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Thomas Bean

Publications and source records attributed to Thomas Bean.

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Thyroid disruption and oxidative stress in American kestrels following embryonic exposure to the alternative flame retardants, EHTBB and TBPH

Brominated flame retardant chemicals, such as 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (EHTBB) (CAS #: 183658–27-7) and bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH) (CAS #: 26040–51-7), have been detected in avian tissues and eggs from remote regions. Exposure to EHTBB and TBPH has been shown to cause oxidative stress and altered thyroid function in rodents and fish, yet no controlled studies have examined potential adverse effects of exposure in birds. Because flame retardants have been detected in wild raptors, we used American kestrels ( Falco sparverius ) as a model raptor to determine whether in ovo exposure to EHTBB or TBPH affected growth, hatching success, oxidative stress, or thyroid function. We exposed kestrel embryos to nominal concentrations (10, 50, or 100 ng g −1 egg weight) of EHTBB and TBPH via egg-injection on embryonic day 5. Embryonic exposure (~23 d) to EHTBB increased thyroid gland mass, reduced glandular colloid and total thyroxine (T4) in hatchling males and females, whereas deiodinase enzyme activity increased in males but decreased in females. Hatchlings exposed to TBPH in ovo exhibited reduced colloid and increased oxidative stress. Although exposure to EHTBB and TBPH caused several physiological effects (e.g., heart and brain mass), only exposure to 50 ng g −1 EHTBB appeared to reduce hatching success. Our results suggest these flame retardants may be hazardous for predatory birds. Future research should evaluate long-term survival and fitness consequences in birds exposed to these chemicals.

Environment International

Environmental contaminants of health-care origin: Exposure and potential effects in wildlife

A diverse range of fauna could be exposed to active pharmaceutical ingredients (APIs) via diet, dermal absorption or bioconcentration. Low level exposures of free-ranging wildlife to APIs has only been demonstrated for a few pathways (e.g., ingestion of fish in estuaries by piscivorous birds), and many remain hypothetical (e.g., ingestion of invertebrates in sludge amended fields by terrestrial vertebrates). Our understanding of API dose-response relationships in wildlife have only been assessed for endocrine disrupting compounds and a few veterinary therapeutics. Drug specific responses at various levels of biological organization are poorly characterized for nearly all wildlife species, and thus our understanding of risk is limited. There is interest in using a read-across approach to fill knowledge gaps for risk. This approach, using data collected in laboratory mammals and humans, would enable predictions for likelihood of adverse effects in wildlife. Given the great diversities in physiologies among species, a combination of in vivo, in vitro and in silico approaches will be required to fill the knowledge gaps for exposure, hazard and risk.

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