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http://www.sciencenews.org/20031025/bob10.asp

 

New PCBs?Throughout life, our bodies accumulate flame retardants, and scientists

are starting to worry

Janet Raloff

 

Polybrominated diphenyl ether (PBDE) is hardly a household phrase. Yet it

probably should be. Household products ranging from kids' pajamas to computers

release these brominated flame retardants. The chemicals have been turning up in

house and yard dust, as well as in specimens collected from sewage sludge,

streams, and even people's bodies. For 3 decades, manufacturers have been

putting these chemicals into a wide variety of products to reduce the risk that

these goods will catch fire.

And indeed, PBDEs have performed reliably, saving an estimated 300 or more lives

each year in the United States alone. However, emerging data on the extent to

which the chemicals pollute the environment have kindled concern that these

useful compounds may have subtle toxic effects, despite having passed standard

safety tests.

Most U.S. chemists trace their initial concern about these compounds to a report

by Swedish scientists at an international chemistry conference in Stockholm 4

years ago. The researchers stunned the audience with data showing that PBDEs

were present in samples of women's breast milk stored over the past quarter

century and that the more recent the sample, the higher the concentration of the

chemicals (SN: 10/13/01, p. 238: http://www.sciencenews.org/20011013/bob18.asp).

Ronald A. Hites of Indiana University in Indianapolis, who attended that

conference, remembers feeling immediate concern because of the close structural

similarity between PBDEs and polychlorinated biphenyls (PCBs)—insulating oils

that were banned in 1979 owing to their toxicity.

As soon as he got home from the meeting, Hites began surveying published studies

that recorded PBDE concentrations in people. Data were available only for

industrial countries. At an Environmental Protection Agency conference in

Chicago this past August, he reported his findings: PBDE concentrations are 10

to 20 times as high in North Americans as they are in Europeans. And the

Europeans' concentrations are about double those of people living in Japan.

Moreover, Hites says, his calculations show that since the 1970s, these body

concentrations have been " exponentially increasing, with a doubling time of 4 to

5 years. "

So what? That's a question scientists and policy makers have been puzzling over.

Animal data reported this summer support concerns that these useful compounds

might, over the long term, prove toxic to people.

A record 80 papers on brominated flame retardants were presented in August at an

international meeting in Boston called Dioxin 2003. Although presentations

linked all five major classes of brominated flame retardants with some animal

toxicity, the majority of studies focused on the three PBDE classes—related

chemicals with different commercial applications and toxicity profiles.

Especially troubling were reports indicating that relatively low-dose exposures

to PBDEs in the womb or shortly after birth could irreparably damage an animal's

reproductive and nervous systems. Earlier test-tube studies had indicated that

the compounds could alter concentrations of thyroid hormones—agents that play a

pivotal role in growth and development.

Blood concentrations of PBDEs eliciting some of these effects in animals are

close to those now being measured in North Americans, observes Linda S.

Birnbaum, EPA's director of experimental toxicology in Research Triangle Park,

N.C. The animal studies are still preliminary and fall well short of proving

that PBDEs pose a major threat to people, Birnbaum says. However, if people

prove as vulnerable, the concentrations showing up in North Americans leave " no

margin of safety, " she told Science News.

Bambi factor

To many toxicologists at the Boston meeting, most troubling were data indicating

that human exposures to PBDEs begin in the womb. Hites had instructed

delivery-room nurses to extract 10 milliliters of umbilical cord blood from each

of 20 Indiana newborns. Each baby's mother also donated blood.

Concentrations of PBDEs in each mother and her baby were virtually identical.

However, the values between mother-baby pairs varied widely. In the July

Environmental Health Perspectives, the Indiana scientists report that although

the average was around 40 parts per billion (ppb) of PBDEs in blood, some moms

and babies showed concentrations up to 450 ppb.

For breastfed infants, mothers' milk continues the PBDE exposure. At the Boston

dioxin meeting, Arnold Schecter of the University of Texas Health Sciences

Center in Dallas previewed his team's data on PBDEs in breast milk recently

donated by 47 women to Texas milk banks.

All PBDEs have a double-ring structure onto which bromine atoms attach at any of

10 positions. Of 209 different PBDEs, called congeners, Schecter and his

colleagues focused on the 13 that occur most commonly in commercial products.

The Texas study is the first to detect the 10-bromine form of PBDE—a congener

known as BDE-209—in human milk. BDE-209 is the primary ingredient of a

commercial flame-retardant product known as the deca mix because the 10-bromine

congener predominates. This congener, among the hardest to measure, has been

studied only recently. Indeed, many toxicologists doubted its large molecules

could enter the body in measurable amounts.

The milk of seven women had concentrations up to 8 ppb. That's disturbing, notes

Birnbaum, a coauthor of the Texas study. Soon-to-be-published animal research,

briefly described at the Boston meeting, indicates that deca may damage nerve

cells during brain development, which in humans occurs not only in the womb, but

also for up to 2 years after birth.

The milk's total mix of PBDEs—from 6.2 to 419 ppb, with an average of 73.9

ppb—proved similar to the totals that Hites' group had measured in blood. The

Texas study is scheduled to appear in the November Environmental Health

Perspectives.

An even newer, nationwide study by the Environmental Working Group, an advocacy

organization based in Washington, D.C., searched samples of human breast milk

from 20 first-time mothers for some 30 PBDE congeners. Every one turned up in at

least one milk sample. Eighty percent contained BDE-209, though none at

concentrations as high as recorded by Schecter's group.

The biggest surprise, says study author Sonya Lunder in the Environmental

Working Group's Oakland, Calif., office, was the high-end exposures, the top 5

to 10 percent of samples. In most PBDE surveys, these samples have proved

surprisingly high. " In Sweden, those much-higher levels may be 30 ppb, " she

notes. " In ours, they were above 500 ppb—with one above 1,000 ppb. "

Highlighting these flame-retardant exposures to the youngest, most vulnerable

segment of society constitutes " the ultimate Bambi factor, " Hites notes. Lunder

and others express hope that the new findings will make investigation of fetal

and neonatal PBDE toxicity a high priority.

Newfound risks

At the Boston dioxin meeting, several researchers linked PBDEs to reproductive

and brain problems. For example, Chris Talsness of Berlin's Free University

reported on reproductive-system impairments in rats after exposures in the womb

to BDE-99, a 5-bromine PBDE.

Her team injected the chemical into the stomachs of females on the sixth day of

their pregnancies, when fetal organs begin developing. The rats received either

60 or 300 micrograms per kilogram of body weight. The latter, Birnbaum points

out, is about 10 times the highest values for PBDEs reported in U.S. residents'

blood or fat.

Although treated rat moms experienced a slightly higher miscarriage rate than

did females that had received an equivalent amount of peanut oil, the big

effects showed up once pups reached adulthood. Ovaries of daughters from both

groups of BDE-treated moms sported cell abnormalities not seen in unexposed

rats.

Some sons of treated animals exhibited low spleen weights, " a flag that the

immune system may be affected, " Talsness says. Compared with sons of untreated

rats, exposed males also had testes weighing less and producing fewer sperm.

In a follow-up study, the researchers mated unexposed rats with offspring of

treated moms. Abnormalities in the offspring of those crosses suggested that the

BDE-99 had caused genetic changes, Talsness says. For example, daughters that

had been exposed to the chemical as fetuses bore pups with unusual birth

defects, such as missing vertebrae and skull bones. Sons exposed as fetuses

showed decreased fertility. These problems turned up far less often in matings

of unexposed pairs.

Per Eriksson of Uppsala University in Sweden and his coworkers also worked with

BDE-99 in their recent studies. Two years ago, the scientists reported that this

chemical, as well as the 4-bromine congener BDE-47 and various PCBs, could

impair learning and memory in rodents if given at a critical period in brain

development. In a newer study, Eriksson's group gave BDE-99 orally to mice 10

days after birth, a period when baby rats are at about the same stage of

development as a human fetus is during the third trimester of pregnancy. The

researchers used a dose of either 0.8 or 8 milligrams per kilogram of an

animal's body weight. When the pups reached adulthood, the researchers ran the

animals through water-maze tests to evaluate their mental skills. Although

animals in the lower-dose group performed much as untreated mice did, those

getting the higher dose showed memory problems.

The scientists also observed how well each mouse familiarized itself to a new

cage. An untreated or low-dose mouse would typically start out agitated, rapidly

explore a novel cage, and then slow down within an hour. However, mice getting

the higher PBDE dose became increasingly hyperactive through the hour. Tested

again 2 months later, these animals became even more hyperactive during the

cage-familiarization test.

More disturbing, in Eriksson's view, was the outcome of a test in which mice got

the low dose of BDE-99 and a similar subtoxic dose of a PCB. Early exposure to

PCBs can cause lasting IQ deficits in children (SN: 6/16/01, p. 374: Available

to rs at http://www.sciencenews.org/20010616/fob6.asp). In the new

tests, animals performed even more poorly on learning and memory tests than had

mice exposed to a dose of the PCB 10 times that given in this experiment. Says

the toxicologist, " I was surprised the [flame retardant] had such a strong and

pronounced interaction with the PCB. " Indeed, he notes, the pollutants' combined

impact appeared " more than additive. "

In a study due out soon in Toxicological Sciences, Eriksson's group shows that

exposure to BDE-209 during that same early period of brain development elicits

similar lasting neurobehavioral effects in mice.

Marcia L. Hardy, a toxicologist with Albemarle Corp., in Baton Rouge, La., which

makes the deca-PBDE product, notes that she has been trying to see those BDE-209

data since 2001. Several months ago, her group obtained a draft version, but she

notes that the report " still leaves a lot of questions unanswered. " However,

even if Eriksson's data hold up, the exposure a mother mouse needed to deliver

PBDE concentrations in milk that are equivalent to what the pups received is

" astronomically huge, " she says. " I don't see how there could be any exposure

like that. "

What to do?

Almost 2 years ago, 126 nations, including the United States, endorsed a new

international treaty to control the production and use of so-called persistent

organic pollutants (POPs). The goal was to limit the release of agents that were

toxic, long-lived, and able to travel long distances (SN: 6/2/01, p. 343:

Available to rs at http://www.sciencenews.org/20010602/fob9.asp). PCBs,

dioxins, and DDT are among the first POPs slated to be banned worldwide under

the treaty. Indeed, owing to their established toxicity, most of the initially

listed chemicals had already been banned in the United States and other

developed countries.

PBDEs and some other brominated flame retardants now in production also deserve

such a global phaseout, argues Åke Bergman of Stockholm University. After all,

he notes, most PBDEs are quite long-lived (see " Flame retardants take a

vacation, " in this week's issue: Available to rs at

http://www.sciencenews.org/20031025/note12.asp) and long-distance travelers. As

several research teams reported at the Dioxin 2003 meeting, PBDEs show up not

only near where they were made or used but also in remote Arctic lakes. Many

toxicologists have begun referring to PBDEs as " the next PCBs. "

Bergman points out that when it comes to PBDEs' toxicity and persistence, " we

know more about these than we knew about PCBs at the time they were banned in

the 1970s. "

The European Union will ban two of the three most popular PBDE formulations

starting next year. These are the penta and octa mixes, containing primarily 5-

and 8-bromine congeners, respectively. In September, California became the only

U.S. jurisdiction to move against PBDEs. It passed a law to ban penta and octa

mixes, but not until 2008. Elsewhere, production and use of these compounds

remain unregulated, and no government has targeted the deca mix for controls.

Bergman expects the toxicity data emerging on the 10-bromine BDE-209 to change

that. " I would be surprised if the deca [mix] isn't going to also be banned [in

Europe] quite soon. " However, a ban on the deca mix won't come easily, he

concedes, " because there is tremendous pressure from industry to keep it. "

Indeed, Hardy told Science News, data on the deca mix—which now accounts for

some 80 percent of PBDEs used globally—indicate its toxicity is so low that

" this is the flame retardant we should be using. "

In the meantime, argues Leif Magnuson of EPA's pollution-control program in San

Francisco, manufacturers should try weaning themselves from brominated flame

retardants. Already, he notes, the electronics companies NEC, Toshiba, Sony, and

Fujitsu have announced a phaseout of the PBDEs from their products.

IKEA, the Swedish furniture maker, has eliminated brominated flame retardants

from its product line. One U.S. maker of mattress foam, Hickory Springs in North

Carolina, tried to switch to a nonbrominated flame retardant this year, but in

summer, the new production processes turned the foam yellow. Mattress makers

balked at accepting anything but snow-white foam.

Moreover, there are problems looming for the two major brominated flame

retardants, ones unlikely to serve as replacements for any banned PBDEs. At the

EPA and Dioxin 2003 meetings last August, toxicologists reported that

tetrabromobisphenol–A impairs the liver and the immune, nervous, and endocrine

systems, and hexabromocyclododecane is detrimental to the nervous system and

also toxic to fish and other aquatic animals.

Manufacturers of flame retardants are already working on a host of potential

alternatives. Though Lunder and others call for extensive safety reviews of

whatever new flame retardants those companies come up with, Bergman argues that

nothing should stall action against PBDEs.

Counters Hardy: " The real risk is fire. " PBDEs have proved valuable at reducing

fire risk, but she says that in discussions of any possible risks, " we're not

really hearing much about their benefits. "

" For heaven's sake, " Bergman counters, " didn't we learn anything from the issues

of DDT and PCBs? It's really time to act. "

 

 

****************

If you have a comment on this article that you would like considered for

publication in Science News, send it to editors. Please include

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To sign up for the free weekly e-LETTER from Science News, go to

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References:

 

2003. 23rd International Sumposium on Halogenated Organic Pollutants and

Persistant Organic Pollutants. August 24-29. Boston.

 

Bromine Science and Environmental Forum. 2000. An introduction to brominated

flame retardants. Available at http://www.bsef.com.

 

Eriksson, O., E. Jakobsson, and A. Fredriksson. 2001. Brominated flame

retardants: A novel class of developmental neurotoxicants in our environment?

Environmental Health Perspectives 109(September):903.

 

Guvenius, D.M. . . . Å. Bergman, et al. 2003. Human prenatal and postnatal

exposure to polybrominated diohenyl ethers, polychlorinated biphenyls,

polycholorobiphenylols, and pentachlorophenol. Environmental Health Perspectives

111(July):1235.

 

Hardy, M.L., et al. 2003. Industry-sponsored research on the potential health

and environmental effects of selected brominated flame retardants. Environment

International 29(September):793-799.

 

Lunder, S., et al. 2003. Mother's Milk: Record levels of toxic fire retardants

found in American mothers' breast milk. Environmental Working Group. September

23. Available at http://www.ewg.org/reports/mothersmilk/.

 

Mazdai, A. . . . R.A. Hites, et al. 2003. Polybrominated diphenyl ethers in

maternal and fetal blood samples. Environmental Health Perspectives

111(July):1249.

 

Schecter, A. . . . L. Birnbaum, et al. In press. Polybrominated diphenyl ethers

(PBDEs) in U.S. mothers' milk. Environmental Health Perspectives.

 

Viberg, H. . . . and P. Eriksson. In press. Neurobehavioural derangements in

adult mice receiving decabrominated diphenyl ether (PBDE 209) during a defined

period of neonatal brain development. Toxicological Sciences.

Further Readings:

 

Lee, J. 2003. California to Ban Chemicals Used as Flame Retardants. New York

Times. August 10.

 

Petreas, M., et al. 2003. High body burdens of 2,2'4,4'-tetrabromodiphenyl ether

(BDE-47) in California women. Environmental Health Perspectives 111(July):1175.

 

Raloff, J. 2003. Flame retardants take a vacation. Science News 164(Oct.

25):269. Available to rs at

http://www.sciencenews.org/20031025/note12.asp.

 

______. 2003. Flame retardants morph into dioxins. Science News 163(May 24):334.

Available to rs at http://www.sciencenews.org/20030524/note15.asp.

 

______. 2001. Fire retardant catfish? Science News Online (Dec. 8). Available at

http://www.sciencenews.org/20011208/food.asp.

 

______. 2001. Memory problems linked to PCBs in fish. Science News 159(June

16):374. Available to rs at

http://www.sciencenews.org/20010616/fob6.asp.

 

______. 2001. Nations sign on to persistent-pollutants ban. Science News

159(June 2):343. Available to rs at

http://www.sciencenews.org/20010602/fob9.asp.

 

______. 1998. Persistent pollutants face global ban. Science News 154(July 4):6.

References and sources available at

http://www.sciencenews.org/sn_arc98/7_4_98/fob6Ref.htm.

 

______. 1996. Because we eat PCBs. Science News Online (Sept. 14). Available at

http://www.sciencenews.org/sn_arch/9_14_96/food.htm.

 

Risk & Policy Analysts Limited. 2003. Decabromodiphenyl ether: Risk reduction

strategy and analysis of advantages and drawbacks, Stage 2 Report. May.

 

______. 2002. Octabromodiphenyl ether: Risk reduction strategy and analysis of

advantages and drawbacks, Final report. June.

 

______. 2000. Risk reduction strategy and analysis of advantages and drawbacks

of pentabromodiphenyl ether, Final report. July.

 

Santillo, D., and P. Johnston. 2003. Playing with fire: The global threat

presented by brominated flame retardants justifies urgent substitution.

Environment International 29(September):725-734.

 

Schubert, C. 2001. Burned by flame retardants? Science News 160(Oct. 13):238.

Available at http://www.sciencenews.org/20011013/bob18.asp.

 

Schubert, C., and J. Raloff. 2001. EU moves against flame retardants. Science

News 160(Sept. 29):207. Avalable to rs at

http://www.sciencenews.org/20010929/note16.asp.

 

Sjödin, A., D.G. Patterson Jr., and Å. Bergman. 2003. A review on human exposure

to brominated flame retardants—particularly polybrominated diphenyl ethers.

Environment International 29(September):928-839.

Sources:

 

Åke Bergman

Department of Environmental Chemistry

Stockholm University

SE-106 91 Stockholm

Sweden

 

Linda Birnbaum

U.S. Environmental Protection Agency

Experimental Toxicology Division

ATTN: MD B143-01

109 T.W. Alexander Drive

Research Triangle Park, NC 27709

 

Per Eriksson

Uppsala University

Department of Environmental Toxicology

Norbyvägen 18 A

Uppsala S-75236

Sweden

 

Marcia L. Hardy

Albemarle Corporation

451 Florida Street

Baton Rouge, LA 70801

 

Ronald A. Hites

Indiana University

School of Public & Environmental Affairs

SPEA 410 H

Bloomington, IN 47405

 

Sonya Lunder

Environmental Working Group

1904 Franklin Street

Suite 703

Oakland, CA 94612

 

Leif Magnuson

U.S. Environmental Protection Agency

Region IX, WST-7

75 Hawthorne Street

San Francisco, CA 94105

 

Arnold Schecter

University of Texas Health Sciences Center

School of Public Health

Dallas Regional Campus

5323 Harry Hines Boulevard

V88.112

Dallas, TX 75390

 

Chris Talsness

Freie Universitä Berlin

Institute for Clinical Pharmocology & Toxicology

Gartstrasse 5

Berlin D-14195

Germany

 

 

 

 

 

From Science News, Vol. 164, No. 17, Oct. 25, 2003, p. 266.

 

 

 

 

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