Continued research has increased understanding of the varied classes and functions in the LT family. LTs may be released from both blood-borne and tissue-residing cells. LTs collectively stimulate the contraction of vascular and nonvascular smooth muscles, enhance vascular permeability, and control the attraction and activation of leukocytes.3Their actions are usually in conjunction with other mediators and modulators of different events, such as vasodilating prostaglandins (PGs), lipoxins, interleukins, and histamine. Levels of many of these compounds can be analyzed in bronchial washing fluid, sputum concentrate, and exhaled breath condensate (EBC). The EBC of asthmatic patients and healthy subjects contains detectable levels of LTB4, LTC4, LTD4, LTE4, and LTF4.5 Stable patients with COPD, COPD exacerbations, and moderate or severe asthma exhibit increased concentrations of LTB4 in EBC,,4,6–7 suggesting that LTB4 may be involved in exacerbations of COPD as well as in those of asthma, and may contribute to neutrophil recruitment. Other eicosanoids are also potent mediators of vasoactivity, plasma exudation, mucus secretion, bronchoactivity, cough, and recruitment of inflammatory cells. For example, the levels of PGs such as PGE2 and PGF2α in EBC are markedly increased in patients with COPD, but not in patients with asthma.9 By contrast, patients with asthma exhibit increased concentrations of thromboxane B2, while patients with COPD and healthy subjects do not.,6 The techniques of EBC analysis are simple to perform and can be repeated over the course of the illness to monitor the patient’s response to therapy. They reflect the degree of oxidative stress and help to determine the degree of reversibility of airway obstruction. Although exhaled and bronchial nitric oxide (NO) has been used the most, other mediators such as LTs may play increasing roles in the diagnosis and management of airway disease.