Have you heard the hype on flame retardants as they relate to pets? Cats, it’s argued in one small study, are sensitive to these PBDE’s (polybrominated diphenyl ethers). They’re a ubiquitous ingredient in computers, electronics and furniture foam padding—and our cats might actually be getting thyroid disease from them.
It’s gotten chic to criticize environmental hazards in vet medicine. That’s generally a good thing, mind you. We vets need to turn a more jaundiced eye towards potential epidemiological risks in household products, among others. Yet epidemiology is a veterinary discipline that’s been slacking, funding-wise, relative to sexier topics like newfangled drugs and challenging new orthopedic surgeries.
That’s in spite of the overwhelming evidence that epidemiology in pets is crucial to understanding many public health hazards for humans. We’ve long known that pets make great sentinels for human disease and other dangers, which is partly why I’m passionate about this statistically rigorous field of study. Talk about killing two birds with one stone. After all, pets do make a difference in human health—especially when we look for environmental connections between the two.
That’s why the EPA funded a study of 23 cats: 11 with hyperthyroidism and 12 without. The 11 cats had marginally higher levels of PBDEs in their blood. No smoking gun with a sample size so small and results so minimally exciting, but enough data to potentially finance another, larger study on the chemical (which is alarmingly seen in higher levels among US citizens).
Hyperthyroidism in cats has become a hot topic since it was discovered (and heavily hyped) that the incidence of this now-common disease has skyrocketed in the past 30 years. The disorder stems from a benign tumor which afflicts this gland so that it produces the metabolism-enhancing thyroid hormone (the one we all wish we had more of when it comes to standing naked in front of a mirror).
But is it really true? Is hyperthyroidism the result of chemicals like PBDEs (as in this recent study)? wet cat foods? (studies demonstrate a correlation) and organophosphates? (another putative variable found in flea collars and other insecticides).
After all, how many cats in 1977 were routinely tested for hyperthyroidism? How many cats back then lived past the age of thirteen? How many cats pre-pet revolution even made it to the vet, even as they died of “age-related” emaciation? So you know, this is a disease of older cats—one that makes them lose weight dramatically in spite of a hefty appetite (and often yields gastrointestinal symptoms, too). In fact, I seldom detect it in cats under twelve years of age.
Sure, I’m concerned. Of course I believe we’re all exposed to higher concentrations of chemicals than ever before. No doubt a wide variety of rising-tide disorders like obesity, cancer and allergies are related to more than just poor diet, pollutants and global warming, respectively. Given all the circumstantial evidence, why shouldn’t we believe we’re almost invariably besieged by post industrial revolution environmental factors? Isn’t the confirmed impact of DDT on our avians enough of a signal?
I spent one winter working for the CDC in both Atlanta and Anchorage. It was heaven—especially the woods surrounding the former city and the back-country north of the latter. I worked with a young PhD epidemiologist studying animals as sentinels for cancer. I’ll never forget her zeal, her Border collies and her depression over the dwindling dollar amounts available for her research.
But this kind of work is exactly where vet medicine should be headed—as much for humans as for pets and other animals. Feline hyperthyroidism is only the tip of the iceberg. Too bad the EPA and NIH so far haven’t seen fit to direct serious funds toward veterinary epidemiology. Without these, how are we ever to tease out the intricacies of exposure-related disease?