Toxicological Responses of alpha-Pinene-Derived Secondary Organic Aerosol and Its Molecular Tracers in Human Lung Cell Lines

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Autores de CIPF

Participantes ajenos a CIPF

  • Khan, F
  • Kwapiszewska, K
  • Zhang, Y
  • Chen, YZ
  • Lambe, AT
  • Kolodziejczyk, A
  • Jalal, N
  • Rudzinski, K
  • Fry, RC
  • Surratt, JD
  • Szmigielski, R

Abstract

Secondary organic aerosol (SOA) is a major component of airborne fine particulate matter (PM2.5) that contributes to adverse human health effects upon inhalation. Atmospheric ozonolysis of alpha-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 alpha-pinene SOA tracers (pinic, pinonic, and 3-methyl-1,2,3-butanetricarboxylic acids) and a full mixture of alpha-pinene SOA in A549 (alveolar epithelial carcinoma) and BEAS-2B (bronchial epithelial normal) lung cell lines. The three aforementioned tracers contributed similar to 57% of the alpha-pinene SOA mass under our experimental conditions. Cellular proliferation, cell viability, and oxidative stress were assessed as toxicological end points. The three alpha-pinene SOA molecular tracers had insignificant responses in both cell types when compared with the alpha-pinene SOA (up to 200 mu g mL(-1)). BEAS-2B cells exposed to 200 mu g mL(-1) of alpha-pinene SOA decreased cellular proliferation to similar to 70% and 44% at 24- and 48-h post exposure, respectively; no changes in A549 cells were observed. The inhibitory concentration-50 (IC50) in BEAS-2B cells was found to be 912 and 230 mu g 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 alpha-pinene SOA. Organic hydroperoxides that were identified in the alpha-pinene SOA samples likely contributed to the ROS and cytotoxicity. This study identifies the potential components of alpha-pinene SOA that likely modulate the oxidative stress response within lung cells and highlights the need to carry out chronic exposure studies on alpha-pinene SOA to elucidate its long-term inhalation exposure effects.

Datos de la publicación

ISSN/ISSNe:
0893-228X, 1520-5010

CHEMICAL RESEARCH IN TOXICOLOGY  AMER CHEMICAL SOC

Tipo:
Article
Páginas:
817-832
PubMed:
33653028

Citas Recibidas en Web of Science: 41

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