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Berylliosis

Berylliosis is a chronic lung disease caused by prolonged exposure to beryllium, a chemical irritant to the lungs.

Symptoms

With prolonged exposure, the lungs become hypersensitive to beryllium causing the development of small inflammatory nodules, called granulomas.

Granulomas are seen in other chronic diseases, such as tuberculosis and sarcoidosis, and it can occasionally be hard to distinguish berylliosis from these disorders.

Ultimately, this process leads to restrictive lung disease, a decreased diffusion capacity.

Clinically patients experience cough and shortness of breath. Other symptoms include chest pain, joint aches, weight loss and fever.

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Silicosis in dental laboratory technicians—five states, 1994-2000
From Morbidity and Mortality Weekly Report, 3/12/04 by K.D. Rosenman

Silicosis is a debilitating, sometimes fatal, yet preventable occupational lung disease caused by inhaling respirable crystalline silica dust. Although crystalline silica exposure and silicosis have been associated historically with work in mining, quarrying, sandblasting, masonry, founding, and ceramics, certain materials and processes used in dental laboratories also place technicians at risk for silicosis (1-3). During 1994-2000, occupational disease surveillance programs in five states identified nine confirmed cases of silicosis among persons who worked in dental laboratories; four persons resided in Michigan, two in New Jersey, and one each in Massachusetts, New York, and Ohio. This report describes three of the cases and underscores the need for employers of dental laboratory technicians to ensure appropriate control of worker exposure to crystalline silica.

Silicosis cases in Michigan, New Jersey, and Ohio were identified through the Sentinel Event Notification Systems for Occupational Risks (SENSOR) surveillance program (4). The case in New York was identified through the state's Occupational Lung Disease Registry, and the case in Massachusetts was identified through the state's Occupational Disease and Injury Surveillance System; both use the SENSOR model. Although cases were identified during 1994-2000, diagnoses preceded state surveillance system identification. State surveillance programs identify suspected cases of silicosis through various sources, including hospital discharge data, death certificate data, workers' compensation reports, and physician reports. Cases are confirmed on the basis of the silicosis surveillance case definition (Box 1) adopted by these state surveillance programs and information from interviews, medical record review, or chest radiograph classification by a National Institute for Occupational Safety and Health (NIOSH)--certified B-reader *.

Case Reports

Case 1. In November 1992, a man aged 65 years in New Jersey died 4 days after being admitted to a hospital with abdominal pain, nausea, and vomiting. The cause of death was shock, pancreatitis, and respiratory failure. At age 48 years, silicosis had been diagnosed in the patient. He had worked for 46 years in dental laboratories, 27 years as an owner, and had performed routine dental laboratory operations. He reportedly was exposed to dust, cobalt, and chemicals, and never wore a respirator. A B-reader classification of a chest radiograph taken 1 day before his death revealed small, rounded opacities involving the upper zones, with a profusion category of 1/2, consistent with silicosis.

Case 2. In September 1995, silicosis was diagnosed in a man aged 66 years in New York. He had worked as a dental technician for 30 years and had been exposed to various mineral and metallic dusts. A chest radiograph taken at a local hospital revealed category 2/3 profusion of small, nodular opacities in the middle and lower lung zones, consistent with silicosis. Asbestosis and berylliosis ([dagger]) also were diagnosed.

Case 3. In November 1992, a man aged 67 years in New Jersey died 3 days after being admitted to a hospital with progressive confusion. The cause of death was urosepsis caused by scleroderma, anemia, and renal failure. He had worked for 28 years in dental laboratories, 24 years as an owner. He reportedly was exposed to various dusts, performed sandblasting in dental laboratories, and never wore a respirator. A chest radiograph taken 10 weeks before his death revealed small, rounded opacities involving the upper zones, with a profusion category of 3/2, consistent with silicosis.

Reported by: KD Rosenman, MD, Michigan State Univ, East Lansing, Michigan. E Pechter, MPH, Massachusetts Dept of Public Health. DP Schill, MS, DJ Valiante, MS, EA Bresnitz, MD, New Jersey Dept of Health and Senior Svcs. KR Cummings, MPH, New York State Dept of Health. E Socie, MX Ohio Dept of Health. MS Filios, ScM, Div of Respiratory Disease Studies, National Institute for Occupational Safety and Health, CDC.

Editorial Note: The findings in this report suggest that dental laboratory technicians might be at risk for silicosis as a result of uncontrolled exposure to airborne crystalline silica dust. For the patients described in this report, the only identified source of crystalline silica exposure was their work as dental technicians. Exposure to respirable crystalline silica in dental laboratories can occur during procedures that generate airborne dust (e.g., mixing powders, removing castings from molds, grinding and polishing castings and porcelain, and using silica sand for abrasive blasting). The proportion of crystalline silica in mold and porcelain materials, by weight, can range up to 70%. A study of dental technicians in South Korea (6) that described materials and processes similar to those used in the United States found exposures during polishing operations that exceeded the NIOSH recommended exposure limit of 0.05 mg/[m.sup.3] (7).

The United States has approximately 14,000 dental laboratories (8), and approximately 6,400 dental laboratory technicians are certified by the National Association of Dental Laboratories (NADL) (NADL, unpublished data, 2004). Because dental laboratories are not registered or licensed, the actual number of dental laboratory technicians is unknown.

The findings in this report are subject to at least three limitations. First, data for some variables (e.g., month or year of diagnosis and job history) were not available for all cases. Second, the risk for exposure to crystalline silica could not be quantified because data on exposure levels among dental laboratory technicians are limited. Finally, silicosis case ascertainment is not complete (9).

Occupational diseases such as silicosis frequently are not recognized or reported by physicians (10). Health-care providers and employers should be educated on the importance of screening and reporting silicosis to their state-based surveillance systems.

Methods to control exposure to silica are well established. Through industrywide educational outreach, state-based surveillance programs can alert employers to a potential occupational hazard and provide guidance for controlling worker exposure. The Occupational Safety and Health Administration (OSHA) requires employers to identify occupational health hazards and control them by instituting engineering and work-practice controls, issuing personal protective equipment (PPE), and ensuring that PPE is working and used properly. As part of an effective OSHA-compliant hazard communication program, dental technicians should be trained in the hazards of crystalline silica exposure and the methods to control exposure (Box 2). Guidance for controlling silica exposure in dental laboratory settings is available at http:// www.state.nj.us/health/eoh/survweb. Additional information about silica and silicosis is available at http://www.cdc.gov/ niosh/topics/silica.

References

(1.) Choudat D. Occupational lung disease among dental technicians. Tuber Lung Dis 1994;75:99-104.

(2.) Rom WN, Lockey JE, Lee JS, et al. Pneumoconiosis and exposures of dental laboratory technicians. Am J Public Health 1984;74:1252-7.

(3.) CDC. Silicosis surveillance--Michigan, New Jersey, Ohio, and Wisconsin, 1987 1990. In: CDC Surveillance Summaries (November 19). MMWR 1993;42(No. SS-5).

(4.) Baker EL. Sentinel Event Notification Systems for Occupational Risks (SENSOR): the concept. Am J Public Health 1989;79(suppl):18-20.

(5.) International Labour Office. Guidelines for the Use of the ILO International Classification of Radiographs of Pneumoconioses, 2000 ed. Geneva, Switzerland: International Labour Office, 2002 (Occupational Safety and Health Series, No. 22, rev. 2000).

(6.) Kim TS, Kim HA, Heo Y, Park Y, Park CY, Roh YM. Level of silica in the respirable dust inhaled by dental technicians with demonstration of respirable symptoms. Ind Health 2002;40:260 5.

(7.) National Institute for Occupational Safety and Health. NIOSH Hazard Review: Health Effects of Occupational Exposure to Respirable Crystalline Silica, 2002. Cincinnati, Ohio: U.S. Department of Health and Human Services, CDC, National Institute for Occupational Safety and Health, 2002; DHHS publication no. (NIOSH)2002-129.

(8.) Marketplace [CD-ROM database]. New York, New York: Dun & Bradstreet, April 2002.

(9.) Rosenman KD, Reilly MJ, Henneberger PK. Estimating the total number of newly-recognized silicosis cases in the United States. Am J Ind Med 2003;44:141-7.

(10.) CDC. Mandatory reporting of occupational diseases by clinicians. MMWR 1990;39(No. RR-9).

* NIOSH B-reader certification is granted to physicians who demonstrate proficiency in classifying chest radiographs for pneumoconioses by using the International Labour Office Classification System (5).

([dagger]) Asbestosis is caused by exposure to asbestos, once commonly used in dental laboratories; berylliosis is caused by exposure to the metal beryllium, a component of some alloys used in dental prostheses.

COPYRIGHT 2004 U.S. Government Printing Office
COPYRIGHT 2004 Gale Group

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