Human Exposure to Environmental

Tobacco Smoke:

Is What You See What You Get??

Roger A. Jenkins, Ph.D.

Presented to the Bloomberg School of Public Health

Johns Hopkins University
February 9, 2005
Sponsors of the ORNL Tobacco Smoke
Characterization Program
National Cancer Institute
Federal Trade Commission
National Institute on Drug Abuse
Council for Tobacco Research USA
University of California-Davis
Center for Indoor Air Research
Brown & Williamson Tobacco Co.
Philip Morris USA
Hotel Association of Canada
 ORNL ETS
“Real World” Studies

¾ Restaurant patron study part of airborne nicotine method development

z 32 venues, published in 1989
¾ Area vs Personal Monitoring
z Variety of venues (ca. 25) included restaurants, laundromats, bowling alleys, etc. Reported
in 1990
¾ 16 Cities Personal Exposure Monitoring
z ca. 1600 subjects geographically dispersed Published in 1996
¾ Waiters/waitresses/bartenders
z ca. 160 subjects, area & personal monitoring. Published in 2000
¾ Demographically representative study
z Personal exposure monitoring of ca. 240 subjects. Reported in 2000
¾ Phoenix/Louisville area monitoring study:
z Intense area monitoring of 6 restaurants and bars. Reported in 1999, some results
published in 2004.
¾ Unrestricted smoking workplace
z 25 subjects in one facility: area vs personal monitoring. Published in 2001
¾ “Black Dog Pub Study
z Area samples demonstrated that one can achieve “regulated non-smoking levels” with
ventilation: Published in 2002
¾ ETS Exposure Variability: on-going
Environmental Tobacco
Smoke 101
 The Two Phases of Tobacco Smoke
¾ Particle Phase, made up of liquid
droplets which are comprised of
higher MW hydrocarbons.
z This is the smoke that is visible,
because the tiny droplets scatter light.

¾ Vapor Phase, made up of volatile

organic chemicals and permanent
gases, such as carbon dioxide, carbon
monoxide, methane, ammonia.
z The vapor phase is not visible to the
human eye.
 Environmental Tobacco
Smoke: What Is It?
Highly diluted mixture of sidestream (70 - 90%)
and
exhaled mainstream (10 - 30%) tobacco smoke

Sidestream Tobacco Smoke Exhaled Mainstream Tobacco Smoke

 Environmental Tobacco Smoke:
What Is It? (continued)

¾ Mainstream, sidestream, and ETS are not the same material.

¾ The term “second hand smoke” is probably misleading, since

most ETS is derived from smoke which is emitted by the
smoldering firecone of the cigarette.

¾ Differences between ETS and mainstream smoke are primarily

due to differences in combustion mechanisms between
sidestream and mainstream tobacco smoke.

¾ Differences between ETS and sidestream smoke are mostly

due to the interactions of various components with the
surrounding environment.
 How Do We Determine
Human Exposure to ETS?
 Cooking
Cleaning

Indoor Air Pollution Can Be Derived

From a Variety of Non-Tobacco Sources

Consumer Products Wood Burning

 All Incomplete Combustion Processes Produce
Smoke Comprised of Thousands of Constituents
Many components are toxic at some level, and all
smokes are likely to contain a few “
signature” components
 Desirable Characteristics of
Marker Compounds
(Taken from the National Academy of Sciences Report on ETS)

¾ Useful for describing the concentration of

complex materials.
¾ Unique to the substance in question.
¾ Behaves like the material or phase of the
substance that is being assessed.
¾ Present in measurable quantities even at low
substance concentrations
Environmental Tobacco Smoke
Markers
N
CH3O
N
CH3 O O
HO
Nicotine Scopoletin

N H

CH2 CH3
CH2OH

3-ethenyl pyridine CH3 CH3

8

N Solanesol
N

Myosmine
60,000 Foot View of the Analytical
Chemistry
¾ Analysis of sub-ppb concentrations of
airborne pollutants still ain’t all that easy.
¾ Nicotine and 3-EP: collection on XAD-4 resin,
extraction with ethyl acetate spiked with an
adsorption blocker, and analyzed via GC-
NPD.
¾ Solanesol: extraction with methanol, reverse
phase HPLC with UV absorption detection at
205 nm.
¾ UV-PM/FPM: Column-less HPLC with UV
and fluorescence detection.
 Area vs Personal Monitoring
Personal

Area
Sample Collection in the Workplace

Sampling Head

Sampling Pump
 Technology is Always Improving:
Opaque Filter Holders May Mitigate Post-
Collection Degradation of Solanesol

Filter Holder

Cyclone
Separator

XAD-4 Vapor
Collection
Cartridge
Clear plastic filter holder
Opaque plastic filter holder
used in 16 Cities Study (1993-94)
used from 1997 on
 16 Cities Study:
Urban Areas Distributed Geographically
Seattle

Buffalo Portland
Boise
Grand Rapids
Philadelphia
Indianapolis
Baltimore
Fresno Columbus
St. Louis
Phoenix Knoxville
San Antonio
Daytona Beach
New Orleans
Distribution of 24-hour TWA RSP Levels
Subject Segregation by Self-Reported Home and Workplace Smoking
Status Confirmed by Diary Observations
(All Subjects with Avg. Cotinine <15 ng/mL)

120
Subject Distribution, %

100
80 Cell 1
Cell 2
60
Cell 3
40 Cell 4
20
0
0.1 1 10 100 1000
3
Respirable Suspended Particulate Matter, (RSP), ug/m
 Distribution of 24-hour TWA Nicotine
Levels
Subject Segregation by Self-Reported Home and Workplace Smoking
Status Confirmed by Diary Observations
(All Subjects with Avg. Cotinine <15 ng/mL)
1.2
S u b je c t D is trib u tio n , F ra c tio n

1
Cell 1
0.8
Cell 2
0.6 Cell 3
Cell 4
0.4

0.2

0
0.001 0.01 0.1 1 10 100
3
24-hr TWA Nicotine Concentration, ug/m
 Concentrations of Selected ETS Markers:
Confirmed Smoking/Non-Smoking Locations
Median 24-hr TWA Levels, ug/m3
10
9
2 4 h r T W A L e v e l, u g /m 3

8
7
3-EP
6
5 Nicotine
4 RSP/10
3 FPM
2 Sol-PM
1
0
Smkg Smkg Home/NS NS Home/Smkg NS Home/NS
Home/Smkg Work Work Work
Work
Median ETS Exposures* in Environments
Where Smoking is Unrestricted
Exposure = Concentration x Time

25
Exposure, ug-hr/m 3

20

15
Home (n = 113)
10 Workplace (n = 139)

0
3-EP Nicotine FPM/10
* Smoking confirmed by diary reports
 Distributions of Bartender TWA Nicotine
Levels:
Multi-Room Bar/Restaurants vs. Single Room Bars
100
90
Percent Subject Distribution

80
70
60 Multi-room
Bars/Restaurants
50
Single Room Bars
40
30
20
10
0

0.01 0.1 1 10 100

TWA Nicotine, ug/m3
 Exposures of Wait Staff and Bartenders vs.
Subjects in Unrestricted Smoking Workplaces
and Homes (16 Cities Study)
Exposures in µg-hr/m3
25
Exposures, ug-hr/m3

20

15 Bartenders
Waiters
10 Urstr Smkg Wrkpl
Unrstr Smkg Home

0
Nicotine 3-EP Sol-PM/10
 Typically Encountered Concentrations
of ETS Are Pretty Low

¾ Highest encountered level of respirable

suspended particulates (RSP) in our wait
staff/bartenders study was about 1/7th of
OSHA Permissible Exposure Limit (PEL).
¾ Median area concentration of nicotine was
0.9 parts per billion.
 Are People Good Observers of their Own
Exposures?
Workplace Nicotine Exposure Concentrations of Subjects Reporting
“A Little” Exposure to ETS
10
Workplace Nicotine Level, ug/m^3

1
0 2000 4000 6000 8000 10000 12000 14000 16000

0.1

0.01

0.001
Subject Number
 How Does Living with a Smoker
Compare to Being a Smoker?

??
¾ Typical smoker will inhale 480 mg/day of smoke
particles, and 32 mg per day of nicotine.
¾ In a home where smoking is unrestricted, the typical
non-smoker will inhale the equivalent of 0.45 mg of
smoke particles and 0.028 mg of nicotine.
Do the Math:
The difference is about a factor of 1100
 Breathing ETS Will Expose You to Toxins,
but Not Like Breathing Urban Air
Confirmed Exposures of
Mean Daily Exposure
Teenagers in Urban
Estimate Based on
Volatile Compound Environments from Non-
Living with a Smoker,
Smoking Homes,
µg/day*
µg/day**

Benzene 14 94

Acetaldehyde 126 260

Formaldehyde 66 230
* Estimate based on 16 Cities exposures to nicotine and Baek/Jenkins chamber study,
Atm. Env, 38, 6583 (2004)

** Estimate based on Kinney et al, Env. Hlth. Persp. 110/S4, 539 (2002)
 Variation of 16 hr TWA Nicotine Concentrations,
Subjects Residing in Smoking Homes
2004 Exposure Study
5.0

4.5

4.0

3.5
Nicotin e, u g /m^3

3.0

2.5

2.0

1.5

1.0

0.5

0.0
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47

Subject

Range of Max/Min Ratios: 1 - 80

Biomarkers for ETS Exposure

It’s Not So Simple

 Avg. Salivary Cotinine Level
as a Function of Nicotine Exposure
All Subjects with Both Markers >95% CL above LOD
Nicotine: 0.063 ug/m3; Cotinine: 1.01 ng/mL
Avg. Salivary Cotinine Level, ng/mL

14 R2 = 0.105
12
10
8
6
4
2
0
0 5 10 15 20 25
24-hr TWA Nicotine Concentration, ug/m3
Key Findings from Some Exposure
Studies
¾ For non-smokers in these environments, exposure at
home is greater than exposure at work.
¾ BUT …. “Living with a smoker” can mean different things
for different people.
¾ Salivary cotinine not a good quantitative indicator of ETS
nicotine exposure.
¾ Humans, as a class, are not good at estimating their
exposure to ETS.
¾ For non-smoking bartenders (if you can find one) who
live with smokers, their exposure to ETS at home is at
least as important as their exposure in the workplace.
¾ Demographics is EVERYTHING!
 How do ORNL Results
Fit into THE BIG PICTURE?
 Ratios of 24-hr Exposures of Never Smoking
Women:
Married to Smokers vs. Married to Non-Smokers
Comparison of EPA Estimate with 16 Cities Data
45
40
3-EP
35
EPA Estimated Ratio: 1.75 Nicotine
30 Myosmine
Z-Factors

25 UVPM
20 FPM
15 Solanesol
Avg. Cotinine
10
RSP
5
0
Calc'd from Medians Calc'd from Means
 Impact of Differences in Z-Factor:
EPA Estimate vs. ORNL 16 Cities Data
Z = Exposure ratio of women exposed from smoking spouse
compared with women not exposed from spouse
1.7
EPA Estimate: Z = 1.75
1.6
Relative Risk Factor

16 Cities
1.5 Solanesol: 33
1.4 FPM Nicotine: 36
3-EP: 24
1.3
1.2
1.1
1
0 5 10 15 20 25
"Z Factor"
 Implications for Risk Assessment:
Never Smoking Female “Misclassification”
Rates

3
EPA Estimated
M isclassificatio n Rate, %

2.5
Estimate from 16
2
Cities Data
1.5

0.5

0
How “Never-Smoker” Misclassification Rates
Impact EPA’s Relative Risk Estimation
16 Cities Females
1.4 Cutoff: 100 ng/mL Point Estimate
1.3 Lower 90% CI
E s tim a te d R e la tiv e R is k

Upper 90% CI
1.2
1.1
1
0.9 EPA’s Point
Estimate
16 cities Females
0.8 Cutoff: 30 ng/mL

0.7
0.00% 2.00% 4.00% 6.00% 8.00% 10.00%

At the ORNL determined mis-classification rate, there is virtually no

statistically significance for increased lung cancer risk to never-smokers
 External “Validation” of ORNL Exposure
Studies by OSHA and Upheld by US Circuit
Court of Appeals for the District of Columbia
“ ….For most of those subjects who worked or lived in smoking environments,
the home appears to be a more important source of ETS exposure.
This appears to be due to the larger amounts of time spent away from work,
as well as somewhat greater ETS constituent levels encountered
outside the workplace……..”
ORNL 16 Cities Study (Jenkins et al, 1996)
The Waters at the Confluence of
Science and Public Policy Get
Pretty Choppy Sometimes
 Oak Ridge Lab to Do Smoke Study
Front Page, Knoxville News Sentinel, Thursday, February 13th, 2003

Four-day monitoring to cover all types of

indoor pollution
By FRANK MUNGER, munger@knews.com
February 13, 2003
OAK RIDGE - Oak Ridge National Laboratory researchers plan
to do a first-of-its-kind study on indoor air pollution, including
but not limited to exposure to secondhand tobacco smoke.
About 65 to 70 nonsmokers of varied backgrounds in the
Knoxville area will be recruited for the project.
The Oak Ridge team will begin screening volunteers this spring,
and the work itself will take place in the summer or fall, said
Dr. Roger Jenkins, an analytical chemist who heads the research
project. Individuals will be monitored over a four-day period so
researchers can better understand how exposures vary from day
to day and under different circumstances, Jenkins said. Most
…………………..
 Oak Ridge National Laboratories
seems to be doing Big Tobacco's dirty
work once again.
Globalink Listserve, Friday, February 14th, 2003

Please remind advocates in your areas to watch out for the Oak Ridge National
Laboratories studies and to proactively inoculate coalition members,
policymakers, and the media against this tobacco industry white-washed
science.

As a reminder, Roger Jenkins is funded by the tobacco industry. This work is

bought and paid for by Philip Morris and is done on a private contracting
basis by the Oak Ridge nuclear energy lab apart from its
official Department of Energy work. It comes with a fine print disclaimer
saying that it does not reflect government opinion.
 The Tobacco Wars

March 5, 1998
Dunn/Wiley et al vs RJR Nabisco
Question: (Dr. Jenkins, you are aware
aren’t you) …. that Oak Ridge is also the facility
known for radiating children, is it not, with
leukemia, conducting those experiments
on children?
When I Start to Hear “Marketing Hype”
in what Should be Scientific
Discussions, my BS Antennae Go Up

¾ “My doctor says that there is nothing better

than Brand X for preventing symptom Y.”

¾ Translation Î Brand X is no better than

any of the other brands at preventing
these symptoms
 “Marketing Hype” #1 Promulgated by
SOME Anti- Smoking Activists
Example Permissible Exposure Limits
¾ “There is NO SAFE
level of ETS Compound Concentration, Concentration,
ppm ug/m3
exposure.”
Acetaldehyde 200 360,000
¾ Translation: no
governing body has Acrolein 0.1 250
established a
“permissible exposure 1,3-butadiene 1
limit” for ETS.
Nicotine 500
¾ In fact, standards exist
for many of the Respirable 5000
components of concern suspended
in ETS. particulate
matter
“Marketing Hype” #2 Promulgated by
SOME Anti- Smoking Activists
¾ “Ventilation can not
remove all traces of
ETS.”

¾ Well, duh! Ventilation

can not remove all
traces of anything,
and nothing can.
 Low Ventilation (CO2 > 1000 ppm) is Often
the Culprit When High ETS Levels are
Observed in Public Places
Phoenix Barbeque Restaurant, Feb 19,1999
CO2 above 1000 ppm usually
indicates inadequate ventilation
1800

1600
CO 2 Concentration, ppm

1400

1200

1000
Inside CO2 Level
800
Outside CO2 level
600

400

200

0
17:00 18:12 19:24 20:36

Time
Determining Meaningful
ETS Levels in Hospitality
Venues Can Pose
Additional “Challenges”

“Recycled” air External Sources

 Intelligently Designed Ventilation
Systems Can Do Quite a Bit
¾ Heat recovery ventilation
system at 3100 cfm
¾ Directional air flow from non-
smoking to smoking section.
¾ 1600 cfm added on west side
NS section
¾ 1500 cfm added at S/NS
boundary through three ceiling
diffusers.
¾ All air exhausted from smoking
section.
 Ventilation Works to Reduce
Exposures
¾ Laboratory scientists
use key principles to
minimize their
exposures to hazardous
volatile chemicals all
the time.
z Segregation of the
source term (object
that causes the
pollution)
z Directional air flow
z Significant replacement
with “clean” air.
 Concentrations of ETS in Non-Smoking Areas
Black Dog Pub vs Comparative Facilities

Concentrations, ug/m3
UVPM FPM Sol-PM Nicotine 3-EP
Black Dog Median 3.4 5.4 0.0 0.00 0.18
Non-
Smoking Mean 3.5 5.8 2.5 0.44 0.23
Areas Std. Dev 1.8 2.5 3.7 0.76 0.28
N = 12
95th %ile 6.4 9.6 8.1 1.75 0.70
Non- Median 5.2 8.6 1.5 0.00 0.00
Smoking
Tavern & Mean 4.6 7.2 2.6 0.21 0.07
Food Court Std. Dev 2.3 4.0 5.5 0.28 0.10
Areas
N = 13 95th %ile 7.9 12.1 7.1 0.64 0.23
Impact of Source 16
Nicotine
Segregation and 14
12
Ventilation on ETS Levels 10
8
Source: US Dept of Transportation Study 6
4
2
0
Distant Boundary Smoking

Boeing 737-400
Distant Boundary Smoking
 Clearly, Prohibition of Smoking in indoor
facilities reduces exposure to a significant
source of Indoor Air Pollution, but ……

¾ Ventilation can
remove other indoor
contaminants,
instead of just one.
 The MAJOR Reasons Why People
Accept/Tolerate/Advocate Smoking Bans
¾ They hate the smell of cigarette smoke, and are
willing to overlook scientific inconsistencies because
the absence of ETS makes for a more pleasant
indoor environment.
¾ They hold a personal grudge against the industry
because their father/mother/uncle died of lung
cancer and they want revenge.
¾ They believe that de-normalizing smoking as
socially acceptable behavior will lead to reduced
health care costs for everyone.
¾ They need to be part of a crusade.
¾ It is easier for them to focus on one source of indoor
air pollution than to understand the complexity of the
“soup” we live in, with or without smoking.
¾ They legitimately believe that banning public
smoking will reduce their exposure to toxic
substances.
Biggest Science-Related Hurdles to
Overcome
¾ Getting the public to understand the difference
between personal opinion/beliefs and science.
z In a society where there are still serious debates about
evolution, this can be a real challenge.

¾ Avoiding the “means justifying the end”

syndrome.
z Distortion/”selective reporting” of science in the name of
preventing teenagers from taking up smoking.

¾ Demanding that public health officials provide

perspective for the information they provide.
z Sure there are 43 carcinogens in ETS, but there are
probably about 40 carcinogens in diesel exhaust, wood
smoke, etc
A Chemist’s Interpretation of
the Heath Effects Studies
 Guiding Principle
¾ “The poison is in the
dose…”
z Paracelsus, early 1500’s
¾ If we did not believe that,
we would not drink tap
water, eat lettuce, etc.
 ETS Exposure and
Lung Cancer

Most of the studies to date have been on a very narrow slice of the
population:
z Women who are truly lifetime never-smokers (< 100 cigts smoked ever)
who have lived with their continuously smoking husbands for their entire life.
(Applies to 2 – 5% of the female population.)
¾ If all the studies are taken together, there MAY be a 25% increased
risk in these subjects relative to lifetime never smokers. (10.8 per
100,000 vs 8.67 per 100,000).
¾ Risk assessment generally irrelevant for former smokers. Health effects
only apply to TRUE LIFETIME NEVER SMOKERS
¾ EPA estimated excess lung cancers due to ETS 1/4th that due to radon
exposure.
¾ Results have NOT been consistent. For example, a broader, more
recent PROSPECTIVE study in California showed NO increase in risk
to lung cancer, heart disease, or COPD.
 ETS Exposure and
Heart Disease
¾ At the current measured exposure levels, it is
very difficult to conceive of a plausible
biological mechanism based on what we
understand today. CO from other sources
much more important, and nicotine levels
from ETS just too low.
¾ Note that “health effects” studies used
questionnaires to assess lifetime exposure.
 ETS Exposure and Lower
Respiratory Disease
¾ Definitely seems to be a factor of 2 – 3
increase among pre-school age children
whose parents smoke at home.
¾ Note that this matches the criteria used by
NCI as a measurable increased risk.
 Why I Remain Very Skeptical
¾ The observed risk factors, if
significant at all, are barely
above “statistical significance.”
¾ The science being done in some
cases – not all – is shoddy at
best.
¾ The smear tactics used by
advocates suggest an
unscientific mindset.
 The Bottom Line
¾ Assessing actual human exposure to ETS can be very
complex.
¾ Studies to date show that overall ETS exposures are
low, and in most cases, you get more from living with
a smoking spouse than anywhere else.
¾ From a chemist’s perspective, some acute
problems (asthma, bronchitis, lower respiratory
disease) associated with ETS are probably real. The
increased risk of chronic diseases (lung cancer, heart
disease) is probably below epidemiology’s detection
limit, given the confounders.
¾ If you like to get verbally abused, study ETS and
publish politically incorrect scientific findings.