Health impact of “reduced yield” cigarettes: a critical ......burden caused by smoking. This...

Health impact of “reduced yield” cigarettes: acritical assessment of the epidemiological evidence

Michael J Thun, David M Burns

AbstractCigarettes with lower machine measured“tar” and nicotine yields have beenmarketed as “safer” than high tarproducts over the last four decades, butthere is conflicting evidence about theimpact of these products on the diseaseburden caused by smoking. This papercritically examines the epidemiologicalevidence relevant to the health conse-quences of “reduced yield” cigarettes.Some epidemiological studies have foundattenuated risk of lung cancer but notother diseases, among people who smoke“reduced yield” cigarettes compared tosmokers of unfiltered, high yield products.These studies probably overestimate themagnitude of any association with lungcancer by over adjusting for the number ofcigarettes smoked per day (one aspect ofcompensatory smoking), and by not fullyconsidering other diVerences betweensmokers of “high yield” and “low yield”cigarettes. Selected cohort studies in theUSA and UK show that lung cancer riskcontinued to increase among oldersmokers from the 1950s to the 1980s,despite the widespread adoption of loweryield cigarettes. The change to filter tipproducts did not prevent a progressiveincrease in lung cancer risk among malesmokers who began smoking during andafter the second world war compared tothe first world war era smokers. Nationaltrends in vital statistics data show declin-ing lung cancer death rates in youngadults, especially males, in manycountries, but the extent to which this isattributable to “reduced yield” cigarettesremains unclear. No studies haveadequately assessed whether healthclaims used to market “reduced yield”cigarettes delay cessation among smokerswho might otherwise quit, or increase ini-tiation among non-smokers. There is noconvincing evidence that past changes incigarette design have resulted in animportant health benefit to eithersmokers or the whole population. Tobaccocontrol policies should not allow changesin cigarette design to subvert or distractfrom interventions proven to reduce theprevalence, intensity, and duration ofsmoking.(Tobacco Control 2001;10(Suppl I):i4–i11)

Keywords: tar and nicotine; lung cancer; changingcigarette

Cigarettes with lower machine measured “tar”and nicotine yields have been marketed as“safer” than high tar products over the last fourdecades,1 2 but there is limited and conflictingevidence about the net impact of theseproducts on the disease burden caused bysmoking. The principal uncertainties are theextent to which compensatory smoking behav-iours induced by “reduced yield” cigarettesmay oVset any putative reductions in the toxic-ity or carcinogenicity of these products, andwhether health claims used to promote “Light”cigarettes may delay cessation among smokerswho might otherwise quit, or increase initiationamong non-smokers. Epidemiological studieshave generally focused narrowly on theintrinsic toxicity and carcinogenicity of“reduced yield” products, rather than on theirindirect eVects on smoking behaviour or thenumber of people smoking.

This paper critically examines the epidemio-logical evidence relevant to the healthconsequences of “reduced yield” cigarettes. Itbegins by briefly reviewing the historical devel-opment of products with lower tar and nicotineyields, as measured by the standard FederalTrade Commission (FTC) protocol ofmachine smoking.3 It then considers theevidence that smokers “compensate” forreductions in machine measured tar and nico-tine by increasing the number of cigarettessmoked per day as well as by increasing thepuV volume and number of puVs per cigarette.It discusses the strengths and limitations ofseveral epidemiological approaches that havebeen used to assess the health eVects of“reduced yield” cigarettes. These include ana-lytic (cohort and case–control) studies thatcompare the risks to smokers who use diVerenttypes of cigarettes; selected cohort studies thatillustrate how the lung cancer risk to smokershas increased over time; and analyses of trendsin national death rates from lung cancer by agein relation to age specific smoking patterns.

Historical development of “lesshazardous” cigarettesThe postulate that cigarettes with lower tardelivery might be less hazardous emerged fromthe early research findings on tobacco relateddiseases. Epidemiological studies repeatedlydemonstrated increased lung cancer risk insmokers beginning in the 1950s4–7; experimentsshowed that painting cigarette smokecondensate on the backs of mice produced skintumours.8 By 1967, independent scientists andpublic health authorities recommended to theUS Congress that cigarettes with lower

Tobacco Control 2001;10(Suppl I):i4–i11i4

American CancerSociety, Atlanta,Georgia, USAM J Thun

Department ofMedicine, Universityof California, SanDiego, California, USAD M Burns

Correspondence to:Michael J Thun MD,American Cancer Society,1599 Clifton Road, Atlanta,GA 30329–4251, [email protected]

www.tobaccocontrol.com

on February 4, 2021 by guest. P

rotected by copyright.http://tobaccocontrol.bm

j.com/

Tob C

ontrol: first published as 10.1136/tc.10.suppl_1.i4 on 1 Decem

ber 2001. Dow

nloaded from



j.com/

Tob C


ber 2001. Dow

nloaded from



j.com/

Tob C


ber 2001. Dow

nloaded from



j.com/

Tob C


ber 2001. Dow

nloaded from



j.com/

Tob C


ber 2001. Dow

nloaded from



j.com/

Tob C


ber 2001. Dow

nloaded from

http://tobaccocontrol.bmj.com/






particulate yield be developed and marketed tosmokers who could not quit.9

The tobacco industry responded to healthconcerns about cigarette use first by adding fil-ters to some brands of cigarettes beginning inthe 1950s, and then by oVering cigarettes thatdelivered progressively less “tar” as measuredby machine smoking.3 10 Much of the reductionin “tar” (total particulate matter minusnicotine and water) was achieved by theaddition of ventilation holes around the filter todilute the smoke with entrained air. A methodof machine smoking that was developed in the1930s11 became codified in the Federal TradeCommission (FTC) annual ratings ofcigarettes.3 This protocol specifies fixed smok-ing parameters for the machine: 35 ml puVvolume, 2 second puV duration, 1 puV perminute frequency, and a fixed butt length towhich the cigarette is smoked.12 Brands thatyield approximately 1–6 mg of tar per cigaretteby the FTC method are referred to as “Ultra-light”; those with approximately 7–15 mg taras “Light”, and those yielding more than15 mg tar as “Regular” or “Full flavoured”.13

Before the mid 1950s, unfiltered cigarettestypically yielded 25–30 mg tar by the FTCmethod.

The FTC ratings do not take into accountvariations in tar and nicotine yield that can beobtained by smokers seeking to maintain aparticular intake of nicotine.3 14–16 Smokers whouse “reduced yield” products can increase theamount of nicotine and tar extracted from eachcigarette by taking more puVs per cigarette,obstructing the ventilation holes around thefilter, and inhaling a larger puV volume moredeeply into the lungs.17 Smokers can also com-pensate for reduced yield by smoking morecigarettes per day.17 Internal documents fromthe tobacco industry express scepticism aboutthe eYcacy of filter tip and “lower yield” prod-ucts in reducing the exposure of smokers, even

during the years when these products were firstheavily marketed to assuage the healthconcerns of smokers.1 2 A memo from HelmutWakeham of Philip Morris (dated 24 March1961) states, “As we know, all too often thesmoker who switches to a hi-fi cigarette windsup smoking more units in order to providehimself with the same delivery which he hadbefore”.18

Compensatory smokingMany experimental studies document thatsmokers who are switched to cigarettes withlower nicotine yield than their usual brand areable to maintain higher plasma concentrationsof nicotine metabolites than would be expectedfrom the FTC ratings. Compensation has beendemonstrated experimentally in both shortterm19–23 and long term studies.24–29 What is lesscertain is the extent to which smokerscompensate by increasing the number of ciga-rettes smoked per day as opposed to otherbehavioural changes that extract more nicotinefrom each cigarette. This distinction isimportant with respect to the epidemiologicalstudies, since most of these studies adjust forthe number of “reduced yield” cigarettessmoked per day, and may thereby over-controlfor one aspect of compensatory smoking.30

We assessed the relation between daily ciga-rette consumption and the FTC rating of nico-tine yield in several additional large studies, theAmerican Cancer Society Cancer PreventionStudy I (CPS-I) cohort, and the 1990 and1996 California Tobacco Surveys (CTS).30 Inthe CPS-I cohort, questionnaires were admin-istered periodically during the follow up todocument changes in smoking behaviour orcigarette brand. Based on these data, fig 1shows the mean change in cigarettes smokedper day in relation to the change in nicotineyield among 169 610 white male smokers whochanged brands between enrollment in 1959and the end of follow up in 1972.27 Each milli-gram decrease in machine measured tar yieldwas associated, on average, with an increase of2.31 cigarettes smoked per day. Thisprospective analysis controlled for age,cigarettes smoked per day before the switch,and tar and nicotine yields of the cigarettesmoked before the switch. A similar relationwas seen in the 1990 and 1996 CTS forcigarette brands with less than 0.95 mgnicotine yield (fig 2). This analysis wasrestricted to adult smokers, age 25–64 years,who smoked at least five cigarettes daily duringthe year before the survey and had notattempted to quit smoking in the previous 12months. The intent was to limit these analysesto persons with relatively stable smokingpatterns31 32 and less likelihood of havingchanged their smoking because of illness.These studies suggest a small but demonstra-ble increase in the number of cigarettessmoked per day among smokers of lower yieldcigarettes. Previous reports14 28 29 33 34 have beenless consistent, perhaps because of smallersample sizes and the inclusion of people withless stable smoking patterns.

Figure 1 Mean change in adjusted cigarettes smoked per day (CPD) reported for subjectschanging brand smoked versus change in machine measured nicotine yield per cigarette:white male smokers (n = 169610), American Cancer Society Cancer Prevention Study I(CPS-I) study, followed 1960 to 1972. Each milligram decrease in machine measured taryield among CPS-I smokers who changed brands between enrollment in 1959 and end offollow up in 1972 was associated with an increase of 2.31 cigarettes smoked per day. Basedon 169610 white male smokers.30

30

10

20

0

–10

–30

–20

Difference in nicotine of one cigarette (mg)between present brand and former brand

Covariates: nicotine, age, cpd, tarSlope of fit line: –2.31 cpd/mg nicotine

Mea

n c

han

ge

in a

dju

sted

CP

D (

95%

CI f

or

mea

ns)

–2 –1.5 –1 –0.5 0 0.5 1 1.5 2

Health impact of “reduced yield” cigarettes i5




j.com/

Tob C


ber 2001. Dow

nloaded from


Epidemiological studiesCOHORT AND CASE–CONTROL STUDIES

COMPARING DIFFERENT TYPES OF CIGARETTES

Over 50 epidemiological studies havecompared disease risks among smokers whouse diVerent types of cigarettes.35–89 Thesestudies, discussed elsewhere,30 typicallymeasure the occurrence of lung cancer,35–78

coronary heart disease,39–42 44 45 51 56 64 67 79–82 andrespiratory diseases caused bysmoking39 42 45 67 83–89 in smokers who use filtertip products compared to those who use unfil-tered, “high yield” products. Most of thesestudies report lower lung cancer risk amongsmokers who use “reduced yield” products,relative to those who smoke unfiltered, “higheryield” cigarettes. They do not consistentlyreport lower risk of coronary heart disease,total stroke, or chronic obstructive pulmonarydisease (COPD).

The studies that compare diVerent types ofcigarettes have at least two limitations thatcomplicate their interpretation. First, theyfocus mostly on diVerences in the intrinsicpathogenicity of “reduced yield” cigarettescompared to unfiltered, higher yield productswithout adequately considering the indirectadverse eVects that lower yield cigarettes mayhave on smoking behaviour. For example, thestudies compare risk among smokers who usediVerent types of cigarettes but do not assesswhether some smokers have deferred quittingbecause of health claims about “reduced yield”products. Lung cancer risk increases exponen-tially with longer duration of smoking.90

Factors that delay cessation may outweigh anyputative reductions in tar yield, increasingrather than decreasing the lung cancer risk foran individual smoker. Furthermore, healthclaims used to market “Light” cigarettes couldworsen the population burden of disease bytrivialising the actual hazards of smoking, thuspromoting initiation or resumption ofsmoking.1 2

Secondly, the published cohort andcase–control studies may overestimate themagnitude of any attenuation in lung cancerrisk by inappropriately controlling for thenumber of cigarettes smoked per day and byunder controlling for other factors that could

reduce risk. In adjusting for the number ofcigarettes smoked per day, the epidemiologicalstudies assume that smokers who switch to“reduced yield” cigarettes do not compensatefor the lower yield by increasing their dailycigarette consumption. Some adjustment forcigarettes per day is needed to assess theintrinsic carcinogenicity of the cigarette, butthis adjustment is inappropriate if it obscuresan adverse eVect of compensatory smoking.Furthermore, smokers who are able to switchto cigarette brands with lower nicotine yield“reduced yield” products may have other char-acteristics that attenuate their lung cancer risk,relative to smokers who cannot switch. Theirchange in brands may reflect comparativelyless dependence on nicotine and otheraddictive components of smoking. Smokerswho switch may have smoked less intensively inthe past and be more likely to quit during thefollow up. Epidemiological studies have nothistorically measured nicotine addiction orrelated parameters such as puV volume, puVsper cigarette, or depth of inhalation.Prospective studies that have assessed smokingbehaviour only at the time of enrolment cannotcontrol for diVerences in cessation rates duringfollow up. Thus, the relatively lower risk of lungcancer among smokers who switch may result,not from switching per se, but rather frombehavioural diVerences related to addiction.Some or all of what has been interpreted aseYcacy may actually reflect selection bias orresidual confounding.

COHORT STUDIES OF LUNG CANCER RISK IN

DIFFERENT GENERATIONS OF SMOKERS

Several major cohort studies of smoking anddisease have bridged the period when thegreatest reduction occurred in the tar ratings ofcigarettes. The British Doctors’ Studyexamined lung cancer rates in relation tosmoking behaviour among British physiciansover a 40 year period.91 Age standardised inci-dence rates among smokers were comparedbetween the intervals 1951–1971 and1971–1991. A similar comparison was made inthe USA where the American Cancer Society(ACS) conducted two large cohort studies ofcomparable design begun 23 years apart: Can-cer Prevention Study I (CPS-I), begun in1959, and CPS-II, begun in 1982.92 93

In both the British Doctors’ Study91 94 andthe two ACS cohorts92 93 lung cancer riskincreased among smokers from the 1950s tothe 1980s. This increase occurred despite adramatic decrease in the machine measured tarlevel of cigarettes in both countries during thistime period.94 Among the British doctors, theage standardised lung cancer incidenceincreased by 19%, from 264 per 100 000 to314 per 100 000 from the first to the second 20year period.94 In the ACS studies, an evenlarger increase occurred in the agestandardised lung cancer death rate amongboth male and female smokers from CPS-I toCPS-II, while this rate remained essentiallyconstant in lifelong non-smokers (fig 3).95 Theage standardised rate increased from 187 to341 (deaths per 100 000 person years) among

Figure 2 Piecewise linear regression of cigarettes smoked per day by sales-weightednicotine yield of the brand smoked (California data), illustrating the inverse relationbetween cigarettes smoked per day and machine measured tar yield below approximately 1mg. Based on the 1990 and 1996 California Tobacco Surveys.30

40

35

30

25

15

20

Sales-weighted nicotine (mg)

Ave

rag

e ci

gar

ette

s p

er d

ay

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

CTS 1990

1.75

CTS 1996Combined CTS

i6 Thun, Burns




j.com/

Tob C


ber 2001. Dow

nloaded from


male current cigarette smokers and from 26 to155 among female smokers from CPS-I toCPS-II. The slope of the increase was reduced,but not eliminated, when the rates wereadjusted for diVerences in the number of ciga-rettes smoked per day and duration ofsmoking, as reported at the time of enrolment.The ACS analyses are restricted to the first sixyears of follow up to enhance comparability.

These cohort studies indicate that the abso-lute risk of lung cancer continued to increaserather than decrease among older smokersdespite the widespread adoption of “reducedyield” cigarettes. The substitution of filter tipproducts among smokers in CPS-II, for theunfiltered, very high yield cigarettes usedextensively by smokers in CPS-I did notprevent a sustained increase in lung canceramong female smokers over age 45 and malesmokers over age 50. Only among youngermale smokers, ages 40–45, were lung cancerdeath rates lower in CPS-II than in CPS-I.95

These studies help to put into perspective therelative attenuation in lung cancer risk seen inthe earlier cohort and case–control studies thatcompare one type of cigarette to another.Whatever the relative impact of “reducedyield” products, their absolute impact wasclearly inadequate to prevent a major increasein lung cancer risk among older smokers.

There are at least three possible explanationswhy lung cancer risk increased among smokersdespite a dramatic decline in the machinemeasure tar yield of the cigarettes beingsmoked. One is that smokers who becameaddicted during and after the first world warpresumably smoked less intensively asadolescents and young adults than did smokerswho initiated smoking during and shortly afterthe second world war.94 95 Manufacturedcigarettes were less available and relativelymore expensive after the first than the secondworld war. Consequently, earlier generations ofsmokers who consumed predominantlyunfiltered, high yield products may have been

spared the full consequences of early life smok-ing that aVected later generations. While theCPS-I and CPS-II analyses adjusted for theusual number of cigarettes smoked per day, asreported at the time of enrolment into thestudies, this might not reflect large diVerencesin early life smoking. Adverse changes insmoking behaviour may have overwhelmed anyputative change in tar yield.

Two alternative explanations for the higherlung cancer risk among smokers in the secondworld war, compared to the first world wargeneration, involve a shift in the demographicsof smokers and/or an increase, rather thandecrease in the carcinogenicity of “reducedyield” cigarettes. Contemporary smokers areless educated and aZuent, and have lesshealthy dietary patterns than previousgenerations of cigarette smokers.96–99 Personswho continue to smoke despite repeated healthwarnings may also be more addicted andsmoke more intensively.95 Neither of theseexplanations would suggest that designchanges in contemporary cigarettes have com-pensated adequately for the increasedvulnerability of smokers or for adverse changesin smoking behaviour.

National trends in lung cancer mortalityat specific agesSeveral analyses100–102 have examined trends innational lung cancer death rates by age in rela-tion to age specific smoking patterns. Studiesbased on national trends are called“ecological” because they lack data onindividual behaviours and outcomes, and can-not separate disease occurrence in currentsmokers from events in former or never smok-ers. However, the trends in national rates doreflect accurately the extent of progresstowards reducing disease occurrence in theoverall population.

One approach is to compare the trend inlung cancer death rates for a particular agegroup with the trends in smoking prevalence atyounger ages. This approach does not integrateall of the relevant parameters of smokingbehaviour, nor does it consider the time lagthat occurs between the initiation of smokingand the onset of lung cancer, but it does allowa visual comparison of trends in age specificprevalence with trends in lung cancer inadjoining birth cohorts. Figure 4 shows thetrends in lung cancer death rates for men andwomen, ages 35–39 in the USA and UKbetween 1965 and 1997, compared to thetrend in cigarette smoking prevalence at ages25–34 over the same time period. Among USmen, the decrease in lung cancer mortalityessentially parallels the decrease in cigarettesmoking prevalence (fig 4A), whereas for menin the UK, the proportionate decrease in lungcancer mortality is much steeper than thedecrease in smoking prevalence (fig 4B).Among US women, the lung cancer death atages 35–39 changed very little over this timeperiod despite a 40% decline in smokingprevalence (fig 4C). Among women ofcorresponding ages in the UK, both lung can-cer and smoking prevalence decreased by 38%

Figure 3 Death rates from all lung cancers by smoking status, CPS-I and CPS-II(adjusted for current amount and duration of smoking). The “non-adjusted” points indicatethe age standardised death rate from lung cancer among male and female current cigarettesmokers and lifelong non-smokers in CPS-I (1959–1965) and CPS-II (1982–1988). The“adjusted” values signify the results adjusted for age, cigarettes smoked per day, and years ofsmoking as reported at enrolment into the study.

350

300

200

250

150

100

0

50

Dea

th r

ate

per

100

000

CPS-I1959–65

Study and year

Never smokers

Female smokers

Non-adjusted

Adjusted

Adjusted

Non-adjusted

Male smokers

CPS-II1982–88





j.com/

Tob C


ber 2001. Dow

nloaded from


over the interval (fig 4D). The temporal trendsin lung cancer mortality in women are morediYcult to interpret than those in men, becauseof the much larger recent changes in the ageswhen women initiated smoking and increasesin the intensity of adolescent smoking.

Reductions in the tar yield of cigarettes areone possible explanation for the very rapiddecline in lung cancer death rates at youngerages among men in the UK94 and the moregradual decreases elsewhere in Europe, NorthAmerica, and Australia100 in recent decades.However, design changes in cigarettes are notthe only potential explanation. The particu-larly high rates of lung cancer that prevailedamong men in the UK until the 1950s andthat are seen presently in some Eastern Euro-pean countries may also reflect the exacerbat-ing eVects of diet, or reductions inoccupational exposures or air pollution fromcoal burning that could potentiate the risksfrom smoking. Other potentially importantparameters that have not been directly consid-ered in these temporal and geographiccomparisons include diVerences in cigarettecomposition across countries, and variationsin the age of initiation, intensity of smoking atvarious ages, and age at cessation, both withinand across countries. Thus, the analyses basedonly on national trends cannot convincinglyseparate the contribution of “reduced yield”cigarettes from other factors that might aVectlung cancer risk.

Furthermore, it should be noted that, whilethe decline in lung cancer death rates atyounger ages is encouraging, there is nocertainty that these trends will be sustainedinto the future. Recent vital statistics data sug-gest that reductions in lung cancer death ratesamong young adults in the USA have slowedand possibly reversed, as a result of adversechanges in smoking behaviour among theyoung.102 To the extent that health claims about“reduced yield” cigarettes defer cessation, thiscould also interfere with the progression offavourable trends into older ages where mostlung cancers occur.

Other comprehensive reviewsRecent reviews by the Institute of Medicine1

and the National Cancer Institute2 have exam-ined the evidence for a reduction in diseaserisks associated with the use of low yieldcigarettes. Their conclusions reinforce the cau-tions raised by the UK Royal College of Physi-cians.103 The Institute of Medicine report onThe scientific base for tobacco harm reductionstated: “There have been many eVorts in thepast to develop less harmful cigarettes, none ofwhich has proved to be successful.”1 TheNational Cancer Institute review concluded:“Epidemiological and other scientific evi-dence, including patterns of mortality fromsmoking caused diseases, does not indicate abenefit to public health from changes incigarette design and manufacturing over thelast 50 years.”2

Figure 4 Lung cancer death rates at ages 35–39 and cigarette smoking prevalence at ages 25–34. The graphs indicate the temporal trend in lung cancerdeath rates at ages 35–39 and in cigarette smoking prevalence at ages 25–34 among men in the USA (A) and UK (B) and among women in the USA(C) and UK (D).

12

8

10

6

4

0

2

80

51% change

54% change

60

40

0

20

A US men

Lung cancer death rate Cigarette smoking prevalence

Dea

th r

ate

per

100

000

Cig

aret

te s

mo

kin

g p

reva

len

ce

1965–69

1970–74

1975–79

1980–84

1985–89

1990–94

1993–97

12

8

10

6

4

0

2

80

48% change

80% change

60

40

0

20

B UK men

Dea

th r

ate

per

100

000

Cig

aret

te s

mo

kin

g p

reva

len

ce1950–

521958–

621968–

721978–

821988–

921993–

97

12

8

10

6

4

0

2

80

40% change

8% change

60

40

0

20

C US women

Dea

th r

ate

per

100

000

Cig

aret

te s

mo

kin

g p

reva

len

ce

1965–69

1970–74

1975–79

1980–84

1985–89

1990–94

1993–97

12

8

10

6

4

0

2

80

38% change

38% change

60

40

0

20

D UK women

Dea

th r

ate

per

100

000

Cig

aret

te s

mo

kin

g p

reva

len

ce

1950–52

1958–62

1968–72

1978–82

1988–92

1993–97

i8 Thun, Burns




j.com/

Tob C


ber 2001. Dow

nloaded from


ConclusionsIn summary, there is no convincing evidencethat changes in cigarette design between the1950s and the mid 1980s have resulted in animportant decrease in the disease burdencaused by cigarette use for either smokers as agroup or for the whole population. While manyepidemiological studies have found attenuatedrisk of lung cancer among people who smokethese products, the extent to which these stud-ies may overestimate the magnitude of the lungcancer association remains unclear. No studieshave adequately assessed whether healthclaims used to market “reduced yield”products delay cessation among smokers whomight otherwise quit or increase initiation orrelapse among non-smokers. The widespreadshift from unfiltered, high yield cigarettes tofilter tip, lower yield products that occurred inthe USA and UK since the 1950s did not pre-vent continuing increases in lung cancer riskamong older smokers in large cohort studies.While one can postulate that lung cancer ratesamong older smokers might have risen evenfurther in the absence of “reduced yield” ciga-rettes, other explanations are also possible. Thetemporal decrease in lung cancer risk atyounger ages has been encouraging, but maybe short lived if health claims about lower yieldcigarettes are allowed to discourage or delaygenuine cessation eVorts by smokers. Further-more, the extent to which changes in agespecific lung cancer death rates reflect modifi-cations in cigarette design versus changes insmoking behaviour including initiation andcessation has yet to be proven. There is noconsistent evidence that “reduced yield”cigarettes have attenuated the risk of othersmoking attributable diseases besides lungcancer.

A central challenge in tobacco policy is toprevent the misuse of unproven health claimsto promote novel products. Alternativenicotine delivery devices may ultimately helpto mitigate the harm caused by smoking to theapproximately 47 million Americans who con-tinue to smoke.1 However, the evidence baserequired to market these products should cor-respond to the evidence required for any newdrug delivery device. Furthermore, the public-ity and marketing of these products must notdistract attention away from interventionsproven to reduce the prevalence, intensity, andduration of smoking.

This paper summarises material from a chapter on disease risksassociated with light cigarettes from the upcoming NationalCancer Institute Monograph 13: Risks associated with smokingcigarettes with low machine-measured yields of tar and nicotine.30

The authors wish to thank the many colleagues who contributedto our thinking on this topic, including Sir Richard Peto, DrsGary Giovino, Theodore Holford, Scott Leischow, Jay Lubin,Jonathan Samet, and Robert Tarone. We thank MichaelPleasant for preparation of the manuscript.

Source of support: American Cancer Society and Universityof California Tobacco-Related Disease Research Program;grant 8RT-0094.

1 Institute of Medicine. Clearing the smoke: the science basefor tobacco harm reduction. In: Stratton K, Shetty P, Wal-lace R, Bondurant S, eds. Committee to assess the science basefor tobacco harm reduction, board on health promotion and dis-ease prevention. Institute of Medicine, National Academy ofSciences, National Academy Press, 2001.

2 National Cancer Institute. Risks associated with smokingcigarettes with low machine-measured yields of tar andnicotine. In: Burns DM, Benowitz NL, eds. Smoking and

Tobacco Control Monograph, No 13. US DHHS, PublicHealth Service, National Institutes of Health, NationalCancer Institute, 2001 (in press).

3 National Cancer Institute. The FTC cigarette test method fordetermining tar, nicotine, and carbon monoxide yields of UScigarettes. Smoking and Tobacco Control Monograph No. 7.Bethesda, Maryland: US Department of Health andHuman Services, Public Health Service, National Insti-tutes of Health, 1996 (NIH Publication No. 96–4028.)

4 Wynder EL, Graham EA Tobacco smoking as a possibleetiologic factor in bronchiogenic carcinoma. A study of sixhundred and eighty-four proved cases. JAMA 1950;143:329–36.

5 Doll R, Hill AB. A study of the aetiology of carcinoma of thelung. BMJ 1952;2:1271–86.

6 Doll R, Hill AB. The mortality of doctors in relation to theirsmoking habits: a preliminary report. BMJ 1954;1(4877):1451–5.

7 Hammond EC, Horn D. Smoking and death rates—a reporton 44 months of follow-up of 187,783 men. II. Death ratesby cause. JAMA 1958;166:1294–308.

8 Wynder EL, Graham EA, Croninger AB. Experimental pro-duction of carcinoma with cigarette tar. Cancer Res1953;13:855–64.

9 US Congress. Hearings before the Consumer Subcommittee ofthe Committee on Commerce. Senate, 90th Congress, 23, 24August 1967, p 7.

10 US Department of Health and Human Services. The healthconsequences of smoking: the changing cigarette. A report of theSurgeon General, 1981. Rockville, Maryland: Public HealthService, OYce of the Assistant Secretary for Health, OYceon Smoking and Health, 1981. (DHHS Publication No(PHS) 81–50156.)

11 Bradford JA, Harlan WR, Hanmer HR. Nature of cigarettesmoke. Technique of experimental smoking. Industrial andEngineering Chemistry 1936;28:836–9.

12 Peeler CE. Cigarette testing and the Federal TradeCommission: a historical overview. The FTC cigarette testmethod for determining tar, nicotine, and carbon monoxideyields of US cigarettes. Smoking and Tobacco ControlMonograph No. 7. Bethesda, Maryland: US Department ofHealth and Human Services, Public Health Service,National Institutes of Health, 1996:1–8 (NIH PublicationNo. 96–4028.)

13 Kozlowski LT, O’Connor RJ, Sweeney CT. Cigarettedesign. In: Risks associated with smoking cigarettes with lowmachine-measured tar and nicotine yields. NCI Smoking andTobacco Control Monograph No 13. Bethesda, Maryland:National Cancer Institute (in press).

14 Jarvis MJ, Boreham R, Primatesta P, et al. Nicotine yieldfrom machine-smoked cigarettes and nicotine intakes insmokers: evidence from a representative populationsurvey. J Natl Cancer Inst 2001;93:134–8.

15 Kozlowski LT. Perceiving the risks of low-yield ventilated-filter cigarettes: the problem of hole-blocking. In: CovelloV, Flamm WG, Rodericks J, TardiV R, eds. Proceedings ofthe International Workshop on the Analysis of Actual vs.Perceived Risks. New York: Plenum, 1983:175–82.

16 Kozlowski LT, Mehta NY, Sweeney CT, et al. Filter ventila-tion and nicotine content of tobacco in cigarettes fromCanada, the United Kingdom, and the United States.Tobacco Control 1998;7:369–75.

17 Benowitz NL. Compensatory smoking of low-yield cigaret-tes.In: Risks associated with smoking cigarettes with lowmachine-measured tar and nicotine yields. NCI Smoking andTobacco Control Monograph No 13. Bethesda, Maryland:National Cancer Institute (in press).

18 Wakeham H. Trends in tar and nicotine deliveries over thelast 5 years. Memo to Mr Hugh Cullman. 24 March 1961.Bates number 1000861953.

19 Russell MA, Wilson C, Patel UA, et al. Plasma nicotine lev-els after smoking cigarettes with high, medium, and lownicotine yields. BMJ 1975;2:414–6.

20 Benowitz NL, Jacob P, III. Nicotine and carbon monoxideintake from high- and low yield cigarettes. Clin PharmacolTher 1984;36:265–70.

21 Benowitz NL, Jacob P, III. Nicotine renal excretion rateinfluences nicotine intake during cigarette smoking. JPharmacol Exp Ther 1985;234:153–5.

22 West RJ, Russell MA, Jarvis MJ, Feyerabend C. Doesswitching to an ultra-low nicotine cigarette induce nicotinewithdrawal eVects? Psychopharmacology (Berl) 1984;84:120–3.

23 Zacny JP, Stitzer ML. Cigarette brand switching: eVects onsmoke exposure and smoking behavior. J Pharmacol ExpTher 1988;246:619–27.

24 Russell MAH, Sutton SR, Iyer R, et al. Long-term switchingto low-tar low-nicotine cigarettes. Br J Addict 1982;77:145–58.

25 Robinson JC, Young JC, Rickett WS, et al. A comparativestudy of the amount of smoke absorbed from low yield(‘less hazardous’) cigarettes. Part 2: Invasive measures. BrJ Addict 1983;78:79–87.

26 Gori GB, Lynch CJ. Smoker intake from cigarettes in the1-mg Federal Trade Commission tar class. Regul ToxicolPharmacol 1983;3:110–20.

27 Peach H, Hayard DM, Ellard DR, et al. Phlegm productionand lung function among cigarette smokers changing targroups during the 1970s. J Epidemiol Community Health1986;40:110–6.

28 Guyatt AR, Kirkham AJT, Mariner DC, et al. Long-termeVects of switching to cigarettes with lower tar andnicotine yields. Psychopharmacology (Berl) 1989;99:80–6.





j.com/

Tob C


ber 2001. Dow

nloaded from


29 Frost C, Fullerton FM, Stephen AM, et al. The tarreduction study: Randomized trial of the eVect of cigarettetar yield reduction on compensatory smoking. Thorax1995;50:1038–43.

30 Burns DM, Major JM, Shanks et al. Smoking lower yieldcigarettes and disease risks. In: Risks associated withsmoking cigarettes with low machine-measured tar and nicotineyields. NCI Smoking and Tobacco Control Monograph No 13.Bethesda, Maryland: National Cancer Institute (in press).

31 Benowitz NL, Henningfield JE. Establishing a nicotinethreshold for addiction. N Engl J Med 1994;331:123–5.

32 ShiVman S. Tobacco “chippers” — individual diVerences intobacco dependence. Psychopharmacology (Berl) 1989;97:539–47.

33 Lynch CJ, Benowitz NL. Spontaneous brand switching:consequences for nicotine and carbon monoxide exposure.Am J Public Health 1987;77:1191–4

34 Peach H, Hayward DM, Shah D. A double-blind rand-omized controlled trial of the eVect of a low- versus a mid-dle tar cigarette on respiratory symptoms-A feasibilitystudy. IARC Scientific Publications 1986;74:251–63.

35 Bross ID, Gibson R. Risks of lung cancer in smokers whoswitch to filter cigarettes. Am J Public Health 1968;58:1396–403.

36 Bross ID. EVect of filter cigarettes on lung cancer risk.Toward a less harmful cigarette. National Cancer InstituteMonograph 28. US Department of Health, Education andWelfare, National Cancer Institute, 1968.

37 Hammond EC, Garfinkel L, Seidman H, et al. Some recentfindings concerning cigarette smoking. Cold Spring HarborConferences on Cell Proliferation, Volume 4. Origins of humancancer. Book A. Incidence of cancer in humans. Cold SpringHarbor, New York: Cold Spring Harbor Laboratory Press,1977;101–12.

38 Hammond EC, Garfinkel L, Seidman H, et al. “Tar” andnicotine content of cigarette smoke in relation to deathrates. Environ Res 1976;12:263–74.

39 Lee PN, Garfinkel L. Mortality and type of cigarettesmoked. J Epidemiol Community Health 1981;35:16–22.

40 Higenbottam T, Shipley MJ, Rose G. Cigarettes, lungcancer, and coronary heart disease: the eVects ofinhalation and tar yield. J Epidemiol Community Health1982;36:113–7.

41 Hawthorne VM., Fry JS. Smoking and health: theassociation between smoking behavior, total mortality, andcardiorespiratory disease in West Central Scotland. J Epi-demiol Community Health 1978;32:260–6.

42 Todd GF, Hunt BM, Lambert PM. Four cardiorespiratorysymptoms as predictors of mortality. J Epidemiol Commu-nity Health 1978;32:267–74.

43 Engeland A, Haldorsen T, Andersen A, et al. The impact ofsmoking habits on lung cancer risk: 28 years’ observationof 26,000 Norwegian men and women. Cancer Causes andControl 1966;7:366–76.

44 Borland C, Chamberlain A, Higenbottam T, et al. Carbonmonoxide yield of cigarettes and its relation to cardiorespi-ratory disease. BMJ 1983;287:1583–6.

45 Tang JL, Morris JK, Wald NJ, et al. Mortality in relation totar yield of cigarettes: a prospective study of four cohorts.BMJ 1995:311:1530–3.

46 Wynder EL, Mabuchi K, Beattie EJ Jr. The epidemiology oflung cancer: recent trends. JAMA 1970;213:2221–8.

47 Wynder EL, Stellman SD. Impact of long-term filtercigarette usage on lung and larynx cancer risk: acase-control study. J Natl Cancer Inst 1979;62:471–7.

48 Augustine A, Harris RE, Wynder EL. Compensation as arisk factor for lung cancer in smokers who switch fromnonfilter to filter cigarettes. Am J Public Health 1989;79:188–91.

49 Kabat GC. Aspects of the epidemiology of lung cancer insmokers and nonsmokers in the United States. Lung Can-cer 1996;15:1–20.

50 Rimington, J. The eVect of filters on the incidence of lungcancer in cigarette smokers. Environ Res 1981;24:162–6.

51 Kuller LH. Cigarette smoking and mortality. MRFITresearch group. Prev Med 1991;20:638–54.

52 Lubin JH, Blot WJ, Berrino F, et al. Patterns of lung cancerrisk according to type of cigarette smoked. Int J Cancer1984;33:569–76.

53 Lubin JH. Modifying risk of developing lung cancer bychanging habits of cigarette smoking. BMJ 1984;288:1953–6; 289:921 [letter—response].

54 Benhamou S, Benhamou E, Tirmarche M, et al. Lung can-cer and use of cigarettes: a French case-control study. JNatl Cancer Inst 1985;74:1169–75.

55 BuZer PA, Contant CF, Pickle LW, et al. Environmentalassociations with lung cancer in Texas coastal counties.Annu Clin Conf on Cancer 1986;28:27–34.

56 Benhamou E, Benhamou S, Flamant R. Lung cancer andwomen: results of a French case–control study. Br J Cancer1987;55:91–5.

57 Benhamou E, Benhamou S, Auquier A, et al. Changes inpatterns of cigarette smoking and lung cancer risk: resultsof a case–control study. Br J Cancer 1989;60:601–4.

58 Benhamou S, Benhamou E, Auquier A, et al. DiVerentialeVects of tar content, type of tobacco and use of a filter onlung cancer risk in male cigarette smokers. Int J Epidemiol1994;23:437–43.

59 Vutuc C, Kunze M. Lung cancer risk in women in relationto tar yields of cigarettes. Prev Med 1982;11:713–6.

60 Vutuc C, Kunze V. Tar yields of cigarettes and male lungcancer risk. J Natl Cancer Inst 1983;71:435–7.

61 Benhamou E, Benhamou S. Black (air-cured) and blond(flue-cured) tobacco and cancer risk. VI: lung cancer. EurJ Cancer 1993;29A:1778–80.

62 Lange P, Nyboe J, Appleyard M, et al. Relationship of thetype of tobacco and inhalation pattern to pulmonary andtotal mortality. Eur Respir J 1992;5:1111–7.

63 Gillis CR, Hole DJ, Boyle P. Cigarette smoking and malelung cancer in an area of very high incidence. I: report of acase-control study in the West of Scotland. J EpidemiolCommunity Health 1988;42:38–43.

64 Alderson MR, Lee PN, Wang R. Risks of lung cancer,chronic bronchitis, ischaemic heart disease, and stroke inrelation to type of cigarette smoked. J Epidemiol Commu-nity Health 1985;39:286–93.

65 Wynder EL, Kabat GC. The eVect of low-yield cigarettesmoking on lung cancer risk. Cancer 1988;62:1223–30.

66 Stellman SD, Muscat JE, Thompson S, et al. Risk ofsquamous cell carcinoma and adenocarcinoma of the lungin relation to lifetime filter cigarette smoking. Cancer1997;80:382–8.

67 Petitti DB, Friedman GD. Cardiovascular and otherdiseases in smokers of low-yield cigarettes. J Chron Dis1985;38:581–8.

68 Sidney S, Tekawa IS, Friedman GD. A prospective study ofcigarette tar yield and lung cancer. Cancer Causes and Con-trol 1993;4:3–10.

69 Wilcox HB, Schoenberg JB, Mason TJ, et al. Smoking andlung cancer: risk as a function of cigarette tar content. PrevMed 1988;17:263–72.

70 Pathak DR, Samet JM, Humble CG, et al. Determinants oflung cancer risk in cigarette smokers in New Mexico. JNatl Cancer Inst 1986;76:597–604.

71 Kaufman DW, Palmer JR, Rosenberg L, et al. Tar content ofcigarettes in relation to lung cancer. Am J Epidemiol 1989;129:703–11.

72 Khuder SA, Dayal HH, Mutgi AB, et al. EVect of cigarettesmoking on major histological types of lung cancer in men.Lung Cancer 1998;22:15–21.

73 Armadans-Gil L, Vaque-Rafart J, Rossello J, et al. Cigarettesmoking and male lung cancer risk with special regard totype of tobacco. Int J Epidemiol 1999;28:614–9.

74 Pezzotto SM, Mahuad R, Bay ML, et al. Variation insmoking-related lung cancer risk factors by cell typeamong men in Argentina: a case-control study. CancerCauses and Control 1993;4:231–7.

75 De Stefani E. Mate drinking and risk of lung cancer inmales: a case-control study from Uruguay. CancerEpidemiology, Biomarkers and Prevention 1996;5:515–9.

76 Agudo A, Barnadas A, Pallares C, et al. Lung cancer andcigarette smoking in women: a case-control study inBarcelona (Spain). Int J Cancer 1994;59:165–9.

77 Matos E, Vilensky M, BoVetta P, et al. Lung cancer andsmoking: a case-control study in Buenos Aires, Argentina.Lung Cancer 1998;21:155–63.

78 Jöckel KH, Ahrens W, Wichmann HE, et al. Occupationaland environmental hazards associated with lung cancer.Int J Epidemiol 1992;21:202–13.

79 Palmer J, Rosenberg L, Shapiro S. Low yield cigarettes andthe risk of nonfatal myocardial infarction in women. NewEngl J Med 1989;320:1569–73.

80 Negri E. Tar yield of cigarettes and risk of acute myocardialinfarction. BMJ 1993;306:1567–9.

81 Powell JT, Edwards RJ, Worrell PC. Risk factors associatedwith the development of peripheral arterial disease insmokers: a case control study. Atherosclerosis 1997;129:41–8.

82 Parish S, Collins R, Peto R. Cigarette smoking, tar yields,and non-fatal myocardial infarction: 14,000 cases and32,000 controls in the United Kingdom. The Interna-tional Studies of Infarct Survival (ISIS) Collaborations.BMJ 1995;311:471–7.

83 Sparrow D, Lee PN, Todd GF. The relationship of tar con-tent to decline in pulmonary function in cigarette smokers.Am Rev Respir Dis 1983;127:56–8.

84 Dean G, et al. Factors related to respiratory and cardiovas-cular symptoms in the United Kingdom. J Epidemiol Com-munity Health 1978;32:86–96.

85 Lange P, Nyboe J, Appleyard M. Relationship of the type oftobacco and inhalation pattern to pulmonary and totalmortality. Eur Resp J 1992;5:1111–7.

86 Alderson MR, Lee PN, Wang R. Risks of lung cancer,chronic bronchitis, ischaemic heart disease, and stroke inrelation to type of cigarette smoked. J Epidemiol Commu-nity Health 1985;39:286–93.

87 Kryanowski M, Sherrill DL, Paoletti P. Relationship of res-piratory symptoms and pulmonary function to tar,nicotine, and carbon monoxide yield of cigarettes. Am RevRespir Dis 1991;143:306–11.

88 Brown CA, Crombie IK, Smith WC. Cigarette tar contentand symptoms of chronic bronchitis: results of the ScottishHeart Health Study. J Epidemiol Community Health1991;45:287–90.

89 Withey CH, Papacosta AO, Swan AV. Respiratory eVects oflowering tar and nicotine levels of cigarettes smoked byyoung male middle tar smokers. II. Results of arandomized controlled trial. J Epidemiol Community Health1992;46:281–5.

90 Doll R, Peto R. Cigarette smoking and bronchial carcinoma:dose and time relationships among regular smokers andlife-long non-smokers. J Epidemiol Community Health1978;32:303–13.

91 Doll R, Peto R, Wheatley K, et al. Mortality in relation tosmoking: 40 years’ observations on male British doctors.BMJ 1994;309:901–11.

i10 Thun, Burns




j.com/

Tob C


ber 2001. Dow

nloaded from


92 Thun MJ, Heath CW Jr. Changes in mortality from smokingin two American Cancer Society prospective studies since1959. Prev Med 1997;26:422–6.

93 Thun M, Myers D, Day-Lally C, et al. Trends in tobaccosmoking and mortality from cigarette use in cancerprevention studies I (1959 through 1965) and II (1982through 1988). In: Burns D, Garfinkel L, Samet J, eds.Changes in cigarette-related disease risks and their implicationfor prevention and control. Smoking and Tobacco ControlMonograph No. 8. Bethesda, Maryland: Department ofHealth and Human Services, Public Health Service,National Institutes of Health, 1997;305–82. (NIH Publi-cation No. 97-4213.)

94 Peto R, Darby S, Deo H, et al. Smoking, smoking cessation,and lung cancer in the U.K. since 1950: combination ofnational statistics with two case-control studies. BMJ2000;321:323–9.

95 Thun MJ, Heath CW Jr. Changes in mortality from smokingin two American Cancer Society prospective studies since1959. Prev Med 1997;26:422–6.

96 Subar AF, Harlan LC, Mattson ME. Food and nutrientintake diVerences between smokers and non-smokers inthe US. Am J Public Health 1990;80:1323–9.

97 Zondervan KT, Ocke MC, Smit HA, et al. Do dietary andsupplementary intakes of antioxidants diVer with smokingstatus? Int J Epidemiol 1996;25:70–9.

98 Midgette AS, Baron JA, Rohan TE. Do cigarette smokershave diets that increase their risks of coronary heartdisease and cancer? Am J Epidemiol 1993;137:521–9.

99 Cade JE, Margetts BM. Relationship between diet andsmoking—is the diet of smokers diVerent? J EpidemiolCommunity Health 1991;45:270–2.

100 Blizzard L, Dwyer T. Declining lung cancer mortality ofyoung Australian women despite increased smoking islinked to reduced cigarette “tar” yields. Br J Cancer 2001;84:392–6.

101 Mannino DM, Ford E, Giovino GA, et al. Lung cancermortality rates in birth cohorts in the United States from1960 to 1994. Lung Cancer 2001;31(2–3):91–9.

102 Jemal A, Chu KC, Tarone RE. Recent trends in lung can-cer mortality in the United States. J Natl Cancer Inst 2001;93:277–83.

103 Tobacco Advisory Group (of the Royal College ofPhysicians). Nicotine addiction in Britain. London: RoyalCollege of Physicians of London, 2000.


Limited space in printed journals means that interesting data and other material are often edited out of

articles; however, limitless cyberspace means that we can include this information online.

Look out for additional tables, references, illustrations.

Data supplements

Want to know more?





j.com/

Tob C


ber 2001. Dow

nloaded from


PostScript..............................................................................................

LETTERS

Tobacco use among schoolpersonnel in Bihar, IndiaTobacco use often starts in adolescent yearswhen school personnel form important rolemodels, potentially influencing tobacco use.To plan effective interventions, it is essential tohave information on the extent and the typeof tobacco use among school personnel, theirattitudes towards tobacco control, and theexistence of school health polices abouttobacco.1

Tobacco use among 13–15 year old studentsis being studied worldwide through theGlobal Youth Tobacco Survey (GYTS)2 whichincorporates the Global School PersonnelSurvey (GSPS). The objectives of GSPS are:(1) obtain baseline information on tobaccouse; (2) evaluate the existence, implementa-tion, and enforcement of tobacco control poli-cies in schools; (3) understand the knowledgeand attitudes towards tobacco control poli-cies; (4) assess training and material require-ments for implementing tobacco preventionand control interventions; and (5) verify someinformation obtained from the GYTS. TheGSPS was piloted in the state of Bihar, Indiaand this report presents the results from thefirst pilot of GSPS.

GSPS is a cross sectional survey thatemploys a cluster sample design to produce arepresentative sample of school personneldrawn from the same schools that wereselected for GYTS. For GYTS, schools weresampled with probability of selection propor-tional to the school enrolment size in grades8–10 (corresponding to ages 13–15 years). Atotal of 50 schools out of 9905 listed for Biharstate were sampled. All school personnel(including all non-teaching staff) in theselected schools were eligible to participate. InIndia, education is a state responsibility andalmost all schools were part of Bihar stateeducational system.

Bihar GSPS was conducted in the monthsof September and October 2000 using thesame survey personnel who had conductedGYTS. The questionnaire contained 46 multi-ple choice questions. Survey procedures al-lowed for anonymous and voluntary partici-pation. School personnel completed the selfadministered questionnaire during the breakhours, recording their responses directly on asheet which could subsequently be opticallyread by machine. The data file obtained wasanalysed using Epi Info. This software tookthe sampling weights into account for produc-ing unbiased estimates of proportions andconfidence intervals.

All selected schools participated in the sur-vey (response rate 100%). Selected schoolsreported having a total of 697 eligible person-nel, out of which 637 returned the completedquestionnaire. The main reason for non-response was absence from school on the dayof the survey. The school personnel responserate was 91.4%.

Out of 637 participating school personnel,73% were men. Some 22.5% were less than 40years old and 38.6% were 50 years or older.Very few were more than 60 as mandatoryretirement age is 60 years. Women were

somewhat younger than men. The majority ofschool personnel (83.5%) were teachers andthere were only two health personnel.

Table 1 shows tobacco use prevalenceamong school personnel. Some 77.4% re-ported using tobacco in one form or the other.The prevalence was almost identical amongmen (77.6%) and women (77.0%). There waslittle difference in smokeless tobacco useamong men (58.7%) and women (53.4%).Although smoking among women in India isgenerally proscribed, prevalence of smokingamong women in this sample was quite high(31%). Most of it was cigarette smoking(26.9%). Among men, overall smoking preva-lence was 47.4%, and cigarette smoking40.5%. It should be noted that prevalence ofcigarette smoking and other smoking habitsdo not add up to the prevalence of smoking,and prevalence of smoking and smokelesstobacco use do not add up to prevalence oftobacco use. This is because many individualsreported using tobacco in multiple forms.

Almost all school personnel (91%) agreedthat tobacco was addictive, and 85% admittedthat it had serious health consequences.While 92% of never users of tobacco believedthat environmental tobacco smoke (ETS) washarmful to people who were repeatedlyexposed to it, 83% of current tobacco usersagreed with that statement. While 83% ofnever tobacco users complained that ETS wasa nuisance, only slightly fewer (77%) currenttobacco users did so.

Except for two people, everyone replied thatthere was no policy on tobacco use either forstudents or personnel. Even though tobaccouse among school personnel was high, a vastmajority was concerned about youth tobaccouse (84.7%). A large proportion (90.4%)wanted a policy prohibiting tobacco use bystudents and, surprisingly, even more wanteda policy prohibiting tobacco use among schoolpersonnel (93.9%).

Another striking finding was that 80%thought that tobacco companies deliberatelyencourage youth to use tobacco. Some 88.3%wanted tobacco companies not to sponsorsports events and 95% wanted a complete banon tobacco advertisements. Surprisingly, eventhough a majority were tobacco users, 78.4%agreed with the need to increase prices oftobacco products, with no difference betweenusers and non-users.

The GSPS study findings reveal an alarmingpicture of very high tobacco use among schoolpersonnel, and a total absence of any tobaccocontrol policy in schools administered by the

state government in Bihar. The results dispelthe myth of smoking as taboo among middleclass women in India in so far as self admin-istered, anonymous questionnaires revealed31% of female school personnel reported cur-rent smoking and 26.9% reported smokingcigarettes. This social change is likely to bedue to several factors such as female emanci-pation and role modelling from westernmedia. The role of marketing strategies bycigarette companies however, cannot beunderestimated. Almost all cigarette advertis-ing imagery includes women, and a cigarettebrand specially targeted at women with thename “Ms” is available on the market. Thiskind of cigarette smoking is still practisedaway from public view—unlike hukka(hubble bubble) and cheroot smoking by ruralwomen—but clearly it may not remain so forlong.

The findings, however, do present anencouraging picture of widespread and neartotal support towards the formulation andimplementation of effective tobacco controlpolicy measures.

D N SinhaSchool of Preventive Oncology, Patna, India

P C GuptaM S Pednekar

Tata Institute of Fundamental Research, Mumbai,India

J T JonesDepartment of Non-communicable Diseases andHealth Promotion, World Health Organization,

Geneva, Switzerland

C W WarrenOffice on Smoking and Health, Centers for DiseaseControl and Prevention, Bethesda, Maryland, USA

Correspondence to: Prakash C. Gupta, TataInstitute of Fundamental Research, Homi Bhabha

Road, Colaba, Mumbai 400 005, India;[email protected]

AcknowledgementsThe Department of Non-communicable Diseases and

Health Promotion, World Health Organisation,

funded this study. Authors wish to acknowledge the

contribution and help from Samira Asma, Lawer-

ence Green, Laura Kann and Leanne Riley.

References1 World Health Organization. WHO

Information series on school health; tobaccouse prevention: an important entry point forthe development of health-promoting schools.Geneva: WHO, 1998:13–14.

Table 1 Prevalence of tobacco use among school personnel in Bihar bysex—Bihar GSPS 2000

Male (%) Female (%) Total (%)

Total number 502 128 630Any tobacco 77.6 (7.8) 77.0 (14.3) 77.4 (7.7)Smokeless 58.7 (6.3) 53.4 (16.1) 57.3 (7.5)Smoking 47.4 (8.7) 31.0 (8.9) 43.0 (7.1)Cigarette 40.5 (5.9) 26.9 (9.9) 36.8 (5.0)Others* 17.4 (4.6) 4.3 (4.7) 13.9 (3.5)

Figures in parentheses denotes confidence intervals (±CI).*Mostly bidi

Tobacco Control 2002;11:82–8582


2 Warren CW, Riley L, Asma S, et al. Tobaccouse by youth: a surveillance report from theGYTS project. Bull WHO 2000;78:868–74.

Exposure to environmentaltobacco smoke in public placesin Barcelona, SpainExposure to environmental tobacco smoke(ETS) has adverse health effects for both chil-dren and adults.1–3 Southern European coun-tries have not had the same level of ETS con-trol measures as other western countries. Thepurpose of this study was to assess currentETS exposure in several locations in Barce-lona, Spain.

We collected airborne nicotine with 31diffusion monitors containing sodium bisul-fate coated filters.4 5 Between September 1999and March 2000 different locations were cho-sen from among the following 18 sites in Bar-celona: five underground (subway) stations(n = 5, one measurement in each station);two restaurants (n = 3, one of the restau-rants, located in one of the two teaching hos-pitals referred to below, had measurementstaken from smoking and non-smoking areas);two large stores (n = 4, two measurements ineach store); two teaching hospitals (n = 4,two measurements from newborns inpatientsand paediatrics outpatients departments fromone hospital, and two from emergency roomsand radiography emergency departmentsfrom the other hospital); one medical school(n = 5), one official language school (n = 2);one secondary school (n = 1); one generalpractice (n = 2); one public health centre(n = 1); and three households (n = 4, onesmoker’s home and two non-smoker’s house-holds). Nicotine concentrations for the threefield blanks all corresponded to airborne con-centrations of less than 0.02 µg/m3.

Monitors were left exposed for periodsranging from 7–13 days, since a minimumperiod of seven days was required to have avalid measure with passive monitors. Onetrained investigator completed a standardform with data concerning the date and time,placement and removal, exposure area, venti-lation and distribution patterns, and distancefrom the person smoking nearby. The highestair nicotine concentration was found inrestaurants, showing a mean of 12.4 µg/m3

(10.6–15.0 µg/m3). The air nicotine concentra-tions in a secondary school and in a smoker’shousehold were 9.5 µg/m3 and 7.9 µg/m3,respectively. In department stores, the averageair nicotine concentration was 2.8 µg/m3

(range 0.4–6.2 µg/m3). ETS exposure in thelanguage school showed a mean nicotine con-centration of 2.3 µg/m3 (range 1.7–3.0 µg/m3).Other results are presented in table 1.

Although these results need to be inter-preted within the limitation of having only 31measurements and a non-random sample,this is the first attempt to obtain an objectivemeasure of ETS exposure in public places inBarcelona. The data may also provide at leastan initial insight into the situation in othersouthern European countries where measure-ments of ETS exposure are not common. Res-taurants showed high concentrations, includ-ing two measurements obtained fromhospital canteens where the average nicotineconcentrations showed no significant differ-ence between smoking and non-smokingareas (15.0 and 11.5 µg/m3, respectively). Thismay reflect a lack of compliance or a weakphysical separation between the two areas,and is especially serious since it involves hos-pitals. Nicotine concentrations in restaurants

were found to be double those found in asmoker’s household. Other studies haveshown higher concentrations of nicotine inworkplaces, including restaurants, as com-pared to smokers’ homes6–8. Our measure-ments are consistent with and even higherthan those found in other studies where meanconcentrations ranged from 2–6 µg/m3 inoffices and from 3–8 µg/m3 in restaurants.8

Since all areas in our study were sampled 24hours a day for at least a full week, concentra-tions were probably much higher during timeof occupancy—that is, when non-smokers,especially children, were exposed. The factthat collection of data was made during thewinter means that the results may have beenless influenced by open windows. The findingof lower concentrations of nicotine in healthcentres and medical schools, where severallocal policies are being put in place, is encour-aging.

The results of this study are intended toraise awareness of involuntary exposure toETS and the need to enforce compliance with

legislation. Such legislation already exists in

Catalonia, affecting the public transport sys-

tem, health and education centres, and large

department stores, where smoking is not

allowed except in designated areas.9 Smoke-

free policies not only protect non-smokers

from second hand smoke, they also create an

environment that makes it easier for smokers

to stop.

M Jané, M Nebot, X Rojano, L ArtazcozInstitut Municipal de Salut Pública, Barcelona,

Spain

J SunyerInstitut Municipal de Investigació Mèdica,

Barcelona

E FernándezInstitut Català d’Oncologia, Barcelona

M Ceraso, J SametJohns Hopkins Bloomberg School of Public Health,

Baltimore, Maryland, USA

Table 1 Concentrations of nicotine recorded in public places in the city ofBarcelona

LocationsSampling time(days)*

Nicotine concentration(µg/m2)

Underground (subway) stations (mean) 2.2Platform 7 0.1Connection 1† 7 3.8Connection 2 7 2.1Connection 3 7 4.1Coach 12 1.0

Restaurants (mean) 12.4Main dining room (no division) 7 10.6Hospital A canteen (non-smoking area) 7 11.5Hospital A canteen (smoking area) 7 15.0

Large stores (mean) 2.8Store A, floor 1 7 0.7Store A, floor 2 7 0.4Store B, information centre 13 6.2Store B, hall 13 3.9

Medical school (mean) 0.9Corridor 1 7 2.1Corridor 2 7 0.0Classroom 7 0.1Cafeteria 7 2.0Hall 7 0.2

Language school (mean) 2.3Hall 1 7 3.0Hall 2 7 1.7

Secondary school (mean) 9.5Teacher’s room 7 9.5

Hospitals (mean) 0.7Hospital B, newborns inpatients 7 0.0Hospital B, paediatric outpatients 11 0.2Hospital A‡, emergency department 7 1.0Hospital A, radiography department (emergencies) 7 1.6

General practice (mean) 1.1Doctor’s room 7 2.0Stairs 7 0.4

Public health centre (mean) 3.7Room 12 3.7

Households, non-smokers (mean) 0.0House A, living room 1 9 0.0House B, living room 2 8 0.0House B, bedroom 8 0.0

Households, smokers (mean) 7.9House C, living room 7 7.9

*The monitors were left exposed for 24 hours a day.†All connections where measures were taken from corresponded to different sites.‡The same hospital where the canteen’s measurement were taken from.

PostScript 83


S K Hammond,School of Public Health, University of California,

Berkeley, California, USA

Correspondence to: Manel Nebot, Institut Municipalde Salut Pública, Plaça Lesseps 1, 08023Barcelona, Spain; [email protected]/

[email protected]

AcknowledgementsWe especially wish to thank Charles Perrino and

Pablo Villegas from the School of Public Health, Uni-

versity of California, Berkeley, and the Institute for

Global Tobacco Control at the Johns Hopkins School

of Public Health, Baltimore, for its support in

carrying out this study.

References1 US Environmental Protection Agency.

Respiratory health effects of passive smoking:lung cancer and other disorders. Washington,DC: Office of Health and EnvironmentalAssessment, 1992. (Publication NoEPA/600/6-90/006F.)

2 Kreuzer M, Krauss M, Kreienbrock L, et al.Environmental tobacco smoke and lungcancer: a case-control study in Germany. Am JEpidemiol 2000;151:241–50.

3 Hackshaw A, Law M, Wald N. Theaccumulated evidence on lung cancer andenvironmental tobacco smoke. BMJ1997;315:980–8.

4 Hammond SK, Leaderer BP. A diffusionmonitor to measure exposure to passivesmoking. Environ Sci Technol1987;21:494–7.

5 Leaderer BP, Hammond SK. Evaluation ofvapor-phase nicotine and respirablesuspended particle mass as markers forEnvironmental Tobacco Smoke. Environ SciTechnol 1991;25:770–7.

6 Siegel M. Involuntary smoking in therestaurant workplace. JAMA1993;270:490–3.

7 Chapman S. Smoking in public places. BMJ1996;312:1051–2.

8 Hammond SK. Exposure of US workers toenvironmental tobacco smoke. Environ HealthPerspect 1999;107:329–40.

9 Llei 10/1991, de 10 de maig, demodificacio de la llei 20/1985 de prevencio iassistencia en materia de substancies quepoden generar dependencia. DOGCnum.1445, maig 1991 [Law restrictingsmoking in Catalonia].

A smoking cessation telephoneresource: feasibility andpreliminary evidence on theeffect on health care provideradherence to smoking cessationguidelinesPhysicians have frequent opportunities tointervene with their smoking patients asapproximately 70% of smokers see a physicianeach year.1 Even brief counselling by aphysician significantly improves the rate ofsmoking cessation according to meta-analyses performed by the Tobacco Use andDependence Guideline Panel and summarisedas “ask, advise, assist, and arrange follow-up”in the Agency for Health Care Policy andResearch (AHCPR) guidelines.2 Despite theseevidence based recommendations, physiciansidentify only about half of current smokers,advise less than half, and assist and arrangefollow up with a small minority.3 There areseveral explanations for this disparity be-tween physicians’ knowledge and their actualbehaviour including inadequate training, re-source and time constraints, and lack ofinformation on community cessation re-sources.

Office systems that screen patients forsmoking status increase the rate of smoking

cessation interventions by health careproviders.4 We hypothesised that providerswould be more likely to adhere to the AHCPRguidelines if they could delegate the timeconsuming steps of assistance and follow up to atelephone cessation resource.

This pilot study assessed the feasibility of acentral telephone smoking cessation resourcethat would proactively call smokers who gavetheir provider consent for referral. We alsoevaluated whether providers would be thenmore likely to adhere to the smoking cessa-tion guidelines. In a quasi-experimental pre-test, post-test design, a sample of patientsseen for any type of visit with a provider inthree participating primary care clinics in Ver-mont were interviewed at exit from the clinic.Only current smokers were asked about theirproviders’ adherence to guidelines. The pri-mary outcome measure was the proportion ofcurrent smokers who reported being asked,advised, assisted, and having follow uparranged at baseline and four months afterimplementation of the resource.

Two hundred and nine patients werereferred to the resource from the three clinicsover the four month duration of resourceavailability. We estimated that this repre-sented 20% of the total number of smokersseen at the clinics during this time period. Weinterviewed 54 smokers at baseline and 111smokers four months after implementation.After the intervention, rates of asking andadvising about smoking were not significantlychanged from baseline (table 1). The increasein the proportion of smokers who wereoffered assistance did not reach significance(p = 0.052). There was a significant increasein those who had follow-up arranged (table1).

Our study demonstrates that a smokingcessation proactive telephone resource isfeasible and that providers will refer patientsto such a resource. The resource had a contactrate of only 52% of referred current smokers,which we attribute to the resource not havingevening calling hours, a significant limitation.Implementation of this proactive smokingcessation telephone resource was associatedwith improved arrangement of follow up.These preliminary data suggest that furtherstudies of the effect of referral resources onadherence of physicians to guidelines arewarranted. Because of the non-randomiseddesign of this pilot study, we cannot attributeimprovements in provider adherence solely tothe availability of the telephone resource, asprovider focus groups, surveys, and trainingalso may have increased adherence to theguidelines. Only a randomised study canaddress this issue.

T W MarcyNational Cancer Institute, Division of Cancer

Prevention, Office of Preventive Oncology,Rockville, Maryland; Office of Health Promotion

Research, University of Vermont College ofMedicine, Burlington, Vermont; Vermont Cancer

Center, University of Vermont, Vermont [email protected]

L J SolomonVermont Cancer Center, and Department of

Psychology, University of Vermont

G S Dana, R Secker-WalkerOffice of Health Promotion Research, University of

Vermont College of Medicine, Burlington, andVermont Cancer Center, University of Vermont

J M SkellyBiometry Facility, University of Vermont

AcknowledgementsFinancial support: Robert Wood Johnson Founda-

tion, Princeton, New Jersey (Award 035850), Univer-

sity of Vermont Patient Oriented Research (Award

6-28529).

References1 Davis R. Uniting physicians against smoking:

the need for a coordinated national strategy.JAMA 1988;259:2900–1.

2 Fiore M, Bailey W, Cohen S, et al. Treatingtobacco use and dependence. Rockville,Maryland: US Department of Health andHuman Services. Public Health Service, 2000.

3 Goldstein M, Niaura R, Willey-Lessne C, etal. Physicians counseling smokers: apopulation-based survey of patients’perceptions of health care provider-deliveredsmoking cessation interventions. Arch InternMed 1997;157:1313–19.

4 Fiore M, Jorenby D, Schensky A, et al.Smoking status as the new vital sign: effect onassessment and intervention in patients whosmoke. Mayo Clin Proc 1995;70:209–13.

Ophthalmologists’ andoptometrists’ attitudes andbehaviours regarding tobaccocessation interventionAlthough health care providers can be effec-tive in motivating and helping patients to quittheir tobacco use,1–7 the potential role of eyecare professionals has been under recognised.Several chronic ocular diseases are associatedwith smoking,8 including formation of cata-racts and age related macular degeneration (aleading cause of blindness).8 9 As a cardiovas-cular risk factor, smoking may also play a rolein the development of anterior ischaemicoptic neuropathy.10 In addition, smoking mayincrease the risk of ocular disease from otherdisorders, such as diabetes, the main cause ofblindness in persons 20–74 years of age.11

Table 1 Adherence of health care providers to smoking cessationinterventions

InterventionBaseline(n=54)

Post-implementation(n=111)

Relative riskPost-implementation vbaseline (95% CI)

Asked 37 (69%) 71 (64%) 0.9 (0.7 to 1.2)Advised to quit 29 (55%)* 65 (59%) 1.1 (0.8 to 1.4)Quit date discussed 5 (9%) 14 (13%) 1.4 (0.5 to 3.6)Assistance offered 14 (26%) 46 (41%)† 1.6 (1.0 to 2.6)Follow up arranged 9 (17%) 38 (34%)‡ 2.1 (1.1 to 3.9)

*One subject’s data missing for this item, n=53.†p=0.052 versus baseline.‡p<0.02 versus baseline.CI, confidence interval

84 PostScript


Before developing a tobacco cessation inter-vention for eye care professionals, it is essen-tial to assess the current status of tobacco ces-sation activities in routine eye care. We sent a12 item questionnaire to all currently licensedophthalmologists (n = 1209) and a randomsample of 1234 optometrists in four westernstates of the USA (Arizona, California, Or-egon, and Washington), assessing demo-graphics and behaviours, attitudes, and barri-ers regarding intervention with tobacco usingpatients. The final return rate was 39% forophthalmologists and 53% for optometrists.Data are presented only for those in currentpractice (90% of the ophthalmologists and95% of the optometrists). Since ophthalmolo-gists were significantly less likely to return thesurvey (χ2 (1, n = 2443) = 48.56, p < 0.001)than optometrists, we report data for eachprofessional group separately without com-paring the two.

As table 1 indicates, both ophthalmologistsand optometrists feel it is appropriate to helptobacco using patients with cessation, thoughfew do so regularly and many barriers areperceived. Optometrists employing supportstaff were more likely to express positive atti-tudes towards providing tobacco interven-tions than those who did not (t(634) = 2.55,p < 0.05), suggesting a correlation betweentime constraints and attitude toward inter-vention.

Both ophthalmologists and optometristscited many barriers to intervening with theirtobacco using patients. Lack of time was mostcommonly cited by ophthalmologists,whereas optometrists were more concernedabout lack of patient materials and lack oftraining. How recently they trained and theirsex were related to barriers. Ophthalmologists

and optometrists who had graduated morerecently from their programmes perceivedfewer barriers to providing cessation services(r = 0.18, p < 0.01 for ophthalmologists;r = 0.16, p < 0.01 for optometrists). Previousstudies1 12 have shown a reduction in percep-tion of barriers due to receiving education intobacco cessation intervention.

Surprisingly, female ophthalmologists wereless likely to believe they should advisepatients to quit (t(381) = 2.16, p < 0.05), andboth female ophthalmologists and optom-etrists perceived more barriers to doing so(t(365) = −2.54, p < 0.05 for ophthalmolo-gists, t(586) = −2.93, p < 0.01 for optom-etrists). This reluctance may be due to femaleeye care providers’ concerns about possiblenegative patient reactions, or fears of losingpatients from their practices.

Although this is a convenience sample, ourresults suggest the feasibility of brief, officebased tobacco cessation interventions for usein eye care settings. An intervention must,however, focus on reducing perceived barriersby training eye care professionals in providingan effective, brief intervention that is readilyreceived by patients, as well as providingresources and materials to practitioners. Ourdata suggest that cooperative agreementswith insurance companies to provide reim-bursement to providers would facilitate theadoption of the intervention.

As summarised by the Clinical PracticeGuidelines,2 many types of general andspecialist providers have successfully incorpo-rated tobacco cessation activities into theirpractices. One way to extend the reach oftobacco cessation interventions is to utiliseother medical specialists to motivate tobaccousers to quit. Ophthalmology and optometry

may provide such an opportunity, given therole of smoking in ocular disease, the fact thatmost visits are for routine rather than acutecare, and the presence of support staff whocan help implement an intervention.

J S GordonJ A Andrews

E LichtensteinH H Severson

L AkersC Williams

Oregon Research Institute, 1715 FranklinBoulevard, Eugene, Oregon 97403, USA

Correspondence to: Dr Judith Gordon;[email protected]

AcknowledgementWork supported in part by grant R01 CA71018 from

the National Cancer Institute.

References1 Andrews JA, Severson HH, Lichtenstein E, et

al. Evaluation of a dental office tobaccocessation program: effects on smokelesstobacco use. Ann Behav Med1999;21:48–53.

2 Fiore MC, Bailey WC, Cohen SJ, et al.Treating tobacco use and dependence.Clinical Practice Guideline. Rockville,Maryland: US Department of Health andHuman Services. Public Health Service, 2000.

3 Hollis JF, Lichtenstein E, Vogt TM, et al.Nurse-assisted counseling for smokers inprimary care. Ann Intern Med1993;118:521–5.

4 Little SJ, Stevens VJ, Severson HH, et al. Aneffective smokeless tobacco intervention fordental hygiene patients. J Dental Hygiene1992;66:185–90.

5 Severson HH, Andrews JA, Lichtenstein E, etal. Reducing maternal smoking and relapse:long-term evaluation of a pediatricintervention. Prev Med 1997;26:120–30.

6 Severson HH, Andrews JA, Lichtenstein E, etal. Using the hygiene visit to deliver a tobaccocessation program: results of a randomizedclinical trial. J Am Dental Assoc1998;129:993–9.

7 Wall MA, Severson HH, Andrews JA, et al.Pediatric office based smoking intervention:impact on maternal smoking and relapse.Pediatrics 1995;96:622–8.

8 Solberg Y, Rosner M, Belkin M. Theassociation between cigarette smoking andocular diseases. Survey of Ophthalmology1998;42:535–47.

9 West S, Munoz B, Emmett EA, et al. Cigarettesmoking and risk of nuclear cataracts. ArchOphthalmol 1989;107:1166–9.

10 Margulies LJ. Ocular manifestations ofcardiovascular and hematologic disorders.Curr Opin Ophthalmol 1995;6:97–103.

11 Alexander LJ, Duenas MR. Eye care forpatients with diabetes in the state of Florida:status in 1988. J Am Optometric Assoc1994;65:552–8.

12 Gordon JS, Severson HH. Tobacco cessationthrough dental office settings. J Dent Educ2001;65:354–63.

CORRECTION

The authors of Health impact of “reducedyield” cigarettes: a critical assessment of theepidemiological evidence (Tobacco Control2001;10(suppl I):i4-i11) would like to correcta statement in figure 1. The legend to figure 1and the corresponding text on page 15 shouldsay “Each milligram decrease in machinemeasured nicotine...” rather than “Each milli-gram decrease in machine measured tar...”.

Table 1 Eye care professionals’ attitudes, beliefs, and perceived barriersregarding intervention with tobacco using patients

Ophthalmologists(n=422) (%)

Optometrists(n=629) (%)

DemographicsYears in practice 23 (SD 11.33) 16 (SD 11.23)Sex 85% male 72% male

Tobacco related behaviours: “How often do you . . .”Ask patients about tobacco use? 71 38Sometimes advise patients to quit tobacco? 91 81Regularly advise patients to quit tobacco? 30 16Provide educational materials on the ocular effects oftobacco use?

5 6

Barriers to intervening with smokersLack of time 83 70Lack of patient materials 67 79Lack of training 64 78Lack of referral resources 63 76Concerns about effectiveness 63 69Concerns about patient resistance or loss 61 72Lack of reimbursement mechanism 57 52Concerns about office staff resistance 32 40

Attitudes about intervening with smokersBelieve it is appropriate for them to document patients’tobacco use

81 69

Believe it is appropriate for them to advise patients toquit tobacco

82 71

Interested in learning new ways to help patients quittobacco

74 80

PostScript 85


Health impact of “reduced yield” cigarettes: a critical ......burden caused by smoking. This...

Documents

Transcript of Health impact of “reduced yield” cigarettes: a critical ......burden caused by smoking. This...