Disease types and pathogenic mechanisms induced by PM2.5 in five human systems: An analysis using omics and human disease databases.

Atmospheric fine particulate matter (PM2.5) can harm various systems in the human body. Due to limitations in the current understanding of epidemiology and toxicology, the disease types and pathogenic mechanisms induced by PM2.5 in various human systems remain unclear. In this study, the disease types induced by PM2.5 in the respiratory, circulatory, endocrine, and female and male urogenital systems have been investigated and the pathogenic mechanisms identified at molecular level. The results reveal that PM2.5 is highly likely to induce pulmonary emphysema, reperfusion injury, malignant thyroid neoplasm, ovarian endometriosis, and nephritis in each of the above systems respectively. The most important co-existing gene, cellular component, biological process, molecular function, and pathway in the five systems targeted by PM2.5 are Fos proto-oncogene (FOS), extracellular matrix, urogenital system development, extracellular matrix structural constituent conferring tensile strength, and ferroptosis respectively. Differentially expressed genes that are significantly and uniquely targeted by PM2.5 in each system are BTG2 (respiratory), BIRC5 (circulatory), NFE2L2 (endocrine), TBK1 (female urogenital) and STAT1 (male urogenital). Important disease-related cellular components, biological processes, and molecular functions are specifically induced by PM2.5. For example, response to wounding, blood vessel morphogenesis, body morphogenesis, negative regulation of response to endoplasmic reticulum stress, and response to type I interferon are the top uniquely existing biological processes in each system respectively. PM2.5 mainly acts on key disease-related pathways such as the PD-L1 expression and PD-1 checkpoint pathway in cancer (respiratory), cell cycle (circulatory), apoptosis (endocrine), antigen processing and presentation (female urogenital), and neuroactive ligand-receptor interaction (male urogenital). This study provides a novel analysis strategy for elucidating PM2.5-related disease types and is an important supplement to epidemiological investigation. It clarifies the risks of PM2.5 exposure, elucidates the pathogenic mechanisms, and provides scientific support for promoting the precise prevention and treatment of PM2.5-related diseases.

Source attribution and quantification of atmospheric nickel concentrations in an industrial area in the United Kingdom (UK).

Pontardawe in South Wales, United Kingdom (UK), consistently has the highest concentrations of nickel (Ni) in PM10 in the UK and repeatedly breaches the 20 ng m-3 annual mean EU target value. Several local industries use Ni in their processes. To assist policy makers and regulators in quantifying the relative Ni contributions of these industries and developing appropriate emission reduction approaches, the hourly concentrations of 23 elements were measured using X-ray fluorescence alongside meteorological variables and black carbon during a four-week campaign in November-December 2015. Concentrations of Ni ranged between 0 and 2480 ng m-3 as hourly means. Positive Matrix Factorization (PMF) was used to identify sources contributing to measured elements. Cluster analysis of bivariate polar plots of those factors containing Ni in their profile was further used to quantify the industrial processes contributing to ambient PM10 concentrations. Two sources were identified to contribute to Ni concentrations, stainless-steel (which contributed to 10% of the Ni burden) and the Ni refinery (contributing 90%). From the stainless-steel process, melting activities were responsible for 66% of the stainless-steel factor contribution.

Sources of particulate-matter air pollution and its oxidative potential in Europe.

Particulate matter is a component of ambient air pollution that has been linked to millions of annual premature deaths globally1-3. Assessments of the chronic and acute effects of particulate matter on human health tend to be based on mass concentration, with particle size and composition also thought to play a part4. Oxidative potential has been suggested to be one of the many possible drivers of the acute health effects of particulate matter, but the link remains uncertain5-8. Studies investigating the particulate-matter components that manifest an oxidative activity have yielded conflicting results7. In consequence, there is still much to be learned about the sources of particulate matter that may control the oxidative potential concentration7. Here we use field observations and air-quality modelling to quantify the major primary and secondary sources of particulate matter and of oxidative potential in Europe. We find that secondary inorganic components, crustal material and secondary biogenic organic aerosols control the mass concentration of particulate matter. By contrast, oxidative potential concentration is associated mostly with anthropogenic sources, in particular with fine-mode secondary organic aerosols largely from residential biomass burning and coarse-mode metals from vehicular non-exhaust emissions. Our results suggest that mitigation strategies aimed at reducing the mass concentrations of particulate matter alone may not reduce the oxidative potential concentration. If the oxidative potential can be linked to major health impacts, it may be more effective to control specific sources of particulate matter rather than overall particulate mass.

Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol.

Ambient air pollution is one of the leading five health risks worldwide. One of the most harmful air pollutants is particulate matter (PM), which has different physical characteristics (particle size and number, surface area and morphology) and a highly complex and variable chemical composition. Our goal was first to comparatively assess the effects of exposure to PM regarding cytotoxicity, release of pro-inflammatory mediators and gene expression in human bronchial epithelia (HBE) reflecting normal and compromised health status. Second, we aimed at evaluating the impact of various PM components from anthropogenic and biogenic sources on the cellular responses. Air-liquid interface (ALI) cultures of fully differentiated HBE derived from normal and cystic fibrosis (CF) donor lungs were exposed at the apical cell surface to water-soluble PM filter extracts for 4 h. The particle dose deposited on cells was 0.9-2.5 and 8.8-25.4 µg per cm2 of cell culture area for low and high PM doses, respectively. Both normal and CF HBE show a clear dose-response relationship with increasing cytotoxicity at higher PM concentrations. The concurrently enhanced release of pro-inflammatory mediators at higher PM exposure levels links cytotoxicity to inflammatory processes. Further, the PM exposure deregulates genes involved in oxidative stress and inflammatory pathways leading to an imbalance of the antioxidant system. Moreover, we identify compromised defense against PM in CF epithelia promoting exacerbation and aggravation of disease. We also demonstrate that the adverse health outcome induced by PM exposure in normal and particularly in susceptible bronchial epithelia is magnified by anthropogenic PM components. Thus, including health-relevant PM components in regulatory guidelines will result in substantial human health benefits and improve protection of the vulnerable population.

Cooking and electronic cigarettes leading to large differences between indoor and outdoor particle composition and concentration measured by aerosol mass spectrometry.

We spend about two thirds of our time in private homes where airborne particles of indoor and outdoor origins are present. The negative health effects of exposure to outdoor particles are known. The characteristics of indoor airborne particles, though, are not well understood. This study assesses the differences in chemical composition of PM1 (<1 µm) inside and outside of an occupied Swedish residence in real time with a High-Resolution Time-of-Flight Aerosol Mass Spectrometer (HR-ToF-AMS) and an Aethalometer. The chemical composition and concentration of particles indoors showed large differences compared to outdoors. The average indoor concentration was 15 µg m-3 and was higher than the outdoor 7 µg m-3. Organics dominated indoor particle composition (86% of the total mass) and originated from indoor sources (cooking, e-cigarette vaping). The average indoor to outdoor ratios were 5.5 for organic matter, 1.0 for black carbon, 0.6 for sulphate, 0.1 for nitrate, 0.2 for ammonium and 0.2 for chloride. The occupancy time accounted for 97% of the total measured period. Four factors were identified in the source apportionment of organic particle fraction by applying positive matrix factorization (PMF): two cooking factors, one e-cigarette factor and one outdoor contribution (OOA) organic factor penetrated from outside.

Quantification of the impact of cooking processes on indoor concentrations of volatile organic species and primary and secondary organic aerosols.

Cooking is recognized as an important source of particulate pollution in indoor and outdoor environments. We conducted more than 100 individual experiments to characterize the particulate and non-methane organic gas emissions from various cooking processes, their reaction rates, and their secondary organic aerosol yields. We used this emission data to develop a box model, for simulating the cooking emission concentrations in a typical European home and the indoor gas-phase reactions leading to secondary organic aerosol production. Our results suggest that about half of the indoor primary organic aerosol emission rates can be explained by cooking. Emission rates of larger and unsaturated aldehydes likely are dominated by cooking while the emission rates of terpenes are negligible. We found that cooking dominates the particulate and gas-phase air pollution in non-smoking European households exceeding 1000 µg m-3 . While frying processes are the main driver of aldehyde emissions, terpenes are mostly emitted due to the use of condiments. The secondary aerosol production is negligible with around 2 µg m-3 . Our results further show that ambient cooking organic aerosol concentrations can only be explained by super-polluters like restaurants. The model offers a comprehensive framework for identifying the main parameters controlling indoor gas- and particle-phase concentrations.

Characterization of Gas-Phase Organics Using Proton Transfer Reaction Time-of-Flight Mass Spectrometry: Residential Coal Combustion.

Residential coal combustion is a significant contributor to particulate urban air pollution in Chinese mega cities and some regions in Europe. While the particulate emission factors and the chemical characteristics of the organic and inorganic aerosol from coal combustion have been extensively studied, the chemical composition and nonmethane organic gas (NMOG) emission factors from residential coal combustion are mostly unknown. We conducted 23 individual burns in a traditional Chinese stove used for heating and cooking using five different coals with Chinese origins, characterizing the NMOG emissions using a proton transfer reaction time-of-flight mass spectrometer. The measured emission factors range from 1.5 to 14.1 g/kgcoal for bituminous coals and are below 0.1 g/kgcoal for anthracite coals. The emission factors from the bituminous coals are mostly influenced by the time until the coal is fully ignited. The emissions from the bituminous coals are dominated by aromatic and oxygenated aromatic compounds with a significant contribution of hydrocarbons. The results of this study can help to improve urban air pollution modeling in China and Eastern Europe and can be used to constrain a coal burning factor in ambient gas phase positive matrix factorization studies.

Characterization of Gas-Phase Organics Using Proton Transfer Reaction Time-of-Flight Mass Spectrometry: Aircraft Turbine Engines.

Nonmethane organic gas emissions (NMOGs) from in-service aircraft turbine engines were investigated using a proton transfer reaction time-of-flight mass spectrometer (PTR-ToF-MS) at an engine test facility at Zurich Airport, Switzerland. Experiments consisted of 60 exhaust samples for seven engine types (used in commercial aviation) from two manufacturers at thrust levels ranging from idle to takeoff. Emission indices (EIs) for more than 200 NMOGs were quantified, and the functional group fractions (including acids, carbonyls, aromatics, and aliphatics) were calculated to characterize the exhaust chemical composition at different engine operation modes. Total NMOG emissions were highest at idling with an average EI of 7.8 g/kg fuel and were a factor of ∼40 lower at takeoff thrust. The relative contribution of pure hydrocarbons (particularly aromatics and aliphatics) of the engine exhaust decreased with increasing thrust while the fraction of oxidized compounds, for example, acids and carbonyls increased. Exhaust chemical composition at idle was also affected by engine technology. Older engines emitted a higher fraction of nonoxidized NMOGs compared to newer ones. Idling conditions dominated ground level organic gas emissions. Based on the EI determined here, we estimate that reducing idle emissions could substantially improve air quality near airports.

Wood combustion particles induce adverse effects to normal and diseased airway epithelia.

Residential wood burning is a major source of poorly characterized, deleterious particulate matter, whose composition and toxicity may vary with wood type, burning condition and photochemical age. The causative link between ambient wood particle constituents and observed adverse health effects is currently lacking. Here we investigate the relationship between chemical properties of primary and atmospherically aged wood combustion particles and acute toxicity in human airway epithelial cells. Emissions from a log wood burner were diluted and injected into a smog chamber for photochemical aging. After concentration-enrichment and removal of oxidizing gases, directly emitted and atmospherically aged particles were deposited on cell cultures at the air-liquid interface for 2 hours in an aerosol deposition chamber mimicking physiological conditions in lungs. Cell models were fully differentiated normal and diseased (cystic fibrosis and asthma) human bronchial epithelia (HBE) and the bronchial epithelial cell line BEAS-2B. Cell responses were assessed at 24 hours after aerosol exposure. Atmospherically relevant doses of wood combustion particles significantly increased cell death in all but the asthma cell model. Expression of oxidative stress markers increased in HBE from all donors. Increased cell death and inflammatory responses could not be assigned to a single chemical fraction of the particles. Exposure to primary and aged wood combustion particles caused adverse effects to airway epithelia, apparently induced by several interacting components.

Characterization of Gas-Phase Organics Using Proton Transfer Reaction Time-of-Flight Mass Spectrometry: Cooking Emissions.

Cooking processes produce gaseous and particle emissions that are potentially deleterious to human health. Using a highly controlled experimental setup involving a proton-transfer-reaction time-of-flight mass spectrometer (PTR-ToF-MS), we investigate the emission factors and the detailed chemical composition of gas phase emissions from a broad variety of cooking styles and techniques. A total of 95 experiments were conducted to characterize nonmethane organic gas (NMOG) emissions from boiling, charbroiling, shallow frying, and deep frying of various vegetables and meats, as well as emissions from vegetable oils heated to different temperatures. Emissions from boiling vegetables are dominated by methanol. Significant amounts of dimethyl sulfide are emitted from cruciferous vegetables. Emissions from shallow frying, deep frying and charbroiling are dominated by aldehydes of differing relative composition depending on the oil used. We show that the emission factors of some aldehydes are particularly large which may result in considerable negative impacts on human health in indoor environments. The suitability of some of the aldehydes as tracers for the identification of cooking emissions in ambient air is discussed.

Toxicity of aged gasoline exhaust particles to normal and diseased airway epithelia.

Particulate matter (PM) pollution is a leading cause of premature death, particularly in those with pre-existing lung disease. A causative link between particle properties and adverse health effects remains unestablished mainly due to complex and variable physico-chemical PM parameters. Controlled laboratory experiments are required. Generating atmospherically realistic aerosols and performing cell-exposure studies at relevant particle-doses are challenging. Here we examine gasoline-exhaust particle toxicity from a Euro-5 passenger car in a uniquely realistic exposure scenario, combining a smog chamber simulating atmospheric ageing, an aerosol enrichment system varying particle number concentration independent of particle chemistry, and an aerosol deposition chamber physiologically delivering particles on air-liquid interface (ALI) cultures reproducing normal and susceptible health status. Gasoline-exhaust is an important PM source with largely unknown health effects. We investigated acute responses of fully-differentiated normal, distressed (antibiotics-treated) normal, and cystic fibrosis human bronchial epithelia (HBE), and a proliferating, single-cell type bronchial epithelial cell-line (BEAS-2B). We show that a single, short-term exposure to realistic doses of atmospherically-aged gasoline-exhaust particles impairs epithelial key-defence mechanisms, rendering it more vulnerable to subsequent hazards. We establish dose-response curves at realistic particle-concentration levels. Significant differences between cell models suggest the use of fully-differentiated HBE is most appropriate in future toxicity studies.

Particulate matter from both heavy fuel oil and diesel fuel shipping emissions show strong biological effects on human lung cells at realistic and comparable in vitro exposure conditions.

BACKGROUND: 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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Source Apportionment of Elemental Carbon in Beijing, China: Insights from Radiocarbon and Organic Marker Measurements.

Elemental carbon (EC) or black carbon (BC) in the atmosphere has a strong influence on both climate and human health. In this study, radiocarbon ((14)C) based source apportionment is used to distinguish between fossil fuel and biomass burning sources of EC isolated from aerosol filter samples collected in Beijing from June 2010 to May 2011. The (14)C results demonstrate that EC is consistently dominated by fossil-fuel combustion throughout the whole year with a mean contribution of 79% ± 6% (ranging from 70% to 91%), though EC has a higher mean and peak concentrations in the cold season. The seasonal molecular pattern of hopanes (i.e., a class of organic markers mainly emitted during the combustion of different fossil fuels) indicates that traffic-related emissions are the most important fossil source in the warm period and coal combustion emissions are significantly increased in the cold season. By combining (14)C based source apportionment results and picene (i.e., an organic marker for coal emissions) concentrations, relative contributions from coal (mainly from residential bituminous coal) and vehicle to EC in the cold period were estimated as 25 ± 4% and 50 ± 7%, respectively, whereas the coal combustion contribution was negligible or very small in the warm period.

Aging of biogenic secondary organic aerosol via gas-phase OH radical reactions.

The Multiple Chamber Aerosol Chemical Aging Study (MUCHACHAS) tested the hypothesis that hydroxyl radical (OH) aging significantly increases the concentration of first-generation biogenic secondary organic aerosol (SOA). OH is the dominant atmospheric oxidant, and MUCHACHAS employed environmental chambers of very different designs, using multiple OH sources to explore a range of chemical conditions and potential sources of systematic error. We isolated the effect of OH aging, confirming our hypothesis while observing corresponding changes in SOA properties. The mass increases are consistent with an existing gap between global SOA sources and those predicted in models, and can be described by a mechanism suitable for implementation in those models.