U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
          Public Health Service
   Office of the Assistant Secretary for Health
       Office on Smoking and Health


    The
Health Consquences
of SMOKING

CtEVV Publication No. (f+t?d 79-50065

U.S. DEPARTMENT OF HEALTH, EDUCATION. AND WELFARE
          Public Health Service
   Office of the Assistant Secretary for Health
      Office on Smoking and Health
      Rockville, Md. Maryland 20857


The Honorable Thomas P. O'Neill
Speaker of the House of Representatives
Washington, D.C. 205 15

Dear Mr. Speaker:

As required by Section 8(a) of the Public Health Cigarette Smoking
Act of 1969, I am submitting the 1977-1978 report on the health
consequences of smoking. The report includes the "Bibliography on
Smoking and Health-l 976," the "Bibliography on Smoking and
Health-1977," and "The Health Consequences of Smoking, 1977-
1978."* The report bears a 2-year designation in order to return the
series to an annual timetable which was altered because of the time
required for the clearance processing of the 1976 report. The Bib-
liographies are prepared annually and routinely to reflect the new
acquisitions to the smoking and health data base which operates at
a cost of $200,000.00 per year; the health consequences of smoking
report, which is a review of this new current information and pre-
pared specifically for Congress, this year cost $9,800.00.

"The Health Consequences of Smoking, 1977-1978" includes re-
cently published data from three classic prospective studies of the
mortality resulting from cigarette smoking. These studies, involving
almost one and a half million persons, continue to document excess
mortality among smokers as compared to nonsmokers.
This part of the report also includes data on the established risks
of low birth weight and increased perinatal mortality for offspring
of women who smoke during pregnancy. In addition, the new evi-
dence is reviewed that shows not only a high rate of heart attacks
among women who smoke cigarettes, but that this effect is particu-
larly critical in women who use oral contraceptives.
The data in this report indicate that former smokers show lower
death rates than continuing smokers and within 10 to 15 years after
quitting come close to the low rates of those who never smoked.
One study supports previous evidence that there is a partial
solution to the health problem in the use of cigarettes with lower
emissions of "tar" and nicotine.

As a result of public demand and a responsive industry, there
has been over recent years a continuing decline in the emissions of
"tar" and nicotine in cigarettes in use.

The data in this report and in previous annual reviews of the
health consequences of smoking have established cigarette smoking
as a habit responsible for an overwhelming level of premature death
and disability in this country. To reduce this preventable and costly

--

*The bibliographies have been published as DHEW Publicati%%mber (CDCj 38-8309,
January and February 1978.


mortality and morbidity, this Department recently announced a
new antismoking program.

The program is one of public education, regulation, and research
with special emphasis on children, teenagers, and young women,
and on occupations where smoking increases risks from occupational
exposure. In undertaking this program, I have invited the coopera-
tion of the major broadcast networks, State and local school offi-
cials, the major corporations of this Nation, State Governors and
legislators, the Federal Trade Commission, the Federal Communi-
cations Commission, the Civil Aeronautics Board, and others whose
involvement and cooperation are crucial to the success of this pro-
gram. In response to the evidence linking the combined use of oral
contraceptives and cigarette smoking, the Food and Drug Admin-
istration, Public Health Service, HEW, has recently required that a
warning statement to that effect accompany oral contraceptives as
they are distributed to those who use them. To provide leadership
and to coordinate this program, an Office on Smoking and Health
has been established in the Office of the Assistant Secretary for
Health. As one of its first tasks, this Office will coordinate the pro-
duction of a comprehensive document which reviews not only the
biomedical but also the behavioral and control data about smoking
and its effects on health. The report will be submitted to Congress
in January 1979.

As the principal health officials of this government, the Surgeon
General and I are committed to fulfilling our responsibilities to pro-
vide information and direction to permit American citizens to make
genuinely free choices about smoking and their own health. In this
regard and as I am required by P.L. 91-222 to make such legislative
recommendations that I deem appropriate based on the scientific
data about the impact of smoking on health, I will submit within
the year a legislative package which I hope will meet with your
approval. With appropriate coordination of legislative action and
program, we can solve this difficult and important public health
problem.

Enclosures

Identical letter sent to The Honorable Walter F. iMondale

. . .
ul


Preface

This tenth report to the Congress on the health consequences of
smoking discusses the special problems incurred by women who
smoke and presents recently published overall mortality data on
smoking.

Smoking was first recognized as a health problem in the 1930's,
when a sharp increase was noted in lung cancer rates for men. No
similar increase was noted for women at that time for several rea-
sons. First, as a group, women did not start smoking when men
did, since such behavior was socially unacceptable for women at
that time. Consequently, until the last decade, there were insuffi-
cient numbers of women who had smoked for a long enough period
of time to provide the size population necessary for meaningful
research.

In recent years, however, the same health risks to men as a re-
sult of smoking have been documented for women who smoke.
These include cardiovascular disease, lung cancer, cancer of other
specific sites, bronchitis, and emphysema. These diseases occur
among smokers at rates far greater than those of nonsmokers. Ad-
ditionally, women have been found to incur unique risks for them-
selves and for their offspring. For example, women over 30 years of
age who smoke and use oral contraceptives have substantially higher
risks of myocardial infarction. Moreover, the offspring of women
who smoke during pregnancy face greater risks of perinatal mortal-
ity and low birth weight. Further understanding of the mechanisms
involved in these health consequences continues to evolve.

Three large prospective epidemiologic studies demonstrate that
overall mortality rates for cigarette smokers are approximately 70
percent higher than those for nonsmokers. These studies also docu-
ment a decrease in overall mortality rates for those who quit smok-
ing, provided they were not ill at the time of cessation. There is
about a 15 percent reduction in overall mortality risk for smokers
of low "tar" and nicotine cigarettes (less than 17.6 mg. "tar" and
less than 1.2 mg. nicotine) compared to those who smoke high
"tar" and nicotine cigarettes (25.8-35.7 mg. "tar" and 2.0-2.7 mg.
nicotine).


Several publications have become available .since the last report
to Congress which review the social, behavioral, legislative, and
health issues related to smoking. A recently published paper by
Daniel Horn, Ph.D., as part of his work with the World Health
Organization, discusses the major barriers to be overcome if further
progress is to be made against the threat of smoking to health, A
copy is included as Appendix A to this report. Two other publica-
tions of note include the U.S. Public Health Service's "Proceedings
of the Third World Conference on Smoking and Health, 1975,"
DHEW Publication No. (NIH) 77-1413, 1977, Volumes I and II,
and the World Health Organization's "Smoking and Its Effects on
Health," Technical Report Series No. 568, Switzerland, 1975.


Table of Contents

Page

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iv.

Table of Contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi
Preparation of the Report and Acknowledgments             . . .
                                            . . . . . . . . . xlll

Chapter 1. Smoking-Related Health
Problems Unique to Women . . . . . . . . . . . . . . . . . . . . . . . . . . Xvii
Introduction. . , . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Effects of Smoking on the Outcome of Pregnancy . . . . . . . . . ,l

Smoking and Birth Weight . . . . . . . . . . . . . . . . . . . . . . . . . 1
Smoking and Perinatal Mortality  . . . . . . . . . . . . . . . . . . . . T
Long-Term Effects on Physical
and Intellectual Development . . . . . . . . . . . . . . . . . . . . . . . 8
Carbon Monoxide and Carboxyhemoglobin Levels
in Maternal and Fetal Circulation and the Possible
Mechanisms of Smoking Effects on Pregnancy . . . . . . . . . . . . p
Smoking and Its Effects on Cardiovascular Disease
Among Women Taking Oral Contraceptives . . . . . . . . . . . . . .13
Effects of Cigarette Smoking on Lactation . . . . . . . . . . . . . . . 15
What Women Know About Smoking and Pregnancy  . . . . . . . 15
Summary of Smoking-Related Health
Problems Unique to Women . . . . . . . . . . . . . . . . . . . . . . . . . .17
References . . . . . . . . . . . . . . . . . , . . . . . . . . . . . , . . . .X . . . .18

Chapter 2. Smoking and Overall Mortality. ............. -21
Introduction......................................2 2

Measuring Mortality  ................................ ?4
Mortality Ratios ................................ .24
Differences in Mortality Rates  ..................... .24
Excess Deaths .................................. .24

vi


Life Expectancy  ...........
Description of the Studies  .......................... .25
The American Cancer Society Study  ................ .25
TheU.S.VeteransStudy  ......................... .26
The British Doctors Study  ........................ .26
Overall Mortality and Cigarette Smoking  ............... .27
Number of Cigarettes Smoked  ..................... .27
Age Began Smoking  ............................. ..2 8
Inhalation Practice  .............................. .29
"Tar" and Nicotine  .............................. 29

Ex-Smokers .................................... ..3 2
PipeandCigarSmoking  ............................ .38
Summary of Smoking and Overall Mortality  .............. 44

References ..................................... ..4 5

Appendix.. .............................. ..1.....4 7



       . s

Index . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..*.......

Figure 1.

Figure 2.

CHAPTER 1
List of Figures

Risks of selected pregnancy complications for
smoking and nonsmoking mothers, by period of
gestational age at delivery for A, abruptio
placentae, B, placenta previa, C, premature rup-
ture of membranes (PROM) . . . . . . . . . . . . . . . . .6
Number of cigarettes normally smoked per day
compared with COHb level at time of sampling
in 93 pregnant women. $ = mean and range of
COHb levels for 129 nonsmokers . . . - . , , . , . . . . 10

vii


Figure 3. - Oxyhemoglobin saturation curves of human
    maternal and fetal blood under control and
    steady-state conditions . . . . . . . . . . . . . . . . . . . . .I2

List of Tables

Table 1 .- Adjusted rates and F ratios for maternal
    smoking and other important factors affecting
    birth weight, gestation, placental complications,
    and perinatal mortality . . . . . . . . . . . . . . . . . . . . .4

Table 2.- Perinatal mortality and selected pregnancy
   complications, by maternal smoking levels . . . . . . `7

Table 3 .- Stillbirths according to cause in relation to
    maternal smoking during pregnancy . . . . . . . . . . .8

Table 4.- Estimated annual mortality rate per 100,000
    women from myocardial infarction and throm-
    boembolism, by use of oral contraceptives,
    smoking habits, and age (in years) . . . . . . . . . . . .I4

Table 5.- Estimated relative risks of nonfatal myocardial
    infarction, by use of oral contraceptives and
    cigarette smoking . . . . . . . . . . . . . . . . . . . . . . . . .14

CHAPTER 2

List of Figures

Figure l.- Annual probability of dying for current
    cigarette smokers, ex-smokers who quit
    less than 5 years ago, and never smokers,
    ages 55-64 . . . . . . . . . . . . . . . . . . . . . . . . ..B... 34

Figure 2.- Annual probability of dying for current
    cigarette smokers, ex-smokers who quit
    5-9 years ago, and never smokers, ages
      55-64  . . . . . . . . . . . . . . . . . . ..*............. 35


Figure 3.- Annual probability of dying for current
    cigarette smokers, ex-smokers who quit
    10-14 years ago, and never smokers, ages
    55-64 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...36

Figure 4.- Annual probability of dying for current

cigarette smokers, ex-smokers who quit
more than 15 years ago, and ex-smokers,
agesSS-64 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .37

Table l.-

Table 2.-

Table 3.-

Table 4.-

Table 5.-

Table 6.-

List of Tables

Age-adjusted mortality ratios for male
cigarette smokers, by amount smoked,
U.S. Veterans Study, 1954 cohort, 16
year follow-up . . . . . . . . . , . . . . . . . . . . . . . . . . .27
Mortality ratios for cigarette smokers, by
number of cigarettes smoked per day,
British Doctors Study . . . . . , . . . . . . . . . . . . . . . .28
Mortality ratios for male cigarette smok-
ers, by age and number of cigarettes
smoked per day, U.S. Veterans Study,
1954 cohort, 16year follow-up . . . . , . . . . . . . . .28
Age-adjusted mortality ratios for male
cigarette smokers, by age began smoking,
U.S. Veterans Study, 1954 cohort, 16
year follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . .29
Age-adjusted mortality ratios for male
cigarette smokers, by number of cigar-
ettes smoked per day and age began
smoking, U.S. Veterans Study, 1954
cohort, 16year follow-up . . . . . . . . . . . . . . . . . . .29
Mortality ratios for cigarette smokers,
by inhalation practice, British Doctors
Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...29

ix


Table 7.- Mortality ratios for all cigarette smokers in
    two time periods, by sex and "tar" and
     nicotine (T/N) content in cigarettes smoked  . . . .30

Table 8.- Mortality ratios for smokers of low "tar" and
    nicotine (T/N) cigarettes and nonsmokers in
     two time periods, by sex  .*a....*........... 31

Table 9.- Mortality ratios for all cigarette smokers and
     nonsmokers in two time periods, by sex and
     "tar" and nicotine (T/N) content of cigarettes
      smoked . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
Table lo.- Mortality ratios for ex-smokers who quit
     smoking on doctor's orders and for other
    reasons, by years since stopping, U.S. Veterans
    Study, 1954 cohort, l&year follow-up  . . . . . . . .33

Table 1 1 .- Mortality ratios for ex-smokers who quit
     smoking on doctor's orders and for other
     reasons, by number of cigarettes smoked per
    day, U.S. Veterans Study, 1954 cohort, 16-
     year follow-up  . . . . . . . . . . . . . . . . . . . . . . . .
Table 12.- Mortality ratios for ex-smokers who quit
     smoking on doctor's orders and for other
    reasons, by age began smoking, U.S. Veterans
     Study, 1954 cohort, 16year follow-up  . . . . .
Table 13.- Mortality ratios for ex-smokers of cigarettes
    only, by years since stopping, number of
     cigarettes smoked per day, and age began
    smoking. U.S. Veterans Study 1954 cohort,
     16-year follow-up . . . , . . . . . . . . . . . . . . . . . . . . .34
Table 14.-Mortality ratios for ex-smokers compared to
     nonsmokers, by number of years since stop
    ping and age, British Doctors Study . . . . . . . . . . .37

.33





.33

X


Table 15 .- Age-adjusted mortality ratios for pipe-only,
    cigar-only, and cigarette-only smokers, U.S.
    Veterans Study, 1954 cohort, 16-year
    follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .38
Table 16.- Age-adjusted mortality ratios for current cigar

Table 17. -

Table 18. -

smokers, by number of cigars smoked per
day, U.S. Veterans Study, 1954 cohort, 16
year follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . .39
Age-adjusted mortality ratios for current cigar
smokers, by age began smoking, U.S. Veterans
Study, 1954 cohort, 16-year follow-up . . . . . . . .39
Age-adjusted mortality ratios for current cigar
smokers, by number of cigars smoked per day
and age began smoking, U.S. Veterans Study,
1954 cohort, 16-year follow-up . . . . . . . , . . . . . .40

Table 19.- Age-adjusted mortality ratios for current pipe
    smokers, by number of pipefuls smoked per
    day, US. Veterans Study, 1954 cohort, 16
     year follow-up , . . . . . . . . . . . , . . . . . . . . . . . .

. .

Table 20.- Age-adjusted mortality ratios for current pipe
    smokers, by age began smoking, U.S. Veterans
    Study, 1954 cohort, 16year follow-up . . . . . .
Table 2 1 .- Age-adjusted mortality ratios for current pipe
    smokers, by number of pipefuls smoked per
    day and age began smoking, U.S. Veterans
                            _ _      ^ --

40




40

. .

Study, 1954 cohort, 16-year tbllow-up . . . . . . . .41

Table 22.-Age-adjusted mortality ratios for current cigar
    smokers, by use of other types of tobacco,
    U.S. Veterans Study, 1954 cohort, 16year
    follow-up . . . . . . . . . . . . . . . , . . . . . . . . . . . . . * .4 1

Xi


Table 23.- Age-adjusted mortality ratios for current pipe
    smokers, by use of other types of tobacco,
    U.S. Veterans Study, 1954 cohort, 16-year
     follow-up  . . . . . . . . . . . . . . . . . . . . . . . . ...**.. 42
Table 24.-Age-adjusted mortality ratios for current cigar-
    ette smokers, by use of other types of tobacco,
    U.S. Veterans Study, 1954 cohort, 16-year
     follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . ..s.. 42

Table 25.- Age-adjusted mortality ratios for all smokers,
    by type of tobacco used, British Doctors Study . .43

Xii


Preparation of the Report
and Acknowledgments

PREVIOUS REPORTS

Reviews of the scientific information linking smoking to health
problems began in 1964 with the publication of Smoking and
Health, Report of the Advisory Committee to the Surgeon General
of the Public Health Service, subsequently referred to as the "Sur-
geon General's Report." Thereafter, Public Law 89-92 was passed
requiring supplemental reports to Congress on this subject, and
the following three reports were published:
1. The Health Consequences of Smoking, A Public Health Service
  Review; I96 7.

2. The Health Consequences of Smoking, 1968 Supplement to
the 1967 PHS Review,

3. The Health Consequences of Smoking, 1969 Supplement to
the I967 PHS Review.

Public Law 9 1-22 amended the previous law in April 1970 and
required a comprehensive review within 18 months, with annual
reports to be submitted thereafter. The result of this review was
The Health Consequences of Smoking, A Report of the Surgeon
General; 1971. Since then, the following annual reports on the
health effects of smoking have been published:

1. The Health Consequences of Smoking, A Report of the Sur-
geon General, 1972.

2. The Health Consequences of Smoking, 1973.
3. The Health Consequences of Smoking, 1974.
4. The Health Consequences of Smoking, 1975.
5. The Health Consequences of Smoking, A Reference Edition,

1976.

Each report since the original "Surgeon General's Report" has
reviewed the scientific literature relevant to the association between

. . .
XIII


smoking and cardiovascular diseases, non-neoplastic bronchopul-
monary diseases, and cancer. Smoking as related to the following
diseases and conditions has been reviewed periodically in these
reports:

Allergy (1972)

Exercise Performance (1973)
Harmful Constituents of Cigarette Smoke (1972)
Noncancerous Oral Disease ( 1969)
Overview: The Health Consequences of Smoking (1975)
Overview: The Health Consequences of Smoking (1976)
Peptic Ulcer Disease (1967, 197 1, 1972, 1973)
Pipe and Cigar Smoking (1973)
Pregnancy (1967, 1969, 1971, 1972, 1973)
Public Exposure to Air Pollution from Tobacco Smoke (1972,

1975)
Tobacco Amblyopia (197 1)

THE 1977- 1978 REPORT

This publication, The Health Consequences of Smoking, 1977-l 978,
contains the most recent data on the health effects of smoking
unique to women and on the effects of smoking on overall mortal-
ity. Although emphasis is on the most recent data, research from
earlier years is included where necessary for clarity.

The report was prepared in the following way by the staff of the
National Clearinghouse for Smoking and Health, a division of the
Bureau of Health Education, Center for Disease Control, Public
Health Service :

1. The Technical Information Center of the Clearinghouse con-
tinually monitors and collects the scientific literature on the
health effects of smoking by means of several established mech-
anisms:

a. An information science corporation is under contract to

Xiv


extract articles on smoking and health from the scientific litera-
ture of the world.

b. The National Library of Medicine, through the MEDLARS
system, provides a monthly listing of articles on smoking and
health. Articles not provided by the information science cor-
poration are obtained for review.
c. Staff members review current medical literature and iden-
tify pertinent articles.

2. Initial drafts for the present report were prepared by the staff
of the National Clearinghouse and sent to experts in the content
area for review and comment regarding the format, the appro-
priateness of the articles selected for discussion, and conclusions.
The drafts were then revised by the Clearinghouse to incorporate
these comments. The final drafts of the complete report were
reviewed by the National Cancer Institute, the National Heart,
Lung, and Blood Institute, the National Institute of Environ-
mental Health Sciences, the National Institute of ChiId Health
and Human Development, and by additional experts both inside
and outside the Public Health Service.

ACKNOWLEDGEMENTS

The National Clearinghouse for Smoking and Health Director, Dan-
iel Horn, Ph.D., was responsible for the preparation of this report.
Medical Staff Director was John J. Witte, M.D. The consulting and
technical editors were Elvin E. Adams, M.D., and Susan J. Dillon,
respectively. The Technical Information Office responsible for the
literature collection was Donald R. Shopland.

The professional staff has had the assistance and advice of the
following experts in the scientific technical fields whose contribu-
tions are gratefully acknowledged:

AUERBACH, Oscar, M.D.-Senior Medical Investigator, Veterans Administra-
tion Hospital, East Orange, New Jersey

xv


COHEN, Lawrence S., M.D.-Professor of Medicine, Chief of Cardiology, Yale
University, School of Medicine, New Haven, Connecticut
FITZPATRICK, Mark J., M.D., M.P.H.-Fairhaven, Massachusetts
FRAZIER, Todd M.-Assistant Director, Center for Community Health and
Medical Care, Harvard Medical School, Boston, Massachusetts
KRETCHMER, Norman, M.D., Ph.D.-Director, National Institute of Child
Health and Human Development, Bethesda, Maryland
KRUMHOLZ, Richard A., M.D.-Medical Director, Institute of Respiratory
Diseases, Kettering Medical Center, Kettering, Ohio
LEVY, Robert I., M.D.-Director, National Heart, Lung, and Blood Institute,
National Institutes of Health, Bethesda, Maryland
MARINE, William M., M.D.-Professor and Chairman, Department of Pre-
ventive Medicine and Comprehensive Health Care, University of Colorado
Medical Center, Denver, Colorado

McMILLAN, Gardner C., M.D.-Associate Director for Etiology of Arterio-
sclerosis and Hypertension, National Heart, Lung, and Blood Institute,
National Institutes of Health, Bethesda, Maryland
MEYER, Mary B.-Associate Professor, The Johns Hopkins University, School
of Hygiene and Public Health, Baltimore, Maryland
NICHOLS, Ervin E., M.D.-Director, Practice Activities, American College of
Obstetrics and Gynecology, Washington, D.C.
PAFFENBARGER, Ralph S., Jr., M.D.-Epidemiologist, Resource for Cancer
Epidemiology, San Francisco Bay Area, California State Department of
Health, Berkeley, California

PETERSON, William F., M.D.-Chairman, Department of Obstetrics and
Gynecology, Washington Hospital Center, Washington, D.C.
PETTY, Thomas L., M.D.-Professor of Medicine and Head, Division of Pul-
monary Medicine, University of Colorado Medical Center, Denver, Colorado
RALL, David P., M.D., Ph.D.-Director, National Institute of Environmental
Health Sciences, Research Triangle Park, North Carolina
REINKE, WiIliam A., Ph.D.-Professor, Department of International Health,
The Johns Hopkins University, Baltimore, Maryland
RENZETTI, Attilio D., Jr., M.D.-Professor of Medicine and Head, Pulmonary
Disease Division, The University of Utah Medical Center, Salt Lake City,
Utah

SCHUMAN, Leonard M., M.D.-Professor and Head, Division of Epidemiology,
School of Public Health, University of Minnesota, Minneapolis, Minnesota
UPTON, Arthur C., M.D.-Director, National Cancer Institute, National Insti-
tutes of Health, Bethesda, Maryland

WYNDER, Ernest L., M.D.-President, American Health Foundation, New
York City, New York

Xvi


Chapter 1
Smoking-Related Health Problems
Unique to Women
Contents

Page

Introduc~on...................................... 1
Effects of Smoking on the Outcome of Pregnancy . , . . . . . . .  1

Smoking and Birth Weight . . . , . . . . . . . . . . . . . . . . . . . . .  1
Smoking and Perinatal Mortality . . . . . . . . . . . . . . . . . . . .  2
Long-Term Effects on Physical
and Intellectual Development , . . . . . . . . . . . . , . , . . , , . , .  8
Carbon Monoxide and Carboxyhemoglobin Levels in
Maternal and Fetal Circulation and the Possible
Mechanisms of Smoking Effects on Pregnancy . . . . . . . . . . . .  9
Smoking and Its Effects on Cardiovascular Disease Among
Women Taking Oral Contraceptives . . . . . . . , . , . . . . . . . . . .  13
Effects of Cigarette Smoking on Lactation . . . . , . . . . . . . . . .  15
What Women Know About Smoking and Pregnancy . . . . . . .  15
Summary of Smoking-Related Health Problems
Unique to Women . . . . . . . . . . . . . . . . . , . . . . . . . . . . . . . . .  17

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  18

xvii


Chapter 1
Smoking-Related Health Problems
Unique to Women

INTRODUCTION

Smoking habits and attitudes among women and teenage girls have
differed in the past from the habits and attitudes among men and
teenage boys. Women tended to smoke fewer cigarettes, were less
likely to inhale, and were more likely to smoke low "tar" and nico-
tine and filter-tipped brands. Surveys have indicated, however, that
the smoking habits of women are becoming more like men's, Women
are taking up the habit at an earlier age and have become heavier
smokers. This has made them more vulnerable not only to lung
cancer and other smoking-related diseases, but also to specific
health problems that are unique to their sex. For example, research
on the relationship between cigarette smoking and the outcome of
pregnancy has established that there are definite risks to both the
fetus and the mother associated with cigarette smoking during
pregnancy. Moreover, women who use oral contraceptives are at
greater risk of cardiovascular disease if they smoke cigarettes. There
is also evidence that nicotine is present in the breast milk of lactat-
ing mothers who smoke. The following is a review of the current
information on these and other health consequences of smoking
unique to women.

EFFECTS OF SMOKING ON THE OUTCOME OF PREGNANCY

There are definite health risks associated with smoking and preg-
nancy, including effects on birth weight, perinatal mortality, and
long-term physical and intellectual development of the child. This
section reviews each of these subjects and also includes information
about the likely mechanism of action of smoke and its contents on
the mother and the products of conception.

Smoking and Birth Weight

In 1957, Simpson published her original finding that babies born
to women who smoke during their pregnancy weigh on the average
200 grams (g) less than the babies born to women who do not smoke

1


(34). Since then, more than 100 articles on this relationship have
led to the general acceptance that smokers' babies generally weigh
150 to 250 g less than nonsmokers' babies, and twice as many of
the former weigh less than 2500 g (13). The 1973 report of The
Health Consequences of Smoking presented evidence to support
a causal association between cigarette smoking and fetal growth re-
tardation (39). A strong dose-response relationship was also estab-
lished in that report, with differences in weight being in direct pro-
portion to the number of cigarettes smoked.
The following additional points were summarized in the 1973
report to further support the causal association between cigarette
smoking during pregnancy and lower birth weight:
1. Results are consistent in all studies, retrospective and pro-
spective, from many different countries, races, cultures, and
geographic settings.

2. The relationship between smoking and reduced birth weight
is independent of other factors that influence birth weight, such
as race, parity, maternal size, socioeconomic status, sex of child,
and all others that have been studied.

3. If a woman gives up smoking by the fourth month of preg-
nancy, her risks of delivering a low-birth-weight baby is similar
to that of a nonsmoker.

Subsequent to the 1973 report, additional reports have further
discussed and corroborated the association between smoking in
pregnancy and low birth weight (19, 25,33, 35).

Smoking and Perinatal Mortality

A strong, probably causal, association between cigarette smoking
and higher late fetal and infant mortality rates among smokers'
infants is now well established (38). Retrospective and prospective
studies have revealed a statistically significant relationship between
cigarette smoking and an elevated mortality risk among the infants
of smokers. In three of these studies of sufficient size to permit ad-
justment for other risk factors, a highly significant independent as-
sociation between smoking and mortality was established. Part of
the discrepancy in results between these studies and those in which
a significant association between smoking and infant mortality was
not demonstrated may be explained by a lack of adjustment for
risk factors other than smoking.

The 1973 report also presented evidence indicating that the
higher relative risks occurred among populations with risk factors
other than smoking being present, such as socioeconomic status,
age, parity, race, and previous pregnancy history.

2


Since 1973, a series of articles by Meyer, et al. analyzed data
from the Ontario Perinatal Mortality Study of all single births in ten
Ontario teaching hospitals in 1960-61 (26, 27, 28). The study in-
volved 5 1,490 births, including 701 fetal deaths and 655 early neo-
natal deaths, and was supplemented by clinical records with inter-
views of mothers in the hospital, interviews with anesthetists and
attending physicians, and autopsy records (29). Perinatal mortality
increased significantly with smoking and was also affected by such
factors as maternal age, parity, socioeconomic status, previous
pregnancy history, hemoglobin level, and other risk factors (29).
Smoking frequencies also varied by many of these characteristics.
Smoking and other risk factors were cross-tabulated among 52
data subgroups. In all subgroups, the mortality increase with
smoking was dose related, but not in a simple, linear way. The
increased risk of perinatal mortality associated with light smoking
among young, low-parity, nonanemic mothers was less than 10
percent. At the other extreme, mothers with other risk factors
of high parity, public hospital status, with previous low-birth-weight
infants, or with hemoglobin less than 11 g had further increased
perinatal mortality risks of 70- 100 percent when they were smokers.
The most significant risk factor (mortality rate of 78 per 1,000
total births) was anemia, defined as a hemoglobin of less than 8.0
g. The failure of some earlier studies to find a significant increase in
perinatal mortality with maternal smoking may be due to selection
of study populations from the end of the spectrum, where light
smoking is associated with only a slight increase in perinatal risk.
This evidence points up how population selection could influence
study findings and shows that exposure to the effects of smoking
during pregnancy is much more dangerous for the babies of some
women than for others. These findings are corroborated by a num-
ber of studies in which fetal, neonatal, or perinatal mortality rates
are compared for smoking and nonsmoking women, controlling for
the effects of various risk factors previously mentioned (1, 12, 22,
36).

Additional data were published in 1976- 1977 (26, 27) and re-
vealed that frequencies of low birth weight (under 2500 g), preterm
delivery (< 38 weeks), perinatal mortality, abruptio placentae, pla-
centa previa, bleeding during pregnancy, and prolonged and pre-
mature rupture of the membranes increased directly and signifi-
cantly (p< 0.00001) as the level of maternal smoking increased
(Tables 1 and 2). The 1976 paper used multiple regression analysis
to measure the independent effect of smoking on the various risk
factors. The probabilities of these complications were also com-
pared (Figure 1). Risks of placenta previa and abruptio placentae
were higher for smokers than for nonsmokers at all gestations, with

3


TABLE 1. Adjusted rates and F ratios for maternal smoking and other impor-
    tant factors affecting birth ,weight, gestation, placental complica.
     tions, and perinatal mortality

Factor            *Adjusted Rates of Outcome            tF Ratio

Maternal Smoking Level
NOIIS
< 1 Pack Per Day
> 1 Pack Per Day

Previous Pregnancy History
No Prwious Pregnancy
Previous Pregnancy, 0 Loss
Previous Pregnancy, Loss

Hospital Pay Status
Private
Public

-

Birth Weight < 2500 Grams
   Per 1000 Births

49.4                       182.8
75.7
113.7

70.0                       123.5
57.8
134.0

60.0
87.4

84.0

Gestation < 38 Weeks
Per 1000 Births

Maternal Smoking Level
None

77.1                         50.6

< 1 Pack Per Day                  92.2
> ' Pack Per Day                 115.9

Previous Pregnancy History
No Previous Pregnancy

69.1                         182.6

Previous Pregnancy, 0 Loss            85.7
Previous Pregnancy, Loss           193.9

Hospital Pay Status
Private

78.9                        120.3

Public

   116.2

Placenta Previa
Per 1000 Births

Maternal Smoking
None

6.5                          11.7

< 1 Pack Per Day                   a.1
> 1 Pack Per Day                  12.5

Previous Pregnancy History
No Previous Pregnancy

8.8

14.4

Previous Pregnancy. 0 Loss            6.6
Previous Pregnancy, Loss             15.8

(Hospital pay status not a significant factor)

4


TABLE 1.

Adjusted rates and F ratios for maternal smoking and other impor-
tant factors affecting birth weight, gestation, placental complica-
tions, and perinatal mortality (con/inu~d)

,",84d Smoking

< 1 Pack Per Day
> I Pack Per Day

Previous Pregnancy History
NO Previous Pregnancy
Previous Pregnancy, 0 Loss
Previous Pregnancy, Loss

Hospital Pay Status
Prwate
Public

Abruptio Placentae
Per 1000 Births

16.4                          17.1
20.3
27.6

18.8                         25.6
17.6
37.4

17.5                        20.7
25.0

Perinatal Mortality
Per 1000 Births

Maternal Smoking
Rone
< 1 Pack Per Day
> 1 Pack Per Day

Previous Pregnancy HistOW
No Previous Pregnancy
Previous Pregnancy, 0 Loss
Previous Pregnancy, LOSS

23.5                           8.4
28.2
31.8



23.1                         97.4
23.6
68.7

Hospital Pay Status
Private

23.3                         44.2

Public                        36.1
*Adjusted rates show independent effect of the factor given, adjusted for all other factors
in regression. They are: maternal smoking, hospital pay status, mothers' bhthpla~,
height, prepregnant weight, sex of child, previous pregnancy history, and age-parity.

tF ratio degrees of freedom: numerator = number of subgroups -1, denominator = infhity.
(All differencesshown are highly significant. F ratios indicate the relative importance of
the factor.)
SOURCE: Personal correspondence, based on data in Meyer, M.B., et al. (26).


    0.02 - -        0
                         A




    0.01 - -
   0.006

   0.008


   0.004 - -

6I
.s
P   0.002 - -
2
9
z  0.001 = =
4 0.0006
ti  0.0006

t 0.0004

  FIGURE l.-Risks of selected pregnancy complica-
  tions for smoking and nonsmoking mothers, by period
  of gestational age at delivery for A, abruptio pla-
  centae, B, placenta previa, C, premature rupture of
  membranes (PROM)
  SOURCE: Meyer M B et al. (27).
            --L -`--r-- ~. .--
4
0.04-e

t :    I    I    I I    I    II    I    II
        I    I    I I    I    II    I    I I

20       24       28      32      36       40      44
Gestation: Weeks

0.004 - -

.s
B   0.001 - -

&  0.0008
f  0.0006
8
$  0.0004--

6
g  0.0002--
%
%
t  0.0001 -L

0
El

I    Ill    I I t I I I    I I
    I I l    Ill1 I    I    I I
20       24      28      32      36       40      44
Gestation: Weeks

6


0.1

0.06

0.06

0
C

0.001
0.0008

0.0008

g 0.0004
L
z
.g 0.0002
D
2
e
0. 0.0001

I    I    I I    I I    I    I    I    I    II
    I    1 I    I I    I    I    I    I    I I
20       24       28       32       36       40      44
Gestation: Waaks

TABLE 2. Perinatal mort&ty and selected pregnancy complications, by
     maternal smoking levels

Smoking level (packs per day)
(rates per 1.000 total births)

Outcome

Perinatal Mortality
Abruptio Placentae
Placenta Previa
Bleeding During Pregnancy
Rupture of Membranes
  > 48 Hours
Rupture of Membranes
Only at Admission

0
23,358
Births)

23.3       28.0
16.1        10.6
6.4         8.2
116.5       141.6


15.8        23.3

30.3        39.3

&`s*
Births)       2*
          X

33.4        27.8*
28.9       47.32
13.1        28.6*
180.1      201.9f

35.8       109.9f

45.0       45.7i

o Cochran's chi square for trends.

*p < 0.00001.

SOURCE: Meyer, M.B.. et al. (27).

7


relatively larger differences in the earlier weeks of pregnancy. The
risk of premature rupture of membranes was more than three times
greater for smokers than for nonsmokers among deliveries that oc-
curred before 34 weeks gestation and remained higher than the
risk for nonsmokers through term (Figure 1C).

A prospective investigation of 9,169 pregnant women was con-
ducted by Goujard, et a.l. (15), and results showed a substantial
increase in stillbirths among smokers. A large proportion of this
increase was due to abruptio placentae. There were 100 stillbirths,
classified into tive categories of causes: vascular, abruptio placen-
tae, mechanical, miscellaneous (syphilis, Rh, malformations, etc.),
and unknown (Table 3). The abruptio placentae category exclu-
sively represented cases without toxemia, the one toxemic case
being classified with the vascular causes. The higher proportion
of smokers is significant for only two of the categories: abruptio
placentae (p = 0.005) and unknown causes (p = 0.0005). Although
the numbers were small, the risk of stillbirths by abruptio placentae
is six times higher among smokers.

TABLE 3. Stillbirths according to cause in relation to maternal smoking
     during pregnancy

                                        Comparison
                      Number of       Percent          With Live
Stillbirths               Deliveries       Smokers         Births*

Cause of Death:

Vaaculer
Abruptio Placentae
Mechanical
Miscellaneous (Syphilis,
Rh, Malformations, . . .)
Unknown
Detailed Records Not

0~
13
13

24
31

2s
46
15
::

p = 0.005




p = 0.0005

Available                    5
    TOTAL               100

2ti

p = 0.0001

Livebirths                   9069

i When p is not given, the difference is not significant.

SOURCE: Goujard, J., et al. (15).

12

Long-Term Effects on Physical and Intellectual Development
Three studies (6, 16, 40) report on long-term effects of smoking
in pregnancy. Data from two of the studies presented below demon-
strate an association between smoking during pregnancy and im-
paired physical and intellectual development in the offspring.
Additional reports further substantiate this association (10, 11).

Butler and Goldstein (6) analyzed the National Child Develop-
ment Study, a longitudinal study of 17,000 children born in Britain
from March 3 to 9, 1958. The test procedures included a reading

8


test at the age of 7 years, and a mathematics test, a reading test,
and a general ability test at the age of 11. At both ages the height
of the child was also measured. Analyses at both ages were based
on smoking habits of the mother after the fourth month of pregnancy

Statistically significant differences in height and reading ability
between smoking categories (0, l-9, or lO+ cigarettes daily) were
found at both 7 and 11 years of age.

When account was taken for such factors as mother's height,
age, social class as determined by father's occupation, number of
older and younger children in the household, and the sex of the
child, there was a deficit of height and reading ability in the off-
spring of mothers who smoked, the extent of which increased with
the amount smoked.

These results establish an association of smoking in pregnancy
with later intellectual development, although the gap between child-
ren of smokers (at all levels of smoking) and nonsmokers does not
appear to change between the ages of 7 and 11 years. Smoking in
pregnancy is associated with an impairment of both mental and
physical growth, although compared with other social and biologi-
cal factors, the effects are small.

In the study by Wingerd and Schoen (40), the net effects of
various factors on length at birth and height at 5 years were deter-
mined in 3,707 single-born, white California children. Children of
smoking mothers were found to be shorter (p< 0.001) at birth and
at 5 years than children of nonsmoking mothers. (Intellectual de-
velopment was not measured in this study.)

In contrast to these results, Hardy and Mellits (16) found very
few significant differences in a number of body measurements and
intellectual functions up to the age of 7 years between children of
smokers and nonsmokers. A possible explanation for this discre-
pancy is that their sample was too small, and a weight-matched con-
trol group could add a bias. Whereas the British study by Butler and
Goldstein involved a sample size of over 5,000 children, Hardy and
Mellits based their t'indings on only 88 matched pairs of children.
Calculations by the authors of the British study show that with the
small sample used by Hardy and Mellits there was only about a 20
percent probability of detecting statistically significant differences
in the heights of children born to smoking and nonsmoking mothers.

CARBON MONOXIDE AND CARBOXYHEMOGLOBIN LEVELS
IN MATERNAL AND FETAL CIRCULATION AND THE POS-
SIBLE MECHANISMS OF SMOKING EFFECTS ON PREGNANCY

There is evidence to show that carboxyhemoglobin (COHb) levels
are substantially elevated in pregnant women who smoke and may
result in damage to placental and fetal blood vessels. Higher levels

9


of COHb in both fetal and maternal blood may also be a factor in
the increased incidence of low birth weight of infants born to
women who smoke.

Cole, Hawkins, and Roberts (7) studies the smoking habits of a
group of pregnant women and related these to the level of COHb in
the circulating blood. A group of 222 patients attending antenatal
clinics at a London hospital were questioned about their smoking
habits. Ninety-three (42 percent) were smokers, and 129 (58 per-
cent) were nonsmokers. Simultaneous maternal and cord blood
samples were taken at normal delivery and at Caesarean section
from 28 patients, and the COHb and fetal hemoglobin levels of
the samples were measured. Results showed that women who
smoke during pregnancy have a significantly higher level of COHb
in their blood than women who do not smoke (p< 0.01). The mean
COHb levels were 1.2 percent (range 0 to 2.4 percent) for the non-
smokers and 4.1 percent (range 0.5 to 14 percent) for the smokers.
There was a positive correlation betwen the number of cigarettes
smoked on the day of sampling and the COHb level (correlation
coefficient 0.82) (Figure 2). With the exception of two patients,

FIGURE 2.-Number of cigarettes normally smoked
per day compared with COHb level at time of sam-
pling in 93 pregnant women. $ = Mean range of
COHb levels for 129 nonsmokers

15  -

o

10           20           30           40
    Cigarettes Smoked Per Day

SOURCE: Cole, P.V., et al. (7)

10


all the fetal COHb 1 evels were demonstrably higher than the re-
spective maternal ones. The mean fetal/maternal COHb ratio was
1.84 to 1 (standard deviation ~0.85). Hemoglobin has a 210 times
greater affmity for carbon monoxide (CO) than for oxygen. It is
obvious, therefore, that cigarette smoking during pregnancy dimin-
ishes the oxygen carrying capacity of both fetal and maternal blood.
This affects maternal oxygenation by increased pulmonary venous
admixture and diminishes the oxygen available to the fetus at the
tissue level by its effect on fetal oxyhemoglobin dissociation.

In a 1975 report by Dow, Rooney, and Spence (1 1), a signifi-
cantly greater rise in COHb concentration in response to smoking a
single cigarette was shown in pregnant women (3.9 percent increase)
as opposed to nonpregnant women (2.1 percent increase). This was
more pronounced when anemia was present (5.0 percent increase)
and appeared to be inversely related to the hemoglobin concentra-
tion. Three groups of women, all smokers, were selected for this
study. The first group consisted of 10 normal, pregnant women late
in the second trimester of pregnancy, with hemoglobin levels of
over 11 g per 100 milliliters (ml). The second group consisted of 10
women also late in the second trimester but whose hemoglobin
levels were less than 10 g/ 100 ml. Apart from anemia at the time of
admission to the study, these patients were normal, The third group
consisted of 10 normal, nonpregnant women with normal hemoglo-
bin levels (over 11 g/l00 ml). The change in COHb was estimated
spectrophotometrically in response to smoking the first cigarette
of the morning, the women having rested for at least 30 minutes. A
sample of venous blood was withdrawn before and 2 minutes after
smoking the cigarette. The cigarettes were of a standard size and of
a "non-mild" (i.e., not low "tar" and nicotine) variety. The women
were instructed to take a puff every 40 seconds, inhaling as deeply
as possible, to a total of 10 puffs.

In the nonpregnant group, the mean rise in COHb concentration
(&standard error of mean) was 2.1kO.2 percent. A significantly
greater increase was found in the normal pregnant group (mean rise
3.950.4 percent; t=3.91; p<O.OOS). The effect was more pro-
nounced in the anemic pregnant women, who had a meaning rise of
5.OkO.2 percent (t=9.9; p<O.O005).

Longo (21) studied the effects of CO on oxygenation of the fetus
in utero. Results showed that the partial pressure of oxygen in fetal
blood decreases in proportion to the COHb concentrations in fetal
and maternal blood (Figure 3).

This decrease in oxygen tension may be a factor in the low
birth weight of infants born to women who smoke or are exposed
to severe air pollution. These results suggest that significant in-
creases in maternal and fetal COHb concentrations can significantly
reduce oxygen deiivery to the fetus.

11


   FIGURE 3.-Oxyhemoglobin saturation curves of
    human maternal and fetal blood under control and
    steady-state conditions*









                      111-------1111-------------









     0    10 20    30    40   50 60 70    60 90 100
              PC+ (torrl
   *With 10 percent fetal and 9.4 percent maternal
   HbCO concentrations. The maternal and fetal hemo-
   globin contents were assumed to equal 12 and 16.3
   per 100 ml of blood, respectively. A normal O2 con-
   sumption of 5 ml per 100 ml of blood was assumed
   for both the uterus and its contents and the fetus.
   SOURCE: Longo, L., (21)
Astrup, et al. (3) carried out experimental studies on animals
which may have a correlation with other data based on human
studies in this report.
The investigation studied the effect of moderate CO exposure
(180p.p.m. and 90p.p.m. CO in atmospheric air) on fetal develop
ment in rabbits. Exposure to 180p.p.m. CO (16-18 percent COHb)
during pregnancy resulted in a 20 percent decrease in birth weight
and a neonatal mortality rate of 35 percent as against 1 percent in
the control group. Exposure to 90p.p.m. CO (8-9 percent COHb)
had a less pronounced effect. There was a negative correlation
between birth weight and maternal COHb concentration (p<O.O5).
The authors conclude that these results indicate that CO in tobacco
smoke might be responsible for the reduced birth weight of babies
whose mothers smoke during pregnancy.

12


A report from Denmark by Asmussen and Kjeldsen (2) studied
the umbilical artery as a possible model for evaluating the vascular
injury provoked by tobacco smoking in humans. Cords from new-
born children delivered by 15 nonsmoking and 13 smoking mothers
were studied in the transmission and the scanning electron micro-
scope. The average weight of children born to smokers was 3,370 g
and that of children born to nonsmokers was 3,695 g, a difference
of 325 g. A difference of 123 g was found in the weights of the
placentas.

Pronounced changes in the intima were found in the umbilical
samples from smokers. The most important findings were degenera-
tive changes in the endothelium, such as swelling, bleeding, contrac-
tion, and subsequent opening of the endothelial junctions, with
formation of subendothelial edema. The basement membranes
were considerably thickened. The smooth muscle cells in the
ecematous subendothelial space often showed vacuolization. Since
similar changes can be induced in arteries of animals by exposure
to CO or perfusion with nicotine, the authors conclude that cigar-
ette smoking is harmful to the vascular endothelium and may pro-
vide some rationale for the mechanism behind low birth weights
and increased perinatal mortality.

SMOKING AND ITS EFFECTS ON CARDIOVASCULAR
DISEASE AMONG WOMEN TAKING ORAL CONTRACEPTIVES
Smoking is a major cause of cardiovascular disease among women,
and it has been found that the use of oral contraceptives potenti-
ates its effect. Therefore, women who smoke and use oral contra-
ceptives are at a much higher risk for cardiovascular disease and
should be encouraged to stop smoking. In a review by Ory (30) of
the original scientific data that exists on the association between
oral contraceptives and myocardial infarction, cigarette smoking
was found to be the most important factor in increasing the proba-
bility of women less than 50 years of age having myocardial infarc-
tion. Although this increased risk is independent of oral contra-
ceptive use, oral contraceptive use appears to be an added risk
factor. The use of these drugs in the absence of other predisposing
factors appears to have only a small effect on increasing the risk
of dying from myocardial infarction.

Jain (18) studied the risk of mortality associated with the use of
oral contraceptives. For women 40-44 who neither use oral contra-
ceptives nor smoke cigarettes, the overall mortality rate from myo-
cardial infarction is 7.4 per 100,000 (Table 4). The comparable
annual mortality rate among women of this age group who use
oral contraceptives but do not smoke is 10.7 per 100,000. This
compares to a rate of 62 per 100,000 for women who take oral
contraceptives and smoke.

13


TABLE 4.

Estimated annual mortality rate per 100,000 women from mycar-
dial infarction and thromboembolism, by use of oral contraceptives,
smoking habits, and age (in years)

  Myocardial Infarction
Women Aged   Women Aged
  30-39         4044

   Thromboembolism
Women Aged   Women Aged
  20-34         3544
                --

Smoking Habits  Users Nonusers Users Nonusers Users Nonusers beers Nonweq
All Smokers     10.2    2.6     62.0    15.9     1.6    0.2      4.1    0.6
Heavy       13.0    5.1     78.7   31.3     4.4    0.2     11.4    0.6
Light        4.7    0.9     28.6    5.7     0.7    0.2      1.9    0.6

Nonsmokers      1.8    1.2     10.7    7.4     1.4    0.2      3.6    0.4

Smokers and
Nonsmokers    5.4    1.9     32.8    11.7     1.5    0.2      3.9    0.5

*Estimated rates for smokers and nonsmokers were 0.24 and 0.16 respectively.
Rates appear the same because of rounding.

SOURCE: Jain, A.K. (18).

In a later study, Jain (17) analyzed the synergistic effect of
smoking and the use of oral contraceptives on myocardial infarc-
tion. The relative risk of nonfatal myocardial infarction among
those who use oral contraceptives and smoke is estimated to be
11.7 to 1 (Table 5). The authors suggest that smoking should be
considered as another contraindication for the prescription of
oral contraceptives.

TABLE 5. E&mated relative risks of nonfatal myocardial infarction, by USe

of oral contraceptives and cigarette smoking.

Smoking Data

Smokers

Current User of Oral Contraceptives
  Yes              No

Total                          11.67
Heavy o                         14.81
Light?                           5.38
Nonsmokers                       2.02

Based on data in Table VII by Mann and associates (25).

2.15
4.23
0.77
1 .oo

*Heavy smokers: at least 15 cigarettes per day.

tLight smokers: less than 15 cigarettes per day.

SOURCE: Jain, A.K. (17).

Results of a study by Beral (4) indicate that oral contraceptive
users who smoke have a 10 times greater risk of dying from cardio-
vascular disease than women who neither smoke nor use the pill.
Smoking by itself was responsible for a Cfold increase in the risk
of dying from cardiovascular diseases. Oral contraceptive use in the
absence of smoking also appeared to increase one's risk, but the dif-
ferences were not statistically significant.

Mann and his colleagues also studied tne relationships between
smoking and myocardial infarction in women (23, 24). Their find-

14


ings show an apparent but not a statistically significant increase in
relative risk of nonfatal myocardial infarction for nonsmokers who
use oral contraceptives (2.02, with a 95 percent confidence interval
of 0.5 to 8.5). In contrast, for smokers who use oral contraceptives,
the relative risk was estimated to be 11.67 compared to that of the
nonsmoking, noncontraceptive user. In addition, these authors re-
ported that the risk of nonfatal myocardial infarction was related
to the amount smoked. It was found that in comparison with non-
smokers and ex-smokers, the relative risk of myocardial infarction
increased significantly to 1.3 in women smoking fewer than 15
cigarettes a day, to 4.4 in women smoking 15 to 24 cigarettes a
day, and to 11.9 in women smoking 25 or more cigarettes a day.

Among nonsmokers, oral contraceptive users have 2.0 (95 per-
cent confidence interval, 0.5 to 8.5) times the risk of having a myo-
cardial infarction. (Because the confidence interval includes 1.0,
chance variation is a possible explanation for this fmding.) Among
smokers, if a woman uses oral contraceptives, she has 5.4 (95
percent confidence interval, 2.0 to 14.7) times the risk of having
a myocardial infarction than if she is a nonuser. This result is highly
statistically significant (p = 0.001).

EFFECTS OF CIGARETTE SMOKING ON LACTATION

Studies by Richer and Giudicelli (31), Rowan (32), and Vorherr
(39), further document the effects of nicotine in breast milk on in-
fants of smoking mothers. Since nicotine has been shown to cause
nausea, vomiting, diarrhea, and tachycardia (38), it is recommended
by the authors that lactating mothers refrain from smoking.

Bradt and Herrenkohl (5) studied the relationship between ciga-
rette smoking and DDT in human milk. A total of 55 human milk
samples from eastern Pennsylvania were studied. Ten of the donors
were cigarette smokers, and they donated 13 of the milk samples.
Results of the study showed that smoking was one of four variables
which contributed to the increase in DDT. Mean total for the non-
smoker was .lOl units versus .146 units for smokers. Four factors
were identified statistically as accounting for 54 percent of the
variance on total DDT levels in human milk. These factors are: (1)
number of children nursed; (2) number of cigarettes smoked daily;
(3) use of nonpersistent pesticides; and (4) diet in calories. The re-
lationship between the number of cigarettes smoked per day and the
total amount of DDT in human milk suggests either that cigarette
smoke may be a source of the human body burden of DDT or that
cigarette smoke may cause more DDT to be excreted in the milk.

WHAT WOMEN KNOW ABOUT SMOKING AND PREGNANCY
There is much information circulating in the scientific community

15


regarding the effects of smoking on health in general and, specifi-
tally, on the outcome of pregnancy. In a survey conducted by the
National Clearinghouse for Smoking and Health (37), an attempt
was made to find out how successfully this information had been
disseminated to the general population and particularly to women.

To what extent was the average woman informed about the con-
sequences of her smoking on her own health and the health of her
unborn child? The questions were designed to find out what women
knew at the time of their last pregnancy (which in some cases was
many years ago) and what they knew at the time of the survey.
At the time of their last pregnancy, 24 percent said they believed
smoking was hazardous to the health of a pregnant woman, and 31
percent said they believed it harmed the developing fetus,
At the time of the survey in 1975, however, 53 percent reported
that they knew smoking was harmful to a pregnant woman, and 60
percent believed it harmed the fetus.

It is clear that the level of knowledge among women about the
effects of smoking on pregnancy is appreciably lower than that in
the scientific community.

16


SUMMARY OF SMOKING-RELATED
PROBLEMS UNIQUE TO WOMEN

1. A strong, probably causal, association exists between ciga-
rette smoking and higher late fetal and infant mortality among
smokers' infants.

2. Perinatal mortality increases significantly with smoking as
well as with other risk factors such as maternal age, parity, socio-
economic status, previous pregnancy history, and hemoglobin level.
3. A dose-response relationship exists between smoking and the
incidence of low birth weight, preterm delivery, perinatal mortality,
abruptio placentae, placenta previa, bleeding during pregnancy, and
prolonged and premature rupture of the membranes.
4. In one study, the risk of premature rupture of membranes
was more than three times greater for smokers than for nonsmokers
among deliveries that occurred before 34 weeks gestation.
5. In another study, the risk of stillbirths by abruptio placentae
was six times higher among smokers.
6. There is an association between smoking during pregnancy
and impaired physical and intellectual development in the offspring.
7. COHb levels are substantially elevated in pregnant women
who smoke and may result in damage to placental and fetal blood
vessels.

8. Higher levels of COHb in both fetal and maternal blood may
be a factor in the increased incidence of low-birth-weight babies
among smokers.

9. The use of oral contraceptives potentiates the harmful ef-
fects of smoking on the cardiovascular system.
10. Results from one study showed that the relative risk of non-
fatal myocardial infarction among women who use oral contra-
ceptives and smoke is approximately 11.7 to 1.
11. Nicotine is present in the breast milk of lactating mothers
who smoke and has been shown to cause nausea, vomiting, diarrhea,
and tachycardia.

12. In one study, smoking was one of four variables which con-
tributed to the increase of DDT in breast milk.
13. As recently as 1975, 40 percent of the women in the United
States were not aware of the hazards to the developing fetus if they
smoked during pregnancy.

17


REFERENCES

1. ANDREWS, J., McGARRY, J.M. A community study of smoking in preg
nancy. Journal of Obstetrics and Gynaecology of the British Common.
wealth 79 (12): 1057-1073, December 1972.
2. ASMUSSEN, I., KJELDSEN, K. Observation on arteries from newborn
children of smoking and nonsmoking mothers. Circulation Research 36:
579-589, May 1975.

3. ASTRUP, P., TROLLE, D., OLSEN, H.M., KJELDSEN, K. Effect of
moderate carbon monoxide exposure on fetal development. Lancet 2
(7789): 1220-1222, December 9, 1972.
4. BERAL, V. Mortality among oral contraceptive users. Lancet 2. (8041):
727-73 1, October 8, 1977.

5. BRADT, P.T., HERRENKOHL, R.C. DDT in human milk. What deter.
mines the levels? Science of the Total Environment 6(2): 161-163, Sep.
tember 1976.

6, BUTLER, N.R., GOLDSTEIN, H. Smoking in pregnancy and subsequent
child development, British Medical Journal 4(5892): 573-575, December
8, 1973.

7. COLE, P.V., HAWKINS, L.H., ROBERTS, D. Smoking during pregnancy
and its effects on the fetus. Journal of Obstetrics and Gynaecology of the
British Commonwealth 79(9): 782-787, September 1972.
8. COLLINGWOOD, J.M. Smoking during pregnancy: effects on perinatai
mortality and on subsequent intellectual and physical development. Health
Visitor 47: 6869, March 1974.

9. DOW, T.G.B., ROONEY, P.J., SPENCE, M. Does anaemia increase the
risks to the fetus caused by smoking in pregnancy? British Medical Journal
4(5991): 253-254, November 1, 1975.

10. DUNN, H.G., McBURNEY, A.K., INGRAM, S., HUNTER, C.M. Maternal
cigarette smoking during pregnancy and the child's subsequent develop-
ment: I. Physical growth to the age of 6% years. Canadian Journal of
Public Health 67(6): 499-505, November-December, 1976.
11. DUNN, H.G., McBURNEY, A.K., INGRAM, S., HUNTER, C.M. Maternal
cigarette smoking during pregnancy and the child's subsequent develop-
ment: II. Neurological and intellectual maturation to the age of 6l% years.
Canadian Journal of Public Health 68: 43-50, January/February 1977.
12. FABIA, J. Regression multiple dupoids de naissance utilisant dix variables
"predictives." Canadian Journal of Public Health 64: 548-55 1, November/
  December 1973.

13. FIELDING, J.E., RUSSO, P.K. Smoking and pregnancy. New England
  Journal of Medicine 298(6): 337-339, February 1978.
14. FORREST, J.M. Drugs in pregnancy and lactation. Medical Journal of
  Australia 2(4): 138-141, July 24, 1976.
15. GOUJARD, J., RUMEAU, C., SCHWARTZ, D. Smoking during preg-
nancy, stillbirth, and abruptio placentae. Biomedicine 23( 1): 20-22, Feb-
  ruary 10,197s.

18


16. HARDY, J., MELLITS, E.D. Does maternal smoking during pregnancy
have a long-term effect on the child? Lancet 2 (7791): 1332-1336. Decem-
ber 23, 1972.

17. JAIN, A.K. Cigarette smoking, use of oral contraceptives, and myocardial
infarction. American Journal of Obstetrics and Gynecology 126 (3): 301-
307, October 1, 1976.

18. JAIN, A.K. Mortality risk associated with the use of oral contraceptives.
Studies in Family Planning 8(3): 50-54, March 1977.
19. KAMINSKI, M., GOUJARD, J., RUMEAU-ROUQUETTE, C. Prediction
of low birthweight and prematurity by a multiple regression analysis with
maternal characteristics known since the beginning of pregnancy. Inter-
national Journal of Epidemiology 2(2): 195204, 1973.
20. KLINE, J., STEIN, Z.A., SUSSER, M., WARBURTON, D. Smoking: a risk
factor for spontaneous abortion.  New England Journal of Medicine
297( 15): 793-796, October 13, 1977.

21. LONGO, L. Carbon monoxide: effects on oxygenation of the fetus in
utero. Science 194(4264): 523-525, October 29, 1976.
22. LUBS, M. Racial differences in maternal smoking effects on the newborn
infant. American Journal of Obstetrics and Gynecology 115( 1): 66-76,
  January 1, 1973.

23. MANN, J.I., INMAN, W.H.W., THOROGOOD, M. Oral contraceptive use
in older women and fatal myocardial infarction. British Medical Journal 2:
  445447, 1976.

24. MANN, J.E., VESSEY, M.P., THOROGOOD, M., DOLL, R. Myocardial in-
farction in young women with special reference to oral contraceptive prac-
tice. British Medical Journal 2: 241-245, 1975.
25. MEREDITH, H.V. Relation between tobacco smoking of pregnant women
and body size of their progeny: a compilation and synthesis of published
studies. Human Biology 47(4): 451-472, December 1975.
26. MEYER, M.B., JONAS, B.S., TONASCIA, J.A. Perinatal events associated
with maternal smoking during pregnancy. American Journal of Epidemi-
ology 103(5): 464-476, 1976.

27. MEYER, M.B., TONASCIA, J.A. Maternal smoking, pregnancy complica-
tions, and perinatal mortality. American Journal of Obstetrics and Gyne-
cology 128: 494-502, July 1, 1977.

28. MEYER, M.B., TONASCIA, J.A., BUCK, C. The interrelationship of ma-
ternal smoking and increased perinatal mortality with other risk factors.
Further analysis of the Ontario Perinatal Mortality Study, 1960-1961.
American Journal of Epidemiology 100(6): 443452, December 1974.
29. ONTARIO DEPARTMENT OF PUBLIC HEALTH. Second Report of the
Perinatal Mortality Study in Ten Teaching Hospitals. Toronto, Canada,
Ontario Department of Health, Ontario Perinatal Mortality Study Com-
mittee, Vol. I., 1967, 275 pp.

30. ORY, H.W. Association between oral contraceptives and myocardial in-
farction. A review. Journal of the American Medical Association 237(24):
  2619-2622, June 13, 1977.

31. RICHER, C., GIUDICELLI, J.F. Exretion des medicaments dans le lait
  maternal. Revue de Medecine 17(2): 1149-I 157, May 17, 1976.
32. ROWAN, J.J. Excretion of drugs in milk. (Letter). Pharmaceutical Journal
217(5885): 184-186, September 4, 1976.
33. RUSH, D. Examination of the relationship between birthweight, ciga-
rette smoking during pregnancy and maternal weight gain. Journal of Ob-
stetrics and Gynaecology of the British Commonwealth 8 1( 10): 746-752,
  October 1974.

19


34. SIMPSON, W.J.A. A preliminary report on cigarette smoking and the inci-
dence of prematurity. American Journal of Obstetrics and Gynecology
  78: 808-815, 1957.

35. SILVERMAN, D.T. Maternal smoking and birthweight. American Journal
  of Epidemiology lOS(6): 513-521, June 1977.
36. SPIRA, A., SPIRA, N., GOUJARD, J., SCHWARTZ, D. Smoking during
pregnancy and placental weight. A multivariate analysis on 3759 cases.
  Journal of Perinatal Medicine 3(4): 237-241, 1975.
37. U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE,
PUBLIC HEALTH SERVICE, CENTER FOR DISEASE CONTROL AND
  NATIONAL INSTITUTES OF HEALTH. Adult use of tobacco-1975.
  Washington, D.C., June 1976.

38. U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE,
  PUBLIC HEALTH SERVICE, HEALTH SERVICES AND MENTAL
  HEALTH ADMINISTRATION. The Health Consequences of Smoking,
  1973. Washington, D.C., DHEW Publication No. (HSM)73-8704, 1973,
  97-149.

39. VORHERR, H. Drug excretion in breast miIlc. Postgraduate Medicine
  56(4): 97-104, October 1974.

40. WINGERD, J., SCHOEN, E.J. Factors influencing length at birth and
  height at five years. Pediatrics 53(5): 737-741, May 1974.

20


Chapter 2
Smoking and Overall Mortality

Contents

Page

Smoking and Overall Mortality ........................  2 1

ln troduction ......................................  22

Measuring Mortality  ................................  24

Mortality Ratios .................................
Differences in Mortality Rates  ...................... i?
ExcessDeaths ...................................  24
Life Expectancy .................................  25

Description of the Studies  ...........................  25

The American Cancer Society Study  .................  25
The U.S. Veterans Study  ..........................
The British Doctors Study  ......................... i:
Overall Mortality and Cigarette Smoking  ................  27
Number of Cigarettes Smoked  ......................  27
Age Began Smoking  ..............................  28
Inhalation Practice  ...............................  29
"Tar" and Nicotine  ..............................  29

Ex-Smokers  ......................................  32

Pipe and Cigar Smoking  .............................  38
Summary of Smoking and Overall Mortality  .............  44

References  .......................................  45

21


Chapter 2

Smoking and Overall Mortality

INTRODUCTION

In 1964, the subject of smoking and overall mortality was examined
in the Report of the Advisory Committee to the Surgeon General of
the Public Health Service (9). This subject was reviewed in 1967
and 1968 in The Health Consequences of Smoking (6,7). Since
then, the updated results of three prospective, epidemiologic studies
concerned with tobacco use and overall mortality have been pub-
lished (1, 3, 5). The following is a review of work previously re-
ported as well as an analysis of the three more recent studies.

Summary of the 1964 Report (9):
1. The death rate for male cigarette smokers was about 70 per-
cent higher than that for nonsmokers.*
2. The death rates increased with the amount smoked.*
3. The ratio of the death rate of smokers to that of nonsmokers
was highest at the earlier ages (40-50) and declined with increas-
ing age.*
4. The mortality ratio was substantially higher for men who
started smoking before the age of 20 than for men who started
after 25.

5. The mortality ratio increased as the number of years of smok-
ing increased.
6. In two studies which recorded the degree of inhalation, the
mortality ratio for a given amount of cigarettes smoked was
greater for inhalers than for noninhalers.
7. Cigarette smokers who had stopped smoking had mortality
ratios of 1.4, compared to 1.7 for current cigarette smokers.
8. The mortality ratio declined as the number of years of cessa-
tion increased.

9. Death rates for men smoking less than five cigars daily were
about the same as those of nonsmokers. For men smoking five
.or more cigars daily, death rates were slightly higher (9 to 27
percent) than those for nonsmokers. Death rates for ex-cigar
smokers were higher than for current smokers in all four studies
in which this comparison could be made. One possible explana-

*Data are derived from seven major prospective studies of male smokers and
nonsmokers. The rate is for smokers of cigarettes only at the time of entry into
the study. These are obtained by subtracting the yearly death rate for non-
smokers from the death rate of a comparable group of smokers. This measure
reflects the added probability of death in a l-year period for the smoker over
that for the nonsmoker.

22


tion may be that a substantial number of cigar smokers quit
smoking due to illness.
10. Death rates for current pipe smokers were little if at all
higher than for nonsmokers, even for those smoking 10 or more
pipefuls per day and for those who had smoked for more than
30 years. Ex-pipe smokers, on the other hand, showed higher
death rates than both nonsmokers and current smokers in four
our of five studies. As similarly noted above, one possible ex-
planation may be that a substantial number of cigar and pipe
smokers quit smoking because of illness.

In the 1967 report of The Health Consequences of Smoking, ad-
ditional conclusions were made relative to the effect of smoking on
overall mortality (6). The highlights of that report are presented
below:

1. The previous conclusions with respect to the association
between smoking and mortality were both confirmed and
strengthened.

2. With respect to effects of smoking on specific age groups, men
45 to 54 years of age were at greatest risk, both in terms of mor-
tality ratios and excess deaths expressed as a percentage of total
deaths. Nevertheless, although both of these measures declined
with advancing age, the increment added to the death rate, which
reflects one's personal chances of being affected, continued to
increase with age.

3. Women who smoked cigarettes had significantly higher death
rates than those who had never smoked regularly. The magnitude
of the relationship varied with several measures of dosage. The
same overall relationships between smoking and mortality were
observed for women as for men, but at a lower level.

4. Previous findings on the lower death rates among those who
had discontinued cigarette smoking were confirmed and
strengthened by the additional data reviewed.

In 1968 report of The Health Consequences of Smoking (7) re-
ported that the life expectancy for a two-pack-a-day or more
smoker at age 25 is 8.3 years less than that for the corresponding
nonsmoker. Even light smokers (those smoking less than 10 cigar-
ettes per day) had 2.8 to 4.6 fewer years of life expectancy than
corresponding nonsmokers.

23


MEASURING MORTALITY

Overall mortality is a term familiar to epidemiologists and statisti-
cians but one which is not commonly used or appreciated by many
who are concerned with the health of the public. To many physi-
cians, dentists, nurses, and other health professionals who have a
primarily clinical orientation, the concept of overall mortality is
often not clearly understood, since it has no immediate applica-
tion to their practice. Individuals die of specific diseases. Disease-
specific mortality rates are of more immediate interest to many
in the health care field. Overall morttity rates are particularly
useful in measuring the effect of agents which affect multiple or-
gan systems and which are capable of causing or contributing to the
cause of several diseases. In contrast, disease-specific mortality
rates measure the effect of an agent on a specific cause of death
but fail to measure the total impact of an agent on the public
health. Overall mortality is, therefore, a good measure of the cumu-
lative or total effect of an agent on health. The problem of how
best to measure the relationship between smoking and mortality
has been discussed in previous reports, as well as in some of the
prospective study reports. A brief discussion of some of the meas-
ures of comparison available and their utility is presented below.

Mortdity Ratios: These are obtained by dividing the death rate
for a classification of smokers by the death rate of a comparable
group of nonsmokers. A mortality ratio has been considered to
reflect the degree to which a classification variable (e.g., smoking)
identifies or may account for variations in death rates. As such,
it is a measure of risk which indicates the relative effect of that
variable on mortality, given that other important factors affecting
mortality (e.g., age) are comparable in the numerator and de-
nominator groups.

Differences In Mortality Rates: These are obtained by subtracting
the yearly death rate for nonsmokers from the death rate of a
comparable group of smokers. This. measure reflects the added
probability of death in a l-year period for the smoker over that for
the nonsmoker. As such, it is a measure of personal health signifi-
cance, a means for the individual to estimate the added risk to
which he is exposed.

Excess Deaths: These are obtained by subtracting from the num-
ber of deaths occurring in a group of smokers the number of
deaths which would have occurred if that group of smokers had
experienced the same mortality rates as a comparable group of
nonsmokers. This measure is an indicator of the public health
significance of the differences found, since it measures the number
of people affected and therefore quantifies the magnitude of the

24


problem for society as a whole.

Life Expectancy: This is a concept which is easier to understand
than it is to calculate. At a given age, it represents the average
number of years one might be expected to live. It identifies the
point in time at which half the population in question theoretically
will be dead and the other half will be alive.

DESCRIPTION OF THE STUDIES

The following is a brief description of the design and methods used
in each of the three studies which are reported in this chapter.
Some comments are made concerning the relative strengths and
weaknesses of each study.

The American Cancer Society

The largest of the three studies discussed here is the American
Cancer Society (ACS) Study (4, 8). In late 1959 and early 1960,
volunteer workers of the ACS enrolled 1,078,894 men and women
in a prospective study. Information was solicited on age, sex, race,
education, place of residence, family history, past diseases, present
physical complaints, occupation, occupational exposures, various
smoking habits, and other factors. Information concerning smoking
habits included: type of tobacco used, number of cigarettes smoked
per day, inhalation practices, age at initiation of smoking, and the
brand of cigarettes smoked from which the "tar" and nicotine
content of the cigarette could be calculated. All segments of the
population were included except migrant workers and similar
groups that could not have been traced easily. Also excluded were
mental patients and those receiving long-term medical care in
institutions. Enrollment was by households, with the specifica-
tion that there be at least one person over age 45 in each house-
hold enrolled. The study area covered 25 states. At the time of
enrollment, each person completed a lengthy questionnaire. At
2-year intervals, for a period of 6 years, brief repeat questionnaires
were administered to each surviving subject. In the follow-up
questionnaires,  information was obtained concerning current
cigarette usage, hospitalization, diseases acquired in the interval
between questionnaires, and several other items. Almost 95 per-
cent of survivors were successfully traced the first 6 years, (that is,
through June of 1966). In October 197 1 and September 1972,
further follow-up questionnaires were distributed to the nearly
900,000 individuals who had been last contacted in September
1965. Nearly 93 percent of the survivors were successfully followed
for the entire 12 years. The time period from July 1, 1960, to June
30, 1966, is referred to as Period 1 and that from July 1, 1966,
to June 30, 1972, is referred to as Period 2.

25


The positive teatures of this study include its prospective design,
the unusually large population enrolled, which included all major
segments of society, the frequency of the follow-up periods, the
variety of the data collected, the thoroughness of follow-up with
loss of but few enrollees, and the relatively long period of observation.

The U.S. Veterans Study

The U.S. Veterans Study (4,5) was initiated by Dom in 1954 and
continued by Kahn and later by Rogot. This study describes the
overall mortality experience of about 250,000 U.S. veterans who
held Government Life Insurance policies in December of 1953. Be-
ginning in January 1954, questionnaires on smoking habits were
mailed to these policy holders and nearly 175,000 (68 percent)
responded. These individuals comprise what in this report is called
the "1954 cohort." In January 1957, a second questionnaire was
mailed to those not responding in 1954, and an additional 50,000
replies were obtained, raising the response rate to 85 percent. These
are referred to as the "1957 cohort." The annual probability of
dying for the 1957 cohort was somewhat greater than that of the
1954 cohort. Because of this, the mortality experience of these
two cohorts was examined separately. Only the data from the 1954
cohort will be considered here, as a separate analysis ~of both
cohorts is beyond the scope, of this paper. The study population
was quite select; almost all policy holders were white males. Most
were white-collar, skilled workers who were veterans of World
War I. This group was questioned as to smoking habits, etc., and
followed for 16 years. Since significant changes have occurred in
the smoking practices of white males in the United States over
the past 20 years, it is likely that similar changes also occurred
in the smoking habits of the subjects of this particular study in
the study period. It is unfortunate, therefore, that the recent mor-
tality experience of this population has to be correlated with
smoking practices of many years ago.

The strengths of this study include its large population, its
prospective design, and its long period of follow-up. Its weaknesses
include its narrow population, which limits the applicability of the
results to the general population, and the lack of information about
more recent changes in smoking habits among members of the
study population which would affect the mortality experience of
the group.

The British Doctors Study
In 195 1, a total of 34,440 male British doctors responded to a
questionnaire distributed by the British Medical Association relative
to smoking habits (1). Nearly all of those enrolled were followed

26


for a period of 20 years. Updated information concerning smoking
practices was obtained in 1957, 1966, and 1972. More than 10,000
deaths occurred in this population in the period of observation.
information was obtained on the type of tobacco used, inhalation
practice, the use of filter cigarettes, and the number of cigarettes
smoked per day. The usual demographic data concerning the back-
ground of the individual were also obtained.

The strengths of this study include its large size, prospective design,
the usually long period of follow-up, the frequent determination of
smoking habits of the subjects enrolled in the study, and the thorough-
ness of follow-up. Perhaps the only significant drawback is that the
study popuIation was so narrow.

The most recent analysis has been limited to overall mortality,
since death certificates were not obtained for those who died in the
last half of the study period, Smoking classifications used in the
latest paper are somewhat different from those used in previous
reports. The occasional smoker was grouped with the nonsmoker,
since their mortality experience was essentially similar. As a result,
occasional smokers who had quit smoking were grouped with those
who had never smoked, and regular smokers who became occasional
smokers were grouped with ex-smokers.

OVERALL MORTALITY AND CIGARETTE SMOKING

Cigarette smoking as related to overall mortality was examined in
these three studies using several different measures of dosage.

Number of Cigarettes Smoked

In the study of U.S. veterans, mortality increased with the number
of cigarettes smoked per day. The mortality ratio was 1.25 for
smokers of less than 10 cigarettes per day and increased to 1.89
for men smoking two packs (40 cigarettes) or more per day (Table
1). In the study of British doctors, the mortality ratio was 1.41 for
smokers of 1-14 cigarettes per day and increased to 2.16 for smok-
ers of 25 or more cigarettes per day. The mortality ratio for all

TABLE 1. Age-adjusted mortality ratios for male cigarette smokers, by amount
     smoked, U.S. Veterans Study, 1954 cohort, l&year follow-up

  Number of
Cigarettes Smoked
  Per Day

Mortality
Ratio

< 10                                 1.25
1 o-20                                1.51
21-39                                1.69
>40                                I .a9

Nonsmokers

1 .oo

Total

1.55

27


cigarette smokers compared to nonsmokers was 1.63 (Table 2). The
mortality experience of U.S. veterans by age and the number of
cigarettes smoked per day are presented in Table 3. Cigarette smok-
ing appears to have a stronger effect on the mortality of younger
smokers than on older smokers. The death rate for smokers in-
creases with age, but since the risk of dying in general increases
more rapidly with advancing age than the risk associated with smok-
ing, the relative contribution of cigarette smoking to overall mor-
tality decreases with time. This relationship is imperfectly demon-
strated when mortality ratios are used.

TABLE 2. Mortality ratios for cigarette smokers, by number of cigarettes
     smoked per day, British Doctors Study

  Number of
Cigarettes Smoked
  Per Day

Mortality
Ratio

Mixed (Cigarette / other)                   1.21
1-14                                 1.41
15-24                                1.51
>25                                2.16

Nonsmokers                            1 .oo

Total                                1.63

TABLE 3. Mortality ratios for male cigarette smokers, by age and number of
    cigarettes smoked per day, U.S. Veterans Study, 1954 cohort, 16-
     year follow-up

  Number of
Cigarettes Smoked
  Per Day

30-34

3544

Age

45-54

5 5-64      65-14

None               1 .oo        1 .oo       1 .oo       1 .oo       1.00
< 10               1.94*       1.44       1.44       I .20       1.1s
10-20               1.27        1.79       1.64       1.49       1.30
21-39               1 .I6        2.23       2.10       1.67      1.42
>40              2.33..      2.72       2.13       1.86       1.65

Total               1.52        1.95       1.83       1.53       1.32

*This f'igure is calculated on the basis of 140 individuals and nine deaths, which is why it
may appear to be somewhat unstable.
**This faure is calculated from 68 individuals and fwe deaths.

Age Began Smoking

The earlier one begins smoking, the more exposure that individual
will have had to cigarette smoke at any subsequent age. In the U.S.
Veterans Study, the overall mortality ratio for those men who be-
gan smoking before the age of 15 was 1.86. This decreased to 1.32
for those who did not start smoking until after the age of 25 (Table
4). Table 5 presents the mortality ratios for males by number of
cigarettes smoked per day and age began smoking. The lowest mor-
tality ratio (1.36) was experienced by those men who smoked fewer

28


than 21 cigarettes per day and who were more than 20 years old
when they began smoking. The highest mortality ratio (1.82) oc-
curred among those who smoked more than 21 cigarettes per day
and began smoking before the age of 20.

TABLE 4.

TABLE 5.

Age adjusted mortality ratios for male cigarette smokers, by age be-
gan smoking, U.S. Veterans Study, 1954 cohort, 16-year follow-up

Age Began
Smoking (Years)

Mortality
Ratio

< 15                                1.86
IS-19                                1.64
20-24                                1.51

Nonsmokers

Total

1 .oo

1.55

Age-adjusted mortality ratios for male cigarette smokers, by num-
ber of cigarettes smoked per day and age began smoking, U.S. Vet-
erans Study, 1954 cohort, 16-year follow-up

  Number of
Cigarettes Smoked
  Per Day

Age Began       Mortality
Smoking (Years)       Ratio

< 21                   >20            1.36
< 21                   < 20            1.56
> 21                   > 20            1.59
> 21                   < 20            1 .a2

Nonsmokers                             1 .oo

Inhalation Practice

Death rates by inhalation practice were examined in the study of
British doctors (Table 6). The mortality ratio for those who did
not inhale was 1.28. This increased to 1.43 for those who did inhale.

TABLE 6.

Mortality ratios for cigarette smokers, by inhalation practice,
British Doctors Study

                             Mortality
Inhalation Practice                       Ratio

Smokers Who Inhaled                      1.43
Smokers Who Did Not Inhale                  1.28

Nonsmokers                             1 .oo

"Tar" and Nice tine

The "tar" and nicotine content of cigarette smoke in relation to
overall mortality was examined by Hammond, et al. (3) using
the ACS data. Several important issues relative to the concept of
less hazardous smoking were settled in this study, It has been
generally accepted that the harmful effects of cigarette smoking

29


are proportional to the "tar" and nicotine levels delivered by the
cigarette. For several years, the "tar" and nicotine levels of all
the popular brands of cigarettes have been checked periodicahy
by the Federal Trade Commission. This information has been made
available to the public through various public and private agencies
and is included in cigarette advertisements. Those who have decided
not to quit or who have not been able to quit have been encouraged
to switch to brands of cigarettes which deliver less "tar" and nico-
tine. This pattern of smoking is thought to be one way of partially
reducing the risks associated with smoking. Some persons in the
scientific community have questioned whether or not there would
be any substantial reduction in risk of mortality associated with
such a switch. Smokers might increase the number of cigarettes
smoked per day, thus keeping their intake of "tar" and nicotine
relatively constant. Smokers switching to low "tar" and nicotine
cigarettes may inhale the smoke more deeply into the lungs, thus
tending to maintain a similar exposure to the toxic elements in the
smoke.

In the study by Hammond, et al. (3), "tar" and nicotine (T/N)
levels were defined as follows: High T/N: 25.8-35.7 milligrams
(mg.) "tar" and 2.0-2.7 mg. nicotine; Medium T/N: 17.6-25.7 mg.
"tar" and 1.2-1.9 mg. nicotine; Low T/N: less than 17.6 mg. "tar"

TABLE 7. Mortality ratios for all cigarette smokers in two time periods, by
      sex and "tar" and nicotine (T/N) content of cigarettes smoked*

Sex           Period

Male             1
Male             2
Female           1

High
TPJ

1 .oo
1 .oo
1 .oo

Mortality Ratio

  Medium
  T/N

  0.90
  0.90
  0.89

Low
T/N

0.88
0.81
0.84

Female           2             1.00           0.87             0.82

Total                         1 .oo           0.91             0.84

SOURCE: Hammond E-C.. et al. (3).

*A matched-group analysis adjusted for several factors. See text.

and less than 1.2 mg. nicotine. A matched group analysis was util-
ized. Subjects within each group were matched for: (1) age, (2) race,
(3) number of cigarettes smoked per day, (4) age began smoking,
(5) place of residence (urban or rural), (6) history of hazardous oc-
cupational exposure, (7) education, (8) history of lung cancer, and
(9) history of heart disease. Matching was done separately for men
and women in both time periods of the study. Within each matched
group, the subjects were divided into three subgroups according to
"tar" and nicotine (high, medium, or low). The entire group was
discarded if it did not contain at least one subject in each "tar"
and nicotine category. The adjusted number of subjects in Period 1

30


was 14,688 men and 30,176 women. In Period 2, there were
6,475 men and 15,342 women. The mean age of subjects in Period
1 was 53.6 years for men and 5 1.6 years for women; in Period 2,
the mean age was 58.4 years for men and 56.7 years for women.

Table 7 shows mortality ratios by sex and "tar" and nicotine
content of the cigarettes smoked. In this instance, the mortality
ratio for the high T/N smokers is represented as 1.00. There is a
small but significant (p< 0.0005) reduction in the risk of dying
with the use of lower T/N cigarettes. The mortality ratio was
reduced to 0.91 for the medium T/N smokers and was further
reduced to 0.84 for the low T/N smokers. A comparison was also
made between the mortality experience of Iow T/N smokers and
nonsmokers. Subjects were matched according to the same factors
as the previous analysis with the exception of the number of
cigarettes smoked per day. The adjusted number of subjects for
Period 1 was 15,346 men and 32,702 women. For Period 2, ad-
justed numbers were 6,822 and 16,803 for men and women, re-
spectively. The mean age of subjects in Period 1 was 53.8 years
for men and 52.3 years for women. In Period 2, the mean ages
for men and women were 58.7 and 57.3 years, respectively. The
mortality ratios for these matched groups are presented in Table
8. The death ratio for the low T/N group is 1.00, and that for
nonsmokers is 0.66. The mortality ratio for the low T/N group
is, therefore, approximately 50 percent higher than that for the
nonsmokers.

TABLE 8. Mortality ratios for smokers of low "tar" and nicotine (T/N) c@-

arettes and nonsmokers in two time periods, by sex

Sex                 Period

Male                    1
Male                    2
Female                   1
Female                   2

Total

SOURCE: Hammond E.C., et al. (3).

      Mortality Ratio
Low T/N            Nonsmokers


1 .oo                 0.51
1 .oo                0.64
I .oo                 0.76
1 .oo                 0.71

I .oo                 0.66

*A matched-group analysis adjusted for several factors. See text.

Assuming that the composition of the two low T/N gOUpS
was quite similar in these separate analyses, whese two sets of
data <an be combined to compare mortality rates of smokers of
various levels of "tar" and nicotine with those of nonsmokers
(Table 9). These results are approximate, however, and are subject
to some error.

Anorher matched group analysis was done comparing mor-
tality ratios of smokers of relatively few (l-19) `high T/N cigar-

31


TABLE 9. Mortality ratios for all cigarette smokers and nonsmokers in two
     time periods, by sex and "tar" and nicotine (T/N) content of
      cigarettes smoked

Sex

Period     Nonsmokers

                           -
       Mortality Ratio
Low T/N    Medium T/N   High T/N

Male        1          1.00
Male        2          1.00
Female       1          1.00
Female       2          1 .oo

Total                  1 .oo

SOURCE: Hammond E.C.. et al. (3).

1.75         1.80     2 .oo-
1.56         1.89         1.92
1.32         1.40         1.57
1.41         1.49         1.73

1.52         1.64         1 .a0

ettes with those smokers of relatively large numbers (20-39) of low
T/N cigarettes. The mortality ratios of these two groups were
very similar, and the difference between them was not statistically
significant.

EX-SMOKERS

The mortality experience of ex-smokers is a subject in which there
has been increasing interest in the past several years. When the
harmful effects of smoking were initially suspected and examined,
the question at first was one of the magnitude of the problem.
More recently, there has been a nationwide recognition of the ad-
verse morbidity and mortality which results from smoking. As
a result, more than 30 million Americans have quit smoking, and
millions more anticipate quitting within the next several years.
One of the questions of greatest concern to the smoker at this
time is not, "How bad is my smoking for my health?" but rather,
"After all these years of smoking will it make any difference if I
quit?" The benefits of stopping smoking are more clearly under-
stood as a result of the studies reviewed here.

The relationship between cessation of smoking and overall mor-
tality was examined in considerable detail in the study of U.S.
veterans. A differentiation was made between ex-smokers who
stopped smoking on the recommendation of a doctor and those
who quit for other reasons (Tables 10, 11, 12). In each cohort,
about 10 percent of the ex-smokers had stopped on doctor's
orders, and this group had much higher mortality levels than those
who stopped for other reasons. There was a direct relationship
between mortality levels and the maximum amount previously
smoked, an inverse relationship between mortality and years
since stopping smoking, and an inverse relationship between mor-
tality and age when smoking began.

The combined effects of these three factors on mortality are
presented in Table 13. The lowest mortality ratio (1.03) was ex-
perienced by ex-smokers who began smoking after the age of 20,

32


smoked fewer than 21 cigarettes per day, and had stopped smoking
for more than 10 years at the time of enrollment in the study.
Conversely, the highest mortality ratio (1.45) was experiened by
ex-smokers who began smoking before the age of 20, smoked
more than 21 cigarettes per day, and had stopped smoking for
less than 10 years at the time of enrollment in the study.

1 `ABLE 10. Mortality ratios for ex-smokers who quit smoking on doctor's
    orders and for other reasons, by years since stopping, U.S. Vet-
    erans Study, 1954 cohort, 16-year follow-up

Mortality Ratio

Years           Quit on         Quit for
Since            Doctor's            Other
Stopping            Orders            Reasons

<5                  1.55              1.23
5-9                1.43              1.23
10-14                1.77              1.14
15-19               1.35              1.04
>20                1.16              1.06

Total                1.52              1.18

TABLE 11. Mortality ratios for ex-smokers who quit smoking on doctor's
    orders and for other reasons, by number of cigarettes smoked per
    day, U.S. Veterans Study, 1954 cohort, 16-year follow-up

Number of
Cigarettes
Smoked Per Day

< 10
1 O-20
21-29

    Mortality Ratio
Quit on         Quit for
Doctor's            Other
Orders            Reasons

1.42              1 .OO
1.48              1.17
1.53              1.30

>40

Total

1.60              I .32

1.52              1.18

TABLE 12. Mortality ratios for ex-smokers who quit smoking on doctor's
    orders and for other reasons, by age began smoking, U.S. Veterans
    Study, 1954 cohort, 16-year follow-up

Age Began
Smoking
(Years)

    Mortality Ratio
Quit on         Quit for
Doctor's            Other
Orders            Reasons

< 15                1.59              1.36
15-19               1.55              1.20
20-24               1.49              1.12
>2s                1.34              1.15

Total                1.52              1.18

A detailed study of the mortality experience of ex-smokers who
stopped smoking for various reasons other than a doctor's order

33


TABLE

13. Mortality ratios for ex-smokers of cigarettes only, by years since
Stopping, number of cigarettes smoked per day, and age began
smoking, U.S. Veterans Study, 1954 cohort, 16-year follow-up

Years       Number of
Since    Ci8arettes Smoked
Stopping      Per Day

< 10          >21
< 10           >21
< 10          < 21
< 10          < 21
> 10           >21
> 10          > 21
> 10           < 21
> 10          < 21

2i02:   Mortality
(Years)     Ratio

  < 20      1.45
  >20      1.27
  < 20      1.21
  >20       1.12
  < 20      1.19
  >20      1.07
  < 20      1.08
  >20      1.03

Nonsmokers                             1.00

         Total                                 1.18

is given in Figures I-4. This information is derived from the U.S.
Veterans Study for men aged 55-64 who used to smoke from

FIGURE l.-Annual probability of dying for current
cigarette smokers, ex-smokers who quit less than 5
years ago, and never smokers, ages 5 5-64*

qx
9.0
8.0
7.0
6.0

5.0

Current smokers

---- Ex-smokers

L Never smokers

0.1 '
     ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,  ,
    0   2   4   6   8  10  12  14  16
   Years of Follow-up
*U.S. Veteransstudy, 1954 cohort, 16-year follow-up.

34


FIGURE 2.-Annual probability of dying for current
cigarette smokers, exsmokers who quit 5-9 years
aeo, and never smokers, ages 55-64*

qx
9.0 -
8.0 -

7.0 -

6.0 -

5.0 -


4.0 -



3.0 -

r"   2.0 -
.-
0"
b

Current smokers

Ex-smokers

Never smokers

2
E1
90"
o"m  1.0
e $ 0.9
" f 0.8
z-
cae
cc
a = 0.1   11111111111111111
      0 2 4 6 8 10 12 14 16
      Years of Follow-up
    *U.S. Veterans Study, 1954 cohort, 16-year follow-up.

21-39 cigarettes per day. The years since stopping smoking is con-
sidered as a variable, and the mortality rates are compared with
those of current cigarette smokers and nonsmokers. Annual proba-
bilities of dying are plotted on a logarithmic scale. This results in
a fairly smooth, linear pattern for both smokers and nonsmokers.
The positive slope indicates increasing mortality with the passing
of time of both smokers and nonsmokers. These lines also appear
to run parallel or perhaps diverge slightly. This indicates an approxi-
mately constant or slightly increasing excess probability of dying
between cigarette smokers and nonsmokers over the 16-year period.
For ex-smokers who quit less than 5 years prior to the beginning
of the study, the probability of dying is at first nearly identical
to that of smokers. (Fwe 1). Over the years, the probability
gradually falls to a position approximately halfway between that of
smokers and nonsmokers. Figures 2 and 3 show that with longer

35


periods of cessation the probability of dying more nearly ap-
proaches that of nonsmokers. The probability of dying for ex-
smokers who had stopped smoking for 15 or more years is virtually
the same as that for nonsmokers for the entire 16year period
(Figure 4).

The mortality experience of British doctors who quit smoking
indicates that there are benefits to quitting no matter how long
one has smoked (Table 14). After 1 O-l 5 years of not smoking, the
risk of dying for ex-smokers is similar to that of those who have
never smoked (1 .l compared to 1 .O). It should be remembered
that overall mortality examines the probability of dying from all
causes. This masks the relative benefits of quitting for specific
diseases. It is known that the risk of dying from ischemic heart
disease is reduced almost immediately after cessation of smoking,

  FIGURE J.-Annual probability of dying for current
  cigarette smokers, ex-smokers who quit lo-14 years
  ago, and never smokers, ages 55-64*
qx

t::- 7
7.0 -
6.0 -

5.0 -

4.0 -

   3.0 -



c"  2.0 -
.-
p'
b

>
.E a
.c -
2; 1.0
2 8
; f 0.9
   0.8
22
=c
a = 0.1    11111111111111111
       0 2 4 6 8 10 12 14 16
      Years of Follow-up

Current smokers

Ex-smokers

Never smokers

*U.S. Veterans Study, 1954 cohort, 16-year follow-up.

36


qx
2
7.0
6.0

5.0

FIGURE 4.-Annual probability of dying for current
cigarette smokers, ex-smokers who quit more than 15
years ago, and never smokers, ages 5 S-64,

0-O Current smokers

---- Ex-smokers

CJY Never smokers

0   2~   4   6   8   10  12  14  16
Years of Follow-up
*U.S. Veterans Study, 1954 cohort, 16-year follow-up.

while the risk of dying from lung cancer decreases more slowly.
Only the net or total effect is demonstrated in overall mortality
figures.

TABLE 14. Mortality ratios for ex-smokers compared to nonsmokers, by
   number of years since stopping and age, British Doctors Study

                 Mortality Ratio
Years
Since         Age        Age         All
Stopping         30-64       >65       As=
0*              2.0         1.6         1.8
1-4              1.7         1.4          1.5
5-9              1.6         1.4          1.5
10-14            1.4         1.2          1.3
> 15             1 .l          1.1          1.1
Nonsmokers        1.0         1 .o          1.0

`Current Smoke-

37


PIPE AND CIGAR SMOKING

Pipe and cigar smoking as related to overall and specific causes of
mortality was last reviewed in the 1973 report of The Health Con-
sequences of Smoking (8). The combustion products of pipe and
cigar smoke contain many of the same chemical compounds found
in cigarette smoke condensate. Since pipe and cigar smokers are
less likely to inhale than cigarette smokers, they experience much
lower mortality from certain diseases strongly associated with
cigarette smoking. These include lung cancer, ischemic heart dis-
ease, and chronic obstructive lung disease. They do have death
rates that are virtually similar to those for cigarette smokers, how-
ever, for cancers of the oral cavity, pharynx, larynx, and esophagus.

It should not be inferred from the above that switching to a
pipe or cigar will necessarily reduce the mortality risks experienced
by a current cigarette smoker, particularly one who inhales. The
reason for this is that a cigarette smoker who inhales would pro-
bably continue to inhale after switching (8). Lower risks for pipe
and cigar smokers may be associated with the lower prevalence of
inhalation among these smokers and not with less hazardous to.
bacco products.

TABLE 15.  Age-adjusted mortality ratios for pipe-only, cigar-only, and cigar-
      ette-only smokers, U.S. Veterans Study, 1954 cohort, 16.year
      folio w-up

Type of                        Mortality
Tobacco                             Ratio

Pipe Only                             1.07
Cigar Only                             1.16
Cigarettes Only                         1.55

Nonsmokers

1 .oo

The U.S. Veterans Study contains the most detailed information
concerning the mortality experience of pipe and cigar smokers. The
mortality ratios for both pipe and cigar smokers are predictably
greater than those for nonsmokers, and they are less than the mor-
tality ratios of cigarette smokers (Table 15). Significant dose-
response relationships were demonstrated for both pipe and cigar
smokers by amount smoked and age began smoking.

38


The mortality ratio for cigar smokers increased from 1 .11 for
those smoking 1-2 cigars per day to 1.39 for those smoking nine or
more cigars per day (Table 16). The mortality ratio was 1.13 for

TABLE 16. Age-adjusted mortality ratios for current cigar smokers, by num-
    ber of cigars smoked per day, U.S. Veterans Study, 1954 cohort,
      16-year follow-up

Number of
Cigars Smoked
Per Day

   l-2
   3-4
   5-8
   >9

Nonsmokers

Total

Mortality
Ratio


1.11
1.13
1.22
1.39

1 .oo
q1.16

those who began smoking after the age of 25 and 1.22 for those
who began smoking before the age of 15 (Table 17). Table 18
combines these variables and shows that the lowest mortality ratio
for cigar-only smokers is 1.07 for those who smoked less than five
cigars per day and began smoking after the age of 25. The highest
mortality ratio of 1.28 was experienced by those who smoked more
than five cigars per day and began smoking before the age of 25.
Somewhat similar dose-response relationships were demonstrated
for pipe-only smokers; however, the risk associated with pipe
smoking is slightly less than that with cigar smoking (Tables 19,
20, and 2 1).

TABLE 17. Age adjusted mortality ratios for current cigar smokers, by age be-
    gan smoking, U.S. Veterans Study, 1954 cohort, 16-year follow-up

Age Began
Smoking
(Years)

< I5
15-19
20-24
>25

Nonsmokers

Total

Mortality
Ratio


1.22
1.23
1.16
1.13

1 .oo

1.16

39


TABLE 18. Age-adjusted mortality ratios for current cigar smokers, by nurn-
     ber of cigars smoked per day and age began smoking, U.S. Vet-
     erans Study, 1954 cohort, 16-year follow-up

nunloer of          430
Cigars Smoked      Began Smoking
Per Day         Wed

<5                  >25
<s                 < 25
Z-5                  >2s
>S                  < 25

Mortality
Ratio

1.07
1.16
1.28
1.23

Nonsmokers                            1 .oo

Total                                1.16

TABLE 19. Age-adjusted mortality ratios for current pipe smokers, by number
     of pipefuls smoked per day, U.S. Veterans Study, 1954 cohort,
      16-year follow-up

Number of
Pipefuls Smoked
  Per Day

<S
5-9
10-19

Mortality
Ratio

0.93
1.12
i .oa

Nonsmokers                            I .oo

Total                                 1.07

TABLE 20. Age-adjusted mortality ratios for current pipe smokers, by age be-
     gan smoking, U.S. Veterans Study, 1954 cohort, 16-year follow-up

Age Began
Smoking
(Years)

Mortality
Ratio

< 1s                                 1.04
15-19                               1.12
20-24                                1.06
>25                                1.06

Nonsmokers                            1.00

Total                                 1 .Ol

40


TABLE 21. Age-adjusted mortality ratios for current pipe smokers, by num-
     ber of pipefuls smoked per day and age began smoking, U.S.
     Veterans Study, 1954 cohort, 16-year follow-up

Number of
Pipefuls Smoked
  Per Day

< 10
< 10
WlO
> 10

Total

   Age
Began Smoking
(Years)

   > 25
   < 25
   > 25
   >25

Mortality
Ratio

1.03
1.05
1.12
1.12

1 .Ol

The above discussion relates to those who have limited their
lifetime smoking to cigars only or pipes only. Frequently, however,
a smoker will have used tobacco in several different forms. For
instance, a cigar smoker may be a former cigarette smoker and may
occasionally smoke pipes. The U.S. Veterans Study contains data
on the mortality ratios'of individuals who use tobacco in various
forms. These data have been arranged so that the various patterns
of smoking are arranged by increasing risk of mortality. Table 22
shows the age-adjusted mortality ratios of current cigar smokers
who have or are using pipes and/or cigarettes. Smoking cigarettes
and cigars is more risky, and smoking pipes and cigars is less risky
than smoking cigars alone.

TABLE 22.

Age-adjusted mortality ratios for current cigar smokers, by use of
other types of tobacco, U.S. Veterans Study, 1954 cohort, 16-
year follow-up

Tvoe of Tobacco Used

Cigarettes        Pipes          Mortality Ratio

Never            Never               1.16
Never             Current              1.10
Never            Former              1.10
Former           Former              1.10
Former           Current              1.13
Former           Never               1.23
Current           Current              1.21
Current           Never               1.30
Current           Former              1.33

41


TABLE 23.  Age-adjusted mortality ratios for current pipe smokers, by use of
     other types of tobacco, U.S. Veterans Study, 1954 cohort, 16-
      year follow-up

Type of Tobacco Used
Cinarettes         Cigars

Mortality Ratio

Never            Never               1 .Ol
Never           Current              1.10
Never           Former              1.11
Former           Former              1.14
Former           Current              1.14
Former           Never               1.10
Current           Current             1.21
Current           Never               1.28
Current           Former             1.36

The mortality experience of pipe smokers is shown in Table 23.
Pipe smoking alone is the least hazardous form of smoking. The
combination of pipes and cigars is a less risky combination than
the combination of pipes and cigarettes. It is interesting to note
that when the pipe smoker divides his smoking three ways and uses
both cigarettes and cigars in addition to pipe smoking, the mortal-
ity ratio is less than if the time devoted to smoking is split two
ways between pipes and cigarettes. Evidently to the extent that
cigarettes are replaced there is a reduction in risk. The mortality
ratios of current cigarette smokers who have or are using pipes
or cigars is shown in Table 24.

TABLE 24. Age-adjusted mortality ratios for current cigarette smokers, by
      use of other types of tobacco, U.S. Veterans Study, 1954 cohort,
      16-year follow-up

  Type of Tobacco Used
Cigarettes        Cigars

Mortality Ratio

Never
Never
Never
Former
Former
Former
Current
Current
Current

Never               1.55
Current             1.28
Former              1.41
Former             1.48
Current              1.36
Never               1.53
Current              1.21
Never               1.30
Former              1.33

42


I,~ the study of British doctors, Doll and Pete (1) reported that
[llose who smoked only pipes or cigars experienced mortality
rJfPs which were similar to, or only slightly above, those of men
,+llo did not smoke at all. Pipe and cigar smokers who a,lso used
iic;lrettes had mortality ratios which were intermediate between
&&e who only smoked pipes and cigars and those who smoked
+arettes. These figures are presented in Table 25.

T,+BLE 25. Age-adjusted mortality ratios for ail smokers, by type of tobacco
     used, British Doctors Study

Type of
Tobacco Used
Pipe or Cigar
Never Cigarettes
Pipe or Cigar
and Cigarettes
Cigarettes Only
Nonsmokers

Mortality
Ratio


  1 .OQ

1.31
1.73

1 .oo


SUMMARY OF SMOKING AND OVERALL MORTALITY

1. Overall mortality rates for cigarette smokers are about 70
percent higher than those for nonsmokers.
2. Overall mortality risk increases with the amount smoked. For
the two-pack-a-day cigarette smoker, the risk of premature death is
approximately twice that of the nonsmoker.
3. Overall mortality ratios of smokers compared to nonsmokers
are highest at earlier ages and decline with increasing age. For cigar-
ette smokers, the risk of premature death is twice that of non-
smokers at age 40.

4. Overall mortality ratios are higher for those who begin smok-
ing at a young age compared to those who begin later. For those
who begin smoking before the age of 15, the risk of premature
death is about 86 percent higher than that for nonsmokers.
5. Overall mortality ratios are higher for those smokers who in-
hale than for those who do not.

6. There is about a 15 percent reduction in overall mortality risk
for smokers of low "tar" and nicotine cigarettes (less than 17.6 mg.
"tar" and less than 1.2 mg. nicotine) compared to those who smoke
high "tar" and nicotine cigarettes (25.8-35.7 mg. "tar" and 2.0-2.7
mg. nicotine).

7. Overall mortality rates of low "tar" and nicotine cigarette
smokers are about 50 percent higher than for nonsmokers.
8. Overall mortality rates of former smokers decline as the num-
ber of years of cessation increase. After 15 years off cigarettes,
death rates for former smokers are nearly identical to those of non-
smokers.

9. Overall mortality rates of former smokers are directly pro-
portional to the number of cigarettes the person used to smoke.
10. Overall mortality rates of former smokers are inversely pro-
portional to the age at which the person began smoking.
11. Regardless of length of time smoked or number of cigarettes
smoked, former smokers have lower mortality rates than continuing
smokers, provided they are not ill at the time of cessation.
12. Overall mortality ratios for cigar smokers are somewhat higher
than for nonsmokers. The U.S. Veterans Study showed a mortality
ratio of 1.16, compared to 1 .O for nonsmokers. The overall mortal-
ity ratio was 39 percent higher than the ratio in nonsmokers for
men smoking nine or more cigars a day. A positive dose-response
relationship exists between cigar smoking and mortality.
13. Overall mortality ratios for male cigar smokers are inversely
proportional to the age at which the individual began smoking.
14. Overall mortality ratios for pipe smokers are only slightly
higher than for nonsmokers. The mortality ratio in the U.S. Vet-
erans Study was 1.07. Overall mortality ratios were 21 percent

44


higher than nonsmokers for men who smoked 20 or more pipefuls
a day than for nonsmokers. A positive dose-response relationship
exists between pipe smoking and mortality.
15. Overall mortality ratios of men who smoke cigarettes in com-
bination with pipes and/or cigars are intermediate between those
who smoke pipes or cigars only and those who smoke cigarettes
only. Cigarette smokers who also smoke cigars or pipes have overall
mortality rates approximately 30 percent higher than nonsmokers.

REFERENCES

1.

2.

3.

4.

5.

6.

7.

8.

9.

DOLL, R., PETO, R. Mortality in relation to smoking: 20 years' observa-
tions on male British doctors. British Medical Journal 2(6OSl): 1525-1536,
December 25, 1976.
HAMMOND, E.C. Smoking in relation to the death rates of one million men
and women. In : Haenszel, W., Editor. Epidemiological approaches to the
study of cancer and other diseases. Bethesda, U.S. Public Health Service,
National Cancer Institute Monograph 19, 1966, pp. 127-204.
HAMMOND, E.C., GARFINKEL, L., SEIDMAN, H., LEW, E.A. "Tar" and
nicotine content of cigarette smoke in relation to death rates. Environmen-
tal Research I2(3): 263-274, December 1976.
KAHN, H.A. The Dom study of smoking and mortality among U.S. veter-
ans: report on 8-s years of observation. In: Haenszel, W., Editor, Epidemio-
logical approaches to the study of cancer and other diseases. Bethesda, U.S.
Public Health Service, National Cancer Institute Monograph 19, 1966, pp.
l-125.
ROGOT, E. Smoking and general mortality among U.S. veterans 1954-1969.
U.S. Department of Health, Education, and Welfare. Washington, D.C.,
DHEW Publication No. (NIH) 74-S44,65 pp.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE, U.S.
PUBLIC HEALTH SERVICE. The Health Consequences of Smoking. A
Public Health Service Review: 1967. Washington, D.C., Public Health Serv-
ice Publication No. 1696, 1967, pp. 7-17.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE, U.S.
PUBLIC HEALTH SERVICE. The Health Consequences of Smoking. 1968
Supplement to the 1967 Public Health Service Review. Washington, D.C.,
1968 Supplement to Public Health Service Publication No. 1696, 1968,
117pp.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE, U.S.
PUBLIC HEALTH SERVICE, HEALTH SERVICES AND MENTAL
HEALTH ADMINISTRATION. The Health Consequences of Smoking,
1973. Washington, D.C., DHEW Publication No. (HSM) 73-8704, 1973,
249 pp.
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE, U.S.
PUBLIC HEALTH SERVICE, CENTER FOR DISEASE CONTROL. Smok-
ing and Health. Report of the Advisory Committee to the Surgeon General
of the Public Health Service. Washington, D.C., Public Health Service Pub-
lication no. 1103, 1964, 387 pp.

45


Appendix

Smoking and Disease
-What Must Be Done
By Daniel Horn, Ph.D.

Director, National Clearinghouse for Smoking and Health
Reprinted from WHO Chronicle, 3 1:355-361(1977)

HOW SMOKING CAUSES DISEASE

Since the early 1950s when cigarette smoking was first implicated
as a major cause of lung cancer in men, further research into the
relationship between smoking and ill health has provided substantial
additional data that support various theories about the mechanisms
caused or enhanced by smoking, with regard to both mortality and
morbidity. The following five mechanisms have been proposed:

(1) Cigarette smoking starts a disease process that progressively
produces irreversible damage, the end-effect of which is more or less
proportional to the total dosage accumulated during the years of
smoking. Cessation of smoking leaves the individual with functional
impairments that neither improve appreciably nor, of themselves,
continue to deteriorate-except perhaps as a result of aging or ex-
posure to other harmful agents. Owing to the interference with
normal mechanisms for clearing the respiratory tract and the de-
struction of peripheral airways, this kind of process probably
accounts for the high rates of chronic obstructive lung disease in
cigarette smokers. A similar process seems to explain the high levels
of atherosclerosis found in cigarette smokers; the almost contin-
uously elevated level of carboxyhaemoglobin found in the blood of
moderate to heavy smokers interacts with high levels of cholesterol
to produce increased formation of atherosclerotic plaques.

(2) Cigarette smoking starts a disease process characterized by
continual repair and recovery until a critical point is reached when
the process is no longer reversible. The total effect is related to
cumulative exposure over the years, so that several short periods of
heavy smoking could lead to the point of irreversibility. Unless this
point has been reached, cessation of smoking results in a rapid
decrease in risk. A mechanism of this kind probably accounts for
both the high dose-response relationship in lung cancer and the ra-
pid relative reduction in risk of lung cancer among populations of
ex-smokers. Other sites of cancer related to cigarette smoking pro-
bably also react in this way, which would correlate with the evi-
dence that tobacco smoke contains both cancer-initiating and
cancer-promoting substances.

47


(3) Cigarette smoking promotes rather than starts the disease
process, either by directly supporting a developing pathological
condition or by diminshing the body's normal capacity to defend
itself against disease. By this mechanism, cigarette smoking could
promote a subclinical disease to a clinically recognizable state or a
mild disease to a more severe form or even increase the fatality
rates of certain diseases. This mechanism might account for the
slightly increased mortality rates for influenza or tuberculosis
among smokers, although cigarette smoking itself is not the cause
of these diseases. Furthermore, unless severe chronic obstructive
lung disease or high levels of atherosclerosis have already developed,
stopping smoking both lessens the severity of heart attacks and im-
proves the recovery rates from them.

(4) Cigarette smoking induces temporary conditions favouring a
critical combination of events, which leads to disease, disability,
and possible fatal consequences. For example, there is substantial
evidence to support a theory that each cigarette can increase the
probability of myocardial damage. This comes about through an
increased demand for oxygen in response to the nicotine in cigar-
ette smoke, at the same time that the carbon monoxide in the
smoke has decreased the supply of oxygen by raising the carboxy-
haemoglobin levels in the blood. Once this imbalance of supply and
demand for oxygen is alleviated, the probability of myocardial
damage would presumably revert to normal levels; in this instance,
stopping smoking should bring about an almost immediate and
sharp decline both in associated morbidity and mortality.

(5) Cigarette smoking may be artificially related to excess disa-
bility or death because of a close association with some other con-
dition, which occurs at a high level in smokers and is itself re-
sponsible for the disease. The generally accepted example of this
mechanism at work is cirrhosis of the liver. Because many heavy
drinkers of alcohol are also heavy smokers, the high rate of cirrhosis
among cigarette smokers has sometimes been attributed to smoking.
Some evidence does suggest that high levels of exposure to both
cigarette smoking and alcohol produce an effect greater than that
for alcohol exposure alone.

Implications for action

The different mechanisms described above are important for the
evaluation of potential public health benefits that could result from
programmes aimed at (i) inducing smokers to stop smoking, (ii)
dissuading young nonsmokers from starting to smoke, or (in)
changing the ingredients of cigarettes to make their smoke less
harmful. For some types of associated morbidity and mortality
there would be no benefits from any of these actions; for others,
rather small benefits or substantial benetits taking place rather

48


rapidly or substantial benefits taking place slowly over a long period
of time. For example, the greatest long-term benefits would result
from dissuading youngsters from taking up smoking, but more im-
mediate, albeit smaller, benefits could be derived from persuading
adults to stop smoking, provided the programme reaches many of
the individuals at greatest risk.

In addition to taking these mechanisms into account in designing
control efforts, there are certain epidemiological findings of special
importance in this respect. First and foremost is the evidence that
cigarette smoking seems to act in concert with many other risk
factors so that the combined risk for almost any disease, on which
cigarette smoking by itself has an effect, is sharply increased. For
example, the radioactivity to which uranium miners under current
mining conditions are exposed appears to have relatively little
effect on lung cancer rates among nonsmokers; for smokers, how-
ever, it appears to produce far higher lung cancer rates than those
for smokers who are not exposed to radioactivity.

Similarly, certain forms of chronic obstructive lung disease
caused by sustained inhaling of particles and fibres are more com-
mon and severe in those who smoke. This applies equally to bys-
sinosis (caused by inhaling cotton fibres) and the fungus-produced
respiratory problems experienced by pigeon breeders. Both smokers
and nonsmokers exposed to asbestos fibres show elevated rates of
asbestosis, but only the smokers manifest extremely high rates of
lung cancer. With ischaemic heart disease also, cigarette smoking
appears to combine with other generally accepted risk factors,
i.e., hypertension and hypercholesterolaemia, to produce a multi-
plicative, rather than simply an additive effect. On the other hand,
there is evidence to suggest that certain endogenous factors, such as
inherited susceptibility, can have an effect opposite to that of the
exogenous factors just noted. Among women, for example, whose
rates of ischaemic heart disease and chronic obstructive lung disease
appear to be lower than those of men in most national and ethnic
groups, even among nonsmokers, the effect of smoking at appar-
ently equivalent dosage levels seems to be less.

In sum, then, the design of specific control programmes needs to
take into account the effect of smoking as an interaction of three
influences:

-dosage, i.e., the effective level of exposure to noxious substances
in cigarette smoke, both accumulated and current
-exposure to other elements that contribute to or produce the
same disease process

-susceptibility to the disease in the host population, presumably
determined by genetic factors.

As smoking habits may be more amenable to control than other
important risk factors or high levels of host susceptibility, measures

49


aimed at reducing exposure to cigarettes can be expected to pro-
duce substantial benefits. But whether to concentrate on short-
term programmes for helping adults whose accumulated exposure
may be approaching the critical point or longer-term efforts aimed
at the youth or some combination of both requires careful identifi-
cation of the groups that will benefit most from the planned con-
trol measures.

SMOKING BEHAVIOUR IN THE INDIVIDUAL

Cigarette smoking represents a category of health problems that can
be called personal choice health behaviour. This class of behaviour
includes many normal ways of increasing the enjoyment of life or
coping with its problems; it includes useful, frequently necessary,
forms of behaviour that have varying degrees of social acceptability.
For a more complete understanding of this sort of behaviour as it
applies to smoking, it is helpful to look at its four stages: initiation,
establishment, maintenance, and cessation or other modification.

The initiation of smoking usually occurs with young people,
frequently rather young children, and depends on how available
cigarettes are to them, the degree of their curiosity about what
smoking is like, and their need to conform with the behaviour of
others-whether parents, older siblings, or peers-or to rebel against
what seems like unreasonable proscriptions against smoking. Ac-
cordingly, smoking is much more common among children of par-
ents who are themselves regular smokers. As cigarette smoking be-
comes widespread in a society, it tends to be taken up with increas-
ing frequency by successive generations of young people. Many
older people may also turn to it, especially if it serves as a substi-
tute for a previously well-established behaviour pattern as was the
case when many males switched to cigarettes from cigars and pipes
in the years between 1920 and 1950.

The establishment of smoking as a continuing habit in adoles-
cents can be influenced by three groups of factors: a cost-benefit
balance, common perceptual stereotypes, and psychological per-
sonal structure and integration. The costs may be either those to
the individual or to society and may reflect health concerns or eco-
nomic or aesthetic values. The benefits are similarly varied, ranging
from easing social contacts and reducing tension to enhancing the
sense of pleasure. The perceptual stereotypes have to do with the
mythology of what smoking is like, what smokers are like, and why
people smoke, and are derived from both the brand-name advertis-
ing of cigarettes and the counter-publicity of antismoking groups.
No one pattern of psychological forces dominates the reasons
either for or against smoking. Either smoking or not smoking can be
a way of expressing the conflict between satisfying one's own de-
sires and conforming to the demands and expectations of society

50


and its leading figures. Similarly, these opposite kinds of behaviour
may reflect the individual's relative need to maintain control over
his own behaviour and destiny as opposed to being subject to the
control of others or the vagaries of chance.

The maintenance of smoking behaviour is usually supported by
the development of habituation or dependence-habituation tend-
ing to reflect simply repetitive behaviour and dependence an in-
creasing desire or need for the effects produced by the behaviour.
In either case, prior to 1950, confirmed smokers tended to continue
smoking unless they became too ill or had their supply of cigarettes
interrupted by wartime shortages or economic deprivation. Since
then, the threat to health posed by cigarette smoking has become
sufficiently well known to millions of smokers to influence many of
them towards trying to give up cigarettes or modifying their smok-
ing in some way that would minimize its potential hazards.

Whether a smoker considers the idea of cessation or other modifi-
cation of his smoking habits and how successful he will be in this
effort depends largely on a number of factors, such as his percep
tion of the threat posed by his continued smoking, how psycho-
logically useful his smoking is to him, and the environmental forces
that either encourage or interfere with his efforts at behavioural
change. Not only must the smoker be aware of a threat to his health,
but he must perceive this as important and personally relevant, as
well as feel able to alter his behaviour and accept as valuable the re-
sults of such alterations. Psychologically, the smoker in the process
of quitting must be able to deal both with the absence of the stimu-
lation provided by cigarettes and with the sense of craving (for to-
bacco) and other withdrawal symptoms. In this, he can be aided by
social forces, interpersonal influences and mass communications,
plus influences generated by health workers and other key groups in
encouraging behavioural change. When these influences become
significant to enough people, action will be taken through legisla-
tion, changes in regulations, and changes in customs. A good exam-
ple is the growing movement to "protect the rights of the non-
smoker" by reducing his exposure to tobacco smoke produced by
others.

SMOKING BEHAVIOUR IN A SOCIETY

New fashions in smoking tend typically to appear first among the
younger, more affluent members of the adult population who form
part of the upper classes of the society. In most developed coun-
tries cigarette smoking increased sharply during the years between
19 10 and 1920 because of the switch to this form of tobacco use
by young males taking up the habit for the first time and by older
men who had hitherto smoked pipes and cigars. The increase in
cigarette smoking was temporarily halted in many countries during

51


the Second World War because of tobacco shortages but soon re-
sumed its upward course after the war and quickly made up for lost
time. Also contributing to this increase were the larger numbers of
women who began smoking cigarettes during and immediately after
the 1940s. As with men thirty years earlier, cigarette smoking
among women was at first confined mainly to the upper and upper-
middle classes, but rapidly moved down the social scale to include
a substantial number of middle and lower-class women.

By the mid-1950s, when new information about the harmful
effects of cigarette smoking began to receive widespread publicity,
the growth of cigarette smoking began to be curtailed, first among
men in the upper classes, then among males in the other social
classes, and finally among adult women by the late 1960s. Of par-
ticular interest is the phenomenon observed in the USA where the
percentage of adolescent boys taking up cigarette smoking has grad-
ually dropped, apparently in response to the intensive educational
efforts begun in the late 195Os, while the percentage of adolescent
girls taking it up has gradually risen. By 1974 the rates for boys and
girls were almost identical and it seems likely that the continuous
increase in the proportion of young girls taking up smoking has
probably reached its limit, perhaps because "equality" in smoking
with boys seems to have been achieved. However, despite the sub-
stantial numbers of adults. who no longer smoke cigarettes, this
increase in smoking by younger women in developed countries-at
rates far higher than for their mothers and grandmothers-has
caused the per capita consumption of cigarettes to continue to rise
in these countries.

The growth of cigarette smoking in developing countries is a sub-
ject on which there is as yet little information. We do know that
there have been large relative increases in smoking in some countries
with low pre-1950 rates, but there are few reliable statistics to indi-
cate the exact rate of growth. From anecdotal material, however, it
is clear that cigarette smoking tneds to be taken up first by persons
having the closest first-hand association with people from the devel-
oped countries, i.e., the professional, political, and business leaders
of those countries. Although the relatively high cost of cigarettes
and the low standards of living in many developing countries may
have prevented cigarette smoking from increasing as rapidly as it
might otherwise have done, recent improvements in the economic
conditions of some of these countries have provided a strong incen-
tive for cigarette makers to launch aggressive marketing campaigns
aimed at offsetting the more static markets for cigarettes in devel-
oped countries, brought on in part by changed attitudes toward
smoking. Although there is no scientifically acceptable evidence to
prove that advertising has contributed to the growth of cigarette
use, and although cigarette smoking has, in fact, grown sharply in

52


some countries without the help of advertising, the overwhelming
aura of respectability and social acceptance conveyed by wide-
spread advertising has almost certainly been an important factor in
stimulating increased smoking.

BARRIERS TO SUCCESSFUL CONTROL

The main barriers to the successful design and implementation of
control programmes are the following:

(1) Gaps in medical and epidemiological knowledge. At present,
the knowledge of the effect of smoking on health and of how this
manifests itself is sufficiently complete to convince the overwhelm-
ing majority of medical scientists and nearly as much of the general
public in developed countries of the hazards involved. However, to
direct control actions toward persons and groups that would benefit
most from them, we need better means of identifying those at
greater risk. At the moment our means of doing this are limited to
identifying persons at the highest level of dosage exposure, those
with concurrent exposure to other risk factors that increase the
likelihood of lung cancer, ischaemic heart disease, or chronic ob-
structive lung disease, and those from ethnic groups with a high
prevalence of these smoking-related diseases. Thus, earlier and mote
precise measurement of the effect of cigarette smoking on an indi-
vidual or a group of individuals would provide an important basis
for sharpening the direction of control action.

(2) Economic and political conflicts. In the early years after
cigarette smoking was identified as a serious health problem, the
economic and political influence of tobacco farmers and the impor-
tance of receipts from the sales and taxation of cigarettes undoubt-
edly impeded the development of political support in this area from
governments. However, as the medical and epidemiologcal case
against smoking became clearer and the costs to society in death
and early disability were better identified, these economic and
political barriers to control action have begun to be lowered, albeit
rather slowly. Similarly, the importance of individual rights has
grown, at first in preventing control actions that would infringe on
the rights of smokers and, more recently, in restricting smoking in
public places so as to protect the rights of nonsmokers.

On another front, efforts to develop less harmful substitutes for
tobacco have recently resulted in the marketing of cigarettes par-
tially made from such substitute materials. With these cigarettes the
problem in health terms is the difficult one of ensuring that they
are at least no more harmful than cigarettes made wholly from
tobacco. In economic and political terms, they pose a significant
threat to tobacco as an agricultural product because if they became

53


widely accepted they could cause the world demand for tobacco to
shrink by as much as fifty per cent.

(3) Lack of knowledge on smoking behaviour. Because of gaps in
our knowledge of smoking behaviour, we are unable to be more help-
ful in assisting individuals who wish to quit smoking. In the USA,
for example, during the decade from the early 1960s to the early
197Os, when the climate of social support for giving up smoking
improved sharply, the spontaneous success rates for those who tried
to give up smoking more or less permanently nearly trebled to
about 40%. However, even in this favourable climate, only about
one person in three who tried to stop smoking was successful.

These figures do not include the many persons who did not even
try to give up smoking; although they accepted the fact that they
would be better off if they did so, they were unwilling to expose
themselves to the risk of failure. Despite the numerous attempts
that have been made to develop systematic therapeutic programmes
for helping people to quit smoking, on either an individual or a
group basis, these have had no better results than the spontaneous
success rates just mentioned, a record probably influenced by the
tendency of these programmes to attract smokers with a history of
previous failure, with whom the prospects of success are quite low.
Much the same can be said of attempts to develop low-cost self-aids
for individuals, as a substitute for costly professional therapy, and
of pharmacological aids; although these aids have had some success,
their effects have been limited and they are in need of further
improvement.

Another area suffering from a lack of knowledge is our ignorance
of the full potential of the effect of various regulatory and legisla-
tive aids such as increasing the price of cigarettes, differential
taxation to promote one type of cigarette as against another,
restrictions on places where smoking is permitted, restrictions on
the ease of purchase and general availability of cigarettes, and the
effect of reducing or banning cigarette advertising and promotional
activities. Although there is some evidence to suggest that these
actions are useful, the benefits achieved have not been adequately
evaluated under controlled conditions.

A third area affected by the lack of knowledge is health educa-
tion of the young and the development of more successful pro-
grammes to dissuade young people from taking up smoking.
Although much is known about some of the principles contributing
to effective health education of the young, these have not yet been
incorporated into programmes, which could provide convincing
evidence of their ability to reduce smoking. Without such evidence,
it is difficult to gain support for making widespread and expensive
changes in educational programmes.

54


(4) Lack of communication and coordination. Occasional inter-
national conferences and sporadic reviews of the smoking problem,
no matter how well thought out, are no substitute for a continuing
system of communication and information exchange. The three
international conferences on smoking that were held in 1967, 1971
and 1975 and the resolutions on the subject adopted by the World
Health Assembly in 1970, 197 1, 1975 and 1976 represent efforts to
support and encourage international action, but they have not
resulted in any system for ensuring that this takes place. National
programmes that have attempted to deal with the total problem,
such as the National Clearinghouse for Smoking and Health in the
USA, have provided systematic annual bibliographical publications
and literature reviews, which have made this task easier, but such
programmes must be augmented by systematic attempts to facili-
tate communication and enhance cooperative efforts.

WHAT IS TO BE DONE?

In the face of these obstacles and the indifferent success of control
efforts to date, it is clear that a much more systematic and multi-
faceted international attack will have to be mounted on the hazards
of smoking if this public health problem is to be reduced; equally,
this attack must be a coordinated one so that maximum benefit is
derived from separate national efforts against different aspects of
the problem. In its coordinating role on international health mat-
ters, WHO is ideally situated to undertake this task. Some of the
key areas in need of immediate attention are:

o Expert advice. Because of the multidisciplinary nature of the
problem, current control efforts are too often fragmented and
piecemeal. What is needed is a small panel of international experts,
operating under the aegis of WHO and comprised of behavioural
scientists, economists, sociologists, toxicologists, pharmacologists,
etc., in addition to public health workers, to provide national,
regional and international programmes with ready access to the best
available advice on the probable effectiveness of various measures.

o Monitoring the problem. Far too little is known about the vari-
ous factors that affect smoking and smoking behaviour in different
countries; the available information is often collected in sufficiently
different ways to make comparisons and extrapolations from na-
tional experience impossible. There is thus the need not only for
greatly expanded collection activities but also for countries to be
informed about what sort of information to collect and in what
way so that national efforts will reinforce one another and provide
the basis for global analyses.


o Information exchange. In addition to the dearth of information,
there is not enough cross-dissemination of available data to permit
making the best use of it. This gap could be fdled by periodic news-
letters, compiled by WHO from national contributions, and by
occasional regional and international conferences. '   i'
o Economic implications. If cigarette smoking i$ reduced by a sub-
stantial amount or the use of tobacco substitutes in cigarettes is
found to be safe and is widely adopted, then the economies of
tobacco-producing countries will be adversely affected. Although
we are far from this point at present, it is none too early to begin
considering alternative employment of tobacco lands and farmers
and the other economic effects of this process.

o Research. Virtually all aspects of the programme to control
smoking can benefit from more systematic research-ranging from
the epidemiological aspects that would identify better predictive
measures of dosage, through research into why people smoke and
what educational and other methods are best calculated to limit
smoking, to the development of various aids and methods to help
people stop smoking. In the latter instance, to cite just one exam-
ple, there has been no reliable or systematic testing of the useful-
ness of the various commercial products that claim to help a person
stop smoking.

56


~cs  03/06/79 informatics inc    6911 Kenil-h *mm    cs IV

INDEX

ABRUPT10 PLACENTAE
(See a&o PERINATAL MORTALITY)
maternal smoking levels and, 3, 7
smokers vs. nonsmokers, 3, 8
ADOLESCENTS
smoking habit, 50, 52
ADVERTISING
effect on cigarette consumption, 52
    53
AGING

effect on mortality ratios in smokers,
  28

effect on mortality ratios in ex-
smokers, 36-37

AMERICAN CANCER SOCImY
  STUDY

methodology, 2526
ANTISMOKING CAMPAIGNS
(See also PREVENTION OF SMOK-
ING)
short and long term strategies, 43-50
BIRTH WEIGHT
effect of carbon monoxide in rabbits,
    12

effect of cewation of smoking during
PEgnanCY, 2

effect of maternal smoking, 14
fetal and maternal carboxyhemoglo-
   bin levels and, 9-10
matemal smoking and, 11, 13
BLOOD VESSELS
effect of carboxyhemoglobin on fetus
   and placenta, 9
effect of smoking, 13
BREAST FEEDING
(See aleo LACTATION)
effect of nicotine on infanta, 15
BRITISH DOCTORS STUDY
methodology, 26!Z7
CARBON MONOXIDE
effect on pregnancy, 9-13

effect on birth weight and neonatal
   mortality in rabbits, L2
low birth weight infants and, 12
CARBOXYHEMOGLOBIN
effect on fetal and placental blood
   vessels, 9

effect on oxygen transport in fetw
  11

CARBOXYHEMOGLOBIN LEVELS
birth weight and, 9-10
birth weight in rabbits and, I2
effect of maternal smoking on fe-
   tavmatemal ratio, 11
effect of smoking in pregnant vs.
  nonpregnant women, 9-10
CARDIOVASCULAR DISEASES
(See also ISCHEMIC HEART DISEASE;
MYOCARDIAL INFARCT;
THROMBOEMBOLISM)
mortality risk in oral contraoeptive
   users and smokers, 13-14
oral contraceptives and smoking and,
   13-15

CESSATION OF SMOKING
(See aho EX-SMOKERS; SMOKERS
vs. Ex-sMOKERs)
effect on biih weight in offspring,
    2

effect on ischemic heart d&ease mar-
tality risk, 36

effect on lung neoplasm mortality
risk, 37

effect on mortality ratea and ratios,
32-37,4142

health benefits, 43-50
CHILDREN
effect of maternal smoking during
  pregnancy on intellectual and
  physical development, &9
smoking habit., 50, 52

57


B                                 hlkmmmRocgino-~
      H,cs 03/06/79 informatics inc    6811 Karmalh A-
                                             R-w20840
                                               .   301 8887700

INDEX

CIGARETTE CONSUMPTION
effect of t&acco industry advertis-
   ing,5%53

CIGARElTES, LESS HAZARDOUS
health benefits, 43-49
mortality ratios in low va medium
   vs. high tar/nicotine smokers, 30-
   31

mortality ratios in low tar/nicotine
   smokers vs. nonsmokers, 31
coNTRAcEPTIvEs, ORAL
eardiovascldar ciileaw and smoking
   and, l3-15

myocardial infarct and smoking and,
    1815
DDT

effect of maternal smoking on levels
   in breast milk, 15
EX-SMOKERS

(See ah CESSATION OF SMOKING;
SMOKERS vs. Ex-sM0KEss)
bii weight in offspring, 2
mortality ratios, 32-33
FETUS

(See aleo BIRTH WEIGHT; PERINA-
TAL MORTALITY)
effect of carboxyhemoglobin on blood
   vessele, 9

effect of maternal smoking on oxy-
   gen transport, 11-12
HEREDITY

role in disease etiology, 49
INHALATION

effect on mortality ratios in ciga-
   rette smokera, 29
effect on mortality ratios in cigar vs.
  pipe smokers, 33
INTELLECTUAL DEVELOPMENT
effect of maternal smoking levels
  during pregnancy on offspring,
   3-9

ISCHEMIC HEART DISEASE
(Ses also CARDIOVASCULAR DIS-
EASES)
mortality risk, effect of cessation of
   smoking, 36
LACTATION
(See also BREAST FEEDING)
effect of maternal smoking, 15
LUNG NEOPLASMS
mortality risk, effect of cessation of
   smoking, 37

MORTALITY

annual probability of dying in smok-
  em va nonsmokers
va ex-smokers, 34-37
cardiovascular diwases, risk in oral
contraceptive users and smoke=,
  13-14

cigarette va cigar vs. pipe smokers,
  38

effect of smoking, 21-45
my&al infarct, rati in orai con-
traceptive users and smokers, l3-
  14

summary of the 1964 Surgeon Gener-
  al's Report findinga, Z-23
summary of the 196'7 He&h Con&?-
   qutmeea of Smoking findings, 29
MORTALITY RATIOS
cigarette va cigar vs. pipe smokers,
   38, 41-45

effect of inhalation, 29$3
effect of smoking duration in cigar
smokers, 39

effect of smoking duration in ciga-
  rette smokers, 2829
effect of smoking duration in pipe
  smokers, 39-41

effect of smoking levels in cigar
smokers, 39-40

effect of smoking levels in cigarette
smoke-m, 27-29

effect of smoking levels in pipe
  smokers, 39-41

ex-smokere, 32-37
low tar/nicotine smokera va non-
smokers, 31-32

low vs. medium va high tar/nicotine
   smokem, 33, 41-43
MYOCARDIAL INFARCT
(See also CARDIOVASCULAR DIS-
  EASES)
mortality rate in oral contraceptive
   users and smokers, 13-14
oral contraceptivea and smoking and,
    13-15

NATIONAL CHILD DEVELOPMENT
  STUDY, 3-9

NATIONAL CLEARINGHOUSE FOR
  SMOKING AND HEALTH
effect of maternal smoking on preg-
   nancy, survey of public aware-
   ness, 16

role in prevention of smoking, 55


HCS 03/06/79 informatics inc           cs `h

INDEX

NICOTINE

rffect on breastcfed infants, 15
effect on mortality ratios, 30-31
NEONATAL MORTALITY
effect of carbon monoxide in rabbits,
   12

ONTARIO PERINATAL MORTALITY
STUDY, 3

OXYGEN TRANSPORT

effect of carboxyhemoglobin on
    fetus, 11
*  effect of maternal smoking on fetus
    and mother, 11-12
' pSRINATAL MORTALITY
(,$ee also ABRUPT10 PLACENTAE;
  BIRTH WEIGHT; PLACENTA
  PREVIA; PREMATURITY; STILL-
  BIRTHS)
effect of maternal smoking, 23, 7
  maternal smoking and, 13
  risk factors, 2-3
PHYSICAL DEVELOPMENT
effect of maternal smoking levels
   during pregnancy on offspring,
     a-9
PLACENTA

effect of carboxyhemoglobin on blood
vessels, 9

PLACENTA PREVIA
(See also PERINATAL MORTALITY)
maternal smoking levels and, 3-4, 7
smokers vs. nonsmokers, 3-4, 8
PREGNANCY

effect of carbon monoxide, 9-13
effect of maternal smoking, 1-13
effect of maternal smoking, public
   awareness, 1516
PREMATURITY
(se also FETUS; PERINATAL MOR-
TALITY)
maternal smoking levels and, 3-4
PREVENTION OF SMOKING
(See atso ANTISMOKING CAM-
PAIGNS)
barriers to successful control, %-%
health benefits, 43-56
international programs, future needs,
    55-56

SMOKE, CIGARETTE
(See also SMOKING)
synergistic action in disease etiology,
   49

SMOKERS, CIGAR
mortaiity ratios, 33-43
mortality ratios, effect of smoking
   duration 33-39

mortality ratios, effect of smoking
levels, 3840

SMOKERS, PIPE
mortality ratios, 33-43
mortality ratios, effect of smoking
   duration, 3341

mortality ratios, effect of smoking
levels, 33-41

SMOKERS vs. EX-SMOKERS
(See a&o CESSATION OF SMOKING;
  EX-SMOKERS)
annual probablity of dying, 34-37
SMOKERS vs. NONSMOKERS
abruptio pI&?en&, 3, 5-6, 8
annual probability of dying, 34-37
birth weight in offspring, 4
membrane rupture during pregnancy,
   7-3

myocsrdial infarct in oral contracep-
  tive users, 13-15
perinatal mortality, 5
placenta previa, 3-4, 6, 3
prematurity, 4

SMOKING (S% o4.so SMOKE, CIGA-
RETTE; SMOKERS, CIGAR;
SMOKERS, PIPE; SMOKING DU-
RATION; SMOKING LEVELS;
SMOKING, MATERNAL)
effect on blood vessels, 13
effect on carboxyhemoglobin levels
  in pregnant vs,
  nonpregnant women, 11
effect on mortality, 21-45
in etiology of disease, review of
   mechanisms, 47-49
synergistic action in disease etiology,
   49

SMOKING AND HEALTH
research needs, 53-56
SMOKING DURATION
(See ah EX-SMOKERS; SMOKERS,
CIGAR; SMOKERS, PIPE; SMOK-
ING; SMOKING LEVELS)
effect on mortality ratios in cigar
   smokers, 3339

effect on mortality ratios in ciga-
rette smokers, 23-29
effect on mortality ratios in ex-
smokers, 3234


INDEX

effect on mortality ratios in pipe
  smokers, 3&11

SMOKING HABIT
children and adolescents, 50, 52
initiation, establishment, maintenance
   and modification, 50-51
research needs, 53-54,56
trends in 20th Century, 51-53
women, 1

SMOKING LEVELS
(See dao SMOKERS, CIGAR; SMOK-
ERS, PIPE; SMOKING; SMOKING
DURATION; SMOKING LEVELS,
MATERNAL)
effect on mortality ratios in cigar
   smokers, 33-40

effect on mortality ratios in ciga-
rette smokers, 2'7-29
effect on mortality ratios in ex-
smokers, 3234

effect on mortality ratios in pipe
  smokers, 3341

effect on myocardial infarct risk in
   oral contraceptive users, 1415
SMOKING LEVELS, MATERNAL
(Sa aiao SMOKING, MATERNAL)
abruptio placentae and, 3, 5, 7
bleeding during pregnancy and, 3, 7
effect on birth weight, 24
effect on carboxyhemoglobin levels,
   10

effect on intellectual and physical
development in offspring, 3-9
effect on perinatal mortality, 3, 5, 7
membrane rupture during pregnancy
  and, 3, 7

prematurity and, 3-4
placenta previa and, 3-4, 7

SMOKING, MATERNAL
(See aleo SMOKING LEVELS, MATER
  Nfi)
effect on birth weight, l-2
effect on DDT levels in breast milk,
    15

effect on fetal/maternal carboxyhem-
oglobin ratio, 11
effect on intellectual and pbyaical
development in offspring, 3-9
effect on lactation, 15
effect on oxygen transport in fetus
  and mother, 11-12
effect on perinatal mortality, 2-3
effect on pregnancy, 1-13
effect on pregnancy, public aware-
ness, 15-16

effect on umbilical artery, 13
low birth weight and, 13
perinatal mortality and, 13
stillbirths and, 8
STILLBIRTHS
(,See also PERINATAL MORTALITY)
maternal smoking and, 8
THROMBOEMBOLISM
(See also CARDIOVASCULAR DIS-
EASES)
mortality rate in oral contraceptive
   users and smokers, 14
TOBACCO INDUSTRY
effect of advertising on cigarette
   sales, 52-53

UMBILICAL ARTERY
effect of maternal smoking, 13
U.S. VETERANS STUDY
methodology, 26
WOMEN

smoking habit, 1
summary of smoking related health
problems, 17