Potential provoking effects of environmental pollutants on food allergy: an issue that is gaining increasing attention

Allergic diseases are widespread globally, affecting over 40% of the population. Food allergy (FA), characterized by an abnormal immune response to harmless proteins in foods, is one of these prevalent conditions. Current estimates suggest that approximately 220 million people worldwide suffer from FA (1). In children, over one-third of parents report their children experiencing hypersensitive reactions to food, with FA affecting around 8% of this demographic. In China, 11.5% of individuals report having a physician-diagnosed FA [95% Confidence Interval(CI): 9.8%, 13.5%]. Notably, the prevalence of FA has increased significantly within a single generation, as evidenced by studies showing a rise in prevalence from 3.5% to 11.1% between 1999 and 2019 (2-3). This sharp increase coincides with rapid industrialization and urbanization, elevating FA to a major public health issue. While genetic factors contribute to around 50% of the susceptibility to allergic diseases (4), the dramatic rise in FA prevalence cannot solely be attributed to genetic changes alone. Environmental factors, particularly pollutants, are increasingly recognized as significant contributors to the development of FA (5). For instance, higher serum levels of perfluoroalkyl and polyfluoroalkyl substances have been associated with increased self-reported FA in adolescents (6-7). The widespread dispersion of pollutants such as persistent endocrine-disrupting compounds, persistent organic pollutants (POPs), fine particulates (FPs), and emerging contaminants like pharmaceutical and personal care products (PPCPs) follows industrial and urban expansion. These pollutants pose considerable health risks (8) and have been linked to the onset of allergic diseases (9-10). They can modify immune responses, leading to immunotoxic effects. The dual allergen exposure hypothesis suggests that disruptions to epithelial barrier integrity, along with microbial dysbiosis and immune dysregulation, are plausible mechanisms for the development of FA (6,11). At the molecular level, processes such as the acute inflammatory response, reactive oxygen species (ROS) generation, neutrophil activation, inflammatory cytokine expression, immune cell signaling disruptions, and apoptosis are implicated in the interaction between environmental pollutants and the immune system (10). However, the long-term effects of these pollutants on FA prevalence remain poorly understood.

This narrative review offers a comprehensive examination of risk factors for FA, particularly emphasizing the role of environmental pollutants.