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Reduced lipid peroxidation and ischemia-reperfusion injury after lung transplantation using low-potassium dextran solution for lung preservation.

Ischemia-reperfusion injury is one of the significant problems in clinical lung transplantation. We investigated the effect of lung preservation with Euro-Collins solution (EC group) or low-potassium dextran solution (LPD group) on lipid peroxidation and ischemia-reperfusion injury in a pig model of lung allotransplantation. The donor lungs were preserved at 4 degrees C for 18 h. Left-sided single lung transplantation was performed, followed by 6 h of reperfusion. Lipid peroxidation was measured as thiobarbituric acid-reactive materials (TBARM) in bronchoalveolar lavage (BAL) fluid and effluent solutions from pulmonary artery (Effluent). After 18 h of ischemia, the LPD group showed lower TBARM in BAL and Effluent than the EC group (p < 0.05). After ischemia plus reperfusion, lung wetto-dry weight ratios and TBARM levels in BAL in the LPD group were lower than those of the EC group (p < 0.05). Lung wet-to-dry weight ratios correlated with TBARM levels in BAL (p < 0.05, r = 0.50). We conclude lipid peroxidation in BAL and Effluent may reflect the degree of ischemia-reperfusion injury, and lung preservation with LPD can reduce lipid peroxidation and lung injury as compared with EC.

Animals↗

Heat stress attenuates ventilator-induced lung dysfunction in an ex vivo rat lung model.

Our laboratory has previously shown decreased mortality rates and the attenuation of lung injury in rats exposed to heat stress (H) 18 h prior to induction of sepsis. In the present study, we examined the hypothesis that heat stress would protect lungs against ventilator-induced lung injury. Male Sprague-Dawley rats were anesthetized and randomly allocated to receive either sham treatment or exposure to heat (rectal temperature 41 degrees C, for 15 min). The lungs were harvested 18 h later, a pressure-volume (P- V) curve was constructed, and the lungs were either lavaged for cytokine and surfactant analyses (preventilation data) or were mechanically ventilated with VT 40 ml/kg in a warmed, humidified chamber. After 2 h of mechanical ventilation, another P-V curve was constructed and the lungs were lavaged for cytokine and surfactant analyses (postventilation data). Mechanical ventilation in control lungs produced a 47% decrease in chord compliance, an increase in lung lavage levels of tumor necrosis factor (TNF)-alpha (722 +/- 306 pg/ml), interleukin (IL)-1beta (902 +/- 322 pg/ml), and macrophage inflammatory protein-2 (MIP-2) (363 +/- 104 pg/ml) as compared with low levels of cytokines detected in preventilation data, and no change in percentage of surfactant large aggregates (LA). In contrast, in mechanically ventilated lungs from animals that were exposed to heat stress we observed a smaller decrease in chord compliance (17%), a significant attenuation in cytokine levels (TNF-alpha 233 +/- 119 pg/ml; IL-1beta 124 +/- 53 pg/ml; MIP-2 73 +/- 52 pg/ml; p < 0.05) and a significant increase in percentage LA compared with control animals. We conclude that exposing animals to heat stress confers protection against the effects of an injurious form of mechanical ventilation, by a mechanism that may involve attenuation of cytokines and preservation of some surfactant properties.

Animals↗

Alveolar macrophage migration. Influence of lung lining material and acute lung insult.

Migration of alveolar macrophages collected by lavage from normal rhesus monkeys was tested in an under agarose migration system. Lung lining material and serum albumin obtained from normal rhesus monkeys enhanced the random migration of alveolar macrophages. A chemotactic effect for alveolar macrophages was demonstrated in response to lung lining material. Gel filtration of lung lining material using Sephadex G-200 indicated the presence of 4 distinct fractions. Fraction IV, which had a molecular weight of less than 5,000 daltons, had the greatest ability to enhance alveolar macrophage migration. Macrophages obtained from lungs of rhesus monkeys after they breathed an oxidant gas (ozone) for 7 days demonstrated decreases in both the number of cells randomly migrating and the distance they migrated. The addition of normal lung lining material to macrophages exposed to ozone enhanced their random mobility but did not restore migration values to control values. Ozonized lung lining material or rhesus monkey serum did not significantly alter alveolar macrophage migration from that of control lung lining material or serum. These data indicate that components of the acellular lining material of the lung can produce directional migration of alveolar macrophages and may serve to direct the central flow and clearance of macrophages from alveolar regions. Intraluminal alveolar macrophage accumulation during lung insult with ozone appeared to be related more to migration inhibition of resident cells than to recruitment of additional cells by chemotaxis.

Animals↗

Dissemination of Pseudomonas aeruginosa during lung infection in hamsters. Role of oxygen-induced lung injury.

Pseudomonas aeruginosa was inoculated into the lungs of normal and oxygen-exposed hamsters. Air-breathing animals developed focal bronchopneumonias but viable organisms were not recovered from the lungs after 3 days; bacteremia was not detected but P. aeruginosa was isolated from the livers of 3 of 12 animals with positive lung cultures. Pseudomonas aeruginosa infection shortened the survival time of oxygen-breathing hamsters, and organisms persisted in the lungs during oxygen exposure. Focal bronchopneumonias were uncommon in animals inoculated after 4 days of oxygen exposure; the predominant histopathologic finding was accentuation of diffuse alveolar damage and increased numbers of scattered neutrophils. Pseudomonas aeruginosa was recovered from the livers of 15 of 18 oxygen-exposed animals in which lung colony counts exceeded 10(3)/lung; only 8 of these animals had demonstrable bacteremia. The concentration of elongation factor-2 in the livers and lungs of oxygen-exposed animals was reduced as colony counts of P. aeruginosa increased in the lungs of infected animals, suggesting exotoxin A activity in these organisms. These findings suggest that bacterial superinfection of injured lungs may account for both worsening lung function and impaired function of other organs.

Animals↗

Increases in lung tissue expression of intercellular adhesion molecule-1 are associated with hyperoxic lung injury and inflammation in mice.

Lung injury caused by breathing enriched oxygen continues to be a major problem in clinical medicine. Experimentally, hyperoxic lung injury is characterized by pulmonary edema and associated neutrophil accumulation. Although extensively investigated, the mechanisms for neutrophil accumulation and the role of this accumulation in hyperoxic lung injury remain controversial. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that when increased on endothelium by inflammatory cytokines leads to increased adhesion of neutrophils to the inflamed endothelium and transendothelial migration. The purpose of this study was to examine the role of inflammation in hyperoxia-induced lung injury by investigating ICAM-1 expression in the lungs of mice exposed to > 95% oxygen continuously. Lung tissue from mice exposed to > 95% oxygen was analyzed for ICAM-1 mRNA by slot blot analysis and for ICAM-1 protein expression. We also examined lungs from mice exposed to hyperoxia for up to 96 h by light microscopy to correlate pulmonary inflammation with ICAM-1 expression. We found that mRNA for ICAM-1 increased 56% over baseline after 48 h of exposure to hyperoxia, that ICAM-1 protein increased by more than 5-fold over baseline after 96 h of exposure to hyperoxia, and that lung inflammation and injury were not evident until 96 h of exposure. Our data demonstrate that exposure to hyperoxia causes an increase in ICAM-1 gene transcription and/or mRNA stability in mouse lungs, and that this increase is followed by an increase in ICAM-1 protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Lung cell oxidant injury. Enhancement of polymorphonuclear leukocyte-mediated cytotoxicity in lung cells exposed to sustained in vitro hyperoxia.

The oxidant damage of lung tissue during in vivo hyperoxic exposure appears to be amplified by neutrophils that release toxic amounts of oxygen metabolites. In our studies cloned lung epithelial cells (L2 cells), lung fibroblasts, and pulmonary artery endothelial cells were cultured under either ambient (Po(2) approximately 140 torr) or hyperoxic (Po(2) approximately 630 torr) conditions for 48 h (24 h for endothelial cells). After cultivation, phorbol myristate acetate- or opsonized zymosan-stimulated neutrophils were added to the cultivated monolayers for 4 h, and lung cell damage was quantitated using (51)Cr release as an index. The data show that stimulated neutrophils are able to injure the three lung cell lines tested, with endothelial cells being highly susceptible to this injury and L2 cells being slightly more susceptible than lung fibroblasts. The studies also demonstrate that all three lung cell lines exposed to sustained hyperoxia are more susceptible to neutrophil-mediated cytotoxicity than their time-matched air controls. Hydrogen peroxide was the main toxic oxygen metabolite because catalase (2,500 U/ml) completely protected the target cells. Equivalent quantities of hydrogen peroxide generated by glucose oxidase instead of by neutrophils gave a similar degree of target cell injury. Superoxide dismutase at high concentrations (250 mug/ml) provided some protection. Other systems that detoxify oxygen metabolites were without protective effect. These findings indicate that the increase in susceptibility of lung cells to neutrophil-mediated oxidant damage is a toxic effect of hyperoxia on lung cells. This specific manifestation of oxygen damage provides insight into the integration between primary mechanisms (oxygen exposure) and secondary mechanisms (release of oxygen metabolites by neutrophils) with respect to the cellular basis for pulmonary oxygen toxicity.

Animals↗

Fetal lamb lung lavage and its effect on lung phosphatidylcholine.

UNLABELLED: The lungs of intrauterine 135--136-day-old lambs were lavaged with amnionic fluid, with or without meconium, to determine the effect on lung phosphatidylcholine (PC) concentration, synthesis, and function. No differences were apparent between animals lavaged with amnionic fluid or amnionic fluid with meconium. When lavaged lungs were compared to nonlavaged controls, no detectable differences were observed in histology or the quantity of saturated (SPC) and unsaturated phosphatidylcholine (UPC). However, the lavaged lungs retained a larger fraction of maximal lung volume at 5 cm H2O distending pressure and the incorporation of (32P) orthophosphate into lung PC was significantly reduced. In addition, two lavaged animals who became acidotic (pH less than 7.20) exhibited decreased incorporation of 14C) palmitate into whole lung unsaturated, and saturated phosphatidylcholine. SPECULATION: These data indicate that amnionic fluid can reduce lamb lung de novo synthesis of PC and may contribute to the alterations in lung PC found in neonatal syndromes of respiratory distress. Acidosis may accentuate this effect.

Amniotic Fluid↗

Lung recruitment improves the efficiency of ventilation and gas exchange during one-lung ventilation anesthesia.

UNLABELLED: Atelectasis in the dependent lung during one-lung ventilation (OLV) impairs arterial oxygenation and increases dead space. We studied the effect of an alveolar recruitment strategy (ARS) on gas exchange and lung efficiency during OLV by using the single-breath test of CO(2) (SBT-CO(2)). Twelve patients undergoing thoracic surgery were studied at three points in time: (a) during two-lung ventilation and (b) during OLV before and (c) after an ARS. The ARS was applied selectively to the dependent lung and consisted of an increase in peak inspiratory pressure up to 40 cm H(2)O combined with a peak end-expiratory pressure level of 20 cm H(2)O for 10 consecutive breaths. The ARS took approximately 3 min. Arterial blood gases, SBT-CO(2), and metabolic and hemodynamic variables were recorded at the end of each study period. Arterial oxygenation and dead space were better during two-lung ventilation compared with OLV. PaO(2) increased during OLV after lung recruitment (244 +/- 89 mm Hg) when compared with OLV without recruitment (144 +/- 73 mm Hg; P < 0.001). The SBT-CO(2) analysis showed a significant decrease in dead-space variables and an increase in the variables related to the efficiency of ventilation during OLV after an ARS when compared with OLV alone. In conclusion, ARS improves gas exchange and ventilation efficiency during OLV. IMPLICATIONS: In this article, we showed how a pulmonary ventilatory maneuver performed in the dependent lung during one-lung ventilation anesthesia improved arterial oxygenation and dead space.

Adult↗

Age-bodyweight relationships to lung growth in the F344 rat as indexed by lung weight measurements.

Measurements of the total lung weights and the individual weights of the lung lobes of male F344 rats ranging in age from about 30 days to 140 days or more were made in order to determine how lung growth and the growths of the individual lung lobes relate to bodyweight over the course of maturation of this species. Additionally, in this study we also compared how each lung lobe grows relative to total lung growth, evaluated the ratios of lung dry weight to wet weight and obtained information on the weights of the trachea and extra-hilar main-stem bronchi as the F344 rat matures. The wet weights WLT of the trachea-lung preparations and the pooled lobe weights WPL as functions of rat bodyweight WB could be readily described by the following logarithmic expressions: WLT = 0.596 ln WB - 1.923, r = 0.95; WPL = 0.464 ln WB - 1.566, r = 0.96. Expressed as percentages of the pooled lobe weights, the individual lobes remained at constant values as the animals grew with the exception of the right caudal lobe which decreased between bodyweights of 72 and 96 g; absolute wet weight measurements of the individual lobes indicated that the right cranial, right middle and right intermediate lobes actually decreased in weight between bodyweights of 300 and 385 g. The dry weights of the lobes consistently represented approximately 22% of the wet weights regardless of animal age or bodyweight, and on average the airways represented about 20% of the weights of the intact airway-lung preparations over the course of animal maturation.

Aging↗

An epidemiological study of lung cancer in Xuan Wei County, China: current progress. Case-control study on lung cancer and cooking fuel.

In Xuan Wei County, Yunnan Province, lung cancer mortality rates are among China's highest in males and females. Previous studies have shown a strong association of lung cancer mortality with air pollution from "smoky" coal combustion. In the present quantitative risk assessment of indoor air pollution study, the result strongly shows an obvious on-site exposure-response relationship between benzo[a]pyrene concentration in indoor air and lung cancer mortality and strongly supports the hypothesis that indoor air pollution is the main risk factor in inducing lung cancer in Xuan Wei County. In the present case-control study, the result shows that in females, the presence of lung cancer is statistically significantly associated with chronic bronchitis and family history of lung cancer. The results also suggest an association of lung cancer with duration of cooking food, but not with passive smoking. In males, the presence of lung cancer is associated with smoking, bronchitis, family history of lung cancer, and personal history of cooking food.

Air Pollution, Indoor↗

Abnormal lung sounds in patients with asthma during episodes with normal lung function.

Even in patients with clinically stable asthma with normal lung function, the airways are characterized by inflammatory changes, including mucosal swelling. In order to investigate whether lung sounds can distinguish these subjects from normal subjects, we compared lung sound characteristics between eight normal and nine symptom-free subjects with mild asthma. All subjects underwent simultaneous recordings of airflow, lung volume changes, and lung sounds during standardized quiet breathing, and during forced maneuvers. Flow-dependent power spectra were computed using fast Fourier transform. For each spectrum we determined lung sound intensity (LSI), frequencies (Q25%, Q50%, Q75%) wheezing (W), and W%. The results were analyzed by ANOVA. During expiration, LSI was lower in patients with asthma than in healthy controls, in particular at relatively low airflow values. During quiet expiration, Q25% to Q75% were higher in asthmatics than in healthy controls, while the change of Q25% to Q75% with flow was greater in asthmatic than in normal subjects. The W and W% were not different between the subject groups. The results indicate that at given airflows, lung sounds are lower in intensity and higher in pitch in asthmatics as compared with controls. This suggests that the generation and/or transmission of lung sounds in symptom-free patients with stable asthma differ from that in normal subjects, even when lung function is within the normal range. Therefore, airflow standardized phonopneumography might reflect morphologic changes in airways of patients with asthma.

Adult↗

Association between lung cancer incidence and family history of lung cancer: data from a large-scale population-based cohort study, the JPHC study.

STUDY OBJECTIVES: To clarify the possibility of a hereditary predisposition to lung cancer, we investigated the association between a family history of lung cancer and subsequent risk of lung cancer in a large-scale, population-based cohort study. DESIGN: We investigated 102,255 middle-aged and older Japanese subjects (48,834 men and 53,421 women) with 13-year follow-up. A total of 791 cases of lung cancer were newly diagnosed during the follow-up period. RESULTS: A family history of lung cancer in a first-degree relative was associated with a significantly increased risk of lung cancer (hazard ratio [HR], 1.95; 95% confidence interval [CI], 1.31 to 2.88). The association was stronger in women than in men (HR, 2.65; 95% CI, 1.40 to 5.01 and HR, 1.69; 95% CI, 1.03 to 2.78, respectively), and in never-smokers than in current smokers (HR, 2.48; 95% CI, 1.27 to 4.84 and HR, 1.73; 95% CI, 0.99 to 3.00, respectively). In addition, family history was more strongly associated with the risk of squamous cell carcinoma than with other histologic types (HR, 2.79; 95% CI, 1.37 to 5.68), while no clear increase in risk was observed in adenocarcinoma and small cell carcinoma. A family history of overall cancer was not associated with an increased risk of lung cancer. CONCLUSIONS: These results suggest that those with a family history of lung cancer are more likely to acquire lung cancer themselves.

Adenocarcinoma↗

Thoracoscopic lung biopsy for diffuse infiltrative lung disease.

Thoracoscopic lung biopsy is becoming the procedure of first choice for the diagnosis of many localized and diffuse lung diseases. We have performed thoracoscopic lung biopsy for 17 patients with diffuse infiltrative lung disease, in Kurume University Hospital. There were 13 females and 4 males with a mean age of 48 years (range: 19-71 years). Thoracoscopic surgical biopsy was performed in the right lung in 12 and in the left lung in 5. Adequate lung tissue from each case was obtained for pathological examination. The mean surgical biopsy time was 49 min (range: 25-72 min) and bleeding was negligible. The mean duration for chest tube drainage was 2.6 days. No postoperative complication such as prolonged air leakage occurred. A specific diagnosis from the biopsy was achieved in 13 (76.4%) of the 17 cases. In only 6 (35.2%) of the 17 cases, the pathological diagnosis was the same as that from the thoracoscopic biopsy. In these 6 cases, the same diagnosis was obtained only in those with idiopathic interstitial pneumonitis or diffuse panbronchitis. Thoracoscopic lung biopsy was safe and useful for diagnosis for diffuse infiltrative lung disease.

Adolescent↗

Methods to evaluate the effects of toxic materials deposited in the lung on immunity in lung-associated lymph nodes.

Intratracheal instillation of sheep red blood cells (SRBC) induced a primary immune response in lung-associated lymph nodes of Chinese hamsters and Fischer-344 rats. Few or no anti-SRBC antibody forming cells (AFC) were found in the spleen or cervical lymph nodes after intratracheal immunization. The number of AFC was significantly suppressed in the lung-associated lymph nodes from hamsters exposed by inhalation of 239PuO2 and in rats exposed by intratracheal instillation of benzo(a)pyrene (BaP). Although the immunologic function of the lung-associated lymph nodes was suppressed by 239PuO2 and BaP exposure, there was no observable increase in the number of AFC in distant lymphoid tissues. These data indicate that damage to lung cells and/or cells in lung-associated lymph nodes can suppress immunity induced by deposition of antigen in the lung. Even though lung-associated lymph nodes in exposed animals contained lower numbers of AFC, antigen instilled into the lungs of exposed animals did not significatnly translocate to distant lymphoid tissues. This indicates that the antigen filtering capacity of the lung-associated lymph nodes was not altered.

Aerosols↗

Evidence for immune responses to a self-antigen in lung transplantation: role of type V collagen-specific T cells in the pathogenesis of lung allograft rejection.

We have reported that lung allograft rejection involves an immune response to a native protein in the lung, type V collagen (col(V)), and that col(V)-induced oral tolerance prevented acute and chronic rejection. In support of these findings col(V) fragments were detected in allografts during rejection, but not in normal lungs. The purpose of the current study was to isolate and characterize col(V)-specific allograft-infiltrating T cells and to determine their contribution to the rejection response in vivo. Two col(V)-specific T cell lines, LT1 and LT3, were isolated from F344 (RT1(lv1)) rat lung allografts during rejection that occurred after transplantation into WKY (RT1(l)) recipients. Both cell lines, but not normal lung lymphocytes, proliferated in response to col(V). Neither LT1 nor LT3 proliferated in response to alloantigens. LT1 and LT3 were CD4(+)CD25(-) and produced IFN-gamma in response to col(V). Compared with normal CD4(+) T cells, both cell lines expressed a limited V-beta TCR repertoire. Each cell strongly expressed V-beta 9 and 16, but differed in expression of other V-betas. Adoptive transfer of each cell line did not induce pathology in lungs of normal WKY rats. In contrast, adoptive transfer of LT1, but not LT3, caused marked peribronchiolar and perivascular inflammation in isograft (WKY) lungs and abrogated col(V)-induced oral tolerance to allograft (F344) lungs. Collectively, these data show that lung allograft rejection involves both allo- and autoimmune responses, and graft destruction that occurs during the rejection response may expose allograft-infiltrating T cells to potentially antigenic epitopes in col(V).

Animals↗

[Diagnosis of small peripheral lung cancers using spiral computed tomography lung cancer screening].

Small peripheral lung cancers can be detected by spiral or helical computed tomography (CT). We applied mobile spiral CT as the first step in further examination (or secondary screening) for lung cancer. We detected 86 lung cancers per 100,000 persons without spiral CT, and 102 patients with spiral CT. Using the latter method, the resection rate and the rate of early-stage lung cancer increased significantly from 48.6% to 67.3% (p < 0.01) and from 21.1% to 35.1% (p < 0.05), respectively. Good results were obtained with mobile CT, especially in women. The mean tumor size of lung cancer detectable with CT was 7 mm smaller than that detected by the previous method. The mean tumor size was only less than 20 mm in females. Overall 787 lung cancers per 100,000 persons were detected using spiral CT for primary screening (1,039 lung cancers/100,000 in men). We must investigate whether the new CT screening system for lung cancer really leads to a lower mortality rate compared with the previous methods. When small nodular lesions with ground-glass opacity could not be diagnosed, the subsequent period up to 10 months can be used to obtain a final diagnosis, regardless of their malignancy. This paper reports specific findings of small peripheral lung cancers, and review the methods of diagnosis for small-sized tumors.

Carcinoma, Small Cell↗

Genetic analysis of three-dimensional shape of mouse lung tumors reveals eight lung tumor shape-determining (Ltsd) loci that are associated with tumor heterogeneity and symmetry.

Most lung tumor linkage studies focus on identifying loci that confer susceptibility or resistance irrespective of the tumor types developed. However, different mouse strains develop different types of lung tumors. A major obstacle for genetic studies of these differences is the lack of reproducible, quantitative, and uniform assessment of tumor type. We have previously described a new variable (Rratio) that assesses the three-dimensional shape of lung tumors in a quantifiable way and showed that nonspherical tumors are correlated with tumor heterogeneity and with a tendency to asymmetrical growth (N. Tripodis and P. Demant, Exp. Lung Res., 27: 521-531, 2001). In the present study, we use the Rratio variable to search for quantitative trait loci affecting tumor phenotype. We tested the F(2) cross between the susceptible strain O20 and the recombinant congenic strain OcB-9. Both develop mixed alveolar and papillary lung tumors, and the OcB9 tumors are, on average, more elongated than the O20 ones. We mapped eight new lung tumor shape-determining loci (Ltsd1-8) involved in mutual interactions. Two of these loci, Ltsd1 and Ltsd3, seem to play a major role in tumor shape formation. The Ltsd4 locus was confirmed in a second F(2) cross between strain O20 and the recombinant congenic strain OcB-6. Genotype-phenotype associations show that nonspherical tumors are correlated with tumor heterogeneity and nonsymmetrical (focal) development of structures. Most of the new Ltsd loci map in regions where susceptibility to lung cancer (Sluc) loci have been previously mapped, raising the question of whether they are identical or closely linked loci. Based on models of tumor growth indicating that supply of nutrients and the ability to create a capillary network may be shape-determining factors (G. P. Pescarmona et al., Med. Hypoth., 53: 497-503, 1999), we suggest as likely candidates for the Ltsd loci genes involved in angiogenesis, vascularization, and capillary patterning. This is the first set of loci that affects qualitative aspects of lung tumors and may provide biologically and clinically interesting indicators of lung tumor progression.

Animals↗

A histologic demonstration of siliceous materials in simian lung mite infected lung tissues by microincineration.

Approximately 90% of freshly imported macaques and other Old World Monkeys are known to be infected with respiratory mites. The lung associated pigments are integral components of pulmonary acariasis in Old World Monkeys; at least three distinctive pigmental bodies are identified in association with lung mite infection. Two major components of pigments are recently identified as silica by using elemental analysis using a high voltage electron microscope and an energy-dispersive X-ray analysis technique. Since a limited number of infected monkey lung tissues and associated pigments can be examined by this tedious procedure, it was important for us to examine much greater number of specimens to verify our initial observation. Ten microincineration technique described provided a unique and practical way to identify the mineral elements in as many 27 histologic sections within a short span of time. Silica and silicates are heat resistant whereas majority of organic materials including lung mite parasites disintegrated under the extreme temperature. Mineral elements were exclusively located within the polarizable white ash. More than 90% of total pigmental bodies identified were found to be related to siliceous materials in 20 incinerated infected monkey lung tissues whereas five noninfected lungs similarly examined did not reveal any pigmental bodies. Other than a small of fine granular mucin substances which were PAS positive, the majority of lung mite associated pigments such as large granules of hemosiderin, needle-like crystals and other fine granules engulfed by macrophages were identified to be siliceous materials as they have persisted even after microincineration. Mite parasites and other organic materials were completely disintegrated. Similar pigmental bodies examined by microscope X-ray analysis were positive for silicate. This finding suggests that lung mite infection in Old Monkeys apparently predisposed silicosis. Therefore, until the link between lung mite infection and silicosis is clarified, experimental inhalation toxicologic findings in mite-infected Old World monkeys should be interpreted cautiously.

Animals↗