Lead inhibits growth and induces apoptosis in normal rat fibroblasts.

The effects on normal rat fibroblasts of lead supplementation (as lead acetate) in the medium were examined. The amount of lead acetate ranged from 0.078 microM to 320 microM, at 14 concentrations. The normal level of lead in the medium was 0.060 microM, and the normal concentration of lead in the fibroblasts was 3.1 +/- 0.1 ng/10(7) cells: these represented the control conditions. On studying fibroblast proliferation and survival after incubation for 48 hours, a lead acetate dose-dependent inhibition of cell proliferation was observed, the results being shown to be significant by ANOVA (p < 0.01), and suggesting a significant dose-response relationship. Apoptosis, evaluated by quantifying cytoplasmic DNA fragments, differs significantly between the lead levels tested. The distribution in the cell cycle, evaluated by using a fluorescence-activated cell sorter, showed a dose-dependent accumulation of cells in the G0/G1 phase, with a compensatory decrease in the percentage of cells in the S phase. Moreover, the occurrence of a subdiploid peak confirmed that apoptosis was more evident when the medium was supplemented with lead acetate at concentrations of 5-20 microM. The inhibition of cell growth is probably due to a direct inhibition of cell proliferation.

Occupational exposure to lead--granulometric distribution of airborne lead in relation to risk assessment.

The amount of airborne lead absorbed by the body during occupational exposure depends not only on lead concentration in workplace air, but also on the granulometric distribution of the aerosol. The Occupational Safety and Health Administration (OSHA) set the lead Permissible Exposure Limit (PEL) at 50 micrograms/m3 on the basis of Bernard's model and a number of assumptions, including assumption "C", which predicts that the first 12.5 micrograms/m3 are made up of fine particles (aerodynamic diameter < 1 micron) whereas the remaining 12.5 micrograms/m3 consist of particles > 1 micron. Occupational exposure to airborne lead at a concentration of 50 micrograms/m3 and a granulometric distribution calculated according to the above mentioned assumption, leads, in the model, to a mean blood level of 40 micrograms/dl. In the present study, we tested the validity of assumption "C" in the environmental air of a factory that manufactured crystal glassware containing 24% lead oxide. An 8-stage impactor was used to measure the particle size of airborne dust collected from personal and area samplings. Results indicate that, on the whole, assumption "C" cannot be considered valid in the work environment investigated in this study. As a result, lead absorption levels in exposed workers may be noticeably different from those predicted by the OSHA model. We therefore suggest that in order to make a correct evaluation of the risk of occupational exposure to lead, it is essential to integrate total airborne lead concentration with a measurement of the granulometric distribution of the aerosol.

Blood lead concentration and biological effects in workers exposed to very low lead levels.

A longitudinal study was carried out on two groups of workers engaged in tin/lead alloy welding in the telecommunication sector. The risk of exposure was evaluated by measuring levels of airborne lead (PbA) and the amount of lead absorbed (PbB). The-correlated effects were assessed by determining zinc protoporphyrin (ZPP) and hemoglobin levels (Hb) and red blood cell (RBC) count. We also recorded subjective symptoms reported by workers. One group of welders composed of 365 subjects underwent two monitoring sessions performed in 1991 and 1995, respectively (Group A). A second group of welders (whose number fluctuated between 148 and 247 subjects) underwent yearly testing for 7 consecutive years (1988-1994; Group B). Results indicated a very low risk of lead exposure during microwelding operations (PbA range, 1.5-24 micrograms/m3). In fact, blood concentrations of Pb (range, 5-55, micrograms/dL) among both groups of welders were significantly higher than those in the general population in Rome (PbB range, 5-16 micrograms/dL); nevertheless, they were significantly lower than the Occupational Safety and Health Administration's permissible exposure limits ZPP determined only in Group B of welders ranged from 5 to 16 micrograms/dL (median, 22 micrograms/dL). No variation was found in the other biological parameters investigated, and no health effects were observed. During the study period, the introduction of some technological innovations led to a further reduction in Pb exposure and, subsequently, to its total elimination. PbB concentrations gradually declined to lower values (6-36 micrograms/dL), and it was interesting to note that ZPP concentrations also decreased to normal levels (range, 2-47 micrograms/dL; median, 11 micrograms/dL), demonstrating that the effect of lead on heme synthesis may occur even at very low levels of Pb exposure.

Occupational exposure to chromium--an assessment of environmental pollution levels and biological monitoring of exposed workers.

In an aircraft construction factory where adhesives containing Cr(VI) compounds were used, the risk of chromium exposure was studied by assessing airborne chromium levels and urinary levels of chromium excretion. Chromium exposure was evaluated by personal sampling over a period of 4 hr in a group of 16 occupational workers selected from a group of 55. Chromium absorption was determined by collecting urine samples from all subjects (n = 55) at 3 different times: prior to the work-shift at the beginning of the working week and prior to and after the workshift at the end of the working week. Each urine sample was tested for chromium and creatinine concentration. Results showed very low exposure to airborne chromium, since values obtained (0.02-1.5 micrograms/m3, GM: 0.17, GSD: 5.34 micrograms/m3) were significantly lower than the ACGIH Hygiene Standard (50 micrograms/m3). Likewise, urinary chromium excretion (0.16-7.74 micrograms/g creat.) was higher than excretion in the general population (0.07-0.17 microgram/g creat.) but lower than BEI-ACGIH (30 micrograms/g creat.). The greatest difference between excretion levels measured before and after the workshift was 2.44 micrograms/g creat, i.e. 4 times lower than the difference proposed by ACGIH (10 micrograms/g creat.).

Vanadate as factor of cardiovascular regulation by interactions with the catecholamine and nitric oxide systems.

The effects of 1 microgram/mL of vanadium, given for 12 mo as sodium metavanadate in drinking water, on cardiovascular and biochemical indices of male rabbits were investigated. At the end of the exposure period, vanadium was more accumulated in bones and kidneys than in spleen and liver; the cardiac ventricles and the aorta contained similar amounts of this element. Blood pressure and heart rate were unchanged in the vanadate-exposed animals since the observed decrease of both cardiac inotropism and stroke volume was counteracted by an increase of peripheral vascular resistance, with reduction of arterial blood flow. The arterial levels of sodium, potassium and aldosterone were unmodified by vanadate which, however, strongly raised those of noradrenaline, adrenaline, L-DOPA, and dopamine. Vanadate caused a marked increase of the activity of monoamine oxidase in renal tubules and liver (probably in relation to the increased plasma catecholamine levels) and a reduction of that of glucose-6-phosphate dehydrogenase in the kidney. There was also evidence that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. It was concluded that vanadium may represent an environmental factor of altered cardiovascular homeostasis.