Although it has been long believed that cigarette smoke is injurious to the lower respiratory tract, the exact early mechanisms and early events responsible for this injury remain unclear. Maternal smoking, particularly in utero, is clearly associated with an increased risk for the later development of childhood atopy and asthma. Smoking is known to increase the inflammatory burden of the lower respiratory tract through a number of related but separate mechanisms. These include the recruitment of increased numbers of inflammatory cells, alteration in cell subtypes, enhancement of some cellular functions, and proinflammatory mediator release. In addition, cigarette smoking in vitro and in animal models appears to promote neurogenic inflammation, increase oxidative stress and lead to the elevation of cysteinyl leukotrienes, all of which could potentially lead to an amplification of the airway inflammation already present in asthmatics. Greater and more consistent effort must be given to encourage the young asthmatic not to smoke. In addition, greater effort must be spent on smoking cessation, especially in pregnant women and young asthmatics.