Traffic- Related Air Pollution: A Critical Review of the Literature on

Emissions, Exposure, and Health Effects

Society for Risk AnalysisNovember 19, 2009

Maria CostantiniHealth Effects Institute

Goals of the ReviewSummarize 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 2009Formal Report published in January 2010

HEI Traffic Review PanelKenneth Demerjian—SUNY, Albany Mark Frampton—U Rochester Michael Jerrett—UC Berkeley 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 CollegeJon Samet—Johns HopkinsIra Tager—UC Berkeley, ChairMichael Walsh—Consultant

Emissions from Motor VehiclesThe 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

more people are near traffic sources of pollution

Emissions from Motor Vehicles

Emissions data and emission inventoriesare 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

• CO

• NO2

• PM2.5

• EC (also referred to as BC, BS, or soot)

• Ultrafine PM

• Benzene

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 NO2 and PM from Source

From Beckerman et al 2008

Spatial Extent Estimates

CO

EC

NO2

UFPM

Road to 100-400 m

Road to 200-500 m

Road to 100-300 m

Assessment of Exposure to Primary Traffic-Generated Air Pollution

Surrogates of traffic exposure used inepidemiologic 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 measuresof traffic

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.)

• 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

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

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

A.Sufficient evidence- all studies were of appropriate quality and at least one study measured traffic density or used modeled exposure

B.Suggestive but not sufficient evidence– as A, but studies only used distance measures

C. Inadequate and insufficient evidence

D. Suggestive of no association

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

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

Synthesis of Evidence

“Suggestive but insufficient” to infer causal association

Reasons

Too few studies

Relative imprecision of most estimates

Traffic Exposure and Asthma Incidence (in Children)

Synthesis of Evidence“Sufficient” OR “suggestive but insufficient” to infer causal associationReasonsStudies including both traffic-specific pollutantsand density measures most consistentStudies on incidence were consistent with studies of prevalence

Exacerbation of Asthma SymptomsIncrease in Wheeze in Children

Exacerbation of Asthma SymptomsIncrease in Wheeze in Children (cont.)

Synthesis of EvidenceExacerbations with asthma—”Sufficient” to infer causal association

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

Other Respiratory Symptoms(in Children)

Traffic Exposure and Allergies(in Children)

Synthesis of evidence“Inadequate and insufficient” to infer a causal association

ReasonWith a few inconsistent exceptions, results based on the skin-prick test or allergen-specific IgE failed to show associations with any of the traffic-pollutionResults for other endpoints (such as hay fever, eczema, itchy rash) were inconsistent

Traffic Exposure and Allergies(in Children)

Conclusions

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

• “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

• “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

Comparison of Epi and Tox ConclusionsCardiovascular morbidity

Epi: Suggestive, but not sufficient Tox: Evidence from tox not sufficient in isolation, but consistent with some epi findings. A case could bemade for a potential causal role of traffic pollutants in cardiovascular-disease morbidity

Exacerbation of asthmaEpi: Sufficient Tox: Evidence supportive of epi conclusions, but

studies are limited in the endpoints evaluatedNon-asthmatic allergy

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

synthesis is not possibleCancers

Epi: Inadequate and insufficient Evidence from in vitro and long-term studies to DEfor DNA damage and carcinogenicity, but it is difficult to relate results to humans; synthesis is premature

For a version of the report go to www.healtheffects.org