MONOGRAPH 13

Risks Associated

with Smoking

Cigarettes with

Low MachineMeasured Yields

of Tar and

Nicotine

U.S. DEPARTMENT OF HEALTH

AND HUMAN SERVICES

Public Health Service

National Institutes of Health

National Cancer Institute

SMOKING

AND

TOBACCO

CONTROL
Risks Associated

with Smoking

Cigarettes with

Low MachineMeasured Yields

of Tar and

Nicotine

SMOKING

AND

TOBACCO

CONTROL

U.S. DEPARTMENT OF HEALTH

AND HUMAN SERVICES

Public Health Service

National Institutes of Health

National Cancer Institute

MONOGRAPH 13

Mono Title Page 11/19/01 11:26 AM Page 1
Smoking and Tobacco Control Monographs Issued to Date

Strategies to Control Tobacco Use in the United States: a blueprint for public health action in the 1990’s. Smoking

and Tobacco Control Monograph No. 1. Bethesda, MD: U.S. Department of Health and Human Services,

Public Health Service, National Institutes of Health, National Cancer Institute. NIH Publication No. 92-3316,

December 1991. 

Smokeless Tobacco or Health: An international perspective. Smoking and Tobacco Control Monograph No. 2.

Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service, National Institutes of

Health. NIH Publication No. 92-3461, September 1992. 

Major Local Tobacco Control Ordinances in the Unites States. Smoking and Tobacco Control Monograph No. 3.

Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service, National Institutes of

Health. NIH Publication No. 93-3532, May 1993.

Respiratory Health Effects of Passive Smoking: Lung cancer and other disorders. The Report of the U.S. Environmental

Protection Agency. Smoking and Tobacco Control Monograph No. 4. Bethesda, MD: U.S. Department of Health

and Human Services, Public Health Service, National Institutes of Health, NIH Publication No. 93-3605,

August 1993

Tobacco and the Clinician. Interventions for Medical and Dental Practice. Smoking and Tobacco Control

Monograph No. 5. Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service,

National Institutes of Health. NIH Publication No. 94-3693, January 1994.

Community-based Interventions for Smokers: The COMMIT Field Experience. Smoking and Tobacco Control

Monograph No. 6. Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service,

National Institutes of Health. NIH Publication No. 95-4028, August 1995.

The FTC Cigarette Test Method for Determining Tar, Nicotine, and Carbon Monoxide Yields of U.S. Cigarettes. Report

of the NCI Expert Committee. Smoking and Tobacco Control Monograph No. 7. Bethesda, MD: U.S.

Department of Health and Human Services, Public Health Service, National Institutes of Health. NIH

Publication No. 96-4028, August 1996.

Changes in Cigarette Related Disease Risks and Their Implication for Prevention and Control. Smoking and Tobacco

Control Monograph No. 8. Bethesda, MD: U.S. Department of Health and Human Services, Public Health

Service, National Institutes of Health. NIH Publication No. 97-4213, February 1997.

Cigars. Health Effects and Trends. Smoking and Tobacco Control Monograph No. 9. Bethesda, MD: U.S.

Department of Health and Human Services, Public Health Service, National Institutes of Health. NIH

Publication No. 98-4302, February 1998.

Health Effects of Exposure to Environmental Tobacco Smoke. The Report of the California Environmental Protection

Agency. Smoking and Tobacco Control Monograph No. 10. Bethesda, MD: U.S. Department of Health and

Human Services, Public Health Service, National Institutes of Health, National Cancer Institute. NIH

Publication No. 99-4645, August 1999.

State and Local Legislative Action to Reduce Tobacco Use. Smoking and Tobacco Control Monograph No. 11.

Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 00-4804, August 2000.

Population Based Smoking Cessation: Proceedings of a Conference on What Works to Influence Cessation in the

General Population. Smoking and Tobacco Control Monograph No. 12. Bethesda, MD: U.S. Department of

Health and Human Services, National Institutes of Health, National Cancer Institute, NIH Publication No.

00-4892, November 2000.

Mono Title Page 11/19/01 11:26 AM Page 2
This monograph, Risks Associated with Smoking Cigarettes with Low

Machine-Measured Yields of Tar and Nicotine, is the 13th report published in

the National Cancer Institute’s (NCI) Smoking and Tobacco Control

Program Monograph Series. The concept for this series was formed by the

late Dr. Joseph W. Cullen, former Deputy Director of the Division of Cancer

Prevention and Control. On the inside front cover of this volume, appears a

list of previously published monographs. In addition to the current monograph, there are two more under development. One will be entitled

Changing Adolescent Smoking Behavior: Where It Is and Why. The other will be

called Is the Target Hardening? The “target” refers to those long-term smokers

who, in many cases, have tried to stop smoking and been unable to do so.

Future monographs will address important and timely issues on tobacco

control, and will reflect our continuing mission to reduce cancer risk, incidence, morbidity, and mortality caused by tobacco use, as well as enhance

the quality of life of current and former users of tobacco. 

The initial meeting of the authors for the Low Tar Monograph took

place in November of 1999. At that meeting, each author presented a preliminary paper or outline. The group discussed each presentation and made

suggestions as to which subtopics might be removed from or added to each

chapter and determined the boundaries of the various chapters. 

One feature of the this monograph is that it blends the old with the

new. Monograph 7, The FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S. Cigarettes, covered the history of

that protocol and recommended changes in its procedures. Chapter 2 of

this publication cites this earlier monograph, brings us up to date on the

FTC method, and provides additional suggestions as to what can be done to

help alert the public to the dangers of smoking. 

The examination of the scientific literature on low-tar and low-nicotine

cigarettes is not unique to this monograph. Several of the earlier volumes

devoted one or more chapters to discussions of the various health aspects of

tar and nicotine levels. However, this monograph includes more than just

the study of amounts of tar and nicotine. Chapter 5 includes a discussion

on the continued health risks to smokers, even those who smoke a lowtar/low-nicotine cigarette, while Chapter 2 describes how changes in the

cigarette design affect an individual’s smoking habit. Chapter 7 points out

how the tobacco companies’ advertisements have changed to match the

emerging public preference for low-tar/low-nicotine cigarettes. 

This monograph is unique in another important aspect. For the first

time, the authors who prepared the various chapters have had extensive

access to the information gleaned from the internal documents of the

tobacco companies. The tobacco industry files now open to the public and

i

Preface

Preface 11/19/01 11:30 AM Page 1
available on the Internet constitute some 33 million pages of formal and

informal memos, meeting notes, research papers, and similar corporate documents. Included are marketing strategies that express the growing concern

among the various tobacco companies of the potential loss of new recruits.

This concern over the potential loss of market was due to the evolving public opinion that smoking is harmful to health and that it is related to many

of the illnesses that smokers experience over the course of their lives. 

The singular message that has been delivered to the public—smoking

causes cancer—is gradually being accepted by more and more people of all

ages. This message has been reported in many scientific papers over the last

50 years. In a historical context, however, the bellwether publication that

galvanized the public opinion was the original 1964 Surgeon General

Report, Smoking and Health: Report of the Advisory Committee to the Surgeon

General of the Public Health Service. The fact that the public has slowly realized and, more importantly, accepted the danger of smoking undoubtedly

concerned the tobacco companies. 

Access to internal industry papers allowed monograph authors to cite a

number of tobacco company documents that show a long-term trend altering the tar and nicotine content of cigarettes by various chemical and

mechanical procedures. The documents further reveal the industry’s efforts

to produce cigarettes that could be marketed as acceptable to health-conscious consumers. Ultimately, these low-tar/low-nicotine cigarettes were

part of the industry’s plan to maintain and expand its consumer base. 

The monograph authors show that the tobacco companies set out to

develop cigarette designs that markedly lowered the tar and nicotine yield

results as measured by the Federal Trade Commission (FTC) testing method.

Yet, these cigarettes can be manipulated by the smoker to increase the

intake of tar and nicotine. The use of these “decreased risk” cigarettes have

not significantly decreased the disease risk. In fact, the use of these cigarettes may be partly responsible for the increase in lung cancer for longterm smokers who have switched to the low-tar/low-nicotine brands.

Finally, switching to these cigarettes may provide smokers with a false sense

of reduced risk, when the actual amount of tar and nicotine consumed may

be the same as, or more than, the previously used higher yield brand. 

This monograph compliments the recently released Institute of

Medicine report entitled Clearing the Smoke: Assessing the Science Base for

Tobacco Harm Reduction. Together, the documents reflect a growing body of

research that has explored the impact of products intended to reduce harm

in an environment where there is near universal recognition of tobacco’s

harmful effects. Both documents reflect the need for more research to better

understand the feasibility and desirability of developing and marketing

products intended to reduce risk, but both also conclude that there is currently no safe tobacco product.

We hope that this evidence-based review will inform any potential recommendations that the Department of Health and Human Services (DHHS)

might make to the FTC regarding the cigarette testing method. 

ii

Smoking and Tobacco Control Monograph No. 13

Preface 11/19/01 11:30 AM Page 2
This monograph, entitled Risks Associated with Smoking Cigarettes with

Low Machine-Measured Yields of Tar and Nicotine, was prepared under the

general editorship of Donald R. Shopland, former Coordinator for the

Smoking and Tobacco Control Program (STCP), National Cancer Institute,

Bethesda, Maryland.

The Senior Scientific Editor for this monograph was David M. Burns,

M.D., Professor of Medicine, School of Medicine, University of California at

San Diego, California. The Co-Scientific Editor was Neal L. Benowitz,

M.D., Professor of Medicine, Chief Division of Clinical Pharmacology and

Experimental Therapeutics, University of California at San Francisco,

California. The Managing Editor for the monograph was Richard H.

Amacher, Project Director, KBM Group Inc., Silver Spring, Maryland. 

The editors and STCP staff members gratefully acknowledge the many

researchers and authors who made this monograph possible through their

many hours of writing and review. Contributors to each chapter are as follows:

iii

Acknowledgements

David M. Burns, M.D.

Professor of Medicine

School of Medicine

University of California,

San Diego School of 

Medicine 

San Diego, CA

Neal L. Benowitz, M.D.

Professor of Medicine and 

Chief

Division of Clinical 

Pharmacology and 

Experimental Therapeutics

University of California at 

San Francisco

San Francisco, CA 

Chapter 1 Overview and Summary

Acknowledgements 11/19/01 10:34 AM Page iii
iv

Smoking and Tobacco Control Monograph No. 13

Lynn T. Kozlowski, Ph.D.

Professor and Head

Department of Biobehavioral 

Health

The Pennsylvania State

University 

University Park, PA

Richard J. O’Connor, B.A.

Research Assistant

Department of Biobehavioral

Health

The Pennsylvania State 

University

University Park, PA

Christine T. Sweeney, M.P.H.,

Ph.D.

Scientist

Pinney Associates, Inc.

Bethesda, MD

Neal L. Benowitz, M.D.

Professor of Medicine and

Chief

Department of Clinical 

Pharmacology and 

Experimental Therapeutics

University of California at

San Francisco

San Francisco, CA

David M. Burns, M.D.

Professor of Medicine

University of California,

San Diego School of Medicine

San Diego, CA

Jacqueline M. Major, M.S.

Statistician

Tobacco Control Policies

Project

University of California at

San Diego

San Diego, CA

Cigarette Design

Compensatory Smoking

of Low-Yield Cigarettes

Smoking Lower Yield

Cigarettes and Disease

Risks

Chapter 2

Chapter 3

Chapter 4

Acknowledgements 11/19/01 10:34 AM Page iv
v

Acknowledgements

Thomas G. Shanks, M.P.H.,

M.S.

Principal Statistician

Tobacco Control Policies

Project

University of California at

San Diego

San Diego, CA

Michael J. Thun, M.D., M.S.

Vice President of

Epidemiology and 

Surveillance Research

American Cancer Society

Atlanta, GA

Dietrich Hoffmann, Ph.D.

Associate Director

American Health

Foundation

Valhalla, NY

Ilse Hoffmann, B.Sc.

Editorial Coordinator

American Health 

Foundation

Valhalla, NY

Neil D. Weinstein, Ph.D.

Professor of Human Ecology

Rutgers, The State University

of New Jersey

New Brunswick, NJ

Richard W. Pollay, Ph.D.

Professor of Marketing,

Faculty of Commerce

Curator of the History of 

Advertising Archives

University of British 

Columbia

Vancouver, Canada

Timothy Dewhirst, M.A.

Ph.D. Candidate

University of British

Columbia

Vancouver, Canada

The Changing Cigarette:

Chemical Studies and

Bioassays

Public Understanding of

Risk and Reasons for

Smoking Low-Yield

Products

Marketing Cigarettes

with Low MachineMeasured Yields

Chapter 5

Chapter 6

Chapter 7

Acknowledgements 11/19/01 10:34 AM Page v
Smoking and Tobacco Control Monograph No. 13

Jeffery Wigand, Ph.D.

President

Smoke-Free Kids

Charleston, SC

Diane Pettitti, M.D., M.P.H.

Director

Division of Research and Evaluation

Kaiser Permanente Medical Care 

Program

Southern California Region

Pasadena, CA

William Farone, Ph.D.

President

Applied Power Concepts, Inc.

Anaheim, CA

Brian Beech, M.S. (OEH), C.I.H. 

(CP), R.O.H.

Tobacco Strategy Branch

Ministry of Health

Government of British of Columbia

British Columbia, Vancouver

Joel B. Cohen, Ph.D.

Distinguished Service Professor and 

Director

Center for Consumer Research

Warrington College of Business 

Administration

University of Florida

Gary A. Giovino, Ph.D., M.S.

Department of Cancer Prevention, 

Epidemiology, and Biostatics

Roswell Park Cancer Institute

Buffalo, NY

David M. Mannino, M.D.

Medical Epidemiologist

National Center for Environmental 

Health

Centers for Disease Control and 

Prevention

Atlanta, GA

Patricia Richter, Ph.D.

Toxicologist

Centers for Disease Control and 

Prevention

Office on Smoking and Health

Atlanta, GA

Ralph Caraballo, Ph.D.

Epidemiologist

Centers for Disease Control and 

Prevention

Office on Smoking and Health

Atlanta, GA

Sir Richard Doll, C.H., F.R.S., F.R.C.P.

Emeritus Professor of Medicine

Nuffield Department of Clinical 

Medicine

Oxford University

Oxford, United Kingdom

Jesse L. Steinfeld, M.D.

Former Surgeon General

C. Everett Koop, M.D., Sc.D.

Former Surgeon General

Senior Scholar

The C. Everett Koop Institute at 

Dartmouth

Hanover, NH

vi

The editors are indebted to a number of distinguished scientists,

researchers, and others in the government, universities, and the private sector who contributed critical reviews during the formation of this final

monograph. We are also grateful for the guidance and support provided by

Stephen Marcus, Ph.D., who has been given the responsibility to continue the STCP monograph series in the future. 

Acknowledgements 11/19/01 10:34 AM Page vi
Acknowledgements

Jonathan M. Samet, M.D., M.S. 

Professor and Chairman

Department of Epidemiology

School of Hygiene and Public Health

Johns Hopkins University

Baltimore, MD

Dorothy K. Hatsukami, Ph.D.

Professor of Psychiatry

University of Minnesota Medical 

School

Minneapolis, MN

Jack E. Henningfield, Ph.D.

Associate Professor

Department of Psychiatry and 

Behavioral Sciences

Johns Hopkins University School of 

Medicine

Baltimore, MD

and

Vice President

Research and Health Policy

Pinney Associates, Inc.

Bethesda, MD

John M. Pinney, B.A.

President

Pinney Associates, Inc.

Bethesda, MD

John R. Hughes, M.D.

Professor

Department of Psychiatry, 

Psychology, and Family Practice

University of Vermont

Burlington, VT

Sir Richard Peto, F.R.S., Hon 

M.R.C.P.

Professor of Medical Statistics and 

Epidemiology

Nuffield Department of Clinical 

Medicine 

Oxford University

Oxford, United Kingdom

David T. Sweanor, J.D.

Legal Counsel

Smoking and Health Action 

Foundation

Ottawa, Canada

Kenneth E. Warner, Ph.D.

Richard D. Remington Collegiate 

Professor of Public Health/Director

University of Michigan Tobacco 

Research Network

University of Michigan

The editors also acknowledge the following individuals at the Tobacco

Control Policies Project, University of California at San Diego, San

Diego, California, for their assistance in the preparation of the monograph:

Robert W. Davignon, M.S.

Production Editor

Christy M. Anderson, B.S.

Statistician

Jerry W. Vaughn, B.S.

Programmer/Analyst

Sharon Buxton

Administrative Assistant

Don F. Harrell

Administrative Assistant

vii

Acknowledgements 11/19/01 10:34 AM Page vii
Finally, the editors and STCP staff would like to acknowledge the contributions of the following staff members at KBM Group, Inc., Silver Spring,

Maryland, who provided technical and editorial assistance in the preparation of the monograph: 

Ann L. Kreske, M.S.

Editor/Graphic Designer

Catherine M. McDermott, B.S.

Copy Editor

Heidi S. Volf, B.A.

Proof Reader/Graphic Designer

Sarah W. Weinstein, B.A.

Graphic Designer

Yaa Nsia Opare-Phillips, B.S.

Administrative Assistant

viii

Smoking and Tobacco Control Monograph No. 13

Acknowledgements 11/19/01 10:34 AM Page viii
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .i

Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .iii

Contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .ix

Chapter 1: Public Health Implications of Changes in Cigarette Design

and Marketing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

How Did It Happen? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

Compensation in Smokers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3

Elasticity of Demand in the Cigarette . . . . . . . . . . . . . . . . . . . . . . .4

Marketing of Low-Yield Cigarettes . . . . . . . . . . . . . . . . . . . . . . . . . .5 

Disease Risks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .6

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .10

Chapter 2: Cigarette Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13

Cigarette-Yield Testing by Smoking Machine Using 

the FTC Protocol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13

Changes in FTC Machine-Smoked Yields Over Time . . . . . . . . . . .13

Design Changes That Reduce Standard Yields . . . . . . . . . . . . . . . .14

Compensation and Cigarette Design: Difference in 

Yield with Different Smoking Patterns . . . . . . . . . . . . . . . . . . .18

More Evidence from Industry Documents Related to Compensation,

Cigarette Design, and the FTC Testing Method . . . . . . . . . . . .33

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .34

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .34

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .35

Chapter 3: Compensatory Smoking of Low-Yield Cigarettes . . . . . .39

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .39

Role of Nicotine in Maintaining Tobacco Addiction . . . . . . . . . . .39

Biomarkers of Tobacco Smoke Exposure . . . . . . . . . . . . . . . . . . . . .41

Nicotine Absorption from Cigarette Smoking . . . . . . . . . . . . . . . .42

Estimating the Extent of Compensation . . . . . . . . . . . . . . . . . . . .44

Studies of Smoking Cigarettes with Different MachineDetermined Yields: Methodological Considerations . . . . . . . . .44

Short-Term Experimental Switching Studies . . . . . . . . . . . . . . . . . .45

Long-Term Experimental Switching Studies . . . . . . . . . . . . . . . . . .47

Studies of Smokers Smoking Self-Selected Brands . . . . . . . . . . . . . .49

Spontaneous Brand Switching . . . . . . . . . . . . . . . . . . . . . . . . . . . .56

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .58

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .60

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .60

ix

Contents

Table of Contents 11/19/01 11:33 AM Page ix
Chapter 4: Smoking Lower Yield Cigarettes and Disease Risks . . . .65

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .65

Historical Development of the Lower Yield Cigarette Issue . . . . . .68

Limitations of Epidemiological Studies in Examining the

Risks of Low-Yield Cigarette Use . . . . . . . . . . . . . . . . . . . . . . .72

Published Epidemiological Studies of Health Endpoints . . . . . . . . .81

Biologic Implications of Compensation for Changes 

in Cigarette Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .109

Correlation of Cigarette Brand Choice with Number of Cigarettes 

Smoked per Day and Duration of Smoking . . . . . . . . . . . . . .111

Temporal Trends in Lung Cancer and Other Diseases in Major 

Cohort Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .119

Temporal Trends in National Lung Cancer Death Rates and

Smoking Behaviors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .123

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .145

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .146

Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .147

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .152

Chapter 5: The Changing Cigarette: Chemical Studies 

and Bioassays . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .159

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .159

Identification of Carcinogens, Tumor Promoters, and

Carcinogens in Tobacco Smoke . . . . . . . . . . . . . . . . . . . . . . .160

Smoking Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .165

Changes in Cigarette Smoke Composition with Various 

Design Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .166

Observations on Cigarette Smokers . . . . . . . . . . . . . . . . . . . . . . .181

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .182

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .184

Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .185

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .185

Chapter 6: Public Understanding of Risk and Reasons for

Smoking Low-Yield Products . . . . . . . . . . . . . . . . . . . . . . . . . . .193

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .193

Perceptions of Light Cigarettes . . . . . . . . . . . . . . . . . . . . . . . . . . .193

Reasons for Smoking or Switching to Light Cigarettes . . . . . . . . .194

The Relationship of Switching to Quitting . . . . . . . . . . . . . . . . . .195

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .196

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .196

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .197

Chapter 7: Marketing Cigarettes with Low MachineMeasured Yields . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .199

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .199

The 1950s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .199

The 1960s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .204

The 1970s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .207

x

Smoking and Tobacco Control Monograph No. 13

Table of Contents 11/19/01 11:33 AM Page x
The 1980s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .223

Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .228

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .231

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .233

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .233

xi

Contents

Table of Contents 11/19/01 11:33 AM Page xi
Table of Contents 11/19/01 11:33 AM Page xii
INTRODUCTION Cigarettes have changed dramatically over the last 50 years, but

the data contained in this volume make it clear that the disease risks associated with smoking have not. Following the demonstration that cigarettes

could cause cancer in the 1950s (Wynder and Graham, 1950; Doll and Hill,

1952, 1954; Hammond and Horn, 1958), cigarette manufacturers added filters to their products. They also embarked on an effort to lower the

machine-measured tar and nicotine yields produced by their cigarettes

when tested under a protocol specified by the Federal Trade Commission

(FTC) (Pillsbury, 1996). These changes led to more than a 60-percent reduction in machine-measured tar yields of U.S. cigarettes over the last 50 years

(see Figure 1-1). 

However, it appears that many of the same changes in cigarette design

that reduced machine-measured tar yields also led to a disassociation

between the machine-measured yield of the cigarette and the amount of tar

and nicotine actually received by the smoker (see Chapters 2 and 3). As a

result, tar and nicotine measurements made by the FTC method for current

cigarettes have little meaning for the smoker, either for how much he or

she will receive from a given cigarette or for differences in the amount of

tar and nicotine received when he or she smokes different brands of cigarettes.

The absence of meaningful differences in smoke exposure when different brands of cigarettes are smoked (see Chapter 3) and the resultant

absence of meaningful differences in risk (see Chapter 4) make the marketing of these cigarettes as lower-delivery and lower-risk products deceptive

for the smoker (see Chapters 6 and 7). The reality that many smokers chose

these products as an alternative to cessation—a change that would produce

real reductions in disease risks—makes this deception an urgent public

health issue.

HOW DID IT HAPPEN? Epidemiological studies established an increased risk of

lung cancer among cigarette smokers in the 1950s (Wynder and Graham,

1950; Doll and Hill, 1952, 1954; Hammond and Horn, 1958). At the same

time, it was discovered that painting tobacco tar on the backs of mice could

produce cancers (Wynder et al., 1953). Widespread public dissemination of

the results of these studies led many smokers to quit (Burns et al., 1997),

but the majority of smokers were addicted and were unable to quit or

unwilling to try. Faced with the continuing exposure of large numbers of

smokers to the cancer-causing substances in tobacco smoke, public health

authorities made the valid conclusion that cigarettes that delivered less tar

1

Public Health Implications of Changes

in Cigarette Design and Marketing

David M. Burns, Neal L. Benowitz

Chapter 01 11/19/01 10:42 AM Page 1
to smokers would be likely to produce less cancer as well (U.S. Congress,

1967), and the effort to produce and market low-tar cigarettes began to

gather momentum.

The recommendations by public health authorities to produce low-tar

cigarettes failed to appreciate two important realities. First, smokers were

powerfully addicted to the nicotine in cigarettes. They actively changed the

way they smoked individual cigarettes (see Chapters 2 and 3)—and some

smokers increased the number of cigarettes they smoked per day (see

Chapter 4)—in order to preserve their moment-to-moment and daily intake

of nicotine. Because cigarettes deliver smoke with a relatively fixed ratio of

tar to nicotine, smokers also preserved their dose of tar when they preserved their dose of nicotine. 

Second, public health authorities dramatically underestimated the ability of cigarette manufacturers to engineer cigarettes that would yield very

low tar and nicotine values when machine smoked, but yielded much higher levels of tar and nicotine when smoked by the smoker. Cigarettes were

designed with an elasticity of delivery that allowed smokers to get much

higher yields of tar and nicotine by altering their pattern of puffing.

Smokers may also obtain higher yields of tar and nicotine by blocking ven2

Smoking and Tobacco Control Monograph No. 13

0

5

10

15

20

25

30

35

40

1955 1960 1965 1970 1975 1980 1985 1990 1995

0

1

1

2

2

3

3

195

TAR

NICOTINE

Tar (mg)

Year

Nicotine (mg)

Figure 1-1

Sales-Weighted Tar and Nicotine Values for U.S. Cigarettes as Measured Using the 

FTC Method 1954*-1998

*Values before 1968 are estimated from available data, D. Hoffmann personal communication.

Chapter 01 11/19/01 10:42 AM Page 2
tilation holes in the filters with their fingers or lips (see Chapter 2). Lowyield cigarettes were designed in such a way that the same alterations in

puff profile (e.g., larger, faster puffs) that resulted from a smoker’s effort to

compensate for a reduced nicotine delivery also generated much higher

deliveries of tar and nicotine from the cigarette. In addition, the ventilation

holes in cigarette filters were placed in locations where they could easily be

blocked by smokers’ lips or fingers. The combination of these two phenomena—compensation on the part of the smoker and elasticity of delivery in

the cigarette—meant that most, perhaps nearly all, smokers who switched

to these low-yield brands did not substantially alter their exposure to tar

and nicotine and, correspondingly, did not lower their risk.

COMPENSATION IN SMOKERS Nicotine intake is a principal reason why most

smokers smoke (U.S. DHHS, 1988). In the absence of nicotine, smokers do

not continue the compulsive use of cigarettes that characterizes addiction.

Tobacco companies recognized early in the process of developing lower

yield cigarettes that smokers would attempt to preserve the amount of nicotine derived from smoking (Wakeham, 1961). Compensation for reduced

delivery of nicotine takes many forms and develops over time after shifting

to lower yield cigarettes (see Chapter 3). Smokers may take larger puffs,

inhale more deeply, take more rapid or more frequent puffs, block ventilation holes in the filters with their fingers or lips, or increase the number of

cigarettes they smoke per day. 

The most important question on compensatory smoking is the extent

to which it occurs when smokers actually switch brands of cigarettes

through their own choice. Unfortunately, this is also the most difficult circumstance under which to obtain detailed measurements of large numbers

of smokers. Many studies have examined smokers when smoking in a laboratory setting or when asked to switch at specific points in time or to specific brands of cigarettes. These studies offer some insight into how smokers

compensate, but may not reflect smokers’ behavior when they are switching of their own volition to a brand of their choice.

Some compensatory smoking changes are evident immediately upon

switching to lower yield cigarettes, but it is common for smokers to require

some time to learn how to smoke lower yield cigarettes in ways that

increase the delivery of nicotine to the smoker. Even under laboratory conditions, when smokers are rapidly switched to lower yield cigarettes, considerable compensation is evident. The extent of compensation increases in

smokers who are allowed longer periods to adapt to smoking the new cigarettes or who are switched under conditions that more closely mimic the

voluntary switching of smokers to lower yield cigarettes. When smokers of

cigarettes with different machine-measured nicotine yields from the general

population are examined, there is little or no relationship between the

nominal nicotine yield of the cigarette smoked and measures of nicotine

intake by the smoker, such as blood cotinine levels (Benowitz et al., 1983:

Benowitz, 1996; Jarvis et al., 2001). These observations suggest that, at least

when considering modern cigarettes, switching from higher to lower yield

cigarettes per se is not likely to reduce tar intake and resultant disease risks.

3

Chapter 1

Chapter 01 11/19/01 10:42 AM Page 3
Early in the 1950s, cigarette manufacturers began to

place filters on the end of the cigarette rod. Many different filters were developed, but the most common type used in the

United States was made of cellulose acetate. A variety of other approaches

to tar reduction was also utilized, including “puffing” the tobacco to reduce

the weight of tobacco in a cigarette, altering the blends of tobacco and

porosity of the paper wrapper, changing the density of the tobacco rod,

using tobacco stems and reconstituted tobacco sheet, and using a wide variety of filter materials (see Chapter 5).

In exploring these approaches, cigarette manufacturers recognized that

approaches to reduction of tar yields that actually reduced the nicotine

(and tar) delivery to smokers resulted in smokers discontinuing the use of

those brands of cigarettes. This led to an effort to design into the cigarette

an elasticity of delivery so that smokers could extract from the cigarette as

much nicotine as they needed by changing the pattern of puffing on the

cigarette (see Chapter 2). The goal of this effort was to develop cigarettes

that would produce very low yields of tar when tested by machine smoking

using the FTC protocol, but would deliver a much higher dose of nicotine

when these cigarettes were smoked by actual smokers with the puffing profiles the companies knew they would use.

An important cigarette design feature allowing a low machine-measured

yield with a higher actual yield is the use of ventilated filters. Holes are cut

into the paper wrapping the filter in locations where they are not covered

when the cigarettes are placed into the smoking machine. However, the lips

or fingers of the smoker can easily cover the holes. When the holes are

uncovered and the low draw rates specified by the FTC protocol are used,

air is drawn into the smoking machine, diluting the smoke coming through

the rod of tobacco and lowering the machine-measured tar values. When

the holes are covered or when the smoker draws more rapidly on the cigarette, much more of the puff volume is composed of smoke drawn through

the rod of tobacco and much less is composed of air drawn from the ventilation holes. The result is a dramatic rise in the tar and nicotine delivered

to the smoker by the cigarette.

A given cigarette can be made to deliver any lower level of tar in

machine measurements by increasing the size or number of the ventilation

holes in the filter. The amount of nicotine in the unburned tobacco is similar for cigarettes with a wide range of machine-measured nicotine yields, as

is the tar-to-nicotine ratios of the smoke from these cigarettes when they

are smoked under conditions that mimic those of actual smokers (see

Chapter 3). This combination of factors, plus the learned compensatory

behaviors of the smoker, allows most cigarettes to deliver similar amounts

of tar and nicotine to cigarette smokers without regard to the amount of tar

and nicotine reported using the FTC method.

This effort by cigarette manufacturers to design cigarettes that could

yield very low levels of tar when smoked by the machine while delivering

full doses of tar and nicotine to smokers was not the only option available

to the cigarette manufacturers. Internal tobacco company documents are

ELASTICITY OF DEMAND

IN THE CIGARETTE

4

Smoking and Tobacco Control Monograph No. 13

Chapter 01 11/19/01 10:42 AM Page 4
replete with descriptions of filters that could selectively remove toxic smoke

constituents, of treatments of tobacco with catalysts like palladium that

reduced levels of carcinogens in the smoke, and of other promising modifications of cigarette toxicity. Many of the changes in cigarette design developed by cigarette manufacturers lowered levels of the toxic constituents in

cigarette smoke, at least as the cigarettes were smoked using the FTC protocol. However, these paths were not pursued to the point of bringing products to market with scientifically established reductions in toxicity or carcinogenicity for smokers. The principal marketing advantage of a cigarette

design scientifically established to cause less harm would be the reduced

toxicity of the product. Because cigarette manufacturers persistently maintained that cigarette smoking did not cause any disease, they could not

advertise a product as safer since it would be necessary to acknowledge the

risks of their existing products. 

One unfortunate outcome of the tobacco companies’ position that cigarettes had not been established to cause any disease is the lost opportunity

to develop cigarettes that have actual reductions in biological toxicity

rather than simply the ability to reassure smokers concerned about the risk

of smoking. The more unfortunate outcome of this position was the marketing of cigarettes with no real difference in disease risks as “safer” products.

The link between tar and cancer risk also led to marketing

of cigarettes with lower machine-measured tar yields as

reduced-risk cigarettes. Terms such as ‘Light’ and ‘Ultra-Light’ were added to

brand names, and substantial numbers of smokers switched to these brands

in an effort to reduce their disease risks (see Chapter 6). Marketing this illusion of risk reduction would have been of concern even if the target for

these brands had been confined to continuing smokers. Instead, these

brands were targeted at those smokers who were thinking of quitting in an

effort to intercept the smokers and keep them smoking cigarettes (see

Chapter 7). The switch to low machine-measured-yield cigarettes with the

illusion of risk reduction was, therefore, substituted for a real risk reduction

that would have occurred had the smoker quit smoking altogether.

Beginning in the 1950s, filter cigarettes were advertised using claims of

scientific discoveries, modern pure materials, and implied endorsements

from medical and scientific organizations. These claims were not supported

by testing that demonstrated lower deliveries of tar and nicotine to smokers

or by studies of actual disease risks. However, the clear message delivered to

smokers by the advertising was that these cigarettes were safer.

With the endorsement of lower tar cigarettes by public health authorities in the 1960s (U.S. Congress, 1967), cigarette marketing began to focus

on machine-measured tar deliveries. Tobacco industry research and engineering efforts recognized that at least two directions were possible with the

development of either a health-image (health reassurance) cigarette or a cigarette with minimal biological activity (one that would actually produce

less disease) (Green, 1968). Unfortunately, the dominant direction taken

was the production of health reassurance cigarettes engineered so that they

MARKETING OF LOWYIELD CIGARETTES

5

Chapter 1

Chapter 01 11/19/01 10:42 AM Page 5
would deliver low yields of tar under FTC

machine-smoking conditions. These low

machine yields were touted in the advertisements and incorporated into cigarette brand

names with terms such as ‘Light’ and ‘UltraLight’. However, the promise of low tar delivery was only valid for the smoking machine.

Smokers received a much higher dose of tar

and enough nicotine to satisfy their addiction.

This dichotomy of delivery between

smokers and machines was the intended

result of the engineering effort to design elasticity of delivery into cigarettes. Testing of

these design concepts on actual smokers

revealed that Light and Regular cigarettes

delivered the same levels of tar and nicotine

when smoked by smokers (Goodman, 1975)

and that advertising these cigarettes as lowtar-yield cigarettes was deceptive (Peeples,

1976). But these cigarettes satisfied the

demand for cigarettes that could be marketed

as low-tar cigarettes with full flavor or taste

(See Figure 1-2). The low-tar claim presented

in the ad only existed for machine smoking and the full flavor received by

the smoker was accompanied by full yields of tar and full disease risks.

DISEASE RISKS Having demonstrated that smokers derive similar amounts of

nicotine from cigarettes with a wide variety of machine-measured nicotine

yields because those cigarettes were designed to deliver a full dose of nicotine (and tar) to the smoker, one might expect that there would be little or

no difference in disease risks among groups of smokers who smoke cigarettes with different machine-measured tar and nicotine yields. However,

epidemiological studies have demonstrated that smokers of lower tar or filtered cigarettes had lower lung cancer risks (see Chapter 4). These findings,

made in the late 1960s and 1970s, were particularly exciting since smokers

had been smoking these reduced-yield cigarettes for only short periods of

time. As more individuals used these products for longer periods of time,

the reduction in disease risk would be expected to increase and national

lung cancer death rates would fall.

Use of lower yield cigarettes grew until they were the dominant type of

cigarette on the U.S. market, with 97 percent of the cigarettes currently sold

in the United States being filtered cigarettes, but lung cancer rates continued to rise. Lung cancer death rates finally peaked in 1990 among White

males; they continue to rise among women in spite of a higher prevalence

of low-yield cigarette use among females. Examination of these trends show

that they are explained by changes in smoking prevalence without postulating reductions in disease risks due to changes in cigarette design (Mannino

et al., 2001; see Chapter 4).

6

Smoking and Tobacco Control Monograph No. 13

Figure 1-2

Low Tar is Important to Me

Chapter 01 11/19/01 10:42 AM Page 6
In addition, prospective mortality studies examining smokers in the

United States (Thun and Heath, 1997; Thun et al., 1997) and the United

Kingdom (Doll et al., 1994) revealed an increase—rather than a decrease—in

the risk of smoking over a period when tar and nicotine yields of cigarettes

were declining. Data from two large prospective mortality studies conducted by the American Cancer Society (ACS) more than 20 years apart are particularly compelling (Thun and Heath, 1997). Machine-measured tar and

nicotine yields of U.S. cigarettes declined dramatically in the interval

between these two studies (see Figure 1-1), and the machine-measured

yields of the cigarettes actually smoked by the participants in these two

studies were dramatically different as a result (see Figure 1-3). Despite the

substantive reduction in tar yield of the cigarettes smoked in CPS (Cancer

Prevention Study)-II, lung cancer disease risks increased, rather than

decreased, compared to CPS-I, even when controlled for differences

between the two studies in number of cigarettes smoked per day and duration of smoking. 

The risk reduction with use of lower yield cigarettes demonstrated in

epidemiological studies and the absence of a risk reduction in U.S. lung

cancer mortality trends or in the two ACS studies with changing cigarette

design are observations that offer apparently conflicting interpretations of

the likely disease consequences of smoking lower yield cigarettes. The epidemiological observation of lower risks with use of filtered and lower tar

cigarettes has been reproduced in multiple populations and cannot be dismissed as an artifact of a single analysis or a single population. Similarly,

national death rate trends are real observations not easily dismissed.

Epidemiological studies and national death rates both measure the

impact of low-yield cigarettes in somewhat different ways. Epidemiological

studies of disease risks compare disease rates among populations of smokers

who use cigarettes with different characteristics. These studies can define

whether the disease experiences of smokers of different types of cigarettes

are different. However, attributing differences in disease experience to the

type of cigarette smoked requires careful consideration of, and adjustment

for, characteristics of the two groups that may influence disease risks other

than the type of cigarette smoked. 

National mortality rate trends are the cumulative result of all of the

changes in smoking behavior over time, changes in cigarette design, demographic changes, and changes in smoking behavior. However, smokers of

different types of cigarettes cannot be examined directly for their contribution to these trends. 

The marketing of low-yield cigarettes as less risky (see Chapters 6 and 7)

results in smokers switching from higher to lower yield cigarettes in an

effort to reduce their disease risks (Cohen, 1996a & b; see Chapters 6 and

7), in an effort to quit, or in an effort to substantially reduce their smoking

(Giovino et al., 1996). Because of these health concerns and an ongoing

interest in cessation, these same low-yield cigarette smokers may also have

higher rates of successful long-term smoking cessation or may voluntarily

reduce the amount that they smoke for health reasons. Risk reductions that

7

Chapter 1

Chapter 01 11/19/01 10:42 AM Page 7
8

Smoking and Tobacco Control Monograph No. 13

6.0-11.9

0

10

20

30

40

50

CPS-II

CPS-I

<6.0 12.0-16.9 17.0-20.9 21.0-25.7 25.8-35.7

Men

Tar Content (mg)

Percentage

0

10

20

30

40

50

CPS-II

CPS-I

<6.0 6.0-11.9 12.0-16.9 17.0-20.9 21.0-25.7 25.8-35.7

Women

Tar Content (mg)

Percentage

Figure 1-3

Percentage Distribution of Tar Content, as Measured by Machine Smoking, of the

Cigarette Brand Smoked at Enrollment

Chapter 01 11/19/01 10:42 AM Page 8
accompany cessation or lowered smoking intensity may appear to be related to the tar level of the cigarette smoked when a population is followed

longitudinally for assessment of disease risk without repeated follow-up

assessment of smoking status. This effect and other differences in healthrelated behaviors linked to low-yield cigarette use may confound the analysis of disease risk in prospective studies of low yield cigarettes.

Many published epidemiological studies of low-yield cigarettes have

adjusted for the number of cigarettes smoked per day because it is the most

readily available quantitative measure of smoking intensity. The potential

for smokers to increase the number of cigarettes they smoke per day when

they switch to lower yield cigarettes can confound analyses of disease risks

among smokers of different types of cigarettes in both case-control and

prospective epidemiological evaluations (see Chapter 4). Data presented in

Chapter 4 show that smokers who switched to low-yield cigarettes in the

ACS CPS-I increased the number of cigarettes that they smoked per day, and

that smokers of ultralow-nicotine-yield cigarettes smoked more cigarettes

per day in recent California tobacco surveys. 

The differences between self-selected populations of smokers of different types of cigarettes and the potential for confounding between type of

cigarette smoked and the number of cigarettes smoked per day may explain

why epidemiological studies have demonstrated a risk difference when one

has not appeared in national death rates. 

However, it is clear that the expected lung cancer risk reduction offered

by the reduction in lung cancer rates in epidemiological studies has not

been realized in national lung cancer death rate trends. When all of the epidemiological evidence is considered in the context of what is currently

known about cigarette design and compensation, it does not support the

conclusion that a reduction in disease risks has occurred in the population

of smokers due to the design changes that occurred in cigarettes over the

last 50 years.

This report reviews evidence on the FTC method for measuring tar and

nicotine yields and the disease risks of machine-measured low-tar cigarettes.

The evidence is derived from research on human behavior and exposures,

cigarette design and yields, smoke chemistry, epidemiological other and

population-based data on human disease risk. In conducting this review,

the objective was to determine whether the evidence taken as a whole

shows that the cumulative effect of engineering changes in cigarette design

over the last 50 years has reduced disease risks in smokers. Traditional scientific judgment requires compelling evidence of a difference before concluding that use of lower yield products reduces disease risk. These judgments

are especially important for harm reduction claims, as they may deter

smokers from cessation of tobacco use. Moreover, there have been previous

public policy statements on the likely benefits of lower yield products.

These prior statements may lead to confusion by creating an implication

that the appropriate standard for judgment would require proof of the

absence of an effect before the policy recommendations should be withdrawn. Given the consequences of being wrong on the advice given to

9

Chapter 1

Chapter 01 11/19/01 10:42 AM Page 9
10

smokers, the burden of proof should not be shifted from proving the presence of an effect. The perspective of this report is whether the existing evidence is sufficient to support claims that disease risks are reduced when

smokers switch to lower yield cigarettes and policy recommendations that

smokers who cannot quit should switch to these products. The answers to

these questions are that current evidence does not support either claims of

reduced harm or policy recommendations to switch to these products.

Many questions remain unanswered. For example, the disease risks of

recently introduced cigarettes or cigarette-like products are not known.

Similarly, the cancer risks for individuals who have only used low and ultralow cigarettes, and who may have different intensities of smoking as a

result, have yet to be fully described. Changes in age-specific lung cancer

death rates at younger ages in the United Kingdom suggest that the future

lung cancer experiences of these young smokers may differ from that of

prior generations of smokers. In addition, the possibility exists that individual product design changes, or future changes in tobacco industry produced

nicotine delivery devices, may reduce disease risks in the future. However,

the burden of proof for these benefits must remain with those who would

make the claims. The proof must integrate both measurements of dose and

measures of actual biological effect. The very real probability that addicted

smokers will seek out and rely upon the promised potential of reduced risk

for products that allow continued smoking creates an obligation to require

clear scientific proof of harm reduction claims before they are communicated to potential product users.

CONCLUSIONS

1. Epidemiological and other scientific evidence, including patterns of

mortality from smoking-caused diseases, does not indicate a benefit to public health from changes in cigarette design and manufacturing over the last

fifty years.

2. For spontaneous brand switchers, there appears to be complete compensation for nicotine delivery, reflecting more intensive smoking of loweryield cigarettes.

3. Widespread adoption of lower yield cigarettes in the United States

has not prevented the sustained increase in lung cancer among older smokers.

4. Many smokers switch to lower yield cigarettes out of concern for

their health, believing these cigarettes to be less risky or to be a step toward

quitting. Advertising and marketing of lower yield cigarettes may promote

initiation and impede cessation, more important determinants of smokingrelated diseases.

5. Measurements of tar and nicotine yields using the FTC method do

not offer smokers meaningful information on the amount of tar and nicotine they will receive from a cigarette. The measurements also do not offer

meaningful information on the relative amounts of tar and nicotine exposure likely to be received from smoking different brands of cigarettes.

Smoking and Tobacco Control Monograph No. 13

Chapter 01 11/19/01 10:42 AM Page 10
Chapter 1

11

REFERENCES

Benowitz, N.L. Biomarkers of cigarette smoking. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.

7. U.S. Department of Health and Human

Services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 96-4028,

1996.

Benowitz, N.L., Hall, S.M., Herning, R.I., Jacob, P.,

Jones, R.T., Osman, A. Smokers of low-yield cigarettes do not consume less nicotine. New England

Journal of Medicine 309(3):139-42, 1983.

Burns, D., Lee, L., Shen, Z., Gilpin, B., Tolley, D.,

Vaughn, J., Shanks, T. Cigarette smoking behavior in the United States. Changes in CigaretteRelated Disease Risks and Their Implication for

Prevention and Control. Smoking and Tobacco

Control Monograph No. 8. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 97-4213, 1997.

Cohen, J. B. Consumer/smoker perceptions of

Federal Trade Commission tar ratings. The FTC

Cigarette Test Method for Determining Tar, Nicotine,

and Carbon Monoxide Yields of U.S. Cigarettes.

Report of the NCI Expert Committee. Smoking and

Tobacco Control Monograph No. 7. U.S.

Department of Health and Human Services,

National Institutes of Health, National Cancer

Institute, NIH Publication No. 96-4028, 1996a.

Cohen, J. B. Smokers’ knowledge and understanding

of advertised tar numbers: Health policy implications. American Journal of Public Health 86(1):18-

24, 1996b.

Doll, R., Hill, A.B. A study of the aetiology of carcinoma of the lung. British Medical Journal 2:1271-

1286, 1952.

Doll, R., Hill, A.B. The mortality of doctors in relation to their smoking habits: A preliminary

report. British Medical Journal 1(4877):1451-1455,

1954.

Doll, R., Peto, R., Wheatley, K., Gray, R., Sutherland,

I. Mortality in relation to smoking: 40 years’

observations on male British doctors. British

Medical Journal 309(6959):901-911, 1994.

Giovino, G.A., Tomar, S.L., Reddy, M.N., Peddicord,

J.P., Zhu, B.P., Escobedo, L.G., Eriksen, M.P.

Attitudes, knowledge, and beliefs about low-yield

cigarettes among adolescents and adults. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.

7. U.S. Department of Health and Human

Services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 96-4028,

1996.

Goodman, B. to Meyer, L.F. September 17, 1975.

Memo by Barboro Goodman. Marlboro—

Marlboro Lights study delivery data. Bates No.

2021544486.

Green, S.J. Research conference held at Hilton Head

Island, S.C. September 24th-30th, 1968.

University of California San Francisco Tobacco

Archive Document I.D. No. 1112.01, 1968.

Hammond, E.C., Horn, D. Smoking and death

rates—Report on forty-four months of follow-up

of 187,783 men. II. Death rates by cause. Journal

of the American Medical Association 166:1294-

1308, 1958.

Jarvis, M.J., Boreham, R., Primatesta, P., Feyerabend,

C., Bryant, A. Nicotine yield from machinesmoked cigarettes and nicotine intakes in smokers: Evidence from a representative population

survey. Journal of the National Cancer Institute

93(2):134-138, 2001.

Mannino, D.M., Ford, E., Giovino, G.A, Thun, M.

Lung cancer mortality rates in birth cohorts in

the United States from 1960 to 1994. Lung

Cancer 31(2-3):91-99, 2001.

Pepples, E. Industry response to cigarette/health controversy. Memo dated February 4, 1976.

University of California San Francisco Tobacco

Archive Document I.D. No. 2205.01, 1976. 

Pillsbury H.C. Review of the Federal Trade

Commission Method for determining cigarette

tar and nicotine yield. The FTC Cigarette Test

Method for Determining Tar, Nicotine, and Carbon

Monoxide Yields of U.S. Cigarettes. Report of the

NCI Expert Committee. Smoking and Tobacco

Control Monograph No. 7. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 96-4028, 1996.

Thun, M.J., Heath, C.W. Changes in mortality from

smoking in two American Cancer Society

prospective studies since 1959. Preventive

Medicine 26(4):422-426. 1997.

Thun, M., Myersm D., Day-Lallym C., Myers, D.G.,

Calle, E., Flanders, W.D., Zhu, B.P., Namboodiri,

M., Heath, Jr, C. Trends in tobacco smoking and

mortality from cigarette use in Cancer

Prevention Studies I (1959 through 1965) and II

(1982 through 1988). Changes in Cigarette-Related

Disease Risks and Their Implications for Prevention

and Control. Smoking and Tobacco Control

Monograph No. 8. U.S. Department of Health

and Human Services, National Institutes of

Health, National Cancer Institute, NIH

Publication No. 97-4213, 1997.

U.S. Congress. Hearings before the Consumer

Subcommittee of the Committee on Commerce.

Senate, 90th Congress, August 23-24, 1967.

Chapter 01 11/19/01 10:42 AM Page 11
Smoking and Tobacco Control Monograph No. 13 

12

U.S. Department of Health and Human Services. The

Health Consequences of Smoking: Nicotine

Addiction. A Report of the Surgeon General.

Washington, D.C.: U.S. Department of Health

and Human Services, Public Health Service,

Centers for Disease Control and Prevention,

Center for Health Promotion and Education,

Office on Smoking and Health, DHHS

Publication No. (CDC) 88-8406, 1988.

Wakeham, H. to Cullman, H. March 24, 1961.

Memo by Hugh Wakeham. Trends in tar and

nicotine deliveries over the last 5 years. Bates

No. 1000861953.

Wynder, E.L., Graham, E.A. Tobacco smoking as a

possible etiologic factor in bronchogenic carcinoma. A study of six hundred and eighty-four

proved cases. Journal of the American Medical

Association 143:329-336, 1950.

Wynder, E.L., Graham, E.A., Croninger, A.B.

Experimental production of carcinoma with cigarette tar. Cancer Research 13:855-864, 1953.

Chapter 01 11/19/01 10:42 AM Page 12
The modern low-yield cigarette is defined by a standardized smoking-machine test commonly referred

to as the FTC method (Peeler, 1996), based on the

Federal Trade Commission protocol. This smoking-machine procedure simulates a precise manner of smoking by fixing puff size (35 ml), puffing rate

(once per minute), puff duration (2 seconds), and butt length to which the

cigarette is smoked (23 mm on an unfiltered cigarette or overwrap, plus 3

mm on a filtered cigarette). The number of puffs to be taken is not specified. The standard yields of tar and nicotine measured are reported in cigarette advertising (according to a cooperative agreement) and on some very

low-tar cigarette packs (as measured by the FTC method) at the manufacturer’s discretion (Peeler, 1996; Kozlowski et al., 1998c). Carbon monoxide

(CO) is also measured, but is not reported in advertising. The same basic

methodology is used for cigarette testing in Canada, Australia, and the

United Kingdom. In the United States, cigarette brands yielding approximately 1-5 or 6 mg tar by this standard method are generally called ‘UltraLight’; brands yielding between approximately 6 or 7-15 mg tar are called

‘Light’; and brands yielding more than 15 mg tar are called ‘Regular’ or ‘Full

Flavor’. By convention, cigarettes yielding 15 mg tar by the FTC method are

called ‘low tar’. 

The origins of the FTC method can be found in the early efforts of

tobacco industry researchers to compare cigarettes of the day. They arbitrarily selected the smoking parameters of a 35-ml puff volume, a 2-second puff

duration, and a one-puff-per-minute frequency (Bradford et al., 1936). At

the time, nearly all cigarettes were unfiltered, lacked overwraps, and were of

similar length, weight, and circumference; presumably, most had similar

burn times, a characteristic closely related to the number of puffs taken.

The past 30 years has seen dramatic growth of variation in the physical

characteristics of cigarettes, with differences in circumference (‘slims’ to

‘wides’), length (70-120 mm), and weights. 

Each year since 1968, the FTC has reported salesweighted yields of tar and nicotine based on the

FTC protocol (Table 2-1). Average sales-weighted standard tar yield

decreased from 21.6 mg in 1968 to 12.0 mg in 1997 (44.4 percent), while

average sales-weighted nicotine yield decreased from 1.35 mg to 0.89 mg

(34.1 percent). Though standard tar and nicotine yields have the status of

official FTC data, it would be wrong to assume that these numbers have any

bearing on smoker exposure to tar and nicotine.

CHANGES IN FTC MACHINESMOKED YIELDS OVER TIME

CIGARETTE-YIELD TESTING

BY SMOKING MACHINE

USING THE FTC PROTOCOL

13

Cigarette Design 

Lynn T. Kozlowski, Richard J. O’Connor, Christine T. Sweeney

Chapter 02 11/19/01 10:52 AM Page 13
Smoking and Tobacco Control Monograph No. 13

Table 2-1

Sales-Weighted Tar and Nicotine Yields: 1968-1997

Year Tar(mg) Nicotine (mg) Tar/Nicotine

1968 21.6 1.35 16.00

1969 20.7 1.38 15.00

1970 20.0 1.31 15.27

1971 20.2 1.32 15.30

1972 19.9 1.39 14.32

1973 19.3 1.32 14.62

1974 18.4 1.24 14.84

1975 18.6 1.21 15.37

1976 18.1 1.16 15.60

1977 16.8 1.12 15.00

1978 16.1 1.11 14.50

1979 15.1 1.07 14.11

1980 14.1 1.04 13.56

1981 13.2 0.92 14.35

1982 13.5 0.89 15.17

1983 13.4 0.88 15.23

1984 13.0 0.89 14.61

1985 13.0 0.95 13.68

1986 13.4 0.93 14.41

1987 13.3 0.94 14.15

1988 13.3 0.94 14.15

1989 13.1 0.96 13.65

1990 12.5 0.93 13.44

1991 12.6 0.94 13.40

1992 12.4 0.92 13.48

1993 12.4 0.90 13.78

1994 12.1 0.90 13.44

1995 12.0 0.87 13.79

1996 12.0 0.88 13.64

1997 12.0 0.89 13.48

Changes in cigarette design have produced the

reductions in standard yields of tar and nicotine

measured over the past several decades. Although it is unlikely that decreases in FTC tar yields of only a few milligrams are toxicologically consequential, cigarette manufacturers can manipulate variables that combine to make

small changes in yields or in the sensory effects of cigarettes. Such reformulations can have important policy implications. For example, changing a

cigarette slightly to reduce the standard tar yield from 16 mg to 15 mg

would increase the percentage of low-tar cigarettes on the market, and

thereby reduce sales-weighted tar levels. However, even without compensatory smoking, such a small change would likely have negligible effects on

health. 

Cigarette design manipulations intended to decrease standard yields can

be divided into those having two broad functional effects: 1) reducing the

number of puffs per cigarette, and 2) reducing the tar and nicotine concentration in smoke per puff (Kozlowski, 1983). Table 2-2 provides a summary

DESIGN CHANGES THAT

REDUCE STANDARD YIELDS

14

Chapter 02 11/19/01 10:52 AM Page 14
of these factors. Manufacturing cigarettes that produce lower FTC tar and

nicotine yields is a complex, multi-factorial process—a complicated recipe.

Manipulating one variable also affects other variables. Cigarette design

involves alteration of elements within a complex system. For example, if

one simply increased filter ventilation greatly, this would cause less tobacco

to be consumed with each standard puff, and thereby cause an increased

number of puffs. Altering design to increase the inter-puff burn rate (e.g.,

chemical treatments of the cigarette paper or using less tobacco) deals with

this issue (Philip Morris, 1980). 

The design features listed in Table 2-2 should not be considered ‘secrets’

of cigarette manufacture. Many of these design characteristics were discussed in a classic book on tobacco and tobacco smoke by Wynder and

Hoffman (1967) and more recently by Browne (1990). Journals such as

Beitrage Zur Tabakforschung and Tobacco Science have been available in

research libraries for decades. Research articles on such design features have

been published by various industry scientists (e.g., Parker and Montgomery,

15

Chapter 2

Table 2-2

Main Ways to Reduce Standard Tar and Nicotine Yields

A. Reduce the number of puffs taken by:

1) decreasing the length of the available tobacco column with 

a. longer filter overwraps,

b. longer filters;

2) increasing the burn rate of the column with

a. chemical additives in paper or tobacco,

b. higher porosity paper,

c. less tobacco (by weight), 

d. lower diameter tobacco column.

B. Reduce concentration of tar and nicotine per puff by:

1) increasing filter efficiency with

a. ventilated filters (by reducing tobacco amount/puff),

b. longer filters,

c. denser filters,

d. ‘active’ filters;

2) increasing air dilution of mainstream smoke with

a. ventilated filters,

b. higher porosity paper;

3) decreasing the density of tobacco with

a. reconstituted sheet tobacco,

b. puffed or expanded tobaccos,

c. flavorings (casings) and additives,

d. smaller circumference cigarettes;

4) tobacco blending with

a. use of lower nicotine yield tobacco strains,

b. flue-cured, burley, oriental tobaccos,

c. different parts/leaf positions of plants.

Chapter 02 11/19/01 10:52 AM Page 15
1979; Shoffner and Ireland, 1982). What is secret, however, is the exact formulation of a particular brand at any given time. Even if details are supplied in some of the formerly secret tobacco company documents, there is

no guarantee, for example, that the Marlboro Light® brand of 1985 is the

same in all attributes as the same named brand in 2000. 

Three design features that can influence standard yield will be discussed. They are: available length of tobacco (which relates to burn rate),

tobacco column nicotine content, and filter ventilation. 

Because the last few puffs on a cigarette have higher deliveries

than the first few puffs, eliminating the last puff by increasing

the burn rate has a relatively large effect on reducing tar and nicotine

yields. The FTC test method has never required the recording or reporting

of the number of puffs taken by the smoking machine, yet industry testing

of cigarettes has routinely done so. The official Canadian cigarette testing

laboratory (Labstat Incorporated, Kitchener, Ontario) has customarily collected the number of puffs taken by the machine for each cigarette smoked.

In one study, 12 best-selling Canadian cigarette brands were shown to have

decreased from 9.8 to 8.8 puffs per cigarette (a 10 percent reduction)

between 1969 and 1974; during the same period, tar yield decreased 13.6

percent, from 22 mg to 19 mg (Kozlowski et al., 1980b). 

There is some evidence that increases in the length of the overwrap (the

distinctive paper wrap covering the outside of the filter) have been used to

decrease the number of puffs taken (Grunberg et al., 1985). Other things

being equal, a longer “filter plus overwrap” will result in a longer butt being

left in the smoking machine. However, tobacco exists under the overwrap

that is still available to be smoked by the human smoker. This additional

tobacco would not be burned in the FTC test, resulting in a lower standard

yield, but a potentially higher yield for the actual smoker. 

Different types of tobacco can contain different amounts of

nicotine, with burley being the highest and flue-cured tobacco

being somewhat lower. Oriental tobaccos and reconstituted tobacco sheet

have substantially lower nicotine contents. Different parts of the same

tobacco plant can contain different nicotine levels based on stalk position,

soil nitrogen, and the curing process. Blends of tobacco strains and tobacco

from particular segments can contribute to the blend of a particular cigarette brand. These blends, combined with the use of fillers, additives, and

reconstituted sheet tobacco in the tobacco column of cigarettes, can lead to

differences in nicotine contents among brands. Kozlowski and colleagues

(1998b) measured the nicotine content of the “tobacco column” (a complex

of tobacco, reconstituted sheet, flavorings, and casings) in American,

British, and Canadian cigarette brands. On the whole, American cigarette

brands contained less nicotine per cigarette (10.2 mg ± 0.25 SEM) than

either British (12.5 mg ± 0.33 SEM) or Canadian (13.5 mg ± 0.49 SEM)

brands (p < 0.008). Among American brands, nicotine contents ranged from

a high of 13.4 mg (Newport Full-Flavor®) to a low of 7.3 mg (GPC Lights®).

The nicotine content of Canadian brands ranged from a high of 18.3 mg

(Players Extra Light®) to a low of 8.0 mg (Players Full Flavour®), while

Nicotine Content 

of Tobacco

Available Length

of Tobacco

16

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 16
British brands ranged from a high of 15.9 mg (Knightsbridge® Super King)

to a low of 9.0 mg (Dorchester®). Brands with the lowest standard nicotine

yield (0.1 mg), such as Carlton®, Carlton® 100, Merit Ultima®, and Craven

Ultra-Mild®, contained between 8.7-11.2 mg nicotine per cigarette

(Kozlowski et al., 1998b). 

These same authors found a significant positive correlation (r = 0.51

[95% CI = 0.20–0.73]) between brand FTC nicotine yield and the nicotine

content of tobacco. In 1997, the state of Massachusetts required testing of

the best-selling cigarettes (N = 15 brand groups) for nicotine content of

whole tobacco (American Cancer Society, 2000). This testing showed no significant differences between brand categories (Full Flavor, Light, or UltraLight). This discrepancy in the relationship between standard yields and

nicotine content may be due to the exclusion of poor-selling, very low FTC

tar brands from the Massachusetts sample. But substantial differences in

nicotine content of tobacco were nonetheless found between some brands.

Values ranged from a low of 8.3 mg for GPC Lights® King Size to a high of

15.48 mg for Marlboro® 100 Soft Pack (an 87 percent difference—low to

high), which cannot be viewed as a small difference. Note that Kozlowski

and associates (1998b) found an 84 percent difference between the lowest

and highest nicotine content observed (see above).

Filter Ventilation Although each of the manufacturing changes listed in Table 2-2

(including those intended to reduce the number of puffs per cigarette) has

contributed to the development of lower tar and nicotine cigarettes, filter

ventilation has been the major innovation behind the modern low-yield

cigarette (Kozlowski, 1983; Kozlowski et al., 1998b). Filter vents, which usually are one or more rings of small holes or perforations, serve to dilute

smoke with air, thereby reducing standard yields of tar, nicotine, and CO. 

A 1956 Philip Morris memo to the company’s most senior executives

maintained that ventilation could serve as a “counter-attack” to negative

health claims about smoking because it reduced “smoke solids,” CO, and

irritation (DuPuis, 1956). 

Vents are placed in the filter by one of three main processes: electrostatic perforation, mechanical perforation, or laser perforation (Helms, 1983;

Helms and Lorenzen, 1984). The method of perforation can influence actual tar and nicotine delivery to the smoker (this issue will be addressed further in the next section). Whatever the method of perforation, the location

of filter vents generally ranges from 11 to 15 mm from the mouth end of

the filter. In a recent study, the filter ventilation levels of 32 U.S. cigarette

brands were tested and found to range from 0 to 83 percent (Kozlowski et

al., 1998b). A cigarette with 0 percent filter ventilation would produce a

puff of smoke undiluted by air from filter vents. A cigarette with 83 percent

filter ventilation would produce a puff that is 83 percent air from vents and

17 percent smoke undiluted by air from vents. 

Increases in ventilation appear to have been important in meeting the

tar-yield maximum in the European Economic Community. Internal Philip

Morris documents indicated that the company’s strategy for reducing the

17

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 17
smoke deliveries of its Marlboro® brands in Europe rested primarily on

increasing filter ventilation (Stolt, 1977). Tests have shown that Full-Flavor

Marlboro® cigarettes are now twice as ventilated in the United Kingdom as

in the United States (19.5 versus 10.2 percent); similar differences are seen

for Marlboro Light® (44.9 versus 22.5 percent) (Kozlowski et al., 1998b).

The observed decreases in standardized

yields of tar and nicotine that have

occurred since 1968 do not seem to

translate into reduced exposures for smokers. Smokers can consciously or

unconsciously compensate for lower standard yields in a number of easy

and effective ways. 

Increasing Puff Number Of course, smokers are not limited in the number of

puffs they may take from a cigarette. Smokers can counteract yield reduction methods that reduce puff number simply by taking more puffs per cigarette. If smokers receive less tar and nicotine per puff from lower yield

products, they can easily compensate by taking more puffs or, of course,

smoking more cigarettes per day. Across 32 studies cited by the Surgeon

General (U.S. DHHS, 1988), the average of the mean inter-puff intervals was

34 seconds, with a range of 18-64 seconds. This contrasts with the 58-second inter-puff interval used with the FTC method. Naturally, the actual

range of inter-puff intervals would be much larger than this range of

means. Results from a recent laboratory study revealed that smokers of lowyield (≤ 0.8 mg nicotine by FTC method) and high-yield (0.9-1.2 mg nicotine by FTC method) cigarette brands had significantly shorter inter-puff

intervals (about 20 seconds) than those of the FTC protocol (Djordjevic et

al., 2000). Clearly, smokers often take more than one puff per minute and

can thereby increase their actual yield. 

Increasing Puff Volume A major and easy way for the smoker to increase smoke

intake is to increase the volume of each puff. Total puff volume per cigarette is a function of puff number and volume per puff. In terms of overall

exposure, total volume per cigarette is a better index and gives insight into

how much ‘work’ the smoker performed in smoking the cigarette. Smokers

are free to take large or small puffs on their cigarettes. The 32 studies summarized in the Surgeon General report (U.S. DHHS, 1988) confirmed that

puff volumes often deviate from the FTC standard. The average of mean

puff volumes across the studies was 43 ml, with a range of 22-66 ml. Again,

because these represent ranges of means, the actual ranges of individual

scores would be broader. 

Published studies confirm that smokers will change their puff sizes in

response to the type of cigarette that they smoke. Herning and associates

(1981) studied smokers who were smoking the first cigarette of the day.

These smokers showed larger puff volumes on the low-nicotine cigarettes

(47.8 ml) than on either the medium- or high-nicotine cigarettes (35.9 ml

and 36.9 ml, respectively). Among 10 participants studied by Tobin and

Sackner (1982), larger puff volumes were taken from the low-tar cigarettes

(52 ml) than from the high-tar cigarettes (39 ml) (P < 0.001). A study by

Moody (1980) reported a mean puff volume of 43.5 ml. Djordjevic and colCOMPENSATION AND CIGARETTE

DESIGN: DIFFERENCE IN YIELD WITH

DIFFERENT SMOKING PATTERNS

18

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 18
leagues (2000) recently reported that the average volumes of smoke per puff

for smokers of low-yield and medium-yield cigarette brands were 48.6 ml

and 44.1 ml, respectively. Other investigators have noted similar findings

(e.g., Zacny et al., 1986, 1987; Zacny and Stitzer, 1988). These studies

showed that the FTC test underestimates the volume of smoke taken from

lower tar cigarettes. Industry studies show that smokers often take far more

in total volume of smoke than is predicted by the FTC test. In two separate

Philip Morris studies, smokers (one in each study) independently took nearly 1,400 ml of smoke from Carlton® cigarettes, in both cases nearly five

times the expected FTC value for a whole cigarette (Wakeham, 1974; Kelley,

1977). 

Additionally, unpublished industry research revealed that puff volumes

increase as standard yields decrease (see Norman and Ihrig, 1980a & b, at

Lorillard, discussed later in the chapter). Clearly, puff volume changes represent a significant and easy mode of compensation for low-yield products. 

Dilution and Puff Volume As discussed earlier, filter ventilation dilutes smoke

with air. One way for the smoker to compensate for the reduced nicotine

delivery that results from air dilution is to increase puff volume. If a smoker

increases puff volume, he or she will receive more smoke from the cigarette

along with more air. This larger puff might feel ‘lighter’ to the smoker than

if they had taken a smaller, more concentrated puff of equivalent yield

from an unventilated or less-ventilated cigarette. This effect of ‘softening’

the taste or reducing the harshness of taste may be an important reason for

the perception of ‘lightness’ in lower standard-yield cigarettes (Kozlowski et

al., 1998a, 1999, 2000).

Consider a simplified model of ventilation and puff volume. A curvilinear relationship exists between the level of dilution and the puff volume

needed to compensate for reduced yield (Sutton et al., 1978). The formula

for puff volume percentage increase needed to compensate is as follows:

percentage increase in puff volume = (% dilution/[100 – % dilution]) x 100.

As dilution increases, puff volume to compensate increases exponentially.

According to Kozlowski and colleagues (1998b), for a cigarette with 13 percent dilution (e.g., Marlboro® Full Flavor), a small puff volume increase (15

percent, from 35 ml to 40 ml) would provide full compensation for the

dilution. To compensate fully for a 40 percent diluted cigarette (e.g.,

Virginia Slims Light® 100), a puff volume of 58 ml (a 67 percent increase)

would be needed. In contrast, with a highly ventilated cigarette such as

Carlton® 100 (83 percent diluted), a large and generally impractical puff

volume of 206 ml would be required. These estimates assume a 35 ml base

puff (the base puff is what is assumed to occur with no ventilation). For

those with a 45 ml base puff, a heroic puff of 265 ml would be required to

compensate for the 83 percent dilution on the 1 mg tar cigarette. The bestselling Marlboro Light® cigarette is just 23 percent diluted, and an easy puff

of about 60 ml (from a 45 ml base) or only 45 ml (from a 35 ml base)

would fully compensate. Increased puff volume is a very likely mode of

compensation when it can be performed without significant additional

effort (i.e., for a Light cigarette with low-to-moderate air dilution). For a

19

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 19
heavily ventilated cigarette (e.g., 83 percent diluted, 1 mg tar), increasing

per-puff volume within acceptable bounds of comfort and effort alone will

not generally provide full or even substantial compensation. (Of course,

smokers are not constrained to simply take bigger puffs; they may also take

more puffs; for more, see Kozlowski et al., 1998b.) 

The phenomenon of compensating with bigger puffs is well known to

industry scientists. For example, Norman and Ihrig (1980a) of Lorillard conducted a series of studies concerning puff volumes and puff velocities on

lower tar cigarettes being greater than those for higher tar cigarettes. These

authors assumed that ultralow-tar brands were more palatable to the smoker if compensatory smoking required a modest amount of additional effort.

To describe this effort, they derived the “puffing power function” (Norman

and Ihrig, 1980b), defined as the product of the flow rate through the cigarette and pressure drop required to produce that flow. 

These authors examined the relationship between puffing power functions (expressed in ‘puffing power units’ or PPU) and puffing regimens (at

standard FTC 35 ml as well as 50 ml puffs). The increase in PPU represented

the “extra effort needed to obtain a given amount of additional [tar] from

the cigarette” (Norman and Ihrig, 1980b). They thought that an understanding of puffing effort is critical for very low-yield brands, since these

are most likely to be smoked with extra effort to obtain more smoke. 

Increasing puff volume can have additional effects, especially if puff

velocity also increases. Other things being equal, a higher velocity puff (i.e.,

> 17.5 ml/sec) will reduce filter efficiency (i.e., the percentage of what

enters the filter that remains in the filter). Further, filter tip ventilation

decreases as flow rate increases. If the cigarette is ventilated with highporosity paper, however, the opposite is true—dilution increases with

increasing flow rate: 

“. . . [A] cigarette constructed with low paper porosity but with

filter tip ventilation would more readily allow a smoker to take a

higher delivery of smoke by increasing the velocity of puffing. Such

a cigarette construction would provide a marketing opportunity to

offer a LOW to LOW TO MIDDLE delivery product when smoked by

machine, which could be a LOW TO MIDDLE to MIDDLE delivery

product when smoked by the smoker.” 

. . . “Alternatively, if a cigarette is manufactured to have no filter

tip ventilation, but high paper porosity, the smoker would not be

able to compensate for reduced delivery by puffing harder; in fact,

the higher the velocity of the puff, the lower the delivery.

Theoretically the smoker would be able to increase delivery by

reducing his puffing velocity and increasing the duration of the

puff. This is unlikely to occur to any marked extent as it would

require a marked change of habit that would probably feel uncomfortable to the smoker.” (See Creighton, 1978a.) 

20

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 20
Air drawn through the vents dilutes the smoke, but also generally

reduces the draw resistance through the filter and tobacco rod (Creighton,

1978a). For example, Zacny and associates (1986) found that the average

“resistance to draw” (RTD—the amount of pressure that must be exerted on

the filter for inhalation) of an unblocked (i.e., fully ventilated) Now® cigarette was 92.5 mm H2O (for Kozlowski et al., 1998b, Now® was 66.3 percent

diluted). In contrast, the same cigarette fully blocked (i.e., unventilated) had

an RTD of 184.4 mm H2O, a 100 percent increase. This lower RTD for the

ventilated cigarette means the smoker can easily take a larger puff on the

cigarette with little added effort and receive more smoke from the cigarette.

Lower RTD, in effect, promotes the use of increased puff volume as a compensation method. Industry studies bear this observation out (Long, 1955;

Goodman, 1977; Creighton and Watts, 1972; Mendell, 1983). The air-diluted smoke would also be less irritating than the same smoke undiluted, and

thereby would also facilitate increased puff volumes because inhibitory oral

and respiratory cues would be milder. 

Additional industry research has looked at interactions between the

type of ventilation used and puff volume. A. B. Norman and others at R. J.

Reynolds Tobacco Co. compared laser, mechanical, and electrostatic perforation types (Norman et al., 1984). Laser perforations were found to promote compensation with increased puff volumes. That is, as puff volumes

increased, filter air dilution decreased most significantly with laser perforations. W. I. Casey (1994) at R. J. Reynolds explored yields from different

tobacco blends with perforations as “holes” versus “slots” (hole versus slot

is not defined). Cigarettes were tested according to FTC procedures as well

as “50/30” procedures (50 ml puff, every 30 seconds); brands had approximately equal air-dilution levels (80-85 percent). Two rows of slots gave the

same nicotine (0.11 mg) as did two rows of holes under FTC conditions, but

gave more nicotine under the 50/30 condition: 0.67 versus 0.53 mg.

Ventilation holes increased yield by 382 percent and ventilation slots

increased yield by 509 percent over FTC estimates, simply by increasing

puff volume and puff number. This effect of slots versus holes was not

found for another tobacco blend. Here, one can see that design features

(e.g., filter ventilation and tobacco blend) can interact dramatically with

smoker behavior (puff volume/puff interval) to produce more elastic products (i.e., giving low values to the smoking machine, but higher values to

smokers).

Blocking Filter Vents Another technique smokers can use to increase smoke concentration is the blocking of filter vents. Research has found that the majority of smokers are unaware of the presence of vents in general or even on

their own brands (Kozlowski et al., 1996, 1998d). At best, filter vents are

placed just millimeters from lips or fingers, and they are often not noticed

by smokers (Kozlowski et al., 1998d). Smokers can and do obstruct the vents

with either their lips or fingers, thereby diminishing or defeating the airdilution effect. The ease with which smokers can unknowingly compensate

for low standard yields by interfering with this important design feature has

long been known within the cigarette industry. Internal company documents from the British American Tobacco Co. indicate that the industry

acknowledges the importance of filter ventilation for designing products to

21

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 21
be compensatable or elastic. For example, in one document, this question

was asked—“Which product/design properties influence elasticity?” The

answer—“1. Tip ventilation: bigger effects at higher degree of ventilation. . .

2. Delivery of the blend . . .” (Brown & Williamson, 1984). 

The earliest of the published studies to examine the

effects of vent blocking used smoking machine estimates to simulate the effect of vent blocking. Blocking half the vents of a 4

mg tar cigarette, for example, increased the smoking-machine yields of tar

by 60 percent (from 4.40 to 7.03 mg), nicotine by 62 percent (from 0.45 to

0.73 mg), and CO by 73 percent (from 4.50 to 7.80 mg) (Kozlowski et al.,

1980a & b). Blocking all of the filter vents of these same cigarettes with

tape increased yields of tar by 186 percent (from 4.40 to 12.60 mg), nicotine by 118 percent (from 0.45 to 0.98 mg), and CO by 293 percent (from

4.50 to 17.70 mg). In another study, Kozlowski and colleagues (1982) completely tape-blocked the vents on different brands of 1 mg tar cigarettes

from Canada, the United States, and the United Kingdom. Cigarettes were

smoked more intensely in the blocked condition (2.4 second puff duration;

44 second puff interval; 47 ml puff volume). Tar yield increased from 1,360

percent (Cambridge® [0.8-11.7 mg]) to 3,800 percent (Viscount No. 1® [0.3-

11.7 mg]). Nicotine yield increased from 720 percent (Cambridge® [0.1-0.82

mg]) to 1,767 percent (John Player Ultra Mild® King Size [0.12-2.24 mg]).

Similarly, CO yield increased from 870 percent (Cambridge® [1.8-17.5 mg])

to 4,180 percent (John Player Ultra Mild® King Size [0.50-21.4 mg]) under

the more intense smoking conditions. Compare this to an unventilated reference cigarette, which saw yield increases of 46 percent for tar, 35.8 percent for nicotine, and 35.7 percent for CO under these intense conditions. 

In a 1983 study, Rickert and associates tested 36 brands of Canadian cigarettes (including 28 brands that had ventilated filters) on a smoking

machine under three experimental conditions to simulate how smokers’

exposure to toxic substances would be affected by smoking patterns of different intensities. In the ‘moderate’ condition (which was used to represent

more typical smoking behavior), puff volume was increased to 48 ml, puff

duration was increased to 2.4 seconds, and puff interval was reduced to 44

seconds. The parameters of the ‘intense’ condition were exactly the same as

the ‘moderate’ condition, except that 50 percent of the vent holes were

covered with tape. Comparing yields obtained under the moderate and

intense conditions, then, shows the effect of blocking 50 percent of filter

vents (Rickert et al., 1983). 

A secondary analysis of these data was performed on the 28 ventilatedfilter brands. These were divided into three standard yield bands: 1-2 mg tar

(n = 4), 3-5 mg tar (n = 11), and 6-14 mg tar (n = 13), roughly corresponding to Lowest Tar, Ultra-Light, and Light designations. Lowest Tar cigarettes showed a nicotine yield increase of 0.22 mg (130 percent), Ultra-Light

cigarettes showed an increase of 0.31 mg (57 percent), and Light cigarettes

showed an increase of 0.43 mg (36 percent). Lowest Tar cigarettes showed

an increase of 2.5 mg tar (160 percent), compared to a 4.0 mg tar (63 perEffects of Vent Blocking

on Smoke Exposure

22

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 22
cent) increase in Ultra-Light and a 5.5 mg tar (38 percent) increase in

Lights. CO yields in Lights were increased by 4.7 mg (36 percent), while

Ultra-Light brands increased 4.9 mg (75 percent) and Lowest Tar brands

increased 2.6 g (150 percent). 

Baker and colleagues (1998) presented an industry experiment on the

effects of differing degrees of vent blocking on smoke yields. Both Light

(9.3 mg tar, 0.89 mg nicotine, 8.7 mg CO at FTC conditions) and UltraLight (4.1 mg tar, 0.35 mg nicotine, 4.0 mg CO at FTC conditions) cigarettes were tested for the effect of vent blocking on yield under the FTC

protocol. The Light cigarette showed an increase of 0.8 mg tar (8.6 percent),

0.08 mg nicotine (9.0 percent), and 1.4 mg CO (16 percent) when smoked

with 50 percent of the vents blocked. The Ultra-Light cigarette showed an

increase of 1.1 mg tar (27 percent), 0.09 mg nicotine (26 percent), and 2.3

mg CO (57.5 percent) with 50 percent vent blockage (Baker et al., 1998). 

Baker and Lewis (1997) provided the results of previously unreleased

industry reports in which smoking machines were used to simulate the

effect of vent blocking with lips and fingers on tar yields. These estimates

were calculated assuming that the maximum coverage of filter vents is

approximately 50 percent for lips and 25 percent for fingers. These

researchers reported that blocking filter vents with fingers would increase

the total particulate matter (TPM—tar plus nicotine, minus water) of a 1.3

mg tar cigarette by 23 percent to 1.6; blocking vents on the same brand

with lips would increase the TPM by 92 percent to 2.5. Blocking filter vents

with fingers would increase the TPM of a 2.2 mg tar cigarette by 32 percent

to 2.9; blocking vents on the same brand with lips would increase the TPM

by 59 percent to 3.5. Blocking filter vents with fingers would increase the

TPM of a 6.7 mg tar cigarette by 10 percent to 7.4; blocking vents on the

same brand with lips would increase the TPM by 21 percent to 8.1. Note

that a negative relationship exists between tar yield and percentage of

increase in TPM (Baker and Lewis, 1997). 

Interestingly, the yield increases seen as a result of 50 percent blocking

were significantly different between the Rickert and associates’ (1983) and

the industry’s (Baker and Lewis, 1997; Baker et al., 1998) studies. For example, nicotine yield in Ultra-Light cigarettes increased 57 percent in the

Rickert and associates (1983) study, but only 26 percent in the Baker and

colleagues (1998) study. Similarly, Rickert and associates found a 63 percent

increase in tar, while Baker and colleagues found only a 27 percent increase.

Baker and Lewis (who downplayed the effects of vent blocking) found that

blocking 50 percent of vents caused a TPM increase of 59 percent, comparable to the Rickert results. However, they found a smaller effect for Lights

(38 percent versus 22 percent increase in tar). 

Why are there such discrepancies in the effects of vent blocking in

these studies? Perhaps smoking conditions contribute to the effect of vent

blocking. In the Rickert and associates (1983) study, cigarettes were smoked

at a larger puff volume with shorter intervals than the FTC conditions used

by Baker and colleagues (1998) and Baker and Lewis (1997). For example, to

approach the 57 percent increase in nicotine yield at 50 percent blockage of

23

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 23
Ultra-Lights seen by Rickert and associates, Baker and colleagues tested their

Ultra-Lights with 100 percent of vents blocked, and even here the yield

increase was only 51 percent. An alternative explanation is that the cigarette designs selected for use in the Baker and colleagues study may be more

resistant to the effect of vent blocking. 

Zacny and associates (1986) evaluated the effect of vent blocking on

smoke exposure in smokers. They found that blocking 0 percent, 50 percent, and 100 percent of the filter vents on a 1 mg tar cigarette with tape,

while holding all other smoking parameters as constant as possible,

increased CO exposure in an orderly fashion. Mean CO boosts (post-cigarette expired air CO level minus pre-cigarette expired air CO level) were

0.83 ppm, 2.87 ppm, and 7.07 ppm when 0 percent, 50 percent, and 100

percent of the filter vents were blocked. 

This research was extended by Kozlowski and colleagues (1996b) to

assess the effect of a behavioral vent blocking maneuver (i.e., blocking vents

with lips) on smoke exposure from the 1 mg tar Ultra-Light brand, Now®.

Blocking filter vents with lips (estimated to be about 50 percent blockage)

more than doubled the CO exposure from these cigarettes: CO boosts for

the unblocked, lip-blocked, and 100 percent tape-blocked conditions averaged 2.7 ppm (SE = 0.52), 6.7 ppm (SE = 1.0), and 12.9 ppm (SE = 2.2),

respectively. 

Sweeney and Kozlowski (1998) examined the effect of blocking the filter

vents of the best-selling cigarette brand, Marlboro Light®. CO boosts for the

unblocked, lip-blocked, tape-blocked (50 percent coverage), and fingerblocked conditions were remarkably similar: 5.0 ppm (SE = 0.47), 4.9 ppm

(SE = 0.86), 4.8 ppm (SE = 0.47), and 4.9 ppm (SE = 0.50), respectively. This

“no-effect” finding for Marlboro Light® was subsequently replicated in a

second study comparing the effects of finger-blocking and not blocking: the

mean CO boosts for the unblocked and finger-blocked conditions were

nearly identical: 6.3 ppm (SE = 0.50) and 6.5 ppm (SE = 0.52). In this same

study, finger-blocking the vents on the 1 mg tar brand Now® led to a significantly higher (P = 0.0004) CO boost (5.4 ppm, SE = 0.64) than when filter

vents were not blocked (2.8 ppm, SE = 0.34). 

Puff number, puff duration, and puff interval were all controlled in

these studies to examine the independent effects of vent blocking on smoke

exposure. What type of an effect does vent blocking have on smoke exposure under more naturalistic conditions when parameters such as puff number and puff duration are free to vary? Zacny and associates (1986) explored

this question with five smokers who smoked 1 mg tar cigarettes ad lib (i.e.,

puff and inhalation parameters were free to vary) under each of three vent

blocking conditions: 0 percent of the filter vents blocked; 50 percent of filter vents blocked with tape; and 100 percent of filter vents blocked with

tape. Participants took significantly more puffs with significantly shorter

interpuff intervals from cigarettes with unblocked filter vents than from cigarettes with blocked filter vents. Puff durations were similar across conditions, but puff volumes were larger when subjects smoked cigarettes with

24

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 24
unblocked filter vents than when smoking cigarettes with blocked filter

vents. Smokers were trying to compensate for smoke dilution by smoking

the unblocked cigarettes more intensely. Nevertheless, participants still had

greater CO exposure when smoking vent-blocked as compared with

unblocked cigarettes, indicating that compensation was not complete.

Mean CO boosts were 4.32 ppm, 6.44 ppm, and 8.96 ppm, when 0 percent,

50 percent, and 100 percent of filter vents were blocked, respectively (standard errors of the mean were not reported). 

The two most recent studies in this area (Sweeney and Kozlowski, 1998;

Sweeney et al., 1999) further extended this research by examining the

effects of behavioral vent-blocking maneuvers under ad lib smoking conditions. In the first study, participants smoked cigarettes from the brands

Now® (1 mg tar by FTC method) and Marlboro Light® (10 mg tar by FTC

method) under each of two vent-blocking conditions: unblocked and finger

blocked. Blocking filter vents with fingers led to an 85 percent increase in

CO exposure from Now®, but had no added effect on CO exposure from

Marlboro Light®. The generalizability of these findings to all brands of

Ultra-Light and Light cigarettes is limited, however, given that only one

brand from each category was examined. A second study examined the

effects of vent blocking using several cigarette brands of varying ventilation

levels and standard tar yields. In a repeated-measures study with female

daily cigarette smokers, the effect of lip-blocking on CO exposure was

examined using four cigarette brands: Carlton® (1 mg FTC tar; 83 percent

ventilated), Now® (2 mg FTC tar; 66 percent ventilated), Virginia Slims

Ultra-Light® (5 mg FTC tar; 56 percent ventilated), and Virginia Slims Light®

(8 mg FTC tar; 40 percent ventilated). Results showed that behavioral blocking caused all four brands to produce similar CO exposures. Blocking vents

increased smokers’ exposure to CO by 239 percent when smoking Carlton®

and by 44 percent when smoking Now®. No significant increases in CO

exposure with blocking were found for either of the Virginia Slims® brands. 

The previous studies have used CO measures as an index of vent blocking because they are more practical and easy to obtain. However, one study

has obtained salivary cotinine levels from self-selected 1 mg tar cigarette

smokers (Kozlowski et al., 1989). Here, large cotinine values were found in

smokers who blocked the vents of 1 mg tar cigarettes; these values are larger

than would be expected given the standard yield of their product and

appear to compensate fully for that reduced yield. No other studies have

been identified that investigated the effects of vent blocking on nicotine or

cotinine levels. Obviously, further studies must be conducted on nicotine

intake before concluding that vent blocking in Light cigarettes is inconsequential to exposure.

Published, peer-reviewed research has shown that a substantial proportion of smokers block vents. Using an unobtrusive indicator of

vent blocking (stain pattern; discussed below), one study found that 58 percent of 135 cigarette filters from various Ultra-Light brands (4 mg tar or

less) gave evidence of at least some vent blocking (Kozlowski et al., 1988).

Using similar procedures, another study found evidence of vent blocking in

Prevalence of 

Vent Blocking

25

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 25
53 percent of 158 filters of Light brands that were collected (Kozlowski et

al., 1994). In a study of ‘high-risk’ smoking practices used by the homeless,

Aloot and colleagues (1993) found that 24 percent reported blocking filter

vents (Aloot et al., 1993). 

The stain pattern technique for determining vent-blocking is straightforward. Trained raters observe the mouth ends of cigarette butts and judge

whether or not vent blocking has occurred based on the extent of the tar

stain on the filter. A “bull’s eye” pattern on the filter indicates that little or

no vent blocking occurred, while a more uniform pattern across the filter

would indicate that filter vents had been blocked. This technique has been

validated and has been shown reliable on a number of brands (e.g.,

Carlton®, Now®, Merit Ultima®, Camel Light®) through numerous refinements (Kozlowski et al., 1980a & b; Pillitteri et al., 1994; Sweeney, 1998). It

must be stressed that this technique detects the presence or absence of any

vent blocking with either fingers or lips. It should not be used to indicate

the extent of vent blocking. 

Industry scientists have objected to the use of the stain pattern technique (Baker and Lewis, 1997). They criticize raters’ accuracy in judging the

presence or absence of blocking and allege that the properties of laser-perforated filter vents produce variant patterns. Instead, the industry touts salivabased measurements of lip placement around the ventilation zone as a better gauge of vent blocking. These techniques use ninhydrin and other biochemical stains to detect remnants of saliva in filters. These saliva-based

techniques can detect vent blocking, but are impaired by factors such as lip

dryness and so may underestimate its extent. Advocates of saliva-based

measures admit that the technique often can fail to give a lip imprint stain

for up to 20 percent of butts (Baker et al., 1998). Another limitation of the

saliva-based measures is that they will only detect lip blocking, totally

ignoring finger blocking (unless the fingers have saliva on them). 

During more than 15 years of published research on vent blocking, no

formal response from the industry was put forth. In 1997, Baker and Lewis,

two industry scientists, published their critique of peer-reviewed work on

the subject. Their assertions were that: 1) vent blocking is not a significant

mode of compensation because it does not occur often; 2) when vent blocking does occur, it hardly increases yields; and 3) mouth insertion depths of

cigarettes do not differ greatly for ventilated and unventilated cigarettes. 

Between 1974 and 1997, 10 studies were conducted by the tobacco

industry in an attempt to measure the depth to which smokers insert cigarettes into their mouths by examining spent cigarette filters from public

areas, such as shopping malls (Baker and Lewis, 1997). In these studies, a

visible imprint of the lip marks on the filter was obtained by spraying the

filter with either iodine or ninhydrin solutions to detect certain enzymes

and amino acids in dried saliva on the filter. Across 10 studies, insertion

depth measures ranged from 3 to 25 mm, with mean values ranging

between 10.1 and 11.5 mm. Using both mouth insertion data based on

2,232 cigarette butts from a pair of 1997 Canadian studies, as well as information on ventilation zone location for leading U.S. brands, Baker and

26

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 26
Lewis (1997) estimated the proportion of smokers that would cover filter

vents while smoking. They concluded that 36 percent of smokers will cover

vents for at least one puff when they are placed at 11 mm, versus 6 percent

of smokers who will cover the vent holes in at least one puff with ventilation zones positioned 17 mm from the mouth end of the filter. 

Brands vary greatly in the placement of vents on the filter, and vent

placement can bear little relationship to the standard yield of the cigarette.

For example, a Marlboro® Full Flavor (16 mg tar) has vents at 12.5 mm from

the mouth end, whereas a Carlton® (1 mg tar) has vents at 15 mm. Merit

Ultima® (1 mg tar) has vents at 11.0 mm, whereas Camel® Full Flavor (17

mg tar) has vents at 14.5 mm (Kozlowksi et al., 1997).

In an unpublished study by Röper (cited in Baker and Lewis, 1997), an

attempt was made to assess more directly the prevalence of lip blocking by

having 52 smokers take 1 puff on 5 cigarettes from each of 3 ventilated-filter brands. Of the 735 visible lip imprints that were obtained, 48 percent

had at least some coverage of the ventilation zone. 

Baker and colleagues (1998) examined 900 British smokers’ filters for

evidence of vent blocking using saliva-based techniques. They report that

15 percent of butts had at least partial vent coverage, while 85 percent

showed no vent zone coverage. More interesting, however, are differences

in coverage and insertion depth among standard (unventilated), Light, and

Ultra-Light cigarettes. Light cigarettes showed partial coverage in 11.5 percent of cases and complete coverage in 1.5 percent of cases. In contrast,

Ultra-Light cigarettes showed partial coverage in 9.6 percent of cases and

complete coverage in 6.5 percent of cases. Further, standard cigarettes were

inserted a mean of 7.8 mm (SD = 3.6) into a smoker’s mouth, whereas

Ultra-Light cigarettes were inserted a mean of 9.5 mm (SD = 5.0) into the

mouth; in these cigarettes, the vents were placed 13.5-14.5 mm from the

mouth end (Baker et al., 1998). 

Porter and Dunn (1998) of Imperial Tobacco examined butts collected

in Montreal, Toronto, and Vancouver, Canada, for signs of vent blocking by

examining mouth insertion depths. They found that the difference in insertion depths between ventilated and unventilated cigarettes was negligible

(10.6 ± 3.6 mm versus 11.0 ± 3.6 mm). Further, they found that between 14

percent and 20 percent showed some evidence of partial vent coverage,

whereas between 4 and 10 percent showed evidence of complete blockage

(Porter and Dunn, 1998). In a similar study, McBride (1985), also of

Imperial Tobacco, found that there were no significant differences in insertion depths between ventilated and unventilated cigarettes. However,

McBride noted that “insertion depths were greatest for cigarettes in the very

low delivery category.” (McBride, 1985)

A study by British American Tobacco/Suisse (1984) examined the depths

to which smokers inserted cigarettes into their mouths. Baker and Lewis

(1997) cited this study along with several others as evidence that insertion

depths are not large enough to interfere with ventilation in most cases.

However, further examination of the results revealed that an interesting

effect was obscured—insertion depths were greatest for the lowest yield cig27

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 27
arettes. The researchers concluded that “highly ventilated cigarettes are

inserted deeply into the smokers mouth and consequently the ventilation

level is reduced during normal smoking” (British American Tobacco/Suisse,

1984). For example, an Ultra-Low delivery cigarette (1 mg tar, 0.1 mg nicotine, 78 percent diluted) showed 43 percent of insertions beyond the vents,

whereas a Full-Flavor brand (16 mg tar, 1.2 mg nicotine, 17 percent diluted)

had only 22 percent of insertions beyond the vents; both brands had vents

at 11-13 mm. By this technique, lip imprints beyond the vents were taken

as evidence of vent blockage. 

Large insertion depths seem to be about twice as common among lesspopular 1 mg tar cigarettes. Given the relative disparity in sales (much

greater for higher yield cigarettes), the ‘few’ blocked 1 mg tar cigarettes can

be ‘hidden’ among the shallow insertion depths of more popular higher

yielding brands. This causes average insertion depths to appear low enough

not to interfere very much with vents. Furthermore, this permits the industry to argue (based on average insertion depths) that vent hole covering is

not a major problem, when, in fact, their data suggest it is a significant

problem for the lowest yield cigarettes. Porter and Dunn (1998) cited

McBride’s prior work, but made no mention of that researcher’s finding of

greater insertion depths for lower yield cigarettes (McBride, 1985), nor did

they address the similar findings of the British American Tobacco/Suisse

study (1984). 

Ferris of the British American Tobacco Co. (cited by Baker and Lewis,

1997) conducted a study in 3 British cities in which 133 smokers of ventilated-filter cigarettes were videotaped. A total of 798 puffs were individually

assessed from the video recordings: during 12 percent of the puffs, smokers’

fingers were in contact with the cigarette for all or part of a puff. During 81

percent of the puffs, there was no finger contact with the cigarette. Ten percent of the puffs could not be assessed. During 29 percent of the final puffs,

however, smokers’ fingers were at least partially in contact with the cigarette. Eleven percent of participants had their fingers in contact with the

cigarette for one or more puffs. However, since finger and lip blocking are

mutually exclusive, it is noteworthy that lip blocking was not included in

this study. 

Baker and Lewis (1997) noted that when smoking an Ultra-Light cigarette (2.2 mg FTC tar), 45 percent of smokers blocked vents to some degree

with their lips. Further, 21 percent of smokers (or nearly half of those who

blocked vents) increased tar yields to at least 3.3 mg tar (50 percent). It was

estimated that approximately 1 in 10 smokers doubled their tar yield from

lip blocking alone; this is not insignificant, yet Baker and Lewis seemed to

downplay these results. 

Table 2-3 outlines the conditions under which different modes of compensation will be likely to occur. Reviewing the literature, vent blocking

appears to be a significant mode of compensation for reduced yield among

smokers of Lowest Tar cigarettes (e.g., 1 mg FTC tar), but not likely among

most smokers of Light and Ultra-Light cigarette brands. 

Brand selection is usually not forced upon smokers. The self-selected

choice of brands is due to many factors. It should be noted that some 28

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 28
smokers of the lowest yield cigarettes appear to have very low nicotine

needs and are disinclined to over-smoke these cigarettes, while other smokers of the lowest yield cigarettes have high nicotine needs and can fully

compensate using these brands (Kozlowski et al., 1989). 

In summary, published, peer-reviewed research has shown that a substantial proportion of smokers block vents and that it is a common mechanism used by smokers to compensate for the reduced nicotine yield of ventilated cigarettes.

During the period 1968-1997, the average salesweighted ratio of tar to nicotine (T/N ratio)

decreased 15.8 percent. Generally, the higher the yield, the higher the T/N

ratio (see Figure 2-1). However, compensatory smoking behaviors (taking

more frequent puffs, taking larger puffs, or vent blocking) can have dramatic effects on T/N ratios (Creighton and Lewis, 1978; Kozlowski et al., 1980b;

Rickert et al., 1983). Given that some researchers have indicated an interest

in using these ratios in the governmental regulation of cigarettes (e.g.,

Russell, 1976; Gori, 1990; Bates et al., 1999), this issue takes on greater

importance.

In their study, Rickert and associates (1983) demonstrated that as intensity of smoking increased, T/N ratios increased. Intensely smoked UltraLight cigarettes provided a nearly identical T/N ratio (12.2) as Light cigaTar/Nicotine Ratios Depend

on Smoking Conditions

29

Chapter 2

Table 2-3

Major Compensatory Behaviors in Relation to Cigarette Designs That Increase Total Smoke

Volume per Cigarette

A. For more-popular lightly and moderately diluted cigarettes (i.e., <60% ventilated, >4 mg FTC

tar yield—“Light” and “Ultra-Light”)

1) Increase volume per puff.

Probably the easiest, most common method; for example, the smoke intake from a 

45 ml puff on a 23% ventilated cigarette can be equivalent to the smoke intake from 

a 35 ml puff on an unventilated cigarette.

2) Increase number of puffs taken.

3) Reduce air dilution (as in Section B below).

This likely will be a lesser-to-negligible compensation mode because (a) the effect is 

relatively small for these brands, and (b) increased puff volume and number can 

achieve all needed/desired compensation.

B. For less-popular heavily diluted cigarettes (i.e., 60-85% ventilated, 1-2 mg FTC tar yield—

“Ultra-Low Tar”)

1) Reduce air diluation by blocking filter vents with lips or fingers.

Filter designs that promote ventilation ‘compromise’ (e.g., Actron®) avoid the need to 

behaviorally block vents.

2) Increase volume per puff.

This technique would be more effective when coupled with some dilution reduction.

Laser filter vents become relatively less effective with increased puff volumes.

3) Increase number of puffs taken.

Chapter 02 11/19/01 10:52 AM Page 29
rettes smoked under standard conditions (11.9). The difference between

standard and intense condition T/N ratios across all brands is significant

(P< 0.0001). The blocking of vents has a greater effect on the change in T/N

ratios in Lowest Tar brands (1.90 or 20.5 percent) than in Lights (0.78 or 6.5

percent) (P = 0.0146). 

Internal tobacco company studies revealed that there is great variability

in the T/N ratios of otherwise equivalent cigarettes. An R. J. Reynolds study

tested the yields of Now® brand cigarettes and comparable experimental

cigarettes (both 1 mg tar/FTC) smoked under two conditions, the standard

FTC method and the previously mentioned “50/30” condition (a 50 ml puff

taken every 30 seconds) (Casey, 1994). The T/N ratio of the Now® blend

under standard conditions was 8.33; however, under 50/30 conditions, the

ratio rose to 10.98 (an increase of 31.8 percent). At the same time, an experimental blend saw its T/N ratio increase from 6.36 at standard conditions to

6.72 at 50/30 conditions (an increase of only 5.7 percent) (Casey, 1994). It

would appear that the trends for reduced “standardized smoking-machine”

T/N ratios may have little relation to the ratios delivered to actual smokers.

Empirical evidence for this proposition is presented in Chapter 3.

Elastic Cigarette Designs The rules or constraints of the FTC measurement regimen can be viewed as obstacles to be overcome by manufacturers that wish

to design cigarettes that deliver lower yields during the course of the stan30

Smoking and Tobacco Control Monograph No. 13

0

5

10

15

20

1 2 to 5 6 to 15 16+

FTC Tar Yield (mg)

Tar / Nicotine Ratio

9.3

11.5

14.4

15.8

Figure 2-1

FTC Tar/Nicotine Ratios for 2,052 Brands Tested as a Function of FTC Tar Yield

Categories (FTC, 1999)

Note: Figure 2-1 shows the T/N ratios for all 2,052 brands tested by the FTC method in 1997 (FTC, 1999) as a function of FTC tar

yield categories. One-way analysis of variance shows that T/N ratios increase as tar yield increases (P<0.0001, all pairwise comparisons significant P<0.001, Bonferroni t-tests) (Ns, SEMs: 15, 0.50; 159, 0.22; 922, 0.07; 156, 0.17).

Chapter 02 11/19/01 10:52 AM Page 30
dardized smoking-machine test, while enabling smokers to achieve yields

higher than would be predicted by smoking machines. A design that gives a

low value to smoking machines but can potentially give higher values to

smokers is termed ‘elastic’. Internal tobacco industry documents revealed a

concern for cigarette elasticity: 

“Smokers have disappointed us in that they have not chosen to

smoke twice as many 10mg cigarettes if they changed from 20mg

products. Thus in order to reinforce the primary pleasures of smoking, I have proposed to make it easier for smokers to take what they

want from a cigarette which might well have a low delivery when

smoked by machine which overcomes current legal constraints and

to enhance the sensations from the first few puffs.” (See Creighton,

1980s.) 

“Irrespective of the ethics involved, we should develop alternative designs (that do not invite obvious criticism) which will allow

the smoker to obtain significant enhanced deliveries should he so

wish” (See British American Tobacco Company, 1984.) 

“Compensation - It exists; most smokers practice it, but we need

to understand it better before advantage can be taken in the marketplace. Here, I believe designing to the subconscious is preferred to

requiring the smoker to commit a conscious act.” (See Sandford,

1985.) 

In a presentation given to marketers at the British American Tobacco

Co., scientist D. E. Creighton described advances in the design of “compensatable” filter products: 

“The design of a cigarette with a compensatable filter will have

a high taste to tar ratio. . . . This [the HH filter] was designed in BAT

Hamburg and has been tested on consumers, who found the cigarettes too strong. As the sample cigarettes had a machine smoked

delivery of about 1mg tar, the product must be very compensatable.

Our own tests both subjective and objective suggested that it is a

compensatable filter, when smoked against conventionally constructed controls. The objective test we have used is to smoke at 35

and 50ml puff volumes and to see if the increase in delivery at the

higher puff volume is pro-rata or more. With HH, the delivery was

more than pro-rata.” [This paper goes on to compare the HH filter

to the Actron filter used in Barclay®, discussed below.] (See

Creighton, 1980s.) 

The ventilated Actron filter makes use of plastic channels to feed air

from vent holes back to the end of the filter. It appears that this channel

system dramatically increased the likelihood of vent blocking because, in

addition to blocking air intake holes, one could also subvert the ventilation

system by either causing the fragile plastic channels to collapse or by blocking air exit holes with lips. This filter design caused competing manufactur31

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 31
ers to complain to the FTC that this cigarette design was classified as 1 mg

but gave much higher actual deliveries. The courts ruled that the FTC test

could not properly provide tar and nicotine numbers for this type of filter

(FTC v. Brown & Williamson Tobacco Corporation, 1985). The Actron filter

can still be found on Brown & Williamson’s Barclay® and Kool Ultra®

brands. 

With some brands, elasticity arose from the ease with which a smoker

could alter their smoking patterns on the product. Internal tobacco company documents show an industry aware that some lower yield products were

smoked more intensely than higher yield products: 

“The smoker profile data reported earlier indicated that

Marlboro Lights cigarettes were not smoked like regular Marlboros.

In effect, the Marlboro 85 smokers in this study did not achieve any

reduction in smoke intake by smoking a cigarette (Marlboro Lights)

normally considered lower in delivery.” (See Goodman, 1975.) 

“Numerous experiments have been carried out in Hamburg,

Montreal and Southampton within the company, as well as many

other experiments by research workers in independent organisations, that show that generally smokers do change their smoking

patterns in response to changes in the machine smoked deliveries of

cigarettes.” (See Creighton, 1978b.)

Cigarette Length In the late 1960s, Philip Morris undertook the Smoke Exposure

Study, termed SEX-1 in their internal documents. While the actual report is

currently unavailable in the company’s Internet document archive, references to the results are available in other documents. In a memo discussing

reasons to publish the SEX-1 report, the effect of cigarette length on exposure is discussed. It appears that smokers of 100 mm cigarettes showed an

increased intake of tar and nicotine compared to 85 mm cigarette smokers.

However, it is noted that this increase was “not as great as would have been

predicted from the increase in available tar” (Dunn, 1971). This issue of cigarette length and exposure was evidently significant, because the design of

a subsequent study (SEX-2) was modified to include smokers who switched

from 85 mm to 100 mm cigarettes to determine changes in daily smoke

intake (Dunn, 1969). While the results of the SEX-1 study are far from clear,

no other findings related to cigarette length are known to exist.

Interestingly, the percentage of cigarettes sold ranging in length from 94 to

101 mm increased from 9 to 39 percent during the period 1967-1997 (FTC,

1999). 

In summary, the tobacco industry has a stake in smokers’ continued use

of their products. Cigarette designs that promote compensation and/or elasticity of yield have been used, both in the research and development laboratories and in the marketplace. These designs allow the smoker to obtain

more smoke (tar, nicotine, and CO) from each cigarette than would be indicated by the FTC testing method.

32

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 32
As shown in previous sections, considerable evidence exists in tobacco industry

documents of knowledge regarding compensation and elasticity. Also revealed in

industry documents are discussions about whether smokers might be misled

by FTC tar and nicotine ratings used in advertisements and league tables.

Particularly of concern were those customers who switched to a lower yield

brand due to health concerns: 

“Should we market cigarettes intended to re-assure the smoker

that they are safer without assuring ourselves that indeed they are

so or are not less safe? For example should we ‘cheat’ smokers by

‘cheating’ League Tables? If we are prepared to accept that government has created league tables to encourage lower delivery cigarette

smoking and further if we make league table claims as implied

health claims—or allow health claims to be so implied—should we

use our superior knowledge of our products to design them so that

they give low league table positions but higher deliveries on human

smoking?” 

. . . “Are smokers entitled to expect that cigarettes shown as

lower delivery in league tables will in fact deliver less to their lungs

than cigarettes shown higher?” (See British American Tobacco

Company, 1977.) 

“It is difficult to ignore the advice of Health Authorities who

advise smokers to give up smoking or change to a lower delivery

brand but there is now sufficient evidence to challenge the advice

to change to a lower delivery brand, at least in the short term. In

general a majority of habitual smokers compensate for changed

delivery, if they change to a lower delivery brand.” (See Creighton,

1978b.) 

“1) Some concern has been expressed concerning the moral

obligation of Philip Morris (and perhaps the tobacco industry) to

reveal to the FTC the fact that some cigarette smokers may be getting more tar than the FTC rating of that cigarette. . . . 2) I believe

that there need be no such concern, at least from a position of

morality. It is obvious that HEW [Department of Health, Education,

and Welfare; now the Department of Health and Human Services]

knows that smokers vary their intake. Otherwise they would not

urge smokers to take fewer puffs. There are published papers which

show that different puffing patterns on the same cigarette will yield

different amounts of tar.” (See Fagan, 1974) 

SUMMARY Many smokers switch to cigarette brands advertised as delivering lower

yields out of concerns for their health, believing them to be less risky or a

step toward quitting (Kozlowski et al., 1998a, 1999; Giovino et al., 1996).

These decisions are often based on the FTC tar ratings, which can be inaccurate in assessing human smoking conditions. Through compensation

MORE EVIDENCE FROM INDUSTRY

DOCUMENTS RELATED TO COMPENSATION, CIGARETTE DESIGN, AND

THE FTC TESTING METHOD

33

Chapter 2

Chapter 02 11/19/01 10:52 AM Page 33
behaviors (i.e., vent blocking on Ultra-Low FTC tar cigarettes, larger puff

volumes, or more frequent puffs), many smokers can obtain adequate nicotine from their new lower yield brand to sustain their addiction. 

Published research results, supplemented by previously unavailable

industry data, show that the 44 percent reduction in standard tar yield and

34 percent reduction in standard nicotine yield seen since 1968 do not necessarily mean that smokers have been receiving less tar and nicotine from

their cigarettes with each passing year. Smokers can and do compensate for

reduced tar and nicotine yield by altering their smoking patterns.

Compensation behaviors can range from simple maneuvers such as taking

more puffs per cigarette, to increasing volume per puff, to blocking filter

vents with fingers or lips. Changes in cigarette design have engineered cigarettes that have an elasticity of delivery, which allows smokers to derive

markedly different amounts of nicotine from the same cigarette by changing the way that they smoke it. This designed elasticity is intrinsic to the

process of compensation when smokers switch to lower yield cigarettes.

Elastic products such as the Actron filter, laser-perforated filters, and invisible filter vents on cigarettes facilitate compensation behaviors in smokers.

Larger puff volumes, increasing puff frequency, and other changes in smoking behavior allow smokers to derive doses of nicotine from cigarettes with

low machine-measured yields sufficient to fully satisfy their addiction.

Smokers are increasingly likely to engage in compensation as the machinemeasured yields of cigarettes fall and the percentages of ventilation

increase.

CONCLUSIONS

1. Several design changes in the way that cigarettes are manufactured

have led to a substantial reduction in the machine-measured tar and nicotine yields of U.S. cigarettes over the last several decades.

2. Many of the same design changes that have reduced machine-measured tar yields, particularly placing ventilation holes in the cigarette filters,

also create an elasticity of delivery for the cigarette, allowing a wide range

of tar and nicotine deliveries from the same cigarette when a smoker alters

his or her smoking behavior.

3. Increasing puff volume and frequency, covering the ventilation holes

with fingers or lips, and other changes in smoking behavior known to

occur with use of low machine-measured-tar cigarettes can dramatically

increase the tar and nicotine delivery of low- and ultralow-yield brands. 

4. Variations in the tar and nicotine delivery that result from the

known compensatory alterations in smoking behaviors make the current

U.S. cigarette tar and nicotine yields as measured by the FTC method not

useful to the smoker either for understanding how much tar and nicotine

he or she is likely to inhale from smoking a given cigarette or for comparing the tar and nicotine intake that is likely to result from smoking different brands of cigarettes.

34

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 34
35

Chapter 2

Aloot, C.B., Vredevor, D.L., Brecht, M. Evaluation of

high-risk smoking practices used by the homeless. Cancer Nursing 16(2):123-130, 1993. 

American Cancer Society. Nicotine content of whole

tobacco. 1997 Cigarette Nicotine Closure Report.

Available at http://www.cancer.org/tobacco/nicotine_report/content.html.

Baker, R.R., Dixon, M., Hill, C.A. The incidence and

consequences of filter vent blocking amongst

British smokers. Beitrage zur Tabakforschung

International 18(2):71-91. 1998. 

Baker, R.R., Lewis, L.S. Filter ventilation—Has there

been a “cover-up”? Recent Advances in Tobacco

Science 23:152-196, 1997. 

Bates, C., McNeill, A., Jarvis, M., Gray, N. The future

of tobacco product regulation and labelling in

Europe: Implications for the forthcoming

European Union directive. Tobacco Control

8(2):225-235, 1999. 

Bradford, J.A., Harlan, W.R., Hanmer, H.R. Nature of

cigarette smoke. Technique of experimental

smoking. Industrial and Engineering Chemistry

28(7):836-839, 1936.

British American Tobacco Company. Research and

Development views on potential marketing

opportunities. September 12, 1984. Minnesota

Trial Exhibit 11,275.

British American Tobaco Company. Suggested

Questions for JH CAC.III, August 26, 1977.

Minnesota Trial Exhibit 11,390. 

British American Tobacco Suisse. Insertion depth

study on Swiss cigarettes. BAT Suisse, 1989. Bates

No. 2501268539. Available at www.pmdocs.com.

Brown & Williamson. Proceedings of the Smoking

Behaviour Marketing Conference, July 9th-12th

1984, Session III. (Minnesota Trial Exhibit

13,431.) 

Browne, C.L. The Design of Cigarettes, 3rd Edition.

Hoechst Celanese Corporate, 1990. 

Casey, W.J. Data related to very high air dilution cigarettes. R.J. Reynolds Tobacco Company, 1994.

Bates No. 512480043. Available at

www.rjrtdocs.com.

Creighton, D.E. Measurement of the degree of ventilation of cigarettes at various flow rates. British

American Tobacco Company, 1978a. Available at

www.cdc.gov/tobacco/industrydocs.

Creighton, D.E. Compensation for changed delivery.

British American Tobacco Company. June 27,

1978b. Minnesota Trial Exhibit 11,089.

Creighton, D.E. Structured creativity group presentation. British American Tobacco Company, 1980s.

BAT No. 102690336-3501. Available at

www.tobaccopapers.org.

Creighton, D.E., Lewis, P.H. The effect of different

cigarettes on human smoking patterns. In:

Smoking Behavior: Physiological and Psychological

Influences. R.E. Thornton (Editors.). Edinburgh,

Scotland: Churchill Livingstone, 1978. 

Creighton, D.E., Watts, R.M. The effect of introducing pinholes in front of the filter on human

smoking pattern. British American Tobacco,

1972. Bates No. 650316736. Available at

www.cdc.gov/tobacco.

Djordjevic, M.V., Stellman, S.D., Zang, E. Doses of

nicotine and lung carcinogens delivered to cigarette smokers. Journal of the National Cancer

Institute 92(2):106-111, 2000. 

Dunn, W.L. to Charles, J.L., Cohen, M., Daylor, F.,

Eichorm, P., Filias, G., Forest, B., Ikeda, R.,

Johnston, M., Osmalov, J., Ryan, F., Tamol, R.,

Thomson, R., Tindall, J., Wakeham, H. April 8,

1969. Memo by W.L. Dunn. Modified design of

SEX-2. Philip Morris, Inc. Bates No. 1003287567.

Available at www.pmdocs.com. 

Dunn, W.L. to Wakeham, H. February 11, 1971.

Memo by W.L. Dunn. SEX-1. Philip Morris, Inc.

Bates No. 2055083000A. Available at

www.pmdocs.com. 

DuPuis, R.H. Untitled memo—CONFIDENTIAL.

Philip Morris, Inc., 1956. Bates No. 1001809856.

Available at www.pmdocs.com.

Fagan, R. to Wakeham, H. March 7, 1974. Memo by

R. Fagan. Moral issue on FTC tar. Bates No.

1000211075.

Federal Trade Commission. “Tar”, nicotine, and carbon monoxide of the smoke of 1262 varieties of

domestic cigarettes for the year 1996. Federal Trade

Commission, Washington, D.C., 1999. 

Federal Trade Commission v. Brown & Williamson

Tobacco Corporation, 250 U.S. App DC 162; 778

F2d 35 (10 and 18 December, 1985). SCB: 580 F

Suppl 981. 

Giovino, G.A., Tomar, S.L., Reddy, M.N., Peddicord,

J.P., Zhu, B.P., Escobedo, L.G., Eriksen, M.P.

Attitudes, knowledge, and beliefs about low-yield

cigarettes among adolescents and adults. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.

7. U.S. Department of Health and Human

Services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 96-4028,

1996. 

Goodman, B. to Meyer, L.F. September 17, 1975.

Memo by B. Goodman. Marlboro—Marlboro

Lights study delivery data. Trial Exhibit 11,564.

Goodman, B.L. to Meyer, L.F. New product development summary of human smoker simulator program. Philip Morris, 1977. Bates No.

1003728025. Available at www.pmdocs.com.

Gori, G.B. Cigarette classification as a consumer

message (Review). Regulatory Toxicology and

Pharmacology 12:253-262, 1990. 

REFERENCES

Chapter 02 11/19/01 10:52 AM Page 35
36

Smoking and Tobacco Control Monograph No. 13

Grunberg, N.E., Morse, D.E., Maycock, V.A.,

Kozlowski, L.T. Changes in overwrap and butt

length of American filter cigarettes. An influence

on reported tar yields. New York State Journal of

Medicine 85:310-312, 1985. 

Helms, A. The concentration of tar, nicotine and carbon monoxide in the smoke of ventilated filter

cigarettes—Comparison of different types of filter ventilations. Hamburg, Germany: HauniWerke Kurbar & Co. KG, 1983. Bates No.

2028562439. Available at www.pmdocs.com. 

Helms, A., Lorenzen, H.C. Latest developments in

the field of cigarette perforation (post-perforation) by laser. Hamburg, Germany: Hauni-Werke

Kurbar & Co. KG, 1984. Available at www.rjrtdocs.com. 

Herning, R.I., Jones, R.T., Bachman, J., Mines, A.H.

Puff volume increases when low-nicotine cigarettes are smoked. British Medical Journal (Clin Res

Ed) 283:187-189, 1981. 

Kelley, M.F. Project Change-2001: Evaluation of a PM

2 mg experimental cigarette versus Now and

Carlton 70. Philip Morris, 1977. Bates No.

1000364294. Available at www.pmdocs.com.

Kozlowski, L.T. Perceiving the risks of low-yield ventilated-filter cigarettes: The problem of holeblocking. Proceedings of the International

Workshop on the Analysis of Actual vs. Perceived

Risks. Covello, V., Flamm, W.G., Rodericks, J.,

Tardiff, R. (Editors.). New York: Plenum, 1983. 

Kozlowski, L.T., Frecker, F.C., Khouw,V., Pope, M.S.

The misuse of ‘less-hazardous’ cigarettes and its

detection: Hole-blocking of ventilated filters.

American Journal of Public Health 70:1202-1203,

1980a. 

Kozlowski, L.T., Goldberg, M.E., Sweeney, C.T.,

Palmer, R.F., Pillitteri, J.L., Yost, B.A., White, E.L.,

Stine, M.M. Smoker reactions to a “radio message” that light cigarettes are as dangerous as

regular cigarettes. Nicotine and Tobacco Research

1:67-76, 1999. 

Kozlowski, L.T., Goldberg, M.E., Yost, B.A., Ahern,

F.M., Aronson, K.R., Sweeney, C.T. Smokers are

unaware of the filter vents now on most cigarettes: Results of a national survey. Tobacco

Control 5(4):265-270, 1996a. 

Kozlowski, L.T., Goldberg, M.E., Yost, B.A., White,

E.L., Sweeney, C.T., Pillitteri, J.L. Smokers’ misperception of light and ultra-light cigarettes may

keep them smoking. American Journal of

Preventive Medicine 15(1):9-16, 1998a. 

Kozlowski, L.T., Heatherton, T.F., Frecker, R.C., Nolte,

H.E. Self-selected blocking of vents on low-yield

cigarettes. Pharmacology, Biochemistry, & Behavior

33(4):815-819, 1989. 

Kozlowski, L.T., Mehta, N.Y., Sweeney, C.T. Filter

ventilation levels in selected U.S. cigarettes—

1997. Morbidity and Mortality Weekly Report

46(44):1043-1047, 1997. 

Kozlowski, L.T., Mehta, N.Y., Sweeney, C.T.,

Schwartz, S.S., Vogler, G.P., Jarvis, M.J., West, R.J.

Filter ventilation and nicotine content of tobacco in cigarettes from Canada, the United

Kingdom, and the United States. Tobacco Control

7(4):369-375, 1998b. 

Kozlowski, L.T., O’Connor, R.J. Official cigarette tar

tests are misleading: Use a two-stage, compensating test. The Lancet 355(9221):2159-61, 2000. 

Kozlowski, L.T., Pillitteri, J.L., Sweeney, C.T. Misuse

of “light” cigarettes by means of vent blocking.

Journal of Substance Abuse 6(3):333-336, 1994. 

Kozlowski, L.T., Pillitteri, J.L., Yost, B.A., Goldberg,

M.E., Ahern, F.M. Advertising fails to inform

smokers of official tar yields of cigarettes. Journal

of Applied Biobehavioral Research 3:55-64, 1998c. 

Kozlowski, L.T., Pope, M.A., Lux, J.E. Prevalence of

the misuse of ultra-low-tar cigarettes by blocking

filter vents. American Journal of Public Health

78(6):694-695, 1988. 

Kozlowski, L.T., Rickert, W.S., Pope, M.A., Robinson,

J.C., Frecker, R.C. Estimating the yield to smokers of tar, nicotine, and carbon monoxide from

the ‘lowest yield’ ventilated filter cigarettes.

British Journal of Addiction 77(2):159-165, 1982. 

Kozlowski, L.T., Rickert, W.S., Robinson, J.C.,

Grunberg, N.E. Have tar and nicotine yields of

cigarettes changed? Science 209(4464):1550-1551,

1980b. 

Kozlowski, L.T., Sweeney, C.T., Pillitteri, J.L. Blocking

cigarette filter vents with lips more than doubles

carbon monoxide intake from ultra-low tar cigarettes. Experimental and Clinical

Psychopharmacology 4:404-408, 1996b. 

Kozlowski, L.T., White, E.L., Sweeney, C.T., Yost,

B.A., Ahern, F.A., Goldberg, M.E. Few smokers

know their own cigarettes have filter vents.

American Journal of Public Health 88(4):681-682,

1998d. 

Kozlowski, L.T., Yost, B., Stine, M.M., Celebucki, C.

Massachusetts advertising against light cigarettes

appears to change beliefs and behavior. American

Journal of Preventive Medicine 18(4):339-342, 2000.

Long, L.L. Summary of results on ventilated cigarettes. Philip Morris, 1955. Bates No.

1001900842. Available at www.pmdocs.com. 

McBride, C. A study to determine the maximum cigarette insertion depth used by Canadian smokers

[Abstract]. Imperial Tobacco, Ltd, 1985. Bates No.

109874617. Available at

www.tobaccopapers.org/documents/psc71e.pdf. 

Mendell, S. 2001 New Product Development. The

relationship between dilution/RTD ratios and

consumer perception. Philip Morris, 1983. Bates

No. 1003638145. Available at www.pmdocs.com. 

Moody, P.M. The relationships of quantified human

smoking behavior and demographic variables.

Social Science Medicine 14A(1):49-54, 1980. 

Chapter 02 11/19/01 10:52 AM Page 36
37

Chapter 2

Norman, A.B., Newsome, J.B., Reynolds, J.H. Effects

of tipping perforation method and vent location

on filter ventilation during smoking. R.J.

Reynolds Tobacco Company, 1984. Bates No.

504017981. Available at www.rjrtdocs.com. 

Norman, V., Ihrig, A.M. A study of human smoking

patterns of ultra-low yield cigarettes. Lorillard

Tobacco Company, 1980a. Bates No. 00782382.

Available at www.lorillarddocs.com. 

Norman, V., Ihrig, A.M. The concept of a power

function to describe smoking effort. Lorillard

Tobacco Company, 1980b. Bates No. 00303446.

Available at www.lorillarddocs.com. 

Parker, J.A., Montgomery, R.T. Design criteria for

ventilated filters. Beitrage zur Tabakforschung

International 10:1-6, 1979. 

Peeler, C.L. Cigarette testing and the Federal Trade

Commission: A historical overview. The FTC

Cigarette Test Method for Determining Tar, Nicotine,

and Carbon Monoxide Yields of US Cigarettes.

Report of the NCI Expert Committee. U.S.

Department of Health and Human Services,

National Institutes of Health, National Cancer

Institute, NIH Publication No. 96-4028, 1996.

Philip Morris. Cigarettes a la carte or how to play

with filter efficiency, filter dilution and expanded tobacco in designing low- and very-low-tar

cigarettes. 1980. Bates No. 2501224987. Available

at www.pmdocs.com. 

Pillitteri, J.L., Morse, A.C., Kozlowski, L.T. Detection

of vent blocking on light and ultralight cigarettes. Pharmacology, Biochemistry, & Behavior

48:539-542, 1994. 

Porter, A., Dunn, P. Mouth insertion depths in

Canadian smokers. Beitrage zur Tabakforschung

International 18:85-91, 1998. 

Rickert, W.S., Robinson, J.C., Young, J.C., Collishaw,

N.E., Bray, D.F. A comparison of the yields of tar,

nicotine, and carbon monoxide of 36 brands of

Canadian cigarettes tested under three conditions. Preventive Medicine 12(5):682-694, 1983. 

Russell, M.A. Low-tar medium-nicotine cigarettes: A

new approach to safer smoking. British Medical

Journal 1(6023):1430-1433, 1976. 

Russell, M.A.H., Sutton, S.R., Iyer, R., Feyerabend, C.,

Vesey, C.J. Long-term switching to low-tar lownicotine cigarettes. British Journal of Addiction

77(2):145-158, 1982. 

Sandford, R.A. to Kohnhorst, E.E. June 28, 1985.

Internal memo by R.A. Sandford. Brown &

Williamson, Research Development and

Engineering. Minnesota Trial Exhibit 13,250.

Shoffner, R.A., Ireland, M.S. Rapid analysis of menthol and nicotine in smoke and the effects of air

dilution on delivery. Tobacco Science 26:109-112,

1982. 

Stolt, P. Update on program for the reduction of

Marlboro smoke deliveries in Europe by means

of filter dilution. Philip Morris Incorporated,

1977. Bates No. 2024270885. Available at

www.pmdocs.com. 

Sutton, S.R., Feyerabend, C., Cole, P.V., Russell, M.A.

Adjustment of smokers to dilution of tobacco

smoke by ventilated cigarette holders. Clinical

Pharmacology and Therapeutics 24(4):395-405,

1978. 

Sweeney, C.T. Experimental Research on the

Behavioral Blocking of Filter Vents on Low-Yield

Cigarettes. Doctoral dissertation, Pennsylvania

State University, 1998. 

Sweeney, C.T., Kozlowski, L.T. Blocking filter vents

increases carbon monoxide levels from ultralight but not light cigarettes. Pharmacology,

Biochemistry, & Behavior 59(3):767-773, 1998. 

Sweeney, C.T., Kozlowski, L.T., Parsa, P. Effect of filter vent blocking on carbon monoxide exposure

from selected lower tar cigarette brands.

Pharmacology, Biochemistry, & Behavior 63(1):167-

173, 1999. 

Tobin, M.J., Sackner, M.A. Monitoring smoking patterns of low and high tar cigarettes with inductive plethysmography. American Review of

Respiratory Disease 126(2):258-264, 1982. 

U.S. Department of Health and Human Services. The

Health Consequences of Smoking: Nicotine

Addiction. A Report of the Surgeon General. U.S.

Department of Health and Human Services,

Public Health Service, Centers for Disease

Control and Prevention, Center for Health

Promotion and Education, Office on Smoking

and Health. DHHS Publication No. (CDC) 88-

8406, 1988. 

Wakeham, H. Some unexpected observations on tar

and nicotine and smoker behavior. Philip Morris,

1974. Bates No. 1000260471. Available at

www.pmdocs.com. 

Wynder, E.L., Hoffman, D. Tobacco and Tobacco

Smoke. New York: Academic Press, 1967. 

Zacny, J.P., Stitzer, M.L. Cigarette brand-switching:

Effects on smoke exposure and smoking behavior. The Journal of Pharmacology and Experimental

Therapeutics 246:619-627, 1988. 

Zacny, J.P., Stitzer, M.L., Brown, F.J., Yingling, J.E.,

Griffiths, R.R. Human cigarette smoking: Effects

of puff and inhalation parameters on smoke

exposure. The Journal of Pharmacology and

Experimental Therapeutics 240(2):554-564, 1987. 

Zacny, J.P., Stitzer, M.L., Yingling, J.E. Cigarette filter

vent blocking: Effects on smoking topography

and carbon monoxide exposure. Pharmacology,

Biochemistry, & Behavior 25:1245-1252, 1986. 

Chapter 02 11/19/01 10:52 AM Page 37
38

Smoking and Tobacco Control Monograph No. 13

Chapter 02 11/19/01 10:52 AM Page 38
INTRODUCTION Most smokers are addicted to nicotine (U.S. DHHS, 1988).

Nicotine addiction results in smokers seeking to take in a constant level of

nicotine from smoking each day (Benowitz, 1988; U.S. DHHS, 1988).

Consequently, when faced with low-yield cigarettes, smokers tend to take in

more nicotine and other tobacco smoke constituents from these cigarettes

than would be predicted by machine testing in order to sustain optimal levels of nicotine intake. This phenomenon of taking in similar levels of nicotine from day to day has been termed ‘regulation' or ‘titration’ of nicotine

intake. The behavior of smoking cigarettes of different machine yields more

or less intensively, and/or smoking more or fewer cigarettes to achieve a

particular intake of nicotine, has been called ‘compensation’. If regulation

of nicotine intake is precise, that is, compensation is complete, then switching to low-yield cigarettes would not be expected to reduce exposure to

tobacco toxins, nor to reduce the risk of disease from smoking. 

Earlier chapters have described the nature of low-yield cigarettes and

the ways in which smokers can modify their smoking behaviors to take in

more tobacco smoke from their cigarettes than predicted by the standard

smoking-machine test. In brief review—when faced with lower yield cigarettes, smokers can smoke more cigarettes per day, can take more and deeper puffs, can puff with a faster draw rate, and/or can block ventilation

holes. Using these last four techniques, a smoker can increase his or her

smoke intake from a particular cigarette several fold above the machine-predicted yields. 

This chapter will review nicotine addiction and the evidence that smokers regulate their intake of nicotine from cigarettes. The focus will be on

primarily studies in which human exposure has been biochemically

assessed. Evidence from both experimental and cross-sectional studies will

be examined. The question of whether or not tar exposure might be

reduced despite compensation for nicotine itself when switching to lowyield cigarettes will also be examined.

Nicotine is the main determinant of tobacco use and addiction. Detailed reviews of

the pharmacology of nicotine and the evidence that nicotine is addictive

have been published in Surgeon General’s reports (for example, the 1988

Surgeon General’s report, The Health Consequences of Smoking: Nicotine

Addiction), as well as in a number of other reviews (Benowitz, 1988, 1999b;

U.S. DHHS, 1988). 

ROLE OF NICOTINE IN MAINTAINING TOBACCO ADDICTION

39

Compensatory Smoking of 

Low-Yield Cigarettes

Neal L. Benowitz

Chapter 03 11/19/01 10:57 AM Page 39
Nicotine is delivered to the smoker in particulate matter and, to some

extent, in the gaseous phase of tobacco smoke. It is rapidly absorbed from

the lungs into the arterial circulation, from which it goes to various organs,

including the brain. Rapid delivery of nicotine to the brain is particularly

important to the issue of compensation because it provides rapid feedback

to the smoker on the dose of nicotine absorbed, and allows minute-tominute titration of nicotine effects. 

In the brain, nicotine binds to and activates nicotinic cholinergic receptors. There are a variety of nicotinic cholinergic receptor subtypes, which

are believed to mediate different actions of nicotine in different parts of the

brain (Picciotto et al., 2000). Nicotinic receptor activation works, at least in

part, by facilitating the release of neurotransmitters, including acetylcholine, norepinephrine, dopamine, beta endorphin, glutamate, gamma

aminobutyric acid (GABA), and others. Nicotine also releases growth hormone, prolactin, and adrenocorticotropic hormone (ACTH). Most of the

behavioral effects of nicotine in people are believed to be mediated by its

actions on central nervous system receptors. 

Nicotine self-administration appears to be motivated both by positive

and negative reinforcement. Positive reinforcement includes pleasure,

arousal, relaxation, reduced stress, enhanced vigilance, improved cognitive

function, mood modulation, and lower body weight. With prolonged exposure to nicotine, there is an increase in the number of nicotinic cholinergic

receptors in the brain that occurs in association with the development of

tolerance to the effects of nicotine (Collins et al., 1994; Breese et al., 1997).

In the tolerant state, nicotine is necessary to maintain normal brain functioning. In the absence of nicotine, brain functioning becomes abnormal

and the individual experiences nicotine withdrawal symptoms, reflecting

physical dependence. Withdrawal symptoms include nervousness, restlessness, irritability, anxiety, impaired concentration, impaired cognitive function, increased appetite, and weight gain. Negative reinforcement refers to

the relief of withdrawal symptoms by nicotine intake. It is difficult to separate positive reinforcement from relief of withdrawal symptoms in smokers.

However, it is clear that nicotine is used by smokers to modulate their levels

of arousal, mood, and performance. 

The cigarette is a drug delivery system for nicotine. Smokers tend to

take in similar doses of nicotine on a day-to-day basis (Benowitz, 1988; U.S.

DHHS, 1988), presumably to optimize the levels of arousal and mood. A

variety of experimental studies support the theory that smokers regulate

daily intake of nicotine. In addition to studies of changed smoking behavior in response to different brands of cigarettes (which was discussed in

detail in Chapter 2), smokers have been shown to change smoking behavior

in response to other interventions that alter nicotine availability. For example, when the excretion of nicotine from the body is accelerated by acidification of the urine, smokers will increase their smoking to take in more

nicotine (Benowitz and Jacob, 1985). Conversely, when nicotine is administered intravenously or by administration of nicotine patches, smokers

reduce their nicotine intake from smoking (Benowitz and Jacob, 1990;

Benowitz et al., 1998).

40

Smoking and Tobacco Control Monograph No. 13

Chapter 03 11/19/01 10:57 AM Page 40
In summary, cigarettes smoking can be viewed as a process of delivering

nicotine to the body. Daily smoking can be viewed as a situation in which

nicotine is taken initially for pleasure, for arousal, and/or for mood modulation. As the day progresses for the smoker, tolerance develops to many of

the effects of nicotine, and further nicotine may be taken to primarily

relieve withdrawal symptoms that emerge between cigarettes. Smokers

appear to have particular desirable levels of nicotine intake throughout the

day that result in optimal functioning. The need for a particular level of

nicotine is central to the concept of compensation for low-yield cigarettes.

As discussed previously, there is considerable individual variability in the way smokers smoke their

cigarettes. Therefore, neither the number of cigarettes smoked per day, nor

the machine-determined yield, nor even a combination of the two can provide complete information on the intake by an individual smoker of tobacco smoke toxins. To determine intake most accurately, one must measure

human exposure to chemicals in tobacco smoke. 

The tobacco smoke constituents that have been most widely used in

quantitating human exposure to smoke are nicotine and carbon monoxide

(CO) (Benowitz, 1996, 1999a). Nicotine can be measured directly in blood,

but more commonly nicotine intake is estimated by measuring levels of its

proximate metabolite, cotinine. Cotinine has a much longer half-life than

nicotine; therefore, cotinine levels in the body vary much less throughout

the day than do nicotine levels. Thus, sampling time for cotinine with

respect to when the last cigarette was smoked is less critical. In addition,

cotinine can be readily measured in blood, saliva, and urine. Measurement

of the sum of nicotine and its metabolites in urine can also be used to

assess nicotine exposure from smoking. 

CO is present in high concentrations in tobacco smoke and is a useful

marker of exposure to the gaseous fraction of tobacco smoke, but the short

half-life of CO excretion makes it a measure that is predominantly influenced by smoking within the most recent several hours. There is no reason

to believe that smokers adjust their smoking to regulate CO levels in the

body. Therefore, discrepancies between CO levels measured in smokers and

those predicted on machine yields are most likely a result of attempts to

regulate nicotine intake. Changes in CO levels in response to different

smoking behaviors may differ from changes in nicotine levels, because CO

absorption is more heavily influenced by depth of inhalation than is nicotine. CO is absorbed across alveolar surfaces, whereas nicotine can be

absorbed across the mucosa in the upper and lower airways, as well as

across the alveolar surface. Levels of CO can be measured in expired air or

in the blood, the latter as carboxyhemoglobin (COHb). CO is a widely used

measure of cigarette smoke exposure, although its level can be influenced

by environmental exposures and the rate of its elimination is markedly

influenced by the level of physical activity. 

Hydrogen cyanide is another component of tobacco smoke. In the

body, cyanide is metabolized to thiocyanate, which can be measured in

blood or saliva. Thiocyanate has been used as a marker of tobacco smoke

BIOMARKERS OF TOBACCO 

SMOKE EXPOSURE

41

Chapter 3

Chapter 03 11/19/01 10:57 AM Page 41
exposure in many studies. Its main limitation is that there are many dietary

sources of thiocyanate, and thiocyanate levels in nonsmokers are substantial. Thus, measurement of thiocyanate yields relatively poor sensitivity and

specificity for tobacco smoke exposure, particularly at low levels of cigarette

smoking.

In considering smoking-related cancer risks, it would be most appropriate to measure exposure to tobacco smoke carcinogens. Such carcinogens in

tobacco smoke include polycyclic aromatic hydrocarbons (PAHs), various

nitrosamines, naphthylamines, polonium-210, and others. The carcinogen

biomarker that has shown the most promise has been a measurement of

nicotine-derived nitrosamines (Hecht, 1998). The nicotine-derived

nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is specific for tobacco smoke exposure and is metabolized to a butanol metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide (NNAL-GLUC). Urine levels of NNAL + NNAL-GLUC are elevated

in smokers (Hecht et al., 1993). The assay for NNAL is technically demanding. As yet, studies of NNAL levels in smokers of different yields of cigarettes have not been published. 

Other potential markers of carcinogen exposure include adducts of 4-

aminobiphenyl to hemoglobin in red blood cells (Bartsch et al., 1990);

adducts of benzo(a)pyrene and other potential carcinogens to DNA in white

blood cells (Jahnke et al., 1990; van Maanen et al., 1994); adducts of PAHs

to plasma albumin (Mooney et al., 1995); and urinary hydroxyproline or Nnitrosoproline excretion (Adlkofer et al., 1984). None of these markers has

been used to date in studying smokers of different yields of cigarettes.

One indirect measure of carcinogen exposure that has been used is the

measurement of mutagenic activity of the urine (Yamasaki and Ames,

1977). This is commonly done using the Salmonella histadine auxotroph

reversion assay. In vitro studies indicate that the mutagenic components of

cigarette smoke are found primarily in the tar rather than in the gaseous

fraction (Florin et al., 1980). It is known that the urine of cigarette smokers

is mutagenic. For an individual smoker, mutagenic activity of the urine

tends to be constant from day to day and there is a relationship between

mutagenic activity and the number of cigarettes smoked per day (Sorsa et

al., 1984; Benowitz, 1989). The test is limited in that it is not specific for

exposure to particular carcinogens, there is considerable variability in

results from assay to assay and from person to person, and dietary and

environmental chemical exposures can influence mutagenic activity.

However, for within-subject comparisons when assays are compared for the

same individual, the test provides a quantitative estimate of exposure to tar

and, thus, potential carcinogen exposure. 

The intake of nicotine from a single cigarette

or while smoking cigarettes throughout the

day can be estimated by measuring blood levels of nicotine at frequent time

intervals. If the clearance (a measure of the rate of metabolism and excretion) of nicotine is known, then blood level data can be converted to actual

intake of nicotine from smoking. Nicotine clearance can be measured by

NICOTINE ABSORPTION FROM

CIGARETTE SMOKING

42

Smoking and Tobacco Control Monograph No. 13

Chapter 03 11/19/01 10:57 AM Page 42
measuring blood levels during and after an intravenous infusion of a

known dose. This technique has been used in the laboratory or on smokers

in a research ward to determine the intake of nicotine from smoking

(Benowitz and Jacob, 1984a; Feyerabend et al., 1985; Benowitz et al., 1991).

On average, smokers take in about 1 mg of nicotine per cigarette. The

intake of nicotine is quite variable from person to person, appears to be

largely independent of machine-determined yield, and can increase threefold or more in response to restricted cigarette availability (Benowitz and

Jacob, 1984a; Benowitz et al., 1986a). 

As noted previously, cotinine can be used as a measure of nicotine

intake from cigarette smoking (Benowitz, 1996). On average, 70-80 percent

of nicotine is metabolized to cotinine. Cotinine has a half-life averaging 16

hours, such that levels are relatively stable throughout the day in smokers.

There is some individual variation in the quantitative relationship between

cotinine levels in blood, saliva, or urine, and the intake of nicotine. This is

because different people convert different percentages of nicotine to cotinine (usual range is 55-92 percent) and because different people metabolize

cotinine itself at different rates (Benowitz and Jacob, 1994). 

The relationship between nicotine intake and cotinine levels can be

expressed mathematically as: 

Intake of nicotine = 

where Css is the steady-state blood cotinine concentration, CLCOT is the

clearance of cotinine, and %ConvNIC→COT is the percent conversion of nicotine to cotinine. 

Rearranging the equation, 

intake of nicotine = 

In adult smokers, the conversion factor K averages 0.08 mg/24

hours/ng/ml (Benowitz and Jacob, 1994). Thus, a cotinine level of 300

ng/ml in a typical smoker corresponds to a daily nicotine intake of 24 mg.

Although cotinine screening levels do not precisely predict nicotine intake

for an individual because of individual variability in the conversion factor,

cotinine levels in groups of smokers are expected to predict average group

exposure to nicotine. Thus, the K factor can be used in population studies

to relate cotinine levels to overall intake of nicotine from particular brands

of cigarettes. 

Another way to estimate nicotine intake from cigarette smoking is to

measure urinary excretion of nicotine and its metabolites (Byrd et al., 1995,

1998). Measurement of all currently known metabolites of nicotine can

43

Chapter 3

Css(CLCOT)

%ConvNIC→COT

CLCOT 

%ConvNIC→COT

Css = K (Css)

Chapter 03 11/19/01 10:57 AM Page 43
account for approximately 90 percent of a dose of nicotine (Benowitz et al.,

1994). Assuming a steady level of smoking from day to day, the sum of

nicotine and its metabolites (as measured in 24-hour urine samples) reflects

the dose of nicotine taken in each day. A related but less precise way to

assess nicotine intake is to measure nicotine and its metabolites in urine

using a nonspecific colorimetric assay (Peach et al., 1985). This assay does

not distinguish particular nicotine metabolites and is less quantitative, but

allows a semi-quantitative comparison of nicotine exposure in populations

of smokers. 

The analysis of biochemical markers after cigarette

brand switching is often expressed as degree of percentage of compensation. Complete compensation means that the same

amount of nicotine or other tobacco smoke constituents is taken in before

and after a switch to a cigarette with a different nominal yield. No compensation means the intake changes in direct proportion to the change in

machine-determined yields relative to the new brand. 

Compensation, defined as the degree to which proportional changes in

a smoker’s intake of a smoke constituent make up for the same proportional

change in the machine-determined yield of that constituent, can be

expressed mathematically in the following equation (Alison et al., 1989):

where C = extent of compensation, marker1 and yield1 represent the levels

of biomarker and yield before the brand change, and marker2 and yield2

represent the levels in the changed brand condition. 

The Zacny and Stitzer (1988) data, which will be described in more

detail later, were used to illustrate the use of this equation. Smokers were

switched from their usual cigarettes with an average nicotine yield of 1.0

mg to cigarettes with an average nicotine yield of 0.4 mg. The average plasma cotinine concentrations were 252 ng/ml while smoking the higher yield

and 188 ng/ml while smoking the lower yield cigarettes. Using the equation

above, 

where data are available, the degree of compensation will be reported for

the various studies discussed in subsequent sections. 

The remainder of this chapter

will review studies of human

exposure to tobacco smoke

chemicals that have used three main types of research designs. The first

STUDIES OF SMOKING CIGARETTES WITH

DIFFERENT MACHINE-DETERMINED YIELDS:

METHODOLOGICAL CONSIDERATIONS

ESTIMATING THE EXTENT 

OF COMPENSATION

44

Smoking and Tobacco Control Monograph No. 13 

log(marker2) - log (marker1)

log(yield2) - log(yield1)

C = 1 -

log(189) - log(252)

log(0.4) - log(1.0)

C = 1 -

Chapter 03 11/19/01 10:57 AM Page 44
design is the experimental forced-switching study, in which smokers are

asked to switch to brands of higher or lower machine-determined yield

compared to their usual brand. These experimental studies have been separated into short term (up to 4 weeks) and long term (more than 4 weeks).

Forced-switching studies are particularly useful in that smoking behavior

and exposure can be assessed under close observation. The limitations of

such studies include the fact that smokers are switching only for the purpose of the research. Motivation and cigarette acceptability are dissimilar

from the natural situation of brand switching. These studies are performed

over periods of time that may not provide adequate duration to adjust to

the taste or puffing characteristics of the new cigarettes. Many of the shortterm studies have been performed in laboratories or on research wards,

environments in which individuals may not smoke cigarettes as they normally do. Longer term forced-switching studies do allow more time to

become accustomed to the new cigarette and are conducted in the smoker’s

natural environment, but they still do not measure the effect of self-determined brand switching. Nonetheless, experimental switching studies have

provided useful information on the mechanism and extent of compensation that can occur.

A second study design is one that follows smokers who smoke selfselected cigarette brands. These are cross-sectional studies of chemical exposures in smokers who have selected the brand of cigarette that they find satisfying. Data from this type of study provide the best estimate of chemical

exposure in smokers smoking different brands of cigarettes, but do not

address the question of what happens if a person switches brands—for

example, if someone switches from high- to low-yield cigarettes.

The third type of study design is one that examines spontaneous brand

switching. These are studies of smokers who have chosen to switch from

higher to lower machine-determined yield cigarettes, or vice versa. In these

studies, the brand of cigarettes has been selected by the smoker, not by the

researchers. Such studies are more informative of smokers’ exposure in the

real world when switching from higher to lower yield cigarettes.

A number of studies have examined the effects

of switching from high- to low-yield cigarettes

over a short period of time, defined for the purposes of this report as up to

one month. The effects of short-term switching to low-yield cigarettes on

how a cigarette is puffed and on vent hole blocking are discussed elsewhere

in this volume. This section will focus on switching studies in which biomarkers of tobacco smoke exposure were measured. 

Russell and coworkers (1975) studied 10 smokers on different days

when they were smoking their usual brand (average yield, 1.34 mg nicotine), or when they were switched to higher yield (2.3 mg nicotine) or to

lower yield (0.14 mg nicotine) cigarettes. The subjects were studied in the

morning while smoking their usual brands, and then again after 5 hours of

smoking either their usual, high-, or low-yield brands. Plasma nicotine concentrations were measured 3 minutes after smoking a cigarette as the indicator of nicotine exposure. Plasma nicotine concentrations were similar

SHORT-TERM EXPERIMENTAL

SWITCHING STUDIES

45

Chapter 3

Chapter 03 11/19/01 10:57 AM Page 45
while smoking the usual and high-yield cigarettes (30.1 and 29.2 ng/ml,

respectively) and significantly lower (8.5 ng/ml) while smoking the lowyield cigarette. The extent of compensation is estimated to be 96 percent

for the high-yield and 20 percent for the low-yield cigarettes, respectively.

The number of cigarettes smoked in the 5 hours of ad libitum smoking

showed a 38 percent reduction while smoking the high-yield cigarettes and

an increase from an average of 10.7 to 12.5 cigarettes per day for low-yield

cigarettes (the latter comparison was not statistically significant). 

Benowitz and Jacob (1984b) studied 11 smokers in a hospital research

ward. They were smoking their own brand of cigarettes (average yield, 16.3

mg tar, 1.1 mg nicotine), or were switched to either Camel® (15.4 mg tar,

1.0 mg nicotine) or True® (4.6 mg tar, 0.4 mg nicotine) for 4 days each.

Cigarette brands were assigned in a balanced order. Nicotine intake was

determined by measuring blood nicotine concentrations throughout the

day. When switched from their usual brand to either Camel® or True®, the

smokers showed an approximately one-third decline in nicotine exposure.

However, the intakes of nicotine and CO were similar when smoking

Camel® or True®. Thus, using Camel®s as a comparator, the degree of compensation when smoking True® was 100 percent. Similar findings were

obtained for CO exposure (based on measurements of COHb) or mutagenic

activity in a 24-hour urine collection (a measure of exposure to potentially

carcinogenic chemicals). 

A similarly designed study was performed where 11 subjects were

switched from their usual brand (average yield, 14.7 mg tar, 1.1 mg nicotine) to Camel® (15.4 mg tar, 1.0 mg nicotine) or to ultra-low Carlton® (tar

0.8 mg, nicotine 0.1 mg) cigarettes (Benowitz et al., 1986b). Compared to

the high-yield Camel® cigarette, when the participants smoked the

Carlton® brand, their nicotine, CO, and mutagenic activity levels were

reduced by 56, 36, and 49 percent, respectively. The percent compensation

based on nicotine exposure was estimated to be 74 percent. 

West and associates (1984) randomized 26 smokers of high-yield cigarettes (average yield, 14.2 mg tar, 1.3 mg nicotine) who either continued

their own brand or switched to an ultra-low-yield cigarette (1 mg tar, 0.1

mg nicotine) for 10 days. Subjects smoked a similar number of cigarettes in

the two conditions. The trough plasma nicotine level averaged 22.8 mg/ml

for the usual brand condition versus 9.4 ng/ml for the ultra-low-yield brand

condition. The latter is consistent with 36 percent compensation. A similar

degree of compensation was estimated based on expired CO levels. 

Zacny and Stitzer (1988) studied 10 smokers of high-yield cigarettes

(average, 1.0 mg nicotine) who smoked five different brands of cigarettes—

their own and cigarettes with yields of 0.1, 0.4, 0.7, and 1.1 mg nicotine—

each for 5 days, in random order. Subjects smoked significantly more cigarettes per day of the two brands with the lowest yields compared to the

three higher yield cigarettes. When smoking low-yield cigarettes, larger and

more frequent puffs were taken as well. The plasma cotinine levels at the

end of each smoking period averaged 152, 188, 221, 252, and 259 ng/ml for

46

Smoking and Tobacco Control Monograph No. 13

Chapter 03 11/19/01 10:57 AM Page 46
the 0.1, 0.4, 0.7, 1.0, and 1.1 mg nicotine brands, respectively. The cotinine

levels measured when smoking the two lowest yield cigarettes were significantly lower than for the three others. Based on group average data, compensation was estimated to be 56, 58, and 60 percent for the 0.1, 0.4, and

0.7 mg nicotine brands, respectively. 

A Benowitz study mentioned previously allowed a comparison of tar-tonicotine ratios as predicted by the smoking machine and as experienced by

the smoker (Benowitz et al., 1986a). The machine-determined tar-to-nicotine ratios for low-yield cigarettes are generally lower than those for highyield cigarettes. For example, the tar-to-nicotine ratios for cigarettes in this

study were 15.4 for Camel®, 11.5 for True®, and 7.3 for Carlton®. Assuming

that urinary mutagenicity is a quantitative measure of tar exposure (which

is reasonable, since most mutagenic activity comes from tar), changes in

the ratio of urinary mutagenicity to the area under the plasma nicotine

concentration time curve over 24 hours can be used as an indicator of

changes in the ratio of actual tar-to-nicotine exposure in the smoker. While

urinary mutagenicity did decline when smokers were switched to ultra-lowyield cigarettes, the ratio of mutagenic activity to nicotine exposure did not

differ for any of the cigarette types. This observation is consistent with

smoking-machine studies in which vent-hole blocking and/or more intensive smoking of low-yield cigarettes resulted in increased tar-to-nicotine

ratios (Rickert et al., 1983). It has been suggested that low-yield cigarettes

may be less hazardous, even if full compensation for nicotine occurs,

because the lower tar-to-nicotine ratio would lead to less intake of tar for

any given level of intake of nicotine. However, based on the urinary mutagenicity data, one must question whether predictions about lower exposure

to tar based on machine-determined tar-to-nicotine ratios are valid. 

In summary, these short-term switching studies demonstrated that

smokers compensate for reduced nicotine deliveries, but the extent of compensation varied in different studies—from 20 percent to 100 percent. The

degree of compensation is likely to be less in short-term switching studies

compared to longer term switching studies, or studies in which smokers

have selected their own brand of cigarettes. This is because 1) smokers have

not chosen to smoke the particular brand of cigarette they are switched to,

2) they often find the low-yield cigarettes to be unsatisfying, and 3) they

may not be smoking the cigarettes long enough to develop effective compensatory smoking behaviors. These short-term switching studies demonstrated that compensation occurs by a combination of smoking more cigarettes per day and by taking in more tobacco smoke per cigarette compared

to smoking-machine predictions. The one study that estimated tar-to-nicotine ratios delivered to the smoker suggested that this ratio is much higher

than is predicted by smoking-machine tests in smokers of low-yield cigarettes, consistent with smoking-machine studies that showed that intensive

puffing increases tar-to-nicotine ratios. 

Several studies have biochemically assessed the

extent of compensation after switching from

higher to lower yield cigarettes for periods of more than a few weeks.

Russell and associates (1982) studied 12 smokers who typically smoked an

LONG-TERM EXPERIMENTAL

SWITCHING STUDIES

47

Chapter 3

Chapter 03 11/19/01 10:57 AM Page 47
average of 38 ‘middle-tar’ cigarettes per day with an average yield of 17.4

mg tar and 1.3 mg nicotine. These subjects were switched to a low-tar cigarette (yield of 10.9 mg tar and 0.7 mg nicotine) for 10 weeks. Compared to

baseline, the average cigarette consumption increased by about three cigarettes per day while smoking the low-yield cigarette, although this was not

statistically significant. Plasma nicotine concentration (measured 2 minutes

after smoking a test cigarette) and plasma cotinine concentrations declined

by an average of 30 percent. There was no change in plasma thiocyanate or

blood COHb. The percentage compensation based on plasma nicotine or

plasma cotinine levels was 36 percent.

Robinson and colleagues (1983) switched a group of smokers of highnicotine cigarettes (average yield, 1.8 to 1.1 mg nicotine) to lower yield

brands over two stages. Six of the subjects, who served as controls, were

switched to cigarettes similar to their usual brand. Sixteen subjects were

switched initially to brands with 33 percent, then to brands with 61 percent

reduction of nicotine yields over 8 weeks. The average serum cotinine level

did not significantly decrease in those who decreased their brand yield (284

versus 244 ng/ml). Likewise, there was no significant reduction in plasma

thiocyanate or blood COHb levels. Thus, the Robinson study demonstrated

nearly complete compensation when switching to lower yield cigarettes.

Some smokers in this study achieved compensation by smoking more cigarettes per day, but for most smokers the main mechanism was smoking cigarettes more intensively and/or blocking ventilation holes.

Peach and associates (1986) studied 183 smokers of middle-tar cigarettes

who were randomized to switch from their own brand to cigarettes of a

similar yield (average, 15.5 mg tar, 1.5 mg nicotine) or a lower yield (9.0 mg

tar, 0.9 mg nicotine). Test cigarettes could be purchased at a discount. The

subjects were followed for 5 weeks and smoked an average of 20 cigarettes

per day, a rate that did not differ between middle- and low-tar cigarettes.

However, urine nicotine metabolite excretion was no different for individuals smoking the two types of cigarettes, indicating 100 percent compensation.

Guyatt and colleagues (1989) studied 29 smokers who smoked their

usual brand for 4 months and then were switched to a lower tar brand for 9

months. The usual cigarette brand had an average yield of 15.6 mg tar and

1.3 mg nicotine. Subjects were switched to cigarettes of at least 3 mg lower

tar than the usual brand—the average switch was to 9.3 mg tar and 0.9 mg

nicotine. Smokers on average smoked a greater number of low-yield cigarettes compared to the usual brand (28.5 versus 24.9 cigarettes per day), but

the difference was not statistically significant. Smokers did take more puffs

and larger puff volumes when smoking the lower yield cigarettes. Plasma

cotinine and COHb levels declined by 18 percent. Compensation was estimated by the authors to be 61 percent based on cotinine and 56 percent

based on COHb levels. The main mechanism for compensation was judged

to be more intensive puffing rather than greater cigarette consumption. 

48

Smoking and Tobacco Control Monograph No. 13

Chapter 03 11/19/01 10:57 AM Page 48
Frost and associates (1995) studied 434 smokers of high-yield cigarettes

who were switched to cigarettes of approximately 50 percent lower yield

compared to their usual brands. One group was switched to the cigarettes

immediately, and another was switched gradually over several months. A

third group, the control group, was switched to cigarettes of 10 percent

lower yield than their usual cigarettes. Subjects were allowed to select the

brand that they would smoke within the specified yield range. The followup was over 6 months. Compared to the preswitching value, levels of serum

cotinine in the fast yield-reduction group declined by an average of 11 percent and COHb declined by 14 percent. In the slow yield-reduction group,

there was a decrease of 6 percent in cotinine and 16 percent in COHb. For

the two groups combined, the extent of compensation was estimated by the

authors to be 79 percent based on cotinine and 65 percent based on COHb.

There was no significant difference in the extent of compensation based on

how fast the yields were reduced. On average, smokers reduced the number

of cigarettes they smoked after switching, which was interpreted by the

authors to reflect the desire of this group of smokers to reduce their smoking in general. The high degree of compensation despite smoking fewer cigarettes per day further demonstrates the point that cigarette yields are substantially increased by smoking lower yield cigarettes more intensively.

In summary, the data from these experimental long-term switching

studies indicated that there was some reduction in smoke exposure, but

that the magnitude of that reduction was small. The larger studies indicated

that the extent of compensation based on nicotine intake was about 80 percent. Compensation occurred primarily by increasing the intensity with

which cigarettes were smoked, in addition to the variable contribution of

increased numbers of cigarettes smoked per day in the different studies. It is

possible that voluntary efforts to cut down on smoking by subjects in some

of these studies may have limited the increase in cigarette consumption

that has been observed in response to switching to lower yield cigarettes in

other studies.

Cross-sectional population studies can provide data on exposure to tobacco smoke constituents in people who have selected the

brand of cigarettes they find satisfying. While

these studies may supply valuable data on tobacco smoke chemical exposure in smokers of different brands, there are limitations in extrapolating

such data to brand switching. For example, the acceptability of nicotine

delivery from a particular cigarette may influence brand selection, and a

highly dependent smoker would choose only those cigarettes that would

provide adequate doses of nicotine. Cross-sectional studies will also include

some people who are in transition—that is, transition to regular smoking,

to cessation, or in the process of relapsing from a previous cessation

attempt. Health concerns may also affect brand selection. All these factors

would be expected to affect the relationship between self-selected brand

and measures of intensity of smoking. Therefore, self-selected brand studies

are not a perfect model for studying compensation in response to brand

switching.

STUDIES OF SMOKERS SMOKING

SELF-SELECTED BRANDS

Studies of Nicotine Exposure

49

Chapter 3

Chapter 03 11/19/01 10:57 AM Page 49
The biomarkers used in cross-sectional studies include markers of nicotine exposure (blood nicotine, blood or saliva cotinine, or urinary nicotine

metabolites) and markers of gas-phase exposure, such as CO and thiocyanate. This section focuses on studies that measured nicotine intake.

Table 3-1 summarizes a number of studies in which nicotine intake was estimated in people who smoked cigarettes with different nominal yields. Most

studies found either weak or no significant correlations between nominal

yields and nicotine intakes. 

Three large studies, which involved general populations of smokers,

warrant particular discussion. Gori and Lynch (1985) recruited 865 smokers

from shopping malls in different areas of the United States. Plasma nicotine

and cotinine concentrations were weakly correlated with the Federal Trade

Commission (FTC) method for machine-measuring nicotine yield (see

Figure 3-1). Woodward and Tunstall-Pedoe (1992) studied 2,754 smokers as

part of the baseline assessment in the Scottish Heart Health Study, which

was conducted between 1984 and 1986. Their main analysis presented plasma cotinine data based on categories of yield: low tar (less than 13 mg/cigarette), middle tar (14-15 mg), and high tar (greater than 14 mg). The mean

cotinine values were no different across categories for males (276, 294, and

278 ng/ml for low-, middle-, and high-tar groups, respectively). For females,

the cotinine level was 26 percent lower in the low-tar group (199 ng/ml)

but similar for the middle- and high-tar groups (270 and 270 ng/ml, respectively). Woodward and Tunstall-Pedoe (1993) performed another analysis of

the same data with comparison of the cotinine concentrations to specific

yields of tar, nicotine, and CO (see Figure 3-2). Multiple regression analysis—which included tar, nicotine, and CO yields as well as cigarette consumption and gender—found that tar was the best predictor of cotinine

level, with an interaction for gender as previously discussed. However, the

best regression model accounted for only 19 percent of the variance in cotinine levels.

Jarvis and colleagues (2001) conducted a study of 2,031 adult smokers

in the United Kingdom as part of the 1998 Health Survey for England.

Smokers were defined as anyone who reported current smoking and included those who smoked only occasionally. Saliva cotinine concentrations correlated weakly with machine-determined nicotine yield (r = 0.19, P <

0.001). After controlling for confounders, machine-determined yield

accounted for 0.79 percent of the variance in saliva cotinine. Using the conversion factor for estimating nicotine intake from cotinine level as

described earlier, Jarvis and associates estimated a nicotine intake per cigarette of 1.17 mg in smokers of brands with machine yields of less than 0.4

mg (average, 0.14 mg), 1.22 mg nicotine for cigarettes with yields of 0.4-

0.75 mg (average, 0.57 mg), and 1.31 mg for brands with yields greater than

0.75 mg (average, 0.91 mg). The authors did not find that smokers of lowyield cigarettes smoked more cigarettes than smokers of higher yield cigarettes. However, in their analysis, most of the occasional smokers fell into

the low-yield cigarette group. Thus, the low-yield group contained a mixture of addicted and nonaddicted smokers, whereas the higher yield groups

included a greater proportion of addicted smokers (Jarvis et al., 2001). 

50

Smoking and Tobacco Control Monograph No. 13

Chapter 03 11/19/01 10:57 AM Page 50
51

Chapter 3

Table 3-1

Studies of Nicotine Intake Compared with Machine Nicotine Yield

Nicotine

Study Population Yields (mg) Results

Russell et al., 1980 330 from smokers’ clinics 0.5-3.5 PNIC vs. Mach-N

or research volunteers r = 0.21*

Rickert and Robinson, 84 during routine medical 0.25-1.3 PCOT vs. Mach-N

1981 exams r = 0.08

Benowitz et al., 1983 272 seeking smoking <0.1-1.9 BCOT vs. FTC-N

cessation therapy r = 0.15 (n = 137)

r = 0.06 (n = 123)

Ebert et al., 1983 76; mix of smoking cessation, 0.1-1.5 PNIC vs. FTC-N

hospital employees, and r = 0.25*

ambulatory patients

Gori and Lynch, 1985 865 recruited from shopping 0.1-1.6 PNIC vs. FTC-N

malls; 10 or more cigarettes r = 0.37*

per day PCOT vs. FTC-N

r = 0.23*

Benowitz et al., 248 seeking smoking cessation 0.1-1.9 BCOT values similar 

1986b (137 from previous study) for FTC-N 0.21 to >1.0

BCOT 2/3 of others 

for FTC-N < 0.20

Russell et al., 1986 392 from smokers’ clinics — BCOT vs. Mach-N

r = 0.13*

BNIC vs. Mach-N

r = 0.26*

Rosa et al., 1992 125 attending military 0.38-1.38 BCOT vs. Mach-N

medical center r = 0.30

Coultas et al., 1993 298 from Hispanic household — SCOT vs. FTC-N

survey r = 0.12

Woodward and 2,754 from Scottish Heart 0.1-1.7 BCOT vs. Mach Tar, N,

Tunstall-Pedoe, 1993 Health Study (1984-1986) and CO and gender 

(multiple regression);

accounted for 19% 

variance 

Byrd et al., 1995 33 volunteers 0.13-1.3 UNIC + metabolites 

vs. FTC-N

N/24 hr: r = 0.68*

N/cig: r = 0.79*

Chapter 03 11/19/01 10:57 AM Page 51
Table 3-1 (continued)

Nicotine

Study Population Yields (mg) Results

Hee et al., 1995 108 volunteers; 5 or more 0.09-1.19 UNIC, UCOT vs.

cigarettes per day Mach-N; NS

Byrd et al., 1998 72 volunteers 0.1-1.4 UNIC + metabolites 

vs. FTC-N

N/24 hr: r = 0.19

N/cig: r = 0.31*

SCOT vs. FTC-N

r = 0.15

Jarvis et al., 2001 2,031 from 1998 Health Survey 0.04-1.06 SCOT vs. Mach-N

for England r = 0.19*

* P < 0.05.

Key: PCOT = plasma cotinine concentration; Mach-N = smoking-machine-determined nicotine yield; PNIC = plasma nicotine concentration; BCOT = blood cotinine concentration; FTC-N = machine yield by Federal Trade Commission method; BNIC = blood nicotine concentration; SCOT = saliva cotinine concentration; UNIC = urine nicotine concentration; UCOT = urine cotinine concentration;

N = nicotine; CO = carbon monoxide.

52

Smoking and Tobacco Control Monograph No. 13

0

5

10

15

20

25

30

35

40

45

50

150 55

200

250

300

350

400

Plasma Nicotine (ng/mL)

FTC Nicotine (mg/cigarette)

0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 1.1 1.2 1.3 1.4 1.5 1.6

Plasma Continine (ng/mL)

Figure 3-1

Plasma Cotinine and Nicotine Concentrations in Cigarette Smokers According to the

FTC Nicotine Yield

Note: Solid line indicates mean; dashed line indicates 95% confidence intervals (from Gori and Lynch, 1985).

Chapter 03 11/19/01 10:57 AM Page 52
53

Chapter 3

5

10

15

20

25

30

35

1 3 5 7 9 11 13 15 17 19 21 23 25

Males

Carbon Monoxide (ppm)

CO Yield (mg/cig)

5

10

15

20

25

30

35

1 3 5 7 9 11 13 15 17 19 21 23 25

Females

CO Yield (mg/cig)

60

80

100

120

140

160

180

200

1 3 5 7 9 11 13 15 17 19 21 23 25

Thiocyanate (mmol/l)

Tar Yield (mg/cig)

60

80

100

120

140

160

180

200

1 3 5 7 9 11 13 15 17 19 21 23 25

Tar Yield (mg/cig)

0

100

200

300

400

500

0.1 0.3 0.5 0.7 0.9 1.1 1.3 1.5 1.7 1.9 2.1 2.3 2.5

Cotinine (ng/ml)

Nicotine Yield (mg/cig)

0

100

200

300

400

500

0.1 0.3 0.5 0.7 0.9 1.1 1.3 1.5 1.7 1.9 2.1 2.3 2.5

Nicotine Yield (mg/cig)

Figure 3-2

Mean Values for Expired Carbon Monoxide v. CO Yield, Serum Thiocyanate v. Tar Yield,

and Serum Cotinine Against Machine-Determined Yields for Men and Women

Note: Bars indicate one standard error (from Woodward and Tunstall-Pedoe, 1993).

Chapter 03 11/19/01 10:57 AM Page 53
Another study by Gori and Lynch (1983) warrants particular discussion

with respect to ultra-low-yield brands of cigarettes. They studied 288 smokers of two ultra-low-yield cigarette brands (1 mg tar). The subjects were

recruited in shopping malls, and plasma cotinine levels were measured. The

cotinine concentrations in smokers averaged 322 and 195 ng/ml for brands

with yields of 0.18 and 0.10 mg nicotine, respectively. The cotinine values

of the second brand were about 30 percent lower than the typical smoker

population value of 300 mg/ml. Smokers of the first ultra-low brand had

cotinine concentrations similar to the smoker population average. These

findings were similar to those of a short-term experimental study, by

Benowitz and associates, in which smokers were switched from regular to

ultra-low-yield cigarettes (Benowitz et al., 1986b). In that study, the intake

of nicotine fell by about 30 percent when switching to ultra-low-yield cigarettes compared to the usual brand.

In summary, most studies of nicotine intake in populations smoking

self-selected brands of cigarettes showed some differences in nicotine exposure when high- and low-yield brands were compared. However, the differences were quite small and not nearly quantitatively proportional to the

changes in nominal yield. Thus, nicotine ratings of cigarettes are poor predictors of actual nicotine intake and of the intake of other toxins as well.

The FTC method generally underestimates human exposure to nicotine,

particularly in smokers who are smoking low-yield cigarettes.

Studies on CO exposure in populations of self-determined

brand smokers are summarized in Table 3-2. An example of

CO data from a large group of smokers recruited from shopping centers is

shown in Figure 3-3 (Gori and Lynch, 1985). Similar data were reported by

Woodward and Tunstall-Pedoe (1992) in the Scottish Heart Health Study

(see Figure 3-2). Most other studies likewise found no relationship between

machine-determined CO yield and CO exposure, although a few studies did

report weak correlations. The conclusions for CO were similar to those discussed above for nicotine; that is, machine-determined yields are poor predictors of human exposure to CO, and presumably to other gaseous components of tobacco smoke as well. 

Several studies have measured plasma or saliva thiocyanate concentrations, and one study measured urinary mutagenic activity. In most studies, thiocyanate concentrations were

no different in smokers of cigarettes with different nominal yields. The

Woodward and Tunstall-Pedoe study (1993) found a weak relationship

between serum thiocyanate and cigarette yield. Benowitz and colleagues

(1986b) found that smokers of ultra-low-yield cigarettes had about 25 percent lower thiocyanate levels compared to other brands, but Maron and

Fortmann (1987) found no difference in thiocyanate concentration comparing smokers of ultra-low and other brands. 

Hee and coworkers (1995) measured urinary mutagenicity in 108 smokers of different yield cigarettes. They found a weak relationship between urinary mutagenicity and nicotine yield (r = 0.22, P > 0.05). 

Studies of Other Tobacco

Smoke Biomarkers

Studies of Carbon

Monoxide Exposure

54

Smoking and Tobacco Control Monograph No. 13

Chapter 03 11/19/01 10:57 AM Page 54
55

Chapter 3

Table 3-2

Studies of Carbon Monoxide Intake Compared with Machine Yield

Machine 

Study Population Yields (mg) Results

Jaffe et al., 1981 200 recruited from 0.2 - >1.0 mg ECO vs. FTC-N

urban workplaces nicotine r = 0.028

Rickert and Robinson, 159 during routine 4-22 mg CO COHb vs. Mach-CO 

1981 medical exams r = 0.10

Sutton et al., 1982 55 volunteers 11-20 mg CO COHb vs. Mach-CO

r = 0.03

Ebert et al., 1983 76; mix of smoking 1-22 mg CO ECO vs. Mach-CO

cessation, hospital r = 0.03

employees, and 

ambulatory patients

Wald et al., 1984 2,455 males during 0.8-28.1 mg CO CO remained 

health screening relatively constant

exams in London regardless of cigarette yield

Gori and Lynch, 1985 865 recruited from 2-18 mg CO ECO vs. FTC-CO;

shopping malls; 10 or virtually no correlamore cigarettes per day tion

Maron and Fortmann, 713 in a community-based <0.2 - >1.0 mg ECO vs. FTC-N

1987 survey NIC Analysis of variance

revealed NSD

Woodward and 2,754 from Scottish Heart 1-19 mg CO ECO vs. Mach Tar, N,

Tunstall-Pedoe, 1992 Health Study (1984–1986) and CO and gender 

(multiple regression)

accounted for 19% of

variance 

Coultas et al., 1993 298 in a population survey, — ECO vs. FTC-CO

primarily Hispanic r = 0.03

Hee et al., 1995 108 volunteers, 5 or more 1.1-15.0 mg COHb vs. Mach

cigarettes per day r = 0.24

Key: CO = carbon monoxide; FTC-N = machine yield of nicotine by Federal Trade Commission method; ECO = expired CO; COHb

= blood carboxyhemoglobin; Mach-CO = smoking-machine-measured CO.

Chapter 03 11/19/01 10:57 AM Page 55
56

Smoking and Tobacco Control Monograph No. 13

Thus, the data on other biomarkers support the overall conclusions of

studies that measured nicotine and CO—that there is very little difference

in tobacco smoke exposure in people smoking cigarettes of different

machine-determined yields. For the general population of smokers who

select their own brand of cigarettes, the extent of nicotine compensation

appears to be almost complete. 

Smokers in their natural environment have chosen the

brand of cigarettes they smoke. A smoker’s choice of cigarette brand is influenced by a variety of factors, including the brand

smoked by peers, the influence of advertising and promotional materials, a

desire to reduce the health risks of smoking (which is, in turn, influenced

by advertising and promotion), and the characteristics of the cigarette (i.e.,

adequacy of nicotine dose, taste, etc.). Experimental studies of brand

switching are, to some extent, artificial in that the researchers select the

brand. Spontaneous brand switching studies are more informative of smokers’ exposures in the real world when they switch to lower yield cigarettes.

SPONTANEOUS BRAND

SWITCHING

0

10

20

30

40

50

60

2 4 6 8 10 12 14 16 18 20

FTC Carbon Monoxide (mg/cigarette)

Expired-Air Carbon Monoxide

(parts per million)

Figure 3-3

Expired Cabon Monoxide Concentrations in Smokers According to FTC CO Yields of

Cigarettes Smoked

Note: Solid line indicates mean; dashed line indicates 95% confidence intervals (from Gori and Lynch, 1985).

Chapter 03 11/19/01 10:57 AM Page 56
Two studies of spontaneous brand switching were reviewed for this chapter.

Lynch and Benowitz (1987) reported on 197 smokers who had measurements of plasma cotinine and COHb while smoking self-selected brands on

2 occasions, 6 years apart. Of these smokers, 104 were smoking cigarettes of

the same or similar machine-determined yields as before, 62 had switched

to a lower yield (0.2 mg or more reduction in nicotine delivery), and 31

had switched to higher yields (0.2 mg or more increase in nicotine delivery). Plasma samples and expired CO were measured on approximately the

same day at baseline and on retesting. Smokers who did not change the

nicotine yield showed a slight decrease in the numbers of cigarettes smoked

per day, but there was no change in cotinine or CO levels (see Figure 3-4).

Smokers who switched to lower yield cigarettes initially smoked cigarettes

with higher nicotine yields (average 1.09 mg) and then switched to cigarettes with an average yield of 0.68 mg, a 38 percent reduction. Brand

switching was associated with a reduction in cotinine and expired CO of

about 20 percent. However, these smokers had also decreased their cigarette

consumption by about 20 percent. Analysis of cotinine concentration or

CO per cigarette showed no change despite reduction in yield. Thus, the

smokers obtained the same dose of nicotine and CO from each cigarette

even though the yield was lower. This observation is consistent with findings described previously showing that when switching from high- to lowyield cigarettes, full compensation from each cigarette is easily achieved.

Reduction in daily exposure to tobacco smoke occurred primarily because

certain smokers who switched to low-yield cigarettes smoked fewer cigarettes. Possibly, switching was part of an attempt by these individuals to

reduce their health risks by smoking both lower yields and fewer cigarettes

per day. 

Switchers to high-yield cigarettes had smoked a low-yield cigarette at

the initial study (average, 0.42 mg nicotine) and switched to cigarettes with

an average yield of 0.85 mg, a 102 percent increase. After switching, cotinine levels increased by 23 percent and expired CO by 5 percent (see Figure

3-5). In this case, smokers did take in more nicotine and CO per cigarette,

although much less than predicted by the relative increase in machine

yield. Because these subjects were smoking lower yield cigarettes and had

lower cotinine levels at baseline compared to subjects who switched to cigarettes of similar or lower yields, it is likely that this group was composed of

smokers in an escalating phase of developing tobacco dependence. This

idea was supported by the observation that, after switching, cotinine levels

rose to levels similar to those of the other two groups at baseline. 

Peach and coworkers studied 599 males over 13 years (from 1971 to

1984) in a study of the effects of brand switching on phlegm production on

pulmonary function tests (Peach et al., 1986a). Average cigarette consumption decreased in all smokers, but less so in those smokers who switched to

lower yield cigarettes. Nicotine intake was estimated by a colorimetric assay

of total nicotine plus metabolite excretion in the urine. At the 1984 assessment, no difference in nicotine metabolite excretion was observed in individuals who had or had not switched from higher to lower yield cigarettes.

This suggests full compensation when switching to lower yield cigarettes. 

57

Chapter 3

Chapter 03 11/19/01 10:57 AM Page 57
Smoking and Tobacco Control Monograph No. 13

58

200

250

300

350

6

8

10

12

400 14

Plasma Cotinine (ng/ml) Plasma Cotinine per cigerette 

(ng/ml)

B S S B

Figure 3-4

Spontaneous Brand Switching Study: Plasma Concentrations of Cotinine and

Cotinine Concentration Normalized for Cigarettes Smoked per Day

Note: B indicates baseline and S indicates follow-up study.

Symbols: Triangles=subjects who did not switch brands (n=109); solid squares=decreasers (n=62); solid circles=increasers (n=32);

asteriks indicate significant change from baseline to follow-up study (from Lynch and Benowitz, 1987).

In summary, these two spontaneous brand-switching studies indicated

that when smokers choose to switch to low-yield cigarettes, their intake of

nicotine and CO (and presumably other smoke constituents) per cigarette

does not significantly change. Thus, for spontaneous brand switchers, there

appears to be a complete compensation for each cigarette smoked, reflecting more intensive smoking. These observations suggest, at least when considering modern cigarettes, that switching from higher to lower yield cigarettes per se is not likely to reduce disease risk. 

SUMMARY Studies of subjects who smoked cigarettes with lower machine-determined yields support the idea that smokers regulate their intake of nicotine

to take in the amount of nicotine that they need to sustain their addiction.

Experimental switching studies show varying degrees of compensation.

Variability from study to study probably reflects the characteristics of the

smokers and the types of cigarettes to which they were switched.

Experimental studies in which smokers were switched from regular to ultraChapter 03 11/19/01 10:57 AM Page 58
low-yield cigarettes suggest a significant but modest reduction in nicotine

exposure. Spontaneous brand-switching studies suggest that there is no

reduction in smoke intake per cigarette, and that any reductions that were

seen in brand switchers depended upon whether or not those individuals

also cut down their cigarette consumption. 

Studies of smokers smoking self-selected brands assessed exposure in

individuals who smoked as many of their cigarettes as they wish. These

studies convincingly showed a weak relationship between nicotine yield

and nicotine, CO, or thiocyanate exposure. An exception may be smokers

of ultra-low-yield cigarettes, for whom in some studies there was an approximately 30 percent reduction of cotinine levels. However, the market share

for ultra-low-yield cigarettes is extremely small. 

59

Chapter 3

Expired CO (ppm) Expired CO 

per cigerette (ppm)

B S S B

30

35

40

45

1.0

1.2

1.4

1.6

50 1.8

Figure 3-5

Spontaneous Brand Switching Study: Expired Air CO Concentration and CO

Concentration Normalized for Cigarettes Smoked per Day

Note: B indicates baseline and S indicates follow-up study.

Symbols: Triangles=subjects who did not switch brands (n=109); solid squares=decreasers (n=62); solid circles=increasers (n=32);

asteriks indicate significant change from baseline to follow-up study (from Lynch and Benowitz, 1987).

Chapter 03 11/19/01 10:57 AM Page 59
Smoking and Tobacco Control Monograph No. 13

60

Adlkofer, F., Scherer, G., Heller, W.D. Hydroxyproline

excretion in urine of smokers and passive smokers. Preventive Medicine 13(6):670-679, 1984.

Alison, S., Frost, C., Thompson, S., Wald, N.

Estimating the extent of compensatory smoking.

Nicotine, Smoking and the Low Tar Programme.

Wald, N., Fruggatt, P. (Editors.). London, Oxford

Medical Publishing, pp. 100-115, 1989.

Bartsch, H., Caporaso, N., Coda, M., Kadlubar, F.,

Malaveille, C., Skipper, P., Talaska, G.,

Tannenbaum, S.R., Vineis, P. Carcinogen hemoglobin adducts, urinary mutagenicity, and metabolic phenotype in active and passive cigarette

smokers. Journal of the National Cancer Institute

82(23):1826-1831, 1990.

Considering the overall exposure data in individuals selecting their own

brands, there is little reason to expect that smokers of low-yield cigarettes

will have a lower risk of disease than those smoking higher yield cigarettes.

Lower tar-to-nicotine ratios could result in reduced risk, in theory, even if

there is full compensation for nicotine, but the few human exposure data

available to date suggest that exposure to tar compared to nicotine is not

different in smokers smoking low-yield cigarettes. 

The majority of smokers appear to compensate by smoking their cigarettes more intensively and/or by blocking ventilation holes. Some studies

show that smokers of low-yield cigarettes smoke more cigarettes per day.

Other studies indicate that occasional smokers are more likely to be in the

low-yield category, which may result in estimates of smoking similar or

even fewer cigarettes in the low-yield group compared to higher yield

groups. Recent data from California suggest that if one looks at addicted

smokers who have been smoking at a stable level for some time, smokers of

low-yield cigarettes do smoke more cigarettes. This type of analysis has not

been performed on other data sets, where cigarette consumption was simply taken for all smokers of a particular yield regardless of level of dependence or the stability of smoking behavior. 

CONCLUSIONS

1. Smokers regulate their intake of nicotine to obtain the amount of

nicotine that they need to sustain their addiction.

2. Spontaneous brand-switching studies suggest that there is no reduction in smoke intake per cigarette, and that any reductions that are seen in

brand switchers depend upon whether or not those individuals also reduce

their cigarette consumption.

3. Studies of smokers smoking self-selected brands showed a weak relationship between machine-measured nicotine yield and a smoker’s nicotine,

CO, or thiocyanate exposure.

4. Considering the overall exposure data for individuals selecting their

own brands, there is little reason to expect that smokers of low-yield cigarettes will have a lower risk of disease than those who smoke higher yield

cigarettes.

REFERENCES

Chapter 03 11/19/01 10:57 AM Page 60
Chapter 3

61

Benowitz, N.L. Pharmacologic aspects of cigarette

smoking and nicotine addiction. The New

England Journal of Medicine 319:1318-1330, 1988.

Benowitz, N.L. Dosimetric studies of compensatory

cigarette smoking. Nicotine, Smoking and the Low

Tar Programme. Wald, N., Froggatt, P. (Editors.).

London, Oxford Medical Publishing, 1989.

Benowitz, N.L. Cotinine as a biomarker of environmental tobacco smoke exposure. Epidemiologic

Reviews 18(2):188-204, 1996.

Benowitz, N.L. Biomarkers of environmental tobacco

smoke exposure. Environmental Health Perspectives

107(Suppl 2):349-355, 1999a.

Benowitz, N.L. Nicotine addiction. Primary Care

26(3):611-631, 1999b.

Benowitz, N.L., Hall, S.M., Herning, R.I., Jacob, P.,

III, Jones, R.T., Osman, A.L. Smokers of low yield

cigarettes do not consume less nicotine. The New

England Journal of Medicine 309(3):139-142, 1983.

Benowitz, N.L., Jacob, P., III. Daily intake of nicotine

during cigarette smoking. Clinical Pharmacology

and Therapeutics 35(4):499-504, 1984a.

Benowitz, N.L., Jacob, P., III. Nicotine and carbon

monoxide intake from high- and low-yield cigarettes. Clinical Pharmacology and Therapeutics

36(2):265-270, 1984b.

Benowitz, N.L., Jacob, P., III. Nicotine renal excretion

rate influences nicotine intake during cigarette

smoking. The Journal of Pharmacology and

Experimental Therapeutic 234(1):153-155, 1985.

Benowitz, N.L., Jacob, P., III. Intravenous nicotine

replacement suppresses nicotine intake from cigarette smoking. The Journal of Pharmacology and

Experimental Therapeutics 254(3):1000-1005,

1990.

Benowitz, N.L., Jacob, P., III. Metabolism of nicotine

to cotinine studied by a dual stable isotope

method. Clinical Pharmacology and Therapeutics

56(5):483-493, 1994.

Benowitz, N.L., Jacob, P., III, Denaro, C. and Jenkins,

R. Stable isotope studies of nicotine kinetics and

bioavailability. Clinical Pharmacology and

Therapeutics 49(3):270-277, 1991.

Benowitz, N.L., Jacob, P., III, Fong, I. and Gupta, S.

Nicotine metabolic profile in man: Comparison

of cigarette smoking and transdermal nicotine.

The Journal of Pharmacology and Experimental

Therapeutics 268(1):296-303, 1994.

Benowitz, N.L., Jacob, P., III, Kozlowski, L. and Yu, L.

Influence of smoking fewer cigarettes on exposure to tar, nicotine, and carbon monoxide exposure. The New England Journal of Medicine

315(21):1310-1313, 1986.

Benowitz, N.L., Jacob, P., III, Yu, L., Talcott, R., Hall,

S. and Jones, R.T. Reduced tar, nicotine, and carbon monoxide exposure while smoking ultralowbut not low-yield cigarettes. Journal of the

American Medical Association 256(2):241-246,

1986.

Benowitz, N.L., Zevin, S., Jacob, P., III. Suppression

of nicotine intake during ad libitum cigarette

smoking by high dose transdermal nicotine. The

Journal of Pharmacology and Experimental

Therapeutics 287(3):958-962, 1998.

Breese, C.R., Marks, M.J., Logel, J., Adams, C.E.,

Sullivan, B., Collins, A.C., Leonard, S. Effect of

smoking history on [3H]nicotine binding in

human postmortem brain. The Journal of

Pharmacology and Experimental Therapeutics

282(1):7-13, 1997.

Byrd, G.D., Davis, R.A., Caldwell, W.S., Robinson,

J.H., deBethizy, J.D. A further study of FTC yield

and nicotine absorption in smokers.

Psychopharmacology (Berl) 13(4):291-299, 1998.

Byrd, G.D., Robinson, J.H., Caldwell, W.S.,

deBethizy, J.D. Comparison of measured and

FTC—Predicted nicotine uptake in smokers.

Psychopharmacology (Berl) 122(2):95-103, 1995.

Collins, A.C., Luo, Y., Selvaag, S., Marks, M.J.

Sensitivity to nicotine and brain nicotinic receptors are altered by chronic nicotine and mecamylamine infusion. The Journal of Pharmacology and

Experimental Therapeutics 271(1):125-133, 1994.

Coultas, D.B., Stidley, C.A., Samet, J.M. Cigarette

yields of tar and nicotine and markers of exposure to tobacco smoke. American Review of

Respiratory Disease 148(2):435-440, 1993.

Ebert, R.V., McNabb, M.E., McCusker, K.T., Snow, S.L.

Amount of nicotine and carbon monoxide

inhaled by smokers of low-tar, low-nicotine cigarettes. Journal of the American Medical Association

250(20):2840-2842, 1983.

Feyerabend, C., Ings, R.M.J. and Russell, M.A.H.

Nicotine pharmacokinetics and its application to

intake from smoking. British Journal of Clinical

Pharmacology 19(2):239-247, 1985.

Florin, I., Rutberg, L., Curvall, M., Enzell, C.R.

Screening of tobacco smoke constituents for

mutagenicity using the Ames' test. Toxicology

15(3):219-232, 1980.

Frost, C., Fullerton, F.M., Stephen, A.M., Stone, R.,

Nicolaides-Bouman, A., Densem, J., Wald, N.J.,

Semmence, A. The tar reduction study:

Randomised trial of the effect of cigarette tar

yield reduction on compensatory smoking.

Thorax 50(10):1038-1043, 1995.

Gori, G.B., Lynch, C.J. Smoker intake from cigarettes

in the 1-mg Federal Trade Commission tar class.

Regulatory Toxicology and Pharmacology 3(2):110-

120, 1983.

Gori, G.B., Lynch, C.J. Analytical cigarette yields as

predictors of smoke bioavailability. Regulatory

Toxicology and Pharmacology 5(3):314-326, 1985.

Guyatt, A.R., Kirkham, A.J.T., Mariner, D.C., Baldry,

A.G., Cumming, G. Long–term effects of switching to cigarettes with lower tar and nicotine

yields. Psychopharmacology (Berl) 99(1):80-86,

1989.

Chapter 03 11/19/01 10:57 AM Page 61
Smoking and Tobacco Control Monograph No. 13

62

Hecht, S.S. Biochemistry, biology, and carcinogenicity of tobacco-specific N-nitrosoamines. Chemical

Research in Toxicology 11(6):559-603, 1998.

Hecht, S.S., Carmella, S.G., Murphy, S.E., Akerkar, S.,

Brunneman, K.D. and Hoffmann, D. A tobaccospecific lung carcinogen in the urine of men

exposed to cigarette smoke. The New England

Journal of Medicine 329(21):1543-1546, 1993.

Hee, J., Callais, F., Momas, I., Laurent, A.M., Min, S.,

Molinier, P., Chastagnier, M., Claude, J.R., Festy,

B. Smokers' behaviour and exposure according to

cigarette yield and smoking experience.

Pharmacology, Biochemistry, and Behavior

52(1):195-203, 1995.

Jaffe, J.H., Kanzler, M., Friedman, L., Stunkard, A.J.,

Vereby, K. Carbon monoxide and thiocyanate

levels in low tar/nicotine smokers. Addictive

Behaviors 6:337-343, 1981.

Jahnke, G.D., Thompson, C.L., Walker, M.P.,

Gallagher, J.E., Lucier, G.W., DiAugustine, R.P.

Multiple DNA adducts in lymphocytes of smokers and nonsmokers determined by 32P-postlabeling analysis. Carcinogenesis 11(2):205-211,

1990.

Jarvis, M.J., Borham, R., Primatesta, P., Feyerabend,

C., Bryant, A. Nicotine yield from machinesmoked cigarettes and nicotine intakes in smokers: Evidence from a representative population

survey. Journal of the National Cancer Institute

93(2):134-138, 2001.

Lynch, C.J., Benowitz, N.L. Spontaneous brand

switching: Consequences for nicotine and carbon monoxide exposure. American Journal of

Public Health 77(9):1191-1194, 1987.

Maron, D.J., Fortmann, S.P. Nicotine yield and measures of cigarette smoke exposure in a large population: are lower-yield cigarettes safer? American

Journal of Public Health 77(5):546-549, 1987.

Mooney, L.A., Santella, R.M., Covey, L., Jeffrey, A.M.,

Bigbee, W., Randall, M.C., Cooper, T.B., Ottman,

R., Tsai, W.-Y., Wazneh, L., et al. Decline of DNA

damage and other biomarkers in peripheral

blood following smoking cessation. Cancer

Epidemiology, Biomarkers & Prevention 4(6):627-

634, 1995.

Peach, H., Ellard, G.A., Jenner, P.J., Morris, R.W. A

simple, inexpensive urine test of smoking.

Thorax 40(5):351-357, 1985.

Peach, H., Hayward, D.M., Ellard, D.R., Morris, R.W.,

Shah, D. Phlegm production and lung function

among cigarette smokers changing tar groups

during the 1970s. Journal of Epidemiology and

Community Health 40(2):110-116, 1986a.

Peach, H., Hayward, D.M., Shah, D. A double-blind

randomized controlled trial of the effect of a

low- versus a middle-tar cigarette on respiratory

symptoms—A feasibility study. IARC Scientific

Publications 74:251-263, 1986b.

Picciotto, M.R., Caldarone, B.J., King, S.L.,

Zachariou, V. Nicotinic receptors in the brain.

Links between molecular biology and behavior.

Neuropsychopharmacology 22(2):451-465, 2000.

Rickert, W.S., Robinson, J.C. Estimating the hazards

of less hazardous cigarettes. II. Study of cigarette

yields of nicotine, carbon monoxide and hydrogen cyanide in relation to levels of cotinine, carboxyhemoglobin, and thiocyanate in smokers.

Journal of Toxicology and Environmental Health

7(3-4):391-403, 1981.

Rickert, W.S., Robinson, J.C., Young, J.C., Collishaw,

N.E., Bray, D.F. A comparison of the yields of tar,

nicotine, and carbon monoxide of 36 brands of

Canadian cigarettes tested under three conditions. Preventive Medicine 12(5):682-694, 1983.

Robinson, J.C., Young, J.C., Rickert, W.S., Fey, G.,

Kozlowski, L.T. A comparative study of the

amount of smoke absorbed from low yield ('less

hazardous') cigarettes. Part 2: Invasive measures.

British Journal of Addiction 78(1):79-87, 1983.

Rosa, M., Pacifici, R., Altieri, I., Pichini, S., Ottaviani,

G., Zuccaro, P. How the steady-state cotinine

concentration in cigarette smokers is directly

related to nicotine intake. Clinical Pharmacology

and Therapeutics 52(3):324-329, 1992.

Russell, M.A., Wilson, C., Patel, U.A., Feyerabend, C.,

Cole, P.V. Plasma nicotine levels after smoking

cigarettes with high, medium, and low nicotine

yields. British Medical Journal 2(5968):414-416,

1975.

Russell, M.A., Jarvis, M., Iyer, R., Feyerabend, C.

Relation of nicotine yield of cigarettes to blood

nicotine concentrations in smokers. British

Medical Journal 280(6219):972-976, 1980.

Russell, M.A., Jarvis, M.J., Feyerabend, C., Saloojee,

Y. Reduction of tar, nicotine and carbon monoxide intake in low tar smokers. Journal of

Epidemiology and Community Health 40(1):80-85,

1986.

Russell, M.A.H., Sutton, S.R., Iyer, R., Feyerabend, C.,

Vesey, C.J. Long–term switching to low–tar

low–nicotine cigarettes. British Journal of

Addiction 77(2):145-158, 1982.

Sorsa, M., Falck, K., Heinonen, T., Vainio, H.,

Norppa, H. and Rimpela, M. Detection of exposure to mutagenic compounds in low-tar and

medium-tar cigarette smokers. Environmental

Research 33(2):312-321, 1984.

Sutton, S.R., Russell, M.A., Iyer, R., Feyerabend, C.,

Saloojee, Y. Relationship between cigarette

yields, puffing patterns, and smoke intake:

Evidence for tar compensation? British Medical

Journal (Clin Res Ed) 285(6342):600-603, 1982.

Chapter 03 11/19/01 10:57 AM Page 62
Chapter 3

63

U.S. Department of Health and Human Services,

Public Health Service. The Health Consequences of

Smoking—Nicotine Addiction: A Report of the

Surgeon General. U.S. Department of Health and

Human Services, Public Health Service, Centers

for Health Promotion and Education, Office on

Smoking and Health. DHHS Publication No. 88-

8406, 1988.

van Maanen, J.M.S., Maas, L.M., Hageman, G.,

Kleinjans, J.C.S., van Agen, B. DNA adduct and

mutation analysis in white blood cells of smokers and nonsmokers. Environmental and Molecular

Mutagenesis 24(1):46-50, 1994.

Wald, N.J., Boreham, J., Bailey, A. Relative intakes of

tar, nicotine, and carbon monoxide from cigarettes of different yields. Thorax 39(5):361-364,

1984.

West, R.J., Russell, M.A., Jarvis, M.J., Feyerabend, C.

Does switching to an ultra-low nicotine cigarette

induce nicotine withdrawal effects?

Psychopharmacology (Berl) 84(1):120-123, 1984.

Woodward, M., Tunstall-Pedoe, H. Do smokers of

lower tar cigarettes consume lower amounts of

smoke components? Results from the Scottish

Heart Health Study. British Journal of Addiction

87(6):921-928, 1992.

Woodward, M., Tunstall–Pedoe, H. Self-titration of

nicotine: evidence from the Scottish Heart

Health Study. Addiction 88(6):821-830, 1993.

Yamasaki, E., Ames, B.N. Concentration of mutagens

from urine by adsorption with the nonpolar

resin XAD-2: Cigarette smokers have mutagenic

urine. Proceedings of the National Academy of

Sciences USA 74(8):3555-3559, 1977.

Zacny, J.P., Stitzer, M.L. Cigarette brand switching:

Effects on smoke exposure and smoking behavior. The Journal of Pharmacology and Experimental

Therapeutics 246(2):619-627, 1988.

Chapter 03 11/19/01 10:57 AM Page 63
Smoking and Tobacco Control Monograph No. 13

64

Chapter 03 11/19/01 10:57 AM Page 64
INTRODUCTION This chapter examines whether the disease risks of smoking

have changed as a result of the changes in cigarette design over the last 50

years. Cigarette design and manufacture have changed substantially over

the last half century, and the relationship of these changes to altered disease risks is an important scientific and public health issue. No cigarette

currently manufactured and sold can be considered safe, and the principal

recommendation for any smoker interested in reducing future disease risks

is to quit smoking. However, approximately 47 million individuals remain

cigarette smokers in the United States (CDC, 2000a), and many of these

smokers have tried to quit and failed. If these continuing cigarette smokers

could alter their risk by choosing cigarettes that differ in machine-measured

tar and nicotine yields or other characteristics, and if this choice did not

interfere with their likelihood of cessation, then advice to switch brands

might be one component of a comprehensive strategy to reduce the disease

consequences of tobacco use. Alternatively, if these lower yield products do

not reduce risks and if smokers switch brands instead of quitting, then the

changes in cigarettes and their marketing as reduced-risk products represent

a cruel deception of current smokers. For those smokers who delay cessation, the increased duration of smoking that results from delayed cessation

is likely to be a more powerful determinant of disease risk than a small, or

nonexistent, reduction in tar exposure from use of these cigarettes.

Prior reviews (U.S. DHHS, 1981; NCI, 1996) of changes in disease risk

with switching from unfiltered or higher yield to filtered or lower yield cigarettes concluded that switching probably reduced lung cancer risk somewhat, but only if smokers did not increase the number of cigarettes that

they smoked per day when they switched to lower yield cigarettes. Ninetyseven percent of the cigarettes sold in the United States currently have filters and the sales-weighted tar yield of cigarettes has declined by more than

60 percent since the 1950s. 

Assessing the consequences of changes in cigarette design and manufacturing is made difficult by the lengthy time period over which these

changes have been made, the difficulty of tracking changes in smoking

behavior over time, and the lack of validity of the FTC yield data as indicators of doses of toxic compounds of cigarette smoke. Nevertheless, epidemiological evidence has provided some insights concerning the consequences

of changes in cigarettes over the last fifty years. The data have three

sources: (1) observations of national rates of lung cancer by age in relation

to age-specific smoking patterns; (2) case-control and cohort studies that

have compared lung cancer risks in smokers of different types of products

at particular points and times; and (3) comparisons of lung cancer in smok65

Smoking Lower Yield Cigarettes and

Disease Risks

David M. Burns, Jacqueline M. Major, Thomas G. Shanks, 

Michael J. Thun, Jonathan M. Samet

Chapter 04 11/19/01 11:00 AM Page 65
ers over time, coming from either a single cohort with lengthy follow-up

(the British Physicians Study) or repeated cohort observations (the two CPS

studies of the American Cancer Society).

Each of these sources of data has strengths and limitations when used

to assess the effect of changes in cigarette design on disease risks. Changes

in age-specific national lung cancer death rates over time measure the actual population burden of disease, and these rates must change if there has

been any substantive benefit resulting from changes in cigarette design.

They also offer the opportunity to examine change in disease rates over

periods of time long enough to allow full expression of the cumulative

effects of all of the changes in cigarette design, which have also occurred

over multiple decades. One major limitation of these data is the absence of

information on smoking status and type of cigarette smoked in national

death registry data. This absence requires comparison of the lung cancer

death rate data with information derived from population surveys on smoking behavior and market data on type of cigarette sold. It limits the examination of these data sets to ecological analyses and comparisons of trends

over time in population measures of smoking behaviors and disease rates.

Epidemiological studies have the strength of being able to collect

detailed information on smoking behaviors, type of cigarette smoked and

other variables of interest that allow differences in these factors to be examined in detail, and controlled, in the analysis of disease risk. However, these

studies are limited by confining their observations to relatively short slices

of time or fixed cohorts of individuals. The cross-sectional nature of casecontrol studies requires extrapolation from differences observed across individuals who smoke different types of cigarettes at one slice of time, with

the presumption that those cross-sectional differences in type of cigarette

smoked reflect the longitudinal changes in cigarette design that preceded

them. For example, the difference in dose of smoke received by a filter cigarette smoker compared to a non-filter cigarette smoker in 1980 may or may

not correspond to the differences in smoke dose received by smokers in the

1950s (almost entirely non-filtered cigarette smokers) compared to the dose

of smoke received by filtered cigarette smokers in the 1980s. A more important limitation of these studies of changing cigarette design is the possibility that the characteristic of the cigarette being studied (machine-measured

yield) may directly influence smoking behavior, including the number of

cigarettes smoked per day. This linkage between the characteristic being

studied and the measures used to control for differences between populations of smokers in the dose of smoke received makes control for intensity

of smoking problematic. In addition, the reasons for choosing the brand

smoked may be linked to other demographic or behavioral characteristics

which may also influence disease outcome (level of addiction, interest in

cutting down or quitting, differences in other health related behaviors,

etc.).

Examination of cohorts with long durations of follow-up (the British

Physicians Study), or comparing similar cohorts separated by a long interval

(the two CPS studies of the American Cancer Society), offer the strengths of

long periods of observation and the availability of individual level data on

66

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 66
smoking behaviors and other characteristics. Limitations of following a single cohort for long periods of follow-up include the fact that the cohort

becomes less and less representative of the entire population over time;

and, in particular, it is limited in its ability to examine the effects of changing cigarette design on smokers who initiate with those products rather

than switch to them. Comparison of similar cohorts separated by more

than 20 years allows inclusion of younger generations of smokers, but is

limited by the possibility that the smokers in the two cohorts are likely to

be of different composition in demographic characteristics and may differ

in other characteristics as well. These differences may occur because the

later cohort of smokers from the 1980s is composed of those who have

been unable or unwilling to quit smoking; and therefore, it may not be

directly comparable to the earlier cohort from the 1960s when the percentage of former smokers was lower.

Each of these sources of epidemiological data can expand our understanding of the disease burden that results from changing cigarette design,

and together they complement each other to counter the limitations present when any one data source is examined in isolation. The question

addressed in this chapter is whether cigarette smoking in the year 2000,

with all of the changes in cigarette design and all of the compensatory

changes in smoking behavior, is more or less hazardous than it was in 1950.

The disease consequences of changes in cigarette design and the consequences of switching type of cigarette smoked can be approached from two

perspectives. First, has the risk of disease per cigarette smoked changed; and

second, has the risk of disease for smokers compared to nonsmokers

changed. From the public health perspective, the latter is the more relevant

question.

The body of existing published literature was examined to answer this

question, and new analyses of data sets from the American Cancer Society

and the California Tobacco Survey are provided to explore and clarify the

differences between epidemiological evaluations and the national trends in

lung cancer death rates.

The chapter begins with a discussion of the historical development of

cigarettes that have produced ever lower machine-measured tar and nicotine yields using the Federal Trade Commission (FTC) protocol1 (Pillsbury,

1996). It then discusses the complexity of epidemiological examination of

the self-selected behavior of smoking lower yield cigarettes and outlines the

potential sources of confounding likely to occur in epidemiological studies.

Next, various epidemiological studies that have assessed the risks of lowyield cigarettes in relation to lung cancer and cardiovascular and chronic

respiratory diseases are examined. The chapter considers the evidence on

compensatory smoking, those changes in smoking behavior that allow

smokers to maintain their customary nicotine intake when they switch to a

cigarette with a lower machine-measured nicotine yield. It discusses two

67

Chapter 4

1 The machine smokes the cigarette with 2-second, 35-ml puffs and a 58-second inter-puff 

interval until a 23-mm butt length or 3 mm from the filter overwrap is reached.

Chapter 04 11/19/01 11:00 AM Page 67
new epidemiological analyses that find higher daily cigarette consumption

among smokers of lower yield cigarettes. Finally, the chapter considers

cohort- and population-based studies that have examined temporal trends

in lung cancer incidence or mortality in relation to changes in cigarette

design and/or smoking behavior.

Greater weight was placed on evidence derived from trends in populations over time than on evidence from cross-sectional epidemiological studies since reductions in general population death rates are the ultimate outcome measure for the effect of changing cigarette design over the last 50

years. If the changes in cigarette design are of public health significance,

they must impact the rates of disease actually occurring in the population

of smokers who use these cigarettes. The true effect of changing cigarette

design requires integration of the information from epidemiological studies

and the population trends in disease rates. If a substantive reduction in disease risk is expected from the epidemiological studies, it should be evident

as a change in population disease rates. If the effect is not evident in the

population data, then one should reconsider the potential for self-selection

and compensatory smoking to bias the epidemiological results or confuse

their interpretation.

While the emphasis in the discussion and analyses presented in this

chapter is on the tar and nicotine yields measured by the FTC protocol, the

question being asked is really whether all of the changes in cigarette design

and manufacture over the last half century have altered the disease risks of

smoking cigarettes. Part of this focus on FTC yields comes from their use,

appropriately, as exposure variables in epidemiological studies. Machinemade measurements of tar and nicotine are used in the discussion simply as

convenient surrogates for the cumulative effect of all of the changes that

have occurred. Arguments can be made to support differences in risk that

might result from individual engineering changes in cigarette manufacturing using evidence based on changes in tobacco smoke chemistry or biological exposure studies, but ultimately, the issue of concern is the net effect of

these cigarette design changes on the total disease burden in human smokers as the cigarettes are smoked by the general public. This chapter is

focused on answering the question: “Have changes in cigarette manufacture

and design over the last 50 years resulted in a meaningful public health

benefit to human smokers?” This overall question has two related but distinct research questions. First, has the risk per cigarette smoked been

changed by these product modifications; and second have the net adverse

consequences of smoking for the population been changed by these product modifications.

Other chapters in this volume describe the marketing and behavioral

issues of cigarettes with low machine-measured yields.

Cigarette smoking was definitively

linked to increased lung cancer risk in

the 1950s (Wynder and Graham, 1950; Doll and Hill, 1952, 1954;

Hammond and Horn, 1958). It was almost simultaneously discovered that

painting cigarette smoke condensate on the skin of animals produced

HISTORICAL DEVELOPMENT OF THE

LOWER YIELD CIGARETTE ISSUE

68

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 68
tumors (Wynder et al., 1953). A logical extrapolation of these observations

was that reducing exposure of smokers to the total particulate matter in cigarette smoke should reduce the risk of developing lung cancer. Independent

scientists and public health authorities recommended that cigarettes which

reduced tobacco smoke delivery to the smoker be developed and marketed

by tobacco companies (U.S. Congress, 1967). The tobacco industry initially

responded by adding filters to cigarettes and then by offering cigarettes that

delivered less tar (the total particulate matter in smoke minus the water and

nicotine) in measurements made by machine smoking of cigarettes using a

fixed pattern of smoking (U.S. DHHS, 1981; NCI, 1996; Warner, 1985). A

variety of approaches to tar reduction were utilized, including ‘puffing’ the

tobacco to reduce the weight of tobacco in a cigarette, altering the blends

of tobacco used and porosity of the paper wrapper, changing the density of

the tobacco rod, using tobacco stems and reconstituted tobacco sheet, and

using a wide variety of filter materials. These changes are detailed more

completely in Chapters 2 and 5. Ultimately, this effort to reduce machinemeasured tar yields led to the introduction of cigarettes with ventilation

holes around the filter. These ventilated filters reduced the tar measured by

machine using the FTC method by diluting the smoke with entrained air.

Ventilation is the principal method by which the very low levels of

machine-measured tar yields of most current light and ultralight cigarettes

are produced (see Chapter 2). 

Both the smoke exposure and the disease risks resulting from smoking

lower yield cigarettes depend on how these cigarettes are used by smokers.

Machine-measured yields are only informative for the smoker to the extent

that they reflect the smoker’s exposure and disease risk either directly or in

relation to other brands of cigarettes. Internal tobacco industry documents

from the 1960s and 1970s, when filtered and lower yield cigarettes were

first heavily marketed to assuage health concerns of smokers, recognized

that these changes in cigarette design might not actually result in delivery

of less tar to smokers. Since smokers were smoking to derive a sufficient

dose of nicotine, they could compensate for reductions in nicotine delivery

by changing the way that they smoked these cigarettes in order to preserve

their nicotine intake. Tar yield is closely correlated with nicotine yield, and

so compensation to preserve nicotine intake preserves tar intake as well. 

A Philip Morris company memo (Wakeham, 1961) expressed concern

about smokers’ likely response to the new highly filtered cigarettes: “As we

know, all too often the smoker who switches to a hi-fi cigarette winds up

smoking more units in order to provide himself with the same delivery

which he had before. In short, I don’t believe the smoking pattern has

changed much, even with the cancer scares and filter cigarettes.” 

A research planning memo by Claude Teague (Teague, 1972) was even

more explicit: “Given a cigarette that delivers less nicotine than he desires,

the smoker will subconsciously adjust his puff volume and frequency, and

smoking frequency, so as to obtain and maintain his per hour and per day

requirement for nicotine . . .” A Brown & Williamson Tobacco Company

memo (Pepples, 1976) commented, “The new filter brands vying for a piece

of the growing filter market made extraordinary claims . . . In most cases,

69

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 69
however, the smoker of a filter cigarette was getting as much or more nicotine and tar as he would have gotten from a regular cigarette. He abandoned the regular cigarette, however, on the ground of reduced risk to

health.” Because tar is delivered in a relatively fixed ratio to nicotine for

most conventional cigarettes (see Chapters 2 and 3), compensation to preserve nicotine intake would also preserve tar exposure, minimizing any

reduction in a smoker’s lung cancer risk from switching to these cigarettes.

There has been a reduction in machine-measured tar-to-nicotine ratios in

ultralow cigarettes when measured by the FTC method, but these same

ratios in ultralow cigarettes increase when smoked under conditions that

mimic those of human smokers (see Chapters 2 and 3). 

The tobacco industry’s response to health concerns about smoking

raised by the public health community was to develop cigarettes with lower

yields of tar and nicotine as measured by the FTC method. The reductions

in tar were marketed as a surrogate for reductions in risk (see Chapter 7).

There is no current evidence that the tobacco companies conducted any

biological or animal testing to test this hypothesis of reduction in risk.

Again, internal tobacco industry documents illuminated the goals and

design directions taken by the industry in this effort. A report on a tobacco

research conference (Green, 1968) noted, “Research staff should lay down

guide lines against which alternative products can be chosen in everyday

operations. Although there may, on occasions, be conflict between saleability and minimal biological activity, two types of products should be clearly

distinguished, viz: 

a) A Health-image (health reassurance) cigarette.

b) A Health-oriented (minimal biological activity) cigarette, to be kept

on the market for those consumers choosing it.” 

Conversion of this line of thinking into cigarette design modifications

was further specified in an undated British American Tobacco Company

memo: “What would seem very much more sensible, is to produce a cigarette which can be machine smoked at a certain tar band, but which, in

human hands, can exceed this tar banding . . .” (BATCO, undated). This

concept is described as “elasticity of delivery,” which has two definitions as

used in this chapter and in tobacco industry documents. First, elasticity is

used to describe the phenomenon of a smoker being able to derive markedly different amounts of tar and nicotine from a cigarette by changing the

way that it is smoked. Inherent in this concept is the understanding that

the elastic cigarette will provide whatever dose of nicotine the smoker

wants if the smoker adjusts his or her pattern of smoking appropriately. A

second, more technical definition was provided in an Imperial Tobacco of

Canada document, which stated, “If the tar delivery increases in direct proportion to the increase in puff volume, the product is inelastic (i.e., elasticity = 1), while if tar delivery increases faster than puff volume, elasticity >

1.” (See Imperial Tobacco Limited, 1993.) 

The importance of ventilation from perforated filters in achieving this

elasticity was clarified by a 1982 Philip Morris memo that described tests on

machine yields of cigarettes with ventilated filters when the holes in the fil70

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 70
ters were covered and uncovered, using different puff volumes to simulate

smoker compensation (Goodman, 1982). The conclusion reached by

Goodman stated, “The decrease in dilution from covering a portion of the

perforated area can result in an increased delivery to the smoker of highlydiluted cigarettes even though the puff parameters decrease.” Implications

of the elasticity of delivery design for actual delivery to the smoker had

been defined in a prior memo by the same individual (Goodman, 1975)

that described a study which examined yields of Marlboro Light® and

Marlboro 85® cigarettes when smoked by smokers who had been switched

to these brands from their regular choice. The smoking puff profile for

these smokers was recorded and then replicated to make measurements on

a smoking machine. The conclusion reached by Goodman (1975) stated:

“In effect, the Marlboro 85 smokers in this study did not achieve any reduction in smoke intake by smoking a cigarette (Marlboro Lights) normally

considered lower in delivery.”

These internal tobacco company documents suggest that the effort to

develop low-yield cigarettes was conducted with a clear appreciation of the

compensation to preserve nicotine intake that was likely to occur in smokers. Cigarettes were designed with elasticity of delivery in an effort to provide low machine yields, allowing marketing of the product as a “healthreassurance” cigarette while continuing to deliver high levels of nicotine to

satisfy the addictive demands of the smokers of these cigarettes. 

However, even though the impact of changes in cigarette design on

actual smoke delivery to smokers was questionable, early studies of the disease risks among smokers of low-yield cigarettes were encouraging. They

demonstrated a somewhat lower lung cancer risk among populations of

individuals who used filtered and low-yield products, albeit a much smaller

reduction in lung cancer risk than the extent of reduction in machinemeasured tar. These studies led to considerable optimism about the likely

public health benefits of changes that had occurred in cigarette design (U.S.

Congress, 1967; U.S. DHEW, 1971, 1979). The early data were particularly

encouraging because the reductions in lung cancer risks were demonstrable

in populations observed during the mid to late 1960s when filtered cigarettes had only been available for a short period of time (Bross, 1968; Bross

and Gibson, 1968; Hammond et al., 1976, 1977). Widespread use of filtered

and lower yield products began in the mid 1950s. Since the reduction in

excess lung cancer risk with cessation continues to increase for 15-20 years

following cessation (U.S. DHHS, 1990; Burns et al., 1997b), it was expected

that these modest changes in risk demonstrable with short-term use of

reduced-tar products would have a growing impact on lung cancer death

rates as more smokers used these products for longer periods of time

(Wynder and Stellman, 1979). 

Over the last 50 years, machine-measured, sales-weighted tar yields for

U.S. cigarettes have declined by over 60 percent. Several careful reviews of

the available scientific data (U.S. DHHS, 1981; NCI, 1996) have suggested

that there is a reduction in lung cancer risk for populations of smokers who

use lower yield cigarettes if they did not increase the number of cigarettes

that they smoked as they decreased the yield of the cigarette that they

71

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 71
smoked. These reviews did not identify reductions in heart or lung disease

risks associated with reductions in tar and nicotine yield of the cigarette

smoked. The lung cancer risk reductions offered the promise of a substantial reduction in U.S. lung cancer death rates. 

A reduction in U.S. lung cancer death rates of the magnitude expected

from the differences in risk found in epidemiological studies of lower yield

cigarettes (15-40%) has not been realized. Lung cancer death rates have

continued to rise among women, and the modest decline in lung cancer

death rates observed among men is generally consistent with the temporal

trends of reduced initiation and increased cessation among males. (Tolley et

al., 1991; Mannino et al., 2001). In addition, two studies performed by the

American Cancer Society 20 years apart (1960s vs. 1980s) have shown an

increase in lung cancer risk among current smokers (Thun and Heath, 1997;

Thun et al., 1997a & b). In these studies, there was no evidence for any

decline in lung cancer risk, even when the subjects were compared controlling for number of cigarettes smoked per day, duration of smoking, and age.

This increase in lung cancer risk over time was confirmed by the results of

the British Physicians Study (Doll et al., 1994) which demonstrated an

increase in lung cancer risk among continuing cigarette smokers during the

last 20 years of the 40 years of follow-up (1951-1991) when compared to

the first 20 years of follow-up, despite a substantial fall in machine-measured tar yield of British cigarettes over this same period. 

The discrepancies between epidemiological studies demonstrating

reductions in risk with the use of low-yield and filtered cigarettes and the

absence of population-based reductions in the hazards of smoking led to a

reexamination of the question: Does the use of lower yield cigarettes result

in meaningful reductions in disease risks compared to use of higher yield

cigarettes? The authors integrated what is known from published epidemiological studies of smokers of low-yield cigarettes with what is known about

compensatory smoking behavior and the characteristics that lead smokers

to choose low-yield products. In addition, a series of new analyses are presented in an effort to resolve the apparent differences between published

epidemiological evaluations and the mortality experience in the United

States. 

Examination of changes in disease risks

that result from changes in cigarette

design raises a set of formidable challenges in human epidemiological studies. These changes come from the

temporally dynamic nature of smoking over the last fifty years. The

changes include changes in the product, changes in the age of smoking initiation, and changes in cessation. Related methodological challenges stem

from the changing demographic distribution of tobacco use; the relationship of duration of smoking and age to disease risks; the cross-sectional

slice of the population experience that is inherent in either retrospective or

prospective epidemiological evaluations; the complexity and wide variety of

changes that have occurred in cigarette design over the last 50 years; the

changes in measures of smoking intensity that result from switching to

lower yield cigarettes; the linkage between reasons for choosing lower yield

LIMITATIONS OF EPIDEMIOLOGICAL

STUDIES IN EXAMINING THE RISKS

OF LOW-YIELD CIGARETTE USE

72

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 72
cigarette brands and other behaviors intended to reduce risks (including

cessation); and the limited availability of information on what changes

were made to which cigarettes, over what periods of time, and their potential impacts on smoking behaviors. The tools used by epidemiologists for

approaching these challenges are rather blunt; obtaining smoking histories

that cover products smoked, age started smoking, and number of cigarettes

smoked per day. FTC yield measurements have been used in some studies as

a surrogate for changes in exposure, in spite of the well-recognized limitations of its use for this purpose (see Chapters 2 and 3).

Cigarette smoking prevalence varies with age, gender, education,

race/ethnicity, and most other demographic characteristics relevant to population risks (U.S. DHHS, 1998). The distribution of smoking prevalence

within demographic characteristic has also varied with calendar year over

the last 50-100 years in ways that influence current differences in disease

rates (Burns et al., 1997a & b; Thun et al., 1997b). For example, women first

began to smoke in large numbers in the late 1930s and 1940s, but during

those years, women initiated smoking across a wide age range (Burns et al.,

1997a). As a result, female smokers who are currently old enough to have

high risks of lung cancer have, on average, shorter durations of smoking

than males of the same age. This difference explains much of the

male/female differences in U.S. lung cancer mortality rates (Mannino et al.,

2001). Demographic and temporal variation in smoking behaviors is also

evident in patterns of smoking cessation (Burns et al., 1997a). 

Superimposed on this complex variation in smoking behaviors are an

equally complex demographic and temporal variations in use of filtered and

lower yield cigarettes, and these patterns do not always parallel those of

smoking prevalence. For example, current survey data show that smoking

prevalence declines with age among adults, but use of low-yield cigarette

increases with age. In addition, older females, who have lower rates of

smoking prevalence than their age-matched male contemporaries, are more

likely to have used filtered and lower yield cigarettes and to have used them

for much more of their smoking histories. 

Some of these differences would be less important if smoking caused

disease instantaneously, or if recent smoking was the principal determinant

of disease risk. However, most diseases caused by smoking are the result of

long periods of cumulative damage to the smoker and are heavily influenced by smoking that occurred 10, 20, or even 30 years or more in the

past. Traditional measures of smoking intensity, such as number of cigarettes smoked per day, are recorded at entry into an epidemiological study.

They have been useful approximations of lifetime smoking intensity in

these studies because of the relative stability of this measure in smokers

over their smoking lifetime. The same stability cannot be assumed when

the smoker switches to a new type of cigarette, particularly when that new

cigarette delivers less nicotine than the smoker is trying to obtain by smoking. What is often measured in epidemiological studies is the number of

cigarettes currently smoked with the current type of cigarette. If the type of

cigarette influences the number of cigarettes, then the current number of

cigarettes smoked per day is not necessarily a valid measure of intensity of

73

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 73
smoking in the past with other types of cigarettes. Similarly, it is also not a

valid measure when comparing current smoking intensities among individuals who smoke different types of cigarettes. Thus, one of the most common measures used to control for smoking intensity in epidemiological

studies may be linked to, and perhaps partly determined by, the characteristics of the cigarette that the epidemiological study is attempting to examine. 

Epidemiological studies examine events during follow-up over defined

slices of time in fixed populations. From these data, investigators attempt to

separate the effects related to age, intensity and duration of smoking from

differences in cigarette design on disease risks produced by smoking. Even

prospective epidemiological studies start with a fixed population defined at

a fixed point in time and follow that population forward in time. These

populations define a temporally specific set of smoking experiences with a

specific set of cigarette products, and these limitations restrict the range of

product changes that can be observed. In other words, any study addresses

only a specific time period and the products used by the smokers observed

in the study. The generalizability of the findings to other time periods and

other products is uncertain. 

Extrapolating effects beyond the range for which one has observations

is always problematic. Generalizability is a particular problem in examining

changing cigarette designs because many design changes occurred simultaneously, and some of them may have influenced cigarette yields in ways

that are contrary to that expected by investigators. For example, some of

the filtered cigarettes introduced in the 1950s and 1960s actually had higher tar deliveries than their nonfiltered brands in the same brand family (see

Chapter 7), making the use of filter cigarette smoking as a measure of lower

tar exposure uncertain. 

Smokers of low-yield cigarettes may differ from smokers of high-yield

cigarettes in important characteristics other than the cigarette smoked.

These differences need to be carefully considered in epidemiological studies

in order to prevent these other characteristics from introducing confounding facts that may bias the results of these studies. If low-yield cigarette

smokers have lower intensities of smoking, are more likely to quit smoking,

or have other characteristics that lower their disease risks, then differences

in disease risks demonstrated between populations of high- and low-yield

cigarette smokers may not be due to the differences in the cigarette that

they smoke. These differences can be considered as confounding, as they

relate to differences between high- and low-yield cigarette smokers reflecting the differences between those selecting and not selecting the product. 

The principal determinant of the chronic disease risks associated with

smoking is the amount of tobacco smoke to which an individual is exposed

as measured by the intensity and duration of smoking. Smoking intensity is

correlated with nicotine levels in the blood (Benowitz et al., 1983;

Benowitz, 1996) and with the need to maintain those levels (U.S. DHHS,

1988). As discussed elsewhere in this monograph (see Chapters 2 and 3),

clinical and pharmacological studies demonstrate that smokers who switch

74

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 74
to cigarettes with low-nicotine yield modify their smoking behavior to

maintain their accustomed nicotine intake. Compensatory behaviors may

include: 1) taking more frequent puffs per cigarette; 2) taking larger puff

volumes and inhaling more deeply; 3) obstructing the ventilation holes

that would otherwise dilute the mainstream smoke; and 4) smoking more

cigarettes per day. Thus, the FTC tar and nicotine ratings do not accurately

reflect the exposure of an individual smoker to the carcinogens in tobacco

smoke, as they do not take account of any of these compensatory behaviors. 

The nicotine yield of the cigarette smoked may be a determinant of the

measure of smoking intensity (number of cigarettes smoked per day) most

commonly used as a control variable in epidemiological studies. If smokers

who switch to lower yield cigarettes increase the number of cigarettes

smoked per day to preserve a constant nicotine intake, then accounting for

the number of cigarettes smoked per day in an analysis misrepresents the

net consequences of changing cigarette type for dose of smoke exposure

and risk. This widely employed strategy addresses the risk of different products conditional on the number of cigarettes smoked per day. For example,

a smoker who smokes 10 high-nicotine cigarettes, and who switches to a

low-nicotine variety, may compensate by smoking 20 low- nicotine cigarettes to maintain exactly the same level of nicotine intake. Measures of

nicotine intake are good measures of total smoke dose; and, if smokers preserve the same nicotine intake, one would expect them to preserve their

total smoke dose and disease risk as well. However, if the number of cigarettes smoked per day is used as a measure of smoke dose, then the smoker

in this example would appear to have doubled his or her smoke dose on

switching to the low-nicotine cigarette, when in reality the smoking intensity or total smoke dose had not changed at all. 

Over the last several decades, there is

substantial evidence showing that

smokers of low yield cigarettes differ

from smokers of high yield cigarettes.

Some of these differences involve other risk factors for cigarette caused diseases, raising the possibility of confounding. Attribution of differences in

risks between the populations to the less hazardous character of the cigarettes that they smoke requires examination of differences between these

two populations of smokers in their use of cigarettes, extent of compensation, reasons for choosing these products, and other behaviors related to

disease risks. 

In the United States, the majority of adolescents begin smoking

Marlboro®, Camel®, or Newport® cigarettes (CDC, 2000b), brands that are

mid-range yield. Thus, it is brand shifting, and the decline in tar and nicotine yields of the same brands over time, rather than brand initiation that

leads to the use of low machine-measured yield cigarettes among adults.

Figure 4-1 presents data from the 1996 California Tobacco Survey for the

fraction of adult smokers with different demographic characteristics who

reported that the brand they smoke is low in tar and nicotine. Similar difComparing Populations of High- and

Low-Yield Cigarette Smokers in

Epidemiological Studies—Population

Differences

75

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 75
ferences across type of cigarette smoked were evident in a national sample

of smokers (Giovino et al., 1996). The fraction of smokers reporting use of

low-tar products increases dramatically with age, education, and income,

and is higher among females than among males. These demographic differences might be expected from the marketing of these products as lower risk

products. 

Low-yield cigarettes have been marketed as delivering less tar, and this

is commonly understood by smokers as resulting in less risk (see Chapters 6

and 7). It is, therefore, not surprising that a substantial fraction of those

who switch from higher to lower yield cigarettes do so in an effort to

reduce their disease risks (Cohen, 1996a & b; see Chapters 6 and 7). In addition, some smokers switch to these products hoping to quit or substantially

reduce their smoking (Giovino et al., 1996; see Chapters 6 and 7). Other

smokers, after a failed cessation attempt, relapse to using low-yield products

in an effort to mitigate the risk from resumption of smoking. Because of

these health concerns, and an ongoing interest in cessation, these same

low-yield cigarette smokers may also have higher rates of successful longterm smoking cessation or may voluntarily reduce the amount that they

smoke for health reasons. Risk reductions that accompany cessation or lowered smoking intensity may appear to be related to the tar level of the cigarette smoked while actually resulting, at least in part, from other factors.

Cohort studies following a population longitudinally for assessment of disease risk without repeated follow-up assessment of smoking status may be

particularly vulnerable to this bias. 

Hammond (1980) examined the American Cancer Society’s first Cancer

Prevention Study (CPS-I) data to look for this association between use of

low-yield cigarettes and smoking cessation. Smokers of low-tar (17.6 mg or

less) cigarettes midway through the study in 1965 were more likely to be

former smokers than medium- or high-tar cigarette smokers at the last follow-up in 1972. 

The higher educational and socioeconomic status of low-yield cigarette

smokers are likely to be correlated with other positive health behaviors

(diet, exercise, etc.) that may lower disease risks for reasons independent of

choice of cigarette type. Giovino and colleagues (1996) showed that smokers of low-yield products have higher levels of formal education than persons who smoke higher yield products. Haddock and associates (1999)

found that Air Force recruits who had switched in the previous year to

lower tar and nicotine brands in order to reduce their health risks were also

more likely to have more nutritious diets. 

The rising level of health concerns that occur in middle age may lead

individuals to a variety of changes in their behavior that are intended to

improve their health, including smoking cessation. It would not be surprising to learn that these same individuals, should they relapse to smoking following a cessation attempt that is part of their efforts to change future disease risks, are more likely to smoke lower yield cigarettes. Any successful

change in their diet, level of exercise, reductions in alcohol or tobacco, as

well as the reductions in disease risks that result from these changes, would

be linked to the use of lower yield cigarettes. 

76

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 76
Conversely, smokers with newly diagnosed disease who are unable to

quit may switch to low-yield cigarettes in the belief that there is less risk

associated with their use. This would have the effect of increasing disease

rates in populations of low-yield cigarette smokers. 

It is also possible that less-intense and less-addicted smokers may either

use, or be more likely to successfully switch to, low-yield cigarettes. Their

demand for nicotine is less, and it may be more easily satisfied by cigarettes

that deliver less nicotine. In contrast, heavy smokers and those who are

strongly dependent may not be able to extract sufficient nicotine from

these lower yield products to satisfy their addiction, so they may preferentially choose higher yield cigarettes. 

These differential characteristics of smokers of different types of cigarettes may affect case-control and cohort studies in different ways. In casecontrol studies of lung cancer, filter or lower yield cigarette smokers are

likely to be better educated, have higher incomes, and have better dietary

habits than will unfiltered or higher tar cigarette smokers. The former may

also be more likely to be less-intense and less-dependent smokers than the

latter. These characteristics may influence the rates of lung cancer occurrence independent of any effect of cigarette type smoked; but unless they

are carefully controlled in the analysis, they may bias toward finding a

lower lung cancer risk among filtered or lower yield cigarette smokers. 

77

Chapter 4

0

10

20

30

40

50

60

70

80

>75,000+

10,001-20,000

20,001-30,000 30,001-50,00050,001-75,000

<=10,000

16+ 13-15

12

<12

Asian/Pacific Islander

African American Hispanic

White

65+

18-24 25-44

45-64

Female

Total

Male

Smokers (%)

Gender Age Race/Ethnicity Education Income

Figure 4-1

Percentage of Smokers Over Age 18 Reporting That Their Brand is Low in Tar and

Nicotine, 1996 California Tobacco Survey

Chapter 04 11/19/01 11:00 AM Page 77
Prospective cohort studies of lung cancer risk in relation to the type of

cigarette smoked follow smokers forward in time to observe lung cancer

risks. If lower yield cigarette smokers are more likely to quit successfully or

adopt other healthy behaviors, and subjects are not tracked repetitively during the follow-up period, then trends toward lower risk smoking behaviors,

cessation and other healthy behaviors may occur with a higher frequency

in the lower yield cigarette group. A reduced rate of disease in lower yield

cigarette smokers may be due to changes in their risk-related behaviors after

the initial entry into the study, rather than to the type of cigarette they

smoked. Many cohort studies have followed populations for a decade or

more, sufficient time for differences to arise in characteristics of smokers of

different types of cigarettes. 

The principal method utilized to control for differences in the intensity of

smoking among different populations

of smokers is to use the number of

cigarettes smoked per day as a measure of smoking intensity or dose of

smoke received. The validity of this approach is supported by the demonstration of higher blood levels of cotinine (the major metabolite of nicotine) among smokers of larger numbers of cigarettes per day (Jarvis et al.,

2001; Benowitz et al., 1983). Current understanding of the compensatory

changes in smoking behavior that occur with the use of low yield cigarettes

suggests that the bulk of compensation occurs by adjusting the topography

of smoking for each individual cigarette (see Chapters 2 and 3). Smokers

take larger puffs, inhale more deeply, and change their smoking pattern in

other ways to extract the same amount of nicotine from cigarettes with

vastly different nicotine yields by the FTC method. Smokers may also compensate by increasing the number of cigarettes smoked per day when they

switch to low yield cigarettes. 

Many published epidemiological studies of low-yield cigarettes have

adjusted for the number of cigarettes smoked per day because it is the most

readily available quantitative measure of smoke dose. It is possible for

smokers who switch to lower yield cigarettes to fully preserve the daily dose

of nicotine and smoke they receive from smoking (see Chapters 2 and 3).

The preservation of a constant daily dose of smoke when shifting to a cigarette with a lower machine-measured yield may occur through changes in

the way the cigarette is smoked, through an increase in number of cigarettes smoked per day, or through a combination of both methods. A smoker who fully compensates, and who increases the number of cigarettes

smoked per day when he or she switches to a lower yield cigarette to

achieve that compensation, will receive the same daily dose of smoke exposure with high and low yield cigarette smoking; but they will report different numbers of cigarettes smoked per day when smoking high and low

yield cigarettes for that same daily dose of smoke. If cigarettes smoked per

day is used in an epidemiological study to estimate the biologic dose of

toxin or carcinogen that this smoker is receiving, then it will appear that

the dose increased when the smoker switched to lower yield cigarettes; and

the true dose of smoke exposure will be overestimated when smoking lower

yield cigarettes as compared to higher yield cigarettes. If a substantial fracUsing Number of Cigarette Per Day to

Control for Intensity of Smoking in

Epidemiological Studies

78

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 78
tion of lower yield cigarette smokers are compensating by increasing the

number of cigarettes smoked per day, then epidemiological studies which

use CPD to control for differences in daily dose will overestimate the dose

received by lower yield cigarette smokers relative to higher yield cigarette

smokers. This overestimation, if present, will bias the risk estimates in favor

of finding lower risks among lower yield cigarette smokers when high and

low yield cigarette smokers are compared in analyses that use CPD to control for daily dose of smoke received by smokers. Even slight compensation

through increasing CPD can substantially bias the risk estimate. 

This potential interaction between number of cigarettes smoked per day

and type of cigarette smoked is illustrated in Figure 4-2 which presents theoretical relationships between disease relative risks and increasing number

of cigarettes smoked per day for high and low yield cigarettes. In theory, a

smoker who compensates fully could do so by either exclusively changing

the pattern of smoking or by increasing the number of cigarettes smoked

per day as part of that compensation. If a smoker compensates entirely by

changing the pattern of smoking and does not increase the number of cigarettes smoked per day, the smoker will drop vertically from the high tar line

to the low tar line. If the level of compensation is only partial, this smoker

would experience a reduction in the daily smoke dose received, and one

would expect a population of smokers who had this form of partial com79

Chapter 4

Number of Cigarettes Smoked per Day

Relative Risk

Compensation without

increasing CPD

Full Compensation with

increasing CPD

High Tar

Low Tar

Figure 4-2

Effect of Increasing the Number of Cigarettes Smoked per Day When Switching to

Low-Yield Cigarettes on the Measurement of Relative Risk in Epidemiological Studies

Which Control for Number of Cigarettes Smoked per Day

Source: Hypothetical.

Chapter 04 11/19/01 11:00 AM Page 79
pensation to have lower lung cancer rates. Their lung cancer risk in relation

to CPD would generate a line similar to that presented as the low tar line in

Figure 4-2, that is a lower risk at any given number of cigarettes smoked per

day. However, if the compensation is complete, one would expect no reduction in daily dose of smoke or in lung cancer risk; and the line representing

their lung cancer risk in relation to CPD would superimpose on that for

high tar cigarette smokers. 

However, a smoker of high-yield cigarettes may also increase the number of cigarettes smoked per day as part of the compensatory changes in

smoking behavior that occur in order to preserve nicotine intake when he

or she switches to low-yield cigarettes. This pattern of complete compensation is represented as a horizontal shift between the two lines in Figure 4-2;

it combines the compensation that occurs due to changes in the pattern of

smoking each individual cigarette with the compensation that occurs

through increasing the number of cigarettes smoked per day. With complete compensation to preserve the same dose of toxic and carcinogenic

intake in this pattern, no change in smoke intake or disease risk would

occur; but when disease risk is plotted against number of cigarettes smoked

per day, the disease risk lines would not superimpose. Instead, they would

look like the two lines in Figure 4-2. The difference between these risk lines

would correctly suggest that a difference in disease risk per cigarette smoked

exists, when there is actually no change in disease risk for individual smokers resulting from switching to the lower yield brand of cigarettes due to

the increase in number of cigarettes smoked. 

Using the number of cigarettes smoked per day to control for the biological dose of smoke intake by the smoker can thus produce an artifactual

difference in disease risk if the question being asked is whether risk declines

when smokers switch to low yield cigarettes rather than if the risk per cigarette smoked declines. If compensatory changes include an increase in

number of cigarettes smoked per day, analyses that control for intensity of

smoking using CPD produce a risk estimate per cigarette smoked per day,

when in reality what is needed is a risk estimate for the total smoking

behavior of the smoker as he or she switches brands of cigarettes. The risk

should be expressed per smoker rather than per cigarette. For example, a

smoker of 20 high-tar cigarettes per day who switches to a low-tar product,

and who increases his or her number of cigarettes smoked to 25 per day to

fully preserve tar and nicotine intake, would also preserve the same disease

risk. However, he or she would appear to have a risk on a per-cigarettesmoked basis that was 80 percent (20 divided by 25) of the risk of smoking

high-tar cigarettes.

While it is possible to argue the legitimacy of expressing risk on a percigarette basis by suggesting that smokers should be educated not to

increase the number of cigarettes smoked per day when they change

brands, a public health benefit from use of low-yield cigarettes can only

accrue if there is a difference in disease risks across individuals as they actually use these low-yield cigarettes. If a cigarette produces a 20-percent

decrease in risk per cigarette, but its use by smokers results in 20 percent

more cigarettes being smoked per day, the net result will likely be no

change in disease risk for the individual or within the population. 80

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 80
81

Chapter 4

The potential for smokers to increase the number of cigarettes that they

smoke per day when they switch to lower yield cigarettes can complicate

analyses of disease risks among smokers of different types of cigarettes in

both case-control and prospective epidemiological evaluations. Data are

presented later in this chapter to show that smokers who switched to lowyield cigarettes in the CPS-I study increased the number of cigarettes that

they smoked per day, and that smokers of ultralow nicotine-yield cigarettes

smoked more cigarettes per day in recent California Tobacco Surveys. 

Even this limited discussion should make it apparent that epidemiological studies which simply compare the disease risks of high- and low-yield

cigarette smokers must be interpreted with great caution when addressing

the question of whether the cigarettes used are themselves the source of the

differences in risks. Some of the published epidemiological studies have recognized this concern, and the studies cited in Tables 4-1 to 4-3 used a variety of design and statistical approaches to adjust for differences in age,

duration of smoking, and intensity of smoking, as well as other characteristics of the populations.

In summary, a number of cautions are appropriate when examining epidemiological data on disease risks among those who smoke cigarettes with

different machine-measured tar and nicotine yields. Comparisons of populations without controlling for differences in intensity of smoking likely to

exist between high- and low-yield smokers can only define the populations

as different, and these comparisons have limited ability to link the differences in risks observed to differences in the product used. However, control

for intensity of smoking across populations using number of cigarettes

smoked per day as the measure of dose may result in model misspecification if smokers who switch to low-yield cigarettes compensate by increasing

the number of cigarettes that they smoke per day. 

Tables 4-1 to 4-3 present epidemiological

evaluations of smokers who used cigarettes

with filters or different levels of machinemeasured tar yield. An effort was made to

include all of the published studies that evaluated individual smokers and

presented numerical risks of disease associated with lower yield cigarettes.

Studies were excluded if they used national consumption data as the measure of smoking, examined black versus blond tobacco, bidis, small cigars,

hand-rolled cigarettes, cigarettes limited predominantly to other countries,

clove cigarettes and other smoking products, Asian-Indian smoking behaviors, or other forms of tobacco use besides cigarettes. 

Table 4-1 shows the studies that have examined lung cancer risks with

low-yield products. While a few studies have not found a relationship, and

several of the relationships identified were not statistically significant, the

clear impression from these studies taken as a whole is that there is a lower

risk of lung cancer among populations of smokers who use lower yield

products. This relationship is evident in case-control studies as well as in

prospective mortality studies (see Table 4-1). The vast majority of these

studies controlled for intensity of smoking using the number of cigarettes

PUBLISHED EPIDEMIOLOGICAL

STUDIES OF HEALTH ENDPOINTS

Lung Cancer

Chapter 04 11/19/01 11:00 AM Page 81
82

Smoking and Tobacco Control Monograph No. 13 Table 4-1 Epidemiological Studies of Low-Yield Cigarettes and Lung Cancer Citation Population Time Period Cigarette Type Relative Risk Comments Bross, I.D., Gibson, R. Case-control study of 974 1960-1966 Filter/Regular 0.59 Stratified by duration of smoking Risks of lung cancer in White male lung cancer and number of cigarettes/day. smokers who switch to patients and hospital Risk for regular is 6.48 and for filter cigarettes. Am. J. controls. filtered is 3.83. Filtered smokers Public Health 58(8): were more likely to smoke more 1396-1403, 1968. than one pack per day, 38% to 35%. Many had been smoking fil- tered cigarettes for leass than 3 years. Bross, I.D. Effect of filter Case-control study of 974 1960–1966 Filter/ Regular 0.59 Stratified by duration of smoking cigarettes on lung cancer White male lung cancer and number of cigarettes/day. risk. National Cancer patients and hospital Risk for regular is 6.59 and for Institute Monograph No. controls. filtered is 3.9. Filtered cigarette 28, Toward a Less Harmful smokers were more likely to Cigarette. U.S. DHEW, NCI, smoke more than one pack per 1968. day, 38% to 35%. Many had 

been smoking filtered cigarettes for less than 3 years.

Hammond, E.C. et al. Some 12-year follow-up of CPS-I. 1960-1972 Tar yield Male low-tar RR=

recent findings concerning A prospective mortality 0.93 for 1960-1966, cigarettes smoking. Cold study of over 1 million men 0.82 for 1966-1972;Springs Harbor Conferences and women. female RR=0.81 foron Cell Proliferation, Volume 1960-1966, 0.81 for4. Origins of Human Cancer, 1966-1972.Book A, Incidence of Cancerin Humans. pp. 101-112, 1977.Hammond, E.C. et al. “Tar” 12-year follow up of CPS-I. 1960-1972 Tar yield Male low-tar RR=

and nicotine content of A prospective mortality 0.93 for 1960-1966,cigarette smoke in relation to study of over 1 million men 0.82 for 1966-1972;death rates. Environ. Res. and women. female RR=p.81 for12:263-274, 1976. 1960-1966, 0.81 for

1966-1973.

Chapter 04 11/19/01 11:00 AM Page 82
Chapter 4

83

Table 4-1 (continued)Citation Population Time Period Cigarette Type Relative Risk CommentsLee, P.N., Garfinkel, L. 12-year follow-up of 1960-1972 Tar yield; Male=0.82; CHD risks are significantly difMortality and type of CPS-I. A prospective low/high female=0.60 ferent, but emphysema risks arecigarette smoked. J. of mortality study of over not.

Epidemiol. Community 1 million men and women.Health 35:16-22, 1981.Higenbottam, T. et al. 10-year follow-up of 1965-1975 Tar yield There was a smallCigarettes, lung cancer, 17, 475 male civil nonsignificant difand coronary heart disease: servants, aged 40-54, and ference in lung The effects of inhalation a sample of male British cancer mortality byand tar yield. J. Epidemiol. residents. tar yield that was

Communty Health 36:113- more evident 117, 1982. among noninhalers.

Hawthorne, V.M., Fry, J.S. Prospective follow-up of 1965-1977 Filter/Regular 0.83 No significant difference in morSmoking and health: The 18,786 people attending a tality rates for filter users for lungassociation between smok- multiphasic screening cancer or cardiovascular disease.ing behavior, total mortality, examination. Smokers of plain cigarettes hadand cardiorespiratory disease lower rates of respiratory sympin West Central Scotland. J. toms than filter smokers.

Epidemiol. CommunityHealth 32:260-266, 1978.Todd, G.F. et al. Four cardio- 12.4-year prospective 1965-1977 Filter/Regular 1.40 The increase in lung cancer morrespiratory symptoms as follow-up of 10,063 tality with filter use was not stapredictors of mortality. J. subjects aged 35-69 tistically significant; there was a

Epidemiol. Community from a random sample statistically significant decrease inHealth 32:267-274, 1978. of the population in all-cause mortality and male CHD

Great Britain. mortality with filter use (stan

dardized for number of cigarettes/day).

Engeland, A. et al. The im- A prospective study of 1966-1993 Filter/Regular Male=0.67; Controlled for age, number of 

pact of smoking habits on 26,126 Norwegian men female=0.91 cigarettes/day, and age at lung cancer risk: 28 years’ and women drawn from initiation.observation of 26,000 a population sample.

Chapter 04 11/19/01 11:00 AM Page 83
Smoking and Tobacco Control Monograph No. 13

84Table 4-1 (continued)

Citation Population Time Period Cigarette Type Relative Risk CommentsNorwegian men and women. Cancer Causes andControl 7:366-376, 1996.Borland, C. et al. Carbon Prospective 10-year 1967-1979 CO yield 0.67 Controlled for age, grade of emmonoxide yield of ciga- follow-up of the White- ployment, cigarettes/day, and tarrettes and its relation to hall study where 4,910 yield. Those who smoked high cardiorespiratory disease. men had known CO CO-yield cigarettes (>20 mg) BMJ 287:1583-1586, 1983. yields of the cigarettes tended to smoke fewer cigarettes/

that they smoked. day.

Tang, J.L. et al. Mortality Four prospective mor- 1967-1982 Filter/Non-filter Tar 0.94 Relative risks for all tobacco-relatin relation to tar yield of tality studies from the and tar level (0.75-1.18) ed diseases combined were stacigarettes: a prospective United Kingdom. tistically significant. RR are adjuststudy of four cohorts. BMJ ed for age, study, and number of

311:1530-1533, 1995. cigarettes/day.Wynder, E.L. et al. The Case-control study of 1968-1969 Filter for at least Decreased risk in smokers of filter

epidemiology of lung 350 lung cancer patients 10 years/Non- cigarettes for 10 or more yearscancer: recent trends. and approximately 700 filter controlled and stratified by numJAMA 213:2221-2228, hospital controls. ber of cigarettes/day.1970.Wynder, E.L., Stellman, Case-control study of 1969-1976 Filter for at least RR for 1-10S.D. Impact of long-term 684 lung cancer patients 10 years/Non- cigarettes/day=filter cigarette usage on and 350 larynx cancer filter 0.61 (M), 0.38 (F);lung and larynx cancer patients. 11-20 cigarettes/risk: A case-control study. day =0.71 (M), 0.79JNCLI 62:471-477, 1979. (F); 31-40 cigarettes/

day=0.66 (M); 30+cigarettes/day=1.03(F); 41+ cigarettes/day=0.86 (M).

Augustine, A. et al. Com- Case-control study of 1969-1984 Filter/Non-filter Compared to those pensation as a risk factor 1,242 lung cancer cases who did not increase 

Chapter 04 11/19/01 11:00 AM Page 84
Chapter 4

85

Table 4-1 (continued)Citation Population Time Period Cigarette Type Relative Risk Commentsfor lung cancer in smokers and 2,300 sex- and age- their cigarette/day Mean changes in cigarettes/daywho switch from nonfilter matched hospital con- when they switched after switching for cases and conto filter cigarettes. AJPH trols. to filtered cigarettes, trols were adjusted by linear 

79:188-191, 1989a the odds ratios for regression for age at switching 

those increased 1- and duration of non-filter smoking10 cigarettes/day utilizing analysis of covariance.wer M=1.19, F=1.66, for those increased 11-20cigarettes/day,the odds ratios were M=1.75, F=2.97, andfor those who increased more than 20cigarettes/day, theodds ratios wereM=2.37, F=3.89.

Kabat, G.C. Aspects of Case-control study of 1969-1991 Filter/Non-filter Non-filter/filter only Reduction in male filter smokers the epidemiology of lung 7,553 lung cancer cases 0.7 (0.4-1.3);non- for Kreyberg I, but not Kreyberg II;cancer in smokers and and 19,992 hospital con- filter/switchers of effect in women not significant;nonsmokers in the United trols. 10+ years 0.7 (0.5- odds ratios adjusted for number ofStates. Lung Cancer 15:1- 0.9). cigarettes/day.20, 1996.Rimington, J. The effect of Follow-up study of 2,393 1970-1976 Filter/Non-filter 0.65 Age standardized.filters on the incidence of non-filter and 3,045 filterlung cancer in cigarette cigarette smokers from asmokers. Environ. Res. sample of mass radio24:162-166, 1981. graphy volunteers aged 

40 or more in England.

Kuller, L.H. et al. Cigarette 10.5-year follow-up of 1972-1985 Tar level, Nicotine RR=1.0 for Adjusted for age, serum cholessmoking and mortality the MRFIT participants. nicotine level nicotine level≤1 mg; terol, diastolic blood pressure, and

MRFIT Research Group. 0.97 (0.62-1.52) for cigarettes/day. Low-tar and lowPreventive Med. 20:638- nicotine cigarette smokers tended 

654, 1991. to smoke more cigarettes/day.

Chapter 04 11/19/01 11:00 AM Page 85
Smoking and Tobacco Control Monograph No. 13

86Table 4-1 (continued)

Citation Population Time Period Cigarette Type Relative Risk CommentsLubin, J.H. et al. Patterns A case-control study of 1976-1980 Filter/Non-filter Male=0.59; Adjusted for years of cigarette 

of lung cancer risk accord- 7,804 cases and 15,207 female=0.50 use, number of cigarettes/day, anding to type of cigarettes hospital-based controls years since cessation.smoked. Int. J. Cancer in seven Western

33:569-576, 1984. European locations.Lubin, J.H. Modifying risk Case-control study of 1976-1980 Filter/Non-filter 0.54 Risks adjusted for duration of useof developing lung cancer 7,181 lung cancer in years.by changing habits of patients and 11,006cigarette smoking. Brit. hospital controls in Med. J. 288:1953-1956, five Western European1984a; Brit. Med. J. 289: countries.

921, 1984b (letterresponse).Benhamou, S. et al. Lung Case-control study of 1976-1980 Filter/Non-filter 0.60cancer and use of cigarettes: 1,625 lung cancer A French case-control study. patients and 3,091JNCI 74:1169-1175, 1985. hospital controls.Buffler, P.A. et al. Case-control study of 1976-1980 13-14 mg/cig- 0.91 No significant difference for filters.

Environmental associations 476 cases and 466 arette (middle)with lung cancer in Texas population-based concoastal counties. Annual trols.Clinical Conference onCancer 28:27-34, 1986.Benhamou, E. et al. Lung Case-control study of 1976-1980 Filter/Non-filter 100% non-filter; Controlled for number of cigacancer and women: Results 96 women with lung RR=0/28 (0.05- rettes/day duration and inhalation.of a French case-control cancer and 192 matched 1.47)study. Brit. J. Cancer 55:91- hospital controls.

95, 1987.Benhamou, E.,et al. Case-control study of 1976-1980 Filter/Non-filter 0.7 (0.5-0.9) Adjusted for age and duration ofChanges in patterns of 1,057 cases and 1,503 cigarette smoking and number of

cigarettes/day.

Chapter 04 11/19/01 11:00 AM Page 86
Chapter 4

87

Table 4-1 (continued)Citation Population Time Period Cigarette Type Relative Risk Commentscigarette smoking and matched hospital conlung cancer risk: Results trols in France.of a case-control study.Br. J. Cancer 60:601-604, 1989.Benhamou, S. et al. Dif- Case-control study of 1976-1980 Filter/Non-filter 0.63 Risk adjusted only by age is 0.38ferential effects of tar con- 1,114 lung cancer for filter smokers only compared tent, type of tobacco and patients and 1,466 to non-filtered and mixed smokers.use of a filter on lung cancer hospital controls. Multivariate analysis shows slightrisk in male cigarette smok- nonsignificant increase withers. Int. J. Epidemiology percentage time smoking high-tar

24:437-443, 1994. cigarettes.Vutuc, C., Kunze, M. Lung Case-control study of 1976-1980 Tar level Tar level <15, odds Adjusted for age, duration, and cancer risk in women in 297 female lung can- ratio=0.29; tar level number of cigarettes/day.relation to tar yields of ciga- cers and neighborhood 15-24, odds ratio=rettes. Preventive Med. 11: controls from 15 lung 0.49; tar level > 24,

713-716, 1982. cancer centers in odds ratio=1.0

Austria.

Vutuc, C., Kunze, V. Tar Case-control study of 1976-1980 Tar level Tar level <15, odds Adjusted for age, duration, and yields of cigarettes and male 252 male lung cancers ratio=0.30; tar 15- number of cigarettes/day.lung cancer risk. JNCI 71: and hospital/neighbor- 24, odds ratio=0.56,

435-437, 1983. hood controls from 15 tar level >24, odds

lung cancer centers in ratio=1.0Austria.

Benhamou, E., Benhamou, Combination of four 1976-1988 Filter/Non-filter 0.91 Adjusted for age, duration, S. Black (air-cured) and case-control studies in cigarettes/day, current smoking,blond (flue-cured) tobacco Cuba, France, Uruguay, and residence.and cancer risk. VI: Lung an Italy.cancer. Eur. J. Cancer29A(12): 1778-1780, 1993.

Chapter 04 11/19/01 11:00 AM Page 87
Smoking and Tobacco Control Monograph No. 13

88Table 4-1 (continued)

Citation Population Time Period Cigarette Type Relative Risk CommentsLange, P. et al. Relationship 6,511 men and 7,703 1976-1989 Filter/Non-filter Male=0.82;

of the type of tobacco and women selected ran- Female=0.61inhalation pattern to pulmo- domly after age nary and total mortality. Eur. stratification from theRespir. J. 5:1111-1117, 1992. general population in

Copenhagen, followedfor 13 years.

Gillis, C.R. et al. Cigarette Case-control study of 656 1977-1981 Low-, medium-, Relative risks did smoking and male lung male lung cancer patients and high-tar not change signifcancer in an area of very and 1,312 age-matched yield icantly with tar high incidence. I: Report of hospital controls. yield for smokersa case-control study in the of 25+ cigarettes/West of Scotland. J. day. For smokers of

Epidemiol. and Community 15-24 cigarettes/Health 42:38-43, 1988. day, risks fell with tar 

yield, but it was notstatistically significant. Smokers of 1-14 cigarettes/day had a significant fall with tar yield.

Alderson, M.R. et al. Risks Case-control study of 1977-1982 Always flter/non- Male 1.48, Adjusted for number of cigarettes/of lung cancer, chronic 12,693 in-patients. filter female 0.85 day.bronchitis, ischaemic heartdisease, and stroke inrelation to type of cigarettesmoked. J. Epidemiol. andCommunity Health 39:286-293, 1985.Wynder, E.L., Kabat, G.C. Case-control study of 1977-1984 Filter/Non-filter Male Kreyberg I, Adjusted for cigarettes/day, age,The effect of low-yield ciga- 1,278 Kreyberg I filter-only smokers, inhalation, and years of education.

Chapter 04 11/19/01 11:00 AM Page 88
Chapter 4

89

Table 4-1 (continued)Citation Population Time Period Cigarette Type Relative Risk Commentsrette smoking on lung cancer patients and 2,408 0.69 (0.37-1.27);risk. Cancer 62:1223-1230, hospital controls and male Kreyberg II, 1988. 807 Kreyberg II partients 0.87 (0.43-1.54)

and 1,543 matchedcontrols.

Stellman, S.D. et al. Risk of Case-control study of 1977-1995 Filter/Non-filter Lifetime filter/non- Reduction in risk for squamous

squamous cell carcinoma 1,442 male and 850 filter: 0.4 (0.2- cell carcinoma in female lifetimeand adenocarcinoma of the female lung cancers 0.8) filter smokers compared to lifetimelung in relation to lifetime from 1977 to 1995 non-filter smokers controlling forfilter cigarette smoking. and hospital control. number of cigarettes/day, noCancer 80(3):382-388, differences for males or for 

1997. adenocarcinoma.Petitti, D.B., Friedman, G.D. 4-year prospective 1979-1982 Tar level and 0.87 (0.68-1.11) Controlled for age, sex, race, andCardiovascular and other follow-up of 16,270 high- and low- for a 5-mg in- number od cigarettes/day.diseases in smokers of current regular smokers (<15 mg tar crease in tarlow yield cigarettes. J. and 42,113 subjects who and 1 mg Chron. Dis. 38:581- never used any form of nicotine) yield588, 1985. tobacco. determined at

the start of thestudy.

Sidney, S. et al. A Prospective follow-up 1979-1985 Tar yield 1.02 (0.98-1.05) Long-term (20+ years) filter use

prospective study of ciga- of 79,946 Kaiser in men; 0.99 was associated with a reducedrette tar yield and lung Permanente Medical (0.96-1.03) in lung cancer risk in women, RR=cancer. Cancer Causes Care group members for women 0.36 (0.18-0.75), but not in men.

and Control 4:3-10, 1993. an average of 5.6 years.Wilcox, H.B. et al. Smoking Case-control study of all 1980-1981 Tar level Tar level 21.1- Adjusted by intensity and durationand lung cancer: Risk as a incidence cases of lung 28.0, odds ratio= of smoking. There was an increasfunction of cigarette tar cancer (763) in six areas 1.0; tar level 17.6- ing intensity of smoking with decontent. Preventive Med. of New Jersey compared 21.0, odds ratio= creasing level of tar among the

17:263-272, 1988. to population-based 1.21 (0.75-1.96); cases when consumption in two 

controls. tar level time periods were compared.

Pathak, D.R. et al. Case-control study of 521 1980-1982 Lifelong filter/ 0.80 Odds ratio was much lower 

Determinants of lung can- lung cancers and 769 con- non-filter

Chapter 04 11/19/01 11:00 AM Page 89
Smoking and Tobacco Control Monograph No. 13

90Table 4-1 (continued)

Citation Population Time Period Cigarette Type Relative Risk Commentscer risk in cigarette smokers trols matched for age, 1980-1982 Lifelong filter/ 0.80 among Hispanics (0.04).in New Mexico. JNCI 76:597- sex, and ethnicity. Non-filter

604, 1986.Kaufman, D. W. et al. Tar Case-control study of 1981-1986 Tar yield: <22, 1, 1.9 (1.0-3.7), Logistic regression controlled for content of cigarettes in 881 lung cancers and 22-28, 29+ 3.1 (1.3-7.1) age, sex, ethnicity, geographic relation to lung cancer. Am. 2,570 hospital controls. region, years of education, year of

J. Epidemiol. 129:703-711, interview, cigarettes/day, and 1989. year smoking started.Khuder, S.A. et al. Effect of Case-control study of 1985-1987 Filter/Non-filter 0.46 Adjusted for number of cigarettes/

cigarettes smoking on 482 male lung cancer day and the confidence intervalsmajor histological types cases and neighbor- overlap.of lung cancer in men. hood controls.Lung Cancer 22:15-21, 1998.Armadans-Gil, L. et al. Case-control study of 1986-1990 Filter/Non-filter 0.40 Adjusted for age and cumulativeCigarette smoking and 325 male lung cancer cigarette consumption.male lung cancer risk patients and agewith special regard to matched hospital contype of tobacco. Int. J. trols.

Epidemiol. 28:614-619, 1999.Pezzotto, S.M. et al. Case-control study of 1987-1991 Filter/Non-filter 0.29 Controlled for age, hospital of 

Variation in smoking- 215 lung cancers and admission, and intensity and durarelated lung cancer 433 hospital controls. tion of smoking.risk factors by cell typeamong men in Argentina:A case-control study.Cancer Causes and Control4:231-237, 1993.

Chapter 04 11/19/01 11:00 AM Page 90
91

Chapter 4

Table 4-1 (continued)Citation Population Time Period Cigarette Type Relative Risk CommentsDe Stefani, E. Mate drinking Case-control study of 1988-1994 Filter/Non-filter 0.72 No significant difference for filters.and risk of lung cancer in 497 cases and 497 males: A case-control study hospital controls.from Uruguay. Cancer Epidemiology, Biomarkers,and Prevention 5:515-519,1996.Agudo, A. et al. Lung Case-control study of 1989-1992 Filter/Non-filter 0.22

cancer and cigarette smok- 101 women with lunging in women: A case-control cancer with two study in Barcelona (Spain). matched hospitalInt. J. Cancer 59:165-169, controls.1994.Matos, E. et al. Lung cancer Case-control study of 1994-1996 Filter/Non-filter Filter 0.34 Filter cigarettes more risky in and smoking: A case-control 200 male lung cancer (CI: 1.09-0.11) black vs. blond comparisons andstudy in Buenos Aires, patients and 397 in comparisons by cell type.Argentina. Lung Cancer 21: hospital controls

155-163, 1998.Jockel, K.H. et al. Case-control study of Not stated Filter/Non-filter 0.41Occupational and environ- 194 lung cancermental hazards associated patients, 194 hospitalwith lung cancer. Int. J. controls, and 194Epidemiol. 21:202-213, population controls in1992. five German cities.

Chapter 04 11/19/01 11:00 AM Page 91
92

Smoking and Tobacco Control Monograph No. 13

smoked per day. Measurement of cigarettes smoked per day was recorded in

these studies at the same time that the brand of cigarettes smoked was

recorded. As a result, the comparison in the studies is between smokers of

equal numbers of different cigarettes smoked per day rather than between

smokers when they are using different products. If smokers increase the

number of cigarettes that they smoke per day when they switch from one

type of cigarettes to another type, then comparing them on a risk per cigarette basis may result in the wrong conclusion if the question being asked is

whether switching to lower yield cigarettes reduces the risk for the smoker.

One of the earliest studies (Bross and Gibson, 1968) was a case-control

study of lung cancer patients diagnosed between 1960 and 1966. The study

demonstrated a relative risk of 0.59 for filter smokers compared to nonfilter

smokers in an analysis stratified by duration and number of cigarettes

smoked per day. This analysis is of interest because it was conducted very

soon following the introduction of filtered cigarettes. Figure 4-3 presents

the number of filtered and nonfiltered cigarettes sold each year from 1925

to 1993, as well as their respective market shares. Essentially all cigarettes

sold prior to 1955 were nonfiltered cigarettes, but the market share for filtered brands increased rapidly thereafter. Because lung cancer is often present for several years prior to its diagnosis, and 5-10 years of cessation are

required to produce a 50-percent reduction in the excess risk of lung cancer,

the presence of such a large reduction in relative risk following so rapidly

after the introduction of filtered cigarettes raises questions concerning the

biological plausibility of these results. Bross and Gibson raised these biological plausibility concerns, noting that many of the filter smokers had been

using filtered cigarettes for less than 3 years. In addition, a table presented

in their article demonstrated that 38 percent of the filter smokers smoked

more than one pack per day in contrast to 35 percent of nonfilter smokers.

This finding was in the opposite direction from the expectation that those

who switched to filtered cigarettes were likely to be lighter smokers on average. It raises the likelihood that smokers who had switched to filtered cigarettes may have compensated for the decreased nicotine delivery of those

cigarettes by increasing the number of cigarettes that they smoked per day,

in effect biasing the analyses by moving less-intense filter smokers into strata where they were compared to more-intense nonfilter smokers.

Perhaps the most influential analyses have been those examining the

12-year follow-up of the American Cancer Society’s CPS-I, which followed

over 1 million men and women for up to 12 years between 1960 and 1972

(Hammond et al., 1976, 1977; Lee and Garfinkel, 1981). These analyses

were conducted using differences in machine-measured tar yields. Salesweighted tar yields declined sharply during this period (see Chapter 5).

Sales-weighted, machine-measured tar yields declined from 36 mg in 1954

to 19 mg in 1972. Figure 4-4 presents the market share of U.S. cigarettes by

the level of machine-measured tar. Prior to 1967, most cigarettes yielded

more than 20 mg of tar, but market shares of 16- to 19-mg tar cigarettes

rose rapidly in the late 1960s and early 1970s. 

The CPS-I compared smokers of high-tar cigarettes with more than 25.8

mg tar to smokers of mid-tar (17.6-25.8 mg) and low-tar (less than 17.6 mg)

Chapter 04 11/19/01 11:00 AM Page 92
93

Chapter 4

cigarettes. However, the ‘high’ group was defined as those who were in the

high category from 1959 to 1960 and the high or mid category from 1965

to 1966; the low category consisted of those who were in the low category

from 1959 to 1960 and either the low or medium category from 1965 to

1966. The comparison categorized smokers into groups with distinct levels

of age, race, number of cigarettes smoked per day, age when smoking

began, residence, occupation, education, and history of heart disease and

cancer. A matched analysis of these groups was performed where the only

difference between pairs was the tar level of the cigarette smoked.

Measurement of the number of cigarettes smoked per day and tar levels of

the cigarette smoked were at the same point in time in the follow-up, and

control for number of cigarettes smoked per day was for the number

smoked after switching to low-yield cigarettes. When smokers of low-yield

cigarettes were compared to smokers of high-yield cigarettes in this

matched analysis, the mortality ratios for lung cancer among males were

0.83 for the first 6 years of follow-up and 0.79 for the last 6 years of followup. Comparable ratios for females were 0.57 and 0.62, respectively.

However, the researchers cautioned that the risk differences between smokers of different-yield cigarettes would disappear if smokers had increased

their number of cigarettes smoked per day when they switched from hightar to low-tar cigarettes. For example, the death rate for subjects who

smoked 1-19 high-tar cigarettes per day was 75.8/100,000, but if individuals

0

20

40

60

80

100

0

200

400

800

1925 1935 1945 1955 1965 1975 1985 1993

600

Year

Share of Market (Percent)

Cigarette Sales (Billions)

Non-Filter Market Share Filter Market Share

Non-Filter Cigarette Sales Filter Cigarette Sales

Figure 4-3

Market Share and Cigarette Sale of Filter and Non-Filter Cigarettes in the United

States, 1925-1993

Source: Maxwell Report (Maxwell, 1994).

Chapter 04 11/19/01 11:00 AM Page 93
had increased to 20-39 cigarettes per day as they switched to low-yield cigarettes, the risk increased to 129.5/100,000. 

This increase in lung cancer risk with compensation was examined

more directly in a case-control study of lung cancer patients that examined

the change in number of cigarettes smoked per day when smokers switched

from nonfiltered to filtered cigarettes (Augustine et al., 1989a & b). In

detailed interviews with the lung cancer patients and hospital controls, the

investigators constructed lifetime smoking histories by brand and number

of cigarettes smoked per day for each brand. The mean number of cigarettes

smoked when using nonfiltered brands was compared to the mean number

of cigarettes smoked per day after switching to filtered brands. Among

males, 45 percent of cases and 41 percent of controls increased the number

of cigarettes that they smoked per day when they switched to filtered cigarettes. Among females, the percentages were even higher, with 59 percent of

cases and 48 percent of controls increasing the number of cigarettes smoked

per day. When compared to those who did not increase their cigarettes per

day (CPD) when they switched to filtered cigarettes (odds ratio = 1), the

lung cancer odds ratios rose with increasing compensation (the odds ratios

for those who increased 1 to 10 CPD were 1.19 for males and 1.66 for

females. The odds ratios for those who increased 11 to 20 CPD were 1.75

94

Smoking and Tobacco Control Monograph No. 13

0

20

40

60

80

100

1965 1970 1975 1980 1985 1990

Year

Share of Market (Percent)

Very Low 1-5

Low 6-10

Medium 11-15

High 16-19

Very High 20+

Figure 4-4

U.S. Market Share of Cigarettes Sold by Tar Yield of the Brand, 1967-1990 (mg of Tar

by FTC Method)

Source: Tar levels for given years are derived from FTC Reports (for years 1967-1990). Sales data by brand are from Maxwell

Report (Maxwell, 1994). Brand-specific market shares are summed by tar level of the brand in the given year to generate the market

share for cigarettes with given tar yields.

Chapter 04 11/19/01 11:00 AM Page 94
for males and 2.97 for females. The odds ratios for those who increased 21

or more CPD were 2.37 for males and 3.83 for females). The analyses were

adjusted for cigarettes smoked per day with nonfiltered cigarette use (before

switching), duration of nonfiltered cigarette use, age at switching, and duration of filtered cigarette use. These data demonstrated the importance of

compensation with increasing number of cigarettes per day following the

switch to filtered cigarettes in defining the change in lung cancer risks.

Other cohort studies have yielded mixed results. Some studies showed

no significant reductions with low-yield products (Higenbottam et al., 1982;

Hawthorne and Fry, 1978; Todd et al., 1978; Tang et al., 1995; Kuller et al.,

1991; Petitti and Friedman, 1985; Sidney et al., 1993), and others showed a

decline in risk (Engeland et al., 1996; Borland et al., 1983; Rimington, 1981;

Lange et al., 1992). All of these studies controlled for intensity of smoking,

using cigarettes smoked per day measured when the yield level of the brand

of cigarettes smoked was entered into the analysis, and most studies controlled for a variety of other smoking (e.g., duration) and demographic characteristics. 

A large U.S. case-control study demonstrated significantly lower lung

cancer odds ratios among filter cigarette smokers who had shifted to filtered

cigarettes 10 or more years prior to diagnosis (Kabat, 1996) as well as for

lifetime filter use (Stellman et al., 1997). The odds ratios were adjusted for

age, education, and number of cigarettes smoked per day. This study also

noted that the risk decline was evident only for lung cancers in the

Kreyberg I classification. Kreyberg II lung cancers showed no risk reduction

with filter use. Kreyberg II lung cancers are predominantly adenocarcinoma,

a form of lung cancer that has been increasing as a fraction of all lung cancers in recent decades. 

Two reports from a large multicountry case-control study in Europe also

reported reductions in lung cancer risk associated with lifetime filtered cigarette use (Lubin et al., 1984; Lubin, 1984a & b). One study adjusted for cigarettes smoked per day at time of interview, duration of cessation, duration

of smoking, and a variety of other demographic characteristics. The second

study adjusted for duration of smoking, but did not adjust for CPD. There

did not appear to be a systematic difference in the number of cigarettes

smoked per day between filter and nonfilter smokers among the lung cancer patients. As would be expected, however, the lifetime filter smokers had

substantially shorter durations of smoking. As is true of most studies of lifetime filtered cigarette users, the validity of self-reported lifetime use is in

question since 63 percent of the lifetime filter smokers with lung cancer

diagnoses between 1976 and 1980 in this study reported durations of filtered cigarette use of 30 or more years. Filtered cigarettes were not used in

large numbers prior to the mid 1950s, making the likely maximum duration of filtered cigarette use approximately 25 years. 

Epidemiological data on reduced risks of developing lung cancer among

lower yield cigarette smokers are supported by a study of the histological

changes in the airways of smokers (Auerbach et al., 1979). The study was

conducted on smokers who died of causes not associated with smoking dur95

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 95
ing two time periods (1955-1960 and 1970-1977). Sales-weighted average tar

yield of cigarettes declined substantially between these two periods of time.

The extent and severity of histological changes in the airways were significantly and substantially less during the second calendar-year period, controlling for number of cigarettes smoked per day. The histological changes

included basal cell hyperplasia, loss of cilia, occurrence of cells with atypical

nuclei, and presence of advanced changes defined as carcinoma in situ.

Comparisons were confined to examination of the airways.

In summary, most case-control and prospective mortality studies conducted in different geographic locations demonstrated differences in lung

cancer risks for filter and low-tar (machine-measured) smokers compared

with nonfilter and high-tar smokers when controlled for cigarettes smoked

per day. The question that remains is whether differences in lung cancer

experience are due to differences in machine-measured tar yield of the cigarettes smoked, due to differences in other characteristics of the smokers

who use these products, or due to differences introduced by model misspecification in these studies. 

A reexamination of the CPS-I data set (see

Appendix) was inconclusive as to whether

compensatory changes in the number of cigarettes smoked per day when smokers switch to a lower nicotine cigarette

introduce a bias sufficient to explain the observed increased lung cancer

risk among smokers of high-yield cigarettes. If a positive gradient in lung

cancer risk with tar level was present in analyses that used the tar level and

number of cigarettes smoked from the most recent follow-up, and that gradient disappeared when controlling for the number of cigarettes smoked

per day at the start of the study (or before smokers changed brands), then

one could postulate that the compensatory shift in number of cigarettes

smoked per day might be biasing the results to show an effect of tar that

was not real. A survival analysis examining lung cancer risks for smokers of

different-yield cigarettes using the yield of the cigarette at the most recent

follow-up was performed, but it did not show a significant effect of tar for

lung cancer risk with either cigarettes smoked per day at baseline or at the

most recent follow-up used to control for intensity of smoking. Since there

was no effect of tar on lung cancer risk to examine, it was not possible to

determine whether controlling for CPD using the number of cigarettes per

day prior to switching brands reduced or eliminated the effect of tar on

lung cancer risk.

A survival analysis of lung cancer risk by tar level of the cigarette

smoked was also conducted among those who changed the brand of cigarettes that they smoked during the CPS-I study. No significant effect was

detected when using either cigarettes smoked per day measured prior to

switching or at the time of the most recent follow-up to control for intensity of smoking. However, the numbers of observed lung cancer deaths were

much smaller than those for the analyses of the entire smoking population. 

CPS-I recorded smoking behaviors at five points during the 12-year follow-up and, therefore, some examination of the interrelationships between

New Analyses of the American

Cancer Society’s Cancer

Prevention Study I Data

96

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 96
tar level, smoking cessation, and number of cigarettes smoked per day was

possible. For the purposes of this monograph, this data set was reexamined

using survival analyses that included age, number of cigarettes smoked per

day, duration of smoking, and first or second 6-year period of follow-up as

variables in the analyses. Three analyses of the CPS-I data set were examined in order to define the potential influences of excess cessation among

low-tar smokers and the influence of shifting numbers of cigarettes smoked

per day during follow-up. Figure 4-5 presents the odds ratios for four different tar levels in the three sets of survival analyses of the CPS-I data using

different criteria to define which smokers are included in the analyses. The

cigarettes smoked per day and tar levels of the cigarettes smoked were those

recorded in the baseline survey for all of these analyses. 

The first set of odds ratios was for the 12-year follow-up of smokers of

cigarettes with different tar yields, with the tar level of the cigarette smoked

and the number of cigarettes smoked per day derived from the baseline survey. These estimates corresponded to the approach utilized by most of the

prospective mortality studies presented in Table 4-1. There was a clear and

97

Chapter 4

0.6

0.8

1

1.2

1.4

1.6

1.8

>25.9

21.5-25.9

18.0-21.5

<18.0

Odds Ratio

Baseline CPD and Tar

with Quits

Baseline CPD and Tar

without Quits

Flat CPD and Tar

without Quits

Tar Level

Figure 4-5

Relationship of Tar Level and Lung Cancer Risk for the American Cancer Society

CPS-I Data

Source: American Cancer Society, CPS-I, White-male current cigarette-only smokers. Tar level interpolated from Reader’s Digest

(Miller & Monahan, 1959, pp.40-41) and FTC (for years 1967-1973) data by brand and year. Tar levels as indicated. Odds ratios are

results of SAS lifereg survival analysis with independent variables of duration, age, CPD, and an indicator variable for first v. second

6 years of follow-up.

Chapter 04 11/19/01 11:00 AM Page 97
statistically significant increase in risk with increasing tar level of the cigarette smoked, and there was a convincing dose-response relationship with

tar level. Smokers who quit were censored in the analysis at the follow-up

when they reported being former smokers. Since the last follow-up interval

was from 1965-72, this analytic approach resulted in all of the smokers who

were listed as current smokers in 1965 being considered current smokers

until the end of the study follow-up, even if they reported being former

smokers in the final follow-up survey in 1972.

The second set of analyses used the same population, but the analysis

censored those smokers who reported being former smokers in the 1972 follow-up as of the date of the next to last follow-up (1965). Because cessation

is known to influence lung cancer risk, removal of those who quit in longterm follow-up is necessary to avoid confounding by the association of

choice of a low tar brand and subsequent cessation of smoking. Hammond

(1980) examined the CPS I data and demonstrated that smokers who were

smoking low-tar (17.6 mg or less) cigarettes in 1965 were more likely than

medium or high tar cigarette smokers to have become former smokers by

the end of the study in 1972. Removal of those who had quit by the last

follow-up did not eliminate the effect of baseline level of tar on lung cancer

risk, but the dose response relationship was less apparent. 

The third set of analyses in Figure 4-5 examined only those smokers

who did not change the number of cigarettes that they reported smoking

per day over the multiple follow-up measurements. This group constituted

approximately one-third of all smokers. When using the baseline values for

tar and cigarettes smoked per day in these analyses, it was impossible to

eliminate the influence of compensatory changes in cigarettes per day that

occurred prior to the baseline measurement. However, by selecting a group

that did not change the number of cigarettes that they reported smoking

during the survey, it is possible that a group may have been identified that

also had more stable smoking practices with regard to number of cigarettes

smoked per day prior to entry into the study. When this group was examined using the baseline number of cigarettes smoked per day and tar levels,

there was no effect of tar level of the cigarette smoked on the odds ratio for

lung cancer risk. This suggested that, at least in this group with stable

smoking behavior, there was no relationship between the type of cigarette

smoked and the degree of lung cancer risk. However, it was not possible to

conclude from these analyses that the difference in lung cancer risk by type

of cigarette smoked in the larger group containing all smokers was due to

compensatory changes in the number of cigarettes smoked per day. 

Cardiovascular Disease Table 4-2 presents the epidemiological studies that examined cardiovascular disease risks. Relative risks of cigarette smoking for

heart disease are in the 2-4 range in contrast to the very high relative risks

for lung cancer. These lower relative risks, and the influence of the other

cardiovascular risk factors, make examination of differences in cardiovascular risks among populations who use different types of cigarettes more difficult. In contrast to the table on lung cancer risks (Table 4-1), there is no

clear consensus on coronary heart disease (CHD) risks in relation to use of

filtered or low-yield cigarettes. Some studies show increased risks and others

98

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 98
99

Chapter 4

Table 4-2Epidemiological Studies of Low-Yield Cigarettes and Heart DiseaseCitation Population Time Period Cigarette Type Relative Risk CommentsLee, P.N., Garfinkel, L. 12-year follow-up of 1960-1972 Tar yield: CHD: Male RR= CHD risks are significantly difMortality and type of CPS-I; a prospective low/high 0.90; female= ferent, but emphysema risks are cigarette smoked.

J mortality study of over 1 0.81 not.

Epidemiol. Community million men and women.Health 35:16-22, 1981.Higenbottam, T. et al. 10-year follow-up of 1965-1975 Tar yield There was a small

Cigarettes, lung cancer, 17,475 male civil servants, effect of tar on CHDand coronary heart aged 40-64, and a sample mortality in the disease: The effects of of male British residents. inhalersinhalation and tar yield.J. Epidemiol. CommunityHealth 36:113-117, 1982.Todd, G.F. et al. Four 12.4-year prospective 1965-1977 Filter/Non-filter 0.75 for males and The increase in lung cancer morcardiorespiratory symptoms follow-up of 10,063 sub- 1.03 for females tality with filter use was not statisas predictors of mortality. jects aged 35-69 from a tically significant, and there was aJ. Epidemiol. Community random sample of the statistically significant decrease inHealth 32:267-274, 1978. population in Great Britain. all-cause mortality and male CHD

mortality with filter use (standardized for number of cigarettes/day).

Hawthorne, V.M., Fry, J.S. Prospective follow-up of 1965-1977 Filter/Non-filter 1.05 for CHD mortal- No difference in mortality rates forSmoking and health: The 18,786 people attending ity filter users for lung cancer or association between smok- a multiphasic screening cardiovascular disease. Smokersing behavior, total mortality, examination. of plain cigarettes had lower ratesand cardiorespiratory dis- of respiratory symptoms than filterease in West Central smokersScotland. J. Epidemiol.Community Health32:260-266, 1978.Borland, C. et al. Carbon Prospective 10-year 1967-1979 CO yield 1.47 for CHD mortality Controlled for age, grade of monoxide yield of cigarettes follow-up of the Whitehall in those smoking ciga- employment, cigarettes/day, and its relation to cardio- study where 4,910 men rettes with less than 18 and tar yield. Those who respiratory disease. BMJ had known CO yields of mg CO yield compared smoked high CO-yield ciga287:1583-1586, 1983. the cigarettes that they to those smoking 20+ rettes (>20 mg) tended to 

smoked. mg CO yield cigarettes smoke fewer cigarettes/day.

Chapter 04 11/19/01 11:00 AM Page 99
100

Smoking and Tobacco Control Monograph No. 13 Table 4-2 (continued) Citation Population Time Period Cigarette Type Relative Risk Comments Tang, J.L. et al. Mortality Four prospective mortal- 1967-1982 Filter/Non-filter Tar CHD: 0.93 Relative risks for all tobacco- in relation to tar yield of ity studies from the and tar yield (0.80-1.07); stroke: related diseases combined were cigarettes: a prospective United Kingdom. 0.81 (0.59-1.12) statistically significant. Relative study of four cohorts. BMJ risks are adjusted for age, study, 311:1530-1533, 1995. and number of cigarettes/day. Kuller, L.H. et al. Cigarette 10.5-year follow-up of 1972-1985 Tar level, CHD: nicotine RR of Adjusted for age, serum choles- smoking and mortality. the MRFIT participants. nicotine level 1.0 for nicotine level terol, diastolic blood pressure, and MRFIT Research Group. ≤1 mg. 1.04 (0.8- cigarettes/day. Low-tar and low- Preventive Med. 20:638- 1.35) for 1.1-1.4 mg, nicotine cigarette smokers tended 654, 1991. and 1.27 (0.92-1.77) to smoke more cigarettes/day. for 1.5+ mg; tar RR of 1.0 for tar level ≤15 mg, 1.08 (0.8-1.45) for 16-19 mg, and 1.19 (0.86-1.65) for 20+ mg.

Benhamou, E. et al. Lung Case-control study of 1976-1980 50+% filter/ 0.31 Controlled for number of cigacancer and women: Results 96 women with lung 100% non-filter rettes/day, duration, and inhalaof a French case-control cancer and 192 tion.study. Br. J. Cancer 55:91- matched hospital 95, 1987. controls.Alderson, M.R. et al. Case-control study of 1977-1982 Always filter/ Age 35-54: Adjusted for number of cigaRisks of lung cancer, 12,693 in-patients. non-filter male=1.78; rettes/day.

chronic bronchitis, female=0.24

ischaemic heart disease, Age 55-74:and stroke in relation to male=2.67;type of cigarette smoked. female=1.32J. Epidemiol. CommunityHealth 39:286-293, 1985.

Chapter 04 11/19/01 11:00 AM Page 100
101

Chapter 4

Table 4-2 (continued)Citation Population Time Period Cigarette Type Relative Risk CommentsPetitti, D.B., Friedman, G.D. 4-year prospective 1979-1982 Tar yield; 1.15 (1.03-1.28) for Controlled for age, sex, race, andCardiovascular and other follow-up of 16,270 high- and low- all cardiovascular number of cigarettes/day.diseases in smokers of low current regular smokers (less than 15 diseases and 1.25 yield cigarettes. J. Chron. and 42,113 subjects who mg tar and 1 mg (0.99-1.58) for 

Dis. 38:581-588, 1985. never used any form of nicotine) yield myocardial infarctobacco. determined at tion for a 5-mg

the start of the increase in tar.study.

Palmer, J. et al. Low yield Case-control study of 1985-1988 Nicotine and CO The estimated re- Included in the model were termscigarettes and the risk of 910 women with a first levels lative risk for wo- for age, hypertension, angina, nonfatal myocardial infarc- myocardial infarction men who smoked diabetes, cholesterol, family histotion in women. NEJM 320: under age 65 and 2,375 cigarettes with the ry of myocardial infarction, body 1569-1573, 1989. hospital controls. lowest level of mass index, type A behavior, exernicotine and CO cise, education, residence, estrowas similar to that gen or oral contraceptive use, coffor women who fee consumption, alcohol consmoked the brands sumption, and number of cigawith the highest rettes/day.

levels of nicotine andCO.

Negri, E. Tar yield of ciga- Case-control study of 1988-1989 Tar level <10 mg=1, 10-15 rettes and risk of acute 916 patients with acute mg=1.2 (0.7-2.1), myocardial infarction. BMJ myocardial infarction >15-20 mg=0.8 

306:1567-1569, 1993. without history of (0.5-1.3), >20 mg=

ischemic heart disease 1 (0.5-1.8).and 1,106 hospital controls in a multi-center Italian study.

Chapter 04 11/19/01 11:00 AM Page 101
102

Smoking and Tobacco Control Monograph No. 13 Table 4-2 (continued) Citation Population Time Period Cigarette Type Relative Risk Comments Powell, J.T. et al. Risk 291 smokers with newly 1988-1992 Tar/Nicotine Peripheral artieral Odds ratios adjusted for age, sex, factors associated with the referred peripheral arterial disease odds ratios and depth of inhalation. development of peripheral disease and 828 controls 1.75 for tar 14+ com- arterial disease in smokers: without the disease from pared to <9 mg; 1.54 A case-control study. outpatient clinics. for 1.2+ mg nicotine Atherosclerosis 129:41-48, compared to <0.8 1997. mg; 1.62 for carboxyhemoglobin 4.5+ compared to <2.7. Parish, S. et al. Cigarette In the United Kingdom in 1990 Two groups: 1.166 (1.025-1.326) Controlled for age, sex, and num- smoking, tar yields, and the early 1990s, 14,000 low-tar users for age 30-59 for ber of cigarettes/day. non-fatal myocardial infarc- cases of nonfatal myo- (<10 mg, 7.5 medium tar com- tion: 14,000 cases and cardial infarctions and mg mean) and pared to low tar. 32,000 controls in the United 32,000 relatives (controls) medium-tar Kingdom. The International (ISIS-3 & -4) responded users (<10 mg, Studies of Infarct Survival to questionnaires. 4,923 13.3 mg mean)

(ISIS) Collaborators. BMJ cases and 6,880 controls 

(Clin Res Ed) were current smokers and 311(7003):471-477, 1995. used in study. Unmatched 

case-control study assessed effects of cigarettes.

Chapter 04 11/19/01 11:00 AM Page 102
show decreased risks, and in many of the studies the risks are not statistically significant. 

In a prospective evaluation of four cohorts from the United Kingdom

(Tang et al., 1995) that included 56,255 males who were followed for an

average of 13 years, a statistically significant reduction in risk of CHD mortality (0.77; 95 percent CI, 0.61–0.97) was demonstrated with decreasing tar

yield, but the decline with filtered cigarette use was not statistically significant. These risks were adjusted for age, study, and number of cigarettes

smoked per day. 

An evaluation of CHD mortality from one of these cohorts (Borland et

al., 1983) revealed that CHD mortality was increased among smokers of

high carbon monoxide (CO)-yield cigarettes in an analysis that controlled

for age, employment grade, amount smoked, and tar yield of the cigarette

smoked. The differences were not statistically significant. Smokers of high

CO-yield cigarettes also tended to smoke fewer cigarettes per day. There was

little correlation between tar yield and CO yield among the different brands

of cigarettes smoked in this study, but these researchers raised the possibility that factors other than tar levels may be important in defining the exposures relevant to CHD risk. 

A case-control study of nonfatal myocardial infarction in women

(Palmer et al., 1989) examined disease risk in relation to nicotine yield and

CO yield of the cigarette smoked at the time of admission to the hospital.

Included in the model were terms for age, hypertension, angina, diabetes,

cholesterol, family history of myocardial infarction, body mass index, type

A behavior, exercise, education, residence, estrogen or oral contraceptive

use, coffee consumption, alcohol consumption, and number of cigarettes

smoked per day. Multivariate relative risk estimates were similar across the

categories of nicotine and CO yields from the highest to the lowest, and the

risks were not significantly different. 

Parish and colleagues (1995) found that the risk ratio of nonfatal

myocardial infarction was 1.104 higher (95 percent CI, 0.998-1.222; P =

0.06) among smokers of medium-tar cigarettes compared to low-tar cigarettes in a case-control study of 14,000 survivors of myocardial infarction,

compared to 32,000 relatives who served as controls. These analyses were

controlled for age, gender, and amount smoked. When the analysis was

limited to those with no previous disease, the risk ratio declined to 1.055

(95 percent CI, 0.910-1.223, P = 0.1), raising the question of whether some

of those smokers with previously diagnosed disease might have switched to

lower yield cigarettes in an effort to reduce their risks of subsequent illness. 

An analysis of the 15-year follow-up of the Multiple Risk Factor

Intervention Trial (MRFIT) participants (Kuller et al., 1991) showed that

either tar or nicotine content of the cigarette smoked was only modestly,

and not statistically significantly, associated with CHD mortality in an

analysis controlled for age, serum cholesterol, diastolic blood pressure, and

cigarettes smoked per day. Petitti and Friedman (1985) found a small but

statistically significant increased risk of CHD and myocardial infarction

related to increased tar yield among 16,270 smokers compared to 42,133

103

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 103
never smokers who were followed for 4 years. These analyses were adjusted

for age, sex, race, and number of cigarettes smoked per day as covariates.

Results were similar when those with prior heart disease were removed and

when the analyses were adjusted for other cardiovascular risk factors.

Higenbottam and associates (1982) found a small increase in CHD mortality

with lower tar yield, but the effect was evident only in the approximately

80 percent of smokers who inhaled. Todd and colleagues (1978) found a

decline in CHD mortality among males, but not among females, who

smoked filtered cigarettes. 

In summary, while the data are not as compelling for alterations in

CHD risk compared to lung cancer risk among populations who smoke lowyield cigarettes, several well-conducted epidemiological studies have

demonstrated a difference in cardiovascular risk among those who smoke

low-yield cigarettes when the analyses were controlled for number of cigarettes smoked per day. The complexity of examining the effect of low-yield

cigarette smoking on CHD risk is exacerbated by the greater independence

of the ratio of CO-to-nicotine yield among different brands of cigarettes in

comparison to the ratio of tar-to-nicotine yield. CO is considered to be a

major etiological agent in cardiovascular disease, and the factors that determine the CO yield of a cigarette are different from those that determine tar

yield. Individual changes in cigarette design may influence tar and CO

yields in different directions. These differences make interpretation of studies of cardiovascular disease risk in relation to tar yield or among filter cigarette smokers more difficult. Once again, the question that remains is

whether this difference in CHD experience is due to the difference in

machine-measured tar yield of the cigarettes smoked, due to the differences

in other characteristics of the smokers who use these products, due to differences in other cardiovascular risk factors among smokers of different

yield cigarettes, or due to differences introduced by controlling for intensity

and duration of smoking in these studies. 

Table 4-3 presents the epidemiological studies that have

examined respiratory disease risks. Since symptomatic

chronic lung disease is commonly present for long periods prior to resulting

in death, and because many smokers will quit smoking once chronic shortness of breath is manifest, it is difficult to evaluate the effect of smoking

low-yield cigarettes on chronic obstructive pulmonary disease mortality. A

reduced death rate from emphysema was demonstrated in the CPS-I 12-year

follow-up (Lee and Garfinkel, 1981) at a point when lower yield products

had not been on the market for an extended period of time. Other mortality outcome studies (Tang et al., 1995; Lang et al., 1992; Petitti and

Friedman, 1985) have not demonstrated a similar reduction in lung disease

mortality. 

Sparrow and colleagues (1983) examined the relationship of tar yield to

pulmonary function measurements in a group of 383 current smokers for

whom pulmonary function measurements were available at two points in

time 5 years apart. In a multivariate regression analysis, tar level of the cigarette smoked was not significantly associated with the forced vital capacity

(FVC) or forced expiratory volume in 1 second (FEV1) in the initial examiChronic Respiratory

Symptoms and Disease

104

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 104
105

Chapter 4

Table 4-3Epidemiological Studies of Low-Yield Cigarettes and Respiratory DiseaseCitation Population Time Period Cigarette Type Relative Risk CommentsLee P.N., Garfinkel, L. 12-year follow-up of 1960-1972 Tar yield: Emphysema: CHD risks are significantly difMortality and type of CPS-I; a prospective mor- low/high male=0.78; ferent, but emphysema risks are cigarette smoked. J. tality study of over 1 female=0.59 not.Epidemiol. Community million men and women.Health 35:16-22, 1981.Hawthorne, V.M., Fry, J.S. Prospective follow-up 1965-1977 Filter/Non-filter 0.61 for chronic No difference in mortality rates Smoking and health: The of 18,786 people for filter users for lung cancer or association between smok- attending a multiphasic cardiovascular disease.ing behavior, total mortality, screening examination. Smokers of plain cigarettes hadand cardiorespiratory dis- lower rates of respiratory sympease in West Central toms than filter smokers.Scotland. J. Epidemiol.Community Health32:260-266, 1978.Tang, J.L. et al. Mortality Four prospective mor- 1967-1982 Filter/Non-filter Tar yield chronic Relative risks for all tobaccoin relation to tar yield of tality studies from the and tar yield obstructive pul- related disease combined were cigarettes: a prospective United Kingdom. monary disease statistically significant. Relative study of four cohorts. BMJ 0.94 (0.64-1.37) risks are adjusted for age, study, 311:1530-1533, 1995. and number of cigarettes/day.Sparrow, D. et al. The 383 current smokers 1969-1980 Tar level In a multiple regres- Controlled for age, height, and 

relationship of tar content enrolled in a longitu- sion analysis, tar level number of cigarettes/day.to decline in pulmonary dinal study of aging did not influence FVC function in cigarette smok- who had spirometry or FEV 1 at baseline ers. Am. Rev. Resp. Dis. performed 5 years or change in these 127:56-58, 1983. apart. measures at follow-up.Dean, G. et al. Factors Sample of 12,736 1972 Filter/Non-filter Of eight respiratory Controlled for age, social class, related to respiratory and men and women aged and cardiovascular number of cigarettes/day, inhalacardiovascular symptoms 37-67 living in England, symptoms, morning tion, and occupation.in the United Kingdom.

J. Scotland, and Wales. cough in men and woEpidemiol. Community men and shortness of

Health 32:86-96, 1978. breath in women were 

lower in filter cigarettesmokers.

Chapter 04 11/19/01 11:00 AM Page 105
106

Smoking and Tobacco Control Monograph No. 13 Table 4-3 (continued) Citation Population Time Period Cigarette Type Relative Risk Comments Lange, P. et al. 6,511 men and 7,703 1976-1989 Filter/Non-filter Chronic obstructive Relationships of the type women selected ran- pulmonary disease: of tobacco and inhalation domly after age strati- male=1.23; female= pattern to pulmonary and fication from the general 1.07 total mortality. Eur. Resp. population in Copenha- J. 5:1111-1117, 1992. gen, followed for 13 years. Alderson, M.R. et al. Case-contrl study of 1977-1982 Always filter/ Chronic bronchitis: Adjusted for number of ciga- Risks of lung cancer, 12,693 in-patients. non-filter male=0.25; rettes/day. chronic bronchitis, female=0.75 ischaemic heart disease, and stroke in relation to type of cigarette smoked. J. Epidemiol. Community Health 39:286-293, 1985. Petitti, D.B., Friedman, G.D. 4-year prospective 1979-1982 High and low 0.97 (0.84-1.13) for Controlled for age, sex, race, and 

Cardiovascular and other follow-up of 16,270 (less than 15 all diseases of the number of cigarettes/day.diseases in smokers of low current regular smok- mg tar and 1 respiratory systemyield cigarettes. J. Chron. ers and 42,113 sub- mg nicotine) for a 5-mg increase

Dis. 38:581-588, 1985. jects who never used yield determined in tar.

any form of tobacco. at the start of

the study

Krzyanowski, M. et al. 690 smokers from a 1981-1988 Tar, nicotine, After adjustment for

Relationship of respiratory sample of households and CO yield intensity and durationsymptoms and pulmonary in Tucson, Arizona; of smoking and depthfunction to tar, nicotine, followed to 1988. of inhalation, thereand carbon monoxide was no effect of taryield of cigarettes. Am. or nicotine on chronic

Rev. Resp. Dis. 143:306- phlegm, cough, or311, 1991. dyspnea. Tar and

nicotine content hadno independent effecton pulmonary function.

Chapter 04 11/19/01 11:00 AM Page 106
107

Chapter 4

Table 4-3 (continued)Citation Population Time Period Cigarette Type Relative Risk CommentsBrown, C.A. et al. 2,801 current cigarette 1984-1986 Tar level Rates of chronic Women in the middle-tar and Cigarette tar content smokers (1,154 males, cough and chronic high-tar group had smoked forand symptoms of chronic 1,647 females), 40-59 phlegm were higher longer and had significantly bronchitis: Results of the years of age, from 22 for women who higher breath CO levels, serumScottish Heart Health districts of Scotland smoked high-tar thiocyanate levels, and dailyStudy. J. Epidemiol. (Scottish Heart Health cigarettes, but not cigarette consumption than Community Health 45: Study): cross-sectional for men. women in the low-tar group. This287-290, 1991. random sample. Ciga- pattern was not seen in men.

rettes smoked by subjects were assigned toone of three tar levelgroups: <12 mg/cig (low); 13-14 mg/cig (middle); 15+ mg/cig(high).

Withey, C.H. et al. Intervention trial in 21 1985-1989 Mid-tar smokers No difference in Analysis of urinary nicotine 

Respiratory effects of local authority districts (>12 mg/ciga- respiratory symp- metabolites showed that smoklowering tar and nicotine in England; male middle- rette) assigned to toms with switching ers allocated to the differentlevels of cigarettes tar smokers aged 18-44 test low-tar/ to different types of cigarette type study adjusted smoked by young male years; 7,029 smokers middle-nicotine, cigarettes. their smoking so that throughoutmiddle tar smokers. II. selected from 265,016 middle-tar/mid- the trial their nicotine inhalationResults of a randomised sent questionnaires; dle-nicotine, differed little from their pretrialcontrolled trial. J. Epidemiol. 643 controls. Assigned or low-tar/low-nic- intakes when they were smoking

Community Health 46(3): 1 of 3 different types of otine cigarettes their usual cigarette for a 6-281-285, 1992. cigarettes for 6 months. for6 months.Three month period.

cigarette groups:LM: low-tar/mid -nicotine, MM: midtar/mid-nicotine, LL:low-tar/low-nicotine. Per cigarette:LM: 9.5 mg tar/1.16 mg nicotine;MM:13.8 mg tar/1.24 mg nicotine;LL: 9.3 mg tar/1.04mg nicotine.

Chapter 04 11/19/01 11:00 AM Page 107
nation, nor to change in these measures over the 5-year interval. The analyses were controlled for age, height, number of cigarettes smoked per day,

and baseline lung function in the follow-up analysis. 

The frequency of respiratory symptoms also has been evaluated in relation to the type of cigarette smoked. Alderson and associates (1985) demonstrated a lower risk of chronic bronchitis among those who had smoked

only filtered cigarettes in an analysis adjusted for number of cigarettes

smoked per day. In contrast, a smaller case-control study (Krzyzanowski et

al., 1991) found no difference in respiratory symptoms in relation to the tar

yield of the cigarette smoked with an analysis adjusted for the duration and

intensity of smoking as well as the depth of inhalation. Brown and colleagues (1991) demonstrated lower rates of chronic cough and phlegm

among female smokers of lower tar cigarettes, but the effect was not evident

in males. In an intervention trial (Withey et al., 1992) that involved switching 7,029 smokers to one of three different types of cigarettes, no difference

in respiratory symptoms after a 6-month interval was noted among those

who switched to lower yield cigarettes. 

In summary, there is little evidence for a substantial difference in mortality from chronic obstructive lung disease among smokers who use lowyield cigarettes. There is equivocal evidence for a reduced rate of respiratory

symptoms. 

Studies published in the epidemiological literature support a difference in lung cancer and possibly heart disease risks, but not

in chronic lung disease risks, between populations of individuals who smoke filtered or lower yield cigarettes compared with individuals

who smoke unfiltered or higher yield cigarettes. However, there is marked

variability among the studies, with many studies finding no effect or an

effect too small to be statistically significant. In some studies, the heart disease and lung cancer risks appeared to change in opposite directions with

low-yield cigarette use, as did risks for male and female smokers. Most of

the major studies that defined this risk used the number of cigarettes

smoked per day as a measure to control for the intensity of cigarette smoking and, therefore, they may be subject to confounding due to a compensatory increase in the number of cigarettes smoked per day by some smokers

when they shifted to lower yield cigarettes. Given the variability of these

results, the potential for confounding and in the analyses, and the difficulty

of examining the continually changing cigarette product, it is difficult to

conclude from these data that there is a clearly demonstrable harm reduction that is due to the use of filtered or lower yield cigarettes in comparison

to unfiltered or higher yield cigarettes. 

These epidemiological data were also recently reviewed by the Tobacco

Advisory Group of the Royal College of Physicians (2000) in conjunction

with the evidence for compensation in smoking behavior with use of lowyield brands. They concluded, “There are therefore reasonable grounds for

concern that low tar cigarettes offer smokers an apparently healthier option

while providing little if any true benefit.” 

Summary of the

Epidemiological

Evidence

108

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 108
The biological significance of

compensatory smoking may be

more complex than is portrayed by measures of nicotine absorption or CO

levels. Addition of a filter to a cigarette lowers the particulate mass passing

into the smoker’s mouth, and that reduction in particulate mass is usually

measured as a reduction in milligrams of tar. The effects of filters and other

changes in cigarette design on the particle-size distribution of the smoke are

complex and somewhat dependent on the compensatory behavior of the

smoker. 

Filtration of cigarette smoke with a cellulose acetate filter alters the distribution of particle size in the smoke, preferentially reducing particles 0.5-

micron mass median diameter (MMD) and larger as well as those particles

below 0.1 micron MMD (Kieth and Derrick, 1960; Keith, 1982). The net

result is a lowering of the MMD of filtered tobacco smoke. The MMD of the

smoke reaching the smoker is concentrated in that range where deposition

in the lung is most efficient and where there is relatively less deposition in

the mouth and throat compared to the lung (International Committee on

Radiation Protection, 1966; Committee on Health Risks of Exposure to

Radon [BEIR VI], 1999). 

Morie and colleagues (1973) examined the fibers in cigarette filters

microscopically to examine the mechanism by which filters would preferentially remove both large and very small particles. They found that fibers oriented parallel to the smoke stream showed heavy deposition of particles

with MMD less than 0.1 micron. Fibers oriented perpendicular to the smoke

stream were coated with particles larger than 0.5 micron MMD. This finding suggests that diffusion of particles smaller than 0.1 micron MMD was

the principal mechanism for deposition of these small particles on filter

fibers oriented parallel to the smoke stream, and that the particles larger

than 0.5 micron were trapped by interception on the fibers oriented perpendicular to the smoke stream. Particle size is a principal determinant of

the deposition site of particles, with particles smaller than 0.5 micron MMD

depositing in the lung rather than the upper airway (International

Committee on Radiation Protection, 1966; Committee on Health Risks of

Exposure to Radon [BEIR VI], 1999). 

An investigation of the effect of filters on particle size, conducted for

Philip Morris soon after filters had been widely introduced (Holmes et al.,

1959; Mitchell, 1958), suggested that filters lowered the particle size of the

smoke produced by cigarettes. For example, Philip Morris regular (unfiltered) cigarettes produced smoke with an MMD of 0.94 micron and Benson

and Hedges® with the filter removed produced smoke with an MMD of 1.0

micron. In contrast, filtered Parliament® cigarettes produced smoke with an

MMD of 0.84 micron and Benson and Hedges® with the filter in place produced smoke with an MMD of 0.82 micron. More recent investigations

(McClusker et al., 1983) revealed that the particle size of the smoke generated by lower yield cigarettes is the same with and without removal of the filters. This difference in results may relate to the effect of filter ventilation on

particle size. Increased ventilation results in an increase in the particle size

of the smoke generated (Kieth, 1982). This effect is thought to occur

BIOLOGIC IMPLICATIONS OF COMPENSATION

FOR CHANGES IN CIGARETTE DESIGN

109

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 109
because the addition of dilution, particularly in the filter, slows down the

rate at which the smoke passes through the cigarette, allowing more time

for coagulation of the smoke particles. This increase in particle size due to

coagulation may counterbalance the reduction in particle size produced by

filtration. Removal of the perforated filters on low-yield cigarettes removes

both the ventilation and the filtration. As discussed elsewhere in this volume (see Chapter 3), smokers of cigarettes with ventilated filters often cover

the filters with their lips or fingers in order to increase the yield of the cigarette. When these ventilation holes are occluded, the result may be filtration without increased ventilation, and particle size may be reduced.

However, no studies of particle size distribution with occlusion of the ventilation holes are available. 

Particles with an MMD larger than 0.75 micron contain much more tar

than do smaller particles because of their larger size, but they are more likely to be deposited in the mouth before reaching the respiratory track. Thus,

a filtered cigarette with a smaller particle-size distribution may deliver much

more of its dose of tar to the lung than will a nonfiltered cigarette with the

same machine-measured tar yield. This may result in a relative preservation

of the carcinogenic dose delivered to the lung when filters are used to

reduce the tar delivered at the mouth. 

Nicotine in smoke is absorbed from both smoke deposited in the mouth

and smoke inhaled into the lung. Venous blood levels of nicotine reflect

the total smoke exposure of the smoker, not where in the respiratory track

the smoke particles are deposited. Large particles contain larger amounts of

nicotine, but will preferentially be deposited in the mouth and throat.

Selective removal of these large particles through filtration will reduce the

fraction of nicotine that is deposited in the upper airway, but may have little effect on the fraction of smoke inhaled into the lung. If the smoker

compensates for the reduction in total nicotine delivery by generating and

inhaling more smoke to preserve total nicotine intake, then the larger mass

of smaller particles delivering that dose of nicotine in filtered smoke might

produce an increased deposition of tar in the lung for the same dose of

nicotine delivered to the bloodstream. 

Changes in pattern of deposition of smoke aerosol have been postulated

(Thun et al., 1997a) as one mechanism underlying the dramatic increase in

adenocarcinoma (a cancer felt to arise from the more peripheral structures

of the lung) seen over the last several decades (Travis et al., 1995) in the

United States and other countries (Russo et al., 1997; Levi et al., 1997). An

additional concern has been increases in the levels of tobacco-specific

nitrosamines in cigarettes over time, particularly NNK, which is a potent

lung carcinogen for adenocarcinoma in animals (Hecht, 1998; see Chapter

5). Recently, it was suggested (Peel et al., 1999) that the formation of tobacco-specific nitrosamines in flue-cured tobacco in the United States is largely

the result of using propane gas heaters in the curing process. Oxides of

nitrogen generated from burning the liquid propane combine with the

nicotine in the tobacco leaf to form the tobacco-specific nitrosamines.

These changes in curing methods were introduced in the mid 1960s and are

110

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 110
likely to have resulted in a substantial increase in the levels of tobacco-specific nitrosamines present in cigarettes containing tobacco cured with this

method. Increased levels of tobacco-specific nitrosamines have the potential

to make cigarettes manufactured after the 1960s more carcinogenic and

may have contributed to the rise in adenocarcinoma, which has become

the most common form of lung cancer. 

As discussed above, examinations of disease risks produced by lower yield cigarettes commonly adjust for differences in

intensity and duration of cigarette smoking. Those adjustments can be complicated if characteristics of the cigarette

itself cause changes in measures of intensity of smoking, or if concerns

about disease risk influence the choice of cigarette smoked. This section

examines cross-sectional and cohort studies of the correlation between type

of cigarette smoked and smoking intensity or duration. 

Data from the CPS-I study for the type of cigarette smoked by White

male smokers of different ages and smoking durations are presented in

Table 4-4 for all of the baseline and follow-up surveys combined. The fraction of smokers who smoked low-yield cigarettes was relatively constant

across different ages, which was in marked contrast to the pattern of

increasing use of low-yield cigarettes with advancing age that was evident

in the California data from 1996 (see Figure 4.1). It is worth noting, however, that the distribution of low-tar cigarette use with duration of smoking,

in contrast to age, is not uniform. When the duration of any cigarette

smoking (cigarettes of any tar level) is examined, those who reported smoking high tar cigarettes at the time of follow-up had been smoking for more

years than smokers of lower tar cigarettes. It is unlikely that this effect is a

function of older age among high tar cigarette smokers as the distribution

of tar level by age is much more uniform in the table.

As part of a case-control study of lung cancer, Augustine and colleagues

(1989a & b) constructed lifetime smoking histories by cigarette brand and

number of cigarettes smoked per day with each brand. They compared the

mean number of cigarettes smoked per day when subjects smoked nonfilCORRELATION OF CIGARETTE

BRAND CHOICE WITH NUMBER OF

CIGARETTES SMOKED PER DAY AND

DURATION OF SMOKING

111

Chapter 4

Table 4-4

Percentage of Smokers of Different Ages and Durations of Smoking Who Smoke Cigarettes

with Different Tar Yields (American Cancer Society’s Cancer Prevention Study I)

Age (Years)

Tar Level (mg) <45 45-55 55-65 65-75 >75 Total

Low ≤17.6 12.82 13.14 14.36 14.36 13.46 13.72

Mid 17.6-25.8 52.24 51.74 53.14 52.23 51.22 52.36

High >25.8 34.94 35.12 32.49 33.41 35.32 33.93

Duration (Years)

<20 20-29 30-39 40-49 50+ Total

Low ≤17.6 16.18 14.60 13.48 13.37 12.77 13.72

Mid 17.6-25.8 53.95 52.25 52.24 52.70 51.28 52.36

High > 25.8 29.87 33.15 34.28 33.93 35.95 33.93

Chapter 04 11/19/01 11:00 AM Page 111
tered cigarette brands to the mean number after they switched to filtered

brands. The differences in cigarettes smoked per day were adjusted for nonfilter cigarettes smoked per day (before switching), duration of nonfilter and

filter smoking, age at diagnosis, and age at switching. Among males, 45 percent of cases and 41 percent of controls increased the number of cigarettes

that they smoked per day when they switched to filtered cigarettes. The

mean increase in cigarettes per day was 5.9 for the cases and 3.9 for the

controls. The percentages were even higher among females, with 59 percent

of cases and 48 percent of controls increasing the number of cigarettes

smoked per day. The mean increase in cigarettes per day was 7.8 for the

cases and 4.7 for the controls. As measured by this study, compensation by

increasing the number of cigarettes smoked per day upon switching to filtered cigarettes was common and involved substantial increases in the

number of cigarettes smoked per day. 

Assessing the impact of switching to low-yield cigarettes on the number

of cigarettes smoked per day from cross-sectional data is complicated by

multiple factors that may influence both choice of cigarette and the number smoked daily. The strength of nicotine addiction is correlated with the

number of cigarettes smoked per day, and it is possible that more-addicted

smokers may not be successful in switching to low-yield cigarettes. Smokers

who are trying to quit, or who are interested in quitting, may smoke fewer

cigarettes per day and shift to low-yield cigarettes as part of their effort to

quit. 

The concentration of cotinine in the blood is correlated with the number of cigarettes smoked per day (Benowitz et al., 1983). Higher nicotine

demand per day is met by smoking more cigarettes per day, and possibly by

smoking each cigarette with more puffs and deeper inhalation. Less-addicted smokers have lower nicotine requirements and generally smoke fewer

cigarettes per day. These lower nicotine requirements may allow the lessaddicted smoker to satisfy their need for nicotine even with cigarettes that

deliver lower levels of nicotine. The more heavily addicted smoker may not

be able to extract sufficient nicotine from a low-yield cigarette to satisfy his

or her addiction, or he or she may have to work so hard to extract the nicotine that the experience of smoking lower yield products is unpleasant. This

effect would tend to concentrate more-addicted smokers who smoke more

cigarettes per day in the higher yield brands. The result of such a phenomenon in cross-sectional examinations of cotinine levels among smokers of

cigarettes with different machine-measured yields would be a slight slope of

increasing cotinine levels with increasing machine-measured nicotine

yields, even if complete compensation occurs at the level of the individual

smoker. 

A similar effect would be expected if smokers who tried to quit switched

to low-yield brands as part of their effort to quit, or as an effort to moderate

their risk upon relapsing to cigarette smoking. Efforts to cut down prior to

quitting may also involve efforts to reduce the number of cigarettes smoked

per day, and those who relapse may smoke fewer daily cigarettes for a period of time after reinitiating smoking. These influences have been reported

as reasons why smokers choose low-yield brands (Giovino et al., 1996), and

112

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 112
they would also be expected to influence the cross-sectional relationship

between machine-measured nicotine yields and biological measures of nicotine intake. 

Even with these influences potentially biasing the results, cross-sectional evaluations of blood cotinine levels have shown little or no relationship

with machine-measured nicotine yields (Benowitz et al., 1983; Benowitz,

1996; see Chapter 2). Benowitz and colleagues (1983) examined cotinine

levels in smokers who smoked cigarettes with different nicotine yields as

measured by the FTC method, and demonstrated a nonstatistically significant positive slope of the relationship between cotinine level in the smoker

and nicotine yield of the brand smoked. In a similar comparison, but on a

randomly selected population sample in the United Kingdom, a small, statistically significant positive slope was demonstrated between cotinine level

in the smoker and nicotine yield of the brand smoked (Jarvis et al., 2001). 

In summary, these data suggest that choice of cigarette brand is only a

relatively minor determinant of the amount of nicotine (and tar) that the

smoker will derive from smoking. This issue is examined in more depth in

Chapter 2. 

The CPS-I recorded cigarette brand

and number of cigarettes smoked

per day at five points during the

12 years of follow-up. Therefore, it

was possible to examine both cross-sectional relationships between the

number of cigarettes smoked per day and the machine-measured yield of

the cigarette smoked, as well as the changes that take place when a smoker

switches brands (see Appendix). 

Table 4-5 presents the observed percentages of smokers of different

numbers of cigarettes per day who smoked low-, mid-, and high-tar yield

cigarettes among the CPS-I population for all of the baseline and follow-up

surveys combined. The relationship between cigarettes per day and tar yield

of the cigarette smoked is complex, as low-tar cigarette smokers were overrepresented in both the 1-9 and 40+ cigarettes per day categories. This may

suggest that choice of cigarette is conditioned by multiple factors, including

the possibility that smokers with greater nicotine demands are less likely to

choose and be satisfied by lower yield cigarettes, and the possibility that

smokers who switch to lower yield brands increase the number of cigarettes

that they smoke per day. 

Hammond and Garfinkel (1964) examined the first 2 years of follow-up

of the CPS-I data (1959-1961). They did not demonstrate a relationship

between an increased, decreased, or unchanged tar and nicotine yield of the

cigarettes smoked and a change in the categorical measure of number of

cigarettes smoked per day. In an analysis that examined change over the

12-year follow-up of the CPS-I data, and which examined continuous as

opposed to categorical measures of numbers of cigarettes smoked per day,

Garfinkel (1979, 1980) showed a modest difference between increasing tar

and nicotine yield of the cigarettes smoked and decreased numbers of cigarettes smoked per day, particularly for females, but the effect was small. 

Change in Number of Cigarettes Smoked

per Day with Differences in MachineMeasured Nicotine Yields in the American

Cancer Society’s Cancer Prevention Study I

113

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 113
The relationship between nicotine yield of the cigarette smoked and the

number of cigarettes smoked per day is reexamined in this report for individual smokers among the CPS-I population of White males. Figure 4-6

presents the mean number of cigarettes smoked per day by all smokers of a

given brand with the machine-measured nicotine yield of the cigarette

brand. Cigarettes smoked per day were adjusted for age because of the influence of age on reported number of cigarettes smoked per day. The results

were similar without the age adjustment. There was a statistically significant slope, with a 0.8 cigarette per day increase for a 1 mg decline in nicotine. 

114

Smoking and Tobacco Control Monograph No. 13

Table 4-5 

Percentage of Smokers of Different Numbers of Cigarettes per Day Who Smoke Cigarettes 

with Different Machine-Measured Tar Yields (American Cancer Society’s Cancer Prevention

Study I)

Cigarettes Smoked per Day

Tar Level (mg) 1-9 10-19 20 21-39 40 >40 Total

Low ≤17.6 17.37 13.91 11.64 14.49 27.27 15.44 13.72

Mid 17.6-25.8 54.64 53 52.63 51.22 54.76 50.7 52.36

High >25.8 27.99 33.08 35.73 34.3 17.97 33.86 33.93

Figure 4-6

Nicotine Level of Brand Smoked versus Mean-Adjusted CPD Reported for All White

Male Smokers (N=169,610): ACS CPS-I Study, Followed 1960-1972

Source: ACS CPS-I, White male current cigarette-only smokers.

Note: Nicotine and tar levels interpolated by year and brand from Reader’s Digest (Miller & Monahan, 1959) and FTC (for years

1967-1973) data, mean CPD by nicotine value using the weighted mean value for each categorical level of CPD. The mean CPD

values are adjusted for age and regressed on nicotine yield per cigarette. For the graph, covariate coefficients are calculated in a

general regression, then points are graphed as adjusted for the covariate with the regression line shown through the adjusted

points.

Chapter 04 11/19/01 11:00 AM Page 114
When the analysis was limited to those who had changed the brand of

cigarettes that they reported smoking in sequential follow-up surveys, the

slope of mean number of cigarettes per day in relation to change in

machine-measured level of nicotine for the brand was -2.31

cigarettes/day/mg nicotine (see Figure 4-7). This analysis controlled for age,

cigarettes smoked per day prior to switching brands, and tar and nicotine

yields of the cigarette smoked before the switch. 

The implications of these shifts in number of cigarettes smoked per day

with changes in nicotine yield of the cigarette are presented in Figure 4-8.

Lung cancer risks from the CPS-I study for smokers of high-tar (more than

25.8 mg) and low-tar (less than 17.6 mg) cigarettes are presented by number

of cigarettes smoked per day at the baseline survey. It is possible to estimate

from this figure how much compensation by number of cigarettes per day

would be required to eliminate the benefit of shifting from one line to the

other (i.e., changing to a low-yield cigarette). In this comparison, it would

require a 20-cigarette-per-day smoker who switched from a high-tar to a

low-tar cigarette to smoke only 4 more cigarettes per day in order to eliminate the benefit in lung cancer risk estimated from the CPS-I data. This difference in number of cigarettes per day is that which would be predicted

from a change in nicotine of 1.7 mg for individuals who switched brands in

115

Chapter 4

-30

-20

-10

0

10

20

30

-2 -1.5 -1 -0.5 0 0.5 1 1.5 2

Covariates: nicotine, age, cpd, tar

Slope of fit line = -2.31 cpd / mg Nic

Delta Nicotine, Difference Present Brand—Former Brand (One Cigarette)

Mean Change in Adjusted CPD

(95% CI for Means)

Figure 4-7

Mean Change in Adjusted CPD Reported for Subjects Changing Brand Smoked v.

Changes in Machine-Measured Nicotine Yield per Cigarettes: White Male Smokers

(N=169,610), ACS CPS-I Study, Followed 1960-1972

Source: ACS CPS-I, White male current cigarette-only smokers.

Note: Nicotine and tar levels interpolated by year and brand from Reader’s Digest (Miller & Monahan, 1959) and FTC (for years

1967-1973) data. Each data point combines subjects with the same change in nicotine (before—after). For each CPD category, the

value used in the calculations is the mean CPD value for the category as calculated across all subjects falling in the category from

the final follow-up questionnaire, which has continuous CPD values available. The mean change in CPD is the average difference

(after—before) in reported CPD level across subjects with the given change in nicotine. Mean change in CPD, adjusted for age, cpd,

and for tar and nicotine level before changing brand, is regressed on change in nicotine yield per cigarette. For the graph, covariate

coefficients are calculated in a general regression, then points are graphed as adjusted for the covariates with the regression line

shown through the adjusted points.

Chapter 04 11/19/01 11:00 AM Page 115
the CPS-I analysis described in the previous paragraph. High tar and nicotine was defined in the CPS-I study as between 2-2.7 mg nicotine, and low

tar and nicotine was below 1.2 mg nicotine. The mean nicotine level for

the high-tar group in Figure 4-8 was 2.36 mg and the mean nicotine level

for the low-tar group was 1.03 mg, a difference of 1.33 mg. In another context, the sales-weighted nicotine yield of U.S. cigarettes has declined from

approximately 2.6 mg in the 1950s to 0.9 mg currently (see Chapter 5), a

change of 1.7 mg of nicotine. The magnitude of this upward compensation,

if it occurred across the entire population using lower yield cigarettes in the

CPS I, is large enough to explain much of the reduction in lung cancer risks

found among low yield cigarette smokers.. 

The relationship between the machinemeasured nicotine yields and the number

of cigarettes smoked per day was also

examined for cigarettes with nicotine

yields similar to those currently used in

the United States. The 1990 and 1996 California Tobacco Surveys (CTS)

were utilized to examine the effects of low tar and nicotine on the number

of cigarettes smoked per day. This analysis was confined to a population of

adult smokers who were not in the process of changing their smoking

Number of Cigarettes Smoked per

Day among Smokers of Cigarettes

with Different Machine-Measured

Nicotine Yields for Current

Cigarettes—California Data

116

Smoking and Tobacco Control Monograph No. 13

0

50

100

150

200

250

300

0 5 10 15 20 25 30 35

High 25.8 mg

Low < 17.6mg

Mean of Cigarettes per Day Category

Lung Cancer Excess Death Rate (per 100,000)

Tar Level

Figure 4-8

Excess Lung Cancer Death Rates for Smokers of Different Numbers of Cigarettes by

Tar Level of Cigarette Smoked, American Cancer Society Cancer Prevention Study I

Source: ACS CPS-I White male current cigarette-only smokers.

Note: Tar levels interpolated by year and brand from Reader’s Digest (Miller & Monahan, 1959) and FTC (for years 1967-1973) data.

Uses base survey (1959) tar and CPD values. Restricted to subjects who smoke throughout study to personal endpoint (end of

study, death, or lost-to-follow-up). The summary rates shown are age-adjusted and duration-adjusted rates for CPD and tar-level categories. For each CPD category, the value used is the mean CPD value for the category as calculated across all subjects falling in

the category from the final follow-up questionnaire, which has continuous CPD values available.

Chapter 04 11/19/01 11:00 AM Page 116
behaviors. Respondents must have smoked at least 100 cigarettes in their

lifetime, smoked cigarettes daily 1 year prior to the survey, and smoked

daily at the time of the survey. The analysis was further restricted to respondents who were 25-64 years old, smoked five or more cigarettes per day,

and who had not tried to quit smoking in the previous 12 months. These

restrictions reduced the possible influences of individuals who were starting

to smoke or trying to quit, were less likely to be using cigarettes because of

their dependence on nicotine as defined by smoking fewer than five cigarettes per day (Shiffman, 1989; Benowitz and Henningfield, 1994), or were

switching brands based on development of an illness (those aged 65 and

older). 

Respondents to the 1996 CTS were asked to read the barcode number

printed on the side of the cigarette package. The brand descriptions for UPC

codes, versions A and E, were provided by Matthew Farrelly of the Research

Triangle Institute. These brand descriptions were used to obtain the corresponding machine-measured nicotine levels provided by the FTC for the

year 1996. The resulting population was 2,140. 

The data were modeled using a multiple linear regression that controlled for the effects of age, gender, race/ethnicity, and level of education,

variables significantly associated with number of cigarettes smoked per day

in the model. This analysis was based on individual subspecies brand data

and cigarettes smoked per day. Figure 4-9 shows an increase in number of

cigarettes per day for smokers of low-nicotine cigarettes (slope = -2.41

cig/mg nicotine, P < 0.005). 

This finding was supported by analyses of the CTS from 1990 and 1996

using sales-weighted nicotine as the measure of the nicotine yield of the

brand smoked. Data on brand smoked were available from the 1990 CTS,

but survey respondents only provided the name of the brand family and

not the specific brand subspecies. An overall sales-weighted nicotine value

was calculated using the 1990 and 1996 CTS for each brand using the sales

and nicotine-yield data for each brand subspecies (see Appendix). The

resulting populations were 2,964 in 1990 and 2,239 in 1996. 

Figure 4-10 demonstrates the relationship of mean cigarettes per day to

the level of nicotine in cigarettes for the 1990 and 1996 CTS. Significantly

more cigarettes were smoked per day by ultralow nicotine cigarette smokers

than by smokers of cigarettes with machine-measured yields of 0.75-0.90,

0.90-1.05, and 1.05+ mg nicotine in both survey years. There were no significant differences between mean cigarettes smoked per day for the 0.75-

0.90, 0.90-1.05, and 1.05+ mg nicotine categories. 

Data from the 1990 and 1996 CTS were modeled using a piecewise multiple linear regression that controlled for the effects of age, gender, race/ethnicity, and level of education. This model allowed for changes in the slope

of the cigarettes per day versus nicotine yield line, with break points dividing the lines at defined levels of nicotine yield. The slopes of the two

regression lines were compared; the left side of the piecewise regression

modeled cigarettes per day for nicotine levels below 0.95 mg, while the

117

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 117
right side modeled cigarettes per day for nicotine levels greater than or

equal to 0.95 mg. Figure 4-11 shows that there was an impact on the number of cigarettes per day for smokers of cigarettes with machine-measured

nicotine yields below 0.95 mg nicotine. The slopes for the lines above 0.95

mg nicotine were not statistically different from zero. The nonstatistically

significant difference in the slope of the lines from the two surveys was an

artifact introduced because Marlboro® had a sales-weighted nicotine value

of 0.94 in 1990 that increased slightly to 0.98 in 1996. This increase shifted

the large population of Marlboro® smokers from one side of the 0.95-mg

point to the other between the two analyses, and this shift resulted in a

slight, nonsignificant shift in the slope of the lines above the 0.95 break

point.

These analyses of the California Tobacco Surveys show a relationship

between average daily cigarette consumption and the FTC nicotine yield of

the cigarette smoked. More specifically, the sales-weighted analyses revealed

that the average number of cigarettes smoked per day varies as a function

of nicotine content below approximately 0.95 mg nicotine per cigarette.

Smokers of cigarettes with ultralow nicotine levels showed a 20 percent

increase in the number of cigarettes smoked per day compared to smokers

of medium-nicotine cigarettes. Yet adults who smoked medium-tar and

-nicotine cigarettes showed no significant difference in the mean number of

118

Smoking and Tobacco Control Monograph No. 13

5

10

15

20

25

30

35

40

45

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9

Piecewise Linear Regression

Multiple Linear Regression

Nicotine (mg)

Average Cigarettes per Day* 

Figure 4-9

Piecewise Linear Regression and Multiple Linear Regression of Cigarettes per Day,

CTS, 1996, Using Individual Brand Nicotine Yield Data

*Controlling for age, gender, race/ethnicity, and education level.

Note: The break point used for the piecewise regression was 0.95 mg of nicotine. FTC data for year 1996 were obtained from the

FTC reports on the tar, nicotine, and carbon monoxide of domestic cigarettes (FTC, 1999). The population consisted of respondents,

aged 25-64, who had smoked 100 cigarettes, smoked daily one year prior to the survey, smoked daily at the time of the survey, had

not made a quit attempt in the past 12 months, and currently smoked 5+ cigarettes per day. The P-values and slopes of the piecewise regresssion are (slope<0.95=-5.61, P<0.95=0.0013) and (slope>0.95=1.51, P>0.95=0.5316).

Chapter 04 11/19/01 11:00 AM Page 118
cigarettes per day when compared to those who smoked relatively high-tar

and -nicotine cigarettes. With current cigarette designs, which depend heavily on ventilated filters to lower the machine-measured yield, smokers

appear to be able to compensate within a single cigarette to maintain nicotine intake obtained from cigarettes that yield more than approximately

0.95 mg nicotine. Below that level of nicotine, compensation with increasing number of cigarettes smoked per day may also play a role. This bifurcated response of cigarettes per day with nicotine yield may be a characteristic

of the engineering of cigarettes for elasticity of delivery described in the

early sections of this chapter, and may not have occurred in cigarettes without ventilated filters. 

Two major prospective mortality studies of

smoking and disease bridged the period of

greatest reduction in tar levels of cigarettes.

Further examinations of these studies have revealed changes in smoking

risks that have occurred as lower yield cigarettes were introduced and

gained widespread acceptance. 

TEMPORAL TRENDS IN LUNG

CANCER AND OTHER DISEASES

IN MAJOR COHORT STUDIES

119

Chapter 4

15

20

25

30

CTS 1996

CTS 1990

0.10-0.75 0.75-0.90 0.90-1.05 1.05-1.70

Sales-Weighted Nicotine (mg)

Average Cigarettes per Day (95% Cl)

Survey Year

Figure 4-10

Cigarettes Smoked per Day by Level of Sales-Weighted Nicotine Yield (California Data)

Source: FTC data for years 1990 and 1996 were obtained from two FTC reports on the tar, nicotine, and carbon monoxide of

domestic cigarettes (FTC, 1992 & 1999). Sales data for 1990 were obtained from the Maxwell Report (Maxwell, 1994). Sales data

for 1996 were not available to the public. The tobacco companies, therefore, provided the 1996 sales-weighted nicotine levels using

the same methodology used for the 1990 analysis. Sales-weighting for overall brand was accomplished by weighting each subbrand nicotine level by its corresponding 1990/1996 market share. The sum of the weighted sub-brand nicotine levels provided the

overall nicotine level for the brand. The population consisted of respondents, aged 25-64, who had smoked 100 cigarettes, smoked

daily one year prior to the survey, smoked daily at the time of the survey, had not made a quit attempt in the past 12 months, and

were currently smoking 5+ cigarettes per day.

Chapter 04 11/19/01 11:00 AM Page 119
The British Physicians Study examined lung cancer mortality rates (Doll

et al., 1994) with a follow-up period of over 40 years. The follow-up interval

was divided into two 20-year periods, 1951-1971 and 1971-1991. Lung cancer death rates in male smokers, age-standardized to the same age distribution in the two follow-up intervals, increased by 19 percent to 314 per

100,000 during the second half of the study compared to 264 per 100,000

during the first 20 years of follow-up. This increase occurred during a period when the tar level of cigarettes in the United Kingdom had fallen dramatically. Lung cancer death rates for the entire U.K. population fell for

males aged 35-54 and 55-74 during the 1971-1991 period (Peto et al., 2000). 

Differences in intensity and duration of smoking for the smokers examined in the two follow-up periods may have contributed to the increase in

lung cancer death rates. Increased rates of cessation in the general population clearly contributed to the discordance of increasing lung cancer death

rates among male smokers in the study as contrasted with decreasing lung

cancer death rates for the male population as a whole. However, these

120

Smoking and Tobacco Control Monograph No. 13

15

20

25

30

35

40

Combined CTS

CTS 1996

CTS 1990

0.15 0.25 0.35 0.45 0.55 0.65 0.75 0.85 0.95 1.05 1.15 1.25 1.35 1.45 1.55 1.65 1.75

Sales-Weighted Nicotine (mg)

Average Cigarettes per Day*

Figure 4-11

Piecewise Linear Regression of Cigarettes Smoked per Day by Sales-Weighted

Nicotine Yield of the Brand Smoked (California Data)

*Controlling for age, sex, race/ethnicity, and level of education.

Note: The break point used was 0.95 mg of nicotine for all three piecewise regressions. FTC data for years 1990 and 1996 were

obtained from two FTC reports on the tar, nicotine, and carbon monoxide of domestic cigarettes (FTC, 1992 & 1999). Sales data for

1990 were obtained from the Maxwell Report (Maxwell, 1994). Sales data for 1996 were not available to the public. The tobacco

companies, therefore, provided the 1996 sales-weighted nicotine levels using the same methodology used for the 1990 analysis.

Sales-weighting for overall brand was accomplished by weighting each sub-brand nicotine level by its corresponding 1990/1996

market share. The sum of the weighted sub-brand nicotine levels provided the overall nicotine level for the brand. The population

consisted of respondents, aged 25-64, who had smoked 100 cigarettes, had smoked daily one year prior to the survey, had not

made a quit attempt in the past 12 months, and were currently smoking 5+ cigarettes per day. The p-values and slopes of the piecewise regression for CTS 1990 are (slope<0.95=-7.12, P<0.95<0.0001) and (slope>0.95=-0.16, P>0.95=0.9517). The p-values and slopes of

the piecewise regression for CTS 1996 are (slope<0.95=-9.13, P<0.95<0.0001) and (slope>0.95=-2.77, P>0.95=0.5117). The P-values and

slopes of the piecewise regression for the combined data are (slope<0.95=-8.69, P<0.95<0.0001) and (slope>0.95=-0.80, P>0.95=0.7171).

Chapter 04 11/19/01 11:00 AM Page 120
increasing death rates among smokers also suggest that smoking may have

become more hazardous over the follow-up interval. If there has been any

benefit of the introduction of lower yield cigarettes in the United Kingdom

for the physicians followed in the British Physicians Study, it is small

enough to have been overwhelmed by the differences in intensity and duration of smoking between the first and second 20-years of the study. 

Findings were similar for a comparison of the two Cancer Prevention

Studies (CPS I and CPS II) which had very similar designs, but were conducted 23 years apart—CPS-I began in 1959 and CPS-II began in 1982.

Comparisons of the first 6 years of follow-up in the two studies (Thun and

Heath, 1997; Thun et al., 1997b) demonstrated that lung cancer death rates

increased between the two follow-up periods, a timeframe where substantial

falls in machine-measured tar yields occurred for U.S. cigarettes. Detailed

examination of the two populations studied showed that there were substantial differences in these two populations in the duration and number of

cigarettes smoked per day, particularly for females (Thun et al., 1997b), and

these differences in smoking behaviors explained some but not all of the

differences in lung cancer death rates. Figure 4-12 presents age-standardized

death rates for male and female participants of CPS-I and CPS-II. There was

no change in the death rates for male and female never smokers between

the two studies, but the lung cancer death rates for current smokers

increased dramatically between the two studies. The increase in lung cancer

death rates between the two time periods was reduced, but not eliminated,

when the rates were adjusted for differences in the number of cigarettes

smoked per day and duration of smoking. 

Nonfiltered cigarette smokers in CPS-I were compared to nonfiltered,

mixed, and filtered cigarette smokers in CPS-II. Among males (see Figure 4-

13), there was a dramatic increase in lung cancer risk for nonfilter smokers

in CPS-II compared to CPS-I, and even the filter smokers in CPS-II had

slightly higher lung cancer rates than the nonfilter smokers in CPS-I.

Among females (see Figure 4-14), there were dramatically higher rates for all

three categories of smokers in CPS-II compared to CPS-I. The rates in

Figures 4-13 and 4-14 were age-standardized, but were not adjusted for differences in the number of cigarettes smoked per day or duration of smoking; it is likely that these differences may have contributed to the differences in lung cancer mortality between the two studies, particularly for

females. However, the comparisons do not suggest that even filter smokers

in CPS-II had any reduction in lung cancer risk when compared to smokers

in CPS-I more than 20 years earlier. Some of this increase in lung cancer

risk between the two studies may have resulted from greater availability of

cigarettes and resultant heavier smoking among adolescents during the

period when smokers in CPS-II were initiating their smoking behaviors.

Alternatively, increased depth of inhalation with lower yield cigarettes and

higher levels of tobacco-specific nitrosamines in the tobacco used in more

recent cigarettes (see Chapter 5) may also have contributed to the increases.

But detailed examination of the risks in these two studies separated by over

20 years does not suggest a reduction in risk resulting from lower yield cigarettes. 

121

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 121
Both of these studies indicate that the lung cancer relative risks associated with smoking increased over the same time period when smokers in the

U.S. and U.K. were switching to lower yield and filtered cigarettes in substantial numbers.

122

Smoking and Tobacco Control Monograph No. 13

CPS-I

1959 - 1965 Study and Year

Death Rate per 100,000

Never Smokers

0

50

100

150

200

250

300

350

CPS-II

1982 - 1988

Male Smokers

Non-Adjusted

Adjusted

Non-Adjusted

Adjusted Female Smokers

Figure 4-12

Death Rates from All Lung Cancers by Smoking Status, CPS-I and CPS-II (Adjusted

for Current Amount and Duration of Smoking)

Note: Death rates from lung cancer by smoking status, CPS-I and CPS-II (adjusted and unadjusted for current amount and duration).

0

100

200

300

400

500

(1896 - 1944) (1919 - 1967)

CPS-I

Non-Filter

CPS-II Non-Filter

CPS-II Filter

CPS-II Mixed

Year Began Smoking

Death Rate per 100,000

Never Smokers

Figure 4-13

Male Lung Cancer Death Rates by Filter Use, CPS-I and CPS-II

Note: Death rates form all lung cancers among men by filter use, CPS-I and CPS-II.

Chapter 04 11/19/01 11:00 AM Page 122
The ultimate measure of a benefit from any

reduction in the risk of smoking is a change

in national death rates. Lung cancer death

rates in both the United States and United Kingdom have declined among

males in recent years. Several investigators have examined the relationships

between smoking behaviors and changes in lung cancer mortality in both

countries, and these analyses are now considered in relation to trends in tar

yields of the cigarettes smoked in both countries. 

In postulating the multi-stage model of

carcinogenesis, Armitage and Doll (1961)

suggested that multiple inheritable changes

in the cell are required to cause malignant transformation. In this model,

successive stages in the transformation of one cell may be separated from

each other by several years, and the factors influencing early stages may be

different from those influencing later stages. In its simplest form, this

model implies that incidence of lung cancer at a given age is a constant

times age raised to a power. Doll and Peto (1978) formulated the equation

for lung cancer as Incidence = 0.273(cigarettes/day + 6)2(age – 22.5)4.5, with

the values in the formula derived from the lung cancer mortality experience

of British physicians. The term (age – 22.5) was derived by assuming a uniform age of smoking uptake of 19 years and a 3.5-year latency from carcinogenic transformation of the cell to death from lung cancer. This term

becomes duration of smoking prior to carcinogenic transformation for current smokers. 

Variations of this model have been used by a number of investigators to

match British national smoking prevalence data with British lung cancer

Published Models Using Smoking

Behavior to Predict National Lung

Cancer Death Rates

TEMPORAL TRENDS IN NATIONAL

LUNG CANCER DEATH RATES AND

SMOKING BEHAVIORS

123

Chapter 4

0

100

200

300

400

500

(1896 - 1944) (1919 - 1967)

CPS-I

Non-Filter

CPS-II Non-Filter

CPS-II Filter

CPS-II Mixed

Year Began Smoking

Death Rate per 100,000

Never Smokers

Figure 4-14

Female Lung Cancer Death Rates by Filter Use, CPS-I and CPS-II

Note: Death rate from all lung cancers among women by filter use, CPS-I and CPS-II.

Chapter 04 11/19/01 11:00 AM Page 123
death rates. Stevens and Moolgavkar (1979, 1984) and Moolgavkar and colleagues (1989) used birth-cohort data on tobacco prevalence and birthcohort-specific, cumulative tar-weighted cigarette consumption to construct

a model that fit British birth-cohort/lung cancer death-rate data. Townsend

(1978) expanded the basic multistage model to include birth-cohort-specific

duration of exposure and number of cigarettes smoked per day. This model

used the prevalence of smoking estimated in 5-calendar-year increments to

divide each birth cohort into strata with different durations of smoking. A

weighted mean of the number of cigarettes smoked per day at each age was

used as the dosage term. 

However, the weighting used assumed that recent smoking was more

important than past smoking, decreasing the weight of duration of smoking. The number of cigarettes was also adjusted by assuming that filtered

cigarettes were 40 percent less carcinogenic and that the carcinogenic risk

of a cigarette was directly proportional to the machine-measured tar yield

of the cigarette. The estimated lung cancer occurrence for each of the fractions with different durations of exposure was summed and added to the

never-smoker risk to predict the lung cancer death rate for the birth cohort.

Never-smoker death rates were taken from the American Cancer Society’s

prospective mortality study of 1 million males and females (Hammond,

1966). 

To test this model, Townsend (1978) varied the constants in the model

over a range and found the values that resulted in the best fit of the model

to the British age-specific lung cancer mortality data. When the exponent

for the duration of exposure term was set at 5 (the best-fit value), the model

explained 98 percent of the variation in excess mortality in the male birth

cohorts but only 84.8 percent of the variation in females. 

Townsend’s study was intended to develop a model of U.K. lung cancer

mortality and was not intended to directly examine the question of risk

reduction with low-yield cigarettes. The author assumed that the risk was

directly proportional to the tar value of the cigarette smoked in creating

their model. Adjustments for filters and tar content of the cigarettes in this

study reduced the predicted risk of cigarettes by almost 40 percent from

1946 to 1966. The fit of the tar data in the model may be the result of the

reduced weight given past smoking behaviors. 

Brown and Kessler (1988) used a multistage model to predict U.S. lung

cancer death rates to the year 2025. This model incorporated terms for calendar-year effects and a term for cohort effects and used a tar-weighted

consumption measure for the number of cigarettes smoked per day. The

model assumed a linear relationship between tar content and lung cancer

risk and used a single cohort term to model the complex effects of differences in age of initiation and duration of exposure that occur across

cohorts. These assumptions resulted in a model that predicted that lung

cancer death rates in males would change very little between 1985 and

2010. The projection was not consistant with the decline in lung cancer

death rates among white males that occurred following a peak in ageadjusted white male death rates in 1990 (Wingo et al., 1999). 

124

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 124
In contrast, Tolley and colleagues (1991) used a compartment model

(i.e., discrete state-discrete time model of health processes) to estimate lung

cancer death rates using birth-cohort-specific smoking initiation, prevalence, and cessation rates for the United States and the relationship of dose

and duration of smoking developed from the British Physicians Study (Peto,

1986). Without any adjustment for tar, they predicted that changes in

smoking prevalence rates alone would project a decline in white male lung

cancer death rates during the mid 1980s, a prediction that closely matched

the actual death rate trends. 

Swartz (1992) used birth-cohort-specific smoking rates estimated by

Harris (1983) and a multistage carcinogenesis model developed by

Whittemore (1988) to estimate U.S. lung cancer mortality. The modeled

estimates predicted a 12-percent decline in lung cancer rates from 1970 to

1985, a period when lung cancer death rates increased by 26 percent.

Substantial declines in tar yield of cigarettes occurred prior to and during

this period, and this model suggested that risks of cigarette smoking

increased rather than decreased over the period when tar yield was falling.

More recently, Mannino and colleagues (2001) examined age- and birthcohort-specific U.S. lung cancer death rates for White males and White

females, adjusting for age- and birth-cohort-specific differences in prevalence and duration of smoking. Differences between male and female lung

cancer rates, and differences in lung cancer rates across birth cohorts, were

eliminated by adjusting for differences in smoking prevalence and duration

of smoking. These researchers noted: “Differences in lung cancer death rates

across birth cohorts of U.S. men and women primarily reflect differences in

the prevalence and duration of smoking. Changes in cigarette design that

have greatly reduced tar yields have a relatively small effect compared with

that of people’s smoking status and duration of smoking.” 

National lung cancer death rate data in the United Kingdom were compared to two lung cancer mortality studies conducted 40 years apart (1950

and 1990) to examine the effects of changes in smoking prevalence (Peto et

al., 2000). The lung cancer risk produced by being a cigarette smoker

increased between 1950 and 1990. This increase was attributed to the

longer durations of smoking experienced by smokers as of 1990. The

changes in smoking prevalence were consistent with the changes in lung

cancer death rates for females and for older males, but younger males had

declines in age-specific lung cancer death rates over time that were much

larger than those in smoking prevalence. Reduction in lung cancer risks

from smoking low-yield cigarettes was suggested as an explanation for this

observation. 

When considering a potential effect of

changing cigarette design over time on

national lung cancer death rates, it is necessary to control for changes in smoking prevalence and intensity over time

because smoking intensity and duration are more powerful predictors of

lung cancer risk in epidemiological studies than is tar yield of the cigarette

smoked. Cigarette smoking was more widely prevalent during the early part

Influence of Smoking Behaviors on

Lung Cancer Death Rates in the

United States and United Kingdom

125

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 125
of the twentieth century in the United Kingdom than in the United States.

For example, per-capita consumption of cigarettes in the United Kingdom

for the year 1905 was 380 cigarettes per adult over age 15 (Wald and

Nicolaides-Bouman, 1991), whereas per-capita consumption in the United

States was only 70 cigarettes per adult over age 18 for the same year (Burns

et al., 1997a). In contrast, filtered and low-yield cigarettes were introduced

and widely accepted in the United States ahead of their use in the United

Kingdom (see Figure 4-15). 

Lung cancer death rates over time reached peak levels that were much

higher in the United Kingdom than in the United States, particularly

among males. However, male lung cancer death rates peaked earlier (around

1970) in the United Kingdom (Peto et al., 2000) compared to the United

States (around 1990), and they declined more steeply in the United

Kingdom than in the United States. Lung cancer death rates in the United

Kingdom are now lower than those in the United States for both males and

females under age 70 (Peto et al., 2000). 

In both the United States and the United Kingdom, the prevalence of

smoking among males born in the early part of the last century exceeded

70 percent, with peak smoking prevalence rates among males in the United

Kingdom being somewhat higher (more than 85 percent) (Burns et al.,

1997a; Wald and Nicolaides-Bouman, 1991). Additionally, males among the

older birth cohorts in the United Kingdom smoked hand-rolled cigarettes in

high percentages (Wald and Nicolaides-Bouman, 1991). The prevalence of

ever smoking has declined among male birth cohorts born after 1930 in

both countries. 

Lung cancer occurs predominantly at older ages due to the powerful

effect of duration of smoking on lung cancer rates. However, because of the

temporal trends in type of cigarettes manufactured and sold, older smokers

also began smoking with much higher yield cigarettes, and they smoked

these cigarettes for much more of their smoking experience than did

younger smokers. As a result, changes over time in age-specific lung cancer

death rates at younger ages have been suggested as a more sensitive measure of the population impact of lower yield cigarettes on lung cancer rates.

Younger smokers are, on average, more likely than older smokers to have

begun their smoking with filtered and lower yield cigarettes and would

have smoked them for a larger fraction of their smoking experience. In

addition, age-specific lung cancer death rates are available from the 1950s

onward allowing a long period of observation during which most of the

changes in cigarette design took place.

The use of temporal changes in age-specific lung cancer death rates at

younger ages as a measure of change in disease risks from low-yield cigarettes is somewhat limited by the observation that most younger smokers in

the United Kingdom (Wald and Nicolaides-Bouman, 1991) and the United

States (CDC, 2000) use cigarettes with mid-range yields of tar rather than

the ultralow yield products. However, the tar values of these mid-range

yield cigarettes are substantially lower than the tar yields of cigarettes sold

20-40 years earlier. In addition, use of low tar-yield cigarettes is currently

126

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 126
more common among older smokers than among younger smokers in both

the U.S. and U.K. (see Figure 4-1 and Wald and Nicolaides-Bouman 1991),

suggesting that a population effect of reduction in risk with use of these

cigarettes, if present, might be larger among these older smokers. Indeed, it

is among older smokers that the epidemiological data presented earlier in

this chapter have suggested a decreased risk. The reduction in disease risk

over time, out of proportion to declines in prevalence, is evident predominantly among younger age groups in the United Kingdom. The decline in

lung cancer risk over time among older age groups is more closely matched

by the decline in smoking prevalence (Peto et al., 2000). 

There is a difference between the United States and the United

Kingdom in the rate of rise of lung cancer with age. This difference is evident across most of the birth cohorts presented in Table 4-6. Figure 4-16

presents age-specific lung cancer death rates for two separate birth cohorts.

Age-specific rates in the United States start lower than in the United

Kingdom but then rise more rapidly with age for both younger and older

birth cohorts. 

This higher rate of lung cancer at younger ages may be due to differences in the distribution of age of initiation among younger male smokers

127

Chapter 4

0

20

40

60

80

100

1925 1935 1945 1955 1965 1975 1985 1995

Year

Share of Market (Percent)

US Non-Filter Market Share UK Non-Filter Market Share

US Filter Market Share UK Filter Market Share

120

Figure 4-15

Market Share of Filter and Non-Filter Cigarettes in the United States and

United Kingdom, 1925-1990

Note: U.S. data were obtained from Maxwell Report (Maxwell, 1994). British data were obtained from UK Smoking Statistics (Wald

and Nicolaides-Bouman, 1991).

Chapter 04 11/19/01 11:00 AM Page 127
in the two countries. Table 4-7 presents self-reported recall of the age of

smoking initiation by smokers who were at different ages at the time of the

survey. Data are presented for three surveys conducted in the United

Kingdom in 1971, 1981, and 1987 (Wald and Nicolaides-Bouman, 1991)

and for data from the National Health Interview Survey of the United States

for the years closest to the U.K. data when the question on age of initiation

was asked. For both sets of surveys, the data presented are for the entire

population and age of initiation is reported for current and former smokers

combined. Initiation rates prior to age 13 are similar for both countries, but

there is a substantially higher rate of initiation among those 14-15 years old

in the United Kingdom. This higher rate of initiation early in adolescence

could contribute to the higher rate of lung cancer deaths at younger ages

observed in Figure 4-16. 

The reasons for the higher rate of rise with age of lung cancer death

rates in the United States compared to the United Kingdom are less clear,

but may relate to cessation during young adulthood in the United Kingdom

occurring earlier in calendar years compared to the United States, thereby

lowering the lung cancer risk as the birth cohort aged. Data are not available to make this direct comparison of cessation, but by 1984, the prevalence rates for 25- to 34-year-old males in the United Kingdom (born

1950–1959) were 39 percent (Wald and Nicolaides-Bouman, 1991), whereas

the rates in comparable cohorts of White males in the United States were

somewhat higher (42-43 percent) (Burns et al., 1997a). This lesser cessation

in the United States could contribute to the more rapid rise in lung cancer

death rates with age. 

The observed difference in lung cancer death rates may also relate to

differences in the pattern of cigarette use at younger ages in the two countries. Differences in age of initiation, intensity of smoking during early adolescence, and rates of cessation during young adulthood all may influence

lung cancer death rates at younger ages. Lung cancer death rates rise with

increasing number of cigarettes smoked per day and even more powerfully

with the duration of smoking (Doll and Peto, 1978), but this increase

occurs with a lag of approximately 20 years from onset of exposure. That is,

approximately a 20-year duration of smoking is required before lung cancer

rates in smokers begin to significantly exceed those in never smokers (Burns

et al., 1997b). As a result, lung cancer death rates at age 35 among smokers

are much more influenced by that group of smokers who began to smoke

before age 15, in contrast to those smokers who first started to smoke in

their mid to late 20s. The epidemiological data would suggest that it is

unlikely that those smokers who began smoking after age 15 make a substantive contribution to lung cancer death rates at age 35, given the 20-year

lag time demonstrated between onset of smoking and increases in the risk

of lung cancer due to smoking. 

Differences in the intensity of smoking at younger ages during the

process of becoming a regular smoker may also play a role. To the extent

that the pattern of early smoking (prior to age 15) is episodic and confined

to a few cigarettes per month, which is the pattern most commonly

described among adolescent smokers currently under age 15 (Johnston et

128

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 128
al., 2000), the exposure would not be expected to contribute substantively

to lung cancer death rates at age 35. To the extent that the pattern of early

smoking is regular smoking of one-half pack or more per day, it would be

expected to contribute relatively more to lung cancer death rates at younger

ages. There are few data available to assess changes over time in the intensi129

Chapter 4

Table 4-6

Age- and Birth-Cohort-Specific Lung Cancer Death Rates for the United States

and United Kingdom

Lung Cancer Death Rate*

Age (Midpoint of 5-Year Age Group)

Midpoint of United Kingdom

Birth Cohort 32.5 37.5 42.5 47.5 52.5 57.5 62.5 67.5 72.5 77.5 82.5

1873 167.30

1878 243.01 259.83

1883 305.25 377.48 391.85

1888 329.25 431.62 506.16 509.23

1893 289.47 428.10 538.81 650.73 679.95

1898 219.13 353.38 512.62 662.33 764.63 812.65

1903 126.17 232.18 374.27 528.11 682.74 796.69 832.76

1908 59.72 125.16 228.23 369.44 514.73 655.69 756.35 767.28

1913 24.87 57.76 120.75 215.69 344.15 479.32 616.24 678.27 669.39

1918 9.78 25.00 55.08 111.60 202.32 316.22 437.96 553.20 592.54

1923 3.76 9.47 22.38 53.96 106.37 184.94 294.74 402.30 475.24

1928 3.53 9.06 21.01 46.80 92.11 158.66 245.40 326.52

1933 2.80 6.29 16.30 36.15 69.26 122.78 184.53

1938 2.49 5.90 12.96 29.62 59.51 102.18

1943 2.24 4.97 11.24 26.26 49.74

1948 1.56 4.07 9.72 20.74

1953 1.09 3.13 8.02

1958 0.77 2.13

1963 0.65

United States

1873 116.80

1878 138.60 176.30

1883 148.90 199.60 222.60

1888 157.80 232.20 268.30 325.40

1893 135.50 219.70 302.60 380.60 431.60

1898 95.90 180.70 277.30 371.00 464.00 477.70

1903 58.20 114.92 199.88 306.95 418.93 502.80 543.33

1908 30.40 68.71 127.55 228.01 329.42 458.80 546.20 584.96

1913 11.60 31.79 76.79 152.13 244.30 359.11 470.70 565.40 580.60

1918 4.90 13.99 38.61 84.32 150.01 255.74 367.06 485.89 529.90

1923 1.70 5.73 17.26 44.03 90.91 162.93 262.46 374.07 470.90

1928 1.97 7.05 21.54 47.86 95.28 167.41 268.18 359.60

1933 2.00 7.34 19.30 45.44 86.59 159.35 233.60

1938 2.03 6.15 17.43 40.26 80.52 132.70

1943 1.80 5.29 15.19 34.64 66.10

1948 1.12 4.32 11.63 26.20

1953 0.98 3.85 9.50

1958 1.16 3.30

1963 1.20

*Deaths per 100,000

Chapter 04 11/19/01 11:00 AM Page 129
ty of smoking during early adolescence in either the United States or

United Kingdom, but it might be expected that the intensity of smoking

during early adolescence may have changed in the direction of reduced

intensity due to the tobacco education and control efforts implemented in

both countries. Data from the Monitoring the Future Study (Johnston et al.,

2000) for high school seniors in the United States showed a decline from

the late 1970s to the present in the percentage of those adolescents who

had smoked within 30 days of the survey who were either daily smokers or

smokers of one-half pack of cigarettes per day or more. These data demonstrate a decline in intensity of smoking among high school seniors over the

last 25 years, and a similar decline may have occurred among all adolescents from the mid 1950s when concerns about the disease risks of smoking

were first widely publicized. 

Patterns of cessation can also influence rates of lung cancer at early

ages. Among birth cohorts born before 1900, the pattern of smoking behavior with age did not include substantial rates of cessation under age 60

(Burns et al., 1997a). However, beginning with the widespread publication

of the disease risks associated with smoking in the mid 1950s, smokers

began to quit at younger ages, so more recent birth cohorts have substantial

fractions of smokers who have quit prior to age 30. These smokers who quit

early would not accumulate a substantial duration of smoking, and therefore would have very low risks. 

130

Smoking and Tobacco Control Monograph No. 13

1

10

100

UK 1926 - 1930

US 1946 - 1950

UK 1946 - 1950

US 1926 - 1930

32.5 37.5 42.5 47.5 52.5

Midpoint of a 5-Year Age Group

Death Rate per 100,000

Figure 4-16

Birth-Cohort-Specific Male Lung Cancer Death Rates by Age

Note: U.S. lung cancer death rates were provided for the years 1960-1994 by D.M. Mannino (personal communication, 2000).

Chapter 04 11/19/01 11:00 AM Page 130
In the United States, most first use of cigarettes occurs before age 18

(U.S.DHHS, 1994). Changes in smoking prevalence after reaching adulthood

reflect rates of cessation almost exclusively. However, data from Table 4-8

suggests that, at least for the period after 1976 and perhaps during the

1950s, the prevalence of smoking among 20-24 year old males in the

131

Chapter 4

Table 4-7

Percentage of Men Starting to Smoke Any Tobacco in the United States and the United

Kingdom at Different Ages (by Age at time of Survey)

Percentage

Age at Time Age at United States United Kingdom

of Survey Initiation Year of Survey: 1970 1980 1987 1971 1981 1987

20-24 13 and less 6.9 8.4 9.7 31 9 10

14-15 8.3 11.6 6.8 15 17

16-17 19.6 18.2 10.0 21 19 17

18-19 18.9 8.7 9.0 11 5 6

20-24 6.9 6.2 3.5 2 2 1

Don’t know 2.5 1.8 0 2 3 3

Never smoked 36.9 45.1 61.0 34 47 47

100 100 100 100 100 100

25-34 13 and less 8.6 7.6 8.8 29 . .

14-15 11.8 11.5 10.8 . .

16-17 16.6 14.6 12.1 24 . .

18-19 17.9 17.1 9.9 13 . .

20-24 12.5 10.7 7.3 8 . .

25-29 1.6 0.8 1.1 1 . .

30-34 0.2 0 0 0 . .

Don’t know 2.8 1.7 0 2 . .

Never Smoked 28.0 36.0 49.9 22 . .

100 100 99.9 100

25-29 13 and less 9.4 8.3 9.1 . 8 9

14-15 11.7 10.1 10.6 . 19 16

16-17 15.9 14.8 12.7 . 21 15

18-19 18.3 16.6 8.8 . 7 6 

20-24 11.0 8.3 6.7 . 5 5

25-29 0.8 1.1 1.3 . 1 1

Don’t know 2.4 1.4 0.0 . 5 3

Never Smoked 30.5 39.4 50.8 . 34 46

100 100 100 100 100

30-34 13 and less 7.5 6.8 8.6 . 9 12

14-15 11.9 13.1 10.9 . 17 14

16-17 17.4 14.4 11.6 . 19 13

18-19 17.3 17.7 11.2 . 8 9

20-24 14.6 13.5 7.8 . 6 4

25-29 2.8 0.4 0.9 . 2 2

30+ 0.4 0 0 . 0 0

Don’t know 3.5 2.1 0 . 4 5

Never Smoked 24.5 32.1 49.0 . 36 42

99.9 100.1 100 100 100

Note: The British data were obtained from UK Smoking Statistics (Wald and Nicolaides-Bouman, 1991). The U.S. data were

obtained from NHIS 1970, 1980, and 1987. The population consisted of United States White males, aged 20+, who were selfrespondents for the above-mentioned NHIS years.

Chapter 04 11/19/01 11:00 AM Page 131
United Kingdom was substantially higher than the prevalence reported four

years earlier for 16-19 year old males. This suggests that a substantial fraction of initiation in the U.K. may have occurred after age 20. These smokers

will not have accumulated twenty years of smoking until they are at least

40-44 years old and are unlikely to meaningfully contribute to the lung

cancer death rate for ages under age forty. 

In summary, a variety of changes in the patterns of cigarette smoking

have occurred in both the United States and the United Kingdom, including changes in smoking initiation as well as smoking cessation. These

changes may be responsible for many of the differences across time and

between the countries in national lung cancer mortality rates. 

Age-specific lung cancer death rates

in the United Kingdom have

declined dramatically in the last

several decades, and these reductions have exceeded the declines in smoking prevalence among the same age groups for those under age 45 (Peto et

al., 2000). One possible explanation for the more rapid decline over time in

lung cancer death rates compared to trends in smoking prevalence is

decreased risk from smoking lower yield cigarettes. A reduced risk from

smoking lower yield products might be first evident among those who are

younger because they would have had a larger proportion of their smoking

experience with these lower yield cigarettes. However, as discussed in the

previous section, it is important to examine other aspects of smoking

behavior that could also account for changes in lung cancer rates before

attributing the differences in lung cancer death rates to changes in cigarette

yield. 

Age- and birth-cohort-specific lung cancer death rates for the United

States and United Kingdom are presented in Table 4-6. The data for the

United Kingdom are those provided by Peto and associates (2000) as the

mean lung cancer death rates for sequential groups of 5 calendar years presented as 5-year age-specific death rates. These rates were converted to

birth-cohort rates by subtracting the mid point of the age group from the 5-

year-calendar period over which the death rates were averaged to approximate the years of birth for that age group. Rates for the United States are

actual birth-cohort- and age-specific lung cancer death rates provided by

Mannino and colleagues (2001). 

It is evident that there have been very dramatic percentage declines in

male lung cancer death rates in the United Kingdom among those under

age 50, with particularly dramatic percentage declines under age 40. Rates

for those aged 40-49 declined by about two-thirds, with rates in the

youngest age group declining by approximately 85 percent. These declines

exceed the approximately 50 percent decline in smoking prevalence over

time at these same ages (see Table 4-8). Among those over age 50 in the

United Kingdom, declines in smoking prevalence and lung cancer death

rates approximate each other more closely. 

In the United States, there have been much less dramatic declines in

lung cancer death rates among white males under age 50, and they more

Examination of Trends Over Time in AgeSpecific Lung Cancer Death Rates in the

United States and United Kingdom

132

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 132
closely match changes in smoking prevalence. Data on smoking prevalence

and lung cancer death rate by birth cohort and age are available for the

United States and are presented in Table 4-9 for White males. At ages 30-34,

the fall in lung cancer death rates across sequential birth cohorts is similar

in magnitude to that observed for the fall in smoking prevalence, particularly for the fall in smoking prevalence for the same birth cohort when the

cohort was age 12. At ages 35-39, lung cancer death rates fall approximately

48 percent from their peak in the 1931-1935 birth cohort to the 1951-1955

cohort, whereas smoking prevalence falls only 39 percent. However, there is

also a 48 percent fall in the prevalence of smoking at age 12 across the

same cohorts. Similarly, there is a 46 percent decline in lung cancer death

rates at ages 40-44 from a peak in the 1926-1930 birth cohort to the last

birth cohort where smoking prevalence data are available, with a decline in

smoking prevalence of 36 percent, but the decline in smoking prevalence at

age 12 is also 36 percent. Given the limited precision of these estimates and

the difficulty in defining the exact measure of smoking behavior that

should be compared (e.g., no measures of intensity of smoking at younger

ages are available), the changes in smoking behaviors across birth cohorts

may well explain the changes in lung cancer death rates in the United

States A more detailed examination of this relationship for all birth cohorts

born after 1910 is presented later in this chapter. 

Examination of the changes in lung cancer death rates at ages 30-34

and 35-39 with sequential birth cohorts in the United Kingdom (see Table

4-6) reveals that rates have fallen dramatically, particularly for those born

after 1945. Lung cancer death rates currently occurring in those age groups

in the United Kingdom approximate rates estimated for nonsmokers in

these age groups by extrapolating retrogressively the rates observed among

older nonsmokers in the CPS-I study to include these age groups. The rates

for never smokers estimated are 1.2 at ages 30-34 and 1.9 at ages 35-39.

These dramatic changes in lung cancer death rates at these younger ages in

the United Kingdom are consistent with the essential elimination of a

smoking effect at ages 30-34 and a near elimination of the effect at ages 35-

39. 

It is theoretically possible that this reduction in age-specific lung cancer

death rates is due to a reduction in the carcinogenicity of the cigarettes

smoked to almost zero in this younger age population, who would have initiated smoking cigarettes with substantially lower tar yields when compared

with older birth cohorts, but this explanation is unlikely. In the United

Kingdom (Wald and Nicolaides-Bouman, 1991), as is true in the United

States, approximately 90 percent of young smokers smoke cigarettes with 10

mg or more tar yields, and approximately one-half smoke cigarettes with

yields of 15 mg tar or higher. This distribution of cigarettes smoked, as well

as the very modest risk reductions demonstrated in epidemiological studies

and the current understanding of compensation (see Chapter 2), make it

biologically implausible that smoking low-yield cigarettes would have

almost no risk. An alternate, explanation is that prevalence of intense

smoking at very young ages has declined dramatically, following demonstration in the 1950s of increased disease risks due to smoking and the

133

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 133
social policy changes that followed the publication of the Royal College of

Physicians’ report on smoking (Royal College of Physicians, 1962). 

Lung cancer death rates for males in the United Kingdom have also

declined for ages 40-44 and ages 45-49 with each age group declining to

one-third of its peak value, a proportionate reduction that exceeds the

134

Smoking and Tobacco Control Monograph No. 13

Table 4-8

Prevalence of Cigarette Smoking among British Males Aged 16 and Over, by Age: ONS General

Household Survey, 1976-1996

Age

Year 16-19 20-24 25-34 35-59 60+

1948 61 74 76 70 39

1949 54 73 71 68 38

1950 51 68 70 66 38

1951 51 68 70 66 42

1952 47 62 67 64 40

1953 47 61 67 64 42

1954 46 63 66 63 42

1955 47 59 67 62 39

1956 52 65 67 65 45

1957 59 61 66 63 45

1958 54 63 65 63 42

1959 60 62 65 63 48

1960 65 67 64 64 46

1961 61 67 60 61 46

1962 61 62 59 60 44

1963 56 65 60 54 42

1964 56 61 55 57 45

1965 50 63 56 56 44

1966 54 60 59 56 44

1967 52 61 56 56 45

1968 57 69 57 57 46

1969 53 62 60 54 44

1970 55 58 60 55 46

1971 53 57 55 50 43

1972 51 60 54 51 42

1973 49 62 53 49 41

1974 48 55 55 51 40

1975 49 53 46 49 41

16-19 20-24 25-34 35-49 50-59 60+

1976 38 46 48 49 49 40

1978 35 46 49 47 47 38

1980 33 44 47 45 45 34

1982 31 39 40 39 41 32

1984 28 39 39 38 38 29

1986 30 41 37 37 34 28

1988 28 37 37 36 32 25

1990 28 39 37 34 27 24

1992 29 39 35 31 27 20

1994 28 42 34 31 26 17

1996 25 43 38 30 27 17

Note: The prevalence of smoking for years 1976 to 1996 was obtained from the Office for National Statistics General Household

Survey, 1976 to 1996 (ONS, 1998).

Chapter 04 11/19/01 11:00 AM Page 134
135

Chapter 4

Table 4-9Comparison of Birth-Cohort-Specific Current Smoking Prevalence at Different Ages with Birth-Cohort- and Age-Specific Lung CancerDeath Rates for White Males in the United States

Age (Years)

Birth-Cohort-Specific Lung Cancer Smoking Lung Cancer Smoking Lung Cancer Smoking Lung Cancer

Current Smoking Prevalence Death Rate Prevalence Death Rate Prevalence Death Rate Prevalence Death Rate

BirthCohort 12 17 22 27 30 30-34 35 35-39 40 40-44 45 45-491906-1910 10.89 41.60 71.20 76.46 77.59 — 76.89 — 72.12 — 69.73 30.401911-1915 8.87 42.42 73.15 78.26 79.31 — 77.57 — 74.43 11.60 70.01 31.791916-1920 9.74 43.11 72.32 78.15 78.45 — 75.65 4.90 71.66 13.99 65.83 38.611921-1925 8.27 40.61 75.36 78.55 77.90 1.70 73.92 5.73 68.20 17.26 60.74 44.031926-1930 7.59 44.64 74.39 75.81 75.06 1.97 70.63 7.05 63.68 21.54 55.76 47.861931-1935 7.55 43.69 71.89 72.75 70.75 2.00 64.61 7.34 56.59 19.30 49.96 45.441936-1940 6.66 40.80 68.38 68.19 65.10 2.03 58.05 6.15 51.72 17.43 45.09 40.261941-1945 6.04 41.40 66.09 62.85 59.67 1.80 53.69 5.29 46.98 15.19 40.14 36.641946-1950 4.85 34.85 58.57 54.81 51.47 1.12 45.78 4.32 40.46 11.63 — 26.201951-1955 3.90 32.48 50.26 47.01 43.91 0.98 39.50 3.85 — 9.50 — —1956-1960 3.85 33.06 44.38 41.59 39.69 1.16 — 3.30 — — — —1961-1965 4.54 28.90 39.36 — — 1.20 — — — — — —

Note: U.S. smoking prevalence was obtained from NCI Smoking and Tobacco Control Monograph No. 8 (Burns et al., 1997a). U.S. lung cancer death rates were obtained for years 1955 to1995. The death rate for 1955 came from the NCI Monograph 59 (NCI, 1982). Death rates for the years 1960-1994 were provided by D.M. Mannino (personal communication, 2000). Thedeath rate for 1995 was obtained from NCHS data.

Chapter 04 11/19/01 11:00 AM Page 135
136

Smoking and Tobacco Control Monograph No. 13

change in smoking prevalence within these age groups. Declines in lung

cancer death rates among older age groups are more modest and are consistent with changes in smoking prevalence. 

Unfortunately, birth cohort analyses of smoking behavior using the

U.K. data are not available to generate a table similar to that provided for

the United States (see Table 4-9). However, data are available on the prevalence of smoking by males of different ages for the calendar years 1948-

1996 (see Table 4-8). These data offer some insight into the changes in age

of smoking initiation and rates of cessation that have occurred among

males in the United Kingdom over the time periods that relate to changes

in lung cancer death rates among sequential birth cohorts of males 40-44

and 45-49 years old, as seen in Table 4-6. 

The smoking prevalence rates estimated prior to 1976 in Table 4-8 for

the United Kingdom are from the Tobacco Research Council/Tobacco

Advisory Council surveys as reported by Wald and Nicolaides-Bouman

(1991). Data after that point are from the General Household Survey (ONS,

1998), which began in 1976. The smoking prevalence estimates for males

16-19 years old prior to 1976 vary substantially from year to year, and they

are too unstable to define year-to-year-to-year changes with precision. The

data for males 20-24 and 25-34 years old are more stable. 

In 1950, the birth cohort born between 1926 and 1930 would have

been 20-24 years old, and that age group had a smoking prevalence of 68

percent in 1950 (see Table 4-8). In 1975, the 1951-1955 birth cohort would

have been 20-24 years old, and that age group had a smoking prevalence of

53 percent in 1975. The decline in smoking prevalence was 22 percent in

contrast to a decline of 62 percent in lung cancer rates at ages 40-44 across

the same cohorts. 

The birth cohort born between 1926 and 1930 had a smoking prevalence of 68 percent in 1950, and 20 years later, when they would have been

ages 40-44, they had a prevalence of approximately 55 percent (as represented by the 35- to 59-year-old age group in Table 4-8). The 1951-1955

birth cohort had a prevalence of 53 percent at ages 20-24; 20 years later in

1996, their smoking prevalence would be approximately 30 percent. These

changes in prevalence rates suggest that at least 19 percent of smokers in

the 1926-1930 cohort had quit smoking by ages 40-44, whereas at least 43

percent of smokers in the 1951-1955 cohort had quit. These estimates are

conservative because any individuals who initiated smoking after age 24

would reduce the estimated rates of cessation prior to age 40 among those

smokers who initiated smoking prior to age 24. This increase in cessation

during young adulthood would be expected to add to the decline in lung

cancer risk produced by the fall in smoking prevalence at ages 20-24

because it would reduce the number of smokers with duration of smoking

sufficient to increase their lung cancer risk. 

A second characteristic of smoking behavior that differs across these

birth cohorts in the United Kingdom is age of smoking initiation, particularly initiation prior to or early in adolescence. Comparison of the smoking

prevalence rates in Table 4-8 at ages 20-24 in a given calendar year to those

Chapter 04 11/19/01 11:00 AM Page 136
of 16- to 19-year-old smokers from 4 calendar years earlier offers some

insight into the fraction of 20- to 24-year-old smokers who initiated after

age 19 and who would, therefore, have had shorter durations of smoking

by ages 40-44. Some caution needs to be exercised in interpreting these

prevalence ratios because of the previously mentioned variability in prevalence rates for the 16- to 19-year-old smokers, but it is generally true that

the fraction of 20- to 24-year-old smokers who are likely to have initiated

after age 19 increased from the early 1950s, peaked in the late 1950s at

approximately 25 percent of the smokers at ages 20-24, and then declined

to the mid 1970s. Data from the General Household Survey have more stable rates for the 16- to 19-year-old group. These data reveal a steady fall in

the ratio of 16- to 19-year-old smoking prevalence compared with the 20-

to 24-year-old prevalence 4 years later. The data in Table 4-8 suggest that as

of 1980, 14 percent of 20- to 24-year-old smokers began smoking after age

19. By 1996, approximately one-third of the 20- to 24-year-old smokers had

begun to smoke after age 19. As described above, these late-initiating smokers will add to the smoking prevalence at age 40, but they are unlikely to

contribute to an increased lung cancer risk at that age due to their short

duration of smoking. They may, however, mask the reduction in smoking

prevalence through cessation for those who have been smoking long

enough to be at increased risk of lung cancer (those who began smoking

before age 20). This masking effect might result in a greater decline in lung

cancer risk at ages 40-44 than would be expected from the decline in smoking prevalence at the same age. 

In summary, a combination of the decline in smoking prevalence and

the increase in late initiation of smoking could explain the excess decline

in lung cancer death rates observed in the United Kingdom. These considerations should be part of an examination of the dramatic decline over time

in lung cancer death rates at younger ages among males in the U.K. The

changes in lung cancer death rates in the United States appear to be consistent with changes in smoking prevalence. 

The question of whether U.S. lung cancer

death rates have declined in a way consistent

with a lowering of the lung cancer risk of smoking due to the use of lower

yield cigarettes can be also examined by modeling the lung cancer death

rate trends expected over time from the smoking behaviors of the U.S. population (see Appendix). The lung cancer risks that result from varying

smoking intensity and duration can be defined using data from the CPS-I

study. These risks can be fit to a model of lung cancer risk developed by

Doll and Peto (1978) and the best fit of the CPS-I data to this model can be

estimated. National birth cohort specific smoking behavior data can be used

to predict national lung cancer death rates by utilizing the model of lung

cancer risk derived from the CPS-I data to estimate the lung cancer rates for

current, former and never smokers. Trends in these predicted estimates can

be compared to the trends in actual observed lung cancer death rates. If the

trends in predicted and observed rates are similar, there is no need to postulate an effect produced by changing cigarette design. If the trends are discordant, a term for changes in the tar yield of the cigarette smoked over

Matching U.S. Smoking Rates to

U.S. Lung Cancer Death Rates

137

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 137
time can be added to the model to determine whether adjusting for the

changing tar yield of the cigarette improves the fit of the model. 

Population data on smoking behavior over time in the United States

provide the smoking intensity and duration estimates that allow the model

to predict the national lung cancer death rates expected from those smoking behaviors. These predicted national rates can be compared with the

actual observed U.S. mortality rates over time to evaluate whether the risks

of smoking measured during the period 1960-1972 (CPS-I) continue to predict current lung cancer death rates, overestimate lung cancer rates over

time suggesting a decline in the risk of smoking as the cigarettes smoked

had lower machine-measured yields, or underestimate lung cancer rates

over time as suggested by the comparison of the risks of smoking in CPS-I

and CPS-II. The purpose of this analysis is not to develop a model of lung

cancer risk, but rather to examine whether lung cancer risks, measured in a

population smoking higher yield cigarettes, overestimates or underestimates

current lung cancer mortality rates in a population smoking cigarettes with

much lower machine-measured tar and nicotine yields than those smoked

by the participants in CPS-I. If the risk is overestimated, it would suggest

that cigarette smoking has become less hazardous over time. If the risk is

underestimated, it suggests that smoking has not become less hazardous

over time and may have become more hazardous. 

Smoking prevalence estimates were based on the National Health

Interview Survey data from 1965 to 1994 (Burns et al., 1997a) and were

adjusted for the differential mortality that occurs in smokers compared with

never smokers. The smoking behaviors were estimated for each 5-year birth

cohort (individuals born within the same 5 calendar years) from 1910

through 1960. Lung cancer risk estimates were derived by fitting the CPS-I

data to a published model of lung cancer risk (Doll and Peto, 1978) that

relates lung cancer death rates to the intensity and duration of smoking.

The formulation of this model is lung cancer death rate = K(cigarettes/day +

6)x(duration – 3.5)y. The best-fit estimate for this equation using the CPS-I

data yields values of K = 0.00000000017196, x = 0.85, and y = 3.71. Lung

cancer death rates were calculated for each single year of age of initiation

(which, when subtracted from age, yields duration of smoking) within each

birth cohort for current smokers. The mean value for cigarettes smoked per

day for all white male smokers in the National Health Interview Survey

(16.45) was used as the term for cigarettes per day. The weighted sum of all

the rates for individual ages of initiation yields the rate for the smokers in

the cohort. 

Rates in former smokers were estimated by modeling the fractional

change in excess lung cancer death rates with duration of cessation using

the CPS-I data (Burns, 1998). The fraction of the excess lung cancer death

rate that remained with each increasing year of smoking duration was then

multiplied by the excess death rate between smokers of that duration and

nonsmokers of the same age. The fraction of the population who quit

smoking in each year was estimated from the National Health Interview

Survey data, and it was assumed that the distribution of smoking duration

for those who quit was the same as that for current smokers in that year.

138

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 138
This generated individual cells of fractions of each cohort that had duration

of smoking and duration of cessation specified by single years. Lung cancer

death rates were calculated for each of these cells by subtracting the risk in

never smokers from that of continuing smokers of the same age of initiation, multiplying the result by the fraction of excess mortality remaining at

the appropriate duration of cessation, and adding back the rate in never

smokers. The prevalence-weighted sum of all of these cells is the lung cancer death rate in former smokers for that birth cohort in that calendar year.

Lung cancer death rates for never smokers were those estimated from CPS-I

data (Burns et al., 1997b). 

Lung cancer death rates for each cohort in each calendar year were generated by summing the rates for current smokers, former smokers, and

never smokers, weighted by their respective prevalence in that year. Figure

4-17 presents an example of these estimates for the cohort born between

1910 and 1914. Rates are presented by calendar year; but because the rates

are for a population born during a fixed set of years, the calendar year axis

also reflects increasing age of the birth cohort. This explains the increasing

never smoker lung cancer death rates with calendar year in the figure, when

age-specific lung cancer death rates in never smokers have not changed

over time (Thun and Heath, 1997; Thun et al., 1997a). 

Actual observed lung cancer mortality rates by birth cohort were

obtained from the U.S. mortality data and are those presented by Mannino

and colleagues (2001). The birth cohorts for smoking and lung cancer are 1-

year discordant, but it is unlikely that this difference contributes substantively to the results. Lung cancer death rates estimated from smoking

behaviors and CPS-I risk data were scaled to the actual U.S. mortality rates

to derive a single exponential scaling factor for all of the cohorts. The value

for this scaling factor was 1.25. Differences between the predicted and actual lung cancer death rates were examined across calendar years for each

birth cohort. A term proportional to the sales-weighted tar yield of U.S. cigarettes for each calendar year was applied to the predicted rates as c times

the tar value, and the optimum value for c was calculated. The resultant taradjusted rates were tested to determine whether the addition of the term

for tar to the predicted rates improved the goodness of fit of the predicted

data to the observed U.S. lung cancer mortality rates by cohort. These three

sets of rates (U.S. mortality, CPS-I predicted, and tar-adjusted CPS-I predicted) are presented in Figures 4-18a to 4-18i, with one graph for each 5-year

birth cohort. 

The fit of the CPS-I predicted rates was improved by the addition of the

tar term, but the improved fit was in the direction of declining tar values

increasing the risk. There was excellent agreement between the CPS-I predicted rates and the real U.S. lung cancer death rates in each cohort until

the late 1970s. However, beginning in 1979 and in later years, there was a

progressive underestimation of U.S. lung cancer mortality when the dose

and duration risk relationships from CPS-I and U.S. smoking prevalences by

birth cohort were used to estimate lung cancer death rates. In order to

account for the difference in timing between transformation of a cell into a

cancer and death from the growth of that cancer, the analysis was repeated

139

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 139
with the tar values lagged by 4 years, and the results were not substantively

nor significantly different. These analyses suggest that, if anything, there

has been an increase rather than a decrease in the carcinogenicity of smoking over the last several decades in the United States. 

In order to address the question of changes in age-specific lung cancer

death rates at younger ages, the difference was examined between the

observed lung cancer death rates and the death rates predicted using the

CPS-I risk data (without a term for tar) at fixed ages across multiple birth

cohorts. If the most recent birth cohorts have lung cancer death rates that

are declining more rapidly than would be predicted from differences in

their smoking prevalence (i.e., an effect suggesting a reduction in risk of

smoking with lower yield cigarettes), then the difference between actual

and predicted lung cancer death rates at fixed ages should have a slope

when plotted across sequential cohorts. When sequential birth cohorts are

examined in this manner for age-specific lung cancer death rates at ages

under 50, there is no discernible slope for cohorts born after 1930, and the

slope for older cohorts and for older ages is in the direction of increasing

risk with the younger cohorts. Therefore, even when the model is examined

in an age-specific format and confined to younger ages, there is no evidence to suggest that there is a decline in risk for smokers who would have

had higher proportions of their smoking experience using filtered or lowyield cigarettes. 

140

Smoking and Tobacco Control Monograph No. 13

0

50

100

150

200

250

Never Smoker

Current Smoker

Former Smoker

1960 1965 1970 1975 1980 1985

Year

Death Rate per 100,000

Figure 4-17

Contribution to White Male Lung Cancer Rates by Smoking Status: Birth Cohort

1910-1914

Note: Prevalence rates of cigarette smoking, initiation, and cessation by year for U.S. White males were obtained from NCI Smoking

and Tobacco Control Monograph No. 8 (Burns et al., 1997a). U.S. population estimates stratified by age, sex, and race were

obtained from CDC and U.S. Bureau of the Census web sites (CDC, 2000c; USBC, 2000). U.S. lung cancer mortality of White males

were provided by D.M. Mannino (personal communication). These risk data were stratified by 5-year birth cohorts for each calendar

year, 1960-1994. The 5-year birth cohorts began with 1901-1905 and ended with 1961-1965. See Appendix for details.

Chapter 04 11/19/01 11:00 AM Page 140
141

Chapter 4

0

100

200

300

400

500

600

ACS/NHIS Data Scaled Exponentially

includes Tar

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

1960 1965 1970 1975 1980 1985 1990

Year

Death Rate per 100,000

0

100

200

300

400

500

600

ACS/NHIS Data Scaled Exponentially

includes Tar

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

1960 1965 1970 1975 1980 1985 1990

Year

Death Rate per 100,000

Projected

Figure 4-18a

Lung Cancer Death Rates: White Males, Birth Cohort 1910-1914

Figure 4-18b

Lung Cancer Death Rates: White Males, Birth Cohort 1915-1919

Chapter 04 11/19/01 11:00 AM Page 141
142

Smoking and Tobacco Control Monograph No. 13

0

100

200

300

400

500

600

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar 

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Year

Death Rate per 100,000

Projected

Figure 4-18c

Lung Cancer Death Rates: White Males, Birth Cohort 1920-1924

Figure 4-18d

Lung Cancer Death Rates: White Males, Birth Cohort 1925-1929

Year

Death Rate per 100,000

0

50

100

150

200

250

300

350

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar 

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Projected

Chapter 04 11/19/01 11:00 AM Page 142
143

Chapter 4

0

50

100

150

200

250

300

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Year

Death Rate per 100,000

Projected

Figure 4-18e

Lung Cancer Death Rates: White Males, Birth Cohort 1930-1934

Figure 4-18f

Lung Cancer Death Rates: White Males, Birth Cohort 1935-1939

0

20

40

60

80

100

120

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar 

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Year

Death Rate per 100,000

Projected

Chapter 04 11/19/01 11:00 AM Page 143
144

Smoking and Tobacco Control Monograph No. 13

Figure 4-18g

Lung Cancer Death Rates: White Males, Birth Cohort 1940-1944

0

10

20

30

40

50

60

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar 

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Year

Death Rate per 100,000

Projected

Figure 4-18h

Lung Cancer Death Rates: White Males, Birth Cohort 1945-1949

0

5

10

15

20

25

30

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Year

Death Rate per 100,000

Projected

Chapter 04 11/19/01 11:00 AM Page 144
145

Chapter 4

In these analyses, tar is a surrogate for the overall changes in cigarette

design and manufacture over the last five decades, rather than a specific

measure of the actual tar intake by the smoker. This analytical approach is

an attempt to answer the question of whether the sum total of the changes

occurring in cigarette design and composition over the last 45 years produced a reduction in carcinogenicity of smoking, and there appears to be

little evidence for a population effect in the direction of a reduced risk.

Moreover, this analysis supports the comparison of the two American

Cancer Society prospective mortality studies (CPS-I and CPS-II) in suggesting that cigarette smoking may have become more, rather than less, hazardous, based on the cumulative effects of all the changes in cigarette

design and manufacture that have occurred over the last half century.

SUMMARY

The three lines of evidence on lung cancer risk in relation to changes in

cigarette design provide somewhat inconsistent findings, perhaps reflecting

methodological limitations and the limited number of studies available.

Detailed examination of lung cancer rates by age in the United States and

the United Kingdom provide seemingly conflicting patterns from the two

countries. Lesser risks for more recent cigarettes are one potential explanation for the rapid decline of lung cancer mortality at younger ages in the

United Kingdom over recent years. However, the temporal pattern of lung

cancer mortality at younger ages in the United States is not consistent with

Figure 4-18i

Lung Cancer Death Rates: White Males, Birth Cohort 1950-1954

2.5

5.0

7.5

10.0

12.5

15.0

1960 1965 1970 1975 1980 1985 1990

ACS/NHIS Data Scaled Exponentially

includes Tar 

ACS/NHIS Data Scaled Exponentially

US Lung Cancer Mortality

Year

Death Rate per 100,000

Projected

0

Note for Figures 18a-18i: Estimated lung cancer death rates were obtained by using a model developed by Peto (Doll and Peto,

1978). U.S. lung cancer death rates were provided for the years 1960-1995 by D.M. Mannino (personal communication, 2000). See

Appendix for further details.

Chapter 04 11/19/01 11:00 AM Page 145
this explanation. The temporally cross-sectional findings from several casecontrol and cohort studies provide some evidence of reduced risk for smokers of lower yield products at time points across the 1960s through the

1980s. These studies, however, provide only relative comparisons of risk

and data analysis methods raise concern about biased findings in some.

Finally, both the British Physician’s Study and the CPS I and II studies provide powerful evidence that both relative and absolute risks of lung cancer

in smokers have risen from the 1950s through the 1980s. The different

findings across these three lines of epidemiological evidence cannot be reconciled with available information. Overall, however, they do not provide

evidence that public health has benefited from changes in cigarette design

and manufacture over the last fifty years.

CONCLUSIONS

1. Changes in cigarette design and manufacturing over the last fifty

years have substantially lowered the sales-weighted, machine-measured tar

and nicotine yields of cigarettes smoked in the United States.

2. Cigarettes with low machine-measured yields by the FTC method are

designed to allow compensatory smoking behaviors that enable a smoker to

derive a wide range of tar and nicotine yields from the same brand, offsetting much of the theoretical benefit of a reduced-yield cigarette.

3. Existing disease risk data do not support making a recommendation

that smokers switch cigarette brands. The recommendation that individuals

who cannot stop smoking should switch to low yield cigarettes can cause

harm if it misleads smokers to postpone serious efforts at cessation.

4. Widespread adoption of lower yield cigarettes by smokers in the

United States has not prevented the sustained increase in lung cancer

among older smokers.

5. Epidemiological studies have not consistently found lesser risk of diseases, other than lung cancer, among smokers of reduced yield cigarettes.

Some studies have found lesser risks of lung cancer among smokers of

reduced yield cigarettes. Some or all of this reduction in lung cancer risk

may reflect differing characteristics of smokers of reduced-yield compared

to higher-yield cigarettes.

6. There is no convincing evidence that changes in cigarette design

between 1950 and the mid 1980s have resulted in an important decrease in

the disease burden caused by cigarette use either for smokers as a group or

for the whole population. 

146

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 146
Appendix

Description of Cancer Prevention Study-I Data

and Methods of Analysis

The first Cancer Prevention Study (CPS-I) was a major cohort study carried out by the American Cancer Society (ACS). Over one million individuals were followed for more than 12 years, from 1959 to 1972. The protocol

included a baseline survey that covered smoking history and present use, as

well as information about health history and behaviors. The major outcome

variable was mortality by specific cause as indicated on the death certificate.

CPS-I provided strong evidence that confirmed relationships between smoking and specific diseases, including lung cancer and coronary heart disease. 

DESCRIPTION OF THE DATA The focus of this analysis is the White male subset

of cigarette smokers. The baseline data were gathered in 1959 and included

174,997 White male current cigarette smokers who were not using other

forms of smoked or oral tobacco. These are the subjects for the present

analysis. Major follow-ups were conducted in 1961, 1963, 1965, and 1972

that included questions about the brand of cigarette smoked and number of

cigarettes smoked per day. This provided enough information to be able to

consider the changing smoking habits during the 12-year period as well as

relationships to disease outcomes. 

TAR AND NICOTINE LEVEL The database available from ACS did not retain the

specific brand smoked from the baseline survey, but it has the brands recoded into categories of tar and nicotine level crossed by filter/nonfilter.

This simplification of the data can be understood by recalling that this was

the era of data entry and analysis using punched cards. For the present

study, this means that the baseline tar and nicotine levels for individuals

are not known explicitly beyond a category of combined tar and nicotine

levels. The subsequent follow-up efforts did retain the specific brand

smoked by the individual, though the particular subspecies of the brand

was not retained, such as king size or regular, low tar versus full flavor, etc. 

The tar and nicotine levels for specific brands were determined in 1959

in laboratory studies commissioned and published by the Reader’s Digest

(Miller and Monahan, 1959). These values were used by the ACS for the

baseline categorizations. Subsequently, brand-specific tar and nicotine

assessments were carried out by the Federal Trade Commission (FTC) in

1967, 1970, and 1974 (FTC, 1967, 1970, 1974). Because these years do not

correspond to the years of the CPS-I follow-up surveys, linear interpolation

was used within brands to estimate tar and nicotine levels for the years of

the follow-up. When multiple subspecies were tested by the FTC within

brands, market share information from the Maxwell Report (Maxwell, 1994)

was used to develop a market-share-weighted tar and nicotine value for

each brand for each survey year. These values allowed a specific tar and

nicotine estimate to be attached to each smoker at each follow-up period

for which he provided a brand. When an individual showed a consistent

147

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 147
148

pattern of smoking the same brand and when the tar and nicotine level for

that brand was consistent with the category assigned to that individual at

baseline, it was assumed that he smoked that brand at baseline and the category values were adjusted to the explicit tar and nicotine values for that

brand. 

CIGARETTES PER DAY At baseline as well as for the follow-up surveys, smokers

were asked how many cigarettes were smoked each day. Responses were categorized into levels 1-9, 10-19, 20, 21-39, 40, 40+ for all except the final follow-up, where the specific number of cigarettes smoked per day was recorded. For most analyses, the final follow-up was also converted to the categorical levels with 40 and 40+ combined. When an explicit value for a category

was needed for graphing or regression, the weighted mean value for the category was used, based on the distribution of observed cigarettes per day values at the time of the final follow-up. These means were: 4.48, 11.97, 20,

29.15, and 43.52, respectively. 

The cross-sectional follow-up surveys provided

estimates of tar and nicotine level and cigarettes

per day for each smoker. By comparing responses

at subsequent surveys, changes over time in the balance of tar and nicotine

and cigarettes per day can be assessed. The baseline and four follow-up surveys provided four sequential measures of change for each subject who

completed the five cross-sectional surveys. The cross-sectional combination

of variables and changes between adjacent surveys allowed analysis of temporal changes in the interrelationships of these variables. 

SAS and Pascal programs were used to assemble simplified

data sets for analysis. For a given subject, the four periods

of follow-up were assembled with the tar and nicotine levels for the beginning of the follow-up period and the reported cigarettes per day level at

that time. Additional criteria were sometimes used to isolate individuals

who: changed brands, did not change brands, never reported an attempt to

quit, changed to a cigarette with a lower tar value, etc. For each individual,

possible endpoints included death with date and international code for

cause of death (WHO, 1957), lost to follow-up, or censored at end of study. 

Several kinds of regression analyses were undertaken. These included survival analysis, regression analysis of log of death rates on tabular data, and regression analysis of interrelationships between factors. 

Survival Analysis Survival analysis was undertaken using the SAS lifereg procedure,

using a database of individual subjects with the combinations of factors

present at the beginning of the interval and an observed time period of follow-up with factors assumed at that level. Generally, the dependent variable

for these analyses was the likelihood of death by a specific cause, such as

lung cancer. The independent variables included combinations of tar level

(continuous or stratified to 3-5 levels), cigarettes per day (continuous or

stratified), age (continuous), and duration of smoking (continuous). 

METHODS OF

ANALYSIS

ASSEMBLING DATA

SET FOR ANALYSIS

CHANGES IN TAR AND NICOTINE AND CIGARETTES PER

DAY ACROSS YEARS OF STUDY

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 148
Alternatively, in some instances the observations were assembled into cells of observations stratified by 5-year age groups,

5-year duration groups, cigarettes per day level, and tar level (3-5 levels),

with observed death rates calculated for each cell. Typically, these cell-wise

analyses were carried out in S-Plus2000, as a glm (generalized linear model)

regression analysis of the log of the death rates or excess mortality rates

(compared to never smokers), and regressed on the explanatory variables. 

Several analyses were also undertaken to examine the

interrelationships between factors, such as the relationship between nicotine level and cigarettes smoked per day. In these analyses, the data points representing combinations reported by individuals at

various points in the follow-up were analyzed. These analyses included

examination of distributions of factors occurring together, and examination

of relationships between changes in one factor as related to changes in

another. For these analyses, the database assembled was similar to that

reported for survival analyses, but sometimes also included changes in factors between consecutive follow-up surveys. Generally, these regression

analyses were undertaken in SAS using the GLM procedure. 

This figure shows the estimated population-based lung cancer death rates for the specific birth cohort by smoking status (current, former, or never smokers). Ever and current smoking prevalence among 5-year birth cohorts of U.S. White males were obtained from

Chapter 2 of the National Cancer Institute’s (NCI) Monograph 8 (Burns et

al., 1997a). Former smoking prevalence in a given year was obtained by

subtracting the current smoking from the ever smoking prevalence in the

same year. The prevalence of never smokers in a given year was obtained by

subtracting the prevalence of ever smokers from 100 percent, where 100

percent represents the entire population. 

To determine the contribution of current and former smokers to the

overall lung cancer death rate, the prevalence rates and risks of death from

lung cancer were linked over time, accounting for changes in initiation and

cessation rates of white males by specific 5-year birth cohorts. 

The age-of-initiation profile for each birth cohort was estimated

using the change in prevalence of ever smoking by year under

age 30. The rate of initiation in a given year was estimated by taking the

difference between the ever smoking prevalence for a given year and that

for the previous year. This generated a distribution of age of initiation by

age/calendar year for those in the cohort who started smoking under the

age of 30. The percentage of the population who are current smokers of

given durations for each calendar year of a birth cohort was obtained by

proportioning the current smokers to the age-of-initiation profile. 

Data on lung cancer death rates among smokers of different durations

along with numbers of cigarettes smoked per day were used to estimate the

parameters for a model of lung cancer risk in relation to smoking behaviors

(Doll and Peto, 1978). These fitting parameters were applied to the data on

birth-cohort-specific smoking prevalence by duration to obtain estimates of

lung cancer death rates for current smokers. An average number of 16.45

Current Smokers’

Contributions

DETAILED NOTES TO

FIGURE 4-17

Regression Analysis of

Combinations of Factors

Regression Analysis

of Tabular Data

149

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 149
150

cigarettes smoked per day was used in this calculation based on the average

number of cigarettes per day reported in the National Health Interview

Surveys (NHIS). These surveys were conducted between 1965 and 1999 and

controlled for age and race. This model required estimation of three parameters. The maximum likelihood procedure was applied to lung cancer

deaths of White male cigarette smokers using data from the ACS CPS-I to

estimate the necessary parameters (a = 0.85285 the exponent on the cigarettes/day term; b = 3.70895 the exponent on the duration term; and c =

1.7196x10-10, a constant). 

The current smokers’ contribution to the national lung cancer death

rate for each calendar year equals the sum of the predicted lung cancer

death rates for smokers of each given duration divided by the white male

population for that year, and it is expressed per 100,000. 

The incidence of smoking cessation in each cohort for each calendar year was estimated by subtracting the prevalence of former

smokers in a given year from the prevalence of former smokers in the previous year. The fraction of the population that quit in a given year is distributed into discrete durations of smoking using the distribution of age of initiation for that cohort and the year of the estimate. 

Modeled estimates were generated for given durations of smoking as

described for current smokers. However, for former smokers, the estimated

lung cancer death rates were reduced using length of time since quitting.

The fractions of excess lung cancer risk (risk in smokers minus the risk in

nonsmokers) that remained after increasing durations of cessation were estimated using data from the ACS CPS-I study (Shanks, 1999). 

To determine the contribution of former smokers to the national White

male lung cancer rate for each birth cohort by calendar year, the predicted

death rates for each duration of smoking at each duration of cessation for

each calendar year were summed and divided by that year’s corresponding

White male population for the birth cohort. The result was expressed per

100,000. 

The observed lung cancer death rates for White male never smokers by 5-year age groups were obtained from NCI Monograph 8,

page 303 (see Burns et al., 1997b), using data from CPS-I. Using the midpoint of each 5-year age group, the observed death rates were modeled

using linear regression of log rates weighted to person-years of observation

to obtain the death rates for each age in 1-year increments (from ages 25 to

88), using S-Plus software (S-Plus 2000, June 1999). 

To determine the contribution of never smokers to the national White

male lung cancer rate for each birth cohort by calendar year, the predicted

death rates were calculated as the product of the prevalence of never smokers in the year, the death rate of never smokers for that cohort in that year

using the median age of the birth cohort at each calendar year, and the corresponding White male population for the birth cohort. The result was

expressed per 100,000. Nine sequential birth cohorts were evaluated, the

first being 1910-1914 and the last being 1950-1954. 

Never Smokers’

Contributions

Former Smokers’

Contributions

Smoking and Tobacco Control Monograph No. 13

Chapter 04 11/19/01 11:00 AM Page 150
The estimated lung cancer death rates by smoking status

(current, former, and never smokers) for individual birth

cohorts of the U.S. White male population were summed to obtain the total

death rates for each birth cohort by year. Total lung cancer death rates were

then scaled to the actual national death rates for each birth cohort and year

strata using a single exponential scaling factor. 

To investigate the effects of tar on lung cancer death rates, a term for

sales-weighted tar was added. Fit of the modeled lung cancer rate data to

actual lung cancer death rates was examined before and after adding tar.

The model was further enhanced by including an additional term for the

mean cigarettes smoked per day for each calendar year. The GLM procedure

in SAS/STAT was used to obtain mean cigarettes per day by year while controlling for age and race. Data sources for the means were the NHIS for the

years 1965-1995. The mean cigarette per day rates for the years 1960-1964

were assumed to equal that of the NHIS for 1965. 

To compare these estimates to the actual lung cancer death rates, the

estimates were scaled exponentially and graphed against the actual national

lung cancer mortality. Sales-weighted average tar deliveries of U.S. cigarettes

for the years 1954-1994 were provided by The American Health Foundation

(Hoffmann, 1997). The modeling procedures were performed using S-Plus

2000 software (S-Plus 2000, June 1999). 

DETAILED NOTES TO

FIGURES 4-18a TO 4-18i

151

Chapter 4

Chapter 04 11/19/01 11:00 AM Page 151
152

Smoking and Tobacco Control Monograph No. 13

Agudo, A., Barnadas, A., Pallares, C., Martinez, I.,

Fabregat, X., Rosello, J., Estape, J., Planas, J.,

Gonzalez, CA. Lung cancer and cigarette smoking in women: a case-control study in Barcelona

(Spain). International Journal of Cancer 59:165-

169, 1994.

Alderson, M.R., Lee, P. N., Wang, R. Risks of lung

cancer, chronic bronchitis, ischaemic heart disease, and stroke in relation to type of cigarette

smoked. Journal of Epidemiology & Community

Health 39:286-293, 1985.

Armadans-Gil, L. Vaque-Rafart, J., Rossello, J., Olona,

M., Alseda, M. Cigarette smoking and male lung

cancer risk with special regard to type of tobacco. International Journal of Epidemiology 28:614-

619, 1999.

Armitage, P., Doll, R. Stochastic models for carcinogenesis. Proceedings of the Fourth Berkeley

Symposium on Mathematical Statistics and

Probability, Vol. 4. Berkeley, CA: University of

California Press, 1961.

Auerbach, O., Hammond, E.C., Garfinkel, L.

Changes in bronchial epithelium in relation to

cigarette smoking, 1955–1960 vs. 1970–1977.

New England Journal of Medicine 300:381-385,

1979.

Augustine, A. Harris R.E., Wynder E.L.

Compensation as a risk factor for lung cancer in

smokers who switch from nonfilter to filter cigarettes. American Journal of Public Health 79:188-

191, 1989a.

Augustine, A. Harris R.E., Wynder E.L.

Compensation as a risk factor for lung cancer in

smokers who switch from nonfilter to filter cigarettes. Progress in Clinical and Biological Research

293:221-230, 1989b.

Benhamou, E., Benhamou, S. Black (air-cured) and

blond (flue-cured) tobacco and cancer risk. VI:

Lung cancer. European Journal of Cancer

29A(12):1778-1780, 1993.

Benhamou, E., Benhamou, S., Auquier, A., Flamant,

R. Changes in patterns of cigarette smoking and

lung cancer risk: Results of a case-control study.

British Journal of Cancer 60:601-604, 1989.

Benhamou, E., Benhamou, S., Flamant, R. Lung cancer and women: Results of a French case-control

study. British Journal of Cancer 55:91-95, 1987.

Benhamou, S., Benhamou, E., Auquier, A., Flamant,

R. Differential effects of tar content, type of

tobacco and use of a filter on lung cancer risk in

male cigarette smokers. International Journal of

Epidemiology 23:437-443, 1994.

Benhamou, S., Benhamou, E., Tirmarche, M.,

Flamant, R. Lung cancer and use of cigarettes: A

French case–control study. Journal of the National

Cancer Institute 74:1169-1175, 1985.

Benowitz, N.L. Biomarkers of cigarette smoking. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.7.

U.S. Department of Health and Human Services,

National Institutes of Health, National Cancer

Institute, NIH Publication No. 96-4028, 1996.

Benowitz, N.L., Hall, S.M., Herning, R.I., Jacob, P.,

Jones, R.T., Osman, A. Smokers of low-yield cigarettes do not consume less nicotine. New England

Journal of Medicine 309:139-42, 1983.

Benowitz, N.L., Henningfield, J.E. Establishing a

nicotine threshold for addiction. New England

Journal of Medicine 331:123-125, 1994.

Borland, C., Chamberlain, A., Higenbottam, T.,

Shipley, M., Rose, G. Carbon monoxide yield of

cigarettes and its relation to cardiorespiratory

disease. British Medical Journal 287:1583-1586,

1983.

British American Tobacco Company. Structured creativity group. Thoughts by C.C. Greig – R&D,

Southampton, Marketing scenario. Florida AG

tobacco litigation, undated. Bates No.

100515909.

Bross, I.D., Gibson, R. Risks of lung cancer in smokers who switch to filter cigarettes. American

Journal of Public Health and the Nations Health

58(8):1396-1403, 1968.

Bross, I.D. Effect of filter cigarettes on lung cancer

risk. Toward a Less Harmful Cigarette. NCI

Monograph No. 28. Wynder, E.L., Hoffmann, D.

(Editors.). U.S. Department. of Health,

Education, and Welfare, National Institutes of

Health, National Cancer Institute, 1968.

Brown, C., Kessler, L. Projections of lung cancer mortality in the United States: 1985–2025. Journal of

the National Cancer Institute 80:43-51, 1988.

Brown, C.A., Crombie, I.K., Smith, W.C., TunstallPedoe, H. Cigarette tar content and symptoms of

chronic bronchitis: Results of the Scottish Heart

Health Study. Journal of Epidemiology and

Community Health 45:287-290, 1991.

Buffler, P.A., Contant, C.F., Pickle, L.W., Burau, K.,

Cooper, S.P., Mason, T.J. Environmental associations with lung cancer in Texas coastal counties.

Lung Cancer: Current Status and Prospects for the

Future. Twenty-eighth Annual Clinical Conference

on Cancer. Mountain, C.F., Carr, D.T. (Editors.).

Houston, Texas, USA, November 7–10, 1984.

Austin, TX: University of Texas Press, 1986.

Burns, D. Primary prevention, smoking, smoking cessation—Implications for future trends in lung cancer

prevention. Proceedings of the International

Conference on Prevention and Early Diagnosis of

Lung Cancer. Varese – Ville Ponti, December 9-

10, 1998. Dominioni, L., Strauss, G. (Editors.),

1998.

REFERENCES

Chapter 04 11/19/01 11:00 AM Page 152
153

Chapter 4

Burns, D., Lee, L., Shen, Z., Gilpin, B., Tolley, D.,

Vaughn, J., Shanks, T. Cigarette smoking behavior in the United States. Changes in CigaretteRelated Disease Risks and Their Implication for

Prevention and Control. Smoking and Tobacco

Control Monograph No. 8. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 97-4213, 1997a.

Burns D., Shanks, T., Choi, W., Thun, M., Heath, C.,

Garfinkel L. The American Cancer Society

Cancer Prevention Study I: 12-year follow-up of

1 million men and women. Changes in CigaretteRelated Disease Risks and Their Implication for

Prevention and Control. Smoking and Tobacco

Control Monograph No. 8. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 97-4213, 1997b.

Centers for Disease Control and Prevention.

Cigarette smoking among adults—United States,

1998. Morbidity and Mortality Weekly Report

49(39):881-884, 2000a.

Centers for Disease Control and Prevention. Ahern,

C.H., Batchelor, S.M., Blanton, C.J., Law, M.,

Loo, C.M., Pevzner, E.S., Ryan, H.A., Stolfus, S.A.,

Tabladillo, M., Warren, C.W., Zinner, L.R.,

Eriksen, M.P., Healton, C.G., Messeri, P.A.,

Reynolds, J.H., Stokes, C., Ross, J.G., Flint, K.,

Robb, W.H. Youth tobacco surveillance—United

States, 1998–1999. Morbidity and Mortality Weekly

Report 49(SS10):1-93, 2000b.

Centers for Disease Control and Prevention. U.S.

Population Estimates by Age, Sex, Race. Centers for

Disease Control and Prevention, 2000. Available

from www.cdc.gov/nchs/datawh/statab/unpubd/

mortabs/pop6079.html.

Cohen, J. B. Consumer/smoker perceptions of

Federal Trade Commission tar ratings. The FTC

Cigarette Test Method for Determining Tar, Nicotine,

and Carbon Monoxide Yields of U.S. Cigarettes.

Report of the NCI Expert Committee. Smoking and

Tobacco Control Monograph No. 7. U.S.

Department of Health and Human Services,

National Institutes of Health, National Cancer

Institute, NIH Publication No. 96-4028, 1996a.

Cohen, J. B. Smokers’ knowledge and understanding

of advertised tar numbers: Health policy implications. American Journal of Public Health 86:18-24,

1996b.

Committee on Health Risks of Exposure to Radon

(BEIR VI). Health Effects of Exposure to Radon:

BEIR VI. National Research Council. Washington,

DC: National Academy Press, 1999.

Dean, G., Lee, P.N., Todd, G.F., Wicken, A.J., Sparks,

D.N. Factors related to respiratory and cardiovascular symptoms in the United Kingdom. Journal

of Epidemiology and Community Health 32:86-96,

1978.

De Stefani, E. Mate drinking and risk of lung cancer

in males: A case-control study from Uruguay.

Cancer Epidemiology, Biomarkers and Prevention

5:515-519, 1996.

Doll, R., Hill, A.B. A study of the aetiology of carcinoma of the lung. British Medical Journal 2:1271-

1286, 1952.

Doll, R., Hill, A.B. The Mortality of doctors in relation to their smoking habits: A preliminary

report. British Medical Journal 1(4877):1451-1455

(June 26), 1954.

Doll, R., Peto, R. Cigarette smoking and bronchial

carcinoma: dose and time relationships among

regular smokers and lifelong non-smokers.

Journal of Epidemiology and Community Health

32:303-313, 1978.

Doll, R., Peto, R., Wheatley, K., Gray, R., Sutherland,

I. Mortality in relation to smoking: 40 years’

observations on male British doctors. British

Medical Journal 309:901-911, 1994.

Engeland, A., Haldorsen, T., Andersen, A., Tretli, S.

The impact of smoking habits on lung cancer

risk: 28 years’ observation of 26,000 Norwegian

men and women. Cancer Causes and Control

7:366-376, 1996.

Federal Trade Commission. Report of Tar and Nicotine

Content of the Smoke of 59 Varieties of Cigarettes.

Federal Trade Commission, Washington, D.C.,

1967. 

Federal Trade Commission. Report of Tar and Nicotine

Content of the Smoke of 126 Varieties of Cigarettes

[for year 1968]. Federal Trade Commission,

Washington, D.C., 1969.

Federal Trade Commission. Report of Tar and Nicotine

Content of the Smoke of 118 Varieties of Cigarettes.

Federal Trade Commission, Washington, D.C.,

1969.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 120 Varieties of

Cigarettes. Federal Trade Commission,

Washington, D.C., 1970.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 130 Varieties of

Cigarettes. Federal Trade Commission,

Washington, D.C., 1974.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 145 Varieties of

Cigarettes [for year 1975]. Federal Trade

Commission, Washington, D.C., 1976.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 166 Varieties of

Cigarettes [for year 1976]. Federal Trade

Commission, Washington, D.C., 1977.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 167 Varieties of

Cigarettes [for year 1977]. Federal Trade

Commission, Washington, D.C., 1978.

Chapter 04 11/19/01 11:00 AM Page 153
154

Smoking and Tobacco Control Monograph No. 13

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 187 Varieties

of Cigarettes [for year 1979]. Federal Trade

Commission, Washington, D.C., 1981.

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 200 Varieties

of Cigarettes [for year 1981]. Federal Trade

Commission, Washington, D.C., 1981.

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 207 Varieties

of Domestic Cigarettes [for year 1982]. Federal

Trade Commission, Washington, D.C., 1984.

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 207 Varieties

of Domestic Cigarettes [for year 1984]. Federal

Trade Commission, Washington, D.C., 1985.

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 370 varieties

of domestic cigarettes [for year 1988]. Federal Trade

Commission, Washington, D.C., 1990.

Federal Trade Commission. Report on Tar, Nicotine,

and Carbon Monoxide Content of the Smoke of 534

Varieties of Domestic Cigarettes [for year 1990].

Federal Trade Commission, Washington D.C.,

1992.

Federal Trade Commission. Report on Tar, Nicotine,

and Carbon Monoxide Content of the Smoke of 1262

Varieties of Domestic Cigarettes [for year 1996].

Federal Trade Commission, Washington D.C.,

1999.

Garfinkel, L. Changes in the cigarette consumption

of smokers in relation to changes in tar/nicotine

content of cigarettes smoked. American Journal of

Public Health 69:1274-1276, 1979.

Garfinkel, L. Changes in number of cigarettes

smoked compared to changes in tar and nicotine

content over a 13-year period. A Safe Cigarette?

Banbury Report 3, Proceedings of a Meeting Held at

the Banbury Center, Cold Spring Harbor Laboratory,

NY, Oct. 14–16, 1979. Gori, G.B., Bock, F.G.

(Editors.). Cold Spring Harbor, NY: Cold Spring

Harbor Laboratory, 1980.

Gillis C.R., Hole, D.J., Boyle, P. Cigarette smoking

and male lung cancer in an area of very high

incidence. I: Report of a case-control study in the

West of Scotland. Journal of Epidemiology and

Community Health 42:38-43, 1988.

Giovino, G.A., Tomar, S.L., Reddy, M.N., Peddicord,

J.P., Zhu, B.P., Escobedo, L.G., Eriksen, M.P.

Attitudes, knowledge, and beliefs about low-yield

cigarettes among adolescents and adults. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.

7. U.S. Department of Health and Human

Services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 96-4028,

1996.

Goodman, B. to Meyer, L.F. September 17, 1975.

Memo by Barboro Goodman. Marlboro-Marlboro

Lights study delivery data. Bates No.

2021544486.

Goodman, B. to Meyer, L.F. October 21, 1982. Memo

by Barboro Goodman. Effect of reduced dilution

on tar delivery to a smoker. Phillip Morris

Archive Document I.D. No. 1003415278/5280. 

Green, S.J. Research conference held at Hilton Head

Island S.C., September 24-30, 1968. University of

California San Francisco Tobacco Archive

Document I.D. 1112.01, 1968. 

Haddock, CK; Talcott, GW; Klesges, RC; Lando, H.

An examination of cigarette brand switching to

reduce health risks. Annals of Behavioral Medicine

21:128-134, 1999.

Hammond, E.C., Horn, D. Smoking and Death

Rates—A report on 44 months of follow-up of

187,783 men. II. Death rates by cause. Journal of

the American Medical Association 166:1294-1308,

1958.

Hammond, E.C., Garfinkel, L. Changes in cigarette

smoking. Journal of the National Cancer Institute

32:49, 1964.

Hammond, E.C. Smoking in relation to the death

rates of one million men and women. National

Cancer Institute Monograph 19:127-204, 1966.

Hammond, E.C. The long term benefits of reducing

tar and nicotine in cigarettes. A Safe Cigarette?

Banbury Report 3, Proceedings of a Meeting Held at

the Banbury Center, Cold Spring Harbor Laboratory,

NY, Oct. 14–16, 1979. Gori, G.B., Bock, F.G.

(Editors.). Cold Spring Harbor, NY: Cold Spring

Harbor Laboratory, 1980.

Hammond, E.C., Garfinkel L., Seidman, H., Lew, E.A.

Some recent findings concerning cigarette smoking. Origins of Human Cancer. Book A: Incidence of

Cancer in Humans. Cold Springs Harbor

Conferences on Cell Proliferation, Volume 4.

1977.

Hammond, E.C., Garfinkel, L., Seideman, H., Lew,

E.A. “Tar” and nicotine content of cigarette

smoke in relation to death rates. Environmental

Research 12:263-274, 1976.

Harris, J. Cigarette smoking among successive birth

cohorts of men and women in the United States

during 1900–1980. Journal of the National Cancer

Institute 71:473-479, 1983.

Hawthorne, V.M., Fry, J.S. Smoking and health: The

association between smoking behavior, total

mortality, and cardiorespiratory disease in West

Central Scotland. Journal of Epidemiology and

Community Health 32:260-266, 1978.

Hecht, S.S. Biochemistry, biology, and carcinogenicity of tobacco-specific N-nitrosamines. Chemical

Research in Toxicology 11:559-603, 1998.

Chapter 04 11/19/01 11:00 AM Page 154
155

Chapter 4

Higenbottam, T., Shipley, M.J., Rose, G. Cigarettes,

lung cancer, and coronary heart disease: The

effects of inhalation and tar yield. Journal of

Epidemiology and Community Health 36:113-117,

1982.

Hoffmann, D., Hoffmann, I. The changing cigarette,

1950–1995. Journal of Toxicology and

Environmental Health 50:307-364, 1997.

Holmes, J.C., Hardcastle, J.E., Mitchel, R.I.

Determination of particle size and electric charge

distribution in cigarette smoke. Tobacco Science

3:148-153, 1959.

Imperial Tobacco Limited. Research & Development

Division, Progress report July 1993-December

1993. Bates No. 402415194-402415196. Available

at www.tobaccopapers.org/documents/psc8.pdf.

International Committee on Radiation Protection,

Task Group in Lung Dynamics. Deposition and

retention models for internal dosimetry of the

human respiratory tract. Health Physics 12:173-

207, 1966.

Jarvis, M.J., Boreham, R., Primatesta, P., Feyerabend,

C., Bryant, A. Nicotine yield from machinesmoked cigarettes and nicotine intakes in smokers: Evidence from a representative population

survey. Journal of the National Cancer Institute

93:134-138, 2001.

Jöckel, K.H., Ahrens, W., Wichmann, H.E., Becher,

H., Bolm-Audorff, U., Jahn, I., Molik, B., Greiser,

E., Timm, J. Occupational and environmental

hazards associated with lung cancer. International

Journal of Epidemiology 21:202-213, 1992.

Johnston, L.D., O'Malley, P.M., Bachman, J.G.

Cigarette use and smokeless tobacco use decline

substantially among teens. University of

Michigan News and Information Services: Ann

Arbor, MI. [On-line], 2000. Available: www.monitoringthefuture.org; accessed 1/16/01. 

Kabat, G.C. Aspects of the epidemiology of lung cancer in smokers and nonsmokers in the United

States. Lung Cancer 15:1-20, 1996.

Kaufman, D.W., Palmer, J.R., Rosenberg, L., Stolley,

P; Warshauer, E., Shapiro, S. Tar content of cigarettes in relation to lung cancer. American Journal

of Epidemiology 129:703-711, 1989.

Khuder, S.A., Dayal, H.H., Mutgi, A.B., Willey, J.C.,

Dayal, G. Effect of cigarette smoking on major

histological types of lung cancer in men. Lung

Cancer 22:15-21, 1998.

Kieth, C.H. Particle size studies on tobacco smoke.

Beitrage zur Tabakforschung International 11:123-

131, 1982.

Kieth, C.H., Derrick, J.C. Measurement of the particle size distribution and concentration of cigarette smoke by the “conifuge.” Journal of Colloid

Science 15:340-356, 1960.

Krzyzanowski, M., Sherrill, D.L., Paoletti, P.,

Lebowitz, M.D. Relationship of respiratory symptoms and pulmonary function to tar, nicotine,

and carbon monoxide yield of cigarettes.

American Review of Respiratory Disease 143:306-

311, 1991.

Kuller, L.H. Ockene, J.K., Meilahn, E., Wentworth,

D.N., Svendsen, KH., Neaton, J.D. Cigarette

smoking and mortality. Cigarette smoking and

mortality. MRFIT Research Group. Preventive

Medicine 20:638-654, 1991.

Lange, P., Nyboe, J., Appleyard, M., Jensen, G.,

Schnohr, P. Relationship of the type of tobacco

and inhalation pattern to pulmonary and total

mortality. European Respiratory Journal 5:1111-

1117, 1992.

Lee, P.N., Garfinkel, L. Mortality and type of cigarette smoked. Journal of Epidemiology and

Community Health 35:16-22, 1981.

Levi, F., Franceschi, S., La Vecchia, C., Randimbson,

L., Te, V. Lung carcinoma trends by histological

type in Valud and Neuchatel, Switzerland,

1974–1994. Cancer 79:906-914, 1997.

Lubin, J.H., Blot, W.J., Berrino, F., Flamant, R., Gillis,

C.R., Kunze, M., Schmahl, D., Visco, G. Patterns

of lung cancer risk according to type of cigarette

smoked. International Journal of Cancer 33:569-

576, 1984.

Lubin, J.H. Modifying risk of developing lung cancer

by changing habits of cigarette smoking. British

Medical Journal 288:1953-56, 1984a. 

Lubin, J.H. [letter-response] British Medical Journal

289:921, 1984b. 

Mannino, D.M., Ford, E., Giovino, G.A, Thun, M.

Lung cancer mortality rates in birth cohorts in

the United States from 1960 to 1994. Lung

Cancer 31(2-3):91-99, 2001.

Matos, E., Vilensky, M., Boffetta, P., Kogevinas, M.

Lung cancer and smoking: A case-control study

in Buenos Aires, Argentina. Lung Cancer 21:155-

163, 1998.

Maxwell, J. C., Jr. Historical Sales Trends in the

Cigarette Industry, a Statistical Summary Covering

69 Years (1925-93). 1994. Richmond, VA, Wheat,

First Securities, Inc. 

McClusker, K., Hiller, F.C., Wilson, J.D., Mazumder,

M.K., Bone R. Aerodynamic sizing of tobacco

smoke particulate from commercial cigarettes.

Archives of Environmental Health 38:215-218,

1983.

Miller, L.M., Monahan, J. The search for “safer” cigarettes. The Reader’s Digest 38:37-45, 1959.

Mitchell, R.I. Second phase report on the determination of particle size in cigarette smoke. Report to

Philip Morris Inc. Battelle Memorial Institute.

October 30, 1958. Bates No. 1001905717.

Moolgavkar, S.H, Dewanji, A., Luebeck, G. Cigarette

smoking and lung cancer: Reanalysis of the

British Doctor’s Data. Journal of the National

Cancer Institute 81:415-420, 1989.

Morie, G.P., Sloan, C.H., Peck, V.G. Study of cigarette

smoke filtration by means of the scanning electron microscope. Beitrage zur Tabakforschung

International 7:99-104, 1973.

Chapter 04 11/19/01 11:00 AM Page 155
156

Smoking and Tobacco Control Monograph No. 13

National Cancer Institute. Cancer Mortality in the

United States: 1959–1977. NCI Monograph 59.

U.S. Department of Health and Human Services,

Public Health Service, National Institutes of

Health, National Cancer Institute, NIH

Publication No. 82-2435. 1982.

National Cancer Institute. The FTC Cigarette Test

Method for Determining Tar, Nicotine, and Carbon

Monoxide Yields of U.S. Cigarettes. Report of the

NCI Expert Committee. Smoking and Tobacco

Control Monograph No. 7. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 96-4028, 1996.

Negri, E., Franzosi, M.G., La Vecchia, C., Santoro, L.,

Nobili, A., Tognoni, G. Tar yield of cigarettes and

risk of acute myocardial infarction. British

Medical Journal 306:1567-1569, 1993.

Office for National Statistics (ONS). Statistics on

Smoking: England. 1976–1996. Statistical Bulletin

1998/25, July 1998.

Palmer, J., Rosenberg, L., Shapiro, S. Low yield cigarettes and the risk of nonfatal myocardial infarction in women. New England Journal of Medicine

320:1569-1573, 1989.

Parish, S., Collins, R., Peto, R., Youngman, L.,

Barton, J., Jayne, K., Clarke, R., Appleby, P.,

Lyon, V., Cederholm-Williams, S., et al. Cigarette

smoking, tar yields, and non-fatal myocardial

infarction: 14,000 cases and 32,000 controls in

the United Kingdom. The International Studies

of Infarct Survival (ISIS) Collaborators. British

Medical Journal (Clin Res Ed) 311[7003], 471-477,

1995.

Pathak, D.R., Samet, J.M., Humble, C.G., Skipper, B.J.

Determinants of lung cancer risk in cigarette

smokers in New Mexico. Journal of the National

Cancer Institute 76:597-604, 1986.

Peel, D.M., Riddick, M.G., Edwards, M.E., Gentry,

J.S., Nestor, T.B. Formation of Tobacco Specific

Nitrosamines in Flue-Cured Tobacco. Presented at

the 53rd Tobacco Science Research Conference.

Montreal, Quebec, Canada. September 12–15,

1999.

Pepples, E. Industry response to cigarette/health controversy. February 4, 1976. University of

California San Francisco Tobacco Archive

Document I.D. 2205.01.

Petitti, D.B., Friedman, G.D. Cardiovascular and

other diseases in smokers of low-yield cigarettes.

Journal of Chronic Diseases 38:581-588, 1985.

Peto, R. Influence of dose and duration of smoking

on lung cancer rates. Tobacco: A Major

International Health Hazard. Zaridze, D.G., Peto,

R. (Editors.). Lyons, France: International Agency

for Research on Cancer, 1986.

Peto, R., Darby, S., Deo, H., Silcocks, P., Whitley, E.,

Doll, R. Smoking, smoking cessation, and lung

cancer in the U.K. since 1950: Combination of

national statistics with two case-control studies.

British Medical Journal 321:323-329, 2000.

Pezzotto, S.M., Mahuad, R., Bay, M.L., Morini, J.C.,

Poletto, L. Variation in smoking-related lung

cancer risk factors by cell type among men in

Argentina: A case-control study. Cancer Causes

and Control 4:231-237, 1993.

Pillsbury, H.C. Review of the Federal Trade

Commission Method for determining cigarette

tar and nicotine yield. The FTC Cigarette Test

Method for Determining Tar, Nicotine, and Carbon

Monoxide Yields of U.S. Cigarettes. Report of the

NCI Expert Committee. Smoking and Tobacco

Control Monograph No. 7. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 96-4028, 1996.

Powell, J.T., Edwards, R.J., Worrell, P.C., Franks, P.J.,

Greenhalgh, R.M., Poulter, N.R. Risk factors associated with the development of peripheral arterial disease in smokers: A case-control study.

Atherosclerosis 129:41-48, 1997.

Rimington, J. The effect of filters on the incidence of

lung cancer in cigarette smokers. Environmental

Research 24:162-166, 1981.

Royal College of Physicians. Smoking and Health.

Summary and Report of the Royal College of

Physicians of London on Smoking in Relation to

Cancer of the Lung and Other Diseases. New York:

Pitman Publishing Corp, 1962.

Russo, A., Crosignani, P., Francheschi, S., Berrino, F.

Changes in lung cancer histological types in

Varese cancer registry, Italy 1976–1992. European

Journal of Cancer 33:1643-1647, 1997.

S-Plus 2000. Guide to Statistics. Data Analysis

Products Division, MathSoft, Inc. Seattle, WA.

June, 1999.

Shanks, T.G. Reduction in disease risks after quitting

smoking. Presentation APHA. Chicago, IL.

November 10, 1999.

Shiffman, S. Tobacco “chippers”—Individual differences in tobacco dependence.

Psychopharmacology (Berlin) 97:539-547, 1989.

Sidney, S., Tekawa, I.S., Friedman, G.D. A prospective

study of cigarette tar yield and lung cancer.

Cancer Causes and Control 4:3-10, 1993.

Sparrow, D., Stefos, T., Bosse, R., Weiss, S.T. The relationship of tar content to decline in pulmonary

function in cigarette smokers. American Review of

Respiratory Disease 127:56-58, 1983.

Stellman, S.D., Muscat, J.E., Thompson, S.,

Hoffmann, D., Wynder, E.L. Risk of squamous

cell carcinoma and adenocarcinoma of the lung

in relation to lifetime filter cigarette smoking.

Cancer 80(3):382-388, 1997.

Stevens, R., Moolgavkar, S. Estimation of relative risk

from vital data: smoking and cancers of the lung

and bladder. Journal of the National Cancer

Institute 63:1351-1357, 1979.

Stevens, R., Moolgavkar, S. A cohort analysis of lung

cancer and smoking in British males. American

Journal of Epidemiology 119:624-641, 1984.

Chapter 04 11/19/01 11:00 AM Page 156
157

Chapter 4

Swartz, J.B. Use of a multistage model to predict

time trends in smoking induced lung cancer.

Journal of Epidemiology and Community Health

46:311-315, 1992.

Tang, J.L., Morris, J.K., Wald, N.J., Hole, D., Shipley,

M., Tunstall-Pedoe, H. Mortality in relation to tar

yield of cigarettes: A prospective study of four

cohorts. British Medical Journal 311:1530-1533,

1995.

Teague, C. Research planning memorandum on a

new type of cigarette delivering a satisfying

amount of nicotine with a reduced “tar”-to-nicotine ratio. March 28, 1972. Engle Plantiffs

Exhibit No. 0111.

Thun, M.J., Heath, C.W. Changes in mortality from

smoking in two American Cancer Society

prospective studies since 1959. Preventive

Medicine 26:422-426. 1997.

Thun, M.J., Lally, C.A., Flannery, J.T., Calle, E.E.,

Flanders, W.D., Heath, C.W. Cigarette smoking

and changes in the histopathology of lung cancer. Journal of the National Cancer Institute

89:1580-1586, 1997a.

Thun, M., Myersm D., Day-Lallym C., Myers, D.G.,

Calle, E., Flanders, W.D., Zhu, B.P., Namboodiri,

M., Heath, Jr, C. Trends in tobacco smoking and

mortality from cigarette use in cancer prevention

studies I (1959 through 1965) and II (1982

through 1988). Changes in Cigarette-Related

Disease Risks and Their Implications for Prevention

and Control. Smoking and Tobacco Control

Monograph No. 8. U.S. Department of Health

and Human Services, National Institutes of

Health, National Cancer Institute, NIH

Publication No. 97-4213, 1997b.

Tobacco Advisory Group (of the Royal College of

Physicians). Nicotine Addiction in Britain. Royal

College of Physicians of London, 2000.

Todd, G.F., Hunt, B.M., Lambert, P.M. Four cardiorespiratory symptoms as predictors of mortality.

Journal of Epidemiology and Community Health

32:267-274, 1978.

Townsend, J. Smoking and lung cancer: A cohort

study of men and women in England and Wales

1935–70. Journal of the Royal Statistical Society

A141[pt 1]:95-107, 1978.

Tolley, H.D., Crane, L., Shipley, N. Smoking prevalence and lung cancer death rates. Strategies to

Control Tobacco Use in the United States: A

Blueprint for Public Health Action in the 1990s.

Smoking and Tobacco Control Monograph No.

1. U.S. Department of Health and Human

Services, National Institutes of Health, National

Cancer Institute, Publication No. [PHS] 92-3316,

1991.

Travis, W.D., Travis, L.B., Devesa, S.S. Lung cancer.

Cancer 75:191-202, 1995.

U.S. Bureau of the Census. U.S. population estimates

by age, sex, race. Washington, D.C., 2000

Available from ww.census.gov/population/www/

estimates/nat_80s_detail.html and

nat_90s_detail.

U.S. Congress. Hearings before the Consumer

Subcommittee of the Committee on Commerce.

Senate, 90th Congress, August 23, 24, 1967.

U.S. Department of Health, Education, and Welfare.

The Health Consequences of Smoking: A Report to

the Surgeon General. U.S. Department of Health,

Education, and Welfare, Public Health Service,

Health Services and Mental Health

Administration, Office on Smoking and Health.

DHEW Publication No. (HSM) 71-7513, 1971.

U.S. Department of Health, Education, and Welfare.

Smoking and Health. A Report of the Surgeon

General. U.S. Department of Health, Education,

and Welfare, Public Health Service, Office of the

Assistant Secretary for Health, Office on Smoking

and Health. DHEW Publication No. (PHS) 79-

50066, 1979.

U.S. Department of Health and Human Services. The

Health Consequences of Smoking: The Changing

Cigarette. A Report of the Surgeon General. U.S.

Department of Health and Human Services,

Public Health Service, Office of the Assistant

Secretary for Health, Office on Smoking and

Health. DHHS Publication No. 81-50156, 1981.

U.S. Department of Health and Human Services. The

Health Consequences of Smoking: Nicotine

Addiction. A Report of the Surgeon General. U.S.

Department of Health and Human Services,

Public Health Service, Centers for Disease

Control and Prevention, Center for Health

Promotion and Education, Office on Smoking

and Health, 1988. DHHS Publication No. (CDC)

88-8406.

U.S. Department of Health and Human Services. The

Health Benefits of Smoking Cessation. A Report of

the Surgeon General. U.S. Department of Health

and Human Services, Public Health Service,

Centers for Disease Control and Prevention,

Center for Chronic Disease Prevention and

Health Promotion, Office on Smoking and

Health, DHHS Publication No. (CDC) 90-8416,

1990.

U.S. Department of Health and Human Services.

Preventing Tobacco Use Among Young People: A

Report of the Surgeon General. U.S. Department of

Health and Human Services, Public Health

Service, Centers for Disease Control and

Prevention, National Center for Chronic Disease

Prevention and Health Promotion, Office on

Smoking and Health, 1994.

U.S. Department of Health and Human Services.

Tobacco Use Among U.S. Racial/Ethnic Minority

Groups: A Report of the Surgeon General. U.S.

Department of Health and Human Services,

Public Health Service, Centers for Disease

Control and Prevention, National Center for

Chronic Disease Prevention and Health

Promotion, Office on Smoking and Health, 1998.

Vutuc, C., Kunze, M. Lung cancer risk in women in

relation to tar yields of cigarettes. Preventive

Medicine 11:713-716, 1982.

Chapter 04 11/19/01 11:00 AM Page 157
158

Smoking and Tobacco Control Monograph No. 13

Vutuc, C., Kunze, M. Tar yields if cigarettes and male

lung cancer risk. Journal of the National Cancer

Institute 71:435-437, 1983.

Wakeham, H to Cullman, H. March 24, 1961. Memo

by H. Wakeman. Trends in tar and nicotine

deliveries over the last 5 years. Bates No.

1000861953.

Warner, KE. Tobacco industry response to public

health concern: A content analysis of cigarette

ads. Health Education Quarterly 12:115-27, 1985.

Wald, N., Nicolaides-Bouman, A. (Editors.). UK

Smoking Statistics. 2nd Edition. Oxford, UK:

Oxford University Press, 1991.

Wilcox, H.B., Schoenberg, J.B., Mason, T.J., Bill, J.S.,

Stemhagen, A. Smoking and lung cancer: Risk as

a function of cigarette tar content. Preventive

Medicine 17:263-272, 1988.

Wingo, P.A, Ries, L.A.G., Giovino, G.A., Miller, D.S.,

Rosenberg, H.M., Shopland D.R., Thun, M.J.,

Edwards, B.K. Annual report to the nation on

the status of cancer, 1973–1996, with a special

section on lung cancer and tobacco smoking.

Journal of the National Cancer Institute 91:675-690,

1999.

Withey, C.H., Papacosta, A.O., Swan, A.V.,

Fitzsimons, B.A., Ellard, G.A., Burney, P.G.,

Colley, J.R., Holland, W.W. Respiratory effects of

lowering tar and nicotine levels of cigarettes

smoked by young male middle tar smokers. II.

Results of a randomised controlled trial. Journal

of Epidemiology and Community Health 46(3):281-

285, 1992.

Whittemore, A.S. Effect of cigarette smoking in epidemiological studies of lung cancer. Statistics in

Medicine 7:223-238, 1988.

World Health Organization. Manual of the

International Statistical Classification of Diseases,

Injuries, and Causes of Death (7th Ed. Rev. of the

International Lists of Diseases and Causes of Death,

adapted 1955). Vol. 1. Geneva: World Health

Organization, 1957.

Wynder, E.L., Graham, E.A. Tobacco smoking as a

possible etiologic factor in bronchogenic carcinoma. A study of six hundred and eighty-four

proved cases. Journal of the American Medical

Association 143:329-336, 1950.

Wynder, E.L., Graham, E.A., Croninger, A.B.

Experimental production of carcinoma with cigarette tar. Cancer Research 13:855-864, 1953.

Wynder, E.L., Kabat, G.C. The effect of low-yield cigarette smoking on lung cancer risk. Cancer

62:1223-1230, 1988.

Wynder, E.L., Mabuchi, K., Beattie, E.J., Jr. The epidemiology of lung cancer: Recent trends. Journal

of the American Medical Association 213:2221-

2228, 1970.

Wynder, E.L., Stellman, S.D. Impact of long-term filter cigarette usage on lung and larynx cancer

risk: A case–control study. Journal of the National

Cancer Institute 62:471-477, 1979.

Chapter 04 11/19/01 11:00 AM Page 158
INTRODUCTION In 1950, the first large-scale epidemiological studies on smoking

and lung cancer conducted by Wynder and Graham, in the United States,

and Doll and Hill, in the United Kingdom, strongly supported the concept

of a dose response between the number of cigarettes smoked and the risk

for cancer of the lung (Wynder and Graham, 1950; Doll and Hill, 1950). 

In 1953, the first successful induction of cancer in a laboratory animal

with a tobacco product was reported with the application of cigarette tara to

mouse skin (Wynder et al., 1953). The particulate matter of cigarette smoke

generated by an automatic smoking machine was suspended in acetone

(1:1) and painted onto the shaven backs of mice three times weekly for up

to 24 months. A clear dose response was observed between the amount of

tar applied to the skin of the mice and the percentage of skin papillomaand carcinoma-bearing animals in the test group (Wynder et al., 1957).

Since then, mouse skin has been widely used as the primary bioassay

method for estimating the carcinogenic potency of tobacco tar and its fractions, as well as of particulate matters of other combustion products

(Wynder and Hoffmann, 1962, 1967; NCI, 1977a, 1977b, 1977c, 1980;

Hoffmann and Wynder, 1977; IARC, 1986a). Intratracheal instillation in

rats of the PAH-containing neutral subfraction of cigarette tar led to squamous cell carcinoma of the trachea and lung (Davis et al., 1975). A cigarette tar suspension in acetone painted onto the inner ear of rabbits led to

carcinoma with metastasis in thoracic organs (Graham et al., 1957).

Dontenwill and colleagues (1973) developed a method that involved

placing Syrian golden hamsters individually into plastic tubes and exposing

them to cigarette smoke diluted with air (1:15) twice daily, 5 days a week,

for up to 24 months (Dontenwill et al., 1973). The method led to lesions

primarily in the epithelial tissue of the outer larynx. Using an inbred strain

of Syrian golden hamsters with increased susceptibility of the respiratory

tract to carcinogens, long-term exposure to cigarette smoke produced a high

tumor yield in the larynx (Bernfeld et al., 1974). A dose response was

recorded between the degree of smoke exposure and the induction of

benign and malignant tumors in the larynges of the hamsters.

In general, inhalation studies have not found that tobacco smoke leads

to squamous cell carcinoma of the lung (Wynder and Hoffmann, 1967;

Mohr and Reznik, 1978; IARC, 1986a & b). Dalbey and associates from the

National Laboratory in Oak Ridge, Tennessee, exposed female F344 rats to

diluted smoke of up to 7 cigarettes daily, 5 times a week for up to 2.5 years.

A high percentage of the smoke-exposed rats developed hyperplasia and

The Changing Cigarette: Chemical

Studies and Bioassays

Dietrich Hoffmann, Ilse Hoffmann

a Throughout the article, the term “tar” is only used as descriptive noun.

159

Chapter 05 11/19/01 11:10 AM Page 159
metaplasia in the epithelium of the nasal turbinates and in the larynx, and

also some hyperplasia in the trachea. The sham-treated rats developed a

small number of lesions in nasal and laryngeal epithelia but none in the

trachea. Ten tumors of the respiratory system were observed in 7 out of 80

smoke-exposed rats. These were 1 adenocarcinoma, 1 squamous cell carcinoma in the nasal cavity, 5 adenomas of the lung, 2 alveologenic carcinomas, and 1 squamous cell carcinoma of the lung (Dalbey et al., 1980). In

the control group of 93 sham-smoked rats, 1 developed an alveologenic carcinoma (Dalbey et al., 1980). In 1952, Essenberg reported that cigarette

smoke induces an excessive number of pulmonary adenomas; whereas, the

sham-exposed mice, as well as the untreated mice, developed significantly

lower rates of pulmonary tumors (Essenberg, 1952). In the following years,

the Leuchtenbergers repeatedly confirmed the findings by Essenberg. They

also demonstrated that even the gas phase increased the occurrence of pulmonary tumors in mice (Leuchtenberger et al., 1958; Leuchtenberger and

Leuchtenberger, 1970). Several additional studies demonstrated the induction of pulmonary tumors in several strains of mice exposed to diluted cigarette smoke (Mühlbock, 1958; Wynder and Hoffmann, 1967; Mohr and

Reznik, 1978; IARC, 1986a & b). Otto exposed mice to diluted cigarette

smoke for 60 minutes daily for up to 24 months. Of 30 mice, 4 developed

lung adenomas and 1 an epidermoid carcinoma of the lung. In the untreated control group, 3 of 60 mice developed lung adenomas (Otto, 1963).

Green and Rodgman (1996) estimated

that there were about 4,800 compounds

in tobacco smoke. In addition, additives out of a list of 599 compounds disclosed by tobacco companies (Doull

et al., 1994) may be added to cigarette tobacco in the process of manufacturing a cigarette in the United States (Green and Rodgman, 1996; Doull et

al., 1994). Tables 5-1 and 5-2 list the major constituents of the vapor phase

(Table 5-1) and the particulate phase (Table 5-2) and their concentrations in

the mainstream smoke (MS) of non-filter cigarettes (Hoffmann and Hecht,

1990; Ishiguro and Sugawara, 1980). The agricultural chemicals and pesticides, as well as their specific thermic degradation products, are omitted

from the two tables because of the many variations in the nature and

amount of these agents in tobacco from country to country and from year

to year (Wittekindt, 1985). Table 5-3 lists the major toxic components in

the MS of cigarettes (Hoffmann et al., 1995).

Development of highly sensitive analytical methods, as well as reproducible short-term and long-term assays, has led to the identification of 69

carcinogens (Table 5-4). Of these, 11 are known human carcinogens (Group

I), 7 are probably carcinogenic in humans (Group 2A), and 49 of the animal

carcinogens are possibly also carcinogenic to humans (Group 2B). This classification of the carcinogens is according to the International Agency for

Research on Cancer (IARC, 1983, 1984, 1986b, 1987, 1988, 1991, 1992,

1994a–e, 1995a & b, 1996, 1999a & b). Two suspected carcinogens have yet

to be evaluated by the IARC.

IDENTIFICATION OF CARCINOGENS,

TUMOR PROMOTERS, AND CARCINOGENS IN TOBACCO SMOKE

160

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 160
Table 5-1

Major Constituents of the Vapor Phase of the Mainstream Smoke of Non-Filter Cigarettes

Compounda Concentration/Cigarette (% of Total Effluent)

Nitrogen 280-320 mg (56-64%)

Oxygen 50-70 mg (11-14%)

Carbon dioxide 45-65 mg (9-13%)

Carbon monoxide 14-23 mg (2.8-4.6%)

Water 7-12 mg (1.4-2.4%)

Argon 5 mg (1.0%)

Hydrogen 0.5-1.0 mg

Ammonia 10-130 μg

Nitrogen oxides (NOx

) 100-600 μg

Hydrogen cyanide 400-500 μg

Hydrogen sulfide 20-90 μg

Methane 1.0-2.0 mg

Other volatile aromatic alkanes (20) 1.0-1.6 mgb

Volatile alkenes (16) 0.4-0.5 mg

Isoprene 0.2-0.4 mg

Butadiene 25-40 μg

Acetylene 20-35 μg

Benzene 12-50 μg

Toluene 20-60 μg

Styrene 10 μg

Other volatile hydrocarbons (29) 15-30 μg

Formic acid 200-600 μg

Acetic acid 300-1,700 μg

Propionic acid 100-300 μg

Methyl formate 20-30 μg

Other volatile acids (6) 5-10 μg

Formaldehyde 20-100 μg

Acetaldehyde 400-1400 μg

Acrolein 60-140 μg

Other volatile aldehydes (6) 80-140 μg

Acetone 100-650 μg

Other volatile ketones (3) 50-100 μg

Methanol 80-180 μg

Other volatile alcohols (7) 10-30 μg

Acetonitrile 100-150 μg

Other volatile nitriles (10) 50-80 μgb

Furan 20-40 μg

Other volatile furans (4) 45-125 μgb

Pyndine 20-200 μg

Pyridine (3) 15-80 μg

3-Vinylpyridine 10-30 μg

Other volatile pyridines (25) 20-50 μgb

Pyrrole 0.1-10 μg

Pyrrolidine 10-18 μg

N-Methylpyrrolidine 2.0-3.0 μg

Volatile pyrazines (18) 3.0-8.0 μg

Methylamine 4-10 μg

Other aliphatic amines (32) 3-10 μg

aNumbers in parentheses represent the individual compounds identified in a given group

bEstimate

161

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 161
Table 5-2

Major Constituents of the Particulate Matter of the Mainstream Smoke of Non-Filter Cigarettes

Compounda μg/Cigaretteb

Nicotine 1.000-3.000

Nornicotine 50-150

Anatabine 5-15

Anabasine 5-12

Other tobacco alkaloids (17) NA

Bipyridyls (4) 10-30

n-Hentriacontane (n-C31H64)c 100

Total nonvolatile hydrocarbons (45)c 300-400c

Naphthalene 2-4

Naphthalenes (23) 3-6c

Phenanthrenes (7) 0.2-0.4c

Anthracenes (5) 0.05-0.1c

Fluorenes (7) 0.6-1.0c

Pyrenes (6) 0.3-0.5c

Fluoranthenes 0.3-0.45c

Carcinogenic polynuclear aromatic hydrocarbons (11)b 0.1-0.25

Phenol 80-160

Other phenols (45)c 60-180c

Catechol 200-400

Other catechols (4) 100-200c

Other dihydroxybenzenes (10) 200-400c

Scopoletin 15-30

Other polyphenols (8)c NA

Cyclotenes (10)c 40-70c

Quinones (7) 0.50

Solanesol 600-1,000

Neophytadienes (4) 200-350

Limonene 30-60

Other terpenes (200-250)c NA

Palmitic acid 100-150

Stearic acid 50-75

Oleic acid 40-110

Linoleic acid 150-250

Linolenic acid 150-250

Lactic acid 60-80

Indole 10-15

Skatole 12-16

Other indoles (13) NA

Quinolines (7) 2-4

Other aza-arenes (55) NA

Benzofurans (4) 200-300

Other 0-heterocyclic compounds (42) NA

Stigmasterol 40-70

Sitosterol 30-40

Campesterol 20-30

Cholesterol 10-20

Aniline 0.36

Toluidines 0.23

Other aromatic amines (12) 0.25

Tobacco-specific N-nitrosamines (6) 0.34-2.7

Glycerol 120 aNumbers in parentheses represent individual compounds identified.

bFor details, See Table 5-4

c

Estimate. NA=Not available.

162

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 162
163

Chapter 5

Table 5-3

Major Toxic Agents in Cigarette Smokea

Concentration/ Non-Filter

Agent Cigarette Toxicity

Carbon monoxide 10-23 mg Binds to hemoglobin, inhibits respiration

Ammonia 10-130 μg Irritation of respiratory tract

Nitrogen oxide (NOx

) 100-600 μg Inflamation of the lung

Hydrogen cyanide 400-500 μg Highly ciliatoxic, inhibits lung clearance

Hydrogen sulfide 10-90 μg Irritation of respiratory tract

Acrolein 60-140 μg Ciliatoxic, inhibits lung clearance

Methanol 100-250 μg Toxic upon inhalation and ingestion

Pyridine 16-40 μg Irritates respiratory tract

Nicotineb 1.0-3.0 mg Induces dependence, affects cardiovascular and 

endocrine systems

Phenol 80-160 μg Tumor promoter in laboratory animals

Catechol 200-400 μg Cocarcinogen in laboratory animals

Aniline 360-655 μg Forms methemoglobin, and this affects respiration

Maleic hydrazide 1.16 μg Mutagenic agent

aThis is an incomplete list.

bToxicity: oral/rat, LD50 free nicotine 50 mg/kg, nicotine bitartrate 65 mg/kg.

Source: Hoffmann et al., 1998.

Table 5-4

Carcinogens in Cigarette Smoke

IARC Evaluation

Evidence of Carcinogenicity

Conc./Non-filter in in

Agent Cigarette Lab Animals Humans Groupa

PAH

Benz(a)anthracene 20-70 ng Sufficient 2A

Benzo(b)fluoranthene 4-22 ng Sufficient 2B

Benzo(j)fluoranthene 6-21 ng Sufficient 2B

Benzo(k)fluoranthene 6-12 ng Sufficient 2B

Benzo(a)pyrene 20-40 ng Sufficient Probable 2A

Dibenz(a,h)anthracene 4 ng Sufficient 2A

Dibenzo(a,l)pyrene 1.7-3.2 ng Sufficient 2B

Dibenzo(a,e)pyrene Present Sufficient 2B

Indeno(1,2,3-cd)pyrene 4-20 ng Sufficient 2B

5-Methylchrysene 0.6 ng Sufficient 2B

Heterocyclic Compounds

Quinolineb 1-2 ng

Dibenz(a,h)acridine 0.1 ng Sufficient 2B

Dibenz(a,j)acridine 3-10 ng Sufficient 2B

Dibenzo(c,g)carbazole 0.7 ng Sufficient 2B

Benzo(b)furan Present Sufficient 2B

Furan 18-37 ng Sufficient 2B

Chapter 05 11/19/01 11:10 AM Page 163
Table 5-4 (continued)

IARC Evaluation

Evidence of Carcinogenicity

Conc./Non-filter in in

Agent Cigarette Lab Animals Humans Groupa

N -Nitrosamines

N -Nitrosodimethylamine 2-180 ng Sufficient 2A

N -Nitrosoethylmethylamine 3-13 ng Sufficient 2B

N -Nitrosodiethylamine ND-2.8 ng Sufficient 2A

N -Nitrosodi-n-propylamine ND-1.0 ng Sufficient 2B

N -Nitroso-di-n-butylamine ND-30 ng Sufficient 2B

N -Nitrosopyrrolidine 3-110 ng Sufficient 2B

N -Nitrosopiperidine ND-9 ng Sufficient 2B

N -Nitrosodiethanolamine ND-68 ng Sufficient 2B

N -Nitrosonornicotine 120-3,700 ng Sufficient 2B

4-(Methylnitrosamino)-1- 80-770 ng Sufficient 2B

(3-pyridyl)-1-butanone

Aromatic Amines

2-Toluidine 30-337 ng Sufficient 2B

2,6-Dimethylaniline 4-50 μg Sufficient 2B

2-Naphthylamine 1-334 ng Sufficient Sufficient 1

4-Aminobiphenyl 2-5.6 ng Sufficient Sufficient 1

N -Heterocyclic Amines

AaC 25-260 ng Sufficient 2B

IQ 0.3 ng Sufficient 2B

Trp-P-1 0.3-0.5 ng Sufficient 2B

Trp-P-2 0.8-1.1 ng Sufficient 2B

Glu-P-1 0.37-0.89 ng Sufficient 2B

Glu-P-2 0.25-0.88 ng Sufficient 2B

PhIP 11-23 ng Sufficient Possible 2A

Aldehydes

Formaldehyde 70-100 μg Sufficient Limited 2A

Acetaldehyde 500-1,400 μg Sufficient Insufficient 2B

Volatile Hydrocarbons

1,3-Butadiene 20-75 μg Sufficient Insufficient 2B

Isoprene 450-1,000 μg Sufficient 2B

Benzene 20-70 μg Sufficient Sufficient 1

Styrene 10 μg Limited 2B

Misc. Organic Compoundsc

Acetamide 38-56 μg Sufficient 2B

Acrylamide Present Sufficient 2B

Acrylonitrile 3-15 μg Sufficient Limited 2A

Vinyl chloride 11-15 ng Sufficient Sufficient 1

DDT 800-1,200 μg Sufficient Probable 2B

DDE 200-370 μg Sufficient 2B

Catechol 100-360 μg Sufficient 2B

Caffeic acid < 3 μg Sufficient 2B

1,1-Dimethylhydrazine Present Sufficient 2B

Nitromethane 0.3-0.6 μg Sufficient 2B

164

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 164
Chapter 5

Table 5-4 (continued)

IARC Evaluation

Evidence of Carcinogenicity

Conc./Non-filter in in

Agent Cigarette Lab Animals Humans Groupa

2-Nitropropane 0.7-1.2 μg Sufficient 2B

Nitrobenzene 25 μg Sufficient 2B

Ethyl carbamate 20-38 μg Sufficient 2B

Ethylene oxide 7 μg Sufficient Sufficient 1

Propylene oxide 12-100 ng Sufficient 2B

Methyleugenol 20 ng

Inorganic Compounds

Hydrazine 24-43 ng Sufficient Inadequate 2B

Arsenic 40-120 μg Inadequate Sufficient 1

Beryllium 0.5 ng Sufficient Sufficient 1

Nickel ND-600 ng Sufficient Sufficient 1

Chromium (only hexavalent) 4-70 ng Sufficient Sufficient 1

Cadmium 7-350 ng Sufficient Sufficient 1

Cobalt 0.13-0.2 ng Sufficient Inadequate 2B

Lead 34-85 ng Sufficient Inadequate 2B

Polonium-210 0.03-1.0 pCi Sufficient Sufficient 1

Abbreviations: ND, not detected; PAH, polynuclar aromatic hydrocarbons; AaC, 2-amino-9H-pyrido[2,3-b]indole; IQ, 2-amino-3-

methylimidazo[4,5-b]quinoline; Trp-P-1, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole; Trp-2, 3-amino-1-methyl-5H-pyrido[4,3-b]indole;

Glue-P-1, 2-amino-6-methyl[1,2-a:3’,2”-d] imidazole; Glu-P-2, 2-aminodipyrido[1,2-a:3’2”-d]imidazole; PhIP, 2-amino-1-methyl-6-

phenylimidazo [4,5-b]pyridine. aIARC Monographs on the Evaluation of Carcinogenic Risks. Volume 1 and Supplements 1-8, 1972-1999. (1) Human carcinogens;

(2A) Probably carcinogenic in humans; (2B) Possibly carcinogenic to humans; (3) Not classifiable as to their carcinogenicity to

humans.

bUnassigned carcinogenicity status by IARC at this time

c

In 1982, the IARC assigned di(2-ethylhexyl)phthalate as sufficient to Group 2B. However, in 2000, re-evaluation of the carcinogenicity was classified as not carcinogenic (IARC 1982, 2000). We cited di(2-ethylhexyl)phthalate as a 2B carcinogen (Hoffmann and

Hoffmann, 1997) and in this article, it is deleted from Table 5-4, “Carcinogenicity in Cigarette Smoke.”

Sources: International Agency for Research on Cancer, 1982, 2000.

In 1936, the American Tobacco Company began using standard

machine smoking conditions, which, to some extent, reflected the

smoking habits of cigarette smokers at that time. The estimated salesweighted average nicotine yields of the cigarettes smoked at that time were

around 2.8 mg (Bradford et al., 1936). In agreement with the U.S. tobacco

industry, the Federal Trade Commission (FTC) adapted the 1936 standard

method in 1969 with only slight modifications. Since then, machine-smoking conditions are one puff/minute with a volume of 35 ml drawn during 2

seconds, leaving a butt length of 23 mm for a non-filter (plain) cigarette,

and length of the filter and overwrap plus 3 mm for a filter cigarette

(Pillsbury et al., 1969). In Canada and the United Kingdom, the standard

smoking conditions of the International Standards Organization (ISO) have

been accepted since 1991 (ISO, 1991). In other European countries, the

standard smoking conditions for cigarettes are those developed by CORESTA (Centre De Cooperation Pour Les Recherches Scientifiques Relative Au

Tabac), which are similar to the FTC standard smoking conditions (CORESTA, 1991). In Japan, the FTC standard smoking conditions are employed for

the machine smoking of cigarettes (Pillsbury et al., 1969). The FTC method

defines tar as smoke particulates minus water and nicotine, whereas CORESTA defines tar as total particulates minus water (Pillsbury et al., 1969; ISO,

1991; CORESTA, 1991). The standard conditions for machine

SMOKING 

CONDITIONS

165

Chapter 05 11/19/01 11:10 AM Page 165
smoking of tobacco products used by the different testing protocols are presented in Table 5-5. Using the FTC method, the sales-weighted average tar

and nicotine yields of U. S. cigarettes decreased from about 37 mg and 2.7

mg in 1954 to 12 mg and 0.85 mg in 1993 (Figure 5-1).

More than 20 years ago, M.A.H. Russell in the United Kingdom and

N.L. Benowitz in the United States reported that long-term smokers of cigarettes with lower nicotine yields took more than one puff per minute, drew

puff volumes exceeding 35 ml, and inhaled the smoke more deeply than

smokers of higher yield cigarettes (Russell, 1976, 1980; Benowitz et al.,

1983). 

Table 5-6 presents the smoking characteristics of 56 volunteer smokers

who regularly consumed low-yield cigarettes (≤ 0.8 mg nicotine/cigarette

according to the FTC smoking machine method) and of 77 volunteer smokers regularly consuming medium-nicotine cigarettes (FTC, 0.9–1.2 mg/cigarette). These two ranges of nicotine yield constituted more than 73.4 percent of all cigarettes smoked in the U.S. in 1993 (FTC, 1995). The results of

this study clearly indicated that the majority of U.S. smokers smoked their

cigarettes much more intensely to satisfy their acquired need for nicotine.

Comparing the yields of the same cigarettes smoked under FTC standard

machine smoking conditions with the smoke inhaled by the consumers of

cigarettes with low- and medium-nicotine content revealed that smokers

inhaled 2.5 and 2.2 times more nicotine/cigarette, 2.6 and 1.9 times more

tar, 1.8 and 1.5 times more carbon monoxide, 1.8 and 1.6 times more BaP,

and 1.7 and 1.7 times more NNK than is generated by the FTC machinesmoking method (Table 5-6; Djordjevic et al., 2000). 

The discrepancy in exposure assessment between recent measurements

and former interpretations of machine-smoking data has led to criticism of

the FTC standard machine smoking method for consumer guidance. The

suggestion that there is a meaningful quantitative relationship between the

FTC-measured yields and actual intake (by the cigarette smoker) is misleading (Benowitz, 1996). In view of these concerns, it appears "that the time

has come for meaningful information on the yields of cigarettes" (Wilkenfeld et al., 2000a & b). The FTC agrees, in principle, that a better and more

comprehensive test program for cigarettes is needed (Peeler and Butters,

2000).

In 1959, Haag et al. reported the selective

reduction of volatile smoke constituents by filtration through charcoal filter tips (Haag et al.,

1959). Several of the compounds that are

selectively removed from mainstream smoke

(MS) in this fashion are major ciliatoxic agents, such as hydrogen cyanide,

formaldehyde, acrolein, and acetaldehyde. Charcoal filters reduce the MS

levels of these agents by up to 66 percent (Kensler and Battista, 1966;

Tiggelbeck, 1976; Battista, 1976). However, for tar reduction, charcoal filters

are less efficient than cellulose acetate filters. Several types of combination

filters are in use. The early charcoal-activated dual and triple filter tips were

cellulose acetate filters with embedded charcoal powder or granulated charCHANGES IN CIGARETTE SMOKE

COMPOSITION WITH VARIOUS

DESIGN CHANGES

Filter Tips

166

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 166
coal sandwiched between cellulose acetate segments. These filters have been

improved by innovative filter designs, incorporating cellulose acetate, charcoal, and cigarette filter paper (Shepherd, 1994). In the United States, however, cigarettes with charcoal filters have accounted for only about 1 percent of all cigarette sales over the past 15 years. In most developed coun167

Chapter 5

Table 5-5

Standard Conditions for Machine Smoking of Tobacco Product

Parameters Cigarettes Bidis Little Cigars Small Cigars Cigars Premium Pipes

FTC CORESTA FTC CORESTA CORESTA CORESTA CORESTA

Weight (g) 0.8-1.1 0.8-1.1 0.55-0.80 0.9-1.3 1.3-2.5 5-17 6-20 *

Puff

Frequency 60.0 60.0 30.0 60.0 40.0 40.0 40.0 20.0

(sec)

Duration 2.0 2.0 2.0 2.0 1.5 1.5 1.5 2.0

(sec)

Volume (ml) 35.0 35.0 35.0 35.0 40.0 40.0 40.0 50.0

Butt length (mm)

Non-filter 23.0 23.0 23.0 23.0 33.0 33.0 33.0

Filter F&OW+3F+8 F&OW+3

Abbreviations: FTC = Federal Trade Commission method; CORESTA = Centre de Cooperation Pour Les Reherches Scientifiques

Relative au Tabac Method; F = filter tip; OW = overwrap.

*One gram of pipe tobacco smoked.

Sources: Hoffmann et al., 1974; International Committee for Cigar Smoking, 1974; Miller, 1963.

0

5

10

15

20

25

30

35

40

1955 1960 1965 1970 1975 1980 1985 1990 1995

0

1

1

2

2

3

3

TAR

NICOTINE

Tar (mg)

Year

Nicotine (mg)

Figure 5-1

Sales-Weighted Tar and Nicotine Values for U.S. Cigarettes as Measured by Machine

Using the FTC Method, 1954*-1998

*Values before 1968 are estimated from available data.

Chapter 05 11/19/01 11:10 AM Page 167
tries, charcoal filter cigarettes have accounted for, at most, a small percentage of the open cigarette market, exceptions are Japan, South Korea,

Venezuela and Hungary, where at least 90 percent of the cigarettes have

charcoal filter tips (John, 1996; Fisher, 2000).

Cellulose acetate filter cigarettes first became popular in Switzerland,

during the early 1950s, and soon thereafter in Germany. Their popularity

spread to the U.S., the UK and Japan, and finally to France. In 1956, the

market share of filter cigarettes in Switzerland was 57.2 percent, in

Germany 16.7 percent, and in the USA 29.6 percent, with only a few percent in Japan, England, and France. By 1965, the filter cigarette market

share in these countries had risen to about 82 percent, 80 percent, 63 percent, 50 percent , 52 percent , and 21 percent, respectively. At this time, cellulose acetate filter cigarettes accounted for at least 95 percent of the cigarette markets in all of the developed countries, except France, where filter

cigarettes remained at 85 percent of all cigarette sales (Wynder and

Hoffmann, 1994; Waltz and Häusermann, 1963; Hoffmann and Hoffmann,

1997).

In the early 1960s, investigators found that cellulose acetate filter tips

retained up to 80 percent of the volatile phenols from the smoke.

Reduction of the emissions of volatile phenols from cigarettes was desirable

because their tumor promoting activity had been demonstrated in carcinogenesis assays (Roe et al., 1959; Wynder and Hoffmann, 1961; Hoffmann

and Wynder, 1971). When tested on a gram-to-gram basis, the tar from cellulose acetate-filtered smoke is somewhat more toxic, but less carcinogenic,

than tars obtained from charcoal-filtered smoke or from the smoke of non168

Smoking and Tobacco Control Monograph No. 13

Table 5-6

A Comparison of Smoke Data for Two Low-Yield U.S. Filter Cigarettes Smoked According to

the FTC-Method and by Smokers

FTC CIgarette Smokers

Parameters Machine Smoking FTC 0.6-0.8 Nicotine FTC 0.9-1.2 Nicotine

Puff

Volume (ml) 35.0 48.6 (45.2-52.3)a 44.1 (40.8-46.8)b

Interval (sec) 58.0 21.3 (19.0-23.8)a 18.5 (16.5-20.6)b

Duration (sec) 2.0 1.5 (1.4-1.7)a 1.5 (1.4-1.6)b

Nicotine (mg/cig) 0.7 (0.6-0.8) 1.74 (1.54-1.98)c

0.1 (1.09-1.13) 2.39 (2.20-2.60)d

Tar (mg/cig) 8.5 (7.7-9.5) 22.3 (18.8-26.5)e

15.4 (14.2-14.9) 29.0 (25.8-32.5)f

CO (mg/cig) 9.7 (9.0-10.4) 17.3 (15.0-20.1)g

14.6 (14.2-14.9) 22.5 (20.3-25.0)h

Ba P (ng/cig) 10 (8.2-12.3) 17.9 (15.3-20.9)i

14 (10.1-19.4) 21.4 (19.2-23.7)j

NNK (ng/cig) 112.9 (96.6-113.0) 186.5 (158.3-219.7)i

146.2 (132.5-165.5) 250.9 (222.7-282.7)j

Test Groups: a56 smokers; b71 smokers; c30 smokers; d42 smokers; e18 smokers; f19 smokers; g15 smokers; h16 smokers; i6 smokers; j

3 smokers.

Source: Djordjevic et al., 2000.

Chapter 05 11/19/01 11:10 AM Page 168
filter cigarettes (Hoffmann and Wynder, 1963; Spears, 1963; Wynder and

Mann, 1957; Bock et al., 1962; NCI, 1977c). Cellulose acetate filter tips also

selectively remove up to 75 percent of the carcinogenic volatile Nnitrosamines (VNA), whereas charcoal-filter tips are much less effective in

removing VNA (Brunnemann et al., 1977). Exposure of Syrian golden hamsters twice daily, 5 days per week, for over 60 weeks to the diluted smoke

from two different cellulose acetate filter cigarettes elicited a significantly

lower incidence of carcinoma of the larynx than exposure to the diluted

smoke from the non-filter cigarette (p<0.01). In contrast, the incidence rate

of carcinoma of the larynx of hamsters exposed to diluted smoke from

charcoal-filter cigarettes did not differ significantly from that of larynx carcinoma in hamsters exposed to diluted smoke from the non-filter cigarette

(Dontenwill et al., 1973).

Filter perforation allows air dilution of smoke during puff drawing. The

velocity of airflow through the burning cone of cigarettes with perforated

filters is slowed down because the negative pressure generated by drawing a

puff is reduced by drawing air through the filter perforations, and the pressure drop across the tobacco rod is reduced, thus slowing the flow of smoke

through the rod. This results in more complete combustion of the tobacco

and a higher retention of particulate matter by cellulose acetate in the filter

tip (Hoffmann and Hoffmann, 1997; Norman et al., 1984; Durocher, 1984;

Baker, 1984). Presently, more than 50 percent of all cigarettes have perforated filter tips. Table 5-7 compares smoke yields of cigarettes without filter

tips, cigarettes with cellulose acetate filter tips, and cigarettes with cellulose

acetate filter tips that are perforated. The filling tobaccos of these experimental cigarettes were made of an identical blend. The conventional filter

tip of cellulose acetate retains more tar, nicotine, and phenol, but releases

more CO and ciliatoxic agents, hydrogen cyanide, acetaldehyde, and

acrolein than does the cigarette with the perforated filter tip (NCI, 1977c).

In mouse skin assays, the tars from both types of filter cigarettes have comparable tumorigenic activity. However, one needs to bear in mind that (a)

these comparative data are generated with tars obtained by the standardized

machine smoking method, with a 35-ml puff, taken once a minute over 2

seconds; (b) more than 60 percent of today’s smokers in the United States

and in many developed countries smoke cigarettes with nicotine yields of

only 1.2 mg or less (according to FTC standards of smoking); and (c) most

of these smokers compensate for the low nicotine delivery. 

Compensation and greater smoke intake is governed by the smoker’s

acquired need for nicotine and, in essence, negates the intended benefits of

reducing smoke yields by technical means (Russell, 1976, 1980; Benowitz et

al., 1983; Benowitz and Henningfield, 1994; Schultz and Seehofer, 1978;

Moody, 1980; Herning et al., 1981; Gritz et al., 1983; Nil et al., 1986;

Djordjevic et al., 1995, 2000; see Chapter 2). 

Paper Porosity Since about 1960, higher cigarette paper porosity and treatment of

paper with citrate have significantly contributed to the reduction of smoke

yields of several smoke components. During and in between puff drawing,

porous paper enhances the outward diffusion through the paper of hydrogen, NO, CO, CO2, methane, ethane, and ethylene. On the other hand, it

169

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 169
accelerates the diffusion of O2 and N2 into the tobacco column; this, in

turn, causes more rapid smoldering during puff intervals (Hoffmann and

Hoffmann, 1997; Owens, 1998). Porous cigarette paper causes a significant

decrease of CO, hydrogen cyanide, nitrogen oxides, volatile aldehydes; yet,

it hardly changes the yields of tar, nicotine, benz(a)anthracene (BaA), and

BaP. Importantly, the significant reduction of nitrogen oxides in the smoke

of these cigarettes reduces the formation and, thus, significantly lowers the

yields of volatile and tobacco-specific N-nitrosamines (TSNA) (Owens, 1998;

Brunnemann et al., 1994).

Cigarette Construction Smoke yields of cigarettes are also dependent on physical

parameters, such as length and circumference of the cigarette, and the

width of the cut (number of cuts per inch) of the tobacco filler. Extending

the cigarette length from 50 mm to 130 mm produces an increase in the

level of oxygen in the mainstream smoke, while the absolute levels of

hydrogen, carbon monoxide, methane, ethane, and ethylene decrease. The

major reason for this lies in the diffusion of oxygen through the paper into

the smoke stream (Terrell and Schmeltz, 1970). This phenomenon is also

reflected in an increased CO delivery with ascending number of puffs

because the available surface area of the paper diminishes as the cigarette is

smoked. With increasing length of the cigarette, the overall yields of tar,

nicotine, PAH, and other particulate components increase (DeBardeleben et

al., 1978). A circumference of cigarettes smaller than the regular 24.8–25.5

mm (e.g., 23 mm or less) translates into less tobacco being burned and a

greater volume of oxygen available during combustion. Thus, the smoke

yields of tar, nicotine, and other particulate components are lowered

(DeBardeleben et al., 1978; Lewis, 1992; Brunnemann et al., 1994;

Hoffmann and Hoffmann, 1997). Cigarettes with small circumference also

have a lower ignition propensity toward inflammable materials than ciga170

Smoking and Tobacco Control Monograph No. 13

Table 5-7

Comparison of Experimental Cigarettes (Yield/Cigarette)a,b

CelluloseAcetate

Unit of Non-FilterCelluloseAcetate CelluloseAcetate Filter w/Perforation &

SmokeComponents Measurement Cigarette FilterCigarette Filter w/Perforation Highly Porous Paper

Carbon monoxide ml 16.2 19.2 8.62 6.66

Hydrogen cyanide μg 368 296 201 109

Nitrogen oxides-NOx μg 406 438 364 224

Formaldehyde μg 36.0 20.9 31.7 21.4

Acetaldehyde μg 1,040 1,290 608 550

Acrolein μg 105 104 58.6 48.6

Tar mg 27.0 14.7 19.2 19.5

Nicotine mg 1.8 0.94 1.31 1.5

Phenol μg 161 61.7 122 129

Benz(a)anthracene μg 40.6 [1.40] 35.3 [2.25] 38.5 [1.88] 40.1 [1.91]

Benzo(a)pyrene ng 29.9 [1.09] 19.6 [1.25] 29.2 [1.13] 23.9 [1.14] aThe composition of the cigarette tobacco is identical in all four experimentsal cigarettes

bNumbers in square brackets = μg/dry tar

Source: National Cancer Institute, 1977c.

Chapter 05 11/19/01 11:10 AM Page 170
rettes that have a 24.8- to 25.5-mm circumference. It has been estimated

that in all fire deaths in the U.S. in 1997, 30% were caused by smoking, and

worldwide, 10% (Lecstikoo et al., 2000).

The number of cuts per inch (width of tobacco strands) applied to the

filler tobacco of cigarettes has an impact on smoke yields and/or on the carcinogenicity of the tars. The first investigation on the importance of tobacco cuts per inch, with regard to smoke yields and tumorigenicity of the

resulting tars, was published in 1965 (Wynder and Hoffmann, 1965). It

compared the smoke yields of tar and BaP when 8, 30, 50, and 60 cuts per

inch of tobacco were applied. Tar yields per cigarette decreased from 29.1 to

23.0 mg and Ba P from 37 to 21 ng. The tumorigenicities of tars derived

from cigarettes made with 8, 30, or 50 cuts per inch of tobacco declined

from 27 percent to 16 percent and 13 percent of tumor-bearing mice. In a

large-scale study of cigarettes filled with an identical blend, cut 20 and 60

times per inch, the smoke yields per cigarette of tar, nicotine, volatile aldehydes, BaA, and BaP were significantly reduced for the fine-cut. However,

hydrogen cyanide was insignificantly increased. Gram-to-gram comparison

of tumorigenicities of both tars on mouse skin revealed statistically insignificant differences (NCI, 1977a). As the large-scale bioassay was repeated

twice, one has to conclude that, in terms of mouse skin carcinogenicity,

activities of tars obtained from coarse-cut and fine-cut tobaccos are comparable.

Tobacco Types The botanical genus Nicotiana has two major subgenera: N. rustica

and N. tabacum. Nicotiana rustica is primarily grown in Russia, the Ukraine,

and other East European countries, including Georgia, Moldavia, and

Poland. It is also grown in South America and, to a limited extent, in India.

In the rest of the world, Nicotiana tabacum is grown as the major tobacco

crop; it is classified into flue-cured type (often called bright, blond, Virginia

or Maryland tobacco), air-cured type (often called burley tobacco; light aircured tobacco grown in Kentucky, and dark air-cured type grown in parts of

Tennessee and Kentucky, South America, Italy, and France) and sun-cured

type (often called oriental tobacco; primarily grown in Greece and Turkey).

In addition, there are special classes of air-cured tobaccos for cigars, chewing tobacco, and snuff (Tso, 1990).

Prior to the last two decades, flue-cured tobaccos were used exclusively

for cigarettes in the United Kingdom and in Finland; they were also the

predominate type used in Canada, Japan, China, and Australia. Air-cured

tobaccos are preferred for cigarettes in France, southern Italy, some parts of

Switzerland and Germany, and South America. Cigarettes made exclusively

from sun-cured tobaccos are popular in Greece and Turkey. In the rest of

Western Europe and in the United States, cigarettes contain blends of fluecured and air-cured tobaccos as major components. Today, in many countries, such as the United Kingdom, France, and other developed nations,

the U.S. blended cigarette is gaining market share. In the United States, the

composition of the cigarette blend has undergone gradual changes. In the

1960s and early 1970s, 45–50 percent of the cigarette blend were flue-cured

(Virginia) tobaccos, 35 percent were air-cured (burley) tobaccos, and a few

171

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 171
percent were Maryland air-cured and oriental tobaccos. By 1980, the average blend was composed of 38 percent flue-cured, 33 percent air-cured, and

a few percent each of Maryland and oriental tobaccos. In the early 1990s,

these proportions were about 35 percent, 30 percent, and, again, a few percent of Maryland and oriental tobaccos (Hoffmann and Hoffmann, 1997;

Spears and Jones, 1981). The blended cigarette is preferred in many countries, in part because each of the three major N. tabacum types adds a certain aroma to the smoke. Some isoprenoids, and a relatively high number

of agents with carboxyl content, are associated with the aroma of flue-cured

tobacco. Other isoprenoids, and especially the composition of the acidic

fraction, are related to the special aroma of air-cured tobaccos (Roberts and

Rowland, 1962; Enzell, 1976; Spears and Jones, 1981; Tso, 1990). 3-

Methylbutanoic acid (isovaleric acid) is considered to impart the most

important flavor characteristic to oriental tobacco (Stedman et al., 1963;

Schumacher, 1970).

However, in regard to the toxicity and carcinogenicity of tobacco and

tobacco smoke, the difference in the nitrate content of the tobaccos is of

primary significance. Flue-cured tobacco can contain up to 0.9 percent of

nitrate; yet, as it is used for regular cigarettes, it contains less than 0.5 percent of NO3. In oriental tobaccos, one finds up to 0.6 percent of NO3, in aircured tobaccos between 0.9 percent and 5.0 percent, but generally below 3

percent in commercial cigarettes. The highest concentration of nitrate is

present in the ribs, and the lowest concentration is in the laminae, especially in the laminae harvested from the top stalk positions of the tobacco

plant (Neurath and Ehmke, 1964; Tso et al., 1982). With the utilization of a

greater proportion of air-cured tobacco in the U.S. cigarette tobacco blend,

the nitrate content of the blended U.S. cigarette tobacco has risen from

about 0.5 percent in the 1950s to 1.2–1.5 percent in the late 1980s (U.S.

DHHS, 1989).

The concentrations of nitrogen oxides (NOx) and methyl nitrite in

smoke depend primarily on the nitrate concentrations in the tobacco, even

though a portion of the nitrogen oxides is also formed during smoking

from amino acids and certain proteins (Philippe and Hackney, 1959; Sims

et al., 1975; Norman et al., 1983). Cigarettes made with flue-cured tobaccos

deliver up to 200 μg of NOx and 20 μg methyl nitrite in the smoke.

Smoking U.S. blended cigarettes produces up to 500 μg NO2 and 200 μg

methyl nitrite, and the smoke of air-cured tobacco cigarettes contains up to

700 μg NOx and 400 μg methyl nitrite. The major source of nitrate is aircured tobacco and, thus, the major source of NOx in its smoke is the nitrogen fertilizers (Sims et al., 1975). The stems of air-cured tobaccos are especially rich in nitrate (≤6.8 percent). Consequently, stems, as components of

expanded and reconstituted tobaccos, contribute in a major way to NOx in

the smoke (Brunnemann et al., 1983).

Freshly generated smoke, as it leaves the mouthpiece of a cigarette, contains NOx virtually only in the form of nitric oxide (NO), and contains

practically no nitrogen dioxide (NO2). However, nitrogen dioxide is quickly

formed upon aging of the smoke. It has been estimated that, within 500

seconds half of the NO in undiluted smoke is oxidized to NO2 (Neurath, 172

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 172
1972). Of major importance is the high reactivity of NOx upon its formation in the burning cone and in the hot zones of a cigarette. The thermically activated nitrogen oxides serve as scavengers of C,H- radicals, whereby

they inhibit the pyrosynthesis of carcinogenic polynuclear aromatic hydrocarbons. Table 5-8 presents data on the smoke yields of tar, nicotine, phenol, and BaP, and the tumorigenicities of the tars on mouse skin (Wynder

and Hoffmann, 1963).

Freshly generated nitrogen oxides also react with secondary and tertiary

amines to form volatile N-nitrosamines (VNA) and several N-nitrosamines

from amino acids, as well as from additives. The NOx also form tobacco-specific N-nitrosamines (TSNA) by N-nitrosation of nicotine and of the minor

tobacco alkaloids (Brunnemann et al., 1977; Brunnemann and Hoffmann,

1981; Tsuda and Kurashima, 1991; Hoffmann et al., 1994). BaP declined

while NNK increased in the smoke of a leading U.S. non-filter cigarette

between 1974 and 1997. Both trends correlate with the use of tobaccos with

higher nitrate content. Recently, it was suggested that the formation of

tobacco-specific nitrosamines in flue-cured tobacco in the United States is,

in part, due to the use of propane gas heaters in the curing process. Oxides

of nitrogen generated during the burning of the liquid propane react with

nicotine in the tobacco leaf to form TSNA. This change in the curing

method, introduced in the mid 1960s, is a likely contributor to the increase

of TSNA levels in cigarette tobacco. Other important factors are the proportionally greater use of air-cured tobacco and the use of reconstituted tobaccos in the cigarette tobacco blend (Neurath and Ehmke, 1964; Brunnemann

et al., 1983; Peel et al., 2001). Increased amounts of TSNA in tobacco compound the carcinogenic potency of the resulting cigarette smoke (Hoffmann

et al., 1994) and are considered to contribute to the rise of adenocarcinoma,

which has become the dominant form of lung cancer in both male and

female smokers during the last three decades (Vincent et al., 1977; Cox and

Yesner, 1979; el-Torkey et al., 1990; Devesa et al., 1991; Stellman et al.,

1997). Increasing concentrations of nitrate in tobacco have also led to an

173

Chapter 5

Table 5-8

Smoke Yields and Tumorigenicity of the Tars from the Four Major N. tabacum Varieties

Flue-Cured Sun-Cured Air-Cured Tobacco

Factors Tobacco Tobacco Kentuckya Maryland

A: Yields/Cigarette

Tar (mg) 33.4 31.5 25.6 21.2

Nicotine (mg) 2.4 1.9 1.2 1.1

Phenol (μg) 95 120 60 43

Benzo(a)pyrene (ng) 53 (1.6)b 44 (1.4)b 24 (0.94)b 18 (0.85)b

B: Tumorigenicityc

Percentage of mice

with skin tumors 34 35 23 18 aLow-nicotine, air-cured tobacco (Kentucky)

bNumber in parentheses = μg BaP/g dry tar c

Bioassayed on a gram-to-gram basis of tar

Source: Wynder and Hoffmann, 1963.

Chapter 05 11/19/01 11:10 AM Page 173
increase in cigarette smoke of the human bladder carcinogens 2-naphthylamine and 4-aminobiphenyl and of other aromatic amines (Patrianakos

and Hoffmann, 1979; Grimmer et al., 1995).

An important aspect relative to the toxicology of cigarette smoke is the

correlation between the nitrate content of tobacco and the pH of cigarette

smoke. Even though the different processes used to flue-cure and air-cure

tobaccos have a significant impact on the smoke composition of the major

types of tobacco, the role of nitrate is of major importance in determining

the pH of the smoke. Whereas flue-cured tobacco and U.S. cigarette tobacco

blends deliver weakly acidic smoke (pH 5.8–6.3), the smoke of cigarettes

made from air-cured tobacco delivers neutral to weakly alkaline smoke (pH

6.5–7.5). A major reason for the range of pH values encountered in the

smoke of the two major tobacco types is the concentration of ammonia in

the smoke, which is directly tied to the concentration of nitrate in the

tobacco. When pH levels of the smoke rise to greater than 6.0, the percentage of free, unprotonated nicotine increases to about 30 percent at pH 7.4

and to about 60 percent at pH 7.8 (Brunnemann and Hoffmann, 1974).

Protonated nicotine is only slowly absorbed in the oral cavity; yet, unprotonated nicotine, which is partially present in the vapor phase of the smoke,

is quickly absorbed through the mucosal membranes of the mouth

(Armitage and Turner, 1970). The pH of cigar smoke rises with increasing

puff numbers from pH 6.5 to 8.5; consequently, the rapid oral absorption of

the free nicotine in the vapor phase gives a primary cigar smoker immediate nicotine stimulation so that he has no need for inhaling the smoke.

Similarly, the smoker of black, air-cured cigarettes tends not to inhale the

smoke at all, or only minimally (Armitage and Turner, 1970; NCI, 1998).

In 1963, the first comparative study on the tumorigenicity on mouse

skin of tars from the four major types of N. tabacum revealed the highest

activity for tars from flue-cured and sun-cured tobaccos, and the lowest for

the two varieties of air-cured tobaccos (Table 5-8; Wynder and Hoffmann,

1963). The concentration of BaP, as an indicator of the concentrations of all

carcinogenic PAH, is correlated with the tumor initiation potential of the

tars. Upon topical application to mouse skin and human epithelia, carcinogenic PAH induces papilloma and carcinoma. In inhalation studies with

Syrian golden hamsters, the smoke of a cigarette made with a particular

tobacco blend was significantly more active in inducing carcinoma of the

larynx than was the smoke of a cigarette with air-cured (black) tobacco

(Dontenwill et al., 1973).

To verify whether a reduction of carcinogenic PAH in the smoke due to

the presence of high levels of nitrate in tobacco leads to reduced mouse

skin tumorigenicity of the tar, sodium nitrate (8.3 percent) was added to the

standard tobacco blend. On a gram-to-gram basis, the tar from the cigarette

with added nitrate (0.6 μg BaP per gram tar) induced skin tumors in only 2

of 50 mice, whereas the tar from the control cigarette (without the addition

of nitrate; 1.05 μg BaP per gram tar) induced skin tumors in 25 of 100 mice

(Hoffmann and Wynder, 1967). In inhalation experiments with Syrian golden hamsters, smoke from the control cigarette plus 8.0 percent of sodium

174

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 174
nitrate induced laryngeal carcinomas in only 25 of 160 animals (15.6 percent), compared to this type of neoplasm in 60 of 200 animals (30 percent)

in assays with the control cigarette (Dontenwill et al., 1973). Thus, all of

these bioassays on the skin of mice and the inhalation studies with hamsters support the concept that increased nitrate content of the tobacco

inhibits the pyrosynthesis of the carcinogenic PAH and that the tars of

these cigarettes, and their smoke as a whole, have a reduced potential for

inducing benign and malignant tumors in epithelial tissues when compared

to the tar or whole smoke of cigarettes with tobacco that is low in nitrate.

In the early 1940s, the technology for making reconstituted tobacco (RT) was developed. Manufacturing RT

enables the utilization of tobacco fines, ribs, and stems in cigarette tobacco

blends (Halter and Ito, 1979). Prior to this technology, tobacco fines and

stems had been discarded. With the utilization of RT as part of the tobacco

blend, less top quality tobacco is needed and, thereby, the cost of making

cigarettes has been reduced. Laboratory studies (Wynder and Hoffmann,

1967) have shown that cigarettes made entirely of RT deliver a smoke with

significantly reduced levels of tar, nicotine, volatile phenols, and carcinogenic PAHs. 

The two major technologies for making RT for cigarettes are the slurry

process and the paper process. Either process leads to RT with low density.

The advantage of RT lies in the creation of a high degree of aeration of the

tobacco which enhances combustibility. Most of the tested tars from reconstituted tobaccos had significantly reduced carcinogenic activity on mouse

skin (Wynder and Hoffmann, 1965; NCI, 1977a). In inhalation assays with

Syrian golden hamsters, diluted smoke from cigarettes made of reconstituted tobacco induced significantly fewer carcinomas in the larynx (19/160)

than the diluted smoke from control cigarettes (60/200). The cigarette with

RT gave only 7 puffs per cigarette and yielded 20.8 mg tar and 16 ng of BaP

compared to 10 puffs, 33.7 mg tar, and 35.4 ng BaP for the control cigarette

(Dontenwill et al., 1973). This result supports the concept that, at least in

the experimental setting, the carcinogenic PAH, with BaP as a surrogate, are

correlated with the induction of papilloma and carcinoma in epithelial tissues. The procarcinogenic TSNA, on the other hand, are not activated by

enzymes to their reactive species in epithelial tissues; thus, they induce few,

if any, tumors in such tissues. Tobacco ribs and stems, the major components of RT, are richer in nitrate (and this applies especially to the ribs and

stems of air-cured tobaccos) than the laminae of tobacco (Neurath and

Ehmke, 1964; Brunnemann et al., 1983; Brunnemann and Hoffmann, 1991;

Burton et al., 1992). Therefore, in general, the nitrate content of today’s

blended U.S. cigarette, which may contain 20–30 percent RT, is at 1.2–1.5

percent—much higher than the nitrate level in cigarettes during the fifties

and sixties when it was ≤0.5 percent (U.S. DHHS, 1989; Spears, 1974).

Cigarettes with RT emit in their smoke significantly greater amounts of

TSNA than cigarettes of the past. These TSNA include the adenocarcinomainducing NNK, which is metabolically activated to carcinogenic species in

target tissues like the lungs (Hoffmann et al., 1994). One major U.S. cigarette manufacturer was awarded a patent in December 1978 for developing

Reconstituted Tobacco

and Expanded Tobacco

175

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 175
a process that reduces more than 90 percent of the nitrate content of the

RT made from ribs and stems (Kite et al., 1978; Gellatly and Uhl, 1978). It is

unclear to which extent this patented method has been applied to the RT

manufacture for U.S. commercial cigarettes. 

There are at least three methods for expanding tobacco by freeze-drying

(NCI, 1977b). As a result of freeze-drying, expanded tobacco has greater filling power than natural tobacco, meaning that less tobacco is needed to fill

a cigarette. An 85-mm filter cigarette, filled entirely with expanded tobacco,

requires 630 mg tobacco; while a regular non-filter control cigarette of the

same dimensions requires 920 mg tobacco. The tar yields in the smoke of

both types of cigarettes amounted to 12.4 mg and 22.1 mg, respectively

(NCI, 1977b, 1980). In 1982, incorporation of all possible modifications in

the makeup of the cigarette required only 785 mg leaf tobacco; in contrast,

in 1950, the blended U.S. cigarette required 1,230 mg leaf tobacco (Spears,

1974). Table 5-9 presents analytical data for the smoke of experimental cigarettes filled with puffed tobacco, expanded or freeze-dried tobacco, and a

control cigarette. Levels of most components measured in the smoke of cigarettes with puffed tobacco, expanded tobacco, or freeze-dried tobacco were

reduced, compared with data for the control cigarette (NCI, 1977b, 1980).

The changes that have occurred between 1950 and 1995 in the makeup

of U.S. cigarettes, have significantly altered smoke composition. Table 5-10

compares data for individual components in the smoke of U.S. blended cigarettes of the 1950s with corresponding data for the cigarette smoke composition profiles that have been established between 1988 and 1995. All of

these cigarettes were smoked using the FTC method (Pillsbury et al., 1969).

Humectants serve to retain moisture and plasticity in cigarette and

pipe tobaccos. They prevent the drying of tobacco, which would

lead to a harsh tasting smoke; importantly, they also preserve those

compounds that impart flavor to the smoke. Today, the principal humectants in cigarette tobacco are glycerol (propane-1,2,3-triol) and propylene

glycol (PG; propane-1-2-diol); of lesser importance are diethylene glycol

(2.2’-di[hydroxyethyl]ether) and sorbitol (Voges, 1984). In the past, ethylene glycol (ethane-1,2,-diol) has been used as a humectant for cigarette

tobacco. However, because this compound leads to the formation of ethylene oxide, which is carcinogenic to both animals and humans, its use has

been prohibited (IARC, 1994a). In 1972, Binder and Lindner reported the

presence of 20 μg ethylene oxide per cigarette in the smoke of the untreated tobacco of one cigarette brand (Binder and Lindner, 1972). In this context, it is noteworthy that Törnqvist and colleagues (1986) found significant

levels of the N-hydroxyethylvaline moiety of hemoglobin in the blood of

smokers ranging between 217 and 690 pmol/g Hb, averaging 389 ± 138

pmol/g, while levels in nonsmokers’ blood ranged between 27 and 106

pmol/g Hb and averaged 58 ± 25 pmol/g Hb. The authors suggest that most

of the ethylene oxide in the hemoglobin adduct is derived from endogenous oxidation of ethene in cigarette smoke (50–250 μg/cigarette)

(Törnqvist et al., 1986).

Humectants may comprise up to 5 percent of the weight of cigarette

Additives

Humectants

176

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 176
177

Chapter 5

Table 5-10

Changes in the Yields of Selected Toxic Agents in the Smoke of U.S. Cigarettes (FTC Smoking

Conditions)

Earlier Cigarettesa Current Cigarettesa

Smoke Component Year Concentration Year Concentration

Carbon monoxide (CO) 1953 33-38 mg (NF) 1994 11 mg (F)

Nitrogen oxides (HNOx) 1965 330 μg (NF) 1994 500 μg (NF)

Benzene 1962 30 μg (NF) 1988 48 μg (NF)

1962 25-30 μg (F) 1990 42 μg (F)

Acetaldehyde 1960 1,000 μg (NF) 1992 400 μg (F)

NDMA 1976 43 ng (NF) 1989 65 ng (NF)

Tar 1953 38 mg (NF) 1994 12 mg (F)

Nicotine 1953 2.7 mg (NF) 1994 0.85 mg (F)

1959 1.7 mg (F) 1994 1.1 mg (F)

Phenol 1960 100 μg (NF) 1994 70 μg (NF)

1960 46 μg (F) 1994 35 μg (F)

Catechol 1965 390 μg (NF) 1994

1976 790 μg (F) 1994 140 μg (F)

2-Naphthylamine 1968 22 ng (NF) 1985 35 ng (F)

BaP 1959 50 ng (NF) 1995 19 ng (NF)

1959 27 ng (F) 1995 8 ng (F)

NNN 1978 220 ng (NF) 1995 300 ng (NF)

1978 240 ng (F) 1995 280 ng (F)

NNK 1978 110 ng (NF) 1995 190 ng (NF)

1978 100 ng (F) 1995 144 ng (F)

aAbbreviations: NF=non-filter; F=filter; NDMA=N-nitrosodimethylamine; BaP=benzo(a)pyrene; NNN=N’-nitrosonornicotine; NNK=4-

(methylnitrosamino)-1-(3-pyridyl)-1-butanone

Source: Pillsbury et al., 1969.

Table 5-9

Smoke Analyses of Cigarettes Made from Puffed, Expanded, and Freeze-Dried Tobacco and

from a Control Cigarette

Smoke Puffed Expanded Freeze-dried Expanded

Component Tobacco Tobacco Tobacco Stems Control

CO (mg) 9.33 11.8 12.3 23.1 18.0

Nitrogen oxides (μg) 247.0 293.0 235.0 349.0 269.0

HCN (μg) 199.0 287.0 234.0 248.0 413.0

Formaldehyde (μg) 20.7 21.7 33.4 58.0 31.7

Acetaldehyde (μg) 814.0 720.0 968.0 803.0 986.0

Acrolein (μg) 105.0 87.7 92.4 93.0 128.0

Tar (mg) 16 18 16 23 37

Nicotine (mg) 0.8 0.7 0.8 0.4 2.6

BaA (ng) 13.7 11.8 15.3 19.5 37.1

BaP (ng) 11.8 8.2 9.2 16.2 28.7

Abbreviations: CO=carbon monoxide; HCN=hydrogen cyanide; BaA=banz(a)anthracene; BaP=benzo(a)pyrene.

Source: National Cancer Institute, 1980.

Chapter 05 11/19/01 11:10 AM Page 177
tobacco. In a 1964 study, 18 U.S. cigarette tobacco blends that were analyzed for humectants contained between 1.7 and 3.15 percent of glycerol,

which is to some extent decomposed to the ciliatoxic acrolein, and between

0.46 and 2.24 percent of PG (Cundiff et al., 1964). The smoke of four

American cigarettes contained between 0.34 and 0.96 mg/cigarette of PG

(Lyerly, 1967). However, PG may be thermically degrading to yield propylene oxide. This would be of concern because propylene oxide is regarded as

possibly carcinogenic to humans (IARC, 1994b). Four U.S. cigarettes contained between 0.34 and 0.96 mg per cigarette (Lyerly, 1967). In 1999,

between 12 and 100 ng of propylene oxide were detected in the smoke of

cigarettes filled with PG treated tobacco. Several commercial samples of

PG, used as a humectant for cigarette tobacco, already contained traces of

propylene oxide (Kagan et al., 1999).

Flavor Additives Natural tobacco is composed of a wide spectrum of components

that, upon heating, release agents, which contribute to the flavor of the

smoke. These include tobacco-specific terpenoids, pyrroles, and pyrazines

among others (Roberts and Rowland, 1962; Gutcho, 1972; Senkus, 1976;

Leffingwell, 1987; Roberts, 1988). The effective reduction of smoke yields

by filter tips and by the incorporation of reconstituted tobacco also brought

about a reduction of flavor components in the smoke. To counteract this

loss of smoke flavor, the tobacco blends are treated with additives that are

essentially precursors to smoke flavors. They include natural agents contributing to minty, spicy, woody, fruity and flowery flavors. In some

instances, such additives also include synthetic agents as flavor enhancers.

While most of the flavor enhancers are chosen indiscriminately, it is realized that some of them may contribute to toxicity or carcinogenicity of cigarette smoke. A case in point was the cessation of the use of deer tongue

extract which contained several percent of the animal carcinogen coumarin

(Voges, 1984). It has been suggested that additives to cigarettes are used to

reduce the perception of environmental tobacco smoke (ETS; Connolly et

al., 2001).

In 1993 and 1994, the tobacco industry convened an expert panel of

toxicologists to screen agents that were in use, or considered for use, as

tobacco additives. The panel established a list of 599 agents that were generally regarded as safe (GRAS), whereby the term ‘safe’ applied to each of

the additives as such without consideration of the fate and reactivity of

these agents during and after combustion (Doull et al., 1994). An exception

was menthol, which was known to transfer into the smoke without yielding appreciable amounts of carcinogenic hydrocarbons (Jenkins et al.,

1970). A recent toxicologic evaluation of flavor ingredients dealt with 170

such agents that are commonly used in the manufacture of American

blended cigarettes, and examined their effects in four sub-chronic, noseonly smoke inhalation studies in rats compared to effects of the smoke of

tobacco blends without additives. Control animals were exposed to filtered

air (Gaworski et al., 1998). Smoke exposure was monitored with internal

dose markers, including carboxyhemoglobin, serum nicotine, and serum

cotinine. The mainstream smoke (MS) of flavored and nonflavored cigarette

types caused essentially the same responses in the respiratory tracts of the

rats; specifically hyperplasia and metaplasia in the nose and larynx. As this

178

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 178
study involved maximally 65 hours of exposure (while induction of tumors

would not be expected until animals reach half their life span), one cannot

deduce with certainty that the addition of these flavoring agents to tobacco

blends has no impact on the development of tumors.

The tobacco companies have undertaken a substantial research

effort to develop new types of nicotine delivery devices. These

devices were intended to generate an aerosol with nicotine in the range of

the levels present in conventional cigarettes but with very low emissions of

tar and other toxic agents. Toward the end of the 1980s, the first prototype

of these new types of cigarettes was on the test market, a product named

"Premier." It was a cigarette that "heats rather than burns tobacco" (R. J.

Reynolds Tobacco Company, 1988; DeBethizy et al., 1990; Borgerding et al.,

1990a & b, 1998). This 80-mm cigarette is comprised of three sections. The

first 40-mm section of this cigarette is made with compressed charcoal,

which is immediately linked to an inner aluminum tube containing tobacco, flavor additives, and glycerol. This tube is embedded in tobacco. Section

2 (~10 mm) is a cellulose acetate filter dusted with charcoal powder. The

third section (~30 mm) is a cellulose acetate filter tip. Under FTC standard

machine smoking conditions, the "Premier" delivers smoke containing 0.3

mg nicotine, 6.3 mg water, 4.6 mg glycerol, 0.4 mg propylene glycol, and

0.7 mg tar. Compared with the reference (conventional) cigarette, and disregarding nicotine, the majority of the known toxic and carcinogenic agents

in the smoke are reduced by more than 90 percent. Known exceptions are

carbon monoxide (CO) (+3.5 percent), ammonia (–5.6 percent), formaldehyde (–35.3 percent), resorcinol (–73.3 percent), quinoline (–56.6 percent),

and acetamide (–18.2 percent). This new type of cigarette did not gain consumer acceptance, possibly because of difficulty in igniting the "Premier,"

the need for frequent puffing to ensure continuous burning, the lack of flavor, and the low nicotine delivery (0.3 mg/cigarette). Nicotine emission was

below the level that would satisfy most smokers’ acquired need for this

agent even with compensatory smoking.

In 1996, a modified "Premier" came on the market. In the United States,

it is known as "Eclipse"; in Germany it is called "HiQ," and in Sweden, it

goes by the name "Inside." The "Eclipse" consists of four sections. Section 1,

the heat source, is a specially prepared charcoal; section 2 consists of tobacco plus glycerol; section 3 contains finely shredded tobacco; and section 4

is a filter tip. Upon ignition, the special charcoal heats the air stream during

puff drawing. The heated air stream enters the tobacco sections and vaporizes glycerol, as well as the volatile and semi-volatile tobacco components,

including nicotine. Under FTC smoking conditions, the "Eclipse" delivers 8

mg CO (low-tar filter cigarette: 6–12 mg), 150 μg acetaldehyde (700 μg), 30

μg NOx (200–300 μg), 180 μg hydrogen cyanide (300–400 μg), 5.1 mg tar

(11–12 mg), and 0.2–0.4 mg nicotine (0.7–1.0 mg). The remainder of the

smoke particulates consists of 33 percent water, 47 percent glycerol, and 17

percent of various other compounds. The concentrations of the major carcinogens, such as BaP, 2-aminonaphthalene, 4-aminobiphenyl, and the

TSNA are lowered by 85–95 percent (Rose and Levin, 1996; Smith et al.,

1996). Currently, the "Eclipse" is being test marketed and it appears that

New Types of

Cigarettes

179

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 179
response is somewhat more favorable than it was to its predecessor, the

"Premier." The products labeled, "Eclipse Full Flavor," "Eclipse Mild," and

"Eclipse Menthol" produce FTC-standardized smoke yields of 0.2, 0.1, and

0.2 mg nicotine and 3, 2, and 3 mg tar per cigarette. Regular cigarette smokers were asked to switch for 2 weeks to "Eclipse." There were four study

groups, each composed of 26–30 volunteers, for a total of 109 smokers.

Smoking of "Eclipse" resulted in about a 30 percent larger puff volume,

about 50 percent more puffs, which added up to a total puff volume per

cigarette that was more than twice that of the total volume drawn from the

control cigarettes (Stiles et al., 1999). These data suggest that the volunteers

smoked "Eclipse" more intensely than their non-filter cigarettes. This observation is also supported in the uptake of nicotine (Benowitz et al., 1997).

The mutagenic activities of the urine of smokers of four types of "Eclipse"

were assayed on two bacterial strains and were reduced by 72% to 100%,

compared with the mutagenic activities of the urine of the same volunteers

after smoking their regular cigarettes (Smith et al., 1996).

An Expert Committee from the Institute of Medicine of the National

Academy of Sciences studied the scientific basis for a possible reduction of

the "harm" induced by "Eclipse" relative to the "harm" induced by smoking

conventional cigarettes. On the basis of the available data, the Committee

came to the following conclusions: "Eclipse" offers the committed smoker

an option that is currently not available. "Eclipse" does not add to the

inherent biological activity of smoke from the range of cigarettes currently

on the market. The elevated COHb levels should be regarded as a potential

risk factor for cardiovascular diseases. The magnitude of this risk remains to

be determined (Gardner, 2000).

The high concentration of glycerol in the "Eclipse" aerosol led to bioassays of glycerol in 2-week (1.0, 1.93, and 3.91 mg/L) and 13-week (0.033,

0.167, and 0.662 mg/L) "nose only" inhalation studies with Sprague-Dawley

rats, testing for toxicity and especially for irritating effects. The investigators detected metaplasia of the lining of the epiglottis (Gardner, 2000). The

13-week inhalation studies with rats and hamsters had also resulted in some

early histopathological changes in the upper respiratory tract in both laboratory animals. These observations signal the need for lifetime inhalation

assays with the smoke of "Eclipse" in rats, preferably Fisher 344 rats, or better yet, in Syrian golden hamsters, possibly with an inbred strain of hamsters susceptible to carcinogens in the respiratory tract (Bernfeld et al.,

1974). Pauly et al., from the Roswell Park Cancer Institute, Buffalo, New

York, caution that harmful glass fibers have been found to migrate into the

filter tip of the "Eclipse" and may be inhaled during puffing (Pauly et al.,

1998).

The Health Department of Massachusetts and the Society for Research

on Nicotine and Tobacco disputed the claims made for "Eclipse." They

requested that the FTC and the FDA institute regulatory procedures to

ensure that insufficiently documented health claims are not made for

tobacco products. Declaring "Eclipse" the "next best choice," or calling

TSNA-reduced tobacco products "safer tobacco" (Anonymous, 2000; Society

180

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 180
for Research on Nicotine and Tobacco, 2000) is deceiving.

In 1998, Philip Morris USA released a new type of cigarette (EHC) that is

heated electrically to release an aerosol. On the basis of chemical analyses

and short-term bioassays, it has significantly lower toxicity and mutagenicity than the smoke of the Kentucky reference filter cigarette, 1R4F. The prototype, containing a tobacco filler wrapped in a tobacco mat, is kept in constant contact with eight electrical heater blades in a microprocessor-controlled lighter. This cigarette contains about half the amount of the tobacco

of a conventional cigarette. Under FTC-standardized smoking conditions,

the cigarette delivers, with an average of 8 puffs, about 1 mg of nicotine,

whereas all other smoke constituents analyzed were significantly lower than

those in the smoke of the low-yield Kentucky reference cigarette, 1R4F

(Terpstra et al., 1998). However, formaldehyde yields were significantly

higher in the smoke of the EHC and emissions of glycerol and 2-nitropropane were comparable to those recorded in the smoke of the 1R4F cigarette. Per gram of tar, the smoke of the EHC had significantly lower mutagenic activity than the smoke of the 1R4F reference cigarette in TA98 and

TA100 tester strains with metabolic activation (Terpstra et al., 1998).

In mice, rats, and hamsters, NNK induces adenomas and

adenocarcinomas (AC) in the peripheral lung. This effect is

independent of route and form of application (Hoffmann et al., 1994). NNK

is metabolically activated primarily to the unstable 4-(hydroxymethylnitrosamino)-1-(3-pyridyl) -1- butanone and to 4-(α-hydroxymethylene)-1-(3-

pyridyl)-1-butanol, which decomposes into methane diazohydroxide and 4-

keto-4-(3-pyridyl)butane diazohydroxide, respectively. The diazohydroxides

react with DNA bases to form 7-methyl guanine, O6-methyl guanine and

O4-methyl thymidine, respectively, and also form a pyridyloxobutyl adduct

of presently unknown structure. Upon acid hydrolysis, this adduct releases

4-hydroxy-1-(3-pyridyl)-1-butanone. These adducts have been found in the

lungs of mice and rats following treatment with NNK, and they have also

been identified in human lungs. The origin of 7-methyl guanine in DNA

from human lungs is unclear; conceivably, in addition to TSNA, nitroso

compounds such as N-nitrosodimethylamine may also have been a source

for this DNA-methylation. However, it is clear that higher levels of 7-

methyl guanine have been found in the lung of smokers than in the lung

of nonsmokers, thus strengthening the evidence that NNK is a major contributor to the methylation of the lung DNA of smokers (Hecht, 1998). 

PAH induce squamous cell carcinoma of the lung in laboratory animals

and in workers with exposures to aerosols that are high in PAH. NNK

metabolites induce primarily AC of the lung in laboratory animals. Reactive

PAH metabolites bind to DNA in epithelial tissues. In laboratory animals,

metabolically activated forms of NNK react with the DNA of Clara cells in

the peripheral lung (Belinsky et al., 1990) to form methylguanine and

methylthymidine, as well as pyridyloxobutylated adducts. 7-Methylguanine

has been found in smokers’ lungs at higher levels than in the lungs of nonsmokers. 

Additional support for the observation that adenocarcinoma of the lung

OBSERVATIONS ON

CIGARETTE SMOKERS

181

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 181
among cigarette smokers has increased relative to squamous cell carcinoma

during the past 25 years, and for the concept that lung cancer risk of smokers of low-nicotine filter cigarettes is similar to that of smokers of non-filter

cigarettes, comes from biochemical studies. In the mouse, the O6-methylguanine pathway of metabolically activated NNK is clearly the major route

for induction of lung tumors; this conclusion is consistent with the high

percentage of GGT→GAT mutations in the K-ras oncogene induced by NNK

(Hecht, 1998; Singer and Essigmann, 1991). A study from the Netherlands

has shown that mutations on codon 12 of the K-ras oncogene are present

in 24–50 percent of human primary adenocarcinoma. These mutations

occur more frequently in AC of the lung in smokers than in nonsmokers.

Twenty percent of the mutations in codon 12 involve GGT→GAT conversions, which supports the concept that NNK plays a role in the induction of

AC of the lung in smokers. Histochemical examination of human lung cancer showed cyclooxygenase (COX)-2 expression in 70 percent of invasive

carcinoma cases (Hida et al., 1998). COX-2 expression was also identified in

adenocarcinoma of the lung in rats treated with NNK (el-Bayoumy et al.,

1999). It is anticipated that future studies in molecular biology will fully

elucidate the significance of TSNA, especially of NNK, and of the carcinogenic PAH in the induction of lung cancer in tobacco smokers.

SUMMARY Major modifications in the makeup of the commercial cigarette were

introduced between 1950 and 1975. Since then, there have been no substantive changes toward a further reduction of the toxic and carcinogenic

potential of cigarette smoke beyond reducing MS yields of tar, nicotine, and

carbon monoxide. Some of these modifications have also resulted in diminished yields of several toxic and carcinogenic smoke constituents. 

Cigarettes with charcoal filter tips deliver MS with significantly lower

concentrations of the major ciliatoxic agents, such as hydrogen cyanide and

volatile aldehydes. However, except in Japan, South Korea, Venezuela, and

Hungary, cigarettes with charcoal filter tips account for less than one percent (USA) and at most for a small percentage of all cigarettes sold worldwide (Fisher, 2000).

Cellulose acetate filters with or without perforation have the capacity

for selective reduction of smoke yields of volatile N-nitrosamines and semivolatile phenols. The latter are major tumor promoters in cigarette tar. In

contrast to cigarettes manufactured in the 1950s, most of the cigarettes on

the market today use a highly porous wrapper of paper treated with agents

that enhance the burning, thus, contributing to the reduction of machinemeasured yields of carbon monoxide, hydrogen cyanide, volatile aldehydes,

volatile N-nitrosamines, PAH, and TSNA. 

Reconstituted tobacco and expanded tobacco today amount to between

25 and 30 percent of the cigarette tobacco blend. Reconstituted tobacco

reduces the yields of smoke components such as tar and CO. The tar from

cigarettes made entirely of reconstituted tobacco is less carcinogenic on

mouse skin and the smoke of these cigarettes reduces significantly the

induction of carcinoma in the larynx of hamsters compared to the smoke

of reference cigarettes made of natural tobacco. Reconstituted tobaccos and

182

Smoking and Tobacco Control Monograph No. 13

Chapter 05 11/19/01 11:10 AM Page 182
expanded tobaccos have a significantly greater filling power than natural

tobacco. An 85-mm filter cigarette that is filled entirely with expanded

tobacco requires 363 mg tobacco while a regular filter-tipped cigarette

requires 667 mg tobacco. The smoke of cigarettes made of expanded tobacco has significantly lower MS yields of tar, nicotine, CO, hydrogen cyanide,

PAH, and TSNA. On the basis of weight-to-weight comparisons, the tar from

these cigarettes is significantly less tumorigenic on mouse skin than the tar

of a reference cigarette made of the corresponding natural tobacco.

Since 1959, each year the levels of tar, nicotine, and benzo(a)pyrene in

the mainstream smoke of a leading U.S. non-filter cigarette have been monitored. Beginning in 1977, the MS was also analyzed for NNK and in 1981,

the determinations of CO in the mainstream smoke were added. For all of

these analyses, the MS was generated with the standardized machine smoking parameters that are mandated by the Federal Trade Commission. Table

5-11 documents the decline of tar levels from 29.8 mg to 24.3 mg in the

years between 1959 and 1984, while nicotine levels fell from 2.4 mg to 1.6

mg between 1959 and 1977. Since then, the smoke yields of tar and nicotine for this non-filter brand have not changed. Carbon monoxide

remained stable at 16 to 18 mg per cigarette since it was first reported in

1981. By 1997, it was clear that significant changes in the smoke yields of

the major lung carcinogens BaP and NNK have occurred since 1977 in that

BaP levels declined from 49 ng to 19 ng, but NNK increased from 120 ng to

195 ng per non-filter cigarette.

It is important to note that we are lacking analytical data regarding the

levels of these major carcinogens and toxins in the mainstream smoke of

leading cellulose acetate filter-tipped cigarettes with and without filter perforation, as well as in the MS of charcoal filter cigarettes. These cellulose

acetate filter cigarettes were actually the ones dominating the U.S. cigarette

market as the use of non-filter cigarettes faded over the years and charcoal

filter cigarettes had only a modest market share. Most importantly, we are

also lacking data on biological activities of the tars of leading brands of filter cigarettes produced since the 1960s because tumorigenicity and carcinogenicity of tars have not been monitored on a regular basis. There is now

also an urgent need for analytical profiles of the toxic and carcinogenic

mainstream smoke constituents that are generated under conditions reflecting the puff drawing profiles actually exhibited by humans who smoke

these cigarettes that give lower yields as per FTC measurements. Such analytical data would have to be established for major U.S. cigarette brands

manufactured since 1960. They would serve as the scientific basis in support of epidemiological observations regarding the risk of cancer of the lung

and upper aerodigestive tract for smokers who have exclusively smoked filter-tipped brands as compared to the risk for smokers who used non-filter

cigarettes.

Changes in the agricultural, curing, and manufacturing processes of cigarettes have resulted in an increase in tobacco-specific nitrosamines in cigarette smoke that may have contributed to the increase in adenocarcinoma

of the lung observed over the past several decades. 

183

Chapter 5

Chapter 05 11/19/01 11:10 AM Page 183
CONCLUSIONS

1. Major modifications in the makeup of the commercial cigarette were

introduced between 1950 and 1975, but since that time there have been

few substantive changes toward a further reduction of the toxic and carcinogenic potential of cigarette smoke.

2. A variety of changes in cigarette design and filtration have resulted in

chemical changes in cigarette smoke, some of which have also demonstrated decreased toxicity in animal assays. Toxicity or carcinogenicity in animal

assays has not been monitored to allow evaluation of changes over time

that have occurred for cigarette smoke produced by commercial brands of

cigarettes. 

3. Changes in the agricultural, curing, and manufacturing processes of

cigarettes have resulted in an increase over the last several decades in the

amounts of tobacco-specific nitrosamines in cigarette smoke. These changes

are considered to have contributed to the increase in adenocarcinoma of

the lung observed over the past several decades.

4. On the basis of the standard machine smoking method for cigarettes

that has been mandated by the FTC, the sales-weighted average nicotine

yields of U.S. cigarettes decreased gradually from 2.7 mg per cigarette in

1953 to 0.85 mg by the mid 1990s. Today, the smoker of filter cigarettes

will greatly increase his/her smoking intensity to satisfy an acquired need

for nicotine. Thus, the inhaled smoke of one cigarette contains 2 to 3 times

the amount of tar, nicotine, and carbon monoxide and 1.6 to 1.8 times the

level of biomarkers for the major lung carcinogens BaP, and NNK, compared

to amounts in the smoke generated by the FTC method. 

184

Smoking and Tobacco Control Monograph No. 13

Table 5-11

Tar, Nicotine, CO, BaP, and NNK in the Mainstream Smoke of a Leading U.S. NF Cigarette,

1959-1997a

Tar Nicotine Carbon Monoxideb Ba P NNKb

Year (mg) (mg) (mg) (ng) (ng)

1959 29.8 2.4 40

1967 27.2 1.6 49

1971 29.0 1.8 22

1977 26.0 1.59 19 120

1981 24.3 1.52 16.7 19 130

1988 24 1.5 16 19 140

1991 25 1.7 16 18 190

1997 26 1.7 18 19 195

Abbreviations: NNK=4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; BaP= benzo(a)pyrene. aThe analytical data were generated by smoking the leading U.S. NF cigarette according to the FTC-mandated standard machine

smoking method (Pillsbury et al., 1969). bThe open fields document the lack of analytical data for the years 1959, 1967, 1971, and 1977 for CO and 1959, 1967, and 1977

for NNK

Sources: Wynder and Hoffman, 1960; Federal Trade Commission, 1971, 1977, 1981, 1988, 1991, 1997; Hoffmann and Hoffmann,

1997.

Chapter 05 11/19/01 11:10 AM Page 184
185

Chapter 5

Anonymous. Massachusetts disputes claims about

Eclipse cigarettes. Tobacco Reporter 127 (No.

11):11-13, 2000.

Armitage, A.K., Turner, D.H. Absorption of nicotine

in cigarette and cigar smoke through the oral

mucosa. Nature (London) 226:1231-1232, 1970.

Baker, R.R.. The effect of ventilation on cigarette

combustion mechanisms. Recent Advances in

Tobacco Science 10:88-150, 1984.

Battista, S.P. Ciliatoxic components in cigarette

smoke. Proceedings of the Third World Conference

on Smoking and Health, New York, June 2-5, 1975.

Vol. 1. Modifying the Risk for the Smoker. Wynder,

E.L., Hoffmann, D., Gori, G.B. (Editors). U.S.

Department of Health, Education, and Welfare,

Public Health Service, National Institutes of

Health, National Cancer Institute, DHEW

Publication No. (NIH) 76-1221, 1976.

Belinsky, S.A., Foley, J.F., White, C.M., Anderson,

M.W., Maronpot, R. Dose-response relationship

between O6-methylguanine formation in Clara

cells and induction of pulmonary neoplasia in

the rat with 4-(methylnitrosamino)-1-(3-pyridyl)-

1-butanone. Cancer Research 50(12):3772-3780,

1990.

Benowitz, N.L. Biomarkers of cigarette smoking. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.

7. U.S. Department of Health and Human services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 96-4028,

1996.

Benowitz, N.L., Hall, S.M., Herning, S.I., Jacob, P. III,

Jones, R.T., Osman, A.-L. Smokers of low yield

cigarettes do not consume less nicotine during

cigarette smoking. New England Journal of

Medicine 309(3):139-142, 1983.

Benowitz, N.L., Henningfield, J.E. Establishing a

nicotine threshold for addiction. The implications for tobacco regulation. New England Journal

of Medicine 331(2):123-125, 1994.

Benowitz, N.L., Jacob, P.J., Slade, J., Yu, L. Nicotine

content of the Eclipse nicotine delivery device.

American Journal of Public Health 87(11):1865-

1866. 1997.

Bernfeld, P., Homberger, F., Russfield, A.B. Strain differences in the response of inbred Syrian hamsters to cigarette smoke inhalation. Journal of the

National Cancer Institute 53(4):1141-1157, 1974.

Appendix

Abbreviations

AC Adenocarcinoma

BaA Benz(a)anthracene

BaP Benzo(a)pyrene

FTC Federal Trade Commission

Hb Hemoglobin

IARC International Agency for Research on Cancer

MS Mainstream Smoke

NNK 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone

NNN N’-Nitrosonornicotine

NOx Nitrogen oxides (NO, NO2, and N2O)

PAH Polynuclear Aromatic Hydrocarbons

RT Reconstituted Tobacco

SCC Squamous Cell Carcinoma

TSNA Tobacco Specific N-Nitrosamines

VNA Volatile N-Nitrosamines

REFERENCES

Chapter 05 11/19/01 11:10 AM Page 185
186

Brunnemann, K.D., Yu, L., Hoffmann, D. Chemical

studies on tobacco smoke XVII. Assessment of

carcinogenic volatile N-nitrosamines in mainstream and sidestream smoke from cigarettes.

Cancer Research 37(9):3218-3222, 1977.

Burton, H.R., Dye, N.K., Bush, L.P. Distribution of

tobacco constituents in tobacco leaf tissue. I.

Tobacco-specific nitrosamines, nitrate, nitrite,

and alkaloids. Journal of Agricultural and Food

Chemistry 40:1050-1055, 1992.

Connolly, G.N., Wayne, G.D., Lymperis, D., Doherty,

M.C. How cigarette additives are used to mask

environmnental smoke. Tobacco Control 9: 283-

291, 2000.

CORESTA Standard Smoking Methods 23:

Determination of total and nicotine-free dry particulate matter using a routine analytical cigarette-smoking machine. Determination of total

particulate matter and preparation for water and

nicotine measurements. CORESTA Information

Bulletin 1991-3:141-151, 1991.

Cox, J.D. and Yesner, R.A. Adenocarcinoma of the

lung. Recent results from the Veterans

Administration lung group. American Review of

Respiratory Disease 120(5):1025-1029, 1979.

Cundiff, R.H., Greene, G.H., Laurene, A.H. Column

elution of humectants from tobacco and determination by vapor chromatography. Tobacco

Science 8:163-170, 1964.

Dalbey, W.E., Nettesheim, P., Griesemer, R., Caton,

J.E., Guerin, M.R. Chronic inhalation of cigarette

smoke by F344 rats. Journal of the National Cancer

Institute 64(2):383-390, 1980.

Davis, B.R., Whitehead, J.K., Gill, M.E., Lee, P.N.,

Butterworth, A.D., Roe, F.J. Response of rat lung

to tobacco smoke condensate or fractions

derived from it ministered repeatedly by intratracheal installation. British Journal of Cancer

31(4):453-461, 1975.

DeBardeleben, M.Z., Claflin, W.E., Gannon, W.F.

Role of cigarette physical characteristics on

smoke composition. Recent Advances in Tobacco

Science 4:85-111, 1978.

DeBethizy, J.D., Borgerding, M.F., Doolittle, D.J.,

Robinson, J.H., McManus, K.T., Rahn, C.A.,

Davis, R.A., Burger, G.T., Hayes, J.R., Reynolds,

J.H., et al. Chemical and biological studies of a

cigarette that heats rather than burns tobacco.

Journal of Clinical Pharmacology 30(8):755-763,

1990.

Devesa, S.S., Shaw, G.L., Blot, W.J. Changing patterns of lung cancer incidence by histologic type.

Cancer Epidemiology Biomarkers and Prevention

1(1):29-34, 1991

Djordjevic, M.V., Fan, J., Ferguson, S., Hoffmann, D.

Self-regulation of smoking intensity, smoke

yields of low-nicotine, low "tar" cigarettes.

Carcinogenesis 16(9):2015-2021, 1995.

Djordjevic, M.V., Stellman, S.D., Zang, E. Doses of

nicotine and lung carcinogens delivered to cigarette smokers. Journal of the National Cancer

Institute 92(2):106-111, 2000.

Smoking and Tobacco Control Monograph No. 13

Binder, H., Lindner, W. Determination of ethylene

oxide in the smoke of untreated cigarettes (in

German). Fachliche Mitteilungen Austria

Tabakwerke 13:215-220, 1972.

Bock, F.G., Moore, G.E., Dowd, J.E. Clark, P.C.

Carcinogenic activity of cigarette smoke condensate. Journal of the American Medical Association

181:668-673, 1962.

Borgerding, M.F., Bodnar, J.A., Chung, H.L., Mangan,

P.P., Morrison, C.C., Risner, C.H., Rodgers, J.C.,

Simmons, D.F., Uhrig, M.S., Wendelboe, F.N.,

Wingate, D.E., Winkler, L.S. Chemical and biological studies of a new cigarette that primarily

heats tobacco. Part 1. Chemical composition of

mainstream smoke. Food and Chemical Toxicology

36(7):169-182, 1998.

Borgerding, M.F., Hicks, R.D., Bodnar, J.E., Riggs,

D.M., Nanni, E J., Fulp, G.W., Jr., Hamlin, W.C.,

Jr., Giles, J.A. Cigarette smoke composition. Part

1. Limitations of FTC method when applied to

cigarettes that heat instead of burn tobacco.

Journal of the Association of Official Analytical

Chemists 73(4):605-609, 1990a.

Borgerding, M.F., Milhous, L.A., Hicks, R.D., Giles,

J.A. Cigarette smoke composition. Part 2.

Method for determining major components in

smoke of cigarettes that heat instead of burn

tobacco. Journal of the Association of Official

Analytical Chemists 73(4):610-615, 1990b.

Bradford, J.A., Harlan, W.R., Hanmer, H.R. Nature of

cigarette smoke; technique of cigarette smoking.

Industrial Engineering and Chemistry 28:836-839,

1936.

Brunnemann, K.D., Hoffmann, D. Chemical studies

on tobacco smoke. XXV. The pH of tobacco

smoke. Food and Cosmetics Toxicology 12(1):115-

124, 1974.

Brunnemann, K.D., Hoffmann, D. Analytical studies

on N-nitrosamines in tobacco and tobacco

smoke. Recent Advances in Tobacco Science 17:71-

112, 1991.

Brunnemann, K.D., Hoffmann, D. Chemical studies

on tobacco smoke. LXIX. Assessment of the carcinogenic N-nitrosodiethanolamine in tobacco

products and tobacco smoke. Carcinogenesis

2(11):1123-1127, 1981.

Brunnemann, K.D., Hoffmann, D., Gairola, C.G.,

Lee, B.C. Low ignition propensity cigarettes:

smoke analysis for carcinogens and testing for

mutagenic activity of the smoke particulate matter. Food and Chemical Toxicology 32(10):917-922,

1994.

Brunnemann, K.D., Masaryk, J., Hoffmann, D. The

role of tobacco stems in the formation of Nnitrosamines in tobacco and cigarette mainstream and sidestream smoke. Journal of

Agricultural and Food Chemistry 31:1221-1224,

1983.

Chapter 05 11/19/01 11:10 AM Page 186
Chapter 5

187

Doll, R., Hill, A.B. Smoking and carcinoma of the

lung. Preliminary report. British Medical Journal

2:739-748, 1950.

Dontenwill, W., Chevalier, H.J., Harke, H.-P., Lafrenz,

U., Reckzeh, G., Schneider, B. Investigations on

the effects of chronic cigarette smoke inhalation

in Syrian golden hamsters. Journal of the National

Cancer Institute 51(6):1781-1832, 1973.

Doull, J., Frawley, J. P., George, W. List of ingredients

added to tobacco in the manufacture of cigarettes by six major American cigarette companies. Washington, D.C. Covington and Burling,

12 April, 1994 (reprinted: Tobacco Journal

International 196:32-39, 1994).

Durocher, D.F. The choice of paper components for

low-tar cigarettes. Recent Advances in Tobacco

Science 10:52-71, 1984.

El-Bayoumy, K., Iatropoulos, M., Amin, S.,

Hoffmann, D., Wynder, E.L. Increased expression

of cyclooxygenase-2 in rat lung tumors induced

by the tobacco-specific nitrosamine 4-(methylnitrosamine)-4-(3-pyridyl)-4-(3-pyridyl)-butanone:

Impact of a high-fat diet. Cancer Research

59(7):1400-1403, 1999.

el-Torkey, M., el-Zeky, F., Hall, J.C. Significant

changes in the distribution of histologic types of

lung cancer. A review of 4,928 cases. Cancer

65(10):2361-2367, 1990.

Enzell, C.R. Terpenoid components of leaf and their

relationship to smoking quality and aroma.

Recent Advances in Tobacco Science 2:32-60, 1976.

Essenberg, J.M. Cigarette smoke and the incidence of

primary neoplasm of the lung in the albino

mouse. Science 116:561-562, 1952.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 121 Varieties of

Cigarettes. Federal Trade Commission,

Washington, D.C., 1971.

Federal Trade Commission. Report of “Tar” and

Nicotine Content of the Smoke of 166 Varieties of

Cigarettes. Federal Trade Commission,

Washington, D.C., 1977.

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 187 Varieties

of Cigarettes. Federal Trade Commission,

Washington, D.C., December 1981.

Federal Trade Commission. Report of “Tar”, Nicotine

and Carbon Monoxide of the Smoke of 272 Varieties

of Domestic Cigarettes. Federal Trade Commission,

Washington, D.C., 1988.

Federal Trade Commission. Tar, Nicotine, and Carbon

Monoxide of the Smoke of 475 Varieties of Domestic

Cigarettes. Federal Trade Commission,

Washington, D.C., 1991.

Federal Trade Commission. Tar, Nicotine, and Carbon

Monoxide of the Smoke of 1,107 Varieties of

Domestic Cigarettes. Federal Trade Commission,

Washington, D.C. 1995.

Federal Trade Commission. Tar, Nicotine, and Carbon

Monoxide of the Smoke of 1,206 Varieties of

Domestic Cigarettes. Federal Trade Commission,

Washington, D.C., 1997.

Fisher, B. Filtering new technology. Tobacco Reporter

127(12):46-47, 2000.

Gaworski, C.L., Dozier, M.M., Heck, J.D., Gerhard,

J.M. Rajendran, N., David, R.M., Brennecke, L.H.,

Morrissey, R. Toxicological evaluation of flavor

ingredients added to cigarette tobacco: 13-week

inhalation exposures in rats. Inhalation

Toxicology10:357-381, 1998.

Gellatly, G., Uhl, R.G. Method for removal of potassium nitrate from tobacco extracts. U. S. Patent

4,131,118, December 26, 1978, 1978.

Gardner, D.E. (Editor). A safer cigarette? Inhalation

Toxicology 12(Supplement 5):1-58, 2000.

Graham, E.A., Croninger, A.B., Wynder, E.L.

Experimental production of carcinoma with cigarette tar. IV. Successful experiments with rabbits.

Cancer Research 17:1058-66, 1957.

Green, C.R., Rodgman, A. The Tobacco Chemists’

Research Conference. A half-century of advances

in analytical methodology of tobacco and its

products. Recent Advances in Tobacco Science

22:131-304, 1996.

Grimmer, G., Schneider, D., Naujack, K.-W.,

Dettbarn, G., Jacob, J. Intercept-reactant method

for the determination of aromatic amines in

mainstream tobacco smoke. Beitrage zur

Tabakforschung International 16:141-156, 1995.

Gritz, E.R., Rose, J.E., Jarvik, M.E. Regulation of

tobacco smoke intake with paced cigarette presentation. Pharmacology, Biochemistry, and Behavior

18:457-462, 1983.

Gutcho, S. Tobacco Flavoring Substances and Methods.

Park Ridge, NJ: Noyes Data Corporation, 1972.

Haag, H.B., Larson, P.S., Finnegan, J.K. Effect of filtration on the chemical and irritating properties

of cigarette smoke. A.M.A. Archives of

Otolaryngology 69:261-265, 1959.

Halter, H.M., Ito, T.I. Effect of reconstitution and

expansion processes on smoke composition.

Recent Advances in Tobacco Science 4:113-132,

1979.

Hecht, S.S. Biochemistry, biology, and carcinogenicity of tobacco-specific N-nitrosamines. Chemical

Research in Toxicology 11(6):559-603, 1998.

Herning, R.I., Jones, R.T., Bachman, G., Mines, A.H.

Puff volume increases when low-nicotine cigarettes are smoked. British Medical Journal (Clin Res

Ed) 283(6285):187-189, 1981.

Hida, T., Yatabe, Y., Achiwa, H., Muramatsu, H.,

Kozaki, K-I., Makamura, S., Ogawa, M.,

Mitsudomic, T., Sugiura, T., Takahashi, T.

Increased expression of cyclooxygenase-2 occurs

frequently in human lung cancers, especially in

adenocarcinoma. Cancer Research 58(17):3761-

3764, 1998.

Hoffmann, D., Brunnemann, K.D., Prokopczyk, B.,

Djordjevic, M.V. Tobacco-specific N-nitrosamines

and Areca-derived N-nitrosamines. Chemistry,

biochemistry, carcinogenicity, and relevance to

humans. Journal of Toxicology and Environmental

Health 41(1):1-52, 1994.

Chapter 05 11/19/01 11:10 AM Page 187
Smoking and Tobacco Control Monograph No. 13 

188

Hoffmann, D., Hecht, S.S. Advances in tobacco carcinogenesis. Handbook of Experimental

Pharmacology. Cooper, C.S., Grover, P.L.

(Editors.). New York: Springer Publications, 1989.

Hoffmann, D., Hoffmann, I. The changing cigarette,

1950–1995. Journal of Toxicology and

Environmental Health 50(4):307-364, 1997.

Hoffmann, D., Hoffmann, I., Wynder, E.L. The

changing cigarette: 1950-1997: facts and expectations. "Report of Canada’s Expert Committee on

Cigarette Toxicity Reduction". W.S. Rickert (Editor.).

Health Canada, Toronto, Ontario, Canada, 1998,

94 p.

Hoffmann, D., Sanghvi, L.D., Wynder, E.L.

Comparative chemical analysis of India bidi and

American cigarette smoke. International Journal of

Cancer 14(1):49-53, 1974.

Hoffmann, D., Wynder, E.L. Filtration of phenols

from cigarette smoke. Journal of the National

Cancer Institute 30:67-84, 1963.

Hoffmann, D., Wynder, E.L. The reduction in the

tumorigenicity of cigarette smoke condensate by

addition of sodium nitrate to tobacco. Cancer

Research 27(1):172-174, 1967.

Hoffmann, D., Wynder, E.L. A study of tobacco carcinogenesis. XI. Tumor initiation, tumor acceleration, and tumor promoting activity of condensate fraction. Cancer 27(4):848-864, 1971.

Hoffmann, D., Wynder, E.L. Chemical analysis and

carcinogenic bioassays of organic particulate pollutants. In: Air Pollution, A.L. Stern (Editor).

Academic Press, New York, 1977, pp. 361-455.

International Agency for Research on Cancer. 1,3-

Butadiene. Occupational Exposures to Mists and

Vapours from Strong Inorganic Acids; and Other

Industrial Chemicals. IARC Monographs on the

Evaluation of Carcinogenic Risks to Humans.

Lyon, France. 54:237-285, 1992.

International Agency for Research on Cancer.

Acrylamide. Some Industrial Chemicals. IARC.

Monographs on the Evaluation of Carcinogenic

Risks to Humans. Lyon, France. 60:389-433,

1994e.

International Agency for Research on Cancer. Amino

Acid Pyrolysis Products in Food. Some Naturally

Occurring and Synthetic Food Components,

Furocoumarins, and Ultraviolet Radiation. IARC

Monographs on the Evaluation of Carcinogenic

Risks to Humans. Lyon, France. 40:233-280,

1986b.

International Agency for Research on Cancer.

Benzofuran. Dry Cleaning, Some Chlorinated

Solvents and Other Industrial Chemicals. IARC

Monographs on the Evaluation of the

Carcinogenic Risks to Humans. Lyon, France.

Vol. 63:431-441, 1995b.

International Agency for Research on Cancer. Coke

Production. Polynuclear Aromatic Compounds, Part

3: Industrial Exposure in Aluminum Production,

Coal Gasification, Coke Production, and Iron and

Steel Founding. IARC Monographs on the

Evaluation of the Carcinogenic Risk of

Chemicals to Humans. Lyon, France. 34:101-131,

1984.

International Agency for Research on Cancer. DDT

and associated compounds. Occupational

Exposures in Insecticide Application, and Some

Pesticides. IARC Monographs on the Evaluation

of Carcinogenic Risks to Humans. Lyon, France.

53: 179-249, 1991.

International Agency for Research on Cancer. Di(2-

ethylhexyl)phthalate. Some Industrial Chemicals

and Dyestuffs. IARC Monographs on the

Evaluation of Carcinogenic Risk of Chemicals to

Humans. Lyon, France. 29: 257-280, 1982.

International Agency for Research on Cancer. Di(2-

ethylhexyl)phthalate. Some Industrial Chemicals.

IARC Monographs on the Evaluation of

Carcinogenic Risk of Chemicals to Humans.

Lyon, France. 77: 41-148, 2000.

International Agency for Research on Cancer.

Ethylene oxide. Some Industrial Chemicals. IARC

Monographs on the Evaluation of Carcinogenic

Risks to Humans. Lyon, France. 60:73-159,

1994a.

International Agency for Research on Cancer. Furan.

Dry Cleaning, Some Chlorinated Solvents and Other

Industrial Chemicals. IARC Monographs on the

Evaluation of the Carcinogenic Risks to Humans.

Lyon, France. 63:393-407, 1995a.

International Agency for Research on Cancer.

Isoprene. Some Industrial Chemicals. IARC

Monographs on the Evaluation of Carcinogenic

Risks to Humans. Lyon, France. 60:215-232,

1994c.

International Agency for Research on Cancer.

Nitrobenzene. Printing Processes and Printing Inks,

Carbon Black and Some Nitro Compounds. IARC

Monographs on the Evaluation of the

Carcinogenic Risks to Humans. Lyon, France.

65:381-408, 1996.

International Agency for Research on Cancer. Overall

Evaluation of Carcinogenicity: An Updating of IARC

Monographs 1 to 42. IARC Monographs on the

Evaluation of Carcinogenic Risks to Humans.

Lyon, France, Supplement No. 7, 1987.

International Agency for Research on Cancer.

Polynuclear Aromatic Compounds. Part 1. Chemical,

Environmental and Experimental Data. IARC

Monographs on the Evaluation of the

Carcinogenic Risk of Chemicals to Humans.

Lyon, France, Vol. 33, 1983.

International Agency for Research on Cancer.

Propylene oxide. Some Industrial Chemicals. IARC

Monographs on the Evaluation of the

Carcinogenic Risks of Chemicals to Humans.

Lyon, France, 60:181-213, 1994b.

Chapter 05 11/19/01 11:10 AM Page 188
Chapter 5

189

International Agency for Research on Cancer. Radon.

Man-Made Mineral Fibres and Radon. IARC

Monographs on the Evaluation of Carcinogenic

Risks to Humans. Lyon, France. 43:173-254,

1988.

International Agency for Research on Cancer.

Styrene. Some Industrial Chemicals. IARC

Monographs on the Evaluation of Carcinogenic

Risks to Humans. Lyon, France, 60:233-320,

1994d.

International Agency for Research on Cancer.

Tobacco Smoking. IARC Monographs on the

Evaluation of Carcinogenic Risks to Humans.

Lyon, France. Vol 38, 1986a.

International Agency for Research on Cancer. 1,3-

Butadiene. Re-evaluation of Some Organic

Chemicals, Hydrzine, and Hydrogen Peroxide. IARC

Monographs on the Evaluation of the

Carcinogenic Risks to Humans. Lyon, France,

71:109-225, 1999a.

International Agency for Research on Cancer.

Acetaldehyde. Re-evaluation of Some Organic

Chemicals, Hydrazine, and Hydrogen Peroxide. IARC

Monographs on the Evaluation of the

Carcinogenic Risks to Humans. Lyon, France,

71:319-344, 1999b.

International Committee for Cigar Smoke Study:

Machine smoking of cigars. Bulletin du

Information CORESTA 1: 31-34, 1974.

International Standards Organization. Routine

Analytical Cigarette Smoking Machine: Part I.

Specifications and Standard Conditions. Geneva,

Switzerland: ISO, 3308, 1991.

Ishiguro, S., Sugawara, S. The Chemistry of Tobacco

Smoke (Japanese). (English translation 1981, 247

p.) Central Institute, Japanese Tobacco

Monopoly Corporation, Yokahama, Japan, 1980,

202 p.

Jenkins, R.W.J., Neroman, P.H., Charms, M.D.

Cigarette smoke formation. II. Smoke distribuion and mainstream pyrolytic composition of

added 14C-menthol (U). Beitrage zur

Tabakforschung International 5:299-301, 1970.

John, A.L. Japan. Always something new. Tobacco

International, p. 30-35, August 1996.

Kagan, M.R., Cunningham, J.A., Hoffmann, D.

Propylene glycol. A precursor of propylene oxide

in cigarette smoke. 53rd Tobacco Science

Research Conference, Abstract #41 and #42,

1999.

Kensler, C.J., Battista, S.P. Chemical and physical factors affecting mammalian ciliary activity.

American Review of Respiratory Disease 93(3):93-

102, 1966.

Kite, G.F., Gellatly, G., Uhl, R.G. Method for removal

of potassium nitrate from tobacco extracts. U. S.

Patent 4,131,117, December 26, 1978. 1978.

Leffingwell, J.C. (ed.). Chemical and sensory aspects

of tobacco flavor. Recent Advances in Tobacco

Science 14:1-218, 1987.

Leuchtenberger, C., Leuchtenberger, R. Effects of

chronic inhalation of whole fresh cigarette

smoke and of its gas phase on pulmonary

tumorigenesis in Snell’s mice. Morphology of

Experimental Respiratory Carcinogenesis. Proceedings

of a Biology Division, Oak Ridge National

Laboratory, Conference, Gatlinburg, Tennesee, May

13-16, 1970. Nettesheim, P., Hanna, Jr., M.G.,

Deatherage, Jr., J.W. (Editors.). Washington, D.C.:

U.S. Atomic Energy Commission, pp. 329-346,

1970.

Leuchtenberger, C., Leuchtenberger, R., Doolin, P.T.

A correlated histological, cytological, and cytochemical study of tracheobronchial tree and

lungs of mice exposed to cigarette smoke. Cancer

11:490-506, 1958.

Lewis, C.I. The effect of cigarette construction

parameters on smoke generation and yield.

Recent Advances in Tobacco Science 16:73-101,

1992.

Lyerly, L.A. Direct vapor chromatographic determination of menthol, propylene glycol, nicotine

and triacetin in cigarette smoke. Tobacco Science

11:49-51, 1967.

Miller, J.E. Determination of the components of pipe

tobacco smoke by means of a new pipe smoking

machine. Proceedings of the 3rd World Tobacco

Congress, Salisbury, Rhodesia, CORESTA,

February 1963, p. 11.

Mohr, U., Reznik, G. Tobacco carcinogenesis.

Pathogenesis and Therapy of Lung Cancer. C.C.

Harris (Editor). Marcel Dekker, Inc., New York,

pp. 263-361, 1978.

Moody, P.M. The relationships of qualified human

smoking behavior and demographic variables.

Social Science & Medicine 14A:49-54, 1980.

Mühlbock, O. Carcinogenicity of cigarette smoke in

mice (Dutch). Nederlands Tijdschrift voor

Geneeskunde 99: 2276-2278, 1958.

National Cancer Institute. Tar and Less Hazardous

Cigarettes. First Set of Experimental Cigarettes.

Smoking and Health Program. DHEW Publication

No. (NIH) 76-905. 148 pages, 1977a.

National Cancer Institute. Toward Less Hazardous

Cigarettes. Second Set of Experimental Cigarettes.

Smoking and Health Program. DHEW Publication

No. (NIH) 76-111. 153 pages, 1977b.

National Cancer Institute. Smoking and Health

Program. Toward Less Hazardous Cigarettes. Third

Set of Experimental Cigarettes. DHEW Publication

No. (NIH) 77-1280, 152 pages, 1977c.

National Cancer Institute. Toward Less Hazardous

Cigarette. Fourth Set of Experimental Cigarettes.

Smoking and Health Program. DHEW Publication

No. (NIH) 80. 213 pages, 1980.

National Cancer Institute. Cigars: Health Effects and

Trends. Smoking and Tobacco Control

Monograph No. 9. Burns, D.M., Hoffmann, D.,

Cummings, K.M. (Editors.). U.S. DHHS, Public

Health Service, NIH-NCI. NIH Publ. No. 98-1302,

Bethesda, MD. 232 pages, 1998.

Chapter 05 11/19/01 11:10 AM Page 189
Smoking and Tobacco Control Monograph No. 13

190

Neurath, G.B. Nitrosamine formation from precursors in tobacco smoke. N-Nitroso Compounds.

Analysis and Formation. Bogovski, P., Preussmann,

R., Walker, E.A. (Editors.). International Agency

for Research on Cancer. Lyon, France, IARC Sci.

Publ. 3: 134-136, 1972.

Neurath, G., Ehmke, H. Studies on the nitrate content of tobacco. [German]. Beiträge zur

Tabakforschung International 2:333-344, 1964.

Nil, R., Buzzi, R., Bättig, K. Effect of different cigarette smoke yields on puffing and inhalation. Is

the measurement of inhalation volumes relevant

for smoke absorption? Pharmacology, Biochemistry,

and Behavior 24(3):587-595, 1986.

Norman, V., Ihrig, A.M., Larson, T.M., Moss, B.L. The

effect of nitrogenous blend components on

NO/NOX and HCN levels in mainstream and

sidestream smoke. Beiträge zur Tabakforschung

International 12:55-62, 1983.

Norman, V., Ihrig, A.M., Shoffner, R.A., Ireland, M.S.

The effect of tip dilution on the filtration efficiency of upstream and downstream segments of

cigarette filters. Beiträge zur Tabakforschung

International 12:178-185, 1984.

Otto, H. Inhalation studies with mice exposed passively to cigarette smoke. (German) Frankfurter

Zeitschrift für Pathologie 73:10-23, 1963.

Patrianakos, C., Hoffmann, D. Chemical studies on

tobacco smoke. LXIV. On the analysis of aromatic amines in cigarette smoke. Journal of Analytical

Toxicology 3:150-154, 1979.

Pauly, J.L., Lee, H.J., Hurley, E.L., Cummings, K.M.,

Lesser, J.D., Streck, R.J. Glass fiber contamination

of cigarette filters: an additional health risk to

the smoker? Cancer Epidemiology, Biomarkers &

Prevention 7(11):967-979, 1998.

Peel, D.M., Riddick, M.G., Edwards, M.E., Gentry,

J.S., Nestor, T.B. Formation of Tobacco Specific

Nitrosamines in Flue-cured Tobacco. Presented at

the 53rd Tobacco Science Research Conference.

Montreal, Quebec, Canada. September 12–15,

1999.

Peele, D.M., Riddick, M.G., Edwards, M.E., Gentry,

J.S., Nestor, N. Formation of tobacco-specific

nitrosamines in flue-cured tobacco. Recent

Advances in Tobacco Science 27: 3-12, 2001.

Peeler, C.L., Butters, G.R. Correspondence re: "It’s

time for a change: cigarette smokers deserve

meaningful information about their cigarettes.

Journal of the National Cancer Institute 92(10):842,

2000.

Philippe, R.J., Hackney, E. The presence of nitrous

oxide and methyl nitrite in cigarette smoke and

tobacco pyrolysis gases. Tobacco Science 3:139-

143, 1959.

Pillsbury, H.C., Bright, C.C., O’Connor, K.J., Irish,

F.W. Tar and nicotine in cigarette smoke. Journal

of the Association of Official Analytical Chemists

52:458-462, 1969.

R. J. Reynolds Tobacco Company. New Cigarette

Prototypes That Heat Instead of Burn Tobacco.

Chemical and Biological Studies. Reynolds Tobacco

Co., Winston-Salem, NC. 744 pages, 1988.

Roberts, D.L. Natural tobacco flavor. Recent Advances

in Tobacco Science 14:49-81, 1988.

Roberts, D.L., Rowland, R.L. Macrocyclic diterpenes,

a- and b- 4, 8, 13-duvatriene-1,3-diol from tobacco. Journal of Organic Chemistry 27:3989-3995,

1962.

Roe, J.F.C., Salaman, M.H. Cohen, J., Burgan, J.C.

Incomplete carcinogens in cigarette smoke condensate. Tumor promotion by phenolic fraction.

British Journal of Cancer 13:623-633, 1959.

Rose, J.E., Levin, E.D. (Eds.). Eclipse and the Harm

Reduction Strategy for Smoking. Conference, Duke

University, Bryan Center, Durham, N.C., August

23, 1996.

Russell, M.A.H. Low-tar, medium nicotine cigarettes:

A new approach to safer smoking. British Medical

Journal 6023:1430-1433, 1976.

Russell, M.A.H. The case for medium-nicotine, lowtar, low-carbon monoxide cigarettes. Banbury

Report 3. Cold Spring Harbor, Cold Spring Harbor

Laboratory, NY, pp. 297-310, 1980.

Schultz, W., Seehofer, F. Smoking behavior in

Germany. The analysis of cigarette butts. In.

Smoking Behavior, Physiological and Psychological

Influences. Thornton, R.E. (Editor.). Edinburgh,

Churchill Livingston, pp. 259-276, 1978.

Schumacher, J.N. The isolation of 6-O-acetyl-2, 3, 4-

tri-O-[(+)-3 methylvaleryl]-b-D-glucopyranose

from tobacco. Carbohydrate Research 13:1-8, 1970.

Senkus, M. (ed.). Leaf composition and physical

properties in relation to smoking quality and

aroma. Recent Advances in Tobacco Science 2:1-

135, 1976.

Shepherd, R.J.K. New charcoal filters. Tobacco

Reporter 121(2):10-14, 1994.

Sims, J.L., Atkinson, W.D., Benner, P. Nitrogen fertilization and genotype effects of selected constituents from all-burley cigarettes. Tobacco

Science 23:11-13, 1975.

Singer, B, Essigmann, J.M. Site-specific mutagenesis:

Retrospective and prospective. Carcinogenesis

12(6):945-955, 1991.

Smith, C.J., McCarns, S.C., Davis, R.A., Livingston,

S.D., Bombick, B.R., Avolos, J.T., Morgan, W.T.,

Doolittle, D.J. Human urine mutagenicity study

comparing cigarettes which burn or primarily

heat tobacco. Mutation Research 361(1):1-9, 1996.

Society for Research on Nicotine and Tobacco. Policy

committee urges regulation on Eclipse. SRNT

Newslett. 6(2-3), 21-22, 2000.

Spears, A.W. Effect of manufacturing variables in cigarette smoke composition CORESTA Bull.,

Montreux, Switzerland, Symp. p. 6, 1974.

Spears, A.W. Selective filtration of volatile phenolic

compounds from cigarette smoke. Tobacco Science

7:76-80, 1963.

Chapter 05 11/19/01 11:10 AM Page 190
Chapter 5

191

Spears, A.W., Jones, S.T. Chemical and physical criteria for tobacco leaf of modern day cigarettes.

Recent Advances in Tobacco Science 7:19-39, 1981.

Stedman, R.L., Burdick, D., Schmeltz, I. Composition

studies on tobacco. XVII. Steam-smoke, volatile

acid fraction of cigarette. Tobacco Science 7:166-

169, 1963.

Stellman, S.D., Muscat, J.E., Thompson, S.,

Hoffmann, D., Wynder, E.L. Risk of squamous

cell carcinoma and adenocarcinoma of the lung

in relation to lifetime filter cigarette smoking.

Cancer 80(3):362-368, 1997.

Stiles, M.F., Guy, T.D., Morgen, W.T., Edwards, D.W.,

Davis, R.W., Robinson, J.H. Human smoking

behavior study. ECLIPSE cigarette compared to

usual brand. Toxicologist 48:119-120, 1999.

Terpstra, P.M., Renninghaus, W., Solana, R.P.

Evaluation of the electrically heated cigarette.

S.O.T. 1998 Annual Meeting, The Toxicologist.

Abstract Issues Toxicological Sciences 42(1S): 295;

#1452, 1998.

Terrell, J.H., Schmeltz, I. Alteration of cigarette

smoke composition. II. Influence of cigarette

design. Tobacco Science 14:82-85, 1970.

Tiggelbeck, D. Vapor phase modification. An underutilized technology. Proc. 3rd World Conference on

Smoking and Health. Vol. 1, Modifying the Risk for

the Smoker. DHEW Publication No. (NIH) 76-

1221. pp. 507-514, 1976.

Törnqvist, M., Osterman-Golkar, S., Kautiainen, A.,

Jensen, S., Farmer, P.B., Ehrenberg, L. Tissue

doses of ethylene oxide in cigarette smokers

determined from adduct levels in hemoglobin.

Carcinogenesis 7(9):1519-1521, 1986.

Tso, T.C. Production, Physiology and Biochemistry of

Tobacco Plant. Beltsville, MD, Ideals, 753 pages,

1990.

Tso, T.C., Chaplin, J.P., Adams, J.D., Hoffmann, D.

Simple correlation and multiple regression

among leaf and smoke characteristics of burley

tobaccos. Beiträge zur Tabakforschung International

11:141-150, 1982.

Tsuda, M., Kurashima, Y. Tobacco smoking, chewing

and snuff dipping. Factors contributing to the

endogenous formation of N-nitroso compounds.

Critical Reviews in Toxicology 21(4):243-253, 1991.

U.S. Consumer Product Safety Commission.

Practicability of Developing a Performance Standard

to Reduce Cigarette Ignition Propensity. Vol. 1,

U.S.C.P.S.C., Washington, D.C., 30 pages, 1993.

U.S. Department of Health and Human Services.

Reducing the Health Consequences of Smoking. 25

Years of Progress. A Report of the Surgeon General.

Anonymous. Massachusetts disputes claims

about Eclipse cigarettes. Tobacco Reporter 127

(No. 11):11-13, 2000.

Vincent, R.G., Pickren, J.W., Lane, W.W., Bross, I.,

Takita, H., Haten, L., Gutierrez, A.C., Rzepka, T.

The changing histopathology of lung cancer.

Cancer 39(4):1647-1655, 1977.

Voges, E. Tobacco Encyclopedia. Tobacco Journal

International, Mainz, Germany. 468 pages, 1984.

Waltz, P., Häusermann, M. Modern cigarettes and

their effects on the smoking habits and on the

composition of cigarette smoke (in German).

Zeitschrift fur Präventivmedizin 8:3-98, 1963.

Wilkenfeld, J., Henningfield, J., Slade, J., Burns, D.,

Pinney, J. It’s time for a change: cigarette smokers deserve meaningful information about their

cigarettes. Journal of the National Cancer Institute

92(2):90-92, 2000a.

Wilkenfeld, J., Henningfield, J., Slade, J., Burns, D.,

Pinney, J. Response to correspondence re: "It’s

time for a change: cigarette smokers deserve

meaningful information about their cigarettes".

Journal of the National Cancer Institute 92(2):842-

843, 2000b.

Wittekindt, W. Changes in recommended plant protection agents for tobacco. Tobacco Journal

International 5:390-394, 1985.

Wynder, E.L., Graham, E.A. Tobacco smoking as a

possible etiologic factor in bronchiogenic carcinoma. A study of six hundred and eighty-four

proved cases. Journal of the American Medical

Association 143:329-336, 1950 (reprinted Journal

of the American Medical Association 253(20)2986-

94). 

Wynder, E.L., Graham, E.A., Croninger, A.G.

Experimental production of carcinoma with cigarette tar. Cancer Research 13:855-864, 1953.

Wynder, E.L., Hoffmann, D. Some practical aspects

of the smoking—Cancer problem. New England

Journal of Medicine 262:540-545, 1960.

Wynder, E.L., Hoffmann, D. A study of tobacco carcinogenesis. VIII. The role of acidic fractions as

promoters. Cancer 14:1306-1315, 1961.

Wynder, E.L., Hoffmann, D. A study of air pollution

carcinogenesis. III. Carcinogenic activity of gasoline engine exhaust. Cancer 152:103-108, 1962.

Wynder, E.L., Hoffmann, D. A contribution to experimental tobacco carcinogenesis. (In German).

Deut. Med. Wochenschr. 88:623-628, 1963.

Wynder, E.L., Hoffmann, D. Reduction of tumorigenicity of tobacco smoke. An experimental

approach. Journal of the American Medical

Association 192:85-94, 1965.

Wynder, E.L., Hoffmann, D. Tobacco and Tobacco

Smoke. Studies in Experimental Carcinogenesis.

New York: Academic Press, 730 pages, 1967.

Wynder, E.L., Hoffmann, D. Smoking and lung cancer: scientific challenges and opportunities.

Cancer Research 54(20):5284-5295, 1994.

Wynder, E.L., Kopf, P., Ziegler, H. A study of tobacco

carcinogenesis. II. Dose-response studies. Cancer

10:1193-1200, 1957.

Wynder, E.L., Mann, J. A study of tobacco carcinogenesis III. Filtered cigarettes. Cancer 10:1201-

1205, 1957.

Chapter 05 11/19/01 11:10 AM Page 191
Smoking and Tobacco Control Monograph No. 13

192

Chapter 05 11/19/01 11:10 AM Page 192
INTRODUCTION Few members of the public understand the probabilities and

odds that form the vocabulary scientists use to discuss risk (Weinstein,

1999). Thus, lay people rely upon other cues, such as the cigarette labels

‘Light’ and ‘Ultra Light’, to help them make decisions about smoking and

other hazards (see Chapter 7). This chapter examines public perceptions of

Light cigarettes, reasons for smoking Lights, and the relationship between

smoking Lights and quitting.

The labels ‘Light’ and ‘Ultra Light’, when applied to cigarettes, imply a variety of benefits. These include lower levels

of tar and nicotine, less risk to health, and milder taste. Cigarette advertising, including the way in which these labels are used in the advertising, further modifies and shapes public perceptions of these products. What ‘Light’

and ‘Ultra Light’ come to mean to members of the public is an empirical

question that can be revealed by careful survey research.

A substantial portion of smokers believe that low-tar cigarettes are less

risky than Regular cigarettes. For example, a nationwide 1987 survey

(Giovino et al., 1996, p. 49) found that 45.7 percent of Ultra-Light smokers,

32.2 percent of Light smokers, and 29.4 percent of Regular smokers said

that low-tar cigarettes reduce the risk of cancer. Nevertheless, smokers’

knowledge about low-tar cigarettes is quite limited.

In 1995, a random sample of 12,371 Canadians adults were asked by

telephone interviewers what the word “light” means in relation to cigarettes (Health Canada, 1995). The most frequently mentioned topics were:

“less tar” (20.1 percent), “less nicotine” (36.2 percent), “safer” or “less

addictive” (3.2 percent), “milder taste” (6.7 percent), “different filter” (2.3

percent), and “nothing” or “ad gimmick” (14.1 percent). A further 21.2 percent had no idea what the term meant. The meanings ascribed to “light”

were generally similar among various subgroups of smokers, although former and never smokers were more likely than current smokers to say that

they had no idea what the term meant (17.8 percent and 28.7 percent versus 12.2 percent, respectively), and former smokers were more likely than

current and never smokers to state that “light” was a meaningless advertising term (22.2 percent versus 16.0 percent and 10.6 percent, respectively).

A 1994 national random telephone survey found that 95% of regular

smokers could identify that they were “somewhat certain” or “very certain”

that they smoked a Regular, Light, or Ultra-Light cigarette (Kozlowski et al.,

1998a & b). However, when asked how much tar their cigarettes contained,

PERCEPTIONS OF

LIGHT CIGARETTES

193

Public Understanding of Risk and

Reasons for Smoking Low-Yield

Products 

Neil D. Weinstein

Chapter 06 11/19/01 11:14 AM Page 193
few smokers knew the answer to this question. For example, Cohen (1996a,

p. 128) reported that 79% of smokers answered that they did not know the

answer to the question. Comparing the estimates given by smokers to the

actual figures for their brands, Kozlowski and colleagues (1998b) found that

only 3% of smokers could correctly state (within 2 mg) the amount of tar in

their cigarettes. In fact, few knew where to look to learn the tar content

(Kozlowski et al., 1998b). Although 67% of smokers said that they would

look on their cigarette package to find the tar content, only 6.3% of cigarettes sold have this information on the package. When asked how many

Light cigarettes someone would have to smoke to get the same amount of

tar as from one Regular cigarette, the most common response from about

half of those surveyed was, “don’t know”; about 40 percent said two cigarettes or more and less than 10 percent said one cigarette (Kozlowski et al.,

1998a).

There are significant differences in knowledge and reported use of tar

numbers among different types of smokers. For example, when Ultra-Light,

Light, and Regular cigarettes were compared, the members of the first group

were found to be somewhat more accurate about their cigarette’s tar number (Kozlowski et al., 1998b). Accuracy was shown by 17% of Ultra-Light

smokers, 2% of Light smokers, and 1% of Regular smokers. Ultra-Light

smokers were also much more likely to say they used this number in making judgments about cigarette safety (Cohen, 1996a, p. 132). Thus,

although only 14% of Cohen’s overall sample said that they used tar numbers to make such judgments, 56% of the smokers of 1- to 5-mg tar cigarettes said that they determined safety from advertised tar values. UltraLight smokers also saw a much bigger difference between the risk of Regular

and Light cigarettes than did other smokers (Cohen, 1996a, p. 130). A large

majority (83%) of Ultra-Light smokers said that switching from a 20-mg to

a 5-mg tar cigarette would significantly reduce health risks, whereas only

about 50% of other smokers shared this belief.

Clearly, knowledge about the reported tar values of their chosen brands,

about where these values can be found, and about vent holes in cigarettes is

largely absent among smokers. Of particular importance is the finding that

a large proportion of smokers believe that switching to a lower tar cigarette

reduces one’s health risks, and since most smokers are only aware of a cigarette’s advertised type—‘Regular’, ‘Light’, or ‘Ultra Light’— and not its tar

number, this classification is used as a surrogate to indicate risk. Attention

to tar numbers is particularly true among Ultra-Light smokers, a majority of

whom say they use these numbers to judge a cigarette’s safety.

A variety of studies have asked smokers about their

reasons for choosing to smoke Light or Ultra Light cigarettes or their reasons for switching to such cigarettes. The results show that the desire to reduce disease risk is one of the

main factors guiding these choices. Although it would be desirable to distinguish in this section between initial cigarette choices, switching as a prelude to quitting, switching as a substitute for quitting, and switching following an unsuccessful quit attempt, the available data do not permit such a

fine-grained analysis. In the 1987 National Health Interview Survey

REASONS FOR SMOKING

OR SWITCHING TO LIGHT

CIGARETTES

194

Smoking and Tobacco Control Monograph No. 13

Chapter 06 11/19/01 11:14 AM Page 194
(Giovino et al., 1996, p. 45), 44 percent of current smokers said that they

had at some time switched to a low-tar/low-nicotine cigarette in order to

reduce their health risk. Similarly, a national survey found that about 60

percent of Ultra-Light smokers and approximately 40 percent of Light

smokers said that they smoked reduced-tar cigarettes “to reduce the risks of

smoking without having to give up smoking” (Kozlowski et al., 1998a)

In this same national telephone survey, the reasons given by current

daily smokers for why they chose to smoke Ultra-Light/Light cigarettes

were: step toward quitting (49/30 percent), reduce risk (58/39 percent),

reduce tar (73/57 percent), reduce nicotine (72/50 percent), and prefer the

taste (69/80 percent) (Kozlowski et al., 1998a). Very similar figures were

obtained in telephone interviews of 266 randomly selected Massachusetts

smokers (Kozlowski et al., 1998a). In a recent experiment involving a randomly selected sample of 568 smokers of Light cigarettes, the reasons given

for smoking Light cigarettes by people in the control or delayed intervention groups were: step toward quitting (25 percent), reduce risk (43 percent), reduce tar or nicotine (70 percent), and prefer taste (81 percent)

(Kozlowski et al., 1999). In these same groups, 39 percent said that Light

cigarettes decreased their risk of having health problems. 

A national survey of adolescents and young adults in 1993 found somewhat less of an emphasis on health issues, with smokers of Light or UltraLight cigarettes saying that they chose their brand because of taste (33 percent), because they were less irritating (29 percent), because they were

healthier than other brands (21 percent), and because they “just liked

them” (19 percent) (Giovino et al., 1996, p. 49).

Not surprisingly, national survey of adults in 1986 showed that those

who have ever switched in order to reduce tar or nicotine are more likely

than those who never switched to believe that some brands are more hazardous than others (54 percent versus 40 percent, respectively) and to

believe that their current brand is less hazardous than other brands (33 percent versus 16 percent, respectively) (Giovino et al., 1996, p. 50). Although

most smokers recognize that smoking is risky to one’s health, those who

chose Light and Ultra-Light cigarettes are more likely to acknowledge the

risk than smokers of Regular cigarettes. For example, 85 percent of those

who had switched to lower tar/nicotine brands said they were concerned

about the health effects of smoking, compared to 70 percent of those who

had never made this switch (Giovino et al., 1996, p. 50). People who had

switched were also more likely to say that their health had been affected by

smoking and that a doctor had advised them to quit (Giovino et al., 1996,

p. 48).

Similarly, when the previously mentioned Canadian smokers were asked

about the likelihood of developing health problems such as emphysema,

asthma, lung cancer, or stroke from smoking for many years, those who

had switched from Regular to Light cigarettes cited more problems as very

likely than those who started and continued smoking Regular cigarettes

(2.13 v. 1.94 problems, respectively) (data from Health Canada, 1995).

195

Chapter 6

Chapter 06 11/19/01 11:14 AM Page 195
Overall, the data are consistent in showing that smokers of Light and

Ultra-Light cigarettes are especially concerned about protecting their health.

The majority of these smokers choose Light or Ultra-Light cigarettes in the

belief that this will reduce their health risks and/or make it easier to quit.

Smokers of low-yield cigarettes not only express

greater concern about the risks of smoking, but they

also show more interest in quitting. In fact, 38 percent of the smoker

respondents to the 1987 National Health Interview Survey who switched to

Light cigarettes saw this change as a step toward quitting (Giovino et al.,

1996, p. 49), and people who smoked Light or Ultra-Light cigarettes tended

to have tried more quitting strategies than those who smoked Regular cigarettes (Giovino et al., 1996, p. 51). Among those smokers who had never

attempted to quit, smokers of low-tar cigarettes were more likely to say that

they had considered quitting.

Similar interest in both quitting and healthy behavior comes from a

study of U.S. Air Force trainees (Haddock et al., 1999). These researchers

reported that individuals who said that they had "switched to a lower

tar/nicotine cigarette just to reduce their health risk" were more likely to

have experienced a successful 24-hour quit attempt in the past, had more

healthy diets, and were less likely to take other kinds of risks. These switchers were also less likely to say that they were addicted to cigarettes.

However, there are no data that show switching to reduced-tar cigarettes increases the likelihood of quitting. In fact, given the perceived

reduction in risk from smoking Light cigarettes, a switch to such brands

may well weaken the motivation to quit. In the Health Canada survey, 32.0

percent of those who started with, and continued to, smoke Light cigarettes

made a quit attempt in the previous 3 months, compared to 15.1 percent of

those who started with, and continued to, smoke Regular cigarettes. But of

those who started with Regular cigarettes and were currently Light cigarette

smokers, only 16.7 percent had tried to quit recently (data from Health

Canada, 1995).

A large 1986 national study of adults in the United States who had ever

smoked found that those who smoked low-yield cigarettes, regardless of

whether they had ever switched to lower yield cigarettes, were less likely to

have quit than those who smoked high-yield brands (Giovino et al., 1996,

p. 49). Persons who had ever switched brands to reduce their level of tar

and nicotine also were less likely to have quit than those who had never

switched brands to reduce their level of tar and nicotine.

When Air Force trainee smokers—who had been required to abstain

from smoking throughout their basic military training—were contacted 12

months later, only 12.5 percent of switchers and 11.1 percent of nonswitchers were still abstinent (Haddock et al., 1999). Controlling for demographic

factors and smoking history, this difference was not statistically significant

(odds ratio = 1.04, p > .5). Among Air Force trainees, switchers did report

THE RELATIONSHIP OF

SWITCHING TO QUITTING

196

Smoking and Tobacco Control Monograph No. 13

Chapter 06 11/19/01 11:14 AM Page 196
smoking fewer cigarettes than nonswitchers. However, in the 1995 Health

Canada survey, people who had started smoking Regular cigarettes and currently smoked Light cigarettes did not smoke fewer cigarettes per day than

those who stayed with Regular cigarettes.

Thus, even among individuals who had switched specifically because

they were concerned about health risks, who had been assisted in long-term

quitting by a mandatory abstinence period, or who said they were less

addicted to cigarettes than did the nonswitchers, the switch to Light cigarettes prior to the abstinence period did not help them stay abstinent.

Switching to Light cigarettes does not seem to be any more of a route

toward quitting than simply staying with Regular cigarettes.

Thus, no data exist that indicate switching to Light or Ultra-Light cigarettes actually assists smokers in quitting.

SUMMARY Overall, the accumulated data are quite consistent. They show that

many consumers use the terms ‘Light’ and ‘Ultra Light’ as a guide to the

riskiness of particular brands of cigarettes. To a considerable extent, smokers

choose Light and Ultra-Light brands because they think that these cigarettes

are not as harmful and cause fewer health problems. Particularly, individuals who are most concerned about smoking risks and most interested in

quitting adopt low-yield brands.

To determine whether switching helps people to smoke less or to quit,

one would ideally examine two groups with the same interest in quitting

and the same smoking history. One would compare the group that

switched with the group that did not, looking at both cessation and smoking rates over time. In reality, however, those who switch are different from

nonswitchers in numerous ways, all of which should facilitate their quitting

and reduce the amount that they smoke. Despite these facilitating factors,

the data show that switchers to a Light or Ultra-Light cigarette are not more

likely to become nonsmokers than are nonswitchers.

Surveys indicate that switching to low-yield cigarettes is viewed by

many smokers as a healthier choice. Given the interest in quitting among

those who make this choice, their failure to quit at rates any higher than

those who do not switch suggests that switching reduces the motivation to

stop smoking. Thus, the advertising of brands designated as ‘Light’ or ‘Ultra

Light’ misleads smokers as to the benefits these brands offer.

The data collected since publication of the 1996 NCI monograph only

reinforce the conclusion reached by Giovino and colleagues (1996) in that

volume that the existence of so called ‘Light’ and ‘Ultra Light’ cigarettes has

kept many smokers interested in protecting their health from quitting.

“The net effect of the introduction and mass marketing of these brands,

then, may have been and may continue to be an increased number of

smoking-attributable deaths.”(Giovino et al., 1996.)

197

Chapter 6

Chapter 06 11/19/01 11:14 AM Page 197
Cohen, J.B. Consumer/smoker perceptions of Federal

Trade Commission Tar Ratings. The FTC Cigarette

Test Method for Determining Tar, Nicotine, and

Carbon Monoxide Yields of U.S. Cigarettes. Report of

the NCI Expert Committee. Smoking and Tobacco

Control Monograph No. 7. U.S. Department of

Health and Human Services, National Institutes

of Health, National Cancer Institute, NIH

Publication No. 96-4028, 1996a.

Cohen J. B. Smokers’ knowledge and understanding

of advertised tar numbers: Heath policy implications. American Journal of Public Health 86:18-24,

1996b.

Giovino, G.A., Tomar, S.L., Reddy, M.N., Peddicord,

J.P., Zhu, B., Escobedo, L.G., Eriksen, M.P.

Attitudes, knowledge, and beliefs about low-yield

cigarettes among adolescents and adults. The

FTC Cigarette Test Method for Determining Tar,

Nicotine, and Carbon Monoxide Yields of U.S.

Cigarettes. Report of the NCI Expert Committee.

Smoking and Tobacco Control Monograph No.

7. U.S. Department of Health and Human

Services, National Institutes of Health, National

Cancer Institute, NIH Publication No. 96-4028,

1996.

Haddock, C.K., Talcott, G.W., Klesges, R.C., Lando,

H. An examination of cigarette brand switching

to reduce health risks. Annals of Behavioral

Medicine 21(2):128–134, 1999. 

Health Canada. Survey on Smoking in Canada. Cycle 4.

Ottawa: Health Canada, June, 1995.

Kozlowski, L.T., Goldberg, M.E., Yost, B. A., White,

E.L., Sweeney, C. T., Pillitteri, J.L. Smokers’ misperceptions of light and ultra-light cigarettes

may keep them smoking. American Journal of

Preventive Medicine 15:9–16, 1998a.

Kozlowski, L.T., Goldberg, M.E., Yost, B.A., Ahern,

F.M., Aronson, K.R. Smokers are unaware of the

filter vents now on most cigarettes: Results of a

national survey. Tobacco Control 5:265–270, 1996.

Kozlowski, L.T., Goldberg, M.E., Sweeney, C.T.,

Palmer, R.F., Pillitteri, J.L. Yost, B.A., White, E.L.,

Stine, M.M. Smoker reactions to a "radio message" that Light cigarettes are as dangerous as

regular cigarettes. Nicotine and Tobacco Control

1:67-76, 1999.

Kozlowski, L.T., Pillitteri, J.L., Ahern, F.M., Yost, B.A.,

Goldberg, M.E. Advertising fails to inform smokers of official yields of cigarettes. Journal of

Applied Biobehavioral Research 3:55-64, 1998b.

Kozlowski, L.T., White, E.L., Sweeney, C.T., Yost,

B.A., Ahern, F.M. Goldberg, M.E. Few smokers

know their cigarettes have filter vents. American

Journal of Public Health 88:681–682, 1998c.

Weinstein, N.D. What does it mean to understand a

risk? Dimensions of risk comprehension. Journal

of the National Cancer Institute—Monograph

25:15–20, 1999.

REFERENCES

CONCLUSIONS

1. Many consumers use the terms ‘Light’ and ‘Ultra-Light’ as a guide to

the riskiness of particular brands of cigarettes.

2. Many smokers choose Light and Ultra-Light brands because they

believe that such cigarettes are less likely to cause health problems. 

3. Individuals who are most concerned about smoking risks and most

interested in quitting adopt low-yield brands.

198

Smoking and Tobacco Control Monograph No. 13

Chapter 06 11/19/01 11:14 AM Page 198
INTRODUCTION During the early 1950s, scientific and popular articles that presented lung cancer research findings initiated what the tobacco industry

termed the “health scare,” as consumers became increasingly concerned

about the potential health risks incurred from smoking. Companies initially

responded to this health scare by introducing filtered products that were

accompanied by advertisements with explicit health-related statements. For

example, Viceroy® maintained that it provided “Double-Barreled Health

Protection” and also claimed that it was “Better for Your Health” in ad

copy. 

In time, the industry became aware that explicit health claims had the

undesirable effects of making health concerns salient or predominant in the

minds of consumers, and encouraged consumers to use “healthfulness” as

the criterion by which they judged cigarettes. Motivation researchers and

other trade analysts advised the industry to shift from explicit verbal assertions of health toward implied healthfulness, an approach that incorporated the use of visual imagery (Pollay, 1989a). 

January of 1964 marked the release of the first Surgeon General’s Report

on smoking, and this event reawakened public concerns about the potential

health consequences of smoking. Tobacco manufacturers needed to reduce

consumer concerns and the ensuing anxious feelings. Quitting was not an

easy option for smokers because nicotine is highly addictive. Switching to a

lower (tar and nicotine) yield cigarette became an attractive alternative for

many smokers once they were convinced by advertising that this would be

a meaningful step toward health and away from risk. Thus, there was a

ready market for “new and improved” cigarettes, or at least for those that

seemed to be that way. 

This chapter will review recently released documents from the tobacco

industry and its consultants, produced during litigation, as well as excerpts

from the relevant trade press, for insights into the firms’ intentions and

actions in marketing their products. Particular attention will be paid to the

period of the mid-1970s, the launch period for most of the new generation

of low-yield products. It will be shown that advertising for reduced-yield

products led consumers to perceive filtered and low-tar delivery products as

safer alternatives to regular cigarettes. 

199

Marketing Cigarettes with Low

Machine-Measured Yields

Richard W. Pollay, Timothy Dewhirst

Chapter 07 11/19/01 11:18 AM Page 199
Advertising during the 1950s promoted filters as the technological fix to the health scare. Filters were heralded with various

dramatic announcements featuring ‘news’ about: scientific discoveries; modern pure materials; research and development

breakthroughs; certification by the United States Testing Company; implied

endorsement by the American Medical Association (see Figure 7-1); “miracle

tip” filters; and descriptions of “20,000 filter traps” or filters made of activated charcoal, “selectrate,” “millecel,” “cellulose acetate” or “micronite”

that were variously described as effective, complete, superior, and producing

mildness, gentleness, smoothness, etc. 

In 1958, for example, a press conference was held at New York’s Plaza

Hotel to launch Parliament® and its new filter, called “Hi-Fi” (“high filtration,” as in high-fidelity state-of-the-art sound reproduction of the 1950s). 

“In the foyers, test tubes bubbled and glassed-in machines

smoked cigarettes by means of tubes. Men and women in long

white laboratory coats bustled about and stood ready to answer any

questions. Inside, a Philip Morris executive told the audience of

reporters that the new Hi-Fi filter was an event of ‘irrevocable significance’. The new filter was described as ‘hospital white’.” (See

Whelan, 1984, p.90) 

The purported product benefit of this new filtration was obviously the

perceived reduction, if not elimination, of cancer and other health risks.

Health benefits were implied through various slogans, such as “Just What

the Dr. Ordered” (L&M®), “Inhale to your Heart’s Content” (Embassy®),

“The Secret to Life is in the Filter” (Life®), “Extra Margin” (of safety protection; analogy to helmets, seat belts, and other safety gear— Parliament®),

and “Thinking Man’s Filter” (Viceroy®). Other slogans were more implicit,

but still provided health inferences to consumers (See Pollay, 1989b). 

If nothing else, the high technology attributes of filtration, and its ability to produce healthful conditions in other media such as water, were communicated (see Figure 7-2). 

“The speed with which charcoal filters penetrated the health

cigarette market shows the effectiveness of a new concept. The public had been conditioned to accept the filtering effects of charcoal in

other fields, and when charcoal was added to cigarette filters it

proved to be an effective advertising gimmick.” (See Johnston, 1966,

p.16) 

“Claims or assurances related to health are prominent in the

(cigarette) advertising. These claims and assurances vary in their

explicitness, but they are sufficiently patent to compel the conclusion that much filter and menthol-filter advertising seeks to persuade smokers and potential smokers that smoking cigarettes is safe

or not unhealthful.” (See the Federal Trade Commission, 1964,

p. 72) 

THE 1950s

Filters Debut as

Health Protection

200

Smoking and Tobacco Control Monograph No. 13

Chapter 07 11/19/01 11:18 AM Page 200
The result in the marketplace

was a dramatic conversion from

‘regular’ (short length; unfiltered)

products to new product forms

(filtered; king sized; 100 mm).

Spending on advertising nearly

tripled from 1952 to 1959, largely

through promoting the virtues of

the new filtered products, thereby

enticing smokers to switch from

their regular unfiltered products

to filtered and, presumably, safer

brands or product-line variants. 

“He had abandoned the

regular cigarette, however, on

the ground of reduced risk to

health. . . . A further consequence of the ‘tar derby’ was

the rapid increase in advertising expenditures during this

period. Advertising expenditures in selected media

jumped from over $55 million in 1952 to approximately

$150 million in 1959.” (See

Pepples, 1976, p. 1)

Gender and age were predictors of who adopted the

new filtered products. Females converted more readily than males, and older concerned smokers adapted more readily than

young starters (O’Keefe and Pollay, 1996). Thus, Philip Morris anticipated

that females would be the largest potential market for a “health cigarette”

following the release of the 1964 Surgeon General’s Report: 

“Women, and particularly young women, would constitute the

greatest potential market for a health cigarette.” (See Johnston,

1966, p. 1) 

Psychology-based consumer research conducted for Brown &

Williamson implied that the females who smoked filters were normal,

whereas the males seemed unusually anxious. In 1967, this research

described women who smoked filter cigarettes as “neither rebels (like

women who smoke plain cigarettes), nor insecure (like females who smoke

menthols).” The males who smoked filter cigarettes were described as “. . .

apprehensive and depressive. They think about death, worry over possible

troubles, are uneasy if inactive, don’t trust others.” (See Oxtoby-Smith, Inc.,

1967, pp. 24-25.)

Once the public accepted filters as an adequate response to at

least assuage their worst fears, there was a market opportunity in providing males with filtered products that delivered ‘full flavor’: 

Filter Cigarette

Marketing to Males

Females and Older Smokers

as Early Filter Smokers

201

Chapter 7

Figure 7-1

Kent—Implied AMA Endorsement

(Circa 1953)

Chapter 07 11/19/01 11:18 AM Page 201
“. . . [O]nce the consumer

had been sufficiently educated on the virtues of filters, a

vacuum was created for a filter with taste; this vacuum

was filled by Winston and

Marlboro.” (See Latimer,

1976, p. 5.) 

Some internal industry documents from the 1970s portray the

filters of the 1950s and the associated risk reduction as essentially

‘cosmetic’: 

“. . . [T]he public began to

accept filters as a way to

reduce the cosmetic risks of

smoking and the attendant

‘ego-status’ risk of appearing

to have an immoral, unclean

habit.” [Emphasis added.] (See

Latimer, 1976, p. 3.)

The Early Tar Wars The period from

the mid-1950s until the mid1960s was tumultuous for the industry. Various new filter products were

launched, many competitive advertising claims used different standards of

measurement, and the Federal Trade Commission (FTC) guidelines concerning what was permissible in cigarette advertising changed as well. Episodes

of intense competitive rivalry of claims and counter-claims about cigarette

yields were dubbed the “tar derby” or “tar wars” within the trade, and the

ensuing publicity in the popular press affected the marketplace. Some manufacturers took advantage of these dynamics to present their cigarettes as

“healthy” to the public during a period of intense advertising claims, then

capitalized on such reputations while selling products that were actually

quite high in tar and nicotine yields. 

“In 1955, the FTC, reacting to conflicting claims as to tar and

filtration, has imposed ‘Cigarette Advertising Guides’ banning all

mention of tar, nicotine and filtration ‘when not established by

competent scientific proof’. This put a stop to such claims in advertising. In July and August of 1957, the Reader’s Digest published two

articles with figures on tar and nicotine mentioning Kent by name.

The August article, written with Kent’s assistance was practically an

ad for Kent. In 90 days, Kent’s sales leaped from 300 million to 3

billion per month. This article broke the dike and set off the famous

Tar Derby. Over the next 4 years, tar levels were drastically cut.

Marlboro dropped from 34 mg. tar in 1957 to 25 mg. in 1958 and

19 mg. in 1961.” (See Cunningham and Walsh, 1980, p. 11) 

202

Smoking and Tobacco Control Monograph No. 13

Figure 7-2

Tareyton—Charcoal Filter (1972)

Chapter 07 11/19/01 11:18 AM Page 202
Kent®, whose advertising of its asbestos-based “Micronite” filter had

been very effective, engaged in a series of product revisions in the 1950s.

With each iteration, the Kent® product yielded more and more tar and

nicotine, and this pattern continued into the 1960s. Similar filter “loosening” was the subject of U.S. Congressional inquiry (Blatnik, 1958).

“In mid 1960, the FTC called off the Tar Derby, rigidly prohibiting tar and nicotine claims. Some of the new low tar brands disappeared. Soon thereafter, the brands stopped reducing tar levels and,

indeed, began to raise them. Kent, for example, went from 14 mg.

in 1961 to 16 mg. in 1963 and 19 mg. in 1966. The FTC prohibition

ended March 25, 1966 initiating a new phase in Hi-Fi development.

Lorrillard [sic] decided not to reduce Kent’s tar level again. Instead it

put out True.” (See Cunningham and Walsh, 1980, p.12.)

Medicinal Menthol During this tar derby period, new menthol-filtered products

were introduced, such as Salem®, Newport®, and Oasis®. Manufacturers of

these new products capitalized on the reputation that menthol already had,

due to its use in cold remedies and related medicinal applications, and the

history of “pseudo-health” claims made in earlier menthol cigarette advertising. The Kool® brand had long been promoted as a medicinal product

with would-be remedial properties that could make the cigarette suitable

when smokers were suffering from coughs, colds, sore throats, etc.: 

“Kool not only remained, but was actively positioned as a remedial/medicinal type product throughout the 1950’s.” (See

Cunningham and Walsh, 1980, p. 9.) 

Salem® was introduced in 1956 as the “first truly new smoking

advance” (see Figure 7-3).

“Salem created a whole new meaning for menthol. From the

heritage of solves-the-negative-problems-of-smoking, menthol

almost instantly became a positive smoking sensation. Menthol in

203

Chapter 7

Figure 7-3

Salem—First Truly New Smoking Advance (1956)

Chapter 07 11/19/01 11:18 AM Page 203
the filter form in the Salem advertising was a ‘refreshing’ taste experience. It can be viewed as very ‘reassuring’ in a personal concern

climate. Undoubtedly, the medicinal menthol connotation carried

forward in a therapeutic fashion, but as a positive taste benefit.”

(See Cunningham and Walsh, 1980, p. 9.) 

“During the ‘tar derby’, menthol styles were perceived as healthier, low ‘tar’ smokes due to the quasi-medical health claims in menthol advertising. . . the first true menthol hi-fi was True Green,

introduced in 1967. . . By 1974, menthol hi-fi styles had a 27%

share of the hi-fi category—close to the proportion of menthols to

all styles.” (See Chambers, 1979.)

The first Surgeon General’s Report on smoking and

health in 1964 established cigarette smoking as a

cause of lung cancer, at least in males. Philip Morris

expressed some regret that the 1964 report did not

strongly endorse the filtered products that had been sold to the public as a

technological fix: 

“The health value of filters is undersold in the report and is the

industry’s best extant answer to its problem. The Tobacco Institute

obviously should foster the communication of the filter message by

all effective means.” (See Wakeham, 1964, p. 8.) 

Consumer Guilt and Anxiety Brown & Williamson’s advertising agency and

market research contractors recognized consumers’ mass sense of being

addicted, as well as the ensuing conflict, guilt, anxieties, and need for reassurance: 

“Most smokers see themselves as addicts . . . the typical smoker

feels guilty and anxious about smoking but impotent to control it.”

(See Oxtoby-Smith, Inc., 1967, p. 6.) 

“Psychologically, most smokers feel trapped. They are concerned about health and addiction. Smokers care about what commercials say about them. Advertising may help to reduce anxiety

and guilt. . . Brand user image may be critical in influencing shifts

in brand loyalty.” [Emphasis in original.] (See Oxtoby-Smith, Inc.,

1967, p. 14.) 

[People who smoke filter cigarettes] “. . . may be receptive to

advertising which helps them escape from their inner conflicts

about smoking.” (See Oxtoby-Smith, Inc., 1967, p. 23.) 

“While unquestionably smokers are concerned about the tar and

nicotine contents and the filtration effectiveness of their brands,

nevertheless, both on the surface and even to some extent unconsciously, they appear to be resisting open involvement with this

‘frightening’ element of smoking.”(See Alex Gochfeld Associates,

Inc., 1969, p. 9.) 

THE 1960s

Implications of the 1964

Surgeon General’s Report

204

Smoking and Tobacco Control Monograph No. 13

Chapter 07 11/19/01 11:18 AM Page 204
Some brands were less successful than others when trying to directly

address consumer conflicts. Kent®, for example, used a visual portrayal of a

smoker’s conscience, and risked their ad being experienced as a nagging

message (see Figure 7-4). 

“. . . [T]he psychological blinders that smokers have donned,

consciously or unconsciously . . . advertising which stresses tar and

nicotine content was received less enthusiastically . . . even in the

Silva Thins commercial where this theme was the major aspect of

the spoken message, a large number of people effectually [sic]

blocked it out of their consciousness retaining only the total image

of the story shown on the screen.” (See Alex Gochfeld Associates,

Inc., 1969, pp. 72-73.)

In order to provide a “foundation upon which marketing

and advertising executions can be built,” Lorillard did a

market segmentation analysis.

“One of the most important revelations of the present study was

the identification of four market segments in the smoker market

who are distinct in terms of their desires in cigarettes and their psychological profile. 

The fundamental basis upon which the market segments were

divided was their desires in the ‘ideal cigarette’. After the market

segments were divided in terms of their smoking needs, they were

then further analyzed in terms of their demography, smoking

behavior, and their personality profile.” [Emphasis in original.] (See

Kieling, 1964, p. 2.) 

The consumer segment most appropriate for Kent® was described in

substantial psychological detail. Despite the label of “social conformist,” of

central concern to these smokers were health consequences: 

“Segment B, the social conformists, represents the prime potential market for development of Kent’s share. 

Compared with the rest of the market, Segment B is less concerned about smoking enjoyment and more concerned about the

health aspect of cigarettes. He cares particularly about a cigarette’s

filter, its king size, and its association with health. 

Type B is a self-controlled person who is willing to compromise

and give up immediate physical gratification for longer range objectives; he is a thinking person who acts deliberately, and is most likely to sacrifice some of the enjoyment of smoking in the interest of

health, about which he is highly concerned. . . These requirements

appear to be compatible with Kent’s current image. 

The other psychological requirement of Type B is the need for

social benefits through association with ‘educated moderns’. . .

‘educated moderns’ include the active, modern people, college graduates, and professionals such as lawyers, doctors, etc.” [Emphasis in

original.] (See Kieling, 1964, pp. 3-5.) 

Segments of

Concerned Consumers

205

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 205
Given that Kent® had a longestablished association with

‘health’ from more than a

decade’s worth of health-themed

advertising, the advertising

deliberately offered reassurances

to targeted consumers of being

seen as “educated moderns,”

with the health promises subtly

made: 

“In the present climate

of opinion after the Surgeon

General’s Report, it may be

desirable to offer reassurance

on ‘association with health’

in Kent’s advertising.”

[Emphasis in original.] (See

Kieling, 1964, p. 14.) 

The “Illusion of Filtration” In their

1966 analysis of the market

potential for a ‘health’ cigarette,

Philip Morris recognized that

while a large proportion of

smokers had health concerns,

they could be assuaged by products with largely illusory filtration systems.

This was helpful since Philip Morris also knew that they had to keep delivering nicotine to those already addicted, as well as to those that they hoped

would become addicted. The report’s conclusions include the following: 

“1. A large proportion of smokers are concerned about the relationship of cigarette smoking to health. . . 

9. Mere reduction in nicotine and TPM [total particulate matter]

deliveries by conventional methods of filtration would not be a

sufficient basis for launching a new cigarette. 

10. The illusion of filtration is as important as the fact of filtration. 

11. Therefore any entry should be by a radically different method

of filtration but need not be any more effective.” (See Johnston,

1966, pp. 1-2.) 

Within this report, Philip Morris’ analyst captured the dilemma

between health concerns and nicotine delivery felt by both smokers and

manufacturers: 

“. . . [A]ny health cigarette must compromise between health

implications on the one hand and flavor and nicotine on the other

. . . flavor and nicotine are both necessary to sell a cigarette. A cigarette that does not deliver nicotine cannot satisfy the habituated

smoker and cannot lead to habituation, and would therefore almost

certainly fail.” (See Johnston, 1966, p. 5.) 

206

Smoking and Tobacco Control Monograph No. 13

Figure 7-4 

Kent—Voice of Wisdom (1955)

Chapter 07 11/19/01 11:18 AM Page 206
Many early brands had been sold with filters that were essentially cosmetic, without meaningful filtration. U.S. Congressional investigations in

1958 found reversals in which some firms’ filtered products delivered even

more tar and nicotine than their unfiltered traditional products. Reversals

occurred even within brand families, with Brand X filtered versions yielding

higher tar and nicotine than the unfiltered Brand X products that they

ostensibly improved upon (Blatnik, 1958, pp. 45-49).

In 1969, R. J. Reynolds articulated concerns about

reducing nicotine delivery and also maintaining a

continuing profitable enterprise. The company

saw nicotine as the sine qua non of smoking satisfaction and worried that

reducing the delivery of nicotine to consumers might have the “self-defeating consequences” of weaning them away from smoking and letting them

off the nicotine hook: 

“In its search for ‘safer’ cigarettes, the tobacco industry has, in

essentially every case, simply reduced the amount of nicotine . . .

perhaps weaning the smoker away from nicotine habituation and

depriving him of parts of the gratification desired or expected. . .

Thus, unless some miraculous solution to the smoking-health problem is found, the present ‘safer’ cigarette strategy, while prudent

and fruitful for the short term, may be equivalent to long term liquidation of the cigarette industry.” (See Teague, 1969, pp. 9-10.) 

This concern with possible ‘weaning’ was still being expressed later by

the British American Tobacco Co. when looking ahead to the 1980s: 

“Taking a long-term view, there is a danger in the current trend

of lower and lower cigarette deliveries—i.e., the smoker will be

weaned away from the habit. . . Nicotine is an important aspect of

‘satisfaction’, and if the nicotine delivery is reduced below a threshold ‘satisfaction’ level, then surely smokers will question more readily why they are indulging in an expensive habit.” (See British

American Tobacco Company, 1976, p. 2)

“Carlton and True appeared in the mid 1960’s, and

Doral and Vantage followed shortly after. . . Lights

and milds [sic] versions of full-taste brands proliferated in the early ’70’s, accounting for 31.6% of hi-fi

business by 1975.” (See Chambers, 1979.) 

By 1973, it was clear to industry participants that a significant number

of brands shared certain characteristics that led them to be described as a

“new low-delivery segment.” Precise relevance to tar and nicotine levels was

elusive, in part because some brands like Kent® and Parliament® were perceived by consumers as being low in delivery due to their product and

advertising histories, even though they were no longer in fact low in delivery. Listed below are some of the guidelines used by Philip Morris to define

low-delivery brands for that company’s internal purposes:

THE 1970s

Early High-Filtration

(Hi-Fi) Brands

Fear that Low-Yield Cigarettes

Would Allow the Consumer to

Wean from Nicotine

207

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 207
“2. All brands in the segment have advertising, if any, focussed on

low delivery. No other brand has advertising focused on low

delivery.

3. Some brands in the segment have tar and nicotine numbers on

their packs. No brand not in the segment has tar and nicotine

numbers on its pack.

4. Some brands in the segment have unusual construction filters

or dilution holes. No brand not in the segment has either of

these characteristics. . . 

6. Brands in the segment which are extensions of ‘flavor’ brands

have names which imply low delivery: Marlboro Light, Kool

Mild, Pall Mall Extra Mild, Lucky Ten, etc.

Note that Kent and Parliament do not qualify for this new low

delivery segment on any of the criteria above. One can still argue,

however, that in the minds of consumers Kent and Parliament are

low delivery cigarettes . . . consumer opinion should be the ultimate

criterion for market segmentation.” [Emphasis in original.] (See

Tindall, 1973, p. 16.)

During the early 1970s, Philip Morris was internally

expressing confidence in its ability to selectively reduce tar

yield while continuing to deliver the all-important nicotine: 

“. . . [T]he tar deliveries of the currently best selling cigarettes

might be reduced somewhat, leaving nicotine as it is, without any

significant overall decrease in the cigarettes’ acceptability.” (See

Schori, 1971, p. 1.) 

R. J. Reynolds was following a similar line of thought in focussing its

product development on nicotine delivery: 

“If nicotine is the sine qua non of tobacco products and tobacco

products are recognized as being attractive dosage forms of nicotine,

then it is logical to design our products—and where possible, our

advertising—around nicotine delivery rather than ‘tar’ delivery or

flavor.” [Emphasis in original.] (See Teague, 1972b, p. 3.) 

“In today’s market it is reasonable to believe that, given the

choice, the typical smoker will chose [sic] and use the cigarette

which delivers the desired, required amount of nicotine, with satisfactory flavor, mildness and other attributes, accompanied by the

least amount of ‘tar’.” [Emphasis in original.] (See Teague, 1972a, p.

4.) 

By 1976, the R. J. Reynolds Market Research Department (MRD) had

joined the research and development (R&D) effort with a clear statement of

their intent to maximize the nicotine satisfaction while maintaining high

profitability by using conventional filters and packaging: 

“MRD and R&D have been working on a sophisticated consumer product testing program to help us ensure that we select the

best blend alternative for our brands to optimize physiological satisfaction.” (See Fitzgerald et al., 1976, p. 1.) 

Nicotine as a Product

Design Feature

208

Smoking and Tobacco Control Monograph No. 13

Chapter 07 11/19/01 11:18 AM Page 208
“Our top priority is to develop and market low ‘tar’ brands (12

mg. ‘tar’ and under) that: Maximize the physiological satisfaction

per puff—the single most important need of smokers. . . [and] yield

higher profitability which means conventional filters and soft packaging for high speed production efficiencies.” (See Fitzgerald et al.,

1976, p. 38.) 

A few years later in 1981, British American Tobacco, the parent company of Brown & Williamson, maintained that, “. . . effort should not be spent

on designing a cigarette which, through its construction, denied the smoker

the opportunity to compensate or oversmoke [sic] to any significant

degree.” [Emphasis added.] (See Oldman, 1981, p. 2.)

During the 1970s, additional evidence of consumer confusion, misinformation, rationalizations, and the corresponding

role played by advertising was gathered by multiple firms.

Market researchers for industry members and their advertising agencies were not even confident that consumers knew

what they were talking about when referring to the ‘taste’ of

a cigarette: 

“. . . [I]t is almost impossible to know if the taste smokers talk

about is something which they, themselves attribute to a cigarette

or just a ‘play-back’ of some advertising messages.” (See Marketing

and Research Counselors, Inc., 1975, p. 2.) 

Apparently, even the so-called ‘taste’ of a product is greatly influenced

by the brand and its reputation. Merit®, as a free-standing brand, had difficulties in being perceived as flavorful, whereas in contrast, product line

extensions like Marlboro Light® had the advantage of being perceived as

more flavorful due to the taste reputation of the ‘parent’ brand: 

“. . . [W]e talked to consumers about Merit’s image and advertising. They told us that Merit, like other free standing low tar brands

such as Kent, Vantage, Carlton, etc., were perceived to be weaker

and have less taste than the line extension low tars: like Marlboro

Lights, Winston Lights, Camel Lights. Apparently, these line extension low tars share the taste heritage of their parent full flavor

brands.” (See Philip Morris, 1990, pp. 13–14.) 

In 1974, Kenyon & Eckhardt Advertising studied “recently starting

smokers” for Brown & Williamson: 

“The purpose of this research was to gain insight into the perceptions, attitudes and behavior of younger, recently starting smokers regarding initial product usage, current smoking and health concerns. In addition, an effort was made to determine reactions to

alternative product positionings [sic].” (See Kenyon & Eckhardt,

1974, p. 1).

“Health concerns exist among younger smokers. . . One type of

smoker rationalized smoking as a pleasure that outweighed the

risks. Another felt that they didn’t smoke enough to be dangerous.

Consumer Reactions

and Behavior

Consumer Ignorance

and Confusion

209

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 209
A third type rationalized his use of cigarettes by feeling he would

quit before it was ‘too late’. A final smoker group said that science

would come to his rescue.” (See Kenyon & Eckhardt, 1974, p. 2).

“In talking to these young smokers about the different brands of

cigarettes they have smoked, we found that they have little knowledge and, in fact, a great deal of misinformation on brand yields. In

all of the sessions, not a single respondent know [sic] the tar and

nicotine level of the cigarette he or she smoked.” (See Kenyon &

Eckhardt, 1974, p. 7). 

Lorillard and their ad agency had the same experience when studying

consumers for Kent®. Lorillard, along with Foote, Cone & Belding, encouraged scores of targeted smokers to talk about their lives, their cigarettes,

their perceptions, and their feelings about tar content for Kent Golden

Light®. They, like Brown & Williamson, found that “practically no one

knew” the tar content of their own regularly smoked brands. This implied

to these firms the need for ads showing comparative packages and data

(O’Toole, 1981, pp. 94-95). 

Philip Morris also knew about smokers’ ignorance of yield levels in the

1970s. Most consumers were not only ignorant of the facts, but even their

general impressions were “not too accurate,” despite their faith in the technology of filters as displayed by shifts to filters and hi-fi products: 

“As yet, there is low awareness among smokers of the tar content of their brand. When asked if they knew the specific milligram

tar content of their brand, the vast majority (89%) said they didn’t

know. . . smokers’ impressions of whether their brand has high,

moderate or low tar content is more on the mark—although still

not too accurate.” [Emphasis in original.] (See The Roper

Organization, Inc., 1976, p. 14.)

As in the 1950s and 1960s, females and older, health-concerned smokers most readily adopted the new, seemingly lowyield products of the 1970s: 

“The modern low ‘tar’ market began in the 1960’s with such

brands as True, Carlton, and Doral . . . initial gains were from

females and older smokers.” (See Brown & Williamson, circa 1977,

p. 4.) 

“The hi-fi smoker demographics tend to be female, older, and

have switched from a full flavor style to its counterpart in the hi-fi

segment.” (See Brown & Williamson, circa 1977, p. 13.) 

This was so much the case that the males who smoked these products

were suspected of being ‘weak’ and somehow wimpish or unmasculine in

the eyes of consumers who were studied for Brown & Williamson: 

“Only women and weak men smoke True or any of those low

tar and nicotine cigarettes.” (See Marketing and Research

Counselors, Inc., 1975, p. 9.) 

Filters Are Still

Perceived As Feminine

210

Smoking and Tobacco Control Monograph No. 13

Chapter 07 11/19/01 11:18 AM Page 210
In 1974, advertising agency advisors to Lorillard tried to counter this

problem with a style of advertising for the True® brand that they felt was

more masculine in its tonality (see Figure 7-5).

“In order to obtain a greater share of males. . . logical, rational

approaches. . . a ‘reasoning’ empathetic approach. . . masculine,

‘macho’ tonality and appeal. Vantage’s tonality can be described as

‘laying it on the line’ in an aggressive, possibly masculine, open

fashion.” (See DeGarmo, Inc., 1974.) 

This problem of low-yield products being perceived as highly feminine

seems to have led R. J. Reynolds to design a marketing strategy that attracted males to a low-yield cigarette that they were developing in 1976: 

“What we want is to portray the feeling and image projected by

Marlboro and Kool advertising on a Vantage/Merit type of cigarette.

In other words, put ‘balls’ (two of them) on a low ‘tar’ and nicotine

cigarette and position.” [Parenthetical clarification of the male genitalia meaning of “balls” as in original.] (See Hind et al., 1976, p. 63.) 

While young male consumers understood that filters seemingly offered

improved health prospects, this was in conflict with their desires to appear

bold and daring: 

“In discussing how a smoker can limit the risks of serious disease without actually giving up smoking, the respondents clearly

recognized the role of high filtration cigarettes. . . the underlying

mechanism working against acceptance of high filtration brands in

this age group is that the image of these cigarettes is contrary to one

of the initial motivations for smoking—to look manly and strong.”

(See Kenyon & Eckhardt Advertising, 1974, p. 10.)

Consumers’ conflicted feelings about smoking cigarettes were

such that they became poor respondents to Brown &

Williamson’s research efforts: 

“. . . [S]mokers themselves falter badly when asked to comment

on the rewards accruing to them from smoking. . . Smokers are so

overwhelmed by the addictive properties of cigarettes and the

potential health hazard that they wax virtually inarticulate when

asked to present a case for the other side. They become guilty and

shame-faced.” (See Kalhok and Short, 1976, p. 8.) 

Smokers were not even aware and/or willing to admit how much they

smoked: 

“Smokers’ own estimates of their daily consumption levels are

extremely unreliable. Many smokers underestimate their actual consumption and certain segments of many populations, notably

young people and women, are often reluctant to admit they

smoke.” (See British American Tobacco Co., 1979, p. 1.) 

Brown & Williamson blamed consumer confusion on advertising, in

part. When contemplating a possible “index of safety” for cigarettes, Brown

& Williamson commented that: 

Continuing

Consumer Conflicts

211

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 211
“Such an index would

have merit for the health-conscious smoker, who otherwise

may well become confused

and increasingly dismayed if

one alleged hazard follows

another, coupled with the

manufacturers’ ‘prescription

for health’ through advertising.” (See Kalhok and Short,

1976, p. 11.) 

Additional market research

conducted for Brown &

Williamson and its advertising

agency, Ted Bates, indicated that

ads needed to be carefully

designed, lest they challenge consumer denials and rationalizations and trigger consumer defensiveness: 

“. . . [S]mokers have to

face the fact that they are

illogical, irrational and stupid

. . . while an ad that depicts

an exciting, invigorating situation could be interesting to the smoke-viewer, the very thin line

separating positive excitement from negative-creating situation

should never be crossed.” [Emphasis in original.] (See Marketing and

Research Counselors, Inc., 1975, pp. 1-2.) 

“. . . [C]ommunication with the smoker that either directly or

indirectly violates and belittles this rationalized need will meet

smoker’s objection—it destroys the rationalization and the smoker

would feel naked and rather stupid.” (See Marketing and Research

Counselors, Inc., 1975, p. 5.) 

One of the problems that advertising could address was the declining

social esteem of smokers, helping them to avoid shame and guilt: 

“Over the period of 20 years, the public and the private image

of the smoker (though exceptions may be found among teenagers

starting to smoke) has changed from being one of an individual

exulting in his positive strength, masculinity and acceptance in the

community, to that of a weak and dependent slave, with prospects

of illness, however distant these may be, unnerved by his children’s

forebodings [sic], and without strength to quit.” (See Kalhok and

Short, 1976, p. 14.) 

212

Smoking and Tobacco Control Monograph No. 13

Figure 7-5

Vantage “Don’t Cop Out”—Macho

Tonality (1971)

Chapter 07 11/19/01 11:18 AM Page 212
In discussing the “elements of good cigarette advertising or how to

reduce objections to a cigarette,” this point was reiterated while stating that

“there are not any real, absolute, positive qualities and attributes in a cigarette,” as noted in the following: 

“Most advertising for other products presents real, or at least

accepted, benefits, values, attributes, end-results, etc., of the product

it ‘pushes,’ sells. Cigarette advertising can not do the same. There

are not any real, absolute, positive qualities and attributes in a cigarette and no one, even the most devout smokers, could believe any

glorification or lies about it. . . The more a cigarette ad is disbelieved, the more it ‘fights’ the defense mechanism of the smoker—

the more the smoker feels challenged. . . The picture, situation presented and the copy should be ambiguous enough to allow the

reader to fill-in his/her illogical-logic which are the results of each

individual defense-mechanism.” (See Marketing and Research

Counselors, Inc., 1975, pp. 12-13.)

Image of Health It was important to the industry that certain cigarette brands

continued to appear to be ‘healthy’, even if this was an image or illusion,

and even if the manufacturing technology did not yet allow for the control

of smoke toxicity: 

“Looking further down the road, the possibility exists that . . .

filters might offer a selective means of controlling smoke toxicity.

Well before that date, however, opportunities exist for filter and

cigarette designs which offer the image of ‘health re-assurance’.”

[Emphases added.] (See British American Tobacco Co., 1976, p. 6.) 

New Product Activity Philip Morris had seen the competitive value of a so-called

“health cigarette” following the first Surgeon General’s Report on cigarettes

in 1964. Over the course of the next 12 years, Philip Morris worked on such

a product, culminating in the 1976 product launch of the Merit® brand.

Just as with Philip Morris’ earlier efforts in the 1950s to develop and consumer-test the Marlboro® product, packaging, and promotion, the product

development process for Merit® was as much focused on consumer and

market testing as on product technologies, per se. The final market launch

strategies used in 1976 gave particular emphasis to the choice of the name

Merit®, obviously communicating apparent virtue, and used an advertising

style that made this product development seem eminently scientific and

newsworthy and less like an ad (see Figure 7-6). The product launch strategy included a very high level of advertising investment ($45 million in

1976) to support a “multi-media blitz.”

“The objective of the advertising campaign was to establish

enough credibility to overcome smoker skepticism towards low-tar

good taste claims. The name ‘MERIT’ was chosen because it was

short, to the point, and it reflected the consumer appeal of good

taste at low tar.” (See John and Wakeham, 1977, p. 13.) 

213

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 213
“Merit was the primary focus

of the sales force for a full year. . .

We spent $45 million on advertising—remember $45 million in

1976! This was a record amount

for a new brand introduction. . .

Creatively, we used provocative

headlines and important looking

copy which looked like it had

real news value. Tar/taste theory

exploded!—Smoke cracked!—

Taste barrier broken!” [Emphasis

in original.] (See Philip Morris,

1990, p. 4.) 

This Merit® launch effort, and its

stunning success, led to a rash of

similar competitive efforts: 

“Merit’s introduction gave

birth to a series of me-too’s. . .

‘Fact’ was introduced in 1976. . .

RJR tried to counter Merit’s technological enriched flavor story

with their all natural ‘Real’

launched in mid 1976. . .

‘Decade’, which was launched

on the platform of ‘the cigarette that took 10 years to create’. . .

Later, Barclay was introduced.” (See Philip Morris, 1990, p. 5.)

Brown & Williamson’s introduction of the Fact® brand was

described by a company spokesman as “a typical new product

introduction as compared to Philip Morris’ sudden national

blitz for Merit. . . Fact is directed to the educated, concerned smoker. Our

copy is straightforward and direct, and there is no gender differentiation or

symbolism.” (See Brand Report 12, 1976, p. 146.) Fact® was using the

“Purite” filter to filter gases, but needed to first inform consumers that gases

were an issue. Their initial effort (see Figure 7-7) was test-marketed in New

England and the North Central States, but did not perform well in the marketplace, despite advertising support of about $30 million over 1976-1977.

The senior brand manager of Brown & Williamson explained: 

“The low gas benefit of the product wasn’t of interest to the

public, and wasn’t understood. The advertising and packaging failed

to reinforce the flavor aspect of the brand. . . The package was perceived by customers as medicinal, like a prescription bottle of

Geritol. The tar level wasn’t low enough by mid-1976 to allow it to

be a talking point in advertising.” (See Brand Report 23, 1977, p.

152.) 

Marketing of Reduced

Gas Phase Cigarettes

214

Smoking and Tobacco Control Monograph No. 13

Figure 7-6

Merit Science Works—“Enriched

Flavor” (1979)

Chapter 07 11/19/01 11:18 AM Page 214
Brown & Williamson’s reconsideration of its Purite gas filter

showed a recognition that in

having to educate consumers

about gas in smoke, they might

raise more anxiety than they

could resolve with this type of

product: 

“While low gas does

offer the opportunity to

make positive health statements to active and passive

smokers alike, it does run

the category risk of raising

another health issue and

perceptively offering lower

taste/satisfaction. . . past

experiences with Lark and

FACT (i.e., good taste and

greater health reassurance

via a new method) demonstrate the inability to immediately proceed with either

of these options.” (Brown &

Williamson, circa 1977, p.

1.)

R. J. Reynolds’ 1976 assessment for their 3-year action plan

acknowledged that they were not yet technologically capable of

producing products that had reduced tar without the undesirable effect of also having reduced nicotine: 

“In general, methods used to reduce ‘tar’ delivery in cigarettes

lead to a proportionate reduction in nicotine. . . It would be more

desirable from our standpoint, i.e., providing satisfaction to the

smoker and maintaining his allegiance to smoking if we could

reduce ‘tar’ to whatever target we choose without a proportionate

drop in nicotine. . . It will take some time to get there by the

approaches we visualize.” (See Fitzgerald et al., 1976, p. 91.) 

Nonetheless, R. J. Reynolds wanted to participate in the rapidly expanding category of concerned consumers, referred to as “worriers” by the company: 

“[The]. . . ‘worrier’ segment of the market (17% of smokers are

so classified). . . ‘Numbers’ products have a growing appeal to these

smokers. Products in the 1-6 mg. ‘tar’ range will continue to build

successful long-term franchises (e.g., Carlton’s growth rate, NOW’s

immediate acceptance—fostered by the intense industry commitment in 1976 to hi-fi brands).” (See Fitzgerald et al., 1976.) 

Marketing Cigarettes

Without Additives

215

Chapter 7

Figure 7-7

Introducing Fact—Low Gas (Before—

1976)

Chapter 07 11/19/01 11:18 AM Page 215
R. J. Reynolds’ product offering was the

Real® brand, with a “natural—no additives”

claim (see Figure 7-8). This ‘natural’ position was thought to convey positive features to both full-flavor smokers and those

seeking effective filtration and health protection. The Real® concept was described as

having, “Broad appeal based primarily on

‘natural’/no additives claim. Connotes taste

to full flavor smokers, low numbers to hi-fi

smokers. No significant negatives.” (See

Fitzgerald et al., 1976.) 

When the Real® brand was launched by

R. J. Reynolds in 1977, it had a budget of

$40 million for “boxcar loads of display

materials, more than 25 million sample

packages, the biggest billboard overlooking

Times Square, the summer long services of

2,000 salesmen. . . and advertising, according to the agency running the campaign,

on everything but painted rocks.” (See

Crittenden, 1977, p. 1ff.) 

That same year, Brown & Williamson

was scheduled to spend $50 million

through the Ted Bates advertising agency on just the product-line extension

of Kool Super Light®. The Kool Super Light® campaign was to appear “in

every conceivable non-broadcast medium, and even an inconceivable

one”—1,500 Beetleboards, i.e., painted up Volkswagen Beetle® cars

(Dougherty, 1977).

The enormous advertising budgets used to launch the

new low-yield products commanded a very disproportionate share of the firms’ total advertising budgets (share

of voice, or SOV), and were seen as creating marketplace

demand for low-yield products. The advertising spending

for new products in 1976-1978 was awesome. New brands and product-line

extensions (variations on familiar brands) were introduced with major

budgets as follows (Source: Lorillard, Inc., 1980): 

Product Budget Year

Merit® $44 million (1976)

Now® $23 million (1976)

Fact® $20 million (1976)

Real® $29 million (1977)

Decade® $24 million (1977)

Camel Light® $25.3 million (1978)

Carlton® $15.3 million (1976)

Vantage® $20.6 million (1976/1977)

Kent Golden Light® $21.0 million (1976-1978)

Marlboro Light® $20.1 million (1976-1978)

Promotional Patterns

Disproportionate

Advertising Budgets

216

Smoking and Tobacco Control Monograph No. 13

Figure 7-8

Real Natural (1977)

Chapter 07 11/19/01 11:18 AM Page 216
“The phenomenal growth of hi-fi brands is, in part, a self-fulfilling prophecy. Hi-fi expenditures have grown from 7% SOV in 1972

to 45% in 1977, much faster than actual segment growth. Spending

per share point now equals $8.3MM.” (See Brown & Williamson,

circa 1977, p. 14.) 

“[The]. . . low tar revolution [of 1976ff] is not ignited by a particular event, such as a Reader’s Digest article, a Surgeon General’s

Report, etc.; it happens quietly based on technologically improved

products and consumers’ desire for a reasonable compromise and

the industry’s massive advertising support leading category development.” (See Cunningham and Walsh, 1980, p. 55.) 

“Lo Fi advertising now (Feb 1980) accounts for only 21% of

total—less than a third of 1974’s share of voice. Reduced tar brands

have increased to 79% share of voice—with ULT’s (Ultra Low Tar’s)

now accounting for 19% of the total. ULT advertising is growing at

a faster rate than any other category.” (See Lorillard, Inc., 1980.)

Executional Aspects The advertising executions that communicated the “lightness”

theme were ‘light’ in many dimensions: 

“ ‘Light-lighter-lightest’ were achieved by insistance [sic] on

lighter presentations—product story imagery—white packs—pale

colours—mildness dominated copy.” (See British American Tobacco

Company, circa 1985, p. 13.) 

This tactic of using color and

imagery to connote product ‘lightness’ had been used earlier with the

introduction of Marlboro Light® in

1971 (see Figure 7-9). 

“. . . [W]hen Marlboro Lights

was first introduced in 1971. . .

the advertising was dramatically

different. . . first using water

color executions, then, big pack

shots, a lot of white space and a

small cowboy visual.” (See Philip

Morris, 1990, p. 6.) 

This means of communicating ‘lightness’ with white or palecolored props, settings, and pristine

environments wasn’t new with

Marlboro Light®, and has proven to

be a durable execution tactic. For

example, Kent® in the early 1960s

showed models all dressed in white,

with both white props and in a pure

white, interior studio environment

(see Figure 7-10).

217

Chapter 7

Figure 7-9

Marlboro Lights (1972)

Chapter 07 11/19/01 11:18 AM Page 217
Through most of the 1990s, the

Parliament® campaign consistently used

models dressed all in white placed in

white environments as well as in outside

pristine environments (see Figure 7-11). 

Artwork for Marlboro Ultra Light® has

featured a pristine environment dominated by fresh air and water, with only minimally sized cowboys or horses (see Figure

7-12). 

Even the packaging design is important in affecting perceptions of relative

safety, as well as taste: 

“Red packs connote strong flavor,

green packs connote coolness or menthol and white packs suggest that a

cigaret [sic] is low-tar. White means

sanitary and safe. And if you put a

low-tar cigaret [sic] in a red package,

people say it tastes stronger than the

same cigaret [sic] packaged in white.”

(See Koten, 1980, p. 22) 

Because of its importance, Brown &

Williamson tested 33 packages before choosing the blue, gold, and red

design used for its Viceroy Rich Light® brand. Philip Morris heightened the

social status appeal of its Benson & Hedges® brand by printing the company’s Park Avenue address on the front and back of each pack. R. J. Reynolds

gave Now® a “modern, chrome-and-glass look designed to appeal to upscale

city and suburban dwellers.” Philip Morris’ successful Merit® connotes a

“flamboyant, young-in-spirit image” (to offset low tar’s dull image) with big

yellow, brown, and orange racing stripes (Koten, 1980). Most “Light” and

“Ultra Light” cigarettes are presented in pure white packaging with minimal

adornments.

To supplement and reinforce their advertising efforts, Brown &

Williamson conceived of public relations and political activities that

encouraged consumers to perceive apparently independent endorsements of

low-yield products. This would reinforce advertising impressions about the

virtues of low-tar products with seemingly independent “news” from credible sources.

“B&W will undertake activities designed to generate statements

by public health opinion leaders which will indicate tolerance for

smoking and improve the consumer’s perception of ultra low ‘tar’

cigarettes (5 mg. or less). . . Through political and scientific friends,

B&W will attempt to elicit. . . statements sympathetic to the concept that generally less health risk is associated with ultra low deliv218

Smoking and Tobacco Control Monograph No. 13

Figure 7-10

Kent—Black Smokers in Pure White

Environment (1964)

Chapter 07 11/19/01 11:18 AM Page 218
ery cigarette consumption. . .

B&W would seek to generate

spontaneous mainstream

media articles dealing with

component deliveries, much

as the old Readers Digest

[sic] articles.” (What are the

obstacles/enemies of a swing

to low “tar” and what action

should we take? Minnesota

Trial Exhibit 26,185, 1982.)

Capturing Consumer Concerns The

continuation of intensive promotion into 1977 involved “a

numbers game that boggles the

mind while promising to relieve

the lungs” (Brand Report 23,

1977, p. 150). Competition was

intense, due in part to the high

stakes and the relatively few

number of switchers. Said

Lorillard’s Tom Mau several

years later: 

“The vast majority of

the cigarette consumers are

brand loyal. . . Only somewhere around 10% of people switch

brands annually. That’s not a lot of people. . . To come out with

something new and successful is difficult.” (See Gardener, 1984, p.

176.) 

It was clear to industry observers that the pace of new product launches

in the mid-1970s was seeking to capitalize on the health concerns of smokers: 

“The current duel between True and Vantage and between

Carlton and Now are other examples of competitive efforts to capitalize on the smoking/health controversy.” (See Pepples, 1976, p. 9.) 

When the motivations for smoking ultra-low-tar cigarettes were studied

by Philip Morris’ contractors in 1978, representatives of the Brand

Management Group, Marketing Research Department, and the advertising

agency all observed the discussion groups from behind a two-way viewing

mirror and tape recordings were made available. The discussions were guided by a detailed outline with extensive probing. The findings were that all

of the reasons for selecting this product form were health-related: 

“. . . [W]ith respect to ultra low tar brands there appear to be

particular additional motivations for smoking this type of cigarette.

These include: 

219

Chapter 7

Figure 7-11

Parliament Lights White on White in

Pristine Environment (1998)

Chapter 07 11/19/01 11:18 AM Page 219
A - Voluntary desire for a safer cigarette. 

B - Increasing awareness and concern about possible hazards of

smoking.

C - Health problem forcing a change to a safer cigarette (as an

alternative to not being able to quit).

D - Peer and family pressure to smoke a safer cigarette (as an

alternative to not being able to stop smoking).

E - Mental commitment to do something about smoking

habits.” (See Goldstein/Krall Marketing Resources, Inc., 1979.) 

Many consumers considered, tried, and even switched to the nominally

lower yield products, and did so primarily in pursuit of better health: 

“More people have switched brands in the past year, and the

largest group of switchers have gone to low tars. Even among those

who have not switched to a low tar brand, there is fairly high disposition among smokers to consider switching to one. This is probably

attributable to the continuing concern over smoking and health.”

(See The Roper Organization, Inc., 1976, p. 3.) 

“Results show that almost two-thirds of smokers are ‘impressed’

by the talk of how cigarettes can seriously affect their health. . .

Women are more concerned about smoking and health than men,

young people more than older people, whites more than blacks, and

the college educated more than those less well educated." [The

growth among low tar brands was] “. . . particularly strong among

two groups who have traditionally been trend setters in the cigarette market—women and the college educated.” (See The Roper

Organization, Inc., 1976, pp. 8, 12.) 

When asked if and why some brands were thought to be better for

health, smokers had

believed the idea

that the nominally

low yields were

meaningful: 

“The low

tar brands have

cornered opinion that to the

extent any

brands are better for your

health, they

are. All smokers

were asked

whether they

thought any

220

Smoking and Tobacco Control Monograph No. 13

Figure 7-12

Marlboro Ultra Light Pristine Environment (1998)

Chapter 07 11/19/01 11:18 AM Page 220
particular brands were better for your health than others, and if so,

which brands. Three in ten of all smokers said some brands were

better for health than others, and almost half of the low tar brand

smokers said this. The brands named were almost exclusively low

tar brands, with the older low tar brands (Vantage, True and

Carlton) getting most mentions. Considering the short length of

time they have been on the market, both Merit and Now had comparatively good mention.” (See The Roper Organization, Inc., 1976,

p. 19.) 

“. . . [I]t is the lower tar content of these brands that make people say they are better for health. When asked why the brands they

named were better for your health, answers overwhelmingly were

concerned with lower tar content.” (See The Roper Organization,

Inc., 1976, p. 20.) 

The reassurance of apparent low yields led many smokers to switch

rather than quit: 

“Smokers needed light brands for tangible, practical, understandable reasons. . . It is useful to consider lights more as a third

alternative to quitting and cutting down—a branded hybrid of

smokers’ unsuccessful attempts to modify their habit on their own.”

[Emphasis in original.] (See British American Tobacco Co., circa

1985, pp. 9, 13.) 

[Many said] “. . . they had tried to quit smoking at some point

in time, they do not appear to have cut down the number of cigarettes they are smoking. The only concession that has been made is

the switch to an ultra low tar brand. These smokers seemed to be

either resigned to the fact or satisfied that they will probably never

quit smoking. In point of fact, smoking an ultra low tar cigarette

seems to relieve some of the guilt of smoking and provide an excuse

not to quit.” (See Goldstein/Krall Marketing Resources, Inc., 1979, p.

12.) 

The True® campaign in the 1970s spoke directly to the desire to quit,

portraying quitting and smoking True® as equivalent alternatives (see Figure

7-13). 

An important strategic reason for adding low-yield products to a product line, also known as a brand family, was to retain the patronage of consumers as they aged and became more concerned about their health: 

[Developing] “. . . new products in the higher end of the

reduced tar category. . . is especially important for Lorillard’s long

term growth. Younger smokers (less than 35) are smoking products

in the higher end of the reduced tar segment and lo-fi. These consumers will move down the tar spectrum, as they get older, with the

probability of staying with the line extensions of products consumed in their youth.” (See Mau, 1981, p. 7.)

221

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 221
Tobacco manufacturers saw advertising,

and marketing efforts more generally, as vital to how consumers perceived the products and themselves; these efforts ultimately

determined how well various firms

succeeded. Lorillard listed marketing’s psychological import right

alongside of the product’s capacity

to deliver the physiological stimulation of nicotine. 

“. . . [L]et me try to define

the elements of product acceptance (given sales distribution

and trial) as they relate to

tobacco products. . . The value

or price of the product is a factor. . . The second element in

acceptance is psychological.

One principle component of

this element arises from our

marketing effort. . . The third

element in acceptance is physiological, being comprised largely of the nicotine-induced stimulation.” (See Spears, 1973, pp. 2-3.) 

With experience, members of the industry realized that the best advertising gave filter smokers ego reinforcement, and didn’t focus solely on

nominal filter effectiveness. This might be appropriate when introducing

new product concepts (e.g., filters), but once the concept was understood, it

was better to avoid any direct addressing of health aspects. 

“1964-1972—The beginning of the high filtration derby. . . In

this type of environment, good new product copy directly addressed

the health arguments by focusing on lowered tar and nicotine while

also claiming to retain real tobacco taste.” [Emphasis in original.]

(See Latimer, 1976, p. 4.) 

“Less effective copy during this period continued to focus on

the filtration process (e.g., selectrate filter, charcoal filters, accu-ray,

etc.) or vacillated between emphasis on taste and emphasis on filter.” (See Latimer, 1976, p. 3.) 

Brown & Williamson articulated the dual objectives of good advertising—providing reassurance about healthfulness (without, of course, doing

so in a heavy-handed way to induce defensiveness) and also providing a

socially attractive brand image that the smoker could acquire when buying

and displaying the package: 

Lessons Learned

About Advertising

222

Smoking and Tobacco Control Monograph No. 13

Figure 7-13

Quit or Smoke True as Equivalent

Options (1976)

Chapter 07 11/19/01 11:18 AM Page 222
“. . . [T]he average smoker often seeks self-justification for smoking. Good cigarette advertising in the past has given the average

smoker a means of justification on the two dimensions typically

used in anti-smoking arguments: 1. High performance risk dimension. . . . 2. Ego/status risk dimension. 

Cigarette advertising. . . provides only justification/rationalization for those who already smoke. . . The smoker’s cigarette brand

choice process is largely an exercise in risk reduction. For some

smokers reduction in physical performance risk is paramount, for

others reduction in ‘ego/status’ risk comes first. . . All good cigarette

advertising has either directly addressed the anti-smoking arguments prevalent at the time or has created a strong, attractive image

into which the besieged smoker could withdraw.” [Emphasis in original.] (See Latimer, 1976, pp. 1-2.) 

The international headquarters of Brown & Williamson’s parent firm,

the British American Tobacco Co., counseled that new marketing approaches should: 

“. . . [C]reate brands and products which reassure consumers, by

answering to their needs. Overall marketing policy will be such that

we maintain faith and confidence in the smoking habit.” (See Short,

1977, p. 1.) 

The advertising campaigns and related communications were central to

how this was to be done: 

“All work in this area [communications] should be directed

towards providing consumer reassurance about cigarettes and the

smoking habit. . . by claimed low deliveries, by the perception of

low deliveries and by the perception of ‘mildness’. Furthermore,

advertising for low delivery or traditional brands should be constructed in ways so as not to provoke anxiety about health, but to

alleviate it, and enable the smoker to feel assured about the habit

and confident in maintaining it over time.” [Emphasis in original.]

(See Short, 1977, p. 3.) 

This attempt to reassure, but not so bluntly as to raise defensiveness,

and to simultaneously offer positive, ego-satisfying, brand imagery, seems

to have been a key to the success of some of the pioneering filter products.

Even the firms being dominated by the more successful marketing efforts of

other firms recognized this. In 1969, American Tobacco noted that: 

“. . . [T]hose ads which make a special point of stressing low tar

and nicotine appear to enjoy less attention and seem to have less

positive impact than those whose advertising has an enjoyment,

fun, or ‘story’ orientation.” (See Alex Gochfeld Associates, Inc.,

1969, p. 18.)

223

Chapter 7

Chapter 07 11/19/01 11:18 AM Page 223
Some very deceptive practices went totally unchecked.

Carlton® had the technology for delivering very low machinemeasured tar yields, and used these low-yield test results in its

advertising. A very desirable brand image was created while

promoting Carlton® in a hard box, emphasizing its very low

numbers (see Figure 7-14). Unfortunately, the boxed product

seems to have been a “phantom brand” and consumers who bought

Carlton® in the store got soft packs. Although consumers might well have

expected that they were getting the same product in a different box, it was

in fact a very different product—one that at times was delivering many,

many more times the tar and nicotine than indicated in the ads.

“FTC’s present system further contributes to consumer deception because it allows some cigarette companies to promote heavily

a ‘box’ brand, without adequately distinguishing it from the soft

pack of the same brand name, which delivers considerably more

‘tar’. In fact, however, the companies produce such a small volume

of the box brand as to make it a phantom brand that is rarely found

in the marketplace. On the other hand, the soft-pack version bearing the identical brand name and package design but testing at a

considerably higher ‘tar’ level, is the version readily available to the

consumer.” [Emphasis in original.] (See Pepples, 1982, p. 4.) 

Now®, like Carlton®, also featured its very low-yield hard box

product in the advertising, while its other product forms delivered

many, many more times higher yield rates (see Figure 7-15).

The only effective policing of deceptive advertising

of low-tar products came

from competitors, rather

than the FTC or any other

agency. In one case,

Lorillard used their data

from a taste comparison test

to imply a consumer preference for its Triumph® brand

over Merit® (see Figure 7-16)

and other brands. Both

Philip Morris and R. J.

Reynolds objected, and had

data of their own to support

their claims. In the court

proceedings, it was learned

that the Lorillard survey

showed 36 percent favored

Triumph® over Merit®, 24

percent rated them even,

and 40 percent favored

Merit®; these preferences

were obtained after subjects

THE 1980s

Policing Deceptive

Advertising

Carlton®

224

Smoking and Tobacco Control Monograph No. 13

Figure 7-14

Carlton Box “Phantom Brand” (1985)

Chapter 07 11/19/01 11:18 AM Page 224
had been informed of the

products’ tar levels. Although

nearly a quarter of the subjects had no preference, the

enjoined statement took

advantage of this and stated,

“An amazing 60% said 3 mg

Triumph tastes as good or

better than 8 mg Merit.” (See

Philip Morris, Inc., v. Loew’s

Theatres, Inc., 1980, p. 1.) 

Barclay® With the FTC yield data providing an apparent accreditation,

consumers were likely to perceive these yield numbers as

valid and meaningful. When

Brown & Williamson brought

the Barclay® product to market

in 1981, it did so with an ad

campaign that called the product 99 percent tar free (see Figure

7-17). The product’s structure,

which was described as

“extremely easy to design and

produce,” allowed for so much

dilution of the smoke column

when tested on machines that it generated phenomenally low-yield data in

the FTC test. This caused alarm among Brown & Williamson’s competitors,

who petitioned the FTC for help. Because of the competitive threat posed

by Barclay®, its competitors disclosed to authorities their awareness that the

FTC testing procedure was flawed and that the yield data were invalid for

human smokers. 

“The next generation of ‘Barclay competitors’ will be spawned

(indeed has already been spawned) in the minds of R&D and marketing people throughout the industry and its suppliers. This generation of products, or the next, could easily be products which will

deliver NO ‘tar’ or nicotine when smoked by the FTC method, and

yet when smoked by humans essentially be unfiltered cigarettes.

Such products could (and would) be advertized [sic] as ‘tar-free’,

‘zero milligrams FTC tar’, or the ‘ultimate low-tar cigarette’, while

actually delivering 20-, 30-, 40-mg or more ‘tar’ when used by a

human smoker! They will be extremely easy to design and produce.

. . . Such cigarettes, while deceptive in the extreme, would be very

difficult for the consumer to resist, since they would provide everything that we presently believe makes for desirable products: taste,

‘punch’, ease of draw and ‘low FTC tar’.” [Emphasis in original.]

(See Reynolds et al., 1982, p. 1.) 

225

Chapter 7

Figure 7-15

Now Box with Substantially Lower Yield

Than Soft Pack (1980)

Chapter 07 11/19/01 11:18 AM Page 225
[As to the threat Barclay represented:] “Here was a 1 mg. tar

product that delivered the taste

of a much stronger cigarette. Of

course we know how they did it,

but to consumers the 99% tar free

claim was intriguing. . . Merit

responded by supporting Merit

Ultra Lights with an $80 million

media budget.” (See Philip

Morris, 1990, p. 8.)

Important Imagery Once the product concept of low-yield filtration had been

communicated, and the previously

discussed brands had established

some corresponding reputation, their

advertising strategies tended toward

more visual, image-oriented forms, as

these could convey enviable

lifestyles, healthy behavior, rewarded

risk-taking, and the social class and

‘intelligence’ of brand users.

When Merit Ultra Light® was

introduced in 1983, the advertising

program had an $80 million media budget, which did not account for retail

promotional efforts. This advertising series featured imagery of large sailing

ships in what was termed the “sea” campaign (see Figure 7-18). The executions not only showed young people in an enviable, carefree, affluent

lifestyle amidst a pristine environment, they also were careful to avoid any

suggestions of danger. 

Images and ad copy had to be carefully selected, lest the

ads reinforce fears rather than offer reassurance. In 1980,

one Vantage® ad made direct reference to “what you may not want” from a

cigarette, only to discover that it alarmed some readers about cancer: 

“The fact that a Vantage ad dares to raise the issue of ‘what you

may not want’ generates defensiveness toward smoking in general,

and a feeling of discomfort. The reference to the taste of Vantage is

lost; overpowered by the implications of tar, nicotine and cancer.”

(See R. J. Reynolds-MacDonald, 1980.) 

The target Vantage® smoker was “female, white collar, extremely concerned about their health, and would like to quit smoking.” A Vantage® ad

headlined “To Smoke or Not to Smoke” (see Figure 7-19) ran in both the

United States and Canada. It stated that, “Vantage is the cigarette for people

who may have second thoughts about smoking and are looking for a way

to do something about it.” According to an R. J. Reynolds operational plan

Vantage®—An Intelligent

Choice

226

Smoking and Tobacco Control Monograph No. 13

Figure 7-16

Triumph Beats Merit with Deceptive

Data (1980)

Chapter 07 11/19/01 11:18 AM Page 226
(1983) and strategic plan (1983-

1987), the basic strategy was to

present Vantage® as an intelligent choice, “positioning

Vantage as the only contemporary choice for intelligent smokers.” (See Pollay, 2000.) The tactic was to influence consumer

perceptions. A 1983 R. J.

Reynolds media plan sought “to

establish a consumer perception

that Vantage is a contemporary

cigarette for intelligent smokers.” (See Pollay, 2000.)

Apparently, this aim was accomplished because, in 1987, an R. J.

Reynolds media plan briefing

document stated that the goal

for a target audience with a

“high amount of quitters” was

“to maintain consumer perception that Vantage is a contemporary cigarette for intelligent

smokers.” (See Pollay, 2000.) 

No doubt envious of the success of Merit® among

“concerned smokers,” as well as that of Marlboro®

among starters, R. J. Reynolds commissioned in-depth psychological

research from Social Research, Inc., in 1982. The purpose of the survey was

to compare the smokers of Vantage® and Merit® based on their smoking histories, their beliefs about the filter and other responses to advertising, and

their personalities. In-depth interviews elicited insights into some of the

psychological subtleties of respondents from Atlanta, Indianapolis, Denver,

Phoenix, and San Francisco. R. J. Reynolds gleaned some useful information

from the research: 

“Both Vantage and Merit smokers have similar early smoking

histories. . . moving from non-filters to filters, switching to lighter

cigarettes to relieve physical symptoms and as an acknowledgement

of increased concerns about alleged health hazards.” [Emphasis in

original.] (See Levy and Robles, 1982, p. 5.) 

“Vantage smokers believe that the filter itself is strong enough

to catch these impurities and that the hole structure is such that

they will not see so much of the resulting discoloration. These ideas

make them think the end product is a milder and more ‘healthful’

smoke.” (See Levy and Robles, 1982, p. 16.) 

“Merit smokers. . . have been influenced by Merit advertising

which so single-mindedly proclaims the brand’s lowered tar and

nicotine. . . Vantage smokers. . . the advertising influenced them by

Psychoanalyzing Merit®

and Vantage® Smokers

227

Chapter 7

Figure 7-17

Barclay—99% Tar Free (1981)

Chapter 07 11/19/01 11:19 AM Page 227
promising real smoking satisfaction from a cigarette, by

not focusing so much on

the low tar aspect.” (See

Levy and Robles, 1982, p.

89.)

Some members of the

industry have

long found

the appearance of Federal

Government vetting to be a

desirable factor usable in advertising. For example, the 1958

advertising for Parliament®

boasted that it was “the first filter cigarette in the world that

meets the standards of the

United States Testing Co.” (see

Figure 7-20). The ad showed the

organization’s official seal,

which included a microscope,

and although the ad was generated by a private firm, the seal

was readily perceived as acceptance by a Government agency. 

Note, too, the Carlton® use of a headline stating that the “Latest U.S.

Gov’t [sic] Laboratory test confirms. . . Carlton is lowest” in 1985, as seen

earlier in Figure 7-14. 

The Federal Government’s adoption of a “uniform and reliable testing

procedure” consistent with the methodology of Philip Morris also seemed

beneficial to that corporation. Philip Morris foresaw in 1964 that such test

results could be used in advertising copy, as they could communicate that

an official Government agency had vetted the products, as well as the possibility that data with a competitive advantage angle could be provided: 

“Apart from possible legal requirements, such a policy would

enhance advertising opportunities.” (See Wakeham, 1964, p. 6.) 

Later, Brown & Williamson saw the benefit to them, even if not to the

public, in using Government evaluations and rating procedures. While the

industry preferred to go unregulated, regulation offered some benefits,

namely prospects for greater stability and the appearance of Government

approval of their products by official testing procedures.

“The tobacco industry, of course, would prefer no regulation at

all. If there must be regulation, the industry is probably better off to

have it at the federal level. . . Even expanded regulatory efforts may

be shared by the industry to [illegible word] stability in the market

DISCUSSION

The Value of Official

Government Ratings

228

Smoking and Tobacco Control Monograph No. 13

Figure 7-18

Merit Ultra Light “Sea” Campaign (1986)

Chapter 07 11/19/01 11:19 AM Page 228
or by individual manufacturers

to bolster market positions—

for example, by capitalizing

on official tar and nicotine

ratings in cigarette advertising.” (See Pepples, 1976, p. 8.) 

The promotional value of the

FTC data meant that the industry

recognized protecting the credibility of the FTC procedure was

in its own interests: 

“Inherent limitations of

the FTC cigarette testing program, and borderline low-‘tar’

advertising practices resulting

from the way the test results

are reported have contributed

to substantial consumer confusion and misunderstanding.

This situation threatens to

erode public confidence in

both the FTC’s test reports

and the industry’s advertising

claims.” (See Pepples, 1982, p.

1.)

Cigarette advertising is notoriously uninformative, with

characteristic forms using veiled health implications and

pictures of ‘health’ along with vague promises of taste and satisfaction

(Pollay, 1994, pp. 179-184). Occasionally, ads for new technological developments in filter design called attention to the filter, with allusions to filter

effectiveness, but almost always without being specific about what constituents of tobacco or its smoke were being filtered, what degree of filtration effectiveness was being realized, or what health or safety consequences

were warranted. Only the tar and nicotine information—as mandated by

regulation and generated by conventional test methods—is given, without

interpretation. For example, Carlton® now encourages smokers to start

“thinking about number 1” and smoke its “Ultra Ultra Light” cigarette (see

Figure 7-21). 

Many cigarette ads contain no information whatsoever, save for the

implicit reminder that a brand exists, e.g., many Marlboro® ads. Some contemporary ads, like a recent campaign for Merit Ultra Light®, take a humorous visual approach to convey that it might be lighter than expected (see

Figure 7-22). 

The cigarette industry has not voluntarily employed its advertising

to inform consumers in a consistent and meaningful way about any

of the following: 1) the technologies employed in fabricating the products,

2) the constituents added in the manufacturing processes, 3) the residues

Consumer

Information

Poor Information, But

Rich Imagery 

229

Chapter 7

Figure 7-19

Vantage “To Smoke or Not To Smoke”

(1974)

Chapter 07 11/19/01 11:19 AM Page 229
and contaminants that may be present

in the combustible column, 4) the

constituents of smoke that may be

hazardous, 5) the addictiveness of

nicotine, or 6) the health risks to

which its regular consumers and their

families are inevitably exposed.

Instead, their advertising for low-yield

products has relied on pictures of

health and images of intelligence, and

has misled consumers into believing

filtered products in general, and lowtar products in specific, to be safe or

safer than other forms without

explaining exactly why. 

While the technological means

to produce low-yield products might

seem important, to industry insiders

it was the marketing sophistication

that was even more crucial in determining the relative success of various

firms: 

[In contrast to the import of marketing] “. . . technology in the

tobacco industry has had virtually no effect on the relative success

of the six companies. . . the industry has become so sophisticated in

marketing that nontechnical developments, while they might have a

large influence on the industry in terms of the types of cigarettes

available, would probably do little to shift shares from one company to another.” [Emphasis added.] (See Ennis et al., 1984.) 

Michael Miles, Chairman and Chief Executive Officer of Philip Morris,

defended advertising eloquently in a trade ad: 

“Those of us in the business of building brands don’t have to be

sold on the importance of advertising or on the necessity for advertising. For me, there is still nothing more exciting in business than

to watch effective advertising work its magic in the marketplace. For

when a brand is acknowledged and accepted by the consumer, it

becomes something much more than what it really is. . . we invest

$2 billion annually in advertising. It’s worth every penny. For we

believe that a strong brand gives the consumer another whole set of

reasons—emotional and personal—to act.” (See Miles, 1992, p. 16.)

SUMMARY This chapter has reviewed many tobacco industry documents and marketing trade sources. The review revealed the importance of marketing and

advertising to the vitality of this industry, and the many means used to create an appearance of healthfulness for various cigarette products, especially

Marketing/Advertising

Gives Cigarettes Vitality

230

Smoking and Tobacco Control Monograph No. 13

Figure 7-20

Parliament—Endorsement of United

States Testing Co. (1958)

Chapter 07 11/19/01 11:19 AM Page 230
those with nominally low yields.

Several tactics were employed by

the tobacco industry that misled

consumers to perceive filtered

and low-tar delivery products as

safe or safer and as a viable alternative to quitting. 

Nicotine delivery is a design

feature of cigarette products, and

an essential part of the design.

Tobacco company documents

reflect a fear of consumers

becoming weaned from smoking

if they are not maintained with

sufficient nicotine. Consumer

acceptance of products that fail

to deliver adequate nicotine satisfaction is also difficult to maintain. 

Health concerns of a serious

nature have been present among

some smokers since at least the

1950s. Females, older, and more

highly educated smokers have

long been more likely to manifest health concerns. The ramifications of these health concerns are anxieties, conflicts, shame, and guilt, leading to a need for reassurance from

advertising. In the 1950s, the promotion of filters provided this reassurance

with very explicit verbal representations about the health protection that

they offered. Once the nominal purpose of filtration was well understood

by the consuming public, the healthfulness of filters was represented by

more implicit means. For example, thinly veiled language (“hospital white”

filters; “Alive with Pleasure”) and visual “pictures of health” images were

used, displaying bold and robust behavior in pristine environments. 

The image or illusion of filtration is essential to the selling of cigarettes,

whereas the fact of filtration is not. Consumer (smoker) opinion and perceptions are what governs their behavior, not the medical or technological

facts known to manufacturers and experts. 

Many deceptive practices have been employed over the years (some

continue to this date) that foster and perpetuate the illusion that various

cigarette brands and product forms are relatively healthy. These tactics

include: 

• Using Medicinal Menthol. Menthol was introduced into some

products capitalizing on its “pseudo-health” benefit, a consumer

perception derived from experiencing menthol elsewhere in the

medicinal context of cough and cold remedies. 

231

Chapter 7

Figure 7-21

Carlton—“Isn’t It Time You Started

Thinking About Number One?” (1999)

Chapter 07 11/19/01 11:19 AM Page 231
• Loosening Filters. Once established in the public’s mind as having effective filtration, Kent® offered several successive generations of product in the 1950s and 1960s that were heralded as

“new and improved,” but in fact contained ever more tar and

nicotine. 

• Using High-Tech Imagery. New filters were offered that seemed

to be the fruits of scientific research and to have meaningful

technological innovations, such as charcoal filters, dual filters,

chambered filters, recessed “safety zoned” filters, gas trap filters,

etc. Almost none of these specified the hazardous elements

being filtered. 

• Using Virtuous Brand Names and Descriptors. Brands were given

names to imply state-of-the-art technology and/or a virtuous

product, e.g., Life®, Merit®, Now®, True®, or Vantage®. Product

variations are described in technically meaningless, but seemingly quantitative, descriptors like “Mild,” “Ultra,” “Light,” or

“Super-Light.” 

• Adding a Very Low-Yield Product to a Product Line. Some product lines had wide-ranging tar and nicotine deliveries in the

same brand family. The best of these levels was used for adver232

Smoking and Tobacco Control Monograph No. 13

Figure 7-22

Merit Ultra Lights—Sumo Ballet Lighter Than Expected (1999)

Chapter 07 11/19/01 11:19 AM Page 232
Chapter 7

233

tising purposes to reassure consumers while selling other product varieties. In some cases, the best product variant was rarely

sold and was known as a phantom brand. 

• Fooling the Machines and Using the Data to Fool Smokers.

Filters and cigarette papers were developed starting in the 1950s

that “air-conditioned” the smoke by diluting the smoke column

with side-stream air. When smoked by machines as in the FTC

tests, low-tar and low-nicotine numbers resulted, a desirable outcome for promotional purposes—but higher yields were ingested

by real smokers, a desirable outcome for maintaining nicotine

addiction. 

Low-yield cigarettes were heavily promoted. Promotional programs for

cigarettes have been lavishly funded in general, with advertising in multiple

media. A disproportionate amount of this funding promoted low-yield

products when they were introduced in the 1970s. 

Little or no meaningful information is contained in promotions for a

given cigarette, such as its ingredients and additives, the technology of filtration, the hazardous constituents of smoke, or the health consequences of

smoking. Consumer ignorance and confusion has been persistent over

many decades. While smokers who switch to low-yield brands manifest

faith in their relative healthfulness, few consumers know the true delivery

characteristics of the brands that they smoke, and even their general

impressions are not very accurate. 

Finally, testing of products by official Government agencies, such as the

FTC, imbues the industry with a certain level of credibility, while providing

Government-rated data that can be used for promotional purposes. 

CONCLUSIONS

1. Advertisements of filtered and low-tar cigarettes were intended to

reassure smokers (who were worried about the health risks of smoking) and

were meant to prevent smokers from quitting based on those same concerns. 

2. Advertising and promotional efforts were successful in getting smokers to use filtered and low-yield cigarette brands. 

3. Internal tobacco company documents demonstrate that the cigarette

manufacturers recognized the inherent deception of advertising that offered

cigarettes as “Light” or “Ultra-Light,” or as having the lowest tar and nicotine yields. 

Chapter 07 11/19/01 11:19 AM Page 233
Alex Gochfeld Associates, Inc. The present competitive position of Pall Mall Gold 100’s and Silva

Thins: A motivational research study. Prepared

for The American Tobacco Company, March,

1969. Bates No. ATXO5 0278907-ATX05

0278953. [101] 

Blatnik, J. Making cigarette ads tell the truth.

Harper’s Magazine 217:45-49, 1958. 

Brand Report 12: Cigarettes. Media Decisions

11(10):141-158, 1976. 

Brand Report 23: Cigarettes. Media Decisions

12(10):149-164, 1977. 

British American Tobacco Co., Ltd. The product in

the early 1980s. March 29, 1976. [080, PSC 42b] 

British American Tobacco Co., Ltd. Year 2000. April

4, 1979. [039, K0137] 

British American Tobacco Co., Ltd. Research & development/marketing conference. Circa 1985. [081,

PSC 60] 

Brown & Williamson. Purite filter. Circa 1977. 

Chambers, R.L. U.S. cigarette history. Brown &

Williamson, September 21, 1979. [038, K0481] 

Crittenden, A. $40 million for a real smoke. The New

York Times, May 15, 1977, Section 3, p. 1 ff. 

Cunningham and Walsh. [Advertising] Kool: 1933-

1980. A retrospective view of Kool. Brown &

Williamson, November 10, 1980. [041, K0478] 

DeGarmo, Inc. Conclusions and implications of True

portfolio research. DeGarmo, Inc., Research

Department; prepared for Lorillard, August,

1974. [102] 

Dougherty, P.H. Advertising, new low-tar, high budget smoke. The New York Times, p. 44, June 20,

1977. 

Ennis, D.M., Tindall, J.E., Eby, L.C. Product testing

short course. Product Evaluation Division,

Research & Development Department, Philip

Morris U.S.A., January 23-24, 1984. [058, K0081] 

Federal Trade Commission. Trade Regulation Rule for

the Prevention of Unfair and Deceptive Advertising

and Labelling of Cigarettes in Relation to the Health

Hazards of Smoking and Accompanying Statement of

Basis and Purpose of Rule. Federal Trade

Commission, Washington D.C., June 22, 1964. 

Fitzgerald, C.W., Senkus, M., Laurene, A., Kecseti,

F.M. (presenters). New product/merchandising

directions: A three year action plan. R. J.

Reynolds, August 19, 1976. [023, K0203] 

Gardner, F. Under siege, cigarette marketers fight

back. Marketing and Media Decisions 19(9):34-37,

175-177, 1984. 

Goldstein/Krall Marketing Resources, Inc. A qualitative exploration of smoker potential for a new

entry in the ultra low tar market category (two

focused group interviews). Prepared for Philip

Morris, January, 1979. [037, K0041] 

Hind, J.F., Fitzgerald, C.W., Ritchy, A.P. New brand

orientation for Ogilvy & Mather, Inc. R. J.

Reynolds Tobacco Company, August 10, 1976.

[103] 

John, J., Wakeham, H. Breakthrough of the high

taste, low tar cigarette—A case history of innovation. Philip Morris Research Center. 1977. [075]

Johnston, M.E. Market potential of a health cigarette. Special Report No. 248, Philip Morris, June,

1966. [004, K0126] 

Kalhok, A.I., Short, P.L. The effect of restrictions on

current marketing on marketing in the future.

Brown & Williamson, May, 1976. [024, K0365] 

Kaplan, M. Inside advertising: Perfect match.

American Photographer October:100-102, 1986. 

Kenyon & Eckhardt Advertising. Young adult smoker

life styles and attitudes. Prepared for Brown &

Williamson, 1974. [018, K0028] 

Kieling, R.F. Implications for Kent. Director of

Market Research. August 31, 1964. [002, K0016] 

Koten, J. Tobacco marketers’ success formula: Make

cigarets [sic] in smoker’s own image. The Wall

Street Journal, p. 22, February 29, 1980. 

Latimer, F.E. Cigarette advertising history. Brown &

Williamson, November 29, 1976. [026, K0358] 

Levy, S.J., Robles, A.G. Vantage and Merit smokers. 

Social Research, Inc., prepared for R. J. Reynolds,

April, 1982. [112] 

Lorillard, Inc. Triumph planning seminar:

Competitive advertising. February 25, 1980.

[111] 

Smoking and Tobacco Control Monograph No. 13 

234

Dr. R. W. Pollay explains the bracketed numbers following some of the World Wide Web/trail-related References: The two numbers

(A, B, [e.g., 026, K0358]) following the descriptive information (author, title, date, etc.) are: (A) a sequence number for the authors’

unique set of documents, and (B) the number that the National Cancer Institute or others used for identifying documents. This latter

sequence is the more helpful for the reader, as it should link to a database at the National Cancer Institute. The Institute provided

the authors with a lengthy inventory of documents from which items were selected by these numbers.

Note as to source of sources: Items 001-064 were supplied by KBM Group as the contractor for National Cancer Institute project on

"Cigarettes with Low Machine-Measured Yields of Tar and Nicotine," and bear both the "TIPS" and "K" numbers in parentheses

(e.g., 001, K0474). Items 065-081 were from sundry alternative sources, including the (Canadian) Physicians for a Smoke Free

Canada Web site. Items 101-114 were from various corporate and trial Web sites, and were provided on request by Ms. Nadine

Leavell, archivist of the Roswell Park Cancer Institute, Buffalo, New York.

REFERENCES

Chapter 07 11/19/01 11:19 AM Page 234
Chapter 7

235

Marketing and Research Counselors, Inc. What have

we learned from people? A conceptual summarization of 18 focus group interviews on the subject of smoking. Prepared for Brown &

Williamson, May 26, 1975. [020, ASH] 

Mau, T.H. August 11, 1981. Lorillard memo. Replies

to 5-year plan questionnaire. [044, K0383] 

Miles, M. 4 A’s advertisement. The New York Times, p.

16, November 24, 1992. 

O’Keefe, A.M., Pollay, R.W. Deadly targeting of

women in promoting cigarettes. Journal of the

American Medical Womens Association 51(1-2):67-

69, 1996. 

Oldman, M. Products/consumer interaction. British

American Tobacco Co., Ltd., May 19, 1981. [043,

K0373] 

O’Toole, J.E. The Trouble with Advertising. New York:

Chelsea, 1981. 

Oxtoby-Smith, Inc. A psychological map of the cigarette world. Prepared for the Ted Bates advertising agency and Brown & Williamson, August,

1967. [005, K0107] 

Pepples, E. February 4, 1976. Brown & Williamson

memo. Industry response to cigarette health controversy. [027, K0125] 

Pepples, E. Low-“tar” cigarette advertising and the

FTC cigarette testing program: A time for reexamination. Brown & Williamson memo, June

9, 1982. 

Philip Morris, Inc. v. Loew’s Theatres, Inc., 511 F.

Suppl. 855 (SDNY 1980). 

Philip Morris, Inc. Merit history (script for slide presentation). August 17, 1990. [065] 

Pollay, R.W. Promotion and Policy for a Pandemic

Product: Notes of the History of Cigarette

Advertising (US). Tobacco Litigator’s Bookshelf

4.7 TPLR, 1989a.

Pollay, R.W. Filters, flavors . . . flim-flam, too!

Cigarette advertising content and its regulation.

Journal of Public Policy and Marketing 8:30-39,

1989b. 

Pollay, R..W. Historical content analyses of cigarette

advertising. Preventing Tobacco Use Among Young

People: A Report of the Surgeon General. U.S.

Department of Health and Human Services,

Centers for Disease Control and Prevention,

Office on Smoking and Health, 1994. 

Pollay, R.W. Targeting youth and concerned smokers:

Evidence from Canadian tobacco industry documents. Tobacco Control 9(2):136-147, 2000. 

R. J. Reynolds-MacDonald (Canada). Vantage Lights

Media Brief, 1980. 

Reynolds, J.H., Norman, A.B., Robinson, J.H. March

4, 1982. R. J. Reynolds interoffice memo.

Possible consequences of failure of the FTC to

act against the Barclay cigarette filter and its

mimics. [050] 

The Roper Organization, Inc. A study of smokers’

habits and attitudes with special emphasis on

low tar cigarettes. Prepared for Philip Morris

U.S.A., May, 1976. [025, K0286] 

Schori, T.R. Tar, nicotine and smoking behavior.

Philip Morris U.S.A. Research Center, November,

1971. [010, K0327] 

Short, P.L. Smoking & health item 7: The effect on

marketing. British American Tobacco Co., Ltd.,

April 14, 1977. [030, Minnesota Litigation] 

Spears, A. Untitled (Re: Costs of making tobacco

products). Lorillard, November 13, 1973. [015,

K0134] 

Teague, C.E. Proposal of a new, consumer-oriented

business strategy for RJR tobacco company.

September 19, 1969. [007, K0083] 

Teague, C.E. A gap in present cigarette product lines

and an opportunity to market a new type of

product. March 28, 1972a. [012, K0416] 

Teague, C.E. Research planning memorandum on

the nature of the tobacco business and the crucial role of nicotine therein. R. J. Reynolds, April

14, 1972b. [011, K0121] 

Tindall, J.E. A new low delivery segment. Philip

Morris U.S.A. Research Center, May 22, 1973.

[014, K0324] 

Wakeham, H. Smoking and health—Significance of

the report of the Surgeon General’s committee to

Philip Morris, Incorporated. Philip Morris

Research Center, February 18. [001, K0474] 

What are the obstacles/enemies of a swing to low

"tar" and what action should we take?

Anonymous—July 2, 1982, Trial Exhibit 26,185,

Minnesota Litigation. [053] 

Whelan, E.M. A Smoking Gun: How the Tobacco

Industry Gets Away With Murder. Philadelphia:

Geo. Stickley, 1984. 

Zoler, J.N. Research requirements for ad claims substantiation. Journal of Advertising Research 23: 9-

15, 1983.

Chapter 07 11/19/01 11:19 AM Page 235
Smoking and Tobacco Control Monograph No. 13 

236

Chapter 07 11/19/01 11:19 AM Page 236