NIOSH Respiratory Diseases Research Program

3.2 Silica-Induced Respiratory Diseases

 3.1d) RDRP Publications of Special Note Relating to Respiratory Diseases Induced by Coal Mine Dust

3.2a) Reduction in Silicosis Deaths through Research and Policy Statements 

In the mid-1980s, NIOSH published estimates of 2.3 to 4.3 million workers at risk of occupational exposure to silica dust in a myriad of occupations including mining, sandblasting, surface drilling, stone cutting, construction, pottery making, silica flour milling, tunneling, and concrete cutting.22 Between 1968 and 2003, there were 15,714 deaths in the U.S. where the death certificate mentioned silicosis. Annual silicosis deaths decreased from 1,065 in 1968 to 179 in 2003,23 but recent estimates show that between 3,600 and 7,300 cases of silicosis are newly recognized each year.24 Also, OSHA and MSHA silica sampling data for 1999 indicate that 47 percent of samples from construction, 38 percent from manufacturing, and eight percent from mining exceeded the PEL for silica and over half of all such silica samples in construction and manufacturing exceeded NIOSH REL for silica (0.05 mg/m3). Thus, while there have been vast improvements in recent decades, silicosis is likely to continue to occur well into the future.

Following a proposal from RDRP scientists of a link between silica exposure and lung cancer in the 1980s, work of RDRP was cited by IARC in support of its determination that evidence was sufficient to list crystalline silica in the forms of quartz and cristobalite as a probable human carcinogen, (2A).25 Silica exposure has been associated with an increased incidence of lung cancer in refractory brick workers, pottery workers, diatomaceous earth workers, foundry workers, granite workers, and miners26 (aspects of silica exposure that relate specifically to lung cancer are discussed in chapter 6).

The increased toxicity of freshly fractured silica has been attributed to siloxyl radicals on the fracture plane, the generation of hydroxyl radicals in aqueous media, and enhanced oxidant stress and inflammation27 and may account for the elevated risk of silicosis among workers exposed to freshly fractured crystalline silica (rock drillers, sandblasters, or silica flour millers). The inflammatory cytokine, Tumor Necrosis Factor-alpha (TNF-a), has been proposed to play a critical role in the development of silicosis.28 Evidence from RDRP scientists has linked a TNF-a gene polymorphism with increased susceptibility to silicosis.29

The objectives of RDRP silica/silicosis initiative were derived from a series of important inputs:

• The Surgeon General’s 1990 “Health Promotion and Disease Prevention Objectives for the Nation,” which included an objective that silicosis should be prevented among workers newly exposed after 1985.30
• The listing by NIOSH in 1980 of the “Top Ten Occupational Diseases and Injuries,” with occupational lung diseases at the top of the list and silicosis prevention flagged as a high priority issue.31
• The 1985 NIOSH-sponsored Symposium on the Leading Work-Related Diseases and Injuries, at which RDRP and external experts in occupational health drafted an “Occupational Lung Disease Prevention Strategy” that listed knowledge gaps and critical issues to be addressed to decrease the incidence of silicosis.32
• RDRP’s “WoRLD Surveillance Reports” documenting silicosis and silica over-exposures in various industries/occupations, based on national mortality data, state-based Sentinel Event Notification System for Occupational Risks (SENSOR) surveillance data from several states, and cases in the Association of Occupational and Environmental Clinics (AOEC) disease surveillance database, and MSHA and OSHA sampling data (A3-28, A3-29, A3-30).33,34,35
• Silicosis-related HHEs conducted by RDRP
• The 1987 IARC monograph indicating that data were insufficient to link silica exposure with lung cancer36

The first coordinated program planning activity in silica-induced lung disease by RDRP was initiated in the mid-1980s and involved the formation of multi-disciplinary working groups of our senior scientists. These groups included surveillance/epidemiology, exposure assessment, toxicology/pathology, and medical monitoring. Each working group developed a list of critical issues. To address these issues, projects were developed by RDRP scientists, evaluated by NIOSH Lead Team, and evaluated by peer-review panels, including a sub-committee of NIOSH BSC. 

RDRP led a renewed silica program planning effort in the 1990s and developed a Silicosis Prevention Initiative in 1992 (A3-31). This initiative emphasized that the persistence of silicosis is a continuing reminder of the failures of prevention; it outlined surveillance and research, disseminating information, and recommending effective actions, both regulatory and legislative, as keys to the prevention of silicosis. The resulting silica research program contained a portfolio of inter-related projects, and semi-annual intramural reviews were conducted to track progress, eliminate less productive projects, and evaluate plans for new studies.

RDRP developed objectives to reduce silicosis through research, policy statements, and education. RDRP made further efforts to introduce substitute materials for sandblasting and demonstrating the relative toxicity of those substitutes. In addition, assessment of exposures and controls, as well as mechanistic data on dose response, freshly fractured silica and oxidant injury has contributed to standard setting and has been a driving force for improved engineering controls.

Key outcomes relating to the six RDRP goals for silica-induced lung diseases as subsequently described in this section have included contributions to the annual reduction in silicosis deaths in the U.S. by 83 percent (from 1968 to 2003)37 (A3-32). The use of silica sand in sandblasting has been reduced by 47 percent (from 1996 to 2004).38 There has been a reduction in the percent of MSHA inspector collected samples for silica that exceed the PEL (Table 8). Freshly fractured silica has been recognized as highly toxic, and considered as especially hazardous due to siloxy-radical formation, which has helped drive improved engineering dust-controls and rulemaking. In turn this has driven additional research that has provided a mechanistic framework for hazard identification and risk assessment with RDRP findings on mineral-dust induced oxidant injury. RDRP has provided some of the data in support of OSHA’s review of the silica standard (planned for 2007).

A coordinated approach described below addresses six objectives:

1. Reduction in silicosis deaths through research and policy statements
2. Promotion of substitutes for silica sand in abrasive blasting
3. Assessment of silica exposures and controls
4. Provision of relevant mechanistic and dose-response data to standard-setting groups
5. Demonstrating that processes generating freshly fractured silica are associated with highly reactive dust
6. Demonstrating that oxidant injury is a critical mechanism for interstitial lung disease