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Biomedical subjects

J P Buchet

Publications and source records attributed to J P Buchet.

At least 19 recordsLinked to original sources
PubMed1992

Impairment of renal function with increasing blood lead concentrations in the general population. The Cadmibel Study Group.

BACKGROUND: Nephropathy is known to occur in persons with heavy exposure to lead. Whether exposure to lead in the general population leads to impaired renal function is not known. METHODS: We studied renal function and indexes of lead exposure in a random population sample of 965 men and 1016 women (age range, 20 to 88 years). In all the subjects we measured creatinine clearance and blood concentrations of lead and zinc protoporphyrin (an indirect measure of blood lead level). RESULTS: The mean (+/- SD) creatinine clearance rate was 99 +/- 30 ml per minute in the men and 80 +/- 25 ml per minute in the women. In the men the geometric mean blood lead concentration was 114 micrograms per liter (0.55 mumol per liter) (range, 23 to 725 micrograms per liter [0.11 to 3.5 mumol per liter]), and in the women 75 micrograms per liter (0.36 mumol per liter) (range, 17 to 603 micrograms per liter [0.08 to 2.9 mumol per liter]); the zinc protoporphyrin values in blood averaged 1.0 and 1.1 micrograms per gram of hemoglobin, respectively. The creatinine clearance rate was inversely correlated with blood lead and zinc protoporphyrin values in the men and the women both before and after adjustments for age, bodymass index, and diuretic treatment. A 10-fold increase in blood lead concentration was associated with a reduction of 10 to 13 ml per minute in creatinine clearance. We also found a positive correlation between serum beta 2-microglobulin (which is inversely related to the glomerular filtration rate) and blood lead in men, between serum beta 2-microglobulin and zinc protoporphyrin in both sexes, and between serum creatinine and zinc protoporphyrin in men. CONCLUSIONS: Exposure to lead may impair renal function in the general population. The alternative hypothesis that renal impairment may lead to an increase in the blood lead concentration cannot be excluded, however.

Adult↗
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

Assessment of the permissible exposure level to manganese in workers exposed to manganese dioxide dust.

The prevalence of neuropsychological and respiratory symptoms, lung ventilatory parameters, neurofunctional performances (visual reaction time, eye-hand coordination, hand steadiness, audioverbal short term memory), and several biological parameters (calcium, iron, luteinising hormone (LH), follicle stimulating hormone (FSH), and prolactin concentrations in serum, blood counts, manganese (Mn) concentration in blood and in urine) were examined in a group of workers (n = 92) exposed to MnO2 dust in a dry alkaline battery factory and a matched control group (n = 101). In the battery plant, the current exposure of the workers to airborne Mn was measured with personal samplers and amounted on average (geometric mean) to 215 and 948 micrograms Mn/m3 for respirable and total dust respectively. For each worker, the lifetime integrated exposure to respirable and total airborne Mn dust was also assessed. The geometric means of the Mn concentrations in blood (MnB) and in urine (MnU) were significantly higher in the Mn exposed group than in the control group (MnB 0.81 v 0.68 microgram/100 ml; MnU 0.84 v 0.09 microgram/g creatinine). On an individual basis, MnU and MnB were not related to various external exposure parameters (duration of exposure, current exposure, or lifetime integrated exposure to airborne Mn). On a group basis, a statistically significant association was found between MnU and current Mn concentrations in air. No appreciable difference between the exposed and the control workers was found with regard to the other biological measurements (calcium, LH, FSH, and prolactin in serum). Although the erythropoietic parameters and serum iron concentration were in the normal range for both groups, there was a statistically significant trend towards lower values in the Mn exposed workers. The prevalences of reported neuropsychological and respiratory symptoms, the lung function parameters, and the audioverbal short term memory scores did not differ between the control and exposed groups. The Mn workers, however, performed the other neurofunctional tests (visual reaction time, eye-hand coordination, hand steadiness) less satisfactorily than the control workers. For these tests, the prevalences of abnormal results were related to the lifetime integrated exposure to total and respirable Mn dust. On the basis of logistic regression analysis it may be inferred that an increased risk of peripheral tremor exists when the lifetime integrated exposure to Mn dust exceeds 3575 or 730 micrograms Mn/m3 x year for total and respirable dust respectively. The results clearly support a previous proposal by the authors to decrease the current time weighted average exposure to Mn dust.

Adolescent↗
PubMed1992

Evaluation of exposure to polycyclic aromatic hydrocarbons in a coke production and a graphite electrode manufacturing plant: assessment of urinary excretion of 1-hydroxypyrene as a biological indicator of exposure.

OBJECTIVES: Characterisation of the airborne concentration of 13 polycyclic aromatic hydrocarbons (PAHs) at various workplaces in a graphite electrode and a coke production plant. Validation of the urinary excretion of 1-hydroxypyrene (hydroxypyrene) as a biological marker of exposure to PAH. DESIGN: Cross sectional study of workers exposed to PAHs (106 in the graphite electrode producing plant and 16 in the coke works). METHODS: Personal air sampling during at least six hours per workshift using a glass fibre filter and a Chromosorb 102 solid sorbent tube and analysis of PAHs by high performance liquid chromatography (HPLC) and spectrofluorometric detection (SFD). Collection of spot urine samples before and after the shift and analysis of 1-hydroxypyrene by HPLC and SFD. RESULTS: The workers most exposed to PAHs were those occupied at the topside area of the coke oven plant and those working in the blending and impregnation areas of the graphite electrode producing plant (mean airborne concentration of total PAHs: 199 and 223 micrograms/m3 respectively). Except for naphthalene and perylene, the relative proportion of the different PAHs did not differ between the plants. Pyrene concentration in air was highly correlated with the total airborne PAH concentration (r = 0.83, p < 0.0001) and the correlation coefficients between hydroxypyrene concentration in postshift urine samples and pyrene or total PAHs in air were 0.67 (p < 0.0001) and 0.72 (p < 0.0001) respectively. Excretion of hydroxypyrene doubled when the exposure to pyrene in air increased 10-fold. The half life for the urinary excretion of hydroxypyrene was around 18 hours (95% confidence interval 16.1-19.8). Smoking habits only explained 2.3% of the variance in hydroxypyrene excretion compared with 45% for the pyrene concentration in air. CONCLUSION: The determination of the urinary excretion of hydroxypyrene in postshift urine samples can be used as a suitable biomarker to assess individual exposure to PAHs in coke ovens and in graphite electrode manufacturing plants.

Air Pollutants, Occupational↗
PubMed1992

Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites.

The relation between exposure to As2O3 fumes and dust, and the urinary excretion of inorganic arsenic metabolites (monomethylarsonic acid, dimethylarsinic acid, unchanged inorganic arsenic) has been studied in 18 workers from a sulphuric acid producing plant. The concentration of arsenic in the breathing zone of each worker was measured during five consecutive days and urine samples were obtained after one shift and before the next. The collection efficiency of the air sampling system exceeded 95%. The time weighted average exposure (TWA) concentrations of As2O3 ranged from 6 to 502 micrograms As/m3 and were log normally distributed. Although exposure probably occurred by ingestion as well as inhalation, statistically significant correlations (log scales) were found between airborne TWA of As2O3 and the inorganic arsenic metabolites in urine collected immediately after the shift, or just before the next shift. For a TWA of 50 micrograms As/m3, the mean concentration of the sum of the three inorganic arsenic metabolites in a postshift urine sample amounted to about 55 micrograms arsenic/g creatinine (95% confidence interval (95% CI) 47-62). Higher estimates of urinary arsenic reported by other authors are probably due either to the influence of dietary organoarsenicals when total arsenic is measured in urine or to a low retention efficiency of the air sampling system for As2O3 in the vapour phase.

Adult↗
PubMed1992

Determinants of serum zinc in a random population sample of four Belgian towns with different degrees of environmental exposure to cadmium.

This report investigated the distribution of serum zinc and the factors determining serum zinc concentration in a large random population sample. The 1977 participants (959 men and 1018 women), 20-80 years old, constituted a stratified random sample of the population of four Belgian districts, representing two areas with low and two with high environmental exposure to cadmium. For each exposure level, a rural and an urban area were selected. The serum concentration of zinc, frequently used as an index for zinc status in human subjects, was higher in men (13.1 mumole/L, range 6.5-23.0 mumole/L) than in women (12.6 mumole/L, range 6.3-23.2 mumole/L). In men, 20% of the variance of serum zinc was explained by age (linear and squared term, R = 0.29), diurnal variation (r = 0.29), and total cholesterol (r = 0.16). After adjustment for these covariates, a negative relationship was observed between serum zinc and both blood (r = -0.10) and urinary cadmium (r = -0.14). In women, 11% of the variance could be explained by age (linear and squared term, R = 0.15), diurnal variation in serum zinc (r = 0.27), creatinine clearance (r = -0.11), log gamma-glutamyltranspeptidase (r = 0.08), cholesterol (r = 0.07), contraceptive pill intake (r = -0.07), and log serum ferritin (r = 0.06). Before and after adjustment for significant covariates, serum zinc was, on average, lowest in the two districts where the body burden of cadmium, as assessed by urinary cadmium excretion, was highest. These results were not altered when subjects exposed to heavy metals at work were excluded from analysis.

Adult↗
PubMed1992

Factors influencing the cadmium body burden in a population study.

The cadmium body burden, as estimated from 24-h urinary cadmium (Cd-U), was determined in 1523 non-occupationally exposed subjects living in five areas of Belgium. It increased with age until 55-65 years in both sexes and thereafter decreased slightly. It was higher in smokers but was inversely associated with alcohol consumption and social class. In men only, it was also positively correlated with body mass index. After the menopause, women showed a significant increase in 24-h Cd-U independently of the other factors. In addition, the cadmium body burden was independently associated with place of residence in both sexes. Highest levels of Cd-U were found in subjects living in an area with soils heavily polluted by cadmium.

Adolescent↗
PubMed1992

Cadmium and health: the Belgian experience.

Studies in the 1970s on chronic cadmium poisoning in man in Belgium showed that the earliest effect was renal dysfunction with proteinuria. Subsequent studies were focused on the characterization of cadmium proteinuria, the diagnosis and prognosis of cadmium nephropathy and the assessment of the concentrations in urine and renal cortex leading to its occurrence. Chronic exposure to cadmium in industry gives rise to a proteinuria which may be tubular, glomerular or mixed in character. This proteinuria may be accompanied or preceded by a variety of other renal effects. In active male workers, three main groups of thresholds for urinary cadmium have been identified for the induction of these effects with corresponding thresholds in the renal cortex. However, these estimates probably cannot be extrapolated to the general population exposed to cadmium mainly by the oral route. The results of a large-scale cross-sectional study (Cadmibel) suggest that subclinical changes in tubular function may occur in the general population above a threshold of urinary cadmium as low as 2 micrograms/24h.

Belgium↗
PubMed1992

Effects of cadmium exposure on the cardiovascular system and on calcium metabolism: results of a cross-sectional population study.

This paper summarizes the findings of the Cadmibel Study, a cross-sectional population study of the health effects of cadmium, but only with respect to the cardiovascular system and calcium metabolism. The study disproved the hypothesis that exposure to cadmium would lead to an increase in blood pressure and in the prevalence of hypertension and other cardiovascular diseases. On the other hand, there was a positive relationship between urinary cadmium (Cd-U) and both serum alkaline phosphatase activity and urinary excretion of calcium. The regression coefficients obtained after adjustment for significant co-variates indicated that, when Cd-U increased two-fold, serum alkaline phosphatase and urinary calcium rose by 4% and 0.25 mmol/24 h, respectively. These findings suggest that calcium metabolism is gradually affected as cadmium accumulates in the body. The morbidity associated with the latter phenomenon is still unknown, and requires further investigation, preferably in a longitudinal prospective population study, in which the incidence of morbid events would be monitored in relation to the cadmium body burden.

Adult↗
PubMed1991

Blood pressure, the prevalence of cardiovascular diseases, and exposure to cadmium: a population study.

In a population study conducted from 1985 to 1989 in Belgium, the authors investigated whether exposure to cadmium is associated with blood pressure elevation and with an increased prevalence of cardiovascular diseases. The participants, aged 20-88 years, constituted a random sample of the households living in two low exposure areas (n = 803) and two high exposure areas (n = 1,283). For each exposure level, a rural and an urban district were selected. The cadmium levels in blood (8.5 vs. 11.0 nmol/liter) and urine (7.2 vs. 8.7 nmol/24 hours) were significantly (p less than 0.001) raised in the two high exposure areas compared with the two low exposure areas (p less than 0.001). Systolic pressure was similar in both rural areas, but in the urban area with high exposure systolic pressure was 5 mmHg (p less than 0.001) higher than in the control town. Diastolic pressure was similar in the four districts and the same was true for the prevalence of hypertension and of other cardiovascular diseases. Adjustment of systolic pressure for blood and urinary cadmium did not remove the difference in systolic pressure between both urban areas, suggesting that it was not related to the cadmium burden on the environment. Further analyses in individual subjects showed that neither blood pressure nor the presence of cardiovascular diseases were significantly and positively correlated with blood and urinary cadmium. Thus, the present population study did not confirm the hypothesis that increased exposure of the population to cadmium is associated with blood pressure elevation and with a higher prevalence of cardiovascular diseases.

Adult↗
PubMed1991

Potentiation of diabetic glomerulopathy in uninephrectomized rats subchronically exposed to cadmium.

The renal effects of diabetes mellitus and cadmium (Cd), separately or in combination, were investigated in unilaterally nephrectomized female Sprague-Dawley rats. Diabetes was induced by injection of streptozotocin and Cd was administered in drinking water at a concentration of 100 p.p.m. for 2.5 months. Cd did not affect the reduction in glomerular filtration rate or the rise in beta 2-microglobulinuria caused by diabetes. By contrast, the effect of diabetes on the urinary excretion of albumin, transferrin or IgG was greatly enhanced by concomitant exposure to Cd. This interaction occurred at Cd levels in the renal cortex which are very similar to those found in the general population of industrialized countries. These observations, in agreement with the results of a recent epidemiological study, suggest that Cd polluting the environment might potentiate the development of diabetic nephropathy.

Animals↗
PubMed1991

Does environmental exposure to cadmium represent a health risk? Conclusions from the Cadmibel study.

Cadmium is a very dispersive pollutant which has progressively accumulated in the environment mainly in the areas where nonferrous smelters have been in operation. An important toxicological feature of cadmium is its exceptionally long biological half-life in the human body. For the general population mainly exposed to cadmium by the diet and smoking, the kidney is the main target organ. Some studies have also suggested that cadmium might play a role in the pathogenesis of hypertension. A cross-sectional study (called Cadmibel) was undertaken to assess whether environmental pollution by cadmium in Belgium might represent a health risk. This paper does not present the detailed results of this study which are published elsewhere but simply report its main conclusions. A total number of 2327 subjects (stratified according to age and sex) was randomly sampled in two urban (Liège and Charleroi) and two rural (Hechtel-Eksel and Noorderkempen) areas, with different environmental pollution by cadmium. After allowing for the various factors known to influence cadmium accumulation, it was estimated that the cadmium body burden of the residents of the most polluted district (Noorderkempen) was 50 to 85% higher than in the less polluted areas. No statistical association was found between environmental exposure to cadmium and blood pressure elevation or the prevalence of cardiovascular diseases. However, the study has shown that the environmental exposure of the general population to cadmium may induce slight renal tubular dysfunction and may probably also affect cadmium homeostasis. The probability of tubular dysfunction (as assessed by sensitive tests) is about 10% when cadmium in urine reaches 2 micrograms/day. The morbidity associated with the changes in the renal proximal tubule and the calcium metabolism observed when the body burden of cadmium exceeds this value remains to be assessed.

Adult↗
PubMed1991

Effects of exposure to cadmium on calcium metabolism: a population study.

The objective was to investigate the hypothesis that environmental exposure to cadmium may affect calcium metabolism in the population at large. The 1987 participants (965 men and 1022 women), from 20 to 80 years old, constituted a random sample of the population of four Belgian districts. The urinary excretion of cadmium, a measure of lifetime exposure, averaged 9.3 nmol/24 h in men (range 0.4-324 nmol/24 h) and 7.1 nmol/24 h (range 0.1-71 nmol/24 h) in women. Serum alkaline phosphatase activity and the urinary excretion of calcium correlated significantly and positively with urinary cadmium excretion in both men and women, and serum total calcium concentration negatively with urinary cadmium excretion in men only. The regression coefficients obtained after adjustment for significant covariates indicated that when urinary cadmium excretion increased twofold, serum alkaline phosphatase activity and urinary calcium excretion rose by 3-4% and 0.25 mmol/24 h respectively, whereas in men serum total calcium concentration fell by 6 mumol/l. After adjustment for significant covariates the relation between serum total calcium concentration and urinary cadmium excretion was not significant in women. The findings suggest that even at environmental exposure levels calcium metabolism is gradually affected, as cadmium accumulates in the body. The morbidity associated with this phenomenon in industrialised countries remains presently unknown and requires further investigation.

Adult↗
PubMed1991

Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.

Unlike inorganic arsenic, inorganic trivalent antimony (Sb) is not methylated in vivo. It is excreted in the bile after conjugation with glutathione and also in urine. A significant proportion of that excreted in bile undergoes an enterohepatic circulation. In workers exposed to pentavalent Sb, the urinary Sb excretion is related to the intensity of exposure. It has been estimated that after eight hours exposure to 500 micrograms Sb/m3, the increase of urinary Sb concentration at the end of the shift amounts on average to 35 micrograms/g creatinine.

Adult↗
PubMed1991

Assessment of the filtration reserve capacity of the kidney in workers exposed to cadmium.

It has been assessed whether an internal dose of cadmium (Cd), as reflected by a Cd concentration in urine not yet sufficient to induce a significantly increased urinary excretion of various plasma proteins (microproteinuria defined as beta 2-microglobulin in urine greater than 300 micrograms/g creatinine, or retinol-binding protein in urine greater than 300 micrograms/g creatinine, or albumin in urine greater than 15 mg/g creatinine, or a combination of these), may affect the filtration reserve capacity of the kidney. The last was determined by measuring the difference between the baseline creatinine clearance and the maximal creatinine clearance after an acute oral load of protein (400 g of cooked red meat). In total 215 men were examined of whom eventually 87 Cd exposed workers (concentration of Cd in urine greater than 2 micrograms/g creatinine) from zinc/cadmium smelters and 92 control workers (concentration of Cd in urine less than 2 micrograms/g creatinine, absence of microproteinuria, normal fasting serum creatinine) were retained for data analysis performed separately for workers aged less or more than 50 years. Microproteinuria was present in 20 Cd workers, all older than 50. This study confirmed the previous observation that the age related decline of the baseline glomerular filtration rate (GFR) is accelerated in male workers with Cd induced microproteinuria; the same observation was made for the maximal GFR. It was found, however, that a renal Cd burden that had not yet caused microproteinuria did not impair the filtration reserve capacity of the kidney. This study therefore validates the previous estimate of the threshold effect concentration of Cd in urine (10 micrograms/g creatinine) that is intended to prevent the occurrence of microproteinuria in male Cd workers. It should be kept in mind, however, that because of the likely interference of the healthy worker effect, this conclusion may not be directly extrapolated to the general population.

Adult↗
PubMed1990

Renal effects of cadmium body burden of the general population.

In a cross-sectional population study to assess whether environmental exposure to cadmium is associated with renal dysfunction, 1699 subjects aged 20-80 years were studied as a random sample of four areas of Belgium with varying degrees of cadmium pollution. After standardisation for several possible confounding factors, five variables (urinary excretion of retinol-binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin, aminoacids, and calcium) were significantly associated with the urinary excretion of cadmium (as a marker of cadmium body burden), suggesting the presence of tubular dysfunction. There was a 10% probability of values of these variables being abnormal when cadmium excretion exceeded 2-4 micrograms/24 h. Excretion reached this threshold in 10% of non-smokers. There was also evidence that diabetic patients may be more susceptible to the toxic effect of cadmium on the renal proximal tubule.

Acetylglucosaminidase↗