In vitro assessment of the pulmonary toxicity of particulate matter emitted during haze events in Chiang Mai, Thailand via investigation of macrophage responses
Issued Date
2023-06-01
Resource Type
eISSN
27525309
Scopus ID
2-s2.0-105020706652
Journal Title
Environmental Research Health
Volume
1
Issue
2
Rights Holder(s)
SCOPUS
Bibliographic Citation
Environmental Research Health Vol.1 No.2 (2023)
Suggested Citation
Maciaszek K., Gillies S., Kawichai S., Prapamontol T., Santijitpakdee T., Kliengchuay W., Sahanavin N., Mueller W., Vardoulakis S., Samutrtai P., Cherrie J.W., Brown D.M., Tantrakarnapa K., Johnston H.J. In vitro assessment of the pulmonary toxicity of particulate matter emitted during haze events in Chiang Mai, Thailand via investigation of macrophage responses. Environmental Research Health Vol.1 No.2 (2023). doi:10.1088/2752-5309/ac9748 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/113018
Title
In vitro assessment of the pulmonary toxicity of particulate matter emitted during haze events in Chiang Mai, Thailand via investigation of macrophage responses
Corresponding Author(s)
Other Contributor(s)
Abstract
Chiang Mai (Thailand) experiences severe haze pollution in the dry season (December–April) each year mainly due to local and regional biomass burning (e.g. of agricultural land). A major component of the haze is airborne particulate matter (PM). During haze events, biomass burning is likely to be the dominant source of PM emissions, and at other times emissions from traffic dominate. The hazard of traffic derived PM has been extensively investigated previously but there are uncertainties regarding the toxicity of PM emitted from biomass burning. The toxicity of PM<inf>10</inf> samples collected during and after haze events in Chiang Mai in 2020 was compared in vitro in J774.1 macrophages as they are responsible for the clearance of inhaled particles. Diesel exhaust particles and ultrafine carbon black were included as benchmark particles as they have been commonly used as a surrogate for PM. Cytotoxicity was evaluated 24 h post exposure at concentrations of 3.9–125µg ml<sup>−1</sup>. Cytokine production (tumour necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-1β, macrophage inflammatory protein (MIP-2)) was assessed and cell morphology visualised using light and scanning electron microscopy. The hydrodynamic diameter, zeta potential and endotoxin content of all particles was assessed as well as the metal content of PM samples. All particles induced a concentration dependent decrease in cell viability and increased TNF-α and MIP-2 production. Only PM samples stimulated IL-6 production and only non-haze PM caused IL-1β production. No change in IL-10 production was detected for any particle. PM samples and DEP caused vacuole formation in cells. The concentrations of endotoxin and metals were highest in non-haze PM, which may explain why it induced the greatest inflammatory response. As non-haze PM was more toxic than haze PM, our results indicate that the source of PM emissions can influence its toxic potency and more specifically, that PM emitted from biomass burning may be less toxic than PM emitted from traffic.