Merced-Nieves Francheska M, Colicino Elena, Coull Brent, Bose Sonali, Redline Susan, Wright Robert O, Wright Rosalind J
Department of Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Environmental Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Department of Environmental Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Environ Res. 2025 Aug 15;279(Pt 1):121707. doi: 10.1016/j.envres.2025.121707. Epub 2025 Apr 25.
Inadequate sleep in childhood can impact long-term neurodevelopmental outcomes; thus, identifying modifiable risk factors amenable to intervention is a priority. Development of sleep neuroarchitecture begins in utero. Manganese (Mn) is a trace element known to be both an essential element for optimal neurodevelopment and, at insufficient or excess levels, a neurotoxicant. We examined associations between prenatal urinary Mn levels and objectively measured sleep outcomes in children aged 6.7 ± 2.0 years and explored sex-specific effects. Sleep was assessed using multi-day actigraphy (n = 222) and single-night in-home polysomnography (PSG) (n = 102). Linear and non-linear associations between prenatal log-transformed Mn levels and sleep outcomes were examined using multivariable linear regression and generalized additive models, respectively. Non-linear associations were examined based on low, moderate (referent group) and high Mn levels indexed by tertiles. Sex-specific effects were evaluated using 2-way interaction terms. A doubling increase in Mn was associated with a 30.9 min (95 % CI = -52.0, -9.86) decrease of average sleep period duration and a 21.9 min (95 % CI = -39.9, -4.02) decrease of average sleep duration on actigraphy; associations were more pronounced in males. Compared to children born to mothers with moderate prenatal urinary Mn levels, children whose mothers had "low" Mn had a percent increase in minutes of wake after sleep onset (WASO) (β = 89.6; 95 % CI = 16.2, 206.5) and a decrease in sleep efficiency percentage (β = -6.47; 95 % CI = -11.3, -1.68) on PSG. Sleep problems may be influenced by environmental exposures, such as metals, and disruption can occur as early as pregnancy.
儿童期睡眠不足会影响长期神经发育结果；因此，确定可干预的可变风险因素是当务之急。睡眠神经结构的发育始于子宫内。锰（Mn）是一种微量元素，已知既是最佳神经发育所必需的元素，在含量不足或过量时又是一种神经毒物。我们研究了产前尿锰水平与6.7±2.0岁儿童客观测量的睡眠结果之间的关联，并探讨了性别特异性影响。使用多日活动记录仪（n = 222）和单晚家庭多导睡眠图（PSG）（n = 102）评估睡眠。分别使用多变量线性回归和广义相加模型研究产前对数转换锰水平与睡眠结果之间的线性和非线性关联。根据三分位数划分的低、中（参照组）和高锰水平检查非线性关联。使用双向交互项评估性别特异性影响。锰增加一倍与活动记录仪测量的平均睡眠时间缩短30.9分钟（95%CI = -52.0，-9.86）和平均睡眠时长缩短21.9分钟（95%CI = -39.9，-4.02）相关；在男性中关联更明显。与产前尿锰水平中等的母亲所生儿童相比，母亲锰水平“低”的儿童在PSG上睡眠开始后觉醒时间（WASO）的分钟数增加百分比（β = 89.6；95%CI = 16.2，206.5），睡眠效率百分比降低（β = -6.47；95%CI = -11.3，-1.68）。睡眠问题可能受环境暴露如金属的影响，而且这种干扰可能早在孕期就会出现。
