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Environmental cadmium exposure may cause male reproductive dysfunction through the renal-testis axisCadmium exposure may harm male fertility and kidney health

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Key Takeaway
Note that environmental cadmium may cause male reproductive dysfunction via the renal-testis axis in animal models.

This narrative review analyzes 40 animal studies to evaluate the effects of environmental cadmium exposure on male reproductive health. The authors synthesize evidence regarding impacts on semen quality, testicular injury, and the hypothalamic-pituitary-testicular axis.

The review identifies a minimum critical human equivalent dose (HED) of 0.002 mg/kg/d for cadmium-induced male reproductive damage, based on a rat LOAEL of 10 $μ$g/kg/d. The authors argue that cadmium exposure may cause significant damage to the male reproductive system and adversely affect semen quality.

A key finding is the impact of the renal-testis axis; cadmium induces renal dysfunction which may indirectly exacerbate testicular injury and disrupt the hypothalamic-pituitary-testicular axis. These results highlight the integrated renal-reproductive toxicity associated with environmental exposure.

Clinical application is limited as the evidence is derived from in vivo studies rather than human clinical trials. The findings suggest that cadmium exposure represents a potential risk factor for male infertility, but direct clinical implications require further investigation.

How this fits prior evidence

This narrative review addresses a gap regarding environmental toxins and male fertility. It complements existing coverage on modifiable risk factors for male infertility and the uncertain links between BPA exposure and male infertility. While previous evidence highlighted risks from lifestyle factors and chemical exposures like BPA, this review specifically focuses on the renal-testis axis as a mechanism for cadmium-induced reproductive damage.

When we think about environmental hazards, we often focus on immediate symptoms. However, some pollutants work quietly over time. A review of 40 animal studies shows that exposure to cadmium—a heavy metal found in the environment—can harm the male reproductive system. This damage can lead to lower semen quality and injury to the testes.

The research highlights a link between kidney health and fertility. It suggests that cadmium causes renal dysfunction, which is a fancy way of saying it harms how kidneys work. This kidney damage then triggers a chain reaction that further damages the reproductive system.

It is important to note that these findings come from animal studies rather than human clinical trials. While the data shows a clear link between cadmium and reproductive issues in animals, the specific impact on humans is still being mapped out by researchers.

What this means for you:
Cadmium exposure can damage both kidneys and male reproductive health through linked biological pathways.

Common questions

What is the link between cadmium and male fertility?

Cadmium exposure can damage the male reproductive system. This damage can lead to problems like testicular injury and lower semen quality. The study reviewed 40 animal experiments to show how this metal impacts reproductive health.

How does cadmium affect the kidneys?

Cadmium causes renal dysfunction, which means it harms the way kidneys function. This damage to the kidneys can then indirectly make it worse for the male reproductive system through a linked pathway between the two organs.

Is this finding based on human clinical trials?

No, these findings are based on animal experiments rather than human clinical trials. The study is a narrative review of 40 different studies involving animals to understand how cadmium affects the body.

Study Details

Study typeSystematic review
EvidenceLevel 1
PublishedJul 2026
View Original Abstract ↓
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: (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.
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