# Tissue levels of persistent organic pollutants and biotransformation enzyme polymorphisms in human stomach cancer

## TL;DR

This study found that certain persistent organic pollutants accumulate in stomach cancer tissues, suggesting a potential link between these environmental chemicals and stomach cancer.

## Contribution

The study directly quantifies POPs in gastric tissue and identifies selective accumulation patterns associated with stomach cancer.

## Key findings

- 13 POPs and chemical classes showed significant differences in gastric tissue between cancer and control groups after FDR correction.
- Systemic POP distribution and genetic polymorphisms showed limited associations with cancer status.
- Tissue-level POP differences were more consistent than systemic or genetic factors in relation to stomach cancer.

## Abstract

Persistent organic pollutants (POPs) are lipophilic environmental contaminants with carcinogenic potential, yet data on their accumulation in human gastric tissue are limited. This study aimed to comprehensively quantify 32 POPs in malignant and non-malignant gastric tissues and to evaluate their distribution across blood and omental adipose tissue, together with metabolic enzyme activity, genetic polymorphisms, and oxidative damage markers.

POP concentrations were measured in gastric tissue, blood, and omental adipose tissue from stomach cancer patients and controls undergoing stomach reduction surgery. Associations were evaluated using multivariable models adjusted for age, sex, and smoking. False discovery rate (FDR) correction was applied to account for multiple testing. Genotyping of CYP1A1, GSTP1, GSTM1, GSTT1, and OGG1 was performed, and CYP1A1 enzyme activity and urinary oxidative damage biomarkers were assessed.

The most robust differences were observed in gastric tissue, where 13 individual POPs and selected chemical classes remained significantly different between cancer and control groups after FDR correction. In blood, five individual POPs remained significant after correction. Several cross-compartment correlations persisted following FDR adjustment, particularly for selected HCH isomers and 4,4′-DDE. CYP1A1 activity did not differ between groups. Among oxidative biomarkers, only urinary o,o′-dityrosine remained significantly lower in cancer patients after FDR correction. In adjusted genetic models, no polymorphism demonstrated a statistically robust association in the overall analysis; the GSTP1 estimate was elevated but imprecise.

Direct quantification of POPs in gastric tissue revealed selective accumulation patterns associated with stomach cancer. While systemic distribution and genetic variability may influence susceptibility, tissue-level POP differences represented the most consistent findings. Larger prospective studies are warranted to clarify temporal and mechanistic relationships.

The online version contains supplementary material available at 10.1007/s10552-026-02154-z.