Sequestration of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin by activated carbon eliminates bioavailability and the suppression of immune function in mice

Abstract The effectiveness of activated carbon in reducing the bioavailability of 2,3,7,8‐tetrachlorodibenzo‐ p ‐dioxin (TCDD) was examined from the context of using in situ sorbent amendments to remediate soils/sediments contaminated with polychlorinated dibenzo‐ p ‐dioxins/dibenzofurans (PCDD/Fs). This technology has gained rapid acceptance based on observations that activated carbon amendments predictably lower PCDD/F concentrations in water and bioaccumulation by simple aquatic organisms and earthworms; it has been assumed that bioavailability to mammals is similarly reduced, although this has been disproven for other sorbent materials. In the present study TCDD was absorbed to a microporous activated carbon (TCDD‐AC) using the incipient wetness method. An aqueous suspension of TCDD‐AC and an equivalent dosage of TCDD in corn oil were administered by oral gavage to B6C3F1 mice. The relative bioavailability of TCDD‐AC was determined by quantifying and comparing the hepatic induction of cyp1A1 (messenger ribonucleic acid) and suppression of the immunoglobulin M antibody‐forming cell immune response by the 2 forms of TCDD. A concentration‐dependent response was observed for both assays when TCDD in corn oil was administered to mice. However, when equivalent masses of TCDD were administered as TCDD‐AC, no induction of cyp1A1 or suppression of the immunoglobulin M antibody‐forming cell response was observed. The absence of these 2 sensitive aryl hydrocarbon receptor–mediated responses in mice provides the first direct evidence that activated carbon can sequester TCDD in a form that eliminates its bioavailability to mammals. These results support the premise that activated carbon can be used to reduce the bioeffective dose of TCDD delivered to mammals and that activated carbon amendments may provide a low‐cost alternative to traditional remediation technologies. Environ Toxicol Chem 2017;36:2671–2678. © 2017 SETAC