NIOSH Programs > Respiratory Diseases > Evidence Package > 3. Interstitial Lung Diseases > 3.2 Silica-Induced Respiratory Diseases
3.2e) Processes that Generate Freshly Fractured Silica are Associated with Highly Reactive Dust3.2d) Provision of Relevant Mechanistic and Dose-Response Data to Standard-Setting Bodies | 3.2f) Oxidant Injury is a Critical Mechanism for Interstitial Lung Disease
Processes that generate freshly fractured silica are associated with dust of high surface reactivity, and sometimes also with high levels of dust. Certain occupations, such as sandblasting, rock drilling, silica flour milling, concrete cutting, and tunneling are associated with a high incidence of silicosis. An important question to answer was: is this high disease rate due only to high airborne dust levels or are freshly fractured silica particles inherently more toxic than aged silica particles?
Three major activities were undertaken to address the issue of silicosis incidence in occupations generating freshly fractured silica dust: field evaluation of exposure levels for rock drillers, surface miners, and cement roofing tile installers; comparisons of the properties of freshly fractured versus aged silica; and research to improve exposure control in mines.
RDRP conducted a recent field investigation of cement roofing tile installers. RDRP industrial hygienists determined that high levels of freshly fractured silica dust can be generated during the cutting, crushing, drilling, or blasting of roofing tile. Recommendations included locating the cutting station on the ground away from roofers, using wet cutting and vacuum systems, avoidance of dry sweeping and compressed air “blow-downs” of settled dust, air monitoring, and use of approved respiratory protection when necessary. RDRP field scientists worked closely with the roofers’ union to reduce exposure.
RDRP research documented that grinding or fracturing crystalline silica in a manner that would occur during rock drilling, sandblasting, silica flour milling, and cement cutting generates siloxyl radicals on the fracture planes where Si-O bonds are broken. These siloxyl radicals exhibit a half-life of about 30 hours in air, representing surface radical decay that is sufficiently slow for inhaled siloxyl radicals to interact with the lung. Upon contact with aqueous media (a situation mimicked by deposition of freshly fractured silica on lung lining fluid), hydroxyl radicals are generated.
In vitro exposure of lung cells to freshly fractured versus aged silica indicates that the freshly fractured silica was more cytotoxic, causing radical-dependent lipid peroxidation and cell damage. Freshly fractured silica also was a more potent stimulant of reactive oxygen species production by alveolar macrophages, thus enhancing oxidant stress. Freshly fractured silica was also a more potent activator of signaling pathways, including transcription factor activation, which results in induction of inflammatory cytokines and growth factors. A water emulsion, containing an organosilane material effectively coats freshly fractured silica, depressing radical generation, and mitigating cytotoxicity. Therefore, organosilane in water sprays represents a potential prevention strategy in cutting, abrasion, and drilling operations.
Inhalation studies in rats were also conducted comparing freshly fractured versus aged silica. These studies, which were a collaborative effort between inhalation technologists, toxicologist, biochemists, and pathologists, indicate that inhalation of freshly fractured silica caused more oxidant injury and inflammation than aged silica (i.e., enhanced pulmonary response occurred to the inhalation of freshly fractured silica as compared to aged silica) (10, 11, A3-67, A3-68). Current standards, which were developed using animals exposed to aged silica may not be adequate to protect workers exposed to freshly fractured silica. There were four other key publications (12-15, A3-69, A3-70, A3-71, A3-72).
RDRP scientists have worked closely with MSHA to develop engineering controls to reduce silica exposures in mining, such as a canopy air curtain system to lower exposure to roofbolters in underground mines and improvements to the Rotoclone dust collector on drills used by highwall drill operators at surface mines. These have been widely disseminated in the form of technical reports.
Outputs and Transfers
Several of the reported outputs for chapter 3.2a are reiterated in this section, these include some materials presented in the appendices (A3-73). In addition, there were three NIOSH Alerts relevant to sandblasters (A3-35), rock drillers (A3-1), and construction workers (A3-36).
Most recently, in 2006 RDRP published a report on the investigation of cement roofing tile installers “Silicosis-Working with Cement Roofing Tiles: A Silica Hazard” (A3-74).
The method developed by RDRP scientists to coat freshly fractured silica to reduce its toxicity was patented (Patent 5,096,733 for use of an organosilane coating to reduce the toxicity of silica dust).
IARC’s 1997 Monograph on the “Evaluation of the Carcinogenic Risk of Chemicals to Humans: Silica, Some Silicates, Coal Dust, and Para-aramid Fibers” cited RDRP’s work on the enhanced toxicity of freshly fractured silica versus aged silica to provide a mechanistic explanation for inconsistencies in findings from epidemiology studies in different occupational settings.73
OSHA considered the data on enhanced toxicity of freshly fractured silica in its currently ongoing review of the silica standard (Perry letter A3-75). Evidence that freshly fractured silica is more toxic than aged silica is driving future research by the scientific community (Donaldson letter A3-66).
RDRP work on the physicochemical characterization of freshly fractured silica led RDRP scientists to more fully elucidate oxidant injury mechanisms associated with silica and other inhaled agents (see “What’s Ahead” in chapter 3.2f below).