Gaseous VOCs rapidly modify particulate matter and its biological effects – Part 1: Simple VOCs and model PM

Abstract

This is the first of a three-part study designed to demonstrate dynamic entanglements among gaseous organic compounds (VOC), particulate matter (PM), and their subsequent potential biological effects. We study these entanglements in increasingly complex VOC and PM mixtures in urban-like conditions in a large outdoor chamber. To the traditional chemical and physical characterizations of gas and PM, we added new measurements of gas-only- and PM-only-biological effects, using cultured human lung cells as model indicators. These biological effects are assessed here as increases in cellular damage or expressed irritation (i.e., cellular toxic effects) from cells exposed to chamber air relative to cells exposed to clean air. The exposure systems permit gas-only- or PM-only-exposures from the same air stream containing both gases and PM in equilibria, i.e., there are no extractive operations prior to cell exposure. Our simple experiments in this part of the study were designed to eliminate many competing atmospheric processes to reduce ambiguity in our results. Simple volatile and semi-volatile organic gases that have inherent cellular toxic properties were tested individually for biological effect in the dark (at constant humidity). Airborne mixtures were then created with each compound and PM that has no inherent cellular toxic properties for another cellular exposure. Acrolein and p-tolualdehyde were used as model VOCs and mineral oil aerosol (MOA) was selected as a surrogate for organic-containing PM. MOA is appropriately complex in composition to represent ambient PM, and it exhibits no inherent cellular toxic effects and thus did not contribute any biological detrimental effects on its own. Chemical measurements, combined with the responses of our biological exposures, clearly demonstrate that gas-phase pollutants can modify the composition of PM (and its resulting detrimental effects on lung cells) – even if the gas-phase pollutants are not considered likely to partition to the condensed phase: the VOC-modified-PM showed significantly more damage and inflammation to lung cells than did the original PM. Because gases and PM are transported and deposited differently within the atmosphere and the lungs, these results have significant consequences. For example, current US policies for research and regulation of PM do not recognize this “effect modification” phenomena (NAS, 2004). These results present an unambiguous demonstration that – even in these simple mixtures – physical and thermal interactions alone can cause a modification of the distribution of species among the phases of airborne pollution mixtures and can result in a non-toxic phase becoming toxic due to atmospheric thermal processes only. Subsequent work extends the simple results reported here to systems with photochemical transformations of complex urban mixtures and to systems with diesel exhaust produced by different fuels.

Epoxide as a precursor to secondary organic aerosol formation from isoprene photooxidation in the presence of nitrogen oxides

“…Measurements from both gas and particle phases were taken periodically until sunset. Detailed operating conditions for chemical and physical monitoring of the chamber have been previously described (44). To detect gaseous MAE formation, chamber air was continuously drawn through two fritted-glass bubblers in series at a sampling flow rate of ∼1 L·min −1 .…”

Cellular RNA is chemically modified by exposure to air pollution mixtures

“…In vitro exposures were performed using the GIVES (gas in vitro exposure system) as previously described (Doyle et al, 2007;Ebersviller et al, 2012;Rager et al, 2011a;Sexton et al, 2004). Briefly, cells were grown on 30 mm Millicell membranes (EMD Millipore Corp., Billerica, MA) in F12-K media with 10% fetal bovine serum (FBS) plus 0.01% penicillin/streptomycin at a density of 850 000 cells/ membrane, 28 h prior to exposure as described (Jaspers et al, 1997;Zavala et al, 2014).…”

“…Its strong reactivity and tendency to generate free radicals, such as hydroxyl (OH) radicals and reactive odd nitrogen species (NO y ), cause damage to a wide range of cellular components (Byvoet et al, 1995;Cataldo, 2006a;Jorge et al, 2002;Weschler et al, 1992). Furthermore, O 3 is created as a byproduct of VOC photolysis and oxidation, degradation of chlorine and nitrogen compounds, and surface reactions on particulate matter (PM) (Crounse et al, 2012;Doyle et al, 2004;Ebersviller et al, 2012;Faxon & Allen, 2013;Meng et al, 1997;Weschler et al, 1992). In addition, it is wellknown that photochemical reactions in air pollution mixtures generate higher levels of O 3 and secondary oxidative compounds (Doyle et al, 2007), an effect which may increase with global climate change (Jacob & Winner, 2009).…”

Early history and rationale for outdoor chamber work at the University of North Carolina

“…A surrogate aerosol to diesel particles was designed to be non-toxic but of similar size and density (aerosolised mineral oil). By conducting a series of experiments where mixing in a dark chamber a non-toxic aerosol of mineral oil with a single toxic gas species, it was demonstrated that the non-toxic mineral oil could be made significantly toxic [73] (Fig. 10).…”

“…Demonstration using a paired gas-only cellular exposure (left) and a particle-only cellular exposure system (right) of a gas-phase toxicant (Tolald, p-tolualdehyde) (left C) making a non-toxic particle (MOA, mineral oil aerosol) (right B, C) become highly toxic to cells (right D). [73,74] Conditions: A are clean air exposures; B are clean air and non-toxic particle; C are gas-phase toxicant, no particles exposure, and D are mixture of gas-phase toxicant and non-toxic particle followed by exposure. Note that in exposure D on left, the gas-phase only toxicity has decreased due to much of the gas-phase toxicant having moved to the particle.…”