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D D McEuen

Publications and source records attributed to D D McEuen.

7 recordsLinked to original sources

Inorganic particulates associated with pulmonary alveolar proteinosis: SEM and X-ray microanalysis results.

Twenty-four cases of pulmonary alveolar proteinosis (PAP) were studied by light microscopy (LM) and scanning electron microscopy (SEM) to test the hypothesis that PAP was related to silica exposure. Increased numbers of birefringent particles (vs. controls) were found in 78% of PAP cases. SEM was used to locate inorganic particulates in situ, which were individually analyzed using energy dispersive X-ray analysis. When analyzed as an aggregate group of cases, no specific inorganic particulate was evidently associated with the PAP reaction. However, analysis of individual cases revealed more specific associations. The concentration of particles determined by SEM exceeded that found by LM by a factor ranging from 2.7 to 964. The concentration of inorganic particulates per cm3 in the areas of PAP ranged from 1.3 X 10(7) to 1.02 X 10(9). Controls all had less than 10(7) particles per cm3. Available environmental history correlated well with particulate analysis results, e.g., silica in a sandblaster, metal fumes in a welder, and cement particles in a cement finisher. Particulates with unique composition were also found in cases with unavailable histories, e.g. metal fumes suggestive of welding or soldering exposure, silicates suggestive of fine particle exposure (greater than 50% of particles less than 1 micron). Only 1 case (the sandblaster) showed greater than 50% of the particles to be silica. Of the 5 infants with PAP, 3 showed the major particulate to be talc, and 1 had evidence of toxic cadmium selenide fume exposure. These results are consistent with the hypothesis that PAP, at least in the majority of cases, is associated with exposure to small inorganic particulates of several types.

Electron Probe Microanalysis↗

Particulate concentrations in pulmonary alveolar proteinosis.

Quantitative birefringent particle counts per 10 high-power fields in lung tissue were correlated with age, sex, and occupational exposure in 37 cases of pulmonary alveolar proteinosis. Counts were significantly higher in pulmonary alveolar proteinosis cases in both regions of alveolar proteinosis (47 +/- 11) and perivascular and peribronchiolar areas (dust retention areas) (275 +/- 65) than in 13 controls (5 +/- 3 and 79 +/- 23, respectively). Of a total of 8619 particles, 4817 were less than 1 micron, and 3771 were 1 to 10 microns in diameter. Fifty-nine percent were round, 19% fibrous, and 22% irregular. When analyzed individually, 20 of 37 cases (78%) had alveolar particle counts significantly higher than controls, and 10 of 26 cases had dust-retention area counts greater than controls (P less than 0.050). Known or possible occupational exposure was ascertained in 13 cases. In the remaining 24 cases insufficient occupational information was available. The mean age of the pulmonary alveolar proteinosis patients was 33 +/- 4 years, and of the controls, 40 +/- 7 years, and there was a male-to-female ratio of approximately 3:1. We propose that many cases of pulmonary alveolar proteinosis will ultimately be shown to be associated with environmental exposures to fine dusts or fumes.

Adolescent↗

Myelopoiesis in the infected burn.

A modified bone marrow clonal cell culture technique was used to study granulocyte production during burn injury and sepsis. When rats were inflicted with a 30 percent third-degree scald burn, marrow cellularity and colony-forming units in culture (CFU-C) per 10(5) marrow cells increased progressively to four times normal by 7 days after injury. Conversely, When animals were burned and the burn wound immediately seeded with 10(8) Pseudomonas organisms, CFU-C declined steadily until the day of death and reflected a progressive loss in marrow cellularity. Further studies were conducted replacing or mixing standard colony-stimulating serum with burn, burn-infected, or normal rat serum. The results indicated that colony-stimulating activity could be supplied by postburn serum, but not with normal or burn-infected rat serum. Additionally, serum from burned-infected animals significantly inhibited colony formation when added to the standard colony-stimulating serum. Marrow failure appears to be the major cause for granulocytopenia in burn infection and may partly be serum mediated.

Animals↗

Correlation between pseudomonas burn wound infection and granulocyte antibacterial activity.

The relationship of granulocyte bactericidal activity with three strains of pseudomonas and the virulence of these same organisms in a scald-burned rat model was investigated. Resistance to bactericidal activity was measured for each strain, using an in vitro assay and normal rat peritoneal granulocytes. Mortality was recorded for rats receiving a 30% third-degree scald burn with simultaneous pseudomonas burn wound infection. A positive correlation between mortality and resistance to bactericidal activity of granulocytes was obtained. These studies stress the importance of pseydomonas strain specificity in burn wound infection and indicate that mortality from these strains may be specifically related to their resistance to the bactericidal activity of leukocytes.

Animals↗

Granulocyte function and Pseudomonas burn wound infection.

Granulocyte function in burn injury has been evaluated with an in vitro animal assay. Bactericidal activity, using this technique, was markedly depressed only when granulocytes from scald burned rats were challenged with each of three strains of Pseudomonas aeruginosa in the presence of autologous postburn serum or heat-inactivated serum. Preincubation of postburn and normal serum at 37 degrees C for 1 h resulted in normal phagocytosis. These studies validate an investigation of plasma and/or granulocyte replacement therapy in the burned patient.

Animals↗