Cadmium on the Job Linked to Falling Testosterone and Vascular Stress in Male Workers

A new cross-sectional study of industrial workers in Türkiye has found that men with occupational exposure to cadmium carry significantly higher burdens of the toxic metal in their bodies and show a distinctive pattern of hormonal and vascular biochemical changes, including lower testosterone and elevated levels of molecules that signal endothelial dysfunction. The research, published in BMC Endocrine Disorders, offers one of the most detailed simultaneous snapshots to date of how chronic cadmium exposure in the workplace may be reshaping both the hormonal axis that governs male reproduction and the biochemical pathways that keep blood vessels healthy.

Cadmium is a heavy metal with no known biological function in the human body, yet it accumulates relentlessly in tissues, particularly the kidneys, with a biological half-life measured in decades. Workers in industries involving metal smelting, battery manufacturing, welding, electroplating, and the processing of zinc and copper ores can inhale cadmium-containing fumes and dust over years of employment. While the metal’s links to kidney damage, bone disease, and cancer have been studied extensively, its effects on the endocrine system and on vascular biology in exposed workers have received comparatively little attention in human studies, a gap the new research set out to address.

The study team, led by Deniz Özkan Vardar of Lokman Hekim University in Ankara together with collaborators from several Turkish universities and occupational health institutions, enrolled 170 adult men: 85 workers with documented occupational cadmium exposure and 85 unexposed controls matched for comparison. To quantify the internal cadmium burden of each participant, the researchers measured urinary cadmium concentrations using inductively coupled plasma mass spectrometry, or ICP-MS, an analytical technique sensitive enough to detect trace metals at parts-per-billion levels. Urinary cadmium is widely regarded as the preferred biomarker of cumulative body burden because the metal accumulates in the kidneys and is slowly excreted, so urine levels reflect decades of exposure rather than recent contact alone.

Beyond the metal itself, the team assembled an unusually comprehensive panel of biomarkers spanning two physiological domains. On the endocrine side, they measured serum total testosterone along with luteinizing hormone and follicle-stimulating hormone, the two pituitary hormones that regulate the testes through the hypothalamic-pituitary-gonadal axis. On the vascular side, they quantified asymmetric dimethylarginine and symmetric dimethylarginine, known as ADMA and SDMA, together with their precursor arginine and related metabolite citrulline. ADMA is of particular interest to cardiovascular researchers because it inhibits endothelial nitric oxide synthase, the enzyme that produces nitric oxide, the signaling molecule responsible for relaxing blood vessels and maintaining vascular health. Elevated ADMA is considered a harbinger of endothelial dysfunction and cardiovascular risk.

The results were striking in their consistency. Cadmium-exposed workers had substantially higher urinary cadmium concentrations than the unexposed controls, confirming that their occupational environment translated into a measurably greater internal body burden. More importantly, the exposed group showed significantly higher serum levels of both ADMA and SDMA, with differences that reached the stringent threshold of p less than 0.001. At the same time, total testosterone, follicle-stimulating hormone, and the arginine-to-ADMA ratio were all significantly lower in the exposed workers, while luteinizing hormone showed a smaller but still statistically significant reduction. The arginine-to-ADMA ratio is a meaningful composite index, because it reflects the balance between the substrate available for nitric oxide production and the endogenous inhibitor that blocks it; a falling ratio suggests a shift toward suppressed nitric oxide bioavailability.

Perhaps most telling were the correlation analyses. Urinary cadmium concentrations were inversely correlated with total testosterone and with follicle-stimulating hormone, meaning that the greater a worker’s internal cadmium burden, the less favorable his endocrine profile tended to be. This dose-response-like relationship strengthens the biological plausibility of a causal link, although the cross-sectional design of the study, which captures a single moment in time, means that it demonstrates association rather than definitive causation. Reverse causation and confounding by other workplace exposures or lifestyle factors cannot be fully excluded, a limitation the authors acknowledge implicitly by framing their findings as a basis for combined biomarker monitoring rather than as proof of harm.

The simultaneous disruption of both endocrine and endothelial markers is what makes the study particularly noteworthy. Cadmium is known from experimental work to interfere with steroidogenesis, the enzymatic machinery inside Leydig cells that converts cholesterol into testosterone, and to damage the seminiferous tubules where sperm are produced. The observed pattern of reduced testosterone alongside reduced LH and FSH suggests that cadmium’s effects may not be confined to the testes themselves but may also involve higher levels of the hypothalamic-pituitary-gonadal axis, since primary testicular failure would typically drive these pituitary hormones upward rather than down. Disentangling whether cadmium acts at the brain, the pituitary, the testes, or all three will require longitudinal and mechanistic follow-up.

On the vascular side, the elevation of ADMA and SDMA in exposed workers fits with growing evidence that heavy metals promote cardiovascular disease in part by degrading nitric oxide signaling. Cadmium generates oxidative stress, and reactive oxygen species accelerate the enzymatic degradation of ADMA’s clearance, raising its circulating levels. Because endothelial dysfunction is an early and reversible stage of atherosclerosis, the finding raises the possibility that cadmium-exposed workers accumulate cardiovascular risk silently, years before any clinical event. The concurrent decline in the arginine-to-ADMA ratio provides a quantitative handle on this shift and suggests a potential monitoring target that could be tracked in occupational health surveillance programs.

The practical implications extend beyond the laboratory. The authors suggest that combined assessment of endocrine and endothelial biomarkers may prove useful for occupational monitoring of workers with chronic cadmium exposure, complementing the traditional reliance on urinary cadmium and kidney function measures such as estimated glomerular filtration rate. If validated in larger and longitudinal cohorts, a panel that includes testosterone, FSH, ADMA, and SDMA could allow occupational physicians to detect subclinical physiological disruption earlier, intervene with exposure controls or job rotation sooner, and ultimately protect a workforce that often has few alternatives to hazardous industrial environments. Regulatory limits on airborne cadmium exist in most industrialized countries, but enforcement varies, and the study is a reminder that even exposures within permissible ranges may leave biochemical fingerprints.

The research also arrives amid broader public concern about endocrine-disrupting chemicals and the slow, cumulative ways in which environmental toxicants shape long-term health. Cadmium does not degrade, persists in soil and tobacco smoke as well as in industrial settings, and enters the general population through food crops grown on contaminated land. For the general public, dietary exposure and smoking dominate; for industrial workers, inhalation can dwarf these routes. As analytical techniques like ICP-MS and liquid chromatography-tandem mass spectrometry make it ever cheaper and easier to measure trace toxicants and their biochemical consequences, studies of this kind are likely to multiply, building the evidence base needed to translate molecular signals into concrete workplace protections. For now, the message from Ankara is clear: the same metal that quietly damages kidneys and bones may also be quietly rewiring the hormonal and vascular chemistry of the men who work with it, and routine blood and urine tests may be able to see it coming.

Subject of Research: Occupational cadmium exposure and its association with endocrine and endothelial biomarker alterations in male workers

Article Title: Occupational cadmium exposure and endocrine biomarker alterations in male workers: a cross-sectional study

Article References: Occupational cadmium exposure and endocrine biomarker alterations in male workers: a cross-sectional study. (n.d.). https://doi.org/10.1186/s12902-026-02605-3

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02605-3

Keywords: cadmium, occupational exposure, testosterone, ADMA, SDMA, FSH, LH, endocrine disruption, endothelial dysfunction, biomarkers, occupational health, toxicology