Environment International 74 (2015) 136–143

Contents lists available at ScienceDirect

Environment International
journal homepage: www.elsevier.com/locate/envint

Review

A review on the human health impact of airborne particulate matter

Ki-Hyun Kim a,⁎, Ehsanul Kabir b, Shamin Kabir c
a
Department of Civil and Environmental Engineering, Hanyang University, Seoul 133-791, Republic of Korea
b
Department of Farm, Power & Machinery, Bangladesh Agricultural University, Mymensingh, Bangladesh
c
LMC Clinic, Mymensingh, Bangladesh

a r t i c l e i n f o a b s t r a c t

Article history: Particulate matter (PM) is a key indicator of air pollution brought into the air by a variety of natural and human
Received 21 July 2014 activities. As it can be suspended over long time and travel over long distances in the atmosphere, it can cause a
Accepted 7 October 2014 wide range of diseases that lead to a significant reduction of human life. The size of particles has been directly
Available online xxxx
linked to their potential for causing health problems. Small particles of concern include “inhalable coarse parti-
cles” with a diameter of 2.5 to 10 μm and “fine particles” smaller than 2.5 μm in diameter. As the source–effect
Keywords:
Particulate matter
relationship of PM remains unclear, it is not easy to define such effects from individual sources such as long-
PM10 range transport of pollution. Because of the potent role of PM and its associated pollutants, detailed knowledge
PM2.5 of their human health impacts is of primary importance. This paper summarizes the basic evidence on the health
Human health effects of particulate matter. An in-depth analysis is provided to address the implications for policy-makers so
Particle size that more stringent strategies can be implemented to reduce air pollution and its health effects.
© 2014 Elsevier Ltd. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
2. Classification and source of PM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
3. Effect of particle size and particle components . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
4. Human diseases associated with PM pollution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
5. Mortality of PM pollution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139
6. Pollution scenario and regulation guidelines for PM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140
7. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141

1. Introduction
Air pollution is a process that introduces diverse pollutants into the
atmosphere that cause harm to humans, other living organisms, and
the natural environment (Kinney, 2008; Brauer et al., 2012; Kim et al.,
2013). The health effects of air pollution, observed from both indoor
and outdoor environments, have been of great concern due to the
high exposure risk even at relatively low concentrations of air pollut-
ants. More than two million deaths are estimated to occur globally
each year as a direct consequence of air pollution through damage to
the lungs and the respiratory system (Shah et al., 2013). Among these
⁎ Corresponding author. Tel.: +82 2 2220 2325.
E-mail addresses: kkim61@hanyang.ac.kr, kkim61@nate.com (K.-H. Kim).
deaths, around 2.1 and 0.47 million are caused by fine particulate matter
(PM) and ozone, respectively (Chuang et al., 2011; Shah et al., 2013).
The presence of PM poses more danger to human health than that of
ground-level ozone and/or other common air pollutants (like carbon
monoxide). Airborne PM consists of a heterogeneous mixture of solid
and liquid particles suspended in air that varies continuously in size
and chemical composition in space and time (WHO, 2013). It is found
that the chemical constituents of PM are diverse enough to include
nitrates; sulfates; elemental and organic carbon; organic compounds
(e.g., polycyclic aromatic hydrocarbons); biological compounds
(e.g., endotoxin, cell fragments); and metals (e.g., iron, copper, nickel,
zinc, and vanadium) (WHO, 2013).
Numerous scientific studies have explained particle exposure as the
source of various health problems including premature death in people

http://dx.doi.org/10.1016/j.envint.2014.10.005
0160-4120/© 2014 Elsevier Ltd. All rights reserved.
 K.-H. Kim et al. / Environment International 74 (2015) 136–143
with heart or lung disease, nonfatal heart attacks, irregular heartbeat,
aggravated asthma, decreased lung function, and increased respiratory
symptoms such as irritation of the airways, coughing, or difficulty
breathing (Atkinson et al., 2010; Cadelis et al., 2014; Correia et al.,
2013; Fang et al., 2013; Meister et al., 2012). This paper provides a com-
prehensive overview of PM pollution and its impact by synthesizing the
newly added information on its source processes, size effect on expo-
sure response, observed health effects, pollution scenario, and regula-
tion guidelines. It also addresses the management skills of this
important pollutant in some areas (such as China and Korea) suffering
from the worst pollution.
2. Classification and source of PM
Although PM can be defined or classified in a number of ways, aero-
dynamic diameter is one of the main criteria to describe its transport
ability in the atmosphere and/or inhaling ability through a respiratory
organism (Esworthy, 2013). EPA has been regulating particles mainly
in two size categories based on their predicted penetration capacity
into the lung as either (i) coarse particulate matter (PM10) with an aero-
dynamic diameter of 10 μm or (ii) fine particulate matter (PM2.5) with
an aerodynamic diameter of 2.5 μm (Esworthy, 2013). These PMs
primarily come from a wide range of sources including road dust, agri-
culture dust, river beds, construction sites, mining operations, and
similar activities (Juda-Rezler et al., 2011).
A comparison of general properties distinguishing fine (PM2.5) and
coarse (PM10) mode particles is summarized in Table 1. Fine particles
with a diameter of less than 0.1 μm are categorized as an ultra-fine parti-
cle (PM0.1), which is still in the early stages of research (Hasheminassab
et al., 2013). Fig. 1 shows a comparison of the size between PM2.5 and
PM10 against the average diameter of a human hair (~70 μm) and fine
beach sand (~90 μm).
The source of PM can be explained as either direct emission into
the air or as conversion from gaseous precursors (such as sulfur dioxide,
oxides of nitrogen, ammonia, and non-methane volatile organic com-
pounds) released from both anthropogenic and natural sources
(Atkinson et al., 2010). Anthropogenic sources are highly variable and
include solid-fuel (coal, lignite, heavy oil, and biomass) combustion, in-
dustrial and agricultural activities, erosion of the pavement by road traf-
fic, and abrasion of brakes and tires (Srimuruganandam and Nagendra,
2012). In contrast, those occurring naturally can be accounted for by
sources including volcanoes, dust storms, forest fires, living vegetation,
and sea spray (Misra et al., 2001). The chemical constituents in PM are
commonly found to include inorganic ions (e.g., sulfates, nitrates, am-
monium, sodium, potassium, calcium, magnesium, and chloride). Its
composition can in fact be expanded further to include all varieties of
constituents such as organic and elemental carbon, crustal material,
particle-bound water, metals (including cadmium, copper, nickel, vana-
dium, and zinc), and polycyclic aromatic hydrocarbons (PAH) (Cheung
et al., 2011). In addition, the environmental significance of biological
components (e.g., allergens and microbial compounds) has also been
emphasized because of their potential health hazards as PM.
Table 1
Comparison of the basic properties of PM with respect to particle size: fine (PM2.5) versus coarse (PM10) mode particles.
Characteristics Fine mode particles (PM2.5)
Diameter Less than 2.5 μm
Composed of Sulfate, SO2 − 4; nitrate, NO−3; ammonium, NH+4; hydrogen ion,
H+; elemental carbon, C; organic compounds; PAH; metals, Pb, Cd,
V, Ni, Cu, Zn; particle-bound water; and biogenic organics.
Sources Combustion of coal, oil, gasoline; transformation products of NOx,
SO2, and organics including biogenic organics, e.g., terpenes; high
temperature processes; smelters, and steel mills
Lifetimes Days to weeks
Travel distance 100 to 1000
(kilometers)
137
Fig. 1. Size comparison of PM2.5 and PM10 against the average diameter of a human hair
(~70 μm) and fine beach sand (~90 μm) (Source: Guaita et al., 2011).
Traffic is the major source of PM mainly originating from the wear of
vehicle components such as brakes and tires as well as suspension of
road dust (De Kok et al., 2006). The inorganic particles of crustal mate-
rial from pavement abrasion are often rich in minerals containing silicon
(Si), aluminum (Al), potassium (K), sodium (Na), and calcium (Ca)
(Lindbom et al., 2006), while brake and tire wear particles may contain
metals such as copper (Cu), antimony (Sb), lead (Pb), cadmium (Cd),
and zinc (Zn) (Hjortenkrans et al., 2006). Because of their small size,
fine particles tend to be suspended in the air for long periods of time
(weeks or months) and can be transported for hundreds (or thousands)
of km (Johansson et al., 2007). If there are changes in wind occurrence
patterns and atmospheric stability, the concentrations of different PM
fractions can fluctuate greatly from one day to the next (or even from
hour to hour) (Johansson et al., 2007).
It is not uncommon to find that PM concentration levels in indoor
environment exceed those of outdoors. A number of activities can gen-
erate particulates in indoor environment ranging from cooking, pets,
walking across the carpet, household products generating liquid aero-
sols (e.g., aerosol cans), and office equipment (e.g., printers and photo-
copiers); the source processes of PM can even be associated with such
factors as house design (e.g., construction materials of the house, the
size and arrangement of rooms, and the number of windows for venti-
lation) (Madureira et al., 2012). Balakrishnan et al. (2002) reported
that the concentrations of respirable PM in households should increase
significantly during cooking activities in the range from 500 to 2000
(biomass heater) and 80 to 160 μg m−3 (kerosene heater). In this re-
spect, fuel and stove type, cooking duration, and smoke from neighbor-
hood cooking were the most important determinants of exposure
across these households. Draggan (2011) observed that the PM emis-
sion rates from individual candles and incenses ranged from 100 to
1700 μg hr−1 and 7 to 202 mg hr−1, respectively.
Coarse mode particles (PM10) Reference
Less than 10 μm Atkinson et al. (2010)
Resuspended dust, soil dust, street dust; coal and oil fly ash; Cheung et al. (2011)
metal oxides of Si, Al, Mg, Ti, Fe, CaCO3, NaCl, sea salt; pollen,
mold spores, and plant parts.
Resuspension of soil tracked onto roads and streets; Suspension Srimuruganandam
from disturbed soils, e.g., farming, mining; resuspension of industrial and Nagendra (2012)
dusts; construction, coal and oil combustion, and ocean spray.
Minutes to hours Cheung et al. (2011)
1 to 10 Srimuruganandam
and Nagendra (2012)
138 K.-H. Kim et al. / Environment International 74 (2015) 136–143
In comparison to the conditions of recognizable source activities, the
indoor pollution of PM can be commonly observed in various livelihood
facilities. In four hospitals in Guangzhou city, China, Wang et al. (2006)
found the average PM10 concentrations of 128 μg m−3. In South Korea,
the concentration of PM10 in several types of indoor environment
(such as child care facility, medical facility, postnatal care center, and el-
ementary school) was found as 77.0 ± 29.9, 74.0 ± 23.6, 93.5 ± 9.47,
and 66.7 ± 15.8 μg m− 3, respectively (Kabir et al., 2012). Similar to
this finding, the mean PM10 concentration inside elementary school
was commonly observed in the range from 66.7 to 77.9 μg m− 3
(Fromme et al., 2007; Heudorf et al., 2009; Yang et al., 2009).
3. Effect of particle size and particle components
It is acknowledged that the exposure effectiveness of PM is greatly
influenced by local conditions such as weather, seasons, topography,
sources of particles, concentrations being emitted, and microenviron-
ments (Casati et al., 2007). Although the effect of PM exposure depends
on physical characteristics (e.g., breathing mode, rate, and volume of a
person), the size of particles has been directly linked to being the
main cause of health problems (Brown et al., 2013). Generally speaking,
the smaller a particle is, the more deeply it will penetrate to deposit on
the respiratory tract at an increasing rate. In nasal-breathing, the cilia
and the mucus act as a very effective filter for most particulates exceed-
ing 10 μm in diameter (coarse PM). Because the coarse PM fraction
settles quickly, it tends to lodge in the trachea (upper throat) or in the
bronchi (Atkinson et al., 2010). If we inhale this PM, it will be initially
collected in our nose and throat. Then, our body will react to eliminate
these intruding PM through such processes as sneezing and coughing
(Cadelis et al., 2014).
To date, particles that have the most impact on human health effects
have been acknowledged to be those less than 10 μm in diameter. These
particles can penetrate within the respiratory tract beginning with the
nasal passages to the alveoli, deep within the lungs due to their exces-
sive penetrability (Londahl et al., 2007). Particles between approxi-
mately 5 and 10 μm are most likely deposited in the tracheobronchial
tree, while those between 1 and 5 μm are deposited in the respiratory
bronchioles and the alveoli where gas exchange occurs (Londahl et al.,
2006) (Fig. 2). These particles can affect gas exchange within the
lungs and can even penetrate the lung. Eventually, these particles will
escape into the blood stream to cause significant health problems (Fu
et al., 2011). Particles smaller than 1 μm in general behave similar to
gas molecules and will therefore penetrate down to the alveoli (deposi-
tion by diffusion forces), and can translocate further into the cell tissue
and/or circulation system (Valavanidis et al., 2008).
It was reported that metals act as possible mediators of PM induced
airway injury and inflammation through the Fenton reaction (Diociaiuti
et al., 2001; González-Flecha, 2004; Jimenez et al., 2000). Transition
metals present in particles, especially iron, increase production of reac-
tive oxygen species (ROS) in vivo (Kadiiska et al., 1997). As the release
of ROS can result in cellular and tissue damage, it can thus initiate or
exacerbate inflammation (Aust et al., 2002; Hitzfeld et al., 1997). More-
over, genotoxic effects attributed to PM may be accounted for by the
content of transition metals such as iron (Gilli et al., 2007). In an animal
model study, Costa and Dreher (1997) found a direct connection for the
in vivo role of soluble transition metals in pulmonary injury induced by
PM. Note that endotoxins found in particulate matter are correlated
with gram-negative bacterial contamination (Traversi et al., 2011). Pirie
et al. (2003) stated that inhaled endotoxin may significantly contribute
to the induction of airway inflammation and dysfunction. In a study con-
ducted in Mexico, Osornio-Vargas et al. (2011) found that PM enriched
with elemental components was predominantly associated with cell
membrane disruption in combination with pro-inflammatory state,
which could result in severe health effects (like pulmonary fibrosis). On
the other hand, PM formed under an enhanced anthropogenic contribu-
tion may have a higher impact on the lung and systemic cardiovascular
Fig. 2. Deposition potential for particles of varying sizes (Source: Londahl et al., 2006).
diseases due to its stronger potential to induce the production of pro-
inflammatory cytokines (Araujo, 2011). PM may also be involved in oxi-
dative stress and inflammation (Møller et al., 2008), which may possibly
lead to TNFa-or mitochondria induced apoptosis (Aggarwal, 2000). In a
previous study in Seoul, Korea, Jung et al. (2012) found that organic ex-
tract of subway PM10 had genotoxic effects on normal human lung cells.
Accordingly, oxidative stress is suspected as one of the major mechanisms
of these genotoxic effects.
4. Human diseases associated with PM pollution
Exposure to PM has been identified as the cause of numerous health
effects including increased hospital admissions, emergency room visits,
respiratory symptoms, exacerbation of chronic respiratory and cardio-
vascular diseases, decreased lung function, and premature mortality
(Guaita et al., 2011; Halonen et al., 2009; Perez et al., 2012; Samoli
et al., 2008). In addition, scientists have suggested that exposure to
high particle levels may also lead to diverse symptoms including low
birth weight in infants, pre-term deliveries, and possibly fetal and infant
deaths. Mild problems associated with inhaling PM2.5 are found to
include shortness of breath (dyspnea), chest discomfort and pain, and
coughing and wheezing (Guaita et al., 2011). A national U.S. epidemio-
logic study found a strong, consistent correlation between adult diabe-
tes and particulate air pollution that persists after adjustment for
other risk factors like obesity and ethnicity (Pearson et al., 2010).
Older adults and children or people with heart (or lung) disease are sub-
ject to much stronger risk from particles than other people. Exposure to
PM was reported to affect lung development in children, including
reversible deficits in lung function, chronically reduced lung growth
rate, and a deficit in long-term lung function (Brauer et al., 2012). The
health impact of PM exposure is briefly depicted in a box plot in Fig. 3.
If children are exposed to an excess level of PM2.5 (e.g., 65 μg m−3 for
24-hours), they are under a significantly high risk of respiratory symp-
toms, asthma medication use, and reduced lung function (Gold et al.,
1999; Guaita et al., 2011). Sofer et al. (2013) reported that those who
were exposed to elevated PM10 levels (N150 μg m−3) suffered from
an approximately 3 to 6% decline in lung function as measured by
peak expiratory flow. Tecer et al. (2008) noticed an 18% rise in admis-
sions of asthma patients with a 10 μg m−3 increase in PM10–2.5 on the
same day of admissions. Cadelis et al. (2014) reported that children
with asthma in Guadeloupe experienced increased risk of visiting the
health emergency department probably due to pollutants contained in
 K.-H. Kim et al. / Environment International 74 (2015) 136–143 139

Particulate matter health impact

Premature death Hospital admission Emergency room visit Asthma attack

Chronic bronchitis Cancer Cardiovascular Disease Diabetes Restricted activity

Fig. 3. Health impacts of PM exposure.

PM10 and PM2.5 of the Saharan dust. McCormack et al. (2011) studied
150 children (predominantly black aged 2 to 6 years old) from east Bal-
timore, Maryland, who were diagnosed as asthma patients by physi-
cians. These authors found statistically significant relationships
between both coarse (and fine) particulate matter levels and asthma
symptoms in both atopic and nonatopic asthmatic children.
It is well known that PM pollution is linked to an increased risk of
hospital admission for myocardial infarction among the elderly and ex-
acerbation of congestive heart failure (Dominici et al., 2006; Wellenius
et al., 2005; Wellenius et al., 2006; Zanobetti and Schwartz, 2005). Sun
et al. (2010) also suggested a possible association between changing
PM levels and transient increases in plasma viscosity, acute-phase reac-
tants, endothelial dysfunction, and altered autonomic control of the
heart (Sun et al., 2010). Moreover, the potent role of PM in increased
cardiac risk is also explained by initiating and promoting atherosclerotic
progression, which is responsible for most cardiovascular diseases
(Suwa et al., 2002). A panel study in Los Angeles using the data for
798 participants (in two clinical trials) found that a 10 μg m−3 increase
in PM2.5 was associated with an increase in carotid intima–media thick-
ness, an ultrasonic measure of atheroma (Kunzli et al., 2005). Bell et al.
(2008) found that short-term exposure to PM2.5 is statistically signifi-
cant to affect cardiovascular and respiratory hospitalizations. In another
study based on a survey of Boston residents, it was seen that exposure
to PM2.5 (with an average concentration of 15.5 μg-m−3) leads to de-
creased vagal tone with reduced heart rate variability (Gold et al.,
2000). Table 2 presents a list of studies that have focused on the effect
of PM exposure and hospital admissions.
Although the impact of PM pollution has been analyzed mainly with
respect to the observable physical damage to human health, its econom-
ic aspect is also significant. PM related illness can ultimately lead to fi-
nancial and non-financial welfare losses of not only patients and their
families but also a significant portion of gross domestic product (GDP)
(Chen et al., 2010; Hou et al., 2011, 2012). China suffered a health-
related economic loss (due to PM10) of US$ 106.5 billion or 2.1% of
China's GDP for the year 2009 (Hou et al., 2012). In another previous
study in China, Zhang et al. (2008) calculated the health effects of pollu-
tion caused by PM10 in 111 Chinese cities in 2004 based on the statistical
data with epidemiological exposure response functions. The total eco-
nomic cost caused by PM10 pollution was estimated to be approximate-
ly US$ 29 billion.
5. Mortality of PM pollution
According to most of the currently available epidemiological studies,
mortality has been used as the indicator of health effects with respect to
PM pollution. Moreover, information on daily admissions to hospital is
also used in time series studies. However, such application is limited
by the lack of intercountry comparisons but used for health impact as-
sessments to reflect differences in national or local practices in hospital
admissions and in the use of other forms of medical care in the case of
acute symptoms (Pope et al., 2009). It is estimated that approximately
3% of cardiopulmonary and 5% of lung cancer deaths are attributable
to PM globally (Fang et al., 2013). Exposure to PM2.5 is estimated to re-
duce the life expectancy of the population by about 8.6 months on aver-
age (Krewski, 2009). Correia et al. (2013) suggested a possible linkage
between reduction in fine particulate matter and improved life expec-
tancy based on data sets collected from 545 counties in the U.S. from
2000 to 2007. Their studies revealed that a decrease of 10 μg m−3 of
PM2.5 should have led to an increase of life expectancy by 0.35 years
on average.
Several studies have provided strong evidence that exposure to PM
can exert direct influences on cardiopulmonary disease (CPD) and
ischemic heart disease (IHD) mortality (Krewski, 2009; Laden et al.,
2006; Pope et al., 2004). Miller et al. (2007) also investigated the effect
of long-term exposure to PM2.5 on cardiovascular disease (CVD) mortal-
ity in post-menopausal women. In a study by Zanobetti and Schwartz

Table 2
Case studies for the human health effects of PM exposure with respect to acute hospital admission.

Order Location Subjects Pollutants Health effect Reference

1 Ontario, Canada
2 204 US counties
3 7 US cities
4 202 US counties
5 UK
6 Taiwan
7 Australia, New Zealand
8 Australia
9 US
10 Cyprus
Not specific PM10, O3, NO2, SO2, CO 11% and 13% increased daily hospitalizations for respiratory and Burnett et al. (1997)
cardiac diseases, respectively
N65 y PM2.5 Increased hospital admission for cardiovascular and respiratory diseases Dominici et al. (2006)
N65 y PM10 Increased hospital admission for chronic heart failure Wellenius et al. (2006)
N65 y PM2.5 1.49% increase in hospitalizations of cardiovascular diseases per 10 g m−3 Bell et al. (2008)
increase in same-day admissions
All ages PM10, O3, NO2, CO Emergency hospital admission for cardiac and respiratory disease Prescott et al. (1998)
Not specific PM10, O3, NO2, CO Increased hospital admissions for cardiovascular disease Chang et al. (2005)
All ages PM10, PM2.5, NO2, CO Adult cardiovascular hospital admissions with five categories of Barnett et al. (2006)
cardiovascular disease
All ages PM10 Respiratory disease and ischemic heart disease admissions Johnston et al. (2007)
N65 y PM2.5, PM10, PM10–2.5 10 g m−3 increase in PM10–2.5 associated with a 0.36% increase in Peng et al. (2008)
cardiovascular disease admissions on the same day
All ages PM10 Every 10 g m−3 increase in daily average PM10 associated with a 0.9% Middleton et al. (2008)
increase in all-cause and a 1.2% increase in cardiovascular admissions
140 K.-H. Kim et al. / Environment International 74 (2015) 136–143

(2009), it was also seen that 10 μg m−3 increases in PM2.5 and PM10 Table 3
from the previous day was associated with 0.8% and 0.6% excess risk in Average annual exposure level (μg m−3) of particular matter between developed and
developing countries (WB, 2013).
all causes of mortality, respectively. Atkinson et al. (2010) reported that
10 μg m−3 increases in PM10 and PM2.5 in London, England was associated Order Name Year
with increases in a 0.5% (95% CI 0.0–0.9) in all-cause mortality and 2.1% Developed countries 2009 2010 2011
(95% CI 0.6–3.7%) in respiratory mortality, respectively. Similarly, in an-
1 Australia 15 14 14
other study in the Netherlands, 10 μg-m−3 increases in PM10 and PM2.5 2 Canada 15 14 14
were related with an increase of 0.5% (95% CI 0.0–0.9) in all causes and 3 Finland 16 16 16
1.6% (95% CI 0.4–2.9%) in respiratory mortality, respectively (Janssen 4 New Zealand 18 17 16
et al., 2013). A 10 μg-m−3 increase in PM2.5 increased all causes of mortal- 5 Ireland 18 17 18
6 United States 20 19 18
ity by (1) 1.4% (95% CI 0.6–2.3) in Barcelona, Spain (Ostro et al., 2011); 7 Japan 20 19 19
(2) 1.5% (95% CI 0.1–2.8) in Stockholm, Sweden (Meister et al., 2012); 8 United Kingdom 20 19 20
and (3) 2.7% (95% CI 1.4–4.1) in Madrid, Spain (Guaita et al., 2011). 9 France 25 24 24
Puett et al. (2009) examined the relationship between long-term 10 Germany 25 24 24
11 Norway 25 23 24
PM2.5 exposure with all-cause mortality among women. They found
12 Russian Federation 30 28 27
an increased risk of all-cause mortality (HR 1.26 [95% CI: 1.02, 1.54]) 13 Italy 36 34 34
and coronary heart disease (CHD) mortality (HR 2.02, 95% CI: 1.07, 14 South Korea 50 48 46
3.78) associated with long-term exposure to PM2.5. In contrast, several 15 Saudi Arabia 113 112 108
studies were not able to demonstrate significant effects of PM2.5 on all 16 United Arab Emirates 131 132 132

causes or cause specific mortality (Branis et al., 2010; Halonen et al., Developing countries
2009; Mallone et al., 2011). The limitations of these studies were gener-
17 Argentina 39 36 36
ally ascribed to relatively small size of population (Garrett and Casimiro,
18 Brazil 41 38 36
2011; Halonen et al., 2009; Stolzel et al., 2007) or short duration of study 19 South Africa 42 40 40
period (1 year) (Branis et al., 2010). 20 Philippines 44 42 43
21 Thailand 45 44 45
6. Pollution scenario and regulation guidelines for PM 22 Indonesia 50 49 47
23 Malaysia 49 49 47
24 Sri Lanka 67 66 62
Urbanization, coupled with increased industrialization, emissions 25 Afghanistan 68 65 63
from vehicles as well as suspension from unpaved roads, and emissions 26 Turkey 70 66 65
from waste and biomass burning for household and commercial needs 27 Kenya 70 71 66
28 China 86 85 82
may lead to substantial increase of PM in ambient air. Table 3 listed
29 India 108 105 100
the average annual exposure level (μg m− 3) of particular matter 30 Zimbabwe 101 104 105
(PM10) in different countries around the world. In most of the cases, 31 Egypt 129 125 120
PM concentrations exceeded the latest air quality guidelines set by the 32 Bangladesh 118 127 121
WHO for mean annual exposures to PM10 (20 μg m−3). As can be ex- 33 Nigeria 153 145 150
34 Pakistan 207 184 171
pected, the particulate matter levels in developing countries are ob-
served to be much higher than those in developed countries. There is
little doubt that increasing concentrations of particulates should cause PM2.5 and PM10, respectively, based on the current three-year average
or contribute to premature mortality and morbidity-related health end- of the 98th percentile data (24 h).
points in such countries. The Chinese standard for the yearly average of particulate material
Clean air is considered to be a basic requirement of human health (PM2.5) is 35 μg m−3 (Cao et al., 2013). In Europe and South Korea, it
and well-being. To protect public health, air quality standards have is 25 μg m−3 (Airkorea, 2014; EU, 2014). Note that the European and
been set in many countries and as such have been an important compo- Chinese emission standard for passenger vehicles for particulate mate-
nent of national risk management and environmental policies. Howev- rial (PM2.5) is 0.025 g km−1 (Hu and Jiang, 2013). In many urban
er, there is no evidence to support a safe or threshold level of exposure areas in the U.S. and Europe, their particle levels are still found to fre-
below which no adverse health effects occur or such effects are per- quently exceed the guideline levels set for the particulate standards,
ceived. As the exposure to PM is ubiquitous and involuntary, it increases although urban air on these continents has become cleaner, on average,
the significance of PM as this determinant of human health. Guidelines with respect to particulates over the last quarter of the 20th century
for regulation should be set for PMs to reduce their potential harmful (Ionescu et al., 2013).
effect on public health and the environment and to offer guidance for It is well known that the status of PM pollution is highly significant in
protecting public health in many other contexts. The regulations for par- some Asian countries. As such, various tactics and techniques have been
ticulate matter set by various governments around the world are listed introduced in those areas to reduce or suppress its pollution in recent
in Table 4. years. In China, the Ministry of Environmental Protection (MEP) report-
In the US, the Environmental Protection Agency (EPA) is responsible ed that the mean concentration of PM2.5 in 74 cities was 76 μg m− 3
for creating, modifying, and enforcing standards for air quality in order which is far higher than the common guidelines (Cheng et al., 2013).
to protect the public from adverse health effects. The EPA considers PM Recently, ‘The Airborne Pollution Prevention and Control Action Plan
one of the six “criteria pollutants” along with ozone, nitrogen oxides, (2013–17)’ has been established by the government of China to reduce
sulfur oxides, carbon monoxide, and lead (Esworthy, 2013). When the PM pollution by installing emissions-cutting exhaust filters, reducing
standard for PM was first introduced in 1971, total suspended particu- coal use, tightening vehicle emission standards, etc. (Sheehan et al.,
late matter (TSP) was chosen as the primary indicator for PM regulation. 2014). The plan's goal is set to reduce 25% of PM emissions from 2012
Since then, such indices for PM have been further modified to enforce levels by the year 2017. It has been proven that the worsening of air
size specific standards (PM10 in 1987 and PM2.5 in 1997). On January pollution in China affects the surrounding countries like Korea and
15, 2013, the EPA published a new regulation for PM. According to Japan as well, with the fine particles moving with the westerly winds
this latest guideline, the annual primary standards for PM2.5 were re- (Ahn et al., 2013). Like the case of China, Korean governmental action
duced to 12 μg m− 3 from the previous criterion of 15 μg m−3. The was concretized by the Ministry of Environment and Korea to build a
EPA retained the daily (24-hour) standard at 35 and 150 μg m−3 for system of information to alert the public by forecasting the pollution
 K.-H. Kim et al. / Environment International 74 (2015) 136–143 141

Table 4
PM regulation guidelines set by various governments.

Order Country Period PM10 (μg m−3) PM2.5 (μg m−3) Reference

1 United States Yearly average None 12 Esworthy (2013)

Daily average (24-hour) 150 35
2 European Union Yearly average 40 25 EU (2014)
Daily average (24-hour) 50 None
3 China Yearly average 70 35 Cao et al. (2013)
Daily average (24-hour) 150 75
4 Hong Kong Yearly average 50 35 Environmental Protection Department, Hong Kong (2013)
Daily average (24-hour) 100 75
5 Japan Yearly average None 15 Ministry of the Environment, Japan (2014)
Daily average (24-hour) 100 35
6 South Korea Yearly average 50 25 Airkorea (2014)
Daily average (24-hour) 100 25
7 Australia Yearly average None 8 Department of the Environment, Australia (2005)
Daily average (24-hour) 50 25

of PM10 (Oh and Kim, 2014). Apart from these purely informative mea-
sures, helpful for alerting the public, other measures focusing on the
reduction of emissions at a national level have been carried out, by
restraining the growth of the fleet of petrol vehicles (development of
recharging station for electric cars and subsidies at purchase) and by
implementing stricter rules for polluting industries (Oh and Kim,
2014). A series of regulations are yet to be exercised by the Seoul city
with regard to restrictions in the use of polluting vehicles and to the
effective control of potential point sources (such as saunas and barbecue
restaurants).
7. Conclusion
The health effects of PM10 and PM2.5 are well documented. Many
lines of evidence point to the fact that exposure to particulate matter
is linked to adverse respiratory and cardiovascular health effects. Epide-
miological and experimental studies have now clearly demonstrated
that not all particles are equally toxic but give different risks for health
effects. There is growing evidence that the most harmful effects of
particulate matter are related to the size of the particle. As particles de-
crease in size, they are hypothesized to increase acidity and their ability
to penetrate into the lower airways. Although we are not yet able to de-
termine a safe level of exposure, the public has become aware of the fact
that even at relatively low concentrations the burden of air pollution on
health is significant. Consequently, effective management of air quality
is necessary to reduce health risk to a minimum. As a means of widening
our knowledge of the seriousness of PM pollution, future research needs
to focus on identification and quantification of the unknown organic
and inorganic compounds present in ambient air particles for a better
understanding of their health effects.
Acknowledgments
This study was supported by a grant from the National Research
Foundation of Korea (NRF) funded by the Ministry of Education, Science
and Technology (MEST) (Grant No. 2009-0093848).
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