Compliance with the clean air act medical aspects: inter-regional symposium on criteria for air quality and methods of measurement, Geneva, 6-12 August 1963

WORLD HEALTH ORGAN IZA 'i-iON INTER-REGIONAL SYIVlPOSrJM ON CRITERIA FOR Am QUALITY AND METHODS . OF. MEASUREMENT Geneva, 6-12 August 1963 MEDICAL ASPECTS by ORGANISATION MONDIALE DE LA SANTE lflHO/AP/16 29 July 1963 P. J. LawtherJ M.B., F.R.C.P. Director, Medical Research Council Air Pollution Research Unit Consultant Phy~ician in Environmental Medicine St. Bartholomew 1s Hospital, London The implementation of the Clean Air Act is leading to the disappearance of smoke from our air whilst pollution by sulfur compounds continues unchecked. In this brief essay an attempt is made to forecast the benefits to health which may be expected to follow the removal of smoke, and to assess the clinical significance of the pollutants which will' still be· emitted. It should be stated firmly at the outset that the reduc- tion of any pollutant should be welcomed by clinicians; the Clean Air Act, admittedly but a partial solution to the problems posed by air pollution, deserves their vigorous support; smoke is certainly not beneficial to man. Before considering the more subtle properties,of air pollutants it is wi~ to remember that smoke is filthy and that this fact is of definite significance to the tired housewife; it obscures the sun and is aesthetically intolerable. Smoke is the result of incomplete combustion of carbonaceous fuels and its chemi- cal and physical composition is comp~ex ~Dd varied. It may consist of tar droplets or tiny particles of carbon or polymers with high carbon content. Electron microscopy . . 1 (Waller, Brooks and Cartwright 1963) has revealed the varied nature of its physical form and, in contrast to the grit and dust measured in deposit gauges, it exists in partic1 ;s which are small enough to be inhaled and reach the depths of the lungs. Whencifer organic matter, however simple, is burnt incompletely, complex polycyclic hydrocarbons may be formed and some of these compounds have been shown to be carcino- genic (cancer produc1nz) when applied to the skin of animals. The occurrence of these compounds in town air has been studied by ''1aller2 (1952) and by Commins3 (1958). Lung -- .. /AP/16 page 2 cancer in man is found more commonly in towns than in the country and many think that this excess is caused by the polycyclic hydrocarbons found in town smoke. 4 This simple hypothesis is inadequate (Lawther and Waller 1958 ) and does not ex- plain the dramatic and continuing rise in the incidence of lung cancer which is definitely linked so closely with the habit of cigarette smoking. It seems like- ly that the difference between urban and rural lung cancer mortality may be due at least in part to the spread of the habit from town to counUybut it would be foolish indeed to say that the carcinogens in town air were not likely to be linked in some manner with the lung cancer problem. Indeed it is possible that cigarette smoke may cause some lung cancer by acting on the bronchial epithelium (cellular lining) in conjunction with the chemicals contained in urban smoke. Many experiments designed to test this hypothesis are at present in progress. But whatever their results the presence in smoke of any compound having carcinogenic properties is surely an cver-whclmingly important reason for the abolition of smoke from the air. It is unfortunate that concern with the carcinogenic components of smoke has overshadowed the many other constituents which may play an important part in the development of chronic bronchitis. This dread disease is, like lung cancer, much commoner in towns than in the country. It is characterized initially by the hyper- secretion of mucus by the cells and glands lining the bronchial tree; this change is followed or accompanied by airway obstruction and chronic infection super- venes which ultimately destroys the lungs. There is good 0vidence, derived from extensive epidemiological studies (College of General Practitioners 19615 ) that the early hypersecretory phase (clinically manifest as cough with production of clear mucus) is closely related to cigarette smoking but that the later phase of the disease (persistent infection, recurrent acute attacks, shortness of breath and ultimate respiratory failure) is linked with urban air pollution. For many years, workers in this field have regarded the sulfurous pollutants to be respon- sible for this change but this belief is at variance with the morbidity seen in chemical industry where gross simple chemical irritation may be experienced (Lawther 19636 ). These findings indicate the need to examine more carefully the constitution and action of the non-carcinogenic components of smoke. These general remarks give support, on clinical grounds, for the Clean Air Act in its efforts to abolish smoke. But there is an urgent need to examine the question of the clinical significance of the pollution left unchecked - the effect of sulfur compounds. AP/16 page 3 Sulfur dioxide and, to a l~sser exi;.ent~ sulfuric acid are cormnon pollutants of 'town air. They are both emitted from fires or fUrnaces burning carbonaceous fuels containing sulfur as an impurity. The sulfuric acid contained in flue gases generally represents only about 1 to 5 per cent of the total sulfur emitted. It seems likely, however; that in certain weather (especially in wet fog) sulfur dioxide may be oxidized in tbc air to sulfuric acid. This acid may persist as droplets, adhere to particles, or fall out as acid rain if the relative humidity rises. Sulfur dioxide~ togctt.er with smokeJ is measured routinely in many towns in Great Britain. 'Ihe D.S.I.R. standard "volumetric set" is cormnonly used. The average amounts found in the City of London vary from about 300 ~m3 (0.105 ppm) in summer to about 500 ~/m3 (0.17 ppm)in winter. The concentrations foUnd at many site_s all over the country are published annually with smoke concentrations by the D.S .I.R. in "The Investigation of Atmospheric Pollution". The concentra- tion of the gas can vary abruptly and peaks can greatly exceed the 24-hour average values. The highQ_st hourly concer>i"r~+Lm measured in London was 5663 pg/m3 (1.98 ppm) in _the "Smog" of 1962. During the 1952 11 Smog11 the highest concentrat;ion 3 measured over a period of 48 hours was 3840 yg/m · (1.34 ppm) and it is possible that peaks in excess of those found in 1962 may well have occurred. Sulfuric acid, determined by micro-titration of filter paper samples of sus- pended matter {Commins 19637 ) is not measured routinely but research observations indicate that in winter in the City of London the air usually contains about 3 ' 15 rs/m •. In the 1962 "Smog11 high concentrations were maintained, the maximum hourly_ ·concentration being 678 pg/m3. The physical state cif this acid is impor- tant; frequently in foggy weather it is seen to occur as large droplets but in normal winter weather the acid particles are much smaller and are usually asso- ciated with crystals, soot or ash. Sulfur dioxide is an irritant gas and if inhaled in sufficiently high con- centrations produces unpleasant effects which are coughing and wheezing. The maximum allowable concentration ~or 8-hour industrial exposure (Conference of 8 ' ' 3 ' American Governmental Hygienists 1961 ) is 5 ppm (14 mg/m )~ It used to be 10 ppm but was recently reduced. These maximum allowable concentrations are published for trre guidance of industrial hygienists and are arrived at after AP/16 page 4 careful consideration of all the literature on toxicology and industrial practice and it is implicit in the definition that a wide margin of safety exists. The maximum allowable concentration for sulfuric acid is 1 mg/m3. Despite the general innocuousness of so2 in concentrations around the maxi- mum allowable concentration (published work on industrial populations does not reveal any sinister effects), there are some people who react unfavourably to still lower concentrations. In some, consistent measurable increases L< airway resistance follow inhalation of concentrations of about 5 ppm; there is some evi- dence that in exceptional cases perceptible increases (measured by delicate tech- niques) ~ve followed the breathing in of 2 ppm (but no less). No such hyper- sensitivity to sulfuric acid has been recorned. Changes in airway resistance (often gross and manifest audible wheezing) sometimes follow exposure to highly polluted town air; this phenomenon is more commonly observed in patients with chronic bronchitis. It is of the utmost im- portance to know what constituent of the pollution causes this change and it is reasonable to suspect these common irritant acids. But it will be remembered that so2 has not yet been found in concentrations exceeding 2 ppm and in laboratory ex- p?rinents on normal and bronchitic volunteers such amounts have not produced mea- surable effects. (It is relevant to state here that patients with chr~nic bron- chitis are sometimes seen to be particularly resistant to so2 probably because their disease~ characterized by a hypersecretion of bronchial mucus, may in rea- lity be a protective mechanism developed by, and in defence against, the inhala- tion of irritant material). Experiments in the laboratory in which normal sub- jects have inhaled sulfuric acid mists of various particle sizes but of concen- trations of approximately 1 mg/m3 have failed to produce significant alterations in airway resistance. There is obviously a need in the experimental approach to the problem to see if the undoubted effect produced by sulfur dioxide in high concentrations can be reproduced by adding a further pollutant to "realistic" concentrations of the gas. The work of Amdur (1959)9 led to the hope that a solution to the problem was in sight. She demonstrated convincingly that the effect of so2 on the airway resis- tance of guinea pigs was enhanced by the addition of an aerosol of sodium AP/16 page 5 chloride containing about 10 mgfm3 . The results of this research reinforced the work on synergism - the working together of factors to produce an effect greater than would be expected from summation- reported by La Belle et al (1955) 10 • Un- fo~tunately attempts to reproduce the effects in man have so far been unsuccess- ful (Amdur3 personal communication, and Lawther, unpublished results). But the continued investigation of this type of phenomenon would appear to be profitable. The failure to produce significant changes in lung function by administra- tion of "realistic" sulfuric acid mists may well be explained by tiJ.e fact that droplets of sulfuric acid grow when the ambient relative humidity is increased and it is likely that acid droplets arc rapidly diluted on inhalation and are already too dilute to be irritant when they hit the bronchial mucosa. Some smoke particles in the air have acid attached in such a way that it may be 11 protected11 against rapid dilution in sudden increases in humidity; such particles might allow the impaction of concentrated acid. They are difficult to prepare in the laboratory but experiments on these lineE are in progress. It is relevant to mention here that aerosols which are relatively chemically inert have been shown to be capable of producing increases in airway resistance (~ Bois and Dautrebande 3 1958)11 • Large doses of particles are probably needed to produce these effects but the demonstration of the occurrence of these changes is of great importanct and cannot be divorced from any consideration of the cli- nical effects of air pollution. Because of variable response of individuals to the experimental exposures briefly described above, and in view of the obvious limitations of laboratory methods, epidemiologicc~l techniques must be used in which many patients are ob- served undisturbed in their carefully defined environments (Lawther, Martin and Wilkins 1962)12 . There is no doubt that chronic bronchitis is more commonly found in large towns that in more sparsely populated areas and there is good reason to believe that air pollution plays an important part in the production of this disease. It is easy to obtain high statistical correlations between the prevalence of chronic bronchitis and sulfur dioxide concentration but obviously this association can- not be assumed to be causal since the degree of pollution of the air by many compounds is closely related to many other noisome factors in urban life. AP/16 page 6 The most dramatic~ and crudest, indication of the relationship between air pollution and disease is the increase in mortality seen to be associated with "Smog" episodes. In the notorious 1952 "Smog" in London (1.34 ppm so2 average for the 48 hours of the two worst days) an excess of 4000 deaths occurred, mostly among the elderly and infirm. Since this episode increases in mortality attendant upon increases in pollution have been studied by many workers. Gore and Shaddick (1958)13 considered the deaths in the City of London during four periods of high pollution between 1954 and 1956 and related the changes in mortality to the mean of the pollution measurements from seven sampling stations operated by the L.C.C. 'Ihey found that significant rises in mortality occurred when air pollution rose to 3 3 levels above 2000 pg/m smoke and 1150 ,pg/m so2 (0.4 ppm). Martin and Bradley (1960) 14 studied the death rates in Greater T,o11r>on for +.be whole period November 1958 to February 1959; they used re-:::: ..A.:..·.:.: from the same sites as were used by Core and Shaddick. It is difficult to extract from this work the same sort of figure as was quoted from Gore and Shaddick since Martin and Bradley considered the changes in pollution which were associated with day by day changes in morta- l:tty. They said "Mc:ny of the increases were small~ some as low as 20 deaths, 10 mg per lOO cubic metres of black suspended matter, or 2.5 ppm so2." We have looked at their figures in terms of absolute measurements of pollution and it would ~eem reasonable to say that deaths increased significantly when smoke rose a~o78 750 pg/m3 and so2 concentrations exceeded 710 pg!m3 (0.25 ppm). Obviously morbidity statistics will provide an index more sensitive than uo~~~ and many studies of illness and pollution have been published or are in progress. The technique used in the author's unit is probably the most sensi- tive (tawther 1959)15; groups of patients with established bronchitis are asked to record, by means of a simple coce in a clary, their own d~ily as3cssment of their health. TI1er.e diary entries are translated into numbers from ~mich a sta- tistic called the "degree of illness of the group" is calculated (in another experirr.ent the "percentage of patients feeling worse than they felt on the pre- ceding day11 was calculated). Fluctuations in these indices followed closely the daily variations in air pollution as measured by smoke and so2 concentrations. When smoke concentrat~ons rose above 300 1~/m3 and so2 above 600 pg/m3 (0.21 ppm) a deterioration of the health of the group was seen to occur (about 1000 v~tie~ts were used in this last experiment). AP/16 page 7 · It is important to remember when considering the results of this type of ex- periment that so2 cannot be specifically incriminated since the concentrations of most pollutants rise together.. 'I'he experiments lack specifici ty at present. Added value may result fr0m studies made in areas where the pattern of pollution is al ter:ing due to the implementation of the Clean Air Act. More fundamental studies of the relationship between air pollution and disease will make use of prospective (as opposed to retrospective) survey techniques. This brief revie\-.r must end with a warning: t..h.e 1952 11 Smog" was thought to be responsible for the death of about 4000 people; preliminary calculations show that the 1962 episode was associated with an excess of about 750 deaths in Greater London. Thc~e can be no doubt that there was less smoke .in December 1962 but the sulfur diox.1.dc levels were approximately the same as those in 1952. Al- ready the difference in mortality has been hailed by many as evidence that the Clean Air Act has removed much of the sting from acute air pollution. This may well be true and the clinician would wish this to be so. But in COJ1templating this reduced death rate we must n0+ fn~e;e·.., -l::!:"..ut mortality in a cormnunity is a function not only of the noxious stimuli applied to the people but also of the susceptibility of the population to stress. It is quite possible tnat in December 1962, London contained fewer people ready to succumb to the ill-effects of air pollution than did the London of 1952. The publicity given to the evil effects of pollution almost ccr-'.:.ainly made susceptible. people take greater care, to avoid exposure and exertion and so diminish their chances of dying. Such empirical pro- tection devices as ll12.Sks and ammo:.1ia not used in 1952 were commonly used last year. So, thoug..l-J the removal of mu8h of 1952 1 s smoke may well have saved many, one must remember ·that we are contemplating a snort series with a moving base-line and our moQd must be one of ca\Jtious optimism. The Clean Air Act is·an eminently sensible law wJ.1ich is already ridding our cities of their disgusting smoke. It deserves the ardent support of.all clini~ians. The wise counsel of the Beaver Committee's report was: " a great deal of work remains to be done on the precise scientific determination of the ill effects of the several elements in air pollution and their :tnter-relationships. This is not purely a medical or a pathological matter, and it'is impo:t>tant that medical~ chemical and physical re- search on this subject should be closely co-ordinated. But action to reduce pol- lution by smoke, grit and dust and sulfur oxides need not and must not be held up while further medical r2search is done." AP/16 page 8 REFERENCES 1. Waller3 R.E., Brooks, A.G.F. and Cartwright, J. An electron microscope study of particles in town air. Int.J. Air Poll.~ 1963 (in press) 2. Waller, R.E. The benzpyrene content of town air. Brit.J. Cancer, 1952, §,8 3. Commins, B.T. Polycyclic hydrocarbons in rural and urban air Int.J. Air Poll., 1958, l' 14 4. Law-:ber, P .J. and V! all er, R .E. Atmospheric pollution and lung cancer Trans. Ass. I::c' .: :__:G.. Off., 1958, _2, No .1 5. College of General Practitioners Chronic bronchitis in Great Britain: a national survey Brit. med.J., 1961, ~~ 973 6. Lawther, P.J. Chronic bronchitis and occupation Proc .Roy .Soc .Hl th, 1963, .C in pro ss) 7. Commins, B.T. Determination of particulate acid in town air The Analyst~ 1963~ 88, 364 8. American Conference of Government Industrial Hygienists Threshold Li~it Values for 1961 Arch.Environ.Hlth, 1961, l• 489 9. Amdur, M.O. The physiological response of guinea pigs to atmospheric pollutants Int.J.Air Poll., 1959, !• 170 10. La Belle, C.W., Long~ J.E. and Christofan, E.E. 11. Synergistic effects of aerosols. Particulates as carriers of toxic vapours A.M.A. Arch. industr. Hlth, 1955, 11, 297 Du Bois, A.B., and ~autrebande, L. Acute effects of breathing inert dust particles and of on the mechanical characteristics of the lungs in man. ponse afbr inhaling f:ympathomimetic aerosols. J. Clin. Inv~ct., 1958, 37, 1746 carbachol aerosol Changes in res- 12. Lawther, P.J., Martin, A.E., and Wilkins, E.T. Epidemiology of air ~ollution WHO Public Health Papers No.l5, 1962 13. Gore, A.T., and Shaddick~ C.W. AP/16 page 9 Atmospheric pollution and mortality in the County of London 1958 Brit. J. Prev. and Soc. Mcd., 12, 104 14. Martin, A .E., and Brad.ley, W .H. Mortality~ fog and atmospheric pollution l"lonth. Bull. Min. Hl th, 1960, 19, 56 15. Lawther, P.J. Climate, air pollution and chronic bronchitis Proc. Roy. Soc. Med., 1958, 51, 262