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Biomedical subjects

R Lauwerys

Publications and source records attributed to R Lauwerys.

At least 55 records · Page 3Linked to original sources
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

Assessment of exposure to inorganic arsenic following ingestion of marine organisms by volunteers.

A study was undertaken to assess whether the consumption of fish and shellfish containing a high concentration (> 1500 micrograms/kg) of organoarsenical compounds was associated with the release of a significant amount of inorganic arsenic (Asi) in vivo. Volunteers were given a known quantity of seafood (ray, cod, plaice, mussel) whose content in total arsenic (As), Asi, monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) was determined. In addition to the total amount of As excreted within 48 hours, that of Asi and its methylated metabolites (MMA, DMA) was also monitored and compared with that expected on the basis of the results of our previous studies on the toxicokinetics of Asi, MMA, and DMA in humans. Ingestion of ray, cod, or plaice does not seem to be associated with a significant release of Asi in vivo. Following consumption of mussels, however, the amount of DMA excreted in urine is significantly higher than that expected on the basis of the amount of Asi and its methylated derivatives already present in the shellfish. It was also noted that among the different marine organisms analyzed (ray, cod, plaice, sole, sea-bream, mussel), the highest proportion of Asi (on the average 3% of the total) was found in mussels. Further metabolic studies are justified to assess the risk of exposure to Asi associated with the consumption of shellfish. In view of the possible release of dimethylarsenic acid from some organoarsenicals, biological monitoring of occupational exposure to Asi by the measurement of its methylated metabolites can provide misleading results if the workers have consumed some marine organisms within 48 hr before urine collection.

Adolescent↗
PubMed1994

Determinants of benzo[a]pyrene diol epoxide adducts to albumin in workers exposed to polycyclic aromatic hydrocarbons.

The present study was undertaken among 260 subjects [133 controls and 127 persons exposed to polycyclic aromatic hydrocarbons (PAHs) from two steel foundries and a graphite electrode producing plant in order to investigate the relationship between the benzo[a]-pyrene-diol epoxide adducts to albumin (BPDE-alb) and the intensity of exposure to PAHs. Blood samples were collected from each subject and BPDE-alb adduct determination was performed using a high-pressure liquid chromatography technique with fluorescence detection. Exposure to PAHs was assessed by measuring airborne concentration of 13 PAHs including benzo[a]pyrene (BaP) using personal air sampling and 1-hydroxypyrene excretion (1-HOP) in postshift urine. Significantly higher BPDE-alb adduct levels were observed in exposed workers compared to controls but wide interindividual variation was observed between subjects with the same level of exposure. BPDE-alb adduct level was weakly but significantly associated with the airborne concentrations of total PAHs (r = 0.35, P = 0.0001) and BaP (r = 0.30, P = 0.0001), and urinary 1-HOP excretion (r = 0.29, P = 0.0001). Alcohol and dietary habits, place of residence, and renal and hepatic status were not found to influence the concentration of BPDE-alb adducts significantly. However, for the same level of exposure to BaP, smokers had a higher probability of having an elevated BPDE-alb adduct level than non-smokers.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Determinants of urinary thioethers, D-glucaric acid and mutagenicity after exposure to polycyclic aromatic hydrocarbons assessed by air monitoring and measurement of 1-hydroxypyrene in urine: a cross-sectional study in workers of coke and graphite-electrode-producing plants.

A cross-sectional epidemiological study was performed on 286 workers from two coke oven and one graphite electrode plants. The aim was to evaluate the usefulness of monitoring 1-hydroxypyrene (1-HOP) in urine for assessing exposure to polycyclic aromatic hydrocarbons (PAHs), and that of the urinary excretion of thioethers and D-glucaric acid, and the mutagenic activity of urine as indicators or biological effects of PAHs. The results confirm that 1-HOP determination in urine probably reflects exposure to PAHs by all routes and is not significantly influenced by the smoking habit. In comparison with the total PAHs in the air and 1-hydroxypyrene in urine, taken as reference exposure parameters, the results indicate that urinary D-glucaric acid excretion is not positively influenced by PAHs exposure; thioethers determination in urine is of poor value, since the smoking habit is a strong confounding factor. The determination of urinary mutagenicity might contribute to the detection of groups of workers exposed to potentially genotoxic PAHs.

Adult↗
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↗
PubMed1994

Determinants of the serum concentrations of low molecular weight proteins in patients on maintenance hemodialysis.

Factors influencing the serum concentrations of low molecular weight proteins (LMWP) during long-term hemodialysis were studied in 112 patients undergoing dialysis for an average of 61.1 months (range 1 to 243). These patients were treated with AN69, cellulose acetate, cuprophan or polysulfone membranes. The following proteins were measured in serum before and after a four hour dialysis session: cystatin C (CYST C), beta 2-microglobulin (beta 2 m), Clara cell protein (CC16) and retinol-binding protein (RBP). Predialysis levels of the four proteins were markedly elevated. In simple regression analysis, pre-dialysis serum concentrations of beta 2 m and CC16 weakly correlated with the duration of dialysis treatment, but these relations completely disappeared when a stepwise regression analysis was performed using as predictors age, sex, residual diuresis, body weight loss (BWL), duration of hemodialysis and the type or ultrafiltration coefficient (UFC) of the membranes. The only significant determinants which emerged from this analysis were the residual diuresis and age which negatively correlated with CYST C, beta 2m and CC16 (residual diuresis only), and sex which influenced CYST C. During the dialysis session, the microproteins underwent changes that were related to their molecular radius, the membrane UFC and the BWL. After adjustment for the latter, high flux membranes (UFC > or = 15 ml/h.m2.mm Hg) allowed up to 50% of CYST C and 25% of beta 2m to be removed. No significant elimination of CC16 and RBP was evident. On the basis of these results, we estimated the effective pore radius of high flux membranes between 1.5 and 1.7 nm and that of low flux membranes as below 1.5 nm.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Proteins↗
PubMed1994

Biological monitoring of workers exposed to cobalt metal, salt, oxides, and hard metal dust.

OBJECTIVE: The aim was to examine the relation between environmental and biological (blood and urine) indices of exposure to different chemical forms of cobalt. METHODS: A cross sectional study was undertaken in workers exposed to cobalt metal, oxides, and salts in a refinery and to a mixture of cobalt and tungsten carbide in a hard metal producing plant. RESULTS AND CONCLUSION: Although biological monitoring of workers exposed to cobalt oxides showed higher blood and urine concentrations than in non-exposed subjects, these indices poorly reflected the recent exposure level. By contrast, when exposure was to soluble cobalt compounds (metal, salts, and hard metals), the measurement of urine or blood cobalt at the end of the workweek could be recommended for the assessment of recent exposure. An eight hour exposure to 20 or 50 micrograms/m3 of a soluble form of cobalt would lead to an average concentration in a postshift urine sample collected at the end of the workweek of 18.2 or 32.4 micrograms of cobalt/g creatinine, respectively.

Adult↗
PubMed1994

Determinants of benzo(a)pyrenediol epoxide adducts to haemoglobin in workers exposed to polycyclic aromatic hydrocarbons.

OBJECTIVE: The aim was to assess the determinants of benzo(a)pyrenediol epoxide adducts to haemoglobin (BaPDE-Hb) in workers exposed to polycyclic aromatic hydrocarbons (PAHs). METHODS: This was a study of the correlations between the concentrations of PAHs in air, 1-hydroxyprene in urine, and BaPDE-Hb adduct concentration in the blood in 206 men working in steel foundries and one graphite electrode producing plant, taking into consideration confounding factors such as smoking and dietary habits. RESULTS: BaPDE-Hb adduct concentration was correlated (r = 0.26; p = 0.0002) with the airborne PAH concentration and was influenced by tobacco consumption but not by dietary habits. Benzo(a)-pyrene concentration in air, 1-hydroxypyrene concentration in urine, and duration of exposure to PAHs were not associated with the adduct concentration. CONCLUSION: Although environmental exposure to PAHs was statistically associated with BaPDE-Hb adduct concentration, differences between individual subjects in the metabolism of benzo(a)pyrene probably play an important part in determining the amount of BaPDE-Hb adducts formed.

Air↗
PubMed1994

Renal function and hyperfiltration capacity in lead smelter workers with high bone lead.

OBJECTIVE: The study was undertaken to assess whether the changes in urinary excretion of eicosanoids (a decrease of 6-keto-PGF1 alpha and PGF2 and an increase of thromboxane) previously found in lead (Pb) exposed workers may decrease the renal haemodynamic response to an acute oral protein load. METHODS: The renal haemodynamic response was estimated by determining the capacity of the kidney to increase the glomerular filtration rate (in terms of creatinine clearance) after an acute consumption of cooked red meat (400 g). A cross sectional study was carried out in 76 male Pb workers (age range 30 to 60 years) and 68 controls matched for age, sex, socioeconomic state, general environment (residence), and workshift characteristics. RESULTS: The Pb workers had been exposed to lead on average for 18 (range 6-36) years and showed a threefold higher body burden of Pb than the controls as estimated by in vivo measurements of tibial Pb concentration (Pb-T) (geometric mean 66 v 21 micrograms Pb/g bone mineral). The geometric mean concentrations of Pb in blood (Pb-B) and Pb in urine (Pb-U) were also significantly higher in the Pb group (Pb-B: 430 v 141 micrograms Pb/l; Pb-U: 40 v 7.5 micrograms Pb/g creatinine). These conditions of chronic exposure to Pb did not entail any significant changes in the concentration of blood borne and urinary markers of nephrotoxicity, such as urinary low and high molecular weight plasma derived proteins (beta 2-microglobulin, retinol binding protein, albumin, transferrin), urinary activities of N-acetyl-beta-D-glucosaminidase and kallikrein, and serum concentrations of creatinine, beta 2-microglobulin, urea, and uric acid. All participants also had normal baseline creatinine clearances (> 80 ml/min/1.73 m2) amounting on average to 115.5 in the controls v 121.3 ml/min/1.73 m2 in the Pb group. Both control and Pb exposed workers showed a significant increment in creatinine clearance (on average 15%) after oral protein load suggesting that the previously found changes in secretion of urinary eicosanoids apparently has no deleterious effect on renal haemodynamics in the examined Pb workers. CONCLUSIONS: The finding that both baseline and stimulated creatinine clearance rates were not only significantly higher in the Pb workers but also positively correlated with Pb-T, suggests that moderate exposure to Pb may be associated with a slight hyperfiltration state, which has been found to attenuate the age related decline in baseline creatinine clearance by a factor of two. Although the relevance of this effect for the worker's health is unknown, it can be concluded that adverse renal changes are unlikely to occur in most adult male Pb workers when their blood Pb concentration is regularly kept below 700 micrograms Pb/l. One should, however, be cautious in extra-polating this conclusion to the general population because of pre-employment screening of the Pb workers for the absence of renal risk factors.

Adult↗
PubMed1994

Competition between albumin and low-molecular-weight proteins for renal tubular uptake in experimental nephropathies.

A controversy presently exists concerning the ability of albumin to inhibit the tubular reabsorption of low-molecular-weight (M(r)) proteins in experimental renal diseases leading to massive proteinuria. We have examined the urinary excretion of albumin and of 2 low-M(r) proteins, beta 2-microglobulin and cystatin C, in rats treated with toxins affecting primarily the glomerulus (puromycin amino-nucleoside and Adriamycin) or the tubule (mercuric chloride and maleic acid). Above a threshold of 100 mg/24 h, albuminuria induced by puromycin aminonucleoside (50 mg/kg) and Adriamycin (5 mg/kg) was associated with a marked increase in the urinary excretion of beta 2-microglobulin and cystatin C peaking at more than 100-fold the baseline levels. These glomerulotoxins did not affect the urinary excretion of the tubular enzyme N-acetyl-beta-D-glucosaminidase. This pattern of effects was completely different from that induced by mercuric chloride (2 mg/kg) and maleic acid (400 mg/kg) which increased the excretion of both N-acetyl-beta-D-glucosaminidase and low-M(r) proteins in rats with albuminuria values below 100 mg/24 h. These results strongly support the hypothesis that at high filtered loads, albumin decreases the tubular uptake of low-M(r) proteins most likely by competition for a common transport mechanism.

Acetylglucosaminidase↗
PubMed1994

Unusual manifestations after malathion poisoning.

We report a case of organophosphate poisoning with a commercial preparation of malathion (deliberate ingestion of Malathane Garden Spray: malathion 15% in isopropyl alcohol) in which the initial cholinergic crisis was followed by cardiac, pulmonary, neurological and renal manifestations. They occurred when erythrocyte and plasma cholinesterases were reactivating. A chemical analysis of the pesticide preparation revealed, apart from malathion itself, the presence of isopropylmalathion and O,O,S-trimethylphosphorothioate. Although pure malathion is regarded as one of the safest organophosphate insecticides, this observation underlines the possibility of severe complications after exposure to a preparation which has been stored for a long period of time.

Aged↗
PubMed1994

Clara cell protein in human amniotic fluid: a potential marker of fetal lung growth.

Clara cell protein (CC16) is a 16-kD protein secreted at the surface of respiratory airways by nonciliated bronchial and bronchiolar cells, including Clara cells. Using the same immunoassay as that recently developed for CC16 in lung lavage, we have measured CC16 in amniotic fluid samples from 100 normal fetuses and 51 fetuses with various pathologies. Ouchterlony immunodiffusion analysis showed a complete identity between CC16 in amniotic fluid and the protein in lung lavages of adults. CC16 was detectable in amniotic fluid from about the 15th wk of pregnancy, then progressively increased until delivery, with a tendency to reach a plateau after the 30th wk. Between the 15th and the 39th wk of pregnancy, the concentration of CC16 in amniotic fluid increased on average 25 times. The sex of the fetus did not influence the concentration of CC16 in amniotic fluid. Compared with expected values, levels of CC16 in amniotic fluid were on average not significantly altered in cases of spina bifida (n = 9), anencephaly (n = 7), and trisomy 21 (n = 6). In contrast, CC16 was on average significantly decreased in cases of diaphragmatic hernia (n = 6), trisomy 18 (n = 14), Turner syndrome (n = 4), and diabetic pregnancy (n = 5). In cases of diaphragmatic hernia, a relation emerged between the concentration of CC16 in amniotic fluid and both the weight of the lungs and the survivorship of the fetuses. The time course of CC16 in amniotic fluid during normal pregnancy and its reduction in pathologies associated with lung hypoplasia suggest that CC16 in amniotic fluid might serve as a marker of bronchial epithelium growth.

Amniotic Fluid↗
PubMed1994

Early indicators of renal dysfunction in silicotic workers.

OBJECTIVES: The aim of this study was to determine whether silicosis is associated with renal alterations detectable in urinary or blood-borne indicators of nephrotoxicity. METHODS: The study used a cross-sectional design. The subjects comprised 116 male workers who had been exposed to silica for at least two years and had been diagnosed as having silicosis and 61 age-matched referents. The considered outcome measures were the concentrations of beta, -microglobulin and creatine in serum and the urinary excretion of albumin, retinol-binding protein, and beta-N-acetyl-D-glucosaminidase. RESULTS: Compared with the referents, the silicotic subjects excreted, on the average, slightly higher amounts of albumin, retinol-binding protein, and beta-N-acetyl-D-glucosaminidase. This increase did not correlate with the duration of exposure or the stage of silicosis and was not associated with an elevation in serum creatinine. The concentration of beta2-microglobulin in the serum of silicotic subjects showed a tendency to rise that became significant in the subgroup with pseudotumoral opacities. This effect, which did not correlate with markers of nephrotoxicity, is however more likely the consequence of silicosis-associated inflammatory reactions than of decreased renal filtration. CONCLUSIONS: The present study confirms that silicosis is associated with some infraclinical renal alterations. However, in the absence of a relationship with length of exposure or severity of silicosis, the implication of silica in their causation needs to be examined further.

Acetylglucosaminidase↗
PubMed1994

Early decrease of serum Clara cell protein in silica-exposed workers.

Clara cell protein (CC16) is a 16 kDa protein secreted by nonciliated cells of the tracheobronchial tree; it has recently been proposed as a peripheral marker of respiratory epithelial injury. The concentration of CC16 was measured in the serum and, when available, in the sputum of 86 miners exposed to silica and of 86 control subjects matched for age, body mass index and smoking status (26 lifelong nonsmokers and 60 current smokers in both groups). Workers were exposed to silica-rich dust in a quarry for 15.2 months on average. No difference between exposed and control workers could be detected with regard to respiratory symptoms, chest radiographs or lung function tests. By contrast, the concentration of CC16 in serum was decreased in silica-exposed workers (geometric mean 12.3 micrograms.l-1) compared to controls (16.3 micrograms.l-1). The decrease was found both in lifelong nonsmokers (14.7 vs 21.9) and current smokers (11.3 vs 14.5). In the latter, tobacco smoking caused a decrease of serum CC16 that was additional to that associated with silica exposure. The determination of CC16 in sputum samples, judged to be reliable on the basis of the CC16/alpha-amylase concentration ratio (mostly from smokers), also revealed a reduction of CC16 following silica exposure (46.2 vs 106 mg.l-1). We conclude that alterations in the serum concentrations of CC16 probably reflect very early toxic effects of silica particles on the respiratory epithelium. This reinforces the view that serum CC16 is a sensitive marker, which might improve our ability to detect exposure to chemicals potentially harmful to the respiratory tract.

Adult↗
PubMed1993

Urinary excretion of homovanillic acid in workers exposed to manganese.

Homovanillic acid, an end product of dopamine catabolism, and manganese (Mn) were measured in the urine of 68 male workers exposed to Mn-containing dust in a dry alkaline battery plant or an Mn oxide and salt producing plant, and in 35 control male subjects. The geometric mean of the airborne concentration of inhalable (total) dust amounted to 0.95 and 1.37 mg/m3 in the dry alkaline battery plant and the Mn oxide and salt producing plant, respectively. In the latter, a higher prevalence of increased values of urinary homovanillic acid concentration was found. In the total population, there was a low but statistically significant positive correlation between the concentration of homovanillic acid and Mn in urine (r = 0.20, P = 0.04) but there was no significant correlation between the level of homovanillic acid in urine and Mn in airborne dust or duration of exposure. This observation might be compatible with the stimulation of dopamine turnover in the brain, which has been observed in the early phase of Mn intoxication in animals. However, the large variability in urinary homovanillic acid excretion in control subjects precludes the use of this biological indicator to detect early interference of Mn with the dopaminergic system.

Adult↗
PubMed1993

Evaluation of the role of reactive oxygen species in the interactive toxicity of carbide-cobalt mixtures on macrophages in culture.

The lung toxicity of a carbide-cobalt mixture is more important than that of each individual component; the mechanism of this interaction is not understood. The capacity of cobalt metal particles alone and mixed with different carbides to generate hydroxyl radicals was examined with the deoxyribose assay. In a chemical system, cobalt ions and cobalt metal particles (Co) were found to catalyse the degradation of deoxyribose in the presence of hydrogen peroxide. Carbides were able to directly oxidize deoxyribose, but their respective activities did not support such a mechanism to explain the carbide-cobalt interactive toxicity, since there was no direct relationship between deoxyribose degradation ability and cytotoxicity toward macrophages. Tungsten, niobium, titanium and chromium carbides (interactive carbides) were only weak oxidants and conversely molybdenum, vanadium and silicon carbides (non-interactive carbides) were the most potent ones. The ability of cobalt metal to produce hydroxyl radicals in the presence of hydrogen peroxide was not increased by tungsten carbide. The role of reactive radical formation in the toxicity of these particles was further assessed in a macrophage culture model. Catalase (4000 U/ml), superoxide dismutase (300 U/ml), sodium azide (1 mM), sodium benzoate, mannitol, taurine and methionine (all 20 mM) were all unable to protect against the cytotoxic effects of cobalt ions and cobalt metal alone or mixed with tungsten carbide. In conclusion, no evidence was found that production of reactive oxygen species contributes to the elective toxicity of carbide-cobalt mixtures.

Animals↗
PubMed1993

Biological markers in PAH exposed workers and controls.

Workers employed in a graphite electrode producing plant (n = 16) and a coke oven (n = 33) were compared with a control population of maintenance workers in a blast furnace (n = 54). The following parameters were analyzed: concentration of 13 different PAHs in the work environment measured by personal air samplers, concentration of hydroxypyrene in the urine, smoking habits (via urinary thiocyanate levels and a questionnaire) and cytogenetic aberrations in lymphocytes (SCE, HFC and MN). On the basis of PAH levels in the work environment and hydroxypyrene concentrations in the urine, the workers from the graphite electrode producing plant were the most exposed. However, statistically significant differences in SCE and HFC and positive correlations between the cytogenetic markers and airborne PAH levels on the one hand, and urinary hydroxypyrene concentrations on the other hand were only detectable in the workers from the coke oven with a lower exposure. No statistically significant effect of smoking was observed. As to the inter-comparison of the different cytogenetic markers, one may consider that SCE and HFC are more sensitive than MN frequencies for the biomonitoring of exposure to PAHs. Whether MN or SCE are the best biomarker for risk assessment of cancer and whether the presence of PAHs in the work environment is really responsible for the cytogenetic effects found in this study could not be ascertained.

Air Pollutants, Occupational↗