Occupational lung cancer.

Exposure to certain industrial agents has been thought to have carcinogenic potential, both for employees who work closely with such agents and for the general population that comes in contact with them. Although case reports, laboratory studies, and epidemiologic analyses help to determine the carcinogenicity of implicated agents, each of these types of investigation has limitations and deficiencies in distinguishing causal from noncausal associations. Asbestos has been linked with bronchogenic carcinoma, but several controversial factors--the degree of risk relative to exposure dose, the synergistic effect of cocarcinogens, and the question of existence of a threshold dose--complicate the understanding of the magnitude of the risk for exposed persons. Several other physical and chemical agents (such as chromium, nickel, and radon) have also been associated with an increased incidence of lung cancer in epidemiologic and animal studies. As with asbestos, the specific type of the agent and exposure conditions are important in determining the degree of carcinogenicity. In studies of exposure to man-made mineral fibers, formaldehyde, and silica, the findings have been inconsistent. Because the degree of health hazard attributable to asbestos and other known and suspected lung carcinogens is controversial, a wide range of opinions exists about the importance of occupational exposures to the overall incidence of lung cancers. Nevertheless, attempting to prevent lung cancers by minimizing or eliminating exposure to carcinogens is preferable to treating existent cases.

Pulmonary disease associated with L-tryptophan-induced eosinophilic myalgia syndrome. Clinical and pathologic features.

Tablets and capsules containing the essential amino acid L-tryptophan are currently being investigated as a cause of the newly recognized eosinophilia/myalgia syndrome. In the five histologically documented cases reported herein, L-tryptophan ingestion was associated with prominent pulmonary complications. All patients were women ranging from 34 to 65 years, and all presented with respiratory symptoms that began after one to nine months of L-tryptophan therapy. Peripheral eosinophilia was present in four patients as were bilateral interstitial infiltrates on chest roentgenograms. One patient had a normal chest roentgenogram. Lung biopsies were done in all patients and biopsy specimens showed a vasculitis and perivasculitis associated with a mild chronic interstitial pneumonitis and eosinophilia. Three patients had clinical and/or histologic evidence of pulmonary hypertension, and one had a follicular bronchiolitis. Four patients recovered promptly with steroid therapy and discontinuation of L-tryptophan therapy, and one patient has had minimal symptomatic improvement.

Chronic obstructive pulmonary disease: a community-oriented program including professional education and screening by a voluntary health agency.

A community program for chronic obstructive pulmonary disease that included detection by screening, professional education, community involvement, and evaluation of results is described. Key figures in the success of this program were senior medical students. In the first community, in which no professional education was offered, 45.3% of persons screened who had abnormal test results came away from their physicians understanding that they did not have a significant health problem. In subsequent communities, in which professional education was a part of the program, this percentage decreased steadily to approximately 11%. Consistently, 25% of the persons screened who had abnormal results did not consult a physician. Twenty-one % of the participants with abnormal results of screening and no previous knowledge of pulmonary disease stopped smoking in the ensuing 2 to 3 yr, whereas only 11.7% of the control group of persons with normal screening results did so.

Pulmonary toxicity recurring after a six week course of busulfan therapy and after subsequent therapy with uracil mustard.

A growing number of drugs, including a number of alkylating agents, have been implicated as the cause of pulmonary diseases. A patient with chronic myelogenous leukemia presented with typical cytology, biopsy, and roentgenologic findings of lung toxicity after only six weeks of therapy with busulfan. There was subsequent clearing. A similar roentgenologic change also occurred after administration of uracil mustard. This has not been reported previously.

Acute respiratory failure and obesity with normal ventilatory response to carbon dioxide and absent hypoxic ventilatory drive.

We measured hypoxic and hypercapnic ventilatory drive in a 64 year old woman with acute respiratory failure, congestive heart failure and obesity when she was in remission. She had a ventilatory response to carbon dioxide (CO2) comparable to that in six obese women without hypoventilation but no ventilatory response to hypoxia or to vital capacity breaths of 15 per cent CO2 in N2. Following weight loss, her ventilatory response to CO2 increased but hypoxic ventilatory response to CO2 increased but hypoxic ventilatory drive remained absent. These findings indicate that attenuation of hypoxic ventilatory drive caused by loss of peripheral chemoreceptor function can be a predisposing factor in the development of acute respiratory failure associated with obesity.

Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnia with aging in normal men.

The response of ventilation and of heart rate to hypoxia and hypercapnia was determined in eight young normal men age 22-30 yr and eight elderly men age 64-73. The elderly men were selected and carefully screened to eliminate the possibility of cardiopulmonary disease. All the subjects were born at low altitude and had no significant prior exposure to hypoxia. The ventilatory response to hypoxia was measured as the exponential slope constant. k, of regression lines relating the logarithm of incremental ventilation to PAo(2) during isocapnic progressive hypoxia. The heart rate response to hypoxia was measured as the percentage change in heart rate between PAo(2) = 100 and PAo(2) = 40 mm Hg. The ventilatory response to hypercapnia was measured as the slope of regression lines relating ventilation to PAco(2) during rebreathing with PAo(2) > 200 mm Hg. The heart rate response to hypercapnia was measured as the percentage change in heart rate between control values at the start of the rebreathing test and PACO(2) = 55 mm Hg. The ventilatory and heart rate responses to both hypoxia and hypercapnia were significantly decreased in the elderly men as compared to the young men. Hypoxic ventilatory drive was decreased by 51+/-6% (mean +/-SEM: P < 0.001) and hypercapnic drive by 41+/-7% (P < 0.025). The percentage change in heart rate produced by hypoxia was 34+/-5% (mean +/-SEM) in the young normals and 12+/-2% in the old normals (P < 0.005). Similar figures for heart rate in response to hypercapnia were 15+/-3% and -1+/-1% for the young and old normal groups (P < 0.001). We conclude that ventilatory and heart rate responses to hypoxia and hypercapnia diminish with age. These alterations in both ventilatory and circulatory controls could make older individuals more vulnerable to hypoxic disease states.