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May 12, 2004

PBDEs - Fire Retardants in Dust: Health Risks of Deca

Most research on the toxic effects of PBDEs has centered on those congeners with five or fewer bromines — the predominant chemicals in Penta. Since these less-brominated PBDEs are readily absorbed by the body, slowly eliminated, highly bioaccumulative, and structurally similar to PCBs, it wasn't that surprising when scientists began to find that low doses of these PBDEs could disrupt the thyroid hormone balance and interfere with neurodevelopment in laboratory animals. [37, 9, 70, 71, 72, 73, 74, 75]

The initial scientific view of Deca was quite different. It was thought that Deca was too large to be absorbed, toxic only at very high doses, and not found in living things. But as more independent scientists examined Deca more closely, this dogma crumbled. Because Deca is challenging to test for, most researchers didn't bother. As one scientist explained in a recent paper: "The 'absence' of [Deca] in the ambient population is likely a result of analytical bias; that is, most studies of the ambient population did not include [Deca] as one of the analytes of interest." [76]

Since researchers have started looking for it more consistently, Deca has been detected in dozens of wildlife species from around the globe as well as human hair, fat, blood and breast milk. Although levels of Deca found in animals and humans are much lower than other PBDEs — on average, five percent of total PBDE concentrations — this is not universally true. Some studies of human tissue found Deca made up as much as one-fourth of PBDEs in people who were not exposed on the job, and as much as 40 percent in people who were occupationally exposed. [76] In Europe, Deca has been found in birds at up to 530 ppb, and in falcon eggs at up to 828 ppb. [38, 39]

According to the EU's draft risk assessment, "The potential for uptake of [Deca] by mammalian systems may be higher than indicated by many of the previous laboratory studies," and the absorption "could be quite large." [39] One study, found that 13.5 percent or more of Deca persisted in the brain, liver, and hearts of mice 24 hours after dosing. [40] Another study indicates that rats absorb 10 percent to 65 percent of a single dose of Deca. [77]

If Deca were truly non-toxic, as the fire retardant industry maintains, or only harmful at very high levels, the fact that it can be absorbed by living things might not matter. But new research is challenging this commonly held notion. A study exposing mice to a single low dose (2.2 mg/kg) of Deca during a "defined critical phase of neonatal brain development" caused "irreversible changes in adult brain function" which worsened with age. [39, 40] These mice, when tested later as adults, showed "neurobehavioral derangements." [40]

Harm at just one dose?

PBDE congener Part of what commercial mixture Test animal PBDE concen-
tration in fat tissue
dose (mg/kg-day)
Toxic effect Source
PBDE-209 Deca Mice Not measured 2.2 (single dose) Caused aberrations in spontaneous motor behavior and habituation capability that worsened with age [40]
PBDE-99 Penta Mice 12 ppb in brain lipid* 0.8 (single dose) Effects on learning and memory, spontaneous motor behavior and habituation capability that worsened with age [9, 10]
Commercial Penta Mixture DE-71 Penta Mice Not measured 0.8 (single dose) Significant decrease in thyroid hormone (T4) levels [70]
PBDE-99 Penta Rats Not measured 0.06 (single dose) Decreased sperm count [95]
PBDE-99 Penta Rats Not measured 0.06 (single dose) Changes in subcellular structure of ovaries [110]

Interestingly, newborn mice exposed during a different phase of development showed no such effects, highlighting the importance of timing in determining whether exposure to PBDEs may cause adverse health effects later in life. Researchers from two different labs found similar neurobehavioral effects when they exposed newborn mice and rats to low doses of tetra and penta PBDEs during certain periods of development. [9, 10, 78] Deca is the only commercial PBDE mixture that has been tested for its ability to cause cancer. In a single study 15 years ago, researchers found high doses of Deca given to rats and mice caused liver, thyroid and pancreas tumors. [79]

The most important question about Deca, however, is its breakdown to less-brominated forms of PBDEs. While there is still debate about whether low doses of Deca are harmful, there is no question that low doses of Penta are. Studies from as far back as the early 1970s clearly show that Deca degrades into less-brominated PBDEs after exposure to sunlight. But the implications of such findings were not recognized until much more recently. [80]

The EU draft ecological assessment concludes: "Available data on photodegradation of [Deca] clearly show that the substance photodegrades under a range of conditions." [81] A leading toxics researcher, Linda Birnbaum of the Environmental Protection Agency, agrees:

"There is now good evidence that Deca can and does break down both in the environment and in fish, as well as in rats. . . . We really don't know if the breakdown products are contributing to the body burdens of these congeners in biota and people. We also don't know the toxicity of these specific congeners, although at least one of them . . . has been shown to be developmentally neurotoxic by studies in Sweden." [82]

Today, numerous studies confirm that Deca can debrominate under a wide range of conditions. [41, 42, 43, 44, 83, 84, 85, 86, 87] One study found that Deca can degrade by 50 percent in as little as 15 minutes, while another found that after five days of exposure to sunlight just six percent of the chemical remained undegraded. [41, 85] These rates are probably much higher than what occurs in the real world, but the bottom line is that these studies found that Deca degradation products were "readily formed on all matrices." [86]

Key Debromination Studies

PBDE congeners tested Part of which commercial mixture(s) Study methodology Source
Study findings
PBDE 209 Deca Deca was dissolved in toluene (solvent) and exposed to artificial ultra-violet (UV) light for four hours. [87]
Deca degraded to nona- to penta-brominated PBDEs. Some dioxin-like compounds (polybrominated dibenzo-furans or PBDFs) were also formed.
PBDE 209 Deca Deca was dissolved in toluene and applied to silica gel, sand, sediment, and soil; exposed to artificial and natural sunlight for 5 to 10 days. [86]
Deca degraded readily to nona- and octa-BDEs (as well as a number of other PBDEs with fewer bromines) on all matrices. A major degradation product was PBDE-183, which is a component of the now banned Octa mixture. Half of the Deca degraded within within 12 hours when applied to sand, and between 2 and 8 days when applied to sediment or soil. Shorter half-life in toluene.
13 congeners (with 3 to 10 bromines) Penta, Octa, Deca Sample was dissolved in toluene and placed in either white or brown glass bottles in sunlight for 2 to 14 days. [85]
Only 6% of deca-BDE remained after 5 days and only 1% after 14 days. PBDEs with 3 to 6 bromines (inlcuding the congener PBDE-47 most prevalent in wildlife and humans) found to be highly stable: they did not degrade significantly even after 14 days.
39 congeners (with 1 to 7 bromines) Penta, Octa Sample was dissolved in a lipid matrix at "biologically relevant concentrations" and exposed to sunlight for 2 or 120 minutes. [44]
Two of the most common congeners found in biota (PBDEs 47 and 99) were formed in significant amounts from the degradation of one hepta-, most hexa- and some penta-BDEs.

PBDEs degrade in steps. Deca, with ten bromines, has been shown to break down into congeners with 9, 8 or 7 bromines in solvent, on silica gel, sand and soil. In one study, researchers found less than half of the original sample of Deca remaining after 20 minutes when Deca was spread on silica gel and exposed to sunlight. [86] They found that Deca persisted longest in soil — but only half remained after just 8 days. And PBDEs with 6 to 9 bromines have also been shown to break down into congeners with 5 or 4 bromines. [85] These less-brominated congeners are not only the most toxic and bioaccumulative, but also seem to be the most resistant to degradation.

It is impossible to ignore evidence of Deca breakdown. In April 2003, the EPA officially acknowledged that "higher brominated forms such as [Deca] can be altered to form more toxicologically active lower brominated forms." [43] While most research has focused on degradation in the environment, a few recent studies have added a twist: Debromination can occur in organisms themselves. [88, 83, 84] When researchers fed Deca to young fish for 60 days, almost none of it was found when the fish was tested 40 days later. But they did find seven different PBDE congeners with fewer bromines, none of which were present in the carp's diet. The researchers concluded that Deca was debrominating in the fish's tissues and converting into congeners "similar to the components in the [Penta] commercial mixtures." Even more importantly, they point out:

"Considering the high levels of [Deca] that have been measured in the environment, it is possible that over long periods of time significant formation of penta- and hexa-BDEs could occur. Therefore, banning the [Penta] commercial mixtures and continuing the use of the [Deca] mixtures may not alleviate the concerns over the presence of lower-brominated PBDEs in the environment." [84]

At this point it is hard to say how much of the Penta and other less-brominated PBDEs in people, animals and the environment originated as Deca. This is specially true given the fact that most studies looking at PBDE breakdown have been two weeks or shorter. But it is clear that allowing Deca to remain on the market may seriously undermine the environmental benefits of getting rid of Penta and Octa. To make matters worse, some data suggests that Deca can degrade into dioxin-like compounds known as PBDFs (polybrominated dibenzofurans) after exposure to ambient sunlight. [87, 89, 42.] Low levels of the very similar polychlorinated dioxins and furans are known to cause cancer and birth defects. PBDFs have recently been measured in human tissue samples and the environment in Japan. [90, 91]

How toxic are Penta and Octa PBDEs?

While research on Deca's health effects is still relatively sparse, there is a substantial body of research on the less-brominated PBDEs. Even low doses of these compounds can cause thyroid hormone disruption, permanent learning and memory impairment, behavioral changes, hearing deficits, delayed puberty onset, and decreased sperm counts in laboratory animals. Scientists have also found that exposures occurring in utero or during infancy lead to more significant harm than exposure during adulthood, and at much lower levels. Some of these studies have found toxic effects at levels lower than are now detected in American women.

Many of the known health effects of PBDEs are thought to stem from their ability to disrupt the body's thyroid hormone balance. Depressed thyroid hormone levels can cause fatigue, depression, anxiety, unexplained weight gain, hair loss and low libido in adults, and even more serious health effects in developing fetuses and infants. [92] A study of women whose levels of thyroid hormones measured in the lowest 10 percent of the population during the first trimester of pregnancy, for example, found that these women were more than 2.5 times as likely to have a child with an IQ of less than 85 (in the lowest 20 percent of the range of IQs). These women were five times as likely to have a child with an IQ of less than 70, meeting the diagnosis of "mild retardation." [93] Although no direct link could be made, one study found higher rates of hypothyroidism among workers exposed to brominated fire retardants on the job. [94]

Scientists are finding that even short-term exposures to commercial PBDE mixtures or individual congeners can alter thyroid hormone levels in animals, with effects being more profound for those animals which were exposed while they were young or in the womb. [70, 71, 72, 73, 74, 75] Other researchers have found subtle reproductive effects, such as decreased sperm count and changes in the sub-cellular structure of the ovaries, at incredibly low doses — just 0.06 mg of PBDEs per kg-day. [95] But some of the most worrisome findings come from experiments that gave young rats a low dose of PBDEs at a critical point in during their brain development. The studies found that just a single dose can cause lasting harm. [9, 11, 10]

In two different studies, one small dose of PBDEs — as little as 0.8 milligrams per kilogram of body weight per day (mg/kg-day) — given to 10-day-old mice caused "deranged spontaneous behavior," significant deficits in learning and memory and a reduced ability to adapt to new environments. These were not transient but rather "persistent neurotoxic effects" which often grew worse with age. [9, 10] Several other animal studies have shown that early-life exposures to PBDEs, often at relatively low levels, can lead to delays in sensory-motor development and hearing deficit. [11, 78, 13] Scientists still do not understand exactly how PBDEs affect neurological development. But there is evidence that they act through several different mechanisms, including mimicking thyroid hormones, increasing their rate of turnover in the body and interfering with intracellular communication. [96]

Most studies on the effects of PBDEs have been short-term — exposures of 14 days or less — so little is known about how longer term exposures may affect thyroid hormones. The answer is important, because the entire U.S. population is exposed daily to low levels of PBDEs, and studies of other thyroid hormone disrupters have found that long-term exposures can cause more serious harm at lower levels of exposure. [97] Recent studies have shown that PBDEs can act in concert with PCBs and other chemicals through similar mechanisms to increase their effects. [98, 99, 75] One study found that exposure to a combination of PCBs and PBDEs affected motor skills of lab animals ten times more strongly than exposure to either chemical alone. [9, 99]

How Safe Are Current Exposures to Penta and Octa?

Penta has been shown to cause permanent impacts to the nervous system of laboratory animals in concentrations of just 4 ppb in brain tissue and 12 ppb in brain fat. [9] One study of newborn mice exposed the animals to a single dose of PBDE-99 in a period that correlates with the third trimester of pregnancy for humans. Thirty percent of the participants in EWG's study and almost 20 percent of women in a Texas study had more than 12 ppb of PBDE-99 in the fat of their breast milk.

Studies have not yet investigated the relationship between contaminant levels measured in brain tissue with breast milk or other body tissues, making it difficult to know for sure if human exposures exceed levels known to permanently damage rodent brains. [9, 99] Scientists are most concerned about the neurological impacts of PBDEs on the fetus and young child, and there are inherent difficulties in detecting subtle impacts to learning, memory and behavior in laboratory animals or humans.

How Safe Are Current Exposures to Deca?

The European Union is completing its risk assessment for Deca, and hopes to publish a final draft sometime in 2004. Preliminary drafts took a hard look at new data on the widespread occurrence of Deca in the environment, recent research showing direct toxicity, and evidence of degradation to more toxic congeners. [39, 81] The draft acknowledges significant uncertainty in assessing Deca's safety: "The substance is persistent and the consequences of low level exposure over the lifetime of long-lived organisms cannot be predicted with any certainty from the current database." [81]

To fill these data gaps, scientists recommend continued monitoring, "for levels of both the substance and its more toxic and bioaccumulate degradation products." [81] They recommend that EU member states make decisions about Deca regulation based on principles of "precautionary risk management" rather than quantitative analysis of the data. The EU risk assessment does not include the cumulative health risks of Deca in combination with those more toxic congeners or with other chemicals such as PCBs.