Flame retardant linked to thyroid disease in cats?

[Tina B and crew]

Traci...I wasn't sure where to post this so feel free to move it to the appropriate location if needed.

There was a small article in the paper the other day about a common flame retardant possibly being linked to thyroid disease in cats. The chemical is polybrominated diphenyl ethers or PBDEs. If what I have read is correct they quit using it in 2004, but it is contained in many foams used as carpet paddings and in furniture as well as in electronics and one article even said it could be in pet food! Please tell me why pet food companies would have a flame retardant in the foods? I'm baffled...I really am. It seems every time we turn around there is something else endangering our pets. With two hyperthyroid cats (one who is still alive) I have to wonder if this is the cause? Personally I will never have carpet again...and I'm looking to alternatives for furniture...but what is a person to do?

Anyway, I just wanted to alert everyone if they hadn't heard this...

Here is a link to one article and if you do a google news search for fire retardant + cats + thyroid you will come up with a bunch...



http://www.sciencedaily.com/releases/20 ... 122354.htm

[Traci]

Tina, let me do alittle research into this and will get back to you.....

[Tina B and crew]

Thanks Traci...I think the studies right now are preliminary and they haven't done widespread research yet. BUT...I have to believe that many of these chemicals are not safe for our animals. I think about the amount of time they spend grooming and in close contact with carpet. I did read on article that alluded to the way it gets in food is through contamination of fish from the ocean. I think most of us know now to feed fish to our cats on a regular basis anyway...but a lot of people still do it! Let me know what you find out. Regardless I will never have carpet simply for the cleanliness factor.

[Traci]

Well, unfortunately, it appears the full report is not available at this time. I can only go by the abstract, which one should not view as a complete report.

Before anything, let me just say that before anyone gets the wrong idea, PBDE's are not intentionally added to pet foods nor human foods. It is theorized that there are many reasons it can end up in the food source, and those theories seem to be getting numerous.

Such examples are via manufacturing processes (storing raw materials in barrels or drums that already contain trace amounts of the chemical, pre-2003 and 2004 rulings by the EPA); or processes where emissions may allow settling of chemical dust on crops, or other food sources where it enters the food chain by other means. This also might or might not correlate with another theory, that being that animal fats in foods may be contaminated (i.e., livestock eating contaminated feed, etc). Some studies done found that animal fats in human foods (mostly fish) was a leading cause, but also followed by meats and dairy products. Another theory (and well-documented) is fish sources, with salmon appearing to be the highest source, although other types of fish are suspect. Yet another theory that might or might not correlate is fish oils in supplements, like cod liver oil, salmon fish oil, etc, since it is theorized the salmon is already contaminated before it is manufacturered into the supplement.

So these are only a few, and mostly theorized ways the chemical gets into the food chain, for both humans and pets.

It should be noted that in the press release, this study notes a couple things that are concerning:

First, the study (abstract) was only done on 23 cats, not a very high control group, and admittedly, a preliminary study. Also, long-term studies must be considered. We don't know if any prior studies were done to monitor PBDE levels in cats: if they were, when, and what was the control group number, what was the route of exposure indicated, what clinical parameters were monitored, and against what number of clinically healthy cats with similar environments. For all we know, PBDE concentrations in serum levels in cats could have been there all along from other sources (which may be impossible to know for certain). I don't know if the authors intended to make a correlation but the following "quote" from the published "article/url" says:

The epidemic of hyperthyroidism in cats began almost 30 years ago, at the same time when PBDEs were introduced into household materials as a fire-prevention measure. Although the disease was first discovered in the U.S., it has since been diagnosed in Canada, Australia, Japan and many parts of Europe.

First, I would not call it an "epidemic". 30 years ago, veterinary medicine was not advanced enough to recognize feline hyperthyroidism on a consistent basis, let alone specific serum tests we have today to test for it. Also, with the advance of veterinary diagnostics and knowledge/clinical research we have available today, we also have to take into account that we know our cats are living longer and therefore new diseases previously undiagnosed or recognized are becoming more distinguishable, as our pets are living longer and will ineviteably develop a disease condition such as hyperthyroidism (amoung various others). Also, pet owners today are more conscious about their pets' health and will be more likely to recognize problems and get them diagnosed sooner than they did 30 years ago. 30 years ago, most pet owners didn't take their ailing pets to a vet and certainly didn't spend the money for additional diagnostics. Pet owners are more willing to spend money on diagnostics and treatments today than they were 30 years ago.

Second, in the actual study's abstract, it quotes:

Co-incident with the introduction of polybrominated diphenyl ethers (PBDEs) into household materials nearly 30 years ago, feline hyperthyroidism (FH) has increased dramatically. Risk of developing FH is associated with indoor living and consumption of canned cat food.

Again, is this a coincidence (as could millions of other coincidences in that period - the 60's and 70's were a hotbed for chemicals and drugs without adequate testing) or fact? While I applaud the authors for wanting to study, as they say, it demands further study and long-term studies, taking various factors into consideration.

Third, and maybe or maybe not so significant, the co-author Birnbaum says to the AP in a similar story one day after the abstract is published:

"The EPA study suggests household dust as the key way PBDE gets into cats, and likely, people. It also found elevated PBDE levels in certain cat food, mostly fish, but tests showed food couldn’t be blamed for the high levels in cats", Birnbaum said.

Which confuses me. Is she talking about a previous EPA study on PBDE on cats (which I could not find at the EPA site or elsewhere), or her own study?

I think both theories (environmental materials vs food supply) should be taken seriously, and studied more closely, particularly long-term studies. I also think both theories may have merit, particularly the first, since virtually everything we use that contain certain plastics and other materials will contain amounts of the chemical. And of course, because all of these materials predate the 2003-2004 EPA ruling on PBDE's, a very large percentage of households will always have this in their homes. Even the electronics sectors continue to use it (per rulings I assume), and some aren't willing to persue alternatives.

So now, I'm even more confused at the canned cat food conundrum. First we learn of pansteatitis, mercury levels in fish, vitamin deficiencies etc. Then we learn that canned cat food fed exclusively may predispose to feline hyperthyroidism. We learn that the theory is because the can (aluminum, whatever) may be of a substance of unkown origin that affects the food via manufacturing process into the food, potentially causing hyperthyroidism. Now we learn there is a new theory that it is a chemical that enters the food supply through various theorized routes of exposure may predispose cats to hyperthyroidism. With exception to the first (fact), it appears nothing further has been studied to confirm or dispute. One can only hope that the second and third remain on a long-term study list and is being studied as we speak and in a few years we will actually be through those long-term studies with results.

Maybe there's a connection, I don't know. Yet.