Inhalation Lung Injury Research Articles

The effect of carbon monoxide on hemodynamics and oxygen metabolism in inhalation lung injury. (Chinese)

The effect of carbon monoxide on hemodynamics and oxygen metabolism in inhalation lung injury. (Chinese)

Environmentally Mediated Disorders of the Respiratory Tract

Although much of the evidence in environmental lung disease remains equivocal, some environmental exposures are known to be clinically relevant. Ambient air pollution remains of concern as a source of morbidity, particularly for susceptible populations such as persons with asthma, chronic obstructive pulmonary disease, or cardiac disease and the elderly. The adverse effects of several components of indoor air pollution have been established. Environmental tobacco smoke contributes to lower-respiratory illness in infants; office workers exposed to thermophilic actinomycetes contaminating ventilation systems have developed hypersensitivity pneumonitis; and in the home, components of house dust and fungus spores may provoke asthma via immediate hypersensitivity. The evidence is less compelling for a link between other exposures and disorders of the respiratory tract. For example, formaldehyde may be responsible for provoking vague respiratory symptoms and even nasal cancers; however, the associations are unproved. Likewise, the relation between low-level exposure to asbestos and the development of lung cancer, although a concern, is not conclusively established. The clinician should be aware of practical measures for patients who inquire about air cleaning. Often, relatively simple solutions are effective. A knowledge of sources and exposures as well as an understanding of the principles of inhalation lung injury should prove useful in directing patient care.

Mortality and lung histopathology after inhalation lung injury. The effect of corticosteroids.

An animal model was used to study the effects of early administration of intramuscular corticosteroids on mortality and lung histopathology induced by a component of smoke. Thirty-six rabbits (mean weight, 2.7 kg) were exposed to acrolein vapor for 15 min; 30 min later the animals were divided into 3 treatment groups. One group received saline placebo intramuscularly at 12-h intervals, a second group was treated intramuscularly with 100 mg methylprednisolone at 12-h intervals, and a third group was treated with a single 100-mg dose of methylprednisolone followed by doses of saline at 12-h intervals. The animals were studied for a 72-h period. There was a significantly lower mortality in the 2 steroid-treated groups than in the nontreated group. A scoring system was developed for evaluating observed histologic changes in the lung. No correlation was seen between survival and histologic score or between score and treatment. High scores for particular histologic features did not explain mortality nor did they predominate in untreated animals; "vascular congestion" was found to be greater in the steroid-treated group. The beneficial effects of steroids in reducing mortality after inhalation of a common smoke constituent was not associated with any evidence of attenuation of lung damage.