Metam sodium is a fumigant often used as a crop pretreatment in agriculture to control a wide array of pests that may inhibit plant yields. Previously, there have only been limited studies conducted on the effects of metam sodium on native soil microbial communities and plant pathogens, and results have been inconsistent. This present study utilized control and metam sodium-treated field plots to examine the effects of metam sodium on soil microbes in terms of numbers, activity, and diversity. Metam sodium did not cause significant changes in culturable heterotrophic numbers, as shown by heterotrophic plate counts, but may have adversely affected non-culturable microbes since metam sodium did affect microbial activity. Specifically, the LuminUltra® and dehydrogenase activity assays both showed a significant decrease in total activity in treated plots one day after soil treatment, with a return to pre-application conditions within seven days. Illumina Next-Generation Sequencing of the 16S rRNA gene showed slight changes in richness and community composition throughout the 28-day study, but initial and final communities were similar in both control and treated soils. Overall, some soil microbes were adversely affected by metam sodium, but the resilience of the soil microbial community allowed for an apparent rapid recovery in terms of numbers, activity, and diversity.

Sodium methyldithiocarbamate (SMD) is commonly reported to cause health risks in humans. Previous reports indicate SMD causes oxidative stress, which can contribute to the activation of NF-êB and cause other characteristics of inflammatory responses to be altered. Almost all pro-inflammatory cytokines require NF-êB activation for full expression and development of an innate immune or inflammatory response. This study evaluated NF-êB activation, providing new information regarding reactive oxygen in macrophages from SMD-treated mice. Studies were conducted in which NF-êB reporter mice were treated with lipopolysaccharide (LPS), SMD, buthionine sulfoximine (BSO), and N-acetyl cysteine (NAC). BSO depletes glutathione (GSH) and increases oxidative stress, whereas NAC spares GSH by acting as a precursor for rapid synthesis to replace oxidized GSH. The work here indicates that NF-êB is not affected directly by increased or decreased reactive oxygen species (ROS), and oxidative stress is not the major mechanism by which SMD inhibits inflammatory responses.