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Toxicological Responses of α-Pinene-Derived Secondary Organic Aerosol and Its Molecular Tracers in Human Lung Cell Lines
Author(s) -
Faria Khan,
Karina Kwapiszewska,
Yue Zhang,
Yuzhi Chen,
Andrew T. Lambe,
Agata Kołodziejczyk,
Nasir Jalal,
Krzysztof J. Rudziński,
Alicia MartínezRomero,
Rebecca C. Fry,
Jason D. Surratt,
Rafał Szmigielski
Publication year - 2021
Publication title -
chemical research in toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 156
eISSN - 1520-5010
pISSN - 0893-228X
DOI - 10.1021/acs.chemrestox.0c00409
Subject(s) - pinene , chemistry , oxidative stress , ozonolysis , aerosol , a549 cell , reactive oxygen species , inhalation , environmental chemistry , in vitro , biochemistry , biology , organic chemistry , anatomy
Secondary organic aerosol (SOA) is a major component of airborne fine particulate matter (PM 2.5 ) that contributes to adverse human health effects upon inhalation. Atmospheric ozonolysis of α-pinene, an abundantly emitted monoterpene from terrestrial vegetation, leads to significant global SOA formation; however, its impact on pulmonary pathophysiology remains uncertain. In this study, we quantified an increasing concentration response of three well-established α-pinene SOA tracers (pinic, pinonic, and 3-methyl-1,2,3-butanetricarboxylic acids) and a full mixture of α-pinene SOA in A549 (alveolar epithelial carcinoma) and BEAS-2B (bronchial epithelial normal) lung cell lines. The three aforementioned tracers contributed ∼57% of the α-pinene SOA mass under our experimental conditions. Cellular proliferation, cell viability, and oxidative stress were assessed as toxicological end points. The three α-pinene SOA molecular tracers had insignificant responses in both cell types when compared with the α-pinene SOA (up to 200 μg mL –1 ). BEAS-2B cells exposed to 200 μg mL –1 of α-pinene SOA decreased cellular proliferation to ∼70% and 44% at 24- and 48-h post exposure, respectively; no changes in A549 cells were observed. The inhibitory concentration-50 (IC 50 ) in BEAS-2B cells was found to be 912 and 230 μg mL –1 at 24 and 48 h, respectively. An approximate 4-fold increase in cellular oxidative stress was observed in BEAS-2B cells when compared with untreated cells, suggesting that reactive oxygen species (ROS) buildup resulted in the downstream cytotoxicity following 24 h of exposure to α-pinene SOA. Organic hydroperoxides that were identified in the α-pinene SOA samples likely contributed to the ROS and cytotoxicity. This study identifies the potential components of α-pinene SOA that likely modulate the oxidative stress response within lung cells and highlights the need to carry out chronic exposure studies on α-pinene SOA to elucidate its long-term inhalation exposure effects.

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