To determine whether
asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of
asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of
amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls.
Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (
asbestosis) occurred. It is concluded that 1)
amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial
fibrosis of the parenchyma (classical
asbestosis); 3)
asbestosis, at least that induced by
amosite, commences at any site in the parenchyma to which the
asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.