Occupational and Environmental Diseases-rev

7/27/2019 Occupational and Environmental Diseases-rev

1/25

11/8/2009

1

OCCUPATIONAL AND

ENVIRONMENTAL DISEASES

Devy Ariany, dr., M.BiomedPathology Anatomy Department

Faculty of Medicine,

UPN Veteran Jakarta

1 November 2009 Devy Ariany, dr, M.Biomed 2

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

PDF created with pdfFactory Pro trial version www.pdffactory.com
http://www.pdffactory.com/http://www.pdffactory.com/http://www.pdffactory.com/


2/25

11/8/2009

2


Personal exposures

Tobacco use

Alcohol abuse

Drug abuse




3/25

11/8/2009

3


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

1 November 2009 6Devy Ariany, dr, M.Biomed



4/25

11/8/2009

4





5/25

11/8/2009

5


Therapeutic drugs


Example

Echinacea

Ginkgo

Ginseng

Saw palmetto

St.John wort



6/25

11/8/2009

6

Exogenous Estrogens And Oral

Contraceptives

1. Exogenous Estrogens ( alone & usually

natural estrogen)

Adverse effects of estrogen therapy :

Endometrial carcinoma

Breast carcinoma

Thromboembolism

Cardiovascular disease


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




7/25

11/8/2009

7

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


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




8/25

11/8/2009

8


Pollutant

Ozone

Nitrogen dioxide

Sulfur dioxide

Acid aerosols

Particulates


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



9/25

11/8/2009

9


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




10/25

11/8/2009

10


Organ

CVS

Nervous

system

GUT

Reproductive

system

Hematopoietic

system

Skin

GIT

Respiratory

system




11/25

11/8/2009

11

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)


Mineral Dust Induced Lung Disease




12/25

11/8/2009

12

Pathogenesis of Pneumoconiosis


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




13/25

11/8/2009

13

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


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




14/25

11/8/2009

14

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)


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




15/25

11/8/2009

15

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.


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




16/25

11/8/2009

16

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


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




17/25

11/8/2009

17

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


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.




18/25

11/8/2009

18



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



19/25

11/8/2009

19


Agricultural hazards


Category

Mycotoxins

Phytotoxins

Animaltoxins

Natural toxins



20/25

11/8/2009

20


Radiation injury




21/25

11/8/2009

21





22/25

11/8/2009

22


Radiation

UVA

UVB

UVC


Physical environment

Mechanical forces

Thermal injuries

Electrical injuries

Injuries related tochanges in atmospheric

pressure



23/25

11/8/2009

23


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


Contusion

Gunshot wounds



24/25

11/8/2009

24


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


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



25/25

11/8/2009


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


Occupational and Environmental Diseases-rev

Documents

Transcript of Occupational and Environmental Diseases-rev