ArticlePDF AvailableLiterature Review

Air Pollution and Children's Health

Authors:

Abstract

Children's exposure to air pollution is a special concern because their immune system and lungs are not fully developed when exposure begins, raising the possibility of different responses than seen in adults. In addition, children spend more time outside, where the concentrations of pollution from traffic, powerplants, and other combustion sources are generally higher. Although air pollution has long been thought to exacerbate minor acute illnesses, recent studies have suggested that air pollution, particularly traffic-related pollution, is associated with infant mortality and the development of asthma and atopy. Other studies have associated particulate air pollution with acute bronchitis in children and demonstrated that rates of bronchitis and chronic cough declined in areas where particle concentrations have fallen. More mixed results have been reported for lung function. Overall, evidence for effects of air pollution on children have been growing, and effects are seen at concentrations that are common today. Although many of these associations seem likely to be causal, others require and warrant additional investigation.
DOI: 10.1542/peds.113.4.S1.1037
2004;113;1037-1043 Pediatrics
Joel Schwartz
Air Pollution and Children’s Health
This information is current as of April 2, 2007
http://www.pediatrics.org/cgi/content/full/113/4/S1/1037
located on the World Wide Web at:
The online version of this article, along with updated information and services, is
rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.
Grove Village, Illinois, 60007. Copyright © 2004 by the American Academy of Pediatrics. All
and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk
publication, it has been published continuously since 1948. PEDIATRICS is owned, published,
PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly
by on April 2, 2007 www.pediatrics.orgDownloaded from
Air Pollution and Children’s Health
Joel Schwartz, PhD
ABSTRACT. Children’s exposure to air pollution is a
special concern because their immune system and lungs
are not fully developed when exposure begins, raising
the possibility of different responses than seen in adults.
In addition, children spend more time outside, where the
concentrations of pollution from traffic, powerplants,
and other combustion sources are generally higher. Al-
though air pollution has long been thought to exacerbate
minor acute illnesses, recent studies have suggested that
air pollution, particularly traffic-related pollution, is as-
sociated with infant mortality and the development of
asthma and atopy. Other studies have associated partic-
ulate air pollution with acute bronchitis in children and
demonstrated that rates of bronchitis and chronic cough
declined in areas where particle concentrations have
fallen. More mixed results have been reported for lung
function. Overall, evidence for effects of air pollution on
children have been growing, and effects are seen at con-
centrations that are common today. Although many of
these associations seem likely to be causal, others require
and warrant additional investigation. Pediatrics 2004;113:
1037–1043; asthma, particles, ozone, lung reaction.
ABBREVIATIONS. PM
10
, particles with aerodynamic diameter
less than 10 mm; NO, nitric oxide; CI, confidence interval.
T
he health effects of air pollution exposure have
become an area of increasing focus in the past
30 years. A growing body of evidence has
demonstrated that there are serious health conse-
quences to community air pollution and that these
consequences are not spread equally among the pop-
ulation. As an example of this differential suscepti-
bility, recent studies have indicated that people with
type 2 diabetes are at higher risk for cardiovascular
effects of airborne particles.
1,2
Similarly, children
have been shown to be at particular risk for other
effects of air pollution, as detailed below.
This article cannot be a comprehensive review of
the literature, because recent reviews of airborne par-
ticles and ozone alone have hundreds of pages sum-
marizing the literature. Rather, I cover the major
health effects in children that have been linked to air
pollution, cite some key papers, and discuss the
strength of the evidence. I particularly highlight ar-
eas where it seems that differences between adults
and children, particularly in the development of the
respiratory and immune system, suggest different
impacts of exposure for children.
BACKGROUND
The lung is not well formed at birth, and develop-
ment of full functionality does not occur until ap-
proximately 6 years of age. During early childhood,
the bronchial tree is still developing. For example,
the number of alveoli in the human lung increases
from 24 million at birth to 257 million at age 4,
3
and
the lung epithelium is not fully developed. This re-
sults in greater permeability of the epithelial layer in
young children. Children also have a larger lung
surface area per kilogram of body weight than adults
and, under normal breathing, breathe 50% more air
per kilogram of body weight than adults. This pro-
cess of early growth and development, the outcome
of which is important for the future health of the
child, suggests that there is a critical exposure time
when air pollution may have lasting effects on respi-
ratory health.
At the same time the child’s lung is developing,
the child’s immune system, immature at birth, is also
beginning to develop. Much recent attention in
asthma research has been focused on this develop-
ment, in particular factors that influence the devel-
opment of TH-2 (humoral immunity dominant) ver-
sus TH-1 (cellular immunity dominant) phenotypes.
4
Another major factor that influences the relative
impact of air pollution on children versus adults is
exposure. Children spend more time outdoors than
adults, particularly in the summer and in the late
afternoon.
5
Some of that time is spent in activities
that increase ventilation rates. This can increase the
exposure to air pollutants compared with adults, as
indoor concentrations of air pollutants of outdoor
origin are usually lower.
PRE- AND PERINATAL EFFECTS OF AIR
POLLUTION
Although historically air pollution has been
thought of as a respiratory toxicant, recent evidence
has broadened our understanding of its full range of
effects. In adults, changes in cardiovascular risk fac-
tors such as C-reactive protein
6
and autonomic con-
trol of the heart
7
have led the way in broadening our
understanding of the range of toxicity. With chil-
dren, perhaps the most unexpected results have been
a range of recent papers reporting that prenatal ex-
posure of populations to prevailing levels of air pol-
lution is associated with early fetal loss,
8
preterm
From the Departments of Environmental Health and Epidemiology, Har-
vard School of Public Health, and Channing Laboratory, Brigham and
Women’s Hospital, Department of Medicine, Harvard Medical School, Bos-
ton, Massachusetts.
Received for publication Oct 7, 2003; accepted Oct 20, 2003.
Reprint requests to (J.S.) Environmental Epidemiology Program, Harvard
School of Public Health, 401 Park Dr, Boston, MA 02215. E-mail:
jschwrtz@hsph.harvard.edu
PEDIATRICS (ISSN 0031 4005). Copyright © 2004 by the American Acad-
emy of Pediatrics.
PEDIATRICS Vol. 113 No. 4 April 2004 1037
by on April 2, 2007 www.pediatrics.orgDownloaded from
delivery,
911
and lower birth weight.
1218
These as-
sociations may or may not be causal but clearly
warrant additional study. The later Bobak study
18
is
notable in that it was nested within a birth cohort
study, allowing good control for social and other
factors that may confound the association. Because
birth certificates in most areas have extensive infor-
mation on maternal medical conditions that may
affect the pregnancy, as well as maternal age, educa-
tion, and smoking, all of these studies are generally
well controlled. Although relatively recent, there is
now considerable evidence that maternal exposure
to air pollution during pregnancy is associated with
adverse birth outcomes. Moreover, particulate air
pollution from combustion sources shares many
characteristics with sidestream tobacco smoke,
which is rich in particles and polycyclic aromatic
hydrocarbons. A recent review by Windham et al
19
found that environmental tobacco smoke was asso-
ciated with low birth weight. This provides support
for the plausibility of the reported association.
The mechanisms involved are as yet unknown but
may include inflammatory processes and oxidative
stress, which have been linked to air pollution. For
example, Salvi et al
20
reported that human volun-
teers who were exposed to diesel particles for 1 hour
had elevated levels of peripheral white cells, as well
as increased vascular cellular adhesion molecule-1
and intercellular adhesion molecule-1 in the lung
epithelium. As noted before, C-reactive protein, an
acute-phase inflammatory marker, was associated
with air pollution exposure in adults. Ozone is a
highly reactive gas, associated with oxidative stress
in many studies.
2124
Additional support is provided by some animal
studies, which provide some ideas about mecha-
nisms. Although these tend to be at high doses, they
can help to supplement the human data. Recently,
Saldiva and co-workers
25,26
reported lung inflamma-
tion associated with particle and particle component
exposure in rats. Carbon monoxide exposure has
been associated with fetal toxicity, including intra-
uterine growth retardation in the rat.
27
Ozone expo-
sure has also been shown to be fetotoxic in an animal
model.
28
Perhaps the most serious thing that can be done to
a childs life is to end it. Recently, a number of
studies have reported that air pollution is associated
with precisely that. In thinking about air pollution
and death, one is inevitably led to the great air pol-
lution episode of December 15, 1952, in London. A
low-level thermal inversion that trapped coal smoke
in the Thames valley, coupled with a stationary front
that dropped wind speed to 0, resulted in a rapid
buildup of pollution to extremely high levels. Ap-
proximately 4000 excess deaths occurred in London
in that week,
29
and elevated death rates continued
for weeks afterward,
30
indicating that there were
delayed as well as prompt effects. Although most of
the deaths were in adults, infant mortality was dou-
bled during that period.
31
This episode is important because it establishes
causality. The influenza epidemic did not arrive in
England until 1 month after the episode, and in
other towns in England, where the weather was as
cold or colder but no inversion occurred, no increase
in deaths was observed. Furthermore, the death rate
increased rapidly in phase with the pollution and
began to come down when the pollution came down.
Hence, it is clear that at very high levels, air pollution
can produce a substantial increase in deaths of chil-
dren.
More recently, Woodruff et al
32
examined infant
deaths in the United States and levels of inhalable
particles (PM
10
) in the air. They excluded infant
deaths in the first month after birth as likely to reflect
complications of pregnancy and delivery and found
that PM
10
was associated with higher death rates in
the next 11 months of life. This excess risk seemed to
be principally from respiratory illness, although sud-
den infant death syndrome deaths were also ele-
vated.
Bobak and Leon
33
recently also examined the
cross-sectional association between air pollution and
infant mortality rates across towns in the Czech Re-
public. A significant association was seen between
infant death rates and particle and SO
2
concentra-
tion. Other studies have examined day-to-day
changes in air pollution and day-to-day changes in
infant deaths. Saldiva et al
34
reported that infant
death from respiratory disease was associated with
air pollution, particularly from traffic. Loomis et al
35
similarly found respiratory deaths in infants associ-
ated with air pollution.
ACUTE EFFECTS OF AIR POLLUTION EXPOSURE
Exposure Issues
As noted above, childrens exposure can be differ-
ent from adults given the same outdoor concentra-
tions. This is particularly important for exposure to
ozone. Ozone is a highly reactive gas, producing
oxidative damage in the lung. Because of that high
reactivity, its half-life in indoor air is only 7 to 10
minutes.
36
Consequently, ozone levels are very low
indoors.
5,37
This is particularly true for locations with
low air exchange rates, such as air-conditioned
homes and workspaces. Ozone also has a distinct
temporal pattern. Because it is not directly emitted
from polluting sources but produced by photochem-
ical reactions in the atmosphere, it shows strong
seasonal and diurnal variations. It is high in the
summer and the afternoon and low in the night,
early morning, and winter. Children tend to be out-
doors in the afternoon and in the summer, which
results in much higher exposure for children than
adults, who are protected by their indoor environ-
ment.
In contrast, fine combustion particles, usually in-
dexed by PM
2.5
(particles 2.5
M in aerodynamic
diameter) penetrate indoors and are not chemically
quenched like ozone (or SO
2
). Recent studies of the
association between personal exposure to particles of
outdoor origins and outdoor concentrations show
that the personal exposures are much more tightly
linked than for ozone,
38
although they do vary with
air exchange rates of the buildings in which the
person spends time. Hence childrens exposure to
1038 AIR POLLUTION AND CHILDRENS HEALTH
by on April 2, 2007 www.pediatrics.orgDownloaded from
PM
2.5
is enhanced by their greater outdoor activity
for this pollutant but to a lesser extent than for ozone.
Health Effects
There is a large body of literature associating
short-term changes in air pollution with short-term
changes in pulmonary health of children, often fo-
cused on individuals with asthma. Of particular in-
terest are a series of summer camp studies
3941
.
These were innovative because the living conditions
of the children in the camp meant that they were
exposed all the time. For most of the day, they were
outdoors, and their indoor quarters had such high air
infiltration rates that indoor concentrations of out-
door pollutants were almost certainly similar to the
outdoor levels. In these studies, lung function de-
clined during air pollution episodes, which were
combinations of ozone and sulfate particulates, some
of which may have been acidic.
Another set of studies examined wintertime epi-
sodes. A study in Steubenville, Ohio, repeated mea-
surements of pulmonary function in schoolchildren
before, during, and after an episode of high-particu-
late air pollution.
42
Lung function declined during
the episode. A similar study was performed in the
Netherlands.
43
These studies were followed up by a different
study design that made it possible to collect large
amounts of data relatively inexpensively. A panel of
children would be recruited and asked to perform
daily peak flow tests and usually to answer ques-
tions on symptom prevalence (wheezing, coughing,
etc) for a period of several months. These measure-
ments were then correlated with air pollution. Often
but not always, these studies would be focused on
children with asthma. In general, significant associ-
ations have been reported with PM
10
,
4448
although
not in every study.
49
Other summer time studies
have reported associations with ozone,
5052
includ-
ing interactions with aeroallergen exposure.
53
Of particular interest are 2 studies from the Neth-
erlands that addressed the question of susceptibility.
Van der Zee et al
54
looked at wintertime air pollution
in panels of 7- to 11-year-old children. A stronger
association was found between particle pollution
and peak flow decrements in children with asthma
symptoms, particularly those on regular medication,
than with nonsymptomatic children. There was also
a significant effect on bronchodilator use in the
symptomatic children. A second analysis looked at
more objective measures than reports of chronic re-
spiratory symptoms as effect modifiers. Children
were stratified into those with measured bronchial
hyperresponsiveness and elevated immunoglobulin
E and those without.
55
The association between dec-
rements in peak flow and air pollution was primarily
in the former group.
A related approach is to use administrative data to
look at more serious outcomes that require physician
contact. For example, Pope
56
examined hospital ad-
missions of children in the Utah valley during 3
consecutive winters. These winters were before, dur-
ing, and after a strike that closed down a steel mill in
the valley that was the largest source of wintertime
air pollution. There was a 50% drop in admissions
of children for asthma and for pneumonia during the
period that the mill was closed and when the pollu-
tion was lower. In the following year, admissions
went back to previous levels. In a neighboring valley,
there was no drop in pollution or admissions in the
middle winter. This is as close to a clinical trial as can
be found in air pollution epidemiology, and the con-
clusions are striking. Air pollution is related to seri-
ous asthma exacerbation and to pneumonia exacer-
bation. Other studies have looked at day-to-day
fluctuations in hospital admissions and day-to-day
changes in air pollution and reported associations
with childhood hospital admissions in Ontario,
57,58
Seattle,
59,60
and elsewhere.
61,62
A different approach is to look at physician visits.
Such data are hard to obtain systematically for large
populations in the United States but are more readily
available in Europe. Medina et al
63
looked at emer-
gency house calls by physicians in Paris and found
that visits for asthma were associated with particu-
late air pollution and ozone and that the association
was stronger for children.
What evidence is there that these associations are
plausible? An important study by Zelikoff et al
64
showed that exposure to urban particles exacerbated
pneumonia in an animal model, supporting the re-
sults of the epidemiologic studies in Utah and else-
where. Other studies have shown ozone to be asso-
ciated with altered macrophage function and
epithelial injury,
65
which could plausibly modify in-
fectivity.
Other evidence points to a role for pollution in
increasing lung inflammation in children, particu-
larly those with asthma. For example, Fischer et al
66
examined a cohort of 68 children (aged 1011) with 7
weekly measurements of exhaled nitric oxide (NO)
and found that increases in several air pollutants
were associated with increased levels of exhaled NO,
a good marker of lung inflammation in individuals
with asthma.
67,68
Giroux et al
69
contrasted exhaled
NO in children who had asthma and lived in urban
areas with others who stayed in a national park in
the mountains, or with children without asthma in
the same city. The exhaled NO concentrations in the
urban children with asthma were more than double
those in the children with asthma in the national
park, and their was no difference in exhaled NO
between children with asthma in the park and
healthy children in the city.
Finally, we have excellent evidence that changing
pollution in the short term produces immediate re-
ductions in asthma exacerbations. In addition to the
Utah study cited above, a more recent study looked
at asthma hospital visits in Atlanta around the period
of the Olympics, when traffic was limited and air
pollution was reduced. A noticeable reduction in
asthma emergency visits occurred during that period
of short-term traffic control.
70
EFFECTS OF LONG-TERM EXPOSURE TO AIR
POLLUTION
Although the role of air pollution in exacerbating
existing illness has been well established, recent ev-
SUPPLEMENT 1039
by on April 2, 2007 www.pediatrics.orgDownloaded from
idence has implicated pollution exposure with the
development of chronic disease or impairments. Ev-
idence has been accumulating for a while about ef-
fects on lung function and bronchitic symptoms.
More recently, studies have begun to implicate air
pollution, particularly from traffic, with the patho-
genesis of asthma.
In the late 1980s, Schwartz
71
examined the associ-
ation between long-term exposure of children to air
pollution and pulmonary function in the Second Na-
tional Health and Nutrition Examination Survey. He
found significant decrements in lung function asso-
ciated with exposure.
Jedrychowski et al
72
also reported that air pollu-
tion was associated with lower levels of lung func-
tion growth in children in Poland. Horak et al
73
made repeated measurements of spirometry during
a 3-year period in Austrian schoolchildren and found
that after adjustment for covariates, including initial
lung function, lung function growth rates were asso-
ciated with PM
10
exposure. An increase of 10
g/m
3
in PM
10
exposure was associated with a decrease in
growth of forced expiratory volume in 1 second of 84
mL/year.
Other studies have implicated ozone exposure
during childhood with reductions in lung function.
For example, Ku¨ nzli et al
74
collected residential ad-
dress histories for freshman at the University of Cal-
ifornia at Berkeley and matched them to monitors
near their homes. Cumulative ozone exposure was
associated with a significant decrement in forced
expiratory volume in 1 second. A similar result was
found for freshmen at Yale.
75
Dockery et al
76
reported that chronic bronchitis
and chest illness in children were associated with
exposure to particulate air pollution. This study com-
pared covariate adjusted rates across 6 communities
in the eastern United States with varying levels of
pollution. No association was seen with asthma or
wheezing. Subsequent studies in the United States
77
and elsewhere confirmed that particulate exposure
was associated with higher rates of chronic cough
and bronchitis symptoms in children and the lack of
association with wheezing and asthma. A similar
large study (n 4470) comparing schoolchildren in
10 communities in Switzerland reported an adjusted
odds ratio for bronchitis of 2.88 (95% confidence
interval [CI]: 1.69 4.89) for PM
10
exposure between
the most and least polluted community.
78
A study of
3676 children across 12 Southern California commu-
nities reported that bronchitis was associated with
PM
10
but only among children with asthma.
77
The
largest study examined 13 369 children in 24 com-
munities in the United States and Canada.
79
Again,
particulate air pollution was associated with bron-
chitis episodes across these communities.
A recent study that looked at eastern Germany,
where there has been a reduction in pollution since
the reunification, shows that this reduction has been
associated with reductions in the rates of chronic
cough and bronchitis symptoms in a new cohort of
children.
80
This demonstrates not merely an associa-
tion but that an intervention produces improvements
in health. A similar dramatic effect of intervention
was seen in a study by Avol et al.
81
Using the South-
ern California cohort study mentioned above, they
identified 110 children who moved from the study
area and followed them up in their new home with
pulmonary function testing identical to that in the
main cohort. Subjects who moved to locations with
higher PM
10
concentrations showed lower rates of
annual growth in lung function, and subjects who
moved to locations with lower PM
10
concentrations
than they had left showed higher rates of growth in
lung function. This effect was increased in subjects
who lived in the new location for at least 3 years.
Of considerable interest are recent studies that
have called into question the previous results indi-
cating that long-term air pollution exposure (mostly
to particles) was associated with bronchitis symp-
toms but not asthma. These studies all used central
monitoring locations in each community to assess
long-term exposure in those communities. Although
these monitoring stations are reasonable surrogates
for long-term exposure to pollutants that are rela-
tively homogeneously distributed across the commu-
nity, that is not true for all pollutants. In particular,
traffic pollutants show strong gradients. Exposure to
diesel exhaust varies greatly with distance from ma-
jor roadways within a community.
82,83
The new stud-
ies have used measurements or models of this mic-
rolevel spatial variability in exposure within
community and returned to the question of whether
air pollution exposure is associated with the devel-
opment of asthma.
Studnicka et al
84
examined 8 small, rural commu-
nities with no industrial sources of pollution. NO
2
was measured in each community and taken as a
measure of exposure to traffic pollution. In areas
without heavy industry, almost all NO
2
is attribut-
able to traffic. Although both gasoline and diesel
engines produce NO
2
, diesel engines produce much
more, so this surrogate is weighted toward diesel
exposure. A strong association between asthma
prevalence and NO
2
levels was found, with odds
ratios reaching 5.81 (95% CI: 1.2726.5), contrasting
the highest and lowest exposures. Kramer et al
85
examined 317 children in 3 German communities.
NO
2
measurements were made outside the homes of
each of the children, and personal NO
2
measure-
ments were collected for each child. The personal
NO
2
measurements reflect exposure to both outdoor
NO
2
and indoor sources (eg, gas stoves). The NO
2
outside the home reflected exposure to NO
2
from
outdoor sources only and therefore was a good sur-
rogate for exposure to traffic pollution. The NO
2
measurements outside each childs home were sig-
nificant predictors of hay fever; symptoms of allergic
rhinitis; wheezing; and sensitization against pollen,
house dust mites, or cats. The personal NO
2
mea-
surements, which were strongly influenced by in-
door sources, were not associated with these out-
comes. This indicates that traffic pollution but
probably not the NO
2
from traffic is associated with
atopy and wheezing. If NO
2
per se is not the relevant
exposure, than diesel particles or some component of
those particles, such as polycyclic aromatic hydrocar-
bons, may be the most important etiologic compo-
1040 AIR POLLUTION AND CHILDRENS HEALTH
by on April 2, 2007 www.pediatrics.orgDownloaded from
nent. In the Netherlands, residence on a high-traffic
street was associated with a 2-fold increase in the
risk of wheezing after control for confounders.
86
Even more recently, Lin et al
87
geocoded the resi-
dential addresses of children who were admitted to
the hospital in Erie County, New York (excluding
Buffalo) for asthma, and age-matched controls who
were admitted for nonrespiratory conditions. These
were linked to Department of Transportation data on
vehicle miles traveled on their street. The odds of
asthma (adjusted for poverty level) for living within
200 m of a street with the highest tertile of traffic
density was 1.93 (95% CI: 1.133.29), and the children
with asthma were more likely to have truck traffic on
their street. Another recent report analyzed data
from 2 birth cohorts totaling 1756 children in Mu-
nich.
88
Geographic Information System modeling
was used to estimate the concentrations of traffic-
related particles and NO
2
outside the birth addresses
of all of the children. These pollutants were associ-
ated with dry cough at night in the first year of life.
Another case-control study of 6147 children in Not-
tingham, England, found increased risk of wheeze
associated with living within 90 m of a roadway.
89
Although some studies showed no increased risk,
90
the overwhelming weight of the recent evidence sug-
gests that traffic pollution is associated with the risk
of developing asthma.
CONCLUSIONS
Air pollution is not the leading cause of death or
morbidity in children in the developed world. How-
ever, there is increasingly strong evidence that air
pollution is associated with nontrivial increases in
the risk of death and chronic disease in children,
worse pregnancy outcomes, and exacerbation of ill-
nesses. It is less clear which pollutants are most
responsible, but particles and ozone have the stron-
gest associations. For the incidence of asthma, traffic
pollution, particularly from trucks, seems to be the
key player.
What is important to realize is that this is an easily
modifiable risk. Sulfate particles, a major fraction of
the particle burden in the air in urban areas, can be
easily removed using scrubbers on powerplants
(their largest source) at a cost that is 1% of the
current price of electricity. NOx reduction, a major
component of an ozone reduction strategy, can also
be retrofitted onto powerplants. In Europe, catalytic
converters on cars can be brought up to US stan-
dards. Traffic particles, NOx, and so forth are dom-
inated by diesel engines. Trap oxidizers and catalysts
can reduce these emissions by up to 90%. Such de-
vices have been on gasoline-powered vehicles for
decades without ending industrial civilization as we
know it. For many of these control strategies, it does
not matter that we are not sure which component of
the pollution mix is principally responsible. Oxida-
tive catalysts reduce carbon soot, polycyclic aromatic
hydrocarbons, CO, and so forth. Given the amount of
money that we spend on the treatment of asthma and
the difficulty that we have in reducing allergen ex-
posures, such straightforward approaches need seri-
ous attention.
REFERENCES
1. Zanobetti A, Schwartz J. Are diabetics more susceptible to the health
effects of airborne particles? Am J Respir Crit Care Med. 2001;164:831 833
2. Bateson TF, Schwartz J. Who is sensitive to the effects of particles on
mortality? A case-crossover analysis of individual characteristics as
effect modifiers. Epidemiology. 2004, in press
3. Dunnill MS. Thorax 1962:17:329, cited in: Altman PL, Dittmer DS.
Respiration and Circulation. Bethesda, MD: Federation of American Soci-
eties for Experimental Biology; 1971
4. Holt PG. Programming for responsiveness to environmental antigens
that trigger allergic respiratory disease in adulthood is initiated in the
perinatal period. Environ Health Perspect. 1998;106(suppl 3):795800
5. US Environmental Protection Agency, National Center for Exposure
Assessment. Exposure Factors Handbook. Washington, DC: Environmen-
tal Protection Agency; 1997 (EPA/600/P95/002Fa)
6. Peters A, Frohlich M, Doring A, et al. Particulate air pollution is asso-
ciated with an acute phase response in men; results from the MONICA-
Augsburg Study. Eur Heart J. 2001;22:1198 1204
7. Gold DR, Litonjua A, Schwartz J, et al. Ambient pollution and heart rate
variability. Circulation. 2000;101:12671273
8. Pereira LA, Loomis D, Conceicao GM, et al. Association between air
pollution and intrauterine mortality in Sao Paulo, Brazil. Environ Health
Perspect, 1998;106:325329
9. Xu X, Ding H, Wang X. Acute effects of total suspended particles and
sulfur dioxides on preterm delivery: a community-based cohort study.
Arch Environ Health. 1995;50:407415
10. Ritz B, Yu F, Chapa G, Fruin S. Effect of air pollution on preterm birth
among children born in southern California between 1989 and 1993.
Epidemiology. 2000;11:502511
11. Lin MC, Chiu HF, Yu HS, et al. Increased risk of preterm delivery in
areas with air pollution from a petroleum refinery plant in Taiwan. J
Toxicol Environ Health A. 2001;64:37 44
12. Wang X, Ding H, Ryan L, Xu X. Association between air pollution and
low birth weight: a community based study. Environ Health Perspect.
1997;105:514520
13. Ritz B, Yu F. The effect of ambient carbon monoxide on low birth weight
among children born in southern California between 1989 and 1993.
Environ Health Perspect. 1999;107:1725
14. Dejmek J, Selevan SG, Benes I, Solansky I, Sram RJ. Fetal growth and
maternal exposure to particulate matter during pregnancy. Environ
Health Perspect. 1999;107:475 480
15. Bobak M, Leon DA. Pregnancy outcomes and outdoor air pollution: an
ecological study in districts of the Czech republic 1986 1988. Occup
Environ Med. 1999;56:539 543
16. Ha EH, Hong YC, Lee BE, Woo BH, Schwartz J, Christiani DC. Is air
pollution a risk factor for low birth weight in Seoul? Epidemiology.
2001;12:643648
17. Bobak M. Outdoor air pollution, low birth weight, and prematurity.
Environ Health Perspect. 2000;108:539543
18. Bobak M, Richards M, Wadsworth M. Air pollution and birth weight in
Britain in 1946. Epidemiology. 2001;12:358 359
19. Windham GC, Eaton A. Hopkins B. Evidence for an association between
environmental tobacco smoke exposure and birthweight: a meta-
analysis and new data. Paediatr Perinat Epidemiol. 1999;13:3557
20. Salvi S, Blomberg A, Rudell B, et al. Acute inflammatory responses in
the airways and peripheral blood after short-term exposure to diesel
exhaust in healthy human volunteers. Am J Respir Crit Care Med. 1999;
159:702709
21. Pryor WA, Church DF. The reaction of ozone with unsaturated fatty
acids: aldehydes and hydrogen peroxide as mediators of ozone toxicity.
In: Davies KJA, ed. Oxidative Damage and Repair: Chemical, Biological and
Medical Aspects. New York, NY: Pergamon Press; 1991:496 504
22. Koren HS, Devlin RB, Graham De, et al. Ozone induced inflammation in
lower airways of human subjects. Am Rev Respir Dis. 1989;139:407 415
23. Mudway IS, Krishna MT, Frew AJ, et al. Compromised concentrations
of ascorbate in fluid lining the respiratory tract in human subjects after
exposure to ozone. Occup Environ Med. 1999;56:473481
24. Saintot M, Bernard N, Astre C, Gerber M. Ozone exposure and blood
antioxidants: a study in a periurban area in Southern France. Arch
Environ Health. 1999;54:34 39
25. Saldiva PH, Clarke RW, Coull BA, et al. Lung inflammation induced by
concentrated ambient air particles is related to particle composition.
Am J Respir Crit Care Med. 2002;165:16101617
26. Rice TM, Clarke RW, Godleski JJ, et al. Differential ability of transition
metals to induce pulmonary inflammation. Toxicol Appl Pharmacol. 2001;
177:4653
SUPPLEMENT 1041
by on April 2, 2007 www.pediatrics.orgDownloaded from
27. Garvey DJ, Longo LD. Chronic low level maternal carbon monoxide
exposure and fetal growth and development. Biol Reprod. 1978;19:8 14
28. Kavlock R, Daston G, Grabowski CT. Studies on the developmental
toxicity of ozone. I. Prenatal effects. Toxicol Appl Pharmacol. 1979;
48(suppl):1928
29. Mortality and morbidity during the London fog of December 1952. Her
Majestys Stationary Office, London. Report No. 95 on Public Health
and Medical Subjects. London, UK: Her Majestys Public Health Service;
1954
30. Anderson HR. Health effects of air pollution episodes. In: Holgate ST,
Samet JM, Koren HS, Maynard RL, eds. Air Pollution and Health. Lon-
don, UK: Academic Press; 1999:461 484
31. Schwartz J. What are people dying of on high air pollution days?
Environ Res. 1994;64:26 35
32. Woodruff TJ, Grillo J, Schoendorf C. The relationship between selected
causes of postneonatal infant mortality and particulate air pollution in
the United States. Environ Health Perspect. 1997;105:608 612
33. Bobak M, Leon DA. Air pollution and infant mortality in the Czech
Republic, 1986 88. Lancet. 1992;340:1010 1014
34. Saldiva PHN, Lichtenfels AJFC, Paiva PSO, et al. Association between
air pollution and mortality due to respiratory disease in children in Sao
Paulo, Brazil. Environ Res. 1994;65:218 225
35. Loomis D, Castillejos M, Gold DR, McDonnell W, Borja-Aburto VH. Air
pollution and infant mortality in Mexico City. Epidemiology. 1999;10:
118123
36. Weschler CJ. Ozone in indoor environments: concentration and chem-
istry. Indoor Air. 2000;10:269288
37. Lee K, Xue J, Geyh AS, et al. Nitrous acid, nitrogen dioxide, and ozone
concentrations in residential environments. Environ Health Perspect.
2002;110:145150
38. Sarnat JA, Schwartz J, Catalano PJ, Suh HH. Confounder or surrogate:
the role of gaseous pollutants in particulate matter epidemiology. En-
viron Health Perspect. 2001;109:10531061
39. Spektor DM, Mao J, He D, Thurston GD, Hayes C, Lippmann M. Effects
of single and multi day ozone exposures on respiratory function in
active normal children. Environ Res. 1991;55:107122
40. Kinney PL, Ware JH, Spengler JD, Dockery DW, Speizer FE, Ferris BG
Jr. Short-term pulmonary function change in association with ozone
levels. Am Rev Respir Dis. 1989;139:56 61
41. Berry M, Lioy PJ, Gelperin K, Buckler G, Klotz J. Accumulated exposure
to ozone and measurement of health effects in children and counselors
at two summer camps. Environ Res. 1991;54:135150
42. Dockery DW, Ware JH, Ferris BG, Speizer FE, Cook NR, Herman SM.
Change in pulmonary function associated with air pollution episodes. J
Air Poll Control Assoc. 1982;32:937942
43. Dassen W, Brunekreef B, Hoek G, et al. Decline in childrens pulmonary
function during an air pollution episode. J Air Poll Control Assoc. 1986;
36:11231127
44. Romieu I, Meneses F, Ruiz S, et al. Effects of air pollution on the
respiratory health of asthmatic children living in Mexico City. Am J
Respir Crit Care Med. 1996;154:300 307
45. Ostro B, Lipsett M, Mann J, Braxton-Owens H, White M. Air pollution
exacerbation of asthma in African-American children in Los Angeles.
Epidemiology. 12:200 208
46. Pope CA, Dockery DW. Acute health effects of PM
10
pollution on
symptomatic and asymptomatic children. Am Rev Respir Dis. 145:
11231128
47. Braun-Fahrlander C, Ackerman-Liebrich U, Schwartz J, Grehm HP,
Rutishausser M, Wanner HU. Air pollution and respiratory symptoms
in pre-school children. Am Rev Respir Dis. 1992;145:42 47
48. Schwartz J, Dockery DW, Neas LM, et al. Acute effects of summer air
pollution on respiratory symptom reporting in children. Am J Respir Crit
Care Med. 1994;150:1234 1242
49. Roemer W, Clench-Aas J, Englert N, et al. Inhomogeneity in response to
air pollution in European children (PEACE project). Occup Environ Med.
1999;56:8692
50. Kinney PL, Lippmann M. Respiratory effects of seasonal exposures to
ozone and particles. Arch Environ Health. 2000;55:210216
51. Jalaludin BB, Chey T, OToole BI, Smith WT, Capon AG, Leeder SR.
Acute effects of low levels of ambient ozone on peak expiratory flow
rate in a cohort of Australian children. Int J Epidemiol. 2000;29:549 557
52. Gold DR, Damokosh AI, Pope CA 3rd, et al. Particulate and ozone
pollutant effects on the respiratory function of children in southwest
Mexico City. Epidemiology. 1999;10:816
53. Higgins BG, Francis HC, Yates C, et al. Environmental exposure to air
pollution and allergens and peak flow changes. Eur Respir J. 2000;16:
6166
54. Van der Zee S, Hoek G, Boezen HM, Schouten JP, van Wijnen JH,
Brunekreef B. Acute effects of urban air pollution on respiratory health
of children with and without chronic respiratory symptoms. Occup
Environ Med. 1999;12:802 812
55. Boezen HM, van der Zee SC, Postma DS, et al. Effects of ambient air
pollution on upper and lower respiratory symptoms and peak expira-
tory flow in children. Lancet. 1999;353:874 878
56. Pope CA III. Respiratory disease associated with community air pollu-
tion and a steel mill, Utah valley. Am J Public Health. 1989;79:623 628
57. Bates DV, Szito R. The Ontario Air Pollution Study: identification of the
causative agent. Environ Health Perspect. 1989;79:69 72
58. Burnett RT, Dales RE, Raizenne ME, et al. Effects of low ambient levels
of ozone and sulfates on the frequency of respiratory admissions to
Ontario hospitals. Environ Res. 1994;65:172194
59. Schwartz J, Koenig J, Slater D, Larson T. Particulate air pollution and
hospital emergency visits for asthma in Seattle. Am Rev Respir Dis.
1993;147:826 831
60. Norris G, Larson T, Koenig J, Claiborn C, Sheppard L, Finn D. Asthma
aggravation, combustion, and stagnant air. Thorax. 2000;55:466470
61. Tenias JM, Ballester F, Rivera ML. Association between hospital emer-
gency visits for asthma and air pollution in Valencia Spain. Occup
Environ Med. 1998;55:541547
62. Sunyer J, Spix C, Que´nel P, et al. Urban air pollution and emergency
admissions for asthma in four European cities: the APHEA Project.
Thorax. 1997;52:760 765
63. Medina S, Le Tertre A, Quenel P, et al. Air pollution and doctorshouse
calls: results from the ERPURS system for monitoring the effects of air
pollution on public health in Greater Paris, France 19911995. Environ
Res. 1997;75:73 84
64. Zelikoff JT, Nadziejko C, Fang T, Gordon C, Premdass C, Cohen MD.
Short term, low-dose inhalation of ambient particulate matter exacer-
bates ongoing pneumococcal infections in Streptococcus Pneumoniae-
infected rats. In: Phalen RF, Bell YM, eds. Proceedings of the Third
Colloquium on Particulate Air Pollution and Human Health. Irvine, CA: Air
Pollution Health Effects Laboratory, University of California; 1999:
894 8 101
65. Devlin RB, McDonnell WF, Mann R, et al. Exposure of humans to
ambient levels of ozone for 6.6 hours causes cellular and biochemical
changes in the lung. Am J Respir Cell Mol Biol. 1991;4:72 81
66. Fischer PH, Steerenerg PA, Smelder JD, Van Loveren H, Van Amster-
dam JG. Association between exhaled nitric oxide, ambient air pollu-
tion, and respiratory health in school children. Int Arch Occup Environ
Health. 2002;75:348 353
67. Kharitonov SA, Yates D, Springall DR, et al. Exhaled nitric oxide is
increased in asthma. Chest. 1995;107(3 suppl):156S157S
68. Massaro AF, Mehta S, Lilly CM, Kobzik L, Reilly JJ, Drazen JM. Elevated
nitric oxide concentrations in isolated lower airway gas of asthmatic
subjects. Am J Respir Crit Care Med. 1996;153:1510 1514
69. Giroux M, Bremont F, Ferrieres J, Dumas JC. Exhaled NO in asthmatic
children in unpolluted and urban environments. Environ Int. 2001;27:
335340
70. Friedman MS, Powell KE, Hutwagner L, Graham LM, Teague WG.
Impact of changes in transportation and commuting behaviors during
the 1996 Summer Olympic Games in Atlanta on air quality and child-
hood asthma. JAMA. 2001;285:897905
71. Schwartz J. Lung function and chronic exposure to air pollution: a
cross-sectional analysis of NHANES II. Environ Res. 1989;50:309 321
72. Jedrychowski W, Flak E, Mroz E. The adverse effect of low levels of
ambient air pollutants on lung function growth in preadolescent chil-
dren. Environ Health Perspect. 1999;107:669 674
73. Horak F, Studnicka M, Gartner C, et al. Particulate matter and lung
function growth in children: a three year followup study in Austrian
schoolchildren. Eur Respir J. 2002;19:838 845
74. Ku¨nzli N, Lurmann F, Segal M, Ngl L, Balmes J, Tager IB. Association
between lifetime ambient ozone exposure and pulmonary function in
college freshmen: results of a pilot study. Environ Res. 1997;72:823
75. Galizia A, Kinney PL. Long-term residence in areas of high ozone:
associations with respiratory health in a nationwide sample of non-
smoking young adults. Environ Health Perspect. 1999;107:675679
76. Dockery DW, Speizer FE, Stram DO, Ware JH, Spengler JD, Ferris BG Jr.
Effects of inhaled particles on respiratory health of children. Am Rev
Respir Dis. 1989;139:587594
77. McConnell R, Berhane K, Gilliland F, et al. Air pollution and bronchitic
symptoms in Southern California children with asthma. Environ Health
Perspect. 1999;107:757760
78. Braun-Fahrlander C, Vuille JC, Sennhauser FH, et al. Respiratory health
and long term exposure to air pollutants in Swiss schoolchildren.
SCARPOL team. Am J Respir Crit Care Med. 1997;155:10421049
79. Dockery DW, Cunningham J, Damokosh AI, et al. Health effects of acid
1042 AIR POLLUTION AND CHILDRENS HEALTH
by on April 2, 2007 www.pediatrics.orgDownloaded from
aerosols on North American children: respiratory symptoms. Environ
Health Perspect. 1996;105:500 505
80. Heinrich J, Hoelscher B, Wichman HE. Decline of ambient air pollution
and respiratory symptoms in children. Am J Respir Crit Care Med.
2000;161:19301936
81. Avol EL, Gauderman WJ, Tan SM, London SJ, Peters JM. Respiratory
effects of relocating to areas of differing air pollution levels. Am J Respir
Crit Care Med. 2001;164:20672072
82. Roorda-Knape MC, Janssen NA, de Hartog J, Van Vliet PH, Harssema
H, Brunekreef B. Air pollution from traffic in city districts near motor-
ways. Atmos Environ. 1998;32:19211930
83. Levy JI, Dumyahn T, Spengler JD. Particulate matter and polycyclic
aromatic hydrocarbon concentrations in indoor and outdoor microen-
vironments in Boston, Massachusetts. J Expo Anal Environ Epidemiol.
2002;12:104114
84. Studnicka M, Hackl E, Pischinger J, et al. Traffic related NO2 and the
prevalence of asthma and respiratory symptoms in seven year olds. Eur
Respir J. 1997;10:22752278
85. Kramer U, Koch T, Ranft U, Ring J, Behrendt H. Traffic related air
pollution is associated with atopy in children living in urban areas.
Epidemiology. 2000;11:64 70
86. Oosterlee A, Drijver M, Lebret E, Brunekreef B. Chronic respiratory
symptoms in children and adults living along streets with high traffic
density. Occup Environ Med. 1996;53:241247
87. Lin S, Munsie JP, Hwang SA, Fitzgerald E, Cayo MR. Childhood asthma
hospitalization and residential exposure to state route traffic. Environ
Res. 2002;88:73 81
88. Gehring U, Cyrys J, Sedlmeir G, et al. Traffic related air pollution and
respiratory health during the first 2 yrs of life. Eur Respir J. 2002;19:
690 698
89. Venn AJ, Lewis SA, Cooper M, Hubbard R, Britton J. Living near a main
road and the risk of wheezing illness in children. Am J Respir Crit Care
Med. 2001;164:21772180
90. English P, Neutra R, Scalf R, Sullivan M, Waller L, Zhu L. Examining
associations between childhood asthma and traffic flow using a geo-
graphic information system. Environ Health Perspect. 1999;107:761767
SUPPLEMENT 1043
by on April 2, 2007 www.pediatrics.orgDownloaded from
DOI: 10.1542/peds.113.4.S1.1037
2004;113;1037-1043 Pediatrics
Joel Schwartz
Air Pollution and Children’s Health
This information is current as of April 2, 2007
& Services
Updated Information
http://www.pediatrics.org/cgi/content/full/113/4/S1/1037
including high-resolution figures, can be found at:
References
http://www.pediatrics.org/cgi/content/full/113/4/S1/1037#BIBL
at:
This article cites 79 articles, 26 of which you can access for free
Citations
rticles
http://www.pediatrics.org/cgi/content/full/113/4/S1/1037#othera
This article has been cited by 9 HighWire-hosted articles:
Subspecialty Collections
logy
http://www.pediatrics.org/cgi/collection/therapeutics_and_toxico
Therapeutics & Toxicology
following collection(s):
This article, along with others on similar topics, appears in the
Permissions & Licensing
http://www.pediatrics.org/misc/Permissions.shtml
tables) or in its entirety can be found online at:
Information about reproducing this article in parts (figures,
Reprints
http://www.pediatrics.org/misc/reprints.shtml
Information about ordering reprints can be found online:
by on April 2, 2007 www.pediatrics.orgDownloaded from
... Children's exposure to air pollutants is especially alarming as they are considered a risk group due to the development of respiratory and the immune systems during childhood and higher inhalation rate (per kilogram of their body weight) than adults, which leave them susceptible to health risks (Branco et al., 2020a;Mudway et al., 2019;Nieuwenhuijsen et al., 2006;Schwartz, 2004;Sousa et al., 2012). The resulting ramifications of this early exposure may have long-term effects on their health as well (Schwartz, 2004). ...
... Children's exposure to air pollutants is especially alarming as they are considered a risk group due to the development of respiratory and the immune systems during childhood and higher inhalation rate (per kilogram of their body weight) than adults, which leave them susceptible to health risks (Branco et al., 2020a;Mudway et al., 2019;Nieuwenhuijsen et al., 2006;Schwartz, 2004;Sousa et al., 2012). The resulting ramifications of this early exposure may have long-term effects on their health as well (Schwartz, 2004). Past research associates children's exposure to poor air quality with adverse health impacts, including reduced lung function, asthma and allergies (Gehring et al., 2013;Mendell, 2007;Schwartz, 2004;Sousa et al., 2012). ...
... The resulting ramifications of this early exposure may have long-term effects on their health as well (Schwartz, 2004). Past research associates children's exposure to poor air quality with adverse health impacts, including reduced lung function, asthma and allergies (Gehring et al., 2013;Mendell, 2007;Schwartz, 2004;Sousa et al., 2012). Hence, monitoring children's exposure to air pollutants is of great significance. ...
Article
Poor indoor air quality has adverse health impacts. Children are considered a risk group, and they spend a significant time indoors at home and in schools. Air quality monitoring has traditionally been limited due to the cost and size of the monitoring stations. Recent advancements in low-cost sensors technology allow for economical, scalable and real-time monitoring, which is especially helpful in monitoring air quality in indoor environments, as they are prone to sudden peaks in pollutant concentrations. However, data reliability is still a considerable challenge to overcome in low-cost sensors technology. Thus, following a monitoring campaign in a nursery and primary school in Porto urban area, the present study analyzed the performance of three commercially available low-cost IoT devices for indoor air quality monitoring in real-world against a research-grade device used as a reference and developed regression models to improve their reliability. This paper also presents the developed on-field calibration models via machine learning technique using multiple linear regression, support vector regression, and gradient boosting regression algorithms and focuses on particulate matter (PM1, PM2.5, PM10) data collected by the devices. The performance evaluation results showed poor detection of particulates in classrooms by the low-cost devices compared to the reference. The on-field calibration algorithms showed a considerable improvement in all three devices' accuracy (reaching up to R² > 0.9) for the light scattering technology based particulate matter sensors. The results also show the different performance of low-cost devices in the lunchroom compared to the classrooms of the same school building, indicating the need for calibration in different microenvironments.
... Several studies have established that children are particularly susceptible and vulnerable to unhealthy air [21,7,16]. Children have an accelerated metabolism which causes them to breathe more frequently and absorb a higher amount of pollutants relative to their body weight [7,16]. Children also have a larger lung surface area per kilogram of body weight than adults [21,7]. ...
... Children have an accelerated metabolism which causes them to breathe more frequently and absorb a higher amount of pollutants relative to their body weight [7,16]. Children also have a larger lung surface area per kilogram of body weight than adults [21,7]. Moreover, stagnation points of toxic particles have been found in the airflow of the cities at locations where there is a greater population concentration [22], including educational institutions increasing the exposure of children to polluting factors. ...
Chapter
According to the World Health Organization, unhealthy air causes respiratory and cardiovascular diseases worldwide, moreover, children are particularly susceptible and vulnerable due to their accelerated metabolism, biological development among other factors. In this work, particle transport and deposition pattern were analyzed using a three-dimensional model of the trachea and bronchi of a child under inhalation condition. The phenomenon is computationally modeling employing fluid-dynamic laws coupled with particle theory to study the two-phase flow. The understanding of inhalation and transport phenomena of toxic particles from 0.5 to 10 μm of diameter through the human respiratory system is also important for investigations into dosimetry and respiratory health effects. From the results it is found that a higher number of particles are deposited at the bifurcation junctions for particles with 5 μm of diameter or higher because of the inertial effect and the shape of the bronchial branching, meanwhile the smaller particles are slightly more randomly attached to the inner walls of the bronchial system. In addition, the heavy particles tended to go to the lower bronchi, as fewer particles circulate to the aligned bronchi against gravity. The results obtained allow us to increase the knowledge of the affectation of the broncho-pulmonary system in young people and children due to air pollutants.
... This gap in research must be filled by more in-depth cohort studies. Even if all the populations living in an urban environment are affected by this pollution, for some authors the health consequences are first of all prejudicial to the health of the children because of the immaturity of their immune and pulmonary system [54,55] . The children with chronic respiratory conditions such as asthma are particularly at risk [10,11] . ...
... In addition, children have a higher respiratory rate and therefore breathe in a larger volume of air and are exposed to a higher proportion of contaminants than adults. Furthermore, children spend more time outdoors playing or exercising in potentially contaminated environments, and they are closer to the ground where the concentration of certain pollutants can be higher [90][91][92][93][94][95]. ...
Chapter
Nowadays, the evolution of the concept of nutrition has acquired a notion of three concurrent dimensions. Nutrition was considered an exclusively biological process while now, it comprises social and ecological aspects. Inadequate nutrition and air pollution are two major nongenetic environmental factors known to cause serious public health problems worldwide. Air pollution does not impact in the same way on the population at large, being particularly the children one of the most vulnerable subpopulations. Additionally, the nutritional status may modify the susceptibility to air pollution exposure and cause a wide range of acute and chronic cardio-respiratory diseases. Moreover, undernutrition is identified as a major health problem with devastating healthcare effects on the individual, social, and economic development. On a global scale, chronic undernourishment affects 144 million children younger than 5 years. However, the mechanism linking undernutrition and air pollution exposure still remains unclear. At present, only few epidemiological studies have been reported associating child malnutrition and air pollution. Therefore, a better understanding of the interactions between undernutrition and air pollution exposure is needed to guide action by individuals and governments.
... Further, because women are often the primary cooks, their personal exposures is driven by emissions during cooking events [7]. In contrast, children's exposure is more closely related to ambient levels given the share of time spent playing outside [35]. Characterizing children's exposure with greater precision and reliability should remain the focus of future studies as evidence of the association between solid fuel use and developmental outcomes continues to emerge [36]. ...
Article
Full-text available
Background Air pollution epidemiological studies usually rely on estimates of long-term exposure to air pollutants, which are difficult to ascertain. This problem is accentuated in settings where sources of personal exposure differ from those of ambient concentrations, including household air pollution environments where cooking is an important source. Objective The objective of this study was to assess the feasibility of estimating usual exposure to PM2.5 based on short-term measurements. Methods We leveraged three types of short-term measurements from a cohort of mother-child pairs in 26 communities in rural Ghana: (A) personal exposure to PM2.5 in mothers and age four children, ambient PM2.5 concentrations (B) at the community level, and (C) at a central site. Baseline models were linear mixed models with a random intercept for community or for participant. Lowest root-mean-square-error (RMSE) was used to select the best-performing model. Results We analyzed 240 community-days and 251 participant-days of PM2.5. Medians (IQR) of PM2.5 were 19.5 (36.5) μg/m³ for the central site, 28.7 (41.5) μg/m³ for the communities, 70.6 (56.9) μg/m³ for mothers, and 80.9 (74.1) μg/m³ for children. The ICCs (95% CI) for community ambient and personal exposure were 0.30 (0.17, 0.47) and 0.74 (0.65, 0.81) respectively. The sources of variability differed during the Harmattan season. Children’s daily exposure was best predicted by models that used community ambient compared to mother’s exposure as a predictor (log-scale RMSE: 0.165 vs 0.325). Conclusion Our results support the feasibility of predicting usual personal exposure to PM2.5 using short-term measurements in settings where household air pollution is an important source of exposure. Our results also suggest that mother’s exposure may not be the best proxy for child’s exposure at age four.
... Although asthma affects persons in all age groups, it is more prevalent among children (9.3%) than adults (7.3%) [6]. Studies have also shown that children are more susceptible to air pollution and at greater risk of asthma exacerbations due to developmental differences such as higher air intake per kilogram of body weight [7][8][9]. However, while correlations between ambient air pollution and risk of asthma attacks have been shown through regional studies [10][11][12][13][14][15] and spatial associations [16][17][18][19], little is known about the direct impact of Nitrogen Dioxide (NO 2 ) exposure in the indoor microenvironment on the progression of the condition [4,5]. ...
Article
Full-text available
Background One of the most common pollutants in residences due to gas appliances, NO2 has been shown to increase the risk of asthma attacks after small increases in short term exposure. However, standard environmental sampling methods taken at the regional level overlook chronic intermittent exposure due to lack of temporal and spatial granularity. Further, the EPA and WHO do not currently provide exposure recommendations to at-risk populations. Aims A pilot study with pediatric asthma patients was conducted to investigate potential deployment challenges as well as benefits of home-based NO2 sensors and, when combined with a subject’s hospital records and self-reported symptoms, the richness of data available for larger-scale epidemiological studies. Methods We developed a compact personal NO2 sensor with one minute temporal resolution and sensitivity down to 15 ppb to monitor exposure levels in the home. Patient hospital records were collected along with self-reported symptom diaries, and two example hypotheses were created to further demonstrate how data of this detail may enable study of the impact of NO2 in this sensitive population. Results 17 patients (55%) had at least 1 h each day with average NO2 exposure >21 ppb. Frequency of acute NO2 exposure >21 ppb was higher in the group with gas stoves (U = 27, p ≤ 0.001), and showed a positive correlation (rs = 0.662, p = 0.037, 95% CI 0.36–0.84) with hospital admissions. Significance Similar studies are needed to evaluate the true impact of NO2 in the home environment on at-risk populations, and to provide further data to regulatory bodies when developing updated recommendations.
... In another study, Cho et al. (2000) conclude that, for respiratory admissions, the relative risk in relation to NO 2 is 1.47 (95% C.I.: 1.03-2.10). Similarly, Schwartz (2004) argues that NO effects on respiratory problems are quite apparent, especially on children, while Braat et al. (2002) link NO to the aggravation of respiratory diseases and allergies, although the significance level of the pollutant could not allow for generalizations. Generalized Linear Models (GLM) assuming Gaussian (normal) distribution for Dhaka city may give the exact scenario as found for the above mentioned cities. ...
Conference Paper
Full-text available
A total of 2 terrestrial molluscs species under the family Helicarionidae, Order - Stylommatophora were collected. Which are new records from Bangladesh. The information on the distribution and ecology, population density and seasonal variation of Sesara diplodon and Sivella castra were provided in this paper. Population density was measured. Pearson correlation among meteorological factors of season (air temperature, rainfall and humidity) and molluscs population density were calculated. Morphometric parameters were measured. Moreover, economic importance and economic role were observed
Article
Climate change‐related disasters have drawn increased attention to the impact of air pollution on health. 122 children ages 9–11 years old, M(SD) = 9.91(.56), participated. Levels of particulate matter (PM2.5) near participants’ homes were obtained from the Environmental Protection Agency. Cytokines were assayed from 100 child serum samples: IL‐6, IL‐8, IL‐10, and TNFα. Autonomic physiology was indexed by pre‐ejection period (PEP), respiratory sinus arrhythmia (RSA), cardiac autonomic regulation (CAR), and cardiac autonomic balance (CAB). IL‐6 was positively related to daily PM2.5 (r = .26, p = .009). IL‐8 was negatively associated with monthly PM2.5 (r = −.23, p = .02). PEP was positively related to daily (r = .29, p = .001) and monthly PM2.5 (r = .18, p = .044). CAR was negatively associated with daily PM2.5 (r = −.29, p = .001). IL‐10, TNFα, RSA, and CAB were not associated with PM2.5. Air pollution may increase risk of inflammation in children.
Article
Full-text available
Background: The impact of environmental pollution (such as air pollution) on health costs has received a great deal of global attention in the last 20 years. Methods: This review aims to summarize the theoretical analysis model of air pollution affecting health costs, and further explore the actual characteristics of the impact of air pollution on health costs. The following main databases were taken into account: Web of Science Core Collection, Medline, SCOPUS, PubMed, and CNKI (China). As of 30 March 2021, we retrieved a total of 445 papers and ended up with 52 articles. Results: This review mainly expounds clarification of the concept of air pollution and health costs, the theoretical model and the actual characteristics of air pollution affecting health costs. In addition, it also discusses other related factors affecting health costs. Conclusion: Our conclusion is that, while academic research on the relationship between air pollution and health costs has made some progress, there are still some shortcomings, such as insufficient consideration of individual avoidance behavior and rural-urban and international mobility. Therefore, the simple use of the original data obtained in the statistical yearbook of the health cost caused by air pollution is also the reason for the errors in the empirical results. In addition, the choice of proxy variables of environmental pollution by scholars is relatively simple, mainly focusing on air pollutants, while the impact of water quality or soil pollution safety on health costs is becoming increasingly prominent, and will become the focus of future research.
Article
Full-text available
The World Health Organization (WHO) estimates that 25% of mortality in developing countries arises from environmental hazards. Over the years, soaring demand for humanity’s essential needs has prompted industrial-scale production and the generation of large quantities of waste. Petroleum refineries generate large quantities of waste which gives rise to health effects such as cancer, eye defects, birth defects, and reproductive defects. Furthermore, the residents living around refineries encounter several hazards arising from operations that generate noise, radiation, chemicals, vibration, dust and toxic pollutant gases. The current research landscape indicates that Petroleum Refinery Emissions or PREs pose significant risks to human health, safety and the environment. Therefore, this paper presents a concise review of the acute and chronic effects of PREs on the health and safety of residents living within the vicinity of petroleum refineries. The reviewed literature revealed that PREs cause various cancers, leukaemia, as well as cardiovascular, respiratory, and reproduction disorders. Hence, numerous approaches to mitigate, eliminate or address the short and long term effects of PREs have been proposed in the literature. The proposed approaches include the bioremediation as well as the monitoring and evaluation of PREs to promptly detect, remediate and eliminate the hazards. However, other measures that could help address the outlined occupational health and environmental safety-related issues will go a long way in mitigating or curbing the socio-economic, environmental, health and safety impacts of PREs and industrial wastes.
Article
Full-text available
Cited By (since 1996): 34 , Export Date: 4 February 2013 , Source: Scopus , The following values have no corresponding Zotero field: Author Address: University of California, School of Medicine, Davis, CA, United States Author Address: Harvard University, School of Public Health, Boston, MA, United States Author Address: Johns Hopkins University, School of Hygiene and Public Health, Baltimore, MD, United States Author Address: Yale University, School of Medicine, New Haven, CT, United States Author Address: University of Medicine, Dentistry of New Jersey/Robert Wood Johnson Medical School, New Brunswick, NJ, United States Author Address: Department of Epidemiology and Preventive Medicine, School of Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95615, United States
Article
Full-text available
A diary study on a random sample of 1,063 Swiss children aged 0-5 y was conducted in four different areas of Switzerland (two urban, one suburban, and one rural area) to investigate the association between air pollution and respiratory symptoms. Passive samplers inside and outside the home measured NOâ concentration during the 6 wk each child was studied. Diaries were completed by parents, and 20% of them were validated with the attending pediatrician's case notes. Other pollutants were measured by city monitor in the two urban locations. Incidence and duration of symptom episodes were examined separately. The study included any episode: episodes of coughing without runny nose, upper respiratory episodes, and episodes of breathing difficulty. Annual average NOâ was associated with the duration of any episode and of upper respiratory episodes in Poisson regressions that controlled for medical history. Nitrogen dioxide (NOâ) was not associated with the incidence of episodes. In regressions using 6-wk average pollution, NOâ measured outdoors, but not indoors, was associated with the duration of any symptom. Total suspended particulates were a more significant predictor of duration in the two urban locations where it was available. Six-week average TSP was also associated with the incidence of coughing episodes. We conclude that duration of respiratory symptom episodes are associated with particulate concentrations, and possibly with NOâ.
Article
Background We enrolled a cohort of primary schoolchildren with a history of wheeze (n = 148) in an 11-month longitudinal study to examine the relationship between ambient ozone concentrations and peak expiratory flow rate. Methods Enrolled children recorded peak expiratory flow rates (PEFR) twice daily. We obtained air pollution, meteorological and pollen data. In all, 125 children remained in the final analysis. Results We found a significant negative association between daily mean deviation in PEFR and same-day mean daytime ozone concentration (β-coefficient = 0.88; P = 0.04) after adjusting for co-pollutants, time trend, meteorological variables, pollen count and Alternaria count. The association was stronger in a subgroup of children with bronchial hyperreactivity and a doctor diagnosis of asthma (β-coefficient = –2.61; P = 0.001). There was no significant association between PEFR and same-day daily daytime maximum ozone concentration. We also demonstrated a dose-response relationship with mean daytime ozone concentration. Conclusions Moderate levels of ambient ozone have an adverse health effect on children with a history of wheezing, and this effect is larger in children with bronchial hyperreactivity and a doctor diagnosis of asthma.
Article
We studied 110 children (59 boys and 51 girls, who were 10 yr of age at enrollment and 15 yr of age at follow-up) who had moved from communities participating in a 10-yr prospective study of respiratory health (The Children's Health Study [CHS]) to determine whether changes in air quality caused by relocation were associated with changes in annual lung function growth rates. The subjects were given health questionnaires and underwent spirometry in their homes across six western states, according to a protocol identical to evaluations performed annually on the CHS cohort in school. Changes in annual average exposure to particulate matter with a mean diameter of 10 mum (PM10) were associated with differences in annual lung function growth rates for FEV1, maximal mid-expiratory flow, and peak expiratory flow rate. As a group, subjects who had moved to areas of lower PM10 showed increased growth in lung function and subjects who moved to communities with a higher PM10 showed decreased growth in lung function. A stronger trend was found for subjects who had migrated at least 3 yr before the follow-up visit than for those who had moved in the previous 1 to 2 yr. We conclude that changes in air pollution exposure during adolescent growth years have a measurable and potentially important effect on lung function growth and performance.
Article
In extreme situations, air pollution episodes cause widespread public apprehension and are associated with measurable effects on health. Air pollution is usually the direct or indirect consequence of burning fuel for transport, industry, or domestic use, but may also come from other sources such as forest fires or volcanic eruptions. Episodes of pollution from the burning of fuel tend to occur not because of an increase in emissions, but because stagnant weather conditions impair their dispersal. In the developed world, episodes that occurred in the postwar decades are unlikely to be repeated, but there remains the risk of less severe episodes and of other disasters such as forest fires and volcanic eruption. Episodes give information about the effects of pollution mixtures in different contexts. Unfortunately, this heterogeneity has not been successfully exploited for identifying the most harmful constituents of pollution or for investigating exposure-response relationships. The epidemiological principles of investigating episodes are straightforward, but in practice, there are many difficulties and assumptions that make comparison of different studies or meta-analysis very difficult.
Article
In order to assess exposure to air pollution from traffic of subjects living near motorways, traffic related air pollutants were measured indoors and outdoors in six city districts near motorways in the West of the Netherlands. Outdoor measurements of PM10, PM2.5, black smoke and benzene were conducted at four different distances from the roadside in two of the six city districts. NO2 was measured in all city districts. Indoor concentrations of PM10 and NO2 were measured in 12 schools in the same six city districts. Reflectance of indoor PM10 filters was measured to get an impression of black smoke concentrations indoors. Outdoor concentrations of black smoke and NO2 declined with distance from the roadside. No gradient was found for PM10, PM2.5 and benzene. The gradients for NO2 and black smoke were curvilinear and more evident in periods that the city districts had been downwind from the motorway for at least 33% of the time. PM10 concentrations in schools were high compared to outdoor concentrations and were not correlated with distance of the school from the motorway, traffic intensity and percentage of time downwind. Indoor black smoke concentrations were significantly correlated with truck traffic intensity and percentage of time downwind. NO2 concentrations in classrooms were significantly correlated with car and total traffic intensity, percentage of time downwind and distance of the school from the motorway.
Article
We assessed the contributions of particulate matter with aerodynamic diameters less than or equal to 10 and less than or equal to 2.5 mu m (PM2.5 and PM10) and ozone (O-3) to peak expiratory flow (PEF) and respiratory symptoms in 40 schoolchildren 8-11 years of age for 59 days during three periods in 1991 at a school in southwest Mexico City. We measured peak expiratory flow in the morning on the children's arrival at school and in the afternoon before their departure from school. Separately for morning and afternoon, we normalized each child's daily measurement of peak flow by subtracting his or her mean peak flow from the daily measurement. Child-specific deviations were averaged to obtain a morning and afternoon mean deviation (Delta PEF) for each day. Mean 24-hour O-3 level was 52 parts per billion (ppb; maximum 103 ppb); mean 24-hour PM2.5 and PM10 were 30 mu g/m(3) (maximum 69 mu g/m(3)) and 49 mu g/m(3) (maximum 81 mu g/m(3)), respectively. We adjusted moving average and polynomial distributed lag multiple regression analyses of Delta PEF us pollution for minimum daily temperature, trend, and season. We examined effects of PM2.5, PM10, and O-3, on Delta PEF separately and in joint models. The models indicated a role for both particles and O-3 in the reduction of peak expiratory flow, with shorter lags between exposure and reduction in peak expiratory flow for O-3 than for particle exposure (0-4 vs 4-7 days). The joint effect of 7 days of exposure to the interquartile range of PM2.5 (17 mu g/m(3)) and O-3 (25 ppb) predicted a 7.1% (95% confidence interval = 11.0-3.9) reduction in morning peak expiratory flow. Pollutant exposure also predicted higher rates of phlegm; colinearity between pollutants limited the potential to distinguish the relative contribution of individual pollutants. In an area with chronically high ambient O-3 levels, school children responded with reduced lung function to both O-3 and particulate exposures within the previous 1 to 2 weeks.