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      Neurotoxicity of e-cigarettes

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          Abstract

          It appears that electronic cigarettes (EC) are a less harmful alternative to conventional cigarette (CC) smoking, as they generate substantially lower levels of harmful carcinogens and other toxic compounds. Thus, switching from CC to EC may be beneficial for smokers. However, recent accounts of EC- or vaping-associated lung injury (EVALI) has raised concerns regarding their adverse health effects. Additionally, the increasing popularity of EC among vulnerable populations, such as adolescents and pregnant women, calls for further EC safety evaluation. In this state-of-the-art review, we provide an update on recent findings regarding the neurological effects induced by EC exposure. Moreover, we discuss possible neurotoxic effects of nicotine and numerous other chemicals which are inherent both to e-liquids and EC aerosols. We conclude that in recognizing pertinent issues associated with EC usage, both government and scientific researchers must address this public health issue with utmost urgency.

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          Most cited references324

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          Is Open Access

          Oxidative Stress: A Key Modulator in Neurodegenerative Diseases

          Oxidative stress is proposed as a regulatory element in ageing and various neurological disorders. The excess of oxidants causes a reduction of antioxidants, which in turn produce an oxidation–reduction imbalance in organisms. Paucity of the antioxidant system generates oxidative-stress, characterized by elevated levels of reactive species (oxygen, hydroxyl free radical, and so on). Mitochondria play a key role in ATP supply to cells via oxidative phosphorylation, as well as synthesis of essential biological molecules. Various redox reactions catalyzed by enzymes take place in the oxidative phosphorylation process. An inefficient oxidative phosphorylation may generate reactive oxygen species (ROS), leading to mitochondrial dysfunction. Mitochondrial redox metabolism, phospholipid metabolism, and proteolytic pathways are found to be the major and potential source of free radicals. A lower concentration of ROS is essential for normal cellular signaling, whereas the higher concentration and long-time exposure of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, ultimately resulting in necrosis and apoptotic cell death. Normal and proper functioning of the central nervous system (CNS) is entirely dependent on the chemical integrity of brain. It is well established that the brain consumes a large amount of oxygen and is highly rich in lipid content, becoming prone to oxidative stress. A high consumption of oxygen leads to excessive production of ROS. Apart from this, the neuronal membranes are found to be rich in polyunsaturated fatty acids, which are highly susceptible to ROS. Various neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), among others, can be the result of biochemical alteration (due to oxidative stress) in bimolecular components. There is a need to understand the processes and role of oxidative stress in neurodegenerative diseases. This review is an effort towards improving our understanding of the pivotal role played by OS in neurodegenerative disorders.
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            A Randomized Trial of E-Cigarettes versus Nicotine-Replacement Therapy

            E-cigarettes are commonly used in attempts to stop smoking, but evidence is limited regarding their effectiveness as compared with that of nicotine products approved as smoking-cessation treatments.
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              Vital Signs: Tobacco Product Use Among Middle and High School Students — United States, 2011–2018

              Introduction Tobacco use is the leading cause of preventable disease and death in the United States; nearly all tobacco product use begins during youth and young adulthood. Methods CDC, the Food and Drug Administration, and the National Cancer Institute analyzed data from the 2011–2018 National Youth Tobacco Surveys to estimate tobacco product use among U.S. middle and high school students. Prevalence estimates of current (past 30-day) use of seven tobacco products were assessed; differences over time were analyzed using multivariable regression (2011–2018) or t-test (2017–2018). Results In 2018, current use of any tobacco product was reported by 27.1% of high school students (4.04 million) and 7.2% of middle school students (840,000); electronic cigarettes (e-cigarettes) were the most commonly used product among high school (20.8%; 3.05 million) and middle school (4.9%; 570,000) students. Use of any tobacco product overall did not change significantly during 2011–2018 among either school level. During 2017–2018, current use of any tobacco product increased 38.3% (from 19.6% to 27.1%) among high school students and 28.6% (from 5.6% to 7.2%) among middle school students; e-cigarette use increased 77.8% (from 11.7% to 20.8%) among high school students and 48.5% (from 3.3% to 4.9%) among middle school students. Conclusions and Implications for Public Health Practice A considerable increase in e-cigarette use among U.S. youths, coupled with no change in use of other tobacco products during 2017–2018, has erased recent progress in reducing overall tobacco product use among youths. The sustained implementation of comprehensive tobacco control strategies, in coordination with Food and Drug Administration regulation of tobacco products, can prevent and reduce the use of all forms of tobacco products among U.S. youths.
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                Author and article information

                Journal
                Food and Chemical Toxicology
                Food and Chemical Toxicology
                Elsevier BV
                02786915
                April 2020
                April 2020
                : 138
                : 111245
                Article
                10.1016/j.fct.2020.111245
                7089837
                32145355
                595c9ab8-3b25-435c-82e6-7e9816a85254
                © 2020

                https://www.elsevier.com/tdm/userlicense/1.0/

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