Occupational asthma.

The seriousness of asthma in the general population has been recognized by increased prevalence, morbidity, and mortality rates in the past 20 years. The effects of occupational asthma on health and productivity in the workplace have been so deleterious that the Occupational Safety and Health Administration targeted 1995 as a crisis year for effective remediation. Several risk factors have been identified, but all asthma is multifactorial. Inhaled chemical, physical, and microbiological agents in the form of dust, fumes, gases, and vapors may cause workplace asthma, which is mediated through pharmacologic, immunologic, or irritant mechanisms. Because of the complexity of these mechanisms after exposure to the offending agents, the clinical manifestations may be classed as immediate, delayed, or dual responses. Evaluating causation and relationship to work requires a thorough history (including detailed job description), physical examination, and definitive studies to determine the presence of bronchospasm, bronchial hyperreactivity, atopy, work-relatedness, and presence of specific sensitization. Goals of treatment for occupational asthma are to maintain pulmonary function as close to normal as possible, to maintain a normal lifestyle, and to prevent exacerbation. In occupational asthma, particularly, the patient (or the inciting cause, if known) should be removed from the offending environment as soon as possible. Specific treatment depends upon the specific offending agent, and antiasthma therapy may be needed following the guidelines of the National Heart, Lung, and Blood Institute.

Post-traumatic upper airway obstruction secondary to a lingual artery hematoma.

An accident victim presented with maxillofacial trauma complicating a head injury. After the airway was secured by tracheostomy, surgical exploration revealed a lingual artery hematoma. This case illustrates the progressive airway occlusion seen with this disorder and the importance of repeated oral examinations.

Comparative pathogenesis of radium-induced intracortical bone lesions in humans and beagles.

Morphologic changes resulting from the effects of chronic radionuclide toxicity (226Ra) in the skeletons of workers in the radioluminescent dial painting industry with preterminal body burdens ranging from about 1.5 to 0.042 muCi were compared with the pathologic alterations in the skeletons of a group of 38 beagle dogs injected with 1.12 muCi/kg. Similarities observed in the skeletal responses of the two species were the presence of (1) dead bone tissue with delayed resolution, (2) a chronic disturbance in the remodeling mechanism of bone tissue, and (3) radiation-induced bone sarcomas. A detailed analysis of sequential changes in radiographic lesions arising in the beagle skeletons, complemented by histopathologic evaluation at the time of limb amputation or at necropsy, has enabled us to examined the disturbance in the bone remodeling process. The perturbation of critical importance in the generation of primary bone tumors appears to lie in the bone tissue formation and deposition phase of the bone remodeling process and gives rise to a spectrum of histologic patterns which we have termed "radiation osteodystrophy." While some of the newly generated patterns demonstrate indolent behavior with fibrous tissue replacement and bone marrow refill, other sites of bone resorption are replaced by a unique fibro-osseous tissue response resembling fibrous dysplasia or osteoblastoma. Some of these proliferative lesions may undergo progressive malignant degeneration. While the more indolent part of the spectrum was also seen in human skeletal tissues, only premalignant and early sarcomatous stages were seen in canine tissues.

Osteometry and autoradiography of the long bones of skeletons of women exposed to internal radiation at 13--19 years of age.

Lengths of long bones of skeletons were examined in 25 women first exposed to large skeletal doses of radiation (alpha particles from radium) at the age of 13--19 years. Mean lengths did not differ significantly between two subgroups based on age at first exposure to radiation (i.e., 13--16 vs. 17--19 years). Autoradiographs of femora of some women who ingested radium at 13-15 years of age showed evidence for bone growth when blood levels of radium were low (i.e., after ingestion of radium). These findings indicate no detectable effect of large skeletal doses of radiation on growth in adolescent and post-adolescent periods.