Ozone is a secondary pollutant which is well established to have significant impacts on crop production and forest vitality in Western Europe and North America (Ashmore, 2003). Its regional-scale distribution means that its overall impact may be widespread; for example, critical levels set to prevent adverse effects to sensitive crops, forest trees and wild plants are exceeded over most of Europe.

Furthermore, increased pollutant emissions coupled with a favourable climate mean that ozone may now pose a significant threat in many developing countries (Emberson et al., 2003). There is evidence of a steady increase in global background concentrations, which is reflected in trends of increased mean concentrations in national records (Coyle et al., 2003).

Furthermore, the global background ozone concentration is predicted to increase further throughout this century (e.g. Stevenson et al., 2000), leading to more widespread and more frequent exceedance of thresholds for effects on the most sensitive species.

In order to predict and quantify the impacts of O3, it is essential to understand its pathways and fate from the ecosystem to the molecular level (Taylor & Hanson, 1992). For example, Busotti and Gerosa (2003) have recently argued that impacts of O3 on forests in the Mediterranean may be substantially lower than in other regions of Europe, despite the higher pollutant concentrations, because of the lower stomatal conductance, denser leaf anatomy and the abundance of primary and secondary metabolites protecting from oxidative stress.

To address such issues air quality guidelines for O3 impacts on vegetation are now introducing the use of flux based indices to characterize O3 dose (UN/ECE, 2003) which is recognised as being far more closely related to damage than simple exposure indices (Fuhrer, 2000). The use of this flux based approach requires in-depth understanding of the processes governing O3 deposition and detoxification of the absorbed stomatal O3 flux and most progress, to date, has been largely dependant on air phase measurements, combined with modelling (Fowler et al., 2001).

Based on current knowledge of O3 deposition processes, a dry deposition module has been developed by Emberson et al. (2001) for use within the photo-oxidant model employed by the UN/ECE to develop European pollution abatement strategies (Simpson et al. 2000). However, key uncertainties in the formulation of this and similar models exist which, until now, were thought intractable using standard empirical methods.

The research proposed here will, for the first time, explain and quantify the processes controlling O3 deposition through the use of 18O as a tracer. Likewise, existing methods are limited in the information which they can provide on the reaction pathways of O3 and its derivatives, in the apoplast, or within the cell.

Current estimates of injury caused by absorbed O3 dose rely on empirical “flux-response” functions that only exist for a very limited number of species. Attempts at modelling detoxification processes (e.g. SODA model of Plochl et al., 2000) have concentrated on the importance of th reactions of O3, and its derivatives, with apoplast ascorbate (ASC; vitamin C; Barnes et al., 2002). However, it is clear from other studies, that additional cell wall components comprise an important, if not vital, forward-defensive barrier which shields the plasmalemma from O3 attack.

This research will use novel 18O tracer methods to identify the principal reaction targets in the leaf apoplast/cell walls, and examine 18O label incorporation into specific apoplast constituents to assess the significance of O3 reactions in the leaf apoplast and the threshold flux at which the apoplast defences are breached by the pollutant.