Accessible in vitro models recapitulating the human airway that are amenable to study whole cannabis smoke exposure are needed for immunological and toxicological studies that inform public health policy as well as medicinal and recreational cannabis use. In the present study, we developed and validated a novel three-dimensional (3D)-printed in vitro exposure system (IVES) that can be directly applied to study the effect of cannabis smoke exposure on primary human bronchial epithelial cells (HBECs). Using commercially available design software and a 3D printer, we designed a four-chamber Transwell insert holder for exposures to whole smoke. COMSOL Multiphysics software was used to model gas distribution, concentration gradients, velocity profile, and shear stress within IVES. Following simulations, primary HBECs cultured at the air–liquid interface on Transwell inserts were exposed to whole cannabis smoke using a modified version of the Foltin puff procedure. Following 24 h, outcome measurements included cell morphology, epithelial barrier function, lactate dehydrogenase (LDH) levels, cytokine expression and gene expression. HBECs exposed to cannabis smoke using IVES showed changes in cell morphology and disruption of barrier function without significant cytotoxicity. Cannabis smoke elevated interleukin-1 (IL-1) family cytokines and elevated CYP1A1 and CYP1B1 expression relative to control. These findings validate IVES to have an effect in HBECs at a molecular level following cannabis smoke exposure. In addition, HBECs stimulated with a viral mimetic, Poly I:C, challenge following cannabis smoke exposure showed a suppression of key antiviral cytokines. The growing legalization of cannabis on a global scale must be paired with research related to potential health impacts on lung exposures. IVES represents an accessible, open-source, exposure system that can be used to model varying types of cannabis smoke exposures with HBECs grown under air–liquid interface culture conditions. / Thesis / Master of Science (MSc) / Despite its recent legalization in Canada, cannabis smoke has been understudied and a lack of evidence exists to inform legislative policies, medicinal and recreational usage. Due to a lack of relevant ways to study cannabis smoke in a lab setting, it is difficult to accumulate literature around its impacts in the lungs. Here, we addressed this gap by engineering and validating a novel model to expose lung cultures to cannabis smoke. In addition, we investigated its impact on the immune response. Our findings suggest exposure to cannabis smoke alters the immune functions of these cells. We also found that in response to a viral mimetic stimulus, cell cultures pre-exposed to cannabis smoke exhibited impaired immune responses. Our novel model to expose cell cultures to cannabis smoke creates a foundation for future researchers to investigate environmental insults, such as cannabis smoke, in the context of respiratory health and infectious disease.

The purpose of this study was to screen the effect of some food-grade ingredients on the off-odors caused by geosmin and 2-methylisoborneol (MIB) compounds in catfish fillets by sensory evaluation. The study revealed that geosmin and MIB odor intensity were reduced to different degrees when fillets were dipped in lime flavor (94% and 67%, respectively), 0.5% acetic acid (AA) (70% and 16%, respectively), hardwood liquid smoke (98% and 86%, respectively), or hickory liquid smoke (98% and 100% respectively) in cooked products. A 0.5% AA proved to be effective in decreasing odor intensity of geosmin (70%) in cooked products, whereas lime flavor (94%), hardwood liquid smoke (98%), and hickory liquid smoke (98%) were very effective in decreasing odor intensity of geosmin in cooked products. These agents added desirable flavors as well, except for AA by panelists? comments. These flavors could be added to a marinade or incorporated in an injection/tumbling solution when catfish fillets are processed.

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Introduction: Multiple sclerosis (MS) is a chronic inflammatory disease which affects approximately 2.5 million people worldwide, including approximately 7,000 children. The etiology of MS is unclear, although researchers generally agree that both environmental and genetic factors are involved. It is also unclear why some patients may only have one demyelinating event (acquired demyelinating syndrome, or ADS) and others develop chronic demyelinating disease (MS). Recent evidence suggests an association between smoking and multiple sclerosis (MS) in adults. A question remains if there is a similar association between secondhand tobacco smoke exposure and MS in children. The purpose of this study is to explore the association between tobacco smoke exposure (TSE) and MS risk in a cohort of children with demyelinating disease. Methods: Data was obtained from the Canadian National Demyelinating Disease Study. This study included two disease groups, which are distinguished by a single (ADS) versus chronic demyelinating attacks (MS). Parents’ self-report of their child’s exposure to smoke in the home, as well as biomarker verification by serum cotinine, classified a child as exposed or not exposed. Logistic regression models were created to determine the association between TSE and the odds of MS compared to healthy controls, the odds of ADS compared to healthy controls, and the odds of MS compared to patients with ADS. In order to determine factors and exposures which distinguish MS from ADS, an assessment of interaction was performed to examine the relationship between TSE and MS risk genes, TSE and serum vitamin D levels, and TSE and prior Epstein Barr Virus exposure on the odds for developing MS compared to ADS patients.. Finally, serum cotinine levels were compared to neurologic functional scores in order to assess if a dose response mechanism exists creating impaired function for pediatric MS. Results: TSE was not significantly associated with increased odds for MS compared to healthy controls (OR= 1.84; 95%CI 0.86, 3.95) but was significantly associated with higher odds of monophasic ADS compared to healthy controls (OR=2.24; 95%CI 1.08, 4.63). TSE alone was not associated with increased odds for MS compared to ADS; however, the presence of both TSE and HLA alleles increased the odds for MS by 3.2 (95%CI 1.04, 9.79) when compared to ADS patients. An additive effect was also found between TSE and lower vitamin D, which together increased the odds for MS compared to patients with monophasic ADS (OR=2.89; 95%CI 1.21, 7.46). EBV was individually associated with MS compared to ADS (OR=4.12; 95%CI 1.62, 10.9) and odds for MS appeared to increase further with the addition of TSE (OR=5.13; 95%CI 1.79, 14.9), however sample size limited interpretation of the interaction analysis. TSE had minimal impact on neurological functional score measures, although long-term follow up with regard to exposure could not be properly assessed. Conclusion: Exposure to tobacco smoke through secondhand sources was not related to MS but TSE may increase the odds of monophasic demyelinating disease occurrence (ADS). The finding of additive effects between TSE and other disease modifying factors (HLA, vitamin D) may provide valuable insight into why some children have only one demyelinating attack (monophasic ADS) while others have multiple attacks and are diagnosed with MS. These effects should be further explored in a larger population of pediatric patients and compared to healthy children. Intervention methods should be tailored to help explain to parents the benefits of reducing their child’s exposures to environmental tobacco smoke. / Public Health

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