Burned by Flame Retardants?

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).

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: https://www.sciencenews.org/sn_arch/9_14_96/fob1.htm; 6/16/01, p. 374: Memory problems linked to PCBs in fish).

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, ke 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 g/g of body weight) to the highest (12 g/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

g/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 g/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 g 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.”

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