{'fraction_non_alphanumeric': 0.01630049610205528, 'fraction_numerical': 0.005669737774627924, 'mean_word_length': 5.331838565022421, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Interstitial accumulation of inhaled chrysotile asbestos fibers and consequent formation of microcalcifications.

Previous studies have shown that inhaled chrysotile asbestos impacts initially at the bifurcations of alveolar ducts in the lungs of rats. Asbestos fibers are transported through alveolar epithelial cells at these bifurcation regions to the interstitium during the 24-hour period after a 1-hour exposure. To further these studies, white rats were exposed to an aerosol of chrysotile asbestos for 1 hour. Animals were sacrificed, and the lungs were fixed by vascular perfusion immediately after and 1 month after exposure. Blocks of tissue were prepared for light and electron microscopy. We report here, at 1 month after exposure, that numerous asbestos fibers had accumulated within the lung interstitium at alveolar duct bifurcations. Many of these interstitial fibers were found in te center of intracellular microcalcifications. The presence of calcifications was proven by X-ray energy spectrometric analysis of the inclusions in situ. Clear X-ray peaks for calcium and phosphorus were demonstrated. The authors propose that 1 month after a 1-hour exposure to chrysotile asbestos, fiber-induced membrane injury in cells of the lung interstitium leads to formation of microcalcifications. This may represent the presence of early cell injury in the initial pathogenetic sequence of asbestosis.