Hypersensitivity pneumonitis from ordinary residential exposures: University of Rochester School of Medicine and Wayne State University College of Pharmacy and Allied Health Professions - Grand Rounds in Environmental Medicine

Environmental Health Perspectives, Sept, 2001 by Michael J. Apostolakos, Harold Rossmoore, William S. Beckett

A previously healthy woman developed hypersensitivity pneumonitis of such severity that she required chronic systemic corticosteroid therapy for symptom control. Detailed investigation of her workplace and home environments revealed fungi in her typical suburban home, to which she had specific serum precipitating antibodies. Efforts to remove mold from the home were unsuccessful in relieving symptoms, and moving to another residence was the only intervention that allowed her to be withdrawn from corticosteroid therapy. Hypersensitivity pneumonitis is commonly associated with occupational or avocational exposures, such as moldy hay in farmers or bird antigen in bird breeders. We propose that hypersensitivity pneumonitis may occur in North America, as it does in Japan, from domestic exposures alone. Key words: Aureobasidium pullulans, extrinsic allergic alveolitis, fungal diseases, humidifier fever, hypersensitivity pneumonitis, indoor air quality, Saccharopolyspora rectivirgula. Environ Health Perspect 109:979-981 (2001). [Online 12 September 2001]

http://ehpnet1.niehs.nih.gov/docs/2001/109p979-981apostolakos /abstract.html

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Case Presentation

A 50-year-old, nonsmoking automobile parts assembly worker presented with summertime cough for 8 years, and breathing difficulty with exercise for several months. She denied fever. The patient's chest X ray was interpreted as being within normal limits (Figure 1). She was initially treated by her primary physician for presumed asthma with an inhaled beta agonist, which brought no relief. The patient was then treated with a brief course of oral prednisone, which brought symptomatic relief. She was referred to a pulmonologist, who heard crackles on her chest exam, but detected no palpable lymphadenopathy. Spirometry on 15 November 2000 was within normal limits (Table 1), but oxygen desaturation occurred with 2 min of brisk walking. Two weeks later (29 November 2000) spirometry showed a 600 mL loss in forced vital capacity (FVC) to 73% predicted (Table 1). High-resolution computed tomography scan of the chest showed ground glass opacities bilaterally and peripherally (Figure 2). Bronchoalveolar lavage fluid contained 60% lymphocytes (normal [less than or equal to] 20%), 30% macrophages, and 10% polymorphonuclear leukocytes. A trans-bronchial biopsy was nondiagnostic due to inadequate tissue. Serum precipitating antibodies were measured on a standard, commercially available hypersensitivity pneumonitis panel of 10 antibodies to 10 common antigens. Serum precipitating antibodies were present to Aureobasidium pullulans and Saccharopolyspora rectivirgula. Symptoms had been most troublesome during hot summer months.

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In her job, the patient assembled small parts using a petroleum distillate lubricant applied from a small squeeze bottle. She did not work with metal working fluids herself, but metal working fluids were used near her work area. A sample of the petroleum metal working fluid from the area closest to her work area was cultured for fungi and thermophilic actinomycetes, and yielded < 1 colony-forming unit (CFU)/mL fluid.

The patient's home was heated by oil forced air and cooled by a window-mounted air conditioner; she had one dog and one cat, but no birds. The unfinished basement of her house had evidence of mold growth on the cement wall (Figure 3). Thick fiberglass insulation, mounted on plastic sheeting, covered all four walls of the basement (Figure 4). The patient reported having a major water leak from the second floor, along a wall surface, to the floors below 2 years earlier, but she noted no water damage to carpets. There were no sources of water aerosol other than faucets and a shower head. Several months before her diagnosis, she had activated 30-40 aerosol cans of insecticide (each containing 71 g 1% pyrethrins and permethrins) indoors because of fleas on her pet dog and cat. She vacated the house for the recommended 30 min and did not note worsening respiratory symptoms with use of this insecticide.

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Water from the basement sump, fiberglass insulation from the basement, and carpeting from the living room were cultured and examined microscopically. Fiberglass produced 3.5 x [10.sup.5] CFU fungi/g, identified as Aureobasidium pullulans; 4.4 x [10.sup.4] CFU/g Humicola species; and 1.0 x [10.sup.3] CFU/g of material identified as thermoactinomycetes with morphology similar to Sacharopolyspora rectivirgula. Carpet produced 6.0 x [10.sup.3] CFU/g Aureobasidium pullulans, Curvularia species, and Humicola species.

After the initial 1 week of 20 mg prednisone bid (twice per day), the patient's symptoms had completely subsided, her lung crackles had cleared, and her diffusing capacity had increased from 45% predicted to 71% predicted (6 December 2000). The prednisone dose was then reduced. The patient remained asymptomatic with normal spirometry and continued to work as before. However, she began to suffer central nervous system effects of the prednisone, which was then discontinued. She traveled to Florida for 1 week. While she was away from her home and job, she felt well. On returning, the patient's spirometry was normal and she had no exercise-induced hypoxemia. After not taking prednisone for 5 weeks and resuming her usual home and work environments for over 4 weeks, the patient's dyspnea on exertion gradually returned, her [FEV.sub.1] and FVC fell, and her [O.sub.2] saturation decreased to 87% with exercise (Table 1). At that time, all fiberglass from her basement was removed and the carpets were cleaned. The patient's condition improved rapidly with reinstitution of 20 mg prednisone daily. However, when the prednisone dose was tapered, she again became symptomatic.