RE: mill effluent chloro-xanthene as toxic as tcdd; great lakes; cardiovascular

["Catalano, Dennis" <catalad@wdni.com>]

  A 1989 paper by Hans-Rudolf Buser, Lars-Owe Kjeller, Stephen Swanson,
  and Christoffer Rappe states that errors were made when the initial
  research was performed on pulp mill effluent and sediment down stream
  from mills.  The compounds initially thought to be chloroxanthene was
  actually methylated chlorofurans.  These compounds can not be
  distinguished  by HRMS and some very good research was performed to
  indicate that the latter compounds were the compounds found in effluent.
   This paper states that the toxicalogical significance of the
  alkyl-PCDFs is not known, but research by Safe and coworkers suggest
  that they act as effective antagonists to TCDD.  They compete with the
  TCDD for binding sites to the Ah receptor and thus block the TCDD
  activity.  These compounds diminish the ability of TCDD to induce enzyme
  activity.
  
  Dennis Catalano
   ----------
  From: ttweed@wildrockies.org
  To: Multiple recipients of list
  Subject: mill effluent chloro-xanthene as toxic as tcdd; great lakes;
  cardiovascular
  Date: Tuesday, July 15, 1997 8:57AM
  
  some may have seen janet ralloff's newest, fascinating as always, dioxin
  research update in _science news_ ('those old dioxin blues', 151:306-7,
  17
  may '97).
  
  after reviewing blue sac syndrome in fish fry, and the acute
  sensitivity--LC50 of 60 ppt--of tcdd to lake trout fry (a top predator
  and
  a key species to great lakes ecosystem balance; 400 ppt for rainbow
  trout),
  she goes on to say that a recently identified paper mill effluent
  compound,
  2,3,6,7-tetrachloroxanthene is as toxic (not quantified here) in
  inducing
  blue sac syndrome as 2,3,7,8-tcdd (work of good old richard peterson,
  and
  erik zabel, @ u. wi/madison).
  
  the brominated 2,3,7,8-tbdd is more potent than it's chlorinated analog
  at
  inducing blue sac.  source is largely the increasing testing of
  brominated
  fire retardants; and, various brominated biphenyls are 10 times as
  potent
  as their pcb analogues.  (peterson et al., october '96 _tox & appl.
  pharm_).
  
  present in an unamed compound used to kill lamprey eel is a fluorine
  substituted--3F, 1 Cl--dioxin (Environment Canada scientist mark
  servos).
  
  john geisy et al. of mich. state u. have evidence that some pcb damage
  immune T cells, which may have contributed to 1989 great lakes fish
  die-offs from bacterial kidney disease [inter alia, presumably].
  
  regarding the mechanism of blue sac syndrome:
  
  consistent w/ finding the Ah receptor in fish, whales, mussels and
  lobsters
  by mark hahn @ woods hole, don tillitt of usgs & mark hannink of u.
  missouri find that the blood vessels of tcdd exposed fry are induced
  into
  inappropriate programmed cell death [a key defence against cancer, btw,
  &
  n.b. because of tcdd's cancer associations], which maybe due to tcdd's
  ability to express genes that produce oxidative enzymes (john stegeman
  and
  jenifer schlesinger @ woods hole).  meanwhile peterson in collaboration
  w/
  unmaned cornell u. scientists have discovered their pollutants slow both
  the blood flow & heart rate of zebra fish, and "prune back" the number
  of
  blood vessels and the ability to maintain new ones.
  
  sounds like excellent work on the mechanistic end of things.
  epidemeologicly, tcdd & pcdd/f are already associated w/ cardiovascular
  disease.  let's see:  mechanistic .. epidemeologic .. and lab animal
  evidence ... hmmn ... dr. lynn goldman, head of epa's oppt, needs to
  stick
  this in her pipe, and smoke it!
  
  
  tony tweedale