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PubMed1994

A 12-month study of policosanol oral toxicity in Sprague Dawley rats.

Policosanol is a natural mixture of higher aliphatic primary alcohols. Oral toxicity of policosanol was evaluated in a 12-month study in which doses from 0.5 to 500 mg/kg were given orally to Sprague Dawley (SD) rats (20/sex/group) daily. There was no treatment-related toxicity. Thus, effects on body weight gain, food consumption, clinical observations, blood biochemistry, hematology, organ weight ratios and histopathological findings were similar in control and treated groups. This study supports the wide safety margin of policosanol when administered chronically.

Administration, Oral↗
PubMed1988

Several aspects of mineral/protein nutrition in relation to consumption of an oil involved in the toxic syndrome.

An oil involved in the 'toxic syndrome' and two similar mixtures of oils, one with and the other without added oleoanilides, were studied for their effects on the utilization of protein, calcium, magnesium, phosphorus, sodium, potassium and zinc. Forty-eight female Wistar rats initially weighing about 75 g were fed for 28 days on the same semi-synthetic diet containing: virgin olive oil, or a mixture of canbra oil (50%), refined olive-pomace oil (20%), grapeseed oil (20%) and animal fat (10%), or the same dietary mixture supplemented with either 700 ppm oleoanilides or the alleged toxic oil. Weight, food intake and nutritional balances were monitored. The food intake of the animals fed the toxic oil began to decrease at the end of the trial, producing a reduction in the amount of nutrients ingested, but no weight loss. This oil also negatively affected the digestion of protein, potassium, sodium and zinc, the mechanism of which, in the case of the first two, appears to be related to the source of the fat. It also decreased metabolic utilization while favouring protein catabolism and the elimination of phosphorus, magnesium and potassium. No substantial modifications were noted in the animals' bones.

Animals↗
PubMed2003

Toxicity evaluation of a commercial bioremediation agent mixed with crude oil.

The toxicity and efficacy of a bacteria-based commercial bioremediation agent (CBA) was assessed through bioassays with juvenile inland silverside minnows, Menidia beryllina, and flask studies of oil degradation. Addition of the CBA to weathered Alaska, USA North Slope crude oil (ANS-521) prior to testing increased toxicity of the water-soluble fraction (WSF) of the oil in both chronic (growth) and acute (mortality) toxicity tests. Time-course toxicity assessment of the water-soluble fraction of the CBA/oil combination indicated increases in effect after 7 to 14 d of mixing that coincided with elevated concentrations of both alkanes and aromatics in the WSF. Under controlled laboratory conditions, the CBA significantly enhanced degradation of the oil compared with a treatment with nutrients alone. The alkane fraction was degraded by nearly 100% over a 42-d period while the aromatic fraction was decreased by 70%. While toxicity testing is not currently required to list bioremediation agents on the product schedule of the National Oil and Hazardous Substances Pollution Contingency Plan, the potential interaction between bioremediation agents and oil should be further investigated and listing requirements reassessed as necessary. Recommendations for future investigations of this issue include characterization of temporal trends in toxicity of CBA and oil mixtures, use of multiple test methods (battery testing) when evaluating toxicity, comparative evaluations of indigenous versus product-derived microorganisms in efficacy studies, and the use of a comparable oil between studies to facilitate comparison of efficacy and toxicity data for different products.

Animals↗
PubMed2005

Short-term ecological risks of depositing contaminated sediment on arable soil.

Sediments act as sinks of suspended material from surface water. Dredging of regional waters and subsequent disposal of the sediment on soil may lead to contamination of the soil, in some cases resulting in exceedance of soil quality standards. Soil quality standards are based on total concentrations. Total levels, however, do not always give an indication of adverse effects in soil ecosystems. Instead, truly bioavailable concentrations should be used as indicators. In this study we aim to test a set of suited indicators. We carried out partition and accumulation assays with metals and polycyclic aromatic hydrocarbons (PAHs) in soils and mixtures of soil and sediment, as well as a limited number of toxicity bioassays. We also investigated the rate of disappearance of PAHs from mixtures of sediments and soils. The experiments confirm that total levels indeed are not indicative of truly occurring toxic effects: mixing of highly contaminated sediments with soil hardly gave rise to either additional accumulation of metals and PAHs or excess toxicity. This indicates that the bioavailability of the metals and PAHs present in the sediment is limited. This general finding is confirmed by the low rate of disappearance of PAHs from the mixtures. It is concluded that inclusion of the aspects of bioavailability, mixture toxicity, and degradation, in the way described in this report, will solve the major limitations of the current methodology of classification of contaminated sediments.

Agriculture↗
PubMed2001

Application of a sigmapolycyclic aromatic hydrocarbon model and a logistic regression model to sediment toxicity data based on a species-specific, water-only LC50 toxic unit for Hyalella azteca.

Two models, a sigmapolycyclic aromatic hydrocarbon (PAH) model based on equilibrium partitioning theory and a logistic-regression model, were developed and evaluated to predict sediment-associated PAH toxicity to Hyalella azteca. A sigmaPAH model was applied to freshwater sediments. This study is the first attempt to use a sigmaPAH model based on water-only, median lethal concentration (LC50) toxic unit (TU) values for sediment-associated PAH mixtures and its application to freshwater sediments. To predict the toxicity (i.e., mortality) from contaminated sediments to H. azteca, an interstitial water TU, calculated as the ambient interstitial water concentration divided by the water-only LC50 in which the interstitial water concentrations were predicted by equilibrium partitioning theory, was used. Assuming additive toxicity for PAH, the sum of TUs was calculated to predict the total toxicity of PAH mixtures in sediments. The sigmaPAH model was developed from 10- and 14-d H. azteca water-only LC50 values. To obtain estimates of LC50 values for a wide range of PAHs, a quantitative structure-activity relationship (QSAR) model (log LC50 - log Kow) with a constant slope was derived using the time-variable LC50 values for four PAH congeners. The logistic-regression model was derived to assess the concentration-response relationship for field sediments, which showed that 1.3 (0.6-3.9) TU were required for a 50% probability that a sediment was toxic. The logistic-regression model reflects both the effects of co-occurring contaminants (i.e., nonmeasured PAH and unknown pollutants) and the overestimation of exposure to sediment-associated PAH. An apparent site-specific bioavailability limitation of sediment-associated PAH was found for a site contaminated by creosote. At this site, no toxic samples were less than 3.9 TU. Finally, the predictability of the sigmaPAH model can be affected by species-specific responses (Hyalella vs Rhepoxynius); chemical specific (PAH vs DDT in H. azteca) biases, which are not incorporated in the equilibrium partitioning model; and the uncertainty from site-specific effects (creosote vs other sources of PAH contamination) on the bioavailability of sediment-associated PAH mixtures.

Animals↗
PubMed2006

Relations between PM10 composition and cell toxicity: a multivariate and graphical approach.

Previous studies have used particle mass and size as metrics to link airborne particles with deleterious health effects. Recent evidence suggests that particle composition can play an important role in PM-toxicity; however, little is known about the specific participation of components (individually or acting in groups) present in such a complex mixture that accounts for toxicity. This work explores relationships among PM(10) components in order to identify their covariant structure and how they vary in three sites in Mexico City. Relationships between PM(10) with cell toxicity and geographical location were also explored. PM(10) was analyzed for elemental composition, organic and elemental carbon, endotoxins and the induction of inhibition of cell proliferation, IL-6, TNFalpha and p53. PM(10) variables were evaluated with principal component analysis and one-way ANOVA. The inhibition of cell proliferation, IL-6 and TNFalpha were evaluated with factorial ANOVA and p53 with the Welch test. The results indicate that there is heterogeneity in particle mass, composition and toxicity in samples collected at different sites. Multivariate analysis identified three major groups: (1) S/K/Ca/Ti/Mn/Fe/Zn/Pb; (2) Cl/Cr/Ni/Cu; and (3) endotoxins, organic and elemental carbon. Groups 1 and 3 showed significant differences among sites. Factorial ANOVA modeling indicated that cell proliferation was affected by PM concentration; TNFalpha and IL-6 by the interaction of concentration and site, and p53 was different by site. Radial plots suggest the existence of complex interactions between components, resulting in characteristic patterns of toxicity by site. We conclude that interactions of PM(10) components determine specific cellular outcomes.

Air Pollutants↗
PubMed2026

Attribution of PM2.5-Induced Transcriptomic Perturbation to Toxic Components.

Ambient fine particulate matter (PM2.5) is a chemically complex mixture whose health impacts are not fully captured by particle mass. Here, we developed an interpretable chemotranscriptomic framework to attribute PM2.5-induced molecular perturbations to toxicity-relevant components. PM2.5 collected from urban roadside and coastal environments was separated into whole, extractable, and unextractable fractions, characterized by LC/GC × GC-HRMS-based nontarget analysis and inductively coupled plasma mass spectrometry (ICP-MS), and evaluated using cytotoxicity testing and transcriptomic profiling in human bronchial epithelial cells. Urban PM2.5 exhibited greater cytotoxic potency per unit mass than coastal PM2.5, with extractable fractions accounting for most cytotoxic and pathway-level responses. Transcriptomics revealed distinct site-specific modes of action: urban PM2.5 preferentially induced oxidative stress, xenobiotic metabolism, and cell cycle suppression, consistent with acute, nonapoptotic injury, whereas coastal PM2.5 elicited weaker cytotoxicity but stronger interferon-mediated immune and apoptosis-related signaling. Integrating chemical abundance with pathway activity using random forest regression, SHAP interpretation, and mechanistic corroboration reduced 5,033 detected features to 444 pathway-linked candidate drivers. Fewer than 5% of features explained ∼95% of cumulative model contribution. Standard-confirmed contributors included plasticizer-related compounds, aromatic and heteroaromatic combustion products, and copper for urban PM2.5 and secondary/aged organics and nickel for coastal PM2.5. These findings support mechanism-informed prioritization of hazardous PM2.5 components beyond mass-based assessment.

Particulate Matter↗
PubMed2001

Differential survival of three mitochondrial lineages of a marine benthic copepod exposed to a pesticide mixture.

In South Carolina estuaries, the harpacticoid copepod Microarthridion littorale (Poppe 1881) consists of three distinct mitochondrial lineages (liI, liII, and liIII), whose distributions may be partially explained by the presence of toxic contaminants in the sampled habitats. The frequencies of liII and liIII are greatly diminished and sometimes absent in South Carolina contaminated tidal creeks where liI is omnipresent. In this study, representatives of these lineages or haplotype groups were collected from sediments of an estuarine creek containing low to undetectable levels of toxicants and then exposed to a toxic (approximately LC90) aqueous mixture containing an organophosphate (chlorpyrifos) and organochlorine pesticide (DDT, mixed isomers). A comparison was conducted for the frequency of each of the three haplotypes among the survivors of the exposed animals relative to that among the survivors of the control group. The haplotype group with the highest frequency in contaminated SC estuaries (liI) was statistically higher in frequency in survivors of the pesticide-exposed group than in the control group. The two rarer groups (liII and liIII) were less abundant among the survivors of the pesticide-exposed group than the control group. The frequencies of liI, liII, and liIII did not change significantly among the survivors of the control group. The differential survival of the three haplotype groups in the pesticide mixture may be one of the reasons that some haplotype groups are more likely to be found in clean or contaminated tidal creeks on the South Carolina coast.

Animals↗
PubMed1999

Capability of serum to convert streptomycin to cytotoxin in patients with aminoglycoside-induced hearing loss.

Individual variations in sensitivity to the ototoxic effects of aminoglycoside antibiotics are well documented. Our research demonstrates that there is an apparent difference in serum from patients who are resistant or susceptible to aminoglycoside ototoxicity. In the first study, the cytotoxicity of sera from patients with and without hearing loss after various time periods following the discontinuation of aminoglycoside treatment was assayed using the isolated outer hair cell toxicity assay. The results indicate that sera from patients with hearing loss were significantly more toxic than sera from patients with normal hearing or minimal hearing loss. This toxicity may persist for up to 1 year after discontinuation of aminoglycoside therapy. In a second study, sera were obtained from patients who had received aminoglycoside therapy several years previously. None of these sera was toxic to isolated outer hair cells in vitro. Streptomycin was then incubated with the sera or a protein fraction isolated from sera, and the incubation mixtures were tested for toxicity. The percentage of damaged outer hair cells was significantly higher when streptomycin had been treated with sera or a serum protein fraction from patients with hearing loss (58+/-10% and 68+/-9%, respectively) than with sera or a serum protein fraction from a control group (10+/-5% and 17+/-4%, respectively). In addition, several incubation mixtures were analyzed using high performance liquid chromatography. A new chromatographic peak was only found in the incubations of streptomycin with serum protein from patients with hearing loss. The results suggest that sera from individuals sensitive to aminoglycoside antibiotics may metabolize these drugs to cytotoxins.

Adolescent↗
PubMedDate not supplied

Acute respiratory effects of diaper emissions.

Mice were monitored with pneumotachographs while they breathed emissions of three brands of disposable diapers (described herein as brands A, B, and C) and one brand of cloth diapers for 1 hr. The authors used a computerized version of the ASTM-E-981 test method to measure changes in the pattern and frequency of respiration. In response to two brands of disposable diapers, many mice exhibited reduced mid-expiratory airflow velocity, sensory irritation, and pulmonary irritation. During the peak effects, brand A caused sensory irritation in 47% of the breaths and reduced mid-expiratory airflow velocity in 17% of the breaths (n = 39 mice), whereas the respective percentages noted for brand B were 20% and 15% of the breaths (n = 28 mice). The effects were generally larger during repeat exposures to these emissions, with up to 89% of breaths showing sensory irritation in response to brand A and up to 35% of breaths showing reduced mid-expiratory airflow velocity with brand B. A third brand of disposable diapers caused increases in respiratory rate, tidal volume, and mid-expiratory airflow velocity. The emissions of cloth diapers produced only slight SI and slight PI. Chemical analysis of the emissions revealed several chemicals with documented respiratory toxicity. The results demonstrate that some types of disposable diapers emit mixtures of chemicals that are toxic to the respiratory tract. Disposable diapers should be considered as one of the factors that might cause or exacerbate asthmatic conditions.

Acute Disease↗
PubMed2005

Joint toxicity of cadmium and phenanthrene in the freshwater amphipod Hyalella azteca.

The joint toxicity of combined metals and polynuclear aromatic hydrocarbons is poorly understood and may deviate from the summed concentration responses of the individual pollutants. The freshwater amphipod Hyalella azteca was exposed to sediment-amended Cd and phenanthrene (Phen) individually and in combination using United States Environmental Protection Agency 10-day sediment toxicity bioassays with lethality and growth end points. The lethal joint toxicity of Cd and Phen was investigated separately in 24-, 48-, and 72-hour aqueous exposures. In sediment exposures, a sublethal concentration of Phen (144 mg kg(-1)) in combination with Cd increased mortality across a range of Cd concentrations and decreased the 10-day LC50 for Cd from 523 mg kg(-1) (461 to 588, 95% confidence interval [CI]) to 263 mg kg(-1) (214 to 312, 95% CI). In contrast, sublethal concentrations of Phen had no effect on the lethal toxicity of Cd in aqueous exposures. Combined sediment-amended Cd and Phen acted independently on growth rate. Rate decreases were driven primarily by Cd. Our findings indicated that association with sediment influences the joint toxicity of Cd and Phen. Thus, mixtures of Cd and Phen may cause synergistic or independent toxicity in H. azteca depending on the end point investigated and the experimental protocol employed. As an implication of these results, the interpretation of standardized toxicity bioassays, including whole-effluent toxicity tests and single-compound toxicity tests, must be made with caution. These assessment protocols may underestimate potentially hazardous mixture effects in sediment environments. Therefore, risk assessment protocols for environments containing metal-PAH mixtures must include robust methods that can detect possible interactive effects among contaminants to optimize environmental protection.

Amphipoda↗
PubMed2000

The application of reporter gene assays for the determination of the toxic potency of diffuse air pollution.

Diffuse air pollution consists of a mixture of numerous compounds. It is emitted by many distributed sources and is omnipresent due to atmospheric transport. Risk assessment of the complex mixture of air pollutants on the basis of the toxicity of the individual compounds is not yet possible because the chemical identity and/or toxicity of the constituencies of a substantial fraction is unknown. In addition, no adequate procedures are available to integrate toxicity data of such complex mixtures, so that an individual risk assessment of the constituents of air pollution disregards possible combination effects. In the present study, an approach has been developed to assess the toxic potency by using in vitro bio-assay techniques. Genotoxicity was assessed in the umu-assay, a reporter gene assay using a strain of Salmonella typhimurium stably transfected with a plasmid (pSK1002) carrying the SOS-gene umuC fused to the reporter gene lacZ. Arylhydrocarbon-receptor activation was assessed in the DR-CALUX-assay, using a stably transfected H4IIE hepatoma cell line containing a plasmid for the luciferase gene under transcriptional control of dioxin-responsive elements. Samples of airborne particulate matter (APM) were collected with a high volume sampler next to a highway and in a natural conservation area. Both assays proved to be applicable to quantify genotoxicity and the presence of polycyclic aromatic hydrocarbons (PAHs) in small extracts from air-filter samples. Results indicate that PAHs from traffic exhausts seem to be largely responsible for an increased genotoxic activity of APM collected down-wind from the highway (western wind). APM collected at eastern wind directions seems to have a different composition of compounds, with a higher genotoxic activity that is less related to highway-emitted PAH-like compounds. At northern wind directions, APM is relatively less genotoxic and contains less PAHs than at other wind directions. Dioxin-like compounds contribute negligibly to the Ah-receptor agonistic potency of APM. Airborne pollutants with genotoxic and/or PAH-like characteristics form an undesired mutagenic risk, which will be evaluated in further in vivo studies.

Air Pollutants↗
PubMed2007

Allelochemical induction of cytochrome P450 monooxygenases and amelioration of xenobiotic toxicity in Helicoverpa zea.

Polyphagous herbivores encounter allelochemicals as complex mixtures in their host plants, and the toxicity of an individual compound may be influenced by the chemical matrix in which it is encountered. Certain plant constituents may reduce toxicity of cooccurring compounds by inducing detoxification systems, including cytochrome P450s, which can metabolize a broad range of substances. The polyphagous corn earworm Helicoverpa zea encounters a diversity of plant allelochemicals in its many host plants and, as well, can encounter aflatoxins, mycotoxins produced by Aspergillus flavus and Aspergillus parasiticus that infect damaged grains. Dietary supplementation of each of three plant allelochemicals that are frequently (coumarin, COU), occasionally (indole-3-carbinol, 13C), or rarely (xanthotoxin, XAN) encountered by H. zea larvae substantially reduced the toxicity of aflatoxin B1 (AFB1) to H. zea. Compared to fourth instars on diets containing 1 microg/g AFB1 that failed to develop and pupate, fourth instars on diets containing I3C and XAN increased in mass by 216.1 and 700% after 6 days, and pupated at rates of 40 and 88%, respectively. Diets containing COU or XAN also significantly reduced the mortality rates of caterpillars exposed to the insecticides, diazinon and carbaryl. Diets containing COU and XAN increased CYP6B8 transcripts 2.6-fold; CYP321A1 transcripts increased 20.7, 8.3, and 10.6-fold in response to COU, I3C, and XAN, respectively. These results indicate that consumption of plant allelochemicals can ameliorate toxicity of natural and synthetic toxins encountered by insects, and they suggest that P450s induced by these allelochemicals contribute to detoxification of these chemicals in H. zea.

Animals↗
PubMed1983

An innovative approach to sampling complex industrial emissions for use in animal toxicity tests: application to iron casting operations.

Sampling of complex mixtures of airborne contaminants for chronic animal toxicity tests often involves numerous sampling devices, requires extensive sampling time, and yields forms of collected materials unsuitable for administration to animals. A method is described which used a high volume, wet venturi scrubber for collection of respirable fractions of emissions from iron foundry casting operations. The construction and operation of the sampler are presented along with collection efficiency data and its application to the preparation of large quantities of samples to be administered to animals by intratracheal instillation.

Air Pollutants↗
PubMed1999

Polychlorinated biphenyls induce meiotic length mutations at the human minisatellite MS32 in yeast.

Polychlorinated biphenyls (PCBs) are lipophilic compounds, several of which are toxic and carcinogenic. Complex mixtures of PCBs (e.g., Aroclor) have been widely used in the industry. The persistence of PCBs, in combination with poor waste management, has led to a large-scale distribution of PCBs in the biosphere. The toxic and carcinogenic effects of PCBs are poorly understood, but are suggested to be associated with Ah receptor binding and induction of the Ah-gene battery. We have previously shown that a higher-chlorinated PCB mixture, Aroclor 1254, significantly increased the germline mutation rate at the mouse minisatellite PC-1. We have recently developed an in vitro model system to study and characterize spontaneous and induced meiotic mutations in human minisatellites integrated in yeast. Here, for the first time, we have used this model system to show that chemicals, in this case Aroclor 1254, can induce meiotic length mutations at the human minisatellite MS32 in a yeast strain harboring 38- and 42-repeat-unit alleles. The results also show that the size distribution of mutant MS32 alleles differs between PCB and the control, with a larger proportion of mutant allele sizes below 29 repeat units in the PCB series. These alleles were not structurally different from the alleles of the same size in the control. We conclude that PCBs induce minisatellite mutations in meiosis and have recombinogenic properties, and that the mutations are induced in an Ah receptor-independent manner. The induction of minisatellite mutations in meiosis as an indication of genomic damage must be taken into account in the risk assessment of PCBs and other environmental contaminants.

Alleles↗
PubMed1998

Lung tumorigenic interactions in strain A/J mice of five environmental polycyclic aromatic hydrocarbons.

The binary, ternary, quaternary, and quintary interactions of a five-component mixture of carcinogenic environmental polycyclic aromatic hydrocarbons (PAHs) using response surface analyses are described. Initially, lung tumor dose-response curves in strain A/J mice for each of the individual PAHs benzo[a]pyrene (B[a]P), benzo[b]fluoranthene (B[b]F), dibenz[a,h]anthracene (DBA), 5-methylchrysene (5MC), and cyclopenta[cd]pyrene (CPP) were obtained. From these data, doses were selected for the quintary mixture study based on toxicity, survival, range of response, and predicted tumor yields. The ratios of doses among PAHs were designed to simulate PAH ratios found in environmental air and combustion samples. Quintary mixtures of B[a]P, B[b]F, DBA, 5MC, and CPP were administered to male strain A/J mice in a 2(5) factorial 32-dose group dosing scheme (combinations of five PAHs each at either high or low doses) and lung adenomas were scored. Comparison of observed lung adenoma formation with that expected from additivity identified both greater than additive and less than additive interactions that were dose related i.e., greater than additive at lower doses and less than additive at higher doses. To identify specific interactions, a response surface analysis using response addition was applied to the tumor data. This response surface model contained five dose, ten binary, ten ternary, five quaternary, and one quintary parameter. This analysis produced statistically significant values of 16 parameters. The model and model parameters were evaluated by estimating the dose-response relationships for each of the five PAHs. The predicted dose-response curves for all five PAHs indicated a good estimation. The binary interaction functions were dominated for the most part by DBA and were inhibitory. The response surface model predicted, to a significant degree, the observed lung tumorigenic responses of the quintary mixtures. These data suggest that although interactions between PAHs do occur, they are limited in extent.

Adenoma↗
PubMed2006

Use of fish in vitro hepatocyte assays to detect multi-endpoint toxicity in Slovenian river sediments.

There is an increasing demand for rapid, sensitive and robust methods for toxicity testing of single chemicals, complex mixtures and environmental samples. The objective of this work was to validate and use a primary culture of rainbow trout (Oncorhynchus mykiss) hepatocytes as a multi-endpoint in vitro bioassay for toxicity characterisation of river sediments from four areas of the Sava and Krupa Rivers (Slovenia). The endpoints were chosen to encompass acute toxicity (cytotoxicity) as well as sub-lethal biomarker and effect endpoints such as metabolic inhibition, DNA damage (Fast Micromethod), endocrine disruption (estrogenicity), and 7-ethoxyresorufin O-deethylase (EROD) activity. Results from these studies show that the primary hepatocyte culture was able to successfully detect effects of single model chemicals in all endpoints analysed. Furthermore, the bioassays were also able to discriminate between contaminated and less contaminated sediments for a number of endpoints such as cytotoxicity, metabolic inhibition and induction of EROD activity, although no increase in DNA damage and estrogenicity was observed above background at any site. The present study shows that primary fish hepatocytes may be used to determine multiple mechanisms of toxic action and that a holistic assessment of effects may improve our understanding of cellular toxicity of complex mixtures such as sediments.

4-Nitroquinoline-1-oxide↗