Pneumoconiosis

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Pneumoconiosis
ICD-10 J60-J65
ICD-9 500-505
DiseasesDB 31746
MeSH D011009

Pneumoconiosis Microchapters

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Pneumoconiosis from other Diseases

Epidemiology and Demographics

Risk Factors

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Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

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Electrocardiogram

Chest X Ray

CT

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Echocardiography or Ultrasound

Other Imaging Findings

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Treatment

Medical Therapy

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Future or Investigational Therapies

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Case #1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Historical Perspective

Classification

Pathophysiology

Pneumoconiosis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Pneumoconiosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Pneumoconiosis On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Pneumoconiosis

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Pneumoconiosis

CDC on Pneumoconiosis

Pneumoconiosis in the news

Blogs on Pneumoconiosis

Directions to Hospitals Treating Pneumoconiosis

Risk calculators and risk factors for Pneumoconiosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Karol Gema Hernández, M.D. [3]

Overview

Pneumoconiosis is an interstitial lung disorder caused by the accumulation of different dust particles in the alveolar space. As the particles accumulate, the body's elimination mechanisms begin to fail, resulting in activation of chemotactic factors that exacerbate the inflammatory response, and therefore cause subsequent fibrosis.

Pathophysiology

The pathogenesis of pneumoconiosis starts with the inhalation of mineral, metallic or dust particles. The most common particles that cause pneumoconiosis are:

  • Asbestos
  • Silica (quartz, cristobalite, or tridymite silica polymorphs)
  • Coal


Other dust particles are also cause of pneumoconiosis, such as hydrated magnesium silicate, hydrous aluminium silicate, bauxite, cobalt, beryllium and iron.


Disease Dust
Asbestosis Asbestos
Silicosis Silica
Coal workers’ pneumoconiosis Coal dust
Talcosis Hydrated aluminium silicate
Mixed dust pneumoconiosis Coal dust, smoke from fires, and silicates
Kaolin- induced pneumoconiosis Hydrous aluminum silicate
Aluminum- induced pneumoconiosis Bauxite (Al2O3)
Hard- metal disease (giant cell pneumonitis) Cobalt
Berylliosis Beryllium
Silicosiderosis Silica and iron


The determinants for the rate of disease progression are the accumulative dose; that is based in duration and intensity of exposure, the fiber type and individual susceptibility. Particles reach the terminal bronquioles and start a cellular reaction, which leads to a chronic inflammatory response based on oxidative injury and profibrotic growth factors and cytokines.

In a normal scenario, when the alveolar and interstitial macrophages in the bronquioles engulf the particles, they are eliminated aided by the mucocilliary system, expelled by mucus or through the lymphatic system. When particles increase in number and exposure continues, the elimination mechanism fails and macrophages begin to accumulate and therefore trigger an immune response. The macrophages, especially in perivascular and peribronquiolar regions, are then entrapped by reticulin, which is secreted by fibroblasts. If the macrophages lyse, more reticulin is released, and the response is augmented. As the accumulation increases the alveolar walls either protrude into alveolar spaces or obliterate them. The fibrogenic potential of dust also causes collagen fibers to develop.

Asbestos fibers need to be greater to 3 μm in diameter in order to penetrate the distal lung. Fibers greater than 5 μm are phagocytosed incompletely and retained in tissues who, initiate cellular reaction resulting in fibrogenesis.

The physiology of macrophage activation is subject to several theories. The macrophages are mainly derived by peripheral blood monocytes and, from local replication. The recruitment of monocytes from peripheral blood occurs in response to several chemotactic factors. Boitelle et al [1] suggested that one of the most potent chemotactic factor for peripheral blood monocytes is monocyte chemoattractant protein- 1 (MCP- 1), suggesting its role in chronic macrophagic infammation. MCP- 1 is a 76 amino acid peptide that results from activation by mediators such as TNF- α. MCP- 1 activates monocytes, and also increases their cytostatic activity, their release of lysosomal enzymes and cytokines (IL1, IL6), and monocyte expression of adhesion molecules (CD11c/CD18, CD11b/CD18).

Some studies in bronchoalveolar lavage made by Vanhée et al [2] showed a large influx of mononuclear phagocytes, with the subsecuent production of neutrophil chemotactic factors, fibronectin, and IL6 and TNF α. The alveolar macrophages in coal miners with massive fibrosis, secreted two main profibrotic factors; platelet-derived growth factor (PDGF) and insulin-like growth factor- 1 (IGF-1), whereas, the patients with simple pneumoconiosis secreted transforming- growth factor- β (TGF- β). This suggested a potential protective effect of TGF- β on the development of pulmonary fibrosis.

The risk for pneumoconiosis among constructions workers is evident, but Tjoe et al concluded there is not a clear-cut relationship between exposure and body’s response. This is hard due to the heterogeneity in exposure levels, as well as dust composition and the possible modification of toxicity by other factors present in dust.

References

2

Causes

Differentiating Pneumoconiosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1

Related Chapters

External links

Template:Respiratory pathology Template:SIB de:Pneumokoniose ko:진폐 it:Pneumoconiosi nl:Pneumoconiose sl:Pnevmokonioza sv:Dammlunga uk:Пневмоконіоз


Template:WikiDoc Sources

  1. Boitelle A, Gosset P, Copin MC, Vanhee D, Marquette CH, Wallaert B; et al. (1997). "MCP-1 secretion in lung from nonsmoking patients with coal worker's pneumoconiosis". Eur Respir J. 10 (3): 557–62. PMID 9072984.
  2. Vanhée D, Gosset P, Boitelle A, Wallaert B, Tonnel AB (1995). "Cytokines and cytokine network in silicosis and coal workers' pneumoconiosis". Eur Respir J. 8 (5): 834–42. PMID 7656959.