Particulate Matter Characteristics, Health Effects and Exposure

Presented by Dr. Linda J. Bonanno Division of Science Research and Technology, NJDEP [email protected]

(609) 984-9480 Slides prepared by Philip Johnson & edited by Dr. Bonanno

NESCAUM Health Effects Workshop

Bordentown, New Jersey July 29 & 30, 2008

Coalbrookdale At Night

, Loutherbourg 1801 2

Over London By Rail

, Dore c1870 3

Some Famous Air Pollution Episodes

• 1948 Donora Smog Disaster, 20 excess deaths, over 7,000 sick • 1952 London Fog estimated 12,000 excess deaths • • 1966 New York City 80 excess deaths – Air Pollution, Geography and Meteorology (inversions) all contributed 4

Overview

1) Characteristics of PM 2) Health effects 3) Biological plausibility, knowledge gaps 4) Temporal and spatial scales of exposure 5) Public health considerations 5

Characteristics of PM

Particles and aerosols, which are a suspension of fine solid or liquid particles in gas) can differ in chemical composition and physical properties.

Particles may derive from many sources and have different fates.

6

Particle origin

Primary: emitted directly from source as particles – Unburned carbon particles from high energy combustion, e.g., autos, wood burning, power generation Secondary: precursor gases or added to existing particles – SO 2 → sulfuric acid + ammonia = sulfate particles • coal-fired power plants, fertilizer – NO 2 → nitric acid + ammonia = nitrate particles • coal-fired power plants, biologicals, autos, fertilizer – Existing particles + VOCs = organic “carbon” particles • autos, vegetation 7

Size

NARSTO 2003 _______________

0.2 μm carbon agglomerate particle

8

Basically…

• TSP-total suspended particles, all particles most mass in larger size • PM 10 - not larger than 10 μm aerodynamic diameter • Coarse or Inhalable PM-between 10 μm and 2.5 μm • PM 2.5

or fine PM-not larger than 2.5 μm • Ultrafine PM- not larger than 0.1 μm, sometimes referred to as nanoparticles 9

TSP, PM 10 , Coarse (PM 10-2.5

): short lifetime (m, h) and travel distance (<10 k); often primary.

– Construction, demo, mining, sea spray dust, dust resuspension Fine (PM 2.5

), : long lifetime (days, weeks); can travel 10 3 – 10 6 k; primary and secondary.

– Combustion, e.g., biomass burning, fossil fuel burning Ultrafine (PM 0.1

) : very short lifetime due to scavenging, nucleation, coagulation, etc. 10

Figure II-4: Average seasonal fine particulate composition, 2000-2002.

Composition

21 18 Other Elemental Carbon Organic Carbon Ammonium Sulfate Ammonium Nitrate 15 0.6

12 0.9

4.2

0.8

1.0

4.4

0.8

4.2

3.2

4.0

9 0.5

2.4

0.4

2.0

0.4

2.1

0.3

2.8

11.4

6 3 0 4.0

5.3

8.7

4.9

2.5

1.0

0.5

0.9

0.2

0.9

0.2

1.0

5.4

1.8

2.7

0.2

1.1

2.9

0.9

0.6

0.3

0.5

0.3

2.0

0.2

1.1

0.2

0.9

0.2

1.1

2.1

2.3

3.3

2.5

0.7

0.4

0.3

0.4

4.4

6.3

5.9

3.5

1.8

0.9

1.8

NESCAUM 2003 Brigantine Lye Brook Acadia Washington, D.C. 1.6

1.1

1.3

5.2

1.2

6.7

4.8

3.7

4.9

5.2

6.9

5.3

4.3

2.5

1.3

2.7

New York City 11

•

Physiochemical Properties

Physical Characteristics

particle surface area, particle number, particle mass, particle size distribution, surface chemistry, surface charge

Chemical Components

biological components (e.g., pollen, microbes) ions (sulfates, nitrates, ammonium) strong acidity (H + ) transition metals (water soluble, bioavailable, oxidant generation) elemental carbon organic carbon (total, nonvolatile, and semivolatile, functional groups and individual species) 12

The Human Lung

excellent delivery device with large surface area 50-100 m 2

court) (80 m 2 is size of tennis

Particle Size & Composition Determine – penetration into body – deposition site in body – clearance mechanisms used by body 13

EPA 1996 14

Health effects

• Overwhelming body evidence from toxicological, epidemiological & clinical work support associations between exposure to PM and a broad range of adverse health effects. • Health effects diverse in – scope – severity – duration – clinical significance • Exacerbation of heart and lung disease; pre-mature death; cancer 15

Short-term effects (days-months)

• mortality from cardiopulmonary diseases • hospitalization and emergency department visits for cardiopulmonary diseases • increased respiratory symptoms • decreased lung function • physiological changes or biomarkers for cardiac changes. U.S. EPA PM Staff Paper 2005 16

Short-term multi-city studies, per 10 µg/m 3 increase:

National Morbidity Mortality Air Pollution Study (NMMAPS) PM 10

– mortality 0.21% – cardiovascular disease – COPD – pneumonia 9.5 % 13.3 % 5.6 %

Harvard Six Cities (PM 2.5

)

– mortality 1.2 %

Air Pollution and Health: A European Approach (APHEA-1,2) black smoke

– mortality 0.6 % 17

Acute exposures (min-hrs)

• Very short-term transient PM 2.5

concern. elevations of • Associations between 1-12 hr exposures and acute cardiovascular and respiratory events, including myocardial infarction in older adults and asthma symptoms in children e.g., Adamkiewicz et al. 2004; Delfino et al. 1998, 2002; Gold et al. 2000; Henneberger et al. 2005; Mar et al. 2005; Morgan et al. 1998; Peters et al. 2001. 18

Long-term effects (years)

• mortality from cardiopulmonary diseases • mortality from lung cancer • effects on the respiratory system such as decreased lung function or the development of chronic respiratory disease.

U.S. EPA PM Staff Paper 2005 19

Long-term multi-city studies, per 10 µg/m 3 increase:

Harvard Six-Cities. Mortality, PM 2.5

– all-cause 14 % – cardiopulmonary – lung cancer 19 % 21 %

American Cancer Society. Mortality, PM

– all-cause 6 % – cardiopulmonary – lung cancer 9 % 14 % 20

Other measures?

Other health indicators

– Out-of-hospital trips to physicians – Lost-work/school days or productivity – Over-the-counter drug consumption Zmirou

et al.

1999 found this was the largest cost from exposure to air pollution .

Total annual effects of PM

– 1,725 premature deaths from both respiratory and cardiac causes – 1,087 hospital admissions – 48,000 visits to emergency departments – 567,000 asthma-symptom days

2.5

– 8.35 million restricted-activity days.

in Ontario:

(MOE 1999, Abelsohn

et al.

2002). 21

Susceptibility

Sensitive subpopulations

(~40% of population) – Infants, children, elderly – Individuals with preexisting cardio respiratory diseases (e.g., asthma, chronic pulmonary obstructive syndrome, atherosclerosis, etc. ) – Individuals with diabetes

Increased vulnerability

– Socioeconomic status (e.g., reduced access to health care, poor nutrition ) – Lifestyle – Elevated exposures, e.g., live/work near major sources (e.g., roadways, industry, 22 wood burning), physical activity, occupation

23

Threshold

No apparent threshold, i.e., no level below which exposure is safe.

Effects seen below current PM 2.5

24-hr - 35 µg/m 3 NAAQS annual - 15 µg EPA revoked annual std for PM 10 , 24-hr is 150 µg/m 3 Small changes in PM 2.5

concentration could result in large public health impacts.

24

Blood

increase coagulation, altered flow reduced O 2 saturation translocate PM

Brain

↑ risk stroke

Lung

inflammation oxidative stress Asthma/COPD reduction lung function increase respiratory symptoms Impact pulmonary reflexes

Heart

↑chance of dysrthythmia altered cardiac repolarization increased myocardial ischemia altered cardiac autonomic function

Systemic Inflammation/Oxidative Stress

Leukocyte & platelet activation ↑C-reactive protein Proinflammatory mediators

Vasculature

Atherosclerosis Destabilization of plaques Endothelia dysfunction Vasoconstriction hypertension 25

Direct pulmonary effects Systemic effects secondary to lung injury Direct effects on the heart

Biological plausibility

Lung injury and inflammation Increased susceptibility to respiratory infections Increased airway reactivity and exacerbation of asthma Lung injury leading to impairment of heart function by lowering blood oxygen levels and increasing the work of breathing Lung inflammation and cytokine production leading to adverse systemic hemodynamic effects (e.g., arrhythmia) Lung inflammation leading to increased risk of heart attacks and strokes due to increased blood coagulability PM/lung interactions potentially affecting hematopoiesis (e.g., blood cell formation) Uptake of particles and/or distribution of soluble components from the lungs into the systemic circulation Effects on the autonomic control of the heart and cardiovascular system

26 EPA 2003

Knowledge gaps

1996 EPA PM Criteria Document – ~35 PM-mortality time-series (short-term) studies published 1988-1996 and Six Cities Cohort study – Concerns: weather, “harvesting”, co-pollutants, mechanical model Most recent EPA NAAQS review – >80 new time-series studies – Six Cities and ACS cohort studies reanalyzed/extended: original findings reenforced • “harvesting” and co-pollutants issues largely addressed • “Splus” controversy addressed • Confounding weather variables not completely resolved – Possible mechanical models developed – Threshold? Does one exist? Absence of “bright line.” 27

True effect estimates likely higher… Ambient measurements from network of centrally located monitors used as surrogate for population exposure. Highly resolved exposure assessment is needed, spatially and temporally, across population segments at greater risk.

28

Temporal, spatial, group scales of exposure

• time scales acute chronic

min, hrs, days, weeks, months, years, lifetime

• space scales personal space, microenvironment, neighborhood, regional, global • individual, group, population scales 29

Figure II-17: Diurnal PM 2.5

seasonal profile for Boston, MA (top), New Haven, CT (middle) and PM 2.5

day-of-week profile for both cities (bottom)

(Note PM 2.5

concentration scale change (y-axis) in each graph)

Fig. 4 - Diurnal Boston TEOM Fine Aerosol Data 20 15 10 5 0 0 1 2 Winter Spring Summer Fall 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Fig. 5 - New Haven Diurnal Fine Aerosol TEOM Data 20 21 22 23 25 20 15 10 5 0 0 1 2 16 Winter Spring Summer Fall 4 5 6 7 8 9 10 11 12 13 14 15 (All available data used from each site ) 16 17 18 19 20 21 22 23 14 12 10

NESCAUM 2003

8 Monday

Boston Daily New Haven Daily Boston Weekly Mean New Haven Weekly Mean

Tuesday Wednesday Thursday Friday Saturday Sunday

30

Figure II-17: Diurnal PM 2.5

seasonal profile for Boston, MA (top), New Haven, CT (middle) and PM 2.5

day-of-week profile for both cities (bottom)

(Note PM 2.5

concentration scale change (y-axis) in each graph)

Fig. 4 - Diurnal Boston TEOM Fine Aerosol Data 20 15 10 5 25 Winter 0 Spring

Local scale, diurnal and seasonal

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Fig. 5 - New Haven Diurnal Fine Aerosol TEOM Data 20 21 22 23 20 15 10 5 0 0 1 2 16 Winter Spring Summer Fall 4 5 6 7 8 9 10 11 12 13 14 15 (All available data used from each site ) 16 17 18 19 20 21 22 23

31

14 12 10 8 Monday

Boston Daily New Haven Daily Boston Weekly Mean New Haven Weekly Mean

Tuesday Wednesday Thursday Friday Saturday Sunday

P Johnson 1999 32

P Johnson 1999 33

P Johnson 1999 Where’s a PM monitor when you need one?

34

Neighborhood variability

CB Ellis Photo 35

Figure II-8a: Back trajectories on 20% worst visibility days at Acadia National Park during 1997-99

NESCAUM 2003

Figure II-8b: Back trajectories on 20% best visibility days at Acadia National Park during 1997-99. 1997-99.

Source: NESCAUM 2002b

Figure II-8a: Back trajectories on 20% worst visibility days at Acadia National Park during 1997-99 Figure II-8b: Back trajectories on 20% best visibility days at Acadia National Park during 1997-99. Figure 2b: Back trajectories on 20% best visibility days at Acadia National Park during 1997-99.

37 Source: NESCAUM 2002b

Global transport

http://www.reuters.com/article/scienceNews/idUSN1545698320070516 38

Spatial gradients – risk reconsidered

Jerrett et al. question: Are health effects greater around sources?

Hypothesis: Community average concentrations lead to measurement error reducing size effects. Method: Analyzed small-area exposure measures in Los Angeles, interpolated 23 fixed site PM 2.5

monitors. 1982-2000. Assessed

within

community comparison of spatial monitoring gradients rather than

across

communities.

39 Jerrett et al.,

Epidemiology

, 2005.

Findings: •

Highest exposures related to proximity to traffic

• Relative risk mortality increase per 10 µg/m 3 : – All-cause: 11-17 % – Ischemic heart disease and lung cancer: 24-60 %

.

depending on model used. Jerrett et al.,

Epidemiology

, 2005.

40

41

42

P Johnson 2004 Upstate NY

Individual, minutes

9000 8000 7000 6000 5000 4000 3000 2000 1000 0 OWF off Real time field measurements of PM2.5 in proximity to an outdoor wood furnace OWF loaded with wood OWF turns on plume away from DataRAM DataRAM 100' from OWF OWF turns off plume moving over and away from DataRAM time (15 sec intervals) Johnson 2006 43

Public health considerations

The Northeast demographic – 15% children ever asthma – 13% adults ever asthma – 4% adults chronic bronchitis preceding 12 months – 10% adults heart disease – 6% adults diabetes – 25% <18 years age – 13% >64 years age 44 Johnson and Graham 2005

Northeast – urban

Most densely populated region in U.S.

72% of population lives in urban areas comprising 6% of landmass.

These areas have the highest PM

2.5

mass in the monitoring network

45

Northeast rural – wood smoke

• 25+ years of studies in variety of locations consistently find RWC has adverse effects on ambient air quality • In local areas, can be chronic and severe • Wood burning has disproportionate effect on air quality relative to other fuel sources – Waterbury, VT: • River valley confluence, night inversions • RWC accounted for up to 40% of ambient TSP • Elevated hourly night-time levels in excess of 100 µg/m 3 .

• 1982 population ~2,000; 28% used wood fuel as primary heating – Rutland, VT: • Wood smoke 24% of PM2.5 mass 46 Sexton et al. (1984) and Sanborn et al. (1981, 1982); Allen et al. 2004

• Overall magnitude of exposure: unknown • Terrain and climate are important factors –River valleys (former water economy: historical mill towns, factory towns, hamlets) –Meteorology: Night-time diurnal inversions (even a small number of woodstoves can affect a large fraction of a community) –Climate: can get very cold • New England has the highest per capita woodstove ownership in the U.S., • The NE Census Region (New England, NJ, NY, PA) consumes over twice the number total cords of wood in woodstoves per year than the Midwest, South, or West (Houck et al. 2001).

47

Summary

• Complex physical & chemical properties • Numerous ubiquitous sources, • Acute & chronic health risks for variety of lung and heart disease endpoints and mortality • Large # of susceptible subpopulations • Diverse exposure scales across time & space • Significant public health consequences 48