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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.

Cytogenetic observations have been performed on male subjects occupationally exposed to elemental mercury in a plant where mercury is amalgamated with zinc and in a chloralkali plant [n = 22; average level of mercury in urine was 117 micrograms/g creatinine and of mercury in blood 3.1 micrograms/100 ml; mean duration of Hg exposure 4 years (range: 0.3-15.3)]. The exposure to mercury vapour did not result in an increased yield of structural chromosomal aberrations in peripheral blood lymphocytes of the workers. These negative results are in agreement with the findings reported for other eukaryotic systems and confirm that population monitoring based on cytogenetic examination of peripheral blood lymphocytes does not always represent a good indicator of damage to genetic material produced by a chemical.

Renal function and psychomotor performance (eye-hand coordination, arm-hand steadiness) of a group of 43 workers exposed to mercury vapor were examined. Their mean age an average duration of exposure to mercury were 38 and 5 years, respectively. The results were compared with those in a matched group of 47 control workers. Increased proteinuria and albuminuria were found slightly more prevalent in the Hg-exposed group than in the control workers. These results are in agreement with those found during a previous study carrier out in another group of workers also exposed to elemental mercury (Buchet et al. 1980). The scores of the psychomotor tests were less satisfactory in the Hg workers than in the control workers, the arm-hand steadiness test being more discriminative than the eye-hand coordination test. Preclinical changes in psychomotor function can be detected independently of the presence of signs of renal dysfunction. No clear-cut relationships were found between the prevalence of abnormal psychomotor scores and the level of mercury in blood (HgB) or in urine (HgU). Increased prevalences of abnormal psychomotor scores seem however to occur for HgB between 1 and 2 micrograms/100 and for HgU between 50 and 100 micrograms/g creatinine. Therefore, a biologic threshold limit value of 50 micrograms/g creatinine in proposed for urinary mercury to prevent the development of preclinical effects on the central nervous system. A similar critical HgU level based on renal dysfunction prevalences has been suggested in a previous study.

The urinary elimination of the metabolites of arsenic has been followed up as a function of time in volunteers who ingested a single oral dose of arsenic (500 microgram As) either as sodium arsenite (Asi), monomethylarsonate (MMA), or cacodylate (DMA). The excretion rate increased in the order Asi less than DMA less than MMA. After 4 days, the amount of arsenic excreted in urine represents 46, 78, and 75% of the ingested dose in the case of Asi, MMA and DMA, respectively. With regard to the in vivo biotransformations, it is concluded that DMA is excreted unchanged; MMA is slightly (13%) methylated into DMA while roughly 75% of the arsenic excreted after ingestion of Asi is methylated arsenic (about 1/3 as MMA and about 2/3 as DMA).

Cadmium in blood (Cd-B) and in urine (Cd-U) and metallothionein (Mt-U) and beta 2-microglobulin in urine (beta 2m-U) were measured in 94 male Cd workers. The results were examined according to the workers' current exposure to cadmium (group C, n = 73, workers currently exposed to Cd; group R, n = 21, Cd workers removed from exposure or retired) and according to their renal status (group N, n = 66, normal beta 2m-U; group I, n = 28, beta 2m-U greater than 200 micrograms/g creatinine). The interrelationships between Mt-U, Cd-U, Cd-B and years of cadmium exposure were examined in the various subgroups. The study of the correlations between these variables demonstrates that Mt-U is directly correlated with Cd-U but not with Cd-B or years of Cd exposure. The association between Cd-U and Mt-U is independent of the status of renal function and the intensity of current exposure to cadmium. Under moderate chronic exposure to cadmium, the fraction of Cd-U which is directly influenced by recent exposure (Cd-B) is small in comparison with that influenced by the cadmium body burden.