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Environmental Toxins
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Ozone (O3) is a highly reactive gas composed of three oxygen atoms. Ozone occurs naturally in the environment but can also be a man-made product that has adverse effects on human health. Stratospheric ozone occurs naturally and reduces the amount of harmful ultraviolet radiation that reaches the Earth’s surface. Ground level ozone is formed from man-made processes and is able to be inhaled by humans. Ground level ozone is mainly formed from photochemical reactions between two major classes of air pollutants, volatile organic compounds (VOC) and nitrogen oxides. Significant sources of VOC in the environment are chemical plants, gasoline pumps, and autobody shops. Nitrogen oxides result primarily from high temperature combustion from sources such as power plants, industrial furnaces and boilers, and motor vehicles (EPA, 2021a).
Inflammatory, Hypersensitivity and Immune Lung Diseases, including Parasitic Diseases.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
The inhalation of nitrogen oxide, solvents or the smoking of drugs such as cannabis or cocaine may produce harmful effects on the lungs. Both acute and chronic changes may occur. Deep inspiration, followed by a prolonged Valsalva manoeuvre and violent coughing may lead to gas leaking from the alveoli and a pneumomediastinum and/or pneumothorax (see also ps. 6.34 - 35). A pneumomediastinum may also result from the rupture of sub-pleural blebs or bullae. In addition free-base cocaine (or 'crack') may cause chest pain and shortness of breath with radiographic findings of localised collapse or lung parenchymal opacification (similar to that seen in Loeffler's syndrome - p. 19.59), acute pulmonary oedema (which can resolve in 24 hours) or barotrauma. Inhaled cocaine may also lead to alveolar damage with haemoptyses and intrapulmonary haemorrhage; the nares may also be inflamed leading to epistaxis and septal perforation. (See further details under Benson and Bentley below).
Acute Lung Injury In Children Due To Chemical And Physical Agents
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Other products of combustion, especially from plastics and other synthetic materials used in furniture and buildings, may be toxic when inhaled.151 Burning polyvinylchloride gives off hydrochloric acid157 which may produce alveolitis, bronchiolitis, and pulmonary edema.151 Burning polyurethane foam decomposes to several toxic substances according to the temperature of combustion, including isocyanates, hydrogen cyanate, ammonia, carbon monoxide, acrylonitriles, and hydrogen cyanide.178 Cyanide (and its metabolite, thiocyanate) were found to be elevated in casualties overcome by smoke inhalation in Glasgow.192 Cyanide is produced by burning silk, wool, and plastics.151 Two of the six children with severe smoke inhalation injury described from Liverpool appeared to suffer from cyanide poisoning, although this was not documented by laboratory investigations.178 Oxides of sulfur and nitrogen are irritating and combine with water to produce corrosive acids and alkalis.157 Nitrogen oxide has been reported to be responsible for the development of bronchiolitis obliterans.151 Aldehydes (irritants that also denature protein) are produced by burning cotton, wood, and furniture.151, 157 Smoke from burning wood is very irritating.171
The rising of allergic respiratory diseases in a changing world: from climate change to migration
Published in Expert Review of Respiratory Medicine, 2020
Benedetta Biagioni, Isabella Annesi-Maesano, Gennaro D’Amato, Lorenzo Cecchi
The evidence that air pollution can cause exacerbations of preexisting asthma is supported by studies and data accumulating for several decades. Nitrogen dioxide, ozone and particulate matter, have been significantly associated with increased asthma exacerbations and higher asthma medication intake [31]. Particulate Matter (PM) is a ubiquitous atmospheric aerosol with both anthropogenic and natural sources that can be classified on the basis of its aerodynamic diameter in PM10 or PM2.5, the latter being also called fine particles. PM2.5 can easily penetrate deeply into bronchial tree, affecting distal airways. Nitrogen oxides gases, such as nitric oxide (NO) and nitrogen dioxide (NO2), are mainly produced from the reaction between nitrogen and oxygen during combustion fuels and are a significant source of air pollution in areas of high motor vehicle traffic.
The toxicology of air pollution predicts its epidemiology
Published in Inhalation Toxicology, 2018
Andrew J. Ghio, Joleen M. Soukup, Michael C. Madden
The interaction between air pollution particles and ozone is suggested to impact human health effects (Figure 2(A)). Air pollution particles include a significant concentration of HULIS (i.e. polycarboxylates), and investigation predicts further carboxylation of this PM following ozone exposure. This results in a particle with a greater capacity to impact (1) iron sequestration resulting in an increased disruption in metal homeostasis and (2) subsequent inflammation and fibrosis. Damage induced by ozone-reacted HULIS is in addition to lung cell injury associated with ozone exposure, which may or may not be a different type of injury and may make the cells more sensitive. Such interaction between particles and ozone is supported by epidemiological, controlled exposure, animal, and in vitro investigation (Bosson et al., 2008; Chen et al., 2007; Jakab & Hemenway, 1994; Kafoury & Kelley, 2005; Madden et al., 2000, 2014; Molhave et al., 2005; Stiegel et al., 2016). Furthermore, it is possible that other components of air pollution (e.g. nitrogen oxides) also participate in modifying the functional groups at the ambient PM surface and subsequently impact human health through the same pathway (Ciobanu et al., 2016). Finally, an additional source of HULIS production could be photooxidation from ultraviolet radiation, which would result in changes comparable to ozone exposure.
S-Nitrosoglutathione formation at gastric pH is augmented by ascorbic acid and by the antioxidant vitamin complex, Resiston
Published in Pharmaceutical Biology, 2018
Vitali I. Stsiapura, Ilya Bederman, Ivan I. Stepuro, Tatiana S. Morozkina, Stephen J. Lewis, Laura Smith, Benjamin Gaston, Nadzeya Marozkina
This work is important because high oral doses of AA and AA-containing antioxidant complexes are commonly used and have benefits in a number of diseases (Cameron and Pauling 1978; Sukolinskii and Morozkina 1989; Morozkina et al. 1991; Du et al. 2012; Rodrigo et al. 2014). Our data suggest that, rather than depleting gastric GSNO levels as we expected, these high exposure levels stabilize GSNO at gastric pH. This could actually augment gastric motility, vascular smooth muscle relaxation and host defence. Additional studies will be required, however, to determine the fate of GSNO under these conditions, and whether GSNO contributes to the beneficial effects of antioxidant complexes. The gastric chemistry of nitrogen oxides is also important because nitric oxide synthase (NOS) deficient mice are viable (Huang 2000). We have hypothesized that exogenous nitrogen oxides in the gut and lung can provide nitrogen oxides in a NOS-independent fashion. For example, the lung lining fluid normally contains near mM levels of reduced GSH and μM levels of nitrite; these are cleared from the airways to the larynx and swallowed. Under conditions of mild acidification in the gut and distal airways, inorganic formation of luminal S-nitrosoglutathione (GSNO) would be predicted (Gaston et al. 1993; Fang et al. 1998; Gaston, Singel, et al. 2006; Marozkina and Gaston 2012, 2015). Our current data suggest that this NOS-independent source of stable nitrogen oxide bioactivity is stabilized, rather than broken down, by oral ingestion of AA given as an antioxidant therapy.