A ir Pollution and Health
SU M M AR Y
(Figures in parenthesis refer to the numbered paragraphs in the
text of the Report)
1. Air Pollution and Health (I. I to I. 9)
For 700 years, at least, British people have protested in one way or
another about the pollution of air through the burning of soft coal. As
long ago as 1273 a Law was passed to prevent this. In the seventeenth
century the great English physician, Thomas Sydenham, was convinced
that the ‘sulphur and fumes of sea coals . . . give occasion for a cough’.
In 1854 Sir John Simon reported to the Court of the City of London his
valid reasons for believing ‘that many persons of irritable lungs find un­
questionable inconvenience from these mechanical impurities of the
atmosphere’. In 1956 the Clean Air Act was passed as a direct conse­
quence of the dense and polluted fog of early December 1952, which, it
is estimated, caused 1,597 more deaths in the Administrative County of
London than would have been expected (Figure 1, Table 1). The Act of
1956 has led to a reduction of air pollution, especially in London.
2. Some Facts about Pollution (2. 1 to 2. 18)
The two major pollutants are smoke and sulphur dioxide. It is easy to
measure their concentrations. They are taken as indices of pollution and
not necessarily as the agents that cause ill-health. In Great Britain air
pollution is due mainly to the burning of carbonaceous fuels. The burn­
ing of soft coal in domestic open fires produces minute droplets of tar
and black smoke. Some smoke also comes from badly designed or badly
operated heating plants and diesel engines. Large quantities of sulphur
dioxide are emitted in the combustion of some solid and liquid fuels, and
in humid conditions may react with other pollutants to form sulphuric
acid and sulphates. Sulphur is present in most coals and crude oil but is
virtually absent from petrol. Small amounts are found in diesel fuel.
Little smoke comes from anthracite burned in open grates, as in parts
of South Wales, or from coke and other manufactured fuels; but the
sulphur content of these fuels is similar to that of coal. Particles in the
air come from industrial processes, wear of roads and tyres, from animals
and plants, from ash escaping from chimneys, as well as from coal smoke.
Measurements of smoke and sulphur dioxide have been made in some
areas for many years, and since 1961 a network of sampling stations has
been set up on a systematic basis throughout the United Kingdom.
Pollution from petrol and diesel engines results from incomplete com­
bustion, additives or impurities in the fuel, and ‘fixation’ of atmospheric
nitrogen. Incomplete combustion in a badly maintained or misused
diesel engine results in the emission of black smoke. Much of the lead
from organic compounds added to petrol as anti-knock agents is emitted
in the exhaust as inorganic lead. The concentrations of lead in the air,
for example, of Fleet Street, London are very small (see also para 7. 1,
p. 58). In combustion, some of the atmospheric nitrogen may be burned
to yield oxides of nitrogen, and in the particular climatic conditions of
I
of the heart and from pneumonia also increased, mostly in older people.
But deaths were also higher than expected in patients under the age of
45 years. Each of several periods of fog during the winter of 1958-59 was
also associated with an immediate increase of mortality, mainly from
bronchitis and pneumonia.
Peaks of Pollution and Cold Weather (4. 5 to 4. 8). A fall in temperature
usually coincides with dense fog, and many observations have shown that
in these circumstances the cold weather increases mortality, especially in
the elderly and the very young. Pollution of the air from domestic fires
will obviously be greater during cold weather than at other times. When
the two are combined the mortality from bronchitis is higher than that
due to either polluted fog or cold separately. During the period 1947-54,
in London and East Anglia the temperatures were similar, but in East
Anglia the amounts of pollution were less, and the increase in the aver­
age number of deaths during periods of intense cold and frequent fogs
was greater in London.
Investigations have shown an increase of absence from work with
increase of air pollution. For example, analysis of medical certificates in
Salford disclosed a doubling of rates for sickness absence from bronchitis
when concentrations of smoke in the air exceeded 1,000 yug/m3. Records
of admissions to London hospitals in 1955-56 show that the demand for
beds for patients with acute diseases of the chest rose during peaks of air
pollution and cold weather.
Long-term Trends (4. 9 to 4. 10). Until the late 1930s death rates from
bronchitis in middle-aged men and women were falling. Since 1940 the
death rate from bronchitis in men has taken an upward turn, and the
decline in the death rate in women has been less marked (Figure 6). It is
believed that these recent changes are due to increased cigarette smoking,
which became more popular, among men especially, during the First
World War and thereafter (Figure 7). The increasing mortality from
bronchitis in men in recent years is more closely linked to increased
cigarette smoking than to any greater exposure to urban air pollution
from the consumption of coal, petroleum, or derv.
Some International Differences (4. 11 to 4. 14). Some of the national differ­
ences recorded may be the result of different methods of certifying death.
British doctors, for example, usually put on the death certificate ‘chronic
bronchitis’, while American and Norwegian physicians use such terms as
‘emphysema’ or ‘bronchiectasis’. Such differences limit the value of
international comparisons. The differences in morbidity rates for bron­
chitis in the rural populations of Denmark and Britain, with less bronchitis
in the former, may be explicable by the Danish preference for pipes and
cigars and the British preference for cigarettes. Surveys of men doing the
same job in different countries but similar in age and smoking habits
showed that men working in London had worse bronchitis and poorer
function of the lung than men in either Bergen in Norway or in Baltimore,
Washington and Westchester (New York) in the USA. Britain has the
unenviable record of the highest death rate in the world from chronic
disease of the lung in middle-aged men.
Differences between Town and Country (4. 75 to 4. 19). All investigations
in Britain have demonstrated a close correlation between presumptive
3
Los Angeles they react with hydrocarbons from exhausts to form a
‘photochemical smog’ that irritates the eyes. Such a combination of
circumstances is very rare in Britain. Concentrations of nitrogen dioxide
above levels considered safe in industrial practice have not been recorded,
e.g. in street air in London (see para 7. 4, p. 59). Petrol engines give out
large quantities of carbon monoxide, almost absent from diesel exhaust.
If a petrol engine is left running in a closed garage the carbon monoxide
may reach a concentration that is fatal because it replaces the oxygen
from the haemoglobin in the blood. Even in heavy traffic the level of
carboxyhaemoglobin (carbon monoxide bound to haemoglobin) found
in the blood of those exposed to its fumes rarely reaches that commonly
found in cigarette smokers. But there is need for investigation of the
possible effects of carbon monoxide from car exhausts on, for example,
perception (see para 7. 2, p. 58).
3. Experiments on Effects of Pollution (3. 1 to 3. 10)
Most of the experimental work on the effects on the lung of inhaled
particles and gases has been done to identify potential hazards in industry.
It is difficult to apply to man the observations made on experimental
animals. It is, however, possible to test the effects of individual com­
ponents of fog, alone or in combination. Particles in the air greater than
10 microns in diameter are trapped in the nose and upper air passages;
smaller particles penetrate farther into the lung. High concentrations of
inert particles can cause increased resistance to the flow of air in the
airways of the lung. There has been no convincing report of any response
in human volunteers to experimental inhalation of less than one part per
million (ppm) of sulphur dioxide, and concentrations of this exceeding
1 ppm are rarely found in urban air. Animal experiments show that the
effect of sulphur dioxide is enhanced in an aerosol in which it is soluble
or which contains salts accelerating its oxidation to sulphuric acid. It is
possible that particles of smoke and sulphuric acid in some special form
increase the irritant effect of sulphur dioxide.
4. Air Pollution and Bronchitis (4. 1 to 4. 30)
Chronic bronchitis is one of the major causes of disablement and death
in Great Britain, particularly among middle-aged and elderly men. In
1967 it caused the death of 5,253 men and 1,134 women between the
ages of 45 and 64. Some 30 million working days are lost to industry each
year because of bronchitis, and the total cost of this amounts to some £65
million a year. It is therefore important to discover the causes of the
disease and ways of preventing it. It seems that the simple recurrent
cough and expectoration of early chronic bronchitis is brought on by
cigarette smoking. Infection of the bronchial tubes follows, and the
patient gradually gets short of breath. The airways of the lung become
narrowed, and oxygen supply to the blood is reduced. Lack of oxygen in
time leads to constriction of the smaller blood-vessels of the lung, which
places an extra strain on the heart; and this is added to the difficulty of
breathing caused by the irritation of the lungs by polluted air. The great
fog of London in December 1952 demonstrated how deadly these effects
can be (Figures 1 and 3). In the Administrative County of London
deaths from bronchitis were nine times the number expected at that
time of the year. Figure 3 in the Report shows that deaths from diseases
2
levels of pollutants in the air and mortality from bronchitis in middle life.
Town air is more polluted than country air. Among postmen, rates for
disablement, premature death, and for absence from work because of
bronchitis were high in those working in the most polluted areas. The
highest rates of disability among postmen and bus crews were among
those working in the centre and north-east of London, where the con­
centration of air pollution was higher than in other parts. A survey in
1961 showed that bronchitis was twice as frequent in large towns as in
rural areas. In general it is commoner in the North of England than in the
South. The differences in mortality from bronchitis in town and country
were brought out in an investigation comparing the experience of Belfast
with that of the surrounding countryside; it illustrated the major im­
portance of smoking habit and social class, as well as of air pollution, in
deaths from this disease.
Effects of Cigarette Smoking and Air Pollution and Cold (4. 20 to 4. 24).
Cigarette smokers are three times more likely to suffer from chronic bron­
chitis than are non-smokers (Figure 9). It is not possible to measure
exactly the relative importance of exposure to cigarette smoking and to
polluted air, but the difference between the rates for non-smokers and
smokers is greatest in the most polluted districts. A survey by the Royal
College of General Practitioners in 1961 demonstrated that cigarette
smoking was associated with chronic cough and expectoration in young
men— the smoker’s cough. After the age of 55 years more serious symp­
toms such as repeated chest illness and breathlessness were commoner in
those living in the more heavily polluted areas. A significant correlation
has been shown between the death rates from pneumonia and the levels
of particulate air pollution in 30 county boroughs in England and Wales.
During very cold weather in London the death rate from pneumonia
doubled when the duration of fog increased from 10 hours to more than
20 hours in the week preceding death. As has already been mentioned,
this pattern was not repeated in East Anglia, where the temperature was
similar but air pollution much less.
Which Pollutant? (4. 25 to 4. 30). Whereas there is no doubt of the illeffects of air pollution, the relative importance of such pollutants as
smoke and sulphur dioxide, used as convenient indices of pollution, has
not been established. It is necessary also to consider the possible effects of
sulphuric acid and of oxides of nitrogen. The significance of different
pollutants may be further elucidated when more is known of the effects of
the Clean Air Acts in changing the nature of pollution of the atmosphere.
5. Chest Diseases in Young People (5. I to 5. II)
In the fog disaster of 1952 the death rate among children rose sharply,
especially in the first year of life. The death rates from bronchitis and
pneumonia in children are higher in England and Wales than elsewhere
in North-western Europe and are double the rates in Scandinavian
countries (Table 4). A complication of infection of the upper respiratory
passages is chronic infection of the middle ear. At examination for
National Service chronic otitis media has been found more often in
youths from towns than in those from the country. Perforated eardrums
and discharging ears were found to be commoner in Sheffield children
4
than in Welsh children of the same social class. In Sheffield itself persist­
ent cough and scarred or perforated eardrums were commoner in districts
where air pollution was high than in those where it was low, an effect
more directly related to pollution than to such social circumstances as
overcrowding in the home. One national survey of schoolchildren
showed a steady rise in the frequency of bronchitis in step with increasing
levels of air pollution. Another survey demonstrated a steady rise of
persistent cough, particularly among children of less skilled workers, from
the lowest rates in the rural areas to maximum rates in the most heavily
polluted areas (see Figure II).
6. Air Pollution and Lung Cancer (6. I to 6. 21)
The evidence that cigarette smoking is the most important factor in
causing lung cancer does not preclude examination of other possible
influences. The death rate from lung cancer is highest in the major
conurbations and decreases with the size of town to the lowest rates in
rural districts. There is a general tendency for death rates from cancer of
the lung to be high in countries where the air is much polluted by smoke
from coal; but the disease is common in some countries (e.g. Finland)
where little coal is used. Some of the earlier statistical work linking lung
cancer with air pollution is open to criticism. Lung cancer is a particular
hazard in certain occupations such as nickel and chromate refining, in
iron foundries and iron mines, and in asbestos works; but men in these
occupations form only a small part of the male urban population and
work only in certain areas. The general excess of mortality from lung
cancer in urban districts cannot therefore be accounted for by workers in
these industries. There is no consistent excess of deaths from lung cancer
in men especially exposed to polluted air in streets, as policemen, bus
conductors, or lorry drivers’ mates. Though the Registrar General has
reported an increased mortality in motor mechanics and drivers of motor
vehicles, there is no increased mortality among mechanics working in
garages and thus exposed to fumes from diesel or petrol engines.
Smoking and the Urban Factor (6. 9 to 6. 14). Cigarette smoking is the
most important of the causes of cancer of the lung. Various studies have
indicated, however, that when allowance is made for the effect of cigar­
ette smoking there remains a degree of association between death rates
from lung cancer and the burning of solid fuels. In Northern Ireland an
inquiry showed that for people with similar smoking habits the risk of
dying from lung cancer rose consistently from rural areas through urban
districts to reach a maximum in central Belfast. The prospective inquiry
into the smoking habits and places of residence of British doctors has
demonstrated that the death rate among cigarette smokers from lung
cancer is higher in conurbations than in rural areas. Similar differences
between rural and urban death rates from cancer of the lung exist in
Norway, where there is little pollution of the air, even in towns. These
observations point to the influence in the incidence of lung cancer of an
‘urban factor’ that is not necessarily related to air pollution. Comparisons
of the experience in Britain and the U SA show that mortality from lung
cancer increases with size of population in both countries, but that in
places of similar size the mortality is twice as great in this country (see
Table 6). This contrast is as marked in rural areas as in urban areas, and
5
implies that in the causation of lung cancer there is a distinct ‘British
factor’ as well as an ‘urban factor’.
Evidencefrom Migration (6. 15). The death rates from cancer of the lung
among British-born people living in the less polluted countries of New
Zealand, South Africa, the United States, and Canada lie between the
lower rates of those born in these countries and the higher rate for Britain
itself (Table 7). In South Africa the British immigrant, with apparently
identical smoking habits and living in the same places as his South
African-born contemporary, still has a higher rate of mortality from
cancer of the lung. There is an enduring effect of British conditions or
habits, and this might be due to exposure to high levels of air pollution in
early life.
Experimental Evidence (6. 16). Experiments on animals have limited
relevance to humans, if only because it is not possible in the laboratory
closely to simulate the conditions of urban air pollution. The cancerproducing substance benzo(a)pyrene is present in small amounts in town
air. Comparatively large amounts introduced directly into the lungs have
resulted in lung tumours in rats. The inhalation of sulphur dioxide and
benzo(a)pyrene together caused tumours to appear in the lungs of rats;
but neither did so when inhaled separately. The inhalation of air
pollutants at ‘realistic concentrations’ has not caused tumours in animals.
Experiments have demonstrated that a cancer-producing substance
might be more effective when inhaled with an irritant such as cigarette
smoke.
7. Other Effects of Air Pollution (7. 1 to 7. 8)
The increasing density of motor vehicle traffic has aroused anxiety about
the possible effects of motor exhausts on health. (See also pp. 1 and 2 of
Summary and paras 2. 5 to 2. 10 of Report.) The concentration of
carbon monoxide in the blood of persons in streets with heavy traffic is
often exceeded in cigarette smokers not exposed to motor exhausts. But
exposure to carbon monoxide in street air may affect the senses and further
research should be carried out on the effects of small concentrations. No
reports of the amount of lead in the blood in Britons exposed to traffic
fumes are available. In places like Los Angeles levels of lead in the blood
have been found to be, in general, below the level at which lead intoxi­
cation arises. Climatic conditions in Britain do not favour the Los Angeles
type of smog. The highest concentration of nitrogen dioxide in London
is well below that considered safe in industrial conditions.
8. Prevention of Air Pollution (8. 1 to 8. 13)
The burning of fuel for heat and power is the prime cause of pollution
of air of British towns. Controls must be applied to the three main sources
of pollution: domestic premises, industry, transport.
Domestic (8. 2 to 8. 5). Most of the pollution likely to affect health
comes from the burning of coal fires in homes. Heating and cooking with
electricity or gas would eliminate this hazard. Little contamination comes
from oil for domestic heating; it has a low sulphur content. As solid fuels
will continue to be used for many years smokeless fuels such as anthracite
or coke are to be preferred; but they contain the same amount of sulphur
6
as raw coal. The heavier grades of oil for large central heating installa­
tions contain more sulphur than coal does. Their chimneys do not always
ensure effective dispersion. District systems in which a large central boiler
house supplies hot water to all the houses of a neighbourhood are em­
ployed in many European cities; local air pollution is greatly reduced in
this way.
Industrial and other Sources (8. 6 to 8. i i ). The large, efficient furnaces
installed in industry and in power stations burn coal so completely that
no smoke should be emitted. Goal and oil from which much of the
sulphur has been removed are too expensive for general use in industry.
Raising the height of chimney stacks to 8oo feet makes dispersion effective.
Sulphurous products can be removed from gases in the chimney stack.
The gas-washing plants at Battersea and Bankside power stations in
London remove some 95 per cent of the sulphur dioxide, but decrease in
buoyancy of the plume may cause pollution of the neighbourhood.
In the street fumes from a diesel engine can be a hazard by obscuring
visibility. Carbon monoxide in vehicle exhausts is a potential hazard in
congested traffic and in enclosed spaces.
Legislative Control (8. 12 to 8. 13). The Glean Air Act of 1956 seeks to
limit the pollution of the air by smoke. The establishment of smokeless
zones in towns and cities is the responsibility of local authorities. The
Glean Air Act of 1968 has widened the scope of some of the original
provisions in relation to industry. When an area is declared to be a
‘smoke control area’ grants of up to 70 per cent of the cost of changing
domestic heating systems may be made to occupiers of houses built
before 1956, when the Glean Air Act was passed.
9. The Effects of the Clean Air Acts (g. 1 to 9. 8)
The emission of smoke from industrial premises has been much reduced
throughout Britain. The control of domestic sources has been less uni­
form. By establishing smoke control areas London and a number of other
large cities have substantially reduced pollution of the air by smoke.
There are still too many ‘black areas’— areas, that is, where smoke
control is urgently needed— in the mining towns of the North (see
Table 8). Improvements in health were shown in the relatively much
fewer deaths in the episode of fog in 1962 in London than in the similar
fog in 1952. There has been a remarkable absence of peaks of pollution in
London for several years. The age-standardised death rate from bron­
chitis in London, which a few years ago was above the national level for
men and women, is now about the same. Similar but less dramatic
changes are taking place in mortality from lung cancer. These changes
could have been due to alterations in smoking habits in the past.10
10. Recommendations (10. 1 to 10. 13)
(a) For Patients (10. 1 to 10. 3). In acute episodes of polluted fog patients
with chronic bronchitis or chronic heart disease, especially the elderly,
should remain indoors. Windows should be closed to keep the foul air
out. Rooms should be warm. A bottle of dilute ammonia opened in a
room may help to neutralise acid mists. Undue exertion should be
avoided. Anyone compelled to go outside should wear a face-mask or a
7
scarf over the nose and the mouth. Advice to patients with chronic
bronchitis to change place of residence should be tempered with caution.
Patients vary in their susceptibility to pollutants. The air in residential
areas of small provincial towns may be more polluted than the air in
large cities. Information about polluted areas may be obtained from the
Warren Spring Laboratory, Stevenage, Herts.
(b) For Central and Local Government (10. 4). The universal and effective
implementation of the Glean Air Acts is the most urgent task confronting
central and local government in the control of air pollution. All new
housing developments should at the outset be designated as smoke control
areas.
(c) For Health Authorities (10. 5 to 10. 7). The Hospital Inpatient Inquiry
should provide data on diseases connected with air pollution. The
Department of Health and Social Security should regularly survey dis­
abling illness among the insured population in this respect. Medical
Officers of Health should conduct surveys of children through the school
medical service to assess the extent and nature of respiratory disorders
among them. There is need for centralised information on changes of air
pollution in different parts of the country and of related changes in health
and disease.
(d) For Research (10. 8 to 10. 11). The Medical Research Council should
ensure the regular assessment of available data on air pollution in re­
lation to health. The Council might extend laboratory studies into the
risks of new forms of pollution, as from asbestos. Research into the
reduction of sulphur in fuels and into methods of removal of sulphur
dioxide from stack gases should be intensified. Further research is needed
into the combined effects on health of air pollution and tobacco smoke
and of exhausts from motor vehicles.
(e) International Co-operation (10. 12). Standardisation of methods of
measuring air pollution and of diagnostic terms and conventions should
facilitate international comparisons, and an exchange of ideas and
information should be carried out through the World Health Organisation.
8
Air Pollution and Health
Stoke-on-Trent 1910
Stoke-on-Trent 1969
Photographs showing the effect of the Glean Air Acts. In the pottery
industry of Stoke-on-Trent coal was replaced by oil, gas and electricity.
(Permission to reproduce these photographs has kindly been given by the
Director of the British Ceramic Research Association and the Director of
the National Society for Clean Air.)
Air Pollution and Health
SUMMARY AND REPORT ON AIR POLLUTION
AND ITS EFFECT ON HEALTH
BY THE COMMITTEE OF THE ROYAL COLLEGE
OF PHYSICIANS OF LONDON
ON SMOKING AND ATMOSPHERIC POLLUTION
LONDON
PITMAN MEDICAL AND SCIENTIFIC
PUBLISHING CO. LTD.
First Published 1970
PITM AN M E D IC A L AND S CIE N T IF IC
COMPANY LTD
31 Fitzroy Square, London, W 1
PUBLISHING
Associated Companies
SIR ISAAC P I T M A N AND SONS L T D
Pitman House, Parker Street, Kingsway,
London, WC2
P.O. Box 6038, Portal Street, Nairobi, Kenya
S IR I S A A C P I T M A N ( A US T . ) P T Y . L T D
Pitman House, Bouverie Street, Carlton,
Victoria 3053, Australia
P I T M A N P U B L I S H I N G C O R P O R A T I O N S . A. L T D
P.O. Box 9898, Johannesburg, S. Africa
PITMAN PUBLISHING CORPOR ATIO N
20 East 46th Street, New York, N Y 10017
SIR ISAAC P ITM A N (CANADA) LTD
Pitman House, 381-383 Church Street, Toronto, 3
TH E COPP CLA R K PUBLISHING COMPA NY
517 Wellington Street, Toronto, 2B
© 1970 The Royal College of Physicians of London
This book is protected under the Berne Convention,
It may not be reproduced by any means, in whole
or in part, without permission. Application with
regard to reproduction should be addressed to the
Publishers.
Paperback Edition : ISBN o 272 76023 4
Library Edition: ISBN o 272 76024 2
Printed in Great Britain by Staples Printers Limited, at their Rochester,
Kent, establishment
21 0005 11
21 0006 11
Contents
Summary
I
Air Pollution and Health
2
3
Sources, Types, and Trends of Air Pollution
7
9
15
Experimental Work on the Effects of Inhaled
Pollution
23
Preface
4
Air Pollution, Chronic Bronchitis, and Allied
Diseases
5
6
7
Respiratory Disorders in Young People
27
43
Air Pollution and Lung Cancer
48
Other Effects of Air Pollution
58
8
Prevention of Air Pollution
61
9
The Effects of the Clean Air Acts
65
Observations and Recommendations
69
References
73
10
Plates
Frontispiece: The effect of the Clean Air Acts
in Stoke-on-Trent
Plate 1 : Electron micrograph of a smoke
aggregate
f.p.
16
Preface
Several serious illnesses, in particular lung cancer, are associated
with smoking or with environment. In April 1959 the Royal
College of Physicians of London set up a Committee t o :
‘Report on the question of smoking and atmospheric
pollution in relation to carcinoma of the lung and other
illnesses.5
The Committee decided that although the effects of air
pollution and smoking might be interrelated the preventive
measures required were so different that the two hazards
should be considered separately. A report on the effects of
smoking, Smoking and Health, was published in 1962. The
College Committee on Smoking and Atmospheric Pollution
now presents its report on Air Pollution and Health. A follow­
up report on smoking is in preparation.
The composition of the Committee is as follows :
Sir Charles Dodds (President and Chairman till 1966)
Sir Max Rosenheim (President and Chairman from 1966)
Sir Aubrey Lewis
Dr J. N. Morris
Dr J. G. Scadding
Dr J. C. Gilson
Dr H. A. Clegg (Co-opted 1969)
Dr P. J. Lawther
Dr F. Avery Jones
Dr D. D. Reid
Dr N. C. Oswald
Dr L. H. Capel
Dr C. M. Fletcher
Sir Kenneth Robson (Registrar)
Mr G. M. G. Tibbs (Secretary of the College)
The Committee wishes to acknowledge the valuable assis­
tance given by M r R. E. Waller of the Air Pollution Unit,
Medical Research Council.
‘A young gentleman who had inked himself by accident,
addressed me from the pavement, and said, “ I am from
Kenge and Carboy’s miss, of Lincoln’s Inn.”
“ If you please, sir,” said I.
He was very obliging; and as he handed me into a fly, after
superintending the removal of my boxes, I asked him whether
there was a great fire anywhere? For the streets were so full
of dense brown smoke that scarcely anything was to be seen.
“ O dear no, miss,” he said. “ This is a London particular.”
I had never heard of such a thing.
“ A fog, miss,” said the young gentleman.
“ O indeed,” said I.'
Bleak House by Charles Dickens
1
A ir Pollution and Health
I. I From Friday 5th December to the morning of Tuesday
9th December 1952, London was enclosed in still, cold air.
The result was a dense fog in which air pollution reached an
unusually high level. There was an immediate increase in the
number of people dying in Greater London, and the mortality
remained higher than was normal for the season (Figure 1). It
was estimated that the fog was responsible for the deaths of
from 3,500 to 4,000 people either during the fog or soon
afterwards.68 In the week ending 13th December deaths in the
Administrative County of London alone, at 2,484, were about
three times the number that might have been expected at that
time of the year. Table 1 shows that the largest relative
TABLE
I.
M O R T A L IT Y INCREASE IN TH E LO N D O N SM O G OF 1952
Cause
Bronchitis
Coronary disease
Myocardial degeneration
Pneumonia
Vascular lesions of CNS
Respiratory tuberculosis
Cancer of lung
Other respiratory diseases
Other causes
All causes
Seasonal
norm
75
N o . o f deaths in
the week after smog
37
98
704
281
244
168
128
17
36
8
410
887
69
52
761
2,484
122
84
77
Relative
increase
9 .4
2-3
2.9
4 .5
1.3
4 .5
1.9
6 .5
1.9
2*8
increases were in deaths from bronchitis, pneumonia, and
tuberculosis and other diseases of the lungs, with bronchitis
heading the list. There was also an increased number of deaths
from heart disease. Most of these deaths were in old people
10
Air Pollution and Health
FIGURE I
DEATH AND POLLUTION LEVELS
IN THE FOG OF DECEMBER 1 952
The fog lasted from 5th December to 9th December. The graphs
show the increased number of deaths during this period and also
the rise in the amounts of sulphur dioxide (S0 2) and smoke in the
air. The figures for death were provided by the Registrar General’s
Office. The pollution levels were measured at twelve different
stations in London.
and the pollution probably hastened their end, but it should
be noted that during December 1952 the number of persons
under the age of 45 dying from bronchitis and pneumonia was
also three times higher than was expected. The winter of
1952 provided a dramatic example of the deadly effect of air
pollution, and was the starting point of a number of inquiries
into the subject.
1.2 As long ago as 1273 a law was passed to prevent or at
least control pollution of the atmosphere by the burning of soft
Air Pollution and Health
11
coal, and complaints against such pollution were frequent in
the thirteenth and fourteenth centuries. A landmark in the
history of this subject was the pamphlet entitled Fumifugium
addressed by John Evelyn to Charles II, in 1661.33 He
described the ‘Evil' as 'epidemicall: indangering as well the
Health of Your Subjects, as it sullies the Glory of this Your
Imperial Seat'. Evelyn suggested that factories using coal
should be moved farther down the Thames valley and that a
green belt of trees and flowers be put round the heart of the
city. ‘But I hear it now objected by some,' Evelyn wrote, ‘that
in publishing this Invective against the smoake of London, I
hazard the engaging of a whole Faculty against me, and par­
ticularly, that the College of Physicians esteem it rather a
Preservation against Infections, than otherwise any cause of
the sad effects which I have enumerated.' The famous seven­
teenth-century physician, Thomas Sydenham, however, had
no doubt about the ill effects of London mists containing, 'the
fumes that arise from the several trades managed here, but
especially sulphur and fumes of sea coals with which the air
is polluted, and these, being sucked into our lungs and insinu­
ating into the blood itself, give occasion for a cough' .121
1.3 Yet three hundred years later there is still uncertainty
about the precise effects on health of fouling of the atmosphere.
This lack of understanding is chiefly due to the complexity of
the problem. The public health movement of the last century
concentrated on drainage, on a clean water-supply, on
sewerage, on housing, and on the control of epidemics of such
diseases as cholera and smallpox and typhoid. The theoretical
justification of sanitary measures at that time was the main­
tenance of pure air, based on a false theory of the spread of
infection. ‘The ultimate end of sewerage, drainage, and a
supply of water adequate to the cleansing of sewers, drains
and streets,' wrote Dr Southwood Smith in 1846, ‘is to main­
tain the air, wherever human beings take up their abode, in a
fit state for respiration.'35 Dr William Farr believed that pol­
lution of the air was responsible for the excess of disorders of
the lung in English cities.14 Sir John Simon, in his City of
London Reports, referred specifically to ‘the flagrant nuisance
of smoke'. ‘I ought likewise to tell you, that there are valid
12
Air Pollution and Health
reasons for supposing that we do not with impunity inhale
day by day so much air which leaves a palpable sediment;
that many persons of irritable lungs find unquestionable incon­
venience from these mechanical impurities of the atmosphere.'
And Simon said that, 'at no distant period' smoke from
domestic chimneys would be controlled, and they would 'cease
to convey to the atmosphere their present immense freight of
fuel that has not been burnt, and of heat that has not been
utilized'. This report was made in 1854 to the Court of the
City of London.109 Since then many other pollutants have
been poured into the atmosphere.
1. 4 Almost exactly a hundred years later, in 1956, the Clean
Air Act was passed.69 This was a direct consequence of the
1952 fog in London. The Beaver Report, which formed the
basis of Government action, had stressed the risk to health
from a heavily polluted atmosphere.6 How serious this might
be had already been shown in 1930, when sixty people died
after a period of intense pollution of the air in a small Belgian
village in the Meuse Valley.36 A similar episode had occurred
in Donora, near Pittsburgh, in 1948,105 and this, with the
emergence of a lachrymatory haze of a different type of
pollution in Los Angeles,40 stimulated the publication in the
U SA of a number of papers on the effects of air pollution on
health.126 127 In the hundred years following John Simon’s
brief reference to the dangers of a smoke-laden atmosphere
there were few reports on the subject in British medical
literature; but some progress had been made in measuring
and charting the nature and amount of contaminants of urban
air in Britain.
1. 5 Anyone who has experienced the dense yellow fog that
used to be known as the 'London particular' is unlikely to be
surprised by the suggestion that it is bad for the lungs. But
a doctor faced with a patient from an area where air pollution
has long been at a high level may find it difficult to determine
the extent to which the patient’s health has been affected by it.
A man with chronic bronchitis may be a heavy smoker, a
worker in heavy industry, live in a crowded home, or have had
repeated attacks of pneumonia. Any additional effects on
health of exposure to polluted air in his surroundings are thus
Air Pollution and Health
13
difficult to assess. The relative influences of cigarette smoking
and air pollution have therefore been studied by comparing,
among large groups of people differing in their exposure to
them, the frequency of the diseases these factors may cause.
The initial approach should be through these epidemiological
comparisons, and the results obtained should be the basis for
public health policy and action. T o say this is not to under­
estimate the need for and value of laboratory research, or the
contribution made by clinical observation.
Some Problems of Measurement and Interpretation
1. 6 The difficulties inherent in the epidemiological approach
to disease stand out prominently in any attempts to measure
the effect of air pollution on disease. Current exposure to
cigarette smoke can be estimated with reasonable accuracy— so
many cigarettes a day. But measurement of exposure of indi­
viduals to air pollution cannot be other than crude. The
concentration of pollutants varies according to the nature and
amount of the fuel used, and to meteorological conditions and
topography of the places where people live. Exposure may be
brief and intense, or be continued for long periods to low
concentrations of the allegedly harmful constituents of the air
breathed.
1. 7 There is, too, no disease that is clearly due to air pollu­
tion alone. The effect of pollutants has thus to be gauged by
the frequency of lung diseases such as bronchitis and emphy­
sema among people exposed to them. But these diseases are not
precisely defined, and diagnostic standards may differ from
time to time or between town and country. To lessen some of
these difficulties of measurement and interpretation surveys of
representative samples of people living in areas differing in
levels of air pollution have been carried out with uniform
methods of investigation and standardised techniques of
measuring lung function. At the same time the individual’s
smoking habits, living conditions, and exposure to industrial
dusts as well as to prevailing levels of local air pollution have
usually been recorded.
1. 8 Modern methods of analysis allow us to disentangle the
presumed effects of these factors and to determine the influence
14
Air Pollution and Health
of pollution on lung and other diseases. In general, evidence
of cause and effect comes from the repeated observation in
similar circumstances of a clear association between the
frequency of disease and the concentration of pollutants to
which people are exposed at different times and places. Such
findings must be assessed in the light of the results of experi­
ments on men and animals, as well as of clinical and patho­
logical experience.
i . 9 Much work on air pollution and health has been done
both in this country and abroad. Some coherent patterns have
emerged. Sufficient evidence has accumulated to justify some
conclusions about the risk to health of general air pollution in
Britain.
2
Sources, Types, and Trends
o f A ir Pollution
2. i Pollution of urban air in Great Britain— and this report
is mainly restricted to British experience— is almost entirely
due to the combustion of carbonaceous fuels. For centuries
raw coal was the main source of heat and other forms of
energy in home and factory. In 1956, the year in which the
Clean Air Act was passed, the consumption of coal rose to its
highest level of 214 million tons. It has since steadily declined.74
Further, a large proportion of the total supply is now burnt
in installations, such as power stations, where smoke emission
is carefully controlled and any other pollutants are dispersed
at a high level. Electricity, gas, and oil play an increasing part
in meeting the national need for energy, fuel oil being more
and more used in central heating plants and in industry. The
discovery of reservoirs of natural gas and the introduction of
nuclear energy will have a growing influence on ways and
means of providing heat and energy in the home and in
industry.
Particulate Matter
2. 2 Most of the particles in the air of British towns come
from the combustion of fuel. Destructive distillation and in­
complete combustion of soft coal on domestic open fires
produce minute tarry droplets and black smoke, which may
remain suspended for long periods. Some smoke comes from
badly designed or wrongly operated heating plants and diesel
engines. In larger installations fuels can be burnt smokelessly,
but the draught may carry particles of ash or of solid fuels up
the chimney. These can be arrested mechanically or electri­
cally, and most of those that escape into the atmosphere are
large enough to fall out near the source; but small ash particles
Air Pollution and Health
i6
are commonly seen in samples collected from town air. The
large quantities of sulphur dioxide produced by the burning of
the sulphur compounds occurring in many solid and liquid
fuels also contribute indirectly to the suspended matter in
urban air, since in humid conditions some reacts with other
pollutants to form sulphuric acid and sulphates. Industrial
processes, building and demolition, wear of road tyres and
other materials, plants and animals, and the burning of vehicle
fuel containing additives, all disperse particles into the air. In
general, most of the particles in urban air have diameters less
than one micron, and it is necessary to use an electron micro­
scope to examine their size and shape.132 Many are complex
structures, and Plate i illustrates the appearance of a single
‘smoke aggregate' from London air at high magnification. In
this sample the individual particles consist of carbon or
complex hydrocarbons each with a diameter of about 0.05
of a micron. Examples of the size and distribution of particles
in London air are given in Table 2.
TABLE 2 .
NUM B ER AND SIZE OF PAR TICLES IN LO N D O N AIR
Sam pling site
City, normal pollution
City, moderate pollution
City, high pollution
Street sample, light traffic
Tunnel sample, heavy traffic
m l= millilitre.
N o. o f
particles/m l
7,800
27,100
154.500
27,300
120,400
ug = a millionth of a gram.
Estim ated
concentration
M a ss median
diameter
(u g /m3)
(um)
100
370
1,970
280
1,260
07
0.8
0.9
0.5
07
um = a millionth of a metre.
Sulphurous and other Pollutants
2. 3 Even with apparently complete combustion most fuels
still pollute the air, particularly with sulphur dioxide. Sulphur
is present in most coals as pyrites and as organic sulphur com­
pounds. The latter also exist in crude oil, and they are concen­
trated in the heavier fractions on refining. Practically all the
sulphur in oil, and between 80 and 90 per cent of that in
coal and coke, go up the chimney as sulphur dioxide, one of
the most important gaseous contaminants in urban air. Some
Electron micrograph of a smoke aggregate x 220,000.
(Permission to reproduce this photograph has kindly been given by
the Air Pollution Unit, M edical Research Council .)
Sources, Types, and Trends of Air Pollution
17
of it— up to 5 per cent— may be further oxidised to sulphuric
acid. Sulphur compounds are virtually absent from petrol, but
small amounts are found in diesel fuel. Motor vehicles con­
tribute very little sulphur dioxide to the air, even in busy
streets, in comparison with that from the combustion of coal
or heavy oil.
2. 4 Minute amounts of polycyclic hydrocarbons are present
in the tarry component of pollution, and some of these (notably
benzo(a)pyrene) have carcinogenic (cancer-producing) proper­
ties. Open coal fires are the main source of these compounds,
with small contributions from motor vehicle exhausts.
2. 5 Some other pollutants of interest in relation to health
are emitted by motor vehicles. There are two types of engine
in common use: spark ignition (petrol), and compression
ignition (diesel). In each case the end-points of combustion are,
ideally, carbon dioxide and water, but undesirable pollution
may be caused b y: (1) incomplete combustion; (2) additives
or impurities in the fuel; and (3) ‘fixation’ of atmospheric
nitrogen. (See also paras 7. 1 to 7. 4)
2. 6 Air is mainly a mixture of oxygen and nitrogen. In
combustion some of the atmospheric nitrogen may also be
burned to yield oxides of nitrogen. The commonest is nitric
oxide (NO), further oxidised to nitrogen dioxide (NO2) in the
air as well as to some extent in the combustion chamber.
Nitrogen dioxide in high concentrations is a suffocating
poisonous gas, but in air polluted by motor vehicles it occurs in
concentrations well below those looked on as safe in industrial
practice.
2. 7 In some conditions (when cold, idling, or decelerating)
petrol engines give out much unaltered petrol, and, when
starting from cold, diesel engines can discharge unburnt fuel.
Often, the petrol is not combusted but discharged in an altered
form : that is, its complex hydrocarbons may be simplified by
rearrangement of the molecules in the process known as
‘cracking’. Contamination of the air by unburnt or by cracked
hydrocarbons is serious in Los Angeles and other cities where
strong sunlight and stable air produce a ‘photochemical smog’.
This results largely from the action of ultraviolet light on
nitrogen oxides and hydrocarbons discharged from the
i8
Air Pollution and Health
exhausts of vehicles. In the presence of some hydrocarbons,
notably olefines, oxides of nitrogen react to form ozone. In
turn, the ozone reacts with more hydrocarbons and other
organic matter to produce compounds that irritate the eyes.
This ‘photochemical smog' is the product of strong sunlight,
stable air conditions, and high concentrations of the necessary
hydrocarbons and oxides of nitrogen— a combination of
circumstances very rare in Britain.
2. 8 With incomplete combustion substances such as alde­
hydes, ketones, and organic acids may be form ed: they are
probably responsible for the typical smell of petrol and diesel
exhausts. Incomplete combustion is also liable to lead to the
formation of carbon in diesel engines, particularly when they
are badly maintained or misused, with the consequent; emission
of clouds of black smoke.
2. 9 Petrol engines emit large quantities of the odourless and
colourless gas carbon monoxide, which is virtually absent from
diesel exhaust. In Britain, concentrations of 10 to 20 ppm are
usual in busy streets, with occasional peaks up to 100 ppm.133
Occupants of vehicles, especially in traffic jams, may be
exposed to high concentrations from exhaust gases from
other cars or leaking exhausts. The degree of absorption can
be measured precisely, by analysis of the blood of exposed
people, with simple and accurate methods that have made
survey work much easier. The much greater affinity of the
haemoglobin of blood for carbon monoxide than for oxygen
constitutes the danger in high concentrations, which may
cause fatal poisoning in a closed garage with the engine
running. Extensive surveys have shown that concentrations
approaching these do not occur even in crowded streets.
2. 10 Organic lead compounds are commonly added to petrol
as ‘anti-knock' agents. Much of the lead is emitted with the
exhaust in inorganic form; the concentrations found in busy
streets are very small. Those in the air of Fleet Street in
London have been found to be about 3 ug/m3, a result in
keeping with assays made abroad.133 (See also para 7. 3)
2. 11 So far as is now known the many other contaminants
of the air constitute no danger to health; but this is a matter
that must be kept under close observation.
Sources, Types, and Trends of Air Pollution
19
Factors Affecting the Distribution of Air Pollutants
2. 12 Measurements of smoke and sulphur dioxide through­
out Britain have shown the effect of various factors on their
distribution in urban air; for example season, weather, size
and position of town, the kind of fuel, and the way it is burnt.
The smoke/sulphur-dioxide ratio is less in town-centres where
offices and shops are centrally heated by plants producing little
or no smoke than in residential areas where coal is incom­
pletely burnt in open grates. A town on a hill or on the coast
will, in general, be swept by winds that make the air cleaner
than in a town inland or in a valley. When the source of heat
is electricity or gas there is little if any pollution of the air,
and little smoke comes from hard coal burned in open grates,
as in parts of South Wales, or from coke and other manufac­
tured fuels. Although the sulphur content of these smokeless
fuels is similar to that of the coal from which they are made,
less of them is needed to provide the same amount of heat. Soft
bituminous coal, which is that chiefly used in houses, cannot
be burnt in open grates without much smoke— a problem of
special significance in places where miners have concessionary
coal.
2. 13 Contamination of the atmosphere from the combustion
of fuels for heating buildings increases in the winter. Seasonal
swings of levels of pollution are less in places where industrial
consumption of fuel is more or less constant throughout the
year, and where domestic fires are used for cooking and for
heating water. The concentration of pollutants in urban air
may increase rapidly when Temperature inversion’ occurs.
Usually, the air is colder the farther it is from the ground.
Warm polluted air from chimney stacks rises rapidy through
the colder layers of air above a city and is quickly dispersed.
But if on a cold, still, cloudless night the earth loses heat by
radiation the air immediately above the ground becomes colder
than the air above the city (Figure 2): the temperature
gradient is inverted. In these conditions contaminated air near
the ground is thus cooler and denser than the air above and
so cannot rise high enough to be effectively dispersed. The
Temperature inversion’ is particularly serious when the cold
ground air in a valley forms a stable pool in which pollutants
FIGURE 2
THE MECHANISM OF TEMPERATURE INVERSION
These illustrations show how change in air temperature can trap
pollutants in a dense fog close to the ground. Many industrial
towns in Britain are by their situation especially exposed to this
hazard..
Sources, Types, and Trends of Air Pollution
21
are trapped. If humid air cools fog may form and shut off the
warmth from the sun. The inversion of temperature persists
until a change in the weather breaks it up. Many industrial
towns in Britain are, unfortunately, situated in valleys and are
therefore especially subject to periods of high air pollution.
The Measurement of Smoke and Sulphur Dioxide
2. 14 Regular measurements of smoke concentrations in
towns were first made more than fifty years ago. The number
of sites making daily measurements of this pollutant, and later
of sulphur dioxide too, has increased. Only since 1961 have
stations for sampling the atmosphere been systematically set
up throughout the United Kingdom. The Warren Spring
Laboratory of the Ministry of Technology organises and
publishes regular reports of this National Survey;76 by Sep­
tember 1969, 1,189 daily sampling instruments were in use.77
Local authorities, as well as other bodies, provide and main­
tain the instruments.
2. 15 A simple apparatus consists of an inlet funnel that
excludes large particles, a clamp holding a filter paper, a
bubbler containing a solution of hydrogen peroxide, a small
pump, and a gas meter to measure the volume of air drawn
through the apparatus. Smoke particles are held back on the
filter paper, and their concentration can be estimated by
reflectance in terms of ‘equivalent standard smoke’. Sulphur
dioxide is converted to sulphuric acid in the bubbler and the
amount is determined by titration.75
2. 16 Samples of air are usually taken over periods of 24
hours, but more frequent measurements may be required.
Acute effects of air pollution may be more closely related to
peak values than to 24-hour averages. At times of high
pollution it is therefore important to supplement routine
measurements of smoke and sulphur dioxide with others made
over short periods (usually one hour). In foggy weather sul­
phuric acid can be determined by titration of samples collected
on filter paper.
2. 17 Since smoke and sulphur dioxide are the major suspect
pollutants and can be measured simply, there is a tendency to
use their concentrations as indices of air pollution in general.
22
Air Pollution and Health
Daily alterations in concentration at any one site are mainly
determined by variations in the weather rather than by short­
term changes in emission. Concentrations of smoke, sulphur
dioxide, and other pollutants usually alter in parallel with
each other. In epidemiological studies concentrations of smoke
or of sulphur dioxide have been used as indices of pollution,
but this does not imply that these pollutants directly cause the
effects that may be observed. Also, in many areas of the
country the relations between smoke, sulphur dioxide, and
other pollutants are gradually changing. For example, in
London there is now much less smoke in the atmosphere as
a result of the implementation of the Clean Air Act; but
concentrations of sulphur dioxide have not decreased to the
same extent. (See Fig. 13, p. 66.)
2. 18 In towns today, the average concentration of sulphur
dioxide over the year is about 200 micrograms per cubic metre
(u g/m 3), ranging from 140 in summer to 260 ug in the
winter.78 Much higher concentrations may occur over short
periods, up to 4,000 u g/m 3 in times of persistent temperature
inversion. Before the Clean Air Act came into force in 1956
concentrations of smoke were often higher than those of
sulphur dioxide, but now they are, in general, lower. It is no
longer true to say that the largest towns have the highest smoke
concentrations: in London they are no higher than those in
many small provincial towns, and are well below those in small
northern mining towns.
3
Experimental Work
on the Effects o f Inhaled Pollution
3. i Most of the work on the effects of inhaled particles and
gases has been done to identify potential hazards in industry,
where men may be exposed for prolonged periods to high
concentrations of pollutants, including some such as sulphur
dioxide that also occur in urban air. Experiments on the
chronic effects of long-term exposures to pollutants are
necessarily confined to animals, but acute effects have been
observed in human volunteers. The use of human beings in
experiments has obvious limitations, especially, for example,
in examining the effects of various pollutants on patients with
bronchitis. It is difficult to apply to man the observations made
in the laboratory on animals, if only for the reason that it is
not possible to simulate in the laboratory the fog as it occurs
in real life. All that can be done is to test the effects of indi­
vidual components of fog, alone or in limited combinations.
3. 2 The American Conference of Governmental Industrial
Hygienists reviews each year the evidence relating to poten­
tially harmful materials. In Britain, the Ministry of Labour
publishes these acceptable ‘threshold limits',72 some of which
are shown in Table 3 alongside the highest hourly concentraTABLE
3.
THRESHOLD L IM IT V ALU ES FO R SOM E PO LLU TA N T S IN
IN D USTRY AND M A X IM U M H O U R L Y C O N C E N T R A TIO N S
IN URBAN A IR
Industrial
lim it
Sulphuric acid, mg/m3
Sulphur dioxide, ppm
Carbon monoxide, ppm
Nitrogen dioxide, ppm
1
5
50
5
M axim u m in
urban air
07
2
55
0.25
24
Air Pollution and Health
tions of pollutants observed in recent years in London air.19
It will be seen that with the exception of carbon monoxide
(discussed in Chapter 7) the concentrations of pollutants in
urban air do not exceed, even for one hour, those considered
acceptable for most workers continuously exposed to them.
Contamination of urban air may exacerbate bronchitis and
hasten the death of patients already seriously ill; hence
industrial limits set for the protection of healthy workers have
limited relevance to those in the same community exposed to
cold and damp and suffering from disabling conditions of the
lung or of the heart, or approaching the end of life. Full
reviews of the epidemiological and experimental evidence on
sulphur dioxide and particulate matter in the air were pub­
lished in 1969 by the United States Department of Health,
Education, and Welfare.126’127
3. 3 The physical phenomena involved in the penetration
and deposition of particles in the lung are complex and depend
on the rate and other aspects of ventilation of the lung, as well
as on the character of the particles themselves. In general,
particles greater than 10 microns in diameter are trapped in
the nose and upper air passages and do not usually reach the
alveoli (or air cells) of the lung. As the size of the particles
diminishes, the proportion that passes beyond the bronchioles
(small branches of the bronchial tubes) increases. Most insoluble
particles of less than 2 microns in diameter reach this region.
Particles containing substances soluble in water grow rapidly
in size in the humid air of the air passages and are thus more
readily deposited there by impaction or sedimentation.
3. 4 O f all parts of the body the respiratory tract is the most
accessible to pollutants in the atmosphere. Inspired air passes
down to the alveoli of the lung, which have a surface of some
50 to 70 square metres, or about twenty-five times the area
of the skin covering the body. An average man breathes about
10 litres of air a minute when seated and up to 50 litres when
working hard for short periods. Retention of small particles
depends on the rate of ventilation of the lungs, which, in turn,
influences the effect on the respiratory tract of noxious matter
in the atmosphere.
3. 5 Though it is possible that aqueous droplets in smoky
Experimental Work on the Effects of Inhaled Pollution
25
fog may cause spasm of the bronchi or oversecretion of mucus
and so increase resistance to the flow of air into and out of the
lungs, there is little doubt that fog droplets are not necessary
for this to happen. Such increased resistance to air flow may
be seen when pollution is high in the absence of fog. It is not
easy to assess the relative importance of smoke particles and
sulphur dioxide. High concentrations of ‘inert’ particles alone
can increase resistance in the airways of the lung in humans
and animals.31 There is little doubt that in animal experiments
the addition of particulate matter to sulphur dioxide and
sulphuric acid can produce increase in airway resistance. These
changes have not been observed in man.
3. 6 There have been no convincing reports of any response
in human volunteers to experimental inhalation of less than
1 ppm of sulphur dioxide. There have been references to slight
transient effects following exposure to concentrations between
1 and 2 ppm,112 124 but these reported positive results are but
few among many thousands of experiments. It must be
remembered, too, that concentrations of SO2 exceeding 1 ppm
are rarely found in town air. A conspicuous feature of the
literature on experiments with sulphur dioxide is the rarity
with which any effects of realistic concentrations have been
reported, despite the performance of a great number of experi­
ments by reputable workers in many countries.
3. 7 One of the difficulties in comparing the results of various
workers is that the pollutants tested have been inhaled in
different ways— through mouth or nose, or through both.
Sulphur dioxide is soluble in water, and the amount absorbed
varies with the route of inhalation and the rate of flow. If the
mixture is inhaled through the nose much of the sulphur
dioxide is absorbed by it, and only minute amounts will there­
fore reach the more remote parts of the respiratory tract.113
According to many observers the bronchoconstrictor effect of
higher concentrations of sulphur dioxide can be abolished by
drugs such as atropine.
3. 8 In town air sulphur dioxide always coexists with par­
ticles, and it has been suggested that these two types of con­
taminant could produce a greater effect in combination than
separately. Animal experiments show that the effect of sulphur
26
Air Pollution and Health
dioxide is enhanced in an aerosol in which it is soluble or
which contains salts that accelerate its oxidation to sulphuric
acid.1 But response to sulphur dioxide is not altered when used
in aerosols of insoluble materials such as carbon and iron
oxide.2 The synergistic effect of particles and sulphur dioxide
has not been seen to occur in men who have been exposed to
mixtures of gas and particles,13 but the possibility that particles
of smoke and sulphuric acid in some special physical forms
may enhance the irritancy of sulphur dioxide must be borne
in mind and must be the subject of continuing research.
3. 9 Episodes of high pollution of the air are often associated
with cold weather. It has been reported that in patients with
a history of sensitivity to cold weather breathing was impaired
when they were exposed to cold air free from any added pollu­
tant.50 Other experiments showed that in patients with asthma
or bronchitis exposure to cold air or to inhaled materials such
as carbon dust rapidly increased airway resistance.110
3. 10 Irritation of the bronchial tubes causes excess secretion
of the mucus, which in normal amounts enables cilia to work.
There is evidence that the phase of over-secretion— simple
chronic bronchitis— is due to the inhalation of cigarette smoke.
These early changes may be reversed by removing the irritant:
that is, by stopping smoking. Control of air pollution will help
to restrain whatever part this may play in causing, or exacer­
bating, chronic bronchitis. Unless preventive measures of this
kind are taken infection is superimposed, in which the bacteria
Haemophilus influenzae and Streptococcus pneumoniae are
often prominent. Possibly urban pollution favours infection
either by encouraging the growth of bacteria or by paralysing
the action of the very fine hairs or cilia lining the airways that
keep mucus on the move. Cigarette smoking also has this
paralysing effect on the cilia. If they are paralysed they cannot
perform their normal function of removing inhaled particles,
including germs, from the lungs. Pollutants may alter the
bacterial inhabitants of the respiratory tract. In animal experi­
ments inhalation of tobacco smoke increases virus and bac­
teria/ infections. Another observation bearing on this was that
particulate pollutants from town air stimulated the growth of
Haemophilus influenzae on culture plates.60
4
A ir Pollution, Chronic Bronchitis,
and A llied Diseases
4. 1
O f diseases affecting the lungs chronic bronchitis is one
of the major causes of disablement and death in Britain, par­
ticularly among middle-aged and elderly men. In 1967, 5,253
deaths in men aged 45 to 64 (6'8 per cent of all male deaths
in the same group) were attributed to bronchitis, and 1,134
deaths in women of the same age (2.6 per cent of all female
deaths in this group).89 Just over thirty million working days
are lost to industry each year because of bronchitis,73 and the
consequent cost of lost production and medical care has been
estimated to amount to £65 million a year. It is therefore of
great importance to the public health and the national
economy to discover the causes of the disease and the effects
on it of contamination of the air.
4. 2 It is appropriate in considering the effect of air pollution
on chronic bronchitis to recall briefly the way in which the
disease develops. At first there is simply persistent or recurrent
cough, with production of phlegm. Infection of the bronchial
tubes is shown by recurrent illnesses in which the phlegm
becomes yellowish or purulent, and in time persistent breath­
lessness may develop. Both the infection and the breathlessness,
often due to an associated emphysema,* tend to increase in
severity and persistence. In many cases heart failure develops
because the circulation of the blood through the lungs is
disturbed.
4. 3 We do not know precisely how air pollution may cause
death in a patient with chronic disease of the lungs and the
heart. Narrowing of the airways by the irritation of contami­
*A condition in which the air spaces in the lung enlarge and break down.
This interferes with the even flow of air, and diminishes the effective gas­
exchanging area of the lung.
28
Air Pollution and Health
nated atmosphere reduces the flow of air in and out of the
lungs and the supply of oxygen to the heart and other tissues.
In such cases examination shows great increase in the difficulty
of breathing, and the oxygen content of the blood is very low.
Even comparatively slight decreases in the diameter of airways
already narrowed by chronic bronchitis may curtail the supply
of oxygen to the blood. It has been repeatedly shown that
reduction of oxygen supply to the lung constricts its smaller
blood-vessels, and this may place an intolerable burden on the
heart. Seriously ill patients may be unable to stand the strain
on breathing brought on by the irritation of polluted air. These
stresses may also be responsible for the gradual deterioration of
many patients with chronic bronchitis during successive years
of exposure to unclean air.
Acute Effects of High Pollution and Cold Weather
4. 4 One of the most dramatic examples of the effect of high
pollution of the air and cold weather, in terms of bronchitic
illness and death, occurred in London in December 1952, and
is referred to at the beginning of this report.68 There, Table 1
shows that in the Administrative County of London deaths
amounted to three times the number expected at that time of
the year. Figure 3 shows that deaths both from lung disease
and from disease of the heart and the blood-vessels followed
a similar time pattern. As has already been stated, most of
these deaths were in elderly people suffering from chronic
disease of the heart and the lungs; but deaths were also higher
than expected in patients under the age of 45 years. There
have been similar if less dramatic episodes before and since
1952 in London and in such large cities as Glasgow and
Manchester.67,98,38,83, 86 For example, in the particularly fogridden winter of 1958-59 several periods of fog were associated
with an immediate increase in mortality, mainly from bron­
chitis and pneumonia.67
4. 5 In 1840 Dr William Farr, the great medical statistician,
noted the influence on mortality of the severe cold that so often
coincides with a fog.86 The same observation has been made
many times since then, and it has been shown that the weekly
death rates from respiratory disease in both infants and the
Air Pollution, Chronic Bronchitis, and Allied Diseases
29
aged are closely related to the temperature recorded in the
preceding week.102,103, 137,138, 142,140,62 Pollution of the air from
domestic fires will obviously be greatest during cold weather.
In London and East Anglia the weekly death rates from
bronchitis and pneumonia during the period 1947-54 were
found to be more closely related to coldness than to the
frequency of fog.8 Nevertheless, the increase in the average
number of deaths during periods of intense cold and frequent
29th
6th
NOV
D
FIGURE 3
13 th
E
C
E
20th
M
B
27th
E
R
3rd
JAN.
DEATHS FROM DISEASES OF THE LUNGS AND THE HEART
AT THE TIME OF THE FOG OF DECEMBER 1 952
It will be seen that the number of deaths from bronchitis, pneu­
monia, and the two forms of heart disease rose during the fog and
continued in excess for the rest of the month.
30
Air Pollution and Health
fogs was greater in London than in East Anglia, where the air
is less polluted.
4. 6 The effects on bronchitis of sudden changes in weather
and contamination of the air have been shown in other ways.
Patients with bronchitis have been asked to record in a diary
changes in their symptoms from day to day.57 Figure 4 shows
that deterioration coincided with increase in the concentration
of both smoke and sulphur dioxide; it was less closely related
to either falls in temperature or variations in relative humidity.
FIGURE 4
EFFECTS OF CHANGES IN WEATHER AND POLLUTION
ON PATIENTS WITH BRONCHITIS
It will be noted that the sharp peak in concentrations of smoke
and sulphur dioxide coincided with aggravation of the disease.
Changes in temperature and humidity had little effect.
Air Pollution, Chronic Bronchitis, and Allied Diseases
31
Statistics of sickness absence have been related to atmospheric
changes. For example, in London during the last war the
monthly absence rate of postmen with bronchitis rose sharply
when fog cut visibility below 1,000 metres.96 A study of factory
and office workers in London showed that rates of absence
from work began to rise when 24-hour averages of 200 ug of
smoke or 250 ug/m3 of sulphur dioxide were reached.3 And
temperature changes had no additional effect. A review of
FIGURE 5
DEATH RATES FROM BRONCHITIS IN MIDDLE AGE IN
RURAL AND URBAN AREAS (ENGLAND AND WALES, I9 5 9 -I9 6 3 )
The above diagram shows the great excess of bronchitis in men
as compared with women. The absolute difference in the death
rate as between rural areas and conurbations is particularly strik­
ing among men. (Data from the Registrar General’s Supplement
on Area Mortality, 1961.)
32
Air Pollution and Health
medical certificates in Salford12 disclosed that there was a
doubling of the rate of absence attributed to bronchitis after
periods when smoke concentration exceeded 1,000 u g/m 3.
4. 7 Records of admissions to London hospitals in 1955-56
made it clear that the demand for beds for patients with acute
chest disease rose during periods of cold weather.48 When
changes in humidity, barometric pressure, and other climatic
factors were taken into account in the statistical analysis, peaks
in air pollution were found to have an effect in addition to that
of cold weather on this demand for beds.
Long-term Effects of Air Pollution
4. 8 High levels of air pollution, especially when combined
with cold weather, certainly affect those already disabled by
disease of the heart or of the lungs. The influence of prolonged
exposure to the concentration of pollutants usually found in
the air of British towns is more difficult to assess. The high
urban excess in mortality from bronchitis is seen in Figure 5.
Reasons for this excess, or for differences in mortality between
town and country, may be found in differences in diagnostic
practice, in the social and occupational structure of the
populations concerned, in the opportunities for cross-infection
in crowded houses and cities, and in cigarette smoking. All
these factors, as well as air pollution, must be taken into
account in making geographic comparisons and in analysing
variations over a period of time.
Long-term Trends in Mortality from Bronchitis
4. 9 Changes in air pollution and factors such as smoking
habits can be compared with long-term trends in the death
rate from chronic bronchitis and related diseases. Interpretation
of changes in the death rates attributed to chronic bronchitis
during the past hundred years is complicated by changes in
diagnostic skills and methods and in the official classification
of causes of death.64 Figure 6 shows the broad trend. The death
rates from bronchitis in both men and women were falling
consistently until 1940, and this fall was at a time when con­
sumption of coal was increasing. Since that date, however, the
death rate from bronchitis in men has taken an upward turn,
Air Pollution, Chronic Bronchitis, and Allied Diseases
33
while in women the decline in mortality has continued, but
less steeply. The difference in mortality between the sexes
became apparent earlier among those of middle age.
4. 10 The changes over a period of time in deaths from
bronchitis among men and women can be looked at in another
way. The ratio of male to female deaths at ages 55 to 59 in
people born in successive five-year periods from 1866-70
onwards is illustrated in Figure 7. The change in mortality from
bronchitis in middle-aged men first appeared in 1935 among
those born around 1880; and increased steadily to a peak in
those bom in succeeding five-year periods. Yet the relative
FIGURE 6 LONG-TERM TRENDS IN MORTALITY FROM BRONCHITIS
RELATED TO CONSUMPTION OF COAL AND TO CIGARETTE SMOKING
Between 1858 and 1940 the death rates from bronchitis in men
and women fell steeply. After 1940 the death rate from bronchitis
in males rose again. In the preceding forty years, cigarette smok­
ing among men had increased rapidly.
34
Air Pollution and Health
exposure to air pollution between men and women was unlikely
to have varied during this time. Cigarette smoking, however,
became more and more popular among men, especially during
the First World War and thereafter. Women took to smoking
later. The increasing mortality from bronchitis in men in recent
years is more closely linked to increased cigarette smoking than
FIGURE 7
TIME TRENDS IN FUEL CONSUMPTION, CIGARETTE
SMOKING, AND EXCESS MORTALITY FROM BRONCHITIS IN MALES
Since the early years of the twentieth century, coal consumption
(excluding that used for generation of power) has declined and
the use of petrol (and more recently derv) has increased. Cigarette
smoking went up sharply until about 1940. Between 1930 and
1955 the ratio of death rates from bronchitis among men to those
among women greatly increased. This growing excess mortality in
males during this period is more closely linked to cigarette smok­
ing than to the consumption of fuels.
Air Pollution, Chronic Bronchitis, and Allied Diseases
35
to any greater exposure of men to urban air pollution, the
consumption of coal, petroleum or derv.
International Differences in Chronic Lung Diseases
4. 11 One study has shown that British physicians, when
certifying death from the same clinical condition, usually state
‘chronic bronchitis’ on the certificate, whereas American and
Norwegian physicians use terms such as ‘emphysema' or
‘bronchiectasis’.97 These and similar differences in diagnostic
classification and differences in certification limit the value of
international comparisons. A detailed comparison of the
hospital and postmortem records of patients dying from all
causes in Bristol and San Francisco has shown, however, that
when the same diagnostic conventions are used there remains
an excess in the death rate from chronic disease of the lung in
Bristol.84 Britain has the highest death rate in the world from
chronic lung disease in middle-aged men.139
4. 12 In one investigation, the death rate from chronic
disease of the lung in the age-group 55 to 64 was found in
different countries to be related more to the consumption of
coal than to cigarette smoking.119 But because the number of
countries included was restricted by the availability of data,
and because of the lack of appropriate measures of life-time
exposure to pollutants, this work is difficult to assess.
4. 13 These indications of international differences in death
rates from bronchitis have been followed up by various
standardised studies of morbidity. A survey of the prevalence
of respiratory symptoms and impaired function of the lung in
similar population groups in Denmark and Britain suggests
that differences in the use of pipe and cigarette could explain
variations in bronchitis rates in rural populations in these two
countries.81 The Danes prefer pipes and cigars, and the British
cigarettes.15 Another standardised survey showed little distinc­
tion between the frequency of simple cough and sputum in
a small New England town, and that in rural and urban
Britain.94 But bronchitis, with recurrent illnesses and breath­
lessness, was commoner in Britain, especially among older
people in the larger towns.
4. 14 Some of the differences in the disease found in samples
36
Air Pollution and Health
of the general population in these countries may be connected
with occupation, with life in factory or farm, and associated
social and economic conditions. Surveys have therefore been
made of men doing the same job (as motor vehicle drivers in
public utilities) in London and elsewhere in Britain,46 in Bergen
in Norway,80 and in Baltimore, Washington, and Westchester
(New York) in the United States.47 49 It was found in groups
similar in age and in smoking habits that men working in
London had worse bronchitis and poorer function of the lung
than those in either Bergen or the cities of the eastern seaboard
of the USA, or in the smaller towns of England. The difference
was most marked in the more serious disease in Londoners
over the age of 45.
Bronchitis in Rural and Urban Britain
4. 15 In rural districts air is cleaner, and there are fewer
people among whom infection might spread. The death rate
from bronchitis of men and their wives, standardised for age,
is about five times greater in the unskilled working classes than
in the professional classes, and intermediate classes have an
intermediate mortality.90 As the gradient is the same for the
men and their wives it must be the result of social and
environmental influences to which both are exposed rather
than to occupational factors affecting only the men. Although
the proportion of people in these social classes varies in dif­
ferent types of district, such differences in social classes are an
unimportant factor in urban/rural differences in bronchitis.136
4. 16 Whatever the index of air pollution employed, all
investigations in Britain have so far shown a close correlation
between presumptive pollution level and mortality from
bronchitis in middle life. One inquiry related it to an index
of smoke based on local consumption of coal by domestic
users.23 Two studies compared the death rate from bronchitis
with current levels of smoke and sulphur dioxide.10,82 In one
of these, crude adjustment for regional differences in cigarette
smoking, or in the proportion of the population formed by
semi-skilled or unskilled workers and their families, reduced
but did not abolish the close correlation between air pollution
and mortality from bronchitis.10
Air Pollution, Chronic Bronchitis, and Allied Diseases
37
4. 17 Another approach was to compare the frequency of
absence of postmen from work because of bronchitis in different
parts of the country with widely differing conditions of pollu­
tion, as indicated by the frequency of thick fog in the districts
where they worked.34 Even after density of population and
domestic overcrowding were taken into account, the rates for
premature death or disablement and for absence from work
because of bronchitis were highest among those working in the
most polluted areas. The same method of study, with uniform
occupational groups, disclosed that among both postmen and
bus crews the highest rates of disability from bronchitis were
among men working in the centre and north-east of London,
where the concentration of air pollution was highest, compared
with the rest of London.91’ 21
The frequency of absence from work because of bronchitis
increases as men grow older. Within the London area, climate is
uniform but inception, i.e. attack, rates are higher in every age
group in districts where smoke concentrations in winter are also
high. (Data from Ministry of Pensions and National Insurance
Morbidity Survey, 1965.)
38
Air Pollution and Health
4. 18 The most recent information on occupied men comes
from the survey of absence from work carried out by the
Ministry of Social Security in 1961-62.73 The rate of disability
attributed to bronchitis was strongly correlated with local levels
of sulphur dioxide and, to a lesser extent, of smoke in the
places where the men worked; but the high bronchitis rate in
South Wales, where pollution was low, was a remarkable
exception to this general rule. There was no consistent associa­
tion between size of town and bronchitis. In general, the
disease was more common in the North of England than in the
South. Within the London region, where climatic conditions
are fairly uniform, the districts where winter pollution was
high had higher sickness absence rates from bronchitis than the
districts where it was moderate (Figure 8).
4. 19 A nation-wide survey of symptoms by standardised
techniques conducted by the Royal College of General Practi­
tioners in 1961 showed that after age, sex, social class, and
tobacco smoking had been taken into account bronchitis was
twice as frequent in large towns as in the rural areas of
Britain.16
Effects of Air Pollution and Cigarette Smoking
4. 20 In Northern Ireland a retrospective inquiry into mor­
tality from bronchitis gave useful information on exposure to
different urban and rural environments as well as to dustiness
of occupation, smoking habits, social class, and other personal
factors.135’ 25 Questions about these aspects of life were put to
the relatives of patients who had died from chronic bronchitis,
and to relatives of a representative control sample of the
population matched for sex and age. The death rates in the
two groups illustrated the major importance of smoking habit
and social class in this disease; but even when age and smoking
differences were taken into account there remained a marked
residential gradient in mortality ranging from 73 per 100,000
in rural districts to 310 per 100,000 for the centre of Belfast.
4. 21 To assess the separate and joint effects of air pollution
and cigarette smoking on symptoms of bronchitis a recent
survey was made of randomly selected samples of the British
population of both sexes between the ages of 35 and 64 years.55
Air Pollution, Chronic Bronchitis, and Allied Diseases
39
Those who responded to a postal inquiry about persistent
cough, bringing up phlegm, and repeated ‘chestiness' were
classified according to the levels of air pollution in their places
of residence and their cigarette smoking. Figure 9 indicates
that cigarette smokers are three times as likely to suffer from
chronic bronchitis as non-smokers, and that twice as many of
those living in heavily polluted districts as of those in the
cleanest areas suffer from this disease; but because of the less
precise measures of exposure used it is not possible to express
the relative importance of individual exposure to cigarette
smoking and air pollution. Specially significant is the combined
effect of smoking and air pollution. This is seen in the widening
FIGURE 9
BRONCHITIS IN RELATION TO SMOKING AND
AIR POLLUTION
The Standardised Morbidity Ratio (%) compares the frequency
of chronic bronchitic symptoms, allowing for differences in age
and sex, in groups of the British population relative to the national
level taken as 100 per cent. These groups are living in areas with
very low (1), low (2), moderate (3), and high (4) prevailing levels
of air pollution. (Data from a survey of respiratory symptoms in
Britain by Lambert and Reid55.)
40
Air Pollution and Health
gap between the rates for bronchitis among smokers and nonsmokers as the level of air pollution rises. The non-smokers are
much less affected.
4. 22 There is some evidence that air pollution is more
important in the aggravation than in the initiation of chronic
bronchitis. In the survey conducted by the Royal College of
General Practitioners, in 1961, for example, cigarette smoking
among the younger men was most clearly associated with
chronic production of phlegm.16 After the age of 55 years,
more serious symptoms such as repeated chest illness and
breathlessness were commoner in those living in the more
heavily polluted areas. Among postmen disabled by bronchitis
complications such as pneumonia were, in early middle life,
more common in the more polluted districts, and the proportion
of men dying within seven years after retiring from work
because of bronchitis was again higher in these parts of
Britain.96
Air Pollution and Intercurrent Infections
4. 23 Winter peaks in the death rate for bronchitis or
pneumonia may of course be associated with epidemics of
influenza and other infections. During a period of dense fog
in London as long ago as 1891 there was a higher mortality
than was expected from measles, whooping-cough, and tuber­
culosis, as well as from bronchitis and pneumonia, according
to the Registrar-General.87’ 83 Many of the 1,400 deaths in
excess of expectation were probably the result of pulmonary
complications of acute infectious disease as well as of chronic
disease of the lungs. Although an epidemic of influenza came
after the fog of 1891, the excess mortality was not attributable
to this infection; nor did it account for the high mortality in
the bad fog of 1952. The simple explanation is probably the
correct one: namely, that the cold weather and the polluted fog
affected the lungs and increased the risks of infection, bringing
on in many cases the pneumonia that so often ends the life of
a person suffering from chronic bronchitis and emphysema.
Pneumonia and other Respiratory Diseases in Adults
4. 24 Investigations have demonstrated a significant correla­
Air Pollution, Chronic Bronchitis, and Allied Diseases
41
tion between pneumonia death rates and the levels of particu­
late air pollution in fifty-three county boroughs in England and
Wales, and the higher death rate from pneumonia in towns is
consistent with the suggestion that air pollutants increase the
risk of serious lung disease.117 During very cold weather in
London, with temperatures below 32° F, the death rate from
pneumonia doubled when the duration of fog increased from
10 hours to more than 20 hours in the week preceding death.8
This pattern was not repeated in East Anglia, where the tem­
perature was similar but air pollution levels were much lower.
In respect of sickness absence, the Ministry of Pensions and
Social Security found in the population at work in England
and Wales no clear rural/urban or regional differences for
pneumonia that could be related to differences in exposure to
pollution of the air.73 This was in sharp contrast with the
correlation between such pollution and absence from work
because of bronchitis.
Conclusions
4. 25 The immediate effects of a rise in pollution above
normal winter levels have been seen in the aggravation of
existing bronchitis, increased sickness absence, more demand
for hospital beds, and greater mortality among patients already
suffering from chronic disorders of the lung. Results from the
many studies on these acute effects reviewed here point to
the direct influence of pollution in addition to any attributable
to low temperatures, but the actual pollutants responsible have
not been identified. Concentrations of smoke and sulphur
dioxide have been used as indices of harmful pollution, but
the relative importance of each has not been established, and
other pollutants, such as sulphuric acid and oxides of nitrogen,
may play some part. The concentrations of most pollutants rise
and fall together in response to day-to-day changes in the
weather, and there is therefore little chance of separating the
influence of any one of them in short-term studies. Thus,
although it has been reported that effects on bronchitis patients
become detectable when the air contains 600 fig/m 3 (about
o.2 ppm) of sulphur dioxide together with 300 /zg/m3 of
smoke, and other associated pollutants, these findings give little
42
Air Pollution and Health
indication of the possible action of one pollutant without the
others.58 The changes in the composition of urban pollution
resulting from the operation of the Clean Air Act may, how­
ever, provide some opportunity of determining the relative
importance of smoke and sulphur dioxide. (See para 9. 5)
4. 26 Although there is no doubt about the immediate harm­
ful effects of high pollution as encountered from time to time
in the larger towns of Great Britain, none of the evidence
presented in this chapter would justify recommendations on
‘air quality standards’ for any one pollutant in isolation from
the others.
4. 27 The influence of long-sustained pollution of the
atmosphere, as indicated by differences in the frequency of
respiratory symptoms or in mortality from bronchitis as
between urban and rural areas, cannot be easily distinguished
from the effects of other environmental factors and smoking
habits. Measurements of air pollution cannot assess anything
more than current exposures, and the development of chronic
respiratory disease may well be influenced by exposure to
pollution early in, or throughout, life. As with acute effects,
the opportunity to investigate the relative importance of smoke,
sulphur dioxide, and other pollutants rests on following up the
effect of changes in the character of pollution resulting from
the operation of the Clean Air Act.
4. 28 Epidemiological studies point to a causal relation
between air pollution and chronic bronchitis, and deaths
from it.
4. 29 Long-term trends in mortality from bronchitis are also
affected by factors such as social improvements and advances
in therapeutic medicine and, in recent decades, by cigarette
smoking.
4. 30 There is some evidence of a combined effect of air
pollution and cigarette smoking on chronic bronchitis. By
irritating the bronchial tubes cigarette smoke brings on cough
and expectoration. High levels of air pollution in British cities
maintain and aggravate the bronchitis thus initiated, with the
risk of further disease of the lung and premature death. In
the absence of cigarette smoking these effects of air pollution
are much less.
5
Respiratory Disorders in Young People
5. I
In the fog disaster of December 1952, mentioned at the
beginning of this report, the death rate of children rose
abruptly, especially in the first year of life.68 Special attention
should be paid to the effect of contaminated air on young
people because a disease that may disable later in life may
have its origins in childhood.
5. 2 Table 4 shows that the death rates from respiratory
disease in children are higher in England and Wales than
TABLE 4.
DEATH RATES (PER 100,000) FR O M INFLUENZA, BRON CH ITIS
AND PN EUM ON IA A T AGES 0-14 YEARS, 1957-61
M a les
Fem ales
40
31
31
28
Northern Ireland
Scotland
England and Wales
France
Norway
Denmark
Netherlands
37
35
33
19
20
18
14
16
15
12
TABLE 5.
BRON CH ITIS D EATH RATES (PER 100,000),
ENGLAND AND WALES (MALES AND FEMALES), 1960-63
Conurbations and Urban 100,000 +
Urban 50,000 to less than 100,000
Rural
0-4
16
13
11
5 -1 4
o -4
0 .5
o.8
1 5 -4 4
2.2
1.9
1.4
4 5 -6 4
75
61
43
elsewhere in North West Europe, and double the rates in
Scandinavian countries. Excess of deaths from bronchitis in
pre-school years in British towns is shown in Table 5; and the
same trend is observed in those over the age of fifteen years.
In the sparser population of the countryside the pre-school
44
Air Pollution and Health
child in rural areas is less exposed to infection and so remains
relatively free from bronchitis. In the school years the picture
changes. The town child has by then been through his ordeal
by infection, probably made worse by air pollution. But the
country child going to school comes into a relatively crowded
community for the first time and is exposed to the respiratory
infections of his schoolmates; and it is he who is now at a
disadvantage, compared with the child in the town, in respect
of bronchitis.93
5. 3 One complication of the infections of the upper respira­
tory tract is chronic infection of the middle ear. Chronic otitis
media was found at examination for National Service to be
higher in youths from towns than in those from the country.61
This trend seems to persist into adult life. When serving away
from home soldiers from towns had more frequent attacks of
respiratory disorders than those from rural areas.100 An urban
cause in common for ear and chest diseases was indicated by
high discharge rates from hospital for both in industrial areas
and low rates in rural areas.03
5. 4 Other factors must be taken into account, such as over­
crowding in the home and in the community, which facilitates
the transfer of infection from one person to another.9 63
Overcrowding is a feature of social class. Semi-skilled and
unskilled workers and their families congregate in the large
industrial centres, and this may to some extent explain the
high rate of respiratory infections in children there.
5. 5 A comparative study of 600 children in Sheffield and
of 400 in a rural district of Wales, at ages of 10 to 12 years,
disclosed that perforated eardrums and discharging ears were
commoner in the Sheffield than in the Welsh children of the
same social class.128,92 The same relation was found in respect
of bronchitis and pneumonia, and in the results of tests of lung
function. Another study in Sheffield itself made it apparent
that persistent cough and scarred or perforated eardrums were
commoner in those districts where air pollution was high than
in those where it was not.65 In this last study it seemed that
social circumstances such as overcrowding in the home had
little effect compared with air pollution.
5. 6 As part of the National Survey of Health and Develop­
Respiratory Disorders in Young People
45
ment health visitors and school doctors have periodically
interviewed and examined 3,866 children out of a national
sample of those born in 1946. They were classified into four
groups according to length of time spent in areas of pollution
varying from very low to very high.30 Little difference in the
frequency of infections of the upper air passages was found
between these groups, though there was some indication that
tonsillitis and discharging ears were less common in rural
areas with low pollution. But repeated infections of the bronchi
and the lungs in infancy that caused admission to hospital or
absence from the infant school were commoner in the more
heavily polluted districts (Figure 10). Similar differences were
found up to the age of 15 years.
5 .7 Since then another survey has been made of 11,000
primary schoolchildren between the ages of 6 and 10 years in
A IR
FIGURE 1 0
P O L L U T I O N
G R O U P
BRONCHITIS IN CHILDREN AT LOCAL LEVELS
OF AIR POLLUTON
The diagram shows that the percentage of children having re­
peated attacks of bronchitis increases with the amounts of air
pollution. (Data from a survey by Douglas and Waller.30)
46
Air Pollution and Health
urban and rural areas in England and W ales: in two cities
with high levels of air pollution (Newcastle and Bolton); in
two with moderate to low levels (Bristol and Reading); and in
rural areas near each centre.17 Questionnaires were issued to
parents and a standardised clinical examination and tests of
lung function were carried out on the children. Figure 11
shows that persistent cough in winter was at its lowest rate
among children of professional and managerial classes and
highest among children of semi-skilled and unskilled labourers.
Among the children of less-skilled workers (Social Classes IV
and V) there is a definite gradient from the lowest rate in the
rural areas to the maximum rates in the most heavily polluted
areas. But in Merthyr Tydfil and rural Glamorgan, where
smoke pollution is relatively low, bronchitis in children is more
frequent than in urban or rural England.
FIGURE 1 1
BRONCHITIS AMONG CHILDREN OF DIFFERENT SOCIAL
CLASSES IN RURAL AND URBAN ENGLAND
The Standardised Morbidity Ratio (%) compares the frequency
of chronic cough in children aged from 6 to 10 years old, living in
rural areas and less and more heavily polluted cities in England,
relative to a rate for all children in the survey of 100 per cent.
(Data from a survey by Colley and Reid.17)
Respiratory Disorders in Young People
47
5.
8 In this survey, children with chronic cough were more
likely also to have blocked noses, discharging ears, or damaged
ear drums. These and other diseases of the upper respiratory
tract were commoner in children from working-class homes
than in those from the homes of professional and managerial
people (social classes I and II) or of skilled workers (social class
III). In each social class the rates for ear disease among children
living in heavily polluted Bolton and Newcastle were three
times as high among rural children. Rates in Bristol and
Reading were, however, lower than those for rural children.
These findings and the conflicting evidence cited in paragraphs
5. 5 and 5. 6 show that there is as yet no conclusive proof that
air pollution in particular, rather than urban conditions in
general, predisposes to infections of the ear, nose, and throat in
children.
Conclusions
5. 9 Death rates from the respiratory diseases (influenza,
bronchitis, and pneumonia) in British children up to the age
of 14 are about double those in Scandinavian countries and the
Netherlands.
5. 10 Surveys in Britain have shown that bronchitis in chil­
dren is especially frequent in areas where there is much air
pollution. But it is also common in South Wales, where pollu­
tion is relatively low. There is some evidence that air pollution
particularly affects children from working-class homes.
5. 11 Children with bronchitis are more liable to disease of
the ear and nose than children free from bronchitis. Dis­
charging ears or damaged ear drums are commoner among
urban than in rural children. Evidence that air pollution affects
the upper as well as the lower respiratory tract is suggestive
but not, as yet, conclusive.
6
A ir Pollution and Lung Cancer
6. i The evidence that cigarette smoking is the most impor­
tant factor in causing lung cancer does not preclude the
examination of other possible influences. Observations suggest
that there might be some additional factor in the British urban
environment. The death rate from lung cancer is highest in
the major conurbations, and decreases with the size of town to
the lowest rates in rural districts. This implies that air pollution
might account for the higher risk of death from lung cancer in
urban areas. But the situation is far more complex than such
a supposition would suggest.
Some Geographical Comparisons
6. 2 Death rates from lung cancer tend to be high in countries
where the air is much polluted by coal smoke. In one study
there was a positive correlation between mortality from lung
cancer and the burning of solid fuel;118 but the disease is
common in some countries (e.g. Finland) where little coal is
burnt. No correlation was found between cancer of the lung
and the use of liquid fuel. International comparisons are, how­
ever, likely to be obscured by differences in diagnostic standards.
6. 3 Early vital statistical studies in England suggested that
local death rates from cancer of the lung were closely related
to an index of pollution given by hours of obscuration of the
sun.114 Further work revealed a close correlation between mor­
tality from the disease and measurements of smoke in a number
of localities in England and Wales.115 Later, more comprehen­
sive studies demonstrated that the scope of this earlier work had
been too narrow, and that the correlation between the prevail­
ing levels of air pollution and mortality from cancer of the lung
had been exaggerated because it was based on the extreme
Air Pollution and Lung Cancer
49
differences between small rural areas in North Wales with low
mortality from lung cancer and large towns in the North West
of England in which the mortality was high and the air heavily
polluted.10,131 Among towns of similar size but different levels
of pollution little correlation was found between these levels
and death rates from cancer of the lung. But within the London
area other investigations showed mortality from lung cancer to
be highest where air pollution was highest as measured by
concentrations of smoke and of sulphur dioxide.41,45
6. 4 In view of the slow evolution of cancer one important
weakness of these studies is that the measurements were related
to current and not past exposures to pollution of the air, and
therefore might be inappropriate. Because of the lack of exact
measurements of pollutants in the air twenty years ago the
frequency of dense fogs at that time has been taken as an
index of pollution, and a rather low correlation has been found
between the presumptive pollution thus estimated and current
death rates from cancer of the lung.34 Recent work, however,
has demonstrated correlation between local levels of consump­
tion of coal ten years previously and death rates from lung
cancer in the larger county boroughs of England and Wales.39
6. 5 The differences between death rates from lung cancer in
country and town— the rural/urban gradient— might be partly
explained by the availability of better diagnostic facilities in
the cities. But the gradient in chronic respiratory diseases with
which lung cancer could be confused suggests that different
diagnostic facilities are not the explanation. Diagnostic methods
and postmortem rates for these two conditions now differ little
as between town and country in Britain.56
Occupational Differences
6.6 For the years around 1961 the Registrar-General re­
ported only a small difference between the lowest death rate
from the disease among the professional and managerial classes
and the higher rates in the skilled, semi-skilled, and unskilled
workers.90 This contrasts with the much greater difference in
the death rate from bronchitis in these social classes (4. 15).
6. 7 There are undoubted increased risks of lung cancer in
men in certain industries that might be thought to be the
50
Air Pollution and Health
cause of raised urban death rates from the disease. Workers
in asbestos, in nickel and chromate refining, in iron foundries
and iron mines, and in tar distillation are all exposed to an
increased risk of the disease, but they form a very small part
of the male urban population and work only in certain areas.
The general excess of mortality from lung cancer in urban
districts cannot be explained by such occupational groups. By
contrast, the low mortality from the disease among coal-miners
accounts for the relatively low rates in some parts of Britain.4’ 52
6. 8 There is no consistent excess of death from lung cancer
in men likely to be particularly exposed to polluted air in
streets. A t the 1951 census policemen had a death rate from
the disease of 7 per cent above the national average, but this
excess is not statistically significant.88 In his last two reports on
occupational mortality the Registrar-General recorded a signi­
ficantly increased mortality from lung cancer of about 20 per
cent in motor mechanics and drivers of motor vehicles.88’ 90
No such excess occurred in bus conductors or in lorry drivers’
mates. Nor was any excess above the national level observed
in a special investigation of mechanics working in garages,
with their inevitable exposure to fumes from diesel engines and
other vehicles.85 Retort-house workers in gas works exposed to
very high levels of known carcinogens (sometimes up to 100
times the peak concentrations of benzo(a)pyrene in towns) have
a relatively small excess of lung cancer in comparison with the
general population : 308 compared with 181 per 100,000 per
annum.2659
Smoking and the Urban Factor
6. 9 By far the most important matter affecting all these
aspects of mortality from lung cancer is cigarette smoking.
Unfortunately we have no detailed information on the smoking
habits among town and country men and women many years
ago, when smoking might have begun to affect people now
dying of lung cancer. More is known about current habits in
different countries and different social classes and areas in this
country.122’123 Much of the international variation in mortality
from lung cancer might be explained by differences in cigarette
smoking; for example, by differences in the length of the stub
Air Pollution and Lung Cancer
51
left after smoking, in the frequency of puffing, as well as in the
quantity and in the type of tobacco used.44 29,141 But. in one of
the studies already discussed some degree of association between
burning solid fuel and lung cancer death rates remained after
differences in smoking habit were taken into account.118 Adjust­
ing the death rates from lung cancer to allow for differences in
current smoking habits between town and country dwellers
makes the urban-rural gradient less prominent but does not
FIGURE 1 2
TRENDS IN FUEL USED, CIGARETTE SMOKING,
AND LUNG CANCER MORTALITY IN MEN
This figure is similar to Figure 7. It shows that malignant disease
of the lung in men follows the upward trend in cigarette consump­
tion much more closely than any of the changes during this
century in the use of either coal or oil fuels. The rise in diesel
fuel consumption followed and did not precede the rise in the
death rate from lung cancer.131
52
Air Pollution and Health
abolish it.10 The contrast between the below-average death
rates among agricultural workers and the higher rates among
mechanics and drivers may be due to the fact that farm
workers smoke 54 cigarettes a week, compared with the
national average of 70, while transport workers smoke 86.123
Possible Causes of Time Trends in Lung Cancer
6. 10 Historical trends in lung cancer mortality in this
country may help in the assessment of any effect of urban
air pollution. Figure 12 illustrates the contrast in the last forty
years between the dramatic rise in death rates from lung cancer
and the decline in coal consumption: this excludes the coal
burnt for generation of power, which does not. as a rule produce
smoke.131 It is obvious, too, that the rise in the use of diesel
fuel (derv) followed and did not precede the increase in lung
cancer. The rise in petrol consumption, it is true, preceded the
rise in mortality from cancer of the lung in men; but the facts
that the mortality rate from this disease began to increase
much later in women, and that men occupationally exposed to
fumes from motor exhausts are not unduly affected, suggest
that the use of petrol plays no part in causing the disease.
Field Surveys of Lung Cancer
6. 11 T o reduce the uncertainty about the relative roles of
cigarette smoking and of urban residence retrospective inquiries
have been made into cigarette smoking and place of residence
of lung-cancer patients as compared with others free from the
disease. In early studies in London hospitals there was little
difference between residence in town or country in the two
groups.27 A survey of lung cancer and other patients living in
either the relatively clean air of rural North Wales or in the
urban areas, including Liverpool in North West England,
brought out the dominant effect of cigarette smoke.120 But,
except among the heaviest smokers, the survey demonstrated
that within each smoking group the death rates rose steadily
from the lowest levels in North Wales and South East Cheshire
to a maximum in the Merseyside conurbation.116 More recently,
in Northern Ireland an inquiry has shown that for people with
similar smoking habits the risk of dying from lung cancer rose
Air Pollution and Lung Cancer
53
from 47 per 100,000 per annum in the rural areas consistently
through urban districts to a maximum of 157 per 100,000
among those who had spent most or all of their lives in central
Belfast.25 135 From the results obtained it was calculated that if
the death rate from lung cancer for a symptomless non-smoker
living in a rural area is taken as the irreducible minimum, the
risk of death from the disease would be about doubled for a
man living in an urban area, but increased twenty-fold if he
smoked more than 20 cigarettes a day.11 Such retrospective
inquiries, of course, have serious limitations, if only because
they depend on the recollection of past events and habits by
patients or by their relatives. Although they appear to point
to an urban factor in the causation of lung cancer, they do not
amount to an indictment of air pollution.
6. 12 Some of the limitations of this method of investigation
are much diminished by prospective inquiries. These have the
advantage that characteristics, habits, and past exposure of
the subject are recorded before the onset of disease; and the
inquiry can be repeated at intervals in the group chosen for
such an investigation. The prospective inquiry into the smoking
habits and residence of doctors is therefore most valuable in
that it can assess the effects of these in a socially and occupa­
tionally homogeneous group.28 Among cigarette smokers the
death rate from cancer of the lung in doctors under the age of
65 rises from 40 per 100,000 in rural areas to 64 per 100,000
in the conurbations of Britain.
6. 13 These results, and those of retrospective inquiries and
comparisons of mortality statistics, demonstrate that there is
an association between urban residence and the risk of dying
from lung cancer, independent of the influence of current
smoking habits. However, there are substantial differences
between urban and rural death rates from lung cancer in
countries such as Norway, where there is little air pollution.53
Pollution is thus unlikely to be the sole cause of the urban
excess. Heavier smoking in towns in the past could be respon­
sible, but up to 1962 the gap between urban and rural death
rates was not closing.10 130
6. 14 As already noted, some of this difference in death rates
from lung cancer as between country and town may be due to
Air Pollution and Health
54
differences in life-time smoking habits. If the death rates from
lung cancer found in a nation-wide survey in the United
States43 are compared (after adjustment for age and current
cigarette consumption) with those in rural and urban areas in
England and Wales, it is found that mortality from lung cancer
increases (Table 6) with size of population in both countries.
TABLE 6 .
RUR AL/U RBAN GRAD IENTS IN LU N G CAN CER M O R T A L IT Y
IN TH E U N ITED STATES AND ENGLAND AND WALES
ADJUSTED FO R AGE AND SM O K IN G
S t a n d a r d is e d M
Population
of area
500,000+
50,000—
< 50,000
Rural
(U S
o r t a l it y
R
Males
national male rate
a t io s
( p e r c e n t) *
(U S
Females
nationalfemale rate
= 100%)
=100%)
US
England & Wales
US
England & Wales
123
111
107
231
132
195
194
177
144
236
216
106
78
149
134
79
* The death rates from lung cancer for non-smokers and those smoking varying
numbers of cigarettes each day found in a US national survey43 have been
used to calculate the number of deaths in corresponding smoking groups in
each type of area in England and Wales that would have occurred if the
inhabitants had the same risk of dying from lung cancer as the Americans as
a whole. The Standardised Mortality Ratio expresses the number of deaths
from lung cancer actually reported in these areas as a ratio to the number
that would have been expected on this basis.
But in places of similar size the death rate in England and
Wales is nearly twice what it is in the USA. This implies that
there is a ‘specific British factor’ as well as a general ‘urban
factor’, especially since this contrast between the national death
rates is just as great in rural as in urban areas. Pollution of the
air in British towns cannot therefore be the whole explanation
of the adverse experience of this country in respect of lung
cancer. As has already been mentioned, there are reports, for
example, of differences in stub length and frequency of puffing
as between American and British smokers, and differences in
the type of tobacco in their cigarettes.44’ 29 141
Experience of British Migrants
6. 15 The death rates from cancer of the lung among Britishborn people living in the less-polluted atmospheres of New
55
Air Pollution and Lung Cancer
Zealand, South Africa, the United States, and Canada, lie
between the lower rates of those bom in these countries and
the higher rate for Britain itself.32’ 24 42,95' 22 This suggests that
there is an enduring effect of British conditions or habits on
the risk of developing lung cancer; and this might be due to
exposure to high levels of air pollution in early life. In South
Africa the British immigrant, with apparently identical smok­
ing habits and living in the same areas as his South-Africanborn contemporary, still has a higher rate of mortality from
cancer of the lung.24 Table 7 shows death rates from lung
TABLE 7 .
AGE-STANDARDISED LU N G CAN CER D EATH RATES
PER 1 0 0 , 0 0 0 PER ANNUM
(M ales aged
-
35 74
)
Norwegian-born residents in Norway
Norwegian-born residents in the United States
US-born residents in the United States
British-born residents in the United States
British-born residents in Britain
31
48
72
94
151
cancer for British and Norwegian migrants to the United
States, for residents in the United States born there, and for
Britons and Norwegians staying in their own countries.95 The
rates are highest for Britons and lowest for Norwegians staying
in their own countries, with United States citizens coming in
between.
Some Experimental Evidence
6. 16 Products from the incomplete combustion or from the
distillation of coal produce tumours when painted on the skin
of laboratory animals. A landmark in this work was the
isolation from gasworks pitch of a substance, benzo(a)pyrene,
which has potent carcinogenic properties.20’51 This carcinogen
is present in small amounts in the smoke of town air.129,18
Many animal experiments have been done to determine
whether by itself or in combination with other materials it
could cause cancer of the lung. Suspensions of comparatively
large amounts of benzo(a)pyrene introduced directly into the
56
Air Pollution and Health
lungs have produced lung tumours in rats.7 Tumours have also
resulted from the insertion into the trachea of this carcinogen
along with particles of carbon.108 The carcinogenic effect
depended on the extent to which the benzo(a)pyrene was
adsorbed on the carbon. When hamsters were given benzo(a)pyrene in suspension with haematite (iron ore), this fine inert
dust seemed to facilitate the penetration of the carcinogen into
the lungs.104 It must be emphasised that such results as these
may have only limited relevance to the human inhalation of
carcinogens from the air. In a recent experiment the inhalation
of sulphur dioxide and benzo(a)pyrene together caused tumours
to appear in the lungs of rats; but neither did so when inhaled
separately.54 This experiment did not simulate the conditions
existing in urban air; nor has the experimental inhalation of
air pollutants at realistic concentrations caused tumours in
animals. However, the experiments have shown that a carcino­
gen might be more effective when inhaled with an irritant such
as cigarette smoke. The possible interaction of cigarette smoke
and carcinogens in urban smoke has been tested by painting
the skin of experimental animals with tobacco smoke conden­
sate and benzo(a)pyrene separately and together: together
they were much more effective than they were separately in
stimulating the production of tumours." The large amount
of work done on the experimental inhalation of cigarette smoke
will be referred to in the further report by the Royal College
of Physicians on smoking.101
Conclusions
6. 17 The evidence on the role of air pollution in the causa­
tion of lung cancer is still inconclusive. Some element in the
British urban environment seems to produce in those sufficiently
exposed to it an increased liability to develop lung cancer. How
much of this liability is due to air pollution alone remains in
doubt.
6. 18 The existence of similar rural-urban gradients in mor­
tality from cancer of the lung in countries where there is little
pollution from coal smoke suggests that pollution of the air by
the products of burning coal is not alone responsible for the
British urban excess in lung cancer. There is conflicting evi­
Air Pollution and Lung Cancer
57
dence on the influence of differences in past smoking habits in
towns and country.
6. 19 Britons who emigrated had an incidence of lung cancer
that was higher than that in the countries they went to but
lower than that of their compatriots who stayed at home.
6. 20 Urban air contains carcinogenic compounds, but the
relatively small excess risk to men occupationally exposed to
large concentrations of these compounds raises doubt about
the relevance to lung cancer of the much lower levels found
in the air of even the most polluted city.
6. 21 The study of the time trends in the death rates of lung
cancer in urban areas demonstrates the overwhelming effect of
cigarette smoking on the distribution of the disease. Indeed,
only the detailed surveys that have taken individual smoking
histories into account have succeeded in separating the rela­
tively very small influence of the ‘urban factor5 on the over­
riding effect of cigarette smoking in the development of cancer
of the lung.
7
Other Effects o f A ir Pollution
Pollutants from Motor Vehicles
7. 1 The increasing density of motor vehicle traffic in British
towns has aroused anxiety about the possible effects on health of
pollutants from motor exhausts. Carbon monoxide and lead are
two of special interest, and the black fumes from diesel engines
the most conspicuously offensive. (See also paras 2 . 5 - 2 . 10)
7. 2 The effects of relatively high amounts of carbon mon­
oxide in the blood are well documented, but recently there has
been a renewal of interest in the possible effects of concentra­
tions below those causing symptoms such as headache. In such
instances visual threshold and discrimination may be impaired,
as, it is suggested, may be the performance of various other
tests of psychomotor performance and perception.66 ,106,5
Surveys have shown that exposure to heavy traffic rarely
produces blood levels of carboxyhaemoglobin (carbon mon­
oxide bound to haemoglobin) greater than 4 per cent satura­
tion. Concentrations in excess of this are very commonly found
in cigarette smokers who are not exposed to motor exhausts.
Much further work is needed to investigate the effects of these
small concentrations on performance.
7. 3 Lead is readily absorbed into the body by inhalation.
Should such absorption exceed excretion, a rise in ‘body
burden' becomes manifest in increased lead levels in blood
and urine. Surveys of 2,300 individuals in Los Angeles, Phila­
delphia and Cincinnati revealed blood levels of over 60 u g/
100 ml in only 11 of them.125 In general, the levels found in
individuals were well below the level of 80 ^Lg/100 ml, at
which danger of lead intoxication arises. No such reports are
available for Britain.
Other Effects of Air Pollution
59
7. 4 Increased motor traffic is raising the amount of many
potentially toxic compounds in urban air. Many exhaust
products are important only in the bright sunlight and still
air of the Los Angeles type of ‘smog’. There, ozone, unburnt
hydrocarbons, 'cracked' hydrocarbons, and oxides of nitrogen
interact to produce substances that irritate the eyes and res­
piratory tract. Such physical effects are seldom, if ever, seen
in Britain. Nitrogen dioxide in high concentrations, as in
industrial accidents, can itself cause acute and often fatal
pulmonary oedema, with damage to the lung in those who
survive. Up to 5 ppm for 8-hour exposures are considered
safe in industrial practice. Such concentrations in street air
have not been recorded. The highest hourly concentration
reported in London is about 0.2 ppm.19
Cardiovascular Disease
7. 5 During the intense fog of December 1952 the death rates
from degenerative heart diseases increased above the normal,
but much less dramatically than the rate for bronchitis.68 These
diseases, and deaths from them, are commoner in the town
than in the country. An analysis of the death rates from
cardiovascular disease in larger county boroughs of England
and Wales showed little correlation with the index of air
pollution as measured by local coal consumption, once social
and other factors were taken into account.39 During the winter
months there is no relation between prevailing concentrations
of smoke and sulphur dioxide in London air and demands on
the Emergency Bed Service by patients suffering from cardio­
vascular disease.48
7. 6 It is often difficult to interpret 'underlying cause' of
death given on the certificate of patients dead from various
diseased conditions of the heart and the lung. For example,
death from heart failure in a patient with chronic bronchitis
and emphysema may be ascribed to chronic bronchitis as the
disease which ultimately led to death, or, alternatively, to
'myocardial degeneration', as the final cause. Some of the
differences in the rates of death from ‘myocardial degeneration'
in town and country may be apparent rather than real.
6o
Air Pollution and Health
Cancer of the Stomach
7. 7 Death rates from cancers of the stomach and intestine
have been found to be significantly related to levels of
smoke pollution in thirty English county boroughs.117 Such
disease might be caused by particulate matter from the air
reaching the alimentary tract from deposits on food or hands
or by the swallowing of smoke-polluted phlegm from the lungs.
Gastric cancer is, however, particularly frequent in semi-skilled
and unskilled labourers and their wives, so that other aspects
of life such as diet may be important in this connexion. In
another analysis of mortality in the larger county boroughs the
adjustment of death rates to allow for differences in the social
class structure in each area reduced the correlation between
air pollution and cancer of the stomach among men, and
abolished it among women.39 In South Africa, British migrants
have a lower death rate from gastric cancer than white South
Africans presumed to have been less exposed to air pollution.24
In the absence of further evidence a causal link between air
pollution and gastric cancer must remain no more than a
speculation.
Arthritis and Rheumatism
7. 8 The inquiry conducted by the Ministry on sickness
absence in the insured population showed a close relation
between absence due to arthritis and rheumatism and local
levels of air pollution as measured by the National Air Pollution
Survey.73 In places where bronchitis was a frequent cause of
absence from work ‘arthritis and rheumatism5 was also a
relatively frequent cause of sickness. Because the more polluted
towns where bronchitis and rheumatic disorders were especially
common were in the North rather than in the South of
England, it was impossible to distinguish the effects of air
pollution from those of different climatic and social circum­
stances in the two parts of the country. Without further field
studies the role, if any, of air pollution in rheumatic disorders
will remain in doubt.
8
Prevention o f A ir Pollution
8. 1
The burning of fuel for heat and power is the prime
cause of the pollution of air of British towns. Complete com­
bustion of all fuels would reduce the emission of smoke and
the amount of fuel needed for these two purposes, and the
result would be an improvement of health and a saving of
money. This is the first step towards control of contamination
of the air. Treatment of either the fuel or the combustion
gases can further reduce contamination by sulphur compounds,
and adequate dispersion will lower the amount of pollution at
ground level. Controls must be applied to the three main
sources of pollution : domestic fires, industry, and transport.
Air Pollution from Domestic Sources
8. 2 Most of the pollution likely to affect health comes from
the burning of coal fires in homes. Electric fires do not con­
taminate the air, and gas fires are almost equally blameless in
this respect. There is little contamination from oil used for
domestic heating; it has a low sulphur content. It is not
possible to burn coal smokelessly on open grates. After each
refuelling volatile matter is distilled off and dispersed as tarry
droplets or bums with a smoky flame. An open coal fire is
a highly inefficient way of heating a room. Nevertheless we
must face the fact that some solid fuels will continue to be
used for many years. Smokeless solid fuels are to be preferred,
such as anthracite, which contains little volatile matter, or
processed fuels. Some of these retain enough volatile matter to
bum freely even in open grates. Others, such as hard cokes,
are practically free of volatile matter and can be burnt only in
deeper fuel beds in stoves or specially designed grates. Closed
62
Air Pollution and Health
stoves are more efficient than open grates, because of increased
efficiency of combustion.
8. 3 Coke and most other solid smokeless fuels contain
approximately the same amount of sulphur as raw coal. Oil
for domestic heating contains little sulphur, but the heavier
grades for large central-heating installations contain more
sulphur than coal does. Sulphur is virtually absent from
domestic gas, and a relatively cheap supply of natural gas
should encourage householders to change their ways of keeping
a home warm. This would greatly reduce pollution of the air
from domestic sources, as, also, would heating by electricity
and oil.
8. 4 Fuels for heating office buildings, commercial premises,
and blocks of flats often contain a high proportion of sulphur,
and although the buildings may be high their chimneys do not
always ensure effective dispersion. In some atmospheric con­
ditions downdraughts of air heavily laden with sulphur dioxide
may enter neighbouring streets and buildings. Efficient chim­
neys are desirable. Fuel of low sulphur content should be used,
especially in conditions that favour temperature inversion.
8. 5 District heating systems in which a central boiler-house
supplies hot water for heating all the houses of a neighbour­
hood are employed in many European cities but in only a few
places in Britain. Local air pollution is greatly reduced, for
a single high chimney disperses contaminants much more
effectively than the low chimneys of many houses.
Pollution from Industrial Sources
8. 6 The large efficient furnaces used in industry and in
power stations can bum coal so completely that no smoke
should be given out, except on lighting up. The control of fuel
and air supply is most important, for uneven firing is respon­
sible for most of the smoke from industrial furnaces. Mechani­
cal stokers and well-designed fire-doors have cut down the
production of smoke even by small boilers.
8. 7 Coal and oil from which much of the sulphur has been
removed are too expensive for general use in industry. Alter­
natively, sulphurous products can be removed from gases in
the chimney stack. This, too, is costly. The gas-washing plants
Prevention of Air Pollution
63
at Battersea and Bankside power stations remove some 95 per
cent of the sulphur dioxide, but the decrease in the buoyancy
of the plume of smoke is often obvious, and it may reach the
ground for short periods. Dry scrubbing processes that do not
cool the plume are being investigated.
8. 8 Raising the height of the chimney stack to as much as
800 feet makes dispersion effective. If the gas velocity is high
the plumes escape even in foggy weather, when contamination
from other sources is trapped close to the ground. High winds
may, of course, bring the plumes down, but the impact is brief,
and high concentration of pollutants is unlikely. The Ministry
of Housing and Local Government has issued a valuable
memorandum on the design of high stacks for the guidance of
local authorities and architects.70
Pollution from Railways, Ships, and Motor Vehicles
8. 9 Steam locomotives, a serious source of pollution for­
merly, have been replaced by diesel and electric engines.
Pollution from suburban diesel trains can still be a nuisance
to those living in the neighbourhood. Improved designs of
fire-doors have reduced the smoke from coal in ships’ boilers,
but most vessels are now oil-fired or have diesel engines, and
pollution from this source in river and sea ports is no longer
a serious problem.
8. 10 Contamination of the air from motor vehicles has
already been mentioned, but it should be stressed once more
that a properly adjusted diesel engine should emit no more
than a faint puff of smoke on acceleration. Diesel fumes may
constitute no direct threat to health, but they are dangerous in
traffic because they obscure visibility; and most people find
their smell offensive. Carbon monoxide in vehicle exhausts
remains a potential hazard in congested traffic and in enclosed
spaces.
8. 11 The customary lack of continued bright sunshine and
the relative rarity of persistently stable air save Britain from
the photochemical reaction that causes the Los Angeles type
of ‘smog’. Therefore, devices designed to reduce the emission
of hydrocarbons from petrol engines are unlikely to be needed;
improvements in engine design are to be preferred.
64
Air Pollution and Health
Legislative Control of Air Pollution
8. 12 The Clean Air Act of 1956 seeks to limit the pollution
of air by smoke, and it puts this responsibility on local
authorities in respect of pollution from the domestic hearth.
It does not try to deal with the emission of sulphur dioxide. It
does not apply to motor vehicles; these are already covered
by the Motor Vehicles (Construction and Use) Regulations,
1 955 , which are enforceable by the police.79 The purpose of
the Clean Air Act is that ‘dark smoke shall not. be emitted from
a chimney of any building' although the Minister may make
regulations specifying the periods for which it may be
permitted (such as during lighting up from cold). The Act
empowers local authorities to forbid the installation of a
furnace, ‘unless it is so far as practicable capable of being
operated continuously without emitting smoke when burning
fuel of a type for which the furnace was designed'. There are,
too, regulations for ‘minimising the emission of grit and dust
from any chimney' that serves a furnace or oven. New furnaces
designed to burn pulverised fuel or solid fuel at a rate of 1 ton/
hour or more must be fitted with approved plant for arresting
grit and dust. The Clean Air Act of 1968 has widened the
scope of some of the original provisions in relation to industry.71
8. 13 An important feature of the Act of 1956 is that for the
first time it gives local authorities powers to deal with domestic
smoke. It states that, ‘any local authority may, by order con­
firmed by the Minister, declare the whole of the district of
the local authority or any part thereof to be a smoke control
area'. The emission of smoke from the chimney of any building
in such an area constitutes an offence. When an area is
declared a ‘smoke control area', many householders must adapt
their equipment to bum smokeless fuel and grants of up to
70 per cent of the cost can be made (30 per cent from the local
authority and 40 per cent by the Government). Grants are not
payable in respect of houses built since the Act was passed in
1956.
9
The Effects o f the Clean A ir Acts
9. i Since the passage of the Clean Air Act the emission of
smoke from industrial premises has been much reduced
throughout the country, but the control of domestic sources
has been less uniform. The use of alternative fuels to coal has
had a marked effect in some areas. Figure 13 shows that both
emission and concentration of smoke in London have fallen.
There has been little fall in the emission of sulphur dioxide,
but in recent years there has been some reduction in its con­
centration. There is some evidence that favourable weather
has contributed to this decline.
9. 2 The resulting improvement in London is obvious. The
air is often as clear as it is in rural areas. Clothes, household
furnishings, and decorations remain clean much longer, and
the cleansing of grime-covered buildings is now economically
justifiable. A wider range of plants and trees can be grown in
city parks and gardens; this, coupled with savings in labour
and expense on laundry and house cleaning, makes family life
both easier and more pleasant in areas where smoke pollution
has been efficiently reduced.
9. 3 In the past decade London has been remarkably free
from episodes of high pollution. This may have been partly
due to reduction of the pall of smoke, thus allowing the sun
to break up temperature inversion. Increased turbulence of
the air induced by large heated buildings may also have helped.
9. 4 By establishing smoke control areas a number of other
large cities apart from London have achieved substantial
reductions in smoke concentration. But unfortunately there
are still too many which have not followed this example, par­
ticularly in the small mining towns of the north, where there
are still far too many ‘black areas' or areas designated by the
66
Air Pollution and Health
Act of 1956 as places in which the establishment of smoke
control areas (domestic) was urgently needed. Big improve­
ments, however, have resulted from the carrying out of the
industrial provisions of the Act. For example, in Stoke-onTrent replacement of coal by oil, gas, and electricity, in the
pottery industry has transformed the scene (see frontispiece).
FIGURE 13
CHANGES IN THE EMISSION OF SMOKE AND SULPHUR
DIOXIDE AND THEIR CONCENTRATION IN LONDON AIR
In London, implementation of the Glean Air Act of 1956 has
markedly reduced the amount of smoke emitted and lowered its
concentration. The emission of sulphur dioxide in the air has
changed little, but better dispersion has also produced lower
concentration of this pollutant in London air.
In London 75 per cent of premises in ‘black areas’ had been
made smokeless by June 1969 (Table 8); the corresponding
figure in the Northern Region less than 25 per cent.111 Although
the proportion was lowest in the South-West (including South
The Effects of the Clean Air Acts
67
TABLE 8 .
SM O KE C O N T R O L PO SITIO N IN REGIONS OF ENGLAND
A T 30 JUNE 1969
(Figures supplied by Ministry of Housing and Local Government)
Region
Percentage of total black
area premises in the region
made smokeless
Northern
Yorkshire and Humberside
East Midlands
Greater London
North Western
West Midlands
South Western
25
47
32
75
43
32
Total (black areas)
51
18
Wales) the need for action here is not as great as was supposed,
since the hard coal used produces little smoke.
The Clean Air Act and Improvements in Health
9. 5 The Clean Air Act has been applied most effectively in
London, where changes in morbidity and mortality (e.g. from
bronchitis) can serve as a measure of the benefits to be obtained
from it. But there are other factors that must also be taken
into account; for example, changes in treatment, improvement
in the standard of living, epidemics of respiratory infections,
and changes in cigarette smoking. The most striking result was
seen in December 1962, when the atmospheric conditions that
caused the fog of December 1952 were closely simulated.107
The fog lasted just as long and the concentrations of sulphur
dioxide were almost identical. There was, however, much less
smoke in the atmosphere in 1962. The excess number of deaths
over the normal expectation was 700 in that episode, as com­
pared with about 4,000 in that of 1952. The numbers of older
people suffering from serious disease of the chest or the heart
may have differed, and many such invalids probably took
warning from the experience of 1952 and stayed indoors; but
at least part of this improvement may be justifiably attributed
to the control of smoke.
68
Air Pollution and Health
Effects on Mortality from Bronchitis
9. 6 Since the passing of the Clean Air Act in 1956 a close
watch has been kept on the relation between fogs and mortality
from bronchitis in London. The definite association observed
in the previous decade between excessive mortality and peaks
in air pollution can no longer be demonstrated. Apart from
the overall reduction in smoke concentration there has for
several years been a remarkable absence of any peaks of
high pollution. The age standardised death rate from bronchitis
in London, which a few years ago was above the national level
for men and for women, is now about the same. This reduc­
tion is particularly marked in men and women below the age
of 45. Similar if less dramatic changes are taking place in
mortality from lung cancer. These changes in death rates from
the two diseases may both be due to alterations in smoking
habits in the past.
Changes in Bronchitis Morbidity
9. 7 During bad fogs there used to be more calls for emer­
gency admission to London hospitals. The correlation between
air pollution and demand for beds has now virtually dis­
appeared. Patients with severe bronchitis who have during
several winters kept a daily record in diary form of their
subjective assessment of fitness have reported deterioration
when levels of air pollution rise. Patients reporting in the
winter of 1964-65 showed less response to changes in pollution
than did those reporting in the winter of 1959-60.134 A long­
term study of bronchitis among middle-aged men working in
West London between 1961 and 1965 demonstrated a decline
in the amount of sputum expectorated during the period when
there was a fall in concentrations of smoke in central London.37
9. 8 The Clean Air Act of 1956 was directed solely against
pollution by particulate matter, but the overall improvement
in the cleanliness of the air— with the absence of peaks of
pollution and decrease of sulphur dioxide— has been greater
than was expected. This abatement in pollution has happily
been associated with some decrease in morbidity.
io
Observations and Recommendations
1 0 . 1 Patients with chronic bronchitis and emphysema or
with chronic heart disease are at special risk in episodes of fog
with intense pollution of the air. The very young and the very
old are also especially vulnerable. Everything should be done
to minimise exposure to the polluted air. Windows should be
closed and the house kept warm. Those likely to be affected
should remain indoors. Undue exertion should be avoided.
Anyone having to go out should wear a face mask or scarf
over nose and mouth. A bottle of dilute ammonia opened in
a room may help to neutralise acid mists,
10. 2 The Meteorological Office provides warnings of fog.
It is thought that the much smaller mortality in the London
fog of 1962, which in other ways resembled the fog of 1952,
may well have been the result of advice over the radio and by
television that those most likely to suffer the effects of the fog
should stay indoors. The Committee would like to commend
this action of the broadcasting authorities and urge them to
repeat this valuable service when fogs or periods of high
pollution are expected in densely populated areas.
10. 3 It is obviously better for health to live in an atmosphere
free from pollutants than in one contaminated by the particles
and gases from the burning of fuel. Nevertheless, advice to
a bronchitic patient to move from a large town should be given
with caution. Individual reactions to polluted air vary greatly,
and concentrations of pollution are no longer closely linked
with size of town. There may be more smoke in suburban areas
or in small towns than in the centres of cities. While the con­
centrations of smoke and sulphur dioxide to be expected in
any given locality can be judged by studying the results of the
National Survey (published by the Warren Spring Laboratory,
70
Air Pollution and Health
Stevenage, Herts.), it is still difficult to assess exposures of
individuals. Sources of pollution close to the patient are impor­
tant, and in particular the possibility of combustion products
escaping indoors (e.g. from leaking flues) must be considered.
Pollution from low-level chimneys in adjacent buildings may
occasionally enter windows in tall blocks of flats.
10. 4 Effective implementation of the Clean Air Acts is the
most urgent task confronting the Government. The public
should be fully informed of the dangers to health of contami­
nated air and urged to bring pressure on local authorities to
put the provisions of the Clean Air Acts into operation. The
domestic coal fire is the major source of air pollution by smoke.
The use of smokeless fuels and of other forms of domestic
heating is essential if the ill effects of coal smoke are to be
abolished. All new housing developments should at the outset
be designated as smoke control areas. District heating schemes
should be considered.
10. 5 Medical Officers of Health should conduct surveys of
children through the school medical service to assess the nature
and extent of respiratory disorders among them. University
departments of epidemiology or social and preventive medicine
might well investigate groups especially susceptible to pollution
of the air, in particular the elderly and those suffering from
chronic diseases of the lungs or of the heart,
io. 6 The National Air Pollution Survey conducted by the
Ministry of Technology should be continued and extended.
Special surveys should where necessary be made to assess the
health effects of particular types of industrial and other forms
of pollution.
10. 7 There is need for centralised information of changes in
pollution in different parts of the country and of changes in
patterns of health and disease, and detailed analyses of mor­
tality from respiratory diseases in relation to air pollution
should continue. The introduction of a national system for
linking vital records from birth to death would also assist in
the assessment of the long-term effects of air pollution. The
Hospital Inpatient Inquiry might usefully supplement this by
providing data on diseases that might be causally connected
with air pollution, and the Department of Health and Social
Observations and Recommendations
71
Security should, from the same standpoint, regularly survey
disabling illness among the insured population.
1o. 8 The Medical Research Council should review the situ­
ation periodically in order to ensure the assessment of available
data. The Council might also consider the extension of labora­
tory studies into the risks likely to be associated with new
forms of pollution, as from asbestos.
1o. 9 Research into the reduction of sulphur in fuels and into
methods of removal of sulphur dioxide from stack gases should
be intensified.
10. 10 Further research is also needed into the combined
effects on health of air pollution and tobacco smoke.
10. 11 On grounds of amenity and of traffic safety, legislation
against unnecessary smoke from badly serviced diesel engines
should be strictly enforced. There is need for further research
into the effects on health of carbon monoxide, oxides of nitro­
gen, lead, and hydrocarbons, from car exhausts in congested
traffic.
10. 12 This report of the committee on Air Pollution and
Health has been principally restricted to conditions in the
United Kingdom. Standardisation of methods of measuring
air pollution, and standardisation of diagnostic terms and
conventions, would facilitate international comparisons and
enhance the value of work done in different countries. Such
an exchange of ideas and information can best, be carried out
through the World Health Organisation, which has set up a
special division on the public health aspects of contamination
of the environment in which man lives. Formal and informal
contacts with governmental and university research centres
abroad should be encouraged.
10. 13 This report, it is suggested, brings forward enough
evidence to justify the vigorous enforcement of existing legis­
lation on the control of various forms of pollution, and
especially the Clean Air Acts of 1956 and 1968, the benefits
of which are now being experienced.
References
1. A m d u r , M. O. (1957). ‘The in­
fluence of aerosols upon the
respiratory response of guinea
pigs to sulphur dioxide.’ Amer.
Indust. Hyg. Ass. Quart., 18, 149-
155 2. A m d u r , M. O. and U n d e r h i l l ,
D. W. (1968). ‘The effect of vari­
ous aerosols on the response of
guinea pigs to sulphur dioxide.’
Arch. Env. Hlth, 16, 460-468.
3. A n g e l , J. H . , F l e t c h e r , G. M.,
H i l l , I. D. and T i n k e r , G. M.
(1965). ‘Respiratory illness in
factory and office workers.’ Brit.
J. Dis. Chest, 59, 66-80.
4. A s h l e y , D. J. B. (1967). ‘The
distribution of lung cancer and
bronchitis in England and Wales.’
Brit. J. Cancer, 21, 243-259.
5. B e a r d , R. R. and W e r t h e i m ,
G. A. (1967). ‘Behavioural im­
pairment associated with small
doses of carbon monoxide.’
J. Publ. Hlth, 57, 2012-2022.
6. B e a v e r C o m m it t e e o n A i r
P o l l u t i o n . (1954). Report,
Gmd. 9322. London: H.M.S.O.
7. B l a g k l o g k , J. W. S. (1957).
‘The production of lung tumours
in rats by 3 : 4 benzpyrene,
methylcholanthrene and the
condensate from cigarette smoke.
Brit.J. Cancer, 11, 181-191.
8. B o y d , J. T. (i960). ‘Climate, air
pollution and mortality.* Brit. J.
prev. soc. Med., 14, 123-135.
9. B r im b l e c o m b e , F. S. W.,
C r u i c k s h a n k , R., M a s t e r s ,
P. L., R e id , D. D. and S t e w a r t ,
G. T. (1958). ‘Family studies of
respiratory infections.’ Brit. med.
J., i, 119-128.
10. B u c k , S. F. and B r o w n , D. A.
(1964). ‘Mortality from lung
cancer and bronchitis in relation
to smoke and sulphur dioxide
concentration, population den­
sity and social index.’ Tobacco
Research Council Research
Paper No. 7.
11. B u c k , S. F. and W i c k e n , A. J.
(1967). ‘Models for use in in­
vestigating the risk of mortality
from lung cancer and bronchitis.’
Appl. Stat., 16, 185-210.
12. B u r n , J. L. and P e m b e r t o n , J.
(1963). ‘Air pollution, bronchitis
and lung cancer in Salford.’
Int. J. Air Wat. Poll., 7, 5-16.
13. B u r t o n , G. G., C o r n , M., G e e ,
J. B . L., V a s a l l o , C . and
T h o m a s , A. P. (1969). ‘Response
of healthy men to inhaled low
concentrations of gas aerosol
mixtures.’ Arch. Env. Hlth, 18,
681-692.
14. C h a r l e s , Sir J. (1953). ‘Atmo­
spheric pollution in relation to
preventive medicine.’ The
Fourth Des Voeux Memorial
Lecture. Proceedings of the
Glasgow Conference, 1953.
London: National Smoke Abate­
ment Society.
Air Pollution and Health
74
15. C h r is t e n s e n , O. W. and W ood,
C. H. (1958). ‘Bronchitis mor­
tality rates in England and
Wales and Denmark.’ Brit, tried.
J., 1, 620-622.
16. C
G eneral Prac­
(1961). ‘Chronic
bronchitis in Great Britain. A
national survey carried out by
the respiratory diseases study
group of the College of General
Practitioners.’ Brit. med. J., 2,
o lleg e of
t it io n e r s .
973 - 9 7 9 *
17. C o l l e y , J. R. T. and R e i d ,
D. D. ‘Childhood bronchitis:
Urban-rural comparisons in
England and Wales.’ (In pre­
paration) .
18. C o m m in s , B. T. (1958). ‘Poly­
cyclic hydrocarbons in rural and
urban air.’ Int.J. Air Poll., 1, 14-
17 *
19. C o m m in s , B. T. a n d W a l l e r ,
R. E. (1967). ‘Observations from
a ten-year study of pollution at a
site in the City of London.’
Atmos. Env., 1, 49-68.
20. C o o k , J. W., H e w e t t , C . L. and
H i e g e r , I. (1933). ‘The isolation
of a cancer-producing hydro­
carbon from coal tar.’ J. Chem.
Soc., Pt. I, 395 - 4 05 .
21. C o r n w a l l , C. J. and R a f f l e ,
P. A. B. (1961). ‘Bronchitis—
sickness absence in London
Transport.’ Brit.J. industr. Med.,
18, 24-33.
22. C o y , P., G r z y b o w s k i , S. and
R o w e , J. F. (1968). ‘Lung cancer
mortality according to birth­
place.’ Canad. M. ^4 ^. J., 99,
476-483.
23. D a l y , C. (1959). ‘Air pollution
and causes of death.’ Brit. J.
prev. soc. Med., 13, 14-27.
24. D e a n , G. (1965). ‘The causes of
death among the South Africanborn and immigrants to South
Africa.’ Supplement 1 to the
South African med. J., 39.
25. D e a n , G. (1966). ‘Lung cancer
and bronchitis in Northern Ire­
land.’ Brit. med.J., 1, 1506-1514.
26. D o l l , R., F i s h e r , R. E. W.,
G a m m o n , E. J., G u n n , W.,
H u g h e s , G . O ., T y r e r , F . H .
and W il s o n , W. (1965). ‘Mor­
tality of gasworkers with special
reference to cancers of the lung
and bladder, chronic bronchitis
and pneumoconiosis.’ Brit. J.
industr. Med., 22, 1-12.
27. D o l l , R. and H i l l , A. B. (1950).
‘Smoking and carcinoma of the
lung.’ Brit. med. J., 2, 739-748.
28. D o l l , R. and H i l l , A. B. ( 1964).
‘Mortality in relation to smoking :
ten years’ observations of British
doctors.’ Brit. med.7 ., 1, 13991410.
29. D o l l , R., H i l l , A. B., G r a y ,
P. G. and P a r r , E. A. (1959).
‘Lung cancer mortality and the
length of cigarette ends.’ Brit,
med. J., 1, 3 2 2 -3 2 5 .
30. D o u g l a s , J. W. B. and W a l l e r ,
R. E. (1966). ‘Air Pollution and
respiratory infection in children.’
Brit. J . prev. soc. Med., 20, 1-8.
31. D u b o is , A. B. and D a u t r e b a n d e ,
L. (1958). ‘Acute effects of
breathing inert dust particles and
of carbachol aerosol on the mech­
anical characteristics of the lungs
in man. Changes in response
after inhaling sympathomimetic
aerosols.’ J. Clin. Invest., 37,
1746-1755.
32. E a s t c o t t , D. F . (1956). ‘The
epidemiology of lung cancer in
New Zealand.’ Lancet, 1, 37-39.
33. E v e l y n , J. (1661). ‘Fumifugium
or the inconvenience of the aer
and smoake of London dissi­
pated.’ Reprinted 1961. London:
National Society for Clean Air.
34. F a i r b a i r n , A. S. and R e i d , D. D.
( i 958) - ‘Air pollution and other
local factors in respiratory dis­
ease.’ Brit. J. prev. soc. Med., 12,
94 _I03 *
75
References
The Life and
Times ofSir E . Chadwick. London:
35. F i n e r , S. E. (1952).
o l l a n d , W. W. a n d R e i d ,
D. D. (1965). ‘The urban factor
in chronic bronchitis.’ Lancet, 1,
46. H
Methuen.
36. F i r k e T j J . (1936). ‘Fog along the
Meuse Valley.’ Trans. Faraday
Soc., 32, 1192-1197.
445-448.
W. W., R e id , D. D.,
R. and S t o n e , R. W.
(!965). ‘Respiratory disease in
England and the United States:
studies of comparative preva­
lence.’ Arch. Environ. Health, 10,
47. H o l l a n d ,
S e lt se r ,
37. F l e t c h e r , G. M. (1967). ‘Recent
clinical and epidemiological
studies of chronic bronchitis.’
Scand.J. Resp. Dis., 48, 285-293.
38. F y f e , P. (1892). The Sewage of the
Air. Glasgow and West of Scot­
land Engine-Keepers Associa­
tion. Glasgow: MacDougall.
39. G a r d n e r , M. J., C r a w f o r d ,
M. D. and M o r r is , J. N. (1969).
‘Patterns of mortality in middle
and early old age in the County
Boroughs of England and Wales.’
Brit. J. prev. soc. Med., 23, 133140.
40. G o l d s m it h , J. R. (1969). ‘Los
Angeles Smog.’ Science J., 5, 44-
4941. G o r e , H. T. a n d S h a d d i c k ,
C. W. (1958). ‘Atmospheric
pollution and mortality in the
County of London.’ Brit. J. prev.
soc. Med., 12, 104-113.
42. H a e n s z e l , W. (1961). ‘Cancer
mortality among the foreignborn in the United States.’
J. nat. Cancer Inst., 26, 37-132.
43. H a e n s z e l , W., L o v e l a n d , D. B.
and S i r k e n , M. G. (1962). ‘Lung
cancer mortality as related to
residence and smoking histories.
I. White Males.’ J. nat. Cancer
Inst., 28, 947-1001.
44. H a m m o n d , E. C. (1958). ‘Lung
cancer death rates in England
and Wales compared with those
in the U.S.A.’ Brit. med. J., 2,
649-654.
45. H e w i t t , D. (1956). ‘Mortality
in the London Boroughs, 195052, with special reference to res­
piratory disease.’ Brit. J. prev.
soc. Med., 10, 45-57.
338-345-
48.
H o l l a n d , W. W., S p i c e r , C. C.
and W il s o n , J. M. G. (1961).
‘Influence of the weather on res­
piratory and heart disease.’
Lancet, 2, 338-341.
49. H o l l a n d , W. W. a n d S t o n e ,
R. W. (1965). ‘Respiratory dis­
orders in United States East
coast telephone men.’ Amer. J.
Epidem., 82, 92-101.
50. H s ie h , Y-C., F r a y s e r , R. and
Ross, J. C. (1968). ‘The effect of
cold air inhalation on ventilation
in normal subjects and in patients
with chronic obstructive pul­
monary disease.’ Amer. Rev. resp.
Dis., 98, 613-622.
51. K e n n a w a y , E. L. (1955). ‘The
identification of a carcinogenic
compound in coal-tar.’ Brit. med.
J-> 2 » 749- 752e n n a w a y , E. L. and K e n n a ­
w a y , N. M. (1953). ‘Incidence
52. K
53.
54.
55.
56.
of lung cancer in coal-miners in
England and Wales.’ Brit. J.
Cancer, 7, 10-18.
K r e y b e r g , L. (1956). ‘Occur­
rence and aetiology oflung cancer
in Norway in the light of patho­
logical anatomy.’ Brit. J. prev.
soc. Med., 10, 145-158.
K u s c h n e r , M. (1968). The J.
Burns Amberson Lecture: ‘The
causes of lung cancer.’ Amer. Rev.
resp. Dis., 98, 573~ 5 9 0 L a m b e r t , P. M. and R e id , D. D.
In preparation.
L a m b e r t , P. M. and R e id , D. D.
In preparation.
Air Pollution and Health
76
57. L a w t h e r , P. J. (1958). ‘Climate,
air pollution and chronic bron­
chitis.’ Proc. roy. Sac. Med., 51,
262-264.
58. L a w t h e r , P. J. (1963). ‘Com­
pliance with the Clean Air Act:
Medical aspects. J . Inst. Fuel, 36,
341-344.
59. L a w t h e r , P. J., C o m m in s , B. T.
and W a l l e r , R. E. (1965). ‘A
study of the concentrations of
polycyclic aromatic hydro­
carbons in gasworks retort
houses.’ Brit. J. industr. Med., 22,
13-20.
60. L a w t h e r , P. J., E m e r s o n , T. R.
and O ’ G r a d y , F. W. (1969).
‘Haemophilus Influenza^:
Growth stimulation by atmo­
spheric pollutants.’ Brit, J. Dis.
Chest, 63, 45-47.
61. L e e , J. A. H. (1957). ‘Chronic
otitis media among a sample of
young men.’ J. Laryng., 71, 398404.
62. L e w i s - F a n in g , E. (1940). ‘A
comparative study of the seasonal
incidence of mortality in Eng­
land and Wales and in the United
States of America.’ M.R.C.
Special Report Series No. 239.
London: H.M.S.O.
63. L id w e l l , O. M. and W i l l i a m s ,
R. E. O. (1961). (1) ‘The Epi­
demiology of the common cold.’
(2) ‘Cross-infection and im­
munity.’ J. Hyg. Camb., 59, 309-
33464. L o g a n , W. P. D. (1951). ‘Mor­
tality in England and Wales
from 1848 to 1947. A survey of
the changing causes of death
during the past hundred years.’
Population Studies, 4, 132-178.
65. L u n n , J. E., K n o w e l d e n , J. and
H a n d y s i d e , A. J. (1967).
‘Patterns of respiratory illness in
Sheffield infant school children.’
Brit. J.prev. soc. Med., 21, 7-16.
66.
M
acFarlan d,
R . A., R
ough-
J. W., H a l p e r i n , M. H .
and N i v e n , J. I. (1944). ‘The
effects of carbon monoxide and
altitude on visual thresholds.’
J. Aviat. Med., 15, 381-394.
ton,
F.
67. M a r t i n , A. E. and B r a d l e y ,
W. H. (1960). ‘Mortality, fog
and atmospheric pollution.’
Mth. Bull. Min. Hlth Lab. Serv.,
* 9. 56- 7268. M
in i s t r y o f
H
ealth
(1954).
‘Mortality and morbidity during
the London fog of December
1952.’ Report on Public and
Medical Subjects No. 95. Lon­
don: H.M.S.O.
69. M i n i s t r y o f H o u s in g a n d L o c a l
G o v e r n m e n t (1956). Clean Air
Act, 1956. London: H.M.S.O.
70. M i n i s t r y o f H o u s in g a n d L o c a l
G o v e r n m e n t (1963). Clean Air
Act, 1956. Memorandum on
Chimney Heights. London:
H.M.S.O.
71. M i n i s t r y o f H o u s in g a n d L o c a l
G o v e r n m e n t (1968). Clean Air
Act, 1968. London: H.M.S.O.
72. M
in is t r y o f
L
abour
(1966).
‘Dust and fumes in factory
atmospheres.’ Safety, Health and
Welfare Booklet. New Series,
No. 8. London: H.M.S.O.
73. M i n i s t r y o f P e n s io n s a n d
N a t i o n a l I n s u r a n c e (1965).
Report on an enquiry into the
incidence of incapacity for work.
Part I I : Incidence of incapacity
for work in different areas and
occupations. London: H.M.S.O.
74. M
in is t r y o f
P o w e r (1962).
Statistical Digest. London:
H.M.S.O.
75. M
W
T ech n ology:
S p r in g L a b o r a t o r y
in is t r y o f
arren
(1966). National Survey of Smoke
and SO 2* Instruction Manual.
London: H.M.S.O.
References
76. M
W
in is t r y o f
arren
T
ech n ology:
S p r in g L a b o r a t o r y
The Investigation of Air
Pollution, 1958-1966. 32nd
(1967).
Report. London: H.M.S.O.
77. M in is t r y o f T e c h n o l o g y
(1969). Information supplied by
the Warren Spring Laboratory.
78. M
W
T ech n ology:
S p r in g L a b o r a t o r y
in i s t r y o f
arren
(1969). ‘The investigation of air
pollution.5 National Survey
Annual Summary, Table I, for
the year ended 1968.
79. M
in i s t r y o f
T
r an spo r t an d
(1955). ‘Motor
Vehicles (Construction and Use)
Regulations.5 Statutory Instru­
ment, 1955, No. 482.
C iv il A
v ia t io n
80. M o r k , T. (1962). ‘A compara­
tive study of respiratory disease
in England and Wales and
Norway.5 Acta med. Scand., 172,
Suppl. 384.
81. O l s e n , H. C. and G il s o n , J. C.
(i960). ‘Respiratory symptoms,
bronchitis and ventilatory capa­
city in men: an Anglo-Danish
comparison, with special refer­
ence to differences in smoking
habits.5Brit. med.J., 1, 450-456.
82. P e m b e r t o n , J. and G o l d b e r g ,
C. (1954). ‘Air pollution and
bronchitis.5Brit. med. J., 2, 567-
57 °83. P o o r e , G. V. (1893). ‘London
fogs and the lessons to be learnt
from them.5 London: The
Sanitary Institute.
84. P u f f e r , R. R. and W y n n e
G r i f f i t h , G . (1967). ‘Patterns of
urban mortality.5 Report of the
Inter-American Investigation of
Mortality. Pan American Health
Organization Scientific Publica­
tion No. 151.
77
85. R a f f l e , P. A. B. (1957). ‘The
Health of the Worker.5 Brit. J.
industr. Med., 14, 73-80.
86. R e g i s t r a r - G e n e r a l (1841).
Appendix to the Third Annual
Report of the Registrar-General
of Births, Deaths and Marriages
in England. London: H.M.S.O.
87. R e g i s t r a r - G e n e r a l (1891).
Weekly returns of births and
deaths for 1891. Vol. 52.
London: H.M.S.O.
88.
e g i s t r a r - G e n e r a l (1954).
Decennial Supplement. England
and Wales, 1951. Occupational
Mortality, Part 1. London:
H.M.S.O.
R
89. R e g i s t r a r - G e n e r a l (1968).
Statistical Review of England
and Wales for the year 1967.
Part 1, Tables, Medical. London:
H.M.S.O.
90. R e g i s t r a r - G e n e r a l . Decennial
Supplement. England and Wales,
1961. Occupational Mortality,
Part 1. London: H.M.S.O. (In
preparation).
91. R e i d , D. D. (1956). ‘General
epidemiology of chronic bron­
chitis.5 Proc. roy. Soc. Med., 49,
767-771.
92. R e i d , D. D. (1964). ‘Air pollu­
tion and respiratory illness in
children. Bronchitis, 2 .5 Second
International Symposium,
Groningen. 3 1 3 -3 1 8 . Royal
Vangorcum, Assen, Netherlands.
93. R e i d , D. D. (1969). ‘The begin­
nings of bronchitis.5 Proc. roy.
Soc. Med., 62, No. 4, 311-316.
94. R
e i d , D. D., A n d e r s o n , D. O.,
F e r r i s , B. G. and F l e t c h e r ,
C. M. (1964). ‘An AngloAmerican comparison of the
prevalence of bronchitis.5 Brit,
med. J., 2, 1487-1491.
78
Air Pollution and Health
95. R e i d , D. D., C o r n f i e l d , J.,
M a r k u s h , R . E., S i e g e l , D.,
P e d e r s e n , E. and H a e n s z e l , W.
(1966). Studies of disease among
migrants and native populations
in Great Britain, Norway and
the United States. III. Preva­
lence of cardiorespiratory symp­
toms among migrants and
native-born in the United States.
Nat. Cancer Inst. Monograph
No. 19, 321-346.
96. R e i d , D. D. a n d F a i r b a i r n ,
A. S. (1958). ‘The natural history
of chronic bronchitis.’ Lancet, 1,
1147-1152.
97. R e i d , D. D. and R o s e , G. A.
(1964). ‘Assessing the compara­
bility of mortality statistics.’
Brit. med. J., 2, 1437-1439.
98. Report of the Medical Officer of
Health for the City of Glasgow,
1925- 1 1 9 -1 2 4 99. R o e , F. J. C. (1962). ‘Role of
314 benzpyrene in carcino­
genesis by tobacco and smoke
condensate.’ Nature, 194, 10891090.
100. R o s e n b a u m , S. (1961). ‘Home
localities of national servicemen
with respiratory disease.’ Brit. J.
prev. soc. Med., 15, 61-67.
101. R o y a l C o l l e g e o f P h y s ic ia n s .
‘Smoking and Health, Second
Report.’ (In preparation).
102. R u s s e l l , W. T. (1924). ‘The
influence of fog on mortality
from respiratory diseases.’ Lancet,
2, 335- 3 3 9 *
103. R u s s e l l , W. T. (1926). ‘The
relative influence of fog and low
temperature on the mortality
from respiratory disease.’ Lancet,
2, 1128-1130.
104. S a f f i o t t i , U., C e f i s , F., K o l b ,
L. H. and S h u b i k , P. (1965).
‘Experimental studies of the con­
ditions of exposure to carcinogens
for lung cancer induction.’ J. Air
Poll. Con. Assn., 15, 23-25.
105. SC H REN K , H. H., H e i MANN, H.,
C l a y t o n , G . D. and G a f a f e r ,
W. M. (1949). ‘Air pollution in
Donora, Pa.’ US Pub. Hlth Bull.,
306.
106. S c h u l t e , J. H. (1963). ‘Effects of
mild carbon monoxide intoxica­
tion.’ Arch. Env. Health, 7, 52453 °.
107. S c o t t , J. A. (1963). ‘The Lon­
don fog of December 1962.’
Medical Officer, 109, 250-252.
108. S h a b a d , L. M. (1967). ‘Studies
in the USSR on the distribution,
circulation and fate of carcino­
genic hydrocarbons in the human
environment and the role of
their deposition in tissues in
carcinogenesis; a review.’ Cancer
Research, 27, 1132-1137.
Public Health
Reports of John Simon, Vol. 1.
109. S im o n , J. (1887).
Sanitary Institute of Great
Britain. London: J. & A.
Churchill.
n o. S im o n s so n , B. G., J a c o b s , F. M.
and N a d e l , J. A. (1967). ‘Role
of autonomic nervous system and
the cough reflex in the increased
responsiveness of airways in
patients with obstructive airway
disease.’ J. Clin. Invest., 46, 18121818.
h i
. S m o k e l e s s A i r (1969). J. Nat.
Soc. for Clean Air, No. 151,
Autumn.
112. S n e l l , R. E. and L u c h s in g e r ,
P. C. (1969). ‘Effects of S O a on
expiratory flow rates and total
respiratory resistance in normal
human subjects.’ Arch. Env.
Health, 18, 693-698.
113. S p e i z e r , F. E. and F r a n k , N. R.
(1966). ‘The uptake and release
of S O 2by the human nose.’ Arch.
Env. Health, 12, 725-728.
References
Regional and
Local Differences in Cancer Death
Rates. Studies on Medical and
114. S t o c k s , P. (1947).
Population Subjects, No. 1.
London: H.M.S.O.
79
Statistics of
Smoking in the United Kingdom.
123. T o d d , G. F. (1969).
Tobacco Research Council
Research Paper, No. 1. 5th
edition.
115. S t o c k s , P. (1952). ‘Epidemiology
of cancer of the lung in England
and Wales.’ Brit. J. Cancer, 6,
9 9 -i11.
116. S t o c k s , P. (1958). Cancer Inci­
124. T o m o n o , Y. (1961). ‘Effects of
S O 2 on human pulmonary func­
tions.’ Jap. J. Ind. Hlth, (Tokyo),
dence in North Wales and Liverpool
Region in Relation to Habits and
Environment. 35th Annual Report
S e r v i c e (1965). Survey of Lead
in the Atmosphere of Three Urban
Communities. Washington: US
of British Empire Cancer Cam­
paign, Suppl. to Part 2.
117. S t o c k s , P. (i960). ‘On the rela­
tions between atmospheric pollu­
tion in urban and rural localities
and mortality from cancer, bron­
chitis and pneumonia, with spe­
cial reference to 314 benzopyrene,
beryllium, molybdenum, vanadian and arsenic.’ Brit. J. Cancer,
397- 4 18.
118. S t o c k s , P. (1966). ‘Recent epi­
demiological studies of lung
cancer mortality, cigarette smok­
ing and air pollution, with dis­
cussion of a new hypothesis of
causation.’ Brit. J. Cancer, 20,
3
.
125. U
-
77 8 5
n it e d
S t a t e s P u b l ic H e a l t h
Government Printing Office.
126. U n i t e d S t a t e s D e p a r t m e n t o f
H e a l t h , E d u c a t io n a n d
W e l f a r e (1969) Air Quality
Criteriafor Sulfur Oxides. Wash­
ington, D.C.
127. U
n it e d S t a t e s D e p a r t m e n t
H e a l t h , E d u c a t io n a n d
W e l f a r e (1969). Air Quality
of
Criteria for Particulate Matter.
Washington, D.C.
128. W
ah dan ,
M. H. M. E-H. (1963).
Atmospheric Pollution and Other
Environmental Factors in Respiratory
Disease of Children. Thesis, Uni­
versity of London.
595-623119. S t o c k s , P. (1967). ‘Lung cancer
and bronchitis in relation to
cigarette smoking and fuel con­
sumption in twenty countries.’
Brit. J. prev. soc. Med., 21, 181185.
129. W a l l e r , R. E. (1952). ‘The
benzpyrene content of town air.’
Brit. J. Cancer, 6, 8-21.
120. S t o c k s , P. and C a m p b e l l , J. M.
(J955). ‘Lung cancer death rates
among non-smokers and pipe
and cigarette smokers.’ Brit. med.
J., 2, 923-929*
131. W a l l e r , R. E. (1967). ‘Bronchi
and lungs— air pollution.’ The
Prevention of Cancer, Chapter 27,
181-186. London: Butterworths.
121. S y d e n h a m , T. (1850). The Works
of Thomas Sydenham, Vol. 2.
London: The Sydenham Society.
Tobacco
Consumption in Various Countries.
122. T o d d , G. F. (1963).
Tobacco Research Council
Research Paper, No. 6. 2nd Edit­
ion Edited byBeese, D. H. (1968).
130. W a l l e r , R. E. (1959) ‘Air pollu­
tion as an aetiological factor in
Lung Cancer.’ Acta Unio. internat.
cancr. (Louvain) 15, 2, 4 3 7 -4 4 2 .
132. W a l l e r , R. E., B r o o k s , A. G. F.
and C a r t w r i g h t , J. (1963). ‘An
electron microscope study of
particles in town air.’ Int. J. Air
Wat. Poll., 7, 779-786.
133. W a l l e r , R. E., C o m m in s , B. T.
and L a w t h e r , P. J. (1965). ‘Air
pollution in a city street.’ Brit. J .
industr. Med., 22, 128-138.
8o
Air Pollution and Health
134. W a l l e r , R. E., L a w t h e r , P. J.
and M a r t i n , A. E. (1969).
‘Glean air and health in London*.
Proceedings of the Clean Air
Conference, Eastbourne, 1969,
Part 1, 71—79. London: National
Society for Clean Air.
i c k e n , A. J. (1966). Environ­
mental and Personal Factors in Lung
Cancer and Bronchitis Mortality in
Northern Ireland, 1960-62.
135. W
Tobacco Research Council
Research Paper, No. 9.
136. W i g k e n , A. J. and B u c k , S. F.
(1964). ‘Report on a study of en­
vironmental factors associated
with lung cancer and bronchitis
mortality in areas of North-East
England.’ Tobacco Research
Council Research Paper, No. 8.
137. W o o d s , H. M. (1927). ‘The
influence of external factors on
the mortality from pneumonia in
childhood and in later adult life.’
J. Hyg., Camb., 26, 36-43.
138. W o o d s , H. M. (1928). ‘On the
statistical epidemiology of respir­
atory diseases.’ Lancet, 1, 539543139. W o r l d H e a l t h O r g a n iz a t io n
(1964). ‘Epidemiological and
Vital Statistics Report.’ 17,
366-401.
140. W
r ig h t ,
G. P. a n d W r i g h t ,
H. P. (1945). ‘Aetiological
factors in broncho-pneumonia
amongst infants in London.’
J. Hyg., Camb., 44, 15-30.
141. W y n d e r , E. L. and F a i r c h i l d ,
E. P. (1966). ‘The role of a his­
tory of persistent cough in the
epidemiology of lung cancer.’
Amer. Rev. resp. Dis., 94, 709-720.
142. Y o u n g , M. (1924). ‘The influ­
ence of weather conditions on the
mortality from bronchitis and
pneumonia in children.’ J. Hyg.,
Camb., 23, 151-175.
A IR P O L L U T IO N AND H EALTH
The dense and polluted fog of early December 1952
killed 2484 people in the administrative County of
London.
This disaster led to the passing of the Clean Air
Act of 1956. The subsequent establishment of smoke
control areas in London has made our capital city
a cleaner and healthier place to live in.
But there are still many “ black areas” in the
small mining towns of the North, where the burning
of soft coal pollutes the air with black smoke and
sulphur dioxide.
Sulphur dioxide is also given off when smokeless
fuels and heavy oils are burnt. Are present con­
centrations of sulphur dioxide in the air harmful to
health ?
Air is also polluted by diesel fumes and by the
exhaust gases of petrol engines. Do diesel fumes
affect health ? What are the risks of concentrations
of carbon monoxide in streets jammed with cars?
Is the possible risk from nitrogen oxides in exhaust
gases such as to call for modifications of the internal
combustion engine ?
These are some of the problems brought to light
in this timely publication by the Royal College of
Physicians on A IR P O L L U T IO N and HEALTH.
£1 1os. od. net