There’s a new study out this week that residents of the Kanawha Valley and surrounding region will want to know about. It was published online Monday in the peer-reviewed journal Environmental Science and Technology and is called Toxicity Assessment of 4-Methyl-1-cyclohexanemethanol and Its Metabolites in Response to a Recent Chemical Spill in West Virginia, USA.
Here’s the abstract:
The large-scale chemical spill on January 9, 2014 from coal processing and cleaning storage tanks of Freedom Industries in Charleston affected the drinking water supply to 300,000 people in Charleston, West Virginia metropolitan, while the short-term and long-term health impacts remain largely unknown and need to be assessed and monitored. There is a lack of publically available toxicological information for the main contaminant 4-methyl-1-cyclohexanemethanol (4-MCHM). Particularly, little is known about 4-MCHM metabolites and their toxicity. This study reports timely and original results of the mechanistic toxicity assessment of 4-MCHM and its metabolites via a newly developed quantitative toxicogenomics approach, employing proteomics analysis in yeast cells and transcriptional analysis in human cells. These results suggested that, although 4-MCHM is considered only moderately toxic based on the previous limited acute toxicity evaluation, 4-MCHM metabolites were likely more toxic than 4-MCHM in both yeast and human cells, with different toxicity profiles and potential mechanisms. In the yeast library, 4-MCHM mainly induced chemical stress related to transmembrane transport and transporter activity, while 4-MCHM metabolites of S9 mainly induced oxidative stress related to antioxidant activity and oxidoreductase activity. With human A549 cells, 4-MCHM mainly induced DNA damage-related biomarkers, which indicates that 4-MCHM is related to genotoxicity due to its DNA damage effect on human cells and therefore warrants further chronic carcinogenesis evaluation.
And here’s the conclusion:
… This study revealed different toxicity and potential mechanisms of 4-MCHM and its metabolites by S9 in yeast and human cells (A549). These results suggested that, although 4-MCHM is considered only moderately toxic based on previous limited acute toxicity evaluation, its metabolites may be more toxic than 4-MCHM and are more relevant to human exposure. Our study at the molecular level revealed some subcytotoxic molecular mechanisms such as DNA damage potential, which indicates that 4-MCHM is related to carcinogenesis and reproductive toxicity due to its DNA damage effect on human cells. Our results suggested that long-term medical monitoring should be considered for the population. It may also provide insights into potential long-term aquatic toxicity issues. The toxicogenomics-based molecular toxicity screening assay employed in this study provides timely information regarding the underlying mechanisms of toxic action of 4-MCHM and its metabolites, especially related to low-dose and chronic exposures, which makes it a useful tool for public health protection and health monitoring needs.