Haijie Tong

Chemical exposure-response relationship between air pollutants and reactive oxygen species in the human respiratory tract.

Air pollution can cause oxidative stress and adverse health effects such as asthma and other respiratory diseases, but the underlying chemical processes are not well characterized. Here we present chemical exposure-response relations between ambient concentrations of air pollutants and the production rates and concentrations of reactive oxygen species (ROS) in the epithelial lining fluid (ELF) of the human respiratory tract. In highly polluted environments, fine particulate matter (PM2.5) containing redox-active transition metals, quinones, and secondary organic aerosols can increase ROS concentrations in the ELF to levels characteristic for respiratory diseases. Ambient ozone readily saturates the ELF and can enhance oxidative stress by depleting antioxidants and surfactants. Chemical exposure-response relations provide a quantitative basis for assessing the relative importance of specific air pollutants in different regions of the world, showing that aerosol-induced epithelial ROS levels in polluted megacity air can be several orders of magnitude higher than in pristine rainforest air.

Release of free amino acids upon oxidation of peptides and proteins by hydroxyl radicals

Hydroxyl radical-induced oxidation of proteins and peptides can lead to the cleavage of the peptide, leading to a release of fragments. Here, we used high-performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS) and pre-column online ortho-phthalaldehyde (OPA) derivatization-based amino acid analysis by HPLC with diode array detection and fluorescence detection to identify and quantify free amino acids released upon oxidation of proteins and peptides by hydroxyl radicals. Bovine serum albumin (BSA), ovalbumin (OVA) as model proteins, and synthetic tripeptides (comprised of varying compositions of the amino acids Gly, Ala, Ser, and Met) were used for reactions with hydroxyl radicals, which were generated by the Fenton reaction of iron ions and hydrogen peroxide. The molar yields of free glycine, aspartic acid, asparagine, and alanine per peptide or protein varied between 4 and 55%. For protein oxidation reactions, the molar yields of Gly (∼32–55% for BSA, ∼10–21% for OVA) were substantially higher than those for the other identified amino acids (∼5–12% for BSA, ∼4–6% for OVA). Upon oxidation of tripeptides with Gly in C-terminal, mid-chain, or N-terminal positions, Gly was preferentially released when it was located at the C-terminal site. Overall, we observe evidence for a site-selective formation of free amino acids in the OH radical-induced oxidation of peptides and proteins, which may be due to a reaction pathway involving nitrogen-centered radicals.

Aerosol Health Effects from Molecular to Global Scales

Poor air quality is globally the largest environmental health risk. Epidemiological studies have uncovered clear relationships of gaseous pollutants and particulate matter (PM) with adverse health outcomes, including mortality by cardiovascular and respiratory diseases. Studies of health impacts by aerosols are highly multidisciplinary with a broad range of scales in space and time. We assess recent advances and future challenges regarding aerosol effects on health from molecular to global scales through epidemiological studies, field measurements, health-related properties of PM, and multiphase interactions of oxidants and PM upon respiratory deposition. Global modeling combined with epidemiological exposure-response functions indicates that ambient air pollution causes more than four million premature deaths per year. Epidemiological studies usually refer to PM mass concentrations, but some health effects may relate to specific constituents such as bioaerosols, polycyclic aromatic compounds, and transition metals. Various analytical techniques and cellular and molecular assays are applied to assess the redox activity of PM and the formation of reactive oxygen species. Multiphase chemical interactions of lung antioxidants with atmospheric pollutants are crucial to the mechanistic and molecular understanding of oxidative stress upon respiratory deposition. The role of distinct PM components in health impacts and mortality needs to be clarified by integrated research on various spatiotemporal scales for better evaluation and mitigation of aerosol effects on public health in the Anthropocene.

Reactive Oxygen Species Formed by Secondary Organic Aerosols in Water and Surrogate Lung Fluid

Reactive oxygen species (ROS) play a central role in adverse health effects of air pollutants. Respiratory deposition of fine air particulate matter can lead to the formation of ROS in epithelial lining fluid, potentially causing oxidative stress and inflammation. Secondary organic aerosols (SOA) account for a large fraction of fine particulate matter, but their role in adverse health effects is unclear. Here, we quantify and compare the ROS yields and oxidative potential of isoprene, β-pinene, and naphthalene SOA in water and surrogate lung fluid (SLF). In pure water, isoprene and β-pinene SOA were found to produce mainly OH and organic radicals, whereas naphthalene SOA produced mainly H2O2 and O2•-. The total molar yields of ROS of isoprene and β-pinene SOA were 11.8% and 8.2% in water and decreased to 8.5% and 5.2% in SLF, which can be attributed to ROS removal by lung antioxidants. A positive correlation between the total peroxide concentration and ROS yield suggests that organic (hydro)peroxides may play an important role in ROS formation from biogenic SOA. The total molar ROS yields of naphthalene SOA was 1.7% in water and increased to 11.3% in SLF. This strong increase is likely due to redox reaction cycles involving environmentally persistent free radicals (EPFR) or semiquinones, antioxidants, and oxygen, which may promote the formation of H2O2 and the adverse health effects of anthropogenic SOA from aromatic precursors.