# Common Environmental Hazards and Male Infertility: Effects on Epididymal Immune Microenvironment

## TL;DR

This paper reviews how environmental hazards disrupt the epididymal immune microenvironment, leading to male infertility, and highlights potential mechanisms for targeted interventions.

## Contribution

The paper provides a comprehensive synthesis of how environmental hazards affect the epididymal immune microenvironment and male fertility from an immunological perspective.

## Key findings

- Environmental hazards disrupt the homeostasis of the epididymal immune microenvironment.
- Chemical, physical, biological, and behavioral hazards share pathophysiological mechanisms leading to male infertility.
- The study identifies molecular mechanisms linking environmental insults to immune dysregulation in the epididymis.

## Abstract

Environmental hazard-induced male infertility has become a major public health issue. The concealment and accumulation of environmental hazards, and their interactions with the endogenous immune network, have long been underappreciated. As the central organ for sperm maturation and motility acquisition, the epididymis plays a vital role in male fertility, and the homeostasis of the epididymal immune microenvironment (EIM) is essential. Nevertheless, a systematic synthesis of common environmental hazards and their impact on EIM, which can lead to male infertility, remains lacking. This review comprehensively summarizes the composition, functionality, and key characteristics of the EIM and underscores its critical role in preserving male reproductive health. We further evaluate and delineate the disruption of EIM homeostasis resulting from major categories of environmental exposures—including chemical, physical, biological, and behavioral hazards—and discuss their shared pathophysiological mechanisms. By integrating evidence linking environmental insults, EIM dysregulation, and male infertility, this work aims to identify pivotal molecular mechanisms from an immunological perspective. The findings provide a mechanistic foundation for the development of targeted interventions and preventive strategies against environmental hazard-induced male infertility.