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RE: mill effluent chloro-xanthene as toxic as tcdd; great lakes; cardiovascular
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
To: Multiple recipients of list
Subject: mill effluent chloro-xanthene as toxic as tcdd; great lakes;
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,
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
a key species to great lakes ecosystem balance; 400 ppt for rainbow
she goes on to say that a recently identified paper mill effluent
2,3,6,7-tetrachloroxanthene is as toxic (not quantified here) in
blue sac syndrome as 2,3,7,8-tcdd (work of good old richard peterson,
erik zabel, @ u. wi/madison).
the brominated 2,3,7,8-tbdd is more potent than it's chlorinated analog
inducing blue sac. source is largely the increasing testing of
fire retardants; and, various brominated biphenyls are 10 times as
as their pcb analogues. (peterson et al., october '96 _tox & appl.
present in an unamed compound used to kill lamprey eel is a fluorine
substituted--3F, 1 Cl--dioxin (Environment Canada scientist mark
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
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
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
jenifer schlesinger @ woods hole). meanwhile peterson in collaboration
unmaned cornell u. scientists have discovered their pollutants slow both
the blood flow & heart rate of zebra fish, and "prune back" the number
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
this in her pipe, and smoke it!