Influence of Environmental Cadmium Exposure on Forearm Bone Density

Wang, Hong-Fu; Zhu, Guoying; Shi, Yongxin; Weng, Shifang; Jin, Taiyi; Kong, Qinghu; Nordberg, Gunnar F.

doi:10.1359/jbmr.2003.18.3.553

Cited by 126 publications

(65 citation statements)

References 12 publications

(17 reference statements)

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“…(3)(4)(5)(6) It should be noted, however, that our results indicate an increased risk of osteoporosis at considerably lower Cd exposures. In addition, the results for BMD at the lumbar spine may indicate a greater public health concern than recognized previously.…”

Section: Discussioncontrasting

confidence: 65%

“…This severe disease was characterized by renal and bone damage, with bone deformities and multiple fractures occurring as a consequence. (2) Recently, Cd has been associated with low bone mass of the forearm (3)(4)(5)(6) and the hip (7) at considerably lower exposure levels in some but far from all studies. (8)(9)(10)(11) Therefore, a possible role of Cd in the public health context of osteoporosis needs to be evaluated.…”

Section: Introductionmentioning

confidence: 99%

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Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women

Engström

Michaëlsson

Suwazono

et al. 2010

Journal of Bone and Mineral Research

127

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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

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Section: Discussioncontrasting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women

Engström

Michaëlsson

Suwazono

et al. 2010

Journal of Bone and Mineral Research

127

View full text Add to dashboard Cite

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“…Clinical features associated with osteoporosis include increased morbidity (ie, pain, physical impairment, and decreased quality of life), increased risk of new fractures, and increased mortality. (7) Studies among populations from Belgium, (4,8) Sweden, (9)(10)(11) Japan, (12) and China (13,14) showed associations between osteoporosis and low-level environmental cadmium exposure. The generally accepted interpretation has been that cadmiuminduced renal tubular damage (2) decreases the calcium reabsorption in the nephron, resulting in hypercalciuria (2) and low BMD and hence increased fracture risk, (4,11) particularly in postmenopausal women (4,8) or men in the older age group.…”

Section: Discussionmentioning

confidence: 99%

Occupational cadmium exposure and calcium excretion, bone density, and osteoporosis in men

Nawrot

Geusens

Nulens³

et al. 2010

Journal of Bone and Mineral Research

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Exposure to cadmium has been associated with osteoporosis and fracture risk in women and the elderly, but studies in middle-aged men are lacking. In 83 male (ex)workers (mean age 45 years; range 24 to 64 years) in a radiator factory using cadmium-containing solder, we investigated the association between urinary cadmium excretion (as an index of lifetime body burden); bone mineral density (BMD) in the distal forearm, hip, and lumbar spine (by dual-energy X-ray absorptiometry); and urinary calcium excretion. Geometric mean urinary cadmium concentration was 1.02 mg/g of creatinine (5th to 95th percentile 0.17 to 5.51 mg/g). BMD was negatively correlated with urinary exposure to cadmium. The partial correlation coefficients (r) adjusted for age, body-mass index, and current smoking were À0.30 ( p ¼ .008) for BMD in the forearm, À0.27 ( p ¼ .017) in the hip, and À0.17 ( p ¼ .15) in the spine. Urinary calcium correlated positively (r ¼ 0.23, p ¼ .044) with the urinary cadmium excretion. Adjusted for the same covariates, the risk of osteoporosis (defined as a T-score below À2.5 in at least one measured bone site) increased dose dependently. Compared with the lowest tertile of urinary cadmium, the risks were 4.8-and 9.9-fold higher in the middle and highest tertiles, respectively. Only four (5%) men had evidence of renal tubular dysfunction (b 2 -microglobulin > 300 mg/g of creatinine). Even in the absence of renal tubular dysfunction, occupational exposure to cadmium is associated in men with lower BMD values, a higher risk of having osteoporosis, and a higher urinary calcium excretion, suggesting a direct osteotoxic effect of cadmium. ß

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“…In addition, an increased risk of fractures was also noted in the Swedish Oscar study, demonstrating an elevated hazard ratio already at exposure levels of 2-4 lg/g creatinine . Studies in China have reported that osteoporosis is related to kidney dysfunction, especially to tubular damage and its severity (Wang et al 2003;Jin et al 2004). Although women are believed to be more susceptible than men, a study in middle-aged men (mean age 45 years) exposed to Cd in an occupational setting showed a dose-dependent increase of osteoporosis.…”

Section: Osteoporosismentioning

confidence: 99%

“…Clinical features associated with osteoporosis include increased morbidity (pain, physical impairment, decreased quality of life), increased risk of new fractures and increased mortality (Van der Klift et al 2002). Studies among populations from Belgium (Staessen et al 1999;Schutte et al 2008b), Sweden (Järup et al 1998a;Alfvén et al 2000;Å kesson et al 2006), Japan and China Jin et al 2004;Wang et al 2003) showed associations between osteoporosis and low-level environmental Cd exposure. The generally accepted interpretation has been that Cd-induced renal tubular damage (Staessen et al 1994) decreases the calcium reabsorption in the nephron, resulting in hypercalciuria and decreased bone mineral density, and hence increased fracture risk (Järup et al 1998c;Staessen et al 1994) particularly in postmenopausal women (Schutte et al 2008b;Staessen et al 1999) or men in the older age group .…”

Section: Osteoporosismentioning

confidence: 99%

Cadmium exposure in the population: from health risks to strategies of prevention

et al. 2010

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We focus on the recent evidence that elucidates our understanding about the effects of cadmium (Cd) on human health and their prevention. Recently, there has been substantial progress in the exploration of the shape of the Cd concentrationresponse function on osteoporosis and mortality. Environmental exposure to Cd increases total mortality in a continuous fashion without evidence of a threshold, independently of kidney function and other classical factors associated with mortality including age, gender, smoking and social economic status. Pooled hazard rates of two recent environmental population based cohort studies revealed that for each doubling of urinary Cd concentration, the relative risk for mortality increases with 17% (95% CI 4.2-33.1%; P \ 0.0001). Tubular kidney damage starts at urinary Cd concentrations ranging between 0.5 and 2 lg urinary Cd/g creatinine, and recent studies focusing on bone effects show increased risk of osteoporosis even at urinary Cd below 1 lg Cd/g creatinine. The non-smoking adult population has urinary Cd concentrations close to or higher than 0.5 lg Cd/g creatinine. To diminish the transfer of Cd from soil to plants for human consumption, the bioavailability of soil Cd for the plants should be reduced (external bioavailability) by maintaining agricultural and garden soils pH close to neutral (pH-H 2 O of 7.5; pH-KCL of 6.5). Reducing the systemic bioavailability of intestinal Cd can be best achieved by preserving a balanced iron status. The latter might especially be relevant in groups with a lower intake of iron, such as vegetarians, and women in reproductive phase of life. In exposed populations, house dust loaded with Cd is an additional relevant exposure route. In view of the insidious etiology of health effects associated with low dose exposure to Cd and the current European Cd intake which is close to the tolerable weekly intake, one should not underestimate the importance of the recent epidemiological evidence on Cd toxicity as to its medical and public health implications.

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Influence of Environmental Cadmium Exposure on Forearm Bone Density

Cited by 126 publications

References 12 publications

Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women

Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women

Occupational cadmium exposure and calcium excretion, bone density, and osteoporosis in men

Cadmium exposure in the population: from health risks to strategies of prevention

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