Chronic granulomatous disease is characterized by recurrent infections that result from an inability of phagocytes to kill organisms effectively. We describe a patient with this disease who developed aspergillus pneumonia after shoveling moldy cedar wood chips. Despite aggressive therapy, the patient's condition deteriorated and he died. At autopsy, the lungs revealed diffuse granulomas, all of the same age, with aspergillus organisms confined to the granulomas. We propose the term "microgranulomatous aspergillosis" for this response, which does not conform to the commonly described aspergillus syndromes. We conclude that susceptible immunosuppressed patients should be advised to avoid occupational situations where high spore concentrations are generated.

We retrospectively evaluated the effect of the Loma Prieta earthquake on calls to 2 designated regional poison control centers (San Francisco and Santa Clara) in the area. In the immediate 12 hours after the earthquake, there was an initial drop (31%) in call volume, related to telephone system overload and other technical problems. Calls from Bay Area counties outside of San Francisco and Santa Clara decreased more dramatically than those from within the host counties where the poison control centers are located. In the next 2 days, each poison control center then handled a 27% increase in call volume. Requests for information regarding safety of water supplies and other environmental concerns were significantly increased. The number of cases of actual poisoning exposure decreased, particularly poison and drug ingestions in children. Most calls directly related to the earthquake included spills and leaks of hazardous materials and questions about water and food safety. Regional poison control centers play an essential role in the emergency medical response to major disasters and are critically dependent on an operational telephone system.

Pulmonary manifestations are not infrequent in the L-tryptophan-induced eosinophilia-myalgia syndrome (EMS). However, previous reports have not described the results of longitudinal pulmonary function, exercise testing, high-resolution computerized tomographic (HRCT) scanning of the chest, or detailed bronchoalveolar lavage (BAL) analysis. We report six patients with EMS who had dyspnea. The diffusing capacity for carbon monoxide was decreased in five patients tested. Exercise testing with arterial blood gas sampling in three patients was consistent with pulmonary vascular or parenchymal disease. Serial exercise testing in two of these patients demonstrated marked improvement temporally associated with corticosteroid treatment. In four patients, HRCT scanning of the chest was abnormal. One of these patients showed no abnormality on routine chest roentgenogram. Two patients undergoing BAL exhibited increased eosinophils in the lavage fluid; a third had elevated lymphocytes. Serial measurements of fibroblast proliferation-stimulating-activity in samples of BAL fluid obtained from serial examinations in two patients exhibited heightened pretreatment activity that returned to the normal range following corticosteroid therapy. In these two patients, increased proportions of T-suppressor/cytolytic (CD8+) cells were observed in the BAL fluid. Despite aggressive immunosuppressive therapy, one of the patients died of respiratory failure. Another remains markedly dyspneic with pulmonary hypertension. Of the remaining four patients, two exhibited resolution of pulmonary symptoms after systemic corticosteroid therapy, and two experienced partial improvement.

Diseases of the lung are among the work-related conditions most widely recognized among nonspecialists and the lay public. Five pulmonary conditions for which occupational or environmental exposures are not typically emphasized are reviewed here in their clinical-pathologic context. These are diffuse alveolar hemorrhage, lipoid pneumonitis, granulomatous lung disease, pulmonary alveolar proteinosis, and pulmonary vascular disease.

In order to indicate priorities for possible occupational health care planning activities, we evaluated occupational health risks, health services, and occupational research and training in Israel from the perspective of occupational medicine in the United States. We used available public information as well as data collected in a previous regional assessment of occupational health in the Negev. We estimated that each year 35% of the workforce in Israel may be exposed to high levels of noise, 4-11% to workplace toxins, and 7% to work injuries, all hazards warranting attention by health planners. Reviewing occupational health services we found that programmatic deficiencies limit the effective use of existing resources. We also evaluated the potential benefits of strengthened expert review in setting funding priorities for research and training in occupational safety and health in Israel.

There is no gold standard for determining poisoning incidence. We wished to compare four measures of poisoning incidence: International Classification of Diseases 9th Revision (ICD-9) principal (N-code) and supplemental external cause of injury (E-code) designations, poison control center (PCC) reporting, and detection by the Drug Abuse Warning Network (DAWN). We studied a case series at two urban hospitals. We assigned ICD-9 N-code and E-code classifications, determining whether these matched with medical records. We ascertained PCC and DAWN system reporting. A total of 724 subjects met entry criteria; 533 were studied (74%). We matched poisoning N-codes for 278 patients (52%), E-code by cause in 306 patients (57%), and E-code by intent in 171 patients (32%). A total of 383 patients (72%) received any poisoning N-code or any E-code. We found that PCC and DAWN reporting occurred for 123 of all patients (23%) and 399 of 487 eligible patients (82%), respectively. In multiple logistic regression, factors of age, hospital admission, suicidal intent, principal poisoning or overdose type, and mixed drug overdose were statistically significant predictors of case match or report varying by surveillance measure. Our findings indicate that common surveillance measures of poisoning and drug overdose may systematically undercount morbidity.

Metal fume fever is a flulike illness caused by zinc oxide inhalation and accompanied by an impressive pulmonary cellular response. We hypothesized that the syndrome is mediated by cytokines released in the lung after exposure to zinc oxide fume. We carried out 26 experimental welding exposures in 23 volunteer subjects, performing postexposure bronchoalveolar lavage (BAL) 3 h (n = 6), 8 h (n = 11), or 22 h (n = 9) after exposure. We detected tumor necrosis factor (TNF), interleukin-6 (IL-6), and interleukin-8 (IL-8) varying in a time- and exposure-related manner. The concentration of TNF in the BAL fluid supernatant was significantly greater at 3 h than at 8 h or 22 h after exposure (p < 0.05), exhibiting a statistically significant exposure-response relationship to airborne zinc at each follow-up time period (p < 0.05). TNF concentrations were statistically correlated with those of IL-6 in BAL supernatant obtained at 22 h (r = 0.78, p = 0.01) and with concentrations of IL-8 in BAL 8 h after exposure (r = 0.85, p = 0.001). IL-6 displayed a significant exposure-response relationship to zinc (p < 0.05) at 22 h. IL-8 exhibited a significant exposure-response relationship to zinc (p < 0.05) at 8 h after exposure, a time at which IL-8 correlated with marked increases in BAL fluid polymorphonuclear leukocytes (PMN) (r = 0.7, p = 0.01). Although we also detected interleukin-1 (IL-1) in BAL samples, this cytokine did not demonstrate a statistically significant exposure response. TNF, IL-6, and IL-8 in BAL fluid supernatant concentrations increased in a time and exposure-dependent fashion after zinc oxide welding fume exposure. The time course of increased cytokines, their correlations with one another and with PMN in the BAL fluid, and the consistency of our findings with the known kinetics and actions of these cytokines support the hypothesis that a network of cytokines is involved in the pathogenesis of metal fume fever.

We conducted a review of the literature detailing the respiratory effects of chlorine, an extremely important but toxic halogen. Historically, the heaviest mass inhalational exposures to chlorine resulted from World War I gassing. Currently potential human exposure to chlorine inhalation occurs in a variety of settings in the workplace, as a result of inadvertent environmental releases, and even in the home due to household cleaning mishaps. Chlorine species are highly reactive; tissue injury results from exposure to chlorine, hydrochloric acid, hypochlorous acid, or chloramines. Acute, high level exposure to chlorine gas in occupational or environmental settings results in a variety of dose-related lung effects ranging from respiratory mucus membrane irritation to pulmonary edema. Pulmonary function testing can reveal either obstructive or restrictive deficits immediately following exposure, with resolution over time in the majority of cases. However, some of those exposed may demonstrate long-term persistent obstructive or restrictive pulmonary deficits or increased nonspecific airway reactivity after high level exposure to chlorine gas. Symptoms and signs following inhalation of mixtures of chlorine-containing cleaners in the home are similar to those after occupational exposures and environmental releases. Although generally less severe, these events may be extremely common. Controlled human exposure data suggest that some subjects may be more responsive to the effects of chlorine gas; epidemiologic data also indicate that certain subpopulations (e.g., smokers) may be at greater risk of adverse outcome after chlorine inhalation. Although these findings are intriguing, additional study is needed to better delineate the risk factors that predispose toward the development of long-term pulmonary sequelae following chlorine gas exposure.

STUDY OBJECTIVE

To estimate the incidence of respiratory symptoms and physiologic abnormalities after inhalation of common irritant chemicals.

DESIGN

Structured interview of 12 months of poison control center (PCC) inhalation cases. Follow-up measurement of pulmonary function and airway responsiveness in a subgroup with symptoms 12 to 24 h postexposure.

SETTING

A regional PCC and clinical pulmonary function laboratory.

PATIENTS

Consecutive sample of 547 inhalation cases. Interviews of 299 subjects. Lung function follow-up in 10 subjects.

MEASUREMENTS AND MAIN RESULTS

Immediate respiratory symptoms were reported by 262 (88 percent) subjects; 12 to 24 h postexposure symptoms were reported by 130 (44 percent). Cigarette smoking was significantly related to immediate onset of cough (relative risk [RR] = 1.3; 95 percent confidence interval [CI], 1.1 to 1.5); both smoking (RR = 1.6; 95 percent CI, 1.1 to 2.1) and prior asthma (RR = 1.3; 95 percent CI, 1.1 to 1.6) were associated with wheeze, exhibiting multiplicative combined risk (RR = 2.8; 95 percent CI, 1.9 to 4.3). Of 10 subjects studied, none had abnormal airflow or lung volumes 8 +/- 4 days postexposure; 8 demonstrated increased airway responsiveness to methacholine. By three months, only one subject's increased responsiveness reversed; in three others, symptoms resolved but increased responsiveness remained.

CONCLUSIONS

Respiratory symptoms following irritant exposure are associated with smoking and asthma and typically resolve quickly. Continuing symptoms are associated with persistent increased airway responsiveness without other pulmonary function abnormalities. This may reflect newly induced airway changes or, alternatively, could represent underlying increased responsiveness in subjects symptomatic after irritant exposure.

OBJECTIVE

To estimate the incidence of work disability among adults with asthma and to evaluate a clinically based illness severity score as a predictor of such disability.

DESIGN

Baseline and follow-up telephone interviews and medical record review.

SETTING

University-based outpatient pulmonary specialty practice.

PATIENTS

Fifty-six patients interviewed at baseline; 42 reinterviewed 2 years later.

MEASUREMENTS

Work disability ascertained by interview report and defined as change in job duties, reduction in pay, or change in job or employment status attributed to asthma. Severity of asthma score derived from medical records and based on respiratory symptom frequency, asthma history, and prescribed medications. Pulmonary function by routine testing. Logistic regression analysis of the 5-year incidence of work disability on severity score and forced expiratory volume in 1 s (FEV1).

RESULTS

The 5-year work disability cumulative incidence was 19 percent for change in duties, 17 percent for reduction in pay, 20 percent for change in job or work status, and 36 percent for any of these measures. The median asthma score was 10 (range, 2 to 26). The mean FEV1 as a percent predicted (FEV1 percent) was 88 +/- 25 percent. Score and FEV1 percent were statistically correlated (r = -0.6, p < 0.0001). Severity of asthma score statistically predicted each measure of work disability (p < 0.01). Addition of FEV1 percent added little additional explanatory power to the logistic regression model (maximum chi 2 = 1.3, p > 0.2).

CONCLUSIONS

Work disability is common among adults with asthma. A severity of asthma score based on clinical variables is statistically correlated with lung function but appears to be a stronger predictor of disability than airflow measured at one point in time.