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Tim S. Nawrot,^1,2,3 Etienne Van Hecke,⁴ Lutgarde Thijs,¹ Tom Richart,^1,5 Tatiana Kuznetsova,¹ Yu Jin,¹ Jaco Vangronsveld,³ Harry A. Roels,⁶ and Jan A. Staessen^1,5

¹Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, and ²School of Public Health, Department of Occupational and Environmental Medicine, University of Leuven, Leuven, Belgium; ³Department of Environmental Biology, University of Hasselt, Diepenbeek, Belgium; ⁴Social and Geography Section, Department of Earth and Environment Sciences, University of Leuven, Leuven, Belgium; ⁵Department of Epidemiology, Maastricht University, Maastricht, the Netherlands; ⁶Industrial Toxicology and Occupational Medicine Unit, Université catholique de Louvain, Brussels, Belgium

Abstract
Background: Few population studies have reported on the long-term changes in the internal cadmium dose and simultaneously occurring mortality.

Objective: We monitored blood cadmium (BCd) , 24-hr urinary cadmium (UCd) , and mortality in an environmentally exposed population.

Methods: Starting from 1985, we followed BCd (until 2003) , UCd (until 1996) , and mortality (until 2007) among 476 and 480 subjects, randomly recruited from low- exposure areas (LEA) and high-exposure areas (HEA) . The last cadmium-producing plant in the HEA closed in 2002.

Results: From 1985–1989 to 1991–1996, BCd decreased by 40.3% and 18.9% in the LEA and HEA, respectively (p < 0.0001 for between-area difference) . From 1991–1996 until 2001–2003, BCd remained unchanged in the HEA (+ 1.8%) and increased by 19.7% in the LEA (p < 0.0001) . Over the entire follow-up period, the annual decrease in BCd averaged 2.7% in the LEA (n = 258) and 1.8% in the HEA (n = 203) . From 1985–1989 to 1991–1996, UCd fell by 12.9% in the LEA and by 16.6% in the HEA (p = 0.22) , with mean annual decreases of 2.7% (n = 366) and 3.4% (n = 364) . Over 20.3 years (median) , 206 deaths (21.5%) occurred. At baseline, BCd (14.6 vs. 10.2 nmol/L) and UCd (14.1 vs. 8.6 nmol/24-hr) were higher in deaths than in survivors. The risks (p≤ 0.04) associated with a doubling of baseline UCd were 20% and 44% for total and noncardiovascular mortality, and 25% and 33% for a doubling of BCd.

Conclusions: Even if zinc–cadmium smelters close, historical environmental contamination remains a persistent source of exposure. Environmental exposure to cadmium increases total and noncardiovascular mortality in a continuous fashion without threshold.

Key words: cadmium, environmental exposure, mortality. Environ Health Perspect 116:1620–1628 (2008) .  doi:10.1289/ehp.11667 available via http://dx.doi.org/ [Online 24 July 2008]

Address correspondence to J.A. Staessen, Studies Coordinating Centre, Laboratory of Hypertension, University of Leuven, Campus Gasthuisberg, Herestraat 49, Box 702, B-3000 Leuven, Belgium. Telephone: 32-16-34-7104. Fax: 32-16-34-7106. E-mail: jan.staessen@med.kuleuven.be

This study would not have been possible without the voluntary collaboration of participants and their general practitioners. The municipality Hechtel-Eksel (Belgium) gave logistic support. We gratefully acknowledge the expert technical assistance of S. Covens, L. Custers, M.-J. Jehoul, H. Truyens, and Y. Zhu (Studies Coordinating Centre) . H. Vandenhoeck and J. Boon (Department of Earth and Environment Sciences, University of Leuven) did the cartography.

The International Lead Zinc Research Organization supported the study from 25 January 1990 until 24 February 1994. The Studies Coordinating Centre, Leuven, Belgium, received support from the European Union (grants IC15-CT98-0329-EPOGH, LSHM-CT-2006-037093 InGenious HyperCare, and HEALTH-F4-2007-201550 HyperGenes) ; the Fonds voor Wetenschappelijk Onderzoek Vlaanderen, Ministry of the Flemish Community, Brussels, Belgium (grants G.0424.03 and G.0575.06) ; and the Katholieke Universiteit Leuven, Belgium (grants OT/00/25 and OT/05/49) . J.A.S. financed measurement of the biomarkers of the internal dose for 2001–2003 from resources generated by work commissioned by pharmaceutical companies.

H.A.R. was a member of the scientific review panel (health) for the Voluntary Risk Assessment Report on Lead and Lead Compounds drafted by the International Lead Zinc Research Organization (Research Triangle Park, NC, USA) , the European Bio-Research Consultants (EBRC Consulting GmbH, Hannover, Germany) , and the Lead Development Association International (LDAint, London, UK) in the framework of the E.C. Chemical Bureau Existing Substances Programme. All other authors declare they have no conflicts of interest.

Received 6 May 2008 ; accepted 23 July 2008.