Developing bird embryos may be affected by a number of thyroid disrupting chemicals through maternal transfer. However, thyroid disruption in developing embryos of wild birds remains largely unstudied, especially with respect to exposure to ubiquitous environmental contaminant classes including halogenated flame retardants (HFRs). The objective of the present study was to investigate responses of the hypothalamic-pituitary-thyroid (HPT) axis of developing birds that are exposed to elevated concentrations of HFRs in their environment. Ring-billed gulls (Larus delawarensis) were collected at the external pipping stage (i.e., just prior to hatching) from two sub-populations that are differentially exposed to HFRs in the St. Lawrence River (QC, Canada). Plasma levels of thyroid hormones (THs) and transcription levels of thyroid-related genes in three tissues (i.e., liver, thyroid gland and brain) were related to liver concentrations of HFRs in pipping gulls from these two colonies. Liver polybrominated diphenyl ether (PBDE) concentrations were negatively correlated with plasma total T4 and total T4/T3 in pipping ring-billed gulls. Moreover, plasma TH levels and hepatic PBDE concentrations were correlated with the transcription of genes involved in metabolism (deiodinases type 1, 2 and 3) and synthesis (sodium iodide symporter and thyroglobulin) in the thyroid gland, negative feedback loop (thyrotropin and corticotropin releasing hormones) in the brain and the pituitary and targeted action (TH receptors) in the three tissues of gulls. The present study suggested that the alteration of TH homeostasis in developing wild birds through changes in the transcription of several thyroid-related genes may be related to potential PBDE-mediated effects.