Genetic markers for occupational asthma

Park, Hae‐Sim; Frew, Anthony J.

doi:10.1067/mai.2002.124664

Cited by 13 publications

(9 citation statements)

References 22 publications

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“…Among the many risk markers associated with susceptibility for the development of TDI asthma, the ability to cope with oxidative stress has been studied recently [13]. Evidence has been presented that TDI exposure might cause oxidative stress at the epithelial surface [20].…”

Section: Discussionmentioning

confidence: 99%

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Long-term follow-up of toluene diisocyanate-induced asthma

Padoan¹,

Pozzato²,

Simoni³

et al. 2003

Eur Respir J

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Eighty-seven cases of occupational asthma induced by toluene diisocyanate (TDI) were diagnosed by an inhalation challenge with TDI and methacholine. After an average follow-up interval of 11 yrs, all subjects were re-examined.Of the 87 subjects examined, 13 (15%) had remained in the same job, 44 (50.5%) had been removed from exposure forv10 yrs and 30 (34.5%) had been removed forw10 yrs. The proportion of subjects who experienced symptoms of asthma and those who were hyperresponsive to methacholine was significantly lower. Of the patients, 59% used short-acting bronchodilators, 8% long-acting bronchodilators and 18% were on regular inhaled glucocorticoids. Thus, multiple regression analysis showed a positive correlation between forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) at follow-up and FVC and FEV1 at diagnosis, and a negative correlation with smoking and with therapy with bronchodilators. Stepwise logistic regression showed that the follow-up provocative dose causing a 20% fall in the FEV1 (PD20) could be predicted from baseline PD20.These results indicate that respiratory symptoms and airway hyperresponsiveness to methacholine persist in subjects removed from exposure to TDI for w10 yrs. A more favourable prognosis was associated with a better lung function and a lower degree of airway hyperresponsiveness to methacholine at diagnosis. Eur Respir J 2003; 21: 637-640.

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Section: Discussionmentioning

confidence: 99%

“…The phenotype characteristics of the subjects are illustrated in order to investigate the outcome of disease. Since OA is a valid model of adult-onset asthma [12,13], information on the outcome of OA can also bring new insights into the natural history of non-OA.…”

mentioning

confidence: 99%

Long-term follow-up of toluene diisocyanate-induced asthma

Padoan¹,

Pozzato²,

Simoni³

et al. 2003

Eur Respir J

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“…Isocyanate exposure induces intracellular hydrogen peroxide production and intercellular adhesion molecule (ICAM)-1 expression on cultured mononuclear cells, suggesting that the production of reactive oxygen species by monocytes at the site of exposure of an isocyanate may contribute to tissue damage [47]. The production of hydrogen peroxide upregulates ICAM-1 expression, which may potentiate the infiltration and adhesion of cells at the site of exposure [3,47]. Therefore, defects in antioxidant defences could contribute to the susceptibility of isocyanate-induced asthma.…”

Section: Oxidative Stressmentioning

confidence: 99%

“…Asthma and allergies are good models for studying complex diseases resulting from the interaction of genetic and environmental factors, and occupational asthma (OA) is a good model for studying the natural history of adult-onset asthma and investigating gene-workplace interactions [2,3]. The amount of time spent in the workplace is an important component of an individual9s environment.…”

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confidence: 99%

The role of genetic factors in occupational asthma: Table 1

Mapp¹

2003

Eur Respir J

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This article explores the influence of genetic factors on the development of sensitisation and occupational asthma (OA).First, several types of studies aimed at examining the role of genes, as well as the role of gene-environment interactions in asthma, including the available data for OA specifically, were reviewed. Genetic approaches include linkage and allele-sharing analysis and segregation analysis. Secondly, deoxyribonucleic acid banking for epidemiological studies was focused upon, highlighting the factors to be considered in choosing the appropriate specimens for genotyping.OA, like asthma, is a multifactorial condition and, to date, no ideal genetic study has been described to examine complex gene-environment interactions. Most studies in OA have examined human leukocyte antigen-associated polymorphisms with some nonreproducible results.The search for genes in occupational asthma is still in progress, and much of the information obtained has been based on small sample sizes, using different strategies for the recruitment of subjects. The best methodological approach still needs to be determined and the results of genetic identification need to be confirmed in different samples.

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“…In addition, the test must search for a gene that is sufficiently penetrant for the test result to have health implications [11,12]. So far, associations found in OA are modest with low odds ratios, indicating that genetic testing alone is not advisable for measuring risk for OA [13][14][15]. Furthermore, because asthma is a complex disease, caused by multiple genetic and environmental factors, information obtained to date by a single gene test is limited for both diagnostic and preventive purposes and, thus, cannot be recommended [16].…”

mentioning

confidence: 99%

What is the role of genetics in occupational asthma?

Mapp¹

2009

Eur Respir J

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Genetic markers for occupational asthma

Cited by 13 publications

References 22 publications

Long-term follow-up of toluene diisocyanate-induced asthma

Long-term follow-up of toluene diisocyanate-induced asthma

The role of genetic factors in occupational asthma: Table 1

What is the role of genetics in occupational asthma?

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