Exposure to ultrafine particles, intracellular production of reactive oxygen species in leukocytes and altered levels of endothelial progenitor cells

Abstract

Exposure to particles in the fine and ultrafine size range has been linked to induction of low-grade systemic inflammation, oxidative stress and development of cardiovascular diseases. Declining levels of endothelial progenitor cells within systemic circulation have likewise been linked to progression of cardiovascular diseases. The objective was to determine if exposure to fine and ultrafine particles from indoor and outdoor sources, assessed by personal and residential indoor monitoring, is associated with altered levels of endothelial progenitor cells, and whether such effects are related to leukocyte-mediated oxidative stress. The study utilized a cross sectional design performed in 58 study participants from a larger cohort. Levels of circulating endothelial progenitor cells, defined as either late (CD34(+)KDR(+) cells) or early (CD34(+)CD133(+)KDR(+) cells) subsets were measured using polychromatic flow cytometry. We additionally measured production of reactive oxygen species in leukocyte subsets (lymphocytes, monocytes and granulocytes) by flow cytometry using intracellular 2',7'-dichlorofluoroscein. The measurements encompassed both basal levels of reactive oxygen species production and capacity for reactive oxygen species production for each leukocyte subset. We found that the late endothelial progenitor subset was negatively associated with levels of ultrafine particles measured within the participant residences and with reactive oxygen species production capacity in lymphocytes. Additionally, the early endothelial progenitor cell levels were positively associated with a personalised measure of ultrafine particle exposure and negatively associated with both basal and capacity for reactive oxygen species production in lymphocytes and granulocytes, respectively. Our results indicate that exposure to fine and ultrafine particles derived from indoor sources may have adverse effects on human vascular health.

A Flow Cytometry‐based Method for the Screening of Nanomaterial‐induced Reactive Oxygen Species Production in Leukocytes Subpopulations in Whole Blood

“…As expected, the exposure to the CB increased the intracellular ROS generation in neutrophils ( p = <0.005). The induction of intracellular ROS after exposure to CB in monocytes and granulocytes has been shown previously , and thus, it was chosen as reference NM.…”

“…This probe has been utilized successfully in previous investigations of ROS generation after exposure of different cells in vitro and ex vivo to a wide range of nano-sized materials (i.e. 9,32,35,37,46,[51][52][53]. Finally, it is important to further state that the flow cytometric evaluation of ROS is an established method and previously used in cell lines to detect NM-induced damage [54,55].…”

The Role of Air Pollution by the Particulate Matter in Pathogenesis of the Chronic Noninfectious Diseases

“…Особенно опасны для здоро-вья человека мелкодисперсные частицы размером ме-нее 2,5 мкм (РМ2,5), которые могут достигать бронхиол и альвеол, и ультрамелкодисперсные частицы с размером частиц 0,1-0,001 мкм (PM0,1), которые включают в себя наночастицы (<100 нм). Обладая малой массой, РМ0,1 имеют большую площадь поверхности, депонируются в альвеолах, могут ускользать от мукоцилиарного клирен-са и макрофагов, в отличие от крупных РМ, проникают в кровоток и затем могут попасть в любую ткань организ-ма человека [8,9]. Однако риск для здоровья человека при воздействии РМ 2,5 и РМ0,1 на молекулярно-клеточном уровне изучен недостаточно.…”

Correlation Between Exposure to Transfluthrin and the Change in Dielectric Properties and Deformed Cells of Mice

“…Cell damage from organs can be caused by oxidative stress and the relation with inflammation [10]. Oxidative stress is a pathological condition that is associated with the increased speed of cell and tissue damage due to the induction of oxygen and its derivatives or ROS (Reactive Oxygen Species) [11].…”