Byssinosis & Other Textile Dust

related Lung diseases

By: Firoozeh M,M.D

 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.
 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.
 Early phases of the process are dustier
( Opening, Picking, Carding)

 Dissemination of respirable fine dusts in

grounding by mechanical separator
Pathogenesis

 Etiologic agents and pathogenesis Remain

unclear.

 The most common hypotheses:

 The release of mediators.
 Immunologic mechanisms.
 Airway reactions to specific dust components.
 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.
 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
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
Clinical features
1- 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
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.
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.
 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
Mortality

 Signficant mortality from non malignant

respiratory diseases, specially chronic lung
diseases.

 Low mortality rates from lung cancer .

Diagnosis

 History
 Physical examination
 Lung function Across shift Reduction in
change in FEV1 FEV1
 Lab evaluation
F0 None(<5%) None(>80%)
 Challenge testing
F1/2 Slight(6-12%) None
 Immunologic testigF1 Definite(>20%) None

F2 Slight/moderate
(60-75%)
F3 Moderate/Severe
(<60%)
Treatment

 Bronchodilating agents
 Antihistamines
 Disodium cromoglycate
 Aerosolized Steroids
Prevention

 Dust abatement
 Medical surveillance with transfer policies for
affected workers
 Treatment of raw cotton to eliminate toxic factors
 Smoking cessation
 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.
COPD
 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
 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.
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.
Occupational risk factors

Chronic or repeated exposure to:

 Organic particulate matter
 Bioaerosols
 Combustion products
 Mineral/metal particulate matter or fume
 Irritant gases & vapours
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
Metal fumes,Irritant gases,Combustion products

 Mining,smelter workers,rubber manufacturing,

welders, fire fighters,…

 Risk higher among atopic workers

Organic dusts

 Textiles, agricultur, baking ,wood & paper

industries.
 Exposure to Allergenic & non allergenic organic
dusts:
Asthma
HP
COPD & chronic bronchitis
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

Environmental tobacco smoke in workplace

In non smoker emploees in high ETS exposure :

Airflow obstruction
 Hair levels of nicotine
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)

 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.
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.