Effects of Mainstream and Environmental Tobacco Smoke on the Immune System in Animals and Humans: A Review

Johnson, Jerry D.; Houchens, David P.; Kluwe, William M.; Craig, D.K.; Fisher, Gerald L.

doi:10.3109/10408449009089870

Cited by 174 publications

(128 citation statements)

References 149 publications

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“…Constituents of cigarettes, including carcinogens, have been found in the cervical mucus of female smokers (Prokopczyk et al, 1997). In addition, exposure to tobacco may have a detrimental effect on the ability of the host to mount an effective immune response against viral infections (Johnson et al, 1990;Geng et al, 1996). It is important to point out that the prevalence of smoking among women in our study was low and that among smokers, intensity of use was moderate.…”

Section: Discussionmentioning

confidence: 99%

HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica

et al. 2001

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The vast majority of cervical cancer cases are attributable to human papillomavirus (HPV) infection (Bosch et al, 1995;Schiffman et al, 1996;Nobbenhuis et al, 1999;Herrero et al, 2000). Our current challenge is to identify factors involved in the rare progression of HPV infection, which is common and usually benign, to cervical cancer and its immediate precursor, high-grade squamous intraepithelial lesions (HSIL).Results from studies of HPV 'co-factors' suggest that reproductive factors, contraceptive use, cigarette smoking, and correlates of sexual behaviour other than HPV infection might be associated with HSIL and cervical cancer (henceforth referred to as HSIL/CA) (Bosch et al, 1992;Munoz et al, 1993;Becker et al, 1994;Moreno et al, 1995;Kjaer et al, 1996;Chaouki et al, 1998;Chichareon et al, 1998;Ho et al, 1998;Kruger-Kjaer et al, 1998;Olsen et al, 1998;Ngelangel et al, 1998;Roteli-Martins et al, 1998). In most of these studies, HPV infection was accounted for through statistical adjustment, i.e. by averaging the impact of other factors in HPV-negative and HPV-positive cases and controls. Given strong association between HPV and HSIL/CA (relative risks of ≥ 50), it is unclear whether effects observed for co-factors (relative risks usually < 3) in these previous studies are real or due to residual confounding by HPV.To address this concern, we conducted a prevalent case-control study within a 10 077 woman population-based study in Guanacaste, Costa Rica. We evaluated factors associated with progression of HPV infection and its early cytologic manifestation (LSIL) by comparing 146 HPV-positive cases of HSIL/CA against a group of 843 HPV-positive cohort members who did not have concurrent HSIL/CA. We chose our control group to include only non-cases (not diagnosed with HSIL) that were truly at risk of becoming a case (infected with HPV). Although this study design likely attenuated the associations of cofactors that are associated with the acquisition and possible persistence of infection, it avoided potential residual confounding by HPV. Thus, by including only HPVinfected women in a strictly population-based study, we were better able to estimate properly the role of possible HPV cofactors. METHODS Cohort baseA population-based cohort was established in Guanacaste, Costa Rica in 1993/4 (Herrero et al, 1997. The study was conducted after approval by the NCI and local institutional review boards, and all participants provided informed consent. Cluster sampling was utilized to select a representative sample of the adult female population of Guanacaste (n = 10 738 eligible women). 10 049 women (94% of eligibles) agreed to visit one of our study clinics. Because few women were expected to have Summary We examined factors associated with high-grade squamous intraepithelial lesions (HSIL) and cervical cancer among human papillomavirus (HPV)-infected women in a prevalent case-control study conducted within a population-based cohort of 10 077 women in Costa Rica. We compared 146 women with HPV-positive HSIL or cance...

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Section: Discussionmentioning

confidence: 99%

HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica

et al. 2001

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“…From a biological viewpoint, smoking may have an adverse effect on fibroblast function (38), chemotaxis and phagocytosis by neutrophils (20,22), immunoglobulin production (17,19) and induction of peripheral vasoconstriction (7). Healing responses are impaired in smokers, and this phenomenon might be related to the reportedly impaired function of fibroblasts in smokers (38).…”

Section: Smokingmentioning

confidence: 99%

How periodontal disease may contribute to cardiovascular disease

Kinane¹,

Lowe²

2000

Periodontology 2000

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“…ETS is composed primarily (95%) of side-stream smoke (emitted from the burning zone) and also (4%) smolder stream smoke (emitted from the puffing zone) (20). The reference-filtered cigarette is known to contain 9.2 mg of tar and 0.8 mg of nicotine.…”

Section: Ag and Ets Exposurementioning

confidence: 99%

Secondhand Smoke Induces Allergic Sensitization in Mice

Rumold

Jyrala²,

Díaz-Sánchez

2001

The Journal of Immunology

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Epidemiological studies have suggested increased prevalence of atopy in children of maternal smokers. Although secondhand smoke or environmental tobacco smoke (ETS) has been shown to augment allergic responses, its role in atopic sensitization is still controversial. We studied whether ETS could initiate a Th2 response and thus induce primary allergic sensitization. Mice were exposed for 10 consecutive days to either 1% aerosolized OVA, ETS (5 cigarettes), or both ETS and OVA. C57BL/6 mice receiving both ETS and OVA developed OVA-specific IgE and IgG1, 12, 14, and 25 days after the initial exposure, whereas those receiving OVA alone did not. Thirty days after the initial challenge (20 days after its completion), mice were re-exposed to OVA. Bronchoalveolar lavage performed 24 h later revealed an influx of eosinophils in the group initially challenged with both ETS and OVA, but not in those exposed to ETS alone or OVA alone. Increases in IL-5, GM-CSF, and IL-2 were observed in bronchoalveolar lavage from this OVA/ETS-exposed group, whereas IFN-γ levels were significantly inhibited. These results suggest that ETS can induce allergic sensitization to a normally harmless Ag, and they may explain why secondhand smoke is a major risk factor for the development of allergy in children.

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Effects of Mainstream and Environmental Tobacco Smoke on the Immune System in Animals and Humans: A Review

Cited by 174 publications

References 149 publications

HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica

HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica

How periodontal disease may contribute to cardiovascular disease

Secondhand Smoke Induces Allergic Sensitization in Mice

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