The COVID-19 pandemic has been an unprecedented public health crisis around the world and has created novel needs in the healthcare industry. Primary among these needs is a vast shortage in personal protective equipment (PPE) such as masks and gloves. This is problematic due to the near constant of COVID-19 cases in hospitals around the United States. In an effort to meet the need for more PPE, new disinfection techniques must be found to "recycle" used PPE. UVC light has previously been used by healthcare facilities for years to disinfect surfaces such as stainless steel and are frequently used in operating room sterilization and dentist offices. UVC light's effectiveness on porous materials such as masks has not been substantially investigated prior to the COVID-19 pandemic. This work shows the effectiveness and efficiency of UVC disinfection on porous surfaces for the COVID-19 virus and other bacteria.

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Photodynamic therapy (PDT) for cancer utilizes the localised delivery of light to activate a photosensitizing drug (such as Photofrin) which is selectively retained by tumour tissues. Although this treatment modality is undergoing clinical trials, the mechanism of PDT cytotoxicity is not fully understood. One approach to understanding the mechanism of action of PDT is to study cell mutants showing alterations in their response to PDT. The capacity of mammalian cells to support virus replication has been used as an assay to compare cellular response to ultraviolet (UV) light and other cytotoxic agents. Cellular capacity has been previously employed to measure cellular recovery following UV irradiation and to predict the sensitivity of cells to several anticancer drugs. In this work, I have examined the use of the capacity assay to examine the sensitivity of cells to PDT treatment. RIF-1 mouse fibrosarcoma cells and a PDT resistant derivative, RIF-8A; as well as Chinese hamster ovary (CHO) cells and CHOMDR (multi-drug resistant) mutant cells were studied. Consistent with the clonogenic survival of these cells after PDT, the viral capacities of RIF-8A and CHO-MDR cells· were greater than those of RIF-1 and CHO cells respectively following PDT treatment. The capacity assay was also used to examine the relative ability of RIF cells to recover from PDT damage. These capacity experiments show that recovery from PDT damage is greater in RIF-SA cells compared to RIF-1 cells, suggesting that RIF-SA cells have an enhanced repair capacity for PDT damage compared to RIF-1 cells. The response of CHO cells and the RIF cells to ultraviolet (UV) light irradiation was also examined. No difference in the UV sensitivity of CHO-N and CHO-MDR cells was found. However, the RIF-SA cell line showed a cross-resistance to UV. The survival of viral DNA synthesis for UV-irradiated virus was also greater in RIF-SA cells compared to RIF-1 cells, suggesting that RIF-SA cells have an increased capacity for the repair of UV-induced DNA damage. It is possible that the increased resistance to PDT of RIF-SA may also result from an increased repair of POT-induced DNA damage in RIF-SA cells. The identification and characterization of a POT-sensitive cell mutant was also investigated. The CHO-AUXB1 cell mutant was found to show an increased sensitivity to PDT and UV compared to the CHO-PRO- parent line. This sensitivity of the CHO-AUXB1 mutant may also result from a deficiency in the repair mechanism of PDT-induced and UV-induced damage. / Thesis / Master of Science (MS)

Photodynamic therapy (PDT) is a new form of cancer treatment that uses the localized delivery of light and a photosensitizing drug, which is selectively retained in tumor tissue, to cause photochemically induced cell death. Although PDT mediated by the sensitizer Photofrin (Ph-PDT) is currently in Phase III trials for a number of human cancers, the exact mechanism(s) involved in PDT induced cytotoxicity is not fully understood. Also, Photofrin has a number of drawbacks including extended cutaneous photosensitization and low absorption in the red region of the spectrum. This has lead to the search for improved sensitizers. In vitro, tumor cells resistant to PDT have been developed from PDT sensitive cell lines to examine the mechanism(s) of PDT action. In this work, the sensitivity of RIF-1 murine fibrosarcoma cells and RIF-1 derived Ph-PDT resistant RIF-8A cells was examined following several damaging agents including PDT mediated by the novel Ruthenium phthalocyanine photosensitizer JM2929 (JM2929-PDT), UV, gamma-radiation, and hyperthermia. Gamma-radiation sensitivity of two other RIF-1 derived Ph-PDT resistant variants, CPR-C1 and RIF-P16CL8, was also examined. RIF-8A cells showed cross resistance to UV but increased sensitivity to gamma-rays compared to RIF-1 cells. RIF-1 and RIF-8A cells showed similar sensitivity to JM2929-PDT and hyperthermia. It is possible that Ph-PDT induces a "UV -like" component of damage and/or there is some overlap in the pathways for the repair of UV and Ph-PDT induced damage, but not JM2929-PDT, hyperthermia, and ionizing radiation damage in RIF-1 and RIF-8A cells. A cross resistance to gamma-rays was observed for CPR-C1 but not RIF-P16CL8 cells. Since Ph-PDT resistant CPR-C1 cells, but not RIF-8A cells or RIF-P16CL8 cells, show a cross resistance to gamma radiation, these results suggest that the cellular changes required for RIF-8A, RIF-P16CL8, and CPR-C1 cells to become resistant to Ph-PDT are different. Survival of RIF-1 and RIF-8A cells following gamma-rays in the presence of either Photofrin or JM2929 was also examined. Results suggest sensitization of RIF-1 cells, but not RIF-8A cells, to gamma-radiation in the presence of Photofrin. Gamma-radiation in the presence of JM2929 had no sensitizing effects on the survival of RIF-1 and RIF-8A cells. DNA repair of a UV-damaged reporter gene was also examined in untreated as well as Ph-PDT, JM2929-PDT, UV, cisplatin, and hyperthermia pretreated RIF-1 and RIF-8A cells. Results suggest an increased repair of UV damaged DNA in untreated RIF-1 cells compared to untreated RIF-8A cells. Ph-PDT, JM2929-PDT, and UV pretreatments resulted in an increased reactivation of a UV damaged reporter gene in RIF-1 cells compared to RIF-8A cells. Enhanced reactivation of a UV damaged reporter gene was not observed in either RIF-1 or RIF-8A cells following cisplatin or hyperthermia pretreatment. Enhanced expression of an undamaged reporter gene was greater in RIF-8A cells compared to RIF-1 cells following Ph-PDT pretreatment, but similar to RIF-1 cells following pretreatment with all other agents. These results suggest that the relation between survival, DNA repair of an actively transcribed gene, and transcriptional enhancement of an actively transcribed gene, varies in RIF-1 and RIF-8A cells depending on the damaging agent used. However, decreased reactivation of a UV damaged reporter gene in RIF-8A cells may be related to Ph-PDT and UV resistance seen in RIF-8A cells. / Thesis / Master of Science (MSc)

Foodborne illnesses caused by Listeria monocytogenes have long been associated with ready-to-eat (RTE) meats contaminated after the primary thermal process has been applied. It is believed that brine solutions used to chill cooked RTE products may serve as a reservoir for L. monocytogenes becoming a potential point of post-processing contamination for RTE meats. Re-circulating ultraviolet light (UV) systems are being used to inactivate L. monocytogenes in chill brines; however very little has been reported on the dose response of healthy and stressed L. monocytogenes to UV in brine solutions. The objectives of this research were to determine 1) minimum dose of UV required to inactivate L. monocytogenes in distilled water, fresh brine, undiluted spent brine, and diluted spent brine, 2) if adaptation to food processing stresses affects the dose response, and 3) if the acquisition of antibiotic resistance mechanisms provides resistance to ultraviolet light 4) effect of stress adaptation on survival in brine solutions. After UV exposure, populations were reduced as follows from greatest to least: water > fresh brine > 5% spent brine > 35% spent brine > 55% spent brine > 100% spent brine (P ≤ 0.05). There were no population differences between acid stressed and antibiotic resistant or healthy and heat shocked (P > 0.05). However, acid-stressed and sulfanilamide-resistant were more resistant to UV light than healthy and heat shocked L. monocytogenes (P ≤ 0.05). Survival in brine solutions (no UV) followed the trend, from greatest to least (P ≤ 0.05): sulfanilamide-resistant > acid-stressed > healthy > heat-shocked. Population estimates decreased from initial inoculation to final sampling for each cell type suspended in spent brine (P ≤ 0.05), but only healthy and heat- shocked cells suspended in fresh brine were significantly reduced (P ≤ 0.05). Knowledge of UV dosing required to control L. monocytogenes in brines used during RTE meat processing, and a greater understanding of the interactions that may influence dose will aid manufacturers in establishing appropriate food safety interventions for these products. / Ph. D.

Chill brines used in ready-to-eat meat processing may be an important source of post-processing contamination by Listeria monocytogenes. The purpose of this study was to determine the efficacy of ultraviolet light (UV) in combination with antimicrobials to reduce L. monocytogenes in fresh and used chill brines. Three different antimicrobials were used in combination with UV; citric acid (CA, 0.2 and 0.5%), dimethyl dicarbonate (DMDC, 250 and 500 ppm), and hydrogen peroxide (HP, 2000 and 4000 ppm). For fresh brine studies, brine (8.0% w/v NaCl) was prepared and inoculated with a cocktail of three L. monocytogenes strains (approximately 6 log CFU/mL). Brine was treated with UV alone, antimicrobials alone, and combination of UV and antimicrobials. Moreover, to observe the effect of treatment temperature and brine circulation through the UV system on survival of listeriae cells, inoculated brine was circulated through the system without any treatment that served as control for all the treatments. For UV treatment, inoculated brine solution was exposed to UV in an Ultraviolet Water Treatment Unit (Model: AMD 150B/1/2T D; Aquionics Inc., Peak output: 254 nm) fitted with an inline chiller to maintain brine temperature of -1°C. Samples were withdrawn at regular intervals for 120 minutes. When L. monocytogenes population was no longer detectable via direct plating on MOX, enrichment was performed and suspect colonies were confirmed using API-Listeria. For antimicrobial-only (i.e., no UV) treatments, a specific concentration of antimicrobial was added in inoculated brine and samples were taken for 120 minutes. For the brine that received combination of UV and antimicrobial treatments, UV was turned on once a specific concentration of antimicrobial was added in inoculated brine and samples were withdrawn at regular intervals for 120 minutes. When treated with UV alone, L. monocytogenes population decreased from approximately 6 log CFU/mL to below the detection limit (i.e., 1 log CFU/mL) in 15 minutes with the reduction rate of 0.87 log CFU/mL per minute. However, cells were detectable by enrichment through 120 minutes. The highest rate of decline (0.90 log CFU/mL per minute) was achieved by the combination of UV and 500 ppm DMDC (UV+500 ppm DMDC), which was not significantly different from the reduction rates of UV and UV+0.5% CA. UV+500 ppm DMDC reduced L. monocytogenes to the detection limit in 15 minutes and the organism was not detected by enrichment after 60 minutes. Though the reduction rate of UV+0.5% CA was not significantly lower than the rate of UV+500 ppm DMDC (P>0.05), the former treatment resulted in non-detectable levels more quickly (45 minutes) than the latter (60 minutes). Thus, based on enrichment studies UV+0.5% CA was the most effective treatment in reducing the population of L. monocytogenes in fresh brine. Moreover, when brine was treated with 0.5% CA alone the population decreased to below detection limit in 15 minutes with the rate significantly lower than UV+500 ppm DMDC and UV+0.5% CA (P<0.05). However, L. monocytogenes was not detectable by enrichment from 60 minutes. To summarize, through enrichment studies we observed that UV+0.5% CA, UV+500 DMDC, and 0.5% CA Control were more effective than other treatments in reducing the listeriae population to a non-detectable level. Spent brine is recycled brine that was obtained from a frankfurter processor after its maximum usage. Results of spent brine studies showed that when brine was treated with UV+4000 ppm HP and UV+2000 ppm HP, L. monocytogenes population decreased to the detection limit in 45 minutes and was not detected by enrichment from 120 minutes. These treatments were observed to be the most effective treatments with a reduction rate of 0.12 log CFU/mL per minute. The reduction rate of some other treatments such as, UV+250 and 500 ppm DMDC, UV+0.2% and 0.5% CA, and UV alone was not significantly different from UV+4000 and 2000 ppm HP. However, the population was detected through enrichment up to 120 minutes in all other treatments. The results of these studies indicate that combinations of UV and antimicrobial may be more effective than either treatment alone (except 0.5% CA treatment) to process fresh chill brines. However, the antimicrobials and UV were less effective for controlling L. monocytgoenes in spent brine; presumably due to the presence of organic matter. / Ph. D.