Environmental tobacco smoke

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 toxic effects of tobacco products are discussed in detail in Chapter 16. It should be noted here, however, that combustion of tobacco indoors 

Acrylamide Acrylic acid Acrylonitrile Hydrocarbon mixtures Ammonia 

Butyl acrylate Butyl butyrate Butyl methacrylate 

2- Chloroethyl acetate Dibutyl ether Diethyl benzenes 

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National Research Council. (1986b). "Environmental Tobacco Smoke Measuring Exposures and Assessing Health Effects." National Academy Press, Washington, DC. 

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. 

Environmental Tobacco Smoke (ETS) mixture of smoke from the burning end of a cigarette, pipe, or cigar and smoke exhaled by the smoker (also secondhand smoke or passive smoking). 

Environmental tobacco smoke mid gasoline vapors both contain mixtures of trace luiiounts of many of the individual compounds regulated as Air Toxics under Title 111, section 112 of the 1990 Clean Air Act Amendnmts. Much of the general public is more likely to be exposed to these mixtures during the course of their lives tlian to specific compounds on the air toxics list. Hence, estimation of the cancer risk resulting from exposure to these mixtures is a useful and relevant exercise. 

Environmental tobacco smoke (ETS) is the diluted mixture of pollutants caused by smoking of tobacco and emitted into the indoor air by a smoker. Constituents of ETS include submicron-size particles composed of a large number of chemicals, plus a large number of gaseous pollutants. Fibers in indoor air include those of asbestos, and man-made mineral fibers such as fiberglass, and glass wool. 

Unvented kerosene and gas space heaters leaking chimneys and furnaces back-drafting from furnaces, gas water heaters, woodstoves, and fireplaces automobile exhaust from attached garages environmental tobacco smoke. Humans are normally the main indoor source of carbon dioxide. Unvented or imperfectly vented combustion appliances can also increase indoor COj concentrations. 

The most common etiology is exposure to environmental tobacco smoke, but other chronic inhalational exposures can also lead to COPD. Inhalation of noxious particles and gases stimulates the activation of neutrophils, macrophages, and CD8+ lymphocytes, which release a variety of chemical mediators, including tumor necrosis factor-a, interleukin-8, and leukotriene B4. These inflammatory cells and mediators lead to widespread destructive changes in the airways, pulmonary vasculature, and lung parenchyma. 

Shima, M. and Adachi, M., Effects of environmental tobacco smoke on serum levels of acute phase proteins in schoolchildren, Prev. Med. 25, 5, 617, 1996. 

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). 

Levels of cyanide and its metabolite thiocyanate in blood serum and plasma, urine, and saliva have been used as indicators of cyanide exposure in humans, particularly in workers at risk of occupational exposures, in smokers or nonsmokers exposed to sidestream or environmental tobacco smoke, in populations exposed to high dietary levels of cyanide, and in other populations with potentially high exposures (see Section 5.6). The correlation between increased cyanide exposure and urinary thiocyanate levels was demonstrated in workers exposed to 6.4-10.3 ppm cyanide in air (El Ghawabi et al. 1975). In another study, blood cyanide concentrations were found to vary from 0.54 to 28.4 pg/100 mL in workers exposed to approximately 0.2-0.8 ppm cyanide in air, and from 0.0 to 14.0 pg/100 mL in control workers... 

Positive correlations between fetal umbilical serum thiocyanate levels and serum thiocyanate levels of smoking mothers (Bottoms et al. 1982 Hauth et al. 1984) and mothers exposed to environmental tobacco smoke in the home (Bottoms et al. 1982) have been reported. Hauth et al. (1984) found that the mean serum thiocyanate concentration (95 pmol/L 5.5 pg/mL) was significantly higher (p < 0.001) in smokers than in passive smokers (35.9 pmol/L 2.1 pg/mL) or nonsmokers (32.3 pmol/L 1.9 pg/mL). Similarly, the mean umbilical thiocyanate concentration in the newborn infants of smoking mothers (72 pmol/L ... 

Baker RR, Proctor CJ. 1990. The origins and properties on environmental tobacco smoke. Environ Int 16 231-245. 

Chen Y, Pederson LL, Lefcoe NM. 1990. Exposure to environmental tobacco smoke (ETS) and serum thiocyanate level in infants. Arch Environ Health 45(3) 163-167. 

Environmental tobacco smokes (ETS) tobacco smoke irritation to mucous membranes chronic and acutes pulmonary effects, cardiovascular effects carcinogenic. 

Sun W, Wu R, Last JA (1995) Effects of exposure to environmental tobacco smoke on a human tracheobronchial epithelial cell line. Toxicology 100( 1-3) 163-174. 

Guerin MR, Jenkins RA, Tomkins BA. 1992. The chemical nature of environmental tobacco smoke Composition and measurement. Chelsea, MD Lewis Publishers. 

Potentials problems with the use of hair include a strong influence of hair pigmentation on nicotine and cotinine binding and uptake (Dehn et al. 2001). Nicotine and cotinine are bound to melanin. As a result, dark hair binds much more nicotine than does blond or white hair. This makes comparison across individuals difficult. Also, hair is exposed to nicotine and cotinine from sweat and from sebaceous gland secretions, and to nicotine from environmental tobacco smoke exposure. Washing the hair before analysis may reduce this problem of environmental contamination, but it is not likely to remove all environmental nicotine and cotiiune. 

Al-Delaimy WK, Crane J, Woodward A (2002) Is the hair nicotine level a more accurate biomarker of environmental tobacco smoke exposure than urine cotinine J Epidemiol Community Health 56(1) 66-71... 

Benowitz NL (1990) Chnical pharmacology of inhaled drags of abuse implications in understanding nicotine dependence. NIDA Res Monogr 99 12-29 Benowitz NL (1996) Cotinine as a biomarker of environmental tobacco smoke exposure. Epidemiol Rev 18(2) 188-204... 

Saliva The use of saliva as a diagnostic fluid has been studied for many years [266]. While the ease and noninvasiveness with which a sample can be obtained make this matrix attractive to the medical community, the use of saliva to detect exposures of persons to environmental contaminants has not been investigated in many studies. However, it has been established that the measurement of cotinine, an indicator of exposure to environmental tobacco smoke, in saliva is correlated with concentrations of cotinine in serum [267]. 

Eatough DJ, Benner CL, Bayona JM, Richards G, Lamb JD, Lee ML, Lewis EA, Hansen LD (1969) Chemical composition of environmental tobacco smoke. 1 Gas-phase acids and bases. Environ Sci Technol 23 679-687... 

Leaderer BP, Hammond SK (1991) Evaluation of vapor-phase nicotine and respirable suspended particle mass as markers for environmental tobacco smoke. Environ Sci Technol 25 770-777... 

Hammond SK (1999) Exposure of U.S. workers to environmental tobacco smoke. Environ Health Perspect 107 329-340... 

Nebot M, Lopez MJ, Gorini G, Neuberger M, Axelsson S, Pilali M, Fonseca C, Abdennbi K, Hackshaw A, Moshammer H, Laurent AM, Salles J, Georgouli M, Fondelli MC, SerrahimaE, Centrich F, Hammond SK (2005) Environmental tobacco smoke exposure in public places of European cities. Tobac Contr 14 60-63... 

Carbon dioxide (CO2) is a colorless and odorless gas. It is an asphyxiant-causing agent. A concentration of 10% can cause unconsciousness and death from oxygen deficiency. The gas can be released from industrial studies [39], automobile exhaust, environmental tobacco smoke (ETS), and inadequately vented fuel heating systems. It is heavy and accumulates at low levels in depressions and along the floor. 

Formaldehyde (HCHO) is a colorless gas with a pungent odor. Formaldehyde has found wide industrial usage as a fungicide and germicide, and in disinfectants and embalming fluids. The serious sources of indoor airborne formaldehyde are furnimre, floor underlayment insulation, and environmental tobacco smoke. Urea formaldehyde (UF) is mixed with adhesives to bond veneers, particles, and fibers. It has been identified as a potential hazardous source. 

Cell signaling. Environmental tobacco smoke, administered to rats during gestation, the early neonatal period, or both, elicited induction of total adenylyl cyclase. In the brain, the specific coupling of p-adren-ergic receptors to adenylyl cyclase was inhibited in the smoke-treated groups, despite... 

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