The developing lung is highly susceptible to damage from exposure to environmental toxicants particularly due to the protracted maturation of the respiratory system, extending from the embryonic phase of development in utero through to adolescence. The functional organization of the lungs requires a coordinated ontogeny of critical developmental processes that include branching morphogenesis, cellular differentiation and proliferation, alveolarization, and maturation of the pulmonary immune, vasculature, and neural systems. Therefore, exposure to environmental pollutants during crucial periods of prenatal and/or postnatal development may determine the course of lung morphogenesis and maturation. Depending on the timing of exposure and pathobiological response of the affected tissue, exposure to environmental pollutants can potentially result in long-term alterations that affect the structure and function of the respiratory system. Besides an immature respiratory system at birth, children possess unique differences in their physiology and behavioral characteristics compared to adults that are believed to augment the vulnerability of their developing lungs to perturbations by environmental toxins. Furthermore, an interaction between genetic predisposition and increased opportunity for exposure to chemical and infectious disease increase the hazards and risks for infants and children. In this article, the evidence for perturbations of lung developmental processes by key ambient pollutants (environmental tobacco smoke [ETS], ozone, and particulate matter [PM]) are discussed in terms of biological factors that are intrinsic to infants and children and that influence exposure-related lung development and respiratory outcomes.