Ocular injuries and diseases at a combat support hospital in support of Operations Desert Shield and Desert Storm.

A retrospective review of all emergency department visits to a combat support hospital (one of four combining to support 150,000 troops) during Operations Desert Shield and Desert Storm was conducted, and all medical records of patients with ocular complaints were analyzed. Ocular injury and/or disease accounted for 14% (108/767) of these visits to the emergency department. Of 108 patients with ocular complaints, corneal foreign bodies (18), ocular burns (14), and traumatic iritis (eight) were the most common injuries treated, while blepharitis and conjunctivitis (16) were the most common diseases. Nineteen (18%) of the 108 patients with ocular complaints were treated during support of the ground war in Iraq (13 were Iraqi prisoners). Ophthalmic injuries accounted for 13% (19/149) of all ground war casualties; however, eight individuals had associated injuries deemed more significant than those of ocular concern. This incidence continues the trend of earlier wars, which has demonstrated a steady increase in ocular injuries. Most US Army troops were issued protective goggles, but only three of 92 American patients wore them at the time of their injury and/or disease.

Pulmonary responses to purified zinc oxide fume.

BACKGROUND: Metal fume fever is a flu-like illness caused by zinc oxide fume inhalation and mediated by unknown mechanisms. It is one of a group of work-related febrile inhalational syndromes. We studied bronchoalveolar lavage (BAL) obtained from cigarette smoking and nonsmoking human volunteers after controlled exposure to purified zinc oxide fume to explore the possible roles of proinflammatory cytokines in this condition. METHODS: We studied 14 volunteers after inhalation exposure to purified zinc oxide fume and after sham exposure to air. The mean cumulative exposure was 537 +/- 232 mg min per cubic meter elemental zinc. Twenty hours after exposure we performed BAL. We analyzed BAL cells and studied BAL supernatant for cytokines including tumor necrosis factor-alpha (TNF alpha), interleukin(IL)-8, and IL-1 by enzyme-linked immunosorbant assay (ELISA). RESULTS: Polymorphonuclear leukocytes (PMNs) were significantly increased in the BAL fluid obtained post-exposure compared to sham (mean difference = 41.3 +/- 16.8 x 10(3) per mL; p < 0.05). Cumulative zinc exposure positively correlated with exposure-sham differences in BAL supernatant concentrations of both TNF (r2 = 0.58; p = .002) and IL-8 (r2 = 0.44, p = 0.01). Exposure-sham concentration differences in BAL supernatant IL-8 and BAL PMNs were also positively correlated (r2 = 0.60; p < 0.001). Cigarette smoking was not associated with exposure-sham differences in BAL TNF or IL-8, but did demonstrate a packs-per-day dependent increase in BAL supernatant IL-1 (t = 2.3, p = 0.04) post-exposure compared to sham, after taking into account the zinc exposure response. CONCLUSIONS: Purified zinc oxide fume inhalation causes an exposure-dependent increase in proinflammatory cytokines and PMNs in the lung. This supports a role for cytokine networking in mediating metal fume fever.

Pulmonary responses after wood chip mulch exposure.

Organic Dust Toxic Syndrome (ODTS) is a flu-like syndrome that can occur after inhalation of cotton, grain, wood chip dusts, or other organic dusts or aerosols. We investigated whether inflammatory pulmonary responses occur, even after relatively brief, low-level wood chip mulch exposure. Six volunteers were exposed to wood chip mulch dust. Total dust and/or endotoxin levels were measured in five subjects. Pulmonary function and peripheral blood counts were measured before and after exposure in each subject. Bronchoalveolar lavage (BAL) was performed in each subject after exposure, and cell, cytokine, and protein concentrations were measured. Control BAL without previous exposure was also performed on three of the subjects. Three of six subjects had symptoms consistent with ODTS. No clinically relevant or statistically significant changes in pulmonary function tests after exposure were found. Three subjects manifested a marked elevation in neutrophil percentage in their BAL (range, 10 to 57%). When these three subjects underwent control BAL, the postexposure comparison demonstrated an increase in neutrophil levels of 154 +/- 89 x 10(3)/mL (mean +/- standard error; P = 0.22). The mean increase in BAL interleukin-8 levels after exposure, compared with paired control values, was 11.2 +/- SE 2.5 pg/mL (P = 0.047). There was also an increase in BAL interleukin-6 levels that reached borderline significance (6.4 +/- SE 2.0 pg/mL; P = 0.08). Tumor necrosis factor levels were increased in all three subjects' BAL as well (0.4 +/- SE 0.2 pg/mL), but this change was not statistically significant (P = 0.2). Our findings of increased BAL proinflammatory cytokine and neutrophil levels are consistent with the theory that cytokine networking in the lung may mediate ODTS.

The inpatient experience of a U.S. Army combat support hospital in the Persian Gulf during non-combat and combat periods.

To identify the key factors that control the workload of a U.S. military hospital during deployment, we studied all 574 admissions to the 46th Combat Support Hospital (CSH) during its deployment during Operations Desert Shield and Desert Storm. Date of admission, admission diagnosis, admitting service, length of hospitalization, disposition, nationality, and sex for each admission were analyzed. The workload of the 46th CSH varied markedly during the different periods of its deployment. Three hundred seventy-eight (66%) of the 574 admissions occurred during Operation Desert Shield, although admissions occurred at the greatest rate during the short Ground War phase of Operation Desert Storm. Iraqis accounted for 82% of the admissions during the Ground War and 51% of the total Desert Storm admissions. The most important factors determining the workload of the 46th CSH were the combat situation, effectiveness of the air-evacuation system, and the obligation to treat enemy soldiers and civilians.

Medical care of Iraqis at a forwardly deployed U.S. Army hospital during Operation Desert Storm.

To evaluate the injuries and diseases and their subsequent care for both Iraqis and U.S. soldiers in the Persian Gulf War, we analyzed all 196 admissions to the 46th Combat Support Hospital during Operation Desert Storm, with primary focus on the 118 admissions during the Ground War. Admission diagnosis was used to classify injury or disease. Percentage of patients who underwent surgery for combat wounds and percentage of patients who were air-evacuated were used as measurements of quality of care. The proportion of Iraqi patients who had been wounded in action was significantly higher than the proportion for Americans (95 vs. 53% for the Ground War). The rate of surgical procedures per wounded patients admitted was the same for Iraqis (28%) as for Americans (27%). Rates of air-evacuation for Iraqis were not statistically different from those for Americans in the same category of admission diagnoses. These last two findings suggest that the quality of care given to Iraqis was the same as that given to Americans.

Occupational asthma.

Occupational asthma is the most common occupational lung disease in the world. Occupational asthma comprises approximately 25-50% of occupational lung diseases and is responsible for up to 15% of all asthma cases. Either immunologic or nonimmunologic causes may be responsible for occupational asthma. There are approximately 250 compounds known to cause occupational asthma. Common examples include flour, animal dander, isocyanates, and latex. The diagnosis of occupational asthma depends on an accurate history of asthma and documentation that the asthma is caused by workplace exposure. Peak flow measurements are commonly used to provide data to define this relationship. Spirometry and bronchial provocation testing are also helpful. The key management tool in occupational asthma is avoidance of the causative agent. Avoidance is more important than treatment with medications. Occupational asthma can have major socioeconomic impacts on an individual, and the diagnostic work-up and management needs to be performed with this in mind.

Cytokines in metal fume fever.

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.