Asbestos: Scientific Developments and Implications for Public Policy

Mossman, Brooke T.; Bignon, J.; Corn, Morton; Seaton, Anthony; Gee, J. Bernard L.

doi:10.1126/science.2153315

Cited by 691 publications

(355 citation statements)

References 76 publications

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“…In this study, we performed a subchronic kinetic study (3,9, and 40 days) with CC10-I B␣ sr (Tg ϩ ) and Tg Ϫ mice using physiological administration of inhaled asbestos fibers at airborne concentrations equivalent to historical occupational exposures (1,2). We characterized novel patterns in differential cell counts in BALF by asbestos over time and profiled cytokines in BALF using a robust Bio-Plex analysis.…”

Section: Discussionmentioning

confidence: 99%

“…A sbestos is a family of naturally occurring mineral fibers associated with the development of lung cancers, mesotheliomas, and fibroproliferative diseases, i.e., pleural and diffuse interstitial fibrosis or asbestosis (1,2). Asbestos-associated lung repair has been compared with models of wound healing wherein early injury to epithelial cells by inhaled fibers leads to compensatory hyperplasia.…”

mentioning

confidence: 99%

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Airway Epithelial NF-κB Activation Modulates Asbestos-Induced Inflammation and Mucin Production In Vivo

Haegens

Barrett

Gell

et al. 2007

The Journal of Immunology

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To investigate the role of bronchiolar epithelial NF-κB activity in the development of inflammation and fibrogenesis in a murine model of asbestos inhalation, we used transgenic (Tg) mice expressing an IκBα mutant (IκBαsr) resistant to phosphorylation-induced degradation and targeted to bronchial epithelium using the CC10 promoter. Sham and chrysotile asbestos-exposed CC10-IκBαsr Tg+ and Tg− mice were examined for altered epithelial cell proliferation and differentiation, cytokine profiles, lung inflammation, and fibrogenesis at 3, 9, and 40 days. KC, IL-6 and IL-1β were increased (p ≤ 0.05) in bronchoalveolar lavage fluid (BALF) from asbestos-exposed mice, but to a lesser extent (p ≤ 0.05) in Tg+ vs Tg− mice. Asbestos also caused increases in IL-4, MIP-1β, and MCP-1 in BALF that were more elevated (p ≤ 0.05) in Tg+ mice at 9 days. Differential cell counts revealed eosinophils in BALF that increased (p ≤ 0.05) in Tg+ mice at 9 days, a time point corresponding with significantly increased numbers of bronchiolar epithelial cells staining positively for mucus production. At all time points, asbestos caused increased numbers of distal bronchiolar epithelial cells and peribronchiolar cells incorporating the proliferation marker, Ki-67. However, bronchiolar epithelial cell and interstitial cell labeling was diminished at 40 days (p ≤ 0.05) in Tg+ vs Tg− mice. Our findings demonstrate that airway epithelial NF-κB activity plays a role in orchestrating the inflammatory response as well as cell proliferation in response to asbestos.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Airway Epithelial NF-κB Activation Modulates Asbestos-Induced Inflammation and Mucin Production In Vivo

Haegens

Barrett

Gell

et al. 2007

The Journal of Immunology

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“…Si 8 O 22 (OH) 2 ], the rodlike amphiboletype asbestos (Mossman et al 1990;Mossman and Gee 1989). Clinical and epidemiologic studies have established that asbestos fibers are associated with the development of pulmonary interstitial fibrosis, lung cancer, and malignant mesothelioma (Mossman et al 1990;Mossman and Gee 1989).…”

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confidence: 99%

Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.

Matsuoka

Ichikawa

Morimoto

2003

Environ Health Perspect

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We examined effects of asbestos exposure on the phosphorylation of p53 protein in human pulmonary epithelial type II cells (A549), which express wild-type p53. In cells exposed to two different types of asbestos, chrysotile (approximately 1-6% iron content) and crocidolite (approximately 27% iron content) fibers, at the doses of 1, 5, and 10 microg/cm2 for 24 hr, the levels of p53 phosphorylated at Ser15 and p53 protein were correlated with the dose. On a per-weight basis, chrysotile was more potent in inducing Ser15 phosphorylation and accumulation of p53 protein than was crocidolite. After exposure to 10 micro g/cm2 chrysotile, the levels of p53 phosphorylated at Ser15 and of p53 protein increased after 18 hr. Among serines in p53 protein immunoprecipitated from A549 cells treated with chrysotile, only Ser15 was markedly phosphorylated. In contrast, no clear phosphorylation was observed at Ser6, Ser9, Ser20, Ser37, Ser46, or Ser392. Blocking of the extracellular signal-regulated protein kinase pathway with U0126 or inhibition of p38 activity with SB203580 did not suppress chrysotile-induced Ser15 phosphorylation. On the other hand, treatment with wortmannin, an inhibitor of DNA-activated protein kinase and ataxia-telangiectasia mutated, suppressed both chrysotile-induced Ser15 phosphorylation and accumulation of p53 protein. Treatment with either catalase or N-acetylcysteine failed to suppress chrysotile-induced Ser15 phosphorylation, suggesting that reactive oxygen species do not play a major role in the phosphorylation of p53 protein. The present results show that asbestos, particularly chrysotile, induces phosphorylation of p53 protein at Ser15 in A549 cells depending on a DNA damage-signaling pathway.

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“…Since free radicals have been considered a potential pathogenetic mechanism in asbestos-related pulmonary diseases, one possibly important determinant in the development of lung injury caused by fibers is the antioxidant capacity of the cells (Mossman et al, 1983(Mossman et al, : 1989a(Mossman et al, : 1989b(Mossman et al, : 1990. There are limited information about the relationship between serum level of antioxidants and mesothelioma.…”

Section: Introductionmentioning

confidence: 99%

Serum Levels of Alpha-Tocopherol, Vitamin C, Beta-Carotene, and Retinol in Malignant Pleural Mesothelioma

Emri

Kılıçkap²,

Kadılar³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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The aim of this study was to investigate the possible relationship between antioxidant vitamin levels and malignant pleural mesothelioma (MPM). For this purpose, we measured the serum levels of 4 antioxidant vitamins, β-carotene, α-tocopherol, retinol, and ascorbic acid, in patients with environmentally induced MPM and in healthy controls from one tremolite village (Kureysler), the biggest erionite village (Tuzkoy) and Ankara. A total of 160 subjects were enrolled in the study, 42 (26.3%) diagnosed with MPM and 118 (73.7%) healthy subjects. A comparison was made between the MPM group and three control groups of which two were exposed and one was unexposed to mineral fibers. The study population consisted of 82 males (51%) and 78 females (49%) with a mean of age of 44.8±14 years (range; 20-65 years). Lowest levels of β-carotene, ascorbic acid, and α-tocopherol were found in MPM patients (MPM vs control groups combined, p<0.0001 for each antioxidant vitamin), without any relation to age or sex. There was no significant difference between the antioxidant levels of healthy controls of Tuzkoy and Ankara. In conclusion; our findings suggested an increased risk of MPM being associated with low levels of α-tocopherol and ascorbic acid in patients with MPM.

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Asbestos: Scientific Developments and Implications for Public Policy

Cited by 691 publications

References 76 publications

Airway Epithelial NF-κB Activation Modulates Asbestos-Induced Inflammation and Mucin Production In Vivo

Airway Epithelial NF-κB Activation Modulates Asbestos-Induced Inflammation and Mucin Production In Vivo

Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.

Serum Levels of Alpha-Tocopherol, Vitamin C, Beta-Carotene, and Retinol in Malignant Pleural Mesothelioma

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