Tobacco smoking and regression of low-grade cervical abnormalities

Koji Matsumoto, Akinori Oki, Reiko Furuta, Hiroo Maeda, Toshiharu Yasugi, Naoyoshi Takatsuka, Yasuo Hirai, Akira Mitsuhashi, Takuma Fujii, Tsuyoshi Iwasaka, Nobuo Yaegashi, Yoh Watanabe, Yutaka Nagai, Tomoyuki Kitagawa, Hiroyuki Yoshikawa

Research output: Contribution to journalArticle

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Abstract

The role of tobacco smoking in the multistage carcinogenesis at the cervix is not fully understood because of a paucity of prospective data. To assess the relationship between smoking and spontaneous regression of cervical precursor lesions, a total of 516 women with low-grade squamous intraepithelial lesion (LSIL) were monitored by cytology and colposcopy every 4 months. Probability of LSIL regression within 2 years was analyzed in relation to smoking behaviors, with regression defined as at least two consecutive negative Pap smears and normal colposcopy. Women's age, initial biopsy results, and human papillomavirus (HPV) genotypes were included in the multivariate models for adjustments. Our study subjects included 258 never-smokers and 258 smokers (179 current and 79 former smokers). During a mean follow-up time of 39.8 months, 320 lesions regressed to normal cytology. Probability of regression within 2 years was significantly lower in smokers than in never-smokers (55.0%. vs 68.8%, P = 0.004). The risk of LSIL persistence increased with smoking intensity and duration and with younger age at starting smoking (P = 0.003, P < 0.001, and P = 0.03, respectively). Smokers had twice as high a risk of persistent HPV infection compared to never-smokers (odds ratio, 2.50; 95% confidence interval, 1.30-4.81; P = 0.006). In young women, passive smoking since childhood reduced probability of regression within 2 years (56.7%. vs 85.9%, P < 0.001). Further adjustments for a wide range of cervical cancer risk factors did not change the findings. In conclusion, tobacco smoking may interfere with regression of cervical precursor lesions. Childhood exposure to second-hand smoke may increase a risk of persistent cervical abnormalities among young women.

Original languageEnglish
Pages (from-to)2065-2073
Number of pages9
JournalCancer science
Volume101
Issue number9
DOIs
Publication statusPublished - 01-09-2010

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Smoking
Colposcopy
Tobacco Smoke Pollution
Cell Biology
Social Adjustment
Papanicolaou Test
Papillomavirus Infections
Cervix Uteri
Uterine Cervical Neoplasms
Carcinogenesis
Odds Ratio
Genotype
Confidence Intervals
Biopsy
Squamous Intraepithelial Lesions of the Cervix

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Matsumoto, K., Oki, A., Furuta, R., Maeda, H., Yasugi, T., Takatsuka, N., ... Yoshikawa, H. (2010). Tobacco smoking and regression of low-grade cervical abnormalities. Cancer science, 101(9), 2065-2073. https://doi.org/10.1111/j.1349-7006.2010.01642.x
Matsumoto, Koji ; Oki, Akinori ; Furuta, Reiko ; Maeda, Hiroo ; Yasugi, Toshiharu ; Takatsuka, Naoyoshi ; Hirai, Yasuo ; Mitsuhashi, Akira ; Fujii, Takuma ; Iwasaka, Tsuyoshi ; Yaegashi, Nobuo ; Watanabe, Yoh ; Nagai, Yutaka ; Kitagawa, Tomoyuki ; Yoshikawa, Hiroyuki. / Tobacco smoking and regression of low-grade cervical abnormalities. In: Cancer science. 2010 ; Vol. 101, No. 9. pp. 2065-2073.
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Matsumoto, K, Oki, A, Furuta, R, Maeda, H, Yasugi, T, Takatsuka, N, Hirai, Y, Mitsuhashi, A, Fujii, T, Iwasaka, T, Yaegashi, N, Watanabe, Y, Nagai, Y, Kitagawa, T & Yoshikawa, H 2010, 'Tobacco smoking and regression of low-grade cervical abnormalities', Cancer science, vol. 101, no. 9, pp. 2065-2073. https://doi.org/10.1111/j.1349-7006.2010.01642.x

Tobacco smoking and regression of low-grade cervical abnormalities. / Matsumoto, Koji; Oki, Akinori; Furuta, Reiko; Maeda, Hiroo; Yasugi, Toshiharu; Takatsuka, Naoyoshi; Hirai, Yasuo; Mitsuhashi, Akira; Fujii, Takuma; Iwasaka, Tsuyoshi; Yaegashi, Nobuo; Watanabe, Yoh; Nagai, Yutaka; Kitagawa, Tomoyuki; Yoshikawa, Hiroyuki.

In: Cancer science, Vol. 101, No. 9, 01.09.2010, p. 2065-2073.

Research output: Contribution to journalArticle

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AU - Matsumoto, Koji

AU - Oki, Akinori

AU - Furuta, Reiko

AU - Maeda, Hiroo

AU - Yasugi, Toshiharu

AU - Takatsuka, Naoyoshi

AU - Hirai, Yasuo

AU - Mitsuhashi, Akira

AU - Fujii, Takuma

AU - Iwasaka, Tsuyoshi

AU - Yaegashi, Nobuo

AU - Watanabe, Yoh

AU - Nagai, Yutaka

AU - Kitagawa, Tomoyuki

AU - Yoshikawa, Hiroyuki

PY - 2010/9/1

Y1 - 2010/9/1

N2 - The role of tobacco smoking in the multistage carcinogenesis at the cervix is not fully understood because of a paucity of prospective data. To assess the relationship between smoking and spontaneous regression of cervical precursor lesions, a total of 516 women with low-grade squamous intraepithelial lesion (LSIL) were monitored by cytology and colposcopy every 4 months. Probability of LSIL regression within 2 years was analyzed in relation to smoking behaviors, with regression defined as at least two consecutive negative Pap smears and normal colposcopy. Women's age, initial biopsy results, and human papillomavirus (HPV) genotypes were included in the multivariate models for adjustments. Our study subjects included 258 never-smokers and 258 smokers (179 current and 79 former smokers). During a mean follow-up time of 39.8 months, 320 lesions regressed to normal cytology. Probability of regression within 2 years was significantly lower in smokers than in never-smokers (55.0%. vs 68.8%, P = 0.004). The risk of LSIL persistence increased with smoking intensity and duration and with younger age at starting smoking (P = 0.003, P < 0.001, and P = 0.03, respectively). Smokers had twice as high a risk of persistent HPV infection compared to never-smokers (odds ratio, 2.50; 95% confidence interval, 1.30-4.81; P = 0.006). In young women, passive smoking since childhood reduced probability of regression within 2 years (56.7%. vs 85.9%, P < 0.001). Further adjustments for a wide range of cervical cancer risk factors did not change the findings. In conclusion, tobacco smoking may interfere with regression of cervical precursor lesions. Childhood exposure to second-hand smoke may increase a risk of persistent cervical abnormalities among young women.

AB - The role of tobacco smoking in the multistage carcinogenesis at the cervix is not fully understood because of a paucity of prospective data. To assess the relationship between smoking and spontaneous regression of cervical precursor lesions, a total of 516 women with low-grade squamous intraepithelial lesion (LSIL) were monitored by cytology and colposcopy every 4 months. Probability of LSIL regression within 2 years was analyzed in relation to smoking behaviors, with regression defined as at least two consecutive negative Pap smears and normal colposcopy. Women's age, initial biopsy results, and human papillomavirus (HPV) genotypes were included in the multivariate models for adjustments. Our study subjects included 258 never-smokers and 258 smokers (179 current and 79 former smokers). During a mean follow-up time of 39.8 months, 320 lesions regressed to normal cytology. Probability of regression within 2 years was significantly lower in smokers than in never-smokers (55.0%. vs 68.8%, P = 0.004). The risk of LSIL persistence increased with smoking intensity and duration and with younger age at starting smoking (P = 0.003, P < 0.001, and P = 0.03, respectively). Smokers had twice as high a risk of persistent HPV infection compared to never-smokers (odds ratio, 2.50; 95% confidence interval, 1.30-4.81; P = 0.006). In young women, passive smoking since childhood reduced probability of regression within 2 years (56.7%. vs 85.9%, P < 0.001). Further adjustments for a wide range of cervical cancer risk factors did not change the findings. In conclusion, tobacco smoking may interfere with regression of cervical precursor lesions. Childhood exposure to second-hand smoke may increase a risk of persistent cervical abnormalities among young women.

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Matsumoto K, Oki A, Furuta R, Maeda H, Yasugi T, Takatsuka N et al. Tobacco smoking and regression of low-grade cervical abnormalities. Cancer science. 2010 Sep 1;101(9):2065-2073. https://doi.org/10.1111/j.1349-7006.2010.01642.x