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At least 19 recordsLinked to original sources
PubMed1992

Comparative toxicity of four chlorinated dibenzo-p-dioxins (CDDs) and their mixture. Part I: Acute toxicity and toxic equivalency factors (TEFs).

There is presently no scientifically proven method to assess the toxicity of environmental samples containing complex mixtures of chlorinated dibenzo-p-dioxins (CDDs) of known composition. Their risk assessment is currently based on the interim concept of toxicity equivalency factors (TEFs), with the unproven assumption that all interactions of CDDs are additive. To address this problem we conducted acute toxicity studies with four different CDDs, viz 2,3,7,8-tetrachlorodibenzo-p-dioxin (tetra-CDD), 1,2,3,7,8-pentachlorodibenzo-p-dioxin (penta-CDD), 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin (hexa-CDD) and 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (hepta-CDD), all containing chlorine substituents in the crucial 2,3,7,8-positions. The homologues, dissolved in corn oil/acetone, were administered to groups of five male Sprague Dawley rats at several doses (at least three) by gastric intubation. The obtained mortality data were employed to calculate the LD20,50 and 80 for each homologue. These data were subsequently used to prepare equipotent doses (expected mortality of 20, 50 and 80%) of a mixture containing all four homologues, each of them contributing one fourth of the toxicity, under the assumption of additive toxicity. The obtained LD50 value and (TEF) was for tetra-CDD 43 micrograms/kg (1), penta-CDD 206 micrograms/kg (0.2) hexa-CDD 887 micrograms/kg (0.05) and hepta-CDD 6325 micrograms/kg (0.007), respectively. The dose-response to the mixture confirmed the hypothesis of strict additivity in the acute toxicity of the four CDD homologues.

Animals↗
PubMed1991

The acute toxicity of pulse-dosed, para-substituted phenols to larval American flagfish (Jordanella floridae): a comparison with toxicity to photoluminescent bacteria and predicted toxicity using log Kow.

The acute toxicity of nine para-substituted phenols was determined using a pulse-exposure testing protocol and 8-day-old larval American flagfish (Jordanella floridae). Relative tolerance was assessed by determining the 2-h pulse exposure concentration causing 20 and 50% mortality (PE LC20 and PE LC50) over the subsequent 94 h. Four bioassays were run for each phenol and yielded the following mean PE LC20 values (mg 1(-1)) in descending order of toxicity: p-aminophenol, 0.06; hydroquinone, 0.13; phenol, 0.70; p-nitrophenol, 0.81; p-cyanophenol, 3.0; p-chlorophenol, 3.3; p-hydroxyacetophenone, 4.2; p-hydroxybenzyl alcohol, 6.4; and p-hydroxybenzoic acid, 170. These toxicities did not correlate significantly with either previously reported toxicity values for the photoluminescent bacteria Photobacterium phosphoreum, or with the log octanol-water partition coefficient. For some of the compounds, however, sensitivities were quite close to previously reported rainbow trout chronic no-observed-effect concentrations based on continuous exposure. Caution is urged with respect to applying "low-level" biota techniques or simple quantitative structure-activity correlations such as Kow when attempting to predict the toxicity of specific chemicals to fish.

Animals↗
PubMed1991

Synergistic vascular toxicity and fatty acid anilides in the toxic oil syndrome.

The underlying etiology of the toxic oil syndrome may be related to any of several toxic contaminants. The hypothesis is made that two or more toxic compounds may act synergistically to cause vascular damage in the toxic oil syndrome. To support this hypothesis, previous studies are reviewed concerning the remarkable synergistic toxic action of allylamine and beta-aminopropionitrile on the media of blood vessels. Although these toxins are not directly related to the toxic oil syndrome, this previous experimental work emphasizes the possibility that unexplored synergistic actions may be important. Furthermore, the hypothesis that contaminating fatty acid anilides in toxic oil undergo alterations during cooking is supported by high pressure liquid chromatographic analysis. The theoretic metabolism of fatty acid anilides is discussed. Recent data concerning the toxic actions of the anilides of oleic and linoleic acid are given. These data suggest that these anilides induce immunologic alterations that may be similar to those seen in the toxic oil syndrome. In addition, the heated anilides appear to have increased toxicity, supporting the concept that the use of toxic oil in cooking may increase its toxicity.

Allylamine↗
PubMed1978

[Mechanism of methamphetamine toxicity in grouped mice and the effects of centrally acting drugs on its toxicity (author's transl)].

The mortality of ddK mice treated with 40 mg/kg i.p. of methamphetamine (MA) was 85% in grouped conditions (10 mice in a cage) and 3% in individually isolated conditions. This mortality was not altered by the social environments even when other mice in the cage were not treated with MA. The mortality of mice individually isolated in cages with transparent walls was significantly higher than that of completely isolated mice. Almost all neuroleptics dose-dependently antagonized the MA toxicity in grouped mice, in small doses. The antagonizing activity of clozapine was somewhat weak, and sulpiride potentiated MA toxicity. Phentolamine and propranolol antagonized the MA toxicity at higher doses than neuroleptics. Reserpine and tetrabenazine previously given to mice remarkably antagonized the MA toxicity. H44/68 (a tyrosine hydroxylase inhibitor) had a considerable effect in antagonizing the MA toxicity, but diethyldithiocarbamate, U-14, 624 and FLA 63 (dopamine-beta-hydroxylase inhibitors) prevented the MA toxicity to a lesser extent than did H44/68. Apomorphine had no effect on the MA toxicity. The present data show that the MA toxicity in grouped mice (the increase in mortality) was enhanced by the presence of other mice, and suggest that the norepinephrine neurons play an important role in promoting the MA toxicity. Neuroleptics antagonize MA toxicity probably by blocking alpha-receptors in the central nervous system.

Adrenergic alpha-Antagonists↗
PubMed1992

Criteria for judging the relative toxicity of chemicals from developmental toxicity data: a workshop summary.

In summary, participants of this workshop confirmed that many criteria need to be considered when interpreting the results of developmental toxicity studies. All aspects of developmental toxicity are of interest, but their importance to the consideration varies along the continuum from hazard detection to risk estimation. As with many other manifestations of toxicity, potential developmental risk to humans is a function of exposure and developmental toxicity, the latter reflecting the inherent potential of a substance to cause an adverse effect under some defined condition. All of the criteria discussed in this workshop were considered to be of some importance in characterizing the developmental toxicity of a substance, their relative importance being a function of the question under consideration. Proper interpretation of developmental toxicity data, which must include prenatal as well as postnatal observations to be considered complete, should take into account the differential toxicity to the mother and the conceptus, the nature of the developmental toxicity observed, and the consistency of response between species. The proximity of human exposure levels to dose levels that are developmentally toxic in animals is a major determinant of the potential for hazard to humans. Mechanistic and pharmacokinetic knowledge can modulate interpretation of descriptive data and refine the prediction of human hazard. Recognizing that in vitro studies will never completely recapitulate the results of in vivo studies, the committee to update the "Smith list" will move forward taking the discussions of this workshop into account.

Animals↗
PubMed1992

The evolution of toxic effluents in fires and the assessment of toxic hazard.

Toxic hazard in fire depends upon three factors: the fire growth curve (mass loss rate of materials, kg/min) and volume dispersal (kg/m3), the yields of toxic products (e.g. kg CO/kg fuel burned) and the toxic potency of the products (exposure dose needed to cause toxic effects, e.g. lethal dose of CO in ppm.min). The first and second sets of data are obtainable from large-scale tests or small-scale tests and mathematical modelling, the third and some information on the second are derived from toxicity studies of combustion products in small-scale tests or of individual fire gases. Small-scale toxicity test data on materials expressed as lethal mass loss exposure doses (LCt50 g min m-3) can be used in Fractional Effective Dose (FED) hazard assessments, providing the decomposition conditions of the test reproduce those in the fire being examined; principally either non-flaming oxidative, early well-ventilated flaming, or vitiated post-flashover. Although bioassays are needed for a full toxicity assessment, it is now possible to predict the toxic potency of materials to some extent from analytical data alone. The suitability of the small-scale test decomposition conditions are determined in terms of non-flaming or flaming behaviour, temperature (or radiant flux), CO2/CO ratio and oxygen concentration. Existing small-scale test methods provide reasonable models for materials under non-flaming oxidative and early flaming conditions, although the data base for the latter is poor. Only the DIN 53436 method is able to model vitiated post-flashover decomposition conditions, but data for this condition are almost non-existent.

Animals↗
PubMed1977

The effects of toxic and non-toxic serum phenytoin levels on carbohydrate tolerance and insulin levels.

The effect of toxic and non-toxic phenytoin levels on carobhydrate tolerance and insulin levels was studied in 18 patients with epilepsy and 17 control subjects. Toxic levels were defined as a serum level greater than 20 microgram/ml. Toxic levels occurred in 11 patients and nontoxic levels in seven patients. Blood glucose and insulin levels were measured at 30-min intervals for a period of 3 h following the ingestion of 50 g glucose. Blood glucose levels were measured by the ferricyanide method, and serum insulin levels by immunoassay of insulin with insulin antibody precipitate. Serum phenytoin levels were measured by gas liquid chromatography. The insulin profiles were the same for all three groups, but there was a significant delay in reaching peak glucose concentrations in patients with toxic levels of phenytoin. It was therefore confirmed that non-toxic levels of phenytoin do not affect carbohydrate tolerance or insulin levels when phenytoin is used in the routine treatement of epilepsy, and it has also been shown that toxic levels of phenytoin do not affect carbohydrate tolerance when the high levels are detected at an early stage.

Adolescent↗
PubMed1992

Strategies for the identification of non-polar toxicants in aqueous environmental samples using toxicity-based fractionation and gas chromatography-mass spectrometry.

Toxicity-based fractionation is a useful tool for the isolation and identification of non-polar organic compounds that are present at toxic concentrations in aqueous environmental samples. Methods for isolating such toxicants from the aqueous sample matrix and techniques for fractionating the compounds for the purpose of reducing the complexity of the sample matrix and thus facilitating identification are evaluated. Strategies for analyzing gas chromatographic-mass spectrometric data and confirming toxicant identification are presented. Studies that use toxicity-based fractionation for identifying the cause of toxicity in aqueous environmental samples such as municipal and industrial wastewater treatment plant effluents and ambient waters are discussed.

Chemical Fractionation↗
PubMed1975

[Investigations on toxic fractions of swine erysipelas bacteria (erysipelothrix rhusiopathiae). 1. Communication: Toxicity investigation on a phenol water extract in chicken embryos (author's transl)].

The watersoluble fractions (WESTPHAL et al., 1952 a, b) of twelve Erysipelothrix rhusiopathiae strains, which differed in virulence were tested for toxicity for ten day old chick-embryos by the route of i.v. injection. The LD50-values ranged from 108 mug to 0.01 mug toxin dry weight/embryo. The different toxicity of these extracts for chick-embryos was compared with the virulence of the corresponding strains in swine: The extracts of four strains with high virulence were very toxic for chick-embryos (LD50:0,01 mug to 0.207 mug) The extracts of four non-virulent strains were low-, respectively non-toxic (LD50:10.95 mug to 108 mug) The extract of one virulent strain showed an intermediate degree of toxicity (LD50:2.8 mug) In tese nine strains there was a correlation between virulence for swine and the toxicity of the extracts for chick-embryos. But this relation could not be found for three other strains.

Animals↗
PubMed1990

Heavy metal toxicity in a N2-fixing cyanobacterium, Anabaena doliolum: regulation of toxicity by certain environmental factors.

The toxic effects of chromium and tin salts on growth, 14C uptake, heterocyst differentiation, and nitrate reductase, nitrogenase, and glutamine synthetase activities of Anabaena doliolum and their regulation by pH, salinity, extracellular metabolites (spent), and organic acids have been studied. The toxicity of the test metals was lowered at alkaline pH and increased at acidic pH. NaCl at 20 mM was found to decrease metal toxicity. Extracellular metabolites (spent) in a 1:1 ratio (v/v) with fresh culture medium and organic acids were found to reduce metal toxicity. Among the various organic acids studied, humic acid was the most effective in regulating metal toxicity, apparently due to its multiple binding sites for metal cations. This study demonstrated that environmental factors, such as pH, salinity, extracellular metabolites, and organic acids, can mediate the toxicity of heavy metals to A. doliolum in a laboratory microcosm.

Acids↗
PubMed1991

Interpreting aquatic toxicity QSARs: the significance of toxicant body residues at the pharmacologic endpoint.

Aquatic QSAR investigations employ bioassay data where a biological response is associated with a toxicant concentration in the exposure water. Although convenient this ignores the fundamental principle that the response is more closely related to an amount present in the organism. This problem has been examined using acute toxicity and bioconcentration QSARs employing log Kow as the molecular descriptor. Combining these QSAR relationships enables estimates of the amount of toxicant in organisms to be made. For acute narcosis (50% mortality) the toxicant level in the hydrophobic (lipid) phase of an exposed organism is, as a first approximation, constant at approximately 50 mmol l-1 of lipid. For the acute toxicity of a variety of hydrophobic narcotic organics examined by US EPA-Duluth in tests with fathead minnows, this corresponds to a whole-body residue of about 4 mmol kg-1. Although the level in the hydrophobic phase remains constant, for hydrophilic chemicals (log Kow less than 1.5) the contribution of the hydrophilic (water) phase of the organism dominates and total body residues should be similar to the respective threshold LC50s. This has important implications in simple pharmacokinetic modelling and in interpreting residue levels in organisms collected in environmental monitoring studies.

Animals↗
PubMed1992

Role of maternal toxicity in assessing developmental toxicity in animals: a discussion.

The belief that any drug or chemical, when administered at a high enough dose, can be expected to produce fetal malformations is not consistent with the facts. However, the stress associated with maternally toxic doses can be expected to result in associated, often transient, fetal abnormalities that may not be the result of deviant organogenesis. Sometimes the toxicity toward the pregnant animal, including her embryos/fetuses since they are hardly in a sanctuary, is severe enough to result in resorption of the embryo or abortion of the fetus. Thus, it is possible that the embryolethality and other indications of developmental toxicity, produced by some drugs and chemicals, may be the result of a mechanism(s) other than selective toxicity toward the embryo. Also, some test materials have been shown to affect maternal homeostasis, thereby disrupting support to the embryo, without causing significant overt toxicity to the embryo or dam; e.g., the endocrine system of the dam is altered. Routine testing has thus far revealed a relatively limited number of true teratogens, although a large number of drugs and chemicals have resulted in fetal effects such as developmental variations when administered at doses that approach lethal levels. Such effects on the fetus should be expected when the maternal animals are stressed by the high dosages usually employed. A better understanding of the etiology and biological relevance of the embryo/fetal deviations often seen in developmental toxicology studies might help to avoid the sometimes unjustified withholding of potentially useful drugs and chemicals from the marketplace.

Abnormalities, Drug-Induced↗
PubMed1978

A study on the toxicity of natural food dyes--toxicity and enzyme inhibition in Paramecium caudatum.

The toxicity of 14 commercial natural dyes which are widely used as food additives in Japan was studied on Paramecium caudatum. Laccaic acid and capsanthin were found to be very toxic to Paramecium caudatum. Some of the commercially available carminic acid and crocin were also toxic. The inhibitory effect of natural food dyes on leucine aminopeptidase, acid phosphatase and esterase in vitro was proportional to the toxic effect of the dyes on the survival time of Paramecium caudatum. Analyses of the commercial natural food dyes by high performance liquid chromatography failed to identify the toxic components.

Acid Phosphatase↗
PubMed1979

Studies on the toxicity of coal-tar dyes. I. Photodecomposed products of four xanthene dyes and their acute toxicity to fish.

The acute toxicity of photodecomposed products of Erythrosine, Eosine, Phloxine and Rose Bengale were studied, since it was found that toxicity of these dyes to fish increased after the dyes had been photoirradiated. Photodecomposed products of the dyes were isolated and identified with UV, IR, NMR spectra and the acute toxicity of those compounds were determined by TLm test. As results of these studies, it became clear that the toxicity of photodecomposed organic products (dehalogenated compounds of dyes) were lower than the mother compounds. The increases in toxicity of the xanthene dyes by photo-irradiation were attributed to the liberated halogens by irradiation.

Animals↗
PubMed1979

Bismuth toxicity in man II. Review of bismuth blood and urine levels in patients after administration of therapeutic bismuth formulations in relation to the problem of bismuth toxicity in man.

A survey of the leterature on bismuth toxicity in man in relation to blood level data, has revealed the necessity of distinguishing between lipid soluble and water soluble organic complexes of bismuth on the one hand and the simple inorganic salts of bismuth on the other hand. A characteristic feature of the former, illustrated by the water soluble bismuth complex triglycollamate, is the high bismuth levels (due to absorption of the complex as such) and the nephrotoxic properties of the compound in man. Bismuth absorption after administration of the simple inorganic salts of bismuth is postulated to occur in the form of ionic bismuth as such, low bismuth levels being characteristic features of such compounds. Bismuth blood and urine levels obtained from patients after administration of a new anti-ulcer drug (Bicitropeptide) in a well controlled clinical trial are discussed and suggest that that this bismuth containing drug behaves pharmacologically in a manner similar to the inorganic bismuth salts in man, low bismuth blood levels and the absence of toxic side effects being conspicuous features of the drug. Based on these considerations, it is proposed that the pharmacologically active bismuth compounds be divided into four different groups depending on structure, stability and solubility. The question as to what constitutes a "toxic bismuth blood level" can only be discussed in relation to the new proposed sub-division of bismuth compounds and is only meaningful if the term is defined to relate only to ionic bismuth (presumably bound to a large extent to blood proteins). Based on information gleaned from the literature and blood level values reported in the clinical trial referred to, it is suggested that bismuth blood level values below 50 micrograms/ml are highly unlikely to be associated with meaningful toxicity in man. Finally, attention is drawn to the reversibility of bismuth toxicity in man as reported by many authors irrespective of the type of bismuth compound concerned.

Animals↗
PubMed1991

The toxicity of waterborne boron to Daphnia magna and Chironomus decorus and the effects of water hardness and sulfate on boron toxicity.

The concentrations of many elements, including boron, are increasing in aquatic ecosystems due to anthropogenic activities. Laboratory studies were undertaken to evaluate the toxicity of waterborne boron to two key freshwater macroinvertebrates and to evaluate the effects of water hardness and sulfate on boron toxicity. Acute toxicity evaluations of waterborne sodium tetraborate resulted in 48 h. LC50 values of 141 and 1376 mg B/L for neonate Daphnia magna and fourth instar Chironomus decorus, respectively. Chronic sublethal studies demonstrated a significant decrease in C. decorus growth rate at 20 mg B/L. Further studies showed that increasing water hardness (10.6 to 170 mg/L as CaCO3) and sulfate (10.2 to 325.4 mg SO4(-2)/L) concentrations did not affect boron toxicity to D. magna. These results, in conjunction with a review of the literature, suggest that aquatic macrophytes may be more sensitive to boron than macroinvertebrates and thus would be better choices for aquatic risk assessment evaluations for this element.

Animals↗
PubMed1979

Serum thyroglobulin in patients with toxic and non-toxic goitres compared to sex- and age-matched control subjects.

To study serum thyroglobulin (Tg) levels in patients with thyroid disorders compared to sex- and age-matched control subjects and to correlate the Tg levels to the thyroid function, 71 patients were investigated before treatment was started. Serum Tg, measured by a double antibody radioimmunoassay, was elevated in all groups with thyroid disorders, as compared to their controls, but the values showed large overlaps between groups. The highest median values were seen in the two groups of patients with toxic goitres (toxic adenoma and Graves' disease). The Tg values in patients with non-toxic goitres (diffuse and nodular) and in controls showed a log normal distribution, whereas the distribution of values from patients with toxic goitres was different. No correlation was found between serum Tg and serum thyroxine, serum triiodothyronine and serum TSH, respectively. It is concluded that determination of serum Tg is of little diagnostic value in thyroid diseases.

Adenoma↗