Aug 2026· Asian Journal of Biology· Vol 22, pp. 86-109· 0 citations
TL;DR
The strongest current inference is that arsenic can damage male reproductive biology and may contribute to impaired semen quality in susceptible or highly exposed populations; the magnitude of risk at common low-level exposure is uncertain.
Abstract
Arsenic is a widespread environmental metalloid whose inorganic forms contaminate drinking water, food chains, soil and air. Male reproductive toxicity is biologically plausible because spermatogenesis, steroidogenesis and post-testicular sperm maturation depend on tightly regulated redox, metabolic and endocrine processes. Yet the evidential basis for attributing human male subfertility to environmental arsenic remains markedly less secure than the experimental literature might suggest. This critical narrative review integrates exposure science, human epidemiology, animal and cell-model evidence, mechanistic research and methodological limitations. Literature published from 1980 to 1 June 2026 was identified through PubMed/MEDLINE, authoritative institutional websites and supplementary scholarly web searching, with backward and forward citation checking. Human studies provide signals of lower sperm concentration or motility, altered seminal biomarkers, infertility-associated urinary arsenic species and perturbation of steroid-hormone excretion. These findings are not uniform: studies are few, often clinic-based and cross-sectional, and differ in arsenic speciation, exposure range, co-exposures, semen assessment and confounder control. Experimental evidence is more coherent, linking arsenite and related compounds to oxidative injury, mitochondrial dysfunction, germ-cell loss, impaired spermatid elongation, acrosomal and flagellar defects, epididymal dysfunction, endocrine disruption, autophagy and altered sperm proteins. Developmental exposure and incomplete recovery after withdrawal raise concern about vulnerable windows, although doses and species frequently limit direct translation to human environmental exposure. The strongest current inference is that arsenic can damage male reproductive biology and may contribute to impaired semen quality in susceptible or highly exposed populations; the magnitude of risk at common low-level exposure is uncertain. Progress requires prospective preconception cohorts, repeated arsenic speciation and semen sampling, mixture-aware analysis, functional sperm and fertility outcomes, and explicit evaluation of reversibility after exposure reduction. Prevention should prioritise exposure control rather than unvalidated arsenic-specific fertility treatments.
Global sperm concentration has declined by over 50% in the past five decades, with environmental pollutants identified as a critical driving factor. This review focuses on testicular-level evidence regarding the effects of microplastics, bisphenol compounds, and air pollution on male reproductive health, with an emphasis on spermatogenic and testicular somatic cell mechanisms. Microplastics have been detected in human testicular tissue, with a causal pathway established linking gut microbiota dysbiosis, immune activation, and blood-testis barrier disruption. Bisphenol A substitutes show comparable or greater reproductive toxicity than BPA, with BCAT1-mediated ferroptosis identified as a novel testicular injury mechanism. For air pollution, spermatogenesis stage I (70-90 days prior to semen collection) has been pinpointed as the critical PM2.5 exposure vulnerability window, with metal constituents of traffic-derived PM2.5 as the primary toxicity drivers. Future research should prioritize prospective cohort studies and clinical intervention trials targeting these emerging mechanistic pathways.
Andong Guo, Yi Lu, Ye Guo et al.· Reproductive Toxicology· 0 citations
This paper is a narrative review focusing on the association between environmental cadmium exposure and male reproductive dysfunction. The relationship between environmental pollutants encountered in daily life and the male reproductive system is attracting increasing attention. Humans are exposed to cadmium through inhalation, dietary intake (food) and other routes, leading to adverse health effects. This study systematically searched PubMed, Web of Science, and CNKI databases from January 1, 2020, to December 31, 2024, and included 40 eligible in vivo studies based on standardized selection criteria. This study reviewed and analyzed relevant animal experiments conducted in recent years. Based on the lowest observable adverse effect level (LOAEL, 10 μg/kg/d) for reproductive toxicity in rats from a chronic 90−day study (Ait Benbella et al., 2025), the minimum critical human equivalent dose (HED) of cadmium−induced male reproductive damage was calculated, All 40 studies in Table 1 were selected according to predefined inclusion/exclusion criteria (see Section 2). The Lowest-Observed-Adverse-Effect Level (LOAEL) was converted to HED using the following formula: HED(mg/kg)=Animal LOAEL (mg/kg)×km of animal km of human (The LOAEL was derived from rat reproductive toxicity data (10 μg/kg/d) (Ait Benbella et al., 2025); km factors of 6 (rat) and 37 (human, 60kg) were applied. The calculated HED was 0.002 mg/kg/d.) Comparisons reveal that cadmium exposure levels in some regions approach or even exceed this threshold. The results suggest that cadmium may cause damage to the male reproductive system, potentially adversely affecting semen quality. Cadmium also induces renal dysfunction that indirectly exacerbates testicular injury via the renal−testis axis, further disrupting the hypothalamic−pituitary−testicular axis and amplifying reproductive toxicity. These findings highlight the integrated renal−reproductive toxicity of environmental cadmium exposure.
Chenming Zhang, Jing Hu, Sicheng Ma et al.· Frontiers in Endocrinology· 0 citations
Infertility is a growing worldwide health issue that cannot be addressed only by hereditary or behavioural causes. Growing research suggests that endocrine-disrupting chemicals (EDCs), which are pervasive environmental pollutants, are substantial contributors to poor male and female reproductive health, particularly in fast industrialising nations like India. The objective was to comprehensively map and synthesise current knowledge on the origins, mechanisms, and clinical reproductive consequences of EDC exposure, with an emphasis on the implications for infertility practice and public health policy. A scoping review was conducted using the PRISMA-ScR framework. The PubMed/MEDLINE, Scopus, and Web of Science databases were searched for systematic reviews, meta-analyses, umbrella reviews, and significant human and animal research published between January 2014 and June 2025. The Endocrine Society, World Health Organisation, and United Nations Environment Programme provided authoritative position statements. Evidence was synthesised thematically based on exposure sources, molecular pathways, and clinical consequences. EDCs, which include bisphenols, phthalates, pesticides, PFAS, and heavy metals, have been linked to poor sperm quality, testosterone shortage, ovulatory dysfunction, decreased ovarian reserve, endometriosis, poor pregnancy outcomes, and possible transgenerational impacts. Disruption of the hypothalamic-pituitary-gonadal axis, interference with hormone receptors, poor steroidogenesis, oxidative stress, mitochondrial dysfunction, and epigenetic alteration were among the mechanisms implicated. Exposure reduction treatments showed short-term reversibility of biomarker load, indicating therapeutic significance. EDCs are controllable yet underappreciated risk factors for infertility. Integrating exposure assessment, preventative counselling, biomonitoring, and regulatory tightening, particularly in India, may improve reproductive outcomes and supplement assisted reproductive technology.
Vinoth Gnana Chellaiyan Devanbu, J. John, Vijayalakshmi Sridharan· International Journal of Rep...· 0 citations
This critical narrative review integrates evidence on major environmental genotoxin classes, exposure routes, molecular mechanisms, human biomonitoring, disease associations and risk-assessment practice for well-established and less mature evidence domains.
Omoighele F. Akhigbe, O. Abutu, N. Y. Wike et al.· Asian Journal of Research in...· 0 citations
Background: Environmental contaminants such as arsenic and microplastics are increasingly associated with male reproductive dysfunction. This article reviews the mechanisms through which arsenic and microplastics affect male reproductive health and highlights the potential protective effects of imperatorin against co-exposure toxicity. Methods: A narrative literature review was conducted using studies published up to June 2026. Relevant experimental and observational studies were identified from major scientific databases to evaluate the effects of arsenic and microplastic exposure on male reproductive health. The review focused on the Nrf2/Keap1, NF-κB, p53, and steroidogenesis signalling pathways and their associated molecular markers involved in oxidative stress, inflammation, apoptosis, hormonal imbalance, and impaired spermatogenesis. The potential cytoprotective mechanisms of imperatorin against environmentally induced testicular injury were also examined. Results: Exposure to arsenic and microplastics negatively impacts male reproductive function by inducing excessive reactive oxygen species production, inhibiting antioxidant defence mechanisms, causing mitochondrial damage, activating inflammation, disrupting endocrine balance, and impairing spermatogenesis. Simultaneous exposure exacerbates oxidative stress, activates nuclear factor-kappa B-mediated inflammatory pathways, disrupts nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 signalling, and intensifies p53-dependent apoptosis. Microplastics may enhance the transit and storage of arsenic in testicular tissue, thus exacerbating its harmful effects on the male reproductive system. Conclusion: The presence of arsenic and microplastics in the environment may significantly affect male reproductive function. Growing evidence suggests that oxidative stress along with interconnected molecular pathways substantially contribute to the toxic effects observed during co-exposure.
Sudha J., Lakshmanan Govindan, Senthil Kumar Sivanesan et al.· Journal of Pioneering Medica...· 0 citations
Rare earth elements (REEs) are increasingly recognized as modulators of male reproductive health. This review presents the first comprehensive and critical analysis of the detrimental and potentially beneficial effects of REEs on male vertebrate reproductive function. In vivo and in vitro studies show that elements, particularly Gadolinium, Lanthanum, and Yttrium, share a toxicological profile characterized by oxidative stress, inflammation, mitochondrial dysfunction, endocrine disruption, and impairment of the blood–testis barrier. These mechanisms converge on both somatic and germ cell populations, ultimately compromising spermatogenesis and hormonal balance. Limited epidemiological data in humans are consistent with experimental findings, indicating inverse associations between seminal REE levels and sperm quality. CeO2 nanoparticles represent an exception, showing dose-dependent duality: although some murine studies describe toxic effects, a broader and more consistent body of evidence indicates their protective action by restoring testicular homeostasis in diabetic models, in rats exposed to pesticides, pharmacological agents or irradiation, and in in vitro-treated spermatozoa. Preliminary data on Yttrium (YO) and Gadolinium (GdVO4) nanoparticles similarly point to protective effects under pathological conditions, whereas Neodymium and Samarium show reproductive toxicity, including hormonal disruption and impaired sperm quality. Overall, REEs cannot be considered a homogeneous class: some pose reproductive hazards, others show potential biomedical utility. A systematic, mechanistic research framework is needed to resolve these dualities. It should contextualise reproductive risks in relation to the growing environmental and occupational exposure to REEs, while simultaneously exploring the biomedical potential of those elements that exhibit protective profiles.
A. Santillo, S. Falvo, Massimo Venditti et al.· International Journal of Mol...· 0 citations
