Animal Derived Thiol Induced Work Exacerbated Asthma: A Brief Case Report of a Unique Workplace Hazard.
A 33 year old female healthcare worker with a history of cough variant asthma presented to the occupational health clinic with 2 weeks of dyspnea and cough that she believed to be due to recurring exposure to skunk spray. The patient reported that her asthma was typically well controlled requiring use of a short acting bronchodilator only twice per year for the past 6 years. Two weeks prior to presentation, she and coworkers began noticing the distinct odor of skunk spray in the temporary clinic building in which they were presently working while their usual location in the main hospital facility underwent renovations. They also witnessed at least one striped skunk traveling under the structure. Repeated attempts by pest control authorities to trap and remove the animal(s) had been unsuccessful. Several coworkers had experienced eye irritation, nausea, and headaches after working in the building, but no others experienced respiratory effects.
The patient's initial physical examination at presentation was remarkable for witnessed conversational dyspnea, but without any obvious adventitious sounds on lung auscultation. Initial spirometry showed a forced expiratory volume at one second (FEV1) of 2.97 L (92% of predicted NHANES III reference values); however, the patient had used her levalbuterol bronchodilator shortly before presenting for evaluation. The patient opted to take a day of sick leave before the weekend, which allowed her to have 3 days away from work. The following Monday, she presented for follow-up evaluation. She reported resolution of symptoms within 12 hours of leaving the temporary clinic, and denied any use of bronchodilators over the weekend. Before this visit, she had worked for less than an hour in the area where the skunk odor persisted. Spirometry at this time noted an FEV1 of 2.62 L (81% predicted). Based on this objective reduction in respiratory function, we recommended to her supervisors that she be temporarily removed from the current work environment, at least until the reported skunks could be captured and removed. Unfortunately, this did not occur immediately and the patient continued to complain daily of cough and dyspnea beginning within one hour of starting work in the temporary clinic building. She managed to work through the day with 3 to 4 bronchodilator administrations each day. The upcoming weekend included a holiday, and the patient spent 4 days away from work over a holiday weekend.
In the interim, occupational health and industrial hygiene conducted a review of organic chemistry literature to better understand what, if any, possible respiratory or mucus membranes irritants were contained within striped skunk spray that might explain the patient's presentation. This review found that 2 thiols, (E)2-butene-1-thiol and 3-methyl-1-butanethiol, are primarily responsible for the odor of striped skunk spray. (1, 2) Thiols are organic compounds containing a carbon-bonded sulfhydryl (R-SH) group that were historically known as mercaptans. (1) The structurally related thiol 1-butanethiol (also known as 1-butyl-mercaptan) is known to have a potent skunk-like odor with a low detection threshold, and was once believed to have been the primary thiol in skunk spray. (1, 3) As such, it has found use as an additive to natural gas to provide the putrid odor for leak detection, and may also be used as an industrial solvent.4 1-butanethiol has established occupational exposure limits by both the Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health and is a known mucus membrane and respiratory irritant. (5) Researchers from the California Environmental Protection Agency had also previously hypothesized that the release of butyl mercaptan, a known degradation product of cotton defoliants, may have contributed to an increased proportion of respiratory-related mortality in cotton-growing areas of the San Joaquin Valley. (6)
The patient returned for follow-up and pre-exposure spirometry following her 4-day absence from the temporary clinic. At this visit, she reported again cessation of symptoms after 12 hours outside the clinic, but stated she had return of cough and subjective dyspnea for about one hour after passing through skunk odor while driving in a rural area. She required no bronchodilator use during this 4-day absence from the temporary clinic. Pre-exposure spirometry was obtained, and the patient was noted to have an FEV1 of 2.97 L (92% predicted) again. She then returned to work in the temporary clinic. Within one hour of exposure, the previously reported developed cough and subjective dyspnea resumed. She then returned, as instructed, to the occupational health clinic after approximately 4 hours of work and before using her bronchodilator. A repeat postexposure spirometry found the FEV1 to be at 2.62 L (81% predicted), again noting a 350 mL and 11% reduction in FEV1. After this second documented detriment in FEV1 following presumed exposure to the noted skunk odor, we obtained permission from the patient to discuss the findings with her supervisors in order to help them understand why the patient was becoming ill at work. We informed the patient's supervisors that she displayed objective evidence of respiratory decline upon returning to the temporary clinic environment, and that we had determined that components of the skunk spray were very likely to cause respiratory irritation at sufficient concentrations. After providing this information, management agreed to relocate the patient to an alternate clinic area until either the skunk(s) could be trapped or until the clinic moved back into its permanent location inside the main hospital facility. Respiratory protection was considered with organic vapor cartridges, but this was rapidly dismissed as unfeasible due to the potential for alarming clinic patients with its appearance, and the reduced ability to communicate. Upon being moved to the alternate clinic facility, the patient again noted cessation of dyspnea, cough, and bronchodilator use within 12 hours after removal from the skunk odor. Pest control efforts continued in the coming weeks at trapping and removal of the skunk(s), but were apparently not successful.
A follow-up visit after working in an alternate clinic for one week found the patient's FEV1 to be 2.90 L (90% predicted) and she had not required bronchodilator use in 6 days. She continued to report no recurrence of cough or dyspnea since no longer being exposed to the skunk odor. Six weeks later, she returned to working with her primary clinic when it was moved back to its location within the main hospital. Symptoms have not returned in the months since return to the primary clinic location.
Work-exacerbated asthma has been reported to occur in up to 25% of working persons with asthma.7 Healthcare workers are a recognized occupation at risk for work-exacerbated asthma, traditionally due to the use of compounds such latex, formaldehyde, glutaraldehyde, chlorhexidine, antibiotics, and detergent enzymes in healthcare.7,8 Thiols would not generally be expected to contribute to work-exacerbated asthma in healthcare workers. However, in this case, we postulate that given the structural similarities among the thiols associated with industrial use and the thiols created in skunk spray, it is likely that the patient experienced thiol-induced respiratory irritation which exacerbated her underlying asthma, initiated symptoms of cough and dyspnea, and induced mild airway obstruction.
Available literature on the specific toxic effects of striped skunk spray in humans is very rare, aside from the expected anecdotal comments about its repulsive odor and resultant success as a deterrent. One physician in rural 19th century Virginia reported a single instance of a schoolboy prank gone wrong when 2 students held down another student, and forced him to inhale from a bottle of "perfume from the skunk or pole-cat." (9) The physician related that the forced inhalational exposure of skunk musk resulted in "A total unconsciousness, relaxation of muscular system, extremities cool, pupils natural, breathing normal, pulse 65, temperature 91[degrees]; in which condition he remained for one hour." Indeed, 1-butanethiol is also recognized as a central nervous system depressant. (3) The veterinary literature suggests that at least canines may be susceptible to a skunk thiol induced hemolytic anemia, but no similar reports are noted in the human medical literature. (10)
We believe this to be the only reported case of skunk thiol irritant-induced, work-exacerbated asthma. Although this is a likely an exceedingly rare occurrence and possibly unique to this particular patient, we felt it appropriate to report this observation as both management and coworkers initially found it difficult to take the patient's respiratory complaints seriously. They believed that the odor was "just a bad smell" and could not possibly have deleterious health effects on workers. It is possible that similar effects could be observed in occupations with greater likelihood of skunk exposure, such as pest control or wildlife management authorities. Our observation of the chemical similarities between skunk-associated thiols and thiols that are known occupational chemical hazards was a key factor in getting the patient removed from what we believed to be a hazardous, albeit unique, working environment for this patient. This case is also a reminder that the investigation of potential causes of occupational asthma or work-exacerbated asthma may require a multidisciplinary approach with occupational medicine, industrial hygiene, safety officers, and pulmonary medicine.
(1.) Wood WF. The history of skunk defensive secretion research. Chem Educat. 2000;4(2):44-50.
(2.) Wood WF. New components in defensive secretion of the striped skunk, Mephitis mephitis. J Chem Ecol. 1990;16(6):2057-2065.
(3.) Occupational Safety and Health Administration. Chemical Sampling Information: Butyl mercaptan [internet]. Available at: https://www.osha.gov/ dts/chemicalsampling/data/CH_223600.html. Accessed October 2, 2018.
(4.) Haz-Map: Occupational Hazards Database [database online]. Bethesda, MD: National Library of Medicine. Last updated October 2018. Available at: https://hazmap.nlm.nih.gov/. Accessed October 2, 2018.
(5.) National Institute for Occupational Safety and Health (NIOSH). n-Butyl mercaptan. NIOSH Pocket Guide to Chemical Hazards. Available at: http://www.cdc.gov/niosh/npg/npgd0083.html. Accessed October 2, 2018.
(6.) Ames RG, Gregson J. Mortality following cotton defoliation: San Joaquin Valley, California, 1970-1990. J Occup Environ Med. 1995;37(7):812-819.
(7.) Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med. 2014;370(7):640-649.
(8.) Szema AM. Work-exacerbated asthma. Clin Chest Med. 2012;33(4):617-624.
(9.) Conway WB. A new anaesthetic. Virginia Medical Monthly. July 28 1881;8:359.
(10.) Zaks KL, Tan EO, Thrall MA. Heinz body anemia in a dog that had been sprayed with skunk musk. J Am Vet Med Assoc. 2005;226(9):1516-1518, 1500.
When this report was prepared, LTC Downs was with the Department of Preventive Medicine, Blanchfield Community Hospital, Fort Campbell, Kentucky.
Mr Renshaw is Chief, Industrial Hygiene Service, Department of Preventive Medicine, Blanchfield Community Hospital, Fort Campbell, Kentucky.
LTC John W. Downs, MC, USA
Joshua M. Renshaw, MS
|Printer friendly Cite/link Email Feedback|
|Author:||Downs, John W.; Renshaw, Joshua M.|
|Publication:||U.S. Army Medical Department Journal|
|Date:||Jul 1, 2018|
|Previous Article:||Application of High Energy Extracorporeal Shockwave Therapy on Musculoskeletal Conditions in US Military Medical Facilities.|