Ozone Reacts With Carbon Black to Produce a Fulvic Acid-Like Substance and Increase an Inflammatory Effect

Abstract

Exposure to ambient ozone has been associated with increased human mortality. Ozone exposure can introduce oxygen-containing functional groups in particulate matter (PM) effecting a greater capacity of the particle for metal complexation and inflammatory effect. We tested the postulate that (1) a fulvic acid-like substance can be produced through a reaction of a carbonaceous particle with high concentrations of ozone and (2) such a fulvic acid-like substance included in the PM can initiate inflammatory effects following exposure of respiratory epithelial (BEAS-2B) cells and an animal model (male Wistar Kyoto rats). Carbon black (CB) was exposed for 72 hours to either filtered air (CB-Air) or approximately 100 ppm ozone (CB-O3). Carbon black exposure to high levels of ozone produced water-soluble, fluorescent organic material. Iron import by BEAS-2B cells at 4 and 24 hours was not induced by incubations with CB-Air but was increased following coexposures of CB-O3 with ferric ammonium citrate. In contrast to CB-Air, exposure of BEAS-2B cells and rats to CB-O3 for 24 hours increased expression of pro-inflammatory cytokines and lung injury, respectively. It is concluded that inflammatory effects of carbonaceous particles on cells can potentially result from (1) an inclusion of a fulvic acid-like substance after reaction with ozone and (2) changes in iron homeostasis following such exposure.

Oxidant-induced epithelial alarmin pathway mediates lung inflammation and functional decline following ultrafine carbon and ozone inhalation co-exposure

“…We and others have previously demonstrated that ultrafine/nano CB particles exhibit the ability to generate oxidants under acellular conditions [ 37 , 56 ]. Moreover, O 3 -interacted CB particles were reported to demonstrate acellular oxidant generation potentials [ 29 , 51 ]. In a recent report demonstrating increased inflammatory reactivity of O 3 -interacted CB particles after intratracheal instillation, fluidized bed approach was used to generate O 3 -interacted particles which were used for intratracheal instillation to elaborate increased inflammatory potential [ 29 ].…”

“…Moreover, O 3 -interacted CB particles were reported to demonstrate acellular oxidant generation potentials [ 29 , 51 ]. In a recent report demonstrating increased inflammatory reactivity of O 3 -interacted CB particles after intratracheal instillation, fluidized bed approach was used to generate O 3 -interacted particles which were used for intratracheal instillation to elaborate increased inflammatory potential [ 29 ]. A recent study described that O 3 alters the composition of the PM and increases its potency to induce lung injury in spontaneously hypertensive rats [ 26 ].…”

“…In the few published co-exposure reports, cardiovascular outcomes (heart rate variability, cardiac arrhythmia, mechanical decrements) were the main focus [ [21] , [22] , [23] , [24] , [25] ]. Previous insights on CB and O 3 pulmonary co-exposure were gained either after intratracheal instillation of relatively high doses O 3 -interacted CB particles or after sequential exposures to O 3 and PM [ [26] , [27] , [28] , [29] ]. Taken together, these studies clearly demonstrate the premise of interactive biological outcomes and warrant further studies to reveal mechanisms underpinning the increased toxicity of O 3 and particle inhalation co-exposures.…”

Transcriptomics of single dose and repeated carbon black and ozone inhalation co-exposure highlight progressive pulmonary mitochondrial dysfunction

“…A limited number of studies previously addressed particle (PM, diesel exhaust particles, CB) and O 3 exposure in a sequential manner and identified potentials for deleterious cardiovascular outcomes and increased lung injury and irritation [ 16 – 19 ]. A recent study demonstrated increased lung injury and formation of a fluvic acid-like substance after intratracheal administration of O 3 reacted CB particles [ 20 ]. To date, only a few PM and O 3 co-exposure studies have been performed, which mainly focused on cardiovascular outcomes and did not address pulmonary inflammatory mechanisms [ 21 – 23 ].…”

Pollution, Inflammation, and Vaccines: A Complex Crosstalk

“…In some cases, the inflammatory effects of different pollutants can act in a synergic fashion: for instance, ozone can react with carbon black, producing a fulvic acid-like substance, which has a high inflammatory potential [ 44 ].…”