Overview of air pollution AProf Bin Jalaludin MBBS
Overview of air pollution A/Prof Bin Jalaludin MBBS, MPH, Ph. D, 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
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’ 1 2 Chlorine and bromine ‘radicals’ destroy ozone molecules Stratospheric ozone layer depleted 3 Increase in ultravioletrelated biological damage Source: Mc. Michael 1993 4 Increase in ultraviolet irradiance at ground level
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 – CO 2, 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 Source: Granier and Shine (1999). 5 700 -11 400
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 - H 2 SO 4, HNO 3 (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, Mt. S) 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 Enhanced greenhouse effect Manifestation Type (direct, indirect) and timinga (early, late) of adverse health effect Direct, early Global warming and other climate change Direct, late Indirect, early Heatwave-related illness and death Extension of vector-borne infections 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 Stratospheric ozone depletion Increased UV-B flux at Earth’s surface Sunburn, conjunctivitis Suppression of immune system increased risk of infection Skin cancer Ocular effects: cataracts, pterygium Acid aerosols (from burning of sulphurous fossil fuels) Acid rain Effects on respiratory system (? ) Consequences of damage to foreshore facilities, roads, etc. Indirect, late Altered viability of (edible) fish in warmed oceans Destruction of wetlands decline in fish stocks Impaired growth of food crops and of marine microorganisms (base of aquatic food web) Aquatic damage (reduced fish) Impaired growth of crops A The designations ‘early’ and ‘late’ are notional, and indicate relative timing. (Based on Mc. Michael, 1993. 3) Impaired forest growth reduced ecosystem productivity
Possible adverse effects upon human health caused by global environmental changes (cont. ) Environmental change Land degradation: intensive agriculture, overgrazing Loss of biodiversity Manifestation Type (direct, indirect) and timinga (early, late) of adverse health effect Direct, early Direct, late Erosion, sterility, nutrient loss, salinity, desertification Decline in agricultural productivity Rural sector depression migration to fringes of cities (see bottom row) Depletion of underground aquifers Lack of water for drinking and hygiene Decline in agricultural productivity Destruction of habitat Deforestation disruption of local culture Loss of potentially edible species Loss of genetic diversity; weakening of ecosystems Other effects of overpopulation (particularly in poor countries) Proliferation of crowded urban slums (due to migration and high fertility) Indirect, early Exposure to pesticides and fertilisers (may also cause algal blooms) Consequences of silting up of dams and rivers Deforestation greenhouse enhancement Loss of medicinals, and other healthsupporting materials Infections Malnutrition Homelessness Antisocial behaviours Indirect, late Social disorder Chronic toxic effects of environmental pollutants A The designations ‘early’ and ‘late’ are notional, and indicate relative timing. (Based on Mc. Michael, 1993. 3) Greater vulnerability of crops and livestock. Reduced vitality of ecosystems Consequences of overload of local ecosystems
Regional/Local Air Pollutants • Criteria (Common) Air Pollutants - (ambient air quality standards established) – Regional • Photochemical smog - Ozone (O 3) • Haze - Particulates (PM) & Nitrogen Dioxide (NO 2) – Local • Sulphur Dioxide (SO 2) • 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 Air pollutant Sc ore (Commonwealth SOE 2001) Health effects Benzene 9 Carcinogenic, causes anaemia 1, 3 -Butadiene 8 Carcinogen Polycyclic aromatic hydrocarbons (PAH) 8 Carcinogen, environmentally persistent Arsenic and compounds 8 Chromium and compounds 8 Nickel and compounds 8 Carcinogen, environmentally persistent Carcinogen, 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 Carcinogen, can affect the respiratory system, environmentally persistent Cadmium and compounds. A 7 Carcinogen 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 5 Probable 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 (1999 c).
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 nonindustrial 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
Relationships between indoor and outdoor concentration of air pollutants (Commonwealth SOE 2001) ci/ca. A g. B NO 2 0. 72 O 3 0. 44 SO 2 0. 34 CO 1 1 Particles 1 1 0. 53 Pollutant Lead A Indoor (c i) and outdoor (c a) concentrations of air pollutants. B Ratio of indoor exposure to outdoor exposure. Source: Beer and Walsh (1997).
Particles in homes - no major sources Source: V Sheppeard, NSW Health
Fine particle (PM 10) levels by number of smokers in house Source: V Sheppeard, NSW Health
Fine particle (PM 10) levels by main heating type 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 Source: V Sheppeard, NSW Health
Peak 1 -hour average concentrations of nitrogen dioxide, indoors & outdoors, 1987 -97 (NSW SOE 2000) Source: Ferrari 1997
In carbon monoxide levels Source: CARB 1998; V Sheppeard, NSW Health
Other in-car exposures (VIC EPA - mean personal concentrations while commuting to CBD (east route) - pilot trial) Source: V Sheppeard, NSW Health
Air toxics in other microenvironments 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
Schedule 2 of the NEPM giving National Environment Protection Standards for ambient air quality (Commonwealth SOE 2001) Pollutant Averaging period Maximum concentration (based on arithmetic means) Maximum allowable exceedences. A (days per year) Carbon monoxide 8 h 9. 0 ppm 1 Nitrogen dioxide 1 h 1 y 0. 12 ppm 0. 03 ppm 10 Photochemical oxidant (as ozone) 1 h 4 h 0. 10 ppm 0. 08 ppm 11 Sulfur dioxide 1 h 1 d 1 y 0. 20 ppm 0. 08 ppm 0. 02 ppm 110 Lead (as TSPs) 1 y 0. 5 g/m 3 0 Particles (as PM 10) 1 d 50 g/m 3 5 A Goal to be achieved by 2008. Source: NEPC (1998).
Primary / secondary pollutants • Primary pollutants – Particles – NOx – SO 2 – CO • Secondary pollutant – Ozone – Particles (gaseous pollutants forming aerosols)
Types of air pollution • Summer episodes (photochemical episodes) – Secondary pollutants – O 3, H 2 SO 4, HNO 3 – Ozone is the index pollutant – “White haze” • Winter episodes – Particles, SO 2 – “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
The role of the atmosphere in the air pollution source sink relationship SOURCE STATE OF ATMOSPHERE SINK DISPERSION Vertical and horizontal – stability, turbulence, wind EMISSIONS Rate, type, source configuration TRANSFORMATION Chemical reactions REMOVAL Settling, scavenging adsorption, impaction RECEPTOR RESPONSE Health effects, vegetation damage, soiling, corrosion
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
Contribution of wood burning to TSP, Sydney Source: Carnovale et al. 1997 (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)
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) Deaths/yr 75 Asthma Hospital Admissions/yr (0. 01% of all adverse impact cases) 265 240 Non-asthma Respiratory Hospital Admissions/yr 3, 500 Respiratory ED Visits/yr 180, 000 Asthma Attacks/yr (i. e. , person-days during which notably increased asthma symptoms, e. g. , requiring extra medication, are experienced) 930, 000 Restricted Activity Days/yr (i. e. , person-days on which activities are restricted due to illness 2, 000 Acute Respiratory Symptom Days/yr (i. e. , person-days during which respiratory symptoms such as chest discomfort, coughing, wheezing, doctor diagnosed flu, etc. are experienced)
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 pests Long-term low-level exposure is of concern; limited studies have been done on effects on Australian native vegetation Damage 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 NO 3 Effects on vegetation, damage to leaf surface, reduced plant growth Limited 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 1997 a
Environmental & human health effects of major air pollutants (cont. ) Pollutant Effects – environmental Effects – human health SO 2 Plant damage and growth inhibition; little known about effects on Australian native vegetation Acid deposition: acidification of soils and lakes change the availability of minerals to plants Corrosion 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 concentrations Compounds may be carcinogenic, mutagenic, teratogenic, neurotoxic, or can cause reproductive dysfunction Source: NHMRC 1996; EPA 1997 a
Size & distribution of particles in the atmosphere 2000) Source: EPA 1993 (data from ANSTO) (NSW SOE
PM 10 – 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/m 3 change in PM 10
Estimated percent changes in daily mortality associated with a 10 g/m 3 increase in PM 10 (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 O 3 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. O 3 (Ito et al. , 1999)
Reported RR of mortality associated with a 100 ppb increase in 1 -h max. O 3 (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 NO 2 Health effect Mechanism Increased 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 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 NO 2 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 levels Pollutant and city Single-pollutant model Multipollutant model Relative risk 95% Confidence interval 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 Carbon monoxide Los Angeles Chicago Philadelphia New York Detroit Houston Milwaukee 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/m 3 increase in 24 hour average SO 2: – 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 General Overall mortality Morbidity index Respiratory Acute and chronic symptoms Acute infections Chronic respiratory diseases Degree of non-specific airways responsiveness Reduced level of lung function Increased rate of lung function decline Decreased rate of lung function growth Exacerbation of a chronic respiratory disease Hospitalization for a chronic respiratory disease Lung cancer Death secondary to a chronic respiratory disease Neuropsychological Reduced performance on neurobehavioural testing Neuropsychological syndrome Neuropsychological 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 exposure Source 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
Study involving modeled air pollution data Bill Physick, CSIRO (personal communication)
A method for exposure assessment Population Exposure Air Pollution
Green Scenarios Work- 9 hours Travel- 3 hours Home- 12 hours TEST CASE- 25% reduction in motor vehicle usage - public transport, car pooling, home office
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. Mc. Michael 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 2000/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
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