NIKEN RAHMATIA-Learning Objective

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 Pathogenesis
• From an occupational health point of view, dust is
classified by
size into following categories:
• Inhalable Dust: is the one which enters the body, but
is trapped in the nose, throat, and upper respiratory
tract. Particle size is usually 6-25μm.
• Respirable Dust: particles that are small enough to
penetrate the nose and upper respiratory system
beyond the body's natural clearance mechanisms
of cilia and mucous and are more likely to be
retained in the lungs. Particle size is usually 1-5μm.
• Particles of <1 μm are exhaled out.
Pathogenesis
Pathogenesis
 Pathophysiology
 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
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
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
 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)

Occupational disease
WHO (1985) :

 Occupational Disease :
“ the relationship to specific causative factors at
work has been fully established and the factors
concerned can be identified, measured and
eventually controlled “
• Work Related Disease :
“ maybe partially caused by adverse working
conditions. They maybe aggravated, accelerated
or exacerbated by workplace exposures and
may impair working capacity.
Personal characteristic, environmental and
socio cultural factors usually play a role as risk
factors and are often more common than
occupational disease “
Occupational Medicine Practice (1996) :

 Occupational Disease :
“ occur as a result of exposure to
physical, chemical, biological,
ergonomic or psychososial
factors in the work place “
Di Indonesia
 Penyakit Akibat Kerja (Occupational Disease)
a. Permennaker No.01/Men/1981  PAK
b. Keppres RI no 22 thn 1993  PAHK
 Perbedaan Occupational Disease dan Work
Related Disease
 Terjadi hanya diantara populasi
pekerja (occurs mainly among
working population)
 Penyebab spesifik
 Adanya paparan di tempat kerja
merupakan hal yang penting
 Tercatat dan mendapatkan ganti
rugi (notifiable and compensable)
 Terjadi juga pada populasi
penduduk (occurs largely in the
community)
 Penyebab multi faktor
 Pemaparan di tempat kerja
mungkin merupakan salah satu
faktor
 Mungkin tercatat dan mungkin
dapat ganti rugi (maybe notifiable
and compensable)
Peraturan Perundangan
 Kep.pres. No.22 tahun 1993
 Per.men. No. Per. 02/Men/1980
 Per.men. No. Per. 01/Men/1981
 Kep.men. No. Kep. 333 th.1989
 Kep.men. No. 62A tahun 1992
 U U No.3 Th.1992 Jamsostek
Pharmacological theraphy Byssinosis

Morbidity & Mortality: 2009 Chart Book on Cardiovascular, Lung and Blood Diseases. 2009.