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

Lockey, James E.; Dunning, Kari; Hilbert, Timothy; Borton, Eric; Levin, Linda; Rice, Carol; McKay, Roy T.; Shipley, Ralph; Meyer, Cristopher A.; Perme, Charles; LeMasters, Grace K.

doi:10.1097/jom.0000000000000373

Cited by 29 publications

(26 citation statements)

References 27 publications

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“…Rohs et al (2008) found that pleural plaques (detected by CXR) were strongly dependent upon cumulative exposure for LAA, which is more in accord with expectation. More recently Lockey et al (2015) used HRCT/CT in a similar analysis of LAA and found that pleural changes (including both localized and diffuse pleural thickening) increased with cumulative exposure and employment duration.…”

Section: Dose-or Exposure-response and Pleural Plaquesmentioning

confidence: 99%

“…These investigators concluded that the weight of evidence indicated that pleural plaques do not have clinically significant impacts on lung function and that the observed association is most likely due to unidentified pleural thickening or other factors. Lockey et al (2015) recently reported results of a careful study of workers employed at a plant that expanded Libby Vermiculite contaminated with LAA in Marysville, Ohio. They identified pleural plaques in the cohort using HRCT/CT and also measured FVC and FEV 1 values.…”

Section: Pleural Plaques and Impairments To Lung Functionmentioning

confidence: 99%

“…The relation between plaques and possible impairment of lung function has been studied extensively (Clark et al, 2014;Jones et al, 1988;Kerper et al, 2014;Kopylev et al, 2014;Lockey et al, 2015;Moolgavkar et al, 2014;Ohlson et al, 1985;Sood & Gee, 1997;Weill et al, 2011;Wilken et al, 2011, Zu et al, 2015 andcontained references). Among the three most recent reviews: Moolgavkar et al (2014) reviewed various studies on the relation between pleural plaques and lung function considered by EPA in their analysis of LAA and concluded:…”

Section: Pleural Plaques and Impairments To Lung Functionmentioning

confidence: 99%

“…Numerous studies have examined the dose-or exposureresponse relation for pleural plaques (Bar-Shai et al, 2012;Boffetta, 1998;Clin et al, 2011;Eisenhawer et al, 2014;Ehrlich et al, 1992;Finkelstein & Vingilis, 1984;Hosoda et al, 2008;Jakobsson et al, 1995;Järvholm, 1992;Karjalainen et al, 1994;Lockey et al, 2015;Mastrangelo et al, 2009;McDonald et al, 1986;Moolgavkar et al, 2014;Paris et al, 2008Paris et al, , 2009Rohs et al, 2008;Sandén & Järvholm, 1986;Shepherd et al, 1997;Soulat et al, 1999;Van Cleemput et al, 2001). Results differ among these studies, 6 but exposure variables found relevant in one or more studies include time since first exposure (TSFE), age at first exposure (Jones, 1997), type (Hillerdal, 1997;Jones, 1997;Sandén & Järvholm, 1986) and dimensions of fiber (Hillerdal, 1997;Jones, 1997), lung fiber burden (Karjalainen et al, 1994;Roberts, 1971), duration of exposure, intensity of estimated asbestos exposure and cumulative exposure (measured in various ways).…”

Section: Dose-or Exposure-response and Pleural Plaquesmentioning

confidence: 99%

See 3 more Smart Citations

Are pleural plaques an appropriate endpoint for risk analyses?

Maxim¹,

Niebo²,

Utell

2015

Inhalation Toxicology

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This review summarizes the literature on the relation between the development of pleural plaques and non-malignant and malignant disease in cohorts exposed to asbestos and other fibers. The available evidence indicates that, absent any other pleural disease, the presence of pleural plaques does not result in respiratory symptoms or clinically significant impacts on lung function. For certain types of asbestos, the development of pleural plaques is statistically correlated with malignant disease, but the evidence is consistent with the hypothesis that pleural plaques without other pleural disease are a marker of exposure, rather than an independent risk factor. Pleural plaques have also developed in cohorts exposed to other fibers that have not proven to be carcinogenic. Risk analyses should be based on the avoidance of known adverse conditions, rather than pleural plaques per se.

show abstract

Section: Dose-or Exposure-response and Pleural Plaquesmentioning

confidence: 99%

Section: Pleural Plaques and Impairments To Lung Functionmentioning

confidence: 99%

Section: Pleural Plaques and Impairments To Lung Functionmentioning

confidence: 99%

Section: Dose-or Exposure-response and Pleural Plaquesmentioning

confidence: 99%

See 2 more Smart Citations

Are pleural plaques an appropriate endpoint for risk analyses?

Maxim¹,

Niebo²,

Utell

2015

Inhalation Toxicology

View full text Add to dashboard Cite

show abstract

“…; Lockey et al. ). In the amphibole‐exposed population of Libby MT, where exposures occurred due to the mining of asbestos‐contaminated vermiculite, pleural fibrosis is the predominant cause of morbidity and mortality (Peipins et al.…”

Section: Introductionmentioning

confidence: 97%

Libby amphibole‐induced mesothelial cell autoantibodies bind to surface plasminogen and alter collagen matrix remodeling

Hanson

Evilia

Gilmer

et al. 2016

Physiological Reports

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Lamellar pleural thickening (LPT) is a fibrotic disease induced by exposure to Libby amphibole (LA) asbestos that causes widespread scarring around the lung, resulting in deterioration of pulmonary function. Investigating the effects of autoantibodies to mesothelial cells (MCAA) present in the study populations has been a major part of the effort to understand the mechanism of pathogenesis. It has been shown in vitro that human mesothelial cells (Met5a) exposed to MCAA increase collagen deposition into the extracellular matrix (ECM). In this study, we sought to further elucidate how MCAA drive increased collagen deposition by identifying the protein targets bound by MCAA on the cellular surface using biotinylation to label and isolate surface proteins. Isolated surface protein fractions were identified as containing MCAA targets using ELISA. The fractions that demonstrated binding by MCAA were then analyzed by tandem mass spectrometry (MS/MS) and MASCOT analysis. The most promising result from the MASCOT analysis, plasminogen (PLG), was tested for MCAA binding using purified human PLG in an ELISA. We report that serum containing MCAA bound at an optical density (OD) 3 times greater than that of controls, and LA‐exposed subjects had a high frequency of positive tests for anti‐PLG autoantibodies. This work implicates the involvement of the plasminogen/plasmin system in the mechanism of excess collagen deposition in Met5a cells exposed to MCAA. Elucidating this mechanism could contribute to the understanding of LPT.

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Reduced lung function in smokers in a lung cancer screening cohort with asbestos exposure and pleural plaques

Lopatin

Tsay

Addrizzo-Harris

et al. 2016

American J Industrial Med

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

Abstract: Exposure to vermiculite containing amphibole fibers is associated with pleural and parenchymal HRCT/CT changes at low cumulative fiber exposure; these changes are associated with spirometric decrements.

Cited by 29 publications

References 27 publications

Are pleural plaques an appropriate endpoint for risk analyses?

Are pleural plaques an appropriate endpoint for risk analyses?

Libby amphibole‐induced mesothelial cell autoantibodies bind to surface plasminogen and alter collagen matrix remodeling

Reduced lung function in smokers in a lung cancer screening cohort with asbestos exposure and pleural plaques

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