Irritant-induced asthma

B. Irritant-induced asthma, work-aggravated asthma, and chronic bronchitis... 

Irritant-induced asthma usually occurs following a single or multiple accidental high-intensity exposures. Repetitive lower intensity exposures to irritants may also cause asthma (Balmes, 2002). Once asthma develops. 

Most household maintenance products contain mixtures of lipophiles and hydrophiles that can produce unanticipated toxic effects. Irritant-induced asthma is an example of such an effect. Solvent-based and waterborne paints contain solvents that are nonsensitizing irritants that are individually not known to induce asthma. Despite this, exposures to both types of paints have been shown to cause the asthma-like condition reactive airways dysfunction syndrome (RADS).I13 14 RADS is discussed in detail in Chapterl8. 

Though asthma is known to be induced by sensitizing chemicals, it is also triggered by irritant chemicals. Significantly, when asthma is induced by sensitizers, it is almost always done so by exposure to a single chemical, but when triggered by irritants, it is almost always following exposures to mixtures of lipophiles and hydrophiles. This connection also holds for the onset of RADS, which is discussed next. 

Tarlo SM. Irritant-induced occupational asthma. Chest 1989 96(2) 297-300. 

Irritant-induced asthma (RADS) occurs in the absence of a latency period, after either a single exposure to toxic concentrations or repetitive exposures to lower concentrations of gases, strong acids and alkalis, organic solvents or wood smoke (Brooks et al., 1985). Such exposures often result in NSBH that may persist for months or years (Brooks and Bernstein, 1993). 

BROOKS, S.M. BERNSTEIN, I.L. (1993) Reactive airways dysfunction syndrome or irritant-induced asthma, in BERNSTEIN, I.L., CHAN-YEUNG, M MALO, J.-L. BERNSTEIN, D.I. (Eds) Asthma in the Workplace, pp. 533-549. New York Marcel Dekker. 

The focus of this chapter is occupational asthma mediated by immunological hypersensitivity, termed occupational asthma with a latency period by Bernstein et al. (1993). This may involve formation of IgE antibody, but not necessarily. Rhinitis, conjunctivitis and urticaria are included because they co-exist commonly with asthma and share common mechanisms. Occupational asthma caused by an irritant exposure sufficient to damage airway mucosa is excluded. There may be immunological epiphenomena, such as formation of specific antibody, in irritant-induced asthma but, when present, these do not imply an immunological causal pathway. 

Work-related asthma is a frequent occupational problem. Classic occupational asthma typically occurs after sensitization to either high-molecu-lar-weight chemicals (eg, inhaled foreign proteins) or to small chemicals that appear to act as haptens (the most common of which are the urethane isocyanates such as toluene diisocyanate [TDI]). After acute, high-level irritant inhalations, for example of chlorine, a chronic irritant-induced... 

Occupational reactive airways dysfunction syndrome (RADS) is defined as persistent respiratory symptoms and nonspecific airway hyperreactivity in patients with a history of acute exposure to an inhaled agent (gas or aerosol) and no prior history of allergies, smoking, or asthma (25). The definition of RADS can usefully be extended in the WTC context (Table 1) to include those with repeated irritant exposure who have developed irritant-induced asthma. RADS can progress to irreversible lower airways obstructive disease. 

McGovern, T.K., Powell, W.S., Day, B.J., et al., 2010. Dimethylthiourea protects against chlorine induced changes in airway function in a murine model of irritant induced asthma. Respir. Res. 11,138. 

Exposure to agents with no immunological potential usually results in OA with no latency period. This irritant-induced asthma most often occurs after single (RADS) or multiple incidents of high exposure. 

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