Tobacco smoke respiratory disease

Effects of indoor air pollutants on humans are essentially the same as those described in Chapter 7. However, there can be some additional pollutant exposures in the indoor environment that are not common in the ambient setting. From the listing in Table 23-1, radon exposures indoors present a radiation hazard for the development of lung cancer. Environmental tobacco smoke has been found to cause lung cancer and other respiratory diseases. Biological agents such as molds and other toxins may be a more likely exposure hazard indoors than outside. 

Respiratory allergies and infections are the most common form of illness in the United States and Europe and account for more missed school and work days than any other disease [1], A substantial body of experimental work has clearly shown that airborne toxicants such as tobacco smoke, ozone, and other air pollutants can alter many aspects of the host defense network to either decrease resistance to infection, or exacerbate respiratory allergies and asthma [2], Exposure to air toxicants can suppress a number of key host defenses including mucociliary clearance in the airways, pulmonary macrophage function, and development of specific immune responses such as IgG antibody production and cell mediated immunity. In contrast, immune stimulation in the form of increased T cell activity and IgE antibody formation has also has been shown to occur under some circumstances, resulting in increased incidence or severity of allergic lung disease. 

Acute Respiratory Infection (ARI), as pneumonia, is one of the biggest causes of death for young children in the Asian region. ARI is also responsible for more episodes of illness than any other disease, with the exception of diarrhoea, and it is well known that ARI is aggravated by exposure to pollutants and indoor environmental tobacco smoke (ETS). 

Respirable suspended particulates (PMin) tobacco smoke emissions from cooking and heating appliances, burnhg incense. respiratory irritation and infection aggravation of existing respiratory or cardiovascular disease nasal and eye irritations. 

In particular, excessive proteolysis of elastin by HLE has been implicated in pulmonary emphysema [19]. In this case, the imbalance appears to result from reduced levels of active extracellular alpha,-proteinase inhibitor (a,-PI), the primary plasma inhibitor of HLE. This decrease is caused either by a genetic disorder (PiZZ phenotype individuals) or by reduction in the elastase inhibitory capacity (EIC) of ai-PI due to its oxidative inactivation by tobacco smoke [20]. The detailed evidence supporting the potential role of elastase in the development of emphysema has been extensively reviewed [21] and will not be repeated here. The fact that HLE is also a potent secretagogue [22] may play a role in several disease states, including cystic fibrosis [23], chronic bronchitis [24], and acute respiratory distress syndrome (ARDS) [25]. The mechanism of the secretagogue activity is not known, but, since the HLE-induced secretion can be blocked by specific HLE inhibitors, it appears to require catalytic activity by the enzyme [26]. 

Coultas, D. B., Stidley, C. A., 8c Samet, J. M. (1993). Cigarette yields of tar and nicotine and markers of exposure to tobacco smoke. American Review of Respiratory Disease, 148, 435—440. 

It is well established that many of the toxic effects of inhaling environmental (second hand) tobacco smoke (ETS) are identical to those of active smoking. ETS is associated with increased risk of lung cancer, 15 respiratory disease (including asthma in children), 16 anc[ cardiovascular disease (including acute myocardial infarction). 17 ... 

The continuing worldwide increase in respiratory disease corresponds to increases in the release of chemicals into the atmosphere. Respiratory irritation, sensitization, asthma, RADS, and lung cancer can be attributed to numerous single chemicals whose toxicological properties are, for the most part, well known. Many unexplained incidences of respiratory disease cannot be attributed to single chemical exposures, but have been shown to occur when exposures are to chemical mixtures that are composed of at least one lipophile and one hydrophile. The sources of such mixtures include diesel exhausts, tobacco smoke, carpet emissions, paint fumes, and cleaning products. Prevention of chemically induced respiratory diseases should include limiting exposures to these chemical mixtures. 

Hoffmann D, Hoffmann I. 1993. Tobacco smoke as a respiratory carcinogen. In Hirsch A, Goldberg M, Martin J-P, et al., eds. Prevention of respiratory diseases. New York, NY Marcel Dekker, Inc., 497-532. 

Passive smoking (also known as secondhand smoke, or ETS) has been shown to produce the same health effects on those exposed to it as to actual smokers, albeit to a lesser degree [46, 47]. ETS is responsible for approximately 3(XK) lung cancer deaths in the United States annually [48], increases the risk of stroke [49], risk of myocardial infarction and other cardiovascular diseases [50, 51], and impacts respiratory health in those exposed [52]. The cardiovascular effect of secondhand tobacco smoke is illustrated by the drastic reduction of acute myocardial infarctions (heart attacks) noted in Helena, Montana when public smoking was banned [53]. This is discussed more thoroughly in Section 29.4. 

Secondhand tobacco smoke has long been associated with respiratory disease in children. The WHO has estabhshed that secondhand smoke can cause sudden death in infants [27] and it has been recently reported that children exposed to it may be at greater risk for developing atherosclerosis as adults [28],... 

In view of the cardiovascular effects of marijuana, including tachycardia and a tendency to orthostatic hypotension, the use of cannabis by patients with cardiovascular disease is most certainly inadvisable. The older the individual, the greater the risk of unpleasant effects, including toxic psychoses. It would also seem better to avoid the use of marijuana in respiratory disease, in which it is likely to have some of the deleterious effects of tobacco smoking (SED VIII, p. 53). Finally, since cannabis passes the placental barrier, and in view of the many unanswered questions as to its basic effects, it would seem very unwise to take the material during pregnancy. The separate data on this topic have been reviewed very recently by Nis-himura and Tanimura (21 ). 

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