Skip to main content
. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: J Allergy Clin Immunol. 2017 Jul;140(1):1–12. doi: 10.1016/j.jaci.2017.05.010
What do we know?
The microbiome differs between atopic and non-atopic people, and these differences are seen in the first few months of life.
Children exposed to farms and biodiversity in green spaces during early life are at reduced risk of developing allergic disease, while early life exposure to HDM, cockroach, mice, and fungi promotes development of allergic disease.
Wheezing episodes associated with RSV and HRV infection increase the risk of asthma in later childhood.
There is no clear evidence that cat or dog exposure promotes or prevents development of atopy.
Prenatal and early life exposure to both indoor and outdoor air pollutants negatively impacts lung development and increases risk of wheezing and asthma.
Maternal smoking or exposure to SHS increases the risk of asthma, allergic sensitization, and atopic dermatitis.
What is still unknown?
Does alteration of the diversity and abundance of commensal microbes in early life directly impact development of allergic disease or are these differences merely markers of immune dysregulation?
What are the mechanisms by which early life farm exposure imparts protection against allergic disease?
Can asthma development be prevented by RSV and/or HRV immunization?
What air quality standards are sufficient to prevent detrimental effects on lung development and atopic disease in children?
When are children most susceptible to the effects of air pollution (prenatal, first year of life, or cumulative lifetime exposure), and what personalized interventions can be developed to reduce the risks associated with pollution exposure?
What are the most cost-effective environmental intervention strategies to prevent allergic disease, and how do these strategies vary geographically?