Semin Respir Crit Care Med 2023; 44(03): 327-339
DOI: 10.1055/s-0043-1764406
Review Article

Pathology and Mineralogy of the Pneumoconioses

Jeremy T. Hua
1   Division of Environmental and Occupational Health Sciences, National Jewish Health, Denver, Colorado
2   Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Aurora, Colorado
,
Carlyne D. Cool
3   Division of Pathology, National Jewish Health, Denver, Colorado
4   Department of Pathology, University of Colorado, Aurora, Colorado
,
Francis H. Y. Green
5   Department of Pathology and Laboratory Medicine, Calgary, Alberta, Canada
› Author Affiliations
Funding J.T.H. was supported by the Reuben M. Cherniack research fellowship at National Jewish Health and a National Institutes of Health fellowship training program grant (grant no.: NIH/NHLBI 2T32HL007085–46).

Abstract

Pneumoconioses represent the spectrum of lung diseases caused by inhalation of respirable particulate matter small enough (typically <5-µm diameter) to reach the terminal airways and alveoli. Pneumoconioses primarily occur in occupational settings where workers perform demanding and skilled manual labor including mining, construction, stone fabrication, farming, plumbing, electronics manufacturing, shipyards, and more. Most pneumoconioses develop after decades of exposure, though shorter latencies can occur from more intense particulate matter exposures. In this review, we summarize the industrial exposures, pathologic findings, and mineralogic features of various well-characterized pneumoconioses including silicosis, silicatosis, mixed-dust pneumoconiosis, coal workers' pneumoconiosis, asbestosis, chronic beryllium disease, aluminosis, hard metal pneumoconiosis, and some less severe pneumoconioses. We also review a general framework for the diagnostic work-up of pneumoconioses for pulmonologists including obtaining a detailed occupational and environmental exposure history. Many pneumoconioses are irreversible and develop due to excessive cumulative respirable dust inhalation. Accurate diagnosis permits interventions to minimize ongoing fibrogenic dust exposure. A consistent occupational exposure history coupled with typical chest imaging findings is usually sufficient to make a clinical diagnosis without the need for tissue sampling. Lung biopsy may be required when exposure history, imaging, and testing are inconsistent, there are unusual or new exposures, or there is a need to obtain tissue for another indication such as suspected malignancy. Close collaboration and information-sharing with the pathologist prior to biopsy is of great importance for diagnosis, as many occupational lung diseases are missed due to insufficient communication. The pathologist has a broad range of analytic techniques including bright-field microscopy, polarized light microscopy, and special histologic stains that may confirm the diagnosis. Advanced techniques for particle characterization such as scanning electron microscopy/energy dispersive spectroscopy may be available in some centers.



Publication History

Article published online:
27 March 2023

© 2023. Thieme. All rights reserved.

Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA

 
  • References

  • 1 Shi P, Xing X, Xi S. et al. Trends in global, regional and national incidence of pneumoconiosis caused by different aetiologies: an analysis from the Global Burden of Disease Study 2017. Occup Environ Med 2020; 77 (06) 407-414
  • 2 Lax MB, Grant WD, Manetti FA, Klein R. Recognizing occupational disease–taking an effective occupational history. Am Fam Physician 1998; 58 (04) 935-944
  • 3 Levy BS, Wegman DH. The occupational history in medical practice. What questions to ask and when to ask them. Postgrad Med 1986; 79 (08) 301-311
  • 4 International Labour Office. Guidelines for the Use of the ILO International Classification of Radiographs of Pneumoconiosis, Revised edition 2011. 2011 . Accessed September 9, 2022 at: https://www.ilo.org/wcmsp5/groups/public/—ed_protect/—protrav/—safework/documents/publication/wcms_168260.pdf
  • 5 Tamura T, Suganuma N, Hering KG. et al. Relationships (I) of International Classification of High-resolution Computed Tomography for Occupational and Environmental Respiratory Diseases with the ILO International Classification of Radiographs of Pneumoconioses for parenchymal abnormalities. Ind Health 2015; 53 (03) 260-270
  • 6 Newman LS. Significance of the blood beryllium lymphocyte proliferation test. Environ Health Perspect 1996; 104 (suppl 5, suppl 5): 953-956
  • 7 US Department of Labor. Black lung program. Accessed September 9, 2022 at: https://www.dol.gov/agencies/owcp/dcmwc
  • 8 US Department of Labor. Energy workers program. Accessed September 9, 2022 at: https://www.dol.gov/agencies/owcp/energy
  • 9 Leung CC, Yu IT, Chen W. Silicosis. Lancet 2012; 379 (9830): 2008-2018
  • 10 Stettler L, Platek S, Groth D, Green F, Vallyathan V. Particle contents of human lungs. In: Basu S, Millette J. eds. Electron Microscopy in Forensic, Occupational, and Environmental Health Sciences. SpringerLink; 1986: 217-226
  • 11 Mastin JP, Stettler LE, Shelburne JD. Quantitative analysis of particulate burden in lung tissue. Scanning Microsc 1988; 2 (03) 1613-1629
  • 12 Krefft S, Wolff J, Rose C. Silicosis: an update and guide for clinicians. Clin Chest Med 2020; 41 (04) 709-722
  • 13 Pavan C, Polimeni M, Tomatis M. et al. Editor's highlight: abrasion of artificial stones as a new cause of an ancient disease. Physicochemical features and cellular responses. Toxicol Sci 2016; 153 (01) 4-17
  • 14 Hua J, Zell-Baran L, Go L. et al. Demographic, exposure and clinical characteristics in a multinational registry of engineered stone workers with silicosis. Occup Environ Med 2022; 79: 586-593
  • 15 Hoy RF, Chambers DC. Silica-related diseases in the modern world. Allergy 2020; 75 (11) 2805-2817
  • 16 Craighead J, Kleinerman J, Abraham J. et al; Silicosis and Silicate Disease Committee. Diseases associated with exposure to silica and nonfibrous silicate minerals. Arch Pathol Lab Med 1988; 112 (07) 673-720
  • 17 McDonald JW, Roggli VL. Detection of silica particles in lung tissue by polarizing light microscopy. Arch Pathol Lab Med 1995; 119 (03) 242-246
  • 18 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
  • 19 Churg A, Wright JL, Wiggs B, Paré PD, Lazar N. Small airways disease and mineral dust exposure. Prevalence, structure, and function. Am Rev Respir Dis 1985; 131 (01) 139-143
  • 20 Schenker MB, Pinkerton KE, Mitchell D, Vallyathan V, Elvine-Kreis B, Green FH. Pneumoconiosis from agricultural dust exposure among young California farmworkers. Environ Health Perspect 2009; 117 (06) 988-994
  • 21 Vallyathan V, Brower PS, Green FH, Attfield MD. Radiographic and pathologic correlation of coal workers' pneumoconiosis. Am J Respir Crit Care Med 1996; 154 (3 Pt 1): 741-748
  • 22 Petsonk EL, Rose C, Cohen R. Coal mine dust lung disease. New lessons from old exposure. Am J Respir Crit Care Med 2013; 187 (11) 1178-1185
  • 23 Kuempel ED, Wheeler MW, Smith RJ, Vallyathan V, Green FH. Contributions of dust exposure and cigarette smoking to emphysema severity in coal miners in the United States. Am J Respir Crit Care Med 2009; 180 (03) 257-264
  • 24 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 (09) 1469-1478
  • 25 Sarver E, Keles C, Rezaee M. Characteristics of respirable dust in eight appalachian coal mines: a dataset including particle size and mineralogy distributions, and metal and trace element mass concentrations. Data Brief 2019; 25: 104032
  • 26 International Agency for Research on Cancer. Asbestos (chrysotile, amosite, crocidolite, tremolite, actinolite, and anthopyhllite). 2018 . IARC Monograph. Accessed September 1, 2022 at: https://monographs.iarc.who.int/wp-content/uploads/2018/06/mono100C-11.pdf
  • 27 Craighead JE, Abraham JL, Churg A. et al. The pathology of asbestos-associated diseases of the lungs and pleural cavities: diagnostic criteria and proposed grading schema. Report of the Pneumoconiosis Committee of the College of American Pathologists and the National Institute for Occupational Safety and Health. Arch Pathol Lab Med 1982; 106 (11) 544-596
  • 28 Hodgson JT, Darnton A. The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg 2000; 44 (08) 565-601
  • 29 Green FH, Harley R, Vallyathan V. et al. Exposure and mineralogical correlates of pulmonary fibrosis in chrysotile asbestos workers. Occup Environ Med 1997; 54 (08) 549-559
  • 30 Roggli VL, Oury TD, Sporn TA. Pathology of Asbestos-Associated Diseases. 2nd ed.. Springer; 2004
  • 31 Roggli VL, Pratt PC, Brody AR. Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases. Br J Ind Med 1986; 43 (01) 18-28
  • 32 Fontenot AP, Maier LA. Genetic susceptibility and immune-mediated destruction in beryllium-induced disease. Trends Immunol 2005; 26 (10) 543-549
  • 33 Newman LS, Kreiss K, King Jr TE, Seay S, Campbell PA. Pathologic and immunologic alterations in early stages of beryllium disease. Re-examination of disease definition and natural history. Am Rev Respir Dis 1989; 139 (06) 1479-1486
  • 34 Mayer A, Hamzeh N. Beryllium and other metal-induced lung disease. Curr Opin Pulm Med 2015; 21 (02) 178-184
  • 35 Oliver LC, Zarnke AM. Sarcoidosis: an occupational disease?. Chest 2021; 160 (04) 1360-1367
  • 36 Müller-Quernheim J, Gaede KI, Fireman E, Zissel G. Diagnoses of chronic beryllium disease within cohorts of sarcoidosis patients. Eur Respir J 2006; 27 (06) 1190-1195
  • 37 Kartaloglu Z, Ilvan A, Aydilek R. et al. Dental technician's pneumoconiosis: mineralogical analysis of two cases. Yonsei Med J 2003; 44 (01) 169-173
  • 38 Taiwo OA. Diffuse parenchymal diseases associated with aluminum use and primary aluminum production. J Occup Environ Med 2014; 56 (5, suppl): S71-S72
  • 39 Hull MJ, Abraham JL. Aluminum welding fume-induced pneumoconiosis. Hum Pathol 2002; 33 (08) 819-825
  • 40 Vallyathan V, Bergeron WN, Robichaux PA, Craighead JE. Pulmonary fibrosis in an aluminum arc welder. Chest 1982; 81 (03) 372-374
  • 41 Carney J, McAdams P, McCluskey J, Roggli VL. Aluminum-induced pneumoconiosis confirmed by analytical scanning electron microscopy: a case report and review of the literature. Ultrastruct Pathol 2016; 40 (03) 155-158
  • 42 Mizutani RF, Terra-Filho M, Lima E. et al. Hard metal lung disease: a case series. J Bras Pneumol 2016; 42 (06) 447-452
  • 43 Naqvi AH, Hunt A, Burnett BR, Abraham JL. Pathologic spectrum and lung dust burden in giant cell interstitial pneumonia (hard metal disease/cobalt pneumonitis): review of 100 cases. Arch Environ Occup Health 2008; 63 (02) 51-70
  • 44 Moriyama H, Kobayashi M, Takada T. et al. Two-dimensional analysis of elements and mononuclear cells in hard metal lung disease. Am J Respir Crit Care Med 2007; 176 (01) 70-77
  • 45 Doig AT. Baritosis: a benign pneumoconiosis. Thorax 1976; 31 (01) 30-39
  • 46 Chong S, Lee KS, Chung MJ, Han J, Kwon OJ, Kim TS. Pneumoconiosis: comparison of imaging and pathologic findings. Radiographics 2006; 26 (01) 59-77
  • 47 Li JJ, Muralikrishnan S, Ng CT, Yung LY, Bay BH. Nanoparticle-induced pulmonary toxicity. Exp Biol Med (Maywood) 2010; 235 (09) 1025-1033