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Biomedical subjects

D Lison

Publications and source records attributed to D Lison.

At least 73 records · Page 4Linked to original sources
PubMed1996

The practice of occupational and environmental health in Belgium.

Occupational medicine and occupational health regulations in Belgium are succinctly presented. Since 1970 a minimum level of appropriate training has been required for conferral of a certificate in occupational medicine. At some universities this training is integrated into a larger programme which meets the requirements of EEC Directive 89/594. The current Belgian legislation relating to the prevention of occupational diseases and injuries is detailed in the Règlement pour la Protection du Travail, first published in 1946 and constantly updated. The occupational physician is supposed to provide advice on the risks to which workers are exposed and the adaptation of working conditions in accordance with the state of health or the abilities of the worker. Employers are obliged by law to cover the risks of accident by subscribing to a private insurance policy which covers any related costs. They also contribute financially to the Fonds des Accidents du Travail (Occupational Accidents Fund) and the Fonds des Maladies Professionnelles (Occupational Diseases Fund). Occupational diseases are recognised and may be financially compensated by the Fonds des Maladies Professionnelles.

Belgium↗
PubMed1996

Assessment of exposure to inorganic arsenic, a human carcinogen, due to the consumption of seafood.

To assess whether regular consumption of seafood, particularly fish and shellfish, by humans may lead to an overexposure to inorganic arsenic, a well-established human carcinogen, the urinary excretion of the relevant As metabolites (Asi, inorganic form; MMA, monomethylarsonic acid; DMA, dimethylarsinic acid) was compared in groups of subjects with different seafood consumption habits and in volunteers after ingestion of a known amount of seafood arsenicals. Studies of Italian cohorts, involving five groups of +/-30 subjects with different seafood consumption habits, and balance studies in Belgian volunteers failed to show a biologically significant absorption of inorganic arsenic either present as such in the food or formed from organoarsenicals during cooking or digestion. The results suggest that the digestion of some seafood, especially mussels, may increase the urinary excretion of the dimethylated arsenic metabolite. Therefore, the biological monitoring of exposure to inorganic arsenic in an industrial context should mainly rely upon specific measurement of the unmetabolized form when recent ingestion of seafood cannot be excluded.

Arsenic↗
PubMed1996

Determination of toluenediamines in urine of workers occupationally exposed to isocyanates by high-performance liquid chromatography.

In recent years, epidemiological evidence that exposure to toluene diisocyanate (TDI) is associated with adverse health effects has led to the development of useful analytical methods for the biological monitoring of TDI. In this paper, an HPLC method is presented that allows accurate determinations of toluenediamines (TDA), urinary metabolites of TDI, in hydrolysed human urine without complicated or time-consuming sample treatment. The procedure requires 5.0 ml of urine and involves the extraction with toluene of TDA and the hydrolysable conjugate fraction followed by further purification with a strong cation-exchange sorbent. Strongly alkaline conditions are chosen for the hydrolysis of urine samples and phenylene-1,3-diamine is used as internal standard to control the sample extraction and clean-up. Separation is performed on a base-deactivated octadecyl reversed-phase column by either ion-suppression or ion-pair chromatography. Chromatographic analysis is complete in less than 20 min and chromatograms with no interfering peaks are obtained. High sensitivity and selectivity are achieved by using electrochemical detection: 2,6- and 2,4-TDA can be detected at the 0.1 and 0.15 microgram l-1 levels, respectively. Absolute recoveries of the method tested with urine samples spiked at 10 micrograms l-1 with phenylene-1,3-diamine and from 1 to 25 micrograms l-1 with 2,6-and 2,4-TDA are greater than 87.6% and 88.3%, respectively. The assay is linear from 0 to 50 micrograms l-1. Within-run precisions evaluated on 10 urine samples ranging from 0 to 10 micrograms l-1 are 7.9% and 5.3% for 2,6- and 2,4-TDA, respectively. Results obtained with urine samples from 12 controls and 15 exposed workers from a flexible polyurethane foam factory indicate that the method is appropriate for the biological monitoring of occupational exposure to TDI.

Chromatography, High Pressure Liquid↗
PubMed1996

Experimental research into the pathogenesis of cobalt/hard metal lung disease.

In recent years clinical, epidemiological and experimental evidence has accumulated indicating that cobalt metal particles, when inhaled in association with other agents such as metallic carbides (hard metals) or diamond dust, may produce an interstitial lung disease termed "hard metal disease" or "cobalt lung". This article summarizes the progress accomplished in our two laboratories to understand the pathogenesis of this disease. Gaps and weaknesses in our current knowledge have also been highlighted in order to suggest potential avenues for further research. Whilst animal models have proved useful for the demonstration of the toxic synergy between cobalt and carbides (e.g. tungsten carbide), most animal models have remained descriptive and have not provided information on the mechanism for this synergy. In particular, the bizarre multinucleated giant cells which are an important hallmark of the human disease, have not been reproduced consistently in experimental animals. Since cobalt is a known sensitizer, there may also be a need to develop experimental models to test the possible involvement of immunological mechanisms in the pathogenesis of the interstitial disease. In vitro systems including macrophage cell cultures and physico-chemical tests have been useful to investigate the mechanism underlying the toxic synergy. The recent finding that, in vitro, cobalt and metallic carbides interact with oxygen to produce toxic activated oxygen species opens a new avenue of research and may offer an alternative interpretation of the fact that only a limited proportion of exposed workers develop interstitial disease. Besides the possible involvement of immunological mechanisms, it may be speculated that individuals with a lower antioxidant defence are more susceptible to the toxic effect of activated oxygen species produced by cobalt-containing dusts from hard metal.

Administration, Inhalation↗
PubMed1996

Occupational hazards for the male reproductive system.

The etiology of male infertilities is largely undetermined, and our knowledge of exogenous factors affecting the male reproductive system is still limited. In particular, the role of specific environmental and occupational factors is incompletely elucidated. Various occupational (physical and chemical) agents have been shown to affect male reproductive functions in animals, but large differences in reproductive function and/or xenobiotic handling between species limit extrapolation to humans. When available, human data are often conflicting and, except in a few instances, usually refer to broad and heterogenous occupational categories or to groups of agents (e.g., solvents). It is often difficult to elucidate the role of a single agent because occupational exposure conditions are often complex and various confounding factors related to lifestyle (smoking, alcohol, and diet) or socioeconomic state may also affect sperm quality, fertility, or pregnancy outcomes. The objective of this work is to summarize the main epidemiological and, where relevant, experimental findings pertaining to agents (physical and chemical) encountered in the occupational environment that might affect the male reproductive system (sperm count, motility and morphology, libido, and fertility) and/or related pregnancy outcomes (spontaneous abortion, stillbirth, low birth weight, and birth defects and childhood malignancy in offspring). Some methodological issues related to research on the reproductive effects of toxicants are also discussed briefly.

Anesthetics↗
PubMed1996

Human toxicity of cobalt-containing dust and experimental studies on the mechanism of interstitial lung disease (hard metal disease).

In the industry, the potential for exposure to cobalt metal dust is particularly important during the production of cobalt powder and the processing and use of hard metals and other cobalt-containing alloys. The different adverse health effects reported in these workers are reviewed. One of the main target organs is the respiratory tract, and this article concentrates on the lung parenchymal reactions induced by cobalt-containing dust. Clinical and epidemiological data indicate that this manifestation is rarely, if ever, induced by pure cobalt metal dust alone, but requires the concomitant inhalation of other compounds such as tungsten carbide in the hard metal industry (hard metal disease). Experimental studies demonstrate that cobalt metal and metallic carbides interact to produce an elective lung toxicity. Recent work on the mechanism of this interaction, which is based on the production of activated oxygen species, is reviewed. A practical implication in industrial hygiene should be that permissible exposure levels to Co dust might have to be different when exposure is to pure Co particles or an association with carbides.

Cobalt↗
PubMed1995

The delayed lung responses to single and repeated intratracheal administration of pure cobalt and hard metal powder in the rat.

Epidemiological and clinical studies suggest that inhalation of cobalt metal dust (Co) mixed with tungsten carbide particles (WC), but not of cobalt dust alone, may cause interstitial pulmonary lesions (hard metal disease). In previous experimental studies in the rat, we have demonstrated the greater acute pulmonary toxicity of a WC-Co mixture compared to Co or WC alone. The present study was undertaken to compare in the same animal model the delayed lung response after intratracheal administration of Co or WC-Co particles (cobalt particle 6.3 wt%). The responses were also compared with those obtained after treatment with arsenic trioxide and crystalline silica used a reference materials producing an acute toxic insult and a progressive fibrogenic response, respectively. Cellular (total and differential counts) and biochemical parameters (LDH, N-acetyl-beta-D-glucosaminidase, total protein, albumin, fibronectin, and hyaluronic acid) were measured in bronchoalveolar lavage fluid following single and repeated intratracheal instillations. The results indicate that the delayed lung response observed after WC-Co is different from that after cobalt metal alone. A single intratracheal dose of WC-Co (1, 5, or 10 mg/100 g body wt) induced an acute alveolitis which persisted for at least 1 month. Four months after a single instillation of WC-Co, no clear histological lung fibrosis could however be evidenced, indicating a reversibility of the lesions. The effects of cobalt (0.06, 0.3, or 0.6 mg/100 g body wt) or tungsten carbide alone (1, 5, 10 mg/ 100 g body wt) were very modest, if any. Following repeated intratracheal instillations (four administrations at 1-month interval), increased lung hydroxyproline content and histopathological evidence of interstitial fibrosis were observed after WC-Co (4 x 1 mg/100 g body wt), but not after administration of each component separately, i.e., Co (4 x 0.06 mg/100 g body wt) or WC (4 x 1 mg/100 g body wt). The mechanism of the fibrotic reaction induced by WC-Co seems different from the progressive inflammatory reaction induced by crystalline silica. We suggest that it might result from a scarring reaction elicited by repeated acute insults as observed after repeated administration of arsenic trioxide.

Acetylglucosaminidase↗
PubMed1995

The role of vitamin E in the susceptibility of rat lung and liver microsomes to iron-stimulated peroxidation.

The production of thiobarbituric acid-reactive substances (TBA-RS) and ethane, two markers of the lipid peroxidation process, was evaluated in rat lung and liver microsomal membranes incubated in the presence of either ferrous ions or a mixture of ferric ions and ascorbate. Microsomal fractions isolated from lung tissue were more resistant than those isolated from the liver. Compared to Fe2+, the association of Fe3+/ascorbate seemed to be totally ineffective in stimulating peroxidation of lung microsomes. The fatty acid profile of lung and liver microsomal membranes could not be responsible for their different susceptibility to free radical degradation. The microsomal fraction isolated from lung showed a higher vitamin E concentration than the liver. The importance of vitamin E in protecting lung membranes was assessed by using lung and liver isolated from vitamin E-deficient and vitamin E-supplemented rats. For both lung and liver microsomal fractions an inverse relationship between vitamin E concentrations and the extent of lipid peroxidation was observed. However, although the vitamin E concentrations in lung and liver microsomes isolated from rats submitted to a vitamin E-deficient diet were not different, lung microsomes still exhibited a lower production of TBA-RS and ethane than liver. In addition to vitamin E, other factors must be involved to explain the resistance of lung microsomes to lipid peroxidation.

Animals↗
PubMed1995

Lung toxicity of hard metal particles and production of interleukin-1, tumor necrosis factor-alpha, fibronectin, and cystatin-c by lung phagocytes.

Hard metal alloys (WC-Co) are made of a mixture of cobalt (Co; 6%) and tungsten carbide (WC; 94%) particles. Chronic inhalation of hard metal dust can lead to the development of a fibrosing alveolitis, the pathogenesis of which is still undefined. The present investigation was undertaken to assess the effect of Co, WC, and WC-Co particles on the release by lung phagocytes of interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), fibronectin, and cystatin-c. The responses were compared with those induced by two other lung toxicants, i.e., crystalline silica (DQ12) and arsenic trioxide (As2O3). IL-1 and TNF-alpha activities produced in the presence and absence of LPS stimulation were measured with the aid of bioassays while fibronectin and cystatin-c were determined by latex immunoassays. In vitro, maximal noncytotoxic doses of As2O3, Co, WC, or WC-Co did not significantly affect the production of these mediators by rat alveolar macrophages. In contrast, DQ12 enhanced the production of TNF-alpha (with and without LPS stimulation) and IL-1 (after LPS stimulation) and decreased cystatin-c release (in the absence of LPS). Following a single intratracheal instillation of the different test preparations in the rat, the response of the lung phagocytes obtained by bronchoalveolar lavage (BAL) 24 hr later was examined. We were unable to detect any consistent effect of Co (0.06 mg/100 g body wt), WC (1 mg/100 g body wt), or WC-Co treatment (1 mg/100 g body wt) on the production of the above mediators. In contrast, after LPS stimulation, As2O3 (0.5 mg/100 g body wt) and DQ12 (1 mg/100 g body wt) stimulated the production of TNF-alpha and IL-1. In the absence of LPS, As2O3 stimulated fibronectin and cystatin-c production and DQ12 stimulated cystatin-c release. Since the dose of WC-Co used in vivo (1 mg/100 g body wt) caused pronounced lung inflammation (increased LDH, protein, and albumin levels in BAL fluid), we conclude that the acute lung toxicity of WC-Co particles is not mediated through enhanced production of the examined mediators by lung phagocytes.

Alloys↗
PubMed1995

Effect of the benzene metabolite, hydroquinone, on interleukin-1 secretion by human monocytes in vitro.

Decreased interleukin-1 (IL-1) production by mononuclear phagocytes has been shown to contribute to benzene myelotoxicity in animals. The study presented here was designed to examine the relevance of this mechanism in humans. Fresh human blood monocytes were exposed to 0.001-10 microM hydroquinone (HQ) and assessed for their ability to release IL-1 alpha and IL-1 beta in response to a stimulation with endotoxin. Both cytokines were measured by specific ELISA. Exposure of human monocytes to micromolar concentrations of HQ for 2 hr resulted in a dose-dependent reduction of IL-1 secretion. For both IL-1 alpha and IL-1 beta, the decreases were statistically significant at concentrations of 5 microM and above. HQ also inhibited RNA and protein synthesis in a dose-dependent manner, with 50% inhibitory concentrations of 21 +/- 11 and 10 +/- 9 microM, respectively. Furthermore, monocytes treated with 5 microM HQ also displayed a reduced total protein content when compared with control cells. These data suggest that the reduction of IL-1 production caused by HQ results from a global impairment of monocyte essential functions such as transcription or translation. Taken as a whole, our results support a mechanism whereby HQ may contribute to the myelotoxicity of benzene in humans by inhibiting the production by mononuclear phagocytes of cytokines involved in the regulation of hematopoiesis.

Benzene↗
PubMed1995

Physicochemical mechanism of the interaction between cobalt metal and carbide particles to generate toxic activated oxygen species.

Hard metal alloys (or cemented carbides) are made of a mixture of tungsten carbide particles (WC, more than 80%) cemented in cobalt metal powder (Co, 5-10%). The inhalation of hard metal particles may cause an interstitial pulmonary disease, the mechanism of which involves an interaction between Co and WC particles. Some epidemiological data also suggest that hard metal dust can induce lung cancer in workers. In a macrophage culture model, butylated hydroxytoluene (1 mM) protected from the cytotoxicity of hard metal particles, suggesting a possible involvement of lipid peroxidation in the toxicity of these powders. In a biochemical system, a mixture of Co and WC particles, but not Co or WC alone, stimulated the production of thiobarbituric acid-reactive substances from arachidonic acid. Using a spin trapping system applied to aqueous particulate suspensions and electrochemical techniques, we present experimental evidence that the association of Co and carbide particles represents a specific toxic entity producing large amounts of activated oxygen species. The mechanism of this interaction proceeds through the oxidation of cobalt metal catalyzed at the surface of carbide particles and resulting in the reduction of dissolved oxygen. This physicochemical property of hard metal particles provides a new basis for interpreting their inflammatory action and their possible carcinogenic effect on the lung.

Animals↗
PubMed1995

Effect of oxygen concentration on production of ethane and thiobarbituric acid-reactive substances by peroxidizing lung and liver homogenates and formation of ethanol by peroxidizing docosahexaenoic acid preparations under hyperoxic conditions.

The oxygen dependence of ethane formation was investigated in rat lung and liver homogenates, incubated in sealed flasks, in which the peroxidation was stimulated by the addition of ferrous ions. For both tissues, the production of ethane was maximal under a 20% oxygenated gas phase, while hyperoxic conditions led to a decreased ethane in the gas phase. The formation of thiobarbituric acid-reactive substances (TBA-RS), another marker of the lipid peroxidation process, in the homogenates of lung and liver was strongly stimulated at 100% compared to 20% oxygen. Experiments were also carried out on iron-stimulated peroxidation of pure docosahexaenoic acid preparations, which under air led to a large production of ethane. As for tissue homogenates, the TBA-RS content was increased in the presence of 100% oxygen. Those conditions, however, did not induce an increase in ethane production but led to the formation of ethanol. Therefore, the quenching of ethyl radical by molecular oxygen seems to be a very attractive hypothesis to explain the lack of increased ethane production in favor of ethanol when iron-induced lipid peroxidation was stimulated by oxygen.

Animals↗
PubMed1995

Study of muscular effects of short-term pyridostigmine treatment in resting and exercising rats.

1. Pyridostigmine (PYR) pretreatment is used by the military to obtain 20-30% whole blood acetylcholinesterase (AChE) inhibition in order to enhance the effectiveness of the standard therapeutic regimen for poisoning by an organophosphate anticholinesterase agent. The present study was undertaken to investigate in a rat model the potential muscle damage produced by this pretreatment when given alone or combined with physical exercise. 2. Grip strength and biochemical measurements, i.e. serum creatine phosphokinase (CPK) activity and creatine urinary excretion rate, together with histological studies, were performed in resting animals during a period of 14 days of PYR administration in a dose producing 20-30% whole blood acetylcholinesterase inhibition. No evidence was found of a deleterious effect of this treatment on the skeletal muscle. 3. In contrast, following physical exercise, the same treatment significantly exacerbated the biochemical changes reflecting a loss of integrity in skeletal muscles, namely, increased CPK and urinary creatine excretion rate. The significance of this observation remains to be clarified.

Animals↗
PubMed1995

Preliminary in vitro investigation into the use of alkaline elution assay for the biomonitoring of humans exposed to genotoxic agents.

1. This in vitro study was undertaken as a preliminary approach before assessing whether the alkaline elution assay can be applied to peripheral blood lymphocytes (PBL) for the monitoring of humans exposed to genotoxic agents such as polycyclic aromatic hydrocarbons (PAH). We have compared in vitro, with the aid of the alkaline elution assay, the formation and the repair of DNA single-strand breaks (ssb) induced by different genotoxic agents [gamma-irradiation, ethyl methanesulfonate (EMS), benzo pyrene diol epoxide (BPDE)] on quiescent and PHA-stimulated human lymphocytes and on a fibroblast cell line. 2. Gamma-irradiation (4 Gy) induced an equivalent amount of DNA ssb in the three cell types. On the other hand, after treatment with EMS (10 mM) and BPDE (50 microM), a higher production of DNA ssb was observed in replicating cells (PHA-stimulated lymphocytes and fibroblasts) when compared with quiescent lymphocytes. 3. After gamma-irradiation, all cell types repaired more than 65% of ssb within 1 h. After treatment with EMS, we noted a deficient DNA repair capacity in quiescent lymphocytes in comparison with replicating cells. In all cell types treated with BPDE, more breaks were observed after a 2 h repair period than immediately after treatment, demonstrating the involvement of a slow repair mechanism after BPDE treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1994

Health risks associated with cobalt exposure--an overview.

Cobalt is an essential oligoelement which enters in the composition of vitamin B12. For the general population, food and beverages represent the main source of cobalt exposure. Traces of cobalt are also present in cement and various household products. In industry, the potential for exposure to cobalt is particularly important during the production of cobalt powder, the production, processing and use of hard metals, the polishing of diamonds with cobalt containing disks and the processing of cobalt alloys. Except in the production of cobalt powders, these activities involve exposure not only to cobalt but also to other substances such as tungsten carbide, iron and diamond which may modulate the biological reactivity of cobalt. Cobalt salts are used for the preparation of enamels and pigments. Cobalt is mainly absorbed from the pulmonary and the gastrointestinal tracts. Absorption through the skin can occur but is low. Concomitant exposure to tungsten carbide increases the pulmonary absorption rate of cobalt metal. Cobalt is not a cumulative toxin and is mainly excreted in urine and to a lesser extent via faeces. Cobalt in blood and urine mainly reflects recent exposure. In the past, outbreaks of cardiomyopathy occurred among heavy consumers of cobalt fortified beer. It is likely that poor nutrition and ethanol had played a synergistic role. Toxic manifestations, however, have mainly been reported following inhalation of cobalt containing dusts in industry. The two main target organs are the skin and the respiratory tract. Cobalt itself may cause allergic dermatitis, rhinitis and asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

Cobalt↗
PubMed1994

Assessment of lipid peroxidation associated with lung damage induced by oxidative stress. In vivo and in vitro studies.

The lung thiobarbituric acid-reactive substances (TBA-RS) content and the amount of ethane exhaled, two potential markers of the lipid peroxidation process, were measured in rats following intratracheal administration of chemicals stimulating the production of free radicals, i.e. paraquat, phorbol myristate acetate and ferrous ions. Five hours after treatment, autopsy revealed gross pulmonary damage but the lung TBA-RS and the ethane exhalation were not different from control animals. On the contrary, a large increase in ethane production was observed 2 hr after intraperitoneal administration of the hepatotoxic carbon tetrachloride. In vitro, incubation of lung and liver homogenates from control rats with ferrous iron led to the development of a lipid peroxidation process in both tissues but the accumulation of TBA-RS and ethane was much lower with homogenates from lung as compared to liver tissue. Those results suggest that the lung may be more resistant than the liver to the initiation and/or propagation of a lipid peroxidation process. The possibility that others markers than ethane and TBA-RS are more appropriate to detect this process in the lung must also be considered.

Animals↗
PubMed1994

Cobalt bioavailability from hard metal particles. Further evidence that cobalt alone is not responsible for the toxicity of hard metal particles.

Hard metal is an alloy of tungsten carbide (WC) in a matrix of cobalt metal (Co). The inhalation of hard metal dust can cause an alveolitis which may progress to interstitial fibrosis. This study was undertaken to compare, both in vivo and in vitro, the bioavailability of cobalt metal when mixed or not with WC and to assess whether this factor had any influence on the cellular toxicity of hard metal particles. In vivo, non-toxic doses of cobalt metal were administered intratracheally in the rat, alone (Co, 0.03 mg/100 g) or mixed with tungsten carbide (WC-Co, 0.5 mg/100 g containing 6.3% of cobalt metal particles). Sequential measurements of cobalt in the lung and in urine demonstrated that the retention time of the metal in the lung was longer in Co- than in WC-Co-treated animals. In vitro, the cellular cobalt uptake was higher when the metal was presented to the macrophages as WC-Co. However, there was no relationship between the cellular uptake of cobalt and the occurrence of toxicity, since the intracellular concentration of cobalt associated with the occurrence of a cytotoxic effect of WC-Co particles was insufficient to exert the same effect when resulting from exposure to Co alone. This clearly indicates that increased bioavailability of cobalt is not the mechanism by which hard metal particles exhibit their cellular toxicity. These observations confirm and extend our previous findings supporting the view that cobalt is not the only component responsible for the toxicity of hard metal particles which should be considered as a specific toxic entity.

Administration, Inhalation↗