ABET Criterion 3.f: how much curriculum content is enough?

Even after multiple cycles of ABET accreditation, many engineering programs are unsure of how much curriculum content is needed to meet the requirements of ABET's Criterion 3.f (an understanding of professional and ethical responsibility). This study represents the first scholarly attempt to assess the impact of curriculum reform following the introduction of ABET Criterion 3.f. This study sought to determine how much professional and ethical responsibility curriculum content was used between 1995 and 2005, as well as how, when, why, and to what effect changes in the amount of content occurred. Subsequently, the study sought to evaluate if different amounts of curriculum content generated differing student outcomes. The amount of curriculum content used by each of the participating programs was identified during semi-structured interviews with program administrators and a review of ABET Self-Study documents. Quantitative methods were applied to determine if a relationship existed between the curriculum content and performance on a nationally administered, engineering-specific standardized examination. The findings indicate a statistical relationship, but a lack of structure between the amount of required content in the curriculum and performance on the examination. Additional findings were also generated regarding the way that programs interpret the Criterion 3.f feedback generated during accreditation visits. The primary impact of this study is that it dispels the myth that more courses or course time on professionalism and ethics will necessarily lead to positive engineering education outcomes. Much of the impetus to add more curriculum content results from a lack of conclusive feedback during ABET accreditation visits.

Relationships among LH, FSH and prolactin secretion, storage and response to secretagogue and hypothalamic GnRH content in ovariectomized pony mares administered testosterone, dihydrotestosterone, estradiol, progesterone, dexamethasone or follicular fluid.

Thirty-five ovariectomized pony mares were used to study the relationships among luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) concentrations in blood (secretion), in pituitary (storage) and in blood after secretagogue administration, as well as the content of gonadotropin releasing hormone (GnRH) in hypothalamic areas, under various conditions of steroidal and nonsteroidal treatment. Five mares each were treated daily for 21 d with vegetable shortening (controls), testosterone (T; 150 micrograms/kg of body weight, BW), dihydrotestosterone (DHT; 150 micrograms/kg BW), estradiol (E2; 35 micrograms/kg BW), progesterone (P4; 500 micrograms/kg BW), dexamethasone (DEX; 125 micrograms/kg BW) or charcoal-stripped equine follicular fluid (FF; 10 ml). Secretagogue injections (GnRH and thyrotropin releasing hormone, TRH, at 1 and 4 micrograms/kg of BW, respectively) were given one d prior to treatment and again after 15 d of treatment. Relative to controls, treatment with T, DHT and DEX reduced (P less than .05) LH secretion, storage and response to exogenous GnRH, whereas treatment with E2 increased (P less than .05) these same characteristics. Treatment with P4 reduced (P less than .05) only LH secretion. Treatment with T, DHT, E2 and DEX reduced (P less than .05) FSH secretion, whereas treatment with P4 increased (P less than .05) it and FF had no effect (P greater than .1). All treatments increased (P less than .05) FSH storage, whereas only treatment with T and DHT increased (P less than .05) the FSH response to exogenous GnRH. Other than a brief increase (P less than .05) in PRL secretion in mares treated with E2, secretion of PRL did not differ (P greater than .1) among groups. Only treatment with E2 increased (P less than .01) PRL storage, yet treatment with T or DHT (but not E2) increased (P less than .05) the PRL response to exogenous TRH. Content of GnRH in the body and pre-optic area of the hypothalamus was not affected (P greater than .1) by treatment, whereas treatment with T, E2 and DEX increased (P less than .1) GnRH content in the median eminence. For LH, secretion, storage and response to exogenous GnRH were all highly correlated (r greater than or equal to .77; P less than .01). For FSH, only storage and response to exogenous GnRH were related (r = .62; P less than .01). PRL characteristics were not significantly related to one another. Moreover, the amount of GnRH in the median eminence was not related (P greater than .1) to any LH or FSH characteristic.

Effects of active immunization against GnRH on LH, FSH and prolactin storage, secretion and response to their secretagogues in pony geldings.

Six pony geldings were actively immunized against GnRH conjugated to bovine serum albumin (BSA) to study 1) the relative dependency of LH and FSH storage, secretion and response to GnRH analog on GnRH bioavailability and 2) the effects of reduced GnRH bioavailability on GnRH storage in the hypothalamus. Five geldings were immunized against BSA. Geldings were immunized in December and 4, 8, 14, 20, 26 and 32 wk later. Ponies immunized against GnRH had increased (P less than .01) GnRH binding in plasma within 6 wk. By June, plasma concentrations of LH and FSH in ponies immunized against GnRH had decreased (P less than .02) by 86 and 59%, respectively, relative to ponies immunized against BSA. The LH response to an injection of GnRH analog, which did not bind to anti-GnRH antibodies, was reduced (P less than .005) by 90% in ponies immunized against GnRH relative to ponies immunized against BSA. In contrast, the FSH response to GnRH analog was similar (P greater than .1) for both groups. Immunization against GnRH reduced (P less than .05) weight of the anterior pituitary (AP) by 31%, LH content in AP by 91% and FSH content in AP by 55% relative to ponies immunized against BSA. There was no effect of GnRH immunization on prolactin characteristics or on GnRH concentrations in the median eminence, preoptic area or body of the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Formation and characterization of vesicles from day-10 horse conceptuses.

The objectives of this research were 1) to determine if cellular vesicles could be formed from Day-10 horse conceptuses similar to trophoblastic vesicles reported for other domestic species and 2) to characterize various aspects of their development in vitro and their ability to withstand the freeze-thaw process. Twenty-five conceptuses were recovered from lighthorse mares on Day 10 after ovulation. After two washes in 0.05% trypsin, each conceptus was placed in 0.25% trypsin until the capsule thinned. Mechanical dispersion with a glass pipette resulted in a combination of individual cells and cell clumps. When cultured in vitro, all preparations exhibited both partially and completely formed vesicles within 24 h. Cellular monolayers also developed within the first 24 h of culture and were predominant by 96 h. Within 13 to 20 d, all monolayers developed dense areas of cells that eventually released from the cell matrix and aggregated to form vesicles. Progesterone and total estrogen concentrations in media samples were lower (P < 0.05) for conceptuses that had required long trypsinization periods for dispersion. Pregnant mare serum gonadotropin was not detectable in any samples. Vesicles cultured in nontreated tissue culture flasks.doubled in size within 24 h but did not increase further by 48 h. Of 234 vesicles frozen after 48 h of culture, the postthaw viability, as measured by the ability to return to prefreeze characteristics, was 34, 21 and 11% after 24, 96 and 168 h in culture, respectively. We conclude that vesicles can be formed by enzymatic dispersion of Day-10 horse conceptuses. However, monolayers were the predominant result of both the initial dispersions and the long-term culture of vesicles. Vesicles showed a limited ability to grow in vitro.

Suppression of lymphocyte proliferation by a greater than 30,000 molecular weight factor in horse conceptus-conditioned medium.

In this experiment we have identified and partially characterized the immunosuppressive activity of preimplantation horse conceptus-conditioned medium (HCCM). Horse conceptuses were nonsurgically flushed from mares at Days 9-10 (n = 6), 15-16 (n = 3), and 25-26 (n = 3). After incubating the conceptuses for 24 h in RPMI-1640 supplemented with 15% fetal calf serum (FCS) and 1% penicillin/streptomycin, HCCM was obtained from cultures and tested for immunosuppressive activity in lymphocyte proliferation assays. Peripheral blood lymphocytes obtained from randomly selected mares were stimulated with mitogens (pokeweed mitogen [PWM], concanavalin A [Con A], and phytohemagglutinin [PHA]) in cultures supplemented with 0%, 25%, or 50% HCCM. HCCM from all cultures suppressed lymphocyte proliferation induced by all three mitogens (p less than 0.001). After being subjected to various treatments (heating, freeze-thawing, and nitrocellulose filtration), HCCM maintained its full biological suppressor activity. Amicon microconcentrators with 10,000 and 30,000 molecular weight (MW) exclusion filter membranes were used to fractionate HCCM by molecular weight. The suppressor factor was found to be in the greater than 30,000 MW fraction. HCCM was further tested interspecifically on donkey and goat lymphocytes stimulated with PWM. HCCM did suppress proliferation of interspecific lymphocytes (p less than 0.01); however, the suppressive capacity of HCCM in caprine lymphocyte cultures was less (p less than 0.05) than that observed in equine cultures. These data support the hypothesis that the horse conceptus produces an immunoregulatory factor. This factor is extremely stabile and appears to exhibit some degree of species-specificity. The production and immunosuppressive effectiveness of such a factor may play an important role in maintaining the fetal allograft throughout gestation.

Effects of sexual stimulation, with and without ejaculation, on serum concentrations of LH, FSH, testosterone, cortisol and prolactin in stallions.

Six lighthorse stallions with previous sexual experience were used to determine the short-term effects of sexual stimulation (SS; 5 min exposure to an estrous mare), SS plus ejaculation (SSE), and no stimulation (control) on serum concentrations of LH, FSH, testosterone, cortisol and prolactin. Stallions received one treatment per day on d 1, 4 and 7. Treatments were assigned such that each stallion 1) received each treatment once and 2) experienced a unique sequence of treatments. Neither SS nor SSE had any consistent effects on LH or FSH concentrations. Testosterone concentrations during control bleedings increased (P less than .05) with time. This increase was suppressed (P less than .05) by both SS and SSE. Cortisol concentrations increased (P less than .05) immediately after SS and SSE. Cortisol concentrations also tended to increase during the control bleedings, but only in stallions that previously had been exposed to SS or SSE. Prolactin concentrations increased (P less than .05) immediately after SS and SSE and tended to rise during control bleedings in stallions previously exposed to SS or SSE. We conclude that 1) prolactin and cortisol were secreted rapidly in response to SS and SSE, 2) the rise in cortisol concentrations likely suppressed testosterone secretion within the next hour, and 3) stallions appeared to associate the distant sounds of other stallions with their own previous exposure to SS and SSE, resulting in a cortisol response (and perhaps a prolactin response) even in the absence of direct stimulation.

Isolation and antigenic identification of hamster lung interstitial macrophages.

Lung interstitial macrophages (IMs) are a large, distinctive population of cells with important proliferative capacities. Characterization of their role in health and disease has been hampered by inadequate methods to separate interstitial from residual alveolar macrophages (AMs) in preparations of individual mononuclear cells from lung tissue. In this study, a specific cell-surface antigen (HAM1) present on more than 90% of hamster AMs, but not expressed by hamster IMs, was used to distinguish these populations. After collagenase digestion of lung tissue slices from exhaustively lavaged and perfused hamster lungs, mononuclear phagocytes were isolated by density gradient centrifugation. The mean yield of lung digest macrophages (3.9 +/- 1.9 (SD) x 10(6] was comparable to the yield of lavaged AMs (4.2 +/- 1.9 x 10(6]. The proliferative capacity of lavaged AMs, blood monocytes, and lung digest macrophages was compared using a soft-agar colony-forming unit (CFU) assay. Both lung digest macrophages and blood monocytes had significantly more CFUs (68.7 +/- 2.6 and 53.5 +/- 8.4 CFU/10(3) cells [mean +/- SEM], respectively) than did AMs (16.5 +/- 1.7) (p less than 0.01). To further define the composition of the lung digest macrophage population, flow cytometric analysis of fixed cells from six experiments was performed using a mouse monoclonal antibody specific for the HAM1 antigen found only on AMs. The lung digest macrophage population consisted of both antigen-negative IMs (78.2% +/- 3.7% [SEM]; n = 6) and antigen-positive, residual AMs (21.8% +/- 3.7%). Morphometric counts confirmed that substantial numbers of AMs are left behind after lavage and contribute to macrophages obtained from lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary effects of blood replacement with a perfluorochemical emulsion followed by exposure to 85% oxygen or air.

Perfluorochemical emulsions (PCE) have been used as blood substitutes because of their high solubility coefficient for oxygen. However, concerns for their clinical use include both the hyperoxia required by PCE to improve oxygen delivery to tissues and the effects of PCE on lung tissue. We addressed 3 questions: (1) What are the combined effects on the lungs of PCE blood replacement and hyperoxia? (2) Does reduction of circulating white cells by PCE blood replacement modify the injurious effects of hyperoxia? (3) Does PCE alone alter the lungs? Adult rats received either partial or complete PCE blood replacement or no PCE and were then exposed to 85% oxygen for 5 days. Other rats received partial PCE or no PCE and breathed air for 5 days. Morphometric and morphologic analyses demonstrated that lung injury was primarily caused by hyperoxia, independent of PCE treatment. Statistical analyses of the data indicated no synergistic effects between PCE and hyperoxia; furthermore, transient reduction of blood inflammatory elements by PCE blood replacement did not modify the extent of injury that occurred later. Importantly, however, rats that received partial PCE and air exposure were virtually identical to those that received no PCE and air exposure. Five days after blood replacement, PCE components were most often seen within alveolar and interstitial macrophages and infrequently within endothelial and epithelial cells. Although PCE itself may have produced functional alterations in lung cells, direct effects were not morphologically evident. Our results suggest that, if PCE are used at moderate FIO2, such as 0.6 or less, structural changes in the lungs could be minimized.

Effects of inhalation of 0.25 ppm ozone on the terminal bronchioles of juvenile and adult rats.

Cells of the terminal bronchioles are particularly susceptible to the effects of inhalation of low levels of ozone (O3). One-day-old (juvenile) or 6-week-old (adult) rats were exposed to 0.25 ppm O3 for 12 h/day or to continuous room air for 6 weeks. Morphometric analysis of perpendicular cross sections of terminal bronchioles demonstrated that exposure to O3 produced alterations in the surface characteristics of ciliated and nonciliated (Clara) cells in both groups of rats. There were significant losses (20-30%) of the surface area contributed by cilia and the luminal surface of Clara cells was decreased by 16-25%. O3 exposure also produced significant decreases in the number of brush cells per square millimeter of terminal bronchiolar basement membrane. The results of this study indicate that the normal structure of terminal bronchiolar epithelial cells is significantly altered by inhalation of 0.25 ppm O3. No statistically significant interactions between the effects of O3 and animal age at the beginning of the exposure were found.

Pulmonary intravascular macrophages in sheep. Morphology and function of a novel constituent of the mononuclear phagocyte system.

Macrophages resident in the pulmonary capillaries of sheep avidly remove injected particles from the circulating blood. Both sheep and rats were injected intravenously with radiolabeled gold colloid and magnetic iron oxide particles. One hour later, particle uptake in various organs was quantified by gamma counting and magnetometry. Organ localization of both gold and iron oxide particles was predominantly hepatic in rats. In marked contrast, sheep had predominantly pulmonary uptake. Ultrastructural morphology showed that pulmonary iron oxide uptake was by intravascular macrophages. Pulmonary intravascular macrophages were present in ruminant lungs in large numbers. Lungs of sheep given no particles were fixed by intratracheal instillation of glutaraldehyde; randomly chosen tissue samples were routinely processed for electron microscopy and studied with stereological methods. We found that these macrophages occupied 15.3% of the intravascular volume, and had 15.9 m2 of free surface available for contact with blood. Intravascular macrophages were closely applied to 7.1% of the endothelial surface, including numerous short segments with 12 to 15 nm of membrane interspace, increased subplasmalemmal cytoplasmic density, and intercellular electron-dense material. We conclude that pulmonary intravascular macrophages in sheep comprise an important component of their mononuclear phagocyte system. Furthermore, we suggest that these macrophages, through phagocytic uptake of bacteria or endotoxin, may contribute to pulmonary inflammation and injury.

Effects of inhalation of 0.12 and 0.25 parts per million ozone on the proximal alveolar region of juvenile and adult rats.

The degree of lung injury caused by prolonged inhalation of low levels of ozone (O3) is of interest since urban environmental levels periodically reach 0.2 to 0.3 ppm. Since the area of the junction of the conductive and respiratory regions of the lung has been reported as the major site of injury due to O3 inhalation, techniques were devised to specifically study alveolar tissue from this region. One-day-old or 6-week-old male rats were exposed to either 0.25 ppm O3 12 hours/day or to continuous room air for 6 weeks. An additional group of 6-week-old rats were exposed to 0.12 ppm O3 for the same time period. All lungs were fixed at the end of the exposure by intratracheal installation of buffered 2% glutaraldehyde. Cylinders of tissue containing a cross-section of a terminal bronchiole were punched out of lung tissue slices using a sharpened cannula. These tissue cylinders were oriented, embedded in Epon, serial sectioned until the first alveolar duct bifurcation was reached, and then thin sectioned for electron microscopy. Qualitative examination of the tissue revealed little observable damage to the proximal alveolar tissues. However, by ultrastructure morphometric analysis, significant changes occurred in the alveolar epithelium of the proximal alveolar region of all exposed animals. In the animals exposed to 0.25 ppm O3 from 1 day of age (juvenile animals), the number of type 1 epithelial cells doubled, their mean surface area decreased 38%, and their mean thickness increased 24%. The number of alveolar type 2 epithelial cells increased, and the number of alveolar macrophages doubled. Adult animals exposed to 0.25 ppm O3 showed similar patterns of changes in the epithelium of the proximal alveolar region and in addition had a doubling of interstitial macrophages, indicating a mild inflammatory stimulus in the interstitium. Adult animals exposed to 0.12 ppm O3 showed smaller, but statistically significant changes in the alveolar type 1 epithelium, suggesting a relatively linear concentration-response relationship. The change in number and size of type 1 cells in all exposed animals is consistent with an increased cell turnover rate due to prolonged O3 inhalation. These results suggest that low concentrations of O3 cause a chronic epithelial injury in the proximal alveolar region and that the extent of these changes occurs in a concentration-dependent manner, even at concentrations as low as 0.12 ppm. No statistically significant age-dependent effects were found.

Patterns of accumulation of platelets and neutrophils in rat lungs during exposure to 100% and 85% oxygen.

The influx of leukocytes into the lung during hyperoxic exposures has been suggested as a significant contributor to alveolar injury because, when activated, they can cause damage by producing oxygen radicals and releasing hydrolytic enzymes. To better understand the relationship between hyperoxic injury and inflammatory responses, morphometric methods were used to quantitate changes in alveolar capillary blood components of rats exposed to 100% and 85% oxygen. After 40 h in 100% oxygen the absolute volume of platelets in the capillary bed increased 78% and there was a 111% increase in the total endothelial cell surface area covered by platelets. There were no significant changes in these parameters for neutrophils until 60 h of exposure of 100% O2. At this point, both the absolute volume and the endothelial surface area covered by neutrophils increased more than threefold. After 3 days in 85% oxygen absolute platelet volume was almost doubled and the surface area covered by platelets increased 79%. No neutrophil increases occurred until 5 days exposure to 85% oxygen, and both absolute volume and surface area dropped to less than control values after 7 days of exposure. The appearance of platelets prior to an influx of neutrophils during both hyperoxic exposures suggests that the initial endothelial cell injury results from an increased intracellular production of oxygen radicals rather than being due to oxygen radicals produced by leukocytes. Endothelial cell membrane changes were associated with the initiation of platelet accumulation in the capillary bed. Platelet components released during platelet activation may be important mediators for the subsequent neutrophil influxes.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhalation studies of Mt. St. Helens volcanic ash in animals: respiratory mechanics, airway reactivity and deposition.

Effects of fine volcanic ash aerosol on pulmonary mechanical properties of awake guinea pigs were evaluated during exposure by inhalation. Ash penetration into the lung as well as tissue response to ash were determined by transmission electron microscopy. The reactivity of airway epithelial irritant receptors following ash exposure was assessed using a histamine bronchoprovocation test. Results indicated that breathing 9,4 mg/m3 of ash for 2 hr did not cause a measurable change in pulmonary function of guinea pigs. Electron micrographs showed that ash particles in the lung below the hilus did not seem to produce any acute tissue reaction and were almost all phagocytized by macrophages. Airways of guinea pigs exposed to ash were significantly less responsive to histamine than were the airways of animals exposed only to air. It appears that even though Mt. St. Helens ash was well tolerated by the guinea pig during the exposure, its presence in the inhaled air did change the "histamine sensitivity" of airway epithelial irritant receptors.

Application of morphometric methods to study diffuse and focal injury in the lung caused by toxic agents.

Morphometric techniques are now being widely applied to a variety of toxicologic problems in order to obtain reproducible and quantitative data about changes in lung structure caused by environmental pollutants. Many environmental pollutants cause lung injury which is concentrated in specific regions of the lung, such as, in small airways and in the proximal portions of alveolar ducts. Morphometric techniques to obtain unbiased estimates of tissue changes occurring in these specific regions are reviewed and contrasted to well-established techniques for morphometric analysis of the distal alveolar regions of the lung. Specific applications of morphometric studies in different toxicologic problems are illustrated and include quantification of the changes in lung tissue and in lung cellular population pattern in response to exposure of small animals to hyperoxic atmospheres and to ozone. Pulmonary oxygen toxicity is an example of a diffuse lesion throughout the distal portion of the acinus whereas ozone exposure is an example of an environmental pollutant causing a greater degree of lung injury in the proximal alveolar region and in the small airways.

Inhalation studies of Mt. St. Helens volcanic ash in animals : Respiratory mechanics, airway reactivity and deposition

This study was conducted to improve speculation of changes in breathing which might be expected while inhaling a dust like Mt. St. Helens volcanic ash. Effects of fine volcanic ash aerosol on pulmonary mechanical properties of awake Guinea pigs were evaluated during exposure by in halation. Ash penetration into the lung as well as tissue response to ash were determinated by transmission electron mycroscopy. The reactivity of airway epithelial irritant receptors following ash exposure was assessed using a histamine bronchoprovocation test. Airways of Guinea pigs exposed to ash were significantly less responsible to histamine tan were the airways of animals exposed only to air (AU)

The distal splenorenal shunt in alcoholic patients. A training program's experience.

Eighteen alcoholic patients who had bled from esophageal varices underwent elective distal splenorenal shunt. None died in surgery, and morbidity was minimal. Two-year survival for the group was 84 per cent. All five patients who have abstained from alcohol remain alive.

Alterations in lung structure caused by inhalation of oxidants.

Morphometric and morphologic methods have been used to evaluate changes in rat lungs caused by the inhalation of a variety of oxidants. Exposure to 100% oxygen causes diffuse pulmonary injury and leads to death after 66-72 h of exposure. The primary insult leading to death in rats exposed to hyperoxia is injury to pulmonary capillary endothelium. Sublethal exposure to hyperoxia was found to cause diffuse injury to all major components of the alveolar septum and was associated with destruction of approximately 50% of the pulmonary capillary endothelial cells. A corresponding decrease in pulmonary capillary surface area and capillary lumen volume also occurred. Exposure to ozone and to nitrogen dioxide in low concentrations did not cause a diffuse injury throughout the alveolar region of the lung, but rather led predominantly to structural alterations in terminal bronchioles and in their adjacent alveoli. Morphometric evaluation of animals exposed to 0.25 ppm ozone and to 2 ppm NO2 demonstrated quantitatively and qualitatively similar lesions. These lesions primarily involve injury and remodelling of the alveolar epithelium. These changes in the alveolar epithelium were also associated with the recruitment of increased numbers of alveolar macrophages to the proximal alveolar region. The different types of lung injury caused by various oxidants are most likely to be related to differences in their reactivity with tissue components and to differences in concentration, distribution, and diffusion characteristics of the oxidant gases.

Morphometric characteristics of cells in the alveolar region of mammalian lungs.

Morphometric procedures have been used to study the characteristics of cells in the alveolar region of the lungs of rats, dogs, baboons, and humans. Compared with the other species, human lungs were found to contain greater numbers of macrophages and to have larger alveolar type II, endothelial, and interstitial cells. The thickness of the interstitium and the pulmonary capillary endothelium were also significantly greater in the human lungs. These differences in human lung anatomy may be due to increased exposure to airborne pollutants and to tobacco smoke. Despite the above differences and the fact that there are large variations in size and functional characteristics of the lungs of these mammals, an overall striking similarity in characteristics of individual lung cells was found. The distribution of cells in alveolar tissue was remarkably constant between species as was the average volume and surface area of most cell types. Computer-aided three-dimensional reconstruction techniques were used to determine the spatial relationship of organelles in individual alveolar type II cells from rats. A three-dimensional reconstruction of cells permits quantification of number, size, surface area, and volume of subcellular organelles and correlations of their three-dimensional spatial relationships.

Reaction of rat lungs to inhaled chrysotile asbestos following acute and subchronic exposures.

Inhalation of asbestos fibers can cause fibrotic and neoplastic diseases in the lung. The early in vivo interactions between fibers and lung tissue that initiate these diseases have received little study. Male and female Fischer 344 rats were placed in inhalation chambers and exposed to 9.06 +/- 1.83 mg/m3 (average respirable mass) of chrysotile asbestos for 1 hr, 1 day, 7 hr/day for 5 days, or 5 days/week for 3 months. Qualitative examination of the tissue showed that, after 1 day, fibers were found not only in the alveolar macrophages, but also in the epithelium and interstitium of the alveolar region. After 3 months, numerous fibers were present in the epithelium and interstitium. Morphometric analysis of this tissue showed that these compartments were also the most significantly changed as a result of asbestos exposure. The majority of epithelial changes were attributable to a 57% increase in the number of type II cells and a 90% increase in their average cell volume. The interstitial cell population increased 58% with a 40% increase in the average cell volume. There was no significant increase in the volume of noncellular interstitium. A morphologic characterization of the interstitial cells showed that interstitial macrophages accounted for almost the entire increase in this population and that 88% of the fiber-containing cells were macrophages. Several interstitial macrophages contained membrane-bound inclusions which were shown by x-ray energy spectrometry to be microcalcifications. They were composed of rings of calcium phosphate granules around asbestos fibers. These microcalcifications may indicate sublethal cell injury caused by the presence of asbestos fibers in the cell cytoplasm. Fibers which enter but do not kil alveolar cells may be an essential component for the pathogenesis of lung disease caused by asbestos inhalation.