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Understanding the pathogenesis of occupational coal and silica dust-associated lung disease

Kanth Swaroop Vanka, Shakti Shukla, Henry M. Gomez, Carole James, Thava Palanisami, Kenneth Williams, Daniel C. Chambers, Warwick J. Britton, Dusan Ilic, Philip Michael Hansbro, Jay Christopher Horvat
European Respiratory Review 2022 31: 210250; DOI: 10.1183/16000617.0250-2021
Kanth Swaroop Vanka
1School of Biomedical Sciences and Pharmacy, The University of Newcastle/Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
2Division of Pulmonary, Allergy, and Critical Care Medicine, Dept of Medicine, University of Pennsylvania, Philadelphia, PA, USA
3Lung Biology Institute, University of Pennsylvania, Philadelphia, PA, USA
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  • ORCID record for Kanth Swaroop Vanka
Shakti Shukla
4Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Sydney, NSW, Australia
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Henry M. Gomez
1School of Biomedical Sciences and Pharmacy, The University of Newcastle/Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
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Carole James
5School of Health Sciences, The University of Newcastle, Newcastle, NSW, Australia
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Thava Palanisami
6Global Innovative Centre for Advanced Nanomaterials, College of Engineering, Science and Environment (CERSE), The University of Newcastle, Newcastle, NSW, Australia
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Kenneth Williams
7Newcastle Institute for Energy and Resources (NIER), School of Engineering, The University of Newcastle, Newcastle, NSW, Australia
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Daniel C. Chambers
8School of Clinical Medicine, The University of Queensland, Brisbane, QLD, Australia
9Queensland Lung Transplant Program, The Prince Charles Hospital, Brisbane, QLD, Australia
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Warwick J. Britton
10Centenary Institute, The University of Sydney, Sydney, NSW, Australia
11Dept of Clinical Immunology, Royal Prince Alfred Hospital, Sydney, NSW, Australia
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Dusan Ilic
7Newcastle Institute for Energy and Resources (NIER), School of Engineering, The University of Newcastle, Newcastle, NSW, Australia
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Philip Michael Hansbro
1School of Biomedical Sciences and Pharmacy, The University of Newcastle/Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
12Centre for Inflammation, Centenary Institute, Sydney, NSW, Australia
13School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia
14P.M. Hansbro and J.C. Horvat have equally contributed as senior authors
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Jay Christopher Horvat
1School of Biomedical Sciences and Pharmacy, The University of Newcastle/Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
14P.M. Hansbro and J.C. Horvat have equally contributed as senior authors
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  • For correspondence: jay.horvat@newcastle.edu
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  • FIGURE 1
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    FIGURE 1

    Pathogenesis of dust particulate matter (PM)-associated occupational lung diseases. Schematic shows the entry of particulate matter (PM10 and below) through environmental/occupational exposure into lungs and development of subsequent respiratory complications, which include increased cellular influx (macrophages, neutrophils, T-lymphocytes and B-cells), alveolar destruction (emphysema) and structural changes (collagen and mucus deposition) leading to chronic bronchitis. PMx: particles with a 50% cut-off aerodynamic diameter of x µm; CWP: coal worker's pneumoconiosis.

  • FIGURE 2
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    FIGURE 2

    Mechanisms of dust particulate matter (PM) toxicity. Schematic representation depicting ambient airborne PM with various cellular mechanisms and triggering cascade reactions, i.e. cellular inflammation, reactive oxygen species (ROS) and reactive nitrogen species (RNS) production, cytokine production and DNA damage, leading to cell death and scar tissue formation. Created with BioRender.com. IL: interleukin; NF-κB: nuclear factor-κB; TNF: tumour necrosis factor.

  • FIGURE 3
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    FIGURE 3

    Pathogenesis of reactive crystalline silica (RCS). The illustration depicts the interaction of RCS with lung epithelial cells and subsequent activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway and production of pro-inflammatory cytokine interleukin (IL)-1β, free radicals and fibroblast-activating factor leading to fibrosis. Created with BioRender.com. ROS: reactive oxygen species; RNS: reactive nitrogen species; ASC: apoptosis-associated speck-like protein containing a caspase activation and recruitment domain; TNF: tumour necrosis factor; NF-κB: nuclear factor-κB.

  • FIGURE 4
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    FIGURE 4

    Occupational exposure limits (OELs) of a) silica (quartz) and b) coal dust particulate matter (PM). The graphs show that the OEL or safe dust exposure limits of respirable and inhalable fractions of silica and coal dust PM vary significantly among different coal-producing countries. These limits are set primarily on particle size. TWA: time-weighted average; ACGIH: American Conference of Governmental Industrial Hygienists; NIOSH REL: National Institute for Occupational Safety and Health recommended exposure limit; OSHA PEL: Occupational Safety and Health Administration permissible exposure limit; TLV: threshold limit value; MSHA: Mine Safety and Health Administration.

Tables

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  • TABLE 1

    Safety standards of particulate matter (PM) in ambient air in different geographical areas

    AgencyPM10PM2.5Reference
    World Health Organization (2018)20 μg·m−3 (annual)
    50 μg·m−3 (24-h)
    10 μg·m−3 (annual)
    25 μg·m−3 (24-h)
    [2]
    US Environmental Protection Agency50 μg·m−3 (annual)
    150 μg·m−3 (24-h)
    12 μg·m−3 (annual)
    35 μg·m−3 (24-h)
    [28]
    New South Wales Environment Protection Authority (Australia)25 μg·m−3 (annual)
    50 μg·m−3 (24-h)
    8 μg·m−3 (annual)
    25 μg·m−3 (24-h)
    [29]
    UK and EUUK/EU: 40 μg·m−3 (annual)
    50 μg·m−3 (24-h)#
    UK: 25 μg·m−3 (annual)[30]
    Scotland: 18 μg·m−3 (annual)
    50 μg·m−3 (24-h)¶
    Scotland: 10 μg·m−3 (annual)

    PMx: particles with a 50% cut-off aerodynamic diameter of x µm. #: not to be exceeded more than 35 times a year in the UK; ¶: not to be exceeded more than seven times a year in Scotland.

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    Understanding the pathogenesis of occupational coal and silica dust-associated lung disease
    Kanth Swaroop Vanka, Shakti Shukla, Henry M. Gomez, Carole James, Thava Palanisami, Kenneth Williams, Daniel C. Chambers, Warwick J. Britton, Dusan Ilic, Philip Michael Hansbro, Jay Christopher Horvat
    European Respiratory Review Sep 2022, 31 (165) 210250; DOI: 10.1183/16000617.0250-2021

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    Understanding the pathogenesis of occupational coal and silica dust-associated lung disease
    Kanth Swaroop Vanka, Shakti Shukla, Henry M. Gomez, Carole James, Thava Palanisami, Kenneth Williams, Daniel C. Chambers, Warwick J. Britton, Dusan Ilic, Philip Michael Hansbro, Jay Christopher Horvat
    European Respiratory Review Sep 2022, 31 (165) 210250; DOI: 10.1183/16000617.0250-2021
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