The Continuing Persistence of Silicosis

Crystalline silica (silicon dioxide) has long been recognized as an occupational hazard. The Occupational Safety and Health Administration (OSHA) estimated in 2003 that over 2 million workers were potentially exposed to crystalline silica dust in general industry, construction and maritime industries. Based on OSHA compliance inspection data, Yassin et al estimated that about 119,000 of such workers were exposed. Inhalation of crystalline silica can cause silicosis, a preventable but incurable type of lung fibrosis. At current U.S. levels of exposure, chronic inhalation generally takes a decade or longer to cause disease. However, high levels of exposure can cause disease more quickly. Severe cases can be disabling or even fatal. Breathing silica dust is also associated with tuberculosis, lung cancer, and chronic obstructive pulmonary disease (COPD). Exposure to silica dust may also cause various autoimmune diseases and chronic renal (kidney) disease.

Silica is the most abundant compound in the earth’s continental crust. It is found in crystalline and non-crystalline (amorphous) forms. Examples of crystalline silica include quartz, tridymite, and cristobalite. Quartz is a major component of soil and rocks. Many occupations and industries create quartz-containing dust through activities like drilling, tunneling, or quarrying, or by cutting, breaking or crushing materials that contain quartz. Sandblasting, a practice outlawed in many countries, is especially hazardous. Cristobalite and tridymite are found in rocks and soil and also produced by heating quartz or amorphous silica (as in foundry work and in manufacturing brick and ceramics). Occupations with hazardous exposures to crystalline silica continue to emerge and occupational exposures that exceed Occupational Safety and Health Administration (OSHA) and Mine Safety and Health Administration (MSHA) permissible exposure limits (PELs) continue to be regularly documented.

There are no surveillance data in the U.S. that permit us to estimate accurately the number of individuals with silicosis. The true extent of the problem is probably greater than indicated by available data. Undercounting of silicosis occurs because there are no national medical monitoring surveillance programs, and there can be a failure to diagnose silicosis or record it as a cause of death on a death certificate. Silicosis often presents long after workers have left causative jobs. Such cases may not be detected in Bureau of Labor statistics as occupational disease and will not be detected if disease presents after retirement. Even so, mortality surveillance shows that an average of 162 individuals died annually from or with silicosis in the U.S. over the period 2000-2005. According to formulas published by Rosenman et al., the 162 silicosis deaths per year would predict about 1,975 newly-recognized living silicosis cases per year. On average, about 29 of the 162 deaths occurred before the age of 65. Mazurek et al. reported that deaths in younger individuals aged 15-44 accounted for 37% of silicosis-related years of potential life lost in the US before age 65 over the period 2000-2005.

In 2002, the National Institute for Occupational Safety and Health (NIOSH) published an extensive review of the Health Effects of Occupational Exposure to Respirable Crystalline Silica. It found “a significant risk of chronic silicosis for workers exposed to respirable crystalline silica over a working lifetime” at current OSHA and MSHA PELs and at the NIOSH recommended exposure limit (REL). It recommended: “Until improved sampling and analytical methods are developed for respirable crystalline silica, NIOSH will continue to recommend an exposure limit of 0.05 mg/m³ as a time-weighted average (TWA) for up to a 10-hr workday during a 40-hr workweek. NIOSH also recommends substituting less hazardous materials for crystalline silica when feasible, using appropriate respiratory protection when source controls cannot keep exposures below the REL, and making medical examinations available to exposed workers.”

People only get silicosis from inhaling respirable crystalline silica dust into their lungs. Thus, every case represents failure to prevent excessive exposure. Sixteen years ago, Wagner published an editorial titled The Inexcusable Persistence of Silicosis. In it, he noted that the scientific bases for preventing silicosis had long been known. He called for a comprehensive workplace standard to eliminate silicosis. Such standards are now on the regulatory agendas of OSHA and MSHA. Although there has already been some controversy about these rulemaking efforts, all should agree with their motivation. Hazardous silica exposures and the diseases they cause should be, and can be, made a thing of the past in the U.S. and elsewhere in the world.

We invite your feedback on chronic work-related diseases like silicosis that take years to develop, often showing up after retirement. Should more be done to determine how often they occur? Or to prevent them and help the people who have them? We look forward to your comments.

David Weissman, MD, and Paul Schulte, PhD

Dr. Weissman is Director of the NIOSH Division of Respiratory Disease Studies.

Dr. Schulte is Director of the NIOSH Education and Information Division.

Web pages of interest

• NIOSH Silica
• NIOSH Engineering Controls for Silica in Construction
• NIOSH Pneumoconiosis
• NIOSH Respiratory Disease Surveillance
• CSTE. Occupational health indicators. Indicator 9: pneumoconiosis hospitalizations.
• NIOSH Work-related lung disease (WoRLD) surveillance system. Volume 1: Silicosis and related exposures.

Selected readings

1. Cohen RA, Patel A, Green FH. Lung disease caused by exposure to coal mine and silica dust. Semin Respir Crit Care Med. 2008 Dec;29(6):651-61.
2. Mazurek JM, Wood JM. Silicosis-related years of potential life lost before age 65 years–United States, 1968-2005. MMWR Morb Mortal Wkly Rep. 2008 Jul 18;57(28):771-5.
3. NIOSH. Health effects of occupational exposure to respirable crystalline silica. DHHS (NIOSH) Publication Number 2002-129 (2002). [http://www.cdc.gov/niosh/docs/2002-129/, accessed 9/22/11].
4. Rosenman KD, Reilly MJ, Henneberger PK. Estimating the total number of newly-recognized silicosis cases in the United States. Am J Ind Med. 2003 Aug;44(2):141-7.
5. Rosenstock L, Cullen M, Fingerhut M. Occupational Health. In: Jamison DT, Breman JG, Measham AR, Alleyne G, Claeson M, Evans DB, Jha P, Mills A, Musgrove P, editors. Disease Control Priorities in Developing Countries. 2nd edition. Washington (DC): World Bank; 2006. Chapter 60.
6. Steenland K. One agent, many diseases: exposure-response data and comparative risks of different outcomes following silica exposure. Am J Ind Med. 2005 Jul;48(1):16-23.
7. Straif K, Benbrahim-Tallaa L, Baan R, Grosse Y, Secretan B, El Ghissassi F, Bouvard V, Guha N, Freeman C, Galichet L, Cogliano V; WHO International Agency for Research on Cancer Monograph Working Group. A review of human carcinogens–part C: metals, arsenic, dusts, and fibres. Lancet Oncol. 2009 May;10(5):453-4.
8. Wagner GR. The inexcusable persistence of silicosis. Am J Public Health. 1995 Oct;85(10):1346-7.
9. Yassin A, Yebesi F, Tingle R. Occupational exposure to crystalline silica dust in the United States, 1988-2003. Environ Health Perspect. 2005 Mar;113(3):255-60.