Organic Pollutants Increase Risk for Feline Hyperthyroidism

In a study recently published in BMC Veterinary Research, researchers determined that several congeners of two persistent organic pollutants—polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs)—are associated with increased risk for feline hyperthyroidism (FH). Study results have broad implications in environmental health, the researchers wrote, given the importance of thyroid hormones in early development and adulthood.

FH is the most common feline endocrinopathy. Its pathogenesis is well known, yet its etiology remains poorly understood. Although multiple factors (environmental, genetic, immune, nutritional) are believed to contribute to FH, no single risk factor has stood out as the dominant etiologic agent. Given the similarities between FH and human toxic nodular goiter, researchers noted that environmental factors affecting the feline thyroid could also affect thyroid health of humans and other animals.

PBDEs and PCBs are structurally similar to tri-iodothyronine (T₃) and thyroxine (T₄) and disrupt thyroid function. Interestingly, they have been found in house dust and canned pet food. Because indoor cats may have increased exposure to PBDEs and PCBs and cannot metabolize these pollutants very well, they may serve as sentinels for prolonged PBDE and PCB exposure, according to the researchers.

Study Design

The researchers collected serum and plasma from 51 pet cats (hyperthyroid, n = 21; control, n = 30). Gas chromatography mass spectrometry was used to detect and measure the concentrations of 13 PBDE and 11 PCB congeners in the samples.

For each congener, researchers measured the detection frequency (DFR), the percentage of samples with a congener concentration above the minimal detection limit. Logistic regression analysis was used to calculate associations between congener concentration and FH.

Sum concentrations for all PBDE and PCB congeners (∑PBDE, ∑PCB), and for those with DFRs above 40% (∑PBDE40, ∑PCB40), were calculated.

Results

Concentrations of 4 of 13 PBDE and 5 of 11 PCB congeners were significantly higher in the hyperthyroid cats than the control cats. In addition, ∑PBDE and ∑PCB values were markedly higher in the hyperthyroid cats than the control cats.

About half of each of the PBDE and PCB congeners had DFRs above 40%. When determining the association between sum congener concentrations and FH, researchers observed that ∑PCB40, not ∑PBDE40, was significantly associated with FH.

The most abundant congeners were BDE47, BDE99, PCB153, and PCB180. Of these, 3 were significantly associated with increased FH risk. Percentages of increased risk are listed below:

• BDE47: 6%
• PCB153: 29%
• PCB180: 48%

Notably, some of the less abundant congeners were also significantly associated with increased FH risk. Several of these congeners are listed below with their percentages of increased risk:

• BDE17: 83%
• BDE49: 72%
• PCB131: 77%

Conclusions and Discussion

Taken together, these study results support the hypothesis that PBDE and PCB play a role in FH etiology. The researchers, though, noted the need for longitudinal studies to observe the lifelong effect of PBDE and PCB exposure on FH pathogenesis. They also proposed conducting structure-activity analyses to determine whether a correlation exists between the structure of PBDE and PCB congeners and disruption of thyroid function.

Given the association between PBDE and PCB congeners and thyroid disease, researchers pointed out that “it is essential to develop a broader understanding of the risk that PBDE and PCB exposure poses to the health of both human and animal populations.”

Dr. JoAnna Pendergrass received her Doctor of Veterinary Medicine degree from the Virginia-Maryland College of Veterinary Medicine. Following veterinary school, she completed a postdoctoral fellowship at Emory University’s Yerkes National Primate Research Center. Dr. Pendergrass is the founder and owner of JPen Communications, a medical communications company.