Postmenopausal bone loss can be exacerbated by environmental contaminants, including the heavy metal cadmium (Cd). We hypothesized that incorporating phosphorus (P) into the diet would lead to the chelation of Cd into P, preventing its absorption and subsequent bone loss.
To test this hypothesis, we used ovariectomized rats as a model of postmenopausal osteoporosis to examine the deleterious effects of Cd on bone with and without added P. Fifty 3-month-old ovariectomized Sprague-Dawley rats were assigned to five treatment groups (n = 10 per group) for 3 months as follows: (1) control; (2) 50 ppm Cd; (3) 50 ppm Cd plus 1.2% P; (4) 200 ppm Cd; and (5) 200 ppm Cd plus 1.2% P.
Cd plus P caused a significant loss of whole body (P = 0.0001 and P < 0.001) and femoral (P = 0.0005 and P < 0.001) bone mineral density (BMD) and bone mineral content, respectively, and a loss of fourth lumbar vertebra BMD and bone mineral content (P < 0.0001 and P < 0.001, respectively). Nonetheless, 200 ppm Cd plus 1.2% P had the most deleterious effects on whole body and femoral BMD. For femoral neck microstructural properties, 50 ppm Cd plus 1.2% P caused an increase in trabecular separation, whereas 200 ppm Cd plus 1.2% P caused a decrease in bone volume–to–total volume ratio, a decrease in trabecular number, and an increase in trabecular separation and structural model index.
Our findings indicate that Cd exposure, along with high intake of P, may be a public health hazard with respect to bone health.