Agricultural chemicals and gut microbiota dysbiosis: implications for the pathogenesis of inflammatory bowel disease.

The global intensification of agriculture has substantially increased human exposure to foodborne and environmental contaminants, including pesticides, heavy metals, endocrine-disrupting chemicals (EDCs), mycotoxins, and fertilizer-related related agricultural exposures. Growing evidence suggests that these agricultural xenobiotics may contribute to inflammatory bowel disease (IBD) pathogenesis through alterations of gut microbiota composition and function. This review examines the current evidence linking major agricultural contaminants to gut microbiota dysbiosis, intestinal barrier dysfunction, immune dysregulation, and chronic intestinal inflammation. Experimental and epidemiological studies indicate that chronic exposure to these compounds may reduce microbial diversity, alter the abundance of beneficial bacterial populations, impair short-chain fatty acid production, and activate oxidative stress and pro-inflammatory signaling pathways, including NF-κB and MAPK-related mechanisms. These alterations may collectively promote epithelial barrier disruption and aberrant mucosal immune activation, which are central processes in IBD pathogenesis. Attention is given to the role of dietary exposure and food-chain contamination as potential mediators of environmentally driven intestinal inflammation. Although most currently available evidence derives from in vitro and animal models, emerging human studies support a possible association between chronic exposure to agricultural contaminants and increased intestinal inflammatory risk. Overall, the evidence reviewed suggests that diverse agricultural contaminants, despite their different chemical characteristics, converge on common pathogenic mechanisms involving gut microbiota dysbiosis, oxidative stress, epithelial barrier dysfunction, and immune dysregulation. These shared alterations may represent a plausible mechanistic link between agricultural chemical exposure and intestinal inflammation, potentially contributing to increased susceptibility to IBD. However, the current body of evidence remains predominantly experimental, and causal relationships in humans have yet to be established. Future research should prioritize longitudinal human studies, exposome-based investigations, and integrated multi-omics approaches to clarify exposure-disease relationships, identify reliable biomarkers of exposure and risk, and support the development of preventive nutritional and environmental strategies targeting microbiota-mediated intestinal inflammation.