All reflection discussions must be 1-2 pages (approx. 500 words) and use APA citation style.
- Provide citations for 2 readings (APA citation style)
- Provide a summary for each reading
- Discuss the major theme(s) or argument(s) of each reading
- In 1-2 paragraphs, discuss your thoughts on the readings and how they connect to the week’s lesson.
11/16/2020 The Role of Highways in American Poverty – The Atlantic
https://www.theatlantic.com/business/archive/2016/03/role-of-highways-in-american-poverty/474282/ 1/5
Sunday tra�ic from New York City to the Jersey Shore in 1941 (LIBRARY OF CONGRESS )
Editor’s Note: is article is adapted from remarks delivered by the author on March 16 at
the University of Arkansas’s Clinton School of Public Service, in Little Rock.
Little Rock is a fascinating city. With its river and renovated warehouses and bustling
River Market district, it reminds me a little bit of Pittsburgh, where I lived a decade ago
when I was starting my journalism career. At that time, Pittsburgh was still the butt of
many jokes, though determined city planners were starting to drive the transformation
that’s made it so popular. Today, there’s a growing population downtown and tech
companies are locating in the city once known for steel.
It’s a funny thing about cities: ey’re all unique, but they sometimes experience busts
and booms in the same way. Just look at all the cities across the country that are
experiencing a craft-beer renaissance and have condos in renovated warehouses
downtown.
Perhaps that’s why policymakers in the 1940s and 1950s thought of cities as human
bodies, bodies that had sicknesses and required cures. Bodies that got sick from the
same diseases and would improve from the same medicine.
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e postwar years were a time of unprecedented prosperity, when Americans were
buying refrigerators and televisions and homes, and wanted to leave the crowded heart
of city centers for space to put all their new belongings. e rise of the automobile
helped them do this. In 1940, 60 percent of Americans owned cars. In 1960, 80
percent did. Today, 95 percent of Americans own cars.
is increase of people heading to the suburbs in their cars caused something else new:
lots and lots of traffic. And to city planners, this was making communities unhealthy.
By the 1950s, highways were being recommended as “the greatest single element in the
cure of city ills,” according to Joseph DiMento, an Irvine professor who has studied
highway construction during that era. To keep cities healthy, planners said, regions
BUSINESS
e Role of Highways in American
Poverty
ey seemed like such a good idea in the 1950s.
ALANA SEMUELS MARCH 18, 2016
What Motivates Companies to Do Good—Altruism, or Guilt?•
e False Promise of Last Year’s Wage Gains•
e Folly of State-Level Tax Cuts•
https://www.theatlantic.com/category/next-economy
http://papers.ssrn.com/sol3/papers.cfm?abstract_id=1392502
https://www.theatlantic.com/business/
https://www.theatlantic.com/author/alana-semuels/
https://www.theatlantic.com/business/archive/2016/03/what-motivates-companies-to-do-good/473511/
https://www.theatlantic.com/business/archive/2016/03/analyzing-2015s-wage-gains/473226/
https://www.theatlantic.com/business/archive/2016/03/state-budget-crisis/473157/
11/16/2020 The Role of Highways in American Poverty – The Atlantic
https://www.theatlantic.com/business/archive/2016/03/role-of-highways-in-american-poverty/474282/ 2/5
needed unclogged arteries for a working circulatory system. In short, cities needed
highways to carry people out of the heart and to the rest of the body.
Luckily for city planners who wanted to keep their cities healthy, there was federal
money available to anyone who wanted to put in modern highways. While the 1944
Federal Highway Act only offered to cover 50 percent of construction costs for
highways, by 1956, the federal government had upped that share to 90 percent. So if
you’re a city planner in the 1950s, you can put in roads from your city to the fast-
growing suburbs for almost no cost at all.
Of course, there were people who couldn’t move to the suburbs. African Americans
were denied home loans by the federal government in certain areas, a practice called
redlining. Restrictive covenants prevented homeowners from selling to certain types of
people, often including African Americans. And they were also denied jobs and other
opportunities that would have allowed them to afford to buy a home in the �rst place.
When I was in Syracuse, I met a man named Manny Breland, who received a
scholarship to play basketball at Syracuse, graduated with a teaching degree, and was
denied job after job because he was black.
In many cities, these restrictions left African Americans crowded into small
neighborhoods. ey essentially weren’t allowed to move anywhere else.
City planners had a solution for this, too. ey saw the crowded African American areas
as unhealthy organs that needed to be removed. To keep cities healthy, planners said,
these areas needed to be cleared and redeveloped, the clogged hearts replaced with
something newer and spiffier. But open-heart surgery on a city is expensive. Highway
construction could be federally funded. Why not use those federal highway dollars to
also tear down blight and rebuild city centers?
e urban planner Robert Moses was one of the �rst to propose the idea of using
highways to “redeem” urban areas. In 1949, the commissioner of the Bureau of Public
Roads, omas MacDonald, even tried to include the idea of highway construction as a
technique for urban renewal in a national housing bill. (He was rebuffed.) But in cities
across America, especially those that didn’t want to—or couldn’t—spend their own
money for so-called urban renewal, the idea began to take hold. ey could have their
highways and they could get rid of their slums. With just one surgery, they could put in
more arteries, and they could remove the city’s heart.
is is exactly what happened in Syracuse, New York. e city had big dreams of
becoming an East Coast hub, since it was close to New York City, Pittsburgh,
Cleveland, and Boston. (In the early days of the car, close was relative.) Use federal
funds to build a series of highways, planners thought, and residents could easily get to
the suburbs and to other cities in the region. After all, who wouldn’t want to live in a
Syracuse that you could easily leave by car? And, if they put the highway in just the
right place, it would allow the city to use federal funds to eradicate what they called a
slum area in the center city.
at neighborhood, called the 15th Ward, was located between Syracuse University and
the city’s downtown. It was predominantly African American. One man who lived there
at the time, Junie Dunham, told me that although the 15th Ward was poor, it was the
type of community that you often picture in 1950s America: fathers going off to jobs in
the morning; kids playing in the streets; families gathering in the park on the weekends
or going on Sunday strolls. He remembers collecting scraps from the streets and
bringing them to the junkyard for pennies, which he would use to buy comics.
To outsiders, though, the 15th Ward was the scene of abject poverty close to two of
Syracuse’s biggest draws—the university and downtown. ey worried about race riots
because so many people were crowded into the neighborhood and prevented from
going anywhere else. ey decided that the best plan would be to tear down the 15th
Ward and replace it with an elevated freeway.
e completion of the highway, I-81, which ran through the urban center, had the
same effect it has had in almost all cities that put interstates through their hearts. It
decimated a close-knit African American community. And when the displaced residents
from the 15th Ward moved to other city neighborhoods, the white residents �ed. It was
easy to move. ere was a beautiful new highway that helped their escape.
But this dynamic hurt the city’s �nances, too. As suburbs grew, they broke off from
cities, taking with them tax revenues, even though their residents still used city services.
Although the Syracuse region was relatively healthy, the city started to get very sick.
http://www.pbs.org/wnet/need-to-know/environment/the-legacy-of-robert-moses/16018/
https://www.theatlantic.com/business/archive/2015/11/syracuse-slums/416892/
11/16/2020 The Role of Highways in American Poverty – The Atlantic
https://www.theatlantic.com/business/archive/2016/03/role-of-highways-in-american-poverty/474282/ 3/5
Between 1940 and 2000, the population of the city of Syracuse shrank 30 percent, from
about 205,000 to 147,000. e population of Onondaga County, where Syracuse is
located, grew 55 percent, from 295,000 to 458,000.
Even today, the region is continuing to sprawl. e population of Onondaga County
peaked in 1970 and has stayed even since then. But residents are moving farther and
farther out. e county has added 7,000 housing units, 147 subdivisions, and 61 miles
of new roads since 2000. Developers build 160 units a year in areas that were once
rural. at’s costing the county money and resources as it adds sewer systems, water
pipes, and stormwater drainage to far-�ung subdivisions. As the county spends money,
the city is struggling to come up with enough revenue for essential things like mass
transit and schools.
What’s more, as the suburbs grow, they’re continuing to make sure that only wealthy
people can live there. ey pass zoning laws that restrict multifamily units. ey require
minimum lot sizes so that their only residents are people who can afford to live in big
houses. It’s a different kind of discrimination than half a century ago, but
discrimination nonetheless.
Today, the city of Syracuse has the highest concentration of poverty in America. What
that means is that large proportions of its population live below the federal poverty line,
and that they’re surrounded by other poor people, too. Nearly two-thirds of the black
poor live in high-poverty neighborhoods in Syracuse. Around 62 percent of the
Hispanic poor live in high-poverty neighborhoods.
Of course, the highway isn’t the only reason there’s so much concentrated poverty in
Syracuse. e economy has changed, and big employers such as the Carrier
Corporation and other manufacturing companies have left for overseas. Wages in
Syracuse and across America have remained stagnant, so even those people who are
employed are �nding it is much harder to make ends meet than it used to be.
Ironically, the people who are left in Syracuse now live in more concentrated poverty
than the people of the 15th Ward, which city leaders saw as so blighted decades ago.
is is bad for the health of the region. We know that people who live in concentrated
poverty have a much harder time succeeding because they’re surrounded by other poor
people. e economist Raj Chetty made this very clear in a series of papers he’s
published in the last two years through the Equality of Opportunity project. He found
that neighborhoods matter, and that a low-income child who is born in certain low-
income neighborhoods has a much smaller shot of achieving upward mobility than a
low-income child born in a better neighborhood.
Now, there are programs that move poor families from areas of concentrated poverty to
wealthy suburbs. I’ve written about some of them. Children thrive when they’re taken
out of housing projects and moved to condos where there are trees, parks, places to ride
their bikes, and good schools nearby. But it’s not realistic to move every family to a
different neighborhood, and besides, many people don’t want to move.
What does work, though, is bringing cities together so that poverty isn’t so
concentrated, so that the rich can’t just leave or wall themselves off from the poor, so
that the poor aren’t trapped in areas of concentrated poverty—what people used to call
slums.
* * *
In the last decade, Americans’ ideas of where they want to live have been changing.
Young professionals and Baby Boomers are moving back to inner cities, fueled by the
desire to live somewhere walkable, near restaurants, bars, and offices, where they don’t
need to have cars. A freeway passing through the heart of a city does not jibe very well
with an urban renaissance.
After all, walkable cities where people want to live probably don’t also have noisy
highways that create physical and psychological rifts that are extremely difficult to
bridge.
In some cities, planners have decided to help that urban renaissance and tear down the
freeways that seemed like a good idea in the 1950s.
Boston tore down its Central Artery in its famous Big Dig, turning a waterfront area of
the city that had long been clogged with traffic into a popular park and walking area.
Milwaukee demolished the Park East freeway in 1999 and urban development has
blossomed in the neighborhoods created by the highway’s removal. Manpower
http://www.syracuse.com/news/index.ssf/2015/09/syracuse_has_nations_highest_poverty_concentrated_among_blacks_hispanics.html
http://equality-of-opportunity.org/images/mobility_geo
http://www.nielsen.com/us/en/insights/news/2014/millennials-prefer-cities-to-suburbs-subways-to-driveways.html
https://www.theatlantic.com/business/archive/2015/11/highways-destroyed-americas-cities/417789/
11/16/2020 The Role of Highways in American Poverty – The Atlantic
https://www.theatlantic.com/business/archive/2016/03/role-of-highways-in-american-poverty/474282/ 4/5
Corporation moved its headquarters to the area, and the average assessed land value
there grew 45 percent. e economically depressed town of New Haven is in the midst
of a project called Downtown Crossing, which has removed parts of Route 34 and is
creating a business district in an area of town bisected by the freeways.
Even some people in Syracuse want to tear down I-81. Like many highways built by
idealistic planners in the 1950s, I-81 is reaching the end of its useful life, according to
engineers. It isn’t wide enough to meet current highway standards, and parts of it are
literally falling apart. Some urban planners want to tear it down to create an urban
boulevard. For more than half a century, the road has divided the city, they say, and it’s
time to knit it together back again.
Some cities are taking the opposite approach. Alabama’s highway department is seeking
to widen parts of a highway that bisect Birmingham, Alabama, though the proposal
faces opposition from business leaders. Florida’s highway department declined to tear
down a highway in Miami called the Overton Expressway.
In the 1950s, when so many highways were built, planners across the country wanted to
help citizens access the prosperity that seemed accessible to everyone in the postwar
years. But starting with the exodus to the suburbs around that time, and continuing to
this day, prosperity has been out of reach for many Americans.
If part of a body is sick, the whole body can’t be healthy, and many cities across America
have parts that aren’t doing very well. But there are regions that are trying to become
healthier by coming together, rather than pulling apart. Tearing down a highway can be
one way to do this. But it’s not the only way. My colleague Derek ompson has
written about the miracle of Minneapolis, where high-income communities share tax
revenues and real estate with lower-income communities to spread prosperity. A year
ago, I visited Louisville, where a court ordered the county and city to combine their
school districts in order to integrate their schools. Today, Louisville is still trying to keep
its county and city schools integrated, even after the Supreme Court told the city it no
longer had to do so. In Chicago, a regional housing authority that covers eight counties,
including Cook County, is working to move families from the inner city to higher-
opportunity neighborhoods. Some cities use inclusive zoning, in which all new
construction must include a certain percentage of housing for low-income residents,
which means that the wealthy can’t separate themselves from the poor.
ese cities have tried to tear down barriers that prevent all of their residents from
reaching their full opportunity. Sometimes those barriers are highways. Sometimes
they’re something else entirely. Tearing down a highway isn’t the only way to make a
city healthy again. But building a new one—or expanding an existing one—seems a
sure�re way to make a city sick.
We want to hear what you think about this article. Submit a letter to the editor or write to
letters@theatlantic.com.
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Special RepoRt 1
7
January 20
10
Traffic-Related Air Pollution: A Critical
Review of the Literature on
Emissions, Exposure, and Health Effects
A Special Report of the HEI Panel on the Health Effects
of Traffic-Related Air Pollution
ExECuTIvE SummARy
ABOuT HEI
The Health Effects Institute is a nonprofit corporation chartered in 1
9
8
0 as an independent
research organization to provide high-quality, impartial, and relevant science on the effects
of air pollution on health. To accomplish its mission, the institute
• Identifies the highest-priority areas for health effects research;
• Competitively funds and oversees research projects;
• Provides intensive independent review of HEI-supported studies and
related research;
• Integrates HEI’s research results with those of other institutions into
broader evaluations; and
• Communicates the results of HEI research and analyses to public and
private decision makers.
HEI receives half of its core funds from the u.S. Environmental Protection Agency and
half from the worldwide motor vehicle industry. Frequently, other public and private
organizations in the united States and around the world also support major projects
or certain research programs. Additional work for this report was funded by the u. S.
Federal Highway Administration.
HEI has funded more than 280 research projects in North America, Europe, Asia, and
Latin America, the results of which have informed decisions regarding carbon monoxide,
air toxics, nitrogen oxides, diesel exhaust, ozone, particulate matter, and other pollutants.
These results have appeared in the peer-reviewed literature and in more than 200
comprehensive reports published by HEI.
HEI’s independent Board of Directors consists of leaders in science and policy who are
committed to fostering the public–private partnership that is central to the organization.
The Health Research Committee solicits input from HEI sponsors and other stakeholders
and works with scientific staff to develop a Five-year Strategic Plan, select research projects
for funding, and oversee their conduct. The Health Review Committee, which has no role
in selecting or overseeing studies, works with staff to evaluate and interpret the results of
funded studies and related research.
All project results and accompanying comments by the Health Review Committee are
widely disseminated through HEI’s Web site (www.healtheffects.org), printed reports,
newsletters, and other publications, annual conferences, and presentations to legislative
bodies and public agencies.
special report 17
INTRODUCTION
Motor vehicles are a significant source of urban air pollu-
tion and are increasingly important contributors of anthropo-
genic carbon dioxide and other greenhouse gases. As awareness
of the potential health effects of air pollutants has grown, many
countries have implemented more stringent emissions controls
and made steady progress in reducing the emissions from motor
vehicles and improving air quality. However, the rapid growth of
the world’s motor-vehicle fleet due to population growth and eco-
nomic improvement, the expansion of metropolitan areas, and
the increasing dependence on motor vehicles because of changes
in land use has resulted in an increase in the fraction of the popu-
lation living and working in close proximity to busy highways
and roads — counteracting to some extent the expected benefits
of pollution-control regulations and technologies.
This Special Report, developed by the Health Effects Institute
(HEI) Panel on the Health Effects of Traffic-Related Air Pollu-
tion, summarizes and synthesizes information linking emis-
sions from, exposures to, and health effects of traffic sources
(i.e., motor vehicles). The term traffic-related exposure is used
in this report to refer to exposure to primary emissions from
motor vehicles, not to the more broadly dispersed secondary
pollutants such as ozone (O
3
) that are derived from these emis-
sions. The report focuses on specific scenarios with a high
aggregation of motor vehicles and people — that is, urban set-
tings and residences in proximity to busy roadways.
EMISSIONS FROM MOTOR VEHICLES
Motor vehicles emit large quantities of carbon dioxide (CO2),
carbon monoxide (CO), hydrocarbons (HC), nitrogen oxides
(NOX), particulate matter (PM), and substances known as mobile-
source air toxics (MSATs), such as benzene, formaldehyde, acet-
aldehyde, 1,3-butadiene, and lead (where leaded gasoline is
still in use). Each of these, along with secondary by-products,
such as ozone and secondary aerosols (e.g., nitrates and inor-
ganic and organic acids), can cause adverse effects on health
and the environment. Pollutants from vehicle emissions are
related to vehicle type (e.g., light- or heavy-duty vehicles) and
age, operating and maintenance conditions, exhaust treatment,
type and quality of fuel, wear of parts (e.g., tires and brakes),
and engine lubricants used. Concerns about the health effects of
motor-vehicle combustion emissions have led to the introduc-
tion of regulations and innovative pollution-control approaches
throughout the world that have resulted in a considerable reduc-
tion of exhaust emissions, particularly in developed countries.
These reductions have been achieved through a comprehensive
strategy that typically involves emissions standards, cleaner
fuels, and vehicle-inspection programs. Recognizing the likely
continued growth in the vehicle fleet and the remaining prob-
lems in traffic-related air quality, the United States, European
countries, Japan, and other countries are continuing to push for
even stricter emissions controls in coming years.
Resuspended road dust, tire wear, and brake wear are sources of
noncombustion PM emissions from motor vehicles. As emissions
controls for exhaust PM become more widespread, emissions from
noncombustion sources will make up a larger proportion of vehi-
cle emissions. Noncombustion emissions contain chemical com-
pounds, such as trace metals and organics, that might contribute
to human health effects. However, current estimates of these emis-
sions are highly uncertain. Thus, although they are not regulated
in the way exhaust emissions are, noncombustion emissions will
need to be considered more closely in future assessments of the
impact of motor vehicles on human health.
The quantification of motor-vehicle emissions is critical in
estimating their impact on local air quality and traffic-related
exposures and requires the collection of travel-activity data
over space and time and the development of emissions inven-
tories. Emissions inventories are developed based on complex
emissions models (of which the U.S. Environmental Protection
Agency’s MOBILE6 has been the most widely used) that pro-
vide exhaust and evaporative emissions rates for total HC, CO,
NOx, PM, sulfur dioxide (SO2), ammonia (NH3), selected air tox-
ics, and green house gases (GHGs) for specific vehicle types and
fuels. The quality of the travel-activity data (such as vehicle-
miles traveled, number of trips, and types of vehicles) and the
complex algorithms used to derive the emissions factors sug-
gest the presence of substantial uncertainties and limitations
in the resulting emissions estimates (NARSTO 200
5
). It should
be noted that estimates of PM emissions have had very limited
field valuation and verification.
The actual measurement of motor-vehicle emissions is critically
important for validating the emissions models. Studies that have
sampled the exhaust of moving vehicles in real-world situations
(specifically, in tunnels or on roadways) have contributed very
useful information about the emissions rates of the current motor-
vehicle fleet and also have allowed the evaluation of the impact of
new emission-control technologies and fuels on emissions.
EXECUTIVE SUMMARY
Traffic-Related Air Pollution: A Critical Review of the
Literature on Emissions, Exposure, and Health Effects
This Executive Summary is excerpted from HEI Special Report 17, Traffic-Related
Air Pollution: A Critical Review of the Literature on Emissions, Exposure, and
Health Effects, by the Institute’s Panel on the Health Effects of Traffic-Related Air
Pollution. The entire report is available at www.healtheffects.org or from HEI.
This document was produced with partial funding by the United States Environ-
mental Protection Agency under Assistance Award CR–8323
4
701 to the Health
Effects Institute; however, it has not been subjected to the Agency’s peer and admin-
istrative review and therefore may not necessarily reflect the views of the Agency,
and no official endorsement by it should be inferred. The contents of this docu-
ment also have not been reviewed by private party institutions, including those
that support the Health Effects Institute; therefore, it may not reflect the views or
policies of these parties, and no endorsement by them should be inferred.
3
ExECuTIvE SummARy
special report 17
Receptor models have been used to estimate the contributions
of various types of sources, including motor vehicles, to ambi-
ent air pollution. Some of the models (those defined as chemi-
cal mass balance models) require the knowledge of the chemi-
cal profile of both the emissions of all the area sources and the
air at the receptor (that is, the impacted location). Other models
(referred to as principal components and factors analyses) do not
require a priori knowledge of the source profiles. The application
of these models has yielded a wide range of results on the contri-
bution of motor vehicles to ambient pollution, depending on the
model, the location of the monitoring sites, and the other sources
present. In U.S. cities, the results show that motor-vehicle con-
tributions range from 5% in Pittsburgh, Pa., under conditions
with very high secondary aerosol, to 49% in Phoenix, Ariz., and
55% in Los Angeles, Calif. Outside the United States, estimates
of the motor-vehicle contribution to PM2.5 (PM # 2.5 µm in aero-
dynamic diameter) range from 6% in Beijing, China, to 53% in
Barcelona, Spain.
Ultimately, an important goal of emissions-characterization
studies is to improve our ability to quantify human exposure to
emissions from motor vehicles, especially in locations with high
concentrations of vehicles and people. Such characterization
requires improving emissions inventories and a more complete
understanding of the chemical and physical transformations on
and near roadways that can produce toxic gaseous, semivolatile,
and particle-phase chemical constituents.
ASSESSMENT OF EXPOSURE TO TRAFFIC-RELATED
AIR POLLUTION
Traffic-related emissions contribute to primary and second-
ary local, urban, and regional (background) pollutant concen-
trations against a background of similar contaminants emitted
from other sources. Traffic emissions are the principal source of
intra-urban variation in the concentrations of air pollutants in
many cities; thus, population-oriented central monitors cannot
by themselves capture this spatial variability. Studies that have
examined gradients in pollutants as a function of distance from
busy roadways have indicated exposure zones for traffic-related
air pollution in the range of 50 to 1500 m from highways and
major roads, depending on the pollutant and the meteorologic
conditions.
Because it is not practical or feasible to measure all the com-
ponents of the traffic-pollutant mix, surrogates of traffic-related
pollution have been used as a reasonable compromise for assess-
ing the contribution of traffic emissions to ambient air pollution
and for estimating traffic exposure. Surrogates can also help in
the assessment of spatial and temporal distributions of ambi-
ent pollution related to motor vehicles and of traffic-mitigation
control strategies.
Two broad categories of surrogates have been used in epide-
miology studies to estimate traffic exposure: (1) measured or
modeled concentrations of pollutant surrogates and (2) direct
measures of traffic itself (such as proximity, or distance, of the
residence to the nearest road and traffic volume within buffers).
The most commonly used traffic-pollutant surrogates include CO,
NO2, elemental carbon (EC; or black carbon [BC] or black smoke
[BS]), PM, benzene, and ultrafine particles (UFP). Exposure mod-
els include geostatistical interpolation, land-use regression, dis-
persion, and hybrid models (the latter combine time–activity data,
personal measurements, and models). They incorporate numer-
ous parameters (such as meteorologic variables, data on land use,
traffic data, and monitoring data or emissions rates depending
on the model) and can improve the spatial representation of the
local impact of traffic against a background of regional and urban
concentrations. However, the accuracy of the inputs is critical to
the usefulness of any given model.
None of the pollutant surrogates considered in the report met
all the criteria for an ideal surrogate. Data are not available to
assess the ratios of the surrogates to emissions from all sources
over time. CO, benzene, and NOx (in this case NO2), found in
on-road vehicle emissions, are components of emissions from all
sources, making it difficult to disentangle the contributions from
motor vehicles from other sources (including some in indoor
environments). Primary, on-road vehicle emissions of PM (PM2.5
or PM10 [PM # 10 µm in aerodynamic diameter]) represent only a
small contribution to emissions from all sources, typically around
3%. EC has been used as a surrogate, primarily for diesel exhaust,
although it is not a specific marker, unless other sources are ruled
out. UFP concentrations are very high in vehicle-exhaust plumes
but decrease rapidly with distance from the source, which poses
a significant challenge for characterization of the spatial and tem-
poral concentration gradients of UFP from roadway traffic.
With regard to exposure models, the Panel noted that,
although proximity models (direct measures of traffic) are the
easiest to implement, they are error prone because they ignore
the parameters that affect the dispersion and physicochemical
activity of the pollutants. Moreover, estimates based on proxim-
ity can be confounded by factors such as socioeconomic status
and noise. Geostatistical interpolation models are best imple-
mented in conjunction with dense, well-distributed monitoring
networks; their chief limitations are the size of the network and
the number of measurements needed over time to estimate the
spatial distribution of pollution surrogates accurately. Land-use
regression is appealing in that it can account for the diversity of
sources that contribute to a surrogate; however, the true contri-
bution (in terms of associated variance) of traffic to the regres-
sion is not always known or reported. Dispersion models utilize
motor-vehicle–emissions and air-quality data and incorporate
meteorologic data, but must be calibrated correctly to realize
their advantages. These models are very data- and computation-
intensive and depend on the validity of the model assumptions.
Hybrid models that combine measurements of personal expo-
sure to traffic surrogates or time–activity data with exposure
models come closest to a logistically feasible “best” estimate of
human exposure.
4
special report 17
ExECuTIvE SummARy
Factors influencing ambient concentrations of a traffic-pollut-
ant surrogate are related to time–activity patterns, meteorologic
conditions, vehicle volume and type, driving patterns, land-use
patterns, the rate at which chemical transformations take place,
and the degree to which the temporal and spatial distribution of
the surrogate reflects the traffic source.
To improve assessment of exposure to traffic-related pollution,
a potential solution is the deployment of a large number of moni-
tors in places where concentrations of air pollutants are expected
to be highly variable and the population density is high. The use
of models that incorporate numerous spatial factors in order to
estimate exposures that are more relevant to the individual’s
exposure situation can also be helpful.
The Panel concluded that the impact of vehicle emissions
extends beyond the local scale to the urban and regional scales.
What people are exposed to is influenced by their proximity to
the sources, the presence of other ambient or microenvironmen-
tal sources, and time–activity patterns. If, as the evidence sug-
gests, groups of lower socioeconomic status experience higher
exposures than groups of higher socioeconomic status, this mer-
its consideration in the interpretation of epidemiologic findings
and in future regulatory actions.
Based on a synthesis of the best available evidence, the Panel
identified an exposure zone within a range of up to 300 to 500 m
from a highway or a major road as the area most highly affected
by traffic emissions (the range reflects the variable influence of
background pollution concentrations, meteorologic conditions,
and season) and estimated that 30% to 45% of people living in
large North American cities live within such zones.
HEALTH EFFECTS OF TRAFFIC-RELATED AIR
POLLUTION: EPIDEMIOLOGY AND TOXICOLOGY
In reviewing the epidemiologic literature on the association
between exposure to traffic-related air pollution and health out-
comes, the Panel developed criteria for the inclusion of stud-
ies based on the characterization of traffic exposure. The Panel
decided to include only studies that investigated associations
between primary emissions from traffic and human health and
that provided specific documentation of a traffic source and
estimates of exposure on a local scale. Thus, studies that relied
exclusively on measurements from a central monitoring site
were not included unless the site was in proximity to traffic. The
Panel also developed criteria for inferring whether associations
between exposure and health outcome were causal by adapting
the criteria used by the U.S. Surgeon General in the report The
Health Consequences of Smoking: A Report of the Surgeon Gen-
eral (U.S. Department of Health and Human Services 2004). In
order to deem the evidence sufficient to conclude that association
between a metric of traffic exposure and an outcome was causal,
it was necessary for the magnitude and direction of the effect esti-
mates to be consistent across different populations and times and
to rule out with reasonable confidence chance, bias in subject
selection, and confounding (in particular, socioeconomic sta-
tus). The four inference criteria applied to this review are listed
in Table 1. To these criteria the Panel added a traffic-specific
coherence criterion (also included in Table 1) to account for the
degree of validity of the traffic-specific exposure metrics. As
noted earlier, the Panel concluded that not all traffic-exposure
measures have equivalent validity and considered simple mea-
sures of proximity to roads or road length and of pollutant sur-
rogates without specific traffic data to be the least specific. The
proximity measures are also likely to introduce confounding.
Modeled estimates of exposure to traffic pollution were thought
to be, a priori, more valid than traffic density estimates alone
because they account for other factors that affect the exposure,
such as geography, land use, and meteorology, when making
estimates for particular locations. In addition, the validity of
estimates can be enhanced by modeling strategies that sepa-
rately estimate the contribution of traffic and background pollu-
tion to personal exposure.
The Panel developed qualitative and quantitative summa-
ries (in tables and figures) for the estimates of the associations
between traffic-related exposure and various health outcomes for
the studies reviewed, but did not derive meta-analytic summaries
by pooling associations estimates because of the lack of equiva-
lence among the exposure measures and populations studied.
The Panel also reviewed the literature on the toxicology of
traffic-related pollution. This included studies of direct expo-
sures to traffic emissions (though there were very few in this cat-
egory), studies that utilized laboratory atmospheres that replicate
aspects of the traffic mix (such as concentrated ambient particles,
or gasoline or diesel exhaust), and studies of specific components
of emissions from motor vehicles. The aim was to identify pos-
sible mechanisms by which exposure to traffic pollutants may
cause effects and provide an understanding of the role of traffic
emissions in the effects being observed in epidemiology studies.
While toxicology studies are limited in their ability to capture the
full complexity of human exposure — because of the small num-
ber of subjects and, in animal studies, the relevance of the results
to humans — they offer the opportunity to explore hypotheses on
specific pathophysiologic mechanisms of action.
The Panel evaluated whether oxidative stress might be the
underlying mechanism of action by which exposure to pollutants
from traffic may lead to adverse health effects. Oxidative stress
results from events occurring in any tissue in the body when
the prooxidant–antioxidant balance is disturbed. This imbal-
ance can happen when the generation of reactive oxygen species,
or free radicals, exceeds the available antioxidant defenses and
is characterized by the presence of increased cellular concen-
trations of oxidized lipids, proteins, and DNA. Oxidative stress
can trigger inflammatory reactions, which lead to an increased
production of oxidants by activated phagocytes recruited to the
airways, perpetuating the cycle of oxidative injury.
The Panel concluded that, although the evidence supported
the hypothesis that oxidative stress is an important determinant
of health effects associated with ambient air pollution in general,
5
ExECuTIvE SummARy
special report 17 6
special report 17
ExECuTIvE SummARy
the extent to which primary traffic-related pollutants contribute
to the burden of reactive oxygen species experienced by humans
near roadways remains undefined.
The Panel’s main conclusions regarding the epidemiologic
associations between exposure to traffic-related air pollution
and health outcomes and the toxicologic evidence (when avail-
able) are presented below for each health outcome. A discussion
of the extent to which toxicology studies do or do not provide
general mechanistic support for the observations and inferences
contributed by epidemiology studies is also provided.
all-caUSe aND caRDioVaScUlaR MoRtalitY
epidemiology
Very few studies of all-cause mortality or cardiovascular mor-
tality and long-term exposure met the criteria for inclusion in
the report. Mostly because of the small number of studies, the
evidence for an association of all-cause mortality with long-
term exposure was classified as “suggestive but not sufficient”
to infer a causal association. Additional factors that led to this
classification were the substantial differences among popula-
tions, time periods, and confounders across studies.
Only four time-series studies of all-cause mortality associ-
ated with short-term exposure met the Panel’s criteria; these,
too, were classified as “suggestive but not sufficient,” largely
on the strength of one well-done study (Maynard et al. 2007).
Two time-series studies based on source-apportionment models
were found to have a number of limitations that prevented a
stronger statement about inferred causality.
Many of the issues that applied to studies of all-cause mortality
applied as well to studies of cardiovascular mortality associated
with long-term exposure and led, similarly, to a classification of
“suggestive but not sufficient.” Only two time-series studies of
cardiovascular mortality met the inclusion criteria, and although
they both show positive associations, the Panel concluded that,
given the overall paucity of studies, the evidence for effects of
short-term exposure was “inadequate and insufficient.”
caRDioVaScUlaR MoRBiDitY
epidemiology
Studies that documented changes in cardiac physiology (such
as heart-rate variability) after short-term exposure to traffic-
related pollution (which was assessed using surrogates, source
apportionment, or pseudo-personal monitoring) provided strong
evidence for a causal association with the exposure. However,
the failure of some studies to consider stress and noise as poten-
tial confounders led the Panel to classify them as “suggestive
but not sufficient” to infer a casual association. Among the stud-
ies that evaluated cardiovascular morbidity, two well-executed
studies on hospitalization for acute myocardial infarction were
identified (Rosenlund et al. 2006; Tonne et al. 2007). In addition,
a prospective study in a German cohort reported an association
between living near a major road and coronary-artery calcifi-
cation as well as higher prevalence of coronary heart disease
(Hoffmann et al. 2006, 2007). Collectively, these studies made a
very strong case for an association between exposure to traffic-
related pollutants and atherosclerosis. However, because of the
small number of studies, the Panel classified them as “sugges-
tive but not sufficient” to infer a causal association.
toxicology
There have been a few toxicology studies that examined the
cardiovascular effects of traffic emissions specifically. However,
the Panel concluded that the recent toxicology literature pro-
vides suggestive evidence that exposure to pollutants that are
components of traffic emissions, including ambient and labora-
tory-generated PM and exhaust from diesel and gasoline-fueled
engines, alters cardiovascular function. There is also evidence,
albeit inconsistent, for acute effects on vascular homeostasis
and suggestive evidence in animal models that repeated expo-
sures to ambient PM in general enhance the development of ath-
erosclerosis. Some studies support the involvement of oxidative
stress. Although the evidence from toxicology studies in isola-
tion is not sufficient in terms of a causal association between
traffic emissions and the incidence or progression of cardiovas-
cular disease, when viewed together with the epidemiologic
evidence, a stronger case could be made for a potential causal
role for traffic-related pollutants in cardiovascular-disease mor-
bidity and mortality. The extent to which these associations
apply to individuals without underlying cardiovascular disease
cannot be determined from the evidence available at this time.
aStHMa aND ReSpiRatoRY SYMptoMS
Asthma is an inflammatory disease of the lung airways char-
acterized by episodic obstruction of the airways, which can lead
to chronic obstructive lung disease. The most prevalent form of
asthma in children and young adults is allergic asthma, which
develops as an immune response to inhaled allergens. Indi-
viduals with asthma and other allergic conditions who have an
increased tendency to develop immediate and localized reac-
tions to allergens (such as pollens) that are mediated by immu-
noglobulin E (IgE) are referred to as “atopic.”
epidemiology
In epidemiology studies, asthma is most frequently identi-
fied by means of responses to questionnaires that do not make
use of a single, universally accepted set of questions, alone or in
combination with other criteria. This is further complicated by
the challenges of distinguishing factors that affect its onset from
those (often the same factors) that lead to its episodic worsening.
A history of asthma symptoms (such a wheezing) often is used
in epidemiology studies as part of the definition both of asthma’s
onset (incidence) and of its prevalence and exacerbation.
Respiratory Health Problems in Children: Asthma Incidence
and Prevalence Seven studies conducted in four separate
7
ExECuTIvE SummARy
special report 17
cohorts and one case-control study qualified as studies of asthma
incidence in children. Eleven studies qualified as studies of
asthma prevalence in children. From these studies, the Panel
concluded that living close to busy roads appears to be an inde-
pendent risk factor for the onset of childhood asthma. The Panel
considered the evidence for a causal relation to be in a gray zone
between “sufficient” and “suggestive but not sufficient.” The
results found across the studies followed a pattern that would
be expected under the plausible assumption that the pollutants
really are causally associated with asthma development, if only
among a subset of children with some accompanying pattern of
endogenous or exogenous susceptibility factors. The conditions
that underlie an increased risk for asthma development among
children exposed to traffic-related pollutants are not known.
Exacerbation of Symptoms in Children with and without
Asthma and Health-Care Utilization for Respiratory Problems
Among the more than 20 cohort and cross-sectional studies
reviewed that examined the association between exposure to
traffic-related pollution and wheezing (an important symptom
in the expression and diagnosis of asthma) in children, there
was a high degree of consistency in finding positive associa-
tions, many of which reached statistical significance (i.e., had
reasonably precise point estimates of associations). This was
true particularly for the large majority of studies that used mod-
els to assign estimates of local concentrations of pollutants,
such as NO2 or soot (the carbonaceous component of PM), to
the place of residence of the study participants. Studies based
on proximity or traffic density also indicated an association
between exposure and wheezing. In addition, exacerbation of
other asthma-related symptoms, such as cough or dry cough,
was consistently associated with exposure across a variety of
exposure measures. Although most studies were not restricted to
children with asthma, all these symptoms were more prevalent
among those with asthma, and it is very likely that the observed
associations were driven by exacerbations of asthma in mixed
groups of participants. The Panel concluded that the evidence
is “sufficient” to infer a causal association between traffic expo-
sure and exacerbations of asthma but that it is “inadequate and
insufficient” to infer a causal association between exposure and
respiratory symptoms in children without asthma.
Nine studies assessed the association between exposure to traf-
fic-related pollution and the use of health-care services to treat
respiratory problems in children. Most of the studies reported
positive associations between exposure and hospital-admission
rates, but the majority had methodologic problems that hampered
their interpretation. The panel concluded that there is “inade-
quate and insufficient” evidence to infer a causal association.
Respiratory Health Problems in Adults: Asthma Onset and Respi-
ratory Symptoms The Panel noted that the evidence between
exposure to traffic-related pollution and new adult asthma was
“inadequate and insufficient” as this was investigated in only one
study (Modig et al. 2006). The Panel reviewed 17 studies on respi-
ratory symptoms, of which all but one relied on proximity to roads
or traffic-density measures, and concluded that the evidence for a
causal association is “suggestive but not sufficient.”
toxicology
The few human studies in which subjects were exposed to
realistic traffic conditions (a road tunnel or busy street) are sup-
portive of the possibility that persons with asthma may be more
susceptible to adverse health effects (such as decrements in lung
function and enhanced responses to allergens) related to such
exposure. The Panel’s evaluation of the toxicologic data on the
respiratory system regarding the effects of components of traffic-
related air pollution was that such exposures result in mild acute
inflammatory responses in healthy individuals and enhanced
allergic responses in allergic asthmatics and animal models.
When the epidemiologic and toxicologic data were viewed
together, the Panel noted that a case could be made that there
are likely to be causal associations related to exposure to traffic-
related air pollution and asthma exacerbation and some other
respiratory symptoms. However, given the lack of a large body
of toxicologic data based on human and animal exposures to
real-world traffic scenarios, the Panel noted that it was hazard-
ous to conclude that causality has been established at this time
for all respiratory symptoms at all ages.
lUNG FUNctioN aND cHRoNic oBStRUctiVe
pUlMoNaRY DiSeaSe
Changes in lung function are considered reliable markers of
health that reflect the effects of endogenous and cumulative
exposure to exogenous factors that might have adverse health
consequences. Reduced lung function is strongly associated
with future morbidity from a variety of causes and is a predic-
tor of life expectancy (Hole et al. 1996); however, the relevance
to health of small, short-term changes has not been assessed.
The Panel considered lung function and chronic obstructive
pulmonary disease (COPD) together in this review, because the
principal criterion for the diagnosis of COPD is based on lung-
function measures.
epidemiology
Lung Function in Children and Adults The studies reviewed
were heterogeneous in their design, approach to exposure
assessment, and lung-function measures. Given their limited
comparability, the Panel concluded that the evidence is “sug-
gestive but not sufficient” to infer a causal association between
short- and long-term exposure to traffic-related pollution and
decrements in lung function. However, in the case of long-
term exposure, there was some coherence in the data, suggest-
ing that (1) long-term exposure is associated with changes in
lung function in adolescents and young adults; (2) lung-func-
tion measures are lower in people who live in more polluted
areas; and (3) changing residence to a less-polluted area in one
study is associated with improvements in lung function (Burr
et al. 2004). The first and second points are consistent with lon-
ger-lasting effects on lung structure and/or function. The third
point can be interpreted to indicate that some component of the
apparent effects on lung function is reversible or is more the
result of short-term exposure.
8
special report 17
ExECuTIvE SummARy
Chronic Obstructive Pulmonary Disease Because only two of
the COPD studies fulfilled the criteria for inclusion in the review
and their results were not consistent, the Panel concluded that
there is “inadequate and insufficient” evidence for causal asso-
ciations between exposure to traffic pollution and COPD.
toxicology
A very limited database of controlled human exposure has
shown short-term reductions in forced expiratory volume in
1 second (FEV1) and increases in inflammation with exposure
to traffic-related air pollution. However, the two end points have
not been associated with each other. Virtually no data are avail-
able from animal models. There are no studies of traffic-related
air pollution and COPD.
While the epidemiology studies do provide suggestive evi-
dence for chronic exposure effects on lung function in adoles-
cents and young adults, there are too few toxicologic data to
indicate what mechanisms underlie these observations. The
aggregate epidemiologic and toxicologic evidence on chronic
exposure to traffic-related air pollution and altered lung func-
tion in older adults and the occurrence of COPD is too sparse to
permit any inference with respect to causal association.
alleRGY
epidemiology
The 16 epidemiology studies on this outcome included in
the review not only had to meet criteria for the quality of their
exposure data but also had to report at least one of the follow-
ing: (1) positive skin-prick testing for common aeroallergens; (2)
serum-specific IgE to common aeroallergens; (3) a physician’s
diagnosis of eczema or allergic rhinitis; or (4) use of question-
naires on the history of symptoms of hay fever, seasonal runny
nose, rhinitis or conjunctivitis, or itchy eyes. With a few incon-
sistent exceptions, results based on the skin-prick test reactivity
or allergen-specific IgE failed to show associations with any of
the traffic-exposure surrogates. Inconsistent results with self-
reported symptoms were also noted. The Panel concluded that
there is “inadequate and insufficient” evidence to infer a causal
association, or even a noncausal association, between exposure
to traffic-related pollution and IgE-mediated allergies. Overall,
the lack of consistency across epidemiology studies might have
reflected a failure to identify susceptible subgroups.
toxicology
The Panel noted that the toxicology data provide strong mech-
anistic evidence with respect to the diesel particle component
of traffic-generated pollution and IgE-mediated allergic reactions
and some evidence for NO2 and late-phase response to allergen.
However, the epidemiology studies were inconsistent. The rel-
evance of the toxicology studies (often by nasal instillation with
diesel exhaust particles) to the actual manifestations of non-
asthmatic allergic phenotypes (e.g., allergic rhinitis or conjunc-
tivitis, eczema, serum-specific IgE, and evidence of sensitization
to aeroallergens) could not be determined.
BiRtH oUtcoMeS
epidemiology
Although a considerable body of data from around the world
has identified consistent associations between exposure to ambi-
ent air pollution in general and various birth-outcome measures
(low birth weight, small for gestational age, and perinatal mor-
tality), only four studies of exposure to traffic-related pollution
met the criteria for inclusion in this review. The small number
of studies and their limited geographic coverage led the Panel to
conclude that there is “inadequate and insufficient” evidence to
infer causality.
toxicology
The toxicology studies reported effects on reproductive organs
and sperm functionality in animals, but these outcomes were not
evaluated in the epidemiology studies. Among the challenges
in interpreting these results are the data limitations and the
almost-universal use of very high exposure concentrations that
have questionable relevance to actual ambient concentrations.
Due to their lack of overlap, the epidemiology and toxicology
studies on reproductive health and birth outcomes do not lend
themselves to any overall synthesis.
caNceR
epidemiology
The Panel focused on general-population exposure studies and
did not review the extensive epidemiologic literature on cancer
from occupational exposure to traffic emission constituents (e.g.,
benzene and diesel exhaust). Among the studies reviewed, five
were of childhood cancers (mainly leukemias, lymphomas, and
cancers of the central nervous system), and four of adult can-
cers (two of lung cancer, one of female breast cancer, and one
of several cancers combined). Data on childhood cancers were
inconclusive in terms of overall consistency and of specific can-
cers. Too few data were available in adults. Overall the Panel
concluded that the evidence was “inadequate and insufficient”
to make inferences for causality between exposure to traffic pol-
lution and cancer.
toxicology
The toxicologic research summarized included in vitro muta-
genicity studies of exposure of cells to PM from traffic pollution,
diesel or biodiesel exhaust, and organic components of some of
these mixtures, as well as animal carcinogenicity studies after
exposure to exhaust from diesel and gasoline-fueled engines.
Although studies in cells demonstrating the capacity of DEP to
induce DNA-strand breaks, base oxidation, and mutagenicity
provide a possible mechanism for the induction of carcinogenic-
ity by traffic-related pollution, the applicability of in vitro muta-
genicity studies to human risk assessment has been questioned.
9
ExECuTIvE SummARy
special report 17
Animal studies have demonstrated the ability of high concentra-
tions of exhaust components in both diesel and gasoline-fueled
engines to cause tumors in animals. However, caution must be
exercised in extrapolating these data to people exposed to much
lower concentrations of pollutants, as seen in the epidemiology
studies. Therefore, the Panel concluded that any statement that
tries to relate the toxicologic to the epidemiologic data is prema-
ture at this time.
OVERALL CONCLUSIONS
Studies have shown that traffic-related emissions affect ambient
air quality on a wide range of spatial scales, from local roadsides
and urban scales to broadly regional background scales. Based
on a synthesis of the best available evidence, the Panel identi-
fied an exposure zone within a range of up to 300 to 500 m from
a major road as the area most highly affected by traffic emissions
(the range reflects the variable influence of background pollution
concentrations, meteorologic conditions, and season).
Surrogates for traffic-related exposure have played, and are
likely to continue to play, a preeminent role in exposure assess-
ments in epidemiology studies. The optimal selection of rel-
evant surrogates (especially surrogates that are single chemicals)
depends on accurate knowledge of the degree to which they rep-
resent the chemical and physical properties of the actual primary
traffic-pollution mixtures to which humans are exposed, which, in
turn, depends on accurate knowledge of motor-vehicle–emissions
composition and near-source transformation and dispersion. The
Panel concluded that none of the pollutant surrogates (CO, NO2,
UFP, EC, and benzene) is unique to emissions from motor vehi-
cles. Among the surrogates based on traffic-exposure models, the
question remains as to the extent to which the proximity model
(i.e., the simple distance-to-road measures) should be employed
in future epidemiology studies because it is particularly prone to
yielding measures potentially containing extraneous information
that can lead to the confounding of associations between health
effects and exposure. In the Panel’s view, the hybrid model is the
current optimal method of assigning exposures to primary traffic-
related pollution.
Many aspects of the epidemiologic and toxicologic evidence
relating adverse human health effects to exposure to primary
traffic-generated air pollution remain incomplete. However,
the Panel concluded that the evidence is sufficient to support a
causal relationship between exposure to traffic-related air pol-
lution and exacerbation of asthma. It also found suggestive evi-
dence of a causal relationship with onset of childhood asthma,
nonasthma respiratory symptoms, impaired lung function, total
and cardiovascular mortality, and cardiovascular morbidity,
although the data are not sufficient to fully support causality. For
a number of other health outcomes, there was limited evidence
of associations, but the data were either inadequate or insuffi-
cient to draw firmer conclusions. The Panel’s conclusions have
to be considered in the context of the progress made to reduce
emissions from motor vehicles. Since the epidemiology studies
are based on past estimates of exposure from older vehicles, they
may not provide an accurate guide to estimating health associa-
tions in the future.
In light of the large number of people residing within 300 to
500 m of major roads, the Panel concludes that the sufficient
and suggestive evidence for these health outcomes indicates that
exposures to traffic-related pollution are likely to be of public
health concern and deserve public attention. Although policy
recommendations based on these conclusions are beyond the
scope of this report, the Panel has tried to organize, summarize,
and discuss the primary evidence in ways that will facilitate its
usefulness to policy makers in the years ahead.
REFERENCES
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Effects on respiratory health of a reduction in air pollution from
vehicle exhaust emissions. Occup Environ Med 61:212–218.
Hoffmann B, Moebus S, Möhlenkamp S, Stang A, Lehmann N,
Dragano N, Schmermund A, Memmesheimer M, Mann K, Erbel
R, Jöckel K-H. 2007. Residential exposure to traffic is associated
with coronary atherosclerosis. Circulation
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Hoffmann B, Moebus S, Stang A, Beck EM, Dragano N, Möhlen-
kamp S, Schmermund A, Memmesheimer M, Mann K, Erbel R,
Jöckel KH. 2006. Residence close to high traffic and prevalence
of coronary heart disease. Eur Heart J 27:2696–2702.
Hole D, Watt G, Davey-Smith G, Hart C, Gillis C, Hawthorne
V. 1996. Impaired lung function and mortality risk in men and
women: Findings from the Renfrew and Paisley prospective
population. Br Med J (Clin Res Ed) 313:711–715.
Maynard D, Coull BA, Gryparis A, Schwartz J. 2007. Mortality
risk associated with short-term exposure to traffic particles and
sulfates. Environ Health Perspect 115:751–755.
Modig L, Järvholm B, Rönnmark E, Nyström L, Lundbäck B, Anders-
son C, Forsberg B. 2006. Vehicle exhaust exposure in an incident
case-control study of adult asthma. Eur Respir J 28:75–81.
NARSTO. 2005. Improving emission inventories for effective air
quality management across North America. NARSTO 05-001.
Pasco, Washington. Available from ftp://narsto.esd.ornl.gov/
pub/EI_Assessment/Improving_Emission_Index .
Rosenlund M, Berglind N, Pershagen G, Hallqvist J, Jonson T,
Bellander T. 2006. Long-term exposure to urban air pollution
and myocardial infarction. Epidemiology 17:383–390.
Tonne C, Melly S, Mittleman M, Coull BA, Goldberg R, Schwartz
J. 2007. A case-control analysis of exposure to traffic and acute
myocardial infarcion. Environ Health Perspect 115:53–57.
U.S. Department of Health and Human Services. 2004. The
Health Consequences of Smoking: A Report of the Surgeon Gen-
eral. U.S. Department of Health and Human Services, Centers
for Disease Control and Prevention, National Center for Chronic
Disease Prevention and Health Promotion, Office on Smoking
and Health. Atlanta, GA.
10
special report 17
EXECUTIVE SUMMARY
Ira Tager, Chair, Professor of Epidemiology, School of Public
Health, University of California–Berkeley; member, HEI Research
Committee
Kenneth Demerjian, Director, Atmospheric Sciences Research
Center; Professor, Department of Earth and Atmospheric Sci-
ences, State University of New York; member, HEI Research
Committee
Mark Frampton, Professor of Medicine and Environmental Med-
icine, University of Rochester School of Medicine and Dentistry
Michael Jerrett, Associate Professor, Division of Environmental
Health Sciences, School of Public Health, University of Califor-
nia–Berkeley
Frank Kelly, Professor of Environmental Health and Director of
Environmental Research Group, King’s College, London, U.K.
Lester Kobzik, Professor of Environmental Health, Harvard
School of Public Health
Nino Künzli, Professor of Social and Preventive Medicine, Pub-
lic Health University of Basel, Institute of Social and Preventive
Medicine at the Swiss Tropical Institute, Basel, Switzerland
Brian Leaderer, Susan Dwight Bliss Professor of Public Health,
Division of Environmental Health Science, Yale University School
of Public Health; former member, HEI Review Committee
Thomas Lumley, Associate Professor, Department of Biostatis-
tics, University of Washington School of Public Health and Com-
munity Medicine
Frederick W. Lurmann, Manager of Exposure Assessment and
President Emeritus, Sonoma Technology, Inc.
Sylvia Richardson, Professor of Biostatistics, Department of
Epidemiology and Public Health, Imperial College School of
Medicine, London, U.K.; member, HEI Research Committee
Jonathan Samet, Director, Professor, and Flora L. Thornton
Chair, Department of Preventive Medicine, Keck School of Medi-
cine, University of Southern California
Michael Walsh, Consultant on vehicle emissions and fuels
issues worldwide; former head of the U.S. EPA Office of Mobile
Source Air Pollution Control
Maria Costantini, Health Effects Institute Principal Scientist,
Project Coordinator
HEI Panel on the Health Effects of Traffic-Related Air Pollution. 2010. Traffic-Related Air
Pollution: A Critical Review of the Literature on Emissions, Exposure, and Health Effects.
HEI Special Report 17. © by the Health Effects Institute, Boston, Mass. The entire report is
available at www.healtheffects.org or from HEI.
Health Effects Institute
101 Federal Street, Suite 500, Boston, MA 02110, USA
Phone: +1-617-488-2300. Fax: +1-617-488-2335. www.healtheffects.org.
Traffic Review Panel
11
Flows: Urban Metabolism
& Human Mobility
Human Mobility &
Urban
Metabolism
• Urban Metabolism
• Linear & Circular Model
• Environmental Impacts
• Human Mobility
•
Transportation
• Ableism & Universal Design
Urban Metabolism
The study of urban metabolism involves ‘big picture’
quantification of the inputs, outputs and storage of energy,
water, nutrients, materials and wastes for an urban region.
Kennedy, C., S. Pincetl, and P. Bunje. “The Study of Urban Metabolism and Its Applications to Urban Planning and
Design.” Environmental Pollution (Barking, Essex: 1987) 159, no. 8–9 (September 2011): 1965–73.
Metabolism
Human Urban
Inputs Outputs
“There is… nothing unnatural about New York City”
–David Harvey–
“There is… nothing unnatural about New York City”
–David Harvey–
“There is… nothing unnatural about New York City”
–David Harvey–
Inputs, Outputs & Transportation
Linear Metabolism (Higher Rate of Pollution)
Inputs Outputs
The City
Inputs Outputs
The City
Circular Metabolism
(Minimize New Inputs and Maximize Recycling)
Trash is Messy
It does not stay in place
Impervious Surfaces
• Pavement
• Concrete
• Asphalt
Natural vs. Impervious Cover
Bioswale
• Reduce flooding
• Stops trash
• Absorbs rainwater
• Aesthetically pleasing
• Provides green space
Transportation
• Cars
• Buses
• Planes
• Trains
• Motorcycles
• Bicycles
• Scooters
• Boats
The Suburbs & Car Centric Society
The Suburbs & Car Centric Society
• Loss of homes
• Loss of businesses
• Air Pollution
• Car Emissions
• Lack of investment in
public transportation
https://www.portlandonline.com/portlandplan/index.cfm?a=288100&c=52256
https://www.portlandonline.com/portlandplan/index.cfm?a=288100&c=52256
Human Mobility Beyond Transportation
These are Important for
Human Mobility Too!
Ableism Defined
Ableism is the discrimination of and social prejudice against people with
disabilities based on the belief that typical abilities are superior. At its heart,
ableism is rooted in the assumption that disabled people require ‘fixing’
and defines people by their disability. Like racism and sexism, ableism
classifies entire groups of people as ‘less than,’ and includes harmful
stereotypes, misconceptions, and generalizations of people with
disabilities.
Americans with Disabilities Act (ADA)
The ADA prohibits discrimination on the basis of disability in
employment, State and local government, public
accommodations, commercial facilities, transportation, and
telecommunications.
Universal Design & Inclusive Infrastructure
Universal Design is the design and composition of an
environment so that it can be accessed, understood and used to
the greatest extent possible by all people regardless of their
age, size, ability or disability. An environment (or any building,
product, or service in that environment) should be designed to
meet the needs of all people who wish to use it.
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