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Biomedical subjects

B Nemery

Publications and source records attributed to B Nemery.

At least 55 records · Page 3Linked to original sources
PubMed2001

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↗
PubMed2001

Interstitial lung disease induced by exogenous agents: factors governing susceptibility.

The purpose of this review is to describe the present state of knowledge regarding host susceptibility factors that may determine the occurrence, development and severity of interstitial lung disease (ILD) caused by exogenous agents. First, host susceptibility may pertain to differences in the delivery and/or persistence of the noxious agent in the lung. The deposition and clearance of inhaled particles or fibres may vary depending on innate anatomical or physiological characteristics, and on acquired changes, such as nasal disease or smoking-induced alterations. Genetically- or environmentally-induced interindividual differences in the expression of pulmonary biotransformation enzymes may form the basis for, or contribute to the risk of, drug-induced interstitial lung disease. Secondly, there are genetic and acquired variations in various enzymatic and nonenzymatic defence systems that protect cells and tissues against oxidative stress, which is often involved in the pathogenesis of interstitial lung disease caused by particles, fibres, metals, organic agents and drugs. Thirdly, the occurrence of immunological sensitization is dependent on both genetic and environmental factors. This has been demonstrated in chronic beryllium lung disease and in hypersensitivity pneumonitis. Fourthly, the propensity of individuals to develop particular types of inflammation, such as granulomas, is probably under genetic control. The regulation and resolution of inflammation and fibrogenesis caused by dust particles are also partly determined by genetic factors, involving cytokine networks and growth factors. In conclusion, although the issue of genetics pervades the entire discussion of host susceptibility, genes are not the only determinants of health and disease. Environmental factors may be equally important in shaping host susceptibility. Therefore, research must be focused on both the genetic bases and the environmental determinants of interstitial lung disease, in order to provide mechanism-based prevention strategies, early detection of, and improved therapy for these conditions.

Air Pollutants↗
PubMed2000

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Journal Article↗
PubMed2000

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↗
PubMed2000

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↗
PubMed2000

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↗
PubMed1999

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↗
PubMed1999

A comparative study of the isolation of type II epithelial cells from rat, hamster, pig and human lung tissue.

Data is reported on the reproducibility and purity of alveolar type II cell isolations from 4 species. Human and pig type II cells were isolated using a tissue slice method to remove blood and contaminating cells, whilst rat and hamster cells were isolated using the method of protease instillation. All cells were purified on Percoll gradients and by differential attachment. Cell type purity was assessed by phase contrast microscopy, electron microscopy (EM), percentage of cells alkaline phosphatase (AP) positive and percentage of cells staining strongly for NADPH dependent nitro blue tetrazolium reductase (NBT). These enzymes are considered as markers for type II and Clara cells respectively. The purity of all cell preparations was enhanced following 24 h culture on a biomatrix and whilst plating efficiency was similar for all species, the human tissue consistently yielded the highest purity of type II cells. All cells with lamellar bodies did not contain AP, and activity was variable between species. Further studies are needed to determine if NBT is equally nonspecific as a cell marker enzyme. In summary, sufficient type II cells of high purity can be isolated thus permitting interspecies comparative studies to investigate the effects of selective and non-specific pulmonary toxins, but more specific marker enzymes are required to identify Type II and Clara cells.

Alkaline Phosphatase↗
PubMed1999

Occupational asthma caused by palladium.

Occupational exposure to complex platinum salts is a well-known cause of occupational asthma. Although there is evidence that platinum refinery workers may also be sensitized to other precious metals, such as palladium or rhodium, no instances of occupational asthma due to an isolated sensitization to palladium have been reported. A case is reported of occupational rhinoconjunctivitis and asthma in a previously healthy worker exposed to the fumes of an electroplating bath containing palladium. There was no exposure to platinum. Sensitization to palladium was documented by skin-prick tests. The skin-prick test was positive with Pd(NH3)4Cl2, but not with (NH4)2PdCl4. Corresponding salts of platinum were all negative. A bronchial provocation test with Pd(NH3)4Cl2 (0.0001% for a total of 315 s, followed by 0.001% for a total of 210 s) led to an early decrease in forced expiratory volume in one second (-35%). A similar exposure (0.001% for a total of 16 min) in an unrelated asthmatic gave no reaction. This case shows that an isolated sensitization to palladium can occur and that respiratory exposure to palladium is a novel cause of metal-induced occupational asthma.

Adult↗
PubMed1999

Investigation of the transport of intact glutathione in human and rat type II pneumocytes.

The aim of the study was to investigate whether there is transmembrane transport of intact glutathione ([3H]-GSH, 0.1 microCi) in rat and human type II pneumocytes (T2P), and if this transport might be dependent on the redox state of the extracellular fluid. The T2P were pretreated with acivicin (250 microM) to inhibit gamma-glutamyltransferase activity and with L-buthionine-[SR]-sulfoximine (1 mM) to inhibit intracellular GSH synthesis. After 48 h in culture, initial GSH influx rate was 0.70 +/- 0.20 nmol/min/mg protein (37 degrees C) and 0.35 +/- 0.04 nmol/min/mg protein (4 degrees C) during the first 5 min in rat T2P. In human T2P, the initial GSH influx rate was 0.36 +/- 0.30 nmol/min/mg protein (37 degrees C) and 0.32 +/- 0.06 nmol/min/mg protein (4 degrees C) during the first 10 min. Thereafter no further influx was found. The influx of 1 mM GSH in freshly isolated rat and human T2P in suspension was 2.3 +/- 0.3 and 1.2 +/- 0.3 nmol/mg protein after 15 min at 37 degrees C, and 2.8 +/- 0.2 and 1.0 +/- 0.3 nmol/mg protein at 4 degrees C, respectively. When GSH influx was studied at different concentrations between 0 and 40 mM, a linear increase without saturation or difference between 37 degrees C and 4 degrees C was found. Pre-exposure to ouabain had no effect on GSH influx. Efflux of GSH was stimulated and influx inhibited by pre-exposure of the cells to reduced thiols, while disulphides inhibited efflux and favoured inward uptake. Thus, in human and rat T2P a GSH-carrier exists which operates as an effluxer. At GSH concentrations in the physiological range no uptake is seen, but some uptake can be observed at GSH concentrations above normal physiological levels. The uptake appears to be energy-independent and non-saturable. Efflux of GSH is stimulated and influx inhibited by reduced thiols, while disulphides inhibit the efflux and favour inward uptake. GSH uptake in T2P thus may depend on concentration gradients and driving forces, such as the redox state of the extracellular fluid.

Animals↗
PubMed1999

In vitro cytotoxicity of textile paint components linked to the "Ardystil syndrome".

The spraying of a paint formula (Acramin F system) had 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 this paint and its main polymeric components, Acramin FWR, Acramin FWN, Acrafix FHN, and Acramoll W, we have undertaken studies using a battery of different cell-types and assessing in vitro cytotoxicity by measuring LDH leakage. This study shows that, as in in vivo studies, the three polycationic paint components, Acramin FWR (a polyurea), Acramin FWN (a polyamide-amine), and Acrafix FHN (a polyamine) exhibited considerable cytotoxicity (LC50 generally below 100 microg/ml for an incubation of 20-24 h) in vitro, while Acramoll W, which is not a polycation, was almost non-toxic (in the concentration range tested). The cytotoxicity was comparable in primary cultures of rat and human type II pneumocytes and alveolar macrophages as well as in the pulmonary cell line A549 and the hepatic cell line HepG2. In human erythrocytes, the toxicity was less pronounced. We speculate that the multiple positive charges play an important role in the toxic mechanism. It is concluded that Acramin FWR and Acramin FWN have similar intrinsic toxicity and that these polymeric compounds, which have no irritant properties or systemic toxicity when given orally, exert a high, unexpected, degree of cytotoxicity.

Adipates↗
PubMed1999

Role of reactive oxygen species in occupational and environmental obstructive pulmonary diseases.

Free radicals and their metabolites, also called reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. Because of its continuous exposure to toxic pollutants in the ambient air, such as cigarette smoke, air pollution, and mineral dusts, the lung is very vulnerable to ROS-induced injury. In this review, the role of ROS in the pathogenesis of obstructive lung diseases is reviewed. A central theme in this review is the pivotal role of transition metals such as iron, vanadium, and nickel in ROS-induced cell damage, not only in exposure to mineral dusts but also in cigarette smoke and air pollution.

Air Pollutants↗
PubMed1999

Sensitization to triglycidylisocyanurate (TGIC) with cutaneous and respiratory manifestations.

The case is presented of a man with allergic contact dermatitis and occupational asthma due to triglycidylisocyanurate (TGIC), which is used as a hardener in thermosetting powder paint. The contact dermatitis was confirmed by patch testing (TGIC 0.5% and 5% in petrolatum), and the occupational asthma was confirmed by bronchial provocation testing: two challenges to an aerosol of lactose containing TGIC (0.05% and 0.1%, w/w, each for 0.5+1+2+4 min) led to a maximal decrease in FEV1 of 22% and 31% after 6 and 4 h, respectively. Skin prick tests with unconjugated TGIC were possibly positive. This case confirms that exposure to TGIC in powder paints may cause not only contact dermatitis, but also occupational asthma.

Adult↗
PubMed1999

Acquisition and extinction of somatic symptoms in response to odours: a Pavlovian paradigm relevant to multiple chemical sensitivity.

OBJECTIVES: Multiple chemical sensitivity is a poorly understood syndrome in which various symptoms are triggered by chemically unrelated, but often odorous substances, at doses below those known to be harmful. This study focuses on the process of pavlovian acquisition and extinction of somatic symptoms triggered by odours. METHODS: Diluted ammonia and butyric acid were odorous conditioned stimuli (CS). The unconditioned stimulus (US) was 7.4% CO2 enriched air. One odour (CS+) was presented together with the US for 2 minutes (CS+ trial), and the other odour (CS-) was presented with air (CS-trial). Three CS+ and three CS-exposures were run in a semi-randomised order; this as the acquisition (conditioning) phase. To test the effect of the conditioning, each subject then had one CS+ only--that is, CS+ without CO2--and one CS- test exposure. Next, half the subjects (n = 32) received five additional CS+ only exposures (extinction group), while the other half received five exposures to breathing air (wait group). Finally, all subjects got one CS+ only test exposure to test the effect of the extinction. Ventilatory responses were measured during and somatic symptoms after each exposure. RESULTS: More symptoms were reported upon exposure to CS+ only than to CS-odours, regardless of the odour type. Altered respiratory rate was only found when ammonia was CS+. Five extinction trials were sufficient to reduce the level of acquired symptoms. CONCLUSION: Subjects can acquire somatic symptoms and altered respiratory behaviour in response to harmless, but odorous chemical substances, if these odours have been associated with a physiological challenge that originally had caused these symptoms. The conditioned symptoms can subsequently be reduced in an extinction procedure. The study further supports the plausibility of a pavlovian conditioning hypothesis to explain the pathogenesis of MCS.

Adult↗
PubMed1999

[Occupational asthma].

Occupational asthma is an important disorder, both for the affected individual and for society. The diagnosis of this condition is not easy and it, therefore, often happens that the occupational origin of asthma is overlooked by physicians. In most instances occupational asthma is due to immunological sensitization to an agent present in the workplace. The numerous possible causes of occupational asthma can be classified in high molecular weight compounds of biologic origin and low molecular weight chemicals. Occupational asthma can also follow from airway irritation, either after an acute inhalational injury, or after chronic or repeated peak exposures to irritants. From a medicolegal point of view, occupational asthma presents problems with regard to establishing a causal relationship between work and asthma and in relation to the generally inadequate compensation of victims. To prevent occupational asthma the best policy is to avoid and minimize exposure to sensitizers at work. Occupational asthma offers interesting models for the study of asthma in general.

Asthma↗