Circulating Microplastics and Electromagnetic/Magnetic Fields: An Expanded Mechanistic Evidence-Mapping Review of Potential Occupational Co-Exposure Pathways

1. Introduction

Microplastics and nanoplastics are persistent, widely distributed emerging contaminants of growing occupational and environmental health concern (Hartmann et al., 2019; Vethaak & Legler, 2021). A recent field-wide retrospective concluded that detection capability has advanced substantially, even as human health risk remains unresolved (Thompson et al., 2024), and the 2025 Lancet Countdown on health and plastics has framed plastic pollution as a systemic public health concern (Landrigan et al., 2025). Global plastic production continues to rise (Plastics Europe, 2023/2024), and human exposure occurs through ingestion, inhalation, and contact with contaminated food, water, dust, and occupational materials (Wright & Kelly, 2017; Kosuth et al., 2018; Cox et al., 2019; Prata et al., 2020).

Human biomonitoring evidence has expanded rapidly. Plastic particles have been reported in blood, lung tissue, placenta, breastmilk, stool, urine, and colon tissue (Schwabl et al., 2019; Ibrahim et al., 2021; Ragusa et al., 2021, 2022; Jenner et al., 2022; Leslie et al., 2022; Pironti et al., 2023; Leonard et al., 2024), and since 2023 in coronary, carotid, and femoral arteries (Liu et al., 2024; Marfella et al., 2024), the frontal cortex of the human brain (Nihart et al., 2025), and human testis and semen (Zhao et al., 2023; Hu et al., 2024), with urinary/seminal burden linked to sperm-quality metrics in a 113-participant study (Zhang et al., 2024). These findings do not establish causation; independent commentary on the brain findings specifically cautions that the sample was small and non-representative (BfR, 2025). Nonetheless, they establish the biological plausibility of internal exposure across an expanding range of tissues, including the bloodstream and vascular interfaces, which are most relevant to this review because circulating particles may interact with immune cells, endothelial cells, and inflammatory mediators.

Microplastic toxicology literature commonly discusses oxidative stress, inflammation, immune modulation, and cellular dysfunction (Lehner et al., 2019; Hirt & Body-Malapel, 2020; Prata et al., 2020; Blackburn & Green, 2022; Li et al., 2023; Kadac-Czapska et al., 2024; Mahmud et al., 2024). This update closes two gaps explicitly flagged in the original evidence map. First, genotoxicity: a 2025 review of more than 85 papers documents microplastic-induced clastogenesis, aneugenesis, and DNA strand breakage (Tang, 2025), corroborated by evidence from human hematopoietic cell lines (Rubio et al., 2020). Second, mitochondrial dysfunction: a 2026 review documents microplastic-induced impairment of oxidative phosphorylation and mitochondrial membrane potential (Microplastics journal, 2026), an animal study shows dose-dependent suppression of tricarboxylic acid cycle and electron transport chain activity after polyethylene microplastic exposure (Kehinde et al., 2026), and a 2026 review links this damage to cardiovascular pathogenesis (Archives of Toxicology, 2026). These mechanisms overlap with broader pathways in chronic inflammation and vascular dysfunction (Simionescu, 2007; Mittal et al., 2014; Sies, 2015; Forrester et al., 2018; Furman et al., 2019; Sies & Jones, 2020; Libby, 2021), supporting a combined-exposure rather than single-agent framework.

EMF/MF are widespread physical exposures from electrical systems, wireless technologies, industrial equipment, and power distribution, with established exposure limits for extremely low-frequency (ELF) and radiofrequency (RF) fields (WHO, 2007; ICNIRP, 2020). The International Agency for Research on Cancer classified RF-EMF as "possibly carcinogenic" (Group 2B) in 2011 based on limited epidemiological evidence (IARC, 2011/2013). This classification continues to generate active debate in risk communication (Wiedemann & Schütz, 2024). Occupational exposure varies substantially by task and equipment (Kim et al., 2001; Choi et al., 2018; Jung et al., 2018; Mailan Arachchige Don et al., 2020), directly paralleling task-dependent occupational microplastic exposure (Murashov et al., 2021; Thongyoo et al., 2023).

EMF/MF biological-effect evidence remains genuinely uncertain. Occupational studies of welders and power-plant workers report measurable oxidative-stress biomarker shifts with long-term ELF-MF exposure (Sharifian et al., 2009; Bagheri Hosseinabadi et al., 2021), while a cytogenetic study of welders found genotoxic markers tracked with co-occurring metal-fume exposure rather than field exposure alone (Dominici et al., 2011) - a direct illustration of the attribution problem this review's framework must anticipate. A 2025 risk-of-bias assessment across ten IARC carcinogen characteristics found that 38% of 159 measurements reported significant effects, while deferring conclusions on genotoxicity/oxidative-stress to reviews reporting inconsistent findings and low certainty (Meyer et al., 2024). Epidemiological evidence on ELF-MF and childhood leukemia remains divided: a 2022 pooled analysis of four recent studies found no association above 0.4 microtesla (Amoon et al., 2022), in contrast to an earlier meta-analysis reporting a dose-dependent association (PLOS ONE, 2021). Therefore, as in the original review, EMF/MF is treated as a possible but unconfirmed physical co-stressor.

Occupational risk assessment has traditionally evaluated stressors individually, yet workers rarely experience single-agent exposure. Cumulative-risk-assessment methodology addresses this gap, distinguishing chemical-mixture from combined chemical/non-chemical stressor assessment (Sexton, 2015; Rider et al., 2018), and has been extended to occupational settings through NIOSH's Total Worker Health framework (Sexton et al./AIHA, 2015) and scoping reviews of combined workplace stressors (NIOSH-affiliated authors, 2021). A Society of Toxicology workshop established that physical stressors can modify both exposure to, and toxicity of, co-occurring chemical/particulate agents (Cory-Slechta et al., 2013/2015) - a precedent structurally analogous to the pairing proposed here.

This review does not claim proven synergistic toxicity. It uses a substantially expanded, structured evidence-mapping approach - 108 sources across eight evidence-type categories and sixteen mechanistic themes, including two mechanisms (genotoxicity and mitochondrial dysfunction) absent from the original 53-source map - to evaluate whether circulating microplastics and EMF/MF exposure may converge on occupational-health-relevant biological pathways, and whether cumulative-risk-assessment methodology can formalize this as a testable research agenda.

2. Methods

2.1. Study Design

This review used a structured evidence-mapping design, appropriate when a field contains heterogeneous study types and the objective is to identify evidence domains and research gaps rather than pooled effect sizes. This update expands a prior 53-source evidence map to 108 sources, expands the mechanism coding scheme from 12 to 16 categories, and adds a new evidence-type category (occupational/combined-exposure risk-assessment framework). No original human, animal, or laboratory data were generated.

2.2. Databases and Search Strategy

Searches covered PubMed-indexed literature, publisher databases (Elsevier ScienceDirect, Springer Nature, Wiley, MDPI, Frontiers), preprint servers (bioRxiv, medRxiv, Research Square), and institutional/regulatory sources (WHO, IARC, ICNIRP, NIOSH/CDC, the German Federal Institute for Risk Assessment, Plastics Europe). Newly added domains were searched for literature published between 2020 and mid-2026; foundational earlier sources from the original bank were retained unchanged. Search terms combined exposure concepts (microplastics, nanoplastics, human blood/brain/testis/semen/artery, electromagnetic fields, magnetic fields, extremely low-frequency fields, radiofrequency fields) with mechanistic terms (oxidative stress, reactive oxygen species, mitochondrial dysfunction, genotoxicity, DNA damage, inflammation, cytokines, endothelial dysfunction, immune response, membrane permeability, endocrine disruption, gut microbiome, reproductive toxicity) and methodological terms (occupational exposure, cumulative risk assessment, combined/mixture stressor exposure), combined with Boolean AND/OR operators (e.g., "microplastic AND (oxidative stress OR genotox OR mitochondri)"; "electromagnetic field AND occupational AND oxidative stress"). Searches were limited to English-language sources.

2.3. Inclusion and Exclusion Criteria

Sources were included if they addressed: detection of microplastics in human biological samples; toxicological mechanisms of microplastics/nanoplastics (including genotoxicity, mitochondrial dysfunction, endocrine/metabolic disruption, gut-microbiome effects); EMF/MF exposure assessment or biological effects; oxidative stress or inflammatory mechanisms; endothelial, vascular, immune, or membrane-related mechanisms; particle behavior relevant to field interaction; or occupational/cumulative-exposure risk-assessment methodology applicable to combined chemical, particulate, or physical stressors. Sources were excluded if unrelated to human, occupational, or environmental health, or if focused only on environmental distribution without biological relevance. Twenty of 108 sources (18.5%) added in this update could not be fully bibliographically verified (complete author list, volume, or page) from the search results alone; these are retained, with key findings intact, but flagged in the supplementary evidence-mapping workbook for verification against primary sources.

2.4. Coding and Synthesis

Each source was coded for citation, title, journal, year, study type, exposure focus, model/population, key mechanism/outcome, relevance, evidence strength, and mechanistic theme. Mechanistic themes were coded using 16 categories (microplastic exposure, EMF/MF exposure, oxidative stress/ROS, inflammation/cytokines, human biomonitoring, endothelial/vascular effects, particle behavior/aggregation, immune effects, cell membrane/permeability, metal additives/contaminants, mitochondrial dysfunction, genotoxicity/DNA damage, endocrine/metabolic disruption, gut microbiome/GI effects, reproductive toxicity, and occupational/cumulative-exposure framework), applied via a documented, case-insensitive keyword-matching procedure across each source's title, key mechanism, exposure focus, and thematic fields (full keyword dictionary in the supplementary workbook); sources could receive more than one tag. This procedure was applied uniformly to all 108 sources, including recoding the original 53 and correcting an internal inconsistency identified in the original evidence-mapping workbook. Evidence types were classified into eight categories: background/contextual evidence; microplastic toxicology mechanisms; human microplastic detection/biomonitoring; EMF/MF biological mechanisms; general oxidative stress/inflammation biology; direct or indirect microplastic-EMF/MF co-exposure relevance (merged here with particle-field interaction analogy, since no direct empirical co-exposure study was identified in either version of this review); and occupational/combined-exposure risk-assessment framework. Mechanism co-occurrence was computed across the full 16-category matrix. A narrative synthesis was combined with descriptive evidence mapping; no meta-analysis was performed due to substantial heterogeneity in study designs, exposure types, and outcome measures across sources. An explicit five-point evidence-strength gradient (very limited to very strong) was applied qualitatively across the distinct evidentiary pillars underlying the review's argument, to make transparent that they are not equally well established.

2.5. Ethics

This review used only previously published literature and publicly available sources; no human participants, animals, biological materials, or identifiable personal data were involved, and institutional review was therefore not required.

3. Results

3.1. Overview

The expanded evidence bank includes 108 sources, more than double the original 53. Table 1 summarizes the updated evidence-type distribution. Microplastic toxicology mechanisms remain the largest category (34 sources, up from 10), reflecting expanded coverage of genotoxicity, mitochondrial dysfunction, endocrine disruption, and gut-microbiome literature. Evidence for EMF/MF biological mechanisms grew to 26 sources (from 7). Human microplastic detection/biomonitoring doubled to 20 sources (from 9), including studies on brain, arterial, and reproductive tissue detection. A new occupational/combined-exposure risk-assessment framework category contributes 7 sources. Evidence of direct or indirect microplastic-EMF/MF co-exposure remains the smallest category (4 sources). It includes no dedicated direct empirical co-exposure study - the central gap identified in the original review persists. Table 2 summarizes study types across the full bank; reviews predominate (32 of 108 sources), followed by human tissue analytical studies (7) and occupational exposure assessments (5).

3.2. Human Microplastic Detection

In addition to blood (Leslie et al., 2022; Leonard et al., 2024), lung (Amato-Lourenço et al., 2021; Jenner et al., 2022), placenta (Ragusa et al., 2021), breastmilk (Ragusa et al., 2022), stool (Schwabl et al., 2019), urine (Pironti et al., 2023), and colon tissue (Ibrahim et al., 2021), this update adds: coronary/carotid/femoral arterial tissue (Liu et al., 2024), extending Marfella et al. (2024); the frontal cortex, where concentrations exceeded liver/kidney and were higher in 2024 than 2016 samples and further elevated with dementia (Nihart et al., 2025), though an independent institutional commentary cautions the autopsy sample was small and non-representative (BfR, 2025); and testis/semen, first reported in a six-testis/thirty-semen Chinese study (Zhao et al., 2023), corroborated by a comparative human-canine study (Hu et al., 2024) and linked to sperm-quality metrics in 113 participants (Zhang et al., 2024). A methodological study that specifically assesses the reliability of blood microplastic quantification highlights ongoing measurement uncertainty (Rauert et al., 2025). Endothelial and microglial cell lines show particular susceptibility to cytotoxic and genotoxic effects from consumer-product-derived microplastics (Janiga-MacNelly et al., 2024/2025). Table 3 summarizes this evidence.

3.3. Microplastic Toxicology Mechanisms

This update closes two gaps explicitly flagged as empty in the original map. For genotoxicity/DNA damage (0 to 10 sources), a 2025 review of more than 85 papers found microplastics cause clastogenesis and aneugenesis through direct and ROS-mediated indirect DNA damage (Tang, 2025), corroborated by human hematopoietic cell-line evidence (Rubio et al., 2020), a review linking intracellular nanoplastics to genotoxic/neurotoxic potential (Casella & Ballaz, 2024), and a carcinogenesis-focused review implicating p53, MAPK, Nrf2, and PI3K/Akt signaling following the first detection of microplastics in human tumor tissue (PMC11545399, 2024). For mitochondrial dysfunction (0 to 4 sources), a 2026 review documents disrupted membrane potential and impaired oxidative phosphorylation converging on NF-kB/NLRP3-mediated inflammation (Microplastics journal, 2026); a rodent study found dose-dependent suppression of testicular tricarboxylic-acid-cycle and electron-transport-chain activity after 28-day polyethylene-microplastic exposure (Kehinde et al., 2026); and a 2026 review connects this damage to pro-atherosclerotic cardiovascular remodeling (Archives of Toxicology, 2026), reinforcing the vascular-interface argument since Marfella et al. (2024).

Two further mechanistic dimensions are new to this update. Endocrine/metabolic disruption is supported by a review characterizing microplastics as vectors for endocrine-disrupting additives (Kannan & Vimalkumar, 2021). Gut microbiome/GI effects are supported by a 2025 systematic review documenting consistent microplastic-induced gut dysbiosis (BMC Gastroenterology, 2025) and a review proposing gut-brain-axis propagation (PMC11120006, 2024) - of particular interest given the new brain-detection evidence. Occupationally relevant evidence includes a 2025 review of exposure-to-mitigation pathways (PMC12142344, 2025) and experimental evidence that inhaled textile microplastic fibers impair lung repair, consistent with occupational respiratory disease patterns among workers in the textile, flocking, and PVC industries (Prata, 2018; bioRxiv preprint, 2021). Table 4 summarizes all 16 coded mechanisms; microplastic exposure (70 coded instances) and oxidative stress/ROS (34) remain dominant, with inflammation/cytokines (19) and the new occupational/cumulative-exposure framework category (19) close behind.

3.4. EMF/MF Exposure and Mechanism Evidence

Exposure guidance and occupational studies (Kim et al., 2001; WHO, 2007; Choi et al., 2018; ICNIRP, 2020; Jung et al., 2018; Mailan Arachchige Don et al., 2020) confirm that field exposure is task- and equipment-dependent. Biological-effect evidence remains uncertain: IARC's 2011 Group 2B classification (IARC, 2011/2013) continues to generate risk-communication debate about public misinterpretation (Wiedemann & Schütz, 2024); a 2025 risk-of-bias assessment across ten IARC carcinogen characteristics found 38% of 159 measurements reporting significant effects while deferring to reviews reporting inconsistent, low-certainty findings on genotoxicity/oxidative stress (Meyer et al., 2024; ScienceDirect, Romeo/Karipidis et al., 2025); and WHO is continuing systematic-review program has extended to RF-EMF and animal cancer bioassays (Mevissen et al., 2025). Childhood leukemia epidemiology remains divided: a 2022 pooled analysis found no association above 0.4 microtesla (Amoon et al., 2022), in contrast to a dose-dependent association reported elsewhere (PLOS ONE, 2021).

Occupationally, power-plant workers and welders show elevated oxidative-stress biomarkers with long-term ELF-MF exposure (Sharifian et al., 2009; Bagheri Hosseinabadi et al., 2021), but a welding cytogenetic study found genotoxic markers tracked with metal-fume co-exposure rather than field exposure (Dominici et al., 2011) - illustrating the attribution problem this review's framework anticipates. Membrane and calcium-channel hypotheses remain proposed but unconfirmed mechanisms (Pall, 2013; Gherardini et al., 2014; arXiv preprint review, 2020). Table 5 summarizes updated EMF/MF evidence domains.

3.5. Occupational/Cumulative-Exposure Frameworks

This new category (7 dedicated sources, 19 coded mechanism instances) formalizes a bridge to concrete occupational practice. Cumulative-risk methodology distinguishes stressor-based from effects-based approaches (Sexton, 2015) and has been extended to combined chemical/non-chemical stressors (NIEHS, 2017; Rider et al., 2018), including a workshop precedent that physical stressors can modify exposure to and toxicity of co-occurring chemical/particulate agents (Cory-Slechta et al., 2013/2015). Occupationally, this has been formalized through NIOSH's Total Worker Health framework (Sexton et al./AIHA, 2015) and a scoping review of combined chemical/physical/psychosocial workplace stressors (NIOSH-affiliated authors, 2021). Independent occupational exposure-assessment literature exists for both stressors: microplastic exposure varies by task in manufacturing, textile, and recycling settings, with no occupational exposure limit yet established (Murashov et al., 2021), and a Thai field study found waste-segregation workers had the highest airborne-microplastic exposure (~3,960 particles/m3) (Thongyoo et al., 2023), directly paralleling task-dependent ELF-MF exposure gradients among Korean workers (Choi et al., 2018; Mailan Arachchige Don et al., 2020). Table 6 presents this synthesis.

3.6. Convergence, Gaps, and Evidence Strength

A publication-year analysis (Figure 1) shows 40 of 108 sources (37%) were published in 2024-2026 alone, reflecting genuine field-wide acceleration rather than search recency bias, since pre-2024 literature was retained unchanged. The mechanism co-occurrence analysis (Figure 2) confirms oxidative stress and inflammation as central cross-cutting themes. At the same time, the occupational/cumulative-exposure category co-occurs most strongly with EMF/MF exposure (13 shared instances) and, less strongly, microplastic exposure (9 instances) - consistent with occupational exposure-assessment methodology having so far been applied more to EMF/MF than to microplastics. Table 7 presents the updated evidence-gap analysis: human detection, toxicological mechanisms (now including genotoxicity and mitochondrial dysfunction), and occupational exposure assessment are well supported; EMF/MF biological effects remain mixed; and direct evidence of microplastic-EMF/MF co-exposure remains absent.

To prevent this expanded evidence base from being misread as uniformly strong, Figure 3 presents an explicit evidence-strength gradient. Human internal-exposure detection and EMF/MF occupational exposure assessment are rated strong-to-very-strong; microplastic toxicology mechanisms and occupational cumulative-exposure methodology are rated moderate-to-strong; EMF/MF biological-effect mechanisms are rated limited; and direct co-exposure evidence is rated very limited - the lowest point on the gradient.

3.7. Updated Conceptual Framework

Figure 4 presents an updated conceptual model adding: an explicit occupational co-location node (settings where both stressors are independently documented at elevated levels); an internal-interface node extended to brain and reproductive tissue; a fourth mechanism branch (endocrine/metabolic disruption, gut-microbiome dysbiosis, reproductive toxicity) alongside particle-related, shared stress-response, and physical co-stressor branches; and expanded testable outcomes (genotoxic/mitochondrial biomarkers, endocrine/metabolic markers, gut-microbiome composition, reproductive endpoints). The framework does not assume EMF/MF directly alters microplastics in blood; it identifies testable possibilities best evaluated within an occupational cumulative-risk-assessment framework in the specific industries identified above.

4. Discussion

This expanded evidence-mapping review indicates that the possible interaction between circulating microplastics and EMF/MF exposure remains biologically plausible but empirically unconfirmed, now supported by more than double the original evidence base and by two mechanistic domains - genotoxicity and mitochondrial dysfunction - absent from the earlier version. Evidence remains strongest for human microplastic detection, now spanning ten tissue/fluid types, and for microplastic toxicological mechanisms, now including genotoxic and mitochondrial pathways. It remains weaker for EMF/MF biological effects, where updated 2024-2025 systematic reviews and epidemiological analyses sharpened rather than resolved long-standing uncertainty, and weakest - unchanged despite a broadened search - for direct co-exposure evidence. This evidence-strength gradient (Figure 3) is important because it prevents overstatement while preserving the practical value of the research question.

Interpret. The primary contribution of this review is to translate a speculative question into a concrete, increasingly specific occupational research agenda, rather than to prove synergistic causation of disease. The hypothesis is that the two exposure domains may converge on oxidative stress, mitochondrial dysfunction, genotoxicity, inflammatory signaling, and vascular biology - a wider convergence footprint than the original review could support - which is sufficient to justify controlled research but insufficient to claim causal risk. If microplastic-induced reactive oxygen species originate substantially at the mitochondrial level, as recent reviews suggest (Kehinde et al., 2026; Microplastics journal, 2026), then any physical co-stressor capable of independently perturbing mitochondrial membrane potential or redox balance - mechanisms repeatedly proposed but not conclusively demonstrated for EMF/MF (Consales et al., 2012; Pall, 2013) - represents a mechanistically coherent, testable candidate for interaction. No study identified here has directly tested this; the value of the observation is that it sharpens the hypothesis into a specific, falsifiable prediction rather than a general statement that both exposures involve oxidative stress.

Integrate. The EMF/MF evidence requires particular restraint. Occupational studies of welders and power-plant workers provide genuine evidence of field-associated oxidative-stress biomarker shifts (Sharifian et al., 2009; Bagheri Hosseinabadi et al., 2021), yet a cytogenetic study in the same occupational literature found genotoxic markers associated with co-occurring metal-fume exposure rather than field exposure (Dominici et al., 2011). This is not evidence against EMF/MF bioeffects; it is a direct methodological warning about attributing effects to any single stressor in real workplaces where multiple exposures co-occur - precisely the problem a formal co-exposure study must solve, and one reason this review locates future work within cumulative-risk-assessment methodology rather than single-stressor toxicology designs. At the population level, divergent 2021-2022 childhood-leukemia analyses (PLOS ONE, 2021; Amoon et al., 2022) show that EMF/MF risk assessment remains an unsettled debate more than four decades after the question was first raised, reinforcing rather than loosening the case for treating EMF/MF as a possible, not confirmed, co-stressor.

Implications. This update's principal practical contribution is to identify occupational cumulative-risk-assessment methodology as the appropriate framework for future empirical work. This methodology was developed specifically because workers are rarely exposed to a single agent at a time (Cory-Slechta et al., 2013/2015; Sexton, 2015) and has already been operationalized occupationally through NIOSH's Total Worker Health program (Sexton et al./AIHA, 2015) and combined-stressor scoping reviews (NIOSH-affiliated authors, 2021). This review identifies a specific, previously unexamined pairing - microplastic particulate exposure and ELF-MF/RF-EMF exposure - for which independent occupational exposure-assessment literature already exists for both stressors (Choi et al., 2018; Jung et al., 2018; Mailan Arachchige Don et al., 2020; Murashov et al., 2021; Thongyoo et al., 2023), and proposes combining these literatures within existing methodology rather than treating them as separate research programs. The public-health message remains cautious: this review does not support claims that EMF/MF and microplastics together cause disease. It supports combined-exposure thinking as routine occupational risk-assessment practice, particularly in polymer processing, textiles, recycling, welding, electroplating, semiconductor, and power-generation industries, where workers are rarely exposed to a single physical or particulate agent at a time.

This study retains limitations from its original version and introduces new ones. It remains based on a structured evidence bank rather than a database-level systematic review with formal risk-of-bias scoring; coding relies on documented keyword-matching criteria and may undercount mechanisms not explicitly captured in the extracted fields. Twenty of 108 sources (18.5%) could not be fully bibliographically verified within this update's search process and are flagged for verification before further use; none were used to support a claim not independently corroborated by at least one fully verified source. No original experimental data were generated, and most importantly, direct co-exposure evidence remains absent despite a substantially broadened search. These findings should therefore be interpreted as hypothesis-generating rather than confirmatory.

Despite these limitations, this update strengthens several original contributions: a more transparent, reproducible evidence map with a single documented coding procedure applied uniformly across 108 sources; mechanistic coverage across sixteen rather than twelve categories; an explicit evidence-strength gradient preventing the expanded base from being misread as uniformly strong; and a formal cumulative-risk-assessment methodology, specific industries, and biomonitoring endpoints for future occupational research. The most important finding, unchanged despite a doubled evidence base, is the research gap itself: no study has directly examined combined exposure to circulating microplastics and EMF/MF. Future research should use controlled in vitro and in vivo studies targeting the mitochondrial and genotoxic endpoints identified here, alongside occupational cohort studies combining personal microplastic and field-exposure monitoring with oxidative-stress, inflammatory, and genotoxicity biomarkers, to test whether EMF/MF modifies microplastic-related cellular uptake, oxidative stress, mitochondrial function, genotoxicity, or endothelial function. Until such evidence exists, the proposed interaction should be treated as a testable occupational-health hypothesis rather than an established causal relationship.