- •Preface to the First Edition
- •Preface to the Second Edition
- •Contents
- •Diagnostic Challenges
- •Expert Centers
- •Patient Organizations
- •Clinical Trials
- •Research in Orphan Lung Diseases
- •Orphan Drugs
- •Orphanet
- •Empowerment of Patients
- •Conclusions
- •References
- •Introduction
- •Challenges to Overcome in Order to Undertake Quality Clinical Research
- •Lack of Reliable Data on Prevalence
- •Small Number of Patients
- •Identifying Causation/Disease Pathogenesis
- •Disease Complexity
- •Lack of Access to a Correct Diagnosis
- •Delay in Diagnosis
- •Challenges But Not Negativity
- •Some Success Stories
- •The Means to Overcome the Challenges of Clinical Research: Get Bigger Numbers of Well-Characterized Patients
- •The Importance of Patient Organizations
- •National and International Networks
- •End Points for Trials: Getting Them Right When Numbers Are Small and Change Is Modest
- •Orphan Drug Development
- •Importance of Referral Centers
- •Looking at the Future
- •The Arguments for Progress
- •Concluding Remarks
- •References
- •3: Chronic Bronchiolitis in Adults
- •Introduction
- •Cellular Bronchiolitis
- •Follicular Bronchiolitis
- •Respiratory Bronchiolitis
- •Airway-Centered Interstitial Fibrosis
- •Proliferative Bronchiolitis
- •Diagnosis
- •Chest Imaging Studies
- •Pulmonary Function Testing
- •Lung Biopsy
- •Mineral Dusts
- •Organic Dusts
- •Volatile Flavoring Agents
- •Infectious Causes of Bronchiolitis
- •Idiopathic Forms of Bronchiolitis
- •Connective Tissue Diseases
- •Organ Transplantation
- •Hematopoietic Stem Cell Transplantation
- •Drug-Induced Bronchiolitis
- •Treatment
- •Constrictive Bronchiolitis
- •Follicular Bronchiolitis
- •Airway-Centered Interstitial Fibrosis
- •Proliferative Bronchiolitis
- •References
- •Background and Epidemiology
- •Pathophysiology
- •Host Characteristics
- •Clinical Manifestations
- •Symptoms
- •Laboratory Evaluation
- •Skin Testing
- •Serum Precipitins
- •Eosinophil Count
- •Total Serum Immunoglobulin E Levels
- •Recombinant Antigens
- •Radiographic Imaging
- •Pulmonary Function Testing
- •Histology
- •Diagnostic Criteria
- •Historical Diagnostic Criteria
- •Rosenberg and Patterson Diagnostic Criteria
- •ISHAM Diagnostic Criteria
- •Cystic Fibrosis Foundation Diagnostic Criteria
- •General Diagnostic Recommendations
- •Allergic Aspergillus Sinusitis (AAS)
- •Natural History
- •Treatment
- •Corticosteroids
- •Antifungal Therapy
- •Monoclonal Antibodies
- •Monitoring for Treatment Response
- •Conclusions
- •References
- •5: Orphan Tracheopathies
- •Introduction
- •Anatomical Considerations
- •Clinical Presentation
- •Etiological Considerations
- •Idiopathic Subglottic Stenosis
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Introduction and Clinical Presentation
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Tracheomalacia
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Tracheobronchomegaly
- •Introduction
- •Clinical Features
- •Pathophysiology
- •Pulmonary Function Studies
- •Imaging Studies
- •Treatment
- •Tracheopathies Associated with Systemic Diseases
- •Relapsing Polychondritis
- •Introduction
- •Clinical Features
- •Laboratory Findings
- •Pulmonary Function and Imaging Studies
- •Treatment
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Tracheobronchial Amyloidosis
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Sarcoidosis
- •Introduction
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Orphan Tracheopathies: Conclusions
- •References
- •6: Amyloidosis and the Lungs and Airways
- •Introduction
- •Diagnosis and Evaluation of Amyloidosis
- •Systemic AA Amyloidosis
- •Systemic AL Amyloidosis
- •Amyloidosis Localised to the Respiratory Tract
- •Laryngeal Amyloidosis
- •Tracheobronchial Amyloidosis
- •Parenchymal Pulmonary Amyloidosis
- •Pulmonary Amyloidosis Associated with Sjögren’s Disease
- •Conclusions
- •References
- •Introduction
- •Pathophysiology
- •Genetic Predisposition
- •Immune Dysregulation
- •Epidemiology
- •Incidence and Prevalence
- •Triggering Factors
- •Clinical Manifestations
- •General Symptoms
- •Pulmonary Manifestations
- •Ear, Nose, and Throat (ENT) Manifestations
- •Neurological Manifestations
- •Skin Manifestations
- •Cardiac Manifestations
- •Gastrointestinal Involvement
- •Renal Manifestations
- •Ophthalmological Manifestations
- •Complementary Investigations
- •Diagnosis
- •Diagnostic Criteria
- •Prognosis and Outcomes
- •Phenotypes According to the ANCA Status
- •Treatment
- •Therapeutic Strategies
- •Remission Induction
- •Maintenance Therapy
- •Other Treatments
- •Prevention of AEs
- •Conclusions
- •References
- •8: Granulomatosis with Polyangiitis
- •A Brief Historical Overview
- •Epidemiology
- •Pathogenesis
- •Clinical Manifestations
- •Constitutional Symptoms
- •Ear, Nose, and Throat (ENT) Manifestations
- •Pulmonary Manifestations
- •Kidney and Urological Manifestations
- •Kidney Manifestations
- •Urological Manifestations
- •Neurological Manifestations
- •Peripheral Nervous System (PNS) Manifestations
- •Central Nervous System (CNS) Manifestations
- •Spinal Cord and Cranial Nerve Involvement
- •Skin and Oral Mucosal Manifestations
- •Eye Manifestations
- •Cardiac Involvement
- •Gastrointestinal Manifestations
- •Gynecological and Obstetric Manifestations
- •Venous Thrombosis and Other Vascular Events
- •Other Manifestations
- •Pediatric GPA
- •Diagnosis
- •Diagnostic Approach
- •Laboratory Investigations
- •Biology
- •Immunology
- •Pathology
- •Treatment
- •Glucocorticoids
- •Cyclophosphamide
- •Rituximab
- •Other Current Induction Approaches
- •Other Treatments in GPA
- •Intravenous Immunoglobulins
- •Plasma Exchange
- •CTLA4-Ig (Abatacept)
- •Cotrimoxazole
- •Other Agents
- •Principles of Treatment for Relapsing and Refractory GPA
- •Outcomes and Prognostic Factors
- •Survival and Causes of Deaths
- •Relapse
- •Damage and Disease Burden on Quality of Life
- •Conclusions
- •References
- •9: Alveolar Hemorrhage
- •Introduction
- •Clinical Presentation
- •Diagnosis (Table 9.1, Fig. 9.3)
- •Pulmonary Capillaritis
- •Histology (Fig. 9.4)
- •Etiologies
- •ANCA-Associated Small Vessel Vasculitis: Granulomatosis with Polyangiitis (GPA)
- •ANCA-Associated Small Vessel Vasculitis: Microscopic Polyangiitis
- •Isolated Pulmonary Capillaritis
- •Systemic Lupus Erythematosus
- •Antiphospholipid Antibody Syndrome
- •Anti-Basement Membrane Antibody Disease (Goodpasture Syndrome)
- •Lung Allograft Rejection
- •Others
- •Bland Pulmonary Hemorrhage (Fig. 9.5)
- •Histology
- •Etiologies
- •Idiopathic Pulmonary Hemosiderosis
- •Drugs and Medications
- •Coagulopathy
- •Valvular Heart Disease and Left Ventricular Dysfunction
- •Other
- •Histology
- •Etiologies
- •Hematopoietic Stem Cell Transplantation (HSCT)
- •Cocaine Inhalation
- •Acute Exacerbation of Interstitial Lung Disease
- •Acute Interstitial Pneumonia
- •Acute Respiratory Distress Syndrome
- •Miscellaneous Causes
- •Etiologies
- •Pulmonary Capillary Hemangiomatosis
- •Treatment
- •Conclusions
- •References
- •Takayasu Arteritis
- •Epidemiology
- •Pathologic Features
- •Pathogenesis
- •Clinical Features
- •Laboratory Findings
- •Imaging Studies
- •Therapeutic Management
- •Prognosis
- •Behçet’s Disease
- •Epidemiology
- •Pathologic Features
- •Pathogenesis
- •Diagnostic Criteria
- •Clinical Features
- •Pulmonary Artery Aneurysm
- •Pulmonary Artery Thrombosis
- •Pulmonary Parenchymal Involvement
- •Laboratory Findings
- •Imaging Studies
- •Therapeutic Management
- •Treatment of PAA
- •Treatment of PAT
- •Prognosis
- •References
- •Introduction
- •Portopulmonary Hypertension (PoPH)
- •Epidemiology and Risk Factors
- •Molecular Pathogenesis
- •PoPH Treatment
- •Hepatopulmonary Syndrome (HPS)
- •Epidemiology and Risk Factors
- •Molecular Pathogenesis
- •HPS Treatment
- •Conclusion
- •References
- •12: Systemic Sclerosis and the Lung
- •Introduction
- •Risk factors for SSc-ILD
- •Genetic Associations
- •Clinical Presentation of SSc-ILD
- •Pulmonary Function Tests (PFTs)
- •Imaging
- •Management
- •References
- •13: Rheumatoid Arthritis and the Lungs
- •Introduction
- •Epidemiology
- •Risk Factors for ILD (Table 13.3)
- •Pathogenesis
- •Clinical Features and Diagnosis
- •Treatments
- •Prognosis
- •Epidemiology
- •Risk Factors
- •Clinical Features, Diagnosis, and Outcome
- •Subtypes or RA-AD
- •Obliterative Bronchiolitis
- •Bronchiectasis
- •COPD
- •Cricoarytenoid Involvement
- •Pleural Disease
- •Conclusion
- •References
- •Introduction
- •Systemic Lupus Erythematosus
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations
- •Pleural Disease
- •Shrinking Lung Syndrome
- •Thrombotic Manifestations
- •Interstitial Lung Disease
- •Other Pulmonary Manifestations
- •Prognosis
- •Sjögren’s Syndrome
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations
- •Airway Disorders
- •Lymphoproliferative Disease
- •Interstitial Lung Disease
- •Prognosis
- •Mixed Connective Tissue Disease
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations
- •Pulmonary Hypertension
- •Interstitial Lung Disease
- •Prognosis
- •Myositis
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations and Treatments
- •Interstitial Lung Disease
- •Respiratory Muscle Weakness
- •Other Pulmonary Manifestations
- •Prognosis
- •Other Therapeutic Options in CTD-ILD
- •Lung Transplantation
- •Conclusion
- •References
- •Introduction
- •Diagnostic Criteria
- •Controversies in the Diagnostic Criteria
- •Typical Clinical Features
- •Disease Progression and Prognosis
- •Summary
- •References
- •Introduction
- •Histiocytes and Dendritic Cells
- •Introduction
- •Cellular and Molecular Pathogenesis
- •Pathology
- •Clinical Presentation
- •Treatment and Prognosis
- •Erdheim-Chester Disease
- •Epidemiology
- •Cellular and Molecular Pathogenesis
- •Histopathology and Immunohistochemistry
- •Clinical Presentation
- •Investigation/Diagnosis
- •Chest Studies
- •Cardiovascular Imaging
- •CNS Imaging
- •Bone Radiography
- •Other Imaging Findings and Considerations
- •Disease Monitoring
- •Pathology
- •Management/Treatment
- •Prognosis
- •Rosai-Dorfman Destombes Disease
- •Epidemiology
- •Etiology/Pathophysiology
- •Histopathology and Immunohistochemistry
- •Clinical Presentation
- •Investigation/Diagnosis
- •Management/Treatment
- •Prognosis
- •Conclusions
- •Diagnostic Criteria for Primary Histiocytic Disorders of the Lung
- •References
- •17: Eosinophilic Pneumonia
- •Introduction
- •Eosinophil Biology
- •Physiologic and Immunologic Role of Eosinophils
- •Release of Mediators
- •Targeting the Eosinophil Cell Lineage
- •Historical Perspective
- •Clinical Presentation
- •Pathology
- •Diagnosis
- •Eosinophilic Lung Disease of Undetermined Cause
- •Idiopathic Chronic Eosinophilic Pneumonia
- •Clinical Features
- •Imaging
- •Laboratory Studies
- •Bronchoalveolar Lavage
- •Lung Function Tests
- •Treatment
- •Outcome and Perspectives
- •Clinical Features
- •Imaging
- •Laboratory Studies
- •Bronchoalveolar Lavage
- •Lung Function Tests
- •Lung Biopsy
- •Treatment and Prognosis
- •Eosinophilic Granulomatosis with Polyangiitis
- •History and Nomenclature
- •Pathology
- •Clinical Features
- •Imaging
- •Laboratory Studies
- •Pathogenesis
- •Diagnosis
- •Treatment and Prognosis
- •Long-Term Outcome
- •Hypereosinophilic Syndrome
- •Pathogenesis
- •Clinical and Imaging Features
- •Laboratory Studies
- •Treatment and Prognosis
- •Eosinophilic Pneumonias of Parasitic Origin
- •Tropical Eosinophilia [191]
- •Ascaris Pneumonia
- •Eosinophilic Pneumonia in Larva Migrans Syndrome
- •Strongyloides Stercoralis Infection
- •Eosinophilic Pneumonias in Other Infections
- •Allergic Bronchopulmonary Aspergillosis
- •Pathogenesis
- •Diagnostic Criteria
- •Biology
- •Imaging
- •Treatment
- •Bronchocentric Granulomatosis
- •Miscellaneous Lung Diseases with Associated Eosinophilia
- •References
- •Introduction
- •Pulmonary Langerhans’ Cell Histiocytosis
- •Epidemiology
- •Pathogenesis
- •Diagnosis
- •Clinical Features
- •Extrathoracic Lesions
- •Pulmonary Function Tests
- •Chest Radiography
- •High-Resolution Computed Tomography (HRCT)
- •Bronchoscopy and Bronchoalveolar Lavage (BAL)
- •Lung Biopsy
- •Pathology
- •Treatment
- •Course and Prognosis
- •Case Report I
- •Introduction
- •Epidemiology
- •Clinical Features
- •Histopathological Findings
- •Radiologic Findings
- •Prognosis and Therapy
- •Desquamative Interstitial Pneumonia
- •Epidemiologic and Clinical Features
- •Histopathological Findings
- •Radiological Findings
- •Prognosis and Therapy
- •Conclusion
- •References
- •19: Lymphangioleiomyomatosis
- •Introduction
- •Pathogenesis
- •Presentation
- •Prognosis
- •Management
- •General Measures
- •Parenchymal Lung Disease
- •Pleural Disease
- •Renal Angiomyolipoma
- •Abdominopelvic Lymphatic Disease
- •Pregnancy
- •Tuberous Sclerosis
- •Drug Treatment
- •Bronchodilators
- •mTOR Inhibitors
- •Anti-Oestrogen Therapy
- •Experimental Therapies
- •Interventions for Advanced Disease
- •Oxygen Therapy
- •Pulmonary Hypertension
- •References
- •20: Diffuse Cystic Lung Disease
- •Introduction
- •Lymphangioleiomyomatosis
- •Pathogenesis
- •Pathologic and Radiographic Characteristics
- •Diagnostic Approach
- •Pulmonary Langerhans Cell Histiocytosis (PLCH)
- •Pathogenesis
- •Pathological and Radiographic Characteristics
- •Diagnostic Approach
- •Birt-Hogg-Dubé Syndrome (BHD)
- •Pathogenesis
- •Pathological and Radiographic Characteristics
- •Diagnostic Approach
- •Lymphoproliferative Disorders
- •Pathogenesis
- •Pathological and Radiographic Characteristics
- •Diagnostic Approach
- •Amyloidosis
- •Light Chain Deposition Disease (LCDD)
- •Conclusion
- •References
- •Introduction
- •Lymphatic Development
- •Clinical Presentation of Lymphatic Disorders
- •Approaches to Diagnosis and Management of Congenital Lymphatic Anomalies
- •Generalized Lymphatic Anomaly
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Course/Prognosis
- •Management
- •Kaposiform Lymphangiomatosis
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Gorham Stout Disease
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Channel-Type LM/Central Conducting LM
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Yellow Nail Syndrome
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Summary
- •References
- •Introduction
- •Historical Note
- •Epidemiology
- •Pathogenesis
- •Surfactant Homeostasis in PAP
- •GM-CSF Signaling Disruption
- •Myeloid Cell Dysfunction
- •GM-CSF Autoantibodies
- •Lymphocytosis
- •Clinical Manifestations
- •Clinical Presentation
- •Secondary Infections
- •Pulmonary Fibrosis
- •Diagnosis
- •Pulmonary Function Testing
- •Radiographic Assessment
- •Bronchoscopy and Bronchoalveolar Lavage
- •Laboratory Studies and Biomarkers
- •GM-CSF Autoantibodies
- •Genetic Testing
- •Lung Pathology
- •Diagnostic Approach to the Patient with PAP
- •Natural History and Prognosis
- •Treatment
- •Whole-Lung Lavage
- •Subcutaneous GM-CSF
- •Inhaled GM-CSF
- •Other Approaches
- •Conclusions and Future Directions
- •References
- •Introduction
- •Epidemiology
- •Gastric Contents
- •Pathobiology of GER/Microaspirate in the Lungs of Patients with IPF
- •GER and the Microbiome
- •Diagnosis
- •Clinical History/Physical Exam
- •Investigations
- •Esophageal Physiology
- •Upper Esophageal Sphincter
- •Esophagus and Peristalsis
- •Lower Esophageal Sphincter and Diaphragm
- •Esophageal pH and Impedance Testing
- •High Resolution Esophageal Manometry
- •Esophagram/Barium Swallow
- •Bronchoalveolar Lavage/Sputum: Biomarkers
- •Treatment
- •Anti-Acid Therapy (PPI/H2 Blocker)
- •GER and Acute Exacerbations of IPF
- •Suggested Approach
- •Summary and Future Directions
- •References
- •Introduction
- •Familial Interstitial Pneumonia
- •Telomere Related Genes
- •Genetic
- •Telomere Length
- •Pulmonary Involvement
- •Interstitial Lung Disease
- •Other Lung Disease
- •Hepatopulmonary Syndrome
- •Emphysema
- •Extrapulmonary Manifestations
- •Mucocutaneous Involvement
- •Hematological Involvement
- •Liver Involvement
- •Other Manifestations
- •Treatment
- •Telomerase Complex Agonists
- •Lung Transplantation
- •Surfactant Pathway
- •Surfactant Protein Genes
- •Pulmonary Involvement
- •Treatment
- •Heritable Forms of Pulmonary Fibrosis with Autoimmune Features
- •TMEM173
- •COPA
- •Pulmonary Alveolar Proteinosis
- •GMCSF Receptor Mutations
- •GATA2
- •MARS
- •Lysinuric Protein Intolerance
- •Lysosomal Diseases
- •Hermansky-Pudlak Syndrome
- •Lysosomal Storage Disorders
- •FAM111B, NDUFAF6, PEPD
- •Conclusion
- •References
- •Introduction
- •Pathophysiology
- •Clinical Presentation
- •Epidemiology
- •Genetic Causes of Bronchiectasis
- •Disorders of Mucociliary Clearance
- •Cystic Fibrosis
- •Primary Ciliary Dyskinesia
- •Other Ciliopathies
- •X-Linked Agammaglobulinemia
- •Chronic Granulomatous Disease and Other Disorders of Neutrophil Function
- •Other Genetic Disorders Predisposing to Bronchiectasis
- •Idiopathic Bronchiectasis
- •Diagnosis of Bronchiectasis
- •Management of Patients with Bronchiectasis
- •Airway Clearance Therapy (ACT)
- •Management of Infections
- •Immune Therapy
- •Surgery
- •Novel Therapies for Managing Cystic Fibrosis
- •Summary
- •References
- •Pulmonary Arteriovenous Malformations
- •Background Pulmonary AVMs
- •Anatomy Pulmonary AVMs
- •Clinical Presentation of Pulmonary AVMs
- •Screening Pulmonary AVMs
- •Treatment Pulmonary AVMs
- •Children with Hereditary Hemorrhagic Telangiectasia
- •Pulmonary Hypertension
- •Pulmonary Hypertension Secondary to Liver Vascular Malformations
- •Pulmonary Arterial Hypertension
- •Background HHT
- •Pathogenesis
- •References
- •27: Pulmonary Alveolar Microlithiasis
- •Introduction
- •Epidemiology
- •Pathogenesis
- •Clinical Features
- •Diagnosis
- •Management
- •Summary
- •References
- •Introduction
- •Hermansky-Pudlak Syndrome
- •Telomerase-Associated Pulmonary Fibrosis
- •Lysosomal Storage Diseases
- •Lysinuric Protein Intolerance
- •Familial Hypocalciuric Hypercalcemia
- •Surfactant Dysfunction Disorders
- •Concluding Remarks
- •References
- •Introduction
- •Background
- •Image Acquisition
- •Key Features of Fibrosis
- •Ancillary Features of Fibrosis
- •Other Imaging Findings in FLD
- •Probable UIP-IPF
- •Indeterminate
- •Alternative Diagnosis
- •UIP in Other Fibrosing Lung Diseases
- •Pleuroparenchymal Fibroelastosis (PPFE)
- •Combined Pulmonary Fibrosis and Emphysema
- •Chronic Hypersensitivity Pneumonitis
- •Other Fibrosing Lung Diseases
- •Fibrosing Sarcoidosis
- •CTD-ILD and Drug-Induced FLD
- •Complications
- •Prognosis
- •Computer Analysis of CT Imaging
- •The Progressive Fibrotic Phenotype
- •Other Imaging Techniques
- •Conclusion
- •References
- •Introduction
- •Bronchoalveolar Lavage (BAL)
- •Technique
- •Interpretation
- •Transbronchial Biopsy (TBB)
- •Transbronchial Lung Cryobiopsy (TLCB)
- •References
- •Introduction
- •Overview of ILD Diagnosis
- •Clinical Assessment
- •Radiological Assessment
- •Laboratory Assessment
- •Integration of Individual Features
- •Multidisciplinary Discussion
- •Diagnostic Ontology
- •Conclusions
- •References
- •Introduction
- •Idiopathic Pulmonary Fibrosis
- •Chronic Hypersensitivity Pneumonitis
- •Connective Tissue Disease
- •Drug-Induced Lung Diseases
- •Radiation Pneumonitis
- •Asbestosis
- •Hermansky-Pudlak Syndrome
- •Risk Factors for Progression
- •Diagnosis
- •Pharmacological Management
- •Conclusions
- •References
- •Historical Perspective
- •Epidemiology and Etiologies
- •Tobacco Smoking and Male Sex
- •Genetic Predisposition
- •Systemic Diseases
- •Other Etiological Contexts
- •Clinical Manifestations
- •Pulmonary Function and Physiology
- •Imaging
- •Computed Tomography Characteristics and Patterns
- •Thick-Walled Large Cysts
- •Imaging Phenotypes
- •Pitfalls
- •Pathology
- •Diagnosis
- •CPFE Is a Syndrome
- •Biology
- •Complications and Outcome
- •Mortality
- •Pulmonary Hypertension
- •Lung Cancer
- •Acute Exacerbation of Pulmonary Fibrosis
- •Other Comorbidities and Complications
- •Management
- •General Measures and Treatment of Emphysema
- •Treatment of Pulmonary Fibrosis
- •Management of Pulmonary Hypertension
- •References
- •Acute Interstitial Pneumonia (AIP)
- •Epidemiology
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Treatment
- •Epidemiology
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Desquamative Interstitial Pneumonia (DIP)
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Treatment
- •Epidemiology
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Treatment
- •References
- •Organizing Pneumonias
- •Epidemiology
- •Pathogenesis
- •Clinical Features
- •Imaging
- •Multifocal Form
- •Isolated Nodular Form
- •Other Imaging Patterns
- •Histopathological Diagnosis of OP Pattern
- •Etiological Diagnosis of OP
- •Treatment
- •Clinical Course and Outcome
- •Severe Forms of OP with Respiratory Failure
- •Acute Fibrinous and Organizing Pneumonia
- •Granulomatous Organizing Pneumonia
- •Acute Interstitial Pneumonia
- •Epidemiology
- •Clinical Picture
- •Imaging
- •Histopathology
- •Diagnosis
- •Treatment
- •Outcome
- •References
- •36: Pleuroparenchymal Fibroelastosis
- •Introduction
- •Epidemiology
- •Clinical Manifestations
- •Laboratory Findings
- •Respiratory Function
- •Radiologic Features
- •Pathologic Features
- •Diagnosis
- •Treatment
- •Prognosis
- •Conclusions
- •References
- •Introduction
- •Acute Berylliosis
- •Chronic Beryllium Disease
- •Exposure
- •Epidemiology
- •Immunopathogenesis and Pathology
- •Genetics
- •Clinical Description and Natural History
- •Treatment and Monitoring
- •Indium–Tin Oxide-Lung Disease
- •Hard Metal Lung
- •Flock Worker’s Disease
- •Asbestosis
- •Nanoparticle Induced ILD
- •Flavoring-Induced Lung Disease
- •Silica-Induced Interstitial Lung Disease
- •Chronic Silicosis
- •Acute and Accelerated Silicosis
- •Chronic Obstructive Disease in CMDLD
- •Simple CMDLD
- •Complicated CMDLD
- •Conclusion
- •References
- •38: Unclassifiable Interstitial Lung Disease
- •Introduction
- •Diagnostic Scenarios
- •Epidemiology
- •Clinical Presentation
- •Diagnosis
- •Clinical Features
- •Radiology
- •Laboratory Investigations
- •Pathology
- •Conclusion
- •References
- •39: Lymphoproliferative Lung Disorders
- •Introduction
- •Nodular Lymphoid Hyperplasia
- •Lymphocytic Interstitial Pneumonia (LIP)
- •Follicular Bronchitis/Bronchiolitis
- •Castleman Disease
- •Primary Pulmonary Lymphomas
- •Primary Pulmonary MALT B Cell Lymphoma
- •Pulmonary Plasmacytoma
- •Follicular Lymphoma
- •Lymphomatoid Granulomatosis
- •Primary Pulmonary Hodgkin Lymphoma (PPHL)
- •Treatment
- •References
- •Introduction
- •Late-Onset Pulmonary Complications
- •Bronchiolitis Obliterans (BO)
- •Pathophysiology
- •Diagnosis
- •Management of BOS
- •Post-HSCT Organizing Pneumonia
- •Other Late-Onset NonInfectious Pulmonary Complications (LONIPCs)
- •Conclusion
- •References
- •Introduction
- •Pulmonary Hypertension Associated with Sarcoidosis (Group 5.2)
- •PH Associated with Pulmonary Langerhans Cell Histiocytosis (Group 5.2)
- •PH in Combined Pulmonary Fibrosis and Emphysema (Group 3.3)
- •PH Associated with Lymphangioleiomyomatosis (Group 3)
- •Hereditary Hemorrhagic Telangiectasia (Group 1.2)
- •Pulmonary Veno-Occlusive Disease (Group 1.5)
- •Small Patella Syndrome (Group 1.2)
- •Conclusion
- •References
- •Introduction
- •Epidemiology
- •Timing, Chronology, Delay Time
- •Route of Administration
- •Patterns of Involvement [3, 4]
- •Drugs and Agents Fallen Out of Favor
- •Drug-Induced Noncardiac Pulmonary Edema
- •Drug-Induced Cardiogenic Pulmonary Edema
- •The “Chemotherapy Lung”
- •Drug-Induced/Iatrogenic Alveolar Hemorrhage
- •Drugs
- •Superwarfarin Rodenticides
- •Transfusion Reactions: TACO–TRALI
- •Acute Eosinophilic Pneumonia
- •Acute Granulomatous Interstitial Lung Disease
- •Acute Organizing Pneumonia (OP), Bronchiolitis Obliterans Organizing Pneumonia (BOOP), or Acute Fibrinous Organizing Pneumonia (AFOP) Patterns
- •Acute Amiodarone-Induced Pulmonary Toxicity (AIPT)
- •Accelerated Pulmonary Fibrosis
- •Acute Exacerbation of Previously Known (Idiopathic) Pulmonary Fibrosis
- •Anaphylaxis
- •Acute Vasculopathy
- •Drug-Induced/Iatrogenic Airway Emergencies
- •Airway Obstruction as a Manifestation of Anaphylaxis
- •Drug-Induced Angioedema
- •Hematoma Around the Upper Airway
- •The “Pill Aspiration Syndrome”
- •Catastrophic Drug-Induced Bronchospasm
- •Peri-operative Emergencies (Table 42.8)
- •Other Rare Presentations
- •Pulmonary Nodules and Masses
- •Pleuroparenchymal Fibroelastosis
- •Late Radiation-Induced Injury
- •Chest Pain
- •Rebound Phenomenon
- •Recall Pneumonitis
- •Thoracic Bezoars: Gossipybomas
- •Respiratory Diseases Considered Idiopathic That May Be Drug-Induced (Table 42.4)
- •Eye Catchers
- •Conclusion
- •References
- •Cancer Mimics of Organizing Pneumonia
- •Lung Adenocarcinoma/Bronchioloalveolar Carcinoma
- •Primary Pulmonary Lymphoma
- •Cancer Mimics of Interstitial Lung Diseases
- •Lymphangitic Carcinomatosis
- •Epithelioid Hemangio-Endothelioma
- •Lymphomatoid Granulomatosis
- •Cystic Tumors
- •Cavitating Tumors
- •Intrathoracic Pseudotumors
- •Respiratory Papillomatosis
- •Pulmonary Langerhans Cell Histiocytosis
- •References
- •Index
37 Interstitial Lung Diseases of Occupational Origin |
661 |
|
|
There is no therapeutic option for established CMDLD, so miners have to be identi ed earlier in the disease process. Therefore, recurring medical monitoring, including spirometry and chest radiography, is of highest importance to identify workers developing complications of CMDLD [293]. Prevention and termination of ongoing exposure is recommended. Bronchodilator therapy, oxygen supplementation, and early diagnosis and therapy of complications like tuberculosis or malignant disease are warranted.
Conclusion
With the enforcement of higher occupational safety standards in industrialized nations the incidence and prevalence of classical occupational interstitial lung diseases like sidero brosis is going down but new entities emerge such as fock worker’s disease or indium–tin oxide interstitial lung diseases, that both have been recognized only
within the last decades. Awareness to potential occupational triggers needs to be high in the diagnostic workup of interstitial lung diseases, since hazards previously thought to affect just the directly exposed worker may be of relevance for bystanders and worker’s family. Such bystander and paraoccupational diseases are frequently caused by the transport of hazardous material in the clothes of workers to other places and home. Outbreaks of paraoccupational diseases caused by beryllium and other compounds have been traced to contamination by industrial dust [25]. The most common hazardous scenario is the cleaning of contaminated work clothing at home. Consequently, the case record of patients undergoing clinical investigations to diagnose interstitial lung diseases need to be extended to occupational details of family members and possible bystander exposure by the dissemination of hazardous materials outside the workplace to recognize paraoccupational diseases. This can only be achieved by a high vigilance of medical professionals.
Diagnostic Box
General clinical and radiological features
•\ Respiratory symptoms e.g., shortness of breath, cough, dyspnea on exertion. •\ Lung function impairment, especially restrictive ventilator defect.
•\ Radiological alterations in HRCT like reticulation, ground glass opacities and noduli.
•\ Detailed anamnesis of occupational environment for exposure to dust from different origins.
Disease-related diagnostic clues:
|
Typical occupation |
Typical radiology |
Typical histology/BAL |
Others |
||||
Chronic |
– |
Electronic industries |
– |
Lymphadenopathy |
– |
Non-caseating granulomata |
– |
Beryllium |
Beryllium |
– |
Ceramic industries |
– |
Perilymphatic noduli |
|
|
|
lymphocyte |
Disease |
– Armaments industries |
– Ground glass opacities |
|
|
|
proliferation test |
||
|
– Atomic industries |
|
|
|
|
|
(BeLPT) |
|
|
|
|
|
|
|
|
|
|
Indium Tin Oxid |
– Production of LCD |
– |
Subpleural reticulation |
– |
Giant cells |
– |
Manifestation as |
|
Lung Disease |
|
displays or solar |
|
and honeycombing |
– Foamy macrophages |
|
alveolar |
|
|
|
techniques |
– |
Emphysema |
– |
Cholesterol clefts |
|
proteinosis |
Hard Metal Lung- |
– Tool maker |
– |
NSIP pattern |
– Multinucleated cells in BAL |
– Cobalt in urine or |
|||
|
– |
Diamond polisher |
– Ground glass opacities |
– Giant cell pneumonitis |
|
blood may help to |
||
|
– |
Steel industry |
– |
Reticulations |
|
|
|
prove exposure |
Flock Worker’s |
– |
Flocking industry |
– |
Reticulation |
– Lymphocytes in BAL |
|
|
|
Disease |
– |
Textile industry |
– |
Consolidation |
– |
Follicular bronchiolitis |
|
|
|
|
|
– Ground glass opacities |
|
|
|
|
|
Asbestosis |
– |
Building construction/ |
– |
Diffuse bilateral |
– |
Peribronchiolar brosis |
– |
Pleura plaques |
|
|
deconstruction |
|
brosis with |
– Asbestosis bodies |
– |
Pleura thickening |
|
|
– |
Shipbuilding |
|
reticulation and |
|
|
|
|
|
– Textile industry |
|
honeycombing |
|
|
|
|
|
Nano-particle |
– |
Different industries |
– |
Fibrosis |
– |
Granulomata |
|
|
induced ILD |
|
including paint spray |
– |
Pleural effusion |
– Detection of nanoparticles |
|
|
|
|
|
industry, fuel industry |
|
|
|
in histological specimens |
|
|
Siderobrosis |
– Welding fumes, e.g. by |
– |
Bronchiolitis |
– |
Macrophages with |
|
|
|
|
|
thermal cutting and |
– |
Desquamative |
|
siderophilic particles |
|
|
|
|
brazing |
|
interstitial pneumonia |
– Mixed dust deposits with |
|
|
|
|
|
|
– Combined pulmonary |
|
brosis and |
|
|
|
|
|
|
|
brosis and emphysema |
|
pseudogranulomata |
|
|
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
662 |
|
|
|
|
|
|
|
A. Prasse et al. |
||
|
|
|
|
|
|
|
||||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
||||
|
|
Typical occupation |
Typical radiology |
Typical histology/BAL |
Others |
|||||
|
Flavoring- |
– Food industry especially |
– |
Bronchiolitis |
– |
Fibrotic obstructive |
|
|
|
|
|
induced lung |
|
in processes related to |
– |
Mosaic attenuation |
|
bronchiolitis |
|
|
|
|
disease |
|
favouring, e.g., coffee |
– |
Centrilobular nodules |
|
|
|
|
|
|
|
|
roasting |
|
|
|
|
|
|
|
|
Coal mine dus |
– |
Coal workers |
– Small nodular opacities |
– Coal dust accumulation |
|
|
|
||
|
lung disease |
– |
Miners |
– |
Irregular opacities |
|
especially in the terminal |
|
|
|
|
|
|
|
– |
Reticular brosis |
|
bronchiole |
|
|
|
|
|
|
|
– Honeycombing |
– Macrophage-rich nodules |
|
|
|
||
|
|
|
|
|
|
|
with dense brosis |
|
|
|
|
Chronic silicosis |
– |
Miners |
– |
Round/irregular |
– Fibrotic leasons with |
– |
May be |
||
|
(simple or |
– |
Quarry workers |
|
nodules with upperlobe |
|
dust-loaded macrophages |
|
complicated by |
|
|
complicated) |
– Tunnel workers |
|
predominance |
– Histiocytes and granuloma |
|
tuberculosis |
|||
|
|
|
|
– Calci cations (i.e. of |
– Concentric brosis in later |
|
|
|
||
|
|
|
|
|
lymphonodes) |
|
stages |
|
|
|
|
|
|
|
– Conglomerate masses |
|
|
|
|
|
|
|
|
|
|
|
and brosis in |
|
|
|
|
|
|
|
|
|
|
complicated silicosis |
|
|
|
|
|
|
Acute and |
– |
Stonemasons |
– |
Consolidations (i.e., |
– |
Bronchoalveolar lavage |
– |
Often short |
|
|
accelerated |
– Arti cial stone workers |
|
perihilar) |
|
with high protein |
|
exposure to high |
||
|
silicosis |
– |
Sandblasters |
– |
Centrilobular nodules |
|
concentrations (milky, |
|
concentrations of |
|
|
|
– |
Stone crushers |
– |
Crazy paving |
|
PAS-positive) |
|
silica |
|
|
|
– |
Polishers |
|
|
– |
Dust-loaded macrophages |
|
|
|
|
|
|
|
|
|
– Silicotic nodules with |
|
|
|
|
|
|
|
|
|
|
|
patchy brosis |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
References
1.\Travis WD, Costabel U, Hansell DM, King TE Jr, Lynch DA, Nicholson AG, et al. An of cial American Thoracic Society/ European Respiratory Society statement: Update of the international multidisciplinary classi cation of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med. 2013;188(6):733–48.
2.\Müller-Quernheim J, Zissel G, Schopf R, Vollmer E, Schlaak M. Differentialdiagnose Berylliose / Sarkoidose bei einem Zahntechniker. Dtsch Med Wochenschr. 1996;121:1462–6.
3.\Balmes JR, Abraham JL, Dweik RA, Fireman E, Fontenot AP, Maier LA, et al. An of cial american thoracic society statement: diagnosis and management of beryllium sensitivity and chronic beryllium disease. Am J Respir Crit Care Med. 2014;190(10):e34–59.
4.\Leung CC, Yu IT, Chen W. Silicosis. Lancet. 2012;379(9830):2008–18.
5.\Awadalla NJ, Hegazy A, Elmetwally RA, Wahby I. Occupational and environmental risk factors for idiopathic pulmonary brosis in Egypt: a multicenter case-control study. Int J Occup Environ Med. 2012;3(3):107–16.
6.\Baumgartner KB, Samet JM, Coultas DB, Stidley CA, Hunt WC, Colby TV, et al. Occupational and environmental risk factors for idiopathic pulmonary brosis: a multicenter case-control study. Collaborating Centers. Am J Epidemiol. 2000;152(4):307–15.
7.\De Sadeleer LJ,Verleden SE, De Dycker E,Yserbyt J,Verschakelen JA, Verbeken EK, et al. Clinical behaviour of patients exposed to organic dust and diagnosed with idiopathic pulmonary brosis. Respirology. 2018;23(12):1160–5.
8.\Ekstrom M, Gustafson T, Boman K, Nilsson K, Tornling G, Murgia N, et al. Effects of smoking, gender and occupational exposure on the risk of severe pulmonary brosis: a population- based case-control study. BMJ Open. 2014;4(1):e004018.
9.\Iwai K, Mori T, Yamada N, Yamaguchi M, Hosoda Y. Idiopathic pulmonary brosis. Epidemiologic approaches to occupational exposure. Am J Respir Crit Care Med. 1994;150(3):670–5.
10.\Izbicki G, Chavko R, Banauch GI, Weiden MD, Berger KI, Aldrich TK, et al. World Trade Center "sarcoid-like" granulomatous pulmonary disease in New York City Fire Department rescue workers. Chest. 2007;131(5):1414–23.
11.\Liu H, Patel D, Welch AM, Wilson C, Mroz MM, Li L, et al. Association Between Occupational Exposures and Sarcoidosis: An Analysis From Death Certi cates in the United States, 1988– 1999. Chest. 2016;150(2):289–98.
12.\Frye BC, Quartucci C, Rakete S, GrubanovicA, Hohne K, Mangold F, et al. A Cluster of beryllium sensitization traced to the presence of beryllium in concrete dust. Chest. 2021;159(3):1084–93.
13.\Ronsmans S, Verbeken EK, Adams E, Keirsbilck S, Yserbyt J, Wuyts WA, et al. Granulomatous lung disease in two workers making light bulbs. Am J Ind Med. 2019;62(10):908–13.
14.\Karkinen-Jaaskelainen M, Maatta K, Pasila M, Saxen L. Pulmonary berylliosis: report on a fatal case. Br J Dis Chest. 1982;76(3):290–7.
15.\Hooper WF. Acute beryllium lung disease. N C Med J. 1981;42(8):551–3.
16.\Cummings KJ, Stefaniak AB, Virji MA, Kreiss K. A reconsideration of acute Beryllium disease. Environ Health Perspect. 2009;117(8):1250–6.
17.\Kriebel D, Sprince NL, Eisen EA, Greaves IA. Pulmonary function in beryllium workers: assessment of exposure. Br J Ind Med. 1988;45(2):83–92.
18.\Newman LS, Mroz MM, Balkissoon R, Maier LA. Beryllium sensitization progresses to chronic beryllium disease: a longitudinal study of disease risk. Am J Respir Crit Care Med. 2005;171(1):54–60.
19.\Eisenbud M, Wanta RC, et al. Non-occupational berylliosis. J Ind Hyg Toxicol. 1949;31(5):282–94.
20.\Hardy HL, Tabershaw IR. Delayed chemical pneumonitis in workers exposed to beryllium compounds. J Industr Hyg Toxicol. 1946;28:197–211.
21.\Müller-Quernheim J, Gaede KI, Fireman E, Zissel G. Diagnoses of chronic beryllium disease within cohorts of sarcoidosis patients. Eur Respir J. 2006;27:1190–5.
37 Interstitial Lung Diseases of Occupational Origin |
663 |
|
|
22.\Newman LS, Kreiss K. Nonoccupational beryllium disease masquerading as sarcoidosis: identi cation by blood lymphocyte proliferative response to beryllium. Am Rev Respir Dis. 1992;145(5):1212–4.
23.\Maier LA, Martyny JW, Liang J, Rossman MD. Recent chronic beryllium disease in residents surrounding a beryllium facility. Am J Respir Crit Care Med. 2008;177(9):1012–7.
24.\Kreiss K, Day GA, Schuler CR. Beryllium: a modern industrial hazard. Annu Rev Public Health. 2007;28:259–77.
25.\Knishkowy B, Baker EL. Transmission of occupational disease to family contacts. Am J Ind Med. 1986;9(6):543–50.
26.\Richeldi L, Sorrentino R, Saltini C. HLA-DPB 1 glutamate 69: a genetic marker of beryllium disease. Science. 1993;262:242–4.
27.\Maier LA, McGrath DS, Sato H, Lympany P, Welsh K, Du Bois R, et al. Infuence of MHC class II in susceptibility to beryllium sensitization and chronic beryllium disease. J Immunol. 2003;171(12):6910–8.
28.\Rossman MD, Stubbs J, Lee CW, Argyris E, Magira E, Monos D. Human leukocyte antigen Class II amino acid epitopes: susceptibility and progression markers for beryllium hypersensitivity. Am J Respir Crit Care Med. 2002;165(6):788–94.
29.\Bailey RL, Thomas CA, Deubner DC, Kent MS, Kreiss K, Schuler CR. Evaluation of a preventive program to reduce sensitization at a beryllium metal, oxide, and alloy production plant. J Occup Environ Med. 2010;52(5):505–12.
30.\Henneberger PK, Goe SK, Miller WE, Doney B, Groce DW. Industries in the United States with airborne beryllium exposure and estimates of the number of current workers potentially exposed. J Occup Environ Hyg. 2004;1(10):648–59.
31.\Statement on sarcoidosis. Joint Statement of the American Thoracic Society (ATS), the European Respiratory Society (ERS) and the World Association of Sarcoidosis and Other Granulomatous Disorders (WASOG) adopted by the ATS Board of Directors and by the ERS Executive Committee, February 1999. Am J Respir Crit Care Med. 1999;160(2):736–55.
32.\Ribeiro M, Fritscher LG, Al-Musaed AM, Balter MS, Hoffstein V, Mazer BD, et al. Search for chronic beryllium disease among sarcoidosis patients in Ontario, Canada. Lung. 2011;189(3):233–41.
33.\Schuler CR, Virji MA, Deubner DC, Stanton ML, Stefaniak AB, Day GA, et al. Sensitization and chronic beryllium disease at a primary manufacturing facility, part 3: exposure-response among short-term workers. Scand J Work Environ Health. 2012;38(3):270–81.
34.\Fontenot AP, Falta MT, Kappler JW, Dai S, McKee AS. Beryllium- induced hypersensitivity: genetic susceptibility and neoantigen generation. J Immunol. 2016;196(1):22–7.
35.\Clayton GM, Wang Y, Crawford F, Novikov A, Wimberly BT, Kieft JS, et al. Structural basis of chronic beryllium disease: linking allergic hypersensitivity and autoimmunity. Cell. 2014;158(1):132–42.
36.\Li L, Silveira LJ, Hamzeh N, Gillespie M, Mroz PM, Mayer AS, et al. Beryllium-induced lung disease exhibits expression pro les similar to sarcoidosis. Eur Respir J. 2016;47(6):1797–808.
37.\Verma DK, Ritchie AC, Shaw ML. Measurement of beryllium in lung tissue of a chronic beryllium disease case and cases with sarcoidosis. Occup Med (Lond). 2003;53(3):223–7.
38.\Tooker BC, Brindley SM, Chiarappa-Zucca ML, Turteltaub KW, Newman LS. Accelerator mass spectrometry detection of beryllium ions in the antigen processing and presentation pathway. J Immunotoxicol. 2015;12(2):181–7.
39.\Wang Z, White PS, Petrovic M, Tatum OL, Newman LS, Maier LA, et al. Differential susceptibilities to chronic beryllium disease contributed by different Glu69 HLA-DPB1 and -DPA1 alleles. J Immunol. 1999;163(3):1647–53.
40.\Van Dyke MV, Martyny JW, Mroz MM, Silveira LJ, Strand M, Fingerlin TE, et al. Risk of chronic beryllium disease by HLA-
DPB1 E69 genotype and beryllium exposure in nuclear workers. Am J Respir Crit Care Med. 2011;183(12):1680–8.
41.\Newman LS. Metals that cause sarcoidosis. Semin Respir Infect. 1998;13(3):212–20.
42.\Newman LS, Kreiss K, King TE, Seay S, Campbell AP. Pathological and immunological alterations in early stages of beryllium disease. Re-examination of disease de nition and natural history. Am Rev Respir Dis. 1989;139:1479–86.
43.\Meyer K. Beryllium and lung disease disease. Chest. 1994;106:942–6.
44.\Handa T, Nagai S, Kitaichi M, Chin K, Ito Y, Oga T, et al. Long- term complications and prognosis of chronic beryllium disease. Sarcoidosis Vasc Diffuse Lung Dis. 2009;26(1):24–31.
45.\Newman LS, Buschman DL, Newell JD Jr, Lynch DA. Beryllium disease: assessment with CT. Radiology. 1994;190(3):835–40.
46.\Newman LS, Lloyd J, Daniloff E. The natural history of beryllium sensitization and chronic beryllium disease. Environ Health Perspect. 1996;104S(5):937–43.
47.\Duggal M, Deubner DC, Curtis AM, Cullen MR. Long-term fol- low-up of beryllium sensitized workers from a single employer. BMC Public Health. 2010;10:5.
48.\Schubauer-Berigan MK, Couch JR, Petersen MR, Carreon T, JinY, Deddens JA. Cohort mortality study of workers at seven beryllium processing plants: update and associations with cumulative and maximum exposure. Occup Environ Med. 2011;68(5):345–53.
49.\Ward E, Okun A, Ruder A, Fingerhut M, Steenland K. A mortality study of workers at seven beryllium processing plants. Am J Ind Med. 1992;22(6):885–904.
50.\Rossman MD, Kern JA, Elias JA, Cullen MR, Epstein PE, Preuss OP, et al. Proliferative response of bronchoalveolar lymphocytes to beryllium. A test for chronic beryllium disease. Ann Intern Med. 1988;108(5):687–93.
51.\Mroz MM, Kreiss K, Lezotte DC, Campbell PA, Newman LS. Reexamination of the blood lymphocyte transformation test in the diagnosis of chronic beryllium disease. J Allergy Clin Immunol. 1991;88:54–60.
52.\Stokes RF, Rossman MD. Blood cell proliferation response to beryllium: analysis by receiver-operating characteristics. J Occup Med. 1991;33(1):23–8.
53.\Stange AW, Furman FJ, Hilmas DE. The beryllium lymphocyte proliferation test: Relevant issues in beryllium health surveillance. Am J Ind Med. 2004;46(5):453–62.
54.\Deubner DC, Goodman M, Iannuzzi J. Variability, predictive value, and uses of the beryllium blood lymphocyte proliferation test (BLPT): preliminary analysis of the ongoing workforce survey. Appl Occup Environ Hyg. 2001;16(5):521–6.
55.\Kreiss K, Mroz MM, Zhen B, Martyny JW, Newman LS. Epidemiology of beryllium sensitization and disease in nuclear workers. Am Rev Respir Dis. 1993;148(4 Pt 1):985–91.
56.\Kreiss K, Newman LS, Mroz MM, Campbell PA. Screening blood test identi es subclinical beryllium disease. J Occup Med. 1989;31:603–8.
57.\Milovanova TN. Comparative analysis between CFSE fow cytometric and tritiated thymidine incorporation tests for beryllium sensitivity. Cytometry B Clin Cytom. 2007;72(4):265–75.
58.\Milovanova TN, Popma SH, Cherian S, Moore JS, Rossman MD. Flow cytometric test for beryllium sensitivity. Cytometry B Clin Cytom. 2004;60(1):23–30.
59.\Pott GB, Palmer BE, Sullivan AK, Silviera L, Maier LA, Newman LS, et al. Frequency of beryllium-speci c, TH1-type cytokine- expressing CD4+ T cells in patients with beryllium-induced disease. J Allergy Clin Immunol. 2005;115(5):1036–42.
60.\Tooker BC, Bowler RP, Orcutt JM, Maier LA, Christensen HM, Newman LS. SELDI-TOF derived serum biomarkers failed to differentiate between patients with beryllium sensitisation and patients with chronic beryllium disease. Occup Environ Med. 2011;68(10):759–64.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
664 |
A. Prasse et al. |
|
|
61.\Sumino K, Hayakawa K, Shibata T, Kitamura S. Heavy metals in normal Japanese tissues. Amounts of 15 heavy metals in 30 subjects. Arch Environ Health. 1975;30(10):487–94.
62.\Wegner R, Heinrich-Ramm R, Nowak D, Olma K, Poschadel B, Szadkowski D. Lung function, biological monitoring, and biological effect monitoring of gemstone cutters exposed to beryls. Occup Environ Med. 2000;57:133–9.
63.\Schepers G. The mineral content of the lung in chronic berylliosis. J Dis Chest. 1962;42:600–7.
64.\Sprince NL, Kazemi H. Beryllium disease. In: Fanburg B, editor. Sarcoidosis and other granulomatous diseases of the lung. Basel: Dekker; 1983. p. 453–68.
65.\Sood A, Beckett WS, Cullen MR. Variable response to long- term corticosteroid therapy in chronic beryllium disease. Chest. 2004;126(6):2000–7.
66.\Bartell SM, Ponce RA, Takaro TK, Zerbe RO, Omenn GS, Faustman EM. Risk estimation and value-of-information analysis for three proposed genetic screening programs for chronic beryllium disease prevention. Risk Anal. 2000;20(1):87–99.
67.\Newman LS, Orton R, Kreiss K. Serum angiotensin converting enzyme activity in chronic beryllium disease. Am Rev Respir Dis. 1992;146:39–42.
68.\Harris J, Bartelson BB, Barker E, Balkissoon R, Kreiss K, Newman LS. Serum neopterin in chronic beryllium disease. Am J Ind Med. 1997;32(1):21–6.
69.\Müller-Quernheim J, Pfeifer S, Strausz J, Ferlinz R. Correlation of clinical and immunologic parameters of the infammatory activity of pulmonary sarcoidosis. Am Rev Respir Dis. 1991;144(6):1322–9.
70.\Sood A. Current treatment of chronic beryllium disease. J Occup Environ Hyg. 2009;6(12):762–5.
71.\Müller-Quernheim J, Kienast K, Held M, Pfeifer S, Costabel U. Treatment of chronic sarcoidosis with an azathioprine/prednisolone regimen. Eur Respir J. 1999;14(5):1117–22.
72.\Baughman RP, Lower EE. Steroid-sparing alternative treatments for sarcoidosis. Clin Chest Med. 1997;18(4):853–64.
73.\Borak J, Woolf SH, Fields CA. Use of |
beryllium lympho- |
cyte proliferation testing for screening of asymptomatic indi- |
|
viduals: an evidence-based assessment. J Occup Environ Med. |
|
2006;48(9):937–47. |
|
74.\Middleton DC, Fink J, Kowalski PJ, |
Lewin MD, Sinks |
T. Optimizing BeLPT criteria for beryllium sensitization. Am J Ind Med. 2008;51(3):166–72.
75.\Middleton DC, Lewin MD, Kowalski PJ, Cox SS, Kleinbaum D. The BeLPT: algorithms and implications. Am J Ind Med. 2006;49(1):36–44.
76.\Homma T, Ueno T, Sekizawa K, Tanaka A, Hirata M. Interstitial pneumonia developed in a worker dealing with particles containing indium-tin oxide. J Occup Health. 2003;45(3): 137–9.
77.\Cummings KJ, Nakano M, Omae K, Takeuchi K, Chonan T, Xiao YL, et al. Indium lung disease. Chest. 2012;141(6):1512–21.
78.\Cummings KJ, Donat WE, Ettensohn DB, Roggli VL, Ingram P, Kreiss K. Pulmonary alveolar proteinosis in workers at an indium processing facility. Am J Respir Crit Care Med. 2010;181(5):458–64.
79.\Xiao YL, Cai HR, Wang YH, Meng FQ, Zhang DP. Pulmonary alveolar proteinosis in an indium-processing worker. Chin Med J. 2010;123(10):1347–50.
80.\Nagano K, Gotoh K, Kasai T, Aiso S, Nishizawa T, Ohnishi M, et al. Twoand 13-week inhalation toxicities of indium-tin oxide and indium oxide in rats. J Occup Health. 2011;53(2): 51–63.
81.\Nagano K, Nishizawa T, Eitaki Y, Ohnishi M, Noguchi T, Arito H, et al. Pulmonary toxicity in mice by 2- and 13-week inhalation exposures to indium-tin oxide and indium oxide aerosols. J Occup Health. 2011;53(3):234–9.
82.\Chonan T, Taguchi O, Omae K. Interstitial pulmonary disorders in indium-processing workers. Eur Respir J. 2007;29(2):317–24.
83.\Cummings KJ, Virji MA, Trapnell BC, Carey B, Healey T, Kreiss K. Early changes in clinical, functional, and laboratory biomarkers in workers at risk of indium lung disease. Ann Am Thorac Soc. 2014;11(9):1395–403.
84.\Nakano M, Omae K, Tanaka A, Hirata M, Michikawa T, Kikuchi Y, et al. Causal relationship between indium compound inhalation and effects on the lungs. J Occup Health. 2009;51(6):513–21.
85.\Amata A, Chonan T, Omae K, Nodera H, Terada J, Tatsumi K. High levels of indium exposure relate to progressive emphysematous changes: a 9-year longitudinal surveillance of indium workers. Thorax. 2015;70(11):1040–6.
86.\Homma S, MiyamotoA, Sakamoto S, Kishi K, Motoi N,Yoshimura K. Pulmonary brosis in an individual occupationally exposed to inhaled indium-tin oxide. Eur Respir J. 2005;25(1):200–4.
87.\Choi S, Won YL, Kim EA. Effect of respiratory protector intervention among indium reclaiming workers. Am J Ind Med. 2015;58(12):1319–20.
88.\Nakano M, Tanaka A, Hirata M, Kumazoe H, Wakamatsu K, Kamada D, et al. An advanced case of indium lung disease with progressive emphysema. J Occup Health. 2016;58(5):477–81.
89.\Nagano K, Nishizawa T, Umeda Y, Kasai T, Noguchi T, Gotoh K, et al. Inhalation carcinogenicity and chronic toxicity of indium-tin oxide in rats and mice. J Occup Health. 2011;53(3):175–87.
90.\Nogami H, Shimoda T, Shoji S, Nishima S. Pulmonary disorders in indium-processing workers. Nihon Kokyuki Gakkai Zasshi. 2008;46(1):60–4.
91.\Watanabe Y, Kawabata Y, Koyama N, Ikeya T, Hoshi E, Takayanagi N, et al. A clinicopathological study of surgically resected lung cancer in patients with usual interstitial pneumonia. Respir Med. 2017;129:158–63.
92.\Maier L, Glazer C, Pacheo K. ILD and other occupational exposures (hard metal pneumoconiosis). In: King T, Schwartz D, editors. Interstitial lung diseases. Denver: People’s Medical Publishing House; 2011. p. 581–93.
93.\Nemery B, Abraham JL. Hard metal lung disease: still hard to understand. Am J Respir Crit Care Med. 2007;176(1):2–3.
94.\Nemery B, Verbeken EK, Demedts M. Giant cell interstitial pneumonia (hard metal lung disease, cobalt lung). Semin Respir Crit Care Med. 2001;22(4):435–48.
95.\Demedts M, Gheysens B, Nagels J, Verbeken E, Lauweryns J, van den Eeckhout A, et al. Cobalt lung in diamond polishers. Am Rev Respir Dis. 1984;130(1):130–5.
96.\Abraham JL, Burnett BR, Hunt A. Development and use of a pneumoconiosis database of human pulmonary inorganic particulate burden in over 400 lungs. Scanning Microsc. 1991;5(1):95– 104; discussion 5-8
97.\Ohori NP, Sciurba FC, Owens GR, Hodgson MJ, Yousem SA. Giant-cell interstitial pneumonia and hard-metal pneumoconiosis. A clinicopathologic study of four cases and review of the literature. Am J Surg Pathol. 1989;13(7):581–7.
98.\Harding HE, Mc LA. Pulmonary brosis in non-ferrous foundry workers. Br J Ind Med. 1955;12(2):92–9.
99.\Adamis Z, Tatrai E, Honma K, Karpati J, Ungvary G. A study on lung toxicity of respirable hard metal dusts in rats. Ann Occup Hyg. 1997;41(5):515–26.
100.\Huaux F, Lasfargues G, Lauwerys R, Lison D. Lung toxicity of hard metal particles and production of interleukin-1, tumor necrosis factor-alpha, bronectin, and cystatin-c by lung phagocytes. Toxicol Appl Pharmacol. 1995;132(1):53–62.
101.\Lison D, Lauwerys R. In vitro cytotoxic effects of cobalt- containing dusts on mouse peritoneal and rat alveolar macrophages. Environ Res. 1990;52(2):187–98.
102.\Lison D, Carbonnelle P, Mollo L, Lauwerys R, Fubini B. Physicochemical mechanism of the interaction between cobalt
37 Interstitial Lung Diseases of Occupational Origin |
665 |
|
|
metal and carbide particles to generate toxic activated oxygen species. Chem Res Toxicol. 1995;8(4):600–6.
103.\Lison D, Lauwerys R, Demedts M, Nemery B. Experimental research into the pathogenesis of cobalt/hard metal lung disease. Eur Respir J. 1996;9(5):1024–8.
104.\Posgay M, Nemeth L, Mester A. Radiological aspects of hard metal disease. Rofo. 1993;159(5):439–43.
105.\Potolicchio I, Mosconi G, Forni A, Nemery B, Seghizzi P, Sorrentino R. Susceptibility to hard metal lung disease is strongly associated with the presence of glutamate 69 in HLA-DP beta chain. Eur J Immunol. 1997;27(10):2741–3.
106.\Cugell DW. The hard metal diseases. Clin Chest Med. 1992;13(2):269–79.
107.\Potolicchio I, Festucci A, Hausler P, Sorrentino R. HLA-DP molecules bind cobalt: a possible explanation for the genetic association with hard metal disease. Eur J Immunol. 1999;29(7):2140–7.
108.\Lewis CP, Demedts M, Nemery B. Indices of oxidative stress in hamster lung following exposure to cobalt(II) ions: in vivo and in vitro studies. Am J Respir Cell Mol Biol. 1991;5(2):163–9.
109.\Cugell DW, Morgan WK, Perkins DG, Rubin A. The respiratory effects of cobalt. Arch Intern Med. 1990;150(1):177–83.
110.\Ruokonen EL, Linnainmaa M, Seuri M, Juhakoski P, Soderstrom KO. A fatal case of hard-metal disease. Scand J Work Environ Health. 1996;22(1):62–5.
111.\Beckett WS. Occupational respiratory diseases. N Engl J Med. 2000;342(6):406–13.
112.\Chiappino G. Hard metal disease: clinical aspects. Sci Total Environ. 1994;150(1-3):65–8.
113.\Maier LA. Clinical approach to chronic beryllium disease and other nonpneumoconiotic interstitial lung diseases. J Thorac Imaging. 2002;17(4):273–84.
114.\Alexandersson R. Blood and urinary concentrations as estimators of cobalt exposure. Arch Environ Health. 1988;43(4):299–303.
115.\Dunlop P, Muller NL, Wilson J, Flint J, Churg A. Hard metal lung disease: high resolution CT and histologic correlation of the initial ndings and demonstration of interval improvement. J Thorac Imaging. 2005;20(4):301–4.
116.\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(2):51–70.
117.\Abraham JL, Hertzberg MA. Inorganic particulates associated with desquamative interstitial pneumonia. Chest. 1981;80(1 Suppl):67–70.
118.\Tanaka J, Moriyama H, Terada M, Takada T, Suzuki E, Narita I, et al. An observational study of giant cell interstitial pneumonia and lung brosis in hard metal lung disease. BMJ Open. 2014;4(3):e004407.
119.\Gotway MB, Golden JA, Warnock M, Koth LL, Webb R, Reddy GP, et al. Hard metal interstitial lung disease: high- resolution computed tomography appearance. J Thorac Imaging. 2002;17(4):314–8.
120.\Chiarchiaro J, Tomsic LR, Strock S, Veraldi KL, Nouraie M, Sellares J, et al. A case series describing common radiographic and pathologic patterns of hard metal pneumoconiosis. Respir Med Case Rep. 2018;25:124–8.
121.\Kelleher P, Pacheco K, Newman LS. Inorganic dust pneumonias: the metal-related parenchymal disorders. Environ Health Perspect. 2000;108(Suppl 4):685–96.
122.\Card JW, Zeldin DC, Bonner JC, Nestmann ER. Pulmonary applications and toxicity of engineered nanoparticles. Am J Physiol Lung Cell Mol Physiol. 2008;295(3):L400–11.
123.\Davison AG, Haslam PL, Corrin B, Coutts II, Dewar A, Riding WD, et al. Interstitial lung disease and asthma in hard-metal workers: bronchoalveolar lavage, ultrastructural, and analytical ndings and results of bronchial provocation tests. Thorax. 1983;38(2):119–28.
124.\Anttila S, Sutinen S, Paananen M, Kreus KE, Sivonen SJ, Grekula A, et al. Hard metal lung disease: a clinical, histological, ultrastructural and X-ray microanalytical study. Eur J Respir Dis. 1986;69(2):83–94.
125.\Chiba Y, Kido T, Tahara M, Oda K, Noguchi S, Kawanami T, et al. Hard Metal Lung Disease with Favorable Response to Corticosteroid Treatment: A Case Report and Literature Review. Tohoku J Exp Med. 2019;247(1):51–8.
126.\Hesterberg TW, McConnell EE, Miller WC, Hamilton R, Bunn WB. Pulmonary toxicity of inhaled polypropylene bers in rats. Fundam Appl Toxicol. 1992;19(3):358–66.
127.\Atis S, Tutluoglu B, Levent E, Ozturk C, Tunaci A, Sahin K, et al. The respiratory effects of occupational polypropylene fock exposure. Eur Respir J. 2005;25(1):110–7.
128.\Kern DG, Crausman RS, Durand KT, Nayer A, Kuhn C 3rd. Flock worker's lung: chronic interstitial lung disease in the nylon focking industry. Ann Intern Med. 1998;129(4):261–72.
129.\Lougheed MD, Roos JO, Waddell WR, Munt PW. Desquamative interstitial pneumonitis and diffuse alveolar damage in textile workers. Potential role of mycotoxins. Chest. 1995;108(5):1196–200.
130.\Sigsgaard T, Pedersen OF, Juul S, Gravesen S. Respiratory disorders and atopy in cotton, wool, and other textile mill workers in Denmark. Am J Ind Med. 1992;22(2):163–84.
131.\Kern DG, Kern E, Crausman RS, Clapp RW. A retrospective cohort study of lung cancer incidence in nylon fock workers, 1998-2008. Int J Occup Environ Health. 2011;17(4):345–51.
132.\Kern DG, Kuhn C 3rd, Ely EW, Pransky GS, Mello CJ, Fraire AE, et al. Flock worker's lung: broadening the spectrum of clinicopathology, narrowing the spectrum of suspected etiologies. Chest. 2000;117(1):251–9.
133.\Boag AH, Colby TV, Fraire AE, Kuhn C 3rd, Roggli VL, Travis WD, et al. The pathology of interstitial lung disease in nylon fock workers. Am J Surg Pathol. 1999;23(12):1539–45.
134.\Washko RM, Day B, Parker JE, Castellan RM, Kreiss K. Epidemiologic investigation of respiratory morbidity at a nylon fock plant. Am J Ind Med. 2000;38(6):628–38.
135.\Burkhart J, Jones W, Porter DW, Washko RM, Eschenbacher WL, Castellan RM. Hazardous occupational exposure and lung disease among nylon fock workers. Am J Ind Med. 1999;1: 145–6.
136.\Turcotte SE, Chee A, Walsh R, Grant FC, Liss GM, Boag A, et al. Flock worker's lung disease: natural history of cases and exposed workers in Kingston, Ontario. Chest. 2013;143(6):1642–8.
137.\Kern D, Crausman R. In: King T, editor. Nylon fock worker’s lung. Alphen aan den Rijn, Netherlands: Wolters Kluwer; 2012.
138.\Porter DW, Castranova V, Robinson VA, Hubbs AF, Mercer RR, Scabilloni J, et al. Acute infammatory reaction in rats after intratracheal instillation of material collected from a nylon focking plant. J Toxicol Environ Health A. 1999;57(1):25–45.
139.\American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 2004;170(6):691–715.
140.\Mossman BT, Gee JB. Asbestos-related diseases. N Engl J Med. 1989;320(26):1721–30.
141.\Churg A, Vedal S. Fiber burden and patterns of asbestos-related disease in workers with heavy mixed amosite and chrysotile exposure. Am J Respir Crit Care Med. 1994;150(3):663–9.
142.\Steele M, Schwartz M. Asbestosis and asbestosis-induced pleuralbrosis. In: King T, Schwartz D, editors. Interstitial lung diseases. Denver: People’s Medical Publishing House; 2011. p. 543–55.
143.\Wagner GR. Asbestosis and silicosis. Lancet. 1997;349(9061):1311–5.
144.\Brody AR, Hill LH, Adkins B Jr, O'Connor RW. Chrysotile asbestos inhalation in rats: deposition pattern and reaction of alveolar epithelium and pulmonary macrophages. Am Rev Respir Dis. 1981;123(6):670–9.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
666 |
A. Prasse et al. |
|
|
145.\Hesterberg TW, Hart GA, Chevalier J, Miiller WC, Hamilton RD, Bauer J, et al. The importance of ber biopersistence and lung dose in determining the chronic inhalation effects of X607, RCF1, and chrysotile asbestos in rats. Toxicol Appl Pharmacol. 1998;153(1):68–82.
146.\Quinlan TR, Marsh JP, Janssen YM, Leslie KO, Hemenway D, Vacek P, et al. Dose-responsive increases in pulmonary brosis after inhalation of asbestos. Am J Respir Crit Care Med. 1994;150(1):200–6.
147.\Churg A, Stevens B. Enhanced retention of asbestos bers in the airways of human smokers. Am J Respir Crit Care Med. 1995;151(5):1409–13.
148.\Rodman T, Rodman MS. Pleural thickening: its signi cance and relationship to asbestos dust exposure. Am Rev Respir Dis. 1983;127(5):656–7.
149.\Sichletidis L, Chloros D, Spyratos D, Haidich AB, Fourkiotou I, Kakoura M, et al. Mortality from occupational exposure to relatively pure chrysotile: a 39-year study. Respiration. 2009;78(1):63–8.
150.\Mossman BT, Craighead JE, MacPherson BV. Asbestos-induced epithelial changes in organ cultures of hamster trachea: inhibition by retinyl methyl ether. Science. 1980;207(4428):311–3.
151.\Coin PG, Osornio-Vargas AR, Roggli VL, Brody AR. Pulmonary brogenesis after three consecutive inhalation exposures to chrysotile asbestos. Am J Respir Crit Care Med. 1996;154(5):1511–9.
152.\Lemaire I, Beaudoin H, Dubois C. Cytokine regulation of lungbroblast proliferation. Pulmonary and systemic changes in asbestos-induced pulmonary brosis. Am Rev Respir Dis. 1986;134(4):653–8.
153.\Rom WN, Travis WD, Brody AR. Cellular and molecular basis of the asbestos-related diseases. Am Rev Respir Dis. 1991;143(2):408–22.
154.\Dostert C, Petrilli V, Van Bruggen R, Steele C, Mossman BT, Tschopp J. Innate immune activation through Nalp3 infammasome sensing of asbestos and silica. Science. 2008;320(5876):674–7.
155.\Gasse P, Mary C, Guenon I, Noulin N, Charron S, Schnyder- Candrian S, et al. IL-1R1/MyD88 signaling and the infammasome are essential in pulmonary infammation and brosis in mice. J Clin Invest. 2007;117(12):3786–99.
156.\Keskitalo E, Varis L, Bloigu R, Kaarteenaho R. Bronchoalveolar cell differential count and the number of asbestos bodies correlate with survival in patients with asbestosis. Occup Environ Med. 2019;76(10):765–71.
157.\Craighead JE, Abraham JL, Churg A, Green FH, Kleinerman J, Pratt PC, 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):544–96.
158.\Kawabata Y, Kasai T, Kobashi Y, Kawahara K, Uekusa T, Kurashima K, et al. Grade 4 asbestosis does not extend directly from the respiratory bronchiole to the peripheral lung. Histopathology. 2018;73(1):29–37.
159.\Copley SJ, Wells AU, Sivakumaran P, Rubens MB, Lee YC, Desai SR, et al. Asbestosis and idiopathic pulmonary brosis: comparison of thin-section CT features. Radiology. 2003;229(3): 731–6.
160.\Kishimoto T, Kato K, Arakawa H, Ashizawa K, Inai K, Takeshima Y. Clinical, radiological, and pathological investigation of asbestosis. Int J Environ Res Public Health. 2011;8(3):899–912.
161.\Gevenois PA, de Maertelaer V, Madani A, Winant C, Sergent G, De Vuyst P. Asbestosis, pleural plaques and diffuse pleural thickening: three distinct benign responses to asbestos exposure. Eur Respir J. 1998;11(5):1021–7.
162.\Roach HD, Davies GJ, Attanoos R, Crane M, Adams H, Phillips S. Asbestos: when the dust settles an imaging review of asbestos- related disease. Radiographics. 2002;22:S167–84.
163.\Lynch DA, Gamsu G, Aberle DR. Conventional and high resolution computed tomography in the diagnosis of asbestos-related diseases. Radiographics. 1989;9(3):523–51.
164.\De Vuyst P, Dumortier P, Moulin E, Yourassowsky N, Yernault JC. Diagnostic value of asbestos bodies in bronchoalveolar lavage
fuid. Am Rev Respir Dis. 1987;136(5):1219–24. |
|
165.\Dodson RF, Williams MG Jr, Corn |
CJ, Brollo A, Bianchi |
C. Asbestos content of lung tissue, |
lymph nodes, and pleu- |
ral plaques from former shipyard workers. Am Rev Respir Dis. |
|
1990;142(4):843–7. |
|
166.\Karjalainen A, Piipari R, Mantyla T, Monkkonen M, Nurminen M, Tukiainen P, et al. Asbestos bodies in bronchoalveolar lavage in relation to asbestos bodies and asbestos bres in lung parenchyma. Eur Respir J. 1996;9(5):1000–5.
167.\Dumortier P, Thimpont J, de Maertelaer V, De Vuyst P. Trends in asbestos body counts in bronchoalveolar lavage fuid over two decades. Eur Respir J. 2003;22(3):519–24.
168.\Miller A, Lilis R, Godbold J, Chan E, Selikoff IJ. Relationship of pulmonary function to radiographic interstitial brosis in 2,611 long-term asbestos insulators. An assessment of the International Labour Of ce profusion score. Am Rev Respir Dis. 1992;145(2 Pt 1):263–70.
169.\Barnikel M, Million PM, Knoop H, Behr J. The natural course of lung function decline in asbestos exposed subjects with pleural plaques and asbestosis. Respir Med. 2019;154:82–5.
170.\Copes R, Thomas D, Becklake MR. Temporal patterns of exposure and nonmalignant pulmonary abnormality in Quebec chrysotile workers. Arch Environ Health. 1985;40(2):80–7.
171.\Becklake MR, Bagatin E, Neder JA. Asbestos-related diseases of the lungs and pleura: uses, trends and management over the last century. Int J Tuberc Lung Dis. 2007;11(4):356–69.
172.\Rytz F, Alexander P, Sabina B, Thomas G, Manuela F-C. Pirfenidone as a treatment for asbestos-related lung brosis? A retrospective case series. ERJ. 2018;52(suppl 62):PA2993.
173.\Tran CL, Buchanan D, Cullen RT, Searl A, Jones AD, Donaldson K. Inhalation of poorly soluble particles. II. Infuence Of particle surface area on infammation and clearance. Inhal Toxicol. 2000;12(12):1113–26.
174.\Nel A, Xia T, Madler L, Li N. Toxic potential of materials at the nanolevel. Science. 2006;311(5761):622–7.
175.\Shvedova AA, Kisin ER, Mercer R, Murray AR, Johnson VJ, Potapovich AI, et al. Unusual infammatory and brogenic pulmonary responses to single-walled carbon nanotubes in mice. Am J Physiol Lung Cell Mol Physiol. 2005;289(5):L698–708.
176.\Lam CW, James JT, McCluskey R, Hunter RL. Pulmonary toxicity of single-wall carbon nanotubes in mice 7 and 90 days after intratracheal instillation. Toxicol Sci. 2004;77(1):126–34.
177.\Bonner JC, Rice AB, Moomaw CR, Morgan DL. Airway brosis in rats induced by vanadium pentoxide. Am J Physiol Lung Cell Mol Physiol. 2000;278(1):L209–16.
178.\Bermudez E, Mangum JB, Wong BA, Asgharian B, Hext PM, Warheit DB, et al. Pulmonary responses of mice, rats, and hamsters to subchronic inhalation of ultra ne titanium dioxide particles. Toxicol Sci. 2004;77(2):347–57.
179.\Cho WS, Duf n R, Bradley M, Megson IL, Macnee W, Howie SE, et al. NiO and Co3O4 nanoparticles induce lung DTH- like responses and alveolar lipoproteinosis. Eur Respir J. 2012;39(3):546–57.
180.\Song Y, Li X, Du X. Exposure to nanoparticles is related to pleural effusion, pulmonary brosis and granuloma. Eur Respir J. 2009;34(3):559–67.
181.\Brain JD, Kreyling W, Gehr P. To the editors: express concern about the recent paper by Song et al. Eur Respir J. 2010;35(1):226–7.
37 Interstitial Lung Diseases of Occupational Origin |
667 |
|
|
182.\Ferri C, Artoni E, Sighinol GL, Luppi F, Zelent G, Colaci M, et al. High serum levels of silica nanoparticles in systemic sclerosis patients with occupational exposure: Possible pathogenetic role in disease phenotypes. Semin Arthritis Rheum. 2018;48(3):475–81.
183.\Ogami A, Yamamoto K, Morimoto Y, Fujita K, Hirohashi M, Oyabu T, et al. Pathological features of rat lung following inhalation and intratracheal instillation of C(60) fullerene. Inhal Toxicol. 2011;23(7):407–16.
184.\Shinohara N, Gamo M, Nakanishi J. Fullerene c60: inhalation hazard assessment and derivation of a period-limited acceptable exposure level. Toxicol Sci. 2011;123(2):576–89.
185.\Bonner JC. Nanoparticles as a potential cause of pleural and interstitial lung disease. Proc Am Thorac Soc. 2010;7(2):138–41.
186.\Buerke U, Schneider J, Rosler J, Woitowitz HJ. Interstitial pulmonary brosis after severe exposure to welding fumes. Am J Ind Med. 2002;41(4):259–68.
187.\Mehrifar Y, Zamanian Z, Pirami H. Respiratory Exposure to Toxic Gases and Metal Fumes Produced by Welding Processes and Pulmonary Function Tests. Int J Occup Environ Med. 2019;10(1):40–9.
188.\Koh DH, Kim JI, Kim KH, Yoo SW. Korea Welders Cohort G. Welding fume exposure and chronic obstructive pulmonary disease in welders. Occup Med (Lond). 2015;65(1):72–7.
189.\Roach LL. The Relationship of Welding Fume Exposure, Smoking, and Pulmonary Function in Welders. Workplace Health Saf. 2018;66(1):34–40.
190.\Cosgrove MP. Pulmonary brosis and exposure to steel welding fume. Occup Med (Lond). 2015;65(9):706–12.
191.\Leso V, Vetrani I, Della Volpe I, Nocera C, Iavicoli I. Welding fume exposure and epigenetic alterations: a systematic review. Int J Environ Res Public Health. 2019;16(10):1745.
192.\Shen S, Zhang R, Zhang J, Wei Y, Guo Y, Su L, et al. Welding fume exposure is associated with infammation: a global metabolomics pro ling study. Environ Health. 2018;17(1):68.
193.\Muller KM, Verhoff MA. lGradation of sideropneumoconiosis. Pneumologie. 2000;54(8):315–7.
194.\Kreiss K, Gomaa A, Kullman G, Fedan K, Simoes EJ, Enright PL. Clinical bronchiolitis obliterans in workers at a microwave- popcorn plant. N Engl J Med. 2002;347(5):330–8.
195.\Starek-Swiechowicz B, Starek A. Diacetyl exposure as a pneumotoxic factor: a review. Rocz Panstw Zakl Hig. 2014;65(2):87–92.
196.\Kreisel D, Gelman AE, Palmer SM. In pursuit of new experimental models of obliterative bronchiolitis. Am J Transplant. 2011;11(5):882–3.
197.\Morgan DL, Jokinen MP, Price HC, Gwinn WM, Palmer SM, Flake GP. Bronchial and bronchiolar brosis in rats exposed to 2,3-pentanedione vapors: implications for bronchiolitis obliterans in humans. Toxicol Pathol. 2012;40(3):448–65.
198.\Palmer SM, Flake GP, Kelly FL, Zhang HL, Nugent JL, Kirby PJ, et al. Severe airway epithelial injury, aberrant repair and bronchiolitis obliterans develops after diacetyl instillation in rats. PLoS One. 2011;6(3):e17644.
199.\Cox CW, Rose CS, Lynch DA. State of the art: Imaging of occupational lung disease. Radiology. 2014;270(3):681–96.
200.\Cavalcanti Zdo R, Albuquerque Filho AP, Pereira CA, Coletta EN. Bronchiolitis associated with exposure to arti cial butter favoring in workers at a cookie factory in Brazil. J Bras Pneumol. 2012;38(3):395–9.
201.\Pierce JS, Abelmann A, Spicer LJ, Adams RE, Finley BL. Diacetyl and 2,3-pentanedione exposures associated with cigarette smoking: implications for risk assessment of food and favoring workers. Crit Rev Toxicol. 2014;44(5):420–35.
202.\Cummings KJ, Boylstein RJ, Stanton ML, Piacitelli CA, Edwards NT, LeBouf RF, et al. Respiratory symptoms and lung function abnormalities related to work at a favouring manufacturing facility. Occup Environ Med. 2014;71(8):549–54.
203.\Kreiss K, Fedan KB, Nasrullah M, Kim TJ, Materna BL, Prudhomme JC, et al. Longitudinal lung function declines among California favoring manufacturing workers. Am J Ind Med. 2012;55(8):657–68.
204.\Bailey RL, Cox-Ganser JM, Duling MG, LeBouf RF, Martin SB Jr, Bledsoe TA, et al. Respiratory morbidity in a coffee processing workplace with sentinel obliterative bronchiolitis cases. Am J Ind Med. 2015;58(12):1235–45.
205.\Hirst DV, Dunn KH, Shulman SA, Hammond DR, Sestito N. Evaluation of engineering controls for the mixing of favorings containing diacetyl and other volatile ingredients. J Occup Environ Hyg. 2014;11(10):680–7.
206.\Barrington-Trimis JL, Samet JM, McConnell R. Flavorings in electronic cigarettes: an unrecognized respiratory health hazard? JAMA. 2014;312(23):2493–4.
207.\Farsalinos KE, Kistler KA, Gillman G, Voudris V. Evaluation of electronic cigarette liquids and aerosol for the presence of selected inhalation toxins. Nicotine Tob Res. 2015;17(2):168–74.
208.\Krefft S, Wolff J, Rose C. Silicosis: an update and guide for clinicians. Clin Chest Med. 2020;41(4):709–22.
209.\Bang KM, Att eld MD, Wood JM, Syamlal G. National trends in silicosis mortality in the United States, 1981–2004. Am J Ind Med. 2008;51(9):633–9.
210.\Linch KD, Miller WE, Althouse RB, Groce DW, Hale JM. Surveillance of respirable crystalline silica dust using OSHA compliance data (1979–1995). Am J Ind Med. 1998;34(6):547–58.
211.\Mazurek JM, Att eld MD. Silicosis mortality among young adults in the United States, 1968–2004. Am J Ind Med. 2008;51(8):568–78.
212.\Rosenman KD, Reilly MJ, Henneberger PK. Estimating the total number of newly-recognized silicosis cases in the United States. Am J Ind Med. 2003;44(2):141–7.
213.\Akgun M, Araz O, Akkurt I, Eroglu A, Alper F, Saglam L, et al. An epidemic of silicosis among former denim sandblasters. Eur Respir J. 2008;32(5):1295–303.
214.\Alper F, Akgun M, Onbas O, Araz O. CT ndings in silicosis due to denim sandblasting. Eur Radiol. 2008;18(12):2739–44.
215.\Carneiro AP, Barreto SM, Siqueira AL, Cavariani F, Forastiere F. Continued exposure to silica after diagnosis of silicosis in Brazilian gold miners. Am J Ind Med. 2006;49(10):811–8.
216.\Nelson G, Girdler-Brown B, Ndlovu N, Murray J. Three decades of silicosis: disease trends at autopsy in South African gold miners. Environ Health Perspect. 2010;118(3):421–6.
217.\Tse LA, Li ZM, Wong TW, Fu ZM, Yu IT. High prevalence of accelerated silicosis among gold miners in Jiangxi, China. Am J Ind Med. 2007;50(12):876–80.
218.\Tse LA, Yu IT, Leung CC, Tam W, Wong TW. Mortality from non-malignant respiratory diseases among people with silicosis in Hong Kong: exposure-response analyses for exposure to silica dust. Occup Environ Med. 2007;64(2):87–92.
219.\Norboo T, Angchuk PT, Yahya M, Kamat SR, Pooley FD, Corrin B, et al. Silicosis in a Himalayan village population: role of environmental dust. Thorax. 1991;46(5):341–3.
220.\Hedlund U, Jonsson H, Eriksson K, Jarvholm B. Exposure- response of silicosis mortality in Swedish iron ore miners. Ann Occup Hyg. 2008;52(1):3–7.
221.\Nagelschmidt G. The relation between lung dust and lung pathology in pneumoconiosis. Br J Ind Med. 1960;17:247–59.
222.\t’Mannetje A, Steenland K, Att eld M, Boffetta P, Checkoway H, DeKlerk N, et al. Exposure-response analysis and risk assessment for silica and silicosis mortality in a pooled analysis of six cohorts. Occup Environ Med. 2002;59(11):723–8.
223.\Cassel SL, Eisenbarth SC, Iyer SS, Sadler JJ, Colegio OR, Tephly LA, et al. The Nalp3 infammasome is essential for the development of silicosis. Proc Natl Acad Sci U S A. 2008;105(26): 9035–40.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
668 |
A. Prasse et al. |
|
|
224.\Fubini B, Hubbard A. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation by silica in infammation andbrosis. Free Radic Biol Med. 2003;34(12):1507–16.
225.\Vallyathan V, Shi XL, Dalal NS, Irr W, Castranova V. Generation of free radicals from freshly fractured silica dust. Potential role in acute silica-induced lung injury. Am Rev Respir Dis. 1988;138(5):1213–9.
226.\Kennedy MC. Aluminium powder inhalations in the treatment of silicosis of pottery workers and pneumoconiosis of coal-miners. Br J Ind Med. 1956;13(2):85–101.
227.\Sharma SK, Pande JN, Verma K. Effect of prednisolone treatment in chronic silicosis. Am Rev Respir Dis. 1991;143(4 Pt 1):814–21.
228.\Wilt JL, Banks DE, Weissman DN, Parker JE, Vallyathan V, Castranova V, et al. Reduction of lung dust burden in pneumoconiosis by whole-lung lavage. J Occup Environ Med. 1996;38(6):619–24.
229.\Barnes H, Goh NSL, Leong TL, Hoy R. Silica-associated lung disease: An old-world exposure in modern industries. Respirology. 2019;24(12):1165–75.
230.\Sherson D. Silicosis in the twenty rst century. Occup Environ Med. 2002;59(11):721–2.
231.\Bakan ND, Ozkan G, Camsari G, Gur A, Bayram M, Acikmese B, et al. Silicosis in denim sandblasters. Chest. 2011;140(5):1300–4.
232.\Sahbaz S, Inonu H, Ocal S, Yilmaz A, Pazarli C, Yeginsu A, et al. Denim sandblasting and silicosis two new subsequent cases in Turkey. Tuberk Toraks. 2007;55(1):87–91.
233.\Hassani E, Bagheri M, Rad IA, Mohebbi I. Association between SNPs at IL-17A and IL-17F and susceptibility to accelerated silicosis. Toxicol Ind Health. 2017;33(9):673–80.
234.\Mohebbi I, Zubeyri T. Radiological progression and mortality among silica four packers: a longitudinal study. Inhal Toxicol. 2007;19(12):1011–7.
235.\Hoy RF, Baird T, Hammerschlag G, Hart D, Johnson AR, King P, et al. Arti cial stone-associated silicosis: a rapidly emerging occupational lung disease. Occup Environ Med. 2018;75(1):3–5.
236.\Kramer MR, Blanc PD, Fireman E, Amital A, Guber A, Rhahman NA, et al. Arti cial stone silicosis [corrected]: disease resurgence among arti cial stone workers. Chest. 2012;142(2):419–24.
237.\Perez-Alonso A, Cordoba-Dona JA, Millares-Lorenzo JL, Figueroa-Murillo E, Garcia-Vadillo C, Romero-Morillos J. Outbreak of silicosis in Spanish quartz conglomerate workers. Int J Occup Environ Health. 2014;20(1):26–32.
238.\Glazer CS, Maier L. Occupational interstitial lung disease. ERS Monograph. 2009:265–86.
239.\Greenberg MI, Waksman J, Curtis J. Silicosis: a review. Dis Mon. 2007;53(8):394–416.
240.\Arakawa H, Johkoh T, Honma K, Saito Y, Fukushima Y, Shida H, et al. Chronic interstitial pneumonia in silicosis and mix-dust pneumoconiosis: its prevalence and comparison of CT ndings with idiopathic pulmonary brosis. Chest. 2007;131(6):1870–6.
241.\Antao VC, Pinheiro GA, Terra-Filho M, Kavakama J, Muller NL. High-resolution CT in silicosis: correlation with radiographicndings and functional impairment. J Comput Assist Tomogr. 2005;29(3):350–6.
242.\ILO. Guidelines for the Use of the ILO International Classi cation of Radiographs of Pneumoconioses, revised Edition 2011. Geneva, Switzerland: International Labour Of ce; 2011.
243.\Lopes AJ, Mogami R, Capone D, Tessarollo B, de Melo PL, Jansen JM. High-resolution computed tomography in silicosis: correlation with chest radiography and pulmonary function tests. J Bras Pneumol. 2008;34(5):264–72.
244.\Mosiewicz J, Myslinski W, Zlomaniec G, Czabak-Garbacz R, Krupski W, Dzida G. Diagnostic value of high resolution computed tomography in the assessment of nodular changes in pneu-
moconiosis in foundry workers in Lublin. Ann Agric Environ Med. 2004;11(2):279–84.
245.\Sun J, Weng D, Jin C, Yan B, Xu G, Jin B, 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):400–5.
246.\Law YW, Leung MC, Leung CC, Yu TS, Tam CM. Characteristics of workers attending the pneumoconiosis clinic for silicosis assessment in Hong Kong: retrospective study. Hong Kong Med J. 2001;7(4):343–9.
247.\Leung CC, Chang KC, Law WS, Yew WW, Tam CM, Chan CK, et al. Determinants of spirometric abnormalities among silicotic patients in Hong Kong. Occup Med (Lond). 2005;55(6):490–3.
248.\Rosenman KD, Reilly MJ, Gardiner J. Results of spirometry among individuals in a silicosis registry. J Occup Environ Med. 2010;52(12):1173–8.
249.\Gibbs A, RaW JC. Diseases due to Silica. Pathology of occupational lung disease. 2nd ed; 1998. p. 209–34.
250.\Lee HS, Phoon WH, Ng TP. Radiological progression and its predictive risk factors in silicosis. Occup Environ Med. 2001;58(7):467–71.
251.\Yang H, Yang L, Zhang J, Chen J. Natural course of silicosis in dust-exposed workers. J Huazhong Univ Sci Technolog Med Sci. 2006;26(2):257–60.
252.\Ng TP, Chan SL, Lam KP. Radiological progression and lung function in silicosis: a ten year follow up study. Br Med J (Clin Res Ed). 1987;295(6591):164–8.
253.\Chong S, Lee KS, Chung MJ, Han J, Kwon OJ, Kim TS. Pneumoconiosis: comparison of imaging and pathologic ndings. Radiographics. 2006;26(1):59–77.
254.\Seaton A, Cherrie JW. Quartz exposures and severe silicosis: a role for the hilar nodes. Occup Environ Med. 1998;55(6):383–6.
255.\Hutyrova B, Smolkova P, Nakladalova M, Tichy T, Kolek V. Case of accelerated silicosis in a sandblaster. Ind Health. 2015;53(2):178–83.
256.\Moreira VB, Ferreira AS, Soares PJ, Gabetto JM, Rodrigues CC. The role of bronchoalveolar lavage in quantifying inhaled particles in silicosis. Rev Port Pneumol. 2005;11(5):457–75.
257.\Sharma SK, Pande JN, Verma K. Bronchoalveolar lavage fuid (BALF) analysis in silicosis. Indian J Chest Dis Allied Sci. 1988;30(4):257–61.
258.\Zhai R, Ge X, Li H, Tang Z, Liao R, Kleinjans J. Differences in cellular and infammatory cytokine pro les in the bronchoalveolar lavage fuid in bagassosis and silicosis. Am J Ind Med. 2004;46(4):338–44.
259.\Ozmen CA, Nazaroglu H, Yildiz T, Bayrak AH, Senturk S, Ates G, et al. MDCT ndings of denim-sandblasting-induced silicosis: a cross-sectional study. Environ Health. 2010;9:17.
260.\Perret JL, Plush B, Lachapelle P, Hinks TS, Walter C, Clarke P, et al. Coal mine dust lung disease in the modern era. Respirology. 2017;22(4):662–70.
261.\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):1178–85.
262.\Laney AS, Att eld MD. Coal workers' pneumoconiosis and progressive massive brosis are increasingly more prevalent among workers in small underground coal mines in the United States. Occup Environ Med. 2010;67(6):428–31.
263.\Suarthana E, Laney AS, Storey E, Hale JM, Att eld MD. Coal workers' pneumoconiosis in the United States: regional differences 40 years after implementation of the 1969 Federal Coal Mine Health and Safety Act. Occup Environ Med. 2011;68(12):908–13.
264.\Ross MH, Murray J. Occupational respiratory disease in mining. Occup Med (Lond). 2004;54(5):304–10.
37 Interstitial Lung Diseases of Occupational Origin |
669 |
|
|
265.\Mo J, Wang L, Au W, Su M. Prevalence of coal workers' pneumoconiosis in China: a systematic analysis of 2001-2011 studies. Int J Hyg Environ Health. 2014;217(1):46–51.
266.\Ates I, Yucesoy B, Yucel A, Suzen SH, Karakas Y, Karakaya A. Possible effect of gene polymorphisms on the release of TNFalpha and IL1 cytokines in coal workers' pneumoconiosis. Exp Toxicol Pathol. 2011;63(1-2):175–9.
267.\Hu W, Zhang Q, Su WC, Feng Z, Rom W, Chen LC, et al. Gene expression of primary human bronchial epithelial cells in response to coal dusts with different prevalence of coal workers' pneumoconiosis. J Toxicol Environ Health A. 2003;66(13):1249–65.
268.\Ulker O, Yucesoy B, Demir O, Tekin I, Karakaya A. Serum and BAL cytokine and antioxidant enzyme levels at different stages of pneumoconiosis in coal workers. Hum Exp Toxicol. 2008;27(12):871–7.
269.\Altin R, Armutcu F, Kart L, Gurel A, Savranlar A, Ozdemir H. Antioxidant response at early stages and low grades of simple coal worker's pneumoconiosis diagnosed by high resolution computed tomography. Int J Hyg Environ Health. 2004;207(5):455–62.
270.\Huang C, Li J, Zhang Q, Huang X. Role of bioavailable iron in coal dust-induced activation of activator protein-1 and nuclear factor of activated T cells: difference between Pennsylvania and Utah coal dusts. Am J Respir Cell Mol Biol. 2002;27(5):568–74.
271.\Huang X, Fournier J, Koenig K, Chen LC. Buffering capacity of coal and its acid-soluble Fe2+ content: possible role in coal workers' pneumoconiosis. Chem Res Toxicol. 1998;11(7):722–9.
272.\Pathology standards for coal workers' pneumoconiosis. Report of the Pneumoconiosis Committee of the College of American Pathologists to the National Institute for Occupational Safety and Health. Arch Pathol Lab Med. 1979;103(8):375–432.
273.\Kuempel ED, Stayner LT, Att eld MD, Buncher CR. Exposure- response analysis of mortality among coal miners in the United States. Am J Ind Med. 1995;28(2):167–84.
274.\Ruckley VA, Gauld SJ, Chapman JS, Davis JM, Douglas AN, Fernie JM, et al. Emphysema and dust exposure in a group of coal workers. Am Rev Respir Dis. 1984;129(4):528–32.
275.\Seixas NS, Robins TG, Att eld MD, Moulton LH. Exposure- response relationships for coal mine dust and obstructive lung disease following enactment of the Federal Coal Mine Health and Safety Act of 1969. Am J Ind Med. 1992;21(5):715–34.
276.\Seixas NS, Robins TG,Att eld MD, Moulton LH. Longitudinal and cross sectional analyses of exposure to coal mine dust and pulmonary function in new miners. Br J Ind Med. 1993;50(10):929–37.
277.\Wang ML, Wu ZE, Du QG, Petsonk EL, Peng KL, Li YD, et al. A prospective cohort study among new Chinese coal miners: the early pattern of lung function change. Occup Environ Med. 2005;62(11):800–5.
278.\Att eld MD. Longitudinal decline in FEV1 in United States coalminers. Thorax. 1985;40(2):132–7.
279.\Miller BG, MacCalman L. Cause-speci c mortality in British coal workers and exposure to respirable dust and quartz. Occup Environ Med. 2010;67(4):270–6.
280.\Laney AS, Petsonk EL. Small pneumoconiotic opacities on U.S. coal worker surveillance chest radiographs are not predominantly in the upper lung zones. Am J Ind Med. 2012;55(9):793–8.
281.\Cockcroft A, Lyons JP, Andersson N, Saunders MJ. Prevalence and relation to underground exposure of radiological irregular opacities in South Wales coal workers with pneumoconiosis. Br J Ind Med. 1983;40(2):169–72.
282.\Collins HP, Dick JA, Bennett JG, Pern PO, Rickards MA, Thomas DJ, et al. Irregularly shaped small shadows on chest radiographs, dust exposure, and lung function in coalworkers' pneumoconiosis. Br J Ind Med. 1988;45(1):43–55.
283.\Antao VC, Petsonk EL, Sokolow LZ, Wolfe AL, Pinheiro GA, Hale JM, et al. Rapidly progressive coal workers' pneumoconiosis in the United States: geographic clustering and other factors. Occup Environ Med. 2005;62(10):670–4.
284.\Cockcroft AE, Wagner JC, Seal EM, Lyons JP, Campbell MJ. Irregular opacities in coalworkers' pneumoconiosis--corre- lation with pulmonary function and pathology. Ann Occup Hyg. 1982;26(1-4):767–87.
285.\Laney AS, Weissman DN. Respiratory diseases caused by coal mine dust. J Occup Environ Med. 2014;56(Suppl 10):S18–22.
286.\Stansbury RC, Beeckman-Wagner LA, Wang ML, Hogg JP, Petsonk EL. Rapid decline in lung function in coal miners: evidence of disease in small airways. Am J Ind Med. 2013;56(9):1107–12.
287.\Brichet A, Tonnel AB, Brambilla E, Devouassoux G, Remy-Jardin M, Copin MC, et al. Chronic interstitial pneumonia with honeycombing in coal workers. Sarcoidosis Vasc Diffuse Lung Dis. 2002;19(3):211–9.
288.\Cockcroft A, Berry G, Cotes JE, Lyons JP. Shape of small opacities and lung function in coalworkers. Thorax. 1982;37(10):765–9.
289.\Thrumurthy SG, Kearney S, Sissons M, HaiderY. Diffuse interlobular septal thickening in a coal miner. Thorax. 2010;65(1):82–4.
290.\Go LH, Krefft SD, Cohen RA, Rose CS. Lung disease and coal mining: what pulmonologists need to know. Curr Opin Pulm Med. 2016;22(2):170–8.
291.\Han L, Han R, Ji X, Wang T, Yang J, Yuan J, et al. Prevalence Characteristics of Coal Workers' Pneumoconiosis (CWP) in a State-Owned Mine in Eastern China. Int J Environ Res Public Health. 2015;12(7):7856–67.
292.\Xia Y, Liu J, Shi T, Xiang H, Bi Y. Prevalence of pneumoconiosis in Hubei, China from 2008 to 2013. Int J Environ Res Public Health. 2014;11(9):8612–21.
293.\Leonard R, Zul kar R, Stansbury R. Coal mining and lung disease in the 21st century. Curr Opin Pulm Med. 2020;26(2):135–41.
294.\Hoy RF, Brims F. Occupational lung diseases in Australia. Med J Aust. 2017;207(10):443–8.
295.\Angus DC, Derde L, Al-Beidh F, Annane D, Arabi Y, Beane A, et al. Effect of Hydrocortisone on Mortality and Organ Support in Patients With Severe COVID-19: The REMAP-CAP COVID-19 Corticosteroid Domain Randomized Clinical Trial. JAMA. 2020;324(13):1317–29.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/