PBDEs and Feline Hyperthyroidism

Chow K., Beatty J.A., Barrs V.R., et al.

Vet Rec, 2014. 175(17): p.433-4.


THE recent Viewpoint article by Hill and Shaw (VR, September 6, 2014, vol 175, pp 228-229) raises interesting questions about the contribution of environmental factors in the development of feline hyperthyroidism, a condition which has increased exponentially since first being described as a clinical disease in the late 1970s (Peterson and others 1979). Our research has sought to investigate a potential link between polybrominated diphenyl ethers (PBDEs) and feline hyperthyroidism (Chow and others 2014). PBDEs are flame-retardants, whose introduction in the late 1970s coincides temporally with the recognition (and increasing frequency) of feline hyperthyroidism (Dye and others 2007). They have been implicated as endocrine disruptors in people (Wang and others 2010), and a potential link has been explored between exposure to various organohalogenated compounds (including PBDEs) and acromegaly in cats (Dirtu and others 2013). In our study, we measured serum PBDE levels (congeners BDE-47, BDE-99, BDE-153, BDE-154 and BDE-183) in 35 hyperthyroid cats and 30 age-matched control cats from Australia. We also measured PBDE levels (congeners BDE-47, BDE-99, BDE-153, BDE-154, BDE-183, BDE-197,BDE-207 and BDE-209) in matched house dust samples from a subset of 25 cats (12 of the hyperthyroid and 13 of the euthyroid control cats). The congener profiles of PBDEs in serum and dust were comparable in both groups, corroborating previous suggestions that dust is the primary route of PBDE exposure in cats (Guo and others 2012). Although there was no significant difference between serum or dust PBDE levels in hyperthyroid and euthyroid cats in our study, we did demonstrate a decreased BDE-47:BDE-99 ratio in the serum of hyperthyroid cats, which has been reported previously (Dye and others 2007). However, our study did not show any difference between PBDE levels or congener profiles in the house dust of hyperthyroid and euthyroid cats. This differs from a previous study, which measured PBDE levels in the house dust of hyperthyroid and euthyroid cats from the USA (Mensching and others 2012). The median serum PBDE levels in the Australian cats (118 ng/g lipid) were more than 20 times lower than median concentrations of 2904 ng/g lipid (Guo and others 2012) and 2683 ng/g lipid (Mensching and others 2012) reported in cats in the USA. Levels of PBDEs in Australian dust samples were also lower than those reported in studies in the USA (Mensching and others 2012). It is possible that the overall lower PBDE levels in Australia may have somewhat obscured a potential link between feline hyperthyroidism and PBDE exposure. However, as feline hyperthyroidism remains an extremely common endocrinopathy of aged cats in Australia (despite lower environmental and sera levels of PBDEs in this country), our research suggests that PBDEs alone are not solely responsible for the development of feline hyperthyroidism. Since it remains possible that PBDEs (or, indeed, other environmental goitrogens) could contribute to the development of feline hyperthyroidism in genetically predisposed individuals, more work should continue investigating potential genetic and environmental causes of this common disease.