{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T22:58:21Z","timestamp":1785538701642,"version":"3.56.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2011,6,1]],"date-time":"2011-06-01T00:00:00Z","timestamp":1306886400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Beryllium sensitization (BeS) and chronic beryllium disease (CBD) are determined by at least one genetic factor, a glutamic acid at position 69 (E69) of the HLA-DPB1 gene, and by exposure to beryllium. The relationship between exposure and the E69 genotype has not been well characterized.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>The study goal was to define the relationship between beryllium exposure and E69 for CBD and BeS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Workers (n = 386) from a U.S. nuclear weapons facility were enrolled into a case\u2013control study (70 BeS, 61 CBD, and 255 control subjects). HLA-DPB1 genotypes were determined by sequence-specific primer-polymerase chain reaction. Beryllium exposures were reconstructed on the basis of worker interviews and historical exposure measurements.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Any E69 carriage increased odds for CBD (odds ratio [OR], 7.61; 95% confidence interval [CI], 3.66\u201315.84) and each unit increase in lifetime weighted average exposure increased the odds for CBD (OR, 2.27; 95% CI, 1.26\u20134.09). Compared with E69-negative genotypes, a single E69-positive *02 allele increased the odds for BeS (OR, 12.01; 95% CI, 4.28\u201333.71) and CBD (OR, 3.46; 95% CI, 1.42\u20138.43). A single non-*02 E69 allele further increased the odds for BeS (OR, 29.54; 95% CI, 10.33\u201384.53) and CBD (OR, 11.97; 95% CI, 5.12\u201328.00) and two E69 allele copies conferred the highest odds for BeS (OR, 55.68; 95% CI, 14.80\u2013209.40) and CBD (OR, 22.54; 95% CI, 7.00\u201372.62).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>E69 and beryllium exposure both contribute to the odds of CBD. The increased odds for CBD and BeS due to E69 appear to be differentially distributed by genotype, with non-*02 E69 carriers and E69 homozygotes at higher odds than those with *02 genotypes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.201002-0254oc","type":"journal-article","created":{"date-parts":[[2011,3,13]],"date-time":"2011-03-13T20:08:41Z","timestamp":1300046921000},"page":"1680-1688","source":"Crossref","is-referenced-by-count":45,"title":["Risk of Chronic Beryllium Disease by HLA-DPB1 E69 Genotype and Beryllium Exposure in Nuclear Workers"],"prefix":"10.1093","volume":"183","author":[{"given":"Mike V.","family":"Van Dyke","sequence":"first","affiliation":[{"name":"National Jewish Health, Denver"},{"name":"Colorado State University, Fort Collins, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John W.","family":"Martyny","sequence":"additional","affiliation":[{"name":"National Jewish Health, Denver"},{"name":"Colorado State University, Fort Collins, and"},{"name":"Colorado School of Public Health, University of Colorado Denver, Denver, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret M.","family":"Mroz","sequence":"additional","affiliation":[{"name":"National Jewish Health, Denver"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lori J.","family":"Silveira","sequence":"additional","affiliation":[{"name":"National Jewish Health, Denver"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matt","family":"Strand","sequence":"additional","affiliation":[{"name":"National Jewish Health, Denver"},{"name":"Colorado School of Public Health, University of Colorado Denver, Denver, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tasha E.","family":"Fingerlin","sequence":"additional","affiliation":[{"name":"Colorado School of Public Health, University of Colorado Denver, Denver, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroe","family":"Sato","sequence":"additional","affiliation":[{"name":"Royal Brompton Hospital and National Heart and Lung Institute, Imperial College London, London, United Kingdom; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee S.","family":"Newman","sequence":"additional","affiliation":[{"name":"Colorado School of Public Health, University of Colorado Denver, Denver, Colorado"},{"name":"University of Colorado Denver School of Medicine, Denver, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa A.","family":"Maier","sequence":"additional","affiliation":[{"name":"National Jewish Health, Denver"},{"name":"Colorado School of Public Health, University of Colorado Denver, Denver, Colorado"},{"name":"University of Colorado Denver School of Medicine, Denver, 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