Toxicity equivalent concentration

A thorough analysis of atmospheric transport and deposition to the Great Lakes has been carried out using the HYSPLIT model developed by the US National Atmospheric and Oceanic Administration (NOAA) [28,29]. An emissions inventory of PCDD/Fs for North America in 1996 was used as input to the model. Factors considered in the fate and distribution were meteorological data, vapor-particle partitioning, aerosol characteristics, reaction with hydroxyl radicals, photolysis, and dry and wet deposition. The model was generally satisfactory at estimating fluxes, except for HpCDD and OCDD, which appeared to be underestimated by about a factor of four. The model output was summarized as 2378-TeCDD toxic equivalent concentrations (TEQs) based on the WHO mammalian 2378-TeCDD toxic equivalent factors (TEFs) [30]. Since HpCDD and OCDD were estimated to contribute only 2% of TEQs, the model was considered to be valid for the purpose intended. 

CDDs = chlorinated dibenzo-p-dioxins CDFs = chlorinated dibenzofurons EPA = Environmental Protection Agency FIpCDD = heptachlorodibenzo-p-dioxin HpCDF = heptachlorodibenzofuran FIxCDD = hexachlorodibenzo-p-dioxin FIxCDF = hexachlorodibenzofuran NA = not applicable PeCDD = pentachlorodibenzo-p-dioxin PeCDF = pentachlorodibenzofuran TCDD = tetrachlorodibenzo-p-dioxin TCDF = tetrachlorodibenzofuran TEQ=Toxicity equivalency concentration... 

Eadon et al.14 devised the toxic equivalency approach. For this, specific dioxin-like compounds are assigned a potency or toxic equivalency factor (TEF) relative to TCDD, which usually has been found to be the most toxic dioxin-like compound and assigned a value of 1.0. The concentration of a specific compound in a sample can then be expressed as a toxic equivalent concentration or quotient (TEQ) by multiplying the concentration of the compound as determined by analytical chemistry techniques by its TEF. Next, the dioxin-like compounds in a sample are assumed to act in an additive manner. Therefore, the TEQ for the sample can be determined by adding together the TEQs for each dioxin-like compound in the sample and the final TEQ can be used in risk assessment. 

Bols, N.C., J.J. Whyte, J.H. Clemons, DJ. Tom, M. van den Heuvel and D.G. Dixon. Use of liver cell lines to develop toxic equivalency factors and to derive toxic equivalent concentrations in environmental samples. In Ecotoxicology Responses, Biomarkers and Risk Assessment, edited by J.T. Zelikoff, Fair Haven, NJ, SOS Publications, pp. 329-350, 1997. 

Sum of measured dioxin and furan congener concentrations converted to the toxic equivalent concentration of 2,3,7,8-tetrachlorodibenzodioxin (T4CDD). 

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. 

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). 

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]. 

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). 

The MRL is based on a NOAEL of 0.5 mg/m3 for decreased acetylcholinesterase activity in rats exposed to disulfoton 4 hours/day for 5 days in a study by Thyssen (1978). The NOAEL was adjusted for intermittent exposure, converted to a human equivalent concentration, and divided by an uncertainty factor of 30 (3 for extrapolation from animals to humans and 10 for human variability). Inhibition of erythrocyte cholinesterase activity and unspecified behavioral disorders were observed at 1.8 mg/m, and unspecified signs of cholinergic toxicity were observed at 9.8 mg/m. Similar effects were observed in rats or mice exposed to higher concentrations for shorter duMtions (Doull 1957 Thyssen 1978). The NOAEL value of 0.5 mg/m is supported by another study, in which no significant decrease in the activity of brain, serum, or submaxillary gland cholinesterase was found in rats exposed to 0.14-0.7 mg/m for 1 hour/day for 5-10 days (DuBois and Kinoshita 1971). Mild depression of erythrocyte cholinesterase activity was reported in workers exposed by the inhalation and dermal routes (Wolfe et al. 1978). 

Although diisobutyl ketone may be more toxic and irritative than lower-molecular-weight ketones at equivalent concentration, it poses less of an inhalation hazard because of its relatively low volatility. ... 

Human subjects exposed briefly to 25 ppm experienced irritation of the eyes, nose, and throat. Workers exposed to 5-8 ppm for 1 month complained of fatigue and malaise, which disappeared when air levels were reduced to l ppm. Repeated or prolonged skin contact with the liquid may cause dermatitis because of its defatting action. Although it may be more toxic and irritative than lower-molecular-weight ketones at equivalent concentrations, it poses less of an inhala-... 

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