Philip Morris
Environmental Tobacco Smoke: A Compendium of Technical Information
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ENVIRONMENTAL TOBACCO SMOKE:
A COMPENDIUM OF TECHNICAL INFORMATION
May 1991 DRAFT
DISCLAIMER
This document is a preliminary draft. Do not cite or quote.
The contents represent only those views of the individual
chapter authors. It should not be construed as representing
the views or policies of the participating organizations.
Draft - Do not cite or quote
PREF'ACE
This compendium of technical perspectives on Environmental
Tobacco Smoke (ETS) is intended to be a useful resource document
for a diverse audience, including: decision-makers such as labor
and management officials concerned with workplace exposures, public
health officials and corporate medical directors who are concerned
with making health policy recommendations, educators, industrial
hygienists and safety officers, ETS researchers, indoor air
pollution investigators, and legislators who are considering
legislation to restrict smoking in workplaces, restaurants, and
public access buildings. Although the technical level varies, even
the more technical treatments do not require a specialist's
knowledge for understanding. There are eleven chapters in this
compilation, including health effects of active smoking in adults
and passive smoking in children and adults, ETS exposure and
dosimetry, comfort aspects, ventilation and ETS, public beliefs
about the harm of ETS and attitudes toward controls, and effective
workplace smoking policies, each of which is aimed at a somewhat
different aud?.ence. Although not all chapters will appeal equally
to such a varied group, it is hoped that the technical information
in this document, written by experts in the field, will provide
information necessary to allow the public, corporations, government
agencies, and legislators to make well-informed choices regarding
exposure to ETS.
This perspective on ETS reflects the viewpoints and expertise
of authors who were selected based upon their publications and
recognition as experts on various aspects of ETS. Accordingly, the
opinions expressed do not necessarily represent the official
policies of the sponsoring agencies.
This document is the result of a coordinated effort jointly
sponsored and produced by the Environmental Protection Agency (EPA)
(chapters 2,3,4,6,7, and 8), the National Cancer Institute (NCI)
(chapters 1,5), the Office on Smoking and Health (Centers for
Disease Control) (chapter 9), the National Heart, Lung, and Blood
Institute (chapter 10), and the Office of Disease Prevention and
Health Promotion (Department of Health and Human Services) (chapter
11).
The editors acknowledge with gratitude the following distinguished
scientists, physicians, and others who lent their support to the
development of this document by contributing critical reviews of
the various manuscripts, by coordinating manuscript preparation,
or assisting in other ways.
Mr. Robert Axelrad, U.S. Environmental Protection Agency,
2
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Washington, DC (Sponsor)
Dr. Lois Biener, Miriam Hospital, Brown University, Providence, RI
Ronald Davis, M.D. Office on Smoking & Health, Centers for Disease
Control, Rockville, MD (Sponsor)
James W. Davis, M.D., Veterans' Administration Hospital, Kansas
City, MO
Ms. Hildy Dillon, American Lung Association, New York, NY
Dr. Cedric Garland, Dept. of Community Medicine, University of
California, San Diego, CA
Dr. Stanton A. Glantz, Department of Cardiology, University of
California Medical School, San Franscisco, CA
Dr. Lawrence Garfinkel, American Cancer Society, New York, NY
Dr. Katherine Hammond, Dept. of Family & Community Medicine
University of Massachusetts Medical Center, Worcester, MA
Dr. Marvin Kristein, State University of New York, Stony Brook, NY
State Univ. of New York, Stony Brook
Dr. Joellen Lewtas, Office of Research & Development, U.S.
Environmental Protection Agency, Research Triangle Park, NC
Dr. Alfred H. Lowrey, Laboratory for the Structure of Matter,
Naval Research Laboratory, Washington, DC
Henry McIntosh, M.D., American College of Cardiology, Washington,
DC
Dr. Michael McGinnis, Office of Disease Prevention and Health
Promotion, Public Health Service, Washington, DC (Sponsor)
Matthew Meyer, Esq., Coalition on Smoking or Health, Washington,
DC
Dr. Gregory Morosco, Health Education Branch, National Heart, Lung,
and Blood Institute,.Bethesda, MD (Sponsor)
Dr. Demetrios Moschandreas,
Research Institute, Chicago, Illinois Institute of Technology
IL
Dr. David Mudarri, , U.S.
Washington, DC
Dr. Terry Pechacek, Smoking, Environmental Protection
Tobacco, and Cancer Program, Agency,
National
~
Cancer Institute, Bethesda, MD (Sponsor) ~
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Mr. James Repace, U.S. Environmental Protection Agency, Washington,
DC (Editor)
Mr. Donald Shopland, National Cancer Institute, Bethesda, MD
(Editor)
John Slade, M.D., Dept. of Medicine, St. Peter's Medical Center,
Rutgers University, New Brunswick, NJ
Dimitri Trichopoulos, M.D., DrPH, Harvard School of Public Health,
Boston, MA
The editors also acknowledge the comments of the tobacco industry.
Mr. Samuel D. Chilcote, Jr., President, The Tobacco Institute,
Washington, DC
Dr. Thomas Borelli, Phillip Morris USA, Richmond, VA
4
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TABLE OF CONTENTS
Chapter 1. Effects of Smoking on Smokers.
Donald Shopland ..............................................9
Chapter 2. Environmental Concentrations of ETS.
John McCarthy, Elizabeth Miesner, and John D.
Spengler ..................................................... 16
Chapter 3.
Smoke.
Measuring Exposure to Environmental Tobacco
Brian P. Leaderer ...................................... ..... 31
Chapter 4. Absorption of Smoke Constituents by
Nonsmokers. Dietrich Hoffmann, Klaus D. Brunnemann,
and Nancy J. Haley ...........................................43
Chapter 5. Environmental Tobacco Smoke and Cancer.
Jonathan M. Samet ........................................... 67
Chapter 6. Passive Smoking and Heart Disease.
Stanton A. Glantz and William W. Parmley ..................... 81
Chapter 7. Exposure Assessment in Passive Smoking.
James L. Repace ...........................................112
Chapter 8. The Odor and Irritation of Environmental
Tobacco Smoke.
William S. Cain ............................................137
Chapter -9. Passive Smoking -- Beliefs, Attitudes,
and Exposures in the United States.
Thomas E. Novotny ...........................................152
Chapter 10. Passive Smoking and Daycare.
Glen L. Bennett .............:..............................180
Chapter 11. No Smoking Policies at the Worksite: A look at
what companies are doing today.
Ruth Behrens ............................................... 197
Chapter 11 Appendix: Economic Justification for
Worksite Smoking Policies.
Ruth Behrens ...............................................219
5
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INTRODUCTION
In 1986, the Surgeon General and the National Research
Council, the latter under contract to EPA, examined the health
effects of the breathing of Environmental Tobacco Smoke (ETS) by
nonsmokers (also known as involuntary or passive smoking). They
agreed that passive smoking caused lung cancer in nonsmoking
adults, caused increased rates of respiratory infections in
children, caused acute noxious effects in many nonsmokers, and was
a major contributor to indoor air pollution. Subsequent to the
publication of these documents, smoking restrictions began to
proliferate. However, a number of diverse technical questions
arose concerning public attitudes toward smoking restrictions,
health and comfort effects, factors affecting exposure, measuring
environmental concentrations of ETS, effects of ventilation on ETS
and'indoor air quality, nonsmokers' uptake of tobacco combustion
products, and corporate experience in effective smoking policy, all
comprise chapters in this compendium. In the interest of providing
answers to this complex of questions, this technical compendium was
commissioned. A brief summary of each chapter followsc
Chapter 1 demonstrates that high dose exposures to tobacco'
smoke, i.e., the effects of smoking on smokers, are very toxic,
causing cancers, cardiovascular diseases, and respiratory diseases.
it is graphically illustrated why cigarette smoking is now
recognized as the Nation's single largest cause of premature death
and disability.
Chapter 2 reviews studies of the concentrations of certain
ETS constituents observed in homes, offices, and other locations
by personal exposure monitors. It is concluded that ETS is the
primary contaminant contributing to respirable particulate air
pollution, and contributes substantially to other indoor
contamininants such as benzene, carbon monoxide, and others. Even
in low doses, tobacco smoke contains a wide variety of toxins,
including many carcinogenso
Chapter 3 treats the methods of assessing nonsmoker's exposure
to environmental tobacco smoke by atmospheric markers, and the
measurement of these marker substances in indoor air. It is
concluded that atmospheric monitoring for respirable particles or
nicotine from ETS is critical for assessing exposures and control
efforts, and that a number of reliable methods are available for
such monitoring.
Chapter 4 provides a detailed treatment of the absorption and
metabolism of tobacco combustion products by nonsmokers. It shows
that absorption has been conclusively demonstrated by studies of
nicotine and its metabolite, cotinine, in the body fuids of
nonsmokers, and that such biomarkers represent a reliable specific
method for assaying the level of uptake of ETS. This exemplifies
6
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that low dose exposure to tobacco smoke leads to the absorption of
toxins from the smoke in amounts sufficient to potentially cause
disease.
Chapter 5 discusses the evidence that low dose exposure to
tobacco smoke has been observed to increase the risk of lung cancer
in nonsmokers, and discusses conclusions of the World Health
Organization, the National Research Council, and the U.S. Surgeon
General that ETS exposure increases lung cancer incidence in
nonsmokers.
Chapter 6 discusses the evidence that low dose exposure to
tobacco smoke has been observed to increase the risk of heart
diseases in nonsmokers, and discusses the epidemiological,
biochemical, and biological bases for this inference. It is
concluded that the combined epidemiological and physiological
evidence suggests that ETS exposure is a cause of heart disease in
nonsmokers.
Chapter 7 investigates the assessment of nonsmokers' exposures
to ETS by mathematical modeling, atmospheric indicators, and
biomarkers in body fluids. Exposures assessed by these various
methods produce consistent results. Because of the large source
strength of tobacco-burning products, exposure to environmental
tobacco smoke is inadequately controlled by measures short of
physical separation of smokers and nonsmokers on different
ventilation systems, making ETS a significant indoor pollutant of
buildings.
Chapter 8 explores the effects of ventilation on the
perception of odor and irritation from ETS in both nonsmokers and
smokers, and shows that attempts to control the odor and irritation
of ETS through ventilation and air cleaning have significant
limitations.
Chapter 9 shows through national surveys of trends in public
attitudes, that the general public, including both smokers and
nonsmokers, believe that tobacco smoke polluted air is harmful and
a large majority find it irritating. There is widespread support
for restrictions against smoking, particularly in the workplace.
Chapter.10 discusses the evidence that smoking both at home
and in daycare centers harms children and infants from tobacco-
smoke polluted air. This has direct -implications for public
education of both parents and daycare providers, as well as for
state policies and regulations affecting facilities which offer
daycare.
Chapter 11 points out the common solution to the problem of
ETS is source control, and examines features of corporate smoking
policies in the workplace, with attention to benefits, incentives,
employee and union involvement, and education. Case histories are
7
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discussed involving several major corporations, detailing problems
encountered and successes. It is concluded that smoke free
workplaces have been achieved in a variety of settings. if
thoughtfully implemented, they enjoy widespread support.
8
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CHAPTER 1
EFFECTS OF SMOKING ON SMOKERS
Donald Shopland
Coordinator
Smoking and Tobacco Control Program
National Cancer Institute, Bethesda, MD
Cigarette smoking is the nation's leading cause of premature
death and disabilityo In 1985, smoking caused approximately
390,000 deaths in the tJnited States (Figure 1). By 1991, this
number had increased to 440,000. In addition, tens of millions of
people suffer from chronic disabling diseases and conditions caused
or aggrevated by smoking. Every medical authority and organization
who has objectively examined the evidence linking smoking to early
death and disability has reached a similar conclusion. The
,evidence that smoking is a major health threat is staggering: over
50,000 citations from dozens of cultures are in the scientific
literature. Smoking causes or is associated with cancers of the
lung and bronchus, larynx, lip and oral cavity, bladder, pancreas,
kidney, stomach and cervix, coronary artery disease,
cerebrovascular disease (stroke), atherosclerotic aortic aneurysm,
atherosclerotic peripheral vascular disease, chronic bronchitis,
emphysema, low birth weight babies, and unsuccessful pregnancy.
This chapter concentrates on the relationship between active
smoking and three diseases caused by ETS -- lung cancer, heart
disease, and nonmalignant lung disease. While there are
qualitative differences between the mainstream smoke inhaied by the
smoker and the ETS nonsmokers inhale, both forms of tobacco smoke
contain the same carcinogens, irritants, and other toxins. The
effects of high doses of smoke on smokers thus provide an
indication of what effects low dose exposures of ETS would be
expected to have on nonsmokers. This connection is particularly
important because the diseases active smoking causes exhibit dose-
response relationships, with higher doses producing greater
effects. Because no threshold has, been demonstrated for the
carcinogenic and other effects of tobacco smoke on tne body, the
existence of a dose-response relationship suugests that ETS would
provide similar, but smaller, dangers than active smoking.
Cancer
Most estimates in the scientific literature indicate that
nearly one-third of all U.S. cancer deaths result from cigarette
smoking. Of the approximately 136,000 cancer deaths which occurred
in 1985 because of smoking, 106,000 are of the lung (Figure 1).
Lung cancer alone is responsible for fully one-quarter of all
9
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cancer mortality; were it not for the increasing number of deaths
from lung cancer produced by smoking, we would be experiencing a
substantial decline in the cancer death rate in the United States.
Approximately 85 to 90 percent of all lung cancer deaths are
smoking related. The evidence linking smoking and excess cancer
mortality is so strong that only the tobacco lobby continues to
claim that no causative role has been established. An examination
of the association between cigarette smoking and lung cancer
graphically illustrates smoking's role in the causation of
neoplastic diseases.
Tobacco smoke contains at least 43 known or suspected human
carcinogens (Table 1), several of which are regulated by the
federal government as environmental toxins. There is no known
threshold for the carcinogenic effects of these agents.
A host of epidemiological studies published during the last
two decades provides an abundance of data which demonstrate that
exposure to these carcinogens because of smoking leads to an
increase in cancer deaths. In particular are the major prospective
studies on smoking and health. These studies, conducted in the
United States, Canada, England, Japan and Sweden represent some of
the largest population based studies ever undertaken by medical
science (Table 2). They involved enrolling healthy men and women
into a study design and then followed these individual over time.
Numerous factor about them were recorded including where they
lived, their occupations, dietary habits, whether they used
tobacco, access to health care, and many other factors. As a
group, these eight studies in the United States, the U.S. Veteran's
Study and the American Cancer Society (ACS) 25-state Study
contained cohorts of 290,000 and 1 million persons respectively.
The Veteran's Study continues to this day and this cohort has been
followed prospectively for 26 years. These studies convincingly
demonstrate that smoking causes cancer.
Lung Cancer
Lung cancer mortality rates are strongly influenced by the
total dose of cigarette smoke received. If one smokes more
cigarettes per day, inhales deeply, if they started smoking at an
early age had has smoked for many years, the risk for lung cancer
.is increased dramatically.
The most often used measure to gauge lung cancer mortality is
the number of cigarettes consumed daily. In the ACS 25-state
study, for example, among males smoking less than 1/2 pack per day
their lung cancer rate was nearly 5 times greater than that of a
nonsmoker. With each increase in the number of cigarettes consumed
daily, a corresponding increase in lung cancer mortality is
observed (Figure 2). For those smokers consuming two or more packs
daily, their lung cancer mortality is about 24 times greater than
10
