Associations between radiographic findings and spirometry in a community exposed to Libby amphibole

Larson, Theodore; Lewin, Michael; Gottschall, E. Brigitte; Antao, Vinicius C.; Kapil, Vikas; Rose, Cecile S.

doi:10.1136/oemed-2011-100316

Cited by 37 publications

(26 citation statements)

References 37 publications

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“…35 A study of urban residents living near a plant using LV also demonstrated an increased risk of pleural changes at lower estimated CFE. 38 Weill and colleagues 39 found that male never smoker Libby residents had a 4.3% and 23.8% loss in percent predicted FVC for LPT and DPT and/or costophrenic angle blunting, respectively. 38 Weill and colleagues 39 found that male never smoker Libby residents had a 4.3% and 23.8% loss in percent predicted FVC for LPT and DPT and/or costophrenic angle blunting, respectively.…”

Section: Discussionmentioning

confidence: 99%

HRCT/CT and Associated Spirometric Effects of Low Libby Amphibole Asbestos Exposure

Lockey

Dunning

Hilbert

et al. 2015

Journal of Occupational &Amp; Environmental Medicine

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Section: Discussionmentioning

confidence: 99%

HRCT/CT and Associated Spirometric Effects of Low Libby Amphibole Asbestos Exposure

Lockey

Dunning

Hilbert

et al. 2015

Journal of Occupational &Amp; Environmental Medicine

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“…We recently demonstrated that the LA-induced autoantibodies alone, in the absence of asbestos, could contribute to the fibrotic process in mice (Gilmer et al 2016). The public health significance of this result is further highlighted by evidence that the LA non-malignant pleural disease is more severe and progressive than what is classically described for general occupational (chrysotile) asbestos exposures, and that the radiographic lesions were clearly associated with pulmonary function decline (Black et al 2014, Larson et al 2012, Whitehouse 2004). …”

Section: Introductionmentioning

confidence: 77%

Mesothelial cell autoantibodies upregulate transcription factors associated with fibrosis

Gilmer

Harding

Woods

et al. 2017

Inhalation Toxicology

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Amphibole asbestos exposure is associated with production of mesothelial cell autoantibodies (MCAA). These MCAA have been linked with pleural fibrotic disease in the asbestos exposed community of Libby, Montana, and induce collagen deposition by cultured mesothelial cells. However, the exact intracellular mechanism by which these autoantibodies cause an increase in collagen deposition remains unknown. This study sought to gain insight into the transcription factors involved in the collagen production after human mesothelial cells are exposed to MCAA. In this study, transcription factor activation profiles were generated from human mesothelial cells (Met5A) treated with serum from Libby subjects, and were compared to cells treated with serum cleared of IgG, and therefore containing no MCAA. Analysis of those profiles indicated C/EBP-beta and hypoxia inducible factor 1 alpha (HIF-1α) are significantly increased in the nucleus, indicating activation, due to MCAA exposure compared to controls. Inhibition of either of these transcription factors significantly reduced collagen 1 deposition by these cells following exposure to MCAA. These data suggest autoantibodies are directly involved in type I collagen deposition and may elucidate potential therapeutic targets for autoantibody mediated fibrosis.

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“…Residents of Libby endured exposure to the vermiculite ore contaminated with amphibole asbestos resulting from past industrial production. While pleural disease has been reported most commonly, parenchymal abnormalities have also been reported [37]. …”

Section: Asbestosismentioning

confidence: 99%

Asbestosis and environmental causes of usual interstitial pneumonia

Gulati

Redlich²

2015

Current Opinion in Pulmonary Medicine

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Purpose of review Recent epidemiologic investigations suggest that occupational and environmental exposures contribute to the overall burden of idiopathic pulmonary fibrosis (IPF). This article explores the epidemiologic and clinical challenges to establishing exposure associations, the current literature regarding exposure disease relationships and the diagnostic work-up of IPF and asbestosis patients. Recent findings IPF patients demonstrate a histopathologic pattern of usual interstitial pneumonia. In the absence of a known cause or association, a usual interstitial pneumonia pattern leads to an IPF diagnosis, which is a progressive and often terminal fibrotic lung disease. It has long been recognized that asbestos exposure can cause pathologic and radiographic changes indistinguishable from IPF. Several epidemiologic studies, primarily case control in design, have found that a number of other exposures that can increase risk of developing IPF include cigarette smoke, wood dust, metal dust, sand/silica and agricultural exposures. Lung mineralogic analyses have provided additional support to causal associations. Genetic variation may explain differences in disease susceptibility among the population. Summary An accumulating body of literature suggests that occupational and environmental exposure can contribute to the development of IPF. The impact of exposure on the pathogenesis and clinical course of disease requires further study.

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Associations between radiographic findings and spirometry in a community exposed to Libby amphibole

Cited by 37 publications

References 37 publications

HRCT/CT and Associated Spirometric Effects of Low Libby Amphibole Asbestos Exposure

HRCT/CT and Associated Spirometric Effects of Low Libby Amphibole Asbestos Exposure

Mesothelial cell autoantibodies upregulate transcription factors associated with fibrosis

Asbestosis and environmental causes of usual interstitial pneumonia

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