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Outbreaks of Respiratory Illness among Employees in Large Office Buildings -- Tennessee, District of Columbia

Recurring outbreaks of respiratory illness among office workers have led to epidemiologic and environmental investigations and to relocation of some or all occupants of the affected office areas. Outbreaks in two cities are summarized below.

Knoxville, Tennessee: An outbreak of febrile illness began during the afternoon and evening of September 21, 1981. About 40% of the 325 office workers in a seven-story building met the case definition of at least three symptoms (headaches, muscle aches, fever, chills, cough, or wheezing) and a time of onset after 11 a.m. (use of this time of onset helped to exclude individuals with preexisting respiratory conditions that were unrelated to exposures in the building). In most affected individuals, these symptoms subsided by the following morning. Subsequent outbreaks of febrile illness occurred in this same building on October 13 and October 15. After the latter outbreak, building occupants were moved to other office facilities.

In each outbreak, a temporal relationship was observed between starting the heating, ventilation, and air-conditioning (HVAC) system and the onset of symptoms. The HVAC system in this building contained two air washers (components of an air-handler unit that emit a water spray) and was contaminated with bacteria, fungi, protozoa, nematodes, and mites. No single microbial agent could be established as responsible for the outbreaks. The HVAC system was the mode of transmission for the organisms. The building remains vacant.

Washington, D.C.: In late January 1982, a persistent, influenza-like illness was reported among occupants of a large office suite on one floor of an eight-story building. Twelve of 41 employees working in the suite met the case definition of at least two of the following symptoms: headache, muscle aches, chest tightness, feverishness, chills, or nausea occurring on consecutive work days, including the last work day (Friday), with relief on weekends. Tests of the carbon-monoxide-diffusing capacity of affected individuals showed that individuals with two or more symptoms had lower single-breath, carbon-monoxide-diffusing capacities than did controls.

The suite was located directly beneath the kitchen of a cafeteria and had been subjected to a series of "floods" from drainage lines, including a drain from the cafeteria dishwasher. Numerous microorganisms, including Acanthamoeba polyphaga and Thermoactinomyces vulgaris, were isolated from the office and the HVAC system. However, attempts through serologic testing to link these agents specifically with illness in individuals produced inconclusive results. Epidemiologic evidence suggested that environmental contaminants present in the water drainage were associated with illness. All workers were removed from the affected office; the office was completely refurbished and is presently being reoccupied. There has been no recurrence of illness. Reported by Div of Respiratory Disease Studies, National Institute for Occupational Safety and Health, CDC.

Editorial Note

Editorial Note: Outbreaks of hypersensitivity pneumonitis (HP), humidifier fever, and similar syndromes among office workers have been described since 1970 (1,2). Symptoms include headache, fatigue, muscle aches, chills, and fever. Manifestations of pulmonary disease, such as chest tightness, coughing, and wheezing, were also observed. These outbreaks have been attributed to thermophilic actinomycetes, nonpathogenic amoeba, several fungi, and endotoxins (3-6). Sources of microbial contamination included humidifiers, air washers, and contaminated filters in air-handling units.

Since October 1981, the National Institute for Occupational Safety and Health has conducted environmental studies in six large multistory office buildings in which HP-like syndromes were reported or were alleged to occur, including those reported here (7). Results of these studies suggest that moisture incursion into occupied spaces and into HVAC system components may have been common to these outbreaks. Engineering measures thought to prevent the occurrence of such outbreaks are straightforward, feasible, and inexpensive. They include: (1) promptly and permanently repairing all external and internal leaks; (2) maintaining relative humidity below 70% in occupied spaces and in low-air-velocity plenums (at higher levels of humidity, the germination and proliferation of fungal spores is enhanced(8,9)); (3) preventing the accumulation of stagnant water under cooling-deck coils of air-handling units through proper inclination and continuous drainage of drain pans; (4) using steam, rather than recirculated water, as a water source for humidifiers in HVAC systems; however, such steam sources should not be contaminated with volatile amines; (5) replacing filters in air-handling units at regular intervals (these should have at least a moderate efficiency rating (50% or more) as measured by the atmospheric-dust spot test (10,11) and should be of the extended-surface type; prefilters (e.g., roll type) should be used before air passage over the higher-efficiency filters); (6) discarding, rather than disinfecting, carpets, upholstery, ceiling tiles, and other porous furnishings that are grossly contaminated; (7) providing outdoor air into ventilation systems at minimum rates per occupant of at least 20 cubic feet per minute in areas where occupants are smoking and at least 5 cubic feet per minute in nonsmoking areas (12). These activities should be considered in on-going preventive-maintenance programs.

References

  1. Arnow PM, Fink JN, Schlueter DP, et al. Early detection of hypersensitivity pneumonitis in office workers. Am J Med 1978;64:236-42.

  2. Kreiss K, Hodgson M. Building associated epidemics. In: J Walsh, C Dudney, E Copenhaver, eds. Indoor air pollution. Boca Raton, Florida: CRC Press, 1984:87-106.

  3. Banaszak EF, Thiede WH, Fink JN. Hypersensitivity pneumonitis due to contamination of an air conditioner. New Engl J Med 1970;283:271-6.

  4. Edwards JH. Microbial and immunological investigations and remedial action after an outbreak of humidifier fever. Br J Ind Med 1980;37:55-62.

  5. Bernstein RS, Sorenson WG, Garabrant D, Reaux C, Treitman RD. Exposures to respirable, airborne Penicillium from a contaminated ventilation system: clinical, environmental and epidemiological aspects. Am Ind Hyg Assoc J 1983;44:161-9.

  6. Rylander R, Haglind P, Lundholm M, Mattsby I, Stenqvist K. Humidifier fever and endotoxin exposure. Clin Allergy 1978;8:511-6.

  7. Morey PR, Hodgson MJ, Sorenson WG, Kullman GK, Rhodes WW, Visvesvara GS. Environmental studies in moldy office buildings: biological agents, sources and preventive measures. Ann Am Conf Gov Ind Hyg (in press).

  8. Block SS. Humidity requirements for mold growth. Appl Microbiol 1953;1:287-93.

  9. Brundrett GW, Onions AHS. Moulds in the home. J Consum Stud Hom Econ 1980;4:311-21.

  10. Barnstable D. Basic considerations for selecting air filters. Plant Engin 1981;45:145-7.

  11. American Society of Heating, Refrigerating, and Air-conditioning Engineers. Method of testing air-cleaning devices used in general ventilation for removing particulate matter. Atlanta, Georgia: ASHRAE, 1976. ASHRAE Standard 52-76.

  12. American Society of Heating, Refrigerating, and Air-conditioning Engineers. Ventilation for acceptable indoor air quality. Atlanta, Georgia: ASHRAE, 1981. ASHRAE Standard 62-1981.



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