The effects discussed in this section are those for which it is not evident whether they
are due to SO2 or SPM, or a combination of the two. Winter-type air pollution episodes, as well as the background situation of winter-type air pollution in some cities, are characterized by increased concentrations of both SPM and SO2. In the Netherlands, lung function decreased transiently by 5 % of aver-age values a few weeks after winter smog epi-sodes in which the 24-hour concentrations of SO2 and total SPM were close to 300 µg/m3 [24, 25]. During an episode in a part of the Federal Republic of Germany in 1985, in which SO2 and SPM reached 24-hour con-centrations of 830 and 600 µg/m3, respect-ively, hospital admissions were 12 % higher than in a control area where the respective concentrations were 320 and 190 µg/m3. Ad-missions due to cardiovascular and respir-atory diseases were 14 % and 7 % higher, re-spectively. A 6 % increase in total mortality was also observed during this episode, due partly to respiratory diseases [26].
The incidence of lung cancer in males in Cracow may provide further evidence of the long-term health effects of mixtures of SPM and SO2 in urban air pollution. Annual mean black smoke levels exceeded 150 µg/m3 and SO2 levels exceeded 104 µg/m3 for several years before registration of the cancer cases.
The incidence of lung cancer among males living for an average of 30 years in polluted parts of the city was 46 % higher than that in residents of less polluted areas [27]. Al-though the risk estimate provided by this study agrees, in general, with that found in recently reviewed studies comparing cancer risk in urban and rural areas [28], quantify-ing the impact of air pollution on cancer incidence remains difficult. In part this is due to the uncertain estimate of past expo-sure to air pollutants.
A study from the Czech Republic sug-gested effects of winter-type air pollution on the health of infants [29]. Postneonatal mor-tality was 20–30 % higher in districts with an-nual mean concentrations of total SPM and SO2 over 85 and 58 µg/m3, respectively, than in those with concentrations below 54 and 13 µg/m3, respectively. The analysis, which considered potential confounding factors,
in-144 Air Pollution
dicated that the relationship was stronger for total SPM than for SO2, and that the risk es-timates were higher for respiratory than for other causes of death.
5.2.2 Lead
Most of the lead in ambient air is in the form of very fine particles, less than 1 µm in diam-eter. Some 30–50 % of inhaled particles are taken up by the respiratory system and ab-sorbed by the body. Larger particles are de-posited in the lungs or absorbed through the gastrointestinal tract. Air is, however, only one of several routes of human exposure to lead; Chapter 10 includes a more extensive discussion of the health effects of lead expo-sure.
Depending on concentrations of lead in ambient air, the exposure from air is esti-mated to range from 17 % to 67 % of total ex-posure in adults, and from 2 % to 17 % in children, with food or ingested dust usually a predominant source. For adults, an increase in exposure to lead in air by 1 mg/m3 is as-sociated with a 10–20 µg/litre increase in the concentration of lead in blood. No such rela-tionship can be established for children [6].
Data from the United States demonstrated a correlation between atmospheric emissions of lead due to the combustion of leaded pet-rol, ambient lead concentrations and levels of lead in blood. All three showed a parallel decline between 1986 and 1990, when both the total lead used in petrol and average blood lead levels decreased by 50 % [30].
Recognizing the multimedia nature of lead exposure, and the role of air as a medium through which lead may be transported to soil, water and food, the WHO guideline level was set at 0.5–1.0 mg/m3 (for an annual mean) [6]. This level is considered to be safe for adults. Since most of the exposure of children to lead occurs through other media, however, the guideline level does not offer sufficient protection.
Even at relatively low levels, lead causes changes in haematological and neurological parameters, and the impairment of
neuro-psychological development in children with associated deficits in cognitive ability. Sev-eral studies conducted after publication of the WHO guidelines confirm the impact in children of relatively low levels of exposure to lead [31]. Exposure producing blood lead levels of 250 µg/l, in cities with elevated con-centrations of lead in air, may affect cogni-tive ability as expressed by the IQ index. The IQs of children with such exposures to lead are estimated to be some 2–10 points lower, on average, than those of children not ex-posed. The shift in the IQ distribution in such an exposed population is estimated to result in a threefold increase in the percen-tage of children with low cognitive ability (an IQ below 80 points), and the proportion of children with high intelligence (an IQ above 125 points) is estimated to be reduced from 5 % to zero. Some studies indicate that neuropsychological development in children is affected at exposure levels corresponding to a level of lead in blood of 100µg/litre and above, but other reports suggest that no threshold exists and that effects can be seen at even lower levels of exposure [32].
5.2.3 Nitrogen dioxide
The evidence related to the health effects of NO2 in concentrations frequently en-countered in ambient air is still not well understood. Upon inhalation, 80–90 % of NO2 can be absorbed and remain within the lung for prolonged periods. An increased susceptibility to infection may be related to exposure.
Animal studies indicate that NO2 at relatively low concentrations (380 µg/m3 for 30 minutes) can trigger biochemical changes, including initiation of lipid perox-idation and an increase in lung enzymes, which may lead to cell injury or death. The biological relevance of these changes, how-ever, is still poorly understood. Animals ex-posed for 1–6 months to NO2 concen-trations of 190–940 µg/m3 showed changes in lung structure and lung metabolism, and impairment of lung defences against
infec-tion. Controlled clinical studies in human subjects and limited epidemiological studies, conducted in the 1970s and early 1980s, pro-duced conflicting results. The lowest NO2 level at which an effect on pulmonary func-tion in humans was seen, after a 30-minute exposure, was 560 µg/m3; this exposure caused a small, reversible decrease in lung function in a group of exercising asthmatics.
In normal subjects the threshold was much higher, about 3000 µg/m3, for 10–15 min-utes. On the basis of this limited evidence, WHO recommended a 1-hour guideline value of 400 µg/m3 and a 24-hour guideline level of 150 µg/m3[6].
Some later studies confirmed the in-creased bronchial responsiveness in asth-matic and non-asthasth-matic subjects exposed for a short time to NO2 concentrations above 500 µg/m3. The results, however, lack consistency, reflecting large variations in in-dividual susceptibility [33]. Nevertheless, a recent study confirmed a deterioration of the defence mechanisms of the lung against influenza viruses after an exposure to relatively high NO2 concentrations (1120 µg/
m3) [34].
Several recent studies evaluated the health effects of short-term increases in NO2 levels.
An increase in the frequency of eye irri-tation, sore throat and phlegm was observed among student nurses in Los Angeles follow-ing an increase in exposure to NO2 for one hour, with maximum concentrations not ex-ceeding 240 µg/m3. The relative risk esti-mates from this study were 1.3 for each 170 µg NO2 per m3[35]. Several studies reported an association between daily NO2 levels and the daily rate of hospital admissions due to acute respiratory diseases. Using data on the hospitalization of children in five German cities, Schwartz et al. [15] found a 28 % in-crease in the number of cases of respiratory tract infection associated with a rise in am-bient NO2 levels from 10 to 70 µg/m3. A number of researchers evaluated the effects of NO2 on ventilatory lung function, but only a few studies demonstrated a decrease in the expiratory flow rate, mainly in sub-jects with underlying chronic respiratory
dis-eases. Quackenboss et al. [36] observed a 3 % decrease in pulmonary expiratory flow rate in a group of asthmatic children per 20 µg/m3 NO2 hourly outdoor concentration.
They also reported prolonged effects, pressed as a 10 % decrease in pulmonary ex-piratory flow rate per increase of 20 µg/m3 in the weekly average outdoor level of NO2. Other studies also observed health effects associated with long-term exposure to NO2. A Swiss study of children aged 5 years or under, living in cities with annual average le-vels of NO2 in ambient air not exceeding 51 µg/m3, found a 20 % increase in the inci-dence of upper respiratory symptoms per 20 µg/m3 increase in NO2 for a continuous period of six weeks [16]. This study also indi-cated a 13 % increase in the duration of any respiratory symptom with an increase in NO2 of 20 µg/m3. Similar results were re-ported for children exposed to NO2indoors.
Several studies found decreased ventila-tory function or accelerated decline of func-tion with aging in residents of areas with high long-term average levels of NO2. An ecological analysis based on data collected in 60 neighbourhoods in the United States indicated a decrease in pulmonary function by approximately 5 % of the predicted value for each 40 µg NO2 per m3 (measured as an annual value) [37].
In most of the studies of short- and long-term effects of NO2, differences in the NO2 levels were correlated with levels of other air pollutants. It can therefore be as-sumed that NO2 concentrations are also in-dicative of levels of some other pollutants, such as those related to road traffic emissions. The combined evidence from all studies, including those on indoor exposure, however, suggests that NO2 at least con-tributes to respiratory effects.
5.2.4 Ozone
Ozone is the predominant photochemical oxidant in summer-type smog, and its most important component in affecting health. It enters the human body through inhalation
146 Air Pollution
and penetrates the respiratory system. Acute O3 exposure causes transient decreases in lung function and an inflammatory response of the lower airways; typical symptoms in-clude cough, chest pain, difficulty in breath-ing and headache. Substantial acute adverse effects undoubtedly occur at exposure to le-vels above 1000 µg/m3 for 1 hour, and more recent studies with ozone levels over 740 µg/
m3 for 2 hours showed an inflammatory re-sponse of the lower airways. Limited data from laboratory and epidemiological studies conducted in the early 1980s indicated that ambient O3 concentrations above 220 µg/m3 could lead to decreases in pulmonary func-tion, especially in children and exercising adults. Some of the other symptoms, includ-ing cough and headache, were associated with O3 concentrations of 160–300 µg/m3. These data led to the recommendation of a 1-hour WHO guideline value of 150-200 µg/
m3, and of an 8-hour value of 100-120 µg/m3 [6].
Since then, several important studies on the health effects of O3 at concentrations similar to the guideline values have been published. Lippmann [38] reviewed some of these and WHO held a consultation in 1990 to evaluate the acute effects of summer-type air pollution episodes [8]. All studies indi-cate large variations between individuals in response to O3 exposure. The effects seem to be more pronounced in children than in adults [39]; no characteristics of the respon-sive group, other than age, have yet been identified. Most studies evaluated acute ef-fects on pulmonary function or symptoms from short-term episodes of elevated O3 le-vels. They showed a 1–4 % decrease in pul-monary function in children for each 100 µg O3per m3 [40–42]. In adults, similar effects were observed but they were limited to measurements taken shortly after exercise and therefore with an increased inhalation rate [43]. Increases in the incidence of cough and eye irritation were seen in children on days with elevated O3 concen-trations. Krzyzanowski et al. [41] reported a 30 % increase in symptoms when 8-hour am-bient O3 levels exceeded 110 µg/m3; Berry et
al. [44] reported that symptoms were twice as frequent in children exposed to 1-hour ambient O3 concentrations over 240 µg/m3 than in those exposed to levels below 160 µg/
m3.
Far fewer studies have attempted to assess long-term effects in people living in areas with high average O3 levels (around 200 µg/
m3). The results indicate a small long-term effect on lung function, including a 6–8 % de-cline in pulmonary function in people aged 6–24 years for each 100 µg O3 per m3 above 90 µg/m3 [37]. A cross-sectional study of children in the Austrian Alps [45] reported a similar relationship. In adults living in the Los Angeles area, with an annual average O3 level over 150 µg/m3, the normal rate of de-cline in pulmonary function, which occurs with age, increased significantly as a func-tion of levels of oxidants in which O3 pre-dominated [46]. A recent analysis of a longi-tudinal study in California, however, did not provide conclusive support for an effect of long-term exposure to O3 on the incidence of respiratory symptoms [23].
It should be noted that, although volatile organic compounds have recently aroused concern as precursors of photo-oxidant formation (such as O3) some of them, such as benzene and 1,3-butadiene, are carcino-genic and have themselves, therefore, im-portant potential health implications.
This section estimates the exposure of popu-lations to the five air pollutants discussed above. These are approximate estimates be-cause relatively few data on air quality were available.
5.3.1 Methodology
Separate estimates of exposure to air pollu-tants are given for populations living in
5.3 Ambient Air Pollution and
Exposure Assessment
urban agglomerations with more than 50 000 inhabitants and in smaller towns and rural areas. The exposure estimates are based on levels of outdoor ambient air pollution and on the assumption that these concentrations are representative of the levels to which people are exposed in their daily lives.
Map 5.1a depicts the density and distribu-tion of populadistribu-tions into urban and rural areas. In total, 700 million people live in the countries of the European Region that lie west of the Ural Mountains, of which 314 million live in large urban areas of more than 50 000 inhabitants and 386 million in rural areas and smaller towns. The large-scale am-bient air pollution models presented in this chapter consider only those people who live inside the modelling grid used by UN ECE EMEPb (as shown in Map 5.1), that is, a total of 656 million people of whom 278 mil-lion live in large urban areas and 378 milmil-lion in the remaining areas. No larger modelling area has yet been used in a consistent way for the whole of Europe.