Using engineered nanomaterial-based toners, laser printers generate aerosols with alarming levels of nanoparticles that bear high bioactivity and potential health risks. Yet, the cardiac impacts of printer-emitted particles (PEPs) are unknown. Inhalation of particulate matter (PM) promotes cardiovascular morbidity and mortality, and ultra-fine particulates (< 0.1 μm aerodynamic diameter) may bear toxicity unique from larger particles. Toxicological studies suggest that PM impairs left ventricular (LV) performance; however, such investigations have heretofore required animal restraint, anesthesia, or ex vivo preparations that can confound physiologic endpoints and/or prohibit LV mechanical assessments during exposure. To assess the acute and chronic effects of PEPs on cardiac physiology, male Sprague Dawley rats were exposed to PEPs (21 days, 5 h/day) while monitoring LV pressure (LVP) and electrocardiogram (ECG) via conscious telemetry, analyzing LVP and heart rate variability (HRV) in four-day increments from exposure days 1 to 21, as well as ECG and baroreflex sensitivity. At 2, 35, and 70 days after PEPs exposure ceased, rats received stress tests. On day 21 of exposure, PEPs significantly (P < 0.05 vs. Air) increased LV end systolic pressure (LVESP, + 18 mmHg) and rate-pressure-product (+ 19%), and decreased HRV indicating sympathetic dominance (root means squared of successive differences [RMSSD], − 21%). Overall, PEPs decreased LV ejection time (− 9%), relaxation time (− 3%), tau (− 5%), RMSSD (− 21%), and P-wave duration (− 9%). PEPs increased QTc interval (+ 5%) and low:high frequency HRV (+ 24%; all P < 0.05 vs. Air), while tending to decrease baroreflex sensitivity and contractility index (− 15% and − 3%, P < 0.10 vs. Air). Relative to Air, at both 2 and 35 days after PEPs, ventricular arrhythmias increased, and at 70 days post-exposure LVESP increased. PEPs impaired ventricular repolarization at 2 and 35 days post-exposure, but only during stress tests. At 72 days post-exposure, PEPs increased urinary dopamine 5-fold and protein expression of ventricular repolarizing channels, Kv1.5, Kv4.2, and Kv7.1, by 50%. Conclusions: Our findings suggest exposure to PEPs increases cardiovascular risk by augmenting sympathetic influence, impairing ventricular performance and repolarization, and inducing hypertension and arrhythmia. PEPs may present significant health risks through adverse cardiovascular effects, especially in occupational settings, among susceptible individuals, and with long-term exposure.

中文翻译：

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吸入打印机发射的颗粒会损害心脏传导、血流动力学和自主调节，并诱发大鼠心律失常和电重构。


激光打印机使用基于纳米材料的工程碳粉，产生含有惊人水平纳米粒子的气溶胶，这些纳米粒子具有高生物活性和潜在的健康风险。然而，打印机发射颗粒 (PEP) 对心脏的影响尚不清楚。吸入颗粒物 (PM) 会促进心血管疾病的发病率和死亡率，而超细颗粒物（< 0.1 μm 空气动力学直径）可能具有较大颗粒物特有的毒性。毒理学研究表明 PM 会损害左心室 (LV) 性能；然而，迄今为止，此类研究需要动物约束、麻醉或离体准备，这些可能会混淆生理终点和/或禁止在暴露期间进行左心室机械评估。为了评估 PEP 对心脏生理学的急性和慢性影响，雄性 Sprague Dawley 大鼠暴露于 PEP（21 天，5 小时/天），同时通过有意识遥测监测左室压力 (LVP) 和心电图 (ECG)，分析 LVP 和心脏从暴露第 1 天到第 21 天以四天为增量的心率变异性 (HRV)，以及心电图和压力反射敏感性。停止接触 PEP 后 2、35 和 70 天，大鼠接受压力测试。在暴露第 21 天，PEP 显着（与空气相比，P < 0.05）增加左心室收缩压 (LVESP，+ 18 mmHg) 和心率-压力-乘积 (+ 19%)，并降低 HRV，表明交感神经支配（均方根）连续差异 [RMSSD], − 21%)。总体而言，PEP 缩短了左室射血时间 (− 9%)、舒张时间 (− 3%)、tau (− 5%)、RMSSD (− 21%) 和 P 波持续时间 (− 9%)。 PEP 增加了 QTc 间期 (+ 5%) 和低：高频 HRV（+ 24%；相对于空气，所有 P < 0.05），同时倾向于降低压力反射敏感性和收缩性指数（− 15% 和 − 3%，P < 0.10与空气）。 相对于 Air，在 PEP 后 2 天和 35 天，室性心律失常均增加，并且在暴露后 70 天 LVESP 增加。 PEP 在暴露后 2 天和 35 天时会损害心室复极，但仅限于压力测试期间。暴露后 72 天，PEP 使尿多巴胺增加 5 倍，心室复极通道 Kv1.5、Kv4.2 和 Kv7.1 的蛋白表达增加 50%。结论：我们的研究结果表明，暴露于 PEP 会通过增强交感神经影响、损害心室性能和复极以及诱发高血压和心律失常来增加心血管风险。 PEP 可能会因心血管不良影响而带来重大健康风险，特别是在职业环境中、易感人群中以及长期接触的情况下。