Burned by Flame Retardants?
Our bodies are accumulating chemicals from sofas,
computers, and television sets
Charlotte Schubert
Two years ago, unnerving news from researchers in
Stockholm hit the European press. An analysis of samples
of women's breast milk since 1972 showed dramatic
increases in a class of relatively unknown chemicals
that toxicologists liken to the notorious pollutants
polychlorinated biphenyls (PCBs).
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The similarity of PBDEs and PCBs
to thyroid hormones may underlie the chemicals'
toxicity. Shown here is a PBDE, a PCB, and a
thyroid hormone.
McDonald |
The lesser-known chemicals, polybromo diphenyl ethers
(PBDEs), had been noted a year earlier in the Swedish
food supply. Soon, researchers in North America also
documented an accumulation of PBDEs in women's milk.
They observed PBDEs in fat, too, where the chemicals
lodge. Furthermore, PBDEs have been reported in human
tissue in Japan, Israel, and Spain.
Studies in Lake Ontario and the Baltic Sea find that
PBDE concentrations in fish are rising rapidly, as they
are in the fat of marine mammals in California and the
Northwest Territories of Canada. The chemicals move up
the marine food chain. Concentrations in Baltic Sea
species increase successively in herring, salmon, and
seals.
Trace amounts of PBDEs leach into the air and sewage,
probably from plastics in appliances and computers, foam
in upholstery, and fabric of carpets and draperies.
Between 5 and 35 percent of such items by weight consist
of PBDE flame retardants.
"This stuff is everywhere," says John Jake Ryan of
Health Canada in Ottawa.
Much of the animal data on the toxicity of PBDEs is
incomplete, and next to nothing is known about their
effects on people. But the results of the animal studies
so far lead toxicologists to an unsettling assessment.
Says Ilonka A.T.M. Meerts of Wageningen University and
Research Center in the Netherlands, "The complete toxic
profile is very much like PCBs," the now-banned
chemicals that cause birth defects, thyroid imbalances,
and neurological damage in animals and people (SN:
4/9/96, p. 165: http://www.sciencenews.org/sn_arch/9_14_96/fob1.htm;
6/16/01, p. 374: http://www.sciencenews.org/20010616/fob6.asp).
Since the 1970s, PBDEs have been in widespread use as
fire retardants in plastics, foam, and textiles.
According to the Bromine Science and Environmental
Forum, an industry group based in Brussels, Belgium, 148
million pounds of these chemicals are produced each
year. Workers in electronics-recycling facilities face
unusually high exposures to PBDEs.
The estimated daily intake of PBDEs by people from
air and food is far below amounts now known to be toxic
to animals. Furthermore, concentrations of PBDEs in
human tissue and breast milk are still only one-tenth to
one-hundredth the concentrations of PCBs present.
Despite PBDEs' relative scarceness today, evidence
that the chemicals are accumulating in people and the
environment raise concerns, given PBDEs' potential for
health effects, says Thomas A. McDonald, a toxicologist
at the California Environmental Protection Agency in
Oakland. "If concentrations in some marine mammal and
human populations continue to rise, PBDEs may be the
PCBs of the future," he says.
In response to such assessments, governments in
Europe have moved toward control of the chemicals. On
Sept. 6, the European parliament voted to ban the use,
manufacture, and import of some forms of PBDE over the
next few years (SN: 9/29/01, p. 207). The legislation
still requires passage by the European Council of
Ministers before it becomes law. The United States and
Canada don't currently regulate the manufacture,
distribution, or disposal of PBDEs.
Toxic effects
Concerns about toxic effects of PBDEs arise from many
lines of research. In 1998, Per Ola Darnerud of Sweden's
National Food Administration in Uppsala and his
colleagues reported to the Nordic Council of Ministers
that PBDEs were in the Swedish food supply, tainting
fish, milk, and eggs.
The next year, Ĺke Bergman of Stockholm University,
Daiva Meironyte Guvenius of the Karolinska Institute in
Stockholm, and their colleagues reported a 60-fold
increase in concentrations of these chemicals detected
in women's milk sampled between 1972 and 1997.
Researchers in North America documented what appeared
to be a similar, dramatic increase in PBDE
concentrations in women's milk. Ryan and Benoit Patry of
Health Canada tested breast-milk samples obtained from
several Canadian cities. At the Dioxin 2000 meeting in
Monterey, Calif., they reported that milk samples from
1992 contained concentrations of PBDEs 100 times as high
as in samples obtained a decade earlier. Preliminary
data indicate there were PBDEs in milk from New York
women in 1997.
Health officials, however, note that the benefits of
breastfeeding an infant outweigh the risks associated
with the presence of PBDEs and PCBs in the milk.
Other scientists have examined fat from women in San
Francisco. Samples contained a wide range of PBDE
concentrations—from 0.017 to 0.462 microgram/gram of
body fat. These samples averaged three times as much
PBDE as in samples from women in Sweden, Jianwen She of
California's Environmental Protection Agency in Berkeley
and his colleagues report in an upcoming issue of
Chemosphere. The United States has strict
flame-retardant standards for furniture and other
household items and uses much of the world's PBDEs.
In animal studies, PBDE exposure results in
pronounced effects on the nervous system. Per Eriksson
at Uppsala University in Sweden tested a pair of
penta-PBDE compounds. He administered single doses of
the compounds to mice 10 days after birth, a critical
time in nervous system development. When the mice had
grown to adults, Eriksson tested their movement,
learning ability, and memory.
Mice that were exposed to any dose of a penta-PBDE
compound, from the lowest in the study (0.7 µg/g of body
weight) to the highest (12 µg/g), showed abnormal
behavior. Those receiving the highest dose of one of the
compounds also performed poorly in navigating a maze.
Eriksson and his colleagues report their results in the
September Environmental Health Perspectives.
At all doses, the nervous system defects worsened as
the mice aged. Eriksson's group has done similar studies
with PCB compounds. Describing effects on the nervous
system of developing animals, he says, "The PBDEs are as
toxic as the PCBs we have investigated."
Exactly how either PBDEs or PCBs affect the nervous
system is unclear. But toxicologists suspect that
imbalances in thyroid hormone might play a role. In
people and animals, proper regulation of this hormone is
critical to the developing nervous system.
Many studies have found that rodents fed high amounts
of PBDEs have thyroid hormone deficiencies. In one
recent study, a group led by Kevin M. Crofton at the
University of North Carolina in Chapel Hill examined
thyroid hormone concentrations in blood from rats fed
penta-PBDE for 4 days. In rats fed 9 to 13 µg/g of body
weight per day, the researchers observed a 20 percent
reduction in T4, the primary thyroid hormone in
circulating blood. Doses of about 100 µg/g reduced T4 by
70 percent, the scientists reported in the May
Toxicological Sciences.
In Crofton's preliminary assessment: "It appears as
if the PBDEs are slightly less potent than the PCBs."
To put the thyroid studies into perspective, Darnerud
estimates that the concentrations of PBDEs that produce
an effect on thyroid hormones in animals are 1 million
times greater than current exposures in people. It's
hard to compare short-term dosage studies with chronic
low-level exposure, he notes, but the gap between animal
exposures in the lab and human exposure is immense.
McDonald agrees with Darnerud's assessment but says,
"There is reason to think that the gap might narrow." He
also suggests that people with slight thyroid imbalances
might be affected by even small doses of PBDEs. He
notes, too, that some animal studies show that toxic
effects of PBDEs and PCBs add to each other.
Similar to hormones
Some of the toxic effects of PCBs and PBDEs may
derive from their structural similarity to thyroid
hormones. PCBs, PBDEs, and thyroid hormones all consist
of two six-carbon rings decorated with halogens. Bromine
attaches to the carbon rings of PBDEs, chlorine to those
of PCBs, and iodine to those of thyroid hormone. In
PBDEs, an atom of oxygen bridges the rings, whereas the
rings of PCBs and thyroid hormones are linked by carbon-
carbon bonds.
The similarity between PBDEs and PCBs, however,
doesn't mean they exert exactly the same effects in the
body, cautions Darnerud. "I think it's perhaps too
simple to say that these compounds are alike," he says.
It's the bromine atoms in the PBDEs that make them
good fire retardants. They quench flames by scavenging
electrons. The number and the placement of the bromine
atoms determine the type of PBDE. The maximum number of
bromines, 10, occurs in deca-PBDE. This substance, which
manufacturers use primarily in hard plastics, accounts
for more than 80 percent of PBDEs in use today.
Deca-PBDE accumulates in human and animal tissue at
far lower concentrations than its cousins with fewer
bromines do. In several analyses, deca-PBDE also seems
to have much less toxicity. However, Eriksson and his
colleagues have found that mice exposed to deca-PBDE as
weanlings show behavioral changes equivalent to those
exposed to penta-PBDE. The researchers presented their
data at the Society for Toxicology meeting in March in
San Francisco.
Penta-PBDE, which has five bromines, is the most
common form in foam products. But commercial
formulations of penta-PBDE contain about 45 percent
tetra-PBDE, with four bromines. Penta- and tetra-PBDE
appear to break down into potentially more toxic
compounds in the body.
Meerts and her colleagues have examined the
interaction of PBDE breakdown products, or metabolites,
with a blood protein that ushers T4 around the body. The
protein, called transthyretin, is one of several T4
escorts in the bloodstream.
In the July 2000 Toxicological Sciences,
Meerts reports that PBDE metabolites bind to
transthyretin, as PCB metabolites do. Compounds
predicted to be metabolic breakdown products of
tetra-PBDE bind even more tightly than T4 itself.
Scientists who study PCBs have speculated that
transthyretin has a special role in carrying PCBs to the
fetus and especially its brain.
Despite PBDEs' structural similarity to thyroid
hormones, McDonald says that "thyroid hormone disruption
is not the whole story."
He notes that laboratory studies of PCBs show that
they can upset the intricate balance of nerve cells'
chemical communication system. Preliminary data from
Prasada Rao S. Kodavanti of the Environmental Protection
Agency in Research Triangle Park, N.C., and his
colleagues suggest that PBDEs may disrupt some of the
same communication processes, reports McDonald in an
upcoming issue of Chemosphere.
Millions of sources
How PBDEs from sofas, carpets, computer monitors, and
television sets get into people is an open question.
"You have millions of point sources in every home, every
bus, every car, and they are slowly making their way
into the environment and up the food chain," says
McDonald.
After analyzing food in Ottawa grocery stores, Ryan
estimates that the average person there eats 0.044 µg of
PBDE per day in meat and dairy. But scientists don't yet
know how food gets contaminated in the first place.
In the United States, spreading sewage waste on
farmland as fertilizer may send PBDEs along to the
dinner table. Robert C. Hale of the Department of
Environmental Science in Gloucester Point, Va., and his
colleagues measured PBDEs in U.S. sewage sludge. They
report in the July 12 Nature that each kilogram
of sludge, by dry weight, carries 1.1 to 2.3 milligrams
of PBDEs with five or fewer bromines. That exceeds
100,000 times the concentration that other researchers
found in some European sludge samples. About 4 million
tons of sewage sludge were applied last year to land in
the United States, according to EPA.
Discarded furniture may contribute to the pollution
in sludge, suggests Hale. As they degrade, couch and
chair cushions release large amounts of penta-PBDE into
dirt, sewers, and sediments, he suspects.
Flame-suppression standards save lives, says Robert
Campbell of the American Chemistry Council in Arlington,
Va.
"We may have to look at issues of risk tradeoff, but
. . . there are flame retardants other than PBDEs," says
Linda Birnbaum, director of the human studies division
at EPA's National Health and Environmental Effects
Research Lab in Research Triangle Park, N.C. She notes,
"We banned the production of PCBs when we had less
information than we do now of the PBDEs."
Fire-squelching substitutes for PBDEs include other
bromine-containing compounds and silicon or
phosphorus-based chemicals. Some of these may gradually
degrade in products, weakening their fire-retardant
properties, notes Campbell.
Birnbaum adds that some substitutes may themselves be
toxic.
Less ambiguous are the data that show PBDEs
accumulating at a rapid rate in the fat of people and
animals in North America. "Current concentrations [of
PBDEs] are still quite low," says Crofton. Like many
other toxicologists, he is particularly concerned about
the future.
Adds Darnerud, "I don't want to see levels get as
high as PCB levels."
Letters:
Couched in language peppered with
mays, the article suggests that we are all being
poisoned with PBDEs from sewage sludge applied to
farmland. However, sludge with high concentrations of
volatile organics isn't qualified in most jurisdictions
of which I am aware for land application. It's usually
sent to a landfill or incinerated.
Couches and chair cushions don't
appear in sewage plants, and therefore PBDEs in those
objects don't appear in the plants' sludge, at least not
directly. Such objects go to landfills, and sludge from
treatment of leachate from such landfills is never
applied to land. Finally, in the United States, sludge
is not supposed to be put on land growing crops for
human consumption or for consumption by animals consumed
by humans. I therefore suspect it to be highly
improbable that there's a direct connection between
sludge and the dinner table in the United States.
McClellan G. Blair
Indiana,
Pa.
The article appears to have a
discrepancy. The text's description of the structural
similarities between the three types of molecules
doesn't agree with the figure of the structures of the
molecules of PBDE-100, PCB-153, and thyroxine.
The text states that the carbon rings
of PBDE are joined by an oxygen atom, while those of PCB
and thyroxine are joined by a carbon-carbon bond. In the
figure, the rings in thyroxine appear to be joined by an
oxygen atom in the same manner as the PBDE-100.
Something seems awry.
Edward Brosius
Saline,
Mich.
Correct. It's incorrect. The text
should have read: "In PBDEs and thyroid hormones, an
atom of oxygen bridges the rings, whereas PCBs are
linked by carbon-carbon bonds." Therefore, says Thomas
A. McDonald of California's Office of Environmental
Health Hazard Assessment, PBDEs structurally resemble
thyroid hormones even more closely than they resemble
PCBs.—The Editors
This article presents incomplete
information on polybrominated diphenyl ethers (PBDEs).
The troubling aspect of this article is its call for
reducing or banning the use of these life-saving
products. The importance of brominated flame retardants
should be pointed out in any article addressing their
use because thousands of people are injured or die in
fires around the globe each year. In the United States
alone, fires kill about 4,000 people annually, with
another 20,000 people suffering serious injury from
burns and property losses totaling about $4.5 billion.
Courtney M. Price
American
Chemistry Council
Arlington, Va.
References:
Hale, R.C., ... and W.H. Duff. 2001.
Persistent pollutants in land-applied sludges.
Nature 412(July 12):140-141.
Meerts, I.A., et al. 2000.
Potent competitive interactions of some brominated flame
retardants and related compounds with human
transthyretin in vitro. Toxicological Sciences
56(July):95.
Zhou, T., et al. 2001. Effects
of short-term in vivo exposure to polybrominated dipher
ethers on thyroid hormones and hepatic enzyme activities
in weanling rats. Toxicological Sciences
61(May):76.
Further Readings:
Raloff, J. 2001. Memory problems
linked to PCBs in fish. Science News 159(June
16):374.
______. 1996. Banned pollutant's
legacy: Lower IQs. Science News 150(Sept.
14):165. Available at http://www.sciencenews.org/sn_arch/9_14_96/fob1.htm.
Sources:
Ĺke Bergman
Department of
Environmental Chemistry
Wallenberg
Laboratory
Stockholm University
106 91
Stockholm
Sweden
Bob Campbell
Great Lakes
Chemical
1801 Highway 52 North
West Lafayette, IN
47906
Kevin M. Crofton
Neurotoxicity
Division
National Health and Environmental Effects
Research Laboratory
U.S. EPA
Research Triangle
Park, NC 27711
Per Ola Darnerud
National Food
Administration
Toxicology Division
P.O. Box
662
751 05 Uppsala
Sweden
William H. Duff
Department of
Environmental Science
Virginia Institute of Marine
Science
P.O. Box 1346
Gloucester Pt., VA 23063
Per Eriksson
University of
Uppsala
Box 256
751 05 Uppsala
Sweden
Daive M. Gevenius
Department of
Medical Biochemistry and Biophysics
Karolinsa
Institute
171 77 Stockholm
Sweden
Robert C. Hale
Department of
Environmental Science
Virginia Institute of Marine
Science
P.O. Box 1346
Gloucester Pt., VA 23062
Prasada Rao S. Kodavanti
Cellular
and Molecular Toxocology Branch
National Health and
Environmental Effects Research Laboratory
U.S.
EPA
Research Triangle Park, NC 27711
Thomas A. McDonald
Office of
Environmental Health Hazard Assessment
California
EPA
1515 Clay Street, 16th Floor
Oakland, CA
94612
Koidu Noren
Department of Medical
Biochemistry and Biophysics
Karolinska
Institute
171 77 Stockholm
Sweden
Jianwen She
Hazardous Materials
Laboratory
California Department of Toxic Substances
Control
California EPA
2151 Berkeley
Way
Berkeley, CA 94704
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