Silicosis natural history, complications and prognosis: Difference between revisions
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{{Silicosis}} | {{Silicosis}} | ||
==Natural history== | ==Natural history== | ||
Silicosis develops very slowly in most cases. Often decades elapse in progression to clinical disease from the beginning. Usually starts as Simple silicosis and progress further after not less than 10 years of exposure to silica. Accelerated silicosis is a variant of silicosis occurred due to intense exposure to silica for 5-10years. | Silicosis develops very slowly in most cases. Often decades elapse in progression to clinical disease from the beginning. Usually starts as Simple silicosis and progress further after not less than 10 years of exposure to silica. Accelerated silicosis is a variant of silicosis occurred due to intense exposure to silica for 5-10years. All forms of silicosis can progress in the absence of continued exposure. | ||
All forms of silicosis can progress in the absence of continued exposure. | |||
==Complications== | ==Complications== | ||
===Tuberculosis=== | ===Tuberculosis=== | ||
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*Silica exposure effects are not just limited to the lungs, it also has a relationship with some rheumatic diseases, such as [[rheumatoid arthritis]] (RA) , [[scleroderma]] , [[systemic lupus erythematosus]] , [[Wegener’s granulomatosis]] and [[polyarteritis nodosa]]<ref name="pmid10741776">{{cite journal| author=De Vuyst P, Camus P| title=The past and present of pneumoconioses. | journal=Curr Opin Pulm Med | year= 2000 | volume= 6 | issue= 2 | pages= 151-6 | pmid=10741776 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10741776 }} </ref> | *Silica exposure effects are not just limited to the lungs, it also has a relationship with some rheumatic diseases, such as [[rheumatoid arthritis]] (RA) , [[scleroderma]] , [[systemic lupus erythematosus]] , [[Wegener’s granulomatosis]] and [[polyarteritis nodosa]]<ref name="pmid10741776">{{cite journal| author=De Vuyst P, Camus P| title=The past and present of pneumoconioses. | journal=Curr Opin Pulm Med | year= 2000 | volume= 6 | issue= 2 | pages= 151-6 | pmid=10741776 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10741776 }} </ref> | ||
*The association with [[scleroderma]] and silicosis is known as [[Erasmus syndrome]] and that with [[rheumatoid arthritis]] is known as [[Caplan’s syndrome]]<ref name="pmid24051915">{{cite journal| author=de Miranda AA, Nascimento AC, Peixoto IL, Scrignoli JA, Cardoso Mdo S, Ribeiro SL| title=Erasmus syndrome: silicosis and systemic sclerosis. | journal=Rev Bras Reumatol | year= 2013 | volume= 53 | issue= 3 | pages= 310-3 | pmid=24051915 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24051915 }} </ref> | *The association with [[scleroderma]] and silicosis is known as [[Erasmus syndrome]] and that with [[rheumatoid arthritis]] is known as [[Caplan’s syndrome]]<ref name="pmid24051915">{{cite journal| author=de Miranda AA, Nascimento AC, Peixoto IL, Scrignoli JA, Cardoso Mdo S, Ribeiro SL| title=Erasmus syndrome: silicosis and systemic sclerosis. | journal=Rev Bras Reumatol | year= 2013 | volume= 53 | issue= 3 | pages= 310-3 | pmid=24051915 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24051915 }} </ref> | ||
==Prognosis== | |||
*Mortality from silicosis in the United States declined from 8.91 deaths per million to 0.66 in the period from 1968 to 2002 [14]. While the number of deaths from silicosis overall has declined since 1968, the number of silicosis-associated deaths reported among persons aged 15 to 44 did not decline substantially prior to 1995 [99]. It is not known to what extent deaths among younger workers were caused by acute or accelerated forms of silicosis. | |||
*Silicosis-related deaths among workers of all ages are associated with significant premature mortality [16]. Between 1996 and 2005, 1746 deaths due to silica exposure resulted in 20,234 years of life lost from life expectancy, with an average of 11.6 years of life lost. For the same period, among 307 decedents who died before age 65, or the end of a working life, there were 3045 years of life lost to age 65, with an average of 9.9 years of life lost from a working life | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 15:17, 23 June 2015
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Natural history
Silicosis develops very slowly in most cases. Often decades elapse in progression to clinical disease from the beginning. Usually starts as Simple silicosis and progress further after not less than 10 years of exposure to silica. Accelerated silicosis is a variant of silicosis occurred due to intense exposure to silica for 5-10years. All forms of silicosis can progress in the absence of continued exposure.
Complications
Tuberculosis
- More recent findings show that exposure to silica, even without silicosis, may also predispose individuals to Tuberculosis[1]The increased risk of both pulmonary and extra-pulmonary TB is lifelong even after the exposure ceases[2]. The risk increases with severity of silicosis. Acute and accelerated silicosis are at increased risk compared to simple chronic. The TB rates can be extremely high in silica-exposed groups with high rates of TB and HIV in the community. In many instances, it is the chest radiograph rather than clinical features that gives the first indication of TB in the presence of silicosis.
- Aggressive treatment of active tuberculosis is indicated as high treatment failure and relapse rates were noted due to direct impairment of macrophage function by crystalline silica and poor drug penetration into silicotic lung nodules.
- Screening for latent TB and early treatment with a 9-month course of Isoniazid is recommended in people with silicosis[3]
Mycosis
- Silica-exposed workers (without silicosis) may be at increased risk for fungal infections, as they are for mycobacterial infections as silica dust impairs cellular defense. Aspergillosis was the most common mycosis among persons with pneumoconiosis[4], in which silica-impaired macrophages are incapable of targeting inhaled conidia [5]
- Silica-exposed workers are protected from exposure to fungi by the following measures :
- Wetting soil and bird droppings to suppress fungal-contaminated dust
- Maintaining good personal hygiene; and,
- In areas with endemic inhaled fungi, use enclosed operator cabs with high-efficiency particulate air filtration or personal respiratory protection for particulates.
Pneumothorax
- Spontaneous pneumothorax is a rare pleural complication that can develop in patients with silicosis. Usually in these cases pneumothorax is unilateral and rarely bilateral[6] Many studies state the association of pneumothorax with the presence of bullae [7] and it can also be due to direct toxic injury by silica, products of inflammatory response affect the elastic fibres of the alveolar wall leading to formation of bleb [8]
Lung cancer
- Many Studies are going on to understand the pathogenesis of silicosis causing lung cancer. One study reports the LTB4 dependent inflammation promotes lung tumour growth [10]
Renal disease
- silica-induced nephropathy has been associated with both glomerular and tubular dysfunction. The hypotheses for the pathophysiology of silica’s effect on the kidney include either a direct toxic effect on the kidney or as an adjuvant to enhance an immunologic mechanism[11]
Rheumatic disease
- Silica exposure effects are not just limited to the lungs, it also has a relationship with some rheumatic diseases, such as rheumatoid arthritis (RA) , scleroderma , systemic lupus erythematosus , Wegener’s granulomatosis and polyarteritis nodosa[12]
- The association with scleroderma and silicosis is known as Erasmus syndrome and that with rheumatoid arthritis is known as Caplan’s syndrome[13]
Prognosis
- Mortality from silicosis in the United States declined from 8.91 deaths per million to 0.66 in the period from 1968 to 2002 [14]. While the number of deaths from silicosis overall has declined since 1968, the number of silicosis-associated deaths reported among persons aged 15 to 44 did not decline substantially prior to 1995 [99]. It is not known to what extent deaths among younger workers were caused by acute or accelerated forms of silicosis.
- Silicosis-related deaths among workers of all ages are associated with significant premature mortality [16]. Between 1996 and 2005, 1746 deaths due to silica exposure resulted in 20,234 years of life lost from life expectancy, with an average of 11.6 years of life lost. For the same period, among 307 decedents who died before age 65, or the end of a working life, there were 3045 years of life lost to age 65, with an average of 9.9 years of life lost from a working life
References
- ↑ Cowie RL (1994). "The epidemiology of tuberculosis in gold miners with silicosis". Am J Respir Crit Care Med. 150 (5 Pt 1): 1460–2. doi:10.1164/ajrccm.150.5.7952577. PMID 7952577.
- ↑ Hnizdo E, Murray J (1998). "Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners". Occup Environ Med. 55 (7): 496–502. PMC 1757613. PMID 9816385.
- ↑ "Adverse effects of crystalline silica exposure. American Thoracic Society Committee of the Scientific Assembly on Environmental and Occupational Health". Am J Respir Crit Care Med. 155 (2): 761–8. 1997. doi:10.1164/ajrccm.155.2.9032226. PMID 9032226.
- ↑ Kato T, Usami I, Morita H, Goto M, Hosoda M, Nakamura A; et al. (2002). "Chronic necrotizing pulmonary aspergillosis in pneumoconiosis: clinical and radiologic findings in 10 patients". Chest. 121 (1): 118–27. PMID 11796440.
- ↑ Segal BH (2007). "Role of macrophages in host defense against aspergillosis and strategies for immune augmentation". Oncologist. 12 Suppl 2: 7–13. doi:10.1634/theoncologist.12-S2-7. PMID 18039634.
- ↑ Mishra P, Jacob SE, Basu D, Panigrahi MK, Govindaraj V (2014). "Bilateral spontaneous pneumothorax in chronic silicosis: a case report". Case Rep Pathol. 2014: 561861. doi:10.1155/2014/561861. PMC 3976776. PMID 24744938.
- ↑ Mohebbi I, Hassani E, Salarilak S, Bahrami AR (2007). "Do bullae and emphysema increase risk of pneumothorax in silicosis?". J Occup Med Toxicol. 2: 8. doi:10.1186/1745-6673-2-8. PMC 2071907. PMID 17868470.
- ↑ Gupta KB, Manchanda M, Kaur P (2006). "Bilateral spontaneous pneumothorax in silicosis". Indian J Chest Dis Allied Sci. 48 (3): 201–3. PMID 18610678.
- ↑ Brown T (2009). "Silica exposure, smoking, silicosis and lung cancer--complex interactions". Occup Med (Lond). 59 (2): 89–95. doi:10.1093/occmed/kqn171. PMID 19233828.
- ↑ Satpathy SR, Jala VR, Bodduluri SR, Krishnan E, Hegde B, Hoyle GW; et al. (2015). "Crystalline silica-induced leukotriene B4-dependent inflammation promotes lung tumour growth". Nat Commun. 6: 7064. doi:10.1038/ncomms8064. PMC 4418220. PMID 25923988.
- ↑ Millerick-May ML, Schrauben S, Reilly MJ, Rosenman KD (2015). "Silicosis and chronic renal disease". Am J Ind Med. 58 (7): 730–6. doi:10.1002/ajim.22465. PMID [ 25940153 [ Check
|pmid=value (help). - ↑ De Vuyst P, Camus P (2000). "The past and present of pneumoconioses". Curr Opin Pulm Med. 6 (2): 151–6. PMID 10741776.
- ↑ de Miranda AA, Nascimento AC, Peixoto IL, Scrignoli JA, Cardoso Mdo S, Ribeiro SL (2013). "Erasmus syndrome: silicosis and systemic sclerosis". Rev Bras Reumatol. 53 (3): 310–3. PMID 24051915.