Publications

The contribution of workplace exposures to the prevalence of asthma in adults has been minimized in the epidemiology of this illness. Analysis of the 1978 Social Security Disability Survey provides a population-based assessment as a novel approach utilizing self-attributed, occupationally related asthma as a measure of disease. Of 6,063 respondents, 468 (7.7 percent) identified asthma as a personal medical condition; 72 (1.2 percent [15.4 percent of all those with asthma]) attributed it to workplace exposures. These subjects were older and included more men and cigarette smokers than groups of both asthmatic and nonasthmatic subjects. The relative risk for occupationally attributed asthma was elevated among industrial and agricultural workers as compared with white collar and service occupations. Analysis of disability benefit status did not indicate that this introduced major reporting bias in this survey. This study suggests that occupational factors may have a greater role in adult asthma than previously thought.

We studied the roentgenograms, pulmonary function tests, and physical findings of 294 shipyard workers to evaluate asbestos exposure-cigarette smoking interactions. Roentgenographic parenchymal opacities, decreased pulmonary diffusing capacity for carbon monoxide, decreased flow at low lung volume, rales, and clubbing were each significantly related to the number of years elapsed since first exposure to asbestos and cigarette smoking status when analyzed by logistic regression. A dose-dependent cigarette smoking response that was consistent with synergism was present only for parenchymal opacities and decreased flow at low lung volume. These findings suggest that decreased flow at low lung volume, possibly reflecting peribronchiolar fibrosis, may be a functional corollary to smoking-associated parenchymal roentgenographic opacities among some asbestos-exposed individuals.

Whether cigarette smoking can cause radiographic opacities indistinguishable from those due to pneumoconiosis remains controversial. The situation becomes clearer when one limits the abnormalities to those that can be standardized under the International Labour Office (ILO) classification system. The bulk of the evidence indicates that, using the ILO system, cigarette smoking alone is not associated with radiographic opacities that would be mistaken for pneumoconiosis with sufficient frequency to be of any practical importance. The effects of cigarette smoking, as a cofactor, in conjunction with occupational dust exposure depend on the type of dust. No relationship has been convincingly demonstrated for coal dust or silica. Only with asbestos exposure does there appear to be a significant cigarette smoking-associated increase in the frequency of irregular radiographic opacities. This increase does not appear to translate into a restrictive impairment in pulmonary function. The limited information available indicates that the features of asbestosis on high-resolution computed tomography are not similarly related to cigarette smoking. Additional research is needed to substantiate the relationship between smoking and occupational exposure to dust of many types, and also the possible imaging and pathophysiologic significance of their interactions.

In the Negev region of Israel, I tested a model approach to occupational health planning. This model included components assessing exposures, measuring adverse health outcomes, and evaluating health services. I analyzed employment survey data, compiled an exposure data base, and carried out site visits covering 10,707 employees (over 50% of the regional industrial work force). Site visits identified exposure hazards of inorganic and organic dusts, heavy metals, chemicals, pesticides, and noise. I identified elevated relative regional injury rates by Standard Morbidity Ratios (SMRs) in a variety of industries, including sixfold increases for mining and non-metallic minerals manufacture (SMR 6.8, 99% CI 6.1-7.7). Review of biological monitoring data suggested deficiencies in pesticide and heavy metals surveillance. A survey of primary care clinics estimated 13,707 cases of occupational injury and illness untreated by existing occupational medical services. Based on these findings, I formulated regional occupational health planning goals, including targeting high-risk industries for increased preventive activities. This regional approach, combining multiple measures of occupational health status, can serve as a model for assessing local public health planning needs.

STUDY OBJECTIVE

To evaluate the usefulness of poison control center detection in occupational illness surveillance.

DESIGN

Case series of all occupationally related exposures referred for poison control center consultation over 6 months. Follow-up structured interviews were done of exposed persons and health care providers. Cases were traced under established occupational illness reporting programs.

SETTING

A regional poison control center.

PATIENTS

Consecutive sample of 461 symptomatic occupational exposure cases. After exclusions and losses to follow-up, interview of 301 patients and the treating physician, physician's assistant, or nurse practitioner for the 223 of the patients under direct medical care.

MEASUREMENTS AND MAIN RESULTS

One hundred and fifty-five persons (61%; CI, 55% to 67%) had systemic or respiratory illness; 109 (36%; CI, 31% to 41%) had eye or skin conditions. Work practices were associated with exposures more often than technical failure; 118 persons (39%; CI, 33% to 45%) reported lack of respirators or other appropriate personal protective equipment. For 223 persons who received direct medical care, only five treating health care providers (2%; CI, 0.2% to 4%) reported occupational specialization, although occupational care was a regular practice activity for 128 of the health care providers (57%; CI, 51% to 63%). Sixty-seven cases (22%; CI, 17% to 27%) were detected by the Doctor's First Report surveillance program; 97 cases (32%; CI, 27% to 37%) comprised the maximal detection estimated for Occupational Safety and Health Administration surveillance.

CONCLUSIONS

Poison control center detection provides a useful surveillance measure for occupational illness. The proportion of case detection failures by established surveillance programs suggests that the incidence of occupational illness in the United States, which is calculated from these incomplete programs, may be three to five times greater than previously estimated.

In a study of occupational illness reported to a regional poison control center and to gauge the center's outreach and services, we did follow-up interviews of 301 case contacts over a 6-month period. We ascertained referral routes, reasons for contacting the poison control center, and awareness of the center's function. For 122 cases a nonphysician was the initial poison control center contact. Of the nonphysician contacts, 41 had already consulted a health care provider and been referred to the poison control center for assistance. Of the 70 persons with exposure, only 21 had been aware before their exposures that poison control center services might include occupational chemical illness consultation. Physicians and nonphysicians expressed similar reasons for contacting the poison control center, with 118 of 301 identifying the need for an exposure hazard risk assessment. These data suggest that although those contacting a poison control center because of occupational illness include a variety of cases, they have many similar service needs.

The radiographic distribution of Pneumocystis carinii pneumonia was studied in 64 consecutive patients with acquired immunodeficiency syndrome to determine the demographic and clinical factors that might be associated with predominance of the disease in the upper zones of the lungs. Twenty-three patients were receiving monthly prophylaxis with 300 mg of aerosolized pentamidine by means of inhalation; the other 41 were not receiving pentamidine and served as a control group. Parenchymal abnormalities were present in 63 of 64 patients. Pleural effusion and cystic lung lesions were uncommon and did not differ between the two groups. Patients receiving aerosolized pentamidine were more likely than control patients to have disease isolated or predominant in the upper lobes (odds ratio = 3.9, confidence interval = 1.1-14.1). After the possible effects of confounding variables were taken into account, prophylaxis remained a significant risk factor. Age and a previous history of P carinii pneumonia were not significant cofactors. The pattern of deposition or retention of the aerosolized pentamidine could be responsible for the finding of predominant P carinii pneumonia in the upper lobes of the lungs.

The pathogenesis of pulmonary edema that occurs during interleukin-2 therapy has often been attributed to an increase in pulmonary capillary permeability. However, renal insufficiency, fluid overload, and hypotension also develop in many patients. These manifestations of systemic toxicity may contribute to the development of pulmonary edema during therapy. Understanding the cause of pulmonary edema during interleukin-2 therapy could directly affect patients' care. Therefore, we reviewed the chest radiographs and clinical course of 54 patients who received high-dose interleukin-2 therapy and lymphokine-activated killer cells for advanced carcinoma. The type, frequency, and course over time of pulmonary abnormalities were recorded and correlated with clinical measures of renal function, fluid status, and blood pressure. Focal or diffuse parenchymal lung opacities were found on radiographs in 43 (80%) of 54 patients. Findings of interstitial pulmonary edema were most common, occurring in 76% of patients. Weight gain, hypotension, and elevation of the serum creatinine level were not associated statistically with interstitial edema. Diffuse air-space disease developed in 20% of patients. Focal consolidation, which was associated with positive central venous catheter cultures (p less than .03), developed in 28% of patients. Pleural effusion occurred in 48% of patients and was associated with all types of parenchymal disease. These data suggest that the frequent development of pulmonary edema during interleukin-2 therapy is not due to renal insufficiency, fluid overload, or hypotension, but is more likely the result of an interleukin-2-related increase in pulmonary capillary permeability.

OBJECTIVE

To examine the pathogenesis of metal fume fever in humans by studying functional, cellular, and biochemical responses after exposure to zinc welding fume.

DESIGN

Clinical experimental study.

PARTICIPANTS

We studied 14 welders recruited through public advertisements.

INTERVENTIONS

Participants welded galvanized steel.

MEASUREMENTS

We measured lung volumes, airflow, diffusing capacity for carbon monoxide, and airway reactivity at baseline as well as either 6 or 20 hours after welding. We carried out bronchoalveolar lavage either 8 hours (early follow-up, 5 participants) or 22 hours (late follow-up, 9 participants) after welding, assaying the fluid for total and differential cell counts and bronchoalveolar lavage supernatant concentrations of interleukin-1 and tumor necrosis factor (TNF).

MAIN RESULTS

Changes in pulmonary function and airway reactivity were minimal. Cumulative zinc exposure and polymorphonuclear leukocyte count in bronchoalveolar lavage fluid at late (r = 0.87; P less than 0.01) and early (r = 0.93; P less than 0.05) follow-up were positively correlated. Among the late follow-up group, the mean proportion of polymorphonuclear leukocytes was 37% (range, 19% to 63%), a statistically greater proportion than the 9% (range, 2% to 21%) seen among the early follow-up group (P less than 0.05). We did not detect TNF or more than a trace amount of interleukin-1 in the bronchoalveolar lavage supernatant.

CONCLUSIONS

Zinc oxide welding fume was associated with a marked dose-dependent increase in the number of polymorphonuclear leukocytes recovered in bronchoalveolar lavage fluid 22 hours after exposure but was not associated with a clinically significant change in pulmonary function or airway reactivity. Although we did not identify increases in either interleukin-1 or TNF levels in bronchoalveolar lavage fluid, cytokines or a cytokine-like mechanism may mediate the syndrome of metal fume fever.