1,374 results on '"LONG-TERM EXPOSURE"'
Search Results
2. Long-term exposure to air pollution and lower respiratory infections in a large population-based adult cohort in Catalonia
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Alari, Anna, Ranzani, Otavio, Milà, Carles, Olmos, Sergio, Basagaña, Xavier, Dadvand, Payam, Duarte-Salles, Talita, Nieuwenhuijsen, Mark, and Tonne, Cathryn
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- 2025
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3. Exposure to submicron particulate matter and long-term survival: Cross-cohort analysis of 3 Chinese national surveys
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Peng, Minjin, Li, Yachen, Wu, Jing, Zeng, Yi, Yao, Yao, and Zhang, Yunquan
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- 2025
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4. Preexisting multimorbidity predicts greater mortality risks related to long-term PM2.5 exposure
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Tang, Ziqing, Ku, Po-Wen, Xia, Yang, Chen, Li-Jung, and Zhang, Yunquan
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- 2025
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5. Safe or unsafe: Role of exposure time and interactions between volatile organic compounds in mixtures
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Li, Xiaoying and Li, Zhenhai
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- 2025
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6. Transcriptome-centric approach to the derivation of adverse outcome pathway networks of vascular dysfunction after long-term low-level exposure of human endothelial cells to dibutyl phthalate
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Stanic, Bojana, Kokai, Dunja, Opacic, Marija, Pogrmic-Majkic, Kristina, and Andric, Nebojsa
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- 2024
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7. Fine particulate matter components associated with exacerbated depressive symptoms among middle-aged and older adults in China
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Wu, Haisheng, Liu, Jiaqi, Conway, Erica, Zhan, Na, Zheng, Lishuang, Sun, Shengzhi, and Li, Jinhui
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- 2024
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8. Coarse particulate air pollution and mortality in a multidrug-resistant tuberculosis cohort
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Feng, Huiying, Ge, Erjia, Grubic, Nicholas, Liu, Xin, Zhang, Hui, Sun, Qiang, Wei, Xiaolin, Zhou, Fangjing, Huang, Shanshan, Chen, Yuhui, Guo, Huixin, Li, Jianwei, Zhang, Kai, Luo, Ming, and Chen, Liang
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- 2024
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9. Untargeted lipidomics uncover hepatic lipid signatures induced by long-term exposure to polystyrene microplastics in vivo
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Ma, Yiming, Zeng, Yao, Sun, Mengqi, Ding, Ruiyang, Yu, Yang, and Duan, Junchao
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- 2024
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10. Multigenerational effects of glyphosate-based herbicide and emamectin benzoate insecticide on the reproduction and gene expression of the copepod Pseudodiaptomus annandalei (Sewell, 1919)
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Kong, Lam, Pan, Yen-Ju, and Hwang, Jiang-Shiou
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- 2024
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11. Exposure to ambient air pollution and elevated blood levels of gamma-glutamyl transferase in a large Austrian cohort
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Wirsching, Jan, Nagel, Gabriele, Tsai, Ming-Yi, de Hoogh, Kees, Jaensch, Andrea, Anwander, Bernhard, Sokhi, Ranjeet S., Ulmer, Hanno, Zitt, Emanuel, Concin, Hans, Brunekreef, Bert, Hoek, Gerard, and Weinmayr, Gudrun
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- 2023
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12. Ambient ozone exposure and depression among middle-aged and older adults: Nationwide longitudinal evidence in China
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Yuan, Yang, Wang, Kai, Wang, Zhen, Zheng, Hao, Ma, Zongwei, Liu, Riyang, Hu, Kejia, Yang, Zhiming, and Zhang, Yunquan
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- 2023
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13. Long-term exposure to elemental components of fine particulate matter and all-natural and cause-specific mortality in a Danish nationwide administrative cohort study
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So, Rina, Chen, Jie, Stafoggia, Massimo, de Hoogh, Kees, Katsouyanni, Klea, Vienneau, Danielle, Samoli, Evangelia, Rodopoulou, Sophia, Loft, Steffen, Lim, Youn-Hee, Westendorp, Rudi G.J., Amini, Heresh, Cole-Hunter, Thomas, Bergmann, Marie, Shahri, Seyed Mahmood Taghavi, Zhang, Jiawei, Maric, Matija, Mortensen, Laust H., Bauwelinck, Mariska, Klompmaker, Jochem O., Atkinson, Richard W., Janssen, Nicole A.H., Oftedal, Bente, Renzi, Matteo, Forastiere, Francesco, Strak, Maciek, Brunekreef, Bert, Hoek, Gerard, and Andersen, Zorana J.
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- 2023
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14. Long-term exposure to ambient air pollutants and their interaction with physical activity on insomnia: A prospective cohort study
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Lin, Yijuan, Gao, Yinyan, Sun, Xuemei, Wang, Jiali, Ye, Shuzi, Wu, Irene X.Y., and Xiao, Fang
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- 2023
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15. Long-term exposure to ambient air pollutants and age-related macular degeneration in middle-aged and older adults
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Ju, Min Jae, Kim, Junghoon, Park, Sung Kyun, Kim, Dong Hyun, and Choi, Yoon-Hyeong
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- 2022
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16. Organophosphate pesticide exposure and risk of SARS-CoV-2 infection
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Lopez, Luis, Kogut, Katie, Rauch, Stephen, Gunier, Robert B, Wong, Marcus P, Harris, Eva, Deardorff, Julianna, Eskenazi, Brenda, and Harley, Kim G
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Environmental Sciences ,Pollution and Contamination ,Emerging Infectious Diseases ,Prevention ,Rural Health ,Health Disparities ,Pediatric ,Clinical Research ,Coronaviruses ,Endocrine Disruptors ,Infectious Diseases ,4.1 Discovery and preclinical testing of markers and technologies ,2.2 Factors relating to the physical environment ,2.1 Biological and endogenous factors ,Good Health and Well Being ,Humans ,COVID-19 ,Female ,Young Adult ,Adolescent ,Environmental Exposure ,Pesticides ,Male ,SARS-CoV-2 ,California ,Pregnancy ,Adult ,Antibodies ,Viral ,Biomarkers ,Organophosphates ,Longitudinal Studies ,Organophosphate pesticides ,Immune system ,Long-term exposure ,Chemical Sciences ,Biological Sciences ,Toxicology ,Biological sciences ,Chemical sciences ,Environmental sciences - Abstract
Several studies have reported immune modulation by organophosphate (OP) pesticides, but the relationship between OP exposure and SARS-CoV-2 infection is yet to be studied. We used two different measures of OP pesticide exposure (urinary biomarkers (N = 154) and residential proximity to OP applications (N = 292)) to examine the association of early-childhood and lifetime exposure to OPs and risk of infection of SARS-CoV-2 using antibody data. Our study population consisted of young adults (ages 18-21 years) from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) Study, a longitudinal cohort of families from a California agricultural region. Urinary biomarkers reflected exposure from in utero to age 5 years. Residential proximity reflected exposures between in utero and age 16 years. SARS-CoV-2 antibodies in blood samples collected between June 2022 and January 2023 were detected via two enzyme linked immunosorbent assays, each designed to bind to different SARS-CoV-2 antigens. We performed logistic regression for each measure of pesticide exposure, adjusting for covariates from demographic data and self-reported questionnaire data. We found increased odds of SARS-CoV-2 infection among participants with higher urinary biomarkers of OPs in utero (OR = 1.94, 95% CI: 0.71, 5,58) and from age 0-5 (OR = 1.90, 95% CI: 0.54, 6.95).
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- 2024
17. Interactive Effects of Long-term Exposure to Air Pollutants on SARS-CoV-2 Infection and Severity: A Northern Italian Population-based Cohort Study.
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Veronesi, Giovanni, De Matteis, Sara, Silibello, Camillo, Giusti, Emanuele M., Ageno, Walter, and Ferrario, Marco M.
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Background: We examined interactions, to our knowledge not yet explored, between long-term exposures to particulate matter (PM
10 ) with nitrogen dioxide (NO2 ) and ozone (O3 ) on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectivity and severity. Methods: We followed 709,864 adult residents of Varese Province from 1 February 2020 until the first positive test, COVID-19 hospitalization, or death, up to 31 December 2020. We estimated residential annual means of PM10 , NO2 , and O3 in 2019 from chemical transport and random-forest models. We estimated the interactive effects of pollutants with urbanicity on SARS-CoV-2 infectivity, hospitalization, and mortality endpoints using Cox regression models adjusted for socio-demographic factors and comorbidities, and additional cases due to interactions using Poisson models. Results: In total 41,065 individuals were infected, 5203 were hospitalized and 1543 died from COVID-19 during follow-up. Mean PM10 was 1.6 times higher and NO2 2.6 times higher than WHO limits, with wide gradients between urban and nonurban areas. PM10 and NO2 were positively associated with SARS-CoV-2 infectivity and mortality, and PM10 with hospitalizations in urban areas. Interaction analyses estimated that the effect of PM10 (per 3.5 µg/m3 ) on infectivity was strongest in urban areas [hazard ratio (HR) = 1.12; 95% CI =1.09, 1.16], corresponding to 854 additional cases per 100,000 person-years, and in areas at high NO2 co-exposure (HR = 1.15; 1.08, 1.22). At higher levels of PM10 co-exposure, the protective association of O3 reversed (HR =1.32, 1.17, 1.49), yielding 278 additional cases per µg/m3 increase in O3 . We estimated similar interactive effects for severity endpoints. Conclusions: We estimate that interactive effects between pollutants exacerbated the burden of the SARS-CoV-2 pandemic in urban areas. Video Abstract EDE.0000000000001792video1.mp4 Kaltura [ABSTRACT FROM AUTHOR]- Published
- 2025
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18. The association between different timeframes of air pollution exposure and COVID-19 incidence, morbidity and mortality in German counties in 2020.
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Hermanns, Sophie, von Schneidemesser, Erika, Caseiro, Alexandre, and Koch, Susanne
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AIR pollutants , *COVID-19 , *COVID-19 pandemic , *PUBLIC health , *PARTICULATE matter , *AIR pollution - Abstract
Background: Ambient air pollution is a known risk factor for several chronic health conditions, including pulmonary dysfunction. In recent years, studies have shown a positive association between exposure to air pollutants and the incidence, morbidity, and mortality of a COVID-19 infection, however the time period for which air pollution exposure is most relevant for the COVID-19 outcome is still not defined. The aim of this study was to analyze the difference in association when varying the time period of air pollution exposure considered on COVID-19 infection within the same cohort during the first wave of the pandemic in 2020. Methods: We conducted a cross-sectional study analyzing the association between long- (10- and 2-years) and short-term (28 days, 7 days, and 2 days) exposure to NO2 and PM2.5 on SARS-CoV-2 incidence, morbidity, and mortality at the level of county during the first outbreak of the pandemic in spring 2020. Health data were extracted from the German national public health institute (Robert-Koch-Institute) and from the German Interdisciplinary Association for Intensive Care and Emergency Medicine. Air pollution data were taken from the APExpose dataset (version 2.0). We used negative binomial models, including adjustment for risk factors (age, sex, days since first COVID-19 case, population density, socio-economic and health parameters). Results: We found that PM2.5 and NO2 exposure 28 days before COVID-19 infection had the highest association with infection, morbidity as well as mortality, as compared to long-term or short-term (2 or 7 days) air pollutant exposure. A 1 μg/m3 increase in PM2.5 was associated with a 31.7% increase in incidence, a 20.6% need for ICU treatment, a 23.1% need for mechanical ventilation, and a 55.3% increase in mortality; an increase of 1 μg/m3 of NO2 was associated with an increase for all outcomes by 25.2 – 29.4%. Conclusions: Our findings show a positive association between PM2.5 and NO2 exposure and the clinical course of a SARS-CoV2 infection, with the strongest association to 28 days of exposure to air pollution. This finding provides an indication as to the primary underlying pathophysiology, and can therefore help to improve the resilience of societies by implementing adequate measures to reduce the air pollutant impact on health outcomes. Trial registration: Not applicable. [ABSTRACT FROM AUTHOR]
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- 2024
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19. Assessment of Respiratory Health Impacts of PM 2.5 by AirQ+ Software in a Sub-Saharan African Urban Setting.
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Ngutuka Kinzunga, Mélanie, Westervelt, Daniel M., Matondo Masisa, Daniel, Bangelesa, Freddy, Kasereka Isevulambire, Paulson, Tangou Tabou, Thierry, Kabengele Obel, Benoit, Kiyombo Mbela, Guillaume, and Kayembe Ntumba, Jean Marie
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AIR pollution , *RESPIRATORY infections , *HEALTH impact assessment , *CHRONIC obstructive pulmonary disease , *AIR quality - Abstract
Background: Ambient air pollution remains a major risk factor for population health worldwide. The impact of PM2.5 air pollution is underestimated in sub-Saharan Africa due to a lack of epidemiological studies. AirQ+ is proposed to reduce these inequalities in research. The aim of this study is to assess, by AirQ+, the impact of prolonged exposure to PM2.5 on respiratory health in Kinshasa in 2019, and to estimate the health benefits of reducing this air pollution. Methods: Population and mortality data were obtained from the Institut National de la Statistique and the Institut de Métrologie et d'Évaluation en santé, respectively. PM2.5 concentrations were measured using PurpleAir PA-II-SD sensors, and average annual concentration was 43.5 µg/m3 in 2019. AirQ+ was used to estimate the health effect attributable to PM2.5 in adults aged over 25 in Kinshasa. Results: In 2019, the proportion of deaths attributable to PM2.5 air pollution was 30.72% for ALRI, 26.55% for COPD and 24.32% for lung cancers. Each 10% reduction in current PM2.5 levels would prevent 1093 deaths (from all causes) per year in Kinshasa. Life expectancy would increase by 4.7 years (CI 3.5–5.3) if the WHO threshold of 5 mg/m3 were respected. Conclusions: The results of this study highlight the major respiratory public health problem associated with air pollution by fine particles in Kinshasa. AirQ+ was used to assess the impact of prolonged exposure to PM2.5 and respiratory deaths among adults in Kinshasa and revealed that this number of deaths could be avoided by improving air quality. [ABSTRACT FROM AUTHOR]
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- 2024
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20. Long-term exposure to PM2.5 and mortality: a national health insurance cohort study.
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Moon, Jeongmin, Kim, Ejin, Jang, Hyemin, Song, Insung, Kwon, Dohoon, Kang, Cinoo, Oh, Jieun, Park, Jinah, Kim, Ayoung, Choi, Moonjung, Cha, Yaerin, Kim, Ho, and Lee, Whanhee
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NATIONAL health insurance , *ESTIMATION bias , *PARTICULATE matter , *MOVING average process , *COHORT analysis - Abstract
Background Previous studies with large data have been widely reported that exposure to fine particulate matter (PM2.5) is associated with all-cause mortality; however, most of these studies adopted ecological time-series designs or have included limited study areas or individuals residing in well-monitored urban areas. However, nationwide cohort studies including cause-specific mortalities with different age groups were sparse. Therefore, this study examined the association between PM2.5 and cause-specific mortality in South Korea using the nationwide cohort. Methods A longitudinal cohort with 187 917 National Health Insurance Service-National Sample Cohort participants aged 50–79 years in enrolment between 2002 and 2019 was used. Annual average PM2.5 was collected from a machine learning-based ensemble model (a test R 2 = 0.87) as an exposure. We performed a time-varying Cox regression model to examine the association between long-term PM2.5 exposure and mortality. To reduce the potential estimation bias, we adopted generalized propensity score weighting method. Results The association with long-term PM2.5 (2-year moving average) was prominent in mortalities related to diabetes mellitus [hazard ratio (HR): 1.03 (95% CI: 1.01, 1.06)], circulatory diseases [HR: 1.02 (95% CI: 1.00, 1.03)] and cancer [HR: 1.01 (95% CI: 1.00, 1.02)]. Meanwhile, circulatory-related mortalities were associated with a longer PM2.5 exposure period (1 or 2-year lags), whereas respiratory-related mortalities were associated with current-year PM2.5 exposure. In addition, the association with PM2.5 was more evident in people aged 50–64 years than in people aged 65–79 years, especially in heart failure-related deaths. Conclusions This study identified the hypothesis that long-term exposure to PM2.5 is associated with mortality, and the association might be different by causes of death. Our result highlights a novel vulnerable population: the middle-aged population with risk factors related to heart failure. [ABSTRACT FROM AUTHOR]
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- 2024
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21. Traffic-related air pollution and Parkinson's disease in central California
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Kwon, Dayoon, Paul, Kimberly C, Yu, Yu, Zhang, Keren, Folle, Aline D, Wu, Jun, Bronstein, Jeff M, and Ritz, Beate
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Environmental Sciences ,Pollution and Contamination ,Neurodegenerative ,Neurosciences ,Brain Disorders ,Climate-Related Exposures and Conditions ,Clinical Research ,Social Determinants of Health ,Parkinson's Disease ,Health Disparities ,2.2 Factors relating to the physical environment ,2.1 Biological and endogenous factors ,Neurological ,Good Health and Well Being ,Sustainable Cities and Communities ,Humans ,Air Pollutants ,Traffic-Related Pollution ,Environmental Exposure ,Parkinson Disease ,Air Pollution ,Particulate Matter ,Dust ,California ,Parkinson's disease ,Air pollution ,Long-term exposure ,Case-control study ,Chemical Sciences ,Biological Sciences ,Toxicology ,Biological sciences ,Chemical sciences ,Environmental sciences - Abstract
BackgroundPrior studies suggested that air pollution exposure may increase the risk of Parkinson's Disease (PD). We investigated the long-term impacts of traffic-related and multiple sources of particulate air pollution on PD in central California.MethodsOur case-control analysis included 761 PD patients and 910 population controls. We assessed exposure at residential and occupational locations from 1981 to 2016, estimating annual average carbon monoxide (CO) concentrations - a traffic pollution marker - based on the California Line Source Dispersion Model, version 4. Additionally, particulate matter (PM2.5) concentrations were based on a nationwide geospatial chemical transport model. Exposures were assessed as 10-year averages with a 5-year lag time prior to a PD diagnosis for cases and an interview date for controls, subsequently categorized into tertiles. Logistic regression models were used, adjusting for various factors.ResultsTraffic-related CO was associated with an increased odds ratio for PD at residences (OR for T3 vs. T1: 1.58; 95% CI: 1.20, 2.10; p-trend = 0.02) and workplaces (OR for T3 vs. T1: 1.91; 95% CI: 1.22, 3.00; p-trend
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- 2024
22. Long-Term Exposure of Fresh and Aged Nano Zinc Oxide Promotes Hepatocellular Carcinoma Malignancy by Up-Regulating Claudin-2
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Yu N, Su M, Wang J, Liu Y, Yang J, Zhang J, and Wang M
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nano zinc oxide ,environmental transformation of nps ,long-term exposure ,malignant progression of tumors ,cldn2 ,Medicine (General) ,R5-920 - Abstract
Na Yu,1,* Mingqin Su,1,* Juan Wang,2 Yakun Liu,1 Jingya Yang,1 Jingyi Zhang,1 Meimei Wang1 1Department of Pathophysiology, School of Basic Medical Science, Anhui Medical University, Hefei, 230032, People’s Republic of China; 2Department of Public Health Inspection and Quarantine, School of Public Health, Anhui Medical University, Hefei, 230032, People’s Republic of China*These authors contributed equally to this workCorrespondence: Meimei Wang, Department of Pathophysiology, School of Basic Medical Science, Anhui Medical University, No. 81, Mei-Shan Road, Hefei, 230032, People’s Republic of China, Email wangmm@ustc.edu.cnBackground: Tumor development and progression is a long and complex process influenced by a combination of intrinsic (eg, gene mutation) and extrinsic (eg, environmental pollution) factors. As a detoxification organ, the liver plays an important role in human exposure and response to various environmental pollutants including nanomaterials (NMs). Hepatocellular carcinoma (HCC) is one of the most common malignant tumors and remains a serious threat to human health. Whether NMs promote liver cancer progression remains elusive and assessing long-term exposure to subtoxic doses of nanoparticles (NPs) remains a challenge. In this study, we focused on the promotional effects of nano zinc oxide (nZnO) on the malignant progression of human HCC cells HepG2, especially aged nZnO that has undergone physicochemical transformation.Methods: In in vitro experiments, we performed colony forming efficiency, soft agar colony formation, and cell migration/invasion assays on HepG2 cells that had been exposed to a low dose of nZnO (1.5 μg/mL) for 3 or 4 months. In in vivo experiments, we subcutaneously inoculated HepG2 cells that had undergone long-term exposure to nZnO for 4 months into BALB/c athymic nude mice and observed tumor formation. ZnCl2 was administered to determine the role of zinc ions.Results: Chronic low-dose exposure to nZnO significantly intensified the malignant progression of HCC cells, whereas aged nZnO may exacerbate the severity of malignant progression. Furthermore, through transcriptome sequencing analysis and in vitro cellular rescue experiments, we demonstrated that the mechanism of nZnO-induced malignant progression of HCC could be linked to the activation of Claudin-2 (CLDN2), one of the components of cellular tight junctions, and the dysregulation of its downstream signaling pathways.Conclusion: Long-term exposure of fresh and aged nZnO promotes hepatocellular carcinoma malignancy by up-regulating CLDN2. The implications of this work can be profound for cancer patients, as the use of various nanoproducts and unintentional exposure to environmentally transformed NMs may unknowingly hasten the progression of their cancers. Keywords: nano zinc oxide, environmental transformation of NPs, long-term exposure, malignant progression of tumors, CLDN2
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- 2024
23. Trajectories of long-term exposure to PCB153 and Benzo[a]pyrene (BaP) air pollution and risk of breast cancer
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Pauline Desnavailles, Delphine Praud, Blandine Le Provost, Hidetaka Kobayashi, Floriane Deygas, Amina Amadou, Thomas Coudon, Lény Grassot, Elodie Faure, Florian Couvidat, Gianluca Severi, Francesca Romana Mancini, Béatrice Fervers, Cécile Proust-Lima, and Karen Leffondré
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Breast cancer ,Long-term exposure ,Polychlorobiphenyl ,Benzo[a]pyrene ,Trajectories of exposure ,Environmental carcinogens ,Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background While genetic, hormonal, and lifestyle factors partially elucidate the incidence of breast cancer, emerging research has underscored the potential contribution of air pollution. Polychlorinated biphenyls (PCBs) and benzo[a]pyrene (BaP) are of particular concern due to endocrine-disrupting properties and their carcinogenetic effect. Objective To identify distinct long term trajectories of exposure to PCB153 and BaP, and estimate their associations with breast cancer risk. Methods We used data from the XENAIR case–control study, nested within the ongoing prospective French E3N cohort which enrolled 98,995 women aged 40–65 years in 1990–1991. Cases were incident cases of primary invasive breast cancer diagnosed from cohort entry to 2011. Controls were randomly selected by incidence density sampling, and individually matched to cases on delay since cohort entry, and date, age, department of residence, and menopausal status at cohort entry. Annual mean outdoor PCB153 and BaP concentrations at residential addresses from 1990 to 2011 were estimated using the CHIMERE chemistry-transport model. Latent class mixed models were used to identify profiles of exposure trajectories from cohort entry to the index date, and conditional logistic regression to estimate their association with the odds of breast cancer. Results 5058 cases and 5059 controls contributed to the analysis. Five profiles of trajectories of PCB153 exposure were identified. The class with the highest PCB153 concentrations had a 69% increased odds of breast cancer compared to the class with the lowest concentrations (95% CI 1.08, 2.64), after adjustment for education and matching factors. The association between identified BaP trajectories and breast cancer was weaker and suffered from large CI. Conclusions Our results support an association between long term exposure to PCB153 and the risk of breast cancer, and encourage further studies to account for lifetime exposure to persistent organic pollutants.
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- 2024
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24. Long-Term Exposure to Nitrogen Dioxide and Ozone and Mortality: Update of the WHO Air Quality Guidelines Systematic Review and Meta-Analysis.
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Kasdagli, Maria-Iosifina, Orellano, Pablo, Pérez Velasco, Román, and Samoli, Evangelia
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CHRONIC obstructive pulmonary disease ,AIR pollution ,NITROGEN dioxide ,RESPIRATORY infections ,CEREBROVASCULAR disease - Abstract
Objectives: We performed a systematic review and meta-analysis on long-term exposure to nitrogen dioxide (NO
2 ) and ozone (O3 ) with mortality, to expand evidence that informed 2021 the WHO Air Quality Guidelines and guide the Health Risks of Air Pollution in Europe project. Methods: We included cohorts investigating NO2 and O3 mortality from all-causes, respiratory diseases, chronic obstructive pulmonary disease (COPD), acute lower respiratory infections (ALRI); and NO2 mortality from circulatory, ischemic heart, cerebrovascular diseases and lung cancer. We pooled estimates by random-effects models and investigated heterogeneity. We assessed the certainty of the evidence using the Grading of Recommendations Assessment Development approach and Evaluation (GRADE). Results: We selected 83 studies for NO2 and 26 for O3 for the meta-analysis. NO2 was associated with all outcomes, except for cerebrovascular mortality. O3 was associated with respiratory mortality following annual exposure. There was high heterogeneity, partly explained by region and pollutant levels. Certainty was high for NO2 with COPD and ALRI, and annual O3 with respiratory mortality. Conclusion: An increasing body of evidence, with new results from countrywide areas and the Western Pacific, supports certainty, including new outcomes. [ABSTRACT FROM AUTHOR]- Published
- 2024
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25. Chromate Affects Gene Expression and DNA Methylation in Long-Term In Vitro Experiments in A549 Cells.
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Fischer, Franziska, Stößer, Sandra, Wegmann, Lisa, Veh, Eva, Lumpp, Tatjana, Parsdorfer, Marlene, Schumacher, Paul, and Hartwig, Andrea
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DNA repair , *DNA methylation , *GENE expression profiling , *OCCUPATIONAL exposure , *GENE expression - Abstract
Chromate has been shown to dysregulate epigenetic mechanisms such as DNA methylation, leading to changes in gene expression and genomic instability. However, most in vitro studies are limited to short incubation periods, although chronic exposure may be more relevant for both environmental and occupational exposure. In this study, human adenocarcinoma A549 cells were treated with 1, 2 or 5 µM chromate for 24 h and compared with incubations with 0.2, 0.5 or 1 µM chromate for 1 to 5 weeks. Chromium accumulated in a pronounced time- and concentration-dependent manner after short-term treatment, whereas a plateau of intracellular chromium content was observed after long-term treatment. While short-term treatment induced a G2 arrest of the cell cycle, this effect was not observed after long-term treatment at lower concentrations. The opposite was observed for global DNA methylation: while short-term treatment showed no effect of chromate, significant dose-dependent hypomethylation was observed in the long-term experiments. Time-dependent effects were also observed in a high-throughput RT-qPCR gene expression analysis, particularly in genes related to the inflammatory response and DNA damage response. Taken together, the results suggest specific differences in toxicity profiles when comparing short-term and long-term exposure to chromate in A549 cells. [ABSTRACT FROM AUTHOR]
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- 2024
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26. Trajectories of long-term exposure to PCB153 and Benzo[a]pyrene (BaP) air pollution and risk of breast cancer.
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Desnavailles, Pauline, Praud, Delphine, Le Provost, Blandine, Kobayashi, Hidetaka, Deygas, Floriane, Amadou, Amina, Coudon, Thomas, Grassot, Lény, Faure, Elodie, Couvidat, Florian, Severi, Gianluca, Mancini, Francesca Romana, Fervers, Béatrice, Proust-Lima, Cécile, and Leffondré, Karen
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AIR pollution potential ,POLYCHLORINATED biphenyls ,BREAST cancer ,CANCER invasiveness ,DISEASE risk factors ,PERSISTENT pollutants ,AIR pollution - Abstract
Background: While genetic, hormonal, and lifestyle factors partially elucidate the incidence of breast cancer, emerging research has underscored the potential contribution of air pollution. Polychlorinated biphenyls (PCBs) and benzo[a]pyrene (BaP) are of particular concern due to endocrine-disrupting properties and their carcinogenetic effect. Objective: To identify distinct long term trajectories of exposure to PCB153 and BaP, and estimate their associations with breast cancer risk. Methods: We used data from the XENAIR case–control study, nested within the ongoing prospective French E3N cohort which enrolled 98,995 women aged 40–65 years in 1990–1991. Cases were incident cases of primary invasive breast cancer diagnosed from cohort entry to 2011. Controls were randomly selected by incidence density sampling, and individually matched to cases on delay since cohort entry, and date, age, department of residence, and menopausal status at cohort entry. Annual mean outdoor PCB153 and BaP concentrations at residential addresses from 1990 to 2011 were estimated using the CHIMERE chemistry-transport model. Latent class mixed models were used to identify profiles of exposure trajectories from cohort entry to the index date, and conditional logistic regression to estimate their association with the odds of breast cancer. Results: 5058 cases and 5059 controls contributed to the analysis. Five profiles of trajectories of PCB153 exposure were identified. The class with the highest PCB153 concentrations had a 69% increased odds of breast cancer compared to the class with the lowest concentrations (95% CI 1.08, 2.64), after adjustment for education and matching factors. The association between identified BaP trajectories and breast cancer was weaker and suffered from large CI. Conclusions: Our results support an association between long term exposure to PCB153 and the risk of breast cancer, and encourage further studies to account for lifetime exposure to persistent organic pollutants. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
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27. A New Method Proposed for the Estimation of Exposure to Atmospheric Pollution through the Analysis of Black Pigments on the Lung Surface.
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Waked, Dunia, Veras, Mariana Matera, Saldiva, Paulo Hilário Nascimento, and Takano, Ana Paula Cremasco
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AIR pollution , *DUST diseases , *PARTICULATE matter , *HUMAN ecology , *REMOTE sensing , *INHALERS - Abstract
Megacities can be considered excellent laboratories for studying the effects of the urban environment on human health. Typically, exposure to pollution is estimated according to daily or annual averages of pollutant concentrations, collected at monitoring stations, using satellite data for remote sensing of pollutant levels, considering proximity to major roads, or through personal exposure monitoring with portable sensors. However, these approaches fall short in identifying individual exposure values over a lifetime. It is well established that individuals living in large urban areas inhale atmospheric particles containing carbonaceous components, resulting in the deposition of black pigments in lung tissue, known as black carbon or anthracosis. This study aims to detail the procedures for assessing the deposition of such pigments, which serve as an estimate of an individual's exposure to atmospheric pollution particles. Data collection involves administering detailed questionnaires and capturing lung images in the autopsy room. The analysis is based on macroscopic quantification of black pigments, supplemented by an evaluation of personal habits and the clinical histories of the individuals. This method of estimating lifetime exposure to inhaled particles provides a valuable tool for understanding the correlation between urban living and its potential health effects. [ABSTRACT FROM AUTHOR]
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- 2024
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28. Exposure to PM2.5 and its constituents is associated with metabolic dysfunction-associated fatty liver disease: a cohort study in Northwest of China.
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Zhao, Yamin, Peng, Yindi, Wang, Minzhen, Zhao, Yanan, He, Yingqian, Zhang, Lulu, Liu, Jing, and Zheng, Shan
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FATTY liver ,AIR pollutants ,AIR pollution ,PROPORTIONAL hazards models ,COHORT analysis ,SPLINES ,CHINA studies - Abstract
Accumulating animal studies have demonstrated associations between ambient air pollution (AP) and metabolic dysfunction-associated fatty liver disease (MAFLD), but relevant epidemiological evidence is limited. We evaluated the association of long-term exposure to AP with the risk of incident MAFLD in Northwest China. The average AP concentration between baseline and follow-up was used to assess individual exposure levels. Cox proportional hazard models and restricted cubic spline functions (RCS) were used to estimate the association of PM
2.5 and its constituents with the risk of MAFLD and the dose–response relationship. Quantile g-computation was used to assess the joint effects of mixed exposure to air pollutants on MAFLD and the weights of the various pollutants. We observed 1516 cases of new-onset MAFLD, with an incidence of 10.89%. Increased exposure to pollutants was significantly associated with increased odds of MAFLD, with hazard ratios (HRs) of 2.93 (95% CI: 1.22, 7.00), 2.86 (1.44, 5.66), 7.55 (3.39, 16.84), 4.83 (1.89, 12.38), 3.35 (1.35, 8.34), 1.89 (1.02, 1.62) for each interquartile range increase in PM2.5 , SO4 2− , NO3 − , NH4 + , OM, and BC, respectively. Stratified analyses suggested that females, frequent exercisers and never-drinkers were more susceptible to MAFLD associated with ambient PM2.5 and its constituents. Mixed exposure to SO4 2− , NO3 − , NH4 + , OM and BC was associated with an increased risk of MAFLD, and the weight of BC had the strongest effect on MAFLD. Exposure to ambient PM2.5 and its constituents increased the risk of MAFLD. [ABSTRACT FROM AUTHOR]- Published
- 2024
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29. Synergistic air pollution exposure elevates depression risk: A cohort study
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Yuqing Hao, Longzhu Xu, Meiyu Peng, Zhugen Yang, Weiqi Wang, and Fanyu Meng
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Air pollution ,Long-term exposure ,Depressive symptoms ,Joint effect ,Mediation analysis ,Environmental sciences ,GE1-350 ,Environmental technology. Sanitary engineering ,TD1-1066 - Abstract
Depression is a leading mental health disorder worldwide, contributing substantially to the global disease burden. While emerging evidence suggests links between specific air pollutants and depression, the potential interactions among multiple pollutants remain underexplored. Here we show the influence of six common air pollutants on depressive symptoms among middle-aged and older Chinese adults. In single-pollutant models, a 10 μg m−3 increase in SO2, CO, PM10, and PM2.5 is associated with increased risks of depressive symptoms, with odds ratios (95% confidence intervals) of 1.276 (1.238–1.315), 1.007 (1.006–1.008), 1.066 (1.055–1.078), and 1.130 (1.108–1.153), respectively. In two-pollutant models, SO2 remains significantly associated with depressive symptoms after adjusting for other pollutants. Multi-pollutant models uncover synergistic effects, with SO2, CO, NO2, PM10, and PM2.5 exhibiting significant interactions, identifying SO2 as the primary driver of these associations. Mediation analyses further indicate that cognitive and physical impairments partially mediate the relationship between air pollution and depressive symptoms. These findings underscore the critical mental health impacts of air pollution and highlight the need for integrated air quality management strategies. Targeted mitigation of specific pollutants, particularly SO2, is expected to significantly enhance public mental health outcomes.
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- 2025
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30. Sensorineural Hearing Loss in Otolaryngology Floor Among Head and Neck Cancer Patients: A Prospective Cohort Study
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Aldaihani, A., Aali, M., Alamodi, U., Taylor, M., Trites, J., and Shoman, N.
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- 2025
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31. Long-term impacts of salinity and temperature changes on Brachionus calyciflorus populations: understanding the role of intraspecific variability
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Wijewardene, Lishani, Venâncio, Cátia, Ribeiro, Rui, and Lopes, Isabel
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- 2025
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32. Sublethal and lethal toxicity assessment of lanthanum and gadolinium to Daphnia magna in a 7-day test method
- Author
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Padilla Suarez, Edith Guadalupe, Revel, Marion, Libralato, Giovanni, Guida, Marco, and Heise, Susanne
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- 2025
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33. Long-term exposure to diesel exhaust particles induces concordant changes in DNA methylation and transcriptome in human adenocarcinoma alveolar basal epithelial cells
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Alexandra Lukyanchuk, Naomi Muraki, Tomoko Kawai, Takehiro Sato, Kenichiro Hata, Tsuyoshi Ito, and Atsushi Tajima
- Subjects
Diesel exhaust particles ,Alveolar epithelium ,Long-term exposure ,Methylation profiling ,Gene expression profiling ,Genetics ,QH426-470 - Abstract
Abstract Background Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns about the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. Although several studies have focused on the effects of short-term DEP exposure on gene expression, research on the transcriptional effects and genome-wide DNA methylation changes caused by long-term DEP exposure is lacking. Hence, in this study, we investigated transcriptional and DNA methylation changes in human adenocarcinoma alveolar basal epithelial A549 cells caused by prolonged exposure to DEP and determined whether these changes are concordant. Results DNA methylation analysis using the Illumina Infinium MethylationEPIC BeadChips showed that the methylation levels of DEP-affected CpG sites in A549 cells changed in a dose-dependent manner; the extent of change increased with increasing dose reaching the statistical significance only in samples exposed to 30 µg/ml DEP. Four-week exposure to 30 µg/ml of DEP significantly induced DNA hypomethylation at 24,464 CpG sites, which were significantly enriched for DNase hypersensitive sites, genomic regions marked by H3K4me1 and H3K27ac, and several transcription factor binding sites. In contrast, 9,436 CpG sites with increased DNA methylation levels were significantly overrepresented in genomic regions marked by H3K27me3 as well as H3K4me1 and H3K27ac. In parallel, gene expression profiling by RNA sequencing demonstrated that long-term exposure to DEP altered the expression levels of 2,410 genes, enriching 16 gene sets including Xenobiotic metabolism, Inflammatory response, and Senescence. In silico analysis revealed that the expression levels of 854 genes correlated with the methylation levels of the DEP-affected cis-CpG sites. Conclusions To our knowledge, this is the first report of genome-wide transcriptional and DNA methylation changes and their associations in A549 cells following long-term exposure to DEP.
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- 2024
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34. Long-term exposure to PM2.5 and its components is associated with elevated blood pressure and hypertension prevalence: Evidence from rural adults
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Ruiyu Wu, Ning Kang, Caiyun Zhang, Yu Song, Wei Liao, Yueling Hong, Jian Hou, Kai Zhang, Hezhong Tian, Hualiang Lin, and Chongjian Wang
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Long-term exposure ,PM2.5 and chemical components ,Blood pressure (BP) ,Hypertension prevalence ,Rural adults ,Medicine (General) ,R5-920 ,Science (General) ,Q1-390 - Abstract
Introduction: The toxicity of fine particulate matter (PM2.5) is determined by its components, while the evidence regarding associations of PM2.5 components with blood pressure (BP) is limited, especially in rural areas. Objectives: This study aimed to explore the associations of PM2.5 and its chemical components with systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP), mean artery pressure (MAP) levels and hypertension prevalence, and to identify key components in Chinese rural areas. Methods: 39,211 adults from the Henan Rural Cohort were included during 2015–2017. Different periods of PM2.5 and chemical components were estimated by hybrid satellite model. The single-pollutant, component-PM2.5 model, component-residual model and component-proportion model were applied to explore the associations of pollutants with BP levels and hypertension prevalence. Exposure-response (E-R) relationships, stratified analyses and sensitivity analyses were used to explore these associations further. Results: 12,826 (32.71%) were identified with hypertension. For each 1 μg/m3 increase of pollutants, the adjusted odds ratio (OR) for hypertension prevalence was 1.03 for PM2.5 mass, 1.40 for BC, 1.16 for NH4+, 1.08 for NO3–, 1.17 for OM, 1.12 for SO42− and 1.25 for SOIL in the single-pollutant model. BC and SOIL were statistically significant in the component-PM2.5 model, component-residual model and component-proportion model. Similarly, associations of these pollutants with elevated BP levels were also found in aforementioned four models. These pollutants produced a stronger association with SBP than DBP, PP and MAP. Most of associations were non-linear in E-R relationships. The groups of older, the men, with lower per capita monthly income, lower educational level and higher BMI were more vulnerable to these pollutants in stratified analyses. The results remained stable in sensitivity analyses. Conclusion: Long-term exposure to PM2.5 and its components, especially BC and SOIL, was associated with elevated BP and hypertension prevalence in rural adults, and decreasing pollutants may provide additional benefits.
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- 2024
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35. Effects of long-term X-ray exposure on CBC among radiological department staff in Sulaimani city
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Salah Q. Mahmood, MSc, Bakhtyar K. Talabany, PhD, and Taib A. Hama-Soor, PhD
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CBC ,Long-term exposure ,Radiology staff ,X-ray ,Medicine (General) ,R5-920 - Abstract
الملخص أهداف البحث: يعتقد أن الأشعة المؤينة المستخدمة في أجهزة الأشعة يمكن أن تؤثر على أنسجة الجسم لدى موظفي قسم الأشعة. تهدف هذه الدراسة إلى مقارنة آثار التعرض طويل الأمد للأشعة السينية على خلايا الدم لدى الموظفين العاملين في أقسام الأشعة المختلفة في المستشفيات المختلفة في مدينة السليمانية / حكومة إقليم كردستان. طريقة البحث: أجريت هذه الدراسة المقطعية في الفترة من 2021 إلى 2022 على 250 موظفا في أقسام الأشعة المختلفة، والتي شملت أخصائيي الأشعة، ومصوري الأشعة، وغيرهم من الطاقم الطبي (طبيب، ممرض، ….إلخ)، وكانت لها معايير الاشتمال، على مستوى المستشفيات في مدينة السليمانية التابعة لحكومة إقليم كردستان. تم جمع البيانات باستخدام استبيان تم ملؤه من قبل المشاركين بعد أخذ الموافقة الشفهية. تم جمع عينة الدم من 250 من موظفي الأشعة ثم إرسالها إلى المختبر للتحقق من مؤشرات الدم. تم تحليل البيانات المجمعة وتم التحقق من المقارنة والعلاقات بين البيانات من خلال الاختبارات الإحصائية الوصفية. النتائج: أظهرت النتائج أن معظم العينات الذكور كانوا من فنيي الأشعة الحاصلين على درجة الدبلوم. كان هناك فروق ذات دلالة إحصائية بين مجموعتي الجنسين فيما يتعلق بمؤشرات الدم من خلايا الدم الحمراء، واختبار الهيماتوكريت، وحجم الكريات، والصفائح الدموية. كان هناك فروق ذات دلالة إحصائية بين المجموعات المهنية من حيث عرض توزيع خلايا الدم الحمراء - معامل التباين وعرض توزيع خلايا الدم الحمراء - الانحراف المعياري وفرق ذو دلالة إحصائية بين الموظفين الذين لديهم تاريخ من التدخين وغير المدخنين و المدخنين سابقاً من حيث متوسط كريات الدم البيضاء والخلايا الليمفاوية ووجود فرق ذو دلالة إحصائية بين الموظفين الذين لديهم تاريخ في استهلاك الكحول وغير الكحوليين ومدمني الكحول السابقين من حيث متوسط كريات الدم البيضاء. الاستنتاجات: بناء على نتائج هذه الدراسة يمكن استنتاج أن متغيرات الدم مثل عرض توزيع خلايا الدم الحمراء - معامل التباين وعرض توزيع خلايا الدم الحمراء - الانحراف المعياري تتأثر بناء على نوع الوظيفة ومدة التعرض لأشعة اكس. Abstract: Objectives: Ionizing rays used in radiology devices are believed to affect the body tissues of radiology department employees. This study was aimed at comparing the effects of long-term exposure to X-rays on the blood cells of staff working in the radiology departments of several hospitals in the Sulaimani City/Kurdistan region government. Methods: This cross-sectional study was conducted from 2021 to 2022 on 250 employees—including radiologists, radiographers, and other medical staff such as physicians or nurses—in the radiology departments of hospitals in the city of Sulaimani, Kurdistan region government. Data were collected with a questionnaire completed by the participants after verbal consent was provided. Blood samples were collected from 250 radiology staff and sent to a laboratory for measurement of blood parameters. The collected data were analyzed in SPSS version 26 software, and relationships in the data were investigated with descriptive statistical tests, Student's t test, and ANOVA. Results: Most male participants were radiographers with a diploma degree. A statistically significant difference in RBC, HCT %, MCV, and PCT blood parameters was observed between sexes. Moreover, statistically significant differences were observed in RDW-CV and RDW-SD between occupational groups; in mean WBC and lymphocytes among staff who were current, never, or former smokers; and in mean WBC among employees who were current, never, or former drinkers (p
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- 2024
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36. Beyond lung cancer: air pollution and bladder, breast and prostate cancer incidence.
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Kayyal-Tarabeia, Inass, Zick, Aviad, Kloog, Itai, Levy, Ilan, Blank, Michael, and Agay-Shay, Keren
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- *
LUNG cancer , *PARTICULATE matter , *BLADDER cancer , *PROSTATE cancer , *BREAST cancer , *AIR pollution - Abstract
Background The carcinogenicity of air pollution and its impact on the risk of lung cancer is well known; however, there are still knowledge gaps and mixed results for other sites of cancer. Methods The current study aimed to evaluate the associations between ambient air pollution [fine particulate matter (PM2.5) and nitrogen oxides (NOx)] and cancer incidence. Exposure assessment was based on historical addresses of >900 000 participants. Cancer incidence included primary cancer cases diagnosed from 2007 to 2015 (n = 30 979). Cox regression was used to evaluate the associations between ambient air pollution and cancer incidence [hazard ratio (HR), 95% CI]. Results In the single-pollutant models, an increase of one interquartile range (IQR) (2.11 µg/m3) o f PM2.5 was associated with an increased risk of all cancer sites (HR = 1.51, 95% CI: 1.47–1.54), lung cancer (HR = 1.73, 95% CI: 1.60–1.87), bladder cancer (HR = 1.50, 95% CI: 1.37–1.65), breast cancer (HR = 1.50, 95% CI: 1.42–1.58) and prostate cancer (HR = 1.41, 95% CI: 1.31–1.52). In the single-pollutant and the co-pollutant models, the estimates for PM2.5 were stronger compared with NOx for all the investigated cancer sites. Conclusions Our findings confirm the carcinogenicity of ambient air pollution on lung cancer and provide additional evidence for bladder, breast and prostate cancers. Further studies are needed to confirm our observation regarding prostate cancer. However, the need for more research should not be a barrier to implementing policies to limit the population's exposure to air pollution. [ABSTRACT FROM AUTHOR]
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- 2024
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37. Inclisiran administration potently and durably lowers LDL-C over an extended-term follow-up: the ORION-8 trial.
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Wright, R Scott, Raal, Frederick J, Koenig, Wolfgang, Landmesser, Ulf, Leiter, Lawrence A, Vikarunnessa, Sheikh, Lesogor, Anastasia, Maheux, Pierre, Talloczy, Zsolt, Zang, Xiao, Schwartz, Gregory G, and Ray, Kausik K
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LDL cholesterol , *SUBTILISINS , *CONFIDENCE intervals , *CARDIOVASCULAR diseases , *ADULTS - Abstract
Aims Data describing the long-term efficacy and tolerability of inclisiran are limited. This was explored in ORION-8, an open-label extension of preceding Phase 2 and Phase 3 placebo-controlled and open-label extension trials. Methods and results Following completion of the parent trial, adult patients with atherosclerotic cardiovascular disease (ASCVD), ASCVD risk equivalent, or heterozygous familial hypercholesterolaemia received open-label inclisiran twice yearly (after initial and 3-month doses) until Day 990, followed by an end-of-study visit at Day 1080 or ≥ 90 days after the last dose. The study endpoints included the proportion of patients achieving pre-specified low-density lipoprotein cholesterol (LDL-C) goals [ASCVD: < 1.8 mmol/L (< 70 mg/dL); ASCVD risk equivalent: < 2.6 mmol/L (< 100 mg/dL)], percentage and absolute changes in LDL-C at end-of-study, and safety of inclisiran. Of 3274 patients, 2446 (74.7%) were followed until end-of-study. Mean age was 64.9 ± 9.9 years, 82.7% (n = 2709) had ASCVD, and mean baseline LDL-C was 2.9 ± 1.2 mmol/L. Mean cumulative exposure to inclisiran (including parent trials) was 3.7 years; maximum exposure was 6.8 years. With inclisiran, 78.4% [95% confidence interval (CI): 76.8, 80.0] of patients achieved pre-specified LDL-C goals and mean percentage change in LDL-C was −49.4% (95% CI: −50.4, −48.3). No attenuation of LDL-C lowering over time was observed. Treatment-emergent adverse events at injection site (all mild/moderate) occurred in 5.9% of the patients. Inclisiran-associated anti-drug antibodies were infrequent (5.5%) and had no impact on the efficacy or safety of inclisiran. No new safety signals were identified. Conclusion In the largest and longest follow-up to date with >12 000 patient-years exposure, inclisiran demonstrated consistent and effective LDL-C lowering with a favourable long-term safety and tolerability profile. Trial Registration number ClinicalTrials.gov identifier: NCT03814187 [ABSTRACT FROM AUTHOR]
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- 2024
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38. Multigenerational exposure to temperature influences mitochondrial oxygen fluxes in the Medaka fish (Oryzias latipes).
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Morla, Julie, Salin, Karine, Lassus, Rémy, Favre‐Marinet, Julie, Sentis, Arnaud, and Daufresne, Martin
- Subjects
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ORYZIAS latipes , *PHYSIOLOGY , *FISH farming , *MITOCHONDRIA , *FACTORIAL experiment designs - Abstract
Aim: Thermal sensitivity of cellular metabolism is crucial for animal physiology and survival under climate change. Despite recent efforts, effects of multigenerational exposure to temperature on the metabolic functioning remain poorly understood. We aimed at determining whether multigenerational exposure to temperature modulate the mitochondrial respiratory response of Medaka fish. Methods: We conducted a multigenerational exposure with Medaka fish reared multiple generations at 20 and 30°C (COLD and WARM fish, respectively). We then measured the oxygen consumption of tail muscle at two assay temperatures (20 and 30°C). Mitochondrial function was determined as the respiration supporting ATP synthesis (OXPHOS) and the respiration required to offset proton leak (LEAK(Omy)) in a full factorial design (COLD‐20°C; COLD‐30°C; WARM‐20°C; WARM‐30°C). Results: We found that higher OXPHOS and LEAK fluxes at 30°C compared to 20°C assay temperature. At each assay temperature, WARM fish had lower tissue oxygen fluxes than COLD fish. Interestingly, we did not find significant differences in respiratory flux when mitochondria were assessed at the rearing temperature of the fish (i.e., COLD‐20°C vs. WARM −30°C). Conclusion: The lower OXPHOS and LEAK capacities in warm fish are likely the result of the multigenerational exposure to warm temperature. This is consistent with a modulatory response of mitochondrial capacity to compensate for potential detrimental effects of warming on metabolism. Finally, the absence of significant differences in respiratory fluxes between COLD‐20°C and WARM‐30°C fish likely reflects an optimal respiration flux when organisms adapt to their thermal conditions. [ABSTRACT FROM AUTHOR]
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- 2024
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39. Long-term exposure to diesel exhaust particles induces concordant changes in DNA methylation and transcriptome in human adenocarcinoma alveolar basal epithelial cells.
- Author
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Lukyanchuk, Alexandra, Muraki, Naomi, Kawai, Tomoko, Sato, Takehiro, Hata, Kenichiro, Ito, Tsuyoshi, and Tajima, Atsushi
- Subjects
GENE expression ,DNA methylation ,TRANSCRIPTION factors ,GENE expression profiling ,DNA analysis ,PREGNANE X receptor - Abstract
Background: Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns about the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. Although several studies have focused on the effects of short-term DEP exposure on gene expression, research on the transcriptional effects and genome-wide DNA methylation changes caused by long-term DEP exposure is lacking. Hence, in this study, we investigated transcriptional and DNA methylation changes in human adenocarcinoma alveolar basal epithelial A549 cells caused by prolonged exposure to DEP and determined whether these changes are concordant. Results: DNA methylation analysis using the Illumina Infinium MethylationEPIC BeadChips showed that the methylation levels of DEP-affected CpG sites in A549 cells changed in a dose-dependent manner; the extent of change increased with increasing dose reaching the statistical significance only in samples exposed to 30 µg/ml DEP. Four-week exposure to 30 µg/ml of DEP significantly induced DNA hypomethylation at 24,464 CpG sites, which were significantly enriched for DNase hypersensitive sites, genomic regions marked by H3K4me1 and H3K27ac, and several transcription factor binding sites. In contrast, 9,436 CpG sites with increased DNA methylation levels were significantly overrepresented in genomic regions marked by H3K27me3 as well as H3K4me1 and H3K27ac. In parallel, gene expression profiling by RNA sequencing demonstrated that long-term exposure to DEP altered the expression levels of 2,410 genes, enriching 16 gene sets including Xenobiotic metabolism, Inflammatory response, and Senescence. In silico analysis revealed that the expression levels of 854 genes correlated with the methylation levels of the DEP-affected cis-CpG sites. Conclusions: To our knowledge, this is the first report of genome-wide transcriptional and DNA methylation changes and their associations in A549 cells following long-term exposure to DEP. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
40. Multi-time-scale surface ozone exposure and associated premature mortalities over Indian cities in different climatological sub-regions.
- Author
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Kumar, Chhabeel, Dogra, Ashish, Kumari, Neelam, Yadav, Shweta, and Tandon, Ankit
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- 2024
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41. Long-Term Exposure to Air Pollution and Risk of Acute Lower Respiratory Infections in the Danish Nurse Cohort.
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Zhang, Jiawei, Lim, Youn-Hee, So, Rina, Mortensen, Laust H., Napolitano, George Maria, Cole-Hunter, Thomas, Tuffier, Stéphane, Bergmann, Marie, Maric, Matija, Taghavi Shahri, Seyed Mahmood, Brandt, Jørgen, Ketzel, Matthias, Loft, Steffen, and Andersen, Zorana Jovanovic
- Subjects
AIR pollution ,RESPIRATORY infections ,CHRONIC obstructive pulmonary disease ,INHALERS ,LUNG diseases ,COMORBIDITY ,RESPIRATORY organs - Abstract
Rationale: Air pollution is a major risk factor for chronic cardiorespiratory diseases, affecting the immune and respiratory systems' functionality, but epidemiological evidence in respiratory infections remains sparse. Objectives: We aimed to assess the association of long-term exposure to ambient air pollution with the risk of developing new and recurrent acute lower respiratory infections (ALRIs), characterized by persistently severe symptoms necessitating hospital contact, and identify the potential susceptible populations by socioeconomic status, smoking, physical activity status, overweight, and comorbidity with chronic lung disease. Methods: We followed 23,912 female nurses from the Danish Nurse Cohort (age >44 yr) from baseline (1993 or 1999) until 2018 for incident and recurrent ALRIs defined by hospital contact (inpatient, outpatient, and emergency room) data from the National Patient Register. Residential annual mean concentrations of fine particulate matter, nitrogen dioxide (NO
2 ), and black carbon were modeled using the Danish Eulerian Hemispheric Model/Urban Background Model/Air Geographic Information System. We used marginal Cox models with time-varying exposures to assess the association of 3-year running mean air pollution level with incident and recurrent ALRIs and examined effect modification by age, socioeconomic status, smoking, physical activity, body mass index, and comorbidity with asthma or chronic obstructive pulmonary disease (COPD). Results: During a 21.3-year mean follow-up, 4,746 ALRIs were observed, of which 2,553 were incident. We observed strong positive associations of all three pollutants with incident ALRIs, with hazard ratios and 95% confidence intervals of 1.19 (1.08–1.31) per 2.5 μg/m3 for fine particulate matter, 1.17 (1.11–1.24) per 8.0 μg/m3 for NO2 , and 1.09 (1.05–1.12) per 0.3 μg/m3 for black carbon, and slightly stronger associations with recurrent ALRIs. Associations were strongest in patients with COPD and nurses with low physical activity. Conclusions: Long-term exposure to air pollution at low levels was associated with risks of new and recurrent ALRIs, with patients with COPD and physically inactive subjects most vulnerable. [ABSTRACT FROM AUTHOR]- Published
- 2024
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42. Long-term exposure to PM2.5 and its components is associated with elevated blood pressure and hypertension prevalence: Evidence from rural adults.
- Author
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Wu, Ruiyu, Kang, Ning, Zhang, Caiyun, Song, Yu, Liao, Wei, Hong, Yueling, Hou, Jian, Zhang, Kai, Tian, Hezhong, Lin, Hualiang, and Wang, Chongjian
- Abstract
[Display omitted] • PM 2.5 and its components is associated with elevated blood pressure and hypertension prevalence. • These pollutants produced a stronger association with the rise of SBP than DBP, PP and MAP. • BC and SOIL were most significant with adverse outcomes in different models. • Reduce the concentrations of PM 2.5 and its components may provide benefits in rural areas. The toxicity of fine particulate matter (PM 2.5) is determined by its components, while the evidence regarding associations of PM 2.5 components with blood pressure (BP) is limited, especially in rural areas. This study aimed to explore the associations of PM 2.5 and its chemical components with systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP), mean artery pressure (MAP) levels and hypertension prevalence, and to identify key components in Chinese rural areas. 39,211 adults from the Henan Rural Cohort were included during 2015–2017. Different periods of PM 2.5 and chemical components were estimated by hybrid satellite model. The single-pollutant, component-PM 2.5 model, component-residual model and component-proportion model were applied to explore the associations of pollutants with BP levels and hypertension prevalence. Exposure-response (E-R) relationships, stratified analyses and sensitivity analyses were used to explore these associations further. 12,826 (32.71%) were identified with hypertension. For each 1 μg/m
3 increase of pollutants, the adjusted odds ratio (OR) for hypertension prevalence was 1.03 for PM 2.5 mass, 1.40 for BC, 1.16 for NH 4+ , 1.08 for NO 3– , 1.17 for OM, 1.12 for SO 42− and 1.25 for SOIL in the single-pollutant model. BC and SOIL were statistically significant in the component-PM 2.5 model, component-residual model and component-proportion model. Similarly, associations of these pollutants with elevated BP levels were also found in aforementioned four models. These pollutants produced a stronger association with SBP than DBP, PP and MAP. Most of associations were non-linear in E-R relationships. The groups of older, the men, with lower per capita monthly income, lower educational level and higher BMI were more vulnerable to these pollutants in stratified analyses. The results remained stable in sensitivity analyses. Long-term exposure to PM 2.5 and its components, especially BC and SOIL, was associated with elevated BP and hypertension prevalence in rural adults, and decreasing pollutants may provide additional benefits. [ABSTRACT FROM AUTHOR]- Published
- 2024
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43. Effects of long-term X-ray exposure on CBC among radiological department staff in Sulaimani city.
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Mahmood, Salah Q., Talabany, Bakhtyar K., and Hama-Soor, Taib A.
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Copyright of Journal of Taibah University Medical Sciences is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2024
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44. Toxic Effects of Triclosan and Triclocarban on Gobiocypris rarus at Various Developmental Stages during Long-term Exposure.
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Zhang Ying, Chen Xiaoqian, and Yang Jing
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TRICLOSAN ,POISONS ,TOXICITY testing ,POLLUTANTS ,YOLK sac ,TRICLOCARBAN ,FISH development - Abstract
Triclosan (TCS) and triclocarban (TCC) are two highly effective broad-spectrum antimicrobial agents having embryo toxicity, endocrine disruption, and reproductive toxicity. These two chemicals are presently emerging pollutants of wide concerns and may cause cancer, DNA damage, and adverse pregnancy outcomes. In 2016, the US Food and Drug Administration (US FDA) has banned market entry of the over-the-counter antibacterial bath products containing antibacterial agents such as TCS and TCC. In China, however, TCS and TCC are still allowed to be used in a limited quantity as quasi-preservatives for cosmetics, and are not restricted for soap products. As emerging exogenous chemical pollutants, TCS and TCC can enter the natural environment with domestic wastewater and pose potential threats to local aquatic lives, ecological security and human health. In order to investigate the toxic effects of TCS and TCC on the long-term exposure and four different developmental stages (i. e., embryo, yolk sac absorption, larval, and juvenile stages) of the Chinese native fish species of Gobiocypris rarus (GR), the fertilized eggs of GR were exposed to TCS and TCC until 60 days post hatching (60 dph) in this study. The results showed that TCS and TCC in the ranges of 6.25 ~ 100 µg ⋅ L
-1 and 0.938 ~ 15 µg ⋅ L-1 , respectively, had no significant toxic effects on the embryo hatchability of GR. In the larval stage, the no observed effect concentration (NOEC) of the 30 dph survival rate in the exposure groups of 6.25 ~ 100 µg ⋅ L-1 TCS and 0.938 ~ 15 µg ⋅ L-1 TCC were 100 µg ⋅ L-1 and 0.938 µg ⋅ L-1 , respectively. According to the national standards of China, the hazards of TCC to the aquatic environment were classified as long-term chronic category 1. In contrast, it is impossible to make a clear judgment for TCS because its maximum testing concentration did not reach 1 mg ⋅L-1 , but the hazards of TCS to the aquatic environment can be judged as the non-long-term chronic category 1. At the juvenile stage, TCS (6.25 ~ 100 µg ⋅ L-1 ) and TCC (0.938 ~ 15 µg ⋅ L-1 ) could induce vitellogenin in both females and males of GR, but did not affect sexual differentiation. During the postembryonic development, TCS of 6.25 ~ 100 µg ⋅ L-1 could significantly affect the fish body weight, which gradually decreased with increasing TCS concentration, indicating that TCS could inhibit the body weight of GR. TCC of 0.938 ~ 15 µg ⋅ L-1 had no significant effect on the fish body weight and body length. In addition, it was found that the toxic effects on the different developmental stages of GR were different. The tolerance of GR at embryonic stage was significantly higher than that at postembryonic development stage, while the tolerance at yolk sac absorption stage and larvae stage was lower than that at the juvenile stage. Therefore, when more of these life stages are included in a test, more toxicity endpoints can be obtained by fewer test animals. Moreover, the toxic effects of different life stages in the tests are all from the same batch of the test animals, making the test results of different life stages more comparable. [ABSTRACT FROM AUTHOR]- Published
- 2024
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45. Evaluation of the Long-Term Exposure to the Magnetic Fields Generated by Overhead Transmission Lines Using Artificial Neural Networks – A Case Study.
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Alihodžić, Ajdin, Mujezinović, Adnan, Turajlić, Emir, Dedović, Maja Muftić, Dautbašić, Nedis, and Turković, Irfan
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ARTIFICIAL neural networks ,ELECTRIC lines ,MAGNETIC fields ,MAGNETIC flux density ,HEIGHT measurement - Abstract
The methodology for the evaluation of long-term exposure to the overhead line magnetic field is presented, in this paper. The developed methodology is based on the ambient temperature measurements and phase conductors' height measurements to find a linear regression model to determine phase conductors' height changes for different ambient temperatures. Based on the overhead transmission line geometry, and datasets about historical overhead line phase current intensity values and ambient temperatures long-term magnetic field exposure can be determined. For magnetic flux density determination, a method based on artificial neural networks is used. The methodology is applied to the case study of overhead line that connect substations Sarajevo 10 and Sarajevo 20. A period of one year is analyzed and magnetic flux density values are determined. The obtained results indicate that during the analyzed period for significant amounts of time magnetic flux density values surpass the recommended values for long-term exposure. [ABSTRACT FROM AUTHOR]
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- 2024
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46. Integrated transcriptomics and proteomics analyses reveal the ameliorative effect of hepatic damage in tilapia caused by polystyrene microplastics with chlorella addition
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Yao Zheng, Haijun Tang, Jiawen Hu, Yi Sun, Haojun Zhu, and Gangchun Xu
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Liver ,Endoplasmic reticulum ,PPAR signaling pathway ,Long-term exposure ,Environmental pollution ,TD172-193.5 ,Environmental sciences ,GE1-350 - Abstract
Fish exhibit varying responses to polystyrene microplastics (MPs) depending on particle size. Previous studies suggested that microorganisms adhering to the surface of MPs can induce toxic effects. In this study, Tilapia were exposed to MPs of control (group A), 75 nm (B), 7.5 μm (C), 750 μm (D), as well as combinations of all sizes (E) and 75 nm MPs with Chlorella vulgaris addition (F) for 7, 10 and 14 days. Histopathological changes in liver of tilapia were assessed using enzyme activities, transcriptomics and proteomics. The results showed that in groups combined MPs of different particle sizes and those supplemented with chlorella, MPs were localized on the surface of goblet cells, leading to vacuoles, constricted hepatic sinuses and nuclei displacement. Exposure to 7.5 and 750 μm MPs significantly increased the contents of fatty acid synthase (FAS), adenosine triphosphate (ATP), acetyl-CoA carboxylase (ACC), lipoprotein lipase (LPL), total cholesterol (TC), total triglyceride (TG) contents at 7 and 10 days. In particular, cytochrome p450 1a1 (EROD), reactive oxygen species (ROS) and superoxide dismutase (SOD) were markedly elevated following exposure to MPs. Apoptotic markers caspase-3, and inflammatory markers, including tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β), had a similar upward trend in comparisons of group C vs A at 7 d, group D vs A at 14 d. The peroxisome proliferator activated receptor (PPAR) signaling pathway, spliceosome, was highly enriched during the 7-day exposure of medium sized MPs, while largest MPs in the comparison of group D vs A at 14 d activated pathways such as phagosome, apoptosis, salmonella infection. Transcriptomic analysis revealed that after 14 days, the kyoto encyclopedia of genes and genomes (KEGG) pathways associated with protein processing in endoplasmic reticulum and the PPAR signaling has been significantly enriched in the Chlorella-supplemented group, which was further confirmed via the proteomic analysis. Overall, the findings highlight the size-dependent effects of MPs on histopathological changes, gene and protein expression in the liver of tilapia, and C. vulgaris effectively attenuated liver damages, likely through modulation of endoplasmic reticulum protein processing and PPAR signaling pathways.
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- 2024
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47. Paralysis caused by dinotefuran at environmental concentration via interfering the Ca2+–ROS–mitochondria pathway in Chironomus kiiensis
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Fenghua Wei, Weiwen Gu, Fengru Zhang, and Shuangxin Wu
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neonicotinoid insecticides ,long-term exposure ,mitochondria ,Chironomidae ,environmental dose ,Public aspects of medicine ,RA1-1270 - Abstract
IntroductionDinotefuran as the third-generation of neonicotinoid insecticides is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration is unclear.MethodsIn this study, the mitochondria damage and oxidative stress of dinotefuran on Chironomus kiiensis were investigated at environmental concentrations by long-term exposure. At the same time, relevant gene expressions of these toxicity indexes were measured as sensitive ecotoxicity biomarkers to reflect the toxic effects of dinotefuran on Chironomidae.ResultsOur present study showed that chronic exposure to environmental concentrations of dinotefuran resulted in behavioral inhibition in the larvae of Chironomidae. For burrowing inhibition of 10 days, the lowest observed-effect concentration (LOEC) and 50% inhibitory concentration (IC50) were 0.01 (0.01–0.04) and 0.60 (0.44–0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ions (Ca2+) in Chironomidae via dysregulating the gene expressions of atp2b, camk ii, and calm. Subsequently, the disruption of the Ca2+ signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H2O2), and malonaldehyde (MDA) levels. Thus, the over-release of Ca2+ and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of atpef0a, sdha, and cyt b.ConclusionOur findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca2+–ROS–mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran.
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- 2024
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48. Long-Term Exposure to Nitrogen Dioxide and Ozone and Mortality: Update of the WHO Air Quality Guidelines Systematic Review and Meta-Analysis
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Maria-Iosifina Kasdagli, Pablo Orellano, Román Pérez Velasco, and Evangelia Samoli
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long-term exposure ,meta-analysis ,mortality ,nitrogen dioxide ,ozone ,Public aspects of medicine ,RA1-1270 - Abstract
ObjectivesWe performed a systematic review and meta-analysis on long-term exposure to nitrogen dioxide (NO2) and ozone (O3) with mortality, to expand evidence that informed 2021 the WHO Air Quality Guidelines and guide the Health Risks of Air Pollution in Europe project.MethodsWe included cohorts investigating NO2 and O3 mortality from all-causes, respiratory diseases, chronic obstructive pulmonary disease (COPD), acute lower respiratory infections (ALRI); and NO2 mortality from circulatory, ischemic heart, cerebrovascular diseases and lung cancer. We pooled estimates by random-effects models and investigated heterogeneity. We assessed the certainty of the evidence using the Grading of Recommendations Assessment Development approach and Evaluation (GRADE).ResultsWe selected 83 studies for NO2 and 26 for O3 for the meta-analysis. NO2 was associated with all outcomes, except for cerebrovascular mortality. O3 was associated with respiratory mortality following annual exposure. There was high heterogeneity, partly explained by region and pollutant levels. Certainty was high for NO2 with COPD and ALRI, and annual O3 with respiratory mortality.ConclusionAn increasing body of evidence, with new results from countrywide areas and the Western Pacific, supports certainty, including new outcomes.
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- 2024
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49. Long-term arsenic exposure decreases mice body weight and liver lipid droplets
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Chengze Lai, Linkang Chen, Xiaoting Zhong, Xianbing Tian, Bin Zhang, Hao Li, Guiwei Zhang, Liping Wang, Yanqin Sun, and Lianxian Guo
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Rice arsenicals ,Metabolomics ,Long-term exposure ,Lipid droplets ,Gut microbiome ,Environmental sciences ,GE1-350 - Abstract
Arsenic (As) is a widespread global pollutant, and there is significant controversy surrounding its complex relationship with obesity, primarily focused on short-term exposure. Recognizing the prolonged nature of dietary arsenic exposure, this study involved feeding mice with arsenic-contained food for 14 months. The results showed that mice exposed to arsenic developed a non-alcoholic fatty liver condition, characterized by a light-yellow hue on the liver surface and various pathological alterations in the liver cells, including enlarged nuclei, cellular necrosis, inflammatory infiltration, dysfunctional mitochondria, and endoplasmic reticulum disorganization. There were also disruptions in biochemistry indices, with a significant increase in total cholesterol (TC) level and a decrease in high-density lipoprotein (HDL) level. However, some contradictory observations occurred, such as a significant decrease in body weight, triglyceride (TG) level, and the numbers of lipid droplets. Several genes related to lipid metabolism were tested, and a model was used to explain these discrepancies. Besides, examinations of the colon revealed compromised intestinal barrier function and signs of inflammation. Fecal 16S rRNA sequencing and pseudo-targeted metabolomics revealed disruptions in internal homeostasis, such as modules, nodes, connections, and lipid-related KEGG pathways. Fecal targeted metabolomics analyses of short-chain fatty acids (SCFAs) and bile acids (BAs) demonstrated a significant upregulation in three primary bile acids (CA, CDCA, TCDCA), four secondary bile acids (TUDCA, DCA, LCA, GUDCA), and total SCFAs level. Oxidative stress and inflammation were also evident. Additionally, based on correlation analysis and mediation analysis, it was assumed that changes in the microbiota (e.g., Dubosiella) can impact the liver metabolites (e.g., TGs) through alterations in fecal metabolites (e.g., LPCs). These findings provide a theoretical reference for the long-term effect of arsenic exposure on liver lipid metabolism.
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- 2024
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50. Ambient fine particulate matter and its constituents may exacerbate the acceleration of aging in adults
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Cui Guo, Jun Yang, Jun Ma, Jie Chen, Siyi Chen, Yiling Zheng, Bo Huang, Jianzhen Yu, Tiantian Li, and Shenjing He
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Biological age ,Fine particulate matter (PM2.5) constituents ,Long-term exposure ,Air pollution change ,Cohort ,Healthy cities ,Environmental sciences ,GE1-350 - Abstract
Both ambient fine particulate matter (PM2.5) and aging are important urban concerns. However, the associations between PM2.5 constituents and the acceleration of aging (AA) remain unclear. We included 16,051 adults (aged 25–80 years) with 19,252 medical observations in Taiwan during 2008−2017. 2-year average PM2.5 and its five major constituents were assessed using a two-stage machine learning model at a resolution of 1 km2. AA was determined by the difference between the Klemera–Doubal biological age and chronological age. A linear mixed model (LMM) with inverse probability weights was used to examine the associations between AA and air pollution. In a semi-randomized study design, we applied a post-matching LMM to assess the impacts of changes in air pollution exposure on AA. Each interquartile range increase in ambient PM2.5, SO4-2, NO3–, NH4+, organic matters (OM), and black carbon (BC) was associated with a 0.20 (95 %confidence interval [CI]: 0.17–0.24), 0.19 (0.15–0.23), 0.14 (0.11–0.18), 0.21 (0.17–0.24), 0.22 (0.19–0.26) and 0.25 (0.21–0.28) year increase in AA, respectively. BC was generally associated with the greatest increase in AA as compared to other constituents. We did not find evident thresholds in their concentration–response associations. Participants exposed to increased levels of PM2.5, SO4-2, NO3–, NH4+, OM, and BC experienced an increase in AA of 0.11 (−0.07–0.29), 0.20 (0.02–0.39), 0.15 (−0.02–0.33), 0.12 (−0.07–0.31), 0.24 (0.07–0.41), and 0.30 (0.07–0.52) years, respectively, compared to those exposed to decreased/unchanged levels. Long-term exposure to ambient PM2.5 and its constituents may accelerate biological aging among Chinese adults. Exposed to increased levels may further aggregate the aging process. This study suggests that reducing exposure to air pollution is beneficial, even for residents within moderately-to-highly polluted regions, such as Taiwan. Rigorous regulation of PM2.5 and its constituents may prevent the acceleration of biological age.
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- 2024
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