Gulls foraging in highly urbanized areas experience disruption in hormones and energetic metabolism
Coralie Turquois1, Marc J Mazerolle2, Sébastien Sauvé3
1Centre de recherche en toxicologie et santé de l'environnement (TOXEN), Département des sciences biologiques, Université du Québec à Montréal, Montréal, QC, Canada.
Abstract:
Studies on birds breeding in highly urbanized environments have reported high plasma levels of a range of halogenated flame retardants (HFRs) and per- and polyfluoroalkyl substances (PFAS). Exposure of birds to these organohalogens may disrupt hormone regulation and energy metabolism, potentially leading to adverse effects on reproduction and health. While the sources and pathways of exposure to certain of these organohalogens have been documented in several bird populations, little information is available on the exposure-related effects on hormones involved in energy metabolism and their cascading effects on metabolism and energy expenditure. This study aimed to assess the linkages between plasma concentrations of PFAS and HFRs, and thyroid hormones, glucocorticoids, as well as other markers of energy metabolism in nesting ring-billed gulls (Larus delawarensis) for which foraging movements were tracked for three years in the Montreal area (QC, Canada). Plasma HFR and PFAS concentrations did not vary with foraging habitat use patterns, suggesting diffuse urban sources. Plasma HFR and PFAS concentrations were associated with sex-specific hormonal and metabolic responses. Specifically, lipid-derived β-hydroxybutyrate levels in plasma of males significantly decreased with increasing PFAS concentrations, whereas this relationship was positive in females. Furthermore, triiodothyronine (T3) and β-hydroxybutyrate levels in males and corticosterone in females both significantly increased with those of HFRs. Results suggest that gulls breeding in densely populated urban environments that are highly exposed to organohalogens may experience perturbations of key hormones involved in energy metabolism leading to metabolic effects.
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