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.