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[Analysis of methodological approach to the evaluation of toxicity of complex mixtures of relatively constant composition used in industry (review of the literature)].

Basing on literature data and the author's personal experience, the article displays current approaches to the toxicological assessment of industrial complex mixtures with permanent compositions. These include two main approaches to the detection of major components: a) the establishment of the individual substances ratio in the toxicological parameters, and b) the application of the regression coefficients and their derivatives. Toxicity assessment against the toxicological parameters of individual substances is also substantiated.

Air Pollutants, Occupational↗

[Joint toxicity on multi-component mixtures of SDS and substituted aromatic compounds].

The toxicity to Photobacterium phosphoreum of different mixture systems of sodium dodecyl sulfate (SDS) and three substituted aromatic compounds according to equiconcentration ratio of 1 : 1, as well as individual toxicity, were determined respectively. The joint toxicity was evaluated by toxicity unit (TU), additive index (AI), similarity parameter (lambda), and mixtures toxicity index (MTI). Four evaluating methods were compared and the modes of joint action of different systems were analyzed primarily. The coherent results were obtained from four different evaluating methods. Conclusions can be drawn that the binary joint effects of phenol and toluene mixed with SDS showed weak synergistic, while the other joint effects of SDS and substituted aromatic compounds were antagonistic. Of the evaluating methods, Toxic Unit is most sensitive with higher value of its parameter. Mechanisms of joint toxicity action could be discussed according to luminescence principle of Photobacterium phosphoreum and molecule structures of the mixture components.

Benzoates↗

[Experimental evaluation of toxicity of selected mixtures used in metallurgy].

The investigation is aimed at evaluation of the effects of copper-coating and bonderizing solutions and oil--emulsion used in technological processes in the metallurgic industry upon hematological and biochemical changes in rats' peripheral blood. The studies were performed on male Wistar rats. The solutions were carried onto hairy and depilated skin. Acute toxicity was evaluated in two-weeks' experiment and chronic toxicity in three--months' experiment. The copper-coating solution was found to be most hazardous, whereas the oil emulsion-the least hazardous. The copper-coating and bonderizing solutions, when chronically applied, result in anaemia and changes in the percentage picture of leucocytes, and also increased blood concentration of uric acid, creatinine and hydroxyproline. No significant changes in concentrations of the remaining biochemical indices were found. The results point to synergistic effects of oil-emulsion and copper-coating solution.

Animals↗

[Clinical effectiveness and systemic toxicity of various mixtures of prilocaine and bupivacaine in axillary plexus block].

The presently existing local anesthetics (LA) do not guarantee a rapid onset and simultaneously a long duration of action. The combination of a medium-long acting LA with bupivacaine, a long-acting LA with slow onset, could be means to achieve these aims. Prilocaine was chosen as the medium-long acting LA because it has the lowest toxicity of this group and for pharmacological reasons. METHODS. In a prospective, controlled double-blind study 100 patients scheduled for axillary block for elective surgical procedures of the hand or wrist were randomly assigned to five groups. Twenty patients in each group received either 40 ml prilocaine 1.5%; 40 ml bupivacaine 0.375%; 20 ml prilocaine 1% + 20 ml bupivacaine 0.5%; 20 ml prilocaine 2% + 20 ml bupivacaine 0.5%; or 20 ml prilocaine 2% + 20 ml bupivacaine 0.375%. The LA mixtures were freshly mixed 15 min prior to the axillary block. The blocks were performed using an immobile, short-beveled needle by anesthesiologists who were familiar with this technique. Analgesia was classified using the pin-prick method with 0 = no analgesia, 1 = analgesia, 2 = anesthesia. Motor blockade was classified with 0 = no motor block, 1 = paresis, 2 = paralysis. The following nerves were analyzed: ulnar, radial, median, musculocutaneous, and medial antebrachial. In 6 patients of each group plasma levels of the LA were measured by gas chromatography and methemoglobinemia was determined. Statistical analysis of the data was performed using the Student t-test and chi-square test on a level of significance of P less than 0.05. Results. All surgical procedures could be performed as planned in regional anesthesia. Twenty minutes after injection of the LA only 15% of the blocks were sufficient in the bupivacaine group, while in the other four groups 40%-50% of the blocks were complete (P less than 0.05). The degree of analgesia was deeper in the groups with 2% prilocaine and prilocaine alone than in the group with 1% prilocaine. Forty minutes after injection there were no significant differences between the groups. Motor blockade after 20 min was significantly lower in the bupivacaine group than in the prilocaine group (P less than 0.05). After 4 h all three prilocaine-bupivacaine mixtures showed a significantly more pronounced analgesia of the median nerve than the prilocaine group (P less than 0.02-0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

Toxicity of a mixture of fatty acids on human blood lymphocytes and leukaemia cell lines.

The effect of a mixture of fatty acids upon lymphocyte and leukaemia cell death was examined. Peripheral lymphocytes from healthy subjects and two human leukaemia cell lines-Jurkat (T lymphocyte) and Raji (B lymphocyte) cells-were treated with increasing concentrations (0.1-0.4 mM) of a fatty acid mixture in a proportion mimicking that of the free fatty acids in plasma. Features of cell death were then evaluated. Phosphatidylserine externalization, and DNA fragmentation (apoptosis), and loss of cell membrane integrity (necrosis) and mitochondrial depolarization (common feature of cell death) were observed in leukaemia cells after the fatty acid treatment for up to 48 h. Human lymphocytes, however, when submitted to the same treatment presented apoptotic feature only. These findings indicate that a free fatty acid mixture (mimicking the proportion found in plasma) triggers apoptosis of leukaemia cell lines followed by loss of cell membrane integrity, whereas in human circulating lymphocytes the same treatment causes apoptosis only. Evidence is presented herein that mitochondria from leukaemic cells are more susceptible to the toxicity of the fatty acids than mitochondria from human circulating lymphocytes.

B-Lymphocytes↗

[Oxygen toxicity in a mixture with helium].

A 3-day exposure of mice to a 20%--80% He-O2 environment at 28--30 degrees C led to an earlier decrease of gas exchange, a faster development of pulmonary inflammatory changes, and an earlier death of the animals as compared with an exposure to similar N2-O2 and He-O2 atmospheres at room temperature. The possible role of the indifferent gas in the toxic effect of oxygen on the animal body is discussed.

Animals↗

Modification of the carbohydrate in ricin with metaperiodate-cyanoborohydride mixtures. Effects on toxicity and in vivo distribution.

Attempts to target antibody-ricin conjugates (immunotoxins) to designated cell types in vivo may be thwarted by their rapid clearance by hepatic reticuloendothelial cells which have receptors that recognise oligosaccharide side chains on the toxin. The B-chain of ricin contains high mannose type oligosaccharides and the A-chain contains a complex unit (GlcNAc)2-Fuc-Xyl-(Man)4-6, all of which potentially could be recognised by the reticuloendothelial system. Treatment of ricin with a mixture of sodium metaperiodate and sodium cyanoborohydride at pH 3.5 resulted in oxidative cleavage of the carbohydrates and reduction of the aldehyde groups thus formed to primary alcohols. By conducting the modification procedure at acidic pH, both the possibility of Schiff's base formation between the aldehyde groups and amino groups in the protein and the possibility of non-specific oxidation of amino acids were minimised. The extent of the carbohydrate modification depended on the duration of treatment, resulting maximally in the destruction of 13 of the 18 mannose residues and of all xylose and fucose. The toxicity of the modified toxin to cells in culture declined by up to 90% as the carbohydrate was destroyed. This was not due to a reduced ability of the B-chain to bind to cells or of the A-chain to inactivate ribosomes. In contrast to the in vitro results, the toxicity of the modified toxin to mice and rats was elevated by up to fourfold. The modification greatly reduced the clearance of the toxin by non-parenchymal cells in the liver and prevented the damage to hepatic Kupffer and sinusoidal cells and to the red pulp of the spleen that is inflicted by the native toxin. The elevated toxicity to animals appears to be because the modified toxin evades the reticuloendothelial system and persists in the bloodstream for longer periods, thus resulting in lethal damage to vital tissues in the animal at lower dosage. The results suggest that immunotoxins prepared from modified ricin would not be readily cleared by the reticuloendothelial system and so be more effective at killing their target cells.

Amino Acids↗

NTP technical report on the toxicity studies of Pesticide/Fertilizer Mixtures Administered in Drinking Water to F344/N Rats and B6C3F1 Mice.

Toxicity studies were performed with pesticide and fertilizer mixtures representative of groundwater contamination found in California and Iowa. The California mixture was composed of aldicarb, atrazine, 1,2-dibromo-3-chloropropane, 1,2- dichloropropane, ethylene dibromide, simazine, and ammonium nitrate. The Iowa mixture contained alachlor, atrazine, cyanazine, metolachlor, metribuzin, and ammonium nitrate. The mixtures were administered in drinking water (with 512 ppm propylene glycol) to F344/N rats and B6C3F1 mice of each sex at concentrations ranging from 0.1x to 100x, where 1x represented the median concentrations of the individual chemicals found in studies of groundwater contamination from normal agricultural activities. This report focuses primarily on 26-week toxicity studies describing histopathology, clinical pathology, neurobehavior/neuropathology, and reproductive system effects. The genetic toxicity of the mixtures was assessed by determining the frequency of micronuclei in peripheral blood of mice and evaluating micronuclei and sister chromatid exchanges in splenocytes from female mice and male rats. Additional studies with these mixtures that are briefly reviewed in this report include teratology studies with Sprague-Dawley rats and continuous breeding studies with CD-1 Swiss mice. In 26-week drinking water studies of the California and the Iowa mixtures, all rats (10 per sex and group) survived to the end of the studies, and there were no significant effects on body weight gains. Water consumption was not affected by the pesticide/fertilizer contaminants, and there were no clinical signs of toxicity or neurobehavioral effects as measured by a functional observational battery, motor activity evaluations, thermal sensitivity evaluations, and startle response. There were no clear adverse effects noted in clinical pathology (including serum cholinesterase activity), organ weight, reproductive system, or histopathologic evaluations, although absolute and relative liver weights were marginally increased with increasing exposure concentration in both male and female rats consuming the Iowa mixture. In 26-week drinking water studies in mice, one male receiving the California mixture at 100x died during the study, and one control female and one female in the 100x group in the Iowa mixture study also died early. It could not be determined if the death of either of the mice in the 100x groups was related to consumption of the pesticide/fertilizer mixtures. Water consumption and body weight gains were not affected in these studies, and no signs of toxicity were noted in clinical observations or in neurobehavioral assessments. No clear adverse effects were noted in clinical pathology, reproductive system, organ weight, or histopathologic evaluations of exposed mice. The pesticide/fertilizer mixtures, when tested over a concentration range similar to that used in the 26-week studies, were found to have no effects in teratology studies or in a continuous breeding assay examining reproductive and developmental toxicity. The California and Iowa pesticide mixtures were tested for induction of micronuclei in peripheral blood erythrocytes of female mice. Results of tests with the California mixture were negative. Significant increases in micronucleated normochromatic erythrocytes were seen at the two-highest concentrations (10x and 100x) of the Iowa mixture, but the increases were within the normal range of micronuclei in historical control animals. Splenocytes of male rats and female mice exposed to these mixtures were examined for micronucleus and sister chromatid exchange frequencies. Sister chromatid exchange frequencies were marginally increased in rats and mice receiving the California mixture, but neither species exhibited increased frequencies of micronucleated splenocytes. None of these changes were considered to have biological importance. In summary, studies of potential toxicity associated with the consumption of mixtures of pesticides and a fertilizer representative of groundwater contamination in agriculturative of groundwater contamination in agricultural areas of Iowa and California failed to demonstrate any significant adverse effects in rats or mice receiving the mixtures in drinking water at concentrations as high as 100 times the median concentrations of the individual chemicals determined by groundwater surveys. NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.

Journal Article↗

Hazard and risk assessment of chemical mixtures using the toxic equivalency factor approach.

There is considerable public, regulatory, and scientific concern regarding human exposure to endocrine-disrupting chemicals, which include compounds that directly modulate steroid hormone receptor pathways (estrogens, antiestrogens, androgens, antiandrogens) and aryl hydrocarbon receptor (AhR) agonists, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds. Based on quantitative structure-activity relationships for both AhR and estrogen receptor (ER) agonists, the relative potency (RP) of individual compounds relative to a standard (e.g. TCDD and 17-beta-estradiol) have been determined for several receptor-mediated responses. Therefore, the TCDD or estrogenic equivalent (TEQ or EQ, respectively) of a mixture is defined as TEQ = sigma[T(i)]xRP(i)or EQ=sigma[E(i)]xRP(i), where T(i) and E(i) are concentrations of individual AhR or ER agonists in any mixture. This approach for risk assessment of endocrine-disrupting mixtures assumes that for each endocrine response pathway, the effects of individual compounds are essentially additive. This paper will critically examine the utility of the TEQ/EQ approach for risk assessment, the validity of the assumptions used for this approach, and the problems associated with comparing low dose exposures to xeno and natural (dietary) endocrine disruptors.

Binding, Competitive↗

Toxicity assessment of cyanobacterial toxin mixtures.

A method is presented for the toxicity assessment of mixtures of cyanobacterial toxins with hepatotoxic, neurotoxic, and carcinogenic effects. The method is based on the derivation of toxicity equivalent factors obtained from toxicological data presented for cyanobacterial toxins in the literature and on the use of toxicity equivalents in analogy with the method used for polychlorinated dibenzo[p]dioxins and dibenzofurans. Because the method easily can include all toxicological data for cyanobacterial toxins at any time, the quality of the toxicity assessment of these toxins can be increased continuously depending on data availability. Generally, all toxicologically relevant cyanobacterial toxins for which data are available should be included in this assessment. The method is considered useful in the toxicity assessment of cyanobacterial toxin mixtures in surface water bodies and in drinking water. When using the total sum of the toxicity equivalents, the approach proposed here seems to lead to a more realistic toxicity assessment of cyanobacterial toxin mixtures than does the worst-case approach. However, the availability of data about acute and, especially, chronic toxicity must be increased significantly in the future in order to establish toxicologically validated exposure limit values for cyanobacterial toxins, especially those with hepatotoxic, neurotoxic, and carcinogenic effects.

Bacterial Toxins↗

Prediction of acute toxicity of chemicals in mixtures: worms Tubifex tubifex and gas/liquid distribution.

The aim of this contribution is to support our proposal of the procedure for predicting acute toxicity of binary mixtures by QSAR analysis techniques. The changes of a mixture composition are described by molar ratio R and visualized in the R-plot (QCAR--quantitative composition-activity relationships). The approach was inspired by Rault and Dalton's laws, their positive and negative deviations in the behavior of a mixture of real gases, by Loewe and Muischnek isoboles and by the Finney test of additivity. Acute toxicity was determined by the laboratory test with woms Tubifex tubifex. The additivity of the acute toxicity in the binary mixture benzene + nitrobenzene was confirmed and a new interaction is described: "mixed interaction" with the binary mixture aniline + ethanol. The "mixed interaction" means that depending on mixture composition, both potentiation and inhibition can occur. As the first physicochemical descriptor of the changes caused by the changing composition of binary mixtures, the gas/liquid equilibrium was studied and a composition of the gaseous phase was determined by a gas chromatographic method. The method for determination of concentrations in the gaseous phase was described. The gaseous phase composition of benzene + nitrobenzene. benzene + ethanol, benzene + aniline and ethanol + aniline mixtures was analyzed. It was found that if the concentrations of the mixture's components in the gaseous phase behave nonideally (they are not additive), the acute toxicity of the same mixture is not additive as well. Another descriptor to distinguish between potentiation and inhibition will be, however, necessary. The properties, both gaseous phase composition and the acute toxicity, of the benzene + nitrobenzene mixture are additive. In mixtures with the mixed interaction, the R-plot of the composition of the gaseous phase is complex with a large variation of results.

Aniline Compounds↗

Safety evaluation of chemical mixtures and combinations of chemical and non-chemical stressors.

Recent developments in hazard identification and risk assessment of chemical mixtures are reviewed. Empirical, descriptive approaches to study and characterize the toxicity of mixtures have dominated during the past two decades, but an increasing number of mechanistic approaches have made their entry into mixture toxicology. A series of empirical studies with simple chemical mixtures in rats is described in some detail because of the important lessons from this work. The development of regulatory guidelines for the toxicological evaluation of chemical mixtures is discussed briefly. Current issues in mixture toxicology include the adverse health effects of ambient air pollution; the application of such modern, sophisticated methodologies as genomics, bioinformatics, and physiologically based pharmacokinetic modeling; and databases for mixture toxicity. Finally, the state of the art of our knowledge on the potential adverse health effects of combined exposures to chemicals and non-chemical stressors (noise, heat/cold, microorganisms, immobilization, restraint, or transportation), research initiatives in these fields, and the development of an indicator for the cumulative health impact of multiple environmental exposures are discussed.

Dose-Response Relationship, Drug↗

An improved in vitro model for testing the pulmonary toxicity of complex mixtures such as cigarette smoke.

Numerous approaches have been employed for testing the biological activity of cigarette smoke in vitro. None of them has managed to expose cultured lung cells in a realistic manner to the complex gaseous and particulate mixture that constitutes cigarette smoke. We have devised a system that makes this possible. The system presented here enables the direct exposure of human lung cells to native, unmodified cigarette mainstream smoke. It consists of a smoking machine, a dilution device for the smoke, analytical devices for online monitoring and a specially adapted exposure module based on the Cultex** cell cultivation system that is equipped with a gas-exposure top. Due to the special design of the exposure device and the optimised exposure conditions, this equipment allows cultured human lung cells to be exposed to freshly generated cigarette mainstream smoke. Exploratory experiments revealed that the smoke could be diluted over a wide concentration range in a reproducible way with respect to gas and particulate phases, and also demonstrated reproducible particle deposition depending on smoke concentration. Furthermore, it was shown that the exposed cells maintained their viability. Native cigarette mainstream smoke induced dose-dependent cellular effects in exposed cells with respect to cellular viability (viable cell number monitored by tetrazolium salt cleavage) and intracellular parameters (ATP and glutathione content). Therefore, fresh, physically and chemically unmodified cigarette mainstream smoke can be tested using this novel system.

Aerosols↗

Toxicity of chemical mixtures: proteomic analysis of persisting liver and kidney protein alterations induced by repeated exposure of rats to JP-8 jet fuel vapor.

Male Sprague-Dawley rats were exposed by whole body inhalation to 1000 mg/m3 +/- 10% JP-8 jet fuel vapor or room air control conditions for 6 h/day, 5 days/week for six consecutive weeks. Following a rest period of 82 days rats were sacrificed, and liver and kidney tissues examined by proteomic methods for both total protein abundance and protein charge modification. Kidney and lung samples were solubilized and separated via large scale, high resolution two-dimensional electrophoresis (2-DE) and gel patterns scanned, digitized and processed for statistical analysis. Through the use of peptide mass fingerprinting, confirmed by sequence tag analysis, three altered proteins were identified and quantified. Numerical, but not significantly different increases were found in total abundance of lamin A (NCBI Accession No. 1346413) in the liver, and of 10-formyltetrahydrofolate dehydrogenase (10-FTHF DH, #1346044) and glutathione-S-transferase (GST; #2393724) in the kidneys of vapor-exposed subjects. Protein charge modification index (CMI) analysis indicated significant alterations (P < 0.001) in expressed lamin A and 10-FTHF DH. These persisting changes in liver and kidney proteins are discussed in terms of possible alterations in the functional capacity of exposed subjects.

Amino Acid Sequence↗