Arsenic Exposure and Toxicology: A Historical Perspective

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.

Toxicological profile for arsenic

The role of smoking as a risk factor for periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of periodontitis was markedly higher among current smokers compared with never smokers (P or = 4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the periodontitis in the 19 to 30 year old group and 32% of the periodontitis in the 31 to 40 year old group, is associated with smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for Cigarette Smoking as a Major Risk Factor for Periodontitis

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.

Vaccination, illness, and smoking history were compiled for a young adult male population. The relationship of cigarette smoking to hemagglutination inhibition antibody response after exposure to a new antigen was assessed in serum specimens collected from 289 volunteers after the 1968 A2/Hong Kong/68 influenza epidemic. Titers were minimally increased among smokers who were sick compared with those of nonsmokers. Among smokers who remained well, titers were significantly increased, probably because of more frequent subclinical infection. The persistence of hemagglutination inhibition antibody after natural infection or vaccination with A2 antigens was significantly decreased among cigarette smokers, as were titers two weeks after vaccination. Serologic response to vaccination did not significantly differ between smoking groups. Smoking, vaccine history, and morbidity status during an influenza epidemic were significant factors in explaining variations in hemagglutination inhibition antibody titers.

V. A. Newill

Papers

Cigarette smoking and hemagglutination inhibition response to influenza after natural disease and immunization.

Mortality among orchard workers exposed to lead arsenate spray: A cohort study