GSF - Forschungszentrum fur Umwelt und Gesunhelt GmbH, Institut fur Biochemische pflanzenpathologie, D-85764 Oberschleissheim, Germany

Soon after the direct ('abiotic') phytotoxic effects of ozone and other air pollutants had been discovered, evidence for interactions of air pollutants with 'biotic' plant diseases also started to accumulate. About as many cases of decreased as of increased biotic diseases caused by ozone were known in 1973 [1], and about the same situation existed in the empirical phytopathological data summarized recently [2]. Tentative generalizations were that pathogens were hardly affected by ambient ozone, and that ozone appeared to weaken biotrophic and to strengthen necrotrophic pathogens by changing the host plant status.

Crop-loss programmes carried out in the USA and in Europe made extensive use of pestcides and therefore lacked significance for the biotic damage pathway of ozone. To what extent ozone alone, or in combination with pathogens, causes damage and population shifts in crop and wild plant populations not treated with pesticides is not clear. Plant primary and secondary metabolism, competitive growth and biodiversity all seem to be affected, making ambient ozone a subtle stress factor or even a selection agent. A complication of the abiotic pathway is that greatly delayed 'memory' effects may occur, and that perennial species may perceive ozone dose integrated over time rather than a short-term ozone concentration [3]. An epidemiological approach to assess the abiotic and biotic damage pathways of ozone at the whole-plant and population levels seems appropriate.

Independent new evidence for a relationship between ozone and biotic plant diseases has recently been obtained at the cellular level [3, 4]. While ozone appears to be largely destroyed in the apoplast, it seems to act through signal chains that affect the chloroplast, whose functions are generally inhibited. The cell nucleus is a second important target. Transcripts are either repressed or induced. About 40 ozone-induced genes have been identified to date. Most can be classified as belonging to one of the following five basic pathogen defence systems of plants: phytoalexins, cellular barriers (lignins, extensins and callose), pathogenesis-related proteins, signal substances (ethylene and salicylic acid), and anti-oxidative systems [3, 4]. The action of ozone is comparable to that of fungal elicitors, and ozone seems to be mistaken for a pathogenic virus or microorganism. These mechanistic results are further strong evidence for an interaction between ozone and biotic disease. The use of biomarkers for ozone should help to develop the above-mentioned epidemiological research strategy.

1. Heagie AS, 1973. Annual Review of Phytopathology 11, 365-388.
2. Manning WJ,von Thedemann A, 1995. Environmental Pollution 88, 219-245.
3. Sandermann H, 1990. Annual Review of Phytopathology 34, 347-356.
4. Sandermann H, Ernst D, Heller W, Langebartels C, 1998. Trends in Plant Science 3, 47-50.