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Biomedical subjects

R Lauwerys

Publications and source records attributed to R Lauwerys.

At least 73 records · Page 4Linked to original sources
PubMed1993

Increased sister chromatid exchanges and tumor markers in workers exposed to elemental chromium-, cobalt- and nickel-containing dusts.

Sister-chromatid exchange (SCE) in blood lymphocytes, serum tumors markers, carcinoembryonic antigen (CEA) and tissue polypeptide antigen (TPA), and urinary excretion of chromium, cobalt and nickel were determined in 26 male workers occupationally exposed to chromium, cobalt and nickel dust and in 25 controls matched for age and smoking habits. The differences in the urinary excretion of metals between exposed persons and controls were statistically significant. An analysis of variance on the SCE rank values revealed that both exposure status (exposed persons vs. controls) and smoking habits (smokers and former smokers vs. never smokers) had a statistically significant effect. For the tumor markers, the analysis of variance did not reveal a statistically significant difference between exposed persons and controls. However, CEA serum levels were significantly correlated not only with smoking habits but also with duration of exposure. As cobalt is only weakly mutagenic, these results suggest that the small amount of absorbed chromium and nickel may have been sufficient to induce SCE. The hypothesis that tumor markers may be increased in groups of subjects exposed to genotoxic substances deserves further study.

Adult↗
PubMed1993

Relationship between atmospheric and urinary nickel in workers manufacturing electrical resistances using nickel oxide: role of the bioavailability of nickel.

The daily concentrations of nickel in total (ie inhalable) and respirable airborne dust (personal sampling) and in post-shift and pre-shift urine samples were monitored during five consecutive work days in 20 workers exposed to NiO in a workshop manufacturing electrical resistances. The individual daily atmospheric nickel concentrations ranged from 0.5 to 9586 micrograms Ni/m3 (geometric mean 22.9) for total dust and from 0.2 to 332 micrograms Ni/m3 (geometric mean 3.5) for respirable dust. The results of the urinary excretion of nickel suggested that the occupationally-related systemic absorption of nickel strongly differed in one subject (worker E) compared to the other 19 workers. In the latter group the nickel concentration in urine never exceeded 5 micrograms Ni/g creatinine, it did not differ between post-shift and pre-shift samples (geometric means: 1.1 versus 1.2 micrograms Ni/g creatinine), and it was only slightly higher than that measured in a group of 17 non-exposed subjects (mean 0.5 micrograms Ni/g creatinine; range 0.1-1.7); furthermore their nickel elimination in urine did not change during the days off or after two weeks of holiday. In worker E, the nickel concentration ranged from 21 to 101 micrograms Ni/g creatinine in post-shift urine, the next morning (after 16 h) it had dropped on average by 50 per cent, it decreased further during the days off, and amounted still to 4.4 micrograms Ni/g creatinine after two weeks of holiday. These divergent patterns of elimination of nickel in urine are most likely related to differences in the nature of exposure to airborne nickel involving both particle size and bioavailability of nickel. Worker E was exposed to NiO powder of 1-8 microns particle size resulting in nickel levels of the respirable fraction on average about 50 times that measured for the 19 other workers (3 micrograms Ni/m3). Transformation of the initial NiO powder into particles of 150 to 600 microns size and associated changes in physicochemical properties of NiO in the particles of the respirable fraction may explain why the urinary excretion of nickel in the 19 workers is hardly influenced by their occupational exposure to this metal. The pattern of urinary nickel elimination in worker E, however, most likely reflects very recent exposure to NiO, suggesting that the degree of bioavailability of nickel from this particular physicochemical form of NiO powder is much higher than that usually accepted for poorly soluble nickel compounds.

Adult↗
PubMed1993

Plasminogen activator activity and fertilizing ability of human spermatozoa.

Mature spermatozoa contain a number of proteases that are supposed to contribute to their fertilizing ability. The present study was directed at plasminogen activator (PA), a protease that belongs to the group of serine proteases and converts the zymogen plasminogen to the active broad-spectrum protease plasmin. To investigate the possible role of PA in the fertilization process, we have measured sperm-bound PA activity in 63 patients included in an in-vitro fertilization (IVF) programme and assessed their relationship to standard semen parameters and the rate of fertilization. PA activity was correlated significantly with the sperm count, as well as with sperm motility and morphology. Using logistic regression analysis, specific PA (pmol pNA 10(-6) cells min-2) was found to significantly influence the probability of fertilization. Other significantly predictive factors were motility and the percentage of spermatozoa with normal morphology. The sperm concentration (10(6) cells ml-1) did not significantly affect the outcome of IVF. We suggest that sperm-bound PA is involved in the fertilization process and may represent a potential indicator of sperm fertilizing capacity.

Female↗
PubMed1993

Serum laminin, hydrocarbon exposure, and glomerular damage.

It has been postulated that occupational exposure to hydrocarbons may damage the kidney and lead to glomerulonephritis and chronic renal failure. As laminin is a ubiquitous basement membrane component that seems to play a central part in the structure and function of basement membranes and as the normal renal filtration process is highly dependent on an intact glomerular basement membrane, the serum laminin concentration was examined in a population of workers exposed to hydrocarbons. The hydrocarbon exposure was assessed by exposure surrogates (exposure duration and exposure score). An interaction between occupational exposure to hydrocarbons and hypertension increased the laminin concentration whereas the laminin concentration decreased in workers exposed for a long time probably because of a selection effect. In a subgroup of printers exposed to toluene whose hippuric acid excretion had been recorded for several years this interaction was confirmed when the hippuric acid excretion was substituted for the other exposure indices. In the exposed group, the age-related decline in creatinine clearance was accelerated. These results seem to confirm that occupational exposure to hydrocarbons is a non-specific factor that may promote a deterioration of renal function.

Adult↗
PubMed1993

Epidemiological survey of workers exposed to cobalt oxides, cobalt salts, and cobalt metal.

Several organs (lung, skin, thyroid, heart, bone marrow) are potential targets of cobalt (Co). Whereas there is no doubt that inhalation of Co alone may cause bronchial asthma, its role in the occurrence of hard metal disease is still controversial because most cases were reported in workers exposed not only to Co but also to other substances such as tungsten carbide, titanium carbide, iron, silica and diamond. To assess whether exposure to pure Co dust (metal, oxides, or salts) may lead to adverse health effects a cross sectional study was carried out among 82 workers in a Co refinery. The results were compared with those in a sex and age matched control group. The Co group had been exposed for 8.0 years on average (range 0.3-39.4). The geometric mean time weighted average exposure assessed with personal samplers (n = 82) was about 125 micrograms/m3 and 25% of the values were higher than 500 micrograms/m3. The concentrations of Co in blood and in urine after the shift were significantly correlated with those in air. Concentration of Co in urine increased during the workweek. A slight interference with thyroid metabolism (decreased T3, T4, and increased TSH), a slight reduction of some erythropoietic variables (red blood cells, haemoglobin, packed cell volume) and increased white cell count were found in the exposed workers. The exposed workers complained more often of dyspnoea and wheezing and had significantly more skin lesions (eczema, erythema) than control workers. Within the exposed group a dose-effect relation was found between the reduction of the forced expiratory volume in one second/vital capacity and the intensity of current exposure to Co assessed by the measurement of Co in air or in urine. The prevalence of dyspnoea was related to the dustiness of the workplace as reflected by statistically significant logistic regression between this symptom and the current levels of Co in air and in urine. No difference between lung volumes, ventilatory performances, carbon monoxide diffusing capacity, and serum myocardial creatine kinase and procollagen III peptide was found between the Co and control groups and no lung abnormalities were detected on the chest radiographs in both groups. The results suggest that exposure to high airborne concentrations of Co alone is not sufficient to cause pulmonary fibrosis. This finding is compatible with experimental studies indicating that interaction of other airborne pollutants with Co particles play a part in the pathogenesis of parenchymal lung lesions.

Adult↗
PubMed1993

Association of cadmium exposure with rapidly progressive emphysema in a smoker.

Rapidly progressive emphysema developed in a 59 year old smoker after exposure to cadmium fumes in a factory. Very high levels of cadmium in air sampled at the workplace and in the patient's blood, urine, and lung tissue confirmed massive exposure. These data strongly suggest an association between the patient's cadmium exposure and the development of emphysema.

Acute Disease↗
PubMed1993

Health effects of environmental exposure to cadmium in a population study.

The Cadmibel Study is a cross-sectional population study, which investigated the hypothesis that environmental exposure of the population to cadmium would result in health effects. The 2,327 participants constituted a random sample of the population of four Belgian districts, chosen to provide a wide range of environmental exposure to cadmium. The urinary cadmium excretion, a measure of lifetime exposure, averaged 9.3 nmol/24h in men (range 0.4-325 nmol/24h) and 7.2 nmol (0.1-71 nmol/24h) in women. The Cadmibel Study refuted the hypothesis that exposure to cadmium would lead to an increase in BP and in the prevalence of hypertension and other cardiovascular diseases. Serum alkaline phosphatase activity and the urinary excretion of calcium correlated significantly and positively with urinary cadmium in both sexes. These findings suggest that the calcium metabolism is gradually affected, as cadmium accumulates in the body. Furthermore, several markers of renal tubular function (urinary excretion of retinol binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin and aminoacids) were significantly and positively associated with urinary cadmium. There was a 10% probability of abnormal values of these markers of tubular function when urinary cadmium exceeded +/- 20 nmol/24h. However, the morbidity associated with the functional changes, observed in the Cadmibel Study, remains presently unknown and requires further investigation, preferably in a longitudinal population studies.

Adult↗
PubMed1992

Incorporation of [35S]sulfate into glomerular membranes of rats chronically exposed to cadmium and its relation with urinary glycosaminoglycans and proteinuria.

The aim of the present work was to assess the effects of long-term exposure to Cd on the sulfatation of glomerular membranes and their relation with proteinuria and urinary glycosaminoglycans (GAG). For this purpose the in vitro incorporation of [35S]sulfate was investigated in female Sprague-Dawley rats given 100 ppm of Cd in drinking water for 7 months. When compared with their controls, glomeruli from Cd-treated rats showed a 12.8% decrease in the incorporation of the label into glomerular membranes. This effect, which was not explained by differences in viability or in sulfate uptake by the glomeruli, suggests that sulfatation of glomerular membranes is impaired in Cd-treated rats. In support of this, in another independent experiment, a decrease, 17.4% on average, of the sulfate content of glomerular membranes was observed in long-term Cd-treated rats (100 ppm in drinking water for 4 months). This effect was significantly correlated with albuminuria and transferrinuria but not with beta 2-microglobinuria, suggesting that a loss of heparan sulfate of the glomerular capillary wall could be involved in the Cd-induced glomerular proteinuria. On the other hand an enhanced urinary excretion of GAG, negatively correlated with the sulfate content of glomerular membranes, was also observed in Cd-treated rats. Moreover GAG excretion was associated with tubular and glomerular proteinuria, which suggests that GAG might be a useful marker of Cd-induced nephrotoxicity.

Animals↗
PubMed1992

Fertility of male workers exposed to cadmium, lead, or manganese.

The effect of exposure to cadmium, lead, or manganese on male reproductive function was examined in 1988-1989 in Belgian blue-collar workers. The workers were exposed to cadmium in two smelters (n = 83; geometric mean urinary cadmium level = 6.94 micrograms/g of creatinine; mean duration of exposure = 24 years), to lead in a battery factory (n = 74; mean blood lead level = 46.3 micrograms/dl; mean duration of exposure = 10.7 years), or to manganese (manganese dioxide) in a dry alkaline battery plant (n = 70; median atmospheric concentration of total manganese dust = 0.71 mg/m3; mean duration of exposure = 6.2 years). Fertility in these workers and in an unexposed population (n = 138) was assessed by examining the birth experiences of their wives through a logistic regression model. The probability of a live birth was not different between the unexposed workers and the cadmium- or manganese-exposed workers before or after the onset of exposure. While the fertility of the lead-exposed workers was somewhat greater than that of the unexposed before the onset of exposure, a significant decrease in fertility was observed during the period of exposure to the metal (odds ratio = 0.65, 95% confidence interval 0.43-0.98).

Adult↗
PubMed1992

Human urinary protein 1: evidence for identity with the Clara cell protein and occurrence in respiratory tract and urogenital secretions.

Protein 1 (P1), a low mol mass urinary protein of unknown function, has been purified, sequenced and quantified in human biological fluids. The molecular size, subunit composition and partial amino acid sequence of P1 are similar to those of the 10 kDa Clara cell protein (CC10), a lung secretory protein. P1 is found in high concentrations in sputum, bronchoalveolar lavages, urine and semen of healthy individuals and in urine of some pregnant women. Contrary to what is claimed, P1 or CC10 is not a specific and unique product of the lung, but like its homologue in rabbits (uteroglobulin) it is also present in urogenital secretions. P1 or CC10 may act as a natural immunosuppressor protecting the respiratory and urogenital tracts from unwanted inflammatory reactions.

Adolescent↗
PubMed1992

Assessment of thyroid, testes, kidney and autonomic nervous system function in lead-exposed workers.

The objective of the study was to assess whether moderate occupational exposure to lead may be associated with early changes in potential target organs (thyroid, testes, kidney, autonomic nervous system). Workers exposed to lead in a lead acid battery factory (n = 98; mean blood lead 51 micrograms/dl, range 40-75 micrograms/dl) and 85 control workers were examined. None of the indicators of kidney function (in urine: retinol-binding protein, beta 2-microglobulin, albumin, N-acetyl-beta-D-glucosaminidase; in serum: creatinine, beta 2-microglobulin), endocrine function (follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, thyroxine, triiodothyronine) and autonomic nervous system (R-R interval variations on the electrocardiogram) were correlated with lead exposure (blood lead or duration of exposure) or showed significantly different mean values between the exposed group and controls. These results and an assessment of the published data suggest that compliance with the Directive of the Council of the European Communities on lead exposure (health surveillance in workers whose lead in blood exceeds 40 micrograms/dl and removal from exposure when blood lead exceeds 70-80 micrograms/dl) would prevent the occurrence of significant biological changes in the majority of lead-exposed workers.

Adult↗
PubMed1992

Renal effects of in utero exposure to mercuric chloride in rats.

The transplacental nephrotoxicity of mercuric chloride has been studied in female Sprague-Dawley rats. Mercuric chloride was injected s.c. to rats at the dose of 1 mg/kg during the last 8 gestational days or the whole pregnancy. Both mothers and newborns developed a transient renal dysfunction resulting in an increased urinary excretion of beta 2-microglobulin and albumin. In mothers and their female offspring, these effects were completely reversible and did not influence the subsequent evolution of the renal function. In the male offspring, however, transitory changes in protein excretion were again observed a few months later, concomitantly with an enhanced accumulation of alpha 2u-globulin in the kidney. The transfer of mercury from maternal to fetal tissues was very small. The kidney concentrations of mercury in newborns were more than 300 times lower than in mothers. The barrier role of the placenta is not sufficient to prevent the occurrence of renal effects in the offspring of rats treated with inorganic mercury during pregnancy.

Alpha-Globulins↗
PubMed1992

Loss of glomerular polyanion correlated with albuminuria in experimental cadmium nephropathy.

The relationship between proteinuria and glomerular polyanion (GPA) charge has been studied in a model of experimental cadmium (Cd) nephropathy. Female Sprague-Dawley rats were administered Cd in drinking water for up to 18 months. From month 2, the animals showed an elevation of albuminuria preceding by about 6 months the rise of urinary beta 2-microglobulin and IgG. The nephrotoxic action of Cd was not readily detectable on the basis of the urinary output of beta-N-acetylglucosaminidase, alanine aminopeptidase and lactate dehydrogenase. These enzymes showed either little variation or were affected late in the intoxication process. Administration of Cd for 12 or 18 months did not impair the GFR. The glomerular origin of the albuminuria induced by Cd was demonstrated by estimating the glomerular filtration of rat or human (injected intravenously) albumin in rats whose tubular reabsorption had been blocked by a saturating dose of cytochrome C. The GPA charge was assessed by measuring the binding of the cationic dye, Alcian blue (AB), to membranes of isolated glomeruli. The sialic and sulfate content of these membranes was also determined. The Cd induced-albuminuria was negatively correlated (r = -0.73; n = 37) with the AB binding to glomerular membranes, their sialic acid content (r = -0.39) but not with their sulfate content (r = -0.15). A negative correlation (r = -0.62; n = 37) was also observed between the albuminuria and red blood cell membrane negative charges largely contributed by sialic acid. All these observations can be interpreted as the evidence that Cd enhances the glomerular filtration of proteins through a GPA depletion involving mainly sialic acid.

Albuminuria↗
PubMed1992

Comparative study of the acute lung toxicity of pure cobalt powder and cobalt-tungsten carbide mixture in rat.

Alveolitis progressing to lung fibrosis has been reported in workers exposed to cobalt containing dust (e.g., tungsten carbide-cobalt mixture as produced by the hard metal industry) but rarely following exposure to pure cobalt dust (e.g., in cobalt-producing factories). We have previously demonstrated that tungsten carbide-cobalt mixture is more toxic toward rat alveolar macrophages in vitro than pure cobalt metal powder. The present study was undertaken to compare in female rats the acute pulmonary response (lung weight, lung histology, cellular and biochemical analyses of bronchoalveolar lavage fluid, and mortality) following the intratracheal instillation of pure cobalt (Co) particles (median particle size, d50:4 microns), pure tungsten carbide (WC) particles (d50:2 microns), tungsten carbide-cobalt (WC-Co) powder (d50:2 microns; cobalt 6.3%, tungsten 84%, carbon 5.4%) and crystalline silica (d50 less than 5 micron) used as pneumotoxic reference material. WC alone (15.67 mg/100 g body wt) behaves as an inert dust producing only a mild accumulation of macrophages in the alveolar duct walls. Co alone (1.0 mg/100 g) only causes a moderate inflammatory response. An identical amount of Co given as WC-Co mixture (16.67 mg/100 g; corresponding to 1.0 mg Co/100 g) produces a severe alveolitis and fatal pulmonary edema. Cellular and biochemical characteristics of bronchoalveolar lavage fluid collected 24 hr after the intratracheal instillation of WC (1.0 mg/100 g) or Co (0.06 mg/100 g) are not significantly different from those of control animals instilled with sterile saline. On the contrary, bronchoalveolar lavage fluid changes following administration of the WC-Co mixture (1.0 mg/100 g; corresponding to 0.06 mg Co/100 g) are very similar to those induced by crystalline silica (1.0 mg/100 g). The amount of cobalt excreted in urine is significantly higher when the animals are exposed to WC-Co powder as compared to an equivalent amount of pure cobalt particles, suggesting an increased bioavailability of cobalt metal when combined with tungsten carbide. This study demonstrates that the acute lung toxicity of tungsten carbide-cobalt mixture is much higher than that of each individual component and may explain why lung fibrosis is rarely if ever induced by exposure to pure cobalt dust.

Animals↗
PubMed1992

Human and experimental studies on renal eicosanoid response to long-term cadmium exposure.

In order to assess the effects of long-term exposure to cadmium (Cd) on the renal metabolism of eicosanoids, the urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), and thromboxane B2 (TXB2) was determined in 37 workers exposed to Cd and in female Sprague-Dawley rats given 100 ppm Cd in drinking water for 10 months. Urinary output of sodium and calcium was also determined. The Cd-exposed workers showed an increased urinary concentration of 6-keto-PGF1 alpha, PGE2, sodium, and calcium. The rise of 6-keto-PGF1 alpha was related to Cd levels in blood and weakly correlated with urinary sodium. Calcium in urine was not related to the concentration of the metal in blood and urine. A slight elevation in urinary TXB2 was also observed in workers with blood Cd higher than 5 micrograms/liter. After 10 months of exposure to Cd, female Sprague-Dawley rats presented an enhanced urinary excretion of albumin, transferrin, beta 2-microglobulin, sodium, and PGE2 in urine. The latter was significantly correlated with albuminuria and transferrinuria. In conclusion the results show that chronic exposure to Cd induces changes in the urinary excretion of some eicosanoids. The possible relation of these changes to Cd-induced kidney dysfunction are discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Monitoring of early nephrotoxic effects of industrial chemicals.

Long-term exposure to certain industrial chemicals (e.g. heavy metals, some halogenated hydrocarbons) may cause progressive degenerative changes in the kidney, possibly leading to renal insufficiency. The screening tests most widely used to assess the integrity of the kidney (i.e. serum creatinine or BUN and the quantitative or semi-quantitative measurement of total proteinuria) lack sensitivity; they do not permit the detection of renal disturbances at a stage when removal from exposure may prevent progression of the disease process and are not suitable to determine the no-effect levels of potentially nephrotoxic chemicals. During the last decades new markers have been proposed for the early detection of structural and/or functional changes at various sites of the renal parenchyma. Some tests mainly attempt to assess the integrity of the glomerulus (e.g. high Mr proteinuria such as transferrinuria and albuminuria; increased excretion of some components of the glomerular basement membrane or the mesangium matrix, increased plasma concentration of low Mr proteins such as beta 2-microglobulin and free retinol binding protein), the proximal tubule (e.g. urinary excretion of several low Mr plasma proteins, tubular enzymes and antigens), the loop of Henle and distal tubule (e.g. excretion of various prostanoids). Currently, the majority of these tests are of limited value at the individual level because their health significance, even when they are persistently abnormal, has not yet been sufficiently studied. In workers exposed to Cd, however, it has been shown that a persistent low Mr proteinuria is predictive of an exacerbation of the age-related decline of the GFR; this biological change should be considered as an adverse effect. Currently, the principal application of these tests lies in the framework of epidemiologic studies designed to assess permissible exposure levels to nephrotoxic pollutants. The study of dose-effects/response relationships based on a large battery of renal markers has allowed the better determination of the internal dose of Cd, which is not associated with significant renal risk.

Animals↗