Occupational and Environmental Diseases-rev
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7/27/2019 Occupational and Environmental Diseases-rev
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OCCUPATIONAL AND
ENVIRONMENTAL DISEASES
Devy Ariany, dr., M.BiomedPathology Anatomy Department
Faculty of Medicine,
UPN Veteran Jakarta
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Injuries and illnesess resulting from exposure to
exogenous chemical or physical agents
Personal exposures
Therapeutic drugs
Outdoor air pollution
Indoor air pollution
Industrial exposures
Agricultural hazards
Natural toxinsRadiation injury
Physical environment
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Personal exposures
Tobacco use
Alcohol abuse
Drug abuse
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Cigarette
smoke
Particulate phase
Gas phase
Chemical carcinogens : tar, polycyclic aromatic hydrocarbons Carcinogenic metals : arsenic, cadmium, nickel, chromium
Potensial promotors : acetaldehyde, phenol
Irritans : NO2, formaldehyde
Cilia toxins : hydrogen cyanide, CO Impaired O2 transport & utilization : CO
Ganglionic stimulation & depression : nicotine
Adverse effects of
smoking
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Therapeutic drugs
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Example
Echinacea
Ginkgo
Ginseng
Saw palmetto
St.John wort
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Exogenous Estrogens And Oral
Contraceptives
1. Exogenous Estrogens ( alone & usually
natural estrogen)
Adverse effects of estrogen therapy :
Endometrial carcinoma
Breast carcinoma
Thromboembolism
Cardiovascular disease
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2. Oral contraseptives
Adverse effects of oral contraseptives
(contain synthetic estrogens & always with progestin)
1.Breast carcinoma 6. Hypertension
2.Endometrial cancer 7. Hepatic adenoma
3.Cervical cancer 8. Gallbladder disease
4.Ovarian cancer 9. Cadiovascular disease5. Thromboembolism
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Acetaminophen
When taken very large doses hepatic
necrosis
The window therapeutic dose : 0,5 gr
Toxic dose : 15-25 gr
Toxicity begins : nausea, vomiting, diarrhea,
sometimes shock and jaundice
Serious overdose : liver failure, renal andmyocardial damage
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Aspirin (Acetylsalicylic Acid)
Overdose ( 2-4 gr) : accidental ingestion of
large number table young children
Suicidal ( 10-30 gr) adult
Effects : at first : respiratory alkalosis
metabolic acidosisdeath
Chronic : take > 3 gr daily headache,
dizziness, tinnitus, difficulty hearing, mental
confusion, nausea, vomiting and diarrhea
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Pollutant
Ozone
Nitrogen dioxide
Sulfur dioxide
Acid aerosols
Particulates
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Patterns of Lung Injury Related to Air Pollution
Lung response Pathogenic Mechanism(s)
Acute or chronic
inflammation (e.c. Chronic
bronchitis)
Emphysema
Ashma
Hypersensivity pneumonia
Pneumoconiosis
Neoplasia
Direct cell injury
Enhanced proteolysis
Allergic or irritant effect
Immunologic injury
Fibrotic reactions caused by
cytokines released from
macrophages & other recruitedleucocytes
Mutagenic & promoting effects
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Carbon Monoxide Nonirritating, colorless, tasteless, odorless
imperfect oxidation of carboneceous materials continues tobe cause accidental & suicidal death
CO kills by inducing CNS depression
CO act as a systemic asphyxiantcarboxyhemoglobin incapable carrying oxygen
Acute Poisoning: generalized cherry-red color skin &mucous membrane
Chronic poisoning : evoke widespread ischemicchanges in the CNS
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Organ
CVS
Nervous
system
GUT
Reproductive
system
Hematopoietic
system
Skin
GIT
Respiratory
system
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Pneumoconiosis
The non-neoplastic lung reaction to inhalation of mineral
dust
Agent : coal dust, silica, asbestos, beryllium
Coal Workers Pneumococoniosis (CWP)
Spectrum of lung finding in coal workers
1. Asymptomatic antracosis
2. Simple Coal workerss pneumoconiosis
3. Progressive massive fibrosis (PMF)
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Mineral Dust Induced Lung Disease
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Pathogenesis of Pneumoconiosis
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Morphology1. Pulmonary anthracosis
Inhaled carbon pigmen is engulfed by alveolar orinterstitial macrophage, then accumulate inconnective tissue linear streak & aggregatespigment identify pulmonary lymphatic & mark thepulmonary lymph node
2. Simple CWP
Characterized : coal macules & coal nodule.
cole macule consist : dust-laden macrophages. Thelession scaterred, but uppers lobes & upper zonesof the lower lobes more heavily involved
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Morphology
3. Caplan syndrome
Coexistence of rheumatoid arthritis with a
pneumoconiosis development distinctive
nodular develop fairly rapidly
The nodular lesions central necrosis
surrounded by palisading fibroblast, plasma
cells, macrophages containing coal dust &
collagenThe syndrome also occur in asbestosis & silicosis
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Clinical course CWP1. CWP usually benign produce little
decrement in lung function
2. Minority casespulmonary dysfunction,hypertension & cor pulmonale
3. CWP PMF (progressive massive fibrosis)linked variety factors : coal dust exposurelevel & total dust burden
4. PMF tendency to progress even absenceexposure
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Silicosis
Caused by inhalation crystalline silica
Occupations associated development silicosis : quarrymining, sandblasting, drilling, tunneling, & stonecutting
Incidence : 1500 cases each year in US
Silica :
1. Crytalline : quartz, cristobalite, tridymite ( mosttoxic and fibrogenic)
2. Amorphous forms (most commonly implicated insilicosis)
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Classification Silicosis1. Acute silicosis : exposure very high level of
silica & develops quickly
2. Chronic ( nodular ) silicosis: exposure overprolonged periods Characteristic fibroticnodules of silicosis
3. Complicated ( conglomerate silicosis)result progression of chronic silicosis
4. Other pulmonary disease : silicosisassociated with TBC
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Morphology
Gross : Characterictic nodule in early stage: tiny,
barely palpable, discrete, pale-to-blackened,
nodules in upper zones
Microscopically : silicotic nodule demontrates
concentrically arranged hyalinized collagen
fibers surrounding an amorphous center.
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Clinical course Chronic silicosis detected routine chest
radiographs (asymptomatic)
Radiographs : fine nodularity in the upper
zones function : normal/ moderately
affected
Most patients do not develop shortness of
breath untill late in the course
The disease slow to kill
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Asbestosis
Asbestos family of crystalline hydrated silicates
Occupational exposure to asbestos, linked to:
1. Parenchymal interstitial fibrosis (asbestosis)
2. Bronchogenic carcinoma
3. Pleural effusions
4. Localized fibrous plaque, rarely diffuse fibrous
plaque
5. Malignant pleural & peritoneal mesothelioma6. Laryngeal carcinoma
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Pathogenesis Asbestosis
Dictate : concentration, size, shape & solubility of different formsasbestos
Two forms asbestos:
1. Serpentine (fiber is curly & flexible) : Chrysotile
2. Amphibole (fiber is straight, stiff,& brittle)more
pathogenic
The greater pathogenicity amphiboles related:
1. Chrysotiles impacted respiratory removed
mucocilliary
trapped
gradually leached from tissue
2. Amphiboles align themselves airstream deliver
deeper penetrate epithelial cells reach interstitium
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Morphology
Gross: diffuse pulmonary interstitial fibrosis
Microscopically : characteristic asbestosbodies : golden brown, fusiform or beadedrods with a translucent center. They consist ofasbestos fibers coated with an iron containingproteinaceous material.
Pleural plaque : well-circumscribes plaque of
dense collagens
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Clinical course Indistinguishable from other diffuse intertitial
lung disease
Typically, progressively worsening dypnea
appears 10-20 years after exposure
The disease may static or progress to
congestive heart failure, cor pulmonale and
death.
1 November 2009 34Devy Ariany, dr, M.Biomed
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Lead causes injury by itsmultiple metabolic
effects:
1. High affinity fir
sulfhydryl groups &
interferes with enzymes
2. Competes with calcium
3. Interferes with
membrane-associated
ezymes4. Inteferes with nerve
transmission and brain
5. Membrane effects
damage the kidneys
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Agricultural hazards
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Category
Mycotoxins
Phytotoxins
Animaltoxins
Natural toxins
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Radiation injury
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Radiation
UVA
UVB
UVC
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Physical environment
Mechanical forces
Thermal injuries
Electrical injuries
Injuries related tochanges in atmospheric
pressure
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Mechanical
forces
Soft-tissue injuries, bone
injuries and head injuries
Bone injuries and head
injuries = chapter 28
Soft-tissue injuries =
superficial, deep, associated
with visceral damage
Abrasion
Laceration
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Contusion
Gunshot wounds
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Thermal injuries
Thermal burns
Hyperthermia
Hypothermia
Heat cramps loss of electrolytes viasweating Heat exhaustion onset sudden, mostcommon hyperthermic syndromefailure of cardiovascular system to
compensate for hypovolemia Heat stroke high ambienttemperatures & high humiditythermoregulatory mechanism fail
Local reactions : Chilling or freezing
of cells & tissues causes injury
in two ways
1. Direct effectsmediated
by physical disruption oforganelles within cells,
high salt consentration
2. Indirect effects exerted
by circulatory changes
Gross inpection on thermal burns :Full-thickness burn are white or charred,
dry and anesthetic; depending on the depth,
partial-thickness burns are pink or mottled withblisters & painful
Microscopically:Devitalized tissue coagulative
necrosis, adjacent vital tissue accumulatesinflammatory cells & exudation
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Electrical injuries
Electrical injuries death arise from low-
voltage or high-power lines or lighting
Two types of injuries :
1. Burns
2. Ventricular fibrilation or cardiac &respiratory paralysis
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Injuries related to changes
in atmospheric pressure
High-altitude
illness
Blast injury
Decompression
disease (Caisson
disease)
Mountain climbers
Rarefied atmosphere of
altitudes above 4000 m
P O2 progressive mental
obtundation
Increased capillary
permeability, pulmonary edema
In atmosphere (air blast) or in
water (immersion blast)
Collapse thorax or abdomen,
with rupture internal organs
Deep-sea divers and underwater workers
Emboli respiratory difficulties, substernal pain Headache, visual disturbances, behavioral disorientation , vertigo
Skeletal manifestations
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