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Exposure to biomass-burning particulate matter (PM) is associated with various adverse health effects, including respiratory and cardiovascular conditions, cancer, and systemic effects. Multiple mechanisms underlying PM toxicity components derived from biomass burning elicit harmful effects, such as reactive oxygen species (ROS) generation, inflammation, genotoxicity, and tissue-specific damage. Specific compounds or families of compounds present in biomass-burning PM, such as polyaromatic hydrocarbons (PAHs) and their derivatives, have been identified as key contributors to the observed health effects. Their roles in oxidative stress, DNA damage, and cell death have been elucidated in various organs, such as the lungs, liver, kidneys, and brain, providing valuable insights into the systemic biological influence of biomass-burning-related diseases. Current knowledge of the impact of biomass burning highlights the imperative need for further research to understand the health implications of this environmental challenge and the importance of mitigating the adverse effects of increased exposure to biomass-burning pollution to protect the well-being of exposed populations worldwide. This review focuses on the crucial roles of oxidative stress and inflammation in mediating health effects, triggered by exposure to biomass-burning aerosols. It examines various aspects of the health-related impacts of biomass-burning emissions, particularly those from PM components. The review highlights the health consequences on exposed populations, emphasizing specific biochemical responses, contributions to toxicity mechanisms, tissue-specific effects, and the families of compounds responsible for these effects. [ABSTRACT FROM AUTHOR]

Background: Secondary organic aerosols (SOAs) formed from anthropogenic or biogenic gaseous precursors in the atmosphere substantially contribute to the ambient fine particulate matter [PM [less than or equal to] 2.5 [micro]m in aerodynamic diameter (P[M.sub.2.5])] burden, which has been associated with adverse human health effects. However, there is only limited evidence on their differential toxicological impact. OBJECTIVES: We aimed to discriminate toxicological effects of aerosols generated by atmospheric aging on combustion soot particles (SPs) of gaseous biogenic ([beta]-pinene) or anthropogenic (naphthalene) precursors in two different lung cell models exposed at the air-liquid interface (ALI). Methods: Mono- or cocultures of lung epithelial cells (A549) and endothelial cells (EA.hy926) were exposed at the ALI for 4 h to different aerosol concentrations of a photochemically aged mixture of primary combustion SP and [beta]-pinene ([SOA.sub.[beta]PIN]-SP) or naphthalene ([SOA.sub.NAP]-SP). The internally mixed soot/SOA particles were comprehensively characterized in terms of their physical and chemical properties. We conducted toxicity tests to determine cytotoxicity, intracellular oxidative stress, primary and secondary genotoxicity, as well as inflammatory and angiogenic effects. Results: We observed considerable toxicity-related outcomes in cells treated with either SOA type. Greater adverse effects were measured for [SOA.sub.NAP]-SP compared with [SOA.sub.[beta]PIN]-SP in both cell models, whereas the nano-sized soot cores alone showed only minor effects. At the functional level, we found that [SOA.sub.NAP]-SP augmented the secretion of malondialdehyde and interleukin-8 and may have induced the activation of endothelial cells in the coculture system. This activation was confirmed by comet assay, suggesting secondary genotoxicity and greater angiogenic potential. Chemical characterization of PM revealed distinct qualitative differences in the composition of the two secondary aerosol types. Discussion: In this study using A549 and EA.hy926 cells exposed at ALI, SOA compounds had greater toxicity than primary SPs. Photochemical aging of naphthalene was associated with the formation of more oxidized, more aromatic SOAs with a higher oxidative potential and toxicity compared with [beta]-pinene. Thus, we conclude that the influence of atmospheric chemistry on the chemical PM composition plays a crucial role for the adverse health outcome of emissions. https://doi.org/10.1289/EHP9413, Introduction Over the past decades, the impact of ambient fine particulate matter [PM [less than or equal to] 2.5 [micro]m (P[M.sub.2.5])] on the global burden of disease has gained substantial [...]

Objective: Surgical removal of third molars is often associated with complications. The aim of the present study was to analyze the incidence of complications following extraction of third molars relative to the risk factors. Method and Materials: This retrospective study included 463 patients who had mandibular third molar extraction (performed by a single surgeon, DSA) in the years 2001 to 2011. In total, 665 mandibular third molars were extracted. The average patient's age was 29 ± 11.30 years, median 26 years, and the patient age ranged from 13 to 75 years. Patients' records were obtained for medical/general data. Results: The overall prevalence of postsurgical complications was 17%. Dry sockets showed the highest incidence (11.6%). Partially impacted teeth showed the highest incidence of complications (67.3%). Cigarette smoking correlated with increased complications and dry sockets, and complications were more prevalent on the left side (62.8%). Conclusion: Complications after mandibular third molar extraction increase with age, level of impaction, side of extraction, and cigarette smoking. [ABSTRACT FROM AUTHOR]

It is being suggested that particle-bound or particle-induced reactive oxygen species (ROS), which significantly contribute to the oxidative potential (OP) of aerosol particles, are a promising metric linking aerosol compositions to toxicity and adverse health effects. However, accurate ROS quantification remains challenging due to the reactive and short-lived nature of many ROS components and the lack of appropriate analytical methods for a reliable quantification. Consequently, it remains difficult to gauge their impact on human health, especially to identify how aerosol particle sources and atmospheric processes drive particle-bound ROS formation in a real-world urban environment. In this study, using a novel online particle-bound ROS instrument (OPROSI), we comprehensively characterized and compared the formation of ROS in secondary organic aerosols (SOA) generated from organic compounds that represent anthropogenic (naphthalene, SOANAP) and biogenic (β-pinene, SOAβPIN) precursors. The SOA mass was condensed onto soot particles (SP) under varied atmospherically relevant conditions (photochemical aging and humidity). We systematically analysed the ability of the aqueous extracts of the two aerosol types (SOANAP-SP and SOAβPIN-SP) to induce ROS production and OP. We further investigated cytotoxicity and cellular ROS production after exposing human lung epithelial cell cultures (A549) to extracts of the two aerosols. A significant finding of this study is that more than 90% of all ROS components in both SOA types have a short lifetime, highlighting the need to develop online instruments for a meaningful quantification of ROS. Our results also show that photochemical aging promotes particle-bound ROS production and enhances the OP of the aerosols. Compared to SOAβPIN-SP, SOANAP-SP elicited a higher acellular and cellular ROS production, a higher OP and a lower cell viability. These consistent results between chemical-based and biological-based analyses indicate that particle-bound ROS quantification could be a feasible metric to predict aerosol particle toxicity and adverse human effects. Moreover, the cellular ROS production caused by SOA exposure not only depends on aerosol type, but is also affected by exposure dose, highlighting a need to mimic the process of particle deposition onto lung cells and their interactions as realistically as possible to avoid unknown biases. [ABSTRACT FROM AUTHOR]