Toxicology of Industrial Compounds

122 PULMONARY TOXICITY STUDIES WITH MAN-MADE ORGANIC FIBRES
Figure 8.1 Continued
exposures and (C) the low-dose exposure groups. A casual glance at the two graphs
B and C indicates that some success was attained in increasing the mean lengths in
the aerosol of the generated chrysotile asbestos sample.
with only occasional centriacinar regions having slight, fibril-associated
thickening of alveolar duct bifurcations. At 1 year postexposure, the lungs
in p-aramid exposed rats were similar to controls. The 1-year chrysotileexposed
animals are still in recovery.
Pulmonary cell proliferation
In chrysotile asbestos-exposed rats, substantial increases compared to
controls in pulmonary cell proliferation indices were measured on terminal
bronchiolar, parenchymal, visceral pleural/subpleural and mesothelial
surfaces, and many of these effects were sustained through 3 months
postexposure. These data demonstrate that 2-week chrysotile exposures
produced a prolonged proliferative response in airway, alveolar and
subpleural cells, as evidenced by the sustained effect through 3 months
postexposure (Table 8.2).
Pulmonary cell proliferation studies demonstrated that 2-week exposures
to the high dose of p-aramid fibrils produced a transient increase in
terminal bronchiolar and visceral pleural/subpleural cell labeling responses.
No increases in lung parenchymal, or subpleural cell labeling indices were
mea sured at any time period relative to sham controls. In addition, no