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Acute Respiratory Illness Following Occupational Exposure to Wood Chips -- Ohio

The inhalation of organic dust contaminated with microbes has been recognized as an occupational hazard for persons who work with decomposing vegetable matter (1-6). An outbreak of illness caused by such inhalation occurred in Ohio in 1983. The investigation that followed is described below.

On June 21, 1983, five employees at a municipal golf course became ill with an influenza-like syndrome within hours after manually unloading a trailer truck full of wood chips. Physicians from the city health department examined and tested all golf-course employees who had helped in the unloading and requested assistance from the National Institute for Occupational Safety and Health in evaluating the outbreak (7). On June 24, a questionnaire was administered to those employees exposed to wood chips, and their medical records were reviewed. The investigators inspected the unloaded wood chips, collected samples, and interviewed the wood chips' vendor.

The wood chips were brought to the golf course in an enclosed, 40-foot trailer. Eleven employees participated in some aspect of the unloading process. Although fresh chips had been ordered, the vendor included old chips that had been stored in the front of the truck for approximately 1 year. Unloaded chips from the front were grossly moldy, and cultures revealed a wide variety of mesophilic and thermophilic bacteria and fungi.

A case was defined as the presence in an employee of at least five of the following six symptoms after exposure to the wood chips: malaise, fever, difficulty breathing, chest tightness, headache, and cough. Except for cough, which was reported by two persons who did not meet the case definitions, each symptom was reported more frequently by ill persons than by well persons (p 0.05) (Table 1).

All five ill employees had worked in very dusty conditions without respiratory protection while unloading the front of the trailer on the afternoon of June 21. The time from beginning of unloading until onset of illness ranged from 4 hours to 16 hours (median 13 hours). None of the workers were hospitalized, but one reported to a local emergency room, and two were too ill to work the following day. Within 48 hours, symptoms were very much improved; within 72 hours, all affected workers had completely recovered.

The other six employees included three who had unloaded fresh chips from the back of the trailer on the morning of June 21, one supervisor who had briefly checked on the unloading process, and two workers who finished unloading the front of the trailer on the morning of June 22 but wore air-purifying respirators. Thus, all five workers who had unloaded the moldy wood chips without respiratory protection became ill, compared with none of the other six workers.

The mean total white blood count in ill workers (11,000) was significantly higher than in those who remained well (8,100); a significantly greater mean absolute polymorphonuclear leukocyte count was also found among the ill (ill: 8,300, well: 5,600) (p = 0.008). The erythrocyte sedimentation rate was elevated in all five ill workers but in only two of the six who did not become ill. Except for one individual who had radiographic changes due to previous surgery, all those who became ill had normal chest radiographs and spirometry. Furthermore, none had positive tests for precipitating antibodies against a standard panel of 11 antigens associated with hypersensitivity pneumonitis extracts of three types of wood chips and 12 microbial organisms isolated from the wood chips (8). Tests for complement fixing antibodies as evidence of histoplasmosis produced low titers in both the acute and convalescent sera of the ill workers.

On the basis of clinical and epidemiologic evidence, the investigators concluded that this episode probably represented an outbreak of self-limited, acute toxic reaction associated with inhalation of large amounts of dust heavily contaminated with microbial toxins from decomposing vegetable matter. Reported by P Asmussen, MPH, WL Duff, ER Heidtman, Middletown City Health Dept, CJ Burress, AM Richmond, MD, Middletown Social and Health Center, Ohio; Hazard Evaluations and Technical Assistance Br, Div of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, CDC.

Editorial Note

Editorial Note:In 1975, an apparent toxic pulmonary illness was reported among 10 farmers who became ill several hours after removing moldy silage (1,2). The authors of that report referred to the illness as "pulmonary mycotoxicosis" because the etiology presumably involved toxic components of inhaled fungal organisms (1). Others have recognized an apparently identical syndrome but have applied other names to it. Thus, it has been variously referred to as (1) "silo unloader's syndrome" to contrast it with silo filler's disease, a toxic pulmonary edema following inhalation of the oxides of nitrogen in freshly filled silos (3); (2) "precipitin test negative farmer's lung" to emphasize its clinical similarities to and its pathogenetic differences from farmer's lung disease, an immunologic lung response to microbial antigens in moldy hay (4); and (3) "organic dust toxic syndrome" (ODTS), a generic designation to emphasize that mycotoxin exposure is not a necessary prerequisite and that the syndrome is not restricted to either silo exposures or farming occupations. A striking similarity has been recognized between ODTS and "mill fever" in cotton textile workers, "grain fever" in grain elevator workers, and "humidifier fever" in building occupants exposed to air from highly contaminated ventilation systems (3,5). Similar to the current report, moldy wood chips were etiologically linked to symptoms of ODTS in individuals exposed to dust from wood chips that had been stored in basements as a fuel source for wood-burning furnaces (6).

Epidemiologically, ODTS often occurs in small outbreaks, with illness affecting all or most individuals who have had intense exposure to microbially contaminated vegetable dust (3,9). The syndrome is clinically characterized as an acute febrile illness with respiratory symptoms; onset usually occurs 4-12 hours after exposure. General malaise, headache, and cough are common symptoms, while dyspnea is variably present. Chest auscultation usually reveals normal breath sounds; the chest x-ray is remarkably clear; and pulmonary function may be only slightly impaired. Leukocytosis with a predominance of polymorphonuclear leukocytes is the rule, and serologic testing for precipitating antibodies associated with farmer's lung disease is usually negative.

With removal from exposure, ODTS is a self-limited illness, occasionally resolving within 24 hours, often within several days, and sometimes only after a few weeks. To date, no deaths have been reported, and there is no evidence for residual pulmonary fibrosis. Some individuals, however, have been hospitalized with severe symptoms, and a few have undergone diagnostic bronchoscopy and lung biopsy. Bronchoalveolar lavage has revealed a predominance of PMNs, and biopsy has demonstrated an acute inflammation without granulomas, as well as an assortment of microorganisms in the airways (1).

ODTS probably occurs much more frequently than is currently recognized. Only serious solitary cases or those that occur in suspicious clusters are likely to come to medical attention, and when a history of environmental exposure is elicited, these are often misdiagnosed by physicians as silo filler's disease or farmer's lung disease (3). Because the incidence, etiologic agent(s), and pathogenesis of ODTS remain unknown, physicians are encouraged to report to appropriate health authorities any influenza-like illness following intense exposures to organic dust. Based on current understanding, symptomatic treatment alone should suffice. Prevention measures should include storing vegetable matter in a way that limits microbial growth and wearing appropriate respiratory protection when intense exposure to organic dusts cannot be avoided.


  1. Emanuel DA, Wenzel FJ, Lawton BR. Pulmonary mycotoxicosis. Chest 1975;67:293-7.

  2. Fink JN. A new lung disease? (Letter). Chest 1975;67:254.

  3. Pratt DS, May JJ. Feed-associated respiratory illness in farmers. Arch Environ Health 1984;39:43-8.

  4. Edwards JH, Baker JT, Davies BH. Precipitin test negative farmer's lung--activation of the alternative pathway of complement by moldy hay dusts. Clin Allergy 1974;4:379-88.

  5. Rylander R, ed. International Workshop on Health Effects of Organic Dusts in the Farm Environment. Am J Ind Med (in press).

  6. Malmberg P, Palmgren U, Rask-Andersen. Relationship between symptoms and exposure to mold dust in Swedish farmers. In: International Workshop on Health Effects of Organic Dusts in the Farm Environment. Am J Ind Med (in press).

  7. National Institute for Occupational Safety and Health. Health hazard evaluation report no. HETA 83-327-1402. Cincinnati, Ohio: National Institute for Occupational Safety and Health, 1984.

  8. American Society for Microbiology. A manual of clinical microbiology. 2nd ed. Washington, DC: American Society for Microbiology, 1974.

  9. Emanuel DA. Toxic reactions (pulmonary mycotoxicosis). In: DiSalvo

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