Air Pollutant Interactions with Pests and Pathogens

Air Pollutant Interactions with Pests and Pathogens


The exponential economic growth in developed countries since the mid-nineteenth century has been accompanied by an increase in the concentrations of various tropospheric trace gases. Among the gaseous pollutants most studied during the past decades are carbon dioxide (CO2) with global distribution, ozone and peroxyacetylnitrate (PAN) with a more regional dimension, and others such as sulfur dioxide, nitrogen oxide (NO2), and hydrogen fluoride (HF), which are associated with emissions from local sources. Besides their potential to influence the global climate and their direct effects on plant growth and important factor affecting plant health. 

However, evaluation of these effects is difficult because of the diverse temporal/spatial distribution and differences in the chemical behavior and because of the complex interactions between the effects of the trace gases and agronomic factors relevant for plant resistance to diseases and insect pests, including fertilizer and pesticide use, crop variety, soil management, water supply, etc. 

Also, the direct effects of gaseous pollutants on the pathogen or insect cannot easily be separated from indirect effects on the host plants through changes in physiological processes. Experiments under controlled conditions can only reveal a limited picture of the multitude of possible effects that may occur in the field. Despite these limitations, a number of studies mainly carried out between 1970 and 2000 have resulted in a significant amount of data describing specific effects of the main trace gases on the incidence of plant diseases and insect pests. These can be compiled and used to formulate some generalizations.


Among the photooxidants, ozone has been the prevalent compound studied for its effects on both plants and plant diseases. Because its photochemical production is favored under conditions of high irradiance, direct effects of ozone on fungal or bacterial pathogens are less likely, as these only grow actively on plant surfaces during wet and cloudy periods. The same applies to soilborne pathogens.

Therefore, the main pathway for ozone effects on diseases occurs indirectly via changes in the physiology of the plant. A number of physiological changes induced by ozone are important with respect to plant disease resistance. Numerous physiological effects of ozone may impair the conditions for the growth of pathogens, particularly of biotrophs, such as accelerated aging/premature senescence, degradation of membrane lipids accompanied by increased cellular leakage, reduced net photosynthesis, increased protein degradation, or enhanced ethylene production, in combination with changes in factors directly affecting resistance. These include elevated antioxidant levels, reinforcement of cell walls (lignin, callose, extensions), induction of phytoalexins, or expression of proteins.

Although these effects may occur in most plant species, they can lead to contrasting effects on the pathogens, according to their parasitic nature. On one hand, ozone stress can cause a reduction in the growth of bacteria and biotrophic fungi such as powdery mildew and rusts, while on the other hand increased infection by necrotrophic parasites can result from ozone predisposing the plants. It has often been observed that the effect of ozone on a particular pathogen is similar to the effect of aging and senescence. The profile of ozone exposure and the dose of ozone is important because the exposure may or may not cause visible injury prior to infection.

For instance, grey mold induced by Botrytis cinerea was enhanced on ozone-injured leaves through the delivery of entry ports, while the disease was restricted on uninjured leaves after exposure to chronic ozone doses. In the latter case, the triggering of plant resistance factors may have been involved in increased resistance against fungal invasion. As the visible injury is less frequent in the field, the latter situation may be of practical importance. A few studies have addressed the interactions of virus diseases with ozone.

These studies consistently looked at changes in ozone sensitivity in virus-infected plants, and they showed that virus infections can protect plants from ozone injury. Most soil fungi can tolerate more than a 10- to 100-fold increase in atmospheric carbon dioxide concentrations. Some pathogenic aerial or soilborne fungi and bacteria were found to be inhibited only at CO2 concentrations exceeding 3–5%, and others were unaffected or even stimulated in growth and/or sporulation under these conditions. This suggests that an increase in atmospheric CO2 from 0.03–0.07% over the next 50 years will probably not have a direct effect on fungal and bacterial plant pathogens but that it may act indirectly via alterations in plant growth, physiology, and metabolic state.

Elevated CO2 can have profound effects on plants, ranging from increased photosynthesis rates to enhanced growth, elevated leaf carbohydrate contents, altered stomata regulation, etc. These changes may favor the growth of biotrophic pathogens, while increased plant growth leading to a denser canopy structure favors foliar pathogens because of more humid microclimatic conditions favoring infection. Increased biomass production will lead to larger amounts of plant litter, which, in turn, has the potential to favor the survival of necrotrophic pathogens during periods with adverse conditions.

Co-occurrence of ozone stress and elevated CO2 may partly counteract inhibitory or stimulating effects of the two trace gases on plants. This has been demonstrated in studies of the combined effects of the two gases on photosynthesis, growth, and yield. However, while CO2 may offset the deleterious effects of ozone on plant growth, the impact of ozone on plant resistance to pathogens seems to be less affected by elevated CO2. 

The point-source-related pollutant gases such as sulfur dioxide and hydrogen fluoride has decreased, but in less developed regions, negative effects may still be of great importance. Effects of SO2 were studied intensively in relation to the occurrence of pathogens associated with forest trees and agricultural crops. In some cases, trees weakened by this pollutant were found to be predisposed to infection, whereas in other cases they were not. 

Conflicting observations were also made with respect to SO2 effects on cereal pathogens. The inconsistencies may be related to whether or not the injury is caused by the pollutant prior to infection. Exposure to atmospheric hydrogen fluoride (HF) leads to an accumulation of fluoride in plant foliage to levels much higher than those present in the atmosphere. Similarly, fluoride accumulation may occur in plants growing on contaminated soils. At high concentrations, fluoride impairs the growth of some representative plant pathogens, both in vitro and in vivo.


Among the herbivorous insects, aphids attracted the most research interest, much more than, for instance, beetles, moths, and butterflies. Earlier field observations along pollution gradients in the vicinity of industrial plants, urban areas, or motorways and more recent experimental investigations using insect suction traps, filtration systems in urban air, open-top chambers, or field fumigation systems have consistently demonstrated that the growth of herbivorous insect populations in terms of their mean relative growth rate is favored by moderate levels of pollution but inhibited in more polluted environments. This general finding mainly refers to the effects of SO2 and NO2 in the vicinity of point sources or alongside motorways.

In particular, various important aphid species on crop plants such as wheat, barley, broad bean, pea, lupin, and brussels sprout or on tree species including apple, beech, pines, and spruces have consistently performed better in atmospheres with moderate levels of the two pollutants, both in the field and in closed fumigation chambers. It is generally believed that an increase in available amino acids in polluted plants leads to the stimulation of the growth of aphid populations.

Direct effects of SO2, NO2, or O3 on insects have been less studied, but the available evidence suggests that insects can largely tolerate these air pollutants at realistic levels when exposed either during feeding on artificial diets or on plants. This has been demonstrated when the host plants were exposed prior to or after the transfer of insects. Consequently, by far the most important effects of air pollutants on herbivorous insect populations are mediated through changes in the host plant. Effects of ozone have been mostly studied in closed chambers, and results have been far more complex than those of SO2 or NO2.

While many experiments have demonstrated increased growth of aphids under ozone stress, this effect was reversed or abolished either at higher temperatures or when applying ozone continuously instead of episodically. Since, in ambient air, peaks in ozone concentrations typically occur episodically, it remains unclear how both the presence of higher temperatures and a diurnal cycle acting in combination would modulate ozone effects on insect pests in the field. Ozone effects on free amino acid content in plants have been found to vary among plant species, pollutant doses, or environmental conditions. Thus, factors other than nutritive traits may be involved in the mediation of ozone effects—for instance, changes in the feeding stimuli on the plant surface.

Limited data on the effects of elevated CO2 demonstrate that insect herbivores, in particular chewing and sucking insects, grow and develop more slowly but consume more plant material. This effect can be attributed to the increased C/N ratio and the reduction in the content of free amino acids in plants grown at elevated CO2. 

While CO2 effects on population growth may be negative or not detectable, enhanced compensatory feeding of chewing insects appears to be a consistent phenomenon and may aggravate the damage to plants. Elevated CO2, a significant growth factor, affects not only the chemical plant composition but also the physical structure and density of the plant canopy, leading to altered microclimatic conditions in the field. Therefore, the combined effects of CO2, temperature, humidity, nutrient supply, and interactions with other pollutants such as ozone determine the outcome of plant-insect relationships, but present knowledge of these complex interactions is limited.


The important effects of ozone and elevated CO2 on plant diseases and insect pests. However, a general evaluation of the risk for enhanced plant diseases caused by air pollution is difficult because effects vary among different plant-pathogen relationships. Moreover, ozone in combination with elevated CO2 is less effective as compared to its effects as a single gas. It seems certain, though, that the effects of pollutants on diseases and insect pests occur preferentially through alterations in the host plants. 

However, plants can acclimate to rising CO2, leading to long-term effects that are different from those observed in controlled short-term experiments. Interacting effects from antagonists, predators, parasitoids, and environmental factors further complicate the evaluation of risks under field conditions. Therefore, a general risk assessment of enhanced diseases and pests caused by ozone stress and/or elevated CO2 is not possible. Specific risks may exist for some insect infestations in the presence of episodic ozone stress and moderate temperatures. 

mportantly, SO2 and NO2 play a major role in regions of the developing world that, at the same time, suffer from insufficient agricultural production, and an elevated risk caused by insect pests under the prevailing climatic conditions seems likely. Hence, these regions may be most threatened by air pollutant effects on insect pests in the future.

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