Our aim was to study the relationship between environmental oxidants (present in our diet and the air and include second hand tobacco smoke) and genes.

Our principle hypotheses were:

1. Asthmatic children with certain antixoidant genes will be at increased risk for troublesome asthma when exposed to environmental oxidants (including tobacco smoke and dietary vitamin E).
2. Asthmatic children with filaggrin null mutations genes will be at increased risk for troublesome asthma when exposed to environmental oxidants (including tobacco smoke and dietary vitamin E).