Assessment of the potential for in-plume sulphur dioxide gas-ash interactions to influence the respiratory toxicity of volcanic ash.

BACKGROUND: Volcanic plumes are complex environments composed of gases and ash particles, where chemical and physical processes occur at different temperature and compositional regimes. Commonly, soluble sulphate- and chloride-bearing salts are formed on ash as gases interact with ash surfaces. Exposure to respirable volcanic ash following an eruption is potentially a significant health concern. The impact of such gas-ash interactions on ash toxicity is wholly un-investigated. Here, we study, for the first time, whether the interaction of volcanic particles with sulphur dioxide (SO2) gas, and the resulting presence of sulphate salt deposits on particle surfaces, influences toxicity to the respiratory system, using an advanced in vitro approach. METHODS: To emplace surface sulphate salts on particles, via replication of the physicochemical reactions that occur between pristine ash surfaces and volcanic gas, analogue substrates (powdered synthetic volcanic glass and natural pumice) were exposed to SO2 at 500 °C, in a novel Advanced Gas-Ash Reactor, resulting in salt-laden particles. The solubility of surface salt deposits was then assessed by leaching in water and geochemical modelling. A human multicellular lung model was exposed to aerosolised salt-laden and pristine (salt-free) particles, and incubated for 24 h. Cell cultures were subsequently assessed for biological endpoints, including cytotoxicity (lactate dehydrogenase release), oxidative stress (oxidative stress-related gene expression; heme oxygenase 1 and NAD(P)H dehydrogenase [quinone] 1) and its (pro-)inflammatory response (tumour necrosis factor α, interleukin 8 and interleukin 1ß at gene and protein levels). RESULTS: In the lung cell model no significant effects were observed between the pristine and SO2-exposed particles, indicating that the surface salt deposits, and the underlying alterations to the substrate, do not cause acute adverse effects in vitro. Based on the leachate data, the majority of the sulphate salts from the ash surfaces are likely to dissolve in the lungs prior to cellular uptake. CONCLUSIONS: The findings of this study indicate that interaction of volcanic ash with SO2 during ash generation and transport does not significantly affect the respiratory toxicity of volcanic ash in vitro. Therefore, sulphate salts are unlikely a dominant factor controlling variability in in vitro toxicity assessments observed during previous eruption response efforts.

Respiratory and Other Hazard Characteristics of Substances in Cleaning Products Used in Healthcare Centres in England and Wales.

Occupational use of cleaning products can cause asthma in healthcare workers but the cleaning agents responsible are not yet known. This study aimed to identify respiratory and other hazards in cleaning products on the National Health Service (NHS) supply chain online catalogue and used in the NHS. Information on cleaning products, their composition, and H-statements that identified hazard characteristics of chemical substances in them was obtained from chemical safety data sheets (SDSs). Furthermore, a quantitative structure-activity relationship model and a published asthmagen list were used to identify potential additional respiratory hazards. 473 cleaning products and 229 substances were identified. SDSs reported only 4 respiratory sensitizers but an additional 51 were suggested by the other 2 methods. In contrast, 25 respiratory irritants were identified using SDSs and only one from the asthmagen list. This comprehensive overview of cleaning agents' hazards has potential use in future risk assessment and epidemiological studies.

Characterization and Hazard Identification of Respirable Cement and Concrete Dust from Construction Activities.

Construction is an important segment of the economy that employs millions of people. Construction dust is an occupational health hazard to millions of construction workers worldwide. The hazards associated with respirable dust depend upon its particulate size distribution and chemical composition, as these determine the deposition pattern in the respiratory tract and reactivity, respectively. This study presents characterization of the size and composition of the dust from two key construction materials-cast cement and poured concrete. The dust was generated by cutting the cured cement and concrete blocks using an 18" hand-held circular saw as used in highway and building construction. Transmission electron microscopy, scanning electron microscopy, dynamic light scattering, and laser diffraction were performed for the size analysis of the particles. Energy dispersive spectroscopy and X-ray photoelectron spectroscopy were used for chemical analysis. X-ray diffraction was used for phase identification. Electron diffraction patterns were obtained to assess the crystallinity of individual particles. They confirm the crystallinity of particles of different size and shapes. With a particle size range between 0.5 µm and 10 µm, greater than 90% of particles fell below 2.5 µm, presenting a respirable health concern. Crystalline compounds including the metals Al, Ca, Fe, Mg, Na, and K were detected. The concrete particles were most enriched in crystalline silica with a concentration of more than 30% by weight. The presence of metals and high crystalline silica content pose a serious health concern to construction workers.

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.

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 ±â€¯0.19 µg/cm2 and 0.39 ±â€¯0.09 µg/cm2 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% CO2). 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-1ß, 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.