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[Cytobiochemical characteristics of the function of pulmonary alveolar macrophages during development of immune reactions after exposure to chemical air pollutants].

Based on an analysis of correlations between variation in the amount of alveolar macrophages of rat lungs and activity of enzymes localized in these cells (acid phosphatase, beta-galactosidase, beta-glucosidase, lactate dehydrogenase), the cytobiochemical changes in the function of pulmonary alveolar macrophages have been defined with the use of a model of permanent inhalation exposure to sulfur dioxide. The use of the model enables the dilimitation of the stages of defence-compensatory reactions and their transition to an unfavourable biological effect. The results obtained may serve as a theoretical basis for recommending a wider experimental application of the tests in question during regulation of environmental factors.

Acid Phosphatase↗

Hot tub lung: presenting features and clinical course of 21 patients.

BACKGROUND: Hot tub lung is an emerging lung disorder associated with exposure to Mycobacterium avium complex organisms contaminating hot tub water. OBJECTIVES: To define the clinical characteristics and outcome of patients with hot tub lung. METHODS: Retrospective review of 21 patients diagnosed with hot tub lung at a tertiary medical center over a 7-year period. RESULTS: The mean (+/-sd) age at presentation was 46 (+/- 15) years; 9 patients were men (43%). All patients described ongoing exposure to hot tubs. The most common referral diagnoses were sarcoidosis, bronchitis, and asthma. Dyspnea and cough were present in all patients, hypoxemia was noted in 10 patients (48%). High-resolution computed tomography of the chest had been performed in 20 patients and demonstrated diffuse centrilobular nodules and/or ground-glass opacities in all patients. M. avium complex was isolated from the hot tub water, respiratory secretions and/or lung tissue in all patients. Bronchoscopic or surgical lung biopsy was obtained in 18 patients and demonstrated bronchiolocentric granulomatous inflammation. With avoidance of exposure, clinical and radiologic improvement was observed in all patients. Additionally, 13 patients (62%) received corticosteroid therapy, 1 (5%) antimycobacterial therapy, 2 (10%) received both, and 5 patients (24%) received no pharmacologic therapy. CONCLUSIONS: Hot tub lung likely represents hypersensitivity pneumonitis due to inhalational exposure to M. avium complex. Antimycobacterial therapy does not appear to be required in the management of this disease. Although corticosteroids may be helpful in the treatment of severely affected patients, others can be managed by avoidance of additional exposure alone.

Adrenal Cortex Hormones↗

CNS depressant effects of volatile organic solvents.

Volatile chemicals used widely as solvents can produce acute effects on the nervous system and behavior after inhalation exposure, and many are subject to abuse. This review considers the nature of the acute effects of volatile organic solvents by comparing their actions to those of classical CNS depressant drugs such as the barbiturates, benzodiazepines and ethanol. Like CNS depressant drugs, selected inhalants have been shown to have biphasic effects on motor activity, disrupt psychomotor performance, have anticonvulsant effects, produce biphasic drug-like effects on rates of schedule-controlled operant behavior, increase rates of punished responding, enhance the effects of depressant drugs, serve as reinforcers in self-administration studies and share discriminative stimulus effects with barbiturates and ethanol. Toluene and 1,1,1-trichloroethane, as well as subanesthetic concentrations of halothane, have been the most extensively studied; however, it is unclear whether important differences may exist among solvents in their ability to produce a depressant profile of acute effects. The possibility that selected solvents can have acute effects similar to those of depressant drugs may shed light on the nature of their acute behavioral toxicology and on their abuse.

Animals↗

Deposition and early disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat.

Little information exists on the metabolism and potential health effects of 233U and 232U, high-specific-activity U isotopes associated with Th breeder systems. This paper describes the distribution and retention of the two isotopes following inhalation of uranyl nitrate, a simulated process solution. The lungs of rats exposed to 233UO2(NO3)2 and 232UO2(NO3)2 aerosols contained from 7 to 23% of the total amount of U retained in the rat after a 30-min inhalation exposure. Uranium was translocated rapidly from the lung and was retained mainly in skeleton, kidney and liver. Amounts equivalent to from one-quarter to one-half the initial lung burden (ILB) of U were excreted in urine the first day after inhalation. Radiation dose estimates based on 233U and 232U retention kinetics indicate that lung and skeleton would be the target organs for delayed radiation effects.

Administration, Inhalation↗

NTP technical report on the toxicity studies of N,N-Dimethylformamide (CAS No. 68-12-2) Administered by Inhalation to F344/N Rats and B6C3F1 Mice.

N,N-Dimethylformamide (DMF), a colorless liquid with a high boiling point, is a solvent used in a large number of industrial processes. Male and female F344/N rats (30/sex/group) and B6C3F1 mice (10/sex/group) were exposed to DMF vapors at concentrations of 0, 50, 100, 200, 400, or 800 ppm, 6 hours/day, 5 days/week, for 13 weeks in whole body exposure inhalation studies. In addition to histopathology, sperm morphology, and vaginal cytology, which were evaluated in both species, the studies examined clinical pathology, cardiovascular, and renal function in rats only. In genetic toxicity studies, DMF was not mutagenic in Salmonella typhimurium strains TA100, TA1535, TA1537, or TA98, with or without S9 activation, nor did it induce germ cell mutations in male Drosophila melanogaster treated by feeding or injection. No induction of sister chromatid exchanges or chromosomal aberrations was noted in cultured Chinese hamster ovary cells treated in vitro with DMF, with or without an S9 metabolic activation system. In one laboratory, a marginal increase in mutant colonies was observed after treatment of mouse lymphoma L5178Y/TK+/- cells with DMF in the absence of S9; results from studies in 2 other laboratories were negative. In the 13-week studies, all rats survived exposures to DMF. Body weight gains were reduced by 50-65% in rats exposed at 800 ppm and to a lesser extent in the 400 ppm group. Evidence of hepatocellular injury was noted as early as day 4, based on increases in activities of liver-specific enzymes in serum in rats of both sexes exposed at 200-800 ppm. Serum cholesterol levels were increased at all exposure concentrations. Relative liver weights were increased in male rats exposed at 100 ppm and higher concentrations, and in female rats at all concentrations. Minimal to moderate centrilobular hepatocellular necrosis was seen in rats of both sexes exposed at 400 and 800 ppm; the lesion was more severe in females. There were no clear, adverse effects seen in urinalyses, in electrocardiographic studies, or in male reproductive system evaluations that could be related to DMF exposure. Hematologic studies showed mild hemoconcentration in males and females. Prolonged diestrus was observed in females exposed at 800 ppm. Among mice exposed to DMF for 13 weeks, there was no chemically related mortality. Body weight gains were approximately 30% less than controls in females exposed at 800 ppm. Relative liver weights were increased in males and females at all exposure concentrations. Centrilobular hepatocellular hypertrophy (minimal to mild) was found in all groups of male mice exposed to DMF, and in female mice exposed at 100 ppm and higher concentrations. The length of the estrous cycle in mice increased with increasing DMF exposure. In summary, DMF-related effects were seen in the liver of both rats and mice, with rats being more severely affected. For rats of both sexes, the no-observed-adverse-effect level (NOAEL) was 200 ppm, based on the absence of liver histopathology, although liver function assays and liver weights showed changes at all exposure levels (as low as 50 ppm). For mice, hepatocellular hypertrophy or increased liver weights occurred at all exposure concentrations. Synonyms: DMF, DMFA.

Journal Article↗

Safety assessment of MIBK (methyl isobutyl ketone).

MIBK (Methyl Isobutyl Ketone) is an aliphatic ketone that functions as both a denaturant and solvent in cosmetic products. Current use in cosmetic products is very limited, but MIBK is reported to be used in one nail correction pen (volume = 3 ml) at a concentration of 21%. The maximum percutaneous absorption rate in guinea pigs is 1.1 micromol/min/cm2 at 10 to 45 min. Metabolites include 4-hydroxy-4-methyl-2-pentanone (oxidation product) and 4-methyl-2-pentanol (4-MPOL) (reduction product). Values for the serum half-life and total clearance time of MIBK in animals were 66 min and 6 h, respectively. In clinical tests, most of the absorbed MIBK had been eliminated from the body 90 min post exposure. MIBK was not toxic via the oral or dermal route of exposure in acute, short-term, or subchronic animal studies, except that nephrotoxicity was observed in rats dosed with 1 g/kg in a short-term study. MIBK was an ocular and skin irritant in animal tests. Ocular irritation was noted in 12 volunteers exposed to 200 ppm MIBK for 15 min in a clinical test. A depression of the vestibulo-oculomotor reflex was seen with intravenous infusion of MIBK (in an emulsion) at 30 microM/kg/min in female rats. The no-observed-effect level in rats exposed orally to MIBK was 50 mg/kg. Both gross and microscopic evidence of lung damage were reported in acute inhalation toxicity studies in animals. Short-term and subchronic inhalation exposures (as low as 100 ppm) produced effects in the kidney and liver that were species and sex dependent. Dermal doses of 300 or 600 mg/kg for 4 months in rats produced reduced mitotic activity in hair follicles, increased thickness of horny and granular cell layers of the epidermis, a decrease in the number of reactive centers in follicles (spleen), an increase in the number of iron-containing pigments in the area of the red pulp (spleen), and a reduction in the lipid content of the cortical layer of the adrenal glands. Neuropathological changes in the most distal portions of the tibial and ulnar nerves were observed in young adult rats which inhaled 1500 ppm MIBK for up to 5 months. No adverse effects were seen in any other neurological end point by any route of exposure in other studies using rats or other animal species. Clinical tests demonstrated a threshold for MIBK-induced irritation of the lungs at 0.03 to 0.1 mg/L after 1 min of respiration. MIBK was not mutagenic in the Ames test or in a mitotic gene-conversion assay in bacteria. Mammalian mutagenicity test results were also negative in the following assays: mouse lymphoma, unscheduled DNA synthesis, micronucleus, cell transformation, and chromosome damage. MIBK did not induce any treatment-related increases in embryotoxicity or fetal malformations in pregnant Fischer 344 rats or CD-1 mice that inhaled MIBK at concentrations of 300, 1000, or 3000 ppm. There was evidence of treatment-related maternal toxicity only at the highest concentration tested. MIBK applied to the tail of rats daily at doses of 300 or 600 mg/kg for 4 months produced changes in the testes, including a reduction in the number of spermatocytes, spermatids, and spermatozoa. An ongoing carcinogenicity study of MIBK being conducted by the National Toxicology Program will be considered when the results are available. On the basis of the information that is currently available, MIBK is considered safe as used in nail polish removers and as an alcohol denaturant in cosmetic products.

Animals↗

Animal model for the study of methanol toxicity: comparison of folate-reduced rat responses with published monkey data.

We attempted to develop a rodent model that exhibits characteristics of human methanol toxicities such as acidosis and visual dysfunction, which are correlated with an accumulation of formate, a toxic metabolite of methanol. Initially three groups of Long-Evans rats with different levels of liver folate were prepared and examined for formate accumulation after methanol administration (3.5 g/kg). The folate-reduced (FR) rats prepared by feeding a folate-deficient diet with 1% succinylsulfathiazole yielded blood formate levels equivalent to those found in methanol-intoxicated humans and developed signs of the visual system toxicity (a manuscript on the latter aspect is in preparation). Responses of FR rats to a variety of methanol exposure scenarios were then investigated, and the results were compared with those reported in the literature for monkeys. Formate accumulation and/or lethality were used as toxic parameters for this comparative evaluation. In FR rats dosed orally with 3 g/kg, the blood formate concentration was 9.2 mmol/L at 24 h postadministration and increased to 15.6 mmol/L at 48 h. The same dose given to monkeys yielded a plateau of 7.4 mmol/L at 12 h after methanol administration, and stayed at this level for an additional 12 h. The area under the concentration vs. time curve for blood formate in FR rats was 2.5-fold greater than that in monkeys when 2.0 g/kg methanol was administered. After a 6-h exposure to 1200 ppm and 2000 ppm methanol, the blood formate concentrations in FR rats were increased by 370% and 636% above the endogenous level, respectively. However, blood formate did not accumulate above the endogenous level when monkeys were exposed to methanol up to 2000 ppm for 6 h. Under acute inhalation exposure conditions, FR rats exposed to 3000 ppm methanol, 20 h/d, could not survive more than 4 d. On the other hand, monkeys exposed to 3000 ppm, 21 h/d, out-lived 20 d. Moreover, monkeys survived for more than 4 d even after an exposure to 10,000 ppm. Thus, these results indicate that FR rats are more sensitive to methanol challenges than monkeys, and suggest that the FR rat could be a congruous animal model for evaluating the health effects of methanol in humans.

Administration, Inhalation↗

Low-level toluene disrupts auditory function in guinea pigs.

Toluene appears to have adverse effects on the human auditory system, but it is difficult to estimate its potency since it is commonly present in the workplace in combination with noise exposure; workplace noise exposures are often highly variable. Studies designed to assess toluene ototoxicity specifically have been limited to high-dose studies in a single laboratory animal model, the rat. Here permanent hearing loss has been observed at concentrations of 1000 ppm toluene and greater after inhalation exposure for 5 days, 6 h/day. The OSHA threshold limit value for toluene is only 100 ppm. The current study focuses on the onset of toluene ototoxicity acutely in the guinea pig and in adducing a mechanism of effect. In this study, evidence is presented for the impairment of auditory function by toluene in the guinea pig, at a concentration substantially lower than that used for studying permanent impairment in the rat. The impaired function was correlated with reduced energy metabolism in outer hair cells. Assessment of auditory function was made using distortion product otoacoustic emissions (DPOAE) with subsequent measurement of succinate dehydrogenase (SDH) staining density in hair cells using surface preparations. Temporary disruption of auditory function in guinea pigs is seen in subjects exposed to 250, 500, and 1000 ppm toluene for 8 h/day, 5 day/week for 1 and 4 weeks. Concentrations as low as 250 ppm toluene were able to disrupt auditory function acutely in the guinea pig, and 500 and 1000 ppm toluene produced greater acute dysfunction. SDH staining suggests that reduced enzyme activity in the midfrequency region of the cochlea occurs acutely following toluene exposure. Although the auditory dysfunction progressed between 1 and 4 weeks of exposure, a permanent loss did not develop for these subjects and hair cell death was not seen. The current study identifies early evidence of auditory system impairment in the guinea pig at low toluene concentration and evidence for impairment of energy production in hair cells. While even a transient auditory impairment has implications for workplace safety, additional study on the transition from such acute effects to permanent impairment is essential.

Animals↗

A physiologically based pharmacokinetic model for inhalation and intravenous administration of naphthalene in rats and mice.

A diffusion limited physiologically based pharmacokinetic model for rats and mice was developed to characterize the absorption, distribution, metabolism, and elimination of naphthalene after inhalation exposure. This model includes compartments for arterial and venous blood, lung, liver, kidney, fat, and other organs. Primary sites for naphthalene metabolism to naphthalene oxide are the lung and the liver. The data used to create this model were generated from National Toxicology Program inhalation and iv studies on naphthalene and consisted of blood time-course data of the parent compound in both rats and mice. To examine the basis for possible interspecies differences in response to naphthalene, the model was extended to describe the distribution and metabolism of naphthalene oxide and the depletion and resynthesis of glutathione. After testing several alternative models, the one presented in this paper shows the best fit to the data with the fewest assumptions possible. The model indicates that tissue dosimetry of the parent compound alone does not explain why this chemical was carcinogenic to the female mouse lung but not to the rat lung. The species difference may be due to a combination of higher levels of naphthalene oxide in the mouse lung and a greater susceptibility of the mouse lung to epoxide-induced carcinogenesis. However, conclusions regarding which metabolite(s) may be responsible for the lung toxicity could not be reached.

Administration, Inhalation↗

Insights into the toxicokinetics and toxicodynamics of 1,3-butadiene.

1,3 Butadiene (BD) is a colorless gas used in the production of synthetic rubber and plastics. BD is carcinogenic in rats and mice, however, there are striking species differences in cancer potency and spectrum of tumors, with mice being more susceptible to tumor induction than rats. Epidemiology studies suggest an excess incidence of leukemia in workers in the styrene-butadiene rubber industry. Consideration of mechanisms of BD carcinogenicity can provide insights into differences in cancer potency between rodents and serve to elucidate the extent to which BD exposure may cause cancer in humans. Mechanistic research in the areas of biochemical toxicology, molecular biology, molecular dosimetry, and susceptibility factors can impact BD cancer risk assessment for humans. This research has focused on quantitating species differences in the metabolism of BD and BD epoxides, defining molecular lesions produced by BD epoxides, identifying biomarkers for BD exposure to explore metabolic pathways in humans, and determining potential risk factors for sensitive subpopulations. BD is activated by P450 isozymes, including CYP2E1, to at least two genotoxic metabolites, epoxybutene (EB) and diepoxybutane (DEB). Dosimetry data from several laboratories on EB and DEB following inhalation exposure to BD indicate that blood concentrations of EB were four-eight-fold higher in mice compared with rats and that blood concentrations of DEB were 25-100-fold higher in mice than in rats. The higher levels of these two DNA-reactive metabolites in mice compared with rats probably contribute to the species differences in carcinogenic effects of BD between mice and rats. In vitro metabolism studies of BD in rats, mice, and human tissues indicate that there are significant quantitative species differences in the metabolic activation of BD to EB and DEB and the detoxication of EB and DEB. Activation/detoxication ratios calculated using in vitro kinetic constants reveal that ratios in mice were greater than in both rats and humans. In vitro data are consistent with in vivo dosimetry data and cancer potency for rodents, and suggest that humans may be at a decreased risk. Data on mutagenicity and mutational spectra of BD epoxides show mechanistic differences between EB- and DEB-induced mutational events suggesting involvement of DEB in the development of cancer. Concentrations of DEB that are genotoxic in vitro are within the range of concentrations measured in mice in vivo, whereas concentrations of EB that are genotoxic in vitro are ten-100-fold greater than concentrations observed in vivo. Characterization of molecular events indicate that EB-induced genotoxicity is due to point mutations and small deletions, while DEB induces point mutations, small deletions, and large-scale deletions involving many base pairs. The extent to which epoxybutanediol is involved in BD carcinogenesis is not known. Molecular dosimetry studies in rodents and humans have focused on urinary metabolites and DNA and hemoglobin adducts. Data from these studies are consistent with in vivo and in vitro metabolism data providing further support for the differences in metabolic activation and deactivation of BD and BD epoxides across species and the role of DEB in tumor development. Research on potential susceptibility factors points to other P450 isozymes, in addition to CYP2E1, that are involved in both the metabolic activation and mutagenicity of BD. Taken together, mechanistic data on BD toxicokinetics and toxicodynamics provide an integrated insight into critical steps in initiation of cancer, metabolites responsible for cancer, sensitive biomarkers for exposure, and potential risk factors for individual susceptibility. Available evidence suggests that BD is unlikely to be a human carcinogen at the low exposure concentrations currently encountered in the environment or workplace.

Animals↗

Current in vivo and in vitro screens for inhalant allergy.

Screening for inhalant allergy requires the use of a rapid, accurate, cost-effective methodology for the detection of the presence or absence of allergic responsiveness. In vivo and in vitro methods have been demonstrated to be sensitive and specific in the diagnosis of inhalant allergy, even with panels as small as seven or eight antigens. There is good concurrence between skin testing techniques and various serum measures of specific IgE, and both methods can be used effectively for screening inhalant allergy, although per-test costs for in vitro methods remain higher than comparable costs for skin testing [28]. Although the rapidity of both methods is acceptable, skin testing allows immediate observation and interpretation of test results, whereas all in vitro methods involve serum processing that delays results for hours to days. In general, both in vitro methods and epicutaneous testing with a device such as the Multi-Test II offer the clinician effective techniques in screening for inhalant allergy. Each technique has benefit and can be used in both primary care practices and in specialists' offices. The choice of the primary technique to be used for screening depends on the type of practice, the practice's familiarity with skin testing, the geographic region, and the relevant payer mix. A review of the relevant research on allergy screening suggests that the number of antigens used should be in the range of 8 to 12 and should include representative allergens from all the significant classes for the specific geographic [table: see text] region. This screen would probably contain one or two grasses, weeds, and trees, two or three molds, cat allergen, and one dust mite allergen. A sample panel is demonstrated in Box 6. It is important to recognize that the diagnosis and treatment of inhalant allergy is a fluid process. In patients who have negative allergy screens but for whom suspicion of inhalant allergy remains high, additional testing with ID techniques is sometimes indicated. This procedure might be suggested in patients for whom there is a high suspicion of mold allergy or who have unusual inhalant exposures. These individuals may represent a failure of the screening process and require additional testing. In these unusual cases, the judgment of the otolaryngic allergist is critical in guiding this further diagnostic work-up. The use of screening procedures for the diagnosis of inhalant allergy provides a rapid, accurate, and cost-effective method for evaluating patients with a history suggestive of allergic disease. Research suggests that a screening panel has strong clinometric properties and has both sensitivity and specificity in excess of 95%. It is statistically unlikely that a patient with negative findings to an allergy screen will demonstrate clinically significant inhalant allergy.

Humans↗

Tremorgenic encephalopathy: a role of mycotoxins in the production of CNS disease in humans?

We describe a young man who, shortly after exposure to moldy silage, developed a neurological syndrome consisting of dementia and a remarkable tremor which was precipitated by movement. All symptoms resolved within one week. Despite investigation, no definitive diagnosis was reached. We propose that this patient's illness may have resulted from inhalation exposure to a tremorgenic mycotoxin.

Adolescent↗

Acute hepatotoxicity of ethylene and halogenated ethylenes after PCB pretreatment.

Previous studies from our laboratory have shown that ethylene, vinyl fluoride monomer (VFM), vinyl chloride monomer (VCM), and vinyl bromide monomer (VBM) are all acutely hepatotoxic in rats pretreated with polychlorinated biphenyl (PCB). The time course of hepatic injury development after exposure and several parameters, environmental and chemical, affecting this toxicity were evaluated in the work reported here. Liver injury, as measured by serum alanine-alpha-ketoglutarate transaminase (SAKT) or sorbitol dehydrogenase (SDH), develops progressively over a 24-hr period following a 4-hr inhalation exposure of PCB-pretreated rats to ethylene or VCM. Environmental temperature during exposure to VCM does not affect hepatotoxicity or mortality below 30.3 degrees C. At 33.8 degrees C, however, mortality and SAKT are dramatically increased. Overnight fasting, which depletes hepatic glutathione (GSH) of PCB-pretreated rats before exposure to ethylene or VCM, significantly increases the hepatotoxicity of these compounds as measured by SDH. The combined effects of fasting and of trichloropropane epoxide (TCPE), an inhibitor of epoxide hydrase (EH), were also examined. TCPE treatment of fasted PCB-pretreated rats immediately before exposure was synergistic in increasing the acute toxicity of ethylene and VCM. TCPE increased mortality in fed or fasted rats exposed to VFM, but there was no effect of fasting alone. Both fasting and TCPE increased the sensitivity of PCB-pretreated rats to VBM, but there was not a clearly synergistic effect of fasting plus TCPE. These data suggest that the acute toxicity of these compounds is mediated through epoxide intermediates.

Animals↗

Methyl methacrylate: inhalation developmental toxicity study in rats.

Methyl methacrylate (99.9% pure) was administered by vapor inhalation exposure to five groups (27 rats/group) of presumed pregnant rats (Crl:CD) at concentrations of 0 (control), 99, 304, 1,178, and 2,028 ppm for 6 hr/day on days 6-15 of gestation (G). Maternal body weight, feed consumption, and clinical signs were recorded throughout gestation. Dams were euthanized on day 20 G. Each uterus was weighed and corpora lutea, implantation sites and resorptions were counted. The number of fetuses per litter were counted and their location within the uterus recorded. All fetuses were weighed, sexed and examined for external and skeletal alterations. One half of the fetuses from each litter were examined for visceral alterations. No treatment-related deaths were noted at any concentration tested. Treatment-related effects on maternal body weight and feed consumption were noted at all exposure levels. The decreases in maternal body weight at 99 and 304 ppm were minimal and transient since they returned to control values by the next weighing period. When exposure was discontinued, body weight gain and feed consumption in all exposure groups returned to control values. There were no treatment-related changes in the number of litters produced or in the mean number per litter of corpora lutea, implantations, resorptions, live or dead fetuses, or sex ratio. Fetal body weights were similar between the control and treated groups. There were no treatment-related increases in the type or incidence of external, visceral, or skeletal malformations, developmental variations, or variations indicative of retarded development. Exposure to methyl methacrylate concentrations up to 2,028 ppm resulted in no embryo or fetal toxicity or malformations even at exposure levels that resulted in maternal toxicity.

Administration, Inhalation↗

Computer simulations of human lung structures for medical applications.

Knowledge of the structure of the human lung has salient health effects applications. The clinical issues encompass: (1) aerosol therapy, the targeted delivery of inhaled particles to enhance the efficacies of pharmacologic drugs; and (2) nuclear medicine, where planar gamma camera imaging, Single Photon Emission Computer Tomography (SPECT) and Positron Emission Tomography (PET) assess the distribution patterns of radiolabeled diagnostic particles and gases. If the resolution of such images could be enhanced, medical regimens would greatly benefit. Therefore, the focused objective of our work was to develop 3-D mathematical descriptions of the complex airway networks within the lung. A Silicon Graphics workstation was used to depict the daedal structures. The computer-generated color illustrations presented herein are intended to complement medical investigation. They will assist the clinician by serving as templates for the lung and, thereby, providing a real basis for the analysis of relatively abstract images. The illustrations identify individual airways and could be of great importance to physicians in the treatment of airway diseases occurring at well defined locations (e.g. bronchogenic carcinomas). To demonstrate that computers can be actively integrated into medical research and practice we have addressed SPECT images of a subject. Computer templates will aid future clinical investigators in two major ways: (1) the interpretation of a planar gamma camera, SPECT and PET images; and (2) the design of drug testing protocols using inhalation exposures. Considering their usefulness for demonstration, the lung simulations have the potential of playing a substantive role in education.

Administration, Inhalation↗

Arsenic in the aetiology of cancer.

Arsenic, one of the most significant hazards in the environment affecting millions of people around the world, is associated with several diseases including cancers of skin, lung, urinary bladder, kidney and liver. Groundwater contamination by arsenic is the main route of exposure. Inhalation of airborne arsenic or arsenic-contaminated dust is a common health problem in many ore mines. This review deals with the questions raised in the epidemiological studies such as the dose-response relationship, putative confounders and synergistic effects, and methods evaluating arsenic exposure. Furthermore, it describes the metabolic pathways of arsenic, and its biological modes of action. The role of arsenic in the development of cancer is elucidated in the context of combined epidemiological and biological studies. However, further analyses by means of molecular epidemiology are needed to improve the understanding of cancer aetiology induced by arsenic.

Arsenic↗

The pulmonary effects of ozone and nitrogen dioxide alone and combined in healthy and asthmatic adolescent subjects.

Separate exposures to 0.12 ppm ozone (O3) or 0.18 ppm nitrogen dioxide (NO2) have not demonstrated consistent changes in pulmonary function in adolescent subjects. However, in polluted urban air, O3 and NO2 occur in combination. Therefore, this project was designed to investigate the pulmonary effects of combined O3 and NO2 exposures during intermittent exercise in adolescent subjects. Twelve healthy and twelve well-characterized asthmatic adolescent subjects were exposed randomly to clean air or 0.12 ppm O3 and 0.30 ppm NO2 alone or in combination during 60 minutes of intermittent moderate exercise (32.5 1/min). The inhalation exposures were carried out while the subjects breathed on a rubber mouthpiece with nose clips in place. The following pulmonary functional values were measured before and after exposure: peak flow, total respiratory resistance, maximal flow at 50 and 75 percent of expired vital capacity, forced expiratory volume in one second and forced vital capacity (FVC). Statistical significance of pulmonary function changes was tested by analysis of covariance for repeated measures. After exposure to 0.12 ppm O3 a significant decrease was seen in maximal flow at 50% of FVC in asthmatic subjects. After exposure to 0.30 ppm NO2 a significant decrease was seen in FVC also in the asthmatic subjects. One possible explanation for these changes is the multiple comparison effect. No significant changes in any parameters were seen in the asthmatic subjects after the combined O3-NO2 exposure or in the healthy subjects after any of the exposures.

Adolescent↗

Inorganic particles induce secretion of a macrophage homologue of platelet-derived growth factor in a density-and time-dependent manner in vitro.

The inhalation of inorganic dust can lead to the development of interstitial pulmonary fibrosis, characterized by the accumulation of fibroblasts and connective tissue matrix in the lung interstitium. The fibrosis causes alterations in the architecture of the lung parenchyma, resulting in abnormal gas exchange and hypoxemia. In a rat model of asbestos exposure, inhaled fibers are deposited on alveolar duct bifurcations, followed by an accumulation of alveolar macrophages at the sites of dust deposition. The alveolar macrophage is thought to be a major mediator of the pulmonary inflammatory response to inhaled dust. Platelet-derived growth factor (PDGF) is a cytokine that has potent chemotactic and mitogenic effects on mesenchymal cells, such as fibroblasts and smooth muscle cells. We studied the secretion of an alveolar macrophage-derived homologue of PDGF in response to carbonyl iron spheres or chrysotile asbestos fibers in vitro. We demonstrate here that rat alveolar macrophages attached to a plastic substrate produce 69 +/- 79 picograms (pg) of PDGF per 10 million macrophages. This is similar to amounts recovered from human platelets. In contrast, macrophages exposed to iron spheres secrete 429 +/- 177 pg of PDGF/10(6) macrophages after 24 h in culture. Exposure to asbestos fibers increased the PDGF production to 628 +/- 213 pg/10(6) cells. PDGF secretion was influenced by the particles in a density- and time-dependent manner. We hypothesize that PDGF and other cytokines secreted by macrophages mediate the development of dust-induced lung disease.

Animals↗