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Fire risk assessment is a crucial step in effective fire control, playing an important role in reducing fire losses. It has remained a significant topic in the field of fire safety. To explore the research hotspots and frontier trends in fire risk assessment and to understand its macroscopic development trajectory, a sample of 1596 papers from 1976 to 2023, extracted from the Web of Science (WoS) database, was utilized to create a knowledge map. The study employed bibliometric methods, visual analysis, and content analysis to uncover the research pulse and hotspots in the field, offering insights into its future development. The findings indicate that research in fire risk assessment has demonstrated continuous growth over the past 50 years. China and the United States are the dominant research forces in the field, while India and Australia show potential as new drivers for development. Expert groups have formed in this field, with intra-institutional cooperation being the primary focus, while inter-institutional collaboration remains limited. The research outcomes exhibit multidisciplinary crossovers, exerting a significant impact on various disciplinary domains. The research hotspots primarily revolve around investigating fire and explosion accidents, assessing the vulnerability of fire subjects, and identifying potential fire hazards. The application of artificial intelligence technology is identified as a pivotal tool for future development. However, to achieve substantial progress, it is important to enhance the importance accorded to fire risk assessment, foster multinational and cross-institutional cooperation, and prioritize research innovation. [ABSTRACT FROM AUTHOR]

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (commonly known as NNK) is one of the most prevalent and potent pulmonary carcinogens in tobacco products that increases the human lung cancer risk. Kava has the potential to reduce NNK and tobacco smoke-induced lung cancer risk by enhancing urinary excretion of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, the major metabolite of NNK) and thus reducing NNK-induced DNA damage. In this study, we quantified N -glucuronidated NNAL (NNAL- N -gluc), O -glucuronidated NNAL (NNAL- O -gluc), and free NNAL in the urine samples collected before and after 1-week kava dietary supplementation. The results showed that kava increased both NNAL-N-glucuronidation and O-glucuronidation. Since NNAL-N-glucuronidation is dominantly catalyzed by UGT2B10, its representative single-nucleotide polymorphisms (SNPs) were analyzed among the clinical trial participants. Individuals with any of the four analyzed SNPs appear to have a reduced basal capacity in NNAL-N-glucuronidation. Among these individuals, kava also resulted in a smaller extent of increases in NNAL-N-glucuronidation, suggesting that participants with those UGT 2 B 10 SNPs may not benefit as much from kava with respect to enhancing NNAL-N-glucuronidation. In summary, our results provide further evidence that kava enhances NNAL urinary detoxification via an increase in both N-glucuronidation and O-glucuronidation. UGT2B10 genetic status has not only the potential to predict the basal capacity of the participants in NNAL-N-glucuronidation but also potentially the extent of kava benefits.

Tobacco smoke remains a serious global issue, resulting in serious health complications, contributing to the onsets of numerous preventive diseases, and imposing significant financial burdens. Despite regulatory policies and cessation measures aimed at curbing its usage, novel interventions are urgently needed for effective damage reduction. Our preclinical and pilot clinical studies showed that AB-free kava has the potential to reduce tobacco smoke-induced lung cancer risk, mitigate tobacco dependence, and reduce tobacco use. To understand the scope of its benefits in damage reduction and potential limitations, this study evaluated the effects of AB-free kava on a panel of health indicators in mice exposed to 2 - 4 weeks of daily tobacco smoke exposure. Our comprehensive assessments included global transcriptional profiling of the lung and liver tissues, analysis of lung inflammation, evaluation of lung function, exploration of tobacco nicotine withdrawal, and characterization of the causal PKA signaling pathway. As expected, Tobacco smoke exposure perturbed a wide range of biological processes and compromised multiple functions in mice. Remarkably, AB-free kava demonstrated the ability to globally mitigate tobacco smoke-induced deficits at the molecular and functional levels with promising safety profiles, offering a unique promise to mitigate tobacco smoke-related health damages. Further pre-clinical evaluation and clinical translation are warranted to fully harness the potential of AB-free kava in combating tobacco smoke-related harms.