Asthma is not a disease children are born with, it has perpetuated through centuries, and from the best we can tell, is still on the rise. Every day we see children and adults who can’t breathe, who can’t work, who can’t participate in phys ed in school, and unfortunately on rare occasion those who unnecessarily die - on average 10 children per day in the US. Despite our advances in asthma genetics, the strongest predictor of developing asthma remains parental history and male gender of the child, non-modifiable risk factors. Yet development of this disease likely has its roots in environmental factors interacting with a susceptible host, interactions which mainly take place during a short period in prenatal and postnatal development. This holds the hope for disease prevention, as environmental exposures can often be modified, and this is the focus of our group’s work. We study ubiquitous and modifiable factors that we have shown to play a causal role in asthma development, respiratory infections and host oxidant defense. Our group has advanced our understanding of the clinical significance of respiratory infections and oxidant defense in the development of asthma, established the infant viral respiratory illness severity-dependent risk on early childhood asthma development and asthma severity, as well as establishing the causal role of respiratory viral infection in asthma development. In addition we have shown that persons with asthma have an increased risk for invasive infections outside the respiratory tract, establishing asthma and allergic diseases as risk factors for vaccine preventable diseases, work that has led to vaccine policy changes for influenza and pneumococcal vaccine. Our current work now extends these findings into proof of concept and early intervention studies moving ever closer to a strategy for primary disease prevention.