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Plasticisers, another burden for asthmatics?
C J Doelman1, P J Borm, A Bast
1Department of Pharmacochemistry, Faculty of Chemistry, Vrije Universiteit, Amsterdam, The Netherlands.
Agents and Actions. Supplements
|January 1, 1990
Summary
Di(2-ethylhexyl)phthalate (DEHP) exposure may lead to bronchial hyperresponsiveness. Its metabolite, mono(2-ethylhexyl)phthalate (MEHP), was shown to increase airway reactivity in rat tracheal tissue.
Area of Science:
- Toxicology
- Pulmonary Medicine
- Pharmacology
Background:
- Di(2-ethylhexyl)phthalate (DEHP) is a widely used plasticizer with known toxicological effects on lung tissue.
- Previous studies indicate DEHP inhalation can cause pulmonary edema and asthma, while intravenous injection leads to lung inflammation and hemorrhage.
Purpose of the Study:
- To investigate the potential of DEHP to induce bronchial hyperresponsiveness.
- To examine the effect of DEHP's metabolite, mono(2-ethylhexyl)phthalate (MEHP), on airway reactivity.
Main Methods:
- In vitro assessment of MEHP's effect on methacholine dose-response curves in rat tracheal tissue.
- Evaluation of dose-dependent changes in EC50 and maximal effect.
Main Results:
- MEHP induced a dose-dependent increase in the negative logarithm of the EC50 for methacholine.
- MEHP also caused a decrease in the maximal effect of the methacholine dose-response curve.
- These findings suggest MEHP alters airway smooth muscle responsiveness.
Conclusions:
- DEHP, through its metabolite MEHP, may cause bronchial hyperresponsiveness.
- The study highlights a potential mechanism for DEHP-induced respiratory issues.
- Further in vivo studies are warranted to confirm these findings in a whole organism context.