10. Occupational asthma

Bardana, Emil J.

doi:10.1016/j.jaci.2007.08.005

Cited by 41 publications

(18 citation statements)

References 28 publications

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“…We also observed that the effect of low-MW agents on non- atopic asthma was higher than on atopic asthma. Our results support the hypotheses of Bardana, who proposed that atopic individuals are more likely to become sensitized and to have allergic OA when exposed to high-MW allergens (10). On the other hand, the relationship between atopic OA and exposure to low-MW agents remains inconsistent (4).…”

Section: Occupational Asthmogens and Atopic And Nonatopic Asthmasupporting

confidence: 84%

“…In some patients with immunologic OA, an IgE-mediated mechanism is involved after sensitization to high-MW agents derived from animal, plant, or microbial origins in the workplace (9,10). Nonimmunologic OA can be induced by exposure to high-level irritants at work, possibly via direct injury to the bronchial mucosa (8)(9)(10). One study investigated long-term outcomes of subjects with irritantinduced OA and reported no significant improvements in measures of lung function.…”

mentioning

confidence: 99%

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Risks of Exposure to Occupational Asthmogens in Atopic and Nonatopic Asthma

Wang¹,

Lin²,

Wu³

et al. 2010

Am J Respir Crit Care Med

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Section: Occupational Asthmogens and Atopic And Nonatopic Asthmasupporting

confidence: 84%

mentioning

confidence: 99%

Risks of Exposure to Occupational Asthmogens in Atopic and Nonatopic Asthma

Wang¹,

Lin²,

Wu³

et al. 2010

Am J Respir Crit Care Med

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“…Beyond infancy, additional exposures are important in establishing risk for asthma, including obesity or high body mass index (BMI)39–41, occupational exposures42, 43, and air pollution44–46. These risks are likely increasing the penetrance of asthma in genetically susceptible individuals, but it is noteworthy that the risk alleles associated with occupational asthma47, 48, for example, are often at loci that have not been implicated in asthma in non-exposed individuals.…”

Section: Asthma As a Model For Studying Geismentioning

confidence: 99%

Gene–environment interactions in human disease: nuisance or opportunity?

Ober¹,

Vercelli²

2011

Trends in Genetics

164

135

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Many environmental risk factors for common, complex human diseases have been revealed by epidemiologic studies, but how genotypes at specific loci modulate individual responses to environmental risk factors is largely unknown. Gene-environment interactions will be missed in genome-wide association studies and may account for some of the 'missing heritability' for these diseases. In this review, we focus on asthma as a model disease for studying gene-environment interactions because of relatively large numbers of candidate gene-environment interactions with asthma risk in the literature. Identifying these interactions using genome-wide approaches poses formidable methodological problems and elucidating molecular mechanisms for these interactions has been challenging. We suggest that studying gene-environment interactions in animal models, while more tractable, is not likely to shed light on the genetic architecture of human diseases. Lastly, we propose avenues for future studies to find gene-environment interactions. The Problem: Accounting for the Heritability of Common Human DiseasesDissecting the genetics of common human diseases with complex etiologies continues to be challenging and the genetic architectures of these diseases remain elusive. Despite the many successes of genome-wide association studies (GWAS) during the past four years (refs.1,2 as examples), there is a growing consensus that the common variants with modest effects on disease risk discovered through GWAS do not account for the majority of the estimated heritabilities of these diseases. This observation was initially termed 'missing heritability'3-5, to suggest that additional genetic variation (such as rare variants or copy number variants) or interactions that are not explicitly modeled (such as epistasis or gene-environment interactions [GEIs]) have been missed by GWAS and may account for a significant proportion of the heritability. More recently, the term 'hidden heritability' 6 was suggested in response to the argument that the joint or simultaneous analysis of individual common risk alleles may account for more of the heritability than the sum of each allele7,8. Of course, it is likely that the genetic architecture of most, if not all, common human diseases will include all of the above components, and it is timely in the post-GWAS era to begin to directly assess the contribution of each to the overall heritability of complex diseases. Here, we will © 2010 Elsevier Ltd. All rights reserved. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. focus on the role of GEIs on risk for human diseas...

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“…Exposure values among crustacean-processing environments are less well established, but exposures of about 3 mg/m 3 seem to induce severe allergic reactions [74]. Not only sensitization but also reactions to food via the inhalational route seem to be common particularly at the workplace, as it is estimated that up to 15% of the asthmatic population in the USA and Europe have occupational asthma [75,76].…”

Section: Sensitization and Provocation Routes: Gut Skin And Lungsmentioning

confidence: 99%

New insights into seafood allergy

Lopata

Lehrer

2009

Current Opinion in Allergy &Amp; Clinical Immunology

170

155

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Although cross-reactivity between crustacean and mollusks as well as mites is demonstrated, the often poor correlation of IgE reactivity and clinical symptoms calls for more detailed investigations. The recent development of hypoallergenic parvalbumin from carp could form the basis for safer vaccination products for treatment of fish allergy. Molecular characterization of more universal marker allergens for the three major seafood groups will improve current component-resolved clinical diagnosis and have a significant impact on the management of allergic patients, on food labeling and on future immunotherapy for seafood allergy.

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10. Occupational asthma

Cited by 41 publications

References 28 publications

Risks of Exposure to Occupational Asthmogens in Atopic and Nonatopic Asthma

Risks of Exposure to Occupational Asthmogens in Atopic and Nonatopic Asthma

Gene–environment interactions in human disease: nuisance or opportunity?

New insights into seafood allergy

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