Biochemical effects of ozone on asthma during postnatal development

Abstract

Background: Ozone exposure during early life has the potential to contribute to the development of asthma as well as to exacerbate underlying allergic asthma.

Scope of review: Developmentally regulated aspects of sensitivity to ozone exposure and downstream biochemical and cellular responses.

Major conclusions: Developmental differences in antioxidant defense responses, respiratory physiology, and vulnerabilities to cellular injury during particular developmental stages all contribute to disparities in the health effects of ozone exposure between children and adults.

General significance: Ozone exposure has the capacity to affect multiple aspects of the "effector arc" of airway hyperresponsiveness, ranging from initial epithelial damage and neural excitation to neural reprogramming during infancy. This article is part of a Special Issue entitled: Biochemistry of Asthma.

Figure 1

Ozone (O₃) reacts with surfactant phospholipids and cellular phospholipids in alveoli to for lipid ozonation products (LOP) that include lipid peroxides, 1-palmitoyl-2-(9′-oxo-nonanoyl)-sn glycero-3-phosphocholine that can stimulate IL-8 release [80], 1-Hydroxy-1-hydroperoxynonane, which activates NF-IL-6 and NF-κB upstream of IL-8 in BEAS-2B cells [81], and others that are capable of inducing local injury and inflammation.