Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Abstract

Biochemically and pathologically, there is strong evidence for both atopic and nonatopic airway sensitization, hyperresponsiveness, and inflammation as a consequence of exposure to tobacco mainstream or sidestream smoke particulate. There is growing evidence for the relation between exposure to mainstream and sidestream smoke and diseases resulting from reactive oxidant challenge and inflammation directly as a consequence of the combined activity of neutrophils, macrophages, dendritic cells, eosinophils, basophils, as a humoral immunological consequence of sensitization, and that the metal components of the particulate play a role in adjuvant effects. As an end consequence, carcinogenicity is a known outcome of chronic inflammation.Smokeless tobacco has been evaluated by the IARC as a group 1 carcinogen. Of the many harmful constituents in smokeless tobacco, oral tissue metallothionein gradients suggest that metals contribute to the toxicity from smokeless tobacco use and possibly sensitization.This work reviews and examines work on probable contributions of toxic metals from tobacco and smoke to pathology observed as a consequence of smoking and the use of smokeless tobacco. Metals and metalloids in tobaccoThough exposure to substances from tobacco use is obviously a complex exposure, the carcinogens in tobacco smoke have been classified for health risk determinations into five major chemical classes. 1 Some of these have been carefully studied, contributing to a strong weight of evidence for associated health risks. 2 Toxic metals and metalloids constitute one of the more understudied major carcinogenic chemical classes in smokeless tobacco products and tobacco smoke. Eight of the top forty substances in the Fowles and Dybing table of cancer risk indices are metals or metalloid compounds. 1 In their table of non-cancer risk indices for individual chemical constituents of mainstream cigarette smoke based on a single cigarette per day, three of the top eight listed for respiratory effect health risk, cadmium, hexavalent chromium, and nickel, were metals. Another metalloid, silicon in the form of silicates, poses serious health risks by inhalation, but limited data is available, likely due to analytical difficulties.Metals and metalloids in smoke from biomass combustion including tobacco are generally considered to be present in ionic form, but may also occur in a gaseous elemental form, as is the case for mercury. 3 Whether a tobacco product is consumed by smoking or in a smokeless form, the exposure to toxic metals is directly related to the concentration in the tobacco leaf, assuming no metal containing additives are included during manufacture. [4][5][6] The soil (including any amendments to the soil such as sludge, fertilizers, or irrigation with

Sex-Based Differences in Multiple Sclerosis (MS): Part II: Rising Incidence of Multiple Sclerosis in Women and the Vulnerability of Men to Progression of this Disease

“…Smoking has been consistently identified to be a detrimental risk factor for MS development with an increase in relative risk of 50 % in ever smokers over never smokers (Sundstrom et al 2008;Hernan et al 2001;Ramagopalan et al 2013b;Hedstrom et al 2009;Riise et al 2003). This enhancing effect of smoking on MS risk is thought to be due to adjuvant effects of smoke particles in the lung, resulting in increased systemic inflammation (Pappas 2011). Coinciding with the rise in MS, the female to male ratio of smoking has also been increasing worldwide since the mid-1930s (Ascherio and Munger 2007b).…”

Toxic Metal Concentrations in Mainstream Smoke from Cigarettes Available in the USA

“…11–14 Fowles and Dybing calculated risk indices for the exposure to toxic substances in tobacco smoke that cause known non-cancer respiratory and cardiovascular health effects. 5 However, they pointed out that the magnitude of non-cancer risks were underestimated due to gaps in dose-response information and corresponding definitive threshold values from authoritative sources for many substances in smoke.…”

Modifiable Risk Factors for Aneurysmal Subarachnoid Hemorrhage

“…25 The formation of carbon monoxide and release of cigarette toxins into the blood stream link smoking with aneurysm formation and rupture. 9,33 Smoking also promotes increased blood levels of proteases such as elastase. Inhalation of smoke from cigarettes irritates the lung tissue and causes an inflammatory reaction with migration of neutrophil granulocytes to the site of inflammation, causing release of elastase.…”