Box 2.1 TEOM and Gravimetric Measurements (continued)
2.5 Health benefits
2.5.2 Quantification methodology: short term exposure
2.5.2.1 Concentration-response coefficients – effects of short term exposure
Because both the concentration of air pollutants and the density of population vary 109.
across the UK, modelling of exposure to pollutants is needed in calculating their effects on health. This was the approach adopted in the report published by COMEAP early in 1998 on the Quantification of the Effects of Air Pollution on Health in the United Kingdom (Department of Health, 1998).
The literature on the effects of air pollutants on health is extensive and has not been 110.
reviewed for this report. This was felt to be unnecessary as the COMEAP report had examined the relevant evidence and had produced a series of coefficients linking concentrations of the major pollutants with effects on health. The coefficients used in this analysis are presented in Table 2.5.
Table 2.5: Concentration response coefficients
Pollutant Health outcome Concentration-response coefficienta
PM10 Loss of life expectancy (long
term exposure)
Deaths brought forward (all causes) (short term exposure)b Respiratory hospital
admissions
Cardiovascular hospital admissions
See later section 2.5.3
+ 0.75% per 10µg.m-3 (24 hour mean) + 0.80% per 10µg.m-3 (24 hour mean) + 0.80% per 10µg.m-3 (24 hour mean) Sulphur
dioxide Deaths brought forward (all causes) Respiratory hospital admissions
+ 0.6% per 10µg.m-3 (24 hour mean) + 0.5% per 10µg.m-3 (24 hour mean) Ozone Deaths brought forward
(all causes)c
Respiratory hospital admissionsc
+ 0.6% per 10µg.m-3 (8 hour mean) + 0.7% per 10µg.m-3 (8 hour mean)
NO2 See noted below See noted below
Notes:
a Note to compare the “relative potency” of the pollutants, the coefficients should be compared on a
molar or volume basis.
b The effects of short term exposure to particles have been considered as a sensitivity analysis in this
report, not because the results are more uncertain than for other pollutants (they are well established), but because the results of the studies on long term exposure to particles probably include the short term effects (see Annex 2, section A2.6.1). Particles concentrations measured by TEOM39 were used
for short term effects and gravimetric particles concentrations were used for long term effects (to match the studies from which the exposure response functions were derived).
c Coefficients of 0.3% per 10µg.m-3 ozone for deaths brought forward were used in a sensitivity
analysis. These are from a more recent WHO meta-analysis that has not yet been discussed by COMEAP.
d COMEAP did not consider that the evidence on NO
2 was sufficiently robust for quantification but
did give a coefficient of 0.5% per 10µg.m-3 for an effect on respiratory hospital admissions. This
coefficient has been used in this report but for sensitivity analysis only. Source: Department of Health (1998; 2001a; 2001b)
Table 2.5 shows that concentration response coefficients were specified for particulate 111.
matter, ozone and sulphur dioxide. The Committee also examined nitrogen dioxide and carbon monoxide but felt that the evidence was not sufficiently strong to allow firm estimates of total effects on health to be made. In the case of nitrogen dioxide, a concentration response coefficient was defined for respiratory hospital admissions. Nitrogen dioxide was also discussed in the EAHEAP report (Department of Health, 1999) which suggested that this coefficient could be used for a sensitivity analysis.
COMEAP
112. (Department of Health, 1998) calculated the ozone impacts using two different assumptions: no threshold or a threshold at 50 ppb. We have followed this here. COMEAP are reviewing the evidence on whether or not there is a threshold for ozone but this is not yet published. WHO concluded that there was evidence that associations existed below the current guideline value (60 ppb), but their confidence in the existence of associations with health outcomes decreased as the concentrations decreased (WHO, 2004a).
In addition to these two assumptions, we have also included an assumption of a 113.
threshold at 35ppb as a sensitivity analysis for comparison with calculations done at a European level. This was not based on direct evidence of a threshold for health effects at 35 ppb. It was recommended on the basis of a combination of the uncertainty in the shape of the concentration response function at low ozone concentrations, the seasonal cycle and geographical distribution of background ozone concentrations and the range of concentrations for which European ozone modelling provided reliable estimates (UNECE/WHO, 2004).
The ozone modelling undertaken for this analysis
114. 40 takes more account of local titration
of ozone with nitric oxide and ozone deposition and is at a finer spatial resolution than the European RAINS modelling. Thus, there is less reason to use a cut-off at 35 ppb. However, the cut-off was included to allow comparison with European calculations. Use of the 35 ppb cut-off omits a lot of the increases in ozone concentrations seen as a result of reducing NOX but it can be useful to distinguish this effect from effects on
decreasing photochemical production of ozone.
For the 50 ppb threshold calculation, days under 50 ppb were set to zero. For other 115.
days, 50 ppb was subtracted from the relevant concentration. The concentrations were then averaged over the year giving the annual mean of concentrations in excess of 50 ppb. The equivalent calculation was also done for concentrations over 35 ppb. A concentration response function of 0.3% per 10µg.m
116. -3 for mortality was used as a
sensitivity analysis. This was based on a more up to date WHO meta-analysis (WHO, 2004b) that has not been considered by COMEAP.
The health effects that were considered to be a result of short term exposure were daily 117.
deaths and admissions to hospital for the treatment of respiratory or cardiovascular diseases. In both cases the COMEAP report made clear that the numbers of events calculated as related to exposure to air pollution could not be simply interpreted as extra events. Deaths are brought forward and hospital admissions may be either brought forward or caused de novo. The extent of advancement of deaths and hospital admissions cannot yet be calculated and estimates of from a few days or weeks to a year have been produced. This inability to calculate the extent of advancement of these events is due to the nature of the epidemiological studies upon which the estimates are based: i.e. time-series studies. Some recent studies have used new statistical techniques to address this in the case of particles and all cause mortality. It was clear that the effect was not solely due to deaths occurring just a few days early but at least some of the deaths could be occurring at least 2 months early and probably more (see Annex 2).
40 Hayman et al (2005) ‘Modelling of Tropospheric Ozone’, AEA Technology, National Environmental Technology Centre.
The 1998 report prepared by COMEAP stressed that other effects on health including 118.
effects on respiratory symptoms and the use of therapeutic drugs might also be increased by exposure to air pollution. The 1999 EAHEAP report also noted that there is data on associations between GP consultations and air pollution. The available data did not allow firm estimates of the size of these effects to be made. The uncertainties and possible omissions of types of effects which may be increased by air pollution are discussed further in Chapter 5.
Ideally, for a cost-benefit analysis, some indication of the relative significance of 119.
the non-quantifiable health effects should be given. This depends on a wide variety of different factors including strength of evidence, size of concentration-response function, ambient concentrations/extent of exceedences, presence or absence of a threshold, numbers of susceptible people and monetary values. For example, minor effects at an individual level may become important in public health terms if large numbers of people are affected and a pollutant with weak effects may be more important if present at higher concentrations.
The strength of evidence and possible size of the concentration response functions is 120.
discussed in the EAHEAP report when suggesting which of the non-quantifiable effects might be examined in a sensitivity analysis.
2.5.2.2 Method of calculation – effects of short term exposure
In calculating the effects of pollutants on health the following sequence of steps has 121.
been adopted. These steps are described in more detail in the COMEAP Quantification Report (Department of Health, 1998); the EAHEAP report (Department of Health, 1999) and a report from Netcen.41
a) The country has been divided into 1km grid squares and the annual average concentration of pollutants and resident population has been estimated for each. The former has been derived from the national mapping of the UK pollution climate42 and the latter from census data.43 Population-weighted mean concentrations are then calculated by region or for the whole of the UK.
b) A baseline level of the given health-related and pollution affected events e.g., daily deaths, hospital admissions for the treatment of respiratory diseases has been obtained from national statistics.44
c) By combining the data from (a) and (b) and applying a coefficient linking the pollutant concentration with the relevant effects, the magnitude of the expected health effects can be derived. For this report, the coefficient is applied to the 41 Stedman et al (2002) ‘Quantification of the Health Effects of Air Pollution in the UK for Revised PM10 Objective Analysis’, a report
produced for the Department for Environment, Food and Rural Affairs, Welsh Assembly Government, The Scottish Executive and the Department of the Environment in Northern Ireland. Contract Number EPG 1/3/146
42 Grice et al (2006); Stedman et al (2006)
43 The calculations performed at Netcen used population data based on the 2001 census giving a total UK population of 58,279,138. 44 Baseline rates were obtained from ONS for mortality (www.statistics.gov.uk) and from the Department of Health (www.hesonline.
nhs.uk) for hospital admissions. The baseline rates used for this report were as follows: all cause deaths excluding external causes 989.7 per 100,000 for 2001; emergency respiratory hospital admissions (ICD10 J00 to J99) 979.7 per 100,000 for 2003/4; emergency cardiovascular admissions (ICD10 I20 to I52) 981.4 per 100,000 for 2003/4. Rates for England and Wales (deaths) or England (hospital admissions) were assumed to apply to the whole of the UK.
expected fall in concentration from the additional policies being assessed. This will give the benefit to health produced by the fall in concentrations of air pollutants expected to occur under the additional policies.
Acute effects calculations are carried out using raw TEOM data for the change in 122.
PM10 concentration as recommended by COMEAP (Department of Health, 1998).
In terms of quantifying the impacts of the different measures, the calculations were done on an annual basis using the 2010 concentration reduction for 5 years, the 2015 concentration results for 5 years and the 2020 concentration results for the remaining 90 years. In terms of presentation of results in both the consultation document and Chapter 3 of this report, the acute effects assessed as part of the central analysis are presented as annual physical impacts: the 2020 estimates are presented for those measures considered to have a sustained effect on pollution and the 2010 estimates are presented for shorter term measures. The way in which the estimates have been used in terms of valuing the impacts is described in section 2.5.5 below.
The COMEAP report in 1998 was based on urban areas only (most studies of health 123.
effects were done in cities). The calculations are based on all areas here but urban areas do in fact dominate the population weighted mean as both population and pollution are higher in urban areas.