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Minutes of the meeting held on Friday 26th November 2004Present:
ITEM 1. OPENING REMARKS, APOLOGIES FOR ABSENCE AND ANNOUNCEMENTS Apologies for absence were received from Dr Paul Harrison, Dr Virginia Murray, Ms Alice Lambert, Prof David Strachan, Prof. Tony Frew, Mr Ronnie Alexander (Welsh Assembly). The Chairman welcomed Dr Robin Fielder, Principal Toxicologist at the HPA who will attend COMEAP as an observer. The Chairman informed Members that Professor Anderson would be attending the meeting after lunch to provide advice on the Cardiovascular Disease and Air Pollution report - paper COMEAP/2004/8 The Chairman reminded Members to submit their expenses claims forms. Blank forms had been tabled. ITEM 2. MINUTES OF THE MEETING HELD ON 25th June 2004 The Chairman took Members through the Minutes of the last meeting page
by page. Members agreed that paragraph 55 needed to reflect that the reason
why hospital admission figures were lower than mortality figures was possibly
due to stroke being managed in the home. Members noted some minor typographical changes. Members agreed that once the above-mentioned changes had been made, the minutes were agreed as an accurate record of the meeting. One Member raised the issue of anonymity within the minutes. The Secretariat and Chairman clarified the situation, stating that opinions given during meetings would not be attributed overtly to the Member who made them. However, where for example, a Member was asked to provide information, then their name could be stated against a particular action point.
It was confirmed that the next meeting of COMEAP would take place on the 18th February 2005. The Chairman, taking into account that this was the Friday of half term, asked Members whether this date was suitable. No Member present at the meeting found this date inconvenient. Dates for meetings throughout the rest of the year were discussed. These were confirmed as follows: June 24th 2005 Annual Air Pollution Meeting - Leicester The Chairman informed Members that this meeting would take place between the 19th - 22nd April 2005. It was brought to Members' attention that the format of this meeting had altered as of this coming year from being a 2 day meeting to a 4 day meeting. The Chairman handed over this item to the Secretariat to provide Members with further information. The Secretariat gave a brief history of the Annual Air Pollution meeting. Recently, however, in liaison with Defra, it had been decided that the meeting should be expanded to include presentations on the chemistry, physics and modelling fields of air pollution during the first 2 days. Work on exposure, epidemiology, clinical and toxicology would be presented on the second 2 days. It was stated that Members would not be required (but would be welcome) to attend all 4 days, but that Members would be expected to attend the last 2 days of the meeting, which, as with previous Annual Air Pollution meetings, would be treated as attendance at a COMEAP meeting. The Secretariat also informed Members that this would be the last Annual Air Pollution Meeting to be held in Leicester. A venue for the 2006 meeting had yet to be decided. Calls for tender would take place later in 2005. Declaration of Interests Finances ITEM 4: REPORT ON OZONE: HEALTH IMPLICATIONS IN THE UK COMEAP/2004/7A, COMEAP/2004/7B, COMEAP/2004/7C Dr Walton introduced the report explaining that it had been agreed to publish the report in two sections. The first section covering the review of the health evidence on ozone was being presented at this meeting. It would be followed at a later meeting by the second section which focussed on the shape of the exposure response relationship for those health outcomes believed to be related to exposure to ozone. Members' comments were invited on the text and conclusions. These comments are given below (minor comments are listed in the annex). General points It was agreed to put the conclusions to each Chapter in bold and to add a Glossary at the end of the report. Chapter 1 Introduction It was suggested that the title to Table 1 should refer to the fact that it was an extract from the 1998 COMEAP report on Quantification of the Effects of Air Pollution on Health in the UK. It should be made clear that quantification of the size of the effect of ozone on health in the UK was planned as part of the forthcoming update of the quantification report rather than in this report. There needed to be a reference to Table 1 in the text. Chapter 2 Ozone levels in the UK It was agreed that it would be made clear that the dashes in Table 2.1 meant that there was no correlation rather than that there was an absence of data. It would need to be checked that the text in paragraph 2.5 reflected this. It was suggested that the conclusions in paragraph 2.15 should be put in bold to highlight that they were the conclusions. (This was suggested for other chapters as well). Chapter 3 Methodology It was noted that the term 'relative rates' in paragraph 3.4 had not been used elsewhere in the report. It was agreed to use an alternative term and to explain how relative risks and percentage increases were related. It was agreed to add a cautionary statement to paragraph 3.9 about the
possible inaccuracy of ICD code allocations on death certificates. The
elderly often had both respiratory and cardiovascular disease and the
primary cause of death might not be obvious. Distinguishing different
types of cardiovascular deaths was also difficult*. It was noted that
it was more common for deaths to be ascribed to arrhythmias in younger
people or in people with less severe disease. On the other hand, deaths
were more likely to be ascribed to progressive forms of heart disease
such as heart failure in older people or in people with more severe disease.
It was queried whether the longer periods of ozone exposure referred to in the third sentence of paragraph 3.12 were 8 hours or 24 hours? The Secretariat explained that this sentence referred to results from chamber studies using a variety of exposure times. It was agreed to make this clear. It was pointed out that ozone could be particularly low at night not only before a high ozone day but also on other nights during a high daytime ozone period. Professor Derwent agreed to redraft the relevant section of paragraph 3.12. It was suggested that the fact that this meant that 24 hour average ozone did not represent high ozone days as well as 8 hour average ozone should be mentioned as a conclusion to Chapter 3. It was agreed that the American Journal of Epidemiology paper by Anderson et al comparing results with and without GAM models would be included in paragraph 3.18. There were still only a relatively small number of multi-pollutant model results for ozone. It was agreed that the general issue of whether to use multi-pollutant models in preference to single pollutant models for meta-analysis if more multi-pollutant model results were available would be discussed in the forthcoming quantification report. Chapter 4 The results in the chapter referred to all ages. It was suggested that some comment should be made about whether there was evidence of an effect on mortality in children. In paragraph 4.5 (iii), the Committee preferred that it was explained that the results for 1 hour average and 8 hour average ozone were strongest rather than that the results for 24 hour average ozone were weakest. The Committee believed that the fact that adjustment for other pollutants
did not result in major changes to the single pollutant model results
strengthened the conclusions in paragraph 4.5 and that this view should
be reflected in paragraph 4.13. The Secretariat explained that further paragraphs to present the results of the recent NMMAPS paper would be added. (A description of the APHEA 2 study was already included). Chapter 5 In paragraph 5.15(i), it was suggested that the phrase 'particularly in the elderly' should be clarified in terms of whether this was due to larger associations or more studies (it was both). The Secretariat explained that the view in paragraph 5.15(ii) that the evidence for asthma admissions was clearer for adults than for children was based on greater consistency between studies. The Secretariat also explained that only a few studies of associations with pneumonia admissions had been performed. These all found positive and statistically significant associations. The sentence in paragraph 5.15 (iv) was not intended to imply that many studies had been performed but only a few were available to the Committee. It was considered that there were many uncertainties in allocating a
heart disease admission to a particular type of heart disease. This was
because many of the cardiovascular health outcomes were inter-related
and could often co-exist. It was therefore agreed to delete the reference
to particular types of cardiovascular admissions in paragraph 5.15 (v).
Professor Poole-Wilson agreed to provide a note to the Secretariat on
this issue. There was discussion of the fact that increases in ozone were not related to increases in cardiovascular admissions but were clearly related to increases in cardiovascular mortality. It was noted that this was not without precedent. Some major studies of treatments for heart disease had found reductions
in cardiovascular deaths without reductions in cardiovascular admissions
(these studies were the COMET trial, the MADIT II trial ). It was agreed
that Professor Poole-Wilson would provide information on these studies.
A paragraph on this issue would be included in Chapter 9 and this paragraph
would be referred to in the appropriate section of Chapter 5. There was discussion of the results for the over 65s which were higher in Table 5.4 than in Table 5.1. The Secretariat explained that the results for the over 65s in Table 5.4 were from single studies (those that also included multi-pollutant models) whereas the results in Table 5.1 were from meta-analyses of several studies. This was explained in a footnote to Table 5.4 but it was agreed that this point should be further emphasised in the text. It was queried why, if particles were correlated with ozone and particles were also linked to hospital admissions, adjustment for particles did not make a difference to the ozone association. It was explained that, using the APHEA 2 study as an example, the summer ozone association was reduced slightly by adjustment for particles but the winter association was increased substantially. Thus, the lack of a major effect of adjustment for particles in all year ozone associations presented in the report was probably the net result of different effects of adjustment in different seasons. It was agreed to make this point in the report (perhaps in a box) and to refer to Table 2.1 in Chapter 2 which indicated positive correlations between particles and ozone in the summer and negative correlations in the winter. Chapter 6 It was suggested that the point that asthmatics were affected by ozone although not more so than the general population should be further emphasised in paragraph 6.36. It was also suggested that reference should be made to the MAAPE report on ozone which came to a similar conclusion based on chamber study evidence. There was also discussion of what this conclusion meant for the advice given in advance of summer smogs which contains specific advice for asthmatics. It was noted that in the case of reductions in lung function, for example, asthmatics already had reduced lung function so the same incremental reduction as in normal subjects could matter more in asthmatic subjects. It was also noted that the baseline rate of symptoms in asthmatics was greater so the same percentage increase as in general subjects would lead to a higher rate of symptoms. It was agreed that the advice in advance of summer smogs would be discussed separately. Although quantification was not being done in this report, it was noted
that prevalence studies were more helpful for quantification. (Odds ratios
based on prevalence could be used to derive numbers of symptom days; odds
ratios based on incidence could be used to derive numbers of symptom episodes
but the duration of the episodes would be unknown.) Mr Hurley agreed to
write a note on this and it would be raised again during discussion of
the forthcoming quantification report. It was agreed to amend paragraph 6.38 to replace 'to a similar degree in both' to 'with no evidence of a difference between'. This was to make clear that the evidence so far was not able to show a difference between asthmatics and the general population - this situation could change in the future. Chapter 7 It was suggested that the part of paragraph 7.46 on the small number of people at the tail end of the distribution should be amended/expanded. It should explain that some people had a greater than average response to ozone and that some people had an average decline in lung function but this decline could matter more if the subject's baseline lung function was already low. It was agreed that this part of the paragraph should be combined with paragraph 7.47. It was noted that paragraphs 7.49 and 7.50 were not conclusions paragraphs. It was suggested that paragraph 7.50 be used as a preamble to the chapter on long term effects. There was discussion of the fact that the lung function changes, but not some inflammatory changes, did not persist with repeated exposure. There was also discussion of studies showing increasing effects over a summer but recovery before the following summer. It was agreed that this would be discussed in the long term effects chapter. Chapter 8 Some members found it confusing that there was no positive association between long term exposure to ozone and mortality when there was an association between short term exposure and mortality. There was discussion of the fact that, if the short term exposure studies were not only affecting the very frail, then some effect might be expected to be seen in the cohort studies. However, the cohort studies might not have been powerful enough to detect a small effect. It was also noted that a long term effect on lung function growth might result in effects on mortality later in life. It was agreed to discuss these issues in the report. Chapter 9 It was suggested that paragraph 9.60 should explain that Bradford Hill's framework had been used for discussion but that the conclusion on causality depended on an overall view rather than any one of Bradford Hill's individual features. Members considered that the positive associations between ozone and reductions
in lung function and increases in symptoms were very likely to be causal.
It was also considered that genetic studies, in addition to toxicological
studies and human volunteer studies added to the plausibility that the
associations were due to ozone. It was agreed to incorporate these views
into paragraph 9.61. Professor Holgate agreed to provide some more detailed
text on the genetic studies to go in an earlier section of the chapter. It was pointed out that paragraph 9.62 did not come to a clear conclusion. It was suggested that the last sentence was amended to 'Given this, we consider that the positive associations between ozone and respiratory admissions are likely to be causal'. It was suggested that less emphasis should be placed on the case fatality argument as this was not the only possible explanation for an association with cardiovascular mortality without an association with cardiovascular admissions. It was agreed that paragraph 9.64 would be amended to take this into account and to make clear that the causality of the associations was less clear for cardiovascular than for respiratory mortality. It was agreed to separate the research recommendation in paragraph 9.64 into another paragraph. The above comments would be incorporated into the conclusions to chapter 9 and a revised version would be circulated soon after the meeting. It was agreed that the Executive Summary and Chapter 8 would be circulated to the main Committee for comments in writing. The Committee was content for the Chairman and subgroup to clear the rest of the report. Annex to Item 4 This annex records minor changes to the text of the ozone report mentioned at the meeting.
The Chairman updated Members on progress to date. He reminded Members that the Sub-group had presented their findings at a British Heart Foundation Workshop on the 5th October to a small group of cardiologists, so initiating formal links with the Cardiological community. The Chairman informed Members that the day had been well received and that the consensus from the audience was that there was some effect of air pollution on the cardiovascular system taking place. The Chairman informed Members that the Secretariat, in their search for the latest paper from the Seventh Day Adventists Study, had found that there had been no further full peer reviewed papers published on this study. The Chairman informed Members that he and the Secretariat had had an editing meeting on the 25th November, during which the report had been substantially modified. Sections of the report were now as follows: Executive Summary The Secretariat informed Members that they had drafted some background
information which was to be edited-in to the mechanisms chapters. The
reference section for this was being written. It was agreed that once
the references had been completed the chapter would be sent to the key
authors for final agreement. The Chairman informed Members that at this meeting, they were required to agree the Summary, Conclusions and Recommendations chapter of the report and that general comments, other than typographical errors, would be noted. Members provided general comment on the report prior to discussion of the summary, conclusions and recommendations chapter. Whole report - general comments Members unanimously agreed that the report had progressed enormously and that generally, it read very well. It was noted that there had recently been a flood of literature in the
cardiological journals on the effects of air pollutants on the cardiovascular
system. This included a statement from the American Heart Association
on air pollution and cardiovascular disease* which contained a good background
section on air pollutants. It was requested that background information
provided within the Committee's report should be retained, as it would
be of great value to cardiologists reading the report. It was suggested
that the inclusion of a picture of a particle in this section of the report
would be useful. It was suggested that the general risk factors for heart disease given
on p21 of the report should be listed in order of importance. It was requested that the word 'clotting' be changed to 'thrombosis'
throughout the document. Given the discussion on ICD codings and cardiovascular event diagnosis
in the ozone report, it was agreed that Professor Poole-Wilson and Professor
Anderson would write a short paragraph for Chapter 2 to explain the difficulties
in precisely allocating ICD codes to the different cardiological outcomes. Members thought that the recommendations given in the Summary, Conclusions and Recommendations chapter were good and that a large range of issues had been tackled. One Member suggested that further research, especially in man was required.
The general consensus was that it was a good piece of work, that the document read well and provided a good overview in terms of the range of issues tackled. However, Members noted the following: i) that the discussion of the Bradford Hill features of causality interrupted
the sequence of questions a) to h). The chapter was not just giving a
summary or conclusions but also substantial amounts of discussion. This
should be reflected in the title of the chapter. ii)that the arguments for causality and mechanisms were much less certain than those for the lung. iii)that the first few paragraphs could be improved. v)that a paragraph providing the discussion and the conclusions from
the animal toxicology chapter had been omitted. vi)that a summarising paragraph in the toxicology section of the report
needed to be brought forward. vii)that some indication of the scale of the problem in public health
terms was needed. This was necessary for policymakers and cardiologists
to put the effects in context. An IOM report which quantified the long-term
effects of particles on cardiovascular mortality was noted. It would also
be useful to be able to draw a parallel with the effects of passive smoking
on heart disease as had been done in the COMEAP report on the long-term
effects of particles and in the annex on smoking. The Secretariat clarified
that it was not planned to undertake a full quantification of the effects
in this report - this would be done in the forthcoming quantification
report QUARK II. However, it would be possible .to include something on
the comparison with passive smoking in paragraph 14. viii)that the comparison between the effects of air pollution and passive
smoking on heart disease also be reflected in the Executive Summary. Page by page discussion of paper COMEAP/2004/8 Paragraph 5 summarised recent developments in the thrombosis and neural
hypotheses and it was questioned by the Secretariat whether either hypothesis
had really been proved or disproved. It was considered that the paragraph
could be strengthened by adding a sentence on the evidence from the animal
toxicology studies. It was also requested that something should be added
on inflammation. It was requested that the word 'falsified' should be changed to 'disproved'
in paragraph 5. Members wished to avoid the use of the terms prudent and imprudent in paragraph 6. It was considered that prudence applied to actions whereas paragraph 6 referred to the Committee's views about causality. The Secretariat agreed to replace paragraph 6 with a paragraph more similar
in style to that of paragraph 11(i).. It was agreed that paragraph 6 would
build firstly the conclusions made from the short-term exposure studies'
data and then the long-term exposure studies' data. Members agreed to
provide comment on the re-drafted paragraph by correspondence. The Committee considered that it was very likely that the positive associations
between short term exposure to pollutants and cardiovascular mortality
and admissions were causal. There was more discussion over how likely
it was that the positive association between long-term exposure to particles
and cardiovascular mortality was causal. Some members considered that
concluding that the associations with long-term exposure were very likely
to be causal was too strong as there were only a few studies. Other members
were more convinced by the results.. It was agreed that the Secretariat
would re-draft paragraph 6 using the term 'likely' or 'very likely' as
appropriate, after which the committee would consider this point again. The Secretariat informed Members that the last sentence of paragraph
7 was to be deleted as it was incorrect. It was requested that the basis
for the term 'convincing' was clarified in paragraph 7 - was this due
to the level of statistical significance of the associations or due to
the support for causality from other evidence? Members' attention was directed towards three tables which summarised
the meta-analysis results from the time series studies. These were: It was agreed that the results from these tables needed to be clearly
reflected in the conclusions. Members wished to ensure that any rearrangements of the table did not result in losing clarity regarding the consistency of the positive associations. It was suggested that the text of paragraph 8a) could specify the proportion of positive associations. The table on page 157 should indicate that the random effects column
was in percentage change per 10 µg/m3 (except CO which was per 10
mg/m3). All pollutants were for 24 hour averages except ozone which was
for an 8 hour average. It was agreed that a paragraph analogous to paragraph 8a) (which referred
to associations with short-term exposure) should be added on the effects
of long-term exposure. It was noted that paragraph 8(b) which provided text on the strength
of the associations, only discussed the acute effects. It was agreed a
sentence on chronic effects would be added by the Secretariat. It was questioned whether the reference to the strength of the associations
given in paragraph 8b was based on the level of statistical significance
or on the size of the coefficients. The Secretariat informed Members that
the magnitude of effects was what was being assessed. It was agreed that
this would be made clear and that the title would be amended to 'How large
are the associations'. It was noted that the importance of the strength of the association in
terms of likely causality was that large associations were less likely
to be substantially altered by the presence of residual confounding. It
was agreed that a sentence on this would be added. It was requested that it should be acknowledged in paragraph 8b) that
the associations between air pollution and cardiovascular outcomes are
not strong in Bradford Hills' terms. Professor Anderson informed the Committee that the results for cardiovascular admissions from APHEA 2 had been published which contained details on effect modification. The results for cause specific mortality had yet to be published. It was requested that Professor Anderson provided the Secretariat with
these papers. A Member requested that a footnote should be added to explain 'confounding'
and 'effect modification'. It was agreed that these would be explained
earlier in the text in Chapter 2. Professor Anderson agreed to edit this
in to the chapter as requested. Specificity Members agreed that the idea of considering specificity of mechanisms
rather than of outcome was good (one mechanism can result in more than
one clinical outcome so associations with several outcomes does not necessarily
mean a lack of specificity). Ideally, this would be tested by specifying
the mechanistic hypothesis a priori. Chapter 2 had explained that it was
difficult to find differences between the results for the different diagnoses
in the time series studies. However, it was noted that specificity might
not always be apparent as there are various types of bias that can affect
the results of epidemiological studies. It was agreed that text on this
could be added to the paragraph. The last sentence of the paragraph on specificity referred to two hypothetical
mechanisms involving clotting or neural mechanisms. Inflammatory mechanisms
could be regarded as a third, although inter-related hypothesis. The Secretariat
agreed to consider this point. Members were generally happy with this section and it was noted that
a recent paper by Peters et al* had given good consideration to
temporality. It was also noted that a paper by Campbell MJ and Tobias A* had considered
whether mortality increased before rather than after days with higher
air pollution levels - this was not the case. An effect preceding the
relevant exposure would not have been supportive of a causal relationship. It was requested that the word 'all' in line 4338 be replaced by 'largely'. Biological Gradient It was requested that 'Exposure Response' should be added in brackets
after this sub-title. Examining biological gradients with non-parametric methods was considered
useful because the methods did not rely on applying a pre-determined shape
to the exposure response relationship. The evidence from these were considered
quite convincing for a linear relationship although some quirks could
appear where data were sparse. Others considered that linearity could
only be tested reliably on very large datasets such as NMMAPS or APHEA.
The Secretariat requested Mr Hurley and Mr Armstrong to re-draft this
section to include some explanation on non-parametric models. This was
agreed. It was requested that it be borne in mind that there may be data
which could be used from the NMMAPS or APHEA studies. It was requested that lines 4346 - 4352 on biological gradients from
laboratory studies be removed from this paragraph. This was agreed. Biological Plausibility It was explained that the conclusions in this section depended on how Members were persuaded by the toxicology. It was agreed that the toxicological mechanisms under consideration were mechanisms operating through inflammation, heart rate variability or thrombosis (although some considered that this was weaker). The Secretariat agreed to add the inflammation hypothesis to the list
at the end of point (iii). Coherence It was noted that the accepted effect of ozone was on cardiovascular
mortality and not on cardiovascular hospital admissions. Previous discussion
of this had raised the point that it was possible to have different mechanisms
applying to deaths and to hospital admissions. The lack of coherence did
not necessarily undermine the case for causality if different mechanisms
were involved for the different outcomes. It was agreed that this point
could be made. It was also agreed that 'however, this does not mean that
causality is not possible' should be added to line 4423 after the sentence
about the lack of an association between ozone and cardiovascular admissions
weakening confidence in the causality of the association between ozone
and cardiovascular deaths. There followed some discussion on the whether the sequence of the coefficients
would run as outlined in the text (with coefficients for cardiac symptoms
greater than for cardiac admissions which were greater than for cardiac
deaths). It was agreed that such a sequence could run in this way if analysing
numbers of cases, but that this did not necessarily follow when looking
at the coefficients. It was agreed that the section on the coefficient
sequence should be removed from the text. Experiment It was agreed that the support from experiment was better in the Hong
Kong study than in the Dublin study. It was agreed that this study should
be added to the text. Support from Analogy There were no comments on this section. Which pollutants are most important? Members thought that the general thrust of this section was good. However,
there were some specific changes requested. One member agreed to modify
the text in paragraph 10 (lines 4492 to 4497), which, members thought,
incorrectly implied that two and multi-pollutant models would be of little
use when establishing the active component of a mixture in which two pollutants
were closely correlated. It was agreed that dissecting out the effects of individual air pollutants from the ambient mixture was difficult. It was noted that the same causal reasoning as Bradford Hill could be applied to deciding which pollutant was most important. Even if the associations for different pollutants could not be disentangled statistically, the biological plausibility of an effect of the different pollutants could be taken into account. In paragraph 11 ii) it was requested that there should be some text added
on the relative importance of primary and secondary particles. This was
agreed. It was then requested that the Committee return to the table which depicted the combined estimates for various pollutants and various cardiovascular outcomes. Members were guided towards the results for CO and SO2 and some of the outcome measures which were striking due to the size of the coefficients. Members agreed that it was difficult to come to firm conclusions about the importance of the associations between cardiovascular disease and these two pollutants especially since much of the mechanistic research to date had concentrated on particles. It was noted that sulphur dioxide was not correlated with particles to the same degree as nitrogen dioxide and that an effect of sulphur dioxide had been picked up in the Hong Kong study. There was discussion of the finding described in Chapter 2 that nitrogen
dioxide associations remained after adjustment for PM10 but not vice versa.
It was mentioned that the multipollutant models from the NMMAPS work showed
that PM10 stood up to adjustment for other pollutants. The Committee were
informed that effect modification had been examined within the APHEA studies
and it had been noted that associations between cardiovascular admissions
and PM10 were greater in cities with higher long term concentrations of
NO2. This could suggest that NO2 was acting as a surrogate for particles
from traffic. It was decided that this could be dealt with in the section
on effect modification in Chapter 2. It was noted that very little consideration had been given to nitric oxide as a pollutant. Although simplistically it would be expected that exposure to nitric oxide would be a good thing for cardiovascular outcomes as it caused vasodilation, it was possible that external exposure to nitric oxide could suppress the bodies own production of nitric oxide which might not return immediately after external exposure stopped. What is the impact on public health? It was agreed that a little more on the scale of the effect including a comparison with passive smoking would be included in paragraph 14 as discussed earlier. It was requested, due to time constraints, that members provide the Secretariat
with their comments on the rest of this chapter via correspondence. The
Secretariat would send members an electronic copy of the chapter to facilitate
this request. Indoor Air Members were reminded that on 14th October 2004 the 'Statement on Assessment of the Heath Implications of Concentrations of Nitrogen Dioxide and Carbon Monoxide Indoors - Advice to HSE and DTI' had been published on the COMEAP website. Members were informed of the imminent publication of the COMEAP Guidance on the Effects on Health of Indoor Air Pollutants on the COMEAP website. AOB The Secretariat reminded the Committee that information on the Freedom of Information Act, which would come into force in January 2005, had been circulated by post. Members were informed that there would be a COMEAP strategy meeting between the Secretariat and the Chairman on the 17th December. Secretariat 2005
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