Environmental Health Perspectives Volume
103, Supplement 6, September 1995
[Citation
in PubMed]
The Effects of Air Pollution on Children
David V. Bates
Department of Health Care and Epidemiology, University of British Columbia,
Vancouver, British Columbia, Canada
Abstract
Air pollutants have been documented to be associated with a wide variety
of adverse health impacts in children. These include increases in mortality
in very severe episodes; an increased risk of perineonatal mortality in
regions of higher pollution, and an increased general rate of mortality
in children; increased acute respiratory disease morbidity; aggravation
of asthma, as shown by increased hospital emergency visits or admissions
as well as in longitudinal panel studies; increased prevalence of respiratory
symptoms in children, and infectious episodes of longer duration; lowered
lung function in children when pollutants increase; lowered lung function
in more polluted regions; increased sickness rates as indicated by kindergarten
and school absences; the adverse effects of inhaled lead from automobile
exhaust. These impacts are especially severe when high levels of outdoor
pollution (usually from uncontrolled coal burning) are combined with high
levels of indoor pollution. In developed countries, where indoor pollution
levels are lower, increasing traffic density and elevated NO2
levels with secondary photochemical and fine particulate pollution appear
to be the main contemporary problem. By virtue of physical activity out
of doors when pollution levels may be high, children may experience higher
exposures than adults. Air pollution is likely to have a greater impact
on asthmatic children if they are without access to routine medical care.
-- Environ Health Perspect 103(Suppl 6):49-53 (1995)
Key words: air pollution, respiratory disease in children, asthma,
postneonatal mortality
This paper is based on a presentation at the Symposium
on Preventing Child Exposures to Environmental Hazards: Research and Policy
Issues held 18-19 March 1994 in Washington.
Address correspondence to Dr. David V. Bates, Department
of Health Care and Epidemiology, University of British Columbia, 5804 Fairview
Avenue, Vancouver, BC, Canada V6T 1Z3. Telephone (604) 822-4530. Fax (604)
822-4994.
Introduction
The description of the impact of air pollutants on children's health
is complicated by the fact that there are a number of types of air pollution
and a variety of indicators of adverse health effects. In the discussion
that follows, the classification is by observed outcome; and the probable
pollutants responsible are noted in each section.
Over the past 5 years, investigators have been increasingly interested
in studying the impact of air pollutants on children. There are several
reasons for this, of which the lack of interference from cigarette smoking
is one, and the increasing evidence that adult chronic respiratory disease
may have its roots in childhood is another. In addition, schoolchildren
can be studied as a particularly accessible group, with spirometric tests
being conducted in the classroom.
Increased Perineonatal Mortality
Premature mortality is generally regarded as the most serious effect
of air pollution, and the end point is specific.
In Acute Episodes
In the London episode in December 1952, there was an increase in observed
mortality in children, as the following data from the official report shows
(Table 1) (1).
Numerically the deaths in those over the age of 45 are, of course, dominant;
but in children below the age of 14, the death rate increased from 38 in
the week before the episode to 67 during it, which is a not inconsiderable
increase.
Increased Mortality Risk in More Polluted Regions
Observations in Britain in 1971 (2) and in the United States in
1977 (3) both indicated that respiratory mortality in children was
increased in more polluted regions. New data reported in 1992 by Bobak and
Leon (4) from the Czech Republic for the years 1986 to 1988 showed
an increasing relative risk for respiratory mortality in the postneonatal
years, in relation to the severity of the air pollution. Forty-six regions
of the country for which TSP, SO2, and NO2 data were
available were included. For quintiles of progressively more severe air
pollution (1 being the least and 5 the most severe), Table 2 shows the relative
risks found after adjustment for socioeconomic factors.
In London in 1952, the pollution was mostly derived from open coal burning;
and the same is true of the air pollution in North Bohemia, which constitutes
the fifth quintile in the table above.
Barker and Osmond (5) from Britain reported that there was a strong
geographic relationship between death rates from chronic bronchitis and
emphysema between 1959 and 1978, and between the infant mortality from bronchitis
and pneumonia in the period 1921 to 1925.
Risks from High Levels of Indoor Pollution
It is well known that respiratory disease is the second most common cause
of death in children in the third world (6). This has often been
attributed to measles; but it seems very probable that the very high levels
of indoor particulate pollution derived from biomass fuel use without adequate
ventilation (7) play a major part in this mortality.
Increased Acute Respiratory Illness
Hospital Admission and Emergency Visit Data
In Provo, Utah, Pope (8) found that hospital admissions of children
for acute respiratory disease were closely associated with levels of fine
particulate pollution (particles less than 10 microns in size or PM10).
In southern Ontario, hospital admissions for children in the summer are
associated with ambient ozone and sulfate levels (9). Data recently
published by Burnett et al. (10) reported on hospital admissions
for 168 hospitals in Ontario over a 6-year period. They noted that in the
summer respiratory admissions were closely associated with ozone levels,
and they observed that among infants 15% of summer admissions were pollutant
associated; whereas among the elderly only 4% were. Recent studies of hospital
admissions in Toronto have indicated that, in addition to ozone and sulfates,
the aerosol hydrogen ion level and the PM10 are associated with increased
admissions (11). In five cities in Germany, Schwartz et al. (12)
found an association between croup and levels of NO2.
Other Indices
In an important longitudinal study in the United Kingdom published in
1966, Douglas and Waller (13) followed 3866 infants adopted at birth
into other families, which randomized any genetic factor. The infants were
being brought up in widely different parts of the country, and the general
air pollution levels of the different regions were divided into four categories.
Over a 3-year period of observation, the occurrence of lower chest infections
was three times higher in the most polluted category than in the cleanest.
It is now realized that such data would have to be corrected for passive
smoking effects and for other sources of indoor pollution such as the use
of gas stoves; these possible influences on the study results are not known.
Lunn et al. (14,15) studied schoolchildren in Sheffield in 1967
and 1970 and concluded that air pollution levels were partly responsible
for respiratory morbidity. More recently, Braun-Fahrlander et al. (16)
in Switzerland reported on a random sample of 625 children aged 0 to 5 years
followed in rural and urban areas. They showed that higher NO2
exposures (confirmed by personal samplers) were associated with a prolongation
of respiratory episodes and that particulate pollution (TSP) was a significant
predictor of symptoms. The asthma prevalence was low in this population.
A similar study of schoolchildren recently reported, found a significant
association between respiratory symptoms and outdoor NO2 exposure
(17). In the Gardanne coal basin in France, Charpin et al. (18)
showed that there were more respiratory symptoms in children in the more
polluted regions. Environmental tobacco smoke exposure has been shown to
be associated with exacerbations of asthma in children (19). It is
not clear whether this effect is to be attributed to particulate exposure
or to increased levels of NO2.
Aggravation of Asthma
Increased Hospital Admissions
Studying hospital admissions in the summer in southern Ontario over a
6-year period from 1974 to 1980 (20), we found that asthma admissions
for children up to the age of 14 were invariably higher after days when
the ambient ozone level had exceeded 80 ppb, compared to all days. More
recent data from Toronto have fully confirmed this relationship (11).
Increased Hospital Emergency Visits
The pioneer study of hospital emergency visits of children in relation
to air pollution was that of Girsch et al. (21) in Philadelphia in
1967. Visits of 1346 patients were analyzed over 676 study days between
July 1963 and May 1965. The hospital was located in a polluted area of the
city. Although aerometric data were very incomplete by modern standards,
the authors concluded, "There was a threefold greater incidence of
bronchial asthma during days of noteworthy higher pollution." Pollen
counts were available in the ragweed season, but the authors noted, "Very
few asthma attacks occurred during the ragweed season."
White et al. (22) studied emergency visits to the Grady Children's
Hospital in Atlanta in the summer of 1990, and reported a 37% increase in
visits for asthma after 6 days when the ozone level exceeded 0.11 ppm. Cody
et al. (23) in New Jersey, in a study of seven hospitals over a 5-year
period, found a consistent increase in emergency visits in relation to ozone
levels during the summer. In Puerto Rico, environmental factors have been
shown to be related to exacerbations of asthma (24); and Puerto Rican
children in the United States have about double the prevalence of asthma
compared to Mexican-American children (25).
In a study of emergency visits in Vancouver in a population of 984,900,
containing 170,300 children below the age of 14 (26), we found that
in a calendar year, there were 2936 visits for all acute respiratory disease
in this age group, of which asthma comprised 1357. In the children, acute
respiratory visits were associated with SO2 levels in the winter;
but in the summer there was no such association, although it was present
for both asthma and acute respiratory visits in the 15- to 60-year-old age
group. No age group showed an association with ozone levels, which were
generally low. Data for fine particulate pollution were not available.
Schwartz et al. (27) showed that emergency visits for asthma in
Seattle were associated year-round with fine particulate pollution (PM10).
Levels of PM10 were always lower than the current U. S. standard of 150
µg/m3 for 1 hr. The association of increased asthma symptoms
with increased particulate air pollution has also been documented by Forsberg
et al. (28).
Increased Medication Use
Following a cohort of schoolchildren with asthma in Provo, Utah, Pope
et al. (29) showed that their medication use cycled with the levels
of PM10. They found the same thing in a panel of young adult asthmatics
and observed that the peak flow rate of normal children was affected by
the PM10 level.
Increase in Respiratory Symptoms
Survey Data
In the cross-sectional comparison of six cities in the United States,
children's symptoms of cough and phlegm were associated with increased levels
of pollutants (30). Dodge et al. (31) found evidence that
respiratory symptoms in children were related to SO2 pollution
levels; the same was true in Charpin's study (18). Dockery and Pope
(32) have recently provided a valuable review of the evidence linking
increased fine particulate pollution (PM10) with a range of outcomes in
adults and children.
There are so many possible confounding factors in cross-sectional comparisons
that this method may be relatively insensitive to differences. For this
reason, the study by Neas et al. (33) of a cohort of 1567 white children
aged 7 to 11 years in the U. S. six-city study, is particularly valuable.
With measurements of NO2 in each home, they were able to show
that there was a 40% increase of risk in lower respiratory symptoms for
a 15 ppb increase in NO2 in the home. In contrast, in a prospective
study of 1205 healthy infants in Albuquerque, New Mexico, Samet et al. (34)
showed that there was no association between NO2 levels in the
home and the occurrence of respiratory infections. There was no passive
tobacco smoke exposure.
Decreases in Lung Function
Summer Camp Data
There is no doubt that ambient ozone, and possibly aerosol acidity, in
northeast North America causes a decrease in lung function in normal children
at summer camps (35). Ozone, sulphate aerosols, and H+
levels are usually all raised in these locations.
Pollution Episode Data
Brunekreef et al. (36) followed a cohort of 1000 children 6 to
12 years of age in rural Holland. For 9 days in January 1987 there was a
pollution episode with increased levels of SO2 and particulates.
Significant decrements in pulmonary function were documented, and the depression
of function continued for some weeks after the episode. This study followed
an earlier one in the same country reported by Dassen et al. (37),
who had also shown an effect on lung function.
More recently, Koenig et al. (38) have shown that woodsmoke air
pollution in the Pacific Northwest has a significant effect on lung function
in children. These authors studied 326 elementary schoolchildren and 24
asthmatic children during and after the winters of 1988 to 1989 and 1989
to 1990. Increases in the fine particulate fraction (PM2.5) were shown to
be related to decreases in the function of the asthmatic children, but the
normal children were not affected. Kinney et al. (39) in the United
States documented changes in lung function in children in relation to episodes
during which the ambient ozone was increased. Halfon and Newacheck (40),
using Health Interview Survey data from the United States, have shown that
the impact of asthma is more severe (in terms of increased school absences,
increased hospital inpatient days, etc.) in children of lower economic status,
presumably because they lack access to routine medication and advice. They
also found that children in the lower socioeconomic category depended more
on hospital emergency departments for routine care and less on private physicians.
Montealegre et al. (24) showed that environmental factors, probably
particulate pollution, were responsible for aggravating asthma in Puerto
Rico. It is of interest that Puerto Rican children resident in the United
States show a high prevalence of asthma (25). The fact that exposure
to environmental tobacco smoke aggravates asthma has been established beyond
doubt (19). It is not clear whether this is due to particulates in
the air or to NO2.
There is a wide variety of aeroallergens that may precipitate severe
asthma in children (41).
Chronically Depressed Lung Function
The French study (42) of men, women, and children showed that
the FEV1 and FVC of children were significantly lower in regions with higher
levels of SO2. The same has recently been shown to be true of
nonsmoking women in Beijing (43) who are exposed to severe outdoor
and indoor pollution. In Wuhan in China (44), there were significant
differences between the FVC values of children between 8 and 12 years of
age as between more and less polluted regions, with girls showing larger
differences than boys. The differences in lung function were not only highly
significant, but of a magnitude to be considered clinically important.
Indirect Indicators
Kindergarten and School Absence Data
Ponka (45) in Helsinki found that absences from school and kindergarten
were related to SO2 levels in the city, but it was difficult
to be sure that effects of temperature changes had been completely eliminated.
Ransom and Pope (46) in Provo, Utah, showed convincingly that school
absences in grades 1 to 6 from 1985 to 1990 were significantly associated
with PM10 levels. The response was greater in those in grades 1 to 3 (6-9
years old) than in the older children. The results were robust to different
model specifications, and weather variables were unlikely to have been responsible
for the findings.
Inhaled Lead from Automobiles
There is controversy over how much of the blood lead in children is directly
derived from lead in automobile exhaust; indirect inhalation is undoubtedly
important (47).
However, the recent demonstration that a fall in the blood lead of the
population in the United States has precisely paralleled the reduction of
lead in gasoline (48) and has indicated beyond question that lead
in gasoline is an important source. There is justifiable current concern
that this problem may be of major importance in the third world (49).
Conclusions
This brief summary of our present understanding of the impact of air
pollution on children shows that, when all the data are taken together,
there is no doubt that relatively low levels of pollution are responsible
for increased morbidity and even mortality in children. This is particularly
true of the pollution that follows uncontrolled coal burning. However, in
the developed world, there is convincing evidence that current levels of
fine particulate pollution are responsible for aggravating asthma and may
well also be responsible for increased lower respiratory illness.
Photochemical air pollution at current levels, particularly when associated
with sulfate aerosols and increased H+ levels, is having an impact
on acute respiratory disease as well as on asthma in children. It seems
probable that when air pollution is severe, the performance of lung function
tests is depressed. It also seems likely that in children growing up in
such polluted environments a "normal" level of FVC and FEV1 may
not be attained--but it remains unclear how much of the cross-sectional
difference in these tests in adults between regions of greater or lesser
air pollution is a reflection of such an effect in childhood.
It is known that schoolchildren may have relatively high ambient pollution
exposures, partly because they are physically active out of doors, but also
because, at the time they may be leaving school in the afternoon, ozone
levels may be at their highest. Low socioeconomic status, with a resulting
lack of routine medical care, may put such children at higher risk if they
have asthma--and it has been shown that children from low-income families
are more often dependent on hospital emergency departments rather than private
physicians for their care and have much more annual morbidity, as judged
by school absences and days spent in the hospital than do "nonpoor"
children (40). In addition, if houses are not air-conditioned, the
concentration of outdoor pollutants in them will be higher. The exposure
of such children to indoor pollutants in regions with cold winters may also
be higher because of relative overcrowding and inexpensive (but dangerous)
heating systems such as kerosene stoves.
There is little doubt that indoor and outdoor air pollution is responsible
for major childhood mortality and morbidity in the third world. Recent research,
however, has shown that there are measurable adverse effects on children
in the developed world; there is a lack of understanding of the precise
mechanisms that underlie the epidemiological data. It is to be presumed
that in all cases events in childhood are not without repercussions in adult
life.
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