Air quality, health impacts and burden of disease due to air pollution (PM10, PM2.5, NO2 and O3): Application of AirQ+ model to the Camp de Tarragona County (Catalonia, Spain).
空气质量、健康影响和空气污染造成的疾病负担 (PM10 、PM2.5 、NO2 和O3): AirQ + 模型在塔拉戈纳营地 (西班牙加泰罗尼亚) 的应用。
- 作者列表："Rovira J","Domingo JL","Schuhmacher M
:The purpose of this study was to assess the impact to human health of air pollutants, through the integration of different technics: data statistics (spatial and temporal trends), population attributable fraction using AIRQ+ model developed by the WHO, and burden of disease using Disability-Adjusted Life Years (DALYs). The levels of SO2, NO, NO2, O3, H2S, benzene, PM10, PM2.5, CO, benzo(a)pyrene and metals, obtained between 2005 and 2017 from the air quality monitoring network across Camp de Tarragona County, were temporally and spatially determined. Health impacts were evaluated using the AIRQ+ model. Finally, the burden of disease was assessed through the calculation of Years of Lost life (YLL) and Years Lost due to Disability (YLD). In general terms, air quality was good according to European quality standards, but it did not fulfil the WHO guidelines, especially for O3, PM10 and PM2.5. Several decreasing (NO, NO2, SO2, PM10 and benzene) and an increasing (O3) temporal trend were found. Correlation between unemployment rate and air pollutant levels was found, pointing that the economic crisis (2008-2014) was a factor influencing the air pollutant levels. Reduction of air pollutant levels (PM2.5) to WHO guidelines in the Camp de Tarragona County would decrease the adult mortality between 23 and 297 cases per year, which means between 0.5 and 7% of all mortality in the area. In this County, for lung cancer, ischemic heart disease, stroke, and chronic obstructive pulmonary disease due to levels of PM2.5 above the WHO threshold limits, DAYLs were 240 years. This means around 80 DALYs for 100,000 persons every year -between 2005 and 2017. Population attributable fraction (PAF) and burden of disease (DALYs) methodologies are suitable tools for regional and national policymakers, who must take decisions to prevent and to control air pollution and to analyse the cost-effectiveness of interventions.
: 本研究的目的是评估空气污染物对人类健康的影响，通过整合不同的技术: 数据统计 (空间和时间趋势)，使用WHO开发的AIRQ + 模型的人群归因分数，以及使用伤残调整生命年 (DALYs) 的疾病负担。SO2 、NO、NO2 、O3 、H2S、苯、PM10 、PM2.5 、CO、苯并 (a) 芘及金属含量，从 2005 年至 2017 年间从塔拉戈纳营地的空气质量监测网络中获得，在时间和空间上进行确定。使用AIRQ + 模型评估健康影响。最后，通过计算生命损失年数 (YLL) 和残疾损失年数 (YLD) 来评估疾病负担。总体而言，根据欧洲质量标准，空气质量良好，但不符合世卫组织指南，特别是O3 、PM10 和pm2.5。结果表明，NO、NO2 、SO2 、PM10 和苯呈下降趋势，O3 呈上升趋势。发现失业率与空气污染物水平之间存在相关性，指出经济危机 (2008-2014) 是影响空气污染物水平的一个因素。根据世卫组织在塔拉戈纳营地的指导方针，降低空气污染物水平 (PM2.5) 将使成人死亡率每年降低 23 至 297 例，这意味着该地区所有死亡率的 0.5 至 7%。在这个县，由于PM2.5 水平超过世卫组织的阈值限制，肺癌，缺血性心脏病，中风和慢性阻塞性肺病的天数为 240 亿年。这意味着每年为 100,000 人提供大约 80 个DALYs，介于 2005 和 2017 之间。人口归因分数 (PAF) 和疾病负担 (DALYs) 方法是区域和国家决策者的合适工具，世卫组织必须作出预防和控制空气污染的决定，并分析干预措施的成本效益。
METHODS::Pulmonary artery sling is a rare congenital anomaly of the origin and course of the left pulmonary artery. Patients with this condition typically present with respiratory failure in young infancy, and asymptomatic cases are uncommon. We describe the case of an adult patient with a lung adenocarcinoma of the right upper lobe, extending into the hilum and superior mediastinum, and with a previously unknown pulmonary artery sling anomaly. The local invasiveness of the tumor and the peculiar vascular anatomy contributed to a unique surgical scenario, wherein multiple reconstructive procedures were required.
METHODS::Patients with idiopathic pulmonary fibrosis (IPF) have higher risk of developing lung cancer, for example, squamous cell carcinoma (SCC), and show poor prognosis, while the molecular basis has not been fully investigated. Here we conducted DNA methylome analysis of lung SCC using 20 SCC samples with/without IPF, and noncancerous lung tissue samples from smokers/nonsmokers, using Infinium HumanMethylation 450K array. SCC was clustered into low- and high-methylation epigenotypes by hierarchical clustering analysis. Genes hypermethylated in SCC significantly included genes targeted by polycomb repressive complex in embryonic stem cells, and genes associated with Gene Ontology terms, for example, "transcription" and "cell adhesion," while genes hypermethylated specifically in high-methylation subgroup significantly included genes associated with "negative regulation of growth." Low-methylation subgroup significantly correlated with IPF (78%, vs. 17% in high-methylation subgroup, p = 0.04), and the correlation was validated by additional Infinium analysis of SCC samples (n = 44 in total), and data from The Cancer Genome Atlas (n = 390). The correlation between low-methylation subgroup and IPF was further validated by quantitative methylation analysis of marker genes commonly hypermethylated in SCC (HOXA2, HOXA9 and PCDHGB6), and markers specifically hypermethylated in high-methylation subgroup (DLEC1, CFTR, MT1M, CRIP3 and ALDH7A1) in 77 SCC cases using pyrosequencing (p = 0.003). Furthermore, low-methylation epigenotype significantly correlated with poorer prognosis among all SCC patients, or among patients without IPF. Multivariate analysis showed that low-methylation epigenotype is an independent predictor of poor prognosis. These may suggest that lung SCC could be stratified into molecular subtypes with distinct prognosis, and low-methylation lung SCC that significantly correlates with IPF shows unfavorable outcome.
METHODS::The role of Fyn-related kinase (FRK) in malignant tumors remains controversial. Our study investigated the function of FRK in lung cancer. Immunohistochemistry staining and generating a knockout of FRK by CRISPR/Cas9 in H1299 (FRK-KO-H1299) cells were strategies used to explore the role of FRK. Immunohistochemistry staining indicated that FRK expression was elevated in 223 lung cancer tissues compared to 26 distant normal lung tissues. FRK contributed to poor survival status in lung cancer patients and acted as a predictor for poor prognosis of lung cancer. Knockout of FRK by CRISPR/Cas9 markedly inhibited proliferation, invasion, colony formation and epithelial-mesenchymal transition (EMT) process in the lung cancer cell line H1299. Further exploration indicated that FRK-KO damaged the stemness phenotype of H1299 by inhibiting CD44 and CD133 expression. Seahorse detection and a U-13 C flux assay revealed that FRK-KO induced metabolism reprogramming by inhibiting the Warburg effect and changing the energy type in H1299 cells. Epidermal growth factor stimulation recovered the expression of FRK and biological functions, metabolic reprogramming and stemness phenotype of H1299 cells. FRK plays an oncogenic role in lung cancer cells via a novel regulation mechanism of enhancing the stemness of H1299 cells by inducing metabolism reprogramming, which finally promotes EMT and metastasis. Our study also indicates that FRK could be used as a potential therapeutic target for drug development.