Stimulation of phagocytosis by ultrafine particles.
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Animals↗
Biomedical subjects
B Nemery
Publications and source records attributed to B Nemery.
Passage of intratracheally instilled ultrafine particles from the lung into the systemic circulation in hamster.
The mechanisms of particulate pollution-related cardiovascular morbidity and mortality are not well understood. We studied the passage of radioactively labeled ultrafine particles after their intratracheal instillation. Hamsters received a single intratracheal instillation of 100 microg albumin nanocolloid particles (nominal diameter < or = 80 nm) labeled with 100 microCi technetium-99m and were killed after 5, 15, 30, and 60 min. In blood, radioactivity, expressed as percentage of total body radioactivity per gram blood, amounted to 2.88 +/- 0.80%, 1.30 +/- 0.17%, 1.52 +/- 0.46%, and 0.21 +/- 0.06% at 5, 15, 30, and 60 min, respectively. Thin-layer chromatography showed only one peak of radioactivity corresponding to unaltered (99m)Tc-albumin nanocolloid. In the liver, radioactivity, expressed as percentage of total radioactivity per organ, amounted to 0.10 +/- 0.07%, 0.23 +/- 0.06%, 1.24 +/- 0.27%, and 0.06 +/- 0.02% at 5, 15, 30, and 60 min, respectively. Lower values were observed in the heart, spleen, kidneys, and brain. Dose dependence was assessed at 30 min following instillation of 10 microg and 1 microg (99m)Tc-albumin per animal (n = 3 at each dose), and values of the same relative magnitudes as after instillation of 100 microg were obtained. We conclude that a significant fraction of (99m)Tc-albumin, taken as a model of ultrafine particles, rapidly diffuses from the lungs into the systemic circulation.
Air Pollutants↗
Polyanions protect against the in vitro pulmonary toxicity of polycationic paint components associated with the Ardystil syndrome.
The polycationic paint components of the Acramin F system have led to severe pulmonary disease in textile printing sprayers in Spain and Algeria (Ardystil syndrome). In order to elucidate the underlying mechanisms of the toxicity of these nitrogen-containing polymeric paint components, Acramin FWR (FWR), Acramin FWN (FWN), and Acrafix FHN (FHN), we have studied the effect of coincubation with polyanionic compounds, Sulodexide (heparin-like substance), DNA and poly-l-glutamic acid (of different lengths) in different pulmonary cell types. This study shows that the cytotoxicity of the three polycationic paint components FWR (a polyurea), FWN (a polyamide-amine), and FHN (a polyamine) is markedly decreased in the presence of the polyanions. It is concluded that the paint components FWR, FWN, and FHN execute their cytotoxicity at least partly by the abundant positive charges these molecules carry at physiological pH.
Adipates↗
The Meuse Valley fog of 1930: an air pollution disaster.
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Air Pollution↗
Genotoxic effects of carbon black particles, diesel exhaust particles, and urban air particulates and their extracts on a human alveolar epithelial cell line (A549) and a human monocytic cell line (THP-1).
The possible genotoxicity of small particulate matter has been under investigation for the last 10 years. Diesel exhaust particles (DEP) are considered as "probably carcinogenic" (IARC group 2A) and a number of studies show genotoxic effects of urban particulate matter (UPM). Carbon black (CB) is carcinogenic in rats. In this study the cytotoxic and genotoxic potency of these three particle types was investigated by exposing human cells (A549 and THP-1 cell lines) in vitro to CB, DEP (SRM 1650, NIST), and UPM (SRM 1648, NIST) for 48 hr. Cytotoxicity was assessed using the Alamar Blue assay, whereas genotoxicity was assessed using the single-cell gel electrophoresis (comet assay). The particles were characterized with regard to their mean diameter in tissue culture medium (CB 100 nm, DEP 400 nm, UPM 2 microm), their total carbon content (CB 99%, DEP 85%, UPM 15%), and their acid-soluble metal composition (UPM >> CB approximately DEP). The concentrations ranged from 16 ng/ml to 16 microg/ml for cytotoxicity tests and from 16 ng/ml to 1.6 microg/ml for genotoxicity tests. In both assays, paraquat was used as a reference chemical. The CB, DEP, and UPM particles showed no significant cytotoxicity. However, all three particles were able to cause significant DNA damage, although to a different extent in the two cell lines. The genotoxicity of washed particles and dichloromethane extracts was also investigated. In THP-1 cells CB washed particles and DEP extracts caused significant DNA damage. This difference in effect may be related to differences in size, structure, and composition of the particles. These results suggest that CB, DEP, and UPM are able to cause DNA damage and, therefore, may contribute to the causation of lung cancer. More detailed studies on influence of size, structure, and composition of the particles are needed.
Air Pollutants↗
Recurrent flu-like illness with migrating pulmonary infiltrates of unknown aetiology.
Migrating pulmonary infiltrates present a difficult diagnostic and therapeutic challenge. We report on eight patients (mean age 51 years, range 32-78 years, with a prolonged history of migrating pulmonary infiltrates of unknown aetiology despite a very elaborate search for infectious causes, hypersensitivity pneumonitis or inhalation fever due to occupational or domestic exposure to fungi, or to other environmental causes, and for humoral or cellular immunological incompetence. These patients (one male, seven females) presented with recurrent episodes (mean 6, range 2-13) of a flu-like illness, often with cough, wheezing and pleuritic chest pain, but without systemic involvement. Previous medical histories were unremarkable. There was no relation with smoking habits, occupation, drug use or other possible exposures. Biochemical data were non-specific. There was no peripheral nor pulmonary eosinophilia; total IgE was normal, with negative RASTs and precipitins to a variety of antigens. Cultures and serological tests for bacteria, viruses, fungi, etc were non-contributory. Chest X-ray and computed tomography (CT) scan showed bilateral migratory pulmonary infiltrates, with a predilection for the middle and lower lung zones, often with a minor-to-moderate pleural effusion. Lung function tests were usually normal; at the most a slight decrease in diffusing capacity was noted in some patients. There was no or only a slight response to antimicrobials; systemic corticosteroids were not given. Further evolution was benign with patients being asymptomatic between the episodes. Despite elaborate investigations, the cause of these 'pneumonias' remains frustratingly unknown.
Adult↗
What happens to the manuscripts that have not been accepted for publication in Occupational and Environmental Medicine?
OBJECTIVES: To evaluate the fate of manuscripts rejected by Occupational and Environmental Medicine (OEM). METHODS: A Medline search was conducted, up to March 2001, to find out whether and where articles submitted to OEM in 1995, 1996, and 1997, but not accepted for publication, were published. The articles were matched by authors and title, sometimes using the abstract to help decide whether the published article was the one that had been previously submitted to OEM. RESULTS: Out of 405 manuscripts rejected (44% of those submitted), 218 articles (54%) were traced in 72 different journals, with more than half being published in seven other major journals dealing with occupational and environmental health (rather than in specialty journals). Most papers were published within 2 years of their initial submission to OEM. Only a small proportion (10%) were published in a journal with a higher impact factor than OEM (1.96 in 1999). CONCLUSION: More than half the articles rejected by OEM found their way into the scientific literature covered by Medline. This figure is comparable with the few available data from other journals. It would be interesting to know the fate of articles published by OEM before they were submitted to our journal.
Bibliometrics↗
Surface of localized pleural plaques quantitated by computed tomography scanning: no relation with cumulative asbestos exposure and no effect on lung function.
To evaluate if there is a relation between the size of asbestos plaques and the level of past exposure and pulmonary function, we measured the surface of localized pleural plaques found on high-resolution (HR) CT scan, using a computerized video display unit-imaging system, in 73 workers (mean age, 43.5 yr) who had worked from 23 to 27 yr in an asbestos-cement factory. Their estimated cumulative exposure to asbestos ranged from 16.4 to 98.7 fiber-years/ ml (mean, 26.3 fiber-years/ml). Lung function measurements included lung volumes, maximal expiratory flows, and diffusing capacity. A control group of 21 workers was examined by the same procedures. Plaques were detected by CT in 51 (70%) asbestos-exposed subjects and in none of the control subjects. The average calculated plaque surface was 47.9 +/- 61.7 cm2 (median, 22.1 cm2; range, 0 to 278.4 cm2). There was no relation between plaque surface and cumulative asbestos exposure (p = 0.24). In the 51 subjects with pleural plaques, the surface of the pleural lesions was not related to cumulative asbestos exposure, or to smoking history or time since first exposure. Neither the presence nor the extent of the plaques was correlated with lung function parameters.
Asbestosis↗
Observer variation in computed tomography of pleural lesions in subjects exposed to indoor asbestos.
To assess the reliability of computed tomography (CT) in detecting discrete pleural lesions, the interobserver and intra-observer variability in reading the conventional and high-resolution CT (HRCT) scans of 100 volunteers, who had worked for > or = 10 yrs in a building with known asbestos contamination, was evaluated. In the first session, pleural abnormalities were detected by a single radiologist (A1) in 13 subjects. In the second session, the scans were read again independently by the same radiologist (A2) and two other experienced radiologists (B, C). The final decision for the presence of pleural lesions was made in a final consensus reading. This gave a diagnosis of pleural abnormalities in 18 subjects, of whom eight (44%) had been detected by all three readers, five (28%) by two readers and four (22%) by only one reader; one scan, rated normal by all readers during the second session, was reconsidered because pleural abnormalities had been noted at the first reading (A1). The intra-observer agreement for reader A was good (kappa (kappa) 0.68) but the interobserver agreement between the readers was only fair to moderate (weighted kappa: A2-B=0.43, A2-C = 0.45, B-C = 0.26) in the second reading session. In conclusion, when looking for the prevalence of pleural lesions in indoor asbestos exposed subjects, the potential lack of consistency in reporting the presence of small pleural abnormalities must be borne in mind and strict precautions must be taken.
Adult↗
Xenobiotic-metabolizing enzyme activities in primary cultures of rat type II pneumocytes and alveolar macrophages.
Because of the evidence for the involvement of xenobiotic bioactivation in pulmonary toxicity and carcinogenesis, it is important to improve our understanding of the xenobiotic-metabolizing enzymes in isolated and cultured specific pulmonary cell populations. Some phase I and phase II xenobiotic-metabolizing enzyme activities, reduced glutathione (GSH), and gamma-glutamyl transferase (gamma-GT) were studied in rat type II pneumocytes and alveolar macrophages cultured for up to 48 h and 3 h, respectively. In type II pneumocytes, 7-ethoxyresorufin activity was not detected. 7-Benzyloxyresorufin (BROD) and 7-pentoxyresorufin (PROD) O-dealkylation decreased at 24 h by 84 and 82%, respectively, and continued to decline over the next 24 h with no measurable PROD at 48 h. The activity of NADPH- and NADH-cytochrome c reductase at 48 h decreased by 31 and 67%, respectively. GST activity decreased by 25 and 42% at 24 and 48 h, respectively. A transient increase in DT-diaphorase activity was observed at 24 h (by 55%). GSH content and gamma-GT activity increased significantly with time in culture. In freshly isolated alveolar macrophages, BROD activity was the only cytochrome P450-dependent alkoxyresorufin-O-dealkylase activity measured. BROD activity decreased by 38% in 3-h-attached macrophages. There were no changes in NADPH- and NADH-cytochrome c reductase, GST, and DT-diaphorase. An increase of GSH (by 24%) was observed in attached macrophages. In conclusion, type II pneumocytes and to a lesser extent alveolar macrophages in primary cultures undergo changes in biotransformation-related enzyme activities and intracellular GSH level that may affect xenobiotic toxicity at different times in culture.
Animals↗
Airborne polyvinyl alcohol (PVA) and cellulose fibre levels in fibre-cement factories in seven European countries.
Because of their relatively high diameter, polyvinyl alcohol (PVA) fibres, as used in fibre-cement, are not fibres as defined by WHO (or other) regulations. Nevertheless, as with all particulate raw materials, it can be questioned if and to what extent particles with critical fibrous dimensions might be generated by the handling or machining of this material. In order to investigate any tendency of PVA fibres to release airborne particles with critical fibrous dimensions (WHO fibres), static and/or personal samples were taken in eight fibre-cement factories at locations where potential exposures to PVA fibres were expected to be the highest. The following locations were surveyed: the PVA fibre weighing station, where PVA bales are opened mechanically and the PVA fibres are dispersed and weighed in a dry state; the fibre-cement slate punching machine; the slate 'riven edge' cutting machine or sheet sawing machine, whichever was present in the respective factories. Since cellulose fibres are an important constituent of fibre-cement, the organic fibre concentrations observed at the machining operations include cellulose. At each factory a control sample was taken in open air. Sampling, sample preparation and sample analysis by scanning electron microscopy (SEM) were performed according to standard German procedures. Only very low number concentrations of organic WHO fibres, ranging from below detection limit to 0.006 f/ml, were found. These levels are lower than the typical levels of organic fibres commonly found in the normal personal environment (0.009-0.02 f/ml), stemming from the release of particles by a person's activities and from clothing and other textiles (bed sheets, blankets, pillow,.). We conclude that the handling of PVA fibres as well as the machining of PVA and cellulose fibre containing cement products in the fibre-cement factories surveyed have a low potential to release fibres with critical fibrous (WHO) dimensions.
Air Pollutants↗
Paracetamol (acetaminophen) cytotoxicity in rat type II pneumocytes and alveolar macrophages in vitro.
Paracetamol (acetaminophen, APAP) liver and kidney cytotoxicity is associated with bioactivation by P450 and/or prostaglandin H synthetase (PGHS) to a reactive metabolite, which depletes GSH, covalently binds to proteins, and leads to oxidative stress. Although APAP may also damage the lung, little is known about the mechanism by which this occurs. We studied the in vitro 24-hr-old type II pneumocytes. A time- and concentration-dependent decrease in intracellular GSH occurred in freshly isolated type II pneumocytes and alveolar macrophages exposed to subtoxic (</= 1 mM) APAP concentrations. In 24-hr-old type II pneumocytes, there were no changes in intracellular GSH concentration after APAP exposure. Potassium ethyl xanthate (a P450 inhibitor) and indomethacin (a PGHS inhibitor) significantly decreased APAP-induced GSH depletion in freshly isolated type II pneumocytes and alveolar macrophages, suggesting that P450 and/or PGHS are involved in APAP bioactivation in these cells.
Acetaminophen↗
In vitro cytotoxicity of various forms of cobalt for rat alveolar macrophages and type II pneumocytes.
It has been shown that cobalt (Co) and the mixture cobalt-tungsten carbide (CoWC) are cytotoxic for alveolar macrophages (AM) and alveolar type II cells (AT-II), but the exact mechanisms of toxicity are not entirely elucidated. In this study, we exposed primary cultures of AT-II and AM, in vitro, to different forms of Co (Co particles, CoWC particles, CoCl(2)) and assessed cell damage using the dimethylthiazol diphenyl tetrazolium bromide test. In some experiments, inserts were used to separate the particles from the cells. The results show that AT-II are twice as sensitive to the effects of 100 microg Co particles/well (1.88 cm(2)) than AM. For this latter cell type, the presence of WC almost doubled (at 25 microg Co/well) the toxic effects compared to pure Co, but this synergy between Co and WC only occurred if the particles were in close contact with the cells. Lactalbumin and, to a lesser degree, EDTA were able to reduce the toxicity of Co, CoWC, and CoCl(2) for AT-II and AM. CoCl(2) showed a similar toxicity for AT-II and AM. The use of Co-conditioned medium revealed that Co particles are "aged" after having been incubated for 24 h in an aqueous medium and are then no longer able to cause the same degree of cell damage as fresh Co particles (71 versus 15% viability for 100 microg Co/well). The time course of the toxicity of the different forms of Co for AT-II and AM showed different patterns in causing cell damage, suggesting different action mechanisms. Evaluation of cell damage by electron microscopy was consistent with biochemical indices. Overall, our results indicate that the Co ion does play a role in the toxicity of both Co particles and CoWC particles.
Animals↗
Polyamines in the lung: polyamine uptake and polyamine-linked pathological or toxicological conditions.
The natural polyamines putrescine, cadaverine, spermidine, and spermine are found in all cells. These (poly)cations exert interactions with anions, e.g., DNA and RNA. This feature represents their best-known direct physiological role in cellular functions: cell growth, division, and differentiation. The lung and, more specifically, alveolar epithelial cells appear to be endowed with a much higher polyamine uptake system than any other major organ. In the lung, the active accumulation of natural polyamines in the epithelium has been studied in various mammalian species including rat, hamster, rabbit, and human. The kinetic parameters (Michaelis-Menten constant and maximal uptake) of the uptake system are the same order of magnitude regardless of the polyamine or species studied and the in vitro system used. Also, other pulmonary cells accumulate polyamines but never to the same extent as the epithelium. Although different uptake systems exist for putrescine, spermidine, and spermine in the lung, neither the nature of the carrier protein nor the reason for its existence is known. Some pulmonary toxicological and/or pathological conditions have been related to polyamine metabolism and/or polyamine content in the lung. Polyamines possess an important intrinsic toxicity. From in vitro studies with nonpulmonary cells, it has been shown that spermidine and spermine can be metabolized to hydrogen peroxide, ammonium, and acrolein, which can all cause cellular toxicity. In hyperoxia or after ozone exposure, the increased polyamine synthesis and polyamine content of the rat lung is correlated with survival of the animals. Pulmonary hypertension induced by monocrotaline or hypoxia has also been linked to the increased polyamine metabolism and polyamine content of the lung. In a small number of studies, it has been shown that polyamines can contribute to the suppression of immunologic reactions in the lung.
Animals↗
Inflammatory effect of intratracheal instillation of ultrafine particles in the rabbit: role of C-fiber and mast cells.
The effects of ultrafine polystyrene carboxylate-modified (fluorospheres) on inflammatory processes are being investigated in rabbit lungs. One milliliter of sterile NaCl (0.9%) containing 4 mg of ultrafine particles (UFP) was intratracheally instilled into anesthetized rabbits. The control animals were only instilled with sterile NaCl (0.9%). Twenty hours after being instilled, the rabbits were killed and their lungs were excised and then tracheally perfused with phosphate-buffered physiological solution (PBS). The lung effluents, collected from small holes made in the pleura, were analyzed for substance P (SP) and histamine content by radioimmunoassay (RIA) methods, after administration of drugs. In addition, in other groups of rabbits, the lung wet/dry (W/D) weight ratio was monitored, as were the cellular and protein contents in bronchoalveolar lavage (BAL). Electron microscopy examination was also performed. In tracheally superfused experiments, UFP induced a significant enhancement of both SP and histamine releases after administration of capsaicin (10(-4) M), to stimulate C-fiber, and carbachol (10(-4) M), a cholinergic agonist. A significant increase in histamine release was also recorded in the UFP-instilled group following the administration of both SP (10(-6) M) plus thiorphan (10(-5) M) and compound 48/80 (C48/80) (10(-3) M) to stimulate mast cells. In addition, the BAL fluid analysis of UFP groups showed an influx of neutrophils and an increase in total protein concentration. An increase in the lung WW/DW ratio was also recorded. Both epithelial and endothelial injuries were observed in the lungs of UFP-instilled rabbits. The pretreatment of rabbits in vivo with a mixture of either SR 140333 and SR 48368, a tachykinin NK(1) and NK(2) receptor antagonist, or a mixture of terfenadine and cimetidine, a histamine H(1) and H(2) receptor antagonist, prevented UFP- induced neutrophil influx and increased total proteins and lung WW/DW ratio. Therefore, it can be concluded that chemicaly inert, electrically charged UFP induce a pulmonary inflammatory process during which the release of SP and histamine from C-fibers and mast cells was enhanced after various stimuli. These latter mediators can also modulate the inflammatory process.
Animals↗
A breathless accountant who blew up balloons.
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Adult↗
Dioxins, Coca-Cola, and mass sociogenic illness in Belgium.
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Adult↗