Early Kidney Damage in a Population Exposed to Cadmium and Other Heavy Metals

Background Exposure to heavy metals may cause kidney damage. The population living near the Avonmouth zinc smelter has been exposed to cadmium and other heavy metals for many decades. Objectives We aimed to assess Cd body burden and early signs of kidney damage in the Avonmouth population. Methods We used dispersion modeling to assess exposure to Cd. We analyzed urine samples from the local population (n = 180) for Cd (U-Cd) to assess dose (body burden) and for three biomarkers of early kidney damage [N-acetyl-β-d-glucosaminidase (U-NAG), retinol-binding protein, and α-1-microglobulin]. We collected information on occupation, intake of homegrown vegetables, smoking, and medical history by questionnaire. Results Median U-Cd concentrations were 0.22 nmol/mmol creatinine (nonsmoking 0.18/smoking 0.40) and 0.34 nmol/mmol creatinine (nonsmoking 0.31/smoking 0.46) in non-occupationally exposed men and women, respectively. There was a significant dose–response relationship between U-Cd and the prevalence of early renal damage—defined as U-NAG > 0.22 IU/mmol—with odds ratios of 2.64 [95% confidence interval (95% CI), 0.70–9.97] and 3.64 (95% CI, 0.98–13.5) for U-Cd levels of 0.3 to < 0.5 and levels ≥ 0.5 nmol/mmol creatinine, respectively (p for trend = 0.045). Conclusion U-Cd concentrations were close to levels where kidney and bone effects have been found in other populations. The dose–response relationship between U-Cd levels and prevalence of U-NAG above the reference value support the need for measures to reduce environmental Cd exposure.