Overview of air pollution A/Prof Bin Jalaludin MBBS, MPH, PhD, MRCP (UK), FAFPHM South Western...
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Transcript of Overview of air pollution A/Prof Bin Jalaludin MBBS, MPH, PhD, MRCP (UK), FAFPHM South Western...
Overview of air pollution
A/Prof Bin JalaludinMBBS, MPH, PhD, MRCP (UK), FAFPHM
South Western Sydney Area Health Service, and
University of New South Wales
This talk
• Will give an overview of air pollution
• Will mainly focus on the common outdoor air pollutants
• Will discuss types of air pollutants
• Will discuss sources of air pollutants
• Will discuss health effects of air pollution
Air pollution – the problem
• Global– Ozone layer depletion– Greenhouse effect
• Regional– Acid rain– Haze and photochemical smog
• Local• Indoor (homes, factories, offices)
Air pollution – the problem
U p p er a tm o sph e reo zon e d ep le tion
C lim a te ch an ge d ue tog ree n ho use e ffe ct
G lo b a l
A c id R a in P h o to che m ica l sm ogH a ze
R e g io n a l
C O , S O 2 , P b , P M A ir T o x ics
L o ca l
P M , N O 2 , E TSA ir T o x icsB io lo g ica l
In do or
Effects of human activities on the atmosphere (NSW SOE 2000)
Ozone Layer Depletion
• Stratospheric ozone reduces harmful UV radiation
• Chloroflurocarbons (CFCs), methyl chloroform, carbon tetrachloride, halons, methyl bromide
• Montreal Protocol on Substances that Deplete the Ozone Layer
The vertical distribution of ozone in the atmosphere at mid-latitudes (Commonwealth SOE 2001)
Source: after WMO (1999)
Postulated steps from the release of halocarbons to increase in UV related biological damage
Halocarbons release chlorine and bromine ‘radicals’
Increase in ultraviolet-related biological damage
Stratospheric ozone layer depleted
Chlorine and bromine ‘radicals’ destroy ozone molecules
Increase in ultraviolet irradiance at ground level
1
2
3
4
Source: McMichael 1993
Average stratospheric ozone concentrations for the month of October (NSW SOE 2000)
Source: Bureau of Meteorology data, as at 1999
Concentrations of ozone-depleting substances, Cape Grim, Tasmania (NSW SOE 2000)
Source: CSIRO data, as at 1999
Past and future stratospheric chlorine levels (ppb, cumulative) of the major ozone-depleting substances (Commonwealth SOE 2001)
Source: Madronich and Velders (1999).
Greenhouse Gases
• Naturally occurring gases - CO, methane
• Anthropogenic gases – CO2, nitrous oxide, chlorofluorocarbons (CFCs)
Source: CSIRO Atmospheric Research.
Annual Australian mean minimum temperature anomalies. (Commonwealth SOE 2001)
Source: Bureau of Meteorology
Global warming potentials of greenhouse gases Potentials are expressed as a multiple of the global warming potential of carbon
dioxide. (Commonwealth SOE 2001)
Gas Global warming potential over 100 years
Carbon dioxide 1
Methane 24
Nitrous oxide 360
Chlorofluorocarbon-11 4 600
Chlorofluorocarbon-12 10 600
Hydrofluorocarbons 10-14 800
Sulfur hexafluoride 22 200
Other perfluorocarbons 5 700-11 400
Source: Granier and Shine (1999).
Carbon dioxide concentrations, Cape Grim, Tasmania (NSW SOE 2000)
Source: CSIRO data, as at 2000
Methane concentrations, Cape Grim, Tasmania (NSW SOE 2000)
Source: CSIRO data, as at 2000
Nitrous oxide concentrations, Cape Grim, Tasmania (NSW SOE 2000)
Source: CSIRO data, as at 2000
Acid Rain
• Emissions of oxides of sulphur and nitrogen produce Acid Aerosols - H2SO4, HNO3 (also regional pollutant)
• Coal fired (and oil fired) power plants
• Trans-boundary issue (especially in Europe and North America)
Annual emissions of sulfur dioxide (as millions of tonnes of sulfur, MtS) and the atmospheric sulfur dioxide cycle. (Commonwealth SOE 2001)
Health Effects of Global Environmental Changes
Possible adverse effects upon human health caused by global environmental changes
Environmental change
Manifestation Type (direct, indirect) and timinga (early, late) of adverse health effect
Direct, early Direct, late Indirect, early Indirect, late
Enhanced greenhouse effect
Global warming and other climate change
Heatwave-related illness and death
Extension of vector-borne infections
Altered viability of (edible) fish in warmed oceans
Natural disasters: cyclones, floods, landslides, fires
Food shortages due to impaired agriculture
Sea-level rise Increased risk of flash floods and surges
Inundation social disorder, impaired sanitation, farmland loss
Consequences of damage to foreshore facilities, roads, etc.
Destruction of wetlands decline in fish stocks
Stratospheric ozone depletion
Increased UV-B flux at Earth’s surface
Sunburn, conjunctivitis Suppression of immune system increased risk of infection
Skin cancerOcular effects: cataracts, pterygium
Impaired growth of food crops and of marine microorganisms (base of aquatic food web)
Acid aerosols (from burning of sulphurous fossil fuels)
Acid rain Effects on respiratory system (?)
Aquatic damage (reduced fish) Impaired growth of crops
Impaired forest growth reduced ecosystem productivity
A The designations ‘early’ and ‘late’ are notional, and indicate relative timing. (Based on McMichael, 1993.3)
Possible adverse effects upon human health caused by global environmental changes (cont.)
Environmental change
Manifestation Type (direct, indirect) and timinga (early, late) of adverse health effect
Direct, early Direct, late Indirect, early Indirect, late
Land degradation: intensive agriculture, overgrazing
Erosion, sterility, nutrient loss, salinity, desertification
Decline in agricultural productivity
Rural sector depression migration to fringes of cities (see bottom row)
Exposure to pesticides and fertilisers (may also cause algal blooms)
Consequences of silting up of dams and rivers
Depletion of underground aquifers
Lack of water for drinking and hygiene
Decline in agricultural productivity
Loss of biodiversity
Destruction of habitat
Deforestation disruption of local culture
Loss of potentially edible species
Deforestation greenhouse enhancement
Loss of genetic diversity; weakening of ecosystems
Loss of medicinals, and other health-supporting materials
Greater vulnerability of crops and livestock. Reduced vitality of ecosystems
Other effects of overpopulation (particularly in poor countries)
Proliferation of crowded urban slums (due to migration and high fertility)
Infections Malnutrition Homelessness Antisocial behaviours
Social disorder Chronic toxic effects of environmental pollutants
Consequences of overload of local ecosystems
A The designations ‘early’ and ‘late’ are notional, and indicate relative timing. (Based on McMichael, 1993.3)
Regional/Local Air Pollutants
• Criteria (Common) Air Pollutants - (ambient air quality standards established)– Regional
• Photochemical smog - Ozone (O3)
• Haze - Particulates (PM) & Nitrogen Dioxide (NO2)
– Local• Sulphur Dioxide (SO2)
• Carbon Monoxide (CO)
• Lead (Pb)
• Air Toxics - (often no standards)
Air toxics or Hazardous Air Pollutants (HAPS) – a definition
“gaseous, aerosol or particulate pollutants (other than the six criteria pollutants)
that are present in the air in low concentrations with characteristics such as toxicity or persistence so as to be a hazard to human, plant or animal life”
Air Toxics / HAPS
• Diverse range of toxic compounds– Volatile Organic Compounds (VOCs)
• formaldehyde: lung, eye, skin irritants
• benzene, 1,3-butadiene: carcinogens
– Persistent organic pollutants (POPs)• DDT, PCB, dioxins: toxic, persistent, bioaccumulate
– Polycyclic Aromatic Hydrocarbons (PAHs)• Benzo[a]pyrene: Incomplete combustion of organic matter –
lung cancer, immune system suppression, respiratory problems
– Toxic Metals (associated with PM or as gases) • Arsenic, cadmium, lead, mercury, nickel, chromium:
persistent, bioaccumulate, toxic - kidney/liver damage, CNS disorders
Air Toxics / HAPs
• Diverse range of point and diffuse sources– point sources: industries and other facilities emitting in
a localised area– diffuse sources: mobile sources (eg: road vehicles,
boats), area based sources (eg: wood burning, dry cleaning, paints, thinners)
• Indoor / in vehicle exposures• Increasing regulatory / public concern• Generally little or no exposure data • US EPA - list of 189 HAPs (1990)
List of priority hazardous air pollutants (Commonwealth SOE 2001)
Air pollutantScore
Health effects
Benzene 9 Carcinogenic, causes anaemia
1,3-Butadiene 8 Carcinogen
Polycyclic aromatic hydrocarbons (PAH)
8 Carcinogen, environmentally persistent
Arsenic and compounds 8 Carcinogen, environmentally persistent
Chromium and compounds 8Carcinogen, affects respiratory system, inhalation can damage nose, throat, lungs, stomach and intestines, environmentally persistent. May lead to asthma, other allergic reactions, stomach upsets, ulcers, convulsions and kidney damage
Nickel and compounds 8 Carcinogen, can affect the respiratory system, environmentally persistent
Cadmium and compoundsA 7Carcinogen linked to prostate and kidney cancer in humans and also to lung and testicular cancer in animals. Smoke from burning cadmium or cadmium oxide can, in severe cases, affect respiratory system, environmentally persistent
Dioxins and furans 7 Carcinogen, skin disease, environmentally persistent and bioaccumulates
Mercury 7 Can cause reproductive problems, environmentally persistent, bioaccumulates
Dichloromethane 5Probable carcinogen, moderately persistent in the environment. High concentrations may cause unconsciousness and death. Exposure may irritate lungs, cause pulmonary oedema and irregular heartbeat. Long-term exposures at high level may damage the liver and brain
Formaldehyde 5 Carcinogen, irritates the skin, eye and respiratory system, and can exacerbate asthma
Styrene 5 Possible carcinogen
1,4-Dichlorobenzene 3 Probable carcinogen, moderately persistent in the environment
Tetrachloroethylene 3 Probable carcinogen
Manganese compounds 3 Can affect brain function, moderately persistent in the environment
A higher score indicates a more serious concern. Source: EPAV (1999c).
NEPMS (standards) to be developed for 5 air toxics in Australia
• benzene
• formaldehyde
• polycyclic aromatic hydrocarbons
• toluene
• xylenes
Criteria for selection for inclusion:
• Excluded air toxics from point sources
• Adequate ambient monitoring data exists
• Significant risk to human health
• Has highest mass emissions to the environment
Review of air toxics and health studies in Australia
• WA Department of Environmental Protection:– Found 10 studies– 9 studies addressed air toxics and health– 1 study measured personal exposure– 1 study in the ambient setting, 9 in
occupational/indoor settings– Formaldehyde was the most researched air
toxic
Source: State of knowledge report: Air toxics and indoor air quality in Australia. (EA, 2001)
Indoor air pollution
• Indoor air can be defined as any non-industrial indoor space where a person spends a period of an hour or more in any day.
• This can include the air space in the office, classroom, motor vehicle, shopping centre, hospital and home.
Indoor air pollution
• The quality of indoor air is influenced by two major factors: – amount and quality of outdoor air getting in
(ventilation rates, deposition and chemical decay)
– indoor sources of emissions of air pollutants
Indoor air pollution
• In winter 80 - 90% of time indoors - mostly in own home
• A number of important indoor air pollutants– Particles – Environmental tobacco smoke (ETS)– Oxides of nitrogen– Formaldehyde– Biological pollutants – house dust mites,
moulds, etc
Pollutant ci/caA B
NO2 0.7 0.72
O3 0.4 0.44
SO2 0.3 0.34
CO 1 1
Particles 1 1
Lead 0.5 0.53A Indoor (c i) and outdoor (c a) concentrations of air pollutants. B Ratio of indoor exposure to outdoor exposure.
Source: Beer and Walsh (1997).
Relationships between indoor and outdoor concentration of air pollutants (Commonwealth SOE 2001)
Particles in homes - no major sources
0
5
10
15
20
25
30
35
40
CentralCoast
CentralSydney
Lithgow Armidale Lismore NorthSydney
South EastSydney
South WestSydney
Tumut WesternSydney
0
0.05
0.1
0.15
0.2
0.25
0.3
0.35
0.4
0.45
indoor PM10
TEOM
Nephelometry
Source: V Sheppeard, NSW Health
Fine particle (PM10) levels by number of smokers in house
0
50
100
150
zero one two three
Source: V Sheppeard, NSW Health
Fine particle (PM10) levels by main heating type
010203040
Source: V Sheppeard, NSW Health
Average levels of total suspended particles in selected Sydney clubs & hotels (NSW SOE 2001)
Source: Cummins et al. 1990
Average weekly nitrogen dioxide levels in homes
0
5
10
15
20
25
30
35
None UnfluedHeating
Cooking Flued Heating Any Both Heatingand Cooking
Mean
nit
rog
en
dio
xid
e (
pp
b)
Living Room Bedroom
Source: V Sheppeard, NSW Health
Peak 1-hour average concentrations of nitrogen dioxide, indoors & outdoors, 1987-97
(NSW SOE 2000)
Source: Ferrari 1997
In car carbon monoxide levels
0204060
meanmax
Source: CARB 1998; V Sheppeard, NSW Health
Other in-car exposures (VIC EPA - mean personal concentrations while commuting to CBD (east route) - pilot trial)
0
2
4
6
8
10
12
14
benzene 1,3 butadiene xylenes
VO
C p
pb
cartrain
Source: V Sheppeard, NSW Health
Air toxics in other microenvironments
02468
10121416
benzenexylenes
Source: WA DEP; V Sheppeard, NSW Health
Burden of disease attributable to indoor smoke from solid fuels
(% DALYs in each subregion)(The World Health Report 2002)
Ambient air pollution
Kuching, Sarawak 1997 Forest Fires
A historical perspective of air pollution
• In 1273, England’s King Edward I passed a law prohibiting the use of at least one type of coal
• In the early 1400's, Henry V formed a commission to oversee the use of coal in the city of London
• In 1661, Charles II ordered the scientist John Evelyn to survey the effects of the increasing air pollution over the city. Evelyn recognised the relationship between the ‘dismal cloud’ over London and a number of fatal diseases but his warnings of the need for control were ignored
A historical perspective of air pollution (cont)
• By the late 1800's industrialisation accompanied by the migration of people into cities increased the quantity and diversity of chemical pollutants entering the air
• In December 1873 weather conditions producing stagnant air and a temperature inversion thick cloud of pollutants covering London for several days about 1,150 deaths, making it one of the earliest air pollution disasters
A historical perspective of air pollution (cont)
• Since 1873 at least 40 episodes of sudden buildups of air pollution have caused widespread casualties in the industrialised world
A historical perspective of air pollution (cont)
• Several air pollution episodes occurred in London, England from December 1952 to 1962, with the most famous air pollution episode in December 1952 being responsible for an estimated 4,000 deaths.
London smog and deaths (1)
London smog and deaths (2)
Early Control Measures
• Government regulation– UK Clean Air Act (1956)
– US Clean Air Act (1963, 1970 amendement)• Standards for 6 air pollutants (called criteria pollutants)
• Reviewed every 5 years
• Cost-benefit analysis
– Victorian Clean Air Act (1958), NSW Clean Air Act (1961)
• Standards to establish “safe” thresholds• Control strategies to reduce/prevent exceedences
Air Quality Standards
• USA – 1970 amendment to the 1963 Clean Air Act
– National Ambient Air Quality Standards (NAAQS)
• UK– Expert Panel on Air Quality Standards established in
1991
• Australia– National standards in 1998
Pollutant Averaging period
Maximum concentration (based on arithmetic
means)
Maximum allowable exceedencesA (days
per year)
Carbon monoxide 8h 9.0 ppm 1
Nitrogen dioxide 1h
1y
0.12 ppm
0.03 ppm
10
Photochemical oxidant (as ozone)
1h
4h
0.10 ppm
0.08 ppm
11
Sulfur dioxide 1h
1d
1y
0.20 ppm
0.08 ppm
0.02 ppm
110
Lead (as TSPs) 1y 0.5 g/m3 0
Particles (as PM10) 1d 50 g/m3 5
A Goal to be achieved by 2008.
Source: NEPC (1998).
Schedule 2 of the NEPM giving National Environment Protection Standards for
ambient air quality (Commonwealth SOE 2001)
Primary / secondary pollutants
• Primary pollutants– Particles– NOx
– SO2
– CO
• Secondary pollutant– Ozone– Particles (gaseous pollutants forming aerosols)
Types of air pollution
• Summer episodes (photochemical episodes)– Secondary pollutants – O3, H2SO4, HNO3
– Ozone is the index pollutant– “White haze”
• Winter episodes– Particles, SO2
– “Brown haze”
Air pollution concentration
• Complex interactions of many influences:– quantities of pollutants emitted, the spatial and
temporal distributions of these emissions– rates of pollutant transport, dispersion and
diffusion in the atmosphere– meteorological conditions such as temperature
and sunlight intensity– atmospheric chemical reactions– topography of the region
DISPERSION
Vertical and horizontal – stability, turbulence, wind
TRANSFORMATION
Chemical reactions
REMOVAL
Settling, scavenging adsorption, impaction
EMISSIONS
Rate, type, source configuration
RECEPTOR RESPONSE
Health effects, vegetation damage, soiling, corrosion
The role of the atmosphere in the air pollution source sink relationship
STATE OF ATMOSPHERESOURCE SINK
Sources of air pollution
• Mobile sources– Motor vehicles, rail, shipping, aviation
• Industry sources– Power stations, petroleum refining, chemical
manufacturing
• Area based sources – small point sources– Service stations, combustion sources, lawn
mowing
Sources of 1995 to 1996 emissions for Port Phillip Region, Vic.
(Commonwealth SOE 2001)
Source: Commonwealth SOE 2001
Sources of emissions and exposure to benzene in the USA. (Commonwealth SOE 2001)
Source: Data from Ott and Roberts (1998).
Anthropogenic emission sources – Sydney and Greater MAQS region
Pollutant emissions & VKT of vehicle fleet, Sydney
Source: Carnovale et al. 1997
Contribution of wood burning to TSP, Sydney (NSW SOE 2000)
Why is air pollution an issue?
• Affects large numbers of people
• Involuntary exposure
• The health costs are enormous
• Also affects the health of flora and fauna
• Other health benefits from air pollution control – road trauma, physical activity
Burden of disease attributable to urban air pollution(% DALYs in each subregion)
(The World Health Report 2002)
Total Annual Economic Costs of Motor Traffic Air Pollution (AUD$m) (Bureau of Transport and Regional Economics 2003)
Capital Cities Mortality Morbidity Base case Lower Upper Base case Lower Upper Sydney 713 441 990 785 782 788 Melbourne 448 276 621 466 465 468 Brisbane 197 122 273 223 222 223 Adelaide 113 70 156 109 109 110 Perth 104 64 144 110 110 111 Hobart 8 5 11 7 7 7 Darwin 5 3 7 10 10 10 Canberra 8 5 12 0 0 0 All capital cities 1596 986 2214 1712 1705 1718
Adverse health effects estimated to be avoided by meeting the US EPA’s 80 ppb 8-h average daily maximum standard in
New York City, NY. (Thurston 1997)
2,000,000Acute Respiratory Symptom Days/yr
(i.e., person-days during which respiratory symptoms such as chest discomfort, coughing, wheezing, doctor diagnosed flu, etc. are experienced)
930,000Restricted Activity Days/yr
(i.e., person-days on which activities are restricted due to illness
180,000Asthma Attacks/yr
(i.e., person-days during which notably increased asthma symptoms, e.g., requiring extra
medication, are experienced)
3,500RespiratoryED Visits/yr
265 240
75Non-asthma Respiratory
Hospital Admissions/yr
Deaths/yr
Asthma Hospital Admissions/yr
(0.01% of all adverse impact cases)
Environmental & human health effects of major air pollutants (NSW SOE 2000)
Pollutant Effects – environmental Effects – human health
Ozone Damage to vegetation, reduced plant growth and crop yields, increased susceptibility to pestsLong-term low-level exposure is of concern; limited studies have been done on effects on Australian native vegetationDamage to fabrics, rubber and construction materials
Irritation of eyes and air passages, decreased function, lung inflammation (potent oxidant), sensitivity of asthma patients to asthma triggers, possible increased susceptibility to infection
NO3 Effects on vegetation, damage to leaf surface, reduced plant growthLimited research has been done on Australian native vegetation
Decreased lung function, lung inflammation, increased sensitivity of asthma patients to asthma triggers, increased susceptibility to respiratory infection
CO - Reduces the capacity of blood to carry oxygen; can lead to decreased exercise capacity and aggravation of cardiovascular disease
Source: NHMRC 1996; EPA 1997a
Environmental & human health effects of major air pollutants (cont.)
Pollutant Effects – environmental Effects – human health
SO2 Plant damage and growth inhibition; little known about effects on Australian native vegetationAcid deposition: acidification of soils and lakes change the availability of minerals to plantsCorrosion of construction materials
Decreased lung function; lung inflammation: may provoke wheezing and exacerbate asthma
Fine particles
Reduced visibility; brown haze Increased rates of respiratory illnesses and symptoms, decreased lung function, excess mortality from heart and lung disease, exacerbation of symptoms in asthma patients
Lead Can accumulate in soil and food chain Altered neurobegavioural function in children, i.e. impaired intellectual development, increase human blood pressure and impair renal function
Air toxics Possible bio-accumulative effects (from accumulation in food chain)
Long-term health effects, even at low concentrationsCompounds may be carcinogenic, mutagenic, teratogenic, neurotoxic, toxic, or can cause reproductive dysfunction
Source: NHMRC 1996; EPA 1997a
Source: EPA 1993 (data from ANSTO)
Size & distribution of particles in the atmosphere (NSW SOE 2000)
PM10 – Health effects
• Acute effects– Decreased lung function
– Increased respiratory symptoms
– Hospitalisation/other health care visit – Mortality
– Increased plasma viscosity,heart rate variability
• Chronic effects– Increased mortality rates, reduced survival times,
chronic cardiopulmonary disease, reduced lung function
Stylized summary of acute exposure studies, percent change in health end-point per 10 g/m3
change in PM10
Estimated percent changes in daily mortality associated with a 10 g/m3 increase in PM10 (with 95% confidence intervals) for a number of cities
Ozone - Acute Health Effects
• Decreases in lung function
• Increase in respiratory symptoms, asthma attacks
• Increase in restricted activity days
• Increase in hospital admissions especially respiratory admissions
• Increase in mortality
The effect of ozone on pulmonary function (after Kleinman et al., 1989)
Effects of ozone on respiratory symptoms (after Kleinman et al., 1989)
Asthma camp associations between O3 levels and both peak flow lung function change and asthma exacerbations (as
indicated by -agonist medication use) (Thurston et al., 1997)
Reported RR of respiratory hospital admission associated with a 100 ppb increase in daily 1-h max.
O3 (Ito et al., 1999)
Reported RR of mortality associated with a 100 ppb increase in 1-h max. O3 (Thurston et al., 1999)
Nitrogen dioxide – Health effects
• Decreases in lung function
• Increase in respiratory symptoms
• Increase in hospital admissions – asthma, COPD
• Increase in mortality – conflicting results
Potential human health effects of NO2
Health effect MechanismIncreased intensity of respiratory infections
Increased severity of respiratory infections
Respiratory symptoms
Reduced lung function
Worsening of the clinical status of persons with asthma, chronic obstructive pulmonary disease or other chronic respiratory conditions
Reduced efficacy of lung defences
Reduced efficacy of lung defences
Airways injury
Airways and alveolar (?) injury
Airways injury
Source: Samet and Utell, 1990
Adjusted prevalence of respiratory infections in children of ten communities in Switzerland according to the mean NO2 level (from Braun-Fahrlander, 1997)
Carbon monoxide – health effects
• Angina and ischaemic heart disease
• Hospital admissions – heart disease, asthma
• Mortality – all cause and heart disease
Relative risks of congestive heart failure admission among Medicare patients as a
function of ambient pollutant levelsPollutant and city Single-pollutant model Multipollutant model
Relative risk
95% Confidence interval
Relative risk
95% Confidence interval
Carbon monoxide
Los Angeles
Chicago
Philadelphia
New York
Detroit
Houston
Milwaukee
1.36
1.29
1.17
1.10
1.24
1.11
1.29
1.25, 1.46
1.16, 1.44
1.05, 1.31
1.03, 1.18
1.11, 1.39
0.97, 1.26
1.07, 1.57
1.39
1.23
1.22
1.05
1.38
1.25
1.26
1.23, 1.56
1.07, 1.43
1.05, 1.41
0.97, 1.14
1.17, 1.63
1.05, 1.49
0.89, 1.77
Note: The multipollutant model included all four pollutants. All models included temperature, month, day of week, and year. Values refer to the relative risk associated with an increase of 10 ppm of carbon monoxide.
From Morris et al. (1995). Reproduced with permission of authors and publisher.
Sulphur dioxide – Health effects
• Decrease lung function – in those with asthma
• Increase in symptoms
• ED presentations
• Hospital admissions - respiratory
• Mortality – all cause, respiratory and CVS
APHEA studies
• For a 50 ug/m3 increase in 24 hour average SO2:
– 3% increase in all cause mortality– 4% increase in cardiovascular mortality– 5% increase in respiratory mortality– 2% increase in respiratory admissions (65+
years)
Types of studies
• Animal studies• Human studies
– Experimental (chamber studies)– Epidemiological (or observational)
• Cross-sectional• Time series• Case-control/ Case-crossover• Cohort• Randomised control trials
Health outcome measures in studies of air pollution
GeneralOverall mortalityMorbidity index
RespiratoryAcute and chronic symptomsAcute infectionsChronic respiratory diseasesDegree of non-specific airways responsivenessReduced level of lung functionIncreased rate of lung function declineDecreased rate of lung function growthExacerbation of a chronic respiratory diseaseHospitalization for a chronic respiratory diseaseLung cancer Death secondary to a chronic respiratory disease
NeuropsychologicalReduced performance on neurobehavioural testingNeuropsychological syndromeNeuropsychological disease
Some other health endpoints of interest
• Cardiovascular disease (AMI, heart failure)– ECG changes – Hospital admissions– Mortality
• Perinatal outcomes– Birth weight and gestational age– Neonatal and infant mortality
• Cancer incidence – lung cancer
Determinants of exposure, dose and biologically effective dose that underlie the development of health effects (Modified from
Jaakkola et al., 1994)
Indirect methods of assessing exposureSource of information Type of information
Source strength Emission rate (mass per time), traffic density
Geographical information Distance of the place of residence from the source
Dispersion models Spatio-temporal concentration distributions from modelling of emission rates, meteorology, air chemistry, geography
Outdoor-indoor penetration Modelling from outdoor concentration, building an ventilation characteristics
Stationary monitoring Concentration over time modelling from concentration of pollutants in microenvironments
Questionnaires and interviews Source strength, distance from the source, time-activity
Personal monitoring Continuous or cumulated concentrations over time
Human samples Concentration of biomarkers of exposure in human tissues and hair
Toxicological models Concentration and dose of pollutants in target organs modelling from concentration, breathing rate, metabolism
Some issues in air pollution
• Multi- pollutant exposure
• Low dose exposure
• Size and composition of particles
• Threshold effects
• Shape of the response function
• Time activity patterns
• Confounding by season and weather
Uses of exposure response relationships
• Standard setting and risk assessment
• Cost benefit analyses
• Air pollution control programs
Bill Physick, CSIRO (personal communication)
Study involving modeled air pollution data
A method for exposure assessment
A lph ing ton
D andenong
C ity B ox.H illFootscrayM t.C ottre ll
P t.C ook
P aisley
B righton
P t.H enryG eelong.S th
G roveda le
0.0
1.0
2.0
3.0
4.0
5.0
Population Air Pollution
0
10000
20000
30000
40000
Exposure
Green Scenarios
144.2 144.4 144.6 144.8 145.0 145.2 145.4
EASTIN G
-38 .4
-38.2
-38.0
-37.8
-37.6
NO
RT
HIN
G
C R AN BO U R N E
FR AN KSTO N
D AN D EN O N G
BR IG H TO N
PAISLEY
SYD EN H AM
M T D AN D EN O N G
SU N BU R Y
PAN TO N H ILL
W ER R IBEE
PORT PHILLIPBAY
BASS STR AIT
MELBOURNE
GEELONG
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
P M10- HOU R 9, 7/3/2001. T EST CASE
144.2 144.4 144.6 144.8 145.0 145.2 145.4
EASTIN G
-38 .4
-38.2
-38.0
-37.8
-37.6
NO
RT
HIN
G
C R AN BO U R N E
FR AN KSTO N
D AN D EN O N G
BR IG H TO N
PAISLEY
SYD EN H AM
M T D AN D EN O N G
SU N BU R Y
PAN TO N H ILL
W ER R IBEE
PORT PHILLIPBAY
BASS STR AIT
MELBOURNE
GEELONG
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
P M10- HOU R 9, 7/3/2001. T EST CASE
144.2 144.4 144.6 144.8 145.0 145.2 145.4
EASTIN G
-38 .4
-38.2
-38.0
-37.8
-37.6
NO
RT
HIN
G
C R AN BO U R N E
FR AN KSTO N
D AN D EN O N G
BR IG H TO N
PAISLEY
SYD EN H AM
M T D AN D EN O N G
SU N BU R Y
PAN TO N H ILL
W ER R IBEE
PORT PHILLIPBAY
BASS STR AIT
MELBOURNE
GEELONG
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
P M10- HOU R 9, 7/3/2001. BASECASE
144.2 144.4 144.6 144.8 145.0 145.2 145.4
EASTIN G
-38 .4
-38.2
-38.0
-37.8
-37.6
NO
RT
HIN
G
C R AN BO U R N E
FR AN KSTO N
D AN D EN O N G
BR IG H TO N
PAISLEY
SYD EN H AM
M T D AN D EN O N G
SU N BU R Y
PAN TO N H ILL
W ER R IBEE
PORT PHILLIPBAY
BASS STR AIT
MELBOURNE
GEELONG
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
P M10- HOU R 9, 7/3/2001. BASECASE
TEST CASE- 25% reduction in motor vehicle usage- public transport, car pooling, home office
144.2 144.4 144.6 144.8 145.0 145.2 145.4
EASTIN G
-38 .4
-38.2
-38.0
-37.8
-37.6
NO
RT
HIN
G
C R AN BO U R N E
FR AN KSTO N
D AN D EN O N G
BR IG H TO N
PAISLEY
SYD EN H AM
M T D AN D EN O N G
SU N BU R Y
PAN TO N H ILL
W ER R IBEE
PORT PHILLIPBAY
BASS STR AIT
MELBOURNE
GEELONG
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
P M10- HOU R 9, 7/3/2001. BASECASE
144.2 144.4 144.6 144.8 145.0 145.2 145.4
EASTIN G
-38 .4
-38.2
-38.0
-37.8
-37.6
NO
RT
HIN
G
C R AN BO U R N E
FR AN KSTO N
D AN D EN O N G
BR IG H TO N
PAISLEY
SYD EN H AM
M T D AN D EN O N G
SU N BU R Y
PAN TO N H ILL
W ER R IBEE
PORT PHILLIPBAY
BASS STR AIT
MELBOURNE
GEELONG
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
P M10- HOU R 9, 7/3/2001. BASECASE
Home- 12 hours
Travel- 3 hours
Work- 9 hours
PM10 CUMULATIVE DOSAGE
0100020003000400050006000700080009000
0 6 12 18 24TIME (hours)
DO
SA
GE
(u
g.m
-3.h
ou
rs) BASE
GREEN+car
Green+train
Selected references:• Department of Environment and Heritage. (2001) State of the Environment
Australia 2001.Canberra, Australia. http://www.erin.gov.au/soe/atmosphere/index.html (accessed October 2003)
• Department of Environment and Heritage. (2001) State of Knowledge Report: Air toxics and indoor air quality in Australia. Canberra, Australia. ISBN 0 642 54739 4.
• Holgate ST, Samet JM, Koren HS, Maynard RL. (eds.) (1999) Air pollution and health. Academic Press. London.
• McMichael AJ. (1993) Planetary overload: Global environmental change and the health of the human species. Cambridge University Press.
• New South Wales Environment Protection Authority. (2000) New South Wales State of the Environment 2000. http://www.epa.nsw.gov.au/soe/soe2000/index.htm (accessed October 2003)
• New South Wales Environment Protection Authority. (1998) Action for air. The NSW Government's 25-year air quality management plan. ISBN 0 7313 0160 9. Chatswood, Australia, Environment Protection Authority.
Thank You