“…Mechanisms of irritant-induced asthma are poorly known, and hypotheses have been formulated mainly in the context of acute-onset IIA 1,15,17 (Figure 2). We review these hypotheses and their relevance or plausibility in the context of possible IIA due to chronic, moderate exposure.…”
Section: Biological Plausibility Of Iia Caused By Chronic Exposure Tomentioning
confidence: 99%
“…Non-allergic asthma, mostly characterized by neutrophilic than eosinophilic inflammation, may be more frequent in persistent adult-onset asthma, but remains less well understood 2,14 . In the context of OA, which is considered a good model to study asthma in general, there is a long-lasting debate regarding whether chronic irritant exposures at a low to moderate level may induce asthma 7,[15][16][17] .…”
Evidence of a causal effect of chronic workplace irritant exposure in new-onset asthma remains limited, mainly because of a lack of longitudinal studies and the difficulty to evaluate irritant exposures. However, recent epidemiological studies strengthen the evidence of an effect of chronic exposure to irritants in work-related asthma. The underlying mechanism remains unknown but may be related to oxidative stress, neurogenic inflammation and dual irritant and adjuvant effects. However, disentangling chronic irritant effects from either acute irritant-induced asthma or immunological low molecular weight agent-induced asthma is difficult for some agents. Further research is needed to improve assessment of irritant exposures and identify biomarkers.
“…Mechanisms of irritant-induced asthma are poorly known, and hypotheses have been formulated mainly in the context of acute-onset IIA 1,15,17 (Figure 2). We review these hypotheses and their relevance or plausibility in the context of possible IIA due to chronic, moderate exposure.…”
Section: Biological Plausibility Of Iia Caused By Chronic Exposure Tomentioning
confidence: 99%
“…Non-allergic asthma, mostly characterized by neutrophilic than eosinophilic inflammation, may be more frequent in persistent adult-onset asthma, but remains less well understood 2,14 . In the context of OA, which is considered a good model to study asthma in general, there is a long-lasting debate regarding whether chronic irritant exposures at a low to moderate level may induce asthma 7,[15][16][17] .…”
Evidence of a causal effect of chronic workplace irritant exposure in new-onset asthma remains limited, mainly because of a lack of longitudinal studies and the difficulty to evaluate irritant exposures. However, recent epidemiological studies strengthen the evidence of an effect of chronic exposure to irritants in work-related asthma. The underlying mechanism remains unknown but may be related to oxidative stress, neurogenic inflammation and dual irritant and adjuvant effects. However, disentangling chronic irritant effects from either acute irritant-induced asthma or immunological low molecular weight agent-induced asthma is difficult for some agents. Further research is needed to improve assessment of irritant exposures and identify biomarkers.
“…However, from a public health point of view, this distinction may not be so important as both OA and WEA have long-term health and socioeconomic consequences. While, following others' suggestion [7], we recommend stopping using the terms 'low dose IIA' and prefer 'chronic exposure IIA', research aiming at improving irritant exposure assessment and measurement, including intensity/ duration, and determining relevant exposure windows may help in this direction. In a workforce-based study in 1,586 domestic cleaners the associations between a wide range of cleaning products and respiratory symptoms were assessed.…”
Section: Discussionmentioning
confidence: 98%
“…Finally, 'low dose' IIA has been described as delayed-onset asthma after chronic exposure to 'low/moderate' concentrations of irritant compounds in the workplace, in absence of exposure to a known sensitizer [5]. However, in a 2014 editorial, Casas and Nemery [7] made a case for stopping using the terms 'low' or 'moderate' dose for irritant exposure to refer to levels that are actually unmeasured, probably common at work, and likely associated with health hazards. Following their suggestion, in the rest of the manuscript we will refer to 'chronic exposure IIA' for this subtype.…”
Purpose of reviewIn this narrative review, we aim to highlight novel research findings on both acute/subacute irritant-induced asthma (IIA) and chronic exposure IIA (also called ‘low dose’ IIA).Recent findingsNovel case series showed that acute and subacute IIA cases had similar causal agents (e.g., acid or base aerosols/fumes, dusts, mixtures) but had occurred in different circumstances (accidents vs. regular work). Acute and subacute IIA cases had similar clinical characteristics but poorer short-term outcomes than sensitizer-induced occupational asthma patients. Novel large epidemiological studies reported associations between chronic occupational exposure to irritants and current adult-onset asthma and poor asthma control, and with a specific asthma endotype characterized by neutrophilic inflammation and oxidative stress. Recent studies reconfirmed the association of the use of disinfectants and cleaning products (especially sprays) with IIA. A role for genetic susceptibility has been suggested.SummaryRecent literature provided further understanding of both acute/subacute and chronic exposure IIA, in terms of causes, possible mechanisms, and consequences such as poor asthma control. Research is needed to clarify several aspects of IIA, including its frequency (still likely underestimated), modulating factors, and mechanisms. Research aiming at improving irritant exposure assessment, including intensity/duration, and determining relevant exposure windows would be welcome.
“…Similarly, occupational rhinitis can be classified as allergic or non-allergic [30]. Irritant-induced asthma or rhinitis can be caused by a single high level (accidental) exposure to irritants or by chronic, lower level ('daily-life') exposure to irritants [30,45,46]. Chronic exposure to inhaled irritants from DCPs may cause injury of the airway epithelium, oxidative stress and neutrophilic airway inflammation [47][48][49], which are also relevant to COPD pathogenesis.…”
Purpose of review: Evidence for adverse respiratory effects of occupational exposure to disinfectants and cleaning products (DCPs) has grown in the last two decades. The relationship between DCPs and asthma is well-documented, but questions remain regarding specific causal agents. Beyond asthma, associations between DCPs and COPD or chronic rhinitis are plausible and have been examined recently. The purpose of this review is to summarize recent advances on the effect of occupational exposure to DCP and chronic airway diseases.
Recent findings:Recent epidemiological studies have often focused on healthcare workers and are characterized by efforts to improve assessment of exposure to specific DCPs. Despite increasing knowledge on the effect of DCPs on asthma, the burden of work-related asthma caused by DCPs has not decreased in the past decade, emphasizing the need to strengthen prevention efforts. Novel data suggest an association between occupational exposure to DCPs and other chronic airway diseases, such as rhinitis, COPD and poor lung function.Summary: Epidemiological and experimental data showed that many chemicals contained in DCPs are likely to cause airway damages, indicating that prevention strategies should target multiple products. Further research is needed to evaluate the impact of DCPs exposure on occupational airway diseases beyond asthma.
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