Tinkelman Naomi E, Spratlen Miranda Jones, Domingo-Relloso Arce, Tellez-Plaza Maria, Grau-Perez Maria, Francesconi Kevin A, Goessler Walter, Howard Barbara V, MacCluer Jean, North Kari E, Umans Jason G, Factor-Litvak Pam, Cole Shelley A, Navas-Acien Ana
Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA; Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, USA.
Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, USA.
Environ Int. 2020 Apr;137:105531. doi: 10.1016/j.envint.2020.105531. Epub 2020 Feb 18.
Experimental and prospective epidemiologic evidence suggest that arsenic exposure has diabetogenic effects. However, little is known about how family exposure to arsenic may affect risk for type 2 diabetes (T2D)-related outcomes in adulthood. We evaluated the association of both maternal and offspring arsenic exposure with fasting glucose and incident T2D in 466 participants of the Strong Heart Family Study. Total arsenic (ΣAs) exposure was calculated as the sum of inorganic arsenic (iAs) and methylated (MMA, DMA) arsenic species in maternal and offspring baseline urine. Median maternal ΣAs at baseline (1989-91) was 7.6 µg/g creatinine, while median offspring ΣAs at baseline (2001-03) was 4.5 µg/g creatinine. Median offspring glucose in 2006-2009 was 94 mg/dL, and 79 participants developed T2D. The fully adjusted mean difference (95% CI) for offspring glucose was 4.40 (-3.46, 12.26) mg/dL per IQR increase in maternal ΣAs vs. 2.72 (-4.91 to 10.34) mg/dL per IQR increase in offspring ΣAs. The fully adjusted odds ratio (95%CI) of incident T2D was 1.35 (1.07, 1.69) for an IQR increase in maternal ΣAs and 1.15 (0.92, 1.43) for offspring ΣAs. The association of maternal ΣAs with T2D outcomes were attenuated with adjustment for offspring adiposity markers. Familial exposure to arsenic, as measured in mothers 15-20 years before offspring follow-up, is associated with increased odds of offspring T2D. More research is needed to confirm findings and better understand the importance of family exposure to arsenic in adult-onset diabetes.
实验和前瞻性流行病学证据表明，砷暴露具有致糖尿病作用。然而，关于家庭砷暴露如何影响成年期2型糖尿病（T2D）相关结局的风险，我们知之甚少。我们在“强心家族研究”的466名参与者中评估了母体和子代砷暴露与空腹血糖及新发T2D之间的关联。总砷（ΣAs）暴露量通过母体和子代基线尿液中无机砷（iAs）和甲基化砷（MMA、DMA）物种的总和来计算。基线时（1989 - 91年）母体ΣAs的中位数为7.6 μg/g肌酐，而基线时（2001 - 03年）子代ΣAs的中位数为4.5 μg/g肌酐。2006 - 2009年子代血糖的中位数为94 mg/dL，79名参与者患了T2D。母体ΣAs每增加一个四分位数间距，子代血糖的完全调整后平均差异（95%CI）为4.40（-3.46，12.26）mg/dL，而子代ΣAs每增加一个四分位数间距，该差异为2.72（-4.91至10.34）mg/dL。母体ΣAs增加一个四分位数间距时，新发T2D的完全调整后比值比（95%CI）为1.35（1.07，1.69），子代ΣAs增加一个四分位数间距时为1.15（0.92，1.43）。对后代肥胖标志物进行调整后，母体ΣAs与T2D结局之间的关联减弱。在子代随访前15 - 20年测量的母亲体内砷的家族暴露，与子代患T2D的几率增加有关。需要更多研究来证实这些发现，并更好地理解家庭砷暴露在成年期糖尿病中的重要性。
