TL: AIR POLLUTION AND CHILD HEALTH SO: Greenpeace UK (GP) DT: August, 1990 Keywords: greenpeace reports atmosphere smog air children human health effects urban cars transportation diseases links gp / AIR POLLUTION AND CHILD HEALTH Dr Catherine Read EXECUTIVE SUMMARY Air pollution is increasing in the UK. Government information shows that though Britain no longer suffers from the kind of notorious smogs that occured in the early 1950s, other types of air pollution, especially emissions from cars, are getting worse. Road traffic in the UK has increased dramatically in the last decade; over the same period, carbon monoxide, and hydrocarbons and nitrogen oxides - the pollutants that lead to the creation of photochemical smog or ozone - have also increased. All of these pollutants are known to be dangerous to health. The extent to which air pollution adversely effects the health of children in the UK is unknown. There are two main reasons for this. Firstly, there is significant shortage of air pollution monitoring equipment in population centres - most of the UK monitoring network is established in rural areas to track the effect of pollutants on plants and agriculture, or to meet the requirements of European Community directives. The monitoring that does take place suggests that children in the UK may regularly experience levels of pollution which have been shown to cause adverse health effects in other countries. Secondly, there has been minimal research in the UK on the effects of the pollution that children experience. Since the dismantling of the Clean Air Council and the Medical Research Council Air Pollution Research Unit more than 10 years ago, virtually no major work done has been done in this country on the effects of air pollution on health. However, a survey of the extensive international research done in this area, when examined in the context of levels of pollution experienced in the UK, suggests these conclusions: * Levels of ozone commonly measured in parts of Southern England in summertime can impair lung function in normal children. This effect is particularly noticeable if the children exercise. The consequences of this exposure are unknown but preliminary research suggests prolonged exposure to ozone may cause long term lung damage. * Levels of air pollutants still found in the UK increase the risk of respiratory infections, particularly among young children. Children with recurrent chest infections lose many hours of schooling and may develop chronic chest disease in later life. * Carbon monoxide interferes with the oxygen carrying capacity of the blood and consequently people with heart disease, pregnant women and their unborn children, and children with congenital heart problems are most at risk. Individuals who spend long periods in heavy traffic may inhale as much carbon monoxide as a smoker. * Low levels of acid aerosols - a pollutant not routinely monitored in the UK - are associated with worsening asthma and bronchitis in children. As there is no routine monitoring for acid aerosols in the UK, it is impossible to determine current levels or to indentify the risks that may result from those levels. * Over the last decade, deaths from asthma among people 5-34 years of age have risen by 30-60% in Australia, France, England and Wales, Canada and the US. Although asthma is a multifactorial disease, physicians around the world are convinced by the evidence that air pollution has contributed to a worsening of this problem. * Levels of nitrogen dioxide found in parts of urban Britain can cause respiratory symptoms including sore throat and cough amongst healthy children, and reduce lung function in those with asthma. * Levels of sulphur dioxide which still occur intermittently in the UK have been associated with increased respiratory symptoms in children, as well increased incidence of asthma and bronchitis. * Hay fever is a potentially disabling condition for many children. Air pollutants worsen the disorder by increasing sensitivity to airborne allergens. * The threat of lead to children's health is popularly thought to be decreasing with the introduction and use of unleaded petrol. Yet children are particularly at risk from lead because of accidental ingestion of dust and soil. Blood levels of lead that are still observed in children in the UK may be associated with mental impairment. CONTENTS PAGE Introduction 1 Summary of UK and International Research 1.1 Summary of UK Research 1.2 Summary of International Research 1.2.1 Nitrogen Dioxide Health Effects Toxicology Clinical Studies Child health 1.2.2 Ozone Health Effects Toxicology Clinical Studies Child health 1.2.3 Sulphur Dioxide and Particulate Matter Health Effects Toxicology Clinical Studies Epidemiology and Child health 1.2.4 Acid Aerosols Health Effects Toxicology Clinical Studies Epidemiology and Child Health 1.2.5 Carbon Monoxide Health Effects Toxicology Clinical Studies Epidemiology Child Health 1.2.6 Lead Health Effects Toxicology and Child Health 1.2.7 Benzene Health Effects Toxicology Child Health I.2 Effects of Air Pollution on Child Health 2.1 Allergic Disease 2.1.1 Asthma A Changing Disease Air Pollution and the Change in Asthma Controlled Chamber Exposure Experiments Epidemiological Studies Major Pollution Episodes Panel Studies of Asthmatics Other Epidemiological Studies Admission and Emergency Room Studies 2.1.2 Hay Fever and Air Pollution 2.2 Air Pollution and Respiratory Infection 2.3 Air Pollution and Cancer References INTRODUCTION The purpose of this report is to examine whether Britain's children are at risk from the air they breathe. The World Health Organisation estimates that millions of Europeans live in areas with air pollution severe enough to cause thousands of premature deaths each year and leave more chronically unwell. (UN ECE, 1990). In the United States 64% of children under the age of thirteen and one third of the nation's unborn children are estimated to be at risk from unhealthy levels of air pollution (ALA 1989a). There is no evidence that Britain's air is significantly cleaner than that in many other areas of developed world. Despite this the Government has assumed for over a decade that air pollution in the UK does not pose any health risk. This report examines that assumption. There is good reason to suppose that children are particularly susceptible to air pollution. Children breathe more air for a given volume of lung tissue than do adults (ALA, 1989b). They are more active than adults and likely to spend a significant amount of leisure time outdoors, particularly during summer when photochemical pollution is at its height. Children's airways may also be more susceptible to the irritant effects of air pollution (Rutishauser et al., 1990). Only outdoor air pollution is considered here. This does not imply that indoor pollution is not a significant health hazard. For some children exposed to indoor air pollution, particularly the effects of passive smoking, the health risk is likely to be significantly greater than that acquired from breathing outdoor air. This report first looks at the research into outdoor air pollution and children's health which has been carried out in Britain. It finds the country which pioneered air pollution research lags seriously behind. Virtually no studies in this area have been conducted since the Government closed the Medical Research Council's Air Pollution Unit over ten years ago. In contrast, extensive research into air pollution and children's health has been carried out in the US, Europe and elsewhere. The pollutants discussed here are carbon monoxide, ozone, nitrogen dioxide, sulphur dioxide, particulate matter, acid aerosols, benzene and lead. The deficit in pollutant monitoring in the UK makes it difficult to define the risk to human health. The bulk of the UK monitoring network is established in rural areas, to track the effect of pollutants on plants and agriculture, or to meet the requirements of European Community directives. The evidence that is available, however, suggests there is cause for concern. Various pollutants are linked with asthma and hay fever, chest infections including croup and childhood cancer. Over the last two decades there has been an increase in illness from asthma and hay fever, particularly among children. Exhaust emissions from motor vehicles have risen dramatically over a similar period (DOE, 1991). Research suggests that pollutants derived from traffic exhaust may exacerbate, and in some circumstances even initiate, both conditions. Finally the report looks at some specific childhood illnesses and assesses whether there could be a link between these and air pollution. 1 SUMMARY OF UK AND INTERNATIONAL RESEARCH 1.1 SUMMARY OF UK RESEARCH During the 1960's and the early 1970's, Britain was at the forefront of research into air pollution and health. This was perhaps appropriate for a country whose capital had earned a reputation as the cradle of air pollution. Britain's research effort was the culmination of over 100 years of winter smogs. Successive temperature inversions trapping smoke from coal fires near the ground regularly claimed the lives of infants and the elderly in London and Britain's other major cities. In 1952 the infamous 'great smog' claimed 4,000 lives and again in 1956, a thousand premature deaths in London were blamed on an extended smog (Martin, 1964). In reaction to the public outcry, Parliament passed a Clean Air Act in 1956 and Britain began a programme to reduce the domestic burning of coal. A Clean Air Council was set up to monitor progress made in abatement control and an Air Pollution Research Unit set up under the auspices of the Medical Research Council to investigate the dangers of air pollution. British researchers made a major contribution to our understanding of the health effects of air pollution through several outstanding field studies (Holland et al., 1979). These studies identified a link between sulphur derived pollutants and the risk of chronic bronchitis in adults and chest infections in children. One study followed up over 5,000 children born during the first week of March 1946. The areas in which children lived were graded into four pollution bands according to domestic coal consumption. The results showed a strong association between lower respiratory tract infection (coughs, bronchitis and pneumonia) and air pollution bands. This association existed for all ages but was most marked in the early years; between ages one and two children from the most polluted areas had three times the amount of illness reported for those in the least polluted areas. Examination by school doctors showed the effects of air pollution persisted up to age fifteen (Douglas & Waller, 1966). A follow up study when the children reached the age of 25 years showed a link between respiratory symptoms and smoking habit, social class and childhood chest illnesses but no effect of childhood exposure to air pollution. A second study of over 800 children in Sheffield supported these findings and identified a further relationship between upper respiratory tract symptoms and air pollution. Children entering the first year of eight local authority schools in four different areas were followed up over a 3 year period from 1963-1965. In the cleanest area, Greenhill, daily smoke - determined by the Black Smoke (BS) method- and SO2 averages were about 100ug/m3 and in the dirtiest area, Attercliffe, they averaged about 300ug/m3 . Upper respiratory tract illnesses, measured in terms of mucopurulent nasal discharge, three or more colds yearly, and scarred or perforated ear drums, were commoner in high pollution areas. Lower respiratory tract illnesses including pneumonia and bronchitis showed a similar pattern (Lunn et al., 1967). Not all the findings were clear cut. A study of over 10,000 children aged 5-14 years in Kent compared the lung function of children living in two urban areas with those living in the country (Holland et al., 1979). The two urban areas had mean levels of smoke of 69 and 50ug/m3. Smoke data for one rural area averaged 34ug/m3; measurements for a second were not available. Children from rural areas did not have the best lung function. The highest peak expiratory flow rates (a standard test of the ability of the brochi to conduct air) were highest in children from the cleaner urban site while children from the dirtier urban and the measured rural area had similar lower peak flow rates. The finding suggested to the investigator that factors other than air pollution must have played a part. Even in the urban areas of Kent, however, levels of air pollutants were considerably lower than those in the Sheffield study. A further study (Colley et al., 1973) investigated urban rural differences in children with bronchitis. Some 10,000 children aged 6-10 years were studied from the cities of Newcastle and Bolton (highly polluted), Bristol and Reading (moderately polluted) and in several country districts in England and Wales. Age standardized morbidity ratios for chronic cough were similar in all areas for social classes 1 to 3. But in classes 4 and 5 there was an increase in ratio from the clean rural to the highly polluted areas. Peak expiratory flow rate adjusted for age, height, weight and social class did not differ with geographical area in those children free of respiratory disease nor in those with respiratory disease. However, the lowest adjusted peak expiratory flow rates were recorded from the children in the clean rural areas. As controls to curb emissions of coal smoke were introduced, studies indicated that deaths and illness from lung disease were subsiding. In response, the British Government abolished the Clean Air Council in 1979 and the Air Pollution Research Unit a year later in 1980. Since the MRC's Unit was closed there have been almost no UK research publications on the health effects of outdoor air pollution from British sources (Read and Green, 1990a). Yet the significance of different forms of air pollution has emerged in the years since those closures. From 1983 to 1989 emissions of primary pollutants from motor vehicles - carbon monoxide, oxides of nitrogen and hydrocarbons - have increased by 39% (DOE, 1991) but the potential health hazard to UK residents from this source of air pollution has barely been addressed. Currently there appears to be a resurgence of interest in investigating health effects of air pollution among a small number of academic centres in the UK. Projects either currently underway or about to start are listed below although none specifically addresses the problem of air pollution and children. Dr Penny Fitzharris at the Department of Immunology, St Mary's Hospital in London and Dr Mike Ashmore of the Centre for Environmental Technology, Imperial College, London are studying the effects of ambient air pollution on hay fever. A pilot study (Gunner et al, 1991) conducted during 1990 indicated that NO2 and O3 made hay fever symptoms worse. The project has funding for two years from the National Asthma Campaign and may include personal monitoring during 1992. Professor Robert Davies, Professor of Respiratory Medicine at St Bartholomew's Hospital in London, is investigating the effect of air pollutants on human epithelial cells which line the upper airways. His group has demonstrated that ambient levels of NO2 could damage these cells and slightly higher concentrations could impair bronchomucociliary clearance (Devalia et al., 1991). Dr John Ayres of the Chest Research Institute, East Birmingham Hospital, is investigating the effect of ambient air pollution on asthmatic symptoms. A pilot study (Rayfield et al., 1990) demonstrated that measurements of peak flow, a standard test of lung function, in asthmatics deteriorated during a pollution episode in Birmingham in September 1989. A larger study will compare asthmatics' lung function with levels of a wider range of ambient air pollution measured at 11 stations with help from Environmental Health Services of Birmingham City Council at Aston Science Park. It is expected to include measurements of acid aerosols. Professor Ross Anderson of the Department of Public Health Sciences at St George's Hospital in London is planning a large epidemiological survey of asthma and air pollution using pollution data from Warren Springs Laboratory and drawing on general practitioner records of attendances for asthma. The British Lung Foundation is planning a major funding initiative for air pollution research projected to begin in autumn 1991. 1.2 SUMMARY OF INTERNATIONAL RESEARCH In terms of human disease, the most important environmental pollutants are nitrogen dioxide (NO2), ozone (O3), sulphur dioxide (SO2) and particulate matter, acid aerosols, carbon monoxide, hydrocarbons (including benzene) and lead. In summarising world research, the information in the following section is broken down into each of these various pollutants. Different kinds of research provide the relevant information. Toxicological studies are usually conducted with laboratory animals and rigorously test the biological response to a given pollutant. However it cannot be assumed that the results extrapolate to human disease. Clinical studies employ human volunteers in the laboratory but can only test the biological response to a pollutant over a narrow range of concentrations. In epidemiological studies, investigators monitor a given population and try to identify correlations between population health and specific factors, in this case air pollutants. This type of study has provided the basis for many advances in preventative medicine, identifying the link between smoking and lung cancer, diet and heart disease, and high blood pressure and stroke. Epidemiological studies are more relevant to public health than clinical and toxicological research because they reflect the real world rather than artificial environments created within the laboratory. However, they are extremely difficult to carry out, and are subject to many confounding factors. This is particularly true of epidemiological studies investigating air pollution. In the past, most studies on the health effects of air pollution depended on a few centrally located outdoor air pollution monitoring stations to reflect the exposure of large populations. In doing so they assumed that outdoor air pollutants provided the greatest contribution to pollutant load and that all individuals in the populations under scrutiny received a similar dose. Subsequent research has shown that exposures to pollutants can differ by orders of magnitude depending on where people spend their time. Most urban dwellers, especially children, spend most time indoors where they may be exposed to potent sources of indoor air pollution such as tobacco smoke. It is now possible to obtain more accurate assessments of exposure to pollutants by using recently developed personal passive monitors which can be placed in areas where individuals spend most time or even worn directly on the body. Other problems still remain. For example epidemiological studies usually only monitor a narrow range of air pollutants where individuals are in fact exposed to a "cocktail" of pollutants which may interact. Individual sensitivity to particular pollutants also varies as does the dose an individual receives. For example, the amount of inhaled carcinogen reaching the small air passages of the lung depends on the rate of respiration which in turn depends on age and the degree of exercise the person is taking. Considering the existence of so many complicating factors, it is hardly surprising the health effects of air pollution are difficult to quantify. 1.2.1 NITROGEN DIOXIDE As a gas, nitrogen makes up almost four-fifths of the atmosphere. During high temperature combustion, nitrogen and oxygen in the air combine to form nitrogen oxides, mainly nitric oxide. The UK emits 2.69 million tonnes of oxides of nitrogen per year and is the third largest source of nitrogen oxides in Europe (PORG, 1990). Nitric oxide is non-toxic to humans but converts rapidly to nitrogen dioxide in the atmosphere. Some nitrogen oxides are also formed by nitrogen components in fuel. Nitrogen oxides (NOx) may undergo further reactions to form tropospheric ozone in the presence of hydrocarbons and sunlight. Nitrogen dioxide is an oxidising agent less powerful than ozone but has similar toxic effects in humans (ALA, 1991b). The most severe outdoor nitrogen dioxide pollution is usually found in heavily trafficked areas. Industries and power plants are also important sources of NOX. In the UK, motor vehicles are the main source (48%) followed by power stations (29%), (DOE, 1991). EC air quality standards for NO2 are: Limit values : 104ppb (200ug/m3), 98 percentile of hourly values throughout year. Guide values : 70ppb (135ug/m3), 98 percentile of hourly values throughout year. 26ppb (50ug/m3), 50 percentile of hourly values throughout year. The limit value is set to protect human health. The guide values aim to improve the protection of human health and contribute to long term protection of the environment. (EC Directive 85/203/EEC) The WHO recommended guidelines for NO2 are: 210ppb (400ug/m3), 1 hr mean. 80ppb (150ug/m3), 24 hr mean. The 1 hr guideline is set to provide a margin of protection for asthmatics and the 24 hr guideline to protect against chronic exposure. Annual mean concentrations of nitrogen dioxide in urban areas throughout the world are typically in the range of 10-50ppb (WHO, 1987). In the US, metropolitan Los Angeles has the highest measured concentrations of up to 400ppb as a one hour average (ALA, 1989b). In London measurements of nitrogen dioxide over the last 12 years show a clear upward trend despite annual fluctuations (LSS, 1989). During 1989 the WHO 1 hour guideline was exceeded at both Central and West London Monitoring sites run by London Scientific Services with a peak of 242ppb at the Central London background site (LSS, 1989). Calculations by scientists at Warren Spring Laboratory predict that an increase in UK traffic growth will offset the tendency of stricter EC vehicle emission limits to reduce total NOx emissions. As a result NO2 concentrations in the year 2000 are likely to be similar to those in 1983/84, implying that the EC's limit value in Central London will still be exceeded (Munday et al., 1989). Indoor exposure to nitrogen dioxide may be more important than outdoor exposures for many people. Tobacco smoking, use of gas stoves and low ventilation rate in modern buildings tend to produce high indoor concentrations of NO2. Levels of oxides of nitrogen in homes using gas cooking are about five times higher than in homes where cooking is by electricity. In addition, researchers have found that NO2 concentrations of up to 500ppb may be inhaled when bending over a gas stove (Goldstein et al ., 1988). HEALTH EFFECTS TOXICITY Laboratory studies have shown that nitrogen dioxide acts like ozone in that it injures the smallest air passages of the lung, stimulates the production of inflammatory substances and increases animal susceptibility to respiratory infections. (Somet, 1987) Emphysema-like changes and changes in collagen, the most abundant structural protein in the lungs, have been observed after long term exposure to relatively low doses (WHO, 1987). Several types of animal study have shown that exposure to nitrogen dioxide increases susceptibility to bacterial lung infections and perhaps viral infections (US EPA, 1982). Non- respiratory effects at higher doses include changes in red blood cell metabolism, liver and kidney function. Laboratory studies on human bronchial epithelial cells show that exposure to 400ppb (levels occasionally found at the roadside) may impair cell function, in theory making the tissue more susceptible to infection (Devalia et al., 1991). CLINICAL STUDIES Human exposure studies in adults have shown mixed results regarding the health effects of nitrogen dioxide exposure. Some studies have not found adverse effects at concentrations from 500ppb to 4000ppb either in healthy volunteers or asthmatics (Linn et al., 1985; Hazucha et al., 1983). Others suggest asthmatics may be effected at much lower doses. In one of the earliest studies (Orehek et al., 1976) 13 out of 20 asthmatic volunteers appeared responsive to NO2 after exposure to 100ppb for one hour. Their change in airway resistance was only marginal after exposure but their airway reactivity to an inhaled muscle-constricting drug showed a more definite increase. This observation suggests that nitrogen dioxide exposure might make asthmatics more susceptible to symptoms caused by other environmental factors even if it does not provoke symptoms directly. CHILD HEALTH Isolating effects due to NO2 in population-based studies is difficult since NO2 in ambient air is usually accompanied by other pollutants of equal or greater toxic potential such as ozone, and other oxidant gases. One study which looked specifically at NO2 effects was conducted near an ammunition plant in Chattanooga, Tennessee in the late 1960's and early 1970's; NO2 was the predominant though not the only the air pollutant emitted by the plant (Shy et al., 1970; Love et al., 1982). In highly polluted areas near the plant both schoolchildren and their parents reported more lower respiratory illnesses than families living in cleaner areas within the same community. When the area was restudied 5 years later, the prevalence of respiratory symptoms was noted to have fallen, corresponding with lowered ambient NO2 levels. A prolonged strike at the munitions plant coincided with a further reduction in symptom reporting. A weakness of this study is that the authors did not take into account indoor sources of NO2 including gas cooking facilities and exposure to tobacco smoke. Furthermore, the standard air monitoring method then in use was eventually found to be inaccurate, so no reliable NO2 concentrations are available. A recent study identified a significant association between outdoor NO2 and respiratory symptoms in 1225 preschool children in Switzerland (Rutishauser et al., 1990). Four regions were chosen to represent different levels of air pollution; two in the cities of Basel and Zurich, one in a suburb (Wetzikon), and one in a rural area of the canton of Zurich (Rafzerfeld). Parents of children participating in the study kept a daily diary of the child's respiratory symptoms including cough, sore throat, fever, running nose and earache for a period of six weeks in 1985 and 1986. Ambient air NO2 was measured with passive samplers (Palmes tubes) located outside the apartment where the child lived and also attached directly to the child. Average weekly NO2 levels for Basel and Zurich were around 26ppb, 17ppb for Wetzikon and 13ppb for Rafzerfeld. The frequency of respiratory symptoms per child per day was found to increase with increasing levels of outdoor NO2. The relationship remained significant even after controlling for factors including passive smoking and indoor NO2. Although numerous epidemiological studies have attempted to find out whether children living in homes with gas cooking stoves have more respiratory illness the evidence is currently inconclusive (Samet et al., 1987). 1.2.2 OZONE Ozone (O3) is a secondary pollutant; it is formed in the atmosphere by a series of photochemical reactions between hydrocarbons and nitrogen oxides. These two primary pollutants are produced during combustion. In the UK, motor vehicles contribute 48% of nitrogen oxides and 37% of hydrocarbons, power stations 35% of nitrogen oxides and industrial processes and solvent evaporation 51% of hydrocarbons (DOE, 1991). The WHO recommended guidelines for ozone are: 76-100ppb (150-200ug/m3) as a 1 hr average. 50-60ppb (100-120ug/m3) as an 8 hr average. Ozone is a natural constituent of the upper atmosphere where it absorbs potentially damaging solar radiation that would otherwise reach the earth's surface. Normal atmospheric mixing brings some stratospheric ozone to the ground and clean air in some remote areas may contain 30-50ppb. (ALA, 1989b) The most severe ozone pollution occurs during still sunny conditions. Concentrations of ozone are often highest outside urban areas, as plumes of pollution move out of urban areas during anti-cyclonic conditions. In Los Angeles which suffers some of the worst photochemical pollution in the world, ozone concentrations frequently exceed 200ppb and sometimes 300ppb for periods of an hour or more (ALA, 1989b), as a result of high levels of both traffic and sunlight, with the pollution trapped bya ring of mountains encircling the city. It was once thought that photochemical smog was confined to Los Angeles. However, during the 1970's photochemical pollution appeared in many of the world's major cities, coinciding with a dramatic growth in emissions of ozone precursors from motor vehicles. Because of the gradual increase of O3 precursor emissions in the northern hemisphere, background levels of O3 are steadily increasing. Over the last three decades measurements in Europe have increased by 1 to 2% a year (Hartmannsgruber et al., 1985). Background levels of O3 are likely to increase still further since emissions of O3 precursors will not decrease dramatically in future, and ultraviolet light intensity may increase due to global changes. In the UK photochemical smogs usually occur when high pressure systems bring low wind speeds and plenty of sunshine. Ozone levels vary throughout the day: in urban areas in the UK levels peak in the early afternoon and fall at night as ozone is 'mopped up' by nitric oxide (NO). In rural areas within the UK, ozone levels peak later in the afternoon due to continuing reactions in pollution plumes moving away from urban centres. Rural areas also tend to experience higher levels of ozone than city centres as there is no NO to remove it. Britain's worst photochemical smog episode occurred during three weeks in summer 1976; peak one hour average rural concentrations exceeded 250ppb and levels in London exceeded 200ppb (Holman, 1989). During 1989, a photochemically active year, the 17-site UK monitoring network for ozone recorded 53 'episode' days when maximum hourly average concentrations exceeded 60ppb at two or more sites. The same year the WHO's upper limit of 100ppb was exceeded for a total of 95 hours at 11 sites monitored by Warren Spring Laboratory. Sites in Southern and South Western England experienced higher levels than more Northerly sites often as a result of long range transport of ozone and its precursors from central Europe (Bower et al., 1990). HEALTH EFFECTS TOXICOLOGY It is hardly surprising that ozone, a powerful oxidant capable of cracking stretched rubber at levels of only 10ppb to 20ppb (0.01 to 0.02ppm) (Elsom, 1987), can also harm the delicate tissue in the lung. Using mathematical models, scientists have calculated that the highest concentrations of ozone occur in the tiniest passages of the lung (Bates, 1990). Animal studies have shown that chronic exposure to levels of 200ppb can cause functional, biochemical and structural changes to the small airways analogous to the changes caused by aging and early chronic obstructive lung disease. Similar concentrations impair defence mechanisms against disease (ALA, 1989b; WHO, 1987). Ozone appears to affect both the immune system and mucociliary clearance, the system through which cells lining the respiratory tract sweep out invading bacteria and other debris. Scientists have recently demonstrated that levels of ozone often experienced during pollution episodes can cause an inflammatory reaction in human lungs (Koren et al ., 1989). Koren and colleagues examined fluid washed out of the lungs of healthy exercising men after they had breathed O3 at levels of 80 and 100ppb for 6.6 hours. At both levels of exposure an increase in inflammatory cells was seen and macrophages - scavenging cells - were less capable of consuming and destroying bacteria than normal. At the higher exposure a variety of inflammatory proteins capable of causing long term lung damage were detected. The significance of this relatively short term finding is unknown. However, research carried out by a Los Angeles pathologist provides a clue. Post mortem examinations of the lungs of 107 healthy young non-smokers killed in accidents showed severe respiratory bronchiolitis in 29 and moderate inflammatory changes in a further 51 cases (Sherwin & Richyers, 1990). The changes are comparable to those seen in the lungs of cigarette smokers and similar to those seen in primates after prolonged exposure to ozone. CLINICAL STUDIES Numerous studies have examined the effects of ozone on healthy young volunteers. Several studies suggest that there is no threshold for an observed ozone effect (WHO, 1987). Short term acute effects start around 100ppb. Eye irritation, due to non- ozone oxidants such as peroxyacetyl nitrate, may occur at slightly lower levels. As levels increase a variety of symptoms may be experienced including, cough, dry throat, chest discomfort, fatigue and nausea. Exposure to ozone may result in an inability to take deep breaths. This is reflected in standard tests of breathing ability. Two measurements commonly used are forced vital capacity (FVC), the volume of a maximum breath forced out, and forced expiratory volume in 1 second (FEV1), the volume of air breathed out in that first second of a forceful exhalation. The degree of unfavourable response depends on O3 concentration, the length of time a person is exposed and the rate of breathing which usually reflects the level of exercise (Hazucha, 1987). In addition some people are more responsive to the effects of O3 than others. At rest no effect is likely under ambient exposure conditions (ALA, 1989b). With light, intermittent exercises, irritation may occur at around 300ppb (concentrations found during severe pollution episodes) after one or two hours' exposure. Several studies have examined ozone effects after either one hour of continuous exercise or two hours' intermittent exercise at concentrations found in ambient air in the United States, (McDonnell et al., 1983; Avol et al., 1984; Kulle et al., 1985; Linn et al., 1986). All these showed losses in lung function in the 150-200ppb range and one suggested slight effects at 120ppb (the US standard). Tolerance appears to occur during prolonged O3 exposure; typically lung function is worse on the second day of exposure but improves on subsequent days. If the frequent exposure stops, tolerance is lost within a week or two (Horvath et al., 1981; Linn et al., 1982). The significance of this remains unknown. Ozone appears to affect asthmatics and people with normal lung function to an equal extent although there is some evidence that a sub group of asthmatics is particulary sensitive. In addition there is evidence that relatively low levels of O3 may lower asthmatics' tolerance to common irritants (Bates, 1990). CHILD HEALTH Numerous epidemiological studies conducted on children in the United States have established a clear link between increasing levels of ambient O3 and impaired lung function. They include four summer camp studies carried out in Indiana and Pennsylvania in 1980 (Lippman et al., 1983) in Mendham, New Jersey in 1982 (Bock et al., 1985; Lioy et al., 1985) and at Fairview Lake, New Jersey in 1984 (Spektor et al., 1988) . All showed an association between a decrease in FVC, FEV1 and peak expiratory flow rate (PEF) and increasing levels of ozone. In the Mendham study an air pollution episode occurred that involved four days of hazy weather and a peak one hour ozone level of 186ppb. Impairments in lung function persisted for a week following the episode. The Fairview Lake study identified significant impairment in lung function tests with increasing O3 levels despite the fact that the US air quality standard was not exceeded during the study and no sustained period during which ozone levels exceeded 100ppb, the WHO's upper guideline limit. There were, however, several periods of 24 hours and longer when O3 levels did not fall below 60ppb (Spektor et al., 1988). Children seem to be as sensitive as adults in terms of lung function changes. They are however less likely to develop symptoms. In a study performed in Chapel Hill, North Carolina, 8-11 year old boys were exposed to 120ppb of ozone for 2 hours during heavy intermittent exercise. (McDonnell et al., 1985). The observed fall in FEV1 was consistent with that demonstrated under similar exposure conditions in adults. However, while adults often develop symptoms at this level of O3 exposure the children did not. In a further study healthy 12 to 15 year olds were exposed to purified air and smoggy Los Angeles air averaging 144ppb of O3 (Avol et al., 1985). The test periods included 1 hour of continuous bicycle exercise. The group's mean FEV1 fell during ambient exposure and only partially recovered over the following hour. The children reported no significant increase in respiratory symptoms accompanying the observed lung function changes. These and other studies suggest children are less aware of respiratory irritation by ozone than adults. As a result, young people living in polluted areas may expose themselves to potentially damaging levels of ozone without being aware of a health problem. (Avol et al , 1985). 1.2.3 SULPHUR DIOXIDE AND PARTICULATE MATTER Sulphur dioxide and particulate matter are produced by the combustion of fossil fuels and are major pollutants in urban areas throughout the world. Because they are emitted by similar sources it is often difficult to ascribe observed health effects to either pollutant alone. The picture is complicated further by acid aerosols which are derived from SO2 under appropriate conditions and often coexist with SO2 and particulates. Airborne particulates consist of a complex mixture of substances originating from a variety of natural or anthropogenic sources. Typical constituents in urban areas include the carbon and hydrocarbon products of incomplete combustion. Coal burning used to be responsible for most visible particulates, especially in urban areas, but today diesel vehicles are a major source accounting for almost one third of total emissions and up to 90% of black smoke in some areas (Van den Hout & Rukeboer, 1986). It has been estimated that a diesel vehicle emits more than 10 times more particulates under urban driving conditions than a petrol vehicle, and up to 100 times more than a petrol vehicle fitted with a 3-way catalytic converter. Diesel particles consist of carbon and are generally under 1 micrometer in diameter. They carry traces of other pollutants such as polyaromatic hydrocarbons (PAH's) (Holman, 1990). Because of the complexity of particulates and the relative importance of size in determining health effects, a variety of descriptive terms exist. Hence particulates may be defined by sampling methods eg. suspended particulate matter, total suspended particulates, black smoke. Other terms refer to the size eg. PM 10 (particulate matter with an aerodynamic diameter of less than 10um). Yet others describe how particulates relate to the respiratory tract, for example thoracic particles which are relatively fine tend to deposit in the lower respiratory tract. A black smoke method is used for measuring particulates in the UK. This measures the darkness of the stain obtained when air has been passed through a white filter paper. In the USA a gravimetric technique is used which measures the weight of total suspended particulates deposited on a filter paper after air has passed through it. For particles the effective dose depends on size as well as concentration. Larger particles, 10um and above, tend to be deposited in the upper airways and are rapidly cleared. Particles below 10um in diameter are able to reach the lungs. The larger particles within this range tend to be deposited in the tracheobronchial region while the smaller particles tend to lodge deep in lung tissue near the alveoli, the air sacs of the lung. Particles within the lung are cleared by the mucociliary system; fine hairlike structures on the surface of cells lining the air passage sweep mucus and debris towards the mouth. Since the alveolar region has a slower clearance system than the upper airways, particles deposited there may remain for months or years. Clearance is impaired in some lung diseases such as cystic fibrosis and may also be impaired by some pollutants, including cigarette smoke. During heavy exercise, when the proportion of mouth breathing to nose breathing increases, more particles penetrate further into the respiratory tract. (ALA, 1989b; WHO 1987) EC air quality standards for SO2 are: Limit : 130ppb (350ug/m3), 98 percentile of daily mean values throughout year. 44ppb (120ug/m3), 50 percentile of daily mean values throughout year. Guide : 37-55ppb (100-150ug/m3), 24 hr mean. 15-22ppb (40-60ug/m3), annual mean. The limit values are set to protect human health, while the guide values serve as long term precautions for health and the environment. (EC Directive 80/779/EEC) The WHO recommends the following guideline to protect public health: 185ppb (500ug/m3) , 10 minute mean 130ppb (350ug/m3), 1 hour mean The WHO Guidelines for particulates are: 125ug/m3 of black smoke or 120ug/m3 TSP as a 24 hour mean in the presence of 125ug/m3 or more of sulphur dioxide. The British Black Smoke Method estimates smoke in the atmosphere by drawing air through a white filter paper and measuring the density of the resulting stain. The "smoke" collected consists of particles of 10um or less. Sulphur dioxide and particulates are often regarded as the 'traditional' pollutants of urban areas. Natural concentrations of SO2 in rural parts of Europe are normally below 1.8ppb to 9ppb. (5-25ug/m3) (WHO, 1987) In contrast, during the London smog of 1952 levels of SO2 reached a peak of nearly 1,480ppb (Elsom, 1987). High levels of winter type pollutants still occur in certain parts of Eastern Europe, and occasionally elsewhere. In a smog episode in the Ruhr District of Germany in 1985, average daily SO2 levels reached 307ppb, coinciding with a significant increase in deaths from heart and lung disease (Wichmann et al., 1989). During this episode schools were closed, the authorities appealed for children and people with heart and lung disease to stay inside, the use of private cars was prohibited and industrial plants were required to reduce emissions significantly or close. In the UK, urban concentrations of SO2 and particulates have fallen dramatically in the last three decades (DOE, 1991) largely due to a decrease in combustion of domestic coal. In the UK, power stations account for nearly three quarters of total SO2 emissions. Annual mean concentrations of SO2 in London are now 7 to 18ppb with roadside levels being slightly higher due to emissions from diesel vehicles (LSS, 1989). Despite relatively low annual means, high peaks of SO2 still occur in London, usually as a result of pollution plumes from power stations grounding under certain weather conditions. In 1989 the WHO 1 hour guideline was exceeded several times at all monitoring stations run by LSS, the maximum recorded value being 607ppb. EC Directives for SO2 and smoke continue to be exceeded in coal mining areas throughout the UK, where the provision of a coal allowance to miners encourages domestic coal burning. HEALTH EFFECTS TOXICOLOGY High concentrations of SO2 slow the respiratory rate and provoke bronchoconstriction, and cause chemical bronchitis and tracheitis in experimental animals. Exposure at SO2 may also increase bronchial reactivity to other agents. Airway resistance usually increases soon after exposure begins and returns to normal a few minutes or hours after exposure ends. Sulphur dioxide may also impair mucociliary clearance. CLINICAL STUDIES High levels of SO2 in excess of 1000 ppb (1ppm) provoke wheezing in normal adults. Asthmatics are more sensitive and may wheeze at levels as low as 200ppb, especially if they are exercising (Linn, 1983). Such levels still occur intermittently in the UK, particularly in coal mining areas (Warren Spring Laboratory, 1989). Exercise often induces wheeziness in asthmatics and SO2 enhances this effect. The wheezing develops within a number of minutes after the start of exercise and does not increase with increasing exposure. Rest usually relieves symptoms within half an hour even if SO2 exposure continues. Some asthmatics are more sensitive to the effects of SO2 than others (Horstman et al ., 1986). Some people without medically diagnosed asthma, but with respiratory allergies, may be nearly as sensitive as typical asthmatics (ALA, 1989b). EPIDEMIOLOGY AND CHILD HEALTH During three major pollution episodes earlier this century, in the Meuse Valley, Belgium in 1930 (Firket, 1931), Donora Pennsylvania in 1948 (Shrenk et al , 1949) and London in 1952 (Ministry of Health, 1954), complex pollutant mixtures of SO2, particulate matter and acid aerosols were blamed for thousands of excess deaths from heart and lung disease. Levels of these pollutants have fallen due to clean air controls and fuel switching for economic reasons. Despite this, over the last decade investigators in many different countries have continued to document adverse health effects of sulphur derived pollution. The adverse health outcomes include respiratory symptoms in children, impaired lung function and increased incidence of asthma and bronchitis (Bates, 1990). Field studies in North America and Europe have shown temporary impairment of lung function in school age children during sulphur dioxide-particulate pollution episodes. The daily average concentrations measured in these episodes are roughly 100 to 200ppb for SO2 and 200-400ug/m3 for particulate matter (US method) (ALA, 1989b). Comparable daily averages of SO2 occur periodically in some industrial northern towns in the UK (Warren Spring Laboratory, 1989). During an air pollution episode affecting the whole of Western Europe in January 1985, the lung function of Dutch primary school children was noted to fall by up to 5% (Dassen et al., 1986). During the episode Total Suspended Particulates (TSP), respirable suspended particulates (RSP) and SO2 concentrations were each in the range of 74 to 92ppb whereas baseline measurements were generally below 37ppb. The children's lung function was still impaired three weeks after the episode but improved over the following days. During January 1987 a second pollution episode affected Central and Western Europe due to the long range transport of pollutants originating in Eastern Europe and the Ruhr. On this occasion daily average concentrations of SO2 reached 111ppb. Measurements of lung function were again noted to fall in a group of 6-12 year old Dutch children (Brunekreef et al., 1989). Lung function was still depressed up to a month after the pollution episode. Field studies have also identified longer term changes in respiratory health associated with sulphur dioxide-pollution. The ongoing Six Cities Study of Air Pollution and Health found a strong association between frequency of chronic cough, bronchitis and chest illness in preadolescent school children and concentrations of particulates and SO2 in six communities in the Eastern United States (Ware et al., 1986). Children with a history of wheeze or asthma had a much higher prevalence of respiratory symptoms and there was some evidence that the association between air pollutant concentrations and symptom rates was stronger with these markers for hyper-reactive airways. 1.2.4 ACID AEROSOLS The potential of acid rain to damage lakes, forests and buildings has received a great deal of attention. Evidence is now accumulating to suggest that airborne acid may have adverse human health effects. Acid aerosols are formed via several mechanisms from common pollutants (sulphur and nitrogen oxides) and may accompany both summer and winter type pollution. In the first, sulphur dioxide produced during combustion reacts with water vapour to form sulphuric acid (H2SO4). Under a second set of conditions the transformation of SO2 into H2SO4 is catalyzed by certain metals within water droplets and carbon on the surface of particulates. This type of reaction can occur rapidly when SO2 and particulate pollution is trapped within a foggy air mass. The third type of reaction is photochemical; nitrogen oxides, produced by motor vehicles and power plants, react in sunlight with hydrocarbons to produce oxidising agents which rapidly interact with SO2 to form H2SO4. Sulphuric and nitric acid is neutralized by atmospheric ammonia. Ammonia is a normal product of animal metabolism which occurs in higher concentrations near the ground. Aerosol acidity tends to increase with height above the ground and aerosols formed within pollutant mixtures emitted from tall stacks may travel thousands of kilometres. Acid aerosols are technically difficult to measure because they are so reactive. Partly because of this, very little monitoring of acid aerosols has taken place and information about ambient levels is not readily available. Limited monitoring for acid aerosol was carried out in London between 1959 and 1972 (Commins & Waller, 1967) The highest reported level in the UK was 680ug sulphuric acid per m3 as a 1 hour average in 1962. Higher levels were almost certainly present in London in earlier years and are now believed to have contributed to the high death rates observed during smoggy episodes (Thurston et al., 1989). Current average acid aerosol levels in Europe are not known but in the US a multi-centre study is currently investigating exposure to particle and vapour phase acid in 24 towns. Data are still limited but 24 hour H+ concentrations in excess of 100 nmoles/m3 (5ug/m3 H2SO4 equivalent) and 12 hour concentrations above 500 n moles/m3 (25ug/m3 H2SO4 equivalent) have been measured. The maximum measured concentration could result in a delivered dose of more than 2000 nmoles (100 ug equivalent H2SO4) of H+ ion in 12 hours for an active child (Dockery et al , 1990). Because of the lack of data there are currently no guidelines limiting acid aerosol exposure. Animal and clinical studies suggest the possibility of adverse health effects at H2SO4 equivalent concentrations of 100ug/m3, comparable to ambient concentrations being measured in the US. HEALTH EFFECTS TOXICOLOGY Sulphuric acid at or near ambient levels increases airway reactivity and reduces the rate at which particles are cleared from the lungs (Schlesinger 1989, 1990). Daily exposure of rabbits to acid aerosols at levels which only transiently impaired bronchociliary clearance following a single exposure produced a persistent reduction of clearance rates. These reductions were similar to those seen in other animals chronically exposed to cigarette smoke, and in human smokers. Other features seen, characteristic of chronic bronchitis in human smokers, included increased airway responsiveness, an increased concentration of mucus secreting cells and airway narrowing. The changes observed suggest persistent exposure to acid aerosols could contribute to the development of chronic bronchitis (Gearhart & Schlesinger, 1989). A number of studies have looked at interactions of acid aerosols and other pollutants. They indicate that sulphuric acid reacts synergistically with low levels of oxidant gases to induce biologically significant changes. An effect has been demonstrated in experimental animals at 40ug/m3 H2SO4 + 200ppb O3. A similar effect occurs at lower levels when the H2SO4 exists as a surface coating on metal oxides, a complex mixture contained in primary emissions from coal combustion (Amdur, 1989). CLINICAL STUDIES Several studies in healthy adults have found no significant changes in lung function or respiratory symptoms following exposure to sulphuric acid at concentrations from 100ug/m3 to 1000ug/m3 for periods of ten minutes to two hours. Others have found impaired lung function and increased respiratory rates at levels between 350-500ug/m3 (WHO, 1987). Asthmatics appear to be especially sensitive but do not react as consistently to sulphuric acid as they do to sulphur dioxide. The lowest demonstrated effect levels for sulphuric acid is 70-100ug/m3 measured in exercising adolescent asthmatics (Koenig et al., 1983; Koenig, 1989). Sulphuric acid also alters bronchomucociliary clearance in healthy non-smoking adults. One study showed low levels of sulphuric acid (100ug/m3 for one hour at rest) appeared to irritate the airways and accelerate clearance, at higher levels (1000ug/m3 ) clearance was slowed (Leikaupf et al., 1981). EPIDEMIOLOGY AND CHILD HEALTH Sulphuric acid was identified as the probable causal agent for around 600 cases of respiratory disease in the Yokkaichi area of Central Japan between 1960 and 1969. The patients lived within 5km of a titanium dioxide plant that emitted between 0.1 million and 3 million kg sulphuric acid per month. The average concentration of sulphur trioxide in February 1965 in a village adjacent to the plant was equivalent to a concentration of 159ug/m3 H2SO4 but it has been estimated that at times concentrations may have been 100 times as high (Kitagawa, 1984). During the five year period of severe air pollution, asthma deaths were double the number which occurred after emissions had been controlled. Sulphuric acid may also have been the component of air pollution responsible for the adverse health effects and deaths seen in the Meuse Valley, Donora and London around the middle of this century. (Dockery and Speizer, 1989) High levels of sulphuric acid are likely to have accompanied the high levels of SO2 and sulphates measured in these episodes. Using historical data, a recent study (Thurston et al., 1989) compared daily mortality rates for Greater London with daily SO2, particulate and aerosol acidity measurements for the winters from 1963 to 1972. Total daily mortality correlated more closely with measurements of acid aerosols than with either of the other two pollutants. In Southern Ontario, there have been studies of the links between hospital admissions for respiratory illness and concentrations of air pollutants over the decade 1974-1984 for the summer and winter months (Bates & Sizto, 1987). Excess respiratory admissions correlated strongly with ozone and sulphates but only for the summer months. Bates and Sizto speculate that the health effects may be due to accompanying sulphuric acid peaks for which the sulphates act as measurement surrogates. Since 1986 (Spengler et al., 1989; Lioy & Waldman, 1989) direct measurements of sulphuric and nitric acid aerosols have been made in different locations across North America. These have shown that in the summer when ozone is elevated and the humidity is high, peaks of acid occur at ground level and last for several hours. At one site, a children's summer camp in Dunsville Ontario, levels have exceeded 50ug/m3 H2SO4. Under these conditions an active child might receive more than 2000 nmoles of H+ ions (100ug/m3 H2SO4) in 12 hours and more than 900 nmoles (45ug/m3 H2SO4) in one hour. Levels close to this have been shown to affect adversely the health of adolescent asthmatics in clinical studies (Spengler et al., 1989). Acid aerosol measurements collected as part of the ongoing Harvard Six Cities Study have been shown to correlate with the prevalence of bronchitis in 10-12 year old children (US EPA, 1988). 1.2.5 CARBON MONOXIDE Carbon monoxide (CO) is a ubiquitous air pollutant that is produced by incomplete combustion of any carbon containing substance. Sources include cars, industry, heating and cooking facilities, and tobacco smoke. Carbon monoxide concentrations in urban areas depend on traffic and weather conditions. Concentrations vary diurnally with the rush hour. Highest concentrations occur near dense traffic in road intersection tunnels, underpasses and underground car parks (Elsom, 1987). Levels within vehicles are higher than outside and may result in surprisingly high blood levels during prolonged periods in dense traffic (Read & Green, 1990b). Carbon monoxide toxicity is related to its affinity for haemoglobin, the oxygen carrying molecules of the blood. Carbon monoxide displaces oxygen from binding sites in the haemoglobin molecule to produce carboxyhaemoglobin (COHb). This impairs delivery of oxygen to brain and other tissues and accounts for most of the toxicological effects. Healthy non-smoking individuals have COHb concentrations of 0.5- 1.5% (Cole, 1975). COHb concentrations are related to the ambient carbon monoxide level, the exposure time, and the degree of physical activity (Coburn et al., 1965). Although levels in the general population may be low, those of individuals occupationally exposed (eg. traffic police and mechanics) may be higher (Read & Green, 1991). Highway inspectors have been reported to have COHb concentrations of 4-7.6% (smokers) and 1.4- 3.8% (non-smokers). It takes 4-12 hours for air levels and blood levels of COHb to equilibrate - exposure to high levels even for brief periods may result in high COHb concentrations that persist for several hours. Unborn children are particularly at risk because foetal blood COHb may be 2.5 times higher than the maternal COHb, ie. it is 'concentrated' in the blood of the foetus (Hoppenbrouwers, 1990). There are no EC air quality standards for carbon monoxide. The WHO recommended guidelines are : Maximum permitted exposure of 86 parts per million (ppm) (100mg/m3) for periods not exceeding 15 minutes. For short term exposure, 50ppm (60mg/m3) for 30 minutes. These guidelines are set up to prevent COHb levels of non-smokers exceeding 2.5-3.0%. HEALTH EFFECTS TOXICOLOGY Moderately high levels of carboxyhaemoglobin (2-4%) decrease the exercise capacity of healthy young men. Higher levels (>5%) cause impairment of concentration, visual perception, ability to learn, headache and decrease of maximal oxygen consumption during strenuous exercise. CLINICAL STUDIES Individuals with heart disease have the best documented vulnerability. Patients with narrowed coronary arteries ischaemic heart disease (IHD) experience chest pain on exertion and are prone to develop abnormal electrical rhythms within heart muscle that can potentially result in sudden death. Low concentrations (2-4%) of COHb increase the likelihood of chest pain in ischaemic heart disease patients who exercise (Allred et al, 1989) in a concentration dependent manner. Similar levels also increase the likelihood of dangerous electrical rythms (dysrythmias) (Shepps et al., 1990). Experimental exposure of normal resting adults to levels expected in urban environments causes no untoward effects until relatively high concentrations of COHb are achieved (Stewart et al., 1970). These include headache and impairment of concentration. EPIDEMIOLOGY A few epidemiological surveys have addressed the relationship between air pollution and death from ischemic heart disease. In one study, of 5529 New York bridge and tunnel workers, a greater than expected rate of death from ischaemic heart disease was found, particularly in those aged over 55 years (Stern et al., 1988). CHILD HEALTH Although studies on mothers exposed to ambient carbon monoxide have not been performed, there are data from women who smoke in pregnancy. It is estimated that foetal COHb concentrations are 7.6-12.6% in women who smoke one packet of cigarettes per day. The placentas in such pregnancies tend to be 10% heavier than expected, which is evidence for impaired blood flow to the foetus and relatively poor foetal oxygenation (Hoppenbrouwers et al, 1990). Although this is perhaps an extreme example, it is reasonable to suggest that mothers who are occupationally exposed to car exhaust, eg. traffic wardens or police, may be at risk. Another group of children potentially at risk are those with congenital heart defects. Many such children have low blood oxygen levels and minor reductions in their oxygen carrying capacity may be hazardous. 1.2.6 LEAD Concern about environmental pollution with lead is warranted because of increasing evidence that low level lead exposure impairs the mental development of young children. Though it is impossible to quantify exactly the contribution of road transport to levels of lead in the environment, it is a major source of environmental lead. Once emitted, lead eventually settles in the soil and surface water. Children are exposed both by inhalation of urban air and ingestion of dust and soil. Other important sources are food and drinking water. Dust ingestion is highest in areas in proximity to dense traffic. Airborne lead levels are in the range 0.5-3ug/m3 for most European cities. In London the annual mean concentration has been in the range 0.1-0.6ug/m3 over the period 1985-1989. There has been a general drop in emissions since the introduction of legislation in 1986 to reduce the lead content of petrol, and the increased availability and use of unleaded petrol (LSS, 1989). There is no reliable equation for calculating the relationship between airborne lead and blood lead in children (partly because of dust ingestion), but in adults a change of 1ug/m3 in airborne lead is associated with a blood lead change of 0.01-0.02ug/ml (Nriagu, 1978). Guidelines: The EC air quality limit value for lead in air is 2ug/m3 The WHO recommends a 1 year mean in the range 0.5-1.0ug/m3 This guideline is set to maintain a blood lead level of <20ug/100ml in 98% of the general population. In urban populations in the UK, blood lead concentrations fall in the range 5-40ug/100ml with the majority being <20ug/100ml. Levels rise steeply over the first 2 years of life, than begin to decrease to a minimum at about 12 years, with levels remaining steady through adult life (Hunter, 1986). HEALTH EFFECTS TOXICOLOGY AND CHILD HEALTH Lead has a range of potential toxic effects. The toxic effects observed depend on dose. At blood levels of 80-100 ug/dl or more they include lead colic (intestinal distress) anaemia due to reduced haemoglobin synthesis, kidney damage and irreversible brain damage. At blood lead levels in the range of 30-60 ug/dl effects include reduced haemoglobin synthesis, peripheral nerve abnormalities and disturbed kidney and reproductive function. (US EPA, 1986). Children may exhibit toxic effects at lower doses than adults. Some unfavourable effects increase with increasing blood lead levels even within the normal range. They include subtle changes in the sythesis of blood cells in adults and children (Piomelli et al., 1982), increased blood pressure in middle aged men (Pocock et al ., 1984) and central nervous system effects in children (Otto et al ., 1982). Most investigations of lead effects in children have focused on intelligence tests and other tests of psychological and social function. This research was pioneered in the USA where children with high levels of lead in teeth scored significantly less well in ability tests than those with low levels (Needleman et al , 1979). Subsequent studies in the UK have yielded equivocal results. Three studies found no statistically significant association between body lead burden and mental ability after allowance for compounding factors (Yule et al ., 1981; Smith et al., 1983; Harvey et al., 1984). A fourth study showed a small but significant effect after the inclusion of compounding variables (Fulton et al., 1987). The effect of blood lead on children's ability remains a source of controversy in Britain (Lansdown, 1986). The US Environmental Protection Agency has considered the better designed studies together and concluded that there is a positive association between lower level lead exposures and cognitive effects with average deficits of one or two IQ points at blood levels of 15-30 ug/dl and four or five points at higher levels. 1.2.7 BENZENE Benzene is one of a complex suite of aromatic hydrocarbons which include toluene and xylene. Benzene is known to cause cancer in humans (WHO, 1987). The major atmospheric sources are emissions from motor vehicles and evaporative losses during the transportation, handling and sale of petrol. Ambient concentrations are highest in the vicinity of petrol stations and near oil refineries (California Air Resources Board, 1984). For this reason, vapour retrieval systems, which limit exposure of the public at filling stations, are mandatory in California, and filling stations are situated away from communities. Additional sources of exposure of humans include tobacco smoke, food, drinking water and household solvents. Industrial exposure occurs in the rubber and petroleum industries. Ambient concentrations are generally between 1 to 50ppb. Children living in urban areas have much higher benzene and toluene blood concentrations (Jermann et al., 1989), than children in rural areas. Information on ambient benzene levels in the UK is scant. In Newham, levels of 130 ppb have been measured on the Romford Road at rush hours and a background level of 2 ppb was measured on derelict land adjacent to London City Airport (Kirkwood, pers. comm.). A level of 13000 ppb was recorded 2 metres from petrol pumps during delivery of bulk fuel to a petrol station in Orpington in the London Borough of Bromley. A level of 2500 ppb was recorded immediately before the delivery and 30 minutes afterwards. A level of 9000 ppb was recorded at a similar distance from pumps at a filling station in Penge during fuel delivery. Levels of 2000 ppb were recorded before delivery with levels falling to 5000 ppb 30 minutes after delivery. Neither station had vapour recovery systems in place (Hawes, pers. comm.). Guidelines: As it is a known carcinogen, the WHO is unable to recommend a safe level for airborne benzene. HEALTH EFFECTS TOXICOLOGY Benzene depresses blood cell formation by the bone marrow of laboratory animals, and causes a variety of tumours in a dose dependent manner (Maltoni et al ., 1985). EPIDEMIOLOGY The assessment of cancer risk in humans exposed to benzene is largely based upon studies of leukaemia rates in two particular cohorts of workers in the United States, one producing rubber film material, and the other working in the Dow Chemical Company. In both cases, a greater than expected incidence of myelogenous leukaemia was observed, in association with an estimated exposure of 16mg/m3 (approximately 5000ppb) (Infante & White, 1985). Data from such studies are used to calculate the risk of leukaemia at the lower concentrations observed in the urban environment. This method of estimating risk is not universally accepted, but in the Los Angeles basin the added lifetime risk is estimated at 101 to 780 cases of leukaemia per million people exposed (CARB, 1984). CHILD HEALTH Comparisons of rates of leukaemia in urban and rural children have had conflicting results. However, one study which analyzed children in urban areas with high traffic density revealed an increased rate of cancers (especially leukaemia) in the high density group. There are a number of obvious potential confounding variables in such a study but the authors postulated that benzene was the aetiological agent responsible for the observed differences (Savitz & Feingold, 1989). Studies in pregnant women have revealed no foetal abnormalities following maternal exposure to low levels of benzene (WHO, 1987). 2 EFFECTS OF AIR POLLUTION ON CHILD HEALTH Our current understanding is that three broad categories of children's health may be affected by air pollution. These are (i) allergic diseases, namely hay fever and asthma, (ii) infection, particularly of the upper and lower respiratory tracts (ie. the nose and throat, and the lung) and (iii) cancer and leukaemia. Of these, there is clear evidence that asthma is worsened by air pollution. Asthma is a very common and potentially dangerous disorder and appears to be increasing. There is therefore a great deal of information on this subject and this is reflected by the attention paid to it in the following discussion. 2.1 ALLERGIC DISEASE One in five teenagers in Britain suffers from hay fever and one in seven primary school children has asthma (Davies & Ollier, 1989). Many physicians are convinced that both conditions are becoming more common and that asthma is now occurring in a more severe form than it did in the past. General practice surveys have shown that the number of people attending their doctors for treatment for both asthma and hay fever doubled between 1971-1981 (Flemming & Crombie, 1987). This trend appears to be continuing; more recent research indicates that the annual average weekly attack rate of asthma in the UK has quadrupled in the last 15 years (Fleming, pers. comm.) (see figure). The number of children admitted to hospital with asthma increased over the last 10 years (Anderson, 1989) and asthma deaths among young people are increasing. Asthma may be even more common than is generally realised; recent studies have suggested that as many as a quarter of the population may be hidden asthmatic sufferers, with symptoms, for example prolonged coughing after chest colds, unrecognised as being due to asthma. 2.1.1 ASTHMA Asthma is a condition in which narrowing of the medium sized air passages of the lung gives rise to wheezing, shortness of breath and cough. A wide variety of stimuli including house dust mite, pollens and air pollutants trigger attacks by irritating inflamed airways in asthmatics' lungs. There is good evidence that susceptibility to asthma is inherited but that environmental agents are necessary to activate the disease. A CHANGING DISEASE Records from the Westminster Hospital from 1873 to 1935 show that although asthma was well recognised in the late 1800's and early 1900's, it was a very rare cause of admission or deaths in adults until just after the First World War (Dr Ian Gregg, pers. comm.). No children were admitted to the paediatric wards with asthma until around 1910. After the Second World War paediatric asthma admissions rose spectacularly and by the 1960's asthma had reached epidemic proportions. Similar epidemics appeared to affect a number of other westernised countries. In Britain hospital admission rates for children with asthma trebled over the 15 year period from 1959-1973 (Anderson, 1987) and asthma deaths were higher than at any time in the previous hundred years. Over the last decade deaths from asthma among 5-34 year olds have risen by between 30-60% in Australia, France, England and Wales, Canada and the US. In a 10 year period in just six countries - the US, Canada, England and Wales, France, West Germany and Japan, 187,000 deaths were attributed to asthma (Sears, 1990). Partly due to inadequate data, studies of asthma prevalence in the UK have been unable to confirm the impression among many clinicians that asthma has recently become more common. A recent overview of studies carried out on children in the UK over the last 20 years has shown a fairly consistent picture; over the course of a year about one school age child in every ten will experience symptoms of wheezing and between three and five per cent will be diagnosed as asthmatic (Anderson, 1989). Observations such as this have led some respiratory physicians to suggest that overall the severity of asthma has increased rather than the prevalence. AIR POLLUTION AND THE CHANGE IN ASTHMA Asthma appears to have increased in severity despite an impressive array of modern drugs available to treat the condition (Gregg, 1989). A number of hypotheses have been put forward but so far none have adequately accounted for the change. They include diagnostic transfer due to recent changes in international disease classification, changing patterns in diagnosis, failure to recognise and treat severe asthma and the suggestion that some of the drugs in modern usage may themselves have contributed to asthma deaths (Burr, 1987). Another possibility advanced by epidemiologists is that some new environmental factor which has been operative during the last 30 to 40 years in westernised countries may be responsible. Of the many agents that could be incriminated, atmospheric pollutants are among the most likely. (Sears, 1990) Air pollutants could affect asthma in a number of ways (Wardlaw, A., pers. comm.): 1 by causing a direct irritant effect on hypersensitive airways. Laboratory studies implicate both O3, SO2 and acid aerosols as potential bronchoconstricting agents; 2 by provoking airway hyperactivity via airway inflammation; 3 by having a direct toxic effect. Oxidants, particularly O3 are toxic to respiratory epithelium. This could aggravate existing asthma or cause asthma in susceptible individuals; 4 by modifying the immune response. For example, air pollutants might have an adjuvant effect increasing specific Ige (antibody) responses to inhaled allergens such as pollens and house dust mite, resulting in enhanced sensitivity to these agents. CONTROLLED CHAMBER EXPOSURE EXPERIMENTS Laboratory studies carried out on adolescents and adults with asthma have demonstrated that ozone, sulphur dioxide and acid aerosols can provoke asthma. Inhalation of SO2 causes wheezing in healthy individuals and asthmatics but asthmatics react at a far lower dose. Normal individuals do not appear to suffer major adverse effects unless concentrations of SO2 are well in excess of 1ppm but concentrations as low as 0.2ppm may affect asthmatics, especially during mouth breathing or undergoing heavy exercise (Linn, 1983). There appears to be no difference between short 5 minute exposures and longer 1 hour exposures, suggesting it is the dose rate which is important rather than total dose. Wheeziness provoked by SO2 appears to be short lived, easily reversed by bronchodilators and without any delayed effects. Studies of SO2 have been carried out on adolescents and adults with relatively mild asthma and it is possible that children or individuals with more severe asthma may react at lower doses. The WHO's 1 hour guideline of 130 ppb, set just below the reported threshold for effects on 'at risk groups', may thus offer only a narrow or non-existent margin of protection (UN ECE, 1990). These guidelines are regularly exceeded in many parts of the UK (Warren Spring Laboratory, 1990). Ozone causes changes in lung function including an increase in nonspecific airway hyper-reactivity and may exacerbate or induce asthma (Richards, 1990). Asthmatics do not appear to be more at risk from ozone than non-asthmatics. The ozone effect is most marked during exercise. With heavy exercise respiratory irritation can occur at concentrations around 200ppb over 1-2 hours (Linn et al , 1986; Folinbee et al., 1984). Exercising cyclists exposed to 210ppb of O3 for 1 hour experienced a significant fall in lung function with symptoms of upper airway irritation and chest tightness. Effects develop more slowly than with SO2 and persist for longer periods. There is some evidence that people exposed to high concentrations of ozone develop tolerance (Farrell et al , 1979) but this appears to subside within a few days of the last exposure (Linn et al , 1982). Although asthmatics do not appear more sensitive to the direct effects of ozone it may facilitate the entry of aero allergens, a phenomenon demonstrated in animal studies (Boushey, 1989). Recently, Drs Noe Zammel and Francis Silverman at the Gage Institute in Toronto found asthmatics sensitive to ragweed, a common allergen in North America, demonstrated an enhanced response after breathing ozone at the US standard of 120ppb. This could prove to be an important mechanism whereby asthma is worsened by ozone exposure (Bates, 1990). Acid aerosols have a variable effect on lung function. Asthmatics appear to be more susceptible; changes in lung function have been documented at concentrations of 100ug/m3 H2SO4 in children and 350ug/m3 in adults (Koenig et al., 1983; Utell et al., 1984). Recent research has shown that the lung function of exercising adolescent asthmatics is impaired at levels between 70-100ug/m3, levels close to those measured in ambient air in summer camps attended by children in the USA (Koenig, 1989). Researchers elsewhere have found asthmatics to be sensitive only at concentrations over 1000ug/m3 (Hackney et al., 1989). Ammonia produced in the mouth neutralises inhaled acid (Larson et al., 1977). Concentrations of oral ammonia vary widely and may explain why some people develop bronchoconstriction at much lower levels of acid aerosol than others. Studies on the effects of NO2 on asthmatics' lung function have produced contradictory results. Orehek et al. (1976) demonstrated that inhalation of 100ppb of NO2 by 20 asthmatics for 1 hour resulted in 13 developing impaired lung function. Other researchers have demonstrated increased responsiveness in asthmatics after breathing 200ppb of NO2 for 2 hour periods with light intermittent exercise (Kleinman et al., 1983; Mohsenin, 1987). However a number of studies have failed to show any effect on asthmatics after inhalation of NO2 up to 4000ppb (Linn et al., 1985; Hazucha et al., 1983). Studies of individual pollutants overlook the fact that in reality, air pollutants virtually always occur in combination. Recent laboratory studies of pollution mixtures suggest 'cocktails' of pollutants may have more profound effects. Koenig et al . of the University of Washington in Seattle recently exposed adolescent asthmatics aged 12-18 to low concentrations of SO2 (100ppb) having previously exposed them to ozone at the US standard of 120ppb for 45 minutes. The exposure resulted in significantly increased airway reactivity (Koenig, 1990). Such levels of both pollutants are regularly recorded in parts of the UK. EPIDEMIOLOGICAL STUDIES MAJOR POLLUTION EPISODES Several major air pollution episodes this century have demonstrated that in some circumstances air pollution may induce asthma but more usually acts as a triggering factor for asthma attacks. During the late 1940's a number of United States Army personnel and their families stationed in Yokohama, a polluted area near Tokyo, developed asthma which was often severe enough to require their transfer. The new disease, initially termed Yokohama Asthma and later Tokyo-Yokohama Respiratory Disease, affected both adults and children, often in families with no previous history of asthma. Symptoms were worse on days when the air pollution was particularly bad but when the families moved out of the affected area, their asthma generally improved and often resolved completely. American airforce crews reported their symptoms seemed to vanish when they flew to a height of five thousand feet or more above the contaminated area but it returned again within minutes of landing (Huber, 1954). Around the middle of the century three famous pollution episodes in the Meuse Valley, Belgium (Firket, 1931), Denora, Pennsylvania (Shrenk et al ., 1949), and London (Ministry of Health, 1954) highlighted the link between pollution and ill health. In each case temperature inversions trapped polluted air near the ground. High levels of SO2 and particulate matter were recorded but many scientists believe acid aerosols formed at the same time were primarily responsible for the excess disease and deaths. Asthma appeared to play a large part in at least the first two incidents. In Donora, 43% of the general population but 88% of asthmatics felt chest discomfort. The part played by asthma in the London episode is less clear as most of 4000 or so excess deaths were attributed to bronchitis and coronary heart disease. However, the deaths were not investigated until two years after the event and it seems likely that many patients labelled as suffering from bronchitis, may actually have suffered from asthma (Dr Andrew Wardlaw, pers. comm.). PANEL STUDIES OF ASTHMATICS A number of panel studies of asthmatics have shown a clear effect of air pollution on asthma. The studies implicate both sulphurous and photochemical pollutants at levels encountered in Europe and the UK. One such study of 51 asthmatics aged 7-55 living in Houston Texas found an increased risk of asthma attacks with increased ozone and decreased temperature. Ozone concentrations were in the range 20 to 160ppb (Holguin, 1985). In a second study (Khan, 1977) 80 children aged 8-15 years kept a log of symptoms, medication and hospital visits for asthma. Ozone, and to a lesser extent SO2, was related to an increase in both the frequency and severity of asthma attacks whereas pollen counts and winter temperature had no effect. OTHER EPIDEMIOLOGICAL STUDIES There is good evidence that children living in polluted conditions suffer more respiratory tract symptoms including cough and wheeze and are more susceptible to respiratory tract infections. However, numerous studies attempting to elucidate the link between air pollution and asthma within larger populations have proved inconclusive. Such studies are hampered by a number of confounding factors which must be taken into account such as weather conditions, personal exposure to tobacco smoke, aero allergens and infectious agents, and lack of information on individual exposure to precise pollutants. A further difficulty is the lack of common guidelines for diagnosing asthma. For example a patient with cough, a common sympton of asthma, may be regarded as having acute bronchitis, rather than asthma, which would result in under-diagnosis of asthma. Several studies have compared respiratory symptom reporting and lung function in children from low and high pollution areas. Not all studies have shown an effect but on balance, the evidence suggests that relatively low level exposure to both photochemical and sulphurous air pollution can impair lung function in normal populations. Some of the most important studies are described below. Researchers in Marseille monitored the effect of daily changes in SO2 levels on respiratory symptoms during winter 1983-84 in 450 children aged 9-11 years living in the Gardanne coal-basin, France. Low pollution areas had mean SO2 levels of 10ppb and high pollution areas 150ppb with daily SO2 levels up to 132ppb. In Biver and Gardanne, the most polluted communities, there was a statistically significant association between daily SO2 levels and prevalence of morning cough and wheezing in the chest (Charpin et al , 1988). A study in Akron, Ohio examined daily 24 hr air pollutants (SO2, NO2) levels and daily diaries in children attending two different schools. The mean SO2 level during the school year was equal to 29ppb in polluted areas and 8ppb in low pollution areas. The incidence of respiratory symptoms, especially cough, runny nose and sore throat was higher in the polluted area (Mostardi et al., 1981). A survey of second and fifth grade school children living in two communities in Israel found that children living in the more polluted community were twice as likely to suffer from asthma. In the higher pollution area, Ashod, an oil fired power station, refineries and a complex industrial zone contributed to monthly average SO2 concentrates in the region of 20ppb with maximal concentrations of 30ppb. In the second community, Hadera, unpolluted in 1980 when the survey was carried out, monthly averages of SO2 were around 2ppb (Goren & Hellman, 1988). A recent survey of 574,878 19-year-old entrants to the Polish army correlated respiratory disease with the mean annual SO2 levels in the recruits' home town. As the SO2 levels increased from an annual mean of less than 5ppb to an annual mean of 28ppb the prevalence of chronic bronchitis rose from 1.18 per thousand to 3.83 per thousand, and the prevalence of asthma from 1.19 per thousand to 6.23 per thousand (Bates, pers. comm.). Recently researchers in Atlanta, Georgia reported a strong correlation between emergency hospital visits for asthma in children and ambient levels of ozone (White et al., 1991). A correlation between childhood asthma, traffic dependent pollutants (NO2, NO, CO) and traffic load has also been identified in Germany (Wichmann et al., 1989). A small number of epidemiological studies suggest levels of air pollutants too low to have direct effect could work indirectly by sensitizing the airways to other bronchoconstricting agents such as aero allergens. Berciano et al (1989) studied 248 children with asthma living in polluted and non-polluted areas in Spain. An area was considered to be polluted when the concentration of sedimentary material (TSP) was above 300mg/m3/day; under 300mg/m3/day was designated a non-polluted area. Children living in polluted areas had significantly more wheezing episodes a year than children in non-polluted areas. In addition, the children living in the more polluted area tended to have more severe asthma. Berciano's report points out that the factors which produced the wheezing episodes were the allergens to which individual asthmatic children were sensitive, mainly house dust mite, and not the air pollutants. These findings are consistent with toxicological studies which indicate that pollutant concentrations needed to induce bronchoconstriction experimentally are usually higher than levels found even in the most polluted cities. The higher frequency of crises and more severe asthma seen in children living in the more polluted areas indicate that air pollution may be acting synergistically through some unknown mechanism. Berciano's study is corroborated by further research linking long term exposure to moderate levels of air pollution with asthma and eczema in children under 15 years of age in Eyrie County between 1946 and 1961 with data from 21 air sampling stations in the same area. The incidence rates of hospitalised cases for each condition produced a definite gradient by air pollution level. An average annual incidence rate of 32.4 hospitalised asthma cases per 100,000 population at risk was found at the lowest air pollution level in comparison to a rate of 50.7 at the highest air pollution level. The average annual incidence rate of hospitalised eczema cases was only 2.9 per 100,000 population at the lowest air pollution level in contrast to an average rate of 10.2 at the highest level. The relationship between air pollution and both diseases was most marked among boys under five - a particularly striking observation in view of the fact that boys are in any case at increased risk of asthma. ADMISSION AND EMERGENCY ROOM STUDIES A study of emergency room visits to St Christopher's Hospital for Children in Philadelphia in the early 1960's showed a 3 times greater incidence of asthma on high pollution days rising to 9 times on days with both high barometric pressure and high pollution. There was no correlation between asthma attacks and ragweed pollen counts (Girsch et al., 1967). In Southern Ontario, hospital admissions data for the 79 acute care hospitals in the region were compared with air pollution levels over a 10 year period for the months January and February and July and August (Bates & Sizto, 1987). Over this period, concentrations of SO2 declined from mean hourly levels of 5000ppb to 2000ppb while concentrations of O3 and NO2 remained stable. Although asthma admissions increased, not much of this was due to the change in the disease classification halfway through the study. In the summer months there was a significant correlation between levels of O3, SO4 and SO2 and admissions for both asthma and other respiratory disease 24-48 hours later. In a follow up study relating emergency visits in Vancouver to air pollution they noted an epidemic of asthma admissions in the autumn similar to that found in other studies but this was unrelated to air pollutants, temperature or known pollens. Concentrations of air pollutants were not markedly raised with hourly maximal concentrations of SO2 generally in the range 10 to 60 ppb (Bates & Sizto 1987 , Bates et al., 1990). However, the authors suggested that in southern Ontario the relationship between hospital admissions in the summer and the summer pollutants, including SO2, ozone and sulphate (SO4) might be due to their co-existence with sulphuric acid aerosol. In contrast in Vancouver, where SO4 levels are less than one quarter those in Ontario, sulphuric acid aerosol is unlikely to exist. A further study found a positive correlation between emergency rooms visits for asthma and NO2, hydrocarbon and COH levels but not with SO2 or O3 in children in Los Angeles. If anything an inverse correlation was seen between photochemical oxidant levels and emergency room visits (Richards, 1981). Tseng (1989) reported a seasonal variation in asthma admissions among 48,000 patients hospitalised in Hong Kong between 1976 and 1985. Hospitalisations for asthma peaked from October to December and to a lesser extent, from April to June. In a follow up study (Tseng, 1990) found an inverse correlation between quarterly admissions for asthma and SO2 but not for other pollutants. The authors concluded that a 'surge' of SO2 in one quarter could have resulted in a 'surge' in hospitalisations for asthma in the next quarter. They suggested the negative correlation between hospital admissions and air pollutant indices imputed that neither ambient SO2 or photo chemical oxidant pollution significantly affected emergency room visits or hospitalisation for asthma. However, they speculated that SO2 exposure in one season may cause increased airway inflammation resulting in increased asthma in the next season. 2.1.2 HAY FEVER AND AIR POLLUTION Hay fever or seasonal allergic rhinitis, has been recognised since the sixteenth century. The symptoms of sore, watering eyes, and nasal blockage or discharge are due to allergy to pollens. Different types of pollen are responsible for these problems in different geographical regions. In the UK timothy and rye grass cause most allergic rhinitis while in Scandinavia, tree pollens, particularly birch are a more usual cause. In the USA grass pollens cause hay fever in the summer months while allergy to ragweed causes problems in the early autumn (Davies & Ollier, 1989). A number of studies have documented an increase in the prevalence of allergic rhinitis this century. In the UK large scale population surveys found the prevalence of hay fever to increase from 5.1 people consulting per 1000 population in 1955 to 20 consultations per 1000 in 1981 (Fleming & Crombie, 1987). This increase cannot readily be explained by increased exposure to allergens as levels of grass pollen have fallen during this period. Recently Japanese scientists have proposed a mechanism which could explain how increasing levels of certain air pollutants may be contributing to an increase in hay fever. Before 1950 allergic rhinitis was extremely rare in Japan. Over the last three decades it has risen sharply; more than 20 different kinds of pollen have been shown to cause the disease but allergy to Japanese cedar pollen is most common. Over the same period the number of diesel powered cars in use in Japan has risen rapidly, from 14,897 in 1951 to 5,151,625 in 1983. Suspicion that some component of diesel exhaust could be connected with the increase of allergic rhinitis was heightened by surveys of school children in rural and urban districts in Japan. They showed that the prevalence of allergic rhinitis was markedly higher among children living in districts polluted by vehicle exhaust; in 1980 more than 1 child in 3 living in polluted areas had hay fever. This observation prompted researchers to study the effect of particulate emissions from diesel cars on the production of IgE antibody, an antibody which is increased in allergic conditions including allergic rhinitis and asthma. They demonstrated that diesel exhaust particulates enhanced the production of specific IgE in respect to an airway irritant in mice. In addition a persistent antibody response to Japanese cedar pollen was observed in mice immunised with cedar pollen mixed with diesel exhaust particulate, but not in animals immunised with cedar pollen alone (Muramaka et al , 1986). Recently researchers at the Department of Immunology, St Mary's Hospital in London in collaboration with the Centre for Environmental Technology at Imperial College London have demonstrated that ambient levels of air pollutants can exacerbate hay fever symptoms. In a pilot study carried out during summer 1990, 65 volunteer hay fever sufferers aged 12-65 years and living within 10 kilometres of central London filled out daily symptom diaries which were subsequently correlated with pollen counts and daily air pollution peaks (Gunner et al., 1991). Although pollen accounted for 70% of nose and eye symptoms, pollutants had an additional effect. No2 and O3 had a further effect on nasal running. The study has received funding for a further two years from the National Asthma Campaign and may include personal monitoring of pollutants during 1992. 2.2 AIR POLLUTION AND RESPIRATORY INFECTION Chronic lung problems in adult life are influenced by the occurence of respiratory tract infection in childhood. Colley et al. (1973) showed that chronic cough was more common at the ages of 20 and 25, both in smokers and non-smokers, in those individuals who had a lower respiratory tract illness before the age of 2. Barker and Osmond (1986) showed a strong geographical relationship in the UK between death rates from chronic bronchitis and emphysema between 1959-78 and infant mortality from bronchitis and pneumonia during 1921-25, again suggesting a causal link between childhood infection and adult chronic bronchitis. There is a clear relationship between childhood infection and air pollution; Waller (1966) demonstrated an increase in the frequency and severity of lower respiratory tract infections of boys and girls exposed to increasing amounts of air pollution. There was no difference in attack rates with social class. An association between lower respiratory tract infection and air pollution was found in each school age group and school examination at age 15 years suggested that respiratory effects persisted until that age. Lunn et al . (1967) showed that both upper respiratory tract infection (manifest as cough productive of green sputum or pneumonia) were associated with geographical area reflecting the pollution levels in Sheffield. Ponka (1990) found that ambient levels of sulphur dioxide and nitrogen dioxide significantly correlated with the number of upper respiratory tract infections reported from health centres, and with absenteeism from child care facilities. Simple croup, a viral infection of the upper airway characterised by acute hoarseness, barking cough and inspiratory stridor, usually occurring in the first years of life, is thought to be influenced by air pollution (Zach, 1990). Laboratory data has revealed that some environmental pollutants weaken the host defences of the respiratory tract which may explain some of the above findings. Sulphur dioxide, acid aerosols, nitrogen dioxide and particles can all depress the ability to clear foreign bodies (including bacteria) from the lung. Bacteria and viruses that enter the lungs are repelled by the local immune system, including some white blood cells (called macrophages). Pollutants, particularly nitrogen dioxide and ozone, have been shown to depress this local immunity (Schlesinger, 1990). 2.3 AIR POLLUTION AND CANCER There are reports of relationships between cancer and occupational exposure to pollutants. Individuals who have worked for many years in oil refineries have an increased risk of leukaemia (Wongsrichanalai et al., 1989; Wong and Raabe 1989). Workers exposed for many years to diesel exhaust such as railroad workers (Garshick et al., 1987) and truck drivers (Steenland, 1986) have a small increased risk of lung cancer. The general population is exposed to the same pollutants, but the ambient levels are much lower. However, for an agent which causes cancer there is no safe level. With respect to benzene which causes leukaemia, it is estimated that there are 100-780 excess deaths per year from leukaemia in the Los Angles area as a result of environmental exposure to this substance, but this is based upon observed effects at much higher levels (CARB, 1984). Attempts to show a relationship between real occurrence of childhood cancer and urban environment have shown either a slight increase (Blair et al., 1980) or a slight decrease (Selvin et al., 1983) in leukaemia rates. 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Notes on units of air pollutant concentrations used: To facilitate comparison and avoid confusion throughout the report, the standard system of unit used is the volume mixing ratio. Thus for SO2, NO2, O3, CO, and benzene (C6H6) concentrations are given in parts per billion or ppb. Conversion into units of mass per unit volume, usually ug/m3, are given for EC and WHO limit/guide values using the factors below: pollutant ppb to ug/m3 ug/m3 to ppb gas multiply by multiply by SO2 2.66 0.37 NO 1.25 0.80 NO2 1.91 0.52 O3 2.00 0.50 CO 1.16 0.86 C6H6 3.24 0.31 [at 20 deg C, 1013 mb] The other pollutants described in the report, such as smoke, particulates, acid aerosols and lead, are present as particles in the air and are not usually expressed in terms of volume mixing ratios. All these pollutants are therefore described in ug/m3. in the case of acid aerosols, acid (H+ superscript) equivalents are also given in nano moles per cubic metre or nmoles/m3. GLOSSARY (Note: the definitions below are intended to assist understanding of certain technical or medical terms within the text. They may be oversimplified for other purposes.) Airway resistance: The resistance offered by the airways to the flow of respiratory gas in and out of the lungs. High resistance may be caused by mucus or other fluid in the air passages, or by excess constriction of the surrounding smooth muscle. It increases the work of breathing and provokes symptoms such as wheezing and shortness of breath. Allergen: Any substance capable of producing specific hypersensitivity in an animal or human. Pollens and housedust mite are examples of common allergens. Alveoli: The air sacs within the lungs through which respiratory gas exchange takes place. Ambient air: In this context, outdoor air. Airway reactivity: The tendency of the airways to constrict in response to certain stresses. Asthmatics have abnormally high airway reactivity even when they are free of symptoms. Airway reactivity is measured by bronchial provocation testing where the subject is asked to inhale aerosols of histamine or methacholine of gradually increasing strength. British Smoke Method (Black smoke or BS method): estimates "smoke" in the atmosphere by drawing air through a white filter paper and measuring the density of the resulting stain. The "smoke" collected consists of particles of 10um diameter or less. Bronchitis: Inflammation of the mucous membrane lining the larger and medium-sized bronchi (the airways between the trachea and the small air passages within the lungs.) Bronchiolitis: Inflammation of the bronchioles, the smaller air passages of the lung. Respiratory bronchiolitis refers to inflammation of the smallest bronchioles which terminate at the alveoli. Bronchoconstriction: Narrowing of the bronchial tubes. Carboxyhaemoglobin (CoHb): Blood haemoglobin that carries carbon monoxide in place of oxygen. Emphysema: A condition in which the alveoli, small air sacs of the lungs, become dilated. Emphysema occurs in a number of conditions including chronic bronchitis. It is also found in the lungs of smokers and elderly people. Epidemiology: The study of disease in defined populations. In this context, the systematic observation of health status and air pollution exposure in communities. Epithelium: Closely packed sheet of cells lining the hollow structures within the body. Bronchial epithelium refers to the cells lining the bronchial passages. Dysrhythmia: Abnormal electrical heart rhythm. Forced expiratory volume (FEV): (A measure of lung function). The maximum volume of air that can be forced out in a given time. It is usually expressed as FEV1 ie. the amount of air forced out in one second. In healthy people FEV1 averages about 80% of forced vital capacity (FVC). A persistently low percentage ( around 65 % or less ) may indicate chronic bronchitis or emphysema. Temporary decreases may result from a decrease in FVC, commonly found in ozone exposures, or from an increase in airway resistance, often found in asthmatics exposed to sulphur dioxide during exercise. Forced Vital Capacity (FVC): (A measurement of lung function.) The volume of a maximum breath forced out. Temporary decreases may indicate irritation of the respiratory tract, a common effect of ozone exposure. Persistent low values may indicate stiffness of the lung or loss of inflatable volume due to scar tissue (pulmonary fibrosis). IgE antibody: An antibody which is increased in allergic conditions including allergic rhinitis and asthma. Inflammation: A localized response of the body to tissue injury. In the respiratory tract it is characterized by swelling of tissues, dilation of small blood vessels with leakage of fluid into air passages and influx of white blood cells. Macrophage: A type of white blood cell which scavenges bacteria and other debris from sites of inflammation. Mucociliary clearance: The natural defense mechanism by which particles (pollutants, bacteria or allergens) are removed from the bronchial passages. Particles are first captured on a blanket of mucus lining the airway. Cilia, tiny hair like projections on the epithelial lining cells, then sweep mucus and residue towards the mouth. Oxidant gas: Highly reactive gas which readily donates electrons to form unstable compounds. (Please check this definition, Charlie). Ozone is the most important oxidant pollutant. Palmes tubes: Passive samplers (diffusion tubes) for measuring nitrogen dioxide. Particulate matter: Finely divided solids or liquids dispersed into air from combustion, industrial activities and natural sources. Airborne particulates consist of a complex mixture of organic and inorganic substances. Various descriptive terms exist which tend to reflect measuring techniques or particle size. In Europe and the UK measurements of suspended particulate matter are based on soiling properties and referred to as 'smoke'. In the USA the monitoring technique is based on weight and the particulates referred to as 'total suspended particulate' (TSP). Respirable particulates are those particles small enough to penetrate the lower respiratory tract. Particles less than 10um in diameter (PM 10) penetrate the lungs fairly efficiently and are considered to be hazardous to health. Passive samplers: Simple devices which collect gaseous pollutants by molecular diffusion. They are reliable, cheap to maintain and portable. Nitrogen dioxide and sulphur dioxide can be measured by this method. Peak Expiratory Flow Rate (PEF): A measure of lung function. The maximum amount of air forced out through the mouth for 10 milliseconds. Personal monitoring: The use of personal equipment such as passive samplers to relate ambient air quality to the health of individuals. Percentile: Percentiles are widely used in reporting pollution data. In a sequence of pollution measurements from a particular site, the 98 percentile is that pollution concentration which is found to be exceeded by 2% of the measured values. Likewise, the 50 percentile (the median) is the value exceeded by 50% of the measured values. Photochemical oxidants (Photochemical smog): The mixture of pollutants formed in a sunlit atmosphere as a result of reactions among hydrocarbons and nitrogen oxides. Stratospheric: Belonging to a layer of the atmosphere which begins approximately 11 kilometres (7 miles) above the surface of the earth. Tropospheric: Belonging to the lower part of the earth's atmosphere.