Dataset Information

The effect of ambient PM2.5 exposure on survival of lung cancer patients after lobectomy.

ABSTRACT: Exposure to fine particulate matter (PM2.5) is linked to lung cancer incidence and mortality. However, the impact of PM2.5 exposure on lung cancer patients after lobectomy, which remains the primary treatment for early-stage lung cancer, is unknown. Therefore, we investigated the correlation between PM2.5 exposure and the survival of lung cancer patients after lobectomy. This study included 3,327 patients with lung cancer who underwent lobectomy procedures. We converted residential addresses into coordinates and estimated individual patients' daily PM2.5 and O3 exposure levels. A Cox multivariate regression model was used to analyze the specific monthly association between PM2.5 exposure and lung cancer survival. Every 10 μg/m3 increase in monthly PM2.5 concentration in the first and second months after lobectomy increased the risk of death (hazard ratio [HR]: 1.043, 95% confidence interval [CI]: 1.019-1.067 and HR: 1.036, 95% CI: 1.013-1.060, respectively). Non-smokers, younger patients, and patients with longer hospitalization durations had worse survival rates when exposed to greater concentrations of PM2.5. High postoperative PM2.5 exposure immediately after lobectomy reduced the survival of patients with lung cancer. Patients living in areas with high PM2.5 should be offered the opportunity to transfer to areas with better air quality after undergoing lobectomies, to prolong their survival times.

SUBMITTER: Liu C

PROVIDER: S-EPMC9990243 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

The effect of ambient PM2.5 exposure on survival of lung cancer patients after lobectomy.

Liu Changpeng C Yang Dongjian D Liu Yuxi Y Piao Heng H Zhang Tao T Li Xi X Zhao Erjiang E Zhang Di D Zheng Yan Y Tang Xiance X

Environmental health : a global access science source 20230307 1

Exposure to fine particulate matter (PM2.5) is linked to lung cancer incidence and mortality. However, the impact of PM2.5 exposure on lung cancer patients after lobectomy, which remains the primary treatment for early-stage lung cancer, is unknown. Therefore, we investigated the correlation between PM2.5 exposure and the survival of lung cancer patients after lobectomy. This study included 3,327 patients with lung cancer who underwent lobectomy procedures. We co ...[more]

PMID: 36879322

Similar Datasets

Project description:Previous studies have shown that long-term exposure to fine particulate matter (PM2.5) increases the morbidity and mortality of pulmonary diseases such as asthma, chronic obstructive pulmonary disease and pulmonary emphysema. Oxidative stress and inflammation play key roles in pulmonary damage caused by PM2.5. Nuclear factor erythroid 2-related factor 2 (Nrf2) could regulate the expression of antioxidant and anti-inflammatory genes and is pivotal for protection against PM2.5-induced oxidative stress. In this study, a real-ambient exposure system was constructed with the outdoor ambient air in north China. Wild-type (WT) and Nrf2-/- (KO) mice were exposed to the real-ambient system for six weeks. After PM2.5 exposure, our data showed that the levels of inflammatory factors and malondialdehyde were significantly increased in WT and KO mice. Moreover, the lung function and pathological phenotype of the WT mice were altered but there was no obvious change in the Nrf2-/- mice. To further explore the potential molecular mechanisms, we performed RNA-sequencing. The RNA-sequence analysis results showed that the CYP450 pathway in the first ten pathways of KEGG was related to the metabolism of PM2.5. In WT and KO mice, the expression of CYP2E1 in the CYP450 pathway showed opposite trends after PM2.5 exposure. The data showed that the expression of the CYP2E1 gene in WT-PM mice increased while it decreased in KO-PM; the expression of the CYP2E1 protein showed a similar trend. CYP2E1 is primarily distributed in the endoplasmic reticulum (ER) where it could metabolize various exogenous substances attached to PM2.5 and produce highly toxic oxidation products closely related to ER stress. Consistently, the expression level of GRP94, a biomarker of ER stress, was increased in WT mice and reduced in KO mice under PM2.5 exposure. Persistent ER stress is a mechanism that causes lung damage under PM2.5 exposure. Nrf2 facilitates lung injury during PM2.5 exposure and CYP2E1 metabolism is involved in this process.

Project description:BackgroundStudies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.MethodsA total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β HSD), 17β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).ResultsExposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.ConclusionConcentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.

Project description:BackgroundThe metabolomic signatures of short- and long-term exposure to PM2.5 have been reported and linked to inflammation and oxidative stress. However, little is known about the relative contribution of the specific PM2.5 species (hence sources) that drive these metabolomic signatures.ObjectivesWe aimed to determine the relative contribution of the different species of PM2.5 exposure to the perturbed metabolic pathways related to changes in the plasma metabolome.MethodsWe performed mass-spectrometry based metabolomic profiling of plasma samples among men from the Normative Aging Study to identify metabolic pathways associated with PM2.5 species. The exposure windows included short-term (one, seven-, and thirty-day moving average) and long-term (one year moving average). We used linear mixed-effect regression with subject-specific intercepts while simultaneously adjusting for PM2.5, NO2, O3, temperature, relative humidity, and covariates and correcting for multiple testing. We also used independent component analysis (ICA) to examine the relative contribution of patterns of PM2.5 species.ResultsBetween 2000 and 2016, 456 men provided 648 blood samples, in which 1158 metabolites were quantified. We chose 305 metabolites for the short-term and 288 metabolites for the long-term exposure in this analysis that were significantly associated (p-value < 0.01) with PM2.5 to include in our PM2.5 species analysis. On average, men were 75.0 years old and their body mass index was 27.7 kg/m2. Only 3% were current smokers. In the adjusted models, ultrafine particles (UFPs) were the most significant species of short-term PM2.5 exposure followed by nickel, vanadium, potassium, silicon, and aluminum. Black carbon, vanadium, zinc, nickel, iron, copper, and selenium were the significant species of long-term PM2.5 exposure. We identified several metabolic pathways perturbed with PM2.5 species including glycerophospholipid, sphingolipid, and glutathione. These pathways are involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair. Results were overlapped with the ICA.ConclusionsWe identified several significant perturbed plasma metabolites and metabolic pathways associated with exposure to PM2.5 species. These species are associated with traffic, fuel oil, and wood smoke. This is the largest study to report a metabolomic signature of PM2.5 species' exposure and the first to use ICA.

Project description:It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM2.5 (particulate matter with aerodynamic diameter 2.5 μm or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM2.5 in the United States (US) and COVID-19 basic reproduction ratio R0- a dimensionless epidemic measure of the rapidity of disease spread through a population. We inferred state-level R0 values using a state-of-the-art susceptible, exposed, infected, and recovered (SEIR) model initialized with COVID-19 epidemiological data corresponding to the period March 2-April 30. This period was characterized by a rapid surge in COVID-19 cases across the US states, implementation of strict social distancing measures, and a significant drop in outdoor air pollution. We find that an increase of 1 μg/m3 in PM2.5 levels below current national ambient air quality standards associates with an increase of 0.25 in R0 (95% CI: 0.048-0.447). A 10% increase in secondary inorganic composition, sulfate-nitrate-ammonium, in PM2.5 associates with ≈10% increase in R0 by 0.22 (95% CI: 0.083-0.352), and presence of black carbon (soot) in the ambient environment moderates this relationship. We considered several potential confounding factors in our analysis, including gaseous air pollutants and socio-economical and meteorological conditions. Our results underscore two policy implications - first, regulatory standards need to be better guided by exploring the concentration-response relationships near the lower end of the PM2.5 air quality distribution; and second, pollution regulations need to be continually enforced for combustion emissions that largely determine secondary inorganic aerosol formation.

Project description:Background: Ambient particulate matter is a public health concern in East Asia as it contributes to a growing number of all-cause and cancer deaths. This study aimed to estimate lung cancer death attributable to ambient particulate matter (PM) < 2.5 μm (PM2.5) in East Asia countries. Methods: The attributable death rates of lung cancer were estimated based on the calculation of population attributable fraction. We performed joinpoint regression analysis and age-period-cohort (APC) model to estimate temporal trends of the attributable death to PM2.5. Results: In 2019, PM2.5 was estimated to have caused 42.2% (nearly 0.13 million) of lung cancer deaths in East Asia men. During 1990-2019, the increase in age-standardized death rates of lung cancer attributable to PM2.5 was highest in China, which increased by 3.50% in males and 3.71% in females. The death rate caused by PM2.5 also significantly increased in the Democratic People's Republic of Korea (2.16% in males; 3.06% in females). Joinpoint analysis showed that the rates generally increased in younger and older people in both the Democratic People's Republic of Korea and Mongolia, while it only increased in elderly people in other countries'. Age effect from APC analysis demonstrated the risk of lung cancer death attributable to PM2.5 generally increased from young to old age. Period effect indicated that from 1994-1998 to 2019-2023 period risk continuously increased by 1.77, 1.68, and 1.72 times in China, the Democratic People's Republic of Korea, and Japan, respectively. The period risk decreased from 1999 to 2009 and subsequently increased from 2009 to 2019 in both the Republic of Korea and Mongolia. Conclusions: The death rate of lung cancer attributable to PM2.5 is increasing in the Democratic People's Republic of Korea, Mongolia, and China. In East Asia, China is facing the highest attributable death rate in recent decades. The period effect suggested a remarkably increased risk of lung cancer death caused by PM2.5 in China, the Democratic People's Republic of Korea, and Japan during the long-term period. It is recommended that the governments of these countries should continuously concentrate on particulate matter pollution governance and improvement.

Dataset Information

The effect of ambient PM2.5 exposure on survival of lung cancer patients after lobectomy.

Publications

The effect of ambient PM<sub>2.5</sub> exposure on survival of lung cancer patients after lobectomy.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets