K. Hiroshima et al., CHARACTERIZATION OF ASBESTOS FIBERS IN LUNGS AND MESOTHELIOMATOUS TISSUES OF BABOONS FOLLOWING LONG-TERM INHALATION, American journal of industrial medicine, 23(6), 1993, pp. 883-901
Changes in the dimensions of inhaled asbestos fibers in the lung and t
ranslocation of intrapulmonary asbestos fibers into mesothelial tissue
s were investigated in 17 baboons (5 exposed to amosite, 4 to chrysoti
le, 5 to crocidolite, and 3 unexposed). The animals received different
cumulative doses of asbestos by inhalation, followed by varying recov
ery periods (0-69 months). All asbestos types induced pulmonary asbest
osis with severity directly related to the cumulative dose. There were
a larger number of asbestos bodies in the lung of the amphibole-expos
ed animals than in those exposed to chrysotile. A tissue burden study,
using transmission electron microscopy on 25-mum paraffin sections, a
shed in a low-temperature asher, was performed. Intrapulmonary amosite
fibers were shorter in geometric mean length compared with a standard
amosite sample (UICC) (3.3 mum). In explanation, it was considered th
at long fibers might not be able to reach the lower respiratory tract
and/or long fibers might be fragmented into shorter fibers. Further, i
n the amosite-exposed group, the mean length of intrapulmonary fibers
increased with the extension of recovery period, suggesting that short
er fibers had been cleared from the lung. The chrysotile standard samp
le (UICC) had a shorter geometric mean length (1.1 mum) than amosite.
The mean length of intrapulmonary chrysotile did not noticeably change
with the extension of inhalation and recovery periods; however, the m
ean width decreased with the extension of these periods. This finding
strongly suggested that separation of thick chrysotile fibers had occu
rred in the lung. The crocidolite standard sample (Transvaal) had a sh
orter geometric mean length (1.4 mum) than amosite. The mean length of
intrapulmonary crocidolite fibers increased with the extension of inh
alation and recovery periods, suggesting that shorter fibers had been
cleared from the lung during both the inhalation and recovery periods.
There was no specific tendency of size distribution among four distin
ct interstitial locations (peribronchiolar, alveolar septal, subpleura
l, and interlobular connective tissue) within the same lung exposed to
either amosite, chrysotile or crocidolite. In four animals, malignant
mesothelioma developed in the pleura (2 amosite and 1 UICC crocidolit
e) and the peritoneum (1 UICC crocidolite). Asbestos fibers were found
in the mesotheliomas. Their size distribution in mesotheliomatous tis
sue and lung was not significantly different in two animals, but the f
ibers were shorter and thinner in another two. The presence of fibers
in the neoplasms was confirmed, and translocation of fibers from the l
ung into the pleura or the peritoneum was strongly suggested.