Aust. N.Z. J. Med. (1977). 7, pp. 78-87 REVIEW
Epidemiological Bases for Ambient Air Quality Criteria* S. R. Leeder? and L. D. Pengellyl From the Department of Clinical Epidemiology and Biostatistics, and the Department of Medicine, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada
Summary: Epidemiological bases for ambient air quality criteria. S. R. Leeder and L. D. Pengelly, Aust. N.z.J. Med., 1977, 7. pp. 78-87,
Epidemiological information about the health consequences of ambient air pollution is adequate at present to set upper limits so that acute deterioration due to pollution can be prevented in patients with chronic lung disease. However, our knowledge is incomplete with respect to what is a safe chronic background level, particularly with regard to reducing and preventing the amount of chronic respiratory disease presently occurring. This review concentrates exclusively on sulphur dioxide and particulate pollution, although the principles used in setting standards for these t w o pollutants may be applied to photochemical pollutants such as ozone which may affect the lung. It is only when the dose-effect relationships between pollution and disease are more clearly understood that the benefit of reducing air pollution to improve health can be predicted.
There are many ways in which we might set acceptable levels of ambient air pollution. If the community is very rich, aesthetic considerations may lead legislators to limit air pollution to small, invisible and, hopefully, innocuous emissions so that the colour of the sky and the amount of sunlight enjoyed by the community are not diminished. By contrast, in a poorer society, the need for industrial production may be so strong that economic constraints over‘Based o n a paper presented at a Specialty Conference on Criteria, Standards and Indices of Air Quality, Ontario Air Pollution Control Association. Toronto, Ontario, April 1976. t N H and MRC (Australia), Clinical Sciences Fellow in Epidemiology. $Associate Professor, McMaster Air Pollution Evaluation Laboratory, Department of Medicine, McMaster University Health Sciences Centre, Hamilton, Ontario. Canada. Correspondence. Dr. S. R . Leeder, Faculty of Medicine, University of Newcastle, NSW 2308, Australia Accepted for publication: 18 October, 1976
ride any air pollution control. Most Western industrial societies find themselves between these two extremes and ambient air pollution criteria are set partly according to what the society can afford. Another consideration is the consequence of pollution upon the health of the community reflecting both the value which these societies place on the individual and his “right to health” and also the realisation that sickness is now a major governmental expense and best avoided for economic reasons as well. This has led some countries, most notably Sweden and the Netherlands, to base their air quality criteria solely on epidemiological grounds. Biological consequences of pollution can be used in several ways in setting the limits of ambient air pollution. Episodes of very severe pollution (e.g. the London fogs) have clearly demonstrated that pollution may affect health and while we have no clear understanding of the underlying mechanisms, we can set limits to pollution to avoid these episodes. Studies of the effects of pollution carried out on cells, small animals or volunteers under the strictly controlled conditions of the laboratory, can suggest health consequences of pollutants, although often the results have proved disappointing because so few changes have been found with exposure‘to realistic, low ambient concentrations of single pollutants. Also the ambient pollution experienced in many communities is often much more complex than used in most laboratory tests. The importance of this complexity is not presently known as far as health is concerned, but it is essential that it be kept in mind if we are to be delivered from simplistic and erroneous answers to complex questions. Thus while toxicological and experimental exposure studies have been helpful in indicating leads as to the way in which air pollution may affect health, the consequences
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of various pollutants in ambient concentrations to which people are exposed in the community need to be assessed epidemiologically. It is only by studying the effects of these pollutants on free-living exercising communities that we obtain data which can be used for setting standards for ambient air pollution in the community. The Epidemiologist’s Task The intimate relationship between the environment in which a person lives and his health is not usually seriously questioned. This relationship exists whether we are considering people in the most technologically advanced society or in a traditional African or Asian village setting, or anywhere between these two extremes. In our studies of the environment in Western societies, we are now “looking for many small things rather than for a few large ones” as Godber (1975)2 put it; small differences in mortality and morbidity among individuals exposed to different environmental factors, small impairments in development and small contributions toward the origins of the chronic diseases which are now responsible for so much ill health. The epidemiologist is faced with the necessity of determining precisely what, and exactly how much, environmental change is necessary for optimal conditions for health. He is expected to be able to predict what benefits may follow from such changes and at what stage in a person’s life such changes must occur to be effective. Once we have acquired this knowledge it still remains to be communicated in such a way that it will motivate a willingness to change the environment by those who are able to change it. The proof of the pudding is in the eating: until a theoretically plausible and desirable change is tried out, we have no way of knowing completely how acceptable it is, what its side effects are or whether its cost is justified by its benefit. The respiratory epidemiologist is principally concerned with the relationship between various environmental factors and those forms of respiratory illness which are common in the community and which are important causes of morbidity and mortality. He is concerned with describing the dose-effect relationship between
SETTING STANDARDS FOR AIR POLLUTION How high bafore causing death or deterioration? ~
A
increased fhronic disease?
FIGURE 1. The issues to be decided with regard to air pollution (solid sawtooth line) are firstly, what are the upper levels (upper dotted line) above which air pollution peaks may cause death or deterioration in chronic patients and, secondly, what are the safe background levels (lower dotted line) which may be tolerated without causing additional cases of chronic disease in the exposed community?
ambient air pollution and the incidence, prevalence and severity of diseases such as chronic bronchitis which may be due in part to ambient pollution (Fig. 1). The establishment and proof of a dose-effect relationship between air pollution and these illnesses can provide useful information by which air pollution standards may be set. Some of the indicators the respiratory epidemiologist may use are listed in Table 1. Dfliculties the Epidemiologist Must Face In attempting to relate levels of ambient air pollution to impairment of health, the epidemiologist is confronted by some very serious problems. The recognition of these problems represents the first step in avoiding conclusions which are simple but false. Otherwise, he will make the mistake, made many times already, of finding associations between pollution and disease which, in truth, are not there or, conversely, missing associations which really exist. The first of these problems is encountered when the epidemiologist tries to obtain information about levels of air pollution in the geographical area he is studying. Very rarely is air pollution in one place due to a single agent. The association of particulate pollution with sulphur dioxide has meant that it has proved impossible so far to separate the effects of these two pollutants in epidemiological studies. Accurate dose-effect relationships thus remain to be determined for both these pollutants. Another problem soon encountered is the technique of
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pollution measurement, a particular difficulty if the epidemiologist is using published air pollution data rather than data which he has collected expressly for the purpose of his own study. Published data which may be used by the epidemiologist are sometimes indirect, e.g. the type and the amount of fossil fuel used over the years in the area which he is studying. Associated circumstances governing the quality and quantity of the pollutants which are emitted, such as the method of combustion employed and seasonal variations in temperature which control heating requirements and factors influencing dispersion are all also important. The latter include the height at which pollutants are emitted, the local topography and the frequency of inversion-type weather conditions.
TABLE I Indicators which the epidemiologist may use to relate air pollution to health (Modified from LTSDHEW Documents AP49 and APSO)' 1. M O R T A L I T I '
-
deaths from all causes deaths from cardiorespiratory disease total deaths age-specific (very old : very youns. etc.) disease-group specific (chronic bronchitics, etc.) ~
~
~
3. hlORBIDIT1'
~
~
~
-
~
prevalence of chronic disorders (diseases or symptoms) in which air pollution may play a part-chronic bronchitis, emphysema, bronchial carcinoma incidence of acute illness (or deterioration) in which air pollution may play a part-exacerbation of chronic lung disease. respiratory illness in childhood, conjunctival irritation measurement of ventilatory capacity including rate of change with age detection of changes in lung function by more sensitive tests, e.g. maximum expiratory flow rate at low lung volumes, heightened bronchial reactivity and bronchial cytopathology detection of changes in function not directly related to respiration (e.g. blood lead levels, etc.)
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If the epidemiologist is taking measurements himself, their placing and timing should be planned to take account of these factors. It is beyond the scope of this paper to evaluate critically the different technical problems encountered in the measurements of pollutants such as sulphur dioxide, particulates, carbon monoxide, oxidants and polycyclic aromatic hydrocarbons but all of these difficulties should be taken into account in any environmental epidemiological s t ~ d y . ~ Another problem frequently encountered in epidemiological studies of the relationship between air pollution and illness is that levels of pollutants rarely remain stable over a period of years. Further, in observing the chronic effects of air pollution on the health of populations, problems are encountered because of the movement of the populations themselves, as Anderson and Ferris" point out in discussing the limitations of their exemplary study of the relationship between pollution and lung function in Berlin, New Hampshire and Chilliwack, British Columbia. People may move from one neighbourhood to another and thus change their exposure to different air pollutants. To find an association between pollution and the development of chronic diseases which require many years to develop, larger samples must be studied to compensate for changing pollution levels and migration, and even this increase in sample size may not entirely solve the problem. Retrospective epidemiological surveys can demonstrate associations but cannot prove "cause and effect" relationships. In studying the relationship of air pollution to illness, it is difficult to be sure that what is causing illness is, in fact, air pollution. Many other urban features commonly vary in parallel with high air pollution levels, including less-than-desirable living conditions, overcrowding, low socio-economic class, and climatic factors. For example, in a three-day fog in London in December 1873, the death rate in the County of London increased suddenly by a factor of 1.4 and similar increases occurred in fogs reported in 1880, 1882, 1891 and 1892.3 Each of these fogs, however, was accompanied by exceptionally low temperatures and the part played by pol-
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lution in the increased death rate is, therefore, not clear. Epidemiological Methods The tools the epidemiologist has to use in these studies include observation of different mortality rates in communities exposed to different levels of air pollution, and similar comparisons of different rates of morbidity based on work absences, hospital admission rates and estimates of consulting rates in general practices according to different pollution levels. Specific surveys may be conducted in communities examining the whole or a sample of the population to determine the prevalence of symptoms of chronic bronchitis, emphysema, etc. or impaired ventilatory function. Mortality rates from the diseases may be compared in places with different pollution burdens over long periods to estimate the likely effects of chronic low levels of pollution. Short-term fluctuations in the mortality rate may be attributable to acute peaks of pollution in large cities. All these studies, with the possible exception of the study of shortterm fluctuations, depend on relating past levels of pollution to disease apparent in the present, but developing more or less insidiously over years. An alternative approach is to study groups, or cohorts of young people and children living in similar environments, differing in respect of a particular pollutant of interest, beginning the study when the subjects are at an age prior to the development of the disease, observing them prospectively over a number of years, studying the inception of chronic bronchitis and emphysema in people exposed to different levels of pollution. Implicit in this approach is the hypothesis that the adult diseases begin in childhood and that children serve as sensitive indicators of pollution effects. A prospective study delivers the investigator from having to make assumptions about uniform levels of exposure to air pollution over the years and provides him with a much better opportunity to allow for factors such as occupational exposure and cigarette smoking. He can then attribute variations in the amount of disease which he is observing to the factor of interest, in this case, air pollution.
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Relationship Between Mortality arid Acute High Leiiels of Pollution Epidemiological studies in London have provided important information about the health consequences of air pollutants such as sulphur dioxide and smoke. Following the episode of the London fog of 5th-8th December, 1952 in which over 4000 unexpected deaths occurred in Greater London, an alert was kept for subsequent increases in mortality which could be related to air pollution. In the 1952 fog, levels of smoke and sulphur dioxide (4460 and 3830 pg/m3 respectively, averaged over 48 hour periods) were recorded. Subsequently, Gore and Shaddick’ related daily records of deaths in the County of London (the inner, densely populated part of Greater London, containing just under half of the total population of eight million) to daily air pollution and observed increased mortality in four fogs that had occurred in 1954, 1955, 1956 and 1957 making adjustments for the season of the year. They demonstrated marked increases in mortality when smoke concentration exceeded 2000 pg/m3 with sulphur dioxide over 1140 pgl m3. Using similar techniques, Martin and Bradley6 demonstrated an increase in deaths with each major change in pollution during the winter 1958-59 when smoke exceeded 750pg,Jm3 and sulphur dioxide exceeded 710 pg/m3.’ As mortality often fell to subnormal levels after a pollution incident, and mortality generally fell on the second day of an incident when pollution remained high, and as the great majority of deaths in fog occurred among people suffering from respiratory or severe cardiac disease, it was argued that some or all of these deaths might have wcurred within a few days even under normal conditions. An examination of daily deaths in London, England, from 1958-1968 failed to detect many changes in daily mortality in response to increased pollution reflecting lower pollution levels and improved care for the chronically
How generally applicable is the technique of relating daily deaths to fluctuations in air pollution levels? Unfortunately, it is a technique not able to be widely used as it is essential that large study populations be available to over-
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come day-to-day random fluctuations in death rates which can otherwise obscure effects of pollution. For example, in London with its population of over eight million, there are some 200-400 deaths a day and the random variations from day-to-day are not so great as to obscure effects of pollution. However, in cities of about one million, although major episodes of pollution have occurred, in general, the random fluctuations in the mortality rate are too large for changes to be identified on a daily basis. In cities including New York, Chicago and Detroit, Andersong was able to show deviations from the moving averages of deaths during different seasons, and to relate these deviations to fluctuations in air pollution. Hechter and Goldsmith" and Breslow" reported that inquiry into the possible relationship of mortality to episodes of high air pollution revealed no significant relationship in Los Angeles. The situation in Los Angeles is also complicated by the wide daily variations in humidity and high daily maxima of temperatureI2, a situation not dissimilar to that in some Australian cities. From these various studies it is possible to conclude that acute peaks in air pollution of sulphur dioxide and smoke are associated in large cities with increased mortality from all causes, particularly cardiac and respiratory, in elderly people but levels of smoke and sulphur dioxide below 750 pg/m3 are not associated with an increased mortality. Workers in the Netherlands, including Brasser et al.' ', interpreted these data to imply that excess mortality did not occur below pollution levels of 400 pg/m3 for SO2 in the presence of soot. Without labouring the controversy, it is necessary to remember that these figures related specifically to the London environment and should be interpreted cautiously in other places.
Acute Exacerbations of Chronic Respiratory Disease and Air Pollution Some studies have tried to relate deterioration in the condition of patients with chronic respiratory disease to sudden increases in the levels of ambient air pollution. Most of these studies have also been carried out in Britain where morbidity statistics, whether relating to
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general practice attendance, hospital admissions or work absence tend to be of better quality than anywhere else in the world. A study. undertaken by Lawther'" in London in which bronchitis patients were asked to keep diaries to record an assessment of their health each day showed that, in winter months, the degree of illness was more closely associated with daily values of atmospheric pollution than with any other factor, though this association disappeared when pollution levels fell in the Spring. Furthermore, a summary of a series of studies of the condition of bronchitic patients during periods of increased pollution has shown that there are relatively few occasions even in London when the health of such patients suddenly deteriorates in recent years8 The minimum concentration of pollutants that could be linked with any definite change in the condition of chronic bronchitis patients were 250 pg/m3 of smoke or when sulphur dioxide exceeded 500 pg/m3 over a 24 hour average. The importance of climatic factors in fluctuation in the state of patients with chronic bronchitis has been emphasized in other studies and can lead to confusion in interpreting the effects of air pollution. However, it appears that when acute exacerbations of chronic respiratory disease are accepted as a reasonable basis on which to determine upper limits of air pollution with sulphur dioxide and smoke, that levels of 250 pg/m3 of smoke and 500 pg/m3 of sulphur dioxide are the limits for which published data suggest action should be taken. Carnow et a l l 5 , in a study of over 500 patients with respiratory disease, developed a personal pollution index for each patient which took account of occupation, social class w d place of residence, and found that pollution played a relatively minor role in causing exacerbations in patients under 55 years unless concentrations of SOz exceeded about 860 pg/m3. It should be emphasized also that not only does climate affect the interpretation of exacerbation data, whether based on health diaries or hospital admission ratcs, but that considerable random fluctuations due to many other factors occurring from dayto-day or week-to-week in patients' symptoms require very substantial sample sizes for thoroughly reliable data to be obtained.
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Studies Relating Air Pollution to Preoalence nj’chronic Respiratory Disease in Adults While a study of the acute effects of high levels of ambient pollution may provide information useful in setting criteria for the acceptable upper limits, a review of the health effects of atmospheric pollution must also attempt to assess the consequences of long-term exposure to ordinary concentrations of ambient air pollution. Here the effects are less dramatic and, consequently, more difficult to identify but are probably felt by a much greater proportion of the population. The effect of air pollution on the mortality from chronic bronchitis and emphysema is grossly overshadowed by the effects of cigarette smoking, and it is impossible to measure lifetime exposure to pollution as accurately as present or past smoking habits. While many studies in Britain and elsewhere have shown that mortality from chronic respiratory disease is more common amongst those living in cities than those in rural areas, it is not yet possible to assign confidently responsibility for this mortality to any particular pollutant or level of air pollution in general. This is not to deny a substantial urban-rural gradient in chronic chest disease but simply to caution against concluding that it is due to pollution. Studies of migrants may enable the effects of pollution exposure in early life to be studied if the levels of pollution are markedly different in the person’s original home and the place to which they have migrated. This method of enquiry has been used by Reid et a l l 6 in the study of respiratory morbidity among British migrants to the United States in which some persistent influence of the British environment in childhood was evident in symptom prevalence in migrants many years later. Because of the difficulties in obtaining accurate information about the lifetime exposure of individuals to pollution and the influence of differing areas of residence unrelated to pollution, and the overpowering effect of cigarette smoking, it is not possible at present to decide safe lower levels of air pollution on the basis of variations in mortality from chronic respiratory disease. The situation may be clarified somewhat by studying non-smokers. However, even though more individuals living in cities
83
may be dying from chronic respiratory disease, the influence of social factors, selective migration to the cities, overcrowding, nutrition and a multiplicity of other unidentified factors may yet explain the excess urban respiratory mortality. It also needs to be recalled that many diseases which do not appear to be causally related in any way to air pollution are often also more common among city dwellers. Studies Relating Air Pollution to Respiratory Illness Mortality in Children Several studies in the UK have shown an association between variations in environmental factors and mortality from respiratory disease in Deaths due to bronchitis, pneumonia and combinations of both have been noted to be more frequent in winter than summer, and occur most commonly in areas where socio-economic circumstances were poor, where living conditions were often crowded and where air pollution was most concentrated?’ In all of these studies it was difficult to separate the effects of individual environmental factors and to be sure that the effects of the environment were specifically upon the respiratory tract. Collins et aLZ0 in their study of the association of several measures of social class, crowding and air pollution, found the effect of these factors to be most marked in the youngest children (i.e. under one year). Death rates due to respiratory disease were compared with those of congenital malformations and accidents as control diseases unrelated to pollution. Domestic pollution and industrial pollution indices were associated to some extent with the number of deaths due to respiratory disease, as were social class, crowding, population density and family educational level. Weaker associations were found with mortality among older children, but the numbers of deaths were smaller and conclusions less certain. Death rates due to the control diseases, particularly congenital malformations, were not associated with the environmental factors to the same extent as respiratory disease mortality. Almost all of the environmental effects were attributed to “domestic” (i.e. ambient pollution due to home heating) and “industrial” air pollution when partial correlation co-efficients
84
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were calculated, but in the absence of detailed measurements of pollution, these findings must be interpreted cautiously biologically, especially when trying to decide which pollutant is responsible. It is not possible to use these data to decide what is the lowest level below which further reduction in air pollution would fail to reduce the number of deaths of children from respiratory diseases. Such a detailed doseeffect study relating pollution to infant mortality is needed. Studies Relating Air Pollution to Respiratory Illness Incidence in Children Beside its immediate mortality, respiratory illness in childhood may mark the beginnings of the lifetime of chronic respiratory disease in some individuals.' Although clinical recovery from acute respiratory illness in childhood is usual, this may not always be as complete as has been assumed. In a number of studies, children with a history of lower respiratory chest illness have been found to have lower ventilatory function than children who escape such Among army recruits, Rosenb a ~ found m ~ a~ greater liability to respiratory infection among those who had spent their childhood in an industrial town. In a birth cohort followed until age 20 years, Colley et found that those with a history of lower respiratory tract illness under two years of age had a higher prevalence of respiratory symptoms at age 20 than those without such a history although the dominant factor associated with symptoms at this age was cigarette smoking. British immigrants in the United States have a small, but significant, persistent excess risk in developing respiratory symptoms due, in part, to adverse environmental factors in earlier life. These findings may be interpreted as evidence of some degree of permanent lung damage in consequence of childhood experience. An association between respiratory illness incidence in childhood and air pollution has been found in a number of community surveys carried out in the United Kingdom, many of which were reviewed by C 0 1 l e y . ~ ~ A study in Kent, England undertaken by Holland et examined the separate effects of different environmental factors and determined the con-
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tribution made by air pollution to respiratory morbidity and impaired ventilatory function in children. Almost 11,000 children aged 10-13 years attending schools in four areas of Kent were examined. Smoke and sulphur dioxide levels were measured at three sites for three months and data about crowding and other social conditions were collected at all four areas. Levels of peak expiratory flow rates were examined in relation to four factors: area of residence, social class, family size and past history of respiratory disease. Small differences in respiratory morbidity could be attributed to the environmental and personal factors, but area of residence played a major part. Because of the limited measurements of pollution however, not all the influence of area of residence could be attributed to air pollution. In a study of nearly 11,000 children aged 6-10 living in contrasting rural and urban areas in England and Wales, Colley and Reid2' found an association of chest conditions with increasing levels of air pollution in children of semi-skilled and unskilled workers. Children in Wales had much more past bronchitis and chronic cough than English children. A gradient in illness incidence was found in the English areas covering the range of 35 to 145 pg/m3 mean winter sulphur dioxide although equally reliable measurements of pollution were not available for all rural areas studied. Douglas and Waller3' found that among nearly 4000 adopted children living in many parts of England, incidence of lower respiratory illness in the first two years of life followed a similar gradient to air pollution with smoke and sulphur dioxide, the incidence ranging from 4.3"" in areas with SO2 levels below 100 pg/m3 annual average up to 12.9"" in children living in areas where annual average for SO2 was over 270 pg/m3 and smoke between 142 and 281 pg/m3. These studies show that the children living in areas with a lower pollution level generally have less respiratory illness, but the exact doseeffect relationship between specific pollutants and respiratory illness or decreased ventilatory function has not yet been determined. A study established by Holland and his colleagues may throw light on the dose-effect relationships between pollution with smoke,
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sulphur dioxide and the incidence of lower respiratory illness and reduced ventilatory capacity in ~ h i l d r e n . ~ Illness ' incidence in children attending primary school in ten areas of England and Scotland is being related to measurements of smoke and sulphur dioxide recorded within I km of each school. The levels of pollutants range from 30-130 pg/m3 of smoke and from 25-135 pg/m3 of SO, in November. Predictions based upon the relationship between respiratory illness in 1816 children and pollution showed that reductions of smoke or SO2 levels from 130 pg/m3 to 10 pg/m3 could result in a decline in respiratory symptom prevalence from 49", to 40°0 in the highest risk group and from 179, to 12", in the lower risk group (Fig. 2). The high and low risk groups were defined by such other factors as social class which had an overriding influence upon respiratory illness prevalence in these children. N o evidence of a thoroughly safe lower level of pollution was found in the data although from these predictions it can be seen that only relatively small reductions in illness would be expected from very substantial changes in pollution. However, this study is important because it attempts to construct a precise doseeffect relationship between certain defined and specifically measured pollutants and respiratory illnesses in children which are known to be INFLUENCE OF POLLUTION O N LOWER RESPIRATORY ILLNESS I N 1,816 CHILDREN (U.K.) AGED 6-10 YEARS
A ' OF GROUP WITH LOWER RESPIRATORY ILLNESS
associated with reductions in lung function. It is of the utmost importance that similar studies be carried out and that the predictions derived from these dose-effect relationships be tested in real life situations. In Port Kembla, Bell32 demonstrated a change in respiratory symptom prevalence following reduction of SO, and particulate pollution after a higher stack was installed at a smelter, exemplifying the value of documenting changes in health following environmental modification. Advantage may be taken of situations where levels of pollution are planned to be reduced, using before-and-after studies to test the validity of the predictions of improved respiratory health following a reduction in pollution. Future Directions-for Epidemiological Contributions in the Determination of Air Pollution Standards Even with two quite common air pollutants, sulphur dioxide and smoke, present information is adequate only for suggesting acceptable upper limits of pollution on the basis of avoiding exacerbations of chronic respiratory disease and deaths in the elderly with chronic respiratory and cardiac problems. While there is a relationship between urban living and the prevalence of chronic chest disease among adults, it is difficult to interpret this in a context in which cigarette smoking exerts an overriding influence and where there are likely to be other unidentified but, nevertheless, very important factors in the urban environment contributing to this excess. In children, a relationship can be described between air pollution and the incidence of lower respiratory illness which, in turn, is known to be associated in some children with diminished ventilatory and a small predisposition to the development of symptoms of chronic bronchitis in the third decade.28 The dose-effect relationships are gradually being described, but in the case of both children and adults, no study thus far is adequate in providing full information about the way in which air pollution causes illness nor in proving that the dose-effect relationship is really due to a specific pollutant. This proof depends upon the demonstration that changing the level of air pollution deliberately will lead
7'
"1
40
30
m
LOW RlSW GROUP
l0I ~
lWg/m'
SMOKE OR SO.
13bg/m'
bard on data from lrwig et a1 119741
FIGURE 2. Dose-response relationship between air pollution and incidence of lower respiratory illness in children aged 5-11 years in the UK living in relatively low polluted areas (10-1 30 pg/m3, November average) obtained from a logistic model by Lrwig et a/. (1974). The high risk group comprised boys, aged 5, of low social class (V) parents, and the l o w risk group girls, aged 11 of high (I) social class parents.
85
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LEEDER AND PENGELLY
to a reduction in either mortality or morbidity of the diseases of specific interest, just as showing a diminished consequent risk of lung cancer in ex-smokers strengthens the case that cigarette smoking is an important cause of lung cancer. If air pollution contributes to the development of chronic bronchitis and emphysema then it probably does this by exerting a longterm effect over many years. If a relationship exists between childhood respiratory illness and that in adults (and this remains hypothetical), childhood illness could be a sensitive indicator used to define the air pollution levels which would reduce chronic bronchitis. Another hypothetical way in which the health effects of air pollution could be studied can be based upon the observation of groups of smokers some of whom eventually develop serious obstructive lung disease. Fletcher et a / . 3 3have shown that, by observing individuals at regular intervals over several years, it is possible to identify those smokers who, as a result of smoking, are tracking towards the development of clinically substantial pulmonary disease in later life (Fig. 3). These “tracking” smokers may include individuals who are losing ventilatory capacity because of quite different patho-
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physiological responses to smoking, but their common feature is their progressive loss of lung function and eventual clinical problems due to it. Fletcher et found a reversion to a more normal rate of loss of lung function (Fig. 3) in those individuals who could be encouraged to give up smoking, although the range of response to ceasing smoking was wide. We do not want to create the impression that pollution necessarily affects the lungs the same way as does smoking. However, if a relationship between air pollution and accelerated loss of ventilatory capacity is established (possibly in certain sensitive individuals) the effects of changing air pollution levels on the rates of loss of ventilatory capacity could be assessed over a period of three or four years, providing the study was well designed statistically, in a similar way to the study referred to above33 dealing with the effects of giving up smoking. The study would have the advantage of relating a reduction in air pollution to a reduction in the main “risk factor” (i.e. accelerated loss of ventilatory capacity) for the development of chronic obstructive lung disease and could have immediate repercussions for the development of suitable air pollution standards. Conclusion
LOSS OF VENTILATORY FUNCTION WITH AGE VENTILATORY CAPACITY
EXPOSED-’
CAUSAL FACTOR REMOVED leg. cigarettes, air pollution)
‘-A-
PRE-DISEASED GROUP CLINICAL DISEASE
+
30
AGE (years)
.. 70
FIGURE 3. Ventilatory capacity normally declines evenly (upper broken line) with increasing age in the fourth and subsequent decades, but the decline may accelerate in patients developing chronic lung disease (solid, lower line), for example, in a cigarette smoker developing chronic obstructive lung disease. If smokers demonstrating accelerated loss of ventilatory capacity stop smoking, ventilatory function loss with age may revert to a more normal rate33 (middle broken line), and the onset of clinical disease delayed. Subjects manifesting these various patterns can be observed by prospective studies. If pollution has the same effect on the lungs as smoking, it is possible that the benefits, if any, of reducing air pollution could manifest in a way similar to stopping smoking in affected individuals.
While the difficulties in using an epidemiological technique to establish air pollution criteria are substantial, it is possible by understanding the natural history of chronic lung disease to design methods which may provide useful information for defining the dose-effect relationship between common pollutants and lung disease. The information which we have at present is useful in setting upper limits of common air pollutants to prevent acute problems due to pollution occurring in patients with chronic lung disease. However, our knowledge is incomplete with respect to what constitutes a safe background level to reduce the amount of chronic respiratory disease presently occurring. Australian ambient air standards are close to those accepted by the Environmental Protection Agency of the USA and the World Health Organisation and are adequate to prevent acute exacerbations of respiratory disease. It is only when the dose-
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effect relationships are more clearly understood that cost-benefit equations relating reduction in air pollution to improvement in health and quality of life can be accurately determined. References I . Air Quality Criteria for Particulate Matter (AP49)and Air Quality Criteria for Sulfur Oxides (AP50). U S. Department of Health. Education and Welfare, Puhlic Health Service Consumer Protection and Environmental Health Service, National Air Pollution Control Association. Washington, D C (January, 1969). 2. G O D B ~ R Sir, G (1975):In: Pediatric3 & the Environmtwr. Report o r t h e 2nd Unigdte Pediatric Workshop: Edited by Donald Barltrop, Fellowship of Postgraduate Medicine, London, p. 3-4. 3. HOLLAND, W.W (1972):Air pollution and respiratory disease Technomi
Epidemiological Bases for Ambient Air Quality Criteria* S. R. Leeder? and L. D. Pengellyl From the Department of Clinical Epidemiology and Biostatistics, and the Department of Medicine, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada
Summary: Epidemiological bases for ambient air quality criteria. S. R. Leeder and L. D. Pengelly, Aust. N.z.J. Med., 1977, 7. pp. 78-87,
Epidemiological information about the health consequences of ambient air pollution is adequate at present to set upper limits so that acute deterioration due to pollution can be prevented in patients with chronic lung disease. However, our knowledge is incomplete with respect to what is a safe chronic background level, particularly with regard to reducing and preventing the amount of chronic respiratory disease presently occurring. This review concentrates exclusively on sulphur dioxide and particulate pollution, although the principles used in setting standards for these t w o pollutants may be applied to photochemical pollutants such as ozone which may affect the lung. It is only when the dose-effect relationships between pollution and disease are more clearly understood that the benefit of reducing air pollution to improve health can be predicted.
There are many ways in which we might set acceptable levels of ambient air pollution. If the community is very rich, aesthetic considerations may lead legislators to limit air pollution to small, invisible and, hopefully, innocuous emissions so that the colour of the sky and the amount of sunlight enjoyed by the community are not diminished. By contrast, in a poorer society, the need for industrial production may be so strong that economic constraints over‘Based o n a paper presented at a Specialty Conference on Criteria, Standards and Indices of Air Quality, Ontario Air Pollution Control Association. Toronto, Ontario, April 1976. t N H and MRC (Australia), Clinical Sciences Fellow in Epidemiology. $Associate Professor, McMaster Air Pollution Evaluation Laboratory, Department of Medicine, McMaster University Health Sciences Centre, Hamilton, Ontario. Canada. Correspondence. Dr. S. R . Leeder, Faculty of Medicine, University of Newcastle, NSW 2308, Australia Accepted for publication: 18 October, 1976
ride any air pollution control. Most Western industrial societies find themselves between these two extremes and ambient air pollution criteria are set partly according to what the society can afford. Another consideration is the consequence of pollution upon the health of the community reflecting both the value which these societies place on the individual and his “right to health” and also the realisation that sickness is now a major governmental expense and best avoided for economic reasons as well. This has led some countries, most notably Sweden and the Netherlands, to base their air quality criteria solely on epidemiological grounds. Biological consequences of pollution can be used in several ways in setting the limits of ambient air pollution. Episodes of very severe pollution (e.g. the London fogs) have clearly demonstrated that pollution may affect health and while we have no clear understanding of the underlying mechanisms, we can set limits to pollution to avoid these episodes. Studies of the effects of pollution carried out on cells, small animals or volunteers under the strictly controlled conditions of the laboratory, can suggest health consequences of pollutants, although often the results have proved disappointing because so few changes have been found with exposure‘to realistic, low ambient concentrations of single pollutants. Also the ambient pollution experienced in many communities is often much more complex than used in most laboratory tests. The importance of this complexity is not presently known as far as health is concerned, but it is essential that it be kept in mind if we are to be delivered from simplistic and erroneous answers to complex questions. Thus while toxicological and experimental exposure studies have been helpful in indicating leads as to the way in which air pollution may affect health, the consequences
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of various pollutants in ambient concentrations to which people are exposed in the community need to be assessed epidemiologically. It is only by studying the effects of these pollutants on free-living exercising communities that we obtain data which can be used for setting standards for ambient air pollution in the community. The Epidemiologist’s Task The intimate relationship between the environment in which a person lives and his health is not usually seriously questioned. This relationship exists whether we are considering people in the most technologically advanced society or in a traditional African or Asian village setting, or anywhere between these two extremes. In our studies of the environment in Western societies, we are now “looking for many small things rather than for a few large ones” as Godber (1975)2 put it; small differences in mortality and morbidity among individuals exposed to different environmental factors, small impairments in development and small contributions toward the origins of the chronic diseases which are now responsible for so much ill health. The epidemiologist is faced with the necessity of determining precisely what, and exactly how much, environmental change is necessary for optimal conditions for health. He is expected to be able to predict what benefits may follow from such changes and at what stage in a person’s life such changes must occur to be effective. Once we have acquired this knowledge it still remains to be communicated in such a way that it will motivate a willingness to change the environment by those who are able to change it. The proof of the pudding is in the eating: until a theoretically plausible and desirable change is tried out, we have no way of knowing completely how acceptable it is, what its side effects are or whether its cost is justified by its benefit. The respiratory epidemiologist is principally concerned with the relationship between various environmental factors and those forms of respiratory illness which are common in the community and which are important causes of morbidity and mortality. He is concerned with describing the dose-effect relationship between
SETTING STANDARDS FOR AIR POLLUTION How high bafore causing death or deterioration? ~
A
increased fhronic disease?
FIGURE 1. The issues to be decided with regard to air pollution (solid sawtooth line) are firstly, what are the upper levels (upper dotted line) above which air pollution peaks may cause death or deterioration in chronic patients and, secondly, what are the safe background levels (lower dotted line) which may be tolerated without causing additional cases of chronic disease in the exposed community?
ambient air pollution and the incidence, prevalence and severity of diseases such as chronic bronchitis which may be due in part to ambient pollution (Fig. 1). The establishment and proof of a dose-effect relationship between air pollution and these illnesses can provide useful information by which air pollution standards may be set. Some of the indicators the respiratory epidemiologist may use are listed in Table 1. Dfliculties the Epidemiologist Must Face In attempting to relate levels of ambient air pollution to impairment of health, the epidemiologist is confronted by some very serious problems. The recognition of these problems represents the first step in avoiding conclusions which are simple but false. Otherwise, he will make the mistake, made many times already, of finding associations between pollution and disease which, in truth, are not there or, conversely, missing associations which really exist. The first of these problems is encountered when the epidemiologist tries to obtain information about levels of air pollution in the geographical area he is studying. Very rarely is air pollution in one place due to a single agent. The association of particulate pollution with sulphur dioxide has meant that it has proved impossible so far to separate the effects of these two pollutants in epidemiological studies. Accurate dose-effect relationships thus remain to be determined for both these pollutants. Another problem soon encountered is the technique of
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pollution measurement, a particular difficulty if the epidemiologist is using published air pollution data rather than data which he has collected expressly for the purpose of his own study. Published data which may be used by the epidemiologist are sometimes indirect, e.g. the type and the amount of fossil fuel used over the years in the area which he is studying. Associated circumstances governing the quality and quantity of the pollutants which are emitted, such as the method of combustion employed and seasonal variations in temperature which control heating requirements and factors influencing dispersion are all also important. The latter include the height at which pollutants are emitted, the local topography and the frequency of inversion-type weather conditions.
TABLE I Indicators which the epidemiologist may use to relate air pollution to health (Modified from LTSDHEW Documents AP49 and APSO)' 1. M O R T A L I T I '
-
deaths from all causes deaths from cardiorespiratory disease total deaths age-specific (very old : very youns. etc.) disease-group specific (chronic bronchitics, etc.) ~
~
~
3. hlORBIDIT1'
~
~
~
-
~
prevalence of chronic disorders (diseases or symptoms) in which air pollution may play a part-chronic bronchitis, emphysema, bronchial carcinoma incidence of acute illness (or deterioration) in which air pollution may play a part-exacerbation of chronic lung disease. respiratory illness in childhood, conjunctival irritation measurement of ventilatory capacity including rate of change with age detection of changes in lung function by more sensitive tests, e.g. maximum expiratory flow rate at low lung volumes, heightened bronchial reactivity and bronchial cytopathology detection of changes in function not directly related to respiration (e.g. blood lead levels, etc.)
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If the epidemiologist is taking measurements himself, their placing and timing should be planned to take account of these factors. It is beyond the scope of this paper to evaluate critically the different technical problems encountered in the measurements of pollutants such as sulphur dioxide, particulates, carbon monoxide, oxidants and polycyclic aromatic hydrocarbons but all of these difficulties should be taken into account in any environmental epidemiological s t ~ d y . ~ Another problem frequently encountered in epidemiological studies of the relationship between air pollution and illness is that levels of pollutants rarely remain stable over a period of years. Further, in observing the chronic effects of air pollution on the health of populations, problems are encountered because of the movement of the populations themselves, as Anderson and Ferris" point out in discussing the limitations of their exemplary study of the relationship between pollution and lung function in Berlin, New Hampshire and Chilliwack, British Columbia. People may move from one neighbourhood to another and thus change their exposure to different air pollutants. To find an association between pollution and the development of chronic diseases which require many years to develop, larger samples must be studied to compensate for changing pollution levels and migration, and even this increase in sample size may not entirely solve the problem. Retrospective epidemiological surveys can demonstrate associations but cannot prove "cause and effect" relationships. In studying the relationship of air pollution to illness, it is difficult to be sure that what is causing illness is, in fact, air pollution. Many other urban features commonly vary in parallel with high air pollution levels, including less-than-desirable living conditions, overcrowding, low socio-economic class, and climatic factors. For example, in a three-day fog in London in December 1873, the death rate in the County of London increased suddenly by a factor of 1.4 and similar increases occurred in fogs reported in 1880, 1882, 1891 and 1892.3 Each of these fogs, however, was accompanied by exceptionally low temperatures and the part played by pol-
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lution in the increased death rate is, therefore, not clear. Epidemiological Methods The tools the epidemiologist has to use in these studies include observation of different mortality rates in communities exposed to different levels of air pollution, and similar comparisons of different rates of morbidity based on work absences, hospital admission rates and estimates of consulting rates in general practices according to different pollution levels. Specific surveys may be conducted in communities examining the whole or a sample of the population to determine the prevalence of symptoms of chronic bronchitis, emphysema, etc. or impaired ventilatory function. Mortality rates from the diseases may be compared in places with different pollution burdens over long periods to estimate the likely effects of chronic low levels of pollution. Short-term fluctuations in the mortality rate may be attributable to acute peaks of pollution in large cities. All these studies, with the possible exception of the study of shortterm fluctuations, depend on relating past levels of pollution to disease apparent in the present, but developing more or less insidiously over years. An alternative approach is to study groups, or cohorts of young people and children living in similar environments, differing in respect of a particular pollutant of interest, beginning the study when the subjects are at an age prior to the development of the disease, observing them prospectively over a number of years, studying the inception of chronic bronchitis and emphysema in people exposed to different levels of pollution. Implicit in this approach is the hypothesis that the adult diseases begin in childhood and that children serve as sensitive indicators of pollution effects. A prospective study delivers the investigator from having to make assumptions about uniform levels of exposure to air pollution over the years and provides him with a much better opportunity to allow for factors such as occupational exposure and cigarette smoking. He can then attribute variations in the amount of disease which he is observing to the factor of interest, in this case, air pollution.
81
Relationship Between Mortality arid Acute High Leiiels of Pollution Epidemiological studies in London have provided important information about the health consequences of air pollutants such as sulphur dioxide and smoke. Following the episode of the London fog of 5th-8th December, 1952 in which over 4000 unexpected deaths occurred in Greater London, an alert was kept for subsequent increases in mortality which could be related to air pollution. In the 1952 fog, levels of smoke and sulphur dioxide (4460 and 3830 pg/m3 respectively, averaged over 48 hour periods) were recorded. Subsequently, Gore and Shaddick’ related daily records of deaths in the County of London (the inner, densely populated part of Greater London, containing just under half of the total population of eight million) to daily air pollution and observed increased mortality in four fogs that had occurred in 1954, 1955, 1956 and 1957 making adjustments for the season of the year. They demonstrated marked increases in mortality when smoke concentration exceeded 2000 pg/m3 with sulphur dioxide over 1140 pgl m3. Using similar techniques, Martin and Bradley6 demonstrated an increase in deaths with each major change in pollution during the winter 1958-59 when smoke exceeded 750pg,Jm3 and sulphur dioxide exceeded 710 pg/m3.’ As mortality often fell to subnormal levels after a pollution incident, and mortality generally fell on the second day of an incident when pollution remained high, and as the great majority of deaths in fog occurred among people suffering from respiratory or severe cardiac disease, it was argued that some or all of these deaths might have wcurred within a few days even under normal conditions. An examination of daily deaths in London, England, from 1958-1968 failed to detect many changes in daily mortality in response to increased pollution reflecting lower pollution levels and improved care for the chronically
How generally applicable is the technique of relating daily deaths to fluctuations in air pollution levels? Unfortunately, it is a technique not able to be widely used as it is essential that large study populations be available to over-
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come day-to-day random fluctuations in death rates which can otherwise obscure effects of pollution. For example, in London with its population of over eight million, there are some 200-400 deaths a day and the random variations from day-to-day are not so great as to obscure effects of pollution. However, in cities of about one million, although major episodes of pollution have occurred, in general, the random fluctuations in the mortality rate are too large for changes to be identified on a daily basis. In cities including New York, Chicago and Detroit, Andersong was able to show deviations from the moving averages of deaths during different seasons, and to relate these deviations to fluctuations in air pollution. Hechter and Goldsmith" and Breslow" reported that inquiry into the possible relationship of mortality to episodes of high air pollution revealed no significant relationship in Los Angeles. The situation in Los Angeles is also complicated by the wide daily variations in humidity and high daily maxima of temperatureI2, a situation not dissimilar to that in some Australian cities. From these various studies it is possible to conclude that acute peaks in air pollution of sulphur dioxide and smoke are associated in large cities with increased mortality from all causes, particularly cardiac and respiratory, in elderly people but levels of smoke and sulphur dioxide below 750 pg/m3 are not associated with an increased mortality. Workers in the Netherlands, including Brasser et al.' ', interpreted these data to imply that excess mortality did not occur below pollution levels of 400 pg/m3 for SO2 in the presence of soot. Without labouring the controversy, it is necessary to remember that these figures related specifically to the London environment and should be interpreted cautiously in other places.
Acute Exacerbations of Chronic Respiratory Disease and Air Pollution Some studies have tried to relate deterioration in the condition of patients with chronic respiratory disease to sudden increases in the levels of ambient air pollution. Most of these studies have also been carried out in Britain where morbidity statistics, whether relating to
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general practice attendance, hospital admissions or work absence tend to be of better quality than anywhere else in the world. A study. undertaken by Lawther'" in London in which bronchitis patients were asked to keep diaries to record an assessment of their health each day showed that, in winter months, the degree of illness was more closely associated with daily values of atmospheric pollution than with any other factor, though this association disappeared when pollution levels fell in the Spring. Furthermore, a summary of a series of studies of the condition of bronchitic patients during periods of increased pollution has shown that there are relatively few occasions even in London when the health of such patients suddenly deteriorates in recent years8 The minimum concentration of pollutants that could be linked with any definite change in the condition of chronic bronchitis patients were 250 pg/m3 of smoke or when sulphur dioxide exceeded 500 pg/m3 over a 24 hour average. The importance of climatic factors in fluctuation in the state of patients with chronic bronchitis has been emphasized in other studies and can lead to confusion in interpreting the effects of air pollution. However, it appears that when acute exacerbations of chronic respiratory disease are accepted as a reasonable basis on which to determine upper limits of air pollution with sulphur dioxide and smoke, that levels of 250 pg/m3 of smoke and 500 pg/m3 of sulphur dioxide are the limits for which published data suggest action should be taken. Carnow et a l l 5 , in a study of over 500 patients with respiratory disease, developed a personal pollution index for each patient which took account of occupation, social class w d place of residence, and found that pollution played a relatively minor role in causing exacerbations in patients under 55 years unless concentrations of SOz exceeded about 860 pg/m3. It should be emphasized also that not only does climate affect the interpretation of exacerbation data, whether based on health diaries or hospital admission ratcs, but that considerable random fluctuations due to many other factors occurring from dayto-day or week-to-week in patients' symptoms require very substantial sample sizes for thoroughly reliable data to be obtained.
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Studies Relating Air Pollution to Preoalence nj’chronic Respiratory Disease in Adults While a study of the acute effects of high levels of ambient pollution may provide information useful in setting criteria for the acceptable upper limits, a review of the health effects of atmospheric pollution must also attempt to assess the consequences of long-term exposure to ordinary concentrations of ambient air pollution. Here the effects are less dramatic and, consequently, more difficult to identify but are probably felt by a much greater proportion of the population. The effect of air pollution on the mortality from chronic bronchitis and emphysema is grossly overshadowed by the effects of cigarette smoking, and it is impossible to measure lifetime exposure to pollution as accurately as present or past smoking habits. While many studies in Britain and elsewhere have shown that mortality from chronic respiratory disease is more common amongst those living in cities than those in rural areas, it is not yet possible to assign confidently responsibility for this mortality to any particular pollutant or level of air pollution in general. This is not to deny a substantial urban-rural gradient in chronic chest disease but simply to caution against concluding that it is due to pollution. Studies of migrants may enable the effects of pollution exposure in early life to be studied if the levels of pollution are markedly different in the person’s original home and the place to which they have migrated. This method of enquiry has been used by Reid et a l l 6 in the study of respiratory morbidity among British migrants to the United States in which some persistent influence of the British environment in childhood was evident in symptom prevalence in migrants many years later. Because of the difficulties in obtaining accurate information about the lifetime exposure of individuals to pollution and the influence of differing areas of residence unrelated to pollution, and the overpowering effect of cigarette smoking, it is not possible at present to decide safe lower levels of air pollution on the basis of variations in mortality from chronic respiratory disease. The situation may be clarified somewhat by studying non-smokers. However, even though more individuals living in cities
83
may be dying from chronic respiratory disease, the influence of social factors, selective migration to the cities, overcrowding, nutrition and a multiplicity of other unidentified factors may yet explain the excess urban respiratory mortality. It also needs to be recalled that many diseases which do not appear to be causally related in any way to air pollution are often also more common among city dwellers. Studies Relating Air Pollution to Respiratory Illness Mortality in Children Several studies in the UK have shown an association between variations in environmental factors and mortality from respiratory disease in Deaths due to bronchitis, pneumonia and combinations of both have been noted to be more frequent in winter than summer, and occur most commonly in areas where socio-economic circumstances were poor, where living conditions were often crowded and where air pollution was most concentrated?’ In all of these studies it was difficult to separate the effects of individual environmental factors and to be sure that the effects of the environment were specifically upon the respiratory tract. Collins et aLZ0 in their study of the association of several measures of social class, crowding and air pollution, found the effect of these factors to be most marked in the youngest children (i.e. under one year). Death rates due to respiratory disease were compared with those of congenital malformations and accidents as control diseases unrelated to pollution. Domestic pollution and industrial pollution indices were associated to some extent with the number of deaths due to respiratory disease, as were social class, crowding, population density and family educational level. Weaker associations were found with mortality among older children, but the numbers of deaths were smaller and conclusions less certain. Death rates due to the control diseases, particularly congenital malformations, were not associated with the environmental factors to the same extent as respiratory disease mortality. Almost all of the environmental effects were attributed to “domestic” (i.e. ambient pollution due to home heating) and “industrial” air pollution when partial correlation co-efficients
84
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were calculated, but in the absence of detailed measurements of pollution, these findings must be interpreted cautiously biologically, especially when trying to decide which pollutant is responsible. It is not possible to use these data to decide what is the lowest level below which further reduction in air pollution would fail to reduce the number of deaths of children from respiratory diseases. Such a detailed doseeffect study relating pollution to infant mortality is needed. Studies Relating Air Pollution to Respiratory Illness Incidence in Children Beside its immediate mortality, respiratory illness in childhood may mark the beginnings of the lifetime of chronic respiratory disease in some individuals.' Although clinical recovery from acute respiratory illness in childhood is usual, this may not always be as complete as has been assumed. In a number of studies, children with a history of lower respiratory chest illness have been found to have lower ventilatory function than children who escape such Among army recruits, Rosenb a ~ found m ~ a~ greater liability to respiratory infection among those who had spent their childhood in an industrial town. In a birth cohort followed until age 20 years, Colley et found that those with a history of lower respiratory tract illness under two years of age had a higher prevalence of respiratory symptoms at age 20 than those without such a history although the dominant factor associated with symptoms at this age was cigarette smoking. British immigrants in the United States have a small, but significant, persistent excess risk in developing respiratory symptoms due, in part, to adverse environmental factors in earlier life. These findings may be interpreted as evidence of some degree of permanent lung damage in consequence of childhood experience. An association between respiratory illness incidence in childhood and air pollution has been found in a number of community surveys carried out in the United Kingdom, many of which were reviewed by C 0 1 l e y . ~ ~ A study in Kent, England undertaken by Holland et examined the separate effects of different environmental factors and determined the con-
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tribution made by air pollution to respiratory morbidity and impaired ventilatory function in children. Almost 11,000 children aged 10-13 years attending schools in four areas of Kent were examined. Smoke and sulphur dioxide levels were measured at three sites for three months and data about crowding and other social conditions were collected at all four areas. Levels of peak expiratory flow rates were examined in relation to four factors: area of residence, social class, family size and past history of respiratory disease. Small differences in respiratory morbidity could be attributed to the environmental and personal factors, but area of residence played a major part. Because of the limited measurements of pollution however, not all the influence of area of residence could be attributed to air pollution. In a study of nearly 11,000 children aged 6-10 living in contrasting rural and urban areas in England and Wales, Colley and Reid2' found an association of chest conditions with increasing levels of air pollution in children of semi-skilled and unskilled workers. Children in Wales had much more past bronchitis and chronic cough than English children. A gradient in illness incidence was found in the English areas covering the range of 35 to 145 pg/m3 mean winter sulphur dioxide although equally reliable measurements of pollution were not available for all rural areas studied. Douglas and Waller3' found that among nearly 4000 adopted children living in many parts of England, incidence of lower respiratory illness in the first two years of life followed a similar gradient to air pollution with smoke and sulphur dioxide, the incidence ranging from 4.3"" in areas with SO2 levels below 100 pg/m3 annual average up to 12.9"" in children living in areas where annual average for SO2 was over 270 pg/m3 and smoke between 142 and 281 pg/m3. These studies show that the children living in areas with a lower pollution level generally have less respiratory illness, but the exact doseeffect relationship between specific pollutants and respiratory illness or decreased ventilatory function has not yet been determined. A study established by Holland and his colleagues may throw light on the dose-effect relationships between pollution with smoke,
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sulphur dioxide and the incidence of lower respiratory illness and reduced ventilatory capacity in ~ h i l d r e n . ~ Illness ' incidence in children attending primary school in ten areas of England and Scotland is being related to measurements of smoke and sulphur dioxide recorded within I km of each school. The levels of pollutants range from 30-130 pg/m3 of smoke and from 25-135 pg/m3 of SO, in November. Predictions based upon the relationship between respiratory illness in 1816 children and pollution showed that reductions of smoke or SO2 levels from 130 pg/m3 to 10 pg/m3 could result in a decline in respiratory symptom prevalence from 49", to 40°0 in the highest risk group and from 179, to 12", in the lower risk group (Fig. 2). The high and low risk groups were defined by such other factors as social class which had an overriding influence upon respiratory illness prevalence in these children. N o evidence of a thoroughly safe lower level of pollution was found in the data although from these predictions it can be seen that only relatively small reductions in illness would be expected from very substantial changes in pollution. However, this study is important because it attempts to construct a precise doseeffect relationship between certain defined and specifically measured pollutants and respiratory illnesses in children which are known to be INFLUENCE OF POLLUTION O N LOWER RESPIRATORY ILLNESS I N 1,816 CHILDREN (U.K.) AGED 6-10 YEARS
A ' OF GROUP WITH LOWER RESPIRATORY ILLNESS
associated with reductions in lung function. It is of the utmost importance that similar studies be carried out and that the predictions derived from these dose-effect relationships be tested in real life situations. In Port Kembla, Bell32 demonstrated a change in respiratory symptom prevalence following reduction of SO, and particulate pollution after a higher stack was installed at a smelter, exemplifying the value of documenting changes in health following environmental modification. Advantage may be taken of situations where levels of pollution are planned to be reduced, using before-and-after studies to test the validity of the predictions of improved respiratory health following a reduction in pollution. Future Directions-for Epidemiological Contributions in the Determination of Air Pollution Standards Even with two quite common air pollutants, sulphur dioxide and smoke, present information is adequate only for suggesting acceptable upper limits of pollution on the basis of avoiding exacerbations of chronic respiratory disease and deaths in the elderly with chronic respiratory and cardiac problems. While there is a relationship between urban living and the prevalence of chronic chest disease among adults, it is difficult to interpret this in a context in which cigarette smoking exerts an overriding influence and where there are likely to be other unidentified but, nevertheless, very important factors in the urban environment contributing to this excess. In children, a relationship can be described between air pollution and the incidence of lower respiratory illness which, in turn, is known to be associated in some children with diminished ventilatory and a small predisposition to the development of symptoms of chronic bronchitis in the third decade.28 The dose-effect relationships are gradually being described, but in the case of both children and adults, no study thus far is adequate in providing full information about the way in which air pollution causes illness nor in proving that the dose-effect relationship is really due to a specific pollutant. This proof depends upon the demonstration that changing the level of air pollution deliberately will lead
7'
"1
40
30
m
LOW RlSW GROUP
l0I ~
lWg/m'
SMOKE OR SO.
13bg/m'
bard on data from lrwig et a1 119741
FIGURE 2. Dose-response relationship between air pollution and incidence of lower respiratory illness in children aged 5-11 years in the UK living in relatively low polluted areas (10-1 30 pg/m3, November average) obtained from a logistic model by Lrwig et a/. (1974). The high risk group comprised boys, aged 5, of low social class (V) parents, and the l o w risk group girls, aged 11 of high (I) social class parents.
85
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LEEDER AND PENGELLY
to a reduction in either mortality or morbidity of the diseases of specific interest, just as showing a diminished consequent risk of lung cancer in ex-smokers strengthens the case that cigarette smoking is an important cause of lung cancer. If air pollution contributes to the development of chronic bronchitis and emphysema then it probably does this by exerting a longterm effect over many years. If a relationship exists between childhood respiratory illness and that in adults (and this remains hypothetical), childhood illness could be a sensitive indicator used to define the air pollution levels which would reduce chronic bronchitis. Another hypothetical way in which the health effects of air pollution could be studied can be based upon the observation of groups of smokers some of whom eventually develop serious obstructive lung disease. Fletcher et a / . 3 3have shown that, by observing individuals at regular intervals over several years, it is possible to identify those smokers who, as a result of smoking, are tracking towards the development of clinically substantial pulmonary disease in later life (Fig. 3). These “tracking” smokers may include individuals who are losing ventilatory capacity because of quite different patho-
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physiological responses to smoking, but their common feature is their progressive loss of lung function and eventual clinical problems due to it. Fletcher et found a reversion to a more normal rate of loss of lung function (Fig. 3) in those individuals who could be encouraged to give up smoking, although the range of response to ceasing smoking was wide. We do not want to create the impression that pollution necessarily affects the lungs the same way as does smoking. However, if a relationship between air pollution and accelerated loss of ventilatory capacity is established (possibly in certain sensitive individuals) the effects of changing air pollution levels on the rates of loss of ventilatory capacity could be assessed over a period of three or four years, providing the study was well designed statistically, in a similar way to the study referred to above33 dealing with the effects of giving up smoking. The study would have the advantage of relating a reduction in air pollution to a reduction in the main “risk factor” (i.e. accelerated loss of ventilatory capacity) for the development of chronic obstructive lung disease and could have immediate repercussions for the development of suitable air pollution standards. Conclusion
LOSS OF VENTILATORY FUNCTION WITH AGE VENTILATORY CAPACITY
EXPOSED-’
CAUSAL FACTOR REMOVED leg. cigarettes, air pollution)
‘-A-
PRE-DISEASED GROUP CLINICAL DISEASE
+
30
AGE (years)
.. 70
FIGURE 3. Ventilatory capacity normally declines evenly (upper broken line) with increasing age in the fourth and subsequent decades, but the decline may accelerate in patients developing chronic lung disease (solid, lower line), for example, in a cigarette smoker developing chronic obstructive lung disease. If smokers demonstrating accelerated loss of ventilatory capacity stop smoking, ventilatory function loss with age may revert to a more normal rate33 (middle broken line), and the onset of clinical disease delayed. Subjects manifesting these various patterns can be observed by prospective studies. If pollution has the same effect on the lungs as smoking, it is possible that the benefits, if any, of reducing air pollution could manifest in a way similar to stopping smoking in affected individuals.
While the difficulties in using an epidemiological technique to establish air pollution criteria are substantial, it is possible by understanding the natural history of chronic lung disease to design methods which may provide useful information for defining the dose-effect relationship between common pollutants and lung disease. The information which we have at present is useful in setting upper limits of common air pollutants to prevent acute problems due to pollution occurring in patients with chronic lung disease. However, our knowledge is incomplete with respect to what constitutes a safe background level to reduce the amount of chronic respiratory disease presently occurring. Australian ambient air standards are close to those accepted by the Environmental Protection Agency of the USA and the World Health Organisation and are adequate to prevent acute exacerbations of respiratory disease. It is only when the dose-
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effect relationships are more clearly understood that cost-benefit equations relating reduction in air pollution to improvement in health and quality of life can be accurately determined. References I . Air Quality Criteria for Particulate Matter (AP49)and Air Quality Criteria for Sulfur Oxides (AP50). U S. Department of Health. Education and Welfare, Puhlic Health Service Consumer Protection and Environmental Health Service, National Air Pollution Control Association. Washington, D C (January, 1969). 2. G O D B ~ R Sir, G (1975):In: Pediatric3 & the Environmtwr. Report o r t h e 2nd Unigdte Pediatric Workshop: Edited by Donald Barltrop, Fellowship of Postgraduate Medicine, London, p. 3-4. 3. HOLLAND, W.W (1972):Air pollution and respiratory disease Technomi
