Chapter 4

INTRODUCTION

The IPCC Report suggests tropospheric ozone concentrations in the northern hemisphere have been rising for the last three decades at an annual rate of 1-2%, and acute exposures of concentrations exceeding 100 nmol mol-1 have been reported across Europe and North America during the vegetative growth periods of spring and early summer (Watson et al., 1990; PORG, 1993). The need to understand and predict the effects of rising carbon dioxide concentrations on wheat and other crops is well recognised, but in reality these effects will be complicated by rising ozone concentrations (Campbell et al., 1988; Drake and Leadley, 1991; Lawlor and Mitchell, 1991; Long 1991; Harley et al., 1992). At present there is a lack of experimental data on the interactive effects of temperature, CO2 and ozone on photosynthesis and forward prediction of such possible effects requires the development of mechanistic models. For example, the mechanistic model of Farquhar et al. (1980) and Farquhar and von Caemmerer (1982) for carbon dioxide uptake and assimilation by leaves has been widely used and validated (von Caemmerer and Farquhar, 1981; Long, 1985; Harley et al., 1992). This mechanistic model of leaf photosynthesis forms the basis of the carbon input sub-models of several key models developed for assessing the impacts of global environmental change at stand to biome level, for example BIOMASS (McMurtie et al., 1990), MAESTRO (Wang and Jarvis, 1990a; b), and WIMOVAC (Humphries and Long, 1995). The mechanistic photosynthesis model provides predictions of the effects and interactions of photon flux, temperature and CO2 on leaf photosynthesis. Perhaps this can be extended to include effects of high ozone episodes.

The earliest manifestations of acute ozone exposure on plants are reduced rates of photosynthesis and stomatal conductance (Hill and Littlefield, 1968; Reich et al. 1985; Olszyk and Tingey, 1986; Amundson et al., 1987; Miller, 1987). Recent work by Farage et al. (1991) and Farage and Long (1995) has established the apparent carboxylation efficiency, determined by the in vivo maximum capacity for carboxylation (Vcmax), as the primary change in the photosynthetic apparatus in wheat, pea and oak leaves following acute ozone exposure. Farage et al. (1991) measured photosynthetic parameters of wheat (Triticum aestivum L. cv Avalon) exposed to acute ozone concentrations. Fully-expanded second leaves of the main stem were separately exposed to 200 and 400 nmol mol-1 of ozone. Measurements were conducted at photon flux densities of 1500 µmol m-2 s-1 and leaf temperature of 20oC, for between 4 and 16 hours (Farage et al., 1991). Although a loss of photosynthetic capacity was measured, the magnitude of this loss cannot be predicted from ozone exposure alone, as ozone must first gain access to the leaf and effects will therefore be a function of stomatal conductance. The effect of ozone is further complicated by stomatal closure, observed as an exponential decline. The work of Farage et al. (1991) and Farage and Long (1995) suggests stomatal closure may be dependent upon changes in the mesophyll. Modelling the effects of ozone on photosynthesis would be greatly simplified should the stomatal response be dependent upon changes occurring in the mesophyll.

The overall aims of this chapter are to present a mechanistic model of photosynthesis incorporating the primary effect of ozone on carboxylation efficiency, and to use this model to predict the interactive effects of concurrent elevated concentrations of ozone and carbon dioxide. The objectives of this chapter are fourfold. First, to develop a basis for a mechanistic model of the effect of acute ozone exposures on leaf photosynthesis, by establishing a relationship between ozone dose and decline in apparent carboxylation efficiency, via changes in Vcmax. The theory and development of the model of acute ozone effects on the Vcmax of wheat are described, followed by a description of model parameterisation and model integration with a leaf CO2 assimilation model. Second, to use this relationship to test the hypothesis that stomatal closure during acute ozone exposure can be predicted from changes in the mesophyll, that is, from changes in Vcmax. The model simulation results are presented and discussed to determine whether the ozone induced stomatal closure under acute exposure can be predicted from the observed changes in the mesophyll. Third, to use the acute ozone model to simulate the interactive effects of a four hour exposure to acute ozone concentrations and elevated [CO2] on the rate of photosynthesis of wheat at the leaf level, via the predicted effects on Vcmax and stomatal closure. Fourth, to scale up the leaf level model of ozone effects to the canopy level in order to assess the interactive effects of ozone and elevated [CO2] on the productivity of a wheat canopy simulated to be growing at a farmland site in the arable region of East Anglia, in the UK.

MODEL THEORY AND DEVELOPMENT

Ozone enters the leaf via the stomata where it is rapidly broken down to form damaging oxidative radicals within the leaf, thereby inducing the production of protective scavenging mechanisms (Heath, 1980; Tingey and Taylor, 1982; Guderian et al., 1985; Scandalios, 1993). The biochemical effects of ozone within the leaf have recently been reviewed by Heath (1994) and a summary of effects at the molecular level can be found in Pell et al. (1994). It has been found that although limited quantities of ozone may be absorbed by the leaf with little or no effect, higher doses damage the photosynthetic apparatus in the mesophyll, initially by reducing the in vivo maximum capacity for carboxylation (Hill and Littlefield, 1969; Heagle et al., 1979; Lehnherr et al, 1987; 1988; Farage et al. 1991; Farage and Long, 1995).

A mechanism for ozone inhibition of photosynthesis is required for prediction of future ozone effects (Heath, 1994). A possible mechanism may be the overloading of the detoxification system above a critical rate of ozone delivery (Heath, 1994). Assuming that protection against O3 within the mesophyll results from metabolism of the derived "active oxygen" species, then it may be expected that the threshold for damage will be determined by the maximum rate of this metabolism. Therefore, the threshold will be determined by the potential rate of removal within the mesophyll, and so it is the flux into the mesophyll, the product of stomatal conductance and external concentration, that will be of importance, and not the external concentrations alone. Therefore, the accumulated amount of ozone entering the leaf above a threshold flux (FO3(0)), here defined as the Effective Ozone Dose (F'O3eff) might be expected to be linearly related to the effect at the initial active site, that is, the reduction in Vcmax.

If such a linear relationship is found between an effective ozone dose and the effects on Vcmax, this may then be used to determine the dependence of ozone-induced stomatal closure on Vcmax. Could the decline in stomatal conductance with ozone exposure be accounted for solely by the decline in Vcmax and resulting change in Ci? If so, this would simplify the problem of modelling ozone effects on plants. A diagram of the proposed model is represented in Figure 4.1.

To test the hypothesis that the acute ozone-induced decrease in Vcmax causes the decline in stomatal conductance via the effects on Ci, Figure 4.1, the measured values of stomatal conductance were to be compared with values predicted by this hypothesis.

4.3.1 Model parameterisation: relating Vcmax to ozone uptake

Total ozone uptake by a leaf (F'O3tot) is determined by the product of ambient ozone concentration and stomatal conductance to ozone, integrated over the time period of exposure:

F'O3tot = ò ( [O3] · gz ) . dt (4.1)

0

Whereas, the proposed effective ozone dose (F'O3eff) is to be calculated as the ozone uptake above a threshold flux (FO3(0)):

F'O3eff = ò ( [O3] · gz ) - FO3(0) . dt (4.2)

0

where stomatal conductance to ozone (gz) is determined from the stomatal conductance to H2O (gs) using the relationship:

gz = gs / 1.67 (4.3)

where 1.67 is the theoretical coefficient to convert the conductance of water to ozone (Laisk et al., 1989). However, stomatal conductance does not remain constant, and declines with the period of ozone exposure, so that the ozone dose will also decline. Farage and co-workers (1991) describe the pattern of decline in stomatal conductance with contiguous exposure to constant ozone concentrations. In order to calculate ozone uptake, exponential curves were fitted to the data of the decline in stomatal conductance with time, at both 200 and 400 nmol mol-1 ozone concentrations, using the relationship:

gz(t) = e(mt+k) + n (4.4)

where k, m and n are constants. This relationship (Equation 4.4) was only used to find the values of stomatal conductance for the calculations to determine the amount of ozone taken up by the leaves during the experiment conducted by Farage et al. (1991). For model simulations stomatal closure was to be predicted by the phenomenological stomatal equations of Ball et al. (1987) (Equation 4.5; A.11).

gs = g(0) + g(1) · (A · RH / Ca) (4.5)

The data points of Farage et al. (1991), together with the fitted curves are illustrated in Figure 4.2. The resulting curvilinear relationships were used to determine the stomatal conductance to ozone at hourly intervals. Thus, the instantaneous flux of ozone into the leaf at hourly intervals, the product of stomatal conductance, found by fitting the exponential curve to the data of Farage et al. (1991) and ambient ozone concentration (Farage et al., 1991), could be determined as follows:

FO3 = [O3] · gz (4.6)

(Figure 4.3). The resulting instantaneous flux data were then integrated using the trapezium rule to find the total dose of ozone at hourly intervals of time (Equation 4.1) which follow curvilinear patterns (Figure 4.4).

The relationship between the ozone-induced reduction in Vcmax measured by Farage et al. (1991) and the calculated total ozone dose for the two concentrations of ozone also follow curvilinear patterns (Figure 4.5). A linear relationship between the reduction in Vcmax and an effective ozone dose, that is a dose above a threshold flux, was sought. In order to determine a threshold flux (FO3(0)) that would give the "best-fit" linear relationship between the percent reduction in Vcmax and effective ozone dose, threshold fluxes, between 20 and 55 µmol m-2 s-1 were simulated, at 5 µmol m-2 s-1 intervals. The calculated effective ozone dose values for each threshold, corresponding to the data of Farage et al. (1991), were plotted against the measured percentage reduction in Vcmax.

Regression analysis (value r2) of the relationships between the effective ozone dose (for each FO3(0) tried) and measured percent reduction in Vcmax were used to determine a best correlation value of threshold flux. Regression analysis determined the "best-fit" value of threshold flux as 40 µmol m-2 s-1, to the nearest 5 µmol m-2 s-1 (r2 = 0.97) (Figure 4.6). The change of effective ozone doses with time for the two concentrations of ambient ozone were calculated (Figure 4.7). The linear relationship between the effective ozone dose, above a threshold flux, and decline in Vcmax, Figure 4.8, can be compared with Figure 4.5, which shows the relatively curvilinear relationships between total ozone dose and decline in Vcmax, at each ozone concentration.

In order to determine the dependency of stomatal closure on reduction in Vcmax, the linear relationship found between the effective ozone dose and reduction in Vcmax (Equation 4.6) was incorporated into the photosynthesis module of WIMOVAC (Humphries and Long, 1995):

D Vcmax = Kz · F'O3eff (4.7)

where Kz is the coefficient for ozone damage, equal to 0.09245.

This acute ozone model was subsequently incorporated as a sub-model within the larger model of Humphries and Long (1995). Equations 4.1 and 4.4 represent functions applied for the purpose of model construction only, and are therefore not included in Table 4.1, which lists the acute model Equations only.

4.3.2 Predicting changes in stomatal conductance

To test the hypothesis that the decline in stomatal conductance is caused by the decrease in Vcmax, via the effects on Ci (Figure 4.1) the ozone dependent decline in Vcmax was incorporated within the biochemical model of leaf photosynthesis (Farquhar et al., 1980), which is included within the leaf assimilation module of WIMOVAC (Humphries and Long, 1995) (Figure 4.9).

Table 4.1: Acute ozone model equations

The equations for the leaf photosynthesis included within the model by Humphries and Long (1995) are common to more than one chapter, and so are listed in Appendix I, Equations A.1 to A.10, and are described in Chapter Two, p.42. A definition of the symbols are listed in Appendix II and values of variables not given in Appendix II are arrived at from equations given in Appendix I.

The regulation of stomatal conductance in WIMOVAC is based on the phenomenological model of Ball et al. (1987), modified by Harley et al. (1992), which relates stomatal conductance to rates of assimilation of CO2, relative humidity (RH) and concentration of CO2 at the leaf surface (Ca) (Equation 4.5 (A.11)).

Stomatal conductance and Ci are both interdependent and in a state of continual flux, with changes in Ci causing changes in stomatal conductance, and vice versa, until equilibrium is reached. The climate change model of Humphries and Long (1995) predicts these changes within a leaf iteratively using the Newton-Raphson approach (Cheney and Kincaid, 1985). The similar interdependence of stomatal conductance and ozone uptake within the new ozone model (Figure 4.1) is also solved iteratively using this approach. The second order Runge-Kutta method of integration is used to integrate the flux of ozone into the leaf that exceeds the threshold flux. Thus the accumulated effective ozone dose is calculated with the simultaneous effects on Vcmax and stomatal conductance via the effects on Ci.

Therefore, the method used by the model to predict ozone effects can be summarised as follows: The photosynthesis model equations of Farquhar and co-workers, existing within WIMOVAC, are first used to calculate the rate of CO2 assimilation. The values of Ci and stomatal conductance are determined iteratively. The stomatal conductance values are then used to calculate the ozone uptake, by conversion to conductance to ozone, and then multiplying by the ambient ozone concentration. From the ozone uptake value, the ozone model equations developed here are used to predict the decline in Vcmax. This decline in Vcmax is determined by the photosynthesis model equations to calculate the stomatal closure, but because this is also dependent upon Ci, Ci and stomatal conductance are again solved iteratively. Another iteration between the stomatal conductance, ozone uptake and effect on Vcmax is performed before a final value for stomatal conductance at the end of a time interval is established. The resulting value of stomatal conductance is used to calculate the uptake of ozone within the passed time interval, and is stored as the stomatal conductance value for the start of the next time interval.

In order to compare the measured and predicted decline in stomatal conductance, the climate change model of Humphries and Long (1995) was parameterised with the control values of Vcmax (51.3) µmol m-2 s-1, as calculated from the data of Farage et al. (1991) and slope coefficient of stomatal conductance (g(1)), estimated as 24.63 using the method of Ball et al. (1987) within WIMOVAC, together with the relevant experimental conditions of photon flux density (1500 µmol m-2 s-1), temperature (20oC), relative humidity (71%) and ambient carbon dioxide concentration (340 µmol mol-1). Thus, the only ozone input values were the ambient ozone concentrations and times of exposure, corresponding to those used in the experiment of Farage et al. (1991).

4.3.3 Sensitivity analysis

To assess the effect of the two main variables of the ozone model on photosynthesis, a sensitivity analysis of the coefficient of ozone damage and threshold flux was conducted. Both Kz and F'O3eff were increased and decreased by 50%, and resulting simulated assimilation rates were compared with those from normal values of Kz and F'O3eff, for 4 hour exposure to ozone concentrations varying between 0 to 400 nmol mol-1. The standard conditions for model simulations were PFD of 1500 µmol m-2 s-1, Ca of 340 µmol mol-1 and temperature of 20oC.

4.3.4 Predicting the interactive effects of elevated [O3] and [CO2] on photosynthesis

The mechanistic model of acute ozone effects on wheat, together with the biochemical equations of CO2 assimilation rates of Farquhar et al. (1980) and the phenomenological model of stomatal conductance of Ball et al. (1987) were used to predict the interactive effects of ozone and elevated CO2 on photosynthesis, via the effects on Vcmax and stomatal conductance. The values of the model variables of light and temperature conditions corresponding to the ozone fumigation experiment of Farage et al. (1991) were used for two simulations of the effects of a four hour exposure to ozone concentrations between 0 and 400 nmol mol-1, first at Ca of 340 and then at 650 µmol mol-1. The values of g(0) and g(1) at elevated [CO2] had to be assumed to be the same as those at ambient [CO2], due to a lack of measured data. Thus, the values for the coefficients of stomatal conductance, g(0) and g(1) were 81.1 and 24.63, respectively, for both ambient and elevated [CO2], Table 4.2.

4.3.5 Predicting the interactive effects of elevated [O3] and [CO2] on a wheat canopy

The leaf model of acute ozone exposure effects was scaled up to the canopy level, using the simple sun-shade canopy model described previously in Chapter Three (p.77) (Table B, Appendix I, p.197). The photosynthesis parameters specifically used for the wheat canopy model are listed in Table 4.3. The [O3] variation during one day was calculated using the simple sinusoidal relationship:

[O3] = [O3]Pk - [O3]B · sin (2p · (Hr - HrPk) / 16) · 12) / 24) + [O3]B (4.8) ()

where peak ozone concentration ([O3]Pk) was set to 120 nmol mol-1, and baseline ozone concentration ([O3]B) was set to 25 nmol mol-1, based on the actual peak and base ozone concentration values measured on a day in late June in 1992, at Sibton, a rural site in Suffolk, described as flat, open cereal farmland (DOE, 1994). The simulation of the effects of ozone on assimilation rates during the day were compared with predicted assimilation rates with no ozone present, at ambient [CO2] of 340 µmol mol-1, on Julian day 180, for latitude 52oN. The corresponding assimilation rates at zero and acute ozone concentrations were then predicted for conditions where [CO2] is elevated to 650 µmol mol-1. The same simulations, at low and high [CO2] for ozone and no ozone present, were repeated at the higher peak ozone concentration of 200 µmol mol-1.

Table 4.2: Values of model parameters used in wheat leaf model simulations.

Table 4.3: Values of model parameters used in wheat canopy model simulations.

4.4.1 Prediction of decline in Vcmax and stomatal closure

Using the empirical relationship between Vcmax and ozone exposure with the assumed mechanism of a threshold flux, and parameterising the stomatal coefficient for only the initial control value of stomatal conductance, the observed change in Vcmax can be closely predicted. Ozone-induced stomatal closure can also be closely predicted (Figure 4.10) in which the decline in measured stomatal conductance is compared with predicted values.

4.4.2 Sensitivity analysis

Changing Kz by 50% alters the magnitude of damage to assimilation rates, above the threshold flux of ozone into the leaf, by altering the sensitivity of Vcmax to the effective ozone dose, Figure 4.11, top. However, changing FO3(0) does not alter the sensitivity of Vcmax to ozone dose, but changes the threshold above which damage occurs, Figure 4.11, bottom.

4.4.3 The interactive effects of elevated [O3] and [CO2] on photosynthesis

The model is used to predict the effects of ozone, at concentrations of up to 400 nmol mol-1, on the rate of CO2 assimilation, Vcmax and stomatal conductance, at both 340 and 650 µmol mol-1 [CO2]. Stomatal conductance is predicted using the equations of Ball et al. (1987), via feedback from reduced Vcmax caused by the damaging effects of ozone.

The model predicts that in elevated [CO2], exposure for four hours will cause a smaller actual and proportionate decrease in A, Vcmax and stomatal conductance than the same exposure in the current atmospheric [CO2] (Figure 4.12). Fours hours exposure at 400 nmol mol-1 [O3] is predicted to decrease A by 28.8% and 38.4% in elevated and current [CO2], respectively. The corresponding decreases in Vcmax and stomatal conductance are 27.8% and 36.5% for Vcmax, and 24.4% and 33.9% for stomatal conductance, in elevated and current [CO2], respectively.

4.4.4 The interactive effects of elevated [O3] and [CO2] on a wheat canopy

At ambient [CO2] of 340 µmol mol-1 the effect of acute ozone at a peak concentration of 120 nmol mol-1 on assimilation rate during the day is negligible, and there is no effect under elevated [CO2] (Figure 4.13). However, at [O3] concentrations of 200 nmol mol-1, the damaging effects of ozone at ambient [CO2] are only slightly greater than at 120 nmol mol-1 [O3], bearing in mind the relatively large difference in acute [O3] (Figure 4.14).

DISCUSSION Two important findings emerge from the construction of this ozone model within the work of this chapter. First, the use of a threshold based on flux rather than concentration allows prediction of effects on photosynthesis at different ozone concentrations (Figure 4.8). The first objective, to relate ozone dose and decline in apparent carboxylation efficiency, via Vcmax, has therefore been satisfied. Second, the decline in stomatal conductance can be predicted from the effects of the ozone-induced decline in Vcmax on intercellular carbon dioxide concentration (Figure 4.11). Therefore the decrease in stomatal conductance can be predicted without the need to simulate any direct effect of [O3]. Thus, the second objective is satisfied, to test the hypothesis that stomatal closure can be predicted from changes in the mesophyll, alone.

The linear relationship between the effective ozone dose, above a threshold flux, and reduction in Vcmax (Figures 4.8a and b) is in contrast to the curvilinear relationship found between the total absorbed ozone dose and reduction in Vcmax, where higher concentrations produce greater damage for equal total absorbed doses of ozone (Figure 4.5). Curvilinear patterns have also been observed for relationships between total absorbed ozone dose and other plant responses, for example, foliar injury of morning glory (Nouchi and Aoki, 1979). However, the inclusion of FO3(0) in the calculation of an effective ozone dose gives a good linear correlation between dose and effect on Vcmax, despite the large difference in ozone concentrations between the two treatments. This linear relationship between the effective ozone dose and decline in Vcmax supports the suggestion that the mechanism of acute ozone effects on photosynthesis is due to an overwhelming of the anti-oxidant protection mechanisms operating within the mesophyll, thereby allowing damage to the photosynthetic apparatus (Heath, 1994). Thus, if ozone enters the leaf too rapidly it exceeds the potential maximum removal rate of damaging radicals. It may be assumed that this maximum rate of metabolism of oxygen radical removal, determines the critical threshold flux of ozone into the leaf.

Although exposure to high concentrations of ozone have been known for some time to cause stomatal closure and reduced photosynthetic rates, the mechanisms for damage had remained unclear (Darrall, 1989; Heath, 1994). Most recent research supports the suggestion that stomatal closure occurs indirectly via the decline in photosynthetic rates, and that Vcmax is the first site of damage (Farage et al, 1991; Pell et al., 1992; Farage and Long, 1995). But a direct effect of ozone on stomatal conductance had also been suggested (Moldau, 1993). The conflicting evidence of sites of initial damage may in part be explained by variation in experimental conditions, as factors known to influence the response to ozone include vapour pressure deficit, growth stage and leaf section (McLaughlin and Taylor, 1981; Beyers et al., 1992; Reiling and Davison, 1992; Nie et al., 1993; Le Thiec et al., 1994; Younglove et al., 1994). Uneven stomatal closure across the surface of a leaf may also generate misleading results (Moldau, 1993). For this study it was assumed that Vcmax was the first site of damage, which is supported by the close linear relationship found between the effective ozone dose and the decline in Vcmax (Figure 4.8). The work of Pell et al. (1992) further supports this assumption. This study indicates that the stomatal closure induced by ozone exposure in fully-expanded second leaves of the main stem of Triticum aestivum L. cv Avalon, exposed to acute ozone concentrations under light saturated conditions, can be simulated without the need to include any direct effect on stomata. This suggests that the effect of ozone on stomatal conductance can be fully accounted for by the feedback through decreased photosynthetic capacity.

This finding simplifies the modelling of acute ozone exposure effects on wheat, by providing a simple but mechanistically based model for simulating the effects of acute ozone exposure on wheat photosynthesis under light-saturating conditions, as only the effect of ozone on Vcmax and control values of stomatal conductance need to be known. The assumptions that are made for the model need to be borne in mind when applying the model to other situations. For example, further research will be required to assess whether the mechanisms for ozone damage and protective mechanisms against damage, which in the model presented here are represented by the values of the Kz and FO3(0), respectively, will be applicable under other sitiuations, where variables as diverse as growth conditions, experimental protocols and genetic variation may influence the biochemical responses of wheat plants to ozone exposure.

The mechanistic basis of this model provides greater confidence for predicting interactive effects than empirical models. Thus, the model can be used to predict the interactive effects of elevated carbon dioxide and ozone concentrations on leaf rates of photosynthesis, so meeting the third objective. At the leaf level, the model predicts, as expected, that under elevated [CO2] the control stomatal conductance (at [O3] = 0 nmol mol-1) is lower than the stomatal conductance at ambient [CO2], due to the higher concentration of substrate for photosynthesis in the ambient air, and thus allowing stomatal closure against water loss from transpiration. The model also predicts ozone to have a less damaging effect on assimilation rates, Vcmax and stomatal conductance under elevated [CO2] (Figure 4.11). This is due to the dependence of ozone uptake on stomatal conductance. So, despite the same ambient ozone concentration at both 340 and 650 nmol mol-1 [CO2], the effective ozone dose is lower under elevated [CO2]. Therefore, in the short-term, the damaging effects of acute ozone exposure would be expected to be less under elevated [CO2] than under ambient [CO2]. However, it should be borne in mind that the interactions between increasing concentrations of O3 and CO2 in the longer time span of global warming will be more difficult to assess, as the acclimation of plants to growth conditions and the effects of genetic and phenotypic adaptation will need to be taken into account.

The predicted effects of acute ozone on a wheat canopy growing at Sibton indicate that acute ozone exposure for one day at the highest concentration that occurred during 1992 was not sufficient to cause a noticeable effect on canopy assimilation, under present carbon dioxide concentrations, and would have no effect under [CO2] elevated to 700 µmol mol-1 (Figure 4.12). Even increasing the peak ozone concentration to the, hitherto, unprecedented level of 200 nmol mol-1, only had a relatively small effect at ambient [CO2], and none at elevated [CO2] (Figure 4.13). Bearing in mind that during that year at Sibton the poor air quality standard was only exceeded on four days during the year, and that the maximum reached was no more than 120 nmol mol-1, it would seem feasible to assume that present wheat crops are adapted to the levels of acute ozone exposure that currently occur. However, different varieties of wheat have different tolerance levels to ozone, and future wheat production might benefit from research into whether the relative ozone sensitivity of various wheat cultivars is related to their values of threshold flux and/or ozone damage coefficients. The attempt to fit the model to another species, gave ambiguous results, with the lowest and highest ozone regime used by Farage et al. (1991) deviating by significant margins from the 1:1 line. However, the results are sufficiently successful to warrant further investigation.

Future research into the effects of acute ozone exposure on crop species will need to be more focused on the objectives of the research to be undertaken. In the past, for example, research has involved diverse approaches to measuring ozone exposure levels, doses and effects, with the result that no one approach has been adopted, or can be applied to all situations. Therefore, any future research into the effects of tropospheric ozone pollution must first establish what question will be answered by the research, and explain why the question is important.

If the model presented here were found to be applicable to other situations, it would provide a valuable tool in the search for methods to unify ozone research, as it would provide a method of relating all types of ozone exposure regimes, artificial or real, to ozone response, via the effective ozone dose, and would therefore have the potential to consolidate ozone information from previous research. Future avenues of research could also include investigations into the applicability of the model to variations in experimental and growth conditions, and phenomenological stage. For example, the interactions between CO2 and ozone are known to depend upon growth stage in wheat (McKee et al., 1995).

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