ED 20,B 295

AUTHOR

. TITLE

'INSTITUTION

PUB DATE

NOTE

BDRS PRICE

DESCRIPTOR,

ABSTRACT,

This report focuses on the evidence about the health

.consequences of smoking for women, and is intended to serve.the

public health and medical communities as 'a unified source of existing

scientific research. The major issues about tobacco use and women's

health are examined, including trends in consumption, biomedical

evidence, and determinants of smoking ititiation, maintenance, and

cessation. The biomedical aspects ofsmoking are presented in terms

of mortality, morbiplity, cardiovasculaidiseases, cancer, pregnancy

and infant,health,, Teptic ulcer disease, drug reactions and , interactions, food constituents, and responses to,diagnostic tests.

The psychosocial and behavioraj. aspects, of smoking in women are

discussed, along with the docffiented increases in- the risk of

contracting lung cancer, heart,disease, or lung disease. The harmful

effects of pregnant mothers smoking behaviors, are also docudented.

Adhitionally, recent data are enumerated to indicate a trend of

,decreasing tobacco usage among women in response to the warnings of

the gavernMent, voluntary agencie, and physicrins. (Author /NRB)'

DOCUMENT RESUME

cc 015 465

Pinney, John M., Ed.:' And Others

The Health Consequendes of Smoking for. Women. A

Report, of the Surgeon General 1979.

Public Health Service (DHHS), Rockville, Md.

.(79]

356p.

MF01/PC15 Plus Postage.

BehaVior, Patterns; *Cancer; *Females; Health

Materials; *Heart Disorders;-*Physical Health;

Pregnancy; Prenatal Influences; Prevention;

Psychological Patterns;,*Smoking:. Tobacco

************4*********************************************************.

* Reproducions supplied by EDRS are the best that can be wade

10' from the original document. *)

0**************J4****************************************************
t-r\ THE HEALTH

s.).; CONSEQUENCES

If, Or SMOKING

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eteport of the Surgeon General

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U S DEPARTMENT OF HEALTH AND HUMAN SEPVI

Pubiu ifedith Serv,co

Office of the Assistant Soc rotary for HPaIth

Office on Smoi,-or) and Heatth . ti

1979
Tp4C C-"AEARY OF .E.PAPE

NSSN C < 0

t1 The Honorable Thomas P, O'Neill,Jr.

1 Speaker of the House of Representatives

'Washington,. D.C. 20515

Dear Mr. Speaker:

I hereby submit to 12th annual report that the Department of Health,,Edudation, and Welfare (DHEW) has prepared for Congress as required by the Public Health

Cigarette Smoking Act Of 1969, Public Law 91-222, and its

predecessor, the Federal Cigarette Labeling and Advertising

Act. This report'is one of the most alarming in the series.

Jok, -tt clearly establishes that women smokers face the same

nisks aS"'"Me...n smoker's of lung cancer, heart disease, lung disease and other consequences. Perhaps more disheartening

is the Harm which mothers' smoking causes to their unborn

babies -and infants.

, The report is not all bad news. It presents recent data showing that women are turning away from smoking in'

response to the warnings of government, voluntary agencies and physicians. The precipitate rise in women's deaths from

lung cancer and chronic lung disease demand that this trend

away from cigarettes be accelerated. Our scrintists expect that by 1983, the lung cancerdeath-rate will exceed.thatof

any other type of cancer among women.

Citigens of our free society may decide for themselves

whether to sMoice cigarettes. The health consequences of

this decision make it imperative for their government to assure that the decision is a informed one. This series /of reports is one way in which EW is striving to meet

this critical. responsibility.

e% your S_1_

Patricia Roberts Harris

tr
PREFACE

This report is more than a factual review of the health conse-*

quinces of smoking for women. It >i a document which, challenges our society and, in particular, our medical and public

health communities.

T is report points out that the first signs of an epidemic of

smo g-related disease among women are now appearing. Because women's cigarette use did nut become widespread untili

the onset of World War II, those women with the greatest inter

sity of smoking are now only in their thirties, forties, and fiftie.

As these women g-rc lder, and continue to ,smoke, their burden of smoking-rel sease-will grow larger. Cigarette smoking now contributes one -fifth of the newly diagnosed cases of

cancer and one-quarter" or all cancer deaths arming wpmen

more cancer and more cancer deaths among women than can be

attributed to any other kriown agent. Within three years, the

lung cancer death rate is expected to surpass that for breast

cancer. A similar epidemic of chronic obstructive lung disease

among women has also begun.

Four rfrain themes emerge from this report to guide future

public kiealth efforts.

First, women are not immune to the aamaging effects cif

smoking already documented for men. The apparently lower

,susceptibility to smoking-related diseases among women smokers is an illusion reflecting the fact that women lagged one

quarter century behind men in thew Ividespread.use of cigarettes:

Second, cigarette smoking is major threat to the outcome of

pregnancy and tvell-being of the newborn baby.

Third, women may not startsmoking, continue to smoke, quit

smoking, or fail to quit smoking for precisely the same reasons

as men. Unless future research clarifies these differences, we

will find it difficult to prevent jnittation of to prvote oessation

of cigarette smoking among women.' t

'Fourth, the reduction of cigvarette smoking is the keystone in

our nation's long term strat to promote a healthy lifestyle

for women and men of all race and ethnic groups.

The Fallacy of Women's Immunity

All of the major prospective studies of smpking and mortality

have reached consistent conclusions.Death rates from coronary

heart disease, chronic lung disease, lung cancer, and overall

mortality rates are significantly increased droungouth women

and men smoky-s. These risks increase 'with the amount

smoked, duration of smoking, depth of Inhalatioh, and the "tar"

V
and nicotine delivery of the cigarette smoked. In these studies, conducted during the past three decades,

relative mortality risks among female smokers' appeared to be

less than those of male smokers. It is now clear, however, that

these tudies were comparing the death rates of a generation of establNhed, lifelong male smokers with a generation of women who had not yet taken up smoking ;cab full intensity Even

those older women whu reported smoking a large number of cigarettes per day .1-iad not smoked cigAettes in the same way as.' their male counterparts. Now that the cigarette smoking char- acteristics of women and men are becoming increasingly similar,' their relative risks of smoking-related illnes become

increasingly similar.

This fallacy of women's apparent immunity is clearly illustrated by differences in the timing of the growth in lung cancer among men and worm in this century. Lung cancer deaths

amon.gmales began to increae during the 1930s, as those men

who had converted from other forms of tobacco to cigarette

smoking before the turn of the century gradually ac'cumglated

decades of inhaled tobacco exposure. By the time of the first retrospective studies of smoking and lung cancer in 1950, two

entire generations of men had already become lifelong cigarette

smokers. Relatively few women from th,ese generations smoked

cigarettes, and even fewerialad smoked cigarettes since their

adolescence. Those young women who had taken up smoking

intensively duxing World War II were only in their twenties and

thirties. In 1950, women accounted for less than. one in twelve

deaths from lung cancer. . Thereaftej, the age adjusted lung cancer death rate among women accelerated, and the male predominance in lung cancer. declined. Lung cancer surpassed uterine cervical cancer as a

cause of death in women. By 1968, as the findings of many large population prospective studies were being published, women

akounted for one-sixth of all lung cancer deaths. These studies

found that women cigarette smokers had 2.5 to 5 times greater death rates from lung cancer than women nonsmokgrs. By 1979, women accounted for fully one-fourth of all lung catcer deaths.

Over the next few years, women cigarette smokers' risk of lung cancer death will approach $ to ,12 tires that of women

nonsmokers, the same relative risk as that of men.

Lung cancer has four main histological types; epidermoid, small cell, adenocarcinoma, and large cell carcinoma, As several studies have shown, the incidence of each of these types of lung

cancer displays a clear relationship to cigarette smoking among

'both men and women Epidermoid and small cell lung cancer appear to be more prominent among men, while adenocar- V1 1 /
i.....,--''' A cinoma of the lung now appears to be more- prominent among

women.

, . , The ecent acceleration of lung cance"r incidenCe among women has in fact IS'e ri more rapid than the corresponding

growth of lung cancer among men in the .1930s. Again, this dif- ference in the initial rate of acceleration.of lung cancer incidence does not refute,the demonstrated causal relation between

cigarettesmoking and lungicancer among both sexes. Instead, differences in therate of increase of lung cancer incidence may

reflect changes in the carcinogenic, properties of cigarette

smoke, th'e style of cigarette smoking, or the interaction of

cigarette. smoking with other environmental hazards. It is

noteworthy that those men who died of lung cancer in the 1930s

came from a generation that had g .radually converted to

cigarettes from other, non-inhaled forms o,( tobacco. By contrast, the first regular tobacco users among women were aintost

exclusively cigarette smokers. . The 1979 Report on Smoking and Health documented numerous instances where cigarette smoking adds to the hazards of

the workplace environment among men. Among women, this

report reveals two such occupational exposuresasbestos and

cotton dustwhich have been clearly demonstrated to interact

with Cigarette smoking. The fact that evidence is limitted among women does not imply that women are protected from the

dangerous interactions of smoking,and occupational exposures.

Pregnancy, Infant Health, and Reproduction

Scientific studies encompassing various races and ethnic

groups, cultures and countries, involving liundreds' of

thousands of pregnanies, have shown that cigarette smoiung

during pregnancy significantly affects the unborn fetus and the

newborn baby. These damaging effects have been repeatedly

shown to operate independently of all other factors that influoce the outcome of pregnancy. The effects are increased by heat'ier smoking and are reduced if a woman stops smoking

during pregnancy.

Numerous toxic Substances in cigarette smoke, such as

nicotine and hydrogen cyanide,. cross the placenta to affect the

fetus directly: The carbon monoxide from cigarette smoke Is

transported into the fetal blood and deprives the growing baby of,oxyge-n. Fetal growth is directly retarded. The resulting reduction in fetal At ight and size his many unfortunate consequences. Women who smoke cigarettes during pregnancy have more spontaneous abortions, and a greater incidence of bleeding during pregnancy, premature and prolonged rupture of am- .

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niotic membranes, abruptiu plac'entae and placenta previa.

Women'who smoke cigarettes during pregnancy have more fetal

and neonatal deaths than nonsmoking pregnantwomen. A Ala:.

nun 4Frtw."een maternal smoking and Sudden Infant Death Syndrome has now been established.

The direct harmful effects of smoking on the fetus have long

term consequences. Children of mothers who smoked during

pregnancy lag measurably in physical growth, there may also

be effects on behavior and cognitive development. The extent of these deficiencies increaseswith the number of cigarettes smoked.

The damaging effects of maternal smoking on infants are not

restricted to pregnancy. Nicotine, a known poison, is found in

the breast milk of smoking mothers Children whose parents

smoke cigarettes have more respiratory infection's and morehospitalizatiAs in the first year of life.

Women who smoke cigarettes have more than three times the

risk of dying of stroke due to subarachnoid hemorrhage, and as

mhch as two times the risk of dying of heart attack in comparison to nonsmoking women The use of oral contraceptives in

addition to smoking, however, causes a Markedly increased risk,

including,a 22-Told increase in'the risk of subarachno'id hemol--

rhagic stroke and a 20-fold increase in heart attack in heavy

smokers.

Why. Do Women Smoke?

Cigarette consumption in this country is now declining. Annual per capita consumption has decreased from 4,258 in 1965 to

an estimated 3,900 in 1979. From 1965 to 1979, the proportion of

adult male cigarette smokers declined from 51 to 37 percent. Not

only have millions men quit smoking, but the rate of minanon of smoking among adolescent males has-no ' slowed.

From 1965 to 19t6, the proportion; of adult w men cigarette

smokears remained virtually unchanged at 32 to 33 percent.

Since 1976, however, the proportion of adult women cigarette

smokers appears to have declined to 28 percent. Although adult

women are now beginning to quit smoking at rates comparable

to adult men, the rate of initiation of smoking amrig- younger

women has not declined.

This report documents numerous differences by sex in the

perceived role of cigarette smoking, in attitudes toward health

and lifestyle, and 1,n methods of coping with stress, anger, and

'boredom. Yet the significance of these differences, and their

relation to differences in smoking patterns, remains poorly understood.

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4
Although it is frequoently observed that women in orgaruz smoking cessation programs have more severe with awal mptoms and lower rates of succe; sful quitting t an men, these observations have not been systematically confirmed for the general population. In the past, women may have attempted to quit or succeeded in quitting smoking less frequently than men The recent decline 1,n the proportion of women smoker'. howel.er, suggests, that womken's attempted and succ.essful quit- ting rates have now increased

Although weight gain is a frequently cited consequence of quitting smoking. the association of weight gain with cessation of smoking has not been the subAct of sufficient scrutiny. Con- trolled studies lkith careful measurement on representative populations of women do not exist. The impact of the fear of weight gain after quitting has not been adequately examined. If *.eight gain does result from cessation of smoking, its exact mechanism must be determined

Even more problematic are marked differences by sex in the distribution of smoking preval e by occupation. Men with ad- anced education and"or ssional occupatior* have taken the lead in quitting ng, but women in administrative and m'anagerial position's ave relatively high smoking prevalence rates Although 20 per nt or fewer male physicians smoke, the proportions of cigarette smokers among women health profes- sionals, especially niirses and psychologists, remain 'disturb- ingly high

Recent changes in smoking prevalence among black women and men have paralleled those of the general population. From 1965 to 1979, the-proportion of black women cigarette smokers declined from 34 to 29 percent, while the proportion of black men smokers declined from 61 to'42 percent. However, differences by race in the onset, maintenance, and cessation of smoking have not been adequately explored Little is known about cigarette making among other ethnic and tinnority

Adolescent Smoking

The health consequences oft

smoking e,..4)Ive over d lifetime. Evidence continues to accumulate, for example, that cigarettes smoking produces measurable lung changes in adolescence and young adulthood Yoking cigarette smokers of both sexes i.ihow more evidence of small airway dysfunction, and a higher preva- lence of cough. wheezing, phlegm production, and other 'respira- tory symptoms The health damage due to cigarette smoking increases when an individual begins regular smoking earlier in life. Yet, as this report documents;the average age of onset of

b

ix Jr
regular smoking among women has continuously declined dun

ing tle last 50 years, and continues to decline.

According to a recent survey'by the National Institute of

Education, cigarette smoking among adolescent girls now exceeds that among adolescent boys. In the 17-19 year age group,

there are almost :5 female cigarette smokers for every 4 male

cigarette smokeri. The causes of this 'invtrsion are far from

clear. We do not yet understand the signal events in the initiation of smoking among young women. It is possible that parents

set examples concerning lifestyle, health attitude, and risktaking much earlier in childhood. The beginning of junior high.

school or entrance into the work force inaY be equally critical

events. We do not know enough about an adolescent's sense of

competence and self-mastery, and how these roles.differ among

women- and men. Although smoking patterns among girls correlate with parental, peer and sibling smoking habit,, educational

level, type of school curriculum, acadeinic performance,

socioeconomic status, and otherformsof,substance abuse, the

practical significance of these empirical correlations is unclear.

Women and the Charging Cigarette

As this report documents,vthe proportion' of men and women

smoker using brands with lowered ;`tar" and nicotine continues to grow. Adolescents of both sexes have foll6wed ,this

trend, to the point wherenonfilter cigarettes are relativelyieare

among yo'ung adults. Although the preponderance of scientific evidence continues

to suggest that cigarettes with lower "tar" and nicotinyare less

hazardous, four serious warnings are in order.

First, the reported "tar" and/nicotine deliveries of cigarettes

are standardized machine measurements. They do not neces:

sarily represent the smoker's actual intake ofthese substances.

Evidence is now mounting that individuals who switch to

cigarettes with lowered "tar" and nicotine inhale m6re deeply,

smoke a greater of their cigarettes, and in some

cases smoke more cigarettes. Second, "tar" and nicotine are not the only dangerous chemical components of cigarette smoke. Many conventio''rial filter

cigarettes, in fact, may deliver more carbon monoxide than non-.

filter cigarettes. Third, it has not been established that lower "tar" and

nicotine cigarettes have less harmful effects on the unborn

fetts and baby; on women and men at high risk for developing

coronary heart disease, such as those with elevated cholesterol

or high blpod pressure; or on orkers with adverse occupational
exposures. It has not been establi lied that switching to a lower "tar" and nicotine cigarette has any, salutary effect on indi- viduals who already have smoking-related illnesses, such as coronary heart disea'se:schronic bronchitis, 'and Emphysema. Fourth, even the lowest yield cigarettes present health hazards for both

- women and men that are very much higher than smoking no cigarettes at all. The single most effectiire way for both women and men smtlic- frs to reduce the-hazards associated with cigarettes is to quit smoking.,

A's this report demonstrates, little is known'about the effects 11 of these product changes on the initiation, maintenance and Cessation of smoking, particularly among women. It has not' been determined whether the availabilitr'of cigarettes with lowered "tar" and nicotine has made it easier for young women to experiment1with and become addicted to Figarettes. It is not known whether smokers of the lowest yield 4igarettes are more or less likely to attempt to quit, orqo succeed in quitting, than smokers of conventional filtertip or nonfilter cigarettes. The extent to which the act of switchin to a lower "tar" cigarette, serves as a substitute for. quitting mad differ among women and men.

Public Health Responsibilities alte

This report,which includes data compiled by individuals from both inside and outside the Government, has confirmed in every 4.3,7ay the judgement of the World Health Organization that there can no longer be any doubt among informed people that cigarette smoking is a major and removable cause of ill health and premature death.

Each individual woman must make her own decision about this significant health issue. Secretary Harris has noted that the role of the 'Government, and all responsible health profes- sionals, is to assure that this decision is an informed tou. In issuing this report, we hope to help the public health community accomplish this purpose.

Julius B. Richmond, M.D.

Assistant Secretary for Health arid

Surgeon General

1

xi
ACKNOWLEIGEMENTS

This report was prepared by agencies of the U.S' Department of Health, Education, and Welfare under the general editorship of the Office on Smoking and Health, John M. Pinney, Director. Consulting scientific editors were David M. Burns, M.D., As- sistant Clinical Professor of Medicine, Pulmonary Division,- ' 1.Jniversity of californiaat San Diego, San Diego, California, and John H. Holbrook, M.D., Associate ProfesSor of Internal Medicine, University of Utah Medical School, Salt Lake City, Utah. Contributing scientific editors were Joanne Luoto, M.D., M.P.H., Medical Officer, Office on Smoking and Health, Rockvill0 Maryland, and Kelley L. Phillips, M.D., M.P.H., Ex- pert Consultant, Office on Smoking and Health,'Rockville, Maryland.

Introduction and Summary

Office on Smoking and Health

Patterns of Cigarette Smoking Office on Smoking and Health

Jeffrey E. Hairis, M.D.,

Ment of Economics, Ph.D., Associate Professor, Depart- Massachusetts Institute of Technology, Cambridge, Massachusetts; Clinical Associate, Medical Serir- ices, Massachusettt General Hospital, Boston, Mas- sachusetts.

Mortality

National Heart, Lung, and Blood InstitkrK

Eugene Rogot, M.A., Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, National Insti- tutes of Health, Bethesda, Maryland. ''' Thomas J. Thom, Division. of Heart and Vascular Diseas s, National Heart, Lung. and Blood, Institute, National In- - tutes of Health, Bethesda, Maryland.

Morbidity

National Center for Health'Statiotics Ronald W. Wilson, M.A., Chief, -Health Status and Demo- graphic Analysis BrItnch, Division of Analysis, National Cen- ter for Health Statistics, Hyattsville, Maryland.

Cardiovascular Diseases

National Heart, Lung, and Bloodi Institute . q

G. C. McMillan, M.D., h.D., Assoate Director for Etiology of Arteriosclerosis and 'Hypertension, Division of Heart and Velar Diseases, National 'Heart, Lung, and Blood Insti- tute, National institutes of 1-1.ealth, Bethesda, Maryland. '

Xiii
r Cancer

National Cancer Institute

Jesse L. Steirifeld, Dean, School of Medicine, Medical

College of Virginia, Virginia Commonwealth Univerkity,

Richmond, Virginia.

Nol?Seoplastic Bronchopulnimwry Diseases

National Heart,:tung, and Blood Institute

Richard A. Bordow, M.D., Associate Director of Respiratory

Medicine, Brookside Hospital, San Pablo, Californra.

Claude J. M. Lenfant, M.D.; Director, Division of Lung Dist'

eases, National Heart, Lung, and Blood Institute, National

Institutes of Health, Bethesda, :Maryland.

Ba7rbara Marzetta Liu, S.M., Division of-Lung Diseases, National Heart, Lung, fr' Blood Institute, National Institutes

of Health, Bethesda, Ma viand.

Eric R. Jurrug, Ph.D., Di ision of Lung Diseases, National

Heart, Lung, and Blood nstitute, National Institutes of

Health, Bethesda, Maryland.

Interaction Between-Smoking and Occupational Exposures

National Institute of Occupational Safety and Health

Jeanne M. Stellman, Associate Professor, Columbia

.Universtty, School of Public Health, New York, New York.

Steven D. Stellman, Ph.D., Assistant Vice- President for

Epidemiology, American Cancer Society, New York, New

Fork.

Pregnancy.and Infant Health

National Institute Of Child Health and Human Development

Eileen G. Hasselmeyer, Ph.D., R.N., Associate Director for

Scientific Revievi, NOlonal Institute of Child Health and

Human Development, National Institutes of Health,

Bethesda, Maryland.

Mary B. Meyer, Sc-.M., Associate Professor of Epidemiology,

Johns Hopkis University, School of Hygiene and"Public

Health, Baltimore, Maryland.

Lawrence D. Longo, M.D., Prof or of Physiology 'of

Obktetrics and Gynecology, Lomalitinda University School of

Medicine, Loma Linda, California. , Donald R. Mattison, M.D., Medical Officer, Pregnancy Re- search Branch, National Institute of Child Health and

Hinman Development, National Institutes of Health,

Bethesda, Maryland.

Peptic Ulcer Disease

National Institute Arthritis, Metabolism an,d Digestive

Diseases

Travis E. SoloWon, M.D., Ph.D., Center for Ulcer Research

xiv 5 \

I
. " .ft - , and Education, Veterans Administotion Wadsworth Medical Center, and University of

Medicine, Los California, Los Angeles School of Angeles, California. , Janet D. Ela§hoff, Ph.D., Center for Ulcer Research and Edu- cation, Veterans Administration' Wadsworth Medical Center and University of.California). Los Angeles School of Medicine, Los Angeles:California.

. , . Interactions of Sinoking with Drugs, Food Constituents, and Responses to Diagno 'tic Tests

ilFqied and Drug Adfni

s

istration

Cheryl Fossl5m Graham, M,D., Division of Drug Experience, Office of Bi etrics and ,Epidemiology,' Food and D Bureau ,of rugs, Administration, Rockville, Maryland. -Psychosoct National Institute

aza1413ehavio4 AsixeCts of ,Srapking ,iii. men, -,0 on Drug Abuse and National Instittte, of '1d. Health and 'Human Development

.

. hi Son 0. ..

. 5' .

. Ellen It . az,. Ph,D.,Research

minigtration Medical Psychologist, Veterans AdCenter, Brentwood, and Associate Re- search Psychologist, Department bf Psychiatry and' -Biobehavioral Sciences, School of Medicine, University 'of California, Los Angeles, California.

, Ann F. Brun'swick, Ph.D., Senior Research Associate (Public Health, Sogiomedical Sciences), Center or Sociocultural Re- search.on Drug Use, York. Columbia Univer ity, N-ew/York, New . -,,. ,

'Maintenanci and Cessation ' .. t Kanen L. Bierman, M.A.; Department oflP1syc,hology, Urriver- Sity of California, Los Angeles, California.' Ellen R, Glitz, PA.D., . 't research Psychologist, Veterans Ad -' ministration Medical Center, Brentwood, and Associate Re, search Psychologist, 'Department of Psychiatry -and Biobehavioral ScienceX, School of Medicine, University of 'California, Los Angeles, California.

, . , 0' .

..., The -editors, acknowledge . wit1gratiAee the many distin-, guished scientists, physfcrans, and other who assisted'in the preparation of this report by coordinating manuscript prepara- tion, contributing critical reviews of the manuscripts or helping th other ways.

b* , Elvin E. Adams, IVI.D., M.P.H., Chairman, Texas Interagency Cb.pincif lit Smoking and Health, Pr4cticing Medicine, Fort Worth, tIntetnak Texas.

Josephine D. Arasteh,Ph.D., Health Scien ist Administrator, Josephine

xv

4
Human Learning and Behavior Branch, Center for Research

for Mothers and Children, ;Cational Institute of Child Health

and Human Development, National Institutes of Health,

Bethesda, Maryland,

Lester Breslow, M.D M.P.H., Dean, School of Public Health,

IUniversity of California at Los Angges, Los Angeles, California. # A. Sonia Buist, M.D., Associate Profe,,,,sor c Medicine and

Physiology, University of Oregon Health Sciences Center,

Portland, Oregon: David M. Burns, M.D., Assistant Clinical Professor of

Medicine, Pulmonary Division, University of California at

San Diego, San Diego, California.

Thomas C. Chalmers, M.D., President and Dean, Mount Sinai

Medical Center, New York, New York.

Florence L. Denmark, eh.D., Professor of Psychdogy, Hunter

College of the City University of New York, and President of

the American, Psychological Association, New York, New

York.

Robert M. Donaldson, Jr., 'M.D., Chief, Medical Services,

Westhaven_yeterans Hospital, and Vice-Chairman; Depart-

,. ,ment of rfiternal Medicine, Yale University School of

Medicine,. New Haven, Connecticut.

Joseph T. Doyle, M.D., Professor of Medicine and Head, Division of Cardiology of the Department of Medicine, Albany

Medical College' of Union University, Albany, New York.

Elizabeth M. Earley, Ph.D., Chief, Section of Cytogenetics,

Division of Pathology, Bureau of Biologics, Food and Drug

Administration, Rockville, naryland,

Bernard H. Ellis, Jr., Program Director for Smoking and Occupational Activities, Office of Cancer Communicapons, National Cancer Institute, National Institutes of Health,*

Bethesda, Maryland. Diane Fink, 14.D., Associate Director, National Cancer Insti

tute, and Coordinator, Smoking, Cancer, and Health Program,

gatibnal,InstituteA of Health, Bethesda, Maryland.

HarOld.E.,Fox, M.D., Associate Professor of Clinical Obstetrics

and Gynecology, Department of Obstetrics and Gynecology,

College of Physic' and Surgeons, Columbia University,

fsP.: and Medical Di Western and Upper Manhattan

Perinatal Netw ork, New York.

Joseph II; gape Veterinary Medical Office?, Divislop of Veterw,ary Medical Research, Bureau of Veterinary

Medicine; Food and Drug Administratioit, Beltsville, Maryland.

Stanley. N. Gershoff, Ph.D,, Director, Wutrition Institute and x `1
Chairman, Graduate Department 101Iutrition, Tufts Univer- sity, Medfoxd, Massachusetts.

Mary E. Guinan, M.D., Clinical Research InVestigator, Clini- cal Studies Section, Venereal Disease Control Division, Center for Disease Control, Atlanta, Georgia: 44., Sharon M. Hall, Ph.D., Assistant Professor in Residence, Uni- versity of California at Sari Francisco, Langley Porter Psy- chiatric Institute, San Francisco, California.

Jane Halpern, M.D., Assistant Secretary for Policy Evaluation and Research, Office of Health and Disability, United States Department of Labor, Washington, D.C. Beatrix A. Hamburg, M.D., Senior Research Psychiatrist, Laboratory of Developmental Psychology, National Institute of Mental Health, National Insti,tutes of Health, Bethesda, Maryland.

Virginia G. Harris, M.D., Director, Maternal and Child Health, Onondaga County Health Department, Syracuse, New York. John H. Holbrook, M.D., Associate Professor of Internal

Medicine, University of Utah Medial School, Salt Lake City, Utah.

L. Stanley,James, M.D., Professor of Pediatrics, and of Obstet- rics and Gynecology, and Director, Division of Perinatal Medicine, College of Physicians and Surgeons, Columbia Uni- versity, New York, New York.

Hersel Jick, M.D., Boston Collaborative' Drug Surveillance Program, Boston University Medical Center, Waltham, Mas- sachusetts.

Reese T. Jones, M.D., Professor of Psychiatry, Department of Psychiatry, University of California at San Francisco, Langley Porter Psychiatric Institute, San Francisco, California.

Philip Kimbel, M.Th., Chairman, Department of Medicine, Graduate Hospital, Philadelphia, Pennsylvania. Jan W. Kuzma, Ph.D., Chairman and Professor of Biostatistics, Department of Biostatistics and Epidemiology, Loma Linda University, Loma Linda, California.

Abraham Lilienfeld; M.D., M.P.H., D.Sc., University Distin- guished Service Professor, Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland. Harold A. Menkes, M.D., Associate Professor of Medicine and

,environmental Health Sciences, Department of Medicine, Johns Hopkins University, Baltimore, Maryland. Kenneth Moser, M.D., professor of Medicine and Director,

Pulmonary Division.,--brniversity of Califorplat San Diego, San Diego, California.

Mariquita Mullan, B.S.N., M.P.H., Special Assistant to the Dixvii

it 1
rector, National Institute of Occupational Safety and Health,

Center for Disease Control, Rockville, Maryland. y. Janyce E. Notopoujos, Program Analyst, Office of`Pldzr ing

and Evaluation, ational Institute_of Child Health and

Human Development, Nationalinstrtes of Health,

Bethesda, Maryland. Abbert Oberman, M.D., Director, Division of Preventive

Medicine, University offttlabarna in Birmingham Medical

Center, BirminghaT,'Atabama. Ralph S. Pafferibargef," M.D., D.R.P.H., Professor of

Epidemiolo'gy; Stanford University, School of,Medicine, Stan-

_ford, California, and Adjunct Profe'Ssor of Epidemiology at the

University of CalifkO, School of Public Health, Berkeley,

California.

Richard Peto, M.D.,* Radcliff Clinic, Oxford University, Oxford, England. '.

Malcolm C. Pike, Ph.D., Professor, Community and Family

Medicine, School of Medicine, University of Southern Califor:

ma at Los Angele§, Los Angeles,

Ovide F. Pomerleau, Ph.D. 1Professor of Psychology and Psychiatry, University of do,nnecticut, School of Medicine, Farmington, Connecticut.

Philp H. Price, M.D.; Medical.. Officer, Metabolic Products

Branch, Division of Metabolism and Endocrine Drugs,

Bureau of Drugs, Food and Drug Administration, Rockville,

Maryland.

Dorothy P. Rice, Director; National Center for Health Statistics,Office of the Assistant Secretary for Health, Hyattsville,

Maryland.

Anthony Robbins, M.D., Director, National Institute of Occupational Safety and Health, Center for Disease Control,

Rockville, Maryland.-

Judith B. Rooks, C.N.MO.P.H., M.S., Office of the Assistant

"Secretary for Hea Rh:Washington, D.C.

Harold P. Roth, M.D., Associate Director for Digestive Diseases and Nutrition.1, National Institute of Arthritis,,

Metabolism, andtpikestive Diseagits, National Institutes of

Health, Bethesda, Ma4land.

Philip Sapir, Special Assistant to the Director for Behavioral

and Social Sciences and Chief, Human Learning and Behavior

Branch, Center fps" Restarch for Mothers and Children, National Institute bf Health and Human Development,

National Institutes of health, Bethesda, Maryland.

Marvin A. Schniederman, Ph.D., Associate Director for Science POlicy, National Cancer Institute, National Institutes of

Health, Bethesda,PMaryland.
4

Irving J. Selikoff, M.D., Professor of Community Medicine and

Professor of Medicine, and Director of Environmental Sci;

elves Laboratory, Mount Sinai Medical Center, New York, New York.

S. I. Shibko, Ph.D., Chief, Contaminants and Natural Toxicants Branch, Division of Toxicology, Bureau of Foods, Food

dnd Drug Administration, Washington, D.C. - Jeremiah Stamler, M.D., Chairman, Department of Community Health and Preventive Medicine, Northwestern Univer, sky Medial School, Chicago, Illinois.

John E. Vanderveen,, Ph.D.., Director, Division of Nutrition, Bureau of Foods, Food. and 'Drug Administration; Washington, D.C.

Eve Weinblatt, Assistant Director for Research, Department of Research and Statistics, Health Insurance Plan of Greater

New YOrk, New "York, New York.

Samilel S. C. Yen, M.D., Profesabr and Chairinan, Department of Reproductive Medicine, University of California, San Di ego, LaJolla, California.

The editors also acknowledge the help of the following'ttaff

who among others assisted in the preparation of the report.

John L. BagioskY, Associate Director for Program Opsica-.

tions, Office on Smoking and Health, Rockville, Maryland.

Jacqueline 0. Blandfyrd, Clerk-Typist, Office on Smoking and Health, Rockville, Maryland.

Betty Bqd, Secretary, Mice on Smoking and Health,

Rockville, Maryland.

John F. Hardesty, Sr., Public Information Officer, Office on

Smoking and Health, Rockville, Maryland.

Patricia E. Healy, Technical Information Clerk, Office on

Smoking and Health, Rockville, Maryland.

Robert S. Hutchings, Associate Director for Information and

Prograr'n DeVelopment, Office on Smoking and Health, Rockville, Maryland.

Margaret 'E, Ketterman, Secrkary; Office on Smoking and Hsalth, Rockville, Maryland.

Richard A., Laso, BUreau of Health Education, Center

for Disease Control, Atlanta, Georgia.

Joanne Luoto, M.D., M.P.H., Medical Officer, Office'on Smoking and HealtTi, Rockville, Maryland.

Judith L. Mullaney, L: S , Technical Information Specialist, ffice on Smoking and Health, Rockville, Maryland.

arjorie L. Olson, Secretary, Office on Smolwilig and Health,

V.ockville; Maryland. . . a

xix
a

Kelley L. Phillips,-M.D., M.P.H., Expert Consultant, Office on

Smoking and Health, Rockville, Maryland.

David L. Pitts, Public Health Advisor, Operations Branch,

Nutrition Division, Bureau of Smallpox Eradication, Center

''' for Disease Control, Atlanta, Georgia.

Donald R. Shopland, Techrtical Information Officer, Office orr

Smoking and Health, Aockville, Maryland.

Linda R. Spiegelman, Administrative Assistant, Office on

Smoking and Health, Rockville, Mary-land.

*Carol M. Sussman: Technical Publication Writer Editor, Office on Smoking and Health, Ito4ville, Maryland.

Ronald G. Thomas, Public HealtK'Analyst, Office on Smoking

and Health, Rockville, Maryland.

'Selwyn M. Waingrow, Public Health Analyst, Office on Smok: Ing and Health, Rokville, Maryland.

Ann E. Wessel, Public Health Analyst. gfAce on Smoking and

Rockv'llle, Maryland.

Car le L. Winn, Assistant Chief, Clinical Chemistry Standard' ation. Section, Clinical Chemistry. Division, Metabolic

Bloc emistry Branch, idureau of Laboratories, Center for

Dis se Control, Atlanta, Georgia.

X X

a
TABLE OF CONTENTS

INTRODUCTION AND SUMMARY # 1 PART I

PATTERNS OF.CIGARETTE SMOKING 15

Introduction 17

The Rise of Cigarette Smoking: 1900-4950 17

The Emergence of Filtertip Cigarettes: 1951-1963 21

Increasing Pubric Health Awareness: 1964-1979 21

Exposure to Cigaretle Smoking Among

Successive Birth Cohorts 28

Cigarette Smoking Among Young Women. 33

Summary 36

References 39

PART II

BIOMEDICAL ASPECTS OF SMOKING N. MORTALITY 44

IntrodWtion and Background 45

Mortality Trends 45

Epiderrifological Studies 46

The American Cancer*Society

25-State Study

1/4 47

The Swedish Study 51

The Canadian Veterans Study 51

. Japanese Study of 29 Health Districts 51

4 The British Doctors Study 51

The Framingham Heart StUdy 52

The British-Norwegian

Migrant Study 52

Overall Mortality for FemalesCigarette Smokers

Versus Nonsmokers 53

Mortality Ratios 53

Amount Smoked and Age 54

Duration of Sm'olwig 57

Age Began Smoking 58

Inhalation , 59

"Tar" and Nicotine Content of

Cigvettes 59

XXI
Comments

Summary

References t MORBIDITY it

61,

61

62

65

Days Lost from WOrk 67

Limitation of Activity 68

Cigarette Smoking, and Occupat4on '69

Summary 70

References v 75

CARD4OVASCULAR DISEASES 77

Introduction", 79

Mortality Rates 79

Atherosclerosis 84

Risk- Factors 86

The Effect of Smoking 86

Atherosclerosis 86

Coronary Heart Disease 88

Cessation of Smoking and "Tar" t' and Nicotine Content of

Cigarettes 92

Angina Pectoris 93_,)

Cereb.rovascular Disease

Arteriosclerotic Peripheral

Vascular Disease 95

Aortic Aneurysm 9,6 6 Hviertension 9

Venous Thrombosis 97

High-Density Lipoprptein 98 . Oral Contraceptive Use, Smoking, an4

Cardiovascular Disease 98

Carbon Monoxide 101

Comment 101

Summary 102

References 103

CANCER 107

Introduction r 109

Lung . 111 . . Geograclhic Differences 116

SmokingPatterns Among Women ( 117

Cessation 4 Smoking 120

Experimental Caccinogensis 121

Larynx , 121

Oral . , 122

Esophagus

xxii n

'123 -
I

Urinary Bladder 125 Kidney 125 Pancreas 126 Summary 126 References 127-

Non-neoplastic Bronchopulmonary

Diseases 133 'Introduction 135 Definitions .4 135' Smoking and Respiratory Mortality 137 Smoking and the Epidemiology and

Pathology of Cold 141 4n-raking and, Respiratory Morbidity '146 8moking and Pulmonary Function 156 Smoking and "Early" Functional

Abnormalities 157

Smoking-and Ventilatory Function 160 Summary 163 References 163

Interaction Between Smoking and

Occupational Exposures 169 Smoking Patterns in Women 172 Patterns of ployment 175 The Reproduc ive Role 177 Specific Interactions Between Occupational Exposure and Smoking 179 Asbestos 179 Caton Dust 181 Summary 186 References 187

PREGNANCY AND INFANT HEALTH 189 Introduction ' 491 Smoking, Birth Weight, and Fetal Growth * 191 Placental Ratios ..,,,i,c, A. 194 Gestation and Fetal ofOwth 195

, Long-Terin Growth and Developme'rit

. 196 Role of Maternal Weight Gain . 202 Smoking; Fetal and Infant Mortality,

'and Morbidity , 206 Spontaneous Abortion 206 (, C9ngential Malformations 207 Nrinatal Mortality ,. 211 Cause of Death _ I 214 Complications of Pregnancy and Labor 214

'alb

)
# ;41i

?reeclampsia .

, . 217

' Preterm Delivery. Pregnancy , Complications, and Perinatal

Mortality by Gestation 217

Long-Term Morbidity and Mortality 221

^Sudden Infant Death SyA-drome 225

Mechanisms . 226

Experimental Studies 229

Tobacco Smoke . 229

Nicotine 229

Carbon Monoxide 231

Polycyclic Aromatic Hydrocarbons 233

Other Components 234

Fertility 235

Smoking and Reproduction in Women . 235

Smoking and Age of Menopause 236

Smoking and Reproduction in Men 236

Fertilization and Conceptus

Transport 237

Summary 238

References 239

PEPTIC ULCER DISEASE 251

Summary 254

References 254

INTERACTIONS OF SMOKING WITH DRUGS,

FOOD CONSTITUENTS, AND RESPONSES

TO DIAGNOSTIC TESTS 25?'''

Women Smokers and Nonsmokers and

Drug Consumption Patterns .. 259

Altered Clinical Response to Drug Therapy

by Snrfo.kers as Compared to Nonsmokers 261

Oral Contraceptives and Smoking 262 4

.Alterations in Normal Clinical Laboratory

Values in Women Smokel 263

The Influence of Smoking on the

Nutritional Needs of Women 264

Summary 265.

References .. 285

PART III ., PSYCHOSOCIAL AND BEHAVIORAL ASPECTSOF SMOKING IN WOMEN 269

IntroduCtion 271

xxiv 4. ) r -, ti ti

._..
p

Initiation of Smoking in Adolescent Girls 271

Concepts of Adolescent Behavior wig 272 Prevalence and Patterns of

Adolescent Cigarette Use t 273 Prevalenc 273 Age at hditiation of Smoking 275

Number of Cigarettes Smoked , 277 Type of Cigarette Srarkea 278 Smoking Cessation 278

Smoking Prevalence and Ethnicity .1. 280

Alcohol and Marihuana Use r 280

Demographic and Psychosocial

.:. Correlate's of Smoking in

Adolescence 281

Socioeconortf(C\ Influences 281 Family Patterns 282

Smoking Among Parents anVblings 282 Peer Group-Influence 2$4

Scholastic Achievement and Aspirations 285

Dynamic, Personality Factors L 286 Prediction of Future Smoking Behavior 288 Prevention of Smoking and

Considerations for Future

Research - 290 Prevention of the Initiation of

Smoking 290 Research Goals 291 Maintenance of Smoking Behavior 293 Patteions of Cigarette Smoking 293

Smoking Prevalence and Ethnicity 296

Pharmacological Effects of

Smoking 297 Nicotine 297 Peripheral Effects 297 Central Effects 298

A Possille- Role for Nicotine in

Smoking Maintenance 298

Dif1krences,in Nicotine Metabolism 300 Smoking and Stimulation Effects 300 Smoking Cessation 302 Demographics 303 Age 303 Education 303

Income 304 Occupation 304

Psychology of Changing Smoking Habits 305

XX V
Treatment Studies : 306

The Smoking Withdrawal Syndrome 315

Smoking and Weight Control 315

Treatment Recommendations , 319\

Conclusions 321

Dissemination of Information About Smoking 321

Health Attitudes and Behaviors , 321

Sources of Information .. 322

Health Care Providers 322

Educators 324 I

Peer Group , 324

Family 325

Media: Television, Radio, Film,

Newspapers, Magazines , 325

Advertising 325

The Failure to Disseminate

Information . 327

Strss at Work 327 '

SmOking Habits of Health Professionals 329

Physicians . 329

. Psychologists 11 , 332

Nurses 333 . , The Pregnant SmokerA Special Target 336

Sources of Information 336

Physician.Advice 337

Prevalrice of Smoking and Quitting .

'2 During Pregnancy 340

s Psychosocial Factors in Quitting 344

Recopmendations . 346

, Summary 346

Re fe r ert.r.k.s 347

A

4*

xxvi
.

'9

t

7

g

INTRODUCTION AND SUMMARY.

4,-

.t.

s

ot,
4,,INTRODUCTION AND SUMMARY

The 1980 Report on the Health Consequences of Smoking fo- cuses upon the evidence relating cigarette smoking to health effects in women. It is not presen'ted as a detailed discussion of the entire range of effects of smoking on health. Such a detailed review of all existing evidence can be found in the 1979 Report of the Surgeon Gejieral on Smoking and Health. Instead, this volume on smoking and women's health is offered, as a review

y

and reappraisal of smoking and major health relationshi s spe- cifrcally in women. It is intended to serve the medical ommu- nay as a unified source of existing sOentific evidence abort health effects of smoking cigarettes for women; As an examina- tion of current knowledge, will logically lend itself to applica- tion in both the personal and public health arenas. , Its content is the work of numerous scientists within the De- partment of Health, Education, and Welfare, 4 well as scien- tific exp'rts ot_pride that organization. Thi, volume examines the major issues ?elating tobacco use to women's health including trends in consumption, the biomed- ical evidence of the health.effeCts of cigarette usage by women, and determinants of smoking initiation, maintenance, and ces- sation.

This section summarizes the principal findings of this report. It is hoped that the entire volume will serve to highlight the established risks of

well as to define thesmoking for women and their children. as areas in need of further inyestigain. t o ,.- ..... Patterns of Cigarette Sinoking

1. Women have differed from men in their historical onset of widespread cigarette use, in the rate of diffusion of smoking among each new birth cohort, in their intensity of cigarette smoking and their use of various types of cigarettes. 2. Men took up cigarette smoking rapidly at the beginning of the twentieth century, especially during World War I. Cigar- ettes rapidly replaced other forms of tobacco. By 1925, approximately .50 percent of adult males were cigarette smokers. Smoking among men accelerated rapidly during World War II. By 1950, the prevalence of cigarette, use among men approached 76 percent in some urban areas. 3. The onset of widespread cigarette use among women lagged behind that of men by 25 to 30 years. The proportion of adult women smoking cigarettes did rbt exceed one quarter until the onset of World War II.

4. Between 1951 and 1963, irWlasing proportions of women

3

l) .
and men smokers 'converted to filtertip cigarettes. By,1964, 79

percent of adult women smokers and 54 percent of adult men

smokers used filter cigarettes. . . 5. After reaching a peak value of 4,3 in 1963; annual per

capita consumption of cigarettes declined'in 1964, 1968-70, and

in the period since 197,5. The most recent. estimate of 3,9.00

cigarettes per capita in 1-9479 is approximately equal to that observed in 1954. , , 6. From 1965 to 1978, the isrloportion of adult men cigarette

'smokers dechnedofrom 51rto 37 perceritN The preliminary estimate of Ault men's smoking prevalence for 1979 is 36.9percent.

----. From 41965 to 1976, the proportion of adult women smokers re-

) ' mained virtually unchanged at 32 to 33 percent. Since 1976, the

i proportion of women smokers ha,s declined to below 30 percent.

For 1979, the prelirninary estimate of adult women's smoking

_prevalence is 28.2 percent. The overall smoking prevalence of

32.3 percent for both sexes in 1979 represents the lowest recorded value in at least 45 years.

7. The proporthori of adult smokers attempting to quit smoking declined from 1970 to 1975, but increased in 1978-1979. In

contrast tofiast years, the proportions of women and men now

attempting to quit smoking, and their reported quitting rates

are indistingujshable. Approximately orre in three adult smokers now makes a serious attempt to quit ,smoking during the

course of a year. Approximately one in five of those who attempt

to quit subsequently succeed.

8. The proportion of adult smokers using Lowe? "tar" anc

nicotine brands has increased substantially. In 1979, 39 per n

of adult women smoker's and 28 percent of adult men °ker.:

reported primary brands with F.T.C. "tar" delivery less thai

15.0 milligrams. It is not known whether smokers of the loves.

"tar" cigarettes are more or less likely to attempt to quit smok

ing, or to succeed*quitting, than smokers of conventional fil

tertip or non-filter cigarettes. . 4 . 9. The average number of cigarettes smoked by, women am

men current smcters 'has increased. The flationship of thi

finding to recent declines in the average F.T.C. "tar" an,

nicotine deliveries of cigarettes is not well understood.

...10. With each successkve generation, the smoking character

'sties of women and men have lAcome increasingly similar.

11. Among women, the avoerage age of onset of regula smol

ing progressively declined, th each successive birth cohort -

from 35 years of age for t e born befOre 1900, to 16 early c

age among those born 1951 o 1960. The average age of Zrnset (

regular smplung among ung women is now virtually identic:

to that of young pen.

4

I ) " 1
12. Maximuin smoking prevalence rates have declined substantially in recent birth cohorts of men. Men born 1931 to 1940

reached a peak smoking proportion of 61 percent during 1960- 62, while men born 1941 to 1950 reached a peak smoking proportionof 58 percent in 1968-69. Men born 1951 to 1960 reached a

peak smoking proportion of 40 percent in 1976. Among recent cohorts of women, peak smoking prevalence rates have declined

to. much smaller extent. Women born 1931 to 1940 reached a

peak smoking proportion of 45 percent in 1966-68, while women

boi-ri 1941 to 1950 reached a peak smoking proportion of 41 perigill cent in 1970 -73. Women born 1951 to 1960 reached a peak smoking proportiOn of 38 percent in 1976. Among-t-4e_generation born 1951 to 1960, the porportions of women and men smoking

cigarettes are now virtually identical.

13. The proportions of women and men munokers in each age group have declined. Among those born beffre 1951, this decline

in smoking prevalence resulted mainly from smoking cessation. By contrast, the observed decline in smoking prevalence among

younger men born 1951 to 1960 has resulted from both smoking

cessation and a lower rate of smoking initiation. This decline in., 'the rate of onset of smoking among young men has not been

observed for yoieng women.

14. Recent survey data on adolescent smoking habits reveal that by ages 17 to 19, smoking prevalence among women ex- ceeds that of men. This finding supports the conclusion that the rate of initiation dfsmoking among young menbut not that of young women2-is declining. The future cigarette use of the

youngest generations of women is uncertain.

15. With each successive birth cohort, the accumulated years of cigarette smoking per woman has progressively approached

the accumulated years of cigarette smoking per man. Each suc- cessive birth cohort has also experienced progressively smaller sex differences in the fraction oflifetime years of smoking that

repreSents filtertip cigarette use.

16. Among men born during this century, each successive

birth cohort has thus far experienced fewer cumulative years of cigarette smoking, higher proportionate entOsure to filtertip

cigarettes, and lower smoking Prevalence rates. This relationship between .birth date and cigarette smoke exposure does not hold for women. Women born 191 to 1940 have exprienced

substantially higher smoking -prevalence rates than earlier

generationq. Unless they quit smoking in substantial numbers, these womenilirrently aged 40 to 59, willsurpass older women

in total years of cigarette smoking per capita, the total years of nonfilter cigarette smoking per capita, and in the total number of cigarettes S'moked. The health consequences of this enhanced

.5
exposure to cigarette smoke among women are likely to be more

prominent in the coming decades."

0- Myr-tality

1. The mortality ratio for women who smoke cigarettes is

about f.2 or 1.3.

2. Mortality ratios for women increase with the afnount

smoked. In the largest prospective study the mortality ratio

was 1.63 for the two-pack-a-day smoker as compar.ed to

nonsmokers.

3. Mortality ratios are generally proportional to the duration

of cigarette smoking; the longer a woman smokes, the greater

the 'excess risk of dying.

4. Mortality ratios tend to be higher for those women who

begin smoking at a young age as compared to those who begin

smoking later. 5. Mortality ratios are higher for those women who report

they inhale smoke than for those who do not inhale.

6. Mortality ratios for women tend to increase with the tar

and nicotine content of the cigarette.

7. Mortality ratios for female smokers are somewhat less

than for male smokers. This may reflect differences in exposure

to cigarette smoke, such as starting smoking later, smoking

cigarettes with lower "tar" and nicotine content, and smoking

fewer cigarettes per day than men.

8. Women demonstrate the same dose esponse relationships

with cigarette smoking as men. An incrYase in mortality occurs

with an increase in number of cigarettes smoked per day, an

earlier age of beginning cigarette smoking, a longer duration of

smoking, inhalation of cigarette smoke, and a higher tar and

nicotine content of the cigarette. Women who have smoking

characteristics similar to men may experience mortality rates

similar to men.

Morbidity

The 1979 Report of the Surgeon General summarized the information on smoking and morbidity as follows:

1. In general, female current cigarette smokers t more

acute and chronic conditions including chronic onchitis

and, or emphysema, chronic sinusitis, pep *c ulcer disease, ana

arteriosclerotic heart disease, than wome who never smoked.

2. There is a dose-response relationship etween the number

of cigarettes smoked per day and the frequency.of reporting for

most of the chronic conditions.

)

40,
v3. The age-adjusted incidence of acute conditions re.g., influenza)'for women smokers is 20 percent higher for women who hadever smoked-than for nonsmokers.

Additional data from the ealth Interview Survey (HIS) is

presented:

1. Currently employe women who smoke cigarettes report more days lost from work due to illness and injury than working women who do not smoke.

2. Limitation of activity is reported more ,commonly among women under the age of 65 who have ever smoked than among those who never smoked.

Cardiovascular Diseases- Coronary heart disease is the major cause of death among

both males and females in the U.S. population. The 1979 Surgeon Genera's Report clearly- demonstrated the close association of cigarette smoking and increased coronary heart disease among males. This report reviews the evidence associating

cigarette Smoking and cardiovascular disease in women:

1. Coronary heart disease, including acute myocardial infarction and chronic ischenlic heart, disease, occurs more frequently

in women who smoke. Ih get-feral, cigarette smoking increases

the risk by El( factor of about two, and in younger women

cigarette snT6king may increase the risk several fold.

'2. Cigarette smoking is a major independent risk factor for coronary heart disease in women; it also acts synergistically with other coronary,heart disease risk factors producing a risk greater than the sum of the individual risks.

3. The use of oral contraceptives by women cigarette smokers

increases therask of a myocardial infarction by a factor of ap- proximately ten.

4' Women who smoke low "tar" and nic^tine cigarettes expe- rience less risk for, coronary heart disease than women who

smoke high. "tar" and nicotine cigarettes, but their risk is still

considerably greater than that of nonsmokers.

5. Increased levels of high-density lipoprotein (HDL) are cor- related with sireduced risk for an acute myocardial infarction; women gigargte smokers have decreased levels of HDL.

6. Cigarette smoking is a major, independent risk factor for

the development of arteriosclerotic peripheral vascular disease

in women Smoking cessation improves the prognosis of the disi order has a favorable impact on vascular patency following reco structive surgecy.

7. omen cigarette smokers experience an increased risk for subar id hemorrhage; the use of both' cigarettes and oral

7

.4 1
contraceptives appears to synergistically increase the risk for

subarachnoid hemorrhage.

8. Women who smoke cigarettes may be more likely to de- velop severe or malignant hypertension than nonsmoking

women.

Cancer

1. Cigarette smoking is causally associated with cancer of the

lungriarynx, oral 'cavity, andlsophagus in women as well as in

rnerr, it is also associated with kidney cancer in women.

2. Cigarette smoking accounts for 18 percent of all cancers

newly diagnosed and 25 percent of all cancer deaths in women.

In 1980, 26,500 of the estimated 101,000 deaths, or over

quarter of the deaths expected from lung cancer, will occur in

women.

3. Women cigarette smokers have been reported to have between 2.5 and 5 times greater likelihood of developing lung

cancer than nonsmoking women.

4. Among women the risk oftleveloping lung cancer increases

with increasing number of cigarettes smoked per day, duration

of the smoking habit, depth of inhalation, and tar and nicotine

content of the cigarette smoked. The risk is inversely related to

the age at which smoking began.

5. A dose-response relationship has been demonstrated between cigarette. smoking and cancer of the lung, larynx, oral

cavity, and urinary bladder in women. 6. The rise in lung cancer death rates is currently much

steeper in women th.an in men. It is projected that the age Adjusted lung cancer death rate will surpass that of breast cancer

in the early'1940s.

7. The rapid increase in lung cancer rates in women is similar

to but steeper than the rise seen in men approximately 25 years

earlier. This probably reflects the fact that women first began

to smoke in large numbers 25-30 years after the increase in

cigarette smoking among men. Thus, neither men nor women

are protected from developing lung cancer caused by cigarette

smoking.

8. Cigarette smoking has been causally related to all four of

the major histologic types of lung cancer in both women and

Men, including epidermoid, small cell, large cell and adenocarcinoma.

9. The use of filter cigarettes and cigarettes with lower levels

of "tar" and nicotine by women is correlated with a lower risk of

cancer of the lung and larynx compared to the use of high-"tal

and-nicotine or unfiltered cigarettes. The risk posed by smoking

8

) _j_
low-".tar" cigarettes, however, .1s clearly greater than that

among females who never smoked.

10. After cessation, of cigarette smoking, a, woman's risk of

developing lung and laryngeal cancer has been, shown to drop

slowly, equ g that of nonsmokers after110- 15 years.

11. ExcestItne ingestion of alcohol acts synergistically with

cigarette smoking to increase the incidence of oral. and

laryngeal cancer in women.

/Non-Neoplastic Bronchopuhnonary.Diseases

1. Recent statistics indicate a rising death rate due to chronic

ObstructiN;e lung diseate (COLD) among women. The data available demonstrate an excess risk of deathfrom COLD among

smoking women over that of nonsmoking women. This excess

/ risk is much greater for heavy smokers than for light smokers.

2. Women's total risk of COLD appears to be somewhat lower

than men's, a difference which may be due to differences in

-prior smoking habits. , 3,' The prevalence of chronic bronchitis varies directly with

cigarette smoking, increasing with the number of cigarettes

smoked per day.

4. There is conflicting evidence regarding differences in the

prevalence of chronic bronchitis in women and men. Several

recent studies suggest that there is no significant difference in

the prevalence of chronic bronchitis between male and female

smokers. This may be the result, however, of increasingly similar smoking behavior of women and men.

5. The presence of emphysema at autopsy exhibits a doseresponse relationsdhip with cigarette smoking during life. _ 6. There is a close Tlationship tetween cigarette smoking

and chronic cough or chronic spufum production in women,

which increases-with total pack-years smoked. . 7. Women current smokers have poorer pulmonary function

by spirometric testing than do female ex-smokers ur nonsmoker' ers, a relationship which is dose-related to the number of

cigarettes Smoked.

Interaction Bets een Smoking and Occupational Exposures

I. The '1979 Surgeon General's Report identified the ways in

-which smoking cigarettes may interact with toe occupational

environment. They include:

a) Facilitation of absorption of physical contamination of

cigarettes,

b) TransfoKmation of workplace chemicals into more toxic

substances, %- C., 9
c) Addition of the exposure to a toxif cons ituent of to

bacco smoke to a concurrent exposure to e same constituent present in the workplace,

d) Addition of a health effect due to environmental expo- sure to a similar health effect due to smoking,

e) Synergy of exposures, and

f) Causation of accident.

2. Women are entering occupational environments with

greater frequency, and thus may be experiencing greater expo- sures to physical and chemical agents.

3. Cohorts of women with a greater prevalence of smoking are currently reaching the ages 'of maximal diseaxe occurrence, re- placing earlier cohorts with lower-cigarette exposures. 4. Physiologic differences in hormonal status between males

and females constitute a potential source of differing responses. 5. In the workplace women who .are pregnant present a nine-month exposure opportunity, including potential

teratogenic and perinatal mortality effects.

6 Concurrent exposure of women to smoking and asbestos,

resulted in a clear excess of cancer of the lung.

7. Women smokers exposed to cotton dust run a higher risk of developing borssinosis, bronchitic syndromes, and abnormal pulmonary function tests than nonsmoking women.

Pregnancy and Infant Health

1. Babies born to women who smoke during pregnancy are, on

the average, 200 grafins lighter than babies born to comparable nonsmoking women.

2. The relationship between maternal smoking and reduced birth weight is independent of all other factors that influence birth weight including race, parity, maternal size, socioeconwic status, and sex of child, it is alsS independent of gestational age.

3. There is a dose-response relationship between maternal

smoking and reduced birth weight; the more the woman smokes

during pregnancy, the greater the reduction in birth weight. 4. If a woman gives up smoking,early d,uring pregnancy, her

risk of delivering a low-birth-weight baby approaches that of a nonsmoker.

5. The ratio of placental weight to birth weight increases with

increasing levels of maternal smoking, reflecting a considerable decrease in mean birth weight and a slight increase in mean

placental mass; this may represent an adaptation to relative

fetal hypoxia.

10

A
.\\\

, - 6. The pattern of fetal growth retardation that occurs wi

maternal smoking is a decrease in all dimensions including body

length, chest circumference, and head circumference.

7. Maternal smoking during pregnancy may adversely, affecr:

the child's long-term growth, intellectual dekreloprnent, and be- ) havioral characteristics.

8. Maternal smoking during pregnancy exerts a direct

growth-retarding effect on the fetus, this effect dues not appear

to be mediated by reduced maternal appetite, eating or weight

gain.

9. The risk of spontaneous abortion, fetal death, and neonatal

death increases directly with increasing levels of maternal

smoking during pregnancy, interaction of maternal smoking with other factors which increase perinatal mixtality may re- sult in an even greater risk.

10. Excess deaths of smokers' infants are found mainly in the

coded causes categories of "unknown" and "anoxia" for fetal

deaths, and the categories of "prematurity- alone'" and "respiratory difficulty" for neonatal deaths; this suggests that the excess deaths are due to problems of the pregnancy, rather than

to abnormalities of the fetus or neonate.

11. Increasing levels of maternal smoking result in a highly

significant increase in the risk.of abruptio placentae, placenta

previa, bleeding early or late in pregnancy, premature'and prolonged rupture of membranes, and preterm deliveryall of

which carry high risks of perinatal loss.

12. Although there is little effect of maternal smoking on

mean gestation, the proportion of fetal deaths and live births

e that occur before term increases directly with maternal smoking level. Up to 14 percent of all preterm decries in the United

States may be attributable to maternal smoking.

13. The incidence of preeclampsia is decreased among women

who smoke during pregnancy; however, if preeclampsia develops in a smoking woman, the risk 'of perinatal mortality is

markedly increased compared to preeclamptic nonsmokers.

14. An infant's risk of developing the "sudden infant death

syndrome" is increased by maternal smoking during pregnancy. 15. There are insufficient data to support a judgement on whether maternal and 'or paternal cigarette smoking increases

the risk of congenital malformatiori,s.

16. Infants and children born to smoking moth s may expe- rience more long-term morbidity than those rn to nonsmoking wathers, however, studies usually cannot distinguish between the effects of smoking during pregnancy and the ef- fects of the infant's or child's passive exposure to cigarette

'smoke afterbirth.

11

e)
17. Studies in women and men. suggest that cigarette smoking may impair fertility.

18. Experimental studies on tobacco smoke, nicotine, carbon

monoxide, polynuclear aromatic hydrocarbons, and other can

stituents of smoke help define pathways by which maternal

smoking during, pregnancy may exert its aforementioned effects.

Peptic Ulcer Disease

The 1979 Surgeon General's port included evidence that

cigarette smoking in males was significantly associated with

the incidence of peptic ulcer disease and increased the risk of

dying from peptic ulcer disease by approximately two-fold. The

effect of smoking on pancreatic secretion and pyloric reflux

demonstrated among men may provide a mechanism by which

peptic ulcers develop.

1. Female smokers show a pre'falence.of peptic ulcer higher

than that of ,nonsmokers by approximately two-fold

2. The effect of cessation on healing is not known

Interactions of Smoking with Drugs, Food Constituents and

Response's to Diagnostic Tests

Most published studies investigating the effects of cigarette

smoking on drug use have been performed on mixed populations, factors specific fur women have not been demonstrated to

date. It has, however, been clearly demonstrated that v.'or'nen

are prescribed and consume more prescription drugs than men.

1. Studies of selected drugs indicate that smoking may affect

clinical responses and alter the dose reIred for an effective

therapeutic result.

2. Smoking interacts with Ural contracep ve_use to inc.rease

the risk of myocardial infarction and sub rachnoid hemorrhage.

3. Common clinical laboratory parameters aloe altered in

smokers compared to nonsmokers, the health significance of

these changes--is unknown.

4. Insufficient information exists for assessment of the im- - pact of smoking on the nutritional needs of women.

Psychosocial and Beha'.ioral Aspects of Smoking in Women

1. The percentage of 17-18 year old omen who smoke has

shown a steady rise between 1968 and 1979. It now appears, however, that the increase in smoking prevalence among all 12-18 year old. females has leveled off and begun to decline.

Younewomen born after 1962 show a substantially reduced

12

t"
initiation of smoking and will probably have a much lower pre- %valence of smoking as adults.

2. Those young women who do begin to smoke are starting to smoke regularly at a younger age, with more than half of the male and female adolescents who begin to smoke starting before the 10th grade.

, 3. The earlier tobacco is Used and the greater the number,of cigarettes smoked per day, the less likely an attempt to quit will be successful.

4. The percentage of women smokers who smoke more than one pack per day is increasing.

5. Adolescent and adult women are more likely to use low-tar and - nicotine cigarettes, smoke fewer cigarettes per day and in- hale less deeply than do men, but the difference between the

sexes in these patterns of smoking is decreasing. Adolescent and adult black women are friore likely to be smokers than their white peers, but they snipke fewer cigarettes per day. 6: Adolescents from low ihcome families, single parent families, and families with lower parental educational levels are more likely to become smokers.

7. Female and male adolescents are -more likely to begin smoking if a parent or older sibling also smokes. 8. Adolescent smokers associate with peers who smoke and

nonsmokers associate with nonsmoking peers. 9. Adolescent girls overestimate the percentage of their peers who smoke and they have a very positive -image of the people in

cigarette advertisements, but they are less likely than adoles- cent boys to see smoking as a social asset.

10. Adolescent girls who smoke tend to be more outgoing but feel less able to influence their future. r Ik 11. Adolescents experience stiress due to feelings ofoanattractiveness,- incompetency in school achievement and personal re- lations, limited opportunity for personal gr,owth and concern over future social and economic roles. This stress may be the

common mechanism pfoducing the increased rates of smoking in some groups.

12. The factors associated with successful quitting by adoles- cents of either sex are lower number of cigarettes smoked per day, higher educational aspirations and achievement, greater acceptance of the health risk of smoking, and hakting more nonsmokers among their friends. 13. It is possible that women and men modify their smoking in order to maintain a constant nicotine level.

14. Women are more likely than .men to srhoke in -ol-der to reduce stress.

15. Women at higher education and income levels are more,

13
likely to succeed in quitting. Additional factors associated with

successful quitting are a strong commitment tO change, the use

of behavioral techniques and reliable social support for quitting. Women have been reported to show lower rates than men

of successful cessation following organized cessation programs,

a difference which is less apparent in those programs that include social support.

1.

k

14
PART I:

:,

Z

----1,t;

PATTERNS OF CIGARETTE SMOKING.

(k... r)-,...,
PATTERNS OF CIGARETTE SMOKING 4

Introduction

This chapter traces the evolution of cigarette smoking among

successive generations of American women and men during the

twentieth century. The available evidence demonstrates that

women have differed from men in their historical onset of widespread cigarette-use, in the rate of diffusion of smoking among

each new birth cohort, in their int?ensity of cigarette smoking, and in their use, of various types of cigarettes.

Four main conclusions emerge from this analysis. First, although men rapidly took up smoking during the early decades of

this century, the proportion of adult female cigarette smokers did not exceed one-quarter until the onset of World War II. The

peak intensity of smok)ng oc rred among women born after 1920. Second, as a restit of igher past rates of quitting and

lower past rates of initiatio among men, as well as changes in

the type of cigarette consumed, the smoking characteristics of

women and men are how becoming increasingly similar. Third, the prevalence of cigarette Snicking : among adult American women and men is declining. This conclusion applies to all age groups, but with less certainty to the youngest generation of women. Fourth, increasing public awareness of the health consequences of smoking has resulted in significant changes in the

nature of the cigarette product. Yet little is known about the

effects of these product changes on the initiation, maintenance

and cessation of smoking, particularly among women. Since the last review of cigarette smoking in the 1979 Report of the Surgeon General (24), two new national surveys have been performed under the sponsorship of the National Center

for Health Statistics and the National Institute of Education.

This chapter relies in part on the recent, preliminary results of these surve4.

The Rise of Cigarette Smoking: 1900U150

Although the use of cigarettes in the United Statres was ob- served as early as 1854 (42,48), consumption did not increase dramatically until after 1900. As shown in Figure 1, per capita consumption of all types of cigarettes increased by more than

tenfold from 1900 to 1920. Despite a transient decline during the Great Depression, consumption increased from 665 cigarettes per capita in 1920 to 3,522 cigarettes per capita in 1950 (50). A continuous, nationally representative' series of smoking

irrtevalence rates during the period 1900 to 1950 is not publicly. liable. Nevertheless, numerous sources can be pieced toID 17

O./
gether to characterize the differential growth of cigarette

smoking among women and men.

Figure 2 depicts estimates of the percentage of rti a 1 e and

female current cigarette smokers in the greater .Milwaukee

area, as compiled by the Milwaukee Journal (38). In 1923, the

first reported year of this survey, 51.8 percent of males aged 18

years and over smoked cigafettes. sixty percent of male

cigarette smokers also smoked pipes or cigars. In total, 87 percent of adult males used some type of tobacco (38).

Although earlier survey estimates of male smoking rates are

unavailable, it appears that the rise of cigarette consumption

prior to 1923 reflected both the conversion of established male

non-cigarette tobacco users to cigarette smoking and the recruitment of a new generation of younger male smokers during

World War I. Innovations in cigarette production and marketing have been cited as influential factors in this rapid growth

(39,48,67). Camel cigarettes, a blend of lighter Burley smoking

tobaccos with previousry dominant Turkish cigarette tobaccos,

were introduced in 1913 and within months attained a national

market. Two similar brands, Lucky Strike and Chesterfield, followed in 1916 and 1919, respectively (39,48,67). During World

War I, the War Industries Board estimated that soldiers of the

Allied Armies consumed 60 to 70 percent more tobacco than

they had used in civilian life (28,29).

Cigarettes continued to dominate other forms of tobacco

among male smokers throughout the 1920s and 1930s. By 1935,

62.5 percent of adult males in the greater Milwaukee area

smoked cigarettes (Figure 2), while the percentages of pipe and

cigar users had declined substantially. Average cigarette consumption frequency among men smokers increased from 3.7

packs per week in 1923 to 4.8 packs per week in 1935 (38).

4tonsumption among men accelerated during World War II

(Figures 1 and 2). In 1944, more than 25 percent of cigarettes

produced in the U.S. were distributed to overseas forces (29),

typically for free or at low cost (39), to the point wheie subsequent shortages developed in the domestic market. By 1948,

67.1 percent of adult males in the Milwaukee area smoked

cigarettes (Figure 2). This estimate of the prevalence of

cigarette use among urban men is confirmed by hirer local consumer surveys performed in that year. For example, in 1948,

adult male smoking rates were 69.1 percent in Omaha, 67.4 percent in Birmingham,'69.4 percent in PhOadelphia, 63.9 percent

in Seattle, and 63.4 percent in San 4!):4-037).

The growth of cigarette smoking among women occurred

much later in the face of strong social taboos. Gottsegen noted

that "the ultra smart set and women social leaders began to

18

1
smoke at the turn of the century" (13). By 1906, erican "girl steniffraPhers" were reported smoking cigarettes clandestinely (5); EV 1919, some -younger women in New York vere reported smoking at dinner phirties "Z:vfth a trace of defice" (48). By 1922, New York women were smoking openly on the streets and

, in bus tops e.48), , . T advertigement showikg a woman smoking was Loril1

lar 19,19 publicity for Helmar cigarettes (43,48). In 1926, a young women in a Liggett and Myers' Chesterfield advertise-' ,ment, did not smoke eb pleaded, "Blow some my way" (6). I)-1 April, 1927, a Philip Mor 's advertisement for Marlboro cigar- ettes noted that "women, when they smoke at all, ,quickly de- -

.lop discrirhinating taste,,) ari'dthat Marlboro cigarettes were as "mild as May" (2). In 1928, a 'Lucky Strike advAisement urged women to "reach fox a Lucky instead 6f a sweet" (31,39,48); In 1934, Eleanor Roosevelt smoked cigarettes pub- licly t26). By 1940, handbags and cosmetic c"empacts were typi- cally 'designed to liold cigarettes (13). - Although the itiWaukee Joiirnal (38) reported that 16.7 pet:- cent of adult women smoked cigarettes in 1934 (Figure 2), Rlior estimates oipromen's smoking prevalence are sporadic. Wessel estimated that women consumed percent Of all cigarette's in 1924 (66). Moody's. Investors Ser,vice estimated that women -smoked 12 percenteof all cigarettes smoked in 1929 (44). The average ddily consumption of women smokers, as compared to 'men smokers, is not documented forhat period. If men smokers I consumed appro;cimately tlfce as many cigarettes per day,a's women smokers (cf. the Milwaukee Journal's 1934 survey report that women's consumption frequency was 135 packs per year as compared to 244 packs per year for male smokers), and if the estimates of male smoking prevalenea..rates in Figure 2 are taken as nationally representative; and if there were approxi- mately 5 percent more adult al than adult females during the 1920 to 1930 decade (51)., essers, estimate yields a 6 i, percent adult female smoking prevalerte in 1924 and Moody's estimate yields a 16' percent 'prevalence in 1929.. The Milwau'kee'Journal series in Figure 2 must be interpreted in light of changes in the type of survey' refpondent and the

. . of. questions designed to elicit smoking practices (see

cap to Figilre 2). Moreo,ier, this urban population series may, nof representative of all American women. Neverthet less, the vailable survey data sources are consistent . with the c n that smoking rates among women did not exceed one-quarter until the onset' of World War II.

Based on 10,00O applications for irnsuAnce policies during 19. to 1940, Ley (32) estimatedage-standardized smoking rates

-.4

19

t
40g

of 63.9 percent of men and 20.8 percent of women aged 15 years

and over. In 1935, Fortune Magazine, in the first nation4i

survey (12), reported that 52.5 percent of adult men and 1:.1

percent of adult women smoked cigarettes. (See Table 1,). Amo g

those under 40 years of age, 65.5 percent of men and 26.2 pert nt

of women were smokers. Among those over 40 years, '.7 percent of men and 9.3 percent of women were smokers. Urbanrural differences in smoking were significant. The proportion of

smokers ranged from 61.4 percent of men and 31.2 percent of

women in cities with population over one million, to -4-4.1 percent.

of men and 8.6 percent of women in rural areas with population

under 2,500. A survey of 250 urban women by the Market Re-

-4 search Corporation in 1937 reported 26 percent regular smokers

and an additional 23 percent occasional smokers (47).

After 1940, women's smoking rates accelerated, as hew g eth;

erations of women, particularly younger women in urban areas,

.entered the labor force (see also title "Occupation and Environment" in this Report). In 1944, the Gallup Poll reported 48

percent adult mule smokers and 36 percerlt adult female smokers (4). In 1949, the Gallup findings were 54 percent male and 33

percent female (4). Local consumer surveys of urban areas in

1948 retealed 37.6 percent adult women cigarette smokers in

Milwaukee (see also Figure 2), 34.3 percent in Omaha, 35.6 percent in Birmingham, 46.7 percent in Philadelphia, 38.3 percent

in Seattle, and 34.0 percent in San Jose (37). Conover, citing

"trade journal" surveys in the three or four years prior to 1950,

reported smoking prevalence rates of 65 to 70 percent among

men and 40 to 45 percent among women (9).

Although the differential growth of cigarette use among various socioeconomic groups is not well documented, the available

data during this pet-Lod suggest that male smoking rates declined with increasing income, while the relation of women's

sfnoking to income was less clear. The Milwaukee Journal in

.1945 noted 58 percent of menwith monthly rents over $50 were

smokers, and 75 percent of men with rents under $30 per month

-were smokers (38). Among women, the corresponding propor-

% nom were 32 and 37 percent respectively. In Mills and Porter's

1947 survey of .Columbus, -Ohio (36), 28.3 percent of white

females and 64.9 percent white males smoked cigarettes,

whereas 36.4 percent black femaales and 68 percent Pack males

smoked cigarettes (estimates calculated from the age distribution data preeoffteTrin Table 6 of (36)). Kirchoff and Rigdon, in a

survey of over 21,000 patients, visitors, and employees of hospitals in Houston and Galveston, noted that 63.2 percent white

males, and 33.4 percent white females, 66.3 percent black males,

and 32.2 black females smoked cigarettes (30).

20

1ti
All of the above finding's reinforce the conclusion that the onset of widespread cigarette use among women lagged behind

that of men by 25 to 30 years' This historicAdelv in the growth of cigarette smoking among women has also been documented

for the United Kingdom (8,46,49).

The Emergence of Filtertip Cigarettes: 1951-1963

As shown in Figure 1, total per capita consumption of cigar- ettes declined during 1953 to 1954. This decline was coincident with the appearance in the popular press of reports seriously

suggesting a link between cigarette smoking and lung cancer (10,33,34,40). Thereafter, the consumption of filtertip cigarettes

increased rapidly (Figure 1). In 1953 filtertip cigarettes consti- tuted 2.9 percent of cigarette production. By 1958, their share of production had increased to 45.3 percent, and by 1963 it was 58.0 percent (50).

The transient decline during 1953 to 1954 in the number of cigarettes consumed was not clearly matched by a decrease in the proportion of cigarette smokers (27). At least in urban areas, the proportion of women smokers continued to increase. From 1953 to 1958, the prevalence of adult female smoking increased from 42.9 to 45A percent in Milwaukee (Figure 2), from 38.4 to 42.6 percent in Omaha, from 47.0 to 50.2 in ashington, D.C., and from 39.6 to 44.4 percent in"'San Jose (37 , At the same time, both women'and men r pidly converted to

filtertip cigarettes. By 1958, filter cigare to use prevailed anfont 61 percent of women smokers and 4 percent of men smoker4 in Milwaukee, 54 percent of women smokers and 43

percent of men smokers in Omaha, 53 percent of women smokeis and 47 percent of men smokers in Washington, D.C., and 59 per- cent of women smokers and 42 percent of men smokers in San Jose (37). Ina nation-wide 1964 survey reported by the National Clearinghouse for Smoking and Health (64), 79 perceht of adult female smokers and 54 percent of adult male smokers used filter

.Cigarettes.

Increasing Public Health Awarene§s: 1964-1979

Per capita consumption reached a peak of 4,336 in 1963 (Fig- ure 1). It declined transiently after the appearance in January 1964 of the first Report of the Advisory Committee- to the Sur- geon General (52). Per capita consumption continued to decline during the subsequent period of increased publicity concerning the health hazards of smoking (24,27). Since 1975, per capita consumption has declined at an average rate of 1.4 percent an21

A

-
year

FIGURE 1.Annual consumption of cigarettes and filtertip

cigarettes per.person oilltd 18 years and over,

1900-11979* . ire. ,te

*Total per capita consumption data for 1917-191-and 1940-79 include o verses;

forces. Total per capita consumption for I351X is,preliminary estimate. Per

capita.consumption. of_fittertipt cigarettekd 44e''d fr'om annual data un the

filtertipshare of tcrty1,1;ciArette pnductiory 3y ,4

SOURCE: U.S. Departrient of Agncultute 4 ).

nually.' The most recant 1919 estimate of 3,900 cigarettes per

capita closely app`rolzimates that pi:Nerved in 1952.

Tabfet1 Summarizes the resultsOt salested, natidnally representative surveys 9"?'adult cigarette use during the period 1935

to 1979. except forikhe.FortuvefrurveAf 1935 (12) and the sup- .

plementl-o the Curierit Pprpt,fatrk Survey in 1955106), these

data weratolleeted under the sponsorship of the 15ational Center for Hplth St cs. The results of other recent national

surveys of adult ci to use (34,57,58,61,62,64), revealing very

similar trends in ;t e r4yeNkj.ence of smoking, were described in

the 1979Ourgeon GvWS"f3 Repoit (24).

Among adult males, thelaevalence of regular cigarette use

has declined contilttitiusifrsive 1965, with more marked decreases in the inter7.41,6, 1965 to 1970 and 1976 to 1978. (The absolute standard errors-for the National Center for Health Statis22

410
tics estimates fdr 1970 to 1976 are less than 0.3 percent. The

absolute standard errors for 1978 and 1979 are 0.6 percent.)

Among adult women, the direction,of change in smoking prevalence is less clear. The estimates for the interval 1976 to 1979,

however, suggest a recent downturn. The preliminary 1979 estimate of 32.3 percent for the overall prevalence of adult

cigarette smoking among both sexes represents the lowest recorded value in at least 45 years. (the overall prevalence of

cigaretteAemoking in the 1935 Fortune Magazine survey was

37.3 percent among adults of both sexes.)

TABLE 1.-Estimates of the prevalence of regular cigarette

smokiong adults, United States, selected

national s-erveys, 1935-1979

Year Females Males

1935 18.1 52 5

1955 24.5 52.6

1965 33.3 51.1

1970 31 1 43.5

1974 31.9 42.7

1976 32 0 4L9

1978 29.9 37.0

1979 28.2 36.9

Data for 1978 are revisips of preliminary estimates reported in Hams t26i.

Data for 1979 are preliminary estimates based on a sample of over 13,000

interviews conducted dunng January-June 1979, provided by Health

Interview Survey. National Center for Health Statistics. 1955 data repre)ent

persons 18 years and over 1976 data represent persons 20 years and over.

Estimates for the years 1965, 1970. 1974, 1978 and 1979 represent persons 17

years and over.

SOURCE Fortune Magazine (12), Haenszel, W.(16), U.S. Department of

Health. Education, and Welfare (54-56, 58 -59).

These patterns of change in smoking prevalence applied to . both white and bllick adults. For white men, the prevalence of

regular smoking declined-from-51.5 percent in 1965 to 36.3 per- cent.in 1979. For black men, the prevalence of regular smoking

declined from 60.8 percent in 1965 to 42.0 percent in 1979. For

white women, smoking prevalerke declined from 34.2 percent in

1965' o 28.2 percent in 1979. For black women smoking prevalence declined from 34.4 percent in 1965 to 28.9 percent in 1979.

Racial differences in cigarette use are discussed in greateoedetail in the chapter in this report entitled "Psychosocial and Behavioral Aspects of Smoking in Women." t

Although the Milwaukee area data for 1964 to 1979 do not

closely match these national estimates, figure 2 does show a

marked decline in smoking rates for both sexes during 1964 to

23
I

10

I

0'

r:co In wo 1940 S50 *60 1970 , *SO

, YEAR

FIGURE 2. Percentitge of adult current cigarette smokers in the

greater Milwaukee area, 1924-1979*

*Prior to 1941, the worchng of the question eliciting cigarette use and the type

of respondent are not recorded. From 1941 to 1954, men were asked, "Do you

smoke cigarets" From 1955 to 1959, all respondents were asked, "Do any

men (women) in your household smoke cigarets with svithout) a filter tip?"'

From 1960 to 1965 and in 1967, both men and women were asked Have you

bought, for your own use, cigarets with (without) a filter tip in the past 30

days" In 1966 and from 1968 to 1979, both men and women were asked,

"Have you bought, for your own use, cigarets with (without) a filtertip in the

past 7 days" All percentages reflect adults aged 18 years and over. Data for

womefrfrom 1976 to 1979 (open circles) represent filtertip cigarette smokers only.

SOURCE: Milwaukee Journal (38).

1970, a deceleration in the decline of smoking prevalence during

1971 to 1975, and a resumption of the decline in prevalence

among men in the last four years.

The cessation of cigarette smoking has been a significant factor in explaining this overall decline in smoking prevalence (24).

Column (i) of Table 2 presents estimates of the percentage of

recent- smokers who made a "fairly serious attempt to quit"

24

4u
TABLE 2. Esti mated rates of attempted and successful quitting

among adult, recent cigarette smokers, United-

. States, 1970:-1979

(1) (Hi (n) Percent of Percent of Percent of

All Recede Smokers All Recent

Smokers Who Attempting to Smokers`Who

Attempted to Quit in Past Reported Quit in Past Year Who Successfully Year Reported Quitting in

Successfully Past Year

Quitting

Women

1970 40 8 2L3 8 7

1975

. 4 30.2 19 5 5.9

1978 32 7 18 8 6.2

1979 32.9 216 70

Men

1970 .44.4 264 117

1975 283 201 57

1978 294..... ,21 5 6 3

1979 31 4 21 3 6.7

1970 and 1975 data from surveys of persons aged 21 years and over, conducted by National Clearinghouse for Smoking and Health 1978 and 1979 data from

the Health Intervie%i Survey of persons aged 17 years and over, conducted by

the U S National Center for Health Statistics. 1979 data are preliminary

-estimates based on interviews during January-June of that year. SOURCE U S Department of Health, Education, and Welfare 154,61,621.

within one year of the interview date. (Recent smokers include

all current smokers plus those former smokers reported to have

stopped within one y r of interview.) Column (ii) shows what proportion of those a empting to quit regarded themselves as

former smokers. Column (iii) shows the proportion of all recent smokers (whether or not they attempted or succeeded quitting) who reported themselves as '1-ecent former smokers. These data

necessarily reflect respondents' self-assessment of both the

seriousness of a quit attempt and their degree of success.

Nevertheless, they do provide an indication of the representative smoker's annual, probability of attempting to quit, the

probability of successful cessation given a uit attempt, and the overall annual smoking cessation rate. (T e absolute standard

errors in Table 4 are approximately 1.0 per ent, 1.5 percent, and

0.3-0.5 percent for columns (i), (ii), and , respectively.)

All three indicators of smoking cessation were highest for men in 1970. Although a relatively large proportion of women

smokers attempted to quit smoking in 1970 (column Om their

25
probability of success in that year was significantly lower than

that of men (column (n)). Quit attempt rates for both sexes (column (1)) declined by 1975, but have increased in 1978 to 1979.

With respect to the probability of attempting to quit and the

success rate, adult men and women cigarette smokers are now

indistinguishable.

Table 3 displays recent changes in the distribution of

cigarette brands according to F.T.C. "tar" contents. The proportion of adults smoking cigarettes with F.T.C. "far" delivery less

than 15 milligrams has increased from 9.5 percent of women and

2.9 percent of men in 19.70 to 38.5 percent of women and 28.1

percent of me in the first half of 1979. A corresponding increase

in the proportion of smokers of cigarettes with F.T.C. nicotine

delivery less than 1.0 milligram was also observed.

T kI3LE 3. Estimated percentage distributibri of adult current

regular cigarette smokers according to F.T.C. "tar"

content of primary brand, United States 1970-1979

Year

Ns ,,rnen

Less Than

o rrtg

5uto

99 mg

10 0 to

1t9 mg

15 0 to

199 mg

20 0 mg

or More

197o o7 2 6x 67I 23 4

1975 1 2 1 2 151, 75I 75

1978 5 .i. x x 21 1 592 57

1979 56 95 234 554 61

Men

1970 o 2 0 9 Is 61 3 28 1

1975 ,i6 1 1 11 0 681 19`2

1978 33 62 135 635 136

1979 26 85 170 601 118

1979 data are preliminary estimates proxided by the National Center for

Health Statistics 1970 and 1975 data represent adults aged 21 years and oxer

1978 and 1979 data represent adnIts aged 17 years and per Estimates

exclude those with unknown primary cigarette brand

SOURCE U S Department of Heajth. Education. and V,elfare (5.4,1.62)

At the same time, the average daily cigarette consumption of

adult smokers has increased. Table 4 shows recent changes in

the distribution of reported daily cigarette consumption among

current smokers. These data must be interpreted in light of

possible underreporting biases (65) and, in particular, a strong

tendency for respondents to round off their reported daily consumption to one park. Nevertheless, the percent of women

smoking less than one pack per day has declined, while the proportion smoking more than one pad( per day has increased. Except fur 1979, a similar trend is observed for men. (The absolute

26
standard errors of the 1978 and 1979 estimates are approxi- mately 1.0 percent.)

The data of Table 4 represent the more recent portion of an apparently long run tren0 toward increasing daily cigarette

consumption among regular smokers. In 1924, Milwaukee men smokers consumed an average of 10 cigarettes per day (38). In

1934, male smokers in Milwaukee consumed an average of 13.4

cigarettes per day, while women smokers consumed 7 per day (38). If cigarette consumption in 1935 was 1,564 per adult (Fig- ure 1 and (50)), and if the overall percentage of adult smokers was 37.3 percent (12), then mean consumption per adult smoker was 11.5 cigarettes per day. If consumption i. per adklt was 3,597 in 1955 and if the prevalence of regular smoking was 37.6 per- cent (16), then mean consumption per adult in that year was 26.2 cigarettes. The corresponding calculation based -on 1979 per capita consumption data and adult prevalence data (Figure 1

and Table 1)7ields 33.3 cigarettes per day. Numerous epidemiological studies and other surveys per - ' formed during the period 1950 to 1965 have shown that for both

I' TABLE 4.Estimated percentage distribution of adult current

cigarette smokers according to reported daily consumptilfrequency, United States, 1965-1979

Year

Women

1965

1970

1974

1976

Percent

Less

Cigarettes

Smoking

Than 15

per Day

Percent

25 Cigarettess

More

Smoking

or per Day

44.5

39 1

38 7

36 5

13 7

18 0

18 5

19 6

1978 360 210

1979 34 6 22.4

Men

1965 .29 6

1 24 5

1970 27R 277

1974 26 ',i 306 1976 7' 24 2 31 1

1978

1979 ,

23 4

26 4

34 2

32 2

Data for 1976 represent persons aged 20 years and over All other year

represent persons aged 17 years and over Data for 1979 are preliminary

estimates based on interviews conducted dunng January -June of that ye f/ .provided by the Health Interview Survey, National Center for Health Statistics

SOURCE Harris, J E i2,6), I, S Department of Health. Education, and Welfare (54-56,58-59)

27
sexes. especially for women, the proportion of hea% y smokers

was larger among the younger age groups i 14,16,19,20,22,

30,36,61,64). These findings .applied to current daily cigarette

consumption and lifetime maximum cigarette consumption.

They are consistent with the hypothesis that regular smokers

in past decades consumed fewer cigarettes per day than contemporary smokers.

The empirical relationships between rates of smoking cessation (Table 2). changes in F.T.C. "tar" and nicotine delivery of

cigarettes !Table 3), and increases in dailt cigarette consumptior, Table. 4)' are poorly understood 125). It is not known

whether smokers of the lowest -ter" cigarettes are more or less

likely to attempt to quit, or to succeed in quitting, than smokers

of conventional filtertip or nonfilter cigarettes. The extent to

which the act of switching to a lower "tar" cigarette may serve

as a substitute for quitting may differ among women and men.

The obser.ed increase in daily cigarette consumption among

current smokers could represent the effect gf higher cessatioti

rates among lighter smokers, an increase in the daily cigarette

consumption of continuing smokers, or an increased daily

cigarette consumption of new entrants into thse smoking population, or a combination of these effects (24). The relationship of

these possible mechanism:, to the observed increase in the proportion of filtertip cigarette and low "tar" cigarette smokers is

not well elucidated

Exposure to Cigarette Smoke Among Successive Birth Cohorts

Figures 3 and 4 depict estimates of the prevalence of current

cigarette smoking from 1900 to 1978 among successive birth

cohorts of men and women. Each continuously graphed time

series corresponds to individuals born dunng a particular decade. For example, among women horn from 1931 to 1940 (Figure

4), who are now 40 to 49 years old, the prevalence pf smoking

rose rapidly during the.post World War II penod and reached a

peak of 45 percent by 1963. Thereafter, their overall prevalence

of smoking declined to 39 percent in 1978.

These prevalence data were constructed from the reported

kifetime,smoking histories of over 13,000 respondents to the

Health Interview Survey during July to December, 1978. (For

related applications of this methodology, see 7,15,27). Although

the accuracy of survey xecullection of age started smoking, age

of smoking cessation, and the duration of significant, temporary

periods of abstinence is not known, no !Articular source of recall

bias has been identified 115,16). However, the .significantly

higher mortality rates of continuing smokers, as compared to
MEN

30

19" 20

6C

30

0

19CC '313 '920

111

94' 5C .

1951 60

1930 19.4/:, '950 t9EC 137C., tgf

YEAR

FIGURE 3.Changes in the pre%alence of cigarette 'smoking

among successive birth cohorts of men, 1900-1978

Calculated from the results of over 13,000 inteniews conducted during the last

two quarters of 137/i, provided by Division of Health Interview Statistics, U S

National Center for Health Statistics'

SOURCE U S Department of Health, Education, and Welfare 60)

nonsmokers or former smokers (1,11,17,18,41,45,46,52), introes a selection bia§ that may understate the prevalence of

past smoking for the oldest cohorts. Fortexample, on the basis of

the insurance life tables recently reported by Cowell and Hirst

(11), a male cigarette smoker at age 32 has an estimated 25

perceniltprobability of surviving to age 80, as compared to 49

29

'1 A
50- MEN

-WO

4

91' 20

20

?921-30

1931-40

-9"

1941-50

1901-10

-190C

9X..) 910 1920 930 940 1950 1960 970 980

YEAR

FIGURE 4.Changes in the prevalence of cigarette smoking

among successive birth cohorts of women,

1900-1978

Calculated from the results of vier 1.300 interviews cunducted during the last

two quarters of 19 76. provided by Division of Health Interview Statistics, U.S.

National Center for Health Statistics

SOURCE U.S Department of Health, Education, and Welfare (60)

percent for a nonsmoker. The estimated probabilities of surviving to age 60 are 80 percent for smokers and 93 percent for

nonsmokers, respectively. Therefore, the peak smoking prevalence rate of men born before 1900, calculated from 1978 survey

responses to be 46 percent in 1937, could actually have been as

high as 65 percent. Since individuals who quit smoking have a

higher survival than continuing smokers (18,45), the actualpoint in time at which smoking rates peaked in this cohort may

have been later than 1937. This effect is less likely to be important among men born after 1910, who are now approaching 70

yettrs old. A similar calculation for men born, for example, between 1911 and 1920 reveals that their peak smoking rate may

have been understated by at most 2 or 3 percentage points.

This source of bias ig likely to be less important for older

women. On the basis of age-specific mortality data reported by

30
/ Hammond in 1966 (18,4ppendix Table 2b),..wortien continuing to

smoke cigarettes from ,age 35 would have an estimated 48 per- cent chance of ,surviving to age 80 years,,..-as compared to 54 percent for nonsmokers. The estimated prObabilities of survival

to age 60 would be 91 percent for smokers and 93 percent for nonsmokers. If these survival data are currently applicable to women smokers and nonsmokers, then the estimated peak pre- valence rate of smoking among women born before 1910 could be

understated by only one to two percentage points. Despite these possible biases, the predicted percentages of current smokers in Figures 3 and 4 are consistent with past survey and epidemiological data on the smoking habits of different age groups (12,14-16,19-23,30,35,36,55).

Comparison of Figures 3 and 4 reveals the following conclU- sions. (a) The most marked differences 'rn smoking prevalence

among men and women appeared in those individuals born before 1910, who are now over 70 years of age. (b) Women born

between 1921 and 1940, who are now approaching 40 to 59 years of age, experienced the highest smoking prevalence rates. These women have not yet reached the age where the absolute excess deeps of smokers over nonsmokers are expected to be- come substantial (1). (c) Among successive cohorts of men and women, the age of peak smoking prevalence has declined.

Among younger cohorts, the peak smoking prevalence rates are declining, although the effect is{ less marked for women. Men

born between 1911 and 1920 reached a peak smoking prevalence of 71 percent during 1946 to 1948, while those born 1941 to 1950

reached a peak smoking prevalence of 58 percent in 1968 to 1969. Women born 1921 tp 1930 reached a peak prevalence of 44 per- cent in 1958 to 1960, while those born in 1941 to 1950 reached a

peak smoking prevalence of 41 percent in 1970 to 1973. ( ) Among men born 1951 to 1960, the rate of increase of smoking

prevalence Eeas slower than in previous cohorts. This slowing of

the diffusion of smoking practices was coincident with the increased publicity concerning the health risks of smoking and

the relatively high rate of quitting smoking among adult males

in the late 1960s. A similar effect is not clearly discernible for young women in this cohort. In both sexes, among individ4als who are now approaching ages 20 to 29, the'prevalence of smoking has apparently peaked. Smoking rates among men and women in this age group are now nearly indistinguishable.

Figure 5 depicts the mean age of sburting regular smoking

among successive birth cohorts, calculated from the same data

as for Figures 3 and .4. The age of onset of smoking among women declined continuously during this century, to the point zwhere it is nearly indistinguishable from that of men. As a re31

nn
49

sK 35

3°-

25fcn

-8 2°

ct) 15

10

ro 5

1901 -10

y.11201921_301

1 1140194150195160

Birth Cohort

FIGURE 5.Mean age of onset of regular smoking among

successive birth cohorts of women and men

SOURCE. U.S. Department of Health, Education, and Welfare (60).

suit, each successive cohort of lifelong continuing women smokers will have an increasing number of years of exposure to

cigarette smoke. a

Figure 6 depicts the accumulated years of cigarette smoking

per capita, up to 1978, for each birth cohort.These magnitudes

cot/respond to the total areas under each'cohort prevalence

curve in Figtires 3 and 4. Among women, individuals born 1911

to 1920 have thus far experienced the largest total exposure per

capita. However, as seen from Figure 4, unless the smoking prevalence rates of women born during 1921 to 1940 decline more

rapidly in the future, the lifetime exposure of these latter

cohorts is likely to exceed that of the 1911 to 1920 cohort. It is

not clear, however, whether the lifetime exposure of men born

32
-r

. 4

from 1921 to 1940, 'now 50 to 69 years of age, will exceed thaQ)f.v._

previpus gederations. With each successive cohort, the ratio

.female to inaleeXposure increasingly approaches one.

Asa result of the rapid diffusion of filtertip cigarettes after e, 1950. (Figure 1), each successive birth cohortAvass exposed to a

different 'proportion of filtertip and nonfilter cigarettes. Details

of the respondent's past history of cigarette brand use were not.

obtained in the 19781-lealth Interview Survey. in-ch data howover, are available from a series of over 2,000 interviews of curand former smokers aged 21 years and over, conducted by

the National Clearinghouse for *-Smoking and Health in 1975

(62). Figdre 7 'depicts, for the same birth cohorts, the proportion

of lifetime years of smoking that represents fiRertip cigarette

use. (The birth dates,of the youngestocohoris in Figures 6 and 7

do n2t mratc0 duel() differences in survey date. and eligible age

grouS.) Among men, thereaisa diitinct, Monotonically increas-

,ing re anon betwpen the prOportion of filtertip cigarette expo- sure and birth. date. e corresponding relationship among

women born before 1930 r fleas their lower smoking c'e.ssation

rates and, therefore7t1 ieir continued use of filter cigarettes (62).

A woman Bora) in 1925, for example, who began smoking at age

21 (Figure 5), and who switched to filtertip cigarettes in 1957

!F" re, has now been smokin4filtertip cigarettes for over

it of tier-smoking career and 40 percent.of her entire

- The prevalence of cigarette smoking, age of initiation, lifetime

rvluration di smoking, and tie extent of use of various types of

8eigarettes are noethe only ,measures of cigaTette Smoke exposui4 among a p rticular poptilation.Trends in depth of inhale-

. tio , fraction o cigarette,a?tually smoked,. and other dimensio s of the style of smoking also affect. smoke exposure. How- eve t as dis ssed in the 197Q Surgeon General's Report (24),

-thes art dif 'cult to determine from survey data. In view of the

cone n ov the accuracy of contemporaneous survey repo

of daily cigarette consumptisin (65), past accounts of the tim

course of daily' cigarette coivsumption would 6e difficult to asseas accurately. Nevertheless, the evidence Presented in the

previous section is cosEtAiritent with the conclusion ehat,the aver0,age daily cigarette consumption among !regular cigarette users

his increased among each successive birth cohart.

CigarThe

more majkeeli:decrine in peak smoking prevalence among

ette Smiling Among Young Women

men born "betwe)ep 1951 and 1960, now approaching 20 to 2.9

years of age, refl:ected a slowing in the rate of initiation of smok33
(13 30

S

25

20-

0

-7 15-

0

F2 10-

elo OD

-1900 1901-10 1911 20 1921-30 1931-40 19411) 0 1951-e0

Beth Cortort

FIGURE 6. Accumulated years of cigarette smoking per person

among successive birth cohorts of women and men,

1978

SOUSA U S.,Department.of Health, Education, and Welfareit0).

ing that was not observed in women of the same age group. This

trend appears to be continuing in the nekt birth cohort.

Table 5 repOrts the results of nation-wide ,,sfumeys of teenage

gigarette smoking during 1968 to 197 The 4nost recent survey, conducted by the National Institute of Education during late 1978 and early 1979, resents the prelitninary results of over

2,600 telephone interviews of individuals aged 12 to 18 years.Th

this survey, but not in the others reported in Table 5, women

and Men 19 years 'of age were also interviewed. Otherwise, the

survey samplini techniques and interview questions regarding

smoking practices were the same for all the surveys. (See notes

to Table 5).

The data' in Table 5 support the conclusion that the rate of

initiation of smoking among even the youngest men is declining,

34

vv
100

a)

290

0 80

A

El

8

1

41=11,

,11

6.

z

-1900 190110' 1911 20 1921 30 1931 40 1941 50 1951 -54

,Birth Cohort

FIGURE 7.Proportion of years smoking filtertip cigarettes

among successive birth cohort of womeitand men,

1975

Calculated from the results of over 2,000 smoking histonetf men and women who had ever smoked, collected by National Clearinghouse for Smoking and Health.

SOURCE- U S, Department of Health, Education, and Welfare,(62),

an effect that is not present among young women. These results must be interpreted in light of sampling variability.-(The abso- lute standard errors on the 1979 estimates for ages 15-16 and _ 17-18 are about 2 percent...) As in adult surveys, non-response biases must also be considered. Nevertheless, the findings in Table 5 are consistent with other nation-wide estimates of smokingyates among young women and men. The prevalenc f current regular smoking among respondents 17 to 19 year o

age in this survey was 28.1 percent for females and 22.8 percent for males. The comparable rates for women and men aged 17 to

19 from khe Health Interview Survey were 29.2 percent and 27.5 percent,'respectively. An analysis of the growth of smoking

prevalence among this group, performed in the same manner as J.

35

yr
TABLE 5.Estimated perceptage of current, regblar cigarette

smokers, ages 12-18, United States, 19681979

Year

Females

Ages r2-14 Ages 15-16 Ages 17-18

"196x 0 6 96 14( 1x6

1970 3 0 14 4 22.8

1972 2 8 163 253

1974 49 202 259

1979 4 4 11 8 26,2

Males

196s 2 9 17.0 30 2

1970 --' 5 7 195 373

1972 46 178 302

1974 4 18I 310

1979 32 13 5 19.3

Nation-wide surveys performed by National Cleannghuuse for Smoking an

Health, 1968-1974, and National Institute of Education, 1979 Current regulE

smokers in all survey s iclude all those who smoke cigarettes at least weekly I

1979, approximately 90 percent of current regular smokers used cigarettes on

daily basis For 1979 only, 29.7 percent males and 31 9 per_Ient feinales, aged 1

were reported as regular smokers

SOURCE U,S, Department of Health tion, and Welfare (63)

that of Figures 3 and 4, suggested that smoking rates amon,

this group of women grew rapidly and exceeded those of men b:

1975. The future sinoking habits of this generation of Nflaunl

women cannot be accurately predicted.

Smoking among adolescent women is discussed in greater de

tail in the chapter entitled "Psychosocial and Behavioral AE

pects of Smoking in Women" in this Report.

Summa

1. Wo en have differed fryn men in their historical onset (

widespr d cigarette use, in the rate of diffusion of smokin

amoRg each new birth cohort, in their intensity of cigarett

smoking and their use of various types of cigarettes.

2. Men took up cigarette smoking rapidly at the beginnin

of the twentieth century, especially during World War I. Cigar

ettes rapidly replaced other forms of tobacco. By 1925, approx

mately 50 percent of adult maleS were cigarette smokers. Smol

ing among )nen accelerated rapidly during World War II. B

1950, the prevalence of cigarette use among men approached '1

percent in some urban areas.

3. The onset of widespread cigarette use among women hal

ged behind th at of men by 25 to 30 years. The proportion of adu

as ,
A*. sr women smoking cigarettes did not exceed one-quarter until the onset of World War II.

4. Between 1951 and 1963, increasing proportions of women and men smokers converted to filtertip cigarettes. By 1964, 79 percent of adult women smokers and 54 percent of adult men smokers used Qlter cigarettes.

. 5. After 'reaching a peak value of 4,336 in 1963, annual per capita consumption of cigarettes declined in 1964, 1968-70, and in the period since 1975. The most recent estimate of :3,900 cigarettes per capita in 1979 is approximately equal to that ob- served in 1952. i 6. From 1965 to 1978, the proportion of adult men cigarette

smokers declined from 51 to 37 percent. The preliminary esti- mate of adult men's smoking prevalence for 1979 is 36.9 percent. From 1965 to 1976, the proportion of adult women smokers re- mained virtually unchanged at 32 to 33 percent. &trice 1976, the proportion of Women smokers has declined to below 30 percent. For 1979, the preliminary estimate of adult women's smoking

prevalence is 28.2 percent. The overall smoking prevalence of 32.3. percent for both sexes in 1979 represents the lowest re- corded value in at least 45 years. 7. The proportion of adu)t smok414 attempting to quit smoking declined from 1970 to 1975, but increased in 1978-1979. In contrast to past years, the proportions of women and men now attempting to 'quit smoking, and _their reported quitting rates, are indistinguishable. Approximately one in three adult smok- ers now makes a serious Attempt to quit smoking during the course of a year. Approximately one in five ofothose who attempt to quit subsequently succeed.

8. The proportion of adultNtrnokers using lower '.:tar" and nicotine brands has increased substantially. In 1979, 39 percent of adult women smokers and 28 percent of adult men smokers reported primary brands with F.T.C. "tar" delivery less than 15.0 milligrams. It is not known whether smokers of the lowest "tar",cigarettes are more or less likely to attempt to quit smok- ing, or to iucceed in quitting, than smokers of conventional fit- tertip or non-filter cigarettes: . 9. The average number of cigarettes smoked-by women and men current smokers has increased. The relationship of this finding to recent declines in the average F.T.C. '`tar" and

nicotine deliveries of cigarettes is not well understood.

10. With each successive generation, the smoking character- istics of women and men have become increasingly similar. 11. Among women, tha,average age of onset of yegular smoking progressively declined with each successive birth cohort from 35 years of age for those born before 19Q0, to 16 years of

37 ', .1. , ,_,
age among those born 1951 to 1960. The average age of onset of

regular smoking among young women is now virtually identical

to that of young men.

12. Maximum smoking prevalence rates have declined substantially in recent birth cohorts of men, Men born 1931 to 1940

reached a peak, smoking proportion of 61 percent dui-mg 1960-

6?, while men born 1941 to. 1950 reached a peak smoking proportion of 58 percent in 1968-69. Men horn 1951 to 1960 reached a

peak smoking proportion of 30 percent in 1976. Among recent

cohorts of women, peak smoking pre\ alence rates have declined

to a much smaller extent. Women Florin 1931 to 1940 reached a

peak smoking proportion of 45 percent in 1966-68. while women

born 1941 to 1950 reached a peak smoking proportion of 31 percent in 1970-73. Women burn 1951 to 1960 reached a peak smoking proportion of 38 percent in 1976. Among the generation born

1951 to 1960, the proportions of women and men smoking

cigarettes are now virtually identical.

13. The proportions of women and men smokers in etch age

group have declined, Among those born before 1951, this decline

in smoking prev alence resulted mainly from smoking cessation.

By contrast, the observed declirke in smoking prevalence among

younger men born 1t51 to 1960 has ulted from both smoking

cessation and a lower rate of smukii initiation. This decline in

the rate of onset of smo"king among yoVng men ha.5 not been

observed for young women.

14. Recent Sur. e,v, data on adolescent Amoking habits refveal

that by ages 17 to 19smoking pre\ alence among women exceeds that of men. This findiiig supports the conclusion that the

rate of initiation of smoking among young menbut not that of

young womenis declining. The future cigarette use of the

youngest generations of women is uncertain

1.5. With each successive birthecohort, the accumulated'ears

of cigarette smoking per woman has progretsively approached

the aecumuLated years of cigarette smoking per man. Each sue- ?

tessive birth cohort has also experienced progress's el,vr smaller

sex.differences in the fraction of lifetime years of smoking that

represents filtertip cigarette use.

16. Among men born during this ,ceritur, each successive

birth cohort has thus far expenencefl fewer cumulativ eyears,of

cigarette smbking, higher proportionate exposure to filtehip

cigarettes, and lower smoking prevalence rates. This relationship between birth date and cigarette smoke exposure does not

hold for women. Women born 1921 to 1940 have expellenced

substantially higher smoking prevalence rates than earlier

generations. Unless they quit smoking in substantial numbers,

these women. c urrentl,v aged 30 to 59, will surpass older women

38
in total years of cigarette smoking per capita, the total' years of

,s nonfilter cigarette smoking per capita, and in the total number of cigarettes smoked. The health consequences of this enhanced exposure to cigarette smoke among women are likely to be more proMinent in the coming decades.

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United States-1976 Vital and Health Statistics. Senes 10. Number

119, No,.ember IT7-7

C S DEPARTMENT OF HEALTH F.DC CA.TION AND WELFARE.

Pj BLI( HEALTH SERF[( E NATIONAL ( ENTER FOR HEALTH

STATISTI( S 'Unpublished dater

s DEPARTMENT OF HEALTH. EDU( ATION, AND WELFARE,

PC BLI( HEALTH SERN, I( E NATIONAL ( LEARINGHOUSE FOR

SMOKING AND HEALTH Adult Use of Tu4mreco 1970 June 1973

S DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE.

PC BLI( HEALTH SERVICE, NATIONAL CLEARINGHOUSE FOR

SMOKKtiG AND HEALTH Adult Use of Tobacco 1975 1976

S DEPARTMENT OF HEALTH EDUCATION. AND WELFARE.

PC BLI( HEALTH SERVICE. NATIONAL ('LEARINGHOUSE FOR

SMOKING AND HEALTH' Patterns and Pre,.alence of Teenage

( igarette Sm4ing- 196x 1970, and 1974 Jill) 1974

C S DEPARTMENT OF HEALTH, EDUCATION. AND WELFARE.

Pt BLI( HEALTH SERN, I( E NATIONAL CLEARINGHOUSE FOR

SMOKING AND HEALTH Use..of Tobacco, Practices, Attitudes,

Knuuledge and Beliefs. United State-, Fail 1964 and Spnng 1966 July

1969

W ARN ER, K E .ntrea.-e tn the Jnderreporting of cigarette

,.insurnptoin Jiiurna, the American Statistical A,,O'CLAtICTI 73,362)

(14 -(1x June

, V E.SSE I. A The first .kxty bilhun, are the hardest for the cigarette

,ndustr) Pnnters Ink 124Y;) 1-6 1 iT- 146, January 31. 1924

HITTEN, I T Brand Performance in the ( igarette I nduit.,-;, and the

Ad% antage of Earl,Entn., '1913-74 U S Federal Trade Cominissio... Jane 19 "4
s'a

BIOMEDICAL ASPECTS OF SMOKING.

AMA
MORTALITY

Introduction and Background

Cigarette smoking has been cited as the single most important environmental factor contributing to premature mortality in the United States (17). A great many epidemiological studies support this statement. The emphasis, in general, has been to

study rratles rather than females. Perhaps the main reason for

this discrepancy is that, in the past, relatively few women

smoked whereas smoking was,common among me,,n. The upward trend in lung cancer death rates in male,s obseried in the 1950s by Dorn and others stimulated epidemiologic studies of smoking and health, especially among males (2,3). According to he 1979 Surgeon Gener'al's Report: It is important that attention be called specifically to the mortality that females experience as a result of cigarette

smoking. There has been an increase in smoking among teen- age girls over the past 10 years. At present, the percentages of

teenage boys smoking and teenage girls smoking are nearly

identical. For some ages, the !. are more teenage girl smokers

than boy smokers. Over t: ; ,st 10 years, there has been a gradual reduction in the percentage of the adult population

that is smoking. Men have quit in greater numbers than women. There has been only a modest drop in the percentage of women who are smoking. In Canada and several European

..countries, smoking is:decreasing among men but increasing

among women.

The present report reviews some of the more important pro- spective epidemiological studies on cigarette smoking and mortality among women. _ Mortality Trends

As background, this section reviews mortality levels by sex and color in the United States, by examining recent trends in overall mortality and in three causes of death which have been

strongly linked to cigarette smokingischemic heart disease, lung 'cancer and the combined category of bronchitis, em- physema and asthma.*. These trends are displayed in Figures 1 through 4.

For all causes of death (Figure 1), the trend for females was downwards over the entire period from 1950 to 1977 with a somewhat steeper decline irNrecent years. The trend in death

rates among males was essentially flat during most of the 1950s and 1960s, but has been sharply downwards since the late 1960s.

The categoily, chronic obstructive lung disease, may include asthma, a dis- ease which' is not causally related to smoking

45
Yr

es.

1

1500

li

co0

coo

cc 1000

__, c

o

7.5 700

0. 0a

o 500 o

0

o

Sa

0

ra

cci

... Nonwhite Mates

.......... ...... 1 .,. ...............

....

`White Mates 1000

c.. .. . ... Now kite Females ' .... , 1 . 700 4.....

White Females--

.....,..

200

1950 1055 1960 1965

..A...._ 500

23,7,

1970 1975

p FI(11 RE 1. Age-adjusted death rates* for all causes of death by

color and sex; United States, 1950-1977

'Adjusted h) the direct method to the U S populationt. 1940

SOURCE National ( enter for Health Statistics (9)

For ;scheme heart disease, the death rate trend for all sa

and color groups was upwards until it flatteked in the 1960s. It

has been sharply downward smce then (Figure 2).

For lung cancer the trend was sharply upwards-durinre

entire period, espesially for females (Figure 3).

For bronchitis, emphysema and asthma, the death rate has

been sharply upwards for all sex and color groups except nonwhite females. In recent .tears there-appears be a leveling otf

for males but not for white females (Figure' 4). Other investigators' hat e studied these trends, especially in relation to

chanties in cigarettes smoking habit's in the United States and

their putenti4 effect upon mortality from the smoking-felated

diseases (8,12). There are, inherent difficulties in interpreting

trend data and in particular in relating one trend to another.

Epidemiological Studies

During the past 30 years, there hav been eight- large pro46

4

) 4.

l/ a
400

..- 300

700

o

-J ^00,

0

RS' 0a

0

100

00

co cc 5C

.

-...

'White Males

.-e--....--

.,.........,

........0"°",

Nonwhite

..... Males

....

. .,

I.**,

.......:-*''

4

4 Nonwhite Females

,.. .......... '' - ...

e White Females

.....

-

.

I,

1950 1955 1960 1965 197Q 1975

.4 6th Rev 7th Rev 0...4.--8th Rev a

FIGURE 2. Age-actjusted death rates* for ischemic heart

disease** by color and sex, United States,

1950-1977'

'Adjusted by the direct method to the U S population, 1940 ICD 6th and 7th Rev No 420 and Rth Rev Nos 4V, 413

SOURCE National Center for Health Statistics (9)

400

300

100

50

spective epidemiological, studies specifically designed to delmeate the relationship between tobacco smoking and the deN elopment of disease. In five of these studies data are available

un women as well as men. These studio are outlined below and

in Table 1 (1.2,447,10). To these publish d results are added

unpublished data from two .other stiudiesAonducted by the National Heart, Lung, and Blood Institiand'from the British

Doctors Study. ,..., THE AMERICACANCER SOCIETY 25-STATE STUDY (6)

The largest stucb, I3S' far is the Amefican Cancer Society study

I .

of men and women in 25 states. rn late 1959 and early 1960, the

American Cancer Society enrolled 1,078,894 men and women in

a prospective study. All segments of the population were

47
411

.A

co 'FABLE 1.Outline of prospective studies of smoking and rnortalitiamongwomen .6

1 Authors

Type of

subjects

Number of .

female . subjects

Age range atb line

Year of

enrollment

Years of

followup

reported

Number of

female

deaths

'Basic it

al measure

eederlof -41# Friberg Be$ Doll British-Norwei

Hrubec JdgieS Gray Framingham Migrant. Stilt Hammond Lorich Walker Hirayama Peto Heart Study - British Norwei

(5) (1) ,5 (4) (2) (10) (10) -- %t.Probability Total pop. Sanwle plu's Probability sar Volunteers (-sample o( Canadian of 29 health v4unteees of British & No

in 25

states

the Swedish

population

pensioners

&,depondents

districts

in JapanBritish

doctors

from Fkamingtiam,,

Mass. \wNtes)

gian migrants

U.S. In 12 stat

562.§71 27,732 - 14,226 142,857

"35-84 18-69 30 to 80 + 40 +

'1959 196g 1955 1966

I. 04 10 6 6

16,773 , 1,955 1,794 1,508

Person-yrs

to

Probability

of death

in 10

Probability

of death

in 6 yrs.

Person-yrs.

death

rate"'

6,192

25 to 75

1951 1948

22 26

1,090 662

Personyrs

death

rate

C

Probability

of death

in 26 yrs.

9,057

45-74

1962 19

5

588 3 Probability o

deacti in

in 5 years.
50

U

co

Co

O

C

O

a. 10

O0O

OO

a) co cc

2

White Males

. .

.... * Noawhite

.

.***

.. ' . Males

i

.

. 4.

Nonwhite

O.

Females

9.

White

4 Females

-

,

1950 1955 1960

-4- 6th Rev ---0--4--70) Rev.----1-4---8th Rev

FIGURE .3. Age ;adjusted death rates* for alignant neoplasm

of trachea, bronchuil, and lung," by color and sex, United States, 1950-1977

1965 1970.

50

1C)

5

2

1975

Adjusted by the direct method to the U S. population. 1940. ICD 6th and 7th Re.v Nos. 162, 163 and 8th Rev No. 162.

SOURCE: National Center for Health Statistics (9).

included except groups that could not be traced easily. A lefigthy

initial questionnaire contained infornbation on age, sex, race,

-4 9
o 30

20

-8, To0

coo

10

r c0

is

a. o

a. Cr480 5

c>o8a

co Ts; ic

2

White Males

, 0--- ,.. .*

. . 0

,. ..

. Nonwhite

. i

.. . .. Males

.

.

. Nonwhite

J

Females

...

..

.

..... :

. .... ,..

.

_ .-- . .

'

4

White Feriales

.

. .....

1950 1955 1960 1965

30

20

10

5

c.

2

1970 .1975

-4----- 6th Rev. 0-4-7th Rev b-114 8th Rev ----o0

FIGURE 4.Ageiadjusted death rats* for bronchitis,

emphysema, and asthma** by color and sex,tnited

. '

States, 1950-1977

''Adjusted by the direct method to the U.S. population, 1940

"1CD 6th and 7th Rev. Nos. 241,501,502,527.1. and 8th Rev Nos. 490,493,549 3

SOURCE National Center for Health Statistics (

education, place of residence, family hi tory,. past- diseases,

present physical complaints, occupational exposures, 'and various habits. Information on smoking included: type of tobacco

----...... used, number of cigarettes smoked per day, degree of inhalation, age i&which smoking began, and the brand of cigarettes

o used frOm pich the "tar" and nicotine content of the cigarette

could be calculated. Nearly 93 percent of the survivors were

successfully followed for a 12-year period. Only limited data

50 0

... f, , -.0V, w.
have been published for the 12-year period for women; the main body of published data for women is based on the first 4-year period of the follow-up.

THE SWEDISH STUDY (I)

A national probability sa#riple of 55,000 Swedish .men and

wonlam was surveyed in 1963, by a mailed questionnaire to

" which 89 percent of the sample responded. Information was collected on smoking status at the time of the query and at specified intervals during the previous 9 years accordingto type

and amount of smoking and degree of inhalation. The question- naire identified age, sex, location (urban, nonurban), income, pfd occuption of each subject. A 10-year follow-up % smoking- related mortality was published in 1975.

THE'CANADIAN VETERANS STUDY (4)

Beginning in 1955, the Department of National Health and

Welfare, Canada, enrolled 78,000 men (veterans on pension) and 14,000 women (mostly widows of xe-terans) in a study Of smoking-related mortality. Information was obtained on age, o detailed smoking history;residerA, and occupation. During the

6 years of follow-up, 9,491 of the men and 1,794 of the women

died. No "recent follow-up has been reported.

. JAPANESE STUDY OF 29 HEALTH DISTRICTS (7)

In late 1965, a total of 265,11$ men and women in 29 health

districts in Japan were enrolled kri a prospective study., This

represented from 91 to\99 percent of the population aged 40 and older in these districts. This study provides a unique opportu- nity to examine' the relationship of cigarette smoking to death

rates in a population with genetic, dietary, and other cultural

differences from previously examined Western populations. At the time of the eighth year of follow-up 4,858 deaths had oc- curred and there werA 1,269,382 Wson-years ttf observation. For women, however, the main body of published data is based

on 5 years of follow-up.

THEIRJTISH DOCTORS STUDY (2)

In 1951, the British Medical Association forwarded to all

British doctors a questionnaire about their smoking habits. A

total of 34,400 men and 6,207 women resTonded. With few exceptions, all men who replied rn 1951 have been followed for 20

years Further inquiries about changes in tobacco use and some

"Aditional demographic characteripcs of the men were made in

51 .
, vt., 19o,, 1966, and 1972. More than 10,000 deaths have occurred irt

This populatiun durmg.tfiejialit 20 years. Fur women, published

-il to are Mailable fur.11,ears of follow-up, and unpublished

to are availablelfor 22 years of follow-up.'

THt FRAMINGHAM HEART STUDY (10)

The Framingham Study began in 1948. with a cohort of 2,336

white men and 2,873 white women who were age 29 to 62 at the

'beginning of- the study and were residents of Framingham,

Massachusetts. Persons were selected by a sample of house-

- holds plus enlistment of volunteers. These individuals were recalled and examined every 2 years 'thereafter.

The routine cardioNascular examination consisted of a medical history, physical examination, blood chemistrii.§, body

easurements, vital capacity, chest x-ray and a 12-lead ,elecrocardiugram. Mortality and morbidity were documented in

etail from the routine biennial examination, hospital records

, death certificates,. physician records and the next-of-kin.

Information un smoking was obtained at the first examination and at seNeral thereafter). A series of monographs and

over 200 articles un the Framingham Study have now become'

part of the ,Scientific literature.

Data on the relationship of cigarette smoking to cardiovascular morbidity and mortality; for both men and women, have

been reported in the Framingham literature, but the longest

repoited follow-up period has been 18 years with relati'ely few

deaths having occurred by then, espeCially among the women

, (11). Data given below aretbased on a jonger follow7Cip period, 26

years, and have not been published. The study is presently in its

16th biennial cycle.

THE BRITISH-NORWEGIAN MIGRANT STUDY(10)

In October 1962, morbidity questionnaires requesting information on itrsunal and demographic characteristics, including

".i.igarette smoking, as well as symptoms of cardlorespiratIry

diserg3e were sent to approximately.32,000 British migrants and

18,0,00 Norwegian migrants to the United States residing-in 12

ttates. These samples 'ere drawn from the 25 percent random

sample of the entire population for 'Ahich country of birth was

recorded In the 1960 United States Census. The 12 states involved contained about three - fourths of the British and 1Corwegian immigrants to the United States. The response rate to the

questionnaire was 86 percept. The respondents were then followed for sun, orshipfnd cause of death data for 5 years, from

January' 1, 1963 through December 31, 1967. The number of

52
morbidity questionnaire respondents and deaths occurring

among them from 1963 to 1967 for ages 45 to 74, by sex, ware as

follOws.

British

Norwegian'

,Males

Respondents Deaths

- 1,181

5,902 643

k

Females

Respondents

9,057

5,337

Deaths

588

354

Several reports dealing with the prevalence surloey, and with

a related cross-section #1 study of mortality, including data on

cigarette smoking for Women as well as for men, have been published (13,14,15,16). The main results of the prevalence study

may be briefly summarized. Four syndromes were considered:

"persistent cough and phlegm," "chronic bronchitto"angina,"

and "possible infarction." The relation of smoking t.6 the prevalence of these symptoms was clearly demonstrated for women

as well as for men. The main results of the cross-sectional mortality study indicated substantial exces.symortality for cigarette

smokers, as compared to nonsmokers: for bothwomen and men.

Overall Mortality for FemalesCigarette Smokers Versus

Nonsmokers

MORTALITY RATIOS

In this report the mortality ratio is the basic means of comparing cigarette smokers with nonsmokers. It is usually obtained by dividing a "death rate" (ur other mortality measure) for a classification \of smokers by the "death rate" (Ur °Cher

mortality measure) of a comparable group of nonsmokers. The

"death rate" may differ markedly from one study to another. In

song t studies it is calculated by means of person-years and is a 1-year measure; in others it is a probability measure, it may be a 5-year, 10-year or, as in the Framingham Study, a 26-year

measure. Differences in mortality ratios may arise because of

these factors.

Because of the arithmetic nature of this ratio, there is a tendency for lower ratios to result with higher underlying levels of . 'mortality. For example, with an underlying mortality level of 10

percent per year for nonsmokers, the mortality ratio for a group of smokers can at most be 10 if all the smokers died Yithin the

year. With a mortality level of 50 percent for nonsmok s, the

maximum possible ratio is 2. Sihce "death rates" incr ith

age, there is a tendency for the mortality ratios to dec

age, since its range is restricted.

53
4 T. BLE 2.Mortality ratios for female cigarette smokers by

number of cigarettes smoked per day and age:

females in 24 states

Number of

tigarette* .Age Total. 15-.4 I ptr da:, (5-44 45- 54, ; 7, 6 4 P-1 .; 74 75-.4 Age ad:Veted'

"Nonlun r,kers I nil 1 Ito 1 o41 1 ilsi 1 olo I (4)

1-'4 '44) :49 1 419 1 1e7 97. 16-1,,, 97 1 2.: 14:1 1, 1 1. I 21 1 19

-.., 20 (9 1 35 1 54 14r 1 51 ,", 1 45

4" I 7,6 1 :el 1 2( 1 42 1 63

:"rnoker,-, 1 12 1 t I 1 27 1 it I 14 1 26

1(iJuted to. the ,lir.tt no th,d 1-,ing a. .tandard t h. age 1..tribution of all u omen Not than "..expetted death.

S(H' R( E Hammond, F.

TABLE 3.Mortality ratios for femaHe cigarette smokers by

number of cigarettes smoked per day and age:

females in the Swedish study

Number ,,f

, Igarette,-, Age Total. 1.-69

per da,!. lilit (9 Ill- .4. -41- .)9 611- 6t, Age-adJu.ted

- Non.mokr. 1 o I o 10 1 0 1 0

1-7 I o 16 1 1 9 I0

,..._1, 2 i , , 1" 1 4 15

14 4 - 2 1", 22 20

... Alt Smoker. 1 . - 1.4 1 i 1 1 1 2

SOUR( E6 eederlof, R (21

Fur simplicity. however. mortality ratios are used throughout

this re% iew. it 1:4, recognized that these ratios are not strictly

comparable fro One study to another nor from one age group

to another

AMOUNT 10KED AND AGE

Overall mort lay ratios by amount smoked and age are presented for several of the studies in Tables 2-7. Except for the

Swedish stud (Table 3). age-acijusted rattos were calculated for

each level of smoking in each study. Adjustment was by the

direct method. using as standard the age distribution of all

54
TABLE 4. Mortality ratios for female cigarette smokers by

number of Cigarettes smoked per day and age; females in the Canadian study

Number of

cigarettes

pee. da,!,

Nonsmokers

1 -9 Ii-

.411 Smokers

4 Age Total. 30-

t0 - * 'W.,- 64 6:, -74 7; - Aige-ad sted'

101)

I -)9

2 2;

1 9;

10 }1

I 09

;ii 1 0 3

I 15) 1

I IC,

1 20

1 10

1)11 92

14",

I1 20

1 43

131

Adjusted by the dire& method using as standard the age distribution of all women Net shevsn"-- less than expe(tesi death. St)rftt E Hest E V. Ft 1. V

TABLE 5.Mortality ratios for female cigarette smokers by . number of cigarettes smoked perliay and age; females in the Framingham Heart Study

Number of

(igarettes Age Total. 24.4 2

per day 29-44 47--)4 Age - Adjusted'

Nonsneikers 1 00 1 00 1 00 1 00

20 1 42 1 21 1 07 1 30

20 1 s4 1 4s 1 13 1 62 21 22 :. 114 1 72

All Smokers 1 62 1 2s 1.07 1.43

'Adjusted by the duxot method using as standard the age distribution of all S441Men

'Not shown less than ; expected deaths

SOUR( 1.2 National Heart. Lung, and Blood Institute 110).

women in the particular study. For the Swedish study the age- adjusted values were taken ditecily from,the report: Mortality ratios shown in Table 2 are considered 'especially

important since they are derived froM the study with ,he largest survivorship experience. Mortiality, ratios generally rose with the amount smoked for eah age group except for the 75 to

8.4 age group. The age-ratios were .97 for the 1-0-9-cigarettes per day group. 1.19 for the 10-to-19 per day group, 1.45"for the 20-39 group, and 1.63 for the 40-plus group.For all cigarette

smokersitthe age-adjusted mortality ratio was 1.26. By age group, mortality ratios were 1.12 for the 35-to-44 -age group,

55 -

i
TABLE 6.Mortality ratios for female cigarette smokers by

number of cigarettes smoked per day and age;

British females

Number of

cigarettes Age Total. 45-74

per day 45-54 55-64 65-74 Ageadjusted'

Nonsmokers 1 00 1 00 1 00 1 00

< 20 1 49 109 79 1 08 %

20 - 1 85 1 51 1 55 1 60

.All Smokers 1 66 1 25 98 125

}Adjusted by the direct method using as standard the age distnbutign of all women SOURCE National Beak, Lung, and Blood Institute (10)

TABLE 7.Mortality ratios for female cigarette smokers by

number of cigarettetismoked per day and age;

Norwegian females

Number of

ci'garettes . Age Total. 45,74

per day ,45 -K4 65-74 'Age-adjusted'

Nonsmokers 1 00 1 00 1 00

-20 154 107 133

20- I41 89 . 118 ---

1 49 1 02 , 128 All smokers

,Adjusted by the direct method using as standard the age distribution of all women S URCE National Heart. Lung. and Blood Institute (10)

1.31 r the 45-to64 age group, 1.27 for the 55-to-65 grodp,

1.31 for the 65-to-I4 group and 1.14 for the 75-to-84 age group.

Data from the Swedish study (Table 3) appear to be reasonably consistent with the ACS data in Table 2. The 1-tb-7-

ogarettes-per-day grOup had.an age-adjusted mortality ratio

of 1.0 (compare*.97 for the 1-to-9 group above) and 2.0 for ,

the 16-plu's Rio ompared with 1.63 for the 40-plus group ,

above). For three of the four age groups, the mortality ratios

were directly associated with level of smoking. By age group,,

the highest mortality ratios werdobserved for the two youngest

age groups and the lowest for the two oldest groups. The overalls

ratio for all cigarette smokers was 1.2.

For the other studies (Tables 4-7) mortality patterns were

generally sitnilar in that mortality ratios tended to be hiKtest

56

'1

s
- TABLE 8.Mortality ratios for female cigarette smokers by

number of cigarettes smoked per day; females in the British Doctors Study

Number of

cigarettes

per day Total,

Age-adjusted' 0

Nonsmokers,

1-14

----,.di

1 00

0 94 15-24 154 25-

i

1 66.

All Smokers 1 23

'Based on annual death rates standardized for age SOURCE Cederlof, R (2)

i

with heaviest smoking and terided to, be lowest ,at the oldest

ages. ,

,..)

For the Japanese study and the British Doctors Study, mor- tality ratios by amount smoked and age were not reported. However, an oVerall age-adjusted mortality ratio for female

cigarette smokers was reported in the Japanese study, while in

the British Doctors Study this ratio was obtained from unpublished data based on 22 years of follow-up-iTable 8). We list these alow with the overall ratios for the other studies:

Study Total rvprtgality ratio agedjusted

American Cancer Society 1.26

Swedish 1.20

--Canadian 1,31 Japanese 1.28 British Doctors 1.23 Framingham 1.43

British Migrants 1.25

Norwegian Migrants 1.28

. e All ratios here are greater than unity. The largest ratio is 1.43. for Framingham. The other 'seven ratios are close to one

another, ranging from 1.2 for ,the Swedish study to 1.31 for the Canadian stud*

0, DURATION OF SMOKING

Overall mortality ratios for women increased° with duration of the smoking habit based on data from the Canadian and

57
TABLE 9.Age-adjusted mortalitzkratios of female cigar4te

smokers, by number of cigarettes smoked perkay

.and age bean smoking; subjects aged 457-54 at start

of study. 25-State Study

Number of Age'began smoking

...garette,

per da:.

lion - maker- I IR) I 00

1-9 093 4) $ifc

1"-19 1 IT 1 23

20- 39 1 33 1 il

-10 1x5

"Ratio not 4hol.,.nle, than 10 expected deathi

SOURCE; Hammond, E

TABLE 10.Age-adjusted mortality ratios of female dgarette

smokers, by number of cigarettes s75/ked per day

and degree of inhalation. Subjects-aged 45-54 at

start of study. 25-State Study

Number of

(Igarette,

per da>

Degree of inhalation of smoke

NoneSItght ModerateDeep

1-9 RF) 1 04

10-19 I2 117

'0-39 1 41 1 58

40; 2 19

"Ratio not ,hov.nle4 than 10 expected deaths

SOUR( E figArn'multij.. '( th4

Swedish studies (1,4). Among Canadian women whp smoked for

10 ur more years the mortality ratio, adjusted for age. was 1.37

compared tl.) a ratio of 1.08 for women smoking tless than 10

years. In the Swedishptud). an excess risk was found fqr women

smoking 30 or more !years (1.4). For those smoking less than 30

years the ratio was 1.0.

AGE BEGAN SMOKING

Tabk 9 shows mortality ratios for women who were 45 to 54 by

number of cigarettes smoked per day and age began smoking

(5). Except for the light cigarette smokers (1-to-9-per-day),

those taking up the habit at ages 15 to 24 had higher mortality

ratios than ttose who started smoking at older ages.

58
TABLE H.Age-adjusted-mortality ratios of female cigarette . smokers, by number of cigarettes smoked per

and degree of inhalation and age. 25-State Studs

Degree

of

9

Atee.

Inhalation 35-44 45-54 55-64 65-74 75-A4

Nonsmoker, 1 00 1 00 I1)0 1 on 1 00

None 1 01 1 11 1 12 96 Slight 1 22 1 21 I 126 12I

M de rate 1 IC, 1 30 1 32 1 41

Deep I 40 1 7s 1 63

"Ratio not ,holxnle than 10 expected death,

SOURCE Hammond, E C (5)

Mortality data for women smokers, according to age started: are also available from the Swedish study ( 1 i; age-adjusted

ratters were reported as 1.7,A.6, and 1.1 for age started less than

17, 17 to 18, and 19 plus, respectively.

INHALATION

Table 10 shows raortAity ratios for female cigarette smokers who were 45 to 54 years of age according to number of cigarettes smoked per day and degree of inhalation of smoke (5). No clear pattern emerges. The "moderate-deep". group had higher mortality ratios than the ';none slight" group in two of three com- parisons.

Table 11 shows mortality ratios for female cigarette smokers by degree of inhalation and age (5. A fairly consistent general

pattern emerges; mortality ratios vary directly with degree of

Inhalation.This is seen in each age group, except perhaps the 35-to--44 age group.

Mortality data for female cigarette smokers according to inhalation are also available from the Swedish study (1); ageadjusted ratios were reported as 1.1, 1:2, and 1.6 for the no inkialation, light inhalation, and deep inhalation groups, respectively.

N

"TAR" AND NICOTINE CONTENT OF CIGARETTES

Tharelationship between overall mortality and the "tar" and , nicotine content of cigarett smoke was recently examined by

Hammond, et al. (6). In thi study, "tart' and nicotine levels

(TN) were defined as follows; 'high" T/N, 25.8 to 35.7 mg "tar"

and 2.0 to 2.7 mg nicotine; "medium" T/N, 17.6 to 25.7 mg "tar" I

59
TABLE 12. Adjusted mortality ratios for males and females, by

" "tar" and nicotine content of cigarettes usually

- smoked

Mortality Ratios

"High" "Medium" -Low"

Sex TN TN TN

Males 1 00 0 94 0.85

Females 1 00 0 88 0.83

i.t Total 081 0.84

SOURCE. Hammond, E.C. ) TABLE 13. Adjusted mortality ratios for males and females

smoking low "tar" and nicotine cigarettes and

subjects who never smoked regularly

Mortality ratios

Sex , "Low" T N . Nonsmokers - N

Wales 1.00 0.61

Females 1.00 0.7-

Total , 1.00 0.66

SOURCE. Hammond, E.(' (6).

TABLE 14.-:10; erall mortality ratios of Cigarette smokers

compared to nonsmokers, WS= and by "tar" and

nicotine content of cigarettes usually smoked

Non- "Low" "Medium" "High"

Sex smokers T'N T'N T,N

Mir Males 4, 1.00 1.66 1.85 --1.96

F(males 1.00 137 1.45 1.65

Total 1.00 1.52 1.64 1.80

SOURCE: Hammond, E C (6).

and 1.2 to 1.9.mg nicotine; "low" TiN, less than 17.6 mg "tar" and b

less than 1.2 mg nicotine.

Table 12 shows the overall mortality ratios of male and female

smokers by these "tar',and nicotine levels. In this instance, the

mortality ratio of the ',high" T,N smokers was represented as

1.00 to illustrate the reduction in overall mortality di* occurred

with lower TAN cigarettes. There was a small reduction in the

risk of dying v h the use of lower TIN cigarettes. The mortality.

60
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. The mortality rativs.were lower for women than for men.

In a separate analysis, a comparison was also made between.,

the mortality ratios of "low" T,'N smokers and nonsmokers.

These data are presented in Table 13. The mortality ratio of the

"low" T'N group was designated as 1.00. Nonsmokers had overall mortality ratios that were considerably less than those of

"low" TIN smokers.

The combined data from Tables 12 and 13 are shown in Table

14 wh re mortality ratios were calculated using nonsmokers as

th= reference. Combining these data from two separate

analyses that are not exactly comparable results in.figures that are only approximate.

Hammond also compared/death rates of smokers of relatively

few (1 to 9) "high" TIN cigarettes with those %I. smokers who

smoked relatively large numbers (20 to 39) of "row" TiN cigar- ettes (17). The death rates of these two groups were very simi1Comments

Mortality ratios for women who smoke cigarettes ranged from

1.2 in the Swedish study to 1.43 in the Framingham study. As

with men, mortality ratios for women who smoke cigarettesvaried directly with amount smoked, depth of inhalation, "tar" and

'nicotine content cif the cigarette and duration of smoking, and

varied inVersely lkith the age when smoking was started.

In attempting to Study cigarette smoking and mortality.

among women, a major difficulty is the lack of large-scale

epidemiological studies addressed specifically to female popula-, tions. The main findings of this review depend heavily on one

study, that of the American Cancer Society. For the other

studies reviewed here, the numbers of women and of deaths

among themare often too sparse to permit meaningful statist;

tical analyses. Thus, for exampled little can be said about the

survivorship experience of women who give up cigarette smo

ing. We strongly recommend: where possible, extending the

length of follow-up of women who are-already enrolled in these

prospective studies. It, s also highly recommended that new

studies, be conducted that are specifically addressed to women

and smoking-related mortality.

Summary

1. The mortality ratio for Women who smoke cigarettes, is

abiout 1.2 or

61
2. MortalityQraltius for women increase with the amount

Smoked. In the largest prospective study the mortality ratio

was 1.63 for the two-pack-a-day smoker as compared---4.9

a non-smokers.

Mor alrt, iflitios are generally proportional to the duration

of eig 1 to uking, the Iurtger a woman smokes, the greater

the excess risk of dying.

4. Mortality ratios tend to be higher for those women who,

begin smukaitig at a young age as compared to those who begin

4; ,smoking Later.

IVIottality ratios are higher for those women who report

they inhale smoke than for those who do not inhale.

6. Mortahty ratios for women tend to increase- with t e tar

and nicotine-coritene of the cigarette. Mortality ratios for female smokers are ,somew at less

than for maleAm'okers. This may reflect differences in exposure

to cigarette smoke, such as starting smoking later, smoking

A cigarettes with lower " ar" and nicotine content, and smtking

fewer ciga/ett4s p y than ruen.

8. WOmen demjnstrate the same dose-respunse relationships

with cigarette smoking as men. ryi increase inymortality occurs

with an increase in number of cigarettes smoked per daypari

earlier age of beginning cigarette smoking, a longer duration

of smoking, inhalation of cigarette smoke, and`a higher "tar"

and nicottine content of the cigarette. Women who haver smoking chargcterietics similar to men' may experiers, mortality

. rates similar to men.

L

Regir 4s

119 BE`ig A*Canadian StutlY-of.Srriokirfg and Health. Department of

N:,,. nal Health and Welfare, Epidemiology Division, Hlalth Seri

Branch, Biestatistics Rksearch..and Statistics Director

1956, 137 pp,

(2) CtIDERLOF, FRIBERG, L., HRUBEZ!, Z., LORICH, U. The Relationthip ofSinoking and Some SocialstOovrables to Mortality and

Cancer Murbichty. A Ten Year Follow-up in a.-.71/obability. Sample of

55,000 SW dish Subjects Age 1.8 to 6?. l'art I and II. Stockholm,

Karatrnsica institute... Department of Environmental Hygiene 1975,

201.pp.

13) DOLL. R.. GRAY.a., PETO, R. Mortality ih Relation to Smokilig 015-

servations on me Du.ctor'S. (Vnp.uhlyikhkd manuscript)

4 ; DORN,11.F.0The tionship of canStrVtie lung and the use"of tobacco. The Ame n atatistic,lan 8(51.71-13,0ecerobpr 1954.

45) HAMMON?. E.( Srp Mit prlatiCin to the death rates .uf one

men ,,and women In. Hae zel, W. (E(1.1t4r Epidemiological Ap

groaches to the Study of Carver and Other Chrunic Diseases, National

river Institute Monograph 1.9 Department of Health, ,EdiAEation,

and WelifirePublic Health Service, National Cancer Institute,

January.1966ep. 127=7294,

62

IS
( 6) HAMMOND, E.C.,IARFINKEL, L., SEIDMAN, H., LEW, EA. "Tar"

and nicotine con nt of cigarette smoke in relation to death rates. Envillonmental Research 12(3): 263-274, December 1976. , (7) 41IRAYAMA, T Smoking in relatiqn to death rates of e9,118 men

and women in Japan. A report of 5 years.° ow -up. Presented at the American Cancer Society's 14th Science Write 'Seminar, Clearwater

Beach, Marclii24-29, L972, 15 pp. (8) NATIONAL

Florida,

'CENTER FOR HEALTH STATISTICS. Mortality from

Diseases Associated with Smoking: United States, 1950-14964. Department of Health, Education, and Welfare, Public Health Service,

National Center for Heatit Statistics, Public Health Service Publication No 1000-Series 20, 50. 4, October 1966,45 pp.

(91 NATIONAL CENTER FOR HEALTH STATISTICS, Office of H41t11.,

Research, Statistics, and Technology, Public Health Service, Depart ment of Health Service, pepartment of Health, Education, and Welfare. (Unpublished data) . (Th) NATIONAL HEART, LUNG, AND BLOOD INSTITUTE. Proceedings of the Conference on the Decline in Coronary Heart Disease Mortality. Department of Health, Education, and Welfare, Public Health Service, a National Institutes of Health, NI H Publication No.79-1610, May 1979, 399 pp.

( L) NATIONAL HEART, LUNG, BLOOD INSTITUTE Some characteristics related ,to the incidence of cardiovascular disease and death.

Framingham Study, 18-year follow-up. In. The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease. Kannel,

W.B., Gordon,ATTE-ditors). DHEW Publication No. (NI H) 74-599, February 1974. . 'r72) NATIONAL HEART, LUNG, AND BLOOD INSTITUTE, Department of Health, Education, and Welfare, Public Hearth Service, National Institutes of Health, 1979: (LinpubliShed data)

( 1f) PEARL. R = EVINE, D.R., GERSON, E.J. Studies of Disease Among Migra and . tive Populations in Great Britain, Norway, aitut the d States 11 Conduct of Field Workin the Unit.ed-Stat,i, National

sneer Institute Monograph 19. Departmerst of HealtIrdducation,

and Welfare, U.S. Public Health Service, National Cancer Institute, 1966, pp. 301-320.

EID, D D Studies of Diseases Among Migrants and Native Populations in-Great Britain, Norway, and the United States. I. Background

and Design National Cancer Institute Monograph 19. Department of Health, Educdtion, and Welfare, Public Health Service, National

Cancer Institute, 1966, pp. 287-199.

REID, CONFI ELD, J., MARKUSH, R.E., et al.'Studia of Disease

among Migtants and Native Population in Great.Britain, Norway, and

the United States. III. plevalence of Cardioiespiratory Symptoms Among Migrants and NaMe R2rn in United States. Natitinal 'Cancer

Institute Monograph 19. Department of Education, and Welfare, Public Health Service, National Caricer Institute, 1966, pp. 321 - 30-..;

(16) ROGOT, E, Gardiorespiratory disease morality among British Norwegian migrants to the United States. American Journal of Epidemiology

108(3);.,181-191, 1978.

(17) U S. PUBLIC HEALTH SERVICE. Smo.king nd Health, A Report of ' the Surgeon General. Department of Health Education, and Welfar2, Public Healthjervice, Office of the Assi ant Secretary for Health, Office on Smorng and Health. DHEW ?ublication No. (PHS) 79-50066, , ois, 1251 pp. 4

. 63

`1
A

:*(

MORBIDITY.

at

11. 1

.
4.4

MORBIDITY

The relationship between cigarette smokingand morbidity

has been summarized, in the 1979 Surgeon General's Rgport. - That report contained data from the National Center for Health,

Statistics Health Interview Survey (HIS) showing the relation- ship for both men and women between smoking and the prevalence of selected chronic diseases, the incidence of acute illness, days lost from work, days of bed disability, and perceived health

status. This section will present additional data from the Health Inte, w Survey on trends in days lost from wv14 and limitation ctivity.

Days Lost from Work

Workers who smoke report losing more work days due twill- ness and injury than do nonsmokers. This relationship hag been observed for both men and women every year that the National Health Interview Sur Vey has included questions on cigarette

smoking. For example, in '1,65 working women whoiamoked reported 6.6 Arrk-loss days; .workirig Women who had never

smoked reported only 4.8 work-loss days (see Table 1). Similarly, in the 1977 HIS women who smoked reported 6.6 days -Iqst from work compared to 5.7 days lost from work by those who never srrioked.

The-National Clearinghouse for Smoking and Health used the

earlier 1965 data to estimate the number of `.;excess"-days lost from work among -cigarette smokers. Thl§ estimation was obtained by calculating the ezpected nurhber of work -loss days if all workers had the same wok -loss experience as those ,CAO had never smoked cigarettes. It was estimated that approximately

20 percent of all work-loss days (rue and injury could be attributed to the higher rates of loss a ng current and former smo ers (2). The 1979 Surgeon Generals Report presented simi- lar culations, ased on 1974'data, and again the estimate was about 20 perce of all work-loss days. These calculations were

not 'sex specific Certain modifications in the collection proce- dures-have Itwere.0 the male response Tate for the smoking data and May; thus, make compatisons of more recent data by sex

less than ideal. However, the data do show that in 1977, the work-loss rate m9ng women who never smoked as higher

than in 1965, while the rates among current smok s remained

"k about the same. This would tendto reduce the n ber of "excess" days among women attributable to Smoki g. There. has been Avbslight .decfease inwork loss among males who never smoked. Former smokers reported fewer work-loss days in 1977 than Although the difference in work-loss days between

g 67
TABLE f.Days hist from work per year due to illness and

injury, per currently emphved persons 17 years

old and older, by smoking status, sex and age

Cfrited States, 1965 and 1977

Female

17 .3

17-144

45-64

Total'

Present

Sm%ket

Former

Smoker

Never

Smoked

55

. 60

_., Percent of work-los, das

1965

66 67

66 60

6.7 77

48

4.5

53

Male

17 .3 . 57 59 68 46

17-44 41 47 36 3.4

45-64 78 79 98 56

. 1977

Female

420 .3 64 66 54 , 5.7

20-44 6 1 6.8 54

45-64 64 65 5c s 65

'Male

20 -' 53 5.9 61 4 2

20-44 51 ' 6.0 55 44

4:5-64 56 5.9 62 3.9 .

'Includes unkitocyn smoking status

2Figlire foes riot meet standards of reliability or prectsion7

'Includes ages 65 and over

SOURCE National Center for HealthtStatistics (1).

196a and 1977 is small, it could be attributed to the assurnption

that in rlecent,years the Omer smoker groups have, a greater

proportion of people who stopped smoking for prevencive reasons, that is, before they had experienced'serrous health consequences.

Further study is needed to determine tite association between

"excess" days lost from work by smokers and specific diseases.

Such an analysis would help .explain the economic impact cJ

smoking in the work place.

Limitation df Activity )

The Health Interview Survey also regularly collects data on

the long-terni impact of chronic illness. Respondents were asked

chronic illness limited their activities (3) Estimates of the

percent of the po ulation with limitation of activity by cigarette

68

.

8
1

smoking status are shown in Table 2 for 1965 and 1977. Detailed

ixtterpretation of rend data is difficult; however, there. appears

to be a relationship between smoking and the impact of chronic

illness. In general, the 1977 data indicate that Vmen under 65 who have ever smoked are more likely to halt a limitation of activity than those who never smoked. There are no marked

differences bet&en current and former smokers. Among eld- erly women in 1077, there were no differences in limitat ns Of activity by smoking status.

TA BLE 2. --i)ercent ofpersons with limitation of activity due to

,thronid conditions, by cigarette smoking status, sex

and age': United States, 1965 and1977

Total'

Present

Smoker

Former

Smoker

sever

Smoked

Female

17-

,17-44

45-64

65 -

17 3

8 3

19.5

45.1

1 Percent with limitation

1965

127 17.3

8.8 9.8,

17.4 22.1

39.8 48.6 '

19.8

7 7

20.2

45 4

Male

17 - 17.3 15.3 23.0 171 ...9 17-44 73 7.7 8.0 6.2 45-64 °20.0 20.9 22.1 15.7 65 - 53.7, , 52.7 56.3 52.9

107 . Female -, 20- 17.6 it , 16.0 18.1 18.3 20-44 , 8.0 9'.2 , 8.4 7.0 45-64 t

, 21.5 24.2 23.9 19.8

65 39.2 36.3 35.6 38.8

Male ib 20 -. 20.0 20'.5 24.1 17.6 20-44 9. 12.4 8.3 7.5 45744 ' 25.7 27.5 25.7 25.7

65 4 . 47.5 52.7 47.6 42.5

1,1141.ulea known smoking status.

SUCRCE. National Center for Health Statistics (1).

Cigarette smoking and Occupation"

The Health Interview Survey providis a considerable data

base on cigarette smoking behavior and occupational status.

See "Interaction Between Smoking and Occupational Exposures" in thus Report.

69
9. The data are iiirtilable from a national simple c

about 40,1100 ilitseholds fur the years 1*-i5, 1966, 1970, 197,=

1976, 1977, 1978, and 1979. Howe\ er. only minimal analysis ha

been conducted on this potentially valuable data base 11). Thi

brief section presents data on smoking patterns fur only two c

these periods 1970 and 1976. Researchers are encou ed t

inestigate these data more fully through the purchase of t

lic use data tapes (1) The importance of this data base increas

as new eidence becomes al. ailable on the increased health ris

experienced b smokers in certain occupations. The problems c

relatively small sample sizes in high-risk occupations can b

partially uiercome by combining severaly ears of the HIS dat

tapes.

Tables 3 and 4 show smoking characteristics of broad occupy

ti5nal groupsi.e., white collar, blue collar. service and fan

workers for 1970 and 1976, respectively. Service and blue co

lar workers, both women and men, are more-likely to smok

than are white collar and farm workers, but the diffeiences ar

much less among female workers. In 1970. there were virtual]

no differences among female white collar, blue collar, and sere

ice workers. more recently. hov:eier, there has been a sligt

increase in smoking among the latter two group. Cautio

should be used in draw ing conclusions from these data based o differences of only a few; percentage points since such di:

ferencescan be well v. ithin sampling error. White collar wort

ers who smoke tend to be heavier smokers than other types s

workers. and this pattern is more marked among female whit

a-r-workers.

The proportions of cigarette smokers b more detailed occt

patiunal classes are shown in Tables 5 nd 6 for 1970 and 19'i1

Within three of four subgroups of white collar workers -

prufessiunals, managers, and sale's peoplethe proportion (

-414-iokers among women is the same as for men in the same occt

pational griiup. This also appears to be true for .laborers, wh

show ,the. highest I, els of smoking among both women and mer

Summary

The I979, Deport of the Surgeon General summarized the. it

formation tm smoking and morbidity as follows.

.1. In general, female current cigarette smokers report mor

. acute and chronic conditions, including' chronic. bronchiti

and or emphysema, chronic sinusitis, peptic ulcer'disease, an

arteriosclerotic heart disease, than women who never smokes.

2. There is a dose- response relationship between the numbe

70

4 fir A
TABLE 3 Percent distribution of,,the population 17 year's and user by cigarette smoking status, accordin

seg and occupation category. United States, 1k0

Sex and

occupation weir- - Percent distribution

_... * Total, Ne,.er Former Present Present smokersno of cigarettes per day poputation' smoked . smokers smokers Total' 15 15-24 25

--- Female

100 0 39 3 Total population 100 0 77:44 11 2 14 9

3x 7

42 4 18 Total currently employed 100 0

White collar workers :.:: 21 11 1 1,1 6

14 2

11(w.i1j1p0 18

Blue collar 1.vorkecx 100 0

100 0 12 6, ,

s 5 ' 4 (1 (0: (0) 40 7

37 6 42 s3 44 4 . 14'. 19. Farm workers 100 0 74 3 '7 5 '1: 627' '49 2 '33 3 19.1

Service workers 100 0 55 ',', ' 9 2 41 6 41 0 it 17 Male

100 0

At

.. ' Total population 100 0 t 24 9 46 2 25 8 45 1 29 Total currently mployed 100 0 2s,s 25 2

100 0

25 5 45 3 29

2' . Blue collar workers ' ..- Mk . 24 s 22 4 52 s

196:(3) 100 0 25 5

White collar workers 100 0 W . 31 6 19.1

110;01 00 23 8 411 4 32.J

Service workers 31 1

. 46 28 100 0 ". 31 1 4s 1 100 a 25 f Farm workers

20 x

100 0 ° 40 7 24 s 34 4

. 100 6 35 5 19

, ,

'Excludes unknown if ever smoked

'Excludes unknown amount of cigarettes smoked - Figure does not meet standards of reliability or precision SOURCE. National Center for Health Statistics

5
C

. TABLE 4- Percent distribution of the population 20 years and o %er by cigarette smolunrstatus, according 1

sex and occupation category, United States, 1976

AY Sex and s '" occupation category

'. Total

population'

Never

smoked

Former

smokers

,tt Present

'smokers

'Present smokers-no of cigarette§ pti day!

Total' X15 15-24 25-

Female

Total population

Total currently emPloyed

`White collar workers

Blue balar workers

Sericce.workess

Farm workers

. Male

Total population

Tolitl currently employed

White collar tvorkera

Blue collar workers

Service workers

arm workers

100.0

100.0

100.0

100.0

100.0

100.0

100.0

100.0

1510,0.

100.0

100.

100.0

)

54 3

50.8

51.1

50.7

49.1

59.8

29.2

29 5

.4 0

24.3

29.4

34.9

13.8

13.3

14.6

10.2

'

11.9

28.9

27 1

29.4

25.3

23.4

28.2

32.0

35.9

34.3

39,0

39.0-

31.3

4... 41. -.9"

'43,e r

36,p;

. 50.41 ' 41.2';

//9- '

100.0

100.0

100.6

109:6

100.0

100.0

. 100.0

'100 0

100.0

100.0

100.0

100.0

36.5

36.5

35.3

38.0

37.9

34.6

24.2

21.9

20.8

21.2

27.6

29 4

_

1

43.8

44.0

42 4

44.3

48.3'

44.8

45.4

43.6

47.4

4Q.0

44.9

. 19.6

19 51'

22.3

, 17.6

13.7

. 31.1

32.8*

65.6

Au In

25.7

'Excludes unknown if ever smoked

','Excludes unknown amount of cigarettes smoked.

Figure does,not meet standards of reliability or precision.

SOURCE: National Center for Health Statistics (1).

.14
TABLE 5 Estimates of the Percentage of current, regulpr cigarette smokers, adult ages 17 'years and of according to labor force status, occupation, d sex, United States, 1970

Total

17-

Female "a

17-44

Total 34 9 36 8 ..... Currently employed / ., 34 6 36 4

White collar total 34 2 34 9 i

, Profespional, technical

stiff kindred 28 1 29.4

Managers & administrators

except farm 48 4'

Sales workers I 34 6 35 3

Clerical Lt kindred workers 35.g 35 9

Blue collar totalP 36 5 39 9

Craftsmen & kindred

workers - . 40 4 44 4

00ratives and kindred

0 P workers ' 36 5 40 0

Laborers, except farm v 23.3 ' '25 6

b

,Service 35.2 39 3

Farm 18'6 '259

45-64

33 7

33 7

34 3

26 3

A 38 3

35 7

36 4

33 5

37 0

33 5

'20.9

33 5

'155

Unemployed 38 4 OS. 32 9

Homemakers 29 7 37 3 32.3

Male r

Tot 1

17 17-44 45-64

46 2 49.0 44.4

46 0 48 7 44 1

;i9 3 41 1 38.4

%. 31 7 32 8 30 6

4

42.8 47 4 40 0

44.9 .. , 46 8 46 1

43.3 45.2 41.5

52 8 ., 56 1 49.2

51 7 56 1 47 2

t 54 7 57.5 50.7

50 9 , 52 0 s 52.9

48 1 48.3 51 7

344 38.7 377

52 3 54 4 53.0

NA NA NA

'NOTE Unknown if ever smoked excluded from calculatiOn 0

'Figure does not meet standards of reliability or precision

SOURCE National Center for Health Statistics (1)

(
TABLE 6. Estimates of the percentage of current, regular cigarette smokers, adults ages 20 years and ose

according to labor force status, occupation, and s-ex, United States, 1976 liz

Total. 2ii

-Female

20-44 45-64' . Total

20-

Male

20-44 45-64

Total 32 0 36 9 348 419 476 413

Ctkrently employed, 35 9 :37 0 16 1 . 43 4 46 8 39 7

White collar total "s 34 3 33 8 '16 9 36 6 38 6 35 3

Professional, technical

and kihdred 291 286 327 300 11 1 299

Managers & administrators

except farm 41 6 42 7 408 41 0 46 4 36 1

Sales workers 38 1 3-70 42 6 39 9 42 6 38 0

Clerical & kindred workers 34 34 7 36 0 40 4 40 1 44 2

Blue collar total 39 0 43 7 33 6V 50 4 54 1 44.3

Craftsmen & kindred workers 40 5 s69 35 6 48 0 52.1 41 6

Operatives and kindred

workers 376 425 31 2 52 3 553 46 2

Laborers, except farm 56 1 52 6 53 7 56 9 517

Service :190 42 8 37 2 47 2 51 1 44

Farm 11 51 0 369 454 35 tr

Uneroplo!,E'd 40 0 41 0 '392 568 599 53 8

Usual activityhomemakers 29 0 37 1 32 2 NA NA NA

NOTE Unknown if ever smoked excluded from calculation

Figure does not meet standards of reliabiliq or precision.

SOURCE National Center for Health Statvitics11) (kJ LI

.1t
)

of cigarettes smoked per day and the frequency of reporting for most of the chronic conditions.

3. The age-adjusted incidence of acute conditions (e.g., in- fluenza) for wome*smokers is 20 percent higlik for women who

had ever smoked than for nonsmokers.

Additional data from the Health Interview Survey HIS is

presented: .

. 1 Currently employed women who sMoke cigarettes report more days lost from work due to-illness and injury than working

women who do not smoke.

2. Limitation of activity is reported more commonly among

women under the age of 65 who have ever smoked than among

those who never smoked.

, References 19

., /) NATIONAL CENTER FOR HEALTH STATISTICS. Standardized

Micro -Data Tape Transcnpt Department of Health. Education, and

Welfare. Public Health Service. DHEW Publication No 781-213, June

1978. -..._

(2, NATIONAL CLEARINGHOUSE FOR SMOKING AND HEALTH. Smoking and Illness Department of Health. Education, and Welfare, Public

Health Seri, ice, Bureau of Disease Prevention and Environmental Con- I

trot, National Center for Chronic DtEre rase Control, National Clearinghouse for Smoking and Health. PHS Publication No. 1662, July 1967, 6

pp

( 3i WILDER, C S Limitation of activit} due to chronic conditions, U S 1974.

Department of Health. Education. and Welfare. Public Health Service.

Health Resource Administration, National Center for Health Statistics,

Senes 10. No 111, Public Health Service Pub No (HRA) 7r1537. June

1977, 65 pp. ',.,

(4i WILSON, R W Cigarette smoking, disability days and respirator} conditions Journal of Occupational Medicine 15(3) 236-240, March 1973.

.cl 75
,

CARDIOVASCULAR DISEASES

- Introduction

While the mortality and morbidity .rates of coronary hear".

disease (acute myocardial infarction and chronic ischemic heart

disease) (CHD) are lower for women than men, CHD still represents the major cause of death among women in the U.S. In 1976

the United States recorded 284,05.5 female deaths as attributir, ble to this cause (Table 2). The difference in mortality

between the sexes is more marked fur acute m -ucard

tion, with males of all ages experiencing 189.ileat s ales

111 deaths per 100,000 (Table 1). Observed differences y sex in

susceptibility to coronary' heart disease are not fully understood

but appear to be affected by multiple specific risk factors within

any demographic group.

McGill and Stern have recently provided an exterKve reiiew

of sex differences in susceptibility to atherosclerosis in huniaus

and in experimental animals, including an analysis of factors known to predispose to atherosclerosis and its dependent

eases

Mortality Rates

In the United States, the ational Center for Health Statistics has reported mortality rates from acut yocardial infarction lip d chronic ischemic heart disease clas ified by age, sex, and r c e , for the years 1968 and 1976 (Tables 1-3) (33). These

tables show that mortality rates for acute myocardial infarction

among adults up to age 64 are highest for white men and are

succeeded by progressively lower rates for other men, other

women, and finally, white women. Mortality rates for chronic

ischemic hart diseases Crary. The rates for white men are second to those for other men and clae to those for nonwhite

women; again, however, rates for white women are by far the

lowest. Both white` and nonwhite women show consistently

D lower rates un it extreme old age. However, the differences narrow markedl in age in comparison with those in young adult- hood and mi dle life (Table 1).

Male-to-fe ale mortality ratios for acute myocardial infarc- tion among Its in their 30's and 40's are approximately 5 to 6 for whites a to 3 for nonwhites; among adults in their 70's and 80's, they are roughly 1.6 and 1.4. The actual number of

deaths involved is very large; their distribution by age, sex, and

race is shown tin Table 2. Between 1968 and 1976, a striking

decline occurred in the acute -myocardial infarctiop mortality

rate for men and women' of all ages and races. These are shown

-.4

79

( 1

t .1 t)
TABLE 1.-Death rates* for acute myocardial infarction and chronic ischemic heart disease for specified groups, bycolor and sex; United States, 196W-1976

Total White All Other , - Year and age

Both Both Both

sexes Male Female sexes Male Female sexes Male Fern:

1976

All ages

25-34 years

35-44 years

45 -54 years

55-64 years

65-74 years

75-84 years

85 years and over

1968

All ages

25-34 years ' 35-44 years

45-54 years

55-64 years

65-74 years

75-84 years

85 years and over .

(

Acute rn-Yocardial infarction

... C14148 189 0 I- Q.8 158.7 202.2 117 3 84.0 100.3 69

2 8 46 1 1 2.6 43 0.9 42 6.4 2 27 0 46.2 8.8 26.6 46.1 7.6 30.4 47.5 '..10 111 7 186 9 41.3 ,, 11%1.8 190.1 37.7 111 2 159 8 .68 309 5

660.1

490.3 147.2 312.2 501 1 142.1 283.2 386.5 Ai.4 '989 8 06 8 674.5 1,024.7 406.5 524.6 667 9 409 1.328 0 1,806 7 1,03 1,364 8 1,881.4 1,054.3 917 0 1,061 1 813 2,038 0 2,564 7 1,7906 2,135.0 2,709.6 1,869:9 1,126.5 1,369 1 990

185 4 243.0 130.6 .195.9 258 0 136 7 109 5 133.2 87

4.6 7.2 22 4 1 6.5 1 7 8.7 13.1 5 42.3 70.9 15 2 40.3 69 6 12.1 57.9 81.6 37 158.5 267 1 56.8 157.6 270.4 51.3 166.6 236.2 105 420 8 668.3 197 1 423.9 684 3 188.4 390.5 512 5 281. 900 5 1,315 0 574.1 1,360.8 574.4 706.7 870.1 571. 1,687 1 2,228.4 1,316.5 1,7 2,306.5 1,342.8' 1,103.1 1,291 4 961 2,911.8 3,5707 2,5530 3,012.9 3,7153 2,637.8 1,782.4 2,163.4 1,526. /

_ (1"
INF

TABLE 1 Death rates* for acute m}ocardial infarction and chronic ischemic heart disease fur specified

age groups, by color and sex; United States, 1968-1976'(Continued)

Year and age

Total A Whit(; Al] Other

Both Both Bath

sexes Male Female sexes Male Female sexes Male Female

1976

All-ages 150 2 153 5 147 0

Chronic isehemi heart disease

155 5 157 7 v 153 4 115 4

a. 125 4 106 4

25-34 years .. 1 6 2 1 0 8 1 2 I Al 0 5 4 2 6 1 24

35-44 years 12% 203 56 106 17.5 39 27 5 410 - 163

45-54 years 57 7 90 9 26 7 50 4 82 6 20 1 116.1 160 7 77 4

55-64 years 173 3 258 5 96 8 159 5 244 3 83 2 302 2 396,1 222 0

65-74 years . 187 1 674 8 343 4 467 8 660 fi 320 4 672 1 805 8 565 2 75-84 years , , 1,621 5 4,947 4 1.422 6 1,626 0 1,968 0 1.420 4 1,572 0 1,742 7 1,448 8

85 yehrs and over 1,647 1 4,945 8 4.507 0 4,859 8 .7,208 0 1,699 1 23;50 8 2,782 4 2,576 9

,1968

, . All ages 150 6 156 3 145 1 1.54 1 158 T 148.2 132 0 141 6 123 3

25 -34 years 16 23 1 1 10 16 04 62 72 53

35-44 years 13 6 2)5 71 '10 4 170 40 38 8 498 29 5

45-54 years 57 0 85 6 30 2 475 760 20 7 142 6 175 8 113 3

55-64 years 190 6 273 4 115 7 169 2 25:3 93 0 39') 1 4(6186 334 8

65-74 years 590 4 ' 769 1 449 7 560 6 742 8 417 9 889 5 10250 777 2

75-84 years 1,826 0 2,075 5 1,655 3' 1.833 9 2,093 7 1,657 8 1,724 6 1,858 1 , 1.628 0

85 years and over 5,523 6 5,636 6 5,468 4 5,695 3 5,831 8 5.629 4 3,605 9 3.736 6 5 518 0

*Rates are deaths per 100,000 population Fur at.ute myocardial infaN tion, rates.ai'v based on deaths assigned tot ategory number 4

of the Eighth Revision of the International Classifo anon of Diseases, adapted for use in the United states, adopted in 1965. and fo

chronic ischemic heart (b4ase, to category number 112 of this revision - SOURCE: Rosenberg, 1.1 MO334

c -
TABLE 2.- Number of deaths* fur acute myocardial infan, tion and ihroniL ischemii hear Cdisease fur specified

age groups, by color and sex; United States, 1968 and 1976

Year and age

1976

Thtal White AIL other

Both I g(iixe, Male FemaleBoth

,e Keg Male Female

A( \Ate mo( ardial infarction

Both

sexes

-"

1 Male Ferrade

All ages 319,477 197,429 122,048 2957.613 183,820 111,793 21,861 11,609 10,255

25-fr4 }ear, 890 718 172 720 598 122 170p 120 50

(5-440ear, 6,223 5.182 1,041 5,138 4,58 780 ' 885 624 261

45-54 ',ear, 26..405 21,361 5,044 23,479 19,407 4,072 2,926 1,954 9:72

55 -64 year, 62,09k 46,516 1),575 56,623 43,072 13,551 5,468 3,444 2,024

65-74 year, 93,695 61,038 -12,657 86,566 ;7,004 29,562 7,129 4,034 3,095

75 -84 year,

year;i and over

89,969

10,068

46,195

16,132

13,574

23,936

84,852

17,939

43,912 40,940

15,201 22,718

dio 5,1f7

2,129,

2,483

931

2,634

1,198

1968

All age, 169,610 216,017 131,593 342,999 220,517 122,482 26,611 15,500 11,111

2544 yearg 1,099 838 261 846 64 182 253 17.1 79

35 -244 }ears 9,980 8,132 1,848 8,412 7,122 1,290 1,563 1,010 558

15-54 Ntars '16,032 29,368 6,664 32,261 26,860 5,401 3,771 2,5(4 1,263

55-64 years 76,108 57,187 18,721 69,504 53,287 16,217 6,604 4,100 2,504

65-74 years 109,672 70,564 39,108 101,863 66,205 35,658 7,809 4,359 3,450

75-81 vearg 100,112 53,838 46,471 95,613 51,4'16 44,177 4,699 2,402 2,297

8; ',ears and io.er 36,135 15,71 t- . 20,424 34017 11,821 19,49, 1 1,818 887 931

1976 , ( hroni( )g( lierm('heart disease

' All ageg' 322,382 "' 160,175 162,007 289,572 141,372 1 146,200 32,810 17,003 15,807

25-34 years ;02 381 121 1:32 266 66 170 , 115 55

35 14 year., 2,917 2,273 6G1 2,137 1,734 403 81,10 539 261
TABLE 2.- Number of deaths* for acute myocardial infarction and chronic ischemic heart disease fur specifi

age groups, by color and sex; United States, 1968 and 1976 - (Continued)

Total I White All other

' Both- Both Both

Year and age sexes Male Female sexes Male Female Male Fema

13,649, 10,391 8,426 1,09

sexes

3,11

45-54 years 10,593 3,056 1,965 5514 years 34,765 24,525 3529

3,25%

10,240

127.564

28,929 20.996

.27:9136:73 5,836

65-74 years 69,176 41,612 60,042 36,745 23,297 4,867 75-84 years 109,860 50,010 6509:8255,40 101,088 45,932 ' 55,156

89:71:7324 5,010

4,018

1,892

4,69

85 years avdlover 91,368 31,109 86,358 29,217 (..._ 57,141

(968

ii All ages 300,216 151,815 . 148,401 268,124 135,333 132,791 32.092 16,482 15,61 /

25-34' years 390 262 128 211 166 45 179 96 8

35-f4 years 3,212 862 1,734 428 616

7,545

2,350

3,541

2,162

2,182

1,050

1,867 ... :21i,:84933985 / 45-K4 yehrs 12,953 9,412 9,727

65-64 years 34,1/5 23,481 - 10,994 27,743 15,732 8,011 3:749

65-74 years 71,905 . '. 41,270 30,635 62,076 36,135 2-4,941 .5,135 4,69 75-84 years . 108:576 50,145 58,431 101,229 46,689 54,540

693,872:223296 85 years and over 68,548 24,801 43,747 64,870 23,269 41,601

7,347

3,678

3,456

1,5.32 2,14

Number of deaths Ifie ti; a. ute 012.ixardial infari tion are those assigned to tategory number 410 of thZ Eighth Revision of the

International Classifiiat ion of Diseases, adapted for use in the I'mteitStates,alopted in 1965, and fors hronii isi.hemu heart disea

to categor\' number 412 of this revision (-

SOURCE Rust erg. H M'.(33)
as percent changes in rate in Table 3. The percent change ha:

been larger at younger ages (Tables 2 and 3). The changes fo.

chronic ischemic heart disease are similar but less dramatp

(Table 3).

/

Atherosclerosis

Differences in heart attack mortality rates among men an(

r women parallel pathology data concerning atherosclerotic plaques of the coronary arteries. The Internatiorra

Atherosclerosis Project systematically collected autopsy obser vations on persons from 14 geographic locations and 19 et nu

groups in differe arts of the world, and, found that womer

from 11 of the 19 s, when compared to their male counter parts, had as mu or even more aortic atherosclerosis. Mer

over age 39 had more raised plaques'in their cor.r.wtary,arterie.F.

than women (24).

These findings indicate that the occurrence of coronary

plaques was parallel to heart attack rates, but that the occurrence of aortic lesions was not. Coronary plaque severity had a male-to-female ratio of 1.61 among whites .and. of 1.14 among blacks.4tudies of a white population in Sweden (40) and of western EUropeans from five locations (18) demonstrate similar findings: a clear excess of coronary atherosclerosis among men and

a similar severity of aortic atherosclerosis "among men compared to women.

Autopsy studies thus show a selective liability of the male

coronary arterial bed for atherosclelosis, as compared to the

female, especially among white men but also among men of other races. The pathological findings are congruent with the

clinical data on heart attack mortality rates. Autopsy studies also show that, among men pr women with manifest coronary heart disease, women patients have roughly the same preyalence of advanced atherosclerotic lesions of the coronaries .as

men (41). These data suggest that the amount 0( atherosclerosis

necessary to precipitate a heart attack is the same, on the average, in both sexes. This generalization about the amount of

coronary atherosclerosis a4ears to hold for heart attacks at

younger ajid older ages, for cent.and old infarcts, and coro- nary occlusion without infarc , and for stenosis, as well as Igor

complicated and calcified lesions and raised plaques in the.cRonary arteries (41).

It should be noted that the grading of atherosclerosis at autopsy is not a simple matter because there are several types of

lesions and several ways of evaluating or measuring them.

,

.., Moreover, the development of the different sorts of lesions is

84
TABLE 3. Percent change* between,1988 and 1976 in death rates for acute myocardial infarction and chronic emir heart diseases for specified age groups, by color and sex: United States

Age

Total White , All Other

Both

Sexes

\

Male Female

Both .

Sexes Male Female.-

Both

SeXes Male Female

Acute myocardial infarction All ages

25-34 years

-1§ 7 -22.2 15 2 ;19 0 -21 6 -14 2 -23 3 24 7 -21 3 39 1 -36.1 -50 0 -36 6 -33 8 -47 1 -51 7

.)

35-44 years 36 2 -34 8 -/ , -51 1 -54 0 - -42 1 II.

45-54 years -29 5 30 0

-34 0 -33.8 -37 2 -.47 5 41.8 -57 (I 55-64 years -264 -266

-27 3 -29 1 -29 7 -26 5 -33 3 -32 3 34 6

65-74 years 26 7 24 7

-25.3 -264 -26 8 -24 6 -275 -24 6 -30'7 -29 1 -26 7 75-84 years -213 -189 -i 7 -29 2 -254t -23 2 -28 2

85 years and over , -213 -21.2 -184 -21 5 -169 -178 -154

/

30 0

- 28 2 29 9 ..-29 1 -27 1' -29 1 ,, Chronic ischernic heart diseases

-36 8 -36 7 -35 1

Akl..ages

25-34 years

-03 18 13 16 -04 , 35 .- 12 6 -114 s -137

35-44 years 59 -10

4 3 -27 3 20 0 18 8 25 0 -32 3 15 3 -52 8

45-54 years 1 2 06 2

-211 19 29 2 5 291 -177 447

55 -64,years 9 1 -5 4

11 6 6 1 A 7 -2 3 19 6 -8 6 31 7

65 -74"years -174 123

16 3 5 7 3.6 10 5 24 1 ,15 5 33 7

75-84 years -236 18 6 11 1 -233 24 4 214 2.73 1 I

85 years and over . -(11 2

159 123

62 141 11 3 -60 ' 143 8& 6 2 ''-11 0 11'6 14 7 -107 -165 265 25.5 .268

Percent changes are based on rates per 100,000 population Fbr 1968 deaths assigned to category number 410 of the El9hth Revision of the aid 1976, rates for acute myocardial infarction fire based on United States, adopted in 1965, International Classification of Diseases, adapted Mr use 'lithe and for chronic ischemic heart disease, on category number SOCRCE Rosenberg, H M (331 412 of this revision
not necessarily parallel Sternby provides a useful discussion o

issues in the 'grading of atherosclerosis (40) Nevertheless, th(

major studies noted above provide strong eidence that wornei

have less coronary Athe'uosclerosis on the average than men o

the same age in the same population

Risk Factors

Factofs present in individuals which correlate with future

liability to disease are risk factors fur that drsease. In the case

of heart attack, for example. tt has been shown That age, male

sex, cigafette smoking, hypertension, elevated blood cholesterol and several other conditions ark positivejy and independently

associated with the probability of heart .ttack. The level w

high-density lipoprotein cholesterol in the serorn4las a nekativE

correlation with heart attack, tha4, is, higher levels are protec

tive The various risk`factors have been identified for both mer

and women and have been shown on multivariate analysis to 4

uffiependent. A combination of risk factors is synergistic, pro- ducing an associated risk greater than the simple sum of the

individual risks Although the data for women are much less

extensive than for men, they indiCate that cigarette smoking is

a major risk factor-for heart attack in women.

The Effect of Smoking

,ATHEROSCLEROSIS

There is little autopsy information about, the amount of

atherosclerosis in women smokers. Sackett and his associates

reported on aortic atherosclerosis among both men and women: of their -15t) female subjects, 309 were nonsmokers, 52 smoked

less than a half,pack per day, and 89 smoked more (34). Mean, age-adjusted aortic atherosclerosis was found to increase in

conjunction lth the amount and duration of smoking., A study c the intrairtyocardial arteries and arterioles of the heart ir) 13 women and 21 men who were nonsmokers, and16

women and 27 Tn who were smokers, indicaled that proliferative lesions in intramyocardial artejies were more advanced

relative to age i'i'i smokers than nonsmokers It was also found

that subendocardial artehores were thickened in smokers. A

separate analysis by sex was -not performed, but the authors

remarked that the lesions de.16ped as rapidly- and as exten- sively in women as in men in bgth smoking and nonsmoking

groups (28).

Studies of the severity of atherosclerotic plaques 4 the arte:ries of women who smoked in comparison with those who did

x6.

1
TABLE 4.Coronary heart disease mortality ratios related to smokingprospectite study

Author, Number and

year. type of Data

country population, (011e( tom

'E ollov, Number

up of

(,ar--,1 deathHammond '15a,5).14 Questionnaire , 14.a19 .and male, and follow up

Garfinkel, 445,0t7i of death cern i

19614, ' female, age' tate . t" S A 40-70 at,

entr,

(Itarettc, d.* Ave No anatatui

M

NS 100 1 00

1-9 I27 0

10-19 100 I 22

20_30 1 75 1 52

411 1 77 0 61

1 9 10-19

20-30

40

t

Male,

30_49 :I0-"9 70-7I

100 1 00 100 I 00

1 WI 1 50 1 1r 114

239 213 182 1 11;

76 240 191 1 49

51 1.79 I 71 1 37

10-49

FerrIA1C,

:.Y0-.)9 60-69 '10...79

NS 1 00 1 00 1 00 1.00

1 9 1 11 1 15 1 01 0 74

10-19 2 01 2 37 1 79 (1 cJK 20-30 Ci 62 2 69 2 00 1 27

10 .1 II 37'3 2 02

Bao1 on 5-9 death,

NS nonsmokers. M male. F female,

SOUR( K S Public Health SerR.e 14.4:o
not smoke involve too few sqbjects to be satisfactory. Inves

tigating the relationhip of these arterial lesions and cigarette

smoking in women ls fundamental to understanding,the occur

rence of heart attack and other ischemic diseases.

CORONARY HEART DISEASE

Coronary heart disease (acute myocardial infarction acid chronic ischemic heart dishse) occurs,with greater freqtiency

in smoking than in nonsmoking women. The prospective study

of Hammond and Garfinkel, published in 1969, included data on

approximately 446,000 women between the ages of 40 and 79 (10). The increase in Mortality ratios in conjunction with in- creasing numbers of cigarettes smoked per day for yarious ages

is shown below in Table 4 (43,44). Mortality ratios were higher

for younger ages and lower for older ages. The one-pack-a-day Esm.oker's risk of death from heart attack was approximately

twice that of the nonsmoker. The prospective data of Shapiro and colleagues are based on a popu4tion cif 120,000 men and

_women (36) Using a sampling factor of about one-thirtieth, they examined 4,301 women at risk of a first my ardial iyifarction

between the years 1962 and 1964. The smoks compared with nonsmokers had roughly twice as many rapidly fatal heart attacks and heart attacks that were not fatal within 48 hours. The

ratio was approximately 2.9 among younger women aged 45 to 54 and 1.8 for the objects aged 55 to 64. Heavy smokers had higher ratios..biit the data did not permit a detailed study of dose relationships or of the experience of female ex-smokers. A recent study examined the cause-specific mortality of 6,194 British women Physicrtns over the period 1951 to 1973 (6). Table 5 presents the results of this stuqy ten conjunction with the pre- viously published FesultY among male. physicians, during the

s same period (7). The clear association of cigarette smoking and ischemic heart disease previously described in males was con- firmed in female physicians. For women who reported smoking 15 or more cigarettes per day, mortality due to ischemic heart disease was more than double that of nonsmokers.

Although the results demonstrated a sirdiiar effect orssmok- ing in the development of ischemic heart disease Ili both male and female physicians, the association of smoking with heart disease was less striking in women physicians. Ischemic heart disease was less promingnt as, a proportional cause of death in

this population of women than in male colleagues (16 percent vs. 32 percent of all deaths). IschemiC heart disease mortality was only 26 percent higher for all ever-pmoked women than for never-snekeq women. However, for females who smoked heav88

I
TABLE 5. Death from ischemic heat't disease and smoking habits when last asked, British physicians 951-1973

. . Annual Death Rate per 100.000

Number Per,lore, Standardized Tor Age X'

Current Smokers Dose Pet Da:, / Total Nonsmoket s of

Popul %.,,, Deaths Nonsmokers

- Ex-smokers 1:11 15-24 - 25 Trend

30'4

otheis

Women 6194 179 -. 126 1:32 2E11",

138

292

Men :34,440 :3191 413 533 501

(number oftgarettes(

598

(any tobaccograms)

trgram = 1 cigarette)*

677 22 51'' 53.56"

"13- 0 001

SOURCE Doll, R (6,7) 5'
25 cigarettes per day). th relative' risk of death fron

ischemic heart disease was 2'.41, a finding consistent with that demonstrated in males, who had a relative risk of 1.6. In such studies, standardization for amount smoked daily by each oT the sexes dues not, however,'correct for differences in age at initiation of smoking and degree of inhalation. This fact

complicates comparison of the magnitude of biologic ef- fect in the two sexes. This "cohontefect- (i.e., unmeasured hurt documented dissimilarities in total smoking experience)may dead to an erryneous interpretation that cigarette smoking is less damaging to women than to men. This issue cannot be re- solved until studies examen ect of smoking in more re

cent cohorts of women Wit-I o se lifetime moking behavior is more similar to that of men

Among 26,467 Swedish women -observed during a 10-year period, the risk of developing fatal coronary heart disease Was sigThficantly higher among .5mukers than nynsmoker (50). The

relative risk'was 1.9 at ages 40 to 49 and 1.3,atpages 50 t?) 59. An

extensive mortality- study in Japan also reported a highly signif- icant increa4e in deaths 'from ischemic heart disease among female smokers, with a mortality ratio for smokers of 1.6 (29). Coronary heart disease morbidity vdata are available on women, from prospective studies ire Framingham., Mas- sachusetts, Tecumseh, Michigan, and the greater New York

areas The Tecumseh data of 1967 do not sjlow a relationship of such morbidiN with smoking (Table 6.) (8). The Framingham Heart Study found an increased risk for women smokers; but

the associations were weak (19.20). The study of Shapiro and colleagues considered troth mortal- ity and morbidity (36). It reported separately on deaths within -18 hours of onset and 0911 definite myocardial infarctions after that time interval. Using this classification. the incidence of coronary heart disease among women smokers was distinctly higher than it was among nonsmokers. While there is some variability , in the strength of thisiassocia- tion, the data from the various prospective studies of mortality and morbidity from coronary h(irt disease establish smoking as a positive Correlate, or risk factor, for women. However, the risk ratios tend to be smaller than for men at a given level of cigarette consumption in all age groups This trend may result from the different smoking patterns reported by men and women who smoke the same number of cigarettes per day (6,7,25). Men generally begin smoking at an earlier age and have thus smoked for a longer time period than women. Men also inhale more often'than women and are more likely to smoke more than half of a cigarette. These smoking

, styles would ex- 90

1ri
0 4 TABLE 6.Coronary heart disease morbidity related to smoking

4 Author, Number Follow- Number

year, and tyk of Data up of

cquntry population collection years' imidents2 Cigarettes day'

1--- . 1+%. Epstein, - 6,568 male Initial medical 4 96 male, 92 Males

1967, and female examination female 40-59

U S A residents of and repeat CHD includ- NS 1 00 (1)

Tecumseh, follow-up .ing deaths, EX 6.33 (10)

Mich examination,. angina, and Cigar4

,. ettes 0., 5 20 (36)

d myocardial

infarct)ens i'emales '

..... Pipes, cigars_ __ _ Males

60 and over 40-59

1 Q0 (71 SM . 1x0 (2)

1 27 (11)

1 90 (23) 60 and over

SM .. 0x0 (6)

rs'

40-59 60 and over

NS \\ 1 00 (21), 1 00 (47)

'''"EX . , 0.89 (3) 1.31 (5) 1 l Cigarettes 1 02 (14) 0 42N2)

'Reexamination of patients was spread ul.(r 11/2-6 year period, but data are reported in. terms of 4 -year incidence rates

'Actual number of CHD incidents derived from data on incidence and total in smoking class

'Risk ratios= actual number of CHD incidents shown in parentheses SM smokers, NS = nonsmokers, EX ex smokers

SOt7RCE S hrhlic Health Service (45(
r- pose men to a larger'dose of ,smuke per cigarette and a large lifeinne amount than that experienced by women. Case control gnd 'retrosfrective studies of women who hay' had heart attacks have suggested an increased incidence o

heart atrack among smokers. For example, 'a case control stud

of 55 women'who had heart attacks before age 50 an uncommpr event in women) found that 89 percent were smokers in contrasl to 55 percent in a control group without Myocardial infarction Heavy smokers (35 or more cigarettes pey day) had an estimatec myocardial infarction rate approximately 20 times that of the nonsmokers As Tar as possible, women using oral contracep times and those with other identifiable risk factors were excluded froth the study (37).

Spain and his associates conducted a retrospective autopsy

study of women who had died suddenly of coronary heart dis- ease and compared this verifiedAiagnosis to the women's smoking habits as reported by the cldsest living relative (38). Only witnessed sUdderi deaths were included in the data. Compari- sons were made between women who had died of coronary heart disease and women who died suddenly of causes other than

heart at4ck. It was fouhd that 62 percent of the women suffer- *fig sudden cardiac death were heavy smokers in contrast with

only 28 percent of the control group. For those who smokedheavily, the mean age at death was 19 years younger than that of nonsmokers; lighter smokers died at an intermediate mean age. In a retrospective study emphasizing psychosoc,ial variables, Talbott and associates reported on 64 white women who cited

suddenly of arteriosclerotic heart disease (42). They found that women who died suddenly smoked more cigarettes than the

comparison group. The relative risk for those sthoking more than a pack a day compared with those smoking less than a pack a day was 3.9 (p< .004).

Smoking, as well as other risk factors, raises the already

somewhat higher risk of myocardial infarction among women ¶ho use oral contraceptives. During the child-bearing years the use of oral contraceptives doubles, tit risk of myocardial

infarction; women who both smoke and cf4 oral contraceptives have approximately 10 times the risk of women who neither

smoke nor use oral contraceptives (14). These issues are consid- ered below in a separate section.

/)

Cessation of Smoking and "Tar" and Nicotine Content of Cigarettes

Existing data are inadequate to determine the effect of smoking,cessatron on the incidence of coronary heart disease in,'

92

1
410

' women. Hammond and associates hale rteported that mortality

rates from coronary heart disease we're lover in women who

smoked ,low "tar's and low-nicotine cigarettes'"(as sold in the

1960s) than in those who smoked medium level products, an&

still lowei than for those who smoked high-"tar" and. highnicotine products, even so,,the nfortality rate for those women

smoking low-"tar", Low-nicotine products was significantly

higher than that of nonsmokers (11).

Evidpce considered tiePpw suggests that stopping smoking is

beneficial in the treatment, of women suffering from periyheral

"vascular disease

/ ' ANGINA PECT IS* e Framingham Heart Stugreported that there was a poSi,

ti _ sociation between smoking and angina pectoris arntrng

men bu of among women (20),, In an extensive study conducted in Ne York .City, Shapiro and colleagues reported a

positive association between the cleelopment of angina pectoris and smoking among men and a nonsignificant positive

trend among women (37), Among patients with angina pectotis,

smoking lowers the exercise threshold fOr the onset of angini

(46). Only male patients have been studied thus far; equivalent

data apparently have not been published for women with angina and angiographically proven coronary atherosclerosis.

CEREBROVASCULAR DISEASE

tThriheidence of stroke as a manifestation of cerebrovascular

disease appears to be somewhat greater in men than in womem

. v but the difference is small (21,30',43).

In an autopsy assessment of cerebrovascular atherosclerosis,

'Sternby reported more atherosclerosis of the common carotid

artery and the carotid sinks in men than- women. There was also

more intracranial atheroscletbsis of certain % essels in men than

Women. However, using the area- ing method,-no sex dif;

ference was found in total intraikrania atherosclerosis (40). The

International Atheroseletosis Pr5ct also reported a slight ex-,

cess of cerebrovascular atherosclerosis among males (2,4 On

the whole, the a% ailable pathological evidence suggests a minor

ihcrease in cerebrovascular atherosclerosis among men in comparison with women, although sonic studies fail to confirm this

conclusion (see 40).

I t not Air whether smoking is a risk fattbr among women i

for t e:development of atherothrombotic stroke. Kalinel ha?

discussed the issue and the current literature in some detail

(19). The Framingham }hart Study has reported a dose-related

1 ' ' .93 i

4

S.
tt)

TABLE 7.--;Death's from cerebrOvasc-ular isease related to smoking

I

Author,

yeah.

country

Hammond

and

:rGaffinkel,

1969,

USA.

' Number

and type

of popu,

lation

358.584

males

445.875

females

40-79 years

of age at

entry,

Data

collection

Questionnaire

and follow -

up of death

certificate

Follow-up

years

Number of

deaths due

underlying to

CVI) as cause Mortality

ratios

6 4,099

Cigarettes day

Age

40-49 50-59 60-69 7

Males

Never smoked 1 00 1.00 1 00

1 -9 2 79 1 95 1 30

10-19 1 14 1 48 +1 44

LO -30 2 21 2.03 '1 62

I64 2.40' 1 72

Females

Never smoked 1 00 1 00 1.00

1 -9 1 50 1 26 1 26

10-19 2.60 2 70 2 15 4

20 -30 290 267 183

40 + 5,70.+ 3 52

SO CE Hetilth Service (44.451'

I
correlation between the incidence of a rothrumbotic stroke

and cigarette smoking in men but not in women. The extensive

prospective study of Hammond and Garfinkel, which involved'

almost 446,000 women and recorded 1,905 deaths from cerebrova "cular disease during a six-year period, found tilttt smoking was a positive correlate for such mortality t1.0), in both men

and women, the mortality ratio was increased by roughly 2 or 2.5 times (Table 7) (44,45).

That some of these deaths may have involved subarachnoid

hemorrhage rather than brain infarction, is suggested by a re-

. cent report that found the incidence of subarachnoid hemorrhage to be positively associated with smoking for both men and

women (2). The relative risk for men was 3.9 and for women, 3.7. The association appeared to relate to hemorrhage from ruptured cerebral aneurysms rather than to other conditions that

may give rise to subarachnoid hemorrhage. A synergism between smoking and the use of oral contraceptives and subarachnoid hemorrhage is noted below (31), The Japanese study

cited in the discussion of iscbemic heft diseaAe has also reported on 366 deaths from cerebrovascular disease among. women who smoked (29) The risk ratios for- subarachnoid

'hemorrhage and cerebral hemorrhage were both significantly

increased among women smokers (p- .001) as was the risk rate foi. the category, "other forms of ,:cerebrovascular disease"

(p .05)

ARTERIOSCLEROTIC PERIPHERAL VASCULAR DISEASE

Clinicians have noted that arteriosclerotic peripheral vascular disease is more common in men than women. Sternby has

reported from autopsy studies that men generally have some- what more atherosclerots of the femoral and pelvic arteries

than women (40).

Kannel has review *d the relationship of smoking to the incl- dence of arteriosclerotic peripheral vascular disease (19). In the Framingham Heart Study the incidence of peripheral vascular disease was increased. among smokers of both sexes; cigarette

smoking was as strong an independent risk factor in women as

, in men. Heavy smokers had a threefold increased incidence.

Weiss studied 245 women with arteriosclerotic peripheral vascular disease (49). Ex-smokers who had not smoked for 5

years or more had nearly a normal risk ratio of 1.06; those who had not smoked for the la1 to" 5 years had a risk of 1.70; continuing smokers of less than a pack a day, 5.15; pack a day

smokers, 11.53; and those smoking more than a pack a day, 15.56

(relative to nonsmokers, 1.00). The increased risk was particu-
larly associated with proximal (aortoiliac) disease, and there

was less association with distal (femuropopnteal) disease: rAf.estandardize.4.4 relative rittik ratios for those smoking a pack a day

were 30.06 ft)) proximal and combined jfilexinfri and distal disease and 6.32 for distal disease alp,rye.

A retrospective study of 2177 patients who underwent arterial

reconstructive procedures'ofpiriotts kinds fur peripheral ascular disease has 'keen reported by Myers and colleagues (27).

Diabetics were excluded from the report. There were 164 male

and 53 female :patients, The-late patency- rate of the ascular

reconstruction was fullov.ed fur 1 to 4 years. The -authors repot-fed that the nutrnbei-tf cigarettes smoked before surgery did

not influence the outaYne, but cessation of smoking after

surgery had a favorable.impact. There were no significant differences in outcome between men and women The -patency rate

4 years after aortofemoral surgery was 90 percent in those who

smoked fire ur fewer cigarettes per day after -surgery and 75

percent in those who smoked a greater amount. Following

femoropuphteal reconstructionbthe 2-year patency rates were

95 percent forthose who s-tOpped smoking', 75 percent for those

.,:,muking as many as 15 cigarettes per day, and 65 percent for

those v.h't, continued to smoke more than 15 cigarettes per day.

AORTIC ANEURYSM

Studies hae nut been reported for v.umen wit respect tc

atherosclerotic aortic arreixrysm and smoking. aths for

women are about one-fifth%thoso for men (10).

HYPERTENSION

Smoking is nut associated with an increased prevalence 01

essential hypertension in myl ur women (39). However, smoking

dues combine with hyperteMion (and/other risk factorsas a

risk factor for heart attack, synergistically compounding the

risk.

Two recent case control studies of rapidry progressive, severe

or malignant hyperterfsion lime found that there is an uverrep

resentatiun of smokers among patients with this uncommOr

phase of hypertension (3,13). In one study of 82 patients whE

deeluped 'malignant hypentension, 67 were ,.,,rno-kers. Thirty

three of those were v.'*en. In the study, 77 percent of the

female patients with malnant hypertension smoked, and only

about 44 percent of those with essential hypertension and of the

general female population sm.pked. The difference is highly sig

nificant. A similar and parallel study of 48 patients with malignant hypertension contained 31 men arid 15 women, 25 men (7f

96

1
percent) and 8 women (53 percent) were smokers cumpared w ith

44 percent and 30 percent, respectively, uf a group uf 4-1 men and

44 worsen with nonmalignant hypertension. The difference is

significant for men but du* hot reach significance fur women. , . VENOUS THROMBOSIS

The section uf the 1979 Surgeon General's Report dealing with

venous td-irombosis noted a case control study by Vessey and

Doll of 84 women w ho had v enuus thrumboembolism (4%). There

was no significant relatiunship to smoking, although there r.as

a trend (p =0 08) reasonably attributable to chance (46). Similarly, Lawson, Davidson, and .Dick repurted nu association with

smoking among 60 premenupausal women whu used oral contraceptives. and who had uncomplicated venous thromboembolism (22).

The is lie is reopened, however,' by a recent paper derived

from the Walnut Creek Contraceptive Drug Study. The authors

analyzed 38 cases uf venous thromboembulie events among the

approxim'ately 16.700 women followed in the study. These,

women were matched with 8,174 controls from the same cohort,

providing each case with 61 to 55 comparison subjects. The

relative risk Q f cigaretti smoking was 2M with a one-sided p value of lTss than 0.01. On multivariate analysis, the smoking

effect was Independent and remand significant. Of the 17

idiopathic cases of thromboembolic disease, 65 percent occurred

in smokrs, while 33 percent of the controls Were smokers. The

elative risk for smokers was -1.2. Both smoking and oral con

traceptive use were independent risk factors.for venous thromboembolic disease in this cohort of women (32).

The same section of the 1979 Surgeon General's Report noted

a controversy about whether smokers whO suffered myocardial

infarctiun had a 'relative protective effect from leg vein thrombosis in the immediate pot infarctiun peri-od (45). The authors

did not provide an analysis for each sex.

A recent inv,estigation of women-undergoing gynecologic operations has studied the incidence of deep vein thrombosis of

the leg in relation to. smoking. In the prospecstive study of 231

women, their stnoking habits during the month before the operation were determined The. occurrence of deep vein thrombosis

(DVT) was assessed by the radioactive fibrinogen technique,

with routine scans un.theVirst, thi3O, and sixth postoperative

(legs. Of the 231 patients, 99 smoked and 132 did not smoke.

Eight of the smokers (8.1 percent) and 29 uf the nonsmokers (22

percent) developed DVT. Following an analysis ol*her factors.

the authors concluded that smoking provided an apparent ''pro97
tective" effect againstpustoperatie DVT, based un .the -fact

that smokers constituted only 21 percent of tile patients with

DVT. They also noted that the women who "de% eloped DVT

weeghed more than those who did nut and that s.mukers who

levelopeti CVT were more overweight than nun,;mukers with

DVT (5) t

In a continuing ptospective stud, of the ielatronship of blood

clotting and blood thrombogenic properties to ischemic heart

dise.se, Meade and associates have repotted on a number of

blo coagulation variables and their relationship to smoking

among 1,426 men and 63ts v,-omen in gland (26) Forty-three

percent of the men and 36 percent of h

r

e women were smokers

Smoking was not found to have an effect in women on factors V

or \'''II, fibrinogen, fibrinolytie activity, antithrombin III,

platelet adhesiveness, or platelet count Smoking decreased fibrinolytic Activity in men and decreased factor VIII activity in

both men and women Oral contraceptive users were found to

how an increaAe in fibrinotytic activity only if the women were

nonsmokers.

r

HIGH-DENSITY LIPOPROTEIN'

High density lipoprotein (HDL) protein complex that

trausports cholesterol in the yowl. A higher level of HDL is

correlated with a reduced risk nf heart attack:It has been observed that women who smoke have lower levels r,f HDL than

expected (1,4,9) ,

Oral Contraceptive Use, Smoking, anclaardioascuslar Disease

The association of oral contraceptive use and an increased

incidence of certain cardiovascular disorders has attracted

much interest Smoking has emerged as a strung synergistic

risk factor, and an additional study has focused on smolitmg as

an independent risk factor

The effects of smgkiltig and of estrogen and progestin c.ontracept-ies on the level of high density lipoprotein in women

have been studied h.t, Bradle;!, and associates. They measured

serum HDL among alm'ost 5,000 women between the ages of 21

and 62 14). They reported that -the use of oral estrogens raised

the level ()HMI, significantly above the level in nonusers while

proge/stin use lowered it Combination drugs tended to chane

the HDL level according to their relative estrogen-progestin

formulation The al.erage HDI, oncentration was redLiced by

smoking Among nonsmoking womentf HDL concentration

was 63 - 16 is mg di, This was reduced by 2.2 mg dl for those

smukin alf a pack per day. and fiy 7 3 mg dl for those smoking

9K

I

1
one or more packs per day. A reduction in the HDL level among

women who smoked was alslo reported from Holland. This study

found an independent negative association with the HDL level

among oral contraceptive users (1). , It has been reported from long-term studies that women

using oral contraception ha% e ,a two to threefold statkti.call

significant increase in risk of venous thromboembolic disease

when compared to those using other form; of contraception (47).

This study concluded that smoking did not significantly increase the incide ce of venous thromboembolism )46). By contragt, the Waln Creek Study reported that smoking contributed to venous romboembolism among both users and nonusers of oral contraceptives (32). Conclusions about the effect of

smoking on venous thromlitembolic phenomena, therefore,

must be regarded as uncertain at this time since there arel.few

rele% ant studies and they provide somewhat contrary conclusions.

In 197;3, the Collaborative Group for the Study of Stroke in

Young Women estimated that the relative risk of cerebral is"-

chernia or thrombosis was approximately nine times greater for

women who use oral contraceptives than for those who do not. A

detailed analysis of smoking was not presented, but one of the

study's striking findings was the high proportion, of women witk

stroke who currently or at some time smoked cigarettes regularly (73.8 percent), compared with smoking rates of 43.4 percent

among neighborhood controls aged 17 to 44. The study also

found an increase in hemorrhagic strokes among white women.

Almost half of the hemorrhagic stro.kes were attributab'le to

bleeding from congenital aneurysms leading, to subarachnoid

hemorrhage,(5). Recehtly an association between smoking and

aneurysmal subarachnoid hemorrhage in both men and women

has been documented (2).

, The Walnut Creek Contraceptive Drug Stuci, reported that in

a cohort of approximately 16,700 women, the risk of sub-.

arachnoid hemorrhage for smokers was 5.7 times that of

nonsmokers, the risk for oral contracepthe users v.as.6.5 times

that of nonusers, and.the relative risk for women who used both

. cigaretstes and oral contraceptives was 22 times as great. Past

users of oraltuntracepties also had an increase in relative risk,

but an analysis of risk was.not ppssible because of the small

number of ca,es (31).

The risk of myocardial inffrction in women is increased by

cigarette smoking, and by the use of oral contraceptives, it is

compounded when both are used together. Fur example, Mann

and associates ieported, a retrospective study of 63 women

below the age bf 45 with acute myocardial infarction. The pro99
4portion of heart attack patients who had used oral contracel

tives in the previous months was significantly higher thane; pected The relative risk for myocardial infarction amen

women smoking 35 ur chore cigarettes per deQ, was 11.3 time

-greater than that 6mong.nUnsmokers. Moreover, there was ev

dence for synergism of the two risks (23)

Jick, et al reported a, 4! as e control study of 107 womcin unde

age 46 IA ho were discharged from the hospital after suffersh

nonfatal, acute myocardial ihfarctions (15.16.17). The annul

* risk of nonfatal m`6cardial infarctiun (MI) among health women aged 39'to 45 who both smoked and Used estrogens fc , noncontraceptp.e pyrposes wai approximately 1 in 750. The

noted that although an acute myocardial infarction is uncurl.

moon in healthy young wumen. the risk appears to be substanti

in v.omeraierth age of 3k who both use estrogens, and smok

cigarettes (17)

In this carne study, a relative risk of 14 was reported for

. oN

contracept(Ye users compared with nonusers (90 percent cunf

dence limits of relatie risk from 5 5 to37) (16) In women smol

iniemore than 25 cigarettes per day the relative risk rose to 3

'times that of wumen v.i-io were both nohusers'cand nonsmoker

Wtlile the number of subjects was small, the authors calculate

that for v.omen_exposed.to either oral contraceptives or smol

ing. but not both, the annual age-specific risk for nonfatal M

were roughly 1 per 190,000 at ages,27 to 37. 1 per 47,000 at age

38 to 40, 1 per 23,000 at ages 4( to 43, and 1 per 16,000 at ages 4

and 45 If. howel.er, both cigar ttes and oral conIraceptives ar

used, the annual age specific, risk is estimated to be muc

higher and the respective risks'become. 1 in 8,400, 1 in 920, 1 i 540. and 1 in 250. The authors report that a dose-response rele

tionship exists between smoking and risk .iong their popule

tion of female myocardial infarction patients, such that smot

ing 1 to 14 cigarettes per Atay carried a relative risk of nonfate

myocardial infarctidn of 9 2, 15 to 25 cigarettes of 7.9; and'26 o

more cigarettes of 21, relative to those who never smoked (15,

In another recent study of 234 pre-menopausal women wh

had suffered a first myocardial infarction and 1,742 control pa r tients drawn from the, hospital population, Shapiru and his cc

workers found an association between recent oral corraceptiv

use and amoking (135). They found no evidence that past use o oral contraceptives was related to heart attack or tha

heightened risk was-associated with incr aced duration of us of the ural cuntracepties For nOnsmu s who used oral con

traceptives, the rate of myocardial infa ction increased fourfoll

compared to nonusers and nonsmokers, in th'use women wh,

smoked 25 or more cigarettes a day but did not use oral con

100
traceptives, the rate increased more than sevenfold; and in

those women who both smoked heavily and used oral contraceptives the rate increased at least twentyfold.

Carbon Monoxide

A study of male and female office workers found no sex dd.

ference in the relationship between carboxyhemoglobin COH b) levels and daily consumption of cigarettes. However, women

smoked fewer cigarettes on the ,average than men. The.study

fund that the COHb levels in smokers were higher among the

sedentary office workers than among ,physically active meat pOrters and that both had higher levels of COHb than pregnant women who smoked (12). The latter had COHb levels approxi-, mately three Knes Higher than that of nonsmokers. Wald re- ported from a cross-sectional study that carboxyhemoglobin levels of smokers are a better indicator of the risk of

atherosclerotic cardiovascular disease than a reported smoking history (48). The proportion of both men and women with

atherosclero,tic disease increased with increasing levels of COHb.

Comment

Women 'are less likely to experience a myocardial infarction

than men. Nevertheless, coronary heart disease is stin a leading

cause of death and disability in women. The lower mortality

rates from acute myocardial infarction and chronic ischemic heart disease of women as compared to men are paralleled 4Ay

less extensive and severe atheroscler6g-rs in the coronary ar-, tierces of adult women. The severity of aortic atherosclerosis, however, is about the game in both sexes.

The relationship of cigarette smoking to atherosclerosis, heart attack,and other 'scheme diseases secondary to

atherosclerosis has not been studied among women as exten- sively asamong meD; moreover, most studies have been limited to white women. is not known whether atherosclerotic

plaques observed at autopsy are more extensive and severe in

women smokers than in nonsmokers. No data ate availAble cone

cerning to incidence of death from atherosclerotic aneurysms of the aorta among women who smoke relative to those who do

not, and inadequate data exist to indicate whether cessation or

smoking by women is associated with a beneficial reduction in

the risk of(heart attack, as has been demopstrated in men. The

effect of smoliing on the threshold for the onset of angina pectoriS and on cardiac function in women with coronary heart disease has not been studied.

1' 101
compelling 'data from prospective coho,

,tudie': and from case control In\ estigations indicate tha

(.igarette smoking is a major risk factor for fatal and nunfata

heart attarks in women. In general, cigarette smoking in

creases the risk b:. a factu'r of abut two, and in younger wdmel

cigarettOs smoking may increase the risk several. fold. Women

who smoke low-"tar" and low-nicotine cigarettes have a greate

risk of suffering heart attacks than nonsmokers but appear II

ha \.e a 'smaller zisk than womk_--n smoking moderate-to-higl

"tar" and nicotine products.

Smoking is a major risk factor fur arteriosclerotic periphera

ascular disease in women, as' it is in men. For both men an

women the successful outcome of surgical rpair of this disorde

is enhanced by cessation of smoking., Smoking is a major ris

factor foi- subarachnoid hemorrhage and for the delfelopment o

malignant hypertension. Smoking is reported to depress th

natural relative ele ation of high-density lipoprotein choles

terul enjoyed by Women In women who use oral contraceptives

smoking is a powerful synergistic risk factor for subarachnon

hemorrhage and for myocardial infarction.

While data implicating smoking as a risk factor fur variou

carlo.ascular diseases in women are neither as extensive no

as complete as for men, the evidence nonetheless clearly estaL

lishes cigarette smoking as a major correlate for myocardia

infarction, arteriosclerotic peripheral vascular diseise an

subaractinoid hemorrhage in women (4 .5).

Su.mmary

coronary heart disease is the r4jor cause of death arnon

both male- a.tid females in the S ,pOpulation The 1979 Su/

goon General's Report clearly demonstrated the close associe

tion of cigarette smoking and increased 'curonarN heart diseas

among males This report reviews the evidence associatin

cigarette smoking and cardiovascular disease in women

1 Coronary heart disease, including acute myocardial infarc

tion and chronic ischemic heart disease;oc(.urs more frequentl

in wome rl who smoke In general, cigarette smoking increase

the risk 1-)N a factor of about two, and in younger wome

cigarette smoking may increase the risk several fold.

( igarette smo.king, is a miiipor independent risk factor fo

coronary heart disease in women, it also acts synergisticall

with other coronary heart disease risk factors producing a ris

greater than the sum of,ttie individual risks

`S The use of oral contraceptives by women cigarette smoker

102
increases the risk of a myo-cai'dial infarction by a factor of ap- proximately ten.

-I. Women who smoke low "tar" and nicotine cigarettes expe- rience less risk for coronary heart disease than women who smoke high "tar" and 7otine cigarettes, but their risk is still 1 considerably greater th n that of nonsmokers.

5 Increased levels of high-density lipoprotein (HDL) are cor- related with a reduced risk for an avute myocardial infarction; worn cigarette smokers have decreased levels of IIDL.

_igarette smoking is a major, independent risk factor for the development of arteriosclerotic peripheral vascular disease

in women. Smokirig cessation improves the prognosis of the dis-- order and has a favorable impact on vascular patency follovring, reconstructive surgery,

7. Women cigarette smoke) experience an increased risk for subarachnoid hemorrhage, the use of both cigarettes and oral contraceptives appears tb increase synergistically the risk for subarachnoid hemorrhage.

Women wiao smoke cigarettes may be more likely to de- velop severe or malignant hypertension than nOnsmokting

women.

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Cerebroy ascular Disc es Proceedings of the Tenth Princeton

Conference. New Jers 1976 New York, Raven Press, 1976. pp 255-245 PETITTI, D B WINGERD, J ['se of oral contraceptlyes, cigarette

smoking, and risk of subarachnoid haemorrhage Lancet 2 234-236,

Jt ly 29. 1978

( 1.2) 1111, 111, D B WINGERD.J PELLEGRIN, F , RAMCHAUAN.S Oral

contracepti'.es, smoking. and other factors in relation to risk of yenous

thromboembolic disease Amencan Journal of Epidemiology 10816,

480-485. December 1978,

( 0) ROSENBERG, H M , KLERBA. A J tin HaYlick. R.J

(Editors) Proceedings of tbie Conference on the Decline in Coronary

Heart Disease Mortality Department of Health, Education, and Welfare, Public Health Ser'.ice, NIH Publication No 79-1610, 1979. pp

11-39

,;) SACKETT. D L . GIBSON, R W , BROSS. I D.J. PICK REN, J W Relation between aortic arbirosclerosis and the use of cigarettes and alcohol An autopsy stu4y Nev. England Journal of Medicine 279(26)

1413-1420, December 26, 1968

r 5) SHAPIRO, S SI,ONE, D ROSENBERG. L , KAUFMAN,ib.W STOLLEY, P D . MIETTINEN. O S Oral-contraceptive use in Lelation to

myocardial infarction Lancet 1 743-747. April 7, 1979 ' Ali WO SHAPIRO, S WF,IN BLATT, E FRANK. ( W , SAGER, R Incidence

of coronary heart disease in a population insured for medical care

(III Pi Myocardial infarction, angina pectoris, and possible myocardial

infarction American Journal of Public Health 59 (Supplement

1-101, June 1969

3;`o) SLONE, D SHAPIRO, S , ROSENBERG, L , KAUFMAN, 11 W

...HARTZ. S(', ROSSI, A STOLLEY, P D MI ETTINF;N. 0 S Rela-

'tion of cigarette smoking to myocardial infarction in -young women

New Englan4 Journal of Medicine 298423) 1273-1276, June 8, 1978

trr) SPAIN:WM , SI EGEL, II , BRADF,SS. Women smokers and sudden

105

12'1
death The !relation...hip ut (igatette ,r(moking to colonart 1i ea e

Journal of the AI», scan MC,11Cal A)( !at 1,n .22417, low, -10117, 14 1;471

Ril()NIBERG4 I' s( 110ENHERGER .1 A , sHEKE1,1,E,

R K D\ ER, A , SHEKELLE, STA.AILE(P. R 55AN \AMAKER,.J

M analt,(1 of the relation...hip of .-re.en (artahle... to Hood

F mdmg 4 the hie ago Heart iarion Den, non Prop, r

1'037-1 :172 Journal of * hroni, 2 in, -,27-",4,,

N o m r sTERN \ H Ather6, a lefirkd popu'atin An auto',

,e. tr, ...(weden Acta Pathologi, a It Alt, robiologi, an-

.11nav1( a nt 1:44 1.; -194;

' :TP,.()N(r F' -(.HER(, I. A RESTREP(), I Athero,(dero,t, In per-

...oh- w,Nn oranar, he trt Lahoraton, In,re,tigation

17 Mat 1101's

T ALB( )TT El I.!, ER I, H , I)ETRE, K , PER PER.1 Biologic and

al r, k fa, tor, of ...widen death from coronary di-ea-rre in

white (sorrier, American Journal of I ardiologt VA hi x,x xi-;-1, 26,

rfiE P Epidempdog, fur ,troke

fa, .11r---- planning Report of the .J.,int ornniii't for Stroke Fa,

171 Mal. -June 1972 , 1,1 HEALTH t(ERA I( F. The Health ( on-erepiem of ,'.-smok

r,g A Refrnt e Edition Department of Health, Edue anon, and V

I'ibu, Health se e, ( et, tor (for ( antral, DFIE \A 1' thref,'

1)( x1-(7, 197e, 657 pp

1'1 HI I' IrEAI TI1 I( E Smoking and Health A Re-po rt of

'he ,urge on (re nera, Department of Health, Education. and Aelfare,

Putdie Health (MK tr. )t" there, A Sc- ( retan, for Health,

ffie or. smoking and Health DH ation No PA, ye.,,0)66,

1.:11 pp

c.,ssir.,} \I I' )( )1,1e: R I ri,.e,digation of relation between Li-er. of oral

ontra( ratite, and thrornt),o,mboht ,h-ea... A turthvr report Briti-rh

Medical Jai,real "(;-(x, 1-1,;1 -0;7(7, June- 14, 19)19

EssE , Irt R PETO, R JOH S(PC,H I' Along

^ tollow-u1! women Lo-ing different method,. of euntra,c-p

Ah intern( re part Journal of Bio...0( :al '17'1-127. 197(',

1,5 ALD, , ARI). S . P , K tA,,,,ociation/

betwe -en nthwn,-( 11,42a,e, and (a u\ }haemoglobin in to ' Brit,...h \fedi( al Journal -11-701i, March 11 197`1

4) V., \ S Cigarette -making and arterio,4 obliteran', art

e.piderniologie approae h Amen, an Journal of Epiderniolog 970(1 17 197.:

;Hi V HAI FA Recent ,t11,11e, on rrioking and I) epidemiology

ar.dirpr. la and -,,unte ,the r We-tern European ountrie- In 'stein

t.i,d 1 (pttfit1, -,55 Ball K Ta(,lor, R M Editor-ri Pro eeding- of the

THrd \,trorld. ariferem e nn :-(rnoking and Health Ne-V. York, lune 2-

N, ',Hill, I I Health 1 on,,,illon e F,din 'anon, (e..atton At ti,.itleand t ton l)ojnirtnif,nt of Health, Education and 14edfarte,

Puhlp He (dth Niational In-titute He alth \at ional ( arc err

I n-t rue, PubliratIon No NIII 7 7 1 11 1977, pp 171 177

22 - ,et
CANCER

Introduction

For more than 40 years cancer has been second,only to cardiovascular disease as a cause of death in the UnIted States.

With the exception of the very elderly, the deidh rate for adult men exceeds that for adult women for both groups of diseases,-

implying a difference in genetic susceptibility, environmental

exposnres or lifestyles Iletween the sexttor a combination of

genetic and environmental factors. Placing these getrralizatons abut cause of dea\tk-in per- spective, current data from the National Center for Health

Statistics (28) reteagi the following Statistics:

Th0-e are 105 male births each year in the United States for every 100 female births, but the higher death rate for males

esults in aratio of 100 men to 1-00V/omen at ages 20 to 24 and of

r, 79:100 at ages 65 to 69, and of 47:100 at age 85. Ltfe expectancy

in the United States in 1976 was 68.7 years for males compared

to 76.1 years for females.

Heart disease and cancer currently account for 60 percent of deaths in the United States. In contrast to the decline in the

age-adjusted death ra/Z for ischemic heart disease, the age- adjusted death rate for cancer has increased. Mean in This

small rise in the overall.- cancer statistics is a remarkable

increasea veritable epidemic,of cancer of the lung in both

men and women. In the past quarter century, deaths from

cancer of the respiratory tract tripled in the white population

and quadrupled in the black population. The remarkable maleto-female preponderence of lung cancer in the 1940s and 1950s

has been decreasing in the 1960s and 197 0s, the rate of increase

in lung cancer in males is slowing while the rate of increase of

-lung'cancer in females is accelerating. As a cause of death, lung

cancer in women is now secon ly to mammary carcinoma and will likely displace breast cance

*

asthe leading cause of cancer mortality in women in the 1980s (1) (see Figure 1).-

Thie 1964 Surgeoili General* Report reached the following

conclusion: "Cigarette smoking is causally related to lung

cancer in men; the magnitude of the effects of cigarette smoking

far outweighs all other factors. The data for women, though less extensive, pornt in the same direction" (IC. Since then, a number of retrospective and prospective epidemiologic studies,

experimental animal carcinogenesis studies, and studies of

human tissues at surgery and autopsy have confirmed a.)id extended those conclusions. Cigarettevno ing is the major cause of cancer of the lung in women. Tha sk_increases with the number of years the individual smoked, the number of ciga1 23 109
83

70

60

50

40

30

20

10

9

8

7

6

5

4

3

2

1950 1955 1960 1965 1970 1975 1980 4198E

-4-6th Rev --*--4-7th Rev.-0-4-8th Rev . 1983

-0.

t--

White Males

.. 4 "Breast ,

.Nonwhite Males

, ,

i---

, White Females

i .,,

i . 'Nonwhite Females *

1

FIGURE 1. Age-adjusted death rates* for malignant neoplas

of trachea, bronchus and lung,** by color and s(

compared to rates for malignant breast neoplasr

United States, 1950-1977; projection for whit

females to 1985.***

*Adjusted by the direct method to the U S population, 1940.

"ICD 6th and 7th Rev Nos 162, 163 and Kth Rev No. 162.

**Projection based on average annual rate of increase user last 10 years

SOURCE National Cancer Institute (25), National (enter fur Health Stati

ties t27)

rettes Voked, the "tar" and nicotine level of the cigarette smolt(

and the degree.of inhalation, and is inversely related to the ag

at which the ind.Ridual began smoking, being higher for tho:

who begin smoking at younger ages. The risk of developin

110 124'
cancer is diminished significantly by qu4ng smoking and is lessened somewhat by switching to low-tar, low-nicotine filter- tip cigarettes (43,45). Considerable evidence has also shown that cigarette smoking is a significant for women, and

bladder, ki ney, and pancreas. Mu-ch of this in

menof carter of the larynx, oral cavity, es hagus,'urinary

as been summarized in previous issues of "The Health Conse- quences of Smoking" or the Surgeon General's Reports (33-43). Table 1 lists the new cases and deaths estimated to occur in 1980 for those cancers which are causally associated with cigarette smoking (1). Smoking will contribute to 43 percent of the male and 18 percent of the female newly diagnosed cancer cases in the United States in 1980 and to 51 percent of the male and 26 percent of the female cancer deaths. This table does not imply that cigarette smoking causes each of these individual

cancers. It does, however, identify the impact of cigarette smok- ing on the major' cancers' now known to be associated with

cigarette smoking. Most of the cases of cancer of the lung and

larynx could 'have been prevented, as could a substantial pro- portion of the cancer deaths at the other sites listed. In this chapter, selected data on cancer and smoking among women will be reviewed and summarized. Where necessary for clarity, data previously reported will be summarized briefly.

Lung

The lung is a compleX organ lined by at least five types of epithelial cells, each of which theoretically mightve rise to one or more types of neoplasm. In addition to the epithelial.cells, blood vessels and connective tissue are prominent in the lungs. Both visceral and parietal portions of the lung are covered by synovial membranes, which also are subject to neoplastic trans- formation. The World Health Organization's classification of malignant tumors (Table 2) includes multiple histologic types, of which epidermoid, small cell, adenocarcinoma, and Large cell carcinoma are causally related to cigarette smoking and display

significant dose-response relationships in epidemiologic studies

(7,43). These four tumors are the most common histologic types of lung cancer in both men and women. However, there are differences in the distribution of the different types of lung cancer in men and women and in smokers and nonsmokers. Epidermoid carcinoma was the most common histologic type Of lung cancer in the male smoker, while adenocarcin4a was most common in the female smoker and in nonsmoker f both sexes in a series recently published from the Mayo Clinic (Table 3) (31). . 4.

125
A

TABLE 1.-Estimated new cancer cases and deaths for sites associated with cigarette smoking, 1980

E'stimak'd New Ca,e, Estimated Death, Site Total Male Female Total " Male Female

All Sites 785,000* 387,000 398,000 405,000 219.500 _A_ 185,500 Lung 117,000 85,000 32,000 101,300 74,800 500

Pancreas 24,000 6 12,500 11,500 '20,900 11,100 9,800

Urinary

Bladder 35,500 26,000 3,500 '10,300 7,000 # 3,300

Oral 25,500 17,900 7,600 8,800 6,100 2,700

Kidney &

Other

Urinary 16,900 10,500 6,400 7,900 4,800 3,100

Esophagus 8,800 6,200 2,600 7,600 5,500 2,106

Larynx 10,700

4 9,0004 1,700 3,500 2,900 600

All Tobacco

Related 238,400 167,100 71,300 160300 112,200 48,1(N) 43

'Carcinoma in SOU is not included There are 45,000 new (!xises of uterine cervical Arcinoma to situ each year Non-melanoma skin

cancer is not included Approximately 400,000 new cases of non-melanoma skin cancer occur annually SOURCE- American Cancer Society
TX131E 2.Worl Health Organization classification of

malignant pleuro - pulmonary neoplasms

I Epidermoid Caonomas

I I Small Cell Anaplastic Carcinomas

III Adenocarcinomas

1 Bronchogenic

a acinar

b papillary with or without mucin formation

IV Large Cell Carcinomas

14' V CoMbined Epidermoid and AdenocarcmoAias VI Carcinold neors

VII BronchiarGlind Tumors

1 Cyhndromas

2 Mucoepidermoid tumors VIII Papillary Tumors of the Surface Epithelium

IX Mixed Tumors and Carinosarcomas

X Sarcomas

XI Unclassified

XII Melanoma

XIII Me,,,othellomas

SOURCE Kreyberg, L ill

TALE 3. Histologic types of pulmonary cancers in smokers

and nonsmokers

Male

NonFemale

Non. Type Total Smokers Smokers Smokers Smokers.

Epidermoid 992 892 7 80 13 Small Cell 640 533 4 100 3 Adenocarcinoma 760 492 39 128 101 Large Cell '466 389 46 46 15 Bronchioloalveolar 6A4 35 4 13 li,

TOTAL 2,926 2,341 70 367 148

SOURCE Resenow, E C (31)

Other centers have similar data, although the proportions by histologic type may vary with the pathologic criteria used, patient population, geographic location, and other factors.

Earlier epidemiologic studies suggested that cigarette smok- ers were more likely to develop squamous-cell and small-cell

lung carcinoma than other types. However, more recent investigat ons indicate that all four major histologic types of lung

cancerincluding adenocarcinoma, which appears to be in- creasing rapidly in recent yearsare related to cigarette smoking`in both men and women (43). , 127 113
In 1980, of the estimated 117,000 newly diagnosed cancers of

the lung in the United States, 32,000 will be among women

There will be an estimated 25,500 deaths from lung cancer in

women 11)

In 1V509omen accounted for approxirtate12: I in 12 of all lung

cancer deaths. 13N 196.8 the proportion was 1 in 3; in 1979 women

dying of lung cancer will represent over one quarter ofall lung

cancer victims White women' hay e death rates from lung cancer

which are similar to those of nonwhite women, while the rates of

white males remai'n below,those of nonwhite males These chfferences may be due to differences in the smoking. habits of

blacks and 'whites described elsewhere in this report

Many prospective studies have found that the lung cancer

death rate for smokers was far in excess of the rates for

,nonsmokers in both sexes, as previously mentioned, te rates

for male smokers dramatically exceeded the rates for female

smokers,. However, E.A. en the nonsmoking male had a higher incidence of, and death rate from, lung cancer than the nonsmoking female (9) This evidence suggested that women might have

a decreased susceptibility to lung cancer A more careful

examination of the data indicates that most of the differences

between male and female lung cancer rates can be explained by

differences in smoking habits and occupational exposures.

As discussed in other ,sections of this report, a smaller percentage of women than men smoke and, when they do smoke,

they are more likely to adopt smoking behaviors that have been

shown to have a lower risk of developing lung cancer. That is,

they smoke fewer cigarettes per day, inhale less, start smoking

later in life, and are more likely to smoke lo-w-tar and lownicotint and filter cigarettes. In addition. it is important to con

sider the cohort effects on the differences in rates between

males and females. O'er 85 percent of those, who smoke regu

larly began between the ages of 12 and 25 (29). Men first began

to smoke in large numbers Just before and during the, First

World War. As each succeeding birth cohort passed through the

,age of initiation 112 to 25), a larger percentage began smokinp

until the groups horn between 1915 and 1930 were reached (17)

In the birth cohorts born after 1930, fewer began to smoke regu

lady., The risk'of developingrinng cancer increases exponen

tially with age and duration Elf smoking, with the increase start

ing 15 to 20 years after the beginning of regular smoking Thi(

accounts for the dramatic nse in the male lung cancer deati

rates noted in the 1930s. As those birth cohorts with highe

smoking rates replaced those with lower smoking rates, thi

age-specific lung cancer rates rose steadily. ands each of au

heavy-smoking birth cohorts grew older, their king cancer risl

114

123 ,
continued to accelerate, resulting in a very steep rise in he . overall male lung ancvr*death rate.The overall cancev ates among men will continue to rise (albeit more slow s those birth cohorts with the he'Sviest smoking prevalence replace those with lower prevalence in the older age groups where the lung cancer death rates are the highest. As these birtli cohorts with high smoking prevalence pass through the age groups and are replaced by birth cohorts with lower smoking 1)revalence, declines in lung cancer rates should be noted

They -hould be noted first in the age-specific death -rates, for the younger age groups and later in the overall lung cancer death rates The first indications of this change have been noted with a decline in the age specific death rates it males born after # 1930 Jt is therefore important to consider this cohort effect 'when examining the differences between lung cancer rates of men and women. , Women began to take up smoking in large numbers 20 to 30 years later than men in the early 1940s) This rise in smoking prevalence w as produced by predominantly young women first using tobacco as cigarettes This is in contrast to the rise in men which included a substantial percentage of men of all ages who switched from other forms of tobacco use to cigarettes. The rise in lung cancer rate, tewomen occurred as those cohorts with high smoking prevalence reached the ages where lung cancer occurs with significant frequency (age 45 and over. Sincemost of these women began smoking cigarettes prior to age 25 they would'have at least 20 years of exposure by age 45 in contrast to the shorter durations of exposure at age 35 for those men who switched to cigarkttes from other forms of tobacco around the time cigarettes first came into widespread use. This greater du- ration of exposure at any given age for women in these first heavy smoking birth cohorts compared to the first cohorts in men. s ould result in a more abrupt rise in lung cancer rates in women . This rapid rise in female lung cancer death rates%egan to be observed in te late 1950s. As birth cohorts with higher smoking prevalence continued to replace those with lower smok- ing prevalence, the rates rose steeply, reproducing the phenomenon noted in males 20 to 30 years earlier with some indication that the rise is even steeper for women. If one sub- tracts 25 years from the female cancer death rates in Figure 1, the rates for women are only slightly below the rates for men. This small difference is explained by lower prevalence of.smok- ing and less hazardous smoking patterns of women and their less frequent exposure to occupational carcinogens Thus,- close scrutiny of the trends reveals no substantial protective effect for women on the risk of developing lung cancer but rather leads to a

115

12,E
TABLE 4.Age-adju.sted lung cancer mortality rAiosag4

began smoking and degree of inhalation

Age Begat Smoking Male Ferna le

15 16* 25

14 7 5 0

20-24 10 1 3 4

2- 4 1 2 3

Depth of in-haiat on Male' Female

None

Slight

Moderate

Heavy

tt 0

13 1

1'70

20

23

35

1 S(tURt_ F. Hammond E

TABLE 5.Age-adjusted relatise risks of lung cancer by number

of cigarettes smoked

Ai S Stud:.

Number of Cigarette,

Smoked Daily

1 10-19 20-39 40-

Male 46 *6 147 Ins

Female L.1 2 4 4,9 7 5

1-14 15-24 25-

Br-lush MaleN 7 ), 12 7 25 1

P1-*gictant., Female 1 3 I/ 6 4 2'9 7

SOUR( E Doll, R ,6,x), Hammond. F (11,

sobering projection of a reproduction of the male lung cancer

epidemic in women (Figure I).

GEOGRAPHIC DIFFERENCES

Lung cancer death rates, including all his logic types, are

highest in industrialized counthes where th e has been e

higher smoking prevalence for longer time. Women in Scotland

have one of the highest death rates from lung cancer of worncen of

any country. Their tobacco consumption persmoker approaches

thatThrEnghsh and Welsh men 1 19). Current tobacco consump

tion by Scottish women is only a little lower than the consump

tion of Scottish men 20 years ago. In England and Scotland

where 'the upper socioeconomic classes have reduced then

116

1;31
TABLE 6.Lung cancer mortality ratios for females by duration

of smoking: Swedish study

Duration of SmokIng Mortallt in Years Rat,o,

Nonsmokers 10

:.ears

1 t' 30- !.ears

' 01:R( E t eqer,of P.

cigarette consumption in recent decades, there is a significantly greater lung cancer mortality rate in the lower socioeconomic classes among women (19).

Age-adjusted death rates for lung cancer in women in select countries indicate that women in Hong Kong have the highest rates, while those in Scotland are second and those in England and %Vales are third The United States ranked sixth world wide (1).

Among nonsmokers, lung cancer is found slightly more often in urban than in rural areas; however, the marked increase in lung cancer among smokers in urban areas suggests that urban living exerts a potentiating rather than an additive effect on the inci- dence of lung cancer. Urban living has little independent effect on lung cancer induction in comparison with even modest smok- ing of filtered low-tar and low-nicotine cigarettes (5,10).

SMOKING PATTERNS AMONG WOMEN

Although women tend to have different patterns of smoking than men, the relative relationships betWeen smoking-and lung cancer are the same. Lung cancer rates for women who smoke

increase with increased dosage as measured by several dosage measures, including number of cigarettes smoked per day, dura- tion of smoking habit, degree of inhalation, age of initiation of smoking, and the "tar" and nicotine level of the cigarettes

smoked. These data, obtained from several prospective investi- gations, are examined in Tables 4, 5, 6, 7, 9, and 10. The more cigarettes an individual smokes, the more likely that individual will die of lung cancer (Table 5). Overall, female cigarette smok- ers have 2.5 to 5.0 times greater likelihood of dying from lung

cancer than nonsmokers (Table 7). As discussed earli.2/-, when the full impact he cohort effect' is felt, this ratio will probably approach that for men (8 to 12). Doll, et al.studied the' cause-specific mortality experience among approximately 6,200 female physiciansin England during

131

117
TABLE 7. Lung cancer mortality prospective studies

At

Agk Atusted Lang I amer Death Relatle R:sks

Ma,e

Fema,e

Br It:sr. Ma,e,

P'r an Ferna,k

SAedIst- Stud; Mate

Femme

(_Igarette,

Nonsmoker- Smokers

u 101

U 14v

1u 50

: x2

10 45

E ederiof R R Hammond, E

the period 1951 to 19:73 ( 6). T e results of this study are presented

.in detail in Table 8, which also includes data from a pie-vious

report on male physicians (8). It is apparent that smoking and lung cancer are similarly

related in men and women. In both sexes, lung cancer mortality

- was at least three times as high in ever-smokers as in neversmokers, at least twice as high in current heavy smokers (more

than 25 cigarettes) as in light smokers (less than 15 cigarettes),

and exhibited a significant dose-response relationship. The

magnitude of the smoking effect on lung cancer for females and

males was approximately the same. The relative risks for mortality from lung cancer for moderate (1:5 to 23 cigarettes per dap

and heavy (more than 25 cigarettes) smokers were 6.3 and 29.7

among females, and 10.6 and 22.4 for males.

. The authors emphasize, however, that no wit lusions can bE

drawn from this data about the ma nitudle of thebrologic effects

of smoking in men comp red to w men. Since the authors doc

umented .differences in lifetime smoke exposure (later age al

initiation and lovier pre,. alence of inhalat on among females)

lifetime smoking exposures between the sees were not directly

comparable. This issue will be resolved only when studiei

ex amin'e the effect of smoking in cohorts of women whos(

lifetime smoking behavior more closely matchesthat of the mer

to whom they are compared. - A number of retrospqtive studies have ;txa`iniried the rela

tionship of smoking andiung cancer in women. The 1971 HealtI

Consequences of Smoking reviewed many of these nivestilka

tfons and showed a smoke -to-nortsmoker risk ratio. rangirn

from 0.2 to 6. 8 fur femalesl.T e reader is referredto this volum,

for a more detailed scussion of these studies. Results of thes,

investigations rove sex differentials similar to those foie u

118

13,
ABLE k.Death rates from lung cancer and smoking Chit when last asked, British physicians 1951-1973

Annual Death Rate per 100,000

Persons Standardized for Age X2 - -

( urrent SmokersDose Per Day Nonsmokers' Trend 'total (is (Dose Popul * Deaths Nonsmokers Ex-Smokers 1-14 15125 25- Others Rey rnse)

Women 6,194 27 ., 23 9 , 45 20kc 13 47* 61 59'

(cigarettes only.

Men 34,440 441 10 43 52 106 224 419' 19704'

(any tobacco grams) "

(1 gram 1 cigarette)

.(p- 001)

SOUR( E Doll, "ft (6,)0`

133
TABLE 9.Age-adjusted lung cancer mortality ratios* for male and females, by tar and nicotine (TIN) in cigarettes smoked

Males Females

High T N

1 00 Medium T N 1 00

0 95 0 79 Low T N 7,1 060

The mortality ratio for the categor!, with highest risk was fnade 1 04 at the relative reductions

'.isualized in risk with the use of over T N cigarettes coupe

SOURCE Hammond, E C 11i

the larger prospective studies, with males having higher overall lung cancer rates compared' to females. However, the lung cancer rates of smokers are significantly higher than those of nonsmokers for both sexes.

The women who smoke low-"tar", low-nicotine cigarettes have ") a lower age-adjusted lung cancer mortality rate than women who smoke high-"tar", high-nicotine cigarettes. Women who smoke medium-"tar", medium-nicotine cigarettes have mortal- ity rates in between (12) (Table 9). However, even the low-"tar" and low-nicotine cigarette smoker has a rate substantially higher than the nonsmoker. These data suggest some benefit from smoking low-"tar", low-nicotine cigarettes. However, a further comparison of women who smoked less than one pack of high-"tar", high- nicotine cigarettes daily with women who smoked more than one pack of low-"tar", low-nicotine cigarettes daily nevealed that thgr smoker of more than a pack a day of low-"tar", low- nicotine cigarettes had over twice the age-adjusted lung cancer mortality rate of the woman who smoked fewer cigarettes, but with high "tar" and nicotine (Table 10). In a retrospective study standardized for duration of smok- ing, number of cigarettes smoked, inhalation and butt lengtit

long-term female smokers of filter cigarettes had a lower rela- tive risk of developing cancer than smokers of non-filter cigarettes (46).

CESSATION OF SMOKING

Although the risk of developing lung cancer increases with age, both for smokers and nonsmokers alike, women in good health who quit smoking will, over a period of years, experience a reduction in their relative risk of developing lung cancer. About 15 years after they have quit smokink, the risk of devel- oping lung cancer approximates that of the nonsmoker.

120
TABLE 10.Age-adjUsted lung cancer mortality ratios* for males and females, comparing those %4ho smoked a

few high tar and nicotine (TN) cigarettesμ ith those vho smoked many lov. TN cigarettes

Malef

1-19 high TN

cigarette, day

I 111)I I 151

TN

igarette, day

1r,

'1

'The rr,,rtaiit2, ran, fur t he ( with was made 1 the n rea,e in risk with -mok,ng more cigarette, day could he illustrated SOUR( E Hammond, E 11,

EXPERIMENTAL CARCINVENESIS

Tt;bacco tars, tobacco smoke, and single or mixtures of chemicals found in tobacco smoke have been used with t arious species of animals in carcinogenesis experiments involving skin paint- ing, subcutitneous injections, tracheobrom)hial implantation, and or instillation and inhalation. Some experiments have re- ported sex differences in the occurrence of lung tumors following exposure to chromium oxide 426,.

However, in a recent monograph on lung cancer, separate re- views on tobacco carcinogenesis, radiation carcinogenesis in the respiratory tract, and experimental models for studies of respi- ratory tract carcinogenesis did not yield informatipn suggesting that the male lung of any of the species studied was more sus- ceptible than the female lung to carcinogenic action by either

tobacco products or radiation (16). The reader is referred to pre- vious Smoking and Health Reports for summaries of experi- mental tobacco carcinogenesis studies.

Larynx

The larynx is a small, complex structure, which produces

speech, controls the flow of air in and out of the lungs, and

prevents aspiration during swallowing. In 1980 there will be an estimated 1,700 new cases of laryngeal cancer and 600 deaths

from that tumor in U.S. women (Table 1). Laryngeal cancer has occurred predominantly in men, but more and More women are developing laryngeal cancer as their smoking and drinking

habits come to approximate those of men. The rrIale-to-female ratio for laryngeal cancer exceeds that of Lung cancer. Laryngeal cancer occurs in'the fifth, sixth, and sevenkdecades both i men and women. While the disease is uncom-ton, its m eld has continued to rise over the past 4uarter century,

121

135
especially in vomen, substantially because of changes in then

smoking habits.

Cancer can occur either in the glottis (true cord. TO percAt u

cases), or in the subglottic or supraglottic region (false curd. 2:

percent of cases). Usually the neoplasm is epidermoid car

cinuma when examinenistulugically. Since a tumor that inter

feres with speech gives rise to early symptoms, gluttic cancer(

are usually di4gnosed at an early stage and are curable in ove)

60 percent of the cases. When the tumor arises in the subglottit

or supraglottic.region. interference with phonation ur speed

ma3. not occur as early as when 'neoplasm begins on the glottis

The tumor ma}. therefore. reach a greater size and be accom

panted b3. significant local tissue invasion and destruction a:

well as metastasis. Patients with tumors discovered when the

are still localized in the larynx have approximately an 80 per

cent cure rate, while ad nct11esions have a 33 percent 3 -yea

urvivairate.

Laryngeal cancer diplays a strovig dose -respunse relation

ship with smoking, increasing with the /number of cigarette'

smoked per day. the "tar" and nicotine content of the cigarette,

smoked, the depth of inhalation and number of years cigarette,

were smoked. The risk of developing laryngeal cancer is in

ter,:el, related to the age at w hich smutting began (43). Aloe

risk for laryngeal cancer has been demonstrated in women wilt

used filtered cigarettes fur 10 years or more compared:to those

v hu smoked nun-filtered cigarettes. Nonetheless, the risk re

mained well in excess of that experienced by nonsmokers (45).

Excessive Utik' of alcohol by nonsmokers also results in an in

creased incidence of laryngeal cancer Heavy drinkers u

alcoholthat is. greater than seven ounces of whiskey or it:

equiwlent per day v;ho also smoke cigarettes have a greate

risk of developing laryngeal cancer than if they either smoke(

ur drank to e...«.ess alone. There is a synergistic effect of smokini

and drinking on laryngeal cancer development (43,44)

When wo quit smoking, their relative risk of developini

larynge' cancer decreases until 10 years after cessation IA hei

their ri approaches that of the nonsmoker (45).

A nu er of investigators have found an association betueel

exposure to asbestos and the submcquent dt,selupment o

laryngeal carcinoma (43).

Oral

Oral neoplasms im ludo ( ancer of the lip, tongue. gums, hucca

mucosa. hard and soft palate, salivary glands. floor of th,

mouth, and orophar3.hx. In the United States for 1980, then

122

13 G
. will be 17,900 new cases in men and 7,600 in women,Jetultibgin 6,100 clecths in-men' and 2,700 deaths in women (1). While dif- ferent histological types of cancer can 'occur in ttis group, squamoUs cell carcinoma is by faAhe most common, except for the tumors of th,e salivary glands. Five-year survival rates range from 25 Derce'nt in those extierits whose tumor is ad"-' vane when first diagnosed to 67 ,percent r those whose tumors localized at diagAsis.

. . In women, oral cancers ac nt for 1.9 percent of all neoplasms, while they account for 4.7 pliknt of all Cancer occurring in men. Deaths from the various oral cancers account for 1.4 percent of cancer deaths in women and 243 percent of all'cancer deaths in mert'Cigarette, pipe and/or cigar smoking are all associated with increased oral cancers. Heavy alcohol use (over rounces pZr day) hag been shown to be an independentCausative factdr (32,42). Wheni,both are used together by women or men, synergism results in an evell'gre.ater incidence of oral cancer (3). PooT oral hygiene or inadequate dentition_Aalso a risk factor (15). M.ost of the prospOrive epidemiologic studies have concen- trated on men. In Japan a large prospective study- showed the Mortality ratio1Por oral cancer,to be 2.88 for the, male cigarette smoker and 1.22 for the female cigarette smoker compaAd with the nonsmoker.

. Leukoplakia or'an abnormal thickening and keratinization of thv oral mucous membrane is recognized as a precancerous condition. While foupd in the western world, it is most common Iin Asian countries where a miOure of tobacco and betel nut or lime ash chewing is common, and in those countries where re- verse chutta (cigar) smoking occurs. Women in certain regions of India are more likely to engage in reverse' chutta smoking ,' than men, although both women and men develop carcinoma of the hard palate after years of revers&chutta smoking Ve (30). Women and men with mouth, p r , and larynx cancer who continue smoking after surgicalrt encof the first neoplasm have a 40 percent probability of developing another neoplasm of the head and neck. Only 6 percent of the patients who quit , smoking develop a sec &id cancer in the region. Less than 10 percent °fora' cancer patients are nonusers of Tobacco; almdst , ,a1) ,ha won:differentiated carcinoma and 4 relatively high cure ra. 43). --\ `----)1

Esophagus

,Carcinoma of the esophagus will be diagnosed in 6,200 men and 2600 women in the United States in- 980 ('l). The American Cancet Society estimates that there will be 5,500 deaths in men

123

1 3
and 2,100 deaths in women from this disease (1). Median survival time once esophageal carcinoma is diagnosed is 6 montis

The 5-year survival rate is only 3 percent. Esophageal ea

cinuma rates have declined in the white population aver t

past 25 years. However, they have increased in the'llaa

in'both sexes. This may reflect genetic ur environmental

factors. In the Caspian littoral, there is dremarkable difference

in esophageal carcinoma incidence in ptrople of comparable

background and sucluecunonlic status living only 400 kilometers

apart. There is a 30 -fold higher incidence in women living in the

desert northwest section of Mazandran, Iran, compared with

the fertile Caspian rainbelt 400 kilometers to the west (20).

Data from a number of retrospective studies show that smoking increases the risk of develop+ng esophageal "carcinoma,

Neither the relative risk of developing esophageal carcinoma

nor the steepness of the dose-response relationship with

cigarette smoking is as great as it is for carcinoma of the lung or

larynx (45). Indixiduals 'who stop smoking pr switch to low-tar,

#1uw-nicotine cigarettes will, afteF a lag period, experience lower

relative risks of developing esophageal carcinoma, although the

fall-off is not as steep as with lung and laryngeal_ cancer. In the

male, both retrospective and prospective studies show that pipe

and cigar smokers have mortality rates from esophageal car-

--onoma similar to cigarette smokers. There are no prospective

epidemiulugic studies of female smokers in this country large

enough to permit development of a mortality ratio comparisor

to nonsmoking females. Ingestion of alcohol is also a major etiological factor in

esophageal carcinoma. A dose- response relationship exists

with increasing alcohol ingestion resulting in an increased incidence of esophageal carcinoma. As in the larynx, synergism of

tl carcinogenic effect un the esophagus occurs with the use of

both tobacco and alcohol 445). Whether or not nutritional deficiencies, which occur frequently with severe, chronic al

coholism, play a role, in carcinogenesis remains unknown, at

does the possible contribution of chronic iron deficiency found ir.

Plummer Vinson's syndrome (Paterson-Kelly syndrome, sid

eropenic dysphag:ia). Ninety-eight percent of esophageal Cancan's are hisologicall3

squamous cell in type. In an autopsy study, Auer ach fount

more abnorm_ the esophageal tissues including atypi

ca.+ nuclei, (7siitregrated nuclei, hyperplasia and hyperactivi

esophageal glandsof tobacco smokers as compared witl

nonsmokers (2). Esophageal carcinoma can be produced experimentally b!

both benz(a)pyrene and the nitrosamines. Both benz(a)pyreni

124

1 vs"
and a group of nitrosamines have been identified in tobacco

smoke. The appearance of experimentailly-duced squamous

cell carcinomas can be accelerated by dissolving dike carcinogen

in alcohol, a laboratory experiment duplicated daily by

thousands if not millions of our citizens (43).

Urinary Bladder

Cancer of the urinary bladder will occur in 26,000 men and

9,500 women in the United States during 1980 and it will kill.

7,000 men and 3,300 women (1). Cancer of the urinary bladder is

frequently multicentric in origin. If found while still localized in

the bladder wall, the 5-year survival rate is 72 percent, in contrast to 14 percent for those patients whose disease had already

spread when the diagnosis was first established (1).

Bladder cancer has been associated with occupational exposure to aniline dyes, leading to the study of aromatic amines as

potential carcinogens. 2-Naphthyla mine, xenylamine, benzidine, and 4-nitrobiphenyl have all been implicated (43).

Numerous retrospective studies have shown a relationship

between smoking and urinary bladder carcinoma in both men

and women (17), The likelihood of either women or men developing bladder cancer increases with the numb r of cigarettes

smoked, the duration of smoking,"and tar an .icotine content

of the cigarette smoked. Changing to I -tar, low-nicoti-ne

cigarettes or more clearly, cessation of smoking, decreases the

relatilvthvisk of developing bladder cancer. The risk of an exsmoker 4veloping urinary bladder cancer approaches that of

the nonsmoker years after cessation (46). In prospective studies 'in Japan and Sweden, women who

smoke are 1,6 to 2.7 times as likely to develop bladder cancer as

nonsmokers (3,N): In an international study of successive bulb

cohorts in the United States, United Kingdom, and Denmark,

Hoover and Cole found increasing rates of bladder cancer assogated with increased cigarette smoking in men and women in

both suburban and rural areas and in all nationalities studied

(17). It has been estimated that 30 percent of urinary bladder cancer in women can be attributed tto cigarette smoking (43).

Kidney

Cancer of the kidney will occur in 10,500 men and 6,400 women

in the United States during 1980 (1). Some 4,800 men and 3,100

women will die of renal carcinoma (1). The 5-year survival rate

is between 40 and 50 percent (1). While the overall classification

of kidney carcinoma includes tumors of the renal pelvis and

125

3,9
ureter, the largest number of kidney carcinomas occur in the

renal parenchyma and are adenocarcinomas.

Ift retrospective studies, adenocarcinomas of the kidney are

found more frequently in smokers compared with nun-smokers

in both men and women (43,44). In a large prospective study

among U teterans, the kidney carver mortality ratio >,nct from 1 0 (the baseline fur nonsmokers) to 1.34 for those

who smoked 10 to 19 cigarettes daily and to 2.75 for men who

smoked two packs or more each day ( 18). :Sularge scale prospective

study of women, and kidney cancer has been 'reported to date.

l'4nc reas

Carcinoma of the pancreas will occur in 12,500 men and 11,300

women in the United States during 1980, and 11,100 men and

1,,so0 women will die of pancreatic c arcinuma (1). During the

past 25 years, there has been a steady increase in both the incidence and mortality due to pancreatic cancer in both men and

women (1,21) Among the common human neoplasms, the rate of

increase of pancreatic ancer ()ter the past quarter century has

been second only to that of the lung.

Most pancreatic carcinomas are adenocarcinomas, arising

from ductal cells (24). Most are relatitely undifferentiated in

cell type. The median sun. Lt al timNtom histologic proof of diagnosis to death io 3.:; ,months in et and 4.5 months in

v.-omen. Sur\ it al time taries little witfiage at time of diagnosis,

duration of symptoms, location of primary lesion (head, body, or %,. tail of pancreas) or eten degree of dIftWptlatiun. The 5-year

survit al rate is onepeNynt," the most fli al survival r - for

any of the common ntoplasins'of eitheme ().f women

Retropective studios relating std g ti) pancreati . carcinorna I5at e been reNlewed in previous reports. In a prospective

study 41143,000 won n, the pancr,sealicsancer mortality ratio

, r, was 1.9i ii)r Japanese women smoKtes eompared to nonsmokers

(14) In Swederko a smaller prospective study' showed that the

mortalityfratio fur panereatic,citu'eT w as fur v.umen- smokers

compared ro //me n. korilltriqkeK; (

In the Urtited Statesc`the male to emalt ratio of,pancreatic

cancer v. ag 1.6 in t 940.s>. It has decreased to the current

estimate 3-1.17 for. . consistent with the decreasing

male to female ralt,los and laryrngeal carcinomas.

Summary 114'.

1 Cigarette smoking is causally associated with cancer of the

lung, larynx. oral Kati ;sand esophagus in women as };,ell as in

men, tt is also associated with kidney cancer in women.

126 (04

. 1 .
. Cigarette smoking accounts for 18 percent of all newly diag- ed cancers and 25 percent of all cancer deaths in women. In 1 80, 26,500 of the estimated 101,000 deaths, or over one-quarter of the deaths expected from lung cancer, will occur in women. 3. Women cigarette smokers have been reported to have be- tween 2.5 and 5 times greater likelihood of developing lung cancer than nonsmoking women.

4. Among women the risk of developing with increasing lung cancer,increases number of cigarettes smoked per day, duration of the,smoking habit, depth of inhalation, and tar and nicotine content of the cigarette smoked. The risk is inversely related to the age at which smoking bega,n. 5. A dose-response relationship has been demonstrated be- tween cigarette smoking and cancer of the lung, larynx, oral cavity, and urinary bladder in women. 6. The, rise in lung cancer death rates is currently much steeper in women than in me,n. It is projected that the age ad- justed lung cancer death rate will surpass that of breast cancer in the early 1980s.

7. The rapid increase in lung cancer rates in women is similar to but steeper than the rise seen in men-approximately 25 years earlier. This probably reflects the fact that women first began to smoke in large numbers 25-30 years after the increase in cigarette smoking among mep. Thus, neither men nor women art protected from developing lung cancer caused by cigarette smokipg.

8. Cigarette smoking has been causally related to all four< the major histologic types of lung cancer in both women aiA men, including epidermoid, small cell, large cell and adenocar- cinoma.

9. The use of filter cigarettes and cigarettes with lower levels of "tar" and nicotine by women is correlated with a lower risk of cancer of the lung and larynx compared to the use of high-"tar" and nicotine or unfiltered cigarettes. The risk posed by smoking low-"tar" Figarettes, however, is clearly greater than that among females who never smoked. 10. After cessation of cigarette smoking, a woman's risk of developing lung and laryngeal cancer has been shown to drop slowly, equalling that of nonsmokers after 10-15 years. 11. Excessive ingestion of alcohol acts synergistically with cigarette smoking to Increase the incidence of oral and laryngeal cancer in women.

1

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I'

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4-

s-

.4.

f

7.

1,45

4

N
NON-NEOPLASTIC BRONCHOPULMONARY DISEASES

Introduction

Chronic non-neoplastic bronchopulmonary disorders are a major cause of death and disability in the United States, Chronic obstructive lung diseasps (COLD), including chronic bronchitis and emphysema, comprise the majority of these illnesses In 1977, they were responsible for nearly 46,000 deaths 11.14 millions of dollars in social security disabilit:.1+payments,- ranking second in ectinomic cost only to heart disease 42). Previous U.S Public Health Service reports on the health A consequences of smoking have presented evidence that cigarette smoking is ..the major cause of COLD (55- 64). The

studies on whi(...h this is based have focused primarily on male populations. This reflects the scienti interest generated by the overwhelming male-to-female ratio the prevalence of COLD at the time these studies began. However, recent mortal- ity statist!cs indicate a substantial increase 'in the death rate from COLD among women (see Mortality action). Although this increased death rate may partially reflect a greater aware- ness and recognition of COLD, its magnitude suggests a true increase in frequency of COLD among women. The follbwing text reviews a large number of studies analyzing the relatain- 'ship of smoking to COLD These studies include appreclrble numbers of women, and many suggest that smoking may affect men and women differently Nevertheless, cigarette smoking remains the most important cause of COLD regardless of sex or other variables.

Definitions

The terms chronic bronchitis and emphysehia have been used, diagnostically for many years Physicians often use these terms interchangeably to describe a patient with chronic airflow

obstruction. These conditions are, however, difficult to distin- guish from each other in patients with chronic airflow obstruction because (a) both conditions may be present in the same patient; (b) both disorders are characterized by expiratory flow obstruction; and lc) patients with either disorder frequently

have the same symptom dj,:spnea on exertion. Consequently, the clinician often labels the patient with chronic airflow, obstruction as having chronic obstrUctive lung disuse cCOLD). Many attempts have been made to establish criteria for the diagnosis of chronic bronchitis and emphysema (1,27,28). The most e12, accepted definitions in the United States are those

135

I IG
.4

TABLE 1.Age-adjusted death rates from COLD tICDA*Ii90 -492

and 519.3) 1960-1977 (per 100,000)

Whnte Nonwhite

Male Female Male Female

1977 334 10 7 r4 i, 35'

19;6 / 335 101 149' 32

1975' 32 1 9 1 13 5 3 3

1974 ;1 1 x4 137 2x

1973 11 4 7 >_< 141 30

1972 299 70 140 29

'.416/71' 2i5 6 6 5 13 2 3 0

1970 2x2 60 133 26

1969 273 54 12e 24

196* 22 3 3r 137 25

1967, 199 31 1:5 200 196. 19 7 30 110 19

1,A5 1x4 27 104 1 5- ,'1964 16 1 2 4 9 2 1 6

1963 159 23 95 ( 19

1962 13 1 20 7 7 1 is 1961 109 17 70 13

1960 4 104 1.7 67 14

SOUR('E National Center for raA '42)

of a joint committee of the American College of Chest Physi

clans and the American Thoracic Society (1).

-Bronchitis. A non-neoplastic disorder of structure or func

tion of the bronchi resulting from Infectious or noninfectious

irritation. The term bronchitis should be modified by appropriate words or phrases to indicate its etiology, its chronicity, the

presence of associated airways dysfunction or type of anatomic

change. The term chronic bronchitis, when unqualified, refer

to a condition associated with prolonged exposure to nonspecific

bronchial irritants and accompanied by mucous hyperseCretior

and certain structural alteratio'ns in the bionchi. Anatomic

changes may include hypertrophy of the mucous-secreting ap

paratus and epithelial-metaplasia, as well as more classic evi

dence of inflammation. In epidemiologic studies, the presenc_e of

cough or sputum production on most days for at least 3 months

of the year has sometimes been accepted as a criterion for drag

nosis.."

"Pulmonary Emphysema. An abnormal enlargement of the

air spaces distal to the terminal nonrespiratory bronchiole, ac companied by destructive changes of the alveolar walls. The

term emphysema may be'modified by words or phrases to indi

cite its etiology, its anatomic subtype, or any associated airway

dysfunction."

136

11
"Chronic Obstructive Lung Disease: This term refers to a disease of uncertain etiology characterized by persistent slowing of airflow during forced expiration. It is recommended that a

more specific term, such as chronic obstructive bronchitis or __!./ chronic obstructive emphysema, be used whenever possible."

It should' be noted that these definitions may have serious

inadequacies, particularly when applied to longitudinal studies assessing the natural history of COLD (29,52). In the following discussion, these limitations are recognized.

Smoking and Respiratory Mortality

Recent mortality statistics indicate a striking increase in

death rate from COLD among women (42). These data presented ,in Table 1 indicate a n6arly fivefold increase in reported mortalities due to COLD from 1962 to 1977 among white females and

a twofold increase among nonwhite females. Mortality rates- from these conditions for white and nonwhite males have also

increased since 1967 (by factors of 1.9 and 1.5, respectively), but the rate of increase has not been as steep as that for women. Seven large prospective studies have shown a greatly in- creased mortality from COLD among smokers as compared to

nonsmokers (14,18,19,31,32,37). These studies, presented in Table 2, represent over 13 million subject years of observation, and approximately 270,000 deaths from all causes. Thentimber

of deaths related to COLD is probably underestimated sing, some of the deaths attributed to pneumonia or myocardial dis- ease may have been due to complications of COLD. In addition, these mortality figures do not include an appreciable number Of

individuals for whom COLD may have been a niajor contribut- ory cause of death. For example, it is not uncommon for individuals to have COLD and lung cancer simultaneously. Two of these prospective studies have included significant numbers of women. Hammond prospectively followed 1,003,229

subjects aged 35 to 84 (31). Nearly 93 percent of the survivOrs were observed for a 12-year period. Death rates from em- physema among women were much higher in cigarette smokers

than nonsmokers. "Heavier" smokers (defined as either smok- ers of 20 or me-re cigarettes a day regardless of age when smOlting was begun, or smokers of 10 or more cigarettes a day who had begun smoking before age 25) had a sevenfold inereaEied mortality rate as compared to nonsmokers. Cederlof et al. followed 55,000 Swedish subjects aged 10 to 69 for 10 years (14). The overall mortality rate from all causes among female smok- ers was 1.2 times higher than that of female nonsmokers. The death rate from bronchitis, emphysema, and asthma among

* . 137

14g .
TABLE 2.COLD morality ratios + in seven prospective studies

Women in 25 Men irr25

Study British States States U S Canadian Men in Califoitua Swedish ISubject (Reference) Doctors 45-65 45-64 65-79 Veterans Veterans 9 States Occupations Fe.knales Male (18) (31) (31) (37) (8) (32) (19) (14),

Emphysema

and or

bronchitis 242 1d08 2 30 4 3

Emphysema

without .._ bronchitis 4 89 6 55 11.41 14 17 7.7

Bronchitis 4:49 11 3

Bronchitis,

emphysema

and asthma

2.2 3 7

Deatate for smokers divided by death rate of a comparable group of nonsmokers. For afrages combined, increased mortality rate significant only for former smokers.

J. 1.

1
female smokers was 2.2 times that of female nonstolie;s. How- ever, the number of deaths due to COLD among women was small in both of these studies; consequently, the relationship with smoking is more difficult to evaluate. Nevertheless, a sig- nificant excess risk for reported mortality from COLD was pres- ent for female cigarette smokers as compared to female nonsmokers.

Data collected by Doll et al. examine the association of smoking and cause-specific mortality in 6,194 women physicians in England, observed prospectively over the period 1951 to 1973 (17). Table 3 presents the results of this study, including previ- ously published results of a similar study among male physi- cians over the same period (18)./The association of smoking and chronic bronchitis clearly observed in males was confirmed in women physicians. For both women and men who reported smoking 15 or more cigarettes per day, the mortality rate due to

emphysema and chronic bronchitis was more than five times as great as in nonsmokers. In both sexes, mortality due to em- physema and chronic bronchitis was more than double that of

nonsmokers, was at least three times as high in ever- 'smokers as in never-smokers, and was at least twice as high in current heavy smokers ( _25 cigarettes) as in light smokers ( -s.15 cigarettes).

The risk of death from emphysema and chronic bronchitis as- sociated with smoking was approximately similar in men and women. For moderate (1 to 14 'cigarettes per day) and heavy ( 325 cigarettes per ,day) smokers, compared with nonsmokers, the relative risk of death was 28.5 and 32 for women, respec- tively, versus 16.7 and 29.3 for men. In this data, as well as that for lung cancer, there is no support for the contention that wolf-len are less susceptible to harmful effects of smoking thah are men. The authors emphasize that no conclusions can be drawn from this data about the magnitude of the biologic effects of smoking in men compared to women. Attempts to document differences in lifetime smoke is posure (later age at initiation and lower prevalence of inhalation among females) demonstrate that lifetime smoking exposures between the sexes are not comparable. This issue will be resolved onlj when

studies examine the effect of smoking in cohorts of women whose lifetime smoking behavior more closelymatches that of the men to whom they are compared. In comparing the relative risks for mortality from COLD in female and male smokers (Table 2), it is apparent that female smokers have lower reported mortality rates than their male counterparts. This difference in mortality rates may be due to differences in female smoking patterns (31). Women tend to

139
4

41.

TABLE 3.. Death rates from dironic bronchitis and emphysema by smoking habit when.last asked, &ILIA

physicians 1951-1973

- .A

Won

'Total

Popul. # Deaths

. 6,194 . 13

a . :4 ,440 254

Annual Death Rate Per 100.000

Persons Standardized for Age

- 60

X2

Non.t

Smplers

23 S.

Ex-

(Smokers

Current SmokersDose Per Day . bnsmokers

v8. N... Trend

( Dose /

1-14 15-25 ) -25 -Response)

64

88

All Other;

' '10

44

21

.38

.57

(cigarettes onry)

50

12.34'

25158'

26.64".

A'

47,23'

any tobacco/grams)

(1 gram = 1 Cigarette)

""

-0,0011

SOURCE: Doll, R. (17,18)

j

4

F
smoke fewer cigarettel, inhale less deeply, and begin smoking

later in life than men. They more frequently smoke filtered and

low-tar and ;nicotine cigarettes and have less occupational exposure to lung irritants than men. Recent data suggest that

women are manifesting smoking patterns similar to those of

men. Moreover, mu omen are joining the labor force, including occupations w e e ex"Rgsure to lung irritants may occur.

(See section on Occu ational Exposures.) Whether these women

will continue to ha e mortality rites different from thuse,f

men remains to be d rmined. , In summary, recent statisticsindicate a rise in the reported

death rate due to COLD among women. The two large prospective studies that included appreciable numbers of women found

significantly higher mortality rates due to COLD among women

smokers as compared to women nonsmokers. This relationship

was accentuated in htavier smokers. Mortality rates from

COLD among female smokers are considerably lower than

among male smokers. This may be due to different smoking patterns and work exposure among men and women.

Smoking and \the E miology and Pathology of COLD

The prevalence of chron konchitis has been d(termined in

several populations in the Lnited States and in other countries

(24,25,26,34,36,41,43,44,46,51). Table 4 lists several studies which

have included appreciable numbers of women. These studies

have documented a close relationship between cigarette smoking and an increased prevalence of chronic bronchitis, and when

looked for, a dose-response relationship was also pretent 1Table

3). The prevalence uf chronic bronchitis-in the United States

was determi in four cohort studies and ranged from 4 to,p10

percent among women and 14..to 18 percent among rffen

(24,25,26,41,41,51). In both men and women a dose - response relationship between the number of cigarettes smoked and the

prevalence of chronic bronchitis was apparent.

The ublened differences between men anewumeti nuted in

these studies may be due in pkrt to the smaller percentage of

wurrA than men who were sr kern in the population studied.

Moreover these women smoked fewer, cigarettes than men.

When comparing current smokers, several studies of different

tiopulations.in' the United States and in England did not find

significant differences iiithe prevalence of chronic bronchitis

be ween men and women (21,33,41).

The relationship- between smoking and pathologic changes in

the lung have largety been obtained by necropsy studies. These

investigations are often skewed by physician and,dr hospital

141

152
T k FILE I Prevalence of chronic bronchitis by smoking classification (numbers in parentheses represent to

number of individuals in particular smoking group)

k,;4' S- Smokers

Author. Year Number and Type

(sounto. (Reference, of Population

Higgins, 1958

England (34(

Oswald, 1955

'Eng (43)

fitibti. 1965

England (16

Remington, 1969

England 16)

94 men and 92 women

randomly chosen from

agriculttlral

communities

3.:602 males and*2.242

female clerical workers

10 65 ,!,rs of age

65,1 men and 84) women

in a Finnish rural

corn man ty 40-60 vr.

of age I 11.729 men and 22.295

women participating in

mass miniature

radiography screening

NS Nonsmokers

\ 1 en

NS 00

EX Ex-Smoker.

Women

NS 0 11 S , 67 S 50

$

NS 155(474) NS 12 1 (6 1 9)

S 18 4 (1.140) S 18 (5791

NS S NS 4 5

16 3 EX 13 3

S 1-11 350 S 1-11 10 1

15-21 11 4 1S-21

25 40 25 57 0

NS 5 1 (9,055) NS 3 4 (12,351)

EX 95 (6,510) EX 3 9 (959) Cigarettes (23,243) Cigarettes (5,955)

5 1-19 91 S 1-9 .51

10-19 IS 0 10-19 106

20 t 20 6 -20 155

omnient

Chronic bronchi'''s

defined by habitual

cough and sputum

production

4:x-smokers represent

those who have Atoppe(

for more than 1 month

Age-adjusted total

prevalence Cigarette

dosage gradient

significant to P 0 001
Ferds, 1962

U S.A (23,25,26) 542 men apd 625 women Overall iN Overall Age-specific rates residents of Neiv NS 13 8 (125) NS 9 4 (378) - Hampshire town chosen EX 11 9 (77) EX 10 8 (37) by random sampling of Cigarettes 40 3 (340) Cigarettes 19.8 (208) census 1-10 , 298 1-10 . 13 1

11-20 - 342 11,20 222 21-30g 423 .21-30

31-40 61 1 31-40 073

(. . -41 75 3 -41 .

, 4

5,140 adult residents of,'' Overall 8 Overall 4 Prevalence rates Tecumseh, Mich estimated from line

-- graph

Payne. 1964

)1 A (44)

Mueller. 1971

USA (41)

Tager. 1976

S.A (51)

281 nien and 328 women Overall 17 (281) Overall 10 (328) residents of Glen.Nodd NS 3 (2) NS, 2 (3) ' Springs, Colo EX 13 (7) EX 5 (1) S f-14 11 (3) S 1-14 14 (7)

15-24 20 (13) 15-21 25 (14)

-25 38 (21) -25 33 (9) -

227 len and 280 women Overall 14 7 (22'f, Overall 7 5 (2851 Age-adjusted in East Boston, Mass . NS 5 8 NS ' L8 prevalence rate age 15 or gre'fiter S 24 2 S 17'6 ....----'
tvk

st

interest and may not accurately represent a random population. Moreover, observer variation occurs frequently, ever

among "experts." Data regarding smoking history are usually derived from a hospital record or from close relatives and

friends; thus they may be unreliable.

Only a few of the studies examining the relationship of

cigarette smoking to the frequency and seeritN of pathologiCal

changes have included significant numbers of female subjects.

Thurlbeck recently reviewed 30 reported surveys of the fre- quency of emphysema at necropsy (53) Emphysema of some

degree was found in about 65 percent of men and45 percent of women The emphysema found. was also more severe in men

than in women.

. The predominant pathological finding in chronic bronchitis is

the hypertrophied mucous gland inthe submucosa of the large

cartilaginous bronchi. The ratio of bronchial gland thickness to

bronchial wall thickness (Reid index) is usually increased. In a

recent survey of 179 consecutive necropsies. Ryder et al. found

significantly greater bronchial mucous gland volume in smok-

. ers compared to nonsmoker,. There was no significant difference in mucous gland volumesIt4fygoir male and female

smokers or male and female nonsmokers (48).

Mueller' et alexamined the prevalence of chronic bronchitis

in one-fifth of the adult population of Glenwood Springs, Col- orado (41). Among current smokers of varying smoking

categories (Table 4) there were no significant differences in the

prevalence of chronic bronchitis. Higgins and Cochran found no

significant difference in the prevalence of chronic bronchitis betwe'en men and women smokers in 186 subjects randomly

chosen from an agricultuN community (Table 4) (34i. Similarly, Oswald atid.Medvel found no significant difference in the prevalence of chronic bronchitis between men and women smokers in

5,844 clerical workers in England (Table 4) (43).

Auerbach et al. examined the relationship of smoking to emphysema in whole-lung Old microscopic sections at necropsy in

1,436.men and 388 women (4,5). Among the women, there were

97 curreri smokers, 16 'tit* whom. smoked two packs a day or more. Data regarding smoking habits were obtained through

interviews with relatives. Female smokers had a significantly

higher rate of emphysema than female nonsmnkers (Table 5).

Furthermore. the severity of the emphysema was dose-related

to the number of cigarettes smoked. The authors found similar

relationships in men.

Spain et al examined consecutive whole-lung mounts from

necropsies of adult victims (49 women, 85 men) of sudden and unexpected death (50) Smoking habits were ascertained by a

144'
4

letter and questionnaire to the next of kin. The degree of emphysema was graded from 0 to 100 1?y two observers independently and without prior knowledge of the source of the specimen or any previous grading. There was a close'relationship between

cigarette smoking and the degree of emphysema in both men

and women. Furthermore, the data (Table 6) demonstrated a

dose-response effect between the number of cigarettes smoked

and the severity of pathological changes.

Thurlbeck et al. examined whole-lung sections in 1,742 random necropsies in three different cities in different countries

with varying climates and environments (54). Using a standard

panel of grading pictures, pathologic changes in the .lung were graded from 0to 100 by the three readers. In men and women

emphysema was more frequent and more severe in smokers

than nonsmokers; however, male smokers had higher average emphysema scores and greater frequency of emphysema than

female smokers and nonsmokers. This difference between men

and women was also true when heavy smokers and ex-smokers

of both sexes were compared. The authors speculate that malefemale differences may exist because. (a) women are prote.cted by hormonal factors; (b) men may smoke- more heavily than women, (c) men may have different smokinapatterns than

women, e.g., inhalation; and (d) men may be eRsed to damaging environmental factors at work. \;

-. 0 T ABLE 3. Means of average degrees of findings* in nonsmokers

and current smokers standardized for age of total study population, women

Subjects Who

Never Smoked

Regularly

Current Cigarette

Smokers

1 Pk 1 +Pk

NuAmber of subjects. 252 33 64

Effiphysema 0 05 1 37 1 70

Fibrosis 0 37 2 89 3 46

Thickening of arttlnoles 0 06 1 26 1 57

Thickening of artenes 001 0 40 0 64

'The pathologic findings recorded were degree of emphysema )four -point

scale ranging from zero for normal to four filr advanced erniphysenia),12)

degree of fibrosis Ise%eri point scale ranging from none to advanced diffuse

fibrosis), (3) degree of thickening of artenoles (four-point scale).' 4) degree of

thickening of artenes (three-point scale). and (5) padlike attachments to

alveolar septa Padlike attachment 1', a thickening of alveolar septa in focal

areas bj fibroblasts, histocjtes and collagen fibrils This is recorded as present or absent

SOURCE Auerbach.(

15G

145.
In summary. the prevalence of chronic bronchitis among

women in the United States has been reported to range from 4

to, lo percent Women who smoke hat e a higher prevalence of

chronic bronchitiswthan those who do not smoke. Overall, hower, chronic brorfth lilt, is less common among women than men

in the United States This rna., reflect the smaller proportion of

women who smoke. differences in their smoking behavior, and

less o«upational exposure to lung irritant--, WherP-comparing

current smokers, seeral studie, Of different population.; in the

United States and England did not find significartt differences

in the prevalence (f chronic bronchits's between men and

women Pathological data suggest that female smokers have a

higher frequency of emphysema and bronchial mucous gland

hypertrophy than female nonsmokers Furthermore. the sever- --It 1,f emph sema is dose-related to the number of cigarettes

smoked Distinct female-male differences in the frequency and

t: \tent Jf emphysema at autopsy ha e been reported, but it is

not clear whether thee differences are due to intrinsic dd.-

ferentes in the way men and women respond to eironmental

injury or to the differences in the degree of environmental injury experienced by men and women

Smoking and Rt.-:orator) Morbidity

A large nurnbel tf re( ent studies have demonstrated a higher

frequent respiratory symptoms, i.e., cough, sputum, wheezing and d, spnea in smokers as compared to nonsmokers Many

ti. Degree of emphysema* and cigarette smoking**

V, Nr Vtitr. Mean Age V. ith

ie,er Mean Orade (,ra:de 20 ("rade 20

Age io of 1Irr.ph,,.-ma Emph!.,kema Ernphy-ema

01 x .11-2111 i ,11C, , 6r, 2,f1 41 14 ,0- ;4I, 16 f 3',-ri 7O) ..rliet 21 2 ,I)-1(1,

.1: o, 6 '0-241, 1 ,17, , To

4 t. -t ,r11J'A an, at the 1-1. les. el for the heal.: ,rnoker, and

Eat lung par r rnount..1 (non wati graded from I) to 1(0) rn

1. T11/1Tt,r,e1t11,f.- of 1, 11, to grade and t hen in enorn,nation, of 10 up to grade

11111Of,.

tit R( I) M

, r

4fx
of these studies have included appreciable numbers, of women

(9,11,15,38,39,40,45,47,65). These investigations have examined populations varying in age, geographic location, social class. and exposure to air pollution.

Leibowitz and Burrows examined the quantitative relation- ships between cigarette smoking and chronic productive cough

in a large randomized sample of the white nonrMexican Ameri- can popufation of Tucson. Arizona (38). Their,data (Table 7) con- firm the ,dose relationship between cigarette smoking and chronic cough and or chronic sputum production in men and women, The effect of cigarette smoking was closely related to the total pack-years smoked (Table 7). These data support the male to female preponderance in prevalence of chronisprian- chitis noted in several other epidemiologic 'surveys

(24.25,26.41.44,51). However. these data also indicate that males and females with equivalent smoking histories have similar rates of chronic cough and or sputum production. Woolf examined the frequency of respiratory symptoms- in women volunteers. aged 25 to 53, drawn from several large

commercial firms (Table 8) (65,66). The prevalence of cough and

sputum production was significantly greater in smokers than in nonsmokers (p< 0.001). Heavier smokers complained of cough and or sputum production more frequently than nonsmokers or ex-smokers. The prevalence of wheezing and exertional dysp. nea increased progressively with the number of cigarettes

smoked. In addition, 'colds that "went to the chest" occurred more frequently in moderate and heavy smokers than in nonsmokers (p <0.005 and p-; 0.001, respectively). Woolf com- pared his data with previously reported data among men (Table 9) and concluded that the relationship of cigarette smoking to respiratory symptoms was similar among men and women. Ferris resurveyed a 1967 sample of Berlin, New Hampshire. residents in 1973 (22). As in 1967, the prevalence of cough and or sputum production in females and males was directly, related to the number of cigarettes smoked daily. When the group evalu- ated in 1967 was examined by current inhaling and smoking status (Figure 1). inhalers had a higherkevalence of symptoms

than nonin hale rs (22) Furtherrnpre, the frequency of symptoms was dose-related to the number of cigaretites smoked. Manfreda et id. studied population samples in an urban and a rural community in Manitoba, Canada (39). Their data presented in Table 10 'demo9strate a higher prevalence of cough, phlegm, and wheezing among men and. women who smoked than in nonsmokers or ex- smokers. However, no significant differences in the prevalence of symptoms were apparent in the two com- munities.

147

"7`,S
TABLE 7. Comparison of pre alence of chronic cough and or chronic sputum production in men and %% omen. by smoking habits*

By ag.- 1&'r".--Ap

arOr 44 It ars

ril ar*,

B F3 pgt k ar- ,f nk r.g

N. %tr.

Smoked path sears

pat k at,

.21 4U pat h ar

pi dr-

_trr.her Sur,,je, t V. tr

r z-rrtorted i*rnok r*,

M..e.. F erna:er Mr1,6-, F eirlair., 1 x2 x 2 ',6 x ; .4-, 17 7

4i ' 'r ..: 12 2 14 -, il I .41 4 x

63, 2,0'1

,4 (_, :04; ir,

Pre*.tr, 1-20 ia Pr. 21) da:

Ma.e, Ferna,e- Ma.e, Fernaa--

,,, 2, s2 2** I4 41 2 17, 41 1 4 ir Y. 'r 40 i; ir E 44r, 47 "r 6

-.7. i i x x3. iF.,, 2 -,3. i1, 1 ',9 ',1

62 -.1 6 x2 .14 t 1r1 x-1 3 14, '',7 1

'7114.12 1 1',41. 10

Pr. -,*nt F.x Srroh rs

ror lo ft 1.* 1. 1 ,zkl. 21 :e 6:* 1*

14 3" ;I', 27.

*Ai 3 . loe to. 1,17

'Sur,,et Ith a h;..tor-> rt ratr pri.rr bt n t*lid from thl Differt nt In rate** 1',2, *-rnoking ,-dgnifi, ant vt.thin *a, tig - gr p X and / Wffer nt, t. h. t ri proport Ion-, and trt rid ith -moking gnifi ant age x X' trend. Trend .,f path >ear, -riznril ant for rna:e irre.( nt and ,, ..n.oher- and female irre-ent -rnoker- X' trend tie,. er -rnr1..« r, AdA,,,4>.rirnifa anti, rilfferr fit from pro-ent or ex -rnoher. (X' and /,

.:41.1.-riptorn, are those reported on d motilfi,at4,,n quekttlonnaire and are.derv.e(1 from the Statr(tnal Heart and Lung In,,taute fth. BrItt-ri WM, a Rt an,r, Win, .1 re .plratr,r, ri re tin hrri t r InItu171 prodt,, t,n rt ft rs t,, the prt.,,e-nc t th rnptorn j dt fr.r t L a-t tnr, rnntL.- of tht ar S( It M
TABLE ti.Pr ev alence of cough and sputum production in 500 omen related to smoking habit

4 NonsmokerNo

Lx-smokers

No cr,

...1.--

mb Light Smokers

No t",

Moderate Smoker,'

Nc,

Healy S'rnoker,,

No

a ( (,ugh'

b Sputum"

c Sputum . oiume

1114 6 o

7 7

1

1 1 6

1 6

r

1112 27 ",

300

32

27 34 k

29 i

66

60

53 7

48 K None

Morning blot,

169 92 ; 61 yx 4 2k 70 0 6:, 70 7 63 31 2 10 1.1 0 0

Tablespoonful' i 17 -, 11 12 0 2IA 23 6 1 6 0 o 0 More than one 14 5 12 11 0 17

I t abrewoonf ul 1 0 7, 0 0 0 0 0 0 4 4 4' 12 9 k

Ira lude« %omen with cough with or without sput...um

1n. lude, a omen v.ith sputum i4ith vithout cough Stet Rt F. V. oo1f R 67o

1 I H
kABLE 9. Presalence of respirator) symptoms in men

. compared with women*

Wr.t. -rn

\ Aerate -ty. -rn - rgip..

.rr

H. a ,OT

Mer

Pubil.0-..ei Data

Omen

Prt...ent

Irr.rtIgatl-n

Y. -r( rt P. r

4 4* .3 -22 47

1424 40,

42 40'; 017-74 47

4).

40') 4...

4 2.7

'Nurnr-r- r par r aw eefer. n,rnner.

RiE, 4S0 R

The relationship between smoking and seNeral respiratory

symptoms was examined by Buist et at. in population samples of

three North American cities (111. Cough, sputum -Production, and wheezing occurred more frequently among smokers than

nonsmokers regardless of sex.

Bewley and Bland examined the relationships between smoktrizand the prevalence of respiratory symptoms in 14,033 chil- dren aged 10 to 121-2 in two separate urban areas of the United

Kingdom Om. In this questionnaire survey, 2.5 percent of the girls acknowledged smoking at least one cigarette per week

("smoker") Boys who smoked outnumbered girls who smoked

by 3.1 and were more frequent smokers of at least one cigarette

a day than were females by 11.1. Table 11 shows that, even in

this young age group, smokers halve a higher frequency of morning cough, cough during the day and night, and cough for 3-months duration than their nonsmoking classmates.

In a questionnaire study of a lArge group of American high

sarnol students in Rochester, Nev. York, Rush found a strong

association between current smoking and respiratory

symptoms in both sexes (4-7). There were minor differences between sexes in the frequency of respiratory symptUms when

150'

1('1
C

0

Males Females

NonInhalers

ifthalers

1 14 15.34

Cigarettes/Day

1 14 15.34 35 +

FIGURE 1.Age-standardized rates (percent) of chronic

nonspecific respiratory disease* by inhaling and

earrent cigarette smoking

ntera for diagni,%1% were follou%

li hronic hero hitis Affirmato.e respon%e to the que,tion Do you bring

up phlegm from hest g,Ix or more times a day for four day% a week for three

months a year for the pa.st three ear, or more'

,2, Asthma Affirmatoce re sp nsr that bronchial asthma had been diagnosed

and uas -.till present

hronic iihstruc tine lung disease Affirmato.e response to On e or more of the follouing wheezing r whistling in the chest o« urred miect days or nights,

the .4 ubje( t had to %top for breath wihen walking at hi% nun pace on the

FIN, Ir.. than Pin per cent of the FV(

These could occur in ,.aroitiie combination, and were nut mutually exclusive

R( E Fern% iite , Jr 22,

smoking his vries were comparable. Rawbone et al., in aques-

.

tionnaire surikey of 10.498 secondary school children aged 11 to

17-in London. f(iu'ild a significantly higher frequency of cough,

151

1 C 2,
TABLE 10. gespiratury symptoms and diseases in male NI) and

female (F) participants inllarleswood

(C)urbanand in Portage La Prairie

(P)ruralexpressed as percent of respondents

'Respiratory Nonsmokers Ex Smokers Smokers

S.,,,mptorn I)(eae

on

.at .ret

montro yrer

/4' 444

444 2b

14)44

'54

20

it 5

it

Pritegrr on mo-kt

.dal. at leat

rriontn year

444 lo 16 9 24 7

4" 5u ,I(12 25 4

4-,eez4ng apart

from ,4,41.

4 2 s o ler , 14 i 26 x il

attar I, of horc

ne of breath

121 2044 25 4 . 2

and ,Abeezing

42' r0 1S5 P 114 11 "i 17

11' 1244 61 1544 li 5 206

Shortne of breath

F,,TTkpared to per

on. of same ex

and age

4u 54 A .,6 12

74/ 124) 61 5u 22.1 175,

.4:4 .0 Ki 1 Manfreda, J

c, lds. and cxertional cl3spnea in regular smokers as compared

to nonsmokers (-15). There was nu appreciable difference in the

frequency of cough between male and female_.okers ur between male and female nonsmokers. Colley et af.Aamimad the

influence of 'smoking, lower respiratory tract illness under 2

Nears of ake, social class,of father, and air pollution on respiratory symptoms in cohort of 20-year-olds followed since birth

(1). Their data (Table 12) suggest that respiratory symptoms\

were tlusuly ;elated to (Ltent smoking. Symptoms were also

related to a history of lower respiratory tract in ection in the

first 2 years of life but were nut related to sou class or air

pollUtion

41tat 152

I f
.er

r TABLE 11 smoking and the pres alence of respiratory Symptoms in gir um two different cit,ies in England

Symptom Residence

Smoker'

N

Prevalen of Symptom With Each Group

7

ExPenmental

Smokekt

N (y,

- Nonsmoker

ti ^1r Significance

Cough in the morning a Kent 10 31 3 9.8 73 6.9 P -4).001 Derbyshare 14 :4'89 50\- 8 4 13 67 P 0 001

Cough day or night, Kent 17 53 1 148 28.0 195 i 1 184 P-0.001

Derbyshire 35 473 176 29.5 458 1 P 0 001

Cough for 3 months of year Kent 5 15.6 43 82 55 t5 2 P- 6.01

Derbyshire 10 13p 32 5.4 82 4 0 P 0.001

Smoker a child who smoked at least one cigarette a week

, Experimental smoker a child who had smoked at sometime but less than one cigarette a week

Test for significant association of cough and smoking habit Chi-square 2 3 table

"Smokers and expenmental smokers combined to give chi-square on a 2 2 table

SOURCE- Bewley. B It (9)

1E 1 . e

1 V
S. 4r

TABLE, Prevalence (percent) of respiratory symptoms by sex and smoking habit in cohort of 3,898 20-year-olds followed since birth

Hiptory

Cigarettt

Smoking

Never

smo'ked,

cigarettes

Ex-smokers

of cigarettes

Present

smoker of

cigarettes

No data on

cigarette

smo#ung

I or All

Population

M F

i.

Winter Cough Day Cough 3 Winter Phlegm Day Morning or *wilt Months in . turning or Night Vough 4n*Winter Winter Phlegm in ntei

Q.1(a' Q.1(b)' Q.1(c)" Q.2(a) Q (b)' ,M. \ Fc M F NI' F M F F

, -

802 1093 1 6 40 1.2 6.5 1 5 3.2 4.8 1.2 6.4

.4

. 101 '57 30 . 1 8 7,1 1d.5 3.0 18 11.0 19 10,2

o 1009 678 13.0 13.2 13.9 16.0 8.1 7.5 14 1 1)1.9 11.6

Va 92- 48 8.7 11.8 9 1 '18.8 4.5 0.0 0:0 6.9 4.8

2022 1876 7 7 7 4 9.8. 10 2 5.0 4.7 9.9 7.6 9.3

9

11 2

0.0

6.7

V

1 (a) Do you usually cough frrst tiling in the morning in the winter?*

(b) Do you usually cough during the day or at night in the winter?

If "'Yes" to *her question 1(a) or (b)

(c) 1 o you csnigh like 10son most days for" uch as three months each winter?

',. .4.

Persistei

Phlegm 3 - Cough al

Months in Pleam

Winter Q.r(e)

Q.2(c)''

4F

+2(c)'

M I r \f , 3.7 3.2 0.9 1 4 0.0 " '2.0'

8.3 5.5 4,9 3.

4.8 0.0 4.8 0.

46,2 .4.3.9 3.0 2.
r4

J

4 2. (a) Do you usually bring up any phlegm (i*it from the chest) first thing in the morning in the winter', (b) Do you usually bring up any phlegm (spit frinn the chest) during the day or at night in the winter' Ife"Yes" to either question 2(a) or (b)

(c) Do yuu bring up .phlegm (spit frontthe chest) on most.days for as much as three months each winter?

SOURCE Colley, J R.T. (15)

.TA1tE 13.Percentages of nonsmokers and smokers with absno'rmal test results in three North America' * cities, using combined reference values*

41/

Upper limit +

Lower limit «

1. Abnormal test

FEVFVC

CV,VC

CC1'LC

AN L'

RWTLC

'

NonsmokTfs

AS S

(95) (27)

1.6 0.2

11.6 20.0

6 11 2 7 2 7

1 7 6 * 11

Total

(122)

Men

AS

(12)

Smokers

S

(115)

Total

(236)

Worn-en

4 Nonsmokers

AS S Total AS'

(145) (46) (191) (107)

Smokers..

S Tot

(98). (20

1.8

10.6

73

3

3

7

1 8

10 6

.k. 5

470'

20

179

1.8

10 9

7 . r

32

13

9

2.6

8.7

6.

15

26

15 .0-

9

2.1

10.0

46

8

7 , 43

0.6

15.0

20

11 4 17 2e

9

; 2.4$

9.1,

8

7. 10

118

1.7

a

11.1

723

20

27

11

1.7

% 11.5

. 25

26

29

37

VAIN 13

2

9.

16

25

25

32

12

*Reference values for nonsmokers derived from asymptomatic nonsmokers in the three cities. **Numbers in parenthesis = number of subjects in each group. Upper and lower limits *the expected 5 perceni abnormal results. AS = asymptomatic; S = symptomatic en

c.n SOURCE' Buist. A.S. (11). 4

e
In a longitudinal study of elderly Edinburgh residents aged

61 to 90, Mi line and Williamson found the prevalence of persistent (co.ugh and sputum production was significantly greater in

smokers Of both sexas than in their nonsmoking counterparts

40). Male prevalence rates were three times higher than those

in females, hum:ever, nu attempt was-made to determine the

relation'ship ut re:spllatury symptoms to life-time tobacco exposure.

In suMmary, many recent studies demonstrate a higher frequency of respiratory symptoms in women who smoke as compared to women who do nut smoke. This is true in surveys,including children, adolescents, young adults, working age, and

elderly worrier The effect of cigarette' smoking is related in

f terms of both the number of cigarettes and,years smoked. The

majority of studies Lptlicate a greater prevalence Of respiratory

symptoms apking men who smoke than among women who

smoke, howeN 'r. these differe'nce's uftwn disappear when the

study is carefully controlled, for smoking history.

Smoking and Pulma6ary Functijor

The insensiti% itN of cough and ,4puturii prudui non in the adult

as a predictor of future de% elupment of COLD has been emphasize,1 by Fletcher and Peto (29). Pulmonary function testing of

fers an abje( ti% t. method fur measuring the atherse effects of

smking. fliA4. eer,i urient tests of pulmonary function displa!,

a marked %ariability between indkiduals and may not detect

the ile%utopMent of (.(11,i) uritil irreNersrble damage of.the lung

has occurred. Also, none of the presently used pulmonary function tests can predict which of those indivnivals with slightly

abnormal pulmonary function will progress to debilitating anc

life-threatening emphysema and chrir4 bronchitis. Becklajic

and Permutt ha% e recently iem. ed the objectives and prob-

. lerns of theikests of lung function commonly used fur early de

teetioriof ('OLD (7).

A large' number of studies ha.- established a higher fre

quen(N of pulmonary functional a.bnor,malities in smokers a.

compared to nonsmokers. These studies hal, e examined (a) the

relationship of smoking t., abnormal tests of small airway funs

non and (In the relatianship of smolling to measurements a:

standard spirometrN. The majority of epidemiologic surveys in

Nestigating the pre% aslerwe of functional abnormalities in smuk

hate' employed spirometro measurements. usually th(

forced expire, orN 1, (Aurae (FED') anti_ vital capkteity (V('). Meas

urements of way resistance, diffusing capacity-, lung solume

and nitrogen mixing ha% e been used much less frequently.

156

167
60 Males

to 40

toa. 20-

0

60

Portage la Prairie

O Charleswood

rl ri 111 fti

Females

a.

RV %TLC CV %VCE CC°Alla

-4ra FIGURE 2.Prevalence of lung function ,abnormalities among

smokers in an urban (Charleswood) and a rural

(Portage La Prairie) community

SOURCE: Manfreda, 3 (39)

Slp III

SMOKING AND "EARLY" FUNcTIONAL

ABNORMALITIES - The most widely used measurements for detecting early

Mange of chronic airflow obstruction are the single-breath nitrogen washout curse or a maximum forced expiratory volume

curve.

A limitedI number of recent studies usinglests.of small airway

function have included appreciable numbers of female subjects.

They ha'e demonstrated a higher frequency of abnormalities in

tests of small airway function in smokers than in nonsAkers or

ex-smokers. A definite dose- response relationship has been

fountitn'some of these studies but not in others (10,11,12). Table

13 shows the data from one of these studies (11). For all measures of small airway function, the frequency of abnormalities

was higher among smokers than nonsmokers in both men and

women. The frequency of abnormal measurements was considqably higher in female smokers than in male smokers except

or closing rapacity, in which equal proportions of male and

1 IGS57
ferhle smokers performed abnormally. Huweer, the frequenc!,

abnormalities among female t onsmukers was also greater

than among male nonsmokers. The authors spec ulate that the

trikditional )em, of irhronlu'airflov. obstruction as being preduminiintly a disease (\f males ma!, be atturate onl!, when male

sm:+ PE. rss outnumber female smokers and when males smoke

more ( igarettes than females. They suggest that when women's

smoking habits become tompurable to those of men. the effect

on lung function may be sinfilar.

Manfreda of al. used the single-breath nitrogen test in a large

group of subjects in two Canadian cities (Figure 2) (39). Almost

-all smokers ix:) percent) reporteq, that they inhaled their

cigarettes. Smokers had a greater pre% alente of abnormalities

ifig-e than nonsmokers regardless of sex. The pre% alent e of aknurmal

%atm, in women who smoke was slightly less than N male

loker's. . In a olunteer population of 530 cigarette smokers attending

n emphyserna screening center. Bust and Russ found an,

eiluis.aq.nt frequern: of abnormalities of the slope of phase III

among male and female smokers of less than 20 cigarettes per

day ( Figure 3) with both sexes has. ing significantly higher prea.lence of abnormalities among stnokers of more than 20

(igarettes per day (12). In the groups smoking more than 20

cigarettes a day, a greater proportion ofTemales demonstrated

abnormalities than males. flowver, thv age composition of

each 1-()up (male and female) was not identical.

A recent stud:s, of small airway function in 205 young volunteer smokers aged Ix to 45 has suggested that smoking may

?exert its effects at different anatomic; locations in the lungs of

men and women (21). All subjects smoked fairly heavily more

than 20 ( igarettes per day) for a short period of time (average.

2.4 pat. k-,s, ears). Male smokers showed frequent. abnormalities in

tests of small airwa,s, function but female smokers did not exhibit these abnormalities. Both'male arid female smokers

showed dtqrlased forted expiratory flows at high lung volumes,

4uggestmg presenttt of large-airway dysfunction in young

smokiars. Male and female 'smokers differed significantly in

their Tesponst4 to He-02 inhalation. Female smokers showed at

Itetsf as great an improvemgnt in forced expiratory flows with He-, as did female nonsmokers. cyntrast male smokers

showed a rnuth smaller response to the He -Or at high lung volumes. Thus. the predominant female response to habitual

cigarette smoki.pg appears to have been inolvement of the

large airwc*s, but men who smoked appeared to have developed

abnormaLities in smaajCirwa,), function. The rason(s) for the

differelpt es in the data deiced from this study and previously

158

1 F 9,
Males

= 350

Females

n=173

100

80

60

40

20

3

40.01007,o 1:177.1

::

42%

= 21 19

<10

137 74

60% =110

173 77

10.20 20-40

ClarettesiDa

100 %

FIGURE 3. Percentage of male and female cigarette smokers

with an abnormal changt in nitrogen concentration

(._.N:) liter according to their daily cigarette

consum tion"

Indicates a significant differrnce between groups using 20 to 40 cigarettes

per dahasihe reference group

Indrcates significant differences between males and females P 0.05).

SOURCE- Buist. A.S. t 12)

cited reports relating smoking to small airway dysfunction

(11,12.39) ix unclear.

In sumniary, a limited number of recent studies have demonstrated a higher frequency of abnormalities in tests of small

airway function in female smokers as compared to female

nonsmokers and ex smokers. It is not clear whether these abnormalities are dose-related. Female smokers may ha've more

frequent Abnormalities in the slope of phase III than male

smokers. Male smoker's may have more frequent abnormalities

in closing sr olume than female stnokers. The meaning of these

differences is unclear. One study hits suggested that the earliest

159

7'0
r t

effcts of smoking un lung function may occur in the large airways in women and small airways in men.

. . 0

SMOKING AND VENTILATORY FUNCTI9X\

The majority of studies examining the relation )hip.of smoking ti,) ventilatory capacity have used some measurement of

forced :iipiratur, volume. Most of these studies have focused on

male populations and have found a kiose relationship between

cigarette smoking and the rreS'ence of abnormal pulmonary

function (2.<16.20). Furthermore, the decrement in perform- ance measured by simple spirometry is dose-related to the

numbers of cigarettes smoked (6,16,20). relatively few studies

have included appreciable numbers of females. , Woolf examined pulmonary function in 500 women voluntq.ers

(63). Smokers demonstrated significantly lower values for FVC,

FEN:, FEF 25-75 percent, and specific conductance than

nonsmokers and ex- smokers who had not smoked for over a

year. this suggests that at least some abnormalities of pulmonary function are reversible with smoking cessation.

Higgins and Keller examined the relationship of smoking to

seven derivatives of the forced vital capacity curve in 3,109

males and 3,256 females aged 10 and older (35). Nonsmokers

performed better than smokers in both sexes. Values consistently decreased w#il increasing cigarette consumption. The

largest differences were in FEV and FEF 25-75 percent.

Seltzer et al. examined the relationship of smoking to FVC in

65,086 white, black, and Asian subjects'aged 20 to 79 who had

attended a Kaiser-Permanente multiphasic health clinic (49).

The authors found a signifieaut reduction in FVC among white

women w hu smoked as co d to nonsmoking white women.

No such differences were found r black and Asian subjects,

however. Nu explanation for this ra 'al difference was apparent

from their data.

In a study by Buist et al., the prevalence of abnormalities of

FEVt FVC was hig.tiel- in female smokers than nonsmokers (11).

The frequency of abnormalities in FEVI FVC among female

smokers was twice that of male smokers (Table 12). Gibson etr al.

vxamined,the relationship of sMokng to measurements of the

forced vital capacity in 18,359 men and women in Australia (30).

Nonsmokers had better lung functions than smokers. Among

smokers of 10 or more cigarettes a day, men showed a greater

decrement in lung function than women.

Burrow's et al. examineethe relationship of smoking to

measurements of forced expiratory volume in 883 men and 1,166

women in Tucson, Arizona (13). Nonsmokers performed better

160

.- 171
3.0

FVC

L

ti

to

.1 0 I 1 I 1 30 40

'

50 60 70 80

Age Years

, FIGURE 4.Changes in forced vital capacity (FIT) by age in

fir S

134)

(38)

(5) (8)

No smoker

He vy Smoker

(39)

(2)

various female cohorts , Results have been standardized to 155 cm and are body temperature and

icessure saturated (BTPS).

:umbers in parentheses are number in that cohort.

Heavy smokers arc those who 'smoke 25 or more cigarettes per day. SOURCE: Ferns. B G., Jr. (23).

than ex-smokers or smokers, and ex-smokers performed better

than smokers in both' sexes. Smokers of more than 20 cigarettes

per day performed worse than smokers of fewer than 20 cigar- ettes per day. There were no significant differences in the regression for FEVI.FVC on pack years iii men and women,

suggesting that' men ant, women with equivalent smoking

habits have similar decrements in FEVIIFVC.

The long-term effects of smoking on pulmonary function have

been scrutinized in tv.0 prospective studies. In tine Framingham

study, 5,209 adults have been followed since 1948 with biennial

examinations including measurements of forced vital capacity

(3). Longitudinally, cigarette smokers showed a more rapid.de- Ane in forced vital capacity than nonsmokers. Men and women

who continued to smoke had a more rapid tlechn.e FVC than

those who had stopped. The rate of decline in pulmonary function was appreciably steeper in mate smokers than fen 1e

smokers. The authors suggest that these 'differences could be

due to differences in smoking habits.

In a 'longitudinal study of.residents of Berlin, New Hampshire, Ferris examined the changes in pulmonary function by

smoking status in the various age cohorts (23). Among females,

heavy and moderate smokers had lower values for. FVC and

FEVI as compared to nonsmokers, and the values fell more

161
30

s'F EV,

L

20

(34)

x(38)

(5)

I.

(39)

(8) (72)

bk. N;-$rnoker

Heavy Sr-ccer

I I 1 40 50 60

Age Years

(2)

(22)

70

4

1at

FIGURE 3. Changes in forced exploratory N olume in 1 second

(FEN', 0) by age in various female cohorts

Reeults ha'e been standardized to 155 4.rn and are body temperature and

presiwre saturated IBTPSi

Numbers in parentheses are number in that cohort

Hea%y smokers are thdse who smoke 25 or more cigarettes per day

SOURCE: Ferris. B G , Jr (Z3)

.rapidly with age. These relationships for heavy smokers (25 or

more cigarettes a day) are presented in Figures 4 alid 5.

In summary, women smokers perform worse on spirometric

testing than do female ex-smokerstor nonsmokers. This relationship appears to be dose-related to the number of cigarettes

smoke . The differential effects of smoking on pulmonary function 1 ales and fendles is unclear: One study demonstrated

that me nd women th equivalent smq)cing habits have similar decrements in F '1 FVC. The,long-term effect of smoking

on pulmonary function has been evaluated in two studies which

included appreciable numbers of females. Langitudinally,

women who smoke show a more rapid decline in forced vital

capacity than w6"malimlio do not smoke. Women who continue to

smoke have a more rapid decline in forced vital capacity than

I those who stop, however, men who continue to smoke have an

even more 'rapid decline in pulmonary function than women

who continue to smoke. The lung -term relationship between

respiratory symptoms and airflow obstruction in women is unknown. One large prospediVe study could not find a relationship between symptoms and the ultimate development ofd

chronic airflow obstruction in men-(29). . ,162

4, .' 173
Summar>

1. Recent statistics indicate a rising death tate due to Chronic

obstructite lung disease (('OLL)) among women. The data al. ailable demonstrate an tYttess 'rrsk of death from ('OLD among

smoking women ol.er that tai nonsmoking women. This excess

risk is mut h greater for hea4 smokers than fur light smokers.

2. `'omens total nsk of NIA) appe;:trs to be somewhat lower

than men's, a difference which may be due to differences in

prior smoking. abets.

3. The pri.,1.aience of thrum(' bronchitis vanes direr; ly with

cigarette smoking. increasing with the number of cigarettes

smoked per day.

4. There is & unflicting eNidente regarding differences `rn the .. pret.alente of t hronit bronchitis in women and men. Several

r* tent studies suggest that there is no significant difference in

the pre,alente of chronic brunchttis between male,and female

smokers Thi).rna!, be the tesultAow ever, of increasingly similar smoking behavior of women and men.

.5. The,,presentel of emphysema at autopsy exhibits a doseresponse relationship ..with tigarette smoking during life.

There ,tti a close relationship between cigarette smoking

and chronic cough or thrum(' sputum production in women,

which increases, with total pack-years smoked.

7, ;'omen current smokers have poorer pulmttnarY function

by 'sp rometrit testing than do fema e ex-smokers or nonsmokers, a relationship w hich is dose-r lated to, bit number of

cigarettes smoked.

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I. V) SELTZER. S1EGELAUB. A B . FRIEDMAti.C.I.D..COLLEN. M.

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23:, -287

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Public Health Seyrfce Office of the As a t Secretary for Health.

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1979. pp. 1251

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26-37, 1971

4

175 167
. , INTERACTION BETWEEN SMOKING-AND OCCUPATIONAL

EXPOSURESTi 1979 Surgeon General's Report on, the health .,conse- quence of smoking,) examines the interaction of smoking

and occnpati&Jsal exPOture. Ways. ip which smoking may inter- acf.with the occIpational environment are'described and

examples, of these interactions are discussed. Briefly, these

types of jnteraction are:

Toilacco7trcgicts mv °serve as vectors by, becoming con44am'inated ,Witth toxic agents found in the'workplace,' thus

facilitating entry of the agent by inhalation, ingestion, and or

skin qbso'rption of the agent.

2' Workpla-ce chemii4als,way be transformed into more harm

fuj agents by smoking.

3, Certain xic agents in tobacco products and or smoke m

also inh the workplace, thus increasing exposure to the

a ent, :Smoking ma contrito. an effect comparable to that

which can resat from exposure to toxic agents found,in the

workplace, thus causing an additive biological effect.

5. Smoking may act synergistically Stith foxic*agerits found in

the workplace to cause a much more profound effect than that

anticipated simply from the sepatate influences of the agent

and strioking added togethm.r.

6: Smoking ni1ay contribute to'accidents in. the workplag.

Although few of the studies discussed in the 1979 Stfrgeon,

General's Report included enough women to Adequately deter-

- mine the he a risks of snang and the occupational environment, it is rea ale to hypothesize that women tvith the saple

occupational ex: ure and smoking behavior as men would de-

' elbp health eff'4" s similar to those dericknstr-ated in men. lioweNer, the interaction of smoking alnd the occupational-environment and its offect'on+en differs in at leaa, two ways:

First, smaking'patberns among women, ate diffevnt from

'Mose among meta --,,--women are less likely to smcike:and if they

do, they smoske fe.lver!clgarettes per day, inhale legs, and are

.more. likely to smoke lower "tar" and nicotine cigarettes

(7,14,1. Second; smokirig and occupational, exposure may ad-,'

versebraffea the fetus thilheellealth of the.rWr during pregnancy: Smoking arid uccu iunal expostitejnay also interact ' watth methods of cOntraceptioNlehosA by,women.

This chapter revielms each or the reasons

health imizact on" men and women ctild examines two occupaexposures where interactions ikith .smoking have been k

dearly detnonstrate&for-worne4:workers.

171

P7J.
TABLE I.-Smiting habits of working women by title and

industry

Irtdustry

Professionals

Health

TeachersOther(

Managerial. Incl.

office, rest..

sales.

administrator

Sales

Clerical

Percent' ./

of

Current Percent ,. Femle

Labor Non. Ex 4 . , Force* Smokers Smokers Present Smokers,:

. \

ks 1 pack .?.. 1 pack

per day4 per day

4.4 4 51.2 16.6 25.2 6.9

4 \

6.8 63.5 , 14.0 '19.8 .7

4.6 IL 53.4 15.1 24.0 '

6.7 42.7 16.4 28.0 12.1

6.2 46.0 16.2 30.0 8.0

.Bookkeepers 4.6 53.1 12.2 26.5 .8.2 .; It Office machin

operators 1.3 52.8 15.7 23.1 - 8.4' Secretaries 13.3 52.0 14.7 26.3 7.0

All other , 14,2 , 50.6 13.6 27.5 s 8.3

Crafts 2.4 46.4 '13.1 31.8 8.6

Operatives 11.8 52.8 .10.1 31.6 / 5.5

. Service

Cleaning 2.5 51.9 12.8 "731.2 4.1

. Food 6.6 40.0 13.4 39.8. 6.8

6.9 52.1 10.5 32.2 5.2

'Private Household

Workers , 2.8 62.4 10.1 24.7 ; 2.8

ir

'Figures are subject to sampling errors and may therefore not agr4e with

those in 'other tables.

, I

SOURCE: National Center for Health Statistics (6).

4 . L Smoking Patterns in Women .041 r

The male-female, differences in moking behavior and the

change in patterns of smoking behavior in women over time are

reviewed in other eections of this report. It is important, however, ter consider the impact of these trends when evaluating the

interaction of smoking and the erivir nment. Regular cigarette

smoking is a behavior that usually gins between the itges,12

and 25 (18). Igs unusual to begin, regular smoking after the Age

172.
P

TABLE 2.7-Estimates of the percentage of current, regular

cigarette smokers. adults eggs 20 years and over.

according tofrlaboi force status and occupation and

sex. U.S.. 1,46 t

. Female

43-64

Total

20- 20-44

Tgtal :32 ir 36.9

.Currently employed '35 9' 37 0

White collar total 34.3 33.8

Professional

`technical

and kindred -\29 1 28.6

Manakers&

administrators

except 'farm 41.6 42.7

Sates workers 38.1 37.0

Clerical & ,

kindred workers 34 8 34.7

14lue collar total 39.0 47,3

" Craftsmen & . 'kindred workers 4(15 46.9

Operatives anal

jundred workers 37 6, 42 5

Laborer. except

farm 56.3 .52 6

,.; Serac, '

(i

karm

39 0 , 32.2

42 8

51.0

Unemployed 40.0 , 41.0

Usual activityhomemaking 29.0 37.1*

;34 rs

36.1

36 9

32.7

40 8

42.6

:36.0

33 6

356

31.2

. :11:2

39.2

.. 32.2

..

Total.

20tMale

20-44 45764.

41 9 47.6 41 3

43.4 46.8 39.7

36.6 38.6 35.3

30 0 31 1 29 9

41 0 , 46 4 36.1

39 9 . 42,6 38.0

40.4 40 1 ',./ 44.2

50.A' ' 54.1, 1, 44.3

48'0, 32.1 . 41.6

:12,3. 55.3 46.2

53 7 - 56.9 , 51.7

'47 2 51,1 44.8

,. 36.9 ...- 45.4

, . ........35.0 -

56.8 51:9 53.8

, NA NA NA

NOTE. Unknown if ever smoked excluded from calculation.

*Figure does not meet standatcls of reliability or preciiion.

SOURCE: National Center for Health Statisti4si64.

,

of 3i1P(7). In a cohort of indiyiduals born in the /arrie year, certain percentage of them will begin smokipg by age. 25. Thehe

preva&nce of smoking in any birth cohort after age 25 is lire-

.dominantly determined by the rate at which people stop smoking Or die. The prevalence changes over time4for (mai 10 year birth cohort since 1910 for both men and women arp-preSented

in the part of this report titled Patterns of Oigarette Shloking.

Women first began smoking cigarettes rarge numbers iih- mtdiately before sand 'during the Secondliqrld War(18). Thus, the observed upswing in smoking among women'occurred 25 to

.30 years after that among men. The birth cohorts with the high-

`) " -, - 173

181 .
4.4 TABLE 3. Occupational distribution of men and women, 19-78, by

percent of each sex employed in each category

Women Men

Professional, Technical 156 14.7 . Sales 6.9 59

Clencal 34 6 6.2

Operatives & Transport 118 17 7,

Service 20.7 8.7

All Other 2.5 11.7.

rafts 18 21.1

nagers 6,r" 14.0

Total' 100 100

SOURCE. Rones,'F.. (14).

est peak smoking pro, ale'nce were born from 1910 to 1930 (men;

and from 1920 to 1950 (wurnep). As these cohorts with high prevalence of smoking grow older, they replace cohorts with...Ulmer

smoking prevalenceir Since both occupational diseases and

smukiit related illnesses increase separatel"ith age, any interaction between the two also could be expected to increase

with age. Men in the blith cobo,rt fronf 1910 to 1930 are now iii

the age range at which a high incidence of di"s'ase would be

eIpected, while those women born from' 1920 to 1954 are just

.01. inning to -enter the ages at which there is abighpeevalence

of disease. As a result, the adverse effects of smoking ancloccu

pational exposure would be expected Co occur more frequently

,in men, reflecting this difference in the age of the average male

and female smoker.Nhis "cohort effect" Might lead to the er

roneous conclusion that women are protected from occupationsmoking interactions, jutt, as it ifas.been used to suggest that women 'are protected from th.e lung cancers induced by

cigarette smoking.

142% A second difference between male andyfernale smoking Eabits

which mkt be ,considered is the prevalence of smoking by occu

pation. Table 1 shows that the prevalence of smoking is reasonably uniform among women employed in many different oct.upations fthe exceptions are education and household area

workers with low .prevatenco and food area workers with high

prevalence). There is not the marked difference in smoking

habits between female blue collar and white ollar workers that

has been observed in men,(13) (Table 2). A . ightly lokver prev a.

lence of smoking among professional ,;vom compared to other

ehite collar workers occurs similar to tha seen in .tnen (7).

The section on behavior in this report discusses the smoking

:habits Of several grodps of ,health professionals. It shows that

174

1 , 2
women physicians and psychologists smoke more heavily than

their malecounterparts. Thus, the relative levels of smoking

observed in the two sexes are reversed for these two occupa- . tional groups in comparison to the general population (14).

Nurses also have been shown to have a much higher prevalence

of smoking than women of the same age in the general population (18). A final notahle difference is that among women, smoking prevalence does.not show the game marked inverse correlation with socioeconomic status (7)1, The reasons for these.;differencef are beyond the scope of this section. However, an understanding of them forms pert. of the background for any discussion of t e interaction of smoking and occupational' exposties among' women. .

. . P.atterns of Employment A.

The pe'rcentage of women In the United States work force is

steadily growing. In 1973 women represented 38.4 percent of the

United States work force and in 1978 th'it percentage had risen

'to 41.2 pircent (15).

Approximately 39 million women are employed outside the

home. Table 3 el -early indicates that the distribution of women

in the labor force by category of work does not parallel that of

men. Women are more likely than hien to be employed in the

clerical and service categories. Men are more likely to be ernployed in the management, crafts and operatives, transport

categories thanornen. Table 4 lists the number of women employed in a wide 'ariety of occupations, including many of_those

traditionally believed to be hazardous foi men. In spite of this

diversity, the bulk of women are employed in a narrow range,f

jobs. Over one-third of women in the paid labor force are ems,

ployed in °tie of the 10 job categories listed in Table 5. All of

these cafego'ries have, been traditional employment areas for

women. Thus, the recent gains by women in employment opportunity' have not yet had a substantial impact on the actual distr,ibutiOn patterns of the female labor force. If a shift does occur

in employment patterns involving greater pi-oportions of

women in occupations with significant exposures, we would expect a cohort effect to be apparent in the development of occupational illness. That is, those women entering hazardous occupationstradition ally limited to male workeis would,be exppcted

to be women newly'entering the work force and, thus, predominaittly in the younger age groups. As these cohorts age:the

duration of both occupational and smoking eXpOsures would increase. It is only after these newer cohorts relish the ages.where

disease is prevalent the/ we would be able to observe the full

. 1 175
TABLE 4.Number of women in the current workforce:

4 classified by occupation (1978)

r.

of Women

Occupation in Thousands

hite-collie workers,

Profession al e.; Technical

Biolog4:al scientists

Chemists

Nurses. dietician,. &

therapists

Health technologists and

techruci an?

Engineering and science

- technicians

Painters and sculptors

Photographer- .13

Managers and adminirtra.-

tors. e.xcept farm 2.365

24.594

6,083

' 17

353

.132

Sales workers

Ales

retail trade

Clerical workers

Bookseeper:. Cashiers

Set retarie,

Typists

2.666

1.672

13.456

1.60

1.222

,561

1.009

Blue-collar v.-00.er, :).770

Craft and kindred workers 694

Printing craft workers 91

Upholsterers 14 Operatives.' except

transport 4,317

At emblers J 606

Bottling and canning,

operatives 25

e-heckers. examiners. and

inspectors. manufacturing. 359

Clothing irfter and - pressers

Cutting operative, n e c

Dressmakers. except

factory. 114

Drillers, earth

Dry wall installers and

lathers , ifolishers. sanders

and buffers 38

Furnace tenders; smelters.

and pourers. metal 3'

Garage workers, and gas

station attendants 20

.176

101 '

1S

Occupan

Blue-collOr workerscont'd

* of Wome

in Thousanc

Laundry and dr, cleaning

operatives. n e

Meat cutters an butchers.

except manufacturing 1 Meat cutters and butchers.

Tanufacto nng 3 Mine operate es, n e.c.

Mixing operatives

Packing and wrappers.

excluding meat and

produce 42

Painters. manufactured

articles 3

Photographic process workers 4

precision machine operatives 4

Drill press operatives 1 Grinding machine operatives 1

Lathe and milling machine

operatives 1 Punch and stamfiing.4ess

operativesSawyer 1 Sewers and statchers

Shoemaking machine

operati%es 6

Furnace tenders and stokers.

except metal

Tetile operatives 22,

Spinners. twisters, and

winders 10i

Welders and Marne cutters 4 Winding operatives, n e.c 3'

All other operatives, except

transport ,06:

Transport equipment

operatives 251 Nonfarm laborers 49:

Service -worker

Private house lds

Child care workers

Cleaners and servants

Housekeepers

Service workers. except

households

Cleaning workers

4:03'

1.13:

47' 5111'

6.90

85:
Table 4 (continued)

* of Women

Occupation in Thousands

# of Woinen

Occupation in Thousands

Service workerscont'd Health service workerscont'd

Lodging quarters cleaners 174 Practical nurses 390 Building Interior cleaners. Personal service workers 1.302 n.e c 462 Attendants 175 Janitors and sextons 222 Barbers 11 Food service workers . 2.951 Child care workers 103 Bartenders 111 Hairdresser and Waiters' assistants 45 cosmetologists 483

Cooks 678 Housekeepers. excluding Dishwashers 42 private households Food counter and Welfare service aides 92 fountain workers 397 Protective service workers 11.5 Waiters 1.252 Firefighters Food service workers. Guards 53 n.e c 384 ,Police and detectives Health service workers 1.660 Shenffs and bailiffs 3 Dental assistants

Health aides, excluding

128 Farm workers 509

n rsing 238 'TOTAL 38,910

Nursing aides. orderlies.

and attendants 902

NOTE n e c is an abbreviation for "not elseWliere classified' and designates broad categories of occupations that cannot'be more specifi ally identified. SOURCE: U.S. Department of Labor (17).

impact of occupational exposures (or their intera tions with

srnoking)-an the- h ealt III of women.

Because of this cohort effect, any failure to d nsAate an

excess risk of a given occupational exposure in w men must be

interpreted with considerable caution. It may mean only that

the women exposed were too young and the exposure too brief

for illness-1'o have yet developed. This caution is doubly impor- tant for those attempting to deinonstrate an ,interaction between occupational exposure and smoking on the development

of disease in women. Thus, little comfort can be taken from the

c ent low prevalence of occupitional disease in women. It is

reasonable to expect that any movement of large numbers of

women into hazarciousi occupations will be followed, after an

appropriate time lag, 13y a dramatic increase in the prevalence

of occupational illneis in women.

The Reproductive Role

A third reason for examining the effects of occupational'expo- sures in women separately from those in men is the difference

177 1 V.
.0" TABLE 5. Most commonfemale job categories, by percentage of

the female work force employed

(

1 Percent of Percentof

Female Female

Woork Foke Job Work Force

4 kola

Secretor>

Retail Sales ( lerk

Bookkeeper

Waitress.

Casper

K 5 PrIvate Household

Worker 2 9

4 3 Registered Nurse 2 8

4 3 Elementary School

Teacher 2 8

3 2 '4' . Typist a 2.6

'Cleaning Workers 2 2

3 1 Sewer & Stitcher 20

SOUR( E *Bones'. P. 114)

, , in their reproductive "roles. Toxic occupational exposures in both men an women can reduce fertility and increase frequenc!, of teratogenic effects l see Table 6). Irk addition, however,

the 9-month duration of gestEttr4. n rovides many oppounities opportunities

for the fetus to share any adv rse toxic exposure of its mothbr. These risks may interact with the -well-established risks of

cigarette smoking during pregnanc!, dziscussed elsewhere in titis

report. Table, 6 provides a list of ht tardtfUs substances in the

work ermronnient, some of which, are suspected of having effects on reproduction.

Another specific concern for omen is that of con-traception.

.... Substantial numbers of worne in-the United States use oral

contraceptives (18). These drpgs have been shown to interact

with cigarette smoking to p oduce a greatly increased risk of

cardiovascular disease, as iscusted in this report. In addition,

It is possible that oral contyaceptives may interact in an adverse

manner with physical (:)t, chemical agents found 'in the work

place, or that.the combynation of smoking, occupational expo- \ure, and oral contractive use may bear special risks. The

answers to those questions can be found only through the study

of populations of wor ing women. . . One study appro ed this issue by examining the health,

status of women in% lved in the manufacture of oral contracepives. PcIller, et al. h ve"shown that women workzng in the man-.

Ufacture of oral co traceptives absorb enough of the drugs to

influence the clot ing mechanism as well as alter menstrual

function (12). 1.: fortunately, the risk of cardiovascular diseaseand the ffects of smoking in relation to its -could not

'be estimated in t is population. Because of the established excess risk of car ovascular disease from concurrent smoking.

178
and oral contraceptive use, examination of cardiovascular risk

in this group would be of interest.

The preceding discussion presents several areas where

female-male differences may significantly litnit the direct applicability of the results of male smoking studies to the

female population. These areas of potential difference present research questions that justify significant, ogoinie research"

activitie4.

Specific Interactions Between Occupational Expbsure and

Smoking

A review of all the potential risks of occupational exposure for

women is beyond the scope of this section. Table. lists a number

Of agents found in the occupational environment and their observed organ toxicity. Table 7 presents selected pulmonary irritants and sensitizers in specific occupational sKtings r ation to the number of women employed' in those settings.

There is little specific data on the health effects-of h'grive

occupational exposure in oinen. Two clear exceptions..e),ust

exposure to asbestos ael to cotton dust. The data from ,studies

of women exposed to these two compounds provde examples of

established interactions between smoking and occupational exposure ni women.

ASBESTOS

N

Selikoff, et al. prospectively followed a group of 370 maie asbestos insulation w_orkers. Theyliernonstrated a multiplicative'

effect of asbestos exposure and cigarette smoking on the risk of

development of lung cancer (4,13). Workers who smoked cigarettes developed lungcancer at a rate 92 times that of non-exposed

nonsmokers. They observed no deaths from lung cancel. among

87 nOnsmokers,.and 24 deaths from bronchogenic cancer among

283 regular smokers, a number well in excess of the 3 deaths

expected. Nev4touse, et Jill. followed, attohort of 900 women first

employed between 1936 and 1942 in an asbestos fattory making

Itth textiles and insulation materials (2,10,11). They analyzed

the group's mortality experience between first emplOyment and

1968, with a minimum of 26 years' follow-up:-There was an ex;

cess overalLekortality partly accounted for by deaths from

cancer, observed even among those who worked in Jobs with

lowto-moderate exposure to asbestos, An excess of cancer of

the lung and pleura was. found among those who were severely

exposed and w4had'worked less than 2 years. In the groups

'with severe eiOgure for ,more than 2 years in the factory, excess deaths from cancer of the lupg.plqura, and non-

\

/57 179

a.
TABLE 6.Chart of toxins and effects

WWI

Y..N... w

N ANIn. %IMMO

SIMOILS3M MO:11, men

-1141 -= 1 1 e.

11.0040144

444~0

.44,447 vc-I I

1G4 41"v.v.

GI MAYA%

1 . 111111/ :10S4. r.1 P.:07W

r t :4.44, 0,0/44. .nno A44 4:. . w sm:24.4,"

itemmt ft.vv !".".".

.sv 0. . coo oaf ...... ...v.

....... . - .44t War Jae

I I: ,........ be Wo

7C. a xr x.-...

.4..,4444011

0 ie.. /44,,

-ow

444 MI. 204 4

.1(

V.114

110

5. 4001.11

MOM 4104 440004

.00:144

.N

X X

0Wcf 7404

PT.Y I -.9 at X ale

.21. 410, sn,-.:S.vo

X.4

terIT 'a X!. X

041 000100

Nay. IGNIO

.10 144 p...

Owls , )

Gen. oGe .1. G.G. ion

V

7.

i 41100 O. %Op G I*0414:0 ... tar,.

....... ',Vv. 2ims wee :$ 11014

t I o PM 00 0.0 004 I X 14, 4-.11., X7.4

ONO, G y; 4tv GIN .0GiMIG -", 44 'GG, .9110

-re. Ventre 4.

6SPCA. ....rely

2X

4.11 PhdSi ZVI weerT0C twact wtti. Ott 05,t4, . Qty 441-Xkli

L,X4 lex *is .P4,1 444 pmt t uqiessta

E.131,:4 Cety T444 .nary 0 COI 4 41114:11 4.

1G wv

SOI;Rl Etiational Institute for Occupational Safety and Health 19i.

.9 180

1
neoplastic respiratory disease were observed. The authors calmisted the excess annual mortality due to lung cancer.'When workers with low-to-moderate exposure experienced a mean ex- cess lung dancer Mortality of '63 deaths (per.100,000 years' expo- sure). Those severely exposed for less than' 2 years experienced

an excess of 44 deaths, and those severely exposed for 2 years or longer experienced an excess of 7241 deaths. Interestingly, an

'examination of deaths did not reveal any significant association with age at first employment in the asbestos factory. In the

`sub- sample of<.workers whose smoking histories were available, those women who had both smoked and were heavily exposed

had a 'risk of developing lung cancer over 30 times that of nonexposed nonsmoking women. The authors concluded that the

data suggested that asbestos and cigarette smoking exert multiplicative rather than merely additive effects.

In summary, the data on smoking and asbestos exposuroin women closely resemble the findings, demonstrated for men.

COTTON DUST

Approximately 250,000 women were employed in the textile

industry in 1978; that population included aPprOximately

100,000 women engaged in spinning, twisting, and winding op- erhtfons. Byssinosis is a syndftme chaActerized by tightness of

the chest and shortness of breath in workers exposed to dust of cotton,. flax, and hemp. In addition to these acute symptoms, workers have been found to develpp chronic. bronchia's', and

some become severely disabled by their obstructive lung disease

(3). Berry et al. studied the workers in 14 cotton and 2 manmade fiber mills in England (1). They found that men had a

greater prevalence of byssinosiS than women, and that smokers of both sexes had 1.4 times greater prevalence of byssinosis

than nonsmokers. ByiSinosis prevalence was also positively as: sociated with length of exposure to cotton dust in both women

and men and was positively associated with dust level in the

working environment in women. Berry, et al. were unable to

determine if the observed difference in prevalence by sex repre- sented a fference in physiologic response or differences in occupational xposure. They also found a higher prevalence of bronchitis i exposed versus nonexposed workers of both sexes.

Smoking wo kers had hilir bronchitis rates than nonsmoking workers.

Bouhuys,,et al. studied 645 active and retired cotton textile

workers (including 372 women), aged 45 and oldero,who had

worked an average of 35 years. Their respiratory symptoms and

flow-volume curves were compared to those of community rem- /7

181

1 SO
TA BLE 7 F'Aample of pulmonary irritants and inorganic sensi them in various owApations wh

Severe

pulmonary irritant

Beryllium & CompoUnds

Phosphorous Tnchloride

Tellundrn (Hexaflouride)

Zinc (Chloride fume)

Ammonia

Chlorine

.Ozone

Sulfuric Am,

Urainum Compounds

Vanadium Compounds

(Pentoxide)

Acrolein

Ammonia

Cadmium dust

Chlorine

Chromatei

Dichloroethyl ether

Ethylene Oxide

Hydrogen Chloride

(4.

' Inorganic

sensitizers

Platinum Salts

Phthalic Anhydnde

Cobalt, metal

fumes & dust

Phthalic Anhydride

Occupation

enw

# of wom

employe

in'

thousazy

Electronic Michinery,

Equipment & Supplies

Hoesehuld Appliances

--Radio, T.V.

Communication Eqilipislept

Electrical Machinery,

+, Equipment & Supplies

Professional & Pho

graphic Equipment

Watches

Scientific & Con oiling

Instruments

Optical & Health Services

Supplies

Photographic Equipment

dis Supplies

Rubber & Misc. Plastic

Products

Rubber Products

Misc. Plastic Products

890

67

216

804

238

65

119

36

257

86

171
Severe

pulmonary irritant Inorganic

sensitizers Occupation

# of wo

employ

in

thousar

Hydrogen Fluoride

Hydrogen Sulfide

Phosgene

Phosphorous Inchlonde

Phthalic Anhydride

Sulfuric Acid

Tellurium (Hexafluondo

Zinc Compounds

Ammonia

Chromic Acid & Chromates

Chromium, metals &

insoluble salts

Hydrogen Sulfide

Phthalic Anhydride

Sulphur Dioxide

Ammonia

Cadmium dustfumes

Chromic Acid & Chromates

Chromium, metal &

insoluble salts

Fluonne

Hydrogen Chloride

Nitrogen Dioxide

Sulfuric Acid

Zinc Chloride fumes

Phthalic Anhydride

Polyvinyl Chloride

Leather & Leather Products 177

Footwear, except rubber 13

Leather Products, except

footwear 40

Falncated Metal Products 299

Cutlery, hand tools, &

other hardware

Fabricated structural

metal products

401 52

78

Screw machine products 26

Metal stamping

fabricated metal

products

43
-a TABLE 7.(Continued)

Severe

pulmonary irritant Inorganic

sensitizers Occupation

# of worn

employ(

in

thousan

CitIonne 4.` Detergents Personal Services Hydrogen Fluoride (Enzymatic> '-Laundering, Cleaning, &

other Garment Services 231

Chlorine Detergents Beauticians 492 Chlorine Dioxide (Enzymatic.; Chromium, metal &

Insoluble salts

Cobalt a Nitric Acid

Sulfur Dioxide

Sulfuric Acid

Ammonia Private Households 1,217 Chlorine Hotels & Motels 424

Beryllium & Beryllium Cobalt, metal Profewional & Related compounds fumes & dust Services 11,931 Chromic Acid & Chromates Detergentes Hospital Workers 2,866 Chromium, metal & (Enzymatic> Offices of Physicians 506 insoluble salts Platinum Salts ffices of Dentists 242 Iodine Health Services 473 Selenium Hexafluoride Convalescent Institutions 869 Zinc Chloride futhes
Se%ere

pulmonary Irritant Inorganic

sensitizers

a

I

Occupation

# of w

emplo

in

thous

Amnion)a

Antimor y i Bromine

Cadmium dust fumes

Chlonne

Chromates

Cotton dust, rt.w

Dichli;roethyl ether

Dunethklomine

Ethylene Chloroh}drin

Ethylene Oxide

Hydrogen Sulfide

Methyl Bromide

Nitric Acid

Nitrogen Dioxide

Sulft. Dioxide

Sulfuric Acid

Zinc Chloride fumes

Hydrogen Sulfide

Cobalt dust

Phthalic Anhydride

)

.1.

r

Textile Mill Products

Knitting N1111-3

Yarn, thread & fabric mills

Mrsc. Tex'ile,mill products

Apparel & other fabricated

textile products .. Apparel & Accessories

M La. fabricated

textile products

. Meat Products

A.

I

12.9

SOURCE: National Clearinghouse for Smoking and Health (8), Rones, P. (14), Stellman, J. (16). f

I r

(

4* in 1
I

Ill IICrt %Slit§ at tell as eon, ols (Aork. 1s of ',tail

had significantly ilit a-t..1 fit 11,1:ct t att l ht .0,1; ( iiiigll, \\ het

III$, "1"111!'1"'". '" k i n Hit' '1' \ \ai t % all aldt ilStNI/eiattd Volt II SPIllat,iii If II

11(1111U-401M! 1.1i ialidt. Tile' HOU! nits. (Lan 41411.4 ( la

ill lard tht a-so. Litton of hodi aro! %to, Ling in the

with de, leased turigfula non. 'vat 1\111111 I 1

slightly mot e to t. tn.lf , Lan f i.,1111,k1/

1114'11, bot ,1114:klily/ 111.11u kit, i e as likely

report this sy .1- .sitikint, %%ono 11 .'t -,totiat fiat tvl II 1411 1."!'"111.(Zlnlr Allif I liv,t t IVflf 1,141 la hit IIN

II, 1'1 1.1 11.11.1 Ili 1111(1 lieu

chitis III 1,tli1i tetiletol is. I -.0 -hotted MI 111111 rat

of smoking and Nit , !II III .1 litt'llcr far % alum

rate of both by ....most, and go.* it this( It.e.1

l it slinimaty , women ha \ 1'4 -hut.% It (AO ha\ e higher risk tit chalking

chronic (distiled\ long di ,ea.e het au -t Tif exposure to cotd

dust in the workgiliate. cue smoking has been ;$140Y,

Intel act 111th sun oi k eposures It, this, risk, 11 though it is nut established w liether this interaction is addith

or multiplicathe. Nten employed In (a. t here they ai

exposed to cotton dust ha\ e a greater pre\ alence of brunch it

and respiratory disability than women. Clarification is nece

sttry to determine witeth& tbis is a sex eifference or a di

feri,nce in exposure (either occupational-or smoking).

Summary

I The 1979.,Surpon General's Report identified the ways

which smoking cigarettes may interact with the occupation environment. They include:

a) Facilitation of absor'ption of physical contamination

:cigarettes.

hi' Transformation of workplace chemicals into more tox sulgtances

ci Addition of the exposure to a toxic constituent of tt

hacco,,smoke to a concurrent exposure to the same col

stititent present in the workplace,

(11; 4ddition'of a health effect due to environmental exp,

sure to a similar health effect due to'smoking,

e) Synergy of exnosures, and

fl Causation of accidents.

2. Women are entering occupational environments wit

greater frequency, and thus may he expel iencing gt eater exp

suVes to physical and chemical agents.

181;

I " i
3. Cohorts of women with a greater prevalenceof smoking are

currently reaching the ages of maximal disease occurelbace, re-.

placing earlier cohorts with lower cigarette exposures.

' 4. Physiologic differences in hormonal status between males

and females constitute a pOtenti'al source of differing responses. 5. In the workplace women who are pregnant present a

9 -month exposure opportunity, including potential teratogenic

aijd perinatal mortality effects.

6. Concurrent exposure of women to smoking and asbestos

-resultcl in a clear excess of cancer of the lung. t.--

.7. Women smokers gxposed to cotton dust run a higher risk of developing byssinosis, bronchitic syndromes, and abnormal p ulmonary function tests than nonsmoking women.

References V

4

(1) BERRY, G MOLYNEUX, M.K .B., TOMBLESON, J.B.L. elationships between dust level and byssinosis and bronchitis in La shire cotton

Bri/ish Journal of Indiistnal Medicine 3L 18- , 1974.

(2) BERRY, GI, NEWHOUSE, M.L., TUROK, M.E. Comb' ede effect of as- bestos exposure and smoking on mortality_ from lung c ncer in factory

workers. Lancet 247775): 476-479, September 2, 19.72. f

(3) ..--litgikkIZYS, A., ScHOENBERG, J.B., BECK, G.J., SC LLING, R.S.F.

Epidemiology of chronic lung disease in a cotton mill ciommunity. Lung

154: 167-10, 1977.

(4) HAMMOND, E.C., SELIKOFF,I:J. Relation'of cigarette smoking to nsr

of death or absestos-associated dISease among insulation workerl in

the United States. In. B,oguvski, P., Gilson, J.C., Zunbrell, V., Wagner, J C', Davis, W (Editors). Biological Effects of Asbestos. InternationalAgency for Research on 'Cancer, Scientific Publication No. 8, Lyon,

France, International Agelicy for Research on Cancer, 1973, pp. 312-

31,7. . (5) KILBURN, K.H., KILBURN, G.G., MUCHANT, J.44yssinosis. Matter from lint to lungs. AMerican Journal of Nursing 73(11). 1954-1956,

November 1973.

(6) NATIONAL, CENTER FOR HEALTIVSTATISTICS. Health Interview

Sttrvey, .1976, Department of Health, Education, and Welfare, Public

Health S6.vice, National Center for Health Statistics. (Unpublished

data).-

(7) NATIONAL CLEARINGH OUSE FOR SMOKING AND HEALTH.

Adult Use of Tobacco, 1975. Department of Health, Education, and

Welfare, Public Health Service, Center for Disease Control, Buneau of

Health Education, National ClEsannghouse for Smoking and Health, June 1976.

(8) NATIONAL CLEARINGHOUSE FOR SMOKING AND HEALTH. Survey of Health Professionals. Smoking and Health, 1975. Department of

HealtlfEducation, and Welfare, Public Health Service, Center for Dis

ease Control, Bureau of Health Education, NationalCleacinghouse for

Smoking and Health, June 1976, 42 pp.

4) NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND

HEALTH Occupational Diseases (Revised Edition). Department of Health ' Education, and Welfare, Public Health Service, Center for Die187

15--
4

ease Control, National Institute for Occupational Safgty and He

June 1977,*608 pp

10) N EWHOUSE, M.L Cancer among workers in the asbestos textile

try In Buguvski, P., Gilson, T C., Timbrell, , Wagner, 4C., Div]

(Editors). Biological Effects of Asbestos I nterroational Agency fur

search on Cancer, ScieScientific -Publication Nu 8, Lion, France, Int' r

tional Agent/ for,Research on Cancer, 1973, pp. 203-208.

(11) NEWHOUSE, M.L., BERRY, G , WAGNER, J C., TUROK, M.E A s

of the mortality of female asbestos workers British Journal of Ir

trial Medicine 29 134-141, 1972.

(12) PULLER, L., THOMSON, J.M., OTRIDGE, B W , YEE. K F., L0(

S.H.M. Effects of manufacturing oral contracepti.es on/ flood dot

British Medical Journal 1 1761-1762, June 30, 1979 /

I H,) PROCTOR, N.H., HUGHES, J.P.'Chemical Hazards ogthe Workp

P elphia, J.B. Lippiricott Company, 1978, 533 pp.

( 14) R P., LEUN, C. Employment and unemployment during 197i- a sis Special Labor Force Report 218 Department of LE

Bureau, of ,Labor Statistics, 1979

(15) SELLOFF, I J.,°HAMMOND, EC., OHURG, J Asbestos expo:

smoking, and neoplasia. Journal of the A mencan Medical Assoc':

204(2) 106-112, Aprkl 8, 1968.

16) ,STELLMAN, J , DAUM, S.M. Work is Dangerous to Healt4New

Pantheon Books, 1973, 448 pp

(17) S DEPARTMENT OF LABOR. Employ ment and unemployment

ing 1978 An analysis Dep4rtment of Labor, 'Bureau of Labor St

tics. Special Labor Force Report 218, 1979.

(is) U S. PUBLIC HEALTH SERVICE Smoking and Health. A Repo

V the Surgeon General Department of Health, Education, and Wel1:ublic Health Service, Office of the Assistant Secretary for He

Office on Smoking and Health, DHEW Publication No (PHS) 79-5(

1979, 1251 pp

188 1

aJ u

OR.

1,6
,PREGNANCY AND INFANT HEALTH

Introduction

'

A woman who smokes during pregnancy -not only risks her own health, but also changes the conditions' under which her

baby develops. Studies have identified specific areas in which

the of is of maternal smoking.during pregnancy may occur. These include etal growth, most oftep.determined by comparing birth weights of smokers' babies with those of otherwise

sinCilar nonsmokers' babies;, spontaneous abortions, fetal deaths, and neonatal deaths; pregnancy complications, including those that predispose to preterm 'delivery, possible effects on lactation; and long term effects on Surviiring children. The

relationships between maternal smoking and these outdbmes

have been established by clinfcal, pathological, and espvcially

epidemiological studies. Understanding of mechanisms by which smoking may. produce the observed effects has been

gained by physiological studies in humans and experimental studies in animals.

The Chapter on Pregnancy and Infant Health ih the 1979

Surgeon Generals Report is adetailed review of past studies of

the effects of smoking in pregnancy, with a comprehensive bibliographi This'sertion suinmarizbs current knowledge in major

areas of study, describes important new studies, and points out areas requiring further resorch (146).

Smoking, Birth Weight, and Fetal Growth

Babies born to women who smoke during pregnancy are, on

the average, 200 grams lighter than babies born to comparable,

Women who do not smoke. Since 1951, When Simpson reported

this finding from her tginal study (138), it has been confirmed

in more than 45'studies ofmore ihan half a uhillion births (146).

sults of these studies are expressed as meal birth weights of

s kers' and nonsmokers' babies of., aLternatively, as the per- ceniage'of babies who weigh less.than 'a specified amount, usu- ally 2,500 grams.

To illustrate the association between maternal smoking and

an increased prop° ion of low-birth-weight infants, the results

of five studies wit a aggrelgated total of almost 113,000 births

in Wales, the U to States, and Canada are summarized in Table 1. In the po ulations, 34 to 54 percent of the mothers

smoked duri pregnancy and on the average the smokers had

twice as ma low-birth-weight babies as.the nonsmokers. Also

.in these po ulations, from 21 td 39 percent of the incidence of

191

.1(3 7
TABLE 1. Btrth weight under 2,500 gramsby maternal smoking habit, relativ e an

from published studies

attributable risks deri

f

Study

Nonsmokers

.., No.

,. .No.

Smokers

. Propor

- _,

tion

'Births< 2,500 grams

Nonsmoker smoker

(%) (%) ,

Relaftwe

risk

smoker

nonsmoker

Arnb

ably

, risk

Mc;

Cardiff

US Collabeorative

White

Blak

California, Kaisers

Permanents

White p/

Black t

Montreal

Ontario

'

.

'

7,176

8,466

11,252

3,189

934

3,954

27,316

*r

,,

6,2.38

9,781

7,777

2,145

479

3,004

21,062

' '

.465

.536

.409

.402

.338

.432

.4:35

7 4.1

, 4.3

10.7.

3.5

. 6.4

5.2

4.5

8.1

9.5

17.5 . 6.4

,1.3.4

'11.4

9.1

1.98

2.21

1.64

1.83

2.09

2.19

2.02

1.;"1

:31 39

21.

25

./27

/ 34

31

*Percentage of total birth weights -- 2,500 gm attributable to maternal smoking. Attributable risk n population = b(r -1) dividt b(r I) I where'b = proportion of mothers who smoky and r - relative risk of low weight =- smoker rate,nonsrsoker rate.

SOURCE: Meyer, M.B. (86).

"vv
If 111111FTIIIITIF

5 6 7 8 9 10 11

Birth Weight (Scale in Pounds. Intervals of 4oz.)

FIGURE 1.Percentage distribution by birth weight of infants of

mothers who did not smoke during pregnancy and of

.thos4who smoked one pack or more of cigarettes per day

SOURCE: MacMahon, B:(77).

low birth weight could be attributed to maternal smoking (3,15,38,86,102,106,107).

One study in which rates of low birth weight were simulta- neously adjusted for multiple factors showed that maternal smoking had a more significant relationship to birth weight than did previous pregnancy history, hospital pay status, mother's prepregnant weight, height, age-parity, or sex of child. Adjusted pates of birth weights under 2,500 grams were 49 per thousand for nonsmokers, 76 per thousand for smokers of less* than a pack per day, and 114 per thousand for smokers of a pack per day or more. The risk of having a low-birth-weight baby therefore increased 53 percent and 130' percent .for light and heavy smokers, respectively, compared with nonsmokers (86). Population studies that illustrate whole distributions of birth weights by maternal smoking levels show a downward shift of all birth weights in proportion to the 'amount smoked (74, 77,83,114,136,160) (see Figure 1).

190 193
4 These studies show that tiRie relationship between smokin

and reduced birth w eight is independent of all other factors the

influence birth weight, such as race, parity, maternal siz

socioeconomic status, sex of child, and other factors that hay

been studied. It i also independent of gestational age. There

a dose-response relationship: that is, the more the woma

smokes during pregnancy, the greater the reduction in birt

' weight. If a woman gives up smoking by .her fourth month

gestation her risk of delivering a low-birth-weight baby is sim

lar to that of a no,nsmoker.

PLACENTAL RATIOS

Analyses of placental weights by maternal smoking habit

have noted that these weights were either not affected or wei

less affected by maternal smoking than were birth weighs

(57,61,91,10_155). The placental ratio, the ratio of placent

weight to birth weight, tended to be larger for smokers than,f(

nonsmokers, mainly because of the dose-related reduction i birth weights with increasins number of cigarettes smoked.

Wingerd and colleagues have studied placental ratios bas(

on data from 7,000 pregnancies among members of the Kaisf

Foundation Health Plan in Oaklatill, Califorpia (156). Smokir

information was obtained early in pregnarrcy, and placenta

were handled according to Benirschke's standardized protocc

Figure 2 shows placental ratios by smoking leiTel and gestatic

for single live births. At each gestational age, from 37 throug

43 weeks'the more the mother smoked during pregnancy, tl

higher was the placental ratio. These ratios were higher f

black than for white women and tended to,increase as matern

hemoglobin level decreased-(156).

Chnstianson's recent report, based on standardized examin

tions of these placentas, has shown that the increase in place

tal ratio with maternal smoking level Was due to considerab

decreases in mean birth weight, accompanied by slight i

creases in mean placental weight. In addition, smokers' place

tas 'were significantly thinner thian those of nonsmokers, ai

their minimum diameters were larger (19). Maternal smoking leads to significant increaSes "in CB

bOxyhemoglobin in maternal and fetal blpod, with a conseque

reduction in the oxygen carrying capacity of both, and a re'clt

ti9n of the.pressure at which oxygen is delivered to the 'et

tissues 70,72,146). Christianson discusses the ,similarity

tween studies of placental ratios by smoking level, altituc

maternal anemia, and maternal cyanotic heart disease. S

suggests that the changes in placental ratio represent an lids

ti

194

200
155

15.0

8 1.4.5

O

14.0

--cts- c

co 13.5

13.9

0 37

Heavy smokers -

No smOteLs....0.00.0../Z)

38 39 . 40 41 42

Week of gestation , 43

FIGURE 2. Ratio of placental w eight to birth weight by 'length of

gestatiqn and maternal smoking category

SOURCE: Wrngerd, J. (1546). ' ry Cation to relative fetal hypoxia (19). An adaptive advantage for survival might occur because a larger placenta with an in- creased area of attachment would deliver more oxygen, and a

smaller.fetus would have a decreased oxygen demand. If so, it is extremely important to 'know whether this reduction in size is

accompanied by any long-term costs in later growth and devel-

'opment.

GESTATION AND FETAL GROWTH'

In early studies the consistent finding that mean birth

00 *eights were lower and the frequency of births under 2,500

ams higher for women who smoked during pregnancy than

r similar nonsmokers raised the obvious question of whether

ttlis might be due to a smoking-related reduction in gestation.

.This is not the case. Studies consistently sho'w that mean gestat on is minimally reduced by maternal smoking (less than 2

d ys) (3,13,146,159) and that birth weight is lower for infants of

s okers than for infants of nonsmokers at each gestational age

( 15,83,146).

. 195

201
The finding that mat rnal smoking does not cause an over

downward shift in the distribution of'gestational ages, as w

shown for birth weigh. If smokers' infants, leads to the conc

sion that the lower weight, must be due to direct retardation

fetal growth. In other words, theie-infants are small-for-dat

rather than preterm. The type of fetal growth retardation ;

sociated with maternal smoking is characterized by an abn,

, mallY short crown-heel length for gestational age (89,9

Smokers' babies are smaller than corresponding non

babies in all dimensions measured, including le ; head c

cumfe-rence, chest circumference, and shoulde rcumferer.

(100,31,52,51,61,102,iO4,146,157).

Previous studies, of these measurements at birth have

ferred that trth size reflects the rate of feral growth; this h

been confirmed by a definitive study in which fetal bipariediameters, were measured serially during gestation. Perss

and coworkers studied 5,715 pregnan6es prospectively, maki

ultrasonic measurements of biparietaldiameters (BPD) from

t., 20 weeks through term. Sepjate growth curves of BPI3 WE

Instructed fur fetuses of sm ers and .rkAmokers whO wf

deiivered between 266 and 294 days after the last menstrt

period! The BPD increased faster in the nonsmoking group; t

difference from the'''smking group was significantly apparE

from the 28th week and wahositively correlated with the av

age num r of cigarettes smoked (Figure 3). Measurattet

taken At llth sho'wed that the distributions of birth weigl

ad lengths. shifted downwafas in proportion to the level

smoking. Figure 4 illustrates this shift (110. These findings c

roborate Miller's characterization of smokers' babies as n

mallys proportioned but short as well as light for dates, a

smaller rn all dimensions than babies of nonsmokers (90). T

data a're also consistent with the speCulation that.relative fe

ma results in a slower mitotic rate, a baby with fewer ce

ands reduced oxygen demand.

LONG-TERM GROWTH AND,DEVELOPIKENT.

Puss' ible lung-term consequences of maternal smoking duri

pregnancy are also of concern. Several lung-term studies p

vide evidence that children of smoking mothers have slight L

measurable deficiencies fri physical growth, intellectual A

emotional development, and behavior (95).

Because thes% complex outcomes are affected by many kno'

and unknown factors, it is important to take these Other fact(

into account in any attempt to measure long-term effects

maternal smoking. Several well-controlled studies have'sho'

196 202
mm

100

BO

70

BPD

7

30

weeks

nonsmokers

CY heavy smokers

ne" 35 # 40

FIGURE 3.Fetal Biparietal Dihmeters (BPD) values [means ' and thaid ard error of means (SE141)1of nonsmokers

and heavy smokers (10 cigarettes/day) plotted in

relation to postinpnstrual age against the normal

range (shaded arel depicts 95% confidence interval)

*OR CE: Persson, P.H. (114).

497

203 ,./
that the p hysical ,growth of smokers' babies remains behin

that of nonsmokers' babies as measured at 7 to 14 days (31);

year, 4 years, and 7 years (pairs of births matched forace, dat

of delivery, maternal age and education, and sex of child) (52);

years (djtisted for other factors) (157); up to 61/z years (prospe

,tive study) (35); and at ages 7 and ,11 (follow-up studies of tl1

17,000 children from the British Perinatal Mortality Study, it

the adjustment for other social and biological factors) (16,30,33

Associations have also been noted between maternal smokiri

and deficiencies in neurological'and intellectual development

the child. Hardy and Mellits Analyzed findings for 88 pairs (

childrep of smokers and nonsmokers, matched for race, 0..te

delivery, maternal age and education, and sex of the child. A

'though they reported no significant differences in intellectu

function between children born to smoking and norzsmokin

mothers, the direction of difference on almost all tests was i favor of the nonsmokebabies. Fewer smokers' tha

nonsmokers',children had normal neurological status at age

year, both in the original 88 matched pairs' and in the addition.

set of 55 pars of children of smokers and nonsmokers, matchE

for birth weight, as well as for the other cited factors. In bot

tsets, smokers' children had lower scores on the majority of tes'

of intelligence and intellectual function at ages 4 and (52,14(

Similarly, Dunn evaluated neurological;intellectual, and b

havioral' status in a prospective study of low-birth-weight is

fants, including 76 who were "small-for-dates" (term and' pr

term), 92 "truly 'p,t4ature" (preterm with birth weight b

tween.11 and 89 percentile) and 151 full-birth-weight contr

infants,'Neurological abnormalities, including minimal cerebr

dysfunction and abnormal or borderline, eledroencephal

grams, were slightly more common among children born

women who smoked (Table 2).

In a battery of psychological tests, the mean scores ofchildr(

of nonsmoking mothers were better than those of smoker's' ch'

dren in 45 out of 48 correlations, and the difference was signi

cant in 14 o these. Some significant difference's' in favor

nonsmokers' children were also demonstrated wttlirespect

behavior ratings and school &cement (35). Tliese results a

very similar to those of Hardijrand Mellits in that the directi(

of the differences was almost always in favor of the nonsmoker

child.

Small numbers and population selection factors were not

problem in the longitudinal follow-tip of the Population

nay included in the British Perinatal Mortality Study, co

prising approximately 17,000 births, an estimated 98 percent

all births in England, Scotland, and Wales during the week

a 198

2 f
'TABLE 2. Incidence of netcrolbgical'al)noimalities at about 61/2

year's, by maternal smokiii habits

POrcg,nt of Children with

Diagnosis

Maternal Stroking.Habits

Diagnosis Smoker Nonsmoker P

Minimal cerebral dysfunction 20.0 1,1.0 '<.05

Total neurological atingrmalities 29.4 19.5 <.05

EEG borderline or abnorma

Lolibirth-weight children) 46.3 32.4 NS

Fullbirth-weig t children 28.2 21.6 , NS

NS not signifi t.

SOURCE: Dun , H.G. (35):'

' rch 3 to 9, 1958. These chil fen have been traced and studied

at ages 7 and 11, to describe their behavior, their health, their, p development, their educational .standard, -and

their home, environment. At ages 7 and 11 years, Physical and mental problems due to maternal smoking during pregnancy were found, and these increased with the number of garettes

smoked. . . s.,:).

Children whose mothers smoked,. 10 or more cigarettes a day

during pregnancy were on average 1.0 centimeter shorter and 3

to 5 months retarded 'in reading, mathematics, and general ability, as compared with the offspring of nonsmokers. After allow-

'nig for associated sociarand biological factors, ag of these dif- ferences were highly significant, as illustrated in Figure

Denson's ase-control study of hyperkinesis reported a highly' significant associatiOn Of hyperkinesis with heavy/ maternal

smoidng, which at a mean level of 23.a cigarettes per day was more than three times the average for two control groups. Pie

authors concluded thatkheir fitidingS.were "consistent with the hypothesis tharsmokingduring pregnancy is an important cause of the hyperkinetic syndrop4! (31).

A recent comparison by Saxton df behavioral patterns ofInfants of Mothers who smoked during pregnancy with infantssof mothers who did not smoke found that these patterns can be

influenced by smoking in pregnancy, and that the auditory

' senses are pdrticularly affected, Fifteen smokers of more than

15 cigarettes per day and 17 nonsmokers were selected rcit

study, matched for maternal age,, social class, and parity. All nts -Atte spontaneous term delfveriets of normal birth

ght. Sex distribution, length of labor, analgesia,'and ObstAtrical factors were similar for the two ,grroupa. Examiners who did

..205 199
Nonsmokers

7- All smokers

Heavy smokers / ,

I

:

:

I

. ,

:

/ .

I

44 46 48 50 52 54. 56"

., Length, cm

FIGURE 4.Distribution of birth lengths

A./ SOURCES Persson, P.H. (114).

not know the smoking status of the mother evaluated the in

fithtscat 4 to 6 days of age, using the Brazelton Neonatal Behav

ioral-Assessment Scale. The scale includes a total of 20 tests am

maneuvers. While many pf these shoveled no statistically signifi

cant differences, all& ory. tests or tests with auditory comps nents were igni different. Recorded "overall' im

pregStons" of the , the end of the test showed that thi

smokers' 'paints .' - 1 Owards "irritability, decreased abilit:

for self-controrte ana a general

to

of interest, whereas th

non'smyke.rF, Liffants tended to be less irritable *sind bette

oriented." The author concluded that some effect on the norms

29.0 206

9,
a) Reading Comprehe won

3

it 2 / . t

co

o:. c 1 13 Test for differences between it 0

F 3 smoking categories after

-;-1 adjusting for other factors

"mom -2 X D F ) = 130 1, P < 0.001 Is2(2,

E TS _3

E E

o \-4

c -5 .

I -,.o _6 ,

.

7°3 -7

a) n = 8,545) (n -_-: 1,981) ( n = 1,489) 0

0 1-9 10+

Amount smoked per day af ter 4th month of pregnancy

b) Mathematics Ability

3 /

ot. ai ' 2

it 1 EN2° 0 732

?2%.g"

-1

-2

.d; -. E > o -3 O E

it

co -5

E .1 -6

6 .5, 1

Test for differences between

3 smoking categories.af ter

adjusting for plhpr factors

X2,(2 D F) = 1WO, P <0 001

(n = 8,543 (n = 1,980) (4-1= 1,489) . 0 1.9 10+

Amount smoked per day after 4th month of pregnancy

c) Height , 144 5- .

.1

..."

143_0-

. Test for differences between) - 3 smoking categories * after adjusting for other factors

X2(2 0 F )= '60.4vP < 0 001

(n = 7,649) (n = 1,729) (n = 1,316)

.

.

6 1.'9 16+

Amount smoked per day after 4th month of pregnancy

J

...

FIGURE 5.Tests of 11-year-old children by mothers' smoking

. habits/after-thefourth month of pregnancy

N

SOURCE: Butler, N.R. (16).

201

.207
t , hearing mechanism had occurred in itif4nts of smokers, possi

due to a, hypoxic effect of carbon monoxide on the cuchl(

organ during development (132).

These studies suggest unfavorable effects oNnaternal sm

ing during pregnancy on the child long-term growth, intell

tual 'development, -ann behayi-ofal Ohracteristics. Althou

these changes are tTifficuk.f4Stddy-tecause of the vast cOmpl

ity of,possible antecedent and confounding variables, h:

priority should be'gi4n Co obtaining conclusive answers ab(

the long4term consequences of fetal exposure to cigare

smoke: f

6

ROLE OF MAT ANAL WEIGHT GAIN.

In,the search foP.mechanisms through which maternal sm

mg reduces birth Nreight, the question has been asked whet!

it might be an inthreyt result of reduced appetite, less intak(

food, and lower Maternal weight gain (84,127). Several ea

studies reported no differences between smoking and nonsm

ing women in intake of food, or in weight gain, and coriclu(

that. the effect of mStqinal smoking on birth weight was

mediated in this Nica4y p46).

Meyer analyzed the relationships between maternal smoki

tiFth weight, maternal weight gain, anti gestation, using d

based on 31,188 births froM the Ontario Perinatal Morta

Study (106,107). She found a significant downward shift in

disthbution of birth' weights as maternal smoking level

creased,. but no similar shift in the distribution of mater

weight gain with Amoki4g. Whereas the usual strong relati

ship between the proportion of births under 2,500 grams

maternal smoking level was found, there was no similar tr(

for the proportion of mothers who gained less than .10 pou

during pregnancy. Finally, the proportion of. infants weigh

, less than 2,500 grims increased directly with the amoi

smoked within each ?aternal weight gain group from less p

5 pounds to 40 pounds or more, as shown in Figure 6 (83). Fr

Figure 6, one might conclude that smoking has a more

flounced effectors lOw birth weight when maternal weight g

during pregnancy s less than 20 pounds.

Other studies have indicalled a lack of relationship'betw

smoking and maternal weight gain, while demonstrating a

rect"Yelationship between smoking and fetal growth rate.

German prospectkve study of 6,200 pregnant women, exami:

every month from the first trimester through delivery,"ehol

no significant.association between smoking habit and \f,Tei

gain. The usual relationships were found between smokiing

zog 0 208

a
25

20

15

10

5

0

r. E

co o 20 0

CV 15

V P.w 10

co 0-

5

0

4

0.4 5-9

4

Private Hospjtal Stat.,

1::1 Nonsmoker

<1 Pack/Day.

Eza 1 + Pack/Day

rig -ER rya- me .,-q

10-14 15.19 20.24.25.29 30.34 35-39 40 +'

Maternal Weight Gain (pounds)

Public liospitakStatus

0.4 -5,9 10-14 J5-19 20-24 25.29 30.34 35.39 40 +

Maternal Weight Gain (pounds)

FIGURE 6.Percentage of birth weights under 2,500 grams by

maternal smoking level within maternal weight gain

group (five-pound intervals) by hospital pay status.

Births of 38,4- weeks gestation (Ontario study)

SOURCE: Meyer, M.B. (83).

small- for-dates babies, with general retardation of weight, length, and head circumference in proportion to the numberbf

cigarettes smoked during pregnancy (80). Miller and Hassanein

also found that the effects of smoking on fetal growth did not

appear to be related to maternal nutrition (93). Persson's study

showing retardation of fetal growth of smokers' babies by serial

measurement of biparietal diameter's and by weight, length,

and other measurements at birth showed that the low birth

weights,were independent of maternal weight gain. These authors concluded that the kal growth retardation resulted from

a direct phaemecOlogical effect of smokitig on the fetus "rather

than an i'bfluence resulting from nutritional deprivation" (114). Hajeri and colleagues studied matemal weight. gain in 105

smokers of 10 or more cigarettes a day.with a control group of nonsmokers who wtre similes with respect to gestation, age, height, parity, and maternal weight at conception. Birth

weights, specific fOr sex, were significantly higher for infants of

*IP ^203

2 (A9
**

TABLE 3.---1Birth weight under 2,500 gm 13) m rnal_smoking

and prepregnant weight

6

Prepregnant

Weight

Total

Btrjhs

Births <2,500 gm per 100

Total Births

Maternal Smoking

(Packs per day)

'Ratio

Smoker:Nonsmoket

0 <- 1 1- <-1 1-

.7

<120 lb

(<54 kg) ,,,,, 120-134 lb

154-61 kg) .

135.4- lb-

(>61 kg)

18.935

, 19,798

10.456

6.1

4.2/

3.3 ,

1.0.2 6.3

5.1

15.8

9.5

8 7

1.7

1,.5

1.6

2.6 ' 2.3

2.6

-r SOURCE: Meyer, M.B. (86).

nonsmokers, with a mean diff'erence for boys of 330 grams an

for girls of 320 grams (p< .01)). Mean extrauteral weight gain

calculated as the difference between maternal weight gain an

the weights of fetus alid placenta, 'vas 7,044 grams for smoker

and 6,899 gramsjor nonsmokers (49).

Garn has compared mein birth weights, specific for gesta

tional age, of babies of obese smokers; all nonsmokers, and al

smokers, using data from the Collaborative Perinatal Project o

the National Institute of Neurological and Communicative Di:

orders and Stroke (NINCDS). Obesity was defined as the top 1.

percent of the dittril;ution oprepregnant weights, shown sepa

rately for black and white women. Babies of the 1,383, obes

white smokers had mean birth weights similar to the tota

group of white nonsmokers and higher than the total group o

white smokers. The 1,001 ()these black smoking mothers ha(

babys whos4 mean birth weights were generally higher thai

those of all black nonsmokers, leading Garn to concludeba

"maternal obesity (weight-defined) apparently cinteracts th,

smoking effect on the conceptus" (43). Because birth weight strongly correated with maternaLsize, a more appropriate

comp\arison would have been between mean birth weights of th

babies of obese smokers and the babies of obese nonsmokers

That such a companson would show the usual relationship t

maternal smoking level is suggested by Meyer's analysis o

birth weight by maternal smoking and prepregnancy weigh

(Table 3). The correlation between maternal weight and th

proportion of logy- birth- weight babies is clear at each smokini

level, and\the independent relatiopship between smoking 'eve

and low birth-weight is Blear at ai c level of maternal w ighi

4.4,7 204 , 2

'6\1
c

TABLE 4. Mean birth weights in successive pregnancies to the

same women, by smoking habit

Smoking Habits Smoking Habits First Second

pregnancy pregnancy

Mean

Birth Weight (gm)

Difference

N * 1 * 2nd- 1st (gm)

Smoker Smoker' 886 3204 3228 -24

Nonsmoker Nonsmoker 988 3356 3388 .32

Difference: Nonsmoker - Smoker (gm. .152 -160

.Srpoker Nonsmoker 119 3171 3381 +110

Nonsmoker Smoker 108 3323 3265 -58

Difference: Nonsmoker - SApker`fgrni +52 -116

SOURCE: Naeye. R. (93).

The relative increases in the proportion of low-weight births

with light and with heavy smoking are almost identical in the

three strata orprepregnant weight (86).

Studies of birth weight, maternal weight, and maternal weight gain should also be ca,refully controlled for maternal age and parity. In studies of successive births to the same mother

included in the Collaborative Perinatal Project of the NINCIJS, Garn found' that prepregnancy weights ,increased with successive pregnancies by similar amounts for smokers andnonsmokers (44)..Naeye, 'using the same database, reported that mater- nal .weight gain was less in the second pregnancy than in the

firgt pregnancy for smokers, for nonsmokers, and for wometl

' who changed habits between pregnancies in either direction

(93). Second babies weighed on the average 24 grams more than

first babielif the.mpther smoked both times, and32 grams more

if he mother smoked neither time (Table 4). If the mother

smoked during the first and not dbring the second pregnancy, the second baby weighed tin average of 110 grams more than the

first baby; in women who smoked during the second pregnancy but not during the first preg'nancy, second babies averaged 58 grams less than first babies (93).

Themost careful analyses indicate that the effect of maternal smoking is a direct one not mediated through an effect on maternal apketite, eating., or weight gain. In coriclusion, as stared in

a Lancet editorial, "iiiitaripeal of the nutritional hypothesis is

that women might be more readily encouraged to eat more durink pregnancy than discouraged from smoking.... However, if,

205 '
= .4

as,now seems moreirkely, the growth-retarding effect, of smok

ing is dile to fetal hkpoxia, there is no.short-cut to removin,

th1s adverse influence" (63). This conclusion in.no way obviate

the enormous importance of dietary factors during pregnancy

Overt maternal malnutrition is associated with inadequat

growth. Recently, It has been suggested that more subtle alter

ations intthe maternal supply of essential nutrients combine(

with compromised uteruplacental circulation may contribute t

reduced fetal growth. Crosby, et al. (26) observed that the con

centraticas'Of each of 14 amino acids and carotene weN reduce

significantly in the=blood of smoking mothers. These worker

postulat4dlihat, while these differences were on the order of 1

,01-20- percent, they could be an important factor in producin.

the small .for-gestational-age infants associated with maternE

smoking. 1'n a study of over 1,100 pregnant women, Schorah, e

al. (1:35) noted an inverse correlation between the number c

cigarettes smoked and the leukocyte ascorbic acid concentrE

tion. For instante, the leukocyte ascorbic acid concentratfo:

was about percent less it the blood of Women who smoke

more than 20 'cigarettes a day as compared with controls. DE

spite a 15 percent increase ip the number of circulating leukc

cytes in the blood of smokers, the blood ascorbic acid concentrE

tion was still 10 percent less than in controls, These difference

were even more marked in women frorp lower socroeconomi

groups. The authors suggested that in addition to the role c

ascorbic acid cn fetal nutrition, these lowered concentration

might be related to the icicreased incidence of premature rur

ture of the amniotic membranes in smoking women.

Smoking, Fetal and Infant Mortality, and Morbidity

'SPON ANEOUS ABORTION

Pa t studies have demonstrated a statistically significant ai

sociation between maternal cigarette smoking and spontaneou

abortion (65,61,104), some showing a strong dose-response r(

lat1onshlp (110,144,162). SpontaneOus*bortions are difficult t

study because 'of problems of ascertainment. In prospectiv

studies, early abortions may be missed, and bias may occur

one group t ncts to register earlier than the other. cc Retrospecwe studies a low more complete ascertainment but are subje(

to errors of recall. Nevertheless, higher rates of spontaneou

abortion have been associated with Maternal smoking in bot

types of studies (61,104,162). Kullander and Kallen found higher rates of "spontaneou

abortion" among smoking women, but noted that many of then

206

21.?
I

pregnancies were unwanted. Analysis of their data showed that the relative risk of spOntanews aboitiOn of smokers compared with nonsmokers was 1.20 for wanted and 1.35 for unwanted

pregnancies (61). A casecontrol study of spontaneous abortion with important variables held constant repdrted an 80 percent

increase in the odds of smoking among the cases compared with

controls (60).

Recent studies corroborated the finding of associations between smoking and spontaneous abortion risk. In a small retro.'

spective study in New Zealand, Fergusson found that women..

vi.ho smoked more than 20 cigarettes a day had almost twice the nonsmoker risk of having had a previous spontaneous abortion#

and that the association could not be explained by differences in

maternal age, educational level,4 parity, race, socioeconomic, status or marital status (42). Ln a study of 12,013 consecutive pregnancies in Dublin, Ireland, Murphy and Mulcahy folind a positive msociation between the number of cigarettes' smoked and the rates of spontaneous abortion, independent of the ef- fects of maternal age and parity. The author stated that induced abortions are a negligible factor in Ireland and conducted

that maternal smoking leads to reduced reproductive efficiency

at all stages of pregnancy (92). Himmellierger and colleagues

surveyed a group of professional women in medicine concerning

the influence of maternal sinoking on their 12,194 pregnancie§

(54). After controlling for interfering variables, the risk of spontaneous abortion for certain subgrdups of heavy smokers was estimated to be as much as 1.7 times that for nonsmokeyr: Spontaneous abortion rates were towest in the 25 to 29 year old cate- gory, increasing with age to levels of 33 and 36 percent for nonsmokers and smokers, respectively, at age 40 plus. The relative increase in\risk associated with maternal smoking was highest at the yoangest ages and decreased* with increasing age

(54),

An editorial in the British M6dical'Jourrial summarized these

findings and stated: "Cigarette smoking, Jie of the first manifestations ,of women's social emancipation, is emerging as a possible threat to her procreative role." The proportion of ab- normal karyitypes in'abortuses of women who smoke appears

to be reduced rather than increased (1). t* he mechanism underlying the smoking- related excess appears to be due to amplicatiobs of pregnancy rather than to any fetal abnormality (13).

'CONGENITAL MALFORMATIONS

Seyeral studies have reported perinatal, fetal, or neonatal motif:114y rate's by cause. In these comparisons, death rates due

P 207

2-1 .e?
VTABLE 5. Incidence of congenital abnormality (a single birtlNonsmokers Sinokers

Number Percent Nuriar Percer

Total abnormal infants

Type of abnormality

Anencephaly

a Spina bifida

Other C.N.S. abnormality

Cardiovascular abnormality

Gut abnormality

Genitounnarrabnormalit;

Bone abnormality

Cleft palate and or hare hp

Other abnormality

18

20

38

34

21

.39

65

10

19

4

2.37

0.2

0.22

0.42

0.37

0.23

0.43

0.72

0.11

0.21

15

23

:36 32

24

25

52

20

18

2.73

0.2

0.3

0.47

0.42

0.32

0.33

0.68

0.26

0.24

x2 (all abnormalities) = 2.22, p >0.05.

x2 (cleft palate and hare lip) = 5.36. 0.01< p <0.05,

SOURCE' Andrews, J. (3).

to congenital malformations have usually been lower for smo

ers' than for nonsmokers' infants (3,22,46,87). This is compatib

with the finding that smoking-related spontaneous abortioi

have a lower frequency of abnorrrial karyotypes and tend

occur later than spontaneous abortions in norwokers. As pr

viously described, increased losses of conceptu7issociated wimaternal smoking, appear to be due to pregnancy problems ai

complications rather than to abnormalities of the embryo

fetus (41). Andrews and McGarry, community study

18,631 pregnancies in Cardiff, Wales, reported that smokers' i

fants had lower mortality rates from malform,ations than tho

of nonsmokers. Rates of stillbirths due to congenital malform

tions were 0.32 and 0.27 per 100 nonsmokers and smokers r

`spectively. Corresponding rates for neonatal deaths were 0.

andp.31 per 100 babies of nonsmoking and smoking mothers.(

the other hand, the incidence of congenital malformatiol

among all single births in Andrews' population was high

among smokers' babies, overall, and Ipecifically higher for c1(

palate and lip. Among other sites, some were higher for smoke

and some for nonsmokers, as is shown in Table 5 (3).'

A significant positive association between cardiac malform

tions and materntl smoking was shown by Fedric1 and c(

leagues, based on firm diagnoses among stillbirths, neonat

deaths, and survivors to age 7 from the British Perinatal Mc

tality Survey. However, this difference was largely due to t]

inclusion of patent ductus arteriosus, which may or may.flot 1

classified as a malformation (80).

208 21 .1,
.09

>. ;1 .08 E

8, .07

Jo

7aa .06

-,q; .05

0

g .04 0

75

,

.03

e

. -.02

.o2

co n .01 a. 0

.

./../4/ 4. ...ND

... .... Heavy Smiker ................

.... ..... .... ...

....., .......

..... -,-- .. Moderate Smoker

-.... ... Nonsioker

...

1 I 1 1 ,1 1 1 1 1 1 1 1 1 1 jr 1 1 1 18 22 26 30 34 38 42 46 ,. 50

-----. ....-A ' Maternal Age

*: .;..1/'

....%

/

FIGURE 7.Risk of congenital abnormality according to age and

smolbig habit r

SOURCE: Himrnelberger, D.t. (54). 1

ale Some recent studies have shown a positive association be-

' tween maternal smoking and congenital malformations, defined

in a variety of ways, Himmelberger and colleagues carried out a . mail survey of professional women in medicine (54). They were

interested in exposure to anesthetic gases in the operating

room, and evaluated possible effect's on pregnancy outcome of a _number of factors including cigarette smoking. Information was obtained and analyzed by a multiple logistic regression based

on 12,914 pregnancies, includhig 10,523 live' births, Which repre- sented a response rate of 53.2 percent. After the effects of age,

e

. xposure to anesthetic gases, and pregnancy history were con- trolled; the risk of congenital abnorinalities for babies of

mothers who smoke was estimated. A statistically significant risk (p-- .05) for aternal smoking was foimd. Figure 7 shows

the utimated risk of congenital .abnormality as a function of

maternal age for ponsmokers, moderate sm'okers (1 to 19 per day), and heavy sinokers (20 plus per day). Relative risks for heavy smoker's compared with nonsmokers were as high as 2.3. ' Rates of abnormalities in each general category were higher for

the children of smokers (see Table 6). The significant increase in

cardiovascular abnbrmalities among smokers' children is in

agreement with Fedrick's findings (40) and in general agree209

Jo o

. n5 X 2
TA13\is. IL Comparison of congenital abnorma lity rates for , babies born of smokers and .nonsmokers, by type of

abnormality

Abnormality

Smokers

No.

Nonsmokers

Flc No.

P*

Carchovascula.4. 19.07+ (68) 13.65 (95) 0.02

Respiratory 15.15 (54) 12.07 (84) 0.10

Musculakeletal 23.84 (85) 19.69 (137) 0.08

Gastrointestinal 13.46 "(48) 9.48 (66) 0.04

Central nervous system 11.50 (41) 10.20 (71) 0.27

Urogenital 21.32 (76) 15.81 (110) 0.02

'One -tail significance level for the test of the difference between two

Proportions.

+Rate is number of congenital a bnormalities pe'r 1,000 hve births. Rates

based upon .3,565 live births amonethe smokers and 6,958 iivceSirths among

the nonsmokers.

SOURCVIiimmelberger, D.U. (54).

ment with the study of Andrews and Mc arry (3)., Himmel

berger, et al. point out that thtir findings are based on retro

spective survey data, obtained by mail, and therefore subject t(

bias from various Sources, including that of a high nonrespong(

rate. Howevelk the Study methods have been designed to elimi

nate those effects (54)..

A recent study by Borlee and Lechat conti-ollej for confound

ing variables by matching births with congenital malformation.

d to control births according to hospital and time of birth, mater

nal age, sex otchild, and socioeconomic level of parents. Tw( hundred and two children with malformations diagnosed a

birth were compared with 175 controls, from a total of 17,97(

consecutive births studied from June 1972 through May 1974

No differences were found between ,cases and controls in th(

dtalribution.of smoking habits, including the number of cigar

ettes smoked' with or without filters. Sixty-six percent o

mothers of malformed infants and 68 percent of mothers of con

trols were nonsmokers. Fathers' smoking habits were also simi

lar among cases and controls. Significantly more mothers .o

malformed infants were heavy coffee drinkers (8 plus cups'pe:

day). Because of the frequent association between heavy coffer

drinking and smoking, both habits should be included iri studies

of environmental factors possibly related to the risk of congeni

tal malformations (10). The same is true for consumption of al

cohol in poptflations where drinking is prevalent. Mau and Netter have reported births by gestation, birtl weight, perinatal mortality, and the incidence of congenita

malformations by smokingchabits of fathers in 3,696 cases ii

210

2i
which the mother was a nonsinoker. Trends toward lower birth

weights and more preterm births with increasing levels of paternal smoking were not statistically significant. In the total

study of 5,200 births, regardless of maternal smoking habits,

there was a significant increase in the incidence ofsevere malformations with increasing levels of paternal smoking, children

of heavily smoking fathers had about twice the expected incidence. Although malformations in all systems were more frequent if the-father smoked over 10 cigarettes per day, only the

'differences in facial malformations were significantly different

(p .91) by smoking level. Theauthors stiate that the trends

with paternal smoking were independent A maternal smoking

level, maternal and paternal age, and social class (120). More studies of these possible relationships are urgently

needed. As serious malformations are relatively rare, the case

control' approach is probably`the method of choice, with careful

matching of ca-§es with suitable controls.

PERINATAL MORTALITY

The 1973 report, The Health Consequences of Smoking and

the 1979 Report have summarized studies demonstrating a direct relationship between level of maternal smoking and risk of perinatal loss. The reports have also clarified reasons for the

variation in risk observed in these studies (146,147).

Two important reasons for variability between studies have

' been demonstrated. First, other important variables such as

age, parity, race,'ands.socioeconomic status influencethe results

if they are unequally distributed between comparison groups of smokers and nonsmokers (89). Second, cigarette smoking is more harniful to the pregnancies of certain Fmen than to

those of others. In general, women with other risk factors were

at greater risk from smoking than otherwise low-risk women

(3,15,22,128,144,159).

Table 7 illustrates these points. It shows that women characterized by low social class, low levelof education, being very

young or during pregnancy, or being black, have higher

risks of perinatal mortality than their counterparts. Their increase in risk due to smoking is relatively greater. Meyer, et al.

measured the perinatal mortality risks of light smokers (less

than a pack of cigarettes per day) anclIO'Of heavy smokers (one

pack or more per day) relative to nonsmoker risks fkithin subgroups of the population. The increased rigk of perinatal mortality for light smokers who were young, low-parity, and nonnemic was less-than 10 percent. At the other extreme, mothers

racterized by high-pa public hospital status, previous

211

21 1;
-/

-TABLE 7.Examples of perinatal mortality by maternal smoking status related to other subgroup

characteristicg

Study

Population

No. of births

Perinatal or neonatal

deaths/1,900 births

NonSmok&'s . Smokers Cakrgory.

Nonsmokers Smokers

British Perinatal Mortality 11,145 4,660__1Social class Survey, England, all births * . 1Z2 (high) 25.8 -26.3 \ 3-5 33.5 46.6

Washington CO, Maryland,

white

7,646 ' 4,641. Father's

education

9+ years 14.4t 16.11

8,years 17.6t 38.0t

Northern Finland, white 8,898 2,346 23.2 23 4

California, middle to Race

upper middle class 6,067 3,726 White .11.0t 11.3t

2,219 1,071 Black 17.11 21.5t

Boston City Hospital //to, ---. Race t. Prenatal Clinic 513 892 f White 29.2 31.4

1,225 636 Black 28.6 54.1

-Quebec, 10% sample of 3,912 2,967 Maternal age registered births 12.1 16.1 0 " 25-34 126 13,2

35+ 23.0 41.7

Relative

risk*

1..02

1.39

1.12

2.16

1.01.

1.03

, 1.26

1.89

1.33

1.05

*R4tio of modality rate for smokers' to nonsmokers' babies.

flkteonaoil onTy.'

B(MRCEhlileyer, M.B. (88).
I

Social Class

40

1 & 2

03 3

4 8,5

30

20

10

0

01, ;;

4 - Para Para Para Para Para Para

1,2,3 0 .4+ 10,3 0 4+

Under 35 years 35 years +

FIGURE 8. Theoretical cumulative mortality risk according to

"smoking habit, in mothers of different age, "parity,

and social class groups

SOURCE: Butler, N.R. (1*.

low-weight births, or anemia had an increased perinatal mortality risk of 'it to 100 percent when they were heavy smoke rs.488).

To help visualize the interacting effects of maternal smoking

and of other factors on perinatal mortality risk, Butler has calculated theoretical mortality risks based on data from the

British Perinatal Mortality Study. In Figure 8, perinatal mortality risks by social class, maternal age, and parity are arranged in order of incraOng magnitude. The differences between smokers' and non okers' risks Are represented by the height of the bars, which varies depending on- other rislefactors

4(15). .o These studies show that the risk of spontaneous abortion, of

fetal death, and of neonatal death increases' :iirectly with in- creasing levels of matetnarsmoking during pregnancy. Studies

of smoking during pregnancy show a"raRge of perinatal mortality risk ratios (smokers versus nonsmok!rs) from a low of 1.01 to

. a high of 2.42. Variability between risk ratios in different study Y

populations may be due to lack of comparability between smokers and nonsmokers in other respects, or to interaction between%

smoking and other,pregnancy ji factors. Studies failing to

I a

213
take account of other important variables may show unusual

high or unusually-low risk ratios.

CAUSE OF DEATH

The increased perthatal mortality associated with matern

smoking is concentrated within a few cause-specific categori(

Excess stillbirths have been associated with antepartu

hemorrhage or abruptio placentae and with "unknown taus

(3,46). Excess neonatal deaths were associated with immaturit

asphyxia, atelectasis (23); and with the respirat distre

syndrome (3).

, Meyer and Tonascia (87) an lyzed fetal and neonatal cleat'

to identify causes of death whi h showed an excess if the moth

smoke etal and neonatal deaths by coded cause and mat(

nal sm king habit are shown in Table 8. For each cause t:

observed numbers fez. smokerwere compared with the numb

expected at nonsmoker rates. The differences between observ.

and expected numbers indicate the number of deaths in ea

categol7 attributable to maternal smoking.

Fetal deaths showed a major smoking-related excess in t:

category of "unknown" cause and some increase fr6m "anoxia

and "maternal cause." By contrast, neonatal deaths related

smoking were in the category of "prematurity alone," or in t:

related dategory of "respiratory difficulty." The tentative co

clusion to be drawn here is that fetuses and neonates who

deatlpWere related to maternal smoking had no recognizat

pathaogy, but had died in utero from anoxia, maternal cause,

unknown cause, or had suffered the consequences of preter

delivery.

Complications of Pregnancy and Labor

Studies have consistently found a direct relationship betwe(

maternal smoking level and the incidence of placenta prev

abruptio placentae,' bleeding during pregnancy ,and prematu

rupture of membranes (3,24,46,61,86,87,94,95,130,144,145). T:

association is independent of socioeconomic and racial bac

ground (144), parity (3) and many other factors (86) (Figure E

These complications carry with them a high risk of fetal al

neonata loss, and are frequently cited as the cause of death amol

the offspring of women who smoke. Kullander and Kallen fount

signifidant increase in frequency of abruptio placentae amol

smokers' children dying before the age of 1 week (61). I n a prosp(

tive study of 9,169 pregnancies by Goujard and colleagues, a lar

reoportion of the increase in stillbirths among smokers w

caused by. abrutio placentae (46).

4t I' 214

)
TABLE 8.-Fetal and treona al deRtis by coded cause and

maternal smoking habit

mothers)

anadian English-speaking

Coded cyse

Obierved

Expected

smoker'

Observed

Expected

difference

P+

Nonsmoker Smoker value

Fetal deaths

Unknown 75 125 81.4 A3.6 0.003

Malformations 32 24 34.7 -10.7 N.S.

Hemolytic disease 11 15 11.9 3.1 N.S.

Anoxia 16 29 17.4 11.6 N.S.

Maternal cause 31 45 33.0 11.3 N.S.

All others 8 13 8.7 4.3 N.S.

Total 173 251 '187.9 63.1 0.003

Neonatal deaths

Unknown 52 51 56.5 -5.5 N.S.

Malformations 22 24 23.9 0.1 N.S.

Hemolytic disease 7 8 7.6 OA N.S.

Respiratory difficulty 46 63 50.0 13.0 N.S.

Prematurity alone 33 65 35.8 29.2 0.005

Maternal cause 2 6 2.2 3.8 N.S.

All others 16 16 17.4 -1.4 N.S.

Total 178 233 193.3 39.6 0.06

Total Births 15,240 16,549

N.S. = not significant.

"Based on nonsmoker rate.

p+ value derived from chi square based on a null hypothesis of no difference i....: between smokers and nonsmokers.

SOURCE: Meyer, M.B. (87).

.41P

Naeye reviewed the 'clinical and postmortem material from

the 3,897 fetal and infant deaths in the Collaborative Perinatal

Project of the NINCDS (102) and reported an association between perinatal mortality rates caused by abruptio placentae,

and number of cigarettes smoked by the mother (95). Abruptio

placentae was the underlying cause identified in 11 percent of

all the deaths in this large study (94). .. Analysis of data from the Ontario Perinatal Mortality Sttidy

corroborated these findings. Increasing levels of smoking resulted,in a highly significant increase in the risks of placental

abruptions, placenta previa, bleeding in pregnancy, and pr

ture and prolonged rupture of membranes. Fetal and ne I,

deaths were analyzed for associations between them nd

smoking-related excesses of yarious coded c plications of f pregnancy and la' bor. Although most diagnoses owed no association with excess mortality for smokers' babi s, a few stood

215

221
4.0

2.5

-0 Nonsmokers

Smokers

MP'

41,

12 16 20

1 I 1 1 25 30 34 38

Gestation (weeks)

FIGURE' 9. Mean plasma olume in nonsmokers and smokers

SOURCE: Pirapi, B.B.K. (117).

out is highly significant. Excess fetal deaths of smokers' babie were strongly associated with bleeding during pregnanc

either,before (1) = 0.01) or after (p = 0.0005) 20 weeks gestatio:

In other coded categories, a significant excess of fetal deati

qccurred among smoking mothers with abruptio placenta

(p = 0.0001) or other obstetrical problems. Similar comparison

were ,made for neonatal deaths. A strong, significient relatioi

ship bet een smoking-related excess neonatal deaths and a hi

tory o1 bleeding before 20 weeks of gestation was foun

(p = 0.0 01). Other Categories that showed significant increase

of smoking-aisociated neonatal deaths were the ad missio

status Of rupture of membranes only, other obstetrical comp]

cations,, a ,pd Oration of rtfPture of membranes over 48 how

(87). ° 2°0)

216 ,y,

, A
PREECLAMPSIA

Several published studies have reported that the incidence of

preeclampsia is declining as the number of cigarettes smoked

increases (109,145). Data from the British Prenatal Mortality

Study were cross-tabulated by parity, severity of preeclampsia,

and maternal smoking status. Smokers had lower rates of all

grades of preeclampsia than nonsmokers, whether they were

primiparae or mu "ltiparae (15). Andrews and McGarry showed

that the inverse relationship between cigarette smoking and

pree'clamptic toxemia was independent of social class, maternal

-weight before pregnancy, inc.!' maternal weight gain during

pregnevey (3). Despite this effect of smoking on the incidence of

preeclahipsia, there is a greatly increased risk of perinatal mor-, tality if preeclampsia does develop in a smoker (3,34,129). Sev- eral authors have suggested that this negative association may ),

be due to the hypotensive effect of thiocyanate, which is derived

from the cyanide present in cigarette smoke and is regularly

found in the blood of smokers (3409). Because preeclampsia is

predominantly a complication o first pregnancies, it is possible

that the occasional finding of reduced rates of perinatal mortality in ydung, primiparous, light smokers who are otherwise

healthy is due to this relationship.

Pirani and MacGillivray performed seven serial meastiements from the end of the second trimester until term in 31

nonsmokers and 29 smokers. After 25 Weeks gestation the plasma volume of smokers failed to keep pace witfi that for nonsmokers, the increases in volume being 25 percent less in

smokers (Figure 9). Plasma volume and total body water expan- sion are related to birthweight, at least in primigravigas. After

30 weeks of gestation, total body water in smokers plateaued in

contrast to nonsmokers, so that by term their body water volume increase was about,25 percent less. Serum heat:stable alkaline phosphate levels in smokers significantly exceeded the

concentration in nonsmokers from the 37th week of pregnancy

onward. This enzyme is of placental origin, and cigarette smoking may contribute to this change biits effects on the placenta

(117). . Whether the reduction in the incidence of preeclampsia with

maternal smoking is due to the hypotensive effects of thiocyanate,

to the reduced size of the baby, to a smaller increase in maternal

blood volurhe, or to another process requires further study.

PRETERM DELIVERY, PREGNANCY COMPLICATIONS,

AND PERINATAL MORTALITY BY GESTATION

Studies of large number's of births to measure mean gestation

by smoking habit have demonstrated differences of only a day

217

223
J

or tivo. This finding led to the conclusion that maternal smoking

does not affect gestation (14,52,74,102,146,159). On the other

hand, abundant evidence has been presented that a smokingrelated increase in preterm delivery plays an important role in

the increased risk of neonatal death for infants of smokers.

When the proportion of preterm births is measured, rather

t the mean gestation, smders have shown consistently

h iglier rates than nonsmokers, as illustrated'ln Table 9. In four

studies in which all births and perinatal deaths- were included,

the risk of early delivery increased froM 3d to 47 percent if the

mother smoked, and 11 to 14 percent of all preterm births could

be attributed to maternal smoking (3,15,38).

Figure, 10, using 'data from the On %ario Perinatal Mortality

'Study, shows percentage distributions by gestational age of

births to nonsmokers, light smokers, and heavy smokers, plotted on a semilogarithmic scale to etnphasize differences between smoking-level groups in very preterm births. There is

little difference between the means of thesesurves because the

great majority of births occur around term in all groups. There

is, however, a significant and dose-related increase in the pro,

portions of preterm babies born to women who smoke. These

preterm deliveries account for a small proportion of total births

tint for a large proportion of the deaths (82,146).

As previously reviewed, Meyer and Tonascia have related the

excess fetal and neonatal mortality of smokers' infants and the

excess incidence of pregnancy complications among women who

smoke to the gestational age of occurrence, using a life-table

approach. A Starting population of all pregnancies in utero at 20

weeks was used to calculate the probabilities of fetal death, live

delivery, followed by survival or death, or the occurrence of a

complication followed by fetal death or .delivery. At 28 week's

,(,the next point defined by the data), the population at risk included those remaining in utero at that point. Figure 11 shows

the probability of perinatal death during each period of gestational age starting at 20 weeks. Risks for smokers' infants were

significantly greater in the earlier weeks, but not different after

38 weeks gestation (87,146).

A similar aPproach was applied to determine the risk by gestation of abruptio placentae, placenta previa, and premature

rupture of membranes for smokers and natsmokers. The risk of

all these complications was higher for smokers throughout gestation, but in all the differences were most significant in the

weeks of pregnancy from 20 to 32 or 30 weeks (87,146). The lower

lirnitof 20 weeks was built tntQthe study design, which included

all single births of at least 20 weeks gestation (106,107).

These studies show that excess deaths-of smokers' infants are

218

2 rvi
TABLE 9.Preterm births by materna smoking habit: relative and attributable risks, derived from publishes studies

----- Preterm Births* Relative

(..." p4r 100 Risk Attributable Smokers Total Births Study Smokers/Non. Risk (proportion)

.Nonsmokers Smokers sinners % i

Cardiff

Great Britain

.465 6.7 9.2 1 36 14 .274

Montreal 4.7 6.9 1.47 ) 11 .432 ' a Ontario . 7.7 10.6 1.38 14 .435 7 4 10.1 1.36 ' 14

1 'Cardiff and Ontario data are for <38 weeks. All others are for <37 weeks.

SOURCE: Andrews, J. (3), Campbell, J.M. (15), Fabia, J. (38), Meyer, M.B. (146). (86), U.S. Department of Health, Education, and Welfare
80.0

1

' 0 2

0 1 } I I I I I I I 1 I I 1 I 20 221 28 32 36 40 44 +

Gestation. Weeks

/ . FIGURE 10. Percentage distrution by weeks of gestation of

births to nonsmokers, smokers of less than one - pack per day, and smokers of one pack per day 'oi

more

SOURCE: Meyer,M.B. (82).

found mainly in the coded cause categOnes of "unknown" any

"anoxia" for fetal deaths, and in the categories of "prematur. t:

alone" and "respiratcry difficulty" for neonatal deaths. i

finding indicates that the excess deaths result not from abno

malities of the fetus or neonate, but from problems related t

''"-----2 20 2:g I
the pregnancy. Increasing levels of maternal smoking result

a highly significant. increase in the risks of placental abruptions, placenta previa, bleeding early or late in pregnancy, pre- mature and prolonged rupture of membranes, and preterm delivery, all of which carry high risks of peririatal loss. Although, there is little effect of maternal smoking on mean gestation, the proportion of fetal' deaths and live births that occur before term

increases directly with maternal smoking level. Up to 14 per- cent of all preterm deliveries in the United States may be attributable to maternal sn'tNcing. According to the results of one..

large study, the most significar4rdifference between smokers'

and nonsmokers' risk of perinital mortality(and pregnancy

complication occurs at the gestational ages from 20 to 32 or 36 weeks.

These findings lead to the conclusion that maternal smoking

can be a direct cause of fetal or neonatal death in an otherwise

normal infant. The immediate cause of most smoking-related

fetal deaths is probably anoxia, which can be attributed to pla- cental complications with antepartum bleeding in 30 percent (tie more of the cases. In other cases, the oxygen supply may simply

fail from reduced carrying capacity and reduced unloading pressures for oxygen causee-by the presence of carbon monoxide in maternal and fetal blood. Neonatal deaths occur as

a result of the increased risk of early delivery among smokers, which may be secondarily related to bleeding early in preg- nancy and premature rupture of membranes (146).

Long-Term Morbidity and Mortality

Studies of infant and child morbidity and mortality by the mother's smoking habits usually cannot distinguish between

the effects of smoking during pregnancy and the e(fect of the

.p-ifant's or child's passive exposure to cigarette smoke after birth. Several studies have found that hospitalization rai.Ils for pneumonia and bronchitis were higher during the first year of

life for infants of smoking mothers (20,21,53). Rates in children

were higher if the smoking parents also had cough and phlegm. Harlap and Davies found that the risk of contracting

pneumonia or bronchitis in the first year of life more than dou- bled if the parents smoked more than 24 cigarettes a day (53). A unique and important study of morbidity and mortality in

smokers' and nonsmokers' children up to the age of five has'now

been published by Rantakallio (11.9). Thepxperience up to age 5 of over 12,000 children born in 1966 in Arthern Finland, com- prising 96 percent of all births in two provinces, was ascertained

through hospital and death records and questionnaires. Smok221

20ti
0.1=

0.08=

0.06 -.-

0.04

0.02'

1

Nonsmokers Smokers

Total Births 27,420 21,465

Total Deaths - 634 624

Probability of Death .023 .029

= 95% CI

0.01,=

0.008 ............ .... 0.006

0.004 *

ea. 0.002

Nonsmokers

0.001

Total Deaths 7-0- (263J On 1121) (110) (152)1149) (187) In)

Smokers and I.

Nonsmokers 20 24 28 32. 36 40 42 +

Gestation: Weeks

A

FIGURE 11.Probability of perinatal death for smoking and

nonsmoking mothers, by period of gestational ag(

(bars show 95% confidence intervals)

SOURCE: Meyer, M.S. (87).

ing was rare in this population, and rthibomokers tended to bt

young and otherwise healthy. Fourteen percent of pregnanwomen smoked fewer than 10 cigarettes per day (mean numlYe:

Lifter the second month of pregnancy 3.b) and 3 percent smoke(

more thin 10 cigarettes per day (mean number 12.2); the re

maining 83 percent of the population were nonsmokers. It wal

therefore possible to remove the usual problems of confounding

variables by close individual matching of 1,750 smokers t(

nonsmoking "controls". Matching factors included marita

status, maternal age within 2 years, and place of residence, witl

the latter category including many socioeconomic variables t(

equalize the probable use of medical facilities and other dif

ferences. Although the author states that perinatal mortaliO.

did not show a, statistically significant. increase for smokers

222

,0 c
rates were 24 per thousand for controls, 26 per thousand for

light smokers, and 33 per thousand for "heavy" smokers (defined as smoking 10 plus cigarettes per day). These rates are

similar to those found in other studies in which differences were

statistically significant. Postneonatal mortality, from 28 days to

5 years, was higher for smokers' children with rates of 11.1 and

3.9 per thousand for smokers' and nonsmokers' children respectively. Overall death rates of 24.7 per thousand births in smoking women and 16.5 per thousand births in nonsmoking women were reported for children under the age of 5, of which 12.6 and 8.8 were neonatal.

In addition, the children of the smokers were hospitalize more frequently, had more visits to doctors, and had longer av

erage durations of hospital stays than children of nonsmokters.

Respiratory diseases caused significantly more hospitalizations among smokers' children. It is of great interest that the chil- dren born to a subgroup of women who stopped smoking dur.ung, the last 3 months of pregnancy showed no increase of post- neonatal mortality or morbidity up to the age of 5, compared' . with controls. However, these women had been very light smok- ers befitre quitting.,Table 10, derived from Rantakallio's study, shows that the various outcomes measured show increasing /

rates of morbidity and mortality with increasing levels of smoky

ing However, it may not be possible to distinguish between the

adverse effects of maternal smolt' during pregnancy and the adverse effects on infants and dren exposed to cigarette

smoke in the home,- liecause women who smoked during preg- nancy probably also continued to smoke after pregnancy. Because of the known carcinogenic potential of tobacco smoke and the evidence that benzo(a)pyrene reaches the placenta, Neutel and Buck investigated the relationship of maternal smoking during pregnancy to the incidence of cancer in children

aged 7 to 10. A combined population of 89,302 births from the Ontario Perinatal Mortality Study and the British Perinatal

Mortality Survey was used as a base population for a prospective study in which 65 cancer deaths and 32 cancer survivors

were identified. For cancer of all sites, the children of smokers

had a relative risk of 1.3, with 95 percent confidence limits of 0.8

to 2 2 dose-response relationship was not observed. The numbers w re not large enough to determine significant differences by site. xcess cancer rates for children of mothers who 'smoke

and a possible dose-related progression wete concentrated at

ages 0 to 24 months, but these rates were based on small numbers of cases. The authors conclude that "although a significant - excess is not demonstrable, a doubling of the cancer risk for

children of smokers cannot be ruled out." Their equivocal re223

29(l 4.0 ,j

r
-,6

1 TABLE 10.Long term effects of morbidity and mortality by level of maternal smoking

Mortality

Nonsmokers

Control 1 Control 2

Light Smkeis

(1.10 per day)

lleavy Smokerl

(10', per day)

Number of children

Doctor visits per child

1300 258 1302 252

(mean number) Alitp .76 .83 Hospitalizations per child

,71

(mean number) .19 .15 .22 .39 <Age 1 14 .08 Age 1-5 1 .17 .30, . .15 .17 .22 .25

B. Perinatal and postneonatal mortality (28 days to 5 years) per 100 births, by maternal smoking 6 Nonsmokers Smokers

Control Light Total Heavy

otal births number

Perinatal mortality per 1,000 births

Postneonatitl mortality

II mortality per 1.000 live births

1844

23.9

3.9

16.5

25.7

1844

26.0

11.1

24.7

( 32.6

SOURCE: Rantakallio, P. (119).

l 2" 0o
sults were reported to encourage other workers to aid to the

data (99). This should certainly be clone, with particular emphasis on th'e first 2 years of life. 4

Rantakallio, et al. also analyzed the use rates of ophthalmological services in their follow-up study of approximately

12,000 children, relating these rates of prenatal factors ascertained during pregnancy. The incidence of squint among smok- ers' children was 22.5 per thousand, compared with 11.5 per

thousand among the children of matched, nonsmoking controls

(p < .05). On fhe other hand, rates of dacryostenosis and of other

congenital ocular malformatitns were higher among the chil- dren of controls. The authoi.% state that squint was inversely

correlated with birth weight and was more common among chil- dren with other diseases, especially nervous or mental diseases

(121).

SUDDEN INFANVEATH SYNDROME

Maternal smoking habits have been ascertained in several

studies of the sudden infant death syndrome (SIDS). In all of

these, an association has been found between maternal smoking

during pregnancy and the incidence of sudden infant death.

Steele and Langworth, in a study of 80 cases, each with two matched controls, which were traced back to the Ontario

Perinataj Mortality Study population of 1960-61, fOund that

sudden infant deaths were strongly associated with the fre- quency and level of maternal smoking during pregnancy

(p < .001). Thirty-nine percent of the cases were nonsmokers versus 60 percent of controls, 36 percent of the cases and 27 percent

of the controls smoked less than a pack per day, 24 percent of

the cases and 10 percent of the controls smoked a pack per day

or more. The habits of the remaining 1 to 2 percent of mothers

were unknown (139).

Bergman and Wiesner studied 56 families who lost babies to

the sudden infant death syndrome and 86 control families. They

reported that a higher proportion of SIDS mothers smoked during pregnancy than controls (61 percent versus 42 percent),

more smoked after pregnancy (59 percent versus 42 percent),

and SIDS mothers smoked a significantly greater number of

cigarettes than controls. These huthors indicate that exposure

to cigarette smoke (passive smoking) appears to enhance the

risk for SIDS for reasons not yet known (8). However, whether

prenatal or postnatal exposure is more important cannot be determined.

Naeye, et al., in their analysis of 125 SIDS victims from the

population of the Collaborative Perinatal Project of the

231 225
NINCDS, stated: "The gestations that produced the SIDS vic

tims were characterized by a greater frequency of mothers wh

smoked cigarettes and had anemia" than was true for the whol

population of 53,721 infants pr for a set of 375 cbntrols matche

for important factors (96). Rhead, commenting on studies put

lished to date which demonstrate an increased incidence c

maternal cigarette smoking in SIDS, states: "It is now ... clea

that maternal cigarette smoking contributes to an infant's ris

of dying from SIDS" (123).

Analysis of data from the prospective study of 19,047(births t

members of the Kaiser Foundation Health Plan (1960-1967

also showed a strong association of SIDS with maternal smok

ing. In the SIDS group, 70.6 percent of mothers smoked dunn

pregnancy, compared with only 35.3 percent of mothers c

babies who did not die of SIDS (p < .001). The relative risk c

SIDS for smokers versus nonsmokers was 4.4 (67). - Mechanisms

Clues to the me chanisms by which smoking may increase th

risk of pregnancy complications are available from pathologies

and physiological studies of placentas, membranes, blood ves,

sels, circulatory patterns, and serum levels of substances im

portant for cell and tissue integrity. For example, it is possibl

that placental changes in smokers that serve as adaptations t

the hypo= effects of carbon monoxide may also increase th

risk of placental complications.

ChristianSon has reported findings from carefully stand

ardized gross examinations of 7,651 placentas from smokers an

.nopsmokers. These examinations revealed that smoker:

placentas were thinner and larger in their minimum diamete

than those of nonsmokers. This significant change effective]:

increased the surface area of the smokers' placentas and must

therefore, have increased their area of attachment to th,

uterine,wall. Tie distance from the edge of membrane ruptur,

to the pla.cente margin was also less for smokers, and signifi

cantly more smokers than nonsmokers had zero distance, whit]

is consistent with the diagnosis of placenta previa (19). Thes,

findings suggest a possible mechanism to account for the signif

icant dose-related increas4 in the frequency of the clinical drag

nosis of placenta previa that accompanies maternal smokini

(86). A similar increase in this condition occurs with increasini

altitude (75).

Christianson's study also reve led that smokers had signifi

cantly more placental calci on, primarily of ate materna

surface, and patchy subchorionic fibrin, as shown in Table 11

226

2
V;

4

t TABLE 11.-teletted results of gross examinations of placentas from smokers and nonsmokers *

Nonsmoker

N=3,461

Calcification

49.5 Patchy Subchorionic Ffbni 26.2 Infarcts

24.6 -------------

Thickneis (mean cm) ., Ratio of smallest diameter'to 2.16 thickness 8.19 ShOrtest distance, ge of rupture of y membranes to pl cental margin (mean cm)...

- 4.32 Pekent with zer distance . . 25.6

Percent of Plallotas with §tated Condition

White

Smoker

N=2,239

60.8

35.3

22.3

2.12

I.. 8..40

4.09

27.9

SOURCE: ristianson, R.E. (19).

p.

let

e

Black

P

Nonsmoker

N=1,300

Smoker

N=652 P

<.0001 43.5 59.0 <.00 <,0001 30,8 37.0 <.01 <.05 14.4 14.5 NE

<.001 . 2.11 2.06 <.01

<0001 . 8.39 g3:68 <.01

<1)25 5.08 4..83 NS

,NS 18.6 20.3 <.05
These changes are characteristic of maturation and aging of the placenta and occur as normal gestation proCeeds; holey r, they

occurred earlier in smokers than in nonsmokers (19). T is finding is compatible with other manifestations of accelera ed aging

reported to be associated with cigarette smoking (28, 8). Asmussen compared placental vesserA in s oking and

nonsmoking mothers by electron microscopy. In the smoking group these vessels were charaaerized by stibintimal edema

with destruction of the intimal elVstic membranes, a marked decrease in collagen content, and .proliferation of myocytes. Asmussen postulated that similar damage may occur in the

fetal and infant vascular system. To what extent such changes may predispose to the subsequent development of vascular dis- -,3 ease remains unknown. The author regarded most of the

changes observed in smoker vessels as degenerative, b mentioned the possibility that the thickening of the basemeRtnembrane observed in smokers might be an attempt at repair (4,5). Naeye (93) has described an increased frequency of placental microscopic lesions associated with smoking. These include:

cy tot rop blastic hyperplasia, obliterative endarteritis, stromal fibrosis, and small villous infai-ction. Smokers also

demonstrated an increased frequency of necrosis and inflammation in the decidua capsularis and in the decidua basal's at

the placental margin. Placental features observed less fre- quently in smokers' placentas were excessive syncytial knots and various thrombotic phenomena.

Naeye found increasing placental enlargement with smoking

level, accompanied by decreasing birth weight and a consequent increase in the placental ratio. The author stated that "as smoking increased, placentas developed microscopic lesions characteristic of underperfusion of the uterus." Naeye's data showed positive trends with maternal smoking level for some findings and negative trends for others (93). Many of the changes cited were of low frequency in all groups, and no clear pattern of possible mechanisms of action emerged.

'Other studies that may shed light on these Complex inttrrelationships include the report by Goujard and colleagues that heavy alcohol consumption as well as smoking contributes to

the risk of stillbirth caused by abruptio placentae. In aprospective survey of 9,1'69 women, the risk oistillbirth kas 21 per 1,000 in smokers who were light or nondrinkers, f0 per 1,000 in

nonsmokingidrinkers of 45 ml equivalents or more of absolute

alcoholand 8.5 per thousand for nonsmokers who drank

less than 45 ml per day. The small number of smokers who were

also heavy drinkers had stillbirth rates of 50.5 per 1,000 (95 women with 5 stillbirths). The proportions of these deaths that

228

2 '1
were attributable to abfuptio placentae increased with smoking

and with drinking, based on data unadjusted for t4e effects of

age, parity, and other factors (122).

More research is needed to define possiblekathways of action

by which the active components of cigarette, smoke affect pregnancy complications that may lead, in turn, to fetal death or to

preterm birth with or without survival.

Experimental Studies

TOBACCO SMOKE

Tobacco smoke contains more than 2,000 compounds including: carbon monoxide, oxides of nitrogen, ammonia, polycyclic

aromatic hydrocarbons, hydrogen cyanide, vinyl chloride, and

nicotine. For the pregnant woman and fetus the most important of these appear to be nicotine, carbon monoxide, and the

polycyclic aromatic hydrocarbons.

NICOTINE

The effect of nicotine on sympathetic and,parasympathetic

ganglia, skeletal muscles, and the central nervous system is

similar to that of acetylcholine. At all three sites it first stimulates, then depresses. Minute doses of nicotine stimulate the

chemoreceptors of the carotid and aortic bodies, causing reflex hypertension. Nicotine also releases epinephrine from the ad- renal medulla, thereby producing cardiovascular changes.

oTiNus, it can produce widely differing effects depending upon the dosage and the particular site that is most sensitive to stimulation.

Nicotine rapidly crtrsses the placenta to affect the fetus (142).

Relatively mature rhesus monkey fetuses respond to nicotine

infusion with a rise in blood pressure, bradycardia, acidosis,

hypercarbia, and hypoxia (141), Maternal nicotine administration in rats also has been shown to affect the fetal central nervous system and its response to electrical stimulation during

the newborn period (56,78).

Quigley, et al. noted that in moderate to heavy smokers, after

34 weeks gestation, smoking two cigarettes in '10 minutes wa,s

associated with a 60 percent increase in maternal plasma

norepinephrine and epinephrine and a 20 percent increase in

serum cortisol concentrations (118). These changes also were associated with an increase in maternal pulse and blood

pressure. Lehtovirta and Forss measured changes in placental

intervillous blood flow using the 133 xenon method (66). Immediately after smoking, intervillous flow decreased 22 percent.

229

235
These data correlate with the tudiesbf Resnik, et al. (122),

showing nicotine:induced increases in catecholamines and decreased uterine blood flow in sheep, and of Haberman, demon-

, stratmg decreased uteroplacental blood flow in women, using

thetmography (48).

Sastry and his colleagues have carried out a series of studies

on the effect of nicotine on the human placenta. Nicotine added

to a calcium-containing medium-pused a 33 percent increase rn

the rate of acetylcholine release from isolated placental villi

(131). The authors postulated that this effect could account for

the decrease in placental amino acid transport (125,154) produced by nicotine-mediated cholinergic blockade (105). Rowell,'

and Sastry also demonstrated that nicotint raised a41 percent

decrease in uptake of alpha amino isobutyric acid in an experimental placental system (126). Their studies indicate that under

normal circumstances acetylcholine exhibits a muscarinic effect facilitating placental amino acid uptake. Nicotine blockade

of the facilitating effects of acetylcholine on amino acid uptake

may result in fetal growth retardation (126). These data agree

with the 1977 work of Crosby, et al. in humans (26).

Nicotine injection in rats results in prolonged gestation with

lower than normal new,born weights. A possible cause of this

prolonged gestation is nicotine-induced delay in ovum implantation. Yoshinaga, et al. tested this hypothesis, administering

7.5 mg nicotine tartrate twice ly from the morning of pioesel-us until the Jay of sacrifice

lti

dfiys 1 to 5 of pregnancy (161).

The nicotine-injected animals dernenstrated a delay of about 12

hours in ovum cleavage from thet'wo- to the four-cell stage, and

each step of development after t114 four-cell stage was thereby

delayed. In;tkdditeion,' ovum eiati- 'into the uterus, blastocyst

formation, shedding ot the zottitt ,114cida, an plantation

N;vere. delayed. Nicotine injecti also was asso ted with a

/crowding" of rinplantation nte§ toward the tubal ends of the

teterin e h or fi

.Apu tIng the preimplantatigft

w

peYi2d the serum concentration

ogeAteratit, luteinizing hormone, and prolactin were lower,

while the concentrationivof estflugen and follicle stimulating

horrnbne went .11i her tat 'n control animal .- These workers

suggested that: e, delayed vum4implanatiori followed a' delayed incre n pri5gesterone secretion required to prepare

the uterus eiraplarifing blastocyst, and that the delayed

progesterone sere n results in part from nicotine-induced

dilOu bed by drills pituitary balance.

Hamosh, dt al. obs yved that, while administtatian of 100 mg

kg 'day-1 nicbtine .ipregnant rats from day 14 gestation onward

failed to affecrawmother or fetus, administration of 1 mg kg- 'day''

230 `)(')
(a dose "comparable" to that of a 20 cigarette-per-day smoker) re- sulted in decrease in titter size and an increase in stillbirth rate.

Although administration of 100 mg kg- 'day"' nicotine failed to affect

newborn birth weight by 12 days of age continued maternal nicotine

admihistration resulted in a'9 percent decrease in body weight and a 40 percent decrease in weight of the stomach contents. These decreases presumably resulted from lower milk production by the

nicotine-treated animals (51).

CARBON MONOXIDE (CO)

Carboxyhemoglobin concentrations of 4 to 5 percent are associated with numerous physiologic alterations in adults.

Cigarette smoking raises the carboxyhemoglobin concentration

4 to 5 percent per pack smoked per day. Although CO diffuses

across the placenta relatively slowly [ the half time equals 1.5 to

2 hr (72)), fetal carboxyhemoglobin concentrations reflect those

'of the mother, and under steady state conditions are 10 to 15

percent higher than maternal levels(71). Elevated carboxyhemoglobin concentrations in the fetus are associated with

'decreased fetal blood oxygen tensions. These decreased oxygen

tensions are associated with a redistribution of fetal blood flowto the brain,.heart, and adrenatglands (146).

Carboxyhemoglobin concentrations have been described

under several conditions of pregnancy. Davies, et al. (31) com- pared carboxyhemoglobin concentrations and "available oxy- gen" (a function of 02 content in ml dl blood-') in women who

stopped smokirig for 48 hours during the last trimester of preg- nancy, with women who did not stop smoking, and with

nonsmoking women. In those women who stopped smaing, car- boxyhemoglobin concentrations decreased. "Available oxygen"

increavefiktbout 8 percent due both to an increase in functioning

hemoglobin and ft shift in the oxyhemoglobin saturation curve; this increase in "available oxygen"- should contribute to improved fetal oxygenation.

Exposure of rabbits (6) and rats (39) to CO during gestation

resulted in decreaked fetal weights and increased perinatal mortality. Such CO-exposed newborn animals showed less activity as well as decreased lung weights and decreased concentrations of brain protein,..DNA, and the neurotransmitters

norepinephrine and serotonin.(45). Cellular hypoxia is the final

common pathway` mediating the adverse effect of CO on the

developing fetus.-

Recent experimental studies have explored various aspects of CO-induced biochemical changes in the fetus and the newborn.

Newby, et al. demonstrfated a persistent effect of CO exposure-in

8- and 13-day-old rats following a single 5-hour exposure to 1,500

231

2`4-' t..)
120

100

17") 80

0

t, 60

z

E 40

&u* CO r =8 i CO n=15

Om.° OONT r n = 9

CONT-rn=9

2 4 16

Intensity (Candlepower/9.4 x 104)

No.

FIGURE 12.Effect of prenatal CO upon peak-to-peak

amplitudes of the first- positiive to the first

negat,ive component of the flash evoked potential

recorded from the rat visual cortex. Vertical bars

represent -± standard error of the means,

SOURCE: Dyer, R.S. (36).

parts per million (0.15 percent CO) (100). In these animals alpha

methyl-p-tyrosine, a potent inhibitor of the enzyme tyrosine

hydroxylase, was injected 1 hour before the CO exposure, and

the extent of catecholamine depletion was taken as an index of

the rate of catecholamine turnover. CO-treated rats showed init..creased steady state dopamine concentrations with decreased

rates of dopamine turnover. In addition, the C0 effect on

dopamine turnover persisted for at least 3 to 6 weeks after a

single exposure of 8-day-old rats. There was no CO effect on

norepinephrine concentrations or turnover rates, and the effect

was not produced in rats exposed to 8 percent oxygen instead of

carbon monoxide. This is consistent with the data'of-Coyle and

Campochiaro, which indicates that a maturational event occurs

in the striatum of the 8-day-old rat (25). Wither this event represents the age of functional maturity, initiation of

. 232 2
dop. aminergic transmission, or maturation of cholinergic inter- neurons is Unclear.

Prenatal CO exposure may have long-term consequences on

central nervous system function. For instance, Dyer, et al. ex- posed female Long-Evans hooded rats to 150 ppm CO through- out pregnancy (36). At birth the litters and mothers were placed

in room air without COlpn day 65 electrodes virere placed in the young rats' skulls, and 2 weeks later visu-ally evoked. potentials were recorded. Figure 12 illustrates the effect of such prenatal

exposure on the peak-to-peak amplitudes of the P1 -NI (first positive to first negative) component of the visual evoked potential from the cortex. Females showed a significant increase in P1 -N1

amplitude,t each of four flash intensities. Although the exact nature of this amplitude increase could not be determined, it

suggests altered cell populations at the retinal, geniculate, and

cortical levelb, and may represent impaired inhibitory mecha- nisms, renderitg other neurons more excitable.

The question of the posibI' teratogenicity of CO has never

beemresolved. Schwetz, et al. exposed mice to 250 ppm CO for 7 or 24 hours per day, from days 6 through 1,5 of gestation, and

rabbits to th same concentration from days 6 through 18 (137). Blood carbo*hemoglobin concentration ranged from 10 to 15

percent. The fetusesof mice exposed to CO for 7 and 24 hours

per day were slightly heavier and lighter, respectively, than

those of the control animals. The only increase in thratogenic effects were minor skeletal variants such as extra lumbar ribs and sputil

POLYCYCLIC AROMATIC HYDROCARBONS

The polycycliC aromatic hydrocarbons (PAH), such as ben- zo(a)pyrene, are 111 dely distributed mutagens and carcinogens. These substances, produced by incomplete combustion of or- ganic material, are important constituents of tobacco 'smoke...

Exposure of cells to PAI-1 induces the enzyme, aryl hydrocarbon hydroxylase. The inducibility of this enzyme system has been used by some workers to demonst!'rate, indirectly, that ben- . zo(a)pyrene and other polycyclic hydroCarbons reach the placenta and fetus.

The placental concentration of benzo(a)pyrene is highly corre- lated with the amount which a pregnant woman smokes (97, 111). In pregnant rats exposed to this substance higher doses were required to induce enzyme activity in the fetus as corn- pared with the dose required to stimulate placental enzyme ac- tivity (153), suggesting that the placenta may protect the fetus

fnom these substances. However, the placenta is not imperme233

2 :p
V

able to benzo(a)pyrene (134), The placenta is involved in complex hormonal interrelations between mother and fetus, and

oxidative enzyme pathways in the placenta are important in

maintaining hormonal and nutrient balance for normal fetal

developMent.The hydroxylation of polycyclic hydrocarbons and

the active transport of various compounds by trophoblast cells

may share common enzyme systems. Thus, the induction of var.-

ious enzymes by polycyclic hydrocarbons may tnterfere *vith

normal transport systems. Another unanswered question concerns the carcinogenic risk

for progeny exposed to utero to po' lycyclic aromatic hydrocarbons. The offspring of mice that were injected with benzo(a)pyrene late in gestation showed an increased incidence of

neoplasms of the lungs, liver, and mammary glands (101). Pelkonen, et al, determined that placental aryl hydrocarbon hydroxylase activity correlated closely with both the amount the

mother smoked and newborn weight (112). These authors

suggested that the placental concentration of this enzyme may

used as a measure of fetal exposure to maternal cigarette

smoking. Vaught, et al.'also reported much higher aryl hydrocarbon hydroxylase activity in the placental microsomes of

smokers compared with nonsmokers (148).

Although currently available data do not allow a quantitative

assessment of the genetic risk to man from cigarette smoking

such risk may occur since so many components of cigarette

smoke are mutagens (as well as carcinogZns) (11). Male

cigarette smokers may have an increased number of abnOrma

spermatozoa (150). Paternal and maternal chromosomal aber

rations (103) and sister chromatid exchanges may be increasec

in smokers (62). Because the proportion of smokers in the population is so high (between 30 and 50 percent), even a relativel3

weak mutagenic effect ckould have a significant effect on th(

gene pool Or).

OTHER COMPONENTS

Cyanide, another'constituent of cigarette smoke, may con

tnbute to retarded infant growth and increased perinatal mor

tality. Smokers have increased levels of cyanide and thiocyan

ate in body fluids. Serum concentrations of vitamin B12, used

cyanide metabolism, are decreased as well. Several worker

have recorded increased thiocyanate concentrations in boti

women who smoke and in their fetuses (2,140,154). Pettigrew, e

al. compared cyanide and thiocyanate concentrations smok

ers and nonsmokers, matched for age, height, panty, any

socioeconomic stattuis (116). Cyanide and thiocyanate concentra

234
tions were two to four times greater in the blood and urine of

smokers and in the urine of smokers' infants as compared with

controls. Meberg, et al. reported that thiocyanate concentrations were correlated with cigarette consumption and inversely

correlated with birth weight (81).

Cadmium, another constituent of tobacco smoke, is concentrated in the placenta of smokers (124). Webster exposed preg- nant mice to 10 to 40 ppm cadmium and noted an inverse correlation between cadmium concentration and fetal weight (152). Lauwerys, et al. 6xamined the effects of epidemiology factors on heavy metal and CO concentrations in the blood, placenta, and fetus of smoking women (65). Cadmium concentrations in maternal blood were twofold greater than concentrations in

fetal blood, suggesting that the placenta acts aa.a barrier to this metal. They reported a correlation between maternal cadmium

and carboxyhemoglobin concentrations (13,65). They also found that the cadmium concentration of smokers' placentas was about 25 percent greater than in a control group' and that the placental cadmium concentration exceeded that of maternal

blood about tenfold (124).

Fertility .

Fertility results from the successful completion of a complex

step-wise process beginning with gametogenesis (sperm and egg production), continuing through gamete, release (ejaculation

and evaluation), gamete interaction (fertilization), conceptus

transport through the fallopian tube into the uterus, and ending with implantation of the embyro into the endometnal wall.

An adverse effect of smoking on any of these steps may impair

fertility.

SMOKING AND REPRODUCTION IN WOMEN

Several epidemiologic studies have suggested that smoking decreases fertility in women (50,115,143,10). The retrospective

study of Tokuhata dettionstratk that 21 pqrcent of women who

regularly smoked cigarettes were infertile ivhile only 14 percent of those who never used tobacco regularly were infertile (143). After several charactOstic's(cause of death, age at and year of dearth;-educatiop, occupation and frequency of marriage as well as husbands' smoking habits, education and occupation) were controlled, a 46 percent excess of infertility was found in women who smoked.

Inn study on the return of fertility after discontinui rIg' contraception, Vessey, et al. found a suggested reducticm in fertility

among women smoking 15 or more cigarettes per day (149).'Pet-

: 241 236
tersson, et al. found a tendency toward a greater prevalence of

secondary amenorrhea among smokers (4.8,100 women) than

among nonsmokers (3.7 100 women) (115). Hammond found that

49 percent of the nonsmoking women between 40 and 49 years

had regular menses while only 40 percent of those smoking

more than one pack a day had a regular menses (50). Conversely

only 18 percent of nonsmokers had irregular menses while 24

percent of those smoking one or more packs of cigarettes per

day said they had irregular menses. Smoking women were also

more likely to have an unusual vaginal discharge and vaginal

bleeding than nonsmokers. Expenniental studies have demon- strated alterations in luteinizing hormone release and a de-

. creased ovulatory responsep rats exposed to tobacco smoke (76).

The effect of smoking on ovulation may result from direct

effects of nicotine on the hypothalamus or pituitar?. This would

alter the release of gonadotropin releasing hormones from the

hypothalamus or impair the pituitary response to releasing

hormones.

SMOKING AND AGE OF MENOPAUSE

Substantial data demonstrate that smoking lowers the age of

spontaneous menopause (7,9,27,58,68,69). The recent study by

.lick, et al. revealed a dose dependent decrease in the age of

menopause in smoking women who live in Sweden and the

United States (58). The median age of opause in nonsmokers was 50, among those smoking one:harrack day it was 49; in

those smoking 1 or more pack day, it was 48. Similar studies

have been published indicating an earlier onset of menopause in

smoking women in the United 'States (29), in England (7), in

Germany (9), and in Sweden (68,69) The mechanism of early

menopause in smokers may be related to ovotoxins in cigarette

smoke (37) or to toxic alterations in the hormonal regulatory

mechanisms controlling the hypothalaitic-pituitary-ovarian

axis (76). One group of ovotoxins may be polycyclic aromatic

hydrocarbons which halve been demonstratedito be metabolized

by ovarian enzyrnes to toxic products which destroy oocytes in

rat and mouse ovaries (47,79).

evidence collected by Daniell (29) and Lindquist (68) suggest

the earlier menopause of smokers is not related to weight

differences between smokers and nonsmokers but is a direct

result of some component of cigarette smoke.

SMOWING AND- REPRODUCTION IN MEN

Spermatogenesis, sperm morptiology, sperm motility

(17,64,133,150) and androgen secretion (12,113) appear to be al236
tered in men who smoke. Viczian (150) has demonstrated decreased sperm density, a cigarette-dose-dependent decrease in

sperm motility, and a cigarette-dose-dependent it eased abnormal sperm morphology among smokers.

In metabolic studies of alcohollf men admitted to a clinical

research center, an inverse relationship between number of

cigarettes smoked and reduction of testosterone levels was seen

(113). Briggs (12) has reported lower plasmg testosterone. among

smoking men compared to matched nonsmoking controls and

has shown that cessation of smoking resulted in increased tesd tosterone levels in these men. Wintermitz and Quillen (158) in a

study on the acute effects of smoking in men demOnstrated increases in plasma cortisol sand growth hormone during the

smoking period. Growth hormone returned to the presmoking

level shortly after the smoking period, and cortisol fell gradually to the presmoking level by 90 minutes after cessation of

smoking. Ur friary catecholamines were higher on the smoking

day than the nonsmoking day. No acute changes were observed

in gonadotropins or testosterone in these men. These studies

demonM.rate stimulatory effects of smoking orcgrowth hormone

and cortisol.

Studies in experimental animals have also shown that tobacco smoke _impairs spermatogenesis (37,151). Smoking also

lowers sexual activity in male rats (18).

These data suggest P.vo possible mechanisms of action of

smoking on male repoduction. A component of cigarette smoke

may have a direct action on the testes, disrupting gamete production. This would be consistent with the suggested effect of

cigarette smoke on the ovary. In addition, cigarette smoke is

known to contain compounds which are mtagenic (59). Alter- natively, cigarette smoke may interfere with the regulatory mechanisms controlling-the hypothalamicpituitarytesticular

axis. * FERTILIZATION AND CONCEPTUS TRANSPORT

The effect of smoking on sperm-egg interaction (fertilization)

has not been studied in mammalian species..gvidence from

sub-mammalian species demonstrates that nicotine promotes

polyspermy (the entrance of more than one sperm into the oo- cyte) (73). Polyipermy would result in abnormal embryonic development and early abortion, which is one known effect of

smoking (60).

The effect of smoking on conceptus transport in the fallopian

tube or entry into the uterus is unknown, however, some evidence suggests that smoking can alter the amplitude and tone

wR 237

243
of contractions,measured during the Rubin uterotubal insufflation test (a combined measure of uterotubal junction and tubal

patency) (98), suggestive that smoking may alter uonceptus

transport in the fallopian tube or its entrance into the uterus.

In summary, cigarette smoking appears to exert an adverse

effect on fertility. Further studies are needed to quantify the

effects, identify etiologic agent(s), and define the mechanism(s)

of action.

Summary

1. Babies born to women who smoke during pregnancy are, on

the average, 200 grams lighter than babies born to comparable

nonsmoking women.

2. The relationship between maternal smoking and reduced

birth weight is independent of all other factors that influence

birth weight including race, parity, maternal size,

socioeconomic status, and sex of child; it is also independent of

gestational age.

3. There is a dose-resptnse relationship between matvniil

smoking andreduced birth weight, the more the woman smokes

during pregnancy, the greater the reduction in birth weight.

-1. If a woman gives up smoking early during pregnancy, her

risk of delivering a low-birth-weight baby approaches that of a

nonsmoker.

5. The ratio of placental wei ht tc ht increases with

increasing levels of na smoking, reflecting a considerable

decrease in mean birth weight anda slight increase in mean

placental mass, this may represe'nt an flaptation to relative

fetal hypoxia. 6. The pattern of fetal growth retardation that occurs with

maternal smoking is a decrease in all dimensions including body

length, chest circumference, and head circumference.

7. Maternal smoking during pregnancy may adversely affect

the child's long-term growth, intellectual development, and behavioralccharacteristics.

8. Maternal smoking during pregnancy exerts a .direct

growth retarding effect on the fetus, this effect does not appear

to be mediated by reduced maternal appetite, eating or weight

gain.

9. The risk of spontaneous abortion, fetal death, and neonatal

death increases directly with increasing levels of maternal

smoking during pregnancy , interaction of maternal smoking

with other factors which increase perinatal mortality may result in an even greater rislk

10. Excess deaths of smokers' infants are found mainly in the

coded cause cAtegories of "unknown" and "anoxia" for fetal

238

2 1 1
deaths, and the categories of "prematurity alone" and "respiratory difficulty" for neonatal deaths; this suggests that the excess deaths are due to problems of the pregnancy, rather than

to abnormalities of the fetus or neonate.

11. Increasing levels of maternal smoking result in a highly

sighificant increase in the risk of abruptio placentae, placenta previa, bleeding early or late in pregnancy, premature and prolonged rupture of membranes, and preterm deliveryall of

which carry high risks of perinatal loss.

12. Although there is little effect of maternal smoking on

mean gestation, the proportion of fetal deaths and live births

that occur before term increases directly with maternal smoking level. Up to 14 percent of all preterm deliveries in the United

States may be attributable to maternal smoking.

13. Theincidence of preeclampsia is decreased among women who smoke during pregnancy; however, if preeclampsia develops in a smoking woman, the ritk of perinatal mortality is

markedly increased compared to preeclamptic nonsmokers.

14. An infant's risk of developing the "sudden infant death

syndrome" is increased by maternal smoking during pregnancy. 15. There are insufficient data to support a judgement on whether maternal and'or paternal cigarette smoking increases

the risk of Congenital malformationi.

16. Infants and children born to smoking m rs may expe- rience more long-term morbidity than th-o'se born to nonsmoking mothers; however, studies usually cannot distinguish between the effects of smok ng during pregnancy and the effects of the infant's or child's assive exposure to cigarette smoke after birth,

17. Studies in women and men suggest that cigarette smoking may impair fertility.

18. Experimental studies on tobacco smoke, nicotine, carbon.

monoxide, polynuclea'r aromatic hydrocarbons, and (4-ier con- stituents of smoke help defifie pathways by which maternal

smoking during pregnancy may exert its aforementioned effects`, References

(1) ALBERMAN, E., CREASY, M., ELLIOTT. M., SPICER. C. Maternal

factors asspciated with fetal chromosal anomalies in spontaneous

abortions British Journal of Obsteincs and Gynecology 83: 621-627, August 1976.

'(2) ANDREWS, J. Thiocyanate and smoking in pregnancy. Bntish Journal

of Obstetrics afid Gynecology 84): 810.814, 1973.

(3) ANDREWS, J,(MCGARRY, J. M. A community study of smoking in pregnancy Journal of Obstetrics and Gynecology of the Bntish Commonwealth 79(12): 1057.1073, December 1972.

245

239
. 'SI /

(..) ASMUSSEN, I Artitnal chan es in infaets of smoking mothers Post-.

graduate Medical Journal 54 00.204, March 1978

(S) ASMUSSEN, I Ultrastructure o human umbilical veins. Acta Obstetnca et Gynecologica Scandeav a, Supplement 57(3) 253-255, 1978.

(6) ASTRUP. P, OLSEN. H' M.. TRO E, D., KJELDSEN, K. Effect of

moderate carbun-munoxide exposure on fetal development Lancet 2

1220-1222, December 9, 1972.

i 7) BAILEY. A , ROBINSON D , VESSEY, M Smoking and age of natural

menopause Lancet 2 722. 1977

1+, I BERGMAN. A B . WIESNER, L A Relationship of passive cigarette-

-,muking to sudden infant death syndrome 58(5) 665-668.

November 1976

(y) BERNHARD, P the Wirkungdgs Rauchers auf Fran and Mutter (The

effect of smoking un women and mothers ) Munchner Medizinische

Wochenschnft 104 1826-1831, 1962

I to) BORLEE. 1 . LECHAT. M F Resultats dune enquete sur les malformations cungenitales dans le Hainaut (Results of a study on congenital malformations in Hainaut ) Beiges de Medicine Sociale, Hygiene,

Medecine du Travail et Medecrne Legate ( Brussels) 36(2). 77-99, February 1979

)11) BRIDGES. B A . CHELMMESEN. 11 , SUGIMURA. T. Cigarette

smokingdues it carry a genetic risk' Mutation Research 65 71-81,

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Journal of Obstetrics and Gynecology 9112). 270.276, January 15, 1965. (145) UNDERWOOD, P B , K,SLER, K. F., O'LANE, J. M., CALLAGAN, D

247

LI Li
A Parental smoking empirically related to pregnancy0cutcume

Obstetric and Gy netology 29i 1; 1 x January 1967

0/..t,i I s DEPARTMENT OF HEALTH, EDIR ATION, AND Xi ELFARE

srnok.rig and Health A Report cc). the Surgeon General Department

of Health, Edw. atom and XX eifare Public Health Sr ei. ice, Office of

the A.sistant Secretary for Health Office on Smoking and Health

DH EP. Public ation No iPHsi 79 50066, 1979; 1251 pp

Pt KJ(' HEALTH SER I( E The Health (onsequences of smuk

,ng 197 i f Department of Health Education and Vielfare DHEV.

P.)1:,c calor HSM 7i s7o4 147 pp 99 149

X Al GHT J B GURTOO H I, PARKER N B LEBOEUF. R,

18)(70R, G Effect, of ,rrnik;ng on rcen7u0apyrene metabolism by

r...iman placenta; micro,ome, ( ancer Research 19s. 1177 31st .Aug_cst 1979

Ess E't M. P RIGHT N H, Mb PHERSON, K P Fert,iity after ,topping different method, of ontraception British Med--

0a, Journa. I 6108 265 267, 1978

X 1( 7.1 A\ M Result, of ,permaeoziont studies in cigarette smoker, Zeit,chrift f..r Halt lr,l Geschiecrt Krankheiten 44,")

1b69

16(15 R ZI AN M The effect of cigarette smoke ;nhatation ur spermatogenes)s ir rats Experientba 24 511 51 196x

5..0 %X ElisTER μ '\ adrni induced fetal growth retardation in the

mo 1,e Arch.,.e, of Eni.ironmentai Health-0 i41 '06-42, January

February 11478

V H R M (,OMMI B .ALX ARES. A P ONNEY A H Effeciof

enzyme on the metatoilsm of her;,zoi aipy rene and

methy 4 morkomethy tarninoazottenzerte in the pregnant and fetall

rat ancer Research 020 t; 9X.978 May 1972

V ENNER.BERG P A , ELS( H, F Effects of cholinergic dug; on

uptake of 14 ( ,arninoisobuti.nc acid by human term placenta fragments implication for acetylcholine recognition ,cite and obsen.ations on the binding of radioartp.e cholinergic ligands Federation

Proceeding, 36 980. 1977

; ;55) N ILSON, E Xik The effect of smoking to pregnancy on'th& placental

co efficient New Zealand Medical Journal 7414750 384-385. 1972

;7;6/ %It IN(ERD, J CHRISTIANSON, R , LOVITT, XX V , SCHODEN. E J

Placental ratio in white and black women relation to smoking and

anemia American Journal of Ob,tetnc, and and Gynecology 124(70

671 675, April I, 1976

I ;70 V, INGER!), J , S( HOEN, E J Factors influencing length at birth and

height at fi'.e year, Pediatric, 3(50 737-741. May 1974

0 I WINTF,RNITZ. Vic t5 , QUILLEN, D Acute riormonal response to

cigarette smoking Journal linical Pharmacology 17(7) 389 -397. July

1977

/ YERI SHALMY J Mother', cigarette smoking and sur.ial of infant

Ametican Journal of Okoitetnc, and Gynecology K844) 505-518. February 15, 1964

0,)6n YERUSHALMY, J The relationship of parents cigarette smoking to

outcome of pregnancyimplications as to the problem of inferring

causation from observed associations American Journal of

Epidemiology 93(6) 443 456. June 1971

/61) YOSHINAGA, K . RI( E. U , KRENN. J , PILOT. R L Effects of

nicotine on early pregnancy in the rat Biology of Reproduction 20

294-303, March. 1979

248

ba.-. 1_1 '1
(162) ZABRISKIE, J R Effect of cigarette smoking dunng pregnancy

b

Study of 2000 cases Obstetrics and Gynecology 2144i 405-411, April 1963

s

2 I-; t..., ,_.,

4

249

1
PEPTIC ULCER DISEASE

4.

There is little information dealing specifically with the relationship between smoking and peptic ulcer disease in women.

The data which are available suggest the same trend toward

higher prevalence gf peptic ulcer disease among women who

smoke as is observed among men who smoke. Table 1, extracted

from the 1979 Surgeon General's Report, shows that the prevalence of "peptic ulcer" in female smokers was higher in two out

of three studies of women, *filch showed a twofold or L6 fold

higher prevalence (7). The one study which failed to denionstrate an increased prevalence was condticted in rural Poland

where very few women smoke (only 7 percent) (6). The median

ratio of smoking ulcer patients to nonsmoking ulcer patients has been reported to be 1.7 for men (7). Thus, women smokers

seem to show greater susceptibility to ulcer disease than do

nonsmokers.

, The population of women with ulcers Contains a greater pro- portion of smokers than does the group of women without ulcers. Alp et al. performed a retrospective analysis of 638 patients with gastric ulcer, 230 of whom were women (2). There

were L9 times as many smokers in the group of women ulcer

patients as in an age-matched control group. However, even

among the ulcer patients, only 39 percent were smokers. In a

smaller genes of 31 female patients admitted to hospitals with

hemorrhage from, or perforation of, gastnc or duodenal ulcers,

the prevalence of smoking was 26 percent in both ulcer patients

' (831) and controls (8131) (1). -, In a report examining the effect of smoking on healing rates

of gastric and duodenal' ulcers, Doll et al. studied 92 women with

gastric ulcer and 54 women with duodenal ulcer (3). Smoking

was 1.6 times more common in women gastric ulcer patients as

in controls matched for age and place of residence (p < 0.01).

There was no significant excess in the proportion of smokers in

the group with duodenal ulcer. The effect of smoking on healing

rate vas reported for men ?nd women grouped together, so no

cdnclusion regarding specific effects on women is possible.

Although some studies' of etiological factors in smokinginduced ulcer disease (gastric acid secretion; pancreatic secretion; etc.) have included women, the number of women has been

small, or the data from women have not been presented sepa- rately. . . Inbsummary, the evidence currently available documents an

increased prevalence of peptic ulcer disease in women who

smoke. No data. are available concerning specific effects of

smoking in women on gastric acid secretion, gastnc emptying,

4 0

v..., 253

1
TABLE 1.Prevalence of peptic ulcer in smoking and

. nonsmoking women (number per 100)

No.

with

Reference ulcers Smokers Nonsmokers Ratio*

Higgins, M.W. " (1966) (5) 47 2.8 1 4 2.0

Fried min'. G.D

(1974) (4) 1092 6.3 3.9 L6

Jedrychowski, W s

f1974)(6) 26 08 1.3 06

'Ratio = Prevalence among smokers

Prevalence among nonsmokers

pancreatic secretion, or other processes which might be involved in the pathogenesis of peptic ulcer disease.

Summary

The 197? Surgeon General's Report included evidence that

cigarette smoking in males was significantly associated with

the incidence of peptic ulcer diease and increased the nsk of

dying from peptic ulcer disease by approximately two-fold. The

effect of smoking on pancreatic secretion and pyloric reflux

demonstrated among men may provide a piechanism by which

peptic ulcers develop.

1. Female smokers show a prevalence of peptic ulcer higher

than that of nonsmokers by approximately two-fold.

2. The effect of cessation on healing is not known.

References

(/) AtLIBONE, A.. FLINT. F J Bronchitis. aspirin, smoking and other

factors in the aetiology ofpeptic ulcer. Lancet 2. 179-182, July 26, 1958.

(2) ALP, M. H., HISLOP, L G., GRANT, A. K. Gastric ulcer in south Australia 1954 1963. 1. Epidemiological factors. Medical Journal ofilkustralia 2. 1128.1132, December 12, 1970.

(Si DOLL, R., JONES, F A.. PYGOTT, F. Effect of smoking on the production and maintenance of kastnc and duodenal ulOers. Lancet 1. 657-

662, March 29, 1958

(4) FRIEDMAN, G D , SIEGELAL'R, A B . SELTZER, C. C Cigarettes,

alcohol. coffee and peptic ulcer. New England Journal of Medicine

290(9) 469.473, February 28, 1974.

(5) HIGGINS, M. W., KJELSBERG. M. Characteristics of smokers in

Tecumseh, :dichigan. II. The distnbution of selected physical measurements and physiological variables and the prevalence of .certain

254

,
diseases in smokers and nonsmokers. Amencan Journal of Epidemiology 86: 60-77, 1967

0 (6) JEDRYCHOWSKI. W., POPIELA, T Association between the occur

rence of peptic ulcers and tobacco smoking. Public Health London

88(.0 195-200, 1974.

(7) C S DEPARTMENT OF HEALTH, EDUCATION. AND WELFARE.

Smoking and Health. a Report of the Surgeon General. Department of

Health, Education, and Welfare, Public Health Services, Office of the Assistant Secretary for Health, Office on Smoking and Health DHEVi Publication No. PHS) 79-54066. 1979. 1251 pp

.i.

A,.

\I' .1

II.

1

i

255
INTERACTIONS OF SMOKING WITH DRUGS, FOOD

CONSTITUENTS, AND RESPONSES TO DI AGNOSTIC TESTS

Since most published studies investigating the effect of cigarette smoking on measures of health were performetrin

mixed populations, it is difficult to demonstrate specific factors

applicable only to women. Neither the differences betreen men

and women regarding the metabolism and action of Th,ugs nor

the ph 'ecological basis for differences between smokers and

_no mokers is well understood. The same is alsoVtrue of the

ob ed variations in laboratory values and nutritional needs.

Thus, the associations for Women between smoking, drugs, variations in clinical laboratory values, and nutritional needs require further study.

Women Smokers and Nonsmokers and Drug Conmption

Patterns

The drug consumption pattern of women as compared to men has been studied by a number of investigators using different methodologies. The results consistently show that women are

prescribed and take more prescription drugs than men (7,17). In

one study where 1-year drug histories were used, the percentage of women using prescription drugs was 29 percent as compared to 13 percent for men (17). Another study which examined

only drugs consumed within 48 hours of the interview showed

that 60.2 percent of the women had taken medication compared

to 41.8 percent of the men (7). The two studies cited are unique

in the realm of drug usage studies because they measure actual

self-administration of drugs rather than counting, physician

prescriptions or pharmacy dispensing patterns. Unfortunately,

neither of these studies quantified informktion according to

whether the subjects were smokers or nonsmokers.

Other reports show that smokers tend to use more drugs, especially of the psychotherapeutic type and drink more coffee

a d' alcoholic beverages than nonsmokers (18,26). In only one

stu y have women smokers and nonsmokers been compared for

use all drug categories, these data were derived from a selfadministered questionnaire asking about d-ruse for the past year (21). As Table 1 shows, women smokers take more of almost

every: type of drug than nonsmokers. When the data were organized according to age groups, the 15-to-19-year-old grpup of women showe/ a marked elevation in drug use among smokers

(Table 2).

. _Although the data are preliminary, a trend that female smokers consume drugs with greater frequefty than female

nonsmokers is suggested. It is beyond the see-Fe of this chapter

25411(

259
TABLE 1.-Ratio of percent usage of dricg..classes, women

smoker/nonsmoker status

Drug class White Black Asian

T Antihistafoine or allergy medicine

Cough medicine

Asthma medicine . Aspinncontaining drugs

Pain medicine

Codeine. itiorphine, Damon,

Percodan Demerol

Pheiilbarbital or other barbiturates

Sleeping pills,

.....,%' G

Tranqui,liers -,,..../ *Anticoagulants

Digitalis or other heart medication

Antihypertensives

Diuretics

. . CortisoneArpe medication

Hormones

Insulin or'diabetic pills

Iron or anemia medications

Thyroid medication

Pills to control pe nods

Contraceptives

Benzedrine or Dexednne

Weight reduction medication

Penicillin or other antibiotics

Sulfa slrugs

Stomach or digestion medicine

--.

*

. 0.8

1 7 0 9

1 2

1 2

1 5 13

1.2

.0*1 5

- 1 3 1 0 0.8

1 1 1.0

1 /.1 09

09

1 1 1 3

1 2 1.6

1 1 1 2 11

1.2

\

N

0 9

1 2

.1.2

1.6 -,

....1.8 1.3

16

01---

0.8

1.1

1 0

1.2

1.3

0.8

0.9

L3

1.2

1.1

1.1

0.9

1.2

12

1.2

;

0.6

0.7

0.9

0.9

14,

1.2

1.6

1.3

1.8

0.0

0.1

0 9

1.3

1.0

1.4

0.9

0.9

2.3

1.5

1.3

1.1

1.3

1.0

0.8

1.3

SOURCE Seltzer, C.G (21)

TABLE 2.- Percentage of positive responses among females in

age group 15-19

Qu4stion Smokers Nonsmokers

Taken phenobubital pr barbiturates? 2.3 1.0

Taken codeine. mo?phine. etc.? 16.0 6.5

Taken Benzedrine or Dexedrine? 4.9 0.3

Taken peniciniffor other antibiotics? 33.0 25.8

Taken pills to prevent pregnancy' 27.0 9.7

SOURCE Seltzer, C.G (21)

Ito "differentiate between' the behavioral components of this

phenomenon or to address the argument that women who

smoke are less healthy than nonsmokers. It is beneficial, how-

: ever, to examine the few reports that address the differences in

260
drug action between smokers and nonsmokers, regardless of the

reasons for druk use.

Altered Clinical Response, to Drug Therapy by Smokers

/Compared to Nonsmokers

Th number of studies investigatin the differences in the

din' responses to a drug by smokers and nonsmokers are far

fewer n number than the studies examining the aitti-attons in

metabolism and biochemistry of drugs in smokers. The 1979

Surgeon General's Report inchiclecf an eKtensive review of the

alterations in drug disposition that occur in smokers,(25). That

information is useful for clarifying mechanisms by which smgking alters drug metabolism, absorption, excretion, and .otli6r

functions, The clinical significance of these alterations his not 1/4 beeli clarified, however.

ical response to drugs was done by Jick and his associated 111

The most ekhaustive examination of alterations in smokers'

The Boston Collaborative Drug Surveillance Program (BCDSP). Over the past several years, this group has investigated the

clinical response of smokers and nonsmokers to sIx d4fferent

-drugs: -pcopoxyphene (Darvon) (4); diaiepam (Valiurp)(3); chlordiazepoxide (Librium) .43), phenobarbital (3), chlorpromazine

(Thorazine) (24);gand theophylline tea (19). The differences observed between smokers an nonsmokers were consistent

among men and wolneh, except for the theophylline study, in

whicla the toxic effects of th py were slightly more frequent among womet.,(13.4 per t)' than among men (9.19.percent).. Only in the t!hlorpro zing study (24) did the study groupPlthosel._

taking chlorpromaline) contain more women than men, an ob- servation that sipports other reports that women use Major

tranquilizing agents more frequently than men (18).

Since the published HC,IDSP data is not organized according to

groups of women smokers and nonsmokers, any difference in drug use between these groups is not reflected in the data

analysis. However,,it is important to note that these studies, . except as noted in the chlorpromazine study, predominantly involved men. It has been shown that waTercreport more fre- q enter use of the inor tranquilizers such as diazeparii zinci cCtlordiazePoxide (1 Thus these studies should not be interpreted as reflecting rug response among the general population (17).

The" sti'dies on chlorpromazine, diazeparh, and chlordiazepoxide showed a lessened frequency of the adverse effect

of drowsiness among smokers as compared to nonsmsOters (4,24). Conversely, no difference waS reported for.,,plienollarbital (3).

, 2*
4 The analgesic effect of propoyphene was reduced in smokers,

an effect which was not observed in smokers on aspirin, codeine,

acetaminophen, or combinations of these drugs (4).

The evidence for increased theophylline metabolism smokers is well established and predicts the observed cl nical response to the9,phylline (13). The BCDSP study of theo vlfiine

showed that smokers not only required larger dosessof then hytline for efficacy, but also were less likely to report advers effects than nonsmokers, even though they required larger do es.

Theoretically, then, because of a decreased clinical res nse

to a drug, the tendency ould be for the smoker to require

creased doses to achieve the same therapeutic effect/as a

nonsmoker.'

Therapeatic efficacy and adverse side effects in relationship

to gender, smoking history, and drug consumption patterns

have of been adequately studied, although the preliminary

evi ence would indicate an area of potential toxic drug effects

d,or therapeutic failures.

Oral Contraceptives and Smoking

Chronic estrogen therapy has a profound interaction with

chronic tobacco use. Again, the BCDSP has been most instrumental in esessing the influence of these two factors on the

health status of women.,

In assessing the relative-risk of stroke in women who smoke

and ,ake oral contraceptives, the data from the Collaborative

Gropp for the StOdy of Stroke in Young Women show that smoking alone increased the risk of hemorrhagic stroke (he., subarachnoid) from 1.0 for a -nonsmoker who did not use oral contraceptives, to 2.6 for a smoker who did not use oral contraceptives. A smoker taking oral contraceptives had a relative risk of

6.1 or 7.6 (depending on the control group) (6). Similar increaser

in risks do not seem to occur for thrombotic stroke in the smoker

taking oral contraceptives, but the risk of a thrombotic stroke'

for a,./ivoman using oral centraceptives alone is about nine times

greater than that for, a noncontraceptive user (5).

Again using the BCDSP Nta, the risk of nonfatal Myocardial

infarction among women under 38 is very low among nonsmokers, whether or not they...use oral contraceptives. However, the

risk to women who both smoke and use oral contraceptives is

substantially higher, rAnging from an estimated one per 8,400

anntielly in Women aged 27 to 37 years tg on ser 250 for women

aged 44 to 45 years (16). In a similar stui of noncontraceptive

estrogens, similar risks were demonstra' d for women who both

smoke and use estrogens (15). These fin*ings are in agreement

262 X I.
with studies done in Great Britain where oral contraceptives

were associated with an overall increase in cardiovascular disene in young women (20).

Another group which has investigated the link between smoking, oral contraception, and myocardial infarction reported that

there is" a considerable interaction between smoking and contraceptive use. The group found that rate of acute myocardial

infarction among female smokers on oral contraceptives is

greater than could be accounted for by either smoking or contraceptives alone. (22). In earlier,studies this same group con- cluded that there was a dose-response relationship between

smoking and myo 'cardial infarction in women, and that among

women smoking 35 or more cigarettes per day, the rate of

myocardial infarction was estimated to be 20 times higher than

among those who never smoked (23).

These data lend themselves to the prediction of risk in only a very general way and provide no particular measures by which

a womansmoker or nonsmokercan 'evaluate her own risk of

experiencing one of the adverse effects 'described..

The following section .reviews some 'of the laboratory values

that are altered by moking. L74pfortunately, many of the largest

studies on the correlation between smoking and alterations in

clinical laboratory values have focused .on men. ,

Alterations in Normal Clinical Laboratory Values in Women

Smokers

Only a few investigators have studied clinical laboratory

values in women smokers and nonsmokers (1,8-12,14,27). Many

of these studies show statistically significant differences in a

variety of common parameters. The clinical significance of

these differences may not be apparent, however, since the actual differences between women smatters and nonsmoker are

small. For exam l study of packed red cell volume (PCN) and

hemoglobin (Hb) wo en smokers and nonsmokers slowed the

PCV and Hb for nonsmo ers to be 41.95 and 13.85 compared to

42.94-and 14.16 for smokers, a difference significant at p < 0.05,

but a discrimination which physician or patient may find difficult to assess (14).

Small differences in laboratory values between 'smokers and

nonsmokers can be seen in a number of serum chemistry and

hematologic tests. One measurement that shows a wide enough

variation between smokers and nonsmokers to be recognized

-----cjinically is the leukocyte count of a smoker (11,12). It is important to recotize that a WBC of 12,-000 per ram' is within the normal rang or a heavy cigarette smoker, and that the dif26) fia

263
ferential count remainsThormal (11). In one study, individuals

with chronic bronchitis were excluded from e luatiorr of leukocyte counts, and the same relative increase fn leukocyte count

was observed (12).

In several studies of triglycende and cholesterol values in

smoking and yrsmoking women, an elevation of both values,

which was not statistically significant, was seen in smokers.

The addition of oral contraceptive use to smoking caused a significant elevation over the nonsmoker, noncontraceptive user.

The noniffeloker values were 79 z_ 6.& mg 100 ml for tnglycendes

and 157 7.5 mg 100 ml for cholesterol. In the smoker they were

110 It 14.8 mg 100 ml and 174.3 8.8 mg 100 ml respectively,

whereas the smoker using oral contraceptives had a tnglycende

value of 150.0 ± 14.1 mg 100 ml and a cholesterol value of 186.1

mg 100 ml. In this same study, there was no significant difference

between the levels of vitamins A, E or C in smoking and

nonsmoking women (27).

A number of investigators have measured vitamin C levels in

smoking and nonsmoking women, with extreme variation in results. Some showed decreased plasma and. leukocyte vitamin C

level.4" in smokers, and others showed no differences between

smokers and nonsmokers. The discrepancies in these results

may in part be related to the amount of dietary vitamin C

habitually consumed by the subjects in the .various studies (27).

Changes in serum proteins were the subject of another study

of women smokers and nonsmokers (26). Significant differences

in all serum protein fractions were found in cigarette smokers

compared to nonsmokers. In general, the effects increased with

the amount smoked, Past smokers showed globulin values that

were significantly below those of women who never smoked, but

there was no difference observed in the other serum protein

fractions between Past smokers and those who had never

smoked.

The Infkience of Smoking on-ithe Nutritional Needs of Women

Outside of a possibly increased need for vitamin C in women

who smoke, there is very little informatv about other nutrient

, requirements in smokers. In recent, years a great deal of time

has been spent studying the influence of smoking on feta! developinent, a subject coVered elsewhere in this volume. The spe-

.cial nutritional needs of the nonpregnant smokirquwpman have

not been dealt with in any systematic way. ,

A recent study involving obese women looked at the influence

of smoking cessation on body weight (2). Although the data are

innately biased because the study group consisted of women

.264

2'

sio
enrolled in a weight loss program, the results showed that Amen who smoked less than a half pack of cigarettes a clgy

-.gained 4 pounds after they quit. Heavy smokers consuming over two packs a day gained an average of 30 pounds over several Itcedes. Moder le smokers gained an intermediate amount. is study does not contradict a commonly held notion. that wtithen gain weight when they stop smoking; however, it pro- vides no behavioral or physiological hypothesis for this phenomenon. 44,

Summary

Most published studies investigating the effects of cigarette

smoking on drug use have been performed on mixed populations; factors specific for women have not been demonstrated to

date. It has, however, been clearly demonstrated thgti, women

are prescribed and consume more prescription drugs than, men. 1. Studies of selected drugs indicatd that smoking tri- ay affect clinical responses and alter the dose required for an effectivs therapeutic result.

2. Smoking interacts with oral contraceptive use to increase the risk of myocardial infarction and subarachnoid hemor-., rhage.

3. Common clinical laboratory parameters are altered in

smokers compared to nonsmokers, the health significance of

these changes is unknown. ' 4 Insufficient information exists for assessment of the impact of smoking on the nutritional needs of women.

ti References

(1) BILLIMORIA, J D, POZNER, H., METSELAAR, B., BEST, F. W., JAMES, D C D Effect of cigarette smoking on lipids, lipoproteins, blood coagulation, fibrinolysis and cellular components of human

blood: Atherosclerosis 21(1) 61.76, January.February 1975

(2) BLITZER, P H.; RIMM, A A., GIFFER, E. E.ThAffect of cessation of

smoking on body weight in 53,032 women. cross sectional and longitud

anal stalysis. Journal of Chronic Diseases 30(7) 415 -429, July 1977. (5) BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM

Clinical depression of the.cntral nervous system due to diazepam Ind

chiordiazepoxide in relation to cigkrette smoking and age. hew Enggsit land Journal of Medicine 288(6) 277.280, February 8, 1973

(4) BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM.

Decreased thrii611 efficacy of propoiyphene in cigarette smokers. Clinical Pharmacology and Therapeutics 14(2) 259.263, March-April 1973. (5) COLLABORATIVE GROUP FOR THE STUDY OF STROKE IN

YOUNG WOMEN Oral contraceptives and increased risk of cerebral

ischemia 6r thrombosis New England Journal of Medicine 2884171

871.878, April 26, 192.3.

(6) COLLABORATIVENGROUP FOR THE STUDY OF STROKE IN

265 2C5
0 YOUNG WOMEN Oral contracept.es and stroke in young women

Jousrnal of the American Medical Association 221(7) 71/44-722, February

17, 1975

47) RAIG;,T VANNATTA, P A ( urrent medication use and symptoms

of depression in a general population' American Journal of Psychiatry

I35(9) 1036 ,039, September 1978

4*/ DALES. L G FRIEDMAN, Q . SIEGELAUB, A B , SELTZER. A C

igarette smoking and serum chemistry tests Journiil of Chronic pisv); eases 27,6i 293-307, August 1973

,Y) DALES L G , FRIEDMAN. Q D SEIGELACB. A B , SELTZER. A (

RY.1-1 K ( igarette smoking habit, and urine charactenstie, Neph

run 20 163.17(1, 1978

10) DESMOND, P.,4 ROBERTS. R K , WILKINSON. Q R , SCHENKER,

a No effect of smoking on metabolism of chlordiazepoxide New Eng

end Journal of Medicine 3004) 199-200 January 25, 1979

FRIEDMAN. Q D , SIEGELAUB. A B SELTZER, C C . FELDMAN,

R ( OLLEN, M F Smoking habits and the leukocyte count ArchRes

of Enironmental Health 264,3i 137.143 March 1973

I I HELMAN, N , Rt. BENSTEIN L S The effects of age, sex, and smoking

on erythrocyte, and leukocyte. American Journal of Clinical PatholOK:. 63 35-44, 1975

(Hi HUNT, S N , JUSKO, W J YUR( HAM, A M Effect of smoking on

thvophyiline disposition Clinical Pharmacology and Therapeutic. 19(5,

Palt r 546.551, %lay 1976

414) 1"AGER. H HAGER' P. L Relationship between cigarette smoking

and high packed cell solume and haemi5gliebin levels Scandinavian

Journal of Haemotology 844) 241-244, 1971

; .JI( K, H , DINAN, B . ROTHMAN. K J Noncontraceptr.e estrogens and

nonfatal myocardial infarction Journal of American Medical Association 2-19414) 14t7 1408, April 1, 1978

)16) JI( K, H , DINAN.43 ROTHMAN, K J Oral contracepto.e,is and nonfatal myocardial infarction Journal of the American Medical Association 239114i, 1403-1406, April- 3. 1978

PARRY. H F, RALTER,.M B. MELLINGER. Q D, CISIN, I H,

MAN HEIMER. D I National patterns of psychotherapeutic drug use

A'rchRe. of Gener'al Psychiatry 28 769483, June 1973

4/),) PARRY, H. F. CISIN, I H, HALTER. M .B, MELLINGER, Q. D,

MAN HELMER. D I Increasing alcohol intake as a coping mechanism

for ptychicaktress In 1_ ooperstock, R I Editor) Social Aspects and Medical C se of Psychotropic Drugs Toronto. Addiction Research Foundation. 1974

(i9) PFEIFER. H J GREgNBLATT, D J Clinical toxicity of theophylline

relation to cigarette smoking Chest 73.44i 455-459. April 1978

e.://), ROYAL. COLLEGE OF GENERAL PRACTITIONERS ORAL CONTRA( EPTION STI DY Mortality among oral contraceptive users

Lancet (4) 727-733. October 8. 1977

(21) SELTZER, ( G FRIEDMAN, Q. D. SIEGELAUB. A B Smoking and

drug consumption in white, black, and oriental men and women

American Journal of Public Health 64(5) 466-473, March 1974

(22( SHAPIRO. S SLONE, D. ROSENBVG, L, KAUFMAN, D, STOLLEY, P D , MIETTINEN, 0 S Oral'contraceptive use in relation to

myocardial infarction Lancet t 1> 743.747. April 7. 1979

1.:4.) SLONE. , SHAPIRO, S S. ROSENBERG, L KAUFMAN, D W

HARTZ, C , ROSSI, A C,STOLLEY'.P D M IETTINEN 0 S Relation of cigarette smoking to myocardial, infarction in young women

266
I

New England Journal of Medicine 298(23) 1273.1276, 1978.

SWETT. D Drowsiness due to chlorpromazine in relation to cigarette

smoking Archjves of General Psychiatry 31 211-213, August 1974, U S PUBLIC HEALTH SERVICE Health A Report of

the Surgeon General U Department of H , Education, and Welfare. Public Health Ser. ice, Office of the Assistant Secretary for

Health. Office on Smokingfrand Health, DHEW Publication No (PHS,

79.50066, 1979. 1251 pp

WINGERD, J , SPONZILL I, E E Concentrations of serum protein fractions In white women effects of age, weight, smoking, tonsillectomy

and other factors Clinical Chemistry 23(7) 1310-1317, 1977,

YEUNG, D L. Relationships betwben cigarette smoking, oral contracepti \es and plasma %itanIns A. E, C and plasma tnglycendes and cholestecol American Journal of Clinical Nutrition 29 1216-1221. 1976

N

2 "V

267
PSYCHOSOCIAL AND BEHAVIORAL ASPECTS OF SMOKING

IN WOMEN

IntrodubtiOn

Currently, women are rapidly approaching men in the rate of

initiation and prevalence of cigarette smoking, but seem to have.

, a lower rate for successful cessation of srrloki (See Is° Part I

of this eport, Patterns of Cigarette Smoking ) increasing percen ge of the S populan n is giving up d mu ing, nationwide

surve and cessation studies gest that a smaller proportion of worrre than men are quitting succe fully

This part, discusses tobacco use by women, with comparative

reference to men's use wherever appropriate,,, Special attention

is directed to the patterns of initiation, the rise in smoking. among girls, and 'the factors important in the maintenance

smoking behavior, including pharmacological effects, -smoking patterns, information dissemination, and)stress management. The differences in successful quitting between men and women

smokers are discussed with the hope of generating new ideas for research and intervention.

A separate analysis of smoking patterns amo women in the

health professions is presented. In addition, a se ion is devoted

to the pregnant smoker because the impact of smoking, both on

the fetus an4 on the pregnant woman, makes this a period of particular importance in the life of the women smoker.

Initiation of Smoking in Adolescent Girls

Cigarette smoking, particularly cigarette smoking among

young girls, is a changing phenomenon. Shifts in smoking at- titudes and behaviors reflect broader social forces, including

changes in sex roles and gender differences in responses to publicinformation programs and to social sanctions against smok- ing.

The trend in adolescent smoking, as in other "adult-like" behaviors such as alcohol use orsexual activity, is toward earlier onset. For example, before the mid-1970s,,girls were less likely

to start smoking than boys, and when they did, they started

later. Neither of these differcinces holds true any l&iger. A number of psychosocial variables correlate hikhly with adolescent smoking trends. These include the attitudes, perceptions, and behaviors of adolescent girls, their social setting

(family, .peer groups) and those broad demographic factors acs, education, familyincome, urbarlicity) that help to define

individual's position within the society.

271

`at
c

CONCEPTS OF ADOLESCENT BEHAVIOR

Discussions of adolescence with its attendant problems have

seldom differentiated between boys and girls, and no theory or

model of adolescent behavior has been developed specifically for

girls. However, gender differences in development, cognitive

processes, sex-role acquisition and achievement have recently

been'examined and a number of psychological differences have

been identified (2 -1,26,51,68,98,211).

The essence of adolescence is growth, transition, and change.

The rate of physical growth in adolescence is more rapid than at

any other stage of development except the neonatal stage. Adolescent development is a complicated process which involves'in--

creasing self-awareness, intellectual and emotional growth, and

physiological changes.

What adults characterize as risk taking in adolescence may be

exploration of the limits of identity and capability. Adolescents

are attempting to resolve the competing and conflicting demands stemming fro ) childhood experience on the one hand

and expectations of a ulthood on the other: dependency and

compliance versus autonomy and independent decision-making;

orientation toward family versus orientation toward peers.

They face increasing demands for social and cognitive achievement and for developing the self-control required to handle new

psychological, physical, and social situations. Inadequate experience with these challenges or failure to meet them may rest

in low self-esteem and increased anxiety and stress.

Numerous formulations contributing to a general model of

adolescent development have emerged. These include life-span

theory and cohort change (52,131), adolescent sexuality (32), and

differences between early and late adolescence (85).

Douvan and Adelson have identified issues that distingikish

adolesce?ee. for girls they are sexuality, interpersonalintimacy, and iderhity issues, for buys they are sexuality,

autunomyl-assertion-indepeltdence and identity issues (51). In

this'audy, conducted in the 1950s, girls evidencid conflict betweeri the social roles for which they were preparing (further education and careers) and the future role they desired

(m,atriiiigi..-mottierhood). La Farge described a similar female

adolescent between social rules and indi% idual:percep;

Lions (109). Research published in the 1970s shows that young

women still have role conflicts different from those of young

men (68).

Research on gen7der -role differentiation in childlitod has

provided some rnsight into developmental differences between

ginks and boys. Maccob!, suggests that these differences may

212 I.... e 2 i' r' t.., it
derive from different role models for boys and girls; from the varying responses of significant adults to their behaviors; from

biological differences; and from a combination of these (116). Block, and Maccoby and Jacklin report that the differences in- clude girls having less confidence in their ability to handle a new task and less se se of control over what happens to' them

(18,117). Girls alsoishow-greater susceptibility to expressed anx- iety, greater need (pr help and reassurance, greater closeness to friends, and more concern for what is socially desirable. Adolescent behaviorssocial or antisocial, adaptive or maladaptivekare a function both ofindividual choice and of the

opportunities for growth and development witech a society pro- vides its youth (36). "Not only is the term 'adolescence' a social . definition; but what society perceives as an adolescent problem

is also .socially defined" (52). Similarly, the development of values, motivations, and controls that foster healthy growth

and dsetenthe onset of smoking and other undesirable behaviors

depends on the opportutities and resources that society makes available to the adoiese4nt.

PREVALENCE-AND PATTERNS OF ADOLESCENT

CIGARETTE USE

National surveys of adolescent smoking behavior have pro- vided information on gender differences, secular trends, and

age stibgroupings within the adolesqnt period. Surveys of smoking patterns, ages 12 to 18, were conducted by the National

Clearinghouse for Smoking and HealZh,.NCSH) in 1968, 1971

1972, and 1974 and by the National Institute of Education (NIP)

in 1979 (130,197). Two other periodic surveys, both sponsored by_ the National Institute on Drug Abuse *(NIDA), included

cigarette consumption (2,101). A number of studies in specific geographic locales or among specific populations, such as high school students, have also been carried out (198). Diffenng defi- hitions of a current regular adolescent smokyr make compari- sons among these studies particularly difficult. In the NCSH and NIE surveys, a regular smoker is defined as one who smokes cigarettes at least weekly. In the NIDA surveys, regu- lar smoking is defined as occurring within thepast 30-days.

Prevalence

TablV summarizes adolescent cigarette smoking prevalence between 1968 and 1979, by age and gender,. as surveyed by NCSH and by NIE. Between 1968 add 1974 there was a signifi- cant increase in the percentage of girl..smokOs in each age cat-- egory at each point in time, in contrast to the relatively stable

,273

.0. 2 7u
prevalence of current rsgular smoking among boys. A decline in

the average age of sinoking initiation foi,both sexes is

suggested by the small but significant increase in smoking prevalence among 12 to 14 year olds. (198 Trends in the data from

a national study of high school seniors also support the

hypothesis of an earlier age of initiation (101.

In the five years from 1974 to 1979, the proportion of 17 .to 18

year old girls who smoked changed little, but the proportion of

boys wio smoked dropped by a third. It was this difference

among 17 to 18 year olds that created the overall higher smoking rate for girls as compared with boys in 1979. However, at

ages 15 to 16, the drop from 1974 to 1979 was greater for girls(

than boys, suggesting that the initiation of smoking is also beginning to decline in those girls born after 1962.

The differences in the within-age-group changes in the smoking prevalence of girls may represent an isolated effect on the

cohort of girls born in 1963 and 1964. The change was essentially

confined to the 15 to 16 year old subgroios who were born during these years. The precise nature o,c the interaction of social

influences on the development and maturation of this cohort is

unclear. However, other data suggest that a marked secular

change occurred in cigarette smoking attitudes and behavior

which was secondary to an increased awareness of the health

risks of smoking. An alternate hypothess's that the isolated decline in the 15

to 16 year old subgroup may be an artifact produced by the

combined trends of reduced initiation of smoking and the initiation at a younger age. Thus, the decline in prevalence among 15

to 16 year ol8 girls would reflect the decreasing percentage of

young wo en who are taking up smoking, but this trend will be

raalkcid r the you'riger age grOup by the tendency of those girls

who are g g to take up smoking to do so at a younger age. The

1979 NI E S rvey reports that:

,The increasing prevalence of teenage smokrng that was observed in the period between 1968 and 1974 has come to a halt,

and a decrease in the smoking rates of both boys and girls has

taken place. The decrease in boNsdsmokng was greater than

that of girls, resulting in a higher smoking rate for rls than

for buys in 1979. Smokrng among boys leveled off in the early

1970s, and then began to decrease. It appears that girls are

now .following this pattern. the smoking rate has level off

among 17 and 18 year olds, and probably can be expected to

decrease over the next few years (130).

Other surveys (Table 2) support these trends in adolescent

girls' smoking behavior. Differences between studies in abso14e prevalence rates reported are at least partly due to the

274
TABLE 1.Estimates of the percentage of current, regular

cigarette smokers, adolescents, aged 12 to 1.8, United

'States, 1968-1979 ., Ages 12-14 Ages 15-16 Ages 17-18 Ages 12-18

Year Ale Female Male Fema18 Male Female Male Female

1968

1970

1972

1974

1979

0

2 9

-57

46

4 2

32

06

30

2 x

4 9

43

170

195

11X135

96

14 4

163

2

II 8

302

37 3

30 2

310

193

1x6

22x

25 3

215 9 26 a

14 7

1x5

157

158

107

V4

1 1 9

133

153

12.7

NOTE Current regtilar smoker includes respondent who smokes cigarettes at least weekly

SOURCE National Cleannghouse for Smoking and Health (197), National Institute of Education (130)

11111 ti

difference in the definition of a sm er, and differences in

survey technique. The National Insti ute of Education Survey included as current regular smokers both those who smoke

one or more cigarettes per week and those who smoke one or

more cigarettes a day. The prevalence rates of Abelson, et al. (2) and Johnston, et al. (101) refer to any cigarette smoking in the past 30 days.

The Abelson, et al. data, which were collected 2 years before

that of NIL, show the predicted decline, but to a lesser degree

(2,130). The Johnston, et al. data suggest that there was an in- crease in adolescent girls' smoking as measured in samples of

'high school seniors between 1975 and 1977 (191). Johnston's fig- ures were retrospectively reported and refer only to youngsters born before and during 1960, and therefore, would not be ex- pected to reflect changes occurring in those cohorts born after

1962 where the decline has occurred. This may explain why the

Johnston, et al. 1977 sample did not reflect a downturn, and re- ports of later cohorts of high school seniors should show a stabilization and then a decline in feinale smoking rates. Re- sults from a study by the same group in 1978 show the predicted downturn in the smoking habits of high school senior girls (from

39.6 percent in 1977 to 38.1 percent in 1978) as well as boys (from

36.6 percent in 1977 to 3416 percent in 1978) (103).

Age of Initiation of Smoking

The data in Table ,1 shol4that the prevalence of smoking in girls aged 12-14 inc eased steadily between 1968 and 1974 to a

level equal to or'slig tly higher than boys of the same age. Between 1974 and 1979 he prevalence of smoking stabilized in

275

2 *
J

girls and may have begun to decline. The prevalence of smoking

by boys of this age peaked in 1970 and has shown a steady der,.

cline since that time,These trends may represent fewer adolescents taking up smoking, with those who do beginning at an

earlier age. Well over one-half of high school seniorsmale and

femalewho smoke regularly, reported first smoking in the

ninth grade or earlier (101). It is hard to know whether this

earlier onset reflects something specific to cigarette smoking or

is attributable to the more general pattern of earlier onset of all

"adult-type" behaviors. This° treridarly initiation of smoking behawior may

have a signifAnt impact on the future health of these adolescents, as many of the health risks associated with smoking increase with both earlier onset of smoking and duration of the

smoking habit. In addition, the earlier the use of a substance is

begun, the longer it is likely to be continued and the more heavily it is likely to be used (26,102,137).

These national surveys do not permit a detailed - ,c,,44vtiation

of the initiation process. "Experimenters," those wTo have

smoked at least a few puffs of a cigarette, but not more than 100

cigarettes, are grouped with "never smokers", those who have

never taken even a few puffs. "Occasional" smokers are defined

as those who smoke less than one cigarette a week but more

than 100 cigarettes in a lifetime. Occasional or intermittent

smoking is rare amortg adults. Examining the proportion of

}experimenters" at each age Sand following their subsequent

smoking behavior might help_elarify the determinants of the

initiation process (126).

In one major British. study, smoking only a few cigarettes

usually led to becoming a regular smoker; only 15 percent of

those who smoked more than a ,single cigarette escaped adoption of smoking as a regular behaviora(,126). The estimate in this

study of 8 percent "occasional smoking" in adolescence is based

on a definition of smoking less than daily, but at least one

cigarette a week for as long as 1 month. The difference in definition of occasional smoking makes comparison with current U. S.

data on adolescents difficult. From 1968 to 1979, the percentage

of current occasional smokers (less than once per week) varied

between 0.4 percent and 1.6 percent for girls, and 0.4 percent

and 2.3 percent for boys (130) McKennell and Thomas estimated

that the mean length of time between`smoking the first

cigarette and adopting regular (daily) smoking was slightly less

than 3 years for boys_and slightly more than 2 years for girls

(126). The difference is probably due to.eailier experimentation

amon\g boys. The transition from experimental or occasional

276 \. 2 ^

a
TABLE 2.Percent of adolescents currently using* cigarettes, , alcohol and marihuana, by sex: three national

surveys compared

Ages 12-18

:CIE (1979)

-Ages 12-17

Abelson, et al.

(1977)

Ages 17-4\9

High School Seniors

Johnson, et al. (1977)-

Ages 1974 1979. Ages 1-974 1977 Ages 1975 1977

4 Current Cigarette Use

12-14 F 5,1 4 3 12-13 13 10

M 4.2 3 2

15-16 F 216. 123 14=15 25 22 C.

MA.8 1 14.6

17-18 F 26.4 27 0 16-17 38 35

M 32.6 19.6

12-18 F 15.9 111 12-17 F 24 22 17-19 ke(.35.9 396 M 16 3 11 1 Ni' 27 23 M 37.2 36 6

$

Qurrent Alcohol Use

16-17 F&M 51 52

12-17 F 29 25 17-19 F 62.2 65.0

M 39 37 M 75.0 77.8

.....- Current Marihuana Use

16-17 F&M 20 29

12-17 F 11 13 17 -19-F 22.5 30.0

34 +2-, 19 M 32 3 40.7

'NOTE: Definition of current use vanes by study. Cigarettes: Nrc

(19791current regular smoker (one or more cigarettes dunng the week

five packs) and current occasional sm er (less over and above a minimum

than one Cigarette per week), Abelson, el al. (1977) and Johnston, t al.

(1977)smoked within the past 30 days. Alcohol and marihuana. use within

the past month (smokers and nonsmokers).

SOURCE- Abelson. H.I. (2), Johnston, L.D.-(101), National Institute of

Education (130). 41

smoking to regular gmoking is an extremely important one to

study because it may provide a crucial period for intervention

before psychosocial or pharmacological dependency is established.

Number of Cigarettes Smoked , In the NCSH/NIE survey (130), a smaller percentage of

female smokers than male smokers smoked ib or more cigar- ettes par day (61.8 percent versus 73.8 percent in 1974 and 59.0

--.. 277
percent versus 65.6 percent in 197 9). The high school senior survey showld male- female rates to be equivalent at the half-pack

per day rate, with boys exceeding girls at heavier levels (101). In

that study; the proportion of females currently smoking as

4 much as a hilii-pack per daiNrvereasei. between 1975 and-1977,

while th.eln5Firtion of males spoking at that rate remained

tar-it:'The Americas Cancer Society survey also suggested

an incrtase in the proportion of heavy smokers among adolescent girls compared with stable rates in boys between 1969 and

1975 (` I6). It reported a,fourfold increasein the percentage of

f ale smokers who smoked at least a pack a day, from 10 per-

, .cerie to 39 percent, compared witt an unchanged rate of 31 percent among males. The equality in smoking behavior may be

extending to the number of cigarettes smoked. 1/4 -*

Type of Cigarette Smoked

In adolesCent smokers uf both sexes, there has been g definite

trend toward smoking cigarettes with lower "tar" yields betweeri.1974 and 1 -9. Figure 1 shows the decline in tha "tar" and

nicotine ,1e v e s of the cigarettes smoked by addlescents. Girls

appear to be slightly ahead of boys in the Use of lower' "tar" cigarettes. The trend cane attributed to three factors: the

increased marketing.of low "tar" cigarettes; the decrea.ged-"tar'

levels of existing cigarettes, and increased awareness crf-differential healtob hazards associated with different kinds .wf

.cigafettes (130), It should to noted, howewer% that the midi-joint

on the cumulative percentage continuum Igs dropped only

about 1 mg "tar" between 1974 and 1979, from approximately

1 m`g to appArn4tely.16.5 mg, and the percentage of adoles-.

ce okingWe lowest category of `tar" (less than or equal to

10 still'very -

ai

Smoking Cessation

, .0

-Are there ylifferences between girls and boys in patterns _of,

mo" king cessatibn comparable, to those observed in adults? A

eat'e'r prtokortion of adult males-0.1in adult females have quit

smokipg (See the section on addlt smoking cessat4n in this

part). Two .pational surveys have shown triore eismOkers

iffofig adolec erii.boys than amonigirls (101,134 Look.ing alp

either the ,peitage of_ex-brripk04amohg all adolescents-tat

the quit rates ilk mber offorrner.smokers divided by number of

ever smokers),,Mb excnd girls in every survey between 1968

and 1.979 (130): Howev4f, i'fexpermin'trital smokers are elimi-

-,n4ted from the anarysis, there are no differences between the

boA and girls. For the two. most recent surveys,' the quit rates

. . 278 r adi
'0*

0/0 100

90

80

70

60

4

rJ

co FIGURE I....Cumulative percentage of adolescent smokers by the tar level of cigarettl smoked, 1974 and 1979

50

40

30

20

10"

Girls

4

x*:,******

s.

<10 11,15 , i6 17 18 19 > 20

(0:6) (0.8) (1.1).(1.1) (1.2)(1.2) (1.45)

Mg "tar" (and median mg nicotine)

1974

4 41, x . x 1979

100

90

80

70.

60'

50

11.15 16 17 18 19 > 20

(0.8) (1.1) (1.1) (1.2)(1.3)41.45)

Mg "tar" (and median mg nicotine)

SOURCE: Federal Trade Commission

k

(61), National institute of Education (130).

;
4

1

t,

were as fol'ows: 33.2 percent of female and '36.0 percent of male

smokers had quit in 1974; 30.5 percent of female and 42.3 per- cent of male smokers ha4 quit in 1979. In contrast, Reeder found no diffel.encein quit rates between boys and girls aged 13 to 19 in natiZal surveys conducted in 1965 (boys 28 percent, gals 29

-percenfrand in 1975 (boys 434 percent; girls 35 percent)7148). Therefore, it is unclear whether adolescent girls show the samtlik patterns of quitting smoking found in adult women. It should, also be remembered that research on both smoking cessation

and illicit drug use has shown that quittmg is often not a per- manent state (100,147,173).

Smoking Prevalence and Ethnicity

There-are nrdata based on a national sample examining adolescerit smoking in different racial groups. However, beginning

in 1969-1970 Brunswick hat conducted a longitudinal personal home interview survey of a representative sample of 668 urban, non!Hispanic black youth's in Harlem, New York City. She found

that more 16 to 17 year old girls than boys smoked (62 percent versus 50 percent). This was well bere national rates had

shown smoking among girls equAling Ad then exceeding that among boys. This greater smoking prevalence in girls continued 4 into he young adult years..* The same subjects were re- interwed 6 to 8 'years later, when the youths were aged 18 to 23. Sixty-two percent of y2ungbiack women (N =25k) were.eur- rent smokers and 18 Rercent were currently smoking at least a Pack a day. This is cailpared with 57 percent of the black mer1,18

to 23 years old (N =277) who were current smokers, 16 percent of whom-regularly smoked atjeast a pack a day: These prevalence

rates are Well above the fates for adult black women found in

national survey data, but are only slightly higher than thetates

found in adult black men 198). This study it of subs_tantial interest, but mak, not be representative of national black adoles- cent smoking patterns.,

Alcohol and Marihuana Use

0,0 _Cigarette use shoUld be viewed in the context of other substance use behaviors. Abelson, et al., Provided information on the use of other substances in the age range of 12 to. 17 by current cigarette smokers and by those not currently sfrkoking

(2). Smokers far exceeded nonsmokers in reporting use of alcohol, marihuana and'or hashish, 61\ "stronger" .drugs (hal

lucinogens, cocaine, heroin, and other opiates): positive reply s

for alcohol were 80.0 percV.Fersus 44.8 percent; for Ahuana

arrd/or hashish, 68.3 percent versus 16.7 percent; and for

280

2 ."
a stronger driigs, 26.3 percent versus 4.1 percent respectively (24,

103,130,216).'Similar figures for alcohol use by 13 to 17 year old girls were reported' by Yankelovich, et al.: 81 percent of the

smokers drank compared with 42 percent of nonsmokers, but

somewhat lower estimates were reported for marihuana use-25 percent of the smokers versus 3 percent of the

nonsmokers (203). Strong associations between alcohol use and

cigarette smoking andOr between marihuana use and cigarette

smoking in adolescents and college students have also been

identified in a number' of other investigations (8697,153,

177,181).

DEMOGRAPHIC AND PSYCHOSOCIAL-CORRELATES OF

SMOKING IN ADOLESCENCE.

Smoking is a complex behavior, and it is likely that adolescents

start to smoke for multiple reasons. Strong correlations between smoking and a number of demographic and psychosocial

variables have been reported, but causal connections have not

been established. Neither has the set pf "predisposing factors"

been often subjected to multivariate analysis. It is rare that'

mor than one or two Variables have been tested simultaneodny. What appear to be separate determinants of smoking behavior (for example,'peer pressurerand socioeconomic status) may actually be reflecting a' single underlying pattern. For

example, aspects of self-confidence, academic achievement,

types of parental andOr peer relations, and;or socioeconomic

factors cluster in certain ways to influence susceptibility to

smoking cigarettes. A few multivariate analyses have been.

conducted (111,113,138).

4

.,

:OPSoeioeconomic Influences - A number of studies.have, examined smoking in relation to

socioeconomic status. The fin gs consistently point to a relationship between lower arental status income and

educationand highdr smoking prevaiente among these par- ents at their children (20,130,14161). Adolescents from lowincome families may also begin to smoke earlier than others

(33,f26). Tie findings that Firls who work have higher rates of smoking may also reflect a relationship to lower economic

status (9,130). Stole and Fischer observed a relationship between downward mobility and smoking ip a ults (180). This may be an impOrtant dynamic to explore in ad lescent initiation of

smoking. - . .. A relationship between parental edu tion and adolescent-

'. smoking also exists (130). When one or both parents attended

. 281
college, 9.9 percent of boys and 10.6 percent of girls smoked,

compared ,with 10.9 percent of boys and 14.8 percent of girls

from homes where neither parent attended college.

Family Patterns

In single-parent households (19.3 percent of those households

surveyed in 1979), adolescent smoking rates were approximately double those of households in which both parents were

- 4 present (130). This.relationship holds for both boys and girls, in

,every age group, Nd across all five NCSI-VME surveys; it has

also.been identified by others (111). In the 1979 survey, 19.3

percent of the boys and 21.2 percent of the girls in singltiparent

i households are smokers, compared to 8.6 percent and 10.7 percent of those in hoines with both paren.ts present.

. Parental modeling may underlie this association in two wa ' Al*

First, adult smoking rates are higher for divorced or separ d

men and women. Second, female single parents who head

households are likely to work outside the home, and smoking is

more prevalent among,working women than among homemakers (182):

Smoking Among Parents and Siblings '- Adolescents are more likely to smoke if either or both parents

smoke than if tlfey do not (9,15,20,161,213). In the 1979 NIE Survey this pattern was found across age and gender (130) (See.

Table 3.) Looking at the data slightly differently, when both parents smoke, 13.5 percent of sons and 15.1 percent of

daughters smoke, when onepdrent_smokes, 9.1 percent of boys

and 12.7 percent of girls smoke,and in homes where neat r

parent smokes, 5.6 percent of boys and 6.5 percent of girls sale

(130).

Ther.e are conflicting reports on the relationship between the

sex of the smoking parent and smoking halpts of the offspring.

In two-parent homes in which only one parent smokes, 17 to 18

years olds appear to be more likely to smoke if the mother does

(130). Other 'studies have identified a relationship between the

child's smoking and that of the Parent of the same sex (9,15,213).

Allegrante, et al. found a relationship between the mother's

smoking behavior and that of sons, but not of daughteirs, and no

relationship of the father's smoking behavior to smoking by

childr,en of eitherrsex (3). In contrast to, all of these findings,

Schneider, et al. were unable to relate parental smoking to that

of offspring (166).

Eocplanations for the 4,ssocikiori between parental and children's smoking behavior incli,tde the effect of role-modelingoa282 1

r
41

TALE 3.Percentage of adolescents who smoke by the smoking behavior of parents and older siblings

. Older Sibling

Ramp No 'Have No Older Older Older ' Older

, Older Sibling

i.. Sibling Sibling Does Sibling Sibling D

One or Both Smokes Not Smoke Smokes Not Smo

Parents

Neither

Parent

One or Both One or Both Neither Neithe

Smoke

- Parents Parents Parent Parent Smokes Smoke Smoke Smokes Smoke

k, Boys

12-14 j 15-16,

2.5 00 63 27 00 00

17-18

176

150

7, 40

79 - 18 8

25'4

6:S

167

211

r0 7

'`f\

2 1

. Total 0.0

Girls

8 2 2 9

. 17 0 7 5 19 5 0 6'

12-14

15-16

37 00 s5 13 3.4 2 9

17-18 29 7

8.2 57 20 0 13 0 15.2 24

Total 97

15 4 32 9 19.6 25 0 67 41 20 3 97 153 41

ti

Base. Both parents present in household

SOURCE National Institute of Education (1301 ' 2
rhs.r

rental perm*siveness (real or imagined), and availability of cigare es in'the home (125).

01 siblings seem equally important or more important

than parents as potential role models for smoking ( 9,130,148). There is a greater likelihood that an adolescent will smoke done

or more older siblings smoke than if no older siblings smoke;

this is true in those households where neither parent smokes as well as in those where one or both parents smoke. In the 1979

survey, boys with older siblings who smoked were more than

three times as likely to smoke as boys with nonsmoking older

siblings, The increase is about twofold for girls. The highest smoking rate for girls was found when at least one parent and

an older sibling smoked (20.3 percent). The corresponding rate

for boys (17,.0 percent) was slightly lower than where an older sibling but neitherparent smoked (19.5 percent) (130). (See Table 3.)

Peer Group Influence

Adolescents' smoking behavior is highly correlated with reports of having friends who also smoke (15,132,133,155,162,216).

Most multivariate analyses have established this factor as

being of prime importance although one such analysis found no

relationship at all (3,113,138). It has been painted out that patterns of drug use in adolescents are very similar among best friends (121). It hhs'not been deMonstrated, however, that it is

the behavior of friends rather than inclinations of the adolescent which influences him or her to smoke (3,130,166).

Inquiring about the smokin behavior of the "four best

friends'.' of adolescent responde s, the NIE study reported that 87.6 percent of boys and 94.0 rcent of girls who smoked stated

that at least one of those friends also smoked. In addition, only

10.2 percent of boys and 5.-9 percent of girls who smoked had no

regular smokers among their four best friends, and an even

smaller fraction (2.2 percent of boys and 0 percent of girls) re- ported that none of their friends had even experimented. In a parallel vein, it was found that nonsmokers also congregate to- gether. Approx,imately one-third of the nonsmokers (33.8 per- cent of boys, 32.9 percent of girls) reported having at least one

best friend who smoked, while over two-fifths (43.0 percent of boys/ 44.1 percent of girls) had no best friend who smoked reguOver one-fifth (22.4 percent of boys, 23.0 percent of girls) had no best friends who had even experimented.

Thus, "peer pressure" to smoke. may be operative when the

adolescent, belongs to or would like to belong to a group in which

smoking is part of the life-style (130). When the peer group be284
havibr does not include smoking, there may be httlepressure on

the adolescent 'to begin to smoke.

'Conformity pressures and peer influence are very strong in

early adolescence. Therefor, if smoking were considered a behavior which was adopted by the majority of adolescents, exper-

/Pentation

and initiation might occur because of the ,impor- aInce of conforraity in this age period (63). Unfortunately, there

are suggestions that most adolescents tend to overestimate the proportion of their peers who are smokers. Eighty-two percent of all girls surveyed in the 1975 American Cancer Society Sur- vey thought of adolescents as smokers rather than nonsmokers

("216). In that same survey, the professions of teachers, execu: tives, housewives, an feminist leaders were all charactenzed

as smokers by approximately two-thirds of girls, with only doctors and athletes considered nonsmokers.

Heterosexual peer considerations may also be important. Girl *smokers are very likely to have boyfriends who also smoke (72

percent), compared with nonsmetking girls (27 percent) (216). Similar percentages apply.to the fractiCm of all male,friendswho

smoke (69 percent jor girl smokers and 32 percent for nonsmok- ers). Yet girls are less Ilk n boys to see smoking as a social , asset (37 percent versus a per ent) and they even consider it a drawback (52 percent girls versus 31 percent boys). The kinds of images projected by the people shd*n in

cigarette advertisements may lend su.pport to peer-influences to

smoke. Girl. smokers characterized such people as attractive (69

percent), 'enjoying themselves (66 percent.), well-dressed (66 per- cent), sexy (54 percent), young (50 percent), and healthy (49 per- cent). :-

_ Prevention efforts alined at making actual statistics n smoking prevalence available to teens in order to correct the above

beliefs may help counter the advertising. Popular personages in various professions and lifestyles which girls mistakenly per- ceive asnsmotter-dominated could be recruited in this effort.

4. Scholastic Achievemtnt and Aspiration

Achievement in school has been one of the most frequently

inyestigated correlates of smokii3g, with a study as early as 1923

showing an association between poor school grades and srnoking (45,83,121,137,143,161,212).. Two studies have reported this

,assalation specifically for girls (35,216). Companng the three

factorsparental smoking, socioeconomic status, and scholastic kerforrhanceBorland and Rudofph identified scholastic, per- formance as the wrongest correlate of smoking.in a sample of high school students (20). Studies of achievement, aspirations

285

282
and expectations in relation to smoking have ,sound that reduced motivation and lower aspiration are associated with a

ihigher prevalence of smoking (3,33,101,1:30). Hitgh school students in college preparatory courses were far less likely to

smoke than students in any other type of curriculum (130).

Smoking rates for boys ,and girls preparing for college ( 9.0' percent and 12.0 percent, respectively) were 50 to 60 percent of

those in other curricula 118 3 percent of boy... 20 1 percent of

Th'e same trend was found in a pre., ious study (216).

Smokers are less involved in extracurricular school activities

and have ti higher rate of abenteeism (9,35,147).

These factors are undoubtedly interrelated with social (4s-s

and other factors. Sense of competency and sense of efficacy (or

personal control) are linked vo school achievement. Srookers

have been reported to hay e less confidence that they can control

what they will become (130). McAlister, et al. comment that high

academic achievement is probably also associated with admis-_

sion into a peer 'group in whit smoking is not accepted (125).

Furthermore, they suite, "Ed ucationapy deprived young people

may be somew hat less aware of the risks ofsmoking, but they

experinte more stress and greater pressure to adopt behavillt that signal independent and maturity" (125).

Dynarriic Personality Factors

Up to this point, adolescent smoking has been described and

analyzed in terms of discrete variables, many of which-a?e truly

not independent of one another. From them, a.composite picture

of the environment of -the female smoker begins to emerge. Par- alleling the behavioral descriptors is a se.t of individual

personality factors which ificlude attitudes, values, beliefs, and

perceptions which relate the adolescent to the world around

her. Vitally important are feelings of self-worth, aspirations and

expectations fur the future, and feelings of 4fficay, competenCe

,,o), apd the girl's viewpf her own smoking behavior. ' ,. Yankelovch, et al. have provided a thought-provoking descnption of the evolution iii values which has occurred 'over the

I)ast 20 year's (216). Smoking is just one behavior which may

have been "suppressed" hi social norms prescriong appropri-

* ate behavior for women in the past, and Which now m,ay be

"disinhibited" in a very real sense.

ACcompanying this shift in sanctions on female behavior is vl

incre4sv in expressed rebelliousness among girl smokers, whi.h

Awas formerly more characteristic of boys. A higher per tentage

if female smokers than nonsmokers are annoyed by "kxperts"

286 . , ,

. . 2
r who define what is good for them (53 percent versus34 percent), agree that 'there ts too much regulation of people's lives (50

percent versus 39 percent), and do notikvant to follow their par- ent's wishes regarding their behavior talpiost 5() percent versus. 26"percent) (21t). Factor scores of male and female smoars

similarly reflect a more negative "feeling toward authority" or dislike of adult-imposed restrictions than those of nonsmokers.

and are apprtximately equal-for both sexes (136). Clausen noted

that girls who smoked were less acquiescent to their parents; more autonomous, and "strikingly higher in quest for power"

than nonsmoking 1(33).

The evolution in es and sex-role belVviors has resulted in

sol;ne interesting differences between male and female smokers

(216). The male smoker remains more socially uneasy. expresses Pa, greater need to be popular with the opposite sex, and consid- ers smoking more of a social asset than the female srrfoker. The

female smoker, compared with her not oking peer, is more

likerto consider parties a favorite leisure time actik-ity, to have a boyfriend, and to have had sexual relationships see also 174).

In addition, she is les's likely to feTl nervous meeting,new people. Finally, while she is more willing to admit that smoking is a

drawback, she shows less acceptance than the male smoker of

the stereotype that adolescents begin to smoke cigarettes to

gain peer acceptance and approval (130,216). Nonsmokers show

the greatest acceptance of this 'stereotype and the one which

describes the smoker as a "show-off" (216), who believes that

smoking makes one look "cool" or "grown-up."

In other studies of smoking behavior, self-esteem has casually been investigated in teLms of the adolescent's self-confidence in

interpersonal relatiorfships. Smokifig is ego enhancing and

facilitates social functioning (122,123). This has been observehl

specifically among adolescent gjrls and female undergraduates

who smoke.(174,216). Smoking is correlated with a wish to be

older (130). Both boys and girls who differed from the norms of

their high school peers on tests of selftconcept were more likely

to smoke cigarettes as well as to use other drugs 495).

Adolescent smoking has been consistently "9-rrelated with low

educational and occupation*1 aspirations. Ins review which in-

' eluded "locus' pf control" as a measured variable, Smith concluded that smokers were moreext'ernally oriented and felt that

they had limit?d. control over what liappened to them (176). Pflaum reviewed findings on the-positive reldtionship between

smoking and 'feelings df helplessness and hopelessness. (143). AdolesCent smokers express less desire and ability than

nonsmokers to control future eventsfor example, to determine.

what kind of pp-ion they will become (130). Girls scored slightly

4

281

21'1'-.1
higher than boys on thas factor:indicating a greater sense of

future control.

Finally, response to stress has bven suggested as a basic

dynamic in cigarette smoking (1221...Feelings of Unattractiveness, a sense of incompetency and inefficacy in school achievement and personal rel4tions, limited opportunities for personal

growth and for future social and economic roles all contribute te.)

stress in adolescence Changes in social settings, such as transition from"elementary to lurqor high- shool, which occur simultaneously with physical and emotional changes must also be acknowledged. Theoretical formulations of lrfe-change events and

their effects on health might also be worth considering in studying the onset of cigarette smoking among girls (47).

Prediction 'of Future Smoking Behavior

In 1979, a longitudinal study was undertaken by the National

Institute of Education involving the re-interview of 46.8 percent

(N= 1,194) of tilt 2,553 adolescents first survey id in 1974 (130).

In 1974, 152 respondents were smokers aid 1,042 were

nonsmokers. By 1979, 27 percent (N = 41) of the smokers had

quit, while 73 percent (N = 111) had continued to smoke. Duting

the same time period, 20.8 perce,nt (N = 2171 of the nonsmokers

had taken up- smoking,, while 79.2 percent'(n = 825) had not.

Thus, 04% proportion of smokers who had quit was greater than

the proportion of nonsmokers who had taken up the habit. However, because the percentage of nonsmokers was much higher

than the percentage of smokers, the., net effect was an increase

in the percentage of the population who,were smokers (12.7 per-

, cent to 27.5 percent).

With each increase in age group, the proportion of boys who.,

initiated smoking became smaller, so that boys who reached age

17 or 18 as nonsmokers were not likely to start in the next five

years. Only 15.4 percent did so, compared with 19.3 percent of 15

to 16 year olds, and 21.6 percent of 12 to 14 year olds. For girls,

the pattern is less clear. Fifteen to 16 year old nonsmokers in

1974 showed the greatest proportion of initiators (27.1 percent)

by 1979. In the 12 to 14 age group, 22.8 percInt took up smoking,

and only 14.7 percent in the 17 to 18 age group did so.

Demographic and psychosocial relationships studied in 1974

were reexamined in this group now aged 17 to 23. The influence

of irder siblings became less powerful than the influence of

pee but educational attainment was still inversely correlated

with smoking status.

Those smokers who had quit had a shorter lifetime history of

smoking and were lighter smokers than those who were current

288

2
smokers in 1979. Of the former smokers, 24.7 percent said they had been smoking less than daily just before quitting; and

another 34.5 percent smoked 1 to 14 cigarettes per day. Only 7.6 percent of current smokers report less than daily consumption. This suggests that the former smokigis may have been less de- pendent (psychologically or physioloMally) upon cigarettes and may have found giving up the habit easier than heavier smokers. In fact, 50 percent of the former smokers succeeded in quitting on their first attempt, while 61.6 percent of current smokers had made one or more unsuccessful attempts to quit.

These young smokers were concerned about health issues.

Sixty percent of current smokers had mad,e at least one attempt, and another 2apercent would have been willing to quit if

there were an easy way to do so. A greater ercentage of young women than men (91.0 percent and 85.2 ent", respectively) d a concern about health effects smoking. The risk

associated with oral contraceptive use and smoking and the

-harmful effects-on the fetus of smoking during pregnancy (130) may be responsible for this increased concern. Young women

were more likely than young memo say that all cigarettes are

equally hazardous (33.7 percent and 25.9 percent, respectively). Multiple regression analysis was used to identify thosle adolescents most likely to take up smoking, and discriminant function analyses were used to predict future smoking for each

stagenonsmoker, experimenter, regular smoker, and exsmoker. The best predictor of future smoking behavior was the

adolescent's own perception of his or her future smoking behavior.

The best predictors of'future smoking for never-smokers and

experimenters were smoking by an older sibling, scores on attitude scales, and age. The chance that a nonsmoker will start

smoking become smaller as the nonsmoker grows older. Once

regular smoking was initiated, the variables of higher dosage, lower educational aspirations, friends who smoked, and lack tfr

acceptance of the health risks of Smoking predicted continued

smoking behavior. ")'-- In summary, this study revealed that former smokers seemed

more similar to experimenters than to regular smokers. Their

smoking histories were sh6rter, and they had a lower dosage and did not have much difficulty quitting. Regular smokers, on

the other hand, tried to quit or expressed an interest in doing so, and were bothered by the health hazards associated'with smoking. Five years previously, they were able to accurately predict their current smoking status. Smoking was also more likely to be a behavior of their older siblings act peers. And lastly, both

educational aspirations and attainments wire lOwer for this

group.

2&C 289
PREVENTION OF SMOKING AND CONSIDERATIONS FOR

FUTURE RESEARCH

Prevention of the Initiation of Smoking

There are a number of ongoing interventions which attempt

to prevent the initiation of smoking (34,1,59,12,5,198). These

studies are directed at elementary, junior high, and high school

students, and use an "inoculation',' approach to prevention. Exposure to a small amount of information About pressures to

smoke is accompanied by practice in copinra.nd assertiveness

strategies. The main types of influences in which students are

instructed are peer pressures, parental modelling, and media

pressures. Peer instructors are often used to maximize influence. Compliance in self-reporting smoking behavior is increased by the use of physiological measures of smoking, for

example, salivary nicotine or expired air carbon monoxide,

which may or may not be an<yzed for the entire subject sample.

Dissemination of information about the health risks of s

ing seems to be successful, at least on a superficial level.

Ninety-six percent of all adolescents (and 91.6 percent of smokers) "strongly or mildly agreed" that smoking is harmful to

health k1,30). Percentages were similar for boys and girls, and

nonsmokets scored higher on all health-related questions thain

smokers. Almost 90 perceiit of adolescent smokers (87.9 percent

of boys and 89.9 percenVof girls) "strongly or mildly agreed"

with the statement, "I believe the health information about

smoking is true." Fishbein has pointed out, however, the potential importance of the difference between strong and mild

agreement with such statements, and the lack of direct personal

attribution involved (63). Only 60 to 65 percent of adolescent

smokers expressed strong agreement, compared with approximately 80 percent of nonsmokers. Either reduction of cognitive

dissonance by denial or actual lack of information may underlie

this response pattern. Finally, a surprisingly high percentage of

smokers feel (strongly or mildly agree) that it is all right to

smoke if "you don't smoke too many." On this item, fewer girls

(25.6 percent) were willing to endorse this statement than boys

(43.3 percent).

somewhat lower estimates of the acceptance of health information comes from the 1975 American Cancer Society (ACS)

Survey (216)t Of all adolescent girls 74 percent agree that smoking is as harmful for women as it is for men, 71 percent agree

that smoking is harmful for young people as well as for older

people, 56 percent agree that it is not safe to smoke low "tar"

cigarettes, kind 56 percent agree,that smoking is as addictive as

290 L Y "4
.4

illegal drugs. Comparable figures are not provided for boys, nor are the data broken down by smoking and nonsmoking

categories. This survey further reports that 68 percent of the girls sampled were not warned about smoking by their doctors. While .4 percent of female smokers began,,to smoke before the

age of 13, only 48 percent attended an antismoking education

program in school, and a mere 4 percent attended such a pro- gram in the sixth grade when they were approximately 12 years old.

These statistics suggest that smoking education and coping

strategies should begin earlier in schools and-should begin earliest for high risk groups.

Research Goals

The best evidence suggests that female cigarette smoking

rate's are declining. 'This cha)Igt,has occurred in more recent

adolescent cohortsthose born after 1962. National surveys are

likely to underestimate true rates, whether school, household, or telephone samples are used. Drop-out, absenteeism, lack of

telephone accessibility, and belonging to a minority group all ' contribute to the sampling errors, which include underrepresentation of population subgroups whose rates are substantially higher than the norm. Accurately measuring these

subgroups would enable scientists t etter. arget interven- interventions. Young black females appear to be Q such group whose - smoking rates well exceed the national average (33). There is good reason to expect the heaviest cigarette use and

other "problem behaviors" among those segments of the adoles- cent population who feel cut Off from socioeconomic opportunity

and mobility. The review of correlates of adolescent smoking

shows that many of the variables that ct cigarette smoking bear a remarkable similarity to ones ntified as predictors of marihuana and/or other illicit drug use It is recommended that

greater attentio.be given to models f behavior and socialization processes.

More prospective longitudinal studies nee41 to be undertaken,

based on varied samples of children. Data need to be collected

about Miysisal and emotdidnal status, psychosocial outlooks and

attitud4s, family and peer relations, academic and recreational

activities, family and school settings, and family and residential

background. This information must be gathered early in childhood to record significant socialization influences which pre- cede the onset of smoking behaviors and should be collected

frequently enough ..to record significant changes close to the

time they occur.

2 Q r

291
A

ZS. TABLE 4.Smoking parameters obser%ed in Hamburg, Germany, in 1971 and 1974

" Puff Number

-,,- Puff Duration

(sec)

Puff Interval

(sec) 10 ot 1 Puff

(sec)

Durath

1974 1971 1974 1971

-2-- 1971 .1974 1971 191 ____ Men 10.2 10.9

. 1.47 . 1.47 ' 529 42.1 15.0 , 16.

Women 10.9 13.3 1 31 1.17 46.0 40,7 14 3 15.

All 10.5 11.8 1.41 1.34 50.3 41 5 14.8 15

SOURCE Schulz, W. (167) F

a

,

,. _J ,/

II
Maintenance of Smoking Behavior

PATTERNS OF CIGARETTE SMOKING

Smokg patterns differ between the sexes. Schulz and

Seehofer studied the moking behavior of male and female

smokers observed surr6ptitiously in public places. Puff number, duration and interval were measured (167). \Vomen'were found

to leave a significantly longer butt length (approximately 2 mm longer and had shorter puff 'durations than men (Table 4). Howeve4, they took a greater number of puffs and, therefore, had the same total puff duration (puff number x puff duration). These authors do not report gender data on inhalation patterns, which are crucial to determining dose. However, Creighton and Lewis reported no sex differences Ili puff voluihe in a small study of the inhalation patterns of eight men and eight women (39). Data on smoking patterns were collected in surveys con- ducted in 4964, 1966, 1970 and 1975 by tFe National Clearing- house for Sficoking and Health- (NCHS) (fee Table 5). In each

survey a greater proprotion of men than ,t;/omen reported inhaling deeply into the chest and inhaling k(most every puff. Men therefore may extract a greater dose of nicotine and the other constituents of cigarette smoke than do Women. However, there

is an increasing proportion of women who repOrt smoking their cigarettes ",as far as possible," in contrast to a decline in the

propoftion of men who reported this behavior (167,192,193,194). A slightly higher proportion of males reported letting "very little"-of their cigarette burn without. smoking it: 1970, 20.6 per-

'

cent Male vs. 18.0 percent female; 1975, 20.9 percent male vs. 18.6 percent female (193,;94). These changes are often a correlate of heavier smoking. In sum, the observational data suggest that men and women have equal total duration of smoking per cigarette, and the national survey data suggest a larger proportion of males inhale deeply. In general, then smoke in a mor

hazardouS way than do women. HoWever, the smoking patterns', of women are changing toward "more hazardous" ,., ). smoking (see Fart I of this Report). \

In contrpst to the minor changes that have occurred in the.

way an individual cigarette is smoked, there have been su6-- stantial changes

smo1e

iin the percentage of both male and female- smokers who smOK more than a pack per day (Table 6). Anumber of ex#nations may be offered for these data: (1) more

tghter than heavier smokers may be quitting, resulting in a mean increase in daily consumption, (2) continuing smokers,

may 'be increasing consumption, (3) smokers newly initiating

the behavior may be smoking more heavily than already estab-.

293,
TABLE 5.Respondent-reported styles of cigarette smoking, current, regular cigarette smokers, selected categories, adults, United States, 1964-1975

4. Inhaling deeply

into the chest /

2. Inhaling almost

every puff

3. Smokin( cigarette

as far as possible

L

1964 1966 1970 1975

Male Female Male Female Male Female Male Female

36 5(7,. 22.59 31 W7c 15 5% 34 3'4 17 5c1t. 30 V? 16.1'4

it

6.3 1 54 g 63 0 1 60 5 47 2 58,5 59.7

15.9 75 135 100 96 104 10.9. 12,9

1.,- In 1964 ancj 1966, the questionnaire response was "as, deeply into the chest as possible " In 1970 and 1975, the questionnaire response was phrased `:deeply into the chest."

2. In each 4urNey year, the queitionnaire response was "inhale 'almost every puff of each cigarette " . 3 In 2964 and 1)-M--the respon/ent was asked to draw a line on a diagram of a cigarittte, indicating the average length of the discarded cigarette butt length- In 1970 and 1975 the verbal questionnaire response was smoking cigarette "a$ far as possible." The data for 1964 and 1966 correspond to those respondents indicating a discarded cigarette &dr length no greater than 20 mm. SOURCE National Cleannghouse for Smoking and Health (192,193394)

291
1

.ts TABLE 6. Estimates of the percentage of current, regular cigarette smokexs w ho consume lore than one pa per day, adults, United States: 1955-1976

4

Year

1935

1 Supplement to ti.rrent

Population SUri:ey

(17 rs and (aer)

21 cigarettes or

mare daily

Total Male Female

23 98

Total

Health Interview

Survey

(17 yrs and oven

23 igarettes

more daily

Male rFemale

-National learinghouse

for Smoking and Health

(21 yrs and os.tsr.

23 ogarett.2s or

more daily

Tbtal Male Fvnal,

1964

1963 _ 25 7 32'4 17 7 199 21 3 Pi 7 1966 21 6 26 :i 137

1967 21 9 26 2 . 272 34 7 169 16 3

196k 224 .26:, "168

1970

1974 23 3 27 6 18 1 23 2 .31 4 17 1

24 72 30.3 18 1973

1976 36 1 36 0 '22.8 233' 308 194

'18 years and over

2Data provided4ty Health Intyrview Survey. National Center for Health Statistic s '20 years ancl(wer.

SO1'R('E 1' S Departikeht of Health, Education, and Wtdfare 1 19isi

ti

CC) cn 2 "'

.f
TABLE 7.Estimates of the percentage of current, regular

cigarette smokers among white and black adults,

aged 20 years and o%er, L'ited States: 1965-,1978

Vvar

1:470

«h;tt

O Male

-1

337

4.1 :4 41 2

4

Fernalr

;4 2

'I '4

;1

;1 4, it) I

Male

Bla(14,

Femalt

RUx

",-1 ),

42 >44

..333

i 3 3 1

3:4 1 ;02

N()TE Re wt,.4-11,pia:. A-d a, per, ntag44 ;,f ,A,p,m14.nt, A itlt kr0_0.4.1:1 pr:ri,king

,tatu, aged 17 year, and ,,.er

Si )1:R4 E t :44 Derlartm. nt aith Edu, ati,n and V4elfare ,1;4X

lished smokers, and )4) declining "tar" and nicotine contents of

cigarettes may be leading to compe.,nsatory increases in number of

cigarettes smoked in order to maintain nicotine dosage (198).

Regarding type of cigarette smoked, the 1975 NCSH survey

reported that more women than men smoked filter tip-cigatettes (all types), 90.6 percent's. 79.3 percent. Women seem 4) be

innovators ircchatiging smoking practices. Sixty -one percent of

women and only 10 percent of men acknowledge changing brands apeast once, and ,women lead the trend in adopting

king-size, filter-tip and 100 mni cigarettes. On the other hand,

women smoke cigarettes almost exclusively. Cigars and pipes

are currently used by 18 percent and 25 percent of men, respectively, but by less than 0.5 percent of women. Less than 2 per-.

Cent of women ash'- .snuff or chewing tobacco compared with 2.5

percent and 4.9 percent of men, respectively.-

, SMOKING PREVAI<ENCe AND ETHNICITY

The prevalence of smoking in the population vtries notsonly

with a'Av, sex, and socioeconomic status,' but also with race and

cultural background. - Table 7 presents smoking prevalence among white and black

adults form 1965 to 1978 (198). Smoking has declined among men

of both races, but prevalence has decreased only slightly among

white and black females. Congfuent estimates of prevalence

and lower cessation rates among blacks have been obtained in

ether studies (66,183,201).

Despite their greater prevalence of smoking, black men nd and

women smoke fewer cigarettes per day than whites (66,183).

Black women may suffer the worst aspects of sexism and rac-

. ism with respect to occupational opportunity and financial compensation. Cigarette smoking may be related to assertion, inde296
pendence, and rebellion Or to identification with behavioral patterns of black males. Adolescent dynamics have been studied

more than those of adults (seettie'section oh adolescent smoking cessation in this Part). Warnecke, et al. found that social and

psychological correlates among black women are similar to

those observed among white women (201).

Friedman, et al. examined smoking prevalence among Asian men and womenChinese, Japanese, Korean or unknown

from the Kaiser PermanerAe Health Plan and found a smaller

percentage of cigarette smokers than among whites or blacks.

Asian women had the least frequency of current, established

cigarette smokers,' 23.1 percent, compared to 39.2 tercent of

white women and 42.1 percent of black women. Athens were also

the least likely to inhale among most age-sex groups of smokers. There were fewer cigarette'smokers among Chinese than

among Japanese; this was particularly true for women and

younger men (66).

PHARMACOLOGICAL EFFECTS OF SMOKING

One or more of the constitutents of cigarette smoke may play

a role in the_ maintenance of smoking behavior and help account

for the,diffigulties many individuals experience when they try

to quit smoking (198).

Nicotine

Nicotine is #bsorbed rapidly from the oral and intestinal mucosa, lungs, and skin. It is distributed throughout the body and

is metabolized by several organs, including the liver. It is then

rapidly cleared, primarily through the kidney. Nicotine has effects on several organ systems, including the autonomic nervous system, voluntary mdscles, stomach, intestines, heart, and

brain. Most of the pharmacological actions of nicotine are

thought to result, from its interaction with receptors of cholinergic nervous systems. Analysis of the physiological ef- fects of nicotine is complicated by the abundance of those effects. Many organs receive input from several neuronal system

which are altered directly/or Indirectly by cholinergic activity. Furthermore, the effects of nicotine itself depend both on the

do.se and on the time course of drug administration. brief expo- sure or low doses cause excitation of cholinergic systems, while

long expose re and high doses result in inittytion and paralysis.

Peripheral Effects

Nicotine produces a variety of changes in the autonomic nervous system "due to simultaneous effects on both'sympathetic

(} 1-* V. I A 297
and parasympathetic systems. The end result is an increased

heart rate and blood pressure, cold, clammy skin, increased acid

, production in the stomach; increased intestinal activity; and

biphasicoanges in salvation, with an initial increase ciillowed

by a decrease. Nicotine also increases respiration.

Cent ral Effects

Nicotine produces tremors and c-auses water retention by 0a

central effect on antidiuretic hormone release. Nicotineinduced nausea and umiting reflect a complex interaction between central and peripheral effects. To date, no specific effects

un complex emotwns and behaviors have been demonstrated.

Animals wily self-administer nicotine under certain circumstances, indicatin5 that it may have pleasurable effects.

A Possible Role for Nicotine in Smoking Maintenance

A strong argument has n made for, classifying smoking as

an addiction. with ntin the leading candidate, for ale addictive,ggent. Inhalation o cigarette smoke offers an effective

wa to administer nicotine. Absorbed rapidly, it travels as a

hig ly concentrated bolus through the heart and directly to the

bra rand is then rapidly cleared. A smoker who smokes one

pa k per day can average around 70,000 such nicotine "injec--

tions" per year. In behavioral terms, smoking has many poten-

.tial conditioned stimuli, ranging from the taste, Sight, and-feel

of the cigarette itself, to the many'social settings in which smoking takeS place.: If, nicotine were a strong unconditioned

stimulus, particul,arly when inhaled, then it would be easily understandable that smoking can become a remarkably persistent

habit through connection of this unconditioned stimulus with

the many associated stimuli-.

Although nicotine has effects on essentially all major organs

in the bode, including the brain, the role of those actions in

maintaining the smoking habit remains an important but unresolved area of research.

The nicotine hypothesis of smoking states that the pharmacological actions of nicotine are "reinforcing." The most

likely site -of this rewarding or reinforcing action is the brain,

with the precise lucuA of reinforcement not yet determined. Inhaling smoke insures rapid delivery of nicotine to the brain. It

takes approximately 13'.5 seconds for an intravenous injection

of nicotine in the arm to reach the brain, but by inhalation, the

delivery time is 7.5 seconds (158). The plasma half-life of nicotine

is approximately 30 minutes, and the pack-a-day smoker lights

298 4)(
t

up approximately every 30 t() 40 minutes of the day. This suggests that the smoker/s attempting to maintain a constant., level of nicotine.

. The nature of the reinforcing effect is sometimes described as an alteration of arousal. Stimulation may be subjectively expe- rienced as increased alertness, a facilitation of,concentration, or an aid to continued efficient performance in fatiguing tasks. Sedation, on the other hand, may a experienced as a tran- qUilizing or calming effect or as a reduction of some dysphoric

state, such as anger. Smoking has been described as distinctly

pleasurable following a meal or accompanying xanthines (coffee and tea)or alcohol. Pharmacologic and psychologic components

to these subjective reports are beginning to be identified (70,78A. There is extensive literature describing 'acute and chronic

nicotine administration in animals including a limited number. -

of self-agninistration models. Tolerance to nicotine has also

been.described (81,88,112). , A number of studies have examined the hypothesis that hu- 01

mans sew-administer tobacco in order tb obt in nicotine. Studies'have also examined compensatory adjustments in the . number of cigarettes and manner of smoking by subjecit in re- sponse to' experimenter- induced increases or decreages in cigarette nicotine content, cigarette size, availability, or sup- plemental nicotine administration. Chewing g- containing nicotine, nicotine tablets, intravenous nicotine an central or'

peripheral nicotinic blocking agents have been used to supple- ment or block the effects of the nicotine absorbed from the smoke. A titration effect is said to occur if subjects change their cigarette smoke intake in the appropriate direction in response

to these experimental manipulations.

A modest amount of compensatiofi has usually been demon- strated (79,158). Smokers seem to titrate along the nicotine, rather than the "tar" continuum but an optimum ratio of nicotine

to "tar': jrobably exists for effective delivery to the lung,Expen- ments involving the intravenous administration of nicotine

have been inconclusive, with both positive and negative effects on the suppression of ,subsequent smc;king having been ob- served. When compensation occurs, it is seldom complete. Thi':; may be dip to a number of factors. (1) the inability to accurately measure the smoker andlor nicotine dose delivered to the subject; (2) technical problems i'n experimental design (79,198); (3) secondary reinforcing effects of smoking which mask titration; and (4) the fact that people may'smoke for 'reasons other than

regulation of nicotine level. ' lo Some have even suggested that nicotine controls smoking beha- vior only at the extremes, and then as an aversive agent (163).

299

r1
Too much smoking might lead to such high serum concentrations of nicotine that toxic effects encourage lower ,intake;

and too little smoking or smoking of low-nicutine cigarettes

could lead t45 such low concentrations that withdrawal side effects encourage resumptipn of smoking. This hypothesis states

that, between those two extremes, other factors such as psychological and social pressures are far more influential in deter-

+ mining smoking patterns.

Differences in Nicotine Metabolism

The metabolism of nicotine may be different in men and

women. Measurement of nicotine and cotinine (the principal

metabolite of nicotine) excreted in the urine after intravenous

administration of nicotine hydrbgen tartrate suggested differences in metabolism based on sex and smoking statue (73). In

nonsmokers, men excreted less nicotine but more cotinine than

women, suggesting greater initial metabolism among men.

However, there were no clear differences, between male and

female smokers.

Schievelbein, et al. studied nicotine and cotinine excretion in

both regular smoker's pnd nonsmokers after they smoked

cigarettes with differink tar and nicotine levels. (165). Women

excreted significantly loWer amounts of nicotine and cotinine

compared v.:1th ?nen for three of the four brands tested. The

gender difference was found for the excretion of nicotine and

cotinine when tested separ4tely and together. The number of

cigarettes smoked per day did not differ between the sexes, but

the carboxyhemoglobin (COHb) levels, which are often taken as

a correlate of depth of inhalation, were lower in the women. The

female subjects, therefore, may have received a lower dose of

nicotine because of a different smoking pattern.

SMOKING AND STIMULATION EFFECTS

The literature suggests that women are more likely to smoke in

situations of hiFh arousal than low arousal and when experiencing "negative affect" (69,96). The effects of smoking, which are

often perceived as tranquilizing, might then be sought as a

major coping mechanism. However, it can also be argued that

the stimulant effects of nicotine, which are usually considered

the predominant central nervous system action, might be

equally useful as a mobilizer. These related and commonly held

beliefs will be examined inesome depth. .

..

4 # Futti..( 69) studied British male and female employee's in a

psychiatric institute, they ranged in age from 28 to 50. Subjects

rated the strength of -the desire o smoke an 22 hypothetical

300 2"-
A

. situations. The 12 high-arousal items involved either emotional strain and anxiety or demanding mental activity; the ten low- arousal items concerned boredom andr.Plaxation or repetitive

tasks and physical fatigUe. A factor ainalysis of the entire qilestionnaire and t-tests performed on male versus female scores

for the most extreme situations on the continuum led Frith to

state that men had a greater desire to smoke in situations inducing boredom and tiredness and women had a greater desire . ot to smoke in stress-inducing situations. 'However, men rated the

desire to smoke signifiCantly higher than did women on all three

of the questions representing low-arousal situations, whereas wtnnen rated the desire' to sinokie significantly higher on only one of the three queslions, representing the high-arousal ex- treme of the continuum (69).

. Using Frith's questionnaire, Barnes and Fishlinsky were un- able to replicate his findings in a sample of Cana ian under- graddates (12). Within the male sample, there was no significant relationship betweeh desire to smoke and 'the arousal value of

the situation in the question, and female subjects indicated a greater desire to smoke in the low-arousal situations. The au- thors point out the possible importance ofsampling differences. Elgerot studied light, medium, and heavy smokers in an at- . tempNo control potential diffatences in inhalation patterns be- tween inen and women (cited br'rith as a possiblefixplanation

for his results) (57). Subjects wen Swedish university students. The 42-item questionnaire was similar, but not identical, to Frith's. There was no gender difference for low-arousal situations. There was no sex difference in the light and medium

smoker subgroups,put wome'n in the heavy smoker subgroup

expressed a greater desi/peto smoke in stress-inducing circum- stances.

' Russell and his co/eagues devised a 34-item questionnaire covering a wide variety of smoking motives. It was administered to 175 norm's' smokers and then subjected to factor' analysis (160). Six factors, representing six types of smoking, were identified. Women scored significantly lower on what was

termed "sensorimotor" smoking, and significantly highu on

"sedative" smoking. Thus, the sex difference on "sedative"

smoking (reduction of arousal) was supported.

Ikaql and Tomkins (96) found evidence that women smoke in

situations involving negative affect. Negative affect smoking is defined as smoking which serves to reduce unpleasant feelings. It includes smoking to reduce the dysphoric feelings accom- panyirig rejection by a social group as well as smoking to,satisfy

a craving for a cigarette (i.e., deprivation negative affect). Posi- tive affect smoking involves the arousal of pleasant feelings.

2(I(' 301

, -)Cd .
For exatifrile, smoking- fi um curiu:sity would be classified this

w;,Q, because of the feelings of excitement and interest generated. Ikard and Tumkins showed twu one intended to

euke positi,.e affect (a slapstick comedy), and anuthei to evoke

negative affect to docitmentaly on Nazi atrocities) to college

s'tii(ents v hu smoke. To be.characterized as either positive- (Jr

negative- affect smokers, the subjects ,had smoke during the

appin.priate indicate a, congruent mood on an affect

checklist The majui finding %vas that C3 percent of the female

sample of 15 subjects exhibited solely negative-affect smoking

compai ed toonl 36 percent'uf the sample of 39 males. While KO

pet cent of the females indicate9 that they were likely to smoke

1n pusiti e as well as negative-affect conditions, their behavior

did nut match the ,elf-lepoit in this experiment--.1t is difficult to

determine if the envii unment of the experiment altered normal

Iur panel ns. oi if ilerhaps smokers iive not accurate in

describing the types of situations in which they smoke.

Nationwide sui veys conducted in 1964, 1966, and 1970 also

suggested thQ.t a highei percentage or women than men are

negato. e-affect smokers and,that little ur no difference exists

between men and women in the percentage: who are positiveaffect smokvs (192,193). A greater percentage of women current smokers endorsed the statement, "It relaxes me.." (192).

This supports the hypothesnz that reduction of negative affect is

a more important factor fur women smukors. The, statements

assessing pusitile-affect smoking did nut show a clear gender

difference. In 1964, slightly mere men than women endorsed the

statement "enjoys it" as a reason for smoking, but in 1966 there

was no difference between se ;es and in 1970 slightly more

female than male current smokers agreed that "cigarettes are

pleasurable" (79.6 percent of women v,ers'qs 77.0 percent of

men).

To summarize. smoking affects arousal; it is nut knowA

whether women smoke to maintain a given arousal level, to

charge that level, (Jr to adjust a, physical blood level of nicotine.,

There are a number of studies which suggest that women use

cigarettes more in highwuusal situations than do men. Studies

which combine self-report with experimental situations providing a good approxii-natiun of natural smoking conditions are

needed to shed sume.light on the validity of evaluation by questionnaire alone.

Smoktircessation

There is an,assumption in the r ekitment literature that men

have greater success than women quitting smoking, Th,

302

ti
basis of this assertia lies partially in the demographic analyzeS`

of cessation rates and partially in the literature on smoking

cessation cliriics and experimental progirams.

° This section yrestrits the results of both demographic and

experimental analyses of smoking cessation. A critical ap- praisal is made of the relative success of men and women in

giving up smoking and in remaining ex-smokers. Psychosocial

and behavioral factors relating to abktinence and difficulties

encountered in quitting are' diScutssed. Finally, recommendations are presented P6r treatment and future research...

DEMOGRAPHICS

.The quitting rates of smokers .are calculated by dividing the number of former smokers by the number of ever smokers

within each, relevant demographic category. The following

statistics are taken from the 1975 U.S. .Department of Health,

Education, and Welfare (USIDHEX) survey on Adult,Use of To- "bacco (194). Former smokers are defined as those who once

smoked but no lorigdr do so. The. term "former smokers" includes bot4-1 those who have quit on their own and those who

have received outside help. Quitting matet-kof women lag behind

those of men, for each category reviewed.

Age

The USDHEW tables dIvide adult age groups into Six

categeries:"ages 21 to 24, 25 to 34, 35 to 44, 45 to 54, 55 to 64, and 65 and over (194). There is a trend toward increasingly larger percentages of former smokers in each sti.ccessive age group cor both men and women. However, within each age group, the per- centage of smokers who have quit is higher for men than it,is for women. For example, in the youngest age category, the per- centage of female smokers who have quit is 22.6 percent while

that form ajes is 27.9 percent. For a middle-aged category (45 to 54), the fedale and male percentages are 32.0 perc and 46.7

percent respectively. In the oldest age group,, 5.,1gercent of

female ever smokers are former smokers, whereas the percent- age is 60 percent for males. Bosse and Rose state that the

sex differences in quitting are vanishing at younger ages, but

Dicke'rt argues persuasively that the absolute amount of convergencois small, and tkat men remain substantially more

likely to stop smoking than women (21,45).

Education

Higher levels of education are associated wall higher rates of

quitting for both men and women. Among those with A college

303

(
4, 7 Q People giwe all*iorts uf/easons for either nut . being able to ur"nut wanting to

star off cigarktes What were your reasons for going back to cigarettes^

(Asked if made a serious 'attempt tostop smoking

\).

I .4

TABLE 8.Most frequently endorsed reasons for resuming

smoking: Fall 1964 and Spring,1966 household

interview suney,.responses of current smokers

Selected total . o wtll power es me Enjoys it

ffelps keep weight down

Smoke to be sociaple

a Current Smokers

1966

N A r.4 1964 M . 705 55 7 772 54 9

14. 542 50 6 588 e7.1

11 4291 113 0 , LIV ' 198

F 209 19 5 191 4e18 M 212 168 181 12, 9

245 2g9 192 " 18 6 M 144 11 4 123 8 7

F 102 95 90 8.7 M 65 5'1 40 2.8

F 75 70 57 . 5.;5 M 998 7.7 43 3 t

F 70 fi 5 46' 4 5

NOTE. More than une answer was 'allowable for each respondent.

SOURCE. U.S. Department of 'Health, Education. and We'lfaiy2;

education or"higher, 52.1 perc^t of the men and 48.1 percent

t thrwrneri who have ever smoked have quit..For all other leve

of educatiol, 40.5 percent of men smokers. aed 31.3 percent o women smokers have giiren up smoking. Although tte discrepncy is lest in the most advanced education category, the percen ..ge of female quitters is smaller at both levels of schooling.

.41 Income

Higher evels of income are aciated in both sexes with

higher rot of cessation. For those ever smokers with incomes

under $10,00 the ratesof quitting for men and women? are 34.7

percent and 3 percent respectively. For those with incomes of

$10,000 or above, the rates are 45.7 percent for men and 36.2

percent fqr women. Quitting rates of men exceed those of women for all but one ($5,000 'Po $7,499) of t1 seven income

kupation

There is a, differencit of only 7.6 percenta 0, between the

proportion of male and fe m are. quitters inote-Uitegory of prw- , 304 . i,

te
4

fessional, technical, and kindred workers, with the male quitting rate at 49.4 percent and the female 4uitting rate at 41.8

ercent. &dramatic increase in.this difference occ rs, however,

among manaq.ers fficials,'and proprietors. In thi ategory the quitting rate fo men is 47.1 percent and that for w en is only 26.5 percee A on sales and clerical workers, 40.1'percent of the men and 25.8 per6nf of the *omen have quit. The quitting

re oi homemakers (33.9 percent) is in the mid range of the rates, for women in other occupations. In general, t 'hen, women are quitting at lower rates than men

'across the, major demographic categories.

PSYCHOLOGY OF CHANGING SMOKING HABITS

A two -year follow-up of over 500 former smokers identifieZ1 in the 1964 nationwide survey.. provides support for the demo- graphic data showing higher proportions dT ex-smoker ong males than females (56). Mehrwere. significantly mois:eFilliely than women to remain successful abstainers.. Men and women made approximately the same number of attempts to quit, and current smokers made more attempts than former. smokers

(168). Furthermore, successful quitters have usually made at least one abortive attempt'to quit before succeeding. A survey

the greatest cess in stopping smoking (216). This finding is

of young aged 18 to 35, revealed that light smokers had

not entirely consistent with,that of Eisinger (56)s however, who reported that long-term smoking was a predictor of successful abstinence. The difference in study samples may account for the lacy of "fit" of the two results, as Ei4iger's sui'Vey, included all adults 21 Years of age and older. The "reinterview" (follow-up) aspect of Eisinger's study gives further credence to his conclu- sions since they are based on data actually obtained at two points in time.

Those factors which consistently seem to differentiate between those wli.o can quit or reduce intake and those who cannot-are: the presence 6? strong motivation and commitment to

change; the Use of behavioral techniques; and the availability of social support. Those whb successfully it or reduce smoking

use behavioral techniques such as sub ting candy ant gum

for cigarlftee-, and some form of self- 41y. ent of deSirable behaviors to maintainabstinen e (1 ccessful reducers ege behavioral techniques n-rb e vons tiftently and for a longer period of time than those who fails:to reduce smoking (140). Suc- cessfuhquitters experience cfavings when theystop, but the use of substitutes seems partially to alleviate these feelings (139). Furthermore, thosesmokers who do reduce intake are more

31 ;305
motivated and committed to personal Change (140), and long- /c . 0

term abstainers have more confidence in their ability to ren)ain

ex-smokers i56),--Successful reducers receive more positive rein;

ftorcement from others and the best known acqpint,.: nces of

successful abstainers are former smokers (56,140).Warn ke, et.

al. reported female relatives to be the primary role models for

women who quit smoking.(201).

TREATMENT STUDIES i Most smokers who attempt to quit do not seek outside help to

stop smoking. The population that seeks treatment may be one

that experiences svere difficulty in giving up smoking.

Thirty-nine treatment studies on smoking have reported success rates for males and females, and have used the criterion of

total abstinence. Two exceptions were made for program,s that

reported "success" in terms of 90 to 100 percent reduction.

The studies reviewed here fall into five categories, of treatment. education, physician advice, pharmacotherapy,

psychotherapy, and behavior muallication (Tables 9-13). The

categorization is, by necessity, only a rough separation of

treatment modalities. Ealuation of the gender difference question, however, does not rest directly on the categorization

schema.

Many of the studies listed in the tables did not report sigwificant

evaluations for male female quitting rates.-Therefore, a chi,

square statistic or Fisher exact probability test was calculated

wherever sufficren/ dala were available. Because of the limited

number of studies identified for analysis and the often limited

sample size, results of borderline (0.05 ,.p ..0.10) and acceptable

(p <-0.05) levels of significa,nce are reported for the-.reader's information. to

The end-of-treatment cessation rates are high for all types af

treatment, but the maintenance of cessation tends to be rpuch

lower. In 1971, Hunt, et al. demonstrated that recidivism curves

of heroin, alcohol, and smoking are almost identical, with longterm cessation falling off steeply from the end of treatment (94).

Within three months approximately 35 percent of successful

quitters are still not smoking, and by one year, the figure is

closer to 20 percent. In 1978, another reviewer.cited virtually

J the same figures (147). There have been reports of improvement

in techniques for obtaining abstinence and in maintaining it,

using rapid smoking an aversive conditioning technique), hypnosis, and group tIjie_pAliy.,The long-term cure rates of 60 percegt

or higher at six months claimed in some studies have not been

reproducible in other settings. The smoking cessation literature

has been recently reviewed in detail (80,147,168,198).

306

I
41,

Across all treatments, women have more difficulty,giving up Smoking than men, both at the end of treatment and at;loi3gterm points of measurement. No studies have be eported in which women do significantly better than men.- ever of the larger studies show, higher abstineric'e ratt$AJKY Men, ut many show no difference. Results in the tables are based primarlly"on those who complete treatment prograp. Attrition rates are very difficult to evaluate because most studies do not disduss the issue of subjects who drop out of fliatMent. Because of the emphasis placed onthe'role of physician advice in increasing smoking education ,ind promoting cessation, an estimate of if's, effectiveness is kevant; From retrospective, data, it is estimated that 35 percent' of people who have been advised by a doctor either to quit Or,, to cutdown sharply, actu- ally do quit (139). Twenty-five percentof those who have not talked to a physician about smoking quit, and only 12 percent who have been told by a physician that' it was permissible to continue smoking quit. The prospective treatment literature !fields :varying esjti- mates of the impact of physician advice. Ten to 25 percent of patients advised by a physician to quit of cut down actually do so (198). Gender dogs not seem to exert a pantic'ular influence. The primary variables associated with the ability to quit after physician admonition were good psychosocial assets, psycholog- ical stability, and the ability to verbalize depression (54). . Success in treatment.in general seems to relate to personal characteristics. A shorter smoking history 4nd lower cigarette consumption also predict a greater likelihood of cessation

(104,144,204). In addition, those subjects most likely to succeed in treatment are highly 'motivated, believe they will succeed, and are confident of their ability to stop smoking (82,136,187). One group of women that seems to have great difficulty in giving up smoking in treatment is honiem'fikers. Homemakers in the age range of 18 to 35 tend to be heavy smokers, and heavy smoking is one predictor of failure in treatment (216). Kanzler, et al. found that homemakers were lebv"succes'sful at quitting, par- ticularly at long-term follow-up (f04).1Howeveri as.previously discussed, homemakers have q_uit rates in the mid-range of those of women in other occupations; therefore, the difference may apply only to those homemakers Arho seek help through

treatment programs.

WilhelMsen found significan male/kmale differences in treatment success,rates and stated thatithe poorer performance of women related almost exclusively to the unsuccessful results . of homemakers (209). These woman explained that,cigarettes served as companions and they repotted the difficulties of being

307

30,:
a

o TABLE 9..Education-Smoking cessation treatment results by sex

oo End--of

Treatment

Study Treatment N (%)

1. Gui Iforil, 19671' (82) Five-Day Plan' unaided 75M

100F

Aided 82M.

91F

2. Petersoh et al, Five-Day Plan 134M&F 79M&F

1968 (141)

3 Berglund, 19g9" (4) Five-Day Plan 895M&F 87M,

84F .

4 Delarue, 1973 (441 -Education, small groups 472M&F

, . 5 Danaheit et al.: Education; skill training group I IF - 50 (of 8 Ss

19781' (41)

'

finishing

treatment)

.N. 6 Ochsner & Da-smrau, Pamphlets' 20M 85M l , 1970 (136) 33F 52F J 1 J

7 Pyszka et al , American Cancer Sockty Clinics 131M 39M&F

1973" (146) 223F

Percent Abstinence

Six

Months Long Term

(%) (%)

23M 1

12F

27M 121 29F

19M (18 mo follow-up

19F on 121 Ss)

32M

27F

} 2 23F3IM } 1 (4-18 mo.)

2

- 34M (12` mo )

21F

50 (9 rip )

28M. (I.Bmo.)

2cIF

(
TABLE 9.EducationSmoking cessation treatment results by sex

Study Treatment

8. Kanzler et al., 1976 (100 Smokenders

ontinued)

Percent Abstinence

End-of- Six

Treatment Months Long Term N '(%) (%) 9 210M 70M. 571 } 1 (48 mo.) :343F 69F 3OF

9, Dubren, 1977* (53) T V. spots 92M 15M ). 1 218F 7F

'p <0.05

20.05 <p <'0 10

*Sucess = 90-100% reduction in smoking. I

"Results based only on those completing treatment or contacted -fo follow-up +Pregnancy interventyin study

3 u C

4
:1

1 TABLE 111Physician adviceSmoking cessation tr,atment results by sex

t. Study

1. Burna, 1969 (27)

Treatment

MD athice to rasp di' pt'

N

) 66M

28F

2. Handel:1973 (87) Antr-smokkg message in 45M

med exam 55F

Percent Abstinenre..

End -ofTreatment Six Months

( (7). )

3 Burnam, 1974 (28) M I) advice . 84M 29M

40F 18F

4 Banc ..4rt al , 1976 (112) . M I) advice 134F . (sprint quitters) 24 83

(Intervention) 63 14

(contriiI) 47 14 5. Donovan, 1977*(49) M D advice :352F *50'7,

rer1uction

(^1. )

'3M !I ( 3 mo ) 32F

Long Term

("2)

381 1 ilZmo , 11F

r

'p. 005

tPregnancy intervention studies

3(c" ,.. r
without adult company all Ity and .of,btiing deprived of outside

activities as obstacles to giving up smoking. Cigarettes have

also beep 'described as a means of temporally partitioning the day, of achieving physical autonomy from children, and of pro- ) viding role differentiation (74).

Frieze, et al. reported women f;xce more life stress than men

and havvmore symptoms of ps,ych,ological distress (68). Waters

reports 0Aat women show rnae.overt signs of neuroticism than

men (203). Furthermore; hefinds an association in women between degree of neiiroticisrft and amount smoked. Burns also

found that felnale smokerShad higher neuroticism scores than did

female nonsmokers. NC) such differences were found in men (27). Some studies have "sho' Wn't4hat women who smoke are both

rriorkject to psychological stress and more outgoing than women \who do not smoke. In a prospective study on women and

smoking, Cherry and. Kiernan measved personality traits in

young women before the onset of sraaing (31). They found that

smokers had high neuroticism aria extroversion scores before

taking up the habit. They add that current women smokers are

more extroverteci and also more neurotic than nonsmokers.

There is evidence that women smokers are more'indep4identmindeol assertive, self-opinionated and forthright (151,216). The

latter authors report that women smokers arelalso characterized by apprehension and tension, and that these characteristics are related to an inability to give up smoking.

The presence of psychological distress has also been shown to

affect the success of women in treatment. Peterson, et al. found

that, while 23 percent of the men who had participated in a

( smoking program cited nervousness as the principal reason for

resuming smoking,..43 per nt of the women cited this reason

(141). Russell reports tha the presence of depression was related to dropping out o treatment, and that depression was

more frequent and severe among the women in his sample 1176).

In a later study, Russell found that within the treatment group, women had worse psychiatric' adjustment scores than did men

(159). Furthermore, although the degree of psychiatric adjust- ment did not differ between male treatment successes or failures, treatment successes amo gwomen were significantly

more likely to have good adju.strient scores. Rode found that

success in a smoking withdrdw'al program was related to lack of

tension and apprehension for women (150). That smoking nAght

indeed act as,a method Of coping with psychological and social

stress is illustrated by the fear reported by many women that they will engage in symptom substitutionspecifically

overeatingif they stop smoking 414,23,27). It is also po'ssible

that underlying stress in women impedes the strength of the

311
TABLE 11.PharniacotherapySmoking cessation treatment results by sex

V

Study Treatment ti

Percent Abstinence

Entl-Of- Six

Treatment 44,onths Long Term

(q) (67( r (%)

1 Turk, 1958' (191) Hydroxyzrne 23F 4F

2 Whitehead and Methylphenidate 10M 20M OM

Davies, 1964 (208) Diazepam 6F OF OF (12 mo )

-3 Wilhelmsen, 1968 (209) Methylscopolamine 291M 56M 11 (12 mo ) tranquilizer 200F 41F

4 Wetterqvist, 71* (207)

1973* (206)

Methylscopolamine 192M

98F

50M }

1 33F (12 19M 9M mo.) -I Om mo

... 12F 9F

5 Arvidsson, 1971* (5r Antichohnergics,

Group aversion therapy - 50M

50F

85M

85F

48M 1 (12 mo ) 22F*1

6 Merry and Preston,

1963'(127)

Lobehne 45M

31F

29M

32F

7 Golledge, 1965*,(72) Lobehne & placebo 19M 63M

8F 73F

8. Ross, 1967 (152) Lobeline

Amphetamine

728M

745F

40M }

1 29F

211 1 (111-57 wks 12F
;TABLE 11PharthacotherapySmoking cessation treatment results by sexContinued

' /

Study , /

Treatment

t N

Percent Abstinence

y Endof- Six

Treatment Months

(%) (%.)

Long Te?rn

-(% )

9. Schaub le et al , 1A7 (164)

10. West et al.,

1977 (204)

Lobeline

Amphetamine

Lobeline, amphetamine

and education

Lobeline, amphetamine

'33M.

35F

14M

17F

255M

288F,

18M

26F]1

5711

26F

43M I

1 33F

22.0M

13 4F 1 (60 mo.

'p <0 05

Results based only on those completing treatment or contacted for followup 1

3 1
.-

TABLE 12.PsychotherapySmoking cessation treatment results by sex

4

Study0

1 Ares, 1964 (129)

. . 2 Mann and Janis, 1968 (119)

3 Streltzer and Koch, 1968 (185)

4 Lichtenstein et al , 1969 (115)

5 Fee and Benson, 1971 (62) p

6 Bozzetti, 1972 (23)

7 Tamertn, 1972 (187)

Treatmlit

Hypnosis, discussion

Emotionahlotetaying

EJAtional role-playing

, Emotional Cole- playing

--...,

ti

35M

15F

26e

30F

54F

306M

204F1

7:t!

7F

16F

End-ofTreatment

(7,)

83M

53F 2

OF (4 wks 1

rpdst)

9F (1-5 wks

post)

561

1 38F

57M. ,

43F

69F

Percent Abstinence

Six

Months

11M

12F

Long Term /

(7, )

--? 8M

12F (2 mo

23-50F (18 mo )*

161

1 (6 12 mo 1 9F

85M (12mo ) 57F

Group therapy

Group therapy

Group therapy

'p 0 05

20 05. p 0.1

Ok reduction in smoking 31
' determination required to cease such behaviors as smoking and

overeating; Weight gain is a frequently reported consequence of

giving up smoking (173).

THE SMOKING WITHDRAWAL SYNDROME

Few of tbe studies reviewed here mentioned gender as a-connection with withdrawal symptoms, and none suggested that men and women differ in the severity of smoking withdrawal

symptoms. However, Shiffman (173) analy4ed Guilford's raw

data (82), and stated that 15 of the 18 major symptoms reported

by .subjects demonstrate sex differences (80,173). Thirteen of

those 15 symptoms were more frequently reported by women.

Other studies show similar, although not statistically significant, trends. (141390,215).

Factors contributing to relapse, such as craving and nervousness, were reported to be similar for men and women (141):

Women who exjerienced the'greatest craving during the initial

five days of ab.stinence were most likely to relapse (82). Since

women score higher than mep on measures of anxiety as a gen- eral rule, it is possible that theylwould be more susceptible to

relapse if smoking had been their customary means of reducing

such dysphoria. Women may also pay more attention to somatic'

symptoms than men, as they male more frequent use of all

health care services, and specifically (because of the relative

symptomatology) for headache and and weight gain (114).

It is likely that tie abstinence syndrome is a major factor in

recidivism during the first few weeks of cessation when ,elapse

is most common, andAhat the number of cigarettes smoked per

day-is an important variable in determining the severity of the

withdrawal. The issuseof a gender difference'in withdrawal severity is a major area where reSeArch is needed.

SMOKING AND WEIGHT CONTROL

Women who smoke are, on the average, thinner than women

who do not smoke. The reported mean weight difference ranges

from 1.2 to 4.5 pounds (7,17,93). Weight gain has been a frequently documented consequence of quitting smoking, both in

males and females, (17,37,65,71,141,190,209,215).

Studies of males have reported weight gains among former

smokers which range from 1. to 12 pounds greater than thosewho continue to smoke. In one such study, the authors observed

that, while 60 percent of continuing smokers gained weight,

among quitting smokers the observed proportiorf was 85 percent

(37). These figures gave rise to an observed-to-expected ratio of

1.4, suggesting that those who quit are 40 percent more likely to

315

31,r-
.

. . . 0 TABLE 13.Behavior modificationSmoking cessation treatment results by sex

Study . Treatment N

Percent Abstinence

End-of- Six

Treatment Months -Long Term,

(%) (%)

. 1. Keutzer, 1968 (105) Breath holding, coverant

control/negative practice,

attention placebo

73M

73F

18M

29F ' 2. Suedfeld and Ikard, 1973

(186) .. Sensory depravation 3M

. ' ' 2F

100M 67M

5OF .50F (+3 mo.)

3. Delahunt and Curran,

1976 (43) negative practice or self-control

Negative, practice and selfcontrol

Control

Nonspecific treatment

50i 61 22

89 56

15 0

56 11

1

4. Tongas et al., 1976*

.. (189) Covert sensit., smoke aversion,

group therapy, combined

treatment

38M

34F

71M

'39F

.

62M 2 (12 mo ) 32F

48M} 2 (24 mo.) 18F

5. Russell, 1970 (156)

.

Electric shock aversion

. 0

.

10M

4F

r 3 ' fr

,., -1-

70M

OF

40M (12 mo.) 50F
TABLE 13. Ffeha%ior modificationSmoking cessation treatment results by sex (Continued)

Percent Abstinen

End-of- Six

Treatment -Months Long Tern

Study Treatment N (%) (%)

6. Chapman et al., 1971 (30) Electric shock, selfmanagement; post - treatment v therapist monitoring: 2 weeks: 4M "g:Cr 25M 25M

8F 100F 37F 29F

11 weeks: 4M 100M 50M 50M

7F 86F fo 57F l 57F

7 Berecz, 1972 (13) Electric shock aversion, , 56M

imagined vs. real Smoking 32F

8. Russell et al., 1976 (159) Electric shock and controls' 28M 64Mt

28F 57Ft

4

(12 mo.)

'p <0.05

'0.05 <p <0.10,,

*Results based only whose completing treatment.

"Percent reduction:little for F; more for Min uhagmed-smoking cond

tTwo weeks post-treatment.

31:
kr;

,ss gain weight than those who continue to smoke; but a significant proportion of observed weight gain among men who quit smoking would have occurred even if they lad continued to smoke. The single major report on lifetime smokirig and weight pat- terns in women examined data provided y approximately

57,000:female members of a national weight-redtiction'prograrri (17). Cross-sectional analysis indicated that current smokers

weighed less than nonsmokbers4by 1.2 pCtinds arid 4.0 pounds less than former smokers. Inhalers wee significantly less obese by 5.7 pounds than current smokers who did riot inhale. A 40-year longitudinal alysis v:eiglit in relation to reported lifetime smoking histo y revealed that betweed ages 30 an 50 (thetwo decades after the majority of those who quit had iscontihued

.) smoking), the former smokers gained more weight han continu- ing smokers, both for inhalers and non-inhalers. The calculated weight gain after cessation varied substantially by amount smoked; heavy smokers who inhaled ( -- 41 cigarettes) gained 30 lbs.,rae light smokers who inlialed (1 to 10 cigarettes) gained only 4 pounds. The observed differences in weight persisted through age 60. Conctusions of this study may not, in fact, be directly applicable to the total female population. This study raises the issues /reporting and recall bias alnong this obese population (rheangroup weights ranging front appr-oximately 171 to 180 pounds)4s well as self-selection into continuing or former smokers.

The implications of such studies are important. The image of the slender, attractive female pervades our culture and cer- tainly present in tobacco advertising (84). Do women perceive weight gain as asignifiCant and unavoidable sequel to dit{conT" tinuing smoking? There is evidence suggesting that fear Of weight gain may keep women from quitting spol-Atig. Women

are more concerned with weight than men 'are. In the 1975 NCSH survey, the perc t ges of female and male smokers who respohded "strongly agtR,Ilk or "mildly agree" to the stqement, "Being afraid of gaining a tot of weight keeps peOkle from, quit- cigarettegr are show in Table 14:

Attempts have been made to examine the cause of such re- ported weight gains. The mechanism of weigh gain with cessa- tion of smoking has not, ho-wever, been elucidated. Trahair and others have reported that appetite increased with smoking ces- sation, and the resulting increased caloric intake caused weight gain (190). Other studies have suggested that smoking may, in fact, directly affect metabolism. Glaitser, "et al.' studiecrseven males before and one month after essation. Body weight and

surface area increased, while h rate, serum calcium, sugar, and oxygen consumption decreased (71). Conversely, however,

318

1 / A
TABLE 11.Percent affirmative responses to statement: "Being

afraid of gaining a lot of weight keeps people from

quitting cigarettes"

Smoking Status Women (<7c ). Men (% )

Never Smoked 59.0 51 5

Formerly Smoked 63 1 53 6

Currently Smoked 59.9 47 3

SOURCE). National Clearinghouse for Smoking and Health (1( 4).

Sims observed no change in resting metabolic rage, thermic re- sponse to exercise or meals, and no change in serum T3 or T4

(175).

Further research is necessary to define the de ee of weight gain after cessation of smoking, the mechanism, by which it occurs and the ability to modify it by educational or behavioral

interventions during and Wafter cessation tempts.

TREATMENT RECOMMENDATIONS

Perri, eeal. recommend that smoking cessation progrpms with

a behavioral emphasit be comprehensive, multifaceted, longterm, and that they include self-reinforcement and problem- solving procedures (140). Gikren the difficulty for some women in

simultaneously dieting attd attempting to quit smoking, smoking withdrawal programs should adopt a total approach to health, including advice on dieting, exercise and the immediate benefits

of abstinence (150).

Marlatt and Gordon write that relapse is greater for

individuals whOse daily schedule fails to include'some rewarding

or pleasurable activity (120). It would appear useful to attend to

this issue in smoking treatment programs. A social support hypothesis is frequently cited in the treatment literature to explain gender differences in quitting. It is often suggested that women do better than men in programs

that provide a maximum amount of social support, and tend to do worse in situations where program support is low or outside

actors militate against quitting. For example, Resnikoffr et al. were able to differentiate, between those women (but not men) who did poorly in group-phis-medication-treatment and those

who did well usinkcthe Social Introversion Scale of the Minnesota

Multiphasic Personality Inventory (149). This scale measures

the degree of.discOmitrt in social situations and the presence of Pc putgoing tendencies. Women scoring high on this scale (shyer; -,\ore socially introverted) Were less likely to quit than low8

31C . 4-

319

s,
'$ .... 0

scoring / g women. This study provides- just one example of the

observation that social support seems tube of lesser consequenc.<

to men in quitting smoking,,although spousal support is important

As th overall categories in Tables 9-13 show, women do more

poorly in treatments characteriZed by less individual attention,

such as education and pharmacotherapy, t ompared with the

categories of psychotherapy and behavior modification, where contact is uS&lly maximized in a small group or in an

individual-to-therapist setting.

Dubren reports that twice as many women as men participated

in a television stop smoking campaign, but that fewer women

stopped smokingpresumably because Of a lack of support (53).

Guilford found that when men and women partiOpated in group

programs, success and failure rates were thesame for both sexes

(78). When they did not attend group programs, men maintained

the same success rates, but women achieved markedly lower

rates. There Is,also support for the notion that groups are particularly effective for women if they are sexually homogeneous

(44,78). Tamerin writes that the group can provide support, empathy, and shared identification with others going through a

similar process (187). The group also provides an avenue for

affe4tive expression, so that the relevance of cigarettes to psychosocial events and the personal meaning of giving them up can be

discussed. Given the differential reaction of men and women to

quitting smoking,as well as the traditionally greater willingness

of women to discuss affective issues, it is not surprising that

all-female smoking-cessation groups have be particularly attractive. , Marlatt and Gordon studied the circumstances under which

smoking relapse is most likely to occur (120). They claim that

experiencing stress in the form of a negative emotional state,

social pressure, or interpersonal conflict is likely to lead to smoking among those who are attempting to abstain. The occurrence

of a full-blown relapse, however, can be attributed to the cognitive reaction to stress-induced smoking. Many individuals who

are trying to abstain view a single slip as eyaclehce that they have

failed,. rather than as a natural and predictable reaction to a

stressful situation. Marlatt and Gordon advocate teaching t e

who are trying to quit the importance of not viewing relaps

all-or-none manner. Rather, they suggest teaching smoke

"plan for a relapse," to become psychologically repared to accept a slip as a natural part of the difficult proc of quitting.

Another factor that appears to influence the Su cess of women

in treatment programs is smoking by significant others in their

environment. Kanzler, et al. found a significant trend for women

320 4', 3 -, 1
5, CZ

to givev,uP smoking if no one it? their daily environment was.a

regular smoker' (104). This trend was only slight for men, although spousal encouragement was related to success in one

large study of smoking cessation treatment in men (170). The

influence of the smoking behayior of significant others on female

attempts to quit has been repeatedly pointed out (14,201,204).

Sensitizing friends and relatives who are smokers to this problem, and advising discretion in smoking behavior on their part,

might increase treatment effectiveness for women. . CONCLUSIONS

Treatment programs should specifically deal with means of

handling anxiety and tension, ways to combat weight gain, and

should prepare smokers for mini- relapses.Social support should

be maximized. It may be increased through choice of treatment

modality, networks of "buddies," friends and relatives, and the

involvement of spouses.

It should be possible to capitalize on the heavy commitment of

women to the health care system, both in terms of their own use

and their role as family providees. Health professionals need to

devise targeted interventions for women with this in mind.

Dissemination of Information About

HEALTH ATTITUDES AND BE' VI

The extraordinarily serious health consequences of smoking

have not deterred almost 30 percent of.the adult female and 37

percent of the adult male population from smoking regularly.

Seventy to 80 percent of these smokers agree that cigarette

smoking is harmful, ilia health hazard that requires action, and

causes disease and death (194). FOrmer smokers and nonsmokers

take a much stronger stand on these three points, ranging from

87 to 96 percent agreement. Gender differences are very slight.

The value placed on health compared to other positive life

goals was slightly lower for smokers than nonsmokers, and highest for ex-smokers'(194). Out of a maximum flictor score of six,

current smokers averaged 4,66 (M = 4.55, F = 4.81), and nonsmokers averaged 4.82 (M.= 4.68, F =4.9) and ex-smokers averaged 4.89

(M 4.78, F= 5.06). The' igher scores of women support their

traditional concern with health in our culture but they are incongruent with recent smoking trends (114).

Fewer current smokers than nonsmokers and ex-smokers report having personally knoivn someone with Coronary heart disease, lung cancer or emPhysemaChronic bronchitis. This finding

may be attributable to a prbcess of denial. Only about one-third

'31C: At 321
of current smokers admitted knowing someone personally whose

"health" was adversely affected by smoking while over 60 peercent of nonsmokers knew such a person. Clearly, mechanisms

must be operating in smokers to reduce cognitive dissonance

caused by their behavior and their knowledge of the health consequences of their behaA ior. One of these mechanisms may be to

deny that the health problems of others are connected to smok

ing.

A related issue is that of complia.oce. The term encompasses a host of behaviors, all related to following medical recommendations! seeking care when serious symptoms appear, taking medications, having follow-up examinations and procedures,

and doing breast self-examination, to name only a few. A large

number of studies ha.,. e been performed in this area, and there is

no evidence that one sex shows greater propensity to be compliant than the other (90,114).

Thus, we would have nc) reason to expect that women and men

would respond differentially to doctors' advice to change their

smoking-behaviors, at least.from this literature.

Women in our society are more in% [lived w oh health care services (114). They arrange for those services and act as role-models

for children. This function would have great information delivery potential.

SOURCES OF INFORMATION

There are a variety of ways that people can learn abodl. the

health consequences of tobacco use. The information gathered

from and effects of tobacco company advertising will be discussed separately- below, The major -ser6rces of information fall into a number of Cattgories.

pealth Care Providers

The influence of physicians and nurses as communicators of

information and as exemplars of healthy life styles has been the

subject of much research (198). The greater concern about health

f among women, and their greater contact with health professionals, provides all obvious avenue of intervention (114). Health

professionals should be continuously reminded of their potential

impact and advised to use it to influence women to reduce smok-'

ing. Physicians are considered the most authoritative source,

with the greatest potential fo1- influencing iSatient behavior.

From the self-report of adults, physicians are not delivering

enough anti-smoking informatiOn and advice. In 1975, a full 64.6

percent of male and 60.8 percent of female current smoke.fs

322

'1 I0A
claimed that they had never received advice from any doctor about quitting, cutting down, or continuing smoking'(194). About 1.9 percentiof male and 21 percent of current female smokers had

been advised to quit. Combining advice to quit anckior Wt. down, the percentages Tosobto 34.8 percent of men and 37.7 percent of women. in 1970, th percentages of men and- women who re- ported such advice were 30.2 percent and 34 percent, respectively

(193). A somewhat lower estimate of physician advice was obtainejofrom an ongoing nationwide study involving approxi- matfly 8,000 people (184),Advice to quit or cut down was reported , by 22.4'pereent of the subjects, and lack ofadvice by 77.6 percent; there were no significant gender differences. , A survey of physicians' opinions about smoking and health in the mid-1960s revealed that 38 percent claimed they advised

"all" 94' "almost all" (95 to 100 percent) of their patients who did not have smoking-related disorders to quit or cut down (76). Eighty-eight percent of physicians claimed they gave- such ad- vice to patients with lung and pulmonary conditions. Nurses spend more time in direct patient contact than do

physicians and can exert a major role in delivering information' as well as serving as exemplars. Most nurses are aware of this

responsibility (60,75,135,195). Only 10 percerit of nurses claimed

to discuss smoking and health with "almost all" or "most" (65 to 99 percent) of their patients or students (135). Another 21.5 per- cent claimed to have discussed it with 35 to 64 percent of patients or students. Only 50 percent of current smokers, compared to 65' percent each of former smokers and nonsmoke'rs, suggested stopping to 5 percent or more of their patients and students. White fheidentical question was not asked of nurses in the 1975

survey, a numberAof valuable questions relating to exemplar status were posed (196). In almost every case, current, smokers

took the weakest position on exemplar role, former smokers were

in between, and nonsmokers were strongest. For all questions, the p4-pportion of nurses who agreed "strongly" or "somewhat" with Orie statements of exernplar role is reported here, Regarding

theifol4 behavior,.69.5, 91.7, and94.5 percent of current, former and nolismoking nurses respectively felt that they should set a good example by not smoking. This percentage varied according

to work location. ,Lowest percentages were given for hospital duty (70.0, 83.3, and 89.2 percent for current, former and

nonsmokers respectively), intermediate for private physician's office (79.9, 86.7, and 90,5 percent, respectively, acid highest for private duly (91.1, 91.4, and 94.4 percent, respectively). A much lower rare of agreement about not smoking in public while in uniform was obtained; only 44.4 percent of current smokers, 6701 percent of former smokers, and 72.8 percent of nonsmokhzig

323
nurses concurred. ti arses believe that it is their repon day to

convince people to stop smoking (64 percent of rs, 74 percent of former smokers, and 6 .8 rcent of nonsmokers).Apprvximately 54 percent of smoke 1.3 percent of former smokeVs,

and 82 percent of nonsmokers said they had tried to persuade

someone other than patients to quit, and a much higher percentIge reported convincing someone notto start (83.4, 78.6, and 75.8

ercent, respectively). Finally, 52.1, 78.2, and 85.4 percent of the

espective, groups agreed strongly or somewhat that nurses

hould be more active in speaking to lay groups.

Given the possible rule mudelingeffect of female nurses, a need

a exists for adequate preparation of all health professionals in

smoking and health counseling This preparation should include

education on the health hazards of smoking as well as effective

methods of counseling patients.

There is little information available about the role played by

other health care providers in dissemination of information or

4iscuuragement of smoking behavior. Nationwide campaigns are

(t currently being aimed at physicians and dentists to increase

th it commitment to and involvement with this task. Other

1 he lth care pro,. idek should be encouraged to take a more active

roe and adopt exemplar status as well.

Educators

Adult educators include those in schools and colleges, job

training, community organizations (churches and other religious groups Young Women's Christian Associations, and Red

Cross, civic organizations, social service groups, cultural groups) and in school-based programs for parents. There are large

number of sources of information about smoking available from

educators in adult settings and in programs for parents. These

have been studod in-depth and reviewed elsewheri (188, 198).

The frequent contact with and involvement of ,women in the

school system should provide excellent opportunities to provide

female-oriented information.'

Peer Group

This group is an important, influential source of information

qn behavior. Evidence is strongest for the effect on initiation

(addressed, earlier in this Part). In two studies of British working class women, the peer group was an important source of

information about smoking and pregnancy (11,74). Other strong

relationships within the lay adult community have also been

reported (118,201). a 324
Significant others, especially within the family, have been

shown to be pnmary sources of information to pregriant women

(11,70 The female relative may serve as a particularly impqrtant role model for black women (201). Smoking initiation is

strongly influenced by parental smoking habits in teenagers

(addressed earlier in thip, Part). In married couples, smoking patterns nd to be consent, this almost enfOroes a sharing of . information and makes it especially important in quitting efforts that couples stop together or are very supportive of the

new ex.smoker (77,118,170,216).

Media: Television, Radio, Film, Newspapers, Magazins

The use of the mass media as a source of information as well

as a tool in effecting cessation has been extensively developed . in recent 'years (55,188,193,198,202,214).

Since women are almost excl-usivelY the target audience of

women's service magazines, effort,..s.hould be devoted to using

this medium to provide'informatio on smoking and health, ces- sation techniques, and clinic availability. These magazines have not adequately disseminated information on smoking and health.

One of the pnncipal reasons suggested for this failure is the.

power that tobacco companies wield through the economic incentive of advertising (178). Only One women's service magazine does not accept cigarette advertising in the United States.

Frank admission of the economic dependency upon spch advertising has been made. Not a single leading national woman's

magazine that accepts cigarette advertising in 7 years of publi- cation printed an article "... that would have given readers any

clear notion of the nature and extent of the medical and social

havoc being wreaked by the cigarette-smoking habit" (178). Smith goes on to point out that those magazines that do not accept cigarette advertising, or have no advertising at all, have

done considerably better at informing their readers of the

health risks of smoking.

Advertising

In recent yearn, a vertising in the United States has been

directed specifically towards the women's market, with themes

as diverse as the emancipation of women, the first woman (biblical reference), romantic love, and the independent single

woman; Most girl smokers have a positive impression of the

325
individuals pictured in cigarette, atheriisements. The latter are

z_z..eri, as attractie by 69 percent). enjoying themselves i by 66

1 percent). well dressed (by 66 percent), sexy lby 54 percent).

young (by 50 percegti, and healthy lb:. 4 percent). There is no

. compara-ble data on hvw girl nonsmoker, or young adult women

i. viu.Advertising (216)

''"/"' Thus. adve'rtisers have been successful in creating a ,ense of

0, mystery, sophistication, and power Around the behavior of

4 smoking Although smoking was oncerrow ned upon for women.

pe.ple no,Ir respond less negatively to a vomah ,nloking (16)

"r here ti, evidence that. fur some women, = moking is linked with

aZttides and behal.iors that comprise a socially valued and

si7.cessful self-image. and that giving up smoking is a threat to

that image'( 123 ).

Aylajority of former smokers and nonsmokers of both sexes

in 4.Pi.t, 1975 Adult Use of Tobacco Sur..ey 1194; agreed with the

sttement. -Cigarette advertising should be stopped c-ompletery The percentages for men were 56.9 percent for

i nonsmokers and 56 4 percent for former smokers, and for

women, 6)s.2 percent for nonsmokers, and 62 5 percent for

former smokers. However, only 42 6 percent of enale smokers

and 42 5 percent of females amokers agreed with the statement.

It appears that adult smokers %alue cigarette advertisements,

but why they dowhether for information abriut brand characterization and mailability. identification with the image portrayed, or some other reasonis not known. Fishbein concluded

that cigarette advertising influences the decision to smoke as

well as the choice of brand. Furthermore, he points out that

cigarette ad,. ertising may ser.e as a discriminative stimulus for

smoking behavior Advertising can- influence the initiation of

smoking. the choice of brands smoked, and the le% el of consumps

tiun. Commenting that the tobacco industry asserts that advertising serves only to influence brand choice and not initiation or

,consumption, Fishbein maintains that it is somewhat unrealistic to assume that an ad% ertisement which can do one of these

things is not also capable of doing the other. While addittonal

research on the effects of cigarette advertising is clearly nec-essary, this re,. iew suggests that cigarette advertising dots affect

Cigarette co sumption (63). ci\

Restricticns ha:.e now been placed, on advertising in many

countries in the world, including the United Atates. There is no

uniform agreement that the ban on televised cigarette advertising in the United States and the United Kingdom significantly

reduced consumption. However. it is generally believed that

each action ,of this sortincluding the U S. Surgeon General's

Reports and the Reports of the Royal College of Physicians, as

326

) --. 1 sir t I).., 1 .
1 welt as other smoking-control measures such as taxation and legislationhas a cumulative effect on per capita consumption

(8,142,202).

THE FAILURE TO DISSEMIN. E INFORMATION

.) Many of the critical evaltions '0f public health campaigns conveying anti-smoking in rmation maintain that little attitudinal or behavioral change is ever effected )188). Fishbein

(63) argues that there is insufficient information describing the

complex relationships between cigarette smoking behavior and beliefs, attitudes, and intentions to make this conclusion. He

further maintains that-it is necessary to know to what extent decisions regarding initiation, reduction, increase or cessation are under attitudinal (individual, personal) or normative

(society-influenced) control. The importance of personalizing

the health message, and the failure of the public to personalize

the health messages that they have received is emphasized. For example. over 80 percent of smokers agree with the statement

that smoking is hazardous to health. However, on the question, "Are you in/any way concerned about the possible effects of cigarette smoking on your health" only 25 percent of current smokers in the 1975 NCSH survey stated that they were "very

concerned," another 22.6 percent were "fairly concerned," 18.9

percent were "only slightly concerned," and a final 31.9 percent were "not concerned" (194). Fishbein maintains that the public

is not effectively informed about the general danger to'health posed by smoking and is even less informed about the connec

Lion with specific diseases. He concludes that the content of an

effective message is fourfold. that continued smoking 1Nds to

negative outcomes, that stopping smokirrg leads to positie out- comes; that personal relevance must be established, and that

normative influences must be appealed to by maintaining that significant others think azi indiVidual should quit.

Stress at Work io A general model of stress at work (38) is worthy of consi ration Examination of the sources of stress at work (Figure 2)

reveals a number of items that are especially salient for women. Discrimination against women in employment, role conflict, authority problems, inequity in promotions, exclusion from

decision-making processes and the "old boys" network have been frequently discussed (68). Indivi ual characteristics may be considered from a gender viewpoint . well; for example, some types of psychological disorders, such as anxiety and de3 2,,

TTT A lir

327
Sources of Stress Individual

At Work Characteristics

Intrinsic to job:

Poor physical working conditions

Workoverload

Time pressures,

Physical danger, etc

Role in organization.

Role ambigititA Role corifTT.

. Responsibility for people , Coigticts re pr garuzational . boundaries (internal

and external/ etc

Cann*velopment

Overpromotion

Underpromotion

Lack of lob security

Thwarted ambition, etc

Relationships4t Work.

Poor relations with boss j

Subordinates or colleagueW

Difficulties in 1;ietegatIng

responsibility etc

Organizational structure and

climate

Little or no participation

in decision.making . Restrictions on behaviour

(budgets etp

Office po),bficsnLack'of effective consultation, etc

The Indjvidual

Leveipf

anxiety

Let

ne rotictsm

olerance for

ambiguity

Type A behavioural

pattern

Extra organizational

sources of stress:

Family problems

Ole crises

Financial dtfflo , etc

FIGURE 2.A model of stress at work

ms marked by astens () are particularly relevant to female workers.

SOURCE: Cooper, C.L. (

it

Symptoms of Occupational Disease

III Health

3 1'

Diastolic blood pressure

Cholesterol Jewel

Heart rate

Smoking

Depressive mood

Escapist drinking

Job dissatisfaction

Reduced aspiration, etc.
pression, are more prevalent among women than men (48,68At The Type A behavior pattern, which is associated with male

cardiovascular disease, has been shown to be unrelated to sex

once socioeconomic status is taken into consideration (172).

An additional set of stressors originates in the extraorganizatianal environment. A prospective study of the relationship of employment status and employment-related behaviors to coronary heart disease (CHD) incidence was conducted by Haynes and Feinleib (91). Working women scored higher on scales measuring daily stress, marital dissatisfaction, and aging wor- ries than men. They were also less likely to display evert anger

than either homemakers or men. While incidence rates of coronary heart disease in working women were not significantly

higher than in homemakers, an excess risk of CHD wits identified aiong women who were employed in clerical jobs and had

childrem,The risk factors for CHD in this group included family

responsibilities, suppressed hostility, a nonsupportive super- visor, awl.,,low job mobility over the preceding 10-year period.

s Smoking Habits of Health Professionals

There are eratively few studies available which present gender-specific smoking rates in various professions. Health

professionals were selected for analysis because they were more

likely to be aware of the health consequences of smoking than the general public; this group has also been studied more exten- sively.

PHYSICIANS

The smoking kabits of male and female physicians in five nations are presented in Table 15. Smoking rates in the general population are provided for comparison wheja supplied by the

authors. No,breakdowns by gender are availgble for the United States. Separate estimates of smoking rate in a small group of women physicians age 36 to 46 at the time ofsurvey (205) and in

a large sample of predominantly male (93 percent) physicians (195) are listed in the table. In addition, the wives of 3,990 physicians were queried about their own smoking habits and those of their husbands; no information is provided on the occupations of these women (77).

Examination of the table shows that smoking rates of

physicians, both male and female, tend to be much lower than

general population rates. The only exception is the higher rate of current smokers among female physicians in Finland (200). The "c'entage of current smokers among the sample of U.S. female physicians ,is higher than that reported in other

329

3 96
t3, TABLE 15.Smoking habits of male and female physicians in selected countries

c> Author Country Number

Percent Smokers

Never

Pop.

Est. Current

Pop.

Est Former

Pop.

Est

1, Bourke, et al., 1972 (22) --r- lrelard M 1359

F 221

17.9

51.5

19 7*

53 2

48 5

26 7

67.6*

38 6"

33 6

22 2

12 7

7.5'

2. Vuori et al , 1 Finland M

F

843 1 38

66

34

26

60

20

27

8

271*

20'

3. Wilhelmsen FaithEll. 1974 (210) \ Sweden

Norway

' 33

54

38

27

29

19

4. Aaro et al., 1977 (1) if M 740

F 398

42

35.3

21 7

53.

36

37'

38'

5. Westling-Wikstrand et al., 1970(205) L SA

USA

US

F 81 35.8 13.6

6. GreenwAldiet al , 19712 (77) M 399.0

F 3990

323

353 _

21

24

36

A

/ 433

273

7 USDHEW. 1976 (195) M 36?,I' 39 64' 43'

34'

*Significant difference between percentages pair d by ( ) 'Stopping rate former smoker

ever smoker

'Sample consisted of physicians and their wives w ose profession was undefined.

'Percentages estimated from graph, not specified text.

'Approximate total of M and F, estimated to by 93 male. )'"
countries and approaches the rates in the general popula9on (205). Prevalence of smoking has a strone relation to demographic variables such as profession, income, and education. We wouleexpect physicians to be in the highest category on each of these variables acrd, therefore, to have lower prevalence rates. Therefore,. it would be relyvant to examine the cross-tabulations for :smoking prevalence by socioeconomic status, according to set. According to the three studiesOrpvidipg comparative data, both female and male phys2a44. are quitting at rates higher than the general pbpuiation. The percentage of former smokers among fema4 physicians, and estimates of quit rate, are lower than among male physicians in all but one of the studies listed. This trend may represent a time lag in the smoking behavtorok---3/4"- women as compared to that of men, or there may be a lower glut rate among women-physicians.

In two studies, female physicians smoked more cigarettes per day than women in the general population (1,22). In co tract, wives of physicians smoked few:er cigarettes on the erage than their husbands (77). A greater percentage of the w ves of physicians than physicians themselves were smokers in every age group except the oldest. The percentage of current smokers appeared to be inversely related to age in the group of wives, but virtually stable across age for the Husbands and physician-husbands. wives tended to have similar smoking habits, Based on a small sample of women graduates of a single U.S. medical school, Westling-Wikstra.nd, et al. (205) reported that 58.8 percent of the current smokers belonged to the category "professor" (academic appointment of assistant professor or above, with or without board attainment) when ranked on pro- fessional attainment. The other categories were "boards" (spe- cialty board certification but not professional appointments), "no boards" (in practice without 'board certification or profes- sional appointment), and "not in practice." The "professor" group was characterized by greater likelihood .of being single and .having fewer "habits of nervous tension." Compar4to other groups, this group had the lowest depression scored, aver- , age anger scores, and the highest anxiety scores. The authors comment that this group of women was the most similar to their male colleagues. They may also have experienced fewer prob- lems with ambivalence about sex rolbs, self-image, or c nflict over aggressive behavioral patterns. The presence ( f t e high anxiety scale,hovvever, casts some doubt on this Women in U.S, medical generalization.

.schools are 'subjected to significant psychological pressures and often experience jmotional prob- lems and lack of confidence about achieving the goal of gradi:ii3al3

4) r,

tiv
0, do (205). Fremale physicians also experience nificant role

corini t (19

The ele>Eance Of indices of stress td smoking wtterns is again

one of inference. If smokmAerves as a copinemechanisma

mieans of reducing negative affectthen it is understandable

t t female hysAcians, ur an, other professional with elevated

ess levels, id h&ve- higher,current smoking rates than the

general populace. It Nalso understandable that they might experience more difficulty in quitting.

PSYCHOLOGISTS . - A survey of psychologists in California sta universities and

colleges found that female psychologists Nve e much more likely

to smoke than their male colleagUes (46). e rate oking

was slightly higher than in male health pro -ssio ls, aed appr&ximately the same for female psychologists percent) and

nurses (195) (s.. Table 16)...

. This' smokinirate is significantly above the rate amongprofessional wchnen in general (25M percent) and was due to lower

. cessation rates among Rsychologists rather than higher initiation rates. The most common reasons given for smoking are the

stress of work ox school, and personal stress. Frieze, et al. state

that professionel women have to exhibit "male-like" charactert istics in order to survive in their jobs, but that these characteristics are often met with criticispi and hostility (67). Thus, social

and occupational demariEls are at odds with each,other -Fur -

thermore, there is evidence that female psycaiologists faCe very

real sex discrimination in the evaluation of f heir work (67).

Dicker) and Bryson (46) report a high degree of power fantasies among female psychologists. who smoke. This support:

Fisher's finding that female smokers in general seem preoc-

' cupied with the issue of 4, o r <64). He speculates that cigarettes.are vitsed defensire

g

ainst feelings of powerlessness

weakness, and inferiority. Elevated suicide rates are another correlate to the evideitc(

of excessive stress and difficulty in coping experienced by som(

emale professionals. These higher Cates, compare() with till

eral female population, hrt;ie been obServed among women

sy.e.ologists, chemists, and physician's (124,164). Factors suc}

as it- b

wer

mine w

1/-a-lelice about success., role conflict and marginalit;

fere as dynamics, However, it is not possible to deter

r these higher suicide rates are due 'to the self

selectiOn of suicide-prone worsen into these and possibly other

- professions, or to the difficulties encountered in professiona

Atraining and practice or 'to an interaction of both).

332

(A. t
NURSES

4 A number of studies have 'shown a higher rate of smoking

among nurses than in the general female population in the

Upited States. The most recent assessment of nurses' smoking

behavior Was. conducted in 1975 (199). In Table 16, srboking

habits of nurses are compared with those of adult U.S. women

and other g-roups.of'fiealth professionals.

Between 1969 and 19T5, the proportion of nurses Who were current smokers rose from 37 to 39 percent. Every other cate- gory of health professional (physician, dentist, and pharmacist)

had-su4tantially reduced smoking rates. The membership of

these three professions is predoininantly male and current

smoking rates vary from 21 to 28 percent. If Me examines quit rates in 1975 among the four" categories of health professionals, it is clear that the majority of physicians, dentists, and pharma- cists who ever smoked cigarettes have a.ait.L64, 61, and 55 per- cent respectively. Among 4-1 urse only 36 percent have quit, which doet, however, compare favorably with adult women (34

percent) and,working women (30 percent) (IP). Noll surveyed smoking behaviors of nurses by work setting

(see Table 17) (135). The overall percentage of current smokers

in this survey Was 37 percent, compared to a national average

(for 1966) ..of 33.7 percent in women. There was a smaller per- centage of never smokers (41.3 percent) among nurses in that survey than among the female population (56.8 percent), suggesting a higher quitting rate at that time as well. From

Table 17 it appears that there is no seltive recruitment into

the various nursing specialties; the proportion of never smokers

is fairly equal across work settings. Differences do appear, how- ever, in the proportion of current smokers according to work

setting. Highest rates of smoking are fSand in psychiatric and pediatric settings, and lowest rates in the four categories con- nected to education and community involvement: nursing edu; cation, working in the community, elementary or high school nursing, and working in a doctor's office.

In GrI>at Britain, only 26 percent of maternity nurses smoked

regularly, compared to 37 percent of those in general nursing

(106). In the United Kingdom, approximatly the same proportion of nurses smoke as women in the general population 44

percent (106,154).

Knopf Elkind reports differences in smoking among different types of ward nursing staff. Trained nurses had 41 percent cur- rent smokers, learners had 28 percent, nursery nurses had 14

percent, and auxiliaries had 61 percent current smokers (106). L'ampman reported a similar excess of smokers among purses

333
TABLE 16 Percentages of cigarette smokers (S), former smokers (FS), and el, er smokers ( ES) and cessation

ratio (FS'ES.) among psychologists, nurses, and other selected health professionals

Sample

Male and predominantly male samples .

('St'(' male psychologists

Eminent experimental psychologii,ts-9(1'7. male

(Lawton and Goldman, 1961)

Psychiatrists '7. male not reported

(Tamann and Eisinger, 1972) . American Public Health Association male membtr,,

(Eyres, 1973)

Physicians-93q male (USPHS, 1977)

t' S adult males (L'SDHEW. 1976)

Female and predominantly female samples

CSUC female psychologiata

American Public Health Association female members

( Eyres. 1973)

'Nurses 98'7. female (USPHS. 1977)

I' S adult females (USDHF.W. 1976)

ti S FS F,S FS..ES

I

2i)8 28 35 62 si5

72 53 11 64 17

309 42 27' 4,9 19

'1.569 21 10 ' 61 66

3,657 21 * 42 63 67

5,702 39 29 69 42

86 38 19 57 .33

1,973 31 31 62 50

2.429 39 22 61 36

6,327 29 14 33

NOTE CSC(' -- California State University and Colleges SOURCE Hicken. (' (46)

t.0
jTABLE 17.Cigarette smoking status by work setting for nurses (percent)

Work Setting Cigarette Smoking Status

Current Former Neer

Total'

Percent N , Surgical Units *-

Medical Unit.,.

41 2 19 4 39 4 100 0 "t29

Operating. Labor. Deli%

37 A Ix 2 43 9 99 9 476 er,

Maternity Unit

Emergency Room 39.5 15 2 45 0' 100 0 455

Pediatrics Unit or Setting

'36 2 17 2 46 6 100 0 4,94

Psychiatric Unit or Seticitig

46 6 5 5 44 6 100 0 50

Nur,ung Education Setting

-49 9 1X 2 '32 0 100 1 135

In the Community 24.6 26 5 45 7 100 1 90

Elementary or High School

26.1 .33.4 40 6 100 1 264

Doctor's Office

27 5 36 4 36 1 100 0 217

Out-Patient Clinic

24 2 33 x 41 9 99 9 335

Other and Mixed 42 5 15 1 42 5 100 1 11:1

41 3 15 4 40'3 100 0 1,075

*Total N -- 6,012

SOURCE Noll. (' E +1'35)

aides (95..2 percent female) in a large metropolitan hospital in the United States (1,10). Fifty-two percent of that group smoked, compared with 36 percent of the medic,a1,.nurs 9;,3 percent female) and -40 percent of the .stude.nt nurses 951'., percent female). This survey was aimed at. identifying snictkoig within the hospital. Thus, true prevalence in this sample can only be higher.

Compared to other.fnale health vofessionals'(sAiable 6)

. ;'," ''''

in the United States,'nurses' c r t t i i rate's are aboaf SOhie4lp

y- chologists, U.S. adult women) and b.elow -others (Avirtkricao 13- b- lic Health Association female members). Knopf Elkind points out that in the British populatfoother female-Ampated pro- fessions, such as prima" iy -school, teachers, heaith visitors and domiciliary midwivd2have notAably lower rates (4f smoking than hospital nurses i'06). entry into the ifrl yession of nursing is associatedwith to ink up dai4., ;:imokinebulktbe degree of occupational stress in,a, pdpulatroti of 300 British student nurses was not different for sm s an&nonsmokers (92). This finding does notrul4nut the of smoking as a-stress- reduction mechanism, howeve ..4,-, Other factors which i ht cont MO a high smoking rate among nurses are wor o erload'and fri,ation in professional

,. relationships with physicians. ",,. 10 Knowledge of health consequenof smoking is/high among nurse's, but it has been shown that "student nurses are less well- ififormed than medical students (154). yrses who quit smoking

335
do cite protection of fiiture health as a major reason (75,92).

Nurses who smoke are less likely than nonsmokers to agree that

not smoking is a preventive measure against cancer (106). Similar refusal to acknowledge health risks of smoking iS found

among smokers in the general population (194). Whether this

represents a real lack of knowledge or a method of reducing

cognitive dissonance through denial is unknown. The problem is)

particularly critical for nurses (and otheryhealth professionals)

since they serve both as exemplars'and as providers of information (106).

The Pregnant Smokera Special Target

The pregnant woman is in a unique life situation. Every substance she ingests and every behavior that she manifests can

affect the present and future health status of the fetus she is

carrying. If she smokes the nicotine, carbon monoxide, and hydrogen cyanide which she inhales all cross ehe placental barrier

and enter the bloodstream of the fetus. The risk factors for both

mother and fetus have been extensively reviewed elsewhere in

this volume as well as in previous reports from the Surgeon

General (198). (See also Pregnancy and Infant Health in Part II

s of this Report),

It is estimated, that between one-quarter and one -third of

pregnant smokers quit smoking for the duration of pregnancy

and that another third cut down.

This section reviews the current literature on source) of information available to the pregnant smoker, summarizes available data on prevalence of current smoking and smoking cessation during pregnancy, and discusses the problem of cessation

from a behavioral viewpoint. , SOURCES OF INFORMATION

The same classes of information discussed in the previous section are available to the pregnant smoker. How the pregnant

smoker uses these sources and her degree of confidence in the

information provided seems to be a function-of socioeconomic

status and panty. 'Information is distributed through health

professionals (primarily physicians and nurses), peers and family. commupity resources, and the media.

Women in lower socioeconomic classes tend to rely more on

lay referral systems, such as peers and family, than upon mass

media or medical sources (10,74). Personal transmission of in

formation seems to be more highly valued and readily adhered

to (71). Middle and upper class women are more likely to utilize

:336 . A

Oa
impersonal sources such as mass media and physician-supplied

information (74).

In one studrof predominantly working class British women, the mode of exposure'to smoking information ranked as follows: 84 percent had seen it on television; 65 percent were told by

famil,y,or friends; 52 percent had seen posters and leaflets; 37

percent had been told by husbands; 34 percent used books and magazines; and 25 percent had been told by a medical source 116 percent from a doctor, and 9 percent from a nurse) (11). The authors comment that television, posters, and leaflets are in- adequate for the delivery of statistical information; books, which are better sources, wer used much less than these other sources. Banc and MacArth present a discussion of health norms in pregnancy (10). enty-nine percent of the sample were aware of some norm r lating to smoking in pregnancy: 39 percent thought they were expected not to smoke at all, and an

additional 40 percent thought they were expected to reduce

their smoking. All of the women co-GM-name at least one source

of information; 98 percent had been expos to mass-media

Messages to quit smoking. Smoling see to be undergoing a change in norm status, from generality to speciffP+ty, i.e., from being a general health menace to on: with specific conse- quences, such as a threat to th-'14-alth o the baby: The issue of normative behavior in II II ing and personalization of message should be crucial to informational campaigns, according to Fish bein's theory (63). Social support from a spouse should also be critical, as would be involvement of significant others.

Women about to have their first baby are more likely to be- lieve educational materials than multiparous women (11,50). This finding suggests that different m des of intervention or

different emphases shpuld be develop d for pnmiparous and multiparous women.

Physician Advice

The physician rerlesents one of the most knowledgeable fig- u'res the pregnant womati will encounter as a source of information. Consequently, estimates of the frequency with which the physician delivers advice on smoking are of-importance. Three such estimates are available from tonal samples in

the United States. In the first study, cond ed in the mid1960s, 37 percent of physicians reported that they advised all or almost all (95 to 100 percent) of their pregnant patients to quit smoking or cut down sharply. Obstetncians were more likely to deliver such advice to pregnant patients (49 percent) than were

,physicians in general practice (38 percent) (76).

337
100

..E. 80

ca0

Ci3 60

a. 40

20

n

Major

Contributing

Association

No Association

ir

NeonatA Coronary Chronic Pulmonary Lung

Death Artery Bronchitis Emphysema Cancer

Disease

FIGURE .3. Beliefs of OB-GYN specialists about the association

of maternal smoking with neonatal death and other

selected diseases . sot R( E Danaher B G ..1(n

, . The PhyNician Advice Survey conducted by the Center for

- Disease Control examined the beliefs and behavior of physicians specializing in Obstetrics and Gynecology (0B -GYM) in

the United States (40). The OB-GYN specialty practice includes

preventive medical care in the form of 'specific suggestions regarding hygiene and family planning and, during pregnancy,

acti'e participation 's directing perinatal care (40). The beliefs

,... of OB-GYN specialists about the relationship between maternal

smoking and neonatal death are presented in Figure 3, a'ong

with their belief about some of the more common diseases associated with smoking. Because neonatal death can result from

a great many factors, the attribution bf causality is somewhat

tower than for the other conditions represented. However, it is

notable that 23.6 percent of thy physicians deny the existence of

any relationship. Congruent with the estimate from the 1960s,

45.3 percent of OB-GYN specialists in this survey claimed to

instruc all or almost all of their patients to quit or cut down on

smoki (see Figure 4). Another 13.1 percent delivered such advicece to most or many 165 to 95 percent). A noticeably smaller fraction of physicians who are current smokers deliver this

message than ex-smokers or nonsmokers.

The 1975 Survey of Adult Use of Tobacco, sponsored by the

National Clearinghouse on Smoking and Health, included a

338 3

:
70

60

50

40

a 30

20

10n

45.3

iAdvise All + Almost All Patients

Most + Many

:: Few + None

37 1

44

Total

in = 3208)

Current

Smokers

(n = 622)

Former

Smokers

(n =,1187)

50

awl

NonSmokers

= 1404)

FIGURE 4.Percentage of patients advised to quit or cut down

their smoking by the smoking behaviorpf the advising obstetrician - gynecologist . SOUR( E Danaher, B G 40t

uestionnaire directed at smoking habits in pregnant women. A

preliminary analysis of the results has been made (89). Out of

12,029 respondents interviewed in 1975, a total of 1,225 women

(814 current smokers and 411 former smokers) were administered questions about their smoking habits during pregnancy. Each of the 983 respondents (664 current smokers and 319

former smokers) who had ever been pregnnt was asked

whether her doctor suggested that she qwt smoking or cut down during her last pregnancy. Table 1.8 displays the results by year of last pregnancy. The percentage of women reporting

suchipdvice from their doctors rose steadily, Only 14.6 percent of

women who had last been pregnant from 1965 to 1969 claimed to

have been advised by their doctor either to stop or cut down, 23.7 percent of women last pregnant from 1970 to 1975 remembered such advice. The estimates are considerably smaller

than those supplied by physicians themselves (40,76). There are

several possible explanations'for the discrepancy. the women

were reporting retrospectively. and memory may have been distorted; a selective under-reporting of advice Cray have occurred, or the populations of p . icians, and patients may be entirely

nonoverlapping. Retr spective data have been shown to he unreliable in one pre nancy study (49). Unfortunately, sample

sizes were too sm I to provide reliable estimates of the per -

339
T 1F31.F. 1,s. Distribution of responses of current former

smokers sAho were eer pregnant to the question

"Did your doctor suggest that you cut dun or stop

smoking eiggrette during your last pregnancy?"

Hd ,*

-.1)1 f l F, N,,

centage Ilf V.Vrlleil V h , follow ed the .rtck;ce of a p1-0,i( t( top moking dunng pregnanc; Su, h data might ha..e Ided an

estimate of.the effe( tierie I,f ,lich e 1r, er 701 perent laim to aci\ie their

pregnant patent to ennonate or harpiN curtail their smoking

(luring pregnant\ . hut a rIlla h smaller percentage of pregnant

women recall such aclic e

PREVALENCE OF SMOKING ANI) QUITTING 1)1RING

PREGNANCY

The pre,. alente smoking in pregnant women 14pefore pedal

cessation hould be roughly equo.a lent to the pre alence of smoking in the female population in the same age

range. corrected for :ocioeconomit status Ten studies conducted in deelcyped countries. reported betwtkn 1571 and 1973.

,how a range from 23 4 pert ent to 47 *1 percent in pre\ alence of

tobacto Uwe 114., The medi4in rate is 42 1.I pelreent smokers for

the entire --ample A ,urey tcondutted during the course of the

pregnant 9.7):;:3 pregpant %;.eayien who represent a cro,,:, section althe genera)population in the Rier,,ide-San BernachnoOntario (California; area wa, recent13, completed

nar. inch( ate that 44 percent of all women sureyed

either tontinued to smoke during pregnant} or had smoked before, bLit not during. thi. pregnano Since the preci-Ac timvof

ce-,,ation not clear, a more con,er. e that/M.3

percent of women continued to smoke for the duration of their pregnano This estimate well within the range of those de- med from the Population Report n- 3.11)

3./ g'4'4
There is a paucity of race-specific rmation on smoking

prevalence during pregnancy. NisWander and Gordon (134), in a study encompassing 14 U.S. cities, reported greater prevalence of smoking among white than black women (53.65 percent vs. 41.85 pircent, respectively). This is a high estimate and reversal of the prevalence rates presented in Table 7. The finding is simi- lar tc the previously presented data, in that white women smoked more cigarettes per day than black women: only 3.3

perszt of black women smokers consume a pack a day 2r more, compared to 13.4 percent of white women in this study. gmoking

is slightly less prevalent in Wad( than in white women in the

sample of Kuzma and Phillip 6 FIN. 57.3 percerit of black women

ared 53.3 percent of white women have never smoked. For His- panic women, the percentage.isom'newhat higher, 61.9 percent never- smokers. Table 19 summarizes the results of 11 studies reporting rates of discontinuing smoking during pregnancy. The overall rate of cessation among regular smokers ranges from 0.9 percent to 35 percent, which is the figure most often

anecdotally cited. The median is closer to 20 percent. Only one study provides ethnic data on smoking cessation

during pregnancy (108). In this study, it should be remembered, stopped smokers are women who smoked prior to:but not dur- ing the pregnancy, so that quitting may not have been

pregnancy:specific. Rates are very similar for white, black and Hispanic women.: 24.5 percent, 24.9 percent and 28.7 percent,

'respectively, were stopped smokers in this study. Even acute abstinence. from cigarette smoking may be of value, if it occurs immediately prior to giving- birth. In the United Kingdom, women are often admitted as early as 48 hours before elective delivery; abstaining from smoking for that period of time was found to result in a net percent increase in

available oxygen as COHb was excreted (42). Such a temporary benefit may actually be critical under acutely stressful conditions, and where there is chronic placental insufficiency. Cutting down on smoking during pregnancy would appear to be better than no change in behavior, especially for those ad- verse effects upon the fetus which show a dose-response relationship. However, cutting down on number of cigarettes does not always imply a reduction in delivered dose of nicotine or

other tobacco smoke constituents (79,80). When smoking behav- ior was measured over the course of pregnancy in regular smokers (5 to 30 cigarettes per day for at least 5 years), de- crease in number of puffs per cigarette occurred as ptegn-iincy progressed (6). Like puffing rate, the COI;lb concentration also decreased over time in pregnancy. However, in these s'ubjects

there wasv significant change in nicotine dose extracted from

341
air

4`

c\:. TABLE 19. Percentage a current smokers who ho altered smoking behavior during pregnancy

\

Author and [)ate N Quit

( hange in Smoking

( ut

Quit Down

Temi'irXril) Only in( reas

laPercent of Women

No Miscellaneous,

Change or Comment

1 kullandt-r ez Kallen. 1971 (107) 2,806 0 9 1 1 97 '3 -0 5 Initiated

2 Andrews & McGarr), 1972 (4) 6,733 14 7 Maternmex only .

, Butler et al 1972 (291 '141 '18 4 QuIt by end of 4&. Mont; 4 Schwartz et at, 1972 (171) 1,188 31 0 100

5 Banc et al 1976' , 1 i4 14 9 st 0 82 1 Quit by It ante-natal s IRIt 6 Graham. 1976 (741 7,0 333 :;3 3 33 3 1 3 quit or cut down,

1 3 cut down temporarily

7 Banc ez MacArthur, 1977' AO( 133 22 5 6 0 C Ti 1 5 3 263 -6 X reduced temporarily

x Oonoi.an, 1977 (49) 959 12 5, 5 6

:# Yankelovich et al 1977 (216i 3.5 0 320
TABLE 19.Percentage of current smokers who altered smoking behavior during pregnancy Cdntinued

Author and Date

10 Harris. 1979'x9)

Change in Smoking HabitPercent of Women

Cut

Quit Down No Miscellaneous, N Quit Temporarily Only Increased Change or Comment

4092 165 24s

11 Kuzma & Phillips. 1979 1087 4.249 25 1'

7 9 36 9 -3 9 changed brand or

switched to filter cigarettes

822 of quitters resumed

smoking after delivery

13 4 of quit smokers were

again smoking at 1-5 mo

post-delivery

NOTE

kt.b. CA:

'These two studies may be composed of oerlapping samples 20f the 506 women in the NCSH sure surt'et whose last during pregnant} pregnancl, occurred during 1965-75, 409 reported snioking either before(

'Percent who stoked prior to. but not during tills pregnancy, calculated as part of smoker sample r

.t
the cigarette over the duration of the pregRancy. Some' alteration in puffing pattern, presumably in inhalation, produced

the compensation. Thus, caution must be exercised in the in-

. terpretatial of "cutting down."

There is even less information available on the percentage of quit-smokers who return to smoking after delivery. Table 19

provides two extremely divergent estimates: 82.2 percent (89) and 13.4 percent (108). Because we are dealing with relatively

small sample sizes, the reliability of such data is not very high. Much more information must be accumulated before any firm

statements about recidivism can be made. Women who quit during pregnancy have an excellent opportunity to change a behavior f'-or life, with benefits both to themselves and to their children (see Recommendations).

PSYCHOSOCIAL FACTORS IN QUITTING

Health reasons, primarily centering around preventing harm

to the fetus, are most often given as reasons for quitting. Yankelovich, et al. (216) report that ,62 percent of young women

smokers beVeve Oita smoking can harm the fetus and norms

against smoking have been discUssed (10). The sickness experi- enced as a part of pregnancy can also be a reason to give, up

smoking (11). It has also been reported that women who smoke

before pregnancy show a signifiOntl increased incidence of

appetite cravings and aversions', ivhich May be associated with

quitting (41).

A closely related aspect of maternal health is weight gain. Preventing excessive weight gain has even been given as a rea- son to continue smoking during pregnancy (50). Banc and MacArthur included control of weight gain as a norm dunes

pregnancy, 24 percent of this,sampl'e expressed awareness of

social expecuations in this area (10). The issue of how much

weight it is appropriate to gain in pregnancy vanes according to

time and culture, so the generality of this finding is unclear.

Little is known about problems in quitting during pregnancy. The role of cigarettes as stimulants or tension reducers may be

altered during this period. Abstinence symptomatology has also

not lieen documented.

A composite picture ofthe successful quitter has been drawn

loy-13aric, et al. and also bF1(uzma and Phillips (11,108). Banc, et al. list educational qualjfications as being positively related to

quitting, followed by/sickness in early pregnancy. Other distinguishing charactenstios are smoking fewer cigarettes before

pregnancy (alsoSee 49,171), having started smoking at an older

age, having stopped previously for at least 6 months, having

344

I t

;
heard about harmful effects of smoking from more, sources, firmly believing that smoking was harmful to the baby, and

finally, being encouraged to stop or being joined in the cessation

effort by their husbands (47,166).

Kuzma and Phillips identified a number of similar characteristjcs: higher educational level; greater family income; being married; being employed; more frequent .church attendance; having 'a spouse who does not smoke; and no illicit drug use (106,108).

The characteristics describedadvanced, educationa' level, 'higher socioeconomic status, wider information base, belief in stopping for the sake of the fetus, and spousal support aH fit with a model of behavior change involving information, per- , sonalization, and social norms (63).

Three studies evaluate smoking cessation interventions for

pregnant women (11;41,49). Tables 9 and 10 show reported abstinence figures for, two studies. One study (11) showed noldif- ference between intervention and control groups, and the sec- ond study (41) showed 50. percent abstinence at 9-month follow- up for those completing treatment (11,41). This latter result is very encouraging but is based on a very small sample in an

affluent community where the aforementioned factors of educa- tiorial level, high socioeconomic status and orientation toward

professional advice are operative.

RECOMMENDATIONS

The receding discussion has revealed a number of findings which may be usefp in improving methods of reaching the pregnant woman anti offering her cessation interventions. ' 1. Pregnant women seem to know that smoking is harmful to health, and most acknowledge that it can be directly harmful to

the fetus. This information about the baby's health should be made as specific as possible, and the mother's own health should

be intricately interwoven in the tilim4. Quitting is for the good of both mother and baby, not the baby alone. The harmful as-j pecrts of smoking and 'the benefits of not smoking milt be

equally emphasized.

2. Mass media, such as television and film, are particularly

good avenues for portraying,women of varying ethnicity in a

number ofgeographical and socioeconomic settings. Because of gender identification it is important to utilize, women as the

transmitters of information and advice. Information should be dispensed by as many different sources of contact in the pre-, natal clin(c (or doctor's office) as possible, not solely by the

346

342 -
\ physician. The awareness of various health prufessiona s

. iaised in this regard.

3. Social ni/rms and lay .1-erral systems should be used as

part of infufm.ation disseirkination an4 modeling influences.

This is particularly .rue for women of letver socioeconomic.

status. It 'is important to'involve the father of 'the child it the

normative- belief system, and in a direct supportive effort of

quitting., This shuitgd be particularly timely' in '..rt-era when more

and.mti.e couples are experiencing pregnancy and birth as a

o-person process.

4. -.7t1tich more emphasis musk t place( Con permanen.t smoking cefsation rath r than ist uri.ng the time of pregnancy.

Pusitie aspects o main ng an eft- smoker include better

health for,the mother am child a,ntl thettuture- impact of role

modelkng its thiz child grOws.

4 A 0 t

t Stimmari

. \

4.1 - 1. The percent,..Rt_. of 17-18 year old women who smoke has

shown a steady rise between .1968 and 1,979. It 'now appears,

howtAer, that the increage in smukii&preyalence among 1 12-18 !,ear old females has Iftled, orb..nd begun to declin

omen -burn after 1962Aow a substantially reduced

tion of stoking and will pr44bably have a mach 104er pro,

fence of smoking as adults' ;

2. Th-ose young women who do begin to smoke are'starting to

smoke riogularlii t a yu'unger age, with More than half of the

male and fenvle 40.1e:went:, who begin to moke starting before

the 10th grad. . 3. The earlier tvbaccci i ased and the grealer the num of

cigareltes.sm'oked pex day, the less likely an attempt to quit will

he successful. 40 4. The percentage of women smoker:: who srnol. more an

one pack pff day is increasing. . j2

5. Adolescent and adult women are more likely to` e low" ar"

and nicotine cigarettes, smoke fewer ctarates per day and in-,

!pie less deeply than do men, but the differerge between the

sexes in these patterns of smoking -.is decreasing. Adolescent

band adult black women are more liktly to be smokers than their

he peers, but they smoke fewereigarettes er day.'

6. Adol...,,e,,cents from 1.6W income, families, single parent

a families with lower pdrental educational lev aPe

more likely to hot-corn' mokers.

7. Female p.pd male dolescents are more likely to be in

smoking if a/parent or old sibling also smokes.

316
A 8. Adolescent smokereas.tociate with pe s who smoke, and nonsmokers associate with nonsmokin

9. Adolescent girls o'vefiestimdte the percenta of their peers

. wlio smoke and they have a very positive image oft people in Cigarette advertisements,*but they are less likely tha adoles- cent boys to see smoki as a social asset.

10. Adolescent girl w o St ke tend to be more outgoing, b

feel less able o influe ce their future.

11. o esc tits exp ience stress die to feelings of unattractive ess, incompetency school achievement and personal re- , at ns, limited opportunity for liprsonal growth and concern

er future social and economic roles.This stress may be the

coMpon mechanism producing the increased rates of smoking

groups.

12. The factors associated with successful quitting by adoles- . cents of either sex are lower number of cigarettes smoked per day, higher educational aspirations and achievement, greater "acceptance of the health risk of smoking, and having more nonsmokers a ng their friends. ."

13. It is possible that women and men modify their smoking

in order to mai tain a onstant nicotine level.

14. Women a e mo 1 than men to smoke i older to reduce stress.

, 15. Worrien at highe, ducatiorli and income levels are more

likely to succeed in quitting. Additional factors associated with

successful quitting are a strong corrainitment to change, the tide of behavioral techniques and reliaTie social support for quitting. Women have been reported to show lower rates than men

of successful cessation following organized cessation prbgrams, a difference which is less apparent in those-progritms that in- clude social sup.

4

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