The effects of metolachlor exposure on the THP-1 alveolar monocyte and macrophage function

The use of additive chemicals such as pesticides has become commonplace in agricultural practices in the Midwestern United States. Metolachlor, an herbicide used to regulate broadleaf weeds in corn and soybeans, is a widely utilized pesticide in the United States. This herbicide is effective in killing broadleaf weeds but has detrimental effects and consequences in non-target organisms. It is a frequent contaminant of ground water due to post application run-off and the air. Inhalation constitutes one route of exposure, in addition to ingestion, adding to the list of unintended targets and consequences. This route of exposure creates an argument for investigation into the effects of metolachlor through inhalation. There is a deficit in research studying the effects that metolachlor has on human health and this presents cause for conducting additional research. In this study, we examined the effects of metolachlor on alveolar monocytes and macrophages; specifically we were interested in determining if there were changes in several functional processes after metolachlor exposure. This study focused on three distinct cellular functions; phagocytosis, apoptosis and production of reactive oxygen species (ROS) after exposure to increasing concentrations of metolachlor, (50 parts per billion (ppb), 100ppb, 500ppb and 1000ppb) at three distinct time points, (24, 48 and 72 hours). We conducted an analysis of the phagocytosis and apoptosis trials by flow cytometry, while ROS we conducted an analysis by measuring a change in fluorescence. Phagocytosis trials yielded no significant differences regardless of concentrations, time points or cell types. Apoptosis experiments yielded results that demonstrated a relationship between metolachlor and a change in function, for monocytes and macrophages during the trials. ROS measurements yielded no significant relationship between metolachlor exposure and production of reactive oxygen species in alveolar monocyte