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ORGANIC DUST TOXIC SYNDROME

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Organic dust toxic syndrome (ODTS), also known as pulmonary mycotoxicosis, is a nonallergic, noninfectious, respiratory illness caused by the inhalation of organic dust from moldy silage, hay, or other agricultural products. It has been suggested that ODTS is a category of inhalation fever, which includes polymer fume fever and metal fume fever.

Specific Substances

    1) Pulmonary mycotoxicosis
    2) Silo unloader's syndrome
    3) Grain fever
    4) Toxin fever
    5) Humidifier fever
    6) Mushroom worker's lung
    7) Bird fancier's lung
    8) Maple bark stripper's disease
    9) Mill fever
    10) ODTS

Available Forms Sources

    A) SOURCES
    1) Organic dust, especially moldy grains, hay, silage, and wood chips, are solid airborne particles that are in the range of 0.1 to 50 microns or larger in diameter and are suspended in air (Boehmer et al, 2009; Meggs et al, 1994; Sullivan et al, 1992; Rosenstock & Cullen, 1986; Malmberg & Rask-Andersen, 1993; Ye Tingting, Shen Yi-e & Huang Jingxiong et al, 1994; Dutkiewicz et al, 1989) Rask-Andersen, 1989; (Schimberg et al, 1992; Malmberg, 1990).
    2) TYPE OF EXPOSURE
    1) Allergens
    2) Animal Dander
    3) Animal Feathers
    4) Animal Feces
    5) Animal Hair
    6) Animal Urine
    7) Bacteria
    8) Chemical Residues:
    9)
    a) Pesticides
    b) Herbicides
    c) Fungicides
    10) Cotton Dust
    11) Endotoxins
    12) Enzymes
    13) Feed Grains
    14) Fungi
    15) Grain Extracts/Dusts
    16) Gram-negative Bacteria
    17) Hay
    18) Humidifier Mists
    19) Insects/Insect Parts
    20) Mites (and body components)
    21) Molds
    22) Moldy Oranges
    23) Mulch
    24) Mycotoxins
    25) Other Plant Products
    26) Plant Debris
    27) Pollen Grains
    28) Poultry Confinement Dusts
    29) Silage (Hay & Others)
    30) Silica
    31) Silocapping Material
    32) Soil Particles
    33) Spores
    34) Starch Granules
    35) Straw
    36) Swine Confinement Dusts
    37) Trichome Particles
    38) Wood Chips
    3) Organic dust is produced by some mechanical process such as crushing, grinding, abrading, or blasting and may be seen with silo unloading, moldy hay baling, swine confinement areas, and humidifiers (Perry et al, 1998; Mamolen et al, 1993; Donham et al, 1990; May et al, 1986).
    4) A study of 2866 farmers in Finland found that 13.6% had suffered from one or more incidents of acute ODTS. Cattle tending was more often associated with symptoms (14%) than swine tending (8.5%). There was no significant difference between grain growers and cattle-tending farmers related to the development of ODTS (Husman et al, 1990).
    5) One thousand and thirty-two workers in nine industries were studied by a cross-sectional survey questionnaire. Significant association between the prevalence of ODTS symptoms and occupation was found in workers in the grain (4.3%), poultry (5.9%), and mushroom (2.5%) industries. Overlap between the symptoms of allergic alveolitis (AA) and ODTS may account for the identification of mushroom workers, where AA is known to occur (Simpson et al, 1998).
    6) One study evaluated inhalable dust and endotoxin levels in 101 samples from 57 workers in grass, cereal, and vegetable seed plants. In personal samples, endotoxin levels were high [mean 1800 EU/m(3); the recommended exposure limit 50 EU/m(3)], especially in the grass seed extracts [levels up to 274,000 EU/m(3)]. Highest levels of dust and endotoxin were measured during the dumping and mixing job tasks. Whole body assay results revealed that most seed extracts induced a pronounced dose dependent cytokine release. The authors concluded that workers handling grass, cereal, or vegetable seeds are at risk of exposure to high levels of endotoxin-containing seed dust. These exposures can induce inflammatory responses, and cause organic dust toxic syndrome (Smit et al, 2006).
    7) Questionnaires sent to 239 pig farmers and 311 rural controls working in nonagricultural occupations were used to establish the prevalence of ODTS in pig farmers. Pig farmers suffered significantly greater rates of ODTS than controls (6.4% vs. 2.6%, p<0.05). ODTS was associated with symptoms of atopy (OR 3.1, 95%CI 1.2-15.6). An inverse relationship between ODTS and the number of years worked as a pig farmer was found (up to 5 years vs. more than 5 years: OR 5.0, 95%CI 0.8-32.9) indicating that farmers learn to avoid unusually heavy exposure situations (Vogelzang et al, 1999).
    8) Of 92 men and 6 women Swedish farmers who had suffered attacks of ODTS, more than 50% had had two or more attacks. The most common exposure was to moldy grain dust. Most cases occurred in autumn, although ODTS was seen year-round. Clusters of cases occurred 11 times (Malmberg, 1990; Rask-Anderson, 1989).
    9) A convenience sample of 297 people (204 men and 93 women), attending a Nebraska agricultural trade show, were surveyed in this cross-sectional study. ODTS symptoms were described by 107 people (36%). A strong association between handling grains (OR 7.5, 95%CI 4.2-13.5) or work in swine confinement (OR 2.0, 95%CI 1.1-3.4) and the development of chest tightness or cough was seen. Grain sorghum was more likely to have been handled than other grains (OR 2.1, 95%CI 1.3-3.5). The mean values for FVC, FEV1, FEV1/FVC and FEF25-75 among people with a history of ODTS were not significantly different from those without such a history (Von Essen et al, 1999).
    10) Corn, soy bean, and oat grains have been implicated in development of ODTS, but WHEAT GRAIN (especially durum wheat) and barley seem to be the most irritating (Levy, 1994; Meggs et al, 1994).
    11) INCLUDED CONDITIONS
    1) Grain Fever
    2) Inhalation Fever
    3) Mill Fever (Cotton Dust Fever, Byssinosis)
    4) Precipitin-Negative Farmer's Lung Disease
    5) Pulmonary Mycotoxicosis
    6) Silo Unloader's Syndrome
    a) REFERENCES: (Rask-Andersen & Pratt, 1992; Jost et al, 1991; Pratt & May, 1994; May et al, 1986).
    b) "INHALATION FEVER" has been proposed as a unifying term for all previously described febrile attack secondary to organic dust(s) inhalation (ODTS), a condition distinct from extrinsic allergic alveolitis (farmers' lung disease)(Rask-Andersen & Pratt, 1992).
    12) ASSOCIATED DISORDERS
    a) In addition to ORGANIC DUST TOXIC SYNDROME, exposure to organic dusts may result in (Sullivan & Kreiger, 1992):
    1) Occupational Asthma (Reactive Airways Disease)
    2) Extrinsic Allergic Alveolitis (Hypersensitivity Pneumonitis; Acute or Chronic Allergic Disease)
    3) "GRAIN ITCH" (the syndrome called grain itch is caused by a mite found in some grains)
    4) Rhinosinusitis (allergic rhinitis and sinusitis)
    5) Allergic Contact Dermatitis
    13) INCIDENCE
    a) It has been estimated that between 30% and 40% of workers exposed to organic dusts will develop ODTS (Seifert et al, 2003; Sullivan & Kreiger, 1992; Meggs et al, 1994). This is in contrast to estimates that only about 8% of exposed individuals will develop Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis; Farmer's Lung Disease)(Meggs et al, 1994). ODTS is thought to be much more common than Hypersensitivity Pneumonitis (Von Essen et al, 1990). ODTS has been said to be 30 to 50 times more common than Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis) in organic dust-exposed workers (Parker et al, 1992; Malmberg et al, 1988; May et al, 1990).
    b) In an epidemiologic study, 5 (12%) of 43 landscape workers developed acute respiratory illness compatible with ODTS, after prolonged exposure to mulch (greater than or equal to 6 hours/day vs less than 6 hours/day; relative risk = 24.7; 95% confidence interval = 3.3 to 184.9). High levels of Aspergillus spores and endotoxin were found in mulch samples (Boehmer et al, 2009).
    c) In as study of slaughterhouse workers, NONE exposed to a mean total airborne dust level of 6.3 mg/m(3) and a mean airborne endotoxin level of 0.4 mg/m(3) developed ODTS, although 50% of these workers complained of cough and 20% had nasal irritation; smokers reported more symptoms than did nonsmokers (Hagmar et al, 1990a).
    d) Four of 15 Danish refuse plant workers developed symptoms of ODTS after exposure to airborne concentrations of organic dust of 8.1 mg/mm(3) and "germs" of 3 x 10(9) cfu/m(3) (Sigsgaard et al, 1990).
    e) Grain fever (ODTS) may present with fever and chills some hours after completing work in as many as 20% of exposed workers, especially if there has been a two-week absence from exposure or a particularly heavy exposure (Levy, 1994).
    f) Amongst Swedish farmers, as many as one out of each 10 grain dust-exposed individuals may develop ODTS: higher attack rates may be seen in gain elevator workers (Pratt & May, 1994; Malmberg et al, 1990).
    g) About 10% of workers in animal confinement facilities describe having symptoms compatible with ODTS(Pratt & May, 1994). Approximately 7% of Swedish farmers and 14% of Finnish farmers have had at least one episode of symptoms compatible with ODTS (Malmberg & Rask-Andersen, 1993; Husman et al, 1990).
    h) The estimated incidence of ODTS varies from 10 to 190 per 10,000 of the exposed population at risk(Sullivan & Kreiger, 1992).
    i) Amongst one group of 349 Chinese grain processing workers in Shanghai, the prevalence of Grain Dust Fever was approximately 18% in males and 13% in females (Ye Tingting, Shen Yi-e & Huang Jingxiong et al, 1994).
    j) While development of Hypersensitivity Pneumonitis (Extrinsic Alveolitis) may require repeated exposures to the components of organic dusts, development of ODTS may be associated with occasional heavy, acute organic dust exposure (Malmberg et al, 1988).
    k) About 34% of a group of 207 swine confinement workers reported symptoms compatible with ODTS (Donham et al, 1990).
    B) USES
    1) Organic dust is a contaminant and has no beneficial use or role.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) TOXICOLOGY: Organic dust toxic syndrome (ODTS) is a noninfectious febrile illness characterized by lung inflammation and self-limiting systemic inflammatory reaction. ODTS occurs most frequently in agricultural workers exposed to moldy grain, silage hay, and wood chips. Workers in hog confinement barns are at greatest risk for ODTS. Level of endotoxin and Aspergillus fumigatus spore exposure correlates with risk of illness.
    B) EPIDEMIOLOGY: Up to 40% of people working in environments with heavy organic dust contamination may develop ODTS. In one study, about 34% of a group of 207 swine confinement workers reported symptoms compatible with ODTS. Deaths are not reported.
    C) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Fever, chills, myalgias, headache, bronchitis, dyspnea, chest tightness, and cough are common. Nausea, vomiting, skin irritation, pruritus, subacute conjunctivitis, keratitis, leukocytosis and neutrophilia may also occur.
    2) SEVERE TOXICITY: Respiratory failure is rare but has been reported.
    3) ONSET: Generally 4 to 12 hours after exposure.
    4) DURATION: Symptoms generally resolve within 24 hours, but may on occasion last 2 to 5 days.

Laboratory Monitoring

    A) Routine blood work is generally not indicated. Leukocytosis is common.
    B) Consider a chest x-ray in patients with more than mild symptoms or if the diagnosis is in question.
    C) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.

Treatment Overview

    0.4.3) INHALATION EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Administer acetaminophen or NSAIDS for fever. Corticosteroids are not indicated. The key is prevention via maintenance of air quality and use of a respirator in high risk environments. Treat bronchospasm with beta-2 agonist aerosols.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Respiratory failure should be treated with ventilator support and symptomatic and supportive care.
    C) DECONTAMINATION
    1) PREHOSPITAL: Move patient to fresh air; administer oxygen as needed.
    2) HOSPITAL: Decontamination is not indicated.
    D) AIRWAY MANAGEMENT
    1) Respiratory failure is rare, but intubation and mechanical ventilation are occasionally required.
    E) ANTIDOTE
    1) None.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild symptoms (eg, fatigue, fever) can be managed at home. Most patients will not present to a healthcare facility. All patients without respiratory failure should be able to be safely managed at home.
    2) OBSERVATION CRITERIA: Patients with dyspnea or respiratory distress should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: Patients with severe respiratory symptoms or severe comorbidities should be admitted.
    4) CONSULT CRITERIA: Consider toxicology consult in the severely ill patient or in the setting of epidemic exposures. An industrial hygiene evaluation of the workplace and evaluation of the patient by an occupational medicine specialist may be useful.
    G) PITFALLS
    1) Failure to obtain adequate history of exposure.
    H) DIFFERENTIAL DIAGNOSIS
    1) Any pulmonary disease including bronchitis, pneumonia and reactive airway disease. Other exposures would include oxides of nitrogen, metal fume fever and cadmium fume fever or hypersensitivity pneumonitis.

Range Of Toxicity

    A) TOXICITY: While higher concentrations and longer exposures to toxic dusts increase the chances of developing symptoms, a specific exposure-response relationship has not been determined.

Clinical Effects

Summary Of Exposure

    A) TOXICOLOGY: Organic dust toxic syndrome (ODTS) is a noninfectious febrile illness characterized by lung inflammation and self-limiting systemic inflammatory reaction. ODTS occurs most frequently in agricultural workers exposed to moldy grain, silage hay, and wood chips. Workers in hog confinement barns are at greatest risk for ODTS. Level of endotoxin and Aspergillus fumigatus spore exposure correlates with risk of illness.
    B) EPIDEMIOLOGY: Up to 40% of people working in environments with heavy organic dust contamination may develop ODTS. In one study, about 34% of a group of 207 swine confinement workers reported symptoms compatible with ODTS. Deaths are not reported.
    C) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Fever, chills, myalgias, headache, bronchitis, dyspnea, chest tightness, and cough are common. Nausea, vomiting, skin irritation, pruritus, subacute conjunctivitis, keratitis, leukocytosis and neutrophilia may also occur.
    2) SEVERE TOXICITY: Respiratory failure is rare but has been reported.
    3) ONSET: Generally 4 to 12 hours after exposure.
    4) DURATION: Symptoms generally resolve within 24 hours, but may on occasion last 2 to 5 days.

Vital Signs

    3.3.3) TEMPERATURE
    A) Fever greater than 38 degrees celsius and chills are classic symptoms (Boehmer et al, 2009; Perry et al, 1998; Patterson & Yunginger, 1994; Rask-Anderson, 1989; Lecours et al, 1986).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Subacute conjunctivitis and keratitis may occur from grain dust exposure, with hyperemia and watery discharge (Hurst & Dosman, 1990).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Stuffy nose and catarrhal rhinitis have been reported (Husman et al, 1990; Hurst & Dosman, 1990).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FAILURE
    1) Respiratory symptoms of a dry cough, dyspnea, and chest tightness are common. Lung sounds are normal or fine, scattered crackles may be heard. Wheezing may occur (Von Essen et al, 1990). Chest X-ray is usually normal or shows minimal interstitial infiltration and pulmonary function tests are normal or show mild restriction.
    2) Impaired respiratory function with arterial oxygen desaturation may occur in the acute phase (Lecours et al, 1986).
    3) Spirometry performed during a symptom-free interval is usually normal (Rask-Anderson, 1989).
    4) Open lung biopsy in patients with ODTS can show multifocal acute inflammation of terminal bronchioles, alveolar and interstitial areas of exudate consisting of neutrophils and macrophages or acute bronchopneumonia. One to 10-micrometer ovoid organisms demonstrable with methenamine silver stains may be seen and cultures may grow fungal species (Perry et al, 1998; Von Essen et al, 1990).
    5) CASE REPORT (ADULT): A 52-year-old male developed fever, myalgia, and marked dyspnea 12 hours after shoveling composted wood chips and leaves. Inspiratory crackles, hypoxemia and bilateral patchy pulmonary infiltrates were seen. Following supportive treatment and systemic steroid administration, the patient improved over three days. He was asymptomatic at one month and acute and convalescent titers to multiple antigens showed no change (Weber et al, 1993).
    6) CASE REPORT (CHILD): An 11-year-old girl developed ODTS after inhalational dust exposure while cleaning out the upper chamber of a corn dryer. Two hours after exposure she developed a nonproductive cough, substernal burning chest pain, and dyspnea. Lungs were clear to auscultation. Peripheral WBC was 26,000 cells/mL. Chest x-ray was normal. By the second hospital day, the leukocytosis, chest pain, and dyspnea had completely resolved (Patterson & Yunginger, 1994).
    7) CASE REPORTS: Three farmers developed ODTS following exposure to moldy silage. Chest x-rays showed bilateral alveolar and interstitial infiltrates. Two of the farmers became hypoxic and required mechanical ventilatory support and were treated with high-dose steroids. The third patient was treated with supportive care without steroids. All three patients recovered without functional deficits or chest x-ray abnormalities (Perry et al, 1998).
    8) LACK OF EFFECT: Ten dairy farmers in central New York State, who had episodes of ODTS at least 5 years prior, were surveyed by questionnaire and the results compared with a matched group (by occupation, gender, age, and smoking status) in which ODTS had not occurred. There was no difference in respiratory symptoms, no increase in airway reactivity or any decrement in pulmonary function between the groups (May et al, 1990).
    B) ACUTE LUNG INJURY
    1) CASE REPORT: A 41-year-old female developed non-cardiogenic pulmonary edema after inhalation exposure to a large amount of moldy oranges in a storehouse. Symptoms began 4 hours after exposure, progressing to frothy pink sputum and severe dyspnea. Chest x-ray showed patchy consolidation typical of pulmonary edema. Peripheral WBC was 14,500/mm(3) and ABG's were pH 7.41, PO2 47 mmHg, PCO2 35 mmHg. Transbronchial biopsy specimens showed normal alveoli and interstitium without alveolitis or granulomas. The patient was treated with oxygen and antibiotics without steroids. Symptoms resolved over 2 days, and chest x-ray, ABG's, and WBC were normal at 4 days. Re-exposure to the work site for 4 days resulted in similar but milder symptoms without chest x-ray changes (Ye Tingting, Shen Yi-e & Huang Jingxiong et al, 1994).
    2) CASE REPORT: A 26-year-old man developed occupational acute lung injury due to Alternaria alternata (an ubiquitous, dematiaceous and hyphae fungus) after exposure to natural cotton powder for 3 weeks. He presented on 2 separate occasions with acute dyspnea, bilateral inspiratory fine crackles without wheezing and fever. Chest X-ray and CT scan revealed bilateral alveolar opacities. Arterial blood gases revealed pH 7.42, PaO2 55 (7.3 kPa), PaCO2 38 (5 kPa), bicarbonate 24 mmol/L, and SaO2 93%. Cytologic examination of bronchoalveolar lavage fluid showed extracytoplasmic macroconidia of Alternaria species. Although no corticosteroids and antifungal agents were administered, his symptoms resolved gradually within 48 hours (Rivoire et al, 2001).
    C) LEUKOCYTOSIS
    1) Bronchoscopy may show inflammation of the mucosa. A leukocytosis with an increased percentage of neutrophils may be seen in bronchoalveolar lavage (BAL) fluid and fungal spores may be cultured in the lavage fluid as well (Lecours et al, 1986).
    2) Neutrophilia in the bronchoalveolar lavage (BAL) fluid may be replaced by a predominantly lymphocytic infiltrate by seven days (Raymenants et al, 1990).
    D) DISORDER OF RESPIRATORY SYSTEM
    1) It has been suggested that byssinosis (cotton dust-related pulmonary disease) is a form of ODTS and that the pulmonary findings are the same as those seen following exposure to other types of organic dusts. There is extensive animal model and human epidemiologic and exposure level data from cotton dust studies that may be applicable to ODTS (Rylander, 1990).
    2) In an epidemiologic study, 5 (12%) of 43 landscape workers developed acute respiratory illness compatible with ODTS, after prolonged exposure to mulch (greater than or equal to 6 hours/day vs less than 6 hours/day; relative risk = 24.7; 95% confidence interval = 3.3 to 184.9). High levels of Aspergillus spores and endotoxin were found in mulch samples. The following adverse effects were also reported: suspected hypersensitivity pneumonitis (n=4), muscle pain (n=4), chest tightness (n=4),, cough (n=3), dyspnea (n=3), fatigue (n=3), and fever (n=2) (Boehmer et al, 2009).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) INCIDENCE: Headache is reported from 28% to 59% of patients in retrospective questionnaire studies (Rask-Anderson, 1989; May et al, 1986).
    B) MALAISE
    1) INCIDENCE: Malaise is reported in up to 60% of organic dust toxic syndrome patients (May et al, 1986).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting may occur (Von Essen et al, 1990).
    B) LOSS OF APPETITE
    1) INCIDENCE: Anorexia was reported by 60% of college students who developed ODTS after exposure to straw dust (Brinton et al, 1987).
    C) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) In a Swedish study, 57% of patients who had celiac disease reported a history of one or more attacks of organic dust toxic syndrome suggesting a possible etiologic relationship (Axmacher et al, 1990).
    2) A case-controlled questionnaire study of patients with gluten intolerance (celiac disease or dermatitis herpetiformis) demonstrated significantly increased odds ratios for exposure to various farm animals (OR range 1.3-1.8) (Axmacher et al, 1991).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) RESPIRATORY ALKALOSIS
    1) Arterial blood gases may be normal or show mild respiratory alkalosis, mild hypoxemia, and increased arterial-alveolar gradient (Von Essen et al, 1990).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) Leukocytosis to 26,000 WBC/mm(3) and neutrophilia are common (Patterson & Yunginger, 1994; Von Essen et al, 1990).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Skin irritation and pruritus are common among grain handlers. Trichome particles, similar in shape to fiberglass, are a dust constituent and may play a part in direct irritation (Hurst & Dosman, 1990).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) INCIDENCE: Myalgias are reported in up to 76% of ODTS cases (May et al, 1986).
    2) In one study, 4 of 43 landscape workers developed muscle pain after prolonged exposure to mulch (greater than or equal to 6 hours/day vs less than 6 hours/day; relative risk = 24.7; 95% confidence interval = 3.3 to 184.9) (Boehmer et al, 2009).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Routine blood work is generally not indicated. Leukocytosis is common.
    B) Consider a chest x-ray in patients with more than mild symptoms or if the diagnosis is in question.
    C) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Routine blood work is generally not indicated. Leukocytosis is common.
    2) Blood and sputum cultures may be needed to distinguish between ODTS and infectious conditions.
    3) Serum allergic precipitin tests should be obtained to distinguish ODTS from hypersensitivity pneumonitis ("Farmer's Lung"). Patients with ODTS will generally not have reactions to antigens (May et al, 1986).
    B) ACID/BASE
    1) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    4.1.4) OTHER
    A) OTHER
    1) CHEST RADIOGRAPH
    a) Consider a chest x-ray in patients with more than mild symptoms or if the diagnosis is in question.
    2) OTHER
    a) Bronchoscopy with bronchoalveolar lavage or lung biopsy may be indicated in severe cases.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Consider a chest x-ray in patients with more than mild symptoms or if the diagnosis is in question.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with severe respiratory symptoms or severe comorbidities should be admitted.
    6.3.3.2) HOME CRITERIA/INHALATION
    A) Patients with mild symptoms (eg, fatigue, fever) can be managed at home. Most patients will not present to a healthcare facility. All patients without respiratory failure should be able to be safely managed at home.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Consider toxicology consult in the severely ill patient or in the setting of epidemic exposures. An industrial hygiene evaluation of the workplace and evaluation of the patient by an occupational medicine specialist may be useful.
    B) Consultation with a pulmonologist should be considered for patients who exhibit severe hypoxia, bronchospasm unresponsive to standard measures or other significant pulmonary dysfunction, pulmonary edema, who do not improve in the expected time frame, or who are suspected of having allergic alveolitis.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients with dyspnea or respiratory distress should be referred to a healthcare facility.

Monitoring

    A) Routine blood work is generally not indicated. Leukocytosis is common.
    B) Consider a chest x-ray in patients with more than mild symptoms or if the diagnosis is in question.
    C) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Move patient to fresh air; administer oxygen as needed.
    B) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    C) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Inhalation Exposure

    6.7.2) TREATMENT
    A) MONITORING OF PATIENT
    1) Routine blood work is generally not indicated. Leukocytosis is common.
    2) Consider a chest x-ray in patients with more than mild symptoms or if the diagnosis is in question.
    3) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    B) CORTICOSTEROID
    1) Corticosteroids have been used to treat some patients with organic dust toxic syndrome (Von Essen et al, 1990), but there are no studies demonstrating the efficacy of steroids. Most patients recover within a few days with only supportive care.
    2) CASE REPORTS: Two patients with bilateral interstitial infiltrates on chest x-ray, and who required mechanical ventilation, were treated with high-dose steroids. A third patient with infiltrates who did not require mechanical ventilation was treated supportively without steroids. All three patients recovered without residual functional deficits or chest x-ray abnormalities (Perry et al, 1998).
    3) CASE REPORT (ADULT): A 52-year-old man developed fever, myalgia, and marked dyspnea 12 hours after shoveling composted wood chips and leaves. Inspiratory crackles, hypoxemia and bilateral patchy pulmonary infiltrates were seen. Following supportive treatment and systemic steroid administration, the patient improved over three days. He was asymptomatic at one month and acute and convalescent titers to multiple antigens showed no change (Weber et al, 1993).
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

Abstracts

Case Reports

    A) ADULT
    1) Sixty-seven fraternity members were exposed to high levels of straw dust that had been laid on the floor for a party. Eighty-two percent became ill between 1.3 and 13 hours after the party, with muscle aches, cough, and a low-grade fever. Duration of illness ranged from 4.5 hours to 7 days. The risk of illness was higher for those who spent more time at the party. The overall attack rate was 82% with the attack rate of 91% for those spending more than 1 hour at the party and 43% for those spending less than 1 hour at the party (Brinton et al, 1987).
    2) An outbreak of ODTS affecting 16 of 28 workers in a print shop was traced to a humidifier found to be contaminated with fungi, amoebae and gram-negative bacteria. Symptom frequency was fever/chills (94%), myalgia (94%), cough (50%), headache (44%), chest tightness/dyspnea (38%), nausea (31%), coryza (19%), wheezing (13%), sore throat (6%), and diarrhea (6%). The risk of illness was correlated with duration of exposure (Mamolen et al, 1993).
    3) In 2 of 6 normal subjects, exposure to 90 to 100 mg/m(3) of respirable-sized grain dust for 1 to 2 hours caused ODTS (Sullivan et al, 1992).
    4) In one case, a patient developed ODTS after shoveling dusty composted wood chips and leaves; endotoxin concentrations in respirable dust fractions ranged from 636 to 16,300 endotoxin units/m(3) (Weber et al, 1993).

Range Of Toxicity

Summary

    A) TOXICITY: While higher concentrations and longer exposures to toxic dusts increase the chances of developing symptoms, a specific exposure-response relationship has not been determined.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) A specific dose-exposure is usually not possible to determine. The incidence of organic dust toxic syndrome (ODTS) from retrospective questionnaires is between 6% and 36% of exposed individuals (Blanc, 1999; Von Essen et al, 1999).
    B) OCCUPATIONAL
    1) Measurements up to 1,000 mg/m(3) of organic dust have been reported in work areas. Usually the range is between 5 and 50 mg/m(3), with 10% being respirable (Hurst & Dosman, 1990).
    2) Exposure to greater than 90 to 100 mg/m(3) of respirable grain dust for 1 to 2 hours provoked ODTS in two of six subjects (Malmberg, 1990).
    3) Six volunteers were exposed to wood chip mulch dust for 60 to 120 minutes. Total dust concentration ranged from 0.3 to 3.6 mg/m(3). For one particular exposure, the respirable fraction comprised 22% of the 0.8 mg/m(3) total dust concentration. Three of the six volunteers had symptoms consistent with ODTS (Wintermeyer et al, 1997).
    4) On six farms where farmers had developed ODTS, air samples averaged 13 +/- 13 x 10(9) spores/m(3) versus 0.12 +/- 0.2 x 10(9) spores/m(3) on reference farms (Malmberg et al, 1993).
    5) Concentrations of bacterial and fungal markers peptidoglycan and lipopolysaccharide, and respirable dust that produced physiologic changes and symptoms of ODTS were 6.5 (2.7 to 13) mcg/m(3), 1.2 (0.9 to 1.4) mcg/m(3), and 21 (16 to 25) mg/m(3), respectively (Zhiping et al, 1996).
    6) Significant decrements in pulmonary function testing were seen when concentrations of total dust and ammonia were above 2.5 mg/m(3) and 7.5 ppm, respectively, in swine workers (Reynolds et al, 1996).
    7) Twenty-three exposed shacklers in the hanging departments of four poultry slaughter-house plants were examined immediately before work on Monday morning and repeated immediately after work the same day. The mean level of total dust was 6.3 mg/m(3) (range 0.4 to 15.3 mg/m(3)). The mean level of endotoxins was 0.40 mcg/m(3) (range 0.02 to 1.50 mcg/m(3)). Total levels of airborne bacteria (mainly coagulase-negative staphylococci) were 4 x 10(5) to 4 x 10(6) cfu/m(3). Total levels of fungi were 500 to 4000 cfu/m(3).
    a) None of the workers developed any symptoms of ODTS (Hagmar et al, 1990).
    8) In as study of slaughterhouse workers, NONE exposed to a mean total airborne dust level of 6.3 mg/m(3) and a mean airborne endotoxin level of 0.4 mg/m(3) developed ODTS, although 50% of these workers complained of cough and 20% had nasal irritation; smokers reported more symptoms than did nonsmokers (Hagmar et al, 1990a).
    9) Four of 15 Danish refuse plant workers developed symptoms of ODTS after exposure to airborne concentrations of organic dust of 8.1 mg/mm(3) and "germs" of 3 x 10(9) cfu/m(3) (Sigsgaard et al, 1990).

Pharmacology Toxicology

Toxicologic Mechanism

    A) The exact mechanism(s) by which organic dusts produce the organic dust toxic syndrome (ODTS) is (are) not known. It is possible that bacterial or fungal endotoxins play a role. Grain dust extracts have been shown to cause alveolar macrophages to produce IL-1, IL-6, and TNF-alpha, which are known endogenous pyrogens (Von Essen et al, 1990).
    B) Peptidoglycan, endotoxin, and lipopolysaccharide (LPS) markers for microbial exposure, were correlated with IL-6 production in 38 swine house workers. Peptidoglycan was correlated with increased peripheral WBC's and body temperature and LPS was correlated with symptoms of ODTS (Zhiping et al, 1996).
    C) Six volunteers were exposed to wood chip mulch dust. Three of the six had symptoms consistent with ODTS. Peripheral WBC was increased. On bronchoalveolar lavage (BAL), IL-8 was increased and there was borderline elevation of IL-6, consistent with the theory that cytokine networking in the lung may mediate ODTS (Wintermeyer et al, 1997).
    D) There may be a "cascading" effect, wherein activation of pulmonary macrophages triggers phagocytic responses with an infiltration of polymorphonuclear leukocytes in the lungs (Sullivan et al, 1992; Pratt & May, 1994). Complement may be activated in this "cascade," and activated T-cells may respond to inhaled organic dust with release of inflammatory mediators (Sullivan et al, 1992; Pratt & May, 1994; Malmberg & Rask-Andersen, 1993). An IgG mediated reaction is unlikely, as there is an absence of specific precipitins in ODTS (Levy, 1994).

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