Tobacco and Public Health - TCSC Indonesia

case–control study nested in a screening cohort, so HPV testing for types 16 and 18
only was performed on archival smears by PCR. A doubling of risk for CIN 3 was
found in current smokers (OR 1.94, 95% CI 1.32–2.85). The effect of smoking
remained significant in women who were HPV positive (OR 2.34, 95% CI 1.28–4.27),
but not in those who were HPV negative.
A similar nested case–control study was carried out by Deacon et al. (2000), and
once again any women without CIN 3 were used as controls for those who had CIN 3.
There were 199 HPV positive cases (by PCR), 181 HPV positive controls, and 203 HPV
negative controls. The risk factors for HPV positivity and having CIN 3 were different,
with smoking significant (with a dose–response) for CIN 3 (OR 2.57, 95% CI
1.49–4.45) but not for HPV infection. The authors suggest that this provides evidence
for a synergism of smoking with HPV to cause cervical neoplasia.
Kjellberg et al. (2000) in Sweden looked at 137 women with high-grade CIN and 253
age-matched controls. HPV testing was performed by PCR. Smoking was significantly
associated with high-grade CIN even after adjustment for the presence of HPV (OR
2.6, 95% CI 1.2–5.6). In addition, there was a dose–response for both duration and
amount of smoking (adjusted OR for >15/day 6.0, 95% CI 2.7–13.3).
Sasagawa et al. (1997) in Japan found that smoking was a significant risk factor for
invasive cancer after adjustment for HPV (OR 5.8, 95% CI 1.8–19.0), but not for CIN
(OR 1.6, 95% CI 0.63–4.0). Smoking significantly elevated the risk of having an HPV
infection (by PCR) in controls (OR 2.7, 95% CI 1.1–6.9) but not cases (OR 1.4, 95% CI
0.38–5.4), most of whom were in any case HPV positive.
Derchain et al. (1999) compared women with biopsy-proven CIN with those whose
biopsies were normal (despite an abnormal colposcopy). After adjustment for the
presence of HPV (by Hybrid Capture I), smoking was still associated with increased
risk of high-grade CIN (OR 4.37, 95% CI 1.48–12.92).
Coker et al. (2002) have looked at both active and passive smoking as risk factors for
CIN, using hybrid capture I as their HPV test. Current smoking was associated with a
non-significant increase in risk of high-grade CIN (OR 1.81, 95% CI 0.71–4.6), with a
similar, but again non-significant odds ratio for passive smoking exposure (OR 2.05,
95% CI 0.77–6.2).
The relationship between smoking and HPV infection
ANNE SZAREWSKI AND JACK CUZICK 467
Ley et al. (1991) investigated HPV prevalence in a screening population, using PCR
methods for HPV detection. The study consisted of a cross-sectional sample of 467
women attending a university health clinic in California for routine screening. The
women were young (median age 22 years), mostly white (72%) and non-Hispanic
(87%). On initial analysis, current smoking was correlated with presence of HPV (OR
2.3, 95% CI 1.1–5.2). The study did not investigate the women further and therefore no
information is available regarding cervical abnormality in the two groups.
Rohan et al. (1991) conducted a similar cross-sectional university health clinic
screening study, in Toronto. In this study, 105 women attending for routine cervical