The carotid body is critical in regulating ventilation in response to changes in oxygen tension, and it provides essential sensory input during early development to stabilize and maintain breathing throughout life. Exposure to chronic sustained or intermittent hypoxia or sustained hyperoxia during early postnatal development differentially modifies breathing responses to acute hypoxic challenges which may be persistent or reversible with maturation. Premature infants are particularly vulnerable to early environmental exposures that modify neuronal circuits that control ventilation; these circuits continue to develop during early postnatal development. Furthermore, premature infants have less antioxidant defenses to counterbalance free radical production that is often associated with oxygen stress. In my presenation, I will compare and contrast the physiological consequences of different paradigms of oxygen stress, the molecular and cellular effects that lead to changes in structure and function of the carotid body and central networks that control breathing during development. Understanding mechanisms that disrupt respiratory reflexes is critical to evaluation and treatment of premature infants who are at high risk for persistent apnea and bradycardic events, reduced arousal responses to an asphyxial event during sleep, and sudden death. All of these adverse physiological events occur because of perturbations of the respiratory network of which the exposure to the extremes of oxygen tension may be operative