Qvarfordt Mikaela, Anderson Martin, Sanchez-Crespo Alejandro, Diakopoulou Maria, Svartengren Magnus
Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
Department of Laboratory Medicine, Division of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Inhal Toxicol. 2022;34(1-2):14-23. doi: 10.1080/08958378.2021.2019859. Epub 2021 Dec 30.
Epidemiological studies indicate association between elevated air pollution and adverse health effects. Several mechanisms have been suggested, including translocation of inhaled ultrafine carbon (UFC) particles into the bloodstream. Previous studies in healthy subjects have shown no significant pulmonary translocation of UFC-particles. This study aimed to assess if UFC-particles translocate from damaged alveolar compartment in subjects suffering from chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF).
Eleven COPD and nine IPF subjects were exposed to a 100 nm UFC-particle-aerosol labeled with Indium-111. Activity in the body was followed up for 10 days using gamma camera planar-imaging as well as in blood and urine samples.
The pulmonary central to periphery activity ratio was significantly higher for COPD as compared to IPF subjects at exposure, 1.8 and 1.4, respectively and remained constant throughout the test period. Ten days after exposure, the estimated median pulmonary translocation of UFC particles was 22.8 and 25.8% for COPD and IPF, respectively. Bound activity was present in blood throughout the test period, peaking at 24-h postinhalation with a median concentration of 5.6 and 8.9 Bq/ml for the COPD and IPF, respectively. Median bound activity excreted in urine (% of inhaled) after 10 days was 1.4% in COPD and 0.7% in IPF. Activity accumulation in liver and spleen could not be demonstrated.
Our results suggest that UFC particles leak through the damaged alveolar barrier to the bloodstream in COPD and IPF patients probably distributing in a wide spectrum of whole-body tissues.
流行病学研究表明空气污染加剧与不良健康影响之间存在关联。已经提出了几种机制，包括吸入的超细碳（UFC）颗粒转移到血液中。先前对健康受试者的研究表明，UFC颗粒在肺部没有明显转移。本研究旨在评估UFC颗粒是否会从患有慢性阻塞性肺疾病（COPD）和特发性肺纤维化（IPF）的受试者受损的肺泡腔转移到血液中。
11名COPD患者和9名IPF患者暴露于用铟-111标记的100纳米UFC颗粒气溶胶中。使用γ相机平面成像以及血液和尿液样本对体内活性进行了10天的随访。
暴露时，COPD患者的肺中央与外周活性比显著高于IPF患者，分别为1.8和1.4，并且在整个测试期间保持不变。暴露10天后，COPD和IPF患者UFC颗粒的估计肺转移中位数分别为22.8%和25.8%。在整个测试期间血液中均存在结合活性，吸入后24小时达到峰值，COPD和IPF患者的中位数浓度分别为5.6和8.9贝克勒尔/毫升。10天后，COPD患者尿液中排出（吸入量的百分比）的结合活性中位数为1.4%，IPF患者为0.7%。未发现肝脏和脾脏中有活性物质蓄积。
我们的结果表明，UFC颗粒可能通过受损的肺泡屏障泄漏到COPD和IPF患者的血液中，并可能分布于全身多种组织中。
