Bactericidal activity of neutral electrolyzed water (NEW), quaternary ammonium (QUAT), and lactic acid‐based solutions was investigated using a manual spraying technique against Salmonella Typhimurium, Escherichia coli O157:H7, Campylobacter jejuni, Listeria monocytogenes and Staphylococcus aureus that were inoculated onto the surface of scarred polypropylene and wooden food cutting boards. Antimicrobial activity was also examined when using cutting boards in preparation of raw chopped beef, chicken tenders or salmon fillets. Viable counts of survivors were determined as log₁₀ CFU/100 cm² within 0 (untreated control), 1, 3, and 5 min of treatment at ambient temperature. Within the first minute of treatment, NEW and QUAT solutions caused more than 3 log₁₀ bacterial reductions on polypropylene surfaces whereas less than 3 log₁₀ reductions were achieved on wooden surfaces. After 5 min of treatment, more than 5 log₁₀ reductions were achieved for all bacterial strains inoculated onto polypropylene surfaces. Using NEW and QUAT solutions within 5 min reduced Gram‐negative bacteria by 4.58 to 4.85 log₁₀ compared to more than 5 log₁₀ reductions in Gram‐positive bacteria inoculated onto wooden surfaces. Lactic acid treatment was significantly less effective (P < 0.05) compared to NEW and QUAT treatments. A decline in antimicrobial effectiveness was observed (0.5 to <2 log₁₀ reductions were achieved within the first minute) when both cutting board types were used to prepare raw chopped beef, chicken tenders or salmon fillets.

Viability of Listeria monocytogenes was monitored during refrigerated (4°C) and/or frozen (i.e., deep chilling at –2.2°C) storage on casing-cooked hams that were commercially prepared with and without potassium lactate and sodium diacetate (1.6%), buffered vinegar (2.2%), buffered vinegar and potassium lactate (1.7%), or a blend of potassium lactate, potassium acetate, and sodium diacetate (1.7%). A portion of these hams were subsequently surface treated with lauric arginate ester (LAE; 44 ppm). In phase I, hams (ca. 3.5 kg each) were sliced (ca. 0.7 cm thick, ca. 100 g), inoculated (ca. 4.0 log CFU per slice), surface treated with LAE, and stored at either 4°C for 120 days or at –2.2°C for 90 days and then at 4°C for an additional 120 days. In phase I, without antimicrobials, the population of L. monocytogenes increased by ca. 5.9 log CFU per slice within 120 days at 4°C; however, pathogen levels increased only slightly (ca. 0.45 log CFU per slice) for hams formulated with potassium lactate and sodium diacetate and decreased by ca. 1.2 log CFU per slice when formulated with the other antimicrobials. For slices held at –2.2°C and then stored at 4°C, but not treated with LAE, L. monocytogenes increased by ca. 4.5 log CFU per slice for controls, whereas when formulated with antimicrobials, pathogen levels decreased by ca. 1.4 to 1.8 log CFU per slice. For product treated with LAE, L. monocytogenes increased by ca. 4.0 log CFU per slice for controls, whereas when formulated with antimicrobials, pathogen levels decreased by ca. 0.9 to 1.9 log CFU per slice. In phase II, whole hams (ca. 1.0 kg each) containing antimicrobials were inoculated (6.8 log CFU per ham) and then stored at –2.2°C for 6 months. Pathogen levels decreased by ca. 2.0 to 3.5 log CFU per ham (without LAE treatment) and by ca. 4.2 to 5.2 log CFU per ham (with application of LAE via Sprayed Lethality in Container) when product was held at –2.2°C. In general, deep chilling hams was listericidal, and inclusion of antimicrobials in the formulation suppressed outgrowth of L. monocytogenes during extended cold storage.