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Elements of Polymer Science
Published in E. Desmond Goddard, James V. Gruber, Principles of Polymer Science and Technology in Cosmetics and Personal Care, 1999
E. Desmond Goddard, James V. Gruber
In polymer analog modifications, a reaction takes place along the polymer chain to convert certain chemical functionalities into different functions, without altering the degree of polymerization of the starting polymer. This approach is particularly useful for the transformation of naturally occurring polymers, but it is applied also to modify synthetic polymers. For example, saturated polymers, such as polyethylene, can be chlorinated or oxidized. Polyenes, such as rubber, can be hydrogenated, halogenated, or epoxidized. Pendant groups, such as the ester groups in poly(vinyl acetate), can be hydrolyzed by transesterification with butanol or methanol to yield poly(vinyl alcohol). The latter can be modified further by reactions typical of alcohols, such as ether formation, esterification, or formation of acetal by treatment with butyraldehyde to form poly(vinyl butyral). The hydroxyl groups in polysaccharides are converted to corresponding ethers and esters. Cellulose ethers, for example, result from the reaction of cellulose with ethylene oxide or propylene oxide (see Chapter 8). Hydrophobically modified polymers such as the cationic cellulose ether derivative, Quatrisoft LM-200 (Amerchol), are obtained via polymer analog reactions (see later chapters).
Extracellular vesicles as actors in the air pollution related cardiopulmonary diseases
Published in Critical Reviews in Toxicology, 2020
Stéphanie Alkoussa, Sébastien Hulo, Dominique Courcot, Sylvain Billet, Perrine J. Martin
Another important source of air pollution is related to smoking. Daily, humans can be exposed to different types of smoke. First of all, mainstream smoke, also known as firsthand smoke, is the direct inhalation of toxic aerosols by a smoker after smoking a cigarette. Second, secondhand smoke or environmental tobacco smoke occurs when tobacco smoke enters an environment, primarily indoor and is inhaled by all smokers or nonsmokers. It is a combination of the smoke exhaled by a smoker and the smoke from the burning end of a cigarette. CS consists of a tar phase, composed mainly of PM1, and a vapor phase. It contains more than 6000 chemicals, most of which are VOCs, including aromatic and oxygenated compounds, highly reactive free radicals, and toxic heavy metals (Kleinstreuer and Feng 2013). The two main ones are CO2 and carbon monoxide (CO) with concentrations around 26.8 and 7.3 mg/cigarette, respectively (Marcilla et al. 2012). Many other compounds are generally detected at concentrations between 5 and 500 μg/cigarette. VOCs, such as methane, benzene, 1,3-butadiene, toluene, and small aldehydes such as acrolein, methyl vinyl ketone, butyraldehyde, acetone, and limonene are primarily constituents of the vapor phase. Nicotine, PAHs, and nitrosamines are associated primarily with the particulate phase, while others as hydrogen cyanide, ammonia, and formaldehyde are found in both phases (Counts et al. 2005).
Design and evaluation of molecular organogel based on folic acid as a potential green drug carrier for oral route
Published in Drug Development and Industrial Pharmacy, 2022
Masar Basim Mohsin Mohamed, Lina A. Dahabiyeh, Mohanad Naji Sahib
To investigate how the FA built their network and what’s the possible interactions of the functional groups of FA molecules with PG; FTIR was executed on the selected organogels, as shown in Figure 3. The carbonyl stretching of –COOH appeared at 1690 cm−1 in FA powder spectrograms and the three selected FA organogels formulations. In addition to the 1690 cm−1 peak, only FA/PG organogels spectrograms showed peaks at 1716–1723 cm−1. These peaks were responsible for acyclic dimerization of carboxylic groups, which in turn help in gelation. Another report showed similar results where the acyclic dimerization through the carboxylic group was referred for the gelation of 12-hydroxystearic acid in butyraldehyde and dodecylaldehyde [38]. Moreover, the FA powder spectrogram showed characteristic peaks at 1601 cm−1 associated with NH bending vibration. In contrast, the spectrograms of organogels exposed a shift to 1607 cm−1, and this shifting could be due to the interactions between FA molecules. Furthermore, FA spectrograms showed bands at 1516 cm−1 and 1481 cm−1 ascribed to the phenyl and pteridine ring [39]. In contrast, the spectrograms of FA organogels of different concentrations showed the disappearance of bands at 1481 cm−1. A possible explanation for this may be due to the interactions between FA molecules with PG molecules. Similar results in another study were observed. The FA-anthracene complex showed a slight shift in the peaks associated with the pteridine ring [39]. In conclusion, the above results were an evidence of organogel formation.
Could E-cigarette vaping contribute to heart disease?
Published in Expert Review of Respiratory Medicine, 2020
Marin Kuntic, Omar Hahad, Andreas Daiber, Thomas Münzel
The major group of toxic compounds in E-cigarette vapor comprises reactive aldehydes and ketones [3]. The carbonyl compounds are generated as degradation products during the heating process of E-cigarette liquid and have well-established adverse health effects by their adduct formation with proteins and DNA, leading to the formation of reactive oxygen species and endoplasmic reticulum stress, impaired mitochondrial function as well as a pro-inflammatory phenotype [50–53]. The major reactive aldehydes and ketones that were detected in E-cigarette vapor, and in E-cigarette liquid at much lower levels, are formaldehyde, acetaldehyde, propionaldehyde, butyraldehyde, acetone, and acrolein [7] as well as minor products such as crotonaldehyde and methacrolein that can be only detected when using superior analytical methods [54,55]. Besides these toxic carbonyls, only trace amounts of transition metals, volatile organic compounds, nitrosamines, and particulates were detected in E-cigarette vapor [56,57] that originate either from contaminations in the E-cigarette liquid or are produced by interaction with the metal heating coil as well as by the heating process itself [3]. In our recent study (human and mouse model), we attributed an appreciable part of the adverse health effects of E-cigarette vapor exposure to the toxic effects of the highly reactive aldehyde acrolein [7], as it stimulates NADPH oxidase activity [58] via protein kinase C activation [59], and NOX-2 isoform, the phagocytic NADPH oxidase, played a central role for adverse cardiovascular health effects in our E-cigarette vapor exposed mice since NOX-2 deficient mice were largely protected [7]. Acrolein levels in E-cigarette vapor also correlated with reactive oxygen species (ROS) formation rates in cultured lung cancer cells [57] as well as ROS and inflammation in primary lung microvascular endothelial cells [60]. In this report, it was also demonstrated that acrolein impairs lung endothelial barrier function that was most likely due to oxidative stress and inflammation. We also know from studies with tobacco cigarette smoke extract that acrolein may cause ferroptosis in vascular smooth muscle cells [61]. In summary, the atherothrombotic effects of acrolein [62], its potential contribution to neurodegenerative processes [63], its carcinogenicity due to DNA damage and inhibition of DNA repair [64] as well as aggravation of respiratory disease complications [65], are all likely increase the chronic disease burden upon long-term use of E-cigarettes.