by: firoozeh m,m.d. work in textile industry, as an occupational hazard from 300 years ago. ...
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Byssinosis & Other Textile Dust related Lung diseases
By: Firoozeh M,M.D
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History
Work in textile industry , as an occupational hazard from 300 years ago.
Peculiar form of asthma among card Flax & hemp workers (Ramazzini 18th century).
Cotton dust standards & medical surveillance in the 1970 in United states.
Increasing prevalence rates in the developing countries.
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Although Natural fibers are common limited numbers can be used for textile:
1-Physical properties Length Strength Pliability Elasticity
2- Difficulty in physically separating cellulose fibers from other vegetable components.
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Early phases of the process are dustier
( Opening, Picking, Carding)
Dissemination of respirable fine dusts in grounding by mechanical separator
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Pathogenesis
Etiologic agents and pathogenesis Remain unclear.
The most common hypotheses: The release of mediators. Immunologic mechanisms. Airway reactions to specific dust components.
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Release of mediators
Cross shift changes in exposure:
Release of both performed & de novo synthesized mediators.
Elevated levels of histamine in cotton workers Higher levels on the first day of re-exposure & related to
level of dust exposure Lower blood levels of histamine in continuouse exposure Histamine associated with only a short time airway response No consistent block of reactions with antihistamines but
mast cell stabilizers blunt the response.
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Immunologic mechanisms
1. Immediate hypersensitivity
2. Immune complex formation
3. Complement activation
Long period of time before onset of symptoms(indicate sensitization)
Slow progressive damage Delay onset of symptoms
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specific cotton dust components At least 50 biologically active components
Endotoxin
- A good index of acute bronchoconstrictor esponse
- Not the principal bronchoconstricting agent
Tannins
- PMN recruitment
- Plt aggregation , mediator release
- Toxic effect on respiratory epithelial & endothelial cells
- Inhibits chloride secretion of airway epithelium
- Desensitizing tracheal epithelial cells to β agonists
- Don’t produce direct airway construction
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Clinical features1- Work related respiratory complaints (Monday symptoms)
2- Changes in pulmonary function
After working a number of years,worker describes chest tightness beginning on the first day of work week afternoons.
The tightness subsides that evening , worker is well in reminder of week , and re-experience symptoms on the first day of following work weeks.
Symptoms may continue unchanged or progress
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Clinical features
At chronic phase :
- Exertional dyspnea
- Non productive cough
Across shift decrease in lung function,which maybe present on other work days even in absence of symptoms.
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Grading
0 : NL,No symptoms of chest tightness or cough. ½ : Occasional chest tightness or cough or both on 1th
day of working week. 1 : chest tightness on every 1th day of working week. 2 : chest tightness on every 1th day & other days of the
working week. 3 : Grade 2 symptoms + permanent ventilatory
incapacity.
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In addition to classic byssinosis ,other symptoms:
Mill fever : Fever,cough,chill,rhinitis at first contact with mill or
return after prolong absence . chest tightness(-)
Weaver’s cough: Asthmatic condition with fever in new &
senior workers,persist for months.
Mattress makers’ fever: Acute outbreak of fever &
constitutional symptoms,in using low grade cotton.
Chronic bronchitis
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Mortality
Signficant mortality from non malignant respiratory diseases, specially chronic lung diseases.
Low mortality rates from lung cancer .
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Diagnosis
History Physical examination Lung function Lab evaluation Challenge testing Immunologic testig
Across shift Reduction in change in FEV1 FEV1
F0 None(<5%) None(>80%)
F1/2 Slight(6-12%) None
F1 Definite(>20%) None
F2 Slight/moderate (60-75%) F3 Moderate/Severe (<60%)
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Treatment
Bronchodilating agents Antihistamines Disodium cromoglycate Aerosolized Steroids
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Prevention
Dust abatement Medical surveillance with transfer policies for
affected workers Treatment of raw cotton to eliminate toxic factors Smoking cessation
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OSHA standards Medical surveillance
- PFT annually
- If baseline Lung function is < 80% predicted
or decrease of FEV1> 5-10% over work shift
PFT semiannually.
- If Lung function is < 60% predicted refer to complete examination.
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COPD
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Definition:
Presence of cough with phlegm at least 3 months, for at least 2 years.
Progressive Airflow limitation that is not fully reversible.
Abnormal inflamatory response of lung to noxious particles or gases.
Morbidity Prevalence :4% in united states
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Risk factors:
- Tobacco smoke
- Occupational dust & chemicals
- Indoor/Outdoor air pollution
Occupational COPD:
Chronic bronchitis in a patient with hx of chronic exposure to pro-inflammatory agents in workplace air.
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Epidemiology
Ranked as the 4th leading cause of death. Ranked as 12th leading cause of disability. Increase with age. Equal prevalence among men & women. The rate increasing faster among women. Occupational exposures:15% of burden of COPD.
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Occupational risk factors
Chronic or repeated exposure to: Organic particulate matter Bioaerosols Combustion products Mineral/metal particulate matter or fume Irritant gases & vapours
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Mineral particulate & fibers
Mining ,tunnelling,building & road construction,cement work,stone carving,farming,…
Prevalence rate of COPD in non-smoker miners:20%
in smoker miners: 60% Silica exposure: Higher COPD retes , mortality from
bronchitis, emphysema & asthma Asbestos & Carbon black exposure: airflow obstruction
& COPD
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Metal fumes,Irritant gases,Combustion products
Mining,smelter workers,rubber manufacturing,
welders, fire fighters,…
Risk higher among atopic workers
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Organic dusts
Textiles, agricultur, baking ,wood & paper industries.
Exposure to Allergenic & non allergenic organic
dusts:
Asthma
HP
COPD & chronic bronchitis
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Agriculture
Inflammatory process in the airway from: Dusts : grains,animal feed,soils Gases & Fumes: manure gases & disinfectants Micro-organisms: endotoxin & fungal components
Chronic airway disease
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Environmental tobacco smoke in workplace
In non smoker emploees in high ETS exposure :
Airflow obstruction Hair levels of nicotine
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Assessment of exposure
Detailed occupational history (specially for dusts,gases,fume exposure)
Ask about the year of beginning & ending the job(duration).
How often exposed to dusts,gases,fume ?(intensity)
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Management
For the patient still exposed to hazards:
recommendation should be made to reduce or eliminate the exposure.
For the patient no longer exposed to hazards:
the disease should be labelled as potentially occupational.
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Prevention
Rapid decline in FEV1(but still in the NL range) in young exposed workers worse prognosis.
Patient should be made aware of his /her decline in Pulmonary function .
Increase recognition & reporting of disease. Willingness of employers to act to reduce
exposure to hazards.
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