Researchers have discovered that the ingredient 2,3-pentanedione (PD), used to promote the flavor and aroma of butter in microwave popcorn is a respiratory hazard, which can also change gene expression in the brain of rats. The study is published in The American Journal of Pathology and suggests that acute PD exposure can lead to respiratory toxicity similar to that of diacetyl in laboratory animals. Before using PD to enhance the flavor of butter, manufacturers used diacetyl. However, diacetyl was found to cause bronchiolitis obliterans, a life-threatening and nonreversible lung disease in those inhaling the substance.

Leading author Ann F. Hubbs, DVM, PhD, DACVP, from the Health Effects Laboratory Division of the National Institute for Occupational Safety and Health at the Centers for Disease Control and Prevention, Morgantown, explains:

“Our study demonstrates that PD, like diacetyl, damages airway epithelium in laboratory studies. This finding is important because the damage is believed to be the underlying cause of bronchiolitis obliterans. Our study also supports established recommendations that flavorings should be substituted only when there is evidence that the substitute is less toxic than the agent it replaces.”

The team conducted animal studies in which they exposed groups of rats for six hours to different concentrations of PD, a comparable concentration of diacetyl, or filtered air. They noted signs of delayed toxicity and exposed additional rats to PD.

They conducted a microscopic examination of the brains, lungs, and nasal tissues from the lab animals at different durations after exposure, i.e. after 0-2 hours, 12-14 hours, and 18-20 hours before assessing these changes in gene expression in certain areas of the brain.

The findings revealed that 12 to 14 hours after exposure PD caused respiratory epithelial injury in the upper nose that was similar to that caused by diacetyl. They also noted that PD exposure caused necrosis and apoptosis in the olfactory neuroepithelium and activation of caspase 3, a protein involved in cell death, in axons of olfactory nerve bundles.

Furthermore, they observed signs consistent with neurotoxicity that showed an elevated expression of the inflammatory mediators, interleukin-6 and nitric oxide synthase-2 and lower expression of vascular endothelial growth factor A in the olfactory bulb, striatum, hippocampus, and cerebellum.

Dr. Hubbs concludes:

“Our study is a reminder that a chemical with a long history of being eaten without any evidence of toxicity can still be an agent with respiratory toxicity when appropriate studies are conducted. It suggests several intriguing potential mechanisms for the toxicity of inhaled volatile α-diketones, reveals mRNA changes in the brain, documents olfactory neurotoxicity, and clearly demonstrates that the remarkable airway toxicity of diacetyl is shared with its close structural relative, PD.”

Written by Petra Rattue