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PubMed1987

Highly toxic coplanar PCBs: occurrence, source, persistency and toxic implications to wildlife and humans.

Isomer-specific determinations of PCB congeners in a wide variety of animal species such as fish, marine mammals (whale, dolphin and porpoise) and terrestrial mammals (dog, cat and human) revealed the environmental occurrence of highly toxic coplanar 3,3',4,4'-tetrachlorobiphenyl (T(4)CB), 3,3',4,4',5-pentachlorobiphenyl (P(5)CB) and 3,3',4,4',5,5'-hexachlorobiphenyl (H(6)CB) within a range of few pg g(-1) to several ten ng g(-1) in fat tissues (except fish) on a wet weight basis. Detection of these toxic residues in wild specimens collected from remote areas such as the North Pacific suggests the already widespread distribution of coplanar PCBs as in the case of general PCB pollution. The clear positive correlations between concentrations of total PCBs and each of the three coplanar PCBs obtained in all mammals analysed suggest that the sources of coplanar PCB contamination to the environment are mainly commercial PCB preparations. Comparison of the composition of three toxic coplanar PCBs in commercial PCB mixtures and in the various animals indicates the relative metabolisability of these congeners as follows: 3,3',4,4'-T4CB>3,3',4,4',5-P5CB>3,3',4,4',5,5'-H6CB. Moreover, marine mammals seem to have lower potency to metabolise the coplanar PCBs in comparison with terrestrial mammals. In human adipose tissues, the concentrations of coplanar PCBs were found to be much higher than 2,3,7,8-tetrachlorodibenzo-p-dioxin (T(4)CDD), 2,3,4,7,8-pentachlorodibenzofuran (P(5)CDF) and other toxic congeners. 'T(4)CDD-equivalent' analysis based on the enzyme induction potencies and the residues of these toxic chemicals indicates that 3,3',4,4',5-P(5)CB may impose a greater toxic threat than dioxins and furans to the humans and probably to wildlife also.

Journal Article↗

PubMed1989

An overview of maternal toxicity and prenatal development: considerations for developmental toxicity hazard assessments.

The objective of testing xenobiotics for potential developmental toxicity is to extrapolate laboratory animal information to the human species, thereby deriving biologically rational regulatory policies. One of the problems that significantly contributes to the difficulty of this task is the possibility that general effects on the maternal organism could affect the developing conceptus. Published data have indicated that factors intrinsic to the maternal organism affect developmental outcome. This overview examines factors which may bear directly or indirectly upon developmental outcome, with emphasis on those of greatest relevance to the hazard assessment process. Standard teratology testing protocols often call for dose levels that induce overt maternal toxicity, and the developmental effects of this toxicity (both alone, and with concurrent embryo/fetal insult) continue to present regulators with considerable interpretive difficulties. In response to these problems there have been both research and literature review efforts dealing with the relationship of maternal and developmental toxicity. Relevant studies are reviewed here, and suggestions for avenues of future research are offered including the identification of any syndromes of developmental effects occurring at maternally toxic levels irrespective of the causative agent, and experimental approaches for the characterization of maternal toxicity.

Animals↗

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↗

PubMed2004

Using multiple metal-gill binding models and the toxic unit concept to help reconcile multiple-metal toxicity results.

Metal-gill binding models and biotic ligand models (BLMs) in general are designed to predict metal toxicity to aquatic organisms. These models calculate the amount of a metal-binding to a sensitive biological membrane, such as a fish gill, which equates with metal toxicity. Cation competition at the metal-binding site and anionic complexation in the water decrease metal-binding to the membrane, decreasing metal toxicity. These models have, to date, been developed for individual metals. To assess how these models handle multiple-metal interactions, metal-gill binding models for two to six metals were created and their behavior tested against the toxic unit (TU) concept assuming strict additivity. The multiple-metal models yield greater than strict additivity at low aqueous metal concentrations (Sigma < 1 TU), strict additivity at intermediate metal concentrations (Sigma = 1 TU), and less than strict additivity at high metal concentrations (Sigma > 1 TU), independent of the combination of metals. Deviations from strict additivity are due to the non-linear nature of the models, where greater than linear filling of binding sites occurs at low metal concentrations, and where strong competition for binding sites occurs at high metal concentrations, with a point of strict additivity between, where the metals sum to one toxic unit. Simulations with natural organic matter (NOM) show similar trends but are complex. Mathematical modeling of multiple-metal interactions may help in the interpretation of toxicity results from mixed-metal exposures to aquatic organisms.

Animals↗

PubMed2005

Statistical evaluation of chronic toxicity data on aquatic organisms for the hazard identification: the chemicals toxicity distribution approach.

Presently, in the Globally Harmonised System of Classification and Labelling of Chemicals the classification of substances for long-term effects to aquatic life is based on acute toxicity in combination with degradation and/or bioaccumulation potential. Recently an OECD Working Group was created to develop the classification scheme to accommodate chronic toxicity data related to aquatic organisms for assigning a chronic hazard category. This study focuses on a new approach for setting chronic toxicity cut-off values based on Chemicals Toxicity Distributions (CTDs). A CTD is obtained through statistical fitting of the data used by regulatory bodies for setting hazard-based classifications. The CTDs were made using the lowest aquatic NOEC value of each chemical. A review of different toxicological sources reporting acute aquatic toxicities was carried out. Initially, the data were arranged according to the specific source and distributions for key taxonomic groups (i.e. fishes, crustaceans and algae) were evaluated separately. In most cases, no significant departures from normality were observed. Thereafter, a compiled database containing >900 values was developed and the CTDs were constructed for each taxonomic group. Significant deviation from normality (P < 0.05) was observed in the fishes and crustaceans' CTDs. However, this deviation was apparently produced by the presence of only seven values with NOECs <1 x 10(-5) mg l(-1), while high correlation between the data and the normal scores (r-values>or= 0.989) indicated that the data were samples from normal distributions. From these observations, potential cut-off values would allow quantitative estimations of the percentage of chemicals falling into each specific category. This approach results in a simple classification hazard scheme where most chemicals are covered in one of the categories, allowing a clear distribution of the chemicals among three categories for chronic toxicity.

Animals↗

PubMed2006

Relative toxicity of dinophysistoxin-2 (DTX-2) compared with okadaic acid, based on acute intraperitoneal toxicity in mice.

When substituting the mouse bioassay for lipophilic marine algal toxins in shellfish with analytical methods, science based factors of relative toxicity for all analogues that contribute to health risk to consumers are necessary. The aim of this paper is to establish the relative intraperitoneal toxicity of dinophysistoxin-2 (DTX-2) compared with okadaic acid (OA). The study was performed as an open, randomised parallel group trial with a four level response surface design within each of the two parallels. In accordance with the response surface design model, the LD50 for DTX-2 and OA was 338 and 206 microg/kg, respectively. By use of common regression analysis, the LD50 of DTX-2 and OA were estimated to 352 microg/kg and 204 microg/kg, respectively. The deviations between the LD50 estimates by the two methods was 4% for DTX-2 and less than 1% for OA. Taken together, these results indicate that the relative toxicity of DTX-2 is about 0.6, compared to OA. Results from the PP2A assay correspond very well with the results obtained by the mouse bioassay. The IC50 concentrations for DTX-2 and OA were 5.94 and 2.81 ng/mL, respectively. This indicates that OA is about twice as toxic as DTX-2. Since inhibition of PP2A is acknowledged as the main mechanism of toxicity of the OA group toxins, this supports the establishment of a relative toxicity factor of DTX-2 of 0.6 compared with OA.

Animals↗

PubMed2000

Comparative culture and toxicity studies between the toxic dinoflagellate Pfiesteria piscicida and a morphologically similar cryptoperidiniopsoid dinoflagellate.

A series of fish bioassays using cultures of the toxic dinoflagellate, Pfiesteria piscicida and a cryptoperidiniopsoid dinoflagellate indicated various degrees of toxicity for Pfiesteria piscicida and no toxicity by the cryptoperidiniopsoid. P. piscicida maintained toxicity in the presence of live fish, and this toxicity was perpetuated following a series of inoculations to other culture vessels. Differences in the onset and magnitude of the fish deaths occurred, requiring 16 days for the initial fish death when using P. piscicida from a culture that had previously been maintained on algal cells, to kills within hours when using a culture that had recently (previous day) killed fish. Autopsies of moribund fish from the test and control fish bioassays indicated a general lack of bacterial infection, which ensued following death of other autopsied fish. Moreover, bacterial comparisons of waters in the fish bioassay and control fish cultures indicated that similar bacterial concentrations were present. Neither oxygen or ammonia levels were determined to be factors in the fish death. Life stages of a cryptoperidiniopsoid dinoflagellate from Virginia estuaries were also identified, including motile zoospore, gametes, planozygote, amoebae, and cyst stages. The cryptoperidiniopsioid did not initiate fish deaths in bioassays conducted over a 14-week period at zoospore concentrations of ca. 700-800 cells ml(-1). Elemental X-ray analysis of the scales from cysts of this dinoflagellate and P. piscicida indicate that they both contain silicon. Overall, the data from this study demonstrate that the cryptoperidiniopsoid possesses several similar life stages and feeding patterns as P. piscicida, but was not toxic to fish.

Journal Article↗

PubMed2001

Effects of toxic and non-toxic cyanobacteria on grazing, zooplanktivory and survival of the mysid shrimp Mysis mixta.

We measured the effect of toxic and non-toxic cyanobacteria strains on grazing, predation rates and survival of the mysid shrimp Mysis mixta by means of laboratory experiments. Juvenile and adult M. mixta fed most actively on the non-toxic strains Aphanizomenon flos-aquae and Nodularia sphaerocarpa as on high quality food, the green flagellate Brachiomonas submarina, whereas grazing on the toxic N. spumigena was significantly lower than on the other strains. The mysids showed normal functional responses; decreasing clearance rates at increasing concentrations of cyanobacteria. In a separate predation experiment, the feeding rates on copepods declined in the presence of aggregated non-toxic cyanobacteria. However, we could not demonstrate increased mortality in a 7-week experiment where mysids were exposed to high concentrations of toxic N. spumigena

Journal Article↗

PubMed2001

Analysis of air toxics emission inventory: inhalation toxicity-based ranking.

Air toxics emission inventories play an important role in air quality regulatory activities. Recently, Minnesota Pollution Control Agency (MPCA) staff compiled a comprehensive air toxics emission inventory for 1996. While acquiring data on the mass of emissions is a necessary first step, equally important is developing information on the potential toxicity of the emitted pollutants. To account for the toxicity of the pollutants in the emission inventory, inhalation health benchmarks for acute effects, chronic effects, and cancer were used to weight the mass of emissions. The 1996 Minnesota emissions inventory results were ranked by mass of emissions and by an index comprised of emissions divided by health benchmarks. The results show that six of eight pollutants ranked highest by toxicity were also the pollutants of concern indicated in environmental monitoring data and modeling data. Monitoring data and modeling results did not show high impacts of the other two pollutants that were identified by the toxicity-based emission ranking method. The biggest limitation in this method is the lack of health benchmark values for many pollutants. Despite uncertainties and limited information, this analysis provides useful information for further targeting pollutants and source categories for control.

Air Pollutants↗

PubMed1985

Acute toxicity, subchronic dermal toxicity, and delayed contact sensitization evaluations of dicyclopentenyloxyethyl methacrylate in rabbits and guinea pigs.

The subchronic dermal toxicity of dicyclopentenyloxethyl methacrylate (DPOMA) was evaluated in young adult New Zealand White rabbits, and its potential to produce delayed contact sensitization was evaluated in Harley guinea pigs by a modified Buehler's closed patch technique. In addition, studies were conducted to evaluate the acute systemic toxicity of DPOMA in rats (oral) and rabbits (dermal), and its eye and skin irritancy in rabbits. In the subchronic dermal toxicity study, 4 groups of rabbits were treated percutaneously with DPOMA at 0 (acetone), 10, 107, and 1067 (undiluted) mg/kg X day in a volume of 1 ml/kg, over a 4-wk period. The application sites were unoccluded. No deaths occurred, and no signs of systemic toxicity were observed. No treatment-related effects were seen on body weights, hematology, clinical chemistry, urinalysis, organ weights, or histopathology (except the treated skin). The only treatment-related effect was slight to moderate skin irritation in the mid- and high-dose groups. The severity of skin irritaton was dependent on the number of applications and the concentration of DPOMA. Maximal skin irritation occurred after 1 wk. No skin irritation was seen in the control and low-dose group. In the DCS study, guinea pigs received 6 induction doses of 0.5 ml 100% DPOMA and were challenged with 0.5 ml of 50% (w/v) DPOMA in acetone 2 wk after the last induction treatment. No erythema or edema was observed in any of the challenged guinea pigs in either the treated and control groups. These acute toxicity studies indicate that DPOMA is practically nontoxic by a single exposure via both oral and dermal routes (the oral LD50 in rat and dermal LD50 in rabbits were greater than 5.0 g/kg body weight), slightly irritating to the skin, and inconsequentially irritating to the eyes. The no-observed-effect level (NOEL) for systemic toxicity of DPOMA applied repeatedly to rabbits skin is at least 1067 mg/kg X d. DPOMA is not a strong or moderate skin sensitizer in guinea pigs.

Acrylates↗

PubMed1986

Toxicity of ozone and nitrogen dioxide to alveolar macrophages: comparative study revealing differences in their mechanism of toxic action.

The toxicity of ozone and nitrogen dioxide is generally ascribed to their oxidative potential. In this study their toxic mechanism of action was compared using an intact cell model. Rat alveolar macrophages were exposed by means of gas diffusion through a Teflon film. In this in vitro system, ozone appeared to be 10 times more toxic than nitrogen dioxide. alpha-Tocopherol protected equally well against ozone and nitrogen dioxide. It was demonstrated that alpha-tocopherol provided its protection by its action as a radical scavenger and not by its stabilizing structural membrane effect, as (1) concentrations of alpha-tocopherol that already provided optimal protection against ozone and nitrogen dioxide did not influence the membrane fluidity of alveolar macrophages and (2) neither one of the structural alpha-tocopherol analogs tested (phytol and the methyl ether of alpha-tocopherol) could provide a protection against ozone or nitrogen dioxide comparable to the one provided by alpha-tocopherol. It was concluded that reactive intermediates scavenged by alpha-tocopherol are important in the toxic mechanism of both ozone and nitrogen dioxide induced cell damage. However, further results presented strongly confirmed that the kind of radicals and/or reactive intermediates, and thus the toxic reaction mechanism involved, must be different in ozone- and nitrogen dioxide-induced cell damage. This was concluded from the observations that showed that (1) vitamin C provided significantly better protection against nitrogen dioxide than against an equally toxic dose of ozone, (2) glutathione depletion affected the cellular sensitivity toward ozone to a significantly greater extent than the sensitivity towards nitrogen dioxide, and (3) the scavenging action of alpha-tocopherol was accompanied by a significantly greater reduction in its cellular level during nitrogen dioxide exposure than during exposure to ozone. One of the possibilities compatible with the results presented in this study might be that lipid (peroxyl) free radicals formed in a radical-mediated peroxidative pathway, resulting in a substantial breakdown of cellular alpha-tocopherol, are involved in nitrogen dioxide-induced cell damage, and that lipid ozonides, scavenged by alpha-tocopherol as well, are involved in ozone-induced cell damage.

Animals↗

PubMed1996

Toxic and non-toxic strains of the cyanobacterium Microcystis aeruginosa contain sequences homologous to peptide synthetase genes.

Toxic strains of Microcystis aeruginosa produce cyclic heptatoxins (microcystins) that are believed to be synthesized non-ribosomally by peptide synthetases. We analysed toxin-producing and non-toxic strains of M. aeruginosa with respect to the presence of DNA sequences potentially encoding peptide synthetases. Hybridizations of genomic DNA of various M. aeruginosa strains with PCR-amplificated fragments possessing homologies to adenylate-forming domains of peptide synthetase genes provided first evidence for the existence of corresponding genes in cyanobacteria. Furthermore we isolated and sequenced from genomic libraries overlapping fragments of M. aeruginosa DNA with a total length of 2982 bp showing significant homology to genes encoding peptide synthetases and hybridizing exclusively with DNA from toxic strains. Our results indicate that both toxic and non-toxic strains of M. aeruginosa possess genes coding for peptide synthetases and that hepatotoxin-producing and non-toxic strains differ in their content of genes for specific peptide synthetases.

Amino Acid Sequence↗

PubMed1984

Presence of toxic shock toxin in toxic shock and other clinical strains of Staphylococcus aureus.

Toxic shock toxin (TST), also known as pyrogenic exotoxin C (Schlievert et al., J. Infect. Dis. 143:509-516, 1981) and staphylococcal enterotoxin F (Bergdoll et al., Lancet i:1017-1021, 1981), was purified from toxic shock strains of Staphylococcus aureus by preparative isoelectric focusing and by chromatofocusing. Neither method produced an absolutely pure protein as determined by silver staining of sodium dodecyl sulfate-acrylamide gels, although chromatofocusing was the better method of the two. Three molecular weight variants of the protein were found in the two toxic shock syndrome strains that were studied, regardless of the purification method that was used. An isoelectric point of 7.15 and molecular weights of 21,400, 22,100, and 23,200 were determined for the different forms of the protein from electrophoresis data. A sedimentation coefficient of 2.3S was determined by sucrose gradient centrifugation, and a Stokes radius of 2 X 10(-7) cm was determined by gel filtration. An average molecular weight of 18,900 for all of the TST forms was calculated from these data by the Stokes-Einstein equation. A survey for TST in 32 control and 46 toxic shock strains of S. aureus by isoelectric focusing and by agarose gel double immunodiffusion with specific rabbit antiserum revealed that the isoelectric focusing method tends to overestimate the number of TST-positive strains because of the detection of non-TST, neutral staphylococcal proteins. Based on immunodiffusion data, the association of TST with toxic shock strains was found to be 100% in vaginal isolates and 62% in non-vaginal isolates. In the control strains, TST was found in 16% of the vaginal strains and 23% of the non-vaginal strains. The value of this toxin as a marker for toxic shock and its relationship to the pathogenesis of this disease are discussed.

Bacterial Toxins↗

PubMedDate not supplied

Influence of previous gold toxicity on subsequent development of penicillamine toxicity.

The incidence of penicillamine toxicity was determined in 250 patients who had never previously received gold, 76 patients who had received gold without toxic reaction, and 79 patients with a previous history of gold toxicity. The results suggest that there may be a higher incidence of penicillamine toxicity in patients who have previously shown toxic reactions. The interval between stopping the gold and starting the penicillamine did not influence incidence of toxicity. The development of a rash during gold treatment does not seem to influence the development of a rash during penicillamine treatment, but patients who have had proteinuria or bone-marrow depression during gold treatment may have an increased likelihood of developing a similar side effect with penicillamine.

Arthritis, Rheumatoid↗

PubMedDate not supplied

Acute verapamil toxicity in a patient with chronic toxicity: possible interaction with ceftriaxone and clindamycin.

OBJECTIVE: To report a case of acute toxicity in a patient with chronic verapamil toxicity, possibly precipitated by intravenous administration of the highly protein-bound drugs ceftriaxone and clindamycin. DATA SOURCES: Case reports, review articles, and relevant laboratory and clinical studies identified by MEDLINE (1984-forward), and relevant cross references from those articles. DATA EXTRACTION: Data were abstracted from pertinent sources by one author and reviewed by the remaining authors. CASE SUMMARY: A 59-year-old man who had been receiving sustained-release verapamil 240 mg q12h for more than two years for hypertension, and phenytoin 300 mg/d for many years for prophylaxis against seizures, was noted to be in junctional rhythm when he presented to the emergency room with bilateral pneumonia. Administration of intravenous ceftriaxone 1 g and clindamycin 900 mg precipitated symptoms of acute verapamil toxicity in this patient. The toxicity led to complete heart block requiring cardiopulmonary resuscitation and insertion of a temporary pacemaker. He spontaneously reverted to normal sinus rhythm after 16 hours. Subsequent cardiac evaluation, including echocardiogram, 48-hour dynamic electrocardiographic recording (Holter), and exercise stress test were normal. The patient has remained in sinus rhythm for more than one year after this episode. CONCLUSIONS: We believe that junctional rhythm on admission was a result of chronic verapamil toxicity. This may have been because of increased bioavailability of the drug or increased sensitivity of the receptors. Administration of ceftriaxone, clindamycin, or both agents might have precipitated acute verapamil toxicity by displacing verapamil from its protein-binding sites. Extreme caution is necessary when a highly protein-bound drug is given to a patient already receiving verapamil.

Blood Proteins↗

PubMed1998

A monoclonal antibody directed against the non-toxic subunit of a dimeric phospholipase A2 neurotoxin, crotoxin, neutralizes its toxicity.

Crotoxin is the main toxic component of the venom of the South-American rattlesnake Crotalus durissus terrificus. It is a phospholipase A2 neurotoxin constituted by the association of two subunits: an acidic, non-toxic and non-enzymatic subunit (CA) and a basic, weakly toxic phospholipase A2 (CB). A murine monoclonal antibody directed to the non-toxic subunit CA, A-56.36, was shown to fully neutralize the toxicity of crotoxin. When the in vitro pharmacological properties of crotoxin were further tested, A-56.36 was shown to enhance the enzymatic activity on negatively-charged phospholipids and to increase the acetylcholine release triggered by crotoxin on Torpedo synaptosomes. These effects were explained by the fast dissociation of the crotoxin complex in the presence of the monoclonal antibody A-56.36 and the immunocomplexation of CA, with CB being released in solution. CB is less toxic than crotoxin, has a higher enzymatic activity and triggers a higher acetylcholine release than crotoxin, due to its strong enzymatic activity. A single-chain variable fragment antibody was prepared from monoclonal antibody A-56.36. It binds to CA with a similar affinity than the parental immunoglobulin and exhibits similar effects on the in vitro pharmacological properties of crotoxin.

Amino Acid Sequence↗

PubMedDate not supplied

Power equation for all-or-none effects of oxygen toxicity and cumulative oxygen toxicity.

Quantification of the level of O2 toxicity may provide a means of setting limits on various hyperoxic exposures. A previously suggested expression for quantitative oxygen toxicity, DMG = a x t2 x PO2c (t-time, DMG-measured level of O2 toxicity), has been adapted for the all-or-none phenomenon: K = t2 x PO2c. A symptom may appear when K reaches a threshold value Kc. Non-linear regression was successfully applied to all-or-none symptoms from the literature: survival, convulsions, substernal distress, reduction in short circuit current and nerve conduction blockade. The generality of these expressions enabled calculation of cumulative oxygen toxicity and a search for the mechanism of oxygen toxicity. Cumulative oxygen toxicity is calculated in three-step calculation loops in three suggested exposure profiles. For a possible recovery period between exposures the expressions took the form: DMGt = DMGc x e-rt, and Kt = Kc x e-rt, where r is the recovery constant. A possibly bimodal distribution of c close to the values of 1 and 4 could be attributed to systemic effects.

Animals↗

PubMed2004

Use of powdered coconut charcoal as a toxicity identification and evaluation manipulation for organic toxicants in marine sediments.

We report on a procedure using powdered coconut charcoal to sequester organic contaminants and reduce toxicity in sediments as part of a series of toxicity identification and evaluation (TIE) methods. Powdered coconut charcoal (PCC) was effective in reducing the toxicity of endosulfan-spiked sediments by 100%. Powdered coconut charcoal also was effective in removing almost 100% of the toxicity from two field sediments contaminated with polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs). Powdered coconut charcoal did not change the toxicity of ammonia or metal-spiked sediments; however, there was some quantitative reduction in the concentrations of free metals (element specific) in metal-spiked sediments. Powdered coconut charcoal is an effective, relatively specific method to sequester and remove toxicity from sediments contaminated with organic contaminants.

Adsorption↗