Terminal Air Research Articles

Air pollution and bronchitic symptoms in Southern California children with asthma.

People who live in cities with dirty air have blacker lungs than people who live in rural areas with less air pollution. This is because, although particulates larger than 10 microm are filtered out when inhaled air passes through the nose, smaller particulates reach the lower airways. The particulates that reach the alveoli (the terminal air pockets of the lungs) stay there permanently. This accounts for the fact that a person who has lived in a polluted city for many years has blacker lungs than one who has lived in a polluted city for a shorter time.

The role of apoptosis in normal and accelerated lung development in fetal rabbits

Background/Purpose: During fetal development, the mammalian lung undergoes progressive parenchymal involution. Intrauterine tracheal occlusion induces accelerated architectural maturation of the fetal lungs associated with depletion of the surfactant-producing type II cells. This study investigates the spatiotemporal pattern of apoptosis during normal fetal lung development and its modulation in tracheal occlusion-induced accelerated fetal lung growth.Methods: Fetal rabbit lungs were studied at 25 to 31 days' gestational age (DGA; term, 31 DGA), corresponding to late pseudoglandular through terminal air sac stages of fetal lung development. Intrauterine tracheal ligation (TL) was performed at 24 DGA. TL fetuses were monitored until 29 DGA, a time-point previously shown to coincide with significant type II cell depletion. Apoptotic cells were identified by light and electron microscopy, as well as terminal deoxynucleotidyl transferase-mediated dUTP-FITC nick-end labeling (TUNEL). Epithelial (type I and II) cell apoptosis was studied by TUNEL labeling in conjunction with antisurfactant protein and anticytokeratin immunohistochemistry. DNA fragmentation was analyzed by gel electrophoresis. Sham-operated littermates served as controls.Results: The number of apoptotic cells progressively increased with advancing lung growth and architectural maturation (apoptotic index [Al] 1.2 ± 0.7 x 10−3 at 25 DGA v 4.2 ± 1.4 x 10−3 at 31 DGA; P < .05, analysis of variance). In TL fetuses, the apoptotic rate was significantly higher than in non-TL fetuses from the third postligation day on, coinciding with the onset of significantly increased airspace distension (Al 4.9 ± 1.3 x 10−3 in TL v 2.6 ± 0.4 x 10−3 in controls at 29 DGA; P < .05, Student's t test). Apoptosis occurred in parenchymal cells and in isolated cells within the airspaces. The apoptotic activity of type II cells was significantly higher in TL fetuses than C fetuses at 29 DGA (type II Al 25.5 ± 6.3 x 10−3 in TL v 2.3 ± 0.8 x 10−3 in C; P < .001). Electron microscopic studies confirmed the presence of apoptotic nuclei in interstitial macrophages and in degenerating intraluminal type II cells. DNA analysis showed nucleosomal bands.Conclusions: Normal fetal lung development is associated with a progressive increase of epithelial and interstitial apoptotic activity, a process enhanced by TL. Tracheal occlusion induces a significant increase of type II cell apoptosis, which likely contributes to the observed type II cell depletion after TL. We speculate that fetal type II cell apoptosis after TL may be induced by mechanical distension (stretch) of the airspaces.

A study of energy use and satisfactory zone ventilation of different outdoor air ventilation strategies for terminal reheat variable air volume systems

Increased building indoor air quality (IAQ) complaints due to reduced outdoor air ventilation rates led to ASHRAE Standard 62–1989. Even though the stipulated standard total outdoor ventilation flow rate may be drawn into the HVAC system, thermal imbalances in the various zones of the building can lead to certain zones being starved of the specified ventilation flow rate, thereby creating localized IAQ problems. The objective of this paper is to compare the differences in energy use and ventilation air flow rates supplied to different zones in the building for three different practical outdoor air ventilation strategies all of which are identical in performance at design conditions but which differ under part-load operation. A simplified simulation methodology (which past studies have demonstrated to be useful for field evaluation of actual buildings) has been used to predict the heating and cooling energy use of a two-zone terminal reheat variable air volume (TRVAV) system during part-load operation specified by varying outdoor temperature and humidity conditions. The trade-off between outdoor air intake and energy use are studied for the following ventilation strategies for a typical 10,000 m 2 commercial building: (i) constant outside air intake based on a value 20% higher than the ASHRAE minimum ventilation rate, (ii) constant ventilation air intake fraction, and (iii) ventilation air intake based on the unfavorable zone requirements (even though the other zone may be over-ventilated). How this trade-off is impacted by bullding size has also been investigated. Finally, we use bin data for Dallas, TX (a moderately hot and humid location) and Seattle, WA (a mild location) in order to study the differences in energy use and zone ventilation flows of different ventilation strategies due to building location. The effect of economizer cycles and of varying ventilation strategies depending upon diurnal building schedules have not been considered in this study. The results of this study which are based on a simplified HVAC simulation approach are consistent with conclusions reached by other researchers Using more detailed simulation models. This suggests that sound and meaningful diagnostic insights of actual building performance and operating strategies can be obtained from such simplified simulations.

Functional and pathological effects of prolonged hyperoxia in neonatal mice.

Bronchopulmonary dysplasia (BPD) commonly develops in premature infants. An improved understanding of the pathophysiology of BPD requires better models. In this study, neonatal FVB/N mice were exposed to room air or 85% oxygen for 28 days. Neonatal hyperoxia resulted in decreased alveolar septation, increased terminal air space size, and increased lung fibrosis. These changes were evident after 7 days and more pronounced by 28 days. Decreased alveolarization was preceded by decreased proliferation of lung cells. After 3 days of hyperoxia, cell proliferation was decreased compared with room air littermates. Cell proliferation continued to be decreased in the first 2 wk but normalized by 4 wk. Hyperoxia caused an increased number of inflammatory cells in lung tissue and in lung lavage fluid. Analysis of lung tissue RNA by RT-PCR showed that hyperoxia increased expression of the proinflammatory cytokines interleukin-1alpha and macrophage inflammatory protein-1alpha. Prolonged neonatal hyperoxia caused functional changes, decreasing lung volume and pulmonary compliance. We conclude that prolonged exposure of neonatal mice to hyperoxia creates a lesion that is very similar to human BPD and suggests that altered cell proliferation may be important in the pathogenesis of chronic neonatal lung disease.

Morphometric estimate of gas-exchange tissue in the new-born tammar wallaby, Macropus eugenii

The lung of the new-born marsupial is at the terminal air sac stage of development. The maturational status of the lung of new-born tammar wallaby was assessed using established morphometric techniques and the results were compared with data from a morphometric study of the lung of the rat. Volume densities of the parenchyma and non-parenchyma, conducting airways and blood vessels, the relative volumes of airspace and tissue, the thickness and the composition of the septa differed between the two species. In addition the volume of capillaries and the surface area of the effective gas-exchange tissue was greater in the new-born rat than in the new-born tammar pouch young. The lung of the new-born tammar appears to be at an earlier phase of the terminal air sac stage than that of the new-born rat. Lung development up to birth appears to be commensurate to the metabolic needs of the organism at birth.

Bronchopulmonary dysplasia of the premature baby: an immunohistochemical study.

Prematurely born infants who required assisted ventilation may develop chronic lung disease or bronchopulmonary dysplasia (BPD). The cells involved in the reparative process of the premature lung are not well defined. The repair of injured tissues is a highly standardized process and the most important cells are activated (modulated) fibroblasts (myofibroblasts). A key cytokine in controlling repair is transforming growth factor-beta (TGF-beta). To characterize the cells involved in the repair process of the premature lung, we employed immunocytochemical techniques and examined the lungs of 39 autopsied premature babies who had neonatal respiratory distress syndrome (RDS). All were treated in neonatal intensive care units and required mechanical ventilation and supplemental oxygen; all survived for at least 12 hours. Antibodies were employed against vimentin, alpha-smooth muscle (alpha-SM) actin, total muscle actin, desmin, MAC387, and TGF-beta. Our study indicates that myofibroblasts are normally present along terminal airways in the developing lung. These cells increase in number some days after lung injury, form bundles of cells encircling terminal air spaces, and acquire desmin contractile filaments shortly thereafter. Myofibroblasts do not lose their contractile filaments with time, suggesting a conversion to smooth muscle metaplasia. The proliferation and migration of such myofibroblasts at sites of lung injury is associated with the presence of TGF-beta. These findings suggest that myofibroblasts play an important role in premature lung repair. They may point the way to experimental and clinical trials that will identify drugs antagonistic to TGF-beta (or other cytokines). Such antagonists may protect the neonates who are at high risk of developing BPD.

Operational Test Results of the Passive Final Approach Spacing Tool

A prototype decision support tool for terminal area air traffic controllers, referred to as the Final Approach Spacing Tool (FAST), was recently evaluated in operation with live air traffic at the Dallas/Fort Worth, Texas Airport. Controllers utilized FAST’s runway and sequence advisories to manage and control arrival traffic during more than twenty-five peak rush traffic periods. This paper presents the results of these tests, describing data on FAST’s impact on airport capacity, in-trail separation on final approach, safety, and controller workload. Results demonstrate airport throughput increases of more than 13 percent with no negative impact on controller workload or safety.

Effect of intrauterine repair of diaphragmatic hernia on the accompanying pulmonary hypoplasia in the fetal rabbit

Severe pulmonary hypoplasia precluding the sustenance of life is often found in newborns with prenatally diagnosed congenital diaphragmatic hernia (CDH). In utero repair of the hernia it is thought to be the sole method of salvaging these patients. To study the efficacy and feasibility of in utero repair of CDH, diaphragmatic hernias (DH) were produced successfully in 81 of 90 fetal rabbits by diaphragmatic perforation via a left thoracotomy at 22 days' gestation (term = 31 days). The DHs were repaired successfully in 25 of 50 fetal rabbits at 26 days' gestation. The rabbits with repaired and non-repaired DHs and their litter-mates (the control group) were delivered at 29 days' gestation by cesarean section. Some of the rabbits were killed and subjected to measurements of body and lung weight, determination of the DNA and surfactant (disaturated phosphatidylcholine; DSPC) contents of the lungs, and light and electron microscopic examination of the lung. Some newborn rabbits underwent endotracheal intubation and measurement of pressure-volume curves and pulmonary compliance. The total lung/body weight ratios and total lung DNA contents in the repair group were greater than those in the non-repair Group (P <0.01). There were no differences among the three groups in regard to body weight. When compared with the control group, both the repair and non-repair groups had increased DSPC content (P <0.01 andP <0.05, respectively), although there was no difference between the repair and non-repair groups. Histologically, the thickness of the terminal air spaces was smaller and the size of the lung acini was larger in the repair group than the non-repair group. Electron-microscopically, the number of type 11 lung cells in both the repair and nonrepair groups tended to be larger than that in the control group. When compared with the non-repair group, the repair group showed increased values for pressure-volume curves (P <0.01) and pulmonary compliance (P <0.01). In conclusion, in utero repair of CDHs is effective in improving the hypoplasticity of the lung accompanying this lesion.

Polarization Options and Terminal Area Multifunction Radars

Multifunction skin track radars utilizing phased array technologies are being considered for terminal area air traffic control surveillance. Augmenting the preferred cooperative beacon-based system, these skin track radars would provide detection and tracking of uncooperative intruders in the terminal area airspace, continued surveillance on any aircraft experiencing a transponder failure, and detection and real-time tracking of potentially hazardous weather cells. An operational limitation on the use of skin track radar is the difficulty in detecting the presence of an aircraft in a range cell that also contains rain clutter. This target to background contrast may be improved by use of circular polarization. The degree of improvement depends upon the rain cancellation ratio and the incremental reduction in aircraft backscatter cross section when viewed with circular polarization. It has also been suggested that alternate use of vertical and horizontal linear polarization could indicate the presence of hail, a particularly hazardous phenomenon. Implementation of high purity polarization flexibility over wide scan sectors may be challenging however. This article presents a parametric examination of potential benefits and limitations associated with the use of polarization flexibility in terminal area surveillance. © 1996 John Wiley & Sons, Inc.

Environmental Control Concepts for Industrial Clean-Room Facilities

Clean rooms rely on the effectiveness of terminal high-efficiency particulate air (HEPA) filters to provide particle-free air to the controlled environment. The filtration modes of HEPA filters are...

The Final Approach Spacing Tool

A system for assisting terminal area air traffic controllers in the management and control of arrival traffic, referred to as the Final Approach Spacing Tool (FAST), is being developed at NASA Ames Research Center. In a cooperative program. NASA and the FAA have efforts underway to install and evaluate the system at the Dallas/Fort Worth Terminal Radar Approach Control facility beginning in 1994. This paper will review the algorithmic components. the human-machine interface, and the results of recent simulations.

Evaluation of lung function changes before and after surfactant application during artificial ventilation in newborn rats with congenital diaphragmatic hernia

Patients with congenital diaphragmatic hernia (CDH) have unilateral or bilateral hypoplasia of the lungs including delayed maturation of the terminal air sacs. Because these lungs are highly susceptible to barotrauma and oxygen toxicity, even in full-term newborns, continued research into optimal ventilatory regimen is essential to improve survival rate and to prevent ongoing lung damage. Against this background, the effect of exogenous surfactant application is evaluated. In newborn rats, CDH was induced after a single dose of 2,4 dichloro-4′-nitrophenyl (Nitrofen) (400 mg/kg) on day 10 of gestation. The newborn rats were intubated immediately after hysterotomy, transferred to a heated multichambered body plethysmograph, and artificially ventilated. Inspiratory peak pressures were initially set at 17 cm H 2O, with positive end-expiratory pressure at 0 cm H 2O and Fio 2 at 1.0. The pressure was raised in steps of 5 cm H 2O, from 5 to 30 cm H 2O, to obtain pressure-volume diagrams at 0, 1, and 6 hours of artifical ventilation. These measurements were obtained in controls and in CDH rats with and without endotracheal installation of bovine surfactant (n = 4 to 10 in each group). Significant differences in lung volume between CDH and control rats were observed at all time-points. Surfactant application had a positive effect on lung volume, especially in control rats at t = 1 hour. No significant differences were observed between the CDH groups at t = 1 or t = 6 hours. In this animal model, the effect of artificial ventilation as well as the beneficial short-term effect of exogenous surfactant application have been evaluated. A continued positive effect on lung volume in CDH lungs could not be determined. Routine administration of exogenous surfactant in human CDH patients is not supported by these experimental results.

Influence of smoking habits on change in carbon monoxide transfer factor over 10 years in middle aged men.

Emphysema is associated with a reduction in carbon monoxide transfer coefficient (TLCO/VA), but little is known about the evolution of changes in TLCO/VA in middle aged smokers at risk of developing chronic airflow obstruction. TLCO/VA (single breath method) was measured on two occasions 10 years apart in 122 middle aged men. Initially TLCO/VA averaged 97% predicted in never smokers (n = 42, mean age 37.2 years), 99% predicted in ex-smokers (n = 21, mean age 41.9 years), and 85% predicted in those who smoked over 15 cigarettes a day (n = 42, mean age 42.0 years). Mean rates of decrease in TLCO/VA over 10 years, however, were similar in the three groups, so that differences between smokers and non-smokers did not increase during the 10 years. Seventeen men (mean age 40.9 years) who initially were smokers became sustained ex-smokers within two years of the first measurement; in these men mean absolute values of TLCO/VA rose, averaging 89% predicted at the first assessment but 102% predicted 10 years later. By the age of about 40 years TLCO/VA was lower in smokers than in never smokers but this difference did not increase over the following 10 years. Sustained ex-smokers had values similar to those of never smokers even when TLCO/VA was known to have been reduced while they were smoking. Changes in TLCO/VA associated with stopping smoking were considerably larger than could be explained by carbon monoxide back pressure, indicating that mechanisms other than irreversible increase in the size of terminal air spaces underlie the lower values in smokers. To detect emphysema in smokers it is necessary to use reference equations that take account of current smoking.

Nutrition and lung structure and function.

Although the effects of malnutrition on various metabolic functions of the body and on disease states have been studied and are well known, the potential influence of nutrition on lung structure and function is not well recognized. Indeed, no human studies related to this subject exist. What little we know comes from experimental animal studies, particularly in rats, dating back to the late 1970s. These studies have revealed that food deprivation influences lung growth and development in growing animals as well as lung structure and function in adults. Due to specific physiologic processes that dominate events during lung growth and adulthood, malnutrition affects these processes differently. In growing animals, food deprivation leads predominantly to the retardation of lung growth and a delay, sometimes nonreversible, in its development into a fully functioning intricate organ. In adult animals, food deprivation alters the architecture of terminal air spaces in a manner similar to what occurs in emphysema.

Residual Volume in a General Population: Effects of Body Size, Age, Cigarette Smoking, and Respiratory Symptoms

Residual volume (RV) was obtained by subtracting vital capacity from total lung capacity determined by the single breath helium dilution (TLCsb) to measure CO diffusing capacity in 2,680 subjects (8 to 64 years old) of a general population sample. There were 712 normal subjects (243 male and 469 female subjects) selected to evaluate the pattern of RV by age and to derive reference values for internal comparisons. From 8 to 20 years old, RV showed an increase because of the cross-sectional body size effect; after 20 to 30 years, RV was still increasing, however, at a lower level. Age and height coefficients were significantly related to RV in younger and older ages, both in male and female subjects. The RV percent predicted and RV/TLC percent were higher in smokers when compared to nonsmokers and exsmokers (the difference was significant in male subjects). A dose-response effect was observed between RV percent predicted, RV/TLC percent, and pack-years. The RV percent predicted and RV/TLC percent were significantly higher in smokers and nonsmokers with FEV1 percent predicted below the normal limit (the difference was significant in male subjects). Moreover, higher values of RV percent predicted and RV/TLC percent were observed in subjects with wheezy symptoms in male smokers and nonsmokers. A negative significant correlation was observed between RV/TLC percent and the diffusing capacity adjusted for lung volume (DL/VA) in smokers, exsmokers and nonsmokers of both sexes, confirming the hypothesis that the decrease in DL/VA may be ascribed to the enlargement of terminal air spaces. In conclusion, determination of RV by the single breath helium dilution method is suitable in epidemiology, and it allows additional important information for understanding the physiopathologic mechanisms related to the pathogenesis of chronic obstructive lung disease.

Transforming growth factor beta 1 is present at sites of extracellular matrix gene expression in human pulmonary fibrosis.

Idiopathic pulmonary fibrosis is an inexorably fatal disorder characterized by connective tissue deposition within the terminal air spaces resulting in loss of lung function and eventual respiratory failure. Previously, we demonstrated that foci of activated fibroblasts expressing high levels of fibronectin, procollagen, and smooth muscle actin and thus resembling those found in healing wounds are responsible for the connective tissue deposition and scarring in idiopathic pulmonary fibrosis. Using in situ hybridization and immunohistochemistry, we now demonstrate the presence of transforming growth factor beta 1 (TGF-beta 1), a potent profibrotic cytokine, in the foci containing these activated fibroblasts. These results suggest that matrix-associated TGF-beta 1 may serve as a stimulus for the persistent expression of connective tissue genes. One potential source of the TGF-beta 1 is the alveolar macrophage, and we demonstrate the expression of abundant TGF-beta 1 mRNA in alveolar macrophages in lung tissue from patients with idiopathic pulmonary fibrosis.

Low-molecular-weight hydrophobic proteins from bovine pulmonary surfactant

Pulmonary surfactant stabilizes the lung by reducing the surface tension in the terminal air spaces. Lipid extract surfactant contains approx. 1% (w/w) low-molecular-weight hydrophobic proteins SP-B (15 kDa: nonreduced) and SP-C (3.5 kDa) and with the remainder being mainly phospholipids. The hydrophobic proteins were purified from bovine lipid extract surfactant using delipidation by phospholipase C digestion followed by hydroxyapatite chromatography. The phospholipase C step removed most of phosphatidylcholine resulting in a 10-fold enrichment of hydrophobic proteins relative to phospholipid. Chromatography of this preparation on a hydroxyapatite column resulted in the elution of phospholipids followed by SP-C and then SP-B. The column chromatography was repeated to remove residual phospholipids and yield purified SP-B and SP-C. The final recovery of SP-B from the lipid extracts was about 15–20% and that of SP-C was 5–10%. The bovine surfactant proteins were reconstituted with phospholipids and examined for their ability to lower the surface tension with a pulsating bubble surfactometer. Reconstituted surfactant preparations containing SP-B and dipalmitoylphosphatidylcholine plus dioleoylphosphatidylglycerol were capable of reducing the surface tension to near zero values at minimum bubble radius while the reconstitutes with SP-C only lowered the surface tension to approx. 20 mN/m. A more rapid decrease in surface tension was observed with reconstituted samples containing both hydrophobic proteins. These results indicate that both SP-B and SP-C can promote the adsorption and spreading of surfactant lipids at the air/liquid interface. In addition, SP-B appears to facilitate the squeeze-out of unsaturated phospholipids leading to an enrichment of dipalmitoylphosphatidylcholine in the monolayer.

Influence of Preexisting Pulmonary Emphysema on Susceptibility of Rats to Inhaled Diesel Exhaust

The susceptibilities of normal rats and rats with preexisting pulmonary emphysema to chronically inhaled diesel exhaust were compared. Rats were exposed 7 h/day, 5 days/wk for 24 months to diesel exhaust at 3.5 mg soot/m3, or to clean air as controls. Emphysema was induced in one-half of the rats by intratracheal instillation of elastase 6 wk before exhaust exposure. Measurements included lung burdens of diesel soot, respiratory function, bronchoalveolar lavage, clearance of radiolabeled particles, pulmonary immune responses, lung collagen, excised lung weight and volume, histopathology, and mean linear intercept of terminal air spaces. Parameters indicated by analysis of variance to exhibit significant interactions between the influences of emphysema and exhaust were examined to determine if the effects were more than additive (indicating increased susceptibility). Although 14 of 63 parameters demonstrated emphysema-exhaust interactions, none indicated increased susceptibility. Less soot accumulated in lungs of emphysematous rats than in those of nonemphysematous rats, and the reduced accumulation had a sparing effect in the emphysematous rats. The results did not support the hypothesis that emphysematous lungs are more susceptible than are normal lungs to chronic exposure to high levels of diesel exhaust. The superimposition of effects of emphysema and exhaust, however, might still warrant special concern for heavy exposures of emphysematous subjects.

USING AIR TO CONVEY MECHANICALLY HARVESTED PEPPERS

ABSTRACT Multiple-slotted conveyors mounted on a mechanical harvester utilized moving air to effectively convey several pepper types. Unlike mechanical conveyors, the design permitted variable conveyor widths. The air velocities required to continuously convey peppers ranged from 30 to 38 m/s requiring 4.4 to 5.8 kW, respectively, for jalapenos and green bells. No single physical property of the peppers was found that could be used to predict terminal velocity nor air velocity needed for effective conveyance. However, the air velocity needed for effective conveyance was, in general, related to pepper mass.

Immature alveolar/blood barrier and low disaturated phosphatidylcholine in fetal lung after intrauterine exposure to O,O,S-trimethylphosphorothioate.

Intrauterine exposure to the potent lung toxicant OOS-TMP was found to result in neonatal lethality attributed to immature lungs (Koizumi et al. 1988). The present study was initiated to investigate biological/pathological profiles of such pulmonary immaturity. OOS-TMP was given p.o. to five pregnant female Sprague-Dawley rats on gestation day (G) 19 at 2.5, 7 or 20 mg/kg. Control (N = 6) or pair-fed dams (N = 5: pair-fed to 20 mg/kg dams) received 2 ml/kg corn oil. On G 22, fetuses were delivered by Cesarean section. The biochemical maturity of lungs was assessed by glycogen content and production of disaturated phosphatidylcholine (DSPC), a major component of pulmonary surfactant. Mean DSPC content was significantly lower in fetuses from dams dosed at 7 or 20 mg/kg while mean glycogen concentration, in contrast, was 3- to 6-fold higher in those fetuses than fetuses from control or pair-fed dams. Pathological examination revealed that in fetuses delivered from dams dosed at 7 mg/kg or 20 mg/kg, glycogen-rich cuboidal epithelial cells completely covered the terminal air space and alveolar/blood barriers stayed at the poorly developed stage. The stage of the pulmonary development in those fetuses was similar to those in fetuses on G19. Therefore it was concluded that intrauterine exposure to OOS-TMP delayed pulmonary development, thereby causing respiratory failure after birth.