Asthma related to cleaning agents: a clinical insight

​Introduction

In recent years, there has been a growing concern about the potential role of exposure to cleaning products in the initiation and aggravation of asthma.1 ,2 Epidemiological surveys have consistently documented increased prevalence3–5 and incidence6–8 rates of asthma in workers exposed to cleaning materials and/or disinfectants, especially in domestic cleaners3,4 and healthcare workers.9–12 In addition, some studies have reported an increased risk of work-related asthma symptoms in exposed workers.5 ,12 ,13

However, there is still limited knowledge on the specific exposures and pathophysiological mechanisms involved in cleaning-related asthma.1 ,2 Cleaning materials typically contain a wide variety of ingredients, some of which are respiratory irritants, such as chlorine-releasing agents and ammonia, while others are potential airway sensitizers.14 ,15 Asthma in cleaners has been mostly associated with the irritant effects of cleaning products, which may exacerbate asthma and, at high exposure levels, cause acute irritant-induced asthma (or 'reactive airways dysfunction syndrome').10 ,16–19 Nevertheless, occasional case reports have ascribed occupational asthma (OA) due to specific airway hypersensitivty to components of detergents or disinfectants.2 Overall the determinants of cleaning-related asthma symptoms remain largely uncertain since most available studies have relied on self-reported symptoms or physician-based diagnosis. Only two studies have investigated the effects of cleaning exposures on peak expiratory flow (PEF) variability with inconsistent results.20 ,21

Therefore, the data of participants who completed specific inhalation challenges (SICs) with the cleaning agents and/or disinfectants suspected of causing their work-related asthma symptoms were reviewed in order: (1) to determine the prevalence and causes of asthmatic reactions induced by these agents and (2) to compare the clinical features as well as the changes in non-specific airway hyper-responsiveness (AHR) and sputum cell counts in participants with positive or negative responses to SIC.

Methods

This study was a retrospective analysis of the charts of all participants investigated through an SIC in our tertiary centre during the period of 1992–2011 for asthma symptoms related to cleaning products and/or disinfectants. The study was approved by the Comité d'éthique médicale of the Centre Hopitalier Universitaire de Mont-Godinne; approval number 84/2012.

Subjects

In our centre, SICs with the occupational agent(s) suspected of causing work-related symptoms are routinely performed to diagnose OA provided that the baseline forced expiratory volume in 1 s(FEV₁) is equal to or above 60% of the predicted value.22 The participants are referred either by their attending physicians or by the Belgian Workers' Compensation Board (WCB). All French-speaking workers submitting a claim for work-related asthma to the WCB are referred to our centre in order to perform an SIC procedure.

The participants were those who completed an SIC procedure with cleaning agents and/or disinfectants were identified from a database of 713 participants who underwent an SIC for possible work-related asthma from 1992 up to 2011. Professional cleaners who had been challenged with latex gloves (n=23) or non-cleaning chemicals present at the workplace (n=3) were excluded from this analysis.

Specific inhalation challenges

SICs were completed according to a standardised protocol, which remained unchanged throughout the study period.23 On the first test day, a 'control' challenge was performed by exposing the participants to a paint diluent containing a mixture of alkyl esters, ketones and aromatic hydrocarbons nebulised in a 5 m³ challenge room for 30 min in order to ensure that fluctuations in FEV₁ were ≤12%. On the following day(s), the participants were challenged with the cleaning product(s) suspected of causing their asthma symptoms at work. Exposure to these products was generated through a 'realistic' approach aimed at reproducing as close as possible the conditions of exposure at the workplace.24 The tested cleaning materials and the mode of exposure during SIC were selected based on the participants' interview, the Material Safety Data Sheets and, most often, an analysis of the job exposure by WCB''s hygienists. The cleaning agents were diluted in cold or heated water, brushed on a cardboard and/or sprayed according to the collected information.

The duration of exposure to the cleaning products was gradually increased (ie, 1, 4, 10, 15, 30 and 60 min) on the same day until a ≥20% fall in FEV₁ occurred or a cumulative exposure of 2 h was completed. Spirometry was obtained at baseline and serially after exposure for a total of at least 6 h. An SIC was considered positive when a sustained ≥20% fall in FEV₁ was recorded. The level of AHR to histamine was determined at the end of the control day (ie, baseline value), 7 h after the end of each active challenge when the FEV₁ was within 10% of baseline value, and 24 h after the last active challenge.25 AHR was expressed as the provocative concentration of histamine causing a 20% fall in FEV₁ (PC₂₀).22 Since March 2006, sputum cell counts were assessed at the end of the control day and 7 h after the end of active challenges (ie, after the assessment of AHR and administration of an inhaled bronchodilator). Sputum was induced through the inhalation of increasing conc

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Asthma related to cleaning agents: a clinical insight

1. Olivier Vandenplas1,2,
2. Vinciane D'Alpaos1,
3. Geneviève Evrard1,
4. Jacques Jamart3,
5. Joel Thimpont2,
6. François Huaux4,
7. Jean-Christophe Renauld5

+ Author Affiliations

1. ¹Department of Chest Medicine, Centre Hospitalier Universitaire de Mont-Godinne, Université Catholique de Louvain,Yvoir, Belgium
2. ²Fonds des Maladies Professionnelles, Brussels, Belgium
3. ³Scientific Support Unit, Centre Hospitalier Universitaire de Mont-Godinne, Université Catholique de Louvain, Yvoir, Belgium
4. ⁴Industrial Toxicology and Occupational Medicine Unit, Université Catholique de Louvain, Brussels, Belgium
5. ⁵Experimental Medicine Unit, Ludwig Institute for Cancer Research, Université Catholique de Louvain, Brussels, Belgium

1. Correspondence to Dr Olivier Vandenplas; olivier.vandenplas@uclouvain.be

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