#ExpBio - Safer Is Not Safe; Just Don't Vape

Apr 23 2017 Published by under [Medicine&Pharma], ExpBio 2017

Electronic cigarettes, or vaping, has been advertised as a safer alternative to smoking tobacco. It provides the addictive ingredient in tobacco (nicotine) in a liquid base that gets heated and delivers it in an inhaled form. Nicotine patches and gum may provide levels of the chemical, but they do not satisfy the ritual of smoking. Vape liquid can contain high amounts of nicotine, often in a flavored liquid base. Heating elements in the devices can release other chemicals into the mix as well.

Tobacco has systemic effects well beyond the lungs. These include cardiovascular disease and kidney dysfunction.

In this study, mice were exposed to vapor generated by a commercial vaping device and then collected and piped into mice. Mice breathed the vapor for 1 hr each day, 5 days each week. In the first experiment, the default laboratory mice (C57Bl6) vaped for 3 months. Findings included a 20% reduction in glomerular filtration rate and an 87% increase in kidney scarring. Changes in heart rate and blood pressure suggested cardiovascular damage as well.

An outbred mouse strain (CD1) received the same exposure for 6 months. This genetically heterogeneous strain might have more resistance to adverse exposures. However, it showed a 64% increase in kidney scarring over control animals. Cardiac scarring increased 2.75-fold over controls. Multiple pro-fibrotic factors studied in each tissue were elevated with exposure to vaping. These patterns of damage were similar to those seen with tobacco smoke exposure in animals from a separate but parallel study (data not included; noted during discussion at poster).

Vaping may not carry the cancer risk of tobacco use, but this animal study strongly suggests it still promotes cardiovascular and kidney disease.

ABSTRACT

Chronic Electronic Cigarette Vapor Inhalation Induces Renal Injury and Functional Decline in Female Mice

Christopher Drummond1, Laura E Crotty Alexander2,3, Jiang Tian1. 1Medicine, University of Toledo, Toledo, OH, 2Pulmonary, Critical Care and Sleep Medicine, University of California San Diego, La Jolla, CA, 3Pulmonary Critical Care, Veterans Affairs San Diego Health System, La Jolla, CA

Clinical studies indicate that combustible cigarette smoke increases renal and cardiac tissue injury progression and functional decline in the setting of chronic kidney disease (CKD). Novel nicotine delivery devices like electronic (e)cigarettes are used by over 10% of the population and produce vapor which may also induce renal injury. To establish whether ecigarette vapor inhalation induced renal injury in the form of fibrosis and decreased renal injury our current study utilized a noseonly

inhalation exposure system to induce 8 weekold female mice to inhale ecigarette vapor containing 24mg/mL of nicotine suspended in a solution of 50% propylene glycol and 50% vegetable glycerin using the following parameters: 12 seconds of vapor exposure every 60 seconds for 60 minutes five days per week for 1, 3 and 6months. Following ecigarette exposure, assessment of renal fibrosis, glomerular filtration rate, and expression of the antifibrotic microRNA miR29b3p were evaluated. Mice exposed to ecigarette vapor suffered a 31% decline in renal tissue expression of miR29b3p vs airexposed

controls (p<0.05). Additionally, mRNA targets of miR29b3p that regulate fibrosis formation or are part of fibrosis were also significantly increased in the kidneys of ecigarette exposed mice versus air controls, i.e., Collagen 1A1 (increased 98%; p<0.05); Collagen 3A1 (129% increase; p<0.05); Collagen 4a1 (72%

increase; p<0.05); Integrin beta 1 (58% increase; p<0.05); and Fibrillin 1 (100% increase; p<0.05). Additionally, we observed a significant increase in renal fibrosis at the 3and 6month

time points as assessed by Trichrome staining in these animals. Lastly, following 3months of

exposure to ecigarette vapor renal function was significantly reduced by 21% versus air exposed controls (p=0.017). These data are the first to indicate that ecigarettes induce renal fibrosis and functional decline. In addition, these data suggest a novel miR29b3p mediated mechanism linking ecigarette vapor exposure and renal injury and functional decline.

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