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Environmental Tobacco Smoke Exposure

Nicotine in tobacco is metabolized to cotinine and urinary cotinine levels serve as indicators of the levels of exposure to environmental tobacco smoke (ETS), also referred to as secondhand smoke. In a Swedish study, a relationship between increased urinary cotinine level and increased risk for SAB was demonstrated. I30l No specific chemical (s) were identified as the causative agent (s). [Pg.387]


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. [Pg.52]

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... [Pg.54]

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... [Pg.54]

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... [Pg.459]

Kabesch, M. and Mutius, E. 2000. Adverse health effects of environmental tobacco smoke exposure in childhood. Allergy Clin Immunol Int J World Allergy Org 12 146-151. [Pg.37]

DiFranza JR, Aligne A, Weitzman M (2004) Prenatal and postnatal environmental tobacco smoke exposure and children s health. Paediatrics, 113 1007-1015. [Pg.260]

Leech JA, Wilby K, McMullen E (1999) Environmental tobacco smoke exposure patterns A subanalysis of the Canadian Human Time-Activity Pattern Survey. Can J Public Health, 90 244-249. [Pg.277]

Windham GC, Eaton A, Hopkins B (1999) Evidence for an association between environmental tobacco smoke exposure and birthweight A meta-analysis and new data. Paediatr Perinat Epidemiol, 13 35-57. [Pg.307]

Law M R, Morris J K, Wald N ] 1997 Environmental tobacco smoke exposure and ischaemic heart disease an evaluation of the evidence. British Medical Journal 315 973-988. [Pg.178]

Mannino DM, Siegel M, Rose D, et al. Environmental tobacco smoke exposure in the home and worksite and health effects in adults Results from the 1991 National Health Interview Survey. Tob Control 1997 6(4) 296-305. [Pg.242]

Gergen PJ, Fowler JA, Maurer KR, et al. The burden of environmental tobacco smoke exposure on the respiratory health of children 2 months through 5 years of age in the United States Third national health and nutrition examination survey, 1988 to 1994. Pediatrics 1998 101(2) E8. [Pg.427]

Quackenboss JJ, Bronnimann D, Camilli AE, et al. 1988. Bronchial responsiveness in children and adults in association with formaldehyde, particulate matter, and environmental tobacco smoke exposures [Abstract]. Am Rev Respir Dis 137 253. [Pg.421]

Gilliland FD, Berhane K, McConnell R, et al Maternal smoking during pregnancy, environmental tobacco smoke exposure and childhood lung function. Thorax 2000 55 271-276. [Pg.98]

It is clear that environmental tobacco smoke exposure has a deleterious effect on asthma control with a 30% increase in frequency of symptoms in preschool children exposed to such pollution [123]. Furthermore, maternal smoking has a significant effect on bronchial hyperresponsiveness and severity of symptoms in children with asthma [124]. [Pg.118]

Bonham AC, Chen CY, Mutoh T, load JP (2001) Lung C-flber CNS reflex Role in the respiratory consequences of extended environmental tobacco smoke exposure in young guinea pigs. Environ Health Perspect 109(Suppl 4) 573-578... [Pg.177]

National Research Council. (1986b). "Environmental Tobacco Smoke Measuring Exposures and Assessing Health Effects." National Academy Press, Washington, DC. [Pg.387]

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. [Pg.388]

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. [Pg.416]

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. [Pg.934]

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). [Pg.239]

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... [Pg.181]

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. [Pg.242]

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. [Pg.254]

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]. [Pg.282]

Hammond SK (1999) Exposure of U.S. workers to environmental tobacco smoke. Environ Health Perspect 107 329-340... [Pg.459]

NT208 Slotkin, T. A., K. E. Pinkerton, M. C. Garofolo, J. T. Auman, E. C. McCook, and F. J. Seidler. Perinatal exposure to environmental tobacco smoke induces adenylyl cyclase and alters receptor-mediated cell signaling in brain and heart of neonatal rats. Brain Res 2001 898(1) 73-81. [Pg.351]

NT224 Lee, C. Z., F. H. Royce, M. S. Denison, and K. E. Pinkerton. Effect of in utero and postnatal exposure to environmental tobacco smoke on the developmental expression of pulmonary cytochrome P450 monooxygenases. J Biochem Mol Toxicol 2000 14(3) 121-130. [Pg.352]

California Environmental Protection Agency, Office of Environmental Health Hazard Assessment, Health Effects of Exposure to Environmental Tobacco Smoke, Final Report, September 1997. [Pg.530]

California Environmental Protection Agency, Health Effects of Exposure to Environmental Tobacco Smoke, Final Report, September 1997. Available from the Office of Environmental Health Hazard Assessment, 301 Capitol Mall, Second Floor, Sacramento, CA 95814 http //www.calepa. cahwnet. gov/oehha/. [Pg.933]


See other pages where Environmental Tobacco Smoke Exposure is mentioned: [Pg.2252]    [Pg.387]    [Pg.2252]    [Pg.387]    [Pg.389]    [Pg.195]    [Pg.1324]    [Pg.17]    [Pg.1150]    [Pg.55]    [Pg.71]    [Pg.32]    [Pg.82]    [Pg.293]    [Pg.479]    [Pg.858]    [Pg.867]    [Pg.480]   


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