The Biophysics of Testicular Cancer

Introduction

Testicular cancer is the most common solid tumor in young men aged 15 to 35, with a median age at diagnosis of 33 years. While relatively rare compared to other malignancies, its incidence has been rising steadily over the past few decades, particularly in Western countries, raising urgent questions about environmental, developmental, and lifestyle influences. In Australia, the incidence is among the highest globally, with approximately 7 new cases per 100,000 men annually. Globally, more than 70,000 men are diagnosed each year, with germ cell tumors accounting for over 95% of all testicular cancers.

Fortunately, when detected early and treated appropriately, testicular cancer is one of the most curable cancers, boasting a five-year survival rate exceeding 95%. However, this statistic belies a deeper story. Treatment, often involving surgery, radiation, or chemotherapy, can bring long-term consequences for fertility, hormonal balance, and mitochondrial health. Moreover, spontaneous regression of testicular germ cell tumors, though rare, is a documented phenomenon, suggesting that unknown intrinsic or environmental biophysical factors may influence tumor behavior and immune surveillance.

This paper explores the often-overlooked environmental and biophysical contributors to testicular cancer. From prenatal chemical exposures and endocrine disruptors to circadian disruption from artificial light and EMF radiation, we will examine the compelling research pointing toward non-genetic, modifiable risk factors that may be driving the modern epidemic. Understanding these influences is not only critical for prevention, it redefines what resilience and risk look like for the next generation of men.

Following the epidemiologic and environmental backdrop, a deeper biophysical lens reveals testicular cancer as a condition profoundly influenced by intergenerational epigenetic signaling. Emerging evidence suggests that both maternal and paternal environments, especially during preconception and gestation, can imprint the germline with patterns of DNA methylation and histone modification that influence testicular development and cancer susceptibility. Aberrant hypermethylation of tumor suppressor genes, including those involved in apoptosis and DNA repair, has been observed in testicular germ cell tumors, suggesting that faulty epigenetic programming may silence critical defense pathways before birth. But epigenetic expression is not shaped solely by chemistry, it is photonic. Recent insights in biophysics show that biophotons, or ultraweak light emissions from DNA and mitochondria, play a role in genomic regulation by orchestrating coherent light-based communication within cells. This endogenous light signaling is sensitive to environmental cues, especially circadian light rhythms. Disruptions to natural light exposure in parents, via artificial lighting, indoor living, or screen-based environments, can lead to altered melatonin secretion and redox status, which in turn affects gamete quality and epigenetic stability. In this view, testicular cancer is not just a localized pathology, but a reflection of broken biophysical coherence across generations.

1. Animal Studies: Research involving animal models, such as the study by Yao et al., has shown that long-term exposure to microwave radiation can lead to testicular damage, affecting sperm motility, morphology, and hormone levels, and inducing oxidative stress. Another study by Bilgici et al. demonstrated that exposure to 2.45 GHz electromagnetic fields in rats resulted in increased inflammation and testicular damage, suggesting potential adverse effects on the male reproductive system.[1-2]

2. In Vitro Studies: In vitro studies, such as the one by Jangid et al., have indicated that radiofrequency electromagnetic radiation can interfere with Leydig cell functions, reducing testosterone production and increasing reactive oxygen species (ROS) levels, which could potentially impact male fertility.[3]

3. A Swedish case-control study examined occupational exposure to extremely low-frequency magnetic fields and found some support for an association with testicular cancer, particularly non-seminoma.[12]

The general concern with ALAN is its potential to disrupt circadian rhythms, which can influence cancer risk through mechanisms involving melatonin suppression and alterations in gene expression related to the circadian clock. Research has shown that exposure to light-emitting diodes (LEDs), which often emit blue-rich light, can disrupt the circadian clock and potentially act as an endocrine disruptor, affecting hormone secretion.[4-6]

One study investigated the association between diagnostic radiation exposure and the risk of testicular germ cell tumors (TGCT). It found that exposure to diagnostic radiation below the waist, such as x-rays or CT scans, was associated with an increased risk of TGCT, particularly when individuals reported three or more exposures. The risk was notably higher for exposures occurring at a young age.[7]

Another study examined the effects of fetal radiation exposure in genetically susceptible mice, demonstrating that radiation exposure during pregnancy significantly increased the incidence of TGCT in offspring. This suggests that radiation exposure during critical periods of fetal development may contribute to testicular cancer risk.[8]

Environmental factors have also been implicated in testicular cancer risk. A systematic review highlighted the potential role of occupational and environmental exposures, such as electromagnetic fields, PCBs, and pesticides, although the evidence was inconsistent and often of lower quality. The review emphasized the importance of prenatal and early-life exposures in the etiology of TGCT, suggesting that these periods may be critical for risk development.[9]

Further research has explored the impact of environmental endocrine disruptors (EEDs) on testicular cancer. Although the evidence is limited and controversial, there is a plausible association between EED exposure and testicular cancer, particularly considering the multifactorial etiology involving both genetic and environmental factors.[10]

Additionally, a population-based case-control study in Denmark investigated the association between long-term residential exposure to air pollution and testicular cancer risk. The study found both positive and negative associations depending on the type of pollutant and the timing of exposure, indicating a complex relationship between air pollution and testicular cancer risk.[11]

References

1. Transcriptomic and Metabolic Profiling Reveals the Effects of Long-Term Microwave Exposure on Testicular Tissue. Yao B, Zeng J, Shi J, et al. Ecotoxicology and Environmental Safety. 2025;293:118040. doi:10.1016/j.ecoenv.2025.118040.

2. What Is Adverse Effect of Wireless Local Area Network, Using 2.45 GHz, on the Reproductive System?. Bilgici B, Gun S, Avci B, Akar A, K Engiz B. International Journal of Radiation Biology. 2018;94(11):1054-1061. doi:10.1080/09553002.2018.1503430.

3. Radio Frequency Electromagnetic Radiations Interfere With the Leydig Cell Functions in-Vitro. Jangid P, Rai U, Singh R. PloS One. 2024;19(5):e0299017. doi:10.1371/journal.pone.0299017.

4. Light Pollution and Cancer. Walker WH, Bumgarner JR, Walton JC, et al. International Journal of Molecular Sciences. 2020;21(24):E9360. doi:10.3390/ijms21249360.

5. Exposure to Artificial Light at Night and Risk of Cancer: Where Do We Go From Here?. Jones RR. British Journal of Cancer. 2021;124(9):1467-1468. doi:10.1038/s41416-020-01231-7. 

6. Effects and Mechanisms of Action of Light-Emitting Diodes on the Human Retina and Internal Clock. Touitou Y, Point S. Environmental Research. 2020;190:109942. doi:10.1016/j.envres.2020.109942.

7. Lower Abdominal and Pelvic Radiation and Testicular Germ Cell Tumor Risk. Nead KT, Mitra N, Weathers B, et al. PloS One. 2020;15(11):e0239321. doi:10.1371/journal.pone.0239321.

8. Fetal Radiation Exposure Induces Testicular Cancer in Genetically Susceptible Mice. Shetty G, Comish PB, Weng CC, Matin A, Meistrich ML. PloS One. 2012;7(2):e32064. doi:10.1371/journal.pone.0032064.

9. Occupational and Environmental Exposures Associated With Testicular Germ Cell Tumours: Systematic Review of Prenatal and Life-Long Exposures. Béranger R, Le Cornet C, Schüz J, Fervers B. PloS One. 2013;8(10):e77130. doi:10.1371/journal.pone.0077130.

10. Environmental Disruptors and Testicular Cancer. Faja F, Esteves S, Pallotti F, et al. Endocrine. 2022;78(3):429-435. doi:10.1007/s12020-022-03171-z.

11. Long-Term Residential Exposure to Air Pollution and Risk of Testicular Cancer in Denmark: A Population-Based Case-Control Study. Taj T, Harbo Poulsen A, Ketzel M, et al. Cancer Epidemiology, Biomarkers & Prevention : A Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2022;:cebp.0961.2021. doi:10.1158/1055-9965.EPI-21-0961.

12. Occupational Exposure to Magnetic Fields in Relation to Male Breast Cancer and Testicular Cancer: A Swedish Case-Control Study. Stenlund C, Floderus B. Cancer Causes & Control : CCC. 1997;8(2):184-91. doi:10.1023/a:1018468112964.

13. Perinatal Factors and the Risk of Testicular Germ Cell Tumors. Cook MB, Graubard BI, Rubertone MV, Erickson RL, McGlynn KA. International Journal of Cancer. 2008;122(11):2600-6. doi:10.1002/ijc.23424.

14. Parental Occupational Exposure to Solvents and Risk of Developing Testicular Germ Cell Tumors Among Sons: A French Nationwide Case-Control Study (TESTIS Study). Guth M, Lefevre M, Pilorget C, et al. Scandinavian Journal of Work, Environment & Health. 2023;49(6):405-418. doi:10.5271/sjweh.4102.

15. Parental Occupations at Birth and Risk of Adult Testicular Germ Cell Tumors in Offspring: A French Nationwide Case-Control Study. Paul A, Danjou AMN, Deygas F, et al. Frontiers in Public Health. 2023;11:1303998. doi:10.3389/fpubh.2023.1303998.

Environmental and Occupational Exposures Linked to Testicular Germ Cell Tumors (TGCT)

Air Pollution

• Ambient Air Pollutants: Recent research suggests that early-life exposure to certain air pollutants may influence TGCT risk. A Danish case–control study found that prenatal and childhood exposure to ozone (O₃) and secondary inorganic aerosols was associated with higher TGCT risk (e.g. O₃: OR ~1.20 per 10 µg/m³), whereas exposure to traffic-related pollutants like NO₂ and organic carbon was linked to a lower risk. [Cite]. This was the first epidemiologic study to report both positive and negative associations depending on the pollutant and exposure timing. [Cite]. 

• Diesel Exhaust and Particulates: Occupations involving heavy traffic or diesel combustion (e.g. transport equipment operators) have been associated with elevated TGCT risk. One case–control study in France observed that fathers working as transport equipment operators around the time of their son’s birth had nearly doubled odds of TGCT in offspring (OR ≈1.96) [Cite] . This suggests possible exposure to diesel exhaust or particulate air pollutants as a contributing factor.

Electromagnetic Fields (EMF)

• Occupational EMF Exposure: Overall, epidemiological studies have not found a consistent link between EMF exposure and testicular cancer. A German population-based study evaluating workplace EMF sources (e.g. working near radar, radio-frequency transmitters, high-voltage lines, or electrical machinery) found no increased TGCT risk in exposed workers (all ORs ~1.0 or below) [Cite] . For instance, men who had ever worked with radar had an OR = 1.0 (95% CI 0.60–1.75), and those near high-voltage lines had OR = 0.7 (0.38–1.18) [Cite] . These null results suggest occupational EMFs are not a major risk factor for TGCT.

• Household EMF Sources: Similarly, domestic exposure to EMFs has shown little effect. A case–control study in the 1980s examined use of electric blankets (a source of prolonged low-frequency EMF) and found no overall association with testicular cancer (RR ~1.0) [Cite] . There was a slight, non-significant trend of lower risk in seminoma and higher risk in non-seminoma among electric blanket users, but these differences were not statistically significant [Cite]. In summary, available evidence indicates that EMF exposure, whether at work or home, contributes little if at all to TGCT risk.

Artificial Light at Night (ALAN) and Circadian Disruption

• Night-Shift Work: Disruption of circadian rhythms via night-shift work (and the corresponding exposure to light at night) has been hypothesized to act as an “environmental endocrine disruptor” by suppressing melatonin [Cite]. However, research specifically linking ALAN or shift work to testicular cancer is very limited. To date, no large epidemiological study has conclusively determined the effect of night-shift work on TGCT risk. In fact, the relationship remains understudied [Cite] . A current international project (ON-Shift) is underway to investigate whether working night shifts is associated with higher incidence of TGCT [Cite]. Early findings or hypotheses from this project emphasize that any potential risk from ALAN has yet to be established.

• Rationale: Although not yet proven in humans, the biological rationale is that circadian disruption could alter hormone levels (e.g. lower nocturnal melatonin, altered testosterone regulation) which might influence testicular tumorigenesis. Until results from ongoing studies are published, ALAN remains a suspected but unconfirmed risk factor for TGCT.

Endocrine Disruptors and Xenoestrogens

• Organochlorine Chemicals: A body of evidence suggests that exposure to endocrine-disrupting chemicals (EDCs), especially during prenatal life, may increase TGCT risk. Persistent organochlorine pollutants are of particular concern. For example, a U.S. study (STEED cohort) reported that men with TGCT had significantly higher serum levels of p,p′-DDE (a DDT metabolite) and trans-nonachlor (an organochlorine pesticide) compared to controls [Cite]. A smaller Swedish study likewise found TGCT cases had higher cis-nonachlor levels than controls [Cite]. These chemicals are known xenoestrogens that can disrupt fetal testicular development. (Notably, the same U.S. study paradoxically found lower PCB levels in cases than controls [Cite], highlighting the complex and sometimes inconsistent nature of EDC effects.) Overall, such findings support the “estrogen hypothesis” of testicular cancer, which posits that elevated estrogenic exposures in utero (potentially via xenoestrogens like DDT/DDE or chlordanes) may predispose to TGCT [Cite].

• Polychlorinated Biphenyls (PCBs): PCBs are another class of persistent chemicals with endocrine activity. While total PCB levels have not shown a clear association with testicular cancer, the profile of PCB congeners may matter. One case–control study of 308 TGCT patients found no overall link with summed PCB concentration, but when PCB congeners were categorized by estrogenic activity, higher serum levels of estrogenic PCBs were associated with a significant increase in TGCT risk (OR ~2.5, 95% CI 1.3–4.7) [Cite]. This suggests that hormonally active PCB subsets (acting as xenoestrogens) could contribute to tumor development.

• Personal Care Products (Phthalates/Parabens): Maternal exposure to everyday endocrine disruptors has also been implicated. A 2018 study by Ghazarian et al. examined mothers’ use of personal care products during pregnancy and breastfeeding. It found that frequent maternal use of face lotions containing parabens and phthalate-related compounds was associated with a 42% higher odds of TGCT in sons (OR = 1.42, 95% CI 1.08–1.86) [Cite]. These chemicals can mimic hormones or alter the endocrine milieu in pregnancy, potentially affecting the developing testes of the fetus. This evidence directly links in utero exposure to certain xenoestrogen-containing products with later TGCT in offspring.

• Other EDCs (Experimental Evidence): Animal and experimental studies bolster the plausibility of EDC effects. For instance, Bisphenol A (BPA), a common plasticizer and known endocrine disruptor, has been shown to promote testicular tumor growth in rodent models. In one study, perinatal exposure to BPA led to accelerated growth of transplanted testicular tumors in mice [Cite]. Such findings (along with known effects of prenatal DES exposure on male reproduction) underscore that environmental estrogens and related chemicals can disturb male reproductive development. In humans, a small Italian study also observed that TGCT patients more often had detectable organochlorine loads (like hexachlorobenzene and PCBs) compared to controls, implicating parental occupational exposures to these pollutants as a risk factor [Cite]. While human data are sometimes conflicting, the majority of epidemiologic studies suggest EDC exposures play a role in testicular germ cell tumor etiology [Cite].

Pesticides

• Household and Domestic Use: Beyond the persistent pollutants mentioned above, more immediate pesticide exposures have been evaluated. A French case–control study (304 cases, 274 controls) investigated parents’ self-reported use of pesticides (insecticides, herbicides, fungicides) in the home or garden during the sons’ early life. The use of fungicides stood out, showing a significant association with TGCT risk in the offspring (OR = 1.73, 95% CI 1.04–2.87). In particular, non-seminomatous TGCT had an even higher risk with domestic fungicide use (OR = 2.44) [Cite]. In contrast, there was no significant risk elevation linked to household insecticide or herbicide use [Cite]. Although details on specific active ingredients were lacking, this suggests that certain antifungal chemical exposures (possibly those with endocrine or genotoxic effects) during childhood or prenatal periods might increase testicular cancer susceptibility.

• Agricultural Exposure (Prenatal): Pesticide exposure in agricultural settings, especially during pregnancy, has been examined as well. A study in California assessed prenatal residential proximity to agricultural pesticide applications among 381 young TGCT cases. It found modest but significant risk increases associated with specific pesticides. Notably, organophosphate insecticides were implicated: Latino mothers living near usage of acephate and malathion during pregnancy had sons with elevated testicular cancer risk (OR 1.30 and 1.19, respectively). Similarly, in non-Latino populations, prenatal proximity to the carbamate insecticide carbaryl was associated with increased TGCT risk (OR ~1.14) [Cite]. These findings, albeit subgroup-specific, tie certain agricultural chemicals to TGCT and may partly explain regional patterns of incidence in heavily farmed areas. (It’s worth noting that this study did not account for postnatal exposures or parental occupational contact with pesticides, which could also contribute to risk [Cite] .)

• Farming Occupations: Consistent with the above, having a parent employed in agriculture has been linked to testicular cancer in offspring. The French nationwide study of parental jobs at birth found that sons of “specialized farmers” had about 2.6-fold higher odds of TGCT [Cite]. The authors suggest pesticide exposure as a likely explanation, given that farming can involve handling of agrochemicals [Cite]. This aligns with earlier observations that men raised in rural, farming communities (or whose mothers had farm/gardening exposures) showed higher incidence of TGCT. Overall, pesticide exposure – whether through parental occupation or environmental contact – is one of the leading environmental suspects in TGCT etiology.

Solvents

• Parental Occupational Solvent Exposure: Organic solvents are widely used chemicals (e.g. in painting, degreasing, chemical manufacturing) and some have endocrine or carcinogenic properties. Several case–control studies have evaluated whether parental jobs involving solvents around the time of a son’s birth are associated with TGCT in the offspring. The recent French TESTIS study (454 cases, 670 controls) found no strong overall link between parental solvent exposure and testicular cancer [Cite]. About 41% of fathers and 21% of mothers had some occupational solvent exposure in the year of birth, but in general this did not translate into higher TGCT rates (paternal exposure to any solvent vs none yielded OR ~0.89, 95% CI 0.68–1.15) [Cite]. Likewise, maternal occupational solvent exposure showed no significant association overall (OR ~0.90)[Cite].

• Specific Solvents and Timing: Although the aggregate results were null, a few specific exposures and subgroups hinted at risk increases. In the French study, sons of fathers with high exposure to trichloroethylene (a chlorinated solvent used in degreasing) had a non-significant trend toward elevated TGCT risk, especially for non-seminomas (OR ≈1.4, 95% CI overlapping 1) [Cite]. More notably, men born in the 1970s showed a significant association if their mother had occupational exposure to petroleum-based fuels/solvents during pregnancy – in that subgroup, TGCT risk was about 2.7 times higher (OR 2.74, 95% CI 1.11–6.76) [Cite]. This latter finding suggests a potential intergenerational effect where maternal exposure to gasoline or similar hydrocarbon solvents in an era of less regulation (1970s) might have affected fetal testis development. It echoes results from a Nordic study (NORD-TEST) which also observed elevated TGCT risk in sons born in 1970–79 to mothers exposed to aromatic hydrocarbon solvents at work [Cite].

• Mechanisms and Interpretation: Some organic solvents (e.g. certain glycol ethers, chlorinated hydrocarbons) are known to be endocrine disruptors or to cause testicular toxicity in animal studies. However, overall epidemiologic evidence in humans is mixed. Large studies in Denmark (1981–2014 births) and France (2015–2018 data) both concluded there is no clear, strong association between parental solvent exposure and TGCT in offspring [Cite] [Cite]. Only subtle increases were seen in specific contexts (like trichloroethylene or combined solvent-heavy metal exposure in certain jobs) [Cite]. Thus, while solvents remain a suspected risk factor – and certain ones like perchloroethylene or methylene chloride showed OR >1 in some analyses[Cite] – current studies provide only limited support. Further research is needed, particularly focusing on high-exposure occupations and on distinguishing different solvent types, to clarify any role in testicular cancer.

Heavy Metals

• General Evidence: Toxic heavy metals such as cadmium (Cd), lead (Pb), chromium (Cr), and others have been postulated to contribute to testicular carcinogenesis. These metals can induce oxidative stress and may disrupt endocrine function or DNA integrity in the testes [Cite]. Recent studies suggest a “significant role” of cadmium and lead in the origin of TGCT [Cite]. For example, cadmium – a known testicular toxin in animal models – has been linked to human TGCT risk by biomonitoring studies. In a 2023 study, TGCT patients had significantly higher blood cadmium levels than healthy controls, and elevated blood Cd was associated with roughly a doubling of risk (OR ~1.98 for top vs bottom levels) [Cite]. This finding reinforces earlier observations that cadmium exposure (from sources like cigarette smoke, industrial emissions, or diet) might be a contributing factor to testicular cancer.

• Cadmium and Lead Mechanisms: Cadmium in particular accumulates in the testis and can cause damage to germ cells. It has estrogen-mimicking effects and interferes with zinc and other essential elements, which may promote malignant transformation in germ cells [Cite]. Lead, another heavy metal, is also suspected to play a role, though evidence is less direct. Both Cd and Pb have been found to correlate with altered hormone levels and oxidative markers in TGCT patients [Cite]. While direct epidemiologic links for lead are not well established, these metals often co-occur in industrial exposures and could collectively contribute to risk.

• Occupational Metal Exposures: Studies of parental occupations provide some support for heavy metal involvement. The Nordic NORD-TEST project reported a modest association between paternal exposure to certain metals and TGCT. Specifically, fathers classified as exposed to a combination of heavy metals (like chromium VI) and solvents had a higher odds of having a son develop TGCT (OR ~1.5, 95% CI 1.01–2.24) [Cite]. Many of these fathers worked in wood-related industries (e.g. carpentry, wood treatment) where they likely encountered chromium-based wood preservatives and solvent mixtures [Cite]. Additionally, that study suggested some risk increase with maternal heavy metal exposure – for instance, mothers exposed to metals such as chromium, nickel, or iron in the workplace had sons with higher TGCT incidence, particularly for those born in the 1980s–90s [Cite]. Although these associations were not very strong, they point toward metals (like Cr(VI)) as potential hazards. Notably, chromium and nickel compounds are established carcinogens and could feasibly affect the developing germ cells if exposure occurs during pregnancy.

• Summary: Heavy metals are considered “relevant toxins” in the context of testicular cancer. Cadmium has the most consistent support, with both biological plausibility and human data (e.g. blood levels) linking it to TGCT [Cite]. Other metals such as chromium and lead are also implicated based on occupational studies and mechanistic understanding [Cite]. Reducing environmental exposure to these metals (via pollution control, workplace safety, and smoking cessation for cadmium) may be a prudent step, given their potential role in testicular tumor development.

Per- and Polyfluoroalkyl Substances (PFAS)

• Firefighting Foam and PFOS: PFAS are a class of persistent man-made chemicals (used in firefighting foams, non-stick coatings, etc.) that have recently been tied to testicular cancer. A notable investigation was conducted among U.S. Air Force servicemen, a group with high PFAS exposure from fire-suppression foams on military bases. Researchers found that airmen who served as firefighters or at installations with PFAS-contaminated water had significantly elevated blood PFAS levels, and importantly, those with higher serum PFOS (perfluorooctane sulfonate) had a greater risk of developing TGCT [Cite]. In this nested case–control study from the Department of Defense serum repository, men in the highest PFOS exposure category showed a clear increase in testicular cancer incidence [Cite]. These findings provide some of the first direct human evidence linking PFAS to TGCT.

• Mechanism and Other PFAS: PFOS and related compounds are believed to act as endocrine disruptors and immunotoxicants. There is evidence that PFAS can interfere with hormonal pathways (some have weak estrogenic or anti-androgenic effects) [Cite]. In the context of TGCT, PFAS exposure might impair testicular development or function, thereby raising cancer risk decades later. While the Air Force study highlighted PFOS, other PFAS like PFOA and PFHxS were also elevated among the servicemen – though their individual associations with TGCT need further study [Cite]. The fact that firefighting personnel had higher PFAS and higher TGCT aligns with this risk factor. As a result, PFAS are now considered emerging environmental carcinogens for testicular cancer, prompting calls for continued research and monitoring [Cite] [Cite].

• Broader Implications: The PFAS–TGCT link is particularly concerning given how ubiquitous and persistent these “forever chemicals” are. Even in the general population (outside of military settings), PFAS are widespread in blood and can come from contaminated water or consumer products. Ongoing studies are examining civilians with high PFAS exposures (e.g. communities near chemical plants) to see if testicular cancer rates are elevated. Early evidence from both epidemiologic data and animal studies has led experts to list testicular cancer as one of the potential outcomes of chronic PFAS exposure [Cite] [Cite]. As regulations on PFAS tighten, we may gain more clarity on whether reducing these exposures will correspondingly lower TGCT incidence in the future.

Sources

The information above is drawn from a range of peer-reviewed studies and reviews. Key sources include epidemiologic studies on perinatal factors and TGCT [Cite], [Cite], occupational case–control studies from Europe [Cite] [Cite] , and research on environmental toxins (e.g. organochlorines [Cite], pesticides [Cite] , solvents [Cite], heavy metals [Cite], and PFAS [Cite]) in relation to testicular cancer risk. Each category of exposure is supported by cited evidence as indicated.