The cadmium concentration in liver (CdL) and in kidney is measured in vivo by neutron capture γ-ray analysis in 309 male workers occupied in two Belgian zinc-cadmium plants. At the same time, blood cadmium (CdB) and the urinary excretion of β2-microglobulin, albumin, total protein, calcium, and cadmium (CdU) is also determined. Among the 264 subjects retained for the statistical analysis 236 are still active at the plants (group A) while 28 others are retired Cd workers or workers removed from Cd exposure (group R). Group A comprises 149 subjects with normal renal function who are engaged in jobs not directly related to Cd production (subgroup Ala) and 87 Cd workers daily occupied with Cd production of whom 72 subjects (subgroup Alb) have not and 15 (subgroup A2) have sign(s) of renal dysfunction. Group R is subdivided into subgroups R1 (n = 10) and R2 (n = 18), subjects without and with renal dysfunction, respectively. Examination of the cumulative frequency distributions and the correlations between the various biological parameters in the different subgroups leads to the following conclusions: (a) calciuria is not much different among the subgroups, (b) CdB mainly reflects recent exposure to cadmium in the absence of Cd-induced renal damage, (c) CdU follows the body burden of cadmium but increases proportionately much more in workers with renal dysfunction particularly when signs of tubular dysfunction are present, (d) CdL is proportional to duration and intensity of Cd exposure in workers without as well as with renal dysfunction, (e) renal cortical cadmium (CdKc) is higher in subgroup Alb and Rl than in subgroup Ala but does not differ between Cd workers without (subgroup Alb) and with (subgroups A2 and R2) renal dysfunction. The latter finding can be explained by a progressive decrease of CdKc after the onset of the renal damage. This hypothesis is supported by the observations that in Cd workers from subgroup R2. CdKc negatively correlates with years of past exposure to Cd (r = −0.59), that Cd workers with renal dysfunction (subgroups A2 and R2) excrete significantly more cadmium in urine, and that they show a much lower slope of CdKc versus CdL than those with normal renal function (subgroup Alb). The results of this investigation suggest that there exists a range of critical CdKc levels, i.e., approximately from 160 to 285 ppm. Beyond a CdKc of 285 ppm the probability is very high that all persons will show sign(s) of renal dysfunction. It has been found that kidney dysfunction is likely to develop in workers with CdL between 30 and 60 ppm and that almost all the Cd workers with CdL above 60 ppm evidence renal dysfunction. This study also demonstrates that in the absence of kidney dysfunction. CdU is correlated with the body burden of cadmium (r = 0.59), but that CdB is not. On the basis of the interrelationships among CdL, CdKc, CdU, and the indicators of renal function, it can be concluded that the probability of developing Cd-induced renal dysfunction in male Cd workers appears to be very low when the critical CdU level of 10 μg/g creatinine is not regularly exceeded. This CdU level corresponds to an average cadmium body burden of 160–170 mg.