ENVIRONMENTALLY

TRIGGERED ILLNESS
Oleh:
dr. Agung S. Dwi Laksana, M.Sc.PH

PENDAHULUAN
AAEM

(200%): kedokteran lingkungan

adalah pelayanan kesehatan
komprehensif, proaktif dan dengan
strategi pendekatan preventif yang
ditujukan untuk evaluasi, manajemen dan
pencegahan akibat buruk yang timbul dari
penyakit yang dipicu oleh lingkungan
(Environmentally Trigerred Illness).

 Environmentally

Trigerred Illness (ETI) adalah

konsekuensi buruk yang terjadi bila interaksi
hemodinamik fungsi-fungsi biologik terganggu
oleh stresor internal maupun eksternal.
Stresor dapat bervariasi, mulai eksposure akut
dan berat terhadap stresor tunggal sampai
akumulasi eksposure derajat rendah terhadap
banyak stresor pada periode waktu yang lama.

MASA KANAK-KANAK
Masa

kanak-kanak merupakan
masa tumbuh kembang yang
cepat
Perubahan

fungsi sistem organ

Perubahan kemampuan
metabolik
Perubahan ukuran fisik
Perubahan perilaku

Potensi
penyakit
akibat
paparan
bahan
toksik

FAKTOR-FAKTOR YANG MEMPENGARUHI

PAPARAN PADA BAYI DAN ANAK-ANAK
Dibandingkan

dengan orang dewasa, bayi

dan anak:
1.
2.
3.

Menghirup lebih banyak udara

Minum lebih banyak air
Makan lebih banyak makanan

Permeabilitas

kulit tinggi

Penetrasi bahan toksik lebih mudah

misal: lindane dan hexachlorophene (neurotoksik)

AGE DEPENDENT TOXICOKINETIC

CHANGES
Perubahan

fisiologis dan komposisi tubuh pada anakanak mempengaruhi absorpsi, distribusi, penimbunan
dan metabolisme serta ekskresi bahan-bahan kimia
Fungsi

sistem organ berubah

Massa otot dan tulang meningkat
organ dalam menjadi bagian kecil tubuh
dosis berubah
kinetika dan toksisitas bahan kimia berubah
Contoh:
Methemoglobinemia karena paparan nitrate lebih mudah
terjadi pada bayi usia 0-4 bulan karena rendahnya
konsentrasi NADH methemoglobin reduktase

Metabolisme xenobiotik seiring perubahan umur

tidak dapat digeneralisasi dengan mudah karena:
1.

Metabolisme bahan kimia yang efisien tidak berarti

menurunkan toksisitasnya

2.

Metabolic by-product dapat lebih toksik daripada susunan

kimia asal
Contoh: methyl parathion dimetabolisir menjadi by-product yg
lebih toksik kerusakan pada organ

Jalur enzymatik tidak matang (mature) secara

bersamaan

T1/2 kafein pada neonatus 4 hari, pada dewasa 4 jam. Usia

7-9 bulan, T1/2 kafein = dewasa.
Metabolisme Teofilin melalui sistem sitokrom P-450 berjalan
lambat pada BBL, meningkat melebihi dewasa pada masa
anak-anak dan menurun secara perlahan pada masa remaja
akhir

3.

Pada usia yang berbeda, ada kemungkinan

berbeda pula jalur enzymatik yang digunakan
untuk metabolisme bahan kimia tertentu

VARIASI SUSCEPTIBILITAS PADA

TIAP TAHAP PERKEMBANGAN
Processes of normal reproduction and
development
MALE FECUNDITY

FEMALE FECUNDITY

CONCEPTION
IMPLANTATION AND
PRECLINICAL GESTATION
CLINICAL PREGNANCY AND
FETAL DEVELOPMENT
BIRTH
POSTNATAL DEVELOPMENT

Adverse outcome
Gangguan fekunditas
Gangguan fertilitas
Subclinical spontaneous
abortion
-Spontaneous abortion
-Fetal death
-Fetal growth retardation
Prematurity
Congenital malformation
-Developmental disorders
-Childhood cancer

PRAKONSEPSI
Male and Female Infertility
Male Fecundity
Hazard
Metals: Lead
Pesticides:
-DBCP
(dibromochloropropane)
-EDB (Ethylenedibromide)
Solvents:
-Ethylene glicol ethers
-2-bromopropene
Pharmaceuticals:
Estrogen
Physical agents:
Ionizing radiation
Heat

Effect
HPG Axis
Toksik terhadap spermatogonia
azoospermia
Kelenjar seks Mempengaruhi kualitas
semen
Toksik terhadap spermatid
Toksik terhadap spermatogonia
azoospermia
Menekan aksis HPG
Efek terhadap Spermatogenesis

 Female

Fecundity

Hazard
Solvents:
-Toluene
-2-bromopropane
Lead

Effect
Menekan sekresi LH dan FSH
Amenorrhea, low estradiol and high
FSH and LH level
Menekan aksis HPO dan toksik
terhadap ovarium dan oocyte

Physical agents:
- Ionizing radiation Menghancurkan oocyte

FETUS

Fetus tidak bisa menghindar dari paparan bahan

toksik melalui placenta
Placenta merupakan membran semipermiabel
yang memungkinkan transport senyawa dengan
berat molekul rendah (misal CO) dan larut lemak
(PAH dan ethanol) dengan mudah
Kemampuan placenta untuk detoksifikasi sangat
rendah
Kontaminan makanan sebelum dan sesudah
hamil dapat membahayakan fetus

FETUS (Cont.)

Perubahan

fisiologi selama hamil memobilisasi

bahan toksik dalam tubuh
Misal:
Mobilisasi

lead dari tulang

Mobilisasi PCBs dari sel lemak
Alkohol

fetal alcohol syndrome

Merokok HbCO fetus meningkat risiko
kematian janin dan penurunan fungsi paru serta
berat badan rendah

FETUS (cont.)

CO gangguan sistem saraf tepi

CO HbCO
Hipoksia
Aktivasi sphingomyelinase
Sphingomyelin

Sphingosine

Akumulasi sphingosine

Gangguan proses seluler:

diferensiasi sel
proliferasi sel
transport protein
apoptosis

FETUS (cont.)

1.

Aborsi spontan

Berbagai jenis bahan kimia dan pekerjaan

dihubungkan dengan terjadinya aborsi
spontan
Mekanisme belum diketahui dengan pasti

BAHAN TOKSIK
Medical hazards:
- Antineoplatik drug
- Anesthetic gases
- Nitrous oxide
- Ethylene oxide

Perawat
Personel ruang operasi
Asisten dokter gigi
Operator sterilisasi

Metals: Lead
Solvents:
- Ethylene glycol ethers

Manufaktur semikonduktor

Aromatic solvents
Mixed organic solvents
Other chemicals:
- PCB
- Pesticides
Physical agents:
- Heavy labor
- Shift work

RISIKO

Pemakaian di tempat kerja

Pemakaian di tempat kerja
Kontaminasi makanan
Keracunan

2.

Cacat

Periode organogenesis otak paling rentan karena

blood brain barrier dan kemampuan detoksifikasi masih
kurang
Keracunan lead kerusakan sistem syaraf
Keracunan ethanol migrasi sel terganggu
malformasi otak
Keracunan methyl mercury cerebral palsy dan
retardasi mental
CO penurunan kognitif permanen dan fungsi
motorik
Pembelahan sel yg cepat pada fetus sensitif
terhadap karsinogen
Diethylstilbestrol (DES) via placenta dan radiasi
kanker

3.

Fetal growth retardation dan prematuritas

BBL (0-2 BULAN), BAYI (2-12 BLN), DAN

TODDLER (1-2 TAHUN)
Pertumbuhan

bayi pada beberapa bulan

pertama merupakan yang tercepat sepanjang
hidup
Jaringan dengan pembelahan sel yang cepat,
termasuk sel hematopoietic, jaringan paru dan
epitel, rentan terhadap kasinogen
Kecepatan pertumbuhan bayi melambat ketika
berusia 9 bulan
Radiasi proliferasi sel
Ethanol migrasi sel
Hypothyroidisme diferensiasi sel

 Exposure

melalui ingesti

Breastfeeding

(ASI): menyusui
mobilisasi toksikan yg larut dalam lemak
kontaminasi ASI.
Formula feeding:
Bayi

mengkonsumsi air dalam jumlah besar

(10%-15% dari berat badannya)
Konsumsi air dari pemberian makanan formula
bayi 180 ml/kgBB/hari setara 35 kaleng
(360 ml) softdrink pada orang dewasa
Paparan logam berat, nitrate, mikroba dan
bahan kimia organik

 Pica

memasukkan benda bukan makanan

ke mulut. Soil-pica dapat terjadi ingesti
bahan toksik: debu, cat mengandung lead,
mercury, produk pembersih lantai, dll.
Solid Food (Makanan Padat): makanan anak <
2 tahun kaya buah, sayur dan padi-padian
exposure residu pestisida

 Exposure
Rasio

melalui kulit (Dermal exposure)

permukaan kulit bayi terhadap berat

badan 3x lebih besar dari orang dewasa
Dosis bahan yg diabsorbsi lebih besar
Kulit bayi lebih mudah mengabsorbsi bahan
kimia karena lapisan keratin tebal pada kulit
bayi baru lahir belum terbentuk
Lapisan keratin baru mulai dibentuk pada hari
ke 3-5 setelah lahir
Hexachlorophene pembersih kulit merusak
dinding sel dan presipitasi protein seluler
vakuolisasi CNS
Betadine hypothyroidisme pada bayi
Anilin methemoglobinemia

 Exposure
Bayi

melalui Inhalasi: Pernapasan

dan anak frekuensi pernafasannya lebih

cepat
Risiko paparan terhadap polutan udara lebih
besar
Paparan terhadap polutan udara meningkatkan
insidensi dan beratnya serangan asthma

ANAK-ANAK USIA 2-6 TAHUN

Aktivitas

anak mulai meningkat: lari,

memanjat, mengendarai sepeda roda tiga
dan aktivitas lain
lingkungan anak lebih luas
Bila diet kurang besi atau kalsium
absorbsi lead lebih tinggi
Risiko soil-pica juga masih tinggi

ANAK USIA SEKOLAH (6-12 TAHUN)

Kegiatan

di luar rumah lebih banyak dari

sebelumnya
Paparan terhadap polutan udara
meningkat
Selama bermain anak-anak dapat
terpapar arsen, merkuri dan bahan toksik
lain melalui ingesti atau inhalasi

REMAJA (12-18 TAHUN)

Risk-taking

behavior paparan terhadap alkohol,

penyalahgunaan obat-obatan, merokok, dsb.
Aktivitas sekolah dan hobby seperti melukis dan
kerajinan paparan bahan kimia
Kecepatan metabolisme xenobiotic menurun karena
peningkatan sekresi hormon pertumbuhan dan
steroid
Perubahan pada masa pubertas pertumbuhan,
pembelahan dan diferensiasi sel yang cepat
kerentanan, terutama gangguan pada perkembangan
sistem reproduksi

AGENT LINGKUNGAN
PENYEBAB GANGGUAN
KARDIOVASKULER

KLASIFIKASI
Gangguan

kardiovaskuler karena agent

lingkungan dapat diklasifikasikan:
1.
2.
3.
4.
5.
6.
7.

Coronary artery disease

Dysrhythmias
Hypertension
Cardiomyopathy
Peripheral vascular disease
ECG Abnormalities
Cor pulmonale

CORONARY ARTERY DISEASE

Acute

cardiac ischemia:

Kerja

berat pada udara yg panas dan lembab

peningkatan kebutuhan oksigen otot
jantung
Chronic

cardiac ischemia:

Berperan

Penyebab

dalam CAD

CAD dan acute cardiac

ischemia: CS2, CO, methylene chloride,
nitrate esters, dan physical inactivity

 CS2
Solvent

dan chemical intermediate pada produksi

rayon
Ambang batas: 10 ppm atau 31 mg/M 3
Mekanisme kerja CS2 belum diketahui, diduga akibat
perubahan pada:
Lipid

darah
Heart rate
Diastolic blood pressure
Carotid artery distensibility

 Nitrate

esters:

Terutama:

nitrogliserin
Digunakan sbg pengobatan dan bahan peledak
Nitrat methemoglobinemia
Nitrat vasodilatasi arteri headache dan confusion
Mekanisme cadiac ischemia karena nitrate tidak
diketahui, tetapi diduga karena efek vasospasme arteri
coronaria
Spasme a. coronaria iskemia dan nekrosis miokard
dan disritmia

 CO
Selain

terikat pada Hb, CO juga terikat pada

sistem sitokrom oksidase pada mitokondria
otot jantung kontraktilitas otot jantung
menurun
Efek: iskemia atau infark miokard, disritmia

HYPERTENSION
Penyebab:
Stress

psikososial: stimulasi sistem syaraf simpatis,

sistem hipothalamus-hipofise-adrenal dan sistem
renin-angiotensin
Agent fisik: kebisingan >90 dB kenaikan tekanan
darah
Agent kimia:
Pb
CS2
CO

aksi pada otot arteri dan aksis renin-angiotensin

COR PULMONALE
Penyakit

jantung karena gangguan pada

paru akibat paparan berbagai agent
Misal:
Silikosis
COPD

(PPOM) karena paparan asbestos

ENVIRONMENTAL
DISEASE OF THE LUNG

GENERAL PRINCIPLES IN THE PATHOGENESIS

OF LUNG DAMAGE CAUSED BY CHEMICALS
Oxidative
Often

Burden (Beban oksidatif)

mediated by free radicals

Ozone, NO2, tobacco smoke
In animal studies the activity of free radicalscavenging enzymes
Reduction of O2 to active O2 metabolites
normally occurs as a by-product of cellular
metabolism during both microsomal and
mitochondrial electron transfer reaction

 Toxic

inhalants, gases

The

sites of deposition of gases in the respiratory

tract define the pattern of toxicity of those gases
Water solubility is the critical factor
Highly soluble gases do not penetrates into the
lung
Ex:

SO2

 Relatively

insoluble gases penetrates deeply

into the lung and reach the smallest airways
and alveoli
Ex:

NO2

Very

insoluble gases efficiently pass through

the respiratory tract and are taken up by the
pulmonary blood supply to be distributed
throughout the body
Ex:

CO and H2S

Particle

deposition and clearance

Particle

size: the larger the number and

mass of particles capable of penetrating
the lung, the greater the probability of a
toxic effect
Deposition mechanism
Interception:

an edge of the particle

contacts the airway surface.
Dependent
ex:

on fiber length

fiber

Impaction
Dependent

on fiber diameter

Sedimentation
In

the smaller bronchi, the bronchioles

and the alveolar spaces, where the
airways are small and the velocity of
airflow is low
Dependent on fiber diameter
Diffusion:

an important factor in the

deposition of sub micrometer particles

1. OCCUPATIONAL ASTHMA
Definisi:

a disease characterised by variable airflow

obstruction and/or airway airway
hyperresponsiveness due to causes and
conditions attributable to a particular working
environment and not to stimuli encountered
outside the workplace
Epidemiology:
The most common occupational lung disease
affect 5-10% of the population worldwide

 Penyebab:
1. Sensitizer-induced

OA (Immunologically

mediated)
2. Irritant-induced OA (non-immunologically
mediated)
3. Workplace aggravation of asthma

 Patofisiologi
1.

Sensitizer-induced OA
Interaction

of both environmental and genetic

factors
High molecular weight compounds (>5 kDa)
induced specific IgE antibodies that mediate
asthmatic response
Low molecular weight agents act as haptens +
amino group on protein antigen

High molecular weight agent

Low molecular weight agent

Animal-derived material:
-Excreta
-Secretion
-Serum
-Dander

Spray paints:
-Toluene diisocyanate
-Hexamethylene diisocyanate

Plant-derived material:
-Flour
- wood dust
-Grain
- latex
-Coffee bean

Wood dust

Enzymes
--amylase
-Papain
-Alcalase

Acid anhydride biocides:

-Formaldehyde
-Glutaraldehyde
-Chloramin T

2.

Irritant-induced asthma

Causes: single exposure to high dose of irritant

The mechanism is not known
Postulate:
Neurogenic

inflamation
Low dose RADS: smoker and allergic rhinitis

3.

Irritant agents: chlorine, acetic acid

Workplace aggravation of asthma

Airway hyper-responsiveness
Low level of respiratory irritant bronchoconstriction

2. COPD AND CHRONIC BRONCHITIS

Epidemiology:
COPD

is predicted to be one of the major causes

of deaths in Indonesia in 2020
Its prevalence increases with age and varies with
the distribution of risk factors in the population
Specific occupational risk factors:
Grain

handler
Asbestos insulator
Aluminium smelter
Wood workers

3. ACUTE INHALATION INJURY

Properties
Physical
Gases,

of irritant:
properties:

vapor, fumes, aerosols and smoke

Water soluble substance: upper airway injury
The size of inhaled particle diameter < 5 m
terminal bronchioles and alveoli
Ex: Zinc chloride (hexite) diameter < 0,1 m

Irritant gas

Water solubility

Mechanism of
injury

Ammonia

High

Alkali burns

Chlorine

Intermediate

Acid burns,
reactive oxygen
species

Hydrogen chloride

High

Acid burns

Oxides of nitrogen

Low

Acid burns,
reactive oxygen
species

Ozone

Low

Reactive oxygen
species

Phosgene

Low

Acid burns

Sulfur dioxide

High

Acid burns

 PATHOGENESIS AND

PRESENTATION
Acute:

CLINICAL

1-2 days of exposure

Laryngeal

edema
Airflow ostruction asthma and bronchitis
Pneumonitis, pulmonary edema
ARDS
Chronic:

weeks to months after the exposure

COPD
Reactive

airways dysfunction syndrome (RADS)

Bronchitis
Bronchiolitis obliterans
Bronchiolitis obliterans organizing Pneumonia

 Upper

airway acute injury

IRRITANT

ACIDIC SUBSTANCES

ALCALOTIC SUBSTANCE

SKIN AND MUCOUS

MEMBRANE

LIQUEFACTION OF
THE SURFACE MUCOSA

COAGULATE TISSUE

DEEPER TISSUE
REACTIVE OXYGEN

LIPID PEROXIDATION
CELLULAR AND TISSUE
DISRUPTION

 Pulmonary
Low water

parenchyma

solubilities: ozone and NO2

exposure are not result in upper airway
irritation
continued exposure to the toxic gases
particle deposition in alveoli
bronchiolar inflammation and pulmonary
edema (alveolar filling)

4. Hypersensitivity Pneumonitis
Definition:
A condition

of granulomatous, interstitial, bronchiolar

and alveolar-filling lung disease caused by repeated
exposure and subsequent sensitization to a variety
organic and chemical antigens

Etiology
Microbial

agent: various bacteria and fungi

Animal protein: avian antigen, rat proteins and dust
from mollusk shells
Low molecular weight chemicals: adhesives and
paints

 Pathogenesis:
HP is

characterized by the presence of

activated T lymphocytes
Host susceptibility: smoking
Exposure factors: Ag concentration, duration
of exposure, frequency of exposure, particle
size, solubility and potency, variability in
workplace, season

5. ASBESTOSIS
Pathogenesis:
Asbestos

fibers are inhaled deep into the respiratory

tract uptake by alveolar epithelial cells
pulmonary interstitium accumulation macrophages
inflamation response alveolitis and
peribronchiolitis
Asbestos fibers are retained in the pulmonary
interstitium or migrate to the pleura
Asbestos fibers generate reactive oxygen
intermediates cytotoxicity lipid peroxidation and
injury to intracellular macromolecul
Activated macrophages produce tumor necrosis
factor, in addition to the production of cytokines,
interleukins and other mediators

FAKTOR LINGKUNGAN
PENYAKIT KULIT

CAUSE OF SKIN DISEASE

Chemical
Mechanical
Physical
Biological
Botanical

CHEMICAL HAZARDS

Chemical agents can be divided into two

main groups:
1.
2.

Primary irritants and

Sensitizers.

Ad.1. Primary Irritants

Irritant:

a substance that produces an

irritating effect when it contacts skin, eyes,
nose, or respiratory system.
Iritan primer mengubah kimia kulit dan
merusak kemampuan proteksinya
kerusakan jaringan
Kerusakan permukaan kulit Dermatitis
Kontak Iritan (DKI)

Ad.1. Primary Irritants

Kebanyakan

bahan kimia iritan larut dalam air

(water soluble) bereaksi dengan unsur lipid
pada kulit
Contoh:

solvent

Primary

irritants act directly on the skin in one of

the following ways:
Chemically

reacting with it,

Dissolving or abstracting from it some of its essential
components,
Denaturing the proteins of the skin, or
Disturbing the skins membrane and its ability to retain
moisture.

Ad.1. Primary Irritants

Yang
1.

termasuk iritan primer:

Keratin Solvents: melunakkan sel keratin kulit

dan kehilangan cairan kulit kulit kering dan
pecah-pecah
Contoh:

2.

Sabun, alkalis dan solvent organik

Fat and Oil Solvents: mengelupas lapisan

lipid kulit dan menurunkan kemampuan kulit
meretensi air
Contoh:

detergent

Ad.1. Primary Irritants

3.

Protein Precipitants: bahan kimia yg

bereaksi dengan sel-sel protein kulit

4.

Dehydrators: menguapkan air dari kulit dan

menghasilkan panas

5.

Contoh: alkohol, formaldehid, fenol dan garamgaram logam berat

Contoh: asam inorganik, alkalis (calcium oxide)

Oxidizers: bereaksi dengan hidrogen dan

melepaskan oksigen dari kulit

Contoh: Nitrat, chlorine, amonia dan hidrogen

peroksida

Ad.1. Primary Irritants

6.

Reducers: bereaksi dengan air pada kulit untuk

melepaskan hidrogen dan melemahkan bagian
luar kulit

7.

Contoh: Tar, karbon aromatik dan alifatik, asam

oksalat

Keratin Stimulants: menstimulasi

pertumbuhan abnormal kulit, menyebabkan
tumor atau kanker

Contoh: produk petroleum, PAH, arsen

Ad.1. Primary Irritants

Two
1.

Major Classes of Primary Irritants

Absolute Primary Irritants are corrosive

substances that injure the skin immediately
following first contact.
Contoh:

2.

asam kuat dan basa kuat

Relative Primary Irritants are less toxic

substances that require either repeated or
prolonged contact to produce inflammation.
Contoh:

sabun, deterjen dan solvent organik

Ad.2. Sensitizer (Alergen)

Sensitizer

: a material that can cause an

allergic reaction of the skin or respiratory
system.
Sensitizers do not cause visible skin
changes following first contact, but
produce a specific acquired alteration in
the capacity of the skin to react, brought
about by an antibody-like mechanism.

Ad.2. Sensitizer
Chemicals

that cause skin sensitization

are far fewer than those that cause
primary irritation.
Contoh:
poison ivy, epoxy, formaldehyde,
ammonia, germicidal agents, nickel
compounds, mercury compounds, cobalt
compounds, and coal tars.
Some compounds, such as turpentine and
chromic acid, cause both primary irritation
and sensitization.

 Workers

can also become sensitized by latex in

rubber gloves
Photosensitizers Certain chemicals are
capable of reacting with specific wave lengths of
natural and artificial light to cause phototoxic or
photoallergic dermatitis. The best known
industrial chemicals with this capacity are
derivatives of coal tar (anthracene,
phenanthrene, and creosote) and certain dyes.

Examples of occupational risk for contact allergy

Industry

Possible sensitizing agents

Textile

Dyes, Formaldehyde, resin

Panting

Epoxy, acrylates

Printing

Acrylates, epoxy, resins

Agriculture

Pesticides, plants, rubber

Food preparation

Flavoring and preservatives

Medical/dental/veterinary Rubber, acrylates, medications

Hairdresser

Nickel, rubber, glyceryl monothioglucolate

Metal workers

Metals, biocides in cutting fluid

Rubber manufacture

Carbamates, mercaptobenzothiazole

Leather tanning

Hromate, formaldehyde

Plastics manufacture

Formaldehyde, phenolic resins, epoxy resins

The Development of Allergic Contact Dermatitis proceeds

in the following steps:
1.

2.

3.

4.

The refractory period is the time during which contact with a

potential allergen occurs without the development of
sensitivity.
The latent or incubation period is the time during which
development of sensitization occurs. Once this process stops,
five to several weeks are required for full sensitization to
occur.
The reaction period occurs when fully sensitized skin is
reexposed to the allergen, resulting in an inflammatory
response at the site of contact. This reaction usually begins
within 12 hours, peaks at 24 to 48 hours, and then slowly
subsides.
The period of persistence of sensitivity is the time during
which no further contact with the allergen occurs, and the
level of sensitivity gradually declines. The rate of decline is
variable: some sensitivities remain for many years, other
disappear rapidly.

PENYAKIT KULIT LAIN KARENA CHEMICAL HAZARDS

1)
2)

Acne dan folliculitis

Disorders of pigmentation

Ad.1). Acne dan folliculitis

a)
b)
c)

Folliculitis
Acne vulgaris
Chloracne

Ad.a). Oil acne (Folliculitis)

Causal:
petroleum

distillate, spt tir, minyak, aspal

Pathogenesis:
Folikel rambut rentan thd iritasi oleh lipid
keratinisasi dinding folikel penyumbatan folikel
(comedo formation) atau menginduksi reaksi
peradangan melalui ruptur dinding folikel
(folliculitis)
Clinical course
Lesi acneiform (follicular) pada daerah yg terpapar,
umumnya pada dorsal tangan dan lengan

Ad.b). Acne vulgaris

Pathogenesis
Dapat

dipicu atu dieksaserbasi oleh stimulus

lingkungan seperti panas, dan keringat, disamping
minyak

Clinical

course

Biasanya

terdapat di wajah, leher, bagian atas dada

dan punggung

Prevention
Menghindari

higiene

Treatment
Sama

kontak dengan bahan penyebab dan

and prognosis

dengan oil acne

Ad.c). Chloracne
Penyebab:

polyaromatic hydrocarbons
Pathogenesis:
Agent

diskeratosis folikel epidermis terbentuk

keratin pada folikel, mirip komedo straw-colored
cystic lesion

Clinical
Lesi

course:

utama: komedo dan straw-colored cystic lesion

Predileksi: lipatan belakang telinga, dagu dan genital
Tanda dan gejala lain: hepatomegali

Chloracne-producing chemicals
Polyhalogenated

naphthalenes

Polychloronaphthalene
Polybromonaphthalene

Polyhalogenated

biphenyl

Polychlorinated

biphenyls (PCBs)
Polybrominated biphenyls (PBBs)
Polyhalogenated

dibenzofurans
Contaminants of polychlorophenol compounds,
especially herbicides (2,4,5-T and
pentachlorophenol) and herbicide intermediate
(2,3,5 trichlorophenol)

PERBEDAAN GAMBARAN ACNE

UMUR

DISTRIBUSI

GAMBARAN
KLINIK

KONDISI
LAIN

Oil acne

Any age

Exposed site

Komedo, pustula None

Acne
vulgaris

Peak
incidence,
age 11 to 20

Face, neck,
chest

Comedo, papula, None

pustula, scar,
cyst

Wajah,
terutama
telinga dan
dagu, aksila,
hidung

Comedo, strawcolored cyst

Chloracne Any age

Xerosis,
conjungtivitis,
peripheral
neuritis, liver
abnormalitis

GANGGUAN PIGMENTASI
1.

Hiperpigmentasi
Penyebab:

logam berat dan senyawa nitrogen

organik dan bahan pencelup
Pathogenesis:
(1) deposisi pigmen eksogen (cairan pencelup,
tato);
(2) deposisi di kulit secara sistematik (logam
berat);
(3) photoeruptions (sinar matahari) ;
(4) hiperpigmentasi pascainflamasi (deposisi
melanin dan hemosiderin)

METALS THAT MAY BE SYSTEMICALLY OR LOCALLY DEPOSITED

IN SKIN

Substance

Color

Location

Arsenic

Bronze

Difuse, especially trunk and proximal

extremities

Chromium

Blue-gray

Diffuse

Copper

Greenish

Hair

Gold

Blue-gray

Sun-exposed areas, especially preorbital

Iron

Brown

Tattoo

Lead

Pallor and Generalized, gingival leadline

vividity

Mercury

Slate gray Skin folds

Silver

Slate gray Sun-exposed area

Gangguan pigmentasi

2.

Hipopigmentasi

Chemical leukoderma: kontak dengan

hidroquinon, derivat elkil phenol dan catechol
Hipopigmentasi pascainflamasi: inflamasi
atau trauma menyebabkan hilangnya
pigmen kulit lokal

Compounds known to produce leucoderma

Hydroquinone
Monobenzyl

ether of Hydroquinone
Monoethyl ether of Hydroquinone
P-isopropylcatechol
P-methylcatechol
P-tert-butylphenol
P-tert-butylcatechol
Mercaptoamines

PREDISPOSING FACTORS

Usia orang tua lebih mudah mengalami iritasi kulit

kronis karena kulitnya lebih kering
Skin types Heavily pigmented skin appears to resist
the harmful effects of external irritants more effectively
than light skin. Workers with naturally dry skin are less
able to tolerate the action of solvents and detergents.
Those with oily skin are predisposed to developing acnelike lesions.
Sweating Increased sweating can irritate the skin and
increase the risk for developing dermatitis. Sweating
softens the skin and opens it up for the development of
secondary fungal and bacterial infection. Sweating can
also be beneficial in diluting concentrations of toxic
substances on the skin.

Predisposing factors

Gender Women usually report fewer occurrences of

dermatitis than men; this could be because of better hygiene
practices and less exposures to toxic substances. However,
women are usually more easily sensitized.
Seasons and Humidity dermatitis is generally more
common during warm weather. During warmer weather
wear less clothing more likely to have skin exposed to
external irritants. When hot less likely to wear personal
protective equipment (PPE). Climates with low humidity dry
out the skin making it easier for toxic agents to attack it.
Personal Hygiene a major factor in the cause of
occupational dermatitis. Unwashed skin and unchanged
clothes can cause prolonged contact to chemicals. Adequate
facilities for maintaining personal cleanliness should be
provided at the workplace.
Preexisting Skin Disease Preexisting skin diseases can
be easily aggravated at the workplace by exposure to
chemicals.