Specific IgE to isocyanates: A useful diagnostic role in occupational asthma☆☆☆★★★

Tee, R D; Cullinan, Paul; Welch, J; Burge, P. Sherwood; Newman-Taylor, A. J.

doi:10.1016/s0091-6749(98)70181-2

Cited by 154 publications

(96 citation statements)

References 22 publications

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“…[3][4][5][6] Allergen-specific IgE, atopy, and elevated total serum IgE, which are strongly associated with common environmental asthma, are not generally associated with isocyanate asthma. 7,8 Thus, in contrast to common allergens, the cell types and effector molecules stimulated by isocyanate exposure remain unclear, including those that promote the development of pathogenic hypersensitivity responses vs. apparent "tolerance". The characteristic differences between isocyanate and common environmental asthma, have lead to the hypothesis that (low molecular weight) isocyanate chemicals elicit immune responses fundamentally distinct from those induced by common environmental allergens, which are generally (high molecular weight) proteins.…”

Section: Introductionmentioning

confidence: 99%

“…9,13,14 However, as mentioned above, antigenic isocyanate-albumin conjugates do not stimulate vigorous in vitro TH2 cellular responses. 4,7 Instead, limited recent studies suggest that human monocyte responses may play an important role in clinical isocyanate exposure outcome. 15,16 Monocytes are crucial cells of the innate arm of the immune system that circulate in an immature form, and differentiate into "tissue macrophages", dendritic cells and alveolar macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Human innate immune responses to hexamethylene diisocyanate (HDI) and HDI–albumin conjugates

Wisnewski

Liu

et al. 2008

Clin Experimental Allergy

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human innate immune responses to hexamethylene diisocyanate (HDI) and HDI–albumin conjugates

Wisnewski

Liu

et al. 2008

Clin Experimental Allergy

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“…The mechanisms by which methylene diphenyl diisocyanate (MDI) causes asthmatic reactions have not been clearly understood. Some investigators have suggested that serum-specific IgE and IgG antibodies are increased in some MDI-sensitized workers [3][4][5][6]. In our previous study, serum-specific IgE and IgG antibodies were shown to be increased in some MDI-induced occupational asthma (MDI-OA) patients, of which specific IgG antibodies were more associated with work-related respiratory symptoms (WRRS) [7].…”

Section: Introductionmentioning

confidence: 74%

Histamine Release and Inflammatory Cell Infiltration in Airway Mucosa in Methylene Diphenyl Diisocyanate (MDI)-Induced Occupational Asthma

et al. 2008

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Introduction Although methylene diphenyl diisocyanate (MDI) is widely used in industries, there have been few studies of the pathogenic mechanisms of MDI-induced occupational asthma (MDI-OA). Methods We performed immunohistochemical analyses, measured inflammatory mediators and cytokines, and quantified histamine release (HR) from peripheral basophils in MDI-OA patients. Thirteen MDI-exposed workers (five MDI-OA, two MDI-induced esoinophilic bronchitis, and six asymptomatic exposed controls, AEC) were enrolled. Results and Discussion Immunochemical analyses indicated significantly increased anti-eosinophilic cationic proteinstained cells in MDI-OA patients as compared with controls (P<0.05). Sputum eosinophil cationic protein levels were increased after MDI-specific inhalation challenge test in MDI-OA/EB patients (P<0.02). Sputum eosinophil counts were highly correlated with IL-8 and MMP-9 levels (P<0.05 and P<0.01, respectively). Basophil HR was significantly increased in MDI-OA patients after stimulations with anti-IgG4 and MDI-human serum albumin conjugates (both P<0.05). Eosinophil activation is a major feature of airway inflammation in MDI-OA patients. Increased HR by MDI may contribute to the pathogenic mechanisms of MDI-OA.

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“…to complex (unconjugate) platinum salts, trimellitic and acid anhydrides [18,19]. In the case of LMW compounds, particularly some of the most common causes of OA, like isocyanates, the sensitivity and specificity of tests assessing the IgE response is variable, being good for some [20] and less satisfactory for others [21,22]. It is also worth noting that results of both skin and in-vitro tests of IgE-mediated sensitivity may fall to a level below detection when workers are removed from exposure [12].…”

Section: Immunological Assessmentmentioning

confidence: 99%

Diagnosing occupational asthma: how, how much, how far?: Table 1

Moscato

Jl²,

Bernstein³

2003

Eur Respir J

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Diagnosing occupational asthma is still a challenge because it is based on a stepwise approach in which the depth of investigative means may vary depending on resources. The authors herewith review the existing investigative means from the approach of outlining controversies and queries.There is no validated clinical questionnaire for diagnosing occupational asthma. Immunological investigation is limited by the lack of standardised extracts for skinprick testing and specific immunoglobulin E assessments. Criteria for interpretation of changes in peak expiratory flow rates and bronchial responsiveness to pharmacological agents are still open to discussion.It is worth improving the methodology of specific inhalation challenges, either in the laboratory or in the workplace, to facilitate more extensive use of these tests. Validation of new means that assess airway inflammation, such as exhaled nitric oxide and induced sputum, needs to be performed. There is a need to increase the use of these diagnostic tests because the diagnosis is still too often based on "clinical impression". Eur Respir J 2003; 21: 879-885.

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Specific IgE to isocyanates: A useful diagnostic role in occupational asthma☆☆☆★★★

Cited by 154 publications

References 22 publications

Human innate immune responses to hexamethylene diisocyanate (HDI) and HDI–albumin conjugates

Human innate immune responses to hexamethylene diisocyanate (HDI) and HDI–albumin conjugates

Histamine Release and Inflammatory Cell Infiltration in Airway Mucosa in Methylene Diphenyl Diisocyanate (MDI)-Induced Occupational Asthma

Diagnosing occupational asthma: how, how much, how far?: Table 1

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