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: Work-related asthma (WRA) includes occupational asthma and work-exacerbated asthma. WRA is by definition preventable. This chapter discusses available tools for prevention of WRA, divided into primary and secondary prevention. For each tool, the available evidence for the effectiveness of the tool is summarized, and examples are provided. Primary prevention addresses healthy workers or persons with asthma due to causes unrelated to work. The principal tool is control of occupational exposure, reached by elimination or reduction in exposure, but vocational guidance and pre-employment screening are also regarded as primary prevention tools. Secondary prevention addresses early detection of work-related sensitization or WRA to prevent further progression. The principal tool for secondary prevention is medical surveillance. Prediction models represent a promising new tool in medical surveillance; this tool is described here in general and by an example. To set priorities for the prevention of WRA, the monitoring of occurrence in populations as well as in specific industries is crucial, and this chapter therefore briefly describes different sources for surveillance data including sentinel reporting systems, population studies, and occupational disease registers. In the future, focus should be on well-conducted intervention studies, improved exposure assessment, improved medical surveillance (e.g., using prediction models) and good quality national surveillance programs.
    02/2011: pages 281-298;
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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. · 3.08 Impact Factor
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    ABSTRACT: The purpose of this article is to critically review the available evidence pertaining to occupational, environmental, and individual factors that can affect the development of occupational asthma (OA). Increasing evidence suggests that exploration of the intrinsic characteristics of OA-causing agents and associated structure-activity relationships offers promising avenues for quantifying the sensitizing potential of agents that are introduced in the workplace. The intensity of exposure to sensitizing agents has been identified as the most important environmental risk factor for OA and should remain the cornerstone for primary prevention strategies. The role of other environmental co-factors (e.g., non-respiratory routes of exposure and concomitant exposure to cigarette smoke and other pollutants) remains to be further delineated. There is convincing evidence that atopy is an important individual risk factor for OA induced by high-molecular-weight agents. There is some evidence that genetic factors, such as leukocyte antigen class II alleles, are associated with an increased risk of OA; however, the role of genetic susceptibility factors is likely to be obscured by complex gene-environment interactions. OA, as well as asthma in general, is a complex disease that results from multiple interactions between environmental factors and host susceptibilities. Determining these interactions is a crucial step towards implementing optimal prevention policies.
    Allergy, asthma & immunology research 07/2011; 3(3):157-67. · 3.08 Impact Factor


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