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Respiratory, endocrine, cardiac, and renal topics
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Cyclophosphamide is used for the treatment of numerous malignant diseases, such as neuroblastoma and acute lymphoblastic leukaemias. It is used before allogenic haematopoietic stem cell transplantation in numerous malignant or non-malignant diseases. Cyclophosphamide is administered either at conventional doses of 100 to 300 mg/m2, or at high doses (1.2 g/m2 or 200 mg/kg) in combination with other cytotoxic agents. During the administration of doses over 1 g/m2, prophylactic measures must be taken to avoid haemorrhagic cystitis. Acrolein is toxic to the bladder mucosa. The occurrence of bladder toxicity depends on the concentration of acrolein present in urine and the duration of the contact between acrolein and the mucosa. This toxicity is aggravated by urine stagnation and previous bladder irradiation. Hyperhydration, resulting in significant diuresis, along with the administration of mesna, which inactivates acrolein by conjugation, minimises toxicity.
The Toxic Environment and Its Medical Implications with Special Emphasis on Smoke Inhalation
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard A. Matthay, G. J. Walker. Smith
Acrolein is present in cigarette smoke, photochemical smog, and fires involving polyethylene, polypropylene, and vinylon materials (Terrill et al., 1978). Because of the irritant effects of acrolein, the Occupational Safety and Health Administration (OSHA) sets the threshold limit value for an 8 hr exposure period at 0.1 ppm. The lungs of animals (rats) exposed for 62 days to an acrolein concentration of 4.0 ppm showed decreased flow-volume curves, a leftward shift of pressure volume curves, and an increase in lung volumes, suggesting airway obstruction of both small and large airways (Costa et al., 1986).
Effect of Neutrophils on Airway Smooth Muscle Responsiveness
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
In the guinea pig and rat, there is evidence that neutrophils are not necessary for ozone-induced increase in airway reactivity. Murlas and Roum38 found that the neutrophil influx into guinea pig airways after ozone lagged behind the increase in airway reactivity and that neutrophils persisted longer than did the increased airway responsiveness. Neutrophil depletion did not affect ozone-induced increases in airway reactivity.39 Likewise, ozone did not alter the small numbers of neutrophils in rat airways, although reactivity measured in isolated perfused lungs increased.40 Acrolein, an unsaturated aldehyde found in cigarette smoke, is a potent respiratory irritant that causes increased airway responsiveness, neutrophil influx, and increased concentrations of TXB2 and PGF2α in BAL fluid from guinea pigs.41 The increased airway reactivity, like that found after ozone in guinea pigs, occurred before neutrophils appeared in BAL fluid in greater number. It may be that, in rodents, airway reactivity is not modulated by neutrophils.42,80
Toxicological assessment of electronic cigarette vaping: an emerging threat to force health, readiness and resilience in the U.S. Army
Published in Drug and Chemical Toxicology, 2022
Marc A. Williams, Gunda Reddy, Michael J. Quinn, Amy Millikan Bell
Acrolein can exert its toxicological effects on inhalational, oral and dermal routes of exposure, and are mediated almost immediately on contact with the exposed tissues and organs. An inhalational exposure to acrolein can provoke intense irritation to the eyes, nose, throat and lungs very quickly following exposure (Weber-Tschopp et al.1977, Buckley et al.1984). Moreover, bronchitis and excess accumulation of fluid in the lung – a process referred to as pulmonary edema, lung hemorrhage, and even death is possible on exposure to high levels of acrolein. Higher airborne concentrations of acrolein might provoke increasingly severe outcomes due to irritation of the entire upper and lower airways system. Both the severity and diversity of observed effects and depth of the respiratory system to which effects extend increases as the exposure level increases.
Conjugated linoleic acid protects brain mitochondrial function in acrolein induced male rats
Published in Toxicology Mechanisms and Methods, 2021
Birsen Aydın, Cansu Güler Şahin, Vedat Şekeroğlu, Zülal Atlı Şekeroğlu
Acrolein (AC) is an environmental pollutant present in automobile exhaust, cigarette, wood, frying of foods in oils and biocides (Moghe et al. 2015; Aydın et al. 2018a, 2018b). Therefore, it poses a serious health threat. Previous studies have demonstrated that AC can cause DNA damage, oxidative damage and mitochondrial dysfunction (Stevens and Maier 2008; Conklin et al. 2011; Moghe et al. 2015; Aydın et al. 2018a, 2018b). AC is a highly reactive neurotoxic substance. Because it has high activity, it causes oxidative stress by adding cellular nucleophilic groups. Increased AC level was detected in damaged brain regions of Alzheimer's patients (Pocernich et al. 2001; Singh et al. 2010). AC can disrupt mitochondrial respiration in the heart, spinal cord and brain tissues. Therefore, AC-induced oxidative stress may disrupt normal bioenergetic metabolism in nerve tissue. Some in vitro studies showed that a decrease in mitochondrial reduced glutathione (GSH) level was found in the brain mitochondria treated with AC. Catalase (CAT) activity is less in brain mitochondria than other tissues, and therefore GSH activity in brain mitochondria is more important than other tissues (Shi et al. 2011).
Could E-cigarette vaping contribute to heart disease?
Published in Expert Review of Respiratory Medicine, 2020
Marin Kuntic, Omar Hahad, Andreas Daiber, Thomas Münzel
Actually there are several ways to calculate the concentrations of acrolein in response to E-cigarette vaping. First, taking into account our measured acrolein concentration in E-cigarette vapor condensate of 0.49 µM (page 6, left column in [7]), we calculate an acrolein mass per volume of 0.49 μmol/L * 56 μg/μmol = 27 μg/L (0.027 μg/mL). In the exposure chamber, we detected a particle/aerosol concentration of 6.5 g/m3 (online supplement, page 16 in [7]). Assuming a density of the aerosol E-cigarette liquid droplets of 1.15 g/ml (propylene glycol and glycerol) we calculate a liquid amount in the vapor-containing air in the exposure chamber of 6.5 g/m3/1.15 g/mL = 5.7 mL/m3 resulting in a total acrolein concentration of 5.7 mL/m3 * 0.027 μg/mL = 0.15 μg/m3, which is only 2.7-fold lower than the recommended upper WHO threshold. Second, assuming an average volume of one breath of 0.5 L and our determined acrolein mass of 0.0032 µg/puff, we find an acrolein concentration in the lung of an E-cigarette vaper of 0.0032 μg/0.0005 m3 = 6.4 μg/m3, which is 16-fold higher than the recommended upper WHO threshold.