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Total Toxic Equivalent

From this equation, it is apparent that the Total MOE is a dose (BMD(l)) with known toxicological characteristics divided by the total toxic equivalent dose (Total TED). Thus, despite the non-transparent form of the usual equation for... [Pg.278]

TCDD is 1. The concentration or dose of each active component in a mixture of concern is multiplied by its TEF to arrive at a TEQ, and the TEQs are added to give the total toxic equivalency of... [Pg.396]

The toxicity of the isomers varies considerably among the different PCDD s and PCDFs. Only about 17 out of the 210 dioxin and fiiran congeners are toxic. The greatest toxicity possesses the 2,3,7,8-tetra-CDD (the so-called Seveso poison ), and the 2,3,7,8-tetra-CDF. By convention, the toxicity of a mixture of PCDD s and PCDF s is determined as Total Toxic Equivalent = TEQ by multiplying the concentration of the different congeners with a specific Toxic Equivalent Factor = TEF ... [Pg.217]

MWCs Organic Emissions The NSPS limits organic emissions to a total dioxin plus furan emission hmit of 30 ng/dscm (at 7 percent O9 diy volume). This level is approximately equivalent to a toxic equivalent (TEQ) of 1.0 ng/dscm, using the 1990 international toxic equivalency fac tor (1-TEF) approach. [Pg.2252]

As shown by several investigations [91], the bromine-rich polybromide phase by itself is hardly flammable and fireextinguishing properties have been reported occasionally. The formation of polybrominated dibenzo-dioxins (PBrDD) and furans (PBrDF) due to the plastic-containing housing of a zinc-flow battery cannot be totally neglected in the case of a fire, but their concentrations are far away from the tetrachloro dibenzodioxine (TCDD) toxic equivalents even in a worst-case scenario. [Pg.191]

Concern has been expressed about the possible formation of dioxins and furans. However, measurements during experiments indicated that the emissions of dioxins and furans were not significantly elevated. Dioxin emissions with or without plastic input appeared to be about a factor of 100 below the standard of 0.1 ng/Nm TEQ TCCD (toxicity equivalent in relation to the toxic dioxin TCCD) (a.7). This might be due to the benefit of the strongly reducing atmosphere and the high temperature of 2100 °C. In total, until now the conclusion has been that at current PVC levels in MSW, pretreatment for chlorine removal is unnecessary. [Pg.9]

The mild (50°C, 1 atm) catalytic multiphasic methodology can reduce the toxicity equivalent (TEQ) of a sample from a total of 572 pgTEQ/mL to less than... [Pg.150]

Barnes DG Toxicity equivalents and EPAs risk assessment of 2,3,7,8-TCDD. Sci Total Environ 104 73, 1991. [Pg.137]

Urban air concentrations were multiplied by relative potencies (REPs) (listed in Table 2) to calculate the contribution of PCNs to dioxin toxic equivalents (TEQ) and to compare the contributions of the dioxin-like PCBs using REPs from Giesy et al. (1997) [143]. On average, PCNs contributed 64% of total PCN and dioxin-like PCB (PCN+PCB) TEQ in downtown air and 48% in north Toronto. The PCN contribution to PCN+PCB TEQ in Chicago air was similar (68%) when recalculated using the same REPs [97,126]. Although PCNs are as important as PCBs in air on a TEQ basis, polychlorinated dioxins and furans remain the dominant contributors of TEQ in downtown Toronto air [126]. [Pg.293]

The procedure involves converting oxon to thion toxicity equivalents by multiplying the oxon value by its relative toxicity (ED of thion r ED,.q of oxon) in Table I. The ED. value is the aermal dose in ug/cnr of total body surface which produces 50% inhibition of red cell ChE activity 72 hours after application. The total thion and oxon level is then divided by the thion toxicity equivalents and the factor is multiplied by the safe level established for thion in Table I. This procedure was conducted for the dislodgeable residues of parathion-paraoxon, methidathion-methidathion oxon, and azinphosmethyl-azinphosmethyl oxon. The safe levels for the total disloggeable residues were determined to be 0.06, 0.2 and 1.6 ug/cm, respectively, for... [Pg.26]

TEQ Toxicity equivalent (TEQ) is defined as the product of the concentration, C , of an individual dioxin-like compound in a complex environmental mixture and the corresponding TCDD toxicity equivalency factor (TEF ) for that compound. The total TEQs is the sum of the TEQs for each of the congeners in a given mixture n Total TEQs = (C TEF ). i=l... [Pg.737]

Because all 2,3,7,8-substituted PCDDs and PCDFs, as well as the planar PCBs, elicit this type of Ah-receptor mediated responses, their toxicity can be expressed relative to that of the most potent congener, which is 2,3,7,8-tctrachlorodibenzo-p-dioxin (TCDD). This concept is known as the toxic equivalence factor (TEF) approach.84,13 The TEF concept can be used to classify each individual congener and, by an additive approach, assess the total risk of environmental or biological levels of PCDDs, PCDFs and planar PCBs. The predictive value of this approach, in particular when PCBs are included, appears to be species- as well as response-dependent.13 This is primarily due to the presence of other PCBs in environmental residues, which may act antagonistically. [Pg.108]

German Studies. Independent confirmation of the possibility of high particulate emissions being accompanied by low dioxin emissions is provided by the monitoring data collected on the TAMARA pilot MSW incineration plant at the Karlsruhe Nuclear Research Centre.22 The pilot plant was fitted with cyclones and a wet scrubber. The particulate and total PCDD/F concentrations in Table 2 are downstream of the cyclones but prior to the wet scrubber. If the reported PCDD/F concentrations are converted to toxic equivalents, values in the region of 1 ng I-TEQ m-3 would be obtained. The data indicate that particulate emission concentrations far in excess of present-day regulatory requirements can be accompanied by low PCDD/F emissions. [Pg.164]

Additivity and no interactions. Additivity concepts that explain a shared adverse effect across chemicals include dose or concentration addition, which assumes chemicals share a common toxic MOA, and RA, which assumes chemicals act by toxicologically (and thus also statistically) independent MOA. There is also a body of research on the use of statistical dose-response modeling of empirical data to examine the joint toxic action of defined mixtures where the claim is that MOA assumptions are not necessary (Gennings et al. 2005). Dose addition methods scale the component doses for relative toxicity and estimate risk using the total summed dose, for example, using relative potency factors (RPFs), toxicity equivalency factors (TEFs), or a hazard index (HI). In contrast, RA (also named independent action ) is... [Pg.168]

This method is also capable of determining the total concentration of all PCDDs/PCDFs in a given level of chlorination (i.e., total TCDD, total PeCDF, etc.), although complete chromatographic separation of all 210 possible PCDDs/PCDFs is not possible under the instrumental conditions described here. The total concentrations are not assigned TEF values in the February 1989 TEF procedure, and therefore are not included in the toxicity equivalence calculations. [Pg.439]

When the Total MOE approach is used and toxic equivalent factors and doses computed, the BMDs should be comparable. Comparability is increased if all of the BMDs are for the same endpoint (or endpoints related to the common mechanism of action and of comparable severity). Comparability is also increased if the BMDs are all ED s (with the same ) as opposed to all NOAELs or all Lowest Observed Adverse Effect Levels (LOAELs), because the NOAELs and LOAELs are influenced by differences in experimental designs. Comparability is also increased if the BMDs all refer to the same species. [Pg.279]

Probabilistic risk assessment methods are described herein for determining a popnlation s distribution of the dose from exposure and the combination of that exposnre characterization with appropriate toxicological information to form aggregate and cumulative risk assessments. An individual s dose from exposure is characterized as a set of chemical- and route-specific dose profiles over time. Toxic equivalence factors (TEFs) that reflect the toxic endpoint and exposure duration of concern are used to scale chemical- and route-specific doses to toxic equivalent doses (TEDs). The latter are combined in a temporally consistent manner to form a profile over time of the Total TED. For each individual, a Total MOE is calculated by dividing a toxicologically relevant benchmark dose (e.g. an EDio) by the individual s Total TED. The distribution of the Total MOE in a popnlation provides important information for risk management decisions. [Pg.312]


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