The experiments demonstrated that relatively low levels of SO2 inhibited shoot yield, and that increasing SO2 conc seemed to have no more of an adverse effect on the plant.

 Plant follicular symptoms to injury include necrotic injury, chlorosis and decreased pss. The extent of damage is related to; the genetic make up of the plant, developmental stage of growth, plant nutrient status, humidity and precipitation.SO2’s first access to the plant is through stomatal openings.

Once inside the leaf it is rapidly dissolved into the aqueous phase of the apoplast to form bisulphate and sulphite. Conversion of toxic sulphite to non-toxic sulphate may occur. The presence of sulphite is inhibitory to peroxidase activity and sulphite oxidation is competitive with the oxidation of phenolic compounds in lignin formation. Necrosis is governed by the accumulation of the oxidation products of phenolic compounds.Part of the SO2 absorbed is re-emitted as H2S, and can be viewed as homeostatic regulation. A certain resistance to SO2 can be built up. Fulber et al (1984) noted that young cucumber leaves absorbing high levels of SO2 were more resistant than mature leaves absorbing smaller amounts. About 60% of the SO2 absorbed were converted to SO42- by oxidation, but the young leaves emitted H2S over 100 times faster.

Short term exposure to SO2 (;50ppb) causes stomata opening; long-term exposure causes stomatal closing. This either enhances or depresses CO2 uptake and water loss. In general acute or chronic exposures to SO2 can result in a reduction in pss rate. Pratt et al (1983) showed an accumulation of total sulphur in SO2 fumigated soybean plants and a reduction in total chloroplast content. Harvey and Legge (1979) found a reduction in total ATP content in pine needles subject to chronic SO2 exposure suggesting a reduction in oxidative phosphorylation or increased energy consumption in stress repair.Plant communities are hierarchies and SO2 pollution affects are related to connectedness of hierarchy.

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Guderian (1979) showed that under SO2 exposure interspecies competition is altered. The primary effect of SO2 on more susceptible species was magnified to such a degree that they could no longer compete effectively for vital growth determining factors. Leading to a decrease in sensitive species and an increase in resistant species.Resistance will evolve when a population contains individuals with heritable differences in characters that effect fitness, e.

g. reproduction of offspring. Murdy (1979) showed that animal weed Peppergrass from a SO2 polluted copper basin in Tennessee, USA, showed significantly less flower sterility after exposure of inflorescence to 0.8ppm SO2 for 9hours, than populations outside the basin.

The population did not differ in sterility in the absence of SO2. However, resistance has energy costs that may reduce yields, or alter the species niche, therefore it would be an error to assume that breeding or evolution of resistance will always compensate for stress from SO2 and other pollutants.There are a number of natural and anthropogenic sources that release SO2 into the atmosphere.

Fuel combustion, metal smelting and oil and natural gas processing produce vast amounts of SO2. Of the 194 tonnes of SO2 emitted annually 83% is duel to fossil fuel combustion. The heat generated by the combustion process carries the SO2 convectively into the atmosphere. SO2 reacts with NO2 and OH in the atmosphere to produce acid rain.

SO2 and acid rain have detrimental effects on vegetation such as chlorosis and reduction of photosynthesis.