Organohalogen compounds such as polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are widely used in industry. Because of their persistence and high bioaccumulative potency, PCBs and PBDEs have been detected in both animal species and humans at significant levels. These halogenated contaminants adversely affect the endocrine system and neurodevelopment. Moreover, hydroxylated metabolites of PCBs (OH-PCBs) and PBDEs (OH-PBDEs) disrupt thyroid hormone (TH) homeostasis and have been implicated in the pathogenesis of feline hyperthyroidism.
In this recent paper from Japan the authors determined the levels and accumulation patterns of PCBs, PBDEs, and their metabolites (OH-PCBs, OH-PBDEs, and MeO-PBDEs) in the blood of pet cats and dogs collected from a veterinary hospital in Japan. To estimate the exposure routes to these chemicals, they determined the levels of dietary exposure of these pets to PCBs, PBDEs, and their derivatives from representative samples of dry and wet pet food products. In addition, they conducted in vitro demethylation experiments to confirm the biotransformation of MeOPBDEs to OH-PBDEs in the livers of dogs and cats. Finally, they compared the biotransformation capacity of PCBs and PBDEs in dogs and cats.
Chemical analyses of PCBs and OH-PCBs showed that the OH-PCB levels were 1 to 2 orders of magnitude lower in cat and dog food products than in their blood, suggesting that the origin of OH-PCBs in pet dogs and cats is PCBs ingested with their food. The major congeners of OH-/MeO-PBDEs identified in both pet food products and blood were natural products (6OH-/MeO-BDE47 and 2′ OH-/MeO-BDE68) from marine organisms. In particular, higher concentrations of 6OH-BDE47 than 2′ OH-BDE68 and two MeO-PBDE congeners were observed in cat blood, although MeO-BDEs were dominant in cat foods, suggesting the efficient biotransformation of 6OH-BDE47 from 6MeO-BDE47 in cats. In vitro demethylation experiments to confirm the biotransformation of MeO-PBDEs to OH-PBDEs was performed using liver microsomes. The results showed that 6MeO-BDE47 and 2′ MeO-BDE68 were demethylated to 6OH-BDE47 and 2′ OHBDE68 in both dogs and, whereas no hydroxylated metabolite from BDE47 was detected.
The present study suggests that pet cats are exposed to MeO-PBDEs through cat food products containing fish flavors and that the OH-PBDEs in cat blood are derived from the CYP-dependent demethylation of naturally occurring MeO-PBDE congeners, not from the hydroxylation of PBDEs. These results suggest that pet cats routinely ingest natural MeO-PBDEs in cat food products containing fish and retain their demethylated metabolites, OH-PBDEs, in the blood for a prolonged time. Further studies are needed to clarify the toxic effects of OHPBDEs such as 6OH-BDE47 on thyroid homeostasis and to establish the relationship between the exposure level and occurrence frequency of FH in pet cats.
Mizukawa H, Nomiyama K, Nakatsu S, et al: Organohalogen Compounds in Pet Dog and Cat: Do Pets Biotransform Natural Brominated Products in Food to Harmful Hydroxlated Substances? Environ. Sci. Technol. 2016, 50, 444−452