There is a subgroup of cigarette smokers who are more susceptible than others to the deleterious effects of cigarette smoke and to chronic airflow obstruction. The study of histopathologic and physiologic differences between these "susceptible" smokers and "resistant" smokers, who do not develop clinically significant airflow obstruction, may lead to better understanding of host factors that determine individual susceptibility to cigarette smoke. This report puts forth the hypothesis that individual differences in number or function of pulmonary neuroendocrine cells may play an important role in determining whether cigarette smokers develop chronic airflow obstruction and perhaps other smoking-related disorders. In this context, pulmonary neuroendocrine cells and bombesin-like peptides are discussed, emphasizing those aspects most relevant to the pathobiologic consequences of cigarette smoking.