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:
- 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 ?
- 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?
- 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 ?
- 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 ?
- 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 ?
- Does the Committee support the proposed
levels of 180 µg/m3 and 240 µg/m3
(1h average) for the information and
alert thresholds, respectively ?
- 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/m
3
are considered similar to those after 4 hrs at
320
mg/m
3.
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
CO
2 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.
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.
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/m
3.
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/m
3.
The exposures lasted several hours.
In controlled exposure studies in healthy
young men engaged in moderate exercise, 160
mg/m
3
for 6.6 hrs resulted in a 5 - 10% decrease in
pulmonary function. The same effects were seen
after 2 hrs at 360
mg/m
3(McDonnell
et al 1983) and after 8 hrs at 240
mg/m
3(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/m
3.
These included the potentiation of bacterial
lung infections at 160
mg/m
3,
inflammation at 240
mg/m
3
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/m
3
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/m
3
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/m
3
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/m
3
x 6.6 hrs) a cumulative dose of
»
1000
mg/m
3
x 1 hour results, or 125
mg/m
3
x 8 hrs or 250
mg/m
3
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/m
3,
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/m
3
x 6.6 hours does produce a change in healthy
individuals. However, this cumulative dose
which is equivalent to
»
1000
mg/m
3
x 1 hour (
»
125
mg/m
3
x 8 hrs or
»
250
mg/m
3
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.
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/m
3
for 8 hours. The committee supports the
conclusion that a level of 120
mg/m
3
is scientifically justified. This level agrees
with the value of 125
mg/m
3
x 8 hrs, which has been calculated from the
cumulative dose of
» 1000
mg/m
3
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/m
3
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/
m
3 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/m
3
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/m
3
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/m
3.
However, from a risk management viewpoint, the
CSTEE acknowledges that it may be useful as an
information level. In contrast, at 240
mg/m
3
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
(O
3) 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