To investigate the mechanism(s) involved in chlordecone (CLD)-induced hypothermia, we examined colonic ( T col) and tail skin ( T sk) temperatures, preferred ambient temperature ( T a), evaporative water loss, and metabolic rate following CLD exposure in the rat. Single ip dosages (0, 50, and 75 mg/kg) in corn oil were administered to Fischer-344 rats. At a T a of 22.5°C, T col was reduced by 50 and 75 mg/kg as early as 0.5 hr, and this effect persisted for 4 hr after dosing. T col was increased 24 hr after both CLD dosages. T sk was elevated 2, 3, 4, and 6 hr after 75 mg/kg and 2 hr after 50 mg/kg. At T a of 30.5°C, T col was decreased at early exposure times after both dosages and was increased 3, 4, and 6 hr after 75 mg/kg. At 10.0°C, an enhanced hypothermia was observed 1–6 hr following 50 and 75 mg/kg CLD. The preferred T a was significantly decreased by ⋍2.8°C following CLD exposure while activity within the temperature gradient was unchanged. At 25.0°C, evaporative water loss was decreased while metabolic rate was not affected by CLD administration. To study the enhanced hypothermia at 10.0°C, metabolic rate was measured continuously for 2 hr following 75 mg/kg CLD and found to be significantly different from controls. The intensified hypothermia in the cold may be due to the inability of the CLD-treated rat to stimulate metabolic thermogenesis in response to cold in addition to the loss of body heat following cutaneous vasodilation. These data suggest that CLD-induced hypothermia at a neutral T a is associated with cutaneous vasodilation and not with a decreased metabolic rate or increased evaporative water loss.