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At least 37 records · Page 2Linked to original sources

The contribution of histamine release to bronchoconstriction provoked by inhaled benzalkonium chloride in asthma.

1. To investigate the possibility that benzalkonium chloride-induced bronchoconstriction results from the endogenous release of histamine, we examined the effect of the selective histamine antagonists terfenadine and astemizole, on the airways response to inhaled benzalkonium chloride and histamine in 12 asthmatic subjects. 2. Double-blind concentration- and time-course studies were undertaken, 3 h after treatment with terfenadine or matched placebo. 3. Benzalkonium chloride and histamine caused concentration-related falls in FEV1 in all subjects with benzalkonium chloride being 7.4 times less potent as a bronchoconstrictor agonist than histamine. Terfenadine displaced to the right the benzalkonium chloride and histamine concentration-response curves by 3.7 and 111 fold respectively. Terfenadine attenuated the initial (5 min) bronchoconstrictor response to benzalkonium chloride by 40%. However, over the whole 45 min period, the response was reduced by only 13% compared with 86% inhibition of the response to histamine. 4. In an open study, eight of the 12 subjects undertook a time course study with inhaled benzalkonium chloride after pretreatment with the chemically unrelated histamine antagonist astemizole. Astemizole inhibited benzalkonium chloride-induced bronchoconstriction to an almost identical degree as that achieved with terfenadine. 5. We conclude that the initial bronchoconstrictor effect of benzalkonium chloride is due, in part, to histamine release. However, the majority of the adverse effect relates to other, as yet unrecognised effects of this bacteriocidal substance.

Adult↗

Contact dermatitis from the epoxy resins tetraglycidyl-4,4'-methylene dianiline and o-diglycidyl phthalate in composite material.

An outbreak of dermatitis occurred in an aircraft factory using epoxy resin composite material. Of 25 operatives, 14 gave positive patch test reactions to the composite material and/or diglycidylether of bisphenol A (DGEBA), tetraglycidyl-4,4'-methylene dianiline (TGMDA), and o-diglycidyl phthalate. This report seems to be the first to demonstrate contact allergy to the two last mentioned epoxy resins. The diglycidylether of bisphenol A used in routine test series picked up only 3 cases of 12 tested.

Aniline Compounds↗

Airborne occupational allergic contact dermatitis from triglycidyl-p-aminophenol and tetraglycidyl-4,4'-methylene dianiline in preimpregnated epoxy products in the aircraft industry.

BACKGROUND: Very little is known about allergic contact dermatitis (ACD) from preimpregnated epoxy products (prepregs). OBJECTIVE: To describe a patient with occupational ACD from prepregs, and report new quantitative data on the content of prepregs. METHODS AND RESULTS: A laminator developed work-related vesicular hand dermatitis. He worked in an aircraft plant assembling aircraft parts, being exposed to preimpregnated carbon fiber and fiberglass sheets (prepregs), and epoxy adhesive tapes and foams. Triglycidyl-p-aminophenol (TGPAP; 1-0.25%, 2+; 0.05%, 1+) and tetraglycidyl-4,4'-methylene dianiline (TGMDA; 1%, 3+; 0.5-0.05%, 2+) provoked allergic patch test reactions, whereas o-diglycidyl phthalate was negative (1-0.05% pet) and standard epoxy provoked a weak (?+) reaction. Six prepreg products provoking allergic patch test reactions were analyzed for their TGPAP, TGMDA and diglycidyl ether of bisphenol A (DGEBA) content using gas and liquid chromatographic methods, showing up to 10% of TGPAP, 19% of TGMDA and 5% of DGEBA in the prepregs. An epoxy primer contained 61% of TGPAP. CONCLUSION: TGPAP and TGMDA caused occupational ACD. These chemicals need to be used when patch testing patients are exposed to prepregs, because patch testing with DGEBA may be negative.

Adult↗

Antioxidant effect of capsaicin on lipid peroxidation in homogeneous solution, micelle dispersions and liposomal membranes.

The antioxidant activity of capsaicin (CAP) was measured in the oxidation of methyl linoleate (ML) in homogeneous solution, of ML micelles in aqueous dispersions and also of soybean phosphatidylcholine liposomal membrane, and was compared to that of alpha-tocopherol (alpha-TOH) which is one of the most important antioxidants in vivo. The reactivity of CAP toward galvinoxyl (a model phenoxyl radical) in acetonitrile solution was found to be much smaller than that of alpha-TOH, suggesting that the radical scavenging activity of CAP is much weaker than that of alpha-TOH. In fact, in homogeneous acetonitrile solution where the antioxidant activity is determined primarily by the chemical activity of the antioxidant toward peroxyl radicals, CAP inhibited the oxidation of ML much less efficiently than alpha-TOH and a clear induction period was not observed. The antioxidant activity of CAP was found to be about 60 times smaller than that of alpha-TOH in homogeneous solution. However, in micelle oxidation, the difference in antioxidant activity of the two antioxidants was much smaller than in homogeneous solution. Furthermore, in the membrane, CAP inhibited the oxidation almost as effectively as alpha-TOH. These results suggest that CAP can act as an antioxidant in the biomembrane.

Acetonitriles↗

[Effect of mixed function oxidases on phthalophos transformation in rat liver].

Phthalophos, organophosphoric pesticide, in the perfused isolated liver of rats transforms to water-soluble oxymethyl phthalimide and phthalimide. The induction of the liver hydroxylating enzymic system with milbex accelerates transformation of phthalophos: in 5 min only 14% of its initial amount is found in perfusate, while in the control--52%. The inhibition of the hydroxylating enzymic system with tetramethylthiuramdisulphide (dithiocarbamate pesticide) inhibits transformation of phthalophos: in 15 min perfusate contains 33% of its initial amount and the control--16%. Induction and inhibition of the hydroxylating enzymic system of the liver affect essentially the phthalophos toxicodynamics, decreasing the degree of the cholinesterase activity.

Animals↗

Review of the genotoxicity and carcinogenicity of 4,4'-methylene-dianiline and 4,4'-methylene-bis-2-chloroaniline.

4,4'-Methylene-dianiline (MDA) and 4,4'-methylene-bis-2-chloroaniline (MOCA) are polycyclic aromatic amines that are currently used in industry. Both compounds have been found to be bacterial mutagens and to be positive in a number of assays for genotoxicity. In animal studies, MDA has induced thyroid and liver neoplasms while exposure to MOCA resulted in a variety of tumors including those of the liver, mammary gland and bladder. Epidemiologic proof of human carcinogenicity of both compounds is lacking; however, there is evidence that MOCA can be metabolized to mutagenic products by human tissue. In this paper, the major finding concerning the biotransformation, genotoxicity and carcinogenicity of MDA and MOCA are reviewed.

Aniline Compounds↗

Mutagenicity studies with o-tolidine and 4,4'-tetramethyldiaminodiphenylmethane.

This paper confirms the mutagenicity of 2 carcinogenic chemicals, o-tolidine and 4,4'-tetramethyldiaminodiphenylmethane (TDDM). o-Tolidine and TDDM were both tested in the Salmonella/mammalian-microsome test and in the sister-chromatid exchange (SCE) test with rabbit lymphocytes in vitro. The number of revertants was increased in the presence of S9 mix by o-tolidine in the Salmonella typhimurium strains TA98 and TA1538, and by TDDM in strains TA98 and TA100. Both compounds showed weak SCE-inducing activity in cultured rabbit lymphocytes in the absence, but not in the presence, of an exogenous metabolic system.

Aniline Compounds↗

A comparison of the mutagenicity and macromolecular binding of the carcinogens Michler's ketone and reduced Michler's ketone.

The mutagenicity of 4,4'-bis(dimethylamino)benzophenone (Michler's ketone, MK, CAS No. 90-94-8) and 4,4'-methylenebis(N,N-dimethyl)benzamine (reduced Michler's ketone, RMK, CAS No. 101-61-1) for Salmonella typhimurium strain TA100 was compared using activated 9000 X g (S9) liver supernatants from 2 animal species. RMK, but not MK, was mutagenic when incubated with phenobarbital-induced B6D2F1 mouse or Osborne-Mendel rat-liver S9. The mutagenic response for RMK was linear at doses from 1 to 33 micrograms/plate. A higher percentage of RMK and MK became irreversibly bound to mouse-liver macromolecules than to rat-liver macromolecules when incubated at 37 degrees C in the presence of reduced nicotinamide adenine dinucleotide phosphate.

Aniline Compounds↗