assessing risk than is the method of using average deposition patterns. In addition to there being increased deposits in the carcina, the streamline cu
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
17-Jun-2003

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