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Sandblasters and Silicosis: Case Studies 1-800-934-2921 Call Now to Find a Lawyer

Case No. 1--One Death

In January 1992, the Ohio Department of Health responded to a physician's report of the death of a 55-year-old worker with accelerated silicosis and associated M. kansasii infection [ODH 1992]. The man was a sandblaster at a metal preparation shop and was reported to have been sandblasting for 10 years, possibly without adequate respiratory protection.

The Ohio Department of Health conducted a site visit at the metal preparation shop. Blasting had always been done manually in an enclosed room and was considered a necessary step to remove the "onion peel skin" that developed after heat stressing the metal.

The shop owner employed 17 workers and operated 3 shifts. All shifts had a designated sandblaster who was given a supplied-air respirator with a hood. Sandblasting was performed for about 6 hours on each shift. During the remainder of the shift, the sandblaster wore only a disposable particulate respirator and shoveled the used sand into a floor pit for recycling. Workers reported that coworkers had developed problems while working as sandblasters and that the employer typically hired six to seven new sandblasters each year to replace those who quit.

A full-shift personal sample collected outside the sandblaster's helmet indicated that the potential exposure to respirable crystalline silica was greater than 200 times the recommended levels. The type of respirator worn during this blasting operation had an assigned protection factor (APF) of 25. The APF, which is discussed further in the section on respiratory protection (p. 9), is the minimum anticipated protection provided by a properly functioning respirator or class of respirators to a given percentage of properly fitted and trained users. Thus, wearing a respirator with an APF of 25 would theoretically provide adequate protection from hazardous concentrations up to 25 times the National Institute for Occupational Safety and Health safety standard -far less protection than needed for a potential exposure greater than 200 times the standards.

An area air sample collected inside the blasting room contained about 500 times the safety standards for crystalline silica. An air sample collected immediately outside the blasting room contained 8 times the safety standards, indicating poor containment of the dust by the blasting room (which was not sealed) and dangerous dust leakage from the sand-handling equipment.

Other problems were noted with regard to airflow pressures at the helmet, improper ventilation, sporadic respirator use, and dust collection. The hopper outlet for the dust collector dumped fine dust directly onto the plant floor. This dust accumulated and exposed many workers as it was dispersed throughout the plant. A currently employed sandblaster stated that although the exposure was a nuisance, he considered the dust to be part of the job.

 

Case No. 2--One Death

In November 1988, a physician in western Texas reported three cases of sandblaster's silicosis to the Ector County Health Department [CDC 1990]. All three patients had been employed at a facility where they sandblasted oil-field drilling pipes. One of the workers, a 34-year-old man, subsequently died as a result of acute silicosis.

Following a later report by the physician in January 1989, the Ector County Health Department and the Texas Department of Health contacted local physicians and identified seven additional sandblasters who had suffered from silicosis since 1985. Of the 10 workers identified, 9 had worked at the same facility, which employed approximately 60 persons.

An investigation by the county and State health departments included a review of personal and occupational histories from each worker. Local radiologists evaluated chest X-rays. For four cases, a B reader also reviewed each patient's most recent chest X-ray for evidence of pneumoconiosis using the 1980 ILO guidelines. The Texas Department of Health reviewed lung tissue pathology reports and conducted an environmental survey of the plant where nine of the workers had been employed.

Each of the 10 workers had histories of occupational exposure to silica and a chest X-ray consistent with pneumoconiosis; 8 had a lung tissue pathology report of silicotic nodules or acute silicosis [Silicosis and Silicate Disease Committee 1988]. All were Hispanic males aged 24 to 50 at the time of diagnosis.

Seven workers were under age 30. Although tuberculosis was considered in all of the reported patients (three of whom had reactive tuberculin skin tests), all sputum and tissue samples from all patients were negative for M. tuberculosis.

All 10 workers had used sandblasting machinery. Duration of exposure to sandblasting ranged from 18 months to 8 years (mean: 4.5 years). Nine workers reported no previous silica exposure; the remaining worker had sandblasted oil-field drilling equipment for 3 years before working at the originally identified facility for 5 years.

The sandblasting process at this facility required that a blasting rod using an equal mixture of flint and garnet (20.5% crystalline silica) be passed through the drilling pipe to remove contaminants and to prepare the interior surface for a new protective plastic coating. Although the sandblasting operation was enclosed by blasting cabinets connected to exhaust systems, the cabinets were in poor repair and permitted clouds of dust to be released throughout the work area.

Protective booths intended to reduce exposures drew air from areas with substantial silica contamination. Workers manually shoveled the used sandblasting material into the machinery for reuse.

In November 1988, air samples from personal breathing zones documented respirable crystalline silica exposures of 400 to 700 µg/m3 for workers in the sandblasting area. These data were consistent with results reported by OSHA during a similar environmental inspection in which exposures substantially exceeded the current OSHA PEL (100 µg/m3) for respirable silica. Supplied-air respirators had not been used during sandblasting, and workers reported wearing only disposable particulate respirators.

Case No. 3--One Death

A 49-year-old nonsmoker who had worked as a sandblaster for 6 years came to a Louisiana hospital complaining of difficult breathing, a nonproductive cough, lack of appetite, fever, and a 20-lb weight loss.

A physical exam, chest X-rays, and sputum stain for bacteria led to a diagnosis of chronic silicosis and a bacterial pneumonia. Although the patient was treated with oxygen and antibiotics, he continued to deteriorate, and a breathing machine was necessary. A lung biopsy showed that the smallest cavities of the lungs were filled with a material composed of fat, protein, and silica particles. Further testing of the sputum revealed that the patient was suffering from tuberculosis, and an appropriate therapy was started. However, the patient continued to require a breathing machine and died on the 20th hospital day.

Case No. 4--Three Deaths

Acute silicosis developed in four men (aged 23, 37, 38, and 47) employed as tombstone sandblasters at a single factory for an average of 3 years. Three of the four men are known to have died of the disease. None of them showed any evidence of tuberculosis.

Investigations revealed that the sandblasters worked in enclosed but vented blasting chambers. Although supplied-air respirators were available to the workers, investigators indicated that they wore only negative-pressure, half-mask respirators with disposable filters. Workers in the blasting room were being exposed outside the mask to 98% crystalline silica sand at a concentration of 15 million particles per cubic foot (5 times the 1974 OSHA standard). A later investigation indicated that workers were using the supplied-air respirators but that they were being exposed to crystalline silica at a concentration of 3,400 µg/m3 as a TWA (18 times the 1974 OSHA standard).

Case No. 5--Eight Deaths

Eighty-three sandblasters in Louisiana were diagnosed as having silicosis. Twenty-two of the 83 had complicating mycobacterial infections. The average age of the patients was 44, with an average silica exposure time of fewer than 10 years. Eight of these patients are known to have died of respiratory failure caused by silicosis.

Almost all of the sandblasters prepared surfaces for painting and then painted them. Most of the workers wore supplied-air respirators, although the hoods were often unattached to an external air supply. When the sandblasting was completed, the workers removed their hoods and immediately began painting, even though large amounts of silica dust were still suspended in the air.

Conclusions

These case studies illustrate the continuing conditions in the American workplace that lead inevitably to the development of silicosis. Four conditions are characteristic of sandblasting worksites where silicosis is a problem:

Failure to substitute less toxic abrasive blasting materials

Inadequate engineering controls (such as ventilation) and work practices

Inadequate respiratory protection for workers

Failure to conduct adequate medical surveillance programs

 

RECOMMENDATIONS

The National Institute for Occupational Safety and Health recommends the following measures to reduce crystalline silica exposures in the workplace and prevent silicosis and silicosis related deaths:

1. Prohibit silica sand (or other substances containing more than 1% crystalline silica) as an abrasive blasting material and substitute less hazardous materials

2. Conduct air monitoring to measure worker exposures.

3. Use containment methods such as blast-cleaning machines and cabinets to control the hazard and protect adjacent workers from exposure.

4. Practice good personal hygiene to avoid unnecessary exposure to silica dust.

5. Wear washable or disposable protective clothes at the work site; shower and change into clean clothes before leaving the work site to prevent contamination of cars, homes, and other work areas.

6. Use respiratory protection when source controls cannot keep silica exposures below the National Institute for Occupational Safety and Health levels.

7. Provide periodic medical examinations for all workers who may be exposed to crystalline silica.

8. Post signs to warn workers about the hazard and to inform them about required protective equipment.

9. Provide workers with training that includes information about health effects, work practices, and protective equipment for crystalline silica.

10. Report all cases of silicosis to State health departments and to OSHA or the Mine Safety and Health Administration (MSHA).

These recommendations are discussed briefly in the following subsections.

Use of Alternative Abrasives

The risk of silicosis is high in workers exposed to abrasive blasting with silica, and the hazard is difficult to control. National Institute for Occupational Safety and Health has therefore recommended since 1974 that silica sand (or other substances containing more than 1% crystalline silica) be prohibited as abrasive blasting material. A variety of materials (corundum, glass beads, pumice, sawdust, slags, steel grit and shot, and walnut shells) are available as alternative blasting media. However, no comprehensive studies have been conducted to evaluate the health effects of these substitute materials. Until comprehensive data are available, engineering controls and personal protective equipment should be used with any of the alternative abrasives.

In addition to the health hazards of abrasive blasting materials, the finely fractured particles of material being removed (lead paint, for example) may also create health risks for workers.

Air Monitoring

Air monitoring should be performed to measure worker exposure to airborne crystalline silica and to provide a basis for selecting engineering controls. Air monitoring should be performed as needed to measure the effectiveness of controls. Air samples should be collected and analyzed according to safety standards or their equivalent.

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