Thirty-one year old female PhD. student exposed to beta-mercapto ethanol inhalation. She is now very sensitive to hydrocarbons and has trouble breathing when outside as well as when she is in the lab. Is this a variant of Reactive Airway Distress Syndrome? Any thoughts about treatment or long term prognosis?


Thank you for your inquiry.

I could find no specific reference of reactive airway disease related to the inhalation of mercaptoethanol. However, according to the Toxicology Data Network, inhalation of mercaptoethanol can be irritating to the respiratory tract. For your interest, copied below is a link to the Toxicology Data Network discussion of the toxicity to mercaptoethanol.

In the meantime, it is not possible for us to say what her diagnosis is, and therefore her prognosis, with the information you have supplied. However, I would be very reassured if her lung functions, including diffusion of carbon monoxide were normal. In that case, I would feel that she did not have any residual lung damage, and had an excellent prognosis. If you continued to be concerned, you could consider either a mannitol or methacholine challenge since most individuals with any significant degree of reactive airway disease will have a positive mannitol or methacholine inhalation challenge test.

There is an excellent review of reactive airway disease related to respiratory irritant exposure in the Mount Sinai Journal of Medicine. I have copied below the abstract of this article. In addition, there are informative case reports of the use of methacholine challenge to diagnosed reactive airway disease. One of these is in Chest, and I have also copied the abstract and a link to this article which can be downloaded free of charge.

Thank you again for your inquiry and we hope this response is helpful to you.

Upper and lower respiratory diseases after occupational and environmental disasters
Mount Sinai Journal of Medicine: Volume 75, Issue 2, pages 89–100, March/April 2008
Respiratory consequences from occupational and environmental disasters are the result of inhalation exposures to chemicals, particulate matter (dusts and fibers) and/or the incomplete products of combusion that are often liberated during disasters such as fires, building collapses, explosions and volcanoes. Unfortunately, experience has shown that environmental controls and effective respiratory protection are often unavailable during the first days to week after a large-scale disaster.

The English literature was reviewed using the key words—disaster and any of the following: respiratory disease, pulmonary, asthma, bronchitis, sinusitis, pulmonary fibrosis, or sarcoidosis.

Respiratory health consequences after aerosolized exposures to high-concentrations of particulates and chemicals can be grouped into 4 major caterogies: 1) upper respiratory disease (chronic rhinosinusitis and reactive upper airways dysfunction syndrome), 2) lower respiratory diseases (reactive [lower] airways dysfunction syndrome, irritant-induced asthma, and chronic obstructive airways diseases), 3) parenchymal or interstitial lung diseases (sarcoidosis, pulmonary fibrosis, and bronchiolitis obliterans, and 4) cancers of the lung and pleura.

This review describes several respiratory consequences of occupational and environmental disasters and uses the World Trade Center disaster to illustrate in detail the consequences of chronic upper and lower respiratory inflammation. Mt Sinai J Med 75:89–100, 2008. © 2008 Mount Sinai School of Medicine.

Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures
Ten individuals developed an asthma-like illness after a single exposure to high levels of an irritating vapor, fume, or smoke. In most instances, the high level exposure was the result of an accident occurring in the workplace or a situation where there was poor ventilation and limited air exchange in the area. In all cases, symptoms developed within a few hours and often minutes after exposure. We have designated the illness as reactive airway dysfunction syndrome (RADS) because a consistent physiologic accompaniment was airways hyperreactivity. When tested, all subjects showed positive methacholine challenge tests. No documented preexisting respiratory illness was identified nor did subjects relate past respiratory complaints. In two subjects, atopy was documented, but in all others, no evidence of allergy was identified. In the majority of the cases, there was persistence of respiratory symptoms and continuation of airways hyperreactivity for more than one year and often several years after the incident. The incriminated etiologic agent varied, but all shared a common characteristic of being irritant in nature. In two cases, bronchial biopsy specimens were available, and an airways inflammatory response was noted. This investigation suggests acute high level, uncontrolled irritant exposures may cause an asthma-like syndrome in some individuals which is different from typical occupational asthma. It can lead to long-term sequelae and chronic airways disease. Nonimmunologic mechanisms seem operative in the pathogenesis of this syndrome.

Phil Lieberman, M.D.

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