Male Reproductive Toxicology and Polycyclic Aromatic Hydrocarbon Exposure

Polycyclic aromatic hydrocarbons (PAHs) are a class of ubiquitous environmental contaminants generated by incomplete combustion of organic material, with common sources including industrial emissions, vehicle exhaust, tobacco smoke and certain cooking processes. Owing to their lipophilic nature, PAHs readily accumulate in biological tissues and can disrupt endocrine and reproductive function by eliciting oxidative stress, perturbing steroidogenic pathways in Leydig cells and inducing DNA damage in spermatozoa. In men, chronic or high-level exposure has been linked to altered sperm motility, morphology and viability, as well as impaired testosterone synthesis. At the molecular level, PAHs activate the aryl hydrocarbon receptor (AhR) and downstream cytochrome P450 enzymes, generating reactive oxygen species (ROS) that overwhelm antioxidant defences and initiate lipid peroxidation, protein adduct formation and apoptotic signalling. This toxic cascade not only compromises spermatogenesis but may also exert transgenerational effects on germline integrity. The global scale of PAH pollution, combined with rising concerns over male infertility rates, underscores the need for robust biomarkers of exposure, mechanistic insight and protective strategies that range from lifestyle interventions to novel therapeutics.

Research from Nature Portfolio

A recent investigation has demonstrated that zinc oxide nanoparticles can mitigate PAH-induced dysregulation of testicular steroidogenesis. In an animal model, co-administration of zinc oxide nanoparticles alongside benzo[a]pyrene reversed oxidative stress biomarkers, restored expression of key steroidogenic enzymes (CYP11A1, StAR, 3β-HSD) and normalised testosterone levels, while preserving testicular histology. This work reveals the potential of nanoparticle-based antioxidants to counteract PAH toxicity at the molecular level and suggests a platform for developing targeted interventions to safeguard male reproductive health.

Male Reproductive Toxicology and Polycyclic Aromatic Hydrocarbon Exposure publication trend

The graph below shows the total number of articles in male reproductive toxicology and polycyclic aromatic hydrocarbon exposure across all publications each year (not limited to Nature Index journals).

Technical terms

Polycyclic aromatic hydrocarbons (PAHs): Lipid-soluble organic compounds formed by incomplete combustion of carbonaceous materials, many of which are endocrine disruptors and carcinogens.

Oxidative stress: A cellular state in which the production of reactive oxygen species exceeds the capacity of antioxidant defences, leading to damage of lipids, proteins and DNA.

Aryl hydrocarbon receptor (AhR): A ligand-activated transcription factor that mediates cellular responses to environmental toxins, including PAHs, by regulating detoxification enzymes.

Reactive oxygen species (ROS): Chemically reactive molecules containing oxygen, such as superoxide anion and hydrogen peroxide, which can induce oxidative damage to cellular components.

Steroidogenic acute regulatory protein (StAR): A mitochondrial protein that controls the transport of cholesterol into mitochondria, a rate-limiting step in steroid hormone biosynthesis.

References

1. Zinc oxide nanoparticles improve testicular steroidogenesis machinery dysfunction in benzo[α]pyrene-challenged rats. Scientific Reports (2021).
2. One-Year Impact of Occupational Exposure to Polycyclic Aromatic Hydrocarbons on Sperm Quality. Antioxidants (2024).
3. Effects of Benzo[a]pyrene on Human Sperm Functions: An In Vitro Study. International Journal of Molecular Sciences (2023).
4. Human sperm proteome reveals the effect of environmental borne seminal polyaromatic hydrocarbons exposome in etiology of idiopathic male factor infertility. Frontiers in Cell and Developmental Biology (2023).