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      Cigarette smoking is an independent risk factor for cervical intraepithelial neoplasia in young women: A longitudinal study

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          Abstract

          Repeated measurements of smoking, cervical human papillomavirus (HPV) status and sexual behaviour were used to measure the risk of high-grade cervical intraepithelial neoplasia (CIN) in relation to changes in smoking and cervical HPV status, and to explore the impact of smoking on the acquisition and duration of incident cervical HPV infection. Included in this longitudinal analysis are 1485 women aged 15–19 years: 1075 were HPV-negative and cytologically normal at recruitment; 410 were HPV-positive, cytologically abnormal or both, at this time. Women re-attended every 6 months, when samples were taken for cytological and virological examination. Current smoking intensity was associated with an increased risk of high-grade CIN, after controlling for cervical HPV status (compared to non-smokers, hazards ratio (HR) for 10 or more cigarettes per day = 2.21, 95% confidence interval (CI) 1.19–4.12, p-trend = 0.008). In women who were HPV-negative and cytologically normal at recruitment, current smoking was not significantly associated with the risk of acquiring a cervical HPV infection, after controlling for life-time number of partners and age of oldest partner (HR = 1.13, 95% CI 0.90–1.41); nor did it prolong the length of time during which HPV could be detected (HR = 1.03, 95% CI 0.78–1.34). Current smoking intensity is an independent risk factor for high-grade CIN in young women, after controlling for cervical HPV infection.

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          Most cited references28

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          Genital human papillomavirus infection: incidence and risk factors in a cohort of female university students.

          Incidence data on human papillomavirus (HPV) infection are limited, and risk factors for transmission are largely unknown. The authors followed 603 female university students in Washington State at 4-month intervals between 1990 and 2000. At each visit, a sexual and health questionnaire was completed and cervical and vulvovaginal samples were collected to detect HPV DNA. At 24 months, the cumulative incidence of first-time infection was 32.3% (95% confidence interval: 28.0, 37.1). Incidences calculated from time of new-partner acquisition were comparable for enrolled virgins and nonvirgins. Smoking, oral contraceptive use, and report of a new male sex partner--in particular, one known for less than 8 months before sex occurred or one reporting other partners--were predictive of incident infection. Always using male condoms with a new partner was not protective. Infection in virgins was rare, but any type of nonpenetrative sexual contact was associated with an increased risk. Detection of oral HPV was rare and was not associated with oral-penile contact. The data show that the incidence of HPV associated with acquisition of a new sex partner is high and that nonpenetrative sexual contact is a plausible route of transmission in virgins.
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            Natural history of cervical human papillomavirus infection in young women: a longitudinal cohort study.

            Laboratory and epidemiological research suggests an association between human papillomavirus (HPV) and cervical intraepithelial neoplasia (CIN). We studied the natural history of incident cervical HPV infection and its relation to the development of CIN. We recruited 2011 women aged 15-19 years who had recently become sexually active. We took a cervical smear every 6 months and stored samples for virological analysis. We immediately referred all women with any cytological abnormality for colposcopic assessment, but postponed treatment until there was histological evidence of progression to high-grade CIN. In 1075 women who were cytologically normal and HPV negative at recruitment, the cumulative risk at 3 years of any HPV infection was 44% (95% CI 40-48): HPV 16 was the most common type. The cumulative risk at 3 years of detecting an HPV type not present in the first positive sample was 26% (20-32). 246 women had an abnormal smear during follow-up, of whom 28 progressed to high-grade CIN. The risk of high-grade CIN was greatest in women who tested positive for HPV 16 (risk ratio 8.5 [3.7-19.2]); this risk was maximum 6-12 months after first detection of HPV 16. All HPV types under consideration were associated with cytologically abnormal smears. Although abnormality was significantly less likely to be associated with low-viral-load samples, the cumulative risk at 3 years of a high-viral-load sample after a low-viral-load sample was 45% (95% CI 35-56). Five women who progressed to high-grade CIN consistently tested negative for HPV. Our findings suggest that attempts to exploit the association between cervical neoplasia and HPV infection to improve effectiveness of cervical screening programmes might be undermined by the limited inferences that can be drawn from the characterisation of a woman's HPV status at a single point in time, and the short lead time gained by its detection.
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              Carcinoma of the cervix and tobacco smoking: collaborative reanalysis of individual data on 13,541 women with carcinoma of the cervix and 23,017 women without carcinoma of the cervix from 23 epidemiological studies.

              Tobacco smoking has been classified as a cause of cervical cancer, but the effect of different patterns of smoking on risk is unclear. The International Collaboration of Epidemiological Studies of Cervical Cancer has brought together and combined individual data on 13,541 women with and 23,017 women without cervical carcinoma, from 23 epidemiological studies. Relative risks (RRs) and 95% confidence intervals (CIs) of carcinoma of the cervix in relation to tobacco smoking were calculated with stratification by study, age, sexual partners, age at first intercourse, oral contraceptive use and parity. Current smokers had a significantly increased risk of squamous cell carcinoma of the cervix compared to never smokers (RR = 1.60 (95% CI: 1.48-1.73), p<0.001). There was increased risk for past smokers also, though to a lesser extent (RR = 1.12 (1.01-1.25)), and there was no clear trend with time since stopping smoking (p-trend = 0.6). There was no association between smoking and adenocarcinoma of the cervix (RR = 0.89 (0.74-1.06) and 0.89 (0.72-1.10) for current and past smokers respectively), and the differences between the RRs for smoking and squamous cell and adenocarcinoma were statistically significant (current smoking p<0.001 and past smoking p = 0.01). In current smokers, the RR of squamous cell carcinoma increased with increasing number of cigarettes smoked per day and also with younger age at starting smoking (p<0.001 for each trend), but not with duration of smoking (p-trend = 0.3). Eight of the studies had tested women for cervical HPV-DNA, and in analyses restricted to women who tested positive, there was a significantly increased risk in current compared to never smokers for squamous cell carcinoma (RR = 1.95 (1.43-2.65)), but not for adenocarcinoma (RR = 1.06 (0.14-7.96)). In summary, smokers are at an increased risk of squamous cell but not of adenocarcinoma of the cervix. The risk of squamous cell carcinoma increases in current smokers with the number of cigarettes smoked per day and with younger age at starting smoking.
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                Author and article information

                Journal
                Eur J Cancer
                Eur. J. Cancer
                European Journal of Cancer
                Elsevier Science Ltd
                0959-8049
                1879-0852
                January 2010
                January 2010
                : 46
                : 2
                : 405-411
                Affiliations
                [a ]Cancer Research UK Clinical Trials Unit, Institute for Cancer Studies, School of Cancer Sciences, The University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom
                [b ]Birmingham Women’s Health Care NHS Trust, Metchley Park Road, Edgbaston, Birmingham B15 2TG, United Kingdom
                [c ]Cancer Research UK Institute for Cancer Studies, School of Cancer Sciences, The University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom
                Author notes
                [* ] Corresponding author: Tel.: +44 (0) 121 414 8876; fax: +44 (0) 121 414 3700. s.i.collins@ 123456bham.ac.uk
                Article
                EJC7296
                10.1016/j.ejca.2009.09.015
                2808403
                19819687
                3973f969-9c82-4dfe-a1a3-20c29c4192a0
                © 2010 Elsevier Ltd.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 6 August 2009
                : 10 September 2009
                : 11 September 2009
                Categories
                Article

                Oncology & Radiotherapy
                cigarette smoking,cervix,human papillomavirus,cervical intraepithelial neoplasia,longitudinal study

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