Volume 40, Issue 4

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.

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.

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.

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.

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.

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.

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.

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.

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.