Public Health and Components of
Particulate Matter: The Changing
Assessment of Black Carbon
Thomas J. Grahame, US Department of Energy
Thomas.Grahame@hq.doe.gov
Rebecca Klemm, Klemm Analysis Group
Richard B. Schlesinger, Pace University
Disclaimer

The views expressed are those of the
authors alone, and do not necessarily
reflect the viewpoint of any U.S.
Government Agency
Caveat


There have been considerable reductions of
particulate vehicular emissions (including black
carbon [BC]), under legislation and regulations
predating and including the Clean Air Act, which
deal with reducing vehicular emissions of all types
(next slide).
As we discuss recently emerging science on health
effects of BC under another section of CAA,
regarding National Ambient Air Quality Standards
(NAAQS), we don’t want to leave impression that
substantial progress hasn’t been made.
Reductions in San Francisco annual
BC concentrations over time
(Kirchstetter, 2008, LBL – black line w/black dots = BC)
Assessments of Black Carbon (BC)
and Diesel Emissions Today



World Health Organization (WHO, EU branch)
suggested consideration of a additional health
standard for BC (2012)
IARC (International Agency for Research on Cancer,
part of WHO) declared diesel exhaust a known
human carcinogen (2012)
Janssen et al. (2011) found that reducing one unit
of BC in air will lengthen survival 4 to 9 times more
than reducing one unit of PM2.5

PM2.5 = Particulate Matter 2.5 micrometers or less
Assessments of BC and Diesel
Emissions Circa 2000




BC barely mentioned in North American air
pollution studies
Vehicular emissions rarely mentioned in air
pollution epidemiology
How did we get from “barely mentioned” to
calling for BC standard, finding BC 4 to 9
times more lethal, labelling diesel emissions
carcinogenic, in a bit more than a decade?
A major theme of the Critical Review
What is Black Carbon (BC)?


BC consists of a core of graphite-like elemental carbon
(EC), on which is adsorbed many carbonaceous
species, metals, etc.
BC is product of incomplete combustion of
carbonaceous materials (diesel, biomass, gasoline,
coal, natural gas [e.g., flaring]) w/o adequate controls



U.S. control requirements for post-2006 on-road diesels
eliminate virtually all BC when in working order
Adsorbed materials add ~ 25% to mass of EC
Polycyclic Aromatic Hydrocarbons (PAHs) are among
adsorbed materials
Representation of diesel particles,
their formation (Courtesy Dr. Ning Li)
Sources of Ambient BC in U.S.
(from EPA Black Carbon Report to Congress)
Mobile sources of BC
(from EPA Black Carbon Report to Congress)




On road diesel:
 153,477
(short tons)
Nonroad diesel
 112,058
On road gasoline
 14,510
Other (e.g., locomotives)


~ another 50,000
Diesel = ~ 80% of mobile sources BC
EC/BC is mostly in ultrafine range
(from Mauderly and Chow, 2008; Fresno)
Particulate Matter (PM) Research in 1970s
through 1990s (very short overview)

1970s and 1980s

A few seminal PM epidemiological studies in
1980s, often noting still current methodological
issues, such as:


health relevance of different pollutants not monitored
at time (e.g., cancer researchers want info on
organics)
A central monitor pollution measurement is a poor
proxy for expressing exposure for everyone in a
metro area, for spatially variable pollutants (BC) –
details to follow
Particulate Matter (PM) Research in 1970s
through 1990s (cont.)

1970s and 1980s (cont.)

Monitoring for many potentially health-relevant
PM2.5 species, including BC/EC, was lacking



Sulfate only PM species routinely monitored
Studies of PM didn’t mention vehicular, diesel,
black carbon, PAHs
Exception of Stern et al., 1988, next, which
looked at vehicular emissions only generally,
in study of tunnel and bridge officers in NYC
The Exception: Stern et al. (1988): Tunnel
Officers vs. Bridge Officers (Risks of ASHD
Disease Mortality)
But….Stern et al (1988) dismissed
particles and organics as cause




Study clearly showed benefits of reducing
exposure to vehicular emissions
But benefits seen by authors as reflecting
reduction in CO
Benefits of reductions of other vehicular
emissions, such as “nitric oxides, hydrocarbons,
particles, lead…highly speculative…”
Lost opportunity to start looking at vehicular PM
emissions
In the 1990s…

Two seminal air pollution studies:



6 Cities Study (Dockery et al., 1993)
American Cancer Society (ACS) Study (Pope et al.,
1995)
Seminal because these were the studies which
convinced people that tiny particles in air, which
often couldn’t be seen, could sicken and kill

But (reflecting lack of monitoring), neither
mentioned BC/EC, PAHs, diesel emissions
1998 “Research Priorities for
Airborne Particulate Matter”


National Research Council (NRC) report
(body of National Academy of Sciences)
Also a seminal work, NRC Reviewed
state of U.S. research on particulates
and made crucial recommendations
Findings of 1998 NRC Report




“The biological basis of most of the [particulate] associations is
essentially unknown . . .”
“There is . . . limited scientific information about the specific
types of particles that might cause adverse health effects…”
Suggested using laboratory and human clinical studies to
explore toxicological mechanisms by which particles may cause
mortality and morbidity
These toxicology tests should examine the “most biologically
important components” of particles, including both size and
chemistry

Suggested expanded monitoring, to avoid issue that “monitoring
is not measuring the most biologically important aspects of
particulate matter…”
Early in 2000s…”Highway
Proximity” Studies

While BC/EC monitoring was beginning, a major
breakthrough in exposure assessment:



People who live near major roads are exposed to
much more pollution than those living further away
Researchers could examine health effects for those
living near roadways (after accounting for socioeconomic and smoking status, age, other potential
confounders), vs. those living farther away
Example of pollutants’ spatial variability (next slide)
Vehicular Pollutants Fall within ~100
to 150 meters of major road
Risks for those living close to
major urban roads, thruways

Starting (slowly) in 2002, many studies:



Found elevated all-cause or cardiovascular
disease (CVD) mortality, or CVD morbidity
(e.g., hospitalization) effects
Most often for those living w/in 100 m of
freeway, 50 m of major urban road
Critical Review (CR) lists ~ 20 such studies
(most post-2006) in Table S2, discusses
several in body of CR
Risks for those living close to major
urban roads, thruways (cont.)

Some examples:



Finkelstein et al. (2004): Living in close proximity to
such roads costs 2.5 years of life (not much less than for
major diseases like ischemic heart disease)
Gan et al. (2010): ~ 30% elevated risk of coronary heart
disease mortality for those living in close proximity to
major roads for length of study, > than risks for those
who moved closer or further during study
Hoffmann et al. CVD morbidity studies

Significantly increased risks of congestive heart disease (2006),
coronary artery disease (2007), peripheral artery disease (2009)
for those living near major roads
Proximity to highways shows importance
of vehicular emissions to health…what
about vehicular emissions per se?


Let’s also look at vehicular emissions specifically,
rather than just proximity to highway…
BC/EC increasingly used in epidemiological
studies, ~ post 2005


Also, to lesser extent, NOx, NO, PAHs, plus in EU black
smoke [similar to BC]
When using chemical/elemental markers such as
BC, there are important methodological issues
that will help us get more reliable results…
Need to compare effects of vehicular PM
emissions vs. other PM2.5 species

1. Why compare many PM2.5 species, including
BC/EC, against same health endpoints in same
epidemiology studies?

Can’t find associations for a PM2.5 species not included in
model (obviously)

Association may “migrate” from a health relevant PM2.5
species not in model, to emissions included in model

Goal: is a given PM2.5 species more strongly, consistently
associated with health effect than other PM2.5 species?
Need reasonably good knowledge of
actual subject exposure

2. Epidemiology results are improved with more
accurate subject exposure information (as with
highway proximity studies, near vs. far)

With poor exposure information (greater exposure
misclassification), effects of locally variable
emissions (e.g., BC) almost always are understated

Example (next slide): Suh and Zanobetti (2010)

Later, pollutants would be modelled to homes of
subjects (hospital admissions, mortality)
When exposure to BC is
accurate….vs. when it isn’t…
Association Between 24-hour Ambient and Personal EC Concentrations
with Different HRV Measures (from Suh and Zanobetti, 2010)
Ambient (Central Monitor)
Personal Monitor
HRV Measure
Change (%), 95% C.I.
Change (%), 95% C.I.
SDNN
RMSSD
PNN50
HF
LF/HF ratio
-1.0
-3.6
-0.34
-2.36
2.60
-4.66
-10.97
-15.16
-13.41
6.22
-3.7 to 1.7
-9.5 to 2.8
-10.55 to 11.04
-11.67 to 7.92
-1.89 to 7.29
(Bold = statistically significant at 95% level)
-7.99 to -1.22
-18.00 to -3.34
-26.33 to -2.29
-23.95 to -1.41
0.15 to 12.64
When you have exposure
misclassification…

Takeaway from Suh and Zanobetti (2010):

If you have large exposure misclassification, you
will understate actual effects in most cases

Does NOT mean that you won’t find some
(smaller) significant associations when using a
central monitor…other studies do….only that they
will very likely be understated
Examine biological mechanisms which
may explain epidemiological associations
for specific PM2.5 species


3. Combine toxicology (finding biological mechanisms
for specific PM2.5 species) with human panel and
controlled human exposure studies, to explain
outcomes (e.g., CVD effects) found in population
based epidemiology (NRC recommendation again)
Illustrative references


Health Effects Institute, 2010
Grahame and Schlesinger, 2010 (BC and CVD)
Monitoring of multiple PM2.5
species, including BC/EC


Widespread monitoring of BC/EC in U.S. got
started in early 2000s, but took until after 2005
(mostly) for epidemiology to use this information
Europe had been measuring black smoke (BS) for
decades because of widespread residential coal use

Thus EU had a head start on measuring dark
carbonaceous material relating to diesels, traffic as
coal use greatly diminished
2006 Critical Review (Pope and
Dockery)

Well over 100 studies discussed in 2006 CR





Great majority examined only size fractions of PM
(PM10, PM2.5, a few ultrafine)
A few EU studies using black smoke (the “head
start”)
Two highway proximity studies
20 studies of heart rate variability (HRV), all using
PM size fractions
None using BC/EC
2006 Critical Review (Pope and
Dockery), cont.


Want to be clear: no criticism implied!
Researchers can’t report on BC/EC
associations if studies using recently available
BC information have yet to be done
What about BC/EC, vehicular emissions
studies now?

Current (2014) CR lists in Tables S2 through S10, and/or
text, ~140 studies of vehicular emission effects in humans




Great majority published after 2005
Most use BC/EC, a small number use other highway emissions,
~ 20 use highway proximity, ~ 5 use traffic density (a few use
more than one indicator)
~ 15 of the most recent studies model vehicular emissions to
the home of subjects (visual of modelled emissions next slide)
~ 20 are controlled human exposure studies using mostly diesel
emissions, some using wood smoke emissions (getting to
biological mechanisms)
NO2 modelled to residences in
Toronto (Jerrett et al., 2009)
Health Outcomes These BC/EC/
Vehicular Emissions Studies Examined

The ~ 140 studies examined:





All-cause, CVD mortality; CVD morbidity (e.g., CVD
emergency hospital admissions, blood pressure);
Intermediate CVD health endpoints (e.g., ~ 20
precursors of CVD such as oxidative stress,
inflammation, adhesion molecules, platelets, etc.);
Cardiac issues (arrhythmias, HRV changes, ST-segment
depression, etc.);
birth outcomes;
brain and central nervous system effects
Health Outcomes These BC/EC/
Vehicular Emissions Studies Examined

Discuss only a few lung cancer studies
very briefly in CR


IARC/WHO 2012 conclusion that diesel
emissions cause lung cancer makes indepth discussion extraneous
Illustrate here with one recent study of
cancer and diesel emissions (next slide)
Cancer risks from air toxics

Morello-Frosch and Jesdale (2006)




Modelled concentrations of 33 Air Toxics
(including DPM, diesel particulate matter) to
census tracts
Estimated cancer risks by multiplying potencies
by amounts of each air toxic
Mobile sources contributed 88% of cancer risks
DPM contributed 82% of cancer risks
Caveat (1)


We do not use source apportionment studies, as
in our judgment, they increase rather than
reduce uncertainty (details in CR)
Researchers routinely come up with different
numbers of factors (“sources”) for same locality


Grahame and Hidy, 2007; HEI, 2010
Not possible to determine, in any case,
differential exposure to a “diesel emissions
factor” (exposure misclassification)
Caveat (2)

For reasons of space, we do not include
in CR (or today) the voluminous
number of studies relating vehicular
emissions to respiratory diseases (see
HEI, 2010)
Caveat (3): Toxicology, Some Observational
Studies: Discussed in Depth in CR (not in Tables)

Also no time for reviewing today:


Several sections in CR on toxicology of diesel and BC
(animal/cells), lengthier versions in Supplemental Material
These link biological mechanisms for health effects in
epidemiological studies


Additional to the ~ 140 epidemiological or controlled human
exposure studies in Tables S2 through S10
Many observational studies in CR (health effects in workers
in trucking companies exposed to different levels of
emissions; oxidative stress at beginning vs. end of work
week in diesel repair, etc.) linking exposure to different
levels of vehicular emissions to health endpoints (example)
Tables S3, S4, S5

Over 30 population-based epidemiology
studies, each using many PM2.5 species
(always including BC/EC), in these tables



S3: mortality associations w/o accurate exposure
information (central monitor concentrations)
S4: hospital admissions (morbidity) associations
w/o accurate exposure information
S5: mortality and morbidity associations when BC
or other vehicular emissions are modelled to home
of subjects (good exposure information)
Some results of studies using many PM2.5
species (multi county studies, from Tables
S3 and S4)
Health Effect
Studied
PM2.5 Species, Other Pollution Variables
MultiCounty
Studies
Geographic
al
Area
1. Peng et
al., 2009
119 counties Daily emergency
CVD hospital
admissions
7 largest PM2.5 components (sulfate, nitrate, silicon, BC,
organic carbon, sodium and ammonium ions)
Component associations: BC
2. Bell et al.,
2009
106 counties Daily CVD
hospital
admissions
20 PM2.5 components (7 in Peng et al. [2009] above, plus
13 elements, mostly metals, incl. Fe, Zn, V and Ni
Component associations: BC, V, Ni
3. Lipfert et
al., 2009
206 rural
and urban
counties
Twelve HAPs (incl. Ni, As, benzene, diesel exhaust
noted by diesel particulates, formaldehyde, polycyclic
organic materials [POM]), sulfate, NOx, EC, traffic
density (proxy for traffic emissions)
Early mortality associations with traffic density, benzene,
formaldehyde, diesel particulate, POM, NOx, EC, Ni
Prospective cohort
study, survival
since enrollment
Human Panel Studies (studies of specific
subjects known to researchers)

Benefits of human panel studies (type of
epidemiological study)


Researchers can know individual subject’s
health in detail (weight, medications,
smoking, conditions, etc.), can control for
these before examining effects of pollutants
Two sets of human panel studies in CR


Harvard School of Public Health (Table S6, 37
studies)
Delfino et al. group (Table S7, 7 studies)
HSPH studies, all including BC/EC

Health endpoints (mostly cardiovascular
intermediate and cardiac endpoints) studied
include:


Oxidative stress, ST-segment reduction, HRV changes,
carotid artery thickness, several circulating markers of
inflammation, systolic and diastolic blood pressure,
soluble adhesion molecules (involved in
atherosclerosis), vascular reactivity, fibrinogen,
homocysteine, LINE-1 methylation, risks of different
arrhythmias, T-wave alternans, telomere length
Cognition: in elderly, in children
HSPH studies, all including BC/EC

In the 10 studies (of 37) with good subject
exposure to BC/EC:





All 10 found BC/EC associations
In 4 studies using PM2.5, half found PM2.5 associations
In 2 studies using sulfate or regional emissions, no
associations
In this limited sample with good exposure, higher % of
BC associations than for either PM2.5 or sulfate
Schwartz et al. (2005) example of benefits of good
exposure, monitoring several PM2.5 species (next slides)
Schwartz et al. (2005) study of 4
HRV measures




8 tests of pollution associations: (two time
periods, 4 different measures of HRV)
Study found associations with BC in 7/8 tests
PM2.5 associations found in 3/8 tests
Authors subtracted BC from PM2.5 on hourly
basis, called the remainder “secondary PM”
 No associations with “secondary PM,”
similar to findings of Suh and Zanobetti
(2010) and others
Monotonic decrease in HRV with
increase in BC (Schwartz et al, 2005)
No HRV associations with regional
PM2.5 with accurate BC exposure
Importance of Schwartz et al.
(2005)


Allows comparing effects of different PM2.5 species,
with good exposure information, thus can show
importance of BC as a result
Before BC monitoring, this study would have been
just one more study simply finding PM2.5
associations, unable to interpret which PM2.5 species
might be harmful
HSPH studies, all including BC

Remaining 27 HSPH studies, which do
NOT have good BC exposure information



Significant BC associations in 20/27 studies
(surprisingly, despite poor exposure information)
Significant PM2.5 associations in 20/25 studies
Significant sulfate associations in 8/14 studies

No metals included, something for future research
HSPH studies, last slide

Several of these 27 studies stated that BC associations
were unexpected, that BC associations should have been
attenuated. Example:
 “Particle measurements with…local sources, such
as mobile source emissions of BC, are typically
more spatially heterogeneous than regional
pollutants ...Therefore, we would have expected
associations to be most attenuated for BC due to
measurement error. This was not the case, as most
of the strongest observed associations involved
BC…” (O’Neill et al., 2007)
Delfino et al. studies






Included BC, EC, OC, particle number, “quasi-ultrafine” PM, secondary
and primary OC
Excellent exposure information (monitors inside and outside
residences of retirees in Los Angeles area)
Studied many intermediate CVD outcomes
Daily averaging times up to 9 days
BC/EC/primary OC associated with outcomes in large majority of
cases
Where compared, secondary organic carbon usually not associated, or
less strongly associated that primary organic carbon
 Among first studies to do such a comparison (need more study)
Introduction of EZ Pass and Birth
Outcomes
(green circles = toll plazas)
Examples: Birth Outcomes Introduction of EZ Pass

When EZ pass was introduced in late 1990s in
New Jersey, and Pennsylvania, two results


Less congestion, less idling, less acceleration = > less
pollution at toll plazas
After EZ pass introduction, for mothers living w/in 2
km of toll plazas, 11% reduction in prematurity, 12%
reduction in lower birth weight, vs. those living w/in 2
km of freeways, but further from toll plazas

(Currie and Walker, 2009, including graphic on previous slide)
Birth Outcomes with Traffic Emissions –
Studies by Ritz, Wilhelm and colleagues,
other researchers

Researchers found associations with a range of adverse
birth outcomes (Table S9, 19 studies):


pre-term birth and measures of low birth weight (most studies),
spontaneous abortion, preeclampsia in mother, small for
gestational age, (childhood cancers - one study)
Outcomes associated with many different measures of
vehicular emissions:




Various vehicular emissions modelled to residence
Proximity to major highways
Cumulative traffic density near residence
Central monitor readings (but only if not too distant from
residence)
Effects on Brain and Central
Nervous System

DNA adduct: bonding of DNA to a carcinogen, such as
PAH, causes mutations and other biological changes,
marker for exposure (courtesy Dr. Frederica Perera)
Maternal PAH exposure and IQ of
child (Perera et al., 2009)


Pregnant women wore personal monitors to
record exposure to PAHs
After controlling for smoking, mother’s IQ and
education level:

Children with prenatal maternal PAH exposure
above the median exposure had full scale and
verbal IQ scores 4.31 and 4.67 points lower
than children with PAH exposure below
median
Maternal PAH exposure and IQ of
child (Perera et al., 2006)

Same conditions (personal monitors,
controlling for potentially confounding
variables) as in previous slide:

Highest quartile of prenatal PAH exposure
significantly associated with lower mental
development at age 3 (Bayley Scales of Infant
Development)
BC associated with
reduced cognition


BC modeled to homes of children (Suglia et al., 2008)
After usual adjustment for socioeconomic
factors, smoking, birth weight, blood level:


Increased BC associated with decreases in 5 tests
of cognition; all results but one (vocabulary)
statistically significant
Previous 3 examples are from 12 CNS studies in
Table S10
How best judge which PM2.5 species are
causally related to mortality, morbidity
outcomes?


EPA uses several appropriate criteria to
determine potential causality of PM2.5
We recommend that their use be extended to
examine effects of different PM2.5 species,
whenever any governing or regulatory body
may wish to go beyond PM mass, regulate
specific PM2.5 species
Several EPA Criteria for judging
Causality of PM2.5

1. “Consistency of the observed
association”

Do many epidemiology studies, using
different designs, in multiple locations, with
different data sets, consistently show
elevated risks for a given mortality or
morbidity endpoint?
Several EPA Criteria for judging
Causality of PM2.5

2. “Coherence”

Are consistent associations in population
based epidemiological studies supported by
other findings from human panel,
controlled human exposure, and animal
toxicology studies? (Emphasis on continuity
across study types)
Several EPA Criteria for judging
Causality of PM2.5

3. “Biological plausibility”

Have biological mechanisms been found
supporting links between exposure to an
agent and adverse effects in humans?
(emphasis on finding biological
mechanisms which explain epidemiological
findings)
Several EPA Criteria for judging
Causality of PM2.5

4. “Experimental evidence” (Natural
Interventions, such as ventilation of
tunnels, introduction of EZ pass)

Does a change in exposure to an emission
bring about a change in occurrence of
health effects?
Assessing BC/EC with these
metrics
So….what do we find?
1. Consistency of Associations for BC




YES
Only handful of ~ 140 studies failed to find BC/EC
association (or associations using other markers for
vehicular emissions)
This was true even for the large majority of studies,
which used central monitor data, which should have
lessened and minimized associations
Associations were more frequent for
BC/EC/vehicular than with any other PM2.5
species, despite less exposure misclassification
for several other species
1. Consistency of Associations for BC


These findings help explain Janssen et al. (2011)
findings that reducing a unit of BC will extend life
by 4 to 9 times as will reducing an equivalent
unit of PM2.5
“Face Mask” studies show that removing diesel
PM abrogates diesel-emission effects in healthy
humans

Use of face mask increases vasodilation,
decreases thrombus formation, increases release
of “clot-busting” tPA (Lucking et al., 2011)
1. Consistency of Associations



Mostofsky et al. (2012), next slide: instead of
different authors, mixes of PM2.5 species,
populations, we have the same authors, PM2.5
species, population
But we have 3 different approaches to
modelling associations in same study, with
same data
Result is still consistent results for BC (but not
for other PM2.5 species, except Ni)
Mostofsky et al., 2012: (3 different
methods of examining ischemic stroke
associations with same data)
2. Coherence


Yes.
Evidence from human panel studies,
controlled human exposure studies,
toxicology supports CVD associations
with BC found in population based
epidemiological studies of all types
examined today
3. “Biological plausibility”



Yes.
Multiple biological mechanisms
(intermediate causes of CVD mortality,
morbidity) found in toxicology studies of
cells, animals;
Many of these same mechanisms found in
human panel studies, controlled human
exposure studies to diesel emissions
4. “Experimental evidence”



Yes.
Bridge and traffic officers (Stern et al.,
1988); EZ Pass study
We might think of highway proximity
studies in the same way (differential
exposures)
Importance of size, chemistry
(NRC 1998 Recommendation)

Both are important to CVD, other outcomes:


Tiniest particles penetrate deeper into lung,
penetrate cell wall more easily; smaller PM often
more harmful than larger PM of same type,
everything else equal
But if the particle doesn’t disrupt cellular activity,
may cause little harm – hence role for chemically
active compounds (next slide)
Examples of importance of
chemistry

Several studies find increased arterial plaque,
lipoperoxidation, or oxidative potential caused by
exposure to BC, by denuded organics from BC, or by
SVOCs, but not by EC core itself:


Kleinman et al., 2013; Verma et al., 2011; Biswas et al., 2009
Other studies have found that tiny ultrafine PM (12
nm) does not cause DNA strand breaks or increases
in DNA repair sites, but slightly larger SVOC PM (23
nm) and ultrafine “soot” PM, enriched in organics (57
nm), do cause one or both (Brauner et al., 2007)
Ultrafine PM causes more oxidative stress
than larger PM, contains more PAHs; more
PAHs => oxidative stress (Li et al., 2003)
Does exposure to BC/diesel emissions
shorten life by shortening telomeres?
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Telomeres are like plastic caps on shoelaces, except
they are at the end of your chromosomes, serve a
similar protective function
When your cells divide, telomeres insure that cells
divide perfectly, but they shorten with each division
When telomeres get too short, your cells don’t
divide any more => senescence, biological aging
Dr. Elizabeth Blackburn won Nobel Prize (2009) for
her work with telomeres
Chromosome with telomere
highlighted
Can diesel/BC cause shortened telomeres,
accelerated biological aging?
Tale of two literatures
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Large biology literature finds that chronic
oxidative stress causes telomeres to shorten
more quickly, thereby accelerating biological
aging, especially CVD states
Air pollution literature finds that diesel
emissions/BC are associated with chronic
oxidative stress

HEI (2010) speculated whether oxidative stress might
be major underlying mechanism by which vehicular
emissions cause harm (telomeres not addressed)
Can diesel/BC cause shortened
telomeres, accelerated biological aging?
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Grahame/Schlesinger (2012) hypothesize that
diesel/BC emissions might cause the accelerated
CVD (mortality and morbidity), observed near
roadways, and with exposure to BC, via oxidative
stress which may shorten telomeres, cause
biological aging, various CVD morbidity states
Theory obviously needs replication, very easily
could be wrong, but has possible advantage of
single explanation for many different CVD effects
(vs. many different explanations)
Very brief look at pollutants,
health effects elsewhere
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Natural experiments
PAHs, BC concentrations
“Natural Experiments” Elsewhere
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Launceston, Australia
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(Johnston et al., 2013)
Town of ~ 67,000, in a valley subject to
inversions, much burning of wood for heating
Big push to convert to electric heat (hydro)
3 years later, wood heat dropped from 66%
to 30% of households
14.4% drop in all-cause, 17.9% drop in CVD
mortality rate among men, not observed in
other locales
Huai River policy: North of river, coal (no
pollution controls) provided free for
heating for decades, equipment still used
Effects of Huai River Policy
Natural Experiment
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Life expectancy north of Huai river 5.5
years less than south of river, mainly
due to cardiorespiratory mortality
Equivalent to 2.5 billion (with a B) life
years lost, based upon 500 million
people living north of river
PAH levels in Northern China, where
coal is used extensively for heating
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Wu et al. (2011): PAH levels in Tianjin were
2165.2 ng/m3 in winter (vs. 11.72 ng/m3 in
autumn)
Wang et al. (2011): 39.4 ng/m3 (“Background
site”), 355 ng/m3 (“rural village”), 1010 ng/m3
(“urban”) annual levels
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Comparison: Boston, MA = 18 ng/m3 (Levy et al.,
2003)
BC Estimated Emissions in Different
Countries (excl. open biomass burning)
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US:
OECD Europe:
China:
India:
294
293
1706
406
Gg/yr
“ “
“ “
“ “
Source: Representative Concentration Pathways
(RCP) database (version 2.0) assembled for the IPCC
Fifth Assessment Report (AR5) – see Table 1 in CR
Conclusion

BC and other traffic emissions (e.g.,
PAHs, SVOCs) appear to be causally
associated with all-cause and CVD
mortality, CVD morbidities, lung cancer
mortality (IARC)
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Probably also with adverse birth outcomes
and central nervous system effects, evidence
appears strong, may need more replication
Thank you!
Remaining slides to be used
only if needed for discussion
Diesel Exhaust as a Hazardous
Air Pollutant
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http://www.epa.gov/ttn/atw/natamain/gloss1.html
(last updated Feb. 22, 2011)
Diesel particulate matter: Diesel particulate matter
(diesel PM) is a mixture of particles that is a
component of diesel exhaust (DE). EPA lists DE as a
mobile source air toxic due to the cancer and
noncancer health effects associated with exposure
to whole DE.
Example: Laden et al, 2000 (sulfates from
different sources are present)
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Study examines associations with daily mortality in
six cities (1979-1988) of markers for:
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vehicular emissions (Pb)
dust (Si)
coal combustion (Se)
For Se, and separately for sulfate as S, findings are
counterintuitive –
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Only Boston (city with lowest Se, and near lowest S) had
significant mortality associations for either Se or S
Localities with considerably higher Se and S (St. Louis,
Steubenville, Knoxville) had no Se or S mortality
associations
Laden et al (2000) Se and S findings
Example: Laden et al., 2000
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Why the “reverse dose response function”?
Long story short:
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Residual oil as burned contains traces of Se
Using EPA data source for ratio of V to Se in asburned residual oils, over 2/3rds of Se in Boston
air from local residual oil (1,700 MW) in 1980s
Calculated that about half Boston sulfate was also
from residual oil combustion, mostly primary V
sulfates, with Ni as well
Residual oil emissions are very toxic relative to
secondary sulfate, coal fly ash
Conclusions re Laden et al (2000)
findings
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Se and S were significantly associated with daily
mortality only in Boston, because only in Boston was
residual oil an important source of each in ambient air
Se and S were not associated with daily mortality in
localities with higher levels of each, because in those
localities, there were no residual oil emissions
Associations per se don’t necessarily point to harm –
have to understand toxicity of different co-emissions, in
this case V and Ni from residual oil
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Reference: Grahame and Hidy, 2004