THE HEALTH
           . 1 I
CONSEQUENCES
OF INVOLUNTARY
SMOKING

a report of the Surgeon General

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
P&k Health Smvke


            `.rtStCstlAs"Or*t.LI*.ND*"UI1ot.",(t~
                  ".s*l*GI"* DL mie,

               MC I 5 1986

The mnorable George Bush
President of the Senetc
W..hington. D.C. 20510

Desr Mr. President:

  It is my pleasure to transmit to the Congress the 1986 Surgeon Gener.1'.
Report on the halt? consequence. of smking, . . mandated by Section g(s) of
the Public Re.lth Cxgsrette S-king Act of 1969.
me "e.lth Consequence* of involunt.ry Smking   The current volume, entitled
                           , exuine. the scientific
evidence on the he.lth effect. re."lttng from mn.mker exposure to
envirollaenr.1 tob.cc" snake.

  The issue of whether or mt tob.cco slake is c.rcinogeaic for humans was
conclusively resolved mre thss 20 ye.=. *go when the first report on *staking
*ad heslth w.. issued in 1964.  Eased on the c"rrent report, the judgment c.n
11)y be tude that exposure to envim-nt.1 tob.cco s-kc csn E.".c disesse,
including lung cancer, in mnstmkers.  It is *la clear th.t simple .ep.r.cioa
of smkers snd mns~ker. within the ..Y sirspsce uy reduce but canmt
elimin.te mnsmker exposure to envirorucnt.1 tobacco slake.

  Ihe report .lw review. *II extensive body of evidence which e.t.bli.he. .O
incressed risk of reapir.tory illness snd reduced lung function in infsnt. .nd
very y~"ng children of p.rent. rbD .oke.  Ihi. effect is ~)re pmmuaced if
both pxent. sake than if only one p.rent sakes. A. . phy.ici.n. I believe
th.t p.reot. should refr.in from -king *round s-11 children both s. . r.n.
of protecting their children'. heslth and to set . pd o rqle for the child.

  Today, only 30 percent of the adult populstion in the United gt.te. .re
*mker.-the 1are.C level of soking in the country since World Ysr II,
reflecting th.t the grest msjority of the populstion h.. never mked or hr.
*"cce**f"lly quit.

  Accompsnying this decline in over.11 prevslence of cigsrette smking h..
been sn Lcrersed cancera for protecting the he.lth .nd well being of
mnsmxker., s. evidenced by the number of lr. and reyl.tion. restricting
soking in public plsces.  Todsy, 40 gtste. snd the District of Dlubi. hsve
enacted some fotn of legislstion to restrict swking in public.  Increasingly,
these lr. pertsin to protecting mnswkcrs in uny different setting.,
including the varkplsce.

  B..ed on the evidence presented in this report. the choice to slake .hD"ld
n"t interfere with the mn.aDker'. choice for sn environment free of tob.cco
.aDke.

                       Sincerely,

                          .
        &gwhNtQ m%

                     Otis B. gown, M.D.
                       secretary

enc1o.ure


DEL 5

The ibnorable Thomas P. O'Neill, or.
Speaker of the H3u.e
of Representatives
Washington, D.C.  20515

Oear Hr. Speaker:

  It is my pleasure co rransmit to the Congress the 1986 Surgeon
General's Report an the health consequences of sroking, . . mandated by
Section B(a) of the Public Health Cigarette Smklng Act of 1969. The
current volume. entitled The Health Consequences of Involuntary Swking,
examines the ocieotific evidence on the health effects resulting from
nonsmoker exposure to environmental tobacco smoke.

  The issue of whether or mt tobscco awke is csrcimgenic for humans
~88 conclusively resolved m)re thsn 20 yesrs .go when the first report on
smking and heslth YBB issued in 1964.  Based on the current report. the
judgment c.n now be made chat exposure to environmental tobscco sswke csn
cause disease. including lung cancer, in mnsmkers. It is also c1e.r
that simple separation of smkers and nonsrmkers within the s.me airap.ce
msy reduce but csnnot eliminate mnsmDker exposure to environment.1
tobscco amke.

  The report also reviews sn extensive body of evidence which
establishes .n incressed risk of respiratory illness and reduced lung
function in infants .nd very young children of psrenta who smoke. This
effect ia mire pmmunced if both p.rents anote th.n if only one parent
amkes.  As . physician, I believe that parents should refrsin from
smoking emend sm.11 children both as . means of protecting their
children's heslth and to set . pod ersmple for the child.

  Today, only 30 percent of the adult popul.tion in the United St.Ces
are srtokers-the lovest level of waking in the country since YDrld Usr
II, reflecting thst the great mjority of the populscion h.. never smked
or has successfully quit.

  Accompanying this decline in overall prevalence of cigarette swking
h.s been an incre.sed concern for protecting the health snd well being of
nonsmokers, as evidenced by the number of lens snd regulstians restricting
smking in public places.  Today, 40 St.tea .nd the District of Columbia
have enacted some form of legislation to restrict smoking in public.
Increasingly, these 1~s pertain to protecting nonawkers in m.ny
different setting., including the workplace.

  Based on the evidence presented in this report, the choice to srmke
should mt interfere with the mnslmker's choice for an environment free
of tobacco woke.

Sincerely,
W fl,a.

Otis R. Bowen, M.D.
secretary


FOREWORD

The data reviewed in 17 previous U.S. Public Health Service
reports on the health consequences of smoking have conclusively
established cigarette smoking as the largest single preventable cause
of premature death and disability in the United States.
The question whether tobacco smoke is harmful to smokers was
answered more than 20 years ago. As a result, many scientists began
to question whether the low levels of exposure to environmental
tobacco smoke (ETS) received by nonsmokers could also be harmful.
The current Report, The Health Consequences of Involuntary
Smoking, examines the evidence that even the lower exposure to
smoke received by the nonsmoker carries with it a health risk. Use of
the term "involuntary smoking" denotes that for many nonsmokers,
exposure to ETS is the result of an unavoidable consequence of being
in proximity to smokers. It is the first Report in the health
consequences of smoking series to establish a health risk due to
tobacco smoke exposure for individuals other than the smoker, and
represents the work of more than 60 distinguished physicians and
scientists, both in this country and abroad.
After careful examin ation of the available evidence, the following
overall conclusions can be reached:

1. Involuntary smoking is a cause of disease, including lung
cancer, in healthy nonsmokers.

2. The children of parents who smoke, compared with the
children of nonsmoking parents, have an increased frequency
of respiratory infections, increased respiratory symptoms, and
slightly smaller rates of increase in lung function as the lung
matures.

3. Simple separation of smokers and nonsmokers within the
same air space may reduce, but does not eliminate, exposure
of nonsmokers to environmental tobacco smoke.

Exposure to environmental tobacco smoke occurs at home, at the
worksite, in public, and in other places where smoking is permitted.

vii


The quality of the indoor environment must be a concern of all who
control and occupy that environment. Protection of individuals from
exposure to environmental tobacco smoke is therefore a responsibili-
ty shared by all:

As parents and adults we must protect the health of our
children by not exposing them to environmental tobacco
smoke.

As employers and employees we must ensure that the act of
smoking does not expose the nonsmoker to tobacco smoke.

For smokers, it is their responsibility to assure that their
behavior does not jeopardize the health of others.

For nonsmokers, it is their responsibility to provide a supportr
ive environment for smokers who are attempting to stop.

Actions taken by individuals, employers, and employee organixa-
tions reflect the growing concern for protecting nonsmokers. The
number of laws and regulations enacted at the national, State, and
local level governing smoking in public has increased substantially
over the past 10 years, and surveys conducted by numerous
organizations show strong public support for these actions among
both smokers and nonsmokers.

As a Nation, we have made substantial progress in addressing the
enormous toll inflicted by active smoking. Efforts to improve and
protect individual health must be not only continued but strength-
ened. On the basis of the evidence presented in this Report, it is clear
that actions to protect nonsmokers from ETS exposure not only are
warranted but are essential to protect public health.

Robert E. Windom, M.D.
Assistant Secretary for Health

. . .
vlll


PREFACE

This, the 1986 Report of the Surgeon General, is the U.S. Public
Health Service's 18th in the health consequences of smoking series
and the 5th issued during my tenure as Surgeon General.

Previous Reports have documented the tremendous health burden
to society from smoking, particularly cigarette smoking. The evi-
dence establishing cigarette smoking as the single largest preventa-
ble cause of premature death and disability in the United States is
overwhelming-totaling more than 50,000 studies from dozens of
cultures. Smoking is now known to be causally related to a variety of
cancers in addition to lung cancer; it is a cause of cardiovascular
disease, particularly coronary heart disease, and is the major cause
of chronic obstructive lung disease. It is estimated that smoking is
responsible for well over 800,000 deaths annually in the United
States, representing approximately 15 percent of all mortality.
Thirty years ago, however, the scientific evidence linking smoking
with early death and disability was more limited. By 1964, the year
the Advisory Committee to the Surgeon General issued the first
report on smoking and health, a substantial body of evidence had
accumulated upon which a judgment could be made that smoking
was a cause of disease in active smokers. Subsequent reports over the
last 20 years have expanded our understanding and knowledge about
smoking behavior, the toxicity and carcinogenicity of tobacco smoke,
and the specific disease risks resulting from exposure to this agent.

This Report is the first issued since 1964 that identifies a chronic
disease risk resulting from exposure to tobacco smoke for individuals
other than smokers. It is now clear that disease risk due to the
inhalation of tobacco smoke is not limited to the individual who is
smoking, but can extend to those who inhale tobacco smoke emitted
into the air. This Report represents a detailed review of the health
effects resulting from nonsmoker exposure to environmental tobacco
smoke (ETS). ETS is the combination of smoke emitted from a
burning tobacco product between puffs (sidestream smoke) and the
smoke exhaled by the smoker. The 1986 Report, The Health
Consequences of Involuntary Smoking, is a critical review of all the
available scientific evidence pertaining to the health effects of ETS
exposure on nonsmokers. The term "involuntary smoking" is used to

ix


note that such exposures often occur as an unavoidable consequence
of being in close proximity to smokers.

Lung Cancer and Environmental Tobacco Smoke

The appropriate framework for an examination of the lung cancer
risk from involuntary smoking is that of a lowdose exposure to a
known human carcinogen. Over 30 years of research have conclu-
sively established cigarette smoke as a carcinogen. This Report
presents evidence that the chemical composition of side&earn
smoke is qualitatively similar to the mainstream smoke inhaled by
the active smoker, and that both mainstream and sidestream smoke
act as carcinogens in bioassay systems. Data related to environmen-
tal levels of tobacco smoke constituents and from measures of
nicotine absorption in nonsmokers suggest that nonsmokers are
exposed to levels of environmental tobacco smoke that would be
expected to generate a lung cancer risk, epidemiological studies of
populations exposed to ETS have documented an increased risk for
lung cancer in those nonsmokers with increased exposure.
It is rare to have such detailed exposure data or human epidemic
logic studies on disease occurrence when attempting to evaluate the
risk of low-dose exposure to an agent with established toxicity at
higher levels of exposure. The relative abundance of data reviewed
in this Report, their cohesiveness, and their biologic plausibility
allow a judgment that involuntary smoking can cause lung cancer in
nonsmokers. Although the number of lung cancers due to involun-
tary smoking is smaller than that due to active smoking, it still
represents a number sufficiently large to generate substantial public
health concern.

It is certain that a substantial proportion of the lung cancers that
occur in nonsmokers are due to EXS exposure; however, more
complete data on the dose and variability of smoke exposure in the
nonsmoking U.S. population will be needed before a quantitative
estimate of the number of such cancers can be made.

Children and Infants

This Report also documents a relationship between parental
smoking and the respiratory health of infants and children (under 2
years of age). Infants of parents who smoke have an increased risk of
hospitalization for bronchitis and pneumonia when compared with
infants of nonsmoking parents. There is a relationship between
parental smoking and an increased frequency of respiratory symp
tams in children. A slower rate of growth in lung function has been
observed in children of smoking parents. In many studies, if both

X


parents smoke, a stronger relationship exists than if only one parent
smokes.

What future respiratory burden these findings may represent for
these children later in life is not known. As a former pediatric
surgeon, I strongly urge parents to refrain from smoking in the
presence of children as a means of protecting not only their
children's current health status but also their own.

Diseases Other Than Lung Cancer

Several studies have provided data on the relationship between
ETS and cancers other than lung cancer and on ETS exposure and
cardiovascular disease. However, further research in these areas will
be required to determine whether an association exists between ETS
exposure and an increased risk of developing these diseases.

Policies Restricting Smoking in Public Places

The growth in our understanding of the disease risk associated
with involuntary smoking has been accompanied by a change in the
social acceptability of smoking and by a growing body of legislation,
regulation, and voluntary action that addresses where smoking may
occur in public. Forty States and the District of Columbia now have
some form of legislation controlling or restricting smoking in various
public settings. Some States limit smoking to only a few designated
areas; however, States are increasingly developing and implement-
ing comprehensive legislation that restricts smoking in many public
settings, including the workplace. Nine States have restrictions that
cover smoking not only by public employees but also by employees in
the private sector.

No systematic evaluation of the effects these measures may have
on smoking behavior has been conducted, but there is little doubt
that strong public sentiment exists for implementing such restric-
tions. A number of national surveys conducted by voluntary health
organizations, government agencies, and even the tobacco industry
have documented that an overwhelming majority of both smokers
and nonsmokers support restricting smoking in public.

Public Health Policy and Involuntary Smoking
The 1986 Surgeon General's Report on the Health Consequences of
Involuntary Smoking clearly documents that nonsmokers are placed
at increased risk for developing disease as the result of exposure to
environmental tobacco smoke.

Critics often express that more research is required, that certain
studies are flawed, or that we should delay action until more
conclusive proof is produced, As both a physician and a public health

xi


official, it is my judgment that the time for delay is past; measures to
protect the public health are required now. The scientific case
against involuntary smoking as a health risk is more than sufficient
to justify appropriate remedial action, and the goal of any remedial
action must be to protect the nonsmoker from environmental
tobacco smoke.
The data contained in this Report on the rapid diffusion of tobacco
smoke throughout an enclosed environment suggest that separation
of smokers and nonsmokers in the same room or in different rooms
that share the same ventilation system may reduce KTS exposure
but will not eliminate exposure. The responsibility to protect the
safety of the indoor environment is shared by all who occupy or
control that environment.
Changes in smoking policies regarding the workplace and other
environments necessitated by the data presented in this Report
should not be designed to punish the smoker. Successful implementa-
tion of protection for the nonsmoker requires the support and
cooperation of smokers, nonsmokers, management, and employees
and should be developed through a cooperative effort of all groups
affected. In addition, changes are often more effective when support
and assistance is provided for the smoker who wants to quit.
Cigarette smoking is an addictive behavior, and the individual
smoker must decide whether or not to continue that behavior;
however, it is evident from the data presented in this volume that
the choice to smoke cannot interfere with the nonsmokers' right to
breathe air free of tobacco smoke. The right of smokers to smoke
ends where their behavior affects the health and wellbeing of
others; furthermore, it is the smokers' responsibility to ensure that
they do not expose nonsmokers to the potential harmful effects of
tobacco smoke.

C. Everett Koop, M.D.
Surgeon General

xii


ACKNOWLEDGMENTS

This Report was prepared by the Department of Health and
Human Services under the general editorship of the Gffice on
Smoking and Health, Donald R. Shopland, Acting Director. Manag-
ing Editor was William R. Lynn, Acting Technical Information
Officer, office on Smoking and Health.
Senior scientific editor was David M. Burns, M.D., Associate
Professor of Medicine, Division of Pulmonary and Critical Care
Medicine, University of California Medical Center, San Diego, San
Diego, California. Consulting scientific editors were Ellen R. Grits,
Ph.D., Director, Division of Cancer Control, Jonsson Comprehensive
Cancer Center, University of California, Los Angeles, Los Angeles,
California, John H. Holbrook, M.D., Associate Professor of Internal
Medicine, Department of Internal Medicine, University Hospital,
Salt Lake City, Utah, and Jonathan M. Same& M.D., Professor of
Medicine, Department of Medicine, The University of New Mexico
School of Medicine, Albuquerque, New Mexico.

The following individuals prepared draft chapters or portions of
the Report.

Neal Benowitz, M.D., San Francisco General Medical Center, San
Francisco, California

A. Sonia Buist, M.D., Professor of Medicine, Department of Physiolo
gy, Gregon Health Sciences University, Portland, Oregon
Charles Hiller, M.D., Pulmonary Division, University Hospital,
Little Rock, Arkansas
Dietrich Hoffmann, Ph.D., Associate Director, Naylor Dana Institute
for Disease Prevention, American Health Foundation, Valhalla,
New York

Ilse Hoffmann, Research Coordinator, Naylor Dana Institute for
Disease Prevention, American Health Foundation, Valhalla, New
York

John R. Hoidal, M.D., Director of Pulmonary Medicine, University of
Tennessee Center for Health Sciences, Memphis, Tennessee
John McCarthy, M.P.H., Harvard School of Public Health, Boston,
Massachusetts

. . .
xlll


Nancy A. Rigotti, M.D., Institute for the Study of Smoking Behavior
and Policy, John F. Kennedy School of Government, Harvard
University, Cambridge, Massachusetts
Jonathan M. &met, M.D., Professor of Medicine, Department of
Medicine, The University of New Mexico School of Medicine,
Albuquerque, New Mexico

John Spengler, Ph.D., Harvard School of Public Health, Boston,
Massachusetts

Annetta Weber, Ph.D., Federal Institute of Technology, Zurich,
Switzerland

Scott T. Weiss, M.D., M.S., Associate Professor of Medicine, Chan-
ning Laboratories, Harvard Medical School, Boston, Massachu-
setts

Anna H. Wu, Ph.D., Department of Preventive Medicine, School of
Medicine, University of Southern California, Los Angeles, Califor-
nia

The editors acknowledge with gratitude the following distin-
guished scientists, physicians, and others who lent their support in
the development of this Report by coordinating manuscript prepara-
tion, contributing critical reviews of the manuscript, or assisting in
other ways.

Elvin E. Adams, M.D., M.P.H., Director, Health and Temperance
Department, General Conference of Seventh-Day Adventists,
Washington, D.C.

Stephen M. Ayres, M.D., Dean, School of Medicine, Medical College
of Virginia, Richmond, Virginia

David V. Bates, M.D., Professor of Medicine and Physiology,
Department of Medicine, Acute Care Hospital, University of
British Columbia, Vancouver; British Columbia
William J. Blot, Ph.D., Chief, Biostatistics Branch, Epidemiology and
Biostatistics Program, Division of Etiology, National Cancer
Institute, National Institutes of Health, Bethesda, Maryland.
Benjamin Burrows, M.D., Professor of Internal Medicine, and
Director, Division of Respiratory Sciences,. The University of
Arizona College of Medicine, Tucson, Arizona
D. M. DeMarini, Ph.D., Genetic Toxicology Division, U.S. Environ-
mental Protection Agency, Research Triangle Park, North Caro-
lina

Vincent T. DeVita, Jr., M.D., Director, National Cancer Institute,
National Institutes of Health, Bethesda, Maryland
Louis Diamond, Ph.D., College of Pharmacy, University of Kentucky,
Lexington, Kentucky
Richard Doll, Cancer Epidemiology and Clinical Trials Unit, Imperi-
al Cancer Research Fund, The Radcliffe Infirmary, University of
Oxford, Oxford, England, United Kingdom

XiV


Manning Feinleib, M.D., Dr.P.H., Director, National Center for
Health Statistics, Office of the Assistant Secretary for Health,
Hyattsville, Maryland

Edwin B. Fisher, Jr., Ph.D., Associate Professor, Department of
Psychology, Washington University, St. Louis, Missouri
William H. Foege, M.D., Executive Director, Task Force for Child
Survival, Carter Presidential Center, Atlanta, Georgia
Joseph F. Fraumeni, Jr., M.D., Associate Director for Epidemiology
and Biostatistics, Division of Cancer Etiology, National Cancer
Institute, National Institutes of Health, Bethesda, Maryland
Lawrence Garfinkel, M.A., Vice President for Epidemiology and
Statistics, and Director of Cancer Prevention, American Cancer
Society, New York, New York

R.A. Griesemer, D.V.M., Ph.D., Director, Biology Division, Oak Ridge
National Laboratory, Oak Ridge, Tennessee
Michael R. Guerin, Ph.D., Organic Chemistry Section, Analytical
Chemistry, Oak Ridge National Laboratory, Oak Ridge, Tennessee
Jeffery E. Harris, M.D., Ph.D., Associate Professor, Department of
Economics, Massachusetts Institute of Technology, Cambridge,
Massachusetts

Millicent Higgins, M.D., Associate Director, Epidemiology and
Biometry Program, National Heart, Lung, and Blood Institute,
National Institutes of Health, Bethesda, Maryland
Takeshi Hirayama, M.D., Director, Institute of Preventive Oncology,
Shinjuku-ku, Tokyo, Japan

Dwight Janerich, D.D.S., M.P.H., Department of Epidemiology and
Public Health, Yale University School of Medicine, New Haven,
Connecticut

Martin Jarvis, M.P.H., Senior Clinical Psychologist, Addiction
Research Unit, Institute of Psychiatry, London, England, United
Kingdom
Brian P. Leaderer, Ph.D., M.P.H., Associate Fellow, John B. Pierce
Foundation Laboratory, Associate Professor, Department of Epide-
miology and Public Health, Yale University School of Medicine,
New Haven, Connecticut

Charles L. LeMaistre, M.D., President, University of Texas Systems
Cancer Center, Houston, Texas

Claude Lenfant, M.D., Director, National Heart, Lung, and Blood
Institute, National Institutes of Health, Bethesda, Maryland
Donald Ian Macdonald, M.D., Administrator, Alcohol, Drug Abuse,
and Mental Health Administration, Rockville, Maryland
James S. Marks, M.D., M.P.H., Assistant Director for Science, Center
for Health Promotion and Education, Centers for Disease Control,
Atlanta, Georgia
James 0. Mason, M.D., Dr.P.H., Director, Centers for Disease
Control, Atlanta, Georgia

xv


J. Michael McGinnis, M.D., Deputy Assistant Secretary for Health
(Disease Prevention and Health Promotion), Office of the Assistant
Secretary for Health, Washington, D.C.
A. J. McMichael, M.D., M.B.B.S., Ph.D., Chairman and Senior
Principal Research Scientist, CSIRO Division of Human Nutrition,
Adelaide, South Australia

D. J. Moschandreas, Ph.D., Research Director, ITT Research Insti-
tute, Chicago, Illinois

David Muir, M.D., Director, Occupational Health Program, Health
Sciences Center, McMaster University, Hamilton, Ontario, Cana-
da

C. Tracy Orleans, Ph.D., Research Associate, Health Services RX+
search Center, University of North Carolina, Chapel Hill, North
Carolina

Richard Pete, M.A., MSc., I.C.R.F., Regius Assessor of Medicine, The
Radcliffe Infirmary, University of Oxford, Oxford, England, Unit-
ed Kingdom
Otto Raabe, M.D., Laboratory for Energy Related Health Research,
University of California, Davis, Davis, California
James L. Repace, Chief of Technical Services, Indoor Air Quality
Program, U.S. Environmental Protection Agency, Washington,
D.C.

M.A.H. Russell, F.R.C.P., Addiction Research Unit, Institute of
Psychiatry, University of London, London, England, United King-
dom

Roy J. Shephard, M.D., Ph.D., Director, School of Physical and
Health Education, University of Toronto, Toronto, Canada
Frank E. Speixer, M.D., Charming Laboratories, Harvard Medical
School, Boston, Massachusetts

Jesse L. Steinfeld, M.D., President, Medical College of Georgia,
Augusta, Georgia

David N. Sundwall, M.D., Administrator, Health Resources and
Services Administration, Rockville, Maryland
Gregory W. Traynor, Staff Scientist, Lawrence Berkeley Laboratory,
Berkeley, California

Dimitrios Trichopoulos, Director, Department of Hygiene and Epide-
miology, School of Medicine, University of Athens, Athens, Greece
Kenneth E. Warner, Ph.D., Professor, and Chairman, Department of
Public Health Policy and Administration, School of Public Health,
The University of Michigan, Ann Arbor, Michigan
Ernst L. Wynder, M.D., President, American Health Foundation,
New York, New York

James B. Wyngaarden, M.D., Director, National Institutes of Health,
Bethesda, Maryland

Frank E. Young, M.D., Commissioner, Food and Drug Administra-
tion, Rockville, Maryland

xvi


The editors also acknowledge the contributions of the following
staff members and others who assisted in the preparation of this
Report.

Erica W. Adams, Chief Copy Editor and Assistant Production
Manager, Health and Natural Resources Department, Sterling
Software, Inc., Rockville, Maryland
Richard H. Amacher, Director, Health and Natural Resources
Department, Sterling Software, Inc., Rockville, Maryland
Margaret L. Anglin, Secretary, Gffice on Smoking and Health,
Rockville, Maryland

John L. Bagrosky, Associate Director for Program Operations, Office
on Smoking and Health, Rockville, Maryland
Charles A. Brown, Programmer, Automation and Technical Services
Department, Sterling Software, Inc., Rockville, Maryland
Clarice D. Brown, Statistician, Office on Smoking and Health,
Rockville, Maryland
Richard C. Brubaker, Information Specialist, Health and Natural
Resources Department, Sterling Software, Inc., Rockville, Mary-
land

Catherine E. Burckhardt, Secretary, Office on Smoking and Health,
Rockville, Maryland

Joanna B. Crichton, Copy Editor, Health and Natural Resources
Department, Sterling Software, Inc., Rockville, Maryland
Stephanie D. DeVoe, Programmer, Automation and Technical
Services Department, Sterling Software, Inc., Rockville, Maryland
Danny A. Goodman, Information Specialist, Health and Natural
Resources Department, Sterling Software, Inc., Rockville, Mary
land

Patricia E. Healy, Technical Information Specialist, Office on
Smoking and Health, Rockville, Maryland
Terri L. Henry, Clerk-Typist, Office on Smoking and Health,
Rockville, Maryland

Timothy K. Hensley, Technical Publications Writer, Office on
Smoking and Health, Rockville, Maryland
Shirley K. Hickman, Data Entry Operator, Health and Natural
Resources Department, Sterling Software, Inc., Rockville, Mary
land

Robert S. Hutchings, Associate Director for Information and Pro-
gram Development, Office on Smoking and Health, Rockville,
Maryland

Maureen Illar, Editorial Assistant, Office on Smoking and Health,
Rockville, Maryland

Julie Kurt, Graphic Artist, Information Center Management De-
partment, Sterling Software, Inc., Rockville, Maryland
Ruth C. Palmer, Secretary, Office on Smoking and Health, Rockville,
Maryland

xvii


Jerome A. Paulson, M.D., Medical Officer, Office on Smoking and
Health, Rockville, Maryland
Russell D. Peek, Library Acquisitions Specialist, Health and Natural
Resources Department, Sterling Software, Inc., Rockville, Mary-
land

Margaret E. Pickerel, Public Information and Publications Special-
ist, Office on Smoking and Health, Rockville, Maryland
Raymond K. Poole, Production Coordinator, Health and Natural
Resources Department, Sterling Software, Inc., Rockville, Mary-
land

Linda R. Spiegelman, Administrative Officer, office on Smoking and
Health, Rockville, Maryland

Evelyn L. Swarr, Administrative Secretary, Automation and Techni-
cal Services Department, Sterling Software, Inc., Rockville, Mary-
land

Debra C. Tate, Publications Systems Specialist, Publishing Systems
Division, Sterling Software, Inc., Riverdale, Maryland
Jerry W. Vaughn, Programmer, University of California, San Diego,
San Diego, California

Mary I. Walz, Computer Systems Analyst, Office on Smoking and
Health, Rockville, Maryland

Louise G. Wiseman, Technical Information Specialist, Gffice on
Smoking and Health, Rockville, Maryland
Pamela Zuniga, Secretary, University of California, San Diego, San
Diego, California

. . .
XVlll


TABLE OF CONTENTS

Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vii

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix

Acknowledgments                                   . . .
               . . . . . . . . . . . . . . . ..*................................ Xl11

1. Introduction, Overview, and Summary and
Conclusions . . . . . . . . . . . . . . . . . . . . , . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2. Health Effects of Environmental Tobacco Smoke Ex-
posure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3. Environmental Tobacco Smoke Chemistry and Expo

  sures of Nonsmokers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121

4. Deposition and Absorption of Tobacco Smoke Constit-
uents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177

5. Toxicity, Acute Irritant Effects, and Carcinogenicity
of Environmental Tobacco Smoke . . . . . . . . . . . . . . . . . . . . . . .225

6. Policies Restricting Smoking in Public Places and the
Workplace . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335

xix


CHAPTER 1

INTRODUCTION, OVERVIEW,
         AND
SUMMARY AND CONCLUSIONS


CONTENTS

Introduction

Development and Organization of the 1986 Report

Overview
  Environmental Tobacco Smoke Constitutents
  Extent of Exposure
  Lung Cancer
  Respiratory Disease
  Cardiovascular Disease
  Irritation
  Determinants of Exposure
  Policies Restricting Smoking

Summary and Conclusions of the 1986 Report
  Health Effects of Environmental Tobacco Smoke
   Exposure

Environmental Tobacco Smoke Chemistry and
Exposures of Nonsmokers
Deposition and Absorption of Tobacco Smoke Constit-
uents

Toxicity, Acute Irritant Effects, and Carcinogenicity
of Environmental Tobacco Smoke
Policies Restricting Smoking in Public Places and the
Workplace


htroductlon

Development and Organization of the 1886 Report
The 1966 Report was developed by the Off&e on Smoking and
Health of the U.S. Department of Health and Human Services as
part of the Department's responsibility, under Public Law 91-222, to
report new and current information on smoking and health to the
unitedstatescongress.
The scientific content of this Report reflects the contributions of
more than 66 scientists representing a variety of disciplines.
Individual manuscripts were written by experts known for their
understanding of and work in specific content areas. These manu-
scripts were refined through a series of meetings attended by the
authors, Office on Smoking Health staff and consultants, and the
Surgeon General.
Upon receipt of the final manuscripts from the authors, the O&e
and its consultants edited and consolidated the individual manu-
scripts into appropriate chapters. These- draft chapters were subjeo
ted to an extensive outside peer review (see Acknowledgments for
individuals and their affiliations) whereby each was reviewed by up
to seven experts. Their comments were integrated and the entire
volume was assembled. This revised edition of the Report was
resubjected to review by 17 distinguished scientists outside the
Federal Government, both in this country and abroad. Parallel to
this review, the entire Report was also submitted to various
institutes and agencies within the U.S. Public Health Service for
review and comment.
The 1966 Report contains a Foreword by the Assistant Secretary
for Health, a Preface by the Surgeon General of the U.S. Public
Health Service, and the following chapters:
Chapter 1. Introduction, Overview, and Summary and Conclu-
        SiOM

Chapter 2. Health Effects of Environmental Tobacco Smoke
     Exposure

Chapter 3. Environmental Tobacco Smoke Chemistry and Expo
      sures of Nonsmokers

Chapter 4. Deposition and Absorption of Tobacco Smoke Con&it+
       uenta

Chapter 5. Toxicity, Acute Irritant Effects, and Carcinogenicity
     of Environmental Tobacco Smoke
Chapter 6. Policies Restricting Smoking in Public Places and the
     Workplace

Overview

Inhalation of tobacco smoke during active cigarette smoking
remains the largest single preventable cause of death and disability

5


for the US. population. The health consequences of cigarette
smoking and of the use of other tobacco products have been
extensively documented in the 17 previous Reports in the health
consequences of smoking series issued by the U.S. Public Health
Service. cSgare* smoking is a major cause of cancer; it is most
strongly associated with cancers of the lung and respiratory tract,
but also causes cancers at other sites, including the pancreas and
urinary bladder. It is the single greatest cause of chronic obstructive
lung dka~3. It c8uf4f33 cardiovascular diseases, including coronary
heart disease, aortic aneurysm, and atherosclerotic peripheral
vascular disease. ~atermd cigarette smoking endangers fetal and
neonatal health, it contributes to perinatal mortality, low birth
weight, and complications during pregnancy. More than 3CQofl
premature deaths occur in the United States each year that are
directly attributable to tobacco use, particularly cigarette smoking.
`Ihis Eteport examines in detail the scientific evidence on involun-
tary smoking as a potential cause of disease in nonsmokers.
Nonsmokers' exposure to environmental tobacco smoke is termed
involuntary smoking in this Fteport because the expcsure generally
occurs as an unavoidable consequence of being in proximity to
smokers, particularly in enclosed indoor environments. The term
"passive smoking" is also used throughout the scientific literature to
describe this exposure.
The magnitude of the disease risks for active smokers secondary to
their "high dose" exposure to tobacco smoke suggests that the "lower
dose" exposure to tobacco smoke received by involuntary smokers
may also have risks. Although the risks of involuntary smoking are
smaller than the risks of active smoking, the number of individuals
injured by involuntary smoking is large both in absolute terms and
in comparison with the number injured by some other agents in the
general environment that are regulated to curtail their potential to
cause human illness.
This Report reviews the evidence on the characteristics of main-
stream tobacco smoke and of environmental tobacco smoke, on the
levels of exposure to environmental tobacco smoke that occur, and
on the health effects of involuntary exposure to tobacco smoke. me
composition of the tobacco smoke inhaled by active smokers and by
involuntary smokers is examin ed for similarities and differences,
and the concentrations of tobacco smoke components that can b
immured in a variety of settings are explored, as is smoke deposition
and absorption in the respiratory tract. The studies that &crib the
risks of environmental tobacco smoke exposure for humans are
carefully reviewed for their fmdings and their validity. `I'he evidence
on the health effects of involuntary smoking is reviewed for biologic
plausibility, and compared with extrapolations of the risks of active

6


smoking to the lower dose of exposure to tobacco smoke found in
nonsmokers. This review leads to three major conclusions:

1.  Involuntary smoking is a cause of disease, including
lung cancer, in healthy nonsmokers.

2.  The children of parents who smoke compared with the
children of nonsmoking parents have an increased
frequency of respiratoryinfections, increased respira-
tory symptoms, and slightly smaller rates of increase in
lung function as the lung matures.
3. The simple separation of smokers and nonsmokers
within the same air space may reduce, but does not
eliminate, the exposure of nonsmokers to environmen-
  tal tobacco smoke.

The subsequent chapters of this volume describe in detail the
evidence that supports these conclusions; the evidence is briefly
summarized here.

Environmental Tobacco Smoke Constituents

Important considerations in e xamining the risks of involuntary
smoking are the composition of environmental tobacco smoke (ETS)
and its toxicity and carcinogenicity relative to the tobacco smoke
inhaled by active smokers. Mainstream cigarette smoke is the smoke
drawn through the tobacco into the smoker's mouth. Sidestream
smoke is the smoke emitted by the burning tobacco between puffs.
Environmental tobacco smoke results from the combination of
sidestream smoke and the fraction of exhaled mainstream smoke not
retained by the smoker. In contrast with mainstream smoke, ETS is
diluted into a larger volume of air, and it ages prior to inhalation.
The comparison of the chemical composition of the smoke inhaled
by active smokers with that inhaled by invohmtary smokers suggests
that the toxic and carcinogenic effects are qualitatively similar, a
similarity that is not too surprising because both mainstream smoke
and environmental tobacco smoke result from the combustion of
tobacco. Individual mainstream smoke constituents, with appropri-
ate testing, have usually been found in sidestream smoke as well.
However, differences between sidestream smoke and mainstream
smoke have been well documented. The temperature of combustion
during side&ream smoke formation is lower than during main-
stream smoke formation. As a result, greater amounts of many of the
organic constituents of smoke, including some carcinogens, are
generated when tobacco burns and forms side&ream smoke than
when mainstream smoke is produced. For example, in contrast with
mainstream smoke, side&ream smoke contains greater amounts of
ammonia, benzene, carbon monoxide, nicotine, and the carcinogens

7


%napthylamine,  4aminobipheny1,   N-nitrosamine,  ~=I+
anthracene, and benzo-pyrene per milligram of tobacco burned.
Although only limited bioassay data comparing mainstream smoke
and sidestream smoke are available, one study has suggested that
sidestream smoke may be more carcinogenic.

Extent of Exposure

~though siclestream smoke and mainstream smoke differ some-
what qualitatively, the differing quantitative doses of smoke compo-
nents inhaled by the active smoker and by the involuntary smoker
are of greater importance in considering the risks of the two
exposures. A number of different markers for tobacco smoke
exposure and absorption have been identified for both active and
involuntary smoking. No single marker quantifies, with precision,
the exposure to each of the smoke constituents over the wide range
of environmental settings in which involuntary smoking occurs.
However, in environments without other significant sources of dust,
respirable suspended particulate levels can be used as a marker of
smoke exposure. Levels of nicotine and its metabolite cotinine in
body fluids provide a sensitive and specific indication of recent whole
smoke exposure under most conditions.
Widely varying levels of environmental tobacco smoke can be
measured in the home and other environments using markers. The
time-activity patterns of nonsmokers, which indicate the time spent
in environments containing EI'S, also vary widely. Thus, the extent
of exposure to ETS is probably highly variable among individuals at
a given point in time, and little is known about the variation in
exposure of the same individual at different points in time.

Llmg cancer

The American Cancer Society estimates that there will be more
than 135,000 deaths from lung cancer in the United States in 1986,
and 85 percent of these lung cancer deaths are directly attributable
to active cigarette smoking. Therefore, even if the number of lung
cancer deaths caused by invohmtary smoking were much smaller
than the number of lung cancer deaths caused by active smoking, the
number of lung cancer deaths attributable to involuntary exposure
would still represent a problem of sufficient magnitude to warrant
substantial public health concern.
Exposure to environmental tobacco smoke has been examined in
numerous recent epidemiological studies as a risk factor for lung
cancer in nonsmokers. These studies have compared the risks for
subjects exposed to MS at home or at work with the risks for people
not reported to be exposed in these environments. Because exposure
to EIS is an almost universal experience in the more developed
~~fhs, theee studies involve comparison of more expased and less

8


exposed people rather than comparison of exposed and unexposed
people. Thus, the studies are inherently conservative in assessing the
consequences of exposure to ETS. Interpretation of these studies
must consider the extent to which populations with different E'JJS
exposures have been identified, the gradient in EXS exposure from
the low-er exposure to the higher exposure groups, and the magni-
tude of the increased lung cancer risk that results from the gradient
in ETS exposure.
To date, questionnaires have been used to classify ETS exposure.
Quantification of exposure by questionnaire, particularly lifetime
exposure, is difficult and has not been validated. However, spousal
and parental smoking status identify individuals 6th different
levels of exposure to ETS. Therefore, investigation has focused on the
children and nonsmoking spouses of smokers, groups for whom
greater ETS exposure would be expected and for whom increased
nicotine absorption has been documented relative to the children
and nonsmoking spouses of nonsmokers.
Of the epidemiologic studies reviewed in this Report that have
examined the question of involuntary smoking's association with
lung cancer, most (11 of 13) have shown a positive association with
exposure, and in 6 the association reached statistical significance.
Given the difficulty in identifying groups with differing ET'S
exposure, the low-dose range of exposure examined, and the small
numbers of subjects in some series, it is not surprising that some
studies have found no association and that in others the association
did not reach a conventional level of statistical significance. The
question is not whether cigarette smoke can cause lung cancer; that
question has been answered unequivocally by examining the evi-
dence for active smoking. The question is, rather, can tobacco smoke
at a lower dose and through a different mode of exposure cause lung
cancer in nonsmokers? The answer must be sought in the coherence
and trends of the epidemiologic evidence available on this lowdose
exposure to a known human carcinogen. In general, those studies
with larger population sizes, more carefully validated diagnosis of
lung cancer, and more careful assessment of M`s exposure status
have shown statistically significant associations. A number of these
studies have demonstrated a dose-response relationship between the
level of M`S exposure and lung cancer risk. By using data on nicotine
absorption by the nonsmoker, the nonsmoker's risk of developing
lung cancer observed in human epidemiologic studies can be
compared with the level of risk expected from an extrapolation of the
d-response data for the active smoker. This extrapolation yields
estimates of an expected lung cancer risk that approximate the
observed lung cancer risk in epidemiologic studies of involud~
smoking.

9


Cigarette smoke is well established as a human carcinogen. The
chemical composition of ETS is qualitatively similar to mainstream
smoke and sidestream smoke and also acts as a carcinogen in
bioassay systems. For many nonsmokers, the quantitative exposure
to ETS is large enough to expect an increased risk of lung cancer to
occur, and epidemiologic studies have demonstrated an increased
lung cancer risk with involuntary smoking. In examining a low-dose
exposure to a known carcinogen, it is rare to have such an
abundance of evidence on which to make a judgment, and given this
abundance of evidence, a clear judgment can now be made: exposure
to ETS is a cause of lung cancer.
The data presented in this Report establish that a substantial
number of the lung cancer deaths that occur among nonsmokers can
be attributed to involuntary smoking. However, better data on the
extent and variability of E!lS exposure are needed to estimate the
number of deaths with confidence.

Respiratory Disease

Acute and chronic respiratory diseases have ah30 been linked to
hvol~ntary exposure to tobacco smoke; the evidence is strongest in
infants. htig the first 2 years of life, infants of parents who smoke
me more Likely than infants of nonsmoking parents to be hospital-
ized for bronchitis and pneumonia. Children whose parents smoke
aho develop respiratory symptoms more frequently, and they show
small, but measurable, differences on tests of lung function when
compared with children of nonsmoking parents.
Respiratory infections in young children represent a direct health
burden for the children and their parents; moreover, these infec-
tions, and the reductions in pulmonary function found in the school-
age children of smokers, may increase susceptibility to develop lung
disease as an adult.

Several studies have reported small decrements in the average
level of lung function in nonsmoking adults exposed to ETS. These
differences may represent a response of the lung to chronic exposure
to the irritants in ETS, but it seems unlikely that ETS exposure, by
itself, is responsible for a substantial number of cases of clinically
significant chronic obstructive lung disease. The small magnitude of
the changes associated with EX'S exposure suggesta that only
Miti~uals with unusual susceptibility would be at risk of develop
kg ClinicallY adent disease from E'I% exposure alone. However,
ETS exposure IMY be a factor that contributes to the development of
clinical disease in individuals with other causes of lug mjury.

cardiovascular Disease
A few studies have examined the relationship hebeen invohrn~
tarY smoking and cardiovascular disease, but no firm conclusion on

10


the relationship can be made owing to the limited number of deaths
in the studies.

Perhaps the most common effect of tobacco smoke exposure is
tissue irrit&.ion. The eyes appear to be especially sensitive to
irritation by EX'S, but the nose, throat, and airway may also be
af%cted by smoke exposure. Irritation has been demonstrated to
occur at levels that are similar to those found in real-life situations.
The level of irritation increases with an increasing concentration of
smoke and duration of exposure. In addition, participants in surveys
report irritation and annoyance due to smoke in the environment
under real-life conditions.

Determinante of Espoi3ure

&pc++ure to EX'S has been documented to be common in the
United States, but additional data on the extent and determi,nanta of
exposure are needed to identify individu& within the population
who have the highest exposure and are at greatest risk. Studies with
biological markers and measurements of EXS components in indoor
air confirm that measurable exposure to l3TS is widespread. How-
ever, within exposed populations, levels of cotinine excretion and
presumably El% exposure vary greatly.
In a room or other indoor area, the size of the space, the number of
smokers, the amount of ventilation, and other factors determine the
concentration of tobacco smoke in the air. The technology for the
cost-effective atration of tobacco smoke from the air is not currently
available, and because of their small size, the smoke particles remain
suspended in the air for long periods of time; thus, the only way to
remove smoke from indoor air is to increase the exchange of indoor
air with clean outdoor air. The number of air changea per hour
required to maintain acceptable indoor air quality is much higher
when smoking is allowed than when smoking is prohibited.
Environmental tobacco smoke originates at the lighted tip of the
cigarette, and exposure to M`s is greatest in proximity to the
smoker. However, the smoke rapidly disseminates throughout any
airspace contiguous with the space in which the smoking is taking
place. Dissemination of smoke is not uniform, and substantial
gradienti in ETS levels have been demonstrated in different parta of
the same airspace. The time course of tobacco smoke dissemination
is rapid enough to ensure the spread of smoke throughout an
airspace within an S-hour workday. In the home, the presence of
even one smoker can GgnEcantly increase levels of respirable
suspended particulates.
These data lead to the conclusion that the simple separation of
smokers and nonsmokers within the same airspace will reduce, but

11


not eliminate, exposure to El%, particularly in those settings where
exposure is prolonged, such as the working environment.

The exposure of an individual nonsmoker to ETS is also deter-
m&xl by that person's time-activity pattern; that is, the amount of
he spent in various locations. For adults, the duration of the
spent in smoke-contaminated environments at work or at home is
the principal dete rminant of E!!`8 exposure, along with the levels of
smoke in those environments. For infants and very young children,
the smoking habit of the primary caretaker, as well as that person's
time-activity pattern, is likely to play a major role in de&mining
ETS exposure.

Policies Restricting Smoking

Pohcies regulating cigarette smoking with the objective of reduc-
ing e~l~ion or fire risk, or of safeguarding the quality of manufac-
tured products, have been in force in a number of States since the
late 1800s. More recently, and with steadily increasing frequency,
pohcies regulating smoking on the basis of the health risk or the
irritation of involuntary smoking have been promulgated.

State and local governments have enacted laws and regulations
restricting smoking in public places. These policies have been
implemented with few problems and at little cost to the respective
governments. !I'he public awareness of these policies that results
from the media coverage surrounding their implementation proba-
bly facilitates their selfenforcement. Public awareness may best be
fostered by encouraging the establishment of these changes at the
local level.

Policies limiting smoking in the worksite have also become
increasingly widespread and more restrictive. However, changes in
worksite policies have evolved largely through voluntary rather
than governmental action. In a steadily increasing number of
worksites, smoking has been prohibited completely or limited to
relatively few areas within the worksite. The creation of a smoke-
free workplace has proceeded successfully when the policy has been
jointly developed by employees, employee organizations, and man-
agement; instituted in phases; and accompanied by support and
assistarm for the smokers to quit smoking.
This trend to protect nonsmokers from ETS exposure may have an
added public health benefithelping those smokers who are at-
tempting to quit to be more successful and not encouraging smoking
by people entering the workforce.

Summary and Conclusions of the 1988 Report
The three major conclusions of this report are the following:

12


1. Involuntary smoking is a cause of disease, including
lung cancer, in healthy nonsmokers.

2. The children of parents who smoke compared with the
children of nonsmoking parente have an iucreased
frequency of respiratory iufectiouq iucreased respira-
tory symptoms, and slightly smaller rates of increase in
lung function as the lung matures.

3. The simple separation of smokers and nousmokers
withiu the same air space may reduce, but doea not
eliminate, the exposure of nonsmokers to enviroumen-
  tal tobacco smoke.

,Individual chapter summaries and conclusions follow.

Health Effects of Euviroumental Tobacco Smoke Exposure
1. Involuntary smoking can cause lung cancer in nonsmokers.
2. Although a substantial number of the lung cancers that occur
  in nonsmokers can be attributed to involuntary smoking, more
  data on the dose and distribution of ETS exposure in the
  population are needed in order to accurately estimate the
  magnitude of risk in the U.S. population.
3. The children of parents who smoke have an increased frequen-
  cy of hospitalization for bronchitis and pneumonia during the
  first year of life when compared with the children of nonsmok-
    ers.

4. The children of parents who smoke have an increased frequen
cy of a variety of acute respiratory illnesses and infections,
including chest illnesses before 2 years of age and physician-
diagnosed bronchitis, tracheitis, and laryngitis, when com-
pared with the children of nonsmokers.

5. Chronic cough and phlegm are more frequent in children
whose parents smoke compared with children of nonsmokers.
The implications of chronic respiratory symptoms for respira-
tory health as an adult are unknown and deserve further
study.
6. The children of parents who smoke have small differences in
tests of pulmonary function when compared with the children
of nonsmokers. Although this decrement is insufficient to
cause symptoms, the possibility that it may increase suscepti-
bility to chronic obstructive pulmonary disease with exposure
to other agents in adult life, e.g., active smoking or cccupation-
al exposures, needs investigation.
7. Healthy adults exposed to environmental tobacco smoke may
have small changes on pulmonary function testing, but are
unlikely to experience clinically significant deficits in pulmo-

13


nary function as a result of exposure to environmental tobacco
smoke alone.
8. A number of studies report that chronic middle ear effusions
are more common in young children whose parents smoke than
in children of nonsmoking parents.
9. Validated questionnaires are needed for the assessment of
recent and remote exposure to environmental tobacco smoke in
the home, workplace, and other environments.
10. The associations between cancers, other than cancer of the
lung, and involuntary smoking require further investigation
before a determina tion can be made about the relationship of
involuntary smoking to these cancers.
11. Further studies on the relationship between involuntary
smoking and cardiovascular disease are needed in order to
determine whether involuntary smoking increases the risk of
cardiovaaculardisease.

Environmental Tobacco Smoke Chemistry and Expcwwes of
Nonsmokera

1. Undiluted sidestream smoke is characterixed by significantly
higher concentrations of many of the toxic and carcinogenic
compounds found in mainstream smoke, including ammonia,
volatile amines, volatile nitr osamines, certain nicotine decom-

position products, and aromatic amines.
2. Environmental tobacco smoke can be a substantial contributor
to the level of indoor air pollution concentrations of respirable
particles, benzene, acrolein, N-nitrosamine, pyrene, and carbon
monoxide. E!l'S is the only source of nicotine and some N-
nitrosamine compounds in the general environment.
3. Measured exposures to respirable suspended particulates are
higher for nonsmokers who report exposure to environmental
tobacco smoke. Exposures to ETS occur widely .in the non-
smoking population.

4. The small particle size of environmental tobacco smoke places
it in the diffusioncontrolled regime of movement in air for
deposition and removal mechanisms. Because these submicron
particles will follow air streams, convective currents will
dominate and the distribution of ETS will occur rapidly
through the volume of a room. As a result, the simple
separation of smokers and nonsmokers within the same
airspace may reduce, but will not eliminate, exposure to ETS.
5. It has been demonstrated that ETS has resulted in elevated
respirable suspended particulate levels in enclosed places.

14


Deposition and Absorption of Tobacco Smoke Constituenta
1. Absorption of tobacco-speciSc smoke constituents (i.e., nicotine)
  from environmental tobacco smoke exposures has been docu-
  mented in a number of samples of the general population of
  developed countries, suggesting that measurable exposure tc
  environmental tobacco smoke is common.
2. Mean levels of nicotine and cotinine in body fluids increase
  with self-reported EX'S exposure.

3. Because of the stability of cotinine levels measured at different
times during exposure and the availability of noninvasive
sampling techniques, cotinine appears to be the shortcterm
marker of choice in epidemiological studies.
4. Both mathematical modeling techniques and experimental
data suggest that 10 to 20 percent of the particulate fraction of
side&ream smoke would be deposited in the airway.
5. The development of specific chemical assays for human expo
sure to the components of cigarette tar is an important
research goal.

Toxicity, Acute Irritant Effects, and Carcinogenicity of
Environmental Tobacco Smoke

1. The main effects of the irritants present in ETS occur in the
conjunctiva of the eyes and the mucous membranes of the nose,
throat, and lower respiratory tract These irritant effects are a
frequent cause of complaints about poor air quality due to
environmental tobacco smoke.

2. Active cigarette smoking is associated with prominent changes
in the number, type, and function of respiratory epithelial and
inflammatory cells; the potential for environmental tobacco
smoke exposure to produce similar changes should be investi-
gated.

3. Animal models have demonstrated the carcinogencity of ciga-
rette smoke, and the limited data that exist suggest that more
carcinogenic activity per milligram of cigarette smoke concen-
trate may be contained in sidestream smoke than in main-
stream cigarette smoke.

Policies Restricting Smoking in Public Places and the
Workplace

1. Beginning in the 19708, an increasing number of public and
private sector institutions have adopted policies to protect
individuals from environmental tobacco smoke exposure by
restricting the circumstances in which smoking is permitted.
2. Smoking in public places has been regulated primarily by
government actions, which have occurred at Federal, State,

15


and local levels. All but nine States have enacted laws
regulating smoking in at least one public place. Since the mid-
19706, there has been an increase in the rate of enactment and
in the comprehensiveness of State legislation. Local govern-
ments have enacted smoking ordinances at an increasing rate
since 1980, more than SO cities and counties have smoking laws
in effect.
9. Smoking at the workplace is regulated by a combination of
government action and private initiative. Legislation in 12
States regulates smoking by government employees, and 9
St&s and more than 70 communities regulate smoking in the
private sector workplace. Approximately 96 percent of busi-
nesses have adopted smoking policies. The increase in work-
place smoking policies has been a trend of the 1980s.
4. Smoking policies may have multiple effects. In addition to
reducing environmental tobacco smoke exposure, they may
alter smoking behavior and public attitudes about tobacco use.
Over time, this may contribute to a reduction in smoking in the
United States. To the present, there has been relatively little
systematic evaluation of policies restricting smoking in public
places or at the workplace.
5. On the basis of case reports and a small number of systematic
studies, it appears that workplace smoking policies improve air
quality, are met with good compliance, and are well accepted
by both smokers and nonsmokers. Policies appear to be
followed by a decrease in smokers' cigarette consumption at
work and an increase in enrollment in company-sponsored
smoking cessation programs.
6. Laws restricting smoking in public places have been imple-
mented with few problems and at little cost to State and local
government. Their impact on smoking behavior and attitudes
has not yet been evaluated.
7. Public opinion polls document strong and growing support for
restricting or banning smoking in a wide range of public places.
Changes in attitudes about smoking in public appear to have
preceded legislation, but the interrelationship of smoking
attitudes, behavior, and legislation are complex.

16


CHAPTER 2

  HEALTH EFFECTS OF
ENVIRONMENTAL TOBACCO
   SMOKE EXPOSURE


CONTENTS

Introduction

Evaluation of Low-Dose Tobacco Smoke Exposures
Extrapolation of Active Smoking Data to Environ-
  mental Tobacco Smoke Exposure
    Comparison of Mainstream Smoke and Side-
      stream Smoke
    Deposition of Mainstream Smoke and Side
     stream Smoke and Environmental Tobacco
      Smoke Dose Estimates
    Dose-Response Relationships and Threshold for
      Risk
Pathophysiologic Considerations
     Cancer
    Lung Disease
Methodological Considerations ip Epidemiologic
   Studies
    Measurement of Exposure
     Atmospheric Markers
     Personal Monitoring
     Questionnaires
    Measurements of Absorption
    Potentially Confounding Variables
     Statistical Issues

Respiratory System Effeds of Involuntary Cigarette
smoke Exposure
  Infants and Children
    Acute Respiratory Illness
     Longitudinal stud&3
      Cross-Sectional Studies
      Case-Control Studies
    Cough, Phlegm, and Wheezing
    Pulmonary Function
     Bronchoconstriction
    Ear, Nose, and Throat
  Adults
    Acute Respiratory Illness
    Cough, Phlegm, and Wheezing

19


Pd.~~onary Function
Bronchoconstriction
Normal Subjects
Asthmatics
Ear, Nose, and Throat

Lung Cancer
  Observed Risk
   General Methodological Issues
   &msal Exposure: Prospective Studies
    Tbe Japanese Cohort Study
    The American Cancer Society Cohort Study
     The Scottish Study
   Spousal Exposure: Cas&!ontrol Studies
     The Greek Study
     The Louisiana Study
     The Hong Kong Studies
    An Ongoing Study of Tobacc&elated Cancers
    The Ios Angeles County Study
     The Four Hospitals Study
     A United Kingdom Study
     The Japanese Case-Control Study
     The Swedish Study
     The German Study
   Other Sources of Tobacco Smoke Exposure
     Parental Smoking
     Coworker's Smoking
   Dose-Response Relationship
Expected Lung Cancer Risk
  S-

Other Cancers

cardiovascular Diseases

                                         ~ ~-
Conclusions

Referencef4

20


Introduction

In 1964, the fmt Report of the Surgeon General on smoking and
health (TJS PHS 1964) determined that cigarette smoking was a
cause of lung cancer in men and probably a cause of lung cancer in
women. That Report also noted causal relationships between smok-
ing and other cancers, as well as chronic lung disease. Subsequent
Reports have described associations, both causal and noncausal,
between tobacco smoking and a wide range of acute and chronic
d&eases. Epidemiological investigations have documented the effects
of tobacco smoking in humans; complementary laboratory investiga-
tions have elucidated some of the mechanisms through which
tobacco smoke causes disease.

More recently, the effects of the inhalation of environmental
tobacco smoke by nonsmokers have become a pressing public health
concern. Nonsmokers, as well as active smokers, inhale environmen-
tal tobacco smoke, the mixture of sidestream smoke and exhaled
mainstream smoke. Various terms have been applied to the inhala-
tion of environmental tobacco smoke by nonsmokers; the terms
"involuntary smoking" and "passive smoking" are the most preva-
lent and are often used interchangeably by researchers and the
public.
Many of the known toxic and carcinogenic agents found in
mainstream cigarette smoke have also been demonstrated to be
present in sidestream smoke. Furthermore, the combustion condi-
tions under which sidestream smoke is produced result in the
generation of larger amounts of many of these toxic and carcinogenic
agents per gram of tobacco burned than the conditions under which
mainstream smoke is generated (see Chapter 3). The characteristics
of environmental tobacco smoke also differ from those of main-
stream smoke because the sidestream smoke ages before it is inhaled
and the mainstream smoke exhaled by the active smoker is modified
during its residence in the lung. There is no evidence to suggest that
environmental tobacco smoke has a qualitatively lower toxicity or
carcinogenicity than mainstream smoke per milligram of smoke
inhaled. In fact, the available evidence suggests that sidestream
smoke contains higher concentrations of many known toxic and
carcinogenic agents per milligram of smoke and is more tumorgenic
than mainstream smoke in animal testing (Wynder and Hoff'mann
1967). As a result, involuntary smoking should not be viewed as a
qualitatively different exposure from active smoking, but rather as a
lowdose exposure to a known hazardous agent-cigarette smoke.

Evaluation of Low-Dose Tobacco Smoke Exposures
Assessment of the health effects of any environmental exposure
poses methodological problems, particularly when exposure levels

21


are low and therefore the magnitude of the expected effect is small.
me ev&ation of an effect due to a low-dose exposure such as
environment& tobacco smoke requires the investigation of popula-
tions with differences in exposure large enough so that an effect
could be anticipated. The population studied must also be of
sufficient size to quantitate the effects in the range of interest with
pr&&n. Failure to fulfill these requirements may produce a false-
negative result in a study of a low-dose exposure.
Exposure to environmental tobacco smoke is a nearly universal
experience in the more developed countries, so the identification of a
truly unexposed population is very difficult. Epidemiological studies
of involuntary smoking have attempted to identify populations with
lower exposure and higher exposure to environmental tobacco
smoke, most notably by examining nonsmokers exposed to tobacco
smoke generated by the smokers of their family. The effects of
environmental tobacco smoke have been investigated in a number of
populations throughout the world. The diversity of these populations
is likely to be accompanied by a similar diversity of their exposure to
envircnmental tobacco smoke. Thus, the gradient in exposure to
environmental tobacco smoke between the "exposed" and %onex-
posed" groups is likely to vary widely among the reported studies.
For example, the husband's smoking status may be a strong
predictor of total exposure to ETS in traditional societies, such as
Japan and Greece, where the wife's exposure outside the home is
limited. In contrast, the husband's smoking status in the United
States, where substantial exposure may occur outside the home, may
not be as predictive.
Sample size considerations are of particular concern for the
epidemiological studies of lung cancer and involuntary smoking.
Because the frequency of lung cancer in nonsmokers is low, many of
these studies often included small numbers of nonsmokers and
lacked the statistical power necessary to fmd the modest effect
expected from this lowdose exposure. Given the constraints of
sample size and the varying gradients of exposure, it would be
expected that some studies would fmd no association between
involuntary smoking and lung cancer, and that other studies would
find associations that lacked statistical significance. Nonunifomity
of the data, however, does not imply a lack of effect; rather, it is the
coherence and trends of the evidence that must be judged. Thus, this
Rep0l-t examines the entire body of evidence on the health effects of
involuntary smoking, as the basis for its conclusions.
In evaluating the hazards posed by an air pollutant such as
environmental tobacco smoke, laboratory, toxicological, human
exposure, and epidemiological investigations provide relevant data.
Each approach has limitations, but the insights each prov&s Me
Complementary. Epidemiological investigations describe the effects

22


in human populations, but their results must be interpreted in the
context of the other types of investigations.
Risk assessment techniques have also been used to characterize
the potential adverse health effects of human exposures to environ-
mental pollutants, particularly those at low levels. The four steps of
risk assessment have been described by the National Academy of
Sciences as hazard identification, dose-response assessment, expo-
sure assessment, and risk characterization (NAS 1983). Risk assess+
ment has also been used to describe the consequences of exposure to
ETS. However, unlike many environmental exposures for which risk
assessment represents the only approach for estimating human risk,
the health effects of ETS exposure can be examined directly using
epidemiological methods. Although this Report reviews several risk
assessmenta done by individual researchers on ETS, its conclusions
are based on the laboratory, toxicological, and epidemiological
evidence.

Extrapolation of Active Smoking Data to Environmental
Tobacco Smoke Exposure

Comparison of Mainstream Smoke and Sidestream Smoke

A detailed comparison of mainstream and side&ream smoke can
be found in Chapter 3. Mainstream smoke (MS) is the term applied to
the complex mixture that is inhaled by the smoker from the
mouthpiece of a cigarette, cigar, or pipe with each puff. Side&ream
smoke (SS) is the aerosol that comes from the burning end of the
cigarette, pipe, or cigar between puffs. Environmental tobacco smoke
(ETS) is the term applied to the combination of SS and exhaled MS,
which is diluted and aged in an area where smoking has taken place.
Most of the existing data on mainstream and sidestream smoke
characteristics relate to cigarette smoking and relatively little
information is available pertaining to cigar and pipe smoking.
&cause both MS and SS are generated from the tip of the burning
tobacco product, it is not surprising that their compositions are
similar. Of the thousands of compounds identified in tobacco smoke,
many have been identified as present in both MS and SS. Among
these are carcinogens, gases such as carbon monoxide and the oxides
of nitrogen, and nicotine. Since there is a wealth of information
relating to the toxicity and carcinogenicity of MS, it should be
emphasized again that ETS cannot be treated as a new environmen-
tal agent for the purpose of assessing health risks. The presence of
the same agents in MS and SS leads to the conclusion that ETS has a
toxic and carcinogenic potential that would not be expected to be
qualitatively different from that of MS. Quantitative differences
between the active smoker's exposure to MS and the involuntary
smoker's exposure to ETS are likely to be. the more important

23


determjnant of the differing magnitudes of risks associated with
them3 two exposures.
werences in the composition of MS and SS primarily reflect
their generation at different temperatures in different oxygen
environments. also, SS is diluted very rapidly, under most circum-
ww, and has the opportunity to age before inhalation. The
h~luntary smoker usually inhales E'IS, not SS, the aerosol that
comes from the tip of a burning cigarette. In considering the
&u&e&tics of SS, it must be emphasii that much of the
existing data about the composition of MS and SS is derived from
studies carried out in special chambers rather than by sampling MS
and SS generated by smokers. In these chamber studies, SS has been
sampled by a probe located close to the burning tip. This experimen-
tal situation clearly differs from that of a room with one or more
smokers freely smoking. In that situation, SS is mixed with exhaled
MS, diluted and aged. Nevertheless, these &amber studies provide
very useful information about the compounds present in the SS.
These studies have established that SS in comparison with MS has a
higher PHI, smaller particle size, and more carbon monoxide,
benzene, toluene, acrolein, acetone, pyridine, ammonia, methyl-
amine, nicotine, aniline, cadmium, radon daughters, beru@ajpyrene
and benzIa]anthracene.
Comparison of the relative concentrations of the various compo-
nents of SS and MS smoke prcvides limited insights concerning the
toxicological potential of ETS in comparison with active smoking. As
described above, SS characteristics, as measured in a &amber, do
not represent those of E!I'S, as inhaled by the nonsmoker under
nonexperimental conditions. Further, the dose-response relation-
sbips between specific tobacco smoke components and specific
diseases are not sufficiently established for the necesssq extrapola-
tions from active smoking to environmental tobacco smoke exposure
for individual agents. For that reason the extrapolations in this
section are confined to the doseresponse relationships of whole
smoke for those diseases with established dose-response relation-
ships.
With regard to the potential of EX'S to cause lung cancer,
UdilUted SS has 20 to 100 times greater concentrations of. highly
carcinogenic volatile. N-nitrosamin es than MS (Brunnemam et al.
1978) as well as higher concentrations of benxopyrenes and
benzCa]anthracenes.
For mum&want effecta on airways and the lung parenchyma,
the agents responsible for the development of acute and chronic
respiratory disease have not been identified, although many tobacco
smoke components have been shown tc cause lung injury (US DHHS
19&Q). Presumably, both vapor phase (gaseous) and particulate phase
kW components of MS are involved. Both airways disease and

24


parenchymal disease are probably a response to the total burden of
respiratory insults, some of which, like active smoking, may be
sufficient by themselves to cause physiologic impairment and
ultimately, clinical disease. Others, such as ETS, may contribute to
the total burden but be insufficient, individually, to cause clinical
disease.

Deposition of Mainstream Smoke and Side&ream Smoke and
Environmental Tobacco Smoke Dose Estimutes

The dose of tobacco smoke delivered to the airways and alveoli
depends, among other factors, on the volume of MS, SS, or E'I'S
inhaled, on the rate and depth of inhalation, and on the sixe, shape,
and density of the individual particles or droplets. Patterns of
deposition of MS in the lungs have been described, but similar
information about deposition patterns for ETS is not yet available.
Without such data, it is necessary to extrapolate from the informa-
tion on MS.

The major factors that affect the pattern of deposition and
retention for particles are particle size distriiution and breathing
pattern. The particle sire range and mean aerodynamic diameter for
particulates in sidestream smoke are similar to those of mainstream
smoke (particle sire range of 0.01 to 0.8 pm for sidestream smoke and
0.1 to 1.0 v for mainstream smoke, and mean aerodynamic
diameter 0.32 p for sidestream smoke and 0.4 pm for mainstream
smoke) (see Cbapters 3 and 4). `l'he deposition site is determined
largely by the size of the particles, with large particles being
deposited preferentially in the nasopbarynx and large conducting
airways. Smaller particles are deposited more peripherally, and very
small particles tend to be exhaled and to have a very low deposition
fraction. The particulates of ETS, because of their size range, are
likely to be deposited peripherally.
The breathing patterns for the inhalation of MS and EYI'S are also
different; MS is inbaled intermittently by the smoker with an
intense inhalation, often followed by a breathhold that resulta in a
more equal distribution. Environmental tobacco smoke, on the other
hand, is inhaled continuously with tidal breaths when the passive
smoker is at rest and with deeper inhalations when the passive
smoker is physically active. Breatbholding does not normally occur
with tidal breathing.
Estimates of the equivalent exposure, in terms of cigarettes per
day, resulting from ETS, as compared with MS, vary quite widely
and depend on the way in which the estimates were made. Bepace
and Lowrey (1985) estimated that nonsmokers in the United States
are exposed to from 0 to 14 mg of tobacco tar (average 1.4 rag) per
day. Vutuc (1984) estimated that the exposure to environmental
cigarette smoke is equivalent to 0.1 to 1 cigarette per day actively

25


smoked. Estimates of ETS exposure, based on cotinine measure-
ments, suggest that involuntary smokers absorb about 0.5 to 1
percent of the nicotine that active smokers absorb (Jarvis et al. 1984,
Haley and Hoffmann 1965; Wald et al. 1984; Russell et al. 1966).

Dose-Response Ret!ationships and Threshold for Risk
-response relationships for active smoking can provide in-
sights into the expected magnitude of disease resulting from the
exposure of nonsmokers to ETS. These data are reviewed to
de&mine whether disease can be expected in association with E'I'S.
Data from cohort and cas+control studies demonstrate dose-
response relationships for lung cancer, which extend to the lowest
levels of reported active smoking. The dose-response relationship of
active smoking with lung cancer risk has been described by several
investigators in several different date sets (Whittemore and Altshu-
ler 1976; Doll and Pet0 1978; Pathak et al. 1986). Although the
mathematical forms of these models vary, none have included a
threshold level of active smoking that must be passed for lung cancer
tc develop.
The dose-response relationship for active smoking and lung cancer
has been used to project the lung cancer risk for nonsmokers (Vutuc
1964). Such projections yield risk estimates of 1.03 to 1.36 for
exposures, considered to be reasonable estimates of involuntary
smoking exposures, i.e., 0.1 t.c 1.0 cigarettes per day. The reference
population for these risk estimates is the risk for nonsmokers as a
group, including those with higher and those with lower exposures to
environmental tobacco smoke. In contrast, the reference population
for the risk estimates in studies of involuntary smoking is the lung
cancer risk in only that group of nonsmokers who have lower
exposure to EITS. Comparisons of lung cancer risk estimates from
active smoking studies with those from involuntary smoking studies
require reference to the same exposure group for proper mterpreta-
tion. In general, the lung cancer experience .of all nonsmokers (i.e.,
those with higher and lower involuntary smoking exposure com-
bined) has been used to establish the reference rate of lung cancer
occurrence (i.e., set as a risk of 1) in studies of active smoking. The
use of all nonsmokers as the reference group averages the lower
risks of nonsmokers with less ETS exposure with the higher risks of
those with more ETS exposure. Thus, with the relative risk for the
entire group of nonsmokers set to unity, the relative risk for
nonsmokers with lower exposure is below 1 and that for the group
with higher exposure is above 1. As a consequence, relative risk
estimates from studies of involuntary exposure cannot be directly
compared with risk estimates extrapolated from active smoking,
unh c(qm%on to a single level of exposure is possible. Failure to

26


consider the differences between the reference populations explains
the apparent discrepancy noted by Vutuc.

Consider, for example, the mortality study reported by Hirayama
(1981a). In this study, the relative risk of lung cancer for nonsmoking
wives of smoking husbands (current and former) compared with
nonsmoking wives of nonsmoking husbands (as calculated from
Figure 1 in Hirayama 1981a) was 1.78. If the relative risk for
nonsmoking wives of nonsmoking husbands were expressed in
relation to the combined group of nonsmoking women, then a value
of 0.63 is obtained, while with a similar calculation, that for
nonsmoking wives of smoking husbands (both current and former),
yields a value of 1.12. Thus, when the appropriate comparison is
made, the risk estimates developed by extrapolation of the active
smoking data (1.03 to 1.36) closely approximate those actually found
in a study of lung cancer risk due to involuntary smoking.
Dose-response relationships between active smoking and the level
of lung function, the rate of decline of lung function in adult life, and
the development of chronic airflow obstruction are well established
(US DHHS 1984). Different measures of dose have provided the
strongest correlation with functional decline in different studies.
Pack-years, a cumulative dose measure, was the strongest predictor
of the level of forced expiratory volume in 1 second (FEVI) in the
Tucson epidemiologic study (Burrows, Knudson, Cline et al. 1977).
Duration of smoking and the amount smoked were found to be the
best predictors in male subjects in a study of three U.S. communities
(Reck et al. 1981), and pack-years was the best predictor in female
subjects. In both of these studies, however, the estimated dose
accounted for only about 15 percent of the variation of age- and
height-adjusted FEW1 levels. The relatively low predictive capability
of cigarette smoking variables in these studies most likely reflects a
lack of information on the dete rminants of individual susceptibility
to tobacco smoke. Further, exposure variables obtained by question-
naire, such as the number of cigarettes smoked daily, may only
roughly approximate the dose delivered to target sites in the
respiratory tract. Many factors, such as puff volume, lung volume at
which inhalation starts, and airways geometry will influence the
smoke dose and its distribution within the lungs. Extrapolation from
the results of these studies to the pulmonary effects of exposure to
ETS is, therefore, likely to be inaccurate.
Another approach for assessing lowdose exposures is to consider
the information available from studies involving children and
teenagers who have recently taken up smoking. Even with brief
smoking experience, cross-set tional studies of active cigarette smok-
ing by children and adolescents have demonstrated an increased
frequency of respiratory symptoms (Rawbone et al. 1978; Rush 1974;
Bewley et al. 1973; Seely et al. 1971) and small but statistically

27


significant reductions in lung function (Seely et al. 1971; Peters and
Ferris 1967; Lim 1973; Walter et al. 1974; &&house 1975; Woolcock
et aL 1984). Longitudinal studies involving children and adolescents
have demonstrated that a physiologic impairment attributable to
smoking may be found in some children by age 14 and may be
present after only 1 year of smoking 10 or more cigarettes per week
in children with previously normal airways (woolcock et al. 1934),
and that relatively small amounts of cigarette use may lead to
significant effects on FEVl and on the growth of lung function in
adolescents (Figure 1) (`l'ager et al. 1935).
When considering the risk of lowdose exposures for the develop
ment of chronic respiratory disease, the existence of a spectrum of
risk and a distribution of dose within the population should be taken
into consideration. The characteristics of the part of the population
most susceptible to involuntary smoke exposure is still being
clarified. Evidence is accumulating that airways hyperrespon-
siveness, atopy, childhood respiratory illness, and occupational
exposures may all influence response to ETS. Current understanding
of lung injury suggests that individuals with one or more of these
characteristics that place them at the most sensitive end of the
susceptibility curve may be the most likely to develop symptoms or
functional changes es a result of ETS exposure. Dose of ETS also
varies in the population, and the coincidence of high dose and
increased susceptibility may convey a particularly high risk. Fur-
thermore, ET3 exposure may damage lungs that are also affected by
other insults.

Pathophysiologic Cbsiderations
Cancer

Carcinogenesis refers to the process by which a normal cell is
transformed into a malignant cell with uncontrolled replication.
Carcinogenesis has been conceptualixed as a multistage process
involving a sequence of alterations in cellular DNA that terminate
with the development of a malignant cell. Agents acting early in this
sequence are referred tc as initiators; those actii later are referred
to as promoters. Compounds with both initiating activity and
promoting activity have been identified in tobacco smoke.
Carcinogenesis reflects DNA damage; although some repair may
take place, biological models have not suggested that there is a
threshold of damage that must be exceeded. Rather, carcinogenesis
has been considered to involve a series of changes, each occurring at
a rate dependent on the dose of a damaging agent. Higher doses
increase the probability that the entire sequence will be completed,
but lower doses may also lead to mahgnancy.


o

0    10,ooo 20300   30,ooo   4o.wo 50,ooo 60,ooo   70,Doo 30,ooo
            Number of cigamtes consumed

150 d

o
?   ?
   o
o

?  ?
?
   o
  o ?

o

o
o

o

o o

o

o

s

+

25

  0    lO,ooa 2a.ooo 30,ooo 40,ow 5o.ooo ewoo   70,ooo 3o.ooo

                Number of cigarettes consumed

FIGURE l.-Relationship between levels of predicted for
      FEW, (A) and FEFSWIJ (B) at examination 8 and
      cumulative number of cigareti smoked
      during examinations 4 through 8
NOTEzMenandwome.nmmbined@J-44).
SOURCE: Tagor et al. (1936).

29


with the PiZZ or other phenotypes, are modest particulate exposures
likely to increase the risk for disease to an appreciable extent.
The development of acute and chronic airzoay disease or symptoms
of cough, phlegm production, and wheeze may require a considerably
smaller exposure than changes in the lung parenchyma, and it is not
unreasonable to hypothesize that these symptoms may be related to
repeated and continuous exposure to EYES in the susceptible individu-
al. Strong evidence that lowdose active smoking causes increased
rates of respiratory symptoms and functional impairment comes
from the studies of children and adolescents discussed earlier
(Woolcock et al. 1984; Tager et al. 1985). Because of the length of
exposure, it is likely that these reflect airway rather than parenchy-
mal effects.

Another pathophysiological mechanism by which exposure to EX'S
may increase an individual's risk for the development of chronic
airflow obstruction is through respiratory viral infections. Mounting
evidence indicates that the very young child (under 2 years of age)
exposed to ETS is at increased risk for lower respiratory tract viral
infections (Harlap and Davies 1974; Colley 1974; Colley et al. 1974;
Leeder et al. 1976a; Fergusson et al. 1981; Dutau et al. 1979; Pedreira
et al. 1985). There is also increasing, though still inconclusive,
epidemiologic evidence that respiratory viral infections in early life
may be associated with an accelerated decline in F'EVl and,
therefore, an increased risk for the development of chronic airflow
obstruction in adult life in smokers (Burrows, Knudson, Lebowitz
1977; Samet et al. 1983). By increasing the occurrence of viral
infections of the lower respiratory tract in early life, exposure to ETS
in childhood may have an appreciable, but indirect, effect on the risk
for the development of chronic airflow obstruction in adult life. The
structural basis for this increased susceptibility has not yet been
elucidated, however. Furthermore, the child whose parents smoke is
also more likely to take up smoking than is the child of nonsmoking
parents. Thus, the child made susceptible to the effecta of active
smoking by prior PITS exposure is also more likely to become an
active smoker.

The possibility that exposure to constituents of tobacco smoke in
utero may exert a prenatal effect must also be considered. This
exposure is clearly not the same as ETS exposure, since the lungs of
the fetus are not being exposed to ETS; rather, the developing fetal
lung is exposed to compounds absorbed by the mother and delivered
to the fetus transplacentally. Evidence of an in utero effect in
pregnant rats has been reported by Collins and coworkers (1985).
These investigators reported that pregnant rats exposed to smoke
from day 5 to day 20 of gestation, in comparison with control rats,
showed reduced lung volume at term and saccules that were reduced
in number and increased in size as a result of the reduced formation

31


Lung Disease

The noncarcinogenic pathophysiologic effects of active smoking on
the respiratory tract can be separated into (1) effects on the airways
and (2) effects on the lung parenchyma. In the airways, the
structural changes include inflammation in the small airways and
mucous gland hypertrophy and hyperplasia. In the parenchyma, the
main structural change is alveolar wall destruction. Both the
airways and the parenchymal changes are caused by active smoking,
but the interrelationships of these changes are not clear. They may
be independent pathophysiologic pi, linked only by their joint
association with tobacco smoking.
As discussed earlier, there is evidence showing an approximately
linear d-response relationship between F'EWl level and amount
smoked; however, the d-response relationships have not been as
well described for the underlying pathophysiologic changes in the
airways or in the lung parenchyma. Host factors and other environ-
mental factors presumably interact with active smoking to affect an
individual's risk for the development of disease. In this regard,
present evidence would suggest that only 10 to 15 percent of smokers
develop clinically significant airflow obstruction, although parenchy-
mal and airways changes can be demonstrated in a substantially
higher percentage at autopsy (US DHHS 1984).
Extrapolation from the evidence on active smoking to the likely
effect of exposure to environmental tobacco smoke on the airways
and parenchyma suggests that pathophysiologic effeds on both the
airways and the lung parenchyma might be expected. Because the
dose of smoke components from ETS exposure is small in comparison
with the dose from active smoking, the extent of lung injury would
most likely also be much smaller than that found in active smokers.
Small changes in the lung may be below the threshold for detection
on pulmonary function testing. If clinically significant chronic
airflow obstruction occurs in nonsmokers exposed to EYES, the risk is
likely to be concentrated among those individuals highly susceptible
to the airway or parenchymal effects of cigarette smoke. This
susceptible group may include individuals with bronchial hyperre
sponsiveness and with other, as yet unidentified, genetic and familial
risk factors. Identifying the risk factors for susceptibility to the
airway and parenchymal effects of both mainstream smoke and EL'S
is an important priority. The dose of environmental tobacco smoke
received by the nonsmoker is unlikely, by itself, to he sufficient to
cause a clinically significant degree of purmchymul disease (em-
physema) unless an individual is at the extreme end of the
susceptibility distribution. Any particulate load is likely to increase
the elaatase burden in the lungs by causing an influx of neutrophils.
However, only in the individual with very inadequate lung defenses,
specificaIly severe deficiency of protease inhibitor (pi) associated

30


of saccule partitions. These hypoplastic lungs showed an internal
surface area that was decreased. Whether this study in rats has any
relevance to humans is not yet clear, but this issue deserves further
investigation.

Whether continued exposure to EX'S during childhood, while the
lung is remodeling and growing, affects the process of growth and
remodeling is not yet clear. In general, rapidly dividing cells and
immature organs are more susceptible to the effects of enviromnen-
tal toxins than are cells undergoing a normal rate of division and
mature organs. Apart from the evidence, cited above, linking lower
respiratory tract viral infections in very early life to an accelerated
decline of F'EVl in adult life, there is no information yet to link the
rate of growth of lung function during childhood to the rate of
decline of hmg function in adult life hecause the nw longitudi-
nal studies have not heen done. More information is needed to
describe the relationship of exposure to ETS at various times during
childhood to the maximal level of lung function achieved at full lung
growth.

Mefiod~logical Considerations in Epidemiologic Studies
Measumnent of Expure

h mamsing the health effects of EX'S exposure, as with other
enknmental pollutant8, accurate assessment of exposure is critical
for obtaining estimates of this agent's effects. Both random and
systematic misclassification of the exposures of subjects in an
investigation are of concern. Random misclassification refers to
errors that occur at random; the consequence of such random
misclassification is to bias toward fmding no effect. Systematic
misclassification refers to nonrandom errors in exposure assessment;
the consequence maybe to bias toward a greater or lesser effect than
is actually present. Biased answers in response to a questionnaire
may introduce systematic misclsssification.
Some misclassification occurs in most observational (nonexperi-
mental) epidemiological studies, and is inherent in all epidemiologi-
cal studies of ETS. Tobacco smoking is ubiquitous in nearly all
environments; few people escape being exposed to EX'S. Thus, the
exposure variables for ETS in epidemiological studies do not
separate nonexposed subjects from exposed subjects, rather, they
identify groups with more or less exposure, or with a qualitative or
semiquantitative gradient of exposure.
In assessing exposure to ETS, the information should cover the
biologically appropriate time period for the health effkct of interest
and be collected in a form that permita the construction of
biologically appropriate exposure measures. However, the collection
of a full lifetime history of IZTS exposure, as in a study of
malignancy, may not he feasible, and the accuracy of the informa-

32


tion may he limited. In evaluating the effects of ETS exposure,
cumulative exposure, duration of exposure, and intensity of exposure
may each influence the magnitude of effects, as may the timing of
exposure in relation to age and level of development.
Because of the difficulties inherent in assessing exposures through
questio maims, increased emphasis has been placed on meamuing
exposure through the use of molecular or biochemical markers. With
available markers, this approach is limited to providing an indica-
tion of recent (within 48 hours) exposure, which may not necessarily
correlate with past exposure. A marker has not yet been devised for
total integrated dose. Nevertheless, biological markers provide
another method for classification of current exposure, and a stan-
dard for validating questionnaires.
The strengths and weaknesses of the existing methods of measur-
ing exposure are further discussed below.

Atmospheric Markers

A number of different markers of atmospheric contamination by
tobacco combustion products can be feasibly measured. Ideally, the
atmospheric levels of the air contaminant or class of contaminants
that are implicated in producing the adverse health effects would be
measured. A variety of contaminants have been measured as
indicators of ETS, but no single measure can adequately index all of
its myriad components. Further, some contaminanta are produced by
sources of environmental contamination other than tobacco smoke.
Nicotine is ahsorbed only from tobacco and tobacco combustion
products.
Some of the pollutants that have heen measured include (1) carbon
monoxide, (2) respirahle suspended particulates CRSP), (3) nicotine,
(4) a number of aromatic hydrocarbons, such as benzene, toluene,
benxopyrene, and phenols, and (5) acrolein. Some of these are in the
vapor phase and some in the particulate phase. Some, such as
nicotine, may exist in one phase (particulate) in MS and in the other
(gas) phase in SS. Until more is learned about the contaminants and
their physical state in ETS, the results of monitoring for a particular
ETS component will be difficult to relate to ita diseasecausing
potential. At a practical level, the technology for measuring nicotine
levels and RSP levels is available and accurate.

Personal Monitoring

Both active and passive personal monitors can be used to measure
an individual's total exposure to an air contaminant at the breathing
xone. Active personal monitoring systems .employ pumps to concen-
trate the air contaminants on a collection medium for laboratory
analysis or to deliver the air to a continuous monitor. Passive

33


personal monitoring systems use diffusion and permeation to
concentrate gases on a collection medium for laboratory analysis.
Personal monitoring should provide a more accurate estimate of the
dose of a contaminant than area mOnitoring, because the actual air
in the breathing zone is sampled and the subject's time-activity
pattern is inherently considered.

As with area monitoring, the results for a particular component of
ETS may not adequately characterize exposure to other components
responsible for a particular disease or effect. Respirable suspended
particulates can be measured with accuracy and give a reasonably
accurate measurement of current exposure.

Questionnaires

me que&ionnaire has heen the most frequently used means of
estimating exposures for epidemiological investigations. Question-
naires typic&y have obtained information about the smoking habits
of parents, spouses, or other family members and often about
exposure outside the home. From this information, the subject is
classified as exposed or not exposed to Errs, and the extent of
exposure may be estimated.
The questionnaire approach for exposure estimation has several
potential limitations. First, the information obtained cannot exhaus-
tively cover lifetime exposure to ETS; therefore, a completely
accurate reconstruction of integrated dose over the years cannot be
achieved. Second, in evaluating El% exposure in the home, the usual
daily smoking of the smokers has often been used as a measure of
exposure intensity at home. This assumption may not be correct,
since smoking does not occur only in the home. For example, a one-
pack-a-day smoker may smoke only five cigarettes a day in the home
environment and smoke the rest at work or elsewhere outside the
home. Third, quantitation of exposure in the workplace is inherently
Sfficult because of changes in jobs and the varying exposure in any
particular workplace.
Despite these shortcomings, the information obtained by question-
taires does discriminate between more exposed and less exposed
ubjects. The evidence validating the questionnaire method is
trongest for domestic exposure. In several studies, levels of cotinine
m body fluids have varied with reported exposure to tobacco smoke
at home (Greenberg et al. 1984; Wald and Ritchie 1984; Matsukura
et al. 1984; Jarvis et al. 1984). In fact, residence with a smoker may
identify a population that is more tolerant of ETS, and therefore
more likely to be exposed outside the home. Evidence in support of
this speculation is provided by a study of urinary cotinine levels in
nonsmoking men in the United Kingdom (`Wald and Ritchie 1984). In
this study, the men married to women who smoked reported a

34


greater duration of exposure outside the home than men married to
women who did not smoke.

Until accurate and inexpensive exposure markers are available for
cumulative ETS exposure, the questionnaire approach will remain
the simplest means of obtaining exposure information. It is, there
fore, important to consider the misclassification that can be intro
duced by using this indirect measure of exposure, In studies of the
effect of ETS exposure, two types of misclassification are of concern:
misclassification of current or former smokers as never smokers and
misclassification of the extent of ETS exposure.
Because active smoking has a greater effect on the lungs than
exposure to ETS? the inclusion of active smokers within a larger
group of nonsmokers may lead to the fmding of a significant effect on
lung function, which is actually attributable to active smoking
rather than to involuntary smoking. Misclassification of undeclared
active smoking is a particularly important source of error in studies
involving teenagers. Misclassification of smoking status is also of
concern in casecontrol studies of the association between exposure
to M`S and lung cancer. Information about smoking habits for these
studies often comes from interviews with a surviving spouse or
surrogate, who may have been a close family member, neighbor, or
friend, or from a review of medical records. The smoking habits of
the subject may he incorrectly reported. Classification of individuals
who are current or former smokers as never smokers would lead to a
spurious increase in the relative risk for lung cancer in nonsmokers
exposed to ETS, because the smoking habits of spouses tend to be
correlated. The extent of this bias in the case-control studies is
uncertain. The proportion of people reported as never smokers, but
who in fact did smoke in the past, is unknown. The proportion of
current smokers who report themselves as nonsmokers can be
estimated from studies using markers to validate questionnaires.
Using biochemical markers of tobacco smoke ahsorption, the propor-
tion would appear to he about 0.5 to 3 percent, depending on the
population studied and the questionnaire used (Wald et al. 1981;
Saloojee et al. 1982).
Misclassification of the extent of ETS exposure can also occur, and
may reduce the observed risk if a nonsmoking spouse of a smoker is
not exposed to smoke at home. Friedman and colleagues (19831,
reporting on a survey of 38,000 subjects, noted that 47 percent of
nonsmoking women married to smokers reported that they were not
exposed to tobacco smoke at home.

Measurements of Absorption

The difficulties inherent in estimating exposure and dose have
provided the impetus for the development of biological markers for
exposure to both MS and ETS. The marker that at present holds the

36


highest promise is cdhine, the mqjor metabolite of nicotine.
Cotinine may he measured in saliva, blood, or urine. Numerous
studies have demonstrated that there is good correlation between
these measures of cotinine and the estimated exposure to tobacco
smoke under laboratory conditions (Russell and Feyerabend 1975;
HofEnann et al. 1984) and under conditions of daily life (Russell and
Feyerabend 1975; Feyerabend et al. 1982; Foliart et al. 1983; Wald et
al. 1984; Wald and Ritchie 1984; Jarvis et al. 1984; Matsukura et al.
1984; Greenberg et al. 1984). Cotinine is probably the best marker for
tobacco smoke intake because it is highly sensitive and specitlc for
t&acc~ smoke and because it can be detected both in active smokers
and in individuals exposed to EX'S. Further details about cotinine
and other markem are to be found in Chapter 4.

Pohntiully Gmfounding Variables

In any epidemiological study, the confounding factors must be
considered and their effects controlled. Confounding refers to the
bii effect of a factor that independently influences the risk for
the disease of concern and is also associated with the exposure under
evaluation. Confounding is of particular concern when the effects of
the exposure of interest are expe&d to be small.
The potential confounding variables depend on the health outcome
of interest. For lung cancer, occupational exposures, diet, and
exposure to other combustion products are of concern. For acute and
chronic pulmonary effects, potential confounders include airways
hyperresponsiveness, other indoor air pollutants, outdoor air pollu-
tion, respiratory tract infections, occupational exposure, and socio
economic status, which may potentially influence disease risk
through its environmental correlau23. While this list is extensive, it
may not be inclusive; in any single investigation it may not be
possible to meesure and control all potentially confounding vti-
able&

In general, the evidence on active smoking in combination with
the dosimetrp of involuntary smoking leads to the conclusion that
the effecta of ETS on a population will be substantially less than the
effecta of active smoking. The effects of E!R3 on infants and young
children are an important exception.
The association of E'IS with an adverse effect in an individual
study may reflect bias, chance, or a causal relationship. Statistical
signiticance testing is used to quantitate the role of chance; by
convention, a p (probability) value less than 0.05 is deemed statisti-
cally significant. A p value less than 0.05 means that the observed
results would occur by chance less than 5 times out of 100, if there is

36


truly no association between ETS and the effect. The choice of 0.05 is
arbitrary, and as the significance level declines, the probability that
the observation could have occurred by chance lessens.
For effects of small magnitude, as may he anticipated for some
consequences of exposure to ETS, a large study population may be
necessary to demonstrate statistical significance. The absence of
statistical significance for an association may refled an inadequate
sample sixe and is not always indicative of the absence of an
association. In this regard, reports describing the absence of effects
of ETS should provide the calculations needed to demonstrate the
study's statistical power (ability to detect effects of the magnitude
expected) or a confidence interval for the estimate of effect.
An additional statistical issue is the directionality of statistical
significance testing. Either one-sided or two-sided tests may he used,
in the fmt, only effects in one direction are considered a possibility,
whereas twosided tests consider the possibility of effects in opposing
directions, i.e., increase or decrease of risk Given the strength of the
evidence on active smoking and disease risk, one-sided testing in the
direction of an adverse effect seems appropriate for most potential
consequences of ETS. However, one-sided tests have not been
performed in all investigations of ETS; the use of two-sided tests
makes these studies conservative, as statistical significance will less
often be attained.

Respiratory System Effects of Involuntary Cigarette Smoke
Exposure

This section reviews the evidence on involuntary smoking and the
adverse physiologic effects, respiratory symptoms, and respiratory
diseases in nonsmoking adults and children. Health effects related to
fetal exposure in utero from active smoking by the mother are not
discussed. Lung growth and development may he influenced by in
utero exposure, and the effects of such exposures have not been
separated from those of exposure after birth. More complete
treatments of this issue have heen published (US DHEW 1979; US
DHHS 1980, Abel 1980; Weinberger and Weiss 1981).
This section begins with a review of the data on infants and
children who are exposed primarily through parental smoking. The
health effects examin ed are increased respiratory illnesses, of both
the upper and the lower respiratory tracts, increased chronic
respiratory symptoms and illnesses, and alterations in lung growth
and development. Studies of adults, whose exposures to environmen-
tal tobacco smoke occur in a variety of settings, are examined with
regard to symptoms and changes in measures of lung function. The
potential for J3TS to produce bronchoconstriction in asthmatic and
nonasthmatic subjects is also examined.

37


InfantsandChildren
Acute Respimtory Illness
Longitudinal Studies

A number of studies, based on a variety of different designs, have
examined the effects of involuntary smoking on the acute respira-
tory illness experience of children (Table 1). Several different end
points have been ev&&ed in these investigations: hospitalization
for bronchitis or pneumonia as 888e88ed by hospital records (Harlap
and Davies 1974; Rantakallio 1978); questionnaire assessment of
hospitalization for bronchitis or pneumonia or of doctor's visits
(Colley 1971; Leeder et al. 1976a) or both G'ergusson et al. 1981;
Fergusson and Horwood 1985); questionnaire assessment of reapira-
tory illness within the last year (Cameron et al. 1969; Schenker et al.
1983; Ware et al. 1984); chest illness before age 2 (Schenker et al.
1983); hospitalization for respiratory syncytial virus 0 infection
(Sims et al. 1978; pullan and Hey 1982); physiciandiagnosed
bronchitis, tracheitis, or laryngitis (Pedreira et al. 1985); and
tonsillectomy as an indication of recurrent respiratory infection
(Said et al. 1978). These diverse end points range from illnesses
associated with a specific etiologic agent, e.g., RSV bronchiolitis, to
clinician&agnosed syndromes, e.g., bronchitis of undetermined
etiology.

The possibility of reporting bias must be considered for the studies
that have used questionnaires to measure iUness experience. In most
of these studies, parents, usually the mother, have responded for the
child and reported on the child's illness experience. Some investiga-
tors have suggested that mothers with respiratory symptoms are
more likely to report symptoms for their children and that stratifica-
tion of subjects by the symptom status of their parents removes this
element of recall bias (Lebowitz and Burrows 1976). Removal of
symptomatic parents, however, may result in overcorrection for
recall bias because cigarette smoking is associated with symptoms in
the adult. This analytical strategy would not be expected to adjust
for biased parental recall of early life events. Additionally, in all
studies in which potential reporting bias was examined, control for
parents' status reduced, but did not eliminate, associations of
involuntary smoking with health -outcomes (Colley et al. 1974;
Leeder et al. 1976a,,b; Schenker et al. 1983; Ware et al. 198.4).
Further, the consistency of these studies, in spite of differing study
populations and methods, weighs against bias as the sole explanation
for the effect of involuntary smoke exposure.
Harlap and Davies (1974) studied 10,672 births in Israel between
1965 ad 1968 and observed that infants, whose mothers, at a
prenatal visit, reported that they smoked, had a 27.5 percent greater
hospital admission rate for pneumonia and bronchitis than children

38


TABLE 1.-E&y childhood reepiratory illnew and involuntary c@arette smoking

0    l-10   11-m m+

C-Y'         2$4x birth& 1963-1966,      fJt&hdm bItmdLiti/          7.6    10.4    11.1    153
(1971)                       prhemo&tIrrtyeuoflifo       10.3    16.1    14.6    292
                         Fa=1.78 for a?m pumt maker
                          RR=280 fbr two puwlt mllokam                         numberaEm&rwx
                                                                           l&d-rhdr


TABLE ~-continued

Study

Saidetal.
w78)

8ohenkeretalal.
mfw

    Eht&b              fihP          Dlneu~ rata per 100            ckllnumb

3,920 children, ajpd lo-!20,    -w ondhr             28.2     41.4     60.9   ~&~notobu
France             edem, geaiemlly before                  pmultmmkiDghmldt~rspac
               age6,Milldi&orof~ueult                    timediredb-~
               mepimtoly tact infedion            r wP== lo+ Y=-

4,071 children, eged 6-14,     che6tiuaembeforeage2           6.7      7.9     11.6    Trend#forbothsirmrhMt
united stata          ChdUblW>SdQ%3iDptlCt         8.8     11.8     13.6
                  Ye=
                                           Parent-

                                          NOMIlWkGI   chrmlt-

camerolJ et al.
w60)

Leederetal
US?Bp, b)

am8 et al.
(1978)

168 children, agmi M;      Reepimtory iuners, rertricted          1.33         1.4      lllneumportednot~
parenta t&phone        activity sad/or medical                      notclearhoymportbgbdult
quationnaire, united stata    conmllhllwhlutyeu                               ml&dtoohud
                                                      -ludy
2J4!3 infant& born l96s-      RR - 2.0 for Wants with two         Not provided        Puew mlponu bin unlikely,
1986, EngLand          amokhg per&a                                  el&cte-Torinfmltod
                                                    -P-P-e-
                                                    Rp&wIul~~not
                                                  invutigatod
                                                 Lcmgiw Btlldy
36 children, hcapitakad,     Bonierline eipifhlt in- in        Not pmided
R8vblvndlioli~36                                         Noh6niCant&ctfor
              matelnalmlloking,6lwtye8rof
colltro~ E&end                                            ?? ???o?*?? o ?
                  life                                  emountemokedorabrfw
                  RR=266                                  IYLm~ofMthncul~
                                                  c---M*


TABLE l.-Continued

lZd&dliO
(1Qw

Pullan and Hey
ww

l&t21 children of amoking     sienifieant incream in       Not `&       FlUBpdiV8fOllOUUpddda
motbera            hapMid for rupiratory                       vidt4hoapi~dmtba
l&322 children of         ilhemduringfimt6yeamoflih                      uPbrsas&-
n-king mothem         RRz1.74                                alldingwal~
FWmd                                                Iaaei-w
190 children hooPitaliced,     8ignis~teffe!ctofmatemal          Not prwidd        c---M-b
B8vinfectioQfh%tywIrof    (Rk1.96) and ~&msJ (RR-1.62)
life; 111 nonhonPi~      smoking at time of rtudo;
-hb FwNd         Eignaant maternal lrmobhg
                effectduringiintyenroflife
                 (RR=l.M)

F&&a et al.
ww

                                             Nommokex hoker
                                                   --
1,144 infanta in prdintric     8ignibntincreer,inrupiratory    Brolrchitis     71     109    l%dia~nothlimkdb
pi-act& united 8tatu      ibUDESunonp~O~                 21      40    eqmuwmaffactmfa
                    childrcm                             4 7  LV"
                                                                        tia


of nonsmoking mothers. In addition, they demonstrated a dose-
response relationship between the amount of maternal smoking and
the number of hospital admissions for these conditions. The infants
were classified by the mothers' prenatal smoking behavior and not
by the mothers' smoking behavior during the first year of the child's
life. Maternal smoking habits would probably have remained
relatively stable across the short observation period.
British. investigators (Colley et al. 1974) followed children born
between 1963 and 1985 in London and also observed an increased
frequency of bronchitis and pneumonia during the first year of life in
the children of parents who smoked. This difference did not persist
at 2 to 5 years of age. Tbis effect was independent of the parents'
personal reports of winter morning phlegm and increased with the
amount of smoking by parents. The annual incidence of bronchitis
and pneumonia during the first year of life also increased with a
greater number of siblings. This variable was not controlled in the
original analysis, however, Leeder and colleagues (1976b) subse
quently reported that, in this same cohort, a dose-response relation-
ship with parental smoking persisted for bronchitis and pneumonia
in the first year of life, after control for parental respiratory
symptoms, the sex of the child, the number of siblings, and a history
of respiratory illness in the siblings.
Fergusson and colleagues (1981) studied 1,265 New Zealand
children from birth to age 3. They demonstrated an increase in
bronchitis and pneumonia and in lower respiratory illness during
the first 2 years of life in children whose mothers smoked compared
with child.ren whose mothers did not smoke. Correction for maternal
age, family size, and socioeconomic status did not affect the
relationship between the amount of maternal smoking and the rate
of respiratory illness. The effect of maternal smoking declined with
increasing age of the child.
In a second report (Fergusson and Horwood 1985) the followup was
extended to include the first 6 years of life. The results conf%rmed the
initial fmdings. Maternal, but not paternal, smoking was associated
with a statistically significant increase in lower respiratory illnesses
during the first 2 years of life. However, after age 2 there was no
signif?cant effect of maternal smoking on respiratory illness occur-
rence.

Rmbkdlio (1978) followed more than 3,696 children during the
first 5 years of life; half of the children had mothers who smoked
cigarettes during pregnancy and half did not. The children of
mothers who smoked had a 70 percent greater chance of hmpi&-
tion for a respiratory illness than the children of nonsmoking
mothers.
Pedreira and associates (1985) prospsctively studied 1,144 infants
and their families in the greater Washington, DC., area. Mate&

42


smoking was associated with an excess frequency of acute bronchitis,
tracheitis, and lary&tis, as diagnosed by the pediatricians caring
for these families. Episodes of croup, pneumonia, and bronchiolitis
were not increased by maternal smoking. A family history of chronic
respiratory symptoms ~88 also associated with excess respiratory
illness.

Ware and coworkers (1984) studied more than 10,009 children in
six American cities. Maternal cigarette smoking was associated with
increased parental reporting of a doctordiagnosed respiratory illness
before the age of 2 years and of an acute respiratory illness within
the past year. The prevalence of positive questionnaire responses
increased consistently with the current daily cigarette consumption
of the mother; the d-response relationships were unchanged by
adjustment for maternal symptoms and educational status.

Cross-Sectional Studies

Schenker and coworkers (1983) studied 4,071 children between the
ages of 5 and 14 years in a cross-sectional study in Pennsylvania.
Both chest illness in the past year and severe chest illness before age
2 were more frequently reported in nonsmoking children of parents
who smoked. These investigators found that symptom and illness
rates were higher in children of parents with respiratory symptoms.
However, a significant effect of maternal smoking on these illness
variables remained after adjustment for the parents' own respira-
tory symptom history.

In a study of 1,355 children between 6 and 12 years of age in the
Iowa public schools, Ekwo and coworkers (1983) found that the
presence in the home of at least one parent who smoked was
significantly associated with reported hospitalization of the child for
a respiratory illness during the first 2 years of life. As in other
studies, the effect was stronger for maternal smoking than for
paternal smoking.

Case-Control Studies

In England, Sims and colleagues (1978) examined 35 children at 8
years of age who had been hospitalized during infancy for RSV
bronchiolitis and compared them with 35 control children of similar
age. Maternal smoking was associated with a relative risk of 2.65 for
hospitalization due to bronchiolitis. The sample size was small, and
this effect of maternal smoking was not statistically significant.

Pullan and Hey (1982) studied children who had been hospitalized
with documented RSV infection in infancy. They found significantly
greater smoking by their mothers at the time of the infection,
compared with children hospitalized for other illnesses, including
respiratory disease for which RSV infection was not documented. At

43


age 10, the children previously ill with RSV infection had an excess
reported occurrence of wheeze and asthma and had lower levels of
pulmonary function in comparison with the controls. The research-
ers could not determine whether the RSV infection had caused
persistent damage that affected the maturation of the lung or
whether these children were already more susceptible to severe RSV
infection because of pulmonary problems that antedated the RN
infection.

In summary, the results of these studies show excess acute
respiratory illness in the children of parents who smoke, particularly
in children under 2 years of age. This pattern is evident in studies
conducted with different methodologies and in different locales. The
increased risk of hospitalization for severe bronchitis or pneumonia
associated with parental smoking ranges from 20 to 40 percent
during the first year of life. Young children appear to represent a
more susceptible population for the adverse effects of involuntary
smoking than older children or adults. The timeactivity patterns of
infants, which generally place them in proximity to their mothers,
may lead to particularly high exposures to environmental tobacco
smoke if the mother smokes.
Acute respiratory illnesses during childhood may have long-term
effects on lung growth and development, and might increase the
susceptibility of the lung to the effects of active smoking and to the
development of chronic obstructive lung disease (Samet et al. 1983;
US DHHS 1984).

Cough, Phlegm, and Wheezing

A number of crossse&onal studies from different countries (Table
2) have shown a positive association between parental cigarette
smoking and the prevalence of chronic cough and chronic phlegm ,in
children; some studies have shown a relationship for persistent
wheeze. However, not all studies have shown a positive relationship
for all symptoms. The results of some of these studies may have been
confounded by the child's own smoking habits (Colley et al. 1974,
Bland et al. 1978; Kasuga et al. 1979). The association with parental
smoking was not statistically &i&ant for all symptoms in all
studies (Lebowits and Burrows 1976; Schilling et al. 1977; Schenker
et al. 1983). However, the majority of studies showed an increase in
symptom prevalence with an increase in the number of smoking
parents in the home.
A recent report (Charlton 1984) provides crosssectional data on
parent-reported cough for 15,000 children, 8 to 19 years of age, in
northern England. Chronic cough in the children was related to their
age and to their own cigarette smoking status. However, with control
of these factors by stratification, the number of parental smokers in
the home was positively associated with the occurrence of chronic

44


TABLE Z.-Chronic respiratory symptoma in children in relation to involuntary smoke exposure

  Bates per 100 by
numb8r of amoking parents

Study             SUhjfXbJ

Beapiitory eymptonu or illness

0     1     2            c!ammellte

Wley et al.
(1974)

2,426 children, agfd 614,      Chronic cough; quentionnaire
blend             completed by parent

16.6

17.1 22.2

Trend eignifican~ reportiog bina
-pcmible result of parent symptoma
or ecth smoking in children,
ldikdYtOC!IpL3blflIU&CtOf
trend

Bland et al.

W378)

3.106 children, awl 12-13,

did not admit-te-ever
emoking cigarettes., England

Couah durina day or at nkht

       - .

Morning oough

16.4

19.0 29.6

1.6 2.8 2.9

Croewectional study
children's self-reported symphme
end emoking hietory a&&d
aimul~ual~ morning end
daytime-&e&-
different dimeen, could be
difference in expoeure (expomre
more likely awnke than deep)
Crowaxtionel study, adju&d for
cbild'e own smoking habita

Wek et al.       8E4 children, aged 6-9,
wm           United States

Chronic wugh end phlegm          1.7    2.1    3.4

Per&tent wheeze               1.8    6.8    11.8

Tread not rign&ant

Tend significant
Cmm-wtional study, edjueted for
parental symptoms and child% ~WII
SmOkiIlg

Charkon
aw

16,ooO children, eged S-19
yeara, E&and

40.0 46.0 66.0


TABLE 2.4htinued

Study             Subject.3

                  Wee per 100 by
                 number of smoking parent-g
Respiratory 6ymptoms or illness       0     1     2            Comment8

Dodge
(1982)

628 children, grades 3-4,
twwparent households;
parent questionnaire
response, United States

Any wheeze               27.6 27.9 40.0

Phlegm                    6.4    10.9    12.0

Cwxh                  14.6 23.0 27.8

Au trends tdgnlfiwn~ some aFect
might relate to po.renM Wm@moa
but no trend influence !ik.ely
&os-e&onal study

Schenker et al.
u9w

Lehowitz and
Burrowx
(1976)

SchiIllng et al.
(1977)

Kaeuga et al.
(1979)

4,071 children, aged 6-14,
United States

1,625 children, <16 yenm
old, United States

816 children, age 7+,
United States

1,937 children, aged 6-11,
Jaw

Chronic cough

chronic phlegm

Persistent wheeze

Pereietent cough

Pen&tent phlegm

whesre
couph, phMm, wheeze

wheeze. asthma

Trend not significant not austed
for parental eymptome, although
parental symptom effect dyr-ed
Croeee&ional study

Hiiher rates in symptomatic
parent .houeebol&, trends persisted
for asymptomatic households; no
adjustment for child`e own smoking
Cros+e&ional etudy
Specific data not provided
-ional study
Adjust.4 for distance of home from
main tratl-ic, highway
cmee-sectional study

Ekwo et al.
(1983)

1,366 children, eged 6-12,
United States

Coughs with adds

Wheeeing apart from c&3

6.2 1.0 8.3

  4.1    4.8    4.0

  1.2    7.7    6.4

  Never    Parent
smoker .  smoker

   3.7       7.2

   10.0      12.8

   23.4       94.1

  No swcant effect

Increased prevalence in
heavy smoker (>21 &/day)
family less clear effect in
light smoker (~21 c&z/day)
family
Odds ratios: 1.4 for smoker
father, I.6 for smoker
mother
2 if only Bnlpker mother

Gasstmeuse measnrd not
contded for; no con&tent doe+
ZEZtional study


cough. The mother's smoking had a greater effect than the father's
smoking.
Burchfiel and colleagues (1986) have conducted a longitudinal
study of 3,482 subjects from Tecumseh, Michigan. Subjects were
initially between the ages of birth and 10 years and were followed up
by questionnaire and examination 15 years after entry into the
study. Age-specific incidence rates were calculated for a number of
chronic respiratory symptoms, including cough, phlegm, wheeze, and
bronchitis. Incidence rates for all symptoms were higher for children
with two parental smokers when compared with children of non-
smokers. Adjustment for potential confounding variables, including
age, parental education, family size, and personal smoking, did not
explain these results.
British researchers &eeder et al. 1976b) studying a birth cohort
over a 5-year period demonstrated an increased incidence of Nheez-
ing among nonasthmatic children with two parents who smoked in
comparison with children whose parents did not smoke, one parent
who smoked, or parents whose smoking changed during the study
(Leeder et al. 1976a). However, when this association was examined
by logistic regression with control for. other factors, parental
smoking was not a significant predictor of wheeze or of asthma.
McConnochie and Roghmann (1984) performed a retrospective
cohort study to examin e the influence of mild bronchitis in early
childhood on wheezing symptoms 8 years later when the subjects had
reached a mean age of 8.3 years. Involuntary smoking was a
significant predictor of current wheezing (odds ratio 1.9). In a related
study (McConnochie and Roghmann 1985) with these same children,
involuntary smoking did not affect lower respiratory tract illness
experience.
In a study of 650 children aged 5 to 10 years (Weiss et al. 19801, a
significant trend in the reported prevalence of chronic wheezing
with current parental smoking was found; the rates were 1.9
percent, 6.9 percent, and 11.8 percent for children with zero, one, and
two parents who smoked, respectively. Although the data given are
for all households, when the analysis was restricted to those
households where neither parent reported symptoms, the results
were identical. The stability of the fmdings with this restriction
suggests that reporting bias introduced by parental symptoms W&B
not responsible for the observed results.
Schenker and coworkers (1983) e xamined the influence of parental
smoking and symptoms on the reporting of chronic respiratory
symptoms of cough, phlegm, and persistent wheezing in children.
These investigators found that the mothers were more likely than
the fathers and symptomatic mothers were more likely than
asymptomatic mothers to report these symptoms in their children.

47


Parental smoking had no significant effects on chronic respiratory
symptoms.

L&,,~z m,j BU~OWB (1976) assessed the effects of household
mea=' smoking on respiratory 8ymptoms in 6% `hwm Chihhn
younger b 15 y- of age. children from homes with current
smoke= m higher symptom rates than those from homes with ex-
smokers ad ee never smokers. However, the effect of household
Bmow w w88 atistically significant only for persistent cough.
h a general population s~u&, &hilling and ~lleagues (1977)
reported no mhtion between wheeze and involuntary smoking.
ware md ~i&,es (1984) enrolled 10,106 children between 6 and
g Y- of we from six U.S. cities in a prospective study. The
pmdene of persistent cough and persistent wheeze, measured at
the second mtion, was higher in children whose parents
smoked. `JJg effect was greater for maternal smoking than for
paternal smoking. Symptom prevalence rates increased linearily
tith the number of cigarettes smoked daily by the mother. In a
multiple logistic model, the effect of maternal smoking persisted
after adjustment for reported ilhess in the parents.
Dodge (1982), studying third and fourth grade children in Arizona,
found that symptoms, including wheeze, were related to both the
presence of symptoms in the parents and the number of smokers in
the household.

In summary, children whose parents smoke had a 30 to 80 percent
excess prevalence of chronic cough or phlegm compared with
children of nonsmoking parents. For wheezing, the increase in risk
varied from none to over sixfold among the studies reviewed. Many
studies showed an exposurerelated increase in the percentage of
children with reported chronic symptoms as the number of parental
smokers in the home increased. Misclassification as nonsmokers of
children who are actively smoking could bias the results of these
studies. Adolescent 8mokers may be reluctant to accurately report
their smoking habits, and more objective measures of exposure may
not help to distinguish active experimentation with cigarettes from
mvohmtary exposure to smoke Cl'ager 1986). Although miscla&fica-
tion of children who are actively smoking as nonsmokers must be
considered, many studies showing a positive association between
P-nM smoldng amI symptoms in children, including children at
4P bdke f%#.ficant experimentation with cigarettes is prevalent.
h addition, many 8tudies (Bland et al. 1978; Weiss et al. 1980;
Chm-hn 19% Schenker et al. 1983, Dodge 1982; Burchfiel et al.
19%) found significant effects of parental smoking after ~~ide~g
active smoking by the children.
chronic resPbtorY symptoms represent an immediate health
h&n for the child. However, the long-term simlcance of chrodc
r@PhtorY sYmPbmS for the health of the child is unclear. &et

48


available data are cross-sectional, and followup studies of chroticdy
symptomatic children are necessaq to determine the long-term
health consequences of chronic respiratory symptoms.

In recent YW, the effect of parental cigare&e smokjng on
pulmonary function in children has been examined in crossgedional
studies (Table 3) and a few longitudinal studies. The crmonal
studies have demonstrated lower values on tests of pulmonary
function (FEV75z, LEVI, FEFLJMS, and flows at low lung volumes) in
children of mothers who smoked compared with cmdren of non-
smoking mothers. The longitudinal studies (Table 4) have confirmed
the cross-sectional results and provide some insight into the imp&+
tions of the cross-sectional data.

Dose-response relationships have been found in both cross-se&on-
al and longitudinal studies Stager et al. 1979; Weiss et al. 1980; Ware
et al. 1964; Berkey et al. 1986); the level of function decreases with
an increasing number of smokers in the home. As would be
anticipated from the mother's greater contact time with the child,
maternal smoking tends to have a greater impact than pa&Id
smoking. Younger children seem to experience greater effects than
older children (Tager et al. 1979; Weiss et al. 1960), and in older
children the effects of personal smoking may be additive with those
of involuntary smoking (Tager et al. 1979,1985).
As noted by Tager (1986), the effect of maternal smoking on lung
function may vary with the child's sex. Some studies have reported
greater effects on flows at lower lung volumes in girls than in boys
(Burchfiel et al. 1986; Tashkin et al. 19% Yamell and St. Leger
1979; Veda.l et al. 1964). Flows at higher lung volumes seem more
affected in boys (Burchfiel et al. 1986, Yarnell and St. Leger 1979;
F&-key et al. 1986; Tad&in et al. 1964). Whether these sex effects
represent differences in exposure, differences in susceptibility to
environmental cigarette smoke, or differences in growth and devel-
opment is unclear.
Tager and colleagues (1983) followed 1,156 children for 7 years to
determine the effect of maternal smoking on the growth of PRO-
nary function in children (Figure 2). After correcting for previous
level of FEVI, age, height, personal cigarette smoking, and correla-
tion between mother's and child's pulmonary function level, mater-
nal smoking was associated with a reduced annual increase in F'EVI
and FEFs75, using two separate methods of analysis. If the effect of
ma&d smoking is maintained to 20 years of age, then a 3 to 5
percent reduction of FEV, and FEFz+75 due to maternal Smoking
would be projected. The validity of this PrOjeCtion remains to be
&&h&ed. Because few mothers changed their smoking habits, the

49


TABLE 3.-~uhonary ~UC&~UI in CII.WEW exposed to involuntary smoking

Study              Subjecta

SchiIling et al.
(1977)

816 children, aged 7-17,
Comwcticut and South
ceroh united statm

FEV, 88 percent pITdictA      No e!Tect of parental amokin    No control for db&ip ab Or
                                    comlntion of eihliug pllmoaur
                               function; for dludren who
                                   nevw enlow vwu60
                               elgdamtly lean in cbikhn
                                 with!Jmokhglnotbm

T-r et al.
om

w&u et al.
a9w

Vddetd.
(lgw

Lebowlte end
BIllTowS
(ls7s)

444 children, e&fed 619,
3ht Bcmfml, Massaehusetb,
united state
&5ochudren,aged~,Eeet
Boston, Memlechueetb,
united state6
r,oca children, aged MS,
united stake
371 houoehol&, complete
hietnriee of parent Emokiug
and pulmonery flmctlon of
children, age >6, Tucson,
Ak-hna. united ststa

MMEF in etadad deviation
units

MMEF in etandard deviation
unite

m,, Fvc, vmuKJl vcdm
VUdO
FBV,, Fvc, o,, vmu7s
derivedfromM?dEPVcune8,
ea etaderd deviation units

signll~t effect of parental
Ml2Oki43

slgnifimt effect of parental
~Okhg

FVC poaitivcly emocietedl flown
negatively omocieti
Noeffectofpnmbdemoking

c!mtmued for oitahip aim and
cadetion of sibling pulmowy
fll&iOll
controlled for nibobip aim and
-htiOlOf&UBgpllmoovy
function
FlowBdaab-raporuewlth
emountarnokedbymother
chggahioa: may bs d
dlfferenm in hdonr leveb of
rlspa_mcomprsdwithmors
no*rly climebe

L8bmitz et al.
(1982)

339 childreb Tuaon,
Arimm, united stat83

FEV,, I acorn

No effect of pan&al wnokhg

Higher lweb of puhoaaq
flulctlon for 4Thikhn of
tmokiqparenbtbanforna-
emokeexpwalchudren


TABLE t.-Continud

subjocte

Pulmonery function meanued

Outcome

668 chilhll, aged 8-10,
Arir.om united St.&n

No effect of parental smoking

PotenW pnrticipation rate
bias;cram+e&onaldatanot
corkroIled for child hei&
allmud FEx,/lP at e 8, 9,
and 11 oonsietently gxater in
nonomoking houoehobio tblm
hreperent smoker hou&o@
0tatica.I tast not lligdbnt

lil&khetal.
ww

Chen and Li
wm

Haaeelblad et al.
(1981).

1,080 noMmoking,
nonasthmatic children, Lctl
Al&e& united stateu
671 children, aged 6-16,
chine

16,689 children, aged 5-17,
eeven geqinphic regione,
u0it.d state3

L, Vmu7~ Vd FE&e-7s

FEV, snd MMEF

FEV, 88 percent pwdkted

Delmamd0~,0~forboys,    Noeffe&ofp&malemoking
and FJZFrm, k,m,a for &la
with mnoking mother at led
Slltly decremd FEV,     Adjuoted for child's own
fC4dMMEFiIlChUdWSl@XpOOd    smotiae~gas~~
to peteal cigarette Emoke     w-d v-mm
Significant effect of mE4ternal     Largenmnherofchihiren
but not paternal smoking      exchdedforinvdidpuImonq
                 tiuxtion data or mieoing
                  porental omoking data

Speizer et al.
ww

Lehowitz
ww

Ekwo et al.
(1983)

8,120 children, eged 6-10,
oix U.S. cltlm

117 femiliea, Tucaon,
Arlmw united stat&i
1,266 chuhn, eged 6-12,
Iowe City, low4 unitad
SW40

FVC end FEV, en percent
predicted

FVC end FFW,

FEV,, Fvc

No effect for FEV, or PVC

No effect of parental smoking

No e.ffect of parental emoking

Recent anelyeie demon&eted
en effezt for FVC end FEV,
Almemeaxd,lWendcaone
rat&3hedIittIeeffect

Data for thin outcome not
epeciflallly enal- innasal
blmchid reepfmlllvene4o emong
imokm children

Spineci et al.      2,386 echoolchildren, Turin,
usw          Italr

statistialuy aigniiamt effect of
metemel omoking

No pemlve emoking effect
diffemna betmen boyo and
l&b


c  TABLE 4.-Pulmonary function in cm&n exposed to involuntary smoking; longitudina\ ddies

  Study             Subjecta         Pulmonary funOti0n mOamld            Outcame               c!ommenta

`l&r et al.
u9w

1,166 children, aged 6-10 at
lnltial mvey, Enat Boston,
Mamachuaetta, United
St&M

FEW,, FEFow

Sicantly decreasai FEW,
and FJ!Tws growth rate for
chUdren of emoking mothem

`I-year followup; no eff$=-t of
paternal amok&; magnitude
roughIy 4 to 6 Pemnt

ware et al.       10,000 children, aged 8-11,
ww           six U.S. cities

WC, ml

WC poeitively aooociaw with
smoking; FEV, ne&ively
amociated with omoke expooure

FEV, dose-response with
amount omoked hy mother;
magnitude of e&ct estimate 6
prant

Berkey et al.
mw

7,834 children, agad 610,
six U.S. cities

WC, FEV,

Slightly higher FVC level,
slightly lower FXV, level in
omcbexposed; gmwth of both
decreased by smoke expomue

coneistent with 3 penxlt
de&it in FEV, growth

Burchfiel et al.
(l=w

3,432 children, aged MO,
Tecumeeh, Michigan, United
Statee

WC, FEV,, vrrdn

FEV, level and growth
decread by maternal smoking

Dwe-reuponoe in maIe chlhimn
with nuder of parental
omokem


LOwmt20%    Mile go%   Highest20%

Dialibution Of syear mean FN,

FIGURE 2.-Percenwe of children with mothers who were
      current cigarette smokers at initial
      examination (black columns) and sixth
      examination (white columns), according to
      distribution of mean age, height, and sex-
       corrected FEV, over the firat six examinations
N(rPE:~20W,middle60%,andhiehat20%nefertoEhildraaarithvllluainthe~ollati(th,middla
tliltxrfiftho, and upper onbflfth, rssp&vely. of the - FEY, diotributio~ nlmlbBnl in parentheua todioate
number of children in each gmup; the three circlen rap&went the BVeraga pbresnt pImdh?d value4 of FEW, for the
the group; remlta for male and famals children were combined, because difference t&mm - vu not
signifmt.
SOURCE: !hget et al. w33).

study could not establish the ages at which children were most
vulnerable to exposure to tobacco smoke.
Ware and colleagues (1964) followed 10,106 white children for two
successive annual examin ations as part of the Harvard Air Pollution
Health Study in six U.S. cities. The forced vital capacity was
significantly higher for children of mothers who were either current
smokers or ex-smokers. However, children whose mothers were
current smokers had a 0.6 percent lower mean FEVl at the first
examination and 0.9 percent lower mean F'EVl at the second
examination. Maternal smoking had a greater effect than paternal
smoking, although the effects of both were sign&ant. The changes
in level of FEYI observed were small. For exposure to a mother who
smoked one pack of cigarettes per day, the FEVl was estimated to be
decreased by less than 1 percent, or 10 to 20 mL for a child with an
F'EVl between 1.5 and 2.5 liters. Projecting the effect cumulatively to
age 20 yields an approximately 3 percent deficit. This effect is
comparable to that observed by Tager and colleagues (1963). These
small average effects may underestimate the effects on populations
of susceptible children.

53


A mom e&hve analysis of longitudinal data from the Harvard
cohort wm performed using a mathematical model to describe lung
growth (Be&y et al. 1966). This ~IM&B~S included 7,834 Children
beben 6 & 10 year6 of age who were evaluated from two to five
hm over a ~-year period. The model estimated that a smoke
expOeed child at age 8 would have an FE571 0.81 percent lower than a
non-emokeexpoa3ed child, and growth of FEVI would be 0.17 percent
lower per year. ~0th effects were statistidy significant. For ~I.I 8
yw& child tith an F'EVl of 1.62 liters, these result-8 translate into
a deficit of 13 J.UL in FEVI and of 3 mL in annual increase in MI.
`&e magnitude of the maternal smoking effect is consistent with a
de&it in J?EVl of 2.8 percent in naturally attained growth, if the
effect, ia sustained throughout ~hildhd.
Burchfiel and colleagues (1966) have conducted a longitudinal
study of 3,462 children observed over a E-year period in Tecumseh,
&.&h&an. The mean increase in FXVI for nonsmoking boys between
the ages of 10 and 19 years was 82.3, 76.2, and 74.5 mL per year for
subjects with zero, one, and two smoking parents, respectively. Boys
with one parent who smoked experienced 92.6 percent and boys with
two parents who smoked experienced 90.5 percent of the growth in
FEVl seen in male children with nonsmoking parents. EXfecta of
parental smoking were not found in girls.
The available data demonstrate that maternal smoking reduces
lung function in young children. However, the absolute magnitude of
the difference in lung function is tnnall on average. A Emall
reduction of function, on the order of 1 to 5 percent of predicted
value, would not be expected to have functional consequences.
However, some children may be affected to a greater extent, and
even small differences might be important for children who become
active cigarette smokers as adults.
A minority of adult cigarette smokers develop chronic obstructive
lung disease, and factors influencing lung growth and development
during childhood might predispose to disease in adulthood (Samet et
al. 1983; Speizer and Tager 1979). In Figure 3 is depicted a model of
growth and decline in pulmonary function from childhood through
adulthood, as measured by the F'EXl. Pulmonary function peaks in
early adult life and declines steadily thereafter in both smokers
(curve B) and nonsmokers (curve A). In people who develop chronic
lung disease (curve CL a more rapid decline has occurred. Childhood
factors could predispose to the development of disease by reducing
the functional level at which decline begins tjr by increasing
SusCePtibfitV to cigarette smoke and increasing the rate of d-be.
Thus, in this model, small decrements in the   ' Ily atwed
led Of PuhnOnary function may be important in identifying &e
susceptible smoker. However, the prerequisite longitudinal stu&es
needed to test this hypothesis have not yet been conducted,


FEV, as percent
of value at
age 2h25

I                 I      I                       L
5     10     15     20     30     40     50     90     70     50
                     Age (uem)

FIGURE 3.-Theoretical curves representing varying rates

of change in FJSV, by age

SOURCE: SpeLer and Tager (1979).

Bronchoconstriction

Nonspecific bronchial responsiveness has been considered a poten-
tial risk factor for the development of chronic obstructive lung
disease in both adults and children (US DHHS 1984). This physiolog-
ic trait may be influenced by environmental exposures such as
involuntary smoking by children and active smoking by adults, and
by respiratory infections at all ages.
Asthma is a chronic disease characterized by bronchial hyperre
sponsiveness. Epidemiologic studies of children have shown no
consistent relationship between the report of a doctor's diagnosis of
asthma and exposure to involuntary smoking. Although one study
showed an association between involuntary smoking and asthma
(Gortmaker et al. 1982), others have not (Schenker et al. 1983;
Horwood et al. 1985). This variability may reflect differing ages of
the children studied, differing exposures, or uncontrolled bias. In
several recent studies (Murray and Morrison 1986; O'Connor et al.

55


1986, web et al. 1985; Martinez et al. 198% Ekwo et al. 19831,
noMpecific broncm responsiveness Was examined in relationship
b ~voluntary smoking. The results of these ytusm .sugge"t that
exposure b matid cigarette smoking b assocmted mth increased
noMpecific wap req&ven~. Some ,repo* suggest that the
hm respoevena is present only m chi&+% kWWn to be
w-tic (Murray and Morrison 1986; o'~nnOr et al. 1986),
whereas othm sw~ that the increased respo~iveness is seen in
4 cmw (~kw~ et al. 1983; Martinez et al. 1985). The pathophysi-
ological magi underlying the increased responsiveness and
the lowm~m consequences of the increased responsiveness remain
horn. m s&ion reviews the studies on asthma and on
bronchial hyperresponsiven~.
&rtln&er amj coworkers (1982) studied the relationship between
paren~ ~&ing and the prevalence of asthma in children up to 17
;years of age. Random community-based populations in Michigan
(3,072 &U.ren) and Massachusetts (894 children) were surveyed.
parents reported on their own smoking habits a&l on the asthma
histories of t&r children. Biased reporting by parents who smoked
~88 d by e=mimng the relationship between parena
smoking and other conditions, and considered not to be present.
A&IM prevakmce declines with age, and asthmatic children are
unlikely to tolerate active smoking; therefore, misclassification of
activelp smoking asthmatic children ss nonsmokers seems unlikely.
In comparison with children of nonsmokers, children whose parents
smoked were more likely to have asthma (relative risks of 1.5 and 1.8
for Michigan and Massachusetts children, respectively) and sevely!
asthma (relative risks of 2.0 and 2.4, respectively). The investigators
estimated that between 18 and 23 percent of all childhood asthma
and 28 and 34 percent of severe childhood asthma is attributable to
exposure to maternal cigarette smoke.
Schenker and coworkers (1983) studied 4,071 children between 5
and 15 years of age in western Pennsylvania. These investigators
found no relationship of parental smoking to the occurrence of
asthma, after adjustment for potential confounding factors.
Horwood and coworkers (1985) conducted a cohort study of 1,058
children in New Zealand who were followed from birth to age 6
ye- A fdy history of allergy and male sex were the ody
significant predictors of incident cases of asthma. Neither parental
smoking nor respiratory illnesses were predictive of the occurrence
Of asthma in this investigation.
A recently reported cross-sectional study by Murray and Morrison
(1986) suggests a mechanism by which maternal cigarette smoking
might influence the severity of childhood asthma. These mvestiga-
h-s StUdkd 94 children, aged 7 to 17 years, with a history of asthma.
The children of mothers who smoked had 47 percent more symp-

56


  41

  2-

  1 -

0.5 -

0.25 -

0.125 -

0.06 -

0.03 -

  049

Nonsmoker smoker

  00

0
0

0   %I?

     0

p=o.o02

FIGURE 4.-P% in two groupa of children with a history

toms, a 13 percent lower FEYI, and a 23 percent lower FEFws than
the children of nonsmoking mothers. Forty-one children, who had
been able to discontinue medication and had no recent respiratory
illness, underwent a histamine challenge test. There was a fourfold
greater responsiveness to hi&amine among the asthmatic children of
mothers who smoked (Figure 4) compared with asthmatic children of
nonsmoking mothers. Dose-response relationships were present for
all outcome variables in this study: symptoms, pulmonary function,
and airways responsiveness. The differences between children of
smoking mothers and children of nonsmoking mothers were greatest
in the older children. The father's smoking behavior did not
influence the child's asthma severity. The sample of asthmatic
children with mothers who smoked was small (N = lo), and only 41 of
96 children had histamine challenge tests. Given the heterogeneity
of asthma, the variable nature of bronchial hyperreactivity in
asthma, and the potential for biased selection, these results must be
interpreted with caution.
O'Connor and coworkers (1986) studied 286 children and young
adults, 6 to 21 years of age, drawn from a community-based sample,

57


and confirmed the findings of Murray and Morrison (1986). Bronchi-
al responsiveness was measured with eucapneic hyperpnea to
subfreezing air. Among the 265 subjects without asthma there was
no significant relationship between maternal cigarette smoking and
nonspecific bronchial responsiveness. However, in the 21 subjects
6th adive asthma, maternal smoking was significantly associated
with increased levels of bronchial responsiveness.

In a study of 1,355 children 6 to 12 years of age, significant
increases in FEW and FF,F25-7s were observed following isoproterenol
administration in children whose parents smoked (E~wo et al. 1983).
Increases after isoproterenol were not observed in children of
nonsmoking parents.
Weiss and coworkers (1985) evaluated 194 subjects between the
ages of 12 and 16 drawn from the same population as those reported
by O'Connor and coworkers (1986), with eucapneic hyperpnea to
subfreezing air as a test for bronchial responsiveness and allergy
skin tests as a test for atopy. Subjects defmed as atopic (any skin test
wheal greater than or equal to 5 mm) had twice the frequency of
lower respiratory illnesses in early childhood and were twice as
likely to have a mother who smoked. However, there was no
relationship between maternal smoking and increased bronchial
responsiveness.
Martinez and associates (1985) studied 170 9-yearold children in
Italy. Nonspecific bronchial responsiveness to methacholine and
allergy prick test positivity in these subjects was significantly
associated with maternal cigarette smoking.
These data suggest that maternal cigarette smoking may influence
the severity of asthma; a mechanism for this effect may be through
alteration of nonspecific bronchial responsiveness. Further investi-
gation is needed to determine whether exposure to environmental
cigarette smoke can induce asthma in children and whether ETS
exposure increases the frequency or severity of attacks of broncho-
constriction in asthmatics. The effect of involuntary smoking on
increased bronchial responsiveness in asthmatics and in norm&h-
matics has only recently been addressed. These initial data are
provocative, but the magnitude of the effect, the target population at
risk, the underlying mechanisms, and the long-term consequences
have not been described. Furthermore, the complex interrelation-
sops ==`u3 respiratory illness, atopy, parental smoking, and
tin-w responsiveness have not been clarified and require further
study.

Ear, Nose, and Thmat

Five studies (Said et al. 1978; Iverson et al. 1985; Kraemer et al.
1983; Black 1985; Pukander et al. 1985) show an excess of chronic

58


middle ear effusions and d&eases in children exposed to parental
smoke.

Said and colleagues (1978) questioned 3,920 children between IO
and 20 years of age about prior tonsillectomy or adenoidectomy,
considered an index of frequent upper respiratory or ear infections.
The investigators reported that, in general, this surgery was
performed before the children were 5 years old. The prevalence of
prior surgery ~INXMS~ with the number of currently smoking
parents in the home.
Iverson and coworkers (1985) prospectively studied 337 children
enrolled in all day-care institutions in a municipality over a 3month
petid to evaluate the importance of involuntary smoking for middle
ear effusion in children. Middle ear effusion was assessed with
tympanometry, and the overall prevalence was found to be approxi-
matsly 23 percent. Although various indoor environmental factors
were assessed in this investigation, only parental smoking was
significantly associated with middle ear effusion. The effect of
parental smoking persisted with control for the number of siblings.
The overall age-adjusted odds ratio was 1.6' (95 percent confidence
interval 1.0-2.6). In 5- to 7-year-old children, 10 to 36 percent of all
chronic middle ear effusions could thus be attributed to smoking on
the basis of these results.

Kraemer and coworkers (1983) performed a cas+control study of
76 children to examin e the relationship of environmental tobacco
smoke exposure to the occurrence of persistent middle ear effusions.
Frequent ear infections, nasal congestion, environmental tobacco
smoke exposure, and atopy were all more frequent in children with
ear effusions. The effect of involuntary smoking was observed only if
nasal congestion was present, and was greatest in children who were
atopic.
Black (1985) performed a case-control study of glue ear with 150
cases and 300 controls. Parental smoking was associated with a
relative risk of 1.64 (95 percent C.I. 1.03-2.61) for glue ear. In
Finland, Pukander and coworkers (1985) conducted a mntrol
study of 264 2 to 3-year-old children with acute otitis media and 207
control children and found an association between parental smoking
and this acute illness.
These studies are consistent in their demonstration of excess
chronic middle ear effusions, a sign of chronic ear disease, in
children exposed to parental cigarette smoke. Potential confounding
factors for middle ear effusions should be examined carefully in
future studies. The long-term implications of the excess middle ear
problems deserve further study.

59


Acute Reqimtory Illness

There are no studies of acute respiratory illness experience in
adulta exposed to environmental cigarette smoke.

cbugh, Phlegm, and wheezing

Few studies have addressed the relationship of chronic respiratory
symptoms in nonsmoking adults with environmental tobacco smoke
exposure. Schilling and colleagues (1977) found that symptoms in
adult men and women were related to personal smoking habits and
that the occurrence of cough, phlegm, or wheeze in nonsmokers was
not related to the smoking habits of their spouses. Schenker and
colleagues (1982) confirmed these results in a telephone survey of
5,000 adult women in western Pennsylvania.

White and Froeb (1980) reported on 2,100 asymptomatic adults
drawn from a population enrolled in a physical fitness program
(Table 5). They reported statistically significant decreases in FEVl
and maximum midexpiratory flow rate 0 as a percent of
predicted in nonsmokers exposed to tobacco smoke in the work
environment for at least 20 years compared with nonsmoking
workers not exposed. The magnitude of effect was comparable to that
of actively smoking 1 to 10 cigarettes per day. However, the absolute
magnitude of the difference in mean levels of function between the
smokeexpoeed group and the unexposed group was smalh 160 mL
(5.5 percent) for FEW1 and 465 I& per second (13.5 percent) for
MMEF. Carbon monoxide levels were measured in selected work-
places and ranged from 3.1 to 25.8 ppm. The study population was
se&selected, and the exposure classification was crude and did not
account for people who changed jobs. It is unclear how the ex-
smokers in the population were handled in the analysis. Kentner
and coworkers (1984) performed a cross+ectionai investigation on
1,351 workers and found no influence of involuntary smoking on
pulmonary function. In this study, involuntary smoking at home and
at work was considered.
Comstock and colleagues (1981) examined 1,724 subjects drawn
from two separate studies in Washington County, Maryland. Male
and female nonsmokers married to smokers did not have a sign&
CaMJy increased risk of having an FEWI less than 80 percent of
Predicted or an F'EJVAWC ratio less than 70 percent. Schilling and
colleagues (1977) also did not find an effect of involuntary smoking in
adults. Effects were not examined within strata defined by age in
either of these studies.

60


TABLE S.-Pulmonary function in adults exposed to involuntary smoking

Study

Subjecta

Pulmonary function measured

Outcome

Comments

White end Froeb    2,100 adults, Sen Diego,
(1980)          California, United States

Fvc, FBV,, end MhfF m
percent predictcd

significant effect of office
exposure to involuntary smoke

Potential e&&ion biaq only
current c@rette emoke
expceure & treatment of
exsmokere unclear

Comtwk et al.
a9811

1,724 adulte, Washington
County, Maryland United
St&S

FEV, 88 percent predicted

No effect of wives' smoking on
hueband's pulmonary function

Includea edulte eged 20+
cmeweetional etudy

Kauffmann et al.
mw

7,818 adulta, mlectd
subgroups, seven cities,
Frence

FFW,, FVC, end MMEF

All meeauw signiEcant effect
in wives of smoking husbands;
only MMEF signGent in
husbands of smoking wives

Not height edjw dear-
reeponmtoamolmtof
husbands' smoking for MMEF
in wivce; no effect below age
40

Brunekreef et al.
w-w

Kentner et al.
(1984)

173 adult.% subaroupe of
larger study, the -
Netherlands

1,851 adult of&e workers,
Germany

Peak flow. in8Diratorv vital

Significant effect in wives of
smoking huebenda for peak
flow FEW, cmmsctionally; no
effect longitudinelly
NO effect of work exposure on
pulmonery function

Chmectionel study
Smell sample .3&e

thmectional .&udy


Kauffmann and colleagues (1983) suggested that the effects of
exposure from a spouse who smoked may be manifest only after
many years of exposure. These investigators asses& the effects of
marriage to a smoker in 7,818 adults drawn from several cities in
France. Among 1,985 nonsmoking women aged 25 to 59,58 percent
of whom had husbands who smoked, the level of MMEF was
significantly reduced in women married to smokers compared with
women married to nonsmokers; this effect did not become apparent
until age 40. The reduction was small, on average.
Recently, studying another population, KaufXnann and colleagues
(1986) suggd,ed that the FEWI/FVC ratio may be a more sensitive
test for detecting differences between exposed and nonexpoeed
subjects, particularly in those with symptoms of wheexing; however,
this suggestion has not been evaluated in other populations.
Rrunekreef and coworkers (1985), from the Netherlands, reported
on 173 nonsmoking women who were participants in a larger
longitudinal study of pulmonary function. The women were classi-
fied by whether they were or were not exposed to tobacco smoke at
study onset or at followup. Cross-sectionally, significant differences
in pulmonary function were observed between smoke-expoeed and
nonexposed women. However, the rate of decline of lung function
king the followup period was not affected by tobacco smoke
exposure in the home. This study had a small number of subjects and
inadequate statistical power to detect effects of exposure on rate of
decline that were not extremely large.
Jones and colleagues (1983) selected women with either high or
low FEVs from a population-based longitudinal study in Tecumseh,
Michigan. Exposure to cigarette smoke at home from husbands who
smoked was not significantly different in the two groups of women.
Nonsmoking men who participated in the Multiple Risk Factor
Intervention Trial had significantly lower levels of pulmonary
function if their wives smoked in comparison with similar men
whose wives did not smoke (Svendsen et al. 1985).
The physiologic and clinical significance of the small changes in
pulmonary function found in some studies of adults remains to be
determined. The small magnitude of effect implies that a previously
healthy individual would not develop chronic lung disease solely on
the basis of involuntary tobacco smoke exposure in adult life.
Whether particular characteristics increase susceptibility, such as
Childhood exposures or illnesses, atopy, reduced pulmonary function
from whatever cause, and increased airways responsiveness, rema,fns
unknown. These sndl changes may also be markers of an irritant
response, possibly transient, to the irritants known to be present in
environmental tobacco smoke.

62


Bronchoconstriction

Normal Subjects

Only limited data have been published on the acute effects of
inhalation of environmental tobacco smoke on pulmonary function
in normal subjects (Table 6) and none on bronchial responsiveness.
The available data have been obtained in exposure chambers under
carefully monitored and controlled circumstances (Pimm et al. 1978;
Shephard et al. 1979; Dahms et al. 1981).

Pimm and colleagues (1978) exposed nonsmoking adults to smoke
in an exposure chamber. Relatively constant levels of carbon
monoxide (approximately 24 ppm) were achieved in the chamber
during involuntary smoking. Peak blood carboxyhemoglobin levels
were always less than 1 percent in these subjects before smoke
exposure, but were significantly greater after the study exposure,
Lung volumes, flow volume curves, and heart rates were measured
for all subjects. Measurements were made at rest and following
exercise under control and smoke-exposure conditions. Flow at 25
percent of the vital capacity was reduced at rest in men and with
exercise in women. Although statistically significant, the magnitude
of the change was small: a 7 percent decrease in flow in men and 14
percent in women.

Shephard and coworkers (1979) utilized a similar cross-over design
in a chamber of exactly the same size as that used by Pimm and
associates. Their results were similar, with a small (3 to 4 percent)
decrease in FVC, FEVI, Vti, and Vma~26. They concluded that these
changes were of the magnitude anticipated from exposure to the
smoke of less than one-half of a cigarette in 2 hours (the exposure
anticipated for an involuntary smoker).
Dahms and colleagues (1981) used a slightly larger chamber and
an exposure with an estimated peak carbon monoxide level of
approximately 20 parts per million. They found no change in FVC,
FEVl, or FEFs76 in normal subjects after 1 hour of exposure.
The active smoker manifests acute responses to the inhalation of
cigarette smoke; thus, highdose involuntary exposure to tobacco
smoke may plausibly induce similar responses in nonsmokers. The
magnitude of these changes is quite small, even at moderate to high
exposure levels, and it is unlikely that this change in airflow, per se,
results in symptoms.

Asthmatics

Dahms and colleagues (1981) exposed 10 patients with bronchial
asthma and 10 normal subjects to cigarette smoke in an environmen-
tal chamber. Pulmonary function was measured at 15-minute
intervals for 1 hour after smoke exposure. Blood carboxyhemoglobin
levels were measured before and after the l-hour exposure. The

63


2  TABLE 6.-Acute effects on pulmonary function of passive exposure to cigarette smoke; normal
        subjects

Study            Type of expceure

Magnitude of expmure

Effecta

Comments

Pimm et al.
(1978)

Chamber 14.6 In, furniture
sparse, smoking machine in
mm

Peak [Co] - 24 ppm;
particulatea >4 mgfni'

Men: 6% increaee PVC, 11%
increnee RV, 4% decrease
0 m.zm during exercise

Women: 7% decreaee V-
after exercise; no effects on
vc, TLC, PVC, FEW,., v,,

No-km; timage age, men
22.7, *omen 21.9; eham
expomm ax control

Shepherd et al.
ww

Dahma et al.
ww

A0 above

Chamber SO m, climate
controlled

Low exposure: peak [CD] - 20
ppm, particulate8 - mg/m';
high expowe: [Co] - 31 ppm

Room levels not meanured;
e&mated at peak [CO] - 20
wm

Low exposure: 3% decmaee
FEW,, 4% decrease vm 6%
decrease V- with exerch
no increaeed effect with high
=poeu~

0.9% increaee in Fvc,
6.2% increaw in m,,
2.2% llmenee in F+EF at 1
hour

Nonmokem: average age, men
23, women 25; sham expoeure
en control; iubjwt eatiited
inhalation - l/2 cigar&e!2
how

10 nonsmokera; a2e range 24-
63 yenm; not blinded; no aham
expmure


carboxyhemoglobin levels in subjects with asthma increased from
0.82 to 1.20 percent. In normal subjects the increase was from 0.62 to
1.05 percent. The increases in carboxyhemoglobin in the two study
groups were not significantly different. Asthmatic subjects had a
decrease in forced vital capacity @`VC), FEVI, and MMEF to a level
significantly different from their preexposure values. The decreases
in asthmatic subjects were present at 15 minutes, but worsened over
the course of the hour to approximately 75 percent of the preexpo
sure values. Normal subjects had no change in pulmonary fundion
with this level of exposure. In this study, subjects were not blinded as
to the exposure and were selected because of complaints about smoke
sensitivity.

Shephard and colleagues (1979), in a very similar experiment,
subjected 14 asthmatics to a Zhour cigarette smoke exposure in a
closed room (14.6 ms). The carbon monoxide levels (24 ppm) were
similar to those predicted in the study of Dahms and coworkers
(1981). Blood carboxyhemoglobin levels were not measured. Subjects
were randomized and blinded to sham (no smoke) and smoke
exposure and tested on two separate occasions. Data were expressed
as the percentage change from the sham exposure. Signi&ant
changes in FVC and FEYI were not observed between the sham and
the smoke exposure periods, although 5 of 12 subjects did report
wheezing or tightness in the chest on the day of smoke exposure.

Wiedemann and associates (1986) examined nonspecific bronchial
responsiveness to methacholine in 9 asthmatic subjects and 14
controls and the effect of acute involuntary smoking on nonspecific
bronchial responsiveness. At the time of the study, all asthmatics
were stable with normal or near normal pulmonary function. The
subjects underwent baseline pulmonary function and methacholine
challenge testing. On a separate day they were exposed to cigarette
smoke for 1 hour at 40 to 50 ppm of carbon monoxide and underwent
pulmonary function and methacholine challenge testing. J?uhnonary
function was not influenced by exposure. Nonspecific bronchial
responsiveness decreased significantly, rather than increasing, as
would be anticipated following an irritant exposure.

Acute exposure in a chamber may not adequately represent
exposure in the general environment. Biases in observation and the
in selection of subjects and the subjects' own expectations may
account for the widely divergent results. Studies of large numbers of
individuals with measurement of the relevant physiologic and
exposure parameters will be necessary to adequately address the
effects of environmental tobacco smoke exposure on asthmatics.

Ear, Nose, and Throat

There are no studies of chronic ear, nose, and throat symptoms in
adults with involuntary smoking exposure.

65


Lung Cancer

This se&ion reviews the epidemiological evidence on invohmtary
smoking and lung cancer in nonsmokers, which has been derived
from retrospective and prospective epidemiological studies. First,
common methodological issues that apply to all these Studies are
considered. Second, for each type of study design, individual studies
are reviewed for their methodological approach (Tables 7 and 81,
findings associated with tobacco smoke exposure (Table 9, Figure 5),
and strengths and limitations. Third, the lung cancer risk associated
with involuntary smoking is e xamined as a low-dose exposure to
cigarette smoke by combining the d-response relationships for
active smoking with the exposure data for involuntary smoking to
predict the expected lung cancer risk due to involuntary smoking.
This expxted risk is then compared with the actual risks observed in
studies of involuntary smoking. Finally, the existing epidemiologicsl
evidence is summarized and the plausibility of the association
between lung cancer and involuntary smoking is evaluated on the
basis of our current knowledge.

ObfBNd Risk

Geneml iUethodological Issues

For both retrospective and prospective studies, the common
methodoltic concerns are disease misclassi&ation and miscla&fi-
cation of the subject's personal smoking status or exposure to ET&
Disease misclassification, for example, refers to the incorrect classifi-
cation of the lung as the primary site of a cancer that originated
elsewhere. Disesss misclassification is of greatest concern in studies
in which the diagn~is of lung cancer was not histologically
confirmed. Such misclsssification tends to be random and to bias
relative risk estimates toward unity (Copeland et al. 1977). Patients
with lung cancer, or any disease associated with cigarette smoke
exposure, may report exposure to ETS more frequently than controls
becauseofbiasinrecall.
Misclassification of the subject's personal smoking status may
occur in both retrospective and prospective studies; this misclassifi-
cation refers to incorrectly classifying a subject as a nonsmoker
when the subject is actually an ex-smoker or a current smoker, or to
incorrectly chdfying the subject as a smoker when the subject is a
nonsmoker. Biochemical markers such as cotinine and nicotine,
which can be used to detect unadmitted active smokers, are sensitive
only to a recent exposure to tobacco smoke; thus, they are not
Ptiicuh+Q useful for identifying ex-smokers who deny their past
SIIlOking hisb?k~. Mis&ss&ation of smokers or ex-smokers as
nonsmokers may produce the appearance of an involuntary smoking
effect when, in fact, the true relationship is with aeve smoking.


&urcz of subjects

Age-

Yeara of earollment

l&St year of followup

Method of followup

VerScation of
diagncei.9

Metbodandtypeof
information obtained

hdex of pamive
smokiug

Number of lung cancer
deaths in nonsmokers

ceusus population, 29
he&h districts, Japan

1966

1961,1962

Recordlinkagebstweaa
ri&factarrecvrdaand
death certitica~

lnterview 0): smoking
auddrinkinghabita,
dietary history,
oocupation, other
health-related variables

Husband's smoking at
entry ooasmoker, ex-
smoker, curteat
smoker (oiglday)

mom

176769 (F)

85-84

196%1960

1972

llIonitored by ACS
volunteers, death
eartificatee from
locallstate hsmlth
departmenta

Verified method of
dlagnosi9aud
tilo6y for 6rat 6
yeam' followup

self -red
qw3tiomlaisz
education, real-
ocoupational
exposure, smokiw
and medical history

H&and's smoking
atentrj? -km
current smoker, and
OigldaJy exsmokers
exoluded

163 0

mea
1,917 (F)

45-64

19724976

1962

Recordlioh@witb

Lomlcauoerre&try

Spouse's smoklug at
eatrJTcurrentm
uever smoker, ex-
smokers edlded
(quit 26 year8 before
atrg)

6 0,8 0

~uRcE:Hirayama(19818,1@33,1964a b), -(1961),~e.tal.(198(1

Misclassification of involuntary smoking exposure refers to the
incorrect categorization of exposed subjects as nonexposed and of
nonexposed subjects as exposed. Most studies of lung cancer to date
have used the number of cigarettes smoked by spouses as a measure
of exposure to involuntary smoking, and thus have disregarded
duration of exposure, exposure from other sources, and factors that
influence exposure, such as proximity to the smokers or size and
ventilation of the room where the exposure occurred. Moreover, all

6'7


TABLE &-Description of case-control studies

Study       cmntry

   case

Source end type

  control

Source end type

            confirmed histology     Iudexofpemd~
Respondent and   Pathologicel/           mole: habita of
type of interview   cytological   Adermarchoma  spouam end others

Trichopouka Greece
et al. (1981,
1983)

C&set and can&
hospitals, 77 NS (FJ

Orthopedic hcepital; 225
Ns; not matched

Selfi not blinded

65%

Correa et al.
(1989)

New Orleans,
United States

Hoepit+ 30 NS (8 M,   Same hospitals, non-~  Self, and proxy        97%     54% among   current spoues
22 F)           related diaeaaes; 313 NS    bm, 23%                   women    RYPe, amount Fk
            (180 M, 133 Q matched for  control, 11%);                      parents
            age, sex, raw hmitd      blinded

Chsn and    Hong Kong    Four hoepit&      Orthopedic, same hoepit&   Self; not blinded       82%       45%     Ndapouee
Fun8 ww             64 NS 0        189 NS; not matched                               w=if-bi-
                                                                     quiwtiom at home
                                                                           andatwork

Koo et al.    Hong Kong     Eight lmpitale;      Population; 137 N&      Self; not blinded      97%       69%      Currentandr-
wa 1981)            88 NS 0        matched for egm, race, sex,                               m b--k
                             emioewllomlc status,                               YmwiP@-B
                                 lwldence dlstrlct                                    other cohablti&
                                                                        am&em (amount
                                                                   PIW

K&at and    united statea    Most from one NY    Same hospital 0; non-     Self; not blinded      10096      M%td     cul7ent spouss
Wynder (19S4)          hoepi~ 134 NS;     tabaamrelated dieeasq 78                         14% F of   @nrentww
               passive smoking data   NS (25 M, 63 p); matched                          134 NS    fmoking habite
               on only 78 NS (26 M,   for age, sex, raa+ hoepital,                              l?urrentwat
                  Mm           date of interview,                                        hnmeandwork
                              nonsmoking status


TABLE 8.-Continued

St&-

country

   caes

Sourceandtype

  Contml

Soweandtype

            confll histology
                           hiexofpamive
Respondent and   Patholo6icaV             srook habit8 of
type of inte.rvlew   ~hw  Adenocarcinonm qouam and othara

wu et al.
w=)

Population; 62 N9; matched  self; not blinded      100%       100%     current and former
for age, ram sex,                                  spa- (amount,
nelghborImcd                                   IT& puent*
                                              cohabitant4
                                        (=mt, Yd,
                                        coworkers &r/day,
                                         P-4

Garfinkel et
al. (1985)

New Jersey,
Ohio, united
St&S

Four hoopit&
134 NS 0

Same haepitale, o~lorectal
cancer patients; 402 NS;
matched for age, hospital,
IlonsmoLiDg status

self (cab& 12%;
control, ?) and
prory; blinded

100%

66%

Current spouse or
cohabitant (total
and at home:
amu& ~3); other
ew-re, a-w
hrdday (at home,
worl, other) 5 and
2syrsbefore
diagm!&chiMhad
em--


d  TABLE &-Continued

Study

Country

   case

Source and type

  Control

Source end type

         confirmed hb3bi~
                           Index of paudve
Respondent and   Patholcgical/             smoke:, habite of
type of interview   cytological   Adenocarcinoma  spousee and others

Lee et al.
wm

United      Ha&al-beeed; 47 NS
KlllgdOlll      (15 M, 32 l9

Same hmpitals, 96 NS (30   Self, hospital         1         1     current spoum
M, 66 F); matched for age,   inpetient                       (smoking habit
sex, marital status, hoepital   interview;                     duriag admission
             spouse, followup                  yr ad maximum
                intarvie-w; not                    during marrio&
              fqecified                        other expceure at
                                           home, at work,
                                        dur@ travel end
                                                leisure

Akiba et al.
ww

Japan

Hllhlma and
Nagasekl bomb
survivors; 103 NS (19
M, 84 F)

Same cohort, noncancer or   self (c-am, 10%;       67%         7     curlent spoum
chronic respiratory disease;   control, 12%) end                  bow llee de
380 NS (110 M, 270 IQ    prow, not blinded                    aBgestop,yra
matched for age, eeq city                         cohabitiS; perenta
of residence, vital statue, yr
of death

Perehagen
et al.
(in press)

Sweden

National census of
Sweden end Swedish
TwlnFhgi&y;
67 NS 0

Two controls from each
soume; 347 Ns; matched
for year of bii, vital
status at followup end for
twin regktry control

Self, and proxy
(case, almost all;
mntrol, 265%);
not applicable,
mailed
questionnaire

99%       57%    spouse lived with
             longeat kImour&
             Yd; parenb


TABLE 9.-Results from selected prospective and cast+
      control studies; lung cancer risk associated with
      spowes' smoking

Study                     Spousee smoking

Nonsmoker

Ex-amoker

Hirayama
(19W

Garfinkel
(1981)

  1.0

Nonsmoker

  1.0

(l.ot:.O)  (l.cy2.4)
<m/&Y           m+/day

1.3                 1.1
(0.9, 1.9)             (0.8. 1.6)

Gillis et al.
ww

   Men
   women

Nonsmoker

Not expomd

     1.0
     1.0

Fa-amoker

Trichopdos et al.      1.0          1.9            1.9           2.5
ww                   (0.9, 4.1)       (1.0, 3.7)       (1.7, 3.8)

Conea et al.
w83~

Nonsmoker

  1.0

l-40 pack-yr          >41 pack-p

  1.6                 3.1
(0.6. 3.8)             (1.1. 8.6)

  No

  1.0

Nonsmoker

  YeS

  0.8
(0.5, 3.1)

&5,ooo hrs'          >wm hln

  1.3                 1.0
(0.8, 2.4)            (0.2, 2.7)

               No            YeS

Kabat and Wynder     1.0
ww          ,.&,

             Nonsmoker       l-20 ym            21+ yrs

wu et al.           1.0
i1985)          (0.4t.4q.9)      (O.`i%

             Nonsmoker   Cigar/pipe    <IO/day    lc-19&y   2 2a/day

Garfinkel et al.        1.0         1.2         1.2      1.1 '    2.1
(1985)                    (0.8. 1.71     (0% 1.6)    (0.8, 1.5)    (1.1, 4.0)

Lee et al.
~1~)

  No

  1.0

Nonsmoker

    YeS

    1.1
  (0.6, 2.4)

l-19/daY       20-29/daY      soo+l~Y

Al&3 et al.
(1966)

Pershagen et al.
(in p-1

  1.0

Nonsmoker

  1.0

1.3
(0.7, 2.3)

   Low*

    1.0
  (0.6, 1.8)

1.5
(0.6, 2.8)

   2.1
   (0.7. 2.5)

High*

3.2
(1.0, 9.5)

' Numbers in parentheses am the 95 percent confidence Ii&e.
=Totd erpmre from spooma, cobabitante, coworkem
* Husband smoked 5 16 cigarettes/day or 1 pack (50 g) of pipe tohncmhmek or any amount duriDg < 30 years of
manillge.

`Husband smoking > 15 cigarettes/day or 1 pack of pipe tobacco/week during 2 30 years ofmarriaga.

                                             71


IO.

  8.

  a,

  7.
x 6.
g5
= 4

  3 ,'

of the published studies have baaed involuntary smoking exposure
measures on questionnaires without validation of these data with
biochemical markers or environmentally measured concentrations
of tobacco smoke constituents. Misclassification of involuntary
emoking exposure is likely to be random and to bias the effect
measures toward the null (Copeland et al. 1977).
Misclassification of exposure to environmental tobacco smoke is
inherent in epidemiological studies of involuntary smoking. Tobacco
smoking has not been re&icted in most indoor environments until
recently, and exposure has been almost inevitable in the home, the
workplace, or other locations. Studies with the biological markem
nicotine and cotinine confirm that tobacco smoke exposure is
widespread; detectable levels of these markers are found even in
people without reported recent exposure. Thus, the exposure vari-
ables employed in epidemiological studies do not separate nonex-
posed subjects from exposed subjeds; instead, they discriminate
more exposed groups from less exposed groups. As a result, the

72


epidemiological approach is conservative in estimating the effects of
involuntary smoking. A truly nonexposed but otherwise equivalent
comparison population has not been identified. The extent of the
resulting bias cannot be readily estimated and probably varies with
the exposure under consideration, which may be one reason for the
variability in risk estimates obtained by different studies.

Information bias is an added concern in cas+control studies, since
neither interviewer nor respondent bias can be ruled out. It is not
feasible to blind interviewers to the case or control status of
respondents because of the usually obvious manifestations of lung
cancer and because of the setting in which some of the interviews are
conducted. Moreover, blinding of interviewers and respondents to
the study hypothesis is difficult because the majority of questions are
concerned with exposure to tobacco smoke. The direction of the
information bias may be dependent on the type of respondent. Self-
respondents may be more apt to interpret their d&ease as related to
exposure to tobacco smoke and thus overreport the exposure.
However, the direction of the information bias is less clear when
interviews are conducted with surrogate respondents. The ability of
a surrogate to provide accurate information may depend on the
relationship of the surrogate respondent to the subject, whether the
surrogate lived with the subject during the time frame of the
questions asked, the degree of detail requested, and the amount of
time elapsed since the event in question @or&s 1982; Pickle et al.
1983; Lerchen and Samet 1986). Surrogate respondents may mini-
mize the reporting of their own smoking because of guilt, or may
overreport about involuntary smoking exposure in an attempt to
explain their relative's illness. Thus, depending on the direction of
the information bias, it may dilute or strengthen the effect being.
measured (Sackett 1979). In general, however, the information on
smoking status and on amount smoked provided by surrogatea has
been found to be fairly comparable to that provided by the
individuals themselves (Blot and McLaughlin 1985).

F'inally, participants and nonparticipants in case-control studies
may be inherently different with respect to their exposure to
involuntary smoking because their awareness of the hypothesis
under study may motivate the decision to participate. However,
participants in cas+control studies are generally not informed of the
hypothesis under study.

Spousal Exposure: Prospective Studies
The Japanese Cohort Study

Hirayama (1981a, 1983, 1984a) has presented data from a large
cohort study that included 91,540 nonsmoking married women who
were residents of 29 health districts in Japan. Subjects were 49 years

73


of age or older at enrollment in 1965; infOrm&iO~ W88 collected on
smoking and drinking habits, diet (e.g., green-yellow vegetables,
meat), occupation, and other health-related variables.
me initial report on invohmtary smoking ~88 baaed on 14 gears of
f&owup (lg6&1979). The husbands' smoking histories were avail-
able for 174 of 240 lung cancer cases identified among the non-
smoking &ed women (Hirayama 1981a); this number increased
to 2~ with 2 additional years of followup -yama 1983, 1984a).
&db p&thing to the association of spouses' lung cancer risk
with the husbands' smoking were essentially identical in the first
and second reports.
On the basis of the smoking habits of the husbands at entry, the
206 nonsmoking women were classified as married to a nonsmoker,
an ex-smoker, or a current smoker. The lung cancer mortality ratios
&d&jzed by husband's age were 1.90,1.36,1.42,1.58, and 1.91 for
women whose husbands were nonsmokers, ex-smokers, and daily
smokers of 1 to 14,15 to 19, and 20 or more cigarettes, respectively
(one-sided p for trend, 0.002). Similarly sign&ant dose-response
trends were observed when the mortality ratios were standardized
by age of the wives, by occupation of the husbands (agricultural,
industrial, other), by age and occupation of the husbands, and by the
time period of observation (19661977 versus 1978-1981). The risk of
lung cancer &ong nonsmoking wives of smokers was reduced to 0.7
(two-sided p=O.O5) if they ate green-yellow vegetables daily com-
pared with 1.0 if they ate such vegetables less often than daily
(Hirayama 1984b). No other characteristic of the wives (e.g., drinking
habits, parity, occupation, nonvegetahle dietary items) or of the
husbands (e.g., drinking habits) was significantly predictive of lung
cancer risk.
Nonsmoking men whose wives were smokers also showed an
elevated lung cancer risk. On the basis of 67 lung cancers in
nonsmoking married men, the lung cancer mortality ratios were
1.00,2.14, and 2.31 if their wives had never smoked or had smoked 1
to 19 cigarettes or 20 or more cigarettes per day, respectively (one-
sided p for trend, 0.023) (Hirayama 198413).
This study has been critically discussed in correspondence since its
initial publication. Because a detailed breakdown of the at-risk
population was not presented in the initial report, the lung cancer
mortality rate was thought by some to be higher in the unmarried
nonsmoking women than in the nonsmoking women marriedto
smokers CRutsch 1981; Grundmann et al. 1981). This impression was
clarified by the researcher (Hirayama 1981b,c,d) and shown to be the
result of incorrect interpretation of data in the original paper. Other
potential problems cited were sampling bias in the study cohort,
misclassification in the diagnosis of lung cancer, misclassification of
the nonsmoking status of wives, misclassification of involuntary

74


smoking exposure, failure to control for potential confounders, and
inadequate statistical treatment of data. Each of these points of
criticism is discussed below.

MacDonald (1981a,b) questioned the representativeness of the 29
health districts selected in the study cohort and suggested that,
industrial pollution, such as asbestos exposure from shipbuilding
industries specific to the selected health districts, may have biased
the results. However, the levels of exposure to this factor would have
to coincide with the husbands' smoking level to explain the effect
observed. Such an association seems unlikely. If the cohort were not
representative, the generalizibility but not the validity of the
findings would be challenged (Criqui 1979).
The accuracy of the diagnosis of primary lung cancer on the basis
of death certificates and the adequacy of the data without informa-
tion on the histology of the tumor were questioned (Grundmann et
al. 1981; MacDonald 1981a). From a sample of 23 cases, Hirayama
(1981b) reported that the distribution by histology of lung cancer in
nonsmoking women whose husbands smoked was similar to that in
women who smoked. Failure to discriminate in some cases between
primary and metatastic lesions to the lung may be a potential
problem with disease diagnosis. Although Hirayama was unable to
assess the accuracy of the diagnosis listed on the death certificate,
there is no reason to believe that error in recording the causes of
death of wives was influenced by the smoking habits of their
husbands, and any misclassification is likely to be random. Inclusion
of nonlung cancer cases would tend to bias the risk ratio toward
unity or no effect (Barron 1977; Greenland 1980).
The relatively high risks observed for nonsmokers whose husbands
smoked led to speculation that Japanese women may report them-
selves as nonsmokers when they actually smoke (Lehnert 1934).
However, some assurance of the reliability of the smoking data
provided by the Japanese women comes from an investigation in
Hiroshima and Nagasaki (Akiba et al. 1986) that found strong
concordance between smoking status reported by the women them-
selves and that reported by their next of km.
Classifying nonsmoking women solely on the basis of the smoking
habits of their current husbands probably does not quantify their
exposure with precision because it accounts for only one of the many
possible sources of tobacco smoke exposure. Moreover, using the
number of cigarettes smoked per day by the husbands as a measure
of exposure dose assumes that the husbands' increasing daily
cigarette consumption is directly related to an increasing ETS
exposure of the wives (Kornegay and Kastenbaum 1981; Lee 1982b).
The analyses were further criticized for not accounting for
potential confounding factors such as socioeconomic status (SES) and
exposure to indoor air pollutants (e.g., from heating and cooking

75


smrces) (Sterling 1981). However, Hirayama showed a fairly consis-
tent relationship between involuntary smoking exposure and lung
mcer across SES categories. The role of indoor air pollutants could
not be addressed directly in the study, but data from one health
distrkt in the study indicated no association between heating or
cooking practices and the smoking habits of the husbands (Hirayama
1981b).
The researcher's failure to specifically describe the methods for
age standardixation in the initial report led to speculation that the
statistical methods used were incorrect (Kornegay and Kastenbaum
1981; Mantel 1981; Tsokos 1981; Lee 1981); however, the calculations
were later confirmed (Harris and DuMouchel 1981; Hammond and
EM&off 1981). The choice of stratification variables used for age
standardixation was also criticixed because the husbands' ages
instead of the wives' ages and U&year age groups instead of narrower
ones were used (Tsokos 1981; MacDonald 1981b). Later publications
confhmed that similar results were obtained regardless of, the
method of standardixation (Hirayama 1984a).

The American Cancer Society Cohort Study
A second prospective study (Garfinkel 1981) that examined the
effects of involuntary smoking was the American Cancer Society
(ACS) study of about 1 million people living in 25 States. A self-
admimstered questionnaire on education, residence, occupational
exposure, and smoking and medical history was completed by the
study subjects upon enrollment.
This report on involuntary smoking was based on 12 years of
followup (1966-1972) and included 176,739 nonsmoking married
women whose husbands' smoking habits were available and whose
husbands were never smokers or current smokers. In the total cohort
of nonsmoking women, 564 lung cancer deaths occurred, and data on
the husbands' smoking habits were available for 153 (27.1 percent).
Wives of ex-smokers and of cigar or pipe smokers were excluded from
the analysis.
A small, statistically nonsignificant increased risk for lung cancer
was found for nonsmokers married to smokers. The mortality ratios
for lung cancer in nonsmoking women were 1.0,1.27, and 1.10 when
the husbands were nonsmokers, daily smokers of fewer than 20
cigarettes, and daily smokers of 20 `or more cigarettes, respectively.
The results were essentially unchanged after accounting for the
potential confounding effects of age, race, education, residence, and
husband's occupational exposure.
The ACS study, like the Japanese study, was not designed to study
the long-term effects of involuntary smoking. However, the ACS
study does provide an estimate of the extent of misclassification of
lung cancer. On the basis of medical record verification, the death

76


certificate diagnosis of lung cancer in nonsmoking women was
incorrect for 12 percent of the cases. Although confirmation of
diagnosis was sought only for the first 6 years of followup, the
available data suggest that some misclassification of lung cancer
occurred. To the extent that passive smoking is related to lung
cancer in nonsmokers, inclusion of nonlung cancers would tend to
dilute a true effect.

A limitation of the ACS study is the nonavailability of smoking
information on the husbands of a large proportion of the nonsmoking
women who died of lung cancer. Because smoking habits are
correlated with various social characteristics, this large loas of
information may have created a bias in this study. The researcher
stated that an index of tobacco smoke exposure based only on
smoking habits of current husbands may be particularly inadequate
for the United States, with its high rate of divorce and substantial
proportion of women working outside the home. This speculation is
supported by data from a group of 37,881 nonsmokers and ex-
smokers who were members of a health plan in California. Friedman
and colleagues (1963) stated that 47 percent of the nonsmoking
women and 39 percent of the nonsmoking men married to smokers
reported no exposure at home. Moreover, being married to a
nonsmoker did not assure the absence of exposure to tobacco smoke,
since 40 percent of the nonsmoking women and 49 percent of the
nonsmoking men married to nonsmokers reported some exposure to
tobacco smoke during the week. Thus, random misclassification
could have biased the results toward unity and led to an underesti-
mate of the effect of passive smoking.

The Scottish Study

Gillis and colleagues (1984) conducted a prospective cohort study of
16,171 Scottish men and women, aged 45 to 64 years, from two urban
areas, who attended a multiphasic health screening clinic between
1972 and 1976. A questionnaire on smoking habits and symptoms of
respiratory and cardiovascular diseases was completed at entry into
the study.
The preliminary analysis of involuntary smoking, representing 6
to 10 years of followup, was based on the 2,744 nonsmokers among
the 8,128 subjects who lived as couples and could be paired according
to smoking habits. Subjects who lived alone or whose partner did not
participate and ex-smokers who had stopped smoking for 5 years or
more were excluded. The nonsmokers were classified as nonsmokers
not exposed to environmental tobacco smoke or as nonsmokers
exposed to environmental tobacco smoke, according to the smoking
habits of their spouses.
A higher age-standardized lung cancer mortality rate was reported
for nonsmoking men exposed to tobacco smoke (13 per 10,006) than

77


for nonsmoking men not exposed (4 per 10,000); however, no
statistical tests were conducted because of the small number of
cancers. Lung cancer rates were similar for nonsmoking women
regardless of the status of their exposure to tobacco smoke (4 per
10,000). The extremely small number of observed lung cancer deaths
(6 men, 8 women) limit the interpretation of the study's findings.

Spu8al Expomre: Case-Control Studies

Table 8 summa&es the car+control studies that have examined
the relationship between involuntary smoking exposure and lung
cancer.

The Greek Study

Trichopoulos and colleagues (1981, 1983; Trichopoulos 1964)
examined the effect of involuntary smoking on lung cancer risk in a
case-control study of 51 Caucasian female lung cancer patients
(excluding adenocarcinoma and terminal bronchiolar carcinomas)
from three chest hospitals and 163 female controls from an
orthopedic hospital in Athens, Greece. All subjects were interviewed
in person by one physician who questioned them regarding their
personal smoking habits and those of their current and former
husbands. Thirty-five percent of the cases were diagnosed only on
the basis of clinical or radiologic information; the remainder were
cytologically (37 percent) or histologically (28 percent) confirmed.
Nonsmoking women were classified by the smoking habits of their
current or former husbands. Husbands were nonsmokers if they had
never smoked or had stopped smoking more than 20 years previous-
ly, ex-smokers if they stopped 5 to 20 years previously, and current
smokers if they were smoking or had stopped less than 5 years before
the interview. Being never married, widowed, or divorced was
equated as being married to a nonsmoker or an ex-smoker, depend-
ing on the length of time in the category.
The initisl report was based on 40 nonsmoking cases and 149
nonsmoking controls. The odds ratios (0R.s) for women married to
nonsmokers, ex-smokers, current smokers of 1 to 20 cigarettes per
by, and current smokers of 21 or more cigarettes per day were 1.0,
1.9,2.4, and 3.4, respectively (two-sided p for trend, < 0.02). In a later
report on 77 nonsmoking cases and 225 nonsmoking controls, the
ORa were somewhat lower: 1.0, 1.9, 1.9, and 2.5, respectively
t'lltchopoulos et al. 1983; Trichopoulos 1984).
The findings of this study were questioned because the diagnosis of
cancer was not pathologically confirmed for 35 percent of the cases
(Hammond and Selikoff 1981; Lee 1982b). The inclusion of cases that
were not lung cancers would tend to dilute the results toward the
null because they may not be related to involuntary smoking.

78


Terminal bronchial (alveolar) carcinoma and adenocarcinoma of the
lung were excluded from the pathologically confirmed group; this
exclusion may have been premature (Hammond and Selikoff 1981;
Kabat and Wynder 19&Q), as the causal association between personal
smoking and adenocarcinoma of the lung is well established (IARC
1986). Because the controls were selected from a different hospital
than were the cases, selection bias cannot be ruled out. Interviewer
bias is also possible, since all subjects were interviewed by a single
physician who knew the case or control status of each subject, and
also knew the hypothesis under investigation.

The index of exposure to tobacco smoke used in this study included
the smoking habits of former and current husbands. Since the
definition of ex-smokers excluded those who had stopped smoking
recently (within the last 5 years), it was unanticipated that the risks
observed for women whose husbands were ex-smokers (i.e., quit 5 to
20 years previously) were as high as for those whose husbands were
current smokers. Additional information on the smoking habits of
these ex-smokers would be valuable.

The Louisiana Study

The cas+control study by Correa and colleagues (1983) was based
on 1,338 primary lung cancer cases, of which 97 percent were
pathologically confirmed. Controls (N= 1,393) were matched to cases
by race, sex, and age (+5 years) and were patients at the same
hospitals as cases but without a diagnosis related to tobacco smoking.

Standard&d interviews were conducted with the subjects (76
percent of cases, 89 percent of controls) or their next of kin.
Questions on occupation, residency, personal smoking and drinking
habits, and smoking habits (including type of tobacco smoked and
amount and duration of smoking) of the current spouse and parents
were asked.

Thirty nonsmoking ever-married lung cancer (excluding bron-
chioalveolar cell) patients (8 men, 22 women) and 313 ever-married
nonsmoking controls (189 men, 133 women) were classified according
to their spouse's total lifetime pack-years and current daily amount
smoked at the time of interview. After adjusting for sex, ORs of 1.60,
1.48, and 3.11 were observed when spouses had smoked none, 1 to 40
pack-years, and 41 or more pack-years, respectively (two-sided
p< 0.05). The results based on current daily number of cigarettes
smoked by spouses were similar.

The study is limited by the small number of nonsmoking cases, but
the consistency of the results for men and women strengthens the
findings. Misclassification of involuntary smoking is possible because
only smoking habits of the current husband were assessed, ignoring
the effect of divorce, remarriage, and exposure from coworkers.
Exposure from parents during childhood was determined, but case

79


numbers were too small for a mea&gful analysis of this factor
among nonsmokers.

The Hong Kong Studies

me high rates of lung cancer, particularly adenocarcinoma of the
lung, among women of Chinese descent in Hong Kong are unexpect-
d in the face of their low rates of tobacco smoking. The role of
involuntary sm&.ng was investigated in two studies conducted in
Hong Kong (Chan et al. 1979; Ghan and Fung 1982; KOO et al. 1983,
1984).
Chm and colleagues (1979) examined the role of involuntary
smoking among 84 female lung cancer patients and 139 orthopedic
control patients, none of whom had ever smoked. Of the 34
nonsmoking cases, 69 (82 percent) were pathologically confirmed,
and 38 of these 69 cases were adenocarcinoma of the lung. The
controls were from the same hospitals as the cases, but were not
individually matched to the cases on any characteristics.
Cases and controls were questioned regarding their residence,
education, occupation, cooking practices, and personal smoking
habit. One question on exposure to others' tobacco smoke was
included: "Are you exposed to the tobacco smoke of others at home or
at work?" The researchers reported that the controls lived with
smoking husbands more frequently (47.5 percent) than the cases
(46.5 percent) (OR 0.771, but did not explain how this question was
used to classifs the habits of the spouse alone. The method used to
classify currently unmarried respondents (i.e., never married, wid-
owed, divorced) with regard to exposure to their spouses' smoking
was not described, and it is not known if the nonsmoking cases and
controls were comparable in terms of current marital and employ-,
ment status. Thus, insufficient information on the measure used to
assess El% exposure, and on the comparability of the nonsmoking
cases and controls, limits interpretation of this study's results.
The study by Koo and colleegues (1983,1934) involved 200 Chinese
female lung cancer patients who were identified from eight hospitals
in Hong Kong; almost all cases were pathologically confirmed (97
percent). Among these women, 68 had never smoked, of whom 52 (59
percent) had adenocarcinomas of the lung. An equal number of
"healthy" population controls, individually matched to cases by age
(f5 years), socioeconomic status, and district of residence, were
interviewed. Among the controls, 137 had never smoked.
Using a sernistructured questionnaire, taped interviews were
obtained and information on residence, occupation, family and
medical history, personal smoking habits, and smoking habits of all
cohabitants and coworkers was elicited. ETS exposure was quanti-
fied in hours and years according to who (i.e., husband, parents, in-
laws, children, others) smoked in the subject's presence and where


(i.e., at home, at work) the exposure occurred. The analysis was based
on a cumulative smoke exposure index (in total hours and total
years) specific to place of exposure.
The investigators concluded that there was no association between
involuntary smoking and lung cancer in nonsmoking Chinese
women, regard&s of the index of smoke exposure used. A small, but
statistically nonsignificant, increased risk (RR 1.24) was associated
with any exposure to tobacco smoke. There were no significant
differences between the cases and the controls in total hours or total
years of exposure. The results remained unchanged when exposure
hours were categorized into three levels of exposure. Odds ratios of
1.09, 1.28, and 1.02 were associated with no, low ( 5 35,900 hours),
and high (> 35,000 hours) exposure levels, respectively. There was no
apparent trend of lung cancer risk with the age when exposure to
tobacco smoke began. The ORs for never exposed and first exposed at
ages 0 to 19,20 to 39, and 40 or older were 1.09,0.96,1.53, and 0.91,
respectively (Koo et al. 1984). AnaIysis by cell type suggested that
the effects of involuntary smoking may be more pronounced for
Kreyberg I tumors (squamous, smallcell, and largeceIl carcinomas)
(OR 1.47, 95 percent C.I. 0.34, 3.33) than for adenocarcinoma (OR
1.11, 95 percent C.I. O-49,2.59) (ILoo et al. 1985), but these numbers
were amaR.
The design of this study addressed the criticisms of other studies
that an index of involuntary smoking exposure based only on
spouses' smoking habits is inadequate, and broadened the exposure
assessment to include alI locations of tobacco smoke exposure.
However, the cumulative exposure index created in this study may
have Iimited validity. Unlike personal smoking, where there is
essentiaIIy one source (personal smoking), one dose (usual or
maximum amount smoked), and one duration of exposure (age at
start and age at stop), EYES exposure derives from diverse sources at
different doses and durations of exposure. The accuracy of the
information on exposure to EIS will depend on the amount of detail
requested, the age of the respondent, the temporal course of the
exposure, and the source of the exposure. Weighing each type of
exposure equally in a cumulative index (in total hours) may be
incorrect because it assumes that all sources of exposure should be
quantified in the same way and that each source of tobacco smoke
contributes equally, disregardiug intimacy of contact and proximity
to smokers and conditions of exposure (e.g., room size, ventilatory
factors). Thus, random misclassification of the expoeure variable by
inclusion of data from less relevant exposures than spousai smoking
may obscure an association of involuntary smoking exposure with
lung cancer risk. In this study, interviewer and respondent bias
should also be considered because a structured questionnaire was not

81


An Ongoing Study of Tobacco-Related Cancers

All of the cases of primary lung cancer in nonsmokers were
selected (Rabat and Wynder 1984) from an ongoing case-control
study of tobacco-related cancer conducted in five U.S. cities between
1971 and 1980 (Wynder and Bellman 1977). For each case, one
control was individually matched by age (r+5 years), sex, race,
hospit,& date of interview (+_2 years), and nonsmoking status.
controls were selected from a large pool of hospitalized patients who
were interviewed over the same time period as the cases and who
had diseases not related to tobacco smoking. Information on demo-
graphic factors, residence, height and weight, drinking habits,
previous diseases, and occupational exposure were obtained. Ques-
tions on tobacco smoke exposure at work, at home, and from current
spouse were added in 1978, and revised in 1979. Information on EYl!S
exposure was available for 25 of 37 nonsmoking male cases, 53 of 97
nonsmoking female cases, and their respective matched controls.
A higher percentage of female controls than of female cases
reported exposure to E'I'S at home (32 percent), at work (59 percent),
and from spouses (66 percent). `Ihe percentages of female cases who
reported exposure at home, at work, and from spouses were 39,49,
and 54 percent, respectively. None of the case-control differences in
women were statistically significant. Male cases reported more
frequent exposure at work (OR 3.27, p= 0.045) and at home (OR 1.26),
but no difference in the smoking status of their spouses (OR 1.60).
The process for selecting the nonsmoking controls from the larger
pool of controls in the ongoing study and for selecting the non-
smoking csses and controls who were questioned with regard to ETS
exposure was not described adequately. It is not clear whether the 25
of 37 male and 53 of 97 female nonsmoking cases and controls who
provided information on involuntary smoking were all interviewed
during or after 1978 when the questions on involuntary smoking
were introduced. `I'he proportion seemed high, since it represented 68
percent of male and 55 percent of female nonsmoking cases
interviewed during the 10 years of data collection. The study was not
designed to specifically address the effect of involuntary smoking,
and a variable subset of questions on involuntary smoking was
asked, depending on when the subjects were interviewed. Misclassifi-
cation of the exposure is possible because it is not clear whether the
cases and controls answered the same set of questions and whether a
comparable amount of information was obtained. The researchers
acknowledged the limitations of this study and presented its results
as prebinary findings.

82


The Los Angeles County Study
In the case-control study by Wu and colleagues (1985), 220 white
female lung cancer patients (149 with adenocarcinoma and 71 with
squamous cell carcinoma) and 220 population controls were individu-
ally matched on sex, race, age (f5 years), and neighborhood of
residence. Cases were identified from the population-based tumor
registry of Los Angeles County. All cases were histologically
confirm& the histological type was based on the pathology report
from the hospital of diagnosis.
Using a structured questionnaire, cases and controls were directly
interviewed by telephone and were asked about their own personal
smoking habits and the smoking habits (amount and years of
smoking) of current and former husbands, parents, and other
household members during childhood and adult life. Exposure to
tobacco smoke at work (in hours per day) was obtained for each job of
at least 6 months' duration. Information on medical and reproduo
tive history, heating and cooking sources, and dietary intake of
vitamin A were obtained.
Of 149 patients with adenocarcinoma of the lung, 29 had never
smoked, nor had 2 of 71 patients with squamous cell carcinoma. The
analysis of involuntary smoking was based on the 29 nonsmokers
among the adenocarcinoma cases and 62 nonsmokers among the
controls.
A subject was classified as married to a smoker if any of her
husbands had ever smoked. Similarly, a subject was considered
exposed at work if she was exposed to tobacco smoke for at least 1
hour per day at any of her jobs. There were small, but nonsign&
cantly increased risks associated with ETS exposure from spouse or
spouses (OR 1.2; 95 percent C.I. 0.2,1.7), and from coworkers (OR 1.3;
95 percent C.I. 0.5,3.3). Increased risk was not associated with smoke
exposure from either parent (OR 0.6; 95 percent C.I. 0.2, 1.7).
Exposure to tobacco smoke from spouses and from coworkers was
combined in an index representing smoke exposure during adult life.
There was an increasing trend in risk with increasing years of
exposure. The ORs were 1.0,1.2, and 2.0 for 0,l to 30, and 31 or more
years of involuntary smoking exposure during adult life, respective
ly, but the results were not statistically significant. Because the
exposures may have occurred concurrently, the years of exposure
represented units of exposure rather than calendar years of expo
sure.
This study is limited by the small number of nonsmoking cases
and controls. Unlike the two case-control studies that excluded
adenocarcinoma or bronchioalveolar cell carcinoma (Trichopoulos et
al. 1981; Correa et al. 1983), cases in this analysis were of these cell
types (17 adenocarcinoma, 12 bronchioalveolar); this case mix may
explain the weak association observed.


The Four Hospitals Study
A Mntrol study by Garfinkel and colleagues (1985) included
134 nOnsmOking female lung cancer cases selected from three
hospitals in New Jersey and one in Ohio over an 11-year period,
1971-1981. Medical records served as the initial source of informa-
tion on smoking status of the subject, and the nonsmoking status of
each case and control was verified at interview. Three controls,
color&al cancer patients matched to cases by age (f5 years) and
hospital, were interviewed for each case, giving a total of 402
controls. All diagnoses of cases and controls were pathologically
confirmed. Interviewers, blinded to the diagnosis of the subjects and
to the study hypothesis, administered a standard questionnaire to
subjects or their next of kin. Information on the smoking habits of
current spouse (total and amount smoked at home), tobacco smoke
from other sources (in hours per day at home, at work, and in other
settings), and exposure to tobacco smoke during childhood were
obtained.
Subjects were classified according to the smoking habits of current
husbands. Smoking habits of a cohabitant in the same household was
used for single women or those who no longer lived with their
spouses. Of the cases, 57 percent were classified according to the
smoking habits of husbands; the corresponding percentage in
controls was not provided. Nonsmoking women living with a smoker
showed an elevated risk for lung cancer (OR 1.31). The ORs for lung
cancer in nonsmoking women were 1.09, 1.15, 1.03, and 2.11 when
the husbands were nonsmokers, daily smokers of less than 10,lO to
19, and 20 or more cigarettes at home, respectively (one-sided p for
trend, <0.025). Similarly, a significant positive linear trend (one-
sided p < 0.025) was shown when the husbands' total amount smoked
was categorized into four levels. However, there was no apparent
dose-related trend by years of exposure to the husbands' smoking (0,
<20,20-29,30-39,40+ years).
There was no apparent association between lung cancer and
tobacco smoke exposure from other sources. Cases and controls did
not differ in their reported exposure to tobacco smoke during
childhood or in their average hours of exposure per day to other's
t&m0 smoke during the last 5 years and 25 yeam before diagnosis.
The results remained unchanged when exposures at home, at work,
and in other settings were e xamined separately. The odds ratios
were highest for exposure in other settings, but they were based on a
small number of positive responses. There was no consistent pattern
by ~tologic type. Squamous cell carcinoma showed the strongest
relationship with involuntary smoking, based on the husbands'
smoking habits at home (RR 5.0,95 percent C.I. 1.4,20.1), but failed
to show any relationship when involuntary smoking exposure was
classifkd by hours of daily exposure.


This caswzontrol study has the largest number of nonsmoking
lung cancer cases to date and provides estimates of the mis&s&ica-
tion of disease and of the smoking status of the subjects. Among the
published studies on involuntary smoking, this is the only one
involving independent verification of the diagnoses of all cases. This
verification showed that 13 percent of the cases classified as lung
cancer were not primary cancers of the lung. This study showed that
40 percent of the women with lung cancer who had been classified as
nonsmokers (or smoking not stated) on hospital records had actually
smoked, compared with 9 percent of the controls. The inclusion of
lung cancer patients who had actually smoked would have substan-
tially increased the odds ratios with involuntary smoking, because 81
percent of the potentially misclassified cases had husbands who
smoked compared with 68 percent of the %ue" nonsmoking patients
with lung cancer. It should be noted that none of the other studies on
involuntary smoking and lung cancer based classification of smoking
status solely on data from medical records. The measure of involun-
tary smoking based on smoking habits of husbands attempted to
differentiate between current total smoking habits and current
smoking habits at home. The interview also included RTS exposure
not only at home but at work and in other settings.
The exposure information presented in this study is potentially
limited by its extensive reliance on surrogate interviews. Owing to
the need to assemble sufficient nonsmoking cases, diagnoses as early
as 1971 were included, so proxies were interviewed for a high
percentage of the deceased cases. Among the cases, 12 percent of the
interviews were conducted with the subject, 25 percent with the
husband, 36 percent with offspring, and 27 percent with an
informant who had known the subject for at least 25 years. The
corresponding distribution of informants in the control series was
not presented. Although the ORs did not. vary consistently by
respondent group, the OR for smoke exposure based on the hus-
bands' smoking tended to be lower when husbands were the
respondents. Presumably, the husbands reported their own smoking
habits, and it cannot be determined whether bias resulted. The
information provided by surrogates may be particularly inaccurate
for exposures outside the home. Systematic bias between personal
and surrogate interviews and systematic bias by informant status
must also be considered. Given that the topic of involuntary smoking
is potentially sensitive for the family of a lung cancer patient, it is
possible that some surrogates may not have provided accurate
histories, particularly with regard to their own smoking habits.
Surrogate respondents for cases might have been more likely to
underreport exposure than those for controls, such differential
reporting would have led to an underestimation of the true effect.
The multiple regression analysis performed in this study did take


respondent status into consideration, and it was determined that this
factor could not account for the relationship with husband's smoking
status (Garfinkel et al. 1965). It is not clear if the colorectal cancer
controls were diagnosed in the same years as the lung cancer cases.
Because the response patterns of relatives who are interviewed after
the recent death of a subject may differ from responses obtained long
after the subject has died, another source of bias may have been
introduced.

A United Kingdom Study

In an ongoing hospital-based cas+control study of lung cancer,
chronic bronchitis, ischemic heart disease, and stroke, Lee and
dIeagues (1986) examined the role of involuntary smoking in a
group of inpatients interviewed after 1979, when, to cover involun-
tary smoking, the questionnaire was extended to married patients.
An attempt was also made to interview the spouses of the married
nonsmoking lung cancer patients and the spouses of the comparison
group.
The interview on involuntary smoking administered to hospital
inpatients included questions on the smoking habits of their first
spouse and on FXS exposure at home, at work, during travel, and
during leisure, based on a subjective four-point scale. Spouses of
nonsmokers were asked about their own smoking habits at the time
of interview, during the year of admission of the subject, and during
the course of their marriage.
A total of 56 lung cancer cases among married lifelong nonsmok-
ers was identified, 2 controls were selected for each case and
individually matched on nonsmoking status, sex, marital status, age,
and hospital. Among the 56 cases and 112 controls, information on
spouses' smoking habits was available for 29 (52 percent) cases and
59 (56 percent) controls from an interview conducted while the
patient was still in the hospital. Interviews with spouses were
obtained for 34 (61 percent) of the cases and 80 (71 percent) of the
controls. Using both of these sources of information, the smoking
habits of spouses were available for 47 (84 percent) of the cases and
96 (86 percent) of the controls. Nine risk estimates were presented
for 8pouses' smoking, for each of the three sources of information
(subject, spouse, and both), for men and women separately and for
both sexes combined. The researchers concluded that spousal
smoking was not associated with lung cancer, because risks were not
consistently elevated. When their spouses reported about their own
smoking, a RR of 1.60 (95 percent C.I. 0.44, 5.78) was found for lung
cancer in the women. In contrast, a RR of 0.75 (95 percent C.I. 0.24,
2.40) was found when the female subjects reported about the
smoking habits of their spouses. On the other hand, a RR of l.Ol(96
percent C-1.0.23,4.41) was found for male lung cancer patients when

86


their spouses reported about their own smoking, whereas the risk
was 1.53 (95 percent CL 0.37,6.34) when the male patients e~aluat&
their spouses' smoking habits. As might be expect&, the combined
risk in relation to spouses' smoking for both sexes and both sources
of information was near unity, at 1.11 (95 percent C.I. 0.59, 2.39).
Using a second group of controls, presumably all of the nonsmokers
who had responded to the hospital inpatient interview on involun-
tary smoking, the researchers reported no significant case and
control differences in exposure to EXS at home, at work, during
travel or leisure, from spouses, or for all sources combined.
This study has several limitations that must be considered in
interpreting its results. Although the study attempted tc verify
involuntary smoking from spouses by using two sources of informa-
tion, dual reports were obtained for only 16 (29 percent) of the cases
and 43 (33 percent) of the controls. The questions on involuntary
smoking included exposure from other sources, but they were based
on a subjective scale, and different groups of controls were used for
the analyses. Information was not presented on the accuracy of the
diagnosis of lung cancer or on the histological types included in the
study. Moreover, the investigators did not verity the smoking status
of the subjects during the interviews with spouses.
The study's inconsistent fmdings by source of information and by
sex may reflect the absence of an association between involuntary
smoking and lung cancer in this population, or may reflect method-
ological problems in the design or conduct of the study. The main
study was not originally designed to investigate the effects of
involuntary smoking. However, because of interest in this issue, the
investigators decided to "increase the number of interviews of
married lung cancer cases and controls." The representativeness of
the cases and the controls cannot be determined because there may
have been differential selection factors in enrolling nonsmoking lung
cancer cases and controls into the study; thus, selection bias cannot
be ruled out. The method for selecting the 112 nonsmoking controls
was not adequately described in the report; it is not clear whether
they were selected from the pool of all controls for lung cancer or
from the pool of controls for the four diseases under study. There is
also an apparent discrepancy in the number of nonsmoking cases
cited in the text and presented in the results. The report cited 44
never smokers among a total of 792 lung cancer patients who
completed the involuntary smoking questionnaires when they were
in the hospital. However, the analysis for an involuntary smoking
effect based on interviews with subjects in the hospital showed only
29 lung cancer patients. This discrepancy was not explained.
The risks in relation to smoking by spouses varied with the source
of information. The risk estimates tended to be higher when the
respondents were men, either reporting about their own smoking

87


habita or the smoking habits of their spouses. This pattern could
result if the male respondents overestimated exposure to environ-
ment& tobacco smoke or if the female respondents underestimated
exposure. An analysis of the patients (16 cases and 43 controls) for
whom data were provided by the spouses and by the subjects
themselves showed a 97 percent concordance for spouses' smoking
during the year of the interview and 85 percent concordance for
spouses' smoking some time during the marriage. Lack of specificity
in the question asked regarding spouses' smoking any time during
the marriage may partly explain the discrepancy in response. To the
extent that there is no consistent pattern in the direction of this
discrepancy, it can be assumed that a spouse was a smoker sometime
during the marriage if either respondent answered positively. On the
basis of this assumption, RRs of 1.47 (spouses of 4 of 7 cases and 7 of
18 male controls smoked) and 1.39 (spouses of 8 of 9 female cases and
16 of 25 female controls) were found for the men and the women,
respectively, in relation to their spouses' smoking. The risk estimates
were not statistically sign&ant, but the number of subjects was
Sldl.

The Japanese CaseControl Study

The study by Akiba and colleagues (1986) included 426 (264 men,
164 women) incident primary lung cancer cases diagnosed between
1971 and 1980 in a cohort of 110,090 Hiroshima and Nagasaki atomic
bomb survivors. Controls were selected among cohort members who
did not have cancer. For deceased cases, corresponding controls were
selected from among cohort members who died of causes other than
cancer or chronic respiratory disease. The controls were individually
matched to cases on a number of factors, including age, sex, birth
year (f2 years), city of residence, and vital status; a variable number
of controls was interviewed, depending on the place of residence. Of
the lung cancers, 29 percent were pathologically confirmed, 43
percent were radiologically or clinically diagnosed, and the remain-
der were found at autopsy.
Subjects or their next of kin were interviewed regarding the
subjects' personal smoking, smoking habits of current spouses and
parents, and occupation. Less than 10 percent of the interviews with
the men and about 20 percent of the interviews with the women
were conducted with the subjects themselves. The distributions of
the next of kin interviewed were similar for the cases and the
controls.
Among the cases, 103 (19 men, 64 women) had never smoked,
compared with 380 controls (110 men, 270 women). An elevated lung
cancer risk associated with smoking habits of spouses was observed
for men and women. An OR of 1.8 (95 percent C.I. 0.5,5.6) was found
for nonsmoking men married to&ves who smoked and an OR of 1.5

88


(95 percent C.I. 1.0,2.5) for nonsmoking women married to husbands
who smoked. Lung cancer risk increased with the amount smoked
per day by the husband, with an OR of 2.1 for women whose
husbands smoked 30 or more cigarettes per day. The OR was higher
(1.8) among women who had been exposed within the past 10 years
compared with those who had been exposed before that time (OR
1.3). However, an increasing duration of exposure to husbands
smoking was not associated with a monotonic trend of increasing
risk. The relation between lung cancer and husbands' smoking was
observed regardless of the occupation of wives (housewife, white-
collar, blue-collar), but the highest odds ratio was for women who
worked in bluecollar jobs and whose husbands were heavy smokers
(OR 3.2).
Despite a high proportion of proxy interviews, the distribution of
informant type was comparable for cases and controls, this compara-
bility minimizes the possibility of recall bias. The high concordance
between the subjects' reported smoking status in a previous survey
and the information from the next of kin is reassuring. Although a
high proportion of cases had no histological confirmation, an
increased risk was observed regardless of the method of diagnosis.
This study also provided an opportunity to test for potential
confounding factors, including radiation exposure and occupation,
but none were identified.

The Swedish Study

The study by Pershagen and associates (in press) included 67
incidents of primary lung cancer cases from a cohort of 27,409
nonsmoking Swedish women who were participants in a national
census survey or in a twin registry. Two controls were selected from
each source and were matched to cases on year of birth, and on vital
status if they were selected from the twin registry.
Subjects or their next of kin (excluding husbands) were mailed a
questionnaire that assessed their exposure to tobacco smoke from
parents and the husband with whom the subject had lived the
longest time. Information on residential and occupational history
was also obtained.
Elevated lung cancer risk associated with the smoking habits of
spouses was observed. For all lung cancers, ORs of 1.0, 1.0, and 3.2
were observed for women who had no, low ( 5 15 cigarettes/day or
< 1 pack of pipe tobacco/week or < 30 years of marriage), and high
exposure to their husbands' smoking, respectively. The increased
risk was found primarily for squamous and small cell carcinomas
(OR 3.3); consistent effects could not be detected for other histologic
types. On the basis of the approximately 75 percent of respondents
who provided information on parental smoking, there was no effect

89


of parental smoking on risk for all lung cancers, after controlling for
the husbands' smoking.
The study is similar in design to the Japanese c88e-control study
(Akiba et al. 1986), except that the Swedish investigators obtained
histologic confirmation for all of the cases under study. Moreover,
this study excluded husbands as informants, so a potential bias
associated with husbands' reporting their own smoking habits could
be eliminated. The investigators contended that the fmding of an
association only for squamous cell and small cell carcinomas argues
against a spurious finding because it is unlikely that the next-of-kin
informers would have been aware of the histologic types diagnosed in
the cases.

The German Study

The last in this description of studies to date based on the cask+
control design is a German study (Knoth et al. 1983), interpreted by
the investigators as showing a role for involuntary smoking in the
etiology of lung cancer. Of 39 nonsmoking women with lung cancer,
24 (62 percent) had lived with smokers. Although a comparison
group was not interviewed, the investigators surmised that this
frequency of smokers in the household was about three times higher
than expected from census-based smoking statistics for men in the
age group 50 to 69. The limitations of this study are evident; the
researchers assumed that smoking prevalences for men were indica-
tive of smoking prevalences for members of the cases' households
and a specific control series was not enrolled.

Other Sources of Tobacco Smoke &posure
Parental Smoking

Recently evaluated as a risk factor for lung cancer, parental
smoking is of interest because of the large number of exposed
children, the age at which it begins, and its duration. Results of this
association are variable, demonstrating no association, association
with just mothers' smoking, or association with both mothers' and
fathers' smoking. Cmea and colleagues (1983) reported an associa-
tion between lung cancer risk and the mothers' smoking in the men,
which persisted after adjusting for personal smoking habits (OR 1.5,
P <O.Ol). This association was not observed in the women, and
increased risk was not related to fathers' smoking in either the men
or the women. A positive association between the mother's smoking
and lung cancer risk was reported in a study of female lung cancer,
but the result was not statistically significant after adjusting for
personal smoking habits (OR 1.7, 95 percent C-1. 0.8, 3.5) (Wu et al.
1985). Another study suggested that the father's smoking (OR 2.5)
and the mother's smoking (OR 1.8) were each related to increased

90


lung cancer risk after a@sting for age and individual smoking
habits (Sandier, Wilcox, Everson 1985b). These results were based on
small numbers, however, particularly for the mother's smoking (in 2
of 15 cases, the mother smoked). Significant associations with
maternal or paternal smoking were not found in two other studies
(Akiba et al. 1986; Pershagen et al. in press); however, information
was lacking for about one-third of the subjects. Since smoking habits
of children are highly correlated with smoking habits of parents, it is
difficult, even at&x adjusting for personal smoking habits, to be
certain that an independent effect of parental smoking has been
Observed.

None of the studies with data on parental smoking had sufficient
numbers to examine the effects of parental smoking on nonsmokers.
In Louisiana, one nonsmoking case had a mother who smoked
(Correa et al. 1983). In Hong Kong, 6 percent (5/88) of the
nonsmoking cases reported that their parents smoked compared
with 2 percent (3/137) of the nonsmoking controls (Koo et al. 1984).
In Los Angeles, the frequencies of smoking by mothers and fathers
were lower for nonsmoking cases (4 percent mothers, 28 percent
fathers) than for nonsmoking controls (11 percent mothers, 35
percent fathers) (Wu et al. 1985). Exposure to tobacco products
during childhood was not significantly different between cases and
controls (OR 0.91, 95 percent C.I. 0.74, 1.12) in another study
(Garfmkel et al. 1985).
It is difficult to obtain accurate information regarding remote
childhood events, so data on parental smoking tend to be crude or
unavailable. Information on maternal smoking during pregnancy
would not be available unless the parents could be interviewed.
Because lung cancer occurs most often among older persons, an
interview with a parent will generally be impossible. Moreover,
information on parental smoking will most likely be unavailable or
meaningless if surrogate interviews are conducted.

Coworker's Smoking

The workplace, an important source of tobacco smoke exposure,
was ,not considered in the early studies on involuntary smoking.
hater case-control studies provided some information on tobacco
exposure at work, but the data were limited and inconclusive. Kabat
and Wynder (1984) reported a statistically significant positive
association between tobacco smoke exposure at work for men but not
for women. In comparison with controls, patients with cancer in
Hong Kong reported more hours and years of exposure at the
workplace, but only two cases and four controls had exposure to
tobacco smoke at work (Koo et al. 1984). Data in the Los Angeles
study suggested that the workplace may be an important source of
exposure to tobacco smoke. A small increased risk was observed for

91


any exposure at work, and an index combining exposure from
coworkers and spouse or spouses indicated a trend of increasing risk
with inc x-easing exposure (Wu et al. 1985). Garfinkel and colleagues
(1985) found no differences between cases and controls in their
exposure to tobacco smoke at work during either the 5 years or the
25 years before diagnosis, and a simiIar lack of an association wm
also reported by Lee and colleagues (1986).

Lkw+Response Relationship

An important factor in the appraisal of the relationship between
~~oluntary smoking and lung cancer ia the assessment of dose-
response relationships. However, this analysis hinges on the defini-
tion of exposure. Data on active smoking and lung cancer suggest
that exposure measures considering amount, duration, and recency
of exposure should be employed in examining dose-response rela-
tionships in active smokers (DoIl and Pet0 1978; Pathak et al. 1986).
Misclassification of exposure to EYTS may be expected when exposure
categorization is based on the amount or the duration of smoking by
the current spouse or cohabitant, as current exposure from one
source may not adequately measure past exposure or cumulative
exposure. Moreover, these exposure variables may not be indicative
of the exposure dose to the respiratory tract because dose deter&
nants such as ventilation rates, breathing pattern, and deposition
factors are unaccounted for.

Research is now being directed toward the integration of informa-
tion from questionnaire responses, biochemical studies, and environ-
mental sampling to determine the most accurate measures of
exposure to the respiratory tract. However, exposure assessments for
epidemiological studies of lung cancer and involuntary smoking will
remain limited by the inaccurate recall of exposures that occurred as
much as 40 to 50 years earlier. Nevertheless, research on exposure
should resolve several points of uncertainty. The comparability
between exposure dose measured by amount smoked and by hours or
years of smoking should be assessed. The relative importance of
sources of ETS should also be clarified, so there will be some
agreement on whether cumulative dose should differentiate between
sources of exposure.
In the absence of data showing a particular exposure measure to
be optimal, an index of involuntary smoking based on the amount
smoked by spouses shows the most consistent do-response relation-
ihip with lung cancer risk (Hirayama 1981a; Trichopoulos et al.
1981; Correa et al. 1983; Garfiiel et al. 1985; Akiba et al. 1986).
Other indices of involuntary smoking exposure have not been as well
studied and have not shown a consistent dose-response relationship
with lung cancer risk. These exposure variables included total years
of exposure to spouses' smoking, average daily hours of exposure

92


from all sources, and cumulative lifetime hours and years of
exposure.
Among the studies that have found a dose-response relationship
with amount smoked by a spouse, three have also examined the
relationship by duration of spouse's smoking (Correa et al. 1966;
Garfinkel et al. 1985; Akiba et al. 1966), but only one study showed
similarly increased risk using a dose and duration variable (&nrea
et al. 1963). In the study by Garfinkel and coworkers (1965), only
years of smoking by the current husband or cohabitant was asked;
therefore, differences in the duration of living with current husband
or cohabitant may account for the less consistent dose-response
relationship. In their Japanese case-control study, Akiba and
colleagues (1966) suggest that intensity (amount smoked per day and
recency of exposure) may be the key index of E?S in studies of lung
cancer risk.

Two studies have assessed total involuntary smoking exposure to
ETS. The method used by Koo and coworkers (1964) relied on
respondents to describe the exposures from each source separately,
and a summary measure of exposure was derived by the investiga-
tors. The method used by Ga&nkel and coworkers (1985) relied on
the respondents to average their exposures from all sources for
specific time periods. The method of Koo and coworkers (1964) may
not have adequately considered intensity of exposure; therefore, an
association may have been obscured by combining low and bigh
intensity exposures as if they were equally important. In the study
by Garfinkel and coworkers (196!5), a high percentage of case
interviews and, presumably, control interviews was conducted with
surrogates. Although information provided by surrogates regarding
demographic variables is generally valid, as are responses on
cigarette smoking status (current, prior, never), more detailed
information on the cigarette smoking of a deceased spouse has more
limited validity (Lerchen and Samet 1966). Surrogate interviews
may provide adequate information about tobacco smoke exposure at
home, but may be inaccurate for describing gradients of total tobacco
smoke exposure from all sources.

Expect& Lung Cancer Risk

An extensive data base describes the relationship between active
smoking and lung cancer (US DHEW 1979, US DHHS 1982; IARC
1966). This information has been utilized to construct mathematical
models to describe the relationship of dose, duration, initiation, and
cessation of active smoking for risk of lung cancer. For several
reasons, comparable models have not yet been developed for
involuntary smoking and lung cancer. First, research on involuntary
smoking and lung cancer is recent. Second, involuntary smoking is
not as read.ily quantified as active smoking; tobacco smoke is

93


ubiq~~~ in the environment and, present in variable but generally
low concentrations in comparison with MS, and inhaled dose varies
with ventilation and other physiological factors @filler 1984; Hoegg
1972; Hoffmann et al. 1984; Schmeltz et al. 1975; St&er 1984; US
DHHS 1984).
Nevertheless, theoretical models, originally developed to describe
the relationship of active smoking and lung cancer, have been used
to predict lung cancer risk from involuntary smoking. Using Doll
and Peto's (1978) model [(OX3 x 1012) (cigarette/day + 6)2 (age
22.5)4.5] for active smoking and lung cancer, Vutuc (1984) cahlbted
expe&d lung cancer risks for various exposure levels, ranging from
0.1 to 5.0 cigarettes per day. For exposure levels of 0.1, 1.0, 2.0, and
5.0 cigarettes per day, the corresponding risk estimates were 1.03,
1.38,1.78, and 3.36, respectively. These lowdoae active smoking risk
estimates are comparisons of active smokers `with all nonsmokers
(those with high ETS exposure and those with low ETS exposure).
The risk estimates in involuntary smoking studies are a comparison
of nonsmokers with higher levels of involuntary smoking exposure
with nonsmokers who have lower levels of involuntary smoking
exposure. As a result, the numerical values of the risk estimates in
active smoking studies are not directly comparable to those in the
involuntary smoking studies.
The appropriateness of extrapolating from the active smoking
model hinges on the actual exposure of a nonsmoker. Estimates of
exposure have been derived from various sources. Experimental
conditions have been used to quantify the involuntary smoker's
exposure to ETS. Hugod and colleagues (1978) reported that under
conditions heavily polluted with sidestream smoke (to maintain a
carbon monoxide concentration of 20 ppm), the particulates of
tohco smoke inhaled by involuntary smokers was small, the
equivalent of one-half to one cigarette per day. Exposures may also
be estimated from biochemical measurements. Studies comparing
cotmine levels in nonsmokers and smokers show cotinine levels in
nonsmokers that correspond to about one-sixth to one-third of a
cigarette per day (Jarvis et al. 1984; Wald et al. 1984). Higher
cothhe levels in nonsmokers, comparable to about two cigarettes
per day, have been reported (Matsukura et al. 1964, 19&j), but the
results were questioned (Acllkofer et al. 1985; Pittenger 1985) and
await Confirmation.
The epidemiologic evidence on the lung cancer risk associated with
marriage of a nonsmoker to a smoker has been criticized as
implausible on the basis of predictions from Doll and Peto's model
(Lee 1982a,b; Vutuc 1984. It has been argued that relative risks of 2
or 3 from involuntary smoking correspond to active smoking of two
to five cigarettes per day and that this equivalent level of active
smoking is too large to be realistic. This argument fails to consider

94


the difference in the comparison groups used to generate the risk
estimates in studies of active smoking and involuntary smoking. The
risk estimates for studies of active smoking use as a comparison
group all nonsmokers, which includes those with and without high
levels of exposure to ETS. Studies of involuntary smoking use risk
estimates that are derived by comparing nonsmokers with higher
levels of exposure to ETS with nonsmokers with lower levels of
exposure to ETS. Decause the risk estimates in active and involun-
tary smoking studies use different comparison groupe, the numerical
values are not directly comparable.

In order to make them comparable, the risk estimates in involun-
tary smoking and active smoking studies would have to be calculated
using the same reference group. If the reference population used is
all nonsmokers, then the risk estimates for nonsmokers married to
nonsmokers are reduced to below 1 (i.e., their lung cancer risk would
be lower than the risk for all nonsmokers as a group). The risk
estimates for nonsmokers married to smokers would be above 1 (i.e.,
would be greater than the risk for all nonsmokers as a group), but
the numerical value of the risk estimate w.ould be reduced from th
value obtained by comparison with nonexposed nonsmokers.
If the data from the Japanese cohort study (Hirayama 1981a) ar
recalculated to use all nonsmokers as the reference population, the
risk estimate for lung cancer in nonsmoking wives of nonsmoking
husbands would be 0.63 and the risk estimate for nonsmoking
women married to smokers (current or former) would be 1.12. The
value of 1.12 compares the risk for nonsmoking wives of smoking
husbands with the risk for all nonsmokers in the studies of active
smoking. This magnitude of risk is within the range of risk that
would be predicted using the Doll and Peto (1978) model for
calculating active smoking risk for smokers of 0.1 (risk estimate 1.03)
and 1 (risk estimate 1.38) cigarette per day. The evidence for
exposure to environmental tobacco smoke based on biologic markers
of tobacco smoke exposure indicate that i.n~~l~ntary smoking
exposure results in levels of biologic markers (e.g., cotinine) that are
similar to levels expected in smokers of 0.1 to 1 cigarette per day.
Thus, estimates derived using similar comparison groups suggest
that the lung cancer mortality experience due to involuntary
smoking is similar to that which would have been expected from an
extension of the dose-response data for active smoking to involun-
tary smoking exposures.
An alternative method of estimating expected lung cancer rates
has been proposed by Repace and Lowrey (1986). They compared the
age-standard&d lung cancer mortality rates of Seventh-Day Ad-
ventists (SDAs) who had never smoked with a demographically
comparable group of nonsmoking nonSDAs and attributed the
difference in lung cancer deaths solely to involuntary smoking. This

96


analysis was based on the following ~SSUI&O~: (1) that SDAs had
no expoeure to passive smoking, whereas alI of the non-SDAa were
exposed, (2) that men and women had equal lung cancer death rates,
and (3) that there were no other d.ifYerences between the two groups.

previous reports of the Surgeon General have reviewed the data
establishing dve cigarette smoking as the major cause of lung
mmr. me &me of a tbreshold for respiratory carcinogenesis in
active ~&hg, the presence of the same carcinogens in mainstream
smoke ad &htream smoke, the demonstrated Uptake Of fxhacco
smoke constituents by invohmtary smokers, and the demonstration
of m b& lung cancer risk in some populations with exposures
to ETs leads to the conclusion that involuntary smoking is a cause of
lung cancer.
me quantification of the risk associated with i.nvolun~ smoking
for the U.S. population -is dependent on a number of factors for which
only a limited amount of data are currently available. The fimt of
these factors is the absolute magnitude of the lung cancer risk
associated with invohmtary smoking. As was previously described,
the studies that have been performed to assess the lung cancer risk
of involuntary smoking do not contain a xero-exposure group. Some
expomre to tobacco smoke is essentially a universal experience;
therefore, studies of involuntary smoking compare a Iowexposure
group with a high-exposure group. The magnitude of the risk
estimate obtained is a function of the increase in risk produced by
the difference in tobacco smoke exposure between the two groups
examined, rather than an absolute measure of the risk of exposure in
comparison wit& no exposure. The magnitude of the difference in
tobacco smoke exposure between groups identified by spousal
smoking habits may vary from study to study; this variation may
padially explain the differences in risk estimates among the studies.
The extrapolation of the risk estimate data to the U.S. population
would therefore require a better understanding of the magnitude of
the exposure to environmental tobacco smoke that occurs in the
popdations examined in the studies of involuntary smoking and
lung cancer. Of particular interest is the magnitude of the difference
in exposure between the high-exposure group and the low-exposure
group-
A second set of data that would be needed to estimate the risk for
the U.S. population is the dose and distribution of exposure to ETS iu
the population. The studies that have been performed have attempt
ed to identify groups with different exposures, but little is known
about the magnitude of the exposures that occur in different
segments of the U.S. population or about the variability of exposure
with time of day or season of the year. !l%e changing norms about

96


smoking in public and the changing prevalence of a&ve smoking
during this century suggest that ETS exposure may have varied
substantially over this century. A better understanding of the
exposures that are actually occurring in the United &atq and of
past exposures, would be needed to accurately assess the risk for the
U.S. population.
The epidemiological evidence that involuntary smoking can signif-
icantly increase the risk of lung cancer in nonsmokers is compelling
when considered as an examina tion of lowdose exposure to a known
carcinogen (i.e., tobacco smoke). Eleven of the thirteen epidemiologi-
cal studies to date show a modest (10 to 300 percent) elevation of the
risk of lung cancer among nonsmokers exposed to involuntary
smoking, in six studies positive associations were statisticahy
significant. The studies showing no or non&nificantly positive
findings were generally the weakest in terms of sample size (Gillia et
al. 1984; Ghan and F'ung 1982; Koo et al. 1984; Kabat and Wynder
19&i; Wu et al. 1985; Lee et al. 1986), study design (Kabat and
Wynder 1984; Lee et al. 1986), or quality of data (Ghan and F'ung
1982).
In Table 10 are shown the sources and types of bias, and in Table
11, the statistical power, of the various case-control studies (Schles-
selman 1982). On the basis of the observed relative risks reported in
the studies, the respective exposure fraction in the control popula-
tions, and an a=0.05 for a two-sided significance test, only the
studies by Trichopoulos and colleagues (1983) and Gorrea and
colleagues (1983) have a probability of above 80 percent of f%xling a
statistically sign&ant result, whereas the majority of the caae-
control studies show a study power of about 0.10 to 0.20. The power
of the study, as expected, improves when a one-sided significance test
is considered. Among the studies in which information on involun-
tary smoking was available to conduct a trend test for dose, the
power for detecting the observed trend was above 50 percent for five
of the studies. However, the power for a twesided test and a one-
sided test, baaed on observed relative risk, and the power for a one-
sided trend test, based on observed results, are difficult to interpret
because the power is a function both of design aspects (sample size,
case-control ratio, exposure prevalence) and of the observed relative
risk. To focus on comparisons of the design differences between
studies, the power estimates for a fixed relative risk of 2 show that
five of the studies would have a power of 0.75 or greater to detect a
statistically significant result. Thus, it is not surprising that some
studies failed to achieve statistical significance, but the lack of
statistical significance in all studies should not invalidate the
positive significant associations for involuntary smoking that have
been observed.

97


TABLE lO.-So~ and types of bias in case-control
       studies

Study

                     . .
                  Tbbd&dbtiOIl
AutboA   rbfh-tion   ofp8mivemoke Interviewer Ihpomht
amclunion   ofhlgcancer                 bh      him

Tricllopoulm     Pocitive     + (1)      + (1)      +(t) -
et al.
ww

cmeaetal.    Positire       -       + (1)         -        -

mS3~

-==dFung  N@iViJ             + (1 or t)      ?        7
w321

xooetd.     NCgBth?             + (1 or 1)      7        ?
mS4)

K&et sad Wynder Negetive
wxu~

Wu et al      WedI
wm      Poeitive

-

+ (1 or t,      ?        7

  -      +(t) -

GMinkeletaL   POEit&       -       + (1 or t,     -    + (1 or t)
(1986)

Akiba et al.    PC&h     + (1)      + (1,         ?    + cc or t)
(1986)

Pershaga et al. Positive
(in press)

+ (1 01 1)     -

Sii epidemiological studies found statistically significant in-
creased risks 888ociated with spouse's smoking; all demonstrated a
dose-response relationship, and several suggested a stronger asso&-
tion with squamous cell and small cell carcinoma than with other
cell types. Three of these studies (Hirayama 1984a, Correa et al.
1983; Akiba et al. 1986) included nonsmoking male lung cancer
patients, and the complementary fmdings in nonsmoking husbands
married to smoking wives strengthen the evidence on involuntary
smoking. The four studies with sign&ant positive findings pub-
lished since 1981 (Correa et al. 1983; Garfiikel et al. 1985; Akiba et
al. 1986; Pershagen et al., in press) not only corroborated the
fmdings of Hirayama (1981a) and Trichopoulos and colleagues
(19811, but answered the many criticisms directed at these two
StUdieS.

9J3


TABLE Il.-Study power for case-control study baaed on an unmatched analysis

                                      ohaerved relative    Power for      Power for       Power for        Power for
                        Proportion of    rick for ever ve.    twosided test    onesided test    one-aided trend      one-sided test
            Number    control:   controla' epouaes   never exposed to     haeed on      haaed 011      test baaed on    baaed on RR=2 for
Study          of eQBe8   case ratio    who smoked    epouew' emoking    ohaerved RR    ohaerved RR    oheerved re3ulta'  ever vu never expmed

T&hop&e et al.
mJ83)

Coma et al.
m63)

Chan and Fug
W2)

Koo et al.
ww

Kabat and Wynder'
ww

wu et a1.s
WJW

Garfmkel et al.
(1986)

Lee et al.
(lgw

Akiha et al.`

77       2.92

xl      10.43

64      1.68

33       1.66

36       1.03

29      1.66

134      3.00

47      2.04

84      2.36

0.62          2.11

0.23           2.97

0.48          0.75

0.71 a          1.23

0.64          0.85

0.60           1.41

0.61          1.23

0.62          1.11

-0.67          1.47

0.79         0.87          0.88           0.89

0.33         0.83          0.97           0.56

0.17         0.26          NA'           0.90

0.10          0.17          0.10           0.64

0.06         0.10          NA'           0.39

0.10         0.17          0.16           0.37

0.24          0.36          0.71            0.94

0.04         0.w)         NA'           0.62

0.26         0.33          0.63           0.76


TABLE ll.-Cbntinued

Study

Number    Control:
of cases   case ratio

            Observed relative     Power for      Power for      Power for        Power for
Proportion of    risk for ever ~8.    twc-Gded test    one-sided test    onesided trend     one-sided test
controls' BpouaeB   never exposed to     based on.      bawd on      test baeed on    bad on RR=2 for
who smoked    SpoueBB' Bmoking    obeerved RR    obeerved RR    observed resulta'  ever vs. never expceed

Per&age" et al.       67       6.18        0.44           1.23          0.12         0.19          0.46'           0.83
(in press)

Pooled*           676      2.96        0.62         153          0.99         LOO          NA            1.00

Pooled a           509      3.40        0.62          1.66          1.M)          1.00          1.M)            1.00

' Based on three levels of passive smoke exposure as defined in respective stud&.
`Data not available for trend test.

`Includes spouses, cohabitanta, and coworkers who smoked.
`Based on nonsmoking caeea and mntrols with information on spouses' smoking.
`Based on cases and controllr who were ever married.
"Based on female casea and controls with information on husbands' smoking (number of cigarettes smoked per day).
`Estimate based on 26 cases and 161 controls in the low exposure category, 7 cases and 12 controla in the hiih exposure category.
`Based on combined results of the 10 we-control studies.
*Based on combined results of the doyen caee-contml studies with data available for trend test.


The most serious criticism is the misclas&cation of the a&ve
smoking status of the subjects, which can produce an apparent
increased risk with involuntary smoking. Moreover, it is likely to
result in differential misclassification because spouses tend to have
similar smoking habits (Burch 1981; Sutton 1981; Higgins et al.
1937). Speculation that the positive results reported in Japan and
Greece were due to cultural bias against the admission of smoking by
women in these more traditional societies may be discounted because
positive significant findings have now been observed in the United
States (Correa et al. 1983; Garfinkel et al. 1985) and in Sweden
(Pershagen et al., in press), where no comparable social stigma
exists. Moreover, in the studies by Garfinkel and coworkers (1985)
and Pershagen and coworkers (in press), the personal smoking status
of each subject was validated and verified at interview, usually by
next of km, who presumably would have no reason to misrepresent
the true smoking status of the subject.
Misclassification of the lung as the primary site and the lack of
pathological confirmation are repeated concerns, but it must be
stressed that this bias would tend to dilute a true effect. Correa
(1983), Garfiiel (198!5), and Pershagen (in press) and their respec-
tive colleagues addressed this issue by including only pathologically
confirmed lung cancers and considering histological cell type in their
analyses. In the study by Garfmkel and associates (1985), after &
independent pathological review was conducted, a significant associ-
ation of excess risk with involuntary smoking remained. Misclassifi-
cation of exposure to RTS cannot be dismissed, since an index based
solely on the smoking habits of a current spouse may not be
indicative of past exposure, cumulative exposure, or the relevant
dose to the respiratory tract.
The magnitude of risk associated with involuntary smoking
exposure is uncertain. Relative risks ranging from 2 to 3 were
generally reported for the highest level of exposure based on the
spouses' smoking habits, but since sample sixes in most studies are
not large, the point estimates of effect are unstable, and confidence
limits are broad and generally overlap from one study tc another. An
index of involuntary smoking based on the smoking habits of the
spouse is a simplistic and convenient measure. There is no reason to
believe, however, that the excess risk associated with involuntary
smoking is restricted to exposure from spouses. Nonsmokers married
to smokers are likely to be more tolerant of EZS exposure and to
experience more exposure to environmental tobacco smoke (Wald
and Ritchie 1984). Higher risk estimates for involuntary smoking
have been obtained in studies restricted to squamous cell and small
cell carcinomas of the lung.
Although involuntary smoking can be established as a cause of
lung cancer, important questions related to this exposure require

101


further research. More accurate estimates for the assessment of
exposure in the home, workplace, and other environments are
needed. Studies of sufficiently large populations should also be
performed. New data from such studies should yield more certain
risk estimates and describe the magnitude of the lung cancer risk in
nonsmokers.

other Cancef8

several recent studies provide data on the relationship of RTS
exposure to cancer at sites other than the lung. Two published
reports address the risk of other cancers in adults from exposure to
tobacco smoke from spouses. Using the same Japanese cohort
described previously, Hirayama (1984a) reported excess mortality for
cancers of the paranasal sinus (N=28) and brain (N=34) among
nonsmoking women who were married to smokers. The standardized
mortality ratios (SMRs) for nasal sinus cancer were 1.00,1.67,2.02,
and 2.65 for women whose husbands never smoked, or had smoked
10 to 14,15 to 19, or 20 or more cigarettes per day, respectively (one-
sided p for trend, 0.03). The corresponding SMRs for brain tumors
were 1.00, 3.03, 6.25, and 4.32, respectively (on+sided p for trend,
0.004). The total number of deaths due to nasa.l cancer and brain
tumors was small, and the numerators in the risk calculations were
unstable, based on five nasal cancers and three brain cancers in
women whose husbands were nonsmokers. In one study (I3rinton et
al. 19&Q, active tobacco smoking was associated with an increased
risk of sinus cancer, particularly squamous cell tumors. Sidestream
smoke has also been suggested to be of etiological importance in
brain tumors in children (Preston-Martin et al. 1982).
In a -ntrol study of adult cancers in relation to childhood
and adult exposure to involuntary smoking, Sandier and coworkers
(1965a, 1986) reported an overall cancer risk of 1.6 (95 percent C.I.
1.2, 2.1) associated with exposure to spouses' smoking, which was
more marked in nonsmokers than smokers. Significant increases
were observed for cancer of the breast (OR 1.8), cervix (OR 1.8), and
endocrine organs (OR 3.2). This study has been criticized in its choice
of controls and in the exclusion of certain cancers by the design of
the study. The biological plausibility of the study's findings was also
questioned because the highest risk estimates were observed for
cancers that have not been consistently related to active smoking
and because higher risks were observed for nonsmokers than for
smkers. Failure to control for potential confounding factors and
kmnvn risk factors for the individual cancer sites under study may
have produced artifact& results QYiedman 1986; Mantel 1986;
Rurch 1966). In a subsequent analysis of the same study population,
Samher, Wilcox, and Everson (1985a,b) reported increasing cancer


risks with incmahg exposure to involuntary smoking as measured
by the number of smokers in the household and by the time periods
of exposure. The biologic plausibility of these findings was aIso
questioned (Burch 1985; Higgins 1985; Lee 1985).

The effect of parental smoking on the development of cancers both
during ~hildhd and in adult life is also of in&eat. The relationship
of parental smoking to overall cancer risk in children or in adults
has been assessed in three studies. A prospective survey (Neubl and
Buck 1971) of about 90,060 infants in Canada and the United
Kingdom followed for a maximum of 10 years found an overa.II
cancer risk of 1.3 (95 percent C.I. 0.8, 2.2) associated with maternal
smoking during pregnancy. No dose-response relationship was
observed, but there were few heavy smokers (>l pack/day) in this
study. A Swedish case-control study (Stjemfeldt et al. 1986) of aII
cancers found a risk of 1.4 (95 percent CL 1.0, 1.9) for maternal
smoking during pregnancy. A do-response relationship was dem-
onstrated; the risk was highest in the most exposed group, those
smoking 10 or more cigarettes per day (RR 1.6, p < 0.01). On the basis
of the smoking habits of the parents of subjects up to 10 years of age,
Samher, Everson, W&ox, and Browder (1985) reported no significant
difference between all cancer cases and controls with respect to the
mother's smoking (RR 1.1, 95 percent CL 0.7, 1.6), but the father's
smoking was related to an overall increased risk (RR 1.5,95 percent
CL 1.1, 2.0). In these three studies, analysis by specific cancer site
revealed an increased risk of leukemia associated with parental
smoking.

Neutel and Buck (1971) found an almost twofold increased risk of
leukemia in &i&en of mothers who smoked during pregnancy, but
the association was not statisticahy significant. Stjernfeldt and
colleagues (1986) reported a sign&ant positive association between
maternal smoking and acute lymphoblastic leukemia. The relative
risks were 1.0, 1.3, and 2.1 (p for trend, <O.Ol) for mothers who
smoked 0, 1 to 9, and 10 or more cigarettes per day, respectively.
Similar significant positive associations with maternal smoking were
not observed for other cancer sites, but the risk assessments were
based on a smalI number of cases. This study suggests that the
relationship between maternal smoking and leukemia was strongest
for smoking during the 5-year period before pregnancy, intermediate
for smoking during pregnancy, and lowest for smoking after
pregnancy. In the study by Sandier, Everson, Wilcox, and Browder
(1985), the mother's smoking and the father's smoking were sepa-
rately and jointly associated with an increased risk for leukemia and
lymphoma. The relative risk was 1.7 when one parent smoked and
4.6 when both parents smoked (p for trend, <O.OOl). The increased
risk with parental smoking was observed regardless of the personal
smoking status of the subject. No other cancer site was associated

103


with the mother's smoking, although the father's smoking was
associated with increased risks for other cancer sites, including the
brain and the cervix. Two studies of leukemia in children found no
relatio&ip with parental smoking (Manning and Carroll 1957; Van
Steensel-Moll et al. 1965). In the study by Manning and Carroll
(1957), the mothers' general smoking habits were assessed, whereas
van Steensel-Mall and colleagues (1985) obtained information on the
smoking habits of both parents in the year before the pregnancy.
Stewart and colleagues (1958) reported a statistically significant risk
of 1.1 (p=O.O4) for leukemia in association with the mothers'
smoking, but cautioned that the smoking information on the
mothers pertained to their habita at the time of interview, which
took place a&r the deaths of the patients and may have been
affected by bereavement.
The effect of parental smoking habits has been examined in
epidemiological studies of brain tumors, rhabdomyosarcoma, and
teeticular cancer in children. Gold and colleagues (1979) reported an
association between maternal smoking prior to and during pregnan-
cy and brain tumors in children. A relative risk of 5.0 (p=O.22) ~88
found, but the result was based on a small number of patients and
was not statistically significant. No relationship between maternal
smoking during pregnancy (RR 1.1, onegided p=O.42) and brain
tumors in children was found in another study Preston-Martin et al.
1982), but a significantly increased risk (RR 1.5, one-sided p=O.W
associated with mothers living with a smoker (usually the child's
father) during pregnancy was observed. A significantly increased
risk with the father's smoking, but not the mother's smoking ~88
also reported in a study of rhabdomyosarcoma (Grufferman et al.
1982). The father's smoking conferred a signScant increase in risk
@R 3.9, 95 percent C.I. 1.3, 9.6), but the mother's smoking during
and after the pregnancy was not significantly different between
Cases and controls (RR 0.8, 95 percent C.I. 0.3, 2.0). A history of
m&d smoking during pregnancy did not differ for testicular
cancer cases and controls (RR 1.0, p=O.57) in one study (Henderson
et al. 1979).
There are at present insufficient data to adequately evaluate the
role of ~voluntary smoking in adult camera other than primary
carcinoma of the lung. In addition, active smokers n&y
receive greater exposure to ETS than nonsmokers. Thus, effects
would not be anticipated in involuntary smokers that do not occur in
active smokers (IARC 1986), and the biological plausibility of
associations between E'l!s exposure and cancer of sites not associated
with active smoking must be questioned. The fmdings of Hirayama
(19%) and Sandier, Everson, and Wilcox (1985) need confirmation
in &xl& that take into account the potential confounding factors
ad *he known risk factors for these individual sites. The evidence

104


for parental smoking and childhood cancer is also not clear, and
evaluation of this association is made difficult by the various
definitions of exposure that have been used, including maternal and
paternal smoking before, during, and after the pregnancy. Mothers
and fathers who smoke during a pregnancy generally smoked before
the conception and continue to smoke after the pregnancy. Thus, an
effect of involuntary smoking after birth cannot readily be distin-
guished from genetic or transplacentally mediated effects.

Cardiovascular Diseases

A causal association between active cigarette smoking and cardio-
vascular disease is well established (VS DHHS 1983). The relation-
ship between cardiovascular disease and involuntary smoking has
been examined in one wntrol study and three prospective
studies. In the case-control study by Lee and colleagues (1986),
described previously, ischemic heart disease cases and controls did
not show a statistically significant difference in their exposure to
involuntary smoking, based on the smoking habits of spouses or on
an index accounting for exposure at home, at work, and during
travel and leisure. In the Japanese cohort study, Hirayama (1984b,
1985) reported an elevated risk for ischemic heart disease (N =494)
in nonsmoking women married to smokers. The standardized
mortality ratios when the husbands were nonsmokers, ex-smokers or
smokers of 19 or more cigarettes per day, and smokers of 20 or more
cigarettes per day were 1.0, 1.10, and 1.31, respectively (one-sided p
for trend, 0.019).

In the Scottish followup study (Gillis et al. 1984), nonsmokers not
exposed to tobacco smoke were compared with nonsmokers exposed
to tobacco smoke with respect to the prevalence of cardiovascular
symptoms at entry and mortality due to coronary heart disease.
There was no consistent pattern of differences in coronary heart
disease or symptoms between nonsmoking men exposed to tobacco
smoke and their nonexposed counterparts. Nonsmoking women
exposed to tobacco smoke exhibited a higher prevalence of angina
and major FCG abnormality at entry, and also a higher mortality
rate for all coronary diseases. However, rates of myocardial infarc-
tion mortality were higher for exposed nonsmoking men and women
compared with the nonexposed nonsmokers. The rates were 31 and 4
per 10,990, respectively, for the nonexposed nonsmoking men and
women, and 45 and 12 per 10,000, respectively, for the exposed
nonsmoking men and women. None of the differences were tested for
statistical signif%ance.
In the Japanese and the Scottish studies, other known risk factors
for cardiovascular diseases, i.e., systolic blood pressure, plasma
cholesterol, were not accounted for in the analysis.

105


ID a study of heart disease, Garland and coworkers (1985) enrolled
82 percent of adults aged 50 to 79 between 1972 and 1974 in a
predominantly white, upper-middle-class community in San Diego,
California Blood pressure and plasma cholesterol were measured at
entry, and all participants responded to a standard interview that
asked about smoking habits, history of heart disease, and other
health-related variables. Excluding women who had a previous
history of heart disease or stroke or who had ever smoked, 695
currently married nonsmoking women were classified by their
husbands' self-reported smoking status at enrollment. After 10 years
of followup, there were 19 deaths due to ischemic heart disease; the
age-standardized mortality rates for nonsmoking wives whose hus-
bands were nonsmokers, ex-smokers, and current smokers were 1.2,
3.6, and 2.7, respectively (one-sided p for trend, <O.lO). After
adjustment for age, systolic blood pressure, total plasma cholesterol,
obesity index, and years of marriage, the relative risk for death due
to ischemic heart disease for women married to current or former
smokers at entry compared with women married to never smokers
was 2.7 (one-sided p 5 0.10).
The study's findings are not convincing from the point of view of
sample stability. The total number of deaths due to ischemic heart
disease was small, and the denominator in the relative risk
calculation is unstable, based on the deaths of two women whose
husbands had never smoked. Moreover, it is well established that the
risk of coronary heart disease is substantially lower among those
who have stopped smoking (US DHHS 1983), although the amount of
time required for this change after cessation of smoking is not clear
(Kennel 1981). In this study, 15 of 19 deaths occurred in nonsmoking
women married to husbands who had stopped smoking at entry, and
the age-standardized rate for ischemic heart disease was highest in
this group. The high proportion of deaths in nonsmoking women
married to men who became ex-smokers implies that the excess
resulted from a sustained effect of involuntary smoking. More
d&&d characterizations of exposure to EI'S and specific types of
~di0~a8cu1ar disease associated with this exposure are needed
before an effect of involuntary smoking on the etiology of cardiovas-
cular disease can be established.
one study (Aronow 1978a,b) suggested that involuntary smoking
aggravates angina pectoris. This study was criticized because the end
point, angina, was based on subjective evaluation, and because other
factors such as stress were not controlled for (Coodley 1978; Robinson
1978; Waite 1978; Wakehan 1978). More important, the validity of
Aronow's work has been questioned (Budiansky 1983).

106


Conclusions

1. Involuntary smoking can cause lung cancer in nonsmokers.
2. Although a substantial number of the lung cancers that occur
in nonsmokers can be attributed to involuntary smoking, more
data on the dose and distribution of ElTS exposure in the
population are needed in order to accurately estimate the
magnitude of risk in the U.S. population.
3. The children of parents who smoke have an increased frequen-
cy of hospitalization for bronchitis and pneumonia during the
first year of life when compared with the children of nonsmok-
ers.

4. The children of parents who smoke have an increased frequen-
cy of a variety of acute respiratory illnesses and infections,
including chest illnesses before 2 years of age and physician-
diagnosed bronchitis, tracheitis, and laryngitis, when com-
pared with the children of nonsmokers.
5. Chronic cough and phlegm are more frequent in children
whose parents smoke compared with children of nonsmokers.
The implications of chronic respiratory symptoms for respira 4
tory health as an adult are unknown and deserve further
study.
6. The children of parents who smoke have small differences in
tests of pulmonary function when compared with the children
of nonsmokers. Although this decrement is insufficient to
cause symptoms, the possibility that it may increase suscepti-
bility to chronic obstructive pulmonary disease with exposure
to other agents in adult life, e.g., active smoking or occupation-
al exposures, needs investigation.
7. Healthy adults exposed to environmental tobacco smoke may
have small changes on pulmonary function testing, but are
unlikely to experience clinically significant deficits in pulm*

nary function as a result of exposure to environmental tobacco
  smoke alone.
8. A number of studies report that chronic middle ear effusions
are more common in young children whose parents smoke than
in children of nonsmoking parents,
9. Validated questionnaires are needed for the assessment of
recent and remote exposure to environmental tobacco smoke in
the home, workplace, and other environments.
10. The associations between cancers, other than cancer of the
lung, and involuntary smoking require further investigation
before a determination can be made about the relationship of
involuntary smoking to these cancers.

11. Further studies on the relationship between involuntary
smoking and cardiovascular disease are needed iu order to

107


determine whether involuntary smoking increases the risk of
cardiovascular disease.

108


References

ABEL, E.L. Smoking during pregnancy: A review of effect.8 on growth and develop-
ment of offipring. Human BiorogV 52(4):593+25, December 1980.
ADLKOFER, F., ScHERER, G., Van HEES, U. Passive smoking. (Ietter). New
England Journal of Medicine 312411):7X3-729, March 14,1985.
AKIBA, S., KATO, H., BLOT, WJ. Passive smoking and lug cancer among Japan*
women. Cancer Reeeamh 46(9):48U4307, September 1986.
ARONOW, W.S. Effect of passive smoking on angina pectoris. New Engla& Jou~l
of Medicine 299G):21-24, July 6,1978a.

ARONOW, W.S. Effects of passive smoking. (ietter). New England Jound of&&&~
299(16):897, October 19.1978b.

BACKHOUSE, C.I. Peak expiratory flow in youths with varying cigarette ~mokbg
habits. British Medical Journal 1(5954):360862, February 15,197s.
BARRON, B.A. The effects of misclassification on the estimation of relative risk.
Biometrics 33(2):414-418, June 1977.

BECK, G.J., DOYLE, CA., SCHACHTER, E.N. Smoking and lung function. American
Review of Respiratory Dr&occ 123(2):14%X5, February 1981.
BERKEY, C.S., WARE, J.H., DOCKERY, D.W., FERRIS, B-G., Jr., SPEIZER, F.E.
Indoor air pollution and pulmonary function growth in preadolescent children.
American Journnl of Epidemiology 123(2):256-269, February 1986.
BEWLEY, B.R., HALIL, T., SNAITH, A.H. Smoking by primary schoolchikkem
prevalence and associated respiratory symptoms. British Journal of Awedive
and Socinl Medicine 27(3):X9-153, August 1973.
BLACK, N. The aetiology of glue ear: A case-control study. Intemational Jownal of
pediatric Otorhindaryngobgy 9(2):121-133, July 1985.
BLAND, M., BEWLEY, B.R., POLLARD, V., BANKS, M.H. EM& of children's and
parents' smoking on respiratory symptoms. Archives of Dkase in Childhood
53(2):10@105, February 1978.

BLOT, W.J., MCLAUGHLIN, J.K. PracticaI issueg in the design and conduct of case
control studies: Use of next-of-kin interviews. In: Blot, W.J., Hirayama, T., Huel,
O.G. (eds). Statistical Issues in Cancer Epidemiology. Hircdims, Sanei Publishers,
1985, pp. 4662.

BRINTON, LA., BLOT, W.J., BECKER, J.A., WINN, D.M., BROWDER, J.P..
FARMER, J.C., Jr., FRAUMENI, J.F., Jr. A mntrol study of cancers of the
nssaI cavity and paranssal sinus. American Journal of Epidemiology 11%6):896-
906, June 1984.

BRUNEKREEF, B., FISCHER, P., REMIJN, B., VAN DER LENDE, R.. SCHOUTEN,
J., QUANJER, P. Indoor air pollution and its effect on pulmonary funtion of adult
nonsmoking women: 3. Passive smoking and pulmonary function. Intemationd
Journal of h'pio!emiology 14(2):227-230, June 1985.
BRUNNEMANN, K.D., ADAMS, J.D., HO, D.P.S., HOFFMANN, D. The influence of
tobacco smoke on indoor atmospheres: 2. Volatile and tobacco-specific nitrosa-
mines in main- and sidestream smoke and their contribution to indoor poRution.
F%ceedinge of the Fourth Joint Conference on Sensing of Environmental Pollu-
tam's, New Orleans, 1977. American Chemical Society, 1978, pp. 876-880.
BUDIANSKY, S. Food and drug d&a fudged. Nature 392(5999):569, April 14,1983.
BURCH, P.R.J. Passive smoking and lung cancer. (letter). British i%fe&.col Jourd
2%X6273):1393, April 251981.

BURCH, P.R.J. Lifetime passive smoking and cancer risk (Ietter). beet 1@433)866,
April 13.1985.

BURCH, P.R.J. Passive smoking in aduIthood and cancer risk. (letter). American
Journal of Epidemiology 123(2):368-369, February 1986.

109


BURmL, C.M., HIGGINS, M.W., KELLER, J.B.. HOWATT, W.F.. BUTLER WJ.,
HIGGINS, I.T.T. Passive smoking in childhood: Respiratory conditions and
pulmonary function in Tecumseh, Michigan. American Review of Respimtory
D&W 133(6):96&973, June 1986.
BURROWS, B., KNUDSON, R.J., CLINE, M.G., LEBOWTIZ, M.D. Quantitative
re~tio&+ b&men cigarette smoking and ventiIatory function. American
Review ofRespimtory Discoar 115(2b19&205, February 1977.
BURROWS, B., KNUDSON, R.J., LEBOWFIZ, MD. The reIationship of childhood
respiratory illness to adult obstructive airway disease. American Reuti of
Respiratory Dieeaee 115(5):751-766, May 1977.
CAIifEftON, P., KOSTIN, J.S., ZAKS, J.M., WOLFE, J.H., TIGHE, G., OSELEPX B.,
sTocI(ER, R, WINTON, J. The health of smokers' and nonsmokers' chihhen.
Jownal of Alkrgy 43(6):336-341, June 1969.
CI-IAN, W.C., COLBOURNE, I&J., FUNG, SC., HO, H.C. Bronchial cancer in Hong
Kong 1976-1977. British Journal of chncer 39(2):18%192, February 1979.
CHAN, W.C., FLING, S.C. Lung cancer in nonsmokers in Hong Kong. In: Gxundmann,
E., CIemmesen, J., Muir, C.S. (eds). 6'eogruphicaZ Pathology in GZMW
Epiokmid~gy. Cancer Campaign, Vol. 6. New York, Gustav Fischer Verlag, 1982,
pp. 199292.

CHARLTON, A. Children's coughs related to parental smoking. British Medid
Journal 2386X31)31647-1649, June 2.1984.
CHEN, Y., LI, W.-X. The effect of passive smoking on chikiren's pulmonary function
in Shanghai. American Journal of Public Health 76(5):5X-518, May 1986.
VOLLEY, J.R.T. Respiratory disease in childhood. British i%dical Bulletin 27(l)%14,
January 1971.

COLLEY, J.R.T. Respiratory symptoms in chi.Idren and parental smoking and phlegm
production. British Medical Journal X5912):201-204, April 27,1974.
COLLEY, J.R.T., HOLLAND, W.W., CORKHILL, R.T. Influence of passive smoking
and paremel phlegm on pneumonia and bronchitis in early chikihood. &mcet
X7888):1031-1934. November 21974.

COLLINS, MI-I., MOESSINGER, A.C., KLEINERMAN, J., BASSI, J., ROSSO, P.,
CCXJ.JNS, A.M., JAMES, L.S., BLANC, W.A. Fetal lung hypopIasia associated
with maternal smoking: A morphometric analysis. Pediatric Research 1%4MO8-
412, April 1985.

COMSlQCK, G.W., MEYER, M.B.. HELSING, K.J., TOCKMAN, M.S. Respiratory
effects of household exposures to tobacco smoke and gas cooking. American Revkw
of Rc+mtory Diaeosc X74(2):143-148. August 1981.
WDm, A. Effecta of passive smoking. Getter). New England Journd of Medicine
WW397, October 19,1978.

co-, K.T., CHECKOWAY, H., McMICHAEL, A.J., HOLBRCOK, R.H. Biee
due tc mieciassification in the e&in&ion of relative risk. American Joumal of
&&mb&~ 105(5):488-495, May 1977.

CQRREA, P., PICKLE, L-W., FONTHAM, E., LIN, Y., HAENSZEL, W. Passive
smoking and lung caner. Lancet 2(8350):595697, September 10,1983.
CRIQUI, M.H. Response bias and risk ratios in epidemiologic studies. Anwim
Joumd of Epidemiology 109(4):394-399, April 1979.
D-8 T.E., BOLIN, J.F., SLAVIN, R.G. Passive smoking: EfMcts on bronchial
~&JM. Chest 80(5):530-534, November 1981.
mDC+J% R. The effecta of indoor pollution on Arizona children. Archives of
EnvimnmentalHeaZth 37(3):161-155, May-June 1982.
DOLL, R., PETO, R. Cigarette smoking and bronchial carcinoma: Dose and time
relationships among regular smokers and lifelong non-smokers. Jourd Of
Epidemiology and Community Health 32(4):303-313, December 1978.

ilo


DUTAU, G., CORBERAND, J., LEOPHONTE, P., ROCHICCIOLI, P. Manifestations
reapiratoires lieee a l'inhalation passive de fumme de #ac chez l'infant d'age pm
scolaire [Regpiratory signs associated with passive inhalation of tobacco smoke in
infants]. Le Poumon et le Cbeur 35(2):63-69,1979.
EKWO, E.E., WEMERGER, M.M., LACHENBRUCH, P.A., HUNTLEY, W.H.
Relationship of parental smoking and gas cooking to respiratory disease in
children. Chest 84(6):66%666, December 1933.
FERGUSSON, D.M., HORWOOD, LJ. Parental smoking and respiratory illness
during early childhood: A six year longitudinal study. P&&ric Pulmo~2ogv
1(2):99-106, March-April 1965.

FERGUSSON, D.M., HORWOOD, LJ., SHANNON, F.T., TAYLOR, B. Parental
smoking and lower respiratory illness in the first three years of life. Journal of
Epidemiology and Community Hecllth 36(3):160-164, September 1931.
FEYERABEND, C., HIG ENBO'ITAM. T., RUSSELL, M.A.H. Nicotine concentrations
in urine and saliva of smokers and nonsmokers. British Medid Journal
2$4(6321):100%1004, April 3,1982.

FOLIART, D., BENOWITZ, N.L., BECKER, C.E. Passive absorption of nicotine in
airline flight attendant& (letter). New E&and Joumd of Medicine 308(16):1106,
May 5,1933.

FRIEDMAN, G.D. Passive smoking in adulthood and cancer risk. (letter). American
Journd ofEpidemiology 123(2):367, February 1936.
FRJEDMAN, G.D., PE'lTITI, D.B., BAWOL, R.D. Prevalence and correlates of passive
smoking. A merican Journal of Public Hwlth 73(4):401-405, April 1933.
GARFINKEL, L. Time trends in lung cancer mortality among nonsmokers and a note
on passive smoking. Journal of the National Cancer Institute 66(6):1061-1066, June
  1931.

GARFINKEL, L., AUERBACH, O., JOUBERT. L. Involuntary smoking and lung
cancer A case-control study. Journal of the National Cancer Institute 75(3):463-
469, September 1936.

GARLAND, C.. BARREIT-CONNOR, E., SUAREZ, L., CRIQUI, M.H., WINGARD,
D.L. Effecta of passive smoking on ischemic heart disease mortality of nonsmokers:
A pmspective study. American Journal of EpidemiorogV 121(6):645-650, May 1935.
GlLLlS, CR., HOLE, D.J., HAWTHORNE, V.M., BOYLE, P. The effect of environ-
mental tobacco smoke in two urban communities in the weat of Scotland. European
Journal of Respimkwy Diseases 66@uppl. 133):121-126,1934.
GOLD, E., GORDIS, L., TONASCLA, J., SZKLO, M. Risk factors for brain tumors in
children. American Journal of Epidemiology 109(3):309-319, March 1979.
GORDlS, L. Should dead casea be matched to dead controls? American Journal of
Epidemiology 1X5(1):16, January 1962.

GORTMAKER, S.L., WALKER, D.K., JACOBS, F.H., RUCB-ROSS, H. Parental
smoking and the risk of childhood asthma. American Jounud of Public Health
72(6):574-579, June 1962.

GREENBERG, R.A., HALEY, N. J., ETZEL, R.A.. LODA, F. A. Measuring the exposure
of infanta t,o t&acm smoke: Nicotine and cotinine in mine and saliva. New
England Journal of M&%&e 310(17):1075-1078, April 26,1934.
GREENLAND, S. The effect of misclassification in the presence of covariatea
American Journal of Epidemiology 112(4):566569, October 1960.
GRUFFERMAN, S., WANG, H.H., DeLONG, E.R., KIMM, S.Y.S., DELZELL, E.S.,
FAUETA, J.M. Environmental factors in the etiology of rhabdomyoearcOma in
childhcud. Journal of the Nationd cclncer Institute 68(1):107-113, January 1962.
GRUNDMANN, E., MULLER, K.-M., WINTER K.D., STERLING, T.D. Non-smoking
wives of heavy smokers have a higher risk of lung cancer. (letter). British bfedid
Journal 2%!(6270):1156, April 4,198l.

111


HALEY, N.J., HOFFMANN D. Analpeis for nicotine and cotinine in hair to
d&.ede cigarette smoker status. C&z&xl Chemistry 31(10):1598-1~, October
  1935.

HA&&@J~), EC., SEIJKOFF, Id. Passive smoking and lung cancer with comments
on ~0 new papers. EnvironmentuZ Research 24l2k444-452, APT 1%~.
HARLAN, s., DAVIES, A.M. Infant admissions to hospital and maternal smoking.
&ncet 1(7857):529-532, NIarch %1974.

HARRIS, J.E., DUMOUCHEL, W.H. Nonsmoking wives of heavy smokers have a
higher &k of lung cancer. (letter). British i%fedicaZ JOUST 283(6296):916, October
3,198l.

HA.SSEI,BLAD, V., HUMBLE, C.G.. GRAHAM, M.G., ANDERSON, H.S. Indoor
environmental dete IZ&IS&S of lung function in children. American Review of
RespiratoryDisease 123(5):479-485, Major 1981.
m=N, B.E., BENTON, B., JING, J., YU, MC, PIILE, ME. Risk &&ax for
-m of tie testis in young men. Internal Journd of Cheer 23(5):698-602,
May 1979.

HIGGINS, 1. Lifetime paesive smoking end cancer risk (letter). Jimwet 1(8433):86&
367, April 13.1985.

HIGGINS, M-W., KIELSBERG, M., METa H. Characteristice of smokers and
nonamokera in Tecumseh Michigan. 1: The distribution of smoking hahite in
pereons and families and their relationship to social characteristica. American
Joumal of EppidemioXo~ 86(1):m9, July 1967.
HULES, F.C. Deposition of side&ream cigarette smoke in the human respiratory
tract. Bwentiue iUiiicine 13(6):602-607, November 1984.
HIRAYAMA, T. Nonsmoking wives of heavy smokers have a higher risk of lung
cancer A study from Japan. British Medical Journal 282(6259):18%X%, January
17,198la.

HIRAYAMA, T. Passive smoking and lung cancer. (letter). British Medical Journal
2%$6273):1393-1394, April 25,198lb.

HlBAYAMA, T. Nonsmoking wives of smokers have a higher risk of lung cancer.
(letter). British Medical JournuZ 28X6296):916-917, October 3,198lc.
HIRAYAMA, T. Nonsmoking wives of smokers have a higher risk of lung cancer.
(letter). British Medical Jounu~l283@304):1465-1466, November 28,198ld.
HIRAYAMA, T. Paeeive smoking and lung cancer Consistency of association. (letter).
Lmcet 2@364):1425-1426, December 17,X%3.
HIRAYAMA, T. Cancer mortality in nonsmoking women with smoking husbands
based on a largescale cohort study in Japan. Preventive Medicine 13(6):-90,
November1984a.

HIRAYAMA, T. Lung cancer in Japanz EXfecta of nutrition and passive smoking. In:
Mizell, M., Correa, P. teds). Lung Gzncerr Causes and Fbvention Deerfield Beach,
Florida, VCH, 1984b, pp. 175-195.

HIRAYAMA, T. Passive smoking: A new target of epidemiology. Joumal of
Eqmimental CZinicaZ Medicine 10(4):287-293,19&35.
HOEGG, U.R. mti smoke in closed spacea. Environmental Health Pecs~tivea
(2):177-E%, October 1972.

HO-, D., HALEY, N.J., ADAMS, J.D., BRUNNEMANN, K.D. Tobacco
sidestream smoke: Uptake by nonsmokers. Preventive Medicine 13(6):6(X3-617,
November 1984.

HORWOOD, LJ., FERGUSSON, D.M, SHANNON, F.T. Social and familial factors in
the development of early childhocd es&ma. Pediatrics 75GW59-868, May 1985.
HUmD, C., mwI(INS, L-H., ASTRUP, P. Expoeure of passive smokers to tobacco
Smoke constituents. Intenudiond Archives of Ckcupatio~l and Environmental
Health 42X1):21-29,1978.

112


INTERNATIONAL AGENCY FOR RESEARCH ON CANCER. To&co Smoking.
IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to
Humans, Vol. 33. Lyon, L4RC. 1986, pp. 163-314.
IVERSON, M., BIRCH, L., LUNDQVIST, G.R., ELBROND, 0. Middle ear effusion in
children and the indoor environment: An epidemiological study. An$im of
Environmentd Health 40(2):74-79, March-April 1985.
JARVIS, M.J., TUNSTALLPEDOE, H., FEYRRABEND, C., VESEY, C., SALOOJEE,
Y. Biochemical markers of smoke absorption and self-reported exposure to passive
smoking. Journal of Epidemi&gy and Community Health 33(4):335~339, Decem-
her 1964.

JONES, JR, HIGGINS, I.T.T., HIGGINS, M.W., KELLER, J.B. Effects of cooking
fuels on lung function in nonsmoking women. Archives of Envimnmntcll E&&h
33(4):219-222, July-August 1983.

KABAT, G.C., WYNDER, E.L. Lung cancer in nonsmokers. Cancer 53(!$:l214-1221,
March 1,1984.

KANNEL, W.B. Update on the role of cigarette smoking in coronary artery disease.
American Heart JournnZ 101(3):31~23, March 1981.
KASUGA, H., HASEBE, A., OSAKA, F., MA'ISUKI, H. Respiratory symptoms in
school children and the role of passive smoking. Tokai Journul of &p-her&al
and Clinical Medicine 4(2):101-114, April 1979.
KAUFFMANN, F., DOCKERY, D.W., SPEIZER, F.E., FERRIS, B.G., Jr. Reepiratory
symptoms and lung function in women with passive and active smoking. (ab&act).
American Review of Respimtory Disease 133(4, part 2):A157, April 1986.
KAUFFMANN, F., TESSIER, J.-F., ORIOL, P. Adult passive smoking in the home
environment: A risk factor for chronic airflow limitation. American Journal of
Epidemiology 117(3):269-280, March 1933.

KENTFR, M., TRIEBIG, G., WELTLE. D. The influence of passive smoking on
pulmonary function: A study of 1351 office workers. Preventive Medicine 13(6):656-
669, November 1934.

KNOTH, A., BOHN, H., SCHMIDT, F. Passiv rauchen als Lungenkreb&Jrsache bei
Nichtraucherinnen [passive smoking as a causal factor of bronchial carcinoma in
female nonsmokers]. Meclizinische Klinik 73(2):66-69, February 11983.
KOO, L.C., HO, J.H.C., LEE, N. An analysis of some risk factora for lung cancer in
Hong Kong. InternationaL Journal of Cancer 35(2):149-156, February 15,1986.
KOO, L.C., HO, J.H.C., SAW, D. Active and passive smoking among female lung
cancer patients and controls in Hong Kong. JownaZ of ExperimentuZ and Clinical
Cancer Research 4.(2):367-375, October-December 1983.
KOO, L.C., HO, J.H.G., SAW, D. Is passive smoking an added risk factor for lung
cancer in Chinese women? Journal of ExperimentaZ and CZiniuzl Cancer Reseamh
3(3):277-233, JuIy-September 1984.

KORNEGAY, K.R., KASTENBAUM, M.A. Non-smoking wives of heavy smokers have
a higher risk of lung cancer. (letter). British Medical JoumuZ 283(6296)z914,
October 3,198l.

KRAEMER, M.J., RICHARDSON, M.A., WEISS, N.S., FURUKAWA, C.T., SHAPIRO,
G.G., PIERSON, W.E., BIERMAN, C.W. Risk factors for pemistent middle
effusions: Otitis media, catarrh, cigarette smoke expcsure, and atopy. Jownul of
the American Medical Association 249(8):102%1OzS, February 25,1983.
LEBOWITZ, M.D. Environmental tobacco smoke: 3.3. The effects of environmental
tobacco smoke exposure and gas staves on daily peak flow rates in asthmatic and
non-esthmatic families. Eumvean Journal of Respimtory Diseases WSuppl.

                                . -
x%3):90-97,1984.

LEBOWITZ, M.D., ARMED, D.B., KNUDSON, R. The effect of passive smoking on
pulmonary function in children. Environment IntemationaZ 8(1-6):371373,1982.
LEBOWITZ, M.D., BURROWS, B. Respiratory symptoms related to smoking habits of
family adults. Chest 69(l):-, January 1976.

113


m, PH. No~~o&J wives of heavy emokera have a higher rick of lung cancer.
(letter). ~ritkh Medical Journal 283@304):1465-1466, November 28,198l.
LEE, P.N. pa&-e making. (letter). Lund 1(8276):791, April 3,1982a.
LEE, P.N. Passive emoking. Food and Cosmetics TaricorogV 200:~229, April
198213.

m P.N. Lifetime passive smoking and c8z1cer risk. (letter). lhzcet 1@443):1444,
June 22,1985.

LEE, P.N., CHAMBERLAIN, J., ALDERSON, MR. Relationehip of pee&e smoking to
risk of lung cancer end other smoking associated dkasea. Britiuh Journal of
Cancer 54(1)97-105, July 1986.

mm &It., CORIMIU, R.T., IRWIG, LX, HOLLAND, W. W. Influence of family
f&m on asthma end wheezing during the first five years of life. British Jm
ofI+ecmtiw and Soeid Medicine 30(4):2X%218, December 1976a.
LEEDER, S.R., CORKHILL, R.T., IRWIG, L.M., HOLLAND, W.W. Influence of family
facto= on the incidence of lower respiratory illneea during the fir& yeer of life.
British Journal of l+eventive and Social Medicine 30(4):203-212, December 1976b.
LEEINERT, G. Roundtable Mon. Arvmtiw Medicine 13(6):73&746, November
1984.

lSXCHEN, ML., SAMET, J.M. An aeewsment of the validity of queetionnaire
reapom provided by a surviving spouse. American Journal of Epidemiology
123(3):461-, Merch 1986.

LIM, T.P.K. Airway obstruction among high school students. American Review of
Respiratory Disease 108(4):985-988, October 1973.
MacDONALD, E.J. Nonsmoking wives of heavy smokers have a higher tik of lung
cancer. (letter). Britiuh Medical Journal 283@296):917, October 3,198la
MacDONALD, E.J. Nonemoking wives of heavy smoke= have a higher rick of hmg
cancer. Oetter). Britbh Medical Journd 283(6304):1465, November 28,198lb.
MANNING, M.D., CARROLL, B.E.. Some epidemiological especta of leukemia in
children. Jownal of the National CIuwer Institute 19(6):1087-1094, December 1957.
m, N. Nonsmoking wives of heavy smokers have a higher rick of lung center.
OetW. British iU&.cal Joumd 283(6296>914-915, October 3,198l.
MANTEL, N. Pee&e smoking in adulthood and cancer risk. &ztter). American
Journal of &idemioL+y 123(2):367368, February 1986.
MARTINEZ, F., ANTOGNONI, G.. MACRI, F., LEBOIVITZ, M., RONCHEXTI, R.
Distribution of bronchial reqoneiveneae to a constrictive drug in a random
pediatric population sample. (abetract). American Review of Respimtory Disease
13X4, part 2U242, April 1985.
UmuKuRA, S., HAMADA, H., SEINO, Y., MURANAKA. H., HIGASHI, E. Peesive
smoking. (letter). New E&and Journal of Medicine 312(11):72&721, March 14,
1985.

~l--U'Rh S., TAMINATO, T., IUTANO, N., SEINO, Y., HAMADA, H.,
UCHMASHI, M., N-, H., HIRATA, Y. Effects of environmental tobacco
mde on UrinarJr cotinine excretion in nonemokem: Evidence for passive smoking.
New England Jownal of i%dicine 311(132828-8%X, September n, 1984.
MaNNOCH& KM., ROGHMANN, K.J. Bronchiolitis as a possible cauee of
wheezing in hildhood: New evidence. Pediutrics 74(1):1-10, July 19&Q.
MdMJNOCH?TE, KM., ROGm, K.J..Predicting clinically s-cant lower
=PhtQrY tract illmsa in childhood following mild bronchiolitis. American
J~wd of Diseases of Children 139(6):625-631, June 1985.
MURRAY, A.B., MORRISON, B.J. The effect of cigerette smoke from the mother on
tmmhid reeponsiveneee and severity of symptoms in children with esthma.
Jow~l of Allergy and Clinical Immunology 77(4):675-581, April 1986.
NATIONAL ACADEMY OF SClENCES. Risk Assessment in the Fedeml Government:
Maw&g he Jhws. Washington, D.C., National Academy Press, 1983.

114


NEUTEL, C.I., BUCK, C. Effect of smoking during pregnancy on the risk of center in
children. Journal of the National Cancer Institute 47(459-63, July 1971.
O'CONNOR, G., WEISS, S.T., TAGER, I., SPEIZER, F.E. The effect of passive smoking
on nonspecific bronchial responsiveneee in a population sample of chiIdren and
young adults. (abstract). CZinicaZ Reseaxh 34(2):581A, April 1986.
PATHAK, DR, SAMET, J.M., HUMBLE, C.G.. SKIPPER, B J. Determinanta of lung
cancer risk in cigarette smokers in New Mexico. Journal of the Natiorud Cancer
Institute 76(4):597X)4, April 1986.

PEDREIRA, F.A., GUANDOLO, V.L., FEROLI, E.J., MELLA, G.W., WEISS, I.P.
Involuntary smoking and incidence of respiratory illness during the first year of
life. Pediatrics 75(3):594-597, March 1985.
PERSHAGEN, G., ZDENEK, H., SVENSSON, C. Passive smoking and lung cancer in
Swedish women. American Journal of Epidemiology, in press.
PETERS, J&I., FERRIS, B.G., Jr. Smoking, puhnonary function, and reepiratory
symptoma in a college-age group. American Review of Respiratory L&ease
95(5):774-782, May 1967.
PICKLE, L.W., BROWN, L.M., BLOT, W.J. Information available from surrogate
respondents in casecontrol interview studies. American Journd of Epidemidgy
118(1):99-108, July 1983.

PIMM, P.E., SILVERMAN, F., SHEPHARD. R.J. Physiological effects of acute passive
exposure to cigarette smoke. Archives of Environmental Health 33(4):201-213,
July-August 1978.

PITTENGER, D.J. Passive smoking. Oetter). New England Journul of Medicine
312(11):720, March 14,1985.

PRESTON-MARTIN, S., YU, MC., BENTON, B.. HENDERSON, B.E. N-nitroso
compounds and childhood brain tumors: A casecontrol study. Cancer Reseamh
42(l2):6240-5245, December 1982.

PULLAN, C.R., HEY, E.N. Wheezing, asthma, and pulmonary dysfunction 10 years
after infection with respiratory syncytiaI virus in infancy. British Medical Joumul
284(6330):166&1669, June 5,198Z.

PUKANDER, J., LUOTONEN, J., TIMONEN, M., KARMA, P. Risk facto= affecting
the occurrence of acute otitia media among 2-3-yearold urban children. Acta W
ZaryngoZiw 100@4):260-265, September-October 1985.
RANTAKALLIO, P. Relationship of maternal smoking to morbidity and mortaiity of
the child up to the age of five. Acta Paediatrica Scandinavica 67(5)621631,
September 1978.

RAWBONE, R.G., KEELING, C.A., JENKINS, A., GUZ. A. Cigarette smoking among
secondary school children in 1975: Prevalence of respiratory symptoms, knowledge
of health hazards, and attitudes to smoking end health. Journal of Epidemiology
and Community Health 32(1):53-X$ March 1978.
REPACX, J.L., LOWREY, A.H. A quantitative e&mate of nonsmokers' lung cancer
risk from passive smoking. Environment InternationaI 11(1X3-22,1985.
ROBINSON, B.F. Effects of passive smoking. getter). New England Joumd of
Medicine 299(16):896, October 19,1978.

RUSH, D. Respiratory symptoms in a group of American secondary echo01 students:
The overwhelming association with cigarette smoking. International Journal of
Epidemidogy 3(2):153-X5, June 1974.

RUSSELL, M.A.H., FEYERABEND C. Blood and urinary nicotine in nonsmokers.
Lumet 7990(1):179-181, January 251975.
RUSSELL, M.AH., JARVIS, M.J., WEST, R.J. Use of urinary nicotine concentration
to estimate exposure and mortality from passive smoking in non-smokers. British
Jownul ofAddiction 81:275-281,1986.

RUTSCH, M. Non-smoking wives of heavy smokers have a higher risk of lung cancer
(letter). British Medical Journd 2%X6269):936, March 21,198l.

11:


SAG, D.L. B& h analptic reeeamh. Journal of Chronic Dkeaeee 32(1-a61-63,
  1979.

SAID, G., ZALOKAR, J., LELLOUCH, J., PATOIS, E. Parental smoking related to
&n&j&,omy and tonsillectomy in ~hildt~~ JOUITUI~ of Epidemiology and
Community He&h 32(2)97-101. June 1973.
SALCGJEE, Y., VESEY, C.J.. COLE, P.V., RUSSELL, M.A.H. Carhoxyhemoglobin
~dp~mathiocyanate:~rnplemen~indicatorsOfSmO~behaviour?Thomr
37(7):521-525, July 1932.

SAMET, JM., TAGER LB., SPEIEER, FE. The reIation8hip between respiratory
fia h CM&,& and chronic air-flow ohetruction in aduhhood. Am&am
Review of Respimtov LXeeaee 127(4X--=% April 1983.
SANDIER, D-P., EVERSON, R.B., WILCOX, AJ. Passive smoking in adulthood and
cancer r+k. Am&can Jownal of Epidemiology 121(1):37-48, January 1935.
smq D.P., EVERSON, R.B., WILCOX, A. J. Passive smoking in aduhhood end
cancer risk. getter). A merican Journal of Epidemiology 123(2):369-370, Fehruary
  1988.

SANDIER, D.P., EVERSON, R.B., WILCOX, A.J., BROWDER, J.P. Cancer ri& in
&&hood from early life exposure to parents' smoking. American Journal of
Public Hwlth 75(5):487-&Z, May 1935.

SANDLER, DP., WILCOX, AJ., EVERSON, R.B. cumulative effects of I&time
passive smoking on cancer risk. Lam-et 1(3424):312314, February 9,198sa
MNDLER, D.P., WILCOX, A-J., EVERSON, R.B. Lifetime passive smoking and
cancer risk. (letter). Lancet 1@433~:857, April 13,1985b.
W, MB., SAMET, J.M., SPEZER, F.E. Effect of cigarette tar content and
smoking habits on respiratory eymptoma in women. American Review of Reepim-
tory Disease 125(6):634-699, June 1932.

ScHENKFlR. M.B., SAMEI', J.M., SPEWER, F.E. Risk factors for childhood re~pira-
tory dkae The effect of host factora and home environmental expomuea
American Review of Reepimtory Disease 1!23(6):1036-1043, December 1933.
8CHIIUNG, R.S.F., LETAI, A.D., HUI, S.L., BECK, G.J., SCHOENBERG, J.B.,
BOUHUYS, A.H. Lung function, respiratory disease, and smoking in families.
American Journal of Epidemialogv 106(4):274-2X& October 1977.
SCHLESSELMAN, J.J. Case-Cbnbul Studies: Design, Conduct, Analysis. Monographs
in Epidemiol~ and Biostatistics, Vol. 2. New York, Oxford University Press,
  1932.
SCHMELTZ. I., HOFFMANN, D., WYNDER, E.L. The infiuence of tobacco smoke on
indoor atmoephereez I. An overview. Prcucntiue Medicine 4(1):66-32, March 1975.
SRELY, J.E., ZUSKIN, E., BOUHUYS, A. Cigarette smokingz Objective evidence for
lung damage in teenagers. Science 172(3934):741-743, May 14,197l.
SBEPHARD, R.J., COLLINS, R., SILVERMAN, F. `*Paggiye" exposure of asthmatic
subjecta to cigarette smoke. Environmental Research 200:392-402, December
  1979.
SIMS, D.G., DOWNHAM, M.A.P.S., GARDNER, P.S., WEBB, J.K.G., WEIGHTMAN,
D. Study of Syearold &i&en with a &tory of respiratory ~yncytiaI virue
bronchiolitis in infancy. Bi-ittih dfedicol J0um1 1(6104):11-14, January 7, 1978.
SPEIZER, FE., FERRIS, B., Jr., BISHOP, Y.M.M., SPENGLER, J. Reapiiatory d&!aee
rates and pulmonary function in children associated with NO, exposure. American
Review of Reepimtory Disease 121(1):3-10, January 1980.
SPEIEER, F.E., TAGER, I.B. Epidemiology of chronic mucus hypersecretion and
obstructive airways disease. Epidemiologic Reviews 1:124-142,1979.
=`INAcI, S., ARGSSA, W., BURGIANI, M., NORTALE, P., BUCCA, C., DeCGNDUS
SION. E. The effects of air pollution on the respiratory health of chikirem A cram-
sectional study. Pediatric Pdm~n~logy 1(5):26%266,1935.
STERLING, T.D. Nonsmoking wives of heavy smokers have a higher risk of lung
cancer. Oetter). British Medical Journal 232(6270):1156, April 4,193l.

116


STEWART, A., WEBB, J., HEWITT, D. A survey of childhood malignancies. British
Medical Journal 59@6):149&1508, June 18,1958.
STJERNFELDT, hf., BERGLUND, K., LINDSTEN, J., LUDVIGSSON, J. Maternal
smoking during pregnancy and rink of childhood cancer. Lancet 1(8494):1359-1352,
June 14,1986.

STGBER, W. Lung dynamics and uptake of smoke constituents by nonsmokers: A
survey. Preventive Medicine 13(6X589-661, November 1984.
SUTTON, G.C. Passive smoking and lung cancer. (letter). British bfcdiciul Joumul
282(6266):733, February 28.1981.

SVENDSEN, K.H., KULLER, L.H., NRATON, J.D. Effecta of passive smoking in the
Multiple Riik Factor Intervention Trial (MBFlT). Cimuhtion, Part H, No. 4,
October 1985.

TAGER, I.B. Passive smoking and reepiratory health in children: Sophistry or carwe
for concern? Ameria n Review of Respimtory D&use 133(6):959-961, June 1986.
TAGER, I.B., MUNOZ, A., ROSNER, B.. WEISS, S.T., CAREY, V., SPEIZER, F.E.
Effect of cigarette smoking on the pulmonary function of children and adolescents.
American Review of Reepimtory Disease 131(5):75%759, May 1985.
TAGER, LB., WEISS, S.T., MUNOZ, A., ROSNER, B., SPEIZER, F.E. Longitudinai
study of the effects of maternal smoking on pulmonary function in children. New
England Journal of Medicine 309(12):699-763, September 22,1983.
TAGER, LB., WEISS, S.T., ROSNER, B., SPElZER, F.E. Effect of parental cigarette
smoking on the pulmonary function of children. American Journal of Epidemiolo-
gy 119(1):1&26, July 1979.

TASHKIN, D., CLARK, VA., SIMMONS, M., REEMS, C., COULSON, A.H.,
BOURQUE, L.B., SAYRE, J.W., DETERS, R, ROKAW, S. The UCLA population
studies of chronic obstructive respiratory dieease: 7. Relationship between perenta
smoking and children's lung function. American Review of Reepimtory LXaeaa
X%X6):891-897, June 1984.

TRICHOPOULOS, D. Pamive smoking and lung cancer. (ietter). Lancet 1(8378):684,
March 24,1984.
TRICHOPOUIDS. D., KALANDIDI, A., SPARROS, L. Lung cancer and passive
smoking. Conclusion of Greek study. (letter). Lancet 2@351):677678, September
17.1983.
TRICHOFOULUS, D., KALANDIDI, A., SPARROS, L., MacMAHON, B. Lung cancer
and passive smoking. Internationul Journd of Ckzncer 27(1):14, January 15,198l.
TSOKOS, C.P. NonamoLiag wives of heavy smokem have a higher risk of lung cancer.
(letter). Britih Me&calJoumuZ 283(6364):146-+1465, November 28.1981.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE. Smoking and
He&k A Rty& of the Surgeon GenemL DHEW Pub. No. @`HS)79-59066. U.S.
Department of Health, Education, and Welfare, Public Health Service, OHice of
the Am&ant Secretary for Health. Of&z-e on Smoking and Health, 1979.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Conse-
quencee of Smoking for Women A Report of the Surgeon Geneml . U.S. Department
of Health and Human Servim, Public Health Service, Office of the Assistant
Secretary for Health, Office on Smoking and Health, 1980.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Conee-
quences of Smoking: Cancer. A Report of the Surgeon GenemL DHHS Pub. NO.
(PHS)82-59179. U.S. Department of Health and Human Services, Public Health
8ervice, Office of the Assistant Secretary for Health, Office on Smoking and
Health, 1982.

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Conse-
quences of Smoking: Car&ovas~ular Disease. A Report of the Surgeon GenemL
DHHS Pub. No. (PHS)84-50264. U.S. Department of Health and Human Service%
Public Health Service, Ofike of the Assistant Secretary for Health, OEce on
Smoking and Health, 1983.

117


U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Cbnee-
qmmm of Smoking Chronic Obstructive Lung Disease. A Report of the Surgeon
&TUZ~Z. DHHS Pub. No. o&dso295. US. Department of Heaith and Human
Services, Public Health Service, Office of the Ass&ant Secretary for Health, OfSce
on Smoking and Health, 1984.

U.S. PLJRLIC HEALTH SERVICE. Smoking and Health. Report of the Advieoory
Committee to the Surgeon GenemI of the F'ublic He&h Service. PHS Pub. NO.
1103. U.S. Department of Health, Education, and Welfare, Public Health Service,
Centers for Disesse Control, 1964.
VAN STRENSELMOLL, H.A., V ALRENBURG, H.A., VANDENBROUCKE, J.P. Are
maternal fertility problems related to cbildbood leukaemia? IntemutionaZ Journal
of Epidemiology 14(4):555-559, December 1985.
VEDAL, S., SCHENKER, M.B., SAMET, J.M., SPEIZER, F.E. Risk factors for
chiMhocd respiratory disease: Analysis of pulmonary function. American Review
of Respiratory Dkeaae 139(2):187-192, August 1984.
VUTUC, C. Quantitative aspects of passive smoking and lung cancer. Prewntiuc
Medicine 13(6):698-794, November 1984.

WAlTE, C.L. Effects of passive smoking. oetter). i&w En&and Journal of Medicine
299(16):897,0&&x 19,1978.

WAKRHAN, H. Effects of passive smoking. (letter). New England Journnl of Medicitae
299(16):896, Octcber 19,1978.

WALD, N.J., BOREHAM, J., BAILEY, A., RITCHIE, C., HADDOW, J.E., RNIGHT, G.
Urinary c&nine as marker of breathing other people's tobacco smoke. getter).
Lancet 1@370):239-231, January 28,1984.
WALD, NJ., IDLE, M., BOREHAM, J., BAILEX, A. Carbon monoxide in breath in
relation to smoking and carboxyhaemoglobm levels. !l7wmx 36(5):366-369, May
1981.
WALL4 N.J., RITCHIE, C. Validation of studies on lung cancer in nonsmokers
married to smokers, getters). Lancet 1(8385):1067, May 12,1984.
WALTER, S., NANCY, N.R., COLLIER, C.R. Changee in forced expiratory ~pirogram
in YOUUJ male smokers. American Review of Respimtov Disease 1X3(5):717-724
1974.

WARE, J.H., DOCKERY, D.W., SPIRO, A. III, SPEIEER, F.E., FERRIS, B.G., Jr.
Passive SmOking, gas cooking, and respiratory health of children living in six cities.
American Review of Respimtvry Dieeaee 129(3):366474, March 1984.
=EWER, S.E., WEISS, S.T. Puhnonary d&ases. bx Burrow, G.N., Ferris, T.F.
(A). Medical Complications During Rugnon~y. 2nd ed. Philadelphia, W.B.
Saunders, 1981, pp. 465-4~.

WEI% ST., TAGER, LB., MUNO& A., SPELZER, F.E. The relationship of respiratory
infections in early childhood to the occurrence of increased levele of bronchial
responsiveness and atopy. A
April 1985.       merican Review of Respimtory D&use 13X4):573-578,

mm, S-T., TAGER, LB., SPEIZER, F.E., ROSNER, B. Persistent wheeze: Its relation
~ZJJ ~Piramry i)biesa, cigarette smoking, and level of pulmonary function in a
population -pie of children. American Review of Reepimtory Disease 122(5X697-
707, November 1980.

WHIT& J-R., FROEB, H.F. Small-airways dysfunction in nonsmokers chronically
exposed ta tobacco smoke. New England Jouma[ of Medicine 392(13):720-723,
March 27,198O.

-MO% A., ALTSHULER, B. Lung cancer incidence in cigarette smokers:
Further adysis of Doll and Hill% data for British physicians. Biometrics
32(4:805-816, December 1976.

mD-3 I-W., MAHLER, D.A., LGRE J., VIRGULTO, J.A., SNYDER, P.,
=mY, R.A. Acute effecta of passive smoking on lung function and airway
r~~ivity in asthmatic subjects. Chest 890:180-185, February 1986.

118


WOOLCOCK, A.J., PEAT, J.K., LEEDER, S.R., BLACKBURN, C.R.B. @de.). The
development of lung function in Sydney children: Effecta of respiratory illness and
smoking. A ten year study. European Joumul of Be8pimtoz-y Diseases 65(Suppl.
132):1-137,X%

WLJ, A.H., HENDERSON, B.E., PIKE, M.C., YU, M.C. Smoking and other risk factora
for lung cancer in women. Journal of the National Cuncer Institute 74(4):747-751,
April 1985.
WYNDER, E.L., HOFFMANN , D. Tobacco and Tobacco Smok Studk in &perimen-
tal Cancinogeneais. New York, Academic Press, 1967.
WYNDER, E.L. STELLMAN, S.D. Comparative epidemiology of totirelated
caners. Cancer Research 37(12):4608-%22, December 1977.
YARNELL, J.W.G., ST. LEGER, A.S. Respiratory illness, maternal smoking habit and
lung function in children. British Joumal of Diseases of the Chest 79(3)%&236,
July 1979.

119


CHAPTER 3

ENVIRONMENTAL TOBACCO
   SMOKE CHEMISTRY
         AND
EXPOSURE OF NONSMOKERS


CONTENTS

Introduction
Laboratory Smoking
  Human Smoking

Sidestream Smoke
  Formation and Physicochemical Nature
  Chemical Analysis

Radioactivity of Tobacco Smoke

Environmental Tobacco Smoke

Comparison of Toxic and Carcinogenic Agents in Main-
stream Smoke and in Environmental Tobacco Smoke

Number and Size Distribution of Particles in Environ-
mental Tobacco Smoke

Estimating Human Exposure to Environmental Tobacco
Smoke

Time-Activity Patterns
Temporal and Spatial Distribution of Smokers

Determinations of Concentration of Environmental
Tobacco Smoke

Microenvironmental Measurements of Concentration
Monitoring Studies

Conclusions

References

123


Introduction

The physicochemical nature of environmental tobacco smoke
(ETS) is governed by the type and form of the tobacco product or
products burned, by the prevailing environmental conditions, and by
secondary reactions. Mainstream smoke (MS) is the complex mixture
that exits from the mouthpiece of a burning cigarette, cigar, or pipe
when a puff is inhaled by the smoker. Sidestream smoke (SS) is
formed between puff-drawings and is freely emitted into the air
surrounding a smoldering tobacco product. Sidestream smoke repre-
sents the major source for ETS. The exhaled portions of MS and the
vapor phase components that diffuse through the wrapper into the
surrounding air constitute minor contributors to ETS.

In the scientific literature, the terms "passive smoking," "involun-
tary smoking," and "inhalation of ETS" are frequently used inter-
changeably (US DHEW 1979; US DHHS 19821964).

Laboratory Smoking

Data on the composition of MS and SS originate from laboratory
studies. For such studies, cigarettes, cigars, or pipes are smoked by
machines under standardized reproducible conditions. It is a major
goal of these measurements to compare the yields of the specific
components in the MS or SS or both of a variety of experimental or
commercial tobacco products and to simulate, though not to repro-
duce, human smoking habits. The most widely used standard
conditions for machine smoking cigarettes and little cigars (5 1.5 g)
are one 35 mL puff of 2-second duration drawn once a minute to a
butt length of 23 mm, or the length of the filter tip plus the over-wrap
plus 3 mm (Brunnemann et al. 1976). The annual reports of the U.S.
Federal Trade Commission on the tar, nicotine, and carbon monox-
ide content of the smoke of U.S. commercial cigarettes are based on
these laboratory smoking conditions. For cigars, the standard
smoking conditions are a 20 mL puff of l&second duration taken
once every 40 seconds, and a butt length of 33 mm CInternational
Committee for Cigar Smoke Study 1974). The most frequently used
pipe-smoking conditions call for the bowl to be filed with 1 g of
tobacco and a 50 mL puff of l-second duration to be taken every 12
seconds (Miller 1964).

A number of devices for collecting sidestream smoke have been
developed (Dube and Green 1982). The most widely used device is a
collection apparatus made of glass and cooled by water circulating
through an outer jacket. The air entering the chamber through a
distributor has a flow rats of 25 mL per second (1.5 L/min)
(Brurmemann and Hoffmann 1974). Under these conditions, the
yields of mainstream smoke components from a cigarette approxi-
mate those obtained from the same cigarette when it is being smoked

125


in the open air. However, the velocity of the airstream through the
chamber has considerable influence on the yields of individual
compounds in SS (Klus and Kuhn 1982).
To collect the particulate phase of MS and SS, the smoke aerosols
are passed through a glass fiber filter (a Cambridge filter with a
diameter of 45 mm) that traps more than 99 percent of all particles
with a diameter of at least 0.1 pm (Wartman et al. 1959). The portion
of the smoke that passes through the glass fiber filter is arbitrarily
designated as vapor phase, although it is realized that this separa-
tion does not fully reflect the actual physicochemical conditions
prevailing in MS and SS. For the analysis of individual components
or a group of components, specific trapping devices and methods
have been developed (Dube and Green 1982).

Human Smoking

The standardized machine-smoking conditions used in the tobacco
laboratory were set up to simulate the parameters of human
smoking as practiced 30 years ago. The examination of current
smoking practices suggests that machinesmoking conditions no
longer reflect current practices. Human smoking patterns depend on
a number of factors, one of which is the delivery of nicotine.
Do&retry of smoke constituents has shown that low nicotine
delivery (~0.6 to 1.0 m&cigarette) generally induces the smoker to
draw larger puff volumes (up to 55 mL per puff), to puff more
frequently (three to five times a minute), and to inhale more deeply
(Heming et al. 1981). Furthermore, many smokers of cigarettes with
perforated filter tips tend to obstruct the holes in these tips by
pressing their lips around them; thus, they inhale more smoke than
would he expected according to the machine-smoking data (Kozlow-
ski et al. 1960). Smokers of cigarettes with a longitudinal air channel
in the filter tip compress the tip in a similar manner so that the
mainstream smoke delivery is increased over that measured with the
laboratory methodology (Hoffmann et al. 1983).
These deviations from machin~moking patterns cause a greater
ammt of tobacco to be consumed during MS generation. Conse
quently, the quantity of tobacco burned between puffs is diminished,
and lower amounts of combustion products are released as SS.
Because of the proximity to the burning tobacco product, the active
smoker usually inhales more of the SS and ETS than a nonsmoker.
It is not known to what extent the different constituents of inhaled
ETS aerosols can be retained in the respiratory tract of nonsmokers.
Studies with MS have shown that more than 90 percent of the
volatile, hydrophilic components are retained by the smoker @al-
hamn et al. 1968a) and that less than 50 percent of the volatile,
hydrophobic MS components are retained by the smoker (Dalhamn
et al. 196813). On the basis of these data, it may be assumed that the

126


passive smoker retains a high percentage of the vapor phase
components of ETS and significantly less of its hydrophobic volatiles.

Sidestream Smoke

Formation7 and Physicochemical Nature

When nonfilter cigarettes are being smoked under standardized
conditions, approximately 45 percent of the tobacco column is
consumed during the generation of MS (puff-drawing), whereas the
remainder is burned between puffs and under conditions of a
strongly reducing atmosphere. In addition, MS and SS is generated
at distinctly higher temperatures than SS (Wynder and Hoffmann
1967). Thus, undiluted SS contains more tobaccoderived combustion
products than does MS, and contains especially greater quantities of
those combustion products that are formed by nitrosation or
amination. Consequently, the composition of SS differs from that of
MS.

The SS of a smoldering cigarette enters the surrounding atmo-
sphere about 3 mm in front of the paper burn line, at about 350" C
(Baker 1984). In Table 1, the MS and the SS from nonfilter cigarettes
are compared. Under standardized conditions, the formation of the
MS of a nonfilter cigarette (80 mm, 1,230 mg) is completed during 10
puffs, requires 20 seconds, and consumes 347 mg of tobacco. The
formation of SS from the same cigarette during smoldering requires
550 seconds and consumes 411 mg of tobacco (Neurath and Horst-
mann 1963).

The pH of the MS of a blended U.S. cigarette ranges from 6.0 to 6.2
and the pH of SS, from 6.7 to 7.5. Above pH 6, the proportion of
unprotonated nicotine in undiluted smoke rises; at pH 7.9, about 50
percent is unprotonated. Therefore, SS contains more free nicotine
in the vapor phase than MS. The reported measurements of the pH
of cigars were 6.5 to 8.5 for MS and 7.5 to 8.7 for SS; measurements
for the pH of SS from pipes have not been published (Brunnemann
and Hoffmann 1974).

Chemical Analysis

In order to establish reproducible chemical-analytical data, ciga-
rette SS is generated in a special chamber. This assures that the
cigarettes burn evenly during puff intervals when an air-stream at a
velocity of 25 mL per second is drawn through the chamber. At this
flow rate in the chamber, MS generation is quantitatively similar to
that measured without the SS chamber (Neurath and Ehmke 1964;
Brunnemann and Hoffmann 1974; Dube and Green 1982). Through-
out this chapter the data refer primarily to MS, SS, and ETS
deriving from cigarettes and not from cigars or pipes, because

127


TAEJLE l.-Comparison of mainstream smoke (MS) and
     sidestream smoke (SS) of a nonfilter cigarette:
     Some physicochemical data

Study                    Parameter3              MS       ss

Neurnth and Horstmarm  Duration of emoke production (see)          20       660
`1963)           Tobaccn burned (m&             347      411

ynder end Hofhann   Peak temperature dm formation ("`3     a900      a600
367)

Brunnemann and
HoEman (1974)

pHoft&alaemi3ol

a-6.2     6.7-75

sceSaellati-SfOlZOlhli
and Savino WE6)

Number of partiolen per ckareW1      10.6 x 10"   36 x 10"

Carter and Haqawa
(1975); Hiller et al.
m82)

Particle s&a cnm)'
Particle meau diameter (rut91

0.1-1.0     0.01-0.8
0.4       0.32

Wynder and Hoffinann   Smoke dilution (~01 %I'
(I967); K&b and
Derrick wo);        carbon momxide                  3-S       2-3
B&or (1964);
Hoffmann, Bnmnemann    carbon dioxide                  6-11       4-6
et al. w34)                                   1!&16      1.6-2

cigarette smoke is the major source of EYE3 in public places. Few data
are available on the SS and ETS from cigars and pipes.
About 300 to 400 of the several thousand individual compounds
identified in tobacco smoke have been quantitatively determined in
both mainstream and, sidestream smoke. A listing of selected agents
iu the MS of nonfilter cigarettes with their reported range of
concentration and their relative ratio of distribution in SS compared
&ith MS is presented in Table 2. Values greater than 1.0 reflect the
greater release of a given compound into SS than intO MS. The
grouping of the compounds in Table 2 into vapor phase components
and particulate phase constituents refers to the makeup of MS, but
does not represent the physicochemical distribution of these corn-
pounds in SS. Some of the volatile compounds in MS and SS are
compared. On the basis of the amount of tobacco burned in the MS
and SS of a nonfilter cigarette (see Table 11, the ratio of SS to MS
should be 1.2 to 1.5 if the combustion conditions during both phases
of smoke generation were comparable. However, this is not the case,

128


as is indicated by the higher SS to MS ratios for carbon monoxide
(2.5-4.7), carbon dioxide W-11), acrolein (3-15), benzene (IO), and
other smoke constituents.

The high yield of carbon monoxide and carbon dioxide in SS
indicates that more carbon monoxide is generated during smoldering
than during puff-drawing. After passing very briefly through the hot
cone, most of the carbon monoxide gas in both MS and SS is oxidised
to carbon dioxide, most likely owing to the high temperature
gradient and the sudden exposure to environmental oxygen upon
emission.,

The higher yields of volatile pyridines in SS compared with MS are
probably caused by the preferred formation of these compounds from
the alkaloids during smoldering (S&melts et al. 1979). In contrast,
hydrogen cyanide (HO is primarily formed from protein at
temperatures above 700" C (Johnson and Kang 1971), and the
smoldering of tobacco at about 690" C does not yield the pyrosynthe-
sis of HCN to the extent that it occurs at the higher temperature
present during MS generation. The very high levels of ammonia,
nitrogen oxide, and the volatile N-nitrosamines in SS compared with
the levels in MS is striking. Studies with `6N-nitrate have under-
scored that the burning of tobacco results in the reduction of nitrate
to ammonia, and that the latter is released to a greater extent during
SS formation than during puff-drawing (Johnson et al. 1973). In a
blended cigarette, this higher level of ammonia in SS causes its
elevated pH to reach levels of 6.7 to 7.5, while the pH of MS is about
6 (Brunnemann and Hoffmann 1974).

The increased release of the highly carcinogenic volatile N-nitrosa-
mines into SS (20 to 100 times greater than into MS) has been well
established (Brunnemann et al. 1977). The carcinogenic potential of
SS may also be affected by the levels of the oxides of nitrogen (NO=).
Four to ten times more nitrogen oxide (NO) is released into the
environment in sidestream smoke than is inhaled with the main-
stream smoke. The smoker inhales more than 95 percent of the NO,
in the form of NO, and only a small portion is oxidized to the
powerful nitrosating agent nitrogen dioxide (NOa). Only a fraction of
NO is expected to be retained in the respiratory system of smokers
by being bound to hemoglobin. The NO, gases released into the
environment are partially oxidized to NO, (Vilcins and Lephardt
1975). Therefore, sidestream smoke-polluted environments are ex-
pected to contain the hydrophilic nitrosating agent NO,.
Data for particulate matter and some of its constituents in MS and
SS are also listed in Table 2. The release of tobacco-specific N-
nitrosamines into SS is up to four times higher than that into MS.
Whether the distribution of these agents in the vapor phase and the
particulate phase of SS is of major consequence with respect to the
carcinogenic potential of SS needs to be determined. It is equally

129


t;
0  TABLE `lo-Distribution of constituents in mainstream smoke (MS) and the ratio of sidestream smoke
       @X3) to MS of noufilter cigarettes

Vapor phase constituents '

MS            SS/MS
range            ratio

Particulate phase constituents'

MS
range

SSIMS
ratio

Carbon monoxide

Carbon dioxide

Carbonyl sulfide

Benzene '

Toluene

Formaldehyde

Acroiein

Acetone

Pyridine
SMethylpyridine
S-Vinylpyridine
Hydrogen cyanide
Hydrazine '

Ammonia

Methylamine

Dimethylamine

Nitrogen oxide

10-23 mg          2.5-4.7

20-40 mg           a11

16-42 pg          0.03-0.13

12-46 pg            10

160 PET             6

70-100 Ilg          o.k&O

6&m I%          8-16

1w250 pg           2-6

16-40 PB           6.5-20

12-36 p.g           3-13

11-30 w          CD-40

4-w         0.1-0.25

32 ng            3

50-130 pg          40-170

11.5-28.7 pg         4.2-6.4

7.610 pg          3.7-5.1

1-W          4-10

Particulate matter *

Nicotine

Anatabine

Phenol

C&echo1

Hydroquinone

Aniline

2-Toluidine

2-Naphthylamine*
4-Aminobiphenyl *
Benz[a]anthracene'
Benzo[a]pyrene s

Cholesterol

y-Butyrolactone'
Quinoline I

Harman

N!-Nitrcsonornicotine'

15-4a mg          1.3-1.9
l-Z.5 mg         2.6-3.3
2-%l%          <0.1-0.6

60-140 pg          1.6-3.0
1-w         0.60.9
110-300 pg         0.749

3130 w            30

160 ng            19

1.7 ng            30

4.6 ng            31

2C-70 ng           2-i

20-W          2.5-3.6

22 w           0.9

10-22 pg          3.k5.0

0.5-2 pg           a11

1.7-3.1 w          0.7-1.7

200-3,~ ng         0.6-3


TABLE 2.-Continued

                        MS       -&SIMS                                       MS
Vapor phase constituents'                                                                           SSIMS
                       range            ratio          Particulate phase constituents'        range           ratio

N-Nitrusodimethylamine'       1040 ng          20-1cQ            NNK'                100-1,006 ng          14
N-Nitrosopyrrolidine'         630 ng           6-30           N-Nitrosudienthanolamine'         20-70 ng           1.2

Formic acid             216-490 ug          1.4-1.6           Cadmium                  100 ng            7.2

Acetic acid            33O-SlO l(g          1.9-3.6           Nickel a                 20-80 ni3          13-30

                                                   ZiiC                    624 w            6.7

                                               Polonium-210'              0.64-0.1 pCi         1.0-4.0

                                               Hensoic acid               14-28 pg         0.67-0.95

                                                 Lactic acid               63-174 Iig          0.3-0.7

                                       Glycolic acid              37-126 pg         0.6-0.96

                                               Succinic acid              110-140 pg         0.43-0.62

' Values are given far fresh and undiluted MS and SS.
*Human carcinogen (IARC 1936).
3Suspxted human carcinogen (IARC 19%).
`Animal carcinogen (IARC 1966).
SOURCE: Elliott and Rowe (1975); Hoffmann et al. (1983); Klw and Kuhn (1982); Sakuma et al. Nfl3); Sakuma, Kusama, Ysmaguchi. Mabuki et al. (1984); Sakuma. K-ma, Yamaguchi,
Sugawara (1994); Schmeltz et al. (1976).


important to examine the significance of the abundant release of
amines into SS (levels are up to 30 times higher than in MS),
indicated by the data for aniline, Ztoluidine, and the alkaloids. This
is of concern because certain amines are readily nitrosated to N-
nitrosamines. However, analytical data on secondary reactions of
amines in polluted environments are lacking.

For a meaningful interpretation of the data on the distribution of
the compounds in cigarette smoke presented in Table 2, certain
aspects of the methodology should be emphasized. First, the data are
baaed on analyses of nonfilter cigarettes that were smoked under
standardized laboratory conditions. Second, the standardized ma-
chine-smoking conditions were established according to human
smoking patterns observed three decades ago and do not reflect the
smoking behavior of contemporary smokers. This caveat applies
particularly to smoking patterns observed with filter cigarettes
designed for low smoke yields. Most consumers of these cigarettes
inhale the smoke more intensely than smokers of nonftiter cigarettes
(Herning et al. 1981; Hill et al. 1983). This change in smoking
intensity affects the delivery of the side&ream smoke. The conven-
tional filter tips of cigarettes influence primarily the yield of MS and
have little impact on SS yield. However, in the case of cigarettes with
specially designed filter tips such as perforations, the yield of SS is
also affected (Table 3) (Adams et al. 1985).

Radioactlvity of Tobacco Smoke

Naturally occurring decay products of radon are found in tobacco
and, therefore, also in tobacco smoke. These include the isotopes of
lead (Pb-2101, bismuth (Bi-210), polonium (Po210), and radon, which
originates from the decay of uranium through radium (Radford and
Hunt 1984; Max-tell 1975). Radon and its short-lived daughters (Po-
218, Pb214, Bi-214, Po214), which precede long-lived daughters in
the decay chain, are ubiquitous in indoor air and are largely derived
from sources other than tobacco smoke. Most of the radon daughters
are attached to particles in the air, but a small proportion, referred
to as the unattached fraction, is not (Raabe 1989; Kruger and
Nijthling 1979; Bergman and Axelson 1983).

It has been suggested that the presence of Pb-210 and subsequent
decay products in tobacco is dependent upon an absorption of short-
lived radon daughters on the leaves of the tobacco plant, especially
where phosphate fertilizers that are rich in radium have been used
and have caused increased leakage of radon from the ground. These
attached short-lived radon daughters then decay to long-lived Pb-210
and subsequent nuclides found in the tobacco (Fleischer and Parungo
1974; Martell 1975). However, the origin of these decay products may

132


TABLE 3.-Distribution of selected components in the sidestream smoke (SS) and the ratio of SS to
      mainstream smoke (MS) of four U.S. commercial cigarettes

components

Cigarette A            Cigarette B             Cigarette (           Cigarette D
85 mm NF               85 mm F               85 mm F              85 mm PF

ss      SWMS          ss      SSiMS          ss      SS/MS          ss     SSIMS

Tar imglgl                       22.6       1.1           24.4        1.6           20.0       2.9           14.1      15.6

Nicotine lmgigl                     4.6       2.2           4.0       2.7           3.4       4.2           3.0      20.0

C'arbon monoxide cmg/g)               28.3       2.1           36.6       2.7           33.2       3.5           26.8      14.9

Ammonia ImyJgl                   524       7.0           8Y3        46           213.1       6.3           236       5.8

(`atecho (pgtgl                    58.2       1.4           89.8        1.9           69.5       2.6           117      12.9

Benzolalpyrenv Ingig                 67       2.6           45.7        2.6           51.7       42           448      20.4

N~N~trosodlmethyumine tng/gl           735       236           597       139           611       50.4           685      167

N-Nitrosopyrrolidtne cng/g~             177       2.7           13Y       13.6           233       71           234      11.7

N -Niirosonornlcotme (ng/yi             857       0.85          307        0.63          1x5       0.68          338       5.1


also depend on the general occurrence of radon in the atmosphere
and not on the local emanation of radon (Hill 1982).

In recent years, it has been shown that relatively high levels of
radon and short-lived radon daughters may occur in indoor air, and
consistent observations in this regard have been made in several
countries (Nero et al. 1985). In the air with a very low concentration
of particles, the proportion of unattached radon daughters is
increased beyond that found with a higher concentration of particles.
The unattached daughters are removed more rapidly than those that
are attached by plating out on walls and fixtures. The addition of an
aerosol, such as tobacco smoke, increases the attached fraction,
elevates the concentration of radon daughters, and reduces the rate
of removal of radon daughters (Bergman and Axelson 1983). The
dose of a radiation received by the airway epithelium depends not
only on the concentration of radon daughters but also on the
unattached fraction and on the size distribution of the inhaled
particles. The interpIay among these factors as they are modified by
KTS has not yet been fully examined.

Environmental Tobacco Smoke

The air dilution of side&ream smoke, and of other contributors to
ETS, causes several physicochemical changes in the aerosol. The
concentration of particles in ET'S depends on the degree of air
dilution and may range from 300 to 500 mg/mg to a few p&ma. At
the same time, the median diameter of particles may decrease as
undiluted SS is diluted to form ETS (Keith and Derrick 1960,
Wynder and Hoffmann 1967; Ingebrethsen and Sears 1936). Further-
more, nicotine volatilizes during air dilution of SS, so that in ET'S it
occurs almost exclusively in the vapor phase (Eudy et al. 1985). This
is reflected in the fairly rapid occurrence of relatively high concen-
trations of nicotine in the saliva of people entering a smokepolluted
room (Hoffmann, Haley et al. 1984). Most likely there are also
redistributions between the vapor phase and the particulate phase of
other constituents in SS due to air dilution, which may account for
the presence of other semivolatiles in the vapor phase of KTS.
However, evidence of such effects needs to be established.

Comparison of Toxic and Carcinogenic Agents in Mainstream
Smoke and in Environmental Tobacco Smoke

The combustion products of cigarettes are the source of both
environmental tobacco smoke and mainstream smoke. Therefore,
comparisons of the levels of specific toxins and carcinogens in KTS
with the corresponding levels in the mainstream smoke are relevant
to an estimation of the risk of E'I'S exposure. Although KTS is a far

134


less concentrated aerosol than undiluted MS, both inhalants contain
the same volatile and nonvolatile toxic agents and carcinogens. This
fact and the current knowledge about the quantitative relationships
between dose and effect that are commonly observed from exposure
to carcinogens have led to the conclusion that the inhalation of ET'S
gives rise to some risk of cancer (IARC 1986).

However, comparisons of MS and ETS should include the consider-
ation of the differences between the two aerosols with regard to their
chemical composition, including pH levels, and their physicochemi-
cal nature (particle size, air dilution factors, and distribution of
agents between vapor phase and particulate phase). Another impor-
tant consideration pertains to the differences between inhaling
ambient air and inhaling a concentrated smoke aerosol during puff-
drawing. Finally, chemical and physicochemical data established by
the analysis of smoke generated by machine-smoking are certainly
not fully comparable to the levels and characteristics of compounds
generated when a smoker inhales cigarette smoke. This caveat
applies particularly to the smoking of low-yield cigarettes, for which
the yields of smoke constituents in machine-generated smoking and
human smoking activities may be most divergent (Heming et al.
1981).
The levels of certain smoke constituents in the mainstream smoke
of one cigarette compared with the amounts of such compounds
inhaled as constituents of ETS in 1 hour at a respiratory rate of 10 L
per minute are presented in Table 4. Unaged MS does not contain
nitrogen dioxide (NO* < 5 &cigarette) because the nitrogen oxides
generated during tobacco combustion in the reducing atmosphere of
the burning cone are transported in the smoke stream (a10 vol %
0,) to the exit of the cigarette mouthpiece in less than 0.2 seconds,
and it takes 500 seconds for half of the nitrogen oxide in MS to
oxidize to nitrogen dioxide (Neurath 1972). The relatively low values
for nicotine reported in ETS may be explained, in part, by the
inefficiency of the trapping devices for collecting all of the available
nicotine; the alkaloid is predominantly in the vapor phase, which
escapes retention by the filters of such devices.

The assignment of benzene as a "human carcinogen," benzo-
[alpyrene as a "suspected human carcinogen," and N-nitrosodi-
methylamine and N-nitrosodiethylamine as "animal carcinogens" is
based on definitions by the International Agency for Research on
Cancer (1986). Accordingly, a human carcinogen is an agent for
which "sufficient evidence of carcinogenicity indicates that there is a
causal relationship between exposure and human cancer." A SUS-
petted human carcinogen is an agent for which "limited evidence of
carcinogenicity indicates that a causal interpretation is credible, but
that alternate explanations, such as chance, bias, or confounding,
could not adequately be excluded." An animal carcinogen is an agent

135


E  TAFHJZ 4-Concentrations of toxic and carcinogetic agents in notilbr cigarette mainstream smoke
       and in environmental tobacco smoke (EiTS) in indoor environments

Agent

.                                      Inhaled ae ETS constituents during 1 hour

          Mainstream Smoke                      Range            Episodic high values'
  Weight             Concentration           Weight        Concentration      Weight   Concentration

Carbon monoxide          lo-23 mg
Nitrogen oxide          100-600M
Nitrogen dioxide          <5 w

Acrolein              60-100 pg

Acetone              KNJ-260 pg

Benzene             1248 pg
N-Nitrosodimethylamine'      10-40 ng

N-NitrosodiethylemineJ       4-25 ng

Nicotine            v.3=2,500 Pl?
Be@alpyre"e'           20-40 ng

2WXQ-5~,300 rm
23O,ooo-1,400,ooO ppb
  <7&Q ppb
75,CG+125,000 ppb
120.~,~ ppb
11$00-43,000 ppb
  s-36 ppb
  3-17 ppb
434I,OGC-1,080,000 ppb
  5-11 ppb

1.2-22 mg
7-90 pg
24-S7Irg
S-72 M

210-720 pg
u-190 pg
6-140 ng
(6120 ng
0.630 pg
1.7-460 ng

l-18.5 ppm
9-120 ppb
21-76 ppb
  6-50 ppb
160-500 wb
  6-9~ wb
0.003-0.072 ppb
<0.00%0.05 ppb
0.15-7.5 ppb

0.0002-0.04 ppb

37 mg
146 w
120 l4z
110 pg
3,500 I%
190 l%
140 ng
120 ng

3cQws

460 ng

32 PP~
196 ppb

106 wb

8~ wb

2,400 wb
98 wb
0.072 ppb
0.05 ppb

76 wb
0.04 ppb

NOTE: Values for inhaled mainstream smoke components were calculated from values in Table 2 and on a respiratory rate of 10 L per minute. Valuea for carbon monoxide and nicotine represent
the range in mainstream smoke of U.S. nonfilter cigarettes 88 reported by the U.S. Federal Trade Commission (19%). Data under EIS are derived from Tables 8 through 16, with data fmm the
unventilated interior compartmenta of automobiles excluded (Badre et al. 1978).
`The designation "episodic high values" was chosen to classify those data in the literature that require confirmation.
*Human carcinogen according to the IARC (Vainio et al. 1986) and suspected carcinogen according to the ACGIH (198%.
`Animal carcinogen according to the IARC (V&do et al. 1995).
4 Suep&.ed human carcinogen, according to the IARC (Vainio et al. 1985) snd according to the ACGIH (1986).


"for which there is sufficient evidence of carcinogenicity in animals
but for which no data on humans are available."
Polonium-210 is not listed in Table 4 because there are no data on

the concentration of this isotope in ETS, although it is a component
of both MS and SS. Whereas in clean air the short-lived radon
daughters tend to plate out on room surfaces, in the presence of an
aerosol such as El's, some of the short&& radon daughters become
attached to particles and consequently remain available for inhala-
tion. Radon daughter background concentration may more than
double in the presence of EYI'S (Bergman and Axelson 1989).

Number and Size Distribution of Particles in EnvIronmentsI
Tobacco Smoke

Environmental tobacco smoke consists of the combined products of
both fresh and aged sidestream smoke and exhaled Ilaainstream
smoke. Coagulation, evaporation, and particle removal on surfaces
occur simultaneously to modify the physical characteristica of the
ETS particles; as a result, the "typical" particle size and chemical
composition of ETS may vary with the age of the smoke and the
characteristics of the environment. Other factors such as relative
humidity, particle concentration, and temperature may also tiect
the characteristics of EYE.

The rapid dilution of SS smoke as it is emitted into a room leads to
a number of physical and chemical changes. For example, the
evaporation of volatile species as the ETS ages reduces the median
diameter of the smoke particles. Several studies have measured the
particle distribution of SS under controlled conditions (Table 5), and
indicate that the mass median diameter (MMD) of ETS is between
approximately 0.2 w and 0.4 v. The differences among the studies
reflect the varying analytical methods. EYE3 particles are in the
diffusioncontrolled regime for particle removal and therefore will
tend to follow stream lines, remain airborne for long periods of time,
and rapidly disperse through open volumes.
As indicated, a number of factors can produce variation in the
mean size of the particles in EYl'S, however, in considering transport,
deposition, and removal in the human lung, it is useful to assume
that the particle sizes of aged ETS will generally be between 0.1 and
0.4 pm. Although the results presented in Table 5 do not permit the
assignment of a single value for the diameter of side&ream smoke
particles, the difference in deposition efficiency in the human
respiratory tract of 0.2 pm particles and 0.4 w particles is negligible
(C&an and Lippmann 1980). Particles in this size range are not
efficiently removed by sedimentation or impaction. Although diffu-
sion is the major removal mechanism for particles of this size, it is

. .

mmnnally efficient in the 0.2 to 0.4 v range. The relatively low

137


iii  TABLE li.-Summary of sidestream smoke size distribution studies

Study

Cigarette

Method

   Chamber
concentration (pg/m sJ

count
median
diameter

Ma.%
median
diameter

Geometric
standard
deviation

Number
per cm'

Keith and Derrick
IlW-ll

Blended

"Conifuge"         Not reported        0.15       Not reported    Not reported     38 x 10"

PorstendGrfer and
Schraub (19721

Not reported

CNUdiffusion tube

Not reported

0.24

Not reported

Not reported

3.3 x 10"

Hiller et al.
(1982J

Not reported

SPART analyzer

5@100

0.32

0.41

1.5

Not reported

Leaderer et al.
(1984)

Commercial       EAA

mcl

Not reported

0.225          21       Not reported

lngebrethsen and
sears (1986)

MCICNC                                        0.2            1.5


particle deposition efficiency for SS particles in human volunteers
observed by Hiller and colleagues (1982) is consistent with particles
in this size range.

Several investigators have measured the size distribution of MS
smoke (Table 6). As is the case with SS smoke, the different
instruments and methodologies employed yielded differing results.
For purposes of comparison, only two sets of studies utilizing
similar instruments are discussed. McCusker and colleagues (19831,
using a single particle aerodynamic relaxation time @PART) analyz-
er to study highly diluted MS smoke particles, found a mass median
diameter of 0.42 pm with a geometric standard deviation (GSD) of
1.38. Hiller and colleagues (1982) used the SPART analyzer on SS
smoke particles and found a mass median diameter of 0.41 pm and
GSD of 1.5. Chang and colleagues (1985) used an electrical aerosol
analyzer (EAA) to measure MS for various dilution ratios and
reported a MMD of 0.27 pm (GSD 1.26) for the highest dilution.
Leaderer and colleagues (1984) used an EAA to determine the size
distribution for SS smoke particles in an environmental chamber
and determined an MMD of 0.23 urn (GSD 2.08). These results also
show that studies utilizing similar instruments provide similar
results for the size distribution of both SS and MS particles. As
discussed in an earlier section, however, the chemical composition of
the MS and ETS particles can be quite different because of the very
different conditions of their generation and the subsequent dilution
and aging ETS undergoes before inhalation.

Estimating Human Exposure to Environmental Tobacco Smoke

Human exposure to ETS can be estimated using approaches
similar to those used for other airborne pollutants. The concentra-
tion of ETS to which an individual is exposed depends on factors such
as the type and number of cigarettes burned, the volume of the room,
the ventilation rate, and the proximity to the source. These factors,
along with the duration of exposure and individual characteristics
such as ventilatory rate and breathing pattern, dictate the dosage
received by an individual.

Ideally, the health effects of exposures to ETS might be assessed by
quantifying the timedependent exposure dose for each of the several
thousand compounds in cigarette smoke and defining the dose-
response relationships for these compounds in producing disease,
both as isolated compounds and in various combinations. The
magnitude of this task, given the number of compounds in smoke,
and the limited knowledge of the precise mechanisms by which these
compounds cause disease have led to a simpler approach, one that
attempts to use measures of exposure to individual smoke constitu-
ents as estimates of whole smoke exposure. The accuracy with which

139


8'  TABLE 6.-s ummary of niainstream smoke size distribution studies

                                                               count         MaSa
                                                              median        median        Geometric
                                                  Dilution        diameter       diameter       etadad     concentration
   Study           cigarem          Method            rati0        k-1        (run)         deviation    (number/cm')

Keith and Derrick
ma3

Blended       "ConIf~"           298           0.23        Not reported     1.6           6.9 I 10

Pomtmdllrfer and
Sehraub (1972)

Not reported     CNC/diffueion tube     Not reported      0.22        Not reported    Not reported    Not regmted

Okada and
Matmnama
(1974)

Blended

Light e&t.ering

Hinds ww

Commercial

Caecade impactor
cascade impactor
Cascade @iactor
Aerosol certifuge
Aeroeol certifuge
Aerosol certifuee
Aemol CeltitilKe

10
60
100
100
320
Ka
700

0.18

Not reported     0.62
Not reported     0.44
Not reported     0.39
Not reported     0.38
Not reported     0.98
Not reported     0.36
Not reported     0.37

0.29

1.5

1.36        Not reported
1.44        Not reportad
1.43        Not reported
1.33        Not reported
1.37        Not mported
1.35        Not rqmrted
1.31         Not revorkd

3 a 10'"

Mdxlsker et al.

2Rl         SPAm analmr       1.2611~       0.36          0.42          1.38     4.2 x t

cbang et al.        2Rl          EAA               6           0.25         0.30          127          4.2 I 10'
mm                                         10           0.24          0.26          1.18          3.6 x 10'
                                            18            0.22          0.96          1.26           7 a 1w


measurements of a single compound reflect exposure to whole smoke
is limited by the changes in the composition of M`s with time and
the conditions of exposure. For this reason, exposures to E'l'S are
often afessed using several measures as markers, including mark-
ers of the vapor phase and the particulate phase as well as reactive
and nonreactive constituents. Although biological markers show
promise as measures of exposure because they measure the absorp
tion of smoke constituents, they too have limitations (diecussed '
Chapter 4). An individual's exposure is a dynamic integration of &:
concentration in various environments and the time that the
individual spends in those environments.
In specifying an individual's exposure to specific components of
EITS, consideration must be given tc the time scale of exposure
appropriate for the response of interest. Immediate exposures of
seconds or hours would be most relevant for irritant and acute
allergic responses. Time-averaged exposures, of hours or days, may
be important for acute contemporary effects such as upper and lowe
respiratory tract symptoms or infections; chronic exposures occur
ring over a year or a lifetime might be associated with increases
prevalence of chronic diseases and risk of cancer.
The spatial dimensions or the proximity of the individual to the
source of smoke is important in assessing that individual's exposure
to ETS. E!lTS is a complex, dynamic system that changes rapidly once
emitted from a cigarette. Physical processes such as evaporation and
dilution of the particles, scavenging of vapors on surfaces, and
chemical reactions of reactive compounds are continuously occurring
and modify the mixture referred to as ETS. An individual located a
few centimeters or a meter from a burning cigarette may be exposed
to a high concentration of ETS, ranging from 200 to 300 mg/m*, and
may inhale components of the mostly undiluted smoke plume and of
the exhaled mainstream smoke. Ayer and Yeager (1982) reported
cigarette plume concentrations of formaldehyde and acrolein in the
core smoke stream emitted from the cigarette of up to 190 times
higher than known irritation levels. Hirayama, as reported by
Lehnert (1984), cites the importance of this "proximity effect" in
assewing exposure. llist.anw on the order of a meter tc tens of
meters from a burning cigarette are relevant for exposures in offices,
restaurants, a room in a how, a car, or the cabin of a commercial
aircraft. At these distances, the mixing of ETS throughout the
airspace and the factors that affect concentration are of importance
in determinin g exposure for people in the space. In many rooms,
mixing is not completely uniform throughout the volume, and
significant concentration gradients can be demonstrated Wizu
1930). These concentration gradients wilI affect an individual's
exposure by modifying the effectiveness of ventilation in diluting or
removing pollutants. The airborne mass concentration may vary by

141


a fa&r of 10 or more within a room. Short-term measurements in
rooms with smokers can yield respirable particulate concentrations
of 100 to 1,000 CLg/mS (Repace and Lowrey 1980). Multihour
measurements average out variations in smoking, mixing, and
ventilation and yield concentrations in the range of 20 to 200 CLg/mS
(Spengler et al. 1981,1985,1986). Finally, on a systems scale, as in a
house or building, concentrations are influenced by dispersion and
dilution through the volume. Most timeintegrated samples are
taken on tbis larger scale.
Using a piexobalance, Lebret (1985) found significant variation in
respirable suspended particulate (R.SP) levels between the living
room, kitchen, and bedroom in homes in the Netherlands during
smoking or within onehalf hour of smoking. Ju and Spengler (1981)
studied the room-toroom variation in 24-hour average concentra-
tions of respirable particles in various residences. Although differ-
ences between some rooms were statistically sign&ant, absolute
differences were relatively small, with a maximum difference of a
factor of 2.

Moscbandreas and colleagues (1978) released sulfur hexafluoride,
a tracer gas, in the living rooms of several residences and observed
uniform concentrations in adjacent rooms within 30 to 90 minutes,
RSP, which is slightly reactive, and nonreactive gases would be
expected to rapidly migrate through adjacent rooms. Therefore, in a
setting such as the work environment, where the duration of
exposure is several hours or more, HTS would be expected to
disseminate throughout the airspace in which smoking is occurring.
Smoke dissemination may be reduced when air exchange rates are
low, as may occur when internal doors are closed.

Time-Activity Patterns

Individual time-activity patterns are a major determinant of
exposure to ETS. The population of the United States is mobile,
spending variable amounts of time in different microenvironments.
Individual activity patterns depend on age, occupation, season, social
class, and sex. For example, Letz and colleagues (1984) surveyed the
time-activity patterns of 332 residents of Roane County, Tennessee,
and found that 75 percent of the person-hours were spent at home,
10.8 percent at work, 8.5 percent in public places, 2.9 percent in
travel, and 2.8 percent in various other places. As expected,
occupation and age were strong determinants of time-activity
patterns. Housewives and unemployed or retired individuals spent
84.9 percent of their time at home, and occupational groups worked
21 to 24 percent of the hours. Students tended to spend the largest
percentage of their time in public places, presumably schools,
ranging from 14.7 percent for the youngest group to 19.17 percent for
the oldest group of students.

142


TABLJZ `I.-Mean percent and standard deviation of time
     allocation iu various locations by work or
     school classification subgroup

                       outdoor ofiice/   Indwtrial/ Thl,aU
Location     HOlIlemaLer   student    worker    ssrvice   c4luhuction perticipant.9

Home       84.34      60.91      49.97      63.74     57.23      64.21
       (2.02l'     (13.92)     (12.24)     (8.72)     c7.05)     (13.99)

outside       5.52       8.62      19.81       2.47      -10.69
       (3-m      6.53     K4.55)     (2491     (10.74)   (Fi

Motor vehicle   4.28       5.11      8.67
        (3.19)      (3.74)     (6.15)  0  (7%       5.51
                                           (4.m

other incLmn   6.01      23.61      21.56      24.99      24.80      21.68
        (3.27)     (10.61)     (5.32)     (10.241     a28a     (11.37)

cooking      4.69                               0.52       1.24
        u.fm   (lit  (iii  (::     @.W      cw

Near mnokem   2.34       5.!20      275      11.73
        (4.32)      c1.88)     (3.38)    (15.19)  (12:   (!z:

Number      8        32        4       12        8        66'

`Numbershparentheemarethe~darddeviation.
' `ho unemployed partioipanta - inchded in the total. but not given a mparate catqmy.
SOURCE: Data f-mm Quaokerlb et al. (1982).

The time allocations for various population subgroups in Portage,
Wisconsin, are summarized in Table 7 (Quackenboss et al. 1982). The
data are consistent with the findings of Letz and colleagues (1984)
and show that the variability of individual nonsmokers' exposure to
smokers can be quite marked between the various occupational
subgroups.
Infants have unique time-activity patterns; their mobility is
limited and the locations where they spend their time depend
primarily on their caretakers. The time-location patterns for 46
infants is illustrated in half-hour segments in E'igure 1 (Harlos et al.
in press). Although infants spend most of their time in their
bedrooms, they are in contact with a caretaker while traveling or in
the living room or the kitchen for approximately half of the day.
These infant time-activity patterns presumably correspond to the
family patterns and may significantly influence the infants' poten-
tial exposure.
Although most people spend approximately 90 percent of their
time in just two microenvironments (home and work) (&alai 1972),
important exposures can be encountered in other environments. For
instance, commuting or being Yn transit" accounts for about 0.5 to
1.5 hours per day for most people. Therefore, additional information

143


-L

--M

-3

,aD

-a
   r

-9

-Lx

-0

FIGURE I.-Time location patterns for 46 infants
SOURCE: HarIm et al. (in prem).

on the time spent and the EZS concentration in various microenvi-
ronments may be useful in defining exposure. This exposure
information can be obtained by questionnaire and validated by
personal monitoring programs. The characterization of concentra-

144


tions or exposures or both in microenvironments should use time
scales appropriate for the health effect of interest. These variations
in location -and time-activity patterns can make the reconstruction of
detailed ETS exposure difficult in studies of long-term health effects.

The limitations in utilizing this timeactivity approach in charac-
terizing exposures to other environmental pollutants also apply for
ETS exposures. They include the following: the extent to which
overall population estimates can be generalized to individual pat
terns is poorly understood; concentrations in various microenviron-
ments are only partially characterized, the variation in time and
activity patterns and their effects on concentration levels are not
established; extrapolation to longer time scales either prospectively
or retrospectively has not been validated; the differences within
structures, i.e., room to room ~variations, are not well established.

Temporal and Spatial Distribution of Smokers

Exposure to ETS can occur in a wide variety of public and private
locations. Approximately 30 percent of the U.S. adult population
currently are cigarette smokers. Nationwide, 46 percent of homes
have one or more smokers (Bureau of the Census 1985). In a survey
of more than 10,000 children in six U.S. cities, the percentage of
children living with one or more smoking adults varied from a low of
60 percent to a high of 75 percent (Ferris et al. 1979). Lebowitx and
Burrows (1976) reported that 54 percent of children in a study in
Tucson had at least one smoker in the home; Schilling and colleagues
(1977) reported that 63 percent of homes in a Connecticut study had
a smoker in the home. These data indicate that the population
potentially exposed to ETS in the home is greater than might be
inferred from aggregated national statistics on the prevalence of
smoking. A variation in the percentage of homes with smokers may
be observed among different regions. Furthermore, within house
holds, smoking does not take place uniformly in time or space.
Smoking patterns may change with activity, location, and time of
day. These variables all serve to modify a nonsmoker's exposure to
ETS.

Exposure to ETS at home may also correlate with ETS exposures
outside the home, possibly because nonsmokers married to smokers
may have a greater tolerance for ETS-polluted environments or may
be in the company of more smokers because of the spouses' tendency
to associate with other smokers. Wald and Ritchie (1984) used a
biological marker and questionnaires to show that nonsmokers
married to smokers reported a duration of exposure to ETS greater
outside the home than was reported by nonsmokers married to
nonsmokers (10.7 hours and 6.0 hours, respectively).

Smoking prevalence varies widely among different groups (e.g.,
teenage girls, nonworking adults, and adults employed in VICIOUS

145


occupations); this variation modifies the exposure of nonsmokers to
EEL Smokers are present in nearly all environments, including
most workplaces, restaurants, and transit vehicles, making it almost
impossible for a nonsmoker to avoid some exposure to ETS. The
number of cigarettes consumed per hour by the smoker may vary at
different times in the day, and the rate and density of smoking will
also differ by the type of indoor environment and activity in such
hales as schools, autos, planes, offices, shops, and bars.
Although there have been numerous measurements of ETS
concentrations in various indoor settings, these data do not repre-
sent a comprehensive description of the actual distribution of ETS
exposures in the U.S. population. Spengler and colleagues (1995) and
Sexton and colleagues (1984) demonstrated by the personal monitor-
ing of respirable particles and the use of time-activity questionnaires
that exposures to EZS both at home and at work are significant
contributors to personal exposures. However, additional data on the
distribution of smokers in the nonsmokers' environment, as well as
the distribution of ETS levels in that environment, are needed in
order to characterize the actual E!CS exposure of the U.S. population.

Determinations of Concentration of Environmental Tobacco
Smoke

Environmental tobacco smoke is a complex mixture of chemical
compmmds that individually may be in the particulate phase, the
vapor phase, or both. ETS concentration varies with the generation
rate of its tobacco-derived constituents, usually given as micrometer
per hour. The generation rate for ETS has been approximated by the
number of cigarettes smoked or the number of people present in a
room who are actively smoking. Room-specific characteristics such
as ventilation rate, decay rate, mixing rate, and room volume also
modify the concentration. Because ETS particles have MMDs in the
0.2 to 0.4 Frn range, convective flows dominate their movement in
air, they remain airborne for long periods of time, and they are
rapidly distributed through a room by advection and a variety of
mixing forces. Under many conditions, the ventilation rate of a space
will dominate chemical or physical removal mechanisms in deter-
mining the levels of ETS particles.
Nonreactive ETS components distribute rapidly through an air-
space volume, and their elimination depends almost solely on the
ventilation rate. For example, Wade and colleagues (1976) simulta-
neously measured carbon monoxide, a nonreactive gas, and nitrogen
&oxide, a reactive gas, in a house and determined their half-lives to
be 2.1 and 0.6 hours, respectively. This study demonstrates the need
for caution in extrapolating from one vapor phase compound to
another. Reactive gases and vapors may be rapidly lost to surfaces or

146


may react with other chemical species. Their removal may be
dotted by their reactiOn Or absorption rates. Furthermore, the
decay of ETsderived Substances can be a function of the chemical as
well as the physical characteristics of room surfaces. For example,
Walsh and colleagues (1977) found that sulfur dioxide removal was
greater for rooms with neutral and alkaline carpets than for rooms
bving carpets with acidic PH. Reactions with furnishings and other
materials may occur for some M`s components as well.

~tx-c-tenvjronmental Measurementa of Conce&r&ion

As was discussed earlier, the complex chemical tieup of ETS
makes the measurements of individual levels for each compound
present in JWS impossible with existing resources; thus, some
individual constituents have been measured as markers of overall
smoke exposure. Because many of these constituents are also
emitted from other sources in the environment, the contribution of
El% to the levels of these constituents is quantified by determining
&e enrichment of specific compounds found in smoke-polluted
environments relative to the concentration measured in nonsmoking
areas. Various ETS components have been measured for this
purpose, including acrolein, aldehydes, aromatic hydrocarbm,
carbon monoxide, nicotine, nitrogen oxides, nitrosamines, phenols,
and respirable particulate matter. A summary of the levels found
and the conditions of measurement are presented in Tables 8
through 15. The major limitation of using most of these gases,
vapors, and particles is their lack of specificity for ETS. The presence
of sources, other than tobacco smoke, of these compounds may limit
their utility for determining the absolute contribution made by EITS
to room concentrations. Levels of nicotine and tobacco-specific
nitrosamines, however, are specific for ETS exposure.
Obviously, no single measurement can completely characterize the
nonsmoker's exposure to ETS, and many studies have measured
several of these components in order to characterize the exposure.
Markers should be chosen both because of their accuracy in
estimating exposure and because of their relevance for the health
outcome of interest.

One widely reported marker of ETS is respirable suspended
particulate (RSP) matter. Although lacking specificity for tobacco
smoke, the prevalence and number of smokers correlates well with
RSP levels in homes and other enclosed areas.

A study of the RSP levels in 80 homes in six cities (Figure 2)
(Spengler et al. 1981) showed that indoor concentrations were higher
on average and had a greater range than the outdoor concentrations.
From these data, it is evident that even one smoker can SigllifiCiUltig
elevate indoor R+SP levels.

147


TABLE EL-Acrolein measured under realistic conditions

Study

Badre et al.
wm

c%fee
&Ken
Hospital lobby
2 train compartment9
car

F&her et al.
(1978) and
Weher et al.
(1979)

lleataurant
Rataurant
Bar
Cafeteria

Varied         Not &em
18 smokers       Not given
12 to a0 amokem    Not given
2to3mokera     Not given
3 smokers       Natural, open
2 mnokem        Natural, cloned

F&80/470 m'
6@-m/440 m*
30 -40/&l ma
NJ-l&Y674 ma

Mechanid
Natural
Natnral, open
11 changeanu

loo n&L. sampled
100 mL eamplen
loo mL mmpla
100 mL .mulplea
loo mL m.mpled
1OOmLsampla
27 x 30 mic samplea
29X3Odlumpla
28 x 30 min analplea
24 x 30 min 8anlpla

            0.03-0.10 m&n'
0.195 m&n*
0.02 mglm'     0.0!&0.12 &In'
0.03 tag/m*
0.20 mg/m'
7PPh
8 Ppb
10 ppb
6 ppb (5 Ppb
non8moking eecticad


TABLE 9.-Aromatic hydrocarbons measured under realistic conditions

Study

Type of
premises

                             Levele       Ncmemcha aatde
          Monitwing
Ventilation        mnditiona       Mean    Ranec-w

Badre et al.
(1978)

cafes
Room
Train compartmente
car

cf&a          Varied            Not given      loo mL sampled
Room          18 amokem          Not @en      loo mL Eamplee
Train wmpartmente  2 to 3 emokem        Not &en      loo mL namplw
car           2 maokern          Natural, clcued    loo mL samples

FXllott and Rowe
(1976)

Arena

Galuakinova
ww

Ileetaurant

Varied            Not given      100 mL Blrmplen
18 smokera          Not given      loo mL Mmples
2 ta 3 amokere        Not given      loo mL amnples
3 nmokera          Natural, open    loo mL Bamph
2 amokere          Natural, clod    loo mL samples

s,647-10,7S9 people
12,00&4S44 people
13,ooO-l4Xl7 people

Not given           Not @en

Not given
Not given
Not &en
Separate non-
=Ktif,Y dsJrs

7.1
9.9
21.7

~dweineummer    6.2
18 daya in the fall       2aHU

Benzene b&m*)

0.102

0.04
0.16

O.W.16

0.oM.10

Toulene (mg/ms)

      0.04-1.04
0.216
1.87
0.60

    Beinclabymae (M/m*)

0.69


TABLE 9.-Continued

Study

Just et al.
(1972)

Coffee houses     Not given           Not given        6 hr wntinuoue         02610.1      4.0-9.3 (outdoola)

  Jhzde~yrone (ng/m")

3.3-23.4      3.0-5.1 (outdoola~
Benmkhihmrylene (ng/m*)

W-10.6      6.9-13.6 (outdoors)
   Perylene bglm*)

o-7-1.3       0.1-1.7 (outdoola)
   F%mne (s&m')

4.1-9.4       2%?.O (outdoom)
  Anthanthrene (&ma)

0.61.9       0.5-1.8 knltdooE3)

   Coronene (rig/d

05-1.2        1.0-2.8

    Phenols b/m')

7.4-11.6

  Beruda$yreae (r&m')

Peny (1973) '

14 public placea

Nat piven

Not given

samples, 6 outdoor
IoCatiOllE

< 20460            (20-43

' The correctn~ of the data ia doubtful (Grimmer et al. 1977).


TABLE lO.-Carbon monoxide measured under realistic conditions

Study

Ventilation

Monibrlng
CWditiOM

  Levela (ppm)

Mean

Nonsmoking contmle @Pm)

Mean

Eadre et al.
(1978)

Bcafea        Varied        Not given    20 mill sempleu                 2-23       (outdoore)        O-15
Room        18 emokma      Not given     20 mln snmplea     60                     0 (0ukJoonl)
Hospital lobby    12 to 90 amokem   Not given     20 mln samples      5
2train        2 to 3 smokers    Not given     20 min namplea                44
wmpartmenta
car         3 amokera      Natural, open   20 min aample     14                      0 (0utdooIu)
          2 Bmokera       Natural, cloeed  20 min samples     !?a                     0 (outdoore)

Can0 et al.
(1970)

Submarines
68 ma

157 c;sarettes
per&Y
94-103 cigarettea
w* &Y

YeS

Ye0

<40 mm

<40 mm

Chappell and
Parker
wl7)

10 offices

16 resteurant3

14 nightclubs
and taverns
Tavern

Not given

Not given

Not 9iven

Not given

value4 not
given
valuea not
given
valuea not
glven
Arti&ial

None

of!?@       1440 ft.'        Natural, open

17x2-3min
samples
17X29min
-Pl-
19 x 2-3 min
mamplm
18XMmiJJ
anmplee
2x2-3min
BEUUPlW
2-3mlnaamplee
3omlnafter
amaking

2.5 f 1.0      1.5-4.6       2.5 f 1.0       1.5-4.5
                      butdoors)
4.0 f 2.5      1.0-9.6       2.5 f 1.6      1.0-6.0
                      (outdwm)
13.0 f 7.0      3.0-29.0      3.0 f 2.0       1.06.0
                     bladom~
8.5

         =tPW

         10.0 (peak)
1.0


t;
RI  TABLE 10.4ntinud

Study

Coburn et al.    ~oorrm       Not given       Not given
(lssa)                                  Not &en                    4.9-9.0
                                          N-oked roome                         2.2 f 0.96      oA-4.6

Cuddeback     Tavern 1     16-294 people     6 changedhr   8 br continuous     11.6          10-l-12
Et)                                                                      2 wdwd
                                 2hrafteremoking -1
          Tavern 2      Not given       l-2 cbangen/br 8 hr amtiauoun     17           -CM?2        valua not given
                                    2brefterMokblg   -12                  valum not given
U.S. Dept. of   18 military     165-219 people     Mecbwlcal    6-7 hr contlnuoue              <Z-6
RansportetiOll    Pbce
(1971) '       8 domeutic     27-11s people      Mechenical    1%2% br       s-2
         Planes                             continuoue

Elliott and     Arena1      ll@X psople      Mechanical    Not &en         9.0
          Arena2      2,ooO people      N&Ud                                9.0 bmwtlvity day)
                                     Not given         26.0                 9.0 bloMctivity day)
                                   No-~                                 9.0

Fischer et al.
(1978) and
Weber et al.
W9)

                                    arena

Reataurent     50-601470 ma      Meehanieal    27X3Oti       6.1          21-9.9         4.8 (outdoon)

Fkataurant

Bar

Cafe&a

60-lOOA ma

80-40/W ma

80-X0/574 m'

        Bamplee
Natural      29X30&l       2.6          1.43.4         1.5 (outdoore)
        aamplm
Natural, open   28XWdIl       4.8          2.4-9.6           1.7 cddoonl)
        =Pl-
11 changee/llr  24XXlmin       1.2          0.7-1.7           0.4 buuoom)
        Nonemoklng                               0.5         0.S0.8
           room


TABLE lO.-Continued

Study

Ventilation

Monitoring
conditions

   Levels burn)

Mean

Nonsmoking controls @pm)

i&an

Godin et al.    Ferryboat      Not given        Not given     11 grab samples     18.4 f 8.7                3.0 f 2.4 (r~onsmoking room)
0972)       Theater foyer   Not given       Not given    Grab samples      3.4 rt 0.8               1.4 f 0.8 (auditorium)

Harke

Gfllca'

-72 ma

236 m'/hr

30 mill samples

< 2.5-4.6

(1974)'

Harke and
Peters
(1974)`

mice 6

car

-78 ms

2 smokers
(4 cw

Natural

Natural

MeChanical

30 mill samples
Samples

Samples

< 2.8-9.0
42 (pdd      (Nonsmokln# mm)
           13.5 (peak)
32 @eak)      (Nollsmoklng mns)
           15.0 (peak)

Harmsen and
Effonberger
mm'

Train

1-18 smokers      Natural

Not &en                   O-40

14 public

Not given

Not 6iven

One grab sample

<lo

(1973)'

Portheine

Ph==

Rooms       Not given       Not given     Not given                   8-26

(1971)'

Sebbcn et al.

9 nightclubs

Not given

Varied       77 X 1 min       13.4          6.5-41.9

(1977)

14 restauranta
45 restaurants
3.3 storea
3 hospital
lobbies

Not given
Not &en
Not given
Not given

Not &en
Not @en
Not 6iven
Not given

samples
outdoors
spot checlo3
spot checks
spot checks
Spot checks

                      9.2         3.0-35.0
9.9 f 5.5               value8 not given
8.2 f 2.2                  7.1 f 1.7 (outdooln)
10.0 -f 4.2                  11.5 zt 6.9 (outdcarn)
           44         Values not @en


E  TABLE lO.-Chntinud

                                                                Level8 bud         Nonsmokina' eon- bran)
              Type of                          MOdWillg
   study         plWli!3H      OccupanCY      Ventilation     conditions        Mesn                    MSan

Intercity bus    Not given

15 cbangea/hr,
23 cigarettes
burning
continuowly
3w
burning
mntinuously

SPpm

18 mm

Slavin end
Hertz
(1975)

i.h_dkOWSki
et al.
(1976)

2 conference
I-OOlIlS

25 officea

Not given

Not given

8 changeslhr   Continuous,               8b-W        l-2 CeePnrate
         morning                           nonwnoking day)
6 changedhr   Continuous,               10 @aaM        1-2 (separate
         morning                          nm &Y)
Not given     continuous       2.78 + 1.42                    2.66f2.23
                                     blYua~ llomdiw
                                           ofiica)

`The Drager tube u.d ia accurate only within f 25 percmt.
`The MSA Molit&e sampler used iu accurate only withio f 26 percent.
*The cigarettes and one cigar smoked in 90 minuted.
`About 40 cigarettes/day were !mloked.
*About 7Ocigarattes/day were smoked.
`Four tiltar cigarettea were smoked.
' No experimentd demiption givsn.


TABLE ll.-Nicotine measured under realistic conditions

Study

Type of
premises

Ventilation

Monitoring
conditions

             Nonsmoking
Leiels (p&m*)        controls

Mean    Range Mean Ranee

Badre et al.
(1978)

Gcafea            Varied         Not given        60 min sample             25-52
Boom             18 smokers        Not given        60 min sample      800
Hospital lobby        12 to 30 smokers     Not given        80 mm sample       37
2 tram compartments   2 to 3 smokers      Not given        80 min sample             36-50
Car             3 smokers         Natural, onen       60 min ssmule       68

Natural; closed

fi0 min sample

1010

Can0 et al.         Submarines
(1970)              66 ma

157 cigarettea
per day
94-m cigarettea
l=* &Y

YeS                       32 pg/m'

YeS                      1535 pg/m;

Hsrmsen and
Effenbwger
(1957)

T&l

Not given

Natural, closed

30-46min
samples

0.741

Hinds end First
(1975) '

Webor and Fiber
wm'

Train
Bus
Bus waiting room
Airline waiting room
Restaurant
Cc&tall lounge
Student lounge

44 offica

Not given
Not given
Not given
Not given
Not given
Not given
Not given

Varied

Not given
Not given
Not given
Not given
Not given
Not given
Not given

Varied

2% hr samples
2'1, hr samples
2'/, hr semplos
2% hr samples
2'1, hr samples
2% hr samples
2% hr samples

14ox3hr
samples

  4.9          valuea not given
  6.3          Values not given
  1.0          valuca not given
  3.1          Valuea not given
  5.2          Values not given
10.3          valuw not given
  2.8          Values not given
0.9 * 1.9  13.8 @AC)  Values not given


TABLE 11.4ntinued

                     Levels t&m')     controls-
          Monitor
ventilation        amdltions       Mean    rbge Man m

First
asw

1 public buildin.
8 public buildiugn

NOMlWLen
Ito6anok4rd

Mechanical
Natural and

                         5.5
Not given
Not given         132     27-30.0

lUuramab3u et al.
ww

oflice
cmoe
IAbomtoly
6 confemace rooms
3 howea
Hcspital lobby
4 hotal lobbits
5 lwtaurants
3 cafeteriaa
3 bun and railway
waitiog roollls
4cara
8trai~
7 alrplene4

Not given         Not &en
Not given        Not given
Not given        Not given
Not given        Not &en
Not given        Not given
Not given        Not glvsn
Not given        Not given
Not given         Not given
Not given        Not given
Not giwm        Not given

Not given
Not given
Not &en

Not given
Not given
Not given

Not &en
Not ghn
Not given
Not given
Not given
Not given
Not &en
Not given
Not givea
Not given

19.4    Sq-sl.6
B.1     14.6a.l
5.8     M-9.6
28.7     16.5-53.0
11.1     7.6-14.6
3.0     1.940
11.2     5.5-18.1
14.8     7.1-37.8
96.4     11.a2.2
19.1     10.1-36.4

Not given         47.7     7.7-83.1
Not given         16.4     8.6-98.1
Not given         16.2     6.3-28.8


TABLE 12.-Nitrogen oxides measured under realistic conditions

study

M of
premises

Ventilation

Fischer et al.
(1678) and
Weber et al.
ww

Weher and
Fischer
ww'

Restaurant

Rwteluant

Eiar

Cafeteria

44omss

50-8Qt470 m'

60-100/440 ma

20-40/50 ma

80-150/574 ma

Varied

Mwlmnical

Natural

NBtUd,
open
11 ch&mgen/hr

Varied

27XiWti
samples
29X8Oltlh
namplea
28X8Oti
samplea
24X2Odl.l
SampIeS
Other-non-
smokers mom

Bamplm

NO,: 76       5%105     62 b3a.dcorl5~
No: 120       26-218     115 (outdoom)
NO,: 66       24-99      60 f~tdoom)
No:80        14-21      11 Mdoom)
NO,: 21        l-61      46 (outdwm)
No: 195       66-414     44 (outdoom)
NO,: 58       25-103     24 (0utdoorB~
No: 9         w6      4 butdoom~
                NO,: 27      15-44

                   No: 5        2-9

NO,: 24 f 22   115 k-w    vehlw not gibwl

No: 62 f 60    =J(peall)    value3 nbt given

1 Contml valua (unoccupied rooms) have bean subtracted.


+
E  TABLE 13.-Nitrosamines measured under realistic conditions

Brunnemann and
Hoffmann
W78)

B~UMWIUIUI et al.
(1976)

!rTBinharwr
Trainbarwr

Bar
sports hall
Bettiug parlor
Ditlwtheque
Bank
IiOUW
HOUBB

Not given       Mechanical
Not given       Natural

Not given      Not given
Not given      Not given
Not given      Not given
Not given      Not given
Not given      Not given
Not given      Not given
Not given      Not given

90 mill continuoue         0.13
90 min amtinuoua         0.11

3 hr wntinuow          0.24
3 lx wntinuow          0.09
90 min wntinuouB         0.05
2v, hr contiMouB         0.09
5 hr amtinuouB          0.01
4 hr amtinuoua        <o.oos
4 hr wntinuoua         <0.003


TABLE 14.-Particulates measured under realistic conditions

Study

Type of
premises

o=UpanCY
(active smokem
perlOOm')

Ventilation

                       Nonsmoking
Monitoring      Levels @g/m')     wntmls @g/m')
conditions
kuin)        Mean SD         Mesa SD

Cocktail party
Lo&x hall
Barandgrill
Firehouse bingo
PizwriB
Bar/cccktail lounge
Church bingo game
Inn
Bowling alley
Hospital waiting Mom
Shopping plara restaurant
Sample 1
Sample 2

0.75         Natural                   15
1.26         MWhanical                 50
1.18         Mechanical                18
2.17         Mechanical                 16
2.94         Mechanical                32
3.24         Mechanical                28
0.47         MeChanieal                 42
0.74         MdWliWl                12
1.53         MWbdCd                20
2.15         Mechaoical                 12

0.18         MeChanical                 18
0.18         MeChanical                 18

153
163

+ a
+ 4

24
60'
63'
51'
40'
50'
30
221
49'
58'

59'
36'

--
-


K?  TABLE 14.-Cbntinued

Study

Typs of
premieen

oocupancy
htive smokera
per 100m.J

                                   NoarmotirrP
           Manitorine      Luvel~ Cpgtm')    f3e0l~ (W/m')
              wnditionm
Ventiletion          0        Mea0 8D        Meanm

Barbeque restaurant
Sandwich rentaurant A
Smokiog eection
Nonsmoking don
F&-food reetaurant
sports arene
Neighborhood restaurant/bar
Hotel bar
Sandwich restaurant B
Smoking section
Nonmoking section
BoadBide reataumnt
Conference room

Repace and     Dinner theater
bmY      Reception hall
(1482)       Bingo hall

0.89

0.29
0
0.42
0.09'
0.40
0.59

0.13
0
1.12
3.54

0.14
1.19
0.93 *
0.93'

MWh_lliWl

Mechanlwl
Mechanical
MWlldCd
MWhBIdd
MWhalliWl
MWM

Mechanical                 8
MWhliCd                21
Mechanical (9.6 a&`)           18
Mwhanical (4.3 a&`)           6

MWlldd                44
MeChanical                20
Natural                  2
Mednical (1.39 ach')          6

10

20
20
40
12
12
12

136 f 17

110 f 36
Mf 5
109 f 38
94 * 1s
93 f 17
93* 2

a6f7
  61
  1M'
1947'

145 f 43
301 f 90
1140
  443'

40'

40%
30
24'
I'
55'
30

55

90
55

4? f 10
33'
40'
40'

`Sequential outdoor meaauem ent (5 minute avelnge~.
`Eatimclted.
`Air changes per hour.
' lrqllibrium level aa determined from mnowtmtion m time curve.


TABLE 14cContinued

Study

Type of
premises

~UpanCY

Ventilation

Monitoring
wnditiiw

  Levels C&m')

Mean

Nonsmoking controls @g/m')

  MWO

Cuddeback et al. Tavern
(1976)
          Tavern

Not given

Not given

6 changedhr   4xahr         310
          continuous
l-2 changealhr  8 hr continuous     986

U.S. Dept. of
Tmrqmtation
(1971)

18 military planes 165-219 people

8 domestic planes 27-113 people

Mechanical

Mechanical

72 x 6-7 hr
eamplw
24 x 1+2y hr
SampIeS

Not given

<lo-120

Dockery and

Residencea

Not given

Varied

24 hr aamplee

32

Spengler
(1W

Elliott end
Bow
(1976)

Arena 1      11,606 people      MWlWliCd    During activities     323               42 (nonactivity day)
Arena 2      %W people      Natural     During activities     620                    92 bM3rativity day)
Arena 3 (smoking  11,090 people      MWhEUliWl    During actlvitiw     148                    71 (nonactivity day)
prohibited)

Harmsen and Traine
Effenberger
(1957)

Just et al.     4 coffee houses
(19721

16120 people      Natural

Not given       Not given

Not given

Nonsmokem' cam

6 hr averages

            46440
        pticledcm'                 20-75
                          pwticlwlcm~

1160        6@-1900     670 (outdoom)    loo-19lxl

Neal et al.    Hospital unit    Not given        Mechanical   48 hr samples       21 f 14       a-58       73 * 25
(1978)       Hospital unit    Not given        MeChanical   48 hr samples       40 + 21      13-79        72 f 25


TABLE Id.- Continued

Study

Type of
premises

ch=wnCY

Ventilation

Monitoring
wnditiona

  Levele -@g/m')

Mean       Range

Nowmokhg control@ (&ma)

  Mean

Spender et al.   Residences     2+ smokers       Natural     24 hr samples      70 + 43                 21 f 12
(1981)                                                                      (outdoom)
                     1 smoker         Natural      24 br earnplea       37 f 15                 21 f 12 (outdoom~
Weher and     44 offii      Veried         Natural and   429 X 2min      133 * 130'
Fischer (1980)                                                 96`2' @eaL)
                         mechanical samples

Quad et al.    Of&e No. 1     0.82*           MWlLSlliWl   Five l@hr workday        45         39.54                   616
(1982)        office No. 2     0.68 =           Mechanical    averagea; continuous       45         37-50                  15-2ll
          Of!& No. 3     1.46'           Mechanical    monitoeg            63         4289                  15-m

Brunekreef and  26 houses      1 to 3 smokers     Natural      2 mo average0          153'        60-340         55        20-m
Boleii (1982)

1 public building  Nonsmokers       Mechanical    2min                                     20
8 public buildings  1 to 6 smokem     Natural end   2min               280
                       mechaniwl

Hawthorne et al.  11 residences    Nonsmokem       o.18-oo.96     5-15 mill                                   9-40
(1984)        8 reaidencea    Nonemokera       0261.98     5-16 min                                  12-M
          2 residences    Smokem         0.27-1.47.     5-15 min            96-196

Nitschke et al.   Outdoor                            166 hr                                     11        11-m
(1985)        19 residences    Nonsmokers       Natural      168 hr                                     26        6-88
          11 residences    Smokers         Natural      168 hr               59         lo-144

Spengler et al.   Outdoor                            24 hr                                  18
(1986)       73 renidencea    Nonsmokers       Natural     24lu                                     28
          24 residences    Smokers         Natural      2dhr               74

Sterling and     1 office       Smokem        Not given    Not given             26         15-36
sterliig       22 Offlws      Smokers        Not given    Not given              32
(1984)

' valua abwa background.
*Habitual smokers per 100111'.
`Wekhtad mean.


TABLE 15.-Residuals measured under realistic conditions

Study

Type of
premisea

                                                NO-
                                           Levels          controla
                        Monitoring
@=panCY          Ventilation          conditions       Mean            hfem R-m

Sadre et al.
(19781'

Gcafea
Floom
Hospital lobby
2 train
compartments
Car
car

Dockery and
Spengler
t1981)

Fwzher et al.
I19781

Restaurant        W-60/470 m'          Mechanical
Restaurant         6&100/440 ms          Natural
Bar             30-4060 ml         Natural. open
Cafeteria          tW150/574 m'          11 ch/hr

    Just et al         4 coffee houses
55    119721

Varied            Not given
16 smokers          Not given
12 to 30 smokers       Not given
2 or 3 smokers        Not given

3 smokers
2 smokers

Natural, open
Natural, closed

Not given            VUied        24 hr earnplea         4.61

Not given           Not given        6 hr continuous      12.0-15.3

103 mL samples
100 mL aample
100 mL samples
100 mL samples

100 mL aample
100 mL 8ample.e

27 x 30 min samples
29 x 30 min samples
28 x 30 min samples
24 x 30 min samples
Other nonsmokers
mm

Acetone (me/m')

     0.915.66
0.51
1.16
     0.36-0.75

0.32
I.20

Sulfatea h/m')

Sulfur dioxide (ppb)

20     9-32        12 Fe
13     5-18        6
30     13-75       I3
15     l-27        12
                7     3-13

Aldehydes h/m')

w

' See original paper for nine other residuals.
SOURCE. Sterling et al. (1982).


  0' , , , I, , , , , , , , , , , , , ,
     NW. ~ec. &n. Fd Mar. Apr. May Jun. Jul. Aug. Sep. Ott Nov. Dec. Jan. Feb. Mar. ~pr.
         1978    1977                             1978

FIGURE 2.-Monthly mean mass respirable particulate
      concentrations &g/m") across six cities
fmJRcEI~etd.(lWl).

TABLE 16.~Respirable particulate levels as a function of
       number of smokers

Smoker status           NumbeI

No smokers      36 homes/l,186 samples

1 em&r       15 homed494 samples

2 amokera       5 homed153 samples

2+ emokera      4 homed? samples

souRcE:~etd.(1981).

Mean (p&m9    standard dwiatlon

24.4             11.6

36.5             14.6

70.4             a.9

51.8             12.3

Spengler and colleagues (1981) collected respirable suspended
particulate samples in 55 homes in six cities. The average concentra-
tions observed between May 1977 and April 1978 are shown in Table
16. The quantity of tobacco smoked was not reported, nor was the
number of hours each smoker spent in the home. The researchers
concluded that the mean WP levels increased by 20 pg/ms per
smoker.
Dockery and Spengler (1981) further analyzed these data and
considered the number of cigarettes smoked in the home. They
concluded that the mean RSP concentration increased by 0.88 w/ma

164


for every cigarette smoked per day in the house. A one-pack-a+lay
smoker in the home thus raises indoor respirable particulate leveE,
by 17.6 w/ma. Air conditioning increased the contribution of each
cigarette by 1.26 w/ma, to a total of 2.11 Clg/ms per cigarette in fully
air-conditioned homes. These values are annual averages; a&ond&
tioned homes, in which air is recirculated during the warmer
months, have higher levels.
Repace and Lowrey (1989) measured RSP concentration using a
piexobalance in several public and private lo&ioris, imh&g
restaurants, cocktail lounges, and halls, in both the presence and the
absence of Bmoking. They then developed an empirical model
utilizing the mass-balance equation. Using both measured and
estimated parameters as input to the model, they validated the
model for predicting an individual's exposure to the RSP constituent
of HIS. The model takes the form: C, = 666 D./n,; where C&equals
the equilibrium concentration of the RSP component of ETS @g/m"),
D. equals the density of active smokers (number of burning cigarettes
per 100 ma), and nv equals the ventilation rate (in air changes per
hour). The ventilation rate is a complex parameter that takes into
account all the room-specific constants affecting the removal of HIS,
such aa ventilation, decay, and mixing.
Measurements in a large number of locations using measures of
smoke generation such as the number of people smoking or the
number of cigarettes being smoked have shown a definite relation-
ship of smoke generation to particulate levels. First (1964) cautioned
again& the use of RSP measurements a~ a measure of El% in public
places because of its nonspecificity for ETS, and noted that other
~ouroes may contribute enough to the levels to invalidate the
determination of the ETS contribution. However, there are few other
sources of RSP in most U.S. homes, and therefore, the relationships
of RSP measurements to HIS levels are generally quite accurate in
this setting.
Nicotine appears to be a promising tracer for ETS because of its
specificity for tobacco and its presence in relatively high concentra-
tions in tobacco smoke. It can also be measured in biological fluids to
provide an indication of acute exposure to tobacco smoke. Cotinine,
nicotine's major metabolite, can be used as an indicator of more
chronic exposure. These biological markers are discussed in a
separate chapter of this Report. Recent studies have indicated that
nicotine may be p rimarily associated with the vapor phase of HI'S
and therefore not a surrogate for the particulate phase as once
thought (Eudy et al. 1986). However, the possible useftiess of this
compound in estimating exposure to EXS warrants further evalu-
ation. The nicotine content of side&ream smoke does not differ
significantly from brand to brand when normalized on a per gram of
tobacco basis (Rickert et al. 1984). The use of nicotine as a marker for


ETS must also give consideration to its loss to surfaces and its
subsequent revolatilization and readmission to the room volume.

Carbon monoxide, a marker for gas phase components, has been
measured extensively as a surrogate for FYI'S There are many
sources of carbon monoxide other than cigarettes, indoors (e.g.,
stoves, grills) and outdoors (e.g., automobile). This nonspecificity for
ETS seriously limits its usefulness for environmental measurements.

In summary, no single compound definitively characterizes an
individual's exposure to ETS. Additional research is currently under
way to quantify the relationships among various constituents and
ETS levels. Because of the complex nature of RTS, investigators may
need to measure several markers or to separately record source
variables (such as number of cigarettes smoked) in order to estimate
exposure to ETS.

Monitoring Studies

Personal monitors can measure the concentrations of ETS in an
individual's breathing zone. Personal monitoring is preferable to
area monitoring because it integrates the temporal and spatial
dimensions of an individual's exposures. At the present time, all of
the studies that have used personal monitors to measure RTS
constituents have utilized active samplers that provide integrated
exposures over differing time periods.

The markers assessed in personal monitoring studies have the
same lack of specificity found in area monitoring studies. However,
in many of the personal monitoring studies, time-activity diaries
were kept to permit greater resolution in attributing exposure to
specific sources.

In Topeka, Kansas, 45 nonsmoking adults carried personal RSP
monitors for 18 days, and area monitors were placed inside and
outside their homes (Spengler and To&son 1981). The indoor RSP
levels were consistently higher than outdoor levels, and the personal
exposures levels were higher than either. The group was divided into
those who reported ETS exposure and those who did not (Figure 3).
Reported exposure to ETS clearly shifts the distribution to the right.
On the average, reported ETS exposure increased an individual's
personal concentration by 20 pg/m3.

Personal RSP monitors were carried by 101 nonsmoking volun-
teers for 3 days in Kingston-Harriman, Tennessee (Spengler et al.
1985). The study population was divided into two groups: those who
lived with a smoker and those who did not. ETS exposure was
reported by 28 of the participants, with the remaining participants
reporting none. The RSP distribution for the ambient samples is
shown in Figure 4. Clearly, exposure to ETS significantly increases
an individual's personal concentration profile.

166


16

NONllOkeexposed

.     lln n             n

$  10
t   6
e:
b   6
CL
   4

2

0

n

0 5 10 15 20 25 30 35 40 45 60 55 60 65 70 75 60 85 60 65

FIGURE 3.-Percentage distribution of personal respirable
     particulate concentrations, non+moke+qwsed
     and smoke-exposed samples, Topeka, Kansas
6OUROE Spqler and Tceteaon (1981).

Sexton and colleagues (1984) monitored personal RSP exposure for
48 nonsmokers in Waterbury, V&mont, every other day for 2 weeks.
The participanta kept activity logs and had simultaneous indoor and
outdoor FC3P samples collected at their homes. The proportion of
time individuals spent exposed to EX'S was the single most important
determinant of their personal exposure. Volunteers who reported
greater than 120 minutes of exposure to ETS had a mean RSP
exposure of 50.1 M/ma, whereas those volunteers who reported no
exposure to EXS had a mean exposure of 31.7 w/m'.

167


2- Ambient
*-..... penona(.
   non-smoke-ewosd
--.- w,
   smoke-eqwed

FXXJRE 4Ahmulative frequency distributions of central
     site ambient and personal smoke-exposed and
     non-smokeaqosed respirable suspended
     ptulhulate concentrations
sG~spannBier~t0@55).

Ni&&, a tobacco-specific compound, should make an excellent
tracer for ETS if its usage can be properly validated. Some
considerations in its usage are detailed in the section on area
sampling. Currently, no published reports are available that utihm
this compound for the type of detailed personal monitoring studies
carried out for PSP. However, a lightweight personal nicotine
monitor has recently been developed (Muramatsu et al. 1994) that
may aid this type of research. The researchers measured average
nicotine concentrations ranging from 9.0 &ma in a hospital lobby to
38.7 H/m3 in a conference room and 47.7 &ma in an automobile,
No information on the duration of exposure or representativeness of
these levels to the general population was given. However, this study
does provide information as to the range of exposures an individual
may encounter and demonstrates that high nicotine levels can be
encountered in various settings. It will be necessary to quantify the
relationship between nicotine, a vapor phase component of El!& and
other components of interest such as RSP in order to fully utilize t&s
tracer.
Chtain organic gasa have been measured as possible indicators of
EZ'S exposure or of specific effects such as irritation. These include
formaldehyde and acrolem Weber and F'ischer 1980) and aromatic
compounds such as benzene, toluene, xylene, and styrene (Higgins et
al. 1983). The U.S. Environmental Protection Agency's recent TEAM
study utilized personal monitors, employing Tenax carkidges, to
develop profiles of individual exposures to volatile organics (Wallace

168


st al. m press). The TEAM study has found significantly increased
exposure to benzene for individuals exposed to E!lS. Again, the
xoxspecificity of these materials for `ET'S limits their applicabi&.
()tber materials such as carbon monoxide and nitrogen &oxide
have heen measured in personal monitoring studies attempting to
sss.sss individuals' exposure to ETS. Their nonspecificity and lack of
sensitivity for low-level ETS exposure make them inappropriate for
pop~ation-based StUdies.
persald monitoring techniques are currently available that will
&cw the assessment of individual exposures to various components
of E'l'S. Although not widely used in the past, they can provide
&u&le input in developing exposure models and in vaM&ing
other monitoring schemes. Their usefulness is primarily that they
sample all of the microenvironments in which individuals find
t&mselves and therefore automatically compensate for the nonurn-
form temporal and spatial distributions of ETS that affect individual
exposure profiles.

Conclusions

1. Undiluted sidestream smoke is characterized by significantly
higher concentrations of many of the toxic and carcinogenic
compounds found in mainstream smoke, including ammonia,
volatile amines, volatile nitrosamines, certain nicotine decom-
position products, and aromatic amines.
2. Environmental tobacco smoke can be a substantial contributor
to the level of indoor air pollution concentrations of respirahle
particles, benzene, acrolein, N-nitrosamine, pyrene, and carbon
monoxide. ETS is the only source of nicotine and some N-
nitrosamine compounds in the general environment.
3. Measured exposures to respirable suspended particulates are
higher for nonsmokers who report exposure to environmental
tobacco smoke. Exposures to JTI'S occur widely in the non-
smoking population.
4. The small particle size of environmental tobacco smoke places
it in the diffusion-controlled regime of movement in air for
deposition and removal mechanisms. Because these submicron
particles will follow air streams, convective currents will
dominate and the distribution of El% will occur rapidly
through the volume of a room. As a result, the simple
separation of smokers and nonsmokers within the same
airspace may reduce, but will not eliminate, exposure to ETS.
5. It has been demonstrated that El% has resulted in elevated
respirable suspended particulate levels in enclosed places.

169


References

ADAMS, J.D., O'MARA-ADAMS, K.J., HOFFMANN, D. On The Mainstnwm-si
stream Diatri&ution of Cigarette Smoke Components. Paper presented at the 5
Tobacco Chemists' Research Conference, Montreal, Canada, October 1966.
AMERKAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENIS
Threshold Limit Values and Btibgical Z&+.wce Indices for 1966-86. Cinch
ACGIH, 1986, p. 114.

AYER, HE., YEAGER, D.W. Irritanta in cigarette smoke plumes. American Joun
ofPublic Health 72(11):128%1285, November 1982.
BADRE, R., GUILLERM, R., ABRAN, N., BOURDIN, M., DUMAS. C. Pollut
atmospherique par la fumee de tabac [Atmospheric pollution by smoking]. Anna
Pharmueeutiques Ftrrncaisea 36(9/10):443X52,1978.
BAKER, R.R. The effect of ventilation on cigarette combustion mechanisms. Reck
Aduances in Tobacco Science l&88-160,1984.
BERGMAN, H., AXFZSON, 0. Passive smoking and indoor radon daughter cow
trations. (letter). I.uncet 2@362):1308-1309, December $1983.
BRUNEKREEF, B., BOLELJ. J.S.M. Long-term average suspended particulate cona
h&ions in smokers' homes. Znternationul Archives of Occupational and Erwin
mental Hdth 50(3~299-302,1982.

BRUNNEMANN, K.D., ADAMS, J.D., HO,D.P.S., HOFFMANN, D. The influenoee
tobacco smoke on indoor atmospheres: 2. Volatile and tobacco-sp~ific nitro
mines in main- and side&ream smoke and their contribution to indoor polhth
Proceedings of the Fourth Joint Confmnce on Sensing of Environmental PO1
tunte, New Orleans, 1977. American Chsmical Society, 1978, pp. 876-880.
BRUNNEMANN, K.D., HOFFMANN, D. The pH of tobacco smoke. Fbod a
Cosmetics Toxicology 12(1):116X&4, February 1974.
BRUNNEMANN, K.D. HOFFMANN, D. Chemical stud& on tobacw smoke: !
Analysis of volatile nitrosamin es in tobacco smoke and polluted indoor envin
msnts. In: Walker, EA., Griciute, L., Castegnaro, M., Lyle, R.E., Davis, W. (ed
Environmental Aspects of N-Nitmso Cbnpounds. IARC Pub. No. 19. Lye
International Agency for Research on Cancer, 1978, pp. M.
BRUNNEMANN, X.D., HOFFMANN, D., WYNDER, E.L., GORI, G.B. Cheti
studies on tobacco smoke: 37. Determination of tar, nicotine, and carbon monoxi
in cigarette smoke. A comparison of international smoking conditions. In: Wyndl
E.L., Hoffmann, D., Gori, G.B. (eds). Modifying the Risk for the Sm.&
w of the Third World Conference on Smoking and Health, New YOI
June 1976, Vol. 1. U.S. Department of Health, Education, and Welfare, Pub
Health Service, National Institutes of Health, National Cancer Institute, DHE
Pub. No. 076-1221,19'?6, pp. 611-449.

BRUNNEMANN, K.D., Y-U, L., HOFFMANN, D. Assessment of carcinogenic volat;
N-nitn#laminea in tobacco and in mainstream and side&ream smoke frc
~karetteS. Cancer Research 37(9):321%$X& September 1977.
BUREAU OF THE CENSUS. Current Population Suruey. U.S. Department
Commerce, Bureau of the Census, 1936.

CmO, J.P., CATALIN, J., BADRE, R., DUMAS, C., VIALA, A., GUHLERME,
Determination de la nicotine par chromatographie en phase -use: 2. Applic
tions [DetATmina tion of nicotine by gas-phase chromatography: 2. Application
kmdw Phannaceutiques I3umaiees 2&11)%33-640, November 1970.
CARTER, W-L HABEGAWA, I. Fixation of tobacco smoke aerosols for si
distribution studiw. J&rnul of Co&d and In&$&e &km 53(1):134-14
Octder1975.

Cm, T-L.9 mPMANI% M. Experimental measurementi and emptid rndellb
of the regional depositions of inhaled particles in humans. American m.wfi
HygieneAssoc&ion Journal 41(6):3QQ#9, June 1980.

170


-G, P.-T., PETERS, L.K., UENO, Y. Particle s& distribution of m&stmam
m smoke undergoing dilution. Aemeol Science a& Technology 4:191-207,
19%

CHApPFLL, S.B., PARKER. R.J. Smoking and carbon monoxide levels m enclosed
public places in New Brunswick &mdicur Jounral ofPublic Health 68(2):159&x,
~-April 1977.

CGBIJRN, R.F., FORSTER, R-E., KANE, P.B. Considerations of the physiological
variablss that determine the blood *boxyhemoglobin concentration in -.
J~urnd of CZinicaI Znvestigation 44(11):18991910, November 1965.
ClJDDEBACK, J.E., DONOVAN, JR, BURG, W.R. Occupational aspects of paseive
poking. American Zndustil Hygiene Association Journal 37(5):263-267, &y
1976.

DALHAMN. T., EDFORS, M.L., RYLANDER, R. Mouth absorption of various
cornpour& in cigarette smoke. Archives of Environmental Health 16(6):831-835,
June 1963a.

DALHAMN, T., EDFOBS, M.L., RYLANDER, R. Retention of cigarette smoke
components in human lungs. Arch&s of Environmental Herr&h 17(5):746-748,
November 196813.

BXKERY, D.W., SPENGLER, J.D. Indooroutdoor relationships of reepirable
sulfates and particles. Atmospheric Environment 15(3):33%343,1981.
DUBE, M.F., GREEN, C.R. Methods of collection of smoke for analytical purposes.
Recent Advarrces in Tobacco Science 8:42X)2,1982.
ELLICfll', L.P.. ROWE, D.R. Air quality during public gatherings. Journul of the Air
pollution Control Aseociution 25(6):635-636, June 1976.
EUDY, L.W., GREEN, C.R., HEAVOR, D.L.. INGEBRETHSE N, BJ., THORNE, F.A.
Studies on the Vapor-Particulate Phaee Distribution of Envimnmental Nicotine By
Meetive llupping and Detection Methoda. Paper presented at the 79th Annual
Meeting of the Air Pollution Control Association, Minneapolis, June 1986.
EUBY, L.W.. THORNE, F.A., HEAVOR, D.L., GREEN, C.R., INGEBRETHSEN, B.J.
Studiee on the VaporPhase Distribution of Envimnmental Nicotine By 5Wected
tipping and L&e&ion Methods. Paper presented at the 39th Tobacco Chemists'
Research Conference, Montreal, Octobsr 1986.
FERRIS, B.G., Jr., SPEIZER, F.E., SPENGLER, J.D., DOCKERY, D.W., BISHOP,
Y.M.M., WOLFSON, M., HUMBLE, C. Effects of sulfur oxides and respirable
particles on human health Methodology and demography of populations in study.
American Review of Respiratory Disease 120(4):767-779, October 1979.
FIRST, M.W. Environmental tobacco smoke measure men& Retrospect and prospect.
European Journal of Respimtory Diseases 65@upp. 133):9-16.1934.
FISCHER, T., WEBER, A., GRANDJEAN, E. LuSxenmreinigung durch Tabakrauch
in Gaststatten [Air pollution due to tobacco smoke in restaurants]. Zntemationnl
Archives of Oocrrpcztional and Environmental Health 4X4):267-280,1978.
J?iSBXER, R.L., PARUNGO, F.P. Aerosol particles on tobacco t&homes. Nature
250(5462h158-169, July 12,1974.

GALUSKINOVA, V. 3,4Benapyrene determination in the smoky atmosphere of social
meeting rooms and reetauranta: A contribution to the problem of the noxiousness
Of SO-C8lled passive smoking. Neopkzsm.a 11(5):465-463,1964.
GODIN, G., WRIGHT, G., SHEPHARD, R.J. Urban exposure to carbon monoxide.
Archives of Environmental Health 26(5):3Q5-313, November 1972.
GRIMMER, G., B&XNKJg, H., HARKE, H.P. Zum Problem des Passivrauchens
Aufnahme von polycyclisehen aromatischen Kohlenwasserstoffen durch Einatmer
von zigarettenrauchhaltiger Luft [problem of passive smoking: Intake of PolYcYCli~
aromatic bydrocarbo~ by breathing air containing &arette smoke]. zntemotionul
Archives of Occupational and~nvimnmental Health 40(2):93-9Q,1977.

171


HARKE, H.P. Zum Problem des Psssivrauchens: 1. Hoer den Einfluss des Raucherm
auf die CO-Konaentration in Biiroraumen me problem of passive smoking. 1. The
influence of smoking on the CO concentration in office rooms]. Int43nation.a~
Archiv fiir Arbeitwnedizin 33(3):199-206,1974.
HARKE, H.P., PETERS, H. Zum Problem dea Passivrauchens: 3. ober den Einfluaa
des Raucbens auf die CU-Konzentration im Kraftfahrzeug bei Fabrten h
stadtgebiet [The problem of passive smokingz 3. The influence of smoking on the
CC concentration in driving automobiles]. Internationales Archiu fir Arbeitumed-
izin 38(3):221-229,1974.

HARLOS, D.P., MARBURY, M., SAMEI?, J., SPENGLER, J.D. ReIating indoor NOs
levels to infant personal e-urea. Atmospheric Environment, in press.
HARMSEN, H., EFFENBERGER, E. Tabakrauch in Verkehmmittehi, Wohn- und
ArbsiterIoxnen pobacco smoke in transportation vehicles, living and working
rooms]. Archiv fir Hygiene und Bakteriologie 141(5):383&Q 1957.
HAWTHOFtNE, R.B. Iadoor Air Quulity Study of Forty East Tennessee Homes. ORNL-
5965. Oak Ridge, Tennessee, Oak Ridge National Laboratory, 1984.
HERNING, R.I., JONES, R.T., BACHMAN, J., MINES, A.H. Puff volume increases
when low-nicotine cigarettes are smoked. British Medioal Journal 283(6285):187-
189, July 181981.

HIGGINS, C.E., GIUEST, W.H., OLERICH, G. Application of Tenax trapping to the
analysis of gas phase organic compounds in ultra-low tar cigarette smoke-
Journal-Association of official Analytical Chemists 66(5):1074-1083, September
  1988.

HILL, C.R. Radioactivity in cigarette smoke. (letter). New England Journal of
Medicine 307(5):311, JuIy 29,1982.

HILL, P., HALEY, N.J., WYNDER, E.L. Cigarette smoking Carboxyhemoglobin,
plasma nicotine, cotinine and thiocyanate vs. seif-reported smoking data and
cardiovascular disease. Journal of Chronic JXseases 36(6):439449,1989.
HILLER, F.C., M&USHER, H.T., MAZUMDER, M.K., WIISON, J.D., BONE, R.C.
Deposition of sidestream cigarette smoke in the human respiratory tract.
American Reuiew of Eespimtory Disease 126(4):406-406, April 1982.
R[NDs, WC. Size characteristica of cigarette smoke. American Industrial Hygiene
Association Journal 39(1):48-54, January 1978.
HDNDs. W.C.. FIRST, M.W. Concentrations of nicotine and tobacco smoke in public
ph. New hgkuui Jownal of Medicine 292(16)%4-845, April 17.1975.
HOFFMANN, D.. BRUNNEMANN, K.D., ADAMS, J.D., HALEY, N.J. Indoor
PdUfhn by tobacco smoke: ModeI studies on the uptake by nonsmokers. In: Indoor
Air, Radon, Passive Smoking Particulates and HousingEpi&mi&gy. Prawsiinge
Of the Third International Conference on Indoor Air Quality and climate.
Stockholm Vol. 2,1984, pp. 313-318.

HO-, D., HALEY, N.J., ADAMS, J.D., BRUNNEMANN, K.D. Tobacco
sidestream smokes Uptake by nonsmokers. preventive Medicine 13(6)608-617.
November 1984.

HO-, D., HALEY, NJ, BRUNNEMANN, K.D., ADAMS, J.D., WYNDER,
E-L. &w=tie %?e&eam Smoke: Formntion, AM&& and Model Studies on the
@take 6-u fimmokenr. Paper presented at the USJapan meeting on the new
etiology of lung cancer, HonoluIu, March 1983.
mGEB=m, BJ.9 SEARS, S.B. Particle Size Distribution of Sidestream Smoke.
Paper Presented at the 39th Tobacco Chemista' Research conference, Montreal,
October 2-5,1988.
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER. Tobacco Smoking.
IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to
Humans, Vol. 38. Lyon, IARC, 1986.
INTERNATIONAL COMMllTEE TIC CIGAR SMOKE STUDY. Machine smoking of
cigars. Gwesta ZnformaGn Bulletin 1:3334,1974.

172


p~mU, Y. General equation for the estimation of indoor pollution. Enema-&l
&km aad Techmlogv l&1254-1257,198O.
JO~E~ON, WE-, HALE, R-W.9 WUGH, S.C., CHEN, P.H. Chemistry of the
conversion of nitrate nitrogen to smoke producte. Nature 243(510433-w, lair
25.1973.

JOLSON, W.R., KANG, J.C. Mechanisms of hydrogen cyanide formation from the
pplysis of amino acids ad related compounds. Joumd of Organic chemistry
36(lh189-192, January 15,197l.

JU, C., SPENGLER, J.D. Room--room vhdions in concentration of respirable
part&e in residences. Envimmentul Science and Teehno&~ 15(5):5g2M)6, ay
1961.

JUST, J., BORKOWSKA, M., MAELARKA, S. Eanieczysmenie dymen tytoniowym
pow&.rza kawisrn Warazawskich ~o~WXXI smoke in the air of Warsaw coffee
rooms]. Roczniki Pantstumuwo Zakludu Hygieny 230:~135,1972.
am, C.H., DERRICK, J.C. Measurement of the. particle s&e distribution and
concentration of cigarette smoke by the "conifuge." Journ& of &&id &ieMe
15(4):340-356, August 1960.

KL,US, H., KUHN, H. Verteibm6 verschiedener Tabakrauchbestandteile auf Haupt-
urxl Nebsnstromrauch (eine obersicht) mtribution of various tobacco smoke
componenta among mainstream and sidestream smoke (a survey)J &itriige .vnr
Tabakfomchung International 1X5):229-265, Nwember 1982.
KOZI.L)WL%& L.T., FRECKER, R.C., KHOUW, V., POPE, MA. The misuse of "lees-
hazardous" cigarettes and its detection: Hole-blocking of ventilg,t& filtere.
American Journal of Public Health 76(11):120%1263, November 1986.
KRUGER, J., NGTHLING, J.F. A comparison of the attachmen t of the decay producte
of radon-226 and radon-222 to monodispereed aerceols. Journal of Aenmol S&me
16(6):571-579,1979.

LEADERER, B.P., CAIN, W.S.. ISSEROFF, R. Ventilation requiremente in buildings:
2. Particulate matter and carbon monoxide from cigarette smokin6. Ahnoarpherie
hrvinwnent X3(1):99-196,1984.

LEBOWlTZ, M.D., BURROWS, B. Respiratory symptoms related to smokiq habits of
family adults. Chest 69(1):46-50, January 1976.
LEBREYI', E. Air Pollution in Lh&ch Homea Ph.D. Theais, Wae;eningen A@zultural
University, The Netherlands, 1985.

LEHNERT, G. Roundtable discussion. Preventive Medicine 13(6):730-746, November
1984.

LEI'Z, R.E., SOCZEK, M.L., SPENGLER, J.D. A survey of timeactiviity patterns in
Kingston/Harriman. Zn: Methods and Supper for Modelled lIhv&a. Paper presented
at Quality Assurance in Air Pollution  Measure menta Conference, Boulder,
Colorado, October 1984.

IdAFtTELL, E.A. Tobacco radioactivity and cancer in smokers. American Scientist
63(4):464412, July-August 1975.

McCUSKER, K., HHLER, F.C., WILSON, J.D., MAZUMDER, I&K., BONE, R.
Aerodynamic sizing of tobacco smoke particulate from commercial cigarettes.
Arch&s of Environmental Health 36(4):2X-218, July-August 1983.
MIT.T.ER J.E. Dete rmination of the componenta of pipe tobacco and cigar smoke by
means of a new smoking machine. Proceedings of the Third Workl Tobacco
Scientific Congress. Salisbury, Southern Rhodesia, February 1963, Sahsbury
Printers, Ltd., 1964, pp. 584-595.

MOSCHANDREAS, D.J., STARK, J.W.C., MCFADDEN, J-E., MORSE, S.S. IndoorAir
Pollution in the Residentid Environment, VoL 1 and 2. U.S. Environmental
Protection Agency Report No. EPA 600/7-7%229a and b, 1978.
MUEAMATSU, M., IJMEMUEA, S., OKADA, T., TOMITA, H. -tio~~ of pe-
axpoeure to tobacco smoke with a ne.wly developed nicotine personal monitor.
Environmental Research 35(1):2X%-227, October 1984.

173


m, A.D., WADDEN, R.A., ROSENBERG, S.H. Eveluation of indoor partirmlate
ConCenftations for gn urban hospital. American ~~u~tnhl Hvgiene w
&wnd 3%7):573-532, July 1978.
NERO, AV., S~I'RO, RG., DOYLE, S.M., MOED, B.A, NAZAROFF, w.w,
REWAN, K.L., 8CHWEHR, M.B. Characterizisg the ~ourcee, range and envimr,e
mend influences of radon 222 and its d-y Products. science of t& Total
Envimnmfmt 45s244, October 1935.
mUR,Am, G.B. Nitroaamine formation from precure0 ra in tobacco smoke. in:
BogovakY, P., prsussmann, R., Walker, E.A. @de). N-Nitmso Compoun&: A&k
& Forma&& mC scientific Publication NO. 3. Lyon, International Agency for
&efmh on Cfmcer, 1972, pp. 134-136.
NEURATH, G., EHMRE, H. Apparatur zur Untereuchung dee Nebenstro~~
[Apparatus for the inve&igation of side-stream smoke]. Beit&ge zur T&&for
schung 2(4):117-121, February 1964.
NEURATH, G., HORSTMANN, H. Einfluas dea Feuchtigkeitsgehaltee van C@mtte,,
  auf die Zueamm ens&ung dea Rauchee und die Glutzonentemperatur [Effect of
mo*re content of &u&tee on the composition of the smoke and the comb-
temperature]. Beit* zur Tabukforschwrg 2(3):93-100, October 1963.
IvnwHKE, LA., CLARKE, W.A., CLARKIN, M.E., TRAYNO~ G.W., WADAm
J.B. Indoor Air Q&i@. Infiltmtion and ventilation in Residential Buildinga
NYSERDA NO. 8510. New York State Energy Research end Development
  Author&y, 1935.
OKADA, T.. MA'I'SUNAMA, K. Dete rmination of particIe-&e distribution and
concentration of cigarette smoke by a Iiiht-ecattering method. Journal of Colloid
and Inteq%ce Sciewe 48(3):461-469, September 1974.
PERRY, J. Fasten your e&belts: No emoking. British Columbia Medical Journal
  15(10~304-306, November 1973.
POSRFER, J., SCHRAUR, A. Concentration and mean particle eize of the
main and side etream of cigarette smoke. Staub Reinhultung der Luft 32(10@
  36, October 1972.
PORTHEINE, F. Zum Problem dee "Passivrauchens" [A contribution to the problem
of "pesive mmoking"]. Mtinchener i@dizinisehe Wochenschrift 113(18):707-709,
  April 30.1971.
QUACKENBOS, J.J., KANABEK, MS., SPENGLER, J.D., LEI'Z, R. Personal
monitoring for nitrogen dioxide exposure: Methodological considerations for a
  mm&Q 8tudy. Envimmnent International 8(1-6)z24%268,1982.
QUANT, F.k NELSON, P.A, SEM. G.J. Experimental meaeure ments of aeroml
~WMMiOna in Officea. Envhnment Intenratiwl8(1-6):223-227,1932.
RAABR 0.0. (hmming the interactions that occur between radon decay prod-
and ae.maoIa. Health Physics 17(2)z177-136, Augur& 1969.
RADmRI& E.P-, Jr., HUNT, V.R. Poloni&21O: A volatile radioelement in eiga-
~ttee. science 143(3603):247-249, January 17,1964.
MACE, J.I+ LOWRE'Y, AH. Indoor air pollution, tobacco smoke. and publk health.
Science 2MA64-472, May 2,1$1&).
REPACE, J-L-. LowR@II, AH. Tobacco emoke, ventilation, and indoor air quality.
A- socictv of Hmhjrg, mmting and Air42mditioning Engineers, Z~C,
!l+m~~~tione 88@art 1)%X5-914,1982.
mC!KEW W-S, ROBINSON, J.C., COLLISHAW, N. Yielb of tar. nicotine, wl
c&m ~!mxid~ in the sideetream smoke from 16 bran& of Canadian cigarettsg
Ad Jownal ofPublic Health 7403228-231, parch 1%.
Sf=UMAs H.9 KuS@fA M., MUNAKATA, S,, OHSUMI, T., SUGAWARA, S. The
dibikb~ Of @!`t?tb EIO& components b-n - and sideetregm
smoke: 1. Acidic componenta. Bei- ZUT T&&forechung ~2):s71, June 1933.


SAKUMA, H., KUSAMA, M., YAMAGUGH& K., MATSUKI, T., SUGAWARA, S. The
&&ibution of cigarette smoke components between mainstream and side&ream
smoke: 2. Bases. Beit?-&@ zur Tabakfomchung 12(4):199-209, July 1984.
SAKU&iA, H., KUSAMA M-3 YAMAGUCHI, K., SUGAWARA, S. The distribution of
cigarette smoke components between mainstream and sidestream smoke: 3. Middle
and- higher boiling component. B&igc zur Tabakfomchung 12(5):251-253,
November 1984.

3&%%SELLATISFORZOLINI, G., SAMNO, A. Evaluation of a rapid index of ambient
~&smination by c&mti smoke in relation to the composition of gas phases of
the smoke. Rivista Itcrliana d'I;qione 280-2)X%%, January-April 1968.
isc%mJNG, R.S.F., LmM, AD., HUI, S.L., BECK, G., SCHOENBERG, J.B.,
BOUHUYS, A. Lung function, respiratory disease and smoking in famihes.
American Journal of Epidemiology 106(4):274-283, October 1977.
f&HhfELTZ, L, dePAOLJS, A., HOFFMANN , D. Phyt&erols in tobacco: Quantitative
analysis and fate in tobacco combustion. Be&&e zur Tabakfomchung 8(4):211-216,
December 1975.

!XBMELTZ, I., WENGER A., HOFFMANN, D., TSO, T.C. On the fate of nitdine
during pyrolysis and in a burning cigarette. Agricultuml and Food Chemi&y
27(3):60%606, May-June 1979.

SEBBEN, J., PIMM. P., SHEPHARD, R.J. Cigareti smoke in enclosed public
facilities. Archives of Environmental Health 32(2):5%X$ March-April 1977.
SEIFF, HE. Carbon Momxide a8 an Indicator of Cigarette-Clawed Pollution Levels in
Intercity Buses. U.S. Department of Transportation, Federal Highway Admini&a-
tion, Bureau of Motor Carrier Safety, April 1973.
SEXTON, K., SPENGLER, J.D., TREITMAN, R.D. Personal exposure to respirable
particles: A case study in Waterbury, Vermont. Atmuspheric Envbvnment
16(7):13851398,1984.

SLAVIN. R.G., HERTZ, M. Indoor Air Pollution Paper preeented at the 39th annual
meeting of the American Academy of Allergy, San Diego, February 1975.
SPENGLER, J.D., DOCKERY, D.W., TURNER, W.A., WOLFSON, J.M., FERRIS,
B.C., Jr. Long-term measurements of respirable sulfatea and particles inside and
outside homes Atmospheric Envirvnment 15(1):23-36,1981.
SPENGLER, J.D., REED, M-P., LEBRET, E., CHANG, B.-H., WARE, J.H., SPEIZER,
F.E., FERRIS, B.G. Harvard's In&or Air Pollution Health study. Paper presented
at the 79th Annual Meeting of the Air Pollution Control Association, Minneapolis,
June 1986.

SPENGLER, J.D., TOSTESGN, T.D. Statistical Modela for Personal Ex0ew-c.s Data.
Paper presented at the Environmetriw 81 conference of the Society for Industrial
and Applied Mathematics, Alexandria, Virgin& April 1981.
8F'ENGLER, J.D., TREMMAN, RD., TOSTESON, T.D., MAGE, D.T., SOCZEK, M.L.
Personal exposures to respirable particulates and implications for air pollution
epidemiology. Envirvnmental Science and Technokgy 1%8):766-707, August 1985.
STERLING, T.D., DIMICH, H., KOBAYASHI, D. Indoor byproduct levels of tobacco
smoke: A critical review of the literature. Journal of the Air Pollution Control
Association 32(3):250-259, March 1982.

STERLING, T.D., STERLING, E.M. Environmental tobacco smoke. 1.2. bnestigations
on the effect of regulating smoking on levels of indoor pollution and on the
perception of health and comfort of office workers. Euweun Jound of hph-
tory Diseases 65fSuppl. 133):17-32,1984.

SZADKOWSKI, D., HARKE, H.P., ANGERER, J. Kohlenmonoxidbelastung durch
Passivrauchen in B&or&unen [Body burden of carbon monoxide from passive
smoking in offices]. Innere M&Gin 3(6)316-313, September 1976.
SZAW, A. The Use of him: &ily Activities of Urban and Suburban Popular in
3fuelve Countries. The Hague, Mouton Publishers, 1972.

175


U.S. DEPMtTMEWP OF HEALTH, EDUCATION, AND WELFARE. Smok+ and
H&th: A Report of the Surgeon Geneml. DHEW Pub. No. 07960066. us.
Department of Health, Education, and Welfare, Public Health Serviw, offi~ e
the h-t ,%mtmy for Health, Offhx on Smoking and Health, 1979.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVLCES. The Health am
~a- of &noking: Cancer. A hfq.wt of the &q&on &neml. DHHS pub. &.
(pHs)8250179. U.S. Department of Health and Human Services, Public I&&b
&IV&, office of the Assistant Secretary for Health Office on Smoking w
Health, 1932.

U.S. DEPARTMENT OF HEALTH AND = s-vK.!E% !t"he Health &-
~uence.g of Smokingz Chmnic Obstrueti~ Lung Disease A Repor of the Sugcon
Ged. DEIHS Pub. No. @%S)34-50205. U.S. Department of Health and Hm
&WV&S, public Healtb Service, office of the Assistant Secretary for Health, OfIiee
on Smoking and Health, 1934.

U.S. DEPARTMENT OF TRANSPORTATION and U.S. DEPARTMENT OF
HEALTH, EDUCATION, AND WELFARE. Health Aspect.9 of Smoking in 32ane
port Aitwaf% U.S. Department of Transportation, Federal Aviation Admi&tm-
tion, and U.S. Department of Health, Education, and Welfare, National Inatit&
for Occupational Safety and Health, December 1971.
U.S. FED- TRADE COIvfIKMION. "Tar, "Nicotine and Gzrbon lldonozide of tke
Smoke of 207 V&i&es of Dm&ic Cigarettes. U.S. Federal Trade Comm%m,
January 1935.

VAINIO, H., HEMMINRI R, WILBOURN, J. Data on the carcinogenici~ of
chemicale in the IARC ddonogmphe p rogramme. Cunzinogenesis 6(11~1653-1665,
November 1935.

VILCINS, G., LEPHAIUYI?, J.O. Aging procewea of cigarette smoke: Formation of
methyl nitrite. C&m&y and I&u&y 223974-975, November 15.1975.
WADE, W.A. III, COTE, W.A., YOCUM, J.E. A study of indoor air quality. Joumai of
Ule Air Pollution Control Association 25(9):93%939, September 1975.
WALD, N., RITCHIE, C. Validation of studies on lung cancer in nonmokers married
by .sders. (letter). Lamt 1@335):607, May 12,191~.
WALLAcE,UpELLIzzARL E.D., HARWEL, T. SPRACINO, C., ZEI.QN, H.
Personal exposures indoor-outdoor relationships and breath levels of volatile
Ogaaics in New J-y. Atmospheric Envinmment, in press.
WALSII, I% BLAcg, A., MORGAN, A., CF&%WSHAW, OH. Absorption of SO, by
tppical indoor sllrfacee including wool carpets, wallpaper, and paint. Aanaepheric
J%virowieent 11(11):1107-1111,1977*

176


CHAPTER 4

   DEPOSITION
AND ABSORPTION
OF TOBACCO SMOKE
  CONSTITUENTS


CONTENTS

Deposition

Size Distribution of Cigarette Smoke
  Mainstream Smoke
  Sidestream Smoke

Particle Deposition in the Respiratory Tract
Total Deposition
Regional Deposition

Respiratory Tract Dose of Environmental Tobacco Smoke
Cigarette Smoke Particulate Mass Deposited
The Concept of "Cigarette Equivalents"

Markers of Absorption
  Carbon Monoxide
Thiocyanate
  Nicotine
  C&nine
Urinary Mutagenicity

Populations in Which Exposure Has Been Demonstrated
Experimental Studies
Nonexperimental Exposures

Quantification of Absorption
Evidence of Absorption in Different Populations
Quantification of Exposure
Comparison of Absorption From Environmental
  Tobacco Smoke and From Active Smoking

Conclusions

References


Introduction

An understanding of the deposition of &arette smoke partick in
the respiratory tract is important because many of the toxic
cmstituents of cigarette smoke are conbined in the particles. me
quantity retained, which c~nstitutea the dose, is some fraction of the
quantity inhaled. Meas~reg of tobacco smoke constituents or their
metabolites are also important because they reflect the absorption of
tobacco smoke by the individual smoker or nonsmoker, and therefore
may be more accurate markers of the actual exposure experienced
by an individual. There is little experimental information describing
the deposition of environmental tobacco smoke in the respiratory
tract (Jarvis et al. 1983). However, cigarette smoke particles
probably behave in a manner similar to other inhaled particles. I,n
contrast, there are a number of observations of different markers in
the biological fluids of smokers and nonsmokers. This review begins
with a discussion of particle deposition in general and the factors
that affect deposition. This understanding is then applied to the
existing data on tobacco smoke deposition in the human respiratory
tract. Subsequently, a variety of biologic markers of smoke absorp-
tion are e namined, and the levels of these markers found in smokers
and nonsmokers under a variety of circumstances are presented.
~inal.ly, an attempt is made to qua&it& the exposure of nonsmok-
ers relative to that of active smokers using levels of these biologic
markers.

Deposition

The term "deposition" refers to the transfer of a particle from
inhaled air to the surface of any portion of the respiratory tract,
from nose to alveolus. "Retention" is the quantity of deposited
material remaining in the respiratory tract at a specified time
following deposition. Retention decreases as clearance mechanisms
such as mucociliary action and absorption reduce the respiratory
tract burden of inhaled particles. Retention is not discussed in this
review.

An aerosol is a suspension of particles in a gaseous or vapor
medium; cigarette smoke is an aerosol. Aerosols are characterized by
such terms as mass median diameter @MD), the diameter below
which lies one-half of the particles by mass, and count median
diameter (CMD), the diameter below which lies one-half of the
particles by number. Most naturally occurring aerosols have a log-
normal size distribution, and the magnitude of the spread of particle
size is the geometric standard deviation @SD). Particle ma88 is a
function of the cube of the diameter; a particle with a diameter of 0.5
pm has one one-thousandth of the mass of a 5 pm particle. Thus, for
au aerosol with a large geometric standard deviation, the mass

181


median heter may be considerably greater than the count
median hemr. The smaller pdicle~ of an aerosol, despite tbeu
relatively small mass, have a large total surface area because of their
great number. A monodisperse aerosol has particles of one size, with
C&ID equal to M&ID, and a G-SD of 1. For practical purposes, a GSD
of 13 or less is accepted as monodisperse. Most naturally oawring
mrmb EU-C? p~lydisperse, with GSDs in the 2 range. A lognormally
&t&&cl aerosol with a GSD of 2 and a CMD of 0.1 will have an
MMD of O.&-Z. In this discussion, when size is referred to, it is the
JMI$D unless otherwise stated. Both the total deposition and the
`deposition site in the respiratory tract vary substantially with
particle size.

site wtributlon of Cigarette Smoke
m Smoke

The size distribution of cigarette smoke hes been of interest to
investigators for many years. The important relationship between
size and respiratory tract deposition is discussed below. Most studier
have been performed using mainstream smoke. Mainstream smoke
is the smoke exiting from the butt of the cigarette during puff-
drawing, and sidestream smoke is the smoke plume that drifts into
the environment from the burning tip of a cigarette between puffk.
Environmental tobacco smoke @TS) is the ambient burden of
side&ream smoke and the smoke exhaled by a smoker. Involuntary
smoking is the consumption of ETS by people, either smokers or
nonsmokers, from the environment. One purpose in discus&g the
size distribution and respiratory tract deposition of particles is to
illustrate the discrepancy between the measured particle size of
mamstresm smoke and its measured deposition in the human
respiratory tract. The deposition fraction of mainstream smoke is
several times higher than would be predicted on the basis of its
particulate size. The measured deposition of side&ream smoke is
more in keeping with its measured size (Hiller, McCusker et al.
1982).
The standard laboratory smoke-generation technique is tc force
air through the cigarette as would be done by a smoker, followed by
the rapid dilution of the resulting mainstream smoke so that particle
size can be measured. A standard 36 cma, 2-second puff is usdY
used, although actual puff volume was shown to average 45 cm' in
one tidy (Mitchell 1962) and 56 cm3 in mother; for individuals, the
Puff vohme can vary from 20 to 30 ems UP to 70 to 80 ems (Hinds et
al. 1983).

The sire distribution of the diluted mainstream smoke aerosol in
then m-u& by one of a variety of techniques such as light
scattering devices, microscopic measurement, or impactor collectipg

182


devices. using various diluting and sizing techniques, particle s&
measurements of mainstream cigarette smoke have been repor-teo
from many laboratories (Table 1). One potential cause of error in
measuring the Sk%3 distribution of main&-e&m cigarette smoke & the
relative insensitivity to ultrafine particles of some previously used
measurement methods. More recent studies using newer measure-
ment techniques support the suggestions by the earlier investigators
(Sinclair 1950) that there is an ultrafine, (< 0.1 pm) component u-~ the
cigarette smoke. Size characteristics have been measured by electron
microscopic methods, following rapid fixation of undiluted fresh
tobacco smoke, as CMD 0.2 pm and GSD 1.5 (Keith 1982). me sb
distribution measured with an electrical aerosol analyzer has been
reported as CMD 0.1 pm, GSD 2.0, suggesting more ultrafine
particles than previously recognized (Anderson and HjJ,ler 19%).
Smaller particles (< 0.4 pm) of tobacco smoke have been shown to
have a chemical composition different from that of larger particles
(St&x 19&I), possibly because of the large surface area of smaller
particles.
Laboratory methods, such as rapid dilution, commonly used to
study mainstream smoke, are highly artificial and may not accurate-
ly duplicate the generation, dilution, and inhalation of mainstream
smoke by the smoker. Smoking technique and respiratory tract
conditions may promote changes in particle size. Therefore, the
particulate sizes in the respiratory tract may differ from the sizes
measured when mainstream smoke is diluted for size analysis or
when diluted sidestream smoke is inhaled by the involuntary
smoker. The smoker's puff is taken as a bolus in a relatively small
volume of air into the humid upper respiratory tract. Smoking
techniques vary widely (Griffrtbs and Henningfield 1982) and have
been shown to vary significantly among groups classified as healthy
smokers compared with those with emphysema and also between
those with emphysema and those with bronchogenic carcinoma and
bronchitis (Medici et al. 1985). Some smokers hold the puff in the
mouth for several seconds prior to deep inhalation. The initial puff is
highly concentrated, with approximately lo8 particles/ems. At this
concentration, particle coagulation can occur rapidly, causing a
tenfold to a hundredfold reduction in particle number and an
increase in particle size (Hinds 1982). Also, the accumulation of
water in or on the particles in the high humidity of the respiratory
tract can increase particle diameter (Muir 1974), and may increase
the diameter as much as 30 percent (Mitchell 1962). Some evidence
suggests, however, that at least for dilute cigarette smoke, hygrc+
scopic growth occurs only under supersaturated conditions (Kousaka
et al. 1982). Coagulation and water uptake by particles in the
respiratory tract may considerably alter particle size distributions so
that measurements under laboratory conditions probably do not

183


!i  `l'ABLE L--Size distribution of mainstream tobacco smoke

Study

Size (pm). concentration
[no. particles/cm']

Dilution

Method

Comment

Wells and Gerke
(1919)

Sinclair
(1950)

DallaValle et al.
(1959)

CMD 0.27

Not given

Oscillation amplitude

CMD 0.0-0.3 fresh
CMD 0.4-0.5 aged

0.1-025

Not given

Light scattering

Electrostatic separation

Agedz size increase attributed to
water accumulation

Langer and Fisher
m53

CMD 0.5 filter
CMD 0.6 plain
12-6 x 1OY

1431

Microscopic impinger
collection

Compared with electrostatic
precipitation
mm 1.75

Keith and Derrick
(1960

CMD 0.23
MMD 0.46

29&l

Aerosol centrifuge
Mic-pio

GSD 1.64
C.dOUl&!d

Porstendijrfer and      ChlD 0.22
Schraub (1972)       [5-7 x 108]

1OO,ocQ1

Related rate of deposition
of radioactive decay
products onto particles to
particle 8ir.e

Also measured deposition

Pomtendiirfer
(1973)

CMD 0.42
CMD 0.22

lo:1
3,loo:l

Radon daughter attached
and deposited in spiral
centrifuge

Okada and
Matsunuma
(19741

CMD 0.16
MMD 0.29

1,50&l

Liiht scattering

GSD 1.46


TABLE l.-Continued

Size (pm), concentration

Study            [no. particleelcm']

Dilution

Method

Comment

Hinds
(1978)

McCusker et al.
(19821

Chang et al.

MMD 0.38-0.62
CMD 0.4
CMD 0.27

MMD 0.29-4.3
[4.2 x lO*]

lO:l-7oo:l
lo:1
3,loozl

126,000:1

Aermol centrifuge

Laser doppler v&&o&y

Size distribution decreases as
dilution incrensee
GSD 1.3-1.6

Aerodynamic diameter OSD 1.4

CMD 0.24-0.26
[3.6 x lay
MMD 5.5 secondary
mode

&l-18:1

Electrical aerosol aaaIyzer
(EAA)
Anderson Cascade Impactor
CD

Bimodal distribution

ww

l-8 I 100

Primary mode @AA) CSD 1.18
  Secoad mode (CD Sk-3046 of
  total mass

NOTE: CMD = count median diameter: MMD = mass medii diimeter; GSD = geometric standard deviation.


TABLE 2.-&e distribution of sidestream tobacco smoke

StudJr         size (pd     DiIUtkUl                  comnl~t

Keith and
Derrick
w6u

CMD 0.16 296zl      AWSOl        Nature of sideetxeam
       centrifuee   centrifuge      smoke generation
                      pmcmamakeadif6cult
                         exact detednation of
                          wncentration at
                       generation and dilution

Pol-sten&rfer
and Schraub
(1972)

CMD0.24   Not given   Rewed rate of
             depceition of
                 mdiwctive
             decay products
              onto prticIee
              taparticIe&e

Hiller,
Mecusker et al.
w32)

CMD 0.31   Not &en

Laser doppler
veIwiIn*

GED 1.6

NUlECMD=axmtmediMdiamaa;~=geometric etamid deviation

represent distributions found in actual mainstream smoking condi-
tions.

Side&ream Smoke

Sidestream smoke is generated by cigarettes burning spontaneous-
ly between puffs and is quantitatively the major contributor to ETS.
Fit+five percent of the tobacco in a cigarette is burned between
puffs, forming sidestream smoke (see Chapter 3). Dilution takes place
as smoke rises in the ambient air currents. This dilution with air
reduces, but probably does not eliminate entirely, the coagulation
that causes the particulate to increase in size, as they may in the
highly concentrated state that occurs when a smoker draws a puff of
mainstream smoke into the mouth and holds it briefly before
inhalation. The size distribution of sidestream smoke might be
expected to resemble that of diluted mainstream smoke. The results
of several reports of sidestream smoke size measurements (Table 2)
support this impression.

Particle Deposition in the Respiratory Tract

Total Deposition

Total deposition haa been studied both theoretically and experi-
mentally. Mathematical equations can be used to predict deposition
by combining mathematical models of lung anatomy with equations
describing the behavior of particles in tubes. The major property to
be considered is particle size and its influence on impaction,
sedimentation, and diffusion. Inertial impaction is the mechanism

186


that causes Particles moving in an airstream to be tile, because of
exceesive mass, to follow the airstream around a bend. Large
particles impact at the bend in the aimtmam or m the lung on or
near a site of airway branching. The Iarger the particle the greater
its chance of depositing by impaction. Impaction ia a relatively
unimportant form of deposition for particles smaller than 0.6 pm.
The effect of gravily on suspended particles causes them to fall, a
process called sedimentation, which also becomes relatively unim-
portant for particles less than 0.6 I.Lm in size. Larger particles fall
faster, end for all particles, the greater the residence time (in the
lung) the greater the likelihood of deposition by sedimentation.
Diffusion is the net transport of particles caused by Brownian
motion. It becomes increasingly important for particles less than 0.5
pm in size (Hinds 1982). The mass median diameter of aide&ream
smoke is in the 0.3 to 0.5 w size range. Total deposition for inhaled
particles is in the 10 to 30 percent range for 0.5 pm sixed particles.
In Figure 1, Lippmann's review (1977) of the measurements of
total deposition of monodisperse aerosols in human subjecta is
modified to include more recent data and data on ultrafine particle
depcsition.
The respiratory pattern clearly affects particle deposition. Most
important for all particles, including environmental tobacco smoke,
is the residence time in the lung. Deposition increases with slow deep
inspiration (Altshuler et al. 1957) and with breath holding (Pahnes et
al. 1966, Anderson and Hiller 1985). In hamsters, the deposition of
0.38 pm particles rises in a nearly linear fashion with oxygen
consumption (Harbison and Brain 1983). These data indicate that
deposition of ETS during involuntary smoking increases with the
increasing activity level of the exposed individual.
The presence of an electrical charge on particles may increase
deposition, Mainstream smoke is highly charged (Corn 1974). The
addition of either a positive charge or a negative charge to inhaled
particles increases deposition in animals (Fraser 19&l), and neutral-
ization of the charge reduces deposition 21 percent in rats (Per-in et
al. 1983). There is little information describing the effect of a charge
on the deposition of either mainstream or side&ream smoke in
human subjects.

Particle growth by water absorption may affect deposition. Mathe-
matical models that describe the effect of humidity on particle
growth indicate the potential for a considerable change in size of
some particles during transit in the humid rt -iratory tract (Perron
1977; Cocks and Fernando 1982; Renninger et al. 1981; Martonen
and Pate1 1981) and that these changes could ~igniikmtly alter
deposition @`err-on 1977). Growth of 0.4 to 0.5 p particles should
increase their deposition fraction, but growth of a 0.07 pm particle to
0.1 pm, for example, would reduce its deposition (see Figure 1). Such

187


     I I I
0.01   0.02 0.03  0.05   0.1    0.2  0.3  0.5 0.7 1.0    2   3   5  7  10    20
               Aerodynembic dim&r-pm

an effect has been shown for laboratory-generated aerosols in human
subjects (Blanchard and Willeke 1983; Tu and Knudson 1984). While
hygroscopic growth has been postulated for tobacco smoke (Muir
1974), it has been demonstrated in the laboratory to occur, at least
for dilute smoke, only in supersaturated conditions (Kousaka et al.
1982).
Many reports describe measured deposition of mainstream ciga-
rette smoke in the human respiratory tract CTable 3). Although few
studies of total sidestream smoke deposition are available, those few
(Table 3) suggest that sidestream smoke does indeed deposit in a
manner similar to that found for laboratoryde&ned research
aerosols. The deposition fraction of mainstream smoke diluted 1:30
and inhaled by rata from chamber air containing 1.68 mg/L
(assuming a rat tidal vo 1 ume of 1.5 mL and a respiratory rate of 85) is

138


8.1 percent @IUU et d. 1978). &positiop for the side&ream smoke
has been measured in mouth-breathing human volunteers at 11
pertint, similar to that for similarly sized polystyrene latex spheres
(Hiller, Mazumder et al. 1982). Environmental tobacco smoke
exposure frequently occurs with breathing through the nose rather
than through the mouth, but inert particles in the size range of ETS
(0.2 to 0.4 pm) are not substantially reduced in number by passage
through the nose. The fraction of inert 0.2 pm particles deposited in
the alveolar region of the lung is similar for mouth breathing and
nasal breathing (Raabe 1984). It is possible that the charged or
reactive particles of J3TS may behave somewhat differently than
inert particles, but it seems unlikely that nasal breathing substan-
tially alters the deposition of the small particles of EY.CS in
comparison with mouth breathing.

Ftegiomd Deposition

Total deposition is subdivided into the fractions depositing in the
upper respiratory tract (larynx and above), the tracheobronchial
region (trachea to and including terminal bronchioles), and the
pulmonary region (respiratory bronchioles and beyond) (Figure 2).
Deposition in these areas is referred to as regional deposition.
Particle size is a major dete rminant of both total and regional
deposition. A mathematical model prediction of regional deposition
of polydisperse aerosols is shown in Figure 2 (ICRP 1966).
Experimental verification of mathematical models of regional
deposition is limited. Using isotope-labeled particles, it is possible to
quantitate the upper respiratory tract deposition as a fraction of
total deposition. By assuming that the aerosol depositing in the
tracheobronchial region will be cleared within 24 hours, it is possible
to measure alveolar deposition as the fraction of the total initial
deposition below the larynx that is remaining at 24 hours and
tracheobronchial deposition as the difference between the initial
deposition and what is remaining at 24 hours. Using this method, the
deposition of 3.5 pm particles was this: total deposition, 0.79; upper
respiratory tract, 0.10; tracheobronchial region, 0.24; and pulmonary
region (alveolar), 0.45 (Emmett et al. 1982). These measurements are
below the estimated regional deposition for upper respiratory tract
deposition and higher for the pulmonary deposition than are the
measurements calculated by using the Task Group on Lung Dynam-
ics model (ICRP 1966).
`The regional deposition of mainstream cigarette smoke in smokers
ha alSo been studied. Subjects inhaled smoke from cigarettes
labeled with radioactive l-iodohexadecane (Black and Pritchard
1984; Pritchard and Black 1984). The results indicate that less than
40 percent of the particulate mass deposited in the pulmonary
region, compared with an expected 90 percent deposition in the


@I  TABLE 3.-R aspiratory tract deposition of mainstream and aide&ream cinarette IWWSQ

    Study

Mainstream smoke

Deposition fraction

Puff volume
CmL)

Smoke dilution

Respiratory pattern

Beumberger
(1923)

Schmahl et al.
(1954

Polydorova (1961)

Mitchell (1962)

Dalhamn et al.
U963)

   88%

   98%

   80%
(22-39 range)

   32%
(70-90 range)

98% + 3.1% SD
@6-99 range)

Not given

46 f 9.8 SD
(33-65 range)

   3s

Puff time
&and)

Not given

1.9 f 0.6 SD

   2

None

None

3OOZl

None

Hinds et al.              41%
m33)            (22-75 range)

53

None

Inhalation

Usual spontaneous
smoking pattern
"Deep inhalation"

Pretrahled
shdard~ pattern
(not dencried)
Ueual epontaneoua
smoking pattern

Side&ream smoke

Binns et al.
(1978)
Hiller, McCusker
et al. (1932)

8%

11%

Not applicable

Not applicable

  3o:l
(in cbarnber~

5I-100 palm'

Spontaneous (rata)

1 L tidal volume, 12
breatheJmin


Figure Z.-Regional deposition of particles inhaled during
     nasal breathing, as predicted using the
     deposition model proposed by the Tack Group
     on Lung Dynamics

pulmonary region for 0.5 pm particles, the size reported for cigarette
smoke (Table 1). This finding further supports the concept that
mainstream smoke particles increase in size in the respiratory tract
by coagulation, hygroscopic growth, or both, and that this growth
affects total and regional deposition. The same group studied the
effect of switching the tar content of cigarettes on regional deposi-
tion. Using. cigarettes with between 16 and 17 mg tar, extrathoracic
deposition was found to be 14 percent of the total deposition and
intrathoracic deposition to be 86 percent, with 51 percent in the
tracheobronchial area and 35 percent in the pulmonary region
(Pritchard and Black 1984). After switching to cigarettes with
between 8 and 9 mg tar, total deposition was 74 percent of that
measured from cigarettes with the higher tar content, the extratho
racic deposition was unchanged, the tracheobronchial deposition was
from 34 to 42 percent, and the pulmonary deposition was 18 to 25
percent of the total mass deposited with the higher tar cigarettes.
With the use of mathematical deposition modeling, the observed
deposition pattern was consistent with one predicted for an aerosol
with an MMD of 6.5 pm, more than 10 times greater than the MMD
described for cigarette smoke (Black and Pritchard 1984).

The deposition of particles is probably not uniform within a lung
region. The mass deposited in the airways, for instance, may vary

191


widely. -4 deposition at specific anatomic sites may ba
eswy important for mme inhalants. For example, the concentra-
tion of carcinogenic subetances at a site may favor that site for
cancer development. This may be e@ecmhY hW"rtant for c*arett@
smoke, hm lung mcer my occur at sites of high deposition such
88 my bifurcations. &p&ion of a 0.3 v laboratory-generated
stable -1 has been shown to favor right upper lobe deposition,
and on t-he ba& of surface density of deposition, the lobar bronchi
(wesmger and Lippmann 1978). The deposition per airway genera-
&n haa been d&~ for large particles, but has not received
sufficient a-eon for p&idea in the size range of main&ream or
Bidegtream smoke. A deposition peak has been Predicted, using a
lung model for the fourth airway generation (trachea is 0) for 5 q
particles, and a peak in airway surface concentration density was
predicted for 8 w particles at the fourth generation (Gerrity et al.
1979). Both of these deposition peaks are calculated for particles
&&&ially larger than those of cigarette smoke.
)3q0&ions may be quite nonuniform even within a single airway
generation. An enhanced deposition at bifurcations with highly
concentrated deposition on carina ridges within bifurcations has
been demonstrated in a five airway generation model of the human
respiratory tract for both cigarette smoke (l&u-tonen and Lowe
1983a) and restxnch aerosols (Martonen and Lowe 1983153.
Epidemiological studies of the pathophysiologic consequences of
involuntary smoking have emphasized, among other things, an
increase in the incidence of respiratory illness in children (see
Chapter 2). The issue of the respiratory tract deposition of particles
in children has been addressed only recently. Using morphometrm
measurements from casts of the lungs of children and young adults
aged 11 days to 21 years, a mathematical growth model was created.
Using this model and conventional methods for predicting the
behavior of particles in tubes, the deposition of particles at various
ag- c-m be presided. On the basis of these calculations, tracheo-
bronchial depositions per kilogram of body weight for 5 p particles
Was &h&d b be six times higher in the resting newborn than m a
resting adult @halen et al. 19851. Differences are predicted &o for
particles the s&e of sidestream smoke, with tracheobroncm
deposition m infancy beii twofold to threefold higher in adulthood.
Total deposition has also been estimated using mathematical model-
ing, with the total deposition estimated at approximately 15 percent
at age 6 months and at 10 percent in adults (XU and YU 1936).

192


ResphtoW Tract Dose of EnvIronmental ~-cc0 smoke
Cigarette Smoke Particulate lbht3 ~epoeited

The dose of environmental tobacco smoke to the respiratory tract
is the product of the mass in inhaled air and the deposition fraction.
To this point, particle size and deposition fraction, which is related to
both size and respiratory pattern as well as to other less understood
factors such as particle charge and hygroscopicity have been
addressed. To estimate dose, the content of smoke in inhaled air-
must be known, as well as the respired minute volume. m content
in inhaled air varies widely, as does minute volume, which depends
considerably on activity level. Sidestream smoke concentrations
have been raised as high as 16.5 mg/m5 in expetiental chambers
(Hoegg 1972). High levels, 2 to 4 mg/ms, have also been estimated
using measured carbon monoxide concentrations for rooms 146 m' in
size containing 50 to 70 persons @ridge and Corn 1972). Such levels
far exceed the EPA air quality standards for total suspended
particulate of 75 w/m* annual average and the 260 w/m* 24-hour
average in the United States and the 250 w/ma 24-hour average for
the United Kingdom.

Measurement8 of environmental smoke concentrations vary wide-
ly, depending upon the location and measurement technique (Tables
4 and 5). Levels of total suspended particulates (TSP) measured
under realistic circumstances have been found to be from 20 to 60
w/m3 in no-smoking areas, and can range from 100 to 700 &ms in
the presence of smokers (Repace and Lowrey 1980). These measure-
ments include all suspended particulates, and so could include
part&e other than tobacco smoke. However, in a smoky indoor
setting where measurements as high as 600 w/m9 have been found,
tobacco smoke is the major contributor to particulate mass, with the
non-tobaccwmoke contribution being small and similar to that
measured for nonsmoking areas, namely in the 20 to 60 @mS range.
This concept is supported by studies in which tobacco smoke
concentration in the environment was determined by measuring the
Gcotme content of suspended particulates. Using this technique
(Hinds and First 1975), EI'S levels have been ehimati to be 20 to
4.80 p,g/ms in bus and airline waiting rooms and as bigh as 640 p&m"
in cocktail lounges. These calculations of smoke concentrations were
based on an average weighted nicotine fraction of 2.6 percent, an
approach that may underestimate tobacco smoke particulate concen-
tration.
The mass deposition in the respiratory tract can be estimated if
the atmospheric burden of cigarette smoke particulates, minute
volume, and deposition fraction is known. Assuming a smoke
concentration of 500 CLg/mS, a minute volume of 12 liters per minute,

193


TABLE 4.--Indoor concentration of total suspended p&cUlates (TSP) meamlred iu OIY%II~ living or
      work.ing situations

Study

Just et al.
(1972)

Hinds and First
(1975)

Location

Coffee shop

Conditions of location,
owupancy, rmloking (5).
   nonsmoking @IS)

4 locations

  TSP

pm/m' x &SD

  1,160

Rackground

pm/m*

  670 '

Comments

Bus waiting

room
Restaurant

Cocktail
lounge

Arena A

Arena B

Arena C

Not given

Not given

40

m-68
200
(51-450)
WE40)

Not applicable

Suspended paarticulates

_ _
collected on filter; nicotine
content measured for
calculation; TSP =
nicotine/O.026

Elliott and Rowe
(1975)

Attendance 9,660
Air conditioned (S)
Attendance 14,300
Air conditioned (S)
Attendance 2,900
Not air conditioned 9X
Attendance 11,990
Natural ventilation (NS)

224              42

461               42

620              92

143              71

High volume sampler for
suspended particulates; also
measured Co at all locations
and benr4alpyrene in arena A

Cuddeback et al.
(1976)

Tavern       6 air changes/hr

Tavern        None apparent

0.31 f 0.05
(0.23-0.34)
  0.99

8hr air sample collected on
filter (6 pm pore size); TSP
measured gravimetrically

Neal et al.
(1976)

Hospital

intensive
care units

    
Independent ventilation

30

66

Anderson personnel sampler

systems                                                  ussd


TABLE 4.-Continued

Study               Location

Conditions of location,
occupsncy, smoking 03,
nonsmoking (NS)

   TSP

pm/m" x &SD

Sackground

pm/m3

Comments

Weber and Fischer
(1930)

Repace and Lowrey
(1980)

44 offices

Residences

Libraries,
churches,
restaurants
Restaurants,
bars, bingo
game

Window ventilation;
32144 allowed unrestricted
smoking
Air conditioned
5 locations, 6 measurements,
10 * 8 persons/l00 m3, all
NS
9 locations; 10 f 10
perwns/100 m', all NS

19 locations, 20 samples, 11
+ 8 persons/100 ms, all S
locations
7 locations with >l
smoker/ms (mean 2.2
smokers/mJ)
18 f 7 persons/lo0 ma, with
1 smoker/l00 ma

,202

  120

38 f 16

38 f 16

242 f 176
m-697)

406 * 188

(187-697)

Subtracted from
   TSP

  Same

Not done

36 + 10'
(4 locations)

47 f 13'
(13 locations)

53 f 8'

TSP measured with
pieeoefectric balance (see
above)

All samples colfected using
pieroelectric balance with very
high collection efficiency at 3.6
pm and 10% at 4 (cm; sample
the l-60 min, outdoom 6-16
min


z  TABLE 4.-Continued

Study              Location

Conditions of location,
occupancy, smoking 6%
nonsmoking (NS)

  TSP

pmhn' I fsD

Background

pm/m'

Comments

Spengler et al.
(1981)

35 homes
16 homes
5 homes

1 home*

No smokers
1 smoker
2 smokers

2 smokers, tightly sealed,
central air conditioning

24.4 f 11.6'
36.6 f. 14.6
70.4 f 42.9

  144

21.1 zlz 11.9
all 55 homes

Annual mean: respirable ma8s
collected on filters after
removal of nonrespirable
fraction; `24-hr sample collected
every 6 days

' Ambient prticulate concentration at site, but outdm~~.
`This home is one of the !ive homes above.


TABLE &-Indoor concentration of total suspended particulates (TPM) generated by smoking
      cigarettes under laboratory conditions

                                           chamber      Cigarette           TPM
Study          Test conditions         Ventiition         Size      consumption        mg/m'           Comment.9

Penkala and    Well mixed          None              9.2 ma    3 simultan~usly, 2 q       3.0
de Oliveira (19'76)                                   puffs
Hoegg       Sealed chamber;       Portable fans          25 ma    24 simultaneously by       16.66
(1972)       experimenter and test    circulated air                                  TPM measured gravimetrically
                                                  machine                   after collection of suspended
        equipment in chamber;                                             particulatea on fdten;
          measured 18 min                                                          sidestream smoke mlIected in
         pcetamoking                                                        chamber; mainstream smoke
                                                                    dischaqp?d
         Same, 150 min        Same                 4 simultaneously by        1.61
          wetsmokina                                   machine

Hugod et al.
(1978)

Sealed room

Unventilated

68 mJ

20 simultaneously by
machine

6.76

TPM measured gravimetrically
from 3hr collection on filter;
mainstream smoke in chamber

Cain et al.
(1983)

Muramahm

4-12 occupants
Climata-controlled
chamber

Climatec0ntr0lled

11 ft3/min/oceupant      11 ma     4/hr (by occupants)        0.350
66 ft'lminloccupant      11 mJ     4/hr fby occupants)        0.16

11 ft'/min/occupant      11 ma     16/hr (by occupants)        1.26
68 ft'/min/occupant      11 mJ     16/hr (by GCGU~MW        0.40

16.4 air changes/hr      34 ms     l/8 min to 60 min       0.19-0.26

F5ezoelectric balance messwed
total mass over 0.01-20 pm

Pieaoelectric balance

et al. (1963)

chamber
Climate-controlled
chamber

16.4 air changeslhr      30 ma

3 simultaneously, then
2/8 min

0.47-0.622


and a deposition fraction of 11 percent (Hiller, McCusker et al. 1982),
mass deposition over an &hour work shift would be 0.317 mg.

The Concept of "Cigarette Equivalents"

Many investigators have attempted to estimate the potential
toxicity of involuntary smoking for the nonsmoker by calculating
"cigarette equivalents" (C.E.). To inhale one C.E. by involuntary
smoking, the involuntary smoker would inhale the same mass
quantity of ETS as is inhaled from one cigarette by a mainstream
smoker. This approach has led to estimates from as low as 0.001 C.E.
per hour to as high as 27 C.E. per day (Hoegg 1972; Hinds and First
1975; Hugod et al. 1978; Repace and Lowrey 1980). These differences
of up to three orders of magnitude seem illogical when most reports
of measurements of environmental concentrations of smoke, from
the most clean to the most polluted with environmental tobacco
smoke, are within tenfold to fiftyfold of each other. The following
discussion demonstrates why the C.E. can vary so greatly as a
measure of exposure.

The calculation of C.E. is as follows: PMIw = TSP (mg/m') x Ox;
where PM&,) equals the particulate mass inhaled by passive smoking,
TSP equals the total suspended particulate, and VE equals the
inhaled volume. C.E. = PMI&PML); where C.E. equals cigarette
equivalent and PML) equals the mass inhaled by (mainstream)
smoking one cigarette. (This is taken to be the tar content of a
cigarette as reported by the U.S. Federal Trade Commission.)
Cigarette equivalents can be calculated for any time interval
chosen, i.e., per hour, per day. Although the example given is for
particulate mass, C.E. can be calculated for any component of
cigarette smoke, such as carbon monoxide and benzo[a]pyrene. The
following calculations illustrate the different results from two
different approaches to the calculation of C.E.
        Example 1      Example 2
   SIB     0.36 mg/hr     20 ma/day
  PMIw    16.1 mg tar/@   0.55 mg tar/cig
  TSP     40 CLg/mS      700 pg/m9

Example 1

PMIcp, = TSP x Ox
     = 40 P /m9 x 0.36 ms/hr
     = 14.  CLg/hr
C.E.   = PMI&PM&ms,
   = (0.0144 mg/hr)/(l6.1 mg/cig)
    = 0.001 cig/hr

198


Example 2

PM&PI  =TSPxOr
   = 700 w/ma x 20 ma/&y
   = 14,990 p&day
C.E.   = PMldwIk4
   = (14 mgklay)/(O.65 mghig)
    = 245 &g/day

These caktitiOn8 of C-E. approximate the approach- d h ho
~~rts-Exanw~e 1 by Kinds and Pi.& (1975) and Example 2 by
Repace and Lowrey (198O)-and the results are similar. The exam-
ples are the extremes used in the two studies, and are at the
extremes Of CommOmy cited rep&a of C.E. Even if the Tsp
concentration used in the two examples were the me, the multx
would differ 24-fold because Example 1 is calculated per hour and
Example 2 is calculated per day; 2%fold because of the aerence in
inhaled minute volume; and 29-fold because of the difference in what
is considered to be a `Wandard" cigarette. Even using the same TSP
concentration, the results would be 1.6 x 10" different. If C.E. is to be
calculated, all of the factors used in the calculation should be
Standardized.

The calculation of C.E. is deficient in several other ways. The
deposition fraction of the total inhaled particulate mass in the
respiratory tract from mainstream smoke is higher than from
involuntary smoking. The deposition fraction for involuntary smok-
ing is approximately 11 percent for mouth breathing (Hiller,
Mazumder et al. 1982). The deposition from mainstream smoke has
been reported to vary from 47 to 90 percent (Table 3). The cigarette
equivalent calculation considers only the quantity inhaled, and if
mm dose depoeited is considered, one C.E. from passive smoking
will cause several times less mass to be deposited than the
mainstream smoke of one cigarette.
The differences in the chemical composition between sidestream
smoke and mainstream smoke make the C.E. concept misleading
unless C.E. is calculated for each smoke constituent. This has been
accomplished (Hugod et al. 1973) using measured levels of various
smoke co&ituente in a chamber filled with sidestream smoke. The
redts indicate that one C.E. for carbon monoxide could b i&&j
5.5 times faster, and for aldehyde, 2.9 times faster, than for
particulate mass. Measurements of total particulate matter and
benxc(a]pyrene taken in an arena with active smoking revealed a
fivefold rise in TSP above background and an eighteenfold increase
in benzo[ajpyrene over background. Using the measured ben-
zo[alpyrene concentration of 21.7 ng/ms, an inhaled volume of 2.4
ma, and 3.2 ng benxo[ajpyrene per cigarette, the occupant of such an
environment would consume 6.4 C.E. for benzo[ajpyrene (IARC 1986,
p. 87). The C.E. TSP would be 1.7. Therefore, a C.E. for the

199


carcinogen bedabyrene would be inhaled 3.6 times more rapidly
w a C.E. for `JSP moth and Rowe 1975).

me *de latitude h the results of C.E. calc~ations demonstrates
the &pen&n= of the C.E. c.ahhtiOn On the numerical VahleS of the
variables chosen, and correspondingly demonstrates the marked
lotion of &e use of C.E. as an atmospheric measure of exposure
b the wnb h en&m&d MOROCCO smoke. When the quantifica-
con of an w ia needed, it is far more precise to use terms that
defiae &e a of exposUre t0 the agent Of interest per unit
he. However, the term cigarette equivalent is frequently used, not
&ply 88 a mwure of exposure, but 88 a unit of disease risk that
~~them~ured~uresintoatikofdiseaseusingthe
known daeresponse relationships between the number of ciga-
re#es~~perdayandtheriskofdiseaee.IfC~.istobeusedasa
tit of risk, the variables used to convert atmospheric measures into
levels of rid for the active smoker need to be determined on the
basis of the depcsition and smoke exposure measures for the average
smoker. The deposition fraction of individual smoke constituents in
t&e population of active smokers is needed rather than the range
ob~rved in a few individuals. In addition, the actual average yield of
the cigarettes smoked by the subjects in the prospective mortality
studies would be needed to compare the dose-reeponse relationships
accurately. The yield using the Federal Trade &nmission (Fl'c
method may dramatically underestimate the actual yield of a
cigarette when the puff volume, rate of draw, or number of puffs is
increeeed; therefore, calculations using the Fl'C numbers may be
inaccurate, particularly for the low-yield cigarettes. These limita-
tions make exlxapolation from atmospheric measurea to c&are*
equivalent units of disease risk a complex and potentially meanin-
BleseP~.

lAaiwa of Absorption

In contrast, measuma of absorption of environmental tobacco
smoke, particularly cotinine levels, can potentially overcome some of
the limitations in translating environmental tobacco smoke expc+
sure3 into expected d&ease risk. Urinary cotinine levels are a
reLatively accurate dosage measure of exposure to smoke; they have
been measured in populations of smokers and nonsmokers, and are
not subject to emrs in estimates of the minute ventilation or yield of
the average cigarette. Potential differences in the half-life of cotinine
in smokers and nonsmokers, differences in the absorption of nicotine
relative to other toxic agents in the smoke, and differences in the
ratio of nicotine to other toxic agents in mainstream smoke and
sidestream smoke remain sources of error, but the accuracy with
which active smoking and involuntary smoking exposure can be

200


compared is almost certainly substantially greater with measures of
absorption than with atmospheric measures.
Tobacco smoke contains many substances, but only a few have
been measured in human biological fluids. of the g-w compo-
nents, markers include carbon monoxide and thiocyanate. The latter
is not a gas but a metabolite of gaseous hydrogen cyanide. Concentra-
tions of nicotine and its metabolite cotinine are markers of nicotine
uptake. In mainstream smoke, nicotine uptake reflects exposure to
particulates. In environmental tobaccc smoke, nicotine becomes
vaporized and therefore reflects gas phase expcsure @udy et al.
1985). Quantitating tar consumption is more difficult urinary
mutagenic activity has been used as an indirect marker.

The relative exposures of nonsmokers to various tobacco smoke
constituents differs from that of smokers. Assuming that exposure to
a single tobacco smoke constituent accurately quantifies the expo-
sure of both smokers and nonsmokers to other constituents is
inaccurate because mainstream smoke and environmental tobacco
smoke differ in composition (see Chapter 3).

To understand the usefulness and limitations of various biochemi-
cal markers, it is important to appreciate the factors that influence
their absorption by the body and their disposition kinetics within it.

Carbon Monoxide

Carbon monoxide is absorbed in the lungs, where it dZfuses across
the alveolar membrane (Lawther 1975; Stewart 1975). It is not
appreciably absorbed across mucous membranes or bronchioles.
Within the body, carbon monoxide binds, as does oxygen, to
hemoglobin, where it can be measured as carboxyhemoglobin.
Carbon monoxide may also be bound to myoglobin and to the
cytochrome enzyme system, although quantitative details of binding
to the latter sites are not available. Carbon monoxide is eliminated
primarily by respiration. The amount of ventilation influences the
rate of elimination. Thus, the half-life of carbon monoxide during
exercise may be less than 1 hour, whereas during sleep it may be
greater than 8 hours (Castleden and Cole 1974). At rest, the half-life
is3to4hour-s.
The disposition kinetics of carbon monoxide explain the temporal
variation of carbon monoxide concentration in active smokers during
a day of regular smoking. With a half-life averaging 3 hours and a
reasonably constant dosing (that is, a regular smoking rate), carbon
monoxide levels will plateau after 9 tc 12 hours of cigarette smoking.
This has been observed in studies of circadian variation of carbon
monoxide concentrations in cigarette smokers (Benowitx, Kuyt et al.
1982). Smoking is not a constant exposure source, but results in
pulsed dosing. There is a smsll increment in carboxyhemoglobin
level immediately after smoking a single cigarette, which then

201


declines mta tie next, cig~tt.e is smoked. But after several hours of
smou, the m@t&e of rise and faR is small compared with the
trough vahres. For this reason, carboxyhemoglobm levels at the end
of a day of smoking are satisfactory indicators of carbon monoxide
exposure during that day.

&bn monoi& e-m may be more'constant during environ-
mental ~~CCCB m&e exposure than during active smoking. The
major limitation m using carbon monoxide as a means of measuring
hrvohmtary smoke exposure is its lack of specificity. Endogenous
carbcn monoxide generation from the metabolism of hemoglobin
results in a low level of carbo~hemoglobin (up to 1 percent)
(Lawther 1975; Stewart 1975). Carbon monoxide is generated by any
source of combustion, including gas stoves, machinery, and automo
bile exhaust. Thus, nonsmokers in a community with moderate home
and industrial carbon monoxide sources may have carboxyhemogb
bin levels of 2 or 3 percent (Woebkenberg et al. 1981). A carbon
monoxide level of 10 in room air results in an increment of 0.4 and
1.4 percent carboxyhemoglobin at 1 and 8 hours of exposure time,
respectively (Lawther 1975; Stewart 1975). Thus, small increments of
carhcn monoxide due to environmental tobacco smoke may be
indistinguishable from that due to endogenous and non-tobacco
related sources.

Measurement of carbon monoxide is straightforward and i,nexpen-
sive. &dar carbon monoxide pressures are proportional to the
concentration of carhoxyhemoglobin in blood, therefore, end&~
carbon monoxide tension accurately reflects blood carboxyhemoglo
bin (Jti and Russell 1980). Expired carbon monofide - &
measured Using an instrument (Ecolyzer) that measures the rate of
conversion of carbon monoxide to carbon &&de 88 it pm over a
catalytically active electrode. Blood carboxyhemoglobin - b
xm~~ured ~~1~ ad quickly wing a differential spectropho~m~
ter.

Hydrogen cyanide is metabolized by the liver to thiooyanate. In
addition to tobacco smoke, certain foods, particularly leafy vegeta-
bles and some nuts, are sources of cyanide. Cyanide is also present in
beer.
Thiocyanatc is distributed in extracellular fluid and is eliminated
slowly by the kidneys. The half-life of thiocyanate is long, about 7 to
14 days. Thiocyanate is also secreted into saliva, with salivary levels
about 10 times that of plasma levels (Haley et al. 1983). The long
half-life of thiocyanate means that there is little flu&ration in
plasma thiocyanate concentrations during a day or from day to day.
Thus, the time of sampling is not critical. On the other hand, a given
level of thiocyanate reflects exposure to hydrogen cyanide over


several we&~ ~mceding the time of sampling. When a smoker stops
smoking, it takes an estimated 3 to 6 weeks for thiocyanate levels to
reach that individual's nonsmoking level.
Because of the presence of cyanide in foods, chiocyanate is not
specific for exposure to cigarette smoke. Although active smokers
have plasma levels of thiocyanate two to four times those of
nonsmokers (vogt et al. 1979, Jacob et al. 1981), light smokers or
involuntary smokers may have little or no elevation of thiocyanate.
When thousands of subjects are studied, involuntary smokers have
been found to have slightly higher thiooyanate levels than those
without exposure (Friedman et al. 1983). Other studies of smaller
numbers of subjects have shown no difference in thiocyanate level
between exposed or nonexposed nonsmokers (Jarvis et al. 1984).

Serum or plasma thiocyanate levels can be measured using
spedrophotometric methods or, alternatively, gas chromatography.

Nicotine

Nicotine ia absorbed through the mucous membranes of the mouth
and bronchial tree as well as across the alveolar capillary mem-
brane. The extent of mucosal absorption varies with the pH of the
smoke, such that nicotine is absorbed in the mouth from alkaline
(cigar) smoke or buffered chewing gum, but very little is absorbed
from acidic (cigarette) mainstream smoke (Armitage and Turner
1970). With aging, environmental tobacco smoke becomes less acidic;
pH may rise to 7.5, and buccal or nasal absorption of nicotine by the
nonsmoker could occur (see Chapter 3).
Nicotine is distributed rapidly to body tissues and is rapidly and
extensively metabolized by the liver. Urinary excretion of unmetabo-
lized nicotine is responsible for from 2 to 25 percent of total nicotine
ehnrination in alkaline and acid urine, respectively; nicotine excre-
tion also varies with urine flow (Rosenberg et al. 1980). Exposure to
environmental tobacco smoke, active smoking, and use of smokeless
tobacco markedly elevate salivary nicotine transiently out of propor-
tion to serum and urinary levels (Hoffiann et al. 1984). Nicotine is
present in breast milk (Luck and Nau 1985), and the concentration
in the milk is almost three times the serum concentration in the
mother (Luck and Nau 1984).
The rate of nicotine metabolism varies considerably, as much as
fourfold among smokers (Benowitz, Jacob et al. 1982). There is
evidence that nicotine is metabolized less rapidly by nonsmokers
than by smokers (Kyerematen et al. 1982). A given level of nicotine
in the body reflects the balance between nicotine absorption and the
metabolism and excretion rates. Thus, in comparing two persons
with the same average blood concentration of nicotine, a rapid
metabolizer may be absorbing up to four times as much nicotine as a
slow metabolizer. To determine daily uptake of nicotine directly,

203


both the nicotine blood concentrations and the rates of metabolism
and excretion must be known. These variables can he measured in
experimental studies (Renowitz and Jacob 1984; Feyerabend et al.
1985), but are not feasible for large-scale epidemiologic studies.
The time course of the decline of blood concentrations of nicotine is
multiexponential. Following the smoking of a. single cigarette or an
intravenous injection of nicotine, blood concentrations of nicotine
decline rapidly owing to tissue uptake, with a half-life of 5 to 10
minutes. If concentrations are followed over a longer period of time
or if multiple doses are consumed so that the tissues are saturated, a
longer elimination half-life of about 2 hours becomes apparent
(Renowitz, Jacob et al. 1982; Feyerabend et al. 1985). Because of the
rapid and extensive distribution in the tissues, there is considerable
fluctuation in nicotine levels in cigarette smokers during and after
smoking. As predicted by the Z-hour half-life, nicotine blood concen-
trations increase progressively and plateau after 6 to 8 hours of
regular smoking (Renowitz, Kuyt et al. 1982). Nicotine concentra-
tions have been sampled in the afternoon in studies of nicotine
uptake during active cigarette smoking (Renowitz and Jacob 1964,
and similar timing might be appropriate in assessing the plateau
levels that result from continuous ETS exposure, such as during a
workday.

Russell and colleagues (1965) quantitated nicotine exposure by
comparing blood nicotine concentrations during intravenous infu-
sions (0.5 to 1.0 mg over 60 minutes) in nonsmokers to the blood
nicotine concentrations in nonsmokers exposed to environmental
tobacco smoke. The data suggest that nicotine uptake in a smoky bar
in 2 hours averaged 0.20 mg per hour.  ..
The presence of nicotine in biologic fluids is highly specific for.
tobacco or tobacco smoke exposure. Nicotine concentration is sensi-
tive to recent exposure because of nicotine's relatively rapid and
extensive tissue distribution and its rapid metabolism. Urinary
nicotine concentration has been examined in a number of studies of
environmental tobacco smoke exposure. Although influenced by
urine pH and flow rate, the excretion rate of nicotine in the urine
reflects the concentration of nicotine in the blood -over the time
period of urine sampling. In other words, nicotine excretion in a
timed urine collection is an integrated measure of the body's
exposure to nicotine during that time. When timed urine collections
are not available, nicotine excretion is commonly expressed as a
ratio of urinary nicotine to urinary creatinine, which is excreted at a
relatively constant rate throughout the day. Urinary nicotine
excretion is highly sensitive to environmental tobacco smoke expo
-sure (Hoffmann et al. 1984; Russell and Feyerabend 1975). Saliva
levels of nicotine rise rapidly during exposure to sidestream smoke
and fall rapidly after exposure has ended (Hoffmann et al. 1984).

204


Presumably, this the course reflects local mouth contamination,
followed by absorption or the swallowing of dcotine.

Blood, urine, or saliva concentrations of nicotine can be measured
by gas chromatography, radioimmunoaaeay, or high pressure liquid
chromatography- sample preparation is problematic in that contam-
ination of samples with even small amounts of tobacco smoke c8n
substantially elevate the normally low concentrations of nicotine in
the blood. Thus, careful Precautions against contamination during
sample collection and processing for analysis are essential. &cause
the concentrations are so low, the measurement of nicotine in blood
has been difficult for many laboratories in the past, but with
currently available assays, it is feasible for largescale epidemiologic
StUdiM.

C&nine

Cotinine, the major metabolite of nicotine, is distributed to body
tissues to a much lesser extent than nicotine, Cotmine is eljmmated
primarily by metabolism, with 15 to 20 percent excreted unchanged
in the urine (Benowitz et al. 1983). Urinary pH does affect the r-end
elimination of cotinine, but the effect is not as great as for nicotine.
Since renal clearance of cotinine is much less variable than that of
nicotine, urinary cotinine levels reflect blood coti.&e levels better
than urinary nicotine levels reflect blood nicotine levels. Plasma,
urine, and saliva cotinine concentrations correlate strongly with one
another (Haley et al. 1983; Jarvis et al. 1984).
The elimination half-life for cotinine averagea 20 hours (range, 10
to 37 hours) (Benowitz et al. 1983). Because of the relatively long
half-life of cotinine, blood concentrations are relatively stable
throughout the day for the active smoker, reaching a maximum near
the end of the day. Because each cigarette adds relatively little to the
overall cotinine level, sampling time with respect to smoking is not
critical. Assuming that smoke exposure occurs throughout the day, a
midafterrmcm or late afternoon level reflect8 the average wtinine
concentration.
The specificity of cotinine as a marker for cigarette smoking ie
excellent. Because of its long -half-life and its high specificity,
cotinine measurements have become the most widely accepted
m&hod for assessing the uptake of nicotine from tobacco, for both
active and involuntary smoking.
Gotinine levels can be used to generate quantitative estimates of
nicotine absorption. Galeazzi and colleagues (1985) defined a linear
relationship between nicotine uptake and plasma cotinine levels in
six healthy volunteers who received several i.v. doses of nicotine
( 5 480 &kg/day) for 4 days. The ability to extrapolate from this
model to levels in nonsmokers is limited, however, because the
elimination half-life of cotinine may be shorter in smokers than in


nsmokers, as is the elimination ha&life of nicotine (Kyerematen
1; al. 1982).
Cotinine can be assayed by radioimmunoassay, gas chromatogra-
phy, and high pressure liquid chromatography.

Urinary Mutagenicity

TO&~ smoke condensate is strongly mutagenic in bacterial test
s-m (ties test) (Kier et al. 1974). A number of compourids,
j&u&g polycyclic aromatic hydrocarbons, contribute to this
mutagenicity. The urine of cigarette smokers has been found to he
mutagenic, and the number of bacterial revertants per test plate is
r&ted to the number of cigarettes smoked per day Wamasaki and
Ames 1977). Urinary mutagenicity disappears within 24 hours after
smoking the last cigarette &do et al. 1986).
For several reasons, the measurement of mutagenic activity of the
urine is not a good quantitative measure of tar absorption. Individu-
als metabolize polycyclic aromatic hydrocarbons and other mutagen-
ic substances differently. Only a small percentage of what is
absorbed is excreted in the urine as mutagenic chemicals. The
bacterial system is differentially sensitive to different mutagenic
compounds. The urine of smokers presumably contains a mixture of
many mutagenic compounds. In addition, the test lacks speciEcity, in
that other environmental exposures result in urinary mutagenicity.
The test may also be insensitive to very low exposures such as
mvobmtary smoking. However, one study, by Bos and colleagues
(1983), indicated slightly increased mutagenic activity in the urine of
nonsmokers following tobacco smoke exposure.
The presence of bedalpyrene and 4-amino biphenyi covalently
bound to DNA and hemoglobin in smokers (Tannenbaum et al., in
press) suggests other potential measures of carcinogenic exposure.
Whether such measures will be sensitive to HIS exposure is
unknown. The development of specific chemical assays for human
exposure to componenta of cigarette tar remains an important
researchgoal.

Populations in Which Exposure Has Been Demonstrated
Absorption of tobacco smoke components by nonsmokers has been
demonstrated in experimental and natural exposure conditions.

Experimental Studies

Nonsmokers have been studied after exposures in tobaccosmoke-
Clled rooms. The smoke may be generated by a cigarette smoking
machine or by active smokers placed in the room by the investigator,
or the location may be a predictably smoke-filled environment such
as a bar. The level of environmental smoke has most often been


quantitated by measuring ambient carbon monoxide concentrations.
In nonsmokers exposed for 1 hour in a test room with a carbon
monoxide level of 33 ppm, carboxyhemoglobin levels increased by 1
percent and urinary nicotine increased about eightfold (Russell and
Feyerabend 1975). Seven subjects in a similar study sat for 2 hours in
a public house (bar) with a carbon monoxide level of 13 ppm; their
expired carbon monoxide increased twofold and their urinary
nicotine excretion increased ninefold (Jarvis et al. 1983). In a study
exposing eight nonsmokers to a smoke-filled room for 6 hours, a
small increase in urinary mutagenic activity was measured (Bos et
al. 1983).

Nonexperimental Exposures

Exposure studies performed in real-life situations have compared
biochemical markers of tobacco smoke exposure in different imiivid-
uals with different self-reported exposures to tobacco smoke. Absorp
tion of nicotine (indicated by urinary cotinine levels) was found to be
increased in adult nonsmokers if the spouse was a smoker (Wald and
Ritchie 1934). In another study (Matsukura et al. I984), urinary
cotinine levels in nonsmokers were increased in proportion to the
presence of smokers and the number of cigarettes smoked at home
and the presence and number of smokers at work. Blood and urinary
nicotine levels were increased after occupational exposure to ETS
such as a transoceanic flight by commercial airline flight attendants
(Foliart et al. 1983). Nicotine absorption, documented by increased
salivary cotinine concentration, has been shown in schoolchildren in
relationship to the smoking habits of the parents (Jarvis et al. 1985),
and using plasma, urinary, and saliva measures, in infants in
relation to the smoking habits of the mother (Greenberg et al. 1934;
Luck and Nau 1985; Pattishall et al. 1935).

Quantification of Absorption
Evidence of Absorption in Different Populations

One questionnaire survey indicated that 63 percent of individuals
report exposure to some tobacco smoke (Friedman et al. 1983).
Thirty-four percent were exposed for 10 hours and 16 percent for 40
or more hours per week. The distribution of cotinine levels in a few
populations has been reported. In men attending a medical screening
examination, there was a tenfold difference in mean urinary
cotinine in nonsmokers with heavy exposure (20 to 80 hours per
week) compared with those who reported no ETS exposure (wald et
al. 1984). The median and 90th percentile urinary cotinine concen-
trations for all nonsmokers who reported exposure to other people's
smoke were 6.0 and 22.0 ng/mL, respectively, compared with a
median of 1645 ng/mL for active smokers, In 569 nonsmoking

207


schoolchildren, salivary cotinine concentrations were widely distrib-
uted. Values were strongly influenced by parental smoking habits
(Jarvis et al. 1985). The median and 25 to 75 percent ranges (in
ng/mL) were 0.20 (O-0.5), 1.0 (O&1.8), 1.35 (0.7-2.71, and 2.7 (l.M.4)
for children whose parents did not smoke or whose father only,
mother only, or both parents smoked, respectively.

Quantification of Exposure

Expired carbon monoxide, carboxyhemoglobin, plasma thiocya-
nate, plasma or urinary nicotine, and plasma, urinary, or salivary
cotinine have been used to evaluate exposure to ETS. However,
successful attempts to quantify the degree of exposure have been
limited largely to measurements of nicotine and cotinine. Expired
carbon monoxide and carboxyhemoglobin have been found to be
increased up to twofold after experimental or natural exposures
(Russell et al. 19731, `but not in more casually exposed subjecta.
Thiocyanate was slightly increased in one very large study of heavily
exposed individuals (Friedman et al. 1983), but most studies report
no differences as a function of involuntary smoking exposure. The
most useful measures appear to be nicotine and cotinine. The data on
nicotine and cotinine measurements are presented in Tables 6 and 7
and suggest the following:

(1) Both nicotine and cotinine are sensitive measures of environ-
mental tobacco smoke exposure. Levels in body fluids may be
elevated 10 or more times in the most heavily exposed groups
compared with the least exposed groups.

(2) The tune course of change in the levels of biochemical markers
depends on which marker is selected and which fluid is sampled.
There ia a lag between peak blood levels of nicotine and peak blood
levels of cotinine, owing to the time required for metabolism
(Hoffmann et al. 1984). Salivary levels of nicotine, because of the
local deposition of smoke in the nose and mouth, peak early and
decline rapidly.

(3) With nicotine, salivary levels increase considerably after
environmental tobacco smoke exposure, but decline rapidly follow-
ing the end of exposure. Blood nicotine levels are too low to be very
useful in quantitating environmental nicotine exposure. Urinary
nicotine is a sensitive indicator of passive smoke exposure, but
because of its relatively short half-life, urinary nicotine levels
decline within several hours of the time of exposure.

(4) Cotinine levels are less susceptible than nicotine to transient
fluctuations in smoke exposure. Blood or plasma, urine, and saliva
concentrations correlate strongly with one another. Because of the
stability of cotinine levels measured at different times during an
exposure and the availability of noninvasive (i.e., urine or saliva)

203


TABLE 6,Nicotine measurea in nonsmokers with environmental tobacco smoke (EIB) sxponve and
      comparisons with active smoking

Numberof Smoking

eubjecta    et&Ii     Rxposum level      BefOr     After    Mom        After        Before     Ahr

Ruassll and
Feyerebend
U~6)

Feyerabend
et al. (1982)

Foliart et al.
M89)

12       NS

14       NS
13       NS
18       S

26       NS
90       NS
8       S
16       S
32       S
27       5

6       Ns

18 min in
enlokem2d room
Hoepad
~~~lw=u
Averege 24 cigdday
No S eqxnum
Work expmum
Nonlnhelem
slight inhalere
Medium bIbden
Dwp inhdm
Flight attendNIb

0.73       0.90

-

- -

        -
        -
-

-
        -
  (1E.S)

-     80 w-2rs)           - -

    12.4 (O&64.3)           - -
    8.9 (o-26)            - -
-    1236 (104-2799)          - -

-     1.5                     lb.9
    21.6                     10.1
     w                    ls2
    1261                    421
    1949                   (64
    1527                     o(#

    lb.2 (8.Sr.4)          - -

.

JAetal.       7       NS     s&m, 1Mo can.        0.8       2.6        10.6.   92.6                1.9    49.6

After, public houm x
2hr

HolTmann et al.     10       NS     Rxpimental chamber
(1980                   2cigaburned          1.1        1.1        24'    Sl'                0     427
                     3cigebumed          ND       1.3        20    94                 1     ma
                     4 cigc burned          0.2       0.5       17    loo               3     790


E  TABLE i&fhntinued
0

                                                Mean or median conoentration and range

Study

Number of   Smoking
subjects      etatus

Expmure level

Plasma nicotine
   ht/mL,

Before      After

     Urine nicotine          Saliva nicotine
     bf+u             WmL,

Before       At&        EdOR     After

Jarvia et al.
ww

Greenberg
et al. (1984)

Luck and Nau
(1986)

48
27
20
7
94

32
19

10
10

10
9

       Hospital clinic patients
  NS     No expmure           -        1.0        -     3.9                -     3.8
  NS     Little expceure         -        0.8             12.2                     4.8
  NS     Some expcmm         -       0.7        -    11.9                    4.4
  NS     Lot of exposure         -        0.9       -    12.2                     12.1
  S                        -       14.8            1760                -     872

  NS     Infanta, mother S        -                 -     as' (O-370)             12.7 (O-188)
  NS     infant, mother NS       -                 -     0 o-89)            -     0 (O-17)
NS, neonates   No exposure           -                 -     0' @14)           - -
NS, neonates  Nuraad by S mother:      -                   14 (&llO)           - -
       no Em expomre
NS, infants   S mother, not nursed      -                 -     36 (4-218)           - -
NS, infants   Nureed by S mother;      -                 -     12 (s-42)            - -
       Em exposure

1 nglmg creatinins.


TABLE V.-Cotini.ne measures in nonsmokers with environmental smoke exposure and comparisons
      with active smoking

                                     ban or median concentration and -
                                        Plaema &hine
        Number                                               Urine cutinine
                                     WmL)                           salivaootin&

         Of    Smoking                                     WmL)           WmL)
Study    eubjecta     atatw        Expoeure level        Before     After     Before        After         More     After

Jarvis       7      NS       Before, 1150 a.m.            1.1 7.3
et al.                                                           4.8       12.9             1.6    8.0
                  After, public houae x 2 hr
GBw

Jarvis                 Hcepital clinic patients
et al.      48      NS       No expmure                     0.8
ww      27     NS                                                    1.6                  0.7
                    Litie expmum                                                     -
                                               -     1.8         -
         20     NS                                                       6.6                   2.2
                   Some expoeure                                                     -
                                               -     2.6         -         8.6
         7      NS                                                                          2.8
                   Lot of expmure                                                    -
                                                     1.8         -         9.4
        94     S                                                                        26
                                               -     276        -        1391             -     810

Hoffmann 10      NS       Rperlmental chamber
et al.                 2 ciga burned              1.7    2.6 (peak     14        21              1.2     28
ww                 Scignburned              1.0    3.0 chenge) 14        88             1.7     2.6
                   4eigsburned              0.9 9.9         14        66             1.0     1.4

Wald and   101      NS        Wife abstinent              - -        8.6 (median 6.0)
Ritchie     20      NS        Wife uaoker               - -        26.2 (median 9.0)


TABLE `I.--continued

        Number
         of    Smoking
Study     subjecte     etatue

Ekpceure level

M~I or median amcantration and raage

       Urine wtinine          sdh mtininc
       b6ld.J           WmL)

BdOl-fJ        After         hf0m    After

Wald
et al.
(1984)

221     NS
43     NS
47      NS

        43     NS
        43     NS
        46     NS
        131      S
        69     S
        42     S

Mataukura  200     NS
et al.      272     NS
ww
        25     NS
        67     NS
        99     NS
         38     NS
         28     NS

        472     NS
        392     S

Med scraening clinic patients
-   ch colleeguex
O-l.6 hr JTTS expaeurejwk
1.6-4.6 hr El?3 exposumlwk
4.5-8.6 hr El% expumlwk
8.6-20 hr ~3% expwlwk
XI-W hr E%?J expmlwk
cigarettes
wm
Pips

No home exposure
All home exposure
Home expmure:
l-9 &/day
lo-19 CigldaY
20-29 CisldaY
So-39 ciglday
> 40 ciglday

All
All

76     NS
201      NS

No workplace exposure
Workplace exposure

-        11.2
-         2.8
         3.4
         6.3
         14.7
        29.6
-        1646 (637-3326)
-         398 (613139)

-      1920 MmS-46@)

-        610 '

790

        310
        4m
-        870
-        1030
        1680

-        880
-        8620

-        220
         720


TABLE 7.-Continued

Mean or median concentration and range

Study

Number
of
aubjocta

Smoking
etatua

Expmure level

Plasma cotinine
   (nghL)

Before     After

Before

urine c&nine
ww

     After

Saliva cotinine
   b&IlL)

Before ARer

Greenberg 32
et al.      19
(1984)

NS, infants

S mother                                   361 (41-1885)        -
NS mother                                                   9 @-261
                                     -        4 0-125)         -    0 6x3)

Jarvie
et al.      269
(1965)
        98
        76
        128

Luck and 10
Nau       19
NW
         10
         9

       Children aged 11-16
NS       Neither parent SM                                                  -     0.4
                                                                     (median 0.2)
NS        SM father                                                       1.9 (1.0)
NS        SM mother                                                       2.0 (1.7)
NS       Both parents SM                                                    -     3.4 (2.4)

NS, neonates  No exposure               - -         -        0' @-w               -
NS, neonates  Nursed by S mother;          -     -                loo Qo-666)         -
       no Fps exposure
NS, infants   S mother, not nursed          - -               327 (117-780)
NS. infants    S mother, nursed;            - -               660 (226870)              -

ITS exp&ure

Serum mtinine

Pattishall 20
et al.       18

NS, children   Smokers in home                4.1                                      -
                                                                      -
NS, children   No smokers in home                1.0         -


E  TABLE CI.-Continued

Mean or median concentration nnd range

Study

Number
of
subjects

Smoking
statue

Expoeure level

PI- cotinhe
   b&W

Before     After

Before

Urine cotinine
wmu

     After

coulta8     88     NSaBed (6   No emokera in home
et al.      41    NS aged (6   1 smoker in home
w66)      21     NS aged <6   2 or more smokera in home
        200     NS aged Cl7  No smokers in home
        98     NS aged 6-17  1 smoker in home
        26     NS aged 617  2 or more mnokem in home
        316     NSaged >17  No smokers in home
        80     NSaged >17  1 emoker in home
        12     NSaged >17  2 or more smokers in home

-     -                      -          -    0, 1.7'
-     -         7                       -    3.8, 4.1
-     -                      -          -    6.4, 6.6
-     -                                0, 1.3
-                            -          -     1.6, 2.4
-     -                      -          -    6.3, 6.8
     -                      -          -    0, 1.6
-     -         -            -          -     0.6. 2.8
-     -         -            -          -     0, 3.7

`rag/me creatinine.
*median. mean.


meats-men% &i&e appears to be the short-term marker of
choice for epidemiological studies.

(6) Mean levels of urinary nicotiue and of cotinine in body fluids
increase with an increasing seKreported E!l'S exposure and with an
increasing number of cigarettes smoked per day. There is consider-
able variability in levels among individuals at any given level of self-
reported exposure.

Comparison Of Abeorption From Environmental Tobacco
Smoke and From Active Smoking

&idemiologic studies show a dose-responss r&tiomGp between
number of cigarettes smoked and lung cancer, coronary artery
disease, and other smoking-related d&eases. Aseuming that dose-
response relationships hold at the lower dose end of the expoeure-
respome curve, risks for nonsmokers can be estimated by using
measures of absorption of tobacco smoke constituenta to compare the
relative exposures of active smokers and involuntary smokers.

As diSCUSStd PreviOuSly, measures Of nicotine uptake (i.e., r&&&e
or cotinine) are the most specific markers for El% exposure a&
provide the best quantitative estimates of the dose of expoeum.
Although the ratio of nicotine to other tobacco smoke constituents
differs in mainstream smoke and sidestream smoke, nicotine uptake
may still be a valid marker of total ETS exposure. Nic@ne uptake in
nonsmokers can be estimated in several ways.

Russell and colleagues (1965) infused nicotine intravenously to
nonsmokers and compared resultant plasma and urine nicotine
levels with those observed iu nonsmokers with E'l'S exposure. An
infusion of 1 mg nicotine over 60 minutes resulted in an average
plasma nicotine concentration of 6.6 ng/mL and an average urinary
mcotine concentration of 224 ng/mL. Using these data in combina-
tion with measured plasma and urinary nicotine levels in nonsmok-
ers after 2 hours in a smoky bar, nicotine uptake was estimated as
0.22 mg per hour. Since the average nicotine uptake per cigarette is
1.0 mg (Renowitz and Jacob 19&i, Feyerabend et al. 1965), 0.22 mg of
nicotine is equivalent to smoking about onefifth of a cigarette per
hour. In m&.ng these calculations, it is assumed that the disposition
~etics of inhaled and intravenous nicotine are similar and that the
rate of nicotine expowre from ETS ifs constant.

Steady state blood cotinine concentrations can also be used to
estimate nicotine uptake. Galeazzi and colleagues (1985) measured
c(ginj.ne levels in smokers receiving various doses of intravenous
nicotine, simulating cigarette smoking, for 4 days. They described
the relationship: [steady state plasma cotinine concentration]
(ng/mL) = (0.783) x [daily nicotine uptake] (w/kg/day). With such
data, a 70 kg nonsmoker with a plasma cotinine concentration of 2.5
ng/mL would have an estimated uptake of 3.2 )~g nicotine/kg/day, or

215


0.22 mg nicotine/day, equivalent to one-f* of a cigarette. This
approach assumes that the half-life for cotinine and nicotine
ewt,iom is similar in smokers and nonsmokers, an assumption
that may not be correct Wyerematen et al. 1982).
A third approach is to compare cotinine levels in nonsmokers with
those in smokers. Jarvis and colleagues (1984) measured plasma,
saliva, and urine nicotine and cotinine levels in 100 nonsmokers
selected from outpatient medical clinics and in 94 smokers. Ratios of
average values for nonsmokers compared with smokers were as
follows: plasma cotinine, 0.6 percent; saliva cotinine, 0.6 percent;
urine &nine, 0.4 percent; urine nicotine, 0.6 percent; and saliva
nicotine, 0.7 percent. These data suggest that, on average, nonsmok-
em absorb 0.5 percent of the amount of nicotine absorbed by
smokers. Assuming that the average smoker consumes 30 mg
nicotine per day (Benowitx and Jacob 1984), this ratio predicts an
exposure of 0.15 mg nicotine, or onesixth of a cigarette per day. The
most heavily exposed group of nonsmokers had levels almost twice
the overall mean for nonsmokers, indicating that their exposure was
quivslent to one-fourth of a cigarette per day. Most studies (see
l'ables 6 and `7) report similar ratios when comparing nonsmokers
with smokers. The exception is Matsukura and colleagues (1984),
who reported urine cotinine ratios of. nonsmokers to smokers of 6
percent. The reason for such high values in this one study is
UllhOWIl.

Personal air monitoring data for nicotine exposure can also be
used to estimate nicotine uptake. For example, Muramatsu and
colleagues (1984) used a pocketable personal air monitor to study
environmental nicotine exposures in various living environments.
They reported air levels of from 2 to 48 cog nicotine/ma. Assuming
that respiration is 0.48 ms per hour and exposure is for 8 hours per
day, nicotine uptake is estimated to range from 8 to 320 w per day.
The average values are consistent with other estimates of onegixth
to onethird cigarette equivalents per day in general populations of
nonsmokers exposed to ETS.
Aa noted before, these estimates must be interpreted with caution.
Rddh absorption of nicotine in smokers and nonsmokers may
substantially underestimate exposure to other components of ETS.

Conclusions

1. Absorption of tobacco-specific smoke constituents (i.e., nicotine)
from environmental tobacco smoke exposures has been docu-
mented in a number of samples of the general population of
developed countries, suggesting that measurable exposure to
environmental tobacco smoke is common.

216


2. Mean levels of nicotine and c&nine in body fluids increase
with self+ep0rted EXS exposure.

3. Because Of the stability of cotinine levels measured at different
times during exposure and the availability of noninvasive
sampling techniques, cotinine appears to be the short-term
marker of choice in epidemiological studies,
4.Both mathematical modeling techniques and experimental
data suggest that 10 to ZO percent of the particulate fraction of
sidestream smoke would be deposited in the airway.
5. The development of specific chemical assays for human ew
sure to the components of cigarette tar is an imp0rtant
research goal.

217


References

ALTSHULER, B., YARMUS, L., PALMES, E.D., NELSON, N. Aerceol deposition in
tie human respiratory tract: 1. Experimental procedurea and total depoeition.
AMA. Archives of Industrid H&&h 15(4):293303, Apfi 1957.
Alq)mN, P.J., HILLER, F.C. Particle Size Distribution of ~aindrtam Tobacco
and Mwijwna Smoke Using the Electrid Aerosol Anal~. Paper presented at
the American Asmciation for Aerc6ol Reseamh, Albuquerque, November 1985.
ANDERSON, P.J., HlLLER F.C., WILSON, FL, Jr., LAU, I.K.T. EBct ofRespimt.ory
&ttem on &p&t& of Ultmfine Aenxds in the Human Respimtory 2)rrct. Paper
preeented at the British Occupational Hygiene Society Sii International
sppi~m on Inhaled Articles, Cambridge, September 1936.
ARMITAGE, AX., TURNER, D.M. Absorption of nicotine in cigarette and cigar
smoke through the oral mwxma Nature 226(5252):l231-1232, June 27.1970.
BAUMBERGER, J.P. The amount of smoke produced from tObacco and it8 abeorption
in smoking 88 determined by electrical precipitation. Journal of PhaTmaco logy and
h?cperimentaZ Thempeutics 21(1):47-67, February 1923.
BmOWl'lZ, N.L., JACOB, P. IlI. Daily intake of nicotine during cigarette smoking.
Clinical Phannaco~ ad Thompeutic.~ 35(4):43Q-604, April 1984.
BENOWlTZ, N.L., JACOB, P. III, JONES, R.T., ROSENRERG, J. Interindividual
variability in the metabolism and cardiovascular effecta of nicotine in man.
3oumal of Phannaco logy and Experimental Thempeutics 221(2):368-372, May
  1982.

BENOWI!lZ, N.L., KUYT, F., JACOB, P. III. Circadian blood nicotine concentrations
&ui.ng cigarette smoking. Clinical Phannacol~gy and Thempeutics 32(6):758-764,
December 1982.

BENOWlTZ, N.L., KUYT, F., JACOB, P. JII, JONES, R.T., OSMAN, A;-L. C&nine
diqmition and effecta. Clinical Pkumacolom and T?wmpeuti 34@:604-611,
November 1983.

BINNS, R., LUGTON, W.GD., WILTON. L.V., DYAS, B.J. Inhalation toxicity studies
on cigarette smoke: 5. Deposition of smoke particles in the respiratory system of
rata under v8rioua expoewe conditions. To&o@y Q(l-2):87-102, February 1976.
BLACK, A., PRITCHARD, J.N. A comparison of the regional deposition and short-
term clearance of tar particulate material from cigarette anoke, with that of 2.5
pm polystyrene micrcepheres. Joumal of Aerosol Science 15(3X224-227,1964.
BLANCHARD, J.D., WILLEKE, K. An inhalation system for characterizing t&d lung
depoeition of ultratine particles. American Indudrial Hygiene Association JOW&
44(11):-, November 1983.

RO8, R.P., THRUWS, J.L.G., HENDERSON, P.T. Excretion of mutagens in human
urine after passive smoking. cbncer Letters 19(1):3CQO, May 1933.
BRIDGE, D.P., CORN, M. Contribution to the aeseasment of exposure of nonsmokers
to air pollution f+om cigarette and cigar smoke in occupied spaces. Environmental
Reseamh 5(2):19%2OQ, 1972.

CAIN, W.S., LEADFXER. B.P., ISSEROFF, R., BERGLUND, L.G., HUEY, Rd.,
LIPSlTF, E.D., PERLMAN, D. Ventilation requirements in buildings: 1. Control of
occupancy odor and tobacco smoke odor. Atmospheric Envimnment 17(6):1X%
1197,1983.

C-DEN, CM, COLE, P.V. Variations in carboxyhaemoglobin levels in smokers.
British Medical Joumd 4(5947):736733, December 28.1974.
CHANG, P.-T., PETERS, L.K., UJDJO, Y. Particle size distribution of mainstreem
cigarette smoke undergoing dilution. In: Liu, B.Y.H., Pui, D.Y.H., Fissan, H.J.
MS.). Aerosols: Science, Techdogy, and Industrial Applications of Airborne
Particles. New York, Eleevier Science Publishing Company, Inc., lQ34, pp. 737-740.
COCKS, AT., F'ERNA@XI, R.P. The growth of sulphate aerosols in the human
airways. Journal of Aerosol Science 13(l)%19, r982.

218


CORN, M. characteristics of tobacw tie smoke and factors influencing its
wncentratiob. and distribution in occupied spaces. In: Rylander, R. (ed.). hviron-
mental T~bacw Effects on the Non-Smoker. Scandinavian JOUST of &epimtoly
Di.3ease8 91(Suppl.):21-36,1974.

COULTAS, D.B., s-, J.M., HOWARD, &A., PEAKE, G.T., SKIPPER, B.J.
salivary wtinine levels and passive tib smoke exposure in the home.
(abstract). America n Review of Respimtorv Disease 133(4, part Z)~Al67-Al58, April
1986.

CUDDEBACK, J.E., DONOVAN, J.R., BURG, W.R. Occupational aspects of paseive
smoking. Am&xm In&&i& Hygiene Association &JUIXUZ 37(&~%7, day
1976.

DALHAMN, T., EDFORS, M.-L., RYLANDER, R. Retention of cigarette emoke
components in human lungs. Archives of Enuimmental Health 17(6):746.-746,
November 1968.

DALLAVALLE, J.M., ORR, C., Jr., HINKLE, B.L. The aggregation of aerowh. Brihh
Journal of Applied Physics MSuppl3):5198-6208,1964.
DAVIES, C.N., HEYDER, J., SUBBA RAMMA, MC. Breathing of halfinicron
aerosols: I. Experimental. Journql of Applied PhyeioZogy 32(5):591-600, May 1972.
ELLIOTT, L.P., ROWE, D.R. Air qu&+y during public gatheringa. JounurZ oft& Air
Pollution Control Aeeociutim 2&6):636-636, June 1976.
EMMETT, PC., AITKEN, R.J., HANNAN, W.J. M eaeurementa of the total and
regional deposition of inhaled particles in the human mpiratory tract. Journal of
Aemsol Science 13(6):64%&O, 1982.

EUDY, L.W., THOME, F.A., HEAVNER, D.L., GREEN, C.R., INGEBRETHSEN, B.J.
Studies on the Vapor-Particulate Phase Dietribution of Environmental Wotine
Paper preeented at the 39th Tobacw Chemists' Research conference, Montreal,
Canada, November 1985.

FEFUN, J., MERCER, T.T., LEACH, L.J. The effect of aeroeol charge on the deposition
and clearance of TiOn particles in rats. Environmental Reeeamh 31(1):1&151,
June 1983.

FERRON, G.A. The size of soluble aerosol particles aa a function of the humidity of
the air: Application to the human respiratory tract. Journal of Aerosol Science
8(4):261-267,1977.

FEYERABEND, C., HIGENBO'ITAM, T., RUSSELL, M.A.H. Nicotine concentrations
in urine and saliva of smokers and nonsmokers. British Medical Journal
284(6321):100%1004, April 3,1982.

FEYERABEND, C., INGS, R.M.J., RUSSELL, M.A.H. Niwtine pharmawkinetica and
its application to intake from smoking. British Journal of Clinical Pharmaeob
19(2):239-247. February 1935.

FOLIART, D., BENOWlTZ, N.L., BECKEF& C.E. Passive absorption of nicotine in
airline flight attendants (letter). New England Journal of Medicine 308(18):1106,
May 6,1983.

FRASER, D.A. The deposition of unipolar charged particles in the lungs of animals.
Archives of Environmental Health 13(2):152-157, August 1966.
FRIEDMAN, G.D., PETITI'I, D.B., BAWOL. R.D. Prevalence and correlates of paaaive
smoking. American Journal of Public Health 73(4):401-406, April 1983.
GALJLUZI, R.L., DAENENS, P., GUGGER, M. Steady&b concentration of coti.nine
aa a measure of nicotine-intake by smokers. European Journd of Chid
Phamuacology 28(3):301304,1985.
GERRITY, T.R., LEE, P.S., HAS8, F.J., MARINELLI, A., WERNER, P., LOURENP,
R.V. Calculated deposition of inhaled particles in the airway generationa of normal
subjects. Journal of Applied Phyeiology 47(4):667-873, October 1979.
GIACOMELLI-MALTONI, G., MXLANDRI, C., PRODI, V., TARROM, G. Deposition
effkiency of monodisperse particles in human respiratory tract. American
Indu&-iaZ Hygiene Association Joumu133(9):603-610, September 1972.

219


GREENBERG,R.A.,HALEY,N.J.,ETZEL,R.A.,~DA,F.AMeaeuringtheexpoeure
of infants to t&acw smoke: Nicotine and wtinine in urine and saliva. New
England Journul of Medicine 310(17):1073-lMg, April 26,19&L.
GFLRTTBS, R.R, HENNINGFIELD, JE Experimental analysis of human cigarette
smoking behavior. &den&on Rvceedinga 41(2X234-240, February 1982.
HALEY, N.J., AXELRAD, C.M., TILTON, K-A. Validation of elf-reported smoking
behavior: Biochemical snalyses of wtinine and thiwyenate. American Jounud of
Public Hmlth 73(10&204-l207, October 1983.

HARBlSON, M-L., BRAJN, J.D. Effects of exercise on particle depoeition in Syriaa
golden hamsters. American Review of Respimtov Dieease 12803904-908, Novem-

ber 6.1983.

HEYDER J., ARMBRU- L.. GEBHART, J., STAHLHOFEN, W. Deposition of
Berm1 pd&s in the human respiratory tract. In: Aemsok in Ph*ik. Mediain
ud T&n& Bad Soden, Federal Republic of GermanY, Geeellechaft fur Aeroeol-
forschung, 1974, pp. 122-l=.

HERDER, J., GEBHART, J., HEIGWER, G., ROTH, C.. STAHLHOFEN, W. Experi-
menu ~&es of the total depceition of aerosol partide~ in the human respiratory
tract. Aem+ Science 4:191-208.1973.
HLLLER, F.C., MAZUMDER, M.K., WILSON, J.D., McLEGD. P.C., BONE, RC.
Human respiratory tract deposition using multimodal aerowls. Jownal of Aemsol
science x3(4):337343,1982.
HlLLEF& F.C., McCUSKER, K.T., MAZUMDER, M& WILSON. J.D., BONE, R.C.
&@tim of side&ream cigarette smoke in the human respiratory tract.
American Review of Respimtq D&use 1!2@4):406-408,1982.
HIND& WC. Aenasol Technobgy. New York, John Wiley and Sons, 1982, pp. 113-119,
143443.

BINDS, W.C. Size chamcteristics of cigarette smoke. Americun Zndustriai Hygiene
Association Journal 39(l):-, Januery 1978.
HINDS, W.C., FIRST, M.W. Concentrations of nicotine and tobacco smoke in public
places. New EngZund Journal of Medicine 29206):844-846, April 17,1975.
HIND8, W., FIRBT, M.W., HUBER, G.L., SHEA, J.W. A method for measur&
respiratory deposition of cigarette smoke during smoking. Anwican 2duetri.d
Hygiene Association Journal 44@):113-118, February 1983.
HOEGG, U.R. Cigarette smoke in clased spaces. Environmental Health Pempectiws
2117-l% October 1972.

HOFFMANN, D., HALEY, N.J., ADAMS, J.D., BRUNNEMANN, K.D. Tobacw
side&rerun smoke: Uptake by nonsmokers. Preventive Medicine 13(6):60&617,
November 1984.

HUGOD, C., HAWKINS, LB., ASTRUP, P. Exposure to passive smokers to t&am
smoke constituents. Internutbnal Archives of Occupational and Environmental
Health 42(1):2130.1978.

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER. Tobacco Smoking
IARC Monographs on the Evaluation of the carcinogenic Risk of Chemicals to
Humans, Vol. 38. Lyon, IARC, 1936.
INTERNATIONAL COIKMITTE E ON RADIATION PRO!tZCTION, TASK GROUP
ON LUNG DYNAMICS. Deposition and retention models for internal doeimetry of
the human respiratory tract. Health Phyeics 12(2):173-207, February 1966.
JACOB, P. III, WILSON, M., BENOWITZ, N.L. Improved gas chromatographic
method for the determination of nicotine and wtinine in biologic fluids. Journal of
Chnwnutography 222(1):61-70, Januaq 2,198l.
JARVIS, M.J., RUSSELL, M.A.H. Expired air carbon monoxide: A simple breath t,&
for tobacco smoke intake. British Medical Journal 231(6233):434-4&, August 16,
1980.


JARVIS, M.J., RUSSELL, MAX., ml%JD, C. Absorption of nicotine and
carbon mnmide from passive smoking under natural CO~~~~OIIS of exposure.
Thonxz 3800829833, November 1983.
JARVIS, M.J., RUSSELL, M.A.H., FEYERABEND, C., EISEZ, J.R., MORGAN, M.,
GAMl@.AGE. P., GRAY, R.M. Passive exposure to tobacco smoke: saliva cotinine
WncB~hatims in a representative population sample of nonsmoking school
children. British Medical J0urna2 291(6606)927-929, October 5.1985.
JARVIS. M.J., T'Ub=TALLPEDOE, H., FEYRRABRND, c., VESN, c., SALLOO-
JR& Y. Biochemical markers of smoke absorption and self-reported exposure t.~
passive smoking. Journal of Epidemiobgy and Community Health 36(4):3364&$
December 1984.

JUST, J., BORKOWSKA, M., MAZIARKA, S. Zaniecxyswenie dymen tytoniowym
powietrra kawiam Warezawskich [Air pollution due to tobacco smoke in Warsaw
coffee houses.] Roczniki Panstwowegv Zakladu Higieny 23(2):129-135,1972.
KADO, N.Y., MANSON, C., EISENSTADT, E., HSIEH, D.P.H. The kinetics of
mutagen excretion in the urine of cigarette smokers. Mutation Reeeanzh
167(2/3):227-232, Augur&September 1985.
KEITH, C.H. Particle size studies on tobacco smoke. Beitr@e cur Z'abakfomdhug
International 11(3):123-131,1982.

KElTH, C.H., DERRICK, J.C. Measurement of the particle sire distribution and
concentration of cigarette smoke by the "conifuge." Joutnol of Cdoid S&ace
15(4):340-366. August 1960.

KIRR, L.D., YAMASAIU, E., AMES, B-N. Detection of mutagenic activity in cig+rette
smoke condensates. Proceedin@ of the Nationul Academy of Scierze USA
71(10):415%4163, October 1974.

KOUSAKA. Y., OKUYAMA, K., WANG, C.-S. Response of cigarette smoke particlee
to change in humidity. Journal of Chemical Engineering of Japan 15(1):76-76,
1982.

KYEREMATEN, G.A., DAMIA.NO,M.D., DVORCHIK, B.H.,VESELL,E.S. Smoking-
induced changes in nicotine disposition: Application of a new HPLC! assay for
nicotine and its metabolites. Clinical Pharmacology and Thenzpeutics 32(6):769-
780, December 1982.

LANDAHL, H.D., TRACEWELL, T.N., LASSEN, W.H. On the retention of airborne
particulates in the human lung. A.MA. Archives of Industrinl Hygiem? and
Ofxupatbnal Medicine 3:359-366,1951.

l.,A,NDAHL, H.D., TRACEWELL, T.N., LASSEN, W.H. Retention of airborne particu-
la* in the human lung. III. AMA. Archives of Industrial Hygiene and
axlbpation4ll Medicine 6508-511,1952.

LANGER, G., FISHER, M.A. Concentration and particle sire of cigarettesmoke
particles. Archives of Industrial Health 13(4):372-378, April 1956.
LAWTHER, P.J. Carbon monoxide. British Medical Bulletin 31(3)%X-260, Septem-
ber 1975.
LEVER, J. (cited in Davies 1974).
LLppMANN, M. Regional deposition of particles in the human respiratory tract. Lx
Lee, D.H.K., Falk, H.L., Murphy, S.D., Geiger, S.R. (eds). Reactions to Enuirunmen-
tal Agenta Handbook of Physiology, Sec. 9. Bethesda, Maryland, American
Physiological Society, 1977, pp. 213-232.

LUCK, W., NAU, H. Nicotine and cotinine concentrations in serum and milk of
nursing mothers. British Journal of Clinical Pharmacobgy 18(l)%15, July 1984.
LUCK, W., NAU, H. Nicotine and cotinine concentrations in serum and urine of
infanta exposed via passive smoking or milk from smoking mothers. Journal of
Pediatrics 107(5)381fX320, November 1985.

221


~mrqs, A., JACOBI, W. Die in vivo Bestimmung der Aerosolteilschendeposition
b A*mtr&. bei Mud- bzw. Naaenatmung. In: Amok in Phyeik, &dizin u?td
Technik. Bad Soden. Federal Republic of Germany, Gesellschaff fur Aeroeolfor-
schung, 1974, pp. 117-121.

MARTONEN, T.B., LOWE, J. Assessment of aerceol deposition patterns in human
mpi&ory tract caste. In: Marple, VA., Liu, B.Y.H. &da). findunwttt~ls and
Sa&. Aerosols in Mining and Industrial Work Environments, Vol. 1. Ann Arbor,
Ann Arbor Science Publishers, 1983a, pp. 151-164.
MARTGNEN, TB., LOWE, J.E. Cigsrette smoke patterns in a human respiratory
tract model. In: Marple, VA, Liu, B.Y.H. (eds). findamentals and Status
Aerosols in Mining and Industrial Work Environments, Vol. 1. Ann Arbor, Ann
Arbor Science Pubiishers, 1983b, p. 171.

MARTGNEN, T.B., PATEL, M. Computation of ammonium bisuifate aerosol deposi-
tion in conducting airways. Journal of Toxicology and Envimnmental Health
8(5/6):1061-1014, November-December 1981.

MATSUKURA, S., TAMU'JATG, T., KITANO, N., SEINO, Y., HAMADA, H.,
UCHIHASHI, M., NAKAJDW H., HIRATA, Y. Effects of environmental tobacco
smoke on urinary cotinine excretion in nonsmokers: Evidence for passive smoking.
New En&ad Journal of Medicine 311(13):828-832, September 27,1984.
M&IJSKER, K., HILLER, F.C., WILSON, J.D., McLEOD, P., SIMS, R., BONE, R.C.
Dilution of cigarette smoke for real time aerodynamic sixing with a SPART
analyzer. Journal ofAenxo1 Science 13(2X103-110,1982.
MEDICI, T.C., UNGER, S., RUEGGER, M. Smoking pattern of smokers with and
without t&a cco-smokerelated lung disease. American Review of Respiratory
Disease 131(3):386888, March 1986.

MITCHELL, R.I. Controiied measurement of smoke-particle retention in the respira-
tory tract. American Review of Respimtory LG~.ws 85(4):526-533, April 1962.
MUIR, D.C.F. Tobacco smoke inhalation. In Rylander, R. (ed.). Environmental
Tobacco Smoke Effects on the Non-Smoker. Scandinavian Journal of Respimtory
Bisea&?.s 91(Suppl.):4446,1974.

MUIR, D.C.F., DAVIES, C.N. The deposition of 0.5 8.m diameter aerosols in the lungs
of men. Annuls of Occupational Hygiene 10:161-l 74, July 1967.
MURAMATSU, M., UMEMURA, S., OKADA, T., TGMITA, H. Estimation of personal
exposure to tobacco smoke with a newly developed nicotine personal monitor.
Environmental Research 35(1):21%227, October 1984.
MURAMATSU, T., WEBER, A, MURAMATSU, S., AKERMANN, F. An experimen-
tal study on irritation and annoyance due to passive smoking. Intemationul
ATchives of Occupational and Environmental Health 51(4):30&317, April 1983.
NEAL, A.D., WADDEN, R.A., ROSENBERG, S.H. Evaluation of indoor particulate
concentrations for an urban hospital. A men&n Industrial Hygiene Association
JownuZ39(7):578582, July 1978.
OKADA, T., MATSUNUMA, K. Determina tion of particle-&e distribution and
concentration of cigarette smoke by a lightscattering method. Journal of Colkid
and Interface Science 48(3)&l-469, September 1974.
PALMEss ED., ALTSI-IUIER, B., NELSON N. Deposition of aerosois in the human
respiratory tract during breath holding. In: Davies, C.N. (ed.). Inhaled Particles
and Vapors LI. Oxford, Pergamon, 1966, pp. 339-349.
PATTZSHALL, E.N., STROPE, G.L., EXZEL, R.A., HELMS, R.W., HALEY, N.J.,
DENNY, F-W. Serum cotinine as a measure of tobacco smoke exposure in children.
American Journal of I)iseasap of Childhood 139(11):1101-1104, November 1985.
PENKALA, S.J., DE OLIVEIRA, G. The simultaneous analysis of carbon monoxide
and suspended particulate matter produced by cigarette smoking. Environmental
Research 9(2):99-114, April 1975.

222


PHALEN, R.F., OLDHAM, M. J., BEAUCAGE, C.B., CWCKER, T.T., MORTENSEN,
J.D. PcetnataI dargament of human tracheobronchial airways and imp~cationa
for particle deposition. Anutomical Record 212(4~36&389, ~uguat 1~.
POLYDOROVA, M. An attempt to determine the retention of tobaoco smoke by
means of membrane filters. In: Davies, C.N. (ed). Inholed Pa&&s o& Vapors n.
Oxford, Pergamon Pieas, 1961, pp. 142-147.
I-3-m. J. Die Beetimmung der Grossenverteibmg von Aerosolen mit
Hilfe der radioektiven Markienmg und der Spiralzentrifuge. ~~~~ science
42wk354.1973.

PORSTENDO~~, J., -Cl'& A. Concentration and mean particle size of the
main and eide beam of cigarette smoke. Stau~Reinhaltung &rLuft 32(10):33-36,
Ocbber 1972..

PRITCHARD, J.N., BLACK, A. An estimation of the tar particulate material
depositing in the respiratory tracb of healthy male middIe. and Iow-t,ar mtte
smokers. In: fill, B.Y.H., hi, D.Y.H., Fieean, H.J. (eda). Aerosols: &ience,
Technology and Inczlrstrirrl Applications of Airborne Part&lee. New York, &tier
Science Publishing Company, Inc., 1984, pp. 989-992.
BAABE, O.G. Size-eelective samphng criteria for the thora& and reepi&Ie r-nam
fradione. Ann& of the American Confemnce of Governmental Ijr.&tnhl flygin-
id3 (ll):M, 1984.

RENNINGER, R.G., HILLER, F.C., BONE, R.C. The evaporation and growth of
droplets having more than one volatile constituent. JournuZ of Aem& &&
12(6):605315,1981.

REPACE, J.L., LOWREY, A.H. Indoor air pollution: Tobacco smoke and public he&h.
Science 208M4-472, May 2,198O.

ROSENBERG, J., BENOWITZ, N.L., JACOB, P. III, WILSON, K.M. Diap&tion
kinetics and effects of intravenous nicotine. Clinicoi Pharmacology and Thenzpeu-
tics 28(4):517-522, October 1980.

RUSSELL, M.A.H., COLE, P.V., BROWN, E. Absorption by nonsmokers of carbon
monoxide from room air polluted by tobacco smoke. Luncet 1(7893)576-579, March
17,1973.

RUSSELL, M.A.H., FEYERABEND, C. Blood and urinary nicotine in nonsmokers.
Lancet 1(7900):179-181, January 25,197s.

RUSSELL, M.A.H., WEST, Rd., JARVIS, M.J. Intravenous nicotine simulation of
passive smoking to estimate dosage to exposed non-emokere. British Joumul of
Addiction 80(2):201-206, June 1985.

SCHILLER, C.F., GEBHART, J., HEYDER, J., RUDOLPH, G., STAHLHOFEN, W.
&position of Momdisperse Aemeol Particles in the O.aMo.2 p Size Range
Within the Human Respimtory !&et. Paper presented at the British Occupational
Hygiene Society Sixth International Sympoeium on Inhaled Particles, Cambridge,
September 1986.

SCHLESINGER, R.B., LIPPMANN, M. Selective particle deposition and bronchogenic
carcinoma. Environmental Research X(3):424-431, June 1978.
SCHMAHL, D., CONSBRUCH, U., DRUCKREY, H. Fluoreszenzmeseungen an
Zigarettenrauch. Anneimittel-Forschung 4(2):71-75. February 1954.
SINCLAIR, D. Optical properties of aerosols. In: Handbook on Aerosols. from the
Summary Technical Report of Division 10, National Defense Research committee,
US. Atomic Energy Commission, 1950, PP. 81-96.
SPENGLER, J.D., DOCKERY, D.W., TURNER, W.A., WOLFSON, J.M., FERRIS,
B.G., Jr. Long term measurements of respirable sulfates and particles inaide and
outside homes. Atmospheric Environment 15(1):23-30,1981.
STEWART, R.D. The effect of carbon monoxide on humane. Annual Review of
Pharmacology 15:409-423,1975.

S'I'GBER, W. Lung dynamics and uptake of smoke conetituents by nonsmokers: A
survey. Preventive Medicine 13(6):689-601, November 1984.

223


T~m &IL, BRYANT MS, SKIPPER. P.L., MACLURE. M. Hemoglobin
Adductr 4 T-&h& A,vm&c Amines Appkxztion to bfOkCUkU' h&ide-
&&gy. Banbury Report Vol. 23, in P==
TV, KU., -N, ~-0. T&l depceition of ultrafine hydrophobic and hygroscopic
d b w hm respiratorg tract. Aerosol Science and Technology ~d63-466,
  1984.

VO(FI: TX., ~VJN, S., w, S.B. Comparison of biochemical and question-
~&imates0ftobacco,. $%mentiw Medicine 8(1X%33, January 1979.
W,U,D, NJ., BOREHAM, J., BAILEY, A-, m, C., -Dow, J.E, KNIGHT. G.
urinnrg as as marker of breathing other people's tobacco smoke. (letter).
,kncct 1(837OM30-231, Jsnuary 2&19M

W&Q N, RITCHIE, C. Vslidation of studies on lung cancer in nonsmokers married
b & (Ietter). icimcet 1(3386~1067, May 12,19!34.
\KIEBQS &, m T. Paseive smoking at work. IntemationaE Arch&s of
QowpotiancJ,&Envimnmentol Health 47(3):209-221,198O.
w&LLs, P.V., GERKE, R.H. An oscillation method for measuring the size of
&eamiugcopic particiee. Journal of the American Chemical Society 41(3):31%
329, Mfu-ch 1919.

WEBON, F.J., Jr., HILLZR, F.C., WIWON, J.D., BONE, R.C. Quantitative deposition
d ultrafine &able ptutides in the human respiratory tract. Journal of Applied
&sbbgy 68@223-229, January 1985.

WB. N-K MOSTARDI, RA. ELY, D.L, WORSTELL, D. Carboxyhem+
gbbin and metbemoglobin levels in residents living in industrial and no&nd&ri-
dtxeninnitiea. Ghvironmenti RescaFch 26(2):347-352, December 1981.
xv. G-h Yu, C9. Effecte of age on deposition of inhaled aerosols in the hw lug,
AemoIScienceand lkdmology 5(3):34%367,1988.
`IIMUSAKE, E, m, RN. Concentration of mutagens from urine by a&rption
W@I the WnpOh reein XA%k @a~%& emokers have mutagenic be.
Aaadin6FB of the Nationnl Academy of Sciences 74(8):3555-3559, August 1977.

224


CHAPTER 5

     TOXICITY,
ACUTE IRRITANT EFFECTS,
AND CARCINOGENICITY
  OF ENVIRONMENTAL
   TOBACCO SMOKE


CONTENTS

Irritation: Acute Exposure
IrritantS in Environmental Tobacco Smoke
Irritating and AMoying Efhta of Environmental
   Tobacco Smoke

Studies of Healthy Individuals
Field Studies
Experimental Studies
Studies of Sensitive Individuals
Children
Allergic Individuals

Effects on the Lung
Effect9 of Cigarette Smoking on Respiratory Epitheli-
   urn: Studies in Humans
Effect of Cigarette Smoking on Lung Inflammatory
   C&f3

  Studies in Humans
  Experimental Models
Effects of Cigarette Smoking on Lung Parenchyma:
Studies in Humans
Summary of Lung Effects

Carcinogenicity of Environmental Tobacco Smoke
Inhalation Experiments
Other In Vivo Bioassays
In Vitro Assays
Summary of Carcinogenicity

Conclusions

Beferehces

227


Irritation: Acute Expoeure
Irritants in Emirogmental Tobacco Smoke
Tobacco smoke is a complex aerosol that contams several thousand
different constituents (Hoffmann, Haley, Brunnemann 1983). Little
is known about the health effects of most of these compounds
individually and even less is known about their interactions. Tobacco
smoke contains compounds established as irritants, toxins, muta-
germ, and carcinogens. The main irritanta identified in environmen-
tal tobacco smoke @Z'S) to date are respirable particulates, certain
aldehydes, phenol, ammonia, nitrogen oxides, sulfur dioxide, and
toluene. The range of concentrations of these irritants measured m
mainstream smoke, in side&ream smoke, and in smoky air under
"realistic" and "natural" conditions or as results of field studies is
summarized in Table 1.
The levels of irritants in air contaminated with ETS vary
considerably (Table 1). Some of this variation is due to differences ir
the number of cigarettes smoked, the amount of ventilation, the
adsorptive properties of the surroundings, and measurement me&
odology. Triebig and Zober (1984) compared the measured concentra-
tions of these irritants with the maximum permissible concentration
(MAK) values for working areas and the maximum emission
concentration (MIK) values for outdoor air pollution in the Federal
Republic of Germany. They concluded that concentrations approxi-
mating or in excess of the MIK values can be found for respirable
particulates, nitrogen dioxide, and acrolein. The other irritants
generally do not reach the existing threshold limit values under
realistic conditions. For phenol there is no MIK value. An evaluation
of the hygienic and medical importance of the compounds in EC'S
based on threshold limit values is problematic for two reasons: first,
MAK values for industries are established for healthy adults with an
Shour exposure per day; MYIK values are for the outdoor environ-
ment, and no indoor limit values exist for "everyday life." Second,
the threshold limit values are valid only for single compounds; E'l'S
contains many different irritants, which might interact to produce
more toxicity than anticipated from the concentrations of individual
compounds.
Many of the constituents of tobacco smoke are also produced by
other sources that contribute contaminants to the indoor or outdoor
environment. For example, sources unrelated to smoking such as
urea formaldehyde foam insulation or certain wood materials can
emit formaldehyde and may give rise to mean air concentrations as
high as 100 to 400 ppb (Triebig and Zober 1984). In measuring the
contribution of tobacco smoke to the levels of these constituents,
some researchers (Weber et al. 1979a; Weber and Fischer 1980) have
subtracted the measured indoor concentrations from the levels


TABLE l.-Major irritants in environmental tobacco smoke
      (ETS), their concentrations in mainstream
     smoke (MS), sidestream smoke (SS) to
      mainstream smoke (MS) ratios, and levels in
     smoky air under realistic and natural
       conditions

kritant

   MS
(per ciweth)

ss/Ms
(ratio)

smoky air
(range)

Acmlein            lo-140 pg
Formaldehyde          ~~Irg

Ammonia

Nitrogen oxides

Pyridine

Sulfur dioxide

Phenol

Toluene

Respirable particulatea

32 w            10

l-75 ppb          NA

20-150 p6         2.6

106 I%           5.6

0.1-40 In6         1.3-1.9

10-20

a50

44-100

4.7-50

6-m Ppb
30-60 Ppb.
CO l-43 pbb)
lOOk pbb"
l-370 ppb NOc
(MO pbb NO,c

NAd

l-69 ppbc
7.4-115 pg/m'
0.04-1.04 n&m'
5962 mg/m*

* Meeaured under experimental conditions only.
b Fischer (1979).

c Difference: indoor concentration minus control value (unoccupied mom or outdoon).
d NA = not available.
SOURCE: Date from Cdlishaw et al. MFA). Remmer W&5). Triebig and zober WM), US DIUB WW, except
where noted.

measured either in the unoccupied room or in the outdoor environ-
ment near the room.

The measured concentrations of irritants listed in Table 1 are
primarily the mean values in air samples collected over intervals of
onehalf hour to several hours. Substantial variation in levels can
occur, depending on the proximity to a smoker and the air-mixing
conditions in the room. Weber and Fischer (1983) measured peak
concentrations of 3,330 to 99,680 ng/ms for the particulates and 41 to
750 ppb for nitrogen oxide in the "blowing cloud" 1 meter from the
smoker immediately after smoke exhalation. These high concentra-
tions decreased very rapidly with time (half-life between 2 and 20
seconds) and distance from the smoker. Ayer and Yeager (1982)
measured formaldehyde and acrolein concentrations in the side
stream smoke plume rising from a cigarette between puffs and
obtained concentrations of some constituents up to three orders of
magnitude above the occupational limits established for more
extended exposures.

230


F  Water       PI&X8
              dtility     otimpact      comparnds
                -----B--w---------
              I   niih       EY=         Ammonis
                               FW
                           TWtChea        Aaolein
                                      Ptilstes

    - -   ------a----------

                 Medium
__3( 1.      Bronchh       6uMvdioxlde
                          Bnmchbleri      Paftiadatea

,,Q   --------------I

                 Low        smlwida     Nurogen dioxide
                          Abdi         Pattidates
                      capiltaliaa

F'IGURE l.-Places of impact, and irritants in the eyes and
      respiratory tract in relation to water solubility
souBcE:vdentin(le86).

Irritating and Annoying Effecta of Environmental Tobacco
Smoke

The main effects of the irritants pr&ent in El's occur in the
conjunctiva of the eyes and in the mucous membranes of the nose,
throat, and lower respiratory tract. The main ocular symptoms are
reddening, itching, and increased lachrymation; the main respira-
tory tract symptoms are itching, cough, and sore throat. The
relationship of the site of the effect of some irritanta in the eyes and
in the respiratory tract to their water solubility is illustrated in
Figure 1. The penetration of the particulatea into the lung depends
on their size; because most of the particulates in tobacco smoke are
smaller than 1 pm, they can penetrate to the smallest airways.

Studies of Healthy Individuals
Field Studies

Several studies have shown that annoyance and irritation are the
most common acute effects of EZ'S exposure. Shephard and Labarre
(1978) surveyed more than 1,000 Canadian citizens aged 10 to 80
years. The interviewed population was representative of southern

231


ontio with respect to both income and profession but underrepre-
sentative of the elderly. Seventy-three percent of the nonsmokers
were disturbed by tobacco smoke in restaurants and 53 percent by
tobacco smoke in offices. The most frequently reported symptom was
eye irritation. Complaints of nausea, dizziues~, and wheezing as well
as rhinorrhea were also reported, although much less frequently
than stinging eyes.
Similar results were obtained in a survey conducted in three
restaurants in Switzerland (Weber et al. 1979a). A multiplechoice
questionnaire was administered to 220 guests. One-third to two-
thirds of the respondents complained about air quality, and up to 12
percent reported eye irritation. In another survey of more than 2,100
white-collar employees, Barad (1979) found that nearly one-fourth of
the nonsmokers reacted to smoke exposure with frustration and
hostility.
Weber and Fischer (1930) surveyed employees in 44 worksite
workrooms, located in seven different companies, that included
offkes, rooms for design and technical and clerical work, and
conference rooms. The choice of companies and worksites was based
on availability and therefore was not a random sample. In all
workrooms, the concentrations of carbon monoxide (CO), nitrogen
oxide (NO), acrolein, particulate matter (PM), and nicotine were
measured in the air. The contribution of tobacco smoke to these
levels was obtained by subtracting background levels obtained before
working hours from the concentrations during working hours. These
differences from the background levels were called SCO, 5N0, and so
on. Measurements were conducted in each room on 2 successive days
(12 l-hour mean values per workroom), and 472 employees were
questioned about irritation and annoyance as well as about their
opinions on involuntary smoking.
Some of the exposure results are summarized in Table 2. The
comparison of these 6 values with the measured absolute indoor
concentrations revealed that 30 to 70 percent of the measured indoor
concentrations of carbon monoxide, .nitrogen oxide, and particulate
matter were due to tobacco smoke. The correlations between the gas
phase components 5CO and &NO were relatively high (Pearson
correlation coefficient r=0.73). However, the correlations of SC0
with Gnicotine and 5PM were low. Nicotine values were generally in
the range of the lower detection limit of the method of measurement
used (gas chromatography). The low correlation of the gaseous
components with the particulate matter is probably due to the
different physical properties (sedimentation, adsorption, and desorp-
tion of the particulates) and to the fact that the &PM values include
particulates from sources other than tobacco smoke.
Approximately one-third of the employees described the quality of
air at work as %ad" with regard to tobacco smoke. Forty percent

232


TABLE %--Air pollution due to tobacco m&e in 44
       workrooms

                 NumberOf      Mean
component            s-d-       veluea     deviation Maximum

6&rbon monoxide @pm)       363          1.1         1.3         6.5

SNitrc@n oxide @pb)         348         32         60         280

6Pa1ticulat.e matter @g/m')      429        133        130         962

were disturbed by smoke. One-fourth reported eye irritation at work
Seventy-two percent of the interviewed nonsmokers and 67 percent
of the smokers were in favor of a separation of the workrooms mt,o
smoking and nonsmoking sections; 49 percent supported a partial or
total prohibition of smoking at work,
Contradictory results were reported by Sterling and Sterling
(1964), who found no relationship between smoking conditions in
ofices and comfort complaints. A self-administered work environ-
ment questionnaire was given to approximately 1,100 employees
working in nine buildings. Data were analyzed according to the
smoking habits of the respondents and the office rules regulating
smoking. The distribution of the responses to questions assessing the
presence of symptoms (headache; fatigue; nose, throat, and eye
irritations; sore throat and cold symptoms) were similar in environ-
ments +ith and without smoking. The researchers concluded that
"smoking is not a pivotal source of indoor pollution of health-related
building complaints." No objective measurements of air pollution
were carried out, however, and there were no descriptions of building
ventilation. The researchers used a "building illness index" that
included several different symptoms in addition to irritation (e.g.,
headache, fatigue), and the irritating effects on the most sensitive
organ-the eyes-may have been masked by this use of an overall
symptom index.

Experimental Studies

Harke and Bleichert (1972) examined the acute physiological
response to ETS in a 170 m3 room. The electrocardiogram, blood
pressure, heart rate, and skin temperature showed no change with
expcsure to ETS, even at extremely high exposure levels (150
cigarettes smoked in 30 minutes, corresponding to a carbon monox-
ide concentration of 60 ppm at the end of the exposure).


The infhrence of the temperature and humidity of room air on odor
perception and irritation was investigated by Kerka and Humphrey
(1956). They found that odor intensity was somewhat reduced by
increasing the temperature at a constant humidity. Both odor and
bfit.ation intensity were reduced by increasing the humidity.
Johansson and Ronge (1966) also observed that acute irritation is
increased in warm and dry air. Johansson (1976) exposed 12 subjects
in a 6.7 m3 climatic chamber for 29 minutes to the El% produced by
the smoking of 10 cigarettes. The air in the chamber was cold (18" or
19" C) or warm (25" or 26" C), and at each temperature, the relative
humidity was evaluated at three levels from 30 to 80 percent. Under
all conditions, subjective irritation, asses& by a questionnaire,
increased during exposure; eye irritation increased more than nose
irritation. No marked effect of temperature on the degree of
irritation was observed, probably owing to the limited temperature
range studied (1P to 26" C). Kerka and Humphrey (1956) demon-
strated a thermal effect when the temperature range was greater
than 8O C. The low relative humidity (7 to 20 percent) in aircraft may
be responsible for the substantial level of perceived irritation due to
TS among passengers, despite the low levels of pollutants measured
n aircraft (WHO 1984).
Basu and colleagues (1978) studied the effects of ETS on human
tear fihu and observed a reduction in the stability of the preccmeal
tear film in subjects exposed to a smoke concentration corresponding
to approximately 20 ppm CO. In the presence of EYE!, the tear fti
breakup time was significantly reduced by 35 to 40 percent com-
pared with baseline measurements without smoke. The researchers
suggested that this reflects an alteration in the relative proportions
of the constituents of tear film.
In these studies, the quantitative exposures to JITS either were not
measured or were determined in a relatively imprecise way. More
systematic studies, including measurements of several compounds of
ETS, were carried out by Weber and collaborators (Weber et al. 1976,
1979a,b; Weber, Fischer, Grandjean 1977; Weber, Fischer, Gierer et
al. 1977; Weber and Fischer 1983) and Muramatsu, Weber, and
colleagues (1983). These experiments were carried out in a climatic
chamber of 30 m3, with an air temperature of 20" to 24" C and a
relative humidity between 40 and 60 percent. The ventilation rate
could be varied between 0.1 and 16 air changes per hour. The smoke
was produced by a Borgwald smoking machine under standardixed
conditions, and only the side&ream smoke of cigarettes was used.
Healthy students were exposed to the sidestream smoke of cigarettes
in groups of two or three in the climatic chamber. They all also
participated in a control exposure with identical conditions, but
without sidestream smoke in the air. The concentrations of the
following compounds were continuously recorded: carbon monoxide,

234


nitrogen oxide, formaldehyde, acrolein, and partictite matter. me
background levels before smoke production were subtracted from the
measured concentrations during smoking; the resultmg values were
called SCO, 5N0, and so forth. The degree of irritating and annoymg
effects of the ~rcposed subjects was determined every 10 minutes by
means of queetion.mires and by measuring the eye bh& rate,
considered an objective measure for eye irritation.
In the first study, 33 subjects were exposed to continuously
increasing smoke concentrations (Weber et al. 1976). `&e majn
re~uh are Summarized in &Ure 2. The concentrations of CC, NO,
formaldehyde (HCHO), and acrolem increased with the number of
cigarettes smoked. Both mean subjective eye irritation and mean eye
blink rate increased with increasing smoke concentration. S&j&ve
nose and throat irritation was also evaluated. Nasal symptoms were
less pronounced than eye symptoms, and the throat was the least
ElffWti?d.
h a second series of studies, acute effects were analyzed in
relation to smoke concentration and duration of exposure (Weber et
al. 1979; Muramatsu, Weber et al. 1983). The tobacco smoke
concentrations corresponded to 1.3, 2.5, 5, and 10 ppm CO @CO).
Subjects were exposed to these smoke concentrations for 1 hour, each
smoke concentration increasing linearly during the first 5 to 10
minutes and then remaining constant at the desired level for the rest
of the hour. Because very high correlations (r > 0.9) were obtained in
the first experimental series between 6CO and each of the other
~m~unds, only 500 was used tc quantify the level of exposure to
E3.S.
The results obtained for subjective eye irritation and eye blink
rati me shown in Figures 3 and 4. The mean reported level of eye
irritation as well as the eye blink rate increased with increasing
smoke concentration. Both irritation parameters E&O increased with
the duration of exposure under conditions of constant smoke
concentration. The same, but less pronounced, results were observed
for nose and throat irritation.
Annoyance increased rapidly as soon as smoke production began
and increased with increasing smoke concentration, but after 10 to
15 minutes the level of annoyance remained approximately constant
during the rest of the exposure. Thus, the intensity of exposure was
important in determining the degree of annoyance and the duration
of exposure was less importam.
mese experiments demonstrated an objective irritant response in
h&thy adult subjects at levels of smoke exposure substantially
lower than the levels at which an airway response has been
demonstrated. Whether this difference represents a difference in
threshold for irritation in the eye and airway or a limitation in the
&l&y to measure subtle changes in the airway is uncertain.

235


Eye blink ratelmin

AC0

AU0

AHW

AAuoleln

,:,,:,I:,
0.06 . . . . .
r    I     I     I     I    1
0.W   0.18   0.32   0.47   0.62   0.64 ppm
r    I     I     I     I    I
0    0.05   0.11   0.16 0.20  0.20 ppm
1         I         I

No.ofriiQmtten 0         10         20

         - EyeiniWhindex
         -*--*-- Eye blinkmte

FIGURE 2.Mean subjective eye irritation, mean eye bliuk
     rate, and concentrations of some pollutants
      during continuous smoke protection in an
       unventilated climatic chamber
NOTE:33eubjectqOmin: mdesnrement before smoke procluction.
SOURCE: WabsretaL(1976).

Hugod and colleagues (1978) and Weber and colleagues (Weber,
Fischer, Grandjean 1977; Weber, Fischer, Gierer et al. 1977; Weber
et al. 1979b) canid out several experiments in order to determine
which compounds in ETS are responsible for irritation and annoy-
ance. The resulta of the two studies were somewhat conflicting.
Hugod and colleagues exposed 10 subjects in an unventilated 68 ma
room to high concentrations of sidestream smoke (concentrations
corresponding to 20 ppm Co), to the gas phase of sidestream smoke
alone, and to acrolein alone at concentrations three times those
found in sidestream smoke alone. Irritation was assessed via a

236


20    30    40    50     60 (min)

Exposure duration

FIGURE 3.-Mean subjective eye irritation related t,o
      smoke concentrations (ppm delta CO) and
      duration of exposure

questionnaire. Both annoyance and irritation were reported at
similar levels in the subjects exposed to the whole sidestream smoke
or to the gas phase only. Exposure to acrolein caused only slight
discomfort.
Weber and colleagues (Weber, Fischer, Grandjean 1977; Weber,
Fischer, Gierer et al. 1977; Weber et al. 1979b) exposed students in
groups of two or three in a 30 mS climatic chamber to whole
sidestream smoke, to acrolein alone, to formaldehyde alone, or to the
gas phase of smoke. Subjective irritation and annoyance as well as
eye blink rate were measured. The results indicated that acrolein
and formaldehyde did not produce substantial irritation or annoy-
ance at the levels used. The gas phase exposure resulted in high
levels of reported annoyance, but was less important as a determi-
nant of irritation. The objectively measured eye blink rate, as well as
subjective eye irritation, was much lower with the gas phase alone

237


40.0

  35.0

  30.0

5"
`E  25.0

g
m

  20.0

  15s

Eye Mink rele

Smokewncentralion
(deltacarbonmonoxide)

I     1     I     I     8 1     1
0     10    20    30     40 50    60 mm
          Exposure duratlon

FIGURE 4.-Mean effecta of environmental tobacco smoke
      on eye blink rate

NOTE: 32 to 43 subjecta; 0 min: measurement before smoke production; 0 to 5 min: increasing smoke
conantrntion; 6 ta 60 min: co&ant smoke production.
SOURCE: Muramatau. Weber et al. (199%.

than with the total sidestream smoke, suggesting that the particu-
late phase is the major determinant of irritation. The researchers
postulated that the irritating effects of the particulate phase are due
to the semivolatile irritant compounds. These compounds, which
volatilize rapidly during the process of combustion, recondense on
the particulates with cooling and may deposit irritants in relatively
high concentrations on the mucous membranes.


Studies of Sensitive Individu&
Children

Several investigators have used questionnaires to examine the
subjective symptoms of children and young people with ElTS
exposure Gameron 1972; Muramatsu 1977; Muramatsu, Muramatsu
et al. 1983). The last group found that 81 percent of B-year-old
children disliked involuntary smoking and 82 percent complained of
one or more kinds of irritation, the most common being eye
irritation. Several epidemiological studies have shown that children
with parents who smoke have an increased risk for respiratory
illness (see Chapter 2).

Allergic Individuals

A few studies have asses& the effects of ETS on allergic
individuals. Speer (1968) found that allergic individuals report
irritation more frequently than healthy individuals. Weber and
Fischer (1980) observed that employees suffering from hay fever
reported significantly more eye irritation at work than those without
hay fever.

Effects on the Lung

Cigarette smoking is associated with prominent changes in the
numbers, types, and functions of respiratory epithelial and i&Jam-
matory cells. These alterations have been implicated in the develop-
ment of pulmonary emphysema, chronic bronchitis, and respiratory
tract cancers and in an increased susceptibility to infections. Chronic
exposure to environmental tobacco smoke might cause similar
changes. Because studies that directly address the effect of chronic
exposure to environmental tobacco smoke on lung structure and
biochemistry have not been conducted, this section reviews those
studies in humans and animals that provide evidence on smoke
exposures that may be relevant to ETS exposure.

Effects of Cigarette Smoking on Respiratory Epithelium:
Studies in Humans

Extensive evidence shows that exposure to cigarette smoke has
adverse effects on respiratory epithelial cells, and dose-respon~
relationships have been established from these changes (Auerbach et
al. 1961; Auerbach, Hammond, Garfinkel 1970). Studies involving
the systematic examination of the bronchial mucosa from large
numbers of human smokers have recorded three principal types of
epithelial changes: epithelial hyperplasia, loss of cilia, and nuclear
atypia. In an autopsy study of 402 adult male subjects (Auerbach et
al. 1961), 98 percent of the sections of the tracheal and bronchial


TABLE 3.Cections with one or more epithelial changes,
      by packs of cigarettes per day

Group

Subjects without lung cancer

Never smoked regularly

Smoked <l/2 pack/day
Smoked 112-l pack/day
Smoked l-2 pack/day
Smoked 22 pack/day

Number of     Number of
subjects       sections

  65         3,324

  36        1,824

  59        3,016

  143         7,062

  36         1,787

Total with one
or more changes

Number   Percentage

  559      16.8

1,683      92.3

2,938      97.4

7,021      99.4

1,780      99.6

Subjects with lung cancer          63        2.764       2,778      99.8

Totals
Average

SOURCE: Auerbach et al (1961).

402        19,797       16,759
                             84.7

epithelium of the men who had smoked had epithelial changes. The
most common abnormality observed was atypical nuclei, and a large
proportion of sections had hyperplasia. Denudation of the ciliated
epithelium was also present in most of those who had smoked. Other
studies have observed that goblet cells were frequently increased in
the airways of cigarette smokers (Regland et al. 1976; Jones 1981).
The extent and severity of the abnormalities have been closely
related to the intensity of smoking. A similar relationship of
smoking habits to laryngeal lesions has been observed (Auerbach,
Hammond, Garfinkel1970), although the laryngeal lesions were less
frequent and less advanced than those in the bronchi for a given
smoking history.

The frequency and severity of epithelial lesions observed in
smokers contrasts sharply with those in individuals who do not
smoke regularly. In the study by Auerbach and colleagues (1961)
(Table 3), 98 percent of the sections from the tracheobronchial tree
from smokers contained abnormal epithelial changes; however,
similar changes were observed in only 16.8 percent of the sections
from nonsmokers. The most common lesion in nonsmokers was
epithelial hyperplasia (9.4 percent); atypical cells were seen in only
4.8 percent of the sections from nonsmokers.

If it is assumed that the nonsmoking group included a subgroup of
individuals who were chronically exposed to environmental tobacco
smoke, an assumption that seems reasonable in light of the largely
U.S. veteran population under consideration in the Auerbach
group's study, then some information on the effect of chronic
exposure to environmental tobacco smoke on the respiratory epithe-

240


lium can be inferred. Epithelial hml&acn; w atypia due to
chronic exposure to environmental~farnabseW.ocau in some
nonsmokers, but these findings a,re not eorrrmDp in the majority of
nonsmokers.
c\igarette smoking also has adverse e&&c&+= @ w w&
                                        `,
beneath the epithelium. Submucosal gagnd hi has been
observed frequently (Auerbach et al. 196l; `&&n&&t& me, Jo-
1981). The prevalence is related to the intensity of- a.
Mucous gland hypertrophy is seen in B, ,w js,. nd
prevalent and is usually not extensive (Au-& & w& ., : .,. ,
The loss of ciliary epithelium, the increased, n~~d!.w
cells, and the mucous gland hypertrophy -t&y qw ti
cigarette smokers would predict muco&ary de w
available evidence indicates that long-term cigarette 6 &
pairs mucociliary transport Wanner 1977). Once a cigarette *
develops chronic bronchitis, mucus transport appears to be w
ibly damaged. Impairment persists even in patients who have
abstained from cigarette smoking for many years (Santa w et +,
1974). Prior to the development of chronic broncwis, howevq
partial recovery of function has been observed (Cam& et al. +?7%
Studies examining mucociliary dysfunction in humaq ,due, s&Q t,o
chronic environmental smoke exposure have not been rqorted.
                                                  
Effect of Cigarette Smoking on Lung Infhm&bti C&
Studies in Humans
One of the earliest pathologic lesions found in the lungs of young
smokers is a respiratory bronchiolitis (Anderson and Foraker 196l;
&Laughlin and `Tueller 1971; Niewoehner et aL 1974). Clusters of
pigment-laden phagocytes, predominantly alveolar macrophages
(AM), lodge in the respiratory bronchioles of cigarette smokers
precisely at the sites of the earliest lung injury. The infiltration' by
AM precedes the development of emphysema and focal fibrosis
(&sio et al. 1978). Analyses of cells harvested by bronchoalveolar
lavage complement the morphologic studies. Lavage fluid yields five
to seven times more AM from the lungs of cigarette smokers than
from nonsmokers' lungs (Harris et al. 1970; Reynolds and Newball
1974; Warr et al. 1976; Hunningbake et al. 1979; Hoidal et al. 1981).
The alveolar macrophages from smokers appear to be activated
morphologically and metabolically. The AM from smokers have
increased size, endoplasmic reticulum, G-olgi apparatus, glucose
metabolism, hydrolytic and proteolytic enzyme activities Pratt et al.
1971; Cohen and Cline 1971; Harris et al. 1970; Rodriguez et al. 1977;
Hinman et al. 1980; Martin 1973; Cantrell et al. 1973), and increased
rates of oxidative metabolism resulting in increased producti& of
reactive oxygen species (superoxide radical, hydrogen peroxide, and
hydroxyl radical) (Hoidal et al. 1981; Hoidal and Niewoehner 1982).


The strategic location of the alveolar macrophages and their
altered function have led to the hypothesis that they may contribute
to the alteration of the protease-antiprotease balance of the lower
respiratory tract and thus foster the development of emphysema in
smokers. Two plausible mechanisms have been identified by which
AM may influence the protease-antiprotease balance in cigarette
smokers. The first is by directly increasing the lung protease burden.
Human AM release enzymes with elastolytic activity in vitro,
whereas those from nonsmokers do not (Rodriguez et al. 1977). The
activity may originate from endogenous or exogenous sources. A
metalloenzyme with activity against synthetic amide substrates,
which have specificity for elastase, was detected in the bronchoalveo
lar washings of cigarette smokers (Janoff et al. 1983; Niederman et
al. 1984) and was also found in the cell culture fluid of smokers' AM
(Hinman et al. 1989). Alveolar macrophages can synthesize a
metalloprotease capable of solubilizing elastin; they also contain a
thiolprotease with such activity (Chapman and Stone 1984). The
metalloprotease, if analogous to that of murine macrophage elastase,
would be resistant to inactivation by alpha,-protease inhibitor (a,PI)
(Banda et al. 1989). These enzymes have not been demonstrated to
csuse emphysema. The content of elastolytic activity in AM at a
given time is less than that of equal numbers of polymorphonuclear
leukocytes (PMN); thus, AM may be only a minor source of enzymes
capable of lung parenchymal destruction. However, their potential
importance must be considered in light of their demonstrated ability
to degrade elastin in the presence of serum protease inhibitors
(Chapman and Stone 1984) and their capability of ongoing synthesis
of elastolytic enzymes. Cell matrix contact may be critical for their
matrix-degrading action, since the AMderived enzymes are likely to
be membrane bound.
Human AM also acquire elastolytic activity from exogenous
sources. AM can bind and internalize neutrophil elastase by virtue of
possessing a specific membrane receptor for this and other neutro-
phi1 glycoproteins (Campbell et al. 1979; Campbell 1982; McGowan et
al. 1983). Studies to date suggest that the scavenged elastase
accounts for much of the elastolytic activity in AM lysates. Seques-
tered PMN elastase may subsequently be released by AM over an
extended period of time.
The second mechanism by which AM may influence the proteas+
antiprotease balance in cigarette smokers is by inactivating a,PI, a
major antiprotease of the lower respiratory tract in humans (Gadek
et al. 1981). Smokers' AM can inactivate a,PI through oxidant
mechanisms in vitro (Carp and Janoff 1989). Studies on bronchoal-
veolar lavage fluids have identified oxidatively inactivated a,PI in
some human smokers (Gadek et al. 1979; Carp et al. 1982), but this
has not been a consistent finding (Stone et al. 1986; Boudier et al.


1983). Studies that directly assess t& a of a,PI activity in the
alveoli space and interstitium of cjsaretts smokers are needed to
clarify this issue.

The phagO@iC Capabilities Of~from~smogerS 4
nonsmokers are similar in most studies m et al. 1970; &hen
and Cline 1971; %ynolck et al. 1975; `&r&o :md @I& lg`&b),
although a few studies (Martin and WAR 1~; ~ et d 1982)
have suggested a modest decrease in the m. -ties of m
from smokers. The experimental desii of these- has differed
considerably, and technical factors may be responsible for the
variable results. In particular, there are merenccs m cehw
culture conditions. In view of the increased number af m in
cigarette smokers, it seems unlikely that a primary m defect
of AM would account for the bacterial colonization observed b some
cigarette smokers.

The possibility that increased numbers of PMN may be present in
the lungs of cigarette smokers has been examined primarily because
of the attention given these cells in the study of the pathogen&sof
emphysema. PMN elastase is the only purified human enzyme +th
ready access to the lung psrenchyma that has been demon&rated to
cause emphysema when admmistered to animals. The ,nu.mber of
PMN is increased in the distal airways and lung parenchyma of
cigarette smokers. Bronchoalveolar lavsge from some smokers yields
increased PMN (Reynolds and Newbsll 1974; Hunninghake &al.
1979). More compelling evidence for incressed PMN in the lungs of
smokers comes from the morphologic evaluation and direct cell*
analysis of the lung parenchyma A fourfold increase in PMN
infiltration has been observed in the lungs of cigarette smokers
compared with the lungs of nonsmokers, using morphometric
techniques (Ludwig et al. 1985). Analysis of cell suspensions from:
lung biopsies has also demonstrated increased PMN in the lung
parenchyma of smokers (H unninghake and Crystal 1983). The
alveolar septa are the primary site of the PMN accumulation.
Increased PMN are present in the alveolar walls of smokers both
with and without emphysema, which suggests that other factors
must also be involved in the development of the destructive lesion.
Factors that might influence the destruction of lung parenchyma
by PMN elastase include the intensity of PMN Mux, the amount of
ela&sse per cell, the quantity and site of elastase released, and local
factors that enhance or inhibit the elsstolytic activity. Investigations
of the relation of PMN elastase levels and the development of
emphysema have provided discrepant results. Some studies have
shown elevated levels of PMN elastase in patients with chronic
obstructive pulmonary disease (Gal&on et al. 1977; Rodriques et al.
1979; Kramps et al. 1980), but others have not CTayJor and Keuppem
1977; Abboud et al. 1979). Other alterations in the PMN function of

243


cigarette smokers include the enhanced generation of reactive
oxygen species in certain smokers (Ludwig and Hoidal 1982). After
stimulation, the release of superoxide anion by PMN was 50 percent
greater from smokers with peripheral white blood counts (WBC)
greater than 9,000 per mm3 than from nonsmokers with similar
WBC or from smokers or nonsmokers with WBC less than 9,000 per
mm'. (Cigarette smokers have increased peripheral WBC counts
compared with nonsmokers.)
The influence of cigarette smoking on many aspects of the immune
system has been examined. Immunoglobulin (Ig) levels in the
peripheral blood of smokers have been reported to be decreased
(Gerrard et al. 1980; Ferson et al. 19791, but similar results have not
been observed in all studies (Bell et al. 1981; Merrill et al. 1985). In
contrast to the decrease of IgG in peripheral blood, cigarette smokers
appear to have increased IgG levels in bronchoalveolar lavage fluid
(Bell et al. 19811, primarily owing to an increase in IgG, (Merrill et
al. 1985). Cell-mediated immunity may also be affected by cigarette.
smoking, but again, the results are somewhat conflicting. Peripheral
blood T-lymphocytes and mitogen responsiveness have been reported
to be increased (Silverman et al. 19751, unchanged (Daniele et al.
19771, or decreased (Petersen et al. 1983). Natural killer-cell activity
in the peripheral blood of cigarette smokers appears decreased
(Ginns et al. 1985; Ferson et al. 1979). Analysis of peripheral blood
lymphocyte populations by monoclonal antibodies has demonstrated
increased T-lymphocytes (OKT3+), with a decreased proportion of
OKT4+ (helper/inducer), and an increased proportion of OKT8+
(suppressor/cytotoxic) subsets in smokers with greater than 50 pack-
years of smoking (Miller et al. 1982). Analysis of bronchoalveolar
lavage fluid from cigarette smokers with a mean smoking history of
14 -- 9 pack-years demonstrated a decreased proportion of
OKT4 + lymphocytes and an increased proportion of OKT8+
lymphocytes (Costabel et al. 1988). In the latter study, the alterations
in T-lymphocyte subsets observed in bronchoalveolar lavage were
not present in peripheral blood. This finding and the increase in IgG
in bronchoalveolar lavage fluid, but not in serum, raise the
possibility of regional effects of cigarette smoking on the immune
system.
The extent to which the alterations of inflammatory cell numbers
and functions observed in smokers are also present in individuals
who are chronically exposed to environmental tobacco smoke
remains unknown. Studies in humans have not directly addressed
this issue. Studies of dose-response relationships are absent, except
for those cited that document a relationship of peripheral white
blood cell count and lymphocyte T-cell subsets. If it is assumed that a
subgroup of nonsmokers is composed of individuals who are chroni-
cally exposed to environmental tobacco smoke, then some inferences

244


are possible. As has been stated, the most common pathologic feature
in the lungs of young cigarette smokers is an accumulation of
pigment-laden macrophages in the respiratory bronchioles. In the
study by Niewoehner and colleagues (1974), all 19 male cigarette
smokers who died suddenly else-where than in a hospital had such
lesions, which were present in all sections studied in 16 of the 19
subjects. In contrast, only 5 of 20 nonsmokers had similar lesions,
and they were minimal in all but 2. One of the two individuals was a
stoker in a foundry and the other was undergoing desensitization for
severe hay fever. Although the inflammatory cell accumulation
cannot be absolutely attributed to these extenuating circumstances,
it is clear that the respiratory bronchiolitis is not common in young,
healthy individuals who do not smoke regularly. In contrast, autopsy
studies have observed focal inflammatory changes quite frequentl:
in older subjects who had not smoked, but the lesions were of much
less severity than in age-matched subjects who had smoked (C&o et
al. 1978). Similar changes have not been observed in studies on
bronchoalveolar lavage fluids. The metabolic activation of the AM
from younger and older nonsmokers is similar (Hoidal and Niewoeh-
ner 1982). These findings suggest that the characteristic inflammato-
ry lesions seen in the lungs of smokers are usually absent or are
modest in those individuals who do not smoke cigarettes and who are
not exposed to an alternative inciting agent.

Experimental Models

The effect of cigarette smoke inhalation on lung inflammation and
inflammatory cell function has been extensively studied in experi-
mental animal models; however, studies have not investigated
inflammatory cell alterations in models intended to simulate chronic
environmental tobacco smoke exposure. Several studies have demon-
strated that chronic cigarette smoke exposure produces an accumu-
lation of AM within the respiratory bronchioles of many animal
species, including dogs (Hernandez et al. 1966; Frasca et al. 1971,
1983; Park et al. 1977), rats (Hendrick et al. 1976; Coggins et al. 1980;
Huber et al. 1981), hamsters (Bernfeld et al. 1979; Hoidal and
Niewoehner 1982), and mice (Matulionis and Traurig 1977), that is
strikingly similar to that seen in human smokers. In most studies,
the accumulation of AM has been dependent on the duration and
intensity of the smoke exposure (Hoidal and Niewoehner 1982;
Huber et al. 1981). Increases in lysosomal enzyme activities have
been observed in rats (Etherton et al. 1979) and mice (Matulionis and
Traurig 1977) following tobacco smoke exposure. Increased elastase
secretion by alveolar macrophages from mice chronically exposed to
cigarette smoke has also been observed (White et al. 1979). Oxygen
consumption, superoxide anion release, hydrogen peroxide produc-
tion, and hexose monophosphate shunt activity were reported to be

245


increased in AM harvested by bronchoalveolar lavage from hamsters
(Hoidal and Niewoehner 1982) and rats (Drath et al. 1978; Huber et
al. 1981) chronically exposed to tobacco smoke. Accumulation of
PMN in the alveolar septa of cigarette smoke-exposed hamsters,
strikingly similar to that observed in human smokers, has also been
reported (Ludwig et al. 1985). In contrast to the focal nature of the
AM accumulation, the accumulation of PMN was diffuse. Studies of
PMN function have not been systematically evaluated in smoke-
exposed animals. One distinctive feature in rats has been a lymph+
cytic periairway infiltration (Innes et al. 1956; Huber et al. 1981).
Similar alterations are not seen in humans. The lymphocytic
infiltration may be due to complicating respiratory infections with
mycoplasma or a respiratory virus, which have been common in rata.

Effects of Cigarette Smoking on Lung Parenchyma: Studies
in Humans

The most striking alteration of the lung parenchyma associated
with cigarette smoking is centrilobular emphysema. The relation-
ships between smoking history, age, and the degree of emphysema
have been examined. The effect of smoking on the development of
emphysema is believed to be cumulative (Anderson et al. 1972;
Auerbach et al. 1974). In a study of 1,824 autopsies from individuals
who had died in the hospital, Auerbach and associates, using a
semiquantitative scoring system, detected emphysematous lesions in
all individuals who had smoked two or more packs of cigarettes per
day, including 111 who had been under 66 years of age at the time of
death. The extent of emphysema strongly correlated with the
number of cigarettes smoked per day. However, some emphysema-
tous changes, usually of a mild degree, were noted in 94 percent of
the individuals who had regularly smoked less than one-half pack
per day. In contrast, no emphysema was detected in 95 percent of the
175 individuals who had not smoked regularly, and only one case of
emphysema of moderate severity had occurred in a person who had
not smoked. These findings suggest that emphysema is rare in
individuals who do not smoke regularly and do not have a genetic
predisposition for the disease.

Summary of Lung Effects

Substantial evidence documents that active cigarette smoking
produces adverse effects on respiratory epithelial cells and causes
lung inflammation and alveolar septal disruption. Whether these
effects occur following chronic exposure to environmental tobacco
smoke cannot be definitively answered by the fragmentary data now
available. It is possible that clinically significant pulmonary conse
quences of chronic exposure to environmental tobacco smoke in
adults might occur only when this exposure interacts with other

246


factors in pad hdarl~ susceptible individuals. In this regard, future
studies directed at W&cted h@-risk populations or animal models
immporating exposure to emi~~xu~~~~tal ~&XCCO SIIIO~B along with
other exposures might be the most fruit&l areas of investigation into
the effects of chronic exposure to environmental tobacco smoke.

Carcinogenicity of Environmental Tobacco Smoke

This section reviews some of the more widely employed m&o& of
evaluation of the carcinogenicity of mains&am smoke that may also
be extended to the evaluation of ETS. The &I&&&J, diffemnces,
and technical difficulties in employing these various bioassays with
MS, smoke condensate, and ETS are discussed.

Inhalation Experiments

Because inhalation is the primary mode of exposure for w he
and in~01~ntav smoking, animal inhalational assays dd appear
to be the ideal approach to developing an animal s&em for
carcinogenicity testing. However, the acute toxicity (mainly due b
carbon monoxide and nicotine) have limited the expos- to wh&
smoke that can be tolerated by laboratory animals.

Two types of passive exposure systems offer the primary ap
proaches to inhalation studies with small laboratory animals. These
systems provide either the forced exposure of the whole body to
tobacco smoke or exposure of the head only. The amount of smoke
that is retained in the lower respiratory tract of the animals is the
dosage variable of interest in assessing these studies. The particulate
matter content of whole smoke is probably of greater importance
than the vapor phase content (Wynder and HoRmann 1967; Davis et
al. 1975) for studies of carcinogenesis. Labeled particulate phase
components have been used for determining the deposition of the
particulate phase in the respiratory tract in smoke inhalation
studies (Mohr and Rexnik 1978). However, since such markers are
applied to the tobacco column, they may be partiahy volatilized
during smoking. Thus, some of the values reported in deposition
studies of inhaled smoke aerosols in mice, rats, and hamsters reflect
the deposition of the trapped particulate phase plus the gas phase of
cigarette smoke in the respiratory tract. A less ambfguow tracer is
decachlorobiphenyl (DCBP). It is added to the tobacco column of
cigarettes, and after exposure of the animals to the smoke of the
treated cigarettes, this tracer can be determined in extra&J of
various segments of the respiratory tract by gas chromatography
with an electron capture detector (GGECD). The detection limit of
DCBP is < 5 x 1011 g (Lewis et al. 1973; Hoffmann et al. 1979). using
these techniques, only a small percentage of the smoke particulates
of cigarette mainstream smoke can be shown to reach regions in the

247


lower respiratory tract of small laboratory animals. This may
explain, at least in part, why the lifetime inhalation exposures of
small animals to tobacco smoke have led only to limited numbers of
lung tumors.

In mice, inhalation assays with cigarette smoke have generally led
to hyperplasia and metaplasia in the trachea and bronchi of the
animals (Wynder and Hoffmann 1967; Mohr and Reznik 1978). In
one of the most extensive studies, the Leuchtenbergers (1970)
induced pulmonary adenoma and adenocarcinoma in Snell's mice.
However, only the gas phase, not the total smoke, induced a
statistically significant number of lung tumors.

In another inhalation bioassay, male and female C57Bl mice (100
in each group) were exposed, nose only, to fresh mainstream smoke
diluted with air (1:39) for 12 minutes every other day for the
duration of their lives. Four lung tumors were detected in both the
treated male mice and the treated female mice. No lung tumors were
found among controls. A similar experimental design was used to
examine the possible differences between the smoke of flu-cured
Bright tobacco cigarettes and the smoke of air-cured Bright tobacco
cigarettes (Harris et al. 1974). Female Wistar rata (408 animals) were
exposed, nose only, to a 1:5 smoketo-air mixture for 15 seconds of
every minute during an 11-minute exposure twice a day, 5 days per
week, for the lifespan of the animals. Three of the rata exposed to
cigarette smoke developed pulmonary squamous neoplasms of uncer-
tain malignancy and one animal had an invasive squamous-cell
carcinoma of the lung. No tumors were found in the 104 sham-
control animals or in the 104 untreated female rats (Davis et al.
1975).

Fischer-344 rats (80 animals) were exposed, nose only, to a 1:lO
smoke-toair mixture for approximately 30 seconds of every minute
that a cigarette was being smoked (Dalbey et al. 1980). In this
manner, the animals were exposed to the smoke of one cigarette per
hour, 7 hours per day, 5 days per week, for 128 weeks. The mean
pulmonary particulate deposition during the smoke-aerosol exposure
was 0.25 mg per cigarette, or 1.75 mg per rat per day. Ten
respiratory tumors were observed in seven smoke-exposed rats. One
alveologenic carcinoma and two adenomatoid lesions were observed
in 3 of the 93 control rats employed in this study. A similar protocol
was used to evaluate the effects of the inhalation of the smoke of
cigarettes with varying tar deliveries. In this study (Wehner et al.
1981), squamous metaplasia of the laryngeal and tracheal epitheli-
urn was significantly increased in the smoke-exposed Fischer-344
rats.

Syrian golden hamsters (80 males and 80 females) were exposed,
nose only, to a 1:7 smoke-toair mixture for 10 to 30 minutes, 5 days
per week, for a period no longer than 52 weeks. The incidence of

248


laryngeal leukoplakias ranged from 11.3 percent for the animal
receiving the low dose to 30.6 percent for those animals receiving the
highest dose of cigarette smoke. Such changes were not observed in
the controls or in the hamsters exposed to the gas phase only
(Dontenwill 1974). Exposing 102 male BIO 87.20 and BIO 15.16
hamsters, nose only, twice a day, 5 days a week, for up to 100 weeks,
resulted in almost 90 percent of the animals having hyperplastic or
neoplastic changes in the larynx (Bernfeld et al. 1974). Laryngeal
cancer was five times more frequent in the BIO 15.16 strain. Two
animals in this strain also developed nasopharyngeal tumors.
Another study using nose-only exposures and similar extents of
exposure reported similar changes in the larynx of the smoke-
exposed animals (Wehner et al. 1974). Increasing the exposure
duration to the lifespan of the animals resulted in the development
of squamous papilloma of the larynx.

Thirty rabbits in an inhalation chamber were exposed to the
smoke generated from 20 cigarettes for up to 5 l/2 years. Thirty-one
animals were used as controls. No tumors were found among the
treated animals that could be related to the exposure to cigarette
smoke (Holland et al. 1963).

Eighty-six beagle dogs, trained to inhale cigarette smoke through
tracheostomata, were actively exposed to smoke from either filter or
nonfilter cigarettes (Auerbach, Hammond, Kirman et al. 1970).
Tumors of the lung were reported in 23 of the 62 dogs exposed to
smoke from the nonfilter cigarettes. Two of the dogs in this group
had small bronchial carcinomas. Noninvasive bronchioalveolar
tumors were reported in 4 of the 12 dogs exposed to the smoke of
filter cigarettes and in 2 of the 8 control dogs. The bronchioalveolar
tumors tended to be multiple, with as many as 20 per lung, and were
reported in 40 of the 203 lung lobes in the 29 dogs with such tumors.

Inhalation studies with SS or ETS have not been reported thus far
with any of the laboratory animal inhalational assays. This lack of
experiments has in large part been due to the absence of exposure
devices that allow the appropriate delivery of the inhalant without
incurring the loss of the test animals due to the toxicity of carbon
monoxide and nicotine.

Other In Vivo Bioassays

Among alternative methods used to assess the relative carcinoge-
nicity of mainstream cigarette smoke, the most widely utilized test is
to collect the cigarette smoke condensate (CSC) and to bioassay this
material for carcinogenicity. In the process of preparing CSC, many
of the volatile and semivolatile components are lost. Furthermore,
there are serious concerns regarding the influence of aging of the
CSC, which can affect both the chemical composition and the
biological activity. Despite these shortcomings, bioassays using CSC

249


have provided insight into mechanisms by which tumor induction in
animal tissues is likely to occur. The application of CSC to mouse
skin haa helped to identify those agents that are active as tumor
initiators and has shown that within the CSC subfractions are
components that can act as tumor promoters or cocarcinogens,
respectively. Thus, this approach allows the comparison of various
condensates, especially when large groups of animals are used (>50
per group).
The application of CSC to mouse skin is the most widely employed
assay for the evaluation of its carcinogenic potential. The mouse skin
bioassays in tobacco carcinogenesis have been reviewed (Hoffmann,
Wynder et al. 1983). A typical experiment uses two to three dose
levels of condensate, generally 25, 50, and 75 mg of CSC, which are
administered topically to the shaved backs of mice three to six times
weekly for approximately 78 weeks. The CSC is most frequently
applied as an acetone suspension (25, 33, or 50 percent). At the
conclusion of such a study, skin tumors, some of which are
malignant, generally are observed among the treated animals in a
dose-related fashion. Such studies have shown that the carcinogenic
activity of CSC! is also a function of tobacco variety, is influenced by
replacement materials such as tobacco sheet or semisynthetics, and
may be influenced by the use of additives. Although such bioassays
have been extensively performed for the tars from mainstream
cigarette smoke, only one study has examined the carcinogenic
potential of the condensate of sidestream cigarette smoke.

Cigarette tar from the sidestream smoke of nonfilter cigarettes
that had settled on the funnel covering a multiple-unit smoking
machine was suspended in acetone and applied to mouse skin for 15
months (Wynder and Hoffmann 1967). Out of a group of 30 Swiss-
ICR mice, 14 animals developed benign skin tumors and 3 animals
had carcinomas. In a parallel assay of MS from the same cigarettes,
a 50 percent CSCacetone suspension applied to deliver a comparable
dose of CSC to 100 Swiss-ICR female mice led to benign skin tumors
in 24 mice and to malignant skin tumors in 6 mice. This indicates
that this smoke condensate of SS had greater tumorigenicity on
mouse skin than MS tar (p > 0.05).

In Vitro Assays

Several short-term bioassays have been performed to evaluate the
genotoxicity of the MS of cigarettes. These studies have been the
subject of two reviews (DeMarini 1983; Obe et al. 1984). Although
most of these studies have evaluated the effects of CSC, some
investigations were focused on either the gas phase or the whole
smoke. In recent years, there has been increased use of short-term
assays to attempt to evaluate the relative genotoxic potential of
environmental tobacco smoke.


The most c=monly employd my for mu~ ectivity is done
with various strains of &l~~~~ e whole irmdta 8%
well as CSC from four types of bh - fauad ;O be mutageaic in
S. typhrimurium TA1533 (Basrur et d 1~8).  -      gmo)reWarr
also found to be mutagenic in a w hy- wLLB -
directly on the bacterial plates (w et d 193~. b etudies lend
support to the extensive assays performed a a w eehaMiah
that tobacco smoke has significant mutagepic *w

Several of the studies with Csc fm em haW besu
aimed at comparing the effects of &ous tobaocas, w -
strains, and various systems selected far m w lost
of the mutagenic activity was m &tb & bagic fnrtion a
CSC (DeMarini 1983). For the CSC! from w e mpta
genie activity was primarily detected with &e m T- and
TA98, thus indicating the presence of &e u - tJped
mutagens. Except for studies on the e&&s af m
cigarettes, metabolic activation was required t.4) demoaastra&e m*
genie activity for most of the CZC studied.

Several short-term tests have been performed in s
systems. A solution of the gas phase of e mm
dissolved in a phosphate buffer induced reciprocal u&c& e
nation in Swcharcmzpc?s ~e~~isiae D3 snd petite mm io m
i&ate of strain D3 (Izard et al. 1980). Whole mainetwam c&are&e
smoke induced mitotic gene conversion, reverse mu&&m, and
reciprocal mitotic recombination in strain M ofS. cenx&& @air&a
1982).
Transformation of mammalian cells was also induced in several
cell systems using the CSC from mainstream  .
&g&t&i 1968; Inui and Takayama 1971; Rhim auE?m
&n&ct et al. 1975; Takayama et al. 1978; Ridal and ti
1980). Transplacental exposure t0 n CSC was WJorted b
trasfom Syrian hamster foeti cells (Raamuseen et ~ ml).
Transforming activity was reported in the acidic and basic fra&~~
                                                    I
as well as the neutral fractions of C&L S~dies on v of
csc have shown that the basic fraction and some of the a&c&
fractions are the most active in Cd tran%formation (Bened& ~4 d
1975). The neutral fraction OfCSCwaS*~ported~~*DNA
repair h normal human lymphocytes (Gadin et al- 197% Transfer
mation of mammalian cells with SS or m has not been repOti

Summary of Carcinogenicity

At present, the scientific literature offers some information on the
physicochernical nature of the sidestream smoke from tobacco
products and of environmental tobacco smoke. Chemical analytical
studies have already demonstrated that SS and FYI'S contain a wfde
spectrum of carcinogens such as polynuclear aromatic hydrocarbons,

261


volatile and tobacco-specific N-nitrosamines, and polonium-210. To
date, only one study has demonstrated the carcinogenic activity of
the particulate matter of sidestream smoke and a few isolated
reports have dealt with the genotoxicity of SS and EX'S. Therefore,
bioassay studies with the mainstream smoke and the environmental
tobacco smoke of cigarettes are needed. Although the resulting
bioassay data will derive from tests of concentrations of environmen-
tal smoke that do not realistically occur in the human setting, these
results will provide information about the relative carcinogenic
potential of sidestream smoke in comparison with the mainstream
smoke of the same cigarettes. In a comprehensive analytical
approach, data should be generated to systematically determine the
concentrations of toxic and tumorigenic agents in the ETS samples
and to simultaneously measure the uptake of tobacco-specific agents
by the body fluids of nonsmokers exposed to ETS.

Conclusions

1. The main effects of the irritants present in EZS occur in the
conjunctiva of the eyes and the mucous membranes of the nose,
throat, and lower respiratory tract. These irritant effects are a
frequent cause of complaints about poor air quality due to
environmental tobacco smoke.

2. Active cigarette smoking is associated with prominent changes
in the number, type, and function of respiratory epithelial and
inflammatory cells; the potential for environmental tobacco
smoke exposure to produce similar changes should be investi-
gated.

3. Animal models have demonstrated the carcinogencity of ciga-
rette smoke, and the limited data that exist suggest that more
carcinogenic activity per milligram of cigarette smoke concen-
trate may be contained in sidestream smoke than in main-
stream cigarette smoke.

252


References

ANDERSON, A& Jr., BWMKER, AG. Pathagenic implicatione of dveo~tie h
pulmonary emphysema-Archives of Pathology 7x6)3620-664, N- 1961.
ANDERSON J.L DUNMLL, MS., RYDER, R.c. udence of the incidence of
edwe- on smoking, age end W.X. !I'hom~ 27(6)~&7~,61, septennber 1972.
AUERBACH, O., GARFINKEL. L HAMMOND, E.C. Rhtkm of smoking and age to
findinga in lung m&m A micfoecopic study. tit 66(l.)~2%38, ~muary
1974.

AUEFCBACH. O., HAMMOND, E.C., GARFlNK& ~Histologicchangeninthe
larynx in relation to 8mOkiW habite. &ncer 25(11:92-104, January 1970.
AUERBACH, O., HAMMON-D, E.C., KlRMAN, D., GARFINgEL. L. effects of
cigar&e 8mOkhW On dm: 2. k'dmonary neoplesma Archim of &nv~~l
Health 21(6):754-763, December 1970.

AUERBACH, O., STOUT, A.P., HAMMOND, E.C., Gm Lfaangesin
bronchial epithelium in relation to cigarette smoking and in &at&~ to Iune
cancer. New England Journal of Medicine 266(6U63-267. August 10,196l.
AYER, HE., YRAGRR, D.W. Irritants in cigerette smoke plumes. Am&con dod
of PrrMic Hecrlth 72(11):1283-1285, November 1982.
BANDA, MJ., CLARK, E.J., W-EBB, 2. Limited proteolysis by macr~phege e~a&aee
inactivates human al-proteinaae inhibitor. Joumal of E.zperi~~~ &fi&e
152(6):1563-1570, December 1930.

BARAD, C.B. Smoking on the job: The controversy heata up. OCCU~&O~ l&&h U&
safety 48(1):21-24, January-February 1979.
BASRUR, P.K.. MCCLURE, S., ZILKEY, B. A comparison of short-term bioeasay
results with carcinogenicity of experimental cigarettes. In: Nieburgs, HX (ed).
Revention and Detection of Cancer, Vol. 1. New York, Marcel Dekker, 1978, pp.
2041-2043.

BASU, P.K., PIMM, P.E., SHEPHARD, R.J., SIIS'ERMAN, F. The effect of cigarette
smoke on the human tear film. Canadian Journal of Ophthdnw&y 13(1)%!2-28,
January 1978.

BELL, D.Y., HASFMAN, J.A., SPOCK, A., McLENNAN, G., HOOK, G.E.R. Plasma
p~~~teine of the bronchoalveolar surface of the 1~8~ of smokera and nonsmokers.
American Review of Reepimtory Disease 124(1):7%79, July 1931.
BENEDICT, W.F., RUCKER, N., FAUST, J., KOURI, R.E. MaEgnant trenaformation
of mouse cells by cigarette smoke condensate. Cancer Research 35(3):357-360,
March 1975.

BER~LD, P., HOMBURGEX, F., RUSSFIEIl), A.B. Strain differences in the
response of inbred Syrian hamsters to cigarette smoke inhalation. Journd of the
Natid Clzncer Institute 53(4):1141-1157, October 1974.
BERNFELIX P., HOMBURGER, F., SOTO, E., PAI, K.J. Cigarette emoke inhalation
&U&S in i&red Syrian golden hamsters. Journal of the National Ckuxr Institute
63(3):675-689, September 1979.

BOOZER, C., PELLETIRR, A., PAULI. G., BIEXH, J.G. The functional activity of a,-
p&&aee inhibitor in bronchoalveolar lavage fluids fi-om healthy human emokers
and nonsmokers. Clinica Chimica Acta 132(3):30%315, August 31,1933.
CAI+fERON, P. Second-hand tobacco smoke: childrex& reactions. Journd of school
Health 62(5):26X%4, May 1972.

C&fNER, P., PHILIPSON, K., ABVIB!XSON, T. Withdrawal of cigerette smoking: A
study on tracheobronchiel clearance. Archives of Rnvinonmental Zidth 26(Z)%-
92, February 1973.

253


CAMPBELL, E.J. Human leukocyte elastase, cathepsin G, and lactoferrin: Family of
neutrophil granule glycoproteins that bind to an alveolar macrophage receptor.
Proceedings of the National Academy of Sciences USA 79(22):6941-6945, November
  1982.

CAMPBELL, E.J, WHITE, R.R., SENIOR, R.M., RODRIGUEZ, R.J., KUHN, C.
Receptor-mediated binding and internalization of leukocyte elastase by alveolar
macrophages in vitro. Journal of Clinical Investigation 64(3):824-833, September
  1979.

CANTRELL, E., BUSBEE, D., WARR, G., MARTIN, R. Induction of aryl hydrocarbon
hydroxylase in human lymphocytes and pulmonary alveolar macrophages: A
comparison. Life Sciences 1x12):1649-1654, December 16,19'73.
CARP, H., JANOFF, A. Potential mediator of inflammation: Phagocytederived
oxidants suppress the elasminhibitory capacity of alpha,-proteinase inhibitor in
vitro. Journal of Clinical Investigation 66@):987-995, November 1980.
CARP, H., MILLER, F., HOIDAL, J.R., JANOFF, A. Potential mechanism of
emphysema: al-Proteinase inhibitor recovered from lungs of cigarette smokers
contains oxidized methionine and has decreased elaatase inhibitory capacity.
Proceedings of the National Academy of Sciences USA 79(6):2041-2045, March
  1982.

CHAPMAN, H.A., Jr., STONE, O.L. Comparison of live human neutrophil and
alveolar macrophage elastolytic activity in vitro: Relative resistance of macro-
phage elastolytic activity to serum and alveolar proteinase inhibitors. Journal of
Clinical Investigation 74(5):1693-1700, November 1984.
COGGINS, C.R.E., FOUILLET, X.L.M., LAM, R., MORGAN, K.T. Cigarette smoke
induced pathology of the rat respiratory tract: A comparison of the effects of the
particulate and vapor phases. Toxicologv 16(2):8%101, August 1980.
COHEN, A.B., CLINE, M.J. The human alveolar macrophage: Isolation, cultivation in
vitro, and studies of morphologic and functional characteristics. Joumal of
Clinical Investigation 50(7):1390-1398, July 1971.
COLLISHAW, N.E., KIRKBRIDE, J., WIGLE, D.T. Tobacco smoke in the workplace:
An occupational health hazard. &n&an Medical Agpociation Journal
131(10):1199-1204, November 15,1984.

COSIO, M., GHEZZO, H., HOGG, J.C., CORBIN, R., LOVELAND, M., DOSMAN, J.,
MACKLEM, P.T. The relations between structural changes in small airways and
pulmonary function tests. New England Journul of Medicine 298(23):1277-1281,
June 8,1978.

COSTABEL, U., BROSS, K.J., REUTER, C., ROHLE, K.-H., MA'ITHYS, H. Alter-
ations in immunoregulatory T-cell subsets in cigarette smokers: A phenotypic
analysis of bronchoalveolar and blood lymphocytes. Chest 900):39-44, July 1986.
DALBEY, W.E., NEFTESHEIM, P., GRIESEMER, R., CATON, J.E., GUERIN, M.R.
Chronic inhalation of cigarette smoke by F344 rats. Journal of the National Cancer
Institute 64(2):383-388, February 1980.

DANIELE, R.P., DAUBER, J.H., ALTOSE, M.D., ROWLANDS, D.T., GORENBERG,
D.J. Lymphocyte studies in asymptomatic cigarette smokers. American Review of
Respiratory Disease 116(6):997-10@5, December 1977.
DAVIS, B.R., WHITEHEAD, J.K., GILL, M.E., LEE, P.N., BU'ITERWORTH, A.D.,
ROE, F.J.C. Response of rat lung to inhaled vapour phase constituents (VP) of
tobacco smoke alone or in conjunction with smoke condensate or fractions of smoke
condensate given by intratracheal instillation. British Journal of Cancer 31(4):462-
468, April 1975.

DeMARINI, D.M. Genotoxicity of tobacco smoke and tobacco smoke condensate.
Mutation Research 114(1):59-89, January 1983.

254


Chcinogenesk and Bioa.sguw. hu
1974. NWV York, Springer-verb ~4, *,h
             -' ~~~Jtpls23-~
DRATH, DB., HARPER, A., GHARIR~, a+:-
The effect of tobacco smoke on the -   i=4atfBgaGL
                   ,. Tima ?mha d rat aIve&r

127(4):165196, April 1979.                  .., 8
FERSON, M., EDWARDS, A., LIND, A., b%%`oIV, a<~{, WY, p- fAl -
kiIIer-ceU activity and immunog~oh~ le,,& ,w &- ?fa hrznrur
subjects. Intenationul Journal of&m B
FISCJ3ER, A. Pawivmuchen: Auamuss u& wgw k .%wyy
Tabakmuch unter experiment&en &&B h hee
smoking: Extent and Iniluence of Air Pouu&a z)rra to :w w:-
Expsrimental Conditions and in Field Stud@ a. m &. && w
Ridgeniissiche Technische Hochschule, Ziirich, -979. I  ., `I:'
FISHER, G.L., McNELLL, K.L., FINCX, G.L., -N, FD., &~~qav~.b
al evaluation of lung macrophages from c&r&& smokers & m
Journal of th.e Reticuloendothelial So&y 32(4)311-&&&,&&, ;, *`:
FBASCA, J.M., AUERBACH. O., CARTER, H.W., PA@& VR aborpboiPpic.&
ations induoed by short-term cigarette smoking, A& J+=!Bfe
111(1):11-20, April 1933.
FRASCA, J.M., AUERRACH, O., PARKS, V.R., JA&HRSoN,J&&&
ic observations on pulmonary fibroeia and emphysema in mm&g'&& w
mental and Mokcuibr Pathology 15(1):168-126, August 1971.
GADEK, J.E., FELLS, G.A., CRYSTAL, RG. Cigar&e amking i&m h&&p&
antiprotease deficiency in the lower respiratory tract of hmmam. h
21X(4424):1316-1316, December 1979.
GADRK, J.E., FELLS, G.A., ZLMMERHAN, RL., RRNNARD, S& GRYSlXT.+ RX%.
&d,ielastases of the human alveolar structmwr Implication thr the pmteww
sntiprotease therapy of emphysema. Jownal of Clinical Inws@&m 08@S6-
898, October 1981.
GAIROJA, C. Genetic effects of fresh cigarette smoke in %cchommm cemsf&e
Mu&on Z&search 102(2):123-X% September 1962.
~~DSJTON, M., MELNICK, E.L., GOLDRING, RM., -R&v-.-GA,
DAVIS, A.L. Interactions of neutrophil elastase, serum trJlpein inhibitors e*
ad smoking history aa rick factors for chronic ob&uoti* m dirmus in
patients with MM, MZ and ZZ phenotypes for alphax-anctryprdn e &?fe~
of Respiratory LXsease 116(5):837-646, November 197'7.
Gaudy, D., Gm&& R.S., YIELDING, K.L. Inhibition of DNA repair bp CCK=&M-
gem. &n&n&al and Biophysical Reswmh &~~~nicatione 48(4)3946849, ~
GERRAR.D, J.W., HEXNEX, D.C., MIMI, J., MEYERS, & w, J-A- -
glob& levels h smokers and nonsmokers. Annal- of Allegy 440~1-2Q, *Y
G$$)- L c  RyU J.H ROGC& P.R., SPRINCE, N.L., OLIVER, Le., =N,
C. J. `p&i& ki;ler ;$11 activity in ciga~ti smokers and * *
American ~evi.ew of Respimtov Disease 131(6):~1*~ Jmelm
wm, H.-P., B~ICHERT, A. Zum Problem dee Psssivrauchens @egarding the
problem of passive sm&&]. Znternattinales Archiv Fir Arbe&med%n %3%2-
322,1972.

                                          255


HARRIS, J.O., SWENSON, E.W., JOHNSON, J.E. III. Human alveolar macrophages:
Comparison of phagocytic ability, glucose utilization and ultrastructure in smokers
and nonsmokers. Journal of Clinical Investigation 49G1):208&2096, November
  1970.

HARRIS, R.J.C., NEGRONI, G., LUDGATE, S., PICK, C.R., CHESTERMAN, F.C.,
MAIDMENT, B.J. The incidence of lung tumors in C57BL mice exposed to
cigarette smoke:air mixtures for prolonged periods. International Journal of
Cancer 14(1):130-136, July 151974.

HERNANDEZ, J.A., ANDERSON, A.E., Jr., HOLMES, W.L., FGRAKER, A.G.
Pulmonary parenchymal defects in dogs following prolonged cigarette smoke
exposure. American Review of Respimtory Diseases 93(1):78-83, January 1966.
HINMAN, L.M., STEVENS, C.A., MAlTHAY, R.A., GEE, J.B.L. Elastase and
lysoxyme activities in human alveolar macrophages: Effects of cigarette smoking.
American Review of Respimtory Disease 121(2):263-271, February 1980.
HOFFMANN, D., HALEY, N.J., BRUNNEMANN, K.D. Cigarette Sidestmam Smoke:
Formation, Analysis and Model Studies on the Uptake by Non-Smokers. Paper
presented at the USJapan Meeting on New Etiology of Lung Cancer, Honolulu,
  March 1983.

HOFFMANN, D., RIVENSON, A., HECHT, S.S., HILFRICH, J., KOBAYASHI, N.,
WYNDER, E.L. Model studies in tobacco carcinogenesis with the Syrian golden
hamster. Progmss in Experimental Tumor Research 24:370-390,1979.
HOFFMANN, D., WYNDER, E.L., RIVENSON, A., LaVOIE, E.J., HECHT, S.S. Skin
bioassays in tobacco carcinogenesis. Rogreee in Experimental %mor Research
26X%67,1983.

HOIDAL, J.R., FOX, R.B., LaMARBE, P.A., PERRI, R., REPINE, J.E. Altered
oxidative metabolic responses in vitro of alveolar macrophages from asymptomatic
cigarette smokers. American Review of Respimtory Disease 123f1):85-89, January
  1981.

HOIDAL, J.R., NIEWOEHNER, D.E. Lung phagocy`e recruitment and metabolic
alterations induced by cigarette smoke in humans and in hamsters. American
Review of Respimtory Disetzse12~3):548-552, September 1982.
HOLLAND, R.H., KOZLOWSKI, E.J., BOOKER, L. The effect of cigarette smoke on
the respiratory system of the rabbit. Cancer 16(5):612-615, May 1963.
HUBER. G.L., DAVIES, P., ZWILLING, G.R., POCHAY, V.E., HINDS, W.C.,
NICHOLAS, H.A., MAHAJAN, V.K., HAYASHI, M., FIRST, M.W. A morphologic
and physiologic bioassay for quantifying alterations in the lung following
experimental chronic inhalation of tobacco smoke. Clinical Respimtory Physiology
17(2):269-327, August 1981.

HUGOD, C., HAWKINS, L.H., ASTRUP, P. Exposure of passive smokers to tobacco
smoke constituents. International Archives of Occupational and Environmental
Health 42(1):21-29.1978.

HUNNINGHAKE, G.W., CRYSTAL, R.G. Cigarette smoking and lung destruction:
Accumulation of neutrophils in the lungs of cigarette smokers. American Review of
Respimtory L&ease 128(5)%33-838, November 1983.
HUNNINGI-IAKE, G.W., GADEK, J.E., KAWANAMI, O., FERRANS, V.J., CRYS
TAL, R.G. Inflammatory and immune processes in the human lung in health and
disease: Evaluation by bronchoalveolar lavage. American Journal of Pathology
97(1):149-206, October 1979.

INNES, J.R.M., McADAMS, A.J., YEVICH, P. Pulmonary disease in rata: A survey
with comments on chronic murine pneumonia. American Journal of Pathology
32(1):141-159, January-February 1956.

INUI, N., TAKAYAMA, S. Acceleration of proliferation and tumor production rate of
L&rain cells by treatment with cigarette tar. Gann 62f4k315-320, August 1971.

256


=, C.9 VALADAuDBARRIEu, D., FAYELE&& J.-P., TESTA, A. influence des
parmetm de fumage SU hdhik genotmiqne da la passe wm de fumee de
cigarette mmee sur le lymphocyte humain et ta Ievure meet of machine
spoking Par-&m on the genotodc activity of gas phase wti emoke toward
human lymphocytes a.nd y-1. Mutation Resemch ~~(~)sr.aai.+a, Apfi 1960.
JANOFF, A., RAJU, L-8 DEARING, R. Levels of e.I&ase activity in bmnchdve&,r
Image fluids of healthy smokers and nonsmokem. A-
D&ease 127(5):540444, May 1983.            Reti ofRespimto8-y

JOHANSSON, C.R. Tobacco smoke in room air: An experimenta investigation of
odour perception and irritating effects. B&fing Say& Engineer #:*262,
March 1976.

JOHANSSON, C.R., RONGE, H. Klbnatinverkan pa lukt och irritationeeffekt av
tobakarok preIiminart meddelande [climatic influence on smell and w&con
effects from tobacco smoke]. Non&k Hygienisk Tidskrifi 47:33+ 1966.
JONES, N.L. The pathophysio1ogiax.l consequencea of smoking on the wv
system. Canadian Journal of Public Health 72(6):366-390, November-December
1961.
KENDRICK, J., -hW P., GUERIN, M., CATON, J., DALBEY, W.,
GRIESEMER, R., RUBM, I., MADDOX, W. Tobacco smoke inhalation stud& in
rats. Toxicology and Applied Pharmac~rogV 37(3):657469, September 1976.
KERKA, W.F., HUMPHREY CM. Temperature and humidity effecta on odour
perception. American Society of Heating, Refrigeruting and Air-Conditioning
Engineem, Inc., Transactions 62:531-552,1956.
KRAMPS, J. A., BAKKER, W., DIJKMAN, J-H. A matched-pair study of the leukocyte
elasta&ike activity in normal persone and in emphysematous patienta with and
without alpha,-antitrypsin deficiency. A meritan Review of Respiratory Disease
121(2):25%261, February 1980.

LASNl!I'ZKI, I. The effect of a hydrcxzarbonenriched fraction of cigarette smoke
condensate on human fetal lung grown in vitro. Cancer Reseamh 26(3>510-513,
March 1966.
LKJCI-ITENBERGER, C., LEU CHTENBERGER, R. Effecta of chronic inhaIation of
whole fresh cigarette smoke and of its gas phase on pulmonary tumorigend~ in
SnelI's mice. In: Nettesheim, P., Hanna, M.G., Jr., Deatherage. J.W., Jr. (eds.).
Morphology of E@erirnental Respimtory Carcinogen&s. Oak Ridge, U.S. Atomic
Energy Co mm&ion, Division of Technical Information, December 1970, pp. 329-
  346.

LEWIS, C.I., McGEADY, J.C., TONG, H.S., SCHULTZ, FJ., SPEARS. A-W. Cigarette
smoke tracers: Gas chromate-graphic analysis of decachIorobipheny1. A&n
Review of Respimtory 0%~ X)6(2):367-370, August 1973.
LUDWIG, P.W., HOIDAL, J.R. Alterations in leukocyte oxidative metabolism in
cigarette smokers. American Review of Respiratory Disease 126@:977-98Q Decem-
ber 1982.

LUDWIG, P.W., $XXlWARTZ, B.A., HOIDAL+ JR, -WOEHNER, D.E. cigarette
smoking causes accumulation of polymorphonuclear leukocytea in alveolar eep
turn. American Review of Respiratory Disease 131(6):826-630, June 1985.
MARTIN, R.R. Altered morphology and increased acid bydrolase content of PuIm*
nary macrophages from cigarette smokers. American Review of Reapimtory
Disease 107(4):596-601, April 1973.

MARTIN, R.R., WARR, G.A. Cigarette smoking and human pulmonary macrophages.
Hospital Practice 12(9):97-104, September 1977.
MATULIONIS, D.H., TRAURIG, H.H. In situ response of lung macrophages and
hydrolase activities to cigarette smoke. Lubomtory Investigation 37(3):314-326,
September 1977.

257


MCGOWAN, SE., STONE, P.J., CALORE, J.D., SNIDER, G.L., FRANZBLAU, C. The
fate of neutrophil elastase incorporated by human alveolar macrophages. Ameri-
can Review of Respimtory Disease 127(4):449-455, April 1983.
MCLAUGHLIN, R.F., TUELLER, E.E. Anatomic and histologic changes in early
emphysema. Chest 5%6):592-599, June 1971.
MERRILL, W.W., NAEGEL, G.P., OLCHOWSKI, J.J., REYNOLDS, H.Y. Immune
globulin G subclass proteins in serum and lavage fluid of normal subjects:
Quantitation and comparison with immunoglobulins A and E. American Review of
Respiratory Disease 131(4):584-587, April 1985.
MILLER, L.G., GOLDSTEIN, G., MURPHY, M., GINNS, L.C. Reversible alterations in
immunoregulatory Tcelle in smoking: Analysis by monoclonal antibodies and flow
cytometry. Chest 82(5):52W%B, November 1982.
MOHR, U., REZNIK, G. Tobacco carcinogenesis. In: Harris, C.C. (ed.). Pathagenesis
and Z'hempy of Lung Cancer. Lung Biology in Health and Disease, Vol. 10. New
York, Marcel Dekker, 1978, pp. 263-367.

MURAMATSU, S., MURAMATSU, T. WEBER, A. A survey on attitudes towards
passive smoking among schoolchildren and students in Switxerland. Social- und
Prliventivmedizin 28(2):82-84,1983.

MURAMATSU, T. A study on smoking experience and smoking habits: Report 3.
Parental smoking habits and second-hand tobacco smoke of high school students.
Gokko Hoken Kenkyu (Japanese Journal of School Health) 19(2):8895,1977.
MURAMATSU, T., WEBER, A., MURAMA'ISU, S., AKERMANN, F. An experimen-
tal study on irritation and annoyance due to passive smoking. Internutional
Archives of Occupational and Environmental Health 51(4):305-317, April 1983.
NIEDERMAN, M.S., FRI'ITS, L.L., MERRILL, W.W., FICK, R.B., MAlTHAY, R.A.,
REYNOLDS, H.Y., GEE, J.B.L. Demonstration of a free elastolytic metalloenxyme
in human lung lavage fluid and its relationship to alpha,-antiprotease. American
Review of Respimtory LX-sense 129(6):943947, June 1984.
NIEWOEHNER, D.E., KLEINERMAN, J., RICE, D.B. Pathologic changes in the
peripheral airways of young cigarette smokers. New England Journal of Medicine
291(15):755758, October 10,1974.

OBE, G., HELLER, W.D., VOGT, H.J. Mutagenic activity of cigarette smoke. In: Obe,
G. ted.). Mutations in Man. Berlin, Springer-Verb% 1984, pp. 223-246.
ONG, T.M., STEWART, J., WHONG, W.Z. A simple in situ mutagenicity test system
for detection of mutagenic air pollutants. Mutation Research 13%4):177-181, April
  1984.

PARK, S.S., KIKKAWA, Y., GOLDRING, I.P., DALY, M.M., ZELEFSKY, M., SHIM,
C., SPIERER, M., MORITA, T. An animal model of cigarette smoking in beagle
dogs: Correlative evaluation of effects on pulmonary function, defense and
morphology. American Review of Respimtory Disease 115(6):971-979, June 1977.
PETERSEN, B.H., STEIMEL, L.F., CALLAGHAN, J.T. Suppression of mitogen-
induced lymphocyte transformation in cigarette smokers. Clinical Immunology
and Zmmunopathology 27(1):135140, April 1983.

PRATT, S.A., SMITH, M.H., LADMAN, A.J., FINLEY, T.N. The ultrastructure of
alveolar macrophages from human cigarette smokers and nonsmokers. Z&oratory
Investigation 24(5):331-338, May 1971.

RASMUSSEN, R.E., BOYD, C.H., DANSIE, D.R., KOURI, R.E., HENRY, C.J. DNA
replication and unscheduled DNA synthesis in lungs of mice expoeed to cigarette
smoke. Cancer Research 41:25&l-2588, July 1981.
REGLAND, B., CAJANDER, S., WIMAN, L.G., FALKNER, S. Scanning electron
microscopy of the bronchial mucosa in some lung diseases using bronchoscopy
specimens: A pilot study including cases of bronchial carcinoma, sarcoidosis,
silicosis, and tuberculosis. Scandinavian Journal of Respimtory Dismses 57(41:171-
182,1976.

258


RHIM, J.S.. HUEBNER, R.J. In -viix, e
cigarette smoke condensate (m iu   ** -wfJf@erfiactkmctif
societyforErpen'mentalBiologycurd~~~~~~~,-~
                  - ~sms*pcoandiytaf~
RIvEDAL,E., SANNER,T. Potentiating~~~apblrctrrrotcll
morphological trensformation of hemeter embryo d by w- -
Letter X)(3):193-198, September 1980.
RODRIGUEZ, J.R, SEALS, J.E., RADIN, A., I,IN, J.&, MANDL, I, m Gy.
Neutrophil lyeoeomel elastaee activi~ b nod eubjeee d b m rith
chronic obf3tructive pulmonary disease. w h of- m
119(3):4@-417, March 1979.
RODRIGUEZ, R.J., WHITE, RX.., SENIOR, RM, w EA, m nlspc ban
human alveolar mamophages: Comparison between b end m
sci.erux 198(4314):3xX314, October 21.1977.
SANTA CRUZ, R., LANDA, J., HIRSCH, J., SACKNER, &&A. M mocQul
velocity in normal man and patiente with obstn&i~ lung diseeet: m d
terbutaline. American Review of Reepimtory llisaee 109(4hw @ ~4.
SHEPHARD, R.J., LAB-, R. Attitudw of the public towa& m h h
public places. Canudian Journal of Public H~lth @(4)53O%l1O, July.- 1918
SILVERMAN, N.A., POTVIN, C., ALExANDw, J-C., Jr., CBRETEN, P.B.iVitl.0
lymphocyte reactivity end T-cell levels in chronic cigarette ~okexa w d
Experimental Immunology 22(2):286-292, November 1975.
SPEER, F. Tobacco end the nonsmoker: A study of subjective eymptoma A&&es qf
Environmental Health 16(3)443-446, March 1988.
STERLING, T.D., STERLING, E.M. Comparison of nonsmokers' and Bmokpd
perception of environmental conditions and health and comfort symptoms in oflice
environments with and without smoking. In: Grandjean, E (ed). &gonoti Md
He&h in Modern office Philadelphia, Taylor end Francis, 1984.
STONE, Pd., CALORE, J.D., McGOWm, S.E., BERN-, J., SNH)ER, G-L.,
FRANZBLAIJ, C. Functional a,-protease inhibitor in the lower respiratory tract aE
cigarette smokers ia not decreased. Science 221(4616):1187-1189, September 1%
  1986.
TAKAYAMA, S., KATOH, Y., HIR,AKAWA, T., TANAKA, M. In vitro morpw
transformation of cryopreserved hamster embryo cells with tobaca, tar- ti
69(1):65-90, February 1978.
TAYLOR, J.C., KEUPPERS, F. Electrophoretic mob*0 of leukocyte elf&se of
nca-& s&j&s and patients with chronic obstructive pulmonary disease. A~PI+-
can Reuiew of Respiratory Disease 116(3):531336, September 1977.
VITO, MC., CiOLDE, D.W. The function of human alveolar maclophsgeg Journal
of the Reticuloendothelid Society 25(1):111-120, January 1979.
TRIEBIG, G., ZOBER, M.A. Indoor air pollution by smoke constituents A -eY.
Preventive Medicine 13(6):570-581, November 1984,
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES m Health conse
quences of Smoking: Chronic Obstructive LUG &w A &@ Qf the Swge~n
Geneml. DHHS Pub. No. (PHS$34-50205. U.S. DePartment of Health and Human
&I-V&S, public Health &rv&, Ofike on Smoking and Health, 1984.
VALENTIN, H. Ar&i&m.e&in. Vol. 2. George Thieme verb, 1985, P* 298-

                                           259


WANNER, A. Clinical aspects of mucocihary transport. American Review of
Respimtory Disease 116(1):73-125, July 1977.
WARR, G.A., MARTIN, R.R., HOLLEMAN, CL., CRISWELL, B.S. Classification of
bronchial lymphocytes from nonsmokers and smokers. American Review of
Respimtory Disease 113(l)%-100, January 1976.
WEBER, A., FISCHER, T. Passive smoking at work. International Archives of
Occupational and Environmental Health 47(3):24%221,1980.
WEBER, A., FISCHER T. Schadstoffkonzentrationen im Blasfeld von Rauchern.
[Concentration of pollutants in the blowing field of smokers]. Znternutional
Archives of Occupational and Environmental Health 63(1):4750,1983.
WEBER, A., FISCHER, T., GIERER, R., GRANDJEAN, E. Experimentelle Reixwir-
kungen von Akrolein auf den Menschen [Experimentally induced irritating effecta
of acrolein in man]. Zntumationul Archives of Occupational and Environmental
Health 40(2):117-136.1977.

WEBER, A., FISCHER, T., GRANDJEAN, E. Objektive und subjektive physiologische
Wirkungen dea Passivrauchens [Objective and subjective physiological effects of
passive smoking]. Znternationnl Archives of Occupationul and Envinmmentul
Health 37(4):277-288, September 6,1976.

WEBER, A., FISCHER, T., GRANDJEAN, E. Reixwirkungen des Formaldehyds
(ECHO) auf den Menschen [Irritating effects of formaldehyde in man]. Znternution-
al Archives of Occupational and Envimnmentul Health 39(4):207-218,1977.
WEBER, A., FISCHER, T., GRANDJEAN, E. Passive smoking in experimental and
held conditions. Environmental Research 2620!%216,1979a.
WEBER, A., FISCHER, T., GRANDJEAN, E. Passive smoking: Irritating effects of the
total smoke and the gas phase. International Archives of Occupational and
Environmental Health 43(3):18%193,1979b.
WEHNER, A.P., BUSCH, R.H., OLSON, R.J., CRAIG, D.K. Effect of chronic exposure
to cigarette smoke on tumor incidence in the Syrian golden hamster. In: Karbe, E.,
Park, J.F. (eds). Experimental Lung Cancer, Carcirwgenesia and Biaassaye. New
York, Springer-Verlag, 1974, pp. 366368.

WEHNER, A.P., DAGLE, G.E., MILLIMAN, E.M., PHELPS, D.W., CARR, D.B.,
DECKER, J.R., FILIPY, R.E. Inhalation bioassay of cigarette smoke in rats.
Toxicology and Applied Pharmacology 61(1):1-17, October 1981.
WHITE, R., WHITE, J., JANOFF, A. Effects of cigarette smoke on elastase secretion
by murine macrophages. Journal of Labomtory and Clinical Medicine 94(3):48%
499, September 1979.

WORLD HEALTH ORGANIZATION. Smoking in Aircmft: Report of a
WHO/ZATA/ZCAO Consultation. WHO/SM0/84.3. Geneva, World Health Organi-
zation, 1984,44 pp.

WYNDER, E.L., HOFFMANN, D. Tobacco and Tobacco Smoke: Studies in Experimen-
tal Curcinogenesis. New York, Academic Press, 1967.

260


CHAPTER 6

POLICIES RESTRICTING
SMOKING IN PUBLIC PLACES
  AND THE WORKPLACE


CONTENTS

Introduction

Current Status of Restrictions on Smoking in Public
Places

Legislative Approaches
  Federal Legislation
  State, Legislation
  Local Legislation
Regulatory Approaches
Smoking Regulation in Specific Public Places
  Public Transportation
   Retail Stores
   Restaurants

Hotels and Motels
Schools
Health Care Facilities

Current Status of Smoking Regulations in the Workplace
  Smoking Policies
  Prevalence of Smoking Policies
  Reasons for Adopting Smoking Policies
  Barriers to Adopting Smoking Policies
  Types of Smoking Policies
    The "Individual Solution" Approach
     Environmental Alterations
    Restrictions on Employee Smoking
    Banning Smoking at the. Workplace
    Preferential Hiring of Nonsmokers
Implementation of Smoking Policies

Impact of Policies Restricting Smoking in Public Places
and in the Workplace
Potential Impacts of Smoking Policies
    Policy Implementation and Approval
    Direct Effects: Air Quality and Smoking Behav-
       ior
    Indirect Effects: Knowledge, Attitudes, Social
     Norms, and Smoking Behatior
Methodologic Considerations in Policy Evaluation


Study Design

  Assessing the Effects of Smoking Policies
Review of Current Eviderice on Impact
  Workplace Smoking Policies
  Policy Implementation
  Air Quality
  Policy Approval
  Smoking Behavior
  Attitudes About Smoking
  Management Issues
  Legislation Restricting Smoking in Public Places
  Policy Implementation and Enforcement
  Policy Approval
  Attitudes tid Social Norms
  Smoking Behavior

Recommendations for Future Research

Conclusions

Appendix: `I'he Comprehensiveness Index of State Laws

References

264


Introduction

Since the 197% the accumulating evidence on the health risks of
involuntary smoking has been accompanied by a wave of social
action regulating tobacco smoking in public places. hntiatives in the
public sector and in the private sector have aimed at protecting
individuals from exposure tc side&ream smoke by regulating the
circumstances in which smoking is permitted. Smoking h public
places has been regulated ~rhmily by government action at the
local level and at the Federal level. Legislation has been the most
common vehicle at the local and State level; agency regulations have
predominated in the Federal Government. There has been relatively
little judicial action to restrict smoking in public places; most cases
have focused on nonsmoking employees' right to a smokefree
workplace (Feldman et al. 1978; Eriksen, in press; Walsh and Gordon
1986). Private sector initiatives have gained momentum in the 1980s.
Businesses in a ,wide variety of industries have adopted smoking
policies to protect employee health. Other private initiatives include
no-smoking sections in restaurants, no-smoking rooms in hotels and
motels, and smoking restrictions in hospitals.
Though this trend was fueled by growing evidence about the
health effects of involuntary smoking, it also reflects the changing
public attitudes about smoking since 1964, when public attention
was focused on the health hazards of cigarette smoking by the
Report of the Advisory Committee to the Surgeon General (US PEIS
1964). The acceptability and desirability of tobacco smoking in public
places has fallen dramatically over time, as reflected in public
opinion surveys. A majority now support the right of nonsmokers to
breathe smoke-free air and favor policies that ensure that right
(ALA 198!jb; Hanauer et al. 1986; BNA 1966; US DHEW 1969).
This chapter addresses the scope and impact of these diverse
pohcies. It begins with a review of the current status of policies
restficting smoking. Issues specific to smoking regulation in trans-
portation vehicles and motels, restaurants, stores, schools, health
care facilities, and the workplace are addressed. The effects of
smoking policies on air quality, attitudes, and smoking behavior are
considered.

Current Status of Restrictions on Smoking in Public Places

Smoking regulations in public places represent a mix of public and
private actions. A public place may be defined as any enclosed area
in which the public is permitted or to which the public is invited.
Smoking restrictions are generally limited to indoor enclosed spaces
(Hanauer et al. 1986). This broad definition of a public place
encompasses a diverse group of facilities that differ in the degree to
which smoking is restricted, the ease of introducing new regulations,


and the methods by which new smoking restrictions have been
proposed and adopted.

Smoking in Federal, State, and local government facilities has
been addressed by legislative and regulatory action. These facilities
include government offices, public schools and libraries, and publicly
owned transport&ion, health care, cultural, and sports facilities. In
public facili&s under private ownership, smoking restrictions are a
mixture of government-sponsored regulation and private initiative.
These facilities include retail stores, restaurants and bars, hotels and
motels, and privately owned transportation, health care, cultural,
and sports facilities.
The extent and ac&ptability of smoking restrictions in public
places is influenced by (1) whether ownership is public or private; (2)
the historical acceptance of smoking in the facility; (3) the degree to
which nonsmokers are exposed to involuntary smoking, determined
by the facility's size, degree of ventilation, and ease of separating
smokers and nonsmokers; and (4) the degree of inconvenience that
smoking restrictions pose to smokers. Smoking restrictions are still
most widespread and least controversial in facilities where smoking
has traditionally been prohibited by fire codes, such as theaters or
libraries, or where smoking is negatively associated with the activity
taking play, such as gyms or health care facilities (Feldman et al.
1978). Small crowded areas with poor ventilation, such as elevators
and public transit vehicles, are also frequently regulated. On the
other hand, the strong association of smoking with eating and
drinking contributes to the controversial nature of smoking re&ic-
Cons in restaurants and bars.

Legislative Approaches
Fe&r-d Legislation

Congress has enacted no Federal legislation restricting smoking in
public places, although bills have been introduced in Congress
several times since 1973 (Feldman et al. 1978).

State Legislation

Most legislation restricting smoking has been enacted at the State
level. Although legislation regulating smoking for health reasons is
largely a phenomenon of the past decade, cigarette smoking has been
the subject of restrictive legislation for nearly a century. Early
legislation had two different rationales. The first, a relatively
noncontroversial rationale, was the protection of the public from fire
or other safety hazards, largely in the workplace (Warner 1981b).
The second, more controversial motivation for early legislative
action was a moral crusade against cigarettes similar in tone and
coincident with the moral crusade against alcohol that emerged at


the tux-n ofthe century Wlow 1981; Nobel 1978). INS goal w~ a total
ban On Cigarettes, which were blamed for social e* and physical
% based 1arge~Y on unfounded claims. By 1887, three States (North
Dakota, Iowa, and Te==ee) had completely banned the de and
use of cig=ett-. At the peak of the movement, cigarettes were
b-cd h a dozen Stat.e~ RJuhing and Markle 1974; sobe 1978).
Most were in the Midwest where cigarette consumption was low and
a~~ticigarette feeling high. The movement lost momentum when
enforcing the regulations proved controversial. AS part of the strong
reaction to alcohol prohibition, ah State laws banmng smoking were
repealed by 1927.
During the 196Os, as the health risks of smoking became widely
`recogn&d, public POLICY on smoking began tc focus on encow
the smoker to quit. However, the few existing State laws regulating
smoking in public places were old and limited in scope. Even newly
enacted laws-in Delaware (1960) and in Michigan (1967, 1968&
restricted smoking in limited areas: public buses and trolleys,
elevators, and retail food establishments (VS DHHS 1985b). Protec-
ting the health or comfort of nonsmokers was not cited as a rationale
of these laws. As Of 1970,~tatuteS restricting smoking were in force
in 14 states (US DHHS 1985b).
In the early 19709, a new wave of smoking legislation emerged. It
covered smoking in a larger number of places and extended for the
first time to privately owned facilities. The language became more
restrictive, moving from permitting a no-smoking section to requir-
ing one and making nonsmoking the principal or assumed condition.
me language also changed to make it clear that the specific intent
was the safety and comfort of nonsmokers.
me pace of new legislation increased in the mid-1970s. Between
1976 and 1974, 9 laws were enacted in 8 States, between 1975 and
1979, 29 new laws were passed and 15 additional States adopted
smoking regulations. Minnesota passed its landmark Clean Indoor
fi Act in 1975 "to protect the public health, comfort, and
environment by prohibiting smoking in public places and at public
meet-s except in designated smoking areas" (M~IUESO~~ Stthte~
Annual 1985). It covered restaurants, private worksites, and a large
number of public places, and soon became the model for other State
legislation. Within the next 5 years, Utah, Montana, and Nebraska
enacted similar comprehensive legislation (US DHHS 1985b). The
language of statutes passed by 11 States during the 1970s made it
clear that the specific purpose was to protect nonsmokers from
involuntary smoking (US DHHS 198523). Model legislation and
advice about the successful enactment of State laws can be found in
several sources (Hanauer et al. 1986; Feldman et al. 1978; Walsh and
Gordon 1986).


1
f  30-
.s
e
$  25-
5
f
z20
b
P  15 -
2

1960 1964   1970            1975            1880            1885

                      Year

FIGURE l.-Prevalence and restrictiveness of State laws

     regulating smoking in public places, 19604986
NOTE See appendix for definitions of mtrictivenem of laws.
S4WRCE: ASH (1SW; OTA (1986); Tri-Agency Tobacco Free Project MSSk US DHHS WS6b).

The rate of enactment of State legislation increased throughout
the seventies (Figure 1, Table 1). The pace of new legislation
continues in the 1980s with 23 new laws enacted by 16 States
between 1980 and 1985 (Table 1). As of 1986, 41 States and the
District of Columbia have enacted laws regulating smoking in at
least one public place (Figure 1). Eighty percent of the U.S.
population currently resides in States with some smoking restric-
tion, compared with 8 percent in 1971 Warner 1981b). Most of the
nine States with no smoking legislation are concentrated in the
southeast United States and include three of the six major tobacco-
producing States (North Carolina, Virginia, and Tennessee) (Figure
a.

Current State legislation varies in comprehensiveness and lan-
guage. The number of public places in which smoking is regulated by
State law ranges from 1 (Delaware, Mississippi, and South Carolina
regulate smoking on public transportation only) to 16 (Minnesota
and Florida) (US DHHS 198513, Tri-Agency Tobacco Free Project

268


1986). State laws most often restrict smoking in public transporta-
tion (35 States), hospitals (33 States), elevator (31 States), indoor
cultural or recreational facilities (29 States), schools (27 Stat.@,
public meeting rooms (21 States), and libraries (19 States) (Table 2).
Other public places specifically mentioned in State smoking legisla-
tion are public restrooms and waiting rooms, jury rooms, polling
places, prisons, hallways, stairwells, and stables. Most laws restriqt
smoking in these places to designated areas, thereby making
nonsmoking the norm; in a few States smoking is banned entirely in
these places. For example, smoking on pqblic transportation is
banned entirely in four States (Florida, Georgia, Massachusetts, and
W&&t& ad one (Washington) bans smoking in theaters,
m-e-, au&t()dm, and indoor sports arenas. Smoking restric-

                                          269


m Nominal
0 No-ns

FIGURE 2.-Geographic variability of State laws regulating
      smoking in public places, 1996

tions extend to restaurants and retail stores, which are largely
privately owned, in 18 States.

Smoking at the workplace is restricted for public sector employees
in 22 States and for private sector employees in 9 States. The
provisions of worksite smoking legislation vary widely, making
direct comparisons of their comprehensiveness difficult.
Currently enacted workplace smoking laws contain provisions to
(1) require a written policy (5 States); (2) limit smoking to designated
areas (8 States); (3) require the posting of signs (10 States); and (4)
give preference to nonsmokers in resolving conflicts over the
designation of a work area (2 States) (OTA 1986). Public or private
worksites are included in the definition of public places in some
States where worksites are subject to the general provisions for
public places. Other States have written separate guidelines for the
worksite, which are usually more stringent. Laws in four States
apply only to State and local government employees; restrictions
apply to the private worksite in an additional nine States.

270


state            AL AK AZ AR     CA     CO (;T DE DC FL GA HI ID   IL IN IA KS KY
                             1971.76         1973                            1925
Year(s) legislation         1975   1973   1977   1960.61    1977   1974             1963             1975
   enacted        -   1964   1981   1963    1962    1985'   1963   1960   1979   1965   1975   1976   1965   -      1978   1975   1972

PUBLIC PLACES WHERE SMOKING IS PROHIBITED (EXCEPT IN DESIGNATED AREAS)
Public transportation       x x    (X)'     X3.4     X     X8 x     X     x3.5 X'         X           X     X     X
Elevators              X' x                 X     X'         X     x1 X' x     X           X     X
Indoor recreational or
cultural facilities'         x x           X      X                    X          X     X           X     X
Retail stores            (X)'             (X)' x     X          X     X              X
Restaurants             X'               X0     X     X'O             X'             X
Schools                X     X     X      X      X     X          X     X              X
Health care facilities
Hospitals              X     X     X      X      X     X         x x          X     X           X     X
Nursing homes          X                X      X     X          X     X              X           X     X
Public meeting rooms       X                X           X          X     X          X     X           X     X
Libraries               X     X                                     X                         X     X
Restrmns              X' x                 X     X              X
Waiting rooms           X     X                 X     X               X                          X
Other               p.27 xn                                     X262-7.30

WORKSITE SMOKING RESTRICITONS "
Public worksites          D"               B      D' B          B    B,D I11       B' B           D
Private worksites          A                            B             BD

IMPLEMENTATION PROVISIONS
Nonsmokers prevail
in disputes             X
No discrimination
against nonsmokers

    ENFORCEMENT
    Penalties for violations      X     X     X      X           X     X     X     X     X     X     X           X     x x
    Smoking              Xm   pa x23.     XS          xm X" x= X21' x23. X"   X2&i          x- 2P x-
Y    Failure to post signs       X@h                                    XUh
c
    Overall State law
     restrictiveness:"      0    3     2     1      3       3     4     1     2     4     1     2     3    0   0    2     2     1


ii   TABLE 2.-Cantinued

St&           LAME MDMAMIMN   IbiB MO MT NE NV NH NJ Nbf   NY NC ND OH
                  1954        1924 1967                                 1955       1921
Year@) legislation         1961,63   1957   1947 1966   1971                     1911        1979       1975           1961
  enacted              1965    1975   1975   1976   1975   1942 -   1979   1979   1976   1961 1965 16%   1976 -   1977 lsec

PUBLIC PLACES WHERE SMOKING I8 PROHIBITED (EXCEPT IN DEslGNATBD AREAS)
Public transportation          X      X    X' 00' x x        X    x x x x x x       x x
ElW&XI                     X    X' x x           x x x x x x            x x
Indoor recreational or
cultural facilities*                      X         X           x x x x x x x       x x
Retail stores              X         cm' x x            x x         X    X
Restaurants                             X    X"           x x             X"   X"           X
Schools                                       X           x x x x x x            x x
Health care facilities
Hospitals               X     x x x x            x x x x x x            x x
Nursing homea            X     x x x x           x x x x x x            x x
Public meeting rooms                            X           x x x x x x            x x
Libra+                          X         X                x x         x x x       X
Rentmoms           x                     X                 X                              x x
waiting rooms             X                    X                 x x x                       X    X
Other                  X'"         X"        Xmm              X"        X"            X"

WORKSITE SMOKING RE!i%`RICl'IONS"
Public worksites           BP                   D"           D "   D"        D'O   B,C" B$F           C     C
Private worksites          4D                  Dl7.21           D"   D17P A"       B,C "       Aal

IMPLEMENTATION PROVISIONS
Nonsmokers prevail
in disputes                                    X                                     X
No discrimination
against nonsmokers          X

ENFURCEMENT


state              OK     OR     PA I.. SC SD TN TX UT VT VA WA WV WI WY
                    1973.76    1927                                            1913               w
Year(s) legislation             1977    1947   1976                     1976                1919               N CC)
   enacted          1975    1961     1977   1977   1937   1974   -   1975   1979   1692   -   1963   1965   1964   -       51 wo)

PUBLIC PLACES WHER?- SMOKING IS PROHIBITED (EXCEPT IN DESIGNATED AREAS)
Public transportation     X                X    (x)* x        X
Elevators            X      X          X         X        X
Indoor recreational or
cultural facilities0      X      X      x x         X        X
Retail stores                 X      X    X
Restaurants                 X          X
Schools                    X           X          X        X
Health care facilities
Hospitals                  X      X    X          X        X
Nursing homes               X      X    X                  X
Public meeting rooms            X
Libraries             X                 X         X        X
Restrooms
Waiting rooms               X
Other                          XS"   X"

X
X
X
X

X'
XL

X'
X'
X
X'

X
X
X'
X
X
X
X"

X     X
     X

     X
     X
     X
X     X

X
X

X

36 (66.6)
31 (60.8)

29 (59.6)
16 (35.3)
16 (35.3)
n (52.9)

33 (64.7)
29 (56.9)
21 (41.2)
19 (37.2)
11 (21.6)
16 (31.4)
12 (23.5)

WORKSITE SMOKING RESTRICI'IONS"
Public worksites               D
Private worksites

D"            D          D"           22 (43.1)
D17.22   A"       D    A"                9 (17.6)

IMPLEMENTATION PROVISIONS
Nonsmokers prevail
in disputes
No discrimination
against nonsmokers

X                                  4 (7.6)

X                                  2 (3.9)

ENFORCEMENT
Penalties for violations    X      X      X    X          X        X     X     X        x x     X            40 (78.4)
Smoking            XW     XWb    X2" x=        X2.%       X2" x=   X23.       XZJ'   psa    X=          39 (76.5)
Failure to post signs            X2&         XW                                       pe                9 (17.6)

Overall State law
restrictivenewzS        2      3      2     3     1     2    0    2     4     1    0    4     1     3    0


Y  TABLE 2.-C!ontinued (Footnotes)

' Executive order.
`School buses only.
a Including school buses.
`California stipulates that at least 50 percent of all passenger seats must be in nonsmoking areas on trains, airplanes. and street railroad cam departing from the State.
`Smoking never permitted in this area.

`Indoor recreational and cultural facilities: museums, auditoriums, theaters, and sports arenas.
`Grocery storea only.
' Beatauranta seating 50 or more persons must have a no-smoking section.
eBestauranta seating 50 or more persons must have e no+moking eection if the restaurant ia in a publicly owned building.
`OBestauranta seating 15 or more persons must have a nwmoking section.
" Restaurants must designate at least 30 percent of their mata aa a no+moking area.
" Reatauranta are encouraged to establish noamoking areas.
`I Ftentauranta must designate at least 50 percent of their seats 88 a no.emoking area.
"Kkleted).

I' No place other than a bar may be designated B smoking area in its entirety.
`* Worksite (only 8, C. and D munt aa having a worksite policy in maculation of totals): A - Employer must post a sign prohibiting smoking at the work&q B - Employer mu& have a (wit&n)

smoking policy; C - Employer must have policy that provides a nonsmoking area; D - No smoking except in designated .wcas.
" Employer must post signs designating smoking and nwmoking arena.
`*Employer mu& vt signs in smoking area.%
`*Employer must post either smoking or nwemoking sign& depending upon their policy.
`"Employer must post Ggna in no-smoking areas.

" State doea not restrict smoking in factories. warehouses. and similar placea of work not usually frequented by the general public.
" Prohibita smoking in any mill or factory in which a no-emoking sign is pasted.
"Pereons who smoke in a prohibited area are subject to a tine or a penalty. Maximum fina or penalties, where applicable, are listed below: a = $5; b = $10, c = 1%; d = $& e = $100, f =
$loO/day; g = $200; h = *urn; i = $5CO; j = $50 or up to 10 days in jail or both; k = $60 or SO daya imprisonment; 1 = civil action; m = minor misdemeanor; n = petty mi&mwnor; o =
misdemefmor; p = petty offense.

" Persona who are required to and fail to pcet smoking and/or no+moking sigma are subjected b a penalty. Maximum finea. where applicable. are listed in footnote 23.
I6 Restrictivenea key: 0 = None, no statewide restrictions; 1 = Nominal, State ragul&en smoking in one to three public placm, excluding restaurants and private vorknita; 2 = B&c, State
regulatea smoking in four or more public places, excluding restaurants and private workaita; 3 = Moderate. State regulatea smoking in restaurants but not private workaitcs; 1 = ENnaive.
State regulates smoking in private work&es.
*`Jury moms.
" Halb and stain.
`*stables.
"Polling plaan.

*`Prisons, at ptin offL%& diiretion.


The least restrictive workplace laws simply empower the employer
to restrict smoking in factories by posting signs. These statutes were
enacted in the early 1900s. The weakest recent laws simply require
an employer to issue a written smoking policy and to post signs.
More restrictive laws require that employers designate no-smoking
areas at work, implying that smoking is the norm. The most
comprehensive laws prohibit smoking except in designated areas,
making nonsmoking the norm. Seven States (Florida, Maine, Minne-
sota, Montana, Nebraska, Utah, and Washington) have this type of
law. In several States, some worksites or some parts of a worksite
(usually private offices) are exempted from the regulations. To
prevent employers from complying with the letter but not the intent
of the law, some States prohibit a workplace from being designated
as entirely smoking.
State laws vary in their provisions for implementation and
enforcement. In most States, the State health department is
responsible for policy enforcement. Nearly all (39 of 42) States with
laws provide penalties for smokers who violate restrictions; the
maximum penalty is $500. In two States violators can be jailed.
Employers or others who fail to designate smoking areas can be fined
in nine States.
The comprehensiveness of State laws, as defined by the number
and nature of places where smoking is restricted or prohibited, has
increased since 1970. In 1981, Warner (1981b) classified State laws
according to their comprehensiveness (restrictiveness) and docu-
mented an increase in the average restrictiveness from 1971 to 1978.
An updated and modified index of the comprehensiveness of State
laws (described in the appendix) demonstrates that the phenomenon
reported by Warner has continued into the mid-eighties. The
comprehensiveness of newly enacted laws increased markedly dur-
ing the mid-seventies, and the average restrictiveness of State laws
in effect has increased more than twofold between 1972 and 1985
(Table 1, Figure 3). As shown in Figure 1 and Table 1, the increase in
comprehensiveness of State laws occurred in two ways. The average
comprehensiveness of first laws in additional States increased, and
existing State smoking laws were replaced with more comprehensive
legislation.
Warner also documented that both the prevalence and comprehen-
siveness of State laws enacted through 1978 varied by geographic
region (Warner 1982). This has not changed (Table 3, Figure 2). Over
90 percent of the States in the Northeast and West have enacted at
least one law regulating smoking, as have three-fourths of the North
Central States. Southern States have fewer laws than other regions,
and the laws they have are less comprehensive than laws in other
regions. The six major tobacco-producing States, all located in the
South, have less restrictive laws than do the other six Southern


0.65

  0.60

  0.55

i
m  0.54
.E
4
s
B
t
g  0.45
P
`S
g
t
Ei
t  0.40
3

  0.35

  0.3c

  0.2c

1            1

T        -L  I I I I    I I 1 I

1960   1965   1970           1975           1960           1965

                      Year

FIGURE 3.-Average restrictiveness of State laws in effect,

1990-1985

NWlW Coding of restrictiveness of law; Extensive = 1.00; Moderate = 0.75; Rasic = 0.50; Nominal = 0.25 ISee
appendix for definitions of ratrictivenw of laws.)

SOURCE: ASH ,1966); WI-A (1966); Tri-Agency Tobacco Free F'mject W366); US DHH6 W35b).

States. Compared with other States, major tobacco States are less
likely to have enacted smoking legislation and more likely to have
enacted less stringent laws.


TABLE 3.-Regional variation in State laws restricting
      smoking

              Total       Stetes                 Average
              Statea      with laws'      Average       restrictiveness
                                  effective date    of laws in effect
Region              N       N CC)       of first law       in 19852.3

Northeast            11       11   (loo)        1944          614

North Central         12        9   (75)        1976          694

west              15       14   (93)         1968          ,714

South              12        7   (58)        1955          357
Major t&am
producing states*      6        3   60)         1961          2.50

Other southern
states             6        4   (67)         1951          438

`Differences in pl'~dence Of laws among four regions: chi .q-; (3 dfj = 6.67, p = 0.03, difference m
~revdence of law, 6011th vs.. all others: chi square (1 dfJ = 5.66, p = 0.04.
' Includes only States with lavm in effect bee Table 1 for Index of Resttictivenea).
' Difference in restrictiveness. South vs. all others: t = 2.76, p = 0.03.
' North Caroline, South Carolina, Virginia, Kentucky, Tennessee, Georgia.

Local L.egislation
In the 198Os, the momentum of nonsmokers' rights legislation
spread from the State to the local level, spearheaded by actions in
California (Warner et al. 1986). Although not the first local action,
the successful passage of San Francisco's Proposition P in 1983 in
spite of heavily subsidized tobacco industry opposition attracted
widespread publicity and was followed by the passage of comprehen-
sive legislation in a number of other local communities (Doyle 1984).
Many local ordinances extend existing State policies to restau-
rants and worksites. According to a March 1986 survey, 74 Califor-
nia cities and counties have passed smoking ordinances, including 62
requiring no-smoking sections in restaurants and 54 restricting
smoking in retail stores (Americans for Nonsmokers' Rights Founda-
tion 1986). In the survey, 66 of these cities and counties rewire
private employers to have a smoking policy or to identify ncwnoking
areas. As a result, 44 percent of California's population lives in
communities that have enacted workplace smoking ordinances even
though California has no State legislation covering the private
workplace.
According to the Tobacco Institute, by the end of 198% 89 cities
and counties nationwide had restricted smoking in the Viva*
workplace. As stated above, three-fourths of these were in California
(BNA 1986). Workplace smoking ordinances have also been passed in
Cincinnati (Ohio), Kansas City (Missouri), Tucson (Arizona), Aspen

                                         277


(Colorado), San Antonio, Austin, and Fort Worth (Texas), Newton
(Massachusetts), and Suffolk County (New York). In New York City,
a bill to prohibit smoking in all enclosed public places has been
proposed by the mayor (New York Times 7/6/86).

Regulatory Approaches

Administrative agencies have become involved in smoking regula-
tion in two ways: (1) the enforcement of smoking legislation enacted
by State and local government is commonly delegated to a specific
agency, usually the public health department; or (2) an agency may
initiate smoking regulation as part of the activities it has been
authorized to supervise (Feldman et al. 1978). Agency regulations
have been the major mode of regulation at the Federal level, where
smoking by Government employees and by passengers in interstate
transportation vehicles have been addressed. Smoking by State and
local employees has also been addressed by the actions of administra-
tors; e.g., smoking by municipal employees and in public areas of
municipal buildings was banned by a recent mayoral order in New
York City (New York Times 6/26/E%).

Smoking Regulation in Specific Public Places

Public Transportation

Because high concentrations of environmental tobacco smoke can
accumulate inside public transport vehicles, smoking is often
restricted or banned in public transportation. Smoking is likely to be
banned entirely in vehicles where smokers spend relatively little
time (e.g., city buses), and confined to designated areas in situations
where smokers spend several hours (e.g., intercity buses, trains, and
airplanes). Such restrictions are relatively well accepted.

Smoking on interstate transportation vehicles is regulated by
Federal agencies. The Civil Aeronautics Board, under its jurisdiction
to "ensure safe and adequate service, equipment, and facilities,"
initially regulated smoking on airplanes, requiring, since 1972, that
every commercial air flight provide a no-smoking section for all
passengers requesting such seating (Feldman et al. 1978; Walsh and
Gordon 1986). Airline control is currently part of the authority of the
U.S. Department of Transportation. Likewise, the Interstate Com-
merce Commission has restricted smoking on buses and trains to
designated areas since the early 1970s (Feldman et al. 1978; Walsh
1984).
Additionally, States and local governments have regulated smok-
ing in public transportation vehicles. Thirty-one States have enacted
legislation to restrict smoking to designated areas in public transit
vehicles; an additional four (Florida, Georgia, Massachusetts, and

278


Washington) ban smoking entirely on these vehicles (Table 2). Local
ordinances also frequently address public transportation.

Retail Stores

In general, State and local legislation prohibiting smoking in retail
stores is well accepted. Eighteen States currently prohibit smoking
in retail stores (Table 2). Proprietors and their trade associations
have generally supported smoking restrictions out of concern for the
costs of cigarette burns to merchandise and facilities and for the
image presented to customers by employees. Furthermore, their
business is less likely to be affected than, for instance, the restaurant
trade because smoking is not as closely associated with shopping as it
is with eating and drinking.

Restaurants

The average American, who according to National Restaurant
Association (NRA) statistics eats out 3.7 times per week, has the
potential for repeated environmental tobacco smoke (ETS) exposure
(NRA 1986). This is a problem particularly in small restaurants,
where ventilation may not be able to remove smoke and room size
precludes a meaningful separation of smokers and nonsmokers.
Public opinion polls document support for restaurant smoking
restrictions among nonsmokers and smokers. Ninety-one percent of
nonsmokers and 86 percent of smokers responding to a 1983 Gallup
poll favored either restricting or banning restaurant smoking, with
most preferring restriction (Gallup 1983). Similar results were
reported by two regional polls in 1984 (UC SRC 1964, Hollander-
Cohen Associates 1984). Roper polls in 1976 and 1978 demonstrated
the growth in this sentiment during the mid-seventies; the propor-
tion of respondents supporting restrictions grew from 57 percent to
73 percent in 2 years (Roper 1978). Yet little is known about how
restrictions affect decisions to dine out or the choice of restaurant. A
1981 telephone survey of 949 individuals conducted by the NRA
(1982) found that the existence of a no-smoking section was near the
bottom of a list of 13 attributes influencing an individual's choice of
restaurant. On the other hand, 47 percent of 1,038 adults answering
a 1984 Gallup Monthly Report on Eating Out stated that one reason
they did not eat out more was that they were bothered by smoke
(Gallup 1984).

As in other privately owned facilities, smoking regulations in
restaurants have come about through private initiative and public
mandate. Private initiatives have sometimes occurred in anticipa-
tion of a local ordinance, but the number of restaurants that have
voluntarily established no-smoking sections is not known. The

279


Ontario Restaurant and Food Services Association (1985) published a
handbook of guidelines for establishing no-smoking sections.
In 1974, Connecticut became the first State to require restaurants
to have no-smoking sections. By 1980, eight other States also
regulated restaurant smoking. At present, laws in 18 States and an
unknown number of localities regulate smoking in restaurants.
Although a nationwide accounting of local regulations is not
available, data are available for several States (Table 2). Most State
and local ordinances specify (1) the minimum number of seats that
must be included in a no-smoking section, (2) the smallest restaurant
for which rules apply, and (3) the manner in which customers are to
be informed about not-smoking sections. Bars that do not serve meals
are uniformly excluded from restrictions. Most current State legisla-
tion specifies that a minimum of 30 percent of seats be designated as
no-smoking and exempts facilities with fewer than 50 seats. Local
ordinances are generally more restrictive, specifying that a higher
percentage of seats be designated no-smoking and extending cover-
age to smaller establishments. Model ordinances (Hanauer et al.
1986) suggest that a minimum of 50 percent of seats be designated as
no-smoking, require the posting of signs inside and outside the
facility, and specify that owners ask patrons about smoking prefer-
ence rather than respond only to customer requests.
There has been more opposition to smoking restrictions in
restaurants than in other privately owned public places (Hanauer et
al. 1986). Opposition has come primarily from restaurant associa-
tions and centers on three concerns: (1) government intrusion into
business practice, (2) practical problems in coordinating seating of
smokers and nonsmokers, and (3) losing the business of smokers who
chose to leave a facility rather than to dine in a no-smoking section
or wait for an available table in a smoking section. These concerns
assume that the supply of no-smoking tables will exceed demand.
While the proportion of tables allocated by most laws to no-smoking
sections greatly underrepresents the proportion of nonsmokers,
mixed parties of smokers and nonsmokers would have to decide
which section to sit in. Restaurant owners appear to perceive little
customer demand for no-smoking areas, or are unaware of the very
high percentage of smokers and nonsmokers responding to public
opinion polls who support smoking restrictions.
In anecdotal reports, the experience of restaurant owners who
have implemented restrictions is that they are well accepted by
customers and less difficult to implement than expected (Lehman
1984). There is little information on the extent of restaurant
compliance with State and local laws. In Park City, Utah, the
Chamber of Commerce polled its 32 member restaurants, and only
25 percent had complied with State law to set up no-smoking areas
(Park Record 6/13/85). However, a random survey of Minneapolis


restaurants in 1976, 1 year after enactment of the comprehensive
Minnesota Clean Indoor Air Act, found near-total compliance with
the State's smoking regulations (Sandell 1984). In a 1978 Minnesota
survey, 66 percent of nonsmokers and 81 percent of smokers felt that
there were adequate no-smoking areas in that State's restaurants
(Minneapolis Tribune 1978).

Hotels and Motels

Over the past decade, hotel and motel operators have begun to
offer guest rooms in which smoking is prohibited. In some facilities,
no-smoking areas in lobbies and restaurants are also provided.
Hotels are unique among public places in the manner and ease with
which smoking has been addressed. Unlike the situation in restau-
rants, among hotels the no-smoking room policy is uniformly a
private initiative, introduced by management in response to per-
ceived customer demand (Linnell 1986). Hotel and motel rooms are
not covered by State and local regulations and have not been
addressed by nonsmokers' rights advocates.

Designating guestrooms as no-smoking began in the early 1970s in
smaller hotel and motel chains. In the 1980s the concept has spread
to larger chains, including Hyatt Hotels in 1984 and Hilton Hotels in
1986 (Los Angeles Times 1986). According to a 1985 survey of 98
hotel and motel chains, 37 of 41 respondents provided no-smoking
rooms, 23 by chainwide policy. The four respondents who did not
offer no-smoking rooms were considering doing so (Linnell1986). The
percentage of rooms allocated as no-smoking varied from 5 to 30
percent, far less than the prevalence of nonsmokers in the adult
population (70 percent). As a result, demand often exceeds supply,
leading several chains to increase the percentage of no-smoking
rooms (Linnell 1986; Vettel 1986). The only entirely no-smoking
facility is the Non-Smokers Inn, a 134-room motel in Dallas, Texas,
which has been open since 1982 and reports a 96 percent occupancy
rate (Vettel 1986). Although there are anecdotal reports of problems
with compliance, hotels do not have penalties for violators. The
exception is the Non-Smokers Inn, where at check-in guests sign an
agreement to abide by the rule; if the management detects smoking
by occupants, $250 is charged to cover the costs of cleaning.

Whether no-smoking guestrooms offer significant protection from
sidestream smoke exposure is not clear. It is not known whether
nonsmokers are exposed to significant. quantities of ETS by staying
in hotel rooms previously, but not currently, occupied by smokers.
Rooms designated as no-smoking may primarily allow nonsmokers to
avoid stale tobacco odors.
The regulation of smoking in hotels and motels is supported by
public opinion. Fifty to sixty percent of respondents to recent opinion
polls favor restrictions on smoking in hotel rooms, and an additional

281


7 to 18 percent favor outright bans on smoking (Gallup 1983, UC
SRC 1984, Hollander-Cohen Associates 1984). In the 1983 Gallup
poll, 60 percent of nonsmokers and 49 percent of smokers supported
smoking restrictions in hotels, with an additional 15 percent of
smokers and 7 percent of nonsmokers favoring outright smoking
bans.

Hotel management regards such policy as a marketing tool. Cost
savings do not appear to be a motivating force in the trend, in spite
of anecdotal reports of reduced cleaning and maintenance costs in
no-smoking rooms (Linnell 1986). Preparing no-smoking rooms
requires an up-front cost for the thorough cleaning of furnishings
and often the repainting of walls. For instance, Quality Inns
estimated that it spent $138 per room when it allocated 10 percent of
its rooms as no-smoking in 1984 (Vettell986).

Schools

Smoking by students in schools has been the subject of State
legislation, State and local school board regulations, and individual
school policies. Colleges and universities are not discussed in this
section. In 27 States, schools are among the public places where
smoking is restricted to designated areas (Table 2). School board
policies often combine restrictions on tobacco use in schools with
educational programs about the hazards of tobacco use. Smoking by
teachers, for whom school is the workplace, is also regulated by
many school boards.

Smoking has traditionally been regulated in schools for reasons
other than concern about sidestream smoke exposure. The two
rationales have been to comply with State law and to prevent the
initiation of smoking by adolescents. The sale or use of tobacco by
minors is prohibited in 35 States (Breslow 1982). Many of these laws
are rendered ineffective by the availability of cigarettes in vending
machines and by cultural norms that discourage the laws' enforce-
ment (US DHEW 1969). Nonetheless, the laws do provide a legal
incentive for schools to regulate student smoking. The second reason
for restricting smoking in schools is that adolescents are making
decisions about whether to begin smoking and the influence of peers
as well as of adult role models who smoke is recognized to be
important (US DHHS 1980,1982).

Recognition of the health effects of involuntary smoking provides
an additional reason to address smoking in schools and a reason to
expand attention from students to faculty. For teachers and staff,
the school is the worksite, a location with the potential for
substantial ETS exposure (Repace and Lowrey 1985). For students,
school is the site where they spend the most time outside of the
home.


A total prohibition of smoking on school grounds provides the
greatest protection from sidestream smoke exposure and unwanted
role modeling effects. In practice, however, this policy has often
proved difficult to enforce effectively (Rashak et al. 1986). In some
cases it has created major discipline problems and required substan-
tial time and personnel for enforcement. School officials, faced with
the management of other social problems, may not wish to devote
much of their resources to enforcement of a strict smoking ban.
Consequently, many schools have established student smoking areas
inside or outside the school building. Use of these areas often
requires parental permission. Smoking areas for students are not
popular with parents or teachers, according to survey data. Over
three-fourths of 603 adults responding to a 1977 Minnesota poll
opposed allowing school boards to establish smoking areas for
students. Only 13 percent of 1,577 public school teachers responding
to a 1976 nationwide survey thought students should be able to
smoke on school grounds.

The nature and extent of school smoking policies nationwide is not
known. Results of the few statewide surveys vary considerably. A
Connecticut survey reported that 75 percent of the State's public
high schools permitted smoking (Bailey 1983). In contrast, in
Arizona, where State law requires schools to restrict smoking on
school grounds, 92 percent of the State's 169 public and private
secondary schools surveyed had written smoking policies for stu-
dents, and most policies prohibited all tobacco use by students
(Rashak et al. 1986).

Smoking by teachers at schools is generally prohibited in the
classroom, but is often permitted in a lounge where students are not
allowed. Ninety percent of Arizona schools permit smoking in
teachers' lounges, 40 percent in private offices, and 19 percent in
meetings (Rashak et al. 1986). Such policies attempt to avoid
negative role modeling effects; however, they create a double
standard that may be a barrier to student compliance with smoking
bans. There has been little concern for protecting teachers from
involuntary smoke exposure at the worksite. Since smoking is
prohibited in the classroom, their exposure is limited to offices and
lounges.

Health Care Facilities

There are strong reasons for health care facilities to have
particularly stringent restrictions on smoking. Many patients treat-
ed in these facilities suffer from illnesses whose symptoms can be
worsened by acute exposure to tobacco smoke. Hospitals also convey
messages about health to patients and visitors; permitting smoking
on the premises may undermine the messages delivered to many
patients about the importance of not smoking (Kottke et al. 1986).

283


Stringent restrictions on smoking in hospitals have been endorsed by
the American Academy of Pediatrics (1986), the American Medical
Association (19&i), and the American College of Physicians (1986).
Hospital smoking policies have been opposed by some who are
concerned about inconveniencing smokers at times of illness and
stress. Proponents of hospital no-smoking policies, on the other hand,
are concerned about inconveniencing the nonsmoking patient or
visitor at these stressful times.

Public opinion supports smoking restrictions in health care
facilities. In the 1978 Roper survey, 69 percent of respondents
favored a ban on smoking in doctors' and dentists' offices and
waiting rooms (AMA 1984). Of the more than 3,000 individuals
interviewed in hospitals and restaurants, 66 percent favored restric-
ting or banning smoking in these areas (Barr and Lambert 1982).
Over 80 percent of patients and faculty and 68 percent of employees
agreed that "a smoke-free hospital would be an improvement in
patient care" at the University of I Minnesota hospital (Kottke et al.
1986).
Smoking in health care facilities has been addressed through State
and local legislation, Federal regulation, and private initiative. In
most States, hospitals and nursing homes are included among public
places where smoking is restricted to designated areas (Table 2). In
many cases, these legislative efforts have not led to strong protection
of patients from involuntary smoke exposure because patient care
areas may be included among the designated areas where smoking is
permitted. Federally run hospitals have adopted increasingly strin-
gent restrictions on smoking. For instance, Veterans' Administra-
tion hospitals and clinics adopted a new smoking policy in 1986, and
a large number of Indian Health Service hospitals are now entirely
smoke free (OTA 1986; Rhoades and Fairbanks 1985). Health care
facilities run by some States, such as Massachusetts, have also
adopted no-smoking policies (Naimark 1986). In nongovernment
hospitals, most smoking restriction has been the result of private
initiative, often spearheaded by the medical staff. Much of this
action has taken place in the 1980s.

Hospital smoking policies can be complex. Within a single
institution, smoking may be handled differently in inpatient, outpa-
tient, and administrative areas. Patients, visitors, and employees
may be subject to different sets of restrictions. Consequently,
smoking policies vary widely among hospitals (Ernster and Wilner
1985). The least stringent policy prohibits smoking only where it is a
safety hazard, such as near oxygen, and may permit the sale of
cigarettes on the premises. Mild policies often assign patients to beds
by smoking status, prohibit staff from smoking in patient care areas,
and provide areas in cafeterias and waiting rooms for nonsmokers.
Moderately stringent policies prohibit smoking in shared patient

284


rooms or in all patient rooms. Some hospitals permit patients to
smoke with a doctor's written order. The most stringent policies,- the
so-called smoke-free hospitals, prohibit smoking throughout the
facility or limit smoking to a single room away from patient care
areas (Kottke et al. 1986). Enforcement of a smoking policy is usually
the responsibility of the nursing staff. Guidelines for implementing
hospital smoking policies have been formulated (Kottke et al. 1986;
Emster and Wilner 1985; AHA 1982).

In spite of anecdotal reports of the adoption of stringent smoking
policies in individual hospitals (Andrews 19831, survey data indicate
that smoking is still widely permitted in patient care areas. A survey
of 360 randomly selected U.S. hospitals published in 1979 found few
restrictions on smoking; fewer than half elicited the patients'
smoking preference on admission or had nosmoking areas in
cafeterias, waiting rczms, or lobbies, and smoking was permitted on
76 percent of the wards (Kelly and Cohen 1979). A 1981 survey of
1,168 community hospitals (Jones 1981) documented some change in
policy prevalence. More than 90 percent of the hospitals had a
written smoking policy, which restricted smoking to designated
areas in 97 percent of cases. Over 85 percent of the hospitals offered
no-smoking patient rooms, subject to availability (Jones 1981). A
recent survey of 185 hospital administrators in Georgia reported
that 70 percent continue to allow smoking in patient rooms,
although only 6 percent permit it at nurses' stations (Berman et al.
1985). The proportion of hospitals allowing cigarette sales on the
premises has declined from 56 to 58 percent in the late seventies
(Kelly and Cohen 1979; Seffrin et al. 1978) to less than 30 percent in
the eighties (Em&x and Wilner 1985; Jones 1981; Berman et al.
1985; Bert&en and Stolberg 1981). While there are little data on the
prevalence of smoking policies in private physicians' offices, guide-
lines for physicians wanting to provide assistance in smoking
cessation are well developed (Lichtenstein and Danaher 1978;
Shipley and Orleans 1982; US DHHS 1984).

Current Status of Smoking Regulations in the Workplace

Policies regulating smoking at the workplace for the protection of
employees' health are a trend of the 1980s. As of 1986, smoking is
restricted or banned in 35 to 40 percent of private sector businesses
(HBPC 1985; BNA 1986; US DHHS 1986) and in an increasing
number of Federal, State, and local government offices (OTA 1986).
Private sector workplace smoking is regulated by law in 9 States and
over 70 communities (OTA 1986; US DHHS 1985b; ASH 1986).
Actions to restrict or ban smoking at the workplace are supported by
a large majority of both smokers and nonsmokers (Gallup 1985).


The workplace has become the focus of particular attention as
evidence about the health hazards of involuntary smoking has
accumulated. Urban adults spend more time at work than at any
other location except home (Repace and Lowrey 1985). For adults
living in a household where no one smokes (Ha+ 19851, the
workplace is the greatest source of FTS exposure. Consequently, an
individual's workplace FTS exposure can be substantial in duration
and intensity. This is of particular concern for individuals also
exposed to industrial toxins whose effects may be synergistic with
tobacco smoke (US DHHS 19854. Furthermore, individuals have less
choice about their ETS exposure at work than they do in other
places, such as restaurants or auditoriums.
The nonsmoker's right to clean air on the job has been supported
by common law precedent (US DHHS 1985a; Walsh and Gordon
1986). Assuring clean air at work has received the growing attention
of policymakers and nonsmokers' rights advocates. The worksite has
also received attention because of its naturally occurring interper-
sonal networks and intrinsic social norms. Behavioral scientists have
attempted to take advantage of the social milieu of the workplace to
increase the success of smoking cessation programs (US DHHS
198%). Smoking policies have the potential to alter worksite norms
about smoking and thereby to contribute to reductions in employee
smoking rates or the prevention of smoking onset. A substantial
fraction of blue-collar workers who smoke report the initiation of
smoking at ages coincident with their entry into the workforce (US
DHHS 1985c).

Smoking Policies

Legislation mandating smoking policies in the private sector
workplace has been more controversial and less widespread than
legislation covering public places. Because a worker's behavior off
the job has traditionally been viewed as beyond the employer's
legitimate concern, private employers have been reluctant to impose
rules on behavior not directly related to employment (Walsh 1984;
Fielding 1986). The concept of workplace smoking restriction has
become more acceptable to employers and legislators as the hazards
of involuntary smoking have become better known and as public
attitudes about smoking have shifted. The rationale for policies has
been reframed as guaranteeing an employee's right to a healthy
work environment.

Prevalence of Smoking Policies

Notwithstanding the recent attention, regulating smoking at work
is not a new idea. There is a long and noncontroversial tradition of
smoking restrictions to insure the safety of the worker, workplace,
and product (OTA 1986). Employers have restricted smoking to

286


prevent fires or explosions around flammable materials or to prevent
product contamination. The policies were supported by State legisla-
tion dating back to 1892, when Vermont authorized employers to
ban smoking in factories so long as a sign was posted (Warner 1982;
US DHHS 198513). New York, Nevada, and West Virginia had
enacted similar legislation by 1921, and in 1924 Massachusetts
banned smoking in stables because of the fire hazard (US DHHS
1985b).
Smoking restrictions remained uncommon throughout the 1960s.
During the 1970s workplace smoking regulations were included in
the comprehensive clean indoor air legislation being proposed at the
State level. In 1975, Minnesota became the first State to enact
regulations for private work&es for the purpose of protecting
employee health. Since then, eight other States have passed laws
covering private sector workplace smoking (T&Agency Tobacco Free
Project 1986; 0T.A 1986; ASH 1986; US DHHS 1985b). Fifteen
percent of the U.S. population lives in these nine States. The scope of
this legislative effort widened in the 1980s to include local govern-
ment. It has been strongest in California, where ordinances in 66
communities cover 44 percent of the State's population (Americans
for Nonsmokers' Rights Foundation 1986).

In spite of this legislative activity, surveys of employers through
the 1970s reveal that worksite smoking regulations remained limited
overall (Table 4). Those in place applied primarily to blue-collar
areas and were motivated by safety concerns (NICSH 198Oa,b,
Bennett and Levy 1980). Policies were more common in industries
with product safety concerns (food, pharmaceuticals) or explosion
hazards (chemicals) (HRPC 1985). Safety was the prime reason for
smoking policies in a survey of 128 large Massachusetts employers in
1978-1979. The potential for an adverse impact on clients, especially
in service industries, was also cited (Bennett and Levy 1980).
Concerns about the impact of smoking on the health of employees or
costs to employers-the focus of the current workplace smoking
action-were not mentioned. Fewer than 1 percent of 855 employers
answering a nationwide survey in 1979 had calculated the costs of
employee smoking (NICSH 1980a,b).

Five surveys of employers conducted between 1977 and 1980
document the situation just prior to the proliferation of workplace
smoking policies. Estimates of the prevalence of smoking policies
ranged from 14 to 64 percent, reflecting differences in types of
businesses sampled and response rates (Table 4). A survey conducted
by the National Interagency Council on Smoking and Health in 1979
had the largest sample size and the only random sample, but had a
low response rate (29 percent) (NICSH 198Oa). Their estimate of a 50
percent prevalence of smoking policies is probably biased upward by
the likelihood that companies with policies were more likely to

287


TABLE I.-Surveys of worksite smoking policies

Survey name    Survey
(pub. date)      year

Number

Business surveyed

Workforce size

Location

Sampling
method

    Interview

Method    who?

               Worksite Incentives
          Restrict   cessation    for
Response rate  smoking  program nonsmoking
  N (%)      (%I      6)     (%)

Dartnell's       1977     250        Large       U.S. and       ?          office            ?        30      11      3
Business (1980)                              Canada                  administrators

Bennett and     197c79    128        Large       Mass.     All Mass.      Mail              88 e+)        64      12
Levy (1980)                     (>lom             business with
                                         >1m
                                  employees

National Inter-    1979    3ooo   Three strata of 1CCO    U.S.    Random sample Mail Top level     855 (29); same     50      15      1

agency Council             small 65@499), medium        stratified by     and  management    for each strata
on Smoking              GCO-22003, large              size       phone and health
and Health             (Fortune Double 500)                          OfGalS
(1980)

Dartnell's       1980     325        Large      U.S.          ?          Administrative       ?        23       9      3
Business (1980)                                                     managers

Administrative    1980     500            ?       US. and  Nonrandom;    Mail Members of    302 60)        14
Management                                Canada   representatives       AMS
Society (Thomas                                   of AMS
19801                                    chapters

Human

1984-85

1100  Larae: l!&une loo0 and U.S.     All members of  Mail CEO or VP for   445 (40)        32      43     8.5

ResolWCM
Policy Corp.
(1985)

hi 100 fastest g-rowing
companies

two selected
Brow

Human
Beaourm


TABLE 4.-C%ntinued

Survey name    SUI-WY
(pub. date)      yeat

NUIdXT

Business surveyed

Workforce size

Location

Sampling
method

    Interview

Method    Who?

               Worksite Incentives
          Restrict   cessation   for
Response rate  smoking  program nonsmoking
  N (%)      (%I     (%I     (%)

U.S. Depart-
ment of Health
and Human
Services (19@4?

1965

1600   Two strata: small (5G   U.S.    Random sample Phone            1358 (65)        36      19
   99). medium-large ( > 100)       stratified by
                        size, location,
                       and industry
                          type

Bureau of
National
Affairs, Inc.
(1966)

1966

1967  Predominantly small-    U.S.     Random      Mail Personnel      662 (34)        36      41      4
    medium 60%-c 1000         sample, selected      executives
                     group: Am. Sot.
                           Pers. Admin.
                          members

Petersen and
M2WkWlgill
( 1966)

1966

1100  Predominantly small-    U.S..          ?      Mail       ?      577 (53)        56      50     5
   medium: 62% - (500;   Canada,
    16% _ 500-loo0, 22% _   and
    >1090             Puerto
                    Rico


TABLE rl.-Continued

Correlates of having a smoking policy

Survey name
(pub. date)

Workplace
sire

Location

Business type

Other

Type of smoking policy                   Duration
(B = ban. R = restrict    Remon for policy   of policy    Comments

Dartnell's                                                                 42% ~5
Business (1960)                                                                           year-

~PlOysss
railed
smoking imue
in 25%

Bennett and
Levy w60)

No

No

No

No

Protect product&
equipment (91%).
worker safety
(3721, customer
contact (17%).
worker health
(0%)

ciearettes
cold on
premises of
95%

National Inter- Large >small
agency Council (54% v* 46%)
on Smoking and
Health (1960)

Blueeollar >   Bluecollar areas 42%R/26%B,   (<I% cnlculate    64% adopted Management-
white-collar   white-collar areas 15%R/ll%B,   costs due to      since 1964    initiated
WWS       cafeterias 19%R12%B,       smoking               policies with
        conference rooms 6%R/7%B.                          rare union
         medical facilities 15%R/25%B                     role; 54%
                                         with policies
                                           bpoee
                                         penalties


TABLE 4.-Continued

Correlates of having a smoking policy

Survey name
(pub. date)

Workplace
sire

Location

Business type

Other

Type of smoking policy
(B = ban, R = restrict

Reason for policy

Duration
of policy

Comments

Dartnell's
Business (1980)

18% R to designated areas
(usually open offices and public
contact areas), 8% R in
cafeterias, 5% limit smoking to
breaks

69% <5
Y-m

Employees
rllid
smoking imue
in 3096.5%
more than in
1977 survey

Administrative
Management
Society (1980)

OfCce areBB 12%R/2%B
B: reception areas (46%).
security areas (35%). open
off&a (27%). hallways (16%),
conference rooms (8%)

Whitecollar

area survey
only; 37%
without policy
had employee
comdaints


TABLE I.-Continued

Correlates of having a smoking policy

Survey name    Workplace
(pub. date)        size

Location

Businees type

Other

Type of smoking Policy
(B = ban, R = restrict

Reason for policy

Duration
of policy

Comments

Human
Resource-6 Policy
Corp. (1985)

west. 45%. >50%:       Locded
NE - 36%,   insurance,      where
NC - 28%.   pharmaceuticals, workplace
South _ 22% finance,      smoking law
       publishing;     in effect
       < 29%: mining,
       consumer goods

3% B while working or on
premises. 35% B by some
employees, 5% do not hire
smokers

Safety G!5%).
health (2O%),
comply with laws
(16%). employee
preference (16%)
nave money (3%,),
increase
productivity (2%)
Reamns r-eject
Policy:
unacceptable to
employees,
employees settle
own problem,
implementation
too difftcult

51% <5
Y-

Spmmred by
Tobacco
Institute;
management
initiated
policies; 70%
encourage
employees to
settle own
diSpWS

U.S. Bepart-   Large >small           Services >     Not unionized                  Comply with regs         Data andysiLT
ment of Health                 other industry   or bluecollar                   (39%). protect             still in
and Human                    types         %                         nonsmokers (39%),            Prognss
services (1986)                                                   protect equipment
                                                          (14%), pmtect
                                                        high ri&
                                                          employees (8%)


TABLE 4.-Chntinued

Correlates of having a smoking policy

Survey name    Workplace
(pub. date)        aim

Location

Businees type

Other

Type of smoking policy
(B = ban, R = restrict

Reason for policy

Duration
of policy

Commer la

Bureau of
National
Affairs, Inc.
(1986)

Large >small   West 52%.  Nonbusiness or Located     Open work areas 19%R/41%B;  Comply with laws   85% <5    2%toadopt
(45% v8 33%)   EN - 42%.   nonmanufacturing where      halls, conference rooms.     (28%). employee   years 85%;   policy in
         NC - 29%,   > manufacturing workplace    restrooms, customer areas 56%-  health, comfort     10% before   1986; 21%
          South . 28%          smoking law   643%B, cafeteriaa 58% partial   (22%), employee    1992      considering
                              in effect     B; total worksite 2%8; 1% hire  complaints (21%),          policy; 23%
                               only nonsmokers, 5% prefer    mandate by             penalties set;
                                      nonsmokers           president (3%)              32%
                                                                  procedures to
                                                                           resolve
                                                                  di.%P"t4%

Petersen and
Mawngill
(1986)

only 33% of
smallest ( < 50
employees) have
policy

Health care     Located     Designated areas only 38%,    Employee pressure 43% ~3     6% made
(93%), retailing   where      client-contact area 13%B, l%B  (21%), comply    ye**, 53%    structural
(83%). finance   workplace    entirely, 2% hire only       with laws (19%).   <6 years    changes; 2790
(61%),      smoking law   nonsmokers            protect employee             use barriers
manufacturing   in effect                      health (19%).               or air
(57%),                                    reduce insurance          purifiers; 45%
transportation                                 Costa (9%)              discipline
GO%), service                                                        violators
(49%),
insurance (18%)


respond. An even higher prevalence of smoking policies (64 percent)
reported in a `survey of large Massachusetts businesses may reflect
similar biases or regional variation or both. Smoking policies were
reported in only 14 percent of white-collar offices in a nonrandom
survey (Thomas 1980) and in 23 to 30 percent of large corporations
responding to two nonrandom surveys by the same group (Petersen
and Massengilll986).

These surveys found that smoking restrictions were moderate,
worksite smoking cessation programs uncommon (9 to 15 percent),
and incentives for nonsmoking rare (< 3 percent). Outright smoking
bans and preferential employment of nonsmokers were not men-
tioned. However, employee complaints about smoking were reported
by one-third of the businesses in two surveys (Petersen and Massen-
gill 1986; Thomas 1980), suggesting a growing pressure on employers
for change. Smoking policies were stricter for bluecollar workers
and larger worksites (NICSH 1980b; Bennett and Levy 1980).

A second set of business surveys, conducted only 5 years later
(1984-1986), shows a different picture (Table 4). Three large surveys,
two based on random samples, reported a remarkably similar
prevalence of workplace smoking restrictions, ranging from 32 to 38
percent (HRPC 1985; US DHHS 1986; BNA 1986). A fourth study
reported that 56 percent of small and medium sixed businesses had
smoking policies, but only 38 percent of businesses restricted
smoking to designated areas (Petersen and Masaengilll986).

Because of uncertainty in the earlier (1977-1980) estimates, it is
difficult to conclude that the most recent estimates of policy
prevalence represent an increase. However, there is suggestive
evidence on this point: half or more of policies reported in the 1984-
1986 surveys were adopted within 5 years, indicating that the
policies are largely products of the 1980s; a sizable number of
companies without policies are considering them; in addition to the
36 percent of companies reporting policies in one 1986 report, 2
percent were planning to implement a smoking policy in 1986 and
another 21 percent were considering adopting a policy (BNA 1986).
Finally, companies that adopt policies rarely reverse them: in the
BNA 1986 survey, only 1 percent of companies without policies had
ever had one and rescinded it. These data support a contention that
workplace smoking policies are a growing trend.

The nature and scope of smoking restrictions also changed during
the 1980s. The most common policy still restricted smoking to
designated areas, but those areas appeared to be shrinking. Despite
several well-publicized examples (Pacific Northwest Bell, Group
Health Cooperative of Puget Sound), total workplace smoking bans
were still rare (1 to 3 percent). An even more stringent smoking
policy now being adopted, giving preference to nonsmokers in hiring
or refusing to hire smokers, was not even considered less than a

294


decade before (BNA 1986, HRPC 1965; Petersen and Massengill
1966). Fewer than 5 percent of businesses have curr&tly adopted
such a policy. Workplace smoking cessation programs were more
common, but incentives for nonsmoking remained rare.

The 1964-1966 surveys suggest that the diffusion of workplace
smoking policies throughout the private sector is occurring in a
nonuniform fashion. Companies with policies differ from those
without policies in workforce size, geographic location, and type of
industry. Smoking policies are slightly more prevalent in large
companies than in small businesses (45 versus 33 percent) (Petersen
and Massengill 1966; BNA 1966). Policies also differ by company
location, being more common in the West and Northeast than in the
North Central region or the South (BNA 1986, HRPC 1935). This
geographic disparity is similar to the pattern of State smoking
legislation, and may in part be explained by it. Businesses in States
with workplace smoking laws are more likely to have adopted
smoking policies than are companies located elsewhere (HRPC 1965;
BNA 1966). Industries are adopting smoking policies at different
rates, with more policies and more recent policies in nonmanufactur-
ing industries (finance, insurance, health care, pharmaceuticals)
(HRPC 1965; Petersen and Massengill 1986; BNA 1996). This
represents a shift from the earlier blue-collar predominance of
smoking restrictions and reflects the change in policy orientation
from workplace safety to employee health.
Two factors may explain the growth of workplace smoking policies
in the 1960s. Recently enacted State and local workplace smoking
legislation is one factor influencing the private sector. Legal
mandates are cited as a major reason for adopting policies, and as
noted above, the prevalence of private sector smoking policies is
higher in regions with legislation in place. Laws may encourage
more rapid private action by putting smoking on the corporate
agenda. A second factor is public support. Support for an employer's
right to restrict smoking to a designated area at work grew from 52
percent to 61 percent during the 1970s (Roper 1978) and continued to
increase in the 1980s (Gallup 1983,1985). In 1985,79 percent of U.S.
adults, including 76 percent of smokers, favored restricting smoking
at work to designated areas. Only 8 percent favored a total
workplace smoking ban (Gallup 1935). These attitudes may also be
manifest as employee pressures to restrict smoking (Petersen and
Massengill1986; BNA 1966; HRPC 1965).

Reasons for Adopting Smoking Policies

It is not always easy to identify the motivations and goals for a
specific workplace policy (OTA 1966). Explicit reasons for imple-
menting policies, according to the most recent employer surveys, are
(1) to protect the health of the employ ee-especially the nonsmok-


er-and assure a safe working environment, (2) to comply with State
and local statutes mandating worksite smoking policies, and (3) to
anticipate or handle demands from nonsmoking employees for a
smoke-free working environment. Other reasons may be the fear of
possible legal liability for illnesses caused by sidestream smoke
exposure in the workplace (Fielding 1982; Walsh 1984). an opportuni-
ty to symbolize a company's concern for employee welfare (Walsh
1984; Eriksen, in press), as part of a general health promotion and
wellness program, and the goal of saving the company money.

Although it is generally agreed that employees who smoke cost
their employers more than do nonsmoking employees, there is as yet
little evidence that implementing policies will reduce the extra
smoking-related costs (OTA 1986; Fielding 1986; Eriksen, in press).
Corporations are keenly interested in stemming the rapid rise in
health insurance costs, but may not see smoking policies as a means
to that end. The top management at Xerox, for example, rejected a
proposed smoking policy because of concerns about the potentially
adverse economic impact of excess smoking breaks on productivity
(Walsh 1984). Actually, economic considerations do not appear to be
a major reason why businesses adopt smoking policies, according to
three recent surveys (HRPC 1985; BNA 1986; Petersen and Massen-
gill 1986).

Barriers to Adopting Smoking Policies

Roth survey data and case reports give insights into reasons why
employers have elected not to implement worksite smoking policies.
According to a Tobacco Institute-sponsored survey, the 24 percent of
large employers who had considered and rejected a smoking policy
gave these reasons: policy not acceptable to employees (59 percent),
employees can handle the problem on their own (58 percent),
implementation too difficult (39 percent) or too costly (5 percent),
policy not acceptable to clients (10 percent), and no employee
complaints about smoking (29 percent) (HRPC 1985).

Fear of worker discontent or union opposition is the major reason
cited by employers who have considered and rejected a workplace
smoking policy. Surveys consistently indicate that smoking policies
are initiated by management, and are often adopted with little or no
employee or union input (HRPC! 1985; BNA 1986; NICSH 198Oa,b).
Although most businesses that have surveyed their employees have
found strong support for smoking restrictions (Pacific Telephone
1983; Robert Finnigan Associates 1985; Addison 1984; Ziady 1986;
Marvit et al. 1980), some unions have actively opposed employer-
mandated policies, both in individual cases and at the national level.
In 1986 the AFL-CIO Executive Council stated its opposition to
unilateral policies and called for the case-by-case handling of
workplace disputes between smokers and nonsmokers (BNA 1986).

296


Roth employee organizations and employers find it difficult to
simultaneously balance the wishes of all their constituents.

Another reason for reluctance to adopt smoking policies is concern
about implementation (HRPC 1985). In some cases, this means
concerns about how to enforce the policy (BNA 1986) or whether it is
enforceable (Eriksen, in press). Other reasons cited by companies
were questions about the legality of limiting employee smoking
(BNA 1986) and the nonsupport of top management who are smokers
(BNA 1986). Some companies are dependent on business relation-
ships with tobacco companies and businesses with tobacco-related
interests, which they do not want to jeopardize (Kristein 1984; Walsh
1984).

Types of Smoking Policies

Private sector businesses have addressed the issue of employee
smoking in a variety of ways. In addition to smoking policies, the
umbrella concept of "worksite smoking control" can include educa-
tional campaigns to motivate workers to quit, self-help and organized
smoking treatment programs, medical advice, and incentives to
encourage nonsmoking (Orleans and Shipley 1982; Windsor and
Bartlett 1984). Smoking programs are sometimes subsumed as part
of broader corporate wellness programs. Worksite smoking cessation
programs were reviewed in the 1985 Report on the Health Conse-
quences of Smoking (US DHHS 1985c).

Businesses have taken a variety of approaches to a worksite
smoking policy. The chClces reflect the individual company's motive
in adopting a policy and assessment of the potential for implementa-
tion and enforcement. When protection from fire or explosion was
the primary motive, policies primarily applied to blue-collar areas;
when the goal was to avoid antagonizing customers, smoking bans
applied only to client-contact areas (Bennett and Levy 1980). A
company's solution also reflects its particular social environment.
Recent study indicates considerable variability among individual
worksites in attitudes and norms about smoking cessation (Sorensen
et al. 1986).

Because smoke travels, the desires of smokers and nonsmokers
will inevitably come into conflict in common areas, and it is difficult
to simultaneously maximize the goals of smoke-free air, minimum
employee disruption, and minimum cost. A business adopting a
policy primarily to avoid employee conflicts is likely to pay greater
heed to smokers' wishes at the expense of smoke-free air, and may
consider solving the problem with increased ventilation (to avoid the
necessity of behavioral change) or may separate smokers and
nonsmokers. A business whose primary goal is to reduce involuntary
smoking hazards will be more willing to sacrifice smokers' conve-
nience and may consider a total smoking ban. A business that aims

297


to reduce costs may choose a minimum of structural changes and a
maximum likelihood that the policy will result in employee smoking
cessation; a total ban on workplace smoking or the hiring of only
nonsmokers would be more likely to achieve these goals. Altemative-
ly, adopting no policy may also be ineqxmiue, so long as there are no
employee conflicts over smoking.
The myriad of current smoking policies have been categorized in
several ways (US DHHS 1985a; BNA 1986; OTA 1986, ALA 1985a,b).
The range, in ascending order of protection for the nonsmoker,
includes these:

(1) No explicit policy (the "individual solution" approach)
(2) Environmental alterations (separating smokers with physical
  barriers, using air filters, or altering ventilation)
(3) Restricting employee smoking, a range with these extremes:
  (a) smoking permitted except in designated no-smoking areas
  (b) smoking prohibited except in designated areas
(4) Banning employee smoking at the worksite
(5) Preferential hiring of nonsmokers.
Options (1) through (3a) effectively state that smoking at work is
acceptable behavior; options (3b) through (5) indicate to employees
that nonsmoking is the company norm. Several groups have
developed model policies of varying degrees of comprehensiveness to
assist employers (ALA 1985a,b; GASP 1985; BNA 1986; Hanauer et
al. 1986).

The "individual Solution" Approach

According to surveys, having no explicit policy is still the most
prevalent approach to smoking in the workplace (HRPC 1985; BNA
1986; US DHHS 1986). Smokers and nonsmokers work out differ-
ences on their own, using so-called common courtesy or finding an
individual solution. According to a 1984 Tobacco Institute-sponsored
survey, `70 percent of large employers encourage employees to work
out differences on their own (HRPC 1985). When there is no explicit
policy, there is the implicit message that environmental tobacco
smoke does not represent a hazard. So long as there are few disputes
and they are easily settled, this approach is expedient. However, it is
not likely to be a successful long-term policy. Nonsmokers in the late
1970s may have been reticent to assert their rights and perceived a
burden of confrontation (Roper 1978; Shor and Williams 1978), but
there is a growing consensus, even among smokers, that supports
abstention in the presence of nonsmokers and smoking restrictions
at worksites (Gallup 1983,1985).

298


Environmental Alterations

Environmental alterations range from simply separating smokers
and nonsmokers to different areas of a room to installing improved
ventilation systems to remove environmental tobacco smoke. The
advantage of this approach is that it requires no behavioral change
of smokers and satisfies some of the wishes of nonsmokers. However,
because tobacco smoke easily diffuses beyond physical boundaries,
simple barriers provide at best a slight reduction in involuntary
smoke exposure (see chapters 3 and 4) (Olshansky 1982). More
sophisticated ventilation systems can be prohibitively expensive, and
even the best may not be able to clean the air adequately (Bepace
and Lowrey 1985; Lefcoe et al. 1983). Workplace modification has
sometimes been utilized as a company's first step in the development
of a more restrictive policy, as happened at the Control Data
Corporation in Minneapolis (OTA 1986).

Restrictions on Employee Smoking

The most common workplace smoking policy is to restrict where
employees may smoke (BNA 1986). This policy has broad public
support; in a 1985 Gallup poll it was the approach favored by 79
percent of U.S. adults, including 76 percent of smokers (Gallup 1985).
Policies differ in (1) the proportion of the workplace in which
smoking is permitted, (2) whether the default condition is smoking,
nonsmoking, or unspecified, (3) who has the authority to designate
the smoking status of an area, and (4) whose wishes prevail when
smokers and nonsmokers disagree. Policies often categorize the
worksite into four areas that are subject to different rules: (1) private
offices, (2) shared offices or work areas, (3) small common use areas
(elevators, bathrooms), and (4) large common use areas (conference
and meeting rooms, auditoriums, cafeterias).

The least restrictive policies permit smoking except in designated
no-smoking areas, indicating that smoking is the company norm.
Who has the authority to designate an area's smoking status and
whether smokers' or nonsmokers' wishes prevail may not be explicit.
The usual pattern is for common use areas to be designated either
totally no-smoking (elevators, bathrooms, conference rooms) or
partly no-smoking (cafeterias, auditoriums). Private offices are left to
the discretion of the occupant, who is often given the authority to
declare it no-smoking. In shared office areas, where the wishes of
smokers and nonsmokers may conflict, each individual may be given
the authority to designate his or her own immediate work area, or
the policy may stipulate that a compromise be reached. However,
this cannot ensure that an employee's self-designated no-smoking
area is free of side&ream smoke. Because the majority of an
employee's time is spent in the immediate work area rather than in


the no-smoking common use areas, a policy that does not specify no-
smoking in shared work areas may not substantially reduce an
employee's environmental tobacco smoke exposure. However, these
policies may satisfy some nonsmokers' wishes with minimal disrup
tion to smokers. In some cases, companies seeking to limit smoking
have adopted this type of policy as a first step to more stringent
restrictions or a total ban (e.g., Boeing, cited in OTA 1986).

The most restrictive policies specify that "smoking is prohibited
except in designated areas," establishing nonsmoking as the work-
place norm. In the strictest policies, smoking is prohibited in shared
work areas (unless all occupants agree to designate an area
"smoking permitted") and in most common use areas. Policies may
limit the areas that can be designated "smoking permitted" and
predetermine that the wishes of nonsmokers prevail when conflict
occurs. Even stricter regulations stipulate not only the location in
which but also the time when smoking is allowed (e.g., work breaks
only). So long as the smoking areas do not contaminate the air of
work areas, these policies provide greater protection of employees
from sidestream smoke at the cost of greater inconvenience to
smokers, who may perceive the restrictions as coercive. The produc-
tivity of smokers may suffer if they are permitted to take extra
smoking breaks or if smoking areas are ~uraI%d too far from the work
station.

The variability of smoking restrictions in common work areas was
demonstrated in a 1985 survey conducted by the Bureau of National
Affairs, Inc. (BNA). Of the 239 companies with smoking policies, 41
percent banned smoking in open work areas, and an additional 20
percent banned it if employees or supervisors wished. Only 8 percent
permitted smoking in all open work areas, and 19 percent divided
areas into smoking and no-smoking sections. There was more
uniformity in treatment of common use areas. Over 50 percent of the
companies banned smoking in hallways, conference rooms, rest-
rooms, and customer contact areas, and smoking was partially
banned in 58 percent of cafeterias (BNA 1986).

In contrast to shared work areas, smoking was permitted in 56
percent of the private offices in that survey, with occupants often
given the authority to designate the office as smoking or no-smoking.
This has the potential for charges of unequal treatment and
problems with employee morale (BNA 1986).

Banning Smoking at the Workplace

Some businesses-including large corporations, among them Pacif-
ic Northwest Bell and the Group Health Cooperative of Seattle-
have recently opted for total bans on smoking at work (US DHHS
1985a; Ziady 1986). Bans may be preceded over several years by
progressively stricter smoking regulations. Notwithstanding these

300


well-publicized successful examples, smoking bans are rare and not
widely supported by public opinion. Only 6 percent of companies
with smoking policies (2 percent of all respondents) in a 1986 survey
totally banned smoking (BNA 1986). Only 12 percent of adults (4
percent of smokers) agreed that "companies should totally ban
smoking at work" in a 1985 Gallup poll. In spite of this hesitancy,
smoking bans are gaining momentum among large employers such
as Boeing, who recently announced an upcoming ban that will cover
its 90,000 employees (Iglehart 1986).

Smoking bans provide the maximum protection for nonsmokers, at
the cost of greater inconvenience for smokers. They send a clear
message that nonsmoking is the company norm. They can reduce
ventilation needs and maintenance costs due to smoking, but pose
potential problems with enforcement and loss of employees who
smoke. Thus, how a ban is planned, prefaced and introduced, and
implemented and enforced is very important. Through a concern for
employee well-being, assistance for smokers who wish to quit should
be implemented along with bans (Orleans and Pinney 1984).

Preferential Hiring of Nonsmokers

The most restrictive workplace smoking policy, preferential hiring
of nonsmokers, was not even discussed several years ago. Explicit
policies favoring nonsmokers are still uncommon. According to the
1986 report of the Bureau of National Affairs, Inc., 1 percent of
businesses hire only nonsmokers, 5 percent give nonsmokers prefer-
ence, and 10 percent permit supervisors to exercise a nonsmoking
preference (BNA 1986). The majority either have no policy (43
percent) or do not permit such a preference (39 percent). On the
other hand, data from small surveys indicate that personnel
managers, the majority of whom are themselves nonsmokers, may
preferentially hire nonsmokers (Weis 1981; Iglehart 1986). In a
unionized setting, selective hiring of nonsmokers may need to be the
subject of collective bargaining (Eriksen, in press).

Hiring only nonsmokers ensures a smoke-free work environment
without conflicts over smoking and makes it clear that nonsmoking
is the company norm. Since the nonsmoking workforce should be
healthier, lower health insurance premiums may also result. On the
other hand, such a policy limits the potential pool of new employees,
raises the issue of what to do about currently employed smokers, and
may present problems with verification of smoking status. Employ-
ers may be reluctant to adopt a policy in which off-the-job activity is
a condition of employment (Walsh 1984).

Assuring compliance with workplace smoking policies is complex.
Model policies usually include three enforcement provisions: (1)
identifying who is responsible for policy enforcement, (2) designating
penalties for noncompliance, and (3) ensuring the protection of an

301


employee bringing a complaint. These provisions are often not
included in practice. Only 23 percent of the policies stipulated
penalties for noncompliance and only 32 percent specified proce-
dures for resolving disputes in the 1986 BNA survey. Approximately
half of the policies outlined in two other business surveys had
provisions for disciplining violators (Petersen and Massengih 1986;
NICSH 198Oa,b).

Implementation of Smoking Policies

Worksites that have adopted smoking policies have differed in the
ease with which policy was implemented. To aid employers, the
American Lung Association and the Office of Disease Prevention and
Health Promotion of the U.S. Department of Health and Human
Services have developed guides with specific recommendations on
how to adopt and implement worksite smoking policies (ALA 1985b;
US DHHS 1985a). These are based on the experience of companies
and can be extremely helpful even though they are not based on
research.

The experiences of 12 corporations that considered smoking
policies are described in a report of the Bureau of National Affairs,
Inc. (1986). Case reports are also included in the guide from the
Office of Disease Prevention and Health Promotion (US DHHS
1985a). According to these case reports, strong support from top
management and having an advisory committee composed of a wide
variety of employees (including both smokers and nonsmokers,
managers, and employee representatives) are common to successful
policies. Surveys of employees can assess distress caused by involun-
tary smoking and support for policy changes. As a rule, such surveys
have generally documented widespread support for smoking restric-
tions from employees, the majority of whom are nonsmokers.

Another correlate of success is 1 well thought out and clearly
articulated communication of the policy. A written document should
give the rationale for the policy implementation, specify where
smoking will be allowed or prohibited, and define responsibility and
procedures for policy enforcement and penalties for violation.
Successful policies avoid criticizing smokers or setting up an
antagonistic situation between smokers and nonsmokers. They make
it clear that the company is not requiring that employees quit
smoking and will help smokers in adjusting to the new regulations.
Giving smokers advance notice of the policy and providing help for
those who want to quit smoking can help gain their support.

Careful plans for implementation are recommended. Allowing
several months between the announcement of the policy and its
effective date gives smokers time to prepare for the change and to
attend smoking cessation programs if they wish to quit. This also
provides time for the posting of adequate numbers of signs and for

302


`making any structural alterations that may be necessary. After
policy implementation, an advisory committee should monitor its
effectiveness and enforcement. A followup survey is helpful to
determine what, if any, adjustments need to be made.

Impact of Policies Restricting Smoking in Public Places and in
the Workplace

Policies that regulate where smoking is permitted may have a
number of direct and indirect effects. In the short term, a policy that
is adequately implemented and enforced will alter the behavior of
smokers in areas where smoking is prohibited and should result in a
reduced concentration of tobacco smoke in that area. Beyond these
direct effects, there is the potential for smoking restrictions to have
broader, indirect effects on smoking behavior and on public attitudes
about tobacco use. This section outlines the possible impacts of
smoking policies, addresses methodologic considerations, and re-
views existing data that bear on these hypotheses.

Potential Impacts of Smoking Policies
Policy Implementation and Approval

The degree to which a smoking policy or law has been implemen-
ted as written is an essential consideration in evaluating its effects
on attitudes, behavior, and air quality. Successful implementation
involves public awareness of the policy, compliance with its regula-
tions, and enforcement of violations. Compliance requires not only
that smokers refrain from smoking where prohibited from doing so,
but also that appropriate decisionmakers develop written policies,
designate areas as no-smoking, and post signs as stipulated. Enforce
ment requires that policy violations be dealt with, either by peer
action or by penalties defined by the policy. Because smoking policies
and laws are approved by the majority of individuals whose behavior
they affect, they are generally held to be self-enforcing, obviating the
need for active policing (Hanauer et al. 1986). When enforcement is
needed, smoking policies and legislation rely primarily on peers,
assuming that the nonsmoking majority of the population will
enforce the policy or statute because it is in their best interest.

Nonsmokers can be expected to favor smoking restrictions, which
offer the benefits of cleaner air and reduced health risks and require
no change in their behavior. The opinions of smokers are expected to
be less favorable because they stand to be inconvenienced. Some
smokers may support the policy to assure themselves of having a
location where smoking is clearly permitted, because of a desire to
quit smoking, or because of concerns about the health hazards of
involuntary smoking. The degree of smokers' support for a policy

303


may also depend on other factors, such as the degree of smoking
restriction or the adequacy of policy implementation.

Direct Effects: Air Quality and Smoking Behavior

The evaluation of a specific policy or piece of legislation must
address whether the policy achieved its stated goals and must also
screen for other effects. The primary goal of policies regulating
smoking in public places or in the workplace is the reduction of
individuals' exposure to environmental tobacco smoke. Measures of
air quality directly assess how well a policy meets this goal. Air
quality also indirectly reflects the behavior of smokers and the
degree of policy compliance.

Smoking policies may have both direct and indirect effects on
smoking behavior. The direct effect of adequately implemented
smoking restrictions is to limit where smoking is permitted, altering
the behavior of smokers in those settings. Smoking policies may have
indirect effects on smoking behavior if they influence the behavior of
smokers outside these settings.

Indirect Effects: Knowledge, Attitudes, Social Norms, and
Smoking Behavior

Policies that restrict or ban smoking in public places or the
worksite convey potentially powerful messages about the role of
cigarettes in society and help to reinforce nonsmoking as the
normative behavior. Restricting smoking to protect nonsmokers may
increase public knowledge of the health risks of smoking and of
involuntary smoking. Smoking restrictions may also alter attitudes
about the social desirability of smoking and the acceptability of
smoking in public. Changes in the knowledge or acceptance of health
risks combined with attitude shifts contribute to changing social
norms about where smoking should and should not occur, as well as
whether it is an acceptable social behavior.

Changes in social norms may influence smoking behavior by
reducing pressures to smoke and increasing social support for
nonsmoking and cessation. The combination of altered social norms
and reduced opportunities to smoke may encourage smokers to quit
and discourage experimentation among nonsmoking youth. Chang-
ing social norms may have their greatest impact on teenagers and
young adults, who might be less inclined to experiment with a
socially undesirable substance. Current smokers are likely to be
prompted by changing social norms to move further through the
stages of self-change that precede cessation (Prochaska et al. 1985).

Smoking restrictions may influence smoking behavior apart from
their influence on social norms. By reducing opportunities for
smoking, restrictions may decrease a smoker's daily cigarette

304


consumption. By reducing the range of settings where smoking
occurs, they reduce the cues and alter the stimulus-response
patterns that help to maintain smoking behavior and that contribute
to relapse among ex-smokers (Orleans 1986). This could increase the
success of quit attempts. Smoking restrictions, especially those at the
workplace, may also help smokers to discover alternatives to
smoking as a stress reduction tool. Likewise, new entrants into the
workforce may not as easily learn to rely on cigarettes to cope with
work-related stressors. This might blunt the increase in smoking
prevalence that occurs at the time of workforce entry, especially
among blue-collar workers (O'Malley et al. 1984; US DHHS 1985c).
Thus, the widespread adoption of smoking restrictions may have a
profound impact on smoking behavior at many points in its natural
history. Hypothesized consequences include reduced cigarette con-
sumption, increased motivation and progress through the stages of
self-change, increased rates of smoking cessation, and decreased
rates of smoking initiation.
Smoking policies may have additional impacts beyond their effects
on attitudes and smoking behavior, such as positive economic effects
for employers by reversing the excess costs associated with employ-
ees who smoke. It is generally agreed that employees who smoke cost
their employers more than nonsmoking employees because of excess
absenteeism, increased health care utilization, and reduced produc-
tivity (OTA 1986; Fielding 1986; Eriksen, in press). This leads to
greater use of sickness, disability, and health care benefits and
ultimately, higher health insurance costs to business. Productivity
losses to business are attributed not only to the individual smoker's
time lost owing to on-the-job smoking, but also to increased
maintenance costs due to cigarette-related damage and refuse.
Estimates of the excess annual cost per smoking employee vary by
an order of magnitude, but even conservative estimates are substan-
tial: $300 to $600 (Kristein 1983, 1984; Solomon 1983; Weis 1981).
Reductions in health care costs are partly dependent on whether
policies lead smokers to quit smoking. Even if smokers quit, the
reduction in health care costs may not be. seen in the short term.
Some employers have been concerned that strict smoking bans may
unfavorably alter employee turnover patterns or productivity.
Smokers' productivity could decrease if, for example, they are
permitted to take extra breaks away from their work stations in
order to smoke (OTA 1986; Michigan Tobacco and Candy Distribu-
tors and Vendor Association 1986). Ccsts involved in adopting a
smoking policy should also be considered. Assessment of these
endpoints is useful because employers may consider them in deciding
whether to implement smoking policies.


Methodologic Considerations in Policy Evaluation
Study Design

Evaluating a new smoking policy in a defined population is similar
to evaluating a smoking cessation intervention, with the addition of
nonsmokers. Impacts on beliefs and attitudes, as well as on behavior,
can be assessed in the population at baseline and at intervals after
implementation. Because smoking policies may influence smoking
behavior gradually, designs must be able to measure delayed effects.

Simultaneous assessment of outcomes in a control population
strengthens confidence in the validity of conclusions. With uncon-
trolled pretest/posttest designs, there is the possibility that changes
in smoking behavior and attitudes are confounded by outside
influences. Worksites, for example, may have concurrent smoking
cessation programs that can affect attitudes and behavior. Popula-
tionwide trends in smoking behavior are another source of confoun-
ding. In practice, random assignment of whole populations will
rarely be feasible, since researchers are rarely in a position to
"assign" the intervention and must rely on natural experiments.
Quasiexperimental designs, which include natural comparison
groups, are the best alternative. Identifying and accessing such
appropriate comparison populations may be difficult in practice.

Either longitudinal or cross-sectional sampling can be employed.
Longitudinal designs, in which the same individuals are interviewed
at two or more points in time, provide the best measure of changes in
outcome measures, but depend on high rates of followup, which may
be practically difficult. Furthermore, individuals' behavior or atti-
tudes may be influenced by repeated assessments in such studies. On
the other hand, when attitudes and behavior are evaluated by
repeated assessments of independently chosen cross-sectional sam-
ples, the possibility exists that smokers and nonsmokers will enter or
leave the population at different rates as a consequence of smo!cing
restrictions. Turnover needs to be followed to assure that changes in
behavior or attitudes are a result of changes in individual behavior
and not changes in the composition of the population.
One-time comparisons of populations with and without policies
can provide suggestive but not conclusive data about impact. The
validity of differences detected in attitudes and behavior is depen-
dent on the degree of similarity between the policy group and the
control group. Uncontrolled one-time assessments done before or
after policy adoption do not permit conclusions about the policy
effects, although they may provide hypotheses for further work.
Postimplementation surveys of a population can, however, provide
useful information about the degree of policy approval, awareness,
compliance, and enforcement.

Assessment of the impact of legislation on smoking behavior is
more difficult because the unit of study is larger and more diverse.

306


Consequently, detailed behavioral or attitudinal data and repeated
assessments are more difficult to obtain. Evaluations are often
limited to analyses of aggregate measures such as smoking preva-
lence and tobacco consumption, which are collected for other
purposes. This approach does not control for potentially confounding
influences on tobacco use or smoking behavior, such as price
fluctuations. Identifying and assessing control groups not subject to
smoking legislation or regulation can strengthen the confidence in
conclusions for the same reasons as above, but is often difficult to
achieve in practice.

Assessing the Effects of Smoking Policies

Ideally, air quality should be measured objectively, but current
technology for measuring the concentration of tobacco smoke in
indoor air is expensive and cumbersome. There is also uncertainty
about which constituent of smoke is best to measure (See chapters 3
and 4 of this volume). Air quality can also be assessed subjectively.
Ratings made by occupants of smoke-free areas can be compared
with those of a control area or to ratings made prior to the ban.
Measurement of an individual nonsmoker's actual exposure to
secondhand smoke, using biochemical measures, is not a specific
measure of the concentration of this smoke in a single area because
an individual may have other sources of smoke exposure. Such
measures might be useful for assessing the concentration of smoke in
areas, like the worksite, that represent a primary source of exposure.
They cannot be used to measure air quality in other places, like an
auditorium, where an individual spends only a few hours.

Many markers of smoking behavior need to be examined in order
to understand the multiple effects of smoking restrictions on
behavior. In a defined population, a new policy may increase
smokers' motivation to quit, confidence in their ability to quit, or the
number, duration, and success of quit attempts. It may also reduce
cigarette consumption among continuing smokers. Workplace poli-
cies may have different impacts on cigarette consumption at work
and outside work. These variables should be separately assessed. As
in other research in smoking behavior, biochemical verification of
self-reported smoking status is desirable.

Public knowledge about the health risks of involuntary smoking
and attitudes about smoking can be assessed by surveys. Data on
social norms can be construed from survey items such as those
measuring the social acceptability of smoking in public places or in
the presence of nonsmokers, the rights of nonsmokers to smoke-free
air, the perceived prevalence of smoking in the environment, and the
perceived social support for cessation or nonsmoking.

The adequacy of a policy's implementation can be assessed by
surveys that measure individuals' knowledge and compliance with a

307


policy. The degree of noncompliance and enforcement can also be
assessed by observations of behavior in public places subject to
smoking restrictions.

Review of Current Evidence on Impact
Workplace Smoking Policies

In 1982, Orleans and Shipley concluded that the evaluation of
worksite smoking policies was limited to a few public opinion polls.
Since then, many policies have been adopted, but evaluation remains
rare. Most common are baseline surveys done by companies consider-
ing smoking policies. The best surveys utilize random or probability
samples and achieve high rates of completion; they provide useful
one-time data on attitudes and behavior prior to policy implementa-
tion. Unfortunately, few companies adopting smoking policies have
done postimplementation surveys to assess impact. To date, the best
evaluations of worksite smoking policies have been done in the
health care setting. There are two controlled and two uncontrolled
studies assessing the effects on employees of adopting a smoking
policy for a hospital (Rigotti et al. 1986; Biener et al. 1986; Andrews
1983; Rosenstock et al. 1986).
One uncontrolled study was reported by Andrews (1983). He
described the process by which the New England Deaconness
Hospital in Boston adopted a restrictive smoking policy in 1977.
Patients and employees were surveyed prior to the policy. Employees
were surveyed again 20 months after the policy took effect. The
survey method and response rate were not specified; presumably it
was not a random sample. Policy approval and smoking behavior
were assessed.

The second uncontrolled study (Rosenstock et al. 1986) evaluated
the impact of a near-total smoking ban adopted in April 1984 by the
Group Health Cooperative of Puget Sound, Washington, the fourth
largest health maintenance organization in the Nation. Four months
after the policy was adopted, they surveyed a systematic probability
sample of 687 employees, assessing smoking behavior, attitudes
toward the policy, and its effect on work performance. Employees
were asked retrospectively about attitudes and behavior prior to the
policy. The response rate was 65 percent.

The two controlled studies of the impact of adopting a restrictive
hospital smoking policy are similar in design. Both involve prepolicy
and postpolicy measurements of intervention and control groups and
assess similar outcomes. Rigotti and colleagues (1986) studied the
impact of a total ban on smoking adopted in November 1984 by the
pediatric service at Massachusetts General Hospital in Boston. All
nurses employed by the service were surveyed at baseline and at 4
and 12 months. Nurses working on the hospital's medical service,
where no policy change occurred, were surveyed concurrently as

308


controls. Response rates to the surveys ranged from 55 to 75 percent;
the prevalence of smoking among respondents and nonrespondents
did not differ. Surveys assessed smoking behavior, attitudes about
smoking, and perceived air quality in both groups. The pediatric
nurses answered additional questions about approval, compliance,
and awareness of the policy. Employment records were reviewed to
assess employee turnover before and after the policy.

Biener and colleagues (19861 studied employees at two Providence,
Rhode Island, hospitals where self-help smoking cessation programs
were being introduced. At one, the Miriam Hospital, there was a
concurrent change in smoking policy. Smoking was prohibited
hospitalwide except in three locations as of August 1985. Separate
random probability samples of 85 employees at each hospital were
surveyed by telephone at baseline (2 to 4 weeks before the policy) and
at 1, 6, and 12 months after the policy. Data were collected in both
hospitals on smoking behavior, attitudes about smoking, and air
quality. Information on policy awareness, compliance, and approval
was obtained at the intervention hospital.

Results of these studies are included in the subsequent sections,
which address the outcomes of workplace smoking policies.

Policy Implementation

According to case reports, organizations that have adopted smok-
ing control policies generally develop careful plans to introduce the
policy, but rarely evaluate how effectively the policy has been
implemented. The findings of Rosenstock and colleagues (1986)
indicate that even careful implementation plans may fall short of
their goals. In their survey of the Group Health Cooperative
employees, only half of the respondents knew of the existence of the
advisory group whose role was to provide information to employees.
Only 36 percent of the smokers and 76 percent of the nonsmokers
felt that they had had an adequate opportunity to express their
views. Not all smokers knew that the decision to prohibit smoking
was an irrevocable one.

Rigotti and colleagues (1986) found that awareness of the smoking
ban on the pediatric service was high; at 4- and 1Zmonth followups,
over 90 percent of employees knew where smoking was not permit-
ted. Employees noted smoky air or smoking in restricted areas on
approximately 20 percent of days worked. Two-thirds of the employ-
ees who smoked admitted at least one personal episode of noncompli-
ance during the year after the policy took effect. Although nonsmok-
ers perceived themselves to be more assertive in enforcing smoking
rules after the smoking ban, many were reluctant to confront a
smoker, especially if the smoker was a coworker.

Biener and colleagues (1986) found a similar high level of policy
awareness and better compliance among the employees of Miriam

309


Hospital in Providence. Six months after the adoption of a policy
prohibiting smoking in all but three areas, 95 percent of the
employees were aware of the policy and half had noted no evidence
of noncompliance. There was no evidence that smokers perceived
more pressure to abstain in the form of increased assertiveness by
nonsmokers; the policy may have reduced the need for assertive
behavior. Rigotti and colleagues (1986) reported that nurses in the
control group described themselves as having to be more assertive
about asking people not to smoke than nurses in the policy group.
Dawley and colleagues (Dawley et al. 1980; Dawley, Carrol et al.
1981; Dawley, Morrison et al. 1981; Dawley and Baldwin 1983;
Dawley and Burton 1985) addressed the question of compliance with
smoking restrictions at the New Orleans Veterans' Administration
Medical Center. Their technique was to unobtrusively observe the
smoking behavior of individuals occupying areas designated as
smoking or no-smoking. In a series of lO-minute periods, an observer
noted the proportion of people smoking among all individuals
occupying a no-smoking area, which sexed as the measure of
noncompliance. Posting no-smoking signs in a hospital lobby reduced
the prevalence of smoking to one-third of its previous level (from 29
percent to 5 to 11 percent, p < 0.01). There was a nonsignificant trend
for better compliance with positively worded signs (e.g., "Please do
not smoke") compared with negatively worded signs (e.g., "No
smoking--Offenders subject to fine") (Dawley, Morrison et al. 1981).
Posting signs designating a no-smoking area in a cafeteria resulted
in a similar decline in smoking prevalence in the area. The
combination of signs and enforcement (polite reminders from staff to
noncompliant patients) achieved greater reductions in smoking
prevalence than were achieved with signs alone; however, the
incremental value of enforcement was not directly assessed in the
study (Dawley and Baldwin 1983). Following a change to a more
restrictive smoking policy (smoking prohibited except in designated
areas, with provisions for enforcement), the noncompliance rate
dropped to under 2 percent (Dawley and Burton 1985). Another
study demonstrated that smoking models reduce compliance with
smoking restrictions. The noncompliance rate doubled when a
smoker was experimentally introduced into the no-smoking area
(Dawley, Carrol et al. 1981).

These studies indicate that there has been good employee compli-
ance with smoking policies in health care facilities, even though
there may be some reluctance by employees to enforce restrictions.
The implementation of smoking policies in other types of worksites
has not been systematically evaluated. Descriptions of the adoption
of policies in a number of worksites do not report major problems
with compliance (BNA 1986).

310


Air Quality

Three studies assessed air quality before and after hospitals
adopted restrictive smoking policies. Both Rigotti and colleagues
(1986) and Biener and colleagues (1986) used a subjective measure,
the frequency that an employee was bothered by smoke at work. In
the Rigotti group's study, perceived air quality was similar in the
intervention group and the control group at baseline. It improved
significantly at 4- and l&month followup on floors where smoking
was banned and did not change on control floors. At 12 months, 79
percent of the nurses on floors with the smoking ban reported
noticing less smoke, and none noted an increase; in contrast, 87
percent of control nurses noted no change in air quality. Biener and
colleagues found a similar pattern; there was a significant difference
in employee assessments of perceived air quality between hospitals
with and hospitals without a smoking policy.

At the New England Baptist Hospital in Boston, the distribution of
respiratory particulates (RSP) was measured before and 1 year after
the adoption of a restrictive smoking policy (Bearg 1984). At
followup, RSP were lower in many hospital areas where smoking
was restricted, most notably in patient care areas and an employee
lounge, but remained high in the cafeteria. Because same-day
measurements of outside air revealed low ambient RSP levels, Bearg
concluded that the high levels inside the building were attributable
to smoking rather than air pollution.

These studies suggest that hospital policies result in less smoking
in work areas designated no-smoking, but that no-smoking areas in
cafeterias may provide little protection from secondhand smoke
exposure because of ventilation problems and the increased smoking
in the few smoking-permitted areas.

Policy Approval

A number of private and public sector organizations considering a
smoking policy have assessed employee attitudes prior to implemen-
tation. Pacific Northwest Bell, Pacific Telephone, New England
Telephone, Texas Instruments, and StrideRite are among businesses
that have done employee surveys (R. Addison, personal communica-
tion, July 21, 1986; Pacific Telephone 1983; Robert Finnegan
Associates 1985; BNA 1986; Ziady 1986). Public sector employers
include the Hawaii and Massachusetts Departments of Public
Health (Marvit et al. 1980; Naimark 1986). The findings of these
surveys are remarkably similar. Over 60 percent of employees report
being at least occasionally bothered by smoke at work (Robert
Finnegan Associates 1985; Pacific Telephone 1983; Ziady 1986; R.
Addison, personal communication, July 21, 1986). There is broad
support for adopting a smoking policy, even among smokers (Pacific

311


Telephone 1983; Robert Finnegan Associates 1985; Marvit et al.
1980, Sorensen and Pechacek 1986).
Assessment of employees' approval of policies after implementa-
tion have been done primarily in health care settings. High rates of
approval are the uniform finding, with smoker-nonsmoker differ-
ences. In the Rigotti group's study (1986), the overall approval of a
smoking ban increased from 72 percent at baseline to 85 percent at 4
and 12 months. Most of the increase was a result of the improved
opinions of the smokers. Only 35 percent of smokers supported the
ban at baseline, but by 1 year this nearly doubled, to 67 percent.
High rates of policy approval at followup by both smokers and
nonsmokers were also reported by Biener and colleagues (1986) (69
percent smokers, 89 percent nonsmokers) and Andrews (1983) (83
percent smokers, 93 percent nonsmokers). Rosenstock and colleagues
(1986) found high overall policy approval at 4 months (85 percent),
but less support by smokers (36 percent). These data indicate that
smoking policies in hospitals are well accepted by employees, and
that smokers' initial reluctance diminishes as they gain experience
with the policy. Generalization from these studies is limited by the
nature of the population studied-health care workers. Followup
surveys in industrial setting would be valuable.

Sorensen and Pechacek (1986) have examined correlates of smok-
ers' approval of smoking restrictions. They surveyed smokers in
eight Minnesota businesses without smoking policies, sampling a
broad cross-section of employees, from blue-collar workers to profes-
sionals. Over three-fourths of the 378 respondents agreed that
employers should establish separate smoking and no-smoking areas
at work. Smokers who favored worksite smoking policies had greater
interest in quitting and more concern for the health risks of smoking
and saw their social environment as supportive of nonsmoking, as
measured by a higher perceived coworker support for quitting and a
greater perceived prevalence of nonsmokers.

Smoking Behavior

Many smokers anticipate that their smoking behavior will change
after a smoking policy is adopted at their worksite. At Pacific
Telephone, 51 percent of the smokers expected that the policy would
lead them to alter their smoking habits, either by cutting down (38
percent) or quitting (13 percent) (Pacific Telephone 1983). In the
Rigotti group's study (1986) of a hospital smoking ban, 72 percent of
the smokers expected the policy to change their habits. All expected
to smoke less at work and most to smoke less outside work.

A successfully implemented smoking policy will provide a smoker
fewer opportunities to smoke. Of course, the smoker may compen-
sate for reduced smoking opportunities at work by more intense
smoking (number of cigarettes, inhalation, puff topography) on

312


breaks or with increased smoking outside work to maintain a
constant overall daily consumption. This is consistent with the
addictive model of smoking behavior (Grit.2 1980; US DHEW 1979).
But if compensation does not occur, the smoker's lower rate at work
would reduce overall daily smoking. Studies at present differ on
which of these alternatives occurs. The results reported below are
entirely self-reports; thus, they suffer from a lack of biochemical
validation of smoking status as well as from an inability to detect
compensation through altered smoking topography (US DHHS
1985c).

Compensation did not appear to occur in the Biener group's
hospital study (1986). Among smokers in the "policy" hospital, the
number of cigarettes smoked daily while at work fell from a baseline
of 8.1 to 4.5 at 1 month and 4.0 at 6 months. Over the same time
period, the at-work cigarette consumption in the control hospital
rose slightly (7.6 to 8.1 cigarettes). The difference in smoking rates
between baseline and l-month followup in the "policy" group was
significant (p=O.O2). At 6 months, the difference in smoking rates at
work between hospitals (8.2 vs. 4.0) was also significant (p=O.Ol).
There were no significant changes in the smoking rate outside work.
Smokers in the hospital study by Rosenstock and colleagues (1986)
reported smoking a mean of 15.6 cigarettes daily, 2 fewer than before
the policy (p <0.003). These data suggest that smokers did not
compensate for reduced smoking opportunities at work by increasing
their smoking at home.

Rigotti and colleagues (1986) found indirect evidence for compen-
sation. The nurses' self-reported cigarette consumption at work
decreased in the policy group, but did not change in the control
group. However, overall cigarette consumption in the policy group
did not change. Both the degree of change and the number of
smokers in the study were small.

In an earlier study, Meade and Wald (1977) compared the smoking
behavior of three British employee groups. Smoking was prohibited
at work for two groups. Smokers who were allowed to smoke at work
had a somewhat higher self-reported average daily cigarette COP
sumption. The maximum rate of smoking occurred at work in the
aft,ernoon, but for workers prohibited from smoking at work, the
maximum rate occurred in the interval between leaving work and
retiring at night.

There has been much speculation that smoking policies will
increase the smoker's motivation and success in quitting. In the
study by Biener and colleagues (1986), the percentage of smokers
considering quitting in the next 6 months increased from 71 percent
at baseline to 91 percent at followup, but there was no change in
motivation in the control hospital group. Two-thirds of the smokers
in Rosenstock and colleagues' uncontrolled study (19861 had a

313


definite desire to quit. However, Rigotti and colleagues (1986) found
no difference in the motivation of nurses between the control group
and the policy group.

Smokers' use of worksite smoking cessation programs before and
after policies go into effect have been used as an index of their
motivation to quit smoking. The results are mixed. In the 6 months
after Pacific Northwest Bell adopted a smoking ban in October 1985,
1,944 employees, representing 25 percent of all smokers, enrolled in
programs reimbursed by the company. This compared with 331 who
attended free onsite programs in the previous 26 months. The cost to
the company per smoker was $142 (Martin 1986; K. Rowland,
memorandum for Len Beil, April 25,1986). At Texas Instruments (R.
Addison, personal communication, July 21, 19861, 486 smokers
enrolled in cessation classes within the first year after the announce-
ment of a smoking policy; this compares with only 11 in 1982, the
last year for which statistics were kept. In both cases, this enthusias-
tic response may in part be due to the employers' new willingness to
pay for the classes, as well as to the incentive provided by a new
policy. For example, only 8 of 148 smokers at the New England
Deaconness Hospital who said they were interested in a smoking
cessation program on their own time actually showed up (Andrew6
1983). Even company sponsorship is not a guarantee of popularity.
At the Group Health Cooperative, only two smokers aware of the
company-sponsored cessation programs had participated within 4
months of policy adoption (Rosenstock et al. 1986). The signup rate
for work&e-based self-help smoking cessation programs was no
greater at a Rhode Island hospital with a new smoking policy than at
one without (Biener et al. 1986).

It is not known whether the cessation rate of smokers who enroll
in worksite programs is affected by the presence of a smoking policy
at the worksite. Only uncontrolled studies with self-report measures
are currently available. At Texas Instruments (R. Addison, personal
communication, July 21, 1986),34 percent of 354 employees enrolled
in the first round of company-sponsored cessation classes quit
smoking by the end of the program; in the second round of classes, 17
percent of 132 enrollees quit. At Pacific Northwest Bell, 44 percent
of 639 respondents quit smoking in a survey of the 1,200 participants
in a company-sponsored program. If nonrespondents are included as
smokers, the cessation rate was 23 percent (Shannon 1986).
There is as yet no conclusive evidence that smoking policies are
associated with increases in smoking cessation attempts or reduc-
tions in smoking prevalence. All reports are based on self-reported
smoking behavior. There are anecdotal reports of smokers quitting
in case reports of company policies (StrideRite, cited in BNA 1986)
and in uncontrolled surveys (Rosenstock et al. 1986; Andrews 1983).
Supporting evidence comes from the New England Deaconness

314


Hospital, where a two-part survey, before and 20 months after the
adoption of a strict smoking policy, demonstrated a reduction in the
prevalence of smoking among employees from 32 to 24 percent, along
with an increase in the prevalence of ex-smokers (27 to 34 percent)
(Andrew6 19831. However, methodologic problems prevent an un-
equivocal conclusion. The first survey included both employees and
patients, but the followup covered only employees; smoking rates for
employees only are not provided. The survey method was not
specified, but it did not appear to be a probability sample, thereby
limiting generalizability of the finding to the entire group. Finally,
because the same group of employees was not surveyed at followup,
an alternate interpretation for the change in smoking prevalence is
that the policy influenced employee turnover rates so that smokers
left and were replaced by ex-smokers. The study did not assess
employee turnover.

Controlled studies by Biener and colleagues (1986) and Rigotti and
colleagues (1986) did not detect an increase in smoking cessation by
employees of hospitals that adopted smoking policies. In the study by
Rigotti and colleagues, nurses in the policy group did not differ from
controls in their motivation to quit, or their expectation of doing so,
or in the number or success of quit attempts. The prevalence of
smoking in the policy group and in the control group was similar at
baseline and did not change in the year after policy adoption.
Similarly, employees in a Rhode Island hospital with a smoking
policy were no more likely to try to quit or to succeed in quitting
than were employees in a control hospital (Biener et al. 1986). The
number of smokers in these two studies was small, and it is possible
that the studies lacked adequate power to detect changes in
behavior. Followup periods of greater than 1 year may also be
required.

Attitudes About Smoking

There has been little assessment of the impact of worksite smoking
policies on attitudes about smoking. The two controlled studies of
hospital smoking policies assessed attitudes about the health risks of
smoking and about involuntary smoking (Biener et al. 1986; Rigotti
et al. 1986). There was no significant change in the smokers' beliefs
about the health risks of smoking or about environmental tobacco
smoke exposure.

Management Issues

There is only sketchy evidence about the impact of worksite
smoking policies on absenteeism, health care costs, productivity, or
employee turnover. No systematic analysis of economic impact has
been done. There is an anecdotal report of cost saving by the Merle

315


Norman Cosmetics Company, which reported lower absenteeism and
housekeeping costs and increased productivity in the year after it
adopted a ban on smoking (ALA of San Diego 1984). In the 6 months
after Pacific Northwest Bell adopted a total smoking ban, no
employees left because of it (Martin 19861. Rigotti and colleagues
(1986) reported no change in employee turnover in the year after the
adoption of a hospital smoking ban. Rosenstock and colleagues (1986)
found that self-reported work performance was unaffected in 75
percent of employees and improved in 21 percent. Costs involved in
implementing a smoking policy have not been systematically mea-
sured, but appear from case reports to have been small (BNA 1986).
Adverse impacts of worksite smoking policies have not been report-
ed.

Legislation Restricting Smoking in Public Places

Legislation restricting smoking in public places has been less well
evaluated than worksite smoking policies. Opinion polls in States
and communities that have passed smoking control regulations
provide some information on attitudes about smoking and smoking
policies. There are no controlled studies of the impact of legislation
on smoking behavior or attitudes.

Policy Implementation and Enforcement

Evaluation of the implementation of State or local smoking control
statutes has been limited. In general, enforcement is delegated to a
State or local agency, such as the department of public health.
Enforcement is handled passively rather than actively; the responsi-
ble agency responds to complaints, but does not actively monitor
policy compliance by surveying worksites, restaurants, or public
places. Nonsmokers rights groups and individual activists are a
major force for informing the public and aiding enforcement by
bringing complaints (Sandell1984).

The experience of cities like San Francisco and States like
Minnesota contradicts tobacco industry estimates of the expense and
intrusiveness required to enforce a smoking law (Martin 1986, New
York Times 4/13/86; Sandell 1984). In the first year after San
Francisco implemented a strict workplace smoking law in March
1984, only 124 complaints were processed and 1 citation was issued;
there were no legal actions. No new employees were hired and no
additional funds were required for enforcement. Policy enforcement
required progressively less of a single employee's time over a l-year
period (Martin 1986). Minnesota enforces its 1975 State smoking law
in a fashion similar to San Francisco's. State public health depart-
ment officials estimate that they handle 1,200 to 1,400 complaints
per year, with costs of enforcement estimated to be under $5,000 per

316


year (Sandell 1984). A survey of 10 California cities with workplace
smoking laws documented that complaint rates were low and
enforcement of these laws was a low priority for all city govem-
men& Officials indicated that they would spend any additional
funds available for enforcement on a public education campaign to
increase awareness of the law rather than initiate active surveil-
lance (Linson 1986).

Because active monitoring of policy compliance is not done, a low
complaint rate is often taken as evidence of a high compliance rate.
Data from Minnesota suggest that this is not always true. In 1976,l
year after the comprehensive Clean Indoor Air Act was enacted, 43
percent of respondents to a statewide poll felt that the law was not
very effective in reducing smoking in public places; 38 percent found
it somewhat effective and 12 percent, very effective (Minneapolis
Tribune 1976). Six years after the law took effect, a survey of
Minnesota businesses with 200 or more employees documented that
only 46 percent of businesses had such a policy. Restaurants,
however, had nearly uniformly conformed to the law within a year of
implementation (Sandell 1984). A statewide opinion poll in 1978
demonstrated that over 70 percent of both smokers and nonsmokers
felt that the Clean Indoor Air Act should be strictly enforced
(Minneapolis Tribune 1978). Two years later, Minnesotans were of
mixed opinion about the law's enforcement: fewer than half (43
percent) considered it very well enforced, 42 percent felt it was not so
well enforced, and 10 percent said it was not enforced at all
(Minneapolis Tribune 1980).

Randolph (1982) studied factors associated with compliance and
enforcement of local ordinances regulating smoking. She asses&
the implementation of a recently enacted San Rafael, California,
smoking ordinance by interviewing proprietors of randomly selected
businesses. Less than 1 year after the ordinance went into effect, 68
percent of 25 proprietors were aware of the policy, but only 44
percent of 30 businesses had complied with the requirement to post
nesmoking signs. The major variable associated with compliance by
businessmen was the type of business; restaurants, retail food stores,
drug stores, banks, and movie theaters were generally posting signs
as required, but department stores and small retail stores were not.
City residents were less well informed. Fewer than half (45 percent)
of 200 randomly selected residents surveyed by telephone were
aware of the ordinance, and only 11 percent could describe its
provisions.

Randolph's study (1982) of implementation also included a 1980
telephone survey of 600 randomly selected residents of three
northern California cities, two with smoking ordinances and one
without. Smokers were classified as compliers or noncompliers
according to whether they refrained from smoking in supermarkets,

317


which was required by State law. Characteristics of smokers who
complied were (1) lower daily cigarette consumption, (2) less per-
ceived need to smoke, (3) greater perception of others' disapproval
for tobacco smoking in public, (4) and greater support for policies
restricting smoking in public places. Smokers' perception of pres-
sures to refrain from smoking in public, awareness of the presence of
a local smoking law, and the duration of the ordinance were not
associated with compliance. Enforcement of smoking laws was
studied in nonsmokers. The best predictor of enforcement behavior
was a nonsmoker's degree of annoyance with tobacco smoke. Other
characteristics associated with enforcement behavior were more
negative attitudes about smoking in public places, greater intoler-
ance of noncompliance, and higher educational level.

Policy Approval

National and regional polls have surveyed public opinion about
where smoking should be restricted or banned. Regional polls have
often been taken when legislation is being considered. There are
little data about public opinion on legislation after its enactment.

Nationwide public opinion about smoking in public places was
assessed by Roper polls in 1976 and 1978 (19781, two Gallup polls
(1978, 19831, and the Harris Prevention Index 85 (Harris 1985). The
Roper polls asked separate questions about preferences for a
smoking restriction or a total ban; the Gallup and Harris polls
offered a choice between the two in the same question. In both Roper
polls, a majority of respondents favored restricting smoking in all
places mentioned: transportation vehicles (airplanes, buses, and
trains), restaurants, workplaces, and indoor arenas. By 1978 three-
fourths of the respondents favored restrictions in all places except
the worksite. Total smoking bans were less popular but still the
choice of at least one-fourth of the respondents.
The 1983 Gallup poll documented increased public support for
smoking restrictions, particularly in restaurants. More than 80
percent of smokers and 90 percent of nonsmokers favored either
banning or restricting smoking in airplanes, buses, and trains and
restaurants. Over half of both smokers and nonsmokers favored
restrictions in motels and at the worksite. Although bans were less
popular than restrictions, they were twice as popular with nonsmok-
ers as with smokers. In 1985, 80 percent of the respondents to the
Harris poll supported restrictions or bans in public places in general.
Regional polls generally support the conclusions of nationwide
surveys.

Minnesota is one State where public opinion of existing legislation
has been measured. Five years after enactment, public opinion of
Minnesota's 1975 Clean Indoor Air Act remained high. Ninety-two
percent of the 1,200 respondents to a statewide poll favored the act,

318


including 87 percent of heavy smokers (two packs per day) and a
larger fraction of lighter smokers (Minneapolis Tribune 1980).

During the first year of the San Rafael, California, smoking
ordinance, nearly 70 percent of 200 randomly selected residents
agreed that there should be laws about smoking in public places and
77 percent said they would have voted for the ordinance had they
had the opportunity Randolph 1982). The reaction of local busi-
nesses was less favorable. Over half (52 percent) did not like the
ordinance, but only 41 percent favored rescinding it. The most
common reason for support was concern for smoking-related damage
to property. Concerns about invading personal rights and fear of
losing business were the major reasons for opposition.

Attitudes and Social Norms

It has been suggested that smoking restrictions will alter public
attitudes and norms about smoking behavior. There are few data
addressing this hypothesis.

Randolph (1982) reported on attitudinal differences between
residents of California communities with and without smoking
ordinances. Smokers in two cities with laws had more negative
attitudes about smoking in public places and were more likely to feel
that there should be laws regarding tobacco smoking in public.
However, there was no difference in smokers' perceptions of social
pressures to refrain from smoking. Nonsmokers in cities with laws
were more likely to believe that tobacco smoke should be regulated
in public, but they were no more annoyed by tobacco smoke,
intolerant of noncompliance, or disapproving of smoking in public
places than residents of the city without a law. Although residents of
communities with and without smoking ordinances did not differ in
their personal support of smoking laws, residents of communities
with laws perceived greater support for these laws by other residents
of their communities. This cross-sectional study cannot differentiate
whether these attitudinal variations were a cause or consequence of
differences in community smoking ordinances.

Data from opinion polls demonstrate that negative attitudes about
smoking generally preceded rather than followed legislation to
restrict smoking in public places. The four Adult Use of Tobacco
Surveys, a series of nationwide surveys conducted between 1964 and
1975, measured attitudes in the decade after the health hazards of
smoking were first widely appreciated (US DHEW 1969, 1973, 1976).
As early as the first survey in 1964, a majority of nonsmokers agreed
with these statements: "It is annoying to be near a person who is
smoking cigarettes" and "Smoking should be allowed in fewer places
than it is now." By 1970, a majority of all respondents agreed with
these statements. By 1975, a majority of smokers agreed with the
idea of further restricting smoking, suggesting that there was wide

319


public support for restricting smoking well before the first compre
hensive Clean Indoor Air Act was passed in Minnesota in 1975. As
early as 1973,73 percent of the nonsmokers in a Minnesota poll felt
that they had the right to a smoke-free environment, and 65 percent
wanted to ask others not to smoke (Minneapolis Tribune 1973). More
recent opinion polls document that negative attitudes about smoking
in public continue to grow. In a 1985 Gallup poll, 75 percent of the
respondents (including 62 percent of the smokers) felt that smokers
should refrain from smoking in the presence of nonsmokers.

However, nonsmokers' attitudes do not translate directly into
action. A smaller proportion of nonsmokers are willing to confront a
smoker whose smoke is bothersome. In three successive Roper polls
between 1974 and 1978, fewer than 10 percent of the nonsmokers
indicated that they would ask an individual smoking indoors to stop
(Roper 1978). Only 32 percent of the nonsmokers in a 1974
Minnesota poll would complain when bothered by another person's
smoking, although an additional 31 percent would take nonconfron-
tational action such as moving away or opening windows (Minneapo-
lis Tribune 1974). These data suggest that in the mid-197Os, despite
strong preferences, many nonsmokers did not perceive that asking a
smoker to stop was socially sanctioned behavior.

Smokers, on the other hand, report an awareness of nonsmokers'
concerns and a willingness to comply with restrictions. Over 90
percent of the smokers in a 1981 Iowa poll (Des Moines Register
1981) extinguished tobacco when they saw a no-smoking sign. Sixty
percent of the smokers in a 1973 Minnesota poll (Minneapolis
Tribune 1973) had at least some misgivings about smoking in the
presence of nonsmokers, and 90 percent would not have been
offended if asked not to smoke. Only 29 to 36 percent of smokers in
three Roper polls (1974-1978) lit a cigarette without looking around,
asking others, or refraining from smoking (Roper 1978).
There may be, therefore, an interaction between attitudes and
policy development. These survey data suggest that attitudes about
smoking in public preceded and may have contributed to the
development of a public policy (Breslow 1982). At the same time,
publicity surrounding campaigns for legislation may increase public
awareness of an issue such as the hazards of involuntary smoking
and therefore contribute to further changing attitudes.

Smoking Behavior

The impact of legislation on smoking behavior has received little
formal attention. There are no controlled studies in which smoking
behavior has been tracked over time in the States or communities
that have enacted smoking legislation. In Randolph's one-time
assessment (1982) of smoking behavior in California communities
with and without smoking control ordinances, there was no differ-

320


ence in smoking prevalence or mean daily cigarette consumption
between the residents of a city with a recent ordinance and one
without. A lower prevalence of smoking in one community with a
longstanding ordinance was probably explained by demographic
differences between that community and the other areas.
Uncontrolled reports of declining smoking prevalence or cigarette
consumption in a State or community with a smoking law cannot
establish a causal relationship. This was particularly the case during
the 197Os, when both smoking prevalence and per capita cigarette
consumption were declining nationally. Warner (1981a; Warner and
Murt 1982) conducted a series of analyses of this decline. In separate
analyses, he estimated the levels of smoking prevalence and ciga-
rette consumption that would have been achieved if previous trends
in these indicators had continued unabated through the 1960s and
1970s. Cigarette consumption in 1978, for example, would have been
36 to 41 percent higher had previous patterns continued. He ascribed
the difference between observed and modeled values to the impact of
the so-called antismoking campaign, defined as the combination of
public events, legislative activity, and Federal regulations that
affected cigarette price, counter-advertising, and the circumstances
in which smoking was allowed.
To assess the relative contributions of components of the anti-
smoking campaign to the decline in adult per capita cigarette
consumption, Warner (1981a) developed a multivariate analysis that
included independent variables to account for price fluctuations,
adverse publicity about smoking, antismoking activities, and the
effectiveness of the nonsmokers' rights movement. The percentage of
adults residing in States restricting smoking in public places was
used as an index of the strength of the nonsmokers' rights
movement. This variable was strongly associated (p <O.OOOl) with
decreases in consumption from 1973 to 1978.

In Warner's view, the temporal relationship between the growth
in legislation restricting smoking in public places and the decline in
cigarette consumption is so close that a causal relationship is
unlikely. He attributed the decline in consumption to the changes in
attitudes and social norms about smoking that were an earlier
consequence of the entire antismoking campaign. He regarded the
legislation as another reflection of changing social norms rather
than the creator of them (Warner 1981b).

Recommendations for Research

Policies restricting the circumstances in which smoking is permit-
ted have been adopted by a broad range of institutions, mostly in the
last decade. Smoking regulations affect the daily lives of a large and
growing number of Americans. Consequently, these policies are of

321


interest to many individuals and groups. For instance, public health
officials are concerned about the health effects of both active and
involuntary smoking; they are most interested in whether these
policies actually reduce a population's exposure to environmental
tobacco smoke and whether they will alter the prevalence of
smoking. Behavioral scientists, primarily concerned with smoking
behavior and attitudes, are chiefly interested in how smoking
policies alter these variables and how this knowledge can increase
our understanding of the dynamics of smoking behavior. Businesses,
unions, and government policymakers have different perspectives.
They are faced with deciding whether to adopt smoking restrictions
and how to improve the implementation and acceptability of existing
ones. Information about the determinants of policy approval and
compliance will be of most interest to them. Businesses may also be
concerned about the economic and managerial impacts of smoking
restrictions.

Understanding the effect of policies on smoking behavior is of
widest interest and deserves attention. Policies may affect the
natural history of smoking behavior at several points, and detailed
behavioral information should be collected to distinguish among
effects on rates of initiation, cessation, and relapse. Studying how
smokers cope with enforced abstinence may provide additional
insights into the maintenance of smoking behavior. Detailed studies
of the influence of policy may advance the state of knowledge about
the determinants of smoking behavior in general. The relationship
between interventions at the social and individual levels is also of
interest. Researchers should consider whether the effectiveness of
individual treatment is enhanced by the presence of a smoking
policy, and whether the impact of a policy is enhanced by the
availability of individual treatment. Concurrent collection of infor-
mation on attitudes about smoking may help to clarify the nature of
the relationships among attitudes, smoking behavior, and smoking
policies.

In addition to considering a variety of outcome measures, re-
searchers should address the determinants of these outcomes.
Characteristics of the policy, the institution, and the population
should be considered. The components of a smoking policy and its
implementation (such as restrictiveness, degree of advance notice,
degree of support for the policy by affected groups, access to smoking
cessation programs) that contribute to its effect-be it on behavior,
attitudes, air quality, acceptability, or compliance-have generally
not been analyzed. Because smoking policies vary widely in their
provisions and implementation, they cannot be evaluated as a
unitary intervention; i.e., better operationalization of "policy" inter-
ventions is needed. The relative strength of policy components on
each outcome measure should be assessed in order to make informed

322


policy recommendations. For example, the degree of protection from
involuntary smoke exposure afforded by policies of different degrees
of stringency in not empirically known. To acquire this knowledge,
researchers will need to develop and validate measures of such
concepts as restrictiveness. The index described in the appendix to
this chapter is a preliminary attempt to do that. The components of a
policy that are most powerful in reducing cigarette consumption,
inducing cessation attempts, preventing relapse, or reducing smok-
ing initiation need to be identified.

Similarly, the components of a policy associated with maximal
acceptability and compliance have been addressed only cursorily.
Dawley and colleagues (Dawley, Morrison et al. 1981; Dawley and
Burton 19851, for example, have examined variables such as the
wording of signs or the presence of active enforcement. Guidelines
for the implementation of smoking policies have not been experi-
mentally derived. Research could empirically support or refute
recommendations on the basis of experience. Interventions such as
the training of managers to handle implementation problems might
then be developed to increase policy acceptability and compliance.

Different types of organizations have presented different climates
for the adoption of smoking regulations. In assessing policy impact,
there may also be substantial interactions between the policy and
type of facility in which it is adopted. Even within a single type of
facility, there may be considerable variability in social norms, social
supports, and characteristics of the population using it. Sorensen
and colleagues (1986) have pointed out these differences among
worksites. Policy evaluations should consider these variables.

Because smoking policies represent a recent social phenomenon,
there is at present relatively little information about their impact.
New policies are being adopted at a growing rate, providing
researchers with the opportunity to study natural experiments that,
up to now, have largely gone unevaluated. The variety of potential
outcomes, number of interested parties, and current lack of informa-
tion make efforts to collect systematic data on new public and
private sector smoking policies a high priority for research. Con-
trolled studies are desirable and permit the firmest conclusions, but
with the current knowledge base, even limited efforts may yield
valuable information. Uncontrolled case studies, for example, can
provide suggestive data and generate hypotheses for further testing.
In some cases, data are already partially collected. For example,
many businesses considering smoking policies survey employees at
baseline, but few repeat the survey after policy adoption. At the
aggregate level, it may be possible to estimate the impact of
legislation on smoking prevalence or cigarette consumption by
relating national survey data on smoking behavior to smoking
restrictions in geographic areas.

323


Conclusions

1. Beginning in the 1970s an increasing number of public and
private sector institutions have adopted policies to protect
individuals from environmental tobacco smoke exposure by
restricting the circumstances under which smoking is permit-
ted.

2. Smoking in public places has been regulated primarily by
government actions, which have occurred at Federal, State,
and local levels. All but nine States have enacted laws
regulating smoking in at least one public place. Since the mid-
197Os, there has been an increase in the rate of enactment and
in the comprehensiveness of State legislation. Local govern-
ments have enacted smoking ordinances at an increasing rate
since 1980; more than 80 cities and counties have smoking laws
in effect.

3. Smoking at the workplace is regulated by a combination of
government action and private initiative. Legislation in 12
States regulates smoking by government employees, and 9
States and over 70 communities regulate smoking in the
private sector workplace. Approximately 35 percent of busi-
nesses have adopted smoking policies. The increase in work-
place smoking policies has been a trend of the 1980s.

4. Smoking policies may have multiple effects. In addition to
reducing environmental tobacco smoke exposure, they may
alter smoking behavior and public attitudes about tobacco use.
Over time, this may contribute to a reduction of smoking in the
United States. To the present, there has been relatively little
systematic evaluation of policies restricting smoking in public
places or at the workplace.

5. On the basis of case reports and a small number of systematic
studies, it appears that workplace smoking policies improve air
quality, are met with good compliance, and are well accepted
by both smokers and nonsmokers. Policies appear to be
followed by a decrease in smokers' cigarette consumption at
work and an increase in enrollment in company-sponsored
smoking cessation programs.

6. Laws restricting smoking in public places have been imple-
mented with few problems and at little cost to State and local
government. Their impact on smoking behavior and attitudes
has not yet been evaluated.

7. Public opinion polls document strong and growing support for
restricting or banning smoking in a wide range of public places.
Changes in attitudes about smoking in public appear to have
preceded legislation, but the interrelationship of smoking
attitudes, behavior, and legislation are complex.

324


APPENDIX


APPENDIX

The Comprehensiveness Index of State Laws

To permit comparisons over time, an index of the comprehen-
siveness of each State's smoking law was created. Laws were
classified on the basis of the number and nature of places where
smoking was restricted or prohibited. The overall principle was that
stronger measures are those that reduce exposure to ETS to the
greatest degree. More comprehensive laws were considered to be
those that restrict smoking in a larger number of public places,
extend to privately owned facilities, and cover places where individu-
als spend a large amount of time.

Laws regulating smoking in private worksites were considered to
be the the most comprehensive, and States with such laws were
assigned the extensive category. Because individuals spend more
time at work than in any other place outside the home, worksite
legislation has the potential for marked reductions in public
exposure to involuntary smoking. Worksite laws also represent an
extension of legislation to the private sector, considered a further
evidence of their comprehensiveness. Nine States are categorized as
having extensive restrictions; the average number of public places
covered by their legislation was 11.0.

The next most stringent category, moderate, was assigned to
States that regulated smoking in restaurants. Restaurants were
chosen because they represent privately owned public places and
because laws covering them have been controversial to enact. It was
felt that States regulating restaurants but not the private workplace
had moderately comprehensive restrictions. The 10 States in this
category also regulated smoking in a large number of public places
(9.5).

The last two categories, nominal and basic, were defined for States
that did not regulate smoking in restaurants or in the private
workplace. They differed in the number of public places covered.
States restricting smoking in one to three public places were
considered to have nominal restrictions. Those restricting smoking
in four or more public places were classified as basic.

327


This number of public places covered by smoking restrictions
increases with increasing comprehensiveness of categories.

                        Mean number of
               Number of
    Category     States   pull;;e;~
      Extensive       9           11.0
      Moderate
      Basic    ::     E
      Nominal             1:4
    No policy   i           0

For the calculation of the comprehensiveness index, categories
were weighted as follows:

Category    Weight
Extensive      1.00
Moderate       .75
Basic         50
Nominal        .25
No policy       .oo

328


References

ACTION ON SMOKING AND HEALTH. Statewide No Smoking Laws Enacted by
State Legislatures. Washington, b.C., Action on Smoking and Health, 1986.
ADDISON, R. New England Baptist Hospital Project, 1983-1984. B&on, Clean Indoor
Air Educational Foundation, September 1984.
AMA COUNCIL ON SCIENTIFIC AFFAIRS. Nonsmoking in hospitals. Connecticut
Medicine 48(5):297-305, May 1984.

AMERICAN ACADEMY OF PEDIATRICS, COMMI'l-l'EE ON ENVIRONMENTAL
HAZARDS. Involuntary smoking: A hazard to children. &&&tics 77(5):755-757,
May 1986.

AMERICAN COLLEGE OF PHYSICIANS. Cigarette Abuse Epidemic. (unpublished
position paper). January 28,1986.

AMERICAN HOSPITAL ASSOCIATION. A Resource to Assist Hospitals in Develop
ing Policies on Smoking. Chicago, American Hospital &sociation, 1962.
AMERICAN LUNG ASSOCIATION. Creating Your Company Policy. New York,
American Lung Association, 1985a.

AMERICAN LUNG ASSOCIATION. Taking Executive Action. New York, American
Lung Association, 1985b.

AMERICAN LUNG ASSOCIATION OF SAN DIEGO. why Smoking Doesn't Work for
Business. The Facts. American Lung Association of San Diego, 1984.
AMERICANS FOR NONSMOKERS' RIGHTS FOUNDATION. California city and
county ordinances. In: Appendix of Legislative Approaches to a Smoke Free Society.
Berkeley, Americans for Nonsmokers Rights Foundation, 1986.
ANDREW& J.L., Jr. Reducing smoking in the hospital: An effective model program.
Chest 84(2):206-209, August 1983.

BAILEY, A. Fewer Connecticut high schools allowing smoking. Connecticut Health
Bulletin 97(4):28&281,1983.

BARR, S.H., LAMBERT, C.A. Smoking regulation in restaurants and healthxare
facilities. (letter). New England Journal of Medicine 306(13):812, April 1, 1982.
BEARG, D.W. 1984 Follow-up Study of Measurements of Respimble Particulates
Genemted From Tobacco Smoke at the New England Baptist Hospital. Life Energy
Associates, August 1984.

BENNFIT, D., LEVY, B.S. Smoking policies and smoking cessation programs of large
employers in Massachusetts. American Journal of Public Health 70(6):629-631,
June 1980.

BERMAN, E.J., RICHARDS, J.W., Jr., FISCHER, P.M., CRETEN, D.A. Tobacco in
hospitals. (letter). Journul of the American Medical Association 254(24):3420,
December 27,1985.

BERTELSEN, J., STOLBERG, C. The hospital's role in smoking prevention: A survey.
Massachusetts Journal of Community Health 20-21, Spring 1981.
BIENER, L., ABRAM& D.B., ROLLICK, M.J., MacNULW, D., DEAN, L. Effects of a
Restrictive Smoking Policy on Hospital Employees. Paper presented at the Society
of Behavioral Medicine, San Francisco, March 1986.
BRESLOW, L. Control of smoking from a public policy perspective. Annual Review of
Public Health 3:129-151,1982.

BUREAU OF NATIONAL AFFAIRS, INC. Where There's Smoke: Problems and
Policies Concerning Smoking in the Workplace. Washington, D.C., Bureau of
National Affairs, Inc., 1986.

DARTNELL'S BUSINESS. Smoking still not policy issue in most offices. Dartnell's
Business 1980 1(4):37-40, June 1980.

DAWLEY. H.H., Jr., BALDWIN, J. The control of smoking: Smoking rate in
designated smoking and no-smoking areas. International Journal of the Addictions
18(7):103%1038,1983.

DAWLEY, H.H., BURTON, MC. Smoking control in a hospital setting. Addictive
Behaviors 10(4):351-355.1985.

329


DAWLEY, H.H., Jr., CARROL, SF., MORRISON, J.E. The discouragement of
smoking in a hospital setting: The importance of modeled behavior. International
Journal ofthe Addictions l&5):905-910,198l.
DAWLEY, H.H., Jr., MORRISON, J., CARROL, S. Compliance behavior in a hospital
setting: Employee and patients' reactions to no-smoking signs. Addictive Behaviors
5(4):32%331, 1980.

DAWLEY, H.H., Jr., MORRISON J., CARROL, S. The effect of differently worded ne
smoking signs on smoking behavior. International Journal of the Addictions
l&8):1467-1471,1981.

DES MOINES REGISTER. Most Iowans won't challenge smokers: Poll. Des Moines
Sunday Register, July 26.1981.

DILLOW, C. Thank you for not smoking: The hundred year war against the cigarette.
American Heritage 32(2):99-107, 1981.

DOYLE, N.C. State and municipalities regulate smoking in work, public places.
Business and Health 2(1):12, November 1984.
ERIKSEN. M. Workplace smoking control: Rationale and approaches. Advances in
Health Education and Promotion. Vol. 1, in press
ERNSTER, V.L., WILNER, S.I. Nonsmoking policies in hospitals. Journal of Public
Health Policy 6(2):197-203, June 1985.

FELDMAN, J., HUANG, S.. LYMAN, J., SOBECK, E. The Legal Aspects of Smoking
Regulation. Stanford, Stanford Environmental Law Society, May 19'78.
FIELDING, J.E. Effectiveness of employee health improvement programs. Journal of
Occupational Medicine 24(11):907-916, November 1982.
FIELDING, J.E. Banning worksite smoking. American Journal of Public Health
76(8):957-959, August 1986.

GALLUP ORGANIZATION. Smoking in America: Public attitudes and behavior.
Gallup Opinion Index 155:1-30, June 1978.
GALLUP ORGANIZATION. Survey of Attitudes Toward Smoking. Princeton, Gallup
Organization, April 1983.

GALLUP ORGANIZATION. Monthly Report on Eating Out. Princeton, Gallup
Organization, January 1984.

GALLUP ORGANIZATION. Survey of Attitudes Toward Smoking. American Lung
Association survey. Princeton, Gallup Organization, July 1985.
GRITZ, E.R. Smoking behavior and tobacco abuse. In: Mello, N.K. 6x0. Advances in
Substance Abuse: Behavioral and Biological Research. A Research Annual, Vol. 1.
Greenwich, Connecticut, JAI Press, 1980, pp. 91-158.
GROUP AGAINST SMOKING POLLUTION. Guide to a Smoke-Free Workplace. New
York, GASP, 1985.

HANAUER, P., BARR G., GLANTZ, S.A. Zxgisla~iue Approaches to a Smoke-Free
Society. Berkeley, Americans for Nonsmokers' Rights Foundation, 1986.
HARRIS ORGANIZATION. Prevention Index 85: A Report on the Nation's Health.
Emmaeua, Pennsylvania, Rodale Press, 1985.
HOLLANDER-COHEN ASSOCIATES. Sun Poll. Baltimore Sun, October 1984.
HUMAN RESOURCES POLICY CORPORATION. Smoking Policies in Large Corpora-
tions. (unpublished report), 1985.

IGLEHART, J.K. The campaign against smoking gains momentum. New England
Journal of Medicine 314(16):1059-1064, April 1986.
JONES, L.D. Advancing the role of hospitals in reducing smoking. In: Proceedings of
the National Conference on Smoking or Health. New York, American Cancer
Society, 1981.

KELLY, N.R., COHEN, F.L. Smoking policies in U.S. hospitals: Current status.
Preventive Medicine 8(5):557-561, 1979.
KO'M'KE, T.E., KNAPP, J., SILVIS, G., SORENSEN, G. Clean Air Health Care: A
Guide to Establish Smoke-Free Health Care Facilities. Minneapolis, University of
  Minnesota. 1986.

330


KRISTEIN, M.M. HOW much can business expect to profit from smoking cessation?
Preventive Medicine 12(2):358-381, March 1983.
KRISTEIN, M.M. Wanted: Smoking policies for the workplace. Business and Health,
pp. 14-17, November 19&i.

LEFCOE, N.M., ASHLEY M.J., PEDERSON L.L., KEAYS, J.J. The health risks of
passive smoking: The growing case for control measures in enclosed environments.
Chest 84(1):9&95, July 1983.

LEHMAN, B.A. Cambridge may limit restaurant smoking. Boston Globe, April 23,
  1984.

LICHTENSTEIN, E., DANAHER, B.G. What can the physician do to assist the patient
to stop smoking? In: Brashear, R.E., Rhodes, M.L. (eds). Chronic Obstructive Lung
Disease: Clinical Treatment and Management. St. Louis, C.V. Mosby, 1978, pp. 227-
241.

LINNELL, R.H. Survey: No-smoking rooms here to stay. Hotel and Motel Munuge-
ment 201(7):1-18, May 19,1986.

LINSON, C.J. Evaluation of Ten Workplace Smoking Regulations in California.
Cambridge, Massachusetts, Harvard University, Institute for the Study of Smok-
ing Behavior and Policy, May 30,1986.

LOS ANGELES TIMES. Hilton chain accomodating nonsmokers. Los Angeles Times,
March 2.1986.

MARTIN, M.J. The San Francisco experience with regulation of smoking in the
workplace: The first twelve months. American Journal of Public Health 76(5):585-
586, May 1986.

MARVIT, R.C., RIGNEY, K.B., YOST, F.N. A good neighbor policy: Controlled
smoking areas and health department attitudes. Hawaii Medical Journal 3%1):7-
10, January 1980.

MEADE, T.W., WALD, N.J. Cigarette smoking patterns during the working day.
British Journal of Preventive and Social Medicine 31(1):25-29, March 1977.
MICHIGAN TOBACCO AND CANDY DISTRIBUTORS AND VENDOR ASSOCIA-
TION. Economic impact of instituting smoking prohibitions in Michigan. In:
Joffman K.B., ted). Study: Ban on smoking expensive. Lansing, Michigan, State
Journal, February 4,1986.

MINNEAPOLIS TRIBUNE. Minnesota poll. Minneapolis Tribune, April 15,1973.
MINNEAPOLIS TRIBUNE. Minnesota poll. Minneapolis Tribune, April 7,1974.
MINNEAPOLIS TRIBUNE. Minnesota poll. Minneapolis Tribune, January 18, 1976.
MINNEAPOLIS TRIBUNE. Minnesota poll. Minneapolis Tribune, June 25,1978.
MINNEAPOLIS TRIBUNE. Minnesota poll. Minneapolis Tribune, May 11,198O.
MINNESOTA STATUTES ANNUAL, Chapter 211 L.1975, Sections 144.41-144.417,
(West Supplement) 1985.

NAIMARK, R.E. Toward a Smoke-Free Environment: Smoking Policy for Massachu-
setts State Facilities. (unpublished manuscript). Cambridge, Massachusetts, Har-
vard University, Institute for the Study of Smoking Behavior and Policy, April
1986.

NATIONAL INTERAGENCY COUNCIL ON SMOKING AND HEALTH. Smoking
and the Workplace: A National Survey. (unpublished manuscript). 198Oa.
NATIONAL INTERAGENCY COUNCIL ON SMOKING AND HEALTH. Smoking
and the workplace: A national survey. Occupational Health and Safety 4%5):31-32,
May 1980b.

NATIONAL RESTAURANT ASSOCIATION. How Consumers Make the Decision to
Eat Out. (survey). Washington, D.C., National Restaurant Association, August
  1982.

NATIONAL RESTAURANT ASSOCIATION. NRA Pocket Fact Book 1985-1986.
Washington, D.C., National Restaurant Association, 1986.
NEW YORK TIMES. San Francisco officials cite success with law. Neul York Times,
April 13, 1986.

331


NEW YORK TIMES. Order by Koch limits smoking in city buildings. New York
Times, June 26.1986.

NEW YORK TIMES. Plan to restrict smoking in NYC faces considerable opposition.
New York Times, July 6,1986.

NUEHRING, E., MARKLE, G.E. Nicotine and norms: The reemergence of a deviant
behavior. Social Problems 21(4):513-526, April 1974.
OFFICE OF TECHNOLOGY ASSESSMENT. Smoking in the Workplace: Selected
Issues. U.S. Congress, Offtce of Technology Asaessment, May 1986.
OLSHANSKY, S.J. Is smoker/nonsmoker segregation effective in reducing passive
inhalation among nonsmokers? American Journal of Public Health 72(7):737-739,
July 1982.

O'MALLEY, P.M., BACHMAN, J.G., JOHNSTON, L.D. Period, age, and cohort effecta
on substance use among American youth, 197-2. American Journal of Public
Health 74(7M82-633, July 1984.

ONTARIO RESTAURANT AND FOOD SERVICES ASSOCIATION. A Restaurateur's
Guide for Establishing a No-Smoking Section. Ontario Restaurant and Food
Services Association, 1985.

ORLEANS, C.S., SHIPLEY, R.H. Work&e smoking cessation initiatives: Review and
recommendations. Addictioe Behaviors 7(1):1-16,1982.
ORLEANS, CT., PINNEY, J. Nonsmoking in the Workplace: A Guide for Employers.
Washington, D.C., Center for Corporate Public Involvement, 1984.
ORLEANS, C.T. Evaluation Research Design for Worksite No-Smoking Policies and
Progmms. Paper presented at the National Cancer Institute Conference, April
  1986.

PACIFIC TELEPHONE. Employee Smoking Study. Project No. 8263. Pacific Tele-
phone, Corporate Research Division, Human Resources Administration, January
  1983.

PARK RECORD. Study shows Park City restaurants are ignoring no smoking area
laws. Park Record, Park City, Utah, June 13,1985.
PETERSEN, D.J., MASSENGILL, D. Smoking regulations in the workplace: An
update. Personnel, pp. 27-31, May 1986.

PROCHASKA, J.O.. DiCLEMENTE, C.C., VELICER, W.F. Predicting change in
smoking status for selfchangers. Addictive Behaviors 10(4):39-, 1985.
RANDOLPH, F.L. The Regulation of Smoking in Public Places: Predictors of
Compliance and Voluntary Enforcement Behavior. IIoctoral Dissertation, Universi-
ty of California, Berkeley, 1982,280 pp.

RASHAK, N.E., OLSEN, L.K., SPEARS, A.K., HAGGERTY, J.M. Smoking policies of
secondary schools in Arizona. Journal of School Health 56(5):180-183, May 1986.
REPACE, J.L., LGWREY A.H. A quantitative estimate of nonsmokers' lung cancer
risk from passive smoking. Enuironment Znternational11:3-22,1985.
RHOADES, E.R., FAIRBANKS, L.L. Smoke-free facilities in the Indian Health
Service. (letter). New England Journal of Medicine 313(24):1548, December 12,
  1985.

RIGO'ITI, N.A., HILL PIKL, B., CLEARY, P., SINGER, D.E., MULLEY, A.G. The
impact of banning smoking on a hospital ward: Acceptance, compliance, air quality
and smoking behavior. (abstract). Chnical Research 34(23:833A, April 1986.
ROBERT FINNEGAN ASSOCIATES. Smoking Policy Preferences of Employees of New
England Telephone: An Employee Opinion Research Suruey. (unpublished report).
April 1985.

ROPER ORGANIZATION. A Study of Public Attitudes Toward Cigarette Smoking
and the Tobacco Industry in 1978. Roper Organization, May 1978.
ROSENSTOCK, I.M., STERGACHIS, A., HEANEY, C. Evaluation of smoking
prohibition policy in a health maintenance organization. American Journal of
Public Health 76(83:1014-1015, August 1986.

332


SANDELL, S.D. The campaign for clean air indoors. Business and Health, pp. 19-21,
November 1984.

SEFFRIN, J.R., BRASHEAR, R.E., SHIRELEY, L.A. A statewide survey of hospital
policy and practice concerning cigarette sales. American Review of Respimtory
Disease 11&6):1105-1107, December 1978.

SHANNON, A.R. Smoking cessation program survey. Pacific Northwest Bell Business
Research, June 1986.

SHIPLEY, R.H., ORLEANS, C.S. Treatment of cigarette smoking. In: Boudewyns,
P.A., Keefe, F.J. (eds). Behavioral Medicine in Genemi Medical Practice. New
York, Addison Wesley, 1982, pp. 237-268.

SHOR, R.E., WILLL4MS, D.C. Normative beliefs about tobacco smoking on campus in
relation to an exposition of the viewpoint of the nonsmokers' rights movement.
Journal of Psychology 100(2nd halfJ:261-274, November 1978.
SOBEL, R. They Satisfy: The Cigarette in American Life. New York, Anchor
Press/Doubleday, 1978.

SOLOMON, L.C. The other side of the smoking worker controversy. Personnel
Administmtor 2fK3):72-73, March 1983.

SORENSEN, G., PECHACEK, T. Support for Nonsmoking Policies Among Employed
Smokers. (unpublished manuscript). August. 1.1986.
SORENSEN, G., PECHACEK, T., PALLONEN, U. Occupational and worksite norms
and attitudes about smoking cessation. American Journal of Public Health
76(5):544-549, May 1986.

THOMAS, E.G. Committee of 500 report. Smoking in the office: A burning issue.
Management World X4):11-12, April 1980.

TRI-AGENCY TOBACCO FREE PROJE(;T. State Legislated Action on Clean Indoor
Air Act. New York, American Cancer Society, American Lung Association,
American Heart Aascciation, February 1986.

UNIVERSITY OF CALIFORNIA SURVEY RESEARCH CENTER. California Poll.
Berkeley, University of California, July, September, October 1984.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE. Ad& Use of
Tobacco, 1970. DHEW Pub. No. (HSMj73-8727. U.S. Department of Health,
Education, and Welfare, Public Health Service, Center for Disease Control,
National Clearinghouse for Smoking and Health, June 1973.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE. Adult Use of
Tobacco, 1975. U.S. Department of Health, Education, and Welfare, Public Health
Service, Health Services and Mental Health Administration, National Clearing-
house for Smoking and Health, June 1976.

U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE. Use of Tobacco,
Practices, Attitudes, Knowledge, and Beliefs, United States: Fall 1964 and Spring
1966. U.S. Department of Health, Education, and Welfare, Public Health Service,
Health Services and Mental Health Administration, National Clearinghouse for
Smoking and Health, July 1969.

U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE. Krasnegor, N.A.
(ed). Cigarette Smoking as a Dependence Process. NIDA Research Monograph 23.
DHEW Pub. No. (ADMl79-800. U.S. Department of Health, Education, and
Welfare, Public Health Service, Alcohol, Drug Abuse and Mental Health Adminis-
tration, National Institute on Drug Abuse, January 1979.

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Conse-
quences of Smoking for Women A Report of the Surgeon General. U.S. Department
of Health and Human Services, Public Health Service, Office of the Assistant
Secretary for Health, Office on Smoking and Health, 1980.

333


U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Conse-
quences of Smoking: Cardiovascular Disease. A Report of the Surgeon General.
DHHS Pub. No. (PHSl82-50179. U.S. Department of Health and Human Services,
Public Health Service, Office of the Assistant Secretary for Health, Office on
Smoking and Health, 1982.

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Conse-
quences of Smoking: Chronic Obstructive Lung Disease. A Report of the Surgeon
Geneml. DHHS Pub. No. (PHSl84-50205. U.S. Department of Health and Human
Services, Public Health Service, Office of the Assistant Secretary for Health, Of&e
on Smoking and Health, 1984.

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. A Decision Maker's
Guide to Reducing Smoking at the Worksite. U.S. Department of Health and
Human Services, Public Health Service, Office on Smoking and Health, 1985a.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. LegisZatiue Overview.
U.S. Department of Health and Human Services, Public Health Service, Office of
the Assistant Secretary for Health, Office on Smoking and Health, 198513.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Cmse-
quences of Smoking: Cancer and Chronic Lung Disease in the Workplace. A Report
of the Surgeon Geneml. DHHS Pub. No. (PHSl85-50207. U.S. Department of Health
and Human Services, Public Health Service, Office on Smoking and Health, 1985c.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. National Survey of
Worksite Health Promotion Activities. U.S. Department of Health and Human
Services, Office of Disease Prevention and Health Promotion, 1988.
U.S. PUBLIC HEALTH SERVICE. Smoking and Health: Report of the Advisory
Committee to the Surgeon General of the Public Health Service. PHS Pub. No. 1103.
U.S. Department of Health, Education, and Welfare, Public Health Service, Center
for Disease Control, 1984.

VETTEL, P. The don't butt inn: Hotels now cater to nonsmokers. Chicago Tribune,
February 23,1986.

WALSH, D.C. Corporate smoking policies: A review and an analysis. Journal of
Occupational Medicine 26(1):17-22, January 1984.
WALSH, D.C., GORDON, N.P. Legal approaches to smoking deterrence. Annual
Review of Public Health 7:127-149,1986.
WARNER, K.E. Cigarette smoking in the 1970's: The impact of the antismoking
campaign on consumption. Science 211(4483):729-731, February 13,198la.
WARNER, K.E. State legislation on smoking and health: A comparison of two policies.
Policy Sciences 13:139-152,198lb.

WARNER, K.E. Regional differences in State legislation on cigarette smoking. Texas
Business Review 56(1):27-29, January-February 1982.
WARNER, K.E., ERNSTER, V.L., HOLBROOK, J.H., LEWIT, E.M., PERTSCHUK,
M., STEINFELD, J.L., WHELAN, E.M. Public policy on smoking and health:
Toward a smoke-free generation by the year 2000. Circulation 73(2):381Aa95A,
February 1988.

WARNER, K.E., MURT, H.A. Impact of the antismoking campaign on smoking
prevalence: A cohort analysis. Journal of Public Health Policy 3(4):374-390,
December 1982.

WEIS, W.L. Can you afford to hire smokers? Personnel Administmtor 26(5):71-78,
May 1981.

WINDSOR, R.A., BARTLETT, E.E. Employee self-help smoking cessation programs: A
review of the literature. Health Education Quarterly 11(4):349359, Winter 1984.
ZIADY, M. A smoke-free workplace: Clearing the air at Pacific Northwest Bell. Good
Health, Good Business (1):1,1988.

334


INDEX

Environmental Tobacco Smoke is abbreviated as ETS throughout this index.

ABSORPTION
biological markers for ETS, 200-
   208

biological markers of smoke absorp
tion in smokers and nonsmokers,
181

RTS vs. active smoking, compari-
son, 215-216

nicotine, tobacco smoke exposure
determination, 203-205

ACROLEIN

measurement under realistic condi-
tions (table), 148

ADOLESCENTS
regulations in schools to prevent
  smoking initiation, 282

AEROSOLS

mainstream smoke, particle size
measurement during laboratory
smoking, 182-183, 186
monodisperse vs. polydisperse, af-
fect on respiratory tract deposi-
tion, 181-182

regional deposition in respiratory
tract, smoke particle size as fac-
tor, 189, 191-192
sidestream smoke, mass median di-
ameter effect on deposition in
respiratory tract, 187

AGE FACTORS
respiratory effects of involuntary
  smoking in infants and children,
   42-44

AIR POLLUTION
(See also ENVIRONMENTAL TO-
  BACCO SMOKE)
hospital smoking policies, assess-
  ment of effect, 311

ALDEHYDES

irritant in ETS, 229

AMMONIA

irritant in ETS, 229

AROMATIC AMINES
sidestream smoke levels higher
  than in mainstream smoke, 14

AROMATIC HYDROCARBONS
measurement under realistic condi-
  tions (table), 149-150

ASTHMA

&e also RESPIRATORY TRACT
DISEASES)

children, maternal smoking as risk
factor, 55-58

pulmonary function in adult asth-
matics exposed to cigarette
smoke, 63, 65

ATTITUDES

public attitudes and social norms,
cigarette consumption relation
ship, 321

public knowledge and attitudes
about smoking, assessment by
surveys, 307

public toward smoking, conclusions
of 1986 report, 324
review of impact of smoking re-
strictions, 319-320
smokers on cessation or reduction,
restrictions and social norms as
factors, 305

BEHAVIOR, HUMAN
(See also SMOKING CHARACTER-
  ISTICS; SMOKING HABIT)
anticipated changes by smokers to
  workplace regulations, 312
assessment of impact of smoking
  policies on smokers, 307

335


INDEX

BEHAVIOR, HUMAN-Contd.
bans on smoking, effect on behav-
  ior of smokers, 16
direct and indirect effects of smok-
  ing policies, 304
hospital employees, smoking behav-
  ior before and after policy im-
  plementation, 315
hospital patients and employees,
  current evidence of smoking pol-
   icies, 308-309

nonsmoking as normative behavior,
reinforcement with smoking poli-
cies, 304

reduction or cessation of smoking,
indirect effect of smoking poli-
cies, 304-305

research recommendations, effect of
smoking restrictions, 322
review of impact of smoking re-
strictions, 320-321
smoking policy impact, evaluation,
306

BIOASSAY

chemical assays for human expo-
sure to cigarette tar components,
206, 217

cotinine levels as measure of nic-
otine absorption, 205206
nicotine in blood for exposure de-
termination, feasibility, 205

BIRTH WEIGHT
maternal smoking as risk factor, 6

BLOOD

cotinine level as marker for ETS
exposure in nonsmokers, 36
cotinine levels as measure of nic-
otine absorption in nonsmokers,
205-206

cotinine levels in ETS-exposed non-
smokers vs. active smokers (ta-
ble), 211-214

nicotine and cotinine levels to
quantify ETS exposure. 208
nicotine levels in ETS-exposed non-
smokers vs. active smokers (ta-
ble), 209-210

nicotine levels in nonsmokers vs.
smokers, 216
white blood cell counts in smokers
vs. nonsmokers, 244

336

BRAIN CANCER
(See also CANCER 1
ETS exposure as risk factor, 102,
   104

BREAST CANCER
(See also CANCER I
spousal smoking as risk factor, 102

BRONCHITIS

(See also RESPIRATORY TRACT
DISEASES)

children, involuntary smoking rela-
tionship, longitudinal studies, 38,
42

children of smokers, conclusions
about risk, 106

infants and children, parental
smoking as risk factor, 10

CANCER

(See also BRAIN CANCER;
BREAST CANCER; CERVICAL
CANCER; LUNG CANCER; RES-
PIRATORY TRACT CANCER)
carcinogenesis, initiators and prc+
moters in tobacco smoke, 28
carcinogens in ETS as risk factors,
135

children, parental smoking as risk
factor for cancers other than
lung cancer, 102-105
ETS exposure risk, 102-104
involuntary smoking relationship
requires further investigation, 14
smoking as major risk factor, 6

CARBON MONOXIDE
acute toxicity in animals as factor
  in smoke carcinogenicity testing,
   247

biological marker for ETS absorp-
tion, 201-202

ETS exposure measurement, lack
of specificity as limitation, 202
involuntary smoking exposure may
be more constant than active
smoking, 202

lung deposition kinetics as factor
in temporal variation in concen-
tration, 201-202
measurement under realistic condi-
tions (table), 151-154
sidestream smoke vs. mainstream
smoke, 129


INDEX

CARBON MONOXIDE--Contd.
workplace level, contribution of to-
  bacco smoke, 232

CARBOXYHEMOGLOBIN LEVELS
biological marker for carbon mon-
  oxide exposure, 202

CARCINOGENESIS
initiators and promoters of cancer
  in tobacco smoke, 28
tumor induction in animal tissues
  with cigarette smoke condensate,
   249-250

CARCINOGENS
environmental vs. mainstream
  smoke, 134-135, 137
ETS vs. mainstream smoke in in-
  door environments (table), 136
human and animal, definition, 135,
   137

mainstream and sidestream smoke,
23-24

sidestream and ETS, 251-252

CARDIOVASCULAR DISEASES
ETS exposure as factor not estab
  lished, 10-11

involuntary smoking as risk factor,
conclusions, 107-108
involuntary smoking relationship
requires further investigation, 14
nonsmokers, prospective and case-
control studies, 105-106

CASE-CONTROL STUDIES
(See also EPIDEMIOLOGICAL
  STUDIES)

cardiovascular disease risk, 105-106
lung cancer risk, 97-98
lung cancer risk in exposed non-
smokers, Hong Kong study, 80-

81

lung cancer risk in spouses of
smokers, Louisiana study, 79-80
lung cancer risk in wives of smok-
ers, Greek study, 78-79
lung cancer risk relationship, Four
Hospitals study, 84-86
lung cancer risk relationship, Ger-
man study, 90

lung cancer risk relationship, Japa-
nese study, 88-89
lung cancer risk relationship,
Swedish study, 89-90

CASE-CONTROL STUDIES
lung cancer risk relationship, Unit-
  ed Kingdom study, 86-88
respiratory disease risk in children,
   43-44

CELLS

inflammatory cell number and
function in smokers, inferences
for involuntary smokers, 244-245
inflammatory, experimental models
of cigarette smoke inhalation,
245-246

inflammatory, need to determine
  effect of ETS exposure, 252
CELLS, EPITHELIAL
chronic ETS exposure, inferred risk
  in nonsmokers, 240-241
ETS exposure effect, research need-
  ed, 252

hyperplasia, loss of cilia, nuclear
atypia, smoking habit relation-
ship, 239-240

CERVICAL CANCER
(See also CANCER)
spousal smoking as risk factor, 102

CESSATION OF SMOKING
public attitudes and smoking poli-
  cies as indirect influences, 304-
   305

research recommendations on effect
of smoking restrictions, 322
workplace programs as part of
smoking control, 297
workplace programs, survey data,
294
workplace smokers motivation and
success, smoking policies as fac-
tor, 313-315

CESSATION OF SMOKING,

METHODS
workplace program, smoking policy
  implementation effect on partici-
  pation, 314-315

CHEMICAL ANALYSIS
sidestream vs. mainstream smoke.
   127

CHILDREN
asthma, maternal smoking as risk
  factor, 55-58
brain tumors, maternal smoking as
   factor, 104

337


INDEX

CHILDREN-Contd.
bronchitis, involuntary smoking re-
  lationship, longitudinal studies,
  38, 42

cancer risk other than lung cancer,
parental smoking as risk factor,
102-105

cough, phlegm, and wheezing, pa-
rental smoking as risk factor,
44, 47-49

ETS exposure, determinants, 12
ETS exposure, reported irritation,
239

health risks of ETS exposure, con-
clusions, 107

health risks of involuntary smok-
ing, summary and conclusions of
1986 report, 12-13
leukemia, maternal smoking during
pregnancy as factor, 103
lung cancer risk, parental smoking
as tactor, 96-91

lung function, information needed
on relationship with ETS expo-
sure, 32
lung function, involuntary smoking
risk relationship (table). 50-52
lung function, maternal smoking
relationship, 49, 53-54
lung function, parental smoking as
factor, 13, 107
middle ear effusions and diseases,
parental smoking risk relation-
ship, 58-59
respiratory diseases, involuntary
smoking relationship (table), 39-
  41
respiratory diseases, parental smok-
ing as risk factor, 10, 13, 4-4
respiratory function tests. maternal
smoking as factor, 53
respiratory symptoms in children
of smokers, 13
respiratory symptoms, relationship
with involuntary smoke exposure
(table), 45-46
respiratory system effects of invol-
untary smoking, 37-59
saliva cotinine concentrations, in-
fluence of parental smoking,
  207-208

338

CIGARETTE EQUIVALENTS
calculation of individual constitu-
  ents needed to determine disease
  risk, 199-200

involuntary smoking toxicity esti-
mation, mathematical modeling,
198-200

CIGARETTE SMOKE
(See also ENVIRONMENTAL TG-
  BACCO SMOKE, MAINSTREAM
  SMOKE; SIDESTREAM SMOKE;
  SMOKE STREAMS; TOBACCO
   SMOKE)

aerosol, suspension of particles in a
gaseous or vapor medium, 181
animal models of carcinogenicity,
247-249

carcinogenicity, condensate bioassay
as alternative to smoke expo-
sure, 24%250

carcinogenicity demonstrated in an-
imal models, 252
carcinogenicity testing in animals,
nicotine and carbon monoxide
toxicity as factor, 247
BTS in public places, major source,
128

inflammatory cell function, experi-
mental models of inhalation ef-
fect, 245-246

particulate mass deposited in respi-
ratory tract, 193, 198
particulate phase constituents, side-
stream to mainstream ratio (ta-
ble), 130-131

regional deposition in respiratory
tract, particle size as factor, 189,
191-192
total suspended particulates gener-
ated under laboratory conditions
(table), 197
toxic and carcinogenic agents in in-
door environments (table), 136
unfiltered cigarette, comparison of
mainstream and sidestream
smoke (table), 128
vapor phase constituents, side-
stream to mainstream ratio tta-
ble), 130-131

CIGARRTTRS
nonfiltered. vapor and particulate
  phase smoke components (table).
   130-131


INDEX

COMBUSTION TEMPERATURE
mainstream and side&ream smoke,
  effect on composition, 24
sidestream vs. mainstream smoke
  generation, effect on component
  levels, 128-129

COTININE

biological marker for EXS absorp
tion, 35-36, 200
blood levels in nicotineinjected vs.
smoke-exposed nonsmokers, 215
216

body fluid level as marker for
smoke exposure in nonsmokers,
8

body fluid levels in nonsmokers as
measure of nicotine absorption,
205

body fluid levels in nonsmokers to
establish lung cancer risk, 95
body fluid levels increase with re-
ported El'S exposure, 15, 217
RTS exposure marker of choice in
epidemiological studies, 217
EX'S exposure marker under real-
life conditions, 207
EI'S exposure quantification, 208,
215

nicotine absorption estimation, 205-
206
plasma, urine, saliva concentra-
tions, correlation, 205
plasma, urine, saliva levels in ETS
exposed nonsmokers vs. active
smokers, 211-214
urinary levels in KTSexposed vs.
nonexposed men, 207

COUGH
(See also RESPIRATORY SYMP-
  TOMS)
children of parents who smoke, re-
  lationship, 44, 4749

EARS
middle ear effusions in children of
  smokers, 58-59, 107

EMPHYSEMA
(See akio RESPIRATORY TRACT
  DISEASES)
nonsmokers vs. smokers, 246

ENVIRONMENTAL TOBACCO
SMOKE
(See akio CIGARETTE SMOKE; IN-
  VOLUNTARY SMOKING;
  MAINSTREAM SMOKE; SIDE
  STREAM SMOKE; TOBACCO
   SMOKE)
absorption of constituents by non-
  smokers under experimental and
  natural exposure, 206-207
active smoking dose-response rela-
  tionships provide insight into
  risks, 26-28
acute exposure, irritation effects,
   229-239
acute physiological response, exper-
  imental studies, 233-239
air dilution effect on particle size
  and distribution, 134
airways hyperresponsiveness and
  other factors in response, 28
annoying and irritating effects of
  exposure, field and experimental
  studies, 231-239
assessment techniques needed of
  recent and remote exposure, 14
atmospheric markers of exposure,
   33
atmospheric vs. biological markers
  of absorption, 201
bioassays needed to determine gen-
  otoxicity, 252
biochemical markers of exposure
  during experimental and natural
  conditions, 206-207
biological markers for absorption,
   200-206
biological markers for estimating
  exposure, 141
brain cancer risk relationship, 102,
    104
cancers other than lung cancer,
  risk relationship, 102-104
carbon monoxide as biological
  marker of exposure, 201-202
carcinogen levels vs. mainstream
   smoke, 134-135, 137
carcinogenicity, 10
carcinogenicity, in vivo and in vi-
  tro experimental determination,
   247-251

339


INDEX

ENVIRONMENTAL TOBACCO
SMOKE-Cad.
cardiovascular disease risk, prospec-
  tive and case-control studies,
   105-106

chemical analysis shows spectrum
of carcinogens, 251-252
chemical composition, comparison
with mainstream smoke, 135,
137

chemical composition, complexity
as factor in exposure determina-
tion, 147

chronic exposure, inferred risk for
respiratory epithelial changes,
240-241

cigarettes as major source in public
places, 128

concentration determination, venti-
lation and other factors, 146
147, 164-165

concentration measurement, 193
concentrations in public transporta-
tion as factor in smoking restric-
tions, 278

constituents from mainstream and
sidestream smoke, 7-6
contribution to indoor air pollution,
conclusions, 169
cotinine as biological marker of ab
sorption, 35-36

cotinine as exposure marker of
choice in epidemiological studies,
217

cumulative, duration, and intensity
of exposure influences effects, 33
determinants of exposure, 11-12
disease risk estimation, value of bi-
ological markers of absorption,
2OC201

dose, product of mass in inhaled
air and deposition fraction, 193
exposure estimation, mathematical
model using "cigarette equiva-
lents", 198-200
exposure expressed as ciga-
rettes/day, variations in esti-
mates, 25-26

exposure, extrapolation of active
smoking data, 23-28
eye irritation in exposed children,
239

eye, nose, throat, respiratory sys-
  tem irritation, conclusions, 252
340

ENVIRONMENTAL TOBACCO
SMOKE-CenM.
genotoxic potential, use of short-
  term in vitro assays, 250-251
health effects, 21-106
health effects, methodological prob
  lems in assessment, 21-22
health effects of exposure, summa-
  ry, 13-14

health risk determination, assess-
ment of exposure critical, 32
health risks of exposure, conclu-
sions, 7, 107-108
human exposure, factors in estima-
tion, 139, 141-142
"individual solution" approach to
workplace smoking implies no
hazard, 298

inflammatory cell functions in
smokers, inferences for exposed
nonsmokers, 244-245
irritant components, whole side-
stream smoke vs. gas phase
only, 236238

irritant effect on allergic persons,
239

irritant effects of exposure in non-
smokers in restaurants and of-
fices, 232

laboratory, toxicological, human ex-
posure, and epidemiological in-
vestigations of hazards, 22-23
lung cancer risk, epidemiological
and case-control evidence, 97-98
lung cancer risk in exposed non-
smokers, Hong Kong case-con-
trol study, 60-61

lung cancer risk in spouses of
smokers, Louisiana case-control
study, 79-60

lung cancer risk in spouses of
smokers, Scottish study, 77-78
lung cancer risk in wives of smok-
ers, Greek case-control study,
78-79

lung cancer risk, need for more ac-
curate estimates of exposure,
102

lung cancer risk relationship, Four
Hospitals case-control study, 84-
86

lung cancer risk relationship, Ger-
man case-control study, 90
lung cancer risk relationship in
nonsmokers, 8-10


INDEX

ENVIRONMENTAL TOBACCO
SMOKE-Contd.
lung cancer risk relationship, Japa-
  nese case-control study, 88-69
lung cancer risk relationship, Los
  Angeles County study, 83
lung cancer risk relationship, pre
  liminary findings of U.S. study,
   82

lung cancer risk relationship, sum-
mary and conclusions, 96-102
lung cancer risk relationship,
Swedish case-control study, 89-
90

lung cancer risk relationship, Unit-
ed Kingdom case-control study,

lung disease risk in nonsmokers as
extrapolation of risk in smokers,
30-31

lung effects, inferences from avail-
able data, 246-247
lung function effects in nonsmok-
ers, 60, 62

lung function in children, more in-
formation needed on relation-
ship, 32

major irritants, concentrations in
mainstream and sidestream
smoke (table), 230
mass deposition in respiratory tract
estimation, 193, 198
mathematical models of lung can-
cer risk in nonsmokers, 93-96
measureable exposure in general
population of developed coun-
tries, 216

misclassification of smoking status
and exposure as factor in deter-
mining risk, 66-67, 72-73
monitoring methods to estimate ex-
posure, 164-167

nasal vs. mouth inhalation, effect
on particle deposition, 189
nicotine and cotinine in body fluids
increase with increasing expo-
sure, 15

nicotine and cotinine to quantify
exposure, 208, 215
nicotine as biological marker of ex-
posure, 202-205
nicotine as tracer, need for proper
validation in personal monitor-
ing, 168

ENVIRONMENTAL TOBACCO
SMOKE4h5td.
nicotine levels in nonsmokers may
  underestimate exposure to other
  components, 216
organic gases and aromatic com-
  pounds as indicators of exposure,
  nonspecificity, 168-169
particle size as factor in dispersion,
   169

particle size distribution and
breathing pattern effect on dose,
25

particle size facilitates rapid distri-
bution, 14

particles, number and size distribu-
tion, 137, 139

particulates, aldehydes, phenol, am-
monia, and other irritants, 229
personal monitors to measure con-
centrations preferable to area
monitoring, 166

physiochemical nature, distribution,
and estimation of human expo-
sure, 125-169

plasma and urine nicotine levels in
nonsmokers vs. intravenous nic-
otine injection, 215
plasma, urine, saliva cotinine in
exposed nonsmokers vs. active
smokers (table), 211-214
plasma, urine, saliva nicotine in
exposed nonsmokers vs. active
smokers (table), 209-210
proximity to smoke source as expo
sure factor, 141

questionnaires for estimating expo-
sure, uses and limitations, 34-35
radioactivity, 134
reduction of exposure as primary
goal of smoking regulation in
public places, 304
respirable suspended particulates in
exposed vs. nonexposed nonsmok-
ers, 169

respiratory disease risk relationship
in infants, children, adults, 10
respiratory infections in infants,
risk relationship, 31
respiratory symptoms in nonsmok-
ers, possible relationship, 31
school smoking regulations tradi-
tionally not to reduce exposure,
282

341


INDEX

ENVIRONMENTAL TOBACCO
SMOKE-Contd.
sidestream smoke as major contrib-
  utor, 186

statistical significance testing of
health risks, 36-37
summary and conclusions of 1986
report, 12-13

temporal and spatial distribution of
smokers in exposure determina-
tion, 145-146

thiocyanates as biological marker
of exposure, 202-203
time-activity patterns as determi-
nant of exposure, 142-145
time period most important deter-
minant of personal exposure, 167
total suspended particulates in in-
door working and living areas
(table), 194-196
toxic and carcinogenic agents in-
doors from nonfilter cigarettes
(table), 136

toxicity, acute irritant effects, and
carcinogenicity, 15
urinary cotinine levels in exposed
vs. nonexposed men, 207
vapor phase, retention by involun-
tary smokers, 126-127
workplace exposure, evidence of
health hazards as factor in
smoking regulations, 286
workplace, lung cancer risk in non-
smokers, 91-92

ENZYME ACTIVITY
lungs of smokers, alveolar macro-
  phages influence on protease-an-
  tiprotease balance, 242-243
polymorphonuclear elastase in
  lungs of smokers, 243
respiratory system of smoke-ex-
  posed animals, 245-246

ENZYMES
elastase, 243

EPIDEMIOLOGICAL STUDIES
(See also CASE-CONTROL STUD
  IlW
confounding variables, 36
lung cancer risk in spouses of
  smokers, 98, 101
methodological considerations, 32-
   37

342

EPIDEMIOLOGICAL STUDIES-Co&d.
questionnaires for estimating ETS
  exposure, uses and limitations,
   34-35

ETS See ENVIRONMENTAL TO-
BACCO SMOKE

EXSMOKERS

(See also NONSMOKERS1
misclassification of status and ETS
exposure as factors in determin-
ing risks, 66-67, 72-73

EYES

annoying and irritating effects of
ETS exposure, 231-239
irritation from ETS exposure, 11
irritation in ETS-exposed children,
239

nonsmokers, irritant effect of invol-
untary smoking in restaurants
and offices, 232

nonsmokers, sidestream smoke as
irritant in laboratory, ventilation
as factor, 234-235
smoke concentration vs. exposure
duration as factors in irritation,
235

tear film in ETS-exposed nonsmok-
ers, experimental study, 234

FETUS

maternal smoking, effect of expo
sure to tobacco smoke constitu-
ents, 31-32

GAS PHASE, CIGARETTE SMOKE
activity in in vitro assays, 251
irritation in nonsmokers vs. whole
  sidestream smoke, 236-238

HOSPITALS

(See akio PUBLIC PLACES)
air quality, effect of smoking poli-
cies, 311

cessation of smoking programs, ef-
fect, 314-315

employee attitudes and approval of
smoking policies, 311312, 315
lung cancer cas+control study in
four hospitals, 84-86
smoking policies, positively worded
signs and enforcement factors in
compliance, 310

smoking policies, review of current
evidence on impact, 308-309


INDEX

HOSPITALS-Co&d.
State legislation restricting smok-
  ing, 269

IMMUNE SYSTEM
cigarette smoking effects, 244

INFANTS

respiratory diseases, parental smok-
ing as risk factor, 10
respiratory system effects of invol-
untary smoking, 38-59
time-location patterns, 144
tracheobronchial smoke particle de-
position, mathematical model
prediction, 192

INVOLUNTARY SMOKING
(See also ENVIRONMENTAL TO-
  BACCO SMOKE; NONSMOK-
  ERS)

absorption vs. active smoking, 215
216

absorption of constituents under
experimental and natural expo-
sure, 206-207

adult asthmatics, lung function ef-
fects, 63, 65

allergic persons, irritant effect, 239
assessment of nonsmoker's expo-
sure, 307

atmospheric vs. biological markers
of ETS absorption in disease
risk estimation, 200-201
bronchoconstriction and asthma in
children of parents who smoke,
55-58

bronchoconstriction in normal adult
nonsmokers, 63
cancers other than lung cancer,
risk relationship, 102-104
carbon monoxide as biological
marker of ETS exposure, 201-
202

cardiovascular disease risk, prospec-
tive and case-control studies,
105-106

children, brain cancer risk, 104
children, lung function effects (ta-
ble), 50-52

children, nonuniform deposition of
particles in respiratory disease
risk, 192

children, parental smoking as fac-
tor in saliva cotinine concentra-
tions, 207-208

INVOLUNTARY SMOKING-Contd.
children, reported eye irritation,
   239

children, respiratory disease rela-
tionship (table), 3941
children, respiratory symptoms re-
lationship (table), 45-46
children, respiratory symptoms
risk, 44, 41-49

children, risk of cancer other than
lung cancer, 102-104
cotinine in body fluids as measure
of nicotine absorption, 205
cotinine level in saliva, blood, and
urine as ETS exposure marker,
36

cumulative, duration, and intensity
influences health risks, 33
disease risk estimation, value of bi-
ological markers of ETS absorp
tion, 200-201

ETS vapor phase components, re-
tention, 126-127
exposure to sidestream and main-
stream smoke components, 8
eye and nasal irritation, smoke
concentration vs. duration as
factors, 235

health effects and public attitudes
as factors in smoking restric-
tions, 265

health hazards, increasing evidence
as factor in regulation, 282, 286
health risks, 6-7, 107-108
infants and children, bronchitis
and pneumonia risk, 38, 42-44
infants and children, respiratory
system effects, 38-59
inflammatory cell numbers and
functions in smokers, inferences,
244-245

irritant effects in nonsmokers in
restaurants and offices, 232
irritation from gas phase VS. whole
sidestream smoke, 236238
lung cancer dose-response relation-
ship, problems in exposure deter
mination, 92-93
lung cancer in spouses of smokers,
prospective and case-control
studies (table). 71
lung cancer in wives of smokers.
Japanese prospective study. 73-
76

343


INDEX

INVOLUNTARY SMOKING-Contd.
lung cancer relationship, relative
  risk, 72

lung cancer risk, American Cancer
Society Cohort Study, 76-77
lung cancer risk assessment, impor-
tance of definition of exposure,
92

lung cancer risk, bias in case-con-
trol studies (table), 98
lung cancer risk, epidemiological
evidence, 97-98
lung cancer risk, evidence from
case-control studies, 97
lung cancer risk factor in children,
90-91

lung cancer risk factor in non-
smokers, 13

lung cancer risk in nonsmokers,
Hong Kong case-control studies,
80-81

lung cancer risk in spouses of
smokers, Louisiana case-control
study, 79-80

lung cancer risk in spouses of
smokers, Scottish study, 77-78
lung cancer risk in wives of smok-
ers, Greek castiontrol study,
78-79

lung cancer risk relationship, case-
control studies (table), 68-70
lung cancer risk relationship, Los
Angeles County study, 83
lung cancer risk relationship, pre-
liminary findings of U.S. study,
62

lung cancer risk relationship, pro-
spective studies (table), 67
lung cancer risk relationship, sum-
mary and conclusions, 96-102
lung cancer risk relationship, the
Four Hospitals case-control
study, 84-86

lung cancer risk relationship, the
German case-control study, 90
lung cancer risk relationship, the
Japanese case-control study, 66-
89

lung cancer risk relationship, the
Swedish case-control study, 89-
90

lung cancer risk relationship, the
United Kingdom case-control
study, 8666

344

INVOLUNTARY SMOKING-Contd.
lung cancer risk, study power of
  case-control studies (table), 99-
   100

lung disease risk, extrapolation
from risk in smokers, 30-31
lung function effects in adult non-
smokers, 60, 62

lung function effects in adults (ta-
ble), 61

lung function effects in healthy
adults (table), 64
mathematical models of lung can-
cer risk, 93-96

middle ear effusions and diseases
in children, risk relationship,
58-59

misclassification of smoking status
and exposure as factors in deter-
mining risk, -7, 72-73
nicotine and cotinine levels as ex-
posure markers under real-life
conditions, 207

nicotine and cotinine to quantify
ET!3 exposure, 208, 215
organization of the 1966 Report, 5
personal monitoring to measure ex-
posure, 33-34

personal monitors to measure KTS
concentrations, 164-167
public and workplace smoking re-
strictions, conclusions of 1966 re
port, 324

public awareness of health hazards
as factor in changing attitudes,
320

quantitative and qualitative differ-
ences in exposure from active
smoking, 23-24

questionnaires for estimating expo-
sure, uses and limitations, 34-35
research recommendations, 321-323
respirable suspended particulate
levels as marker of smoke expo-
sure, 8

respiratory system effects in chil-
dren, caswontrol studies, 43-44
respiratory system effects in chil-
dren, cross-sectional studies, 43
respiratory system effects in in-
fants and children, longitudinal
studies, 38, 42-43

State legislation in 1970s aimed at
protecting nonsmokers, 267


INDEX

INVOLUNTARY SMOKINC--Contd.
summary and conclusions of 1986
  report, 12-13

thiocyanate levels not specific for
exposure, 203

toxicity, mathematical model for
estimating using "cigarette
equivalents", 198-200
urinary nicotine and expired car-
bon monoxide in nonsmokers fol-
lowing exposure, 207
workplace, lung cancer risk rela-
tionship, 91-92

workplaces, current status of smok-
ing regulations, 285-303

IRRITATION

(See also RESPIRATORY SYMP-
TOMS)

acute effects of ETS exposure, 229
239

allergic persons, ETS exposure ef-
fect, 239

annoying and irritating effects of
ETS, 231-239

children exposed to E'I'S, 239
ETS exposure effects, conclusions,
252

nonsmokers, experimental studies
of ETS exposure effects, 233-239

LABORATORY SMOKING
chemical analysis of sidestream
  smoke in special chambers, 127-
  129, 132

mainstream and sidestream compo-
sition data collection, 125
mainstream smoke particle size dis-
tribution (table). 184-185
particle size of mainstream smoke
aerosol, measurement, 182-183,
186

sidestream smoke particle size dis-
tribution (table), 186

LEGISLATION
(See also SMOKING REGULA-
  TIONS)
average restrictiveness of State
  laws, 1960-1985 (figure), 276
comprehensiveness index of State
  laws, 327-328
current State smoking regulations,
  variations, 268-270
early restrictions as moral crusade
  and fire protection, 266-267

LEGISLATION--Contd.
emphasis shift and increase in
  State legislation during the
   1970s. 267

Federal, State, and local to restrict
smoking, 266-278
impact on smoking behavior, as-
sessment, 306-307
local, California's nonsmokers'
rights movement as factor, 277
Minnesota, landmark Clean Indoor
Air Act of 1975, model for other
States, 267

nonsmoking sections in restaurants
mandated by State laws, 260
rate of new State legislation con-
tinues into 1986s 268
regional variation in State laws
against smoking (table), 277
restrictions and bans on smoking,
16

review of impact on smoking be-
havior, 32&321
smoking regulations, conclusions of
1986 report, 324
social norms and public attitudes
as factors in passage, 321
State and local laws and Federal
regulation in health care facili-
ties, 284-285

State and local laws on public
smoking, influence on private
sector, 295

State and local smoking control
statutes, implementation evalu-
ation, 316318

State, increase in comprehensive-
ness of smoking regulations
since 1970, 275
State laws regulating smoking in
public places and workplaces &a-
ble), 271-274

State laws restricting smoking,
197&1965 (table), 269
States with no regulations against
smoking, 268
student smoking, legal incentive for
regulation by schools, 282
tobacco-producing States have less
restrictive laws on smoking,
275-276
workplace smoking, early contro-
versy, 286

345


INDEX

LEGISLATION-Contd.
workplace smoking, private sector,
  State and local laws, 285
workplace smoking regulation, vari-
  ations in State laws, 270, 275

LEUKEMIA

children of women who smoked
during pregnancy, risk relation-
ship, 103-104

LEUKOCYTES
polymorphonuclear. lung disease
  risk relationship in smokers,
   243-244

LUNG CANCER
(See also CANCER)
animals exposed to cigarette
  smoke, 248-249
confounding variables in studies of
  ETS risk in nonsmokers, 36
ETS as risk factor in nonsmokers,
   8-10

ETS exposure as risk in nonsmok-
ers, Hong Kong case-control
studies, 80-81

ETS risk relationship, need for
more accurate estimates of expo-
sure, 102

involuntary smokers, study power
of case-control studies (table),
99-100

involuntary smoking as factor,
American Cancer Society Cohort
Study, 76-77

involuntary smoking as factor, Los
Angeles County study, 83
involuntary smoking as factor, pre-
liminary findings of U.S. study,
82

involuntary smoking as factor, rela-
tive risk, 72

involuntary smoking as factor, the
Four Hospitals case-control
study, 84-86

involuntary smoking as factor, the
German case-control study, 90
involuntary smoking as factor, the
Japanese case-control study, 8%
89

involuntary smoking as factor, the
Swedish case-control study, 89-
90

346

LUNG CANCERXontd.
involuntary smoking as factor, the
  United Kingdom case-control
  study, 86-86

involuntary smoking as risk factor,
bias in case-control studies (ta-
ble), 98

involuntary smoking as risk factor,
case-control studies (table), 68-
70

involuntary smoking as risk factor,
prospective studies (table), 67
involuntary smoking as risk factor,
summary and conclusions, 96-
102, 107

involuntary smoking dose-response
relationship, problems in expo-
sure determination, 92-93
mathematical models of ETS expo-
sure risk in nonsmokers, 93-96
methodological issues in assessing
involuntary smoking risk, 66-67,
72-73

mortality in nonsmoking wives of
smokers, 27

nonsmokers, case-control study evi-
dence of ETS exposure as risk
factor, 97

nonsmokers, epidemiological evi-
dence of KTS exposure as risk
factor, 97-98

nonsmokers, involuntary smoking
as risk factor, 13, 66-101
nonsmokers, projection of EX'S risk
from relationship with smoking
in smokers, 26-27
nonsmoking spouses of smokers,
Louisiana case-control study, 79-
80

nonsmoking spouses of smokers, po-
tential bias in Japanese study,
74-75

nonsmoking spouses of smokers,
Scottish study, 77-78
nonsmoking wives of smokers, Jap
anese prospective study, 73-76
nonuniform carcinogenic particle
deposition as possible risk factor,
192

parental smoking as risk factor,
90-91

sample size of concern in studies of
nonsmokers, 22

smoking as major risk factor, 6


INDEX

LUNG CANCER-Contd.
spousal smoking as risk factor, pro-
  spective and case-control studies
  (table), 71

women married to smokers, Greek
case-control study, 78-79

LUNG DISEASES
(See also RESPIRATORY TRACT
  DISEASES)

active smokers, extrapolation of
risk in involuntary smokers, 30
bronchiolitis, early pathologic le-
sions in smokers, 241

LUNG FUNCTION
adult asthmatic nonsmokers ex-
  posed to cigarette smoke, 63, 65
adults exposed to involuntary
  smoking (table), 61
asymptomatic adults, long-term
  workplace exposure as risk fac-
  tor, 60

children and adolescents who start
to smoke, 28

children and adults, conclusions
about ETS exposure risk, 107
children, information needed on re-
lationship with ET'S exposure, 32
children, involuntary smoking risk
relationship (table), 50-52
children, maternal smoking rela-
tionship, 49, 53-54
healthy nonsmokers exposed to cig-
arette smoke (table), 64
nonsmokers, ETS as factor in de-
cline, 10

nonsmokers, extrapolation of ETS
risk from risks in smokers, 27

LUNGS

(See also RESPIRATORY SYSTEM)
carbon monoxide deposition kinetics
as factor in variations in concen-
tration, 201-202

children of parents who smoke,
possible long-term effects, 44
cigarette smoking effect, implica-
tions for chronic ETS exposure,
239

cigarette smoking effects, summary,
246-247
inflammatory cell function, experi-
mental models of cigarette
smoke inhalation, 245-246

LUNGS-Contd.
inflammatory cells, cigarette smok-
  ing effect, 241-246
inflammatory lesions in smokers
  vs. nonsmokers, 245
parenchyma alterations in smokers,
   246

parenchyma destruction by poly-
morphonuclear elastase in smok-
ers, 243

regional deposition of mainstream
smoke particles in smokers, 189,
191

respirable particle deposition, non-
uniformity. 191-192
sidestream smoke particle deposi-
tion, mass median diameter as
factor, 187

MAINSTREAM SMOKE
(See akro CIGARETTE SMOKE;
  SIDESTREAM SMOKE; SMOKE
  STREAMS; TOBACCO SMOKE)
condensates, in vitro assays of mu-
  tagenic activity, 250-251
definition, 7
electrical charge as factor in parti-
  cle deposition, 187
particle size distribution studies,
   140

particle size distribution (table),
184-185

regional deposition in respiratory
tract of smokers, 189, 191
respiratory system deposition vs.
sidestream smoke (table), I90

MATERNAL SMOKING
(See nlso PARENTAL SMOKING)
asthmatic children, risk relation-
  ship, 55-58

brain tumors in children, risk rela-
tionship, 104

cancer other than lung cancer in
children, risk relationship, 103-
104

health risks for fetus and neonate,
6

leukemia in children of women
who smoked during pregnancy.
103

lung function in children, risk rela-
tionship, 49, 53-54
lung function in children, risk rela-
tionship (table), 50-52

347


INDEX

MATERNAL SMOKING-Contd.
respiratory illness in children,
  case-control studies of risk, 43-
   44

respiratory illness in children,
cross-sectional studies of risk, 43
respiratory illness in infants and
children, 38, 42-43

MATHEMATICAL MODELS
airways deposition of sidestream
  smoke suggested, 217
humidity effect on particle size and
  deposition, 187-188
lung cancer risk of ETS exposure,
   93-96

particle deposition patterns, effect
of cigarette tar content, 191
regional deposition of polydisperse
aerosols, 189

respirable suspended particulate
constituent of ETS for exposure
prediction, 165

respiratory tract deposition of side-
stream smoke particles, 186-187
tracheobronchial smoke particle de
position prediction, age as factor,
192

MINNESOTA

landmark Clean Indoor Air Act,
model for other States, 267
public approval of 1975 Clean In-
door Air Act, 318-319

MORTALITY

cancers other than lung cancer,
standard ratios for wives of
smokers, 102

lung cancer, establishing risk in
nonsmokers, 95-97
lung cancer in ETS exposed non-
smokers, American Cancer Soci-
ety Cohort Study, 76-77
lung cancer in nonsmoking wives
of smokers, 27

lung cancer in spouses of smokers,
Scottish study, 77-78
lung cancer in wives of smokers,
Japanese prospective study, 73-
76

maternal smoking as risk factor
for infant mortality, 6

348

MOTIVATION
cessation of smoking, public atti-
  tudes and restrictions as rein-
  forcement, 305

worker safety not health as factor
in early smoking regulations,
287

workplace smoking policies, effect
on smoking cessation attempts,
313-314

workplace smoking regulation, 295-
296

NICOTINE

(See also TOBACCO SMOKE CON-
STITUENTS)

absorption in nonsmokers to assess
lung cancer risk, 9
absorption in populations suggests
ETS exposure is common, 15
acute toxicity in animals as factor
in smoke carcinogenicity testing,
247

atmospheric levels as marker of
ETS exposure, 33
biological fluid levels, promising
tracer of ETS exposure, 165-166
blood levels, metabolism, and excre-
tion rate to determikne intake,
203-204

body fluid levels as marker of
smoke exposure in nonsmokers,
8

body fluid levels increase with re-
ported El's exposure, 15, 217
body fluid levels specificity for to-
bacco or tobacco smoke expo-
sure, 204

BTS as source in general environ-
ment, 14, 169

ETS exposure determination, speci-
ficity, 147

ETS exposure quantification, 208,
215

ETS tracer, need for proper valida-
tion, 168

measurement under realistic condi-
tions (table), 155-156
personal air monitoring for intake
determination, 216
plasma and urine levels from in-
travenous infusion vs. ETS expo-
sure in nonsmokers, 215


INDEX

NICOTINELContd.
plasma,* urine, saliva levels in non-
  smokers vs. active smokers, 209-
  210, 216

suspended particulate levels as
measurement of ETS exposure,
193
tobacco smoke exposure determina-
tion, absorption, distribution, me
tabolism, 203-205
vapor phase of sidestream vs.
mainstream smoke, 127

NITROGEN OXIDES
carcinogenic potential of oxides of
  nitrogen in sidestream smoke,
   129

irritant in ETS, 229
measurement under realistic condi-
tions (table), 157
nitrogen dioxide in sidestream
smoke, carcinogenic potential,
129

NITROSAMINE CONTENT
N-nitrosamines in sidestream vs.
  mainstream smoke, 129

NITROSAMINES
ETS as only source of some N-ni-
  trosamine compounds in general
  environment, 169
ETS exposure determination, speci-
  ficity, 147

measurement under realistic condi-
tions (table), 158
sidestream smoke levels higher
than in mainstream smoke, 14

NONSMOKERS
absorption of smoke constituents
  under experimental and natural
  exposure, 206-207
blood cotinine levels, nicotine injec-
  tion vs. smoke exposure, 215-216
California nonsmokers' rights move-
  ment as factor in local smoking
  regulation, 277

cardiovascular disease, prospective
and case-control studies of ETS
risk, 105-106

chronic ETS exposure, inferred risk
for respiratory epithelium, 24&
241

cotinine elimination half-life VS.
smokers, 205-206

NONSMOKERS-Contd.
emphysema risk vs. smokers, genet-
  ic predisposition as factor, 246
ETS as lung cancer risk factor,
  problems in exposure determina-
  tion, 92-93

ETSexposed, plasma, urine, saliva
cotinine vs. active smokers &a-
ble), 211-214

ETS-exposed, plasma, urine, saliva
nicotine vs. active smokers (ta-
ble), 209-210

ETS exposure, experimental studies
of irritant effects, 233-239
ETS exposure, relationships with
active smoking provide insight
into risks, 26-28
ETS exposure toxicity, mathemati-
cal model using "cigarette equiv-
alents", 193-200
ETS exposure, wide variations, 14
health risks of ETS exposure, con-
clusions, 107-108
health risks of involuntary smok-
ing, summary and conclusions,
12-13

irritant effects of involuntary
smoking in restaurants and of-
fices, 232

irritation from sidestream smoke
vs. gas phase sidestream smoke,
236238

irritation from smoke exposure,
concentration vs. duration as
factors, 235

lung cancer, establishing risk of
ETS exposure, 95
lung cancer, ETS exposure as fac-
tor, Four Hospitals case-control
study, 64-66

lung cancer, ETS exposure as fac-
tor, German case-control study,
90

lung cancer, ETS exposure as fac-
tor, Hong Kong case-control
study, 80-81

lung cancer, ETS exposure as fac-
tor, Japanese case-control study.
88-89

lung cancer, ETS exposure as fac-
tor, Los Angeles County study.
33

349


                  INDEX

NONSMOKERS-Contd.
lung cancer, ETS exposure as fac-
  tor, preliminary findings of U.S.
  study, 82

NONSMOKERS-Co&d.
plasma, saliva, and urine nicotine
  and cotinine levels vs. active
  smokers, 216

lung cancer, ETS exposure as fac-
tor, Swedish case-control study,
89-90

lung cancer, ETS exposure as fac-
tor, United Kingdom case-con-
trol study, 36-88
lung cancer in spouses of smokers,
prospective and case-control
studies (table), 71
lung cancer, involuntary smoking
as risk factor, 13
lung cancer risk from ET'S expo-
sure, S-10

preferential hiring, most restrictive
smoking policy, 301302
private, local, governmental actions
for protection from smoke expo
sure, 265

lung cancer risk from ETS as pro-
jection of relationship of smok-
ing in smokers, 26-27
lung cancer risk in spouses of
smokers, Japanese prospective
study, 73-76

lung cancer risk in spouses of
smokers, Louisiana case-control
study, 79-30

respirable suspended particulates in
JZT!kxposed vs. nonexposed, 169
review of impact of smoking re-
strictions on attitudes, 320
separation from smokers for risk
reduction, effectiveness, 11-12
State antismoking legislation in
1970s aimed at protection, 267
temporal and spatial distribution of
smokers in ETS exposure deter-
mination, 145-146
urinary cotinine levels in ETS-ex-
posed vs. nonexposed men, 207
urinary nicotine and expired car-
bon monoxide, effects of smoke
exposure, 267

lung cancer risk in spouses of
smokers, Scottish study, 77-78
lung cancer risk of ETS exposure,
American Cancer Society Cohort
Study, 76-77

workplace bans for maximum pro-
tection, momentum growing
among large employers, 301
workplace demands for clean air as
motivation for smoking regula-
tions, 296

lung cancer risk of involuntary
smoking, case-control studies (ta-
ble), 68-70

workplace smoking as eye irritant,
233

lung cancer risk of involuntary
smoking, more accurate data
needed, 102

workplace smoking as lung cancer
risk factor, 91-92

NOSE

lung function in healthy adults ex-
posed to cigarette smoke (table),
64

mathematical models of lung can-
cer risk with ETS exposure, 93-
96

misclassification of status and ETS
exposure as factors in determin-
ing risk, 66-67, 72-73
nicotine and cotinine to quantify
ETS exposure, 208, 215
odor perception and irritation, in-
fluence of room temperature and
humidity, 234

annoying and irritating effects of
ETS exposure, 231, 235
ET'S particle deposition, effect of
nasal inhalation, 189
smoke concentration vs. exposure
duration as factors in irritation.
235

PARENTAL SMOKING
(See also MATERNAL SMOKING)
cancers other than lung cancer in
  children, risk relationship, 102-
   105

plasma and urine nicotine levels,
intravenous vs. ETS exposure ef-
fect, 215

cough, phlegm, and wheezing in
children, 44, 47-49
lung cancer risk relationship, 90-91
lung function in children, relation-
ship (table), 50-52

350


PARENTAL SMOKING-Cad.
lung function in children, risk rela-
  tionship, 53-54

middle ear effusions and diseases
in children, risk relationship,
5849

respiratory illness in infants and
children, 38, 42-44
respiratory symptoms in children,
13

respiratory symptoms in children,
relationship (table), 45-46
respiratory system effects in chil-
dren, 38-59

saliva cotinine concentrations in
children, effect, 207-208

Passive Smoking See INVOLUN-
TARY SMOKING

PHYSICAL ACTIVITY
EXS deposition increase with in-
  creasing activity, 187

PREGNANCY

fetal exposure to tobacco smoke
constituents, possible effects, 31-
32

leukemia risk in children of smok-
ers, 103

PUBLIC PLACES
(See also HOSPITALS; WORK-
  PLACE)

current status of smoking regula-
tions mix of public and private
actions, 265-266

employee attitudes before smoking
policy implementation, 311
health care facilities, public sup
port of smoking restrictions, 284
health care facilities, smoking regu-
lations, 283-285

hotels and motels, smoking regula-
tions, 231-282

impact of public and workplace
policies restricting smoking, 303-
321

interstate transportation, smoking
regulated at Federal level, 278
legislation restricting smoking,
evaluation of impact, 316-318
local smoking regulations, 277-278
public transportation, smoking reg-
ulations, 278-279

PUBLIC PLACXS-Contd.
research recommendations on ef-
  fects of smoking regulations, 321
restaurants, opposition, acceptance,
  and implementation of smoking
  restrictions, 280
restaurants, smoking regulations,
   279-281
retail stores, smoking regulations,
   279
schools, smoking regulations, 282-
   283
smoking regulation, State laws (ta-
  ble), 271-274
smoking regulations, conclusions of
   1986 report, 324
smoking regulations, factors in ac-
  ceptability, 266
smoking regulations in specific
  public places, 278-285
smoking regulations, public approv-
  al, national and regional polls,
   318-319
smoking restrictions, variations in
  current State legislation, 268-
   270
State laws regulating smoking,
  comprehensiveness index, 327-
   323
State legislation to restrict smok-
  ing, increase during the 1970s
   267
States restrict smoking in transpor-
  tation, hospitals, elevators, and
   others, 269
total suspended particulates (table),
   194-195

PULMONARY ALVEOLAR MAC
ROPHAGBS
lung injury relationship in smok-
  ers, 241-243, 245
protease-antiprotease balance in
  lungs of smokers, influence,
   242-243
respiratory bronchioles of smoke-ex-
  posed animals, 245-246

PYRIDINES
sidestream vs. mainstream smoke
  levels, 129

RADIATION
decay products of radon in tobacco
  smoke, 132, 134
ETS radioactivity, 134

INDEX

351


REDUCTION OF SMOKING
(See also CESSATION OF SMOK-
  ING)

public attitudes and smoking poli-
cies as indirect influences, 304
305

RESPIRATORY SYMPTOMS-ConM.
cough, phlegm, wheezing in chil-
  dren, parental smoking as factor,
  44, 4749

involuntary smokers, 31

RESIDENCES

total suspended particulates (table),
195-196

RESPIRATORY SYSTEM
(See also LUNGS)
animals, carcinogenicity of cigarette
  smoke, 247-248

RESPIRABLE SUSPENDED PAR-
TICULATES

breathing pattern and particle size
distribution effect on ETS dose,
25

enclosed places, ETS role, 169
ETS-exposed and nonexposed sam-
ples, percentage distribution, 167
hospital before and after adopting
restrictive smoking policy, 311
irritants in ETS, 229
marker for RTS exposure, 33-34
personal monitors to measure ETS
exposure, 166-168
residental levels as function of
number of smokers (table), 164
respiratory disease risk in children
of smokers, 192

breathing patterns as factor in
sidestream smoke deposition, 187
bronchoconstriction in children, pa-
rental smoking as risk factor,
5558

bronchoconstriction in normal
adults exposed to involuntary
smoking, 63

INDEX

cigarette smoking effects, implica
tions for involuntary smoking
risks, 239-241

tracheobronchial deposition in in-
fants vs. adults, prediction, 192

RESPIRATORY FUNCTION TESTS
children, involuntary smoking as
  risk factor, 53-54
nonsmokers exposed to involuntary
  smoking, 62-63

deposition and absorption of tobac-
co smoke constituents, 181-216
deposition of mainstream and side-
stream smoke, 25
enzyme activity in smoke-exposed
animals, 245

predicted levels, relationship with
number of cigarettes smoked, 29

epithelial cells, dose-response effect
of cigarette smoking, 239
ETS deposition, 193-216
ETS dose, product of mass in in-
haled air and deposition frac-
tion, 193

RESPIRATORY SYMPTOiifS
(See also COUGH; IRRITATION;
   NOSE)

annoying and irritating effect of
ETS exposure, 231-232, 236-239
children and adolescents who start
to smoke, 27

hyperplasia and metaplasia in tra-
chea and bronchi of smokeex-
posed animals, 248
involuntary smoking effects, 37-65
mass deposition of ET'S, estimation,
193

children and adults, ETS exposure
as factor, conclusions, 167
children, parental smoking as fac-
tor, 13

children, relationship with involun-
tary smoke exposure (table), 45
46

cough, phlegm, and wheezing in
adults, ETS exposure as risk not
established, 60

nasal vs. mouth inhalation of RTS,
  effect on particle deposition, 189
nose, throat, and airway irritation
  from smoke exposure, 11
particle size of cigarette smoke as
  factor in deposition, 182
puffing and inhalation patterns as
  factor in particle deposition, 183
regional deposition of smoke parti-
  cles, 189, 191

352

sidestream and mainstream .smoke
deposition (table), 196


INDEX

RESPIRATORY SYSTEM-Contd.
sidestream smoke particle deposi-
  tion, 186-189

smoke particle size as factor in re-
gional deposition, 189, 191-192

RESPIRATORY TRACT CANCER
animals exposed to cigarette
  smoke, 248

RESPIRATORY TRACT DISEASES
acute illness in children, parental
  smoking as risk factor, 38, 42-44
asthma in children, maternal
  smoking as risk factor, 55-58
children, case-control studies of pa-
  ternal smoking as risk factor,
   43-44

children, nonuniform deposition of
smoke particles as risk factor,
192

children, parental smoking as fac-
tor, 13

children, parental smoking as risk
factor, 38-59

early childhood, involuntary smok-
ing relationship (table), 3941
involuntary smoking as risk factor,
10

nonsmoking adults and children,
involuntary smoking as factor,
37-66

pneumonia in children of smokers,
conclusions about risk, 107
population characteristics as factor
in ETS risk, 28

smoking as major risk factor, 6

RESPIRATORY TRACT INFEC
TIONS

children of smokers, conclusions
about risk, 107

infants, ETS exposure as risk fac-
tor, 31

SALIVA

cotinine level as marker for ET'S
exposure in nonsmokers, 36
cotinine levels in ET&exposed non-
smokers vs. active smokers (ta-
ble), 211-214

nicotine and cotinine levels to
quantify ETS exposure, 208, 215
nicotine levels as sidestream smoke
exposure indicator, 204-205

SALIVA-Contd.
nicotine levels in ETS-exposed non-
  smokers vs. active smokers (ta-
  bleJ, 209-210

nicotine levels in nonsmokers vs.
smokers, 216

SIDESTREAM SMOKE
(See also CIGARETTE SMOKE;
  MAINSTREAM SMOKE;
  SMOKE STREAMS; TOBACCO
  SMOKE)

bioassays needed to determine gen-
otoxicity, 252

carbon monoxide and carbon diox-
ide levels vs. mainstream smoke,
129

carcinogen levels vs. mainstream
smoke, 24

carcinogenic potential, effect of lev-
els of oxides of nitrogen, 129
carcinogenicity vs. mainstream
smoke in animal models, 252
chemical analysis, 127-129, 132
chemical composition as factor in
estimating exposure using "ciga-
rette equivalents", 199
component levels, combustion tem-
perature effect vs. mainstream
smoke, 128129
constituent formation vs. main-
stream smoke, 7-8
definition, 7
experimental and mathematical
models show deposition in air-
ways, 217

formaldehyde and acrolein concen-
trations above occupational lim-
its, 230

formation and physiochemical na-
ture, 127

inhalation effects in laboratory ani-
mals not reported, toxicity fac-
tor, 249

irritation in nonsmokers vs. gas
phase sidestream smoke vs. acro-
lein, 236-237

irritation of nonsmokers in labora-
tory, ventilation as factor, 234-
235

laboratory collection devices, 125
126

major source of ETS, 125

353


INDEX

SIDESTREAM SMOKE-Contd.
mass median diameter, effect on
  deposition in respiratory tract,
   187

mathematical models of particle de-
position in respiratory tract,
186-187

nicotine in vapor phase vs. main-
stream smoke, 127
particle distribution in respiratory
tract, 186-189

particle size distribution studies (ta-
ble), 138

particle size distribution (table),
186

particles, number and size distribu-
tion, 137, 139

particulate matter vs. mainstream
smoke, 129, 132
particulate phase as major determi-
nant of irritation in nonsmokers,
237-238

physiochemical nature and spec-
trum of carcinogens, summary,
251-252
regional deposition in respiratory
tract, particle size as factor, 189,
191-192
respiratory system deposition vs.
mainstream smoke (table), 190
saliva nicotine levels as indicator
of exposure, 204-205
toxic and carcinogenic agents, 21
toxic and carcinogenic compounds,
14
toxic and carcinogenic compounds
vs. mainstream smoke, conclu-
sions, 169
tumor induction by condensate on
mouse skin vs. mainstream
smoke condensate, 250
vapor and particulate phase con-
stituents, sidestream to main-
stream ratio (table), 130-131

SMOKE INHALATION, ANIMAL
carcinogenicity testing, 247-250
laryngeal leukoplakias in hamsters,
   24a249
lung and respiratory cancers in
  mice and rata, 248
lung inflammatory cell function,
  experimental models, 245-246

354

SMOKE STREAMS
(See also CIGARETTE SMOKE;
  MAINSTREAM SMOKE; SIDE
  STREAM SMOKE; TOBACCO
  SMOKE)

combustion temperature effect on
components of side&ream vs.
mainstream smoke, 128-129
mainstream and sidestream smoke,
comparison, 23-25
mainstream smoke vs. ETS, chemi-
cal composition, 135, 137
mainstream vs. sidestream smoke
from unfiltered cigarette, com-
parison (table), 128
particulate matter in mainstream
and sidestream smoke, 129, 132
sidestream and mainstream smoke
inhalation by smokers and invol-
untary smokers, 126127
toxic and carcinogenic agents in in-
door mainstream vs. ETS (table),
136

vapor and particulate phase con-
stituents, sidestream to main-
stream ratio (table), 130-131

SMOKING

immune system effects, 244
public knowledge and attitudes,
policy impact assessment by sur-
veys, 367

public places and workplaces, State
regulations (table), 271-274
regulatory approaches of State and
local governments, 278

SMOKING CHARACTERISTICS
compensatory smoking by workers
  following smoking policy imple-
  mentation, 312-313
machine smoking simulation, incon-
  sistency with current patterns,
   126127
puffing and inhalation effect on
  particle deposition, vs. machine
  smoking, 183

SMOKING CONTROL PROGRAMS
evaluation, methodological consider-
  ations, study design as factor,
   306-308

guides on how to adopt and imple-
ment regulatory policies, 302


SMOKING CONTROL
PROGRAMS-Contd.
"individual solution" approach to
  control workplace smoking, 298

separating smokers and nonsmok-
ers, improving workplace ventila-
tion, 299
workplace cessation of smoking
programs as part of control poli-
cies, 297
workplace restrictions on where
smoking is allowed, variations,
299-300

SMOKING HABIT
consumption decline, effect of pub-
  lic attitudes and social norms,
   321

population group differences in
EXS exposure determination,
145146

research recommendations on effect
of smoking restrictions, 322
smoking restrictions with most im-
pact on behavior, research need-
ed, 323

SMOKING MACHINES
We also LABORATORY SMOK-
  ING)
human smoking simulation incon
  sistent with current patterns,
   126-127
standard conditions for machine
  smoking cigarettes, 125

SMOKING REGULATIONS
(See akro LEGISLATION)
assessment of effect on air quality,
   307
average restrictiveness of State
  laws, 1960-1985 (figure,, 276
case-control studies of impact on
  human behavior, evaluation, 306
current State legislation, variations,
   268270
designated smoking or no-smoking
  areas to control workplace smok-
  ing, 299-300
employer-mandated policies in the
  private sector, opposition, 296-
   297
enforcement costs, experience con-
  tradicts tobacco industry esti-
   mates, 316

SMOKING REGULATIONS-ConM.
geographic variability of State laws
  on smoking in public places (fig-
  ure), 270

health care facilities, 283-285
health care facilities, public sup
port, 284

health care facilities, variations in
policies, 284-285
hospitals, awareness and compli-
ance, 309-310

hospitals, effect on air quality, 311
hospitals, employee approval of pol-
icies, 312

hospitals, positively worded signs
and enforcement factors in com-
pliance, 310

hospitals, review of current evi-
dence of impact, 308-309
hotels and motels, private initiative
in response to perceived demand,
281-282

hotels and motels, public support,
281-282
impact on air quality, behavior, at-
titudes, 303-321
implementation, 309-310
implementation, assessment of im-
pact, 307-308
implementation of workplace poli-
cies, 302-303
implementation, smokers' support
as factor, 303-304
legislation to restrict smoking in
public places, 266-276
local legislative restrictions, 277-
278
local restrictions, California's non-
smokers' rights movement as
factor, 277
nonsmoker's exposure to second-
hand smoke, assessment of im-
pact, 306
policy components that impact on
smoking behavior, research need-
ed, 323
preferential hiring of nonsmokers
as most restrictive policy, 301-
302
public and private organizations.
employees' attitudes, 311-312
public and workplace. conclusions
of 1986 report, 324

355


SMOKING REGULATIONS-Contd.
public and workplace control poli-
  cies, indirect effects, 304-306
public and workplace restrictions,
  review of impact, 303-321
public approval, national and re-
  gional polls, 318-319
public awareness, compliance, and
   enforcement of violations in im-
  plementation, 303
public places and workplaces, Fed-
  eral, State, and local action, 15-
   16

public places and workplaces, State
laws (table), 271-274
public places, current status mix of
public and private actions, 265%
266

public places, factors in acceptabili-
ty, 266

public places, role of public atti-
tudes and social norms, 321
public support, 16
public transportation, 278-279
regional variation in State laws
against smoking (table), 277
research must consider policy char-
acteristics. institution, and popu-
lation, 321323

research recommendations, 321-323
restaurants, 279-281
restaurants, opposition, acceptance,
and implementation, 280
retail stores, 279
review of impact on attitudes and
social norms, 319-320
schools, difficulties in enforcement,
283

schools, double standard of teacher
smoking vs. student restrictions,
283

schools, traditionally not to reduce
sidestream smoke exposure, 282
social phenomenon, impact infor-
mation lacking, need for re-
search, 323

specific public places, 278-285
State and local governments, re-
strictions, 12

State and local statutes, implemen-
tation evaluation, 316-318
State laws, comprehensiveness in-
dex, 327-328

356

SMOKING REGULATIONthChtd.
State laws restricting smoking,
  1970-1935 (table), 269
State legislation, emphasis shift
  and increase during the 19709,
   267

State legislation in 1970s aimed at
protecting nonsmokers, 267
State legislation, increase in
comprehensiveness, 275
States with no smoking legislation,
268

tobacco-producing States, fewer
enacted and less restrictive, 275
276

worker safety as motivation for
early policies, 287
workplace ban, complexity of assur-
ing compliance, 301-302
workplace bans, usually preceded
by progressively stricter regula-
tions, 300-301

workplace, barriers to adopting pol-
icies, 296-297

workplace, categories of policies,
298

workplace compliance with local or-
dinances, type of business as fac-
tor, 317

workplace, current evidence of im-
pact, 308-309

workplace, current status, 285-303
workplace, early controversy in the
private sector, 286
workplace, economic considerations
apparently not a factor, 296
workplace, effect on smoking cessa-
tion motivation and success,
313-315

workplace, employee attitudes be
fore policy implementation, 311
workplace, impact on absenteeism,
health care costs, productivity,
turnover, 315-316
workplace, impact on health care
and maintenance costs, 305
workplace, influence of nonsmok-
ers` demand for clean air, 286
workplace, nature, scope, and prev-
alence in the 1980s. 294-295
workplace, policy implementation
effect on smokers' behavior, 312-
313


SMOKING REGULATIONS-Contd.
workplace, prevalence, 286-287,
   294-295

workplace, public vs. private sector,
270

workplace, worker health, State
legislation, nonsmokers' demands
as factors, 295-296
workplace, workforce size, industry
type, geographic location as fac-
tors, 295

workplaces, survey data 1977-1986
(table), 288-293

SMOKING STATUS
(See also SMOKING HABIT)
misclassification as factor in deter-
  mining EI'S risk, 98, 101
misclassification as factor in deter-
  mining health risks of involun-
  tary smoking, 6667, 72-73

SMOKING SURVEYS
workplaces, 287, 294-295

STATISTICS
significance testing of ETS risks,
   36-37

TARS, CIGAREX-TE
carcinogenicity testing in animals,
   247-243
chemical assay for human exposure
  to components, research goal,
   217
tumor induction on mouse skin,
   sidestream vs. mainstream con-
  densates, 250

TABS, TOBACCO
particulates measured under realis-
  tic conditions (table), 159-162
sidestream smoke particle size dis-
  tribution studies (table), 138

THIOCYANATES
sources, metabolism, elimination,
  half-life, 202-203

TOBACCO SMOKE
(See also CIGARETI'E SMOKE;
  MAINSTREAM SMOKE; SIDE
  STREAM SMOKE; SMOKE
  STREAMS)
absorption during active smoking
  vs. involuntary smoking, 215-216

TOBACCO SMOKE-Contd.
biological markers of smoke absorp
  tion in smokers and nonsmokers,
   181

machine vs. human smoking, non-
comparability of chemical and
physiochemical data, 135
mainstream vs. environmental,
characteristics, 6
nicotine in vapor phase, sidestream
vs. mainstream, 127
odor perception and irritation, in-
fluence of room temperature and
humidity, 234

particle sire distribution of main-
stream smoke (table), l&1-185
particle size distribution of side-
stream smoke (table), 186
quantitatively determined com-
pounds in sidestream and main-
stream smoke, 128
radioactivity, 132, 134
residuals, measured under realistic
conditions (table), 163
vapor phase, retention by smokers
vs. involuntary smokers, 126-127
workplace air pollution, contribu-
tion (table), 233

TOBACCO SMOKE CONSTITU-
ENTS

(See also COTININE; NICOTINE)
absorption in nonsmokers under
experimental and natural expo-
sures, 206-207

chemical assay for human exposure
to tar components. research goal,
217

deposition and absorption, 181-216
deposition fraction of individual
components needed to determine
disease risk, ZOO
STS and mainstream differences as
factor in exposure of nonsmokers
vs. smokers, 201
ETS exposure quantification, 208,
215

irritants also produced by other
sources, 229-230
irritants in ET& 229
nicotine, absorption, distribution,
metabolism, and body fluid lcv-
els, 203-205

357


INDEX

TOBACCO SMOKE CONSTITU-
ENTS-Cad.
particle deposition in lung areas,
  nonuniformity, cancer risk rela-
  tionship, 192

trapping devices to analyze individ-
  ual components, 126
TOBACCO SMOKE PARTICU-
LATES

carcinogenicity testing in animals,
247-248

indoor concentrations by cigarette
smoking under laboratory condi-
tions (table), 197
irritation in nonsmokers vs. gas
phase of sidestream smoke, 237-
238

potential toxicity estimation using
"cigarette equivalents", deficien-
cies, 199

total suspended particulates in in-
  door working and living environ-
  ments (table), 194-196
URINE

cotinine level as marker for ETS
exposure in nonsmokers, 36
cotinine levels in BTS-exposed non-
smokers vs. active smokers (ta-
ble), 211-214

cotinine levels in ETS-exposed vs.
nonexposed men, 207
mutagenic activity not good mea-
sure of tar absorption, 206
nicotine and cotinine levels to
quantify ETS exposure, 208, 215
nicotine excretion, individual me-
tabolism as factor in smokers
and nonsmokers, 203-205
nicotine levels in BTS-exposed non-
smokers vs. active smokers &a-
ble), 209-210

nicotine levels in nonsmokers vs.
smokers, 216

VENTILATION
ETS components elimination, major
  factor, 146-147, 164-165
ETS, determinant of exposure, 11
ETS, effect on levels, 229
ETS, factor in estimating human
  exposure, 139, 141-142
involuntary smoking exposure, fac-
   tor, 67

restaurants, inadequate control of
ETS levels, 279

358

VENTILATION-ConM.
sidestream smoke in laboratory, ef-
  fect on perceived irritation in
  nonsmokers, 234-235

WOMEN

cancers other than lung cancer in
nonsmokers married to smokers,
102

lung cancer in wives of smokers,
Greek case-control study, 78-79
lung cancer, involuntary smoking
as factor, German case-control
study, 90

lung cancer risk in wives of smok-
ers, Japanese prospective study,
73-76

lung cancer risk with ETS expo-
sure, Hong Kong case-control
studies, 60-81

WORKPLACE

(See also PUBLIC PLACES)
barriers to adopting smoking poli-
cies, 296-297

carbon monoxide, nitrogen, and
particulate matter levels due to
tobacco smoke, 232
categories of smoking policies, 298
compliance with local smoking or-
dinances, type of business as fac-
tor, 317

health care and maintenance cost
reduction as benefit of smoking
policy, 305

hospitals, employee approval of
smoking policies, 312
involuntary smoking, irritant ef-
fects, 232

irritants, tobacco smoke and other
sources, 229-230
preferential hiring of nonsmokers
as most restrictive smoking poli-
cy, 301-302

research recommendations on effect
of smoking regulations, 321
safety as motivation for early regu-
lations against smoking, 287
smoking policies, survey data 1977-
1986 (table), 288-293
smoking restrictions, conclusions of
1986 report, 324
State laws regulating smoking,
comprehensiveness index, 327-
328


INDEX

WORKPLACE--Contd.
surveys of smoking policies, 287,
   294-295

tobacco smoke contribution to air
pollution (table), 233
total suspended particulates (table),
194-195

WORKPLACE SMOKING
(See also ENVIRONMENTAL TO-
  BACCO SMOKE; INVOLUN-
  TARY SMOKING1
bans, usually preceded by progres-
  sively stricter regulations, 30%
   301

business type as factor in compli-
ance with local smoking ordi-
nances, 317

cessation programs as part of pri-
vate sector smoking control, 297
control by restricting where smok-
ing is allowed, variations, 299
300

H'S exposure determination, factor,
142

eye irritation reported in nonsmok-
ers, 233

government offices, smoking regula-
tion increasing, 285
guides on how to adopt and imple-
ment smoking policies, 302
hospitals, awareness and compli-
ance of employees, 309-310
hospitals, review of current evi-
dence on impact of smoking reg-`
ulations, 308-309

impact of public and workplace re-
strictions, 303-321

WORKPLACE SMOKING-Contd.
"individual solution" approach to
  regulation, 298

legislated restriction, early contro-
versy, 286

lung cancer risk factor in non-
smokers, 91-92
lung function effects of exposure in
nonsmokers, 60

motivation for regulation, 295-296
nature, scope, and prevalence of
regulation in the 1980s 294-295
policy implementation effect on
smokers, 312313
private sector regulation, legislation
and public support as factors,
295

private sector, State and local leg-
islation, 285

regulation, impact on absenteeism,
health care costs, productivity,
turnover, 315-316
regulations, current status, 285-303
regulations supported by smokers
and nonsmokers, 285
regulations, workforce size, geo-
graphic location, type of indus-
try as factors, 295
restrictions, 16
restrictions, voluntary vs. govern-
mental, 12

schools, restrictions to reduce facul-
ty/staff exposure to EXS, 282
State regulation, public vs. private
sector, 270

State regulations (table), 271-274
urinary cotinine levels as marker
of exposure in nonsmokers, 207

359