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Humans cessation

In humans, inhaled insoluble barium salts are retained in the lung (47,49). Inhalation of high concentrations of the fine dusts of barium sulfate can result in the formation of harmless nodular granules in the lungs, a condition called baritosis (49). Baritosis produces no specific symptoms and no changes in pulmonary function. The nodulates disappear upon cessation of exposure to the barium salt. However, it is possible that barium sulfate may produce benign pneumoconiosis because, unlike barium carbonate, barium sulfate is poorly absorbed (21). [Pg.483]

Fiore MC, Smith SS, Jorenby DE, et al The effectiveness of the nicotine patch for smoking cessation. JAMA 271 1940-1947, 1994 Fiore MC, Bailey WC, Cohen SJ, et al Smoking Cessation. Clinical Practice Guideline No 18 (ACHPRPublNo 96-0692). Rockville, MD, U.S. Department of Health and Human Services, 1996... [Pg.335]

Hematological Effects. Humans exposed to acrylonitrile at concentrations where nausea, vomiting and weakness occurred (16 to 100 ppm for 20 to 45 minutes), were also reported to have low grade anemia. However, complete recovery after cessation of exposure was reported (Wilson 1944 ... [Pg.31]

Human toxicity data are limited to secondary citations. Because these citations provided no experimental details, they cannot be considered reliable. Deaths have occurred from aniline ingestion and skin absorption, but doses were unknown. Reviews of the older literature indicate that a concentration of 5 ppm was considered safe for daily exposures, concentrations of 7 to 53 ppm produced slight symptoms after several hours, a concentration of 40 to 53 ppm was tolerated for 6 h without distinct symptoms, a concentration of 130 ppm may be tolerated for 0.5 to 1 h without immediate or late sequalae, and 100 to 160 ppm was the maximum concentration that could be inhaled for 1 h without serious disturbance. In studies of accidents with unknown exposure concentrations, methemoglobin levels of up to 72% were measured. Recoveries occurred with a minimum of medical intervention following cessation of exposure. [Pg.42]

The nonlethal effects of acute exposure of laboratory species to arsine are summarized in Table 2-6. Many of the effects observed appear to occur from one to several days following cessation of exposure and, to some extent, increase in severity as post-exposure time increases. This is consistent with clinical observations for human poisonings with arsine. [Pg.102]

Humans given zinc supplements should be aware of possible complications (Fosmire 1990). Low intakes of 100 to 300 mg of zinc daily in excess of the recommended dietary allowance of 15 mg Zn daily may produce induced copper deficiency, impaired immune function, and disrupted blood lipid profiles. Patients treated with zinc supplements (150 mg daily) to control sickle cell anemia and nonresponsive celiac disease developed a severe copper deficiency in 13 to 23 months normal copper status was restored by cessation of zinc supplements and increased dietary copper (Fosmire 1990). [Pg.711]

Chlordane is readily absorbed by warm-blooded animals through skin, diet, and inhalation. It is quickly distributed in the body and tends to concentrate in liver and fat (WHO 1984). Up to 75% of a single oral dose of chlordane administered to rats and mice was absorbed in the gut, and up to 76% of an aerosol dose was absorbed in the respiratory tract (Nomeir and Hajjar 1987). Rabbits absorbed 33% in the gut following oral administration (USEPA 1988). Chlordane residues in mammals were usually not measurable 4 to 8 weeks after cessation of exposure (Ingle 1965). Chlordane persistence in human serum and whole body was estimated at 88 days and 21 days, respectively this compares to a Tb 1/2 of about 23 days in rats fed chlordane for 56 days (USEPA 1980). [Pg.831]

Plasma levels of cyanide in unexposed, healthy adults average 0 to 10.7 figHOO mL (mean, 4.8, g/100 mL) (Feldstein and Klendshoj 1954). Following mild exposures to cyanide, plasma levels return to this normal range within 4 to 8 h after cessation of exposure the half-life for the conversion of cyanide to thiocyanate from a nonlethal dose in humans was between 20 min and 1 h. [Pg.257]

Excretion. Some -hexane is exhaled following cessation of exposure. This could amount to approximately 10% of that absorbed (Mutti et al. 1984 Veulemans et al. 1982). Excretion is rapid and biphasic with half-lives of 0.2 hours and 1.7 hours. Most -hexane is excreted in the urine as metabolites. Radiolabeled 14C02 in exhaled air has been detected after animal exposure to l4C] -hexane (Bus et al. 1982), indicating that intermediary metabolism of some metabolites takes place. 2,5-Hexanedione and 4,5-dihydroxy-2-hexanone are the major urinary metabolites of -hexane in humans. Half-lives of excretion have been estimated to be 13-14 hours (Perbellini et al. 1981, 1986). [Pg.118]

Histochemical studies of bone marrow samples show that peroxidase-containing granules are detectable in promyelocytes. The human promyelo-cytic leukaemia cell line HL-60 grows easily in culture, and the cells resemble promyelocytes both structurally and functionally. Furthermore, they can be induced to differentiate in vitro upon addition of various agents, such as retinoic acid and phorbol esters, and these differentiated cells resemble more mature forms of neutrophils. HL-60 cells possess almost the same amount of myeloperoxidase (4.4 fig per 106 cells) as mature neutrophils, and the enzyme purified from these cells has the same subunit structure. The cells thus actively synthesise the enzyme only until they are induced to differentiate. This cell line has been extensively used to study the molecular events controlling the expression of enzymes such as myeloperoxidase, and also to investigate the molecular controls that lead to a cessation of their expression. [Pg.61]

Behavioral and emotional Nicotine has a number of behavioral and emotional effects. It increases locomotor activity, which is mediated by increased dopamine in the nucleus accumbens (Mirza 1996). Nicotine suppresses appetite and decreases weight gain in rats (Grunberg et al. 1986). Conversely, cessation of smoking causes increases in body weight. Nicotine increases sexual receptivity in female rats, but whether this occurs in humans has not been studied—or at least not formally (Fuxe et al. 1977). [Pg.112]

Nicotine reduces anxiety in humans, more so in females than males (Stewart et al. 1997). Similar to nicotine, the nicotinic channel activator ABT-418 has anxiolytic effects (Brioni et al. 1994). Nicotine reduces anxiety and right hemisphere EEG activation in subjects watching a stress-inducing movie (Gilbert et al. 1989). Conversely, smoking cessation is commonly associated with increases in anxiety and dysphoria (West and Hajek 1997). [Pg.112]

Franks FIM, Flagedorn FI, Flensley VR, Flensley WJ, Starmer GA. (1975). The effect of caffeine on human performance, alone and in combination with ethanol. Psychopharmacologia. 45(2) 177-81. Franks P, Flarp J, Bell B. (1989). Randomized, controlled trial of clonidine for smoking cessation in a primary care setting. JAMA. 262(21) 3011-13. [Pg.451]

A possible case of chronic intoxication by 1,2-dibromoethane occurred in a worker involved in 1,2-dibromoethane production (Kochmann 1928). Symptoms were nonspecific. Upper respiratory symptoms consisted of pharyngitis and bronchitis other symptoms were lymphadenopathy, conjunctivitis, anorexia, headache, and depression. The worker s condition improved upon cessation of exposure. No other studies were located regarding respiratory effects in humans after inhalation exposure to 1,2-dibromoethane. [Pg.24]

An understanding of the pharmacology of nicotine and how nicotine produces addiction and influences smoking behavior provides a necessary basis for therapeutic advances in smoking cessation interventions. This chapter provides a review of several aspects of the human pharmacology of nicotine. These include the presence and levels of nicotine and related alkaloids in tobacco products, the absorption of nicotine from tobacco products and nicotine medications, the distribution of nicotine in body tissues, the metabolism and renal excretion of nicotine, nicotine and cotinine blood levels during tobacco use or nicotine replacement therapy, and biomarkers of nicotine exposure. For more details and references on the pharmacokinetics and metabolism of nicotine, the reader is referred to Hukkanen et al. (2005c). [Pg.30]

Rose JE, Behm FM, Westman EC, Kukovich P (2006) Precessation treatment with nicotine skin patch facilitates smoking cessation. Nicotine Tob Res 8(1) 89-101 Ross B, Bluml S (2001) Magnetic resonance spectroscopy of the human brain, Anat Rec 265(2) 54-84... [Pg.142]


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See also in sourсe #XX -- [ Pg.15 , Pg.16 , Pg.21 ]




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