The formula for ozone (O3) looks very similar to that of molecular oxygen, but O3 is a much stronger oxidezer than O2 -- let's examine why. The Lewis structures in Figure 1 indicate that the ozone molecule has two equivalent resonance structures, which means the electrons are delocalized. From the Lewis structure, we see that the bond order for O2 is 2 (a double bond), whereas the bond order for O3 is 1.5 (one and a half bonds). Recall that a smaller bond order means a weaker (longer) bond. When the bond order is lower, electrons are held less tightly. The lower bond order of O3 indicates that delocalized p-electrons will be more available to react with other molecules.
The prediction of relative reactivities from the Lewis structure is confirmed by the standard reduction potentials for oxygen and ozone. Reduction potentials measure the tendency of a substance to accept electrons relative to some standard, generally H+ + e- ---> 1/2H2. Both O2 and O3 accept electrons and hydrogen ions to produce water (see reduction half-reactions in Equations 1 and 2). Note: the reduction of O2 is the basis of the electron transport chain, which is discussed in the tutorial Energy for the Body: Oxidative Phosphorylation.
O2 (g) + 4H+ + 4e- ---> 2H2O (l)
eo=1.23 V at 298 K (1)
O3 (g) + 2H+ + 2e- ---> O2 (g) + H2O (l)
eo=2.07 V at 298 K (2)
The more positive the standard reduction potential, the more readily the substance accepts electrons. (Recall that DG = -nFe. DG is a measure of spontaneity, and negative values for DG indicate a spontaneous reaction. Negative values of DG correspond to positive values for the reduction potential, e.) Hence, we see that O3 is a stronger oxidizing agent than O2.
Our knowledge of chemistry predicts that high concentrations of ozone might be unhealthy because it is a stronger oxidizer than oxygen and might therefore damage lung tissue. A number of tissue culture and animal studies confirm this hypothesis. In vitro exposure to ozone causes airway epithelium damage and lipid oxidation. Human bronchial epithelial cells exposed to ozone in tissue culture release molecules that cause inflammation. Asthma is essentially an inflammation of the airways, and air pollution that causes inflammation is suspected of triggering asthma attacks. However, there is clinical evidence both for and against ozone as a cause of asthma. In vivo exposure of guinea pigs to ozone causes DNA strand breaks in tracheobronchial epithelial cells. This may mean that high ozone concentrations will contribute to increased incidence of lung cancer. The relationship between ozone levels and public health is an active area of research, and we are sure to learn more in the next few years.