What is the role of genetics in occupational asthma?

Dipartimento di Medicina Clinica e Sperimentale, Università degli Studi di Ferrara, Via Fossato di Mortara 64 B, 44100 Ferrara, Italy. .
European Respiratory Journal (Impact Factor: 7.13). 04/2009; 33(3):459-60. DOI: 10.1183/09031936.00183508
Source: PubMed
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    ABSTRACT: Occupational exposures are thought to be responsible for 10-15% of new-onset asthma cases in adults, with disparities across sectors. Because most of the data are derived from registries and cross-sectional studies, little is known about incidence of occupational asthma (OA) during the first years after inception of exposure. This paper describes the design of a study that focuses on this early asthma onset period among young workers in the bakery, pastry making and hairdressing sectors in order to assess early incidence of OA in these "at risk" occupations according to exposure duration, and to identify risk factors of OA incidence. The study population is composed of subjects who graduated between 2001 and 2006 in these sectors where they experience exposure to organic or inorganic allergenic or irritant compounds (with an objective of 150 subjects by year) and 250 young workers with no specific occupational exposure. A phone interview focusing on respiratory and 'Ear-Nose-Throat' (ENT) work-related symptoms screen subjects considered as "possibly OA cases". Subjects are invited to participate in a medical visit to complete clinical and lung function investigations, including fractional exhaled nitric oxide (FENO) and carbon monoxide (CO) measurements, and to collect blood samples for IgE (Immunoglobulin E) measurements (total IgE and IgE for work-related and common allergens). Markers of oxidative stress and genetic polymorphisms exploration are also assessed. A random sample of 200 "non-cases" (controls) is also visited, following a nested case-control design. This study may allow to describ a latent period between inception of exposure and the rise of the prevalence of asthma symptoms, an information that would be useful for the prevention of OA. Such a time frame would be suited for conducting screening campaigns of this emergent asthma at a stage when occupational hygiene measures and adapted therapeutic interventions might be effective. Clinical trial registration number is NCT01096537.
    BMC Public Health 04/2010; 10:206. DOI:10.1186/1471-2458-10-206 · 2.32 Impact Factor
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    ABSTRACT: The burden of asthma attributable to occupational exposures is significant. A better evaluation of markers of asthma and rhinitis in occupational settings may help reduce the frequency of occupational asthma (OA) and rhinitis (OR). This publication reviews articles published in 2008 and 2009 to provide an update on aspects related to markers of asthma and rhinitis. Markers derived from occupational exposure assessment, questionnaires, clinical data, and noninvasive tests such as functional tests or measures of serum antibodies are used to develop prediction models for the likelihood of OA and OR development. Findings from prospective studies highlight the course of preclinical signs and markers of airway inflammation in the natural history of OA and OR. Airway inflammation, evaluated by quantification of cells and mediators in induced sputum or nasal lavage and by exhaled nitric oxide, is associated with OA and OR; however, the sensitivity and specificity of these means, especially exhaled nitric oxide, have not been sufficiently assessed.
    Current Allergy and Asthma Reports 09/2010; 10(5):365-72. DOI:10.1007/s11882-010-0131-1 · 2.45 Impact Factor
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    ABSTRACT: A genetic polymorphism of the beta 2-adrenergic receptor is a major factor associated with the asthmatic phenotype. The association of this polymorphism with toluene diisocyanate (TDI)-induced asthma has not been investigated. We examined 103 TDI-induced asthma patients (TDI-OA), 60 asymptomatic exposed controls (AEC), and 263 unexposed healthy controls (NC) in order to identify beta 2-adrenergic receptor gene (ADRB2) polymorphisms and the possible association with TDI-induced asthma. Single nucleotide polymorphisms (SNPs) of ADRB2 were genotyped by direct sequencing. Serum-specific IgE and IgG levels were measured using an enzyme-linked immunosorbent assay. Phenotypes and clinical patient parameters were compared. SNPs were identified (-47 T>C, -20 T>C, Arg16Gly A>G, Gln27Glu C>G, Leu134Leu G>A, Arg175Arg C>A) during ADRB2 screening (from -231 to 793 bp). No significant differences in allelic and genotypic frequencies were noted for any of the six ADRB2 SNPs. The Arg16Gly A>G, Leu134Leu G>A, and Arg175Arg C>A SNPs and haplotype 1 [TTACGC] were significantly associated with specific IgE antibodies to the TDI-human serum albumin (HSA) conjugate in TDI-exposed subjects (P<0.05). Exposed workers with the ADRB2 ht1/ht1 homozygote had a significantly higher TDI-HSA conjugate-specific IgE sensitization rate than did those with the null ht1 haplotype (odds ratio, 15.40; 95% confidence interval, 1.81-131.06). ADRB2 polymorphisms may affect IgE-specific sensitization to TDI-HSA conjugate in TDI-exposed workers.
    Allergy, asthma & immunology research 10/2010; 2(4):260-6. DOI:10.4168/aair.2010.2.4.260 · 3.08 Impact Factor


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