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. 2008 Dec;116(12):1620-8.
doi: 10.1289/ehp.11667. Epub 2008 Jul 24.

Cadmium-related mortality and long-term secular trends in the cadmium body burden of an environmentally exposed population

Tim S Nawrot  1 , Etienne Van Hecke, Lutgarde Thijs, Tom Richart, Tatiana Kuznetsova, Yu Jin, Jaco Vangronsveld, Harry A Roels, Jan A Staessen
Affiliations

Cadmium-related mortality and long-term secular trends in the cadmium body burden of an environmentally exposed population

Tim S Nawrot et al. Environ Health Perspect. 2008 Dec.

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 < or = 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.

Keywords: cadmium; environmental exposure; mortality.

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Figures

Figure 1
Figure 1
Geographic representation of UCd at baseline (1985–1989) and spatial analysis of mortality up to 30 September 2007, in participants 50–69 years of age at enrollment. Dots represent the homes of the deceased participants. The diameters in the lower left diagram represent the number of participants per area.
Figure 2
Figure 2
Flow chart of the Flemish cohort from 1985–1989 until 2007. FU, follow-up.
Figure 3
Figure 3
BCd (A) and UCd (B) in the cohort analysis. The horizontal bar (deaths) indicates the geometric mean (solid line) with 95% CI (dashed lines) of the internal dose in subjects who died before 30 September 2007 (significance of the difference with survivors, p < 0.0001). *Significant difference between consecutive measurements.
Figure 4
Figure 4
Ten-year risk of death in relation to the BCd (A and C) and UCd (B and D) at baseline with standardization to the distribution (mean or ratio) of sex, age, body mass index, smoking, γ-glutamyltransferase as index of alcohol intake, and SES: risk function for the 5th, 25th, 50th, 75th, and 95th percentiles of the 24-hr urinary excretion of RBP (A and B) and the SCrt (C and D). p-Values are for the independent effects of cadmium (pCd), urinary RBP (pRBP), and serum creatinine (pSCrt). The range of the internal cadmium dose plotted along the horizontal axes corresponds with the 1st to 99th percentile of BCd and UCd.
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