Surface Free Radical Activity of PM<sub>10</sub> and Ultrafine Titanium Dioxide: A Unifying Factor in Their Toxicity?

Abstract

Epidemiological evidence has been accumulating showing a strong relationship between particulate environmental air pollution (PM10) and end-points of respiratory ill health such as attacks of asthma, COPD, diminished lung function and cardio-vascular deaths (Pope et al., 1995). To date there has been no plausible biological hypothesis to explain this relationship at the very low airborne mass concentrations of particulate air pollution that are found (< 50 \ig ml). We recently hypothesised (Seaton et al., 1995) that an ultrafine (< 100 nm diameter) component of PM10 is responsible for its adverse effects. This is based on the initial studies of Oberdorster and colleagues (Feirin et al., 1992) who demonstrated that titanium dioxide in the ultrafine form (20 nm diameter) was highly inflammogenic to the lungs of rats compared to fine (200 nm diameter) TiO2 particles at the same airborne mass concentration. We now hypothesise that the adverse effects of PM10 on the lung result from free radical activity at the surface of an ultrafine fraction. We further hypothesise that the interstitialisation that was seen with UFTiO2 (Ferin et al., 1992) could similarly occur with the ultrafine component of PM10. If the ultrafine material has free radical activity then the increased surface area that is presented to the epithelial surface by a relatively small mass of ultrafine particles could compromise epithelial integrity leading to interstitialisation. We demonstrate here that ultrafine TiO2 and PM10 both have hydroxyl radical activity and that UFTiO2 is capable of causing hydroxyl radical-mediated membrane damage to erythrocytes; fine TiO2 has much less of these properties. Additionally PM10 hydroxyl radical activity is either in the ultrafine fraction or is released in soluble form.