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Smoke exposure

Techniques for handling sodium in commercial-scale appHcations have improved (5,23,98,101,102). Contamination by sodium oxide is kept at a minimum by completely welded constmction and inert gas-pressured transfers. Residual oxide is removed by cold traps or micrometallic filters. Special mechanical pumps or leak-free electromagnetic pumps and meters work well with clean Hquid sodium. Corrosion of stainless or carbon steel equipment is minimi2ed by keeping the oxide content low. The 8-h TWA PEL and ceiling TLV for sodium or sodium oxide or hydroxide smoke exposure is 2 mg/m. There is no defined AID for pure sodium, as even the smallest quantity ingested could potentially cause fatal injury. [Pg.168]

Exposure to cigarette smoke Exposure to ozone Exposure to ionizing radiation... [Pg.201]

Prolonged use of computer or reading Contact lenses Air travel Smoke exposure... [Pg.945]

The majority of people who smoke never develop lung cancer. Genetic risk factors may predispose certain smokers to lung cancer. After adjustments for age, smoke exposure, occupation, and gender, relatives of a lung cancer patient have approximately a twofold risk of developing lung cancer. The... [Pg.1324]

Li, S., Park, M., Bahk, J., Kim, M. Chronic nicotine and smoking exposure decreases GABAb1 receptor expression in the rat hippocampus. Neurosci. Lett. 334 135, 2002. [Pg.49]

Chronic bronchitis is a result of several contributing factors, including cigarette smoking exposure to occupational dusts, fumes, and environmental pollution and bacterial (and possibly viral) infection. [Pg.480]

Belin, R.M. et al., Smoke exposure is associated with a lower prevalence of serum thyroid autoantibodies and thyrotropin concentration elevation and a higher prevalence of mild thyrotropin concentration suppression in the third National Health and Nutrition Examination Survey (NHANES III), J. Clin. Endocrinol. Metab., 89, 6077, 2004. [Pg.452]

A number of studies of the toxicity of zinc oxide/hexachloroethane smoke have been conducted (Brown et al. 1990 Karlsson et al. 1986 Marrs et al. 1983). These studies demonstrate that smoke exposure results in pulmonary inflammation and irritation. When male Porton Wistar rats were exposed to hexachloroethane/zinc oxide smoke for 60 minutes, the lungs showed pulmonary edema, alveolitis, and areas of macrophage infiltration 3 days later. At 14 days, there was interstitial fibrosis and macrophage infiltration. At 28 days, increased fibrosis and macrophage infiltration were noted. However, these same symptoms occurred when the animals inhaled zinc chloride there was no apparent synergism between the zinc chloride and residual hexachloroethane (Brown et al. 1990 Richard et al. 1989). This is consistent with the fact that smoke contains little hexachloroethane and the observation that acute exposure to 260 ppm hexachloroethane had no effects on the lungs of rats (Weeks et al. 1979). [Pg.98]

Aii SF, Newport GD, Scaiiet AC, Pauie MG, Baiiey JR, Siikker W Jr. (1991). Chronic marijuana smoke exposure in the rhesus monkey IV. Neurochemicai effects and comparison to acute and chronic exposure to deita-9-tetrahydrocannabinoi (THC) in rats. Pharmacol Biochem Behav. 40(3) 677-82. Bachman JA, Benowitz NL, Herning RI, Jones RT. (1979). Dissociation of autonomic and cognitive effects of THC in man. Psychopharmacology (Berlin). 61(2) 171-75. [Pg.555]

Paule MG, Allen RR, Bailey JR, Scallet AC, Ali SF, Brown RM, Slikker W Jr. (1992). Chronic marijuana smoke exposure in the rhesus monkey II. Effects on progressive ratio and conditioned position responding. J Pharmacol Exp Ther. 260(1) 210-22. [Pg.564]

Chetiyanukornkul T, Toriba A, Kizu R, Kimura K, Hayakawa K. 2004. Hair analysis of nicotine and cotinine for evaluating tobacco smoke exposure by liquid chromatography-mass spectrometry. Biomed Chromatogr 18 655. [Pg.169]

Owen, M.J., et al. (1993). Relation of infant feeding practices cigarette smoke exposure and group children care to the onset and duration of otitis media with effusion in the first years of life, J. Pediatric., 123, 702-710. [Pg.124]

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]

Dietary sources of nicotine have been alleged to be a potential confounder of cotinine levels used in measurement of secondhand smoke exposure. Several foods contain small amounts of nicotine (Siegmund et al. 1999). However, the levels of nicotine in foods are quite low. Based on nicotine levels in foods and the usual daily consumption of various nicotine-containing foods, it has been determined that... [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]

Of all the design characteristics of cigarettes, filter ventilation may be the most important in determining machine-smoked yields (Djordjevic et al. 1995), as well as the most important determinant of the differences in machine-smoked yields and human smoking behavior and smoke exposure. Filter ventilation dilutes mainstream... [Pg.469]

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]

There is some USEPA precedent for use of statistical meta-analysis in a regulatory context, including the recent meta-analysis of organophosphate-related acetylcholinesterase inhibition data and meta-analysis of epidemiological studies on effects of 2nd hand tobacco smoke exposure. Warren-Hicks and Moore (1998) provide some discussion of the potential applicability of meta-analysis to ecological risk assessments. [Pg.47]

Respiratory Effects. Although the SMR for respiratory diseases was 1.31 among workers at a thorium refinery (Polednak et al. 1983), the increase may have been attributable in part to smoking Exposure level estimates for inhalation intakes ranged from 0.003-0.192 nCi/m (0.001-0.007 Bq/m ) for a period of 1 -33 years. Because the workers were exposed to other toxic compounds (uranium dust) as well as other radioactive metals, toxic effects cannot necessarily be attributed to thorium. Therefore, no quantitative information from the study is reported in Table 2-1 or Figure 2-1. [Pg.28]

Arterial endothelial injury. Environmental smoke, administered to ovariectomized rats treated with subcutaneous placebo or 17 p-estradiol pellets for 6 weeks, produced a more than fourfold increase of carotid artery low-density lipoprotein (LDL) accumulation compared with filtered air exposure. The effect was largely mediated by increased permeability. No protective effect of estradiol was observed. Acute smoke exposure of a buffer solution containing LDL produced a more than sixfold increase in the highly reactive carbonyl glyoxal. Perfusion of this solution through carotid arteries produced 105% increase in permeability. Perfusion of glyoxal alone produced a 50% increase in carotid artery permeability ... [Pg.290]

Carboxyhemoglobin effect. Cigarette smoke was administered by inhalation with a modified Walton horizontal smoke exposure machine to mice at intermittent doses. During the first 30 seconds of each 1-minute cycle, the subjects were exposed to smoke diluted either 1 10 or 1 5 with air. This treatment produced carboxyhemoglobin... [Pg.292]


See other pages where Smoke exposure is mentioned: [Pg.1062]    [Pg.1068]    [Pg.1324]    [Pg.427]    [Pg.429]    [Pg.471]    [Pg.473]    [Pg.477]    [Pg.8]    [Pg.314]    [Pg.111]    [Pg.30]    [Pg.49]    [Pg.50]    [Pg.53]    [Pg.383]    [Pg.187]    [Pg.85]    [Pg.286]    [Pg.286]    [Pg.288]    [Pg.289]    [Pg.293]    [Pg.295]    [Pg.298]    [Pg.301]    [Pg.305]    [Pg.305]    [Pg.305]   
See also in sourсe #XX -- [ Pg.420 ]




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