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PubMed1999

Beryllium contamination inside vehicles of machine shop workers.

Inhalation of beryllium particles causes a chronic, debilitating lung disease--chronic beryllium disease (CBD)--in immunologically sensitized workers. Evidence that very low concentrations of beryllium may initiate this chronic disease is provided by incidences of the illness in family members exposed to beryllium dust from workers' clothes and residents in neighborhoods surrounding beryllium refineries. This article describes the results of a cross-sectional survey to evaluate potential take-home beryllium exposures by measuring surface concentrations on the hands and in vehicles of workers at a precision machine shop where cases of CBD had recently been diagnosed. Many workers did not change out of their work clothes and shoes at the end of their shift, increasing the risk of taking beryllium home to their families. Wipe samples collected from workers' hands and vehicle surfaces were analyzed for beryllium content by inductively coupled argon plasma-atomic emission spectroscopy (ICP-AES). The results ranged widely, from nondetectable to 40 micrograms/ft2 on workers' hands and up to 714 micrograms/ft2 inside their vehicles, demonstrating that many workers carried residual beryllium on their hands and contaminated the inside of their vehicles when leaving work. The highest beryllium concentrations inside the workers' vehicles were found on the drivers' floor (GM = 19 micrograms/ft2, GSD = 4.9), indicating that workers were carrying beryllium on their shoes into their vehicles. A safe level of beryllium contamination on surfaces is not known, but it is prudent to reduce the potential for workers to carry beryllium away from the work site.

Adult↗

PubMed1991

Dosimetry of beryllium in cultured canine pulmonary alveolar macrophages.

This study was designed to determine the dosimetry within macrophages of beryllium compounds administered at sublethal doses. Information on the dosimetry of beryllium within macrophages is required to guide further efforts to isolate and characterize beryllium-containing haptens. Inhalation of beryllium aerosols can cause chronic berylliosis, a progressive, granulomatous fibrosis of the lung. Studies in laboratory animals indicate that alveolar macrophages take up beryllium compounds and participate in a hypersensitivity immune response to beryllium-containing antigen. Beagle dog macrophage cultures were incubated with 7BeSO4 in solution or with suspensions of 7BeO particles that had been calcined at 500 or 1000 degrees C. Beryllium-7 was measured in fractions collected from cultures after successive centrifugation and filtration steps at 2, 6, 20, and 48 h after addition. An insignificant percentage of BeSO4 was taken up by the cells and did not cause cytotoxicity. Maximum BeO uptake occurred within 6 h, was 60 +/- 6% of added BeO, and was independent of BeO calcination temperature or specific surface area. Approximately 22% of 500 degrees C BeO dissolved within 48 h after addition to cell culture, concurrent with 39% cell killing. Dissolved beryllium remained associated with cells until a cytotoxic concentration was reached (2.2 x 10(-5) M, 15 nmol Be/10(6) cells), when the beryllium was released into the medium. There was no significant dissolution of the 1000 degrees C BeO within 48 h, and no significant cell killing. The results indicate that beryllium dissolved from phagocytized BeO was more cytotoxic than soluble beryllium added extracellularly. The data support an interactive mechanism in which phagocytized BeO particles were dissolved, and dissolved beryllium remained associated with the macrophage until a cytotoxic concentration accumulated, whereupon the beryllium was released to the medium and not appreciably taken up by viable cells.

Animals↗

PubMed2006

Exposure pathway assessment at a copper-beryllium alloy facility.

Controlling beryllium inhalation exposures to comply with regulatory levels (2 micro g m(-3) of air) does not appear to prevent beryllium sensitization and chronic beryllium disease (CBD). Additionally, it has proven difficult to establish a clear inhalation exposure-response relationship for beryllium sensitization and CBD. Thus, skin may be an important route of exposure that leads to beryllium sensitization. A 2000 survey had identified prevalence of sensitization (7%) and CBD (4%) in a beryllium alloy facility. An improved particulate migration control program, including dermal protection in production areas, was completed in 2002 at the facility. The purpose of this study was to evaluate levels of beryllium in workplace air, on work surfaces, on cotton gloves worn by employees over nitrile gloves, and on necks and faces of employees subsequent to implementation of the program. Over a 6 day period, we collected general area air samples (n = 10), wipes from routinely handled work surfaces (n = 252), thin cotton glove samples (n = 113) worn by employees, and neck wipes (n = 109) and face wipes (n = 109) from the same employees. In production, production support and office areas geometric mean (GM) levels of beryllium were 0.95, 0.59 and 0.05 micro g per 100 cm(2) on work surfaces; 42.8, 73.8 and 0.07 micro g per sample on cotton gloves; 0.07, 0.09 and 0.003 micro g on necks; and 0.07, 0.12 and 0.003 micro g on faces, respectively. Correlations were strong between beryllium in air and on work surfaces (r = 0.79), and between beryllium on cotton gloves and on work surfaces (0.86), necks (0.87) and faces (0.86). This study demonstrates that, even with the implementation of control measures to reduce skin contact with beryllium as part of a comprehensive workplace protection program, measurable levels of beryllium continue to reach the skin of workers in production and production support areas. Based on our current understanding of the multiple exposure pathways that may lead to sensitization, we support prudent control practices such as use of protective gloves to minimize skin exposure to beryllium salts and fine particles.

Air Pollutants, Occupational↗

PubMedDate not supplied

Application of beryllium antibodies in risk assessment and health surveillance: two case studies.

This paper demonstrates that current standards used by the Occupational Safety and Health Administration (OSHA) to establish an area free from potential beryllium contamination may be inadequate. Using the Beryllium Antibody Assay, it was shown that workers exposed to former beryllium work areas, thought to be sanitized and to meet OSHA standards, experienced statistically significant rises in blood beryllium antibody titers. This finding raises the question of whether the equipment currently required to protect workers in beryllium-laden environments is sufficient. The project mission of decommissioning/decontaminating the former nuclear weapons plant at Rocky Flats Environmental Technology Site (RFETS), instituted in 1992, has necessitated development of new technology directed toward safe and responsible cleanup. Challenges have been posed not only by the need to dispose of radioactive and chemical waste, but also by the problem of cleaning up hazardous metals such as the element beryllium. Beryllium was used extensively in research and the manufacture of nuclear weapons components at Rocky Flats for over 40 years. Since inhalation of this element can induce chronic beryllium disease (Eisenbud and Lisson, 1983), an antibody assay was developed to screen workers for internal exposure to beryllium. Exposure is indicated by a titer of antibodies greater than two standard deviations above a normal population control (defined as the mean titer of pooled samples from 51 individuals with no known exposure to beryllium) and a p-value of < 0.05. This paper describes two new applications for the assay: risk assessment and health surveillance. Case study 1 involves a team of three workers who cleaned a beryllium plenum and whose beryllium antibody titers provided a quantitative assessment of their exposure. Case study 2 describes the use of the antibody assay to determine the probable manner in which one worker was exposed to beryllium while performing his duties as an architectural engineer.

Air Pollutants, Occupational↗

PubMed1993

Beryllium disease screening in the ceramics industry. Blood lymphocyte test performance and exposure-disease relations.

We identified nine new cases of biopsy-confirmed chronic beryllium disease among 505 employees and ex-employees in a company that had manufactured beryllia ceramics from 1958 through 1975. Of tests commonly used in medical surveillance, only a confirmed blood beryllium lymphocyte transformation test had a high positive predictive value for beryllium disease (100%). However, two beryllium disease cases had either a normal or inconsistently abnormal blood test and were identified for diagnostic workup by abnormal chest radiograph. The only risk factor for beryllium disease was beryllium exposure; smoking or allergic history did not affect risk. Degree of beryllium exposure was associated with disease rates, which ranged from 2.9% to 15.8% for beryllia-exposed subgroups. One case of beryllium disease occurred in a "dust-disturber" who did not report past beryllium exposure and who began employment 8 years after commercial beryllia production had stopped. Our data support efforts to prevent beryllium disease by lowering beryllium exposures and to identify subclinical and early disease by broad-based medical surveillance using the blood beryllium lymphocyte test and chest radiograph in beryllium-using industries.

Adult↗

PubMed2002

Beryllium colorimetric detection for high speed monitoring of laboratory environments.

The health consequences of beryllium (Be2+) exposure can be severe. Beryllium is responsible for a debilitating and potentially fatal lung disease, chronic beryllium disease (CBD) resulting from inhalation of beryllium particles. The US Code of Federal Register (CFR), 10 CFR 850, has established a limit of 0.2 microg beryllium/100 cm(2) as the maximum amount of beryllium allowable on surfaces to be released from beryllium work areas in Department of Energy (DOE) facilities. The analytical technique described herein reduces the time and cost of detecting beryllium on laboratory working surfaces substantially. The technique provides a positive colorimetric response to the presence of beryllium on a 30.5 cm x 30.5 cm (1 ft(2)) surface at a minimum detection of 0.2 microg/100 cm(2). The method has been validated to provide positive results for beryllium in the presence of excess iron, calcium, magnesium, copper, nickel, chromium and lead at concentrations 100 times that of beryllium and aluminum and uranium (UO2(2+)) at lesser concentrations. The colorimetric detection technique has also been validated to effectively detect solid forms of beryllium including Be(OH)2, BeCl2, BeSO4, beryllium metal and BeO.

Beryllium↗

PubMed2001

Beryllium Exposure Control Program at the Cardiff Atomic Weapons Establishment in the United Kingdom.

The Cardiff Atomic Weapons Establishment (AWE) plant, located in Cardiff, Wales, United Kingdom, used metallic beryllium in their beryllium facility during the years of operation 1961-1997. The beryllium production processes included melting and casting, powder production, pressing, machining, and heat and surface treatments. As part of Cardiff's industrial hygiene program, extensive area measurements and personal lapel measurements of airborne beryllium concentrations were collected for Cardiff workers over the 36-year period of operation. In addition to extensive air monitoring, the beryllium control program also utilized surface contamination controls, building design, engineering controls, worker controls, material controls, and medical surveillance. The electronic database includes 367,757 area sampling records at 101 locations and 217,681 personal lapel sampling records collected from 194 employees over the period 1981-1997. Similar workplace samples were collected from 1961 to 1980, but they were not analyzed because they were not available electronically. Annual personal mean sampling concentrations for all workers ranged from 0.11 to 0.72 micrograms per cubic meter (microg/m3) with 95th percentiles ranging from 0.22 to 1.89 microg/m3; foundry workers worked in the highest concentration areas with a mean of 0.87 microg/m3 and a 95th percentile of 2.9 microg/m3. Area sampling concentrations, as expected, were lower than personal sampling concentrations. Mean annual area sample concentrations for all locations ranged from 0.02 to 0.32 microg/m3. The area sample 95th percentile concentrations for all years were below 0.5 microg/m3. For the overwhelming majority of samples, airborne beryllium concentrations were below the 2.0 microg/m3 standard. Although blood lymphocyte testing for beryllium sensitization has not been routinely conducted among these workers, this metal beryllium processing facility is the only large scale beryllium facility of its kind to have experienced only one unique a case of clinical chronic beryllium disease (CBD) ascertained by traditional medical monitoring procedures. The treating physician determined that this lung disease was likely caused by a systems reaction resulting from a mound contaminated with beryllium. However, he could not rule out the potential for inhalation exposure. Over the 17 years of measurement data analyzed, on occasion, airborne beryllium concentrations have exceeded 2.0 microg/m3; however, the Cardiff experience demonstrates that strict and consistent adherence to exposure control measures that emphasized airborne and surface levels and appropriate engineering controls, work practices, and use of personal protective equipment appears to have successfully prevented the incidence of clinical CBD with the exception of one unique case.

Air Pollutants, Occupational↗

PubMed2003

Summary of historical beryllium uses and airborne concentration levels at Los Alamos National Laboratory.

Beryllium operations and accompanying medical surveillance of workers at Los Alamos National Laboratory began in the 1940s. In 1999 a Former Workers Medical Surveillance Program that includes screening for chronic beryllium disease was initiated. As part of this program, historical beryllium exposure conditions were reconstructed from archived paper and electronic industrial hygiene data sources to improve understanding of past beryllium uses and airborne concentration levels. Archived industrial hygiene sampling reports indicated beryllium was principally used in technical areas-01 and -03, primarily being machined. Beryllium was also used at 15 other technical areas in activities that ranged from explosives detonation to the manufacture of X-ray windows. A total of 4528 personal breathing zone and area air samples for beryllium, combined for purposes of calculating summary statistics, were identified during the records review phase. The geometric mean airborne beryllium concentration for the period 1949-1989 for all technical areas was 0.04 microg Be/m(3) with 97 percent of all sample below the 2.0 microg Be/m(3) occupational exposure limit (OEL). Average beryllium concentrations per decade were less than 1 microg Be/m(3) and annual geometric mean concentrations in technical area-03, the largest user of beryllium, were generally below 0.1 microg Be/m(3), indicating exposure was generally well-controlled, that is, below the OEL. Typical of many retrospective exposure assessments, not all archived data could be extracted and summarized. Despite this, we report a reasonable summary of potential beryllium uses and airborne concentration levels a worker may have encountered from 1949-1989. These data can be used to more effectively identify former worker populations at potential risk for chronic beryllium disease and to offer these workers screening as part of the Former Worker Medical Surveillance Program, and in the event that a case is diagnosed, help to understand historical exposure conditions.

Air Pollutants, Occupational↗

PubMed2003

Skin as a route of exposure and sensitization in chronic beryllium disease.

Chronic beryllium disease is an occupational lung disease that begins as a cell-mediated immune response to beryllium. Although respiratory and engineering controls have significantly decreased occupational beryllium exposures over the last decade, the rate of beryllium sensitization has not declined. We hypothesized that skin exposure to beryllium particles would provide an alternative route for sensitization to this metal. We employed optical scanning laser confocal microscopy and size-selected fluorospheres to demonstrate that 0.5- and 1.0- micro m particles, in conjunction with motion, as at the wrist, penetrate the stratum corneum of human skin and reach the epidermis and, occasionally, the dermis. The cutaneous immune response to chemical sensitizers is initiated in the skin, matures in the local lymph node (LN), and releases hapten-specific T cells into the peripheral blood. Topical application of beryllium to C3H mice generated beryllium-specific sensitization that was documented by peripheral blood and LN beryllium lymphocyte proliferation tests (BeLPT) and by changes in LN T-cell activation markers, increased expression of CD44, and decreased CD62L. In a sensitization-challenge treatment paradigm, epicutaneous beryllium increased murine ear thickness following chemical challenge. These data are consistent with development of a hapten-specific, cell-mediated immune response following topical application of beryllium and suggest a mechanistic link between the persistent rate of beryllium worker sensitization and skin exposure to fine and ultrafine beryllium particles.

Administration, Topical↗

PubMed2002

Genetic and exposure risks for chronic beryllium disease.

Exposure to beryllium results in beryllium sensitization, or development of a beryllium-specific, cell-mediated immune response, in 2% to 19% of exposed individuals. Sensitization usually precedes the development of the scarring lung disease, chronic beryllium disease. The development of granulomatous inflammation in patients with CBD is associated with the production of numerous inflammatory cytokines, including IFN-gamma, IL-2, and TNF-alpha (see Fig. 1). In some individuals this can result in increased granulomatous inflammation and a more severe form of the disease. Although the exposure response relationship in sensitization and disease is nonlinear, in some studies, higher exposures were associated with higher rates of sensitization and CBD. Machinists usually have higher levels of beryllium exposure and increased risk of developing sensitization and disease. The impact of the physicochemical properties of beryllium, such as form, solubility, and particle size, on the risk of sensitization and disease are less well understood. It is clear from numerous studies that genetic susceptibility affects risk of beryllium-related health effects. The role of HLA-DPB1 Glu69 in the proliferative response to beryllium and risk of sensitization has been the most well-studied. Some genes, such as Glu69, are important in the development of an antigen-specific, cell-mediated immune response to beryllium or sensitization, whereas others may be important in the development of beryllium-specific granulomatous inflammation or CBD (see Fig. 1). Two copies of the Glu69 gene may be a disease-specific genetic risk factor. The TNF-alpha -308 A variant is associated with beryllium-stimulated TNF-alpha production, which, in turn, is associated with more severe CBD. Whether the TNF-alpha -308 A is a genetic risk factor in CBD, sensitization, or more severe disease still needs to be determined. It is likely that sensitization and CBD are multigenetic processes, and that these genes interact with exposure to determine risk of disease. Current genetic markers are not ready for clinical use as a screening test for beryllium-related health effects because of the low specificity of the markers and the low prevalence of BeS and CBD.

Berylliosis↗

PubMed2003

Beryllium chemical speciation in elemental human biological fluids.

The understanding of beryllium chemistry in human body fluids is important for understanding the prevention and treatment of chronic beryllium disease. Thermodynamic modeling has traditionally been used to study environmental contaminant migration and rarely in the examination of metal (particularly beryllium) toxicology. In this work, a chemical thermodynamic speciation code (MINTEQA2) has been used to model and understand the chemistry of beryllium in simulated human biological fluids such as intracellular, interstitial, and plasma fluids, a number of airway surface fluids for patients with lung conditions, saliva, sweat, urine, bile, gastric juice, and pancreatic fluid. The results show that predicted beryllium solubility and speciation vary markedly between each simulated biological fluid. Formation of beryllium hydroxide and/or phosphate was observed in most of the modeled fluids, and results support the postulation that beryllium absorption in the gastrointestinal tract may be limited by the formation of beryllium phosphate solids. It is also postulated that beryllium is potentially 13% less soluble in the airway surface fluid of a patient with asthma when compared to a "normal" case. The results of this work, supported by experimental validation, can aid in the understanding of beryllium toxicology. Our results can potentially be applied to assessing the feasibility of biological monitoring or chelation treatment of beryllium body burden.

Berylliosis↗

PubMed2006

Validation of a standardized portable fluorescence method for determining trace beryllium in workplace air and wipe samples.

Beryllium is widely used in industry for its unique properties; however, occupational exposure to beryllium particles can cause potentially fatal disease. Consequently, exposure limits for beryllium particles in air and action levels on surfaces have been established to reduce exposure risks for workers. Field-portable monitoring methods for beryllium are desired in order to facilitate on-site measurement of beryllium in the workplace, so that immediate action can be taken to protect human health. In this work, a standardized, portable fluorescence method for the determination of trace beryllium in workplace samples, i.e., air filters and dust wipes, was validated through intra- and inter-laboratory testing. The procedure entails extraction of beryllium in 1% ammonium bifluoride (NH(4)HF(2), aqueous), followed by fluorescence measurement of the complex formed between beryllium ion and hydroxybenzoquinoline sulfonate (HBQS). The method detection limit was estimated to be less than 0.02 microg Be per air filter or wipe sample, with a dynamic range up to greater than 10 microg. The overall method accuracy was shown to satisfy the accuracy criterion (A< or = +/-25%) for analytical methods promulgated by the US National Institute for Occupational Safety and Health (NIOSH). Interferences from numerous metals tested (in >400-fold excess concentration compared to that of beryllium) were negligible or minimal. The procedure was shown to be effective for the dissolution and quantitative detection of beryllium extracted from refractory beryllium oxide particles. An American Society for Testing and Materials (ASTM) International voluntary consensus standard based on the methodology has recently been published.

Air Pollutants↗

PubMed1968

Uptake, distribution and binding of beryllium to organelles of the rat liver cell.

1. Male rats were injected intravenously with amounts ranging from 0.08 to 111.0mumoles of [(7)Be]beryllium sulphate/kg. body wt. The distribution in the rat and the subcellular distribution of beryllium in the liver were determined. 2. Within the entire dose range a higher specific activity of beryllium was present in a mitochondrial fraction containing the lysosomes. Purification of this fraction confirmed that beryllium is taken up by lysosomes. 3. With doses approaching the LD(50), beryllium was also found in increasing amounts to be present in the liver cell nuclei. Beryllium also showed affinity towards isolated cell nuclei in vitro. Evidence is presented that they have one class of binding sites for beryllium. Mitochondria have less affinity for beryllium. 4. No evidence could be obtained of an affinity of beryllium for DNA or RNA by fractionation of nuclei and dialysis experiments. 5. The presence of beryllium in liver cell nuclei may be relevant to the effects of beryllium on nuclear structure and function.

Acid Phosphatase↗

PubMed2001

Contribution of incidental exposure pathways to total beryllium exposures.

Beryllium manufacturing processes are associated with the immune-mediated chronic beryllium disease (CBO). Recent workplace epidemiological studies have been relatively unsuccessful in correlating disease with workplace air concentrations of beryllium, thereby failing to support the hypothesis that dose by the respiratory route determines the risk of disease. This has led to consideration of the hypotheses that dermal or oral exposures to beryllium can influence disease risk, either as a cause of sensitization or to induced tolerance to beryllium. If so, the control of dermal and/or ingestion exposure to beryllium, which has heretofore been widely disregarded in the United States, would be of practical importance. Most of the literature of the past 50 years indicates that ingestion and dermal uptake of beryllium are unimportant routes of exposures. The toxicology data generally support this position. However, research is under way to determine whether sensitization to beryllium may occur following exposure via routes other than inhalation, raising the question of whether this sensitization from other routes of exposure makes the lungs more susceptible to inflammation when inhaled doses are encountered. Using published data on other metals, this article describes the likely range of doses that a worker might incur in the workplace due to incidental exposure pathways (i.e., exposures not directly related to inhalation of workplace air), such as hand-to-mouth exposure, dermal contact, and resuspension following deposition of beryllium onto clothing. This analysis indicates that these incidental routes of exposure could contribute to total absorbed doses of beryllium that exceed simple airborne inhalation exposures. Because the doses presented by these alternative exposure pathways could be appreciable compared with the airborne inhaled dose, and could continue even when respirators are worn, these pathways may represent the primary routes of entry of beryllium into the body. We believe that the potential for exposure from these incidental exposure pathways merits additional study.

Administration, Oral↗

PubMed2004

Industries in the United States with airborne beryllium exposure and estimates of the number of current workers potentially exposed.

Estimates of the number of workers in the United States occupationally exposed to beryllium were published in the 1970s and 1980s and ranged from 21,200 to 800,000. We obtained information from several sources to identify specific industries with beryllium exposure and to estimate the number of current workers potentially exposed to beryllium. We spoke with representatives from the primary beryllium industry and government agencies about the number of exposed workers in their facilities. To identify industries in the private sector but outside the primary industry, we used data from the Integrated Management Information System (IMIS), which is managed by the Occupational Safety and Health Administration, and the Health Hazard Evaluation program of the National Institute for Occupational Safety and Health. We used IMIS data from OSHA inspections with a previously developed algorithm to estimate the number of potentially exposed workers in nonprimary industries. Workers potentially exposed to beryllium included 1500 current employees in the primary beryllium industry and 26,500 individuals currently working for the Department of Energy or the Department of Defense. We identified 108 four-digit Standard Industrial Classification (SIC) categories in which at least one measurement of airborne beryllium was > or = 0.1 microg/m3. Based on the subset of 94 SIC categories with beryllium > or = 0.1 microg/m3, we estimated 26,400 to 106,000 workers may be exposed in the private sector (outside the primary industry). In total, there are as many as 134,000 current workers in government and private industry potentially exposed to beryllium in the United States. We recommend that the results of this study be used to target at-risk audiences for hazard communications intended to prevent beryllium sensitization and chronic beryllium disease.

Air Pollution, Indoor↗

PubMed1997

Comparison of in vivo and in vitro measures of beryllium sensitization.

Chronic beryllium disease (CBD) diagnosis hinges on demonstrating a cell-mediated immune response to beryllium salts in vitro with the beryllium lymphocyte proliferation test (BeLPT). The BeLPT has found widespread application in screening for CBD and beryllium sensitization in populations of exposed workers. We hypothesized that the in vivo beryllium salt patch test may be of value as an adjunct to the BeLPT, rectifying false negative or ambiguous blood test results. We studied subjects with CBD (n = 11), beryllium sensitization without disease (n = 3), and control subjects with dermatitis (n = 20). Evaluation included completion of a demographic questionnaire, blood BeLPT (if CBD or beryllium-sensitized), and beryllium patch testing with 0.1% and 1% beryllium sulfate (BeSO4) in petrolatum and in aqueous vehicles. Biopsies were performed at abnormal patch test sites in five subjects. The 1% aqueous BeSO4 proved superior either to 1% petrolatum or 0.1% solutions, producing positive reactions in all CBD and beryllium-sensitized subjects. We observed no long-term adverse reactions. Biopsies demonstrated spongiotic changes early, followed by noncaseating granulomas within 18 days. We conclude that the beryllium patch test can be used safely to clarify the sensitization state and diagnosis of CBD.

Adrenal Cortex Hormones↗

PubMed2005

Beryllium exposure: dermal and immunological considerations.

OBJECTIVE: People exposed to beryllium compounds are at increased risk of developing beryllium sensitization and chronic beryllium disease (CBD). The purpose of this short communication is to present information regarding the potential importance of skin exposure to beryllium, an exposure and alternate immune response pathway to the respiratory tract, which has been largely overlooked in epidemiologic and exposure assessment studies. METHODS: We reviewed the published literature, including epidemiologic, immunologic, genetic, and laboratory-based studies of in vivo and in vitro models, to assess the state of knowledge concerning skin exposure to beryllium. RESULTS: Reduction in inhalation exposure to beryllium has not resulted in a concomitant reduction in the occurrence of beryllium sensitization or CBD, suggesting that continued prevalence may be due, in part, to unchecked skin exposure to beryllium-containing particles. CONCLUSIONS: Recent developments in our understanding of the multiple exposure pathways that may lead to beryllium sensitization and CBD suggest that a prudent approach to worker protection is to assess and minimize both skin and inhalation exposures to beryllium.

Berylliosis↗

PubMed2000

Development of an eight-hour occupational exposure limit for beryllium.

This article recommends an 8-hour occupational exposure limit (OEL) for beryllium. It responds to growing concerns about the continuing incidence of chronic beryllium disease despite the long-standing OEL for beryllium: 2 micrograms of beryllium per cubic meter of air (microgram/m3), 8-hour time-weighted average (TWA). Current 8-hour TWA beryllium OELs are not based on chronic beryllium disease toxicology and an increasing number of studies report incidence of chronic beryllium disease at exposure levels apparently below 2 micrograms/m3. The experience of the beryllium-exposed population of Lorain, Ohio, in the late 1940s, and the ambient air regulatory standards derived from that event provide evidence that establishing a protective level is possible. These levels are used as the basis for a new recommended beryllium exposure standard. A correspondingly protective 8-hour TWA level of 0.1 microgram/m3 has been derived, which, for commonly encountered workplace conditions (in terms of geometric standard deviation and percent-compliance), should provide long-term mean exposure protection comparable to that received by the unaffected Lorain subpopulation and provided by the Environmental Protection Agency (EPA) ambient standard. It is concluded that an exposure limit of 0.1 microgram/m3 combined with exposure monitoring to assure a high rate of day-to-day compliance would provide better control of both long-term mean exposure levels and short-term levels than do current occupational exposure limits. The health data available, while certainly not conclusive, support further reductions in exposure levels to help minimize the incidence of chronic beryllium disease.

Air Pollutants, Occupational↗