Occupational lung disease pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Occupational lung diseases include the pneumoconioses (interstitial lung diseases), hypersensitivity pneumonitis, bronchiolitis, byssinosis, and occupational asthma. Pneumoconiosis is an [[interstitial lung disease]] 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 subsequently lead to [[fibrosis]]. Hypersensitivity pneumonitis, bronchiolitis, bysinnosis and occupational asthma are all part of the respiratory systems’ over reactivity towards inhalants. | Occupational lung diseases include the pneumoconioses (interstitial lung diseases), hypersensitivity pneumonitis, bronchiolitis, byssinosis, and occupational asthma. Pneumoconiosis is an [[interstitial lung disease]] 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 subsequently lead to [[fibrosis]]. Hypersensitivity pneumonitis and its subcategories of, bronchiolitis, bysinnosis and occupational asthma are all part of the respiratory systems’ over reactivity towards inhalants. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis of pneumoconioses=== | ||
* The pathogenesis of pneumoconiosis starts with the inhalation of mineral, metallic or dust particles.<ref name="pmid10931786">{{cite journal| author=Castranova V, Vallyathan V| title=Silicosis and coal workers' pneumoconiosis. | journal=Environ Health Perspect | year= 2000 | volume= 108 Suppl 4 | issue= | pages= 675-84 | pmid=10931786 | doi= | pmc=PMC1637684 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10931786 }} </ref><ref>name="pmid9072984">{{cite journal| author=Boitelle A, Gosset P, Copin MC, Vanhee D, Marquette CH, Wallaert B et al.| title=MCP-1 secretion in lung from nonsmoking patients with coal worker's pneumoconiosis. | journal=Eur Respir J | year= 1997 | volume= 10 | issue= 3 | pages= 557-62 | pmid=9072984 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9072984 }} </ref><ref name="pmid7656959">{{cite journal| author=Vanhée D, Gosset P, Boitelle A, Wallaert B, Tonnel AB| title=Cytokines and cytokine network in silicosis and coal workers' pneumoconiosis. | journal=Eur Respir J | year= 1995 | volume= 8 | issue= 5 | pages= 834-42 | pmid=7656959 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7656959 }} </ref> | * The pathogenesis of pneumoconiosis starts with the inhalation of mineral, metallic or dust particles.<ref name="pmid10931786">{{cite journal| author=Castranova V, Vallyathan V| title=Silicosis and coal workers' pneumoconiosis. | journal=Environ Health Perspect | year= 2000 | volume= 108 Suppl 4 | issue= | pages= 675-84 | pmid=10931786 | doi= | pmc=PMC1637684 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10931786 }} </ref><ref>name="pmid9072984">{{cite journal| author=Boitelle A, Gosset P, Copin MC, Vanhee D, Marquette CH, Wallaert B et al.| title=MCP-1 secretion in lung from nonsmoking patients with coal worker's pneumoconiosis. | journal=Eur Respir J | year= 1997 | volume= 10 | issue= 3 | pages= 557-62 | pmid=9072984 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9072984 }} </ref><ref name="pmid7656959">{{cite journal| author=Vanhée D, Gosset P, Boitelle A, Wallaert B, Tonnel AB| title=Cytokines and cytokine network in silicosis and coal workers' pneumoconiosis. | journal=Eur Respir J | year= 1995 | volume= 8 | issue= 5 | pages= 834-42 | pmid=7656959 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7656959 }} </ref> | ||
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* The physiology of macrophage activation is subject to several theories: | * The physiology of macrophage activation is subject to several theories: | ||
** The macrophages are mainly derived from peripheral blood monocytes and, from local replication. | ** The macrophages are mainly derived from peripheral blood monocytes and, from local replication. | ||
** The recruitment of monocytes from peripheral blood occurs in response to several chemotactic factors suggest that one of the most potent chemotactic factors for peripheral blood monocytes is monocyte chemoattractant protein- 1 (MCP- 1), suggesting its role in chronic macrophage inflammation. | ** The recruitment of monocytes from peripheral blood occurs in response to several chemotactic factors suggest that one of the most potent chemotactic factors for peripheral blood monocytes is monocyte chemoattractant protein - 1 (MCP - 1), suggesting its role in chronic macrophage inflammation. | ||
** TNFα activates MCP- 1 expression. MCP-1 is a 76 amino acid peptide that activates monocytes, and also increases its cytostatic activity, and the expression of monocyte adhesion molecules such as CD11c/CD18 and CD11b/CD18. | ** TNFα activates MCP - 1 expression. MCP - 1 is a 76 amino acid peptide that activates monocytes, and also increases its cytostatic activity, and the expression of monocyte adhesion molecules such as CD11c/CD18 and CD11b/CD18. | ||
* As exposure continues, the elimination system begins to fail, leading to release of reactive oxygen species. These in turn exacerbate the inflammatory response, with the release of more cytokines, such as TNF and interleukins, which subsequently lead to fibrogenesis. | * As exposure continues, the elimination system begins to fail, leading to release of reactive oxygen species. These in turn exacerbate the inflammatory response, with the release of more cytokines, such as TNF and interleukins, which subsequently lead to fibrogenesis. | ||
* The determinants for the rate of disease progression are the accumulative dose; that is based on duration and intensity of exposure, the fiber type and individual susceptibility. | * The determinants for the rate of disease progression are the accumulative dose; that is based on duration and intensity of exposure, the fiber type and individual susceptibility. | ||
* The underlying pathogenic mechanisms that lead to pulmonary fibrosis in pneumoconiosis suggest a potential protective effect of TGF- β on the development of pulmonary fibrosis. | * The underlying pathogenic mechanisms that lead to pulmonary fibrosis in pneumoconiosis suggest a potential protective effect of TGF- β on the development of pulmonary fibrosis. | ||
* 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 reinforces that TGF- β has a possible protective effect against the development of pulmonary fibrosis. | * 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 reinforces that TGF- β has a possible protective effect against the development of pulmonary fibrosis. | ||
=== Pathogenesis of hypersensitivity pneumonitis === | |||
* | |||
===Biological Reactivity of Different Dust Particles=== | ===Biological Reactivity of Different Dust Particles=== | ||
Revision as of 15:01, 12 February 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: ;Hadeel Maksoud M.D.[2]
Overview
Occupational lung diseases include the pneumoconioses (interstitial lung diseases), hypersensitivity pneumonitis, bronchiolitis, byssinosis, and occupational asthma. Pneumoconiosis is an interstitial lung disease 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 subsequently lead to fibrosis. Hypersensitivity pneumonitis and its subcategories of, bronchiolitis, bysinnosis and occupational asthma are all part of the respiratory systems’ over reactivity towards inhalants.
Pathophysiology
Pathogenesis of pneumoconioses
- The pathogenesis of pneumoconiosis starts with the inhalation of mineral, metallic or dust particles.[1][2][3]
- The most common particles that cause pneumoconiosis are:
- Asbestos
- Silica (quartz, cristobalite, coesite or tridymite silica polymorphs)
- Structural differences between the polymorphs of silica, are important because of the different degrees of biological reactivity they present, making some of them more toxic than others. The biological reactivity makes quartz more toxic, followed by tridymite, cristobalite, coesite, and finally stishovite.
- Coal
- Other dust particles may also lead to pneumoconiosis, such as hydrated magnesium silicate, hydrous aluminum silicate, bauxite, cobalt, beryllium and iron.
- When particles reach the distal lung, the mucocilliary and lympathic system take care of their elimination.
- Dust fibers must be less than 3 μm in diameter in order to penetrate the distal lung.
- Fibers greater than 5 μm are phagocytosed incompletely and retained in tissues.
- When particles increase in number, macrophages are activated to engulf those particles.
- Reticulin is then secreted by fibroblasts to entrap macrophages, as an attempt to control the excess of dust particles.
- The physiology of macrophage activation is subject to several theories:
- The macrophages are mainly derived from peripheral blood monocytes and, from local replication.
- The recruitment of monocytes from peripheral blood occurs in response to several chemotactic factors suggest that one of the most potent chemotactic factors for peripheral blood monocytes is monocyte chemoattractant protein - 1 (MCP - 1), suggesting its role in chronic macrophage inflammation.
- TNFα activates MCP - 1 expression. MCP - 1 is a 76 amino acid peptide that activates monocytes, and also increases its cytostatic activity, and the expression of monocyte adhesion molecules such as CD11c/CD18 and CD11b/CD18.
- As exposure continues, the elimination system begins to fail, leading to release of reactive oxygen species. These in turn exacerbate the inflammatory response, with the release of more cytokines, such as TNF and interleukins, which subsequently lead to fibrogenesis.
- The determinants for the rate of disease progression are the accumulative dose; that is based on duration and intensity of exposure, the fiber type and individual susceptibility.
- The underlying pathogenic mechanisms that lead to pulmonary fibrosis in pneumoconiosis suggest a potential protective effect of TGF- β on the development of pulmonary fibrosis.
- 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 reinforces that TGF- β has a possible protective effect against the development of pulmonary fibrosis.
Pathogenesis of hypersensitivity pneumonitis
Biological Reactivity of Different Dust Particles
- Each dust particle has a different degree of biological reactivity.
- This variability is due to properties in the surface of the particles.
- In the case of silica, there are two theories explaining their biological reactivity:
- One theory states that silica is a hydrogen donor, whereas biological macromolecules are hydrogen acceptors, creating strong hydrogen bonds that contribute to the damage.
- The second theory states that at a pH of 7.0, silica is negatively charged, and therefore attracts alveolar macrophages, and activates the generation of reactive oxygen species and cytokines.
Shown below is a table summarizing the dust exposure associated with pneumocociosis:
| Disease | Dust |
|---|---|
| Coal workers’ pneumoconiosis | Coal dust |
| Silicosis | Silica |
| Asbestosis | Asbestos |
| Talcosis | Hydrated magnesium silicate |
| Kaolin - induced pneumoconiosis | Hydrous aluminum silicate |
| Mixed dust pneumoconiosis | Coal dust, smoke from fires, and silicates |
| Aluminum - induced pneumoconiosis | Bauxite (Al2O3) |
| Berylliosis | Beryllium |
| Silicosiderosis | Silica and iron |
| Hard - metal disease (giant cell pneumonitis) | Cobalt |
Associated Conditions
- Asthma
- Chronic bronchitis
- Emphysema
- Allergic rhinitis
- Interstitial pulmonary fibrosis
- Hives
- Eczema
- Mesothelioma
- Non-small cell lung cancer
Gross Pathology
- On gross pathology, dilated airways, destruction of lung tissue, and discoloration of lung tissue are characteristic findings of occupational lung disease.
Microscopic Pathology
- On microscopic histopathological analysis, calcification, central necrosis, dense collagen and, sometimes malignant cells are characteristic findings of occupational lung disease.
References
- ↑ Castranova V, Vallyathan V (2000). "Silicosis and coal workers' pneumoconiosis". Environ Health Perspect. 108 Suppl 4: 675–84. PMC 1637684. PMID 10931786.
- ↑ name="pmid9072984">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.
- ↑ 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.