Environmental tobacco smoke (ETS) exposure is a common health concern despite legislation to limit its presence, especially in public environments. ETS exposure is associated with changes in lung development and morphology, airway hyperresponsiveness and obstruction and development of asthma and its increased severity. However these effects of ETS exposure are not universally supported. Clinical data as well as studies in laboratory animals report ETS exposure may even attenuate airway hyperresponsiveness (AHR). Therefore, we lack complete understanding of ETS effects on pulmonary function as well as its mechanism of action. Disparate clinical and laboratory reports likely result from variables of ETS exposure, degrees of atopy and mechanisms of sensitization. The present review addresses the effects of ETS on AHR reported in humans and animal models. ETS role as an adjuvant to AHR as well as it contribution to development of antigenic tolerance is also reviewed. Possible neurogenic, cellular and intracellular mechanisms of ETS-induced ARH are proposed based on the existing literature. Enhanced understanding of the effects and mechanism of ETS will enhance therapy strategies in treatment of ARH and related disease such as COPD as well as enhancing public presentation of convincing evidence to avoid ETS.