Flame Retardant Chemicals in House Dust Linked to Hyperthyroidism

The Feline Thyroid Gland: A Model for Endocrine Disruption by Polybrominated Diphenyl Ethers (PBDEs)?

D. A. Mensching, M. Slater, J. W. Scott, D. C. Ferguson, and V. R. Beasley

Journal of Toxicology and Environmental Health 2012;75:201–212.

Hyperthyroidism is the most common endocrine disorder of cats and is a frequently diagnosed disease in small animal practice. However, despite the high rate of this disease in cats (over 10% of cats aged > 10 years), hyperthyroidism is a new disease that was first described in only 1979 (1,2). The sudden appearance and subsequent increase in the prevalence of this disorder has prompted numerous epidemiology studies searching for a potential underlying cause(s). Although such investigations point to a number of environmental and nutritional factors that could play a role in the pathogenesis of this disorder, the underlying causes remain unclear (3).

One group of environmental chemicals that may contribute to thyroid disease in man includes the polybrominated diphenyl ethers (PBDEs), synthetic brominated compounds used as flame retardants in a variety of consumer products such as electronics, furniture, textiles, and construction materials (4-7).

In both man and experimental animals, PBDEs clearly disrupt thyroid hormone metabolism. Studies of rats and mice report that exposure to PBDEs lowers free and total T4 concentrations in a dose-dependent manner (8-10). In contrast, epidemiological studies in humans suggest that higher exposure to PBDEs reduces serum TSH values and may increase serum T4 concentrations (11-14).

Because PBDEs are known thyroid disruptors, these chemicals may play a role in the pathogenesis of thyroid tumors and hyperthyroidism in cats. In support of that hypothesis, major PBDE production began just before the time that hyperthyroidism was first recognized in 1979.

The purpose of this study by Mensching et al (15) was to investigate the role of PBDEs in the occurrence of hyperthyroidism in cats. To that end, they evaluated euthyroid and hyperthyroid cats and measured PBDEs in each cat's serum, diet (i.e, cat food), and environment (house dust).

Objectives of study
The role of polybrominated diphenyl ethers (PBDE) was investigated in the occurrence of feline hyperthyroidism (FH). We postulated that PBDE play a role in the development of FH, with ingestion of canned cat food and household dust serving as sources of exposure. Specific research objectives for this pilot project included the following:

1. Compare PBDE burdens in serum in age- matched euthyroid versus hyperthyroid domesticated cats to determine if hyperthyroidism correlated with heavier contaminant loads.
2. Determine the PBDE content of commercial canned cat foods and household dust to identify predominant exposure sources for domestic cats.
3. Investigate possible disruption of the hypothalamic–pituitary–thyroid axis by examining an association between serum PBDE concentrations or environmental or nutritional PBDE exposure with thyroid function tests.

Methods
The role of polybrominated diphenyl ethers (PBDE) in FH was investigated by evaluating 15 PBDE congeners in serum from 62 client-owned (21 euthyroid, 41 hyperthyroid) and 10 feral cats. Ten samples of commercial canned cat food and 19 dust samples from homes of client-owned cats were also analyzed.

Results of study
Total serum PBDE concentrations in euthyroid cats were not significantly different from those of hyperthyroid cats. Total serum PBDE in feral cats, however, were significantly lower than in either of the groups of client-owned cats. Total serum PBDEs did not correlate with serum total T4 concentrations.

Total PBDEs in canned cat food ranged from 0.42 to 3.1 ng/g, and total PBDEs in dust from 510 to 95,000 ng/g. Total PBDEs in dust from homes of euthyroid cats ranged from 510 to 4900 ng/g. In dust from homes of hyperthyroid cats, total PBDEs concentrations were significantly higher, ranging from 1100 to 95,000 ng/g. Dust PBDEs and serum total T4 concentrations were also significantly correlated.

Conclusions of study
Estimates of PBDE exposures calculated from canned cat food and dust data suggest that domestic cats are primarily exposed through ingestion of household dust. These findings indicate further study of the role of PBDE is needed in the development of FH, which might identify the cat as a model and sentinel for humans with toxic nodular goiter.

Discussion
Over the last 30 years, PBDEs have become major global contaminants. Levels of PBDEs have been detected in human adipose tissue, serum, and breast milk samples collected in Asia, Europe, North America, Oceania, and the Arctic (6,7). Exposure occurs in particular through the diet (PBDEs are present in both food, milk, and water) and the indoor environment (particularly dust) (11).

Like the PCBs, some of the toxic effects of PBDEs may derive from their structural similarity to thyroid hormones (see Figure 1) (6,7). The PCBs, PBDEs, and thyroid hormones all consist of two six-carbon rings decorated with halogens. Bromine attaches to the carbon rings of PBDEs, chlorine to those of PCBs, and iodine to those of thyroid hormone. In PBDEs, an atom of oxygen bridges the rings, whereas the rings of PCBs and thyroid hormones are linked by carbon-carbon bonds.

Figure 1. Chemical structure of PBDEs, PCBs, and T4.  The similarity of PBDE and PCBs to T4 may underlie chemicals' toxicity.

Because PBDEs are known thyroid disruptors, these chemicals may play a role in the pathogenesis of thyroid tumors and hyperthyroidism in cats. In one earlier study (16) designed to determine whether body burdens of PBDEs in hyperthyroid cats were greater than that of non-hyperthyroid cats, serum samples were collected from 11 hyperthyroid and 12 euthyroid house cats for PBDE measurement. The overall PBDE levels in cats were 20- to 100-fold greater than median levels in U.S. adults. However, due to high variability within each group, no association was detected between hyperthyroid cats and serum PBDE levels. In a follow-up study by the same group (17), the investigators again found that both normal and hyperthyroid cats had extremely high serum PBDE levels (approximately 50-times higher than levels in human residents living in California). PBDE congener patterns in these cats resembled patterns found in house dust, similar to findings in human patients (11). These results suggested that house dust, rather than diet, is the most likely route of exposure for PBDEs in the cats.

In this latest study from the University of Illinois, Mensching and colleagues measured serum PBDE in euthyroid, hyperthyroid, and feral cats (15).  Although no difference in serum PBDE concentrations was detected between the two groups of house cats, serum PBDE concentrations in the feral cats were significantly lower than in either of the groups of client-owned cats suggesting that the cat's home environment was the source of their exposure.

They also found significantly higher PBDEs in dust from homes of hyperthyroid cats, compares to the homes of euthyroid cats. A significant correlation was also found between dust PBDE levels and serum total T4 concentration in the cats (15). Estimates of PBDE exposures calculated from canned cat food and dust data strongly suggest that domestic cats are primarily exposed through ingestion of household dust, in agreement with the previous findings in cats (16,17)

My Bottom Line
Overall, these studies show that cats can be highly exposed to PBDEs, presumably through ingestion of household dust during their normal grooming behavior. These findings also provide provocative evidence for the possible role of PBDEs in the development of thyroid tumors and hyperthyroidism in cats. That said, additional investigation into the role of PBDEs in the development of hyperthyroidism in cats is certainly warranted. 

So it appears that house dust could be an important source of these chemicals for cats. They are likely ingesting PBDEs when they groom the dust out of their fur (a similar route is used to explain the linkage between environmental tobacco smoke and lymphoma in cats) (18). But what does this mean for cat owners? Should we all get rid of our flame-resistant furnishings, turn our indoor cats into outdoor cats, or vacuum and clean our houses more often? Only the last option seems to be a practical one for most of us.

Another issue concerns our own heath. Shouldn't we all be concerned about our own PBDE exposure?  Remember that this chemical doesn't act as a thyroid disruptor only in cats— it also affects all of us (4-7,11)!

References

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