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At least 73 records · Page 4Linked to original sources
PubMed2003

The influence of time on lead toxicity and bioaccumulation determined by the OECD earthworm toxicity test.

Internationally agreed standard protocols for assessing chemical toxicity of contaminants in soil to worms assume that the test soil does not need to equilibrate with the chemical to be tested prior to the addition of the test organisms and that the chemical will exert any toxic effect upon the test organism within 28 days. Three experiments were carried out to investigate these assumptions. The first experiment was a standard toxicity test where lead nitrate was added to a soil in solution to give a range of concentrations. The mortality of the worms and the concentration of lead in the survivors were determined. The LC50s for 14 and 28 days were 5311 and 5395 microgPb g(-1)soil respectively. The second experiment was a timed lead accumulation study with worms cultivated in soil containing either 3000 or 5000 microgPb g(-1)soil. The concentration of lead in the worms was determined at various sampling times. Uptake at both concentrations was linear with time. Worms in the 5000 microg g(-1) soil accumulated lead at a faster rate (3.16 microg Pb g(-1)tissue day(-1)) than those in the 3000 microg g(-1) soil (2.21 microg Pb g(-1)tissue day(-1)). The third experiment was a timed experiment with worms cultivated in soil containing 7000 microgPb g(-1)soil. Soil and lead nitrate solution were mixed and stored at 20 degrees C. Worms were added at various times over a 35-day period. The time to death increased from 23 h, when worms were added directly after the lead was added to the soil, to 67 h when worms were added after the soil had equilibrated with the lead for 35 days. In artificially Pb-amended soils the worms accumulate Pb over the duration of their exposure to the Pb. Thus time limited toxicity tests may be terminated before worm body load has reached a toxic level. This could result in under-estimates of the toxicity of Pb to worms. As the equilibration time of artificially amended Pb-bearing soils increases the bioavailability of Pb decreases. Thus addition of worms shortly after addition of Pb to soils may result in the over-estimate of Pb toxicity to worms. The current OECD acute worm toxicity test fails to take these two phenomena into account thereby reducing the environmental relevance of the contaminant toxicities it is used to calculate.

Animals↗
PubMed1996

Situational smoke toxicity testing: hazard assessment as the 'front end' of a smoke toxicity test.

Traditionally, the toxic potency of the smoke from a material or product is part of the assessment of the fire hazard in a given scenario. The assessment also requires a knowledge of virtually all the details of the fire environment and, until they are identified, a 'safe' or 'acceptable' level of smoke toxicity is a term without meaning. This paper suggests a method of using the knowledge of these factors to simplify smoke toxicity testing. Faster, cheaper, and better-targeted smoke toxicity tests would result if the rest of the hazard assessment were carried out first. This is accomplished by determining or specifying all the relevant fire properties except the toxic potency, identifying the other environmental conditions (such as those typical of an aircraft cabin interior) and the desired tenability limits (such as the minimum necessary escape time), and then solving the equations for the buildup of toxic conditions in terms of the single remaining unknown, the toxic potency. The result is the greatest toxic potency which would meet the requirements of the analysis. In this approach, a material or product is acceptable if its smoke is no more toxic then the computed result and unacceptable if it is not. It would not be necessary to obtain an EC50 (product concentration which will cause an effect in half the animals) or dose-response profile, only the response at whatever dose is dictated by the analysis. Two sample cases are presented to illustrate the technique.

Administration, Inhalation↗
PubMedDate not supplied

Development of a high throughput in vitro toxicity screen predictive of high acute in vivo toxic potential.

At an early stage of drug discovery high throughput screens are an invaluable tool to de-select compounds with undesirable properties. A high throughout in vitro toxicity screen has been developed and validated to identify compounds that have a high potential to be acutely toxic in vivo. This screen is based on treating Chinese hamster ovary (CHO) cells with test compounds for 24 h and then determining the degree of cytotoxicity by the reduction of Resazurin. Twenty-six structurally unrelated compounds were chosen that spanned a range of acute LD(50) values and mechanisms of toxicity. The acute LD(50) values (intraperitoneal and intravenous routes) from rat and mouse were taken from the RTECS database. Experimentally derived in vitro IC(35) results were compared to the 'most toxic' (lowest) LD(50) values for each compound. The resulting correlation was statistically significant (r=0.8475). However, due to the scatter of the data points, it was considered not appropriate to rank compounds according to their degree of in vivo toxicity on the basis of the in vitro result. However, by defining cut-off concentrations for both the in vivo (LD(50)) and the in vitro (IC(35)) values it was possible, using the in vitro result (IC(35) <10 microM), to identify compounds that had a high potential to be acutely toxic in vivo ('most toxic' LD(50) <25 micromol/kg). Further development led to a high throughput screen capable of giving a 'Yes', 'No' or 'Borderline' classification as to whether a compound has a high acute in vivo toxic potential. This screen is highly specific (no false positive classifications) and has a sensitivity of approximately 80%. This is deemed acceptable for a first tier toxicity screen at an early stage in the drug discovery process. Transfer of this screen from GlaxoSmithKline UK to sites in Italy, Spain and the USA resulted in very similar findings indicating the inter-laboratory robustness of this screen and therefore the ability to compare results across the GlaxoSmithKline sites.

Animal Testing Alternatives↗
PubMed2000

Toxicity of various amyloid beta peptide species in cultured human blood-brain barrier endothelial cells: increased toxicity of dutch-type mutant.

The amyloid beta peptide (A beta) is the major component of the neuritic and cerebrovascular amyloid plaques that are one of the characteristic features of Alzheimer's disease (AD). This peptide has been shown to be toxic to several relevant cell types, including neurons, cerebrovascular smooth muscle cells, and endothelial cells. We have studied the toxic effects of both soluble and aggregated species of A beta(1-40) and the mutation A beta(1-40)Glu-->Gln(22), which is the major species deposited in the cerebrovascular blood vessels of victims of hereditary cerebral hemorrhage with amyloidosis, Dutch type. We find that aggregates of both peptides, as well as of A beta(1-42) and A beta(25-35), are toxic to cultured human cerebrovascular endothelial cells (hBEC) obtained from the brain of a victim of AD (at doses lower than those that are toxic to CNS neurons or leptomeningeal smooth muscle cells). Soluble A beta(1-40) Gln(22) is equally toxic to hBEC, whereas wild-type A beta(1-40) is toxic only at higher doses. This toxicity is seen at the lowest dose of A beta(1-40) Gln (22) used, 20 nM. The soluble A beta(1-40)Gln(22) aggregates on the surface of the cells, in contrast to A beta(1-40), and its toxicity can be blocked both by an inhibitor of free radical formation and by Congo red, which inhibits amyloid fibril formation. We discuss the possibility that the enhanced toxicity of A beta(1-40)Gln(22) is mediated by a A beta receptor on the endothelial cells.

Amyloid beta-Peptides↗
PubMed1992

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

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

Animals↗
PubMed2006

Cell culture models for the investigation of NRTI-induced mitochondrial toxicity. Relevance for the prediction of clinical toxicity.

The introduction of highly active antiretroviral therapy (HAART) for treatment of human immunodeficiency virus (HIV) infection has led to substantial reduction in morbidity and near-complete suppression of HIV-1 replication. But since HAART is unlikely to eradicate HIV-1, antiviral therapy may be required a lifelong, leading to an increase in attention on the long-term safety of HAART. A major toxicity of HAART is the mitochondrial toxicity. Mitochondrial toxicity becomes apparent particularly over the medium-term to long-term therapy and is attributed to treatment with nucleoside reverse transcriptase inhibitors (NRTIs), leading to a wide range of severe adverse events in HIV-infected patients. These include lactic acidosis, hepatic steatosis, neuropathy, (cardio-) myopathy, pancreatitis, and probably lipodystrophy. Furthermore, lactic acidosis and encephalopathy have been reported in children exposed in-utero and/or postnatally to NRTIs. Mitochondrial toxicity could pose a major threat to long-term success of HIV-therapy, and is of great concern for children exposed in-utero and/or postnatally to NRTIs. Therefore, investigation of mitochondrial toxicity of new compounds or new combinations is of growing interest for the clinical application of antiretroviral agents. However, at present no standardized and validated screening model system exists for the investigation of NRTI-induced mitochondrial toxicity. There is a need for the generation of a relevant in vitro assay system that can assess the mitochondrial toxicity in early preclinical development. This paper gives an overview of cell culture models currently used for the investigation of NRTI-induced mitochondrial toxicity and discusses the relevance and suitability of these models for prediction of clinical toxicity.

Animals↗
PubMed2003

Catechol-O-methyltransferase inhibition protects against 3,4-dihydroxyphenylalanine (DOPA) toxicity in primary mesencephalic cultures: new insights into levodopa toxicity.

Inhibition of catechol-O-methyltransferase (COMT) has protective effects on levodopa (L-DOPA), but not D-DOPA toxicity towards dopamine (DA) neurons in rat primary mesencephalic cultures [Mol. Pharmacol. 57 (2000) 589]. Here, we extend our recent studies to elucidate the mechanisms of these protective effects. Thus, we investigated the effects of all main L-DOPA/DA metabolites on survival of tyrosine hydroxylase immunoreactive (THir) neurons in primary rat mesencephalic cultures. 3-O-Methyldopa, homovanillic acid, dihydroxyphenyl acetate and 3-methoxytyramine had no effects at concentrations up to 300 micro M after 24h, whereas DA was more toxic than L-DOPA with toxicity at concentrations of >or=1 micro M. The coenzyme of COMT, S-adenosyl-L-methionine (SAM), and its demethylated product S-adenosylhomocystein caused no relevant alteration of THir neuron survival or L-DOPA toxicity. In contrast, inhibition of SAM synthesis by selenomethionine showed time- and dose-dependent increase of THir neuron survival, but did not affect L-DOPA toxicity. L-DOPA-induced lipid peroxidation in mesencephalic cultures was not modified by the COMT inhibitor Ro 41-0960 (1 micro M). Increased contamination of the cultures with glial cells attenuated L- and D-DOPA toxicity, but caused significant enhancement of protection by COMT inhibitors against L-DOPA toxicity only. Investigations of L-DOPA uptake in rat striatal cultures using HPLC revealed a significant reduction of extracellular L-DOPA concentrations by Ro 41-0960. Our data confirm that L-DOPA toxicity towards DA neurons is mediated by an autooxidative process, which is attenuated by glial cells. In addition, we demonstrate a second mechanism of L-DOPA toxicity in vitro mediated by a COMT- and glia-dependent pathway, which is blocked by COMT inhibitors, most likely due to enhanced glial uptake of L-DOPA.

Animals↗
PubMed1994

Toxicity grading systems. A comparison between the WHO scoring system and the Common Toxicity Criteria when used for nausea and vomiting.

BACKGROUND: The Common Toxicity Criteria adopted by the NCI in the USA for grading toxicity in cancer clinical trials have been compared to the WHO scoring system which is still in use in Europe. PATIENTS & METHODS: Sixty-six patients undergoing emetic chemotherapy at the Netherlands Cancer Institute completed questionnaires, 32 according to the WHO criteria and 34 to the Common Toxicity Criteria, on the severity, frequency and duration of gastro-intestinal toxicity. Their answers were then compared to the scores coded by research nurses and physicians. The nurses coded acute toxicity when the patients were discharged, and the doctors coded overall toxicity when the patients returned for the subsequent course of chemotherapy. To evaluate the coding systems, an estimate was made of the percentage agreement between the patients' answers and the nurses' and doctors' ratings. RESULTS: The percentage agreement of the Common Toxicity Criteria with the patients' own experiences of nausea and vomiting was considerably better than that of the WHO score. The Gamma statistic confirmed this. The Common Toxicity Criteria have now been adopted for grading toxicity in studies of the Early Clinical Trials Group of the EORTC and are recommended for use in other clinical trials.

Adult↗
PubMed2005

Ecological implications of the emergence of non-toxic subcultures from toxic Microcystis strains.

Two toxic, microcystin-producing, Microcystis sp. strains KLL MG-K and KLL MB-K were isolated as single colonies on agar plates from Lake Kinneret, Israel. Two non-toxic subcultures, MG-J and MB-J spontaneously succeeded the toxic ones under laboratory conditions. Southern analyses showed that MG-J and MB-J are lacking at least 34 kb of the mcy region, encoding the microcystin synthetase. Analyses of the 16S rRNA genes, the intergenic spacer region between cpcB and cpcA and the patterns of the polymerase chain reaction products of randomly amplified polymorphic DNA and highly iterated palindrome, and presence of mobile DNA elements did not allow unequivocal distinction between toxic and non-toxic subcultures. Laboratory and field experiments indicated an advantage of the toxic strain over its non-toxic successor. When grown separated by a membrane, which allowed passage of the media but not the cells, MG-K severely inhibited the growth of MG-J. Furthermore, when MG strains were placed in dialysis bags in Lake Kinneret during the season in which Microcystis is often observed, cells of MG-J lysed, whereas MG-K survived. Mechanisms whereby the non-toxic subcultures emerged and prevailed over the corresponding toxic ones under laboratory conditions, as well as a possible role of microcystin under natural conditions, are discussed.

Bacterial Toxins↗
PubMed2006

Photoinduced toxicity of polycyclic aromatic hydrocarbons to Daphnia magna: ultraviolet-mediated effects and the toxicity of polycyclic aromatic hydrocarbon photoproducts.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants known for their photoinduced toxicity. This toxicity may occur through two mechanisms: Photosensitization, and photomodification. Photosensitization generally leads to the production of singlet oxygen, a reactive oxygen species that is highly damaging to biological molecules. Photomodification of PAHs, usually via oxidation, results in the formation of new compounds and can occur under environmentally relevant levels of actinic radiation. The toxicities of 16 intact PAHs to Daphnia magna were assessed under two ultraviolet radiation conditions. The toxicity of intact PAHs generally increased in the presence of full-spectrum simulated solar radiation relative to that in the presence of visible light plus ultraviolet A only. Despite the knowledge of a bipartite mechanism of phototoxicity that includes photosensitization and photomodification, few studies have examined the effects of PAH photoproducts on animals. To expand the existing data, 14 PAH photoproducts (oxy-PAHs) also were assayed, most of which were highly toxic without further photomodification. Two photoproducts of benzo[a]pyrene, 1,6- and 3,6-benzo[a]pyrenequinone, were the most toxic compounds tested, followed closely by benz[a]anthraquinone. Each of these three compounds had a median effective concentration in the low nanomolar range. The data presented highlight the effects of ultraviolet radiation on mediating PAH toxicity and the need to analyze absorption spectra of contaminants in the prediction of photoinduced toxicity. The importance of the role of photomodification also is stressed, because several oxy-PAHs, an unregulated group of contaminants, were highly toxic to D. magna, a key bioindicator species in aquatic ecosystems.

Animals↗
PubMed2001

A multi-channel continuous toxicity monitoring system using recombinant bioluminescent bacteria for classification of toxicity.

A multi-channel system for continuous toxicity monitoring and classification of toxicity was developed based upon a previously developed two-stage minibioreactor system. The multi-channel system consists of a series of a two-stage minibioreactor systems connected by a fiber optic probe to a luminometer. Each channel was used for cultivating different recombinant bacterial strains, such as TV1061 (grpE::luxCDABE), DPD2794 (recA::luxCDABE), and DPD2540 (fabA::luxCDABE), which are induced by protein-, DNA-, and cell membrane damaging-agents, respectively. GC2 (lac::luxCDABE) is a bacterium expressing bioluminescence constitutively, which shows a reduction in its light level as cellular toxicity increases. Artificial wastewater samples were made by combining toxic chemicals, including Mitomycin C (a representative DNA damaging agent), phenol (a representative protein damaging agent), and cerulenin (a representative cell membrane damaging agent), and injecting this sample into each channel in order to simulate the detection of toxicity for mixed chemical samples. Each channel showed a specific bioluminescent response due to the toxic chemicals contained in the sample wastewater, while GC2 showed a general response to cellular toxicity. By using this multi-channel continuous toxicity monitoring system, classification of toxicity in field samples was found to be possible.

Bioreactors↗
PubMed2006

Acute toxicity of leachates of tire wear material to Daphnia magna--variability and toxic components.

Large amounts of tire rubber are deposited along the roads due to tread wear. Several compounds may leach from the rubber and cause toxicity to aquatic organisms. To investigate the toxic effects of tire wear material from different tires, rubber was abraded from the treads of twenty-five tires. Leachates were prepared by allowing the rubber to equilibrate with dilution water at 44 degrees C for 72 h. Then the rubber was filtered from the leachates, and test organisms (Daphnia magna) were added. Forty-eight hour EC50s ranged from 0.5 to >10.0 g l(-1). The toxicity identification evaluation (TIE) indicated that non-polar organic compounds caused most of the toxicity. UV exposure of the filtered tire leachates caused no significant increase in toxicity. However, when tested as unfiltered leachates (the rubber was not filtered from the leachates before addition of D. magna) photo-enhanced toxicity was considerable for some tires, which means that test procedures are important when testing tire leachates for aquatic (photo) toxicity. The acute toxicity of tire wear for Daphnia magna was found to be <40 times a predicted environmental concentration based on reports on the concentration of a tire component found in environmental samples, which emphasizes the need for a more extensive risk assessment of tire wear for the environment.

Animals↗
PubMed2004

Development of new toxicity identification evaluation by assessing toxicity reduction on adsorption and ion-exchange treatments.

A new toxicity identification evaluation method for water exhibiting toxicity has been suggested by evaluating toxicity reduction resulting from adsorption and ion-exchange treatments. Adsorption using various adsorbents such as activated carbon, chitosan and zeolite, and ion-exchange using cationic and anionic ion-exchange resins were performed. In addition, toxicity was evaluated by a cell survival test using human liver cancer origin cells (HepG2), and the dose response data was applied to treatment characteristics. The amount of toxicity adsorbed by the various adsorbents was defined based on adsorption isotherm. Parameters of the toxicity adsorption isotherm provided information that allowed us to identify the toxicity-controlling chemicals in environmental water containing various chemicals. The method is promising for water quality management because it can be used to identify toxicity-controlling chemicals among various environmental pollutants.

Adsorption↗
PubMed2006

Use of carboxylesterase activity to remove pyrethroid-associated toxicity to Ceriodaphnia dubia and Hyalella azteca in toxicity identification evaluations.

Increases in the use and application of pyrethroid insecticides have resulted in concern regarding potential effects on aquatic ecosystems. Methods for the detection of pyrethroids in receiving waters are required to monitor environmental levels of these insecticides. One method employed for the identification of causes of toxicity in aquatic samples is the toxicity identification evaluation (TIE); however, current TIE protocols do not include specific methods for pyrethroid detection. Recent work identified carboxylesterase treatment as a useful method for removing/detecting pyrethroid-associated toxicity. The present study has extended this earlier work and examined the ability of carboxylesterase activity to remove permethrin- and bifenthrin-associated toxicity to Ceriodaphnia dubia and Hyalella azteca in a variety of matrices, including laboratory water, Sacramento River (CA, USA) water, and Salinas River (CA, USA) interstitial water. Esterase activity successfully removed 1,000 ng/L of permethrin-associated toxicity and 600 ng/L of bifenthrin-associated toxicity to C. dubia in Sacramento River water. In interstitial water, 200 ng/L of permethrin-associated toxicity and 60 ng/L of bifenthrin-associated toxicity to H. azteca were removed. The selectivity of the method was validated using heat-inactivated enzyme and bovine serum albumin, demonstrating that catalytically active esterase is required. Further studies showed that the enzyme is not significantly inhibited by metals. Matrix effects on esterase activity were examined with municipal effluent and seawater in addition to the matrices discussed above. Results confirmed that the esterase retains catalytic function in a diverse array of matrices, suggesting that this technique can be adapted to a variety of aquatic samples. These data demonstrate the utility of carboxylesterase treatment as a viable step to detect the presence of pyrethroids in receiving waters.

Ammonia↗
PubMed2006

A larval medaka (Oryzias latipes) acute toxicity assay combined with solid-phase extraction to efficiently determine the toxicity of organic contaminants in river water.

Using a larval medaka (Oryzias latipes) acute toxicity assay combined with solid-phase extraction, we proposed a method for efficiently determining the fish toxicity of organic contaminants in river water. Organic toxicants were 10, 20, 50 and 100-fold concentrated from 4 L of the sample with adsorption cartridges. The lethal effect was observed by exposing every ten individuals of 48-72 h old larval medaka to 20 mL of each solution for 48h. The median lethal concentration rate (LCR50) was used as an indicator for the toxicity. With the developed toxicity test method, more than seven times difference was found in the LCR50 of the river water samples. LCR50 distribution profiles were compared with 125 samples in two typical rivers. The result revealed a lower toxicity level in the mainstream than in the confluences, and a lower toxicity level in Sagami River than in Ayase River. LCR50 proved unique as a toxicity indicator, which was impossible to speculate from the conventional water quality indicator of the dissolved organic carbon concentration. As an effective screening test for priority settings, the method can help us with an efficient planning for the environmental investigation and management.

Animals↗
PubMed1988

Toxic properties of the mushroom Cortinarius orellanus. I. Chemical characterization of the main toxin of Cortinarius orellanus (Fries) and Cortinarius speciosissimus (Kühn & Romagn) and acute toxicity in mice.

The toxins of the mushrooms Cortinarius orellanus (Fries) and Cortinarius speciosissimus (Kühn & Romagn) were isolated by extraction procedures and Sephadex chromatography. All intermediate and end products of the purification process were tested in mice for acute toxicity after oral and i.p. administration. In both species a fluorescent main toxin and a nonfluorescent compound of minor toxicity were found. The main toxin of both species was identified by mass spectrometric and nuclear magnetic resonance analyses as the 2,2'-bipyridine-3,3',4,4'-tetrol-1,1'-dioxide, which is identical to orellanine. The purified compound was toxic when administered either orally or i.p. When given orally the LD50 was 33 mg/kg body weight in mice. The oral LD50 of Cortinarius orellanus (2.20 g dried mushroom/kg) and of Cortinarius speciosissimus (3.12 g/kg) depended on the orellanine content (14 mg/g in Cortinarius orellanus and 9 mg/g in Cortinarius speciosissimus). The second toxic component was ineffective in mice when given orally. It caused acute toxicity when administered i.p., but toxicity was low when compared to the main toxin. Thus it appears to be of minor importance. Intraperitoneal testing of both isolated toxins and of the extract containing the whole toxic potential of the mushrooms revealed that toxicity, time dependency and expression of toxicosis is accounted for by the sum of these two toxins. No peptidic main toxin as described by other mycologists could be detected.

2,2'-Dipyridyl↗
PubMed1992

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

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

Animals↗