There is evidence that dietary factors may be important in the etiology of asthma and chronic obstructive pulmonary disease (COPD) in both smokers and nonsmokers. However, the existing data on the role of diet in the etiology of asthma and COPD come predominantly from cross-sectional studies. Prospective data are needed to properly address the role of diet in the development of asthma and COPD. Air pollution clearly exacerbates existing lung disease, but a role in the incidence of asthma and COPD in adults is not established. Prospective data are necessary to properly examine this association, but such data are few. Genetic factors are likely to play a role in modulating the effects of diet, smoking, and ambient air pollution on the risk of adverse respiratory outcomes in adults. Genetic factors may influence the metabolism of nutrients in food that are responsible for health effects. Both diet and genetics may combine to influence susceptibility to adverse effects of air pollution. Effects of air pollution are likely to be weak when averaged over whole populations and identification of susceptibility factors will help to clarify health consequences of air pollution. I am establishing two high-quality population resources to prospectively investigate effects of diet, smoking, air pollution, genetics and their interactions in relation to asthma and COPD in adults. The first population is a cohort of 63,000 older adults of Chinese ethnicity in Singapore. The cohort was established with NCI extramural funding to examine the relationship between diet and cancer. I have expanded the study to include the assessment of asthma and chronic bronchitis. Chronic bronchitis is a COPD outcome. Field staff are beginning to recontact subjects and review records to validate asthma outcomes. The Singapore Chinese cohort is of particular interest because of the prospective collection of risk factor data. Another major strength of the study is the high quality dietary assessment, which was developed specifically for, and validated in, this population. The Singapore cohort also follows dietary patterns quite distinct from the Western populations included in existing adult respiratory studies. Other strengths of the study are the large proportion of nonsmokers and the availability of genetic samples. Although the current follow-up cycle of the Singapore study is not yet complete, we have begun to produce manuscripts. We have identified interesting associations between soluble fiber and soy intake and the risk of chronic bronchitis. After the current follow-up cycle and asthma validation is complete, we will begin analyses of genetic polymorphisms that may influence risk of asthma and chronic bronchitis and modulate effects of diet and air pollution. The second study is a collaboration with an extramurally funded cohort, the Atherosclerosis Risk in Communities (ARIC) study. We will examine relationships between traffic-related air pollution and the decline in pulmonary function over time, asthma and COPD in adults. The ARIC study is a cohort of 16,000 adults assembled in the late 1980?s in four US communities. It is one of the few large studies with longitudinal measures of pulmonary function. To examine the feasibility of investigating traffic-related air pollution as a risk factor for health outcomes in the ARIC study, we have begun a pilot study to examine the variation in traffic related air pollution at the residences of subjects. If the pilot study shows the variation in traffic density to be sufficient, we will prepare a proposal to perform a full investigation of traffic-related air pollution in the ARIC cohort. We have also sought and obtained approval for a collaboration with the ARIC study to investigate whether obesity modifies the effect of smoking on decline in pulmonary function. Obesity has recently been appreciated to be a risk factor for asthma in children and adults and appears to be related to enhanced age-related decline in pulmonary function. If obesity modifies the well-described effect of smoking, then it is possible that obesity might modify the adverse effects of air pollution.