Respiratory hazard assessment of combined exposure to complete gasoline exhaust and respirable volcanic ash in a multicellular human lung model at the air-liquid interface

Abstract

Communities resident in urban areas located near active volcanoes can experience volcanic ash exposures during, and following, an eruption, in addition to sustained exposures to high concentrations of anthropogenic air pollutants (e.g., vehicle exhaust emissions). Inhalation of anthropogenic pollution is known to cause the onset of, or exacerbate, respiratory and cardiovascular diseases. It is further postulated similar exposure to volcanic ash can also affect such disease states. Understanding of the impact of combined exposure of volcanic ash and anthropogenic pollution to human health, however, remains limited. The aim of this study was to assess the biological impact of combined exposure to respirable volcanic ash (from Soufrière Hills volcano (SHV), Montserrat and Chaitén volcano (ChV), Chile; representing different magmatic compositions and eruption styles) and freshly-generated complete exhaust from a gasoline vehicle. A multicellular human lung model (an epithelial cell-layer composed of A549 alveolar type II-like cells complemented with human blood monocyte-derived macrophages and dendritic cells cultured at the air-liquid interface) was exposed to diluted exhaust (1:10) continuously for 6 h, followed by immediate exposure to the ash as a dry powder (0.54 ± 0.19 μg/cm and 0.39 ± 0.09 μg/cm for SHV and ChV ash, respectively). After an 18 h incubation, cells were exposed again for 6 h to diluted exhaust, and a final 18 h incubation (at 37 °C and 5% CO). Cell cultures were then assessed for cytotoxic, oxidative stress and (pro-)inflammatory responses. Results indicate that, at all tested (sub-lethal) concentrations, co-exposures with both ash samples induced no significant expression of genes associated with oxidative stress (HMOX1, NQO1) or production of (pro-)inflammatory markers (IL-1β, IL-8, TNF-α) at the gene and protein levels. In summary, considering the employed experimental conditions, combined exposure of volcanic ash and gasoline vehicle exhaust has a limited short-term biological impact to an advanced lung cell in vitro model.

The Biological Effects of Complete Gasoline Engine Emissions Exposure in a 3D Human Airway Model (MucilAirTM) and in Human Bronchial Epithelial Cells (BEAS-2B)

“…Although there were no changes in the expression of oxidative stress- and inflammation-related genes observed after exposure to gasoline exhaust, diesel exhaust induced the expression of HMOX1 , GSR , and IL-8 [27]. Finally, the exposure to complete gasoline exhaust for 2 × 6 h during a 48-h incubation had no effect on the expression of oxidative stress- and inflammation-related genes in a co-culture of lung cells, monocytes, and dendritic cells growing at the ALI [37]. Overall, these studies indicate that the gene expression is induced by exposure to diesel exhaust, while gasoline emissions have hardly any effect.…”

Assessing the biological reactivity of organic compounds on volcanic ash: implications for human health hazard

“…Accordingly, populations are commonly exposed to volcanic ash concomitantly with additional substances, notably urban air pollutants such as vehicle and industry emissions, which are composed of a mixture of particulate matter and gaseous/volatile species. Currently, limited understanding exists regarding the human health hazards associated with the combined exposures to volcanic particulate matter and the polluted urban environment (Tomašek et al 2016(Tomašek et al , 2018. Of particular importance is how volcanic ash interacts with urban pollutants and if this association may influence its biological reactivity and, in this way, contribute to an increase in adverse health effects for exposed populations.…”

Health Impact Assessment of Volcanic Ash Inhalation: A Comparison With Outdoor Air Pollution Methods

“…A review of 419 source apportionment datasets of urban ambient PM 2.5 , published during 1990-2014, generated the following global averages: 25% traffic, 15% industrial activities, 20% domestic fuel burning, 22% unspecified anthropogenic sources, and 18% from natural dust and salt (Karagulian et al, 2015). Similarly, the composition of dusts from volcanic eruptions may vary according to the chemical and physical properties of a given eruption and level of adsorption of volcanic, atmospheric, and anthropogenic elements (Damby et al, 2013;Durant et al, 2010;Horwell et al, 2013;Tomašek et al, 2016Tomašek et al, , 2018Tomašek et al, , 2019. While PM composition and toxicity are likely to vary by source, the evidence concerning how components affect toxicity, and to what extent, is 10.1029/2020GH000256…”

“…No substantial difference was observed post-eruption, though a decrease in lung function was apparent from subsequent exposure to relatively lower concentrations of urban air pollution (Johnson et al, 1982). More recently, an in vitro study using a multicellular lung culture found combined exposure to volcanic ash and diesel particles produced a greater, but minimal, pro-inflammatory response than to that from ash alone (Tomašek et al, 2016), though a follow-up study with gasoline exhaust found no such effect (Tomašek et al, 2018). Cardiorespiratory hospital admissions in Iceland were elevated on days of high PM 10 concentrations (>50 μg/m 3 ) caused by volcanic ash, but were only borderline significant after adjustment for such days (Carlsen et al, 2015).…”