Title: A comparison of toxicity equivalency (TEQ) results obtained using rapidscreen and the DIPS-CALUX bioassay with EPA method 8290 and 1668A calculated TEQS

Auteur(s): Chandramouli B ; Tochacek LE ; Harvan D ; Hass JR ;  ; 

Year: 2003

Journal: Organohalogen Compounds

Subject(s): bioassay ; CALUX ; TEQ ; toxicity ; dioxins ; dioxin ; furans ; 2,3,7,8-TCDD ; food ; monitoring ; PCB ;  ; 

Summary: Toxic Equivalency (TEQ) describes the toxicity of a sample in terms of one representative compound. Among dioxins and furans, Toxicity Equivalency Factors, or TEFs, are used to describe the relative toxicity of 16 specific congeners in comparison to 2,3,7,8-TCDD. The TEQ of a sample is typically determined from the sum of each congener's concentration (or detection limit) multiplied by its TEF. While HRGC/HRMS is the definitive analytical method used for determining the TEQ of an environmental, food or serum sample at part-per-trillion levels (ppt), it is time consuming and expensive. Cost barriers may undermine the thoroughness of a sampling or monitoring program. Screening methods for the TEQ of samples from a variety of matrices are becoming increasingly important due to concerns about dioxin/furan/PCB contamination. Screening methods promise cost-effective, more rigorous sampling and monitoring by greatly reducing the number of samples that have to be tested using full-scale quantitative methods.The RapidScreen method for TEQI developed by Triangle Laboratories, Inc., USA and the DIPS-CALUX Bioassay developed by Xenobiotic Detection Systems, Inc., USA2, are two methods available to screen samples from a variety of matrices for dioxin toxicity. The RapidScreen method uses isotope dilution HRGCIHRMS to screen samples as positive or negative based on a threshold TEQ. Seven dioxin/furan congeners (shown in Table I) that contributed 62% to an environmental sample's overall 8290 measured TEQ 77% of the time3, and three PCB congeners are used in the calculations. The DIPS-CALUX bioassay quantitates the TEQ based on the activation of aryl hydrocarbon receptor (AhR)-mediated gene transcription.