Epidemiology
Association between smoking and genital warts:
1
Department of
Screening-based Research,
Cancer Registry of Norway,
Oslo, Norway
2
Institute of Cancer
Epidemiology, Danish Cancer
Society, Copenhagen, Denmark
3
Department of Obstetrics and
Gynaecology, Rigshospitalet,
University of Copenhagen,
Denmark
4
Icelandic Cancer Society,
Reykjavik, Iceland
5
Department of Medical
Epidemiology and Biostatistics,
Karolinska Institute, Stockholm,
Sweden
6
Merck Research Laboratories,
Merck & Co, Inc, Upper
Gwynedd, Pennsylvania, USA
Correspondence to
Dr Bo Terning Hansen, Cancer
Registry of Norway, PO Box
5313 Majorstuen, N-0304 Oslo,
Norway; bo.terning.hansen@
kreftregisteret.no
Accepted 22 January 2010
258
longitudinal analysis
Bo Terning Hansen,1 Maria Hagerup-Jenssen,1 Susanne Krüger Kjær,2,3
Christian Munk,2 Laufey Tryggvadottir,4 Pär Sparén,5 Kai-Li Liaw,6 Mari Nygård1
ABSTRACT
Objectives To assess the association between smoking
and the reported clinical diagnosis of genital warts.
Methods A sample of 58 094 women (aged 18e45)
randomly drawn from the general female population of
Denmark, Iceland, Norway and Sweden answered
a questionnaire on lifestyle and health. Longitudinal data
were reconstructed based on self report of age-specific
events. In a Cox regression model, women who reported
having been clinically diagnosed with genital warts were
followed up until the age at first diagnosis, while women
who reported never having been diagnosed with genital
warts were censored at the age of interview. Age-
specific smoking doses and ages at onset of smoking,
sexual intercourse, condom use, hormonal contraceptive
use, first pregnancy and alcohol drinking were included in
the model as time-dependent covariates. The model also
included lifetime number of coital partners and country of
origin as fixed covariates.
Results Ever-smokers reported a lower age at first
intercourse and more coital partners than never-smokers.
The adjusted model showed that sexual behaviour
strongly influenced the risk of being diagnosed with
genital warts, and that smokers in addition had an
increased risk compared with non-smokers (adjusted
HR¼1.27, 95% CI 1.17 to 1.37). There was also
a modest additional doseeresponse effect of smoking,
with smokers experiencing a 0.6% increased risk of being
diagnosed with genital warts for each additional
cigarette smoked daily (adjusted HR¼1.006, 95% CI
1.001 to 1.012).
Conclusions Smokers experienced a moderately
increased risk of being diagnosed with genital warts. This
finding could be explained by the immunosuppressive
effects of nicotine, or by confounding not accounted for
in the adjusted model.
INTRODUCTION
Genital warts affect some 11% of Nordic women1
and are the most common clinical manifestation of
human papillomavirus (HPV) infection of the
genitalia. Genital warts are sexually transmitted,
and they are caused by low-risk HPV types 6 and
11,2 which do not cause cancer. In women, genital
warts are mainly found on the external genitalia
and adjacent anal and perianal areas, but may also
occur on the cervix and in the vagina. Genital warts
are detrimental to quality of life.3 At the population
level, there are considerable costs associated with
the diagnosis and treatment of genital warts.4
Numerous studies show that smokers have an
increased risk of developing precancerous and
cancerous cervical lesions caused by infection with
high-risk HPV types.5 Less is known about the
influence of smoking on the risk of acquiring genital
warts. Some studies report no significant associa-
tion between smoking and acquisition of genital
warts among women,6e8 whereas others report an
increased risk of genital warts among female
smokers,9e11 ranging up to a fivefold increased risk
for current smokers compared with non-smokers.12
Investigations of smoking and clearance/remission
of genital warts similarly report mixed results.13e15
The studies examining a potential doseeresponse
effect of cigarette smoking on the risk of acquiring
genital warts have used rather crude interval cate-
gorisations of current smoking dose or smoking
duration and have not taken into account the fact
that individual smoking status and intensity often
change with time. Such categorisation may mask
variation which might be of importance if smoking
is associated with the disease. More studies are thus
needed to examine the role of smoking for the
acquisition of genital warts. Smoking may influ-
ence the susceptibility to genital warts through a
causal immunosuppressive effect,16 and/or through
an association with risk taking that extends to
sexual behaviour.17
The aim of this study is to assess the association
between smoking and genital warts. Our analysis
takes into account the fact that smoking behaviour
may vary with time within subjects. We use
a prospective analysis on reconstructed longitudinal
data that was collected cross-sectionally.
METHODS
A random sample of women aged 18e45 from
Denmark, Iceland, Norway and Sweden were asked
to participate in a survey on lifestyle and health
during 2004e5. Data on enrolment and data
collection have previously been provided.1 Briefly,
in total 69 486 women participated in the study by
responding to a self-administered questionnaire
(participation rate 66.9%). The women were asked
whether they ever had been told by medical
personnel that they had genital warts, and if so, the
age at first diagnosis. They were also asked about
smoking status (ie, current, former or never-
smoker) and age-specific smoking doses measured
by the number of cigarettes smoked daily in the age
intervals <13, 13e16, 17e20, 21e24, 25e29,
30e34, 35e39 and 40e45 years. Further, they were
asked about age at first pregnancy, and debut age of
smoking, drinking alcohol, sexual intercourse,
condom use and hormonal contraceptive use. A
total of 11 392 participants did not respond to at
least one of these questions, and were hence
Sex Transm Infect 2010;86:258e262. doi:10.1136/sti.2009.038273
 Epidemiology

excluded from the analyses, leaving a total of 58 094 women to Table 1 Characteristics of never- and ever-smoking Nordic women
be included. aged 18e45
Since the timing of the first onset of genital warts and several Never-smokers Ever-smokers
lifestyle parameters were available, we could reconstruct longi- (n[31908) (n[26186) p Value*
tudinal data on the reported diagnosis of genital warts and some Genital wartsy
of its potential predictors. We used a Cox regression model with Ever (%) 8.8 12.5 <0.0001
time-dependent covariates to this end. Integer age was treated as Age at first diagnosis 22.04 (4.65) 21.92 (4.75) 0.4
the temporal unit, thus the baseline hazard function describes Sexual intercoursey
the effect of age on the risk of being diagnosed with genital Ever (%) 94.5 99.0 <0.0001
warts. Subjects with genital warts changed status from not Debut age 17.48 (2.71) 16.12 (2.03) <0.0001
having to having genital warts at the age when they were first Condom usey
diagnosed. Events subsequent to the first diagnosis of genital Ever (%) 86.4 90.4 <0.0001
warts were not included in the model. Subjects never diagnosed Debut age 18.19 (3.49) 17.25 (3.42) <0.0001
with genital warts were censored at the age of interview. Sexual Hormonal contraceptive usey
intercourse, condom use, hormonal contraceptive use, pregnancy Ever (%) 87.2 92.6 <0.0001
Debut age 18.36 (3.50) 17.36 (3.30) <0.0001
and alcohol drinking were each dichotomous and time-depen-
Pregnancyy
dent covariates. Subjects who experienced these events changed
Ever (%) 57.8 71.3 <0.0001
status permanently at the age of onset of the event. Smoking
Age, first 24.89 (4.57) 23.07 (4.83) <0.0001
status was also dichotomous and hence changed at the age of
Drinking alcoholy
onset for smokers, but subjects who stopped smoking before Ever (%) 92.9 98.7 <0.0001
a diagnosis of genital warts or censoring changed status twice. Debut age 16.78 (2.06) 15.99 (1.86) <0.0001
Smoking dose was separately included in the model as the Number of lifetime
number of cigarettes smoked daily by each individual at each Coital partners 5.81 (7.48) 10.68 (11.54) <0.0001
age. A positive dose identifies a smoker at a particular age. A dose
Results are shown as mean (SD) unless stated otherwise.
of zero could pertain to never-smokers as well as ever-smokers *c2 test or unpaired t test.
who did not smoke at that particular age, and smokers smoking ystatus and age refer to the period until the onset of genital warts, or censoring.
less than one cigarette a day at that particular age. Lifetime
number of coital partners, country of origin and level of educa-
tion were included as fixed covariates in all multivariate models.
Level of education was dropped from the models and is hence increased risk. In contrast, having been pregnant had a protec-
not reported since it did not influence model estimates. Model- tive effect. Finally, the adjusted model showed that the HR for
ling was done with R 2.7.2. being diagnosed with genital warts was somewhat higher
among women in Iceland, Norway and Sweden than among
women in Denmark.
RESULTS
In total, 6077 of the 58 094 women included in the analyses DISCUSSION
reported having been clinically diagnosed with genital warts (ie, Smoking was associated with an increased risk of being diag-
10.5%). Ever-smokers and current smokers at the onset of genital nosed with genital warts in our large randomly selected study
warts or censoring constituted 45.2% and 29.3% of the sample, population of Nordic women, with smokers experiencing a 27%
respectively. Mean age of smoking initiation was 16.4 (SD 3.12) higher risk than non-smokers. There was a modest additional
years. Ever-smokers generally preceded never-smokers in experi- doseeresponse relationship between smoking and the risk of
ences related to sexual behaviour, as well as in debut age for being diagnosed with genital warts, the risk increasing by 0.6%
drinking alcohol. A higher percentage of smokers ever experi- for each additional cigarette smoked daily. Hence, a woman in
enced genital warts, sexual intercourse and pregnancy, and ever our population-based sample who smoked, for example, 20
used condoms, hormonal contraceptives and alcohol. In addi- cigarettes a day was overall at a 39% greater risk of being diag-
tion, ever-smokers reported more lifetime coital partners than nosed with genital warts than a non-smoker.
never-smokers (table 1). From our model and from previous studies,6 8 it is obvious that
The association between smoking and the other behaviours the risk of genital warts is strongly influenced by sexual behaviour.
was adjusted for by the inclusion of various time-dependent and Our data also confirm that smoking is associated with various
fixed covariates in a Cox regression model. This multiple model aspects of sexual behaviour as well as the initiation of alcohol use.
showed that smokers had an adjusted hazards ratio (HR) of 1.27 Since smoking may be associated with other types of risk-taking
(95% CI 1.17 to 1.37) for being diagnosed with genital warts behaviour, such as substance use and risky sex,17 it may be difficult
compared with non-smokers (table 2). There was a modest to identify the individual contributions of these linked behaviours
additional doseeresponse effect of smoking; the risk of being to the risk of disease. In our adjusted model we included a range of
diagnosed with genital warts increased by 0.6% per additional covariates related to sexual behaviour, as well as the onset of
cigarette smoked daily (HR¼1.006, 95% CI 1.001 to 1.012). alcohol drinking and country of origin, in an attempt to control for
The strongest predictors for the risk of being diagnosed with potential confounders that may relate both to smoking and to the
genital warts were associated with sexual behaviour. Having had reported diagnosis of genital warts. This model showed that
sexual intercourse and having used condoms and hormonal smoking explained some variation in the risk of being diagnosed
contraceptives increased the risk substantially. Moreover, the with genital warts that was additional to that explained by the
lifetime number of coital partners (a fixed covariate) was posi- other covariates. However, this could result from incomplete
tively associated with an increased risk of being diagnosed with control of the confounders of the association between smoking
genital warts. This effect was strong, as indicated by a very and genital warts.18 Although we included several covariates
narrow CI. Having drunk alcohol was also associated with an related to sexual behaviour, our model does not capture all aspects

Sex Transm Infect 2010;86:258e262. doi:10.1136/sti.2009.038273 259

 Epidemiology

Table 2 Risk of being diagnosed with genital warts among 58094 doseeresponse effect documented in this study lends some
Nordic women aged 18e45 support to a causal link between smoking and the risk of being
Crude HR Adjusted HR Adjusted diagnosed with genital warts. However, we cannot exclude the
Covariates (95% CI) (95% CI) p value possibility that an increase in smoking dose coincides with
Time-dependent covariates* changes in risk factors not accounted for by our adjusted model.
Smoking status The association between smoking and genital warts has not
Non-smoker 1 1 e been extensively investigated, and results from different studies
Smoker 1.70 (1.62 to 1.79) 1.27 (1.17 to 1.37) <0.0001 vary.6e12 The inconsistencies may be explained by differences in
Smoking dosey 1.032 1.006 0.02 sampling, sample size and analytical approach. The studies
(1.028 to 1.035) (1.001 to 1.012) reporting the highest risks for smokers have relatively low
Sexual intercourse sample sizes. There does not appear to be a trend for prospective
Never 1 1 e
studies to be more or less likely to report an effect of smoking
Ever 37.17 12.76 <0.0001
(26.37 to 52.40) (8.94 to 18.20)
than retrospective studies. Our study adds to the evidence that
Condom use there is a relationship between smoking and genital warts after
Never 1 1 e adjustment for potential confounders. A previous cross-sectional
Ever 3.26 (3.00 to 3.55) 1.57 (1.44 to 1.70) <0.0001 analysis from the same survey showed a weaker association
Hormonal contraceptive use between smoking and genital warts.1 Like the other studies that
Never 1 1 e have examined this association, it did not take the time-varying
Ever 3.42 (3.13 to 3.72) 1.81 (1.67 to 1.98) <0.0001 nature of smoking behaviour into account. Moreover, it
Drinking alcohol employed a crude lifetime measure of smoking dose rather than
Never 1 1 e the dose acquired before the onset (or not) of disease.
Ever 4.16 (3.62 to 4.79) 1.79 (1.56 to 2.06) <0.0001 Women who had had sexual intercourse were at an increased
Pregnancy risk of being diagnosed with genital warts, confirming the
Never 1 1 e sexually transmitted nature of the infection. In addition, oral
Ever 0.88 (0.82 to 0.94) 0.72 (0.68 to 0.77) <0.0001 contraceptive use, drinking alcohol and condom use were asso-
Fixed covariates ciated with an increased risk of being diagnosed with genital
Lifetime number of 1.016 1.014 <0.0001 warts, perhaps owing to more risky and/or a higher sexual
coital partners (1.016 to 1.017) (1.013 to 1.015)
activity among those who ever experienced these events than
Country
Denmark 1 1 e
among those who never did so. Moreover, women using
Iceland 1.21 (1.13 to 1.30) 1.34 (1.25 to 1.44) <0.0001
condoms may have had partners with a higher risk profile,
Norway 0.95 (0.88 to 1.02) 1.10 (1.02 to 1.18) 0.01 which could have increased the risk of these women being
Sweden 1.13 (1.05 to 1.21) 1.21 (1.12 to 1.29) <0.0001 diagnosed with genital warts, especially since any genital
contact is sufficient for the transmission of genital warts and
HR, 95%s CIs and p-values from Cox regression models with time-dependent and fixed
covariates. Crude estimates refer to univariate models, adjusted estimates refer to condoms hence offer limited protection. Hormonal contracep-
a multivariate model which included all covariates in the table. tive users may also have been more exposed to HPV if the use of
*All statuses refer to the period until the onset of genital warts, or censoring.
yNumber of cigarettes smoked daily.
hormonal contraceptives reduced the frequency of condom use.
Alcohol consumption24 and oral contraceptive use25 may also
have reduced individual immunocompetence, and hence
of sexual behaviour that may be of importance for the acquisition increased the risk of being diagnosed with genital warts. Women
of genital warts. For instance, we do not have information on the who had been pregnant had a reduced risk of being diagnosed
sexual risk profile of the partners of the women included in this with genital warts compared with those who never had been
study, nor do we have information on age-specific frequencies of pregnant. Possibly, ever-pregnant women overall had a reduced
alcohol, condom or hormonal contraceptive use until the time number of sex partners subsequent to the pregnancy, and/or
of disease or censoring. Moreover, we include the lifetime number partners with a lower risk profile, and hence experienced
of coital partners as a fixed effect, which is suboptimal since only a somewhat reduced exposure to HPV. We also found that the
the partners who were acquired before the onset of genital warts HR for being diagnosed with genital warts differed somewhat
are relevant for the outcome. Reliable information on such between the countries, and that it was highest among Icelandic
detailed aspects of behaviour is hard to obtain from a large sample women. Some of this variation might be explained by differ-
of participants. If some of this missing information is related to ences in sexual behaviour, since Icelandic women report more
the risk of being diagnosed with genital warts and also is differ- coital partners.1
ently distributed between smokers and non-smokers, the effects This study has a large sample size and a high participation
attributed to smoking in our analyses may in fact be due to rate considering the sensitive nature of the questions asked. A
differences in other behaviours. further strength of this study is the registration of complete
Alternatively, our documentation of an increased risk for being individual smoking histories. This gives a detailed account of
diagnosed with genital warts among smokers could result from smoking behaviour that allows for inclusion of temporal aspects
a causal effect of smoking itself. A recent study suggests an in the consideration of smoking as a potential predictor for
independent effect of smoking in the development of HPV- genital warts. Using lifetime or current measures of smoking
induced invasive cervical cancer.19 Smoking may damage the status or intensity, as has been the rule, may obscure real effects
cervical epithelium20 and impact on the humoral and cell- with respect to the event of acquiring/not acquiring genital
mediated immune response.16 It changes the density of warts, since individual smoking status and intensity often vary
Langerhans cells,21 T lymphocytes22 and immunomodulating over time. Here, we specifically examine time-dependent
agents23 in the cervical epithelium, and may thus increase the behaviour until the onset of disease (or age at interview for
susceptibility to infection and act synergistically with HPV to women who reported never having been diagnosed with genital
increase the risk of acquisition of genital warts. The modest warts).

260 Sex Transm Infect 2010;86:258e262. doi:10.1136/sti.2009.038273


In order to minimise misclassification of disease, we asked
whether participants had been diagnosed with genital warts by
medical personnel, thereby avoiding potential imprecision
introduced by self diagnosis. However, some of the women may
have had undiagnosed cases of genital warts. Vaginal and
cervical warts may be particularly likely to have escaped notice
among women who have rarely had gynaecological examina-
tions. Since smoking may be more common among individuals
with a relatively low socioeconomic status,26 and low socio-
economic status could be associated with reduced access to
certain healthcare services,27 there is a possibility that undiag-
nosed cases of genital warts may have occurred more frequently
among smokers than among non-smokers in our sample. If so,
we may have underestimated the effect of smoking on the risk
of being diagnosed with genital warts. However, since socio-
economic status in a Nordic setting does not appear to be
a strong predictor of the propensity to visit a general practi-
tioner,28 or to attend screening for cervical cancer,29 the potential
for a bias in undiagnosed cases of genital warts between smokers
and non-smokers may be limited in our study.
The main limitation of this study is that it is based on self
report of retrospective events. Although collected cross-section-
ally, most of the data used in this investigation are longitudinal,
reconstructed by the participants’ reports of the timing of
events. The validity of this approach hinges on the respondents’
ability to recall the retrospective events of interest with
reasonable accuracy. Moreover, self report of topics that
implicitly relate to social norms, like the occurrence of genital
warts, may be erroneous. Recall of age-specific smoking doses is
perhaps particularly susceptible to imprecision, but information
on individual smoking histories is very hard to obtain by other
means than self report. Some studies show that recall of
smoking history,30 including age at smoking initiation,31 is
reliably accounted for by self report. Moreover, current smoking
status generally seems to be reliably reported.32 33 Mistakes in
the relative ordering of smoking initiation and the onset of
genital warts is unlikely to represent a major problem here, since
the average age of smoking initiation and the first onset of
genital warts were widely separated. Smoking initiation is
largely a teenage phenomenon while the first onset of genital
warts tends to occur somewhat later. However, an ideal design
to examine the association between genital warts and smoking
would be a prospective study in which smoking, sexual behav-
iour and disease status were closely tracked to minimise recall
error and misclassification of disease.
We conclude that smokers experienced a moderately increased
risk of being diagnosed with genital warts. This finding could be
Key messages
< The risk of being diagnosed with genital warts was strongly
influenced by sexual behaviour among women from the
general population in Denmark, Iceland, Norway and Sweden.
< Smokers experienced an additionally increased risk of being
diagnosed with genital warts.
< The risk of being diagnosed with genital warts was modestly
affected by smoking dose.
< The associations between smoking and the risk of being
diagnosed with genital warts may be due to biological effects
of smoking, or residual confounding with sexual behaviour.
Sex Transm Infect 2010;86:258e262. doi:10.1136/sti.2009.038273
Epidemiology
explained by the immunosuppressive effects of nicotine, or by
confounding not accounted for in the adjusted model.
Acknowledgements We thank Björn Hagmar and Ole Klungsøyr for comments on
a previous draft of this paper.
Funding Merck & Co Inc (grant number: EPO 8014.016).
Competing interests None.
Ethics approval This study was conducted with the approval of the national data
protection boards and ethics committees in Denmark, Iceland, Norway and Sweden.
Contributors SKK, CM, LT, PS, KLL, MHJ and MN designed the questionnaire and
coordinated the collection of data. SKK, CM, MN and BTH conceived and designed the
study. BTH did the statistical analyses and wrote the manuscript. All authors critically
revised the manuscript for intellectual content and approved the final version.
Provenance and peer review Not commissioned; externally peer reviewed.
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