Objectives Cadmium (Cd) toxicity of the kidney varies between individuals despite similar exposure levels. In humans Cd is mainly bound to metallothioneins (MT), which scavenge its toxic effects. Here we analysed whether polymorphisms in MT genes MT2A influence Cd-related kidney damage.

Methods In a cross-sectional study N = 566 volunteers were selected from three areas in South-Eastern China, which to varying degree were Cd-polluted from a smelter (control area [median Cd in blood B-Cd = 1.38 μg/L], moderately [B-Cd = 4 μg/L] and highly [B-Cd = 9.5 μg/L] polluted areas). (control area [median Cd in urine U-Cd = 2.01 μg/g Cr], moderately [U-Cd = 4.17 μg/g Cr] and highly [U-Cd = 11.39 μg/g Cr] polluted areas). B-Cd, U-Cd concentrations were measured by graphite-furnace atomic absorption spectrometry. Polymorphisms in MT2A (rs10636 G/C, rs1610216 C/T and rs28366003 A/G) were determined by Taqman assays. Urinary N-Acetyl-beta-(D)-Glucosaminidase (UNAG) was determined by spectrometry, urinary β2-microglobulin (UB2M) and albumin (UALB) by ELISA.

Results BCd and UCd had an association with variant alleles for MT2A (rs10636) in female living in the highly polluted group (p = 0.017 and 0.004, respectively). UCd had a weak association with variant alleles for MT2A (rs28366003) in the highly polluted group (p = 0.08,). An association wasn’t found between renal dysfunction and MT2A polymorphisms variation in polluted group.

Conclusions The finding indicates genetic variation in the MT2A genes may not associate with renal dysfunction caused by cadmium exposure.