Except for those who live near cadmium-emitting industries,
inhalation of cadmium in the ambient air may occur but is not a
major source of exposure. Smokers and people living in contaminated
areas have higher urinary cadmium concentrations, with
smokers having about twice as high concentrations as nonsmokers
[35]. Blood cadmium tends to reflect recent exposures and urinary
cadmium reflects cumulative cadmium exposure and body burden
(particularly, kidney cadmium levels). Sensitive areas are the kidney
and bone following oral exposure, and the kidney and lung
following inhalation exposure. Effects that have been observed in
humans and/or animals include reproductive toxicity, hepatic effects,
hematological effects, and immunological effects. Although
acute pulmonary effects and deaths are uncommon, sporadic cases
still occur [36]. Because the toxicity of cadmium is dependent on its
concentration in the kidney, adverse effects in humans are typically
not observed after shorter durations. Drawing inferences from the
present results, the mean cadmium (Cd) urine concentration of
50 mg/L detected in urine samples from paint factory workers was
eight times (and significantly) higher than that found in nonfactory
workers (6 mg/L). Cadmium excretion in urine of occupationally
exposed workers increases proportionally with body burden of
cadmium, but the amount of cadmium excreted represents only a
small fraction of the total body burden unless renal damage is
present; in this case, urinary cadmium excretion markedly increases
[37]. It has been suggested that the tubular damage is
reversible [38], but there is overwhelming evidence that the cadmium-
induced tubular damage is indeed irreversible [35]. Baring
cases of renal damage, our results suggest that workers in paint
factories have on average six times the cadmium body burden of
the general population.