Transcript Slide 1

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
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
Kenneth 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 College
Jon Samet—Johns Hopkins
Ira Tager—UC Berkeley, 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
more people are near traffic
sources of pollution
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
•
•
•
•
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
Road to 100-400 m
NO2
Road to 200-500 m
UFPM
Road to 100-300 m
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.)
Direct measures
– Traffic exposure models
of traffic
• 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
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 association
Reasons
Studies including both
traffic-specific pollutants
and density measures most
consistent
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.)
Synthesis of
Evidence
Exacerbations with
asthma—”Sufficient”
to infer causal
association
Reasons
Large 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
Reason
With a few inconsistent
exceptions, results based on the
skin-prick test or allergenspecific IgE failed to show
associations with any of the
traffic-pollution
Results 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 nearsource 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
• “Inadequate and
insufficient” evidence to
Infer causal associations
• “Suggestive but insufficient”
evidence
– Mortality (all-cause and
cardiovascular)
– Cardiovascular morbidity
– Decreases in lung function
– General respiratory symptoms
– Adult onset asthma
– Health care utilization for
childhood and adult
respiratory diseases
– COPD
– Non-asthmatic allergy
– Birth outcomes
– Cancers
Comparison of Epi and Tox Conclusions
Cardiovascular morbidity
Epi: Suggestive, but not sufficient
Tox: 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 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 outcomes
Epi: Inadequate and insufficient
No overlap in outcomes between epi and tox;
synthesis is not possible
Cancers
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
For a version of the report go to
www.healtheffects.org