Genetic susceptibility to beryllium: a case–referent study of men and women of working age with sarcoidosis or other chronic lung disease

Cherry, Nicola; Beach, Jeremy; Burstyn, Igor; Schouchen, Janine; Svenson, Larry; Tamminga, Jan; Yiannakoulias, Niko

doi:10.1136/oemed-2014-102359

Cited by 13 publications

(7 citation statements)

References 25 publications

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“…Epidemiological evidence on the proportion of chronic beryllium disease misdiagnosed as sarcoidosis is limited to a few case series (188)(189)(190)(191)(192) and one case-referent study (193). Combining beryllium-focused studies of sarcoidosis Overall (I^2 = 94.54%, p = 0.00) Figure 4.…”

Section: Occupational Burden Of Hp (Extrinsic Allergic Alveolitis) Anmentioning

confidence: 99%

“…with other studies that estimated occupational risk, we identified seven studies to use to estimate the occupational burden of sarcoidosis (Table 8) (181,183,184,(188)(189)(190)193). The pooled estimated occupational proportion of sarcoidosis ranged from 0% to 54%, with a weighted metaproportion of 30% (95% CI, 17-45%).…”

Section: Occupational Burden Of Hp (Extrinsic Allergic Alveolitis) Anmentioning

confidence: 99%

See 1 more Smart Citation

The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement

Blanc¹,

Annesi‐Maesano²,

Balmes³

et al. 2019

Am J Respir Crit Care Med

323

204

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Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections. Methods: Relevant literature was identified for each respiratory condition. The occupational population attributable fraction (PAF) was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group. Results: Workplace exposures contribute substantially to the burden of multiple chronic respiratory diseases, including asthma (PAF, 16%); chronic obstructive pulmonary disease (PAF, 14%); chronic bronchitis (PAF, 13%); idiopathic pulmonary fibrosis (PAF, 26%); hypersensitivity pneumonitis (occupational burden, 19%); other granulomatous diseases, including sarcoidosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (occupational burden, 2.3% in silica-exposed workers and 1% in healthcare workers); and community-acquired pneumonia in working-age adults (PAF, 10%). Conclusions: Workplace exposures contribute to the burden of disease across a range of nonmalignant lung conditions in adults (in addition to the 100% burden for the classic occupational pneumoconioses). This burden has important clinical, research, and policy implications. There is a pressing need to improve clinical recognition and public health awareness of the contribution of occupational factors across a range of nonmalignant respiratory diseases.

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Section: Occupational Burden Of Hp (Extrinsic Allergic Alveolitis) Anmentioning

confidence: 99%

Section: Occupational Burden Of Hp (Extrinsic Allergic Alveolitis) Anmentioning

confidence: 99%

The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement

Blanc¹,

Annesi‐Maesano²,

Balmes³

et al. 2019

Am J Respir Crit Care Med

323

204

View full text Add to dashboard Cite

show abstract

“…The process can be dissected epidemiologically and pathologically, in a dose-response and temporal fashion, from exposure to sensitisation to overt granulomatous inflammation. A common genetic polymorphism of the human leukocyte antigen (HLA)-DP1 gene (Glu69) markedly elevates risk for beryllium sensitisation and CBD [7,8], facilitating assessment of gene-environment relationships and identification of at-risk populations [9]. Antigen-specific immunological responses can be characterised in cells obtained by bronchoalveolar lavage [10], and there are viable animal models for some aspects of CBD [6,11].…”

mentioning

confidence: 99%

Beryllium disease and sarcoidosis: still besties after all these years?

Culver

2016

Eur Respir J

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“…Differences in the lengths of microsatellite sequences in the promoter region of PLA2G4A were reported between patients with severe asthma and healthy controls, with a direct impact on mRNA and protein expression, suggesting a role in asthma pathogenesis ( Sokolowska et al 2010 ). Few candidate G × occupational exposure interaction studies have been published for asthma ( Kauffmann et al 2010 ; Kogevinas 2014 ; Smit et al 2014 ; Cherry et al 2015 ). In a GWAS focusing on occupational exposures, CTNNA3 (catenin alpha 3, alpha-T catenin) was reported to be the strongest candidate gene for toluene diisocyanate (TDI)-induced asthma in Korean patients ( Kim et al 2009 ), and only one GEWIS has been published that identified novel susceptibility loci for occupational exposure to biological dust, mineral dust, and gases and fumes in relation to forced expiratory volume in 1 sec (FEV 1 ) levels ( de Jong et al 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Genes Interacting with Occupational Exposures to Low Molecular Weight Agents and Irritants on Adult-Onset Asthma in Three European Studies

Rava

Ahmed

Kogevinas

et al. 2017

Environ Health Perspect

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Background:The biological mechanisms by which cleaning products and disinfectants—an emerging risk factor—affect respiratory health remain incompletely evaluated. Studying genes by environment interactions (G × E) may help identify new genes related to adult-onset asthma.Objectives:We identified interactions between genetic polymorphisms of a large set of genes involved in the response to oxidative stress and occupational exposures to low molecular weight (LMW) agents or irritants on adult-onset asthma.Methods:Our data came from three large European cohorts: Epidemiological Family-based Study of the Genetics and Environment of Asthma (EGEA), Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults (SAPALDIA), and European Community Respiratory Health Survey in Adults (ECRHS). A candidate pathway–based strategy identified 163 genes involved in the response to oxidative stress and potentially related to exposures to LMW agents/irritants. Occupational exposures were evaluated using an asthma job-exposure matrix and job-specific questionnaires for cleaners and healthcare workers. Logistic regression models were used to detect G × E interactions, adjusted for age, sex, and population ancestry, in 2,599 adults (mean age, 47 years; 60% women, 36% exposed, 18% asthmatics). p-Values were corrected for multiple comparisons.Results:Ever exposure to LMW agents/irritants was associated with current adult-onset asthma [OR = 1.28 (95% CI: 1.04, 1.58)]. Eight single nucleotide polymorphism (SNP) by exposure interactions at five loci were found at p < 0.005: PLA2G4A (rs932476, chromosome 1), near PLA2R1 (rs2667026, chromosome 2), near RELA (rs931127, rs7949980, chromosome 11), PRKD1 (rs1958980, rs11847351, rs1958987, chromosome 14), and PRKCA (rs6504453, chromosome 17). Results were consistent across the three studies and after accounting for smoking.Conclusions:Using a pathway-based selection process, we identified novel genes potentially involved in adult asthma by interaction with occupational exposure. These genes play a role in the NF-κB pathway, which is involved in inflammation.Citation:Rava M, Ahmed I, Kogevinas M, Le Moual N, Bouzigon E, Curjuric I, Dizier MH, Dumas O, Gonzalez JR, Imboden M, Mehta AJ, Tubert-Bitter P, Zock JP, Jarvis D, Probst-Hensch NM, Demenais F, Nadif R. 2017. Genes interacting with occupational exposures to low molecular weight agents and irritants on adult-onset asthma in three European studies. Environ Health Perspect 125:207–214; http://dx.doi.org/10.1289/EHP376

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Genetic susceptibility to beryllium: a case–referent study of men and women of working age with sarcoidosis or other chronic lung disease

Cited by 13 publications

References 25 publications

The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement

The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement

Beryllium disease and sarcoidosis: still besties after all these years?

Genes Interacting with Occupational Exposures to Low Molecular Weight Agents and Irritants on Adult-Onset Asthma in Three European Studies

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