Chemical composition and bioreactivity of PM_2.5 during 2013 haze events in China

Highlights

• Significant increases of sulfate, nitrate and ammonium were observed during episodes.

• High contributions of biomass burning emissions to organic carbon (OC) were estimated in this study.

• BJ PM_2.5 samples has the highest bioreactivity although PM_2.5 levels are not the highest.

• The OC, urea and levoglucosan are associated with oxidative-inflammatory responses.

Abstract

Chemical composition and bioreactivity of PM_2.5 samples collected from Beijing (BJ), Xi'an (XA), Xiamen (XM) and Hong Kong (HK) in China during haze events were characterized. PM_2.5 mass concentrations in BJ, XA, XM and HK in the episodes were found to be 258 ± 100 μg m⁻³, 233 ± 52 μg m⁻³, 46 ± 9 μg m⁻³ and 48 ± 13 μg m⁻³, respectively. Significant increase of sulfate, nitrate and ammonium concentrations in northern cities were observed. High contributions of biomass burning emissions to organic carbon (OC) in northern cities were estimated in this study implying frequent biomass burning during the haze periods. The urea concentrations in PM_2.5 were 1855 ± 755 ng m⁻³ (BJ), 1124 ± 243 ng m⁻³ (XA), 543 ± 104 ng m⁻³ (XM) and 363 ± 61 ng m⁻³ (HK) suggesting higher or close to upper limits compared to other regions in the world. Dose-dependent alterations in oxidative potential, IL-6, IFN-γ and TNF-α levels were also investigated. The oxidative potential levels are BJ > XM > XA > HK, whereas levels of IL-6, IFN-γ and TNF-α were BJ > XA > XM > HK. The sulfate, nitrate, ammonium, OC, urea and levoglucosan are associated with oxidative-inflammatory responses. These experimental results are crucial for the policymakers to implement cost-effective abatement strategies for improving air quality.

Introduction

Very recent studies report that more than 2 million premature deaths around the world each year are associated with anthropogenic PM_2.5 (particulate matter with an aerodynamic diameter <2.5 μm) related cardiopulmonary diseases and lung cancer (Silva et al., 2013). Numerous epidemiological and toxicological studies have also shown correlation between exposure to particulate matter (PM) and adverse health effects (Brunekreef and Holgate, 2002, Pope et al., 2002, Pun et al., 2014). The underlying mechanism of particle-induced health effects is believed to be driven by the production of reactive oxygen species (ROS, e.g. superoxide (O²⁻), hydrogen peroxide (H₂O₂), and hydroxyl radical (OH)) and the interaction of PM with epithelial cells and macrophages in the lung environment (Li et al., 2003, Nel, 2005). Adverse human health effects occur when an overproduction of ROS impacts on the body's anti-oxidative defenses (oxidative stress, OS) leading to cell dysfunction, inflammation and cardio-pulmonary disease (BeruBe et al., 2007). The oxidative stress can activate signaling pathways leading to the release of pro-inflammatory mediators (e.g. interleukin 6 (IL-6), interleukins 8 (IL-8), tumor necrosis factor α (TNF-α) and interferon γ (IFN-γ)) (Mitschik et al., 2008). Previous studies have focused on airborne particles with an aerodynamic diameter smaller than 2.5 μm (PM_2.5) because these fine particles can penetrate into the airways of the respiratory tract, reaching the alveoli and diffusing to other extrapulmonary target organs (Semmler et al., 2004). It is found that the size of particles is an important parameter in inducing cardiovascular and respiratory effects (Boldo et al., 2011). The ultrafine and fine particles are more potent than coarse particles on per mass basis (Cho et al., 2005, Ntziachristos et al., 2007). Besides particle size, there is growing evidence that the chemical composition of particles is also an important factor mediating cellular oxidative stress (Daher et al., 2014, Yang et al., 2014).

The PM_2.5 concentrations observed in Chinese urban air are often one to two orders of magnitude higher than those observed in urban areas in the US and European countries (Huang et al., 2014b). Despite such high level of particulate pollution, studies related to particle toxicities are still very scarce in China (Deng et al., 2013, Huang et al., 2014a, Wei et al., 2011, Xu and Zhang, 2004). Especially, the toxicity of particles during haze events (visibility range is less than 10 km, RH < 80%) is not clear. The objective of this study was to investigate the toxicity of particles collected during severe haze events in China during January–February 2013. These haze events received worldwide media attention, with daily PM_2.5 concentration higher than 700 μg m⁻³. The PM_2.5 samples were collected in four Chinese megacities with the total mass, organic and elemental carbon (OC and EC) content being analyzed in order to determine the PM_2.5 cytotoxicity. Certain organic compounds such as levoglucosan, water soluble organic nitrogen (WSON) species (e.g. amino acids, amines and urea) were also measured in the aerosol samples. WSON consists of a broad array of nitrogen-containing organic species that are derived from both anthropogenic and natural emissions (Cornell et al., 2003, Neff et al., 2002). There are concerns about toxicity of organic nitrogen compounds such as nitrophenols (Natangelo et al., 1999), nitrated polycyclic aromatic hydrocarbons and other N-containing combustion products or industrial emissions which are present in the atmosphere (Albinet et al., 2008, Cheng et al., 2006) and how all of these compounds have effects on human health. Therefore, the PM_2.5 toxicity was tested in vitro in human alveolar epithelial A549 cells that are considered as the relevant target cells. PM biological activities were characterized by measuring the expression of a panel of biomarkers. The IL-6, TNF-α and IFN-γ were further used as effective biomarkers for investigating PM exposure to the occurrence of oxidative stress and pro-inflammatory responses. The above biological results were combined with chemical analysis to elucidate the difference in aerosol bioactivities during haze episodes in four Chinese megacities.