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
Background: Exposure to arsenic via drinking water has been associated with adverse pregnancy outcomes and infant morbidity and mortality. Little is known, however, about the effects of arsenic on child growth.Objective: We assessed potential effects of early-life arsenic exposure on weight and length of children from birth to 2 years of age.Methods: We followed 2,372 infants born in a population-based intervention trial in rural Bangladesh. Exposure was assessed by arsenic concentrations in urine (U-As) of mothers (gestational weeks 8 and 30) and children (18 months old). Child anthropometry was measured monthly in the first year and quarterly in the second. Linear regression models were used to examine associations of U-As (by quintiles) with child weight and length, adjusted for age, maternal body mass index, socioeconomic status, and sex (or stratified by sex).Results: Median (10th–90th percentiles) U-As concentrations were about 80 (25–400) µg/L in the mothers and 34 (12–159) µg/L in the children. Inverse associations of maternal U-As with child’s attained weight and length at 3–24 months were markedly attenuated after adjustment. However, associations of U-As at 18 months with weight and length at 18–24 months were more robust, particularly in girls. Compared with girls in the first quintile of U-As (< 16 µg/L), those in the fourth quintile (26–46 µg/L) were almost 300 g lighter and 0.7 cm shorter, and had adjusted odds ratios (95% confidence interval) for underweight and stunting of 1.57 (1.02–2.40) and 1.58 (1.05–2.37), respectively, at 21 months.Conclusions: Postnatal arsenic exposure was associated with lower body weight and length among girls, but not boys.
The prevalence and risk factors for acquisition of human T-cell lymphotropic virus type I and II (HTLV-I and II) were investigated in a prospective study of 913 injecting drug users (IDUs) in Stockholm in 1994. Epidemiologic data were recorded, and blood samples were tested for antibodies against HTLV-I and HTLV-II; human immunodeficiency virus (HIV) types 1 and 2; and hepatitis A (HAV), B (HBV), C (HCV), and D (HDV). Positive serologic results for HTLV were confirmed by Western blot (WB) and polymerase chain reaction (PCR). Of the 905 participants with conclusive HTLV-II status, 29 (3.2%) were HTLV-II positive, and all but three were of Nordic descent. None was HTLV-I infected. One person was infected as early as 1981, before HIV had reached the IDU population in Sweden. The prevalence of HTLV-II infection was 12% among HIV-1-seropositive and 1.8% among HIV-1-seronegative participants. The overall seroprevalences were 14% for HIV-1, 0% for HIV-2, 41% for HAV, 75% for HBV, 92% for HCV, and 8% for HDV. Although amphetamine has been the main injecting drug in Sweden for several decades, heroin abuse combined with a debut of injecting drugs before 1975 was identified as the most important risk factor associated with HTLV-II infection. HAV and HIV seropositivity were also independent risk factors.
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