Levels Three Times Higher in Toddlers Than Moms
Fire Retardants in Toddlers and Their Mothers: Deca Risks
This study presents evidence that U.S. children are widely exposed to Deca PBDE. Deca was measured in more than half of our participants, with higher levels in children. Median concentrations in children were 1.74 ppb. Average levels in children with detectable Deca was 4.7 ppb, with 2 children between 10 and 20 ppb lipid. Deca made up about 20 percent of the total PBDE measurements in 6 of our participants when congeners were evaluated on a molar basis. As with the other PBDEs children had higher concentrations than adults.
Deca is the most widely used PBDE, and the only form still produced in the United States. Yet Deca has evaded regulation due to the fact that it is not commonly measured in biomonitoring studies. Few laboratories have the capability to reliably detect it, due to its chemical structure and because it is a common contaminant in laboratory equipment which often complicates the quantification of low parts per billion concentrations.
Deca also passes through the body quickly, with an estimated half life of just 2 weeks, as opposed to other PBDEs with longer half-lives (Thuresson 2005). The short-residency time complicates biomonitoring studies because 75 percent of a single day exposure will be gone one month later. The finding of this chemical in more than half of participants indicates frequent ingestion of Deca via contaminated dust or foods.
We found higher Deca concentrations in kids than their mothers
Source: EWG's tests of 20 children and mothers
Like other PBDEs, Deca upsets the developing brain and reproductive system (EPA 2008d). But recent studies indicate that it also impacts the reproductive system, possibly at even lower exposure levels (Van der Ven 2008). In addition to its direct toxicity there are serious concerns that Deca breaks down in the environment to form PBDEs with fewer bromines which are more persistent and bioaccumulative in people. Deca is quickly transformed in humans even though it is still unclear into exactly which breakdown products. In workers exposed to Deca there was a clear accumulation of PBDEs with 8 or 9 bromines (Thuresson 2005). Similar results were found in rainbow trout and rats fed Deca in controlled studies (Kierkegaard 1999, Huwe 2007).
Deca manufacturers have claimed that the chemical does not pose a health risk because it is poorly absorbed, quickly excreted and therefore much less of a health concern than other PBDEs (ACC 2003). They also dismiss concerns that Deca breaks down in the environment to form Penta-type PBDEs (BSEF 2006). But these claims have been disputed by dozens of scientific publications and recent reviews by environmental and health agencies in the European Union, Canada and U.S. States of Maine, Michigan, Illinois and Washington.
Minnesota's Pollution Control Agency recently concluded that Deca shows potential to accumulate and concentrate in the food chain, is toxic, and breaks down in the environment to more harmful forms. They also found that effective alternatives are available (Minnesota PCA 2008). The Canadian government echoes these findings (Canada 2006). Michigan's 2008 summary and Washington State's 2006 review both find similar risks of harm and support a legislative ban on Deca-BDE contingent on the availability of a safe alternative (Michigan 2008, Washington 2006). The State of Maine also concurred with findings of Deca toxicity and breakdown and concludes that safer alternatives exist (Maine 2007). In 2007 Maine became the first U.S. state to fully ban Deca in its major uses.
What do biomonitoring studies tell us about Deca risks?
The measurements for young children indicate that Deca may pose a greater health threat than previously thought. Concentrations in 1/3rd of our child participants exceeded the CDC’s estimate of about 2 ppb for adults and older children. This estimate is calculated from pooled blood samples that do not give information about highly exposed sub-populations (Sjödin 2008).
The highest concentrations of Deca in our children were 12 and 19 ppb lipid, and were comparable to the only other tests of young children in the U.S., which was 2 siblings in California. The California study reported concentrations of 9 and 12 ppb in the older sibling, and 19 and 26 ppb in the younger, though much higher concentrations were reported in analysis by a different laboratory for samples taken 3 months prior (roughly 10 times higher in every family member) (Fischer 2006). Since Deca has a rapid metabolism in people, concentrations could vary widely within the 3 month sampling period. Like our test subjects these children's parents did not report any unusual sources of exposure.
Deca PBDE has now been reported in human blood from residents of Sweden, Nicaragua, Norway, the Faroe Islands, Belgium, the United Kingdom and Mexico (as reviewed by Athanasiadou 2008). Toxic metabolites of Deca, including hydroxylated PBDEs, are also detected as evidence of recent Deca exposure (Athanasiadou 2008). It appears to be detected more in umbilical cord blood, breast milk, and placenta than other body fluids (Frederiksen 2008, Gomara 2007).
Recent detections in wildlife, specifically top predators including grizzly bears and hawks, raise the issue of biomagnification in the food chain and additional concerns about the safety of this chemical for wildlife and ecological systems (Voorspoels 2006, Voorspoels 2007, Christensen 2005).
Deca breakdown has been documented in the bodies of fish and mice in laboratories and in wild animals (Stapleton 2004 Huwe 2007, Kierkegaard 1999, Van den Steen 2007). It also occurs in the environment by sunlight or bacteria, and has been documented in plastics, household dust, wastewater, and soil (Ahn 2006, He 2006, La Guardia 2007, Stapleton 2007, Kajiwara 2008).
We detected PBDEs with 7 and 8 bromines which are not commonly reported in U.S. studies and could indicate Deca breakdown or contact with items containing the seldom used Octa PBDE mixture.
PBDE-183, a type with 7 bromines, was found 6 children (30%) and 4 mothers (20%). All but one of these participants had detectable Deca, and the highest concentrations of BDE-183 was measured in the child with the highest Deca level. BDE-183 is not in the Deca mixture but would be an expected breakdown product. It is also a major component of the less common Octa mixture (La Guardia 2006).
Another trace congener, PBDE-197, containing 8 bromines was detected in every participant. Maximum concentrations were 2 ppb in lipid. PBDE-197 has been reported as part of the Octa mixture (LaGuardia 2006). Additionally rodents fed Deca had 10-fold increase of PBDE-197 in their bodies, which authors concluded was due to debromination (Huwe 2007). PBDE-197 and other PBDEs with 8 or 9 bromines have been detected in Deca-spiked dust exposed to sunlight, indicating debromination under real-world conditions (Stapleton 2007). PBDE-197 and Deca have been reported at elevated levels in the serum of Chinese electronics dismantlers (median of 310 and 83.5 ppb and a maximum of >3,000 ppb) (Qu 2007, Bi 2007). Scientists conclude that the level of these trace congeners is too high to be from impurities in the Deca mixture (Stapleton 2006).