Acetaldehyde at a Low Concentration Synergistically Exacerbates Allergic Airway Inflammation as an Endocrine-Disrupting Chemical and as a Volatile Organic Compound

Abstract

Background: Acetaldehyde is an endocrine-disrupting chemical (EDC) and a volatile organic compound (VOC). It is also a carcinogen and teratogen that causes bronchoconstriction in a subset of asthmatics. However, the mechanism through which acetaldehyde acts as an EDC/VOC causing allergic airway inflammation remains unknown. Objectives: To determine the effects of a low concentration of acetaldehyde, which itself did not trigger airway inflammation, on extant allergic airway inflammation in a murine model of allergic asthma. Methods: We compared airway hyperresponsiveness (AHR), lung pathology, serum IgE and airway concentrations of cytokines among four groups of BALB/c mice [control, Dermatophagoides farinae(Df) allergen-sensitized (AS), intranasally acetaldehyde-injected (ALD) and AS-ALD mice]. Results: Physiological and histological differences were not evident between ALD and control mice. AS mice developed AHR and allergic airway inflammation characterized by goblet cell hyperplasia and eosinophilic infiltration. Both AHR and airway eosinophilia were significantly enhanced in AS-ALD compared with AS mice. Serum total and Df-specific IgE were significantly increased in both AS and AS-ALD mice compared with control and ALD mice, but comparable between AS and AS-ALD mice. Mite allergen sensitization significantly increased interleukin-5 and granulocyte macrophage colony-stimulating factor, and decreased interferon-γ levels in the airways; injecting acetaldehyde into airways with allergic inflammation significantly increased the levels of these inflammatory cytokines. Conclusions: Exposure to acetaldehyde can enhance allergic airway inflammation in asthma.

Icariin attenuates asthmatic airway inflammation via modulating alveolar macrophage activation based on network pharmacology and in vivo experiments

“…112,113 This may explain why Kawano et al 114 reported that acetaldehyde exacerbates allergic airway inflammation in asthma. 114 Corticosteroids inhibit the formation of acetaldehyde adducts and reduce cytokine production to reduce inflammation. 115 Nevertheless, the production F I G U R E 1 1 Schematic of ICA attenuates the inflammatory response by involving arginine and proline metabolism pathway and macrophage activation/ polarization via regulation of Aldh2, Nos3, Nos2, Aldh9a1, Nos1, Jun, Syk, Jak2 and Tnf in asthmatic mice.…”

“…Remarkably, acetaldehyde induces histamine release from airway mast cells, resulting in increased inflammatory factors and AHR 112,113 . This may explain why Kawano et al 114 reported that acetaldehyde exacerbates allergic airway inflammation in asthma 114 . Corticosteroids inhibit the formation of acetaldehyde adducts and reduce cytokine production to reduce inflammation 115 .…”

Towards practical indoor air phytoremediation: A review

“…Exposure to VOCs in the indoor environment has been associated with several health effects, such as contributing to sick building syndrome (Brinke et al, 1998) and exacerbating asthma symptoms (Fuentes-Leonarte et al, 2009;McGwin Jr et al, 2010), while several common VOCs, such as acetyl aldehyde, have been identified as endocrine disruptors (Kawano et al, 2012), whilst others have been linked to problems with the nervous, hepatic, renal and respiratory systems (Sriprapat et al, 2014). Several VOCs, such as benzene and formaldehyde, are known carcinogens (Khanchi et al, 2015).…”

Effects of Endocrine Disrupters on Immune Function and Inflammation

“…Finally, exposure to some PCB congeners appears to affect the risk of non-Hodgkin lymphoma [105]. [106][107][108][109][110][111][112][113][114][115][116]. The categories include products from antimicrobial soap (triclosan), naturally occurring phytoestrogens in food (genistein), antimollusk (tributyltin) and antifungal (vinclozolin) compounds, drugs (valproate), mycotoxins (zearalenone), and industrial organics (acetaldehyde and nonylphenol).…”