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COTTON DUST

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Cotton dust is dust present in the air during the handling or processing of cotton. This dust may contain a mixture of many substances including ground up plant matter, fiber, bacteria, fungi, soil, pesticides, non-cotton matter, and other contaminants.

Specific Substances

    A) No Synonyms were found in group or single elements

Available Forms Sources

    A) SOURCES
    1) Cotton dust is generated into the air as a result of the processing of cotton fibers combined with any naturally occurring materials such as stems, leaves, bracts, and inorganic matter which may have accumulated on the fibers during growing or harvesting.
    2) Dust generated from cotton processing through weaving of fabric and dust generated in other manufacturing processes or operations using new or waste cotton fibers or cotton fiber byproducts from textile mills is considered cotton dust (Sittig, 1985).
    B) USES
    1) Cotton is used in apparel, industrial and household fabrics, upholstery, thread, and medicine (Sax & Lewis, 1987).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Byssinosis is an occupational respiratory disease that occurs in workers who process cotton, hemp, and flax (Levy, 1975).
    B) Inhalation of cotton dust causes chest tightness, cough, wheezing, varying degrees of dyspnea, bronchial asthma, and chronic bronchitis. Smoking may contribute to the severity of respiratory symptoms. Long-term exposure may result in irreversible ventilatory impairment.
    0.2.3) VITAL SIGNS
    A) Fever may be present.
    0.2.4) HEENT
    A) Blepharitis or conjunctivitis may develop in workers.
    0.2.5) CARDIOVASCULAR
    A) Cardiac failure may occur in those with advanced byssinosis.
    0.2.6) RESPIRATORY
    A) Inhalation of cotton dust may cause chest tightness, cough, wheezing, varying degrees of dyspnea, bronchial asthma, and chronic bronchitis.
    B) Smoking may contribute to the severity of respiratory symptoms. Long-term exposure may result in irreversible ventilatory impairment.
    0.2.10) GENITOURINARY
    A) An increase in morbidity of renal disease may be seen in workers.
    0.2.13) HEMATOLOGIC
    A) An increase in white blood cell count may occur.
    0.2.14) DERMATOLOGIC
    A) Eczema may occur.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) There are no know documented reports of specific neoplasms related to cotton.
    0.2.22) OTHER
    A) Workers are susceptible to an increase in the morbidity of rheumatoid arthritis.

Laboratory Monitoring

    A) A decline in FEV1 may be noted. Progressive impairment in lung function may be noted over long periods of time.
    B) There are no specific chest x-ray abnormalities noted in patients with byssinosis.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Due to the nature of this material, ingestion is unlikely.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) OTHER -
    1) Antihistamines and/or bronchodilators may be beneficial in certain limited circumstances (see TREATMENT, INHALATION EXPOSURE SECTION in main document for more information).
    C) PULMONARY EDEMA/NON-CARDIOGENIC -
    1) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.

Range Of Toxicity

    A) In general, toxicity is related to chronic exposure.

Clinical Effects

Summary Of Exposure

    A) Byssinosis is an occupational respiratory disease that occurs in workers who process cotton, hemp, and flax (Levy, 1975).
    B) Inhalation of cotton dust causes chest tightness, cough, wheezing, varying degrees of dyspnea, bronchial asthma, and chronic bronchitis. Smoking may contribute to the severity of respiratory symptoms. Long-term exposure may result in irreversible ventilatory impairment.

Vital Signs

    3.3.1) SUMMARY
    A) Fever may be present.
    3.3.3) TEMPERATURE
    A) Fever may be present (Hathaway et al, 1991; Lewis, 1992).

Heent

    3.4.1) SUMMARY
    A) Blepharitis or conjunctivitis may develop in workers.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Blepharitis or conjunctivitis may develop in workers in processing rooms (Lewis, 1992).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac failure may occur in those with advanced byssinosis.
    3.5.2) CLINICAL EFFECTS
    A) HEART FAILURE
    1) In patients with advanced byssinosis, increasing shortness of breath on exertion causes right ventricular strain that may ultimately lead to cardiac failure (Clayton & Clayton, 1982; Finkel, 1983).

Respiratory

    3.6.1) SUMMARY
    A) Inhalation of cotton dust may cause chest tightness, cough, wheezing, varying degrees of dyspnea, bronchial asthma, and chronic bronchitis.
    B) Smoking may contribute to the severity of respiratory symptoms. Long-term exposure may result in irreversible ventilatory impairment.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) CHEST TIGHTNESS - Symptoms in workers exposed to cotton dust begin with chest tightness, often occurring after a few hours of work (Finkel, 1983; Pickering, 1987; Hathaway et al, 1991).
    2) DYSPNEA - Cough, wheezing, and varying degrees of dyspnea may occur after a few hours of work (Finkel, 1983; Pickering, 1987; Hathaway et al, 1991).
    3) ASTHMA - Bronchial asthma may occur. In a study of cotton textile mill workers, the prevalence of bronchial asthma ranged from 8.5% to 20.5% (Woldeyohannes et al, 1991; Lewis, 1992).
    4) SMOKING - There is evidence to suggest that cigarette smoking contributes to the severity of respiratory symptoms (Levy, 1975; (Clayton & Clayton, 1982).
    5) CHRONIC BRONCHITIS - In a study of cotton textile mill workers, the prevalence of chronic bronchitis ranged from 4% to 24% (Woldeyohannes et al, 1991).
    6) LONG-TERM EXPOSURE - Exposure to cotton dust for at least 10 years -- usually more than 20 years -- may result in irreversible ventilatory impairment; this stage of the disease may be indistinguishable from emphysema or chronic bronchitis (Levy, 1975).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) INHALATION - Increases in stored intraepithelial mucosubstances in the rat respiratory tract were produced by inhalation of 5.3 and 14.5 mg/m(3) endotoxin-contaminated cotton dust for 2 hours/day for 3 days, equivalent to 2.8 and 8.9 mcg/m(3) endotoxin (Gordon & Harkema, 1995).

Genitourinary

    3.10.1) SUMMARY
    A) An increase in morbidity of renal disease may be seen in workers.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) RENAL DISEASE - Workers exposed to cotton dust are susceptible to an increase in morbidity from renal disease (Koskela et al, 1990).

Hematologic

    3.13.1) SUMMARY
    A) An increase in white blood cell count may occur.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) The white blood cell count may be slightly elevated in the acute stage (Rylander, 1982).

Dermatologic

    3.14.1) SUMMARY
    A) Eczema may occur.
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) Eczema may occur in sensitized persons (Lewis, 1992).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) There are no know documented reports of specific neoplasms related to cotton.
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) There are no known documented reports of specific neoplasms related to cotton dust exposure (Clayton & Clayton, 1982).

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A decline in FEV1 may be noted. Progressive impairment in lung function may be noted over long periods of time.
    B) There are no specific chest x-ray abnormalities noted in patients with byssinosis.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) A decline in FEV1 may be noted, particularly during the first day of the working week (Pickering, 1987; Hathaway et al, 1991).
    b) In a long-term study of respiratory function in cotton textile workers, progressive impairment of lung function was noted over a 10-year period (Zuskin et al, 1991).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) There are no specific chest x-ray abnormalities noted in patients with byssinosis (Finkel, 1983; Pickering, 1987).

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) Hospital admission is suggested for patients with moderate symptoms, chest signs, radiologic abnormalities, or impaired oxygenation.

Monitoring

    A) A decline in FEV1 may be noted. Progressive impairment in lung function may be noted over long periods of time.
    B) There are no specific chest x-ray abnormalities noted in patients with byssinosis.

Oral Exposure

    6.5.3) TREATMENT
    A) AT RISK - FINDING
    1) Due to the nature of this material, ingestion exposure is unlikely.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) AIRWAY MANAGEMENT
    1) If symptoms are not relieved by exposure to fresh air, oxygen should be administered until blood gases can be measured. Assisted ventilation may be required if symptoms are severe or prolonged.
    B) 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).
    C) SUPPORT
    1) REDUCTION - COTTON DUST EXPOSURE - PRINCIPAL THERAPEUTIC MODALITY - Transfer to lowest risk areas of mill may be insufficient to alter significantly natural history of disease, and the worker may continue to have symptoms, even after removal from exposure.
    a) Pharmacologic therapy is not a substitute for reduction of exposure and may mask a progressive process (Rosenstock & Cullen, 1986).
    b) Workers who have chest tightness and/or dyspnea on most first working days, those who exhibit a decrease in FEV1 over the work shift of >10% of the preshift value, and those with a preshift FEV1 of <60% of the predicted value should be removed from further dust exposure (Schilling, 1983).
    1) Workers who show less severe effects (eg, preshift FEV1 >60% but less than 80% of predicted value or a work shift decrement of FEV1 >5% of the preshift value) should be reexamined in six months (Schilling, 1983).
    c) Cigarette smokers should not be permitted to work in areas of high exposure to cotton dust (Levy, 1988).
    2) PHARMACOLOGIC TREATMENT - There is no specific pharmacologic therapy for acute byssinosis. Pharmacologic therapy is not a substitute for reduction of cotton dust exposure and may mask a progressive process. Long-term efficacy of pharmacologic intervention, particularly the effect on long-term prognosis, is not known (Rosenstock & Cullen, 1986; Levy, 1988).
    a) Prophylactic preshift administration of bronchodilators and antihistamines to block bronchoconstriction (particularly in individuals with large acute reductions in ventilatory function) may be of value if continued exposure cannot be avoided.
    b) However, symptomatic therapy is not recommended unless dust can be removed from the working environment because of the possibility that continued exposure to cotton dust may lead to the development of persistent or even life-long asthma (Chan-Yeung et al, 1987) Ong, 1987).
    3) BRONCHODILATORS - Use of disodium cromoglycate or beclomethasone, together with beta-adrenergic stimulants, before and during exposure has been recommended to help prevent the recurrence of symptoms (Zuskin, 1975).
    a) However, pharmacologic therapy is not a substitute for reduction of exposure and may mask a progressive process. Long-term efficacy of this intervention is not known (Rosenstock & Cullen, 1986; Schilling, 1983; Levy, 1988).
    4) RECOMMENDATION - (Chan-Yeung et al, 1987) Ong, 1987) - Prophylactic preshift administration of bronchodilators to block bronchoconstriction in workers with large acute reductions in ventilatory function may be of value if continued exposure cannot be avoided.
    a) However, symptomatic therapy is not recommended unless dust can be removed from the working environment because of the possibility that continued exposure to cotton dust may lead to the development of persistent or even lifelong asthma
    b) HISTAMINE ANTAGONISTS - Because antihistamines reduce the effects of dust inhalation on the lungs by blocking the bronchoconstrictor effect, these agents have been recommended to help prevent the recurrence of symptoms (Zuskin, 1975).
    1) However, pharmacologic therapy is not a substitute for reduction of exposure and may mask a progressive process. Long-term efficacy of this intervention is not known (Rosenstock & Cullen, 1986; Schilling, 1983; Levy, 1988).
    a) RECOMMENDATION - (Chan-Yeung et al, 1987) Ong, 1987) - Prophylactic preshift administration of antihistamines to workers with a large acute reduction in ventilatory function may be of value if continued exposure cannot be avoided.
    b) However, symptomatic therapy is not recommended unless dust can be removed from the working environment because of the possibility that continued exposure to cotton dust may lead to the
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) 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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) 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).
    6.9.2) TREATMENT
    A) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) In general, toxicity is related to chronic exposure.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)RAT:
    1) 2 gm/kg (RTECS, 1993)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Work-related respiratory symptoms among 410 grain handlers were more strongly related to the concentration of endotoxin in the dust than to the total dust concentration (Schwartz et al, 1995).
    B) Workers with positive skin tests to cotton dust extract showed greater decreases in FEV(1) over the first year of exposure than did workers who were did not react on skin testing (Li et al, 1995).

Physicochemical

Physical Characteristics

    A) TENACITY (Sax & Lewis, 1987) :
    1) 3 to 6 g/denier (dry)
    2) 4 to 8 g/denier (wet)
    B) ELONGATION: 3% to 7% (Sax & Lewis, 1987)

Molecular Weight

    A) Not applicable

References

General Bibliography

    1) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
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    3) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
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    7) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2C. Toxicology, 3rd ed, John Wiley & Sons, New York, NY, 1982, pp 4380-4383.
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