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 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

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 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%)

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.