Background Infectious diseases may rival cancer, heart disease, and chronic lung disease as sources of morbidity and mortality from smoking. We reviewed mechanisms by which smoking increases the risk of infection and the epidemiology of smoking-related infection, and delineated implications of this increased risk of infection among cigarette smokers. Methods The MEDLINE database was searched for articles on the mechanisms and epidemiology of smoking-related infectious diseases. English-language articles and selected cross-references were included. Results Mechanisms by which smoking increases the risk of infections include structural changes in the respiratory tract and a decrease in immune response. Cigarette smoking is a substantial risk factor for important bacterial and viral infections. For example, smokers incur a 2- to 4-fold increased risk of invasive pneumococcal disease. Influenza risk is severalfold higher and is much more severe in smokers than nonsmokers. Perhaps the greatest public health impact of smoking on infection is the increased risk of tuberculosis, a particular problem in underdeveloped countries where smoking rates are increasing rapidly. Conclusions The clinical implications of our findings include emphasizing the importance of smoking cessation as part of the therapeutic plan for people with serious infectious diseases or periodontitis, and individuals who have positive results of tuberculin skin tests. Controlling exposure to secondhand cigarette smoke in children is important to reduce the risks of meningococcal disease and otitis media, and in adults to reduce the risk of influenza and meningococcal disease. Other recommendations include pneumococcal and influenza vaccine in all smokers and acyclovir treatment for varicella in smokers.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/217624/ira30766.pdf

Cigarette smoking and infection.

Aim: To review the potential biological mechanisms underlying the effects of tobacco smoking on periodontitis.

Main findings: Smoking has major effects on the host response, but there are also a number of studies that show some microbiological differences between smokers and non-smokers.

Smoking has a long-term chronic effect on many important aspects of the inflammatory and immune responses. Histological studies have shown alterations in the vasculature of the periodontal tissues in smokers. Smoking induces a significant systemic neutrophilia, but neutrophil transmigration across the periodontal microvasculature is impeded. The suppression of neutrophil cell spreading, chemokinesis, chemotaxis and phagocytosis have been described. Protease release from neutrophils may be an important mechanism in tissue destruction. Tobacco smoke has been found to affect both cell-mediated immunity and humoral immunity. Research on gingival crevicular fluid has demonstrated that there are lower levels of cytokines, enzymes and possibly polymorphonuclear cells in smokers. In vitro studies have shown detrimental effects of nicotine and some other tobacco compounds on fibroblast function, including fibroblast proliferation, adhesion to root surfaces and cytotoxicity.

Conclusion: Tobacco smoking has widespread systemic effects, many of which may provide mechanisms for the increased susceptibility to periodontitis and the poorer response to treatment.

Mechanisms of action of environmental factors – tobacco smoking

Tobacco smoking is associated with increased prevalence of various diseases, both in the respiratory tract and in distal organs. The possibility that tobacco smoke induced changes in immune and inflammatory processes may play a part in the aetiology and pathogenesis of many of these diseases was first recognised in the mid 1960s. The ensuing decade witnessed a steadily increasing research effort centred on toxicological aspects of chronic inhalation of tobacco smoke in relation to immune and inflammatory cell function in experimental animals. This work (reviewed by Holt and Keast') defined a discrete pattern of change in animals during the course of tobacco smoke exposure, with the following salient features: (1) systemically, biphasic fluctuations were observed in primary T cell dependent humoral and cellular immune responses, initial enhancement during the first few months of exposure eventually giving way to suppression in chronically exposed animals; (2) T cell independent immune responses (for example, to bacterial polysaccharide antigens) and secondary immune responses dependent on T memory cells remained normal in these animals; (3) an immediate and profound suppression of T cell function was noted in the respiratory tract, together with (4) the steady development of an expanded and functionally altered population of alveolar macrophages. Recognition of the possibility that similar effects occur in man has provided the impetus for various direct studies on aspects of immune and inflammatory cell functions in human smokers. Furthermore, it has become accepted practice to segregate the smokers within \"control\" populations, particularly in studies using bronchoalveolar lavage. The available data from these human studies are reviewed below in the light of the information available from earlier animal experiments.

https://thorax.bmj.com/content/thoraxjnl/42/4/241.full.pdf

Immune and inflammatory function in cigarette smokers.

Immunomodulatory effects of cigarette smoke

Numerous investigations of the relationship between smoking and periodontal disease have been performed over the last 15 years, and there now exists a substantial body of literature upon which this current review is based. From both cross-sectional and longitudinal studies, there appears to be strong epidemiological evidence that smoking confers a considerably increased risk of periodontal disease. This evidence is further supported by the data emanating from patients who stop smoking. These patients have levels of risk similar to those of non-smokers. Numerous studies of the potential mechanisms whereby smoking tobacco may predispose to periodontal disease have been conducted, and it appears that smoking may affect the vasculature, the humoral immune system, and the cellular immune and inflammatory systems, and have effects throughout the cytokine and adhesion molecule network. The aim of this review is to consider the evidence for the association between smoking and periodontal diseases and to highlight the biological mechanisms whereby smoking may affect the periodontium.

Smoking and Periodontal Disease

Antibodies to antigens in humidifier water were detected by double immunodiffusion in 30 of 63 (47.6%) persons who were exposed to aerosols from a water humidification unit in a cigar plant, whereas no antibodies could be detected in 49 unexposed blood donors (P less than 0.001). The presence of antibodies could not be related to fever or pulmonary symptoms (cough, expectoration, dyspnoe). Antibodies were found in 14 (93.3%) of 15 nonsmokers and in only 13 (31.7%) of 41 smokers (P less than 0.001), and the titres were highest in nonsmokers. Serum IgG and IgA levels were higher in nonsmokers than in smokers, and the variances within the groups were significantly different (F less than 0.05 and F less than 0.05, respectively). The mean serum IgM values were not significantly different in the two groups. Antibodies to Candida albicans and Escherichia coli 04 and 075 were detected with equal prevalences and titres in smokers and nonsmokers. These findings suggest that tobacco smoking may suppress the humoral immune response to inhaled antigens but not to antigens which are supposed to be absorbed through membranes other than those of the bronchopulmonary system. They may partly explain the reported increased incidence of allergic alveolitis in nonsmokers.

Serum antibodies and immunoglobulins in smokers and nonsmokers.

In a field study, 75 workers from a cheroot factory were compared with 50 reference workers from a large telephone company. Questionnaire responses revealed higher prevalences of cough and shortness of breath on exercise among the tobacco workers than controls. Cigarette smoking was the same in the two groups, but tobacco workers also smoked cheroots. Significantly decreased values (p < .01) of forced expiratory volume in 1 sec (FEV, 1.0) and forced vital capacity (FVC) were found among tobacco workers compared to referents. After adjusting for number of cigarettes and cheroots smoked, there remained no significant differences. There was a suggestion (p < .10) of decreased FEV1.0 among light or nonsmoking tobacco workers. When cigarette consumption only was considered, this difference was significant (p < .01). Lung function values were not associated with the very low measured dust exposures. Bronchial reactivity to inhaled histamine, diurnal and weekly changes in FEV1.0, skin-prick tests with t...

Respiratory Disease and Lung Function in a Tobacco Industry

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Serum antibodies and immunoglobulins in smokers and nonsmokers.

Respiratory Disease and Lung Function in a Tobacco Industry