PBDEs have been shown to have hormone-disrupting effects, in particular, on estrogen and thyroid hormones.[10] A 2009 animal study conducted by the US Environmental Protection Agency (EPA) demonstrates that deiodination, active transport, sulfation, and glucuronidation may be involved in disruption of thyroid homeostasis after perinatal exposure to PBDEs during critical developmental time points in utero and shortly after birth.[11] The adverse effects on hepatic mechanism of thyroid hormone disruption during development have been shown to persist into adulthood.[citation needed] The EPA noted that PBDEs are particularly toxic to the developing brains of animals.[11] Peer-reviewed studies have shown that even a single dose administered to mice during development of the brain can cause permanent changes in behavior, including hyperactivity.[12]

Swedish scientists first reported substances related to pentaBDE were accumulating in human breast milk.[13] Studies by the Swedish Society for Nature Conservation found for the first time very high levels of more highly brominated PBDEs (BDE-209) in eggs of peregrine falcons.[14] Two forms of PBDEs, penta- and octaBDE, are no longer manufactured in the United States because of health and safety concerns. Based on a comprehensive risk assessment under the Existing Substances Regulation 793/93/EEC, the European Union has completely banned the use of penta- and octaBDE since 2004.[15] However, both chemicals are still found in furniture and foam items made before the phase-out was completed. The most common PBDEs used in electronics are decaBDE. DecaBDE is banned in Europe for this use and in some U.S. states. For PBDE, EPA has set reference dose of 7 micrograms per kilogram of body weight, which is "believed to be without appreciable effects". However, Linda Birnbaum, PhD, a senior toxicologist formerly with the EPA (now at NIEHS) notes concern: "What I see is another piece of evidence that supports the fact that levels of these chemicals in children appear to be higher than the levels in their parents; I think this study raises a red flag."[16]

Increasing levels of PBDEs in the environment may be responsible for the increasing incidence of feline hyperthyroidism.[17] A study in 2007 found PBDE levels in cats 20- to 100-fold greater than median levels in U.S. adults, although it was not adequately powered to establish an association between hyperthyroid cats and serum PBDE levels.[18] Subsequent studies have indeed found such an association.[19][20][21]

An experiment conducted at Woods Hole Oceanographic Institution in 2005 showed that the isotopic signature of methoxy-PBDEs found in whale blubber contained carbon-14, the naturally occurring radioactive isotope of carbon. Methoxy-PBDEs are produced by some marine species.[22] If the methoxy-PBDEs in the whale had come from artificial (human-made) sources, they would have contained only stable isotopes of carbon because virtually all PBDEs that are produced artificially use petroleum as the source of carbon; all carbon-14 would have long since completely decayed from that source.[23] The isotopic signatures of the PBDEs themselves were not evaluated. The carbon-14 may instead be in methoxy groups enzymatically added to man-made PBDEs.

A 2010 study found that children with higher concentrations of PBDE congeners 47, 99 and 100 in their umbilical cord blood at birth scored lower on tests of mental and physical development between the ages of one and six. Developmental effects were particularly evident at four years of age, when verbal and full IQ scores were reduced 5.5 to 8.0 points for those with the highest prenatal exposures after correcting for sex, ethnicity, tobacco smoke exposure, and mother's IQ.[24]