Accelerated silicosis in sandblasters: Pathology, mineralogy, and clinical correlates.
accelerated silicosis
crystalline silica
lung pathology
microanalysis
mineralogy
occupational disease
sandblasting
scanning electron microscopy
Journal
American journal of industrial medicine
ISSN: 1097-0274
Titre abrégé: Am J Ind Med
Pays: United States
ID NLM: 8101110
Informations de publication
Date de publication:
24 Jan 2024
24 Jan 2024
Historique:
revised:
29
11
2023
received:
03
08
2023
accepted:
22
12
2023
medline:
24
1
2024
pubmed:
24
1
2024
entrez:
24
1
2024
Statut:
aheadofprint
Résumé
With increasing reports of accelerated and acute silicosis, PMF, and autoimmune disease among coal miners and silica-exposed countertop workers, we present previously incompletely-described pulmonary pathology of accelerated silicosis and correlations with mineralogy, radiography, and disease progression in 46 Texas oilfield pipe sandblasters who were biopsied between 1988 and 1995. Worker examinations included pulmonary function tests, chest X-ray (CXR), high-resolution computed tomography (HRCT), and Gallium-67 scans. Quantitative mineralogic analysis of pulmonary parenchymal burden of silica, silicates, and metal particles used scanning electron microscopy with energy dispersive x-ray spectroscopy (SEM EDS). Workers had clinical deterioration after <10 years exposure in dusty workplaces. Although initial CXR was normal in 54%, Gallium-67 scans were positive in 68% of those with normal CXR, indicating pulmonary inflammation. The histology of accelerated silicosis is diffuse interstitial infiltration of macrophages filled with weakly birefringent particles with or without silicotic nodules or alveolar proteinosis. Lung silica concentrations were among the highest in our database, showing a dose-response relationship with CXR, HRCT, and pathologic changes (macrophages, fibrosis, and silicotic nodules). Radiographic scores and diffusing capacity worsened during observation. Silica exposure was intensified, patients presented younger, with shorter exposure, more severe clinical abnormalities, higher lung particle burdens, and more rapid progression in a subset of patients exposed to recycled blasting sand. Accelerated silicosis may present with a normal CXR despite significant histopathology. Multivariable analyses showed silica, and not other particles, is the driver of observed radiologic, physiologic, and histologic outcomes. Eliminating this preventable disease requires higher physician, public health, and societal awareness.
Sections du résumé
BACKGROUND
BACKGROUND
With increasing reports of accelerated and acute silicosis, PMF, and autoimmune disease among coal miners and silica-exposed countertop workers, we present previously incompletely-described pulmonary pathology of accelerated silicosis and correlations with mineralogy, radiography, and disease progression in 46 Texas oilfield pipe sandblasters who were biopsied between 1988 and 1995.
METHODS
METHODS
Worker examinations included pulmonary function tests, chest X-ray (CXR), high-resolution computed tomography (HRCT), and Gallium-67 scans. Quantitative mineralogic analysis of pulmonary parenchymal burden of silica, silicates, and metal particles used scanning electron microscopy with energy dispersive x-ray spectroscopy (SEM EDS).
RESULTS
RESULTS
Workers had clinical deterioration after <10 years exposure in dusty workplaces. Although initial CXR was normal in 54%, Gallium-67 scans were positive in 68% of those with normal CXR, indicating pulmonary inflammation. The histology of accelerated silicosis is diffuse interstitial infiltration of macrophages filled with weakly birefringent particles with or without silicotic nodules or alveolar proteinosis. Lung silica concentrations were among the highest in our database, showing a dose-response relationship with CXR, HRCT, and pathologic changes (macrophages, fibrosis, and silicotic nodules). Radiographic scores and diffusing capacity worsened during observation. Silica exposure was intensified, patients presented younger, with shorter exposure, more severe clinical abnormalities, higher lung particle burdens, and more rapid progression in a subset of patients exposed to recycled blasting sand.
CONCLUSIONS
CONCLUSIONS
Accelerated silicosis may present with a normal CXR despite significant histopathology. Multivariable analyses showed silica, and not other particles, is the driver of observed radiologic, physiologic, and histologic outcomes. Eliminating this preventable disease requires higher physician, public health, and societal awareness.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, USA
Informations de copyright
© 2024 The Authors. American Journal of Industrial Medicine published by Wiley Periodicals LLC.
Références
Leung CC, Yu ITS, Chen W. Silicosis. Lancet. 2012;379(9830):2008-2018.
Rosner D, Markowitz G. Deadly Dust: Silicosis and the On-going Struggle to Protect Workers' Health. 2nd ed. University of Michigan Press; 2006.
Kambouchner M, Bernaudin JF. The pathologist's view of silicosis in 1930 and in 2015. The Johannesburg Conference legacy. Am J Ind Med. 2015;58(suppl 1):S48-S58.
Cohen RA, Petsonk EL, Rose C, et al. Lung pathology in U.S. coal workers with rapidly progressive pneumoconiosis implicates silica and silicates. Am J Respir Crit Care Med. 2016;193(6):673-680.
Hoy RF, Chambers DC. Silica-related diseases in the modern world. Allergy. 2020;75(11):2805-2817.
Leso V, Fontana L, Romano R, Gervetti P, Iavicoli I. Artificial stone associated silicosis: a systematic review. Int J Environ Res Public Health. 2019;16(4):568.
Fazio JC, Gandhi SA, Flattery J, et al. Silicosis Among Immigrant Engineered Stoneamong immigrant engineered stone (Quartz) Countertop Fabrication Workerscountertop fabrication workers in California. JAMA Intern Med. 2023;183(9):991-998.
Abraham JL, Wiesenfeld SL. Two cases of fatal PMF in an ongoing epidemic of accelerated silicosis in oilfield sandblasters: lung pathology and mineralogy. Ann Occup Hyg. 1997;41(suppl 1):440-447.
Buechner HA, Ansari A. Acute silico-proteinosis. Dis Chest. 1969;55(4):274-284.
Craighead JE, Kleinerman J, Abraham JL, et al. Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and silicate disease committee. Arch Pathol Lab Med. 1988;112(7):673-720.
Abraham JL. Analysis of fibrous and non-fibrous particles. In: Rom W, ed. Environmental and Occupational Medicine. 4 ed. Lippincott Willliams & Wilkins; 2007:277-297.
Abraham JL, Wiesenfeld SL. Pathology and microanalysis of the ongoing epidemic of subacute silicosis in West Texas oilfield sandblasters. Mod Pathol. 1995;8:146A.
Wiesenfeld SL, Abraham JL. Epidemic of accelerated silicosis in Texas sandblasters: clinical, pathologic and microanalytic observations. Am J Respir Crit Care Med. 1995;151:A710.
Fleming D, Maynard D, McKinney B, Perrotta DM, Schulze L, Pichette J. Current trends silicosis: cluster in sandblasters-Texas, and occupational surveillance for silicosis. MMWR Morb Mortal Wkly Rep. 1990;39(25):433-437.
Abraham JL, Crawford JA, Sanyal S, Burnett BR, Wiesenfeld SL. Relevance of accelerated silicosis in sandblasters to rapidly progressive pneumoconiosis. Am J Respir Crit Care Med. 2019;199:A1177.
Antao VCS, DeVuyst P. ILO classification. In: Gevenois PA and DeVuyst P, eds. Imaging of occupational and environmental disorders of the chest. Springer; 2006:93-99.
Liddell FDK. Assessment of radiological progression of simple pneumoconiosis in individual miners. Occup Environ Med. 1974;31(3):185-195.
Liddell FDK, Morgan WKC. Methods of assessing serial films of the pneumoconioses: a review. Occup Med. 1978;28(1):6-15.
Bergin C, Muller N, Vedal S, Chan-Yeung M. CT in silicosis: correlation with plain films and pulmonary function tests. Am J Roentgenol. 1986;146(3):477-483.
Siemsen JK, Sargent EN, Grebe SF, Winsor DW, Wentz D, Jacobson G. Pulmonary concentration of Ga67 in pneumoconiosis. Am J Roentgenol. 1974;120(4):815-820.
ATS. Single breath carbon monoxide diffusing capacity (transfer factor): recommendations for a standard technique. Am Rev Respir Dis. 1987;136(5):1299-1307.
Crapo RO, Morris AH. Standardized single breath normal values for carbon monoxide diffusing capacity. Am Rev Respir Dis. 1981;123(2):185-189.
Abraham JL, Burnett BR. Quantitative analysis of inorganic particulate burden in situ in tissue sections. Scanning Electron Microsc. 1983;2(Pt):681-696.
NIOSH. Request for Assistance in Preventing Silicosis and Deaths From Sandblasting. US Department of Health, Education and Welfare, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health; 1992.
Abraham JL, Burnett BR, Hunt A. Quantification of non-fibrous and fibrous particulates in human lungs: twenty-year update on pneumoconiosis database. Ann Occup Hyg. 2002;46(suppl 1):397-401.
Abraham JL. Analysis of fibrous and nonfibrous particles. In: Rom W, ed. Environmental and Occupational Medicine. Lippincott, Williams & Wilkins; 2007:286.
Cohen RA, Rose CS, Go LHT, et al. Pathology and mineralogy demonstrate respirable crystalline silica is a major cause of severe pneumoconiosis in U.S. coal miners. Ann Am Thorac Soc. 2022;19(9):1469-1478.
NIOSH. Health effects of occupational exposure to respirable crystalline silica. U.S. Department of Health and Human Services CfDCaP, National Institute for Occupational Safety and Health. NIOSH Publications Dissemination; 2002:23.
Rees D, Murray J. Silica. In: Taylor AN, Cullinan R, Blanc PD, Pickering A, eds. Parkes' Occupational Lung Disorders. 4th ed. CRC Press; 2017:188.
Akgun M, Araz O, Ucar EY, et al. Silicosis appears inevitable among former denim sandblasters. Chest. 2015;148(3):647-654.
Quan H, Wu W, Yang G, et al. Risk factors of silicosis progression: a retrospective cohort study in China. Front Med. 2022;9:832052.
Craighead JE. Cryptic pulmonary lesions in workers occupationally exposed to dust containing silica. J Am Med Assoc. 1980;244(17):1939-1941.
Ehrlich R, Murray J, Rees D. Subradiological silicosis. Am J Ind Med. 2018;61(11):877-885.
Newbigin K, Parsons R, Deller D, Edwards R, McBean R. Stonemasons with silicosis: preliminary findings and a warning message from Australia. Respirology. 2019;24(12):1220-1221.
Sun J, Weng D, Jin C, et al. The value of high resolution computed tomography in the diagnostics of small opacities and complications of silicosis in mine machinery manufacturing workers, compared to radiography. J Occup Health. 2008;50(5):400-405.
Martinez Gonzalez C, Prieto Gonzalez A, Garcia Alfonso L, et al. Silicosis in artificial quartz conglomerate workers. Arch Bronconeumol. 2019;55(9):459-464.
Parks CG, Conrad K, Cooper GS. Occupational exposure to crystalline silica and autoimmune disease. Environ Health Perspect. 1999;107(suppl 5):793-802.
Pollard KM. Silica, silicosis, and autoimmunity. Front Immunol. 2016;7:97.
Honma K, Abraham JL, Chiyotani K, et al. Proposed criteria for mixed-dust pneumoconiosis: definition, descriptions, and guidelines for pathologic diagnosis and clinical correlation. Hum Pathol. 2004;35(12):1515-1523.
Seaton A, Legge JS, Henderson J, Kerr KM. Accelerated silicosis in scottish stonemasons. Lancet. 1991;337(8737):341-344.
Kefeli M, Akpolat I, Zeren H, et al. Clinical, histopathological and mineralogical analysis findings of an unusual case of pneumoconiosis. Turk J Pathol. 2012;28(2):184-188.
Nugent KM, Dodson RF, Idell S, Devillier JR. The utility of bronchoalveolar lavage and transbronchial lung biopsy combined with energy-dispersive X-ray analysis in the diagnosis of silicosis. Am Rev Respir Dis. 1989;140(5):1438-1441.
Hutyrová B, Smolková P, Nakládalová M, Tichý T, Kolek V. Case of accelerated silicosis in a sandblaster. Ind Health. 2015;53(2):178-183.
Sahbaz S, Inönü H, Ocal S, et al. Denim sandblasting and silicosis two new subsequent cases in Turkey. Tuberk Toraks. 2007;55(1):87-91.
Mohebbi I, Aslan-Abadi N, Booshehri B, Zubeyri T, Ghavam F. Rapidly progressive silicosis. Tanaffos. 2007;6(2):73-76.
Nakládalová M, Štěpánek L, Kolek V, Žurková M, Tichý T. A case of accelerated silicosis. Occup Med. 2018;68(7):482-484.
Cox-Ganser JM, Burchfiel CM, Fekedulegn D, Andrew ME, Ducatman BS. Silicosis in lymph nodes: the canary in the miner? J Occup Environ Med. 2009;51(2):164-169.
Murray J, Webster I, Reid G, Kielkowski D. The relation between fibrosis of hilar lymph glands and the development of parenchymal silicosis. Occup Environ Med. 1991;48(4):267-269.
Gardner LU. Pathology of so-called acute silicosis. Am J Public Health Nations Health. 1933;23(12):1240-1249.
Gibbs AR, Wagner JC. Diseases due to silica. In: Churg A, Green FH, eds. Pathology of Occupational Lung Disease. 2nd ed. Williams & Wilkins; 1998:214.
Green FH, Vallyathan V. Pathologic responses to inhaled silica. In: Castranova V, Vallyathan V, Wallace WE, eds. Silica and Silica-Induced Lung Disease. CRC Press; 1996:43.
Hoy RF, Jeebhay MF, Cavalin C, et al. Current global perspectives on silicosis-convergence of old and newly emergent hazards. Respirology. 2022;27(6):387-398.
Levin K, McLean C, Hoy R. Artificial stone-associated silicosis: clinical-pathological-radiological correlates of disease. Respirol Case Rep. 2019;7(7):e00470.
Abraham JL, Crawford JA, Scalzetti E, Kramer LG. Analysis of lung particle burden in a 28 year old man with rapidly progressive coal worker's pneumoconiosis [abstract]. Am J Respir Crit Care Med. 2016;193:A7074.
Nagelschmidt G. The relation between lung dust and lung pathology in pneumoconiosis. Occup Environ Med. 1960;17:247-259.
Dufresne A, Loosereewanich P, Bégin R, et al. Tentative explanatory variable of lung dust concentration in gold miners exposed to crystalline silica. J Exposure Anal Environ Epidemiol. 1998;8(3):375-398.
Samimi B, Ziskind M, Weill H. The relation of silica dust to accelerated silicosis. Ecotoxicol Environ Safety. 1978;1(4):429-436.
Castranova V, Pailes WH, Dalai NS, et al. Enhanced pulmonary response to the inhalation of freshly fractured silica as compared with aged dust exposure. Appl Occup Environ Hyg. 1996;11(7):937-941.
Merewether ERA. The risk of silicosis in sand-blasters. Tubercle. 1936;17(9):385-391.
Barnes H, Goh NSL, Leong TL, Hoy R. Silica-associated lung disease: an old-world exposure in modern industries. Respirology. 2019;24(12):1165-1175.
Akgün M. Denim production and silicosis. Curr Opin Pulm Med. 2016;22(2):165-169.
Bakan ND, Özkan G, Çamsari G, et al. Silicosis in denim sandblasters. Chest. 2011;140(5):1300-1304.
Tse LA, Li ZM, Wong TW, Fu ZM, Yu ITS. High prevalence of accelerated silicosis among gold miners in Jiangxi, China. Am J Ind Med. 2007;50(12):876-880.
Jiang CQ, Xiao LW, Lam TH, Xie NW, Zhu CQ. Accelerated silicosis in workers exposed to agate dust in Guangzhou, China. Am J Ind Med. 2001;40(1):87-91.