Reviews on Environmental Health

Editor-in-Chief: Kelly G. Pennell
Edited by: Tahir Rafique and Alexander Sergeev

Language: English

First published: January 1, 1986

Publication Frequency: 4 issues per year

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About this journal

It is with great pleasure and excitement that we announce Dr. Kelly G. Pennell (kellypennell@uky.edu) has taken over as our new Editor-in-Chief. Dr. Pennell steps into this role following the exceptional tenure of David Carpenter, and we are confident that her leadership will usher in a new era of growth and innovation.

About Dr. Kelly G. Pennell

Dr. Kelly G. Pennell is the Earl Parker Robinson Chair Professor of Sustainability and Environment in the Department of Civil Engineering at the University of Kentucky. Dr. Pennell is a licensed professional engineer with previous experience working for an international consulting firm on hazardous waste site clean-ups. She earned her degrees from Purdue University (PhD 2005, Civil Engineering), Rose-Hulman Institute of Technology (MS 2021, Environmental Engineering) and Lawrence Technological University (BS 1997, Civil Engineering). Dr. Pennell is internationally recognized for her research involving stakeholder engagement, modeling fate and transport processes, and re-(defining) chemical exposure conceptual models in communities. She is a leading expert in vapor intrusion processes, which involve the migration of subsurface vapors into indoor air spaces. Her research has fostered informed decision-making in many communities and influenced policy framework changes at multiple jurisdiction levels.

Objective
Reviews on Environmental Health (REVEH) is an international peer-reviewed journal that aims to fill the need for publication of review articles on hot topics in the field of environmental health. It is intended to be an inspiring forum for scientists, environmentalists, physicians, engineers, and students who are concerned with aspects of human health, including quality of life, that are determined by physiological and psychosociological interactions between humans and physical, chemical, biological, and social factors in the environment. One major challenge is to link the research on environmental causes of disease to the clinical practice of medicine.
REVEH is a hybrid journal, published quarterly in print and online. All contributions submitted for publication in REVEH are subject to single-anonymized peer review by at least two experts in the field, selected and invited by the Editor-in-Chief and a dedicated Editorial Team. REVEH publishes only English-language articles.

Topics
Environmental toxicology // Neurotoxicology // Immunology // Oncology // Dermatology // Epidemiology // Molecular biology // Pharmacogenetics // Child health // Medicine, occupational health and risk assessment // Water, air, and soil quality control // Climate change// Methods for biomonitoring and remediation

Article formats
Review, Opinion Paper, Point/Counterpoint Paper, Letter to the Editor and Reply, Editorial

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Specialized, comprehensive and cutting-edge review articles
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Authors have the option of publishing their articles under the Creative Commons Attribution (CC-BY-4.0) open access license. Open access allows authors to retain copyright and share their findings with the scientific community without restrictions. Authors who belong to an institution that has an agreement with the publisher can publish open access without paying an article processing charge (APC) or at a considerable discount

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m6A methylation – a new target of metabolic diseases induced by environmental pollutants

September 26, 2025

Runfeng Chang, Jinyun Li, Lu Fang, Miaocui Xi, Yue Huang, Jiahang Li, Wenjun Zhang, Qiuhui Qian, Zejun Wang, Jin Yan, Huili Wang

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Exposure to environmental pollutants is closely associated with the development of obesity and related metabolic diseases. As the most prevalent form of eukaryotic chemical modification, N6-methyladenosine (m6A) methylation regulated by series enzymes plays an important role in the pathogenesis of metabolic diseases such as obesity, non-alcoholic fatty liver disease (NAFLD), atherosclerosis (AS), and type 2 diabetes (T2D). Therefore, investigating the specific mechanisms of m6A methylation in obesity and related metabolic diseases and its relationship with environmental pollutants is vital for developing treatment and prevention strategies. This article summarizes the latest research on m6A methylation in glucose and lipid metabolism-related diseases and elucidates the specific molecular mechanisms of metabolic disorders regulated by m6A methylation-related enzymes. More importantly, we highlight that m6A methylation process is a target for environmental pollutants in inducing human metabolic diseases. Our review aims to provide new insights into understanding the underlying mechanisms of environmental pollutant-induced metabolic diseases and to explore preventive and therapeutic measures.
Open Access
Genetic susceptibility to adverse arsenic-related cardiometabolic outcomes: a systematic review

June 27, 2025

Kim R. van Daalen, Jeenan Kaiser, Nusrat Khan, Maša Josipović, Clare T. Oliver-Williams, Adam S. Butterworth

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Millions of people worldwide are chronically exposed to environmental arsenic through drinking water, increasing their risk of various adverse cardiometabolic outcomes. To understand the inter-individual variation in arsenic susceptibility, this systematic review explores all epidemiological evidence on interactions between single nucleotide polymorphisms (SNPs) and arsenic exposure in relation to cardiometabolic health. Five electronic databases were searched until April 2023. From 42,202 retrieved publications, 18 candidate gene-environment (cGxE) studies were included, and no genome-wide association studies were found. Of 676 SNPs in 148 genes tested, 40 SNPs in 24 genes, 4 haplotypes and combined SNPs in MCP-1/APOE , were reported to statistically significantly interact with arsenic exposure. These genes were involved in arsenic metabolism , oxidative stress or defence, DNA damage repair, endothelial (dys) function, inflammation or immune function, tumour suppressor activity, or were previously implicated in cardiometabolic disease pathways. Most studies did not explore the same SNPs (or strong proxies), and none of the identified SNP-arsenic interactions were replicated for the same arsenic species and cardiometabolic outcome. Whilst some SNPs are suggestive of influencing susceptibility to arsenic for various cardiometabolic outcomes, further research is needed to understand the interplay between arsenic and genetic variants, identify at-risk populations, and improve risk assessment.
Open Access
Exposure to air pollution from coal-fired power plants and impacts on human health: a scoping review

March 6, 2025

Nomfundo Mahlangeni, Thandi Kapwata, Candice Webster, Chantelle Howlett-Downing, Caradee Y. Wright

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Communities living in proximity to coal-fired power plants (CFPPs) may be at greater risk of negative health impacts from exposure to air pollution than communities living further away. The aim of this scoping review was to provide an update on the evidence of the health risks of air pollution exposure associated with living in proximity to CFPPs and to evaluate the relationship between residential proximity and the extent of the health burden. We followed the PRISMA-ScR guidelines and searched Google Scholar, PubMed, ScienceDirect, Scopus and Web of Science for relevant studies from inception up to 31 January 2024. Fifty-six studies were included with most articles published from 2016 to 2023 (n=33, 59 %) and 35 were in high income countries (63 %). Living close to CFPPs was frequently associated with increased odds or likelihood of respiratory disorders, adverse birth outcomes and child developmental issues. Interventions such as emission control systems or total shutdown of CFPPs led to improved health among communities living near CFPPs. The review highlights the health impacts from air pollution associated with living in proximity to CFPPs and the need for policy measures to reduce air pollution by installing emission control technologies or transitioning to cleaner energy sources.
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Corrigendum to: Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder

October 26, 2016

Dominique Belpomme, Christine Campagnac, Philippe Irigaray

Article number: 20158888

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Rachel Carson and Theo Colborn: two pioneering women of science opposing an epoch of toxic entanglement

January 1, 2000

Steven L. Ogden, David O. Carpenter

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A changing of the guard at Reviews on Environmental Health

January 1, 2000

David O. Carpenter

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Potential effects of MPs and their co-pollutants on human intestinal tract

January 1, 2000

Lixiang Wang, Jiayu Li, Chao Liu, Wanshun Li, Yi Lu, Zhenghui Yang, Zhendong Jin, Haojie Huang

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Microplastics (MPs), which are tiny plastic particles measuring less than 5 mm, have sparked public concern in recent years. When exposed to the environment, MPs absorb a variety of pollutants, leading to joint damage to human digestive system and other tissues. Human exposure to MPs mainly through food intake, resulting in potential risk of intestinal tract. Research have demonstrated that MPs compromise intestinal integrity and disrupt microbiota, as well as traverse into systemic circulation, posing threat to other tissues in our body. Morever, the MPs also serve as the “carrier” of the pollutants in the environment, such as organic compound, heavy metal and marine pollutant. The interaction between co-pollutants and MPs will influence their physical and chemical properties, producing dual toxic effects on intestinal system. However, the uptake and digestion process of MPs and their co-pollutants in the human body, the extent and mechanism of intestinal damage remain obscure. This review synthesizes current knowledge on MPs’ uptake and digestion process in the gut, elucidating the pathogenesis of MPs and their co-pollutant induced damage on intestinal physical, microbiota and immune barrier.
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Metals exposure and biomarkers of liver damage: a systematic review and meta-analysis of observational studies

January 1, 2000

Ibrahim Issah, Serwaa A. Bawua, John Arko-Mensah, Mabel S. Duah, Shirley V. Simpson, Thomas P. Agyekum, Olalekan A. Uthman, Julius N. Fobil

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Introduction Environmental exposure to metals represents a significant global health concern, yet the hepatotoxic potential of these contaminants remains incompletely characterized. This systematic review and meta-analysis aimed to quantify the association between exposure to metals and liver damage as indicated by liver enzyme alterations. Content We conducted a comprehensive search of electronic databases for epidemiological studies that examined associations between metal exposure and liver enzymes. Using random-effects models, we calculated pooled standardized mean differences (SMDs) with 95 % confidence intervals (CIs) for each metal. Subgroup analyses explored variations by geographical region, exposure assessment methodology, liver biomarkers, and study characteristics. Summary Thirty-nine studies met inclusion criteria. All four metals showed significant positive associations with liver damage, with cadmium exhibiting the strongest association (SMD=5.98, 95 % CI: 2.16–9.87), followed by lead (SMD=5.48, 95 % CI: 0.63–10.33), mercury (SMD=5.15, 95 % CI: 0.21–10.51), and arsenic (SMD=1.52, 95 % CI: 0.53–2.52). Metal-specific patterns of liver enzyme alterations were observed: arsenic primarily affected transaminases (ALT, AST), while cadmium, mercury, and lead showed stronger associations with AST and GGT. Outlook This systematic review and meta-analysis provides robust evidence that environmental exposure to arsenic, cadmium, mercury, and lead is significantly associated with liver damage across diverse populations.
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Impacts of PM_2.5 on stillbirth and the potential mechanism: a narrative review

January 1, 2000

Zhan Li, Ruixia Liu, Enjie Zhang

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Air pollution has attracted widespread attention as one of the major environmental health problems worldwide. In recent years, recognized as one of the major environmental risk factors for the increased global burden of disease, fine particulate matter (PM 2.5 ) increased risk of adverse pregnancy outcomes such as stillbirth. Stillbirths impose a substantial burden on both families and society. Although the existing evidence has revealed the association between PM 2.5 exposure and stillbirth, the underlying mechanism behind this is a lack of clarity. In this review, epidemiological evidence regarding the effects of PM 2.5 on stillbirth, as well as the sensitive windows of exposure, has been summarized. For the potential mechanism, the generation of reactive oxygen species was recognized as the molecular initiating event (MIE), and trigged oxidative stress, mitochondrial dysfunction, regulated cell death (RCD), inflammation and hyper coagulation, which can lead to pathological changes in the placenta and further lead to stillbirth. The purpose is to provide scientific evidence for developing early prevention strategies, reducing the stillbirth rate, and alleviating the social burdens of stillbirth.
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Prevalence of foodborne pathogens in ready-to-eat foods: systematic review, meta-analysis and meta-regression

January 1, 2000

Pavel V. Berezhanskiy, Amirhossein Mahmoudizeh, Yadolah Fakhri

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Ready-to-eat (RTE) foods are highly susceptible to microbial contamination, posing significant public health risks. This study aimed to conduct a systematic review, meta-analysis, and meta-regression to evaluate the prevalence of foodborne pathogens in RTE foods, assess trends over time, and examine the impact of the Global Food Security Index (GFSI). The search was conducted across Scopus, Web of Science, Embase, and PubMed until 2025. Studies reporting pathogen prevalence in RTE foods were included. Meta-analysis in defined subgroup and meta-regression assessed the effects of time and GFSI on prevalence trends. Sixty-five papers with 858 datasets comprising a total of 232,760 samples were included in the meta-analysis. Gram-negative pathogens (ES=18.32, 95 % CI: 15.29–21.53) were more prevalent than Gram-positive pathogens (ES=8.08, 95 % CI: 7.17–9.02). The African Region had the highest prevalence (ES=30.02, 95 % CI: 25.75–34.44), while the Americas had the lowest (ES=4.56, 95 % CI: 2.28–7.34). Contamination increased over time (C=0.018, p<0.001) but decreased with GFSI implementation (C=−0.005, p<0.001). RTE foods are highly vulnerable to contamination, particularly by Gram-negative pathogens. Regional disparities highlight the need for improved food safety infrastructure, especially in high-risk areas. Adopting global standards like GFSI and addressing emerging challenges such as antimicrobial resistance and climate change are essential for reducing foodborne illnesses.
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Fine particulate matter exposure and cancer risk: a systematic review and meta-analysis of prospective cohort studies

January 1, 2000

Yuting Feng, Jiaoyuan Li, Yi Wang, Tongxin Yin, Qiankun Wang, Liming Cheng

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Studies examining the relationship between fine particulate matter (PM 2.5 ) exposure and cancer risk is inconclusive, with an evident scarcity of comprehensive data on the overall cancer risk. Given the emergence of new evidence, updated meta-analyses is essential. A search was performed on multiple databases including PubMed, Embase, Scopus, Web of Science, and the Cochrane Library up to Jan 2025. Hazard ratios (HRs), relative risks (RRs), or incidence rate ratios (IRRs) with their 95 % confidence intervals (CIs) were extracted and pooled. Moreover, a comprehensive and detailed quality assessment of the included studies was conducted to validate the plausibility of the findings. Overall, 57 original studies were included, covering 36 cancer categories and including overall cancer and malignancies specific to particular anatomical sites. For each increase of 10 μg per cubic meter in PM 2.5 concentration, there was an observed pooled HR of 1.07 for overall cancer (95 %CI:1.02–1.13). In the case of site-specific cancers, the pooled HRs were 1.11 (95 %CI:1.07–1.15), 1.06 (95 %CI:1.02–1.11), 1.17 (95 %CI:1.07–1.28), and 1.14 (95 %CI:1.03–1.26) for lung, breast, liver and esophageal cancers, respectively. Furthermore, PM 2.5 exposure may potentially correlate with the risk of cancers at other anatomical locations including upper aerodigestive tract, oral cavity, kidney, skin, as well as digestive organs. In light of available evidence, it is inferred that PM 2.5 exposure could potentially raise overall cancer risk with moderate certainty. As for site-specific malignancies, there is very low certainty evidence for lung cancer, low certainty evidence for breast cancer, and moderate certainty evidence for both liver and esophageal cancers.
Open Access
The effects of bushfire smoke exposure on oxidative stress and inflammatory biomarkers: a systematic review

January 1, 2000

Siti Nurshahida Nazli, Gaurav Langan, Sophie Iles, Leron Rathnayake, Dhiya Rampersad, Iyanuoluwa Araba, Peter D. Sly, Dwan Vilcins

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Introduction Bushfire smoke (BFS) is an escalating global health concern, with increasing bushfire frequency due to climate change. Exposure to BFS significantly impacts public health due to worsening respiratory and cardiovascular conditions, causing increased of hospitalizations and mortality. While BFS exposure is linked to morbidity of these conditions, the underlying biological mechanisms, particularly oxidative stress and inflammation, remain unclear. Content This systematic review (PROSPERO ID: CRD42024554409) synthesized evidence on oxidative stress and inflammatory biomarkers from BFS exposure. Comprehensive searches of PubMed, Embase, Web of Science, Scopus, and Cochrane Library were conducted. Fourteen studies met inclusion criteria, encompassing occupational and non-occupational populations. Risk of bias was assessed using NIH tools, and findings were synthesized narratively due to study heterogeneity. Commonly examined biomarkers included IL-8, IL-6, TNF- α , 8-isoprostane, malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Summary IL-8 emerged as the most consistent inflammatory biomarker, with a pooled random-effects analysis of three firefighter studies showing an acute post-shift increase in blood IL-8 (mean difference 9.76 pg/mL, 95 % CI –8.26 to 27.79), though with substantial heterogeneity. Other inflammatory and oxidative stress biomarkers showed mixed or inconsistent associations with BFS exposure. Small sample sizes, heterogeneous exposure assessment, inconsistent exposure metrics, and unadjusted confounding limited generalizability. Outlook This review identifies IL-8 as the most consistent short-term biomarker of BFS exposure in occupational settings but highlights inconsistent evidence for other biomarkers. Future research should use standardized biomarker protocols, larger sample size, longitudinal designs, and include vulnerable populations to clarify biomarker responses to BFS and strengthen the evidence base for public health and occupational safety measures.
Open Access
Radiofrequency radiation-induced gene expression

January 1, 2000

Henry Lai, B. Blake Levitt

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Genes are differentially expressed in cells in response to changes in the internal or external environment. The response is generally an adaptive mechanism to the environmental challenge to restore cell functions to homeostasis. There are numerous studies reporting changes in gene expression in cells exposed to radiofrequency radiation (RFR), the type of energy emitted by wireless communication devices. The major genes affected are those involved in: repair of damaged proteins, response to stress, oxidative changes, apoptosis, DNA damage detection and repair, and changes in neural functions. Gene expression data supports the notion that RFR is a stressor that causes oxidative changes and DNA and protein damage in cells under different exposure conditions, in many biological systems. Changes in all these significant gene expression effects are supported by results of other biological studies of RFR exposure in the literature. They should be considered in the setting of RFR-exposure guidelines.
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Prenatal exposure to bisphenol-A and neurocognitive changes in children aged 2 to 5 years: a systematic review

January 1, 2000

Isabella Vian Matias de Oliveira, Fernanda Martins de Albuquerque, Amanda de Jesus Fernandes, Priscila Berti Zanella, Mariane Alves Silva

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Bisphenol-A (BPA) is a synthetic organic compound considered an endocrine disruptor. Childhood exposure to BPA has been linked to impaired memory and learning, as well as Attention Deficit Hyperactivity Disorder. The aim of this study was to review the available literature on prenatal exposure to BPA and its relationship to the neurocognitive development of children aged 2–5 years. This systematic review (CRD42023494940 registration PROSPERO) was conducted between December 2023 and May 2024, following the recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) guidelines. The Web of Science, Embase, and PubMed databases were used for the search, with no publication date limit. The following terms, with the respective Boolean operators, were searched: ((bisphenol A) OR (BPA)) AND ((pregnancy) OR (pregnant woman)). Twenty-one longitudinal studies were selected for this review. Most studies have demonstrated negative effects of prenatal BPA exposure on the neurocognitive development of children aged 2–5 years. These results differed between the sexes, with females having lower emotional control, reduced language dominance and problem solving, and males having lower psychomotor development and higher prosocial behavior, among other differences. Overall, BPA exposure during pregnancy has been associated with hyperactivity, aggression, anxiety, depression, inattention, and sleep problems. It is concluded that maternal exposure to BPA during pregnancy results in adverse health effects in children aged 2–5 years, with impairments in their neurocognitive development.
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The nail salon workforce: a systematic scoping review of carcinogen exposure assessments, health outcome, and workforce intervention research

January 1, 2000

Thoin F. Begum, Robin Taylor Wilson, Leuna Sarah, Ayan Labrooy, Emma Marie Porcaro, Grace X. Ma

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Nail salon workers are routinely exposed to occupational hazards, including volatile organic compounds (VOCs), ultraviolet radiation, fine particulate matter (PM 2.5 ), and heavy metals. With the industry projected to double in size over the next decade, identifying exposure risks and intervention gaps is essential for workforce protection. This systematic scoping review synthesized peer-reviewed exposure assessments, health outcome studies, and intervention research in nail salons published between 2013 and 2024. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses and the National Institute of Environmental Health Sciences National Toxicology Program Handbook for Conducting Systematic Reviews. Risk of bias was assessed using the Strengthening the Reporting of Observational Studies in Epidemiology guidelines. Forty-two studies met inclusion criteria: 29 exposure assessments, 11 health outcome studies, and two intervention evaluations. Most were conducted in the U.S. (88 %), with sample sizes ranging from 20 to 150 workers. Common findings included inadequate ventilation (71 %), VOC concentrations above Occupational Safety and Health Administration limits, and persistent detection of methyl methacrylate, despite its U.S. Food and Drug Administration ban. PM 2.5 was evaluated in one study and exceeded World Health Organization guidelines. Heavy metals were infrequently measured, though one study raised concerns about chronic exposure. Only 17 % of studies examined exposure–health outcome associations, with limited evidence on cognitive and psychosocial impacts. Two intervention studies reported improved knowledge and reduced exposures but lacked randomized designs. This review highlights the urgent need for evidence-based interventions, stronger regulatory oversight, and comprehensive evaluation of health impacts in this socially vulnerable workforce.
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Triazole fungicides induce genotoxicity via oxidative stress in mammals in vivo: a comprehensive review

January 1, 2000

Lucas Vilas Bôas Correia, Gabriel Carvalhal de Aguiar, Aparecida Marta Regina dos Santos Pereira, Lucas de Santana Cardoso Thomaz, Isabelly Cristina Correia dos Santos de Oliveira, Renata de Britto Mari, Juliana Elaine Perobelli, Daniel Araki Ribeiro, Regina Cláudia Barbosa da Silva

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This systematic review aimed to assess the genotoxic effects of triazole compounds authorized for use in Brazil in in vivo studies involving mammalian tissues and organs. A comprehensive search was conducted in specialized literature databases, including Embase, Google Scholar, Medline, PubMed, and Scopus using the following keywords: “triazoles,” “mutagenicity,” “genotoxicity,” “mammals,” “mammalian cells,” “eukaryotic cells,” “rodents,” “rats,” “mice,” and “ in vivo ” for all data published until February 2025. A total of 15 studies were included. The findings demonstrated that exposure to triazole fungicides (BRO, DFC, EPX, PPZ and TEB) induce genotoxicity in different mammalian tissues or organs in vivo . This genotoxic effect was manifested through various biological alterations, including increased DNA damage, the formation of micronuclei and adducts, as well as elevated rates of genetic mutations. Furthermore, these chemicals demonstrated the ability to induce oxidative stress, suggesting that this mechanism plays a central role in the genotoxicity associated with these chemicals. This review demonstrated that triazole fungicides induce genotoxicity in mammalian tissues and organs in vivo , with oxidative stress acting as a possible key mechanism in this process. Additionally, these findings underscore the importance of maintaining national pesticide residue monitoring programs (PARA), promoting good agricultural practices, and enforcing maximum residue limit (MRLs) programs, as well as conducting further research on the chronic effects of triazole fungicides, particularly among vulnerable populations in Brazil and worldwide. Such measures are crucial for safeguarding human health and protecting the environment.

Journal Impact Factor	4.5	2024, Journal Citation Reports (Clarivate, 2025)
5-year Journal Impact Factor	4.8	2024, Journal Citation Reports (Clarivate, 2025)
Journal Citation Indicator	0.47	2024, Journal Citation Reports (Clarivate, 2025)
CiteScore	10.2	2024, Scopus (Elsevier B.V., 2025)
SCImago Journal Rank	0.956	2024, SJR (Scimago Lab, 2025; Data Source: Scopus)
Source Normalized Impact per Paper	1.383	2024, CWTS Journal Indicators (CWTS B.V., 2025; Data Source: Scopus)

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