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Plant-driven strategies for mitigating microplastic pollution in agricultural ecosystems 减轻农业生态系统中微塑料污染的植物驱动战略
IF 2.7 Pub Date : 2025-12-01 DOI: 10.1016/j.heha.2025.100160
Anindita Banerjee , Pranav Kumar , Arkaprobha Ghosh , Soumita Reja , Surjit Singh
Microplastics (MPs) have become a widespread and novel threat to agriculture by degrading soils, damaging plant productivity and ultimately threatening food security. Research on MP contamination paths through plastic mulching, biosolids, compost, and wastewater irrigation has led to a greater understanding the problem, but the physiological and ecological impacts on plants have not been quantified and explained. MPs affect the biophysical properties of the soils, including the water and nutrients, which impacts their flow to the MP-affected plants. Biophysical changes caused by the MPs to the soils include changes to bulk density, porosity, and hydraulic conductivity. In the rhizosphere, they cause disruption to the microbial networks, suppression of enzymes, and the destabilization of symbiotic relationships, which impacts the plants’ ability to biogoechemically cycle and mitigate stress. MP-affected plants result in reduced germination, depressed photosynthetic productivity, oxidative stress leading to altered carbon distribution, secondary metabolites, and loss of other metabolites.
While there are many studies on the microbial and physicochemical approaches to remediation, the plant pathway and approaches to remediation are still largely unexplored and present a novel opportunity to address the problem. Symbiotic microbial consortia associated with root systems will help with enzymatic transformation of aggregating, immobilizing, and in some cases, biochemically transforming MPs. The detoxification capacity of PGPR and rhizosphere biochar are often situational and short-lived. Most importantly, the short-term laboratory studies using pristine MPs and over concentrated MPs will not accurately influence or predict the ecological impact and applicability to the field.
This review underscores the need for an integrated, nature-based strategies to combat MP pollution and protect agroecosystem integrity by bridging microbiology, soil science, and sustainable agriculture. Furthermore, a comprehensive understanding of the root system physiology, chemical exudation patterns, and microbial associations has been explored to determine the fate of the MP in deriving implementable plant-driven approaches. Such a framework is necessary to develop resilient self-remediating agroecosystems that can degrade plastic waste while maintaining productive agriculture.
微塑料(MPs)通过降解土壤、破坏植物生产力并最终威胁粮食安全,已成为对农业的广泛和新的威胁。通过塑料覆盖、生物固体、堆肥和废水灌溉对多酚污染途径的研究使人们对这一问题有了更深入的了解,但对植物的生理和生态影响尚未得到量化和解释。MPs影响土壤的生物物理特性,包括水分和养分,从而影响它们流向受MPs影响的植物。MPs对土壤造成的生物物理变化包括体积密度、孔隙度和水力导电性的变化。在根际,它们会破坏微生物网络,抑制酶,破坏共生关系,从而影响植物的生物化学循环和缓解胁迫的能力。受mp影响的植物会导致发芽降低、光合生产力下降、氧化胁迫导致碳分布、次生代谢物和其他代谢物的改变。虽然有许多关于微生物和物理化学修复方法的研究,但植物途径和修复方法仍在很大程度上未被探索,并提供了解决问题的新机会。与根系相关的共生微生物联合体将有助于聚合、固定化和在某些情况下生化转化MPs的酶转化。PGPR和根际生物炭的解毒能力往往是情境性的和短暂的。最重要的是,使用原始MPs和过度浓缩MPs的短期实验室研究不能准确地影响或预测生态影响和对现场的适用性。这篇综述强调了需要一个综合的、基于自然的战略,通过连接微生物学、土壤科学和可持续农业来对抗土壤污染和保护农业生态系统的完整性。此外,对根系生理、化学渗出模式和微生物关联的全面了解已经被探索,以确定MP的命运,从而获得可实施的植物驱动方法。这样一个框架对于发展有弹性的自我修复农业生态系统是必要的,这些生态系统可以在保持农业生产的同时降解塑料废物。
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引用次数: 0
Perfluorooctanoic acid impairs myogenic differentiation and muscle function via activation of the hippo-YAP pathway in mice and C2C12 myoblasts 在小鼠和C2C12成肌细胞中,全氟辛酸通过激活海马- yap通路损害成肌分化和肌肉功能
IF 2.7 Pub Date : 2025-11-28 DOI: 10.1016/j.heha.2025.100162
Gaowei Duan , Hong Hong , Yuanhang Liu , He Xiao , Yuan Ding , Muhammad Amjad , Peixuan Wu , Li Zhong , Xu Wang , Xin Meng , Haiyan Zhang
Perfluorooctanoic acid (PFOA), a widely distributed environmental pollutant, exerts toxic effects on multiple human organs and tissues. However, its impact on skeletal muscle function and the underlying molecular mechanisms remain poorly understood. In this study, we first observed that PFOA exposure caused muscle dysfunction in juvenile mice, characterized by reduced grip strength and impaired motor coordination; to explore the underlying mechanism, we further conducted in vitro experiments using C2C12 myoblasts. Long-term treatment with 100 μacid (PFOA), a widely distributed environmental pollutant, exerts toxic effects on multiple human organs and tissues. However, its impact on myotubes. Transcriptome sequencing revealed a significant decrease in the expression of key myogenic regulatory factors (e.g., myosin heavy chain MYHC and myogenin) in PFOA-treated cells, findings that were confirmed by RT-qPCR and Western blot analyses. Mechanistically, PFOA treatment activated the Hippo signaling pathway, as evidenced by increased phosphorylation of the YAP protein. Treatment with taurine, an indirect activator of YAP, significantly restored the expression of myogenic genes and effectively promoted myotube formation. In summary, this study demonstrates that PFOA impairs muscle function by activating the Hippo signaling pathway and suppressing the transcription of key myogenic factors, providing new insights into PFOA-induced myotoxicity.
全氟辛酸(PFOA)是一种广泛分布的环境污染物,对人体多个器官和组织具有毒性作用。然而,其对骨骼肌功能的影响和潜在的分子机制仍然知之甚少。在这项研究中,我们首先观察到PFOA暴露导致幼年小鼠肌肉功能障碍,其特征是握力下降和运动协调受损;为了探究其潜在的机制,我们进一步利用C2C12成肌细胞进行了体外实验。100 μ酸(PFOA)是一种广泛分布的环境污染物,长期处理会对人体多个器官和组织产生毒性作用。然而,它对肌管的影响。转录组测序显示,pfoa处理的细胞中关键的肌生成调节因子(如肌球蛋白重链MYHC和肌原蛋白)的表达显著降低,RT-qPCR和Western blot分析证实了这一发现。机制上,PFOA处理激活了Hippo信号通路,正如YAP蛋白磷酸化增加所证明的那样。牛磺酸是YAP的一种间接激活剂,用牛磺酸治疗可以显著恢复成肌基因的表达,并有效促进肌管的形成。综上所述,本研究表明PFOA通过激活Hippo信号通路和抑制关键肌生成因子的转录来损害肌肉功能,为PFOA诱导的肌毒性研究提供了新的见解。
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引用次数: 0
Estimated burden of disease and health effects attributable to fine particulate matter and ozone exposure in relation to COPD and cardiovascular disease in Upper Northern Thailand 泰国北部地区与慢性阻塞性肺病和心血管疾病相关的细颗粒物和臭氧暴露造成的疾病负担和健康影响的估计
IF 2.7 Pub Date : 2025-11-27 DOI: 10.1016/j.heha.2025.100161
Sarawut Sangkham , Nattapon Pansakun , Patipat Vongruang , Mohammad Nayeem Hasan , Saksin Simsin
Fine particulate matter (PM2.5) is a significant contributor to air pollution and is associated with many diseases of global public health concern. In this study, the burden of lung cancer and cardiopulmonary disease attributed to PM2.5 exposure in Thailand's upper northern region is estimated. Additionally, generalised additive models (GAMs) were used to examine the relationship between PM2.5 and ozone (O3) levels and the incidence of cardiovascular diseases (CVDs) and chronic obstructive pulmonary disease (COPD). The results indicated all eight provinces showed a positive relative risk (RR) for lung cancer and cardiopulmonary disease. The estimated long-term exposure to PM2.5 during 2015–2023 showed that the regional average relative risk (RR) was 1.558 (95 % CI: 1.530–1.586) for lung cancer and 1.344 (95 % CI: 1.328–1.361) for cardiopulmonary disease. This study examined the short-term effects of PM2.5 and ozone (O3) exposure on morbidity from COPD and CVD. PM2.5 exposure was significantly associated with increased COPD risk only in Lampang province, where the incidence rate ratio [IRR] was 1.009 (95 % CI: 1.002–1.017), p < 0.05. Ozone exposure showed significant associations with COPD risk in Chiang Mai, Chiang Rai, and Nan provinces, with the IRRs of 1.021 (95 % CI: 1.009–1.033), 1.020 (95 % CI: 1.007–1.032), and 1.026 (95 % CI: 1.012–1.040), respectively (p < 0.05). Ozone exposure was associated with an increased IRR for CVD risk in Chiang Mai, Chiang Rai, and Nan provinces; however, the association was not statistically significant. In contrast, no significant association in IRR was observed for short-term PM2.5 exposure in relation to CVD. Joint exposure to PM2.5 and O3 was significantly associated with increased risk of COPD in Chiang Mai, Chiang Rai, and Nan provinces (p < 0.05). Interaction analyses revealed synergistic effects on COPD in Nan and CVD in Chiang Rai and Nan. Male sex, older age (≥ 60 years), and seasonal variation of particulate matter and ozone concentration were identified as significant effect modifiers. These findings elucidate the differential impacts of air pollutants on respiratory and cardiovascular health in upper northern Thailand. Furthermore, they emphasise the heightened vulnerability of older adults and males, underscoring the urgent need for targeted, region-specific public health interventions.
细颗粒物(PM2.5)是造成空气污染的重要因素,与许多引起全球公共卫生关注的疾病有关。在本研究中,估计了泰国北部上地区PM2.5暴露导致的肺癌和心肺疾病负担。此外,还使用广义加性模型(GAMs)来研究PM2.5和臭氧(O3)水平与心血管疾病(cvd)和慢性阻塞性肺疾病(COPD)发病率之间的关系。结果显示,所有8个省份的肺癌和心肺疾病的相对危险度(RR)均为正。2015-2023年期间PM2.5的估计长期暴露表明,肺癌的区域平均相对风险(RR)为1.558 (95% CI: 1.530-1.586),心肺疾病的区域平均相对风险(RR)为1.344 (95% CI: 1.328-1.361)。本研究考察了PM2.5和臭氧暴露对慢性阻塞性肺病和心血管疾病发病率的短期影响。PM2.5暴露与COPD风险增加的显著相关仅在南邦省,其发病率比[IRR]为1.009 (95% CI: 1.002-1.017), p < 0.05。在清迈、清莱和南省,臭氧暴露与COPD风险显著相关,irs分别为1.021 (95% CI: 1.009-1.033)、1.020 (95% CI: 1.007-1.032)和1.026 (95% CI: 1.012-1.040) (p < 0.05)。在清迈、清莱和南省,臭氧暴露与CVD风险的IRR增加有关;然而,这种关联在统计学上并不显著。相比之下,没有观察到短期PM2.5暴露与CVD的显著关联。在清迈、清莱和南省,PM2.5和O3的联合暴露与COPD风险增加显著相关(p < 0.05)。相互作用分析显示,清莱和南的慢性阻塞性肺病和CVD具有协同作用。男性、年龄(≥60岁)、颗粒物和臭氧浓度的季节变化被认为是显著的影响因素。这些发现阐明了空气污染物对泰国北部北部呼吸和心血管健康的不同影响。此外,它们强调老年人和男性的脆弱性增加,强调迫切需要有针对性的、针对特定区域的公共卫生干预措施。
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引用次数: 0
Pre-existing pulmonary function abnormality exacerbates the impact of occupational dust exposure on incident hypertension: Evidence from a large occupational cohort 先前存在的肺功能异常加剧了职业性粉尘暴露对高血压事件的影响:来自大型职业队列的证据
IF 2.7 Pub Date : 2025-11-09 DOI: 10.1016/j.heha.2025.100157
Zhongzhi Xu , Xin Xu , Shao Lin , Bing Xia , Shanyu Zhou , Shu Wang , Yawei Guo , Lulu Lin , Huiyuan Zhong , Lerong Liu , Yongshun Huang , Wangjian Zhang
This study aimed to examine the independent and joint effects of occupational dust exposure (ODE) and pulmonary function abnormalities (PFA) on the incidence of hypertension, and to assess whether pre-existing PFA modifies the ODE–hypertension relationship. A prospective cohort design was used, drawing data from the Guangdong Key Occupational Diseases Surveillance Project (2021–2023), which included 144,627 workers from 21 cities in Guangdong, China. ODE and PFA were assessed using standardized protocols, and hypertension was defined as elevated blood pressure or use of antihypertensive medication. Cox proportional hazards models, restricted cubic splines, and interaction analyses were performed to evaluate associations, and Mendelian randomization (MR) using UK Biobank data was conducted to assess causality. At baseline, 33,766 participants (23.3 %) had PFA, and during follow-up, 14,996 (10.4 %) developed hypertension. Both ODE (HR = 1.12, 95 % CI: 1.08–1.16) and PFA (HR = 1.19, 95 % CI: 1.14–1.23) were independently associated with increased hypertension risk (P < 0.001), with a higher combined effect (HR = 1.39, 95 % CI: 1.31–1.47). A positive trend was observed between dust exposure duration and hypertension risk (HR = 1.11 for ≥6 years vs. <2 years; P for trend = 0.017). Respirable dust (≤10 μm) and inorganic dust were significantly associated with increased hypertension risk (HR = 1.16 and 1.13). MR analysis supported a causal relationship between ODE, PFA, and hypertension. These findings indicate that pre-existing PFA amplifies the hypertensive effects of ODE, highlighting the importance of respiratory health interventions to reduce hypertension risk among dust-exposed workers.
本研究旨在探讨职业性粉尘暴露(ODE)和肺功能异常(PFA)对高血压发病率的独立和联合影响,并评估先前存在的PFA是否会改变ODE与高血压的关系。采用前瞻性队列设计,数据来源于广东省重点职业病监测项目(2021-2023),包括来自广东省21个城市的144,627名劳动者。采用标准化方案评估ODE和PFA,并将高血压定义为血压升高或使用抗高血压药物。采用Cox比例风险模型、受限三次样条和相互作用分析来评估相关性,并使用UK Biobank数据进行孟德尔随机化(MR)来评估因果关系。在基线时,33,766名参与者(23.3%)患有PFA,在随访期间,14,996名参与者(10.4%)患有高血压。ODE (HR = 1.12, 95% CI: 1.08-1.16)和PFA (HR = 1.19, 95% CI: 1.14-1.23)与高血压风险增加独立相关(P < 0.001),合并效应更高(HR = 1.39, 95% CI: 1.31-1.47)。粉尘暴露时间与高血压风险呈正相关(≥6年HR = 1.11 vs. 2年P = 0.017)。呼吸性粉尘(≤10 μm)和无机粉尘与高血压风险增加显著相关(HR = 1.16和1.13)。磁共振分析支持ODE、PFA和高血压之间的因果关系。这些研究结果表明,先前存在的PFA放大了ODE的高血压效应,强调了呼吸健康干预措施对降低粉尘暴露工人高血压风险的重要性。
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引用次数: 0
What drives toilet cleanliness in urban schools? Roles of infrastructure, resources, and hygiene promotion in Kampala 是什么促使城市学校的厕所保持清洁?坎帕拉的基础设施、资源和卫生推广的作用
IF 2.7 Pub Date : 2025-11-09 DOI: 10.1016/j.heha.2025.100158
Jude Zziwa Byansi , Swaib Semiyaga , Alex Yasoni Katukiza , Najib Lukooya Bateganya , Frank Kansiime , Robinah Nakawunde Kulabako
Access to clean toilets in schools is essential for a conducive learning environment and safeguarding pupils' health. Urban schools often face sanitation challenges stemming from overcrowding, inadequate facilities, and differences in management practices across school categories such as public or private, primary or secondary, day or boarding, and service level classifications. Identifying key factors influencing toilet cleanliness is vital for improving urban school sanitation. This study investigated the drivers of toilet cleanliness through a cross-sectional study conducted in Kampala City, in Uganda. Kampala City has 852 schools of which 274 were selected for this study. Data collection comprised 274 structured observations guided by a checklist, 548 questionnaires administered to Head Teachers and Sanitation Teachers, and 40 key informant interviews. Logistic regression and decision tree modeling were used for data analysis. Across all school types, significant associations were observed between toilet cleanliness and facility privacy, sex segregation, presence of health clubs, handwashing facilities with soap and water, rainwater harvesting systems, sanitation budget, and toilet paper availability. The decision tree model identified rainwater harvesting, handwashing facilities, and health clubs as the strongest predictors of toilet cleanliness, in that order. Findings indicate that policymakers and school administrators should prioritize investment in water access, hygiene infrastructure, and health clubs to improve and sustain toilet cleanliness in urban schools.
在学校使用干净的厕所对于营造有利的学习环境和保护学生的健康至关重要。城市学校往往面临卫生方面的挑战,这些挑战源于过度拥挤、设施不足以及公立或私立、小学或中学、走读或寄宿以及服务水平分类等学校类别之间管理实践的差异。确定影响厕所清洁度的关键因素对于改善城市学校卫生条件至关重要。本研究通过在乌干达坎帕拉市进行的横断面研究调查了厕所清洁的驱动因素。坎帕拉市有852所学校,其中274所被选中参加这项研究。数据收集包括在核对表指导下进行的274次结构化观察,向校长和环卫教师发放的548份问卷,以及40次关键信息提供者访谈。采用Logistic回归和决策树模型进行数据分析。在所有类型的学校中,厕所清洁度与设施隐私、性别隔离、健康俱乐部的存在、带肥皂和水的洗手设施、雨水收集系统、卫生预算和厕纸的可用性之间存在显著关联。决策树模型将雨水收集、洗手设施和健身俱乐部确定为厕所清洁度的最强预测因子。研究结果表明,决策者和学校管理者应优先投资于供水、卫生基础设施和健康俱乐部,以改善和维持城市学校的厕所清洁。
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引用次数: 0
Exposure to cadmium and cerebrovascular mortality in the United States 美国的镉暴露与脑血管死亡率
IF 2.7 Pub Date : 2025-10-01 DOI: 10.1016/j.heha.2025.100156
Xin Wang , Ziqin Cao , Kelly M. Bakulski , Henry L. Paulson

Background

Cerebrovascular diseases are a leading cause of death in the U.S., and emerging evidence suggests that environmental toxicants such as cadmium may contribute to cerebrovascular risk. This study investigates the association between cadmium exposure and cerebrovascular mortality in a nationally representative sample of U.S. adults.

Methods

We analyzed data from adults aged ≥40 years in the National Health and Nutrition Examination Survey (NHANES) 1999–2016 cycles, with mortality follow-up through 2019. Blood cadmium was measured in 23,455 participants, and urinary cadmium was measured in 8929 participants. Cerebrovascular deaths were identified through linkage with the National Death Index. Survey-weighted Cox proportional hazards models evaluated associations between cadmium concentrations and cerebrovascular mortality.

Results

Over a mean follow-up of 10.2 years, 247 cerebrovascular deaths were observed. Each interquartile range increase in blood cadmium (0.40 µg/L) was associated with a 23 % higher risk of cerebrovascular mortality (HR = 1.23, 95 % CI: 1.04–1.46). Urinary cadmium was also associated with higher cerebrovascular mortality, although marginally significant (HR = 1.36 per doubling, 95 % CI: 0.99–1.87). Associations appeared stronger among former and current smokers, though interaction terms were not statistically significant.

Conclusions

Cadmium exposure is associated with increased cerebrovascular mortality in the U.S. population. These findings support cadmium as a modifiable environmental risk factor and underscore the need for public health interventions to reduce exposure through tobacco control, dietary regulations, and environmental policy.
背景在美国,脑血管疾病是导致死亡的主要原因之一,而且越来越多的证据表明,镉等环境毒物可能会增加脑血管风险。本研究调查了镉暴露与脑血管死亡率之间的关系,在美国成年人的全国代表性样本。方法分析1999-2016年国家健康与营养调查(NHANES)周期中年龄≥40岁的成年人的数据,并随访至2019年的死亡率。在23,455名参与者中测量了血镉,在8929名参与者中测量了尿镉。脑血管死亡是通过与国家死亡指数的联系来确定的。调查加权Cox比例风险模型评估了镉浓度与脑血管死亡率之间的关系。结果平均随访10.2年,共发生247例脑血管死亡。血镉浓度每增加四分位数(0.40µg/L),脑血管死亡风险增加23% (HR = 1.23, 95% CI: 1.04-1.46)。尿镉也与较高的脑血管死亡率相关,尽管有边际意义(HR = 1.36 / 2倍,95% CI: 0.99-1.87)。尽管相互作用项在统计上不显著,但在曾经和现在的吸烟者之间的关联似乎更强。结论:在美国人群中,镉暴露与脑血管死亡率增加有关。这些发现支持镉是一种可改变的环境风险因素,并强调需要通过烟草控制、饮食法规和环境政策进行公共卫生干预,以减少镉的暴露。
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引用次数: 0
Assessment of particulate matter exposure associated with biomass storage in urban heating plant 与城市供热厂生物质储存有关的颗粒物暴露评估
IF 2.7 Pub Date : 2025-10-01 DOI: 10.1016/j.heha.2025.100154
Daniel Tomčík , Miloš Gejdoš
This study assessed the airborne particulate matter (PM) in urban heating plants, potentially affecting respiratory health in workers and nearby residents. The objectives of this study were to characterize occupational exposure during chip-loading activities and to evaluate ambient PM concentrations in the surrounding environment. Occupational exposure was assessed in accordance with the relevant standards using the Temtop M2000C, while continuous ambient monitoring was conducted with the AirNote device. The results indicate a significant increase in PM concentrations during woodchip loading activities. Mean PM2.5 concentrations were 24.03 µg/m3 during loading and 8.07 µg/m3 during non-loading, while PM10 levels were 38.75 µg/m3 and 12.80 µg/m3, respectively. Continuous monitoring revealed that daily mean PM2.5 concentrations were above the WHO 24-h guideline value of 15 µg/m3 on 3 days. The maximum daily mean PM2.5 concentration was 43.7 µg/m3, while the median daily mean was 22.5 µg/m3. For PM10, the maximum daily mean reached 70.9 µg/m3 and the median daily mean was 35.6 µg/m3, with exceedance of the WHO 24-hour guideline of 45 µg/m3 observed on one day. Distance from the woodchip pile also had a significant effect on PM concentrations (p < 0.001), with short-term mean levels at 50 m exceeding the WHO 24-h guideline value by 2.9 times for PM2.5 and 1.6 times for PM10. These guideline values are provided for context only, as they represent 24-hour mean concentrations and not instantaneous limits. Beyond 100 m, no further significant reduction in PM levels was observed. Biomass storage operations can cause temporary PM exceedances, particularly during handling and near storage areas. These findings underscore the importance of implementing mitigation strategies to reduce airborne particulate emissions.
本研究评估了城市供热厂空气中的颗粒物(PM),这些颗粒物可能影响工人和附近居民的呼吸健康。本研究的目的是表征在芯片装载活动期间的职业暴露,并评估周围环境中的PM浓度。使用Temtop M2000C按照相关标准评估职业暴露,同时使用AirNote设备进行连续环境监测。结果表明,在木屑装载活动期间,PM浓度显著增加。加载期间PM2.5的平均浓度为24.03µg/m3,非加载期间为8.07µg/m3, PM10的平均浓度分别为38.75µg/m3和12.80µg/m3。连续监测显示,有3天PM2.5日均浓度高于WHO 24小时指导值15µg/m3。PM2.5日平均浓度最大值为43.7µg/m3,日平均中位数为22.5µg/m3。PM10最大日平均值为70.9µg/m3,中位日平均值为35.6µg/m3,有一天超过了WHO 24小时指导值45µg/m3。距离木屑堆的距离对PM浓度也有显著影响(p < 0.001), 50 m处的短期平均水平PM2.5是WHO 24小时指导值的2.9倍,PM10是1.6倍。这些指标值仅供参考,因为它们代表24小时平均浓度,而不是瞬时限值。超过100米,未观察到PM水平进一步显著降低。生物质储存操作可能导致暂时的PM超标,特别是在处理和储存区域附近。这些发现强调了实施减缓战略以减少空气中微粒排放的重要性。
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引用次数: 0
Air pollution mixtures and stillbirth: k-means cluster analysis 空气污染混合物与死产:k均值聚类分析
IF 2.7 Pub Date : 2025-09-19 DOI: 10.1016/j.heha.2025.100153
Naomi O. Riches , Ramkiran Gouripeddi , Robert M. Silver , Julio C. Facelli

Background

Preventing stillbirths starts with identifying modifiable risk factors, such as air pollution (AP). Most research has focused on individual components of AP (e.g. PM2.5) to assess the linear relationship between air pollutant concentration and stillbirth, with mixed results. However, the air we breathe is a mixture of gases and particles. The purpose of this study was to assess how mixtures of criteria air pollutants are associated with stillbirth in the United States.

Materials and Methods

Air pollution data from the US Environmental Protection Agency and individual US birth and fetal death data from the CDC National Vital Statistics System were used. Air pollutant exposures were clustered using k-means clustering. A categorical variable linking each patient to one of these clusters was used in a regression analysis.

Results

Four AP clusters were identified through k-means. Exposure to air pollution mixtures included in Clusters 1, 2, and 4 during pregnancy was associated with a 40%, 13%, and 43% increase in the odds of stillbirth, compared to Cluster 3 (reference), (OR = 1.40, 95% CI: 1.36-1.44, p<0.001; OR = 1.13, 95% CI: 1.09-1.16, p<0.001; OR = 1.43, 95% CI: 1.38-1.49, p<0.001), respectively.

Discussion

The air pollution cluster associated with the greatest odds of stillbirth was high in PM2.5 and SO2, which may indicate industrial sources. To our knowledge, this is the first study to assess the impact of air pollution mixtures on stillbirth using k-means clustering. This method can be used to identify non-linear relationships between mixtures of air pollution and a health outcome.
预防死产始于确定可改变的风险因素,如空气污染(AP)。大多数研究都集中在AP的单个成分(例如PM2.5)上,以评估空气污染物浓度与死胎之间的线性关系,结果好坏参半。然而,我们呼吸的空气是气体和颗粒的混合物。本研究的目的是评估美国标准空气污染物的混合物与死产的关系。材料和方法使用美国环境保护署的空气污染数据和美国疾病控制与预防中心国家生命统计系统的美国出生和胎儿死亡数据。采用k-均值聚类对空气污染物暴露进行聚类。在回归分析中使用了将每个患者与其中一个集群联系起来的分类变量。结果通过k-means鉴定出4个AP聚类。与聚类3(参考文献)相比,妊娠期间暴露于聚类1、2和4中的空气污染混合物与死产几率分别增加40%、13%和43%相关(OR = 1.40, 95% CI: 1.36-1.44, p<0.001; OR = 1.13, 95% CI: 1.09-1.16, p<0.001; OR = 1.43, 95% CI: 1.38-1.49, p<0.001)。与死产几率最高相关的空气污染集群PM2.5和SO2含量较高,这可能表明工业来源。据我们所知,这是第一个使用k均值聚类来评估空气污染混合物对死胎影响的研究。这种方法可用于确定空气污染混合物与健康结果之间的非线性关系。
{"title":"Air pollution mixtures and stillbirth: k-means cluster analysis","authors":"Naomi O. Riches ,&nbsp;Ramkiran Gouripeddi ,&nbsp;Robert M. Silver ,&nbsp;Julio C. Facelli","doi":"10.1016/j.heha.2025.100153","DOIUrl":"10.1016/j.heha.2025.100153","url":null,"abstract":"<div><h3>Background</h3><div>Preventing stillbirths starts with identifying modifiable risk factors, such as air pollution (AP). Most research has focused on individual components of AP (e.g. PM<sub>2.5</sub>) to assess the linear relationship between air pollutant concentration and stillbirth, with mixed results. However, the air we breathe is a mixture of gases and particles. The purpose of this study was to assess how mixtures of criteria air pollutants are associated with stillbirth in the United States.</div></div><div><h3>Materials and Methods</h3><div>Air pollution data from the US Environmental Protection Agency and individual US birth and fetal death data from the CDC National Vital Statistics System were used. Air pollutant exposures were clustered using k-means clustering. A categorical variable linking each patient to one of these clusters was used in a regression analysis.</div></div><div><h3>Results</h3><div>Four AP clusters were identified through k-means. Exposure to air pollution mixtures included in Clusters 1, 2, and 4 during pregnancy was associated with a 40%, 13%, and 43% increase in the odds of stillbirth, compared to Cluster 3 (reference), (OR = 1.40, 95% CI: 1.36-1.44, p&lt;0.001; OR = 1.13, 95% CI: 1.09-1.16, p&lt;0.001; OR = 1.43, 95% CI: 1.38-1.49, p&lt;0.001), respectively.</div></div><div><h3>Discussion</h3><div>The air pollution cluster associated with the greatest odds of stillbirth was high in PM<sub>2.5</sub> and SO<sub>2</sub>, which may indicate industrial sources. To our knowledge, this is the first study to assess the impact of air pollution mixtures on stillbirth using k-means clustering. This method can be used to identify non-linear relationships between mixtures of air pollution and a health outcome.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100153"},"PeriodicalIF":2.7,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145159073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Blood cadmium and lead concentrations in association with homocysteine and all-cause and cardiovascular mortality 血镉和铅浓度与同型半胱氨酸、全因死亡率和心血管死亡率的关系
IF 2.7 Pub Date : 2025-09-19 DOI: 10.1016/j.heha.2025.100148
Shaohui Liu , Ziqi Zeng , Quanhong Chen , Anan Zhou , Yunan Xu , Hao Chen , Yunfeng Zou
Cadmium and lead exposure are reported to associate with elevated plasma homocysteine concentrations. However, whether homocysteine plays a role in the associations of cadmium and lead with all-cause and cardiovascular mortality is unclear. We conducted a cohort study using data from 6456 participants in the National Health and Nutrition Examination Survey (NHANES) (2003–2006). Cox regression models and restricted cubic splines (RCS) were used to examine the associations between cadmium, lead, and homocysteine and all-cause and cardiovascular mortality. Mediation analysis was conducted to evaluate the indirect effect of homocysteine in the associations between cadmium, lead and all-cause and cardiovascular mortality. During a median of 14.33 years of follow-up, 1642 (25.43 %) all-cause deaths and 575 (8.91 %) cardiovascular deaths were observed. When compared with the first quartile, cadmium, lead, and homocysteine levels in the fourth quartile were associated with increased all-cause mortality risk [hazard ratios (HRs) with 95 % confidence interval (CI) 1.91 (1.60, 2.29), 1.38 (1.16, 1.64), and 1.74 (1.42, 2.14), respectively] and cardiovascular mortality [1.85 (1.37, 2.50), 1.55 (1.15, 2.09), 1.67 (1.17, 2.37), respectively]. RCS analysis suggested nonlinear associations of cadmium, lead, and homocysteine with all-cause mortality, nonlinear relationships between cadmium and cardiovascular mortality, and linear associations between lead, homocysteine and cardiovascular mortality. Changes in homocysteine levels accounted for approximately 4.11 % and 5.81 % of the observed associations between cadmium exposure and all-cause and cardiovascular mortality, respectively. Similar observations were made for homocysteine on the associations of lead exposure and all-cause (11.05 %) and cardiovascular (7.69 %) mortality. Furthermore, lead concentrations modified the associations of cadmium and homocysteine with cardiovascular and all-cause mortality. Our findings suggested that plasma homocysteine was associated with the observed relationships between cadmium and lead exposure and increased all-cause and cardiovascular mortality, potentially reflecting underlying pathways relevant to heavy metal-related cardiovascular risk.
据报道,镉和铅暴露与血浆同型半胱氨酸浓度升高有关。然而,同型半胱氨酸是否在镉和铅与全因死亡率和心血管死亡率的关联中起作用尚不清楚。我们使用2003-2006年国家健康与营养检查调查(NHANES)的6456名参与者的数据进行了一项队列研究。使用Cox回归模型和限制性三次样条(RCS)来检查镉、铅和同型半胱氨酸与全因死亡率和心血管死亡率之间的关系。进行了中介分析,以评估同型半胱氨酸在镉、铅与全因死亡率和心血管死亡率之间的间接影响。在中位14.33年的随访期间,观察到1642例(25.43%)全因死亡和575例(8.91%)心血管死亡。与第一个四分位数相比,第四个四分位数的镉、铅和同型半胱氨酸水平与全因死亡风险增加相关[95%可信区间(CI)分别为1.91(1.60,2.29)、1.38(1.16,1.64)和1.74(1.42,2.14)]和心血管死亡率[分别为1.85(1.37,2.50)、1.55(1.15,2.09)、1.67(1.17,2.37)]。RCS分析表明,镉、铅和同型半胱氨酸与全因死亡率呈非线性关系,镉与心血管死亡率呈非线性关系,铅、同型半胱氨酸与心血管死亡率呈线性关系。在观察到的镉暴露与全因死亡率和心血管死亡率之间的关联中,同型半胱氨酸水平的变化分别占约4.11%和5.81%。同型半胱氨酸对铅暴露与全因死亡率(11.05%)和心血管死亡率(7.69%)之间的关系也进行了类似的观察。此外,铅浓度改变了镉和同型半胱氨酸与心血管和全因死亡率的关系。我们的研究结果表明,血浆同型半胱氨酸与观察到的镉和铅暴露、全因死亡率和心血管死亡率增加之间的关系有关,可能反映了与重金属相关的心血管风险相关的潜在途径。
{"title":"Blood cadmium and lead concentrations in association with homocysteine and all-cause and cardiovascular mortality","authors":"Shaohui Liu ,&nbsp;Ziqi Zeng ,&nbsp;Quanhong Chen ,&nbsp;Anan Zhou ,&nbsp;Yunan Xu ,&nbsp;Hao Chen ,&nbsp;Yunfeng Zou","doi":"10.1016/j.heha.2025.100148","DOIUrl":"10.1016/j.heha.2025.100148","url":null,"abstract":"<div><div>Cadmium and lead exposure are reported to associate with elevated plasma homocysteine concentrations. However, whether homocysteine plays a role in the associations of cadmium and lead with all-cause and cardiovascular mortality is unclear. We conducted a cohort study using data from 6456 participants in the National Health and Nutrition Examination Survey (NHANES) (2003–2006). Cox regression models and restricted cubic splines (RCS) were used to examine the associations between cadmium, lead, and homocysteine and all-cause and cardiovascular mortality. Mediation analysis was conducted to evaluate the indirect effect of homocysteine in the associations between cadmium, lead and all-cause and cardiovascular mortality. During a median of 14.33 years of follow-up, 1642 (25.43 %) all-cause deaths and 575 (8.91 %) cardiovascular deaths were observed. When compared with the first quartile, cadmium, lead, and homocysteine levels in the fourth quartile were associated with increased all-cause mortality risk [hazard ratios (HRs) with 95 % confidence interval (CI) 1.91 (1.60, 2.29), 1.38 (1.16, 1.64), and 1.74 (1.42, 2.14), respectively] and cardiovascular mortality [1.85 (1.37, 2.50), 1.55 (1.15, 2.09), 1.67 (1.17, 2.37), respectively]. RCS analysis suggested nonlinear associations of cadmium, lead, and homocysteine with all-cause mortality, nonlinear relationships between cadmium and cardiovascular mortality, and linear associations between lead, homocysteine and cardiovascular mortality. Changes in homocysteine levels accounted for approximately 4.11 % and 5.81 % of the observed associations between cadmium exposure and all-cause and cardiovascular mortality, respectively. Similar observations were made for homocysteine on the associations of lead exposure and all-cause (11.05 %) and cardiovascular (7.69 %) mortality. Furthermore, lead concentrations modified the associations of cadmium and homocysteine with cardiovascular and all-cause mortality. Our findings suggested that plasma homocysteine was associated with the observed relationships between cadmium and lead exposure and increased all-cause and cardiovascular mortality, potentially reflecting underlying pathways relevant to heavy metal-related cardiovascular risk.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100148"},"PeriodicalIF":2.7,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145416428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Unraveling co-contamination characteristics of heavy metals in soil-crop system and collaborative management of their health risk across China 中国土壤-作物系统重金属共污染特征及其健康风险协同管理
IF 2.7 Pub Date : 2025-09-18 DOI: 10.1016/j.heha.2025.100151
Wenzhuo Deng , Fei Li , Xiyao Chen , Jinyuan Guo , Chang Gao , Junrui Zhao , Tianwei Sun , Jingdong Zhang
Heavy metal pollution in farmland soil and crops directly affects the food safety and public health. A comprehensive national-scale assessment from an integrated soil-crop perspective in China remains limited. To address this gap, this study conducted a systematic review using an optimized bibliometric approach enhanced with uncertainty control and case mining. 1157 publications reporting on eight heavy metals (As, Cd, Cr, Cu, Hg, Ni, Pb, and Zn) in agricultural soils, grains, and vegetables across China were analyzed. Key findings include: (1) Cadmium (Cd) was the most widespread pollutant in soils, whereas mercury (Hg) showed highly concentrated hotspots. (2) A discrepancy was observed between soil pollution levels and the corresponding crop contamination indicating that the relationship between them is not fully synergistic. (3) Health risk assessment revealed that the total carcinogenic risk from soil exposure (10⁻⁶ - 10⁻⁵) was significantly lower than that from ingestion of contaminated grains and vegetables (10⁻⁴ - 10⁻³). Arsenic (As) and Cd were identified as the primary risk contributors in most provinces. (4) Geographically, integrated high-risk areas were classified as Class I (Guangdong, Guizhou, Yunnan) and Class II (Hunan). Risk sources in Yunnan and Guizhou were attributed to both geogenic and anthropogenic activities, with exposure dominated by vegetable and grain ingestion, respectively. In contrast, risks in Guangdong and Hunan were primarily linked to human activities (industrial, mining, and agricultural), with comparable exposure from both crops. Based on these findings, tailored risk mitigation strategies are proposed for the identified high-risk provinces, considering their distinct exposure pathways and contamination sources.
农田土壤和农作物重金属污染直接影响食品安全和公众健康。在中国,从土壤-作物综合角度进行全国范围的综合评估仍然有限。为了解决这一差距,本研究使用优化的文献计量学方法进行了系统回顾,并加强了不确定性控制和案例挖掘。分析了中国农业土壤、粮食和蔬菜中8种重金属(As、Cd、Cr、Cu、Hg、Ni、Pb和Zn)的1157份出版物。主要发现包括:(1)镉(Cd)是土壤中分布最广的污染物,而汞(Hg)则呈现高度集中的热点。(2)土壤污染水平与作物污染水平之间存在差异,表明两者之间的关系并非完全协同。(3)健康风险评估显示,接触土壤(10⁻6 - 10⁻5)的总致癌风险明显低于摄入受污染的谷物和蔬菜(10⁻4 - 10⁻3)。在大多数省份,砷(As)和镉被确定为主要的危险因素。(4)综合高风险区域在地理上划分为一类(广东、贵州、云南)和二类(湖南)。云南和贵州的风险源主要为地质和人为活动,暴露主要为蔬菜和谷物摄入。相比之下,广东和湖南的风险主要与人类活动(工业、采矿和农业)有关,两种作物的风险相当。在此基础上,针对已确定的高风险省份,考虑到其不同的暴露途径和污染源,提出了量身定制的风险缓解策略。
{"title":"Unraveling co-contamination characteristics of heavy metals in soil-crop system and collaborative management of their health risk across China","authors":"Wenzhuo Deng ,&nbsp;Fei Li ,&nbsp;Xiyao Chen ,&nbsp;Jinyuan Guo ,&nbsp;Chang Gao ,&nbsp;Junrui Zhao ,&nbsp;Tianwei Sun ,&nbsp;Jingdong Zhang","doi":"10.1016/j.heha.2025.100151","DOIUrl":"10.1016/j.heha.2025.100151","url":null,"abstract":"<div><div>Heavy metal pollution in farmland soil and crops directly affects the food safety and public health. A comprehensive national-scale assessment from an integrated soil-crop perspective in China remains limited. To address this gap, this study conducted a systematic review using an optimized bibliometric approach enhanced with uncertainty control and case mining. 1157 publications reporting on eight heavy metals (As, Cd, Cr, Cu, Hg, Ni, Pb, and Zn) in agricultural soils, grains, and vegetables across China were analyzed. Key findings include: (1) Cadmium (Cd) was the most widespread pollutant in soils, whereas mercury (Hg) showed highly concentrated hotspots. (2) A discrepancy was observed between soil pollution levels and the corresponding crop contamination indicating that the relationship between them is not fully synergistic. (3) Health risk assessment revealed that the total carcinogenic risk from soil exposure (10⁻⁶ - 10⁻⁵) was significantly lower than that from ingestion of contaminated grains and vegetables (10⁻⁴ - 10⁻³). Arsenic (As) and Cd were identified as the primary risk contributors in most provinces. (4) Geographically, integrated high-risk areas were classified as Class I (Guangdong, Guizhou, Yunnan) and Class II (Hunan). Risk sources in Yunnan and Guizhou were attributed to both geogenic and anthropogenic activities, with exposure dominated by vegetable and grain ingestion, respectively. In contrast, risks in Guangdong and Hunan were primarily linked to human activities (industrial, mining, and agricultural), with comparable exposure from both crops. Based on these findings, tailored risk mitigation strategies are proposed for the identified high-risk provinces, considering their distinct exposure pathways and contamination sources.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100151"},"PeriodicalIF":2.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145159072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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Hygiene and environmental health advances
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