Micro‐ and nanoplastics in the human genitourinary system: oncological impact – a systematic review

Abstract

Objectives

To systematically assess the prevalence, distribution, and quantitative burden of micro‐ and nanoplastics (MNPs) in human tissues of the urinary tract and male reproductive organs, with particular attention to their potential oncological implications.

Methods

This systematic review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines. A systematic search of PubMed, Embase, and Scopus was performed to identify human observational studies reporting detection and/or quantification of MNPs in the urinary tract and male reproductive organs. Risk of bias was assessed in the included studies.

Results

A total of 14 cross‐sectional human studies were included. MNPs were detected across all investigated tissues, including the kidney, prostate, testis, penis, ureter, and, incidentally, the urinary bladder. All studies comparing malignant and adjacent non‐malignant tissues (kidney, prostate, and penis) consistently reported significantly higher microplastic concentrations, particle counts or greater polymer diversity in tumour tissue. Considerable heterogeneity was observed across studies with respect to analytical techniques, digestion protocols, and reporting metrics.

Conclusions

Micro‐ and nanoplastics are widely present in tissues of the urinary tract and male reproductive system and show consistent enrichment in urological malignancies compared with adjacent non‐malignant tissue, suggesting potential oncological relevance. Substantial methodological heterogeneity currently limits comparability across studies, underscoring the need for standardised analytical approaches to advance research in this field.

Abbreviations

BPA

bisphenol A

ccRCC

clear cell RCC

COX‐2

cyclooxygenase‐2

EDS

energy‐dispersive X‐ray spectroscopy

(ATR‐)FTIR

(attenuated total reflection) Fourier transform infrared spectroscopy

HNO₃

nitric acid

KOH

potassium hydroxide

LDIR

laser direct infrared imaging

LNCaP

lymph node carcinoma of the prostate

MNPs

micro‐ and nanoplastics

NF‐κB

nuclear factor kappa B

NOS‐xs2

Newcastle–Ottawa Scale for cross‐sectional studies

PA

polyamides

PA6

polyamide 6

PA66

polyamide 66

PC

polycarbonate

PE

polyethylene

PET

polyethylene terephthalate

PI3K/Akt

phosphoinositide 3‐kinase/protein kinase B

PP

polypropylene

PRISMA

Preferred Reporting Items for Systematic Reviews and Meta‐Analyses

PS(‐MPs)

polystyrene (microplastics)

PVC

polyvinyl chloride

Py‐GC/MS

pyrolysis–gas chromatography–mass spectrometry

SEM

scanning electron microscopy

TGF‐β

transforming growth factor‐β

Introduction

The modern era is characterised by widespread plastic overabundance. The total weight of plastic debris currently present in the environment is estimated to exceed the biomass of the entire human population by roughly 25 fold [1] and it has been estimated that humans ingest an amount of microplastics equivalent to the weight of a credit card each week [2].

Given the rapid growth of plastic production, understanding the potential health risks posed by plastic degradation products, particularly micro‐ and nanoplastics (MNPs), has become an urgent scientific priority. This need is underscored by the fact that, in 2019, the WHO stated that MNPs in drinking water do not pose a risk to human health, while emphasising that the available scientific evidence remains highly limited [3].

Micro‐ and nanoplastics are now detected across all environments, from soil and marine ecosystems to the atmosphere, and have also been identified in the tissues of living organisms, including humans [4]. Definitions of MNPs vary across organisations: microplastics are typically described as particles <5 mm, sometimes restricted to <1 mm, whereas nanoplastics are defined using different cut‐offs, most commonly <100 nm or <1 μm [3, 5]. Growing evidence suggests that MNPs disrupt key cellular processes, such as oxidative stress, inflammation, mitochondrial dysfunction, endoplasmic reticulum stress and autophagy, leading to tissue damage, fibrosis, chronic inflammation and potentially carcinogenic effects [5, 6, 7]. MNPs may promote carcinogenesis by activating pro‐inflammatory and pro‐proliferative pathways, including nuclear factor kappa B (NF‐κB) [8], signal transducer and activator of transcription 3 (STAT3) [9] and cyclooxygenase‐2 (COX‐2) [10]. They may also impair genomic stability through downregulation of breast cancer susceptibility gene 1 (BRCA1) and ataxia–telangiectasia mutated (ATM) [11], and reduce immune surveillance by disrupting macrophage and T‐cell function [5, 12].

The urinary system represents a particularly compelling target for studying MNPs because it serves as a major route for the elimination of chemicals and particles that enter the bloodstream. The kidneys, which produce ~180 L of primary urine through glomerular filtration per day, provide substantial opportunity for trapping MNP particles, while excreting ~1.5 L of final urine that may also contain MNPs [13, 14]. Therefore, the upper and lower urinary tract is continuously exposed to any particles excreted in urine [5]. In 2021, there were 2.25 million new cases and 815 546 deaths from urological cancers globally, and these numbers continue to rise each year, driven by population ageing, lifestyle factors and advances in diagnostic detection [15]. Yet this raises an important question: could another hallmark of modern civilisation, the escalating plastic crisis and the accumulation of MNPs in human tissues, also play a role in this trend? Growing evidence suggests that microplastic exposure may be implicated in tumorigenesis across multiple non‐urological malignancies [12, 16, 17]. Microplastics have been reported to be enriched in tumour tissue and play a role in tumour biology and therapeutic response in several cancers such as colorectal [18], gastric [19], breast [20], liver [21], skin [17] and cervical cancer [22], and has been linked to enhanced tumour proliferation [17, 19], invasion and migration [19], disease progression [22] and resistance to chemotherapy [16] or targeted therapies [19] in experimental models. These observations raise the possibility that MNP accumulation may represent a previously underappreciated environmental factor contributing to cancer biology, with potential relevance also for malignancies of the genitourinary tract [12].

The aim of this systematic review was to synthesise evidence from human studies on the presence of MNPs in tissues of the urinary tract and male reproductive system. We aimed to compare microplastic characteristics between organs, with particular emphasis on cancer‐related studies, while critically evaluating methodological heterogeneity and identifying key knowledge gaps.

Methods

This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) 2020 guidelines. The final protocol was registered prospectively at the International Prospective Register of Systematic Reviews (PROSPERO; registration number: CRD420261280143).

Eligibility Criteria

Studies were eligible for inclusion if they reported the detection, quantification, or characterisation of MNPs in tissues of the urinary tract or male reproductive system. For the purposes of this review, we examined MNP accumulation across the urinary tract (kidney, ureter, bladder, urethra) and male reproductive organs (prostate, penis, testis, epididymis).

Studies were included if they met the following criteria:

1. Observational design: case–control, cross‐sectional, cohort studies.

2. Population: human participants from whom tissue specimens of the urinary tract (kidney, ureter, bladder, urethra) or male reproductive organs (prostate, penis, testis, epididymis) were obtained.

3. Exposure: environmental exposure to MNPs, assessed by validated analytical methods, such as Raman spectroscopy, laser direct infrared imaging (LDIR), Fourier transform infrared spectroscopy (FTIR), pyrolysis–gas chromatography–mass spectrometry (Py‐GC/MS), scanning electron microscopy (SEM) or other techniques confirming MNP identity or characteristics.

4. Comparator: studies with or without a comparator group were eligible.

5. Outcomes: (primary) detection and/or quantification of MNPs in tissues of the urinary tract and male reproductive organs; (secondary, when reported) particle characteristics (polymer type, size, morphology) and exploratory associations with clinical, pathological, or disease‐related features.

Exclusion criteria:

1. Animal or in vitro studies without analysis of human samples.

2. Studies lacking direct detection of MNPs in human samples.

3. Studies using techniques unable to confirm MNP identity.

4. Book chapters, case reports, commentaries, conference abstracts, editorials, errata, guidelines, letters to the editor, notes, protocols, and reviews (systematic, narrative, scoping, meta‐analyses).

5. Duplicate data (the most comprehensive and/or updated report was considered).

6. Insufficient data reporting to extract MNP prevalence or concentration.

7. Publications in languages other than English.

Search Strategy

On 11 January 2026 two investigators (N.A. and J.K.) independently searched for relevant studies in databases including PubMed, Scopus, and Embase without restrictions on language or publication date, under the supervision of another reviewer (A.Ś.). The search strategy (Appendix S1) was constructed using two primary concept blocks, each expanded with relevant synonyms and Medical Subject Headings (MeSH) terms: (i) urinary and male reproductive system‐related terms (e.g., ‘bladder’, ‘kidney’, ‘ureter’, ‘urethra’, ‘prostate’) and (ii) microplastic‐related terms (e.g., ‘microplastics’, ‘nanoplastics’, ‘polymer particles’).

Study Selection

Title and abstract screening was performed independently by two reviewers (N.A. and J.K.). Full‐text articles were then assessed for eligibility according to the pre‐defined inclusion and exclusion criteria. Any conflicts between the two reviewers were resolved through discussion with another (A.Ś.). All citation management, deduplication and screening procedures were conducted using EndNote 21 (Clarivate Analytics, Philadelphia, PA, USA).

The database search yielded 2484 records (652 from PubMed, 736 from Embase, and 1096 from Scopus). After automatic deduplication, 1419 records remained and an additional 174 duplicates were removed manually, resulting in 1245 unique records for title and abstract screening. This process yielded 26 articles for full‐text assessment, of which 12 were excluded [23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34], resulting in 14 studies included in the review. The PRISMA flow diagram is presented in Fig. 1 [35].

Fig. 1.

Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) flow diagram of the study selection process. Adapted from Page et al. [35].

Data Extraction and Synthesis

Two reviewers (N.A. and J.K.) independently completed a standardised data extraction form. A detailed description of all extracted variables and data synthesis is provided in Appendix S2.

Risk of Bias

Two reviewers (N.A. and J.K.) independently assessed study quality using a modified Newcastle–Ottawa Scale for cross‐sectional studies (NOS‐xs2) [36], adapted for studies investigating the presence of MNPs in urological organs and the male reproductive system. Any disagreements were resolved through discussion with a third reviewer (A.Ś). Detailed scoring criteria are provided in Appendix S3. The NOS‐xs2 was modified to include explicit criteria relevant to MNPs research, including sample contamination control, adequacy of analytical detection methods and transparency of sample preparation. Studies were classified as having low risk of bias (3–4 stars), moderate risk of bias (2 stars), or high risk of bias (0–1 star).

Results

Summary of Included Studies Characteristics

A total of 14 observational cross‐sectional studies published between 2023 and 2025 were included (Table 1 [8, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49]), mainly from China (eight studies), with fewer from the USA (three) and Europe (three). Five studies conducted paired analyses of tumour and adjacent normal tissue.

Table 1.

Characteristics of included studies.

Reference	Country	Type of study	Sample type	Population			Sample size, n	Analytical method
				Description	N, sex	Age, years
Cao et al. (2025) [37]	China	Cross‐sectional (ex vivo)	Kidney	Deceased organ donors	8M	75.0 ± 6.0*	8 (kidney)	Raman microspectroscopy
Codrington et al. (2025) [38]	USA	Cross‐sectional with a procedural contamination control	Penis	Men undergoing IPP implantation	6	67.7 ± 11.8*	6 (penile corpus; 1 procedural control)	LDIR, SEM
Demirelli et al. (2024) [39]	Turkey	Cross‐sectional	Prostate	Men undergoing TURP	12	70.0 ± 9.8	12 (prostate)	ATR‐FTIR, light microscopy
Deng et al. (2024) [40]	China	Cross‐sectional (paired tissue comparison)	Prostate (tumour, adjacent normal tissue)	Men with prostate cancer undergoing RARP	22	66.8 ± 7.2	44 (prostate: 22 tumour, 22 adjacent normal)	LDIR, Py‐GC/MS, SEM
Hu et al. (2024) [41]	USA	Cross‐sectional (ex vivo)	Testis	Post‐mortem human testis specimens	23	[16–88]	23 (testis)	Py‐GC/MS
Krafft et al. (2023) [42]	Germany	Cross‐sectional (ex vivo, paired tissue comparison)	Bladder (tumour, adjacent normal tissue)	Human bladder specimens (tissue bank)	10 (sex NR)	ND	20 (bladder: 10 tumour, 10 adjacent normal)	Raman microspectroscopy (incidental detection)
Massardo et al. (2024) [43]	Italy	Cross‐sectional	Kidney	Patients undergoing nephrectomy (healthy renal tissue)	10 (6F/4M)	41.8 ± 8.9*	10 (kidney)	Raman microspectroscopy
Nihart et al. (2025) [44]	USA	Cross‐sectional (ex vivo)	Kidney	Post‐mortem individuals (autopsy)	52 (20F/31M/1U)	48.0 ± 16.7*	52 (kidney)	Py‐GC/MS, SEM‐EDS, TEM, light microscopy, polarisation wave microscopy
Wang et al. (2025) [45]	China	Cross‐sectional (paired tissue comparison)	Penis (tumour, adjacent normal tissue)	Men diagnosed with penile cancer	17	58.06 ± 8.38	34 (penis: 17 tumour, 17 adjacent normal)	LDIR
Wang et al. (2025) [46]	China	Cross‐sectional (ex vivo)	Kidney; ureter	Deceased kidney transplant donors	28 (sex NR)	[25–65]	56 total (28 kidney; 28 ureter)	LDIR, Py‐GC/MS, SEM
Yang et al. (2024) [47]	China	Cross‐sectional	Testis	Men attending a reproductive medicine centre (azoospermia)	18	[25–44]	18 (testis)	Py‐GC/MS
Ye et al. (2025) [8]	China	Cross‐sectional (paired tissue comparison)	Kidney (tumour, adjacent normal tissue)	Adults with ccRCC undergoing nephrectomy	6 (sex NR)	[18–75]	12 (kidney: 6 tumour, 6 adjacent normal)	Py‐GC/MS, SEM
Zhang et al. (2025) [48]	China	Cross‐sectional (paired tissue comparison)	Kidney (tumour, adjacent normal tissue)	Adults with ccRCC undergoing nephrectomy	32 (9F/23M)	58.06 ± 12.52	43 (kidney: 33 tumour, 10 adjacent normal; 1 IVC thrombus)	LDIR, Py‐GC/MS, SEM
Zhao et al. (2023) [49]	China	Cross‐sectional	Testis	Men providing testicular tissue (NOA)	6	32.8 ± 3.9*	6 (testis)	LDIR

F, female; IPP, inflatable penile prosthesis; IQR, interquartile range; IVC, inferior vena cava; M, male; ND, no data; NOA, non‐obstructive azoospermia; NR, not reported; TEM, transmission electron microscopy; U, undetermined.

Numerical values are given as mean ± SD or median (IQR or lower–upper quartile). Values in square brackets [] indicate range, while asterisks (*) denote values calculated by the authors from data reported in the original studies.

The studies covered heterogeneous populations, including healthy individuals and clinical cohorts undergoing urological procedures, infertility evaluation, cancer treatment, or post‐mortem tissue donation. Kidney tissue was most frequently examined (six studies), followed by testis (three), prostate and penis (two each), with other urological tissues assessed sporadically.

A total of 250 participants were included (170 men, 35 women and 45 with sex not reported or undetermined). Reported participant ages ranged from 26.6 to 75.0 years, and sample sizes were generally small, most commonly <20 participants providing urological tissue (nine studies).

Across included studies, three main analytical approaches were used: (i) spectroscopic polymer identification, including Raman microspectroscopy, attenuated total reflection‐FTIR (ATR‐FTIR), and LDIR (10 studies); (ii) thermal degradation–based mass quantification using Py‐GC/MS (seven); and (iii) electron microscopy, including SEM, SEM‐energy‐dispersive X‐ray spectroscopy (SEM‐EDS), and transmission electron microscopy (six). Six studies employed multimodal workflows combining two or more of these approaches, most commonly spectroscopy with SEM and/or Py‐GC/MS, enabling integrated assessment of particle morphology, polymer composition, and total polymer load.

Most studies were judged to have a low risk of bias (nine of 14), with four rated as moderate and one as high. Detailed assessment is provided in Table S1.

Main Findings

Sample Preparation Protocols and Analytical Methodological Heterogeneity

Sample digestion and preparation methods varied widely (Table 2 [8, 37–49]). Alkaline potassium hydroxide (KOH) digestion was the most common approach (five studies), followed by nitric acid (HNO₃) digestion (four). Enzymatic digestion and solvent extraction were less frequently used, each applied in two studies. Notably, in four studies no digestion was performed, and intact biological material was analysed, including bladder [42], kidney [8, 44], and testis [47].

Table 2.

Analytical and methodological characteristics of included studies.

Reference	Sample type	Analytical method	Digestion, extraction	Py‐GC/MS target polymers	Method‐related size limit/range, μm	Filter pore size, μm	Practical size limit, μm
Cao et al. (2025) [37]	Kidney	Raman microspectroscopy	H2O2/FeSO4	–	–	0.45	1.52
Codrington et al. (2025) [38]	Penile tissue	LDIR, SEM	KOH + NaClO	–	20–500 (LDIR); 2 (SEM)	0.8	2
Demirelli et al. (2024) [39]	Prostate	ATR‐FTIR, light microscopy	KOH	–	–	2.5	2.5
Deng et al. (2024) [40]	Prostate (tumour, adjacent normal tissue)	LDIR, Py‐GC/MS, SEM	HNO3 (LDIR, SEM); solvent extraction (Py‐GC/MS)	PS, PE, PP, PVC, PMMA, PC, PET, PA6, PA66, PLA, PBAT	20–500 (LDIR)	13 (LDIR, SEM); no filtration (Py‐GC/MS)	20
Hu et al. (2024) [41]	Testis	Py‐GC/MS	KOH	PE, PVC, PA66, PA6, SBR, PU, PP, ABS, PMMA, PET, PC, PS	–	No filtration	–
Krafft et al. (2023) [42]	Bladder (tumour, adjacent normal tissue)	Raman microspectroscopy (incidental detection)	No digestion	–	–	No filtration	–
Massardo et al. (2024) [43]	Kidney	Raman microspectroscopy	KOH	–	1	0.2	3
Nihart et al. (2025) [44]	Kidney	Py‐GC/MS, SEM‐EDS, TEM, polarisation wave microscopy, light microscopy	KOH (Py‐GC/MS, TEM); no digestion (SEM‐EDS, light microscopy, polarisation wave microscopy)	PE, PP, PS, PVC, PET, PMMA, PC, PA6, PA66, ABS, SBR, PU	–	No filtration	0.1 (100 nm)
Wang et al. (2025) [45]	Penile tissue (tumour, adjacent normal tissue)	LDIR	HNO3	–	20–500 (LDIR)	1	20
Wang et al. (2025) [46]	Kidney; ureter	LDIR, Py‐GC/MS, SEM	HNO3 + solvent extraction (Py‐GC/MS); enzymatic (LDIR, SEM)	PE, PVC, PS, PMMA, PP, PA66, PA6, PC, PET, PBAT, PLA	20–500 (LDIR)	0.45 (LDIR, SEM); no filtration (Py‐GC/MS)	20
Yang et al. (2024) [47]	Testis	Py‐GC/MS	No digestion	PVC, PS, PMMA, PET, PE, PP, PC, PA66, PA6, PLA, PBAT	–	No filtration	–
Ye et al. (2025) [8]	Kidney (tumour, adjacent normal tissue)	Py‐GC/MS, SEM	No digestion (Py‐GC/MS); ND for SEM	PS, PE, PP, PVC, PA	–	No filtration (Py‐GC/MS); ND for SEM	–
Zhang et al. (2025) [48]	Kidney (tumour, adjacent normal tissue)	LDIR, Py‐GC/MS, SEM	HNO3	PS, PA6, PA66, PC, PE, PET, PMMA, PP, PVC, ABS, SBR	20–500 (LDIR)	13 (LDIR); filtration, but pore size NR (Py‐GC/MS)	20
Zhao et al. (2023) [49]	Testis	LDIR	Enzymatic	–	–	0.45	20

ABS, acrylonitrile butadiene styrene; H₂O₂/FeSO₄, Fenton's reagent; H₂O₂, hydrogen peroxide; NaClO, sodium hypochlorite; ND, no data; NR, not reported; PA, polyamides; PBAT, polybutylene adipate terephthalate; PLA, polylactic acid; PMMA, polymethyl methacrylate; PU, polyurethane; SBR, styrene‐butadiene rubber; TEM, transmission electron microscopy.

Particle size limits apply exclusively to particle size‐based analytical techniques. Py‐GC/MS does not measure particle size; any size‐related detection limitations arise from pre‐analytical sample preparation (e.g., filtration).

Across Py‐GC/MS studies, polyethylene (PE), polystyrene (PS), polypropylene (PP), polyvinyl chloride (PVC) and polyamides (PA) were targeted in all analyses (seven of seven). Polyethylene terephthalate (PET), polymethyl methacrylate, and polycarbonate (PC) were also commonly included (six of seven studies). In contrast, acrylonitrile butadiene styrene, styrene‐butadiene rubber, polylactic acid, polybutylene adipate terephthalate, and polyurethane were assessed less frequently.

Filtration pore sizes ranged from 0.2 to 13 μm, with most studies using 0.2–1 μm filters, whereas three studies used >1‐μm filters. Filtration was not applied in seven studies, primarily in Py‐GC/MS workflows. Methodological differences in digestion and filtration resulted in substantial variability in practical MNP detection limits, which in size‐dependent approaches (excluding Py‐GC/MS) ranged from about 1.5 to 20 μm.

Urinary Tract Organs

Detailed MNP detection outcomes and particle characteristics across included studies are provided in Table 3 [8, 37–49], while Fig. 2 presents an overview of microplastic accumulation across the genito‐urinary system. Cancer‐related findings are summarised separately in a dedicated section below.

Table 3.

Microplastic detection outcomes and particle characteristics in the included studies.

Reference	Sample type	Polymer types	Number of positive samples/all (%)	Particle count	Concentration	Size, μm	Shape
Cao et al. (2025) [37]	Kidney	PP, PP, PLA	7/8 (87.5)	58.63 ± 16.5 particles/g, PP predominant	–	25.89 ± 15.63 [4.03–54.52]	Fragments, fibres, pellets
Codrington et al. (2025) [38]	Penile tissue	PET, PP, PS, PVC, APV, PMMA, PTFE	5/6 (83.3)	46 particles/6 samples, PET predominant (47.8%)	–	20–100 (84% of particles); SEM: 2 to >100	Spheres, fibres, fragments
Demirelli et al. (2024) [39]	Prostate	PA6, PP, PAA, PDMS	6/12 (50.0)	21.5 ± 10.13 particles/sample ≈12.43 ± 5.86 particles/g*, PA6 predominant	–	2.5–26	Pellets, spheres, fibres
Deng et al. (2024) [40]	Prostate (tumour, adjacent normal tissue)	Tumour and adjacent normal tissue: PA, PET, PVC, PP, PE, EVA, FKM, FMQ, PU, CPE, ACR, SBS, POM, BR, PI, PS; PS tumour only by LDIR	Tumour: 22/22 (100); Adjacent normal tissue: 22/22 (100)	Tumour: [39–100] particles/g; Adjacent normal tissue: [76.4–179.5] particles/g	Tumour: 290.3 μg/g; Adjacent normal tissue: 181.0 μg/g PS/PE/PVC significantly ↑ in tumour (PE predominant in both)	20–100	Irregular particles, fragments, fibres
Hu et al. (2024) [41]	Testis	ABS, PA6, PA66, PC, PE, PET, PMMA, PP, PS, PU, PVC, SBR	23/23 (100)	–	328.44 ± 135.29 μg/g, [161.22–695.94] μg/g, PE predominant (35.2%)	–	–
Krafft et al. (2023) [42]	Bladder (tumour, adjacent normal tissue)	Tumour: PS, PPS	Tumour: 2/10 (20); Adjacent normal tissue: 0/10 (0) Incidental detection	Tumour: 2 particles/10 samples	–	–	–
Massardo et al. (2024) [43]	Kidney	PE, PS	2/10 (20)	2 particles/10 samples ≈0.08 particles/g*	–	3–11	–
Nihart et al. (2025) [44]	Kidney	PE, PP, PVC, PS, PET, PA6, PA66, SBR, ABS, PMMA, PU, PC	52/52 (100)	–	404 (213.7–1186) [47.80–1741] μg/g (2024 samples); 402.5 (310.6–786.1) [59.06–1848] μg/g (2016 samples), PE predominant	<0.4–5	Nanofragments
Wang et al. (2025) [45]	Penile tissue (tumour, adjacent normal tissue)	Tumour: PE, PVC, PA, PP, POM, PU, PS; Adjacent normal tissue: PP, PMMA, PE, PVC, PA, PC	Tumour: 16/17 (94.1), PE predominant (24.4); Adjacent normal tissue: 13/17 (76.5), PP predominant (26.9)	Tumour: 7.43 ± 3.70 particles/g; Adjacent normal tissue: 5.07 ± 4.31 particles/g significantly ↑ in tumour	–	Tumour: 20–100 (80%), >100 (20.0%); Adjacent normal tissue: 20–100, (80.8%), >100 (19.2%)	–
Wang et al. (2025) [46]	Kidney; ureter	Kidney: NR, PU, SR, PE, PVC, PET, PA66; Ureter: ACR, PE, PET, PMMA, PP, PU, PVC, BR, SR, PTFE	Kidney: 28/28 (100); Ureter: 28/28 (100)	Kidney: 293 particles/28 samples ≈10.46 particles/g*, NR predominant (23.2%); Ureter: 1672 particles/28 samples ≈59.71 particles/g*, SR predominant (11.0%)	Kidney: 6.67 [5.18–7.95] μg/g, PA66 only detected; ureter: 146.3 μg/g*, PE predominant	Kidney: 20–100 (54.9%), 100–500 (45.1%); Ureter: 20–100 (48.7%), 100–500 (51.3%)	–
Yang et al. (2024) [47]	Testis	Testis: PS, PVC, PA66, PMMA	Testis: 18/18 (100)	–	Testis: 2207 (1792–3954) μg/g, PA66 predominant (38.48%)	–	–
Ye et al. (2025) [8]	Kidney (tumour, adjacent normal tissue)	Tumour and adjacent normal tissue: PS, PE, PP, PVC, PA	Tumour: 3/3 (100); adjacent normal tissue 3/3 (100)	–	Tumour: 64.815 μg/g; Adjacent normal tissue: 12.986 μg/g, total/PE/PP/PS significantly ↑ in tumour (PE predominant in both)	–	–
Zhang et al. (2024) [48]	Kidney (tumour, adjacent normal tissue)	Tumour and adjacent normal tissue: PE, PP, PVC, PS, PET, PMMA, PC, PU, PA, ABS, EVA, POM, FKM, FMQ, BR, ACR, EAA, SBR; PVC, PS tumour only by Py‐GC/MS Adjacent normal tissue only: PLA	Tumour: 33/33 (100); adjacent normal tissue: 10/10 (100); 1 IVC thrombus positive	↑ quantity (particles/g) in tumour vs. adjacent normal tissue	Tumour: 1175.63 μg/g**; Adjacent normal tissue: 175.26 μg/g**, total/PE/PVC significantly ↑ in tumour (PE predominant in both); Highest PE/PS in IVC thrombus	<100 (mostly), <200 (overall)	Fibres, fragments
Zhao et al. (2023) [49]	Testis	PS, PVC, PE, PP	4/6 (66.7)	11.60 ± 15.52 particles/g, PS predominant	–	83.15 ± 56.25	Fragments predominant, fibres, subspherical particles

ABS, acrylonitrile butadiene styrene; ACR, acrylate polymer; APV, acrylates/polyurethanes/varnish; BR, butadiene rubber; CPE, chlorinated polyethylene; EAA, ethylene acrylic acid; EVA, ethylene vinyl acetate; FKM, fluoroelastomer; FMQ, fluorosilicone rubber; IQR, interquartile range; IVC, inferior vena cava; NR, natural rubber; PA66, polyamide 66 (nylon 66); PA6, polyamide 6 (nylon 6); PAA, polyacrylic acid; PDMS, polydimethylsiloxane; PI, polyimide; PLA, polylactic acid; PMMA, polymethyl methacrylate; POM, polyoxymethylene; PPS, poly(phenylene sulphide); PTFE, polytetrafluoroethylene; PU, polyurethane; SBR, styrene‐butadiene rubber; SBS, styrene–butadiene–styrene copolymer; SIS, styrene–isoprene copolymer; SR, silicone rubber.

Numerical values are given as mean ± SD or median (IQR or lower–upper quartile). Mean values reported without SD are presented alone, whereas median values reported without IQR are marked with double asterisks (**). Values in square brackets [] indicate range, while single asterisks (*) and the ≈ symbol denote values calculated by the authors from data reported in the original studies. ↑ denotes higher values in the indicated group.

Fig. 2.

Accumulation of MNPs across the human genitourinary system in included studies. ↑ denotes higher values in the indicated group. Created with Biorender.com.

Kidney

Six studies assessed MNP accumulation in human kidney tissue, including paired clear cell RCC (ccRCC) with adjacent normal tissue [8, 48], and non‐malignant samples [37, 43, 44, 46]. In normal kidney tissue, MNPs were detected in most samples, with reported positivity rates ranging from 20% [43] to 100% [44, 46] and an overall detection rate of 90.8% (89/98 samples).

In normal kidney tissue, MNP concentrations ranged from 6.67 [46] to 404 μg/g [44], while reported particle abundance varied from very low counts [43] to ~60 particles/g [37]. Predominant polymer types varied across studies, including PP, PE and polyamide 66 (PA66).

Reported particle sizes spanned a wide range, from <0.4 [44] to 500 μm [46]. In one study of kidney transplant recipients, polymer‐specific microplastic measures in kidney‐associated tissues were associated with early postoperative blood pressure changes [46].

Bladder, Ureter

The bladder and ureter were grouped due to limited available evidence. No study targeted MNP accumulation in non‐malignant bladder tissue; microplastics were only incidentally detected in bladder cancer [42].

In ureter tissue, MNPs were detected in 100% of samples, with substantially higher particle count than in kidney tissue (1672 vs 293 particles across 28 samples) and higher PE and PVC concentrations [46]. Detected particles were predominantly large (mainly 100–500 μm). Predominant polymers varied by analytical approach (silicone rubber after enzymatic digestion with LDIR; PE after HNO₃ digestion with solvent extraction) [46].

Male Reproductive Organs

Testis

Micro‐ and nanoplastics accumulation in the testes was assessed in three studies [41, 47, 49], with microplastics detected in 66.7% [49] to 100% of samples [41, 47] and an overall detection rate of 95.7% (45/47 samples).

Reported mass‐based concentrations were high, ranging from ~330 [41] to ~2200 μg/g [47], while particle abundance reached ~12 particles/g [49]. One study reported an average testicular microplastic particle size of ~83 μm [49]. Predominant polymer types varied across studies, including PE, PA66, PVC and PS. Exploratory analyses reported higher total testicular microplastic levels in humans than in dogs in one study [41], and associations between testicular microplastic burden and selected lifestyle factors (city residence, home‐cooked meals, scrub‐cleanser use, and body mass index) in another study [47].

Prostate

Two studies examined MNP accumulation in the prostate, one in non‐cancerous tissue [39] and one in prostate cancer tissue with adjacent normal tissue [40]. In non‐cancerous prostate tissue, MNPs were detected in six of 12 samples (50%), with a mean (SD) abundance of 21.5 (10.13) particles/sample (12.43 (5.86) particles/g), particle sizes ranging from 2.5 to 26 μm, mostly pellet‐like and polyamide 6 (PA6) predominance [39].

Penis

Two studies assessed MNP accumulation in penile tissue, including one analysis of non‐cancerous tissue [38] and one comparing tumour tissue with adjacent normal tissue [45]. In the non‐cancer study, microplastics were detected in five of six samples, mostly PET and PP. A total of 46 particles were identified, predominantly within the 20–100 μm size range and exhibiting heterogeneous morphology [38].

Cancer‐Related Studies

Five studies examined MNP accumulation in urological cancers using paired tumour and adjacent non‐malignant tissues. Tumour tissues showed higher MNP concentrations, particle counts or polymer diversity than corresponding healthy tissues in kidney, prostate and penile cancers [8, 40, 45, 48].

In a single prostate cancer study, MNPs were detected in all samples, with higher total concentrations in tumour than in adjacent normal tissue and significantly higher tumour levels of PS, PE and PVC. Notably, PS was detected exclusively in tumours by LDIR. Particle size distributions were comparable between tissues. Exploratory correlations linked higher PP abundance with elevated PSA levels, higher PE abundance with lower Gleason scores, and increased PS abundance with take‐out food consumption [40].

In a penile cancer study, MNPs were detected more frequently in tumour than in adjacent normal tissue (94.1% vs 76.5%), with a higher particle count in tumours. Polymer profiles differed between tissues, with PP predominating in normal tissue and PE in tumours. Malignant samples showed slightly greater polymeric diversity, with comparable particle size distributions [45].

Two studies investigated MNP accumulation in ccRCC [8, 48]. In one study of 32 patients, all samples were MNP‐positive, with markedly higher total MNP concentrations in tumour tissue than in adjacent normal tissue. PE predominated in malignant tissue, with substantially higher PE and PVC concentrations in tumours and greater polymeric diversity. In ccRCC, higher microplastic burden was associated with male sex, urban residence or indoor occupational exposure and was linked to transcriptomic alterations with potential implications for therapeutic sensitivity [48]. Ye et al. [8] also analysed MNPs in ccRCC, detecting microplastics in all samples with markedly higher total concentrations in tumours than in normal tissue. Tumour tissue showed increased levels of PE, PP, and PS, with PE predominating. Functional experiments demonstrated that cytoplasmic accumulation of PS microplastics promoted ccRCC progression through activation of the NF‐κB and transforming growth factor‐β (TGF‐β) pathways [8]. Notably, Zhang et al. [48] also reported that higher microplastic burden in ccRCC was associated with male sex, representing the only sex‐stratified analysis among the included urological studies.

In contrast, bladder cancer evidence is limited to incidental microplastic detection in a study primarily evaluating confocal Raman spectroscopic imaging for differentiating malignant from non‐malignant bladder tissue, with only two particles identified in 10 tumour samples [42]. This study was therefore considered to have a high risk of bias, limiting quantitative interpretation.

Microplastic Distribution Across Urological and Non‐Urological Tissues

Across studies directly comparing multiple tissues, the kidney generally exhibited intermediate microplastic accumulation: higher than in the heart, lungs or spleen, comparable to the liver or small intestine, and lower than in the brain or adrenal tissues [37, 44, 46]. Notably, markedly higher microplastic levels in the ureter than in the kidney were reported, but evidence is limited to a single study [46].

Discussion

This systematic review summarises human evidence on MNPs in the urinary tract and male reproductive organs, with all included studies published between 2023 and 2025 despite the absence of date restrictions, highlighting the rapidly emerging nature of this field. Collectively, the evidence supports a widespread presence of microplastics across the urological and male reproductive tissues examined, despite a predominant research focus on the kidney and testis. PE was the most frequently reported polymer overall, although polymer profiles varied across tissues and studies. Cancer‐related studies consistently demonstrated higher MNP concentrations and altered polymer profiles in tumour compared with adjacent normal tissue.

Microplastic Distribution Across the Human Urinary Tract and Male Reproductive System

Human exposure to MNPs occurs primarily via the gastrointestinal tract, with additional contributions from inhalation and dermal contact [50, 51]. Ingestion of contaminated food and beverages is the main exposure route [52]. Smaller microplastics, especially <150 μm, can cross the intestinal barrier [53], with particles <10 μm showing the highest ability to enter the bloodstream, particularly when intestinal barrier integrity is impaired [54]. Inhaled small airborne MNPs may reach the alveoli and enter systemic circulation [55]. Dermal exposure is considered a minor route and occurs predominantly via skin pores [51, 52].

Once absorbed into the systemic circulation [56], MNP distribution appears to be shaped by organ‐specific blood flow. Highly perfused organs, including the kidneys, liver, small intestine, and brain, consistently show higher MNP accumulation than less vascularised tissues, supporting a circulation‐driven deposition pattern [29, 37, 44]. Within the urinary system, the kidneys represent a key target due to their high perfusion and filtration function [46, 57], which likely contributes to the intermediate‐to‐high MNP levels reported in renal tissue (up to 404 μg/g [44]; mean [SD] 58.63 [16.5] particles/g [37]).

Histological analyses indicate preferential localisation of MNPs within renal glomeruli and tubules, mainly in the 1–5 μm range [44], suggesting that a substantial fraction may escape detection by conventional light microscopy. Experimental evidence supports biological relevance, as microplastics are taken up by renal tubular epithelial cells and induce oxidative stress, inflammatory and autophagy‐related responses in vitro [58]. In vivo, rodent studies associate repeated oral microplastic exposure with renal accumulation, oxidative and inflammatory injury, and impaired renal function, suggesting a potential contribution to chronic kidney disease progression [57, 59, 60, 61].

Recent evidence links MNPs in kidney‐associated tissues to blood pressure regulation. In human transplanted kidneys, polymer‐specific microplastic levels in renal vessels, adrenal tissue, and the ureter were correlated with early postoperative blood pressure changes [46], with positive associations for natural rubber (adrenal tissue) and PP (renal veins) and inverse associations for PC (renal arteries) and butadiene rubber (ureter), although causality cannot be established.

Micro‐ and nanoplastics accumulation may depend on blood flow normalised to tissue mass. Smaller organs with high perfusion per gramme of tissue, such as the thyroid gland [29], may therefore exhibit higher microplastic concentration than larger organs. Consistent with this concept, adrenal tissue showed higher microplastic levels than the kidney [46].

Despite lower perfusion compared with the kidney, the blood–testis barrier may limit microplastic clearance once particles enter testicular tissue, potentially promoting their retention [47]. This may explain the relatively high microplastic concentrations reported in human testes by Py‐GC/MS (mean [SD] 328.44 [135.29] μg/g [41]; median [interquartile range] 2207 [1792–3954] μg/g [47]). The higher concentration was reported in men with azoospermia, suggesting potential selection bias [47], whereas the lower estimate was derived from post‐mortem testicular tissue from a unselected population [41]. Lower concentrations observed in men aged >55 years and the absence of clear age‐dependent accumulation may reflect continuous spermatogenesis and sperm release, consistent with the detection of microplastics in seminal fluid [41]. Experimental data suggest functional relevance, with PVC and PET concentrations negatively correlating with testicular mass and sperm count in dogs, and human testicular concentrations reported to be approximately threefold higher [41]. Mechanistic studies indicate that MNPs can induce oxidative stress, inflammation, mitochondrial dysfunction, and disruption of the blood–testis barrier, ultimately impairing spermatogenesis [62].

Micro‐ and nanoplastics burden in normal prostate tissue appears intermediate relative to other urological organs (prostate: mean [SD] 12.43 [5.86] particles/g [39]; kidney: up to mean [SD] 58.63 [16.5] particles/g [37]; testis: mean [SD] 11.60 [15.52] particles/g [49]), although interpretation is limited by single‐study data [39]. Prostate particles were predominantly small and enriched in PA, contrasting with the kidney where PE predominates [39]. Prostate microplastic accumulation may contribute to microplastics detected in semen [47], although its biological and clinical relevance remains unclear.

Evidence on microplastic accumulation in normal penile tissue is limited to a small human study reporting microplastics in most samples [38]. In the absence of luminal exposure, these findings are consistent with haematogenous delivery to erectile tissue. While no association with erectile dysfunction has been demonstrated in humans [38], animal models suggest that PS nanoplastics can accumulate in corpus cavernosum and impair erectile function in a dose‐dependent manner [63].

Evidence on microplastic accumulation in urothelial tissues remains extremely limited. To date, only one study has quantitatively assessed ureteric tissue, reporting microplastics in all samples and markedly higher polymer concentrations and particle abundance than in kidney tissue (1672 vs 293 particles/28 samples) [46]. Ureteric microplastics were predominantly large (100–500 μm), contrasting with the smaller size ranges typically reported in urinary microplastic studies [43, 64, 65, 66], although particles approaching 400 μm have been described [14]. The predominance of large particles may suggest deposition within the ureteric wall following systemic delivery and could partially explain the presence of large microplastics reported in urine, although this remains speculative. In contrast, bladder microplastics have been reported only incidentally [42] and without quantitative assessment, underscoring a major knowledge gap in urothelial tissues.

Sex‐stratified data in urological tissues remain scarce. Among included studies, only Zhang et al. [48] reported sex‐specific findings, demonstrating higher microplastic burden in ccRCC in males. Interestingly, this contrasts with studies investigating other systems and organs, as Zhu et al. [67] reported significantly higher microplastic accumulation in females across lung, intestinal, and tonsillar tissues. These discrepancies suggest that sex‐specific accumulation patterns may be tissue‐ or disease‐specific, potentially influenced by differences in body composition, hormonal factors, or occupational exposures. However, the mechanisms underlying potential sex‐related differences in MNP accumulation remain unknown. It is also possible that sex has no true effect on MNP accumulation and that these preliminary observations are hypothesis‐generating only. Further sex‐stratified research in urological tissues is warranted.

Microplastic Accumulation in Urological Neoplasms

As outlined earlier, MNP exposure has been linked to adverse biological effects, including inflammation, oxidative stress, DNA and epigenetic damage [52, 54]. These observations raise questions about the oncological implications of MNP accumulation in human tissues. Particular attention has focused on plastic additives, which are weakly bound compounds that can be released from polymer matrices [68]. Examples include vinyl chloride associated with PVC, dioxins and benzene associated with PS‐based plastics, and bisphenol A (BPA) from PCs [52].

Most evidence linking MNPs and plastic‐associated chemicals to carcinogenesis originates from studies on lung, skin, colorectal, breast, and liver cancers [69]. MNPs activate key oncogenic signalling pathways, including NF‐κB, mechanistic target of rapamycin (mTOR), Wnt/β‐catenin, and phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) [12, 70]. Experimentally, MNP exposure enhances autophagy in colorectal cancer cells and promotes oxaliplatin resistance [16], promotes breast cancer progression [20], intensifies inflammatory signalling in skin cancer models [12, 17] and induces resistance to chemotherapy and monoclonal antibody therapy in gastric cancer [19].

In contrast, evidence on the oncological relevance of MNP accumulation in urology remains limited [3]. However, studies directly comparing MNP levels in tumour and adjacent non‐malignant tissues in prostate [40], renal [8, 48], and penile cancers [45] consistently demonstrate higher accumulation in malignant tissue.

Deng et al. [40] showed that prostate cancer tissue accumulates higher microplastic levels than adjacent normal tissue, with enrichment of specific polymers, particularly PS, PE, and PVC. In a subsequent study, low‐dose exposure to 1‐μm PS microplastics enhanced proliferation, migration, and invasion in human prostate cancer cell line lymph node carcinoma of the prostate (LNCaP) and primary human prostate cancer cells without inducing apoptosis [71]. This is clinically relevant, as environmentally realistic microplastic concentrations may promote malignant progression, unlike the high, non‐physiological doses commonly used in experimental studies [59, 72]. Integrated transcriptomic analyses of PS‐exposed LNCaP cells and human prostate tumours revealed concordant molecular signatures, characterised by redox‐ and glutathione‐related pathway enrichment and suppression of apoptosis‐ and immune‐associated signalling. Analyses indicated glutathione peroxidase 4 (GPX4)‐dependent attenuation of ferroptosis, suggesting that low‐dose PS exposure supports redox adaptation and survival of prostate cancer cells rather than cytotoxic stress [71].

As noted earlier, MNPs can act as carriers for biologically active chemical additives. In prostate cells, BPA has been associated with disrupted steroid receptor signalling [73], centrosome dysregulation [74], increased proliferation, and reduced apoptotic responses [75, 76]. Other plastic‐associated compounds, including phthalates, have also been investigated in the context of prostate cancer, while polycyclic aromatic hydrocarbons have been linked to oxidative stress [77, 78, 79]. Notably, PS‐microplastics (PS‐MPs) can adsorb arsenite, potentially enhancing its bioavailability and prostate cancer risk [80]. Consistent with these observations, combined exposure to low‐dose microplastics and a high‐fat diet was shown to exacerbate inflammatory responses and epithelial apoptosis in the mouse prostate [81].

Zhang et al. [48] reported that, compared with adjacent non‐malignant tissue, ccRCC exhibits higher abundance, concentration, and diversity of MNPs. Patients were stratified by tumour microplastic burden for transcriptomic analysis. Interestingly, microplastic‐rich tumours showed enrichment of genes involved in complement and coagulation cascades, platelet activation, and PI3K/Akt signalling, together with higher Tumour Immune Dysfunction and Exclusion (TIDE) scores, which are indicative of reduced predicted responsiveness to immune checkpoint blockade. In parallel, activation of PI3K/Akt signalling, a pathway central to ccRCC biology and a validated therapeutic target, may help explain the increased predicted sensitivity to axitinib and rapamycin observed in this group [48]. This interpretation is supported by experimental evidence showing that PS‐MPs and plastic‐associated additives, including BPA, can modulate PI3K/Akt and mitogen‐activated protein kinase (MAPK) signalling in renal epithelial models [58, 82, 83, 84].

Another ccRCC study reported that tumour tissue exhibited higher MNP concentrations than adjacent normal tissue, with pronounced enrichment and cytoplasmic accumulation of PS‐MPs [8]. PS‐MP exposure markedly promoted ccRCC cell proliferation, migration, and invasion while suppressing apoptosis. Transcriptomic profiling followed by functional validation revealed activation of both NF‐κB and TGF‐β signalling pathways in PS‐MP‐exposed ccRCC cells. Importantly, pharmacological inhibition of these pathways using NF‐κB and TGF‐β inhibitors significantly attenuated PS‐MP‐induced proliferative and invasive effects, findings that were further confirmed in preclinical models, including patient‐derived organoids and cell‐derived xenografts, without evidence of overt treatment‐related toxicity [8]. Taken together, findings in renal cancer highlight potential links between microplastic burden, tumour biology and therapeutic response [8, 48], while underscoring the need to extend these observations to other urological malignancies.

Evidence linking MNPs to penile cancer remains limited. In penile cancer, only a single human study by Wang et al. [45] demonstrated significantly higher microplastic levels in tumour tissue compared with adjacent normal tissue, together with greater polymer diversity, predominantly PE, PA and PVC, while preclinical models and additional human studies are currently lacking.

Evidence linking microplastics to bladder cancer is extremely limited and confined to incidental detection in human tumour tissue [42]. As considerable concentrations of MNPs are found in urine [43, 64, 65, 66], which is stored in the bladder, we may suspect that urine MNPs exert an effect on bladder urothelium, similar to smoke carcinogens. Preclinical evidence indicates that microplastic exposure induces NF‐κB‐mediated inflammatory injury in non‐neoplastic murine bladder epithelium [85] and that aromatic microplastics trigger oxidative stress‐related cytotoxicity in urine‐derived epithelial cells [86]. Dedicated cancer‐specific models and human studies investigating microplastic involvement in bladder carcinogenesis are currently lacking.

Across all human tissue‐based studies of urological malignancies, PE was consistently elevated in tumour tissue compared with adjacent normal tissue and emerged as the most frequent polymer in penile cancer [45] and ccRCC [8, 48]. PVC was also repeatedly enriched in tumour tissue [40, 45, 48], while PS showed tumour‐associated enrichment in prostate cancer and ccRCC [8, 40]. The recurrent predominance of PE, PVC and PS across different urological malignancies suggests a non‐random pattern of microplastic accumulation, potentially shaped by features of the tumour microenvironment and cancer‐specific tissue alterations.

Strengths, Limitations and Methodological Considerations

This systematic review has several important strengths. It integrates evidence from both normal and cancerous urological tissues, providing a comprehensive overview of MNP accumulation across the urinary tract. By synthesising recent human studies and explicitly addressing methodological heterogeneity, it enables critical interpretation of current findings and highlights key gaps for future research. Most studies applied carefully designed methodologies with procedural blanks, quality control and detailed reporting, with the majority assessed as having a low overall risk of bias.

The main limitation of this review is substantial methodological heterogeneity. Differences in digestion protocols can selectively affect polymer recovery [87]. In kidney Py‐GC/MS studies, marked differences in reported concentrations likely arose from differences in digestion protocols and the application of additional solvent extraction in one study (404 μg/g, KOH [44] vs 6.67 μg/g HNO₃ with solvent extraction [46]). Detection criteria also influenced reported prevalence, with kidney positivity ranging from 20% under strict Raman‐based identification [43] to 100% in other studies [44, 46]. Moreover, the same analytical technique could serve different roles across studies, as SEM was most often used for morphological characterisation [40, 48] but in one study functioned as an independent detection method [38]. In addition, studies were often limited by small sample sizes, in several cases involving <10 individuals, which restricts generalisability of the findings. Limited sensitivity for nanoscale particles likely led to underestimation of smaller MNPs, despite evidence that the smallest size fractions are often the most abundant and contribute substantially to total particle burden [88]. No standardised laboratory practices currently exist for MNP extraction and analysis from human tissues. As a result, the potential for laboratory‐induced contamination – particularly from plastic consumables such as pipette tips, centrifuge tubes, filtration units, and other plasticware – cannot be fully excluded [89]. While most included studies employed procedural blanks and contamination controls, the absence of universally adopted protocols means that the extent to which laboratory‐derived MNPs may contribute to reported particle counts and polymer profiles remains uncertain. In addition, the ability to detect such contamination may vary according to the analytical platform used and its sensitivity threshold, potentially leading to under recognition of low‐level laboratory‐derived particles. Finally, the majority of included studies did not report sex‐stratified analyses, precluding systematic evaluation of potential sex differences in MNP accumulation.

Conclusions

This systematic review demonstrates that MNPs are consistently detected across human urinary system and male reproductive organs, with the highest burdens reported in the kidney and testis. Studies comparing malignant and adjacent non‐malignant tissues consistently show enrichment of MNPs in urological cancers, particularly renal, prostate, and penile cancer, suggesting potential oncological relevance that warrants further investigation. Substantial methodological heterogeneity and the absence of standardised analytical protocols remain the principal barriers to advancing this field.

Author Contributions

Conceptualisation: Aleksander Ślusarczyk; methodology: Aleksander Ślusarczyk, Nicole Akpang and Jakub Kwiatkowski; validation: Aleksander Ślusarczyk, Łukasz Zapała, Piotr Zapała and Piotr Radziszewski; investigation and data interpretation: Aleksander Ślusarczyk, Nicole Akpang and Jakub Kwiatkowski; writing – original draft preparation: Nicole Akpang and Jakub Kwiatkowski; writing – review and editing: Aleksander Ślusarczyk, Nicole Akpang, Jakub Kwiatkowski, Łukasz Zapała, Piotr Zapała and Piotr Radziszewski; visualisation: Nicole Akpang and Jakub Kwiatkowski; supervision: Aleksander Ślusarczyk, Łukasz Zapała, Piotr Zapała and Piotr Radziszewski. All authors have read and agreed to the published version of the manuscript.

Disclosure of Interests

None declared.

Funding

This research received no external funding.

Supporting information

Appendix S1. Search strategy.

Appendix S2. Data extraction and synthesis.

Appendix S3. Modified Newcastle–Ottawa Quality Assessment Scale (NOS‐xs2).

Table S1. Quality assessment of the included studies using the modified Newcastle–Ottawa Scale (NOS‐xs2).

Data Availability Statement

The datasets generated during and/or analysed during the present study are available from the corresponding author on reasonable request.