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At least 19 recordsLinked to original sources
PubMed2006

Enhanced preventive programme at a beryllium oxide ceramics facility reduces beryllium sensitisation among new workers.

BACKGROUND: A 1998 survey at a beryllium oxide ceramics manufacturing facility found that 10% of workers hired in the previous 6 years had beryllium sensitisation as determined by the beryllium lymphocyte proliferation test (BeLPT). In response, the facility implemented an enhanced preventive programme to reduce sensitisation, including increased respiratory and dermal protection and particle migration control. AIM: To assess the programme's effectiveness in preventing sensitisation. METHODS: In 2000, the facility began testing newly hired workers for beryllium sensitisation with the BeLPT at time of hire and during employment. The sensitisation rate and prevalence for workers hired from 2000 to 2004 were compared with that for workers hired from 1993 to 1998, who were tested in the 1998 survey. Facility environmental conditions for both time periods were evaluated. RESULTS: Newly hired workers in both cohorts worked for a mean of 16 months. Of the 97 workers hired from 2000 to 2004 with at least one employment BeLPT result, four had abnormal results at time of hire and one became sensitised during employment. Of the 69 workers hired from 1993 to 1998 and tested in 1998, six were found to be sensitised. The sensitisation rate for the 2000-4 workers was 0.7-2.7/1000 person-months of employment, and that for the 1993-8 workers was 5.6/1000 person-months, at least 2.1 (95% confidence interval (CI) 0.6 to 8.4) and up to 8.2 (95% CI 1.2 to 188.8) times higher than that for the 2000-4 workers. The sensitisation prevalence for the 2000-4 workers was 1% and that for the 1993-8 workers was 8.7%, 8.4 (95% CI 1.04 to 68.49) times higher than that for the 2000-4 workers. Airborne beryllium levels for production workers for the two time periods were similar. CONCLUSIONS: A comprehensive preventive programme reduced beryllium sensitisation in new workers during the first years of employment, despite airborne beryllium levels for production workers that were similar to pre-programme levels.

Adolescent↗
PubMed1990

Clearance, translocation, and excretion of beryllium following acute inhalation of beryllium oxide by beagle dogs.

Beagle dogs inhaled radiolabeled beryllium oxide (7BeO) particles that were calcined at either 500 or 1000 degrees C, resulting in either high (mean of 50 micrograms/kg body wt) or low (mean of 17 micrograms/kg body wt) initial lung burdens (ILBs) of both preparations of BeO. Levels of beryllium in whole body, tissue, and excreta were measured by external gamma-ray counting. Dogs were euthanized in pairs at 8, 32, 64, and 180 days after exposure to determine beryllium distribution in tissues. Beryllium oxide calcined at 1000 degrees C was retained more tenaciously in the lungs (62% of the ILB retained at 180 days after exposure) than BeO calcined at 500 degrees C (14% of the ILB retained at 180 days after exposure). Most of the beryllium that was cleared from the lungs and not excreted was translocated to the tracheobronchial lymph nodes, skeleton, liver, and blood. More beryllium was translocated to the skeleton and liver at 180 days after inhalation of BeO prepared at 500 degrees C than at 1000 degrees C. The predominant mode of excretion at early times after exposure was through the feces, with urinary excretion assuming predominance at later times. These data are important for interpreting the toxic effects of beryllium in the exposed dogs. Furthermore, because little is known concerning the retention and clearance of inhaled beryllium in man, these results provide information that may be used to understand the disposition of beryllium in accidentally exposed humans.

Administration, Inhalation↗
PubMed1994

The comparative pulmonary toxicity of beryllium metal and beryllium oxide in cynomolgus monkeys.

Inhalation of beryllium (Be) may result in an immune-mediated, chronic granulomatous pulmonary disorder known as chronic beryllium disease (CBD). The physicochemical form of Be may affect the incidence and severity of CBD. We exposed cynomolgus monkeys, by bronchoscopic, intrabronchiolar instillation, to either beryllium oxide (BeO; heat-treated at 500 degrees C) or Be metal at concentrations selected to achieve equimolar concentrations of available Be2+ ions dissolving from the particles. Monkeys underwent bronchoalveolar lavage of the right and left diaphragmatic lobes at 14, 30, 60, 90, and 120 days post exposure (dpe). Monkeys were sacrificed at 80 and 180 dpe for evaluation of histopathological pulmonary changes. Numbers of lymphocytes from lung lobes of Be metal-exposed, but not BeO-exposed, monkeys were increased at 14, 30 and 90 dpe. Lung lymphocytes were increased for BeO exposed monkeys only at 60 dpe. In vitro, Be-specific, lung lymphocyte proliferation occurred at 14, 60, and 90 dpe for lymphocytes from Be metal-exposed lung lobes only. At no time were values from BeO-exposed lung lobes different from values from control lobes. Lung lesions in Be metal-exposed monkeys were characterized by focally intense, interstitial fibrosis, marked Type II cell hyperplasia, and variable lymphocyte infiltration. Some Be-metal-exposed monkeys had discrete immune granulomas consisting of tightly organized lymphocytic cuffs surrounding nodular aggregates of epithelioid macrophages. Lesions were rarely present in BeO-exposed monkeys and were much less severe. These data suggest that Be metal produces more severe pulmonary lesions than does BeO and that these lesions are accompanied by Be-specific immune responses.

Animals↗
PubMed1997

Immunologic specificity of lymphocyte cell lines from dogs exposed to beryllium oxide.

We have reported that dogs exposed twice to aerosols of beryllium oxide (BeO) developed Be-specific immune responses within the lung, along with granulomatous and fibrotic lung lesions. To evaluate the specificity of the immune response, lymphocytes from lungs and blood of BeO-exposed dogs were co-cultured over an irradiated blood monocyte layer, alternately with interleukin 2 and BeSO4. Resultant cell lines were then tested for their response to different metal cations, common canine recall antigens, and BeSO4 in an in vitro cell proliferation assay. The cell lines responded to BeSO4 in a dose-dependent fashion, with mean stimulation indices of 7, 58, 119, and 112 at concentrations of 0.01, 1.0, 10, and 100 microM BeSO4 respectively. Cells not proliferate when incubated with ZnSO4 or NiSO4, or with canine distemper, leptospira, adenovirus 2, parvovirus, or parainfluenza antigens. Lymphocytes from normal vaccinated dogs proliferated markedly when cultured with these antigens. Cells from the cultured cell lines (91%) stained with Thy-1 (a pan T-cell marker) and 96% stained with DT2 (a helper T-cell marker). Furthermore, the Be-induced proliferative response was restricted by major histocompatibility (MHC) class II antigens. These data reinforce the premise that inhalation exposure of dogs to BeO produces lung lesions and MHC class II restricted immunologic responses mediated by Be-specific, helper T-Cells. These data further confirm the hypothesis that antigen localized to the lung results in the recruitment of T-cells to the lung, followed by localized antigen-specific, cell-mediated immune responses.

Administration, Inhalation↗
PubMed1983

[Studies on the effects of beryllium oxide in purity and fired temperature to the occurrence of chronic pulmonary berylliosis].

Among various beryllium (Be) compounds, beryllium oxide (BeO) has so far been noted as a causative substance which introduce chronic pulmonary berylliosis. In our study, chronic pulmonary berylliosis was experimentally evoked by using two species of BeO with individual purity and fired temperature (A group: 95.0% in purity, and 1,300 degrees C or above in fired temperature, B group: 99.9% in purity, and 800-1,000 degrees C in fired temperature), and demarcation of prepared Be concentration involving in the genesis of the disorder was examined. BeO with various concentrations ranging from 200 micrograms to 0.1 micrograms were mixed with 0.1% agar solution and infused into right thorax cavity of male guinea pig, following which variation of the body weight was checked and pulmonary histo-pathological findings, peripheral hematological tests, and sero-biochemical tests were carried out on a periodical basis at 8 weeks, 16 weeks, and 32 weeks. The results obtained are outlined herein. 1) Body weights of test animals in both A group and B group were significantly decreased as compared with that of the control. 2) Pulmonary histo-pathological findings revealed the genesis of epitheloid-cell granuloma in the lungs where non-infusion sides were included, which resembled to non-caseating granuloma in the human pulmonary berylliosis. 3) The frequency in the genesis of epithelaid-cell granuloma was 1/36 (2.8%) in A group and 4/35 (11.4%) in B group, granuloma formation being marked in the latter. 4) Examination of the frequency in terms of BeO dosages revealed no results suggesting the dose-response relationship between pulmonary granuloma formation and the dosage. 5) There were no changes worthy of note in peripheral hematological tests. 6) Sero-biochemical tests revealed that alkaline phosphatase value together with total protein in each was significantly decreased in B group at 32 weeks following the infusion.

Berylliosis↗
PubMed1991

[Rabbit osteosarcoma induced by hydroxypropylcellulose mixed beryllium oxide pellet--comparison between implantations into bone marrow cavity and into fracture callus of the femur].

Hydroxypropylcellulose mixed beryllium oxide pellets were implanted into the distal metaphysis in the right femurs of 30 rabbits (3 groups, 10 rabbits each): in Group 1 into the internal callus 1 week after production of artificial fracture at a dose of 300 mg, in Group 2 into the bone marrow cavity at a dose of 300 mg, and in Group 3 into the bone marrow cavity at a dose of 50 mg. Osteosarcoma was induced in all of 10 rabbits in Group 1, 7 out of 10 in Group 2, 1 out of 10 in Group 3 at 56 weeks after implantation of BeO. In Group 1, the emergence of tumor and the increase of serum alkaline phosphatase appeared significantly earlier and 80% of the animals with osteosarcoma showed lung metastasis. This experimental method, especially that used in group 1, appears to be useful for the study of human osteosarcoma.

Alkaline Phosphatase↗
PubMed2005

Bioavailability of beryllium oxide particles: an in vitro study in the murine J774A.1 macrophage cell line model.

Beryllium metal and its oxide and alloys are materials of industrial significance with recognized adverse effects on worker health. Currently, the degree of risk associated with exposure to these materials in the workplace is assessed through measurement of beryllium aerosol mass concentration. Compliance with the current mass-based occupational exposure limit has proven ineffective at eliminating the occurrence of chronic beryllium disease (CBD). The rationale for this research was to examine the mechanism of beryllium bioavailability, which may be pertinent to risk. The authors tested the hypothesis in vitro that dissolution of particles engulfed by macrophages is greater than dissolution in cellular medium alone. Physicochemical changes were evaluated in vitro for well-characterized high-purity beryllium oxide (BeO) particles in cell-free media alone and engulfed by and retained within murine J774A.1 monocyte-macrophage cells. The BeO particles were from a commercially available powder and consisted of diffuse clusters (aerodynamic diameter range 1.5 to 2.5 microm) of 200-nm diameter primary particles. Following incubation for 124 to 144 hours, particles were recovered and recharacterized. Recovered particles were similar in morphology, chemical composition, and size relative to the original material, confirming the relatively insoluble nature of the BeO particles. Measurable levels of dissolved beryllium, representing 0.3% to 4.8% of the estimated total beryllium mass added, were measured in the recovered intracellular fluid. Dissolved beryllium was not detected in the extracellular media. The BeO chemical dissolution rate constant in the J774A. 1 cells was 2.1 +/- 1.7 x 10(-8)g/(cm2 . day). In contrast, the BeO chemical dissolution rate constant in cell-free media was < 8.1 x 10(-9)g/(cm2 . day). In vivo, beryllium dissolved by macrophages may be released in the pulmonary alveolar environment, in the lymphatic system after transport of beryllium by macrophages, or in the alveolar interstitium after migration and dissolution of beryllium particles in tissue. These findings demonstrate a mechanism of bioavailability for beryllium, are consistent with previously observed results in canine alveolar macrophages, and provide insights into additional research needs to understand and prevent beryllium sensitization and CBD.

Animals↗