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Exposure to perfluoroalkyl and polyfluoroalkyl substances and risk of stroke in adults: a meta-analysis. 接触全氟烷基和多氟烷基物质与成人中风风险:一项荟萃分析
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-09-04 DOI: 10.1515/reveh-2023-0021
Min Cheol Chang, Seung Min Chung, Sang Gyu Kwak

Introduction: Evidence of the adverse metabolic health effects of perfluoroalkyl and polyfluoroalkyl substances (PFAS) is increasing. However, the impact of PFAS on cardiovascular diseases remains controversial. This meta-analysis aimed to analyze the impact of PFAS on the stroke risk.

Content: Databases were searched for studies published up to November 1, 2022, which report the association between stroke and exposure to at least one of four main PFAS (perfluorooctanoic acid [PFOA], perfluorooctanesulfonic acid [PFOS], perfluorononanoic acid [PFNA], and perfluorohexane sulfonic acid [PFHxS]). Data extraction and quality assessment were performed according to the Newcastle-Ottawa scale.

Summary and outlook: Four studies were included in this systematic review. Multivariate adjusted odds ratios (ORs) for incident stroke per 1-log unit increment in each serum PFAS were combined in the meta-analysis. The risk of development of stroke was not significantly associated with PFOA, PFOS, or PFNA exposure (PFOA: pooled odds ratio [OR]=1.001, 95 % confidence interval [CI]=0.975-1.028, p=0.934; PFOS: pooled OR=0.994, 95 % CI=0.972-1.017, p=0.601; PFNA: pooled OR=1.016, 95 % CI=0.920-1.123, p=0.752), whereas a moderately lower risk was associated with PFHxS exposure without statistical significance (pooled OR=0.953, 95 % CI=0.908-1.001, p=0.054). PFOA, PFOS, and PFNA exposure showed a neutral association, while PFHxS showed a possible inverse association with the risk of stroke. Therefore, this finding should be interpreted with caution. Further prospective observational studies with PFAS mixture analyses are warranted.

导言:全氟烷基和多氟烷基物质(PFAS)对代谢健康不利影响的证据越来越多。然而,PFAS对心血管疾病的影响仍存在争议。本荟萃分析旨在分析PFAS对卒中风险的影响。内容:检索截至2022年11月1日发表的研究数据库,这些研究报告了中风与暴露于四种主要PFAS(全氟辛酸[PFOA]、全氟辛烷磺酸[PFOS]、全氟壬酸[PFNA]和全氟己烷磺酸[PFHxS])中的至少一种之间的关系。根据纽卡斯尔-渥太华量表进行数据提取和质量评估。综述与展望:本系统综述纳入4项研究。在荟萃分析中,将各血清PFAS每增加1 log单位的卒中事件的多因素校正优势比(ORs)结合起来。卒中发生风险与PFOA、PFOS或PFNA暴露无显著相关(PFOA:合并优势比[or]=1.001, 95 %置信区间[CI]=0.975-1.028, p=0.934;PFOS:合并OR=0.994, 95 % CI=0.972 ~ 1.017, p=0.601;PFNA:合并OR=1.016, 95 % CI=0.920-1.123, p=0.752),而中度低风险与PFHxS暴露相关,但无统计学意义(合并OR=0.953, 95 % CI=0.908-1.001, p=0.054)。PFOA、PFOS和PFNA暴露与卒中风险呈中性相关,而PFHxS与卒中风险呈可能的负相关。因此,应该谨慎地解释这一发现。PFAS混合物分析的进一步前瞻性观察研究是有必要的。
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引用次数: 0
Impacts and potential mechanisms of fine particulate matter (PM2.5) on male testosterone biosynthesis disruption. 细颗粒物(PM2.5)对男性睾酮生物合成干扰的影响及其潜在机制
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-09-01 DOI: 10.1515/reveh-2023-0064
Shaokai Zheng, Nannan Zhao, Xiaojun Lin, Lianglin Qiu

Exposure to PM2.5 is the most significant air pollutant for health risk. The testosterone level in male is vulnerable to environmental toxicants. In the past, researchers focused more attention on the impacts of PM2.5 on respiratory system, cardiovascular system, and nervous system, and few researchers focused attention on the reproductive system. Recent studies have reported that PM2.5 involved in male testosterone biosynthesis disruption, which is closely associated with male reproductive health. However, the underlying mechanisms by which PM2.5 causes testosterone biosynthesis disruption are still not clear. To better understand its potential mechanisms, we based on the existing scientific publications to critically and comprehensively reviewed the role and potential mechanisms of PM2.5 that are participated in testosterone biosynthesis in male. In this review, we summarized the potential mechanisms of PM2.5 triggering the change of testosterone level in male, which involve in oxidative stress, inflammatory response, ferroptosis, pyroptosis, autophagy and mitophagy, microRNAs (miRNAs), endoplasmic reticulum (ER) stress, and N6-methyladenosine (m6A) modification. It will provide new suggestions and ideas for prevention and treatment of testosterone biosynthesis disruption caused by PM2.5 for future research.

PM2.5是对健康危害最大的空气污染物。男性体内的睾酮水平易受环境毒物的影响。过去研究人员更多关注PM2.5对呼吸系统、心血管系统和神经系统的影响,很少有研究人员关注生殖系统。近年来有研究报道,PM2.5与男性睾酮生物合成干扰有关,与男性生殖健康密切相关。然而,PM2.5导致睾酮生物合成中断的潜在机制尚不清楚。为了更好地了解其潜在机制,我们在现有科学出版物的基础上,对PM2.5参与男性睾酮生物合成的作用和潜在机制进行了批判性和全面的回顾。本文综述了PM2.5引发男性睾酮水平变化的潜在机制,包括氧化应激、炎症反应、铁亡、焦亡、自噬和有丝自噬、microrna (miRNAs)、内质网(ER)应激和n6 -甲基腺苷(m6A)修饰。为今后的研究提供预防和治疗PM2.5引起的睾酮生物合成中断的新建议和思路。
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引用次数: 0
Frontmatter 头版头条
4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-09-01 DOI: 10.1515/reveh-2023-frontmatter3
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引用次数: 0
The European Union assessments of radiofrequency radiation health risks - another hard nut to crack (Review). 欧洲联盟对射频辐射健康风险的评估——另一个需要解决的难题(审查)。
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-23 DOI: 10.1515/reveh-2023-0046
Rainer Nyberg, Julie McCredden, Lennart Hardell

In 2017 an article was published on the unwillingness of the WHO to acknowledge the health effects associated with the use of wireless phones. It was thus stated that the WHO is 'A Hard Nut to Crack'. Since then, there has been no progress, and history seems to be repeating in that the European Union (EU) is following in the blind man's footsteps created by the WHO. Despite increasing evidence of serious negative effects from radiofrequency radiation on human health and the environment, the EU has not acknowledged that there are any risks. Since September 2017, seven appeals by scientists and medical doctors have been sent to the EU requesting a halt to the roll-out of the fifth generation of wireless communication (5G). The millimeter waves (MMW) and complex waveforms of 5G contribute massively harmful additions to existing planetary electromagnetic pollution. Fundamental rights and EU primary law make it mandatory for the EU to protect the population, especially children, from all kinds of harmful health effects of wireless technology. However, several experts associated with the WHO and the EU have conflicts of interest due to their ties to industry. The subsequent prioritizing of economic interests is resulting in human and planetary health being compromised. Experts must make an unbiased evaluation with no conflicts of interest. The seven appeals to the EU have included requests for immediate protective action, which have been ignored. On the issue of wireless radiation and the health of citizens, the EU seems to be another hard nut to crack.

2017年,一篇关于世卫组织不愿承认与使用无线电话相关的健康影响的文章发表。因此,有人说世界卫生组织是“一个难以攻克的难题”。从那时起,没有任何进展,历史似乎在重复,欧盟正在跟随世界卫生组织创造的盲人的脚步。尽管越来越多的证据表明射频辐射对人类健康和环境有严重的负面影响,但欧盟尚未承认存在任何风险。自2017年9月以来,科学家和医生已经向欧盟发出了七份呼吁,要求停止推出第五代无线通信(5G)。5G的毫米波(MMW)和复杂波形对现有的行星电磁污染造成了巨大的有害影响。基本权利和欧盟主要法律规定,欧盟有义务保护民众,特别是儿童,免受无线技术对健康的各种有害影响。然而,与世界卫生组织和欧盟有关的一些专家由于与工业界的关系而存在利益冲突。随后对经济利益的优先考虑导致人类和地球健康受到损害。专家必须在没有利益冲突的情况下做出公正的评估。向欧盟提出的七项上诉包括要求立即采取保护措施,但都被忽视了。在无线辐射与公民健康的问题上,欧盟似乎又是一块难啃的硬骨头。
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引用次数: 0
Research progresses on the effects of heavy metals on the circadian clock system. 重金属对生物钟系统影响的研究进展。
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-14 DOI: 10.1515/reveh-2022-0104
Qian Xue, Rui Wang, Ruijian Zhu-Ge, Li Guo

Environmental pollution with heavy metals is widespread, thus increasing attention has been paid to their toxic effects. Recent studies have suggested that heavy metals may influence the expression of circadian clock genes. Almost all organs and tissues exhibit circadian rhythms. The normal circadian rhythm of an organism is maintained by the central and peripheral circadian clock. Thus, circadian rhythm disorders perturb normal physiological processes. Here, we review the effects of heavy metals, including manganese, copper, cadmium, and lead, on four core circadian clock genes, i.e., ARNTL, CLOCK, PER, and CRY genes.

重金属对环境的污染十分普遍,其毒性作用日益引起人们的重视。最近的研究表明,重金属可能影响生物钟基因的表达。几乎所有的器官和组织都有昼夜节律。生物体的正常昼夜节律是由中央和外周生物钟维持的。因此,昼夜节律紊乱扰乱了正常的生理过程。本文综述了锰、铜、镉和铅等重金属对四种核心生物钟基因(即ARNTL、clock、PER和CRY基因)的影响。
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引用次数: 0
Diagnosing and managing heat exhaustion: insights from a systematic review of cases in the desert climate of Mecca. 诊断和管理中暑:来自麦加沙漠气候病例系统回顾的见解。
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-04 DOI: 10.1515/reveh-2023-0059
Saber Yezli, Yara Yassin, Sujoud Ghallab, Mashan Abdullah, Bisher Abuyassin, Ramesh Vishwakarma, Abderrezak Bouchama

Heat exhaustion (HE) is a common, yet obscure, heat-related illness that affects millions of people yearly and its burden is projected to rise due to climate change. A comprehensive literature synthesis is lacking despite previous studies on various HE aspects. This systematic review aims to fill this gap by identifying and synthesizing available evidence on the risk factors, symptoms, biomarkers, treatment options, and outcomes for HE. The review focused on HE during the Muslim (Hajj) pilgrimage where the condition is endemic. We conducted a structured search of MEDLINE/PubMed, Embase, Web of Science Core Collection, SCOPUS, and CINAHL databases. We summarized the data from eligible studies and synthesized them in narrative form using pooled descriptive statistics. Ten studies were included between 1980 and 2019, reporting over 1,194 HE cases. HE cases presented with elevated core temperature (up to 40°C) and mainly affected older males from the Middle East and North Africa region, with overweight individuals at a higher risk. Clinical symptoms included hyperventilation, fatigue, dizziness, headaches, nausea, and vomiting, but not central nervous system disturbances. HE was associated with cardiac stress, and with water, electrolyte, and acid-base alterations. Cooling and hydration therapy were the primary management strategies, leading to a low mortality rate (pooled case fatality rate=0.11 % [95 % CI: 0.01, 0.3]). Most cases recovered within a few hours without complications. HE is associated with cardiac stress and changes in homeostasis, leading to distinct clinical symptoms. Early diagnosis and treatment of HE are crucial in reducing the risk of complications and mortality. The review provides insights into the pathophysiology and outcomes of HE, adding to the scarce literature on the subject. Prospero registration number: CRD42022325759.

中暑衰竭(HE)是一种常见但鲜为人知的与热有关的疾病,每年影响数百万人,由于气候变化,其负担预计会增加。尽管前人对高等教育的各个方面进行了研究,但缺乏全面的文献综合。本系统综述旨在通过识别和综合关于HE的风险因素、症状、生物标志物、治疗方案和结果的现有证据来填补这一空白。审查的重点是穆斯林(朝觐)朝圣期间的HE,那里的情况是地方性的。我们对MEDLINE/PubMed、Embase、Web of Science Core Collection、SCOPUS和CINAHL数据库进行了结构化检索。我们总结了符合条件的研究的数据,并使用汇总描述性统计以叙述形式将其综合起来。1980年至2019年期间纳入了10项研究,报告了1194例HE病例。HE病例表现为核心温度升高(高达40°C),主要影响中东和北非地区的老年男性,超重个体的风险更高。临床症状包括换气过度、疲劳、头晕、头痛、恶心和呕吐,但无中枢神经系统紊乱。HE与心脏应激、水、电解质和酸碱改变有关。冷却和水合治疗是主要的治疗策略,导致低死亡率(合并病死率= 0.11% [95% CI: 0.01, 0.3])。大多数病例在几小时内恢复,没有并发症。HE与心脏应激和体内平衡的改变有关,导致明显的临床症状。HE的早期诊断和治疗对于降低并发症和死亡率的风险至关重要。该综述提供了对HE的病理生理学和结果的见解,补充了关于该主题的稀缺文献。普洛斯彼罗注册号:CRD42022325759。
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引用次数: 0
Association of the ACE2-Angiotensin1-7-Mas axis with lung damage caused by cigarette smoke exposure: a systematic review. ace2 -血管紧张素- 1-7- mas轴与香烟烟雾暴露引起的肺损伤的关联:一项系统综述
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-03 DOI: 10.1515/reveh-2023-0028
Maryam Maleki, Alireza Aliboroni, Amin Kheiri, Mohammad Reza Kaffashian, Maryam Kheiry

Through the Mas receptor, angiotensin-(1-7) [Ang-(1-7)] has been shown to have a key role in the development of lung inflammation. This systematic review (SR) sought to identify the relationship between lung damage brought on by exposure to cigarette smoke (CS) and the ACE2-Ang-(1-7)-Mas pathway. In this investigation, relevant keywords were used to search PubMed (MEDLINE), Scopus (Elsevier), and Institute for Scientific Information (ISI) Web of Science up to December 2022. Nine studies were chosen because they satisfied the inclusion/exclusion criteria. The majority of research concluded that exposure to CS increased the risk of lung damage. Smoking cigarettes is the main cause of COPD because it causes massive amounts of reactive oxygen and nitrogen species to enter the lungs, which stimulate the production of inflammatory cytokines like IL-1 β, IL-6, and TNF-α, as well as the invasion of inflammatory cells like neutrophils and macrophages. These findings support the renin-angiotensin system's (RAS) involvement in the pathophysiology of smoking-induced damage. Additionally, via stimulating pro-inflammatory mediators, aberrant RAS activity has been linked to lung damage. Lung inflammation's etiology has been shown to be significantly influenced by the protective known RAS arm ACE2-Ang-(1-7)-Mas. In conclusion, these are important for informing policymakers to pass legislation limiting the use of smoking and other tobacco to prevent their harmful effects.

通过Mas受体,血管紧张素-(1-7)[Ang-(1-7)]已被证明在肺部炎症的发展中起关键作用。本系统综述(SR)旨在确定暴露于香烟烟雾(CS)引起的肺损伤与ACE2-Ang-(1-7)- mas途径之间的关系。在本次调查中,使用相关关键词检索PubMed (MEDLINE)、Scopus (Elsevier)和Institute for Scientific Information (ISI) Web of Science,截止日期为2022年12月。选择了9项研究,因为它们符合纳入/排除标准。大多数研究得出的结论是,接触CS会增加肺部损伤的风险。吸烟是导致慢性阻塞性肺病的主要原因,因为它会导致大量活性氧和活性氮进入肺部,从而刺激IL-1 β、IL-6和TNF-α等炎症细胞因子的产生,以及中性粒细胞和巨噬细胞等炎症细胞的入侵。这些发现支持肾素-血管紧张素系统(RAS)参与吸烟引起的损伤的病理生理过程。此外,通过刺激促炎介质,异常的RAS活性与肺损伤有关。肺部炎症的病因已被证明受到已知的RAS保护性臂ACE2-Ang-(1-7)- mas的显著影响。总之,这些对告知决策者通过立法限制吸烟和其他烟草的使用以防止其有害影响是很重要的。
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引用次数: 0
Impacts and mechanisms of PM2.5 on bone. PM2.5对骨骼的影响及其机制。
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-03 DOI: 10.1515/reveh-2023-0024
Yuqing Tian, Yunpeng Hu, Xiaoli Hou, Faming Tian

Osteoporosis is a metabolic bone disease, which is characterized by a decreased bone mass and deterioration of bone microstructure, resulting in increased bone fragility and a higher risk of fracture. The main pathological process of osteoporosis is the dynamic imbalance between bone absorption and bone formation, which can be caused by various factors such as air pollution. Particulate matter (PM)2.5 refers to the fine particles in the atmosphere, which are small in volume and large in specific surface area. These particles are prone to carrying toxic substances and have negative effects on several extrapulmonary organs, including bones. In this review, we present relevant data from studies, which show that PM2.5 is associated with abnormal bone turnover and osteoporosis. PM2.5 may cause or aggravate bone loss by stimulating an inflammatory response, inducing oxidative damage, reducing estrogen efficiency by competitive binding to estrogen receptors, or endocrine disorder mediated by binding with aromatic hydrocarbon receptors, and affecting the synthesis of vitamin D to reduce calcium absorption. The cellular and molecular mechanisms involved in these processes are also summarized in this review.

骨质疏松症是一种代谢性骨病,其特点是骨量减少,骨微结构恶化,导致骨脆性增加,骨折风险增加。骨质疏松症的主要病理过程是骨吸收与骨形成之间的动态失衡,可由空气污染等多种因素引起。颗粒物(PM)2.5是指大气中体积小、比表面积大的细颗粒物。这些颗粒容易携带有毒物质,并对包括骨骼在内的几个肺外器官产生负面影响。在这篇综述中,我们提供了相关研究数据,这些数据表明PM2.5与异常骨转换和骨质疏松症有关。PM2.5可能通过刺激炎症反应、诱导氧化损伤、通过与雌激素受体竞争结合降低雌激素效率、或通过与芳烃受体结合介导内分泌紊乱、影响维生素D的合成从而减少钙的吸收等途径导致或加重骨质流失。本文对这些过程所涉及的细胞和分子机制也进行了综述。
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引用次数: 1
Ancient medicine and famous iranian physicians. 古代医学和著名的伊朗医生。
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-03 DOI: 10.1515/reveh-2023-0077
Mehdi Shafiei Bafti, Farzane Safa
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引用次数: 0
Para-occupational exposure to chemical substances: a systematic review. 化学物质的职业性接触:系统综述。
IF 3.9 4区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2023-08-02 DOI: 10.1515/reveh-2023-0019
Soleiman Ramezanifar, Afsane Azimian, Elahe Khadiv, Seyed Husein Naziri, Noradin Gharari, Mehdi Fazlzadeh

Today, many health problems related to work have overshadowed workers and their families. In the meantime, chemicals are among the risk factors that have created many problems due to para-occupational exposure. In para-occupational exposures, family members are exposed to work pollutants transferred to the home environment. This study was conducted to investigate para-occupational exposure to chemicals. To conduct this systematic review, databases such as "Web of Science", "Google Scholar", "Scopus", and "SID" were used. Relevant articles in these databases were extracted by searching keywords such as "take-home exposure", "para-occupational exposure", and "chemicals" from 2000 to 2022. To extract the required data, all parts of the articles were reviewed following the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA 2020). Among the 44 identified articles, 23 were selected as final articles, of which 10 were related to agriculture workers and their families, and 13 were related to other occupations. These studies mainly investigated para-occupational exposure to pesticides (14 studies) and metals (four studies). Also, contaminated work clothes, the washing place of contaminated clothes, and storage of working clothes, equipment, and chemicals were proposed as the main routes of contamination transmission. As a result of these para-occupational exposures, problems like neuro-behavioral disorders in children, end-stage renal disease, black gingival borders, and autism spectrum disorder were created or aggravated. Limiting the transmission routes and taking measures such as training and providing facilities like devoting places for washing and storing clothes in the workplaces can decrease this type of exposure.

今天,许多与工作有关的健康问题给工人和他们的家庭蒙上了阴影。与此同时,化学物质是由于职业性接触而产生许多问题的风险因素之一。在准职业暴露中,家庭成员暴露于转移到家庭环境的工作污染物。本研究旨在调查职业性接触化学品的情况。为了进行系统评价,使用了“Web of Science”、“Google Scholar”、“Scopus”和“SID”等数据库。通过检索关键词“带回家暴露”、“准职业暴露”、“化学物质”等,提取2000 - 2022年数据库中的相关文章。为了提取所需的数据,按照系统评价和荟萃分析的首选报告项目(PRISMA 2020)对文章的所有部分进行了审查。在确定的44篇文章中,23篇被选为最终文章,其中10篇与农业工人及其家庭有关,13篇与其他职业有关。这些研究主要调查了职业性接触农药(14项研究)和金属(4项研究)。被污染的工作服、被污染的洗涤场所、工作服、设备和化学品的存放处是污染传播的主要途径。由于这些准职业暴露,儿童神经行为障碍、终末期肾病、黑牙龈边界和自闭症谱系障碍等问题产生或加剧。限制传播途径和采取培训等措施,并在工作场所提供专门的洗涤和存放衣服的场所等设施,可减少这类接触。
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引用次数: 0
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