Heavy metals and human reproductive toxicity: Mechanisms, pregnancy outcomes, and mitigation strategies

Heavy metals are environmental pollutants with well-documented systemic toxicity. Emerging evidence highlights their detrimental effects on human reproductive health. This narrative review aims to synthesize current scientific literature on the reproductive toxicity of arsenic (As), cadmium (Cd), chromium (Cr), mercury (Hg), and lead (Pb), focusing on their impact on fertility, pregnancy outcomes, fetal development, and neonatal health. The analysis includes cellular, molecular, and endocrine mechanisms, and considers both chronic environmental and acute occupational exposures. Inclusion criteria comprised peer-reviewed experimental, clinical, and review studies involving human subjects, providing direct translational relevance. Key endpoints included gametogenesis, hormonal regulation, fertility outcomes, and pregnancy complications. The main mechanisms of heavy metal-induced reproductive toxicity include DNA damage, oxidative stress, apoptosis, ionic mimicry, and hormonal disruption. In males, exposure is associated with reduced sperm quality, altered morphology, and impaired motility. In females, heavy metals interfere with oocyte maturation, ovarian function, and hormonal balance, increasing the risk of infertility, miscarriage, and adverse pregnancy outcomes. In addition to summarizing toxic effects, the review also discusses emerging protective and mitigation strategies-such as micronutrient and antioxidant supplementation-that may counteract reproductive damage. Heavy metal exposure, even at low levels, poses a significant risk to human reproductive health. The findings underscore the urgent need for preventive strategies, environmental regulation, and targeted health monitoring, particularly among vulnerable populations. Future research should explore the long-term and transgenerational effects of exposure.