Cadmium exposure in tobacco workers: possible renal effects

Cadmium is a nephrotoxic metal widely used in industry and the main source of Cd in general population is smoking. Considering that the source of Cd in cigarettes is the tobacco leaf, the exposure to Cd was evaluated in workers employed at a tobacco leaf processing factory. Blood and urinary Cd levels were measured by flameless atomic absorption spectrometry in 87 workers and 35 controls. Urinary enzymes, total protein, albumin and uric acid were also determined to investigate the possible nephrotoxic effects of Cd. Blood Cd levels were significantly higher in workers (1.63 +/- 1.95 microg/L) than in controls (0.91 +/- 1.15 microg/L) (p = 0.044). The increase observed in urinary Cd levels of workers was non significant (0.56 +/- 0.5 microg/g creatinine in workers and 0.46 +/- 0.5 microg/g creatinine in controls). Both in workers and in controls, subjects smoking >10 cigarettes/day showed significantly increased blood Cd levels compared to non-smokers (p = 0.000 and p = 0.011, respectively). In workers, urinary alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total protein, and uric acid were observed to be significantly increased (p = 0.013, p = 0.000, p = 0.000, p = 0.025, respectively), ALP, GGT and total protein being positively correlated with Cd in urine. In conclusion, the workers in the tobacco leaf processing factory were found to be exposed to Cd compared to the general population. The increase in the urinary enzymes and proteins suggests that an exposure to Cd affects kidney functions even below the toxic limits generally accepted.