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Sample records for berylliosis

  1. Interaction of genetic and exposure factors in the prevalence of berylliosis.

    Science.gov (United States)

    Richeldi, L; Kreiss, K; Mroz, M M; Zhen, B; Tartoni, P; Saltini, C

    1997-10-01

    Prevalence of berylliosis, a lung disorder driven by the activation of beryllium-specific T cells, is associated with a major histocompatibility complex (MHC) class II marker (HLA-DPB1Glu69) and with the type of industrial exposure. We evaluated the interaction between marker and exposure in a beryllium-exposed population in which the prevalence of berylliosis was associated with machining beryllium. The presence of the marker was associated with higher prevalence (HLA-DPB1Glu69-positive machinists 25%; HLA-DPB1Glu69-negative machinists 3.2%, P = 0.05) and predicted berylliosis independent of machining history (odds ratios 11.8 and 10.1). The study shows that in berylliosis the carrier status of a genetic susceptibility factor adds to the effect of process-related risk factors.

  2. [Asthma, alveolitis, aspergillosis, berylliosis. What to do when there is allergic reaction of the lung?].

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    Vier, H; Protze, M; Brunner, R; Gillissen, A

    2003-03-06

    Among the major allergic pulmonary disorders are bronchial asthma, extrinsic allergic alveolitis, allergic aspergillosis and berylliosis. Asthma is diagnosed on the basis of clinical symptoms (wheezing, respiratory distress, tight chest, coughing) and lung function tests possibly supplemented by allergic and provocative testing. Asthma treatment is differentiated into long-term medication and as-required medication. Specific immunotherapy is considered the sole causal therapy. Extrinsic allergic alveolitis is work- or hobby-related (farmer's/cheese worker's/bird-fancier's lung) and manifests as diffuse pneumonitis with dyspnea, coughing and fever. For the diagnosis, the antigen provocative test in particular plays a major role. In the main, treatment comprises strict avoidance of allergens. The diagnosis of allergic pulmonary aspergillosis is based on the history, clinical findings, skin tests, serology and radiography. Treatment is stage-related by means of immunosuppressive agents. In terms of radiographic and pulmonary function findings, berylliosis is similar to sarcoidosis. Here, too, immunosuppressive agents are to the fore.

  3. Immunogenetic basis of environmental lung disease: Lessons from the berylliosis model

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    Saltini, C.; Richeldi, L. [Univ. di Modena, Dept. di Scienze Mediche, Modena (Italy); Amicosante, M. [Univ. di Roma `Tor Vergata`, Dept. di Biologia, Roma (Italy); Franchi, A. [Univ. de Modena, Dept. Medicina Interna, Modena (Italy); Lombardi, G. [Hammersmith Hospital, Dept. of Immunology, London (United Kingdom)

    1998-12-01

    The role of genetic factors has been hypothesized in the pathogenesis of a number of chronic inflammatory lung diseases. The genes of the major histocompatibility complex (MHC) locus on human chromosome 6 have been identified as important determinants in diseases caused both by inorganic and organic compounds such as beryllium, gold, acid anhydrides, isocyanates and grass pollens. Since many environmental factors are the determinants of the immunopathogenesis of asthma, pulmonary granulomatous disorders, hypersensitivity pneumonitis and fibrotic lung disorders, an understanding of the interaction between environmental factors is crucial to epidemiology, prevention and treatment of these disorders. Berylliosis is an environmental chronic inflammatory disorder of the lung caused by inhalation of beryllium dusts. A human leukocyte antigen class II marker (HLA-DP Glu69) has been found to be strongly associated with the disease. In in vitro studies, the gene has been shown to play a direct role in the immunopathogenesis of the disease. In human studies, the gene has been shown to confer increased susceptibility to beryllium in exposed workers, thus suggesting that HLA gene markers may be used as epidemiological probes to identify population groups at higher risk of environmental lung diseases, to identify environmental levels of lung immunotoxicants that would be safe for the entire population and the prevent disease risk associated with occupation, manufactured products and the environment. Studies on the associations between human leukocyte antigens and chronic inflammatory lung disorders are reviewed in the context of the berylliosis model. (au) 123 refs.

  4. Identification of HLA-DRPheβ47 as the susceptibility marker of hypersensitivity to beryllium in individuals lacking the berylliosis-associated supratypic marker HLA-DPGluβ69

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    Rogliani Paola

    2005-08-01

    Full Text Available Abstract Background Susceptibility to beryllium (Be-hypersensitivity (BH has been associated with HLA-DP alleles carrying a glutamate at position 69 of the HLA-DP β-chain (HLA-DPGlu69 and with several HLA-DP, -DQ and -DR alleles and polymorphisms. However, no genetic associations have been found between BH affected subjects not carrying the HLA-DPGlu69 susceptibility marker. Methods In this report, we re-evaluated an already described patient populations after 7 years of follow-up including new 29 identified BH subjects. An overall population 36 berylliosis patients and 38 Be-sensitization without lung granulomas and 86 Be-exposed controls was analysed to assess the role of the individual HLA-class II polymorphisms associated with BH-susceptibility in HLA-DPGlu69 negative subjects by univariate and multivariate analysis. Results As previously observed in this population the HLA-DPGlu69 markers was present in higher frequency in berylliosis patients (31 out of 36, 86% than in Be-sensitized (21 out of 38, 55%, p = 0.008 vs berylliosis and 41 out of 86 (48%, p However, 22 subjects presenting BH did not carry the HLA-DPGlu69 marker. We thus evaluated the contribution of all the HLA-DR, -DP and -DQ polymorphisms in determining BH susceptibility in this subgroup of HLA-Glu69 subjects. In HLA-DPGlu69-negatives a significant association with BH was found for the HLA-DQLeu26, for the HLA-DRB1 locus residues Ser13, Tyr26, His32, Asn37, Phe47 and Arg74 and for the HLA-DRB3 locus clusterized residues Arg11, Tyr26, Asp28, Leu38, Ser60 and Arg74. HLA-DRPhe47 (OR 2.956, p Conclusion We conclude that HLA-DPGlu69 is the primary marker of Be-hypersensitivity and HLA-DRPhe47 is associated with BH in Glu69-negative subjects, likely playing a role in Be-presentation and sensitization.

  5. Beryllium detection in human lung tissue using electron probe X-ray microanalysis.

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    Butnor, Kelly J; Sporn, Thomas A; Ingram, Peter; Gunasegaram, Sue; Pinto, John F; Roggli, Victor L

    2003-11-01

    Chronic berylliosis is an uncommon disease that is caused by the inhalation of beryllium particles, dust, or fumes. The distinction between chronic berylliosis and sarcoidosis can be difficult both clinically and histologically, as both entities can have similar presentations and exhibit nonnecrotizing granulomatous inflammation of the lungs. The diagnosis of chronic berylliosis relies on a history of exposure to beryllium, roentgenographic evidence of diffuse nodular disease, and demonstration of beryllium hypersensitivity by ancillary studies, such as lymphocyte proliferation testing. Additional support may be gained by the demonstration of beryllium in lung tissue. Unlike other exogenous particulates, such as asbestos, detection of beryllium in human lung tissue is problematic. The low atomic number of beryllium usually makes it unsuitable for conventional microprobe analysis. We describe a case of chronic berylliosis in which beryllium was detected in lung tissue using atmospheric thin-window energy-dispersive X-ray analysis (ATW EDXA). A woman with a history of occupational exposure to beryllium at a nuclear weapons testing facility presented with progressive cough and dyspnea and a nodular pattern on chest roentgenograph. Open lung biopsy showed nonnecrotizing granulomatous inflammation that was histologically indistinguishable from sarcoidosis. Scanning electron microscopy and ATW EDXA demonstrated particulates containing beryllium within the granulomas. This application of EDXA offers significant advantages over existing methods of beryllium detection in that it is nondestructive, more widely available, and can be performed using routine paraffin sections.

  6. Some results of medical researches at Ulba Metallurgical Plant

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    Artemieva, G.I.; Novikov, V.G.; Savchuk, V.V. [Ulba Metallurgical Plant, Ust-Kamenogorsk (Kazakhstan)

    1998-01-01

    The results of 45-years medical researches at beryllium production of Ulba Metallurgical Plant are summarized in this report. Statistic data on different kinds of occupational diseases, related to beryllium production and the dynamics of changing occupational diseases with the development of beryllium production, are given there. Data on average duration of life of occupational disease patients are presented in the report. It includes the description of problems, related to berylliosis diagnosis. Issues, connected to beryllium production effect on health of man, located nearby beryllium production are also discussed there as well. (author)

  7. High-resolution CT in the evaluation of occupational and environmental disease

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    Akira, M. [National Kinki Central Hospital for Chest Diseases, Osaka (Japan). Dept. of Radiology

    2002-01-01

    CT has an increasing role in the radiologic evaluation of occupational/environmental lung disease. The high-resolution CT (HRCT) findings of silicosis, mixed dust pneumoconiosis, coal worker's pneumoconiosis, graphite pneumoconiosis, asbestosis, talcosis, welder's lung, berylliosis, aluminum lung, and hard metal pneumoconiosis are described. Hypersensitivity pneumonitis and lung damage caused by exposure to toxic fumes also are described. HRCT pathologic correlation with each type of pneumoconiosis is focused on. HRCT is useful in achieving an accurate categorization of the parenchymal changes in each type of pneumoconiosis.

  8. Analysis of HLA-DP association with beryllium disease susceptibility in pooled exposed populations

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    Cesare Saltini, Massimo Amicosante

    2009-12-19

    Berylliosis or Chronic Beryllium Disease is a chronic granulomatous disorder primarily involving the lung associated with the exposition to low doses of Beryllium (Be) in the workplace. Berylliosis risk has been associated with the presence of a glutamate at position 69 of the HLA-DP beta chain (HLA-DPbetaGlu69) that is expressed in about 97% of disease cases and in 27% of the unaffected Be-exposed controls (p<0.0001) (Richeldi et al. Science 1993; 262: 242-244.12). Since this first observation of an immunogenetic association between berylliosis and HLA-DPbetaGlu69 a number of studies have confirmed the role of this marker as the primary gene of susceptibility of berylliosis (Richeldi et al Am J Ind Med. 1997; 32:337-40; Wang et al J. Immunol. 1999; 163: 1647-53; Saltini et al Eur Respir J. 2001 18:677-84; Rossman et al Am J Respir Crit Care Med. 2002 165:788-94). Moreover, a structure/function interaction between HLA-DP molecules carrying Glu69 and beryllium in driving and developing the immune response against beryllium itself has been observed as: (1) Be-specific T-cells clones obtained from berylliosis patients recognize beryllium as antigen only when presented in the context of the HLA-DP{beta}Glu69 molecules but not in the context of HLA-DP allelic variants carrying Lys69 (Lombardi G et al. J Immunol 2001; 166: 3549-3555), and (2) beryllium presents an affinity for the HLA-DP2, carrying the berylliosis marker of susceptibility HLA-DPGlu69, from 40 to 100 times higher that the HLA-DP molecule carrying Lys69 (Amicosante M. et al Hum. Immunol. 2001; 62: 686-93). However, although the immunogenetic studies performed have been addressed a number of different questions about the genetic association between berylliosis and/or beryllium sensitization, exposure levels to beryllium and HLA markers, a number of questions are still open in the field mainly due to the limitation imposed by the low number of subjects carrying berylliosis or beryllium sensitization enrolled

  9. Interstitial granulomatous pulmonary diseases: a diagnostic approach for the general pathologist

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    Silva Aloísio S. Felipe da

    2003-01-01

    Full Text Available Some kinds of interstitial pneumonia present a histopathological pattern dominated by sarcoid - necrotizing or non-necrotizing - granulomas, which can be divided into two main groups: infectious and non-infectious. The infectious causes include tuberculosis, histoplasmosis, fungi in general, paracoccidioidomycosis, ascaridiasis, echinococcosis and dirophilariosis. The non-infectious causes include histiocytosis-X, hipersensitivity pneumonia, vasculitis, lymphomas, sarcoidosis, and pneumoconioses such as silicosis and berylliosis. The purpose of this review is to provide a practical guideline to enable general pathologists to make the differential diagnosis of granulomatous pulmonary diseases. For this purpose, anatomical-clinical-radiological correlations will be presented and targeted to each diagnosis discussed. Whenever a granulomatous inflammatory process is in progress, the search for infective agents by direct observation, by culture, and by histochemical methods should be mandatory. The histological aspects of infectious granulomas to be analyzed should include their random histo-anatomical location, the type of inflammatory reaction, and necrosis. A panel of complementary reactions (immunohistochemistry and PCR should identify the infectious agent and, whenever their results and the culture are negative, the possibility of non-infectious granulomatous diseases has to be evaluated. In such cases, the histo-anatomical distribution (bronchocentric, lymphangitic, angiocentric, random, the qualitative characteristics of the lesions (type of necrosis and inflammatory reaction, and the correlation with the X-ray findings will help the diagnosis.

  10. The Angiotensin Converting Enzyme Insertion/Deletion polymorphism is not associated with an increased risk of death or bronchopulmonary dysplasia in ventilated very low birth weight infants

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    Baier R John

    2004-12-01

    Full Text Available Abstract Background The ACE gene contains a polymorphism consisting of either the presence (insertion, I or absence (deletion, D of a 287 bp alu repeat in intron 16. The D allele is associated with increased ACE activity in both tissue and plasma. The DD genotype is associated with risk of developing ARDS and mortality. The frequency of the D allele is higher in patients with pulmonary fibrosis, sarcoidosis and berylliosis. The role of this polymorphism has not been studied in the development of BPD in the premature newborn. Methods ACE I/D genotype was determined in 245 (194 African-American, 47 Caucasian and 4 Hispanic mechanically ventilated infants weighing less than 1250 grams at birth and compared to outcome (death and/or development of BPD. Results The incidence of the D allele in the study population was 0.58. Eighty-eight (35.9% infants were homozygous DD, 107 (43.7% were heterozygous ID and 50 (20.4% were homozygous II. There were no significant differences between genotype groups with respect to ethnic origin, birth weight, gestation, or gender. There was no effect of the ACE I/D polymorphism on mortality or development of BPD (O2 on 28 days or 36 weeks PCA. Secondary outcomes (intraventricular hemorrhage and periventricular leukomalacia similarly were not influenced by the ACE ID polymorphism. Conclusions The ACE I/D polymorphism does not significantly influence the development of BPD in ventilated infants less than 1250 grams.

  11. Medical Surveillance for Former Workers

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    Tim Takaro

    2009-05-29

    The Former Hanford Worker Medical Monitoring Program, directed by the Occupational and Environmental Medicine Program at the University of Washington, served former production and other non-construction workers who were potentially exposed to workplace hazards while working for the USDOE or its contractors at Hanford. The USDOE Former Workers Program arose from Congressional action in the Defense Authorization of 1993 (Public Law 102). Section 3162 stated that, “The Secretary shall establish and carry out a program for the identification and ongoing medical evaluation of current and former Department of Energy employees who are subject to significant health risks as a result of exposure of such employees to hazardous or radioactive substances during such employment.” (This also covers former employees of USDOE contractors and subcontractors.) The key objective has been to provide these former workers with medical evaluations in order to determine whether workers have experienced significant risk due to workplace exposure to hazards. Exposures to asbestos, beryllium, and noise can produce specific medical conditions: asbestosis, berylliosis, and noise-induced hearing loss (NIHL). Each of these conditions can be identified by specific, non-invasive screening tests, which are widely available. Treatments are also available for individuals affected by these conditions. This project involved two phases. Phase I involved a needs and risk assessment, characterizing the nature and extent of workplace health hazards which may have increased the risk for long-term health effects. We categorized jobs and tasks by likelihood of exposures to specific workplace health hazards; and located and established contact with former Hanford workers. Phase II involved implementation of medical monitoring programs for former workers whose individual work history indicated significant risk for adverse health effects. We identified 118,000 former workers, employed from 1943 to 1997