Tobacco and Public Health - TCSC Indonesia

466
SMOKING AND CERVICAL NEOPLASIA
Morrison et al. (1991) used a combination of Southern blotting and polymerase
chain reaction (PCR) techniques to assess HPV status in his study, conducted in
New York. This case–control study did not include cancer cases, restricting itself to CIN
(of any grade). Once again, a high proportion of both cases (53%) and controls (44%)
were of Hispanic origin and relatively few women (20% of cases and 9% of controls)
smoked more than 10 cigarettes per day. The study showed an increased risk in
smokers (OR 3.0, 95% CI 1.1–8.1) and a dose–response relationship, but the association
was no longer significant after adjustment for HPV.
Schiffman et al. (1993) reported a case–control study from a health screening clinic in
Oregon, using consensus PCR for determination of HPV status. Cases and controls were
chosen on the basis of cytology results, which introduced misclassification problems in
both case and control groups. Although not all cases had colposcopy and biopsy, of those
who did, the majority were low-grade lesions. Based on cytology, there were 450 lowgrade
lesions and 50 of high grade. Thirty-five per cent of cases and 20 per cent of controls
were current smokers; no data were presented regarding amount or duration of smoking.
An increased risk in current smokers was observed (RR 1.7, p < 0.05), but this was no
longer significant after adjustment for HPV (RR 1.2, 95% CI 0.8–1.8). However, an ancillary
analysis showed that among HPV positive women, current smokers were almost three
times as likely to have CIN 2/3 as non-smoking women (RR 2.7, 95% CI 1.1–6.5).
Kjaer et al. (1996) showed that even after adjustment for sexual behaviour and the
presence of HPV (detected by consensus PCR), smoking remained an independent risk
factor for both low- and high-grade cervical abnormalities (as measured by cytology).
The adjusted relative risks (RR) were 1.8 (95% CI 1.1–2.8) for low-grade abnormalities
and 2.3 (95% CI 1.3–4.2) for high-grade abnormalities. The study also showed that
current smoking was a significant risk factor in both HPV positive (OR 1.9, 95% CI
1.2–3.2) and HPV negative women (OR 2.4, 95% CI 1.3–4.6).
Roteli-Martins et al. (1998) compared risk factors in women with biopsy-proven CIN
1 with those who had high-grade CIN, in their study in Brazil. HPV testing was performed
by Hybrid Capture I. The 77 women were between 20 and 35 years of age.
Smokers were significantly more likely to have high-grade CIN (35 per cent of women
with CIN 1 smoked vs. 78 per cent of those with CIN 2/3, p < 0.001) and there was a trend
towards an increasing risk with increasing duration of smoking (p = 0.07). In addition,
smokers were significantly more likely to test positive for high-risk HPV types (p = 0.046).
Ho et al. (1998) also used women with CIN 1 as controls for those with high-grade
CIN in their study from New York. In this larger study of 348 women, 90 per cent were
Hispanic or Black. HPV testing was performed by PCR and Southern blotting. It was
found that the risk of having CIN 3 was significantly greater in smokers (OR 2.37, 95%
CI 1.09–5.15) and increased with the number of cigarettes smoked per day (p = 0.03)
and duration of smoking (p = 0.02). This was not the case for CIN 2, however (OR for
current smoking 1.46, 95% CI 0.67–3.19).
Ylitalo et al. (1999) in Sweden used all women without CIN 3 as controls for those
with CIN 3 (thus the control group included even those with CIN 2). This was a