Inhalation toxicology
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Inhalation toxicology · Aug 2010
Malondialdehyde and superoxide dismutase correlate with FEV(1) in patients with COPD associated with wood smoke exposure and tobacco smoking.
Tobacco smoking is the primary risk factor for chronic obstructive pulmonary disease (COPD). However, recent epidemiological studies have established domestic exposure to wood smoke and other biomass fuels as additional important risk factors, characteristic in developing countries. Oxidative stress is one of the mechanisms concerned with pathogenesis of COPD. ⋯ No differences were shown regarding GPx, GR, and GST activities between COPD and control groups. Inverse correlations were founded between MDA and SOD with FEV(1) in both COPD patients and control subjects (P < 0.001). These results indicate a role for oxidative stress in COPD associated with wood smoke similar to that observed with tobacco smoking in subjects who ceased at least 10 years previous to this study.
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Inhalation toxicology · Aug 2010
Montelukast prevents vascular endothelial dysfunction from internal combustion exhaust inhalation during exercise.
Associations between high particulate matter (PM) pollution and increased morbidity and mortality from coronary heart disease have been identified. This study assessed leukotriene (LT) participation in PM-induced vascular endothelial dysfunction. Ten healthy males exercised 4 times for 30 min in both high PM (550,286 +/- 42,004 particles x cm(-3)) and low PM (4571 +/- 1922 particles x cm(-3)) after ingesting placebo (PL) or 10 mg montelukast (MK; half-life 3-6 h), a leukotriene receptor antagonist. ⋯ At 4 h, high PM MK FMD blunting increased (p = .1). At 24 h, high PM FMD blunting persisted (p < .05); no difference was observed between high PM PL or MK treatment, but was different that low PM PL/MK treatments (p < .05). MK blocked high PM post-exercise FMD blunting and maintained normal response, suggesting that leukotrienes are involved in PM-initiated vascular endothelial dysfunction.
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Inhalation toxicology · Aug 2010
Pulmonary function and histological impairment in mice after acute exposure to aluminum dust.
Along the aluminum refining process, alumina (Al2O3) constitutes the main source of dust. Although aluminum refinery workers present respiratory symptoms with lung functional changes, no conclusive data about lung function impairment after alumina exposure has been so far reported. We examined the pulmonary alterations of exposure to material collected in an aluminum refinery in Brazil. ⋯ ALUM also presented significantly higher fraction area of alveolar collapse (69.7 +/- 1.2%) and influx of polymorphonuclear cells (27.5 +/- 1.1%) in lung parenchyma than CTRL (27.2 +/- 1.1% and 14.6 +/- 0.7%, respectively). The composition analysis of the particulate matter showed high concentrations of aluminum. For the first time it was demonstrated in an experimental model that an acute exposure to dust collected in an aluminum producing facility impaired lung mechanics that could be associated with inflammation.
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Inhalation toxicology · Jun 2010
Comparative StudyMetered-dose inhaler efficiency enhancement: a case study and novel design.
The efficiency of the metered-dose inhaler (MDI) is a critical issue in aerosol medicine because it deals with delivering a life-saving medication to patients with various lung diseases. Mouthpiece diameter, air flow rate, and entrance angle are among many parameters that influence the MDI penetration efficiency. It is well known that inertial impaction accounts for the massive aerosol deposition in the oral airway. ⋯ The experiments are conducted at three different air flow rates (30, 60, and 90 L/min) and five entrance/spray angles (0 degrees, 10 degrees, 20 degrees, 30 degrees, and 40 degrees). The results show that the new modified mouthpiece has higher aerosol penetration efficiency than the ones with the conventional mouthpiece. A second type of experiment is conducted to evaluate the relative strength of the aerosol impaction.
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Inhalation toxicology · Jan 2010
A transport model for nicotine in the tracheobronchial and pulmonary region of the lung.
Nicotine in mainstream cigarette smoke is predominantly present in the particulate phase. Interestingly, however, the deposition efficiency of smoke particles in the respiratory tract is less effective than is the nicotine retention. In the literature, four nicotine deposition mechanisms are identified: (a) direct gas deposition, (b) evaporative gas deposition, (c) particle deposition with evaporation, and (d) particle deposition with diffusion. ⋯ The model incorporates nicotine mass transport through estimates for the diffusion time across the epithelial layer and the time for nicotine vapor diffusion from the gas volume to the tissue surfaces in the tracheobronchial and pulmonary regions of the respiratory tract. The model comprises four mass transfer processes for nicotine at the surface of the respiratory tract epithelium: (1) conversion of free base nicotine from protonated nicotine; (2) free base nicotine transport across the epithelium; (3) free base nicotine evaporation; and (4) diffusion of free base nicotine vapor from the surface gas layer into the airway lumen. Results of the nicotine mass transport model suggest that the principal mechanism of nicotine delivery to the lung is by direct deposition of particles to the alveolar fluid lining, followed rapidly by evaporation into the lumen and then gas diffusion back to the surface as nicotine depletes in the surface layer through its transport across the epithelium.