Sequence of bronchoalveolar lavage and histopathologic findings in rat lungs early in inhalation asbestos exposure

Smith, Cecilia M.; Batcher, Sharon; Catanzaro, Antonino; Abraham, Jerrold L.; Phalen, Robert F.

doi:10.1080/15287398709530968

Cited by 9 publications

(3 citation statements)

References 22 publications

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“…LA exposure was often associated with a greater incidence of intra-alveolar and interstitial AM aggregation, while the amosite-exposed lungs demonstrated greater incidence of large giant cells and interstitial fibrosis. These histopathological findings are consistent with previous studies (Smith et al 1987;Hurbánková and Kaiglová 1997;Petruska et al 1991).…”

Section: Discussionsupporting

confidence: 95%

“…The temporal pattern of inflammatory responses to LA and amosite was similar to that found in previous rat asbestos inhalation (Smith et al 1987) and IT studies (Li et al 1993;Hurbánková and Kaiglová 1997), including an early inflammatory response due to the neutrophil recruitment to the airways. Markers of cellular permeability and damage were also augmented at most of the time points both in the amosite and in the high-dose LA groups.…”

Section: Discussionsupporting

confidence: 74%

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Pulmonary Inflammatory and Fibrotic Responses in Fischer 344 Rats After Intratracheal Instillation Exposure to Libby Amphibole

Padilla-Carlin

Schladweiler

Shannahan

et al. 2011

Journal of Toxicology and Environmental Health, Part A

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Increased incidences of asbestosis have been reported in workers from Libby, MT, associated with exposures to amphibole-contaminated vermiculite. In this study pulmonary and histopathological changes were investigated following Libby amphibole (LA) exposure in a rat model. Rat respirable fractions of LA and amosite (aerodynamic diameter <2.5 μm) were prepared by water elutriation. Male F344 rats were exposed to single doses of either saline (SAL), amosite (0.65 mg/rat), or LA (0.65 or 6.5 mg/rat) by intratracheal instillation. At times from 1 d to 3 mo after exposure, bronchoalveolar lavage (BAL) was performed and right and left lungs were removed for reverse-transcription polymerase chain reaction (RT-PCR) and histopathological analysis, respectively. Data indicated that 0.65 mg amosite resulted in a higher degree of pulmonary injury, inflammation, and fibrotic events than LA at the same mass dose. Exposure to either amosite or high dose LA resulted in higher levels of cellular permeability and injury, inflammatory enzymes, and iron binding proteins in both BAL fluid and lung tissue at most time points when compared to SAL controls. However, mRNA expression for some growth factors (e.g., platelet-derived growth factor [PDGF]-A and transforming growth factor [TGF]-1β), which contribute to fibrosis, were downregulated at several time points. Furthermore, histopathological examination showed notable thickening of interstitial areas surrounding the alveolar ducts and terminal bronchioles. On a mass dose basis, amosite produced a greater acute and persistent lung injury for at least 3 mo after exposure. However, further testing and analysis of LA are needed with regard to the dose metric to fully evaluate its potential fibrogenicity and carcinogenicity.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionsupporting

confidence: 74%

Pulmonary Inflammatory and Fibrotic Responses in Fischer 344 Rats After Intratracheal Instillation Exposure to Libby Amphibole

Padilla-Carlin

Schladweiler

Shannahan

et al. 2011

Journal of Toxicology and Environmental Health, Part A

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“…After inhalation or intratracheal administration of asbestos fibers to rodents, an initial inflammatory response, characterized by increases in PMNs in BALF and lung tissues, is observed (1,(16)(17)(18). Increases in PMNs are also observed in the BALF and lungs of workers exposed to asbestos and individuals with a variety of pneumoconiosis (19,20).…”

Section: Introductionmentioning

confidence: 80%

Asbestos-Induced Lung Inflammation and Epithelial Cell Proliferation Are Altered in Myeloperoxidase-Null Mice

Haegens¹,

Vliet²,

Butnor³

et al. 2005

Cancer Research

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Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers. In comparison with sham mice, asbestos-exposed myeloperoxidase-null (MPOÀ/À) and normal (MPO+/+) mice exhibited comparable increases in polymorphonuclear leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation. Differential cell counts on BALF revealed decreased proportions of macrophages and increased lymphocytes in all mice exposed to asbestos, but numbers were decreased overall in asbestosexposed myeloperoxidase-null versus normal mice. Asbestosassociated lung inflammation in myeloperoxidase-null mice was reduced (P V 0.05) in comparison with normal asbestosexposed mice at 9 days. Decreased lung inflammation in asbestos-exposed myeloperoxidase-null mice at 9 days was accompanied by increases (P V 0.05) in Ki-67-and cyclin D1-positive immunoreactive cells, markers of cell cycle reentry, in the distal bronchiolar epithelium. Asbestos-induced epithelial cell proliferation in myeloperoxidase-null mice at 30 days was comparable to that found at 9 days. In contrast, inflammation and epithelial cell proliferation in asbestos-exposed normal mice increased over time. These results support the hypothesis that myeloperoxidase status modulates early asbestos-induced oxidative stress, epithelial cell proliferation, and inflammation.

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Experimental Models of Asbestos-Related Diseases

Fattman¹,

Chu²,

Oury³

Pathology of Asbestos-Associated Diseases

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Sequence of bronchoalveolar lavage and histopathologic findings in rat lungs early in inhalation asbestos exposure

Cited by 9 publications

References 22 publications

Pulmonary Inflammatory and Fibrotic Responses in Fischer 344 Rats After Intratracheal Instillation Exposure to Libby Amphibole

Pulmonary Inflammatory and Fibrotic Responses in Fischer 344 Rats After Intratracheal Instillation Exposure to Libby Amphibole

Asbestos-Induced Lung Inflammation and Epithelial Cell Proliferation Are Altered in Myeloperoxidase-Null Mice

Experimental Models of Asbestos-Related Diseases

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