Characterization of atrazine transport across nasal respiratory and olfactory mucosae

The herbicide atrazine is one of the most commonly used pesticides in United States. Atrazine was banned in the European Union in 2005 because of its ubiquity in drinking water; however, in The United States more than 75 million pounds of atrazine are used annually, especially in the Midwest. Atrazine has many adverse health effects including enhancing developmental, immunologic endocrine alterations. Studies have reported that exposure to atrazine causes dopaminergic toxicity and mitochondrial dysfunction; these cellular changes have been linked to an increase in the incidence of Parkinson's disease. The objective of this study is to characterize atrazine effect on the respiratory and olfactory mucosae with specific attention to the potential for atrazine transfer to the brain via the olfactory system. Uptake of atrazine was investigated across excised nasal mucosal tissues equilibrated in Krebs's buffer (KRB) or in a co-solvent system containing propylene glycol (PG), similar to the commercial herbicide product. Active uptake pathways were probed using 2,4-dinitrophenol (2,4-DNP) as a metabolic inhibitor. Brightfield microscopy was used to assess the effects of ATZ exposure on the tissues. ATZ was found to be transported across the nasal tissues in a manner consistent with passive diffusion, and 2,4-DNP did not reduce the overall uptake of ATZ. Microscopy results showed erosion of the epithelial surface following exposure to ATZ-PG-KRB when compared to control and ATZ -KRB. These results suggest a negative effect of the ATZ co-solvent formulations on nasal tissues with the potential for increased systemic and CNS exposure.