Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex

Hsiao Chi Chuang; Ruei Hao Shie; Chii Hong Lee; Chia Pin Chio; Tzu Hsuen Yuan; Jui Huan Lee; Chang Chuan Chan

doi:10.1007/s11356-020-09644-w

Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex

Hsiao Chi Chuang, Ruei Hao Shie, Chii Hong Lee, Chia Pin Chio, Tzu Hsuen Yuan, Jui Huan Lee, Chang Chuan Chan

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12 Citations (Scopus)

Abstract

Adverse health effects have been observed in nearby residents due to exposure to petrochemical-derived chemicals. The objective of this study was to examine associations of soluble metals with lung and liver toxicity in fine particulate matter (PM_2.5) in the vicinity of a petrochemical complex. PM_2.5 was collected in the vicinity of a petrochemical complex of Mailiao Township (Yunlin County, Taiwan) to investigate lung and liver toxicity in BALB/c mice. The PM_2.5 concentration was 30.2 ± 11.2 μg/m³, and the PM_2.5 was clustered in major local emissions (19.1 μg/m³) and minor local emissions (14.1 μg/m³) using a k-means clustering model. The PM_2.5 (50 and 150 μg/kg) and PM_2.5-equivalent soluble nickel (Ni), vanadium (V), and lead (Pb) concentrations were intratracheally instilled into BALB/c mice. PM_2.5 and V significantly decreased the tidal volume after exposure (p < 0.05). The peak expiratory flow (PEF) and peak inspiratory flow (PIF)/PEF ratio were significantly altered by 150 μg/kg V (p < 0.05). V and Pb significantly increased total protein and lactate dehydrogenase (LDH) levels in bronchoalveolar lavage fluid (BALF) (p < 0.05). Interleukin (IL)-6 in BALF significantly increased after exposure to Pb (p < 0.05) accompanied by lung inflammatory infiltration. PM_2.5 and Pb significantly increased levels of 8-isoprostane (p < 0.05). The level of caspase-3 activity significantly increased after exposure to Pb (p < 0.05). LDH in the liver was significantly increased by PM_2.5 (p < 0.05). 8-Isoprostane in the liver was significantly increased by PM_2.5 and Pb (p < 0.05). IL-6 in the liver was significantly increased by PM_2.5, Ni, V, and Pb after exposure (p < 0.05), accompanied by liver inflammatory infiltration. Our results demonstrated that V in PM_2.5 was associated with an increase in 8-isoprostane for all emissions and major local petrochemical emissions. In conclusion, V contributes to in vivo liver toxicity induced by PM_2.5 in the vicinity of a petrochemical complex.

Original language	English
Pages (from-to)	34442-34452
Number of pages	11
Journal	Environmental Science and Pollution Research
Volume	27
Issue number	27
DOIs	https://doi.org/10.1007/s11356-020-09644-w
Publication status	Published - Sept 1 2020

Keywords

Air pollution
Inflammation
Liver
Lung
Oxidative stress

ASJC Scopus subject areas

Environmental Chemistry
Pollution
Health, Toxicology and Mutagenesis

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10.1007/s11356-020-09644-w

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@article{02a77c8f7f2b43739387f801e3b65e89,

title = "Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex",

abstract = "Adverse health effects have been observed in nearby residents due to exposure to petrochemical-derived chemicals. The objective of this study was to examine associations of soluble metals with lung and liver toxicity in fine particulate matter (PM2.5) in the vicinity of a petrochemical complex. PM2.5 was collected in the vicinity of a petrochemical complex of Mailiao Township (Yunlin County, Taiwan) to investigate lung and liver toxicity in BALB/c mice. The PM2.5 concentration was 30.2 ± 11.2 μg/m3, and the PM2.5 was clustered in major local emissions (19.1 μg/m3) and minor local emissions (14.1 μg/m3) using a k-means clustering model. The PM2.5 (50 and 150 μg/kg) and PM2.5-equivalent soluble nickel (Ni), vanadium (V), and lead (Pb) concentrations were intratracheally instilled into BALB/c mice. PM2.5 and V significantly decreased the tidal volume after exposure (p < 0.05). The peak expiratory flow (PEF) and peak inspiratory flow (PIF)/PEF ratio were significantly altered by 150 μg/kg V (p < 0.05). V and Pb significantly increased total protein and lactate dehydrogenase (LDH) levels in bronchoalveolar lavage fluid (BALF) (p < 0.05). Interleukin (IL)-6 in BALF significantly increased after exposure to Pb (p < 0.05) accompanied by lung inflammatory infiltration. PM2.5 and Pb significantly increased levels of 8-isoprostane (p < 0.05). The level of caspase-3 activity significantly increased after exposure to Pb (p < 0.05). LDH in the liver was significantly increased by PM2.5 (p < 0.05). 8-Isoprostane in the liver was significantly increased by PM2.5 and Pb (p < 0.05). IL-6 in the liver was significantly increased by PM2.5, Ni, V, and Pb after exposure (p < 0.05), accompanied by liver inflammatory infiltration. Our results demonstrated that V in PM2.5 was associated with an increase in 8-isoprostane for all emissions and major local petrochemical emissions. In conclusion, V contributes to in vivo liver toxicity induced by PM2.5 in the vicinity of a petrochemical complex.",

keywords = "Air pollution, Inflammation, Liver, Lung, Oxidative stress",

author = "Chuang, {Hsiao Chi} and Shie, {Ruei Hao} and Lee, {Chii Hong} and Chio, {Chia Pin} and Yuan, {Tzu Hsuen} and Lee, {Jui Huan} and Chan, {Chang Chuan}",

note = "Funding Information: The authors wish to thank Ms. Yi-Syuan Lin, Mr. Guan-Che Wu, and Mrs. Yu-Hua Liao for technical assistance with this research. This paper was financially supported by the “Innovation and Policy Center for Population Health and Sustainable Environment (Population Health Research Center, PHRC), College of Public Health, National Taiwan University” from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan. Funding Information: This study was funded by the Ministry of Science and Technology of Taiwan (MOST104-2621-M-038-002-MY3). Acknowledgments Publisher Copyright: {\textcopyright} 2020, Springer-Verlag GmbH Germany, part of Springer Nature.",

year = "2020",

month = sep,

day = "1",

doi = "10.1007/s11356-020-09644-w",

language = "English",

volume = "27",

pages = "34442--34452",

journal = "Environmental Science and Pollution Research",

issn = "0944-1344",

publisher = "Springer",

number = "27",

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TY - JOUR

T1 - Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex

AU - Chuang, Hsiao Chi

AU - Shie, Ruei Hao

AU - Lee, Chii Hong

AU - Chio, Chia Pin

AU - Yuan, Tzu Hsuen

AU - Lee, Jui Huan

AU - Chan, Chang Chuan

N1 - Funding Information: The authors wish to thank Ms. Yi-Syuan Lin, Mr. Guan-Che Wu, and Mrs. Yu-Hua Liao for technical assistance with this research. This paper was financially supported by the “Innovation and Policy Center for Population Health and Sustainable Environment (Population Health Research Center, PHRC), College of Public Health, National Taiwan University” from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan. Funding Information: This study was funded by the Ministry of Science and Technology of Taiwan (MOST104-2621-M-038-002-MY3). Acknowledgments Publisher Copyright: © 2020, Springer-Verlag GmbH Germany, part of Springer Nature.

PY - 2020/9/1

Y1 - 2020/9/1

N2 - Adverse health effects have been observed in nearby residents due to exposure to petrochemical-derived chemicals. The objective of this study was to examine associations of soluble metals with lung and liver toxicity in fine particulate matter (PM2.5) in the vicinity of a petrochemical complex. PM2.5 was collected in the vicinity of a petrochemical complex of Mailiao Township (Yunlin County, Taiwan) to investigate lung and liver toxicity in BALB/c mice. The PM2.5 concentration was 30.2 ± 11.2 μg/m3, and the PM2.5 was clustered in major local emissions (19.1 μg/m3) and minor local emissions (14.1 μg/m3) using a k-means clustering model. The PM2.5 (50 and 150 μg/kg) and PM2.5-equivalent soluble nickel (Ni), vanadium (V), and lead (Pb) concentrations were intratracheally instilled into BALB/c mice. PM2.5 and V significantly decreased the tidal volume after exposure (p < 0.05). The peak expiratory flow (PEF) and peak inspiratory flow (PIF)/PEF ratio were significantly altered by 150 μg/kg V (p < 0.05). V and Pb significantly increased total protein and lactate dehydrogenase (LDH) levels in bronchoalveolar lavage fluid (BALF) (p < 0.05). Interleukin (IL)-6 in BALF significantly increased after exposure to Pb (p < 0.05) accompanied by lung inflammatory infiltration. PM2.5 and Pb significantly increased levels of 8-isoprostane (p < 0.05). The level of caspase-3 activity significantly increased after exposure to Pb (p < 0.05). LDH in the liver was significantly increased by PM2.5 (p < 0.05). 8-Isoprostane in the liver was significantly increased by PM2.5 and Pb (p < 0.05). IL-6 in the liver was significantly increased by PM2.5, Ni, V, and Pb after exposure (p < 0.05), accompanied by liver inflammatory infiltration. Our results demonstrated that V in PM2.5 was associated with an increase in 8-isoprostane for all emissions and major local petrochemical emissions. In conclusion, V contributes to in vivo liver toxicity induced by PM2.5 in the vicinity of a petrochemical complex.

AB - Adverse health effects have been observed in nearby residents due to exposure to petrochemical-derived chemicals. The objective of this study was to examine associations of soluble metals with lung and liver toxicity in fine particulate matter (PM2.5) in the vicinity of a petrochemical complex. PM2.5 was collected in the vicinity of a petrochemical complex of Mailiao Township (Yunlin County, Taiwan) to investigate lung and liver toxicity in BALB/c mice. The PM2.5 concentration was 30.2 ± 11.2 μg/m3, and the PM2.5 was clustered in major local emissions (19.1 μg/m3) and minor local emissions (14.1 μg/m3) using a k-means clustering model. The PM2.5 (50 and 150 μg/kg) and PM2.5-equivalent soluble nickel (Ni), vanadium (V), and lead (Pb) concentrations were intratracheally instilled into BALB/c mice. PM2.5 and V significantly decreased the tidal volume after exposure (p < 0.05). The peak expiratory flow (PEF) and peak inspiratory flow (PIF)/PEF ratio were significantly altered by 150 μg/kg V (p < 0.05). V and Pb significantly increased total protein and lactate dehydrogenase (LDH) levels in bronchoalveolar lavage fluid (BALF) (p < 0.05). Interleukin (IL)-6 in BALF significantly increased after exposure to Pb (p < 0.05) accompanied by lung inflammatory infiltration. PM2.5 and Pb significantly increased levels of 8-isoprostane (p < 0.05). The level of caspase-3 activity significantly increased after exposure to Pb (p < 0.05). LDH in the liver was significantly increased by PM2.5 (p < 0.05). 8-Isoprostane in the liver was significantly increased by PM2.5 and Pb (p < 0.05). IL-6 in the liver was significantly increased by PM2.5, Ni, V, and Pb after exposure (p < 0.05), accompanied by liver inflammatory infiltration. Our results demonstrated that V in PM2.5 was associated with an increase in 8-isoprostane for all emissions and major local petrochemical emissions. In conclusion, V contributes to in vivo liver toxicity induced by PM2.5 in the vicinity of a petrochemical complex.

KW - Air pollution

KW - Inflammation

KW - Liver

KW - Lung

KW - Oxidative stress

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Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex

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