# Persistent organic pollutants and prostate cancer: multiple mechanisms and comprehensive control strategies

## TL;DR

This paper reviews how persistent organic pollutants may contribute to prostate cancer through multiple biological mechanisms and suggests comprehensive strategies for prevention and control.

## Contribution

The paper constructs a comprehensive mechanism analysis framework and proposes a full-chain prevention and control strategy for POPs-related prostate cancer.

## Key findings

- Multiple POPs are associated with prostate cancer risk, progression, and poor outcomes.
- POPs interfere with endocrine signaling, induce epigenetic changes, and disrupt metabolism.
- A full-chain prevention strategy is proposed, integrating POPs exposure assessment into clinical management.

## Abstract

Persistent organic pollutants (POPs) are a class of chemical substances with environmental persistence, bioaccumulation, and high toxicity, which are widely present in the environment and food chains. Prostate cancer (PCa) is a highly prevalent malignant tumor in the male reproductive system, and the association between its incidence and POPs exposure has attracted increasing attention. This review systematically summarizes recent epidemiological and experimental research evidence, indicating that multiple POPs are associated with the incidence risk, invasive progression, and poor clinical outcomes of PCa. A comprehensive mechanism analysis framework is constructed to clarify that POPs are associated with the occurrence and development of Pca mainly through four synergistic biological pathways: as endocrine disruptors, they interfere with androgen and aryl hydrocarbon receptor signaling pathways; potentially inducing epigenetic reprogramming including DNA methylation, histone modification, and non-coding RNA expression; may contribute to abnormal reorganization of cellular energy metabolism, lipid, and amino acid metabolism; and being linked to oxidative stress, which may lead to damage to the antioxidant defense system and genomic instability. Based on the above understanding of the mechanisms, we further propose a comprehensive prevention and control strategy covering the entire chain, including multi-dimensional public health intervention measures from source emission reduction, transmission pathway interruption to protection of susceptible populations. Moreover, we integrate the POPs exposure assessment into the whole-process clinical management of PCa, including the practical pathways for prevention, diagnosis, treatment, and prognosis. This review not only deepens the understanding of the complex mechanisms through which POPs are associated with PCa, but also provides a crucial theoretical basis for formulating evidence-based, precise prevention and treatment strategies.