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"This is a chicken's brain; this is a chicken's brain on TCDD"

  apologies for any duplicates to folks who've already received this.  Makes
  me wonder what it's doing to OUR brains if we eat dioxin-contaminated
  Unfortunately, EHP is no longer available on-line for free and this piece
  is FULL of graphics and tables. I'd be happy to send hard copies (when I
  get my mail copy of july EHP) to folks who don't subscribe, or you can
  contact the researchers at the address noted in teh abstract.
  Environmental Health Perspectives  Volume 105, Number 7, July 1997
  Brain Asymmetry as a Potential Biomarker for Developmental TCDD
  Intoxication: A Dose�Response Study
  Diane S. Henshel, J. William Martin, and Jamie C. DeWitt
  School of Public and Environmental Affairs, Indiana University, Bloomington,
  Indiana 47405 USA
  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, 10th 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.
  Jackie Hunt Christensen
  Food Safety Project Director
  Institute for Agriculture and Trade Policy
  2105 1st Avenue South
  Minneapolis,  MN 55404
  612-870-3424 (direct line)
  612-870-4846 (fax)
  e-mail: <jchristensen@igc.apc.org>
  IATP's Endocrine Disrupter Resource Center: http://www.sustain.org/edrc