Association of Combined Tobacco Smoking and Oral Contraceptive Use With Cervical Intraepithelial Neoplasia 2 or 3 in Korean Women.

Hea Young Oh,Jae-Kwan Lee,Mi Kyung Kim,Sang-Soo Seo

doi:10.2188/jea.je20150047

Hea Young Oh, Jae-Kwan Lee + Show 2 more

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https://doi.org/10.2188/jea.je20150047

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Abstract

BackgroundCigarette smoking and oral contraceptive (OC) use have been associated with cervical neoplasia, and the combination of smoking and OC use could influence cervical carcinogenesis. We aimed to assess the joint effect of smoking and OC use on the risk of cervical intraepithelial neoplasia (CIN).MethodsFrom a cohort of human papillomavirus-positive subjects recruited from 6 hospitals in Korea from March 2006 to November 2012, a total of 678 subjects (411 control, 133 CIN 1, and 134 CIN 2 or 3 cases) were selected for this study (mean age, 43 years). The risk of CIN associated with smoking and OC use on additive and multiplicative scales was estimated via multinomial logistic regression after adjustment for potential confounding factors. The relative excess risk due to interaction (RERI) and the synergy index (S) were used to evaluate the additive interaction.ResultsOC users (odds ratio [OR] 1.98; 95% confidence interval [CI], 1.07–3.69) and long-term OC use (≥20 months; OR 2.71; 95% CI, 1.11–6.59) had a higher risk of CIN 2/3, but had no association with CIN 1, compared to non-OC users. Smokers and heavy smoking (≥8 cigarettes/day) were not associated with any CIN grade. Combined smoking and OC use (OR 4.91; 95% CI, 1.68–14.4; RERI/S, 3.77/27.4; P for multiplicative interaction = 0.003) and combined heavy smoking and long-term OC use (OR 11.5; 95% CI, 1.88–70.4; RERI/S, 9.93/18.8; P for multiplicative interaction = 0.009) had a higher risk of CIN 2/3 but had no association with CIN 1 compared to combined non-smoking and non-OC use.ConclusionsOC use and smoking acted synergistically to increase the risk of CIN 2 or 3 in Korean women.

Highlights

Oncogenic human papillomavirus (HPV) is a major risk factor of cervical cancer, but cofactors, such as cigarette smoking, long-term oral contraceptive (OC) use, high parity, and coinfection with human immunodeficiency virus, Chlamydia trachomatis, or herpes simplex virus type 2, have been established as risk factors in cervical carcinogenesis.[1]
The International Collaboration of Epidemiological Studies of Cervical Cancer evaluated the risk of cigarette smoking and found that current smoking increased the risk of cervical squamous cell carcinoma, but not that of adenocarcinoma.[4,5]
We demonstrated that any OC use and long-term OC use (≥20 months) was associated with elevated risk of cervical intraepithelial neoplasia (CIN) 2/3 but not with CIN 1

Summary

Introduction

Oncogenic human papillomavirus (HPV) is a major risk factor of cervical cancer, but cofactors, such as cigarette smoking, long-term oral contraceptive (OC) use, high parity, and coinfection with human immunodeficiency virus, Chlamydia trachomatis, or herpes simplex virus type 2, have been established as risk factors in cervical carcinogenesis.[1] Smoking and OC use are the most widely studied epidemiological co-factors in cervical cancer development. The International Agency for Research on Cancer (IARC) has determined that tobacco smoking is causally associated with cervical cancer.[2] In a prospective study including 1800 women with oncogenic HPV DNA, a high smoking intensity among current smokers was associated with an increased risk of CIN 3 or cervical cancer.[3] The International Collaboration of Epidemiological Studies of Cervical Cancer evaluated the risk of cigarette smoking and found that current smoking increased the risk of cervical squamous cell carcinoma, but not that of adenocarcinoma.[4,5] The risk increased up to 3-fold with increasing number of cigarettes smoked per day and years smoked. Conclusions: OC use and smoking acted synergistically to increase the risk of CIN 2 or 3 in Korean women

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