During winter 2013, extremely high concentrations (i.e., 4–20 times higher than the World Health Organization guideline) of PM_2.5 (particulate matter with an aerodynamic diameter < 2.5 μm) mass concentrations (24 h samples) were found in four major cities in China including Xi'an, Beijing, Shanghai and Guangzhou. Statistical analysis of a combined data set from elemental carbon (EC), organic carbon (OC), ¹⁴C and biomass-burning marker measurements using Latin hypercube sampling allowed a quantitative source apportionment of carbonaceous aerosols. Based on ¹⁴C measurements of EC fractions (six samples each city), we found that fossil emissions from coal combustion and vehicle exhaust dominated EC with a mean contribution of 75 ± 8% across all sites. The remaining 25 ± 8% was exclusively attributed to biomass combustion, consistent with the measurements of biomass-burning markers such as anhydrosugars (levoglucosan and mannosan) and water-soluble potassium (K⁺). With a combination of the levoglucosan-to-mannosan and levoglucosan-to-K⁺ ratios, the major source of biomass burning in winter in China is suggested to be combustion of crop residues. The contribution of fossil sources to OC was highest in Beijing (58 ± 5%) and decreased from Shanghai (49 ± 2%) to Xi'an (38 ± 3%) and Guangzhou (35 ± 7%). Generally, a larger fraction of fossil OC was from secondary origins than primary sources for all sites. Non-fossil sources accounted on average for 55 ± 10 and 48 ± 9% of OC and total carbon (TC), respectively, which suggests that non-fossil emissions were very important contributors of urban carbonaceous aerosols in China. The primary biomass-burning emissions accounted for 40 ± 8, 48 ± 18, 53 ± 4 and 65 ± 26% of non-fossil OC for Xi'an, Beijing, Shanghai and Guangzhou, respectively. Other non-fossil sources excluding primary biomass burning were mainly attributed to formation of secondary organic carbon (SOC) from non-fossil precursors such as biomass-burning emissions. For each site, we also compared samples from moderately to heavily polluted days according to particulate matter mass. Despite a significant increase of the absolute mass concentrations of primary emissions from both fossil and non-fossil sources during the heavily polluted events, their relative contribution to TC was even decreased, whereas the portion of SOC was consistently increased at all sites. This observation indicates that SOC was an important fraction in the increment of carbonaceous aerosols during the haze episode in China.

Ship engine emissions are important with regard to lung and cardiovascular diseases especially in coastal regions worldwide. Known cellular responses to combustion particles include oxidative stress and inflammatory signalling. To provide a molecular link between the chemical and physical characteristics of ship emission particles and the cellular responses they elicit and to identify potentially harmful fractions in shipping emission aerosols. Through an air-liquid interface exposure system, we exposed human lung cells under realistic in vitro conditions to exhaust fumes from a ship engine running on either common heavy fuel oil (HFO) or cleaner-burning diesel fuel (DF). Advanced chemical analyses of the exhaust aerosols were combined with transcriptional, proteomic and metabolomic profiling including isotope labelling methods to characterise the lung cell responses. The HFO emissions contained high concentrations of toxic compounds such as metals and polycyclic aromatic hydrocarbon, and were higher in particle mass. These compounds were lower in DF emissions, which in turn had higher concentrations of elemental carbon (“soot”). Common cellular reactions included cellular stress responses and endocytosis. Reactions to HFO emissions were dominated by oxidative stress and inflammatory responses, whereas DF emissions induced generally a broader biological response than HFO emissions and affected essential cellular pathways such as energy metabolism, protein synthesis, and chromatin modification. Despite a lower content of known toxic compounds, combustion particles from the clean shipping fuel DF influenced several essential pathways of lung cell metabolism more strongly than particles from the unrefined fuel HFO. This might be attributable to a higher soot content in DF. Thus the role of diesel soot, which is a known carcinogen in acute air pollution-induced health effects should be further investigated. For the use of HFO and DF we recommend a reduction of carbonaceous soot in the ship emissions by implementation of filtration devices.