Ambient Air Toxics & Acute Human Health Effects

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Ambient Air Toxics Acute Human Health Effects

• Air Toxics What We Know, What We Dont Know, and
  What We Need to Know
• University of Houston Hilton, Houston, Texas
• October 17-18, 2005

Winifred J. Hamilton, PhD, SM Assistant Professor
and Director Environmental Health Section Chronic
Disease Prevention and Control Research
Center Baylor College of Medicine, Houston,
Texas 713.798.1052 hamilton_at_bcm.tmc.edu
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OUTLINE

• AIR TOXICSWHAT ARE THEY?
• HOW DO WE MEASURE EXPOSURE?
• ACUTE VS CHRONIC DISEASE?
• HOW DO WE STUDY HEALTH EFFECTS?
• THE 3 WORKSHOP QUESTIONS
• Do better exposure estimates lead to stronger
  associations?
• Is it preferable to focus on acute or chronic
  health effects?
• Do diseases correlate with exposure?
• SELECTED AAT HEALTH STUDIES
• BCM HC AP ADMITS STUDY
• THE AH, DUH FACTOR

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1. AIR TOXICSWHAT ARE THEY?

• Air Toxics (ATs)
• Definition Gaseous, aerosol or particulate
  pollutants (other than the six criteria
  pollutants) which 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 (EPHC NEPM,
  Australia)
• Lists of key ATs vary and change
• - HAPs ( ATs N 188) - NATA (N 33)
• - TRI (N 650) - NEPM-AT (N 6)
• - Calif TACs (N 224) - Calif Hot Spot Program
  (N 18)
• - Manmade chemicals on the market (N 60,000)
• Criteria Air Pollutants (CAPs)
• O3, NO2, SO2, CO, PM, Pb
• What differentiates the 6 CAPs from the ATs?

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The 188 HAPS
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The 188 HAPS continued
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2. HOW DO WE MEASURE EXPOSURE?

• Survey (eg, use of pesticides)
• Microenvironments (eg, RIOPA)
• Personal monitors
• All outdoors (eg, Six City)
• Ambient monitoring network
• Geospatial
• Proximity, dispersion, CMAQ, TRI facilities,
  roadways
• Variables that affect exposure
• Events (accidents, fireworks)
• Activity, vehicle use, age, smoking
• Which chemicals? What averaging schemas?...

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http//www.epa.gov/triexplorer
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13.45 ug/m3 6.1 ppbV 1,3-butadiene
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Monitored Concentrations of Outdoor HAPs
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The Big ThreeHC a strong contenderBUT lower PM
levels?
http//www.epa.gov/air/data/geosel.html 30
minutes ESLEffect Screening Level NDNo Data
RBRisk Based
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Measuring Risk

• U.S. Rating Systems
• EPAs NAAQSs
• OSHA/NIOSH
• LD50
• EPAs IRIS
• TCEQs ESLs
• International
• WHO (IARC)
• Australias EPHC is developingNEPM standards for
  5 ATs benzene, formaldehyde, benzo(a)pyrene,
  toluene and xylenes
• Weak areas in our understanding
• Low exposure, long duration
• Subtle effects (cognition, endocrine
  disruption...)
• Multipollutant and cumulative effects
• Windows of harm, latency, lag times
• Differences in susceptibility

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Measuring Health Risk from Air Toxics

• National Air Toxics Assessment (NATA)
• Assesses risk from 32 of the 188 HAPS, plus
  diesel PM
• Air Toxics Emissions Inventory?
• Estimate ambient concentrations across US?
• Estimate population exposures across US?
• Characterize public health risk (cancer and
  noncancer)?

Relationship of estimated cancer risk from air
toxics with median household income among
Maryland census tracts, 2000 (Apelberg 2005)
http//www.epa.gov/ttn/atw/nata/
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3. ACUTE VS CHRONIC DISEASE

• Acute Disease / Health Effects
• An illness or clinical symptoms that have a rapid
  onset and short but often severe course (eg,
  asthma or heart attack)
• Chronic Disease / Health Effects
• An illness or clinical symptoms that are
  prolonged, do not resolve spontaneously, and are
  rarely cured completely (eg, diabetes, cancer,
  multiple sclerosis, hypertension)
• What differentiates chronic from acute disease?
• Reversibility? Easier causal connection?
• Considerable blurring
• Exacerbations (acute) often require chronic
  disease substrate
• What of acute exposure (eg, Bhopal) that leads to
  subsequent chronic disease state (eg, emphysema
  and CHF)?
• Is premature death an acute or chronic effect?

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Measuring Disease

• What endpoint?
• Biomarkers
• BLLs, cotinine, DNA damage, PSA
• Community health questionnaire / survey
• Medication usage
• Clinic Visit
• Signs (measurable, eg, FEV, eosinophils)
• Symptoms (questionnaire, medical history)
• Diagnosis
• Hospitalization
• Emergency room visit
• Death
• Who, What, When and Where?

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4. THE E-D RELATIONSHIP
Example 1,3-Butadiene
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4. THE E-D RELATIONSHIP continued

• Types of studies
• Experimental and clinical trials
• Population (epidemiologic) studies
• Case-control (retrospective)
• Cohort (prospective)
• Ecologic
• Mixed
• Study methodologies
• Randomization, matching, spatial patterns,
  time-series, surveillance, questionnaire,
  molecular changes, controlling for confounding
• Money, time and availability of data are major
  constraints
• Take an environmental health / exposure history!
  Use a standardized form.

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5. THE 3 WORKSHOP QUESTIONS

• Do better exposure estimates lead to stronger
  associations?
• Probablyif youre measuring the right things, if
  you understand the causal pathway (if it exists),
  if you adjust for confounders, if you have
  sufficient numbers.
• Guard against waiting for the definitive study
• Is it preferable to focus on acute or chronic
  health effects?
• Intertwined. Chronic disease is of more public
  health importance, but acute effects easier and
  cheaper to measure and more likely to find useful
  associations for regulatory decisions.
• Do mortality and morbidity correlate with
  exposure?
• Correlation with CAPs, esp PM, strong across
  studies.
• CAPs may in part be surrogates for ATs.
• AT risk analyses suggest yes, but epi studies
  conflicting

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6. SELECTED HEALTH STUDIES

• CAP Major Prospective Studies
• CAPs ATTs?
• Ongoing methodological refinement confounder
  control
• Harvard 6-Cities Study (Dockery 1992, Lippman
  2003, Krewski 2004)
• 8,111 adults in 6 US cities
• FU 14-16 yr initial (b 1974-77)
• 26 mortality PM, sulfates
• Re-analyses find same
• American Cancer Society Study (Pope 1994,
  Lippman 2003, Krewski 2004)
• 295,223 adults in 50 US cities
• FU 6 yr initial (b 1982)
• 17 mortality PM
• Re-analyses find same

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6. SELECTED HEALTH STUDIES continued

• Major Retrospective Studies
• CAPs ATTs? Large Ns refinement of
  methodologies
• APHEA Air Pollution and Health - European
  Approach
• 30 European cities, extensive shared db and
  methodologies
• Multiple studies, publications (gt 40),
  re-analyses
• NMMAPS National Morbidity, Mortality, and Air
  Pollution Study
• 90 US cities chosen by size 14-yr period
• Multiple studies, publications, re-analyses
• 10-ppb O3 in previous week 0.52 mortality
  (Bell 2004)
• 0.41 mortality per 10 µg/m3 in PM10 (old
  GAM) 0.27 (new GAM) 0.21 (GLM) (Dominici
  2005)

(right) hospital admissions for ischemic
heart disease in persons gt65 yr per 10 µg/m3
PM10 for 0 1 average lag
Samoli 2003
Le Tertre 2003
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6. SELECTED HEALTH STUDIES continued

• Ambient Air Toxics
• Paucity of studiesfocus on clarifying exposure
• Oxygenated urban air toxics and asthma
  variability in middle school children A panel
  study (Delclos G, in review)
• 29 labile asthmatic children, age 10-13, in the
  Aldine school district. Examines measures of lung
  function with personal exposure to air toxics,
  especially aldehydes. Confounders measured
  included other indoor and outdoor pollutants, air
  exchange rate, temperature, humidity and activity
  level. 
• Increased risk of preterm delivery among people
  living near the three oil refineries in Taiwan
  (Yang 2004)
• Compared 7,095 first-parity singleton births to
  mothers living within 3 km (1.86 miles) of 3
  refineries with 10 random sample of births in
  rest of Taiwan (N50,388) between 1/1/1994 and
  12/31/1997. Controlled for multiple confounders.
• Outcome variable of interest preterm delivery
  (lt 37 weeks).
• AOR 1.14 (1.01-1.28)

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6. SELECTED HEALTH STUDIES continued

• Ambient Air Toxics continued
• The impact of polycyclic aromatic hydrocarbons
  and fine particles on pregnancy outcome (Dejmek
  2000)
• Compared birth outcomes (IUGR) in two communities
• Teplice and Prachatice N 3378 and 1505
• Similar levels of c-PAHs but Teplice has higher
  PM2.5
• Similar results for each 10 ng c-PAH in first
  gestational month, AOR 1.22 (1.07 1.39) for
  IUGR
• Suggests earlier association seen with PM due to
  PAH component

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6. SELECTED HEALTH STUDIES continued

• Ambient Air Toxics continued
• Asthma symptoms in Hispanic children and daily
  ambient exposures to toxic and criteria air
  pollutants (Delfino 2003)
• Panel study of 22 Hispanic asthmatic adolescents
  in LA
• Measured CAPs plus EC-OC, 10 ATs, asthma symptoms
  
• Significant AORs of asthma exacerbation
  associated with interquartile increase in
  pollutant concentrations included1.27
  (1.05-1.54) for 8-hr NO2 1.23 (1.02-1.48) for
  benzene1.37 (1.04-1.80) for formaldehyde 1.85
  (1.11-3.08) for EC1.88 (1.12-3.17) for OC

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6. SELECTED HEALTH STUDIES continued

• Ambient Air Toxics
• Effect of motor vehicle emissions on respiratory
  health in an urban area (Buckeridge 2002)
• SE Toronto. Ecologic study design
• Age- and gender-adjusted 1990-1992 hospital
  admission (respiratory vs genitourinary) rates
  by 334 EAs
• GIS used to create 10-m street buffers to
  estimate EA PM2.5 exposure based on daily
  traffic counts
• Adjusted for SES
• RR 1.24 (1.05-1.45) for respiratory subset
  (asthma, bronchitis, COPD, pneumonia, URI) for
  log10 in PM2.5

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7. BCM HC AP ADMITS STUDY

• Objective
• To analyze spatial relationships between hospital
  admissions and air pollution, with special
  attention to air toxics, in 337 4 x 4 km domains
  in Harris County, Texas.
• Year 1 August 2000 year 2 August October 2000
• Study Design
• Mixed-level ecologic correlation analysis

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7. BCM HC AP ADMITS STUDY continued

• Key collaborators
• Baylor College of Medicine (Hamilton WJ,
  Ningthoujam SS)
• University of Houston (Byun DW, Coarfa V, Kim S)
• UT School of Public Health (Chan W, Li Y)
• US Environmental Protection Agency (Ching JKS)
• Data sources
• Hospital admissions from THCIC RUDF
• Pollutant concentrations
• CMAQ-AT model hourly concentrations for each cell
• Concentrations from are monitors (TCEQ)
• Census 2000 data
• Median household income, minority, housing
• IRB approvals from TDSHS and BCM

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7. BCM HC AP ADMITS STUDY continued

• Hospital Admissions
• Hospital coverage
• 95 hospitals (77.6 of hospitals, 96.0 of beds)
• Two significant omissions LBJ (324
  beds)Quentin Meese (75 beds)
• HC residents admitted 44,078
• Exclusions 7,350
• Newborns 6,885
• Accidents 465
• No discharge diagnosis 40
• Total for geocoding 36,688
• Total geocoded 29,900 (81.5)

N 36,688
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7. BCM HC AP ADMITS STUDY continued

• Geocoded hospital admissions (N 29,900)

Cardiovascular6,284 (17.1) Respiratory2,946
(8.0) Cardiorespiratory7,467 (20.4) Other22,43
3 (61.2)
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7. BCM HC AP ADMITS STUDY continued

• EPAs CMAQ-AT Eulerian nested photochemical model
• MM5 meteorology
• NEI99, augmented by NTI99 and TEI2000
• SMOKE
• SAPRC99
• BCM receives text files for each pollutant with
  hourly concentrations
• Generate for each cell for August 2000
• Mean maximum
• Mean of 24-hr avg
• 12-hr AM (6 a 6 p)
• 12-hr PM (6 p 6 a)
• AT score from rankings

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7. BCM HC AP ADMITS STUDY continued

• Pollutant concentrations from area monitors
• Use IDL to run correlations

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7. BCM HC AP ADMITS STUDY continued
Mean 24-hour CMAQ-AT generated ozone
concentrations on August 1, 2000, in 337 4 x 4-km
cells in Harris County. Red denotes the highest
concentrations (35-45 ppbv) and the dark green
denotes the lowest (9-25 ppbv).
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7. BCM HC AP ADMITS STUDY continued
Median household income by cell. Dark green lt
25,000 red gt 70,000.
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THE AH, DUH FACTOR

• Convincing research is helpful
• Drives regulations
• Significantly increases compliance
• Great education tool
• However
• Research should not be used to delay
  implementation of commonsense regulations or
  education to reduce exposure
• Incentives for conservation, decreased vehicle
  use, decreased emissions
• Elimination of unnecessary toxic processes /
  practices
• Education about personal exposure
• and political leadership needed to implement
  the Ah, Duh Stuff, now, while continuing
  research

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Selected Sources

• Apelberg BJ, Buckley TJ, White RH. Socioeconomic
  and racial disparities in cancer risk from air
  toxics in Maryland. Environ Health Perspect
  113693-9(2005)
• Australias EPHC NEPM-AT program
  http//www.ephc.gov.au/nepms/air/air_toxics.html
• EPAs HAPs Database http//www.epa.gov/air/data/
• Buckeridge DL, Glazier R, Harvey BJ, et al.
  Effect of motor vehicle emissions on respiratory
  health in an urban area. Environ Health Perspect
  110293-300.(2002)
• Delfino RJ, Gong H, Jr., Linn WS, Pellizzari ED,
  Hu Y. Asthma symptoms in Hispanic children and
  daily ambient exposures to toxic and criteria air
  pollutants. Environ Health Perspect
  111647-56(2003)
• Dominici F, McDermott A, Daniels M, Zeger SL,
  Samet JM. Revised analyses of the National
  Morbidity, Mortality, and Air Pollution Study
  mortality among residents of 90 cities. J Toxicol
  Environ Health A 681071-92(2005)
• EPAs Integrated Risk Information System
  http//www.epa.gov/iris/
• EPAs TRI Explorer http//www.epa.gov/triexplorer/
  
• Leikauf GD. Hazardous air pollutants and asthma.
  Environ Health Perspect 110 Suppl 4505-26(2002)
• Le Tertre A, Medina S, Samoli E, et al.
  Short-term effects of particulate air pollution
  on cardiovascular diseases in eight European
  cities. J Epidemiol Community Health
  56773-9(2002)
• Lippmann M, Frampton M, Schwartz J, et al. The
  U.S. Environmental Protection Agency Particulate
  Matter Health Effects Research Centers Program A
  midcourse report of status, progress, and plans.
  Environ Health Perspect 1111074-92(2003)
• National Air Toxics Assessment (NATA)
  http//www.epa.gov/ttn/atw/nata/
• Payne-Sturges DC, Burke TA, Breysse P,
  Diener-West M, Buckley TJ. Personal exposure
  meets risk assessment a comparison of measured
  and modeled exposures and risks in an urban
  community. Environ Health Perspect
  112589-98(2004)
• Yang CY, Chang CC, Chuang HY, Ho CK, Wu TN, Chang
  PY. Increased risk of preterm delivery among
  people living near the three oil refineries in
  Taiwan. Environ Int 30337-42(2004)