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Tobias Alfvén,¹ Lars Järup,^1,2 and Carl-Gustaf Elinder³

¹Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; ²Department of Epidemiology and Public Health, Imperial College School of Medicine, London, United Kingdom; ³Department of Renal Medicine, Huddinge University Hospital, and Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden

Abstract

Long-term exposure to cadmium may cause kidney and bone damage. Urinary cadmium is commonly used as the dose estimate for the body burden of cadmium. However, elevated levels of cadmium in the urine may reflect not only high levels of cadmium dose but also renal dysfunction. In this study we used blood cadmium as the dose estimate. In addition, we analyzed blood lead. We examined 479 men and 542 women, ages 16-81 years, who were environmentally or occupationally exposed to cadmium and lead. We used urinary protein 1-microglobulin as a marker for tubular proteinuria and measured forearm bone mineral density using dual-energy X-ray absorptiometry. The relationship between blood cadmium and tubular proteinuria was strong, even when we excluded occupationally exposed participants. The subgroup with the highest blood cadmium levels had a 4-fold risk of tubular proteinuria compared to the subgroup with the lowest blood cadmium levels. In the older age group (age > 60) , the risk of low bone mineral density (z-score < -1) for the subgroup with the highest blood cadmium levels was almost 3-fold compared to the group with lowest blood cadmium levels. We found no similar associations for lead. The observed effects may be caused by higher cadmium exposure in the past. This study strengthens previous evidence that cadmium exposure may affect both bone mineral density and kidney function. Key words: bone density, cadmium, environmental exposure, heavy metals, lead, occupational exposure, osteoporosis, proteinuria. Environ Health Perspect 110:699-702 (2002) . [Online 3 June 2002]

http://ehpnet1.niehs.nih.gov/docs/2002/110p699-702alfven/ abstract.html

Address correspondence to T. Alfvén, Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE-171 77 Stockholm, Sweden. Telephone: +46-8-728-75-08. Fax: +46-8-30-45-71. E-mail: tobias.alfven@student.ki.se

We thank all the participants in the study and the other team members in project OSCAR: D. Carlsson, L. Hellström, B. Persson, C. Pettersson, and G. Spång. We also thank A. Grubb, Department of Clinical Chemistry in Lund, who analyzed the protein HC ; the late A. Schütz, Department of Occupational and Environmental Medicine in Lund, who analyzed the cadmium and lead ; A-C. Palmqvist and A-K. Thunberg, who collected the data ; and M. Blomberg for entering data into computer files.

The study was supported by a grant from the Swedish Environmental Protection Agency.

Received 20 September 2001 ; accepted 15 January 2002.

Tables 2 and 3 were corrected on 7 August 2002.