Overview: A Metabolomics Look at Food Additives and Childhood Asthma
Researchers are increasingly examining how everyday food additives may influence childhood asthma. A recent study published in Frontiers in Immunology used metabolomics to explore the mechanisms behind the association between additives and asthma in children. The findings suggest that preservative and sweetener exposure could disrupt immune balance and gut-lung interactions, potentially contributing to airway inflammation.
What the study did
The investigation combined statistical analyses with a non-targeted metabolic profile of serum samples from children aged 15 and younger. By measuring ten common additives in serum and assessing asthma status, researchers sought to identify metabolic signatures linked to asthma. They also explored how additives might affect immune cell development, focusing on CD4+ T-cells and dendritic cells (DCs), pivotal players in allergic responses.
Serum analysis revealed that several additives were rarely absorbed and were therefore poorly detected in the bloodstream. Yet others, such as dehydroacetic acid, benzoic acid, and cyclamate, appeared frequently and were higher in children with asthma. This pattern prompted analyses that connected specific metabolites with asthma risk, hinting at immune and metabolic pathways that could be altered by exposure to these substances.
Key findings: when additives meet the immune system
Among the standout results were 73 metabolites significantly associated with asthma risk. Some acted as mediators in the link between additive exposure and asthma, including molecules involved in airway inflammation and immune signaling, such as components of glycerophospholipid metabolism and amino acids like glutamine and histidine. Importantly, these metabolites aligned with broader immune markers: immunoglobulin E (IgE), interleukins IL-4 and IL-17A, and profiles of CD4+ T-cell differentiation.
The study also incorporated animal experiments. Mice exposed to food additives showed elevated inflammatory cells in lung tissues, higher levels of eosinophils and IL-17A in bronchoalveolar lavage fluid, and increased IgE and IL-4—hallmarks of allergic inflammation. Immune cell shifts were observed as well, with more allergic dendritic cells and Th2/Th17 cells in the additive-exposed groups, suggesting a potential mechanism for how additives might skew immune responses toward allergy and asthma.
The gut-lung axis and metabolic disruption
Researchers propose that the gut-lung axis could mediate these effects. Additives may alter gut permeability and the microbiota, allowing inflammatory metabolites and immune signals to travel to the lungs and upset the balance of airway immunity. In CD4+ T-cells isolated from gut-associated lymphoid tissues, distinct metabolic changes emerged depending on the additive: for example, acesulfame altered lipid and phospholipid metabolism, while saccharin changed amino acid and nucleotide pathways. These changes could influence how immune cells differentiate and respond to inhaled or environmental allergens.
Despite these insights, the authors cautioned that the study does not establish causality. The cohort was limited to participants in Nanjing, China, and factors such as parental smoking and body mass index were not fully controlled. They call for broader studies to confirm findings across diverse populations and to validate the mechanistic links in humans.
Implications for parents and policymakers
The results add to a growing body of evidence that ultra-processed foods and their additives may affect child health beyond weight and nutrition. For families, this could mean paying closer attention to additive-heavy foods, especially for children with a history of allergies or asthma. For policymakers and food manufacturers, the study underscores the need for transparent labeling and ongoing research into the health consequences of common additives.
Next steps in research
Future work should expand to include more populations, assess additional additives, and employ causal study designs to confirm whether the observed metabolic and immune changes directly drive asthma development. Integrating metabolomics with longitudinal data could help determine whether reductions in exposure translate to measurable improvements in respiratory health.
