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PubMedDate not supplied

Long-term effects of toluene inhalation on rat behavior.

The effect of inhalation exposure to toluene (3700 mg/m3, 1000 ppm, 21 h/day, 5 days/week, during 4 weeks) on male Sprague-Dawley rats was tested. A wide range of test situations was used, including an operant test with baseline performance and extinction, motor coordination, and exploratory activity. All tests were made 11 to 35 days after the end of the exposure. The results indicate that toluene exposure causes a long-lasting impairment on the extinction process and reduction in the variability of the baseline response in the operant behavior situation. Toluene also had an effect on the water regulation.

Administration, Inhalation↗
PubMed1997

Pulmonary retention and clearance of inhaled biopersistent aerosol particles: data-reducing interpolation models and models of physiologically based systems--a review of recent progress and remaining problems.

During the last 40 years, most models of long-term clearance and retention of biopersistent particles in the pulmonary region of the lung were phenomenologically oriented and accounted for only a small portion of the growing insight into lung dynamics by pulmologists, histologists, and biochemists. In this review, theoretical developments of modeling pulmonary dynamics for biopersistent particles during or after inhalation exposure are discussed. Several characteristic examples are given of the present state of the art. Most of the models presently in use are pragmatical compartmental models with a single compartment for the pulmonary region. They relate to observed data and facilitate an interpolation within the range covered by observation. Occasionally, these models are unjustifiably used for extrapolations in efforts to derive hypothetical risk assessments. Modeling efforts aiming at models of physiologically based pulmonary systems with a potential for extrapolations are not common and were published only during the last decade. Of this kind of approach, the review covers four examples. Promising progress has been made, but scarcity of supporting experimental data slows validation and extension. The two most recent model developments are based on a hypothesis by P.E. Morrow. According to Morrow, alveolar clearance is accomplished by mobile alveolar macrophages after phagocytosis of particles on the alveolar surface. The macrophage mobility, however, and thus the efficiency of the transport to the mucociliary escalator of the tracheobronchial tract will eventually decline towards total loss of mobility after the particle burden of the macrophages exceeds a critical value. The POCK model has been evaluated for a variety of chronic and subchronic rat exposure studies with noncytotoxic aerosols and gave good simulation results. The model by Tran et al. appears to be still in the developing stage of facilitating simulations for cytotoxic aerosols, but the combination of both model approaches seems to be a sound route of future efforts.

Administration, Inhalation↗
PubMedDate not supplied

Time-varying concentration profile as a determinant of the inhalation toxicity of carbon tetrachloride.

Certain limitations on the flexibility of small-animal inhalation exposure systems are overcome by the machine control and monitoring of the concentration of the gas or vapor of interest. Computer assistance of chamber operation allows the user to simulate time-varying concentration profiles accurately and repeatedly. We exposed rats to seven different profiles in which the maximum concentration of carbon tetrachloride (CCl4) was 1500 ppm and the product of concentration times time (C X T) was 4500 ppm X h. The purpose was to determine the effects of systematically varying the shape of the concentration profile on the expression of hepatotoxicity of a chemical about which much was already known. All of the exposures were conducted within a span of 6 h. Examination of the severity of vacuolation and pattern of necrosis could be used to distinguish some of the exposure profiles from others. For example, vacuolation was less severe when two equal pulses were presented with an interval of 60 min, rather than 180-240 min. The indexes of necrosis varied in a more complex way, and the differences among the profiles that accounted for the differences in the patterns of the histopathological changes were not immediately apparent. We concluded that the characteristic of a time-related variation in concentration is one of the determinants of the inhalation hepatotoxicity of CCl4 and that the simple, time-weighted, average concentration may not always fairly represent the best model for the study of problems in inhalation toxicology.

Animals↗
PubMed1991

The nitric oxide/heme protein complex as a biologic marker of exposure to nitrogen dioxide in humans, rats, and in vitro models.

In an effort to develop a biologic marker of exposure to nitrogen dioxide (NO2), we investigated the in vivo formation of a complex between heme proteins and nitric oxide (NO). In aqueous solution, NO2 disproportionates to NO and nitrate. The NO binds to the iron of heme proteins to form an electron spin resonance (ESR)-detectable complex. We have shown that when rat liver, lung, or nasal microsomes are exposed to 20 ppm NO2 in vitro, an ESR signal attributable to an NO/heme protein complex is detected. After inhalation exposure of rats to 20 ppm NO2 for 6 h, this same ESR signal was detected in microsomes prepared from the exposed rats' lungs or liver; microsomes prepared from the nasal tissue failed to yield any detectable signal. When we lavaged the lungs of rats exposed for 6 h to 0, 5, 10, 20, or 30 ppm NO2 and isolated the bronchoalveolar cell pellets, the NO/heme protein complex was detected in the cell pellets. We were able to demonstrate a dose-dependent relationship between the ESR signal intensity of the NO/heme protein complex and the NO2 exposure concentration. Finally, we used ESR to examine bronchoalveolar lavage cell pellets obtained from human volunteers exposed to either 1.5 or 4 ppm NO2, for 20 min every other day, for six exposures. No signal was found in any of the samples taken 3 wk prior to NO2 exposure, but an ESR signal attributable to the NO/heme protein complex was detected in every sample obtained after the 4 ppm NO2 exposure and in five of eight samples obtained after the 1.5 ppm NO2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

A comparison of the acute behavioral effects of inhaled amyl, ethyl, and butyl acetate in mice.

The acute neurobehavioral effects of three acetates (amyl, ethyl, and n-butyl acetate) were investigated after 20-min inhalation exposures in mice using locomotor activity and a functional observational battery (FOB). Ethyl and n-butyl acetate produced significant decreases in locomotor activity at the highest concentrations examined, while amyl acetate was without effect. Minimally effective concentrations for activity-decreasing effects were 2000 ppm for ethyl acetate and 8000 ppm for n-butyl acetate. The potency order was similar in the FOB where ethyl acetate was more potent in disrupting the neurobehavioral measures. The FOB profile of effects for all three acetates included changes in posture, decreased arousal, increased tonic/clonic movements, disturbances in gait, delayed righting reflexes, and increased sensorimotor reactivity. Furthermore, handling-induced convulsions were produced in some mice acutely exposed to each of these acetates. Recovery from the acute effects of these acetates was rapid and began within minutes of removal from the exposure chamber. The acetates produced a profile of neurobehavioral effects that were different from those reported for depressant solvents (i.e., toluene, 1,1,1-trichloroethane) that are subject to abuse. Evidence is emerging for qualitative differences in the acute neurobehavioral effects of various volatile chemicals.

Acetates↗
PubMed1984

Development of rodent peripheral blood lymphocyte culture systems to detect cytogenetic damage in vivo.

Peripheral blood lymphocytes (PBLs) offer many advantages for in vivo cytogenetic studies. They can be removed nonlethally from the animal allowing a subject to serve as its own control, permitting the analysis of cytogenetic damage over time. Furthermore, mature PBLs normally do not divide, and some populations are long-lived. Thus, they have the potential to accumulate DNA lesions during chronic exposures to genotoxicants. We have developed standard methodologies for the whole blood culture of rat and mouse PBLs to serve as models for determining the sensitivity of PBLs to cytogenetic damage. The cultures obtained with these protocols give reproducible results with high mitotic indices, stable baseline sister chromatid exchange (SCE) frequencies, and ample numbers of first-and second-division methaphases for scoring both chromosomal aberrations and SCEs. The methodologies have been especially useful for examining cytogenetic damage after inhalation exposures to toxicants such as ethylene oxide, formaldehyde, benzene, and nitrobenzene. Of these compounds, only benzene and ethylene oxide were found to induce significant dose-dependent increases in SCEs in PBLs. Also, dose-response curves have been obtained for several carcinogens administered by ip injection. These studies show that PBLs are sensitive indicators of the genotoxic effects of the carcinogens benzo (a)pyrene, 2-acetylaminofluorene, cyclophosphamide (CP), N-nitrosomorpholine, and ethylmethanesulfonate (EMS). In addition, because subpopulations of lymphocytes can be stimulated to divide using different mitogens, it has been possible to compare the sensitivity of murine B and T lymphocytes following in vitro and in vivo cyclophosphamide exposure. Once the sensitivity and selectivity of rodent lymphocyte cultures are determined, these assays should be valuable not only as a means for predicting which environmental agents could lead to increases in human cytogenetic damage, but also as a way to corroborate human cytogenetic studies.

Alkylating Agents↗
PubMedDate not supplied

Two-generation reproduction study on commercial hexane solvent.

The reproductive effects of inhalation exposure to commercial hexane vapors were evaluated in Sprague-Dawley rats. Males and females were exposed to commercial hexane vapor at target concentrations of 0, 900, 3000 or 9000 ppm for 6 h a day, 5 or 7 days a week, over two generations. In addition to pre-breed exposures of 10 weeks' duration, exposures continued through mating, gestation and lactation. At both the F0 breed to produce F1 litters and the F1 breed to produce F2 litters, reproductive parameters were unaffected by commercial hexane exposure. The mating, fertility and gestational indices, as well as litter size and postnatal survival, were not significantly different between exposure groups. However, reductions in body weight and body weight gain were observed in both F1 and F2 litters exposed to 9000 ppm. Effects on body weight were not observed in offspring exposed to the two lower concentrations of commercial hexane. Histopathological examination of selected tissues revealed hyaline droplet nephropathy in adult F0 and F1 males exposed to 9000 ppm. This finding was anticipated and is not believed to be relevant for the assessment of human health effects. No other treatment-related histopathological lesions were observed. Thus, exposure of rats to commercial hexane for two generations resulted in reduced body weight gains at 9000 ppm but no adverse effects on reproduction. These findings suggest that occupational exposure to commercial hexane vapors at currently recommended threshold limit value concentrations (i.e. TLV for n-hexane is 50 ppm and TLV for other hexane isomers is 500 ppm) should not pose a reproductive hazard.

Administration, Inhalation↗
PubMed1999

Characterization of hepatocellular resistance and susceptibility to styrene toxicity in B6C3F1 mice.

Short-term inhalation exposure of B6C3F1 mice to styrene causes necrosis of centrilobular (CL) hepatocytes. However, in spite of continued exposure, the necrotic parenchyma is rapidly regenerated, indicating resistance by regenerated cells to styrene toxicity. These studies were conducted to test the hypothesis that resistance to repeated styrene exposure is due to sustained cell proliferation, with production of hepatocytes that have reduced metabolic capacity. Male mice were exposed to air or 500 ppm styrene (6 h/day); hepatotoxicity was evaluated by microscopic examination, serum liver enzyme levels, and bromodeoxyuridine (BrdU)-labeling index (LI). Metabolism was assessed by measurement of blood styrene and styrene oxide. Both single and repeated exposures to styrene resulted in mortality by Day 2; in mice that survived, there was CL necrosis with elevated BrdU LI at Day 6, and complete restoration of the necrotic parenchyma by Day 15. The BrdU LI in mice given a single exposure had returned to control levels by Day 15. Re-exposure of these mice on Day 15 resulted in additional mortality and hepatocellular necrosis, indicating that regenerated CL cells were again susceptible to the cytolethal effect of styrene following a 14-day recovery. However, in mice repeatedly exposed to styrene for 14 days, the BrdU LI remained significantly increased on Day 15, with preferential labeling of CL hepatocytes with enlarged nuclei (karyomegaly). If repeated exposures were followed by a 10-day recovery period, CL karyomegaly persisted, but the BrdU LI returned to control level and CL hepatocytes became susceptible again to styrene toxicity as demonstrated by additional mortality and acute necrosis after a challenge exposure. These findings indicated a requirement for continued styrene exposure and DNA synthesis in order to maintain this resistant phenotype. Analyses of proliferating-cell nuclear-antigen (PCNA) labeling were conducted to further characterize the cell cycle kinetics of these hepatocytes. The proportion of cells in S-phase was increased by repeated exposure. However, PCNA analysis also revealed an even larger increase in the G1 cell compartment with repeated exposures, without a concurrent increase in G2 phase or in mitotic cell numbers. These data indicate that resistance to styrene-induced necrosis under conditions of repeated exposure is not due to sustained cell turnover and production of new, metabolically inactive cells, but rather is due to some other, as yet unknown, protective phenotype of the regenerated cells.

Administration, Inhalation↗
PubMed2004

Animal models for diisocyanate asthma: answers for lingering questions.

PURPOSE OF REVIEW: Diisocyanates are the leading cause of occupational asthma, the most commonly reported lung disease associated with the workplace. Clinical studies have implicated the immune system in the pathogenesis of occupational asthma, but ethical and moral issues prevent mechanistic investigations in humans. For this reason, the development and characterization of animal models are germane to further understanding of diisocyanate occupational asthma and to identify avenues for therapeutic intervention. This review will highlight important features of existing experimental animal models with emphasis on new developments. RECENT FINDINGS: Experimental animal models of diisocyanate occupational asthma have demonstrated an immunological basis for the disease. Mice can be sensitized by dermal or respiratory exposure, suggesting that either exposure route may be important in the workplace. Recent findings show that sensitized mice develop airway hyperreactivity and inflammation, reflective of human disease. The transfer of lymphocytes or serum from sensitized mice can cause clinical disease in naive mice. Transgenic animals have identified a role for specific immunity, including the involvement of T-helper type 1/2 responses as well as CD4 and CD8 T cells in diisocyanate occupational asthma. Recent animal models have shown that sensitization can occur through subchronic inhalation of vapor-phase diisocyanate at levels as low as 20 ppb. SUMMARY: Recent progress using animal models has been instrumental in furthering current understanding of the involvement of the immune system in disease pathogenesis. The demonstration of diisocyanate occupational asthma in a murine model after sub-chronic inhalation exposure at relevant exposure levels should provide opportunities for more accurate risk assessment data.

Air Pollutants, Occupational↗
PubMed1989

The ultrastructure and reversibility of testicular atrophy induced by ethylene glycol monomethyl ether (EGME) in the rat.

Inhalation exposure to 300 ppm ethylene glycol monomethyl ether (EGME) for 3 days produced degenerative changes in spermatocytes of pachytene and meiotic division at spermatogenic stage XIV in rats. However, a wide range of germ cell types including spermatogonia was affected and the stage-specific damage was not discernible after 2 weeks exposure to 300 ppm EGME. The stage-specific damage was related to exposure concentration-time course. In early stages, degenerating spermatocytes showed nuclear chromatin clumping around synaptonemal complexes, cytoplasmic vesiculation with electron-dense material deposition, and disruption of the plasma membrane. Chromosomal microtubules in the meiotic division of spermatocytes were discontinued with deposition of electron-dense chromatin material. Sertoli cells showed cytoplasmic vacuolization, contact loss to germ cells, and cytoplasmic processes fragmentation with disrupted microtubules. Degenerative pachytene or meiotic spermatocytes were associated with disrupted Sertoli-germ cell relationship, chromosomal microtubules, and synaptonemal complexes. Spermatid degeneration and giant cell formation were observed after spermatocyte degeneration. Spermatid degeneration appeared to be a secondary change resulting from disrupted Sertoli-to-germ cell association. After 14 days post-exposure (PE) following 2 weeks exposure, some tubules were lined with regenerating spermatocytes with or without round spermatids. By 42 days PE, many tubules regained normal germinal epithelium, but some tubules were still atrophic even after 84 days PE. Reversibility of testicular atrophy was inversely proportional to severity of damaged stem cells.

Administration, Inhalation↗
PubMed1983

Inhalation carcinogenesis of high-fired 241AmO2 in rats.

Wistar rats were given a single inhalation exposure to high-fired 241AmO2 particles and examined over their life span. A total of 310 rats were used: 259 exposed to 241Am for life-span study, 30 exposed to 241Am for early metabolism study, and 21 unexposed life-span controls. The activity median aerodynamic diameter of the aerosols was 0.75-1.39 microns. About 55% of alveolarly deposited 241Am was cleared from the lung with a half-life of 0.5 days, 37% with a half-life of 7 days, and 8% with a half-life of 580 days. Group mean lung doses ranged from less than 5.7 rad up to 1500 rad. Significant early mortality due to radiation pneumonitis was seen only in the highest exposure group. The percentage of rats with lung tumors was 0% for controls (21 rats), 1% at lifetime lung doses less than 10 rad (139 rats), 7% at 10-50 rad (86 rats), 0% at 50-100 rad (9 rats), 60% at 100-500 rad (10 rats), and 7% at 500 rad (15 rats). Only one liver and one bone tumor were found in all exposed rats, both at lifetime tissue doses less than 10 rad. The fate and carcinogenicity of inhaled 241AmO2 in the lung of rats were similar to what has previously been described for inhaled 244CmO2.

Aerosols↗
PubMed1991

Dichloroacetonitrile, a by-product of water chlorination, induces aneuploidy in Drosophila.

Nitriles have been shown to be potent inducers of aneuploidy in yeast and Drosophila test systems. Haloacetonitriles are by-products of water chlorination that have been shown to be mutagenic and carcinogenic following topical application. In this report we show that dichloroacetonitrile, but not dibromoacetonitrile, is an effective inducer of aneuploidy in oocytes of Drosophila melanogaster. Following inhalation exposure of ZESTE adult females, dichloroacetonitrile (8.6 ppm) induced highly significant increments in the frequencies of sex chromosome loss and gain. Sodium cyanide was also found to be a highly effective inducer of germline aneuploidy, suggesting that cyanide toxicity may contribute to potency of nitriles as inducers of aneuploidy.

Acetonitriles↗
PubMed2003

World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.

Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass median aerodynamic diameter < 2.5 microm (PM2.5)] has detrimental respiratory effects in mice to contribute to the risk assessment of WTC-derived pollutants. Samples of WTC PM2.5 were derived from settled dust collected at several locations around Ground Zero on 12 and 13 September 2001. Aspirated samples of WTC PM2.5 induced mild to moderate degrees of pulmonary inflammation 1 day after exposure but only at a relatively high dose (100 microg). This response was not as great as that caused by 100 microg PM2.5 derived from residual oil fly ash (ROFA) or Washington, DC, ambient air PM [National Institute of Standards and Technology, Standard Reference Material (SRM) 1649a]. However, this same dose of WTC PM2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to that from SRM 1649a and to a greater degree than that from ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that exposure to high levels of WTC PM2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM2.5 that would cause comparable doses in people are high (approximately 425 microg/m3 for 8 hr) but conceivable in the aftermath of the collapse of the towers when rescue and salvage efforts were in effect. We conclude that a high-level exposure to WTC PM2.5 could cause pulmonary inflammation and airway hyperresponsiveness in people. The effects of chronic exposures to lower levels of WTC PM2.5, the persistence of any respiratory effects, and the effects of coarser WTC PM are unknown and were not examined in these studies. Degree of exposure and respiratory protection, individual differences in sensitivity to WTC PM2.5, and species differences in responses must be considered in assessing the risks of exposure to WTC PM2.5.

Air Pollutants↗
PubMed1994

Analysis of sister chromatid exchange, micronucleus and chromosomal aberration frequencies in rodents exposed to mosquito coil smoke by inhalation route.

Mosquito coil smoke emitting from a mosquito repellent, was tested for its mutagenic effect in bone marrow cells from mouse and rat after 4 h acute inhalation exposure. Coil smoke with suspended particulate concentrations of 99-129 mg/m3, significantly elevated the frequencies of sister chromatid exchanges in bone marrow cells and micronuclei in polychromatic erythrocytes. Analysis of chromosomal aberrations in metaphases also revealed a significantly higher incidence of chromosomal aberration frequency in exposed rats and mice.

Administration, Inhalation↗
PubMed1996

Pharmacokinetic model of dioxin and furan levels in adipose tissue from sawmill work involving chlorophenate fungicides.

Sawmill workers in British Columbia (B.C.), Canada, have been exposed to chlorophenate fungicides which are known to be contaminated with polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). Due to concern about the potential of these workers to have significant body burdens of PCDD/Fs, and the absence of measurements in these workers, a single-compartment pharmacokinetic model was developed to estimate the concentration of PCDD/Fs in the fat tissue of the sawmill workers. Data from a large cohort of B.C. sawmill workers and literature-based data on chlorophenate exposures and PCDD/F concentrations in chlorophenates were used in Monte Carlo simulations to predict a PCDD/F body burden distribution. The median concentrations of HxCDF and HpCDF predicted using the model for the B.C. sawmill worker population exceeded the range measured in unexposed populations. PeCDF and OCDF concentrations exceeded the range measured in unexposed populations at the 70th percentile of the model-predicted distribution, and PeCDD at the 90th percentile. The primary limitation of the model was the scarcity of input data about actual dermal and inhalation exposures to chlorophenates.

Adipose Tissue↗
PubMed1988

The effect of inhaled sulfur dioxide and systemic sulfite on the induction of lung carcinoma in rats by benzo[a]pyrene.

In a previous study at this Institute, inhaled sulfur dioxide (SO2) was shown to enhance the induction by inhaled benzo[a]pyrene (BaP) of squamous cell carcinoma (SQCA) of the respiratory tract of rats (S. Laskin, M. Kuschner, A. Sellakumar, and G. V. Katz, 1976, In "Air Pollution and the Lung," pp. 190-213). We attempted to confirm and extend this finding by using an experimental protocol intended to illuminate the role of SO2. Rats were treated with BaP by 15 consecutive weekly intratracheal instillations. Some of these rats were simultaneously exposed either to SO2 by inhalation or to sulfite/bisulfite anions that accumulated systemically from endogenous generation in rats with induced sulfite oxidase deficiency. The total treatment period spanned 21 weeks, after which the rats were observed for the development of tumors. BaP-treated rats began to die with SQCA of the respiratory tract at approximately 200 days after the first BaP treatment and at 2 years after the first treatment nearly all rats in the BaP-treated groups had died, most with SQCA. Survival in the control groups was excellent and the health of all groups (aside from pulmonary SQCA in BaP-treated groups) was also excellent. The probability of dying with a pulmonary SQCA in the experimental groups treated with BaP, BaP plus inhaled SO2, and BaP plus systemic sulfite/bisulfite was calculated by the logrank analysis. The data sets of SQCA probability from these groups were not statistically different (i.e., P greater than 0.05) by the chi 2 test indicating that, in this experiment, neither inhalation exposure to SO2 nor systemic exposure to sulfite/bisulfite anions affected the induction of SQCA of the lung by intratracheally instilled BaP. We conclude that the results of this study do not support an etiological role for either SO2 or sulfite/bisulfite anions in the induction of SQCA of the respiratory tract by BaP.

Administration, Inhalation↗
PubMed1996

Detection of aldehydes in bronchoalveolar lavage of rats exposed to ozone.

We report the detection of hexanal, heptanal, and nonanal in the bronchoalveolar lavage (BAL) of rats exposed to 0.5 to 10 ppm ozone with or without simultaneous 5% CO2. These three aldehydes primarily result from the Criegee ozonation of specific mono- or polyunsaturated fatty acids that are present in significant amounts in the rat lung; e.g., palmitoleic acid gives heptanal, oleic gives nonanal, and linoleic and arachidonic can give hexanal. Hexanal also is produced in the ozone-initiated autoxidation of any n-6 polyunsaturated fatty acid, and thus is a measure of generalized oxidative stress. (Monounsaturated fatty acids do not undergo appreciable autoxidation.) This detection and quantitation of aldehydes directly demonstrates for the first time that unsaturated fatty acids undergo Criegee ozonation in the lung when ozone is inhaled. Exposure to ozone alone produced smaller apparent yields of the three aldehydes than did exposure to ozone plus 5% CO2. Hexanal, heptanal, and nonanal can be detected in BAL of rats 5 hr after the end of the ozone exposure, but after more than 5 hr only hexanal can be found, probably from ozone-induced autoxidation of n-6 PUFA that continues after ozone exposure. The measured amounts of aldehydes are low, and that, coupled with inherent biovariability, suggests that aldehydes may not be useful as quantitative dosimeters. However, they can be useful biomarkers, since some of these aldehydes (e.g., nonanal) are produced in ozone-specific pathways and aldehydes are the most easily detected among the lipid ozonation products (LOP). Furthermore, our identification of these aldehydes by BAL, coupled with our recognition that ozone itself cannot penetrate far enough into the lung to cause many of the effects associated with the inhalation of ozone, suggests that these aldehydes, as well as other types of LOP (such as hydroxyhydroperoxides and Criegee ozonides), may act as signal transduction molecules, activating lipases and causing the release of inflammatory molecules by a variety of pathways not yet entirely elucidated.

Aldehydes↗
PubMed1989

Acrylic resin pneumoconiosis: report of a case in a dental student.

Pneumoconiosis in dental laboratory workers has been associated with exposure to metal alloys and silica used in the manufacturing of dental prosthetics. In this report, we describe a 27-yr-old dental student who was found to have bilateral basal pulmonary interstitial infiltrates and nodules on a chest roentgenogram after a brief episode of upper respiratory infection. An open lung biopsy revealed interstitial pneumonitis with an abundance of vacuolated macrophages in the alveolar spaces. Ultrastructural analysis showed in the alveolar and interstitial spaces the accumulation of macrophages laden with electron-lucent bodies resembling plastic beads. An inhalation exposure history, taken subsequent to these findings, revealed exposure to high levels of acrylic plastic in a dental school laboratory. Removal from the site of exposure has resulted in the gradual resolution of the roentgenographic abnormalities.

Acrylic Resins↗