U.S.

113 ANAK
$14 MILYARD
KELUHAN:
NAPAS PENDEK+WH
LIFE-THREATING
ECES: HEALTH: ASTHMA, ALLERGIES, AND OTHER RESPIRATORY DISORDERS, 23/12/2002

ODONNELL:
- INCREASE CASE
- ONE HAS EVER BEEN ABLE TO
SAY WHAT CAUSES ASTHMA
-POLLUTAN IS A CAUSE IS A
VERY SIGNIFICANT STATEMENT
NORMAN H. EDELMAN:
OZON ASSOCIATED WITH ASTHMA

BRITISH SCIENTIST:

DAVID KING:

SMOKE GUN

POLLUTANT
CAUSE

POLLUTANT

DEVELOPMENT OF
ASTHMA

ASTHMA

GLOBAL
WARNING
ECES: HEALTH: ASTHMA, ALLERGIES, AND OTHER RESPIRATORY DISORDERS, 23/12/2002

U.K.:
1. 17 ANAK
(INCRESE 6X THAN
25 YR AGO
2. 5 JUTA
3. 18.000 BARU
DIAGNOSED/WEEK
4. 1.500 DEATH/YR

PREVALENSI ASMA
(ERJ, 2002)
SELURUH NDIVIDU, 2 12%
PADA PENDERITA RHINITIS ALERGIKA
10 40 %
PENDERITA BRONKIAL
HIPEREAKTIVITI, 3,5 28 %
RENDAH U.K., U.S., AUSTRALIA, NEW
ZELAN, IRLANDIA
TINGGI DI MEDITERIAN COUNTRIES,
ICELAND, EROPA TIMUR DAN INDIA

FAKTOR MENINGKATNYA PREVALENSI

(CHRISTER JANSON, 2002)

GENETIK
EVIRONMENTAL
POLLUTAN
FOOD PEOPLE EAT
GAYA HIDUP
OCCUPATIONAL
EXPOSURE:
BIOLOGICAL &
MINERAL DUST

HYGIENE
INFECTION
EATING HABIT
RURAL
URBAN
ENVIROMENTS
IKLIM
(PADA ANAK)

POLUSI UDARA
Dr. Marian Frieri, can contribute to
asthma inflamation ozon biang keladi
utama
Dr. Jonatan Patz, Johns Hopkins
Blooberg School of Public Health an
important conclution

AGENT

HOST

ENVIRONMENT

AGENT
(ALERGEN)

INFEKSI
NONINFEKSI

HOST:
GENETIK

VIRUS
NONIN
FEKSI

KUMAN

LINGKUNGAN:
POLUTAN
IRITAN

INFLAMASI
HYPERRESPO
NSIVENESS

SESAK

HIPOTESA INFLAMASI
ALERGEN

O3

PAM
SEL MAST

EPITIL
CHEMOTATIC MEDIATOR
LTD4 , PAF, NCF
NETROFIL

O2
RADIKAL

ENZYM
TXA2

Smooth muscle constriction

NERVE

SEKRESI
MENINGKAT

KESEMBABAN
MUKOSA

PENYEMPITAN
S.N
KELUHAN ASMA

SPASME OTOT
POLOS S.N

INFLAMASI
ACTH
IL-1
ECF

INFLAMASI

CORTISOL
KRONIS

RANGSANGAN

TNF
LT
TX
KININ

MEDIATOR
INFLAMASI

AKUT

PATOFISIOLOGI ASMA
-EXAGERATED
CONSTRICTION
-INCREASE
SMOOT MUSCLE
MASS

ACUTE
INNFLAMATION:

SMOTH
MUSCLE
DYSFUC
TION

-INCREASE
RELEASE OF
MEDIATOR

AIRWAY
INFLMATION

AIRWAY
REMODELLING
- CELLULAR ROLIFERATION
>SMOOTH MUSCLE-CELL
>MUCOUS GLAND
-INCREASE MATRIX PROTEIN DEPOSITION

-BASEMEMBRANE THICKENING
-ANGIOGENESIS

-INFLAMATORY
CELLS
ACTIVATION
-INFLAMATORY
MEDIATOR
RELEASE

CHRONIC
INFLAMATION:
-INCREASE
INFLAMATORY
NUMBER
-EPITHELIAL
DAMAGE

ACUTE
INFLAM
ATION

BRONCHOCONSTRI
CTION

CHRONIC
INFLAMA
TION

AIRWAY
REMODELLING

-INCREASE
INFLAMATORY
CELL NUMBER

-CELLULER
PROLIFERATION
INCREASE

-EPITHELIAL
DAMAGE

-EXTRACELLULAR
MATRIX

MUCOSAL OEDEM
AIRWAY
SECRESION

AIRWAY
NARROWING

SYMTO
MES

BRONCHIAL
HYPERREACTIVITY

REDUCED AIRWAY
REVERSIBILITY

EXACER
BATION

KOMPONEN AIRWAY REMODELING

BECKETT PA, HOWARD PH; THORAX, APRIL 2003. (WWW.THORAXJNL.COM)
MCUS METAPLASIA

EPITHELIAL DISRUPTION
ELASTIC FIBRE
FRAGMENTATION

INCREASE VASCULARITY
EXTRACELLULAR MATRIX
GLYCOPROTEIN

SMOOTH MUSCLE HYPERTROPHY AND

HYPERLASIA

SUB-BASEMEMBRANE
THICKENING
SUB-EPITHELIAL
FIBROSIS
DEPOSISI CLAGEN I,
COLAGEN II DAN
FIBRONECTIN

PROLIFERATION INDUCED BY
INFLAMATORY MEDIATOR
NERVE

CYTOKINES
GROWTH FACTOR

MYOFIBROBLAST

TERGANTUNG PADA PROSES INFLAMASI

SMOOTH
MUSCLE
DYSFUNC
TION

AIRWAY
INFLAMATI
ON

CS

LABA

RONCHOCONSTICTI
ON

INFLAMATORY CELL
INFILTRATION ACTIVITY

BRONCHOHYPERRE
ACTIVITY

MUCOSA OEDEMA

HYPERPLASY
INFLAMATORY
MEDIATOR RELEASE

CELLULAR
PROLIFERATION
EPITHELIAL DAMAGE
BASEMEMBRANE
TICKENING