Air pollution is considered the most serious environmental concern on Earth, as 99% of the world population were living in the places where WHO air quality guidelines levels were not met (24). The development in urbanization, population, and industrialization has significantly increased ambient air pollution in urban cities, both locally and globally, causing some of the most serious air quality challenges. At once, India was considered as the world’s second most polluted country (25). The elevated levels of air pollution in many regions of the world were profound enough to have genuine impacts on human health and have also led to numerous diseases, including respiratory (26), cardiovascular (27), cancer (28), liver (29), and reproductive diseases (30, 31). The sources of air pollution are classified into two categories: natural and anthropogenic sources, which include industrial emissions, motor vehicle exhaust, dust from construction and mining, residential activities like burning of coal, and natural sources, such as wood, wildfire, volcanic eruptions, etc. (32). Pollutants that are emitted directly into the atmosphere are termed primary pollutants, including carbon monoxide (CO), Sulphur dioxide (SO_₂), nitrogen dioxide (NO_₂)_, and particulate matter (PM). Secondary pollutants are formed through interactions with other components in the atmosphere. Some of the secondary pollutants include ozone (O_₃) and secondary particulate matter (sulphates, nitrates, ammonium salts, and secondary organic aerosols). Also, many pollutants coexist and vary spatially and temporally, hence it is challenging to separate their effects (33). Numerous recent research studies have shown the adverse effects of air pollution on human reproductive health. Air pollutants, when inhaled, have their absorption and distribution depend on the mode of entry and solubility. It was determined that increased ROS can impact the semen quality parameters through different pollutants as showed in Table 1. The most explored mechanisms are inflammation, the induction of apoptosis, destruction of the blood-testis barrier, and oxidative stress (34, 35). Oxidative stress can be defined as the state of imbalance in the ROS production and antioxidant activity (36). It is well established that most of the air pollutants have different mechanisms but ultimately end in the production of ROS. Excessive ROS production amplifies the recruitment of proinflammatory cytokines, thereby inducing inflammation, oxidative stress, and lipid peroxidation; increases the binding of PAHs to their receptors; or interacts with PAHs to trigger DNA strand breaks and apoptosis. All these pathways contribute to the pathophysiology of diminished male reproductive potential (37, 38).

Air pollutants, especially the particles that are >2.5 and <10 μm in diameter, which are commonly known as PM_2.5 and PM_10, can disrupt the blood-testis barrier and cause oxidative stress. Recent studies have shown that exposure to PM_2.5 and PM₁₀ has significantly decreased the sperm concentration, motility during the entire spermatogenesis period (39). The major air pollutant, O_₃ exposure, is associated with declined sperm concentration (40). The PM and CO are associated with declined sperm count, motility, and elevated morphological defects (41). Exposure to CO and SO_₂ appeared to influence sperm motility parameters and influence semen quality throughout spermatogenesis (42). A recent study reveals that exposure to ambient SO_₂ was negatively associated with all semen quality parameters except for the sperm concentration progressive motility (43). A recent Meta-analysis reveals that the higher exposure to outdoor air pollution is associated with abnormal semen quality and increased DNA fragmentation index (44). A notable trend observed that predominance of studies linking air pollution and semen quality originate from China, shows high industrial activity, and availability of large clinical cohorts. However, the predominance of data from a single region raises questions about global generalizability. Air pollution composition varies geographically; for example, Pollution profiles differ significantly by geography; for instance, particulate matter in rapidly industrializing regions often contains higher concentrations of heavy metals (arsenic, lead) and sulfates from coal combustion, whereas pollution in Western urban centers is primarily driven by nitrate-rich vehicular emissions (45). These differences influence particulate matter constituents, including metals, PAHs, and secondary organic aerosols, which may have biological effects on the male reproductive system. In addition, inter-population variation in genetic background, particularly in oxidative stress–response genes and xenobiotic-metabolizing enzymes, may modify individual susceptibility to pollution-related reproductive toxicity. This geographical bias limiting the global generalizability of the findings, so this highlights the need for similar studies in other regions, especially in countries with rising pollution levels and limited reproductive health data, such as in South Asia, the Middle East, and Africa. Diverse environmental exposures, genetic backgrounds, and lifestyle factors across populations could lead to different susceptibility patterns and outcomes, which are currently underrepresented in the literature.

Several metals and metalloids (elements that lie in the intermediate state between metals and non-metals) are essential for living organisms, playing crucial roles in cell division and metabolism while also facilitating endocrine signaling between organs. However, excessive concentrations of certain metalloids can lead to heavy metal toxicity (46). Heavy metals are naturally occurring elements with a large atomic weight and density of at least 5 times greater than that of water (47). Heavy metals such as cadmium (Cd), lead (Pb), chromium (Cr), and mercury (Hg) are among the most dangerous for male reproductive health and fertility. Chronic exposure to these metals can potentially impact male fertility by causing severe oxidative stress and cellular toxicity, even at low concentrations (48–50).

Phthalates are synthetic organic chemicals that are used in almost wide variety of products in industries as solvents, plasticizers, and additives in polyvinyl chloride (PVC) plastics or personal care products (PCPs) (81). The difference in molecular weight of phthalates makes it to be useful for different purposes. The high molecular weight phthalates (for example, di-isodecyl phthalate, benzyl butyl phthalate (BBP), and di-2-ethylhexyl phthalate) are used primarily in PVC polymers and plastisol applications, plastics, food packaging, and food processing materials, vinyl toys and vinyl floor coverings, and building products. The low molecular weight phthalates (for example, diethyl phthalate, di-isobutyl phthalate, and di-n-butyl phthalate) are often used in non-PVC applications, such as certain dietary supplements, personal care products and enteric-coated tablets (82). Though the phthalates are essential in useful commercial products, both types are toxic. High molecular weight phthalates are considered more harmful due to their stronger anti-androgenic effects, leading to reduced sperm quality and testicular damage. However, low molecular weight phthalates also cause significant harm, particularly in disrupting hormone function (80, 83). Phthalates have been implicated in compromising semen quality through several mechanisms. One primary pathway involves endocrine disruption, where phthalates interfere with hormonal balance, particularly by reducing testosterone levels. This hormonal imbalance adversely affects spermatogenesis, leading to decreased sperm count and motility. Emphasizing the negative effect on male reproductive health, a systematic review and meta-analysis found that exposure to phthalates and their metabolites is linked to a decrease in sperm quality (84). Furthermore, demonstrated to cause oxidative stress in the testes are phthalates. Further compromising sperm function is this oxidative environment’s destruction of sperm DNA and cellular membranes. Studies show that phthalate exposure lowers sperm motility, capacitance, and the acrosome reaction, therefore lowering fertilization rates and so compromising embryonic development (17). Many human research has been done on connections involving phthalate exposure and semen quality and/or circulating hormone levels among adult men. Among studies of semen quality parameters, a systematic review of the human epidemiological data concluded that there was moderate to robust evidence for reductions in semen quality in relation to phthalate exposure levels on the basis of consistent findings across up to 14 different studies (83). Delayed time to pregnancy in relation to male phthalate exposure or sperm DNA damage and sperm aneuploidy is seen for various reproductive endpoints in adult men (79). Furthermore, investigations have shown that phthalates can change the expression of genes important for reproductive purpose, therefore compromising the structural integrity and functionality of sperm. These disturbances taken together draw attention to the possible risk phthalate exposure to male fertility presents (85–87).

Bisphenol A (BPA) is a chemical molecule, widely utilized in many daily use products including containers to line food and beverage, thermal sheets, dental sealants, fillers and cooking utensils. BPA is also present on the internal coating of cans used in canned food which is considered as the main route of exposure. Reutilization and exposure of those containers to temperatures greater than 70 °C results in BPA leakage to food and beverage which ultimately leads to the dietary ingestion of BPA to humans (88). However, the risk of exposure through inhalation and skin contact, especially through thermal paper is also considerable. BPA induces DNA damage by elevating intracellular ROS levels, resulting in DNA breakage and enhanced migration of DNA towards the tails from the sperm nucleus (80). By mimicking the estrogen, BPA throws off hormonal equilibrium. It messes with the androgen receptor system, which lowers testosterone and generates less sperm (89). Recent research has underlined the negative consequences of EDCs especially BPA on sperm quality and general reproductive health as showed in Table 3, implying that these substances help to explain the rising male infertility frequency.

Pesticides are compounds used to either prevent, eradicate, or manage insects, weeds, fungus, and rodents. They are extensively applied in residences, public health, and agriculture to preserve crops, lower disease spread, and uphold hygienic conditions (90). Excessive or improper use can lead to release of pesticide compounds to the environment such as organochlorines, organophosphates and pyrethroids, etc. Recent scientific studies have established a significant link between pesticide exposure and male infertility, particularly concerning semen quality. Pesticides significantly impact male reproductive health primarily via endocrine disruption and oxidative stress. Numerous pesticides function as endocrine-altering chemicals (EDCs), disrupting the body’s hormonal systems. Organochlorine pesticides and their metabolites can bind to androgen receptors, so suppressing testosterone activity and altering the hormonal regulation of spermatogenesis (91). A thorough meta-analysis has shown that exposure to organophosphate pesticides significantly diminishes sperm count, concentration, motility, and normal morphology (92). The pesticides have direct harm to spermatozoa, as it interferes with hormonal regulatory processes leading to impairment of Sertoli and Leydig cell activities. Additionally, exposure to various pesticides, including organochlorines and organophosphates, is associated with a tangible decline in semen quality (93).

Due to their diminutive size, microplastics can rapidly infiltrate an organism through the food chain, negatively impacting normal physiological activities. The quality of human semen has been eventually decreased from the last few decades as a result of urbanization (102). The mechanism by which it enhances the reproductive toxicity is by creating oxidative stress (103). The toxicity of microplastics is contingent upon size, with the potential for ROS formation escalating with larger plastic particle dimensions (104). Initially, it elevates the concentration of reactive oxygen species in bodily tissues and cells. Furthermore, it modifies the antioxidant systems, including Superoxide dismutase (SOD), Catalase (CAT), and glutathione (GSH), resulting in increased ROS levels that adversely affect spermatogenesis and reduce fertility (103). Recent research has identified the presence of MPs in both testes and semen, with an average concentration of 0.23 ± 0.45 particles/mL in semen and 11.60 ± 15.52 particles/g in testes (105). A recent study identified MPs ranging in size from 2 to 6 μm, suggesting their potential to breach the blood-testis barrier and induce inflammation (106). This may facilitate the uptake and release of MPs via endo- and exocytosis by macrophages within the testes, thereby disrupting spermatogenesis (107). In a study assessing the reproductive toxicity of microplastics, drinking water containing 5 μm polystyrene microplastics was administered to young male mice (1-5 weeks) during a 35-day period. After exposure the ratio of viable spermatozoa to the total number of sperm in the epididymis was found to have significantly decreased (108). Histological assessment of the testes revealed detachment of germ cells, a decrease in spermatid counts, and structural damage to the germinal epithelium (109). A subsequent investigation corroborated similar findings. Mice were subjected to oral gavage of polystyrene microplastics with diameters of 0.5, 4, and 10 μm for 28 days, resulting in bioaccumulation within testicular tissue, inflammatory responses, alterations in sperm morphology, impairment of testosterone biosynthesis, disruption of spermatogenesis, and weight reduction (110). Notably, in vitro studies revealed that polystyrene MPs could enter Leydig, Sertoli, and germ cells, indicating that these reproductive abnormalities could be caused by direct cellular contacts. Data still indicates that ingested MPs may accumulate in the testes and other mammalian tissues, however it is still in the early stages (111). In animal studies, this build-up has been associated with decreased semen quality, most likely due to inflammation and oxidative stress-induced damage. Several studies have demonstrated that it can translocate from the gastrointestinal tract to tissues, potentially affecting metabolism, immunity, and reproduction in aquatic organisms (112). Furthermore, these plastic particles act as carriers for hydrophobic pollutants and microbial infections, intensifying their toxicological impact (113). To present, only a limited number of research have been undertaken on the possible effects of MPs on the human reproductive system (108–111, 114, 115). Further empirical evidence is required on the entry of MPs into the human body, the concentration in human tissues (such as testes, epididymis and blood), the correlation of this concentration with semen quality, the threshold that induces harm to the male reproductive system, and the precise mechanisms via which reproductive system damage occurs (115).

Rising average local temperatures and the increasing frequency of heatwaves exemplify the swiftly evolving impacts of climate change on the global thermal environment (122). These changes are continuing to have serious effects on the distribution and abundance of natural populations and species, and they possess a serious threat to biodiversity (91). Climate change has emerged as a significant factor influencing male reproductive health (123). The core temperature is regulated above all other physiological functions in mammals, which are homeotherms with body temperatures between 35.8 °C and 39.8 °C (124). The specific thermoregulatory system of the suspended scrotum in men sustains an intratesticular temperature slightly below body temperature, essential for spermatogenesis. Superoxide dismutase, catalase, and glutathione peroxidase are antioxidant defenses activated by heat-induced oxidative stress in the testes, mostly via lipid peroxidation and ROS (125). It has been observed that high scrotal temperatures might result genetic and morphological damage, such as DNA damage, decreased sperm viability, and altered steroidogenesis (126). Elevated ambient temperatures, particularly during heatwaves, have been linked to decreased semen quality. A retrospective study in Argentina (2005–2023) involving over 54,000 men found that exposure to prolonged heatwaves during spermatogenesis led to significant reductions in sperm concentration, motility, and normal morphology (127). Statistical research has been conducted between 2000 and 2019 to investigate the global relationship between temperature change and the age-standardized prevalence rate (ASPR) of male infertility. The researchers found a U-shaped association using geographic detectors and restricted cubic spline curves, showing that higher male infertility ASPR is linked to both high and low ambient temperatures with the lowest prevalence noted at 16 °C (128). In particular, geographic locations, such as Southeast Asia and the Middle East, and those with higher Socio-demographic Indexes (SDI) showed a stronger correlation. According to Shared Socioeconomic Pathways (SSP) models, future projections indicate that rising temperatures might contribute to even higher frequency of male infertility (129). Elevated scrotal temperatures disrupt spermatogenesis by inducing oxidative stress, impairing mitochondrial activity, and diminishing the production of proteins essential for sperm movement (125). A multi-Centre study in China examining 78,952 semen samples from 33,234 donors indicated that both thermal extremes negatively impacted sperm parameters, with heat-related anomalies during the warm season significantly diminishing sperm concentration and motility (130). These findings emphasize the susceptibility of spermatogenesis to temperature variations, illustrating the possible effects of global warming on male fertility (131).

Effective measures require political will, financial resources, and international cooperation to implement laws on ongoing greenhouse gas emissions, while individuals can initiate or endorse climate-friendly mitigation efforts (132). Advanced prediction models capable of accurately forecasting biological and ecological responses to current and anticipated future climate conditions must be incorporated to evaluate the long-term impacts of climate change on populations (133). The temperature range at which reproductive capacity is forfeited is referred to as the Thermal Fertility Limit (TFL), a broader counterpart to the Critical Thermal Limit (CTL) (134). The CTL delineates the upper and lower temperature limits beyond which an organism cannot sustain physiological activities, typically resulting in mortality. Conversely, TFL concentrates exclusively on fertility loss. While survival remains unchanged, it includes both upper (TF Max) and lower (TF Min) thresholds beyond which fertility is not sustained (135). The TFL functions as a comprehensive framework for unifying the effects of heat stress on reproductive function across several species (Figure 4). The significant distinction between the thermal thresholds for reproduction and survival is underscored by the observation that fertility may be impaired at temperatures far lower than those that induce mortality (136).

High-resolution climate models coupled with multi-omics predictive frameworks transcriptome-wide association studies (TWAS), genome-wide association studies (GWAS) and expression quantitative-trait-loci (eQTL) mapping can forecast individual susceptibility by integrating baseline environmental exposures with host genetics. These algorithms may ultimately identify males at increased risk of heat-induced subfertility and guide personalized mitigation actions. (Abbreviations: TF, thermal fertility; TWAS, transcriptome-wide association study; GWAS, genome-wide association study; eQTL, expression quantitative trait locus).

Identifying this distinction is crucial for accurately assessing a species’ vulnerability to climate change and for informing more targeted conservation and management strategies (137). Predictive models that incorporate transcriptome-wide association studies (TWAS), genome-wide association studies (GWAS), and expression quantitative trait loci (eQTL) mapping are dependable instruments for assessing the effects of climate change on infertility and other reproductive health outcomes (138). These models offer a data-driven basis for evaluating genetic and regulatory elements vulnerable to heat stress in the context of changing environmental conditions. It offers insight into elevated temperatures that may impact male fertility by modifying genes and transcriptomes at critical developmental stages. By identifying specific genes and regulatory networks linked to heat-induced sterility, these models enhance the understanding of biological pathways that are temperature-sensitive (139). Comparable techniques may be employed to identify individuals or communities that have genetic susceptibility to reproductive complications under thermal stress in humans (140). This prediction ability is essential for determining the long-term reproductive risks associated with global warming and for guiding targeted therapies to maintain fertility among populations (141). Predictive genomics is therefore a promising tool for tackling new climate-related risks for human reproductive health. Recent breakthroughs in artificial intelligence (AI) have markedly improved our capacity to forecast male fertility risks through the integration of environmental, behavioral, and biological data (142). A 2024 study presented an explainable AI model that used Extreme Gradient Boosting (XGB) in conjunction with the Synthetic Minority Over-sampling Technique (SMOTE) to forecast male fertility based on adjustable lifestyle and environmental variables (143, 144). This model attained elevated accuracy and offered clear insights into the influence of certain exposures, including heat stress and endocrine-disrupting chemicals, on fertility outcomes (145). Furthermore, studies have indicated that environmental variables such as heavy metals, phthalates, electromagnetic radiation, and temperature can induce sperm DNA damage, resulting in epigenetic alterations that hinder spermatogenesis (7, 146). These findings highlight the imperative for predictive models that evaluate present reproductive status while also forecasting future risks by accounting for both direct environmental influences and heritable epigenetic alterations. Incorporating these models into practice may enable early interventions and guide public health measures to alleviate the negative impacts of environmental variables on male reproductive health (147).

Reproductive health is a vital component of both social and individual well-being, and the development of dependable biomarkers is crucial for detecting various reproductive illnesses (155). Recent research breakthroughs have underscored the significance of integrative biomarkers that amalgamate several biological methodologies to improve diagnostic precision (156). Integrative biomarkers encompass several biological indicators, including as epigenetic, proteomic, genomic, and metabolomic profiles, which might elucidate the fundamental mechanisms of reproductive health and disease (157). Identified a new array of circRNAs that may serve as diagnostic biomarkers for male infertility and offers molecular insights that could enhance diagnostic and treatment strategies (158). Furthermore, research conducted by Soubry (159) indicated that DNA methylation patterns in sperm may function as possible biomarkers for male infertility. This discovery highlights the necessity for a holistic strategy that incorporates both genetic and epigenetic elements in evaluations of reproductive health (159). The amalgamation of several biomarker categories presents a potential opportunity for the advancement of reproductive diagnostics. Integrating genetic, epigenetic, proteomic, and metabolomic data enables healthcare professionals to attain a more thorough comprehension of reproductive health. Ongoing research in this domain is crucial for the advancement of improved diagnostic instruments that can enhance patient outcomes (160, 161).

Developments in artificial intelligence (AI) and machine learning (ML) have created fresh opportunities for evaluating and forecasting male fertility hazards linked with environmental exposures (162). One important advancement is the Mojo AISA (Artificial Intelligence Semen Analysis) system, which effectively analyses semen samples using artificial intelligence and deep learning algorithms. By automating sperm parameter evaluation including concentration, motility, shape, and viability, this method lowers human error and inter-observer variability (163). Mojo AISA provides a complete evaluation of sperm quality by including sample preparation, imaging, and analysis into a single automated process, therefore enabling early identification of reproductive problems and guiding therapy plans (164). Additionally, some models utilize deep learning techniques to analyze sperm images and estimate DNA fragmentation index (DFI) values, offering a non-invasive and accurate alternative to traditional assays (165). Such AI-assisted evaluations have demonstrated strong correlations with manual assessments, indicating their potential in clinical settings (166). Emerging studies has increasingly approached the role of AI in the clinical management of male infertility, highlighting its applications in diagnosing hypogonadism, analyzing semen parameters, and predicting outcomes of assisted reproductive technologies (167). It advocates for the integration of AI into clinical workflows to enhance diagnostic accuracy and treatment personalization. A systematic review highlighted the efficacy of AI algorithms in sperm selection, reporting that convolutional neural networks (CNNs) achieved up to 90.73% accuracy in automating morphological classification of sperm images (168, 169). These findings highlight the potential of AI to enhance objectivity and efficiency in sperm analysis. Furthermore, AI algorithms have been applied to predict Johnsen scores, which assess spermatogenic potential based on testicular histology. By analyzing histological images, these models can classify Johnsen scores with high accuracy, aiding in the diagnosis and management of male infertility (170). Machine learning models, including gradient boosted trees and logistic regression, have been employed to predict the presence of spermatozoa in testicular biopsies of patients with non-obstructive azoospermia (NOA). These models achieved Area Under the Receiver Operating Characteristic Curve (AUC-ROC) up to 0.807, aiding in clinical decision-making for sperm retrieval procedures (171). A recent study introduced a deep learning model utilizing VGG-16 architecture to predict semen parameters such as sperm concentration, motility, and morphology based on testicular ultrasonography images. The model achieved area under the receiver operating characteristic curve values of 0.76 for oligospermia, 0.89 for asthenozoospermia, and 0.86 for teratozoospermia, indicating its potential as a non-invasive diagnostic tool (172). Although AI- and ML-based systems and deep-learning semen analysis platforms promise diagnostic accuracy, they have limitations on clinical adoption. Most models are trained on relatively small, single-center datasets, which raise concerns across ethnicities, geographic regions, and laboratory protocols. Deep-learning systems function as “black boxes,” providing limited interpretability, these challenges clinician trust, patient counselling, and regulatory approval. Medicolegal and ethical considerations are unresolved for data privacy, informed consent for AI-assisted decision-making, and algorithmic bias arising from training datasets. The AI output must be updated with current WHO semen analysis guidelines and incorporated into clinician-decision pathways rather than functioning as standalone diagnostics (173). Addressing these challenges is essential for clinical translation of AI/ML technologies in male infertility assessment.

Animal models and in vitro experiments have provided a foundation in understanding microplastics and climate-driven heat stress that compromises reproductive physiology. However, emerging human study shows that follicular fluid contains microplastics, which may pose a risk to reproduction. To verify clinical significance, more human research is required (174). Reducing contact with plastic containers and packaging known to contain endocrine-disrupting chemicals, avoiding high-pollution environments, and exposure to airborne pollutants through indoor air filtration are actionable recommendations based on human evidence in clinical practice. Addressing microplastic toxicity requires detection and precise quantification. This can be done by multi-centric case–control studies on testicular biopsies taken during testicular sperm extraction using Raman or FTIR techniques (175). Studies have linked exposure to synthetic fibers with cancer and respiratory disease in textile workers, but there is still insufficient evidence to directly associate microplastic exposure with specific health problems in humans (176). Animal trials and population-level temperature data have been the primary sources for research on climate-related heat exposure and male fertility. Direct human clinical evidence remains insufficient. Since most existing research depends on wide area temperature averages, one significant challenge is accurately assessing personal heat exposure during the whole spermatogenic cycle (177). Future studies would benefit from personal monitoring devices that quantify heat exposure in daily and occupational environments and relate these measurements to repeated semen analyses. In Japan, temperature changes related to climate change had more male stillbirths, but the reasons are still unclear (178). Certain elements of air pollution can cause health impacts through immunological, inflammatory, and excessive oxidative stress pathways. According to an Australian study, there was a 6.6% increase in emergency room visits during heat waves resulting from PM2.5 exposure (179). Large, long-term cohorts are required to clarify exposure–response relationships and to determine whether heat-related declines in semen quality are transient or persistent.

When a significant amount of research focuses on diagnosis, biomarker recognition and predictive modelling, dietary practices should be revised to reduce the Western-style diet, which is highly processed foods that lacks in vitamins. Conversely, eating a diet low in saturated and trans fats and high in antioxidants and anti-inflammatory agents like vitamin C, vitamin E, vitamin D, folate, β-carotene, selenium, zinc, cryptoxanthin, and lycopene could prevent male infertility (180). Lifestyle-based approaches are equally important and involve avoiding scrotal hyperthermia, reducing excess body weight, quitting smoking, limiting alcohol consumption, improving sleep quality, and engaging in regular physical activity, all of which help maintain hormonal balance and lower systemic inflammation. According to a recent study, endogenous coenzyme Q10 levels and platelet mitochondrial activity are indicators of mitochondrial health in infertile males (181). Data obtained using such markers may serve as a basis for patient-tailored antioxidant preventive therapy and the long-term evaluation of its effects. For male fertility, the effects of exposure to various environmental and lifestyle factors may be reversible. Using personal protective equipment at workplace, reducing the intake of highly processed and hot foods packed in plastic, and indoor air quality through filtration are examples of practical solutions. Many symptomatic men who stop such exposure exhibit spontaneous improvements in fertility. For example, a recent study found that quitting smoking improved sperm concentration, semen volume, and overall sperm count (182). Additionally, medical treatments such as aromatase inhibitors, gonadotropins, and selective estrogen receptor modulators may be taken into consideration (183). Assisted reproduction is required if neither lifestyle changes nor the non-invasive therapies are successful in increasing male fertility. The current understanding on health risks posed by environmental factors should motivate policymakers to implement legal frameworks that mitigate their adverse effects on human health (184). Moreover, this raises the need for enhanced education of children and adolescents aimed at reducing environmental exposure. In order to lower population-level reproductive risk, policy measures including tighter regulation of endocrine-disrupting chemicals, microplastic management, better air quality standards, and monitoring heavy metal pollution in water and food systems are important. Rather than analyzing semen parameters, therapeutic approaches should be evaluated in well-designed randomized controlled trials (185). AI can assist with diagnosis, individualized care, treatment prediction, and recovery tracking.