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Abstract

Over the past 250 years-since the Industrial Revolution accelerated the process of pollutant emission, which, until then, had been limited to the domestic use of fuels (mineral and vegetal) and intermittent volcanic emissions-air pollution has been present in various scenarios. Today, approximately 50% of the people in the world live in cities and urban areas and are exposed to progressively higher levels of air pollutants. This is a non-systematic review on the different types and sources of air pollutants, as well as on the respiratory effects attributed to exposure to such contaminants. Aggravation of the symptoms of disease, together with increases in the demand for emergency treatment, the number of hospitalizations, and the number of deaths, can be attributed to particulate and gaseous pollutants, emitted by various sources. Chronic exposure to air pollutants not only causes decompensation of pre-existing diseases but also increases the number of new cases of asthma, COPD, and lung cancer, even in rural areas. Air pollutants now rival tobacco smoke as the leading risk factor for these diseases. We hope that we can impress upon pulmonologists and clinicians the relevance of investigating exposure to air pollutants and of recognizing this as a risk factor that should be taken into account in the adoption of best practices for the control of the acute decompensation of respiratory diseases and for maintenance treatment between exacerbations.
J Bras Pneumol. 2012;38(5):643-655
Air pollution and the respiratory system*
A poluição do ar e o sistema respiratório
Marcos Abdo Arbex, Ubiratan de Paula Santos,
Lourdes Conceição Martins, Paulo Hilário Nascimento Saldiva,
Luiz Alberto Amador Pereira, Alfésio Luis Ferreira Braga
Abstract
Over the past 250 years—since the Industrial Revolution accelerated the process of pollutant emission, which,
until then, had been limited to the domestic use of fuels (mineral and vegetal) and intermittent volcanic
emissions—air pollution has been present in various scenarios. Today, approximately 50% of the people in
the world live in cities and urban areas and are exposed to progressively higher levels of air pollutants. This
is a non-systematic review on the different types and sources of air pollutants, as well as on the respiratory
effects attributed to exposure to such contaminants. Aggravation of the symptoms of disease, together with
increases in the demand for emergency treatment, the number of hospitalizations, and the number of deaths,
can be attributed to particulate and gaseous pollutants, emitted by various sources. Chronic exposure to air
pollutants not only causes decompensation of pre-existing diseases but also increases the number of new cases
of asthma, COPD, and lung cancer, even in rural areas. Air pollutants now rival tobacco smoke as the leading
risk factor for these diseases. We hope that we can impress upon pulmonologists and clinicians the relevance
of investigating exposure to air pollutants and of recognizing this as a risk factor that should be taken into
account in the adoption of best practices for the control of the acute decompensation of respiratory diseases
and for maintenance treatment between exacerbations.
Keywords: Respiratory System; Air pollution; Pregnancy; Pulmonary disease, chronic obstructive; Asthma;
Respiratory tract Infections.
Resumo
A poluição atmosférica encontra-se presente nos mais diferentes cenários ao longo dos últimos 250 anos, desde
que a Revolução Industrial acelerou o processo de emissão de poluentes que, até então, estava limitado ao uso
doméstico de combustíveis vegetais e minerais e às emissões vulcânicas intermitentes. Hoje, aproximadamente 50%
da população do planeta vivem em cidades e aglomerados urbanos e estão expostas a níveis progressivamente
maiores de poluentes do ar. Este estudo é uma revisão não sistemática sobre os diferentes tipos e fontes de
poluentes do ar e os efeitos respiratórios atribuídos à exposição a esses contaminantes. Podem ser creditados
aos poluentes particulados e gasosos, emitidos por diferentes fontes, aumentos nos sintomas de doenças, na
procura por atendimentos em serviços de emergência e no número de internações e de óbitos. Mais do que
descompensar doenças pré-existentes, exposições crônicas têm ajudado a aumentar o número de casos novos
de asma, de DPOC e de câncer de pulmão, tanto em áreas urbanas quanto em áreas rurais, fazendo com
que os poluentes atmosféricos rivalizem com a fumaça do tabaco pelo papel de principal fator de risco para
estas doenças. Na rotina de clínicos e pneumologistas, esperamos contribuir para consolidar a importância da
investigação sobre a exposição aos poluentes do ar e o reconhecimento de que esse fator de risco merece ser
levado em conta na adoção da melhor terapêutica para o controle das descompensações agudas das doenças
respiratórias e para a sua manutenção entre as crises.
Descritores: Sistema respiratório; Poluição do ar; Gravidez; Doença pulmonar obstrutiva crônica; Asma;
Infecções respiratórias.
* Study carried out at the Center for Environmental Epidemiology Studies, Air Pollution Laboratory, Department of Pathology,
University of São Paulo School of Medicine, São Paulo, Brazil.
Correspondence to: Marcos Abdo Arbex. Rua Dr. Arnaldo, 455, sala 1304, CEP 01246-903, São Paulo, SP, Brasil.
Tel. 55 11 3061-8530 or 55 16 9714-2882. Email: arbexma@techs.com.br
Financial support: None.
Submitted: 23 July 2012. Accepted, after review: 22 August 2012.
Review Article
644 Arbex MA, Santos UP, Martins LC, Saldiva PHN, Pereira LAA, Braga ALF
J Bras Pneumol. 2012;38(5):643-655
atmosphere, whereas secondary pollutants result
from chemical reactions among primary pollutants.
The major primary pollutants monitored by
the major environmental agencies in Brazil and
worldwide are nitrogen oxides (NO2 or NOx), volatile
organic compounds (VOCs), carbon monoxide
(CO), and sulfur dioxide (SO2). One example of
a secondary pollutant is ozone (O3), formed by
the photo-oxidation-induced chemical reaction
of VOCs and NO2 in the presence of ultraviolet
rays from sunlight.(6,7)
The most studied pollutant is PM, which can
be primary or secondary. It varies in number, size,
shape, surface area, and chemical composition
depending on its place of production and its
emission source. The deleterious effects of PM on
human health depend on PM size and chemical
composition. The multiple chemical components
of PM include a core of elemental or organic
carbon; inorganic compounds, such as sulfates
and nitrates; transition metal oxides; soluble salts;
organic compounds, such as polycyclic aromatic
hydrocarbons; and biological materials, such as
pollen, bacteria, spores, and animal remains. On
the basis of total suspended particle size, PM is
classified as follows: constituent particles of up
to 30 µm in diameter; constituent particles of
less than 10 µm in diameter (PM
10
or inhalable
fraction); constituent particles of less than 2.5 µm
in diameter (PM
2.5
or fine PM); and constituent
particles of less than 10 nm in diameter (PM0.1
or ultrafine PM).(6,7)
Chart 1 shows the major pollutants monitored
by environmental protection agencies in urban
areas, as well as their sources, their sites of action
in the respiratory system, and their effects on
human health.
How air pollutants affect the
respiratory system
Several mechanisms have been suggested
to explain the adverse effects of air pollutants.
The most consistent and most widely accepted
explanation is that, once in contact with the
respiratory epithelium, high concentrations of
oxidants and pro-oxidants in environmental
pollutants such as PM of various sizes and
compositions and in gases such as O3 and
nitrogen oxides cause the formation of oxygen
and nitrogen free radicals, which in turn induce
oxidative stress in the airways. In other words, an
increase in free radicals that are not neutralized
Introduction
Although the effects of pollution had been
described since antiquity, pollution began to
have a major impact on the population with the
advent of the Industrial Revolution. The rapid
urbanization seen worldwide brought about a
large increase in energy consumption and in
pollutant emissions from stationary fossil fuel
burning sources, such as industries, and from
mobile sources, such as motor vehicles. Currently,
approximately 50% of the people in the world
live in cities and urban areas and are exposed
to progressively higher levels of air pollutants.
(1)
The other half, especially in developing countries,
uses solid fuels derived from biomass (wood,
charcoal, dried animal dung, and agricultural
residues) and, to a lesser extent, liquid fuels,
as a source of energy for cooking, heating, and
lighting.(1,2)
Because of the large contact area between
the surface of the respiratory system and the
environment, air quality directly affects respiratory
health. In addition, a significant quantity of
inhaled pollutants reach the systemic circulation
through the lungs and can cause deleterious
effects on various organs and systems.(3)
Global estimates suggest that external
environmental pollution (outdoor pollution) causes
1.15 million deaths worldwide (corresponding to
nearly 2% of the total number of deaths) and is
responsible for 8.75 million disability-adjusted
life years,
(4)
whereas pollution inside homes causes
approximately 2 million premature deaths and
results in 41 million disability-adjusted life years.
(5)
For Brazil, the World Health Organization
has estimated that air pollution causes nearly
20,000 deaths/year, a value that is five times as
high as the estimated number of deaths from
environmental/passive smoking, and that indoor
air pollution leads to 10,700 deaths/year.(4,5)
Air pollution: sources, site of action,
and pathophysiology
Air pollution is a mixture of particles—
particulate matter (PM)—and gases released
into the atmosphere mainly by industries, motor
vehicles, and thermoelectric power plants, as
well as from biomass and fossil fuel burning.
Pollutants can be classified as primary or secondary.
Primary pollutants are released directly into the
Air pollution and the respiratory system
J Bras Pneumol. 2012;38(5):643-655
645
Chart 1 - Major air pollutants, their sources, their sites of action in the respiratory system, and their effects
on human health.
Pollutants Source Penetration into the
respiratory system Pathophysiology
TSP Anthropogenic sources: street
dust; road dust; agricultural
activities; and construction
activities. Natural sources: sea salt;
pollen; spores; fungi; and volcanic
ash.
Nose and throat It impairs mucociliary and macrophage
activity. It causes airway irritation.
It induces oxidative stress and,
consequently, pulmonary and systemic
inflammation. Chronic exposure causes
bronchial remodeling and COPD. It can
be carcinogenic.
PM
10
Trachea, bronchi, and
bronchioles
PM
2.5
Burning of fossil fuels and
biomass; thermoelectric power
plants
Alveoli
PM
0.1
Alveoli, lung tissue,
and bloodstream
O
3
It is not emitted directly into
the atmosphere. It is produced
by complex chemical reactions
between volatile organic
compounds (VOCs) and nitrogen
oxides (NO
x
) in the presence of
sunlight. Sunlight and temperature
stimulate such reactions, so
that, on hot sunny days, O
3
concentrations peak.
The sources of VOC and NO
x
emissions are vehicles, chemical
industries, laundries, and activities
that use solvents.
Trachea, bronchi,
bronchioles, and
alveoli
It is a photochemical oxidant that
is extremely irritating. It induces
respiratory tract mucosal inflammation.
At high concentrations, it irritates
the eyes, the nasal mucosa, and
the oropharynx. It causes cough
and chest discomfort. Exposure for
several hours produces damage to the
epithelium lining the airways. It induces
inflammation and airway obstruction in
the presence of stimuli such as cold and
exercise.
NO
x
, NO
2
Anthropogenic sources: nitric acid;
sulfuric acid; and combustion
engine industries (major source);
fuel burning at high temperatures,
in thermal power plants that
use gas or incineration. Natural
sources: electrical discharges in the
atmosphere.
Trachea, bronchi,
bronchiole, and
alveoli
An irritant. It affects the mucosa of the
eyes, nose, throat, and lower respiratory
tract. It increases bronchial reactivity
and increases susceptibility to infections
and allergens. It is considered a good
marker of vehicular pollution.
SO
2
Anthropogenic sources: petroleum
refineries; diesel vehicles; furnaces;
metallurgy; and papermaking.
Natural sources: volcanic activity.
Upper airways,
trachea, bronchi, and
bronchioles
An irritant. It affects the mucosa of
the eyes, nose, throat, and respiratory
tract. It causes cough and increases
bronchial reactivity, facilitating
bronchoconstriction.
CO Anthropogenic sources: forest
fires; incomplete combustion
of fossil fuels or other organic
materials; and road transportation.
Urban areas with heavy traffic are
the major contributing source of
CO emissions.
Natural sources: volcanic eruptions
and chlorophyll decomposition.
Alveoli and
bloodstream
It binds to hemoglobin, interfering
with oxygen transport. It causes
headache, nausea, and dizziness. It
has a deleterious effect on the fetus.
It is associated with low birth weight
neonates and fetal death.
TSP: total suspended particles; PM: particulate matter; PM
10
: PM of less than10 µm in diameter; PM
2.5
: PM of less than
2.5 µm in diameter; and PM0.1: PM of less than 0.1 µm in diameter. Adapted from Kunzli et al.(6)
646 Arbex MA, Santos UP, Martins LC, Saldiva PHN, Pereira LAA, Braga ALF
J Bras Pneumol. 2012;38(5):643-655
Individuals with pre-existing chronic
diseases
The third most susceptible group, regardless of
age, comprises individuals with pre-existing chronic
diseases affecting mainly the respiratory system
(asthma, COPD, and fibrosis) or the circulatory
system (arrhythmias, hypertension, and ischemic
heart diseases), as well as those with chronic
diseases such as diabetes and collagen diseases.
(3)
Genetic susceptibility
The production of free radicals and the
induction of inflammatory response by pollutants
in the respiratory system can be neutralized by
the antioxidant agents present in the aqueous
layer lining the respiratory epithelium—glutathione
S-transferase (GST), superoxide dismutase, catalase,
tocopherol, ascorbic acid, and uric acid—which
can prevent oxidative stress and represent the
first line of defense against the adverse effects of
pollutants.
(11)
Of the antioxidant agents present
in the respiratory epithelium, GST is considered
the most important(11) and is represented by three
major classes of enzymes: GSTM1; GSTP1; and
GSTT1.(11)
Polymorphisms in genes encoding the enzymes
of the GST family can change the expression
or function of these enzymes in the lung tissue
and result in different responses to inflammation
and oxidative stress and, consequently, in
increased susceptibility to the adverse effects
of air pollutants.(11) Studies conducted in Mexico
showed that children with asthma with a deletion
polymorphism of genes encoding the GSTM1 and
GSTP1 enzymes had increased susceptibility to
O
3
exposure, this increased susceptibility being
characterized by an increase in biomarkers of
nasal inflammation, reduced peak expiratory
flow, and increased dyspnea.(12,13)
Effects of air pollution during
pregnancy
Exposure to air pollutants during pregnancy can
impair fetal development and cause intrauterine
growth retardation, prematurity, low birth weight,
congenital anomalies, and, in cases that are
more severe, intrauterine or perinatal death.(14)
The biological mechanisms underlying the
effects of air pollutants during pregnancy
have yet to be fully elucidated. Extensive cell
by antioxidant defenses initiates an inflammatory
response with release of inflammatory cells and
mediators (cytokines, chemokines, and adhesion
molecules) that reach the systemic circulation,
leading to subclinical inflammation, which not
only has a negative effect on the respiratory
system but also causes systemic effects.(6,7)
Latency effects
The effects of pollutants on health can be
acute or chronic. Acute effects are manifest
shortly after exposure (hours or days). Chronic
effects are usually assessed in longitudinal studies
over years or decades.
(8)
Chart 2 summarizes the
acute and chronic effects of pollutants on the
respiratory system.
Susceptible groups
Children
Children are highly susceptible to exposure
to air pollutants. Minute ventilation is higher
in children than in adults because children
have higher basal metabolic rates and engage
in more physical activity than do adults, as well
as because children spend more time outdoors
than do adults. On the basis of body weight,
the volume of air passing through the airways
of a child at rest is twice that of an adult under
similar conditions. Pollutant-induced irritation
producing a weak response in adults can result
in significant obstruction in children. In addition,
the fact that their immune system is not fully
developed increases the possibility of respiratory
infections.(6,7,9)
Elderly individuals
Elderly individuals are susceptible to the
adverse effects of exposure to air pollutants
because they have a less efficient immune
system (immunosenescence) and a progressive
decline in pulmonary function that can lead
to airway obstruction and exercise limitation.
There is decreased chest wall compliance and
lung hyperinflation requiring additional energy
expenditure to perform respiratory movements,
as well as functional decline of organ systems.
(10)
Air pollution and the respiratory system
J Bras Pneumol. 2012;38(5):643-655
647
and fetal prematurity associated with higher levels
of traffic-generated NOx and PM2.5.(19)
Effects of pollutants on the
respiratory system
Effects on respiratory symptoms
Epidemiological studies have shown that
exposure to gaseous pollutants and PM is
associated with a higher incidence of upper
airway symptoms, such as rhinorrhea, nasal
obstruction, cough, laryngospasm, and vocal
fold dysfunction,
(20)
and lower airway symptoms,
such as cough, dyspnea, and wheezing, especially
in children.(21) This exposure is also associated
with an increase in cough and wheezing in adults
with chronic lung disease and in healthy adults.
(21)
Effects on pulmonary function
Pulmonary function is an important marker
of the effects of air pollution on the exposed
proliferation, physiological immaturity, accelerated
organ development, and changes in metabolism
increase fetal susceptibility to maternal inhalation
of air pollutants, and the maternal respiratory
system can, in turn, be compromised by the
action of pollutants, thereby affecting placental
transport of oxygen and glucose.(15) In addition,
pollutants can affect maternal blood coagulation
because of an inflammatory response resulting
from oxidative stress, increasing the possibility
of placental infarction and chronic villitis.(16)
A meta-analysis of studies published between
1994 and 2003 revealed that a 10-µg/m
3
increase
in PM
10
exposure was associated with a 5% increase
in postnatal mortality from all causes and a 22%
increase in mortality from respiratory diseases.
(17)
A study conducted in São Paulo, Brazil, revealed
that a 1-µg/m3 increase in PM10 concentration
and a 1-ppm increase in CO concentration were
associated with a 0.6-g and a 12-g reduction in
birth weight, respectively.
(18)
A study conducted
in California, USA, and evaluating 81,186 births
found an increased risk of maternal preeclampsia
Chart 2 - Acute and chronic effects of pollutants on the respiratory system.
Effects of acute exposure (hours and days after increasing pollution)
Increased mortality
Symptom exacerbation in individuals with COPD or asthma
Increased mortality from respiratory diseases
Higher frequency of acute respiratory infections
Increased number of hospitalizations for pneumonia
Increased prevalence of symptoms and signs of eye, nose, and throat irritation
Increased prevalence of acute respiratory symptoms (wheezing, cough, and expectoration)
Need for increasing the dose of medication
Acute changes in pulmonary function
Increased number of medical visits, emergency room visits, and hospitalizations
Higher rates of work and school absenteeism
Effects of chronic exposure (years of chronic exposure)
Increased mortality from respiratory diseases
Increased incidence and prevalence of asthma and COPD
Increased incidence of and mortality from lung cancer
Increased incidence of and mortality from pneumonia and influenza
Chronic changes in pulmonary function
Chronic reduction in FEV
1
and FVC
Impaired lung development in children and youths
Increased prevalence of below-normal FEV
1
Increased rate of decline in FEV
1
Other effects
Low birth weight
Preterm delivery
Changes in the cognitive development of children
Adapted from Kunzli et al.(6)
648 Arbex MA, Santos UP, Martins LC, Saldiva PHN, Pereira LAA, Braga ALF
J Bras Pneumol. 2012;38(5):643-655
with those residing in less polluted areas. The
effects were significant even in children without
bronchial asthma. The proportion of children with
an FEV1 < 80% at age 18 years was five times
higher in more polluted communities than in less
polluted communities (mean PM
2.5
concentrations
of 29.0 µg/m3 and 6.0 µg/m3, respectively).(24)
Those same authors investigated pulmonary
function in 3,677 individuals, who were followed
over an 8-year period (between ages 10 and
18 years) and who lived within 500 m or 1,500 m of
a high-traffic road. At age 18 years, the adolescents
living closer to the high-traffic road showed
an 81.0-mL deficit in FEV1 and a 127.0-mL/s
deficit in FEF
25-75%
when compared with those
living farther away.(25)
A cross-sectional study conducted in Germany
evaluated 2,593 women (mean age, 54.5 years) in
7 communities. Levels of NO
2
and PM
10
showed
significant negative associations with FEV
1
, FVC,
and FEV
1
/FVC. An annual increase of 7.0 µg/m
3
in PM
10
was associated with a 5.0% reduction in
FEV
1
and a 1.0% reduction in FEV
1
/FVC, and, for
an annual increase of 16.0% in NO
2
, there was
a 4.0% reduction in FEV1 and a 1.0% reduction
in FEV1/FVC.(26)
A prospective study conducted in Switzerland
evaluated 4,742 adults in the 18-60 year age
bracket in 8 communities over an 11-year period.
Over the study period, there was a mean drop
of 5.3 µg/m3 in PM10 levels. A 10-µg/m3 decline
in the mean annual PM
10
concentration was
associated with statistically significant reductions
in the annual rates of decline in FEV1 (of 9%),
FEF25-75% (of 16%), and FEV1/FVC (of 6%).(27)
Pollution and bronchial asthma
Epidemiological and toxicological studies
have demonstrated the association between air
pollution and bronchial asthma.
(21)
Air pollutants
are associated with an increase in the number of
emergency room visits and hospitalizations for
acute asthma attacks, as well as with an increase
in expiratory wheezing, respiratory symptoms,
and use of rescue medication.(21)
The prevalence of bronchial asthma has
increased worldwide, especially in highly
industrialized urban areas. Prospective studies
suggest that exposure to air pollutants can lead
to the development of new cases of asthma.
One example of this is the large increase in the
incidence of asthma in China after the recent
population, as well as being an early, objective,
and quantitative predictor of cardiorespiratory
morbidity and mortality. Studies have demonstrated
the acute and chronic effects of pollutants on
pulmonary function in children, adolescents,
healthy adults, and individuals with a history
of respiratory disease.(6,7)
Effects associated with acute exposure
Chang et al.
(22)
investigated the effects of
variations in daily concentrations of PM10, SO2,
CO, and NO2 on the pulmonary function of
2,919 students in the 12-16 year age bracket
in the city of Taipei, Taiwan. A 1-ppm increase in
CO concentration was associated with a 69.8-mL
reduction in FVC (95% CI: −115.0 to −24.4) and
a 73.7-mL reduction in FEV
1
(95% CI: −118.0 to
−29.7), with a 1-day lag effect. A 1-ppb increase in
SO
2
concentration was associated with a 12.9-mL
reduction in FVC (95% CI: −20.7 to −5.1) and
an 11.7-mL reduction in FEV
1
(95% CI: −19.3 to
−4.2), also with a 1-day lag effect. Variations
in O3 and PM10 concentrations showed a small
but significant negative association with FVC
and FEV1 on the day of exposure.
A study conducted in London, England,
compared pulmonary function parameters in
60 adults with mild or moderate asthma on
two different occasions: after a two-hour walk
along Oxford Street, the city’s main commercial
corridor, where only diesel-powered buses and
taxis are allowed; and after a two-hour walk
through Hyde Park (a city park). At the time of
the study, PM
2.5
and NO
2
levels were, respectively,
3.0 and 6.5 times higher on Oxford Street than
in Hyde Park. There was a 6.1% reduction in
FEV
1
(p = 0.04) and a 5.4% reduction in FVC
(p = 0.001) after exposure on Oxford Street in
relation to exposure in Hyde Park.(23)
Effects associated with chronic
exposure
Gauderman et al. conducted a prospective
study following 1,759 children in the 10-18 year
age bracket in 12 communities in California,
USA, with different levels of NO
2
, acid vapor,
PM
2.5
, and elemental carbon. After controlling
for confounding factors, the authors found that
children residing in areas with higher environmental
levels of PM showed a significant decline in
FEV
1
(of approximately 100 mL) when compared
Air pollution and the respiratory system
J Bras Pneumol. 2012;38(5):643-655
649
of asthma-related visits to the emergency rooms
of the city among individuals of all ages.(33)
During the Olympic Games in Beijing, PM
2.5
and
O3 concentrations decreased from 78.8 µg/m3
to 46.7 µg/m
3
and from 65.8 ppb to 61 ppb,
respectively, and the number of asthma-related
emergency rooms visits decreased by 41.6%.(34)
Effects associated with chronic
exposure
In a prospective study conducted in
12 communities with different O3 levels in
California, USA, 3,535 schoolchildren with no
history of asthma were followed over a 5-year
period. In the follow-up period, 265 children
developed asthma. In communities with high O
3
concentrations, the risk of developing asthma was
3.3 times higher (95% CI: 1.9-5.8) in children
who played three or more sports than in those
who did not play any sports. In areas with low O3
concentrations, the number of sports played was
not a risk factor for the development of asthma.
The same was true for time spent outdoors,
which was shown to be a direct risk factor for
the development of asthma only in areas with
high O3 concentrations.(35)
Ghering et al. followed the first 8 years of life
of 3,863 children in communities in the north,
west, and center of the Netherlands. At age
8 years, the children underwent allergy testing
and bronchial hyperresponsiveness testing. Levels
of PM
2.5
were associated with a 28% increase
in the incidence of asthma, a 29% increase in
the prevalence of asthma, and a 15% increase
in asthma symptoms.(36)
In Munich, Germany, 2,860 children were
followed from birth to age 4 years and 3,061
were followed to age 6 years. The authors
categorized residential distance to a main road
as follows: < 50 m; 50-250 m; 250-1,000 m;
and > 1,000 m. The study showed significant
inverse associations between residential distance
to a main road and the outcomes analyzed.
Among those living less than 50 m from a main
road, the highest ORs were for asthma (OR = 1.6;
95% CI: 1.03-2.37), hay fever (OR = 1.6; 95%
CI: 1.1-2.3), and allergic sensitization to pollen
(OR = 1.4; 95% CI: 1.2-1.6).(37)
A cohort study conducted in Switzerland
between 1991 and 2002 and evaluating
2,725 nonsmoking adults in the 18-60 year age
bracket showed that those living in more polluted
industrial development and, consequently, the
large increase in the concentration of pollutants.
(28)
Effects associated with acute exposure
In Athens, Greece, one group of researchers
investigated the acute effects of PM10 and SO2
exposure on the number of emergency room visits
by children and adolescents in the 0-14 year age
bracket between 2001 and 2004. A 10-µg/m
3
increase in PM10 and SO2 levels was associated
with a 2.2% increase (95% CI: 0.1-5.1) and a
6.0% increase (95% CI: 0.9-11.3), respectively,
in the number of asthma-related visits.(29)
A study involving children and adolescents
in the 0-18 year age bracket and conducted in
Copenhagen, Denmark, between 2001 and 2008,
revealed an increase in the number of asthma-
related hospitalizations due to increased levels
of NO
x
(OR = 1.11; 95% CI: 1.05-1.17), NO
2
(OR = 1.10; 95% CI: 1.04-1.16), PM
10
(OR = 1.07;
95% CI: 1.03-1.12), and PM
2.5
(OR = 1.09; 95%
CI: 1.04-1.13).(30)
An association between increased pollutant
levels and hospitalizations for asthma has been
observed in the city of Araraquara, located in
the center of the sugarcane-producing area of
the state of São Paulo, Brazil. During the harvest
period, when sugarcane straw burning is the
largest pollutant emission source, the number
of hospitalizations for asthma was 50% higher
than was that during the period when there is no
burning (p < 0.001). A 10-µg/m
3
increase in the
concentrations of PM of up to 30 µm in diameter
was associated with an 11.6% increase in the
number of hospitalizations (95% CI: 5.4-17.7),
with a 1-day lag effect.(31)
A study conducted in the city of Rio Branco,
Brazil, showed that, in the forest biomass
burning season, the number of asthma-related
visits among children under 10 years of age
increased in parallel with the increase in PM2.5
concentrations measured in the city.(32)
During the Olympic Games in Atlanta,
USA, measures to reduce urban pollution were
implemented. During the three weeks of games,
traffic counts dropped around 22%. Peak daily
levels of O
3
, NO
2
, CO, and PM
10
decreased 28%,
7%, 19%, and 17%, respectively, in comparison
with the three weeks before and the three weeks
after the Games. There was a 40% reduction in
the number of consultations for asthma among
children and an 11-19% decline in the number
650 Arbex MA, Santos UP, Martins LC, Saldiva PHN, Pereira LAA, Braga ALF
J Bras Pneumol. 2012;38(5):643-655
as being more pronounced in the winter than
in the summer.(40)
A study conducted between 1986 and 1999
and involving 36 American cities showed that
a 5-ppb increase in O
3
levels and a 10-µg/m
3
increase in PM
10
levels were associated with an
increase of 0.27% (95% CI: 0.1-0.5) and 1.5%
(95% CI: 0.9-2.0), respectively, in the number
of hospitalizations for COPD. Use of central air
conditioning was found to reduce the adverse
effects of air pollution.(41)
A study conducted between 2001 and 2003
in city of São Paulo, Brazil, and evaluating
1,769 patients over 40 years of age showed
that an increase in the number of COPD-related
emergency room visits was associated with increases
in air concentrations of PM
10
and SO
2
. Variations
in PM
10
and SO
2
concentrations (28.2 µg/m
3
and
7.8 µg/m
3
, respectively) were associated with
a cumulative 6-day increase of 19% and 16%
in COPD admissions, respectively. A 10-µg/m3
increase in PM10 concentration was associated
with a 6.7% increase in the number of visits on
the day of exposure.(42)
Effects of chronic exposure
Schikowski et al. followed 4,757 women in
the 54-55 year age bracket in Germany, using
diagnostic criteria for COPD established by the
Global Initiative for Chronic Obstructive Lung
Disease. The prevalence of COPD (stages I-IV)
was found to be 4.5 %. A 7-µg/m
3
increase in the
5-year mean PM
10
concentration was associated
with a 1.33 OR (95% CI: 1.03-1.72) for the
development of COPD and a 5.1% decline in
FEV
1
(95% CI: 2.5-7.7). Women living less that
100 m from a high-traffic road were at a higher
risk of developing COPD than were those living
farther away (OR = 1.8; 95% CI: 1.1-3.0).
(26)
Those authors suggest that chronic exposure
to traffic-generated PM10 increases the risk of
developing COPD and accelerates pulmonary
function loss.
A study conducted in Denmark followed
57,053 individuals between 1993 and 2004
and showed that 1,786 (3.4%) developed
COPD. The authors found a positive association
between COPD and exposure to traffic-generated
pollutants after controlling for confounding
factors, including smoking. The incidence of
COPD was associated with the 35-year NO
2
mean
areas were at a higher risk of developing asthma
(a 30% increase in risk for every 1-µg/m
3
increase
in the concentration of traffic-generated PM10).(38)
Pollution and COPD
Patients with COPD are particularly vulnerable
to additional stress on the airways caused by
aggressive agents. Smoking is recognized as the
most important factor for the development of
COPD, especially in developed countries. However,
over the last 10 years, an increasing number of
studies have suggested that there are risk factors
other than smoking in the genesis of COPD. These
factors include exposure to indoor and outdoor
air pollutants, occupational exposure to dust and
fumes, history of recurrent respiratory infections
in childhood, history of pulmonary tuberculosis,
chronic asthma, intrauterine growth retardation,
poor nutrition, and low socioeconomic status.
(1)
Exposure to air pollution is associated with
an increase in respiratory morbidity from COPD,
including an increase in respiratory symptoms
and a decrease in pulmonary function, as well as
being a common cause of exacerbations leading
to emergency room visits or hospitalizations.
(39)
Indoor biomass burning is a significant cause of
COPD in nonsmoking women who are exposed to
high concentrations of pollutants during cooking
activities, especially in rural areas of developing
countries, and this significantly contributes to the
global increase in the disease.
(1,2)
While women with
COPD caused by smoking have emphysema and
goblet cell metaplasia more commonly than do
those exposed to biomass burning, the latter group
has more severe interlobular septal thickening,
more pigment deposition in the lung parenchyma,
more small airway fibrosis, and more severe intimal
thickening of the pulmonary artery.(39)
Effects associated with acute exposure
An ecological study conducted in Hong Kong,
China, investigated the association between air
pollutants and hospitalizations for COPD between
2000 and 2004. Significant associations were
observed between hospitalizations for COPD
and levels of pollutants. The relative risk (RR)
of hospitalization for every 10-µg/m
3
increase
in SO
2
, NO
2
, O
3
, PM
10
, and PM
2.5
concentrations
was, respectively, 1.007, 1.026, 1.040, 1.024,
and 1.031. The effect started on the day of
exposure and lasted until the fifth day, as well
Air pollution and the respiratory system
J Bras Pneumol. 2012;38(5):643-655
651
(95% CI: 0.9-8.0) and 2.5% (95% CI: 0.1-4.8),
respectively. Children under 15 years of age
constituted the most susceptible age group.(48)
Belleudi et al. investigated the effects of PM
on the number of hospitalizations for pneumonia
among individuals over 35 years of age admitted
to any of five Roman hospitals between 2001 and
2005. A 10-µg/m
3
increase in PM
2.5
concentration
was associated with a 2.8% increase in the number
of hospitalizations for pneumonia, with a 2-day
lag effect.(49)
Medina-Ramón et al., in a study conducted
between 1986 and 1999 and involving 36 American
cities, showed that, during the hottest period,
a cumulative 2-day increase of 5 ppb in O3
concentration was associated with a 0.41%
increase (95% CI: 0.26-0.57) in the number
of hospitalizations for pneumonia. Similarly, a
10-µg/m
3
increase in PM
10
concentration was
associated with a 0.8% increase in the number
of hospitalizations for pneumonia on the day
of exposure (95% CI: 0.5-1.2).(41)
Effects associated with chronic
exposure
Between 2003 and 2005, Neupane et al.
conducted a case-control study in Canada in
which they investigated long-term exposure to
NO
2
, PM
2.5
, and SO
2
and the risk of hospitalization
for pneumonia in individuals over 65 years of
age. They evaluated 365 elderly individuals with
radiologically confirmed community-acquired
pneumonia and 494 controls. The groups were
compared on the basis of individual exposure
to NO2, PM2.5, and SO2 in the previous year.
Long-term ( 1-year) exposure to high levels
of NO
2
and PM
2.5
was significantly associated
with hospitalization for community-acquired
pneumonia.(50)
A cohort study conducted in the USA showed
that a 10-µg/m³ increase in PM
2.5
concentration
was associated with a 20% increase in the risk
of death from pneumonia and influenza in
nonsmokers.(51)
Pollution and lung cancer
The World Health Organization estimates
that, in 2008, there were 12.7 million new
cases of cancer that caused 7.6 million deaths
worldwide, the number of new cases of lung
cancer and the number of deaths from lung
concentration (RR = 1.08; 95% CI: 1.02-1.14 for
an interquartile range of 5.8 µg/m3).(43)
A meta-analysis of 15 studies showed that
individuals exposed to biomass burning have a 2.4
higher OR (95% CI: 1.9-3.3) for the development
of COPD than do those who were not exposed.(44)
A recent meta-analysis of 25 studies showed that
the risk in women exposed to biomass burning
is similar to that in women who used another
type of fuel (OR = 2.4; 95% CI: 1.5-9.9).(2)
In a meta-analysis, Kurmi et al. showed a
positive association of use of solid fuel with
COPD (OR = 2.8; 95% CI: 1.8-4.0) and chronic
bronchitis (OR = 2.3; 95% CI: 1.9-2.8) when
compared with use of other types of fuels.
(45)
The risk is similar to that reported for smokers
who developed COPD (OR = 2.5) and is higher
than that for individuals who developed COPD
because of passive smoking or alpha-1 antitrypsin
deficiency. On the basis of a comparison of the
1.1 billion smokers with the 3 billion individuals
exposed to high concentrations of pollutants
generated by solid fuel burning, Kodgule & Salvi
hypothesized that the latter exposure is a more
significant risk factor for the development of
COPD.(46)
Pollution and acute respiratory
infection
Acute lower respiratory tract infection is
the leading cause of death in children up to
5 years of age. In this age group, this type
of infection causes 2 million deaths per year.
Half of such deaths are attributed to indoor
exposure to pollutants from solid fuel burning.
(46)
A meta-analysis of 24 studies showed that
indoor exposure to biomass burning increases
the risk of pneumonia in children (OR = 1.8; 95%
CI: 1.5-2.1).
(47)
Similarly, a recent meta-analysis
of 25 studies found a significant and robust
association between indoor biomass burning and
acute respiratory infection in children (OR = 3.5;
95% CI: 1.9-6.4).(2)
Effects associated with acute exposure
Host et al. investigated the association of PM
10
and PM
2.5
concentrations with hospitalization for
respiratory infection in 6 French cities between
2000 and 2003. The excess RR of hospitalization
for respiratory infection for every 10-µg/m
3
increase
in PM10 and PM2.5 concentrations was 4.4%
652 Arbex MA, Santos UP, Martins LC, Saldiva PHN, Pereira LAA, Braga ALF
J Bras Pneumol. 2012;38(5):643-655
equivalent to those resulting from smoking
10 cigarettes/day) and reduces aerobic performance
in athletes.(58)
Although the major recommendations of sports
medicine societies do not include precautions
against exercising in polluted environments,
a recent statement from the American Heart
Association(3) on the effects of pollution
recommends that intensive exercise be avoided
when air quality is unsatisfactory.
A recent review
(60)
investigating the effects
of pollution on athlete performance concluded
that exercising in environments with high levels
of pollutants sharply reduces pulmonary and
vascular function in individuals with asthma
and in healthy individuals, and that long-term
exercise in polluted environments is associated
with reduced pulmonary function and can induce
vascular dysfunction, probably due to systemic
and airway oxidative stress, leading to reduced
exercise performance. In brief, it is recommended
that susceptible individuals (those with asthma,
those with COPD, patients with cardiovascular
disease, elderly individuals, and children) avoid
exercising when air quality is poor.
Final considerations
Exposure to air pollutants poses a risk to
human health as early as in intrauterine life.
Health professionals should recognize the
importance of the effects of pollutants in clinical
practice and properly assess the exposure profile
of patients at home, in the workplace, and in
the region of residence. If it is not possible
to reduce the emission of pollutants in the
short or medium term, it is perfectly possible
to counsel patients regarding the adoption of
preventive measures to reduce the effects of
indoor and outdoor pollutants, reducing the
adverse effects associated with this exposure. In
addition, physicians should, as appropriate, not
only make adjustments to the standard treatment
when increases in air pollutant concentrations
can aggravate pre-existing diseases but also, as
citizens, use their knowledge to promote the
adoption of measures to reduce pollutant levels
in urban and rural areas.
References
1.
Salvi SS, Barnes PJ. Chronic obstructive pulmonary disease
in non-smokers. Lancet. 2009;374(9691):733-43. http://
dx.doi.org/10.1016/S0140-6736(09)61303-9
cancer being 1.61 million and 1.18 million,
respectively.
(52)
Studies have shown the effects
of exposure to pollutants and the development
of lung cancer, which is attributed to the direct
action of carcinogens present in pollution and
to the chronic inflammation induced by such
carcinogens.(7,53)
A prospective study involving 500,000 adults
in 50 states in the USA
(54)
showed that a 14%
increase in the incidence of lung cancer was
associated with a 10-µg/m3 in PM2.5 concentration.
In a study conducted in European countries, 5%
and 7% of the various types of lung cancer in
nonsmokers and former smokers, respectively,
were attributed to the effects of pollution.
(55)
An
analysis of several cohort and case-control studies
suggested that, on average, chronic exposure to
air pollution increases the risk of lung cancer
incidence by 20-30%.(7,56)
Air pollution and mortality
In a review of studies conducted in various
countries and investigating the effects of acute
changes in pollution levels, it was suggested
that a 0.4-1.3% increase in the RR of death is
associated with a 10-µg/m
3
increase in PM
2.5
levels or a 20-µg/m3 increase in PM10 levels.(57)
The largest impact on mortality occurs among
children under 5 years of age (RR = 1.6%) and
among elderly individuals (RR = 2.0%), for every
10-µg/m3 increase in PM10 concentration.(57)
In the USA, the most relevant studies on the
chronic effects of air pollution on mortality have
estimated a 6-17% increase in cardiopulmonary
mortality for a 10-µg/m³ increase in PM2.5 levels.(57)
Effects of air pollution on exercise
Air pollution and physical
exercise - risks and benefits
During aerobic exercise, the inhaled air enters
the airways mostly through the mouth and minute
volume and diffusing capacity increase, facilitating
the penetration of pollutants.(58) The quantity of
ultrafine particles deposited in the respiratory
tract is nearly five times higher during moderate
exercise than at rest and increases as particle
size decreases.(59)
Exercising near a high-traffic road increases
carboxyhemoglobin levels (a 30-min run can
increase carboxyhemoglobin levels to levels
Air pollution and the respiratory system
J Bras Pneumol. 2012;38(5):643-655
653
16.
Kannan S, Misra DP, Dvonch JT, Krishnakumar A.
Exposures to airborne particulate matter and adverse
perinatal outcomes: a biologically plausible mechanistic
framework for exploring potential effect modification by
nutrition. Environ Health Perspect. 2006;114(11):1636-42.
PMid:17107846 PMCid:1665414.
17.
Lacasaña M, Esplugues A, Ballester F. Exposure to
ambient air pollution and prenatal and early childhood
health effects. Eur J Epidemiol. 2005;20(2):183-99.
PMid:15792286. http://dx.doi.org/10.1007/
s10654-004-3005-9
18.
Medeiros A, Gouveia N. Relationship between low
birthweight and air pollution in the city of Sao
Paulo, Brazil [Article in Portuguese]. Rev Saude
Publica. 2005;39(6):965-72. PMid:16341408. http://
dx.doi.org/10.1590/S0034-89102005000600015
19.
Wu J, Ren C, Delfino RJ, Chung J, Wilhelm M, Ritz
B. Association between local traffic-generated air
pollution and preeclampsia and preterm delivery in
the south coast air basin of California. Environ Health
Perspect. 2009;117(11):1773-9. PMid:20049131
PMCid:2801174. http://dx.doi.org/10.1289/ehp.0800334
20.
Shusterman D. The effects of air pollutants and
irritants on the upper airway. Proc Am Thorac
Soc. 2011;8(1):101-5. PMid:21364227. http://dx.doi.
org/10.1513/pats.201003-027RN
21.
Kelly FJ, Fussell JC. Air pollution and airway disease.
Clin Exp Allergy. 2011;41(8):1059-71. PMid:21623970.
http://dx.doi.org/10.1111/j.1365-2222.2011.03776.x
22.
Chang YK, Wu CC, Lee LT, Lin RS, Yu YH, Chen YC. The
short-term effects of air pollution on adolescent lung
function in Taiwan. Chemosphere. 2012;87(1):26-30.
PMid:22189374. http://dx.doi.org/10.1016/j.
chemosphere.2011.11.048
23.
McCreanor J, Cullinan P, Nieuwenhuijsen MJ, Stewart-
Evans J, Malliarou E, Jarup L, et al. Respiratory effects
of exposure to diesel traffic in persons with asthma. N
Engl J Med. 2007;357(23):2348-58. PMid:18057337.
http://dx.doi.org/10.1056/NEJMoa071535
24.
Gauderman WJ, Avol E, Gilliland F, Vora H, Thomas
D, Berhane K, et al. The effect of air pollution on
lung development from 10 to 18 years of age. N Engl
J Med. 2004;351(11):1057-67. Erratum in: N Engl J
Med. 2005;352(12):1276. PMid:15356303. http://dx.doi.
org/10.1056/NEJMoa040610
25.
Gauderman WJ, Vora H, McConnell R, Berhane K, Gilliland
F, Thomas D, et al. Effect of exposure to traffic on
lung development from 10 to 18 years of age: a cohort
study. Lancet. 2007;369(9561):571-7. http://dx.doi.
org/10.1016/S0140-6736(07)60037-3
26.
Schikowski T, Sugiri D, Ranft U, Gehring U, Heinrich
J, Wichmann HE, et al. Long-term air pollution
exposure and living close to busy roads are associated
with COPD in women. Respir Res. 2005;6:152.
PMid:16372913 PMCid:1352358. http://dx.doi.
org/10.1186/1465-9921-6-152
27.
Downs SH, Schindler C, Liu LJ, Keidel D, Bayer-Oglesby
L, Brutsche MH, et al. Reduced exposure to PM10 and
attenuated age-related decline in lung function. N Engl
J Med. 2007;357(23):2338-47. PMid:18057336. http://
dx.doi.org/10.1056/NEJMoa073625
28.
Watts J. Doctors blame air pollution for China’s asthma
increases. Lancet. 2006;368(9537):719-20. http://dx.doi.
org/10.1016/S0140-6736(06)69267-2
2.
Po JY, FitzGerald JM, Carlsten C. Respiratory disease
associated with solid biomass fuel exposure in rural
women and children: systematic review and meta-analysis.
Thorax. 2011;66(3):232-9. PMid:21248322. http://
dx.doi.org/10.1136/thx.2010.147884
3.
Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR,
Bhatnagar A, Diez-Roux AV, et al. Particulate matter
air pollution and cardiovascular disease: An update to the
scientific statement from the American Heart Association.
Circulation. 2010;121(21):2331-78. PMid:20458016.
http://dx.doi.org/10.1161/CIR.0b013e3181dbece1
4.
World Health Organization. Global health risks. Mortality
and burden of disease attributable to selected major
risks. Geneva: World Health Organization; 2009.
5.
Oberg M, Jaakkola MS, Woodward A, Peruga A, Prüss-
Ustün A. Worldwide burden of disease from exposure
to second-hand smoke: a retrospective analysis of data
from 192 countries. Lancet. 2011;377(9760):139-46.
http://dx.doi.org/10.1016/S0140-6736(10)61388-8
6.
Künzli N, Perez L, Rapp R. Air quality and health. Lausanne:
European Respiratory Society; 2010.
7.
World Health Organization. Air quality guidelines.
Global update 2005. Particulate matter, ozone, nitrogen
dioxide and sulfur dioxide. Copenhagen: World Health
Organization; 2005. http://dx.doi.org/10.3201/
eid1110.050644
8.
Braga AL, Zanobetti A, Schwartz J. The lag structure
between particulate air pollution and respiratory and
cardiovascular deaths in 10 US cities. J Occup Environ
Med. 2001;43(11):927-33. PMid:11725331. http://dx.doi.
org/10.1097/00043764-200111000-00001
9.
Salvi S. Health effects of ambient air pollution in children.
Paediatr Respir Rev. 2007;8(4):275-80. PMid:18005894.
http://dx.doi.org/10.1016/j.prrv.2007.08.008
10.
Sharma G, Goodwin J. Effect of aging on respiratory
system physiology and immunology. Clin Interv
Aging. 2006;1(3):253-60. http://dx.doi.org/10.2147/
ciia.2006.1.3.253
11.
Minelli C, Wei I, Sagoo G, Jarvis D, Shaheen S, Burney P.
Interactive effects of antioxidant genes and air pollution
on respiratory function and airway disease: a HuGE review.
Am J Epidemiol. 2011;173(6):603-20. PMid:21343247.
http://dx.doi.org/10.1093/aje/kwq403
12.
Romieu I, Sienra-Monge JJ, Ramírez-Aguilar M, Moreno-
Macías H, Reyes-Ruiz NI, Estela del Río-Navarro B, et al.
Genetic polymorphism of GSTM1 and antioxidant
supplementation influence lung function in relation
to ozone exposure in asthmatic children in Mexico City.
Thorax. 2004;59(1):8-10. PMid:14694237 PMCid:1758856.
13.
Romieu I, Ramirez-Aguilar M, Sienra-Monge JJ, Moreno-
Macías H, del Rio-Navarro BE, David G, et al. GSTM1
and GSTP1 and respiratory health in asthmatic children
exposed to ozone. Eur Respir J. 2006;28(5):953-9.
PMid:16870661. http://dx.doi.org/10.1183/0903193
6.06.00114905
14. Srám RJ, Binková B, Dejmek J, Bobak M. Ambient air
pollution and pregnancy outcomes: a review of the
literature. Environ Health Perspect. 2005;113(4):375-82.
PMid:15811825 PMCid:1278474. http://dx.doi.org/10.1289/
ehp.6362
15.
Ritz B, Wilhelm M. Ambient air pollution and
adverse birth outcomes: methodologic issues
in an emerging field. Basic Clin Pharmacol
Toxicol. 2008;102(2):182-90. PMid:18226073. http://
dx.doi.org/10.1111/j.1742-7843.2007.00161.x
654 Arbex MA, Santos UP, Martins LC, Saldiva PHN, Pereira LAA, Braga ALF
J Bras Pneumol. 2012;38(5):643-655
disease in Hong Kong. Thorax. 2007;62(9):780-5.
PMid:17311838 PMCid:2117326. http://dx.doi.org/10.1136/
thx.2006.076166
41.
Medina-Ramón M, Zanobetti A, Schwartz J. The effect of
ozone and PM10 on hospital admissions for pneumonia
and chronic obstructive pulmonary disease: a national
multicity study. Am J Epidemiol. 2006;163(6):579-88.
PMid:16443803. http://dx.doi.org/10.1093/aje/kwj078
42.
Arbex MA, de Souza Conceição GM, Cendon SP, Arbex
FF, Lopes AC, Moysés EP, et al. Urban air pollution
and chronic obstructive pulmonary disease-related
emergency department visits. J Epidemiol Community
Health. 2009;63(10):777-83. PMid:19468016. http://
dx.doi.org/10.1136/jech.2008.078360
43.
Andersen ZJ, Hvidberg M, Jensen SS, Ketzel M, Loft
S, Sørensen M, et al. Chronic obstructive pulmonary
disease and long-term exposure to traffic-related
air pollution: a cohort study. Am J Respir Crit Care
Med. 2011;183(4):455-61. PMid:20870755. http://dx.doi.
org/10.1164/rccm.201006-0937OC
44.
Hu G, Zhou Y, Tian J, Yao W, Li J, Li B, et al. Risk of
COPD from exposure to biomass smoke: a metaanalysis.
Chest. 2010;138(1):20-31. PMid:20139228.
45.
Kurmi OP, Semple S, Simkhada P, Smith WC, Ayres JG.
COPD and chronic bronchitis risk of indoor air pollution
from solid fuel: a systematic review and meta-analysis.
Thorax. 2010;65(3):221-8. PMid:20335290. http://
dx.doi.org/10.1136/thx.2009.124644
46.
Kodgule R, Salvi S. Exposure to biomass smoke as a cause
for airway disease in women and children. Curr Opin
Allergy Clin Immunol. 2012;12(1):82-90. PMid:22157154.
http://dx.doi.org/10.1097/ACI.0b013e32834ecb65
47. Dherani M, Pope D, Mascarenhas M, Smith KR, Weber
M, Bruce N. Indoor air pollution from unprocessed solid
fuel use and pneumonia risk in children aged under five
years: a systematic review and meta-analysis. Bull World
Health Organ. 2008;86(5):390-398C. PMid:18545742
PMCid:2647443. http://dx.doi.org/10.2471/BLT.07.044529
48.
Host S, Larrieu S, Pascal L, Blanchard M, Declercq
C, Fabre P, et al. Short-term associations between
fine and coarse particles and hospital admissions for
cardiorespiratory diseases in six French cities. Occup
Environ Med. 2008;65(8):544-51. PMid:18056749.
http://dx.doi.org/10.1136/oem.2007.036194
49.
Belleudi V, Faustini A, Stafoggia M, Cattani G, Marconi
A, Perucci CA, et al. Impact of fine and ultrafine particles
on emergency hospital admissions for cardiac and
respiratory diseases. Epidemiology. 2010;21(3):414-23.
PMid:20386174. http://dx.doi.org/10.1097/
EDE.0b013e3181d5c021
50.
Neupane B, Jerrett M, Burnett RT, Marrie T, Arain A,
Loeb M. Long-term exposure to ambient air pollution
and risk of hospitalization with community-acquired
pneumonia in older adults. Am J Respir Crit Care
Med. 2010;181(1):47-53. PMid:19797763. http://dx.doi.
org/10.1164/rccm.200901-0160OC
51.
Pope CA 3rd, Burnett RT, Thurston GD, Thun MJ, Calle EE,
Krewski D, et al. Cardiovascular mortality and long-term
exposure to particulate air pollution: epidemiological
evidence of general pathophysiological pathways of
disease. Circulation. 2004;109(1):71-7. PMid:14676145.
http://dx.doi.org/10.1161/01.CIR.0000108927.80044.7F
52.
Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D.
Global cancer statistics. CA Cancer J Clin. 2011;61(2):69-90.
29.
Samoli E, Nastos PT, Paliatsos AG, Katsouyanni K,
Priftis KN. Acute effects of air pollution on pediatric
asthma exacerbation: evidence of association and
effect modification. Environ Res. 2011;111(3):418-24.
PMid:21296347. http://dx.doi.org/10.1016/j.
envres.2011.01.014
30.
Iskandar A, Andersen ZJ, Bønnelykke K, Ellermann T,
Andersen KK, Bisgaard H. Coarse and fine particles but not
ultrafine particles in urban air trigger hospital admission
for asthma in children. Thorax. 2012;67(3):252-7.
PMid:22156960. http://dx.doi.org/10.1136/
thoraxjnl-2011-200324
31.
Arbex MA, Martins LC, de Oliveira RC, Pereira LA,
Arbex FF, Cançado JE, et al. Air pollution from
biomass burning and asthma hospital admissions in
a sugar cane plantation area in Brazil. J Epidemiol
Community Health. 2007;61(5):395-400. PMid:17435205
PMCid:2465679. http://dx.doi.org/10.1136/
jech.2005.044743
32.
Mascarenhas MD, Vieira LC, Lanzieri TM, Leal AP,
Duarte AF, Hatch DL. Anthropogenic air pollution
and respiratory disease-related emergency room
visits in Rio Branco, Brazil--September, 2005. J Bras
Pneumol. 2008;34(1):42-6. PMid:18278375. http://
dx.doi.org/10.1590/S1806-37132008000100008
33.
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 childhood asthma.
JAMA. 2001;285(7):897-905. PMid:11180733. http://
dx.doi.org/10.1001/jama.285.7.897
34.
Li Y, Wang W, Kan H, Xu X, Chen B. Air quality
and outpatient visits for asthma in adults during
the 2008 Summer Olympic Games in Beijing. Sci Total
Environ. 2010;408(5):1226-7. PMid:19959207. http://
dx.doi.org/10.1016/j.scitotenv.2009.11.035
35.
McConnell R, Berhane K, Gilliland F, London SJ, Islam T,
Gauderman WJ, et al. Asthma in exercising children exposed
to ozone: a cohort study. Lancet. 2002;359(9304):386-91.
Erratum in: Lancet 2002;359(9309):896. http://dx.doi.
org/10.1016/S0140-6736(02)07597-9
36. Gehring U, Wijga AH, Brauer M, Fischer P, de Jongste
JC, Kerkhof M, et al. Traffic-related air pollution
and the development of asthma and allergies
during the first 8 years of life. Am J Respir Crit Care
Med. 2010;181(6):596-603. PMid:19965811. http://
dx.doi.org/10.1164/rccm.200906-0858OC
37.
Morgenstern V, Zutavern A, Cyrys J, Brockow I, Koletzko
S, Krämer U, et al. Atopic diseases, allergic sensitization,
and exposure to traffic-related air pollution in children.
Am J Respir Crit Care Med. 2008;177(12):1331-7.
PMid:18337595. http://dx.doi.org/10.1164/
rccm.200701-036OC
38.
Künzli N, Bridevaux PO, Liu LJ, Garcia-Esteban R,
Schindler C, Gerbase MW, et al. Traffic-related air pollution
correlates with adult-onset asthma among never-smokers.
Thorax. 2009;64(8):664-70. PMid:19359271. http://
dx.doi.org/10.1136/thx.2008.110031
39.
Ko FW, Hui DS. Air pollution and chronic obstructive
pulmonary disease. Respirology. 2012;17(3):395-401.
PMid:22142380. http://dx.doi.
org/10.1111/j.1440-1843.2011.02112.x
40.
Ko FW, Tam W, Wong TW, Chan DP, Tung AH, Lai
CK, et al. Temporal relationship between air pollutants
and hospital admissions for chronic obstructive pulmonary
Air pollution and the respiratory system
J Bras Pneumol. 2012;38(5):643-655
655
Crit Care Med. 2006;173(6):667-72. PMid:16424447
PMCid:2662950. http://dx.doi.org/10.1164/
rccm.200503-443OC
57.
Pope CA 3rd. Mortality effects of longer term exposures
to fine particulate air pollution: review of recent
epidemiological evidence. Inhal Toxicol. 2007;19
Suppl 1:33-8. PMid:17886048. http://dx.doi.
org/10.1080/08958370701492961
58.
Carlisle AJ, Sharp NC. Exercise and outdoor ambient air
pollution. Br J Sports Med. 2001;35(4):214-22. http://
dx.doi.org/10.1136/bjsm.35.4.214
59.
Daigle CC, Chalupa DC, Gibb FR, Morrow PE,
Oberdörster G, Utell MJ, et al. Ultrafine particle
deposition in humans during rest and exercise. Inhal
Toxicol. 2003;15(6):539-52. PMid:12692730. http://
dx.doi.org/10.1080/08958370304468
60.
Rundell KW. Effect of air pollution on athlete health
and performance. Br J Sports Med. 2012;46(6):407-12.
PMid:22267572. http://dx.doi.org/10.1136/
bjsports-2011-090823
Erratum in: CA Cancer J Clin. 2011;61(2):134.
PMid:21296855. http://dx.doi.org/10.3322/caac.20107
53.
Yang W, Omaye ST. Air pollutants, oxidative stress
and human health. Mutat Res. 2009;674(1-2):45-54.
PMid:19013537. http://dx.doi.org/10.1016/j.
mrgentox.2008.10.005
54. Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski
D, Ito K, et al. Lung cancer, cardiopulmonary mortality,
and long-term exposure to fine particulate air pollution.
JAMA. 2002;287(9):1132-41. http://dx.doi.org/10.1001/
jama.287.9.1132
55.
Vineis P, Hoek G, Krzyzanowski M, Vigna-Taglianti
F, Veglia F, Airoldi L, et al. Lung cancers attributable
to environmental tobacco smoke and air pollution in
non-smokers in different European countries: a prospective
study. Environ Health. 2007;6:7. PMid:17302981
PMCid:1803768. http://dx.doi.org/10.1186/1476-069X-6-7
56.
Laden F, Schwartz J, Speizer FE, Dockery DW. Reduction
in fine particulate air pollution and mortality: Extended
follow-up of the Harvard Six Cities study. Am J Respir
About the authors
Marcos Abdo Arbex
Senior Researcher. Center for Environmental Epidemiology Studies, Air Pollution Laboratory, Department of Pathology, University
of São Paulo School of Medicine, São Paulo, Brazil; and Professor of Pulmonology.
Centro Universitário de Araraquara
– Uniara,
Araraquara University Center – School of Medicine, Araraquara, Brazil.
Ubiratan de Paula Santos
Senior Researcher. Center for Environmental Epidemiology Studies, Air Pollution Laboratory, Department of Pathology,
University of São Paulo School of Medicine, São Paulo, Brazil.
Lourdes Conceição Martins
Senior Researcher. Center for Environmental Epidemiology Studies, Air Pollution Laboratory, Department of Pathology,
University of São Paulo School of Medicine, São Paulo, Brazil; and Assistant Professor. Graduate Program in Public Health,
Universidade Católica de Santos
– UNISANTOS, Catholic University of Santos – Santos, Brazil.
Paulo Hilário Nascimento Saldiva
Full Professor. Department of Pathology, University of São Paulo School of Medicine, São Paulo, Brazil.
Luiz Alberto Amador Pereira
Senior Researcher. Center for Environmental Epidemiology Studies, Air Pollution Laboratory, Department of Pathology,
University of São Paulo School of Medicine, São Paulo, Brazil; and Assistant Professor. Graduate Program in Public Health,
Universidade Católica de Santos
– UNISANTOS, Catholic University of Santos – Santos, Brazil.
Alfésio Luis Ferreira Braga
Senior Researcher. Center for Environmental Epidemiology Studies, Air Pollution Laboratory, Department of Pathology,
University of São Paulo School of Medicine, São Paulo, Brazil; and Assistant Professor. Graduate Program in Public Health,
Universidade Católica de Santos
– UNISANTOS, Catholic University of Santos – Santos, Brazil.
... PM is a complex airborne mixture of solids, liquids or mixed-phase particles that vary in number, size, shape, surface area, chemical composition, solubility and origin. PM consists of an inner elemental or organic carbon core with various high molecular weight organic and inorganic chemical pollutants, biological materials and/or heavy metals around the core [16]. The composition of ambient PM differs geographically depending on the predominant source of particles and prevailing weather conditions at any given time. ...
... The inhalation of particulate pollutants targets the natural defence of the lung by increasing epithelial permeability that ultimately leads to epithelial barrier dysfunction [16]. Further, PM damages the airway cilia and reduces their capability to carry out airway clearance and averts the timely elimination of PM from the airway and lungs [77]. ...
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Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder with substantial patient burden and leading cause of death globally. Cigarette smoke remains to be the most recognised causative factor behind COPD pathogenesis. Given the alarming increase in prevalence of COPD amongst non-smokers in recent past, a potential role of air pollution particularly particulate matter (PM) in COPD development has gained much attention of the scientists. Indeed, several epidemiological studies indicate strong correlation between airborne PM and COPD incidence/exacerbations. PM-induced oxidative stress seems to be the major player in orchestrating COPD inflammatory cycle but the exact molecular mechanism(s) behind such a process are still poorly understood. This may be due to the complexity of multiple molecular pathways involved. Oxidative stress-linked mitochondrial dysfunction and autophagy have also gained importance and have been the focus of recent studies regarding COPD pathogenesis. Accordingly, the present review is aimed at understanding the key molecular players behind PM-mediated COPD pathogenesis through analysis of various experimental studies supported by epidemiological data to identify relevant preventive/therapeutic targets in the area.
... The combination of suspended organic and inorganic particles emit various precursors-such as nitrogen oxides (NO x ), sulphur dioxide (SO 2 ), ozone (O 3 ), carbon monoxide (CO), lead, and volatile organic chemical compounds-which is a serious problem faced by developing as well as developed countries [2,4]. According to the World Health Organization (WHO), it is estimated that the presence of the most dangerous particulate matter (PM)-that is particles having a 2.5-micrometre diameter (PM) 2.5 -in the The unwanted gift of the industrial revolution, population explosion, and the rapid expansion of metropolitan areas is air pollution, which is a problem being faced globally, especially in developing countries [10]. Air pollution produces smog and acid rain, which depletes the ozone layer of the atmosphere causes global warming [11]. ...
... Similarly, the PM 2.5 concentration for marble dust areas (Darmangi and Malagori) are 189 µg/m and 195 µg/m 3 , which exceeds the WHO standard limits of 25 µg/m 3 . Additionally, the PM 10 concentration values for the same marble dust areas were calculated as 620 µg/m 3 and 730 µg/m 3 as compared to 50 µg/m 3 recommended values of PM 10 . While the NMD areas (Mattani and Jalozai) were not quite so affected. ...
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All over the world, increasing anthropogenic activities, industrialization, and urbanization have intensified the emissions of various pollutants that cause air pollution. Marble quarries in Pakistan are abundant and there is a plethora of small- and large-scale industries, including mining and marble-based industries. The air pollution caused by the dust generated in the process of crushing and extracting marble can cause serious problems to the general physiological functions of plants and it affects human life as well. Therefore, the objectives of this study were to assess the air quality of areas with marble factories and areas without marble factories, where the concentration of particulate matter in terms of total suspended particles (TSP) was determined. For this purpose, EPAM-5000 equipment was used to measure the particulate levels. Besides this, a spectrophotometer was used to analyze the presence of PM2.5 and PM10 in the chemical composition of marble dust. It was observed that the TSP concentrations in Darmangi and Malagori areas of Peshawar, Pakistan—having marble factories—were 626 µg/m3 and 5321 µg/m3 respectively. The (PM2.5, PM10) concentration in Darmangi was (189 µg/m3, 520 µg/m3) and in Malagori, it was recorded as (195 µg/m3, 631 µg/m3), which was significantly higher than the non-marble dust areas and also exceeded WHO recommended standards. It was concluded that the areas with the marble factories were more susceptible to air pollution as the concentration of TSP was significantly higher than the recommended TSP levels. It is recommended that marble factories should be shifted away from residential areas along with strict enforcement. People should be instructed to use protective equipment and waste management should be ensured along with control mechanisms to monitor particulate levels.
... Several mechanisms underpinning children's susceptibility have been suggested. For example, air pollutants can lead to increased oxidative stress and immune cell recruitment and distal airway inflammation (Schraufnagel et al., 2019;Wu et al., 2018;Arbex et al., 2012), which, in turn, reaches the circulation and causes systemic inflammation (Arbex et al., 2012). ...
... Several mechanisms underpinning children's susceptibility have been suggested. For example, air pollutants can lead to increased oxidative stress and immune cell recruitment and distal airway inflammation (Schraufnagel et al., 2019;Wu et al., 2018;Arbex et al., 2012), which, in turn, reaches the circulation and causes systemic inflammation (Arbex et al., 2012). ...
Article
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Background Evidence from developed countries suggests that fine particulate matter (≤2.5 µm [PM2.5]) contributes to childhood respiratory morbidity and mortality. However, few analyses have focused on resource-limited settings, where much of this burden occurs. We aimed to investigate the cross-sectional associations between annual average exposure to ambient PM2.5 and acute respiratory infection (ARI) in children aged <5 years living in low- and middle-income countries (LMICs). Methods We combined Demographic and Health Survey (DHS) data from 35 countries with gridded global estimates of annual PM2.5 mass concentrations. We analysed the association between PM2.5 and maternal-reported ARI in the two weeks preceding the survey among children aged <5 years living in 35 LMICs. We used multivariable logistic regression models that adjusted for child, maternal, household and cluster-level factors. We also fitted multi-pollutant models (adjusted for nitrogen dioxide [NO2] and surface-level ozone [O3]), among other sensitivity analyses. We assessed whether the associations between PM2.5 and ARI were modified by sex, age and place of residence. Results The analysis comprised 573,950 children, among whom the prevalence of ARI was 22,506 (3.92%). The mean (±SD) estimated annual concentration of PM2.5 to which children were exposed was 48.2 (±31.0) µg/m³. The 5th and 95th percentiles of PM2.5 were 9.8 µg/m³ and 110.9 µg/m³, respectively. A 10 µg/m³ increase in PM2.5 was associated with greater odds of having an ARI (OR: 1.06; 95% CI: 1.05–1.07). The association between PM2.5 and ARI was robust to adjustment for NO2 and O3. We observed evidence of effect modification by sex, age and place of residence, suggesting greater effects of PM2.5 on ARI in boys, in younger children, and in children living in rural areas. Conclusions Annual average ambient PM2.5, as an indicator for long-term exposure, was associated with greater odds of maternal-reported ARI in children aged <5 years living in 35 LMICs. Longitudinal studies in LMICs are required to corroborate our cross-sectional findings, to further elucidate the extent to which lowering PM2.5 may have a role in the global challenge of reducing ARI-related morbidity and mortality in children.
... The effects of air pollution on people have been the subject of research around the world to correlate the photochemical effects of air and health, the respiratory system, and the aggravation of allergic diseases. According to Arbex et al. (2012), the individuals most susceptible to diseases caused by pollutant emissions are children, the elderly, people with chronic diseases, and people with genetic susceptibility. In addition, pollutants can affect the human fetus during pregnancy by causing intrauterine growth retardation, prematurity, low birth weight, and-in the most severe cases-congenital anomalies and intrauterine or perinatal death. ...
... CETESB used beta radiation to determine PM 2.5 and PM 10 , pulse fluorescence to determine SO 2 , chemiluminescence to determine NOx, non-expendable infrared to determine CO, and the ultraviolet method to determine O 3 . The air pollutants emitted monthly with the most impact on the population's health were monitored according to the relationship presented by Arbex et al. (2012) and Santana et al. (2020), as cited by the WHO (2019) and CONAMA (2019). ...
Article
Full-text available
This work aims to obtain an artificial neural network to simulate hospitalizations for respiratory diseases influenced by pollutant gaseous such as CO, PM10, PM2.5, NO2, O3, and SO2 emitted from 2011 to 2017, in the city of São Paulo. The hospitalization costs were also be calculated. MLP and RBF neural networks have been tested by varying the number of neurons in the hidden layer and the type of equation of the output function. The following pollutants and its concentration range were collected considering the supervision of Alto Tiete station set, in several neighborhoods in the city of São Paulo, from in the period 2011 to 2017: 28–63 µg/m3 of PM2.5, 52–110 µg/m3 of PM10, 49–135 µg/m3 of O3, 0.8–2.6 ppm CO, 41–98 µg/m3 of NO2, and 3–16 µg/m3 of SO2. Results showed that a RBF neural network with 6 input neurons, 13 hidden layer neurons, and 1 output neuron, using BFGS algorithm and a Gaussian function to neuronal activation, was the best fitted to the experimental datasets. So, knowing the monthly concentration of gaseous pollutions was possible to predict the hospitalization of 1464 to 3483 ± 510 patients, with costs between 570,447 and 1,357,151 ± 198,171 USD per month. This way, it is possible to use this neural network to predict the costs of hospitalizing patients for respiratory diseases and to contribute to the decision-making of how much the government should spend on health care.
... The environmental company from SP state (Companhia Ambiental do Estado de São Paulo; CETESB, 2019) described the period between May and September as the most adverse for dispersion of primary pollutants in the SP state and that the 2018 winter was considered the most adverse when compared with the last 3 years. In the Metropolitan Region of São Paulo, most of the automatic stations registered a slight increase (compared to 2017) in the mean concentrations of the fine particulate matter 2.5 (PM2.5), which is extremely harmful to the respiratory system (Arbex et al., 2012). ...
Article
Full-text available
Dry conditions occurred over São Paulo state (southeastern Brazil) from February to July 2018, causing the driest semester in 35 years. Socioeconomic impacts included a record number of fire spots, most adverse conditions to pollutant dispersion in 3 years and the winter's lowest water reservoirs stored volume in 17 years. This paper discusses climate drivers to the onset and persistence of the dry conditions, with special attention to the intraseasonal forcing. Barotropic atmospheric circulations forced by the intraseasonal Pacific-South America teleconnection pattern, embedded in the lower frequency setup of the Pacific Decadal Oscillation and the Atlantic Multidecadal Oscillation, were identified as main large-scale forcings to reduce precipitation. Drought evolution was modulated by other intraseasonal drivers such as the Madden Julian, Antarctic and 10–30 days Oscillations. A break in the 6-month dry condition, in March 2018, highlighted the important role of such oscillations in determining precipitation anomalies over SP. Results show that intraseasonal phenomena and their interactions control drought characteristics such as magnitude, persistence and spatial distribution within a setup determined by lower-frequency oscillations. The intraseasonal timescale seems to be key and must be considered for a complete description and understanding of the complex drought evolution process in São Paulo.
... The particulate matter (PM) from outdoor air pollution has been classified as members of Group 1 carcinogens (agents carcinogenic to humans) by the International Agency for Research on Cancer [1]. Air pollutants have been previously reported to be associated with adverse health conditions, including cardiovascular diseases, diabetes, neurodegenerative disorders, reduced life expectancy, and the development of several types of cancers [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. ...
Article
Full-text available
Out of eight deaths caused worldwide, one death is caused due to air pollution exposure, making it one of the top global killers. Personal exposure measurement for real-time monitoring has been used for inhaled dose estimation during various modes of workplace commuting. However, dose-exposure studies during long commutes are scarce and more information on inhaled doses is needed. This study focuses on personal exposures to size-fractionated particulate matter (PM1, PM2.5, PM4, PM7, PM10, TSP) and black carbon (BC) inside a bus traveling more than 270 kms on a highway between Albany, NY and Boston, MA. Measurements were also made indoors, outdoors, and while walking in each city. Mean PM (PM1, PM2.5, PM4, PM7, PM10, TSP) and mean BC concentrations were calculated to estimate the inhaled exposure dose. The highest average PM2.5 and PM10 exposures concentrations were 30 ± 12 and 111 ± 193 µg/m3, respectively, during Boston to Albany. Notably, personal exposure to BC on a bus from Albany to Boston (5483 ± 2099 ng/m3) was the highest measured during any commute. The average inhaled dose for PM2.5 during commutes ranged from 0.018 µg/km to 0.371 µg/km. Exposure concentrations in indoor settings (average PM2.5 = 37 ± 55 µg/m3, PM10 = 78 ± 82 µg/m3, BC = 5695 ± 1774 ng/m3) were higher than those in outdoor environments. Carpeted flooring, cooking, and vacuuming all tended to increase the indoor particulate level. A high BC concentration (1583 ± 1004 ng/m3) was measured during walking. Typical concentration profiles in long-haul journeys are presented.
... Forest firehaze is a globally important source of particulate matter (PM)pollution but its public health effects are challenging to assess 3,7 . PM is associated with a higher incidence of upper airway symptoms, such as rhinorrhoea, nasal obstruction, cough, laryngospasm, and vocal fold dysfunction, and lower airway symptoms, such as cough, dyspnoea, and wheezing 8 .The respiratoy distress syndrome is one of the cause to induce premature rupture of membrane (PROM) to result preterm delivery 9 . ...
Article
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Over the past 30 years, forest fire has been one of main ecological issues in Indonesia. Human-caused deforestation was accused to be the reason behind this matter, apart from the drastic changing in global climate. Palangkaraya is one of the citiesaffected by haze of the forest fire in 2015; considered to be the worst year of forest fire with the value of PM10 was above the normal threshold. As the impact to the community wellbeing, the prevalence of acute respiratory infection (ARI) in October 2015was increasing especially in children. The research aimed to analyse the spatial distribution of children with ARI in October 2015 at Palangkaraya City. Data onARI number were collected from Primary Care under Public Health Office of Palangkaraya City. The PM 10 value was collected bythe Environmental Agency of Palangkaraya City. The spatial analyse method was conducted using theAverage Nearest Neighbour (ANN) method. The result shows that the number of ANN ratio is 0.761801. It means that the distribution pattern of children with ARI in Central Kalimantan during the forest fire in October 2015 was in cluster form. Bangladesh Journal of Medical Science Vol. 21(1) 2022 Page : 171-174
... Air pollution exposure for extended periods should be associated with allergy and other diseases. Particulate matter and other air pollutants have detrimental effects on the respiratory system and studies conducted have shown that exposure to particulate matter is associated with respiratory diseases, such as chronic bronchitis, emphysema and airflow obstruction [49,50]. ...
Article
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This quantitative exploratory baseline study aimed to investigate whether allergy among adolescents was associated with household living conditions, including living near gold mine tailing dumps in South Africa. A questionnaire based on the International Study of Asthma and Allergies was used to collect information on allergy and household risk factors among adolescents (n = 5611). A chi-square test was applied to determine the relationship between community (exposed/unexposed) and confounding variables. Crude and adjusted odds ratios (ORs) and 95% confidence intervals (CI) were calculated using univariate and multiple logistic regression analysis (LRA) to estimate the likelihood of having doctor-diagnosed allergies. The overall prevalence of doctor-diagnosed allergies was 25.5%. The exposed communities had a higher prevalence of doctor-diagnosed allergies (26.97%) compared with the unexposed (22.69%) communities. The study found an association between doctor-diagnosed allergy and having fungus in the house, being female, currently having pets in and around the house, residing in the community for more than three years and living in communities located close to gold mine tailing dumps. Actions to implement buffer zones between gold mine tailing dumps and communities would support Sustainable Development Goals 3 (health) and 11 (sustainable cities and communities), while failing to address the current potential identified risk factors may pose a significant public health challenge. Local policymakers should also apply the precautionary principle to protect the health of children, especially with the location of human settlements relative to air pollution sources.
... Air pollution is associated with adverse health conditions, including cardiovascular diseases, diabetes, neurodegenerative disorders, reduced life expectancy, and the development of several types of cancers [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15]. ...
Article
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The goal of this research was to investigate the health effects of winter pollution on various occupations in Lahore and its neighboring peri-urban areas. A questionnaire survey, key informants, and focused group discussions were employed to collect data, which included demographic, socioeconomic, and health-related information. Descriptive statistics and the multivariate logistic regression model (MLRM) were used to examine the effects of pollution on exposed occupational groups who experienced symptoms such as coughing, shortness of breath, and eye discomfort. According to data from interviews, MLRM revealed that individuals working in various occupations with outdoor and indoor environments are equally affected by winter smog, but being middle-aged (odds ratio OR = 5.73), having a history of a respiratory ailment (OR = 4.06), and location (OR = 2.26) all play important roles in determining health. However, less educated people, elders, and people who already live in polluted areas are more likely to develop respiratory health symptoms. During the smog incident, it was determined that diverse health and socioeconomic factors exacerbate an individual’s negative health impact more than others.
... High concentrations of oxidants and pro-oxidants in nitrogen dioxide lead to the formation of oxygen and nitrogen free radicals. An increase in these radicals initiates an inflammatory response by releasing inflammatory cells and mediators (cytokines, chemokines, etc.) that reach the circulatory system, cause subclinical inflammation that negatively affects the respiratory system [30]. ...
Article
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Introduction: Air pollution is one of the main causes for the significant increase of respiratory infections in Tehran. In the present study, we investigated the associations between short-term exposure to ambient air pollutants with the hospital admissions and deaths. Materials and methods: Health data from 39915 hospital admissions and 2459 registered deaths associated with these hospital admissions for respiratory infections were obtained from the Ministry of Health and Medical Education during 2014-2017. We used the distributed lag non-linear model (DLNM) for the analyses. Results: There was a statistically positive association between PM2.5 and AURI in the age group of 16 years and younger at lags 6 (RR 1.31; 1.05-1.64) and 7 (RR 1.50; 1.09-2.06). AURI admissions was associated with O3 in the age group of 16 and 65 years at lag 7 with RR 1.13 (1.00-1.27). ALRI admissions was associated with CO in the age group of 65 years and older at lag 0 with RR 1.12 (1.02-1.23). PM10 was associated with ALRI daily hospital admissions at lag 0 for males. ALRI admissions were associated with NO2 for females at lag 0. There was a positive association between ALRI deaths and SO2 in the age group of 65 years and older at lags 4 and 5 with RR 1.04 (1.00-1.09) and 1.03 (1.00-1.07), respectively. Conclusion: Exposure to outdoor air pollutants including PM10, PM2.5, SO2, NO2, O3, and CO was associated with hospital admissions for AURI and ALRI at different lags. Moreover, exposure to SO2 was associated with deaths for ALRI.
Article
Full-text available
Rationale: In vitro studies, animal experiments, and human exposure studies have shown how ambient air pollution increases the risk of atopic diseases. However, results derived from observational studies are inconsistent. Objectives: To assess the relationship between individual-based exposure to traffic-related air pollutants and allergic disease outcomes in a prospective birth cohort study during the first 6 years of life. Methods:We studied 2,860 children at the age of 4 years and 3,061 at the age of 6 years to investigate atopic diseases and allergic sensitization. Long-term exposure to particulate matter (PM2.5), PM2.5 absorbance, and long-term exposure to nitrogen dioxide (NO2) was assessed at residential addresses using geographic information systems based regression models and air pollution measurements. The distance to the nearest main road was used as a surrogate for traffic-related air pollutants. Measurements and Main Results: Strong positive associations were found between the distance to the nearest main road and asthmatic bronchitis, hay fever, eczema, and sensitization. A distance-dependent relationship could be identified, with the highest odds ratios (ORs) for children living less than 50 m from busy streets. For PM2.5 absorbance, statistically significant effects were found for asthmatic bronchitis (OR, 1.56; 95% confidence interval [CI], 1.03-2.37), hay fever (OR, 1.59; 95% CI, 1.11-2.27), and allergic sensitization to pollen (OR, 1.40; 95% CI, 1.20-1.64). NO2 exposure was associated with eczema, whereas no association was found for allergic sensitization. Conclusions: This study provides strong evidence for increased risk of atopic diseases and allergic sensitization when children are exposed to ambient particulate matter
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Unfavourable effects on the respiratory and the cardiovascular systems from short-term and long-term inhalation of air pollution are well documented. Exposure to freshly generated mixed combustion emissions such as those observed in proximity to roadways with high volumes of traffic and those from ice-resurfacing equipment are of particular concern. This is because there is a greater toxicity from freshly generated whole exhaust than from its component parts. The particles released from emissions are considered to cause oxidative damage and inflammation in the airways and the vascular system, and may be related to decreased exercise performance. However, few studies have examined this aspect. Several papers describe deleterious effects on health from chronic and acute air pollution exposure. However, there has been no research into the effects of long-term exposure to air pollution on athletic performance and a paucity of studies that describe the effects of acute exposure on exercise performance. The current knowledge of exercising in the high-pollution environment and the consequences that it may have on athlete performance are reviewed.
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A mass screening of lung function associated with air pollutants for children is limited. This study assessed the association between air pollutants exposure and the lung function of junior high school students in a mass screening program in Taipei city, Taiwan. Among 10,396 students with completed asthma screening questionnaires and anthropometric measures, 2919 students aged 12-16 received the spirometry test. Forced vital capacity (FVC) and forced expiratory flow in 1s (FEV(1)) in association with daily ambient concentrations of particulate matter with diameter of 10 μm or less (PM(10)), sulfur dioxide (SO(2)), carbon monoxide (CO), nitrogen dioxide (NO(2)), and ozone (O(3)) were assessed by regression models controlling for the age, gender, height, weight, student living districts, rainfall and temperature. FVC, had a significant negative association with short-term exposure to O(3) and PM(10) measured on the day of spirometry testing. FVC values also were reversely associated with means of SO(2), O(3), NO(2), PM(10) and CO exposed 1 d earlier. An increase of 1-ppm CO was associated with the reduction in FVC for 69.8 mL (95% CI: -115, -24.4 mL) or in FEV(1) for 73.7 mL (95% CI: -118, -29.7 mL). An increase in SO(2) for 1 ppb was associated with the reductions in FVC and FEV(1) for 12.9 mL (95% CI: -20.7, -5.09 mL) and 11.7 mL (95% CI: -19.3, -4.16 mL), respectively. In conclusion, the short-term exposure to O(3) and PM(10) was associated with reducing FVC and FEV(1). CO and SO(2) exposure had a strong 1-d lag effect on FVC and FEV(1).