Foundation Course on

Air Quality Management in Asia

Impacts

Edited by
Gary Haq and Dieter Schwela

5
Editors
Dr Gary Haq, Stockholm Environment Institute, University of York
Dr Dieter Schwela, Stockholm Environment Institute, University of York

Module Contributors
Professor Bingheng Chen, School of Public Health, Fudan University, Shanghai
Dr Dilip Biwas, Former Chairman, Central Pollution Control Board, New Delhi
Dr David L. Calkins, Sierra Nevada Air Quality Group, LLC, San Francisco Bay Area, CA
Dr Axel Friedrich, Department of Transport and Noise at the Federal Environment Agency (UBA), Berlin
Mr Karsten Fuglsang, FORCE Technology, Copenhagen
Dr Gary Haq, Stockholm Environment Institute, University of York, York
Professor Lidia Morawska, School of Physical and Chemical Sciences, Queensland University of Technology, Brisbane
Professor Frank Murray, School of Environmental Science, Murdoch University, Perth
Dr Kim Oanh Nguyen Thi, Environmental Technology and Management, Asian Institute of Technology, Bangkok
Dr Dieter Schwela, Stockholm Environment Institute, University of York, York
Mr Bjarne Sivertsen, Norwegian Institute for Air Research, Olso
Dr Vanisa Surapipith, Pollution Control Department, Bangkok
Dr Patcharawadee Suwanathada, Pollution Control Department, Bangkok
Mr Harry Vallack, Stockholm Environment Institute, University of York

Production Team
Howard Cambridge, Web Manager, Stockholm Environment Institute, University of York, York
Richard Clay, Design/layout, Stockholm Environment Institute, University of York, York
Erik Willis, Publications Manager, Stockholm Environment Institute, University of York, York

Funding
The modules were produced by the Stockholm Environment Institute (SEI) and the University of York (UoY) as
part of the Clean Air for Asia Training Programme. The programme was led by the SEI and UoY in collaboration
with the Pollution Control Department (Thailand), Vietnam Environment Protection Agency (VEPA), and Clean
Air Initiative for Asian Cities (CAI-Asia). The Clean Air for Asia Training Programme was funded under the
European Union’s Asia Urbs programme (TH/Asia Urbs/01 (91000)). Additional funding was received from the
Norwegian Agency for Development Cooperation (NORAD), International Atomic Energy Agency (IAEA),
World Health Organization, Norwegian Institute for Air Research (NILU), and Force Technology.

Stockholm Environment Institute

Kräftriket 2B
Stockholm
Sweden SE 106 91
Tel: +46 8 674 7070
Fax: +46 8 674 7020
E-mail: [email protected]
Web: www.sei.se

Copyright © 2008 Stockholm Environment Institute

This publication may be reproduced in whole or in part and in any form for educational or nonprofit purposes, without special permission from
the copyright holder(s) provided acknowledgement of the source is made. No use of this publication may be made for resale or other commercial
purpose, without the written permission of the copyright holder(s).

DISCLAIMER
All text, photographs, and graphics in this manual are provided for information purposes only.Whilst every reasonable effort has been made to ensure
that the information is complete, correct and up-to-date, this cannot be guaranteed, and the Stockholm Environment Institute shall not be liable
whatsoever for any damage incurred as a result of its use. The Stockholm Environment Institute takes no responsibility for the content of websites
that are linked to this document.The existence of a link to an external website does not imply that the Stockholm Environment Institute endorses the
activities or views of that organisation. In no event shall the Stockholm Environment Institute be responsible or liable, directly or indirectly, for any
damage or loss caused or alleged to be caused by or in connection with the use of or reliance on any such content, goods, or services available on or
through any such site or resource.The mention of specific organisations or of certain manufacturers’ products does not imply that they are endorsed
or recommended by the Stockholm Environment Institute in preference to others of a similar nature that are not mentioned.
 Foundation Course on Air Quality Management in Asia

The Foundation Course on Air Quality Clean air is recognised as a key component of a
Management in Asia is for adult learners studying sustainable urban environment in international
the issue without the support of a class room agreements and increasingly in regional
teacher. It is aimed at students with some basic environmental declarations in Asia. National
knowledge of environment and air pollution and local governments have begun to develop
issues, acquired in a variety of ways ranging from air quality management strategies to address the
conventional study, working in an environmental deterioration in urban air quality. However, the
related field or informal experience of air scope and effectiveness of such strategies vary
pollution issues. widely between countries and cities.

The course provides you with an opportunity The aim of air quality management is to maintain
to develop your understanding of the key the quality of the air that protects human health
components required to develop a programme and welfare but also to provide protection for
to manage urban air pollution and to achieve animals, plants (crops, forests and vegetation),
better air quality. By working through the six ecosystems and material aesthetics, such as
modules you will gradually achieve a higher natural levels of visibility. In order to achieve
level of understanding of urban air pollution and this goal, appropriate policies, and strategies
the measures taken to monitor air quality and to to prevent and control air pollution need to be
prevent and control urban air pollution. developed and implemented.

Urban Air Pollution in Asia Module Structure

Urban air pollution affects the health, well-being The foundation course consists of six modules
and life chances of hundreds of million men, which address the key components of air
women and children in Asia every day. It is quality management. An international team of
responsible for an estimated 537,000 premature air pollution experts have contributed to the
deaths annually with indoor air being responsible development of the course. Each module is
for over double this number of deaths. It is often divided into a number of sections each devoted
the poor and socially marginalized who tend to a different aspect of the issue, together with
to suffer disproportionately from the effects of examples and key references.
deteriorating air quality due to living near sources
of pollution.
 Module 5 - Impacts

Introduction 1

Section 1 Air Pollution and Health 2

1.1 Measuring Exposure to Air Pollution 4
1.2 Health Impacts of Key Air Pollutants 6
1.3 Global Burden of Disease and Air Pollution 13
1.4 Climate Change and Health 14

Section 2 Design of Health Studies 17

2.1 Information from Toxicological Animal Studies 17
2.2 Information from Epidemiological Studies 18
2.3 Health Endpoints 20

Section 3 Economic Assessment of Air Pollution and Health 21

3.1 Cost-Benefit and Cost-Effectiveness Analysis 22

Section 4 Managing Indoor Air Pollution 24

4.1 Indoor Air Pollution 24

Section 5 Environmental Impacts of Air Pollution 27

5.1 Effects on Visibility 27
5.2 Effects on Economic Material and Structures 28
5.3 Effects on Vegetation 30

Summary 33
Information Sources 34
Learning objectives
In Module 5 Air Pollution Impacts you will examine the impacts of common air pollutants on human
health and environment. In particular, you will learn about the methods used to study and assess
the impact of air pollution on the health of a given population and the associated economic costs. At
the end of the module you will have a better understanding of:
• the effect of key air pollutants on health
• different approaches used to undertake health studies
• information required to undertake health studies
• approaches used to assess the economic impacts associated with air pollution and health
• approaches used to manage indoor air pollution
• environmental impacts of air pollution.
List of Acronyms and Abbreviations
ABC Atmospheric brown cloud ETS Environmental tobacco smoke PESA Proton elastic scattering analysis
ACFA Asian Clean Fuels Association EU European Union PID Photo ionisation detector
ACS American Cancer Society FID Flame ionisation detector PIGE Particle induced gamma ray
ADAC Automatic data acquisition system FOE Friends of the Earth emission
ADB Asian Development Bank FST Foundation for Science and PILs Public interest litigation
ADORC Acid Deposition and Oxidant Technology PIXE Particle induced X-ray emission
Research Center GBD Global burden of disease PM Particulate matter
AirQUIS Air quality information system GDP Gross domestic product PM10 Particulate matter less than 10
ALAD Aminolaevulinic acid dehydrase GHG Greenhouse gas microns in diameter
AMIS Air quality management GIS Geographic information system PM2.5 Particulate matter less than 2.5
information system GTF Global Technology Forum microns in diameter
APHEA Air Pollution and Health, A HAP Hazardous air pollutant PMF Positive matrix factorisation
European Approach HC Hydrocarbon POP Persistent organic pollutant
API Air pollution index HCA Human capital approach PPM Parts per million
APINA Air Pollution Information Network HCMC Ho Chi Minh City PRC People’s Republic of China
APMA Air pollution in the megacities of HEI Health Effects Institute PSAT Particulate matter source
Asia project HEPA Ho Chi Minh City Environmental apportionment technology
APNEE Air Pollution Network for Early Protection Agency PSI Pollutant standard index
warning and on-line information Hg Mercury PSU/NCAR Pennsylvania State University /
Exchange in Europe HIV/AIDS Human immunodeficiency virus/ National Center for Atmospheric
AQG Air quality guideline Acquired Immunodeficiency Research
AQM Air quality management Syndrome PVC Polyvinyl chloride
AQMS Air quality management system I&M Inspection and maintenance QA/QC Quality assurance/quality control
AQO Air quality objective IBA Ion beam analysis QEPA Queensland Environmental
AQSM Air quality simulation model ICCA International Council of Chemical Protection Agency
As Arsenic Associations ROS Reactive oxygen species
ASEAN Association of South East Asian IFFN International Forest Fire News RBS Rutherford backscattering
Nations IPCC Intergovernmental Panel on spectrometry
ASG Atmospheric Studies Group Climate Change SA Source apportionment
ATD Arizona test dust IQ Intelligent quotient SACTRA Standing Advisory Committee on
AWGESC ASEAN Working Group on IR Infrared Trunk Road Assessment
Environmentally Sustainable ISO Organization for Standardization SAR Special Administrative Region
Cities IT Interim target SMC San Miguel Corporation
AWS Automatic weather station IUGR Intrauterine low growth restriction SMS Short message service
BaP Benzo[a]pyrene IUPAC International Union of Pure and SO2 Sulphur dioxide
BBC British Broadcasting Corporation Applied Chemistry SOx Sulphur oxides
BMR Bangkok Metropolitan Area IVL Swedish Environmental Research SPCB State Pollution Control Board
BRT Bus rapid transit Institute TAPM The Air Pollution Model
BS Black smoke km kilometre TEA Triethanolamine
BTEX Benzene, toluene, ethylbenzene LBW Low birth weight TEAM Total Exposure Assessment
and xylenes LCD Less developed country Methodology
CAI-Asia Clean Air Initiative for Asian Cities LPG Liquid petroleum gas TEOM Tapered element oscillating
CAIP Clean air implementation plan LPM Lagrangian particle module microbalance
CARB Californian Air Resources Board MAPs Major air pollutants TSP Total suspended particulate
CAS Chemical Abstract Service MCIP Meteorology-Chemistry Interface UAM Urban airshed model
CBA Cost benefit analysis Processor UCB University of California at
Cd Cadmium MMS Multimedia messaging service Berkeley
CD Compact disc MOEF Ministry of Environment and UF Ultra fine
CDM Clean development mechanism Forests UK United Kingdom
CEA Cost-effectiveness analysis MOPE Ministry of Population and UNDESA United Nations Department of
CER Certified emissions reduction Environment Economic and Social Affairs
CMAS Institute for the Environment, MT Meteo-Technology UNDP United Nations Development
Chapel Hill MW Molecular weight Programme
CMB Chemical mass balance NAA Neutron activation analysis UNECE United Nations Economic
CNG Compressed natural gas NAAQS National Ambient Air Quality Commission for Europe
CO Carbon monoxide Standards UNEP United Nations Environment
CO2 Carbon dioxide NASA National Aeronautics and Space Programme
COHb Carboxyhaemoglobin Administration UNFCCC United Nations framework on
COI Cost of illness NDIR Non-dispersive Infrared climate change
COPD Chronic obstructive pulmonary NILU Norwegian Institute for Air UN-Habitat United Nations Habitat
disease Research US United States
CORINAIR CORe INventory of AIR emissions NKBI Neutral buffered potassium iodide USEPA United States Environmental
CPCB Central Pollution Control Board NMMAPS National Morbidity and Mortality Protection Agency
CSIRO Commonwealth Scientific and Air Pollution Study UV Ultra violet
Industrial Research Organisation NO Nitric oxide UVF Ultra violet fluorescence
CVM Contingent valuation method NO2 Nitrogen dioxide VOC Volatile organic compound
DALY Disability-adjusted life years NOx Nitrogen oxides VOSL Value of statistical life
DAS Data acquisition system NYU New York University VSI Visibility Standard Index
DDT Dichloro-Diphenyl-Trichloroethane O2 Oxygen WAP Wireless Application Service WHO
DETR Department for Transport and the O3 Ozone World Health Organization
Regions OECD Organization for Economic WMO World Meteorological
DQO Data quality system Cooperation and Development Organization
DQO Data quality objective PAH Polycyclic aromatic hydrocarbons WRAC Wide ranging aerosol collector
DWM Diagnostic wind model PAN Peroxyacetyl nitrate WTP Willingness to pay
EB Executive board Pb Lead XRF X-ray fluorescence
EC European Commission PbB Level of blood lead YLD Years of life with disability
EEA European Environment Agency PCB Polychlorinated biphenyl YLL Years of life lost
EGM Eulerian Grid Module PCD Pollution Control Department
EIA Environmental impact assessment PDR People’s Democractic Republic
List of Tables, Figures and Boxes

Table 5.1 A Summary of Major Impacts (scale and sources) for Key Pollutants

Figure 5.1 The impact of air pollution on human health

Figure 5.2 The size of various particles in comparison with human hair
Figure 5.3 Climate change and health
Figure 5.4 Direct and indirect health impacts of air pollution and greenhouse gases
Figure 5.5 Dose response relationship between health effects and carboxyhaemoglobin in blood
Figure 5.6 Cohort studies scheme
Figure 5.7 Case-control studies scheme
Figure 5.8 Technical interventions for reducing health impacts from use of biomass fuel in households
Figure 5.9 Social-behavioural interventions for reducing health impacts from use of biomass fuels in
households
Figure 5.10 Effectiveness of potential exposure interventions and typical values
Figure 5.11 Average visual range versus relative humidity at Los Angeles International Airport, California
Figure 5.12 Uptake and deposition of ozone on plants

Box 5.1 Composition of the Air

Box 5.2 Typical PM10 Concentrations
Box 5.3 WHO PM Guideline Values
Box 5.4 WHO SO2 Guideline Values
Box 5.5 WHO NO2 Guideline Values
Box 5.6 WHO O3 Guideline Values
Box 5.7 WHO CO Guideline Values
Box 5.8 WHO Lead Guideline Values
Box 5.9 Health-based Economic Assessment of Air Pollution in Metropolitan Shanghai, China
Box 5.10 The Structure of a Leaf
 Introduction

A ir pollution is a major environmental health

problem affecting both developed and
developing countries. Concern focuses not only
Many people are vulnerable to the adverse effects
of air pollutants because they are highly exposed
to pollutants and/or have increased sensitivity to
on ambient air quality in cities but also on indoor exposure (e.g., children, the fetus, older people or
air quality in the home and workplace. the sick). A study of the global burden of disease
demonstrated that 67 per cent of the estimated
Levels of air pollution in Asian cities regularly
number of deaths for acute respiratory diseases
exceed World Health Organization (WHO)
occurs before 15 years of age (Murray and Lopez,
guidelines with smoke, dust and particles double
1996).
the world average. Pollutants emissions have
direct and indirect effects (e.g. acidification, The world’s poorest people suffer most from
eutrophication, ground-level ozone) on air quality adverse environmental conditions and are exposed
with a wide range of impacts on human health, to high levels of indoor as well as ambient air
ecosystems, agriculture and materials. pollution. Most of the poor, especially in the less
developed countries, live and work in rural areas
In 2001 the total number of deaths was estimated to
and at the margins of expanding urban centres.
be approximately 56.55 million. Approximately 2.5
million deaths per year are the result of exposure This module provides an understanding of the key
to particulate matter (WHO, 2002). Indoor smoke environmental of impacts associated with urban air
from solid fuels in developing countries represents pollution. It examines the impact of different air
65 per cent of these 2.5 million deaths and is the pollutants on human health, materials, buildings
major cause of excess deaths due to air pollution and crops. It discusses the different methodological
world-wide. Ischaemic heart disease, acute approaches used in air pollution and health
lower respiratory infections, chronic obstructive studies. It also examines the methods used to assess
pulmonary disease and perinatal conditions the economic cost of air pollution and health, which
are the main causes leading to death, with air is important in persuading decision-makers to take
pollution being one of the contributing causes of action to address air pollution.
these diseases.

1
5
Section 1 Air Pollution and Health

A ir is a colourless and odourless mixture of

gases that constitutes the earth’s atmosphere.
Air also contains water vapour in amounts that
expansion of motorized road transport, and
to a lesser extent, building construction. If
combustion of fossil fuels is complete, it produces
vary depending on atmospheric conditions. The carbon dioxide (CO2) and water, together with
oxygen in the air is vital for life but humans can nitrogen oxides (NOx) generated by oxidation of
only survive for any extended period of time atmospheric nitrogen at high temperatures. But if
within a comparatively narrow range of oxygen the combustion is incomplete, it will lead to visible
content (19-21 per cent) . black smoke comprising fine carbon particles and/
or complex hydrocarbons (HC), CO and partially
The tolerance limit for ozone (O 3) or carbon
oxidized organic compounds. Since fossil fuels
monoxide (CO) is even less. Several hundred
contain organic or inorganic sulphur compounds
µg  O3/m3, or a few hundred mg CO/m3, could
in varying amounts, most of the sulphur in fossil
mean severe illness or even death, depending on
fuels is emitted as sulphur dioxide (SO2). Removal
the exposure. Argon, neon, krypton and xenon are
of sulphur at source is still quite expensive and
odourless, colourless, tasteless and inert gaseous
difficult to achieve for coal.
elements naturally found in the atmosphere, but
their amount is very small and their impact on air Indoor air pollution has a number of sources,
quality, health and environment is negligible. including combustion of fossil fuels or biomass
fuels indoors, tobacco smoking in closed premises,
The amount of air we breathe depends on age,
and various kinds of chemicals released from
gender and the type of activity we are engaged
furniture, carpets and other household sources,
in. On average, an adult inhales approximately
as well as radon from building materials and
22 m3 of air per day (WHO, 1994). Many of our
basements (depending on the construction
daily activities release particles and chemicals into
material and surrounding soil).
the air we breathe. Particles and chemicals that are
undesirable and have the potential to affect our Occupational exposure to industrial air pollutants
health and the environment are called pollutants. varies from industry to industry. People affected
Air pollutants may be emitted from both natural generally form the work force and are relatively
and human produced sources. A primary younger and stronger than people in a community.
air pollutant is one emitted into the air from In most cases the exposure time is limited to
identifiable sources. A secondary air pollutant is eight hours each week day. Pollutants involved
a pollutant formed by chemical reaction(s) in the range from metallic fumes, fibres and dusts to
atmosphere. Generally, combustion of fossil fuels organic solvents at concentrations much higher
is the major source of both ambient (outdoor) than those encountered in a suburban or an urban
air pollution and indoor air community.
Box 5.1 pollution.
Composition of the Air Exposure to environmental pollutants is a
Ambient air pollution is problem of increasing concern due to a diversity
Nitrogen 78 per cent
usually understood as outdoor of pollutants and the vast number of people at
Oxygen 20.95 per cent
air pollution. Deterioration of risk. Since individuals differ widely in genetic
Argon 0.93 per cent
air quality or increase in air pre-disposition and physiological response,
Carbon dioxide 0.038 per cent
pollution has followed the the effects of air pollution can sometimes be
The composition varies according to observed even when the pollution level is below
growth in modern industry,
local environmental conditions.
domestic combustion of coal, the level indicated by air quality guidelines.

2
Young and elderly, patients with cardio-vascular The most common air pollutants in our daily life
and pulmonary disease and workers in certain are particulate matter (PM), SO2, NOx, CO, CO2
industries may be at higher risk due to their and O3. Figure 5.1 shows the pathway of how
increased biological sensitivity and different source emissions leading to exposure can affect
exposure pattern. human health.

Determining the Health Hazards

due to air pollution
To understand the impact of air pollution on human • population groups which are exposed;
health a number of questions can be posed:
• level to which they are exposed;

What is a health hazard due to air pollution? • duration of exposure;

• A health hazard is a source of danger or • health impacts that these hazards could
an agent that can harm human health cause or do have caused, i.e. dose-
(qualitative notion). (exposure-) response relationships.

What is a health risk due to air pollution? Which environments do we have to consider in
• The health risk is the probability that health the assessment of risks due to air pollution?
impact will occur (quantitative notion). • home environment

• workplace environment
Which information do we need to assess health
risks presented by hazards? • community environment
• hazards as they occur in a particular
• larger-scale environment.
environment;

Figure 5.1 The impact of air pollution on human health

3
5
1.1 Measuring Exposure to Air b) individual exposure based upon diaries and
micro-environment concentration estimates.
Pollution

T he assessment of human exposure to air Integrated models may use measurement data
pollutants is a part of total risk assessment, and statistical interpolation procedures to produce
and a necessary part of air quality management concentrations in each square kilometre (km2).
(AQM) where it contributes to information on These concentrations can then be used together
prioritising abatement measures. Exposure with the population distribution to estimate an
assessment is currently a bottleneck in risk approximate exposure of the population for each
assessment since it involves not only the estimation km2. When added for all grid squares the method
of concentrations but also the determination of becomes a fairly robust method for obtaining a
exposure factors such as duration of exposure, complete picture of the population exposure to air
time use pattern of human populations, personal pollutants. This method has been applied in Oslo
vulnerability and lifestyle. Exposure assessment (Norway) where the number of people living within
has been a research topic in its own right (USEPA, areas of concentrations exceeding given levels was
1997), inside and outside of epidemiological presented on maps.
studies. The general idea is to look at: Personal exposure to NO2 and PM10 was estimated
• outdoor air conditions in ambient air where by a combination of exposure calculations in
people move; and observation points along major roads and for each
grid square. The total number of persons exposed
• indoor air conditions where people
to PM10 was 320,000 persons in 1995, and reduced
normally spend most of their time through
to 220,000 persons in 2001 (Bøhler et al., 2003).
measurements of personal exposure.
Each of these refinements often adds a layer of The individual exposure approach assumes that
complexity to exposure assessment. Some major each person is exposed to a contaminant represented
questions include: by the measured or estimated concentration in the
• Which of the complicating factors are most micro-environment that he/she is in at the moment.
important? For example, the exposure is dependent on whether
that geographical area is in the proximity of heavy
• How do we quantify them and arrive at a
traffic or whether the individual is indoors or
suitable population exposure model?
outdoors, travelling or shopping.
This is a particular challenge if only monitoring
data are to be used in the exposure assessment. A micro-environment can be a location outside
Normally these tasks are undertaken in a (e.g a street) or inside (e.g. office). Without doubt
combination of measurement data for air quality the best method of measuring exposure is by
and air pollution modelling. The WHO (WHO, the use of personal monitors, especially when
2000a) discussed exposure assessment in general people move from place to place. However, this
terms, and concluded that it is probably best is impractical when several compounds are being
carried out with a combination of measurements studied simultaneously. In addition, it is uncertain
and models. how much people change their routines when they
have to carry some of the larger portable units. It
In general, two different methods are being applied
can therefore be more practical to use computer
to estimate human exposure to air pollutants. The
models based upon data from diaries to estimate
two main models have been used to estimate:
each individual’s exposure to each pollutant for
each prescribed time span. This model has used as
a) integrated number of people living within little as one hour as the unit of time. With this time
areas of given concentration levels; and resolution, it is possible to reflect major changes in

4
micro-environments without requiring a diary that • classification of individual exposure (high
is impossible for people to complete. versus low);

The major elements of a practical concentration • measured or modelled outdoor

exposure model are: concentrations;

• geographical location • measurement of indoor and outdoor

concentrations;
• proximity to traffic
• estimation of personal exposure using
• being indoors or outdoors
indoor, outdoor and other micro-
• shopping environmental concentrations along with
• travelling. time–activity diaries;
In this approach the number of micro-environments • direct measurement of personal exposure;
of importance and interest is normally large. and
The study therefore will have to be made • measurement of biomarkers of exposure
manageable by judiciously reducing the number such as blood levels of heavy metals,
of measurements within each micro-environment carboxy-haemoglobin or endocrine
type. Institutional and public micro-environments disruptors.
lend themselves easily to a reduced number of
Clearly, the least sophisticated approach in
measurements. Decisions on how much reduction
classifying exposure groups using a categorical
in measurements can be achieved can largely be
variable (such as homes with gas versus electric
made through site visits, walk-through surveys,
cooking stoves for NO2 impact assessment) could
and analysis of information existing for the specific
lead to significant exposure misclassification bias.
micro-environment.
However, many existing environmental health
Air quality standards and guidelines have been studies are based on ambient or community
established based upon air pollution impact to surveillance monitoring data. Humans are exposed
human health and well-being (see Module 6 to many types of pollutants involving different
Governance and Policies). The best available pollutant sources and locations other than outdoor
background material for the evaluation of health pollutants and monitored ambient environments,
impacts is the US Environmental Protection e.g. PM, NO2, and volatile organic compounds
Agency (USEPA) criteria documents (e.g. USEPA, (VOCs). For reactive pollutants, such as O3, indoor
2006) and the guidelines for air quality (WHO, pollution levels are significantly lower than the
2000b; 2005). WHO’s guideline values for air outdoor concentrations. Since people spend more
quality are set to ensure that the population time indoors, personal O3 exposure is more closely
exposed to concentrations lower than the guideline related to indoor than outdoor O3 concentrations.
values should be subject to negligible or - in the In general, therefore, exposure models based
case of PM10 and PM2.5 – relatively small risks of on ambient data only are less accurate than the
adverse effects. In cases where the guideline for a micro-environmental models that combine indoor
pollutant is exceeded, the probability of harmful and outdoor concentration measurements (or
effects will increase. predictions) with time-activity patterns.
A number of different approaches to exposure Human exposure modelling for environmental
assessment have typically been used in pollutants has received considerable attention over
environmental epidemiology investigations. In the past decade. A number of human exposure
terms of increasing order of sophistication, these assessment field studies, such as the Total Exposure
include: Assessment Methodology (TEAM) studies of the

5
5
USEPA, have provided an important foundation less than 0.1 µm). PM10 include inhalable particles
for models of human exposure to CO, VOCs, which can penetrate to the thoracic region. PM2.5
pesticides and PM10. The results from these field has high probability of deposition in the airways
studies have produced greater understanding of and alveoli. Particles with different aerodynamic
the variation in the indoor, and outdoor pollutant diameters differ in their overall contributions to
concentrations, and concentrations obtained from airborne particle mass and in their origin, physical
personal monitoring. However, the measurements characteristics, chemical composition, and health
can usually be generalized and technically effects. Total suspended particulate matter (TSP)
interpreted in terms of human exposure using and black smoke (BS) were used as indicators
exposure models. of airborne particles in the past, and TSP is still
used as an indicator of particulate matter in some
The exposure models provide an analytic structure
countries.
for combing data of different types collected from
disparate studies in a manner that may make Coarse particles contain earth crustal materials, dust
more complete use of the existing information on from roads, industries and construction activities,
a particular pollutant than is possible from direct and biological material, such as pollen grains and
study methods. The uncertainty about various bacterial fragments. PM2.5 contains combustion
components of environmental health assessment particles, the secondarily formed aerosols (gas to
can be incorporated into such models to estimate particle conversion), and recondensed organic and
uncertainty about the prediction endpoint (e.g. metal vapours. Diesel trucks emit particles primarily
exposure, dose or health outcome), to identify the in the range of 0.1-0.2 µm. The composition of
components that influence prediction accuracy particles varies substantially across cities around
and precision by comparing predicted values to the world depending upon local geographical,
those measured in the field. Validated models can meteorological conditions and specific sources.
then be used to investigate the effectiveness of Figure 5.2 illustrates the sizes of various particles
various strategies to manage the public health risks in comparison with human hair.
associated with exposure to key air pollutants.
Health effects.
1.2 Health Impacts of Key Air
Pollutants Bacteria: 10 µm

Particulate matter
Road dust: 5 µm
Airborne PM is a complex mixture of particles with
components having diverse chemical and physical
Coal dust: 2 µm
characteristics. Particles are generally classified
by their aerodynamic diameters since size is a Human hair: 100 µm
critical determinant of site of deposition within
the respiratory tract. PM10 are particles less than
10 microns in aerodynamic diameter1. They can Viruses: 0.4 µm

further be divided into coarse particles (from 2.5

to 10 µm), fine particles (PM2.5, less than 2.5 µm) Vehicle emissions: 0.2 µm
and ultrafine (UF) particles (particles of diameter

Figure 5.2: The size of various particles in

1 More accurately: particles for which the peak of ths size
distribution is at 10 µm with at least 50% of sizes below 10 µm. comparison to the width of a
Particles of sizes 2.5 and 0.1 µm have an analogous definition. human hair

6
There has long been evidence showing that high cancer mortality, respectively.
Box 5.2
levels of PM and other pollutants affect health. The coarse particle fraction Some Typical PM10
Air pollution episodes in the last century provide (PM10-2.5) and TSP were not Concentrations
evidence of their adverse consequences. Recent consistently associated with Me an PM 10 concent r a t ions in
epidemiological studies showed an independent mortality. Thresholds were northern Europe and North America
are approximately 15 to 30 µg/m3.
role of PM in causing adverse health effects, and not apparent in these studies.
However, higher concentrations
toxicological studies demonstrated the mechanisms However, PM2.5 annual mean (45 to 98 µg/m3) have been found
of PM toxicity thus supporting the findings from level of 10 µg/m is found to be
3 in certain areas of some European
cities. In urban areas of developing
epidemiological studies. the lowest level at which all- countries, the PM 10 levels may
cause, cardiopulmonary and b e subs t a n t i a l l y h igh e r. For
Many time-series studies have explored the example, measurements from four
lung cancer mortality have been Chinese cities indicated annual
acute health effects associated with exposure to
shown to increase with more mean PM10 concentrations ranged
airborne particulates. PM10 is used as an indicator from 115-275  µg/m 3 . In Bangkok,
than 95 per cent confidence in mean 24-hr PM10 concentrations of
for air borne particulates as there are extensive
response to PM2.5. Although 80-100 µg/m3 have been reported.
measurement data of PM10 throughout the world. Developing country cities in Asia
adverse health effects cannot tend to have high PM concentrations
Substantial evidence shows that PM exposure is
be entirely ruled out even at (HEI, 2004).
linked to a variety of adverse effects on mortality
such low level, these levels are
(non-accidental all-cause mortality, cardiovascular
expected to effectively reduce health risks (Dockery
and respiratory mortality) and morbidity (hospital
et al., 1993; Pope III et al., 2002).
admissions, out-patient and emergency visits,
asthma attacks and acute respiratory infection). The A wide range of morbidity indicators has been
association between PM and adverse health effects investigated in epidemiological studies. These
is consistent in various cities, both in developed include hospital admissions, emergency room or
and developing countries. The risk for adverse clinic visits, symptoms in persons with underlying
health outcomes has been shown to increase with chronic heart or lung diseases, pulmonary function,
exposure and there is no evidence to suggest a and various biomarkers. The risk for acute events,
threshold below which no adverse health effects including myocardial infarction (heart attack) and
would be anticipated. stroke, has also been assessed.

Several meta-analyses have been conducted to In addition to PM10 and PM2.5, there is considerable
examine the relative risk of short-term mortality toxicological evidence of potential adverse effects
associated with a 10 µg/m3 increase of PM10. Meta- of UF particles on human health, but the available
analyses on European studies, US studies and Asian epidemiological evidence is insufficient to derive an
studies showed that for each increase of 10 µg/ exposure-response relationship to UF particles.
m3 PM10 the estimates for short-term all-cause
mortality were 0.62 per cent, 0.46 per cent and 0.5 Mechanisms of toxicity
per cent, respectively (HEI, 2004) . The epidemiological evidence of the adverse health
Evidence also showed chronic adverse health effects effects of PM is supported by toxicological research.
associated with long-term exposure to air pollution. Toxicological studies on PM toxicity involved the
Two long-term exposure studies, i.e. the US respiratory and cardiovascular systems, as well as
American Cancer Society (ACS) study and Harvard immunological and inflammatory responses, which
Six-Cities cohort study, reported associations provide abundant mechanisms by which PM may
between long-term exposure to PM2.5 and mortality. adversely affect health. Inflammation by Reactive
A 10 µg/m3 increase of PM2.5 was associated with Oxygen Species (ROS) is emerging as a central and
approximately a 4 per cent, 6 per cent and 8 per cent underlying potential mechanism for a variety of
increase risk of all-cause, cardiopulmonary, and lung adverse effects.

7
5
Toxicological studies have nose and upper respiratory tract. During exercise,
Box 5.3
WHO PM Guideline shown that ambient PM may SO2 tends to reach the lower airways because the
Values (WHO, 2000b) have direct effects on the increased flow rates and mouth breathing reduce
The available information for short- respiratory tract. These effects the percentage of inspired SO2 absorbed in the nose
term and long-term exposures to mainly involve production of and upper airways.
PM 10 and PM 2.5 does not allow
an inflammatory res­p onse,
the setting of a threshold for the In controlled chamber studies, short-term exposure
onset of adverse effects. For this exacerbation of exis­ting airway
reason no guideline values were to high level SO 2 has been found to induce
diseases, or impairment
recommended, but inst ead risk adverse health effects, including reduced lung
estimates and exposure-response of pulmonary defence
relationships were provided. function and increased respiratory symptoms on
mechanisms. Inhaled PM may
both healthy and asthmatic volunteers. Response
increase production of antigen-
WHO PM Guideline to inhaled SO2 is rapid, usually within a few
Values (WHO, 2005) specific immunoglobulins,
minutes. Lung function returns to normal after
alter airway reactivity to
PM10 50 µg/m3 for 24-hour mean several minutes to several hours, varying with the
antigen challenge or enhance
20 µg/m3 for annual mean individual and severity of the response. However,
suscepti­bility of the lungs to
PM2.5 25 µg/m3 for 24-hour mean continued exposure does not seem to increase the
microbial infection. There are
10 µg/m3 for annual mean response, and there seems to be a tendency for it
also extrapulmonary effects of
to decline gradually. Asthmatics are particularly
PM. One potential pathway is
sensitive to SO2. During exercise, the percentage
via systemic transport of cytokines produced in
of SO2 penetration to the lower respiratory tract
the lungs by an inflammatory response. Another
increases.
potential pathway is through adverse effects on
coagulation properties that lead to increased risk of Approximately 60 per cent of time-series studies
stroke or myocardial infarction (heart attack). There that have been conducted to explore the association
is also the possibility that PM may have a direct between PM and daily mortality and morbidity
effect on the heart, resulting in changes in blood also examined the impacts of SO2. Associations
pressure, heart rate, and heart rate variability. between SO 2 exposure and daily mortality
(including all-cause, cardiovascular and pulmonary
Sulphur dioxide (SO2) mortalities) were found in most of these studies,
SO 2 is emitted from combustion of sulphur- but the consistency of SO2’s association with
containing fossil fuels from power plants, various daily mortality appeared to be less than that for
industries, and motor vehicles. It has been one PM. Some researchers argued that SO2 serves as
of the major air pollutants worldwide. In recent a “surrogate” for urban air pollution from fossil
years, as a result of stringent controls on emissions fuel combustion. In an intervention study in Hong
and changes in fuel use, concentrations of SO2 in Kong, where the sulphur content of fuels was
developed countries have significantly declined. reduced to 0.5 per cent over a weekend in July
Annual mean concentrations in such areas are 1990, the ambient SO2 concentration decreased
now in the range of 12-45 µg/m3, with daily means from 44 to 21 µg /m3. The reduced SO2 level led
seldom exceeding 70 µg/m3. However, in some to reductions in adverse health effects such as
developing countries, the use of high-sulphur throat irritation, hospital admission and excess
containing coal is still increasing, thus ambient mortality for respiratory-cardiovascular diseases.
SO2 concentrations there remain high. This suggests a causal relationship between SO2
exposure and adverse health outcomes (Hedley
Health Effects et al., 2002).
SO2 is readily soluble in water. After inhalation,
Associations between emergency hospital
SO2 is absorbed in the mucous membranes of the
admissions for asthma and SO2 have been reported

8
in some studies, but not in others. Likewise, levels of NO2 vary according
Box 5.4
associations between hospital admissions for to time of the day, season of
WHO SO2 Guideline
chronic obstructive pulmonary disease (COPD) and the year, and meteorological Values (WHO 2000b)
SO2 were found to be significantly positive in some factors. The NO2 levels near • 500 µg/m3 for 10-minute mean
studies, but not in others. Association between SO2 main thoroughfares are
• 125 µg/m3 for 24-hour mean
and cardiac disease hospital admissions was found generally much higher than
• 50 µg/m3 for annual mean
both in London and Hong Kong despite their those monitored in stationary
differences in climate and ethnicity. A meta-analysis monitoring stations. WHO SO2 Guideline
Values (WHO, 2005)
examined the time series studies performed in Asia
3
• 500 µg/m for 10-minute mean
on SO2 and respiratory and cardiovascular hospital Health effects
admissions, in which positive associations were NO 2 is a strong oxidant, • 20 µg/m3 for 24-hour mean

also found. However, it could not be concluded relatively soluble in water. • no guideline value for the annual
mean
whether SO2 per se is positively correlated with Toxicological data show
hospital admissions or acts as a surrogate for a that NO 2 can induce toxic
mixture of urban air pollutants. respiratory effects, including reduced host
defence against infectious pulmonary disease and
Prospective cohort studies have been performed
enhanced airway responsiveness in exercising
to analyse the long-term effects of air pollution.
healthy subjects to bronchoconstrictive agents,
SO2 was found to be associated with mortality in
and in asthmatics to allergens and irritant stimuli.
the ACS cohort study in which the follow-up data
These effects were observed in controlled human
of approximately half a million subjects during
studies with NO2 concentrations much higher than
1982–1998 were linked to fine particles, sulphate,
the ambient levels. The result of a meta-analysis
and gaseous pollutants data.
has indicated adverse effects when the levels
exceed 200 µg/m3.
Nitrogen oxides (NOx)
Since NO 2 is strongly related to PM, as both
Although NOx include many chemical species,
come from the same combustion sources, and is
the sum of NO and NO2 is generally referred to as
converted to nitrates, it contributes to fine particle
NOx, and NO2 is the most important of them. Most
mass in ambient air. Therefore it is very difficult
atmospheric NOx is emitted as nitric oxide (NO),
to discriminate the effects of NO2 from those of
which is rapidly oxidized by O3 to NO2. NO2 is the
other pollutants in epidemiological studies. Many
main source of tropospheric ozone in the presence
epidemiological studies used NO2 as a marker or
of hydrocarbons and ultraviolet light, thus playing
a surrogate for air pollutant mixture from fuel
an important role in determining ambient O3
combustion.
concentrations. NO2 is also a key precursor of
nitrate particles which form an important fraction Respiratory symptoms in children and bronchitic
of the ambient air PM 2.5 mass. Emissions of symptoms in asthmatic children have been
NOx are from both natural and anthropogenic found to increase with outdoor annual NO 2
sources. The major anthropogenic source of NOx concentrations. Reduced lung function growth in
is combustion of fossil fuels both in stationary children has also been reported linked to increased
sources and in motor vehicles. NO2 concentrations.
Natural background annual mean concentrations Many time-series studies have been conducted
for NO2 range from 0.4 to 9.4 µg/m3. In urban areas to explore the association between NO2 exposure
annual mean NO2 concentrations are generally and daily mortality. NO2 daily concentrations
in the range of 20 to 90  µg/m3, with an hourly are found to be significantly associated with
maximum of 75 to 1015  µg/m3. Urban outdoor increased all-cause, cardiovascular and respiratory

9
5
Box 5.5
mortality. A meta-analysis on Ozone (O3)
daily mortality and 24-hour
WHO NO2 Guideline O3 and other photochemical oxidants are secondary
Values (WHO, 2000b;2005) NO2 levels indicated that the
air pollutants formed by the action of short-
overall effect estimate from
• 200 µg/m3 for 1-hour mean wavelength radiation from the sun on NO2. O3 is
the single pollutant model for
• 40 µg/m3 for annual mean formed by reacting with NO, forming NO2 and
all-cause mortality was 2.8 per
oxygen (O2). Background ambient concentrations
cent per 45 µg/m3 NO2 which
of O 3 vary with time and location. O 3 tends
fell to 0.9 per cent in multi-
to travel with the prevailing wind. Generally,
pollutant models, including particles (Stieb et al.,
its concentration is higher in suburban areas.
2002). The European APHEA-1 (Air Pollution and
O3 concentration levels could reach 400  µg/m3
Health, a European Approach) study found a 1.3
in summer in large cities with heavy traffic in
per cent increase in daily deaths per 50  µg/ m3
developing countries. Indoor O3 are generally
NO2 (1-hour maximum) (Touloumi et al., 1997).
significantly lower than those measured outdoors
The effect remained statistically significant after
due to absorption by walls and floors.
adjusting for black smoke. The APHEA-2 study
(Katsouyanni et al., 2001) found that PM effects on
daily mortality were stronger in areas with high Health effects
NO2. The US National Morbidity and Mortality O3 is a potent oxidant and may induce either direct
Air Pollution Study (NMMAPS) showed that daily or indirect oxidative stress through inflammatory
mortality increased from 0.3 to about 0.4 per cent per reaction to the respiratory tract. Short-term acute
18.8 µg/m3 increase of NO2. effects include respiratory symptoms, pulmonary
function changes, increased airway responsiveness
The results of most of the time series studies on and airway inflammation. Exposure to ambient
NO2 and hospital admissions/emergency room levels of O3 induces a significant inflammatory
visits for respiratory and cardiovascular diseases, reaction including cellular influx and release
as well as doctor visits for asthma in children show of inflammatory mediators and cytokines. The
an independent NO2 effect. Controlling for other association between O3 exposure and pulmonary
pollutants lowers the effect estimates at times, and inflammation seems to be dose dependent.
at other times makes them statistically insignificant. Controlled chamber studies show changes in lung
In some studies, NO2, rather than PM, was found to function and lung inflammation among young
be associated with asthma hospital admissions. An healthy adults when exercising.
effect of NO2 has been noted in most panel studies
evaluating aggravation of asthma in children, O 3 affects pulmonary defence mechanisms
showing a clear effect of NO2 on the incidence of because of impairment of mucociliary clearance,
viral infections among asthmatics. decreased macrophage activity and effects on
circulating lymphocytes. O3 may disrupt normal
Health risks from NOx may result from NO2 per se function of the airways and pulmonary immune
or its products, including O3 and secondary fine system by suppressing or enhancing the host’s
particles. It is difficult to determine whether the immune responsiveness. Exposure to O 3 may
independent effects observed for NO2 and PM increase bronchial responsiveness to allergens in
are effects due to NO2, or regionally transported subjects with airway allergy. However, there is
particles and locally produced fine and ultrafine considerable individual variation in the response
particles. However, NO 2 levels are generally to O3. Pre-existing pulmonary diseases, asthma,
considered a reasonable marker of exposure to age and genetic factors may influence the host’s
traffic-related emissions. susceptibility to O3.

10
Combined evidence from time-series studies show Health effects
positive associations between daily mortality and After inhalation, CO diffuses Box 5.6
WHO O3 Guideline Values
O3 levels, independent of the effects of PM. An r a p i d l y a c r o s s a l ve o l a r
(WHO, 2000b)
increase of 10 µg/m3 in the 8-hour O3 concentration and capillary membranes.
• 120 µg/m3 for 8-hour mean
is associated with a 0.3 to 0.5 per cent increased daily Approximately 80  -  90 per
mortality. There is no clear evidence of a threshold cent of the absorbed CO WHO O3 Guideline Values
(WHO, 2005)
for O3. Time-series studies have shown effects at O3 binds with haemoglobin to
• 100 µg/m3 for 8-hour mean
concentrations below 120 µg/m3. form carboxyhaemoglobin
(COHb). The affinity of CO
Combined evidence shows that O 3 exposure to haemoglobin is 200-250 times higher than that
is significantly associated with an increase in of O2. Consequently, the formed COHb reduces
morbidity. The most common health end-points are the oxygen-carrying capacity of the blood and
school absenteeism, hospital or emergency room impairs the release of O2 from oxyhaemoglobin to
admissions for asthma, respiratory infections, and extravascular tissues, thus causing tissue hypoxia.
exacerbation of chronic airway diseases. Children, Tissue hypoxia is the main toxicity mechanism of
elderly people, asthmatics and those with chronic CO. Therefore, in organs and tissues with high
obstructive airway diseases are more sensitive to O2 consumption such as brain, heavy exercising
O3 exposure. Effects of O3 on respiratory hospital skeletal muscles and developing fetus, toxic effects
admissions seem stronger during the warmer of CO are more prominent.
season.
COHb is a specific biomarker of exposure to CO
There is some evidence indicating that long-term in blood. In healthy, non-smoking populations
exposure to O3 may have chronic effects. Animal the COHb levels are about 0.5-1.5 per cent due
data, as well as some autopsy studies indicate that to endogenous CO production and exposures to
chronic exposure to O3 induces significant airway background environmental CO. During pregnancy,
changes at terminal and respiratory bronchioli. due to increased endogenous production, maternal
However, epidemiological evidence of its chronic COHb levels are elevated to 0.7-2.5 per cent.
effects is less conclusive. However, for car drivers, traffic policemen, garage
attendants, tunnel workers and firemen, their COHb
Carbon monoxide (CO) levels could be as high as 10 per cent.
CO is a colourless and odourless gas. The main source
Exposure to CO may contribute to cardiovascular
of environmental CO is anthropogenic, mainly
mortality and the early course of heart attack.
due to emissions from incomplete combustion of
Patients with coronary artery disease are considered
fossil fuels. Global background concentrations of
as most sensitive to CO exposure, with aggravation
CO range between 0.06  mg/m3 and 0.14  mg/m3
of angina occurring in patients at COHb levels
(0.05-0.12  ppm). In cities with heavy traffic the
of 2.9 - 5.9 per cent. In addition to shortening in
8-hour average CO concentrations are generally
the time to onset of angina, electrocardiographic
lower than 20 mg/m3 (17 ppm) with short-lasting
changes and impaired left ventricular function,
peak below 60 mg/m3 (53 ppm). Some indoor CO
ventricular arrhythmias may be increased at higher
concentrations could reach much higher levels, such
COHb levels. Exposures to CO do not seem to have
as in underground car parking areas, road tunnels,
atherogenic (causing a fatty deposit on or within
and in homes with gas stoves. CO concentrations
the inner lining of an artery) effect on humans. It is
inside motor vehicles are generally higher than those
unlikely that CO has direct adverse effects on lung
monitored in outdoor air. Indoor tobacco smoking
tissue except for extremely high concentrations
can also raise the CO concentration indoors.
associated with CO poisoning. However, the effects

11
5
of CO exposure on lung function and disposal. Lead water pipes, lead-containing
and respiratory symptoms are containers and leaded-gasoline also contribute to
Box 5.7
WHO CO Guideline still inconclusive. the environmental burden of lead. Humans are
Values (WHO, 2000b) exposed to lead through air, food, water and soil/
Severe hypoxia due to acute
Well-documented evidence has dust. Average lead levels in air are usually below
CO poisoning may cause
shown various adverse effects in 0.15 µg/m3 at non-urban sites. For infants and
connection with different COHb both reversible, short-lasting
young children, lead in dust and soil, as well as
levels. A COHb level of 2.5 per neurological deficits and delayed
cent is recommended to protect lead-containing paint are also important exposure
non-smoking, middle-aged and neurological damage. The
sources.
elderly population groups with neurobehavioural effects include
coronary heart disease from
acute ischaemic heart attacks, impaired coordination, driving
Health effects
and to protect the fetuses of ability, vigilance and cognitive
non-smoking pregnant women The level of blood lead (PbB) is the best available
performance when COHb levels
from hypoxic consequences.The indicator of current and recent past environmental
following guideline values for CO reach 5 - 8 per cent. Increased
in ambient air were recommended lead exposure, and may also be a reasonably good
COHb levels decrease the
by WHO in 2000 in such a way that indicator of lead body burden with stable lead
the COHb level of 2.5 per cent maximal exercise performance
would not be exceeded: exposure. PbB is used as an indicator to relate with
in a healthy population.
• 100,000 µg/m3 for 15 minutes
various adverse effects of lead exposure.
The fetus is extremely sensitive
• 60,000 µg/m3 for 30 minutes In experimental animal studies, lead has been
to CO exposure. The absorbed
• 30,000 µg/m3 for 1 hour shown to cause adverse effects on haematopoietic,
CO can diffuse through placental
• 10,000 µg/m3 for 8 hours nervous, renal, cardiovascular, reproductive,
membrane. During pregnancy,
immune and bone systems. Impaired learning/
endogenous production of CO
memory abilities, and visual and auditory
increased, and maternal COHb
impairments have been reported (WHO, 1995).
levels are usually about 20 per cent higher than the
non-pregnant values. At steady state, fetal COHb In humans, lead has been shown to have a wide
levels are up to 10-15 per cent higher than maternal range of biological effects. Adverse effects on haem
COHb levels. The elimination half-life of COHb in synthesis have been reported in both adults and
the fetus is much longer than that in the pregnant children. Anaemia has been observed in children
woman. There is a well-established and probably at PbB levels above 40 µg/dl. Increased levels of
causal relationship between maternal smoking serum erythrocyte protoporphyrin and increased
and low birth weight at fetal COHb levels of 2-10 urinary excretion of coproporphyrin and delta-
per cent. In addition, maternal smoking seems to aminolaevulinic acid are observed when PbB
be associated with a dose-dependent increase in concentrations are elevated. Inhibition of delta-
perinatal deaths and with behavioural effects in aminolaevulinic acid dehydrase (ALAD) and
infants and young children. dihydrobiopterin reductase has been observed at
lower levels.
CO causes a large number of accidental poisonings
and suicidal deaths in the general population Lead exposure impairs neurobehavioural and
(Fabre et al., 1999; Shepherd and Klein-Schwartz, psychological functions. Children are more
1998). vulnerable to adverse effects of lead due to
neurological, metabolic and behavioural reasons.
Lead (Pb) Evidence has shown that PbB levels are related to
Sources of lead in the environment include natural intelligence quotient (IQ). Combined evidence from
and anthropogenic origins. Anthropogenic sources cross-sectional and prospective epidemiological
include lead mining, smelting, use, recycling studies show that PbB levels even below 25 µg/dl​
might be related to decrements in IQ (WHO, 2000a).

12
Long-term high level occupational lead exposure unit of measurement of the
Box 5.8
in workers has been shown to be associated with overall “burden of disease” WHO Pb Guideline
peripheral neuropathy, such as reduction in on the population. The GBD Values (WHO, 2000b)
peripheral nerve conduction velocity, impaired also presents a first estimate • 0.5 µg/m3 for annual mean
sensory motor function, and impaired autonomic of the proportion of mortality
nerves system function. and disability that can be
attributed to certain risk factors for the disease,
Recent studies using more sensitive indicators of
in this case air pollution. This approach can be
renal function suggest renal effects at lower levels
modified to reach a “country” or “city” burden of
of lead exposure. Some but not all epidemiological
disease, if needed (WHO, 2006).
studies show an association between lead exposure
and pre-term delivery and some indices of fetal To reflect various disease burdens it is critical
growth and maturation. The reproductive effects of to provide a single measure of disease burden
lead in the male are limited to sperm morphology to capture the impact of both premature death
and count. In the female, some adverse pregnancy and disability. The Disability-Adjusted Life Year
outcomes have been attributed to lead. (DALY) is adopted as a common measuring index
in this context. DALY is the sum of years of life lost
WHO Guidelines for lead in air have been based on
to premature death (YLL) and years lived with a
the concentration of lead in blood. Critical effects
disability of specified severity and duration (YLD).
to be considered in the adult organism include
Thus, one DALY is equal to the loss of one healthy
elevation of free erythrocyte protoporphyrin,
life year, that is, time lived with a disability and
whereas for children cognitive deficiency, hearing
time lost through premature death, i.e.:
impairment and disturbed vitamin D metabolism
are taken as the decisive effects. A critical level of DALY = YLL + YLD
lead in blood of 10 µg/dl was proposed based on
A “premature” death is defined as one that occurs
the earliest adverse effects of lead in young children
before the age to which the dying person could
beginning at 10-15 µg PbB/dl. It is assumed that
have expected to survive. However, disability is
approximately 1 µg Pb/m3 of air would contribute
difficult to define and quantify. All non-fatal health
to 5 µg PbB/dl in blood (WHO 1995).
outcomes of disease are different from each other
in their causes, nature, and especially severity. In
1.3 Global Burden of Disease and order to calculate the YLD for different category
Air Pollution of disability, it is crucial to set weights for each

W hen setting priority and intervention category of disability based on their nature and
targets on air pollution from the public severity.
health standpoint, it is important for decision
Combined evidence shows that almost all diseases
makers to know what the total impact of air
are caused by the interaction of genetic and
pollution related disease is and to compare the
environmental factors. The amount of disease,
impacts of different risk factors contributing to
disability and death in the world today can
such diseases. The Global Burden of Disease (GBD)
be attributed to a selected number of the most
approach of WHO provides policy-makers with a
important risks to human health. This burden
comprehensive picture of the world’s current and
could be lowered if the attributable risk factors
future health needs and a method to assess the
are reduced. Risk is defined as the probability of
situation (WHO, 2002). This method quantifies
an adverse outcome.
not only the number of deaths but also disability
in a population, and combines these into a single Estimating the contributions of selected major risk
factors to global, regional or country specific burden

13
5
of disease in a unified manner can help set priorities and industrial practices, have led to increased
for research and policy action in respective areas. atmospheric concentrations of a number of
greenhouse gases (GHGs).
The ten leading causes of global disease burden
worldwide estimated by the WHO (2002) are GHGs include CO 2 , CH 4 (methane, natural
underweight, unsafe sex, high blood pressure, gas), N 2 O (nitrous oxide), O 3 , and CFCs
tobacco consumption, alcohol consumption, unsafe (Chlorofluorocarbons). CO2, the most important
water, sanitation and hygiene, iron deficiency, greenhouse gas, absorbs heat and acts like a blanket
indoor smoke from solid fuels, high cholesterol, to keep our planet warm, and thus increases the
and obesity. Together, these account for more than global temperature. The use of fossil fuels currently
one third of all deaths worldwide. accounts for 80 to 85 per cent of the CO2 being
added to the atmosphere. CH4 is the second most
WHO also estimated numbers of premature deaths
important GHG, produced by rice cultivation, cattle
and DALYs attributable to various environmental
and sheep ranching, and by decaying material in
risks: unsafe water, sanitation and hygiene may
landfills. CH4 is also emitted during coal mining
attribute to 1.7 million deaths and 54.2 million
and oil drilling, and by leaky gas pipelines.
DALYs; urban air pollution may attribute to 0.8
million deaths and 7.9 million DALYs; lead may N2O is produced by denitrification processes in
attribute to 234,000 deaths and 12.9 million DALYs. oceans, nitrification and denitrification pathways
Indoor air pollution was estimated to be 1.6 million in soils, and by various agricultural and industrial
excess deaths annually. Taking necessary actions to practices. Based on current data, tropospheric
control and prevent environmental risks could lead O3 is an important contributor to the enhanced
to up to 10 years more of life expectancy globally greenhouse effect. However, because of its relatively
(WHO, 2002). short atmospheric lifetime, the magnitude of this
contribution is uncertain. Sulphates and nitrates,
on the other hand, may limit climate change
1.4 Climate Change and Health
in some areas. Within this context, fossil fuel
C limate change has drawn the attention of
scientists, decision makers and the general
public in recent years. Climate is usually defined
combustion related air pollution is considered as
climate forcing.
as the statistical description of weather in terms
of the mean and variability of relevant quantities Health effects
(e.g. temperature, precipitation, and wind) over The consequences of climate change might be
a period of time (e.g. 30 years). Global average indirectly related to human health, (see Figure
temperatures are generally quite stable. The 5.3). The likely negative consequences of climate
Intergovernmental Panel on Climate Change (IPCC), change include extreme weather events, changing
a group established by the World Meteorological patterns of precipitation, droughts, floods, rising
Organization (WMO) and the United Nations sea levels, and spread of disease-transferring
Environment Programme (UNEP), has reported vectors (e.g. mosquitos). Changing regional climate
that the average surface temperature of the earth could alter forests, crop yields, water supplies,
has increased during the twentieth century by biodiversity, and ecosystems. Heat waves and
approximately 0.6 - 1.1 °C (IPCC, 2007). heavy precipitation events are likely to increase;
droughts are likely to increase in total area affected;
Both natural events and human activities tropical cyclones are likely to tend towards larger
contribute to climate change. Human activities, lifetimes and greater storm intensity; extreme
most importantly the burning of fossil fuels, as extra-tropical storms are likely to show a net
well as deforestation and various agricultural increase in frequency and intensity (IPCC, 2007).

14
Figure 5.3 Climate change and health

All these events could affect human and animal temperatures may make air and water pollution
health (see Figure 5.3). more pronounced, which in turn may harm human
health. Some scientists believe that algal blooms
Extreme temperature is a risk factor for mortality.
could occur more frequently as temperatures warm
Statistics on mortality and hospital admissions
up (WHO, 2003). Figure 5.4 details the indirect
show that death rates increase during extremely
health impacts of climate change.
hot days, particularly among the elderly and young
children (WHO, 2003). For example, extreme The reduction of air pollution from motor vehicles
heat waves caused more than 52,000 deaths in and power plants will significantly help reduce
Europe and more than 2,800 deaths in India in the amount of GHG emitted, especially CO 2.
2003 (EPI, 2003; 2006). People with cardiovascular Cleaner cars, stricter emission standards for
and respiratory diseases are more vulnerable. stationary sources and motor vehicles, modern
Climate change may also increase the risk of electricity generators and increasing the use of
certain infectious diseases, particularly those renewable energy sources will all contribute to
that appear only in warm areas. Diseases spread reducing GHG emissions. By doing so, not only the
by mosquitoes and other insects could become amount of CO2 will be significantly reduced, other
more prevalent. Such vector-borne diseases pollutants emitted from fossil fuel combustion
include malaria, dengue fever, yellow fever, and such as PM, NO2 and SO2 will also be reduced,
encephalitis. Disease-carrying mosquitoes are thus bringing about significant associated health
spreading as climate shifts allow them to survive and environmental co-benefits (see Module 6
in previously inhospitable areas. Moreover, warm Governance and Policies).

15
5
Emissions
Soil & surface Wet & dry of gases & Climate
water deposition particles

Visual Heat, cold, Biological Sea level

Plants extreme
range disease rise
and soil weather events agents

Ground
water Health
effects

Figure 5.4: Direct and indirect health impacts of air pollution and greenhouse gases

16
Section 2 Design of Health Studies

2.1 Information from Toxico- period may not be sufficiently long for the
logical Animal Studies study purpose.

F or most environmental chemicals,

epidemiological studies or human control
studies are generally not available. For key air
• Genetic disposition, metabolic processes,
sensitivity, disposition towards diseases
and other properties may differ between
pollutants, such as PM, recent epidemiological humans and animals.
and time-series studies have shown statistically
significant associations between PM exposure and
In recent years, animal models have been
mortality and morbidity. More evidence is still
used to explore the mechanisms of toxicity
needed to establish a causal relationship and to
of air pollutants, and to investigate the host
further explore the underlying mechanisms that
susceptibility. An “animal model” refers to an
result in health impacts.
animal useful for laboratory medical research
Animal studies have the unique advantage of that has specific characteristics for developing
exposing laboratory animals to a particular a human disease or disorder (NHGRI, 2007).
chemical of interest and seeing the specific toxic Animal models of chronic obstructive pulmonary
effects on a target organs/systems and establishing disease (COPD) remain a critical experimental
dose-response relations (WHO, 1994; 1999). A tool in studying various aspects of COPD and
dose-response relation is a relationship between air pollution. Using a mouse model, long-
the amount of an agent administered to, taken up term exposure to low concentrations of PM2.5
by, or absorbed by an organism, system, or (sub-) altered vasomotor tone, and induced vascular
population and the change developed in that inflammation, and atherosclerosis, thus providing
organism, system, or (sub-) population in reaction the potential mechanisms of cardiovascular
to the agent. Figure 5.5. is an example of a dose- susceptibility to PM2.5.
response relationship.

Thus animal studies play an important role in risk

assessment for the purpose of hazard identification
of chemicals. Such data are most useful if they are
of good quality and obtained in compliance with
standard animal test guidelines, good laboratory
practice, and the numbers of animals for test
groups and the control group are adequate for
thorough toxicological examination and statistical
evaluation. However, limitations of animal studies
include the following:

• Exposure levels in animal studies

are usually much higher than those
encountered in the real environment; the
exposure route may not be relevant with
Figure 5.5: Dose-response relationship between
respect to human exposure; the exposure
health effects and carboxyhaemoglobin in
blood

17
5
Human data from volunteer studies or to exist, an analytical study can then be conducted
epidemiological studies are normally used a priori to evaluate the quantitative relationship between
for establishing environmental health criteria/ exposure and health effect by following a population
standards wherever possible. However, animal data over a period of time. If the study design incorporates
can contribute to establishing the causal relationship all the information contained in the person-time
and to further exploring the underlying mechanism experience of the study population, it is called a
for the development of diseases due to exposure to cohort study. If the study design attempts to obtain
a toxic chemical. the same findings by comparing cases of the disease
with people without the disease (selected as a
sample of the person-time experience of the source
2.2 Information from Epidemio­
population that generated the cases), it is called a
logical Studies case-control study. Studies are termed “prospective”

T he findings of toxicological studies have

the advantage of being able to identify
the adverse health effects specifically and to
if the population is observed over time as events
occur. Studies are termed “retrospective” or
“historical” if existing records are used and
pin-pointing the dose/effect relationship more
exposure and health outcome are ascertained after
precisely. It is both unfeasible and unethical to
they have occurred (Beaglehole et al., 1993).
try to test the result on humans. Findings from
epidemiological studies are based on observations Most descriptive studies are based on existing
of human subjects only and therefore are more mortality or morbidity data, and patterns of health
directly representative and applicable to actual outcome are examined for specific geographical areas
situations in our daily life. or specified time periods. The main disadvantage
of using existing records is that the information
Environmental epidemiological they provide may not be fully appropriate for the
studies particular study objective and may not have the
The 1952 London smog episode received worldwide required precision for the study purpose.
attention and highlighted the association between
ambient air pollution and mortality. Since the 1952 Cross-sectional studies
smog numerous environmental epidemiological Cross-sectional studies examine the association
studies have been undertaken. Epidemiology is between an environmental exposure and prevalence
the study of the distribution and determinants of a certain disease (the proportion of the population
of health-related states or events in specified affected) at a particular point in time or during a
populations. Environmental epidemiology is the short period of time. Estimates of exposure and
branch of epidemiology that specifically deals with measurement of personal disease characteristics
environmental exposure as determinants. are made at the same time. This approach is usually
undertaken before undertaking a cohort study or a
Epidemiological studies can further be classified as case-control study because generally it takes less
either observational or experimental. Observational time to complete and, therefore, is less expensive.
studies are studies in which the investigator Since cross-sectional studies examine the prevalence
observes but takes no action to intervene. They can of diseases, symptoms, and biomarkers of exposure
be descriptive or analytical. These studies are mostly and/or effects rather than their incidence, they are
descriptive; they define the population group of used to describe long-term conditions of health
interest, estimate prevalence or incidence of the outcomes (health endpoints) rather than their daily
disease, and identify any potential environmental changes.
determinants that might have caused the disease.
If a specific cause-effect relationship is suspected

18
Ecological studies
In ecological studies the investigator compares
aggregate measures of exposure (average exposure
or proportion of population exposed) with aggregate
measures of health outcome rates for the same
population. The investigator analyses associations
between environmental exposure and health
outcomes using groups of people instead of Figure 5.6: Cohort studies scheme
individuals as the unit of analysis. It is used in
performing exploratory analyses using existing though also a sample of the source population from
population data. which the cases are identified, do not develop the
health outcome (called “controls”). Case-control
Cohort studies studies are efficient for studying rare disease cases,
The study population in a cohort study consists especially those with a long induction period. For
of individuals who are at risk of developing instance, it has been used extensively to study the
a particular disease or health outcome. The impact of environmental determinants for various
individuals are divided into groups (“cohorts”) cancers (see Figure 5.7).
according to their exposure status. A cohort is
a group of individuals, identified by a common Time-series studies
characteristic, who are studied over a period of time In time-series studies repeated observations of
in an epidemiological investigation. Cohort studies exposure and health endpoints are made over time
are studies in which two groups of people with within the same study population. The analysis
different levels of exposure are followed up and the centres on comparing variations in exposure status
effects are recorded. Thus cohort studies are also over time with changes in health outcome status
known as follow-up studies. They are then followed over time. A time-series study based on aggregate
over time to ascertain the subsequent incidence of data is essentially a temporal comparison study that
the health outcome in each group (see Figure 5.6). examines an association between a variable exposure
It is called a prospective cohort study if the relevant and a concomitant variable health outcome. This
data are collected as the events unfold and a method has been used extensively in recent decades
retrospective or historical cohort study if past events in the study of atmospheric air pollution and its
are examined using existing health-related records. impact on health. Since observations are made
A non-exposed group is used for comparison with within the same population, the influence of many
the exposed groups and the exposed groups can confounding factors can thus be avoided.
further be divided into sub-groups based on their
degree of exposure. Cohort studies are used to
assess long-term health effects of acute exposures
to environmental hazards. Cohort studies are
also used to measure chronic effects of long-term
exposure to environmental toxic chemicals.

Case-control studies
A case-control study is a study that examines
the association between exposure and the health
outcome by comparing individuals who develop
the health outcome (called “cases”) and those who, Figure 5.7: Case-control studies scheme

19
5
Summarizing Study Information The main disadvantage of the crude mortality rate
There is a considerable amount of information is that it takes no account of the fact that the chance
on air pollution and its impact on health (WHO, of dying varies with age, sex, socio-economic
2000b; 2005). With different objectives, study status, ethnic group and other factors. Therefore it
types and methodology of various researchers, it is not appropriate to compare the crude mortality
is conceivable that the findings are anything but rate of one group of people against that of another
uniform. In order to reach a workable summary group of people when their age structure and
interpretation of several individual studies on a other contributing factors differ. Comparisons of
related topic, a method has been developed and mortality rates between different groups of people
refined over years towards this goal. The method with diverse age structures should be based on
is called “meta-analysis”, a quantitative analysis of age-standardized mortality rates or morbidity
the combined results of several individual studies. rates which eliminate the influence of different age
The basic steps include: locate all relevant studies distribution of the populations compared.
pertaining to the specific research topic, resolve
issues of study quality and conflicting results, Morbidity
calculate summary weights and finally reach a Morbidity data are based on out-patient consultation
summary effect or summary risk estimate. Though records and hospital admission records. However,
a meta-analysis method has its limitations, it is a hospital admission rates may be influenced by
useful technique for summarizing environmental factors other than the disease itself. Factors such
epidemiological studies, and for helping people as accessibility to medical care, social-economic
to reach a consensus when the results of several status of the population, service radius of medical
studies conflict with one another. facilities and availability of hospital beds may
influence the accuracy of morbidity rates.

2.3 Health Endpoints Birth outcomes

A dverse health effects due to air pollution range
from sub-clinical changes or manifestations
to illness and death. The following health endpoints
Recent evidence shows that air pollution might
be a risk factor of adverse birth outcomes, which
include low birth weight (LBW), pre-term delivery,
have been widely reported in the air pollution and intra-uterine growth retardation (IUGR), birth
health literature: acute and chronic mortality defects, and stillbirth. The characteristics and
(Rabl, 1998; 2006), morbidity (acute and chronic severity of adverse birth outcomes depend upon
bronchitis, acute respiratory infections, respiratory the air pollutant, exposure period and exposure
and cardiovascular hospital admissions, out- concentration. LBW refers to a live new-born’s
patient visits for internal medicine and pediatrics, weight less than 2,500 grams. Studies have shown
emergency-room visits, asthma attacks, etc.), birth that CO, PM10, PM2.5, SO2 and NO2 are potential
outcomes, and lung function tests. risk factors of LBW. It was found that exposure to
PM10, SO2 and formaldehyde during pregnancy
Mortality may be a potential risk factor of pre-term birth.
The death rate or crude mortality rate is calculated
from the number of deaths in a specified period in After controlling risk factors, such as, pre-delivery
a specific population against the total population health care, maternal education status, sex of new-
during that period. Death and cause of death are born infants, season, etc., air pollution exposure
recorded on standard death certificates in which (e.g., CO, SO2) also is a risk factor in IUGR.
age, sex, date of birth, place of residence, as well
as ethnic group are recorded. The usefulness of the
data depends on its accuracy and completeness.

20
Section 3 Economic Assessment of Air Pollution and Health

V aluation of health outcomes is a critical

component in assigning the social cost of
air pollution. Cost-benefit and cost-effectiveness
or the results of CVM studies (Ashenfelter, 2006).
The result of applying these methods is not the
value of an identifiable life, but instead the value
analysis provide a basis for setting priorities for
of reducing fatal risks in a population.
next-step actions.
So far, studies on the WTP for reducing the health
There are several existing methods that could be
risk of air pollution are mostly conducted in
used to estimate the monetary values of health
developed countries, but sparse in developing
outcomes associated with air pollution. The
countries. Economic analysis conducted in
willingness-to-pay (WTP) approach measures
developing countries has to rely on estimated
how much the concerned individuals are willing
values from studies in developed countries. This
to pay in order to reduce their own health risk
procedure is often termed as benefit transfer or
due to air pollution exposure (Johannesson, 1996;
value transfer in economics. Characteristics of
Drummond et al., 1997; Mansfield, 1997). The main
the concerned population (e.g. age distribution,
advantage of the WTP approach lies in its focus
income, health status and culture) may have
on the individual viewpoint and wishes of the
contextual effects on the valuation results. For
concerned population. The main difficulty of the
example, different social and health insurance
WTP approach lies in obtaining reliable and correct
systems greatly influence the risk perception of
empirical estimation.
local populations, resulting in a different WTP to
A variety of valuation techniques have been avoid the risk. Therefore, it might be inappropriate
used to measure the WTP value: labour-market to transfer the WTP values from developed
studies, contingent valuation method (CVM) and countries to developing countries directly.
various types of market-based analysis (Golan
There is also substantial information on the
and Shechter, 1993; Klose, 1999). Labour-market
valuation of health outcomes in which the
studies attempt to infer the compensation required
human capital approach (HCA) and the cost
in exchange for the increased risk associated with
of illness (COI) approach are adopted (Becker,
particular occupations while standardizing for all
1993; Houtven et al., 2005). The HCA considers
other attributes of the job and the worker. CVM
individuals as units of human capital that produce
uses survey information to determine what people
goods and services for society. Therefore, HCA
are prepared to pay to reduce the likelihood of
assesses the costs of a premature death by counting
premature death or certain diseases. The market-
the discounted values of future production which
based approach attempts to infer the WTP for
the “victims” could have generated if they had not
reductions in risk from the purchase of goods
died prematurely. The COI approach is used in
of which the sole purpose is to reduce the risks
morbidity studies and is consistent with the human
confronting an individual.
capital approach. The COI approach estimates the
Death is the most important health endpoint medical treatment costs plus the loss of production
associated with air pollution exposure. For due to possible incapacity to work. The main
mortality valuation, the most commonly applied advantage of these two approaches lies in their
approach is the value of a statistical life (VOSL). simple and transparent calculation concept, thus
The VOSL measures the value of given reduction resulting in higher social acceptance. The HCA
in risk and an individual’s WTP to reduce the risk, and COI, however, neglect a basic principle of the
relying on wage and occupational risk tradeoff data welfare economics theory, according to which each

21
5
valuation of positive or negative impacts has to be be presented based on the benefits and costs for
based on variations in the utility of the individuals which monetary values can be assigned, and a
concerned. Actually, HCA and COI are not entirely discussion of non-monetized or unquantifiable
related with the WTP concept. It has been shown benefits and costs should also be provided (Nas,
that HCA/COI provides a lower estimate of WTP 1996).
(Tarricone, 2005).
The net social benefit of each major alternative
Generally, the preferred approach is based on the can be estimated by subtracting the present value
individual’s WTP for risk reduction, while HCA/ of monetary social costs from the present value of
COI could also be used as an alternative approach monetary social benefits. The same baseline must
for certain morbidity endpoints due to absence of be used in both the benefit and cost analyses.
existing WTP literature on these endpoints. Plausible upper- and lower-bound estimates of
net benefits should be provided. The “best” or
3.1 Cost-Benefit and Cost- most-likely estimate should be identified and
sensitivity of the net benefits estimate to variations
Effective­ness Analysis in uncertain parameters should be examined.

A QM refers to all the activities a regulatory

authority undertakes to ensure that the air
we breathe is safe. The AQM process is the system
Other considerations for presenting and
summarizing the results from CBA include the
of understanding all the sources that contribute to following:
air pollution and the health and environmental • Discounting benefits and costs at a certain
effects of the pollutants, and then taking necessary time-point is the preferred method for
steps to reduce or control the pollution sources summarizing benefits and costs that
to reach or maintain certain agreed-upon target accrue over several years. Alternatives to
pollution levels in the air. An effective AQM discounting include annualizing costs and
strategy is dependent on a number of factors, benefits, and accumulating the costs and
which include emissions inventories (Module benefits through time to a designated future
2), air quality prediction models (Module 3), air year.
quality monitoring networks (Module 4), exposure • Present and evaluate non-monetized and
and damage assessments, as well as health- and non-quantified effects. There should be a
environment-based standards. Along with these presentation and evaluation of all benefits
factors are a range of cost-effective pollution control and costs that can only be quantified but
measures and legislative powers and resources to not valued, as well as all benefits and costs
implement and enforce these measures. It should that can be only qualitatively described.
be noted that AQM not only aims to maintain
• Present the incremental benefits, costs, and
the air quality that protects human health and
net benefits of moving from one regulatory
welfare but also provides protection of animals,
alternative to more stringent ones.
plants, ecosystems, materials and aesthetics, such
as visibility, (see Modules 1 and 6). • Discuss other potential costs and benefits
that may be the by-products of the
proposed action. These include transfer of
Cost-benefit Analysis
the pollution problem from one medium
Cost-benefit analysis (CBA) is a way of estimating
to another or possible exacerbation of
and totalling equivalent monetary value of benefits
exposure for specific sub-populations not
and costs. The decision is then made as to whether
included in the economic impact analysis.
the proposed AQM actions are beneficial. In this
process, estimates of the net social benefits should

22
Cost-effectiveness Analysis The CEA of a policy option in AQM is calculated by
When many benefits cannot easily be monetized, dividing the annualized cost of the option by non-
or when authorities set forth a specific policy monetary benefit measures. Such measures range
objective, cost-effectiveness analysis (CEA) should from the amount of reduction in air pollution to
be conducted. This will also provide useful improvement in human health or the environment,
information to policy makers. as well as damages avoided. DALY is one of the
measures currently in popular use.

Box 5.9
Health-based Economic Assessment of Air Pollution in Metropolitan
Shanghai, China
To study the impact of air pollution on human health and its subsequent economic costs in
Metropolitan Shanghai, the attributable number of cases due to air pollution in urban areas of
Shanghai in 2001 was calculated and the corresponding economic costs of the health damage
were estimated based on unit values of the health outcomes (Kan and Chen, 2004). The effect of
air pollution on mortality was assessed by using the VOSL. The literature on VOSL, or on WTP to
avoid a statistical premature death, however, is mainly adopted from the United States data. The
researchers relied on a previous contingent valuation study conducted in Chongqing, China, in
estimating the VOSL of Shanghai residents. In the Chongqing study, an average WTP of US$ 34,750
for saving a statistical life was reported. The marginal effect of income on WTP value was also
reported. With an annual increase in income of $145.80, the marginal increase for saving a statistical
life was $14,550. Therefore, taking the annual income difference between Chongqing and Shanghai
residents into account, a conversion based on Chongqing’s coefficient between marginal WTP and
income was reached, and the VOSL in Shanghai was estimated at $108,500.
For different endpoints of morbidity, since there have been no WTP studies on these endpoints
in China, an alternative approach was used to infer the value from those used by USEPA after
conversion (USEPA, 1999). COI was also calculated for hospital admissions and outpatient visits,
using actual data from Shanghai.
Using the unit values and quantified health effects, the economic costs were computed. The total
economic cost of health impacts due to air pollution in Metropolitan Shanghai in 2001 was estimated
to be approximately 625.40 millions US dollars, which accounted for 1.03 per cent of gross domestic
product (GDP) of the city in that year.

23
5
Section 4 Managing Indoor Air Pollution

U rban AQM has traditionally only addressed

the sources of, and mitigation of exposure
to, outdoor air pollution. However, indoor air
however, have been of limited success (Basnyat
and Shrestha, 2003).

As an integrated part of AQM, along with the

pollution can be a major source of exposure
management of outdoor air quality, indoor air
for many people. This is especially the case in
quality has yet to become a central focus of
developing countries where the poorest people
research, development aid and policy-making
are typically exposed to smoke from open stove
including - as formulated at the Fifteenth Session
cooking or heating in private homes. According
of the United Nations Commission on Sustainable
to the WHO, approximately 2.5 billion people are
Development (CSD) - action to (PA, 2007):
exposed to smoke from solid fuel use (WHO, 2002).
Addressing indoor air quality is often considered • Provide financial support to programmes
as beyond the scope of urban AQM. One of the and other activities that address adverse
reasons for this obvious shortcoming is probably health impacts of indoor air pollution
the fact that the management of indoor air quality including public awareness campaigns in
in private homes is not considered to be the developing countries.
responsibility of the public community.
• Improve the dissemination of information
However, mechanisms are available for and knowledge about the health impacts
governmental authorities to reduce the impact of indoor air pollution, in particular on
from certain indoor air pollution sources, such as women, children and workers.
incentives to install improved stoves or buy cleaner • Accelerate the transition from inefficient
fuels such as kerosene, to introduce biogas, or to utilization of biomass to cleaner energy
tax highly polluting fuels such as high-sulphur sources, technology, and appliances for
coal. As the poorest communities have little ability cooking and heating and support efforts
to switch to more expensive fuels, it is certainly a to disseminate improved biomass-based
political challenge to introduce fuel taxes on cheap technologies.
fuels and subsidise cleaner but more expensive
fuels. However, the introduction of improved
stoves has been very successful in China, where
4.1 Indoor Air Pollution
more than 175 million improved stoves have been
introduced during the period 1982-1999 (UNDP,
H uman beings in urban areas tend to spend
most of their time indoors, where they
can be exposed to poor air quality. Pollution and
2000). In India, a heavily subsidised programme
degradation of indoor air cause illness, increased
(the government met 50 per cent of costs) led to
mortality, loss of productivity and can have major
the installation of 30 million stoves. It ran from
economic and social implications. Indoor air
1984 until 2002, when funding was discontinued.
problems can be reduced by better urban planning,
This generated very mixed results and follow-up
design, operation and maintenance of buildings,
research showed only 10 million stoves remained in
and through the use of less-polluting materials
use (SF, 2003). Up to 2003 95,000 improved cooking
and equipment in buildings. Indoor air quality
stoves (ICS) have been distributed or installed at
problems affect all types of buildings, including
various districts in rural Nepal by the Community
homes, schools, offices, health care facilities and
Forest Development Programme (CFDP) and other
other public and commercial buildings.
organisations. ICS programmes in rural Nepal,

24
Health effects can include increased rates of lung a health promoting way by means of technical and
disease, allergy and asthma, and cancer as well behavioural interventions. WHO has summarized
as fatal conditions such as CO poisoning and technical and social-behavioural interventions in
legionnaires’ disease. The medical and social a publication on indoor air pollution from the use
costs associated with these illnesses, and the of biomass fuels (WHO, 1992; 2000). Both types of
related reduction in human productivity, result in interventions are depicted in Figures 5.8 and 5.9
significant economic losses.
Figure 5.8 provides an overview of the effectiveness
The management of indoor air pollution in of major technical interventions for reducing ill-
developing countries is a very important task for health from the use of household solid fuel.
the building’s occupants if adverse impacts from
Major technical options include:
open stove cooking and heating are to be avoided.
The decisions of the building’s occupants, however, • improved ventilation;
will often be driven by the household economy,
• improved stoves - chimneys;
convenience or habits rather than by minimal
health risk considerations with respect to activities, • improved stoves - combustion; and
facilities, and materials used indoors. Legislative
• fuel upgrade and use of renewable
and economic mechanisms should encourage
energies.
individuals to manage the indoor environment in

TECHNICAL INTERVENTION

Change of Change of Fuel

kitchen layout stoves alternatives

General Hoods Kerosene

house
layout Chimneys Liquid
petroleum
Hood gas
location Alternative
stove Electricity
Chimney designs
location Biogas

Transmission Biofuel
of emissions upgrading

Ventilation Solar
energy

ASSESSMENT OF INTERVENTION

REDUCTION OF HEALTH IMPACTS

Figure 5.8 Technical interventions for Figure 5.9 Social-behavioural

reducing health impacts interventions for reducing
from use of biomass fuel in health impacts from use of
households biomass fuels in households
Source: WHO (2000b) Source: WHO (2000b)

25
5
While technical interventions are, in principle, easily interventions in households relative to using a
accomplished, social-behavioural interventions traditional cookstove without flue gas venting
(see Figure 5.9) are much more difficult to (exposure = 100 per cent). Low-cost improved
implement because they require stakeholder cookstoves (ICs) reduce exposure already by 50 per
involvement and acceptance, compromises in the cent and high-cost ICs reduce it further to less than
community and change of behavioural patterns 30 per cent. Exposure is lowest for use of kerosine
and cultural traditions. Figure 5.10 shows the and liquid petroleum gas (WHO, 2000b).
percentage reduction of exposure due to different

Figure 5.10: Effectiveness of potential exposure interventions and typical values

Source: WHO (2000b)

26
 Section 5 Environmental Impacts of Air Pollution

A ir pollution has an effect on visibility

and has long been a significant source of
damage to non-living materials. Air pollution has
coloured smoke such as from open-hearths and
soot, absorption becomes an important factor in
light reduction. In addition to the factors that affect
contributed to the corrosion of metals, cracking of visual range through changes in the dispersion of
rubber, soiling and eroding of building surfaces, materials, meteorological factors can also affect
deterioration of works of art, and fading of dyed visibility. These include relative humidity, the size
materials. Injury to vegetation has been one of of hygroscopic particles, wind and mixing depth.
the earliest signs of air pollution, for example due Figure 5.11 provides an example of the relationship
to the effects of SO2 emitted from smelters, and between visual range and relative humidity at Los
fluoride gases. Angeles International Airport.

In Figure 5.11 the visual range decreases with

5.1 Effects on Visibility increasing relative humidity. With increasing

T he visual range (or visibility) depends

upon the transmission of light through the
atmosphere and the ability of the eye to distinguish
relative humidity, hygroscopic particles increase
in size and thus become more effective in reducing
visual range.
an object against its background. When the contrast
The sharp decrease in visual range above a relative
between the object and the background approaches
humidity of 67 per cent is mainly due to the
zero, the object cannot be seen, and it is said to be
occurrence of sea salt particles as the airport is
“beyond the limit of visual range”. On clean and
located 2-3 kms from the Pacific Ocean.
clear days, the visual range may be several tens of
kilometres, up to 110 kilometres. On moderately Aerosols are generally classified by their size. The
polluted and hazy days the visual range is reduced classification is divided into three categories:
considerably to less than 20 km, and still visible
• ultra fine particles with diameters less then
objects appear diffused. On very polluted and hazy
0.1 µm;
days, visual range is reduced to a few kilometres,
under extreme conditions even to a few tens of • fine particles with diameters anywhere
metres. Changes in the visual range do occur under from 0.1 to 2.5 µm ; and
the conditions of uniform haze, layered haze and
plumes. • coarse particles with diameters above
2.5 µm.
The alteration of contrast or light intensity is due
to the absorption and scattering of light by the Aerosols are important within the atmosphere
atmosphere. The scattering due to particulate air with respect to cloud formation, precipitation, fog
pollutants in the atmosphere is usually attributed frequency and persistence, radiation, atmospheric
to particles of a size comparable to the wavelength chemistry and atmospheric electricity. Cloud
of the incident light. This is called Mie scattering formation and precipitation are dependent on all
which depends on the particle radius, the three sizes of aerosols.
wavelength of the light, and the refractive index Aitken nuclei (solid and liquid particles of the
of the particulate material (e.g. aerosols of sulphur, order of a few tenths of a micron to a few microns)
water, and oil). are too small to compete with large aerosols
Many air pollutants such as wood smoke reduce for water vapour but they can stick together to
light primarily by scattering. However, for form larger aerosols which play a major role in

27
5

(%)
Figure 5.11: Average visual range versus relative humidity at
Los Angeles International Airport, California
Source: Robinson (1977)

cloud formation. Giant aerosols (particles of a • Abrasion by solid particles of sufficient size
dry radius larger than 1 µm) can also serve as and travelling at high velocities.
cloud condensation nuclei but not as effectively
• Deposition on a surface of solid and liquid
due to their short lifetime from dry fall out. An
particles which may spoil the material´s
aerosol becomes a cloud condensation nucleus
appearance. Frequent removal from a
when water vapour in the atmosphere condenses
surface of solid and liquid particles may
onto it. The condensation of water vapour onto
cause noticeable deterioration.
an aerosol can happen in a number of different
ways. The aerosols’ role in precipitation is much the • Direct chemical attack - direct and
same. The difference is that there must be enough irreversible reaction of air pollutants
water vapour in the cloud for aerosols to become with materials to cause deterioration (e.g.
precipitation size. tarnishing of silver with hydrogen sulphide
Liquid aerosols can absorb gases within the or the etching of a metallic surface by an
atmosphere that can then react to form a solution. acid mist).
These gases can also adhere to the surface of solid • Indirect chemical attack - pollutants are
aerosols and cause other chemical reactions. absorbed by the material and undergo
chemical changes (e.g. SO2 is absorbed by
5.2 Effects on Economic Material marble and converted to sulphuric acid,
and Structures which deteriorates the stone structure).

A ir pollution has been a significant source

of damage to non-living materials. The
mechanisms which result in damage include:
• Electrochemical corrosion occurring in
ferrous metal surfaces in the presence

28
 of water films contaminated with air produces abrasion. Wind direction is important
pollutants. when sources of air pollutants are present near the
exposed material.
There are several important factors that influence
the attack rate of damaging pollutants. These
Corrosion
include moisture, temperature, sunlight and air
For determining background corrosion rates
movement.
and exposure-response relationships for testing
materials, their position in space is an important
Moisture variable. Corrosion test samples are often mounted
Without moisture little, if any, corrosion occurs. at 45o from the horizontal. In such situations the
For several metals, there seems to be a critical under surfaces are often more corroded than the
atmospheric humidity, which when exceeded, upper surfaces because corrosive agents are not
produces a sharp rise in corrosion. Depending on washed off by the rain. Devices for rotating metal
the metal, the critical value lies between 60 and test samples, mounted vertically on a carousel,
90 per cent relative humidity. With increasing have also been developed avoiding this problem.
humidity, the protective oxygen film on the metal
Deterioration of materials manifests itself and is
surface breaks down and corrosion begins. This
observed in many ways. Building and artwork
happens with or without air pollutants. In some
materials such as stone and mortar may be
countries, e.g. England, the controlling factor in
discoloured or leached away by pollutants.
atmospheric corrosion of metals is mainly air
Demonstrations of such deterioration can be made
pollutants. Moisture in the form of rain often
by comparing photographs of buildings before and
reduces corrosion rates, probably as a result of
after cleaning, or by comparing photographs of the
dilution and washing away of corrosive agents.
same artwork taken at different times.

Temperature Corrosion of metals is frequently detected by

The influence of temperature on corrosion of weight change. Changes in the thickness of a
materials is twofold: increased temperatures may sample can also be measured by a micrometre but
increase the rate of the chemical reactions resulting reproducibility of results depends on irregular
in deterioration. Lowered temperatures may changes in thickness, reducing the validity of
increase the probability of damage, because the this technique. In industrial monitoring electrical
surface temperature may fall below the dew point, resistance measurements are used to detect
and the surface becomes moist and, in the presence corrosion. Maintenance frequency is another
of corrosive pollutants, conducive to damage. measure to estimate corrosion losses.

Protective coatings such as paints are affected by

Sunlight pollutants such as SO2, O3, hydrogen sulphide,
Sunlight can cause direct deterioration of rubber tarry and greasy aerosols, and metal salts. Paint
by cracking, or the fading of dyes. In addition, it pigments provide hiding power and durability.
produces O3 in reactions of ambient NOx and HC. Binder and additives hold the pigment to the
Direct sunlight damage on rubber or dyes cannot surface. Both protect the underlying material from
necessarily be distinguished from that caused by corrosion and weathering. Air pollution may limit
O3. both of these functions by damaging the protective
coating and by exposing the underlying surface
Air movement
to attack. Typical examples for such attacks are
Wind speed determines if PM impacts on vertical
discolorations of paints of buildings exposed to
surfaces, deposits on horizontal surfaces, or
hydrogen sulphide. Another example is car soiling

29
5
where cars are observed to be covered with mostly To gain a better understanding of the vegetation
brown spots from iron particles that washing failed effects of air pollutants it is necessary to understand
to remove. the structure of a leaf (see box 5.10).

The cracking of rubber is caused by O 3 and Acute injury from air pollutants results in
ultraviolet (UV) radiation. It can be measured by plasmolysis (shrinking of the cell structure outside
determining the depth of cracks. Both, UV radiation the cell nucleus caused by loss of water) of the
and O3 attack the long HC chains of the rubber and cells and subsequent collapse of the tissue. The
by breaking these bonds, shorten the molecules injury may occur in the spongy parenchyma from
with resulting loss of elasticity and other problems. exposure to peroxyacetyl nitrate, in the palisade
Tyre manufacturers add two primary protective cells from exposure to O3, and in both cell types
substances to the rubber. To protect against UV, from exposure to fluorides or SO2. Tissue collapse
they add carbon black. The carbon black will turn and necrotic patterns may also be associated with
white/grey as it absorbs the UV and dissipates chronic injury.
the energy as heat. Thus rubber parts turn grey as
they age. To protect against O3, tyre manufacturers Chlorosis is the loss or reduction of the green
add a wax based protective substance. The O3 plant pigment, chlorophyll. The loss of chlorophyll
attacks the wax and depletes it. As the tyre rolls, usually results in a pale green or yellow pattern.
additional wax is forced to the surface of the tyre. Chlorosis generally indicates a deficiency of some
This is referred to as “blooming”. This blooming nutrient required by the plant. Tissue severely
refreshes the surface wax. A tyre that has not been injured by air pollutants often has a characteristic
flexed will have the wax depleted by the O3 and colour; bleaching is associated with SO 2 , a
thus begin to degrade and suffer “dry rot”. yellowing with ammonia, and a browning with
fluoride. Chlorosis may appear in association with
necrotic tissue after exposure to SO2 or oxidants.
5.3 Effects on Vegetation

T he effects of air pollutants on vegetation,

crops, and forests include visible symptoms
such as identifiable changes in the colour of the
Reduction in growth caused by air pollutants is
well established. In general, growth reductions
have been related to visual injury symptoms.
leaf. Subtle effects do not result in visible injury Herbicides that are not applied properly may lead
measured in terms of plant growth, reproduction, to growth abnormalities such as twisting and/
yield and effects on populations and communities or elongation of leaves and stems. Physiological
of plants. and biochemical processes are a prerequisite to
measurable visual and growth effects. Stomata
are the principal avenue of pollutant uptake by
Visible injury
plant leaves. Closure of the stomata will effectively
Visible injury is classified as acute or chronic.
protect plants from pollutant injury. The acute
Acute symptoms are associated with short-term
response of plants to air pollutants results from
exposures to higher concentrations of air pollutants
a massive dose that causes disruption of the
and usually appear within 24 hours after exposure.
cell membranes and a loss of the differential
Chronic symptoms are associated with long-term
permeability of the membrane. Cellular water
or intermittent exposures to low concentrations
and solutes may be lost and the cell plasmolyzed,
of an air pollutant. However, repeated short-
or water may enter and cause cell rupture. Either
term exposure will cause physiological changes
disruption or rupture may cause cell death.
indicative of chronic symptoms.
Recovery may take place if exposure is minimal
and environmental conditions are non-severe.

30
The extent of recovery depends upon the severity Air pollution effects on plant populations and
of external stresses and the ability of the cells to communities may consist of:
initiate repair mechanisms.
• changes of plant populations by eliminating
Major air pollutants such as O3, oxidants and more sensitive plants; and
fluorides can affect plant reproductive structures • replacement of sensitive plants by resistant
and pollen germination and thus initiate genetic plants.
abnormalities and affect yield. Conditions under
which seeds are formed may influence the Only a few studies have been performed relating
susceptibility of the next generation to various to the effects of air pollutants on either plant
stresses. Certain air pollutants may thus affect populations or communities.
reproduction. Figure 5.12 shows various uptake Factors affecting the response of vegetation to air
and deposition processes leading to the effect of pollutants include:
O3 on crops.

Box 5.10
The Structure of a Leaf
The leaf consists of a network of denser structures, the veins, all interconnecting back to the base or stem of the leaf.
Specialized cells within these veins serve as transport systems of the leaf.
In the areas between the veins, there are normally three specialized layers: epidermis, palisade, and spongy parenchyma
cells.The epidermis is a single layer of thick-walled cells on the upper and lower surfaces of the leaf. Under the epidermis
of the upper surface of the leaf one or more rows of rather uniform, elongated cells stand on end and are closely packed
together (palisade layer). Between the lower edge of the palisade layer and the epidermis of the lower leaf surface, a
loosely packed area of cells exists that are somewhat irregularly shaped (spongy parenchyma). The epidermis is covered
with a layer of waxy material. In the epidermis, specialized guard cells (stomata) exist edging an opening. They are able
to change shape, thus regulating the opening or closing of the stomata. The stomata regulate the mechanism for gas
exchange between the plant tissues and the air (BBC, 2007).

31
5
• genetic variability with respect to
morphological, physiological, and
biochemical characteristics, and plant
sensitivity;

• climatic factors before, during, and after

exposure such as light duration, light
intensity, light quality, temperature, relative
humidity, and CO2 concentrations within
the leaf;

• edaphic (i.e. pertaining or indigenous to soil)

factors such as soil, water, and fertility.

A full understanding of air pollution effects on

vegetation is difficult to gain because of the many
factors that determine plant response.

Table 5.1 lists the major impacts which damage crops

and forests and lead to a reduction in crop yield Figure 5.12 Uptake and deposition of ozone
and quality, carbon reserves, and forest decline, on plants
increased water stress, and reduction of nutrient Source: Emberson et al. (2003)

availability. Reduced crop yields may cause local

food shortages and famine and altered food quality
which may be detrimental to human health.

Table 5.1 A summary of major impacts (scale and sources) for key pollutants

Pollutant Major sources Major impacts Scale of effects

Sulphur dioxide Power generation; commercial Visible foliar injury; altered plant growth; Local
(SO2) and domestic heating elimination of lichens and bryophytes; forest
decline
Nitrogen oxides Power generation; transport Altered plant growth; enhanced sensitivity Local
(NOx) to secondary stresses; eutrophication
Ozone (O3) Secondary pollutant formed Visible foliar injury; reduced growth; forest Regional
from NOx and hydrocarbons decline
Suspended Transport; power generation; Altered plant growth; enhanced sensitivity Local
particulate industry; domestic heating to secondary stresses
matter (SPM)
Fluorides Aluminium manufacturing and Reduced plant growth; fluorosis in grazing Local
smelting animals

Source: Emberson et al. (2003).

32
 Summary

I n this module you have learnt about how

exposure to air pollution is assessed and the
impact of key air pollutants on human health and
The key messages you should take away from this
module on impacts are:

► Only careful estimates of exposure can

environment. You have also learnt about the:
lead to meaningful assessments of health
• importance of a sound estimation of impacts.
exposure to air pollutants and GHGs
► The local and national burden of disease
• health impacts of the key air pollutants due to air pollution should be estimated,
including the consideration of vulnerable
• indirect health impacts of GHGs
sub-populations such as women and
• burden of disease approach children, the poor, the elderly and the
diseased.
• economic assessment of air pollution and
health and cost benefit/effectiveness ► Use of rapid methods for health impact
analysis assessment may lead to useful estimations
of health impacts.
• environmental impacts of air pollution.
► Uncertainties of rapid assessment methods
You have also learnt about the design of
should be carefully considered.
epidemiological health studies and their use in
rapid health impact assessment including: ► Economic valuation of impacts is necessary
for cost-benefit analysis in air quality
• Cross-sectional studies
management.
• Ecological studies

• Cohort studies
Module 6 Governance and Policies is the final module
• Case-control studies in this series. In this module you will examine the
issues which need to be addressed in an overall
• Time-series studies.
policy framework to achieve better air quality.
In addition, this module has examined the economic The module will consider air quality guidelines
assessment of air pollution and health and the and standards, clean air implementation plans,
variety of methods available (e.g. willingness-to- roles of stakeholders and policy instruments
pay, contingent valuation and the human capital in reducing air pollution. The module will also
approach). Providing information to policy-makers examine the institutional arrangements for air
on the human and economic cost of air pollution quality governance.
is important in order to facilitate the adoption of
appropriate policies to combat the problem.

33
 5
Information Sources

Ashenfelter, O. (2006) Measuring the value of a statistical life: Problems and prospects. NBER Working Paper
Series No 11916. National Bureau of Economic Research Inc., Cambridge, MA
Basnyat, M.B., Shrestha, S.K. (2003) Government Policy and Strategies of Improved Cook Stove for Dissemination
in Nepal. Alternate Energy Promotion Centre, Kathmandu. http://www.arecop.org/zip/
Govt_pol.pdf
BBC (2007) Leaf structure. http://www.bbc.co.uk/scotland/education/bitesize/standard/biology/world_of_
plants/making_food_rev3.shtml
Becker, G.S. (1993) Human Capital: A Theoretical and Empirical Analysis, with Special Reference to Education.
3rd edition, Chicago, University of Chicago Press.
Bøhler T., Laupsa H., McInnes H. (2003) Trend analysis of air pollution exposure in Oslo 1995, 1998 and 2001.
Norwegian Institute for Air Research, Kjeller, Norway. http://www.nilu.no/data/inc/leverfil.
cfm?id=6387&type=6
Dockery, D., Pope, A. and Xu, X. (1993) An association between air pollution and mortality in six US cities.
New England Journal of Medicine, 329: 1753-1759
Drummond, M.F., O’Brien, B.J., Stoddart, G.L., Torrence, G.W. (1997) Methods for the economic evaluation of
health care programmes. 2nd ed., Oxford University Press, New York
EPI, (2003) Record heat wave in Europe takes 35,000 lives - far greater losses may lie ahead. Earth Policy institute,
Washington D.C. Website: http://www.earth-policy.org/Updates/Update29.htm
EPI, (2006) Setting the record straight: More than 52,000 Europeans died from heat in Summer 2003. Earth Policy
institute, Washington D.C. Website: http://www.earth-policy.org/Updates/2006/Update56.
htm
Fabre, M, Cabot, C., Ducasse, J.L., Virenque, C., Cathala, B. (1999) Carbon monoxide poisoning in the
Midi-Pyrenees. Indoor Built Environment 8: 176-178.
Golan, E.H. and Shechter, M. (1993) Contingent valuation of supplemental health care in Israel. Medical
Decision Making 13:302-310.
Hedley, A.J., Wong, C.M., Thach, T.Q., Ma, S., Lam, T.H. and Anderson, H.R. (2002) Cardiorespiratory and
all-cause mortality after restrictions on sulphur content of fuel in Hong Kong: an intervention
study. Lancet, 360: 1646-1652
HEI (2004) Health effects of outdoor air pollution in developing countries of Asia: a literature review, Health Effects
Institute, Special Report 15, Boston
IPCC (2007) Intergovernmental Panel on Climate Change Fourth Assessment Report, Synthesis Report,
Summary for Policymakers, IPCC, Geneva. www.ipcc.ch/pdf/assessment-report/ar4/syr/
ar4_syr_spm’.pdf
Johannesson, M. (1996) A note on the relationship between ex ante and expected willingness to pay for
health care. Social Science and Medicine 42: 305-311

34
Kan, H. and Chen, B. (2004) Particulate air pollution in urban areas of Shanghai, China: health-based
economic assessment. Science of the Total Environment, 2004; 322(1-3):71-9
Katsouyanni, K., Touloumi, G., Samoli, E., Gryparis, A., Le Tertre, A., Monopolis, Y., Rossi, G., Zmirou,
D., Ballester, F., Boumghar ,A., Anderson, H.R., Wojtyniak, B., Paldy, A., Braunstein, R.,
Pekkanen ,J., Schindler, C. and Schwarta, J. (2001) Confounding and effect modification in
the short-term effects of ambient particles on total mortality: results from 29 European cities
within the APHEA2 project. Epidemiology, 12: 521-531
Klose, T. (1999) The contingent valuation method in health care. Health Policy 47: 97-123
Mansfield, E. (1997) Preference regarding risk. In: Microeconomics. Theory and Applications, 9th ed. W.W.
Norton and Company,Inc. New York.1997
Nas, T.F. (1996) Cost-Benefit Analysis: Theory and Application. Thousand Oaks, CA: Sage Publications Inc
NHGRI, 2007 Talking glossary – animal model. National Human Genome Research Institute,National Institues
of Health, Bethesda, MD. Website: http://www.genome.gov/glossary.cfm?key=animal%20
modelStern (1977a)
OECD (2000) OECD’s guidelines for the testing of chemicals, http://www.oecd.org/ehs/test/health.htm
PA (2007) UN stalls action on the killer in the kitchen. Practical Action, Rugby. Website:
Pope, C.A. III, Burnett, R.T., Thun, M.J., Calle, E.E., Krewski, D., Ito, K., Thurston, G.D. (2002) Lung cancer,
cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal
of the American Medical Association, 287: 1132-1141
Rabl, A. (1998) Mortality risks of air pollution: the role of exposure–response functions, Journal of Hazardous
Materials 61, 91-98
Rabl, A. (2003) Analysis of air pollution mortality in terms of life expectancy changes: relation between time series,
intervention, and cohort studies. Environmental Health: A Global Access Science Source 2006,
5:1. Website: http://www.ehjournal.net/content/5/1/1
Robinson, E. (1977) Effects on physical Properties of the Atmosphere. In: Stern A.C. Air Pollution. Third
edition. Volume II, The Effects of Air Pollution. Academic Press, New York
SF (2003) Who works on indoor air pollution? Shell Foundation, London. http://www.shellfoundation.org/
index.php?newsID=370
Shepherd, G. and Klein-Schwartz, W. (1998) Accidental and suicidal adolescent poisonings in the United
States. Archives of Pediatrics and Adolescent Medicine 152: 1181-1185. http://archpedi.ama-assn.
org/cgi/content/full/152/12/1181?ck=nck
Stieb, D.M., Judek, S. and Burnett, R.T. (2002) Meta-analysis of time-series studies of air pollution and
mortality: effects of gases and particles and the influence of cause of death, age, and season.
Journal of the Air & Waste Management Association, 52: 470-484
Tarricone, R, (2005) Cost-of-illness analysis: What room in health economics? Health Policy 77, 51-63
Touloumi, G., Katsouyanni, K., Zmirou, D., Schwartz, J., Spix, C., De Leon, A.P., Tobias, A., Quennel, P.,
Rabczenko, D., Bacharova, L., Bisanti, L., Vonk, J.M. and Ponka, A. (1997) Short-term effects of
ambient oxidant exposure on mortality: a combined analysis within the APHEA project. Air
Pollution and Health: a European Approach. American Journal of Epidemiology, 146: 177-185

35
5
UNDP (2000) World Energy Assessment: Energy and the Challenge of Sustainability, Chapter 10, Rural energy
in developing Countries, pp. 367-389. United Nations Development Programme, New York,
NY.
http://www.energyandenvironment.undp.org/undp/indexAction.cfm?module=Library&ac
tion=GetFile&DocumentAttachmentID=1020,
http://www.undp.org/energy/activities/wea/pdfs/chapter10.pdf
USEPA (1999) The Benefits and Costs of the Clean Air Act: 1990 to 2010. Office of Air and Radiation, United
States Environmental Protection Agency, Washington, DC
USEPA (2006) Air Quality Criteria for Particulate Matter (October 2004) National Center for Environmental
Assessment, United States Environmental Protection Agency, Research Triangle Park, NC.
http://cfpub2.epa.gov/ncea/cfm/recordisplay.cfm?deid=87903
Van Houtven, G., Honeycutt, A., Gilman B., McCall, N., Throneburg, W. (2005) Cost of illness for
environmentally related health effects in older Americans. Final report. RTI International Health,
Social, and Economic Research, Research Triangle Institute International, Research Triangle
Park, NC. http://www.epa.gov/aging/resources/coi/2005_04_coi_older_am_dr_01title.pdf
WHO (1992) Indoor air pollution from biomass fuel. WHO/PEP/92-3A. World Health Organization, Geneva
WHO (1994) Environmental Health Criteria 170: Assessing human health risks of chemicals: derivation of guidance
values for health-based exposure limits, World Health Organization, Geneva
WHO (1995) Inorganic Lead. Environmental Health Criteria 165. International Programme on Chemical Safety,
World Health Organization, Geneva.
WHO (1997) Environmental Health Criteria 188: Nitrogen oxides (2nd edition), World Health Organization,
Geneva
WHO (1999) Environmental Health Criteria 210: Principles for the assessment of risks to human health from
exposure to chemicals, World Health Organization, Geneva
WHO (2000a) Human exposure assessment. Environmental Health Criteria 214. International Programme on
Chemical Safety, World Health Organization, Geneva
WHO (2000b) Guidelines for Air Quality, WHO/SDE/OEH/00.02, World Health Organization, Geneva.
http://whqlibdoc.who.int/hq/2000/WHO_SDE_OEH_00.02_pp1-104.pdf, http://whqlibdoc.
who.int/hq/2000/WHO_SDE_OEH_00.02_pp105-190.pdf
WHO (2000c) Air quality guidelines for Europe, 2nd edition, WHO Regional Publications, European Series,
No. 91, World Health Organization, Regional Office for Europe, Copenhagen
WHO (2002) Reducing risks, promoting healthy life. The World Health Report 2002, World Health Organization,
Geneva. http://www.who.int/whr/2002/en/index.html
WHO (2003) Climate change and human health – Risks and Responses. World Health Organization, Geneva
WHO (2005) ‘WHO Air Quality Guidelines Global Update 2005’Particulate matter, ozone, nitrogen dioxide and
sulphur dioxide. Regional Office for Europe, World Health Organization, Copenhagen. http://
www.euro.who.int/Document/E90038.pdf
WHO (2006) Environmental burden of disease: Country profiles. World Health Organization, Geneva. http://
www.who.int/quantifying_ehimpacts/countryprofiles/en/index.html

36
The Foundation Course on Air Quality Management in Asia is for adult learners studying the issue
without the support of a class room teacher. It is aimed at students with some basic knowledge of
environment and air pollution issues, acquired in a variety of ways ranging from conventional study,
working in an environment related field or informal experience of air pollution issues. It provides
the opportunity to develop an understanding of the key components required to manage urban air
pollution and to achieve better air quality.

The course consists of six modules which address the key components of air quality management.
An international team of air pollution experts have contributed to the development of the course.
Each module is divided into a number of sections devoted to a different aspect of the issue together
with examples and key references.

www.sei.se/cleanair