Cadmium-induced bone effect is not mediated via low serum 1,25-dihydroxy vitamin D

Cadmium is a widespread environmental pollutant, which is associated with increased risk of osteoporosis. It has been proposed that cadmium's toxic effect on bone is exerted via impaired activation of vitamin D, secondary to the kidney effects. To test this, we assessed the association of cadmium-induced bone and kidney effects with serum 1,25-dihydroxyvitamin D (1,25(OH) 2D); measured by enzyme immunoassay. For the assessment, we selected 85 postmenopausal women, based on low (0.14–0.39 μg/L) or high (0.66–2.1 μg/L) urinary cadmium, within a cross-sectional population-based women's health survey in Southern Sweden. We also measured 25-hydroxy vitamin D, cadmium in blood, bone mineral density and several markers of bone remodeling and kidney effects. Although there were clear differences in both kidney and bone effect markers between women with low and high cadmium exposure, the 1,25(OH) 2D concentrations were not significantly different (median, 111 pmol/L (5–95th percentile, 67–170 pmol/L) in low- and 125 pmol/L (66–200 pmol/L) in high-cadmium groups; p=0.08). Also, there was no association between 1,25(OH) 2D and markers of bone or kidney effects. It is concluded that the low levels of cadmium exposure present in the studied women, although high enough to be associated with lower bone mineral density and increased bone resorption, were not associated with lower serum concentrations of 1,25(OH) 2D. Hence, decreased circulating levels of 1,25(OH) 2D are unlikely to be the proposed link between cadmium-induced effects on kidney and bone.