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At least 19 recordsLinked to original sources
PubMed1976

Bioassay of 2, 4, 5-trichlorophenoxyacetic acid for carcinogenicity in mice.

Adult mice of strains C3Hf and XVII/G received 2, 4, 5-T by continuous oral administration (80 ppm in the diet). The 2, 4, 5-T preparation contained less than 0-05 ppm of dioxins. In 2, 4, 5-T -treated C3Hf mice a significant increase in the incidence of neoplastic lesions was found. No significant difference was found in the XVII/G strain between the treated and control mice. Rare forms of tumours, which were not observed in the controls, were present in the 2, 4, 5-t -treated C3Hf mice.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMedDate not supplied

A review of the genetic toxicology of chlorinated dibenzo-p-dioxins.

Information from both published and unpublished sources considered relevant to the understanding of the genetic toxicology of chlorinated dibenzo-p-dioxins is summarized in this review. Interest in writing this paper was stimulated by the fact that this class of compounds, particularly 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has gained notoriety as an extreme environmental and industrial hazard. The potential for human exposure occurs in the work place when dioxins are formed during the synthesis of a number of commercially important compounds such as 2,4,5-trichlorophenoxyacetic acid, hexachlorophene, and pentachlorophenol. Environmental contamination may result from manufacturing processes and from dioxin contaminants in marketed products. Research on dioxins as potential mutagens was initiated because of their structural similarity to acridines, a class of known intercalating agents. To date, only 4 dioxin compounds have been evaluated for mutagenicity: the di-, tetra-, and octa-chlorinated derivatives and the unsubstituted dibenzo-p-dioxin. Since only a few of the many possible structural forms of dioxins have been tested, no definite conclusions can be made about their potential mutagenicity. Furthermore, the positive mutagenicity and cytological effects reported thus far with the few dioxin isomers examined seems to depend on the position of chlorine substitution. The most active form of the molecule is the 2,3,7,8-derivative (TCDD). Data available for assessing the mutagenic potential of TCDD are conflicting and scarce. Differences in testing results reported in these studies could be attributed to solubility problems with the test chemical, treatment protocols, purity of test samples, or toxicity. Because there are conflicting data, additional experiments are needed before the mutagenic potential of TCDD and other dioxins can be determined. Studies exploring the promoting effect of dioxins on the mutagenicity of other compounds are also recommended because experiments have shown TCDD to be an extremely active liver enzyme inducing agent that enhances the mutagenicity of certain polycyclic hydrocarbons such as 3-methylcholanthrene in vitro. The importance of discerning the hazards to human health from dioxin compounds became apparent after an accidental release of TCDD from a chemical plant contaminated the Seveso, Italy area in July 1976. This accident revealed that insufficient data were available to properly evaluate the long-term health risks posed by dioxin compounds. Several research projects were therefore initiated after the Seveso incident; it is hoped that many of the questions concerning the mutagenicity of TCDD and possibly of other dioxin congeners will be answered as a result of this work.

Acridines↗
PubMed1978

Multinationals and health: reflections on the Seveso catastrophe.

On July 10, 1976, a cloud of vaporized products containing dioxin escaped from a deposit of a plant of the Icmesa firm in the northern suburbs of Milan. The fallout was deposited on a vast zone in the municipalities of Desio, Seveso, Meda, and Cesano. Dioxin was not the desired product of the industrial process, but rather an impurity which generally accompanies trichlorophenol, and, to a smaller extent, the products synthesized from trichlorophenol. Among these there are hexachlorophene and the herbicide 2,4,5-trichlorophenoxyacetic acid, which was used as a defoliant in the Vietnam War. After describing toxicological properties of dioxin, this paper examines the role of multinational corporations and of capitalist governments in exploiting not only the people of underdeveloped lands, but also workers of developed countries, transforming into capital not only the increased value of man, but also the conditions, harmfulness, and risks of work.

Accidents↗
PubMedDate not supplied

Renal transport and renal metabolism of 2, 4, 5-trichlorophenoxyacetate by the chicken.

In vitro and in vivo renal tubular transport of 2,4,5-trichlorophenoxyacetate (2,4,5-T), a hormone-type herbicide, was studied in the chicken. Renal cortical slices incubated with 14C-labeled 2,4,5-T demonstrated a slice-to-medium ratio of the 14C-label of 26 after 2 hr of incubation. This accumulation was inhibited significantly by probenecid, phenol red, dinitrophenol and iodoacetamide. In vitro metabolism of 2,4,5-T was apparent in the renal slice studies; at least two metabolites were found by electrophoretic analysis. Even though chicken liver slices were able to accumulate 2,4,5-T, the accumulated herbicide was not metabolized. In addition, chicken kidney slices metabolized 2,4,5-T to a much greater extent than did rat or rabbit kidney slices, which produced only negligible amounts of metabolites. When [14C]-2,4,5-T was infused into the renal portal system of the chicken, the 14C-label originally associated with 2,4,5-T was shown to be secreted by the renal tubule. Probenecid inhibited the transport of the 14C-label without affecting the simultaneous transport of tetra-ethylammonium, an organic cation transported by the renal proximal tubule. At the present infusion rate of 2,4,5-T (2.9 X 10(-10) mol/min), the excreted label was associated primarily with an acidic metabolite(s). It can be concluded that the chicken transports 2,4,5-T by a probenecid sensitive mechanism; however, this transport appears to be associated with the metabolism of the herbicide.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1975

[Polychlorodibenzo-p-dioxins (author's transl)].

Polychlorodibenzo-p-dioxins (chlorodioxins) appear most frequently by heating of chlorophenols in alkaline solution specially when producing organic derivatives. Consequently chlorodioxins may contaminate several industrial chemical products largely used, for instance, as pesticides. Occasionally, chlorodioxins are also synthesized from chlorophenols or their derivatives in situ during industrial processes. Chlorodioxins are the cause of chloracne and chick edema which killed thousands of broiler chickens in the U.S.A. Furthermore chlorodioxins seem to be foetotoxic possible even for man. The present paper is the first part of our work. It is a review of the chemical and toxicological properties of chlorodioxins. We hope to publish later a review of analytical methods and the results of our analyses.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1979

2,4,5--T.

Explore the source record for details and available documents.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1976

[Chloracne, porphyria cutanea tarda, and other poisonings due to the herbicides].

In 80 industrial workers producing herbicides (2,4,5-trichlorphenoxyaceticacidsodium and sodiumpentachlorphenolate) in Czechoslovakia the following signs of intoxication caused by 2,3,6,7-tetrachlordibenzodioxin were found: Dermatological: Chloracne and Porphyria cutanea tarda. Internal: Disorders of the metabolism of porphyrins, fats, carbohydrates, plasmaproteins. Neurological: Mainly lesions of the peripheral neurone. Psychiatric: Neurasthenic syndrome and organic lesions. Differences from the usual course of chloracne were observed. Porphyria cutanea tarda acquisita was most obvious, one patient suffered and died from severe atherosclerosis, hypertension and diabetes. Many patients developed polyneuropathy, as verified both by EMG and autopsy. Two patients died from bronchogenic carcinoma.

2,4,5-Trichlorophenoxyacetic Acid↗