2017
DOI: 10.1016/j.yrtph.2017.08.018
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Chemical-induced asthma and the role of clinical, toxicological, exposure and epidemiological research in regulatory and hazard characterization approaches

Abstract: Uncertainties in understanding all potential modes-of-action for asthma induction and elicitation hinders design of hazard characterization and risk assessment methods that adequately screen and protect against hazardous chemical exposures. To address this challenge and identify current research needs, the University of Cincinnati and the American Cleaning Institute hosted a webinar series to discuss the current state-of-science regarding chemical-induced asthma. The general consensus is that the available dat… Show more

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Cited by 15 publications
(11 citation statements)
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“…VOCs cannot act as antigens due to their low molecular weight but may still initiate an adaptive immune response by acting as haptens through carrier protein binding as reported for occupational exposure to toluene, one of the VOCs released by the fuel oil blend employed in our study (Karol 1983). In the absence of an adaptive immune response, VOCs may interact with innate immunity pathways through contact with the airway epithelium and elicit inflammation, as described for reactive airways dysfunction (Vincent et al 2017). Given the various possibilities by which VOCs may potentially activate immune system pathways, our working hypothesis was that airway hyperresponsiveness was underlain by an inflammatory response as generally is the case in airway disease.…”
Section: Environmental Health Perspectivesmentioning
confidence: 99%
“…VOCs cannot act as antigens due to their low molecular weight but may still initiate an adaptive immune response by acting as haptens through carrier protein binding as reported for occupational exposure to toluene, one of the VOCs released by the fuel oil blend employed in our study (Karol 1983). In the absence of an adaptive immune response, VOCs may interact with innate immunity pathways through contact with the airway epithelium and elicit inflammation, as described for reactive airways dysfunction (Vincent et al 2017). Given the various possibilities by which VOCs may potentially activate immune system pathways, our working hypothesis was that airway hyperresponsiveness was underlain by an inflammatory response as generally is the case in airway disease.…”
Section: Environmental Health Perspectivesmentioning
confidence: 99%
“…Occupational and chemical exposures comprise a less common, but well-known source of irritants and allergens that cause asthmatic disease. In occupational health, the term "reactive airways dysfunction syndrome" (RADS) is often used to refer to bronchial reactivity without an initial latency or sensitisation period [108]. Examples of culprit chemicals include isocyanates, acid anhydrides, azodicarbonamide, dyes, enzymes, and metals [109].…”
Section: The Exposome and Environmental Exposuresmentioning
confidence: 99%
“…Examples of culprit chemicals include isocyanates, acid anhydrides, azodicarbonamide, dyes, enzymes, and metals [109]. Potential mechanisms of disease are highly-variable, and may involve type I (allergic) hypersensitivity vs. non-allergic/irritant, or Type IV (T cellmediated) mechanisms; "inducers" vs. "inciters"; dermal vs. respiratory sensitisers; and low molecular weight (LMW, hapten-like) vs. high molecular weight (HMW) allergens [108]. It is likely that many culprits drive disease through mixed mechanisms.…”
Section: The Exposome and Environmental Exposuresmentioning
confidence: 99%
“…Chronic airway conditions downstream of excessive irritant exposure in humans include nonallergic rhinitis, chronic cough, and asthma-like airway hyper-responsiveness. 137 These conditions are thought to be related by a common etiology involving inflammation of respiratory epithelium in nasopharynx (rhinitis), larynx/throat (laryngitis), and conducting airways (asthma) and aberration of sensory nerve responses in those regions. 138 Changes in the human respiratory epithelium associated with these conditions include neutrophilia, basement membrane thickening (fibrosis of basal lamina), and migration of mast cells to airway smooth muscle.…”
Section: Chronic Adverse Outcomes and Airway Diseasesmentioning
confidence: 99%