The influence of thermoreceptors in human facial skin on thermoeffector responses is equivocal; furthermore, the presence of thermoreceptors in the respiratory tract and their involvement in thermal homeostasis has not been elucidated. This study tested the hypothesis that hot air directed on the face and inhaled during whole-body passive heat stress elicits an earlier onset and greater sensitivity of cutaneous vasodilation and sweating than that directed on an equal skin surface area away from the face. Six men and 2 women completed 2 trials separated by ~1 week. Participants were passively heated (water-perfused suit; core temperature increase ~0.9°C) while hot air was directed on either the face or on the lower leg (counterbalanced). Skin blood flux (laser-Doppler flowmetry) and local sweat rate (capacitance hygrometry) were measured at the chest and one forearm. During hot-air heating, local temperatures of the cheek and leg were 38.4 ± 0.8 °C and 38.8 ± 0.6 °C, respectively (p=0.18). Breathing hot air combined with facial heating did not affect mean body temperature onsets (p=0.97 and 0.27 for arm and chest sites, respectively) or slopes of cutaneous vasodilation (p=0.49 and 0.43 for arm and chest sites, respectively), or the onsets (p=0.89 and 0.94 for arm and chest sites, respectively) or slopes of sweating (p=0.48 and 0.65 for arm and chest sites, respectively). Based on these findings, respiratory tract thermoreceptors—if present in humans—and selective facial skin heating do not modulate thermoeffector responses during passive heat stress.