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Assessing the cancer risk from environmental PCBs.

A new approach to assessing the cancer risk from environmental polychlorinated biphenyls (PCBs) considers both toxicity and environmental processes to make distinctions among environmental mixtures. New toxicity information from a 1996 cancer study of four commercial mixtures strengthens the case that all PCB mixtures can cause cancer, although different mixtures have different potencies. Environmental processes alter PCB mixtures through partitioning, chemical transformation, and preferential bioaccumulation; these processes can increase or decrease toxicity considerably. Bioaccumulated PCBs are of greatest concern because they appear to be more toxic than commercial PCBs and more persistent in the body. The new approach uses toxicity studies of commercial mixtures to develop a range of cancer potency estimates and then considers the effect of environmental processes to choose appropriate values for representative classes of environmental mixtures. Guidance is given for assessing risks from different exposure pathways, less-than-lifetime and early-life exposures, and mixtures containing dioxinlike compounds.

Environmental Exposure↗

Toxicity measurement of orthopedic implant alloy degradation products using a bioluminescent bacterial assay.

The toxicity of aqueous metal solutions representative of ionic degradation products from orthopedic implant alloys was determined using a bacterial bioluminescence assay, Microtox. The toxicity of forms of the individual elements released from ASTM F75 Co-Cr-Mo (Co-Cr-Mo), F138 316L stainless steel (316L), and F136 Ti-6Al-4V (Ti-6Al-4V) was first determined, and a mathematical model was developed to predict the toxicity of mixtures of these ions. Aqueous metal solutions were then mixed according to the proportions of the ions found in these alloys, and their toxicity was measured with Microtox. Mixture behavior was classified as synergistic, antagonistic, or additive by comparing measured toxicity to predicted toxicity. Since relating these tests to actual implant corrosion processes can be confounded by selective leaching, the predicted and measured toxicity of aqueous metal solutions mixed according to proportions representative of selective leaching were next determined, and the mixture behaviors were classified as before. The most toxic individual alloying elements were found to be hexavalent Cr, Ni, and Co, in that order: a finding in accord with prior biocompatibility research. Co-Cr-Mo was found to be the most toxic alloy mixture of both those combined according to alloy composition and those combined to reflect selective leaching. The Ti-6Al-4V mixtures were found to behave synergistically, while the Co-Cr-Mo and 316L mixtures behaved antagonistically. By providing insight into degradation product toxicity and elemental interaction, these experiments demonstrate the utility of employing bioluminescent bacterial assays to investigate biocompatibility of implant materials. Further studies to more closely simulate in vivo conditions, though, are required to fully gauge their potential in this regard.

Algorithms↗

Central nervous system toxicity of local anesthetic mixtures in the rat.

Local anesthetics are often administered as mixtures during regional anesthesia. This study investigated whether a synergistic or antagonistic interaction between amide/amide or amide/ester local anesthetic combinations is present with respect to central nervous system toxicity. For surgical preparation, rats were anesthetized with 0.8% halothane in 30% O2/balance N2O and mechanically ventilated. Mean arterial blood pressure and the electroencephalogram were continuously monitored. After surgery, the halothane was discontinued for 15 min. An intravenous infusion of solutions containing lidocaine alone, bupivacaine alone, or any of three mixtures of the two drugs was then begun and continued at a fixed rate until seizure activity was observed on the electroencephalogram. Total administered doses of both drugs were compared by isobolographic analysis. After a similar protocol, a second experiment was performed evaluating lidocaine, tetracaine, or any of three mixtures of those two drugs. In both experiments, normocapnia, normoxia, and normothermia were maintained for all rats. For mixtures of lidocaine/bupivacaine (P = 0.40) and lidocaine/tetracaine (P = 0.24), there was no evidence that a significant degree of either synergism or antagonism was present. At the onset of seizures, mean arterial pressure was lowest in the lidocaine-alone groups in both experiments. Increasing doses of either bupivacaine or tetracaine (with correspondingly decreasing doses of lidocaine) were associated with greater mean arterial pressure values at onset of seizures. We conclude that central nervous system toxic effects of amide/amide or amide/ester anesthetic combinations, such as might occur during accidental intravascular injection, are no more than when the drugs are administered alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗

The effects of motorway runoff on freshwater ecosystems: 3. Toxicant confirmation.

Previous studies have demonstrated that small streams receiving road runoff have reduced water and sediment quality. These changes in quality are associated with alterations in the structure and functioning of stream communities. Laboratory studies have indicated that the community changes are due to sediment-associated contaminants, and toxicant identification evaluations have shown that the major toxicants are contained probably in a fraction of sediment extract that contains polycyclic aromatic hydrocarbons (PAHs). The aim of the present study was to determine whether PAHs were indeed the major toxicants in sediment extracts. Toxicity tests were performed with PAH mixtures, the toxic fraction of an extract of runoff-contaminated sediment, and a whole sediment extract. These indicated that three PAHs accounted for the toxicity of a sediment extract: pyrene, fluoranthene, and phenanthrene. The possibility of spatial or temporal variation in major toxicants was also investigated and tests on a number of sediment extracts obtained from a number of sites at different times demonstrated that the three PAHs accounted for 30.8 to 120% of an extract's toxicity. When the PAHs were considered individually, pyrene was shown to account for most of the toxicity (44.9%), followed by fluoranthene (16%) and phenanthrene (3.5%).

Animals↗

Ozonation of chrysene: evaluation of byproduct mixtures and identification of toxic constituent.

The effects of chrysene and the ozonated byproducts on in vitro gap junctional intercellular communication (GJIC) were evaluated using the scrape loading/dye transfer (SL/DT) technique. A 1 mM solution of chrysene was ozonated at dosages of 1.75, 3, 4.25, and 5 mol O3/mol chrysene (Chr). The early ozonation mixture, 1.75 mol O3/mol Chr, exhibited greater inhibition to GJIC than chrysene and irreversible damage to cells leading to cell death. To determine the compounds potentially responsible for the increase in toxicity, the byproducts formed upon treatment with 1.44 mol O3/mol Chr were separated into 14 fractions using RP-HPLC. The major compounds identified in the fractions were 2-(2'-formyl) phenyl-1-naphthaldehyde, 2-(2'formyl) phenyl-1-naphthoic acid, and 2-2-carboxyphenyl-1-naphthoic acid. 2-(2'-Formyl) phenyl-1-naphthaldehyde was determined to be the compound causing GJIC inhibition in sample fractions and byproduct mixtures.

Animals↗

The potentiating effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on paraquat-induced neurochemical and behavioral changes in mice.

Although the etiology of Parkinson's disease (PD) is not fully understood, there are numerous studies that have linked the increased risk for developing PD to pesticides exposure including paraquat (PQ). Moreover, the exposure to a combination of compounds or chemical mixtures has been suggested to further increase this risk. In the current study, the effects of PQ on the nigrostriatal dopaminergic system in male C57BL6 mice exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were examined to assess the impact of toxic substance mixtures exposure on neurochemical and behavioral changes. In this study, a low non-toxic dose of MPTP (10mg/kg) was injected once a day for 5 days and was followed by PQ (7 mg/kg) once a day for 6 days (subacute protocol) or once a week for 10 weeks (chronic protocol). The results from the subacute protocol showed that PQ reduced the turnover of dopamine (DA) as indicated by a 21% and a 22.3% decrease in dihydroxyphenyl acetic acid (DOPAC), homovanillic acid and increased S-adenosyl methionine/S-adenosyl homocysteine index (SAM/SAH) by 100%. However, the administration of PQ to MPTP primed mice resulted in the decrease of DOPAC, HVA, DA, by 35.8%, 35.2% and 22.1%, respectively. In addition, PQ decreased the total number of movements (TM) by 28% but MPTP plus PQ decreased TM by 41%. The SAM/SAH index showed that MPTP increased methylation by 33.3%, but MPTP plus PQ increased methylation by 81%. In the chronic protocol, the data showed that MPTP administration did not affect DA, DOPAC, and HVA levels. The administration of PQ led to significant decrease in DOPAC, HVA, and TD by 31.6%, 19.9%, and 21.2% respectively with no effect on DA levels. The MPTP plus PQ group showed reduced DA, DOPAC, HVA, and total distance traveled by 58.4%, 82.8%, 55.8%, and 83.9%, respectively. Meanwhile, PQ administration caused a reduction in tyrosine hydroxylase immunoreactivity in the substantia nigra, and this effect was more pronounced in MPTP pretreated mice. It was concluded from this study that prior treatment with MPTP potentiated the effects of PQ in reducing DA, DOPAC, HVA, TH immunoreactivity, locomotor activity, and increasing the methylation index. The enhanced effects of PQ following MPTP administration further support the role of toxic substance mixtures in causing Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

Toxicity of cadmium and zinc mixtures to cercarial tail loss in Diplostomum spathaceum (Trematoda:Diplostomidae).

The effects of cadmium and zinc mixtures on tail loss of the free-living cercarial stage of the parasitic fluke Diplostomum spathaceum were investigated at concentrations ranging from 0.1 to 10,000 microg/L. Cercariae were exposed to metal mixtures of equal concentrations, metal mixtures of unequal concentrations, and a low-dose pretreatment followed by high-dose exposure mixtures. Under control conditions as the cercarial population aged tail loss occurred naturally a few hours before death, with an increasing tail loss over time associated with a decrease in cercarial survival. Under all mixture exposures the period of tail loss was prolonged compared to single-metal exposures. In most test solutions this was associated with a similar increase in survival of cercariae. Inhibition of tail loss occurred in low concentrations (0.1-100 microg/L) of equal mixed exposures. In some unequal, and in all pretreatment mixture exposures, a significant stimulation of tail loss occurred compared to the pattern of decreasing survival over time within the cercarial population. The importance of toxic metal mixtures to cercarial tail loss and potential implications for successful parasite transmission are discussed.

Animals↗

Toxicity assessment of environmentally relevant pollutant mixtures using a heuristic model.

In this study, 9 chemicals were chosen from a recent report on surface water concentrations of a variety of xenobiotics to test the hypothesis that the toxicity of chemical mixtures could be estimated using a model based on the toxicity of the individual chemicals. Concentration-response curves for the endpoints of lifespan, growth rate, and fecundity were generated for each chemical experimentally using the crustacean, Daphnia magna. From this data, a mathematical model for the combined toxicity of these chemicals was generated that merged the concepts of concentration addition and independent joint action. Toxicity of a mixture was modeled at various levels at which the ratio of the chemicals within the mixture was maintained at that reported for median detected environmental levels. Toxicity of the mixture was then determined experimentally and compared to model predictions. The model accurately predicted the most sensitive endpoint, as well as the lowest toxic effect level of the mixture. Results demonstrated that, for this mixture of chemicals, toxicity was not influenced significantly by interactions among the chemicals and a single constituent dominated toxicity. According to model predictions and experimental results, the median detected environmental concentrations of chemicals constituting this mixture provided no margin of safety.

Animals↗

Toxicity characterization of complex mixtures using biological and chemical analysis in preparation for assessment of mixture similarity.

In the United States, several proposed approaches for using bioassays for the risk assessment of complex hazardous mixtures require that selected mixtures be "sufficiently similar" to each other. The goal of this research was to evaluate the utility of a protocol using in vitro bioassays and chemical analysis as a basis for assessing mixture similarity. Two wood preserving wastes (WPWs) containing polycyclic aromatic hydrocarbons and pentachlorophenol were extracted and fractionated to generate potentially similar mixtures. Chemical analysis was conducted using gas chromatography/mass spectrometry. Genotoxicity was evaluated using the Salmonella/microsome and Escherichia coli prophage induction assays. The crude extract of one WPW was also tested in the chick embryotoxicity screening test (CHEST) assay. The CHEST assay provided the most sensitive measurement of toxicity. Overall, the biological potency of the samples was not well correlated with predicted potency based on chemical analysis. Although several mixtures appeared similar based on chemical analysis, the magnitude of the response in bioassays was often dissimilar. Fractionation was required to detect the genotoxicity of mixture components in vitro. The results confirm the need for an integrated protocol, combining chemical analysis, fractionation, and biological testing to characterize the risk associated with complex mixtures.

Biological Assay↗

Genetic toxicity of a standardized mixture of citrus polymethoxylated flavones.

Flavonoids are a ubiquitous family of phytochemicals that display a variety of biological effects, both beneficial and adverse depending on the individual compound. Certain flavonoids are genotoxic while others inhibit the genotoxicity of other mutagens. In the present studies, the mutagenicity of a mixture of polymethoxylated flavones (PMFs) purified from citrus peel oil was evaluated. The mixture consisted of nobiletin (32.5%), 3,3',4',5,6,7,8-heptamethoxyflavone (25.0%), tangeretin (14.0%), trimethylscutellarein (9.1%), sinensetin (3.9%), 5-demethyl-nobiletin (2.8%), hexa-O-methylquercetagetin (3.3%), 5-demethyl-tetramethylscutellarein (0.7%), 5-hydroxy-3,3',4',6,7,8-hexamethoxyflavone (0.7%), and a small quantity of unidentified flavonoid compounds (3.9%). In vitro addition of the PMF mixture over a concentration range that spanned four log doses (0.0005-5.0 mg/plate) did not reveal any evidence of mutagenicity in five bacterial tester strains (Salmonella typhimurium TA98, TA100, TA102, TA1535 and TA1537) either in the absence or presence of S9 activation. The PMF mixture exhibited a statistically significant increase in mutagenicity of L5178Y tk(+/-) mouse lymphoma cells at 0.05 (38.5 x 10(-6); P<0.05) and 0.1 mg/ml (61 x 10(-6); P<0.01) compared with vehicle-treated controls (mutation frequency=19.7 x 10(-6)). However, these responses were within historical values observed in negative control cultures and extremely small compared to the positive control (EMS 0.5 microl/ml; 1685.3 x 10(-6)). Furthermore, in the presence of S9 there was no indication of genetic toxicity in L5178Y tk(+/-) cells. These results demonstrate that the PMF mixture is not genotoxic in in vitro assay systems.

Animals↗

Mechanism of concentration addition toxicity: they are different for nonpolar narcotic chemicals, polar narcotic chemicals and reactive chemicals.

According to the toxicity mechanism of the individual chemicals, the concentration addition toxicity mechanism is revealed for nonpolar-narcotic-chemical mixtures, polar-narcotic-chemical mixtures and reactive-chemical mixtures, respectively. For nonpolar-narcotic-chemical mixtures, the partitioning of individual chemicals from water to biophase was determined, and the result shows that their concentration additive effect results from no competitive partitioning among individual chemicals. For polar-narcotic-chemical mixtures, their toxicity are contributed by two factors (the total baseline toxicity and the hydrogen bond donor activity of individual chemicals), and it is the concentration additive effect for either of these two factors that leads to their concentration addition toxicity. In addition, the interactions between the reactive chemicals and the biological macromolecules are discussed thoroughly. The results suggest that the net effect of these interactions is zero, and it is this zero net effect that leads to the concentration addition toxicity mechanism for reactive-chemical mixtures.

Drug-Related Side Effects and Adverse Reactions↗

NTP technical report on the toxicity studies of a Chemical Mixture of 25 Groundwater Contaminants Administered in Drinking Water to F344/N Rats and B6C3F(1) Mice.

Toxicity studies were performed with a chemically defined mixture of 25 groundwater contaminants, using dose levels considered to have environmental relevance. The mixture contained 19 organic compounds and six metals (shown below); the selection of these compounds was based primarily on the frequency of their occurrence in United States Environmental Protection Agency surveys of groundwater contamination in the vicinity of hazardous waste disposal sites. This report focuses primarily on 26-week drinking water toxicity studies with male and female F344/N rats and B6C3F(1) mice. The endpoints evaluated included histopathology, clinical pathology, neurobehavioral studies, and reproductive toxicity. Additional studies using this same chemical mixture are briefly reviewed in this report and include an evaluation of spermatogenesis in B6C3F(1) mice exposed to the chemical mixture for 13 weeks, a continuous breeding study with Sprague-Dawley rats and CD-1(R) Swiss mice, studies of myelotoxicity in B6C3F(1) mice exposed to the chemical mixture for up to 31.5 weeks, studies of immunosuppression in B6C3F(1) mice exposed for up to 13 weeks, in vitro mutagenicity assays in Salmonella typhimurium and Escherichia coli, and measures of genetic damage in bone marrow and peripheral blood of F344/N rats and B6C3F(1) mice in 2-week drinking water studies. In a 26-week drinking water study in which rats were administered the chemical mixture at composite contaminant concentrations of 0, 11, 38, 113, or 378 ppm, no deaths occurred and the body weight gain of high-dose males was slightly less than that of the controls. Water consumption decreased with dose and was 24% to 28% less than that of the controls at the highest concentration. Changes in organ weights occurred primarily in high-dose rats and included increased absolute and relative liver and kidney weights in females, increased relative kidney weight in males, and decreased absolute and relative thymus weights in males and females. Hematologic assessments indicated that rats receiving 378 ppm developed a microcytic anemia consistent with that accompanying iron depletion. Multiple foci of inflammation occurred in the liver of exposed rats. In high-dose females, these liver lesions were especially prominent and included bile duct and oval cell hyperplasia. Inflammation also occurred in the mesenteric lymph nodes, the adrenal gland, and the spleen. The amount of hemosiderin in the spleens of rats receiving the higher concentrations of the chemical mixture was less than normal. Components of a chemical mixture of 25 groundwater contaminants include acetone, aroclor 1260, arsenic, benzene, cadmium, carbon tetrachloride, chlorobenzene, chloroform, chromium, 1,1-dichloroethane, 1,2-dichloroethane, 1,1-dichloroethylene, 1,2-trans-dichloroethylene, di(2-ethylhexyl) phthalate, ethylbenzene, lead, mercury, methylene chloride, nickel, phenol, tetrachloroethylene, toluene, 1,1,1-trichloroethane, trichloroethylene, xylenes. In a 26-week study in which mice were exposed to the chemical mixture at concentrations of 0, 11, 38, 113, and 378 ppm in drinking water, there were no clear adverse effects noted in survival, weight gain, clinical pathology parameters, or histopathologic evaluations. Water consumption decreased with increasing dose, and water consumption by high-dose mice was approximately 40% less than that by the controls. In neurobehavioral assessments, no clear treatment-related effects were observed in measures of forelimb and hindlimb grip strength, hindlimb footsplay, motor activity, response to a thermal stimulus, or startle response in rats or mice evaluated at 6-week intervals throughout the 26- week drinking water studies. There were no effects on sperm morphology or motility or on estrous cycle length in rats or mice receiving the chemical mixture during the 26-week studies. Sperm concentration was decreased in F(1) CD-1(R) Swiss mice during continuous breeding studies, although there were no clear adverse effects on the fertility of Sprague-Dawley rats or CD-1(R) Swiss mice in th CD-1&reg; Swiss mice in these studies. Pup weight, the number of live males, and the number of male pups per litter were slightly decreased in dosed rats in the continuous breeding study in rats; the number of live female mouse pups in litters born of the F(0) and F(1) generations was decreased in the 378 ppm group. The significance of these observations, if any, is not known. F(1) mice receiving 378 ppm had increased incidences of hepatic inflammation compared to the controls. In female B6C3F(1) mice that received the chemical mixture in drinking water at concentrations as high as 756 ppm for 2 weeks or 378 ppm for 13 weeks, assessments of immune function showed suppression of hematopoietic stem cells and antigen-induced antibody-forming cells. This was manifested by impaired resistance to challenge with a nonlethal strain of mouse malaria, Plasmodium yoelii. Additional evidence of an adverse effect on hematopoietic stem cells was demonstrated by decreases in the in vitro colony-forming ability of granulocyte-macrophage progenitor cells and erythroid precursor cells isolated from female mice that had received the chemical mixture at a concentration of 378 or 756 ppm in 31.5 week studies. Potential genotoxic effects of the chemical mixture to the bone marrow of F344/N rats and B6C3F(1) mice were assessed in 2-week drinking water studies with concentrations as high as 756 ppm. Small increases in sister chromatid exchanges and micronucleated polychromatic erythrocytes occurred in the bone marrow of dosed male mice, and micronucleated polychromatic erythrocytes were also increased in dosed female mice. The chemical mixture did not induce mutations in Salmonella typhimurium strains TA98 and TA100 and did not induce DNA damage in Escherichia coli with or without metabolic activation. In summary, rats receiving drinking water containing a mixture of 25 common groundwater contaminants at levels of potential environmental relevance developed inflammatory lesions in the liver, spleen, lymph nodes, and adrenal gland, as well as evidence of an iron deficiency anemia. The inflammatory lesions could not be predicted based on the known toxic effects of the individual components of the chemical mixture. Mice exposed to similar concentrations of the chemical mixture did not show adverse effects in a standard toxicity study but developed deficits in bone marrow function, evidence of genetic damage, hepatic inflammation, and immunosuppression in other studies that generally included exposures to higher concentrations or exposures of longer duration. A no-observed-adverse-effect level for histologic injury (granulomatous inflammation of the liver) was 11 ppm in rats; however, no clear evidence for histologic injury was seen in mice exposed to concentrations of the chemical mixture as high as 378 ppm in a standard 26-week study. 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↗

Toxicity to Tradescantia of technogenic radionuclides and their mixture with heavy metals.

The genotoxic effects on Tradescantia of (137)Cs, (90)Sr, and (236, 242)Pu, a heavy metal mixture [Cd, Cr(VI), Cu, Mn(II), Ni, Pb, Zn] and of a complex mixture of these toxicants were determined. The impact of radionuclides on plants subjected to ionizing radiation exposure was estimated. The number of somatic mutations and the quantity of nonviable stamen hairs were used as end points in the testing. An increase in the quantity of nonviable stamen hairs was observed with increasing internal exposure to (137)Cs, (90)Sr, and (236, 242)Pu; however, the number of somatic mutations was not observed to be dependent on ionizing radiation. The internal dose of individual radionuclides necessary to decrease the quantity of viable stamen hairs in Tradescantia by 50% can be arranged in the following sequence: (236, 242)Pu > (137)Cs > (90)Sr. Tradescantia died in the mixture of the radionuclides (90)Sr, (137)Cs, and (236)Pu (5 x 10(-2), 7 x 10(-5), and 4 x 10(-10) Gy, respectively) after 14 days, whereas the heavy metal mixture caused somatic mutations in 3% of the Tradescantia and nonviable stamen hairs in 7% but no mortality. However, the Tradescantia died in a combined mixture of these heavy metals and the radionuclides after 14 days. On the basis of all these observations, it can be concluded that the toxic effect of radionuclides was more significant than that of heavy metals.

Cesium Radioisotopes↗

Assessment of dermal absorption and penetration of components of a fuel mixture (JP-8).

Occupational and environmental multi-chemical exposures are extremely common. Methods for assessment of the risks from dermal exposures to complex mixtures vary depending on the information available. The composition of a volatile mixture (such as JP-8 jet fuel) can change radically, depending on the phase of the mixture - vapor, liquid or aerosol. Assessing the absorption (into the skin) and penetration (through the skin) of components of the mixture can reduce uncertainty in the risk assessment process. Permeability coefficients of the 12 individual components that could be detected to penetrate the skin could be used to assess the toxicity of each individual component in the JP-8. The penetration of each of these components is related to and can be predicted from molecular weight and octanol water partition coefficients of that component. The composition of the components that penetrate the skin would be different from the composition of JP-8 because the permeability of the components differs by two orders of magnitude. Concentrations of the aliphatic chemicals found in the skin correlated well with carbon number. The JP-8 jet fuel is used as an example of how component data on absorption and penetration can be integrated into an assessment (McDougal et al., Toxicol Sci 2000; 55: 247-255). The component approach shows promise for estimating systemic toxicity of mixtures. Local toxicity (irritation, sensitization, etc.) may be better understood in the future when quantitative information becomes available about the duration and magnitude of chemical exposures required to cause local effects.

Absorption↗

Increased toxicity to invertebrates associated with a mixture of atrazine and organophosphate insecticides.

This study examined the joint toxicity of atrazine and three organophosphate (OP) insecticides (chlorpyrifos, methyl parathion, and diazinon) exposed to Hyalella azteca and Musca domestica. A factorial design was used to evaluate the toxicity of binary mixtures in which the lethal concentration/lethal dose (LC1/LD1, LC5/LD5, LC15/LD15, and LC50/LD50) of each OP was combined with atrazine concentrations of 0, 10, 40, 80, and 200 microg/L for H. azteca and 0, 200, and 2,000 ng/mg for M. domestica. Atrazine concentrations (> or = 40 microg/L) in combination with each OP caused a significant increase in toxicity to H. azteca compared with the OPs dosed individually. Acetylcholinesterase (AChE) activity also was examined for the individual OPs with and without atrazine treatment. Atrazine in combination with each of the OPs resulted in a significant decrease in AChE activity compared with the OPs dosed individually. In addition, H. azteca that were pretreated with atrazine (> or = 40 microg/L) were much more sensitive to the OP insecticides compared with H. azteca that were not pretreated with atrazine before being tested. Topical exposure to atrazine concentrations did not significantly increase OP toxicity to M. domestica. The results of this study indicate the potential for increased toxicity in organisms exposed to environmental mixtures.

Acetylcholinesterase↗

Evaluation of methods for predicting the toxicity of polycyclic aromatic hydrocarbon mixtures.

Risk assessments of polycyclic aromatic hydrocarbon mixtures are hindered by a lack of reliable information on the potency of both mixtures and their individual components. This paper examines methods for approximating the toxicity of polycyclic aromatic hydrocarbon (PAH) mixtures. PAHs were isolated from a coal tar and then separated by ring number using HPLC. Five fractions (A-E) were generated, each possessing a unique composition and expected potency. The toxicity of each fraction was measured in the Salmonella/mutagenicity assay and the Chick Embryo Screening Test (CHEST). Their abilities to induce ethoxyresorufin-O-deethylase and to inhibit gap junction intercellular communication in rat liver Clone 9 cells were also measured. In the Salmonella/mutagenicity assay, fractions were predicted to have potencies in the order C > D > E > B > A. Toxic equivalency factors (TEFs) for fractions A-E were in the order E > or = D > C > B > A. TEF values were 20,652, 20,929, 441, 306, and 74.1 micrograms of BaP equiv/g, respectively. A lack of agreement between assay-predicted potencies and chemical analysis-predicted potencies was observed with other assays and other methods of calculation. The results demonstrate the limitations of using a single method to predict the toxicity of a complex PAH mixture.

Animals↗

Sensitivity of epigean and hypogean freshwater macroinvertebrates to complex mixtures. Part I: Laboratory experiments.

The impact of waste storage on aquatic systems is a regulatory requirement in Europe, but it is nowadays only considered to a limited extent. The complexity of mixtures, which contain many inorganic and organic compounds, requires the use of combining chemical measurements with ecotoxicological observations. This research employed an integrated laboratory and outdoor mesocosms approach to assess the effects of mixtures on freshwater macroinvertebrates. The effects of percolates coming from water having percolated through maturated secondary smelting slags, on freshwater macroinvertebrates (molluscs, crustaceans and insect larvae) were investigated under laboratory conditions using a continuous flow-through testing apparatus. Lethality (LC50 96 and 240 h) was chosen as the endpoint. The results indicate that the difference in sensitivity of macroinvertebrates is correlated with their ability to regulate or neutralize contaminants in the mixture during short-term exposure. Moreover, differences in sensitivity were dependent on duration of exposure. Because of the variability of toxicity among mixtures coming from the same waste, bioassays are required to determine the toxicities of these mixtures.

Animals↗