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Editorials |

Can We Alter the Natural History of Silicosis?Silicosis FREE TO VIEW

LTC Daniel E. Banks, MC, USA, FCCP; Surinder K. Jindal, MD, FCCP
Author and Funding Information

From the Department of Medicine (Dr Banks), Uniformed University of the Health Sciences; and Jindal Clinics (Dr Jindal).

CORRESPONDENCE TO: LTC Daniel E. Banks, MC, USA, FCCP, 2478 Stanley Rd, Ft Sam Houston, TX 78234-6120; e-mail: dbanks49@yahoo.com


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(3):574-576. doi:10.1378/chest.15-0591
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In 2007, Akgun and colleagues1 reported on 145 men who sandblasted denim for at least 1 month with a latency period of at least 10 months; 77 (53%) showed silicosis based on accepted diagnostic criteria for silicosis as a profusion category of opacities of 1/0 or greater. Now, these same authors provide a 4-year follow-up of this cohort in this issue of CHEST (see page 647).2 Of the 83 who participated in the follow-up evaluation, nine died (at a mean age of 24 years), and of the remaining 74, 71 (95.9%) had radiographic evidence of silicosis based on the same criteria.

Epidemics of silicosis like the one reported in this issue have been reported throughout the 20th century and in the early years of this century in cultures around the world. In the United States, the number of deaths attributable to silicosis has lessened, but cases persist in the United States and other countries.3-6 It is always difficult to be certain about the true prevalence of this illness in the United States because no organized national morbidity surveillance program for silicosis exists, and mortality surveillance depends on death certificate data that often are inaccurate. Although silicosis has been categorized as an untreatable disease, a great amount of understanding of the pathogenesis of this disease has been gained through lavage and cellular investigations of the lungs in animal models as well as the rare attempt to address the disease in humans. Yet, only limited efforts have been made to develop interventions that challenge the gradual decline in lung function and often early mortality in those with this illness. There is not even an option to provide potentially beneficial compassionate use therapy.

Are there comparable models of interstitial lung diseases where therapies have been tried? The answer is complicated by the different pathogenetic mechanisms leading to interstitial lung disease. Sarcoidosis, although granulomatous like silicosis, often has a variable course (unlike silicosis) yet has been shown to respond to steroid therapy. Idiopathic pulmonary fibrosis, a disease with an expected survival time similar to this population of silicotics, has been the subject of 15 trials suitable for analysis.7 Scleroderma, an interstitial lung disease with primary vascular involvement, has benefited from the initiation of the Scleroderma Patient-Centered Intervention Network8 to identify patients and develop clinical trials. All these diseases, like silicosis, are relatively rare, and in none of the therapeutic trials has there been evidence that the inciting reason for the illness was altered.

In contrast to the efforts expended to develop therapeutic approaches to the aforementioned interstitial lung diseases, efforts to develop treatments for silicosis have been modest. What ideas have been put forth? The Chinese have been the most active in attempting silicosis therapy. They have pioneered the use of whole-lung lavage in the treatment of silicosis, comparing outcomes in patients who underwent this procedure to matched patients who did not.9 After 2 years, respiratory symptoms, the rate of lung function decline, and the rate of progression shown on chest radiograph were less in the patients undergoing lavage. Analysis of the lavagate showed that a substantial amount of dust and number of inflammatory cells can be removed. The authors commented that the approach is practical in both early and accelerated silicosis but should be used cautiously in advanced silicosis. Other reports suggested that steroid therapy can effectively limit progression, but when steroids were tapered, the disease became aggressive and progressed dramatically.10,11

There are opportunities for untested new therapies with the potential to prevent even heavily exposed individuals from progressing to end-stage disease, where lung transplantation becomes the sole therapeutic option. What are these possible therapies? On the basis of our understanding of the pathogenetic mechanisms of silicosis brought to light through animal models, antibodies to tumor necrosis factor-α or its receptor site IL-1 and, to a lesser extent, transforming growth factor-β all have potential therapeutic roles by diminishing inflammatory and fibrotic responses to silica dust. Numerous agents are commercially available. Of course, the physician who prescribes these therapies must recognize that they lessen immunity and may predispose to infection.12 Even if effective therapies can be developed, they will not serve as a replacement for limiting exposures, including removal of affected individuals from additional exposure.

The work of Akgun and colleagues2 has again provided strong evidence of the need to intervene and alter the natural history of silicosis. Clinical trials of these therapies may need to take place outside developed countries because there are fewer cases of silicosis in the United States compared with previously. It is time for us to address this illness in a way that may offer those affected a chance for a better life.

Acknowledgments

Other contributions: The opinions contained in this editorial are the personal views of the authors and are not to be construed as the views of the US Army or Department of Defense.

Akgun M, Araz O, Akkurt I, et al. An epidemic of silicosis among former denim sandblasters. Eur Respir J. 2008;32(5):1295-1303. [CrossRef] [PubMed]
 
Akgun M, Araz O, Ucar EY, et al. Silicosis appears inevitable among former denim sandblasters: a 4-year follow-up study. Chest. 2015;148(3):647-654.
 
Bang KM, Mazurek JM, Wood JM, White GE, Hendricks SA, Weston A. Silicosis mortality trends and new exposures to respirable crystalline silica—United States, 2001–2010. MMWR Morb Mortal Wkly Rep. 2015;64(5):117-120. [PubMed]
 
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):8612-8621. [CrossRef] [PubMed]
 
Churchyard GJ, Ehrlich R, teWaterNaude JM, et al. Silicosis prevalence and exposure-response relations in South African goldminers. Occup Environ Med. 2004;61(10):811-816. [CrossRef] [PubMed]
 
Jindal SK. Silicosis in India: past and present. Curr Opin Pulm Med. 2013;19(2):163-168. [CrossRef] [PubMed]
 
Richeldi L. Clinical trials of investigational agents for IPF: a review of a Cochrane report. Respir Res. 2013;14(suppl 1):S4. [CrossRef] [PubMed]
 
Kwakkenbos L, Jewett LR, Baron M, et al. The Scleroderma Patient-centered Intervention Network (SPIN) Cohort: protocol for a cohort multiple randomised controlled trial (cmRCT) design to support trials of psychosocial and rehabilitation interventions in a rare disease context. BMJ Open. 2013;3(8):e003563. [CrossRef] [PubMed]
 
Zhang YM, Zhang HT, Wang CY, Wang W, Wu J, Wang C. Long-term therapeutic effects of whole lung lavage in the management of silicosis [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2012;30(9):690-693. [PubMed]
 
Sharma SK, Pande JN, Verma K. Effect of prednisolone treatment in chronic silicosis. Am Rev Respir Dis. 1991;143(4 pt 1):814-821. [CrossRef] [PubMed]
 
Goodman GB, Kaplan PD, Stachura I, Castranova V, Pailes WH, Lapp NL. Acute silicosis responding to corticosteroid therapy. Chest. 1992;101(2):366-370. [CrossRef] [PubMed]
 
Jalloul A, Banks DE. Can we translate our understanding of the pathogenic mechanisms of silicosis into a therapeutic plan? Clin Pulm Med. 2010;17(6):266-275. [CrossRef]
 

Figures

Tables

References

Akgun M, Araz O, Akkurt I, et al. An epidemic of silicosis among former denim sandblasters. Eur Respir J. 2008;32(5):1295-1303. [CrossRef] [PubMed]
 
Akgun M, Araz O, Ucar EY, et al. Silicosis appears inevitable among former denim sandblasters: a 4-year follow-up study. Chest. 2015;148(3):647-654.
 
Bang KM, Mazurek JM, Wood JM, White GE, Hendricks SA, Weston A. Silicosis mortality trends and new exposures to respirable crystalline silica—United States, 2001–2010. MMWR Morb Mortal Wkly Rep. 2015;64(5):117-120. [PubMed]
 
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):8612-8621. [CrossRef] [PubMed]
 
Churchyard GJ, Ehrlich R, teWaterNaude JM, et al. Silicosis prevalence and exposure-response relations in South African goldminers. Occup Environ Med. 2004;61(10):811-816. [CrossRef] [PubMed]
 
Jindal SK. Silicosis in India: past and present. Curr Opin Pulm Med. 2013;19(2):163-168. [CrossRef] [PubMed]
 
Richeldi L. Clinical trials of investigational agents for IPF: a review of a Cochrane report. Respir Res. 2013;14(suppl 1):S4. [CrossRef] [PubMed]
 
Kwakkenbos L, Jewett LR, Baron M, et al. The Scleroderma Patient-centered Intervention Network (SPIN) Cohort: protocol for a cohort multiple randomised controlled trial (cmRCT) design to support trials of psychosocial and rehabilitation interventions in a rare disease context. BMJ Open. 2013;3(8):e003563. [CrossRef] [PubMed]
 
Zhang YM, Zhang HT, Wang CY, Wang W, Wu J, Wang C. Long-term therapeutic effects of whole lung lavage in the management of silicosis [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2012;30(9):690-693. [PubMed]
 
Sharma SK, Pande JN, Verma K. Effect of prednisolone treatment in chronic silicosis. Am Rev Respir Dis. 1991;143(4 pt 1):814-821. [CrossRef] [PubMed]
 
Goodman GB, Kaplan PD, Stachura I, Castranova V, Pailes WH, Lapp NL. Acute silicosis responding to corticosteroid therapy. Chest. 1992;101(2):366-370. [CrossRef] [PubMed]
 
Jalloul A, Banks DE. Can we translate our understanding of the pathogenic mechanisms of silicosis into a therapeutic plan? Clin Pulm Med. 2010;17(6):266-275. [CrossRef]
 
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