Cadmium exposure and male reproductive health: a systematic review of mechanisms and reproductive outcomes (2020–2026)

Cadmium is a non-essential heavy metal and an environmental and occupational toxicant with potential adverse effects on male reproductive health. Although cadmium-induced reproductive toxicity has been widely investigated, the recent evidence on its effects on testicular structure, spermatogenesis, sperm quality, reproductive hormones, and related molecular pathways has not been comprehensively synthesized. This systematic review aimed to synthesize recent evidence on the effects of cadmium exposure on the male reproductive system, with emphasis on reproductive outcomes, underlying mechanisms, and potential protective interventions. A systematic literature search was conducted on January 15, 2026, in PubMed, Scopus, Web of Science, and Google Scholar for studies published between 2020 and 2026. Search terms included cadmium, male reproductive system, testicular toxicity, spermatogenesis, sperm quality, and related terms. Eligible studies included human observational studies and animal studies investigating the effects of cadmium exposure on male reproductive outcomes. Data were synthesized narratively because of substantial heterogeneity in study designs, exposure levels and durations, experimental models, and outcome measures. Risk of bias was assessed using study-design-appropriate approaches, with SYRCLE used for experimental animal studies and JBI critical appraisal tools used for human observational studies. The non-experimental animal study and in-vitro component of the mixed-design study were considered narratively. Twenty primary studies met the inclusion criteria, comprising five human observational studies and 15 animal studies, of which 14 were experimental studies and one was an environmental observational study. Across the evidence base, cadmium exposure was associated with testicular structural alterations, impaired spermatogenesis, reduced sperm quality, reproductive hormonal changes, oxidative stress, apoptosis, and molecular alterations. The five human observational studies generally supported associations between cadmium exposure and adverse sperm or oxidative-stress outcomes, although findings were not entirely consistent, and several studies involved potential confounding or co-exposure to other toxicants, limiting attribution of the observed reproductive outcomes specifically to cadmium. Animal studies provided broader mechanistic evidence and suggested that antioxidant, zinc, and plant-derived interventions may attenuate selected cadmium-associated reproductive effects. However, evidence for the effectiveness of these interventions in humans was limited. The available evidence indicates that cadmium exposure is associated with adverse effects on male reproductive health across experimental and human observational studies. However, the predominance of animal evidence, limited longitudinal human data, heterogeneity between studies, and potential confounding in observational research limit causal inference in humans. Further longitudinal human studies with standardized exposure assessment, careful control of confounding factors, and investigation of molecular and epigenetic mechanisms are needed. Efforts to reduce occupational and environmental cadmium exposure and strengthen exposure monitoring remain important for protecting male reproductive health. Not applicable.