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Diane S. Henshel, J. William Martin, and Jamie C. DeWitt

School of Public and Environmental Affairs, Indiana University, Bloomington, Indiana 47405 USA

Abstract

Previous studies have indicated that in ovo exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds is correlated with the development of grossly asymmetric brains. This asymmetry is manifested as a difference between the two halves of the forebrain and the tecta. Previously, only wildlife species (heron, cormorant, and eagle) had been shown to manifest this response. In the wildlife studies, the frequency and degree of left-right interhemispheric differences had been correlated with the levels of polychlorinated dibenzo-p-dioxin toxic equivalency factors (TEFs) in eggs from the same nest (heron, cormorant) . We studied the effect of in ovo exposure to TCDD on the brain throughout development in a sensitive laboratory model (chicken) . Embryos from chicken eggs (Gallus gallus) injected with one of several doses of TCDD or vehicle control were sacrificed after 9, 11, 13, 15, 17, or 20 days of incubation, or incubated to hatch and then sacrificed either within 24 hr or at 3 weeks post-hatch. Measurements of both chicken embryo and hatchling brains indicated that 1) TCDD alone induced the brain asymmetry in developing chickens ; 2) this brain asymmetry was similar to that observed in animals exposed in the wild to a mixture of TCDD-related contaminants ; 3) there was a dose-related increase in both the frequency and severity of brain asymmetry observed at all ages measured ; and 4) the asymmetry was measurable in embryonic brains at an age when the braincase was a thin, flexible layer (embryonic day 9) , implying that the effect of TCDD was directly on the developing brain and not indirectly via an effect on the braincase. Key words: asymmetry, brain, development, dioxin, embryo, TCDD. Environ Health Perspect 105:718-725 (1997)

Address correspondence to D.S. Henshel, School of Public and Environmental Affairs, 10^th and Fee Lane, Room 340 SPEA Building, Indiana University, Bloomington, IN 47405 USA.

This work was supported by the Wildlife Toxicology Fund (World Wildlife Fund, Canada) , the Sustainable Development Research Initiative of British Columbia, NSERC (Canada) , the British Columbia Ministry (Environment) , the Arde Bulova Foundation, and a Biological Research Support Grant. J.W.M. and J.C.D. were supported by research assistantships from the School of Public and Environmental Affairs, Indiana University.

Received 16 October 1996 ; accepted 3 March 1997.