Mandate of the CSTEE

In view of the recommendation by the DG XI Ad-Hoc Working Group, in particular the recommendations given in the ozone position paper section 3 (risk assessment), the CSTEE is invited to advise the Commission on the following questions:

1. Does the Committee support the proposed critical level for vegetation and ecosystem protection of AOT 40 = 3 ppm.h as a long term objective, with the same AOT 40 with a higher excess level to be used for the interim objective in the model analysis and the (interim) target value for the daughter directive ?
2. With respect to human health, does the Committee support the view that no clear no-effect level for ozone exists and that in particular below an ozone concentration of 160 µg/m³ (8-hour average) significant health effects are evident?
3. Does the Committee support the conclusion that, in order not to neglect a significant proportion of health risk, a long term objective for human health should be set at 120 µg/m³(8 hour average) (the WHO guideline level for human health) rather than at a higher level ?
4. Does the Committee agree that, with regard to the previous question, the interim target for the modelling exercise should be expressed as an AOT 60 ?
5. Does the Committee agree that health effect considerations support the framing of the interim target value as a concentration of 120 µg/m³ averaged over 8 hours with a defined number of allowed exceedances ?
6. Does the Committee support the proposed levels of 180 µg/m³ and 240 µg/m³ (1h average) for the information and alert thresholds, respectively ?
7. Does the Committee, with regard to risk assessment, support the ranking of the effects accounted for in the cost/benefit analysis, based on an uncertainty and relevance, in particular the relevance given to premature mortality from ozone exposure (sections 3.3.2 and 3 of the consultant report)?

Ozone has a variety of effects in humans and animals. Oxidative stress/damage deriving primarily from its reaction with sulphydryl groups, formation of aldehydes, and reaction with unsaturated molecules has been reported. Signs of inflammation, such as elevated levels of PGE, interleukin 6, PMNs in bronchoalveolar lavages, and immune suppression, which may be related to damage to the T-cell dependant system, are frequent following exposure to high levels of ozone. Ozone is also able to induce cellular changes such as altered membrane permeability and damage, for example to lung type I pneumocytes and ciliated epithelial cells. Even at low levels, reduced respiratory functional capacity can be observed. The available data on mutagenicity and carcinogenicity are not conclusive. It is not fully established how interdependent the above effects are, though it is a not unreasonable assumption that all may stem from initial oxidative stress.

Experimental data support the assumption that the toxicity of ozone is adequately described by Haber´s rule (effect = concentration x time) at least at environmental concentrations. Consequently, effects seen after 8 hrs exposure at 160 mg/m³ are considered similar to those after 4 hrs at 320 mg/m³.

In view of the uncertainty regarding the interdependency of these effects the following questions need to be considered for each effect.

• What is the significance for health of each of these changes? For each is there an acceptable level of change below which the effect may be regarded as insignificant in human health terms?
• What is the dose response relationship and how is it affected by duration of exposure and respiration rate? Is there an identifiable threshold dose?
• After acute exposure, is the effect reversible and, if so, how rapidly and completely?
• Does tolerance/adaptation occur on extended exposure, if so what are the implications in human health terms of this tolerance?
• Is there an identifiable at risk group(s)?
• What is the relationship between the effects arising from acute and chronic exposure?

The effects of ozone on vegetation are also documented. Similarly to humans, oxidative stress/damage due to reaction with unsaturated organic compounds, sulphydryl compounds, formation of aldehydes, hydrogen peroxide, as well as cellular changes including altered membrane permeability are described. More specifically, reduced photosynthesis, impaired CO₂ fixation and altered cell growth leading to reduction in root/shoot ratios and in flower formation are observed. This may result in ecological balance shifts as less ozone-sensitive species are favoured.

Presumably a tolerance phenomenon occurs in plants with continual exposure, though it appears to be poorly documented.

• General comments on the report

The overview of effects of ozone is quite thorough and well balanced. In regard to humans the reference concerning the likelihood of the existence of ozone exposures at which excess risk is very low and therefore not detectable, or does not exist (Anderson HR, et al. BMJ 312, 1996, 665-669) should be mentioned specifically. Although this is only one study, it nonetheless indicates the possibility and the range of concentrations at which excess risk may approach zero. The concept of dose in humans and animals is complicated by the fact that tidal volume has been shown to have a substantial influence on the effect of ozone on pulmonary function. This implies that the exercise will tend to increase the magnitude of the effect for a particular level and duration of ozone exposure compared with the at rest effect. Other factors may also influence the available dose to cause an effect.

A major difficulty in establishing the significance of slight changes in the effects in all species and in determining the lower end of the dose response relationship is that current ambient air levels of ozone in many countries are already sufficient to produce biological changes.

It is widely assumed for ozone that response is linear with dose, but the evidence does not establish this for each of the effects identified above.

Answers to questions

General remarks

From a scientific viewpoint (which is the only one appropriate for the CSTEE) standards and guidelines must have a sound basis. For neither man, animals nor for plants has a threshold been established for either acute or chronic effects. This raises the issue of what type and degree of change is of health significance

From an environmental management viewpoint there is a major additional problem as indicated above that in many areas, ozone levels are above those levels where some biological effects are known to occur. Furthermore, reducing ozone levels, in contrast to the situations for other ambient air pollutants, cannot be achieved by local action. While it is a reasonable approach to set interim target values in management terms (as proposed by the DG XI Ad Hoc Working Group) it is important to be clear whether or not they have a scientific basis.

• Question 1

PRELIMINARY CONSIDERATIONS

Accumulated exposure Over the Threshold (AOT) is defined as the sum of all excess concentrations above a specified threshold occurring within a specific period of time. It counts the exceedances weighted by their exceedance rate (ER). ER being the difference between the recorded level and the threshold.

AOT is a new concept which has not been applied previously by the CSTEE, the EC or WHO in setting ambient air standards for other pollutants. Alternative approaches set threshold and a level for significant effects or a threshold with the number of exceedences.

From an environmental management viewpoint the use of different standards for human/animals and plants is undesirable and the case for using AOT values for vegetation instead of the conventional approach of setting a value, a measuring period and exceedence limits is not founded on a good understanding of the toxicological mechanisms underlying the damage. The CSTEE has concerns on the lack of information to establish real ecotoxicological thresholds for ozone but it noted that it is frequently the case in ecotoxicology that mechanisms information is not available. The argument is based on several studies showing a linear relationship between ozone levels, using AOT as an indicator, and reduction in biomass. Whether AOT is the best indicator of the relationship between ozone exposure and other effects in plants has not been substantiated directly. However the CSTEE considers that a good correlation is likely and therefore that it currently represents the best possible approach considering the available information.

Furthermore the rationale to consider an AOT based proposal as scientifically sound is based on the use of higher tier (field, semi-field) assays using ecologically relevant end-points.

Answers to question 1

Given the limited amount of available information, both the position paper on tropospheric ozone (CSTEE/99/1 - Add. 2A) and the WHO guideline recognise that it is not possible to set a true ecotoxicological threshold for ozone. The CSTEE agrees that the selection of 40 ppb as an exposure threshold for practical purposes is a best estimate that is internationally accepted and the CSTEE considers it appropriate for the development of European criteria. From a scientific viewpoint the CSTEE acknowledged that an AOT value was a valid approach for integrating information on threshold exceedences for the protection of plants though it queried why ozone should be singled out among ambient air pollutants for this approach. It also considered that the number and spacing of exceedences was important information in predicting effects and that this data was not fully embodied in an AOT value.

The long term objective value recommended by the WHO represented the highest levels of exposure (expressed as AOT 40, at 3ppm.h) for which no statistically or ecologically relevant reduction in biomass has been found under field-semifield conditions. No additional uncertainty factor (uncertainty factor =1) was employed. The selected endpoints for observable-relevant effects were a yield reduction of more than 5% for crops and a decrease of 10% in biomass for forests. Changes below these levels were considered to be statistically not significant and of low relevance in ecological terms. The use of an uncertainty factor of 1 for field studies has been proposed in other assessments and considered acceptable in other opinions of the CSTEE when the available information was considered to cover the most sensitive species/systems. Unfortunately, the information summarised in the report does not include the results of laboratory exposures which could be useful to determine if the field/semifield studies on crops/forests correspond to the most sensitive species-systems. It is considered that these data could be highly useful as additional information to support the proposed standard.

The position paper proposes the Long-Term Objective as the most restrictive WHO guideline value setting the value of AOT 40 (daylight hours, 3 months) at 3ppm.h. This single objective also covers the effects on forest, assuming that forests are similar or less sensitive than crops and semi natural vegetation.

The proposed interim Target Value is set at a higher value than the Long-Term Objective, and therefore, must be recognised as higher than the estimated ecotoxicological threshold. This proposal must be understood as a regulatory arrangement based on cost/benefit analysis which is not supported specifically by the outcome of the scientific risk analysis.

The proposal of a single Long-Term Objective for the protection of vegetation is considered pragmatic, and the use of the most restrictive value is in agreement with the Precautionary Principle. However, the CSTEE noted that there are several factors that can affect the toxicity of ozone for plants and large differences in the actual threshold must be expected for different environmental and ecological conditions.

As a general rule, the CSTEE considers that in order to provide comparable levels of protection across the Community, when there is clear evidence of the amelioration effects of environmental factors (air, water or soil quality, weather conditions, etc.) on the toxicity of environmental pollutants, the proposed ecotoxicological thresholds should be adapted, if possible, to reflect these conditions. These adapted criteria should, as far as possible, incorporate the critical environmental parameters in their definition (e.g. some ecotoxicological thresholds for metals in water are related to the water hardness). If this approach is not possible, the criteria should be defined for the worst-case conditions while recognising that higher ecotoxicological thresholds can be accepted at the local scale if information is available to confirm the validity for the local situation.

In our current state of knowledge the scientific basis of the proposed long-term objective value (5% of yield reduction; 10% loss in biomass) is considered appropriate for the regulatory application of this objective. The CSTEE suggests the use of the proposed value, AOT 40 of 3ppm.h, as a default Long-Term Objective that must be used unless specific information for the particular environmental and/or ecological conditions is available. If this local information allows estimation of the level of exposure that produce 5% of yield reduction in agricultural crops, reductions of shoot biomass or seed production for natural vegetation or 10% loss of biomass in the most sensitive ecosystem of a particular area/region, a Local Long-Term Objective and/or Local Target Value for this particular area/region may be justified.

Recommendations:

Taking into account the present status of knowledge on ozone effects on vegetation, a critical level of AOT 40 = 3ppm hours may be assumed as suitable for protection against biomass reduction of crops and natural vegetation.

There are no particular reasons for not using the same format (i.e. AOT 40) for the interim target value. The proposed provisional range (8-9 ppm hours) is acceptable.

More research is obviously needed, particularly information on reactions of ozone with or passage through plasma membranes. The development of more precise tools (monitoring, modelling, etc.) capable of clarifying the relationships between plant yield and actual concentrations, as well as to better quantify the role of local, regional and global emissions is needed. The development of endpoints more sensitive and accurately measurable than reduction in biomass should be encouraged.

• Question 2

Ozone mostly exerts its effects on cells by producing oxidative stress (Menzel 1994). In vitro and in vivo, ozone has been reported to induce enzymes that are associated with protection of cells against oxidative stress (Boehme et al 1992, Rahman et al 1991). This explains the clinical and experimental observations of adaptive responses of the lung upon repeated exposure. Since the ozone concentrations which overwhelm the antioxidative capacity of the lung are not known, nor is there information on the dose response of the oxidative effects, a threshold of adverse ozone effects cannot be identified.

Field studies in children, adolescents, and young adults have indicated that pulmonary function is impaired after short-term ozone exposure in the range of 120-240 mg/m³. A no effect level has not been detected. Mobile laboratory studies have observed associations between impaired pulmonary function in children or asthmatics and ozone concentrations of 280-340 mg/m³. The exposures lasted several hours.

In controlled exposure studies in healthy young men engaged in moderate exercise, 160 mg/m³ for 6.6 hrs resulted in a 5 - 10% decrease in pulmonary function. The same effects were seen after 2 hrs at 360 mg/m³(McDonnell et al 1983) and after 8 hrs at 240 mg/m³(Hazucha et al 1992). This agrees with Haber´s rule, that short-term exposure to higher concentrations has similar effects to longer exposures at lower concentrations.

It is well documented that functional changes caused by ozone are subject to adaptation (Lippmann 1992). During repeated daily exposure to higher environmental ozone concentrations the effects have been shown to be most severe on day 2 and then become less pronounced every day until day 5 when practically no more effects on functional parameters were detected. Whether other lung changes are also subject to such adaptation reactions is not known.

Animal experiments

Long term inhalation exposure produced adverse effects on lung function in all species investigated at ozone concentrations down to 200 mg/m³. These included the potentiation of bacterial lung infections at 160 mg/m³, inflammation at 240 mg/m³ and morphological changes in the centriacinar region of the lung.

Since marginal effects have been found at low concentrations none of these studies which were performed at ozone concentrations found in the environment can be used to derive a NOEL. Ozone concentrations of 240 mg/m³ for 6 hrs induced in the nose of rats an increased number of inflammatory cells which were still found 18 hrs after exposure. At higher concentrations and longer exposure times these effects were increased (Hotchkiss et al 1989). An increase in DNA synthesis and epithelial hyperplasia was also seen at such exposure levels (Henderson et al 1993, Hotchkiss et al 1991, Johnson et al 1990). Using a cumulative dose of 2,880 mg/m³ x hour Rajini and Witschi (1995) still observed effects in the rat lung.

REFERENCES

Boehme DS, Hotchkiss JA, Henderson RF, Glutathione and GSH-dependent enzymes in bronchoalveolar lavage fluid cells in response to ozone. Exp Mol Pathol 56: 37-48, 1992

Hazucha MJ, Folinsbee J, Seal jr E, Effects of steady state and variable ozone concentration profiles on pulmonary function. Am Rev Respir Dis 146: 1487-1493, 1992

Henderson RF, Hotchkiss JA, Chang IY, Scott BR, Harkema JR, Effect of cumulative exposure on nasal response to ozone. Toxicol Appl Pharmacol 119: 59-65, 1993

Hotchkiss JA, Harkema JR, Sun JD, Henderson RF, Comparison of acute ozone-induced nasal and pulmonary inflammatory responses in rats. Toxicol Appl Pharmacol 98: 289-302, 1989

Hotchkiss JA, Harkema JR, Henderson RF, Effect of cumulative ozone exposure on ozone-induced nasal epithelial hyperplasia and secretory metaplasia in rats. Exp Lung Res 15: 589-600, 1991

Johnson NF, Hotchkiss JA, Harkema JR, Henderson RF, Proliferative responses of rat nasal epithelia to ozone. Toxicol Appl Pharmacol 103: 143-155, 1990

Lippmann M, Ozone. in: Lippmann M (Ed.) Environmental toxicants. Human exposures and their health effects, Van Nostrand Reinhold, New York, 465-519,1992

McDonnell WF, Horstmann DH, Hazucha MJ, Seal E, Haak ED, Abdul-Salaam S, House DE, Pulmonary effects of ozone exposure during exercise: Dose-response characteristics. J Appl Physiol 54: 1345-1352, 1983

Menzel DB, The toxicity of air pollution in experimental animals and humans: The role of oxidative stress. Toxicol Lett 72: 269-277, 1994

Rahman I-U, Clerch LB, Massaro D, Rat lung antioxidant enzyme induction by ozone. Am J Physiol 260: L412-L418, 1991

Rajini P, Witschi H, Cumulative labelling indices in epithelial cell populations of the respiratory tract after exposure to ozone at low concentrations. Toxicol Appl Pharmacol 130: 32-40, 1995

Conclusions

Exposure of healthy test persons to an ozone concentration of 160 mg/m³ for 6.6 hrs produced changes in lung function parameters and release of inflammatory cells and inflammatory mediators. These changes were reversible, subject to adaptation and have been observed under conditions of mild to moderate physical activity. Considering Habers rule (concentration x time: 160 mg/m³ x 6.6 hrs) a cumulative dose of » 1000 mg/m³ x 1 hour results, or 125 mg/m³ x 8 hrs or 250 mg/m³ x 4 hrs.

From animal experiments which showed a NOEL in the nasal epithelium of rats, Henderson et al (1993) calculated a cumulative dose of 2,880 mg/m³, however in rat lung this cumulative dose still induced effects.

It can be concluded that a NOEL cannot be defined either from the studies in man or from animal experiments. 160 mg/m³ x 6.6 hours does produce a change in healthy individuals. However, this cumulative dose which is equivalent to » 1000 mg/m³ x 1 hour (» 125 mg/m³ x 8 hrs or » 250 mg/m³ x 4 hrs) reflects marginal and reversible effects which are obtained under mild to moderate exercise. Whether they are significant in health terms for such subjects is controversial.

The CSTEE noted that the data to support this figure is largely from a single paper on healthy individuals taking exercise. In addition it is not established whether this is the most sensitive population group. Account needs to be taken of this and of the potential for longer exposures.

Recommendations:

Further work is needed to identify whether individuals taking moderate to heavy exercise are the most sensitive population group.

• Question 3

In view of the limited data-base and uncertainty about the nature of the most sensitive population group such as adults taking heavy and prolonged exercise, the long term objective for human health should be lower than 160 mg/m³ for 8 hours. The committee supports the conclusion that a level of 120 mg/m³ is scientifically justified. This level agrees with the value of 125 mg/m³ x 8 hrs, which has been calculated from the cumulative dose of » 1000 mg/m³ x 1 hour, a value being supported by the cumulative information from animal experiments and human exposure studies. The same argument has been used to define a workplace standard. The CSTEE is concerned that the data base is inadequate to identify whether a long term standard is needed and if so the level that should be used to protect human health.

Recommendations:

The CSTEE recommends more research into the possible long-term effects of chronic ozone exposure.

The CSTEE draws attention to the possible additive/synergistic effects at this dose with other pollutants which are frequently present together with ozone, especially PM10 particulates but also SOx, NOx... Research is needed to evaluate these possible interactive effects.

Question 4

In the recognised absence of a scientifically based assessment of the correlation between data from toxicological monitoring and AOT, the CSTEE does not see the benefits of expressing the exposure limits for man as AOT 60 as an alternative to 120 mg/m³ x 8 hrs although this can be acceptable until modelling of the latter is achievable. The CSTEE noted that this standard does not take into account possible long term effects from chronic ozone exposure. In order to model the consequence of long term human exposure the CSTEE recommends the use of the 8 hrs average concentration of 120 mg/ m³ as a starting point.

Recommendations:

There is a need for research:

• to verify whether or not the use of AOT is the most appropriate indication of the risk to human health from exceedences of the ozone threshold. The CSTEE also considered that it is very important to evaluate the relative merits of using AOT values, threshold exceedence values or another parameter to protect human health from ambient air pollutants.
• to identify whether there is a need for a long term standard to protect against chronic effects to human health.
• Question 5

A new standard should be expressed in a similar way to other standards. Typically other ambient air standards are expressed as a maximum or mean value with a number of permitted exceedences expressed as a percentage. Given the available data, the CSTEE considers that 120 µg/m³ represents an acceptable target value, and considers that frequency and extents of exceedances must be limited as much as possible. From a health view point defining the number of exceedences of a tentative threshold value alone has limited meaning. If the CxT value of 1000 mg/m³ is taken as a benchmark, it is the number and magnitude of exceedences of this value which are important and needs to be recorded.

Question 6

Because no science-based rationale can be provided for it, the CSTEE does not support the proposed 1-hour value of 180 mg/m³. However, from a risk management viewpoint, the CSTEE acknowledges that it may be useful as an information level. In contrast, at 240 mg/m³ average over 8 hours there are indeed sufficient scientifically relevant data demonstrating a significant adverse effect, and this therefore is accepted by the CSTEE as an alert threshold.

Question 7

Ranking in cost benefit terms, although no doubt valid for identifying environmental management options is not an area where the CSTEE presently has specific expertise. It is therefore not appropriate for the CSTEE to comment on this aspect. Premature mortality has been widely used in other contexts for cost benefit estimates, however, the population group involved and the extent to which death has been hastened is important.

Recommendations:

Regarding other health effects, the CSTEE agrees that a ranking of the effects of ozone on human health can be carried out, taking into consideration that at low levels (starting at 120mg/m3) impairment of lung function is the first reported change and that at higher exposures, other effects such as irritation, inflammatory reactions, immune dysfunctions and asthma attacks may progressively show up. Each of these effects must be examined keeping in mind the possibilities of reversibility.

The CSTEE recognises that risk/benefit evaluation will gain increasing prominence in making judgements on priorities for environmental improvements. It is concerned that assessment benefits should be subjected to the same scientific criteria as the evaluation of risk. The CSTEE proposes that detailed discussions are initiated by DG XXIV to identify how this might be achieved.

List of documents made available to the Scientific Committee on Toxicity, Ecotoxicity and the Environment via its Secretariat to help it reach the opinion requested by the services of the Commission on the subject of

"Risk assessment underpinning new standards and thresholds in the proposal for a daughter directive for tropospheric ozone"

CSTEE/99/1

Note from P. Perera (Head of Unit XI/D/3) to Mrs de Solà and Mr. Delogu on consultation of the CSTEE on the risk assessment underpinning new standards and thresholds in the proposal for a daughter directive for tropospheric ozone (with terms of reference/mandate).

CSTEE/99/1 - Add. 1/A

Position Paper on Tropospheric Ozone (Rev. 4.2, 23.01.99)

CSTEE/99/1 - Add. 1/B

Executive Summary

CSTEE/99/1 - Add. 1/C

Introduction

CSTEE/99/1 - Add. 1/D

Basic Legislative Concept For An Ozone Daughter Directive

CSTEE/99/1 - Add. 1/E

Risk Assessment

CSTEE/99/1 - Add. 1/F

Ozone Monitoring and Assessment Strategy

CSTEE/99/1 - Add. 1/G

Abatement Strategy and Cost Implications

CSTEE/99/1 - Add. 1/H

Reporting Ozone Levels

CSTEE/99/1 - Add. 1/I

Annex A : Structure and members of the Ad-Hoc Working Group

CSTEE/99/1 - Add. 1/J

Annex B : Ozone in mountainous regions and in southern Europe

CSTEE/99/1 - Add. 1/K

Annex C : Relating EMEP/RAINS scenario results to measured ozone levels

CSTEE/99/1 - Add. 1/L

Annex D : The effect of local and regional emission reductions

CSTEE/99/1 - Add. 1/M

Annex E : Urban and regional scale measures

CSTEE/99/1 - Add. 1/N

Annex F : Information to be disseminated to the public in case of exceedance of the information threshold or the general alert threshold

CSTEE/99/1 - Add. 2

WHO-guideline

Ozone and Other Photochemical Oxidants

Final draft, November 1997

CSTEE/99/1 - Add. 3

WHO-guideline

Ozone Effects on Vegetation

Final draft, December 1996

CSTEE/99/1 - Add. 4

Economic Evaluation of the Control of Acidification and Ground-Level Ozone

AEA Technology

Final Report for DG XI of the European Commission corresponding to IIASA Fifth Interim Report, Addendum 2 to Part B

July 1998.

CSTEE/99/1 - Add. 5

Appendix I - Abbreviations and Terminology.

CSTEE/99/1 - Add. 6/A

Letter from Jochen Brandt, Secretary General CONCAWE - "CONCAWE's submission concerning the basis for setting EU ozone air quality targets - 10/3/1999.

CSTEE/99/1 - Add. 6/B

Fax from the European Centre for Environment and Health Bilthoven Division (16/12/1997) - "Health effects of ozone exposure in Europe".

CSTEE/99/1 - Add. 6/C

Report no. 95/60 from CONCAWE "Determination of air quality standards bands for ozone".

CSTEE/99/1 - Add. 6/D

CONCAWE Review - Volume 5 - Number 1 - April 1996.
"Air quality standards - a focus on ozone".

CSTEE/99/1 - Add. 6/E

CONCAWE Review - Volume 6 - Number 2 - October 1997.
"An ozone abatement strategy for Europe".

CSTEE/99/1 - Add. 7

Plant Response to Air Pollution
Set of articles sent by Prof. Chambers.

CSTEE/99/1 - Add. 8

Report from Franco De Santis (1999) - CNR - Istituto Inquinamento Atmosferico (Italy)
"New Directions - Will a new European vegetation ozone standard be fair to all European countries ?"

CSTEE/99/1 - Add. 9

Understanding AOT
AOT versus NET (Number of Exceedences of the Threshold)
From K.D. van den Hout, TNO, 22 January 1998.

CSTEE/99/1 - Add. 10

The critical level for effects of ozone on crops, and the transfer to mapping
Report from J. Fuhrer - Swiss Federal Research Station for Agroecology and Agriculture - Institute of Environmental Protection and Agriculture (IUL).

CSTEE/99/1 - Add. 11

Rapid Communication in 'Environmental Pollution 87 (1995) 119-126 - "Ambient ozone (O₃) and adverse crop response: a unified view of cause and effect" by S. V. Kruppa, L. Grunhage, H.-J. Jäger, M. J. Manning, A. H. Legge & K. Hanewald (July 1994).

CSTEE/99/1 - Add. 12

An evaluation of indices that describe the impact of ozone on the yield of spring wheat (Triticum Aestivum L.)
Report from J.M. Finnan and J.I. Burke (IRL) and M. B. Jones (IRL) - 1997

CSTEE/99/1 - Add. 13

Ozone critical levels for agricultural crops - Analysis and interpretation of the results from the UN-ECE International Cooperative Programme for Crops by G. Sanders, G. Balls and C. Booth - ICP Crops Co-ordination Centre, Nottingham University

CSTEE/99/1 - Add. 14

Critical levels for ozone - a UN-ECE workshop report N° 16 - Bern, 1-4/11/1993 - Edited by Jürg Fuhrer and Beat Achermann