Externality on Theory

Air Pollution and HealthImpact

Y. MatsukiAugust 8, 2009Presented at NTUU “KPI”

What’s new on the public healthissue?

Loss of life expectancy for chronicmortality from air pollution[Dockery et al 1993, Pope et al 1995]have found positive correlationsbetween exposure to particles andtotal mortality

Epidemiology of Acute HealthEffects

Table of contents- Introduction

- Studies of air pollution episodes- Health effects at low levels of air pollution

- Acute Morbidity- Daily time-series mortality studies- Slope of the mortality exposure-response relationship and

lead-lag relationships- Acute Morbidity

- Hospital usage- Exacerbation of asthma- Respiratory symptoms- Lung function- Restricted activity

Introduction

It’s about human health andpollution.Where in the world is this storyabout?When did this story start?What changed for the last 10-15years?

Air pollution episodesWhere the most dramatic episode occurredand when?What happened?Mortality and morbidityHow?Respiratory and cardiovascularCardiopulmonary diseaseWhat was the level of particle and SO2?500 g/m3 – 2 mg/m3

If not old days, where do these levels exist?

Health effects at low level of airpollution

What was the primary interest to airpollution policy among the mostdeveloped nations for the last 20years?To determine the lowest levelThe length of exposure to causehealth impactsThreshold was often assumed.

Health effects at low level of airpollution

With improved air monitoring, isthreshold proven?No threshold, or bellow ambient levelin the US in 1996.Many of the studies suggest linearmodel.What is necessary to prove it?Number of time-series studies

What are the health effects?

MortalityHospitalization for respiratory andheart diseaseAggravation of asthmaIncidence and duration of respiratorysymptomsLung functionRestricted activity

Acute MortalityDaily time-series mortality studies

US EPA reviewed Ostro 1993,Schwartz 1994c, Dockery & Pope1994, Pope et al. 1995b.What these studies observed?Changes in daily death countsassociated with short-term changesin particulate air pollution.a near linear function.

What do you see from those tableand figures?

Consistency in estimated effectsStatistically significant effectEstimated Range?0.5 percent – 1.6 percent in dailymortality for each 10 g/m3 increasein PM10 concentration.Weighted mean?About 0.8 percent

Percent increase in Mortalityper 10 g/m3 increase in PM10

Mortality Cases/ g/m3 ?0.5 percent – 1.6 percent in dailymortality for each 10 g/m3 increasein PM10 concentration.5 x 10-4 – 1.5 x 10-3 Cases/ g/m3

Weighted mean about 0.8 percent8 x 10-4

Mortality by respiratory disease andcardiovascular disease

Large effect on respiratory diseasemortalityAlso cardiovascular disease causingdeath

Shape of the mortality exposure-responserelationship and lead-lag relationships

PM10 concentration in typical UScities10 to 120 g/m3

Max 365 g/m3 in the Utah ValleyHow is in Ukraine?

Shape of the mortality exposure-responserelationship and lead-lag relationships

What does it say?Typically near linear or log-linearThree possibilities:(1) no threshold(2) threshold is bellow existingpollution levels(3) looking more linear than it reallyis.

Shape of the mortality exposure-responserelationship and lead-lag relationships

Increased mortality occurredconcurrently or within 1-5 daysfollowing an increase in air pollution.

Acute MorbidityHospital usage

What happened in the Utah Valley duringthe winter of 1986-1987?A labor dispute resulted in the closure ofthe local steel mill, the largest single sourceof particulate emission.This winter PM10 ave. 51 g/m3 , max. 113g/m3

Previous year ave. 90 g/m3 , max 365g/m3

Children hospital admission for respiratorydisease dropped 50 percent.

Acute MorbidityHospital usage

What was the argument by Lamm etal. (1994)?Not closure of the steel mill, butRespiratory Syncytial Virus (RSV)What was the argument by Pope(1991)?Not by the virus.

Acute MorbidityHospital usage

What is the exposure-response of thehospital admission of all respiratorydiseases?0.8 – 3.4 % increase per 10 g/m3 byPM108 x 10-4 – 3.4 x 10-3 Cases/ g/m3 byPM10

Acute MorbidityHospital usage

Emergency department visit %increase by 10 g/m3 increase ofPM100.5 – 3.4 (ave. 1.0) % increase/ 10g/m3

Exacerbation of asthmaRespiratory symptoms

Asthma, BronchodilatorCough

Exacerbation of asthmaWhat is the exposure-response relation ofasthmatic attack?3 % increase in asthmatic attacks with 10g/m3 increase of PM10

3 x 10-3 cases/ g/m3

What is the exposure-response relation ofbronchodilator use?1.1 – 12 % (ave. 3.0) increase with 10g/m3 increase of PM10

3.0 x 10-3 cases/ g/m3

Respiratory symptomsLower Respiratory symptoms

Wheezing, dry cough, phlegm, shortness of breath,chest discomfort/pain

What is the exposure-response relation of lowerrespiratory symptoms?Ave. 3.0 % increase in lower respiratory symptomswith 10 g/m3 increase of PM103.0 x 10-3 cases/ g/m3

Upper Respiratory symptomsRunny nose, stuffy nose, sinusitis, sore throat, wetcough, head cold, hay fever, red eyes

Statistically insignificant association observed.

Key words

PneumoniaCOPD: chronic obstructive pulmonary(lung) diseaseCoronary Artery DiseaseDisrythmias (such as slow heart rate)Congestive Heart Failure

Lung function

FEV: forced expiratory volume (ameasure of lung function)FVC: forced vital capacityPEF: Peak expiratory flow

Epidemiology of Chronic HealthEffects

Table of contents- Introduction- Mortality Studies

- Population-based (ecologic) mortality studies- Research needs for improved study designs- Prospective Cohort Mortality Studies- Harvard six-cities study- Implication of prospective cohort mortality results

- Chronic Health Effects; Morbidity- Chronic differences in lung function- Chronic respiratory symptoms and disease

Introduction

What is the difference between the acuteeffects and the chronic effects?Acute: associated with short term (day today change)Chronic = long-term: a long time +cumulative effects of repeated exposureIf acute effect exists, is there also chroniceffect by the same pollutant?Not automatically

Mortality StudiesPopulation-based mortality studies

What is the summary of the population-based cross-sectional study?Average mortality is higher in cities with higher fineparticulate and sulfate particulates.How the other risks were controlled?Smoking rate, education levels, income levels,poverty rates, housing density, etc were included inthe regression models.What is the coefficients of air pollution relatedmortality?About 3 % per 10 g/m3

4 x 10-3 per g/m3

What are limitations of Population-based Studies?

Systematic and/or analytical biasStudy designsData setsAnalytic techniquesRegression analysisHypothesis testingControlling some other factors

Size of the estimated associationComparison with the current pollution level to thechronic mortality is not appropriate,Because now the pollution level is lower than yearsago.

Cannot control for individual differences in cigarettesmoking, and other risk factors.

What are limitations of Population-based Studies?

Age, poverty, health care,occupations, cigarette smoking,housing quality, cooking fuels varyamong cities and potentially could beconfounding the apparent airpollution associations.

Improved study designs

What are 2 important issues 1970s –1980sThresholdStudy design – what evidenceneeded?If threshold, what will become easier?To establish the acceptable goal forpollution control

Prospective Cohort MortalityStudies

3 cohort mortality studiesWith improved study design

Prospective Cohort MortalityStudies

Not on the data available for thepopulation as a whole,But, it analyzes the incidence ofhealth effects in a sample ofindividuals.Negative aspect:It relies on community-based airpollution monitoring.Costly and time-consuming

Harvard six-cities study14-16 follow up of 8,111 adults living in 6 cities of theUSTSP, PM10, PM2.5, SO4, H+, SO2, NO2 and O3 levelswere monitored.What is most strongly associated with mortality risk?SmokingBut, after controlling for individual differences (age,sex, smoking, body mass, education, occupationalexposure),Differences in relative mortality risks across 6 citieswere strongly associated with difference in pollutionlevels in those cities.PM10, PM2.5, SO4 than TSP and SO2, H+, or ozone.

Shape of the figure

Mortality risk and fine particulateNearly linearNo threshold

Implications of prospective cohortmortality results

The increased risk from air pollutionbigger or smaller than cigarettesmoking?SmallBut, there is a correlation.

Summary

MortalityAcute exposure Total 0.5-1.5%/10 g/m3

5 x 10-4 – 1.5 x 10-3 (cases/ g/m3)Chronic exposure 3 – 9 %/10 g/m3

3 x 10-3 – 9 x 10-3 (cases/ g/m3)

Exposure-Response Function f(r,C(r,Q))

PM10 and NitratesHealth impact cases/(year.person. g/m3)

Long-term Mortality 2.60E-4

Chronic Bronchitis 7.65E-5

Restricted Activity Days 5.0E-2

Work Days Lost 1.0E-2

Hospital AdmissionsCardiovascular, Respiratory 6.00E-5, 2.56E-6

Asthmatic adultsBronchodilatorLower respiratory symptoms

6.00E-2

1.63E-1

Infant Mortality 2.78E-5

Asthmatic childrenCardiovascular, Respiratory 7.8E-2, 1.0E-1

f(r,C(r,Q)) SO2

Health impact cases/(year.person. g/m3)

Short-term Mortality 2.30E-6

Hospital AdmissionsAdmissions 2.84E-6

Source: Rabl 2001

Concentration of the pollution( g/m3)C(x,Q) Gaussian Plume Model

Q - h2

C = ---------------- exp [--------]21/2 3/2 ux z z

2

z

z

Atmospheric Stability

Surface WindSpeed(meter/second)

Day Night

Incoming Solar Radiation ThinlyOvercastor clearsky

HeavyCloudStrong Moderate Slight

< 2 A A-B B

2-3 A-B B C E F

3-5 B B-C C D E

5-6 C C-D D D D

> 6 C D D D D

Weather observationDay Wind Speed

(meter/second)Wind DirectionE, ESE, SSE, S…..

Atmospheric Stability(A,B… .F)

Aug 7 1800

1900

2000

2100

2200

2300

2400

Aug 8 0600

0700

0800

0900

2100

0900