The effect of stopping smoking on cervical Langerhans'cells and lymphocytes

Szarewski, Anne; Maddox, P.; Royston, Patrick; Jarvis, M. J.; Anderson, M. C.; Guillebaud, John; Cuzick, Jack

doi:10.1016/s0306-5456(00)00074-7

Cited by 27 publications

(24 citation statements)

References 32 publications

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“…It seems that smoking affects the interaction between the virus and the host in some manner that increases the likelihood of premalignant change but the exact biological mechanism of this interaction is uncertain. Given the presence of smoke carcinogenic metabolites in cervical secretions, smoking could increase the risk of CIN3 either by increasing the chance of viral persistence via immune modulation (23,24) or of genomic damage via genotoxins (5,25). Increased risk may be the result of ''geneenvironment'' interactions of genotoxic smoking metabolites and the inherited ability to detoxify them via metabolic pathways (26).…”

Section: Discussionmentioning

confidence: 99%

Smoking Is a Risk Factor for Cervical Intraepithelial Neoplasia Grade 3 among Oncogenic Human Papillomavirus DNA–Positive Women with Equivocal or Mildly Abnormal Cytology

McIntyre‐Seltman

Castle²,

Guido³

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

115

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Background: Smoking is a potential risk factor for cervical cancer and its immediate precursor, cervical intraepithelial neoplasia grade 3 (CIN3), but few studies have adequately taken into account the possible confounding effect of oncogenic human papillomavirus (HPV) infection. Methods: Women (n = 5,060) with minimally abnormal Papanicolaou smears were enrolled in the ASCUS and LSIL Triage Study, a clinical trial to evaluate management strategies, and were seen every 6 months for the 2-year duration of the study. Cervical specimens were tested for HPV DNA using both Hybrid Capture 2 and PGMY09/11 L1 consensus primer PCR with reverse line blot hybridization for genotyping. Multivariate logistics regression models were used to assess associations [odds ratio (OR) with 95% confidence intervals (95% CI)] between smoking behaviors and rigorously reviewed cases of cervical intraepithelial neoplasia grade 3 or cancer (zCIN3) identified throughout the study (n = 506) in women with oncogenic HPV (n = 3,133).

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Section: Discussionmentioning

confidence: 99%

Smoking Is a Risk Factor for Cervical Intraepithelial Neoplasia Grade 3 among Oncogenic Human Papillomavirus DNA–Positive Women with Equivocal or Mildly Abnormal Cytology

McIntyre‐Seltman

Castle²,

Guido³

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

115

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“…One of these mechanisms is the induction of a local immunosuppressive effect caused by tobacco metabolites which could produce a detrimental effect on the ability of the host to develop an effective immune response against viral infections, increasing the risk of persistent infections in the cervix. 14,35,36 In addition, the chemicals found in cigarettes, such as nicotine and its metabolite cotinine, which can cause DNA damage in squamous epithelial cells, have also been found in the cervical mucus of female smokers. 22,37 Our study has important strengths but also several limitations that need to be taken into account.…”

Section: Epidemiologymentioning

confidence: 99%

Smoking as a major risk factor for cervical cancer and pre-cancer: Results from the EPIC cohort

et al. 2014

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A total of 308,036 women were selected from the European Prospective Investigation into Cancer and Nutrition (EPIC) study to evaluate the association between tobacco smoking and the risk of cervical intraepithelial neoplasia of grade 3 (CIN3)/carcinoma in situ (CIS) and invasive cervical cancer (ICC). At baseline, participants completed a questionnaire and provided blood samples. During a mean follow‐up time of 9 years, 261 ICC cases and 804 CIN3/CIS cases were reported. In a nested case–control study, the baseline sera from 609 cases and 1,218 matched controls were tested for L1 antibodies against HPV types 11, 16, 18, 31, 33, 35, 45, 52, 58, and antibodies against Chlamydia trachomatis (CT), and Human Herpes Virus 2 (HHV‐2). Cervical samples were not available for HPV‐DNA analysis in this study. Multivariate analyses were used to estimate associations between smoking and risk of CIN3/CIS and ICC in the cohort and the case–control studies. In the cohort analyses smoking status, duration and intensity showed a two‐fold increased risk of CIN3/CIS and ICC, while time since quitting was associated with a two‐fold reduced risk. In the nested case–control study, consistent associations were observed after adjustment for HPV, CT and HHV‐2 serostatus, in both HPV seronegative and seropositive women. Results from this large prospective study confirm the role of tobacco smoking as an important risk factor for both CIN3/CIS and ICC, even after taking into account HPV exposure as determined by HPV serology. The strong beneficial effect of quitting smoking is an important finding that will further support public health policies for smoking cessation.

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“…Changes in cervical immune cell counts [128], smoke constituents found in cervical mucus [129] Immune system Impaired function of leucocytes [124,130] Alterations in lymphocyte subpopulations in CD4 and CD8 cells [131] Depressed cytotoxic activity of natural killer cells [132] Decreased levels of immunoglobulins [133] Increased levels of inflammatory mediators [134] Enhanced oxidative stress [135] The effects of environmental tobacco smoke (ETS) exposure…”

Section: Periodontal Tissuesmentioning

confidence: 99%