Variable effects of chemical allergens on serum ige concentration in mice. Preliminary evaluation of a novel approach to the identification of respiratory sensitizers
- 1 October 1992
- journal article
- research article
- Published by Wiley in Journal of Applied Toxicology
- Vol. 12 (5), 317-323
- https://doi.org/10.1002/jat.2550120505
Abstract
A wide variety of chemicals may induce allergic contact dermatitis (contact sensitivity). Some chemical allergens may, in addition, cause respiratory sensitization. Topical exposure of mice to contact and respiratory chemical sensitizers results in the initiation of divergent immune responses characteristic of preferential activation of different functional subpopulations of T helper (TH) cells. In the present study we have sought to make use of these differences, particularly differences in the ability of contact and respiratory allergens to provoke IgE responses, and to question whether opportunities exist for the identification of chemicals with the potential for respiratory sensitization. We have examined alterations in the serum concentration of IgE following topical exposure of mice to seven chemical allergens; trimellitic anhydride (TMA), phthalic anhydride, diphenylmethane‐4,4′‐diisocyanate (MDI), dicyclohexylmethane‐4,4′‐diisocyanate (HMDI), isophorone diisocyanate (IPDI), oxazolone and 2,4‐dinitrochlorobenzene (DNCB). Three of these—TMA, phthalic anhydride and MDI—are known human respiratory sensitizers. The other four—HMDI, IPDI, oxazolone and DNCB—appear not to cause respiratory allergy, or at least have a very limited potential to do so. At the concentrations tested, exposure to all chemicals caused a lymphocyte proliferative response in lymph nodes draining the site of application. However, exposure only to TMA, phthalic anhydride and MDI resulted in a substantial increase in the concentration of serum IgE. Treatment with HMDI and IPDI failed to induce any change in serum IgE concentration. DNCB and oxazolone caused only small and transient elevations of IgE that were considerably less marked than those observed with respiratory sensitizers. These data suggest that it may be possible not only to identify chemical allergens as a function of immune responses induced in mice but also to determine the form that allergic reactions may take. It is proposed that analysis of induced alterations in the serum concentration of IgE may provide a method for the identification of those chemicals that have a significant potential to cause respiratory sensitization.Keywords
This publication has 29 references indexed in Scilit:
- Contact Hypersensitivity Response to Isophorone Diisocyanate in MiceDrug and Chemical Toxicology, 1989
- Respiratory effects of inhaled isocyanatesCRC Critical Reviews in Toxicology, 1986
- Detection of IgE-mediated respiratory sensitization in workers exposed to hexahydrophthalic anhydrideJournal of Allergy and Clinical Immunology, 1985
- Tetrachlorophthalic anhydride asthma: evidence for specific IgE antibodyJournal of Allergy and Clinical Immunology, 1983
- Extensive skin sensitization with minimal antibody production in guinea pigs as a result of exposure to dicyclohexylmethane-4,4′-diisocyanateToxicology and Applied Pharmacology, 1982
- Clinical and immunologic evaluation of trimellitic anhydride- and phthalic anhydride-exposed workers using a questionnaire with comparative analysis of enzyme-linked immunosorbent and radioimmunoassay studies1Journal of Allergy and Clinical Immunology, 1982
- Immunoglobulin E—mediated asthma and hypersensitivity pneumonitis with precipitating anti-hapten antibodies due to diphenylmethane diisocyanate (MDI) exposureJournal of Allergy and Clinical Immunology, 1980
- Immunologic sensitization and pulmonary hypersensitivity by repeated inhalation of aromatic isocyanatesToxicology and Applied Pharmacology, 1980
- Pulmonary hypersensitivity to hexyl isocyanate-ovalbumin aerosol in guinea pigsToxicology and Applied Pharmacology, 1979
- Isocyanate asthma: respiratory symptoms caused by diphenyl-methane di-isocyanateThorax, 1973