Effects of inhalants

The primary site of action is postulated to be the Hpid matrix of cell membranes. The Hpid properties which are said to be altered vary from theory to theory and include enhancing membrane fluidity volume expansion melting of gel phases increasing membrane thickness, surface tension, and lateral surface pressure and encouraging the formation of polar dislocations (10,11). Most theories postulate that changes in the Hpids influence the activities of cmcial membrane proteins such as ion channels. The Hpid theories suffer from an important drawback at clinically used concentrations, the effects of inhalational anesthetics on Hpid bilayers are very small and essentially undetectable (6,12,13). 

Utell, M. J. (1985). Effects of inhaled acid aerosols on lung mechanics an analysis of human exposure studies. Environmental Health Perspect. 63, 39-44. 

Holma, B. (1989). Effects of inhaled acids on airway mucus and its consequences for health. Environ. Health Perspect. 79, 109-113. 

Inhaled steroids (commonly used are beclomethasone, budesonide, triamcinolone, fluticasone, flunisolide) appear to attenuate the inflammatory response, to reduce bronchial hyperreactivity, to decrease exacerbations and to improve health status they may also reduce the risk of myocar dial infar ction, but they do not modify the longterm decline in lung function. Whether- steroids affect mortality remains unclear. Many patients appear to be resistant to steroids and large, long-term trials have shown only limited effectiveness of inhaled corticosteroid ther apy. Certainly, the benefit from steroids is smaller in COPD than in asthma. Topical side-effects of inhaled steroids are oropharyngeal candidiasis and hoarse voice. At the normal doses systemic side-effects of inhaled steroids have not been firmly established. The current recommendation is that the addition of inhaled gluco-coiticosteroids to bronchodilator treatment is appropriate for patients with severe to veiy sever e COPD. 

No systematic studies of tolerance to the reinforcing effects of inhaled nitrites have been reported. However, anecdotal observations in workers with high exposure to nitrites have suggested that tolerance to the subjective effects of this compound occurs after a few days of exposure (Marsh and Marsh... 

Although, to our knowledge, the effects of inhalation of amyl nitrite or butyl nitrite on glutamatergic neurotransmission have not been studied, NO, the potent compound that mediates the peripheral effects of nitrites in blood vessels, if released in the CNS when nitrites are inhaled, may potentially affect the glutamatergic system. NO has been reported to act directly on the postsynaptic NMDA receptor, where it can increase or decrease NMDA-mediated currents and subsequent calcium influx (Aizenman et al. 1990 Dingledine et al. 1999 Manzoni et al. 1992). 

Laboratory tests can help in assessing the effects of inhalant use. Laboratory tests that measure hepatic function, renal function, and hematopoietic... 

Rea TM, Nash JF, Zabik JE, et al Effects of toluene inhalation on brain biogenic amines in the rat. Toxicology 31 143-1450, 1984 Rebert CS, Matteucci MJ, Pryor GT Acute electrophysiologic effects of inhaled toluene on adult male Long-Evans rats. Pharmacol Biochem Behav 33 157—165, 1989 Reynolds JEF Martindale The Extra Pharmacopoeia, 28th Edition. London, Pharmaceutical Press, 1982, pp 745-746... 

Although a number of studies have reported the effects of inhalation exposure to methyl parathion in humans, no inhalation MRLs were derived based on human data because of the lack of adequate quantitative exposure information. Animal data were also insufficient to support the derivation of an acute-, intermediate-, or chronic-duration inhalation MRL. 

The database for the health effects of methyl parathion after ingestion in experimental animals is substantial. However, as can be seen in Figure 3-5, only limited information is available on the effects of inhalation and dermal exposure to methyl parathion in animals. Furthermore, the health effects such as death and neurotoxicity resulting from acute exposure in animals are more fully studied than systemic and immunotoxic effects associated with acute exposure. 

Irregular respiration was observed in both male and female rats after a 4-hour nose-only inhalation exposure to aerosolized endosulfan (Hoechst 1983a). In both male and female rats, dyspnea was observed at the lowest concentrations tested (12.3 and 3.6 mg/m for males and females, respectively). Autopsies of the rats that died revealed dark-red, pinhead-sized foci on the lungs. It is unclear whether these effects represent direct effects of inhaled endosulfan on respiratory tissues or whether they are secondary to central nervous system effects on respiratory function. No treatment-related effects were... 

Carbon monoxide seriously impedes transport of oxygen. The deadly effect of inhaled CO results from its reaction with hemoglobin. A CO molecule is almost the same size and shape as O2, so it fits into the binding pocket of the hemoglobin molecule. In addition, the carbon atom of CO forms a stronger bond to than does O2. Under... 

Studies of workers and volunteers in experiments have provided most of the data on health effects of inhaled trichloroethylene in humans. Most of the information on reported effects in humans following oral exposure... 

Beliles et al. 1980 Land et al. 1981). Studies for oral exposure indicate no adverse reproductive effects (NTP 1985, 1986). More research on the reproductive effects of inhalation exposure to trichloroethylene, especially effects on miscarriage in humans is needed. Additional animal studies via the inhalation and dermal routes are needed to further characterize reproductive effects. 

Aranyi C, O Shea WJ, Graham JA, et al. 1986. The effects of inhalation of organic chemical air contaminants on murine lung host defenses. Fundam Appl Toxicol 6 713-720. 

Bushnell PJ. 1997. Concentration-time relationships for the effects of inhaled trichloroethylene on signal detection behavior in rats. Fund Appl Toxicol 36 30-38. 

Kylin B, Axell K, Samuel HE, et al. 1967. Effect of inhaled trichloroethylene on the CNS as measured by optokinetic nystagmus. Arch Environ Health 15 48-52. 

Much of the pulmonary NEP activity is believed to reside in the epithelium, as has been demonstrated in the ferret (Borson et al., 1986), and thus it is likely that inhaled ozone would preferentially destroy luminal NEP before affecting any enzymes in the vasculature, which may degrade peptides delivered by the intravenous route. This may explain the route-dependency of BHR after ozone in guinea pigs. Further evidence that the oxidant effects of inhaled ozone are selective is provided by the findings that pressor responses to angiotensin I (which requires conversion by ACE to angiotensin II) were not altered by ozone exposure (Yeadon et eU., 1992). 

Local adverse effects of inhaled corticosteroids include oral candidiasis and dysphonia. The incidence of local adverse... 

Buldakov LA, Kalmykova ZI, Nifatov AP, et al. 1972. Metabolism and biological effects of inhaled 241Am and 239Pu in dogs. Health Phys 22 873-874. 

Talbot RJ, Nicholls L, Morgan A, et al. 1989. Effect of inhaled a-emitting nuclides on mouse alveolar macrophages. Radiat Res 119 271-285. 

S. P. Newman, Deposition and Effects of Inhalation Aerosols, AB DRACO (subsidiary to ASTRA), Lund, Sweden, 1983. 

Lopez A, Prior MG, Reiffenstein RJ, et al. 1989. Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. Fundam Appl Toxicol 12 367-373. 

Saillenfait AM, Bonnet P, de Ceaurriz J. 1989. Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats. Toxicol Lett 48 57-66. 

Oberdorster G. 1992. Pulmonary deposition, clearance and effects of inhaled soluble and insoluble cadmium compounds. In Nordberg GF, Herber RFM, Alessio L, eds. Cadmium in the human environment Toxicity and carcinogenicity. Lyon International Agency for Research on Cancer,... 

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