Scintigraphic assessment of renal function in steel plant workers occupationally exposed to lead.

Objectives: Occupational exposure to lead may produce kidney damage, but existing data on the dose range associated with nephrotoxicity are inconclusive. We here assessed renal function under conditions of low to moderate lead exposure using renal scintigraphy.

Methods: Fifty-three male foundrymen (exposed group) and fourty male office workers (control group) from a steel plant were included in the study.

Oxidative DNA damage and oxidative stress in subjects occupationally exposed to nitrous oxide (N(2)O).

Objectives: Occupational exposure to nitrous oxide (N(2)O) and/or halogenated hydrocarbons has been suggested to induce damage of genetic material, but the underlying mechanisms remain obscure. This study investigated the role of oxidative processes in the genotoxicity associated with exposure to waste anaesthetic gases.

Methods: The study was performed in 36 female nurses and in 36 unexposed female health care workers matched for age and employment duration.

DNA damage induced by nitrous oxide: study in medical personnel of operating rooms.

Occupational exposure to anaesthetics such as nitrous oxide (N(2)O) and halogenated hydrocarbons has been suggested to increase risk of genetic damage. However, the dose-dependency of genotoxic effects has not been unequivocally established and their relation to occupational exposure limit (OEL) remain obscure. In this study, the genotoxicity associated with occupational exposure to anaesthetics has been investigated in a group of 55 female nurses and 29 male anaesthesiologists active for at least 5 years in a working environment containing variable concentrations of N(2)O and halogenated hydrocarbons.

Impaired vitamin B12 metabolic status in healthcare workers occupationally exposed to nitrous oxide.

Background: Previous studies demonstrated inactivation of vitamin B12 by nitrous oxide (N(2)O). The intraoperative exposure to N(2)O was shown to induce megaloblastic anaemia and myelopathy in subjects with subclinical vitamin B12 deficiency. In contrast, no data concerning the influence of occupational exposure to N(2)O on vitamin B12 metabolic status are available to date.

Evidence for oxidative stress at elevated plasma thiol levels in chronic exposure to carbon disulfide (CS2) and coronary heart disease.

Objectives: Oxidative stress in plasma may be promoted by plasma thiols such as homocysteine. However, other thiols such as glutathione may also exert antioxidant effects in vitro and in vivo. To further investigate whether plasma thiols act as prooxidants or antioxidants, we compared plasma oxidative status in patients with coronary heart disease (CHD) and in subjects occupationally exposed to carbon disulfide (CS(2)).

Occupational exposure to nitrous oxide - the role of scavenging and ventilation systems in reducing the exposure level in operating rooms.

Objectives: The aim of this study was to assess the level of occupational exposure to nitrous oxide (N(2)O) in operating rooms (ORs), as related to different ventilation and scavenging systems used to remove waste anaesthetic gases from the work environment.

Methods: The monitoring of N(2)O in the air covered 35 ORs in 10 hospitals equipped with different systems for ventilation and anaesthetic scavenging. The examined systems included: natural ventilation with supplementary fresh air provided by a pressure ventilation system (up to 6 air changes/h); pressure and exhaust ventilation systems equipped with ventilation units supplying fresh air to and discharging contaminated air outside the working area (more than 10 air changes/h); complete air-conditioning system with laminar air flow (more than 15 air changes/h).

Increased incidence of micronuclei assessed with the micronucleus assay and the fluorescence in situ hybridization (FISH) technique in peripheral blood lymphocytes of nurses exposed to nitrous oxide.

It has been postulated that exposure to nitrous oxide and halogenated anaesthetics is associated with various adverse health effects such as neurological and reproductive abnormalities or impairment of hepatic functions. In spite of the quite well known genotoxic effects of exposure to nitrous oxide in vivo, the mechanisms of these effects are still not clear. The aim of this study was to assess the frequency of micronuclei and to identify the type of chromosomal damage (clastogenic or aneugenic) in peripheral blood lymphocytes of operating-room nurses exposed to nitrous oxide.

Combined exposure to m-xylene and ethanol: oxidative stress in the rat liver.

Objectives: Ethanol may be a significant combined factor in human solvent toxicity. Lipid peroxidation has been suggested to be an important contributing mechanism involved in experimental alcohol-induced liver injury. The aim of the study was to investigate whether a short-term ethanol ingestion in rats chronically exposed to m-xylene vapor may influence the lipid peroxidation rate in the intracellular hepatic membranes, the level of glutathione and the activity of glutathione-related enzymes in the liver.

Increased oxidative stress in subjects exposed to carbon disulfide (CS2)--an occupational coronary risk factor.

There is considerable epidemiological evidence that workers exposed to carbon disulfide (CS2) develop premature atherosclerosis leading to increased rates of coronary heart disease (CHD), but mechanisms underlying this association remain obscure. The present study documents that occupational exposure to CS2 modifies the oxidative status of plasma, which is a major determinant of the susceptibility to atherosclerosis. Concentrations of thiobarbituric reactive substances (TBARS), which reflect lipid peroxidation processes in plasma, were determined in 29 men who were exposed to CS2 for more than 20 years, in 24 patients with peripheral atherosclerosis, and in 30 unexposed, healthy control subjects.

Updating of hygiene standards for carbon disulfide based on health risk assessment.

In 1995 the hygiene occupational standard values of carbon disulfide (CS2) were established in Poland: the maximum allowable concentration, eight-hour time weighted average (MAC-TWA)--18 mg/m3, and the short time exposure level (STEL)--30 mg/m3. For lack of reliable retrospective data on the CS2 exposure levels in the work environment and the dose-response relationship, the following have been taken into account in establishing these values: the nervous and vascular systems are recognized as the main CS2 exposure targets; long-term exposure to CS2 in the work environment, exceeding 30 mg/m3, induces the toxic effect in the nervous and cardiovascular systems; chronic exposure to CS2 at concentration below 20 mg/m3 does not produce adverse effects in the peripheral nervous and vascular systems; coronary heart disease does not occur more frequently in workers exposed to CS2. Aiming at updating the 1995 MAC value for CS2 the authors carried out an analysis of the recent literature data on the relation between exposure levels and health risk.

Genotoxicity of industrial dyes under the inductive effect of ethanol on monooxygenase system in mice.

The genotoxic effects of triarylmethane (Acid Green 16, C.I.44025) and arylmonoazo (Basic Orange 28, developed by Boruta Pigment Plant, Poland, C.

Carbon disulfide-induced modification and cytotoxicity of low-density lipoproteins.

The secondary oxidation of biologically modified low-density lipoproteins (LDL) was demonstrated to contribute to the cytotoxicity and thereby to the atherogenicity of modified lipoproteins. Previously we have shown that chemical modification of LDL by carbon disulfide (CS(2)) mimicked the naturally occurring process of LDL modification. In the present study the cytotoxicity of CS(2)-modified LDL and their susceptibility to the secondary oxidative modification was investigated.

Cytochrome P-450 mediated genotoxicity of triarylmethane dye in mice fed ethanol liquid diet.

Genotoxic effect of synthetic triarylmethane dye (Acid Green 16) was evaluated in Balb C mice fed nutritionally adequate liquid diet (1 kcal/ml) or isocaloric alcoholic diet containing 5% (w/v) ethanol (36% of total calories) for 6 days. Dye compound was given intraperitoneally at dose 150 mg/kg body wt. 30 h before test.

Biological markers of oxidative stress induced by ethanol and iron overload in rat.

Studies on rats treated for 15 months with ethanol (10%, w/v, solution in drinking water) revealed that the stimulation of hepatic cytochrome P-450 monooxygenases activity was accompanied by enhanced microsomal malondialdehyde formation, a lipid peroxidation index and a decreased level of the antioxidant, alpha-tocopherol. The other components of the prooxidant/antioxidant system, diene conjugates and catalase, glutathione peroxidase and superoxide dismutase activities were unaffected. Oxidative stress in blood was shown by a significant decrease in the alpha-tocopherol level whereas lipid peroxidation and antioxidant enzyme activity remained unchanged.

Urinary excretion of copper bound to low molecular weight proteins in the population exposed to cadmium in community and occupational environments.

People living in Cd-polluted areas excrete increased amounts of copper with urine. A substantial quantity of this is eliminated with metallothionein the concentration of which in urine increases in people exposed to cadmium. Therefore, the measurement of metallothionein in urine is applied as a marker of renal function in people exposed to cadmium in addition to other low molecular weight proteins, beta 2-microglobulins (beta 2MG) and retinol binding proteins (RBP).

[Nephrotoxic action of cadmium].

Functional state of kidney in persons exposed to cadmium (Cd) is estimated mostly by determination of low molecular proteins in urine (beta 2MG, RBP) they are sensitive but not specific indicators of Cd exposure effects. The usefulness of a new indicator of renal functional disorders which is similar to metallothionein was studied. The test involved the determination of the urinary excretion of cadmium bound to low molecular specific protein.

Metabolic disposal of antipyrine and lipid peroxidation indices in volunteers jointly exposed to industrial organic solvents and ethanol.

Each of twelve volunteers, at 2 week intervals, received 1 g of antipyrine, a test drug, and were exposed for 4 h either to toluene (375 mg/m3) or xylene (435 mg/m3) singly or in combination with ethanol (0.45 g/kg body wt. before the onset of exposure and 0.

Genotoxic effect of triarylmethane dye--acid green 16 after chronic ethanol consumption in mice.

Genotoxic effect and hepatic microsomal monooxygenase activities were assessed in mice treated with Acid Green 16 (single i.p. injection at dose 75 mg/kg) superimposed on prolonged ethanol consumption (10% solution in drinking water for 2-4 months).

Interaction of ethanol and xylene in their effects on erythrocytes and other haematological parameters in the rat.

Rats were given ethanol in drinking water for 8 months, followed by inhalation exposure (5 h daily) to 12,000 mg m-3 xylene for 9 days. Combined exposure to xylene and ethanol induced the same changes in the haematological, biochemical and biophysical parameters of the erythrocyte membrane as those found previously in our experiment with toluene-ethanol. Macrocytosis, a decrease in sedimentation rate and erythrocyte packing difference, as well as decreased fluidity of the erythrocytes membrane in the middle zone of the lipid bilayer, were the most significant changes of exposure to ethanol and xylene.

[Stimulation of microsomal lipid peroxidation as the effect of combined action of xylene and ethanol].

The aim of the study was to evaluate if in the case of combined exposure of rats to xylene and ethanol stimulation of lipid peroxidation in the liver microsomes (an index of interaction with lipids and derangements of integrity/fluidity of membranes) might occur. Experiments were carried out on male Wistar rats in the conditions of prolonged, inhalatory preexposure to m-xylene at concentration of 4000 mg/m3 for 6 and 12 weeks, and next joint 5-fold treatment with ethanol (2.5 g/kg oral doses in 12 hours intervals for 3 days).

[Induction of cytochrome P-450 monooxygenase after combined exposure of rats to xylene and ethanol].

Increased biological risk following from combined exposure to xylene, an industrial solvent, and ethanol, the most likely additional factor to occupational exposure, may result from inductive effects of the chemicals on cyt. P-450 monooxygenase, where biotransformation of xylene and, in part of ethanol, takes place. Studies were carried out on rats: 1) preinduced with ethanol (10% solution in drinking water for 8 months) and for next 9 days jointly exposed to xylene vapour at concentration of 12,000 mg/m3; 2) preexposed to m-xylene vapours at concentration of 4,000 mg/m3 for 6 and 12 weeks or at concentration of 400 mg/m3 for 5 months and for next 3 days jointly administered ethanol (5 doses of 2.

The effect of combined exposures to ethanol and xylene on rat hepatic microsomal monooxygenase activities.

Studies on rats treated for 8 months with ethanol (10% solution in drinking water) and simultaneously exposed to xylene vapour (12,000 mg/m3, 5 hr daily) for the last 9 days revealed that the chemicals exert additive stimulatory effect on hepatic microsomal monooxygenase: the activity of aniline p-hydroxylase increased by 380%, microsomal ethanol oxidizing system by 92%, NADPH-cyt. c reductase by 30% and the level of cytochrome P-450 by 70%. The changes were accompanied by a marked proliferation of smooth endoplasmic reticulum (a subcellular site of cytochrome P-450 monooxygenases in the hepatocytes) and an increased NADPH-Fe2+- and ascorbate-Fe2+-driven lipid peroxidation in microsomal membranes--a potential toxic mechanism.

Studies on the effect of ethanol and/or toluene on rat erythrocytes.

Rats were subjected to a chronic ethanol exposure in their drinking water for 8 months and then a short subacute toluene exposure to 12,000 mg/m3 for 5 h/day for nine days. Combined exposure increased the reticulocyte count and the concentration of haemoglobin, and changed the biochemical/biophysical properties of red blood cells. Macrocytosis and a decrease in erythrocyte membrane lipid fluidity in the middle zone of the lipid bilayer were the most useful indices of exposure.

Silica earth provoked lung fibrosis with stimulation of lysosomal enzymes and lipid peroxidation in rats.

The dynamics of the biological response of pulmonary tissue to silica dust (silica earth from Piotrowice, Poland, recommended as a domestic reference fibrogenic standard) was studied in rats after single-shot intratracheal instillation of a suspension of 20 mg of the dust for one, three, and seven months. Silica dust provoked pronounced pulmonary fibrosis as inferred from increased collagen content together with pathomorphological alteration (silicotic nodules). The lung burden of silica dust affected the lysosomal subfraction as manifested by an increase in its protein content with concomitant stimulation (release and presumably induction) of beta-glucuronidase and cathepsin D and a transient (up to three months) stimulation of lipid peroxidation.