Toxic equivalents and

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

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... 

A tiered system for mixture extrapolation is proposed. The lowest tier is based on extrapolation using toxicological point-estimate information such as EC50 values. This translates into the use of toxic units, toxic equivalencies, and similar techniques. The use of the entire concentration-response relationships of the separate compounds is recommended for Tier-2, in conjunction with the use of either concentration or response addition as a modeling approach. In Tier-3, a mixed-model approach can be considered, to more specifically address considerations on toxic modes of action. In the latter case, the approach may be extended to allow incorporation of the responses of different ecological receptors (Tier-4). Research needs have been clearly identified in community-level mixture assessments. 

As one example of endocrine disrupter work, EPA has been involved in dioxin reassessment for the last 11 years. This is an incredibly complex issue, with a huge amount of available information—from the chemistry of toxicity equivalents and understanding how dioxin-like congeners can play into the total load in the environment to an understanding of how dioxin works to affect cells essentially as an environmental hormone. 

Fe(CO)s is a highly toxic substance discovered in 1891, the only previously known metal carbonyl being Ni(CO)4. Like its thermally unstable Ru and Os analogues, its structure is trigonal bipyramidal (Fig. 25.10a) but its C nmr spectrum indicates that all 5 carbon atoms are equivalent and this is explained by the molecules fluxional behaviour (p. 914). 

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. 

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. 

Ah-receptor-mediated toxicity is particularly associated with the highly toxic compound 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD), commonly referred to as dioxin. TCDD, and the concept of toxicity equivalency factors (TEFs) based on TCDDs, will be dealt with in Chapter 7. The main point to make at this juncture is that the toxicity of each individual coplanar congener in a mixture can be expressed in terms of a toxic equivalent calculated relative to the toxicity of dioxin. Summation of the toxic equivalents of the individual coplanar PCBs gives a measure of the toxicity of the whole mixture, as expressed through the Ah receptor mechanism. 

Safe, S. (1990). An authoritative account of the toxicology of PCBs, and the development of toxic equivalency factors. 

Toxic equivalency factors (TEFs) are estimated relative to 2,3,7,8-TCDD, which is assigned a value of 1. They are measures of the toxicity of individual compounds relative to that of 2,3,7,8-TCDD. A variety of toxic indices, measured in vivo or in vitro, have been used to estimate TEFs, including reproductive effects (e.g., embryo toxicity in birds), immunotoxicity, and effects on organ weights. The degree of induction of P450 lAl is another measure from which estimations of TEF values have been made. The usual approach is to compare a dose-response curve for a test compound with that of the reference compound, 2,3,7,8-TCDD, and thereby establish the concentrations (or doses) that are required to elicit a standard response. The ratio of concentration of 2,3,7,8-TCDD to concentration of test chemical when both compounds produce the same degree of response is the TEF. Once determined, a TEF can be used to convert a concentration of a dioxin-like chemical found in an environmental sample to a toxic equivalent (TEQ). 

PCDDs and PCDEs, together with coplanar PCBs, can express Ah-receptor-mediated toxicity. TCDD (dioxin) is used as a reference compound in the determination of TEFs, which can be used to estimate TEQs (toxic equivalents) for residues of PHAHs found in wildlife samples. Biomarker assays for Ah-receptor-mediated toxicity have been based on the induction of P450 lAl. TEQs measured in field samples have sometimes been related to toxic effects upon individuals and associated ecological effects (e.g., reproductive success). 

Ahlborg, U.G., Becking, G.C., and Birnbaum, L.S. et al. (1994). Toxic equivalency factors for dioxin-like PCBs. Chemosphere 28, 1049-1067. 

Safe, S. (1998) Hazard and Risk Assessment of Chemical Mixtures Using the Toxic Equivalency Factor Approach. Environmental Health Perspectives, 106(Suppl. 4), 1051-1058. 

To control the emission of organics, these units must comply with similar DRE requirements to the other hazardous waste combustion units. Owners or operators of MACT combustion units must select POHCs and demonstrate a DRE of 99.99% for each POHC in the hazardous wastestream. Sources that bum hazardous waste have a required DRE of 99.9999% for each POHC designated. Additionally, for dioxins and furans, U.S. EPA promulgated more stringent standards under MACT. For example, MACT incinerators and cement kilns that bum waste with dioxins and furans must not exceed an emission limitation of either 0.2 ng of toxicity equivalence per dry standard cubic meter (TEQ/m3) or 0.4 ng TEQ/m3 at the inlet to the dry particulate matter control device. This unit of measure is based on a method for assessing risks associated with exposures to dioxins and furans. 

In tree bark from Luqiao of Taizhou (Fig. 1), the mean concentrations of PCDD/ Fs (List 4 of Appendix) and PCBs (List 8 of Appendix) were 0.1 and 6.5 pg/g lipid weight, respectively. Among all the target analytes, 2,3,4,7,8-PeCDF and PCB-126 were the dominant contributors to toxic equivalency (TEQ). The high levels of PCDD/Fs and PCBs in tree bark suggested the impact of e-waste recycling operations on the local environment [50]. 

Proposed toxicity equivalency value (TEF) relative to 2,3,7,8-TCDD of non-ortho, mono-ortho, and di-ortho planar PCBs... 

Data on the bioavailability of PCDDs are limited. It is known that PCDDs incorporated into wood as a result of chlorophenol (preservative) treatment are bioavailable. Swine and poultry using chlorophenol-treated wooden pens or litter have been found to be contaminated with PCDDs (NRCC 1981). Toxicities of individual PCDD isomers can vary by a factor of 1000 to 10,000 for isomers as closely related as 2,3,7,8-TCDD and 1,2,3,8-TCDD, or 1,2,3,7,8-penta-CDD and 1,2,4,7,8-penta-CDD (Rappe 1984). Isomers with the highest biological activity and acute toxicity have four to six chlorine atoms, and all lateral (i.e., 2,3,7, and 8) positions substituted with chlorine. On this basis, the most toxic PCDD isomers are 2,3,7,8-TCDD, 1,2,3,7,8-penta-CDD, 1,2,3,6,7,8-hexa-CDD, 1,2,3,7,8,9-hexa-CDD, and 1,2,3,4,7,8-hexa-CDD (Rappe 1984). Ishizuka et al. (1998) have assigned toxic equivalencies for various PCDDs, with 2,3,7,8-TCDD given a value of 1 (highest biological activity), followed by a value of 0.5 for 1,2,3,7,8-penta-CDD a value of 0.1 for three PCDD isomers (1,2,3,4,7,8-hexa-CDD, 1,2,3,4,7,8-hexa-CDD, 1,2,3,7,8,9-hexa-CDD), a value of 0.01 for 1,2,3,4,6,7,8-hepta-CDD and a value of 0.001 for 1,2,3,4,6,7,8,9-octa-CDD. 

Newsted, J.L., J.P. Giesy, G.T. Ankley, D.E. Tillitt, R.A. Crawford, J.W. Gooch, P.D. Jones, and M.S. Denison. 1995. Development of toxic equivalency factors for PCB congeners and the assessment of TCDD and PCB mixtures in rainbow trout. Environ. Toxicol. Chem. 14 861-871. 

Commercial PCB mixtures frequently contain impurities that may contribute to the 2,3,7,8-TCDD toxic equivalency factor. These impurities may include other PCBs, dioxins, dibenzofurans, naphthalenes, diphenyl ethers and toluenes, phenoxy and biphenyl anisoles, xanthenes, xanthones, anthracenes, and fluorenes (Jones etal. 1993). PCB concentrations in avian tissues sometimes correlate positively with DDE concentrations (Mora et al. 1993). Eggs of peregrine falcons (Falco peregrinus) from California, for example, contained measurable quantities of various organochlorine compounds, including dioxins, dibenzofurans, mirex, hexachlorobenzene, and / ,//-DDE at 7.1 to 26.0 mg/kg FW PCB 126 accounted for 83% of the 2,3,7,8-TCDD equivalents, but its interaction with other detectable organochlorine compounds is largely unknown (Jarman et al. 1993). 

Bryan, A.M., W.B. Stone, and P.G. Olafsson. 1987b. Disposition of toxic PCB congeners in snapping turtle eggs expressed as toxic equivalents of TCDD. Bull. Environ. Contam. Toxicol. 39 791-796. 

Clemons, J.H., L.E.J. Lee, C.R. Myers, D.G. Dixon, and N.C. Bols. 1996. Cytochrome P4501A1 induction by polychlorinated biphenyls (PCBs) in liver cell lines from rat and trout and the derivation of toxic equivalency factors. Canad. Jour. Fish. Aquat. Sci. 53 1177-1185. 

Green, N.J.L., K.C. Jones, and J. Harwood. 1996. Contribution of coplanar and non-coplanar polychlorinated biphenyls to the toxic equivalence of grey seal (Halichoerus grypus) milk. Chemosphere 33 1273-1281. 

Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibcnzo-p-dioxins PCDDs), dibenzofurans (PCDFs), and related compounds environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21 51-88. 

Zabel, E.W., P.M. Cook, and R.E. Peterson. 1995. Toxic equivalency factors of polychlorinated dibenzo-p-dioxin, dibenzofuran and biphenyl congeners based on early life stage mortality in rainbow trout (Onco-rhynchus mykiss). Aquat. Toxicol. 31 315-328. 

Schecter, A., et al. Congener-specific levels of dioxin and dibenzofurans in U.S. food and estimated daily dioxin toxic equivalent intake, Environ. Health Perspect., 102,962, 1994. 

Analysis of the contaminants in herring and in the seals at the end of the study revealed that PCBs accounted for the majority of Toxic Equivalents to 2,3,7,8-tetrachlo-rodibenzo-p-dioxin (TEQ). Combined with the pattern of immunotoxic effects at the level of the thymus and the T-cell, and a literature indicating an AhR-mediated immunotoxic vulnerability of the thymus [59, 60], the authors concluded that AhR-mediated effects, caused in large part by PCBs, led to the observed effects [57, 61]. They speculated that... 

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