All people are exposed to cadmium (Cd) via food; smokers are additionally exposed. High Cd exposure is associated with severe bone damage, but the public health impact in relation to osteoporosis and fractures at low environmental exposure remains to be clarified. Within the population-based Swedish Mammography Cohort, we assessed urinary Cd [U-Cd, mg/g of creatinine (cr)] as a marker of lifetime exposure and bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA) among 2688 women. Register-based information on fractures was retrieved from 1997 to 2009. Associations were evaluated by multivariable regression analyses. In linear regression, U-Cd was inversely associated with BMD at the total body ( p < .001), femoral neck ( p ¼ .025), total hip ( p ¼ .004), lumbar spine ( p ¼ .088), and volumetric femoral neck ( p ¼ .013). In comparison with women with U-Cd < 0.50 mg/g of cr, those with U-Cd ! 0.75 mg/g of cr had odds ratios (ORs) of 2.45 [95% confidence interval (CI) 1.51-3.97] and 1.97 (95% CI 1.24-3.14) for osteoporosis at the femoral neck and lumbar spine, respectively. Among never-smokers, the corresponding ORs were 3.47 (95% CI 1.46-8.23) and 3.26 (95% CI 1.44-7.38). For any first fracture (n ¼ 395), the OR was 1.16 (95% CI 0.89-1.50) comparing U-Cd ! 0.50 mg/g of cr with lower levels. Among never-smokers, the ORs (95% CIs) were 2.03 (1.33-3.09) for any first fracture, 2.06 (1.28-3.32) for first osteoporotic fracture, 2.18 (1.20-3.94) for first distal forearm fracture, and 1.89 (1.25-2.85) for multiple incident fractures. U-Cd at low environmental exposure from food in a general population of women showed modest but significant association with both BMD and fractures, especially in neversmokers, indicating a larger concern than previously known. ß