A Global Perspective of Fine Particulate

Matter Pollution and Its Health Effects

Arideep Mukherjee and Madhoolika Agrawal

Contents
1 Introduction
2 Method
3 PM2.5 Guidelines and Standards
4 Global PM2.5 Status and Exceedance
4.1 Asia
4.2 Africa
4.3 Europe
4.4 South America
4.5 North America
5 Source Apportionment for PM2.5
5.1 Asia
5.2 Europe and Africa
5.3 North and South America
6 Gas to Particle Conversion and Secondary Aerosol Formation in Atmosphere
7 Health Effects of PM2.5
7.1 Evidences from Recent Reviews and Meta-Analysis of Health Effects of Fine PM
7.2 Evidences from Recent Health Effects Studies of Fine PM
7.3 Evidences from Global Health Effects Estimates of Fine PM
7.4 Evidences from Fine PM Exposure Health Effects Estimates
7.5 Evidences from Genotoxic Health Effects Estimates of Fine PM
8 Health Effects of Chemical Constituents of PM2.5
9 Mechanism of Fine PM Toxicity
10 Suggestions
11 Conclusion
12 Summary
References

A. Mukherjee • M. Agrawal (*)

Laboratory of Air Pollution and Global Climate Change, Department of Botany, Banaras
Hindu University, Varanasi 221005, India
e-mail: arideep@[Link]; [Link]@[Link]

© Springer International Publishing AG 2017

Reviews of Environmental Contamination and Toxicology,
DOI 10.1007/398_2017_3
 A. Mukherjee and M. Agrawal

Abbreviations

CI Confidence interval
CPCB Central Pollution Control Board
HR Hazard ratio
IQR Interquartile range
NAAQS National ambient air quality standard
OR Odds ratio
PI Posterior interval
PM Particulate matters
PM2.5 Particulate matters of 2.5 μm size or less
WHO World Health Organization

1 Introduction

The particulate matter (PM) pollution is a global burden, which not only affects the
physical atmosphere, but also has drastic effects on human civilization since the
beginning of anthropogenic interferences to the natural ecosystems. The greatest
concern lies over the negative impact on human health as exposure to ambient PM
pollution is ranked 12th among the Global DALYs (disability-adjusted life-years)
risk factors according to Global burden of disease study in 2013 (Forouzanfar et al.
2015). An aerosol is a suspension of a solid or liquid particle in the air. For health
purposes, aerosol or particulate matter (PM) is typically defined by size, with the
smaller particles having more health impacts. Particles with a diameter <10 μm are
called PM10 and with a diameter <2.5 μm PM2.5.
Climate change combined with air pollution reduces the healing capacity (intrinsic
ability to restore back to its earlier state in time) of natural systems, and causes extreme
variability (variations over a wide range) leading to more serious health effects (Fig. 1).
PM in air is cosmopolitan in distribution in all types of ecosystems from desert to oceans.
PM has both direct and indirect effects on the earth by both cooling and heating of the
atmosphere. Aerosols in the atmosphere impact both climate and biogeochemistry in the
earth’s surface after deposition (Von Schneidemesser et al. 2015). It is estimated that
anthropogenic changes in aerosols contribute to
40.0 % change in short wave radiative
forcing and
60.0 % increase in the number of Cloud Condensation Nuclei (CCN), the
small particles on which water vapor condenses (Mahowald et al. 2011). Aerosols have
a short atmospheric lifetime (about a week), so their effects are more evident than
greenhouse gases (GHGs) (Kopp and Mauzerall 2010). Most PM occurs naturally in the
environment as desert dust, forest fire, sea salt, and sulfates from volcanoes, but
increasing anthropogenic interferences in the environment have significantly increased
the PM burden (Zhang et al. 2015). Large cities with higher traffic and poor air pollutant
dispersion are more susceptible to negative health effects due to PM. High traffic density
in urban areas contributed up to 140 % higher PM2.5 levels compared to suburban
background area (Dongarra et al. 2010).
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

Fig. 1 Effects of particulate matter on different components of the atmosphere

The major component of PM having potential negative health effects are traffic
and combustion related fine PM (Mills et al. 2009; Pope and Dockery 2013). Earlier
reports have mostly highlighted PM exposure and short- or long-term effects with
PM-related hospital admissions, mortality and morbidity (Samet et al. 2000; Pope
et al. 2002; Dominici et al. 2006), but recent scientific findings have identified
several health effects of PM as fine particles trigger inflammatory response, plaque
formation in the blood vessels, lung cancer, term low birth weight, mutagenicity,
changes in gene expression, and immune responses (Coronas et al. 2009;
Wichmann et al. 2009; Raaschou-Nielsen et al. 2013; Dadvand et al. 2014; Ding
et al. 2014; Hennig et al. 2014; Apte et al. 2015; Chafe et al. 2014).
As fine PM is one of the major air pollutants in the world and most severe to
health, it is of utmost important to summarize a global scenario of PM status and its
health effects. So considering these points the manuscript attempts to cover a global
perspective of the current status of fine particulate matter pollution (PM2.5) particles
with an aerodynamic diameter of 2.5 μm or less. Their range of concentrations and
 A. Mukherjee and M. Agrawal

sources and their health effects in urban, suburban, rural, and remote areas of the
world are well documented and analyzed. The major objective of this review is to
collate the information on spatial variations in fine PM concentrations and their
exceedances in different continents of the world, with special reference to country
and city specific variations. Since fine PM is mainly responsible for negative health
impacts, source apportionment of fine PM, its constituents, and different health
impacts were also reviewed.

2 Method

World Wide Web was searched for combinations of key words such as fine
particulate matter pollution, PM2.5, source apportionment of fine PM, constituents
of PM2.5, health effects of fine PM in PubMed, Scopus, Google scholar, and
SciVerse. We selected 500 peer-reviewed articles published after year 2000
containing information on fine PM concentrations and related health effects.
Among the articles searched, only those satisfying the criteria such as measurement
of fine PM and source apportionment by standard methodology, health effects using
human subjects and relevant statistical analyses for health assessment were further
screened for the review. Local studies with only limited data for specific season or
location were excluded with exception of a few studies having no long-term data
available for comparison at such locations. For global and country specific varia-
tions in fine PM, databases from government organizations like Central Pollution
Control Board (CPCB) in India, United States Environmental Protection Agency
(US EPA) in the USA, Chinese National Environmental Monitoring (CNEM) in
China, European Environment Agency (EEA) for Europe, and World Health
Organization (WHO) for global database were also screened (CPCB 2013;
CNEM 2013; EEA 2013, US EPA 2015; WHO 2014). Relevant published reviews
and meta-analysis were also searched to identify the health effects of PM2.5 and its
constituents.

3 PM2.5 Guidelines and Standards

PM2.5 and below in ambient air significantly cause severe health concern, even in
low concentrations. Several national and international monitoring agencies have
proposed guideline values to reduce health effects caused by PM2.5. The values
above the guidelines are suggested to be toxic or causing severe negative effects on
breathing for both short and long durations, but no concentration is identified at
which no health effect is recorded (WHO 2005). These values are suggested based
on scientific evidences of toxicity of specific pollutant, geographic location, emis-
sion sources, economic conditions, and monitoring duration. These guidelines are
implemented to reduce or control the pollutant under the specific conditions of a
country. Selected PM2.5 guideline values for 24-h average (short term) and annual
average (long term) of national and international agencies are given in Table 1.
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

Table 1 PM2.5 ambient air quality guideline values (μg m3)

Agency/country 24-h Annual References
WHO 25.0 10.0 WHO (2005)
75.0 (IT-1) 35.0 (IT-1)
50.0 (IT-2) 25.0 (IT-2)
37.5 (IT-1) 15.0 (IT-1)
US EPA 35.0 12.0 (Primary) US EPA (2015)
15.0 (Secondary)
China 35.0 Class 1 15.0 Class 1 GB-3095 (2012)
75.0 Class 2 35.0 Class 2
India 60.0 40.0 CPCB (2009)
Europe 25.0 EEA (2013)
Australia 25.0 8.0 NEPM (2002)
Canada 30.0 (Old) 10.0 (2015) ECC (2013)
28.0 (2015) 8.80 (2020)
27.0 (2020)
Mexico 65.0 15.0 NOM (2005)
Bangladesh 65.0 15.0 Begum et al. (2013)
Thailand 50.0 25.0 PCD (2010)
Japan 35.0 15.0 EQSJ (2009)
IT-1 interim target-1, IT-2 interim target-2, IT-3 interim target-3

4 Global PM2.5 Status and Exceedance

4.1 Asia

Asia is the largest and most populated continent in the world with varying land-
scapes. Most of the developing countries in Asia have very high levels of air
pollutants (WHO 2014). West and South Asia are the most populated and polluted
zones in the world. In South Asia, Pakistan, Bangladesh, and Afghanistan have very
high PM2.5 concentration and values were 8.00–10.0 times above the World Health
Organization (WHO) annual mean standard of 10.0 μg m3 (WHO 2005). In India,
fine PM level was 5.00 times higher than the WHO annual mean standard. In West
Asia, fine PM levels were very high in Qatar, Iran, and in United Arab Emirates
although levels were significantly lower in Oman, Lebanon, and Israel (Fig. 2). In
East Asia, Mongolia has very high PM level of 64.0 μg m3 followed by China
(41.0 μg m3), whereas Japan is the only country having PM2.5 levels below the
WHO annual mean standard (Fig. 2d). South-East Asia is comparatively less
polluted by fine PM as most of the countries showed values below 25.0 μg m3
except Vietnam and Myanmar (WHO 2014).
 A. Mukherjee and M. Agrawal

a b c

d e

PM2.5
< 10
10 to 25
25 to 50
50 to 75
>= 75

Fig. 2 Global distribution of PM2.5 concentration (μg m3) in different continents of the world (a)
North America, (b) South America, (c) Europe (d) Asia, and (e) Africa. (Data source WHO 2014)

4.1.1 India

Most of the major metropolitan cities in India violate the annual mean WHO and
national mbient air quality standard (NAAQS) of India (CPCB 2009) for PM2.5
(CPCB 2013) (Fig. 3). Major cities like Delhi, Ahmedabad, and Patna showed
levels higher than 100 μg m3 (CPCB 2013). Southern and northeastern part of
India showed lower levels of PM2.5 compared with other regions mostly due to
higher vegetation cover, lower emissions, and planned urbanization (CPCB 2013;
Tian et al. 2014). Most cities in north India are unplanned with huge population and
poor road conditions that are ideal conditions for higher particulate episodes
throughout the year. Seasonal variations were distinct with higher pollution load
in winter and lower in rainy season (CPCB 2013). Chennai was found to be the least
polluted with PM2.5 and maximum levels were found in Delhi. Traffic is identified
as a major cause of such higher PM2.5 level in India (CPCB 2013).
Northern parts of India are highly polluted with PM levels in ambient air (Fig. 4).
New Delhi, the capital of India, showed very high PM2.5 levels ranging between
27.0 and 227 μg m3 in urban atmosphere which exceeded the annual mean
NAAQS of India (CPCB 2009) by 2.40 times (Tiwari et al. 2009). Further Tiwari
et al. (2013) reported a higher annual mean of 122 μg m3, with variations between
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

Fig. 3 Mean annual PM2.5 concentrations for year 2013 in China and the USA and for 2011 for
India and Europe (Data Source CPCB 2013; CNEM 2013; EEA 2013, US EPA 2015, WHO 2014)

54.3 and 338 μg m3 in New Delhi. Higher concentration of fine PM in northern
India is a direct result of excessive biomass burning, coal burning, traffic, and dust
storms in summer from Thar Desert of Rajasthan (Kulshrestha et al. 2009; Tiwari
et al. 2013). Mean PM2.5 concentrations in both urban and rural areas in Agra were
more than double the annual mean NAAQS of India (CPCB 2009), and annual
average levels were 10.5 and 9.10 times higher than annual mean WHO standard,
respectively (Kulshrestha et al. 2009). Similarly, in Kanpur ambient PM2.5 levels in
commercial, residential, and control sites were well above the annual mean national
standard of India and 14.0, 9.50, and 6.00 times of WHO annual mean standard at
respective sites (Sharma and Maloo 2005).
PM2.5 levels ranged between 34.5 and 112 μg m3 in the largest city of eastern
India, Kolkata, with annual mean value, almost 1.80 times the annual mean national
standard (CPCB 2009), and maximum exceedance occurred during winter season
(2.30–2.80 times) (Chatterjee et al. 2012). In Raipur, another growing urban center
in eastern India, PM2.5 levels ranging from 24.0 to 269 μg m3 with a mean value of
150 μg m3, which was more than three times higher than annual mean NAAQS
(CPCB 2009). But the most concerning factor was that PM2.5 levels exceeded the
annual mean standard for 94.0 % of sampling days (Deshmukh et al. 2013).
 A. Mukherjee and M. Agrawal

Fig. 4 Variations in PM2.5 concentrations at different urban locations throughout the world.
Concentrations are mean values based on measurements performed in different years (varying
from 1999 to 2013)

Monitoring data from heavily urbanized area of Ahmedabad, one of the largest
city in western India, revealed PM2.5 concentrations to be 1.30 times the NAAQS
and 5.00 times of WHO annual mean standard during the study period from 2006 to
2007 (Sudheer and Rengarajan 2012). A study based on different land use patterns
in Mumbai city by Joseph et al. (2012) reported 59.0, 76.0, 67.0, and 80.0 %
exceedance of NAAQS (CPCB 2009) for PM2.5 at control, kerb, residential, and
industrial sites, respectively.

4.1.2 China

China showed higher PM2.5 concentrations in all major cities with violation of annual
mean Class I Chinese ambient air quality standards (CAAQS) of 15.0 μg m3 and Class
II standard of 35.0 μg m3 (GB3095 2012) (Fig. 3). Shijiazhuang and Jinan showed
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

values above 100 μg m3 in north, whereas apart from Haikou and Fuzhou in south-east
and Yinchuan, Lhasa, and Kunming in western China, all other cities showed PM2.5
levels above 50.0 μg m3 (WHO 2014). Seasonal variations were distinct with maxi-
mum concentration during winter and lowest during summer season. Higher exceedance
levels of PM2.5 concentrations were mostly in northern part compared to south-east and
west and exceedance rates were more in winter than in summer season.
In urban and suburban areas in Tianjin, PM2.5 mass concentration was above
CAAQS (GB3095 2012) and almost 13.0 times the WHO annual mean standard
(Li et al. 2012). PM2.5 mean concentrations were just above 24-h CAAQS at suburban
sites near two largest cities, Beijing and Shanghai (Zhou et al. 2009), however, at an
urban site in Shanghai, concentrations varied from 8.00 to 389 μg m3 with annual mean
level exceeding annual mean CAAQ Class II standard by 1.60 times during the study
period of 2004–2008 (Chen et al. 2013). Hu et al. (2014) studied short-term PM2.5 levels
during June–August 2013, in 13 cities located in North China Plain (NCP) and in
20 cities in Yangtze River Delta (YRD). Average PM2.5 levels were 77.0 μg m3 in
NCP region and 42.8 μg m3 in YRD region and in both the regions, annual mean CAAQ
Class I standard was exceeded by 83.0 % and 51.0 % of times, respectively. Mean annual
level of PM2.5 in Chengdu was 10.0 times of the WHO annual mean standard and almost
three times of annual mean CAAQ Class II standard of 35.0 μg m3.

4.1.3 Other Asian Countries

PM2.5 levels were recorded very high in Lahore, Pakistan with annual average
concentration of 194 μg m3 during 2007–2008, and PM2.5 levels were above
100 μg m3 for 84.0 % of sampling days (Stone et al. 2010). Khwaja et al. (2015)
reported PM2.5 concentrations varying between 30.0 and 279 μg m3 with an
annual mean of 101 μg m3 in the megacity of Karachi, Pakistan during
2008–2009. Long-term monitoring results of PM2.5 concentrations from 1996 to
2011 in Dhaka, Bangladesh showed values ranging between 5.26 and 240 μg m3
with a mean value of 36.7 μg m3, which was 3.70 times higher than WHO annual
mean standard and 2.40 times of Bangladesh annual standard of 15.0 μg m3
(Begum et al. 2013) (Fig. 4). In an urban traffic-influenced site in Dhaka, annual
mean PM2.5 concentration level was 82.5 μg m3, which was ascribed to high traffic
under urban influence (Begum et al. 2012). Alolayan et al. (2013) in Kuwait City
reported PM2.5 levels to be 5.00 times the WHO annual mean standard and
exceedance of 78.0 % days above WHO 24-h mean value. In Jeddah, Saudi Arabia,
PM2.5 levels were 3.40 times of the WHO annual mean standard (Hussein et al.
2014). PM2.5 concentrations varied between 23.0 and 186 μg m3 with an average
of 74.2 μg m3 during 2000–2001 in Jeddah, Saudi Arabia (Hussain et al. 2014).
Compared to other Asian megacities, PM2.5 levels were comparatively lower in
Singapore with annual mean PM2.5 concentrations of 27.2 μg m3 and levels
exceeded only 30.0 % times, the value of 30.0 μg m3, although the mean level
was 2.70 times higher than WHO annual mean standard (Balasubramanian et al.
2003). In urban residential site in Karachi, Pakistan, PM2.5 concentration varied
 A. Mukherjee and M. Agrawal

from 27.4 to 175 μg m3 with annual mean level, 8.35 times higher than the annual
mean WHO standards (Mansha et al. 2012). Han et al. (2011) monitored PM2.5
levels at a rural site in Chuncheon, Korea and reported that about 37.0 % of samples
exceeded 24-h US NAAQS of 35.0 μg m3 and annual mean level was 3.00 times
the annual mean WHO standard (Fig. 6). Urban residential site in Kaohsiung City,
Taiwan showed PM2.5 levels ranging from 0.80 to 162 μg m3 with annual mean
value three times of the annual mean WHO standard during 2006–2010 (Cheng
et al. 2014).

4.2 Africa

In the African continent, fine PM levels were above 30 μg m3 in Senegal,

Mauritius, and Ghana whereas in South Africa, level was below 30 μg m3
(Fig. 2e). Compared to other countries in Africa, Ghana showed high mean PM2.5
value of around 49 μg m3 (WHO 2014). Due to lack of data in the most of the
countries in this region, limited information is available on fine PM levels in Africa.
Poor air quality in African continent is not new with excessive biomass burning for
cooking and dusty roads. African dust storms add more concern to the already
severely affected continent.
High PM2.5 levels were observed by Doumbia et al. (2012) at a traffic-influenced
site in Dakar, the capital and the largest city of Senegal in West Africa, where daily
mean levels varied between 24.0 and 80.0 μg m3 and annual mean concentration
was several times higher than WHO annual mean standard. Dionisio et al. (2010)
reported about 8.00–14.0 μg m3 higher PM2.5 levels in roadside compared to
residential site in Accra, the capital of West African country of Ghana. Fine PM
levels ranged between 3.00 and 53.0 μg m3 at an urban background site and from
1.90 to 36.0 μg m3 at a suburban site in Nairobi, Kenya, and both sites exceeded
the 24-h WHO standard by 29.0 and 7.00 %, respectively (Gaita et al. 2014). PM2.5
at a kerb side in Dares Salaam, the largest city of Tanzania ranged between 5.10 and
66.0 μg m3 (Mkoma et al. 2010). Around an urban industrial area in Harare,
Zimbabwe Kuvarega and Taru (2008) found mean PM2.5 concentration of
40.5 μg m3, which exceeded the WHO annual mean limit throughout the moni-
toring period. Owoade et al. (2015) found fine PM ranging between 14.4 and
986 μg m3 around scrap iron and steel smelting industries in South Western
Nigeria during 2011–2012, with a mean value of 300 μg m3 around the main
production unit.
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

4.3 Europe

Europe seems to have much better air quality related to fine PM concentration
compared to other regions of the world primarily due to planned development,
green technology, reduction in emissions, and lower population density (Maas and
Grennfelt 2016). Fine PM levels were least in Northwestern Europe with only
United Kingdom, Denmark, and Lithuania having values above WHO guideline
(Fig. 2c). In Western Europe, most of the countries have PM2.5 values ranging
between 15.0 and 20.0 μg m3 (WHO 2014). In Eastern Europe, fine PM values
above 20.0 μg m3 were recorded in most of the countries except Romania and
Belarus and maximum concentration was reported from Turkey, with annual
average level of 39.0 μg m3 (WHO 2014). In Southern European countries, annual
fine PM values were just above the annual mean WHO levels of 10.0 μg m3 in
Spain, Portugal, and Malta, above 20.0 μg m3 in Slovenia and Italy, above
30.0 μg m3 in Serbia, and above 40.0 μg m3 in Bulgaria (WHO 2014).
PM2.5 levels in most European cities were well below the annual mean European
Union (EU) PM2.5 standard of 25.0 μg m3 (Fig. 4). In some of the cities like
Dublin (Ireland), Stavanger (Norway), Stockholm (Sweden), and Helsinki (Fin-
land), the levels were even below the annual mean WHO PM2.5 standard of
10.0 μg m3. In Madrid (Spain), Lisbon (Portugal), and Glasgow (UK), levels
were just above or around the annual mean WHO standard. Only few cities showed
values above the annual mean EU PM2.5 standard like Sofia (Bulgaria) and Istanbul
(Turkey), where annual mean levels were twice the EU permissible limit. Larger
European cities like Paris, Berlin, Barcelona, Prague, Moscow, and London also
showed PM2.5 values below EU permissible limit, but were well above WHO,
PM2.5 annual mean standard.
Rajšić et al. (2008) reported PM2.5 concentration to be three times higher than
the European Commission (EC) annual limit of 20.0 μg m3 and six times of the
WHO annual limit in Belgrade, Serbia. Roadside monitoring of PM2.5 in Athens,
Greece, showed levels ranging from 8.00 to 135 μg m3 with annual mean level
almost four times of the annual mean WHO and 1.60 times of the annual mean
European Union (EU) standards (Chaloulakou et al. 2005). In dense traffic area
around a highway in Istanbul, Turkey, Onat et al. (2013) found PM2.5 levels ranged
from 23.8 to 81.5 μg m3 whereas PM2.5 value was observed above 35.0 μg m3
during 60 % of the total monitoring period.
Mean annual PM2.5 concentration was twice the EU and five times of the WHO
annual mean standards in industrialized city of Bursa, Turkey (Kendall et al. 2011).
Mean PM2.5 concentrations were 24.11 and 64.3 μg m3, respectively, in suburban
and urban areas in Izmir, Turkey during 2004–2005 (Yatkin and Bayram 2008). In
three cities, Pavia, Verona, and Torino in Northern Italy, PM2.5 levels were 1.4, 1.5,
and 1.9 times of the annual mean EU standard whereas exceedance in daily air
quality value was more than 50 % in all these cities (Traversi et al. 2009). Lazaridis
et al. (2008) found PM2.5 concentration close to the EU annual mean, but were
2.50–2.70 times higher than the annual WHO standard at Akrotiri station, an urban
 A. Mukherjee and M. Agrawal

Fig. 5 Variations in PM2.5 concentrations at different urban, urban traffic, and urban background
locations throughout the world. Concentrations are mean values based on measurements
performed in different years (varying from 1998 to 2013)

background area of the island of Crete, Greece (Fig. 5). In suburban areas in
Cartagena, Spain, PM2.5 concentrations ranged from 7.00 to 47.0 μg m3 with
annual mean below the EU standard and 2.20 times the annual mean WHO standard
(Fig. 6) (Negral et al. 2008). Long-term monitoring results from 2003 to 2012 at a
rural site in Melpitz, Germany showed that PM2.5 levels were consistently above the
annual mean WHO standard (Spindler et al. 2013) (Fig. 6). Hazenkamp-Von Arx
et al. (2004) monitored PM2.5 levels in 21 cities in Europe for 1 year and found
PM2.5 levels ranging from 3.70 to 44.9 μg m3 with lowest concentration in
Reykjavik, the capital of Iceland and maximum in Turin, Italy. In most of the
major cities like Paris, Barcelona, and Antwerp, PM2.5 levels were above the annual
mean WHO standard. A similar study from 20 European sites during 2008–2011
found that 16 out of 20 sites showed PM2.5 levels above the WHO annual limit,
whereas except Turin, Italy, all other cities were below the EU annual limit (Eeftens
et al. 2012).
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

Fig. 6 Variations in PM2.5 concentrations at different urban residential, suburban, rural, and
remote location throughout the world. Concentrations are mean values based on measurements
performed in different years (varying from 1994 to 2013)

4.4 South America

Unlike Asia and Africa, South American countries have regulated fine PM levels up
to a significant level (WHO 2014). In most of the countries, PM2.5 levels were
below 30.0 μg m3 with exception of Peru where concentration was 39.0 μg m3. In
Brazil and Columbia, values were below 25.0 μg m3, whereas in Uruguay,
Argentina, Ecuador, and Paraguay levels were even below 20.0 μg m3 (Fig. 2b).
PM2.5 estimation in highly traffic area in six Brazilian state capitals revealed that
concentration was maximum in Sao Paulo (28.1 μg m3) and least in Recife
(7.10 μg m3). In all the cities except Recife, levels were higher than the annual
mean WHO and USEPA standards (de Miranda et al. 2012).
Mariani and de Mello (2007) reported PM2.5 concentration of 17.0 μg m3 at a
costal urban site in Rio de Janeiro, Brazil. Short-term study of PM2.5 levels by
Lemos et al. (2012) in urban, industrial, and residential areas in Rio Grande city,
 A. Mukherjee and M. Agrawal

Brazil showed that levels were below the Brazilian standard, but higher than 24-h
WHO standard on few occasions during the study period. PM2.5 mean concentration
was 71.0 and 61.0 μg m3 in urban and semiurban areas of the Córdoba, the second
largest city of Argentina which was three times higher than the EU and seven times
higher than the annual mean WHO standards during the period of July 2009–April
2010 (López et al. 2011).

4.5 North America

PM2.5 levels in North American continent were variable with countries. Levels in
Canada were below the WHO annual mean standard and were just above the
standard in the USA (WHO 2014). In countries like Mexico levels were 2.50
times higher than the annual mean WHO standard (Fig. 2a).
According to US EPA dataset for PM2.5 (Weighted Annual Mean) for year 2013
(US EPA 2015), levels in most of the areas in the USA were below NAAQS
(US EPA 2012) annual mean standard of 15.0 μg m3 (Fig. 3). Only few areas
having higher PM2.5 levels are Bakersfield, CA; Fairbanks, AK; Fresno, CA based
on Core Based Statistical Area (CBSA) in the USA. The database clearly showed
that PM2.5 is under control in most of the areas in the USA. In many areas values
were even below 5.00 μg m3. When 98th percentiles of the daily average mea-
surement values for the whole period were compared, exceedance of 24-h NAAQS
of 35 μg m3 was more prominent (US EPA 2012). It indicates that short-term
effects of PM2.5 are more realized than the long-term ones. Results of 537 monitor-
ing sites for PM2.5 from 2000 to 2013 indicate a 34.0 % national decrease in fine PM
concentration in the USA (US EPA 2014).
Saldarriaga-Nore~ na et al. (2009) in Guadalajara, Mexico found PM2.5 levels to be
2.90 and 3.50 times the annual mean Mexican standard of 15.0 μg m3 in industrial
and traffic-influenced sites, with values ranging from 2.00 to 181 μg m3 during the
study period (Fig. 4). Raysoni et al. (2011) analyzed PM2.5 levels outside schools in
US-Mexican border and found higher concentrations at schools in Ciudad Juárez,
Mexico compared to El Paso, USA during January to May 2008. A short-term study
by Olson et al. (2008) at a residential outdoor in Tampa, USA showed that PM2.5 level
was three times below the USEPA 24-h standard during October and November 2002.
Long-term monitoring results in both New York City and Rochester, USA showed
decreasing pattern of PM2.5 level from 2003 to 2012 with values within the annual
mean WHO and US EPA levels in Rochester and just above WHO level in New York
City (Rattigan et al. 2013). In four cities in Connecticut and one in Massachusetts,
PM2.5 levels ranged between 11.9 and 17.0 μg m3 with maximum concentration of
18.3 μg m3 during cold season in New Heaven and lowest concentration of
11.6 μg m3 at Hartford (Lee et al. 2011). Qin et al. (2006) found average PM2.5
concentration of 13.0–15.0 μg m3 in different urban commercial area in
New York City.
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

5 Source Apportionment for PM2.5

Source apportionment studies help to recognize or characterize those factors that

contribute to pollution levels. The composition of PM depends upon its origin and
transformations that happen under different environmental conditions (Hyder et al.
2014). An effect of PM is elicited based on its chemical nature and toxicity. PM2.5 is
mostly generated due to combustion and emissions from automobiles (Fleisch et al.
2014). Major components of PM2.5 are black carbon (BC), polycyclic aromatic
hydrocarbons (PAHs), heavy metals, organic carbon, hydrocarbons, volatile
organic hydrocarbons (VOCs), minerals, inorganic ions, and biological material
(Tiwari et al. 2009; Traversi et al. 2009; de Miranda et al. 2012; Fleisch et al. 2014).

5.1 Asia

In New Delhi, India, Tiwari et al. (2009) reported that PM2.5 was made up of
undetermined fractions (40.9 %), secondary inorganic aerosols (27.1 %), salt aero-
sols (23.3 %), and mineral matter (8.70 %) indicating sources such as biomass and
fossil fuel burning and soil derived particles. Source apportionment through prin-
cipal component analysis (PCA) of PM2.5 revealed that major contributors were
vehicular emission (38.0 %), biomass burning (27.0 %), dust aerosols (18.0 %), and
secondary anthropogenic components (11 %) in the eastern Indian megacity of
Kolkata in 2006 (Chatterjee et al. 2012). PM2.5 mass was mostly contributed by
organic matter (36.0–52.0 %), secondary inorganic aerosols (21.0–27.0 %), crustal
(6.00–12.0 %), non-crustal (4.0–8.00 %), and sea salt (6.00–11.0 %) in Mumbai,
India (Joseph et al. 2012). Sudheer and Rengarajan (2012) in urban atmosphere of
Ahmedabad, India reported that anthropogenic sources (80.0 %) contributed to
PM2.5 mass and identified industrial emission, biomass burning, vehicular emis-
sions, and resuspended or long range transported dust as the major sources of
particulate pollution.
Major contributors to high PM2.5 in Karachi, Pakistan were industrial emissions
(53.0 %), road dust (16.1 %), and secondary aerosols (12.4 %) (Mansha et al. 2012).
Source apportionment study by Raja et al. (2010) in Lahore, Pakistan detected
secondary particles (30.2 %), diesel emissions (28.3 %), biomass burning (14.8 %),
coal combustion (13.3 %), and two-stroke vehicles (7.70 %) as the major contrib-
utors to observed PM2.5 mass. Alolayan et al. (2013) in Kuwait City found maxi-
mum contribution of soil/sand dust (54.0 %) followed by oil combustion (18.0 %),
petrochemical industry (12.0 %), local traffic (11.0 %), and transported traffic/
smelter emissions (5.0 %) to PM2.5, indicating that major sources in Kuwait city are
of crustal origin which is approximately 50.0 % mass of PM2.5, and were attributed
to dust storm events in this area (Alolayan et al. 2013). Major sources of fine
particles in Kuala Lumpur, Malaysia were two-stroke engines (35.7 %), motor
vehicles (31.9 %), smoke/biomass burning (17.5 %), soil dust (8.30 %), and
 A. Mukherjee and M. Agrawal

industry (16.7 %) (Rahman et al. 2011). At a traffic site in Bangkok Metropolitan

Region, Thailand, Chuersuwan et al. (2008) observed maximum contribution from
automobiles (32.0 %), followed by biomass burning (26.0 %). PCA analysis
revealed six major sources of PM2.5 in Singapore as soil dust, metallurgical
industry, emissions from biomass fires and local traffic, sea spray, and fuel oil
combustion processes (Balasubramanian et al. 2003).

5.2 Europe and Africa

Rogula-Kozłowska et al. (2013) found that apart from industrial, power plants, and
soil/road dust, combustion of fuels in domestic uses and automobiles contributed to
36.0–78.0 % PM2.5 mass at two sites in Poland. In urban traffic and background
sites, Voutsa et al. (2014) found secondary inorganic aerosols (SIA) to be a major
part of PM2.5 mass and identified local sources and long range transport as major
contributors to SIA formation in Thessaloniki, Greece. In Barcelona Metropolitan
area, Spain, vehicular-secondary sources contributed 73.0 % of PM2.5 mass (Querol
et al. 2001). Rajšić et al. (2008) reported combustion sources from traffic and
resuspended road dust mostly contribute to trace metals in coarse and fine fraction
of PM in a central urban area in Belgrade, Serbia. Negral et al. (2008) identified
sources of PM2.5 as crustal, traffic, secondary, marine, Zn metallurgy industry, and
shipyard in Cartagena, Spain. Source profile of fine PM using positive matrix
factorization (PMF) technique, in Izmir, Turkey, showed contributions of
unidentified fraction (38.0 %), fuels and steel (37.0 %), traffic (12.0 %), mineral
(9.00 %), and marine (4.00 %) sources in suburban area whereas unidentified
(48.0 %), fuels and steel (22.0 %), traffic (15.0 %), marine (14.0 %), and mineral
(1.00 %) in urban area Yatkin and Bayram (2008).
Zakey et al. (2008) identified waste burning to be a significant source of PM2.5 in
different environments of Greater Cairo area in Egypt. In Nairobi, Kenya, source
apportionment by PMF identified five major sources of fine PM as traffic (39.0 %),
mineral dust (35.0 %), mixed factor (13.0 %), industrial (7.0 %), and combustion
(6.0 %) (Gaita et al. 2014). Around scrap iron and steel smelting industries in South
Western Nigeria, Owoade et al. (2015) identified coking coal (83 %) as the major
source of fine PM followed by soil (10.0 %), metallurgical industry (6.00 %), and
electronic waste processing (1.00 %).

5.3 North and South America

Source apportionment analysis by Olson et al. (2008) in residential outdoors of

Tampa, Florida identified sulfate (55.0 %), gasoline-powered motor vehicles
(32.0 %), diesel-powered vehicles (8.00 %), and road dust (5.00 %) as major
sources of PM2.5 by using EPA Chemical Mass Balance Model. Pancras et al.
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

Fig. 7 Source apportionment of PM2.5 in selected cities of the world

 A. Mukherjee and M. Agrawal

(2013) in Dearborn, Michigan, USA identified automobiles, road dust, and indus-
tries, secondary sources as the major sources of PM2.5 pollution. Sources of PM2.5
in four cities in Connecticut and one in Massachusetts in the USA were sulfur-
related pollution, motor vehicle, road dust, oil combustion, and sea salt (Lee et al.
2011).
A study by Murillo et al. (2013) to identify sources of EC and OC in PM2.5 mass
characterized gasoline vehicles (10.0 %), on-road diesel emissions (16.0 %), rail-
road traffic (4.0 %), industrial combustion (9.0 %), and wood smoke (5.0 %) as
major contributors to PM2.5 in Costa Rica, Central America. Major sources of PM2.5
in urban area of Córdoba City, Argentina were traffic (32.0 %), urban dust (54.0 %),
soil dust (1.00 %), metallurgical industries and diesel (13.0 %), whereas in subur-
ban site major contributors were urban dust (56.0 %) followed by traffic (28.0 %)
and metallurgical industries and diesel (11.0 %) (López et al. 2011).
Different sources of fine PM in different regions of the world mostly depend on
local activities, population density, atmospheric condition, and land use pattern. In
Fig. 7 a detailed source profile of PM2.5 at selected cities of the world, where
exceedances are high is shown.

6 Gas to Particle Conversion and Secondary Aerosol

Formation in Atmosphere

PM in the atmosphere is either directly generated through primary sources or by

secondary formation due to gas to particle conversion. Secondary generation of PM
contributes significant portion of fine PM in the atmosphere, as most of the
secondary aerosols are formed from particles of size 0.10–2.50 μm (Baek et al.
2006; Hallquist et al. 2009; Zhang et al. 2015; Yao et al. 2016).
Major secondary aerosols in the atmosphere are organics, sulfate, nitrate, ammo-
nium, and other inorganic salts, which are formed either by gas to particle conver-
sion or by particle phase reactions (Zhang et al. 2015; Huang et al. 2016). Primary
emitted gases in the atmosphere such as sulfur dioxide (SO2), nitrogen dioxide
(NO2), ammonia (NH3), ozone (O3), and VOCs undergo photochemical oxidation,
hydration, peroxyradical self-reaction, and condensation to produce various short
lived intermediate molecules, which by process of nucleation, transformation, and
coagulation ultimately produce secondary aerosols (Baek et al. 2006; Hallquist
et al. 2009; Zhang et al. 2015). Secondary aerosol formation is a complex process
controlled by concentrations of precursor atmospheric gases, particle size of
existing PM, relative humidity, temperature, wind speed and direction, boundary
layer height, and solar radiation (Huang et al. 2016). Higher relative humidity
increases higher secondary formation by increasing oxidation of sulfur and nitrogen
species in the atmosphere (Huang et al. 2016).
Secondary aerosol formation and their lifetimes in the atmosphere is variable
with higher concentrations during day time which is correlated with higher
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

emissions of precursor gases and suitable atmospheric conditions for secondary

aerosol formation. Mancilla et al. (2015) found 32.0 % higher organic carbonaceous
aerosol during day hours compared to night time in an urban area of Monterrey,
Mexico.
Inorganic aerosols such as sulfate and nitrate are formed through initial reactions
of hydroxyl radicals (OH) with SO2 and NO2 by intermediate formation of sulfuric
and nitric acid. Nitric acid may further react with ammonia gas to form ammonium
nitrate aerosol. Sulfuric acid may further nucleate or may be absorbed at existing
particle surfaces or form salts with other inorganic species such as ammonia (Baek
et al. 2006; Hallquist et al. 2009; Zhang et al. 2015). In Beijing, China, secondary
inorganic aerosols such as sulfate, nitrate, and ammonium contributed almost
82.8 % of total inorganic mass of water soluble inorganics in fine PM compared
to 61.8 % contribution in coarse particle fraction, indicating higher secondary
formation in fine mode aerosols (Zhang et al. 2015). Further, during polluted
days contributions of secondary inorganic aerosols (sulfate, nitrate, and ammo-
nium) were much higher (82.0–90.0 %) than in non-polluted days (64.0–81.0 %) in
total PM inorganic mass.
In comparison to inorganic aerosols, reaction mechanisms of VOCs are much
more complicated. Different VOCs released into the atmosphere undergo further
oxidation to produce less volatile organics, such as aldehydes, carboxylic acids,
ketones, and hydroperoxides, by photo-oxidation in the presence of hydroxyl
radicals, ozone, nitrate, water vapor through several chemical reactions such as
aldol condensation, ozonolysis, and peroxyradical self-reaction to form secondary
organic species (Zhang et al. 2015). Significant contributions of around
11.0–52.0 % of secondary organic aerosols in PM2.5 were observed in an urban
metropolitan area of Monterrey, Mexico by Mancilla et al. (2015), whereas in an
urban area of Ahmedabad city, 34.6 % and 45.0 % contributions to the total
carbonaceous aerosol mass in PM2.5 were reported by Sudheera et al. (2015),
respectively, during day and night time.

7 Health Effects of PM2.5

Among outdoor air pollutants, PM2.5 is the most prevailing contributor to the global
health liability (Anenberg et al. 2010). PM2.5 has the ability to cross the alveoli of
the lung and can finally enter into the blood stream to produce inflammatory or
oxidative damage, leading to more drastic and long-term secondary effects on both
cardiovascular and nervous systems (Araujo 2011; Breysse et al. 2013; Øvrevik
et al. 2015). These health effects mostly depend upon age, lifestyle, health status,
medical care, and exposure concentrations of the pollutants and climate. Percentage
change in PM2.5 mean annual exposure data between 1990 and 2010 showed a
global increase of PM2.5 exposure by 9.90 % (World Bank 2015). This global
increase is directly correlated with 8.00 % increase in South Asia and 34.0 %
increase in East Asia and Pacific. Significant reductions have, however, occurred in
 A. Mukherjee and M. Agrawal

European Union (42.0 %), Latin American countries (7.00 %), and the USA
(29.0 %) in the last two decades (Fig. 8). A detailed summary of studies examining
the association between PM2.5 and health effects is presented in Table 2. It is
beyond the scope of this article to assess all the health effects of PM2.5, therefore
in this section we have only discussed recent studies suggesting association of
PM2.5 and health effects from article published between 2004 and 2017.

7.1 Evidences from Recent Reviews and Meta-Analysis

of Health Effects of Fine PM

Sun et al. (2015) assessed a relationship between fine particulate matter exposure during
pregnancy and preterm birth based on 18 studies before 2014 and found a positive
association between fine PM and preterm birth. Hamra et al. (2014) suggested outdoor
air pollution and PM to be classified as Group-1 carcinogen based on the systematic
review and meta-analysis of outdoor particulate matter exposure and lung cancer risk. In
a systematic review and meta-analysis of short-term exposure to PM Bell et al. (2013)
reported a higher risk of PM associated hospitalization and death for elderly persons and
indicative evidence of higher risk of death for lower education and income group
individuals. In a systematic review and meta-analysis of epidemiological time-series
studies (61 studies, 40 investigated daily mortality, and 27 hospital admissions)

Fig. 8 Percentage change in mean annual exposure concentration of PM2.5 between 1990 and
2010. Darker region indicates positive increase in PM2.5 exposure, whereas lighter region indicates
decrease in PM2.5 exposure in the last two decades (World Bank 2015)
Table 2 Summary of studies examining the association between PM2.5 and health impacts
Data
collection Sample
Study period Location size Age Method/model Results Findings References
Global burden of Global All ages Global atmo- 3.50  0.90 million Anthropogenic Anenberg
mortality due to spheric chemical cardiopulmonary PM2.5 contrib- et al.
PM2.5 transport model and utes substantially (2010)
220,000  80,000 to global prema-
lung cancer mortal- ture mortality
ities annually
Source-specific 2001–2002 New York 65.0 Time-series gen- Source-related Toxicity of Lall et al.
daily PM2.5mass City, USA eralized linear PM2.5 (specifically PM2.5 depends (2011)
and hospital model steel and traffic) was on the source
admissions significantly associ-
ated with hospital
admissions
Mortality effects 2005–2009 Beijing, China Poisson general- 10.0 μg m3 Significant asso- Li et al.
from PM size ized additive increase in PM2.5 ciations between (2013)
fractions models levels is associated daily mortality
with a 0.65 % (95 % with PM2.5
CI: 0.29–0.80 %),
0.63 % (95 % CI:
0.25–0.83 %), and
1.38 % (95 % CI:
0.51–1.71 %)
increase in
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

non-accidental,
respiratory and cir-
culatory mortality,
respectively
(continued)
Table 2 (continued)
Data
collection Sample
Study period Location size Age Method/model Results Findings References
Short-term asso- 2000–2006 9 French cities 548,474 15.0–74.0, >74.0 Poisson regres- 10.0 μg m3 Significant asso- Pascal
ciations between sion model increase in PM2.5 ciation between et al.
PM2.5 and results in increase of short-term (2014)
mortality (+0.7 % [0.1; 1.6]) impacts of PM2.5
on all-ages on mortality
non-accidental
mortality
Traffic related 2004–2006 Los Angeles, 220,528 Logistic Approximately Significant asso- Wilhelm
air toxics and USA regression 5.00 % increase in ciation between et al.
low birth weight adjusted odds of PM2.5 with fetal (2012)
(LBW) term LBW per IQR growth
increase was associ-
ated with exposures
to PM2.5
PM exposure 2000–2003 Bochum, 4291 45.0–75.0 Generalized IQR increase in Significant asso- Fuks et al.
with arterial BP Essen, and additive models PM2.5 (2.40 μg m3) ciation between (2011)
and hypertension Mülheim, was associated with long-term expo-
Germany estimated increases sure to PM with
in mean systolic and increased arterial
diastolic BP of BP and
1.40 mmHg (95 % hypertension
CI: 0.5, 2.3) and
0.9 mmHg (95 % CI:
0.4, 1.4),
respectively
A. Mukherjee and M. Agrawal
Ambient air and 2005–2008 Boston, USA 765 65.0 Epidemiological OR of CESD-R No association Wang
traffic pollution studies depres- score  16.0 of 0.67 between expo- et al.
and the presence sion scale (95 % CI: 0.46, 0.98) sure to ambient (2014)
of depressive per IQR (3.04 μg m air pollutants
3
symptoms ) increase in PM2.5 with depressive
over the 2 weeks symptoms
preceding assessment
Fine particulate 1999–2002 204 US urban 11.5 > 65.0 Bayesian 2-stage 1.28 % (95 % CI, Significant asso- Dominici
air pollution and counties Million hierarchical 0.78 %–1.78 %) ciation between et al.
hospital models and sin- increase in risk of short-term expo- (2006)
admission gle lag and dis- heart failure per sure to PM2.5
tributed lag over 10.0 μg m3 increase with increases
dispersed in same-day PM2.5 the risk for hos-
Poisson regres- pital admission
sion models for cardiovascu-
lar and respira-
tory diseases
Association 1998–2004 New Jersey, 1719 20.0–40.0 Time-stratified The relative odds of Significant asso- Faiz et al.
between ambient USA case-crossover stillbirth increased ciation between (2013)
air pollution and design and con- with IQR increases in increased risk of
stillbirth ditional logistic the mean concentra- stillbirth with
regression tions of PM2.5 short-term
(OR ¼ 1.07, 95 % increases in air
CI ¼ 0.93–1.22) pollutants in the
2 days before previous few
delivery days
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

(continued)
Table 2 (continued)
Data
collection Sample
Study period Location size Age Method/model Results Findings References
Long- and short- 2000–2008 Massachusetts, Time-series 10.0 μg m3 increase Short-term Kloog
term effects of USA analysis in PM2.5 exposure effects of PM2.5 et al.
PM2.5 exposures was associated with a exposures was (2013)
on population 2.80 % increase in more severe on
mortality PM-related mortality population
(95 % CI ¼ 2.0–3.5) mortality
for short-term expo-
sure and 1.6
(CI ¼ 1.50–1.80) for
long-term exposure
Reduction in 2008, 2010 661 Eight busy urban Airway resistance Reduction in Boogaard
(traffic policy- and four subur- decreased with a (traffic policy- et al.
related) air pol- ban background decline in PM related) air pol- (2013)
lution concentra- locations were (9.0 % per IQR) lution concentra-
tions with selected for air tions may lead to
changes in respi- pollution and small improve-
ratory health respiratory ments in respira-
health tory health
measurement
Long-term expo- 2008–2011 9 European 312,944 Cox regression Hazard ratio of 118 Significant asso- Raaschou-
sure to ambient countries models (096–146) with per ciation between Nielsen
air pollution and 5.00 μg m3 long-term expo- et al.
lung cancer increase in PM2.5 sure to ambient (2013)
incidence air pollution and
lung cancer
A. Mukherjee and M. Agrawal
Long-term expo- 1979–1983 Columbia and 1.2 Million 30.0 Cox proportional Each 10.0 μg m3 Significant asso- Pope et al.
sure to fine PM and Puerto Rico hazards survival increase in fine par- ciation between (2002)
and all cause, 1999–2000 model ticulate air pollution long-term expo-
lung cancer and was associated with sure to fine par-
cardiovascular approximately a 4.0, ticulate air
mortality 6.0, and 8.0 % pollution and
increase risk of all lung cancer and
cause, cardiopulmo- cardiovascular
nary and lung cancer mortality
mortality
Association 2008–2009 Karachi, 40.0 < Age < 60.0 Generalized lin- 1.60 % Increase in Higher levels of Khwaja
between particu- Pakistan ear model both hospital admis- fine PM were et al.
late air pollution (GLM) using sions and emer- associated with a (2012)
and cardiovascu- negative bino- gency room visits striking eleva-
lar diseases mial regression for cardiovascular tion in rates of
disease with each ER visits and
10.0 μg m3 hospitalizations
increase in PM2.5 for cardiovascu-
concentration lar diseases
IQR interquartile range, CI confidence interval, HR hazard ratio, PI posterior interval, OR odds ratio
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects
 A. Mukherjee and M. Agrawal

Atkinson et al. (2015) assessed daily mortality and hospital admissions due to PM
pollution. Morakinyo et al. (2016) identified the role of biological and chemical
components of inhalable and respirable PM toxicity.

7.2 Evidences from Recent Health Effects Studies

of Fine PM

In a recent study by Wu et al. (2017) in Chinese men, sperm concentration and

count were found to be adversely effected by fine PM whereas no changes were
observed in sperm motility. The study concludes that fine PM pollution effects
sperm development specifically semen quality. Lu et al. (2017) identified a positive
association between PM2.5 exposure and glucose homeostasis during pregnancy in
3589 pregnant women in Chiayi City, Taiwan although short-term effect was
non-significant. Chen et al. (2017) reported association between ambient PM2.5
and influenza incidence in China and found that a 10.0 μg m3 increase in PM2.5
was associated with relative risk (RR) of 1.01 (95 % CI: 1.00, 1.02), of influenza
incidence that appeared at lag day 2. The authors also estimated that exposure to
fine PM may contribute to 10.7 % of incident influenza cases. Ajmani et al. (2016)
reported significant association between worsening of olfactory function with
PM2.5, 6-month average exposure (per 1-IQR increase in PM2.5: OR 1.28, 95 %
CI 1.05, 1.55) in home-dwelling US adults age 57–85 years. Mehta et al. (2016)
studied long-term PM2.5 exposure effects on renal function in a cohort of older men
in the Boston Metropolitan area and found a 2.10 μg m3 interquartile range higher
1-year PM2.5 was associated with a 1.87 mL min1/1.73 m2 lower estimated
glomerular filtration rate [95 % confidence interval (CI): 2.99, 0.76] suggesting
a reduction in renal function due to fine PM. In Seoul, Korea, Kim et al. (2016)
assessed the relationship between long-term PM2.5 exposure and major depressive
disorder in 27,270 participants 15–79 years of age from 2002 to 2010 and found risk
of major depressive disorder was positively associated with long-term exposure to
PM2.5.
Results of meta-analysis by Flores-Pajot et al. (2016) found changes in autism
spectrum disorder of 1.34 (95 % CI: 0.83, 2.17) with a 10.0 μg m3 increase in
PM2.5 exposure. In a short-term PM2.5 exposure and infant mortality study in Japan
Yorifuji et al. (2016) reported odds ratios of 1.06 (95 % confidence interval:
1.01–1.12) for infant mortality and 1.10 (1.02–1.19) for post-neonatal mortality
for a 10.0 μg m3 increase in PM2.5. Luo et al. (2015) in their systematic review and
meta-analysis of short-term exposure to particulate air pollution and risk of myo-
cardial infarction (MI) identified that 10.0 μg m3 increment in PM2.5 was associ-
ated with risk of MI (OR ¼ 1.02; 95 % CI 1.01–1.03). Meta-analysis of
25 published epidemiological studies between maternal exposure to PM2.5 and
pregnancy outcomes found a positive association between increase in PM2.5 con-
centrations and increase in the risk of low birth weight, preterm birth (PTB), and
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

small for gestational age (SGA) whereas the association was non-significant for
stillbirth (Zhu et al. 2015). In a 5-year study from 2005 to 2009, in six counties in
South-western Pennsylvania, authors found an increase in risk of childhood autism
spectrum disorder for both prenatal and postnatal exposure to PM2.5 (Talbott et al.
2015).

7.3 Evidences from Global Health Effects Estimates

of Fine PM

Evans et al. (2013) derived global PM2.5 exposure levels by utilizing remote sensing
data of MODIS and MISR satellites, and found that the anthropogenic component
of PM2.5 was responsible for a global fraction of adult mortality by 8.00 %
(5.30–10.5) due to cardiopulmonary disease and 9.40 % (6.60–11.8) due to ische-
mic heart disease. Climate change can modify these effects more strongly than what
was expected. Fang et al. (2013) found that twenty-first century climate change
results in approximate global increases of 100,000 premature mortalities associated
with PM2.5. Satellite derived pollution data showed that the anthropogenic compo-
nent of PM2.5 (95 % CI) was solely responsible for 12.8 % (5.90–18.5) increase in
lung cancer-based adult mortality in the world (Evans et al. 2013). According to
estimates of a global atmospheric chemical transport model (CTM) and health
impact function, 75.0 % of excess mortalities in Asia and 17.0 % in Europe
occurred because of high PM2.5 concentrations (Anenberg et al. 2010).

7.4 Evidences from Fine PM Exposure Health Effects

Estimates

Hennig et al. (2014) found significant associations between long-term exposure to

PM2.5 with high-sensitive C-reactive protein (hs-CRP), a marker of systemic
inflammation with 4.53 % increase in hs-CRP concentration (95 % CI: 2.76,
6.33 %) per 1.00 μg m3 increase in total PM2.5 in three German cities (Table 1).
The study on short-term associations between PM2.5 and mortality in nine French
cities by Pascal et al. (2014) clearly indicated that PM2.5 had a significant impact on
cardiovascular mortality and the impact was highest during summer season. Fleisch
et al. (2014) evaluated the association of second trimester and PM2.5 exposure in
pregnant women in Boston, USA and found that PM2.5 exposure was significantly
associated with impaired glucose tolerance (IGT), but not with gestational diabetes
mellitus (GDM) and indicated the direct effect of PM in abnormal glycemia during
pregnancy.
Harrison et al. (2004) found a significant association between long-term expo-
sures to PM2.5 and mortality due to lung cancer based on American Cancer Society
 A. Mukherjee and M. Agrawal

cohort study. A significant association was found between long-term exposures to

PM2.5 with cardiovascular events in women in 36 US metropolitan areas (Miller
et al. 2007). A 24.0 % increase in the risk of a cardiovascular event [Hazard Ratio
(HR) ¼ 1.24; 95 % CI, 1.09 to 1.41] and 76.0 % increase in the risk of death from
cardiovascular disease (HR ¼ 1.76; 95 % CI, 1.25 to 2.47) were associated with a
10 μg m3 increase in PM2.5 (Miller et al. 2007). In Karachi, Pakistan, Khwaja et al.
(2012) found an increase in hospital admissions by 1.60 % and emergency room
visits for cardiovascular disease by 1.60 % with each 10.0 μg m3 increase in PM2.5
concentrations. The Heinz Nixdorf Recall Study, a population-based prospective
cohort in Germany found a positive association between long-term urban back-
ground PM2.5 and arterial BP and hypertension, which may induce atherosclerosis
(Fuks et al. 2011). Short-term effects of PM2.5 on cause-specific hospital admission
were investigated by Dominici et al. (2006) in 204 US urban counties and they
reported that reducing PM2.5 concentrations by 10.0 μg m3 would reduce the
number of hospitalizations for heart failure by 3156.

7.5 Evidences from Genotoxic Health Effects Estimates

of Fine PM

Human bronchial epithelial (HBE) cells when exposed to PM2.5 samples collected
from Wuhan, China showed changes in 970 and 492 genes at lower and higher
exposures (Ding et al. 2014). These changes were mostly associated with genes of
inflammatory and immune responses, oxidative stress response, and response to
DNA damage. Similar variable responses in inflammation-related genes in the
bronchial epithelial cell line were also observed by Øvrevik et al. (2009). Baulig
et al. (2009) and Cachon et al. (2014) also found associations between
pro-inflammatory response in airway epithelial cells and aqueous extracts of
PM2.5. Cachon et al. (2014) observed cell cycle alterations by fine PM in human
bronchial epithelial cells.

8 Health Effects of Chemical Constituents of PM2.5

Major components present in the fine PM are typically similar in different geo-
graphic regions of the world but proportions of different components vary signif-
icantly with different emissions and local sources (Chatterjee et al. 2012; Gaita
et al. 2014; Raja et al. 2010). The composition and properties of PM influence its
toxicity apart from its aerodynamic diameter, exposure pathway, and alveolar
deposition capacity (Mazzoli-Rocha et al. 2010). PM contains a diverse array of
chemical and biological constituents such as carbonaceous (organic and elemental
carbon, aldehydes, PAH, nitro-PAH, ketones, quinones, hydrocarbons), inorganic
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

(sulfate, nitrate, ammonia, quartz, silica, sea salt, mineral oxides), and biological
(bacteria, pollen, fungi, virus, plant debris) components (Ghio et al. 2012) (Fig. 9).
Rohr and Wyzga (2012) reviewed 48 independent epidemiological studies to
assess different health effects of PM components. Among different PM components
studied, carbonaceous components of PM were found to be maximally associated
with negative health effects. The study also identified that effects were more
prominent for cardiovascular anomalies. Metals such as nickel (Ni), vanadium
(V), zinc (Zn), copper (Cu), silicon (Si), and potassium (K) showed maximum
negative health effects. V and Ni were found to be more toxic for both respiratory
and cardiovascular diseases whereas Al and Si were more prominent in respiratory
anomalies. Iron (Fe), Zn, sulfur (S), and lead (Pb) showed the least associations
with negative health effects amongst the metals studied. Authors also found con-
tradictions in health effects related to sulfate which were probably due to spatial
variations in those studies. Cakmak et al. (2014) reported acute changes in cardio-
vascular and respiratory physiology with metals in PM2.5. There were significant
increases in heart rate and blood pressure and decrease in lung function with IQR
increases in calcium (Ca), cadmium (Cd), Pb strontium (Sr), tin (Sn), V, and Zn
levels in fine PM. Greene and Morris (2006) found lifetime excess lung cancer risk
due to chromium (Cr) and arsenic (As) in PM2.5 in Washington, DC, USA (Fig. 9).
Mazzoli-Rocha et al. (2010) reviewed the association between oxidative stress
and impairment of the function of the lung exposed to PM and found PM constit-
uents specifically PAH and HM as the major elicitors of oxidative stress and
respiratory diseases. Breysse et al. (2013) identified BC, OC, SVOCs, Ni, and V
as important components of PM toxicity and also concluded that the secondary
aerosol formation may enhance PM toxicity. Miyata and van Eeden (2011) identi-
fied major soluble metals such as Fe, V, Ni, and Zn to be mainly responsible for
ROS generation. de Kok et al. (2006) reported PAH concentration as the most
important factor in determining the radical generating capacity compared to total
metal content or transition metal content in PM.
In a review Valavanidis et al. (2008) identified almost 500 different organic
compounds with mutagenic potential. Mutagenicity was mostly due to the presence
of polar or highly polar compounds with an aromatic nitro group, amines, and
aromatic ketones. DNA-reactivity was found to be positively correlated with
concentrations of total PAH and transition metals indicating that chemical compo-
nents of PM directly influence DNA strand break (de Kok et al. 2006). Significant
quantitative and qualitative differences in cytokine/chemokine responses to PM
components in bronchial epithelial cell line were observed when effects of PM
components were assessed on the expression of 84 inflammation-related genes
Øvrevik et al. (2009).
Stanek et al. (2011) examined relationships between PM components and health
effects from 29 epidemiological studies and found vehicular emission, biomass
burning, and road dust sources contributing maximally to cardiovascular diseases
but no such clear associations were observed with metals, secondary sulfate, and
salt components in PM. SOA represents a significant part of PM2.5, as we have
already discussed in Section 6 but health effects of SOA are limited and only
 A. Mukherjee and M. Agrawal

reported from a few regions of the world. Rappazzo et al. (2015) studied associa-
tions between chemical component of PM2.5 with risk of preterm birth (PTB) in
three cities of the USA and found consistent associations between EC and sulfate
with risk of PTB, whereas for nitrate, an association was only found for the first
trimester and no significant association was observed for organic carbon. Nitrate
levels in PM2.5 showed an association with an increase in monthly mortality in a
7-year study of 12.5 million Medicare enrollees in eastern USA for the age group
above 65 years (Chung et al. 2015). In a traffic related air toxic study, major
components of SOAs such as organic carbon and ammonium nitrate in PM2.5
showed a positive association with preterm birth in women living in Southern
California, USA (Wilhelm et al. 2011).
Exposure to airborne PAHs was found to be adversely affecting the children’s
cognitive development by 5 years of age in a prospective cohort study in Krakow,
Poland (Edwards et al. 2010). Results of a New York City cohort study showed
distinct effects in child behavior with prenatal exposure to PAH (Perera et al. 2012)
(Fig. 9). Perera et al. (2009) observed a significant inverse relationship between
high/low PAH exposure and full-scale and verbal IQ score (Fig. 10). Hong et al.
(2016) estimated the lung cancer risk of atmospheric PAH in five Asian countries
and found a higher lung cancer risk in China and Vietnam compared to India, Japan,
and South Korea.
Biological components in PM can also cause severe health effects directly
through allergic pollens in PM or by the presence of bacterial or fungal toxin in
PM that after inhalation can induce several inflammatory responses (Morakinyo
et al. 2016). Degobbi et al. (2011) reviewed the role of endotoxin (cell wall
component of gram-negative bacteria) in PM toxicity and found endotoxin as a
modulator for immunological response by increasing pro-inflammatory cytokine
expression. The study also identified an increment in response of several cytokines
and chemokine’s expressions due to the presence of endotoxin in PM.
Krall et al. (2015) reviewed the current methods and challenges in epidemio-
logical studies on associations between PM constituents and health effects and
found three major challenges like spatial–temporal variations in exposure, identi-
fying effects of individual PM components and error in measurement techniques.
Based on the epidemiological and toxicological findings it is clear that the toxicity
of PM depends on the combination of all PM components and their interactions
with each other. The information is still limited due to heterogeneity in PM
components concentrations in different studies, exposure doses, and specific mea-
surement techniques. Therefore, further researches are required to identify stronger
associations between PM components and health effects.
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

9 Mechanism of Fine PM Toxicity

Most of the studies have reported oxidative stress as the primary effect of
PM-related toxicity (Salvi and Holgate 1999; Øvrevik et al. 2015). Reactive oxygen
species (ROS) cause significant damage to tissues and further induce different
signaling cascades in this process. The mechanism follows the activation of tran-
scription factors which induce genes of pro-inflammatory response in most cases.
The intensity of oxidative stress depends upon the size of fine PM as well as its
chemical constituents. PAH, organic constituents, and heavy metals severely inten-
sify these effects (Bai et al. 2007; Øvrevik et al. 2015). When PM interacts with
airway epithelial cells and alveolar macrophages it raises the levels of cytokine like
IL-interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor
(GMCF), IL-1b which results in local or systematic inflammation (Block and
Calderón-Garcidue~ nas 2009).
Araujo (2011) reviewed the association of PM and its components with systemic
oxidative stress, inflammation, and atherosclerosis based on epidemiological and
experimental evidences. The author suggested three different mechanisms by which
PM causes systemic cardiovascular irregularities; pulmonary and systemic inflam-
mation; activation of receptors of pulmonary receptors that alters the autonomic
nervous system, and entree of PM components to systemic circulation. It was
further suggested that the effects of PM and its components are collaborating and
even gaseous pollutants play a significant role in health effects.
Mazzoli-Rocha et al. (2010) reviewed the role of oxidative stress in signaling
and inflammation by PM. It was found that PM-induced generation of ROS
activates the redox responsive signaling pathway (mitogen-activated protein kinase
(MAPK) family) and Ca++ influx, which further stimulate transcription factor and
expression of genes related to inflammation or DNA damage in inflammatory cells
and alveolar macrophages that ultimately result in cell injury or apoptosis, leading
to respiratory morbidity and mortality. Similar observations were also made by
Ghio et al. (2012) and Breysse et al. (2013) in their studies of uncertainties in the
health effects caused by airborne particulate matter. Major outcomes of the studies
were (1) identification of the role of epigenetic mechanisms in PM-induced toxicity,
(2) role of respiratory inflammation by fine PM induces asthmatic responses,
(3) ROS as an important modulator in induction of cellular response, (4) increment
in pro-inflammatory and immune responses, (5) changes in concentrations of
plasma high-density lipoprotein, (6) increase in coronary vascular resistance and
decrease in myocardial perfusion causing acute myocardial infraction, (7) induction
in expression of genes related to innate immunity, genes of complement system
pathways and chemotaxis, (8) intrusion of eosinophil and neutrophil to airways, and
(9) elevated secretions of cytokines (Breysse et al. 2013).
Ghio et al. (2012) further identified PM-induced responses such as the role of
kinase cascade (ERK, p38, and Jun kinases) in PM-induced cell responses, oxidant
generation by activation of NADPH oxidases, the role of metals in electron
transport and ROS generation, induction in expression of stress response enzymes
 A. Mukherjee and M. Agrawal

(glutathione transferase, heme oxygenase, and superoxide dismutase) in epithelial

cells and macrophages, mitochondrial dysfunction, and increased expression of
cytochrome P-450.
In their review on the toxicological assessment of airborne PM, Valavanidis
et al. (2008) identified several different mechanisms of toxicity such as ROS
generation, DNA oxidative damage, mutagenicity, and induction of
pro-inflammatory factors (cytokines and chemokines). Valavanidis et al. (2008)
in their review concluded that all the studied relationships between PM and
genotoxicity showed positive DNA damage, oxidative DNA damage, micronuclei
sister chromatid exchange, and single-strand breaks. de Kok et al. (2006) also found
fine PM to exert high DNA-reactivity.
Miyata and van Eeden (2011) reviewed the immunological interactions between
alveolar macrophages and PM and found fine PM to induce innate immune
responses by ROS generation through activation of different transcription factors.
After particles are internalized, adaptive immunity is induced through expression of
major histocompatibility complex Class II and modulation in response of T helper
cells. Feng et al. (2016) identified oxidative stress and inflammation with alteration
in immune responses as the major mechanism behind fine PM-induced respiratory
effects. Oxidative stress and inflammation in hypothalamus may cause alteration in
its neuroendocrine function and ultimately may lead to neuroendocrine disorders.
Alteration in immune response in pregnant women due to PM exposure may induce
adverse effects in childhood or at maturity (Feng et al. 2016). Increase in expression
of phase I xenobiotic-metabolizing cytochrome P450 enzymes due to organic
components of fine PM and inflammatory response in other organs such as spleen,
heart, kidney, and liver due to fine PM are reported (Feng et al. 2016) (Fig. 9).
Øvrevik et al. (2015) identified interactions of particles with lipid bilayer, cell
surface receptors, intracellular molecules, and direct formation of ROS, resulting in
activation of genes responsible for process of inflammation in airway mucosa cells.
This inflammation itself can trigger cardiovascular effects by transport of inflam-
matory mediators through circulation (Øvrevik et al. 2015). Laing et al. (2010)
observed that PM2.5 exposure resulted in endoplasmic reticulum stress and unfolded
protein response (UPR) signaling pathway in lung and liver tissues and in mouse
macrophage cells and they concluded that PM2.5 can activate UPR-related branches
which further lead to apoptosis by the PERK-eIF2-CHOP pathway. The mecha-
nisms of toxicity of PM and their effects are shown in Fig. 10.
Based on the above evidences, it can be concluded that the actual mechanisms
and components of fine PM responsible for such health effects after exposure of
biological systems to PM are still not completely known and further evidences at
gene and molecular levels should be studied.
 Cd Hg Pb As Ba Cr Zn

Cancer Kidney Child Lung

Heavy damage behavior cancer Muscle Liver Pediatric
weakness damage asthma
Metal Lung
Cardiovascular Neurological Neurological Neurological Kidney
disease disorders disorders disorders damage injury
Cardiovascular
Bone deformity Oxidative
Lung Cardiovascular disorders Skin ulcers
Lower IQ stress
Kidney damage damage disease

Oxidative Lung Child

Asthma
stress Cancer behavior
PAH
Teratogenic Morbidity and
Damage to
DNA Cognitive development Mortality
blood vessel
damage in children Epigenetic endothelium
alterations

Telomere attrition
Decreased Blood
lung function pressure
BC, Atherosclerosis
Acute
OC, Attention
Epigenetic respiratory Cardiovascular
SO4
modification inflammation reduction in
children disease
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

Fig. 9 Health effects of different PM2.5 chemical constituents

 COPD
E-selectin CYP1A1 Asthma
Cardiovascular mortality PTGS2 ALDH1A3 Lung Cancer
Acute coronary syndrome CXCL-2 TIPARP
Myocardial ischaemia CCL-2
Myocardial inflammation Histamine Systemic Inflammation
Bronectin Neuro Inflammation
Neutrophils
Lymphocytes
Enhance gene expression
Endothelial permeabilty Mast cells
and transcription
ROS IL-6
Leukocyte IL-8
Platelet activation GM-CSF
ET1 IL-6
Blood pressure IL-1β Blood vessel
Plasma viscosity GM-CSF
Coagulation factor VII PAH
CRP

JNKs-AP1
NFκβ Epithelial
Endothelial cell cells
TLR4
IgE

SOA
DPM
PM
Enhance gene expression
Fatty acid Liver and transcription
β oxidation
HM
Anti inflammatory BC
response Macrophage
Vasodilation
Kupffer Cell CD-68
NO
CD-163
TNFα HLA-DR TNFα
PGE2 IL1-β TNFβ
Peripheral IL-6
IFNγ COX2
UPR pathway Systematic Interferon-g
Metabolic disorders Endoplasmic Inflammation Aβ42 deposition TGF-β
Cancer NFκβ
reticulum NFκβ expression
Inflammation PERK ICAM-1
hsp 70
Neuron injury
Apoptosis C3a
CHOP factors
Neuron degeneration AP-1
CNS disorders AP-2
Neural disorders
PM IL-6 HETE ROS GM-CSF IL-1β Ca+2

Fig. 10 Different pathways of PM toxicity and their effects in different organ systems. PM particulate matter, PAH polycyclic aromatic hydrocarbons, DPM
diesel particulate matter, SOA secondary organic aerosol, HM heavy metal, BC black carbon, ROS reactive oxygen species, ET-1 endothelin-1, CRP C-reactive
protein, JNKs-AP1 c-Jun N-terminal kinases activation protein 1, NO nitric oxide, NF-κB nuclear factor-κB, TLR-4 toll-like receptor 4, IgE
immunoglobulin E, UPR unfolded protein response, PERK protein kinase-like ER kinase, CHOP C/EBP homologous protein, IL-6 interleukin 6, IL-1β
interleukin 1β, GM-CSF granulocyte-macrophage colony stimulating factor, TNFα tumor necrosis factor α, PGE2 prostaglandin E2, IFNγ interferon γ, CCL-2
chemokine (C-C motif) ligand 2, CXCL-2 chemokine (C-X-C motif) ligand 2, PTGS2 prostaglandin-endoperoxide synthase 2, CYP1A1 cytochrome P450,
family 1, subfamily A, polypeptide 1, ALDH1A3 aldehyde dehydrogenase 1 family, member A3, TIPARP TCDD-inducible poly(ADP-ribose) polymerase,
AP-1 activator protein 1, AP-2 activator protein 2, C3a complement component 3a, HSP70 heat shock protein 70, ICAM1 intercellular adhesion molecule-1,
TGF-β transforming growth factor beta, NFκβ nuclear factor κβ, Aβ42 amyloid beta-42, COX2 cyclooxygenase 2, HLA-DR human leukocyte antigen-D related,
HETE hydroxyicosatetraenoic acid. (Modified from Bai et al. 2007; Block and Calderón-Garcidue~ nas 2009; Laing et al. 2010; Aung et al. 2011)
A. Mukherjee and M. Agrawal
A Global Perspective of Fine Particulate Matter Pollution and Its Health Effects

10 Suggestions

Cleaning our environment is the biggest and topmost priority in the current sce-
nario; choices should be economical and implementable with long-term solutions.
Identifying problems is the first step to solution. We know the consequences that we
are facing every day, so we must bring new ideas to overcome this burden. The
following suggestions can help to mitigate the PM levels and consequently improve
human health. Suggestions are proposed from best to least effective measure:
1. Strict emission standards for fine PM emission from vehicles and industries.
2. Prevention of biomass burning.
3. More emphasis should be given on health effects study especially in Asian and
African countries.
4. School building should not be near highway or any major roadway.
5. More scientific research on passive monitoring techniques should be conducted
as it is economical and easy to implement in developing countries.
6. Large urban forestry development programs.
7. Use of bio-filters to reduce emissions from industry or around traffic sites.
8. Creating a global PM10, PM2.5, and PM1 standards for different regions based
on its topography and history.
9. Epidemiological monitoring of air quality effects as a part of national ambient
air quality monitoring program especially for developing countries.
10. Creating a global database of PM levels and their sources.

11 Conclusion

Fine PM has become a major public health issue, particularly in large cities. Most of
the large cities in the world showed PM levels above the respective standards of
their own countries as well as the WHO standards. Levels were less elevated in the
USA and European cities. Asian cities are mostly critical with consistently higher
PM2.5 levels and exposure. Most of the major cities in Asia have exceeded the
threshold levels. Even rural and remote areas have higher PM levels, which indicate
a rapid dispersion from urban centers. High population density and urbanization are
the major drivers of poor air quality around the world. Automobiles along with
combustion activities are major sources of PM2.5.
Epidemiological studies provided evidence that there is an increasing trend of
fine PM-related health issues all over the world. Traffic seems to be the major factor
behind health anomalies around the globe with children and pregnant women being
most vulnerable. Several studies indicated the carcinogenic or mutagenic nature of
chemical constituents associated with fine PM that have severe health consequences
even at lower concentrations. African and Asian countries require more epidemi-
ological studies to provide a broader perspective of health effects. More scientific
 A. Mukherjee and M. Agrawal

studies on gene and metabolic levels will further be able to discover the yet hidden
health effects of fine PM.

12 Summary

Global status, trend, and health effects of fine particulate matter (PM2.5) were
reviewed. Asian and African continents have higher exceedance of fine PM than
the standards compared to Europe and the USA. Traffic, biomass burning, road
dust, and local sources affect fine PM concentrations. Epidemiological studies
provided clear evidence of increasing fine PM-related health issues all over the
world. Fine PM causes several health effects such as increase in inflammatory
responses, lung cancer, heart rate variability, term low birth weight, mutagenicity,
changes in gene expression, and immune responses. Chemical constituents of fine
PM such as polycyclic aromatic hydrocarbons, heavy metals, and elemental carbon
are mostly responsible for PM2.5 toxicity. Emission reduction policies should be
more emphasized with epidemiological studies to combat negative effect of
fine PM.

Acknowledgements The authors are thankful to the Department of Science and Technology
(DST), India for providing financial support in the form of an Inspire fellowship (IF120768). The
authors are also grateful to anonymous reviewers and editor for their valuable suggestions for
improving the quality of the manuscript.

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