The hypothesis we would like to test is that children with autism, and perhaps those with other forms of developmental delay (DD), may have elevated body polybrominatd diphenylether (PBDE) concentrations, compared to typically developing (TD) controls. Using samples of umbilical cord tissue to measure PBDE leadings is highly relevant to what the foetus would have received from the mother via the placenta. In the first instance we would like to obtain 3 samples of cord tissue of varying mass, between 0.3 and 1.5g, so that we can find out what PBDEs we can measure in samples of this size. Hopefully we will be able to meaure most of the important PBDEs in these samples so that we could proceed with a funding application to measure samples from the different study groups described above.

PBDEs have been used as flame retardants in textiles, including carpets, curtains and household furnishings, as well as in plastics and computer components, since the mid-1980s, around the time that autism prevalence began to increase globally. While the causative factors involved in an individual becoming autistic are likely to be multi-factorial, the timing of PBDE introduction in homes and workplaces, their rapid rise in the environment since the 1980s and a parallel rise of PBDE concentrations in human tissues and fluids along with their known affects on metabolism makes them environmental factors that are very worthy of further investigation. Unlike many of the other neuroendocrine and elemental toxins such as dioxins, PCBs, Hg and Pb, that are all decreasing in the environment, PBDEs have risen rapidly over the same time frame as the recorded increased prevalence of autism. While around 43 PBDE congeners have been identified the contribution to overall tissue concentrations in humans is largely represented by 10 congeners namely PBDEs 28, 47, 49, 66, 99, 100, 153, 154,183 and 209. The measurement of tissue PBDE concentrations will be conducted using state-of-the-art analytical equipment including automated solvent extraction (ASE(tm)) and gas-chromatography/mass spectrometry (GC/MS). PBDEs have known endocrine disrupting activity including alteration of thyroid hormone concentrations [they deplete T4 levels and function, as well as reducing vitamin A (retinol)]. In addition, PBDEs stimulate pro-oxidant activity resulting in an increase in the oxidised/reduced glutathione ratio (GSSG/GSH). Increased GSSG/GSH ratio and antioxidant dysfunction have been reported in patients with autism. PBDEs induce hepatic cytochrome P450 IIB1 and 1A1 hepatic detoxifying systems. Possible impairments in this metabolic detoxification in individuals with autism and/or developmental delay might make these individuals more susceptible to elevated tissue levels of PBDEs. Perhaps the greatest concern of damaging effects of PBDEs relate to developmental neurotoxicity in mice and rats. These effects include disruption of spontaneous behaviour, impaired learning and memory, hearing and memory impairments and behavioural changes. The mechanisms for these affects on behaviour and cognition are unknown but may be associated with alterations to cholinergic receptors (Viberg et al., 2002).