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Traffic- Related Air Pollution: A Critical Review of the Literature on Emissions, Exposure, and Health Effects. Society for Risk Analysis November 19, 2009 Maria Costantini Health Effects Institute. Goals of the Review. Summarize and synthesize relevant information on

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Traffic- Related Air Pollution:A Critical Review of the Literature on Emissions, Exposure, and Health Effects

Society for Risk Analysis

November 19, 2009

Maria Costantini

Health Effects Institute

goals of the review
Goals of the Review

Summarize and synthesize relevant information on

air pollution from traffic and its health effects linking

  • Information on tailpipe emissions with human exposure to traffic –related pollution
  • Human exposure to traffic pollution with human health effects (epidemiology)
  • Epidemiologic associations with toxicological results

A preprint of the report released in May 2009

Formal Report published in January 2010

hei traffic review panel
HEI Traffic Review Panel

Kenneth Demerjian—SUNY, Albany

Mark Frampton—U Rochester

Michael Jerrett—UCBerkeley

Frank Kelly—King’s College

Lester Kobzik—Harvard SPH

Nino Künzli—IMdM, Barcelona

Brian Leaderer—Yale SPH

Thomas Lumley—U of Washington SPH

Frederick Lurmann—Sonoma Tech. Inc

Sylvia Richardson—Imperial College

Jon Samet—Johns Hopkins

Ira Tager—UCBerkeley, Chair

Michael Walsh—Consultant

emissions from motor vehicles the current context
Significant progress has been made in reducing pollutant emissions from motor vehicles despite increases in number of vehicles and vehicle miles traveled

Increased urbanization and urban populations and changes in land use have:

Increased dependence on motor vehicles and traffic congestion

Emissions from Motor VehiclesThe Current Context

more people are near traffic sources of pollution

emissions from motor vehicles
Emissions from Motor Vehicles

Emissions data and emission inventories

are needed to:

  • Understand the relative contribution of motor vehicles emissions to air pollution in total and at specific locations
    • Contribution to PM, CO, NOx,, VOCs
  • Describe exposure
    • Trends in emissions in the context of transportation plans and introduction of new control technologies and new fuels
  • Improve the quality and range of pollutant surrogates
pollutant surrogate traffic pollution
Pollutant Surrogate Traffic Pollution
  • CO
  • NO2
  • PM2.5
  • EC (also referred to as BC, BS, or soot)
  • Ultrafine PM
  • Benzene
size distribution of pm
Size Distribution of PM

3 main classes of PM

Coarse - PM2.5-10 mass

Fine - PM2.5 mass

Ultrafine – PM0.1 number

Courtesy of David Kittelson and Winn Watts, 2009

gradients of no 2 and pm from source
Gradients of NO2 and PM from Source

From Beckerman et al 2008

spatial extent estimates




Road to 100-400 m

Road to 200-500 m

Road to 100-300 m

Spatial Extent Estimates
assessment of exposure to primary traffic generated air pollution
Assessment of Exposure to Primary Traffic-Generated Air Pollution

Surrogates of traffic exposure used in

epidemiologic studies

  • Pollutant surrogates (e.g., NO2, PM, EC/BS, CO, benzene, etc.)
  • Traffic exposure models
    • Estimate of traffic density or intensity
    • Distance from and/or length of roadways
    • Complex models that provide surrogate concentrations
      • Geostatistical interpolation, dispersion, land-use, and hybrid model

Direct measures

of traffic

conclusions on traffic exposure surrogates
Conclusions on Traffic Exposure Surrogates
  • None of the pollutant surrogates considered met all criteria for an ideal surrogate
    • CO, benzene, and NOx [NO2] found in on-road vehicle emissions are components of emissions from all sources and are also contributed by indoor sources. They have substantial variability across locations. Can be useful if measured with final spatial resolution.
    • PM2.5 as a surrogate of traffic pollution is of limited value because it is emitted by many sources and is well mixed within a region
    • UFPM have not been used in epidemiologic studies so far because the characterization of their spatial concentration gradients pose a significant challenge
conclusions on traffic exposure surrogates cont
Conclusions on Traffic Exposure Surrogates (cont.)
  • Exposure models have various degrees of utility to health studies depending on the quality of the input data
    • The measure of distance to road is the most error-prone and the least specific
    • Measures of traffic density and traffic flow are more specific
    • The hybrid model provides a feasible “best” estimate of exposure
      • Combines a model with time-activity data or personal monitoring
epidemiology criteria for inclusion of studies
Epidemiology Criteria for Inclusion of Studies

Based on type of exposure metric

  • Only studies in which the pollutant surrogates of exposure used were documented to have derived primarily from traffic or were measured in proximity of the residences and the roadways
  • Studies based direct measures or models of traffic

Exposure based on traffic density or derived from exposure

models (other than proximity) considered to be “best” surrogates”

epidemiology criteria for causal inference
Epidemiology Criteria for Causal Inference

4 categories1 used to infer causal association based on how well studies controlled for confounding, on the consistency of the findings across studies, and on the quality of the method to estimate exposure to primary traffic-generated pollutants

  • Sufficient evidence- all studies were of appropriate quality and at least one study measured traffic density or used modeled exposure
  • Suggestive but not sufficientevidence– as A, but studies only used distance measures
  • Inadequate and insufficient evidence
  • Suggestive of no association

1Adapted from US Surgeon General on the health consequences of ETS

epidemiology health outcomes evaluated
Epidemiology Health Outcomes Evaluated
  • Mortality (all cause, cardiopulmonary)
  • Cardiovascular morbidity
  • Respiratory outcomes (children and adults)
    • Asthma—childhood/adult
    • Respiratory symptoms
    • Health care utilization for respiratory problems
    • Lung function
    • COPD
  • Non-asthmatic allergy (children)
  • Birth outcomes
  • Cancer (children and adults)
long term traffic exposure and cardiopulmonary mortality
Long-Term Traffic Exposure and Cardiopulmonary Mortality

Synthesis of Evidence

“Suggestive but insufficient” to infer causal association


Too few studies

Relative imprecision of most estimates

traffic exposure and asthma incidence in children
Traffic Exposure and Asthma Incidence (in Children)

Synthesis of Evidence

“Sufficient” OR

“suggestive but insufficient”

to infer causal association


Studies including both

traffic-specific pollutants

and density measures most


Studies on incidence were consistent with studies of prevalence


Exacerbation of Asthma Symptoms

Increase in Wheeze in Children

exacerbation of asthma symptoms increase in wheeze in children cont
Exacerbation of Asthma SymptomsIncrease in Wheeze in Children (cont.)

Synthesis of Evidence

Exacerbations with asthma—”Sufficient” to infer causal association


Large number of studies with adequate control for confounding and mostly precise effect estimates

traffic exposure and allergies in children
Traffic Exposure and Allergies(in Children)

Synthesis of evidence

“Inadequate and insufficient”

to infer a causal association


With a few inconsistent exceptions, results based on the skin-prick test or allergen-specific IgE failed to show associations with any of the traffic-pollution

Results for other endpoints (such as hay fever, eczema, itchy rash) were inconsistent

exposure area of impact
Exposure – Area of Impact
  • Traffic-related pollutants impact ambient air quality on a broad spatial scale ranging from roadside, to urban, to regional background
  • Based on synthesis of evidence, 300-500 meters from a major road was identified as the near-source area most impacted by traffic; variations exist depending on meteorology, background pollution, and local factors
conclusions from epidemiologic studies
Conclusions From Epidemiologic Studies
  • “Inadequate and insufficient” evidence to Infer causal associations
    • Adult onset asthma
    • Health care utilization for childhood and adult respiratory diseases
    • COPD
    • Non-asthmatic allergy
    • Birth outcomes
    • Cancers
  • “Sufficient ” evidence to Infer causal associations
    • Exacerbation of asthma
    • Asthma incidence in children
  • “Suggestive but insufficient” evidence
    • Mortality (all-cause and cardiovascular)
    • Cardiovascular morbidity
    • Decreases in lung function
    • General respiratory symptoms
comparison of epi and tox conclusions
Comparison of Epi and Tox Conclusions

Cardiovascular morbidity

Epi: Suggestive, but not sufficientTox: Evidence from tox not sufficient in isolation, but

consistent with some epi findings. A case could be

made for a potential causal role of traffic pollutants in cardiovascular-disease morbidity

Exacerbation of asthma

Epi: Sufficient Tox: Evidence supportive of epi conclusions, but studies are limited in the endpoints evaluated

Non-asthmatic allergy

Epi: Inadequate and insufficientTox: Data supported a stronger inference that the epi (by

providing mechanistic evidence for associations

of traffic pollution and IgE-mediated allergic reactions),

but studies used non relevant exposure routes and doses

Birth outcomes

Epi: Inadequate and insufficient No overlap in outcomes between epi and tox;

synthesis is not possible


Epi: Inadequate and insufficient Evidence from in vitro and long-term studies to DE

for DNA damage and carcinogenicity, but it is difficult

to relate results to humans; synthesis is premature