Occupational poisoning
By:
Sotoudeh manesh MD
Occupational medicine specialist
Introduction
Poison:

– Any substance that, when administered to a living organism, causes a harmful
effect.
Poisoning:

– The morbid condition produced by a poison.
Toxic:
– Term used to describe a chemical that has the ability to cause harmful or
fatal effects upon exposure to humans, animals, or plants.
• Toxicity:
– The capacity of a substance to induce damage to living tissue. Toxicity
can be acute, chronic, local, or systemic.
(Lewis Dictionary of Occupational and Environmental Safety and Health)
Introduction
•
Common occupational toxic substances can be divided into
4 groups:
1. Heavy metals
2. Pesticides
3. Organic solvents
4. Gases, vapors and particulates
Particulates
Classification of particles by size:

1. Non-inhalable particle



– Larger than 200 μm (0.2mm)
2. Inhalable particle (nasopharyngeal region)

– Smaller than 200 μm (0.2mm)

– Deposit in nose or trachea
3. Respirable particle (alveolar region)

– Smaller than 10 μm (0.01mm)

– Deposition in alveolar area (e.g. pneumoconiosis)
Water Solubility
gases
Example
Site of injury
High
Ammonia,formaldehyde
Upper airway
Moderate
Chlorine,sulfur dioxide
Lower airway
Low
NOx ,phosgene
Lung parenchyma
>10
Dust
Upper airway
2.5 – 6
Fire smoke particle
Lower airway
< 2.5
Fume ,asbestos fibers
Lung parenchyma
Particle size
Gases, vapours and particulates

Definitions:

• gas is a term usually applied to a substance that is in the gaseous state at room
temperature and pressure

• vapour is applied to the gaseous phase of a material that is ordinarily a solid or
liquid at room temperature and pressure

• aerosol is applied for a relatively stable suspension of solid particles in air, liquid
droplets in air or solid particles dissolved or suspended in liquid droplets in air

• mists and fogs are aerosols of liquid droplets formed by condensation of liquid
droplets on particulate nuclei in the air

• fumes are solid particles formed by combustion, sublimation or condensation of
vaporised material

• dusts are solid particles in air formed by grinding, milling or blasting

• fibres are solid particles with an increased aspect ratio (the ratio of length to
width); they have special properties because of their ability to be suspended in air
for longer periods than dusts and other aerosols.

Smog :
Toxic gas
 General
consideration
 Odors
 Asphyxiant
 solubility
Factors affecting the dose of inorganic
gas delivered to the respiratory system
 Physicochemiacal
factors
 Concentration
 Duration
 Minute
of exposure
ventilation
Toxicity of Gases and vapours

• Asphyxiation:

simple asphyxiation


– ability of a gas or vapour to displace oxygen from air by dilution

• Carbon dioxide

• Nitrogen (N2)

• Inert gases such as helium, argon and neon.
toxic asphyxiants

– by interfering with the ability of the body to transport oxygen.

• Carbon monoxide

• Cyanides

• Hydrogen sulfide

• Irritation to the tissues in respiratory system

– Ammonia

– Chlorine

• Sensitisation – asthma
‫‪CASE1‬‬
‫‪ ‬آقاي ‪26‬ساله با سردرد يك ماهه در آذرماه مراجعه كرده‪.‬دو مرتبه توسط متخصص‬
‫مربوطه با تشخيص سردرد ناشي از استرس و تشديد در اثر فيومهاي محيط كار بررسي‬
‫شده است‪.‬‬
‫‪: PHx ‬سابقه يك مرتبه سردرد در نوجواني مي دهد‪.‬سردرد اخير در حدود‪4‬ماه قبل‬
‫شروع شده كه به تدريج از نظر شدت و تواتر بيشتر شده و به‪OTC‬پاسخ مناسب نمي‬
‫دهد‪.‬سردرد رترواربيتال با انتشار به پشت سرهمراه باحساسيت به نور و سروصدا و‬
‫گاهي تهوع مي باشد‪.‬‬
‫‪OHx ‬شغل نجار و كار بر روي محصوالت روكش داربه مدت ‪ 6‬ماه‪10.‬نفر همكار ديگر هم‬
‫دارد‪.‬فضاي کارگاه ‪ 100*25‬مترمي باشد‪.‬در داخل كارگاه يك اتاقك كوچك باز جهت‬
‫اسپري كردن و استفاده از مواد جال دهنده با تهويه و يك بخاري گازي وجود دارد‪.‬درب‬
‫كارگاه در فصل زمستان كامال بسته مي شود‪.‬‬
‫‪:Task ‬استفاده از مواد جال دهنده‬
‫‪ :MSDS ‬حدود ‪ %70‬متيلن كلرايد‪،‬تولوئن‪،‬متيل اتيل كتون‪،‬ايزوپروپيل الكل‪،‬اتيل استات‬
‫‪،‬ايزوپروپيل الكل‬
CO poisoning

Colorless, odorless and non irritant

40000 emergency visit in USA

CoHb:0.5%in nonsmoker adult and 1% in adult that
typically exposed in environment
CO poisoning
Exposure setting

Incomplete combustion

Smoking:400ppm(0.04%)

PEL:50 ppm

CoHb:3-8% occasionally up to 15%

Inadequate ventilation

Methylene chloride
CO poisoning
Environmental measurement

Colorimetric device

Electronic short testing devices

CO2 measurement(in home)
CO poisoning
Biologic monitoring

CoHb

COHb=[Co]air*KT

220 times affinity co for Hb as O2

Half time=320min
CO poisoning
pathophysiology

Reduce the oxygen-carrying

Alter arterial oxygen tension and
hemoglobin saturation

Cytochrome effect

Reoxygenation and demyelination
CO poisoning
Acute clinical effect

Non-specific =viral infection

COHb 5%:visual perception , +hypoxia without hyeperventilation

COHb>5%:tissue hypoxia,vasodilation ,…syncope….lactic asidosis and
hyperventilation…..seizure,coma,cardiac arrhythmia,MI,Sudden death

Cherry red lips

Retinal hemorrhage

Erythematous lesions with bullae over bony prominences

Sweat gland necrosis

Lab:PaO2,Pulse oximetry,CO oximetry
CO poisoning
Delay effects

Incidance:10-30%

2-40days

Mental deterioration, mood dis,unusual behavior, gait and other movement
disturbance, parkinsonian deficit ,focal neurological sings
CO poisoning
Chronic effects

Erythrocytosis

Angina

Atherosclerosis???
CO Poisoning
Signs and symptoms closely resemble those of
other diseases.
 Often misdiagnosed as:



Viral illness (e.g., the “flu”)

Acute coronary syndrome

Migraine
Estimated that misdiagnosis may occur in up to
30-50% of CO-exposed patients presenting to the
ED.
Source: Raub JA, Mathieu-Holt M, Hampson NB, Thom SR. Carbon Monoxide Poisoning: A
Public Health Perspective. Toxicology 200;145:1-14
Cherry red skin
Signs and
Symptoms
color
is not
always present
when
Severityand, CO-Hb
Signs & Symptoms
present, Level
is often
COHb levels do not
Mild a late finding.
< 15 - 20%
Headache, nausea, vomiting, dizziness, blurred
always correlate
vision.
symptoms
nor
Moderate
21 - 40%
Confusion, syncope,with
chest pain,
dyspnea, weakness,
tachycardia, tachypnea,
rhabdomyolysis.
predict
sequelae.
Severe
41 - 59%
Fatal
> 60%
Palpitations, dysrhythmias, hypotension, myocardial
ischemia, cardiac arrest, respiratory arrest,
pulmonary edema, seizures, coma.
Death
CO poisoning
Clinical evaluation

Clinical suspicion

COHb measurement or CO measurement in exhaled air

Neurology neuropsychology evaluation
CO poisoning
Management

Remove

O2 100%

Mechanical ventilation

Hyperbaric oxygen therapy

any period of unconsciousness

COHb>40%

Pregnancy and COHb>15%

Sign of cardiac ischemia and arrhythmia

PHx of IHD and COHb>20%

Symptom don’t resolved after 4-6h with 100%O2

RECURRENT SYMPTOM after 3W
‫‪case2‬‬
‫‪‬‬
‫آقاي ‪40‬ساله با شرح حال تماس با پودر و مواد جواهرسازی‬
‫توسط همكاران به اورژانس آورده مي شود‪.‬وي داراي يك مغازه‬
‫طالسازي و پرداخت كننده طال مي باشد‪.‬در روز حادثه در هنگام‬
‫كار با مواد صيقل دهنده ‪fan‬باالي سرش را روشن مي كند و پودر‬
‫در داخل مغازه پراكنده مي شود‪.‬بالفاصله فرد سريعا دچار تهوع‬
‫‪،‬استفراغ و احساس سوزش در سراسر بدن مي شود‪ .‬توسط‬
‫همكاران به بيمارستان ارجاع مي شود‪ .‬در هنگام مراجعه فرد‬
‫هوشيار و اورينته ‪ PR=80‬و ‪.BP=100/60‬معاينه شكم و ريه نرمال‬
‫است‪ 4.‬مرتبه ‪LOOSE STOOL‬داشته است ‪.‬سرگيجه تنگي نفس‬
‫و خونريزي و تشنج نداشت‪.‬بعد از ‪ 2‬ساعت ‪BP‬كاهش مي يابد‪.‬‬
‫‪pH 7.30, pO2 50, pCO2 23, HCO3=11.6, ABG‬بود‪ .‬اقدامات‬
‫ساپرتيو موثر نبود و فرد در نهايت فوت نمود‬

Hydrogen cyanide is a
colorless or pale blue
liquid or gas with a
faint bitter almond
like odor
Cyanide

Hydrogen cyanide is formed during the incomplete
combustion of nitrogen- containing polymers, such as
certain plastics, polyurethanes, and wool. Hydrogen
cyanide is present in cigarette smoke

HUMAN EXPOSURE: Cyanides are well absorbed via the
gastrointestinal tract or skin and rapidly absorbed via the
respiratory tract. Once absorbed, cyanide is rapidly and
ubiquitously distributed throughout the body, although the
highest levels are typically found in the liver, lungs, blood,
and brain.
Cyanide

Usage
 Insecticides
& rodenticide
 Electroplating
 Nylon
 Metal
cleaning

PEL:10PPM,

IDHI:50PPM
Cyanide
measurement

Difficult

BM:thiocyanate level in blood or urine
Cyanide
pathophysiology

Cytochrome oxidase enzyme
Cyanide
clinical features

Mild: bitter almond taste, irritation of mucous membrane, dyspnea,headache,
dizziness, nausea and vomiting, agitation

Severe:hypotention ,arrhythmias, cardiogenic and non-cardiogenic pulmonary
edema,lactic acidosis,seizure,coma,

Cherry red skin color

Acute cyanid exp :hyperpnea,respiratory arrest

Delay effect:leukoencephalopathy
Cyanide
chronic clinical effects

Skin and MM irritation and ulcer

Thyroid gland enlargement

Rash, bitter almond ,headache

Smokers amblyopia
Cyanide
management

Sodium nitrate: 10ml of
30%solution(300 mg) over 5-20 min

Amyl nitrate:0.3ml ampoule
crushed every minute inhalation

Sodium thiosulfate:50ml
25%solution(12.5g)IV over 10
minute

Hydroxycobalamine:10ml of 40%
solution(4g) iv over 20 min
‫‪Case3‬‬
‫‪‬‬
‫آقاي ‪ 27‬ساله –كارگر دامپروري ‪-‬به منظور تميز كردن پمپ داخل‬
‫گودالي از كود به عمق ‪ 6‬متر مي شود‪.‬پس از پايين رفتن در‬
‫حدود ‪ 3‬متر داخل گودال سقوط مي كند‪.‬همكار فرد داخل گودال‬
‫مي شود تا وي را نجات دهد كه او نيز به داخل گودال سقوط مي‬
‫كند‪20.‬دقيقه بعد نيروي امداد مي رسد و با كمك آپارات هردو را‬
‫خارج مي كند ولي هردو نفر در مسير بيمارستان فوت مي كنند‬
Hydrogen sulfide
general consideration

Irritant

Asphyxiant in cellular level and
inactive cytochrome oxidase

Odor threshold: 5ppm :rotten eggs

Irritant threshold: 10ppm

>100ppm: toxic effect on the
olfactory nerve
Hydrogen sulfide
exposure

Decay of organic sulfur-containing material: sewer gas

Petroleum process
Hydrogen sulfide
acute clinical effects

CNS abnormality :rapid loss of consciousness“knockdown”

Respiratory paralysis

Tachycardia and hyperpenea,cv collapse

Irritation effects: from MM to pulmonary edema
Hydrogen sulfide
chronic clinical effects

Irritation

Loss of odor sensation

Cognitive and personality
H2S Awareness
Concentration
Health Effects
10 ppm
Beginning eye irritation
50-100 ppm
Slight respiratory tract irritation after 1 hour exposure.
100 ppm
Coughing, eye irritation, loss of sense of smell after 2-15
minutes. Altered respiration, pain in the eyes, and drowsiness
after 15-30 minutes followed by throat irritation after 1 hour.
Several hours exposure results in gradual increase in severity of
these symptoms and death may occur within the next 48 hours
200-300 ppm
Severe respiratory tract irritation after 1 hour of exposure.
Possible pulmonary edema (fluid in the lungs).
Loss of consciousness and possibly death in 30 minutes to 1
hour.
Rapid unconsciousness, loss of respiration, and death after 1-3
minutes.
Unconsciousness at once, loss of respiration and death in a few
minutes. Death may occur even if individual is removed to fresh
air at once.
500-700 ppm
700-1,000 ppm
1,000-2,000ppm
Hydrogen sulfide
clinical evaluation

Awareness of the circumstances: patients breath , clothing

Urinary thiosulfate??
Hydrogen sulfide
management

O2 100%

nitrate
‫‪CASE4‬‬
‫‪‬‬
‫آقاي ‪49‬ساله تكنسين تعميرات يخچال با تنگي نفس شديد‬
‫‪،‬سرفه و ويز مراجعه كرده است‪.‬نامبرده عنوان مي كند در هنگام‬
‫جوشكاري بر روي لوله هاي پشت يخچال دچار اشك ريزش و‬
‫احساس سوزش در دهان و گلو شده است كه به تدريج بدتر‬
‫شده است‪.‬در هنگام جوشكاري بوي سبزي گنديده به مشامش‬
‫رسيده است‪.‬در هنگام مراجعه ديسپنه و ويز بازدمي دارد‪.‬قرمزي‬
‫‪HR=95 BP=110/60‬‬
‫چشم و به نظر كانژكتويت دارد‪.‬‬
‫‪O2sat=98%‬مي باشد‪ CBC.‬و بيوشيمي خون طبيعي است‪.‬‬
‫‪‬‬
‫تشخيص‪:‬‬
Phosgene
general consideration

Synonyms: carbonic acid dichloride ,carbonyl chloride,chloroformyl chloride,
carbon oxychloride

Colorless ,low solubility, oxidant gas, odor rotting vegetables
Phosgene
exposure

Usages: isocyanate ,coal tar, dyes, pharmaceuticals,insecticidesd

Chlorinated hydrocarbon are heated: welding of metals degreased with
solvent(trichloroethylene &trichloroethane) or carbone teracholoride as a fire
fighting
Phosgene
measurement

IR spectrophotometry ,

GC,

phosgene indicator badges
Phosgene
clinical effects


acute

Irritation of MM,

Alveolar injury: acute pneumonitis , pul edema

Delay??
Chronic

PFT abnormalities
Phosgene
managements

Observe at least for 24h

Patent of airway

O2

Positive pressure ventilation

Corticosteroids

Supportive: theophylline, salbutamol
‫‪CASE5‬‬
‫‪ ‬آقاي ‪ 59‬سال شاغل در كارخانه استحصال مس به علت ضعف عمومي‪ ،‬دردشديد‬
‫عضالني ‪،‬تعريق شديد ‪،‬لرز همراه با ادرار تيره(شبيه خون)همراه با تهوع‪،‬استفراغ‬
‫صفراوي توسط همكاران آورده شده است‪.‬هوشيار است و هرگونه درد شكمي و‬
‫تروماي شكم‪،‬سابقه بيماري خوني و يا كليوي را انكار مي كند‪.‬سابقه گاستريت مزمن‬
‫دارد كه گاهي اومپرازول مصرف مي كند‪.‬‬
‫‪T=36.8 HR=78 BP=130/80 RR=18 ‬‬
‫‪Hb=13.8 WBC=18000 PLAT=109000 Cr=1.55 Urea=80 ‬‬
‫‪Pro(+3) WBC=80 RBC=1-2 Epi=more ‬‬
‫‪ ‬سونو‪:‬مختصر ادم اطراف كليه راست‪.‬ساير موارد‪،‬مثانه و پروستات نرمال‬
‫‪ ‬به بخش ارولوژي منتقل شد‪.‬ولي بعد از چند ساعت وضعيت عمومي فرد بدتر‬
‫شد‪.‬يرقان‪،‬تب‪،‬اسهال‪،‬كاهش سطح هوشياري پيدا كرد‪Hb=8 Bill=5.8(indirect) .‬‬
‫‪WBC=20000 Cr=3.59 urea=188‬‬
‫‪ ‬تشخيص؟ اقدام؟‬
Arsine gas (AsH3)

A colorless & odorless gas at low
concentration but smell of “garlic”
at high concentration
• Generated when arsenic containing
metals contact with strong acid
• Intravascular hemolysis ( abdominal
pain, vomiting, hemoglobinuria,
renal failure)
Arsine gas (AsH3)


Acute effect of arsine

Abdominal pain,oliguria,jaundice

Headache,vertigo,hemathemesis,EKG change
Laboratory findings

Anemia,LDH ,reticolositosis,billirobin hemoglobinuria
Arsenic (As)•

Three forms: Inorganic, organic, arsine gas
• Used as insecticides and herbicides, in glassware, alloy and
pigment production, and in the semiconductor industry
• Occupational exposure mostly to inorganic arsenic: – those
involved in the processing of copper, gold, and lead ores. –
Agriculture (pesticides)
• The organic arsenic[V] forms are less toxic than the
inorganic arsenic[III] forms
Acute Arsenic Poisoning

May follow the ingestion of deliberately or accidentally contaminated food or
drink
• Gastrointestinal: metallic or garlic taste, dry mouth, dysphagia, abdominal
pain, profound vomiting, and diarrhea with rice water stools – Shock → multi
organ failure → death
• Survivors often develop:
• Bone marrow suppression (anemia, leukopenia)
– Hemolysis
– Hepatomegaly
– Melanosis
– Polyneuropathy
Chronic arsenic poisoning
• More common form of arsenic poisoning
• Skin : pigmentation, depigmentation, cancer
• Peripheral nerves: sensorimotor neuropathy
• Liver: Cirrhosis
• CVS: hypertension
• Blood: Megaloblastic anemia
• Others: nasal perforation
Ozone’s Effects on Health:
A Story of Good and Bad
Where Healthcare Meets Policy
We Must First Understand Ozone to
Understand the Effects It Has on Our Health
Ozone:
Discovered in a lab in the mid 1800s
From the Greek ozein – “to smell”
A pungent blue gas, detectable in small amounts
Chemical Formula:
O3
Highly reactive with many chemicals
Source: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005.
What Are the Differences Between Ozone in
the Stratosphere and the Troposphere?
Stratospheric Ozone
• 90% of all ozone exists in “ozone layer”
– Naturally forms during chemical reactions between UV
sunlight and O2
– 12,000 ozone molecules per billion air molecules
– Shields humans from harmful UV rays/stabilizes weather
Tropospheric Ozone
• 20–100 ozone molecules per billion air molecules
• It’s the result of human pollution
– Irritates the heart and lungs and traps heat (global warming)
Sources: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005.
Bell ML, McDermott A, Zeger SL, Samet JM, Dominici F. Ozone and short-term mortality in 95 US urban communities, 1987-2000. JAMA. 2004;292:2372-2378.
Some Human-Produced Chemicals
Can Destroy Stratospheric Ozone
 UV protection
 Weather stabilization
Deplete ozone
Refrigerants
Air conditioning
Foam blowing
Industrial cleaning
Chlorofluorocarbons (CFCs)
(Stable in troposphere)
Release chlorine
Stratosphere
CFCs Broken Down by UV
Rays
Bromine-containing
compounds are even
more destructive
Sources: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005.
US Environmental Protection Agency. Ozone Depletion Glossary. Available at: http://www.epa.gov/Ozone/defns.html. Accessed February 9, 2005.
Pollution Produces Bad
Ozone in the Troposphere
Naturally degraded by
chemicals, soils, plants
Fossil fuel
combustion
Hydrocarbons
+
Nitric Oxides
+
Sunlight
Little escape
to stratosphere
 Hospitalization
Emergency room visits
 Respiratory disease
Lung function
 Death rates
Ozone
Source: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: http://www.epa.gov/ozone/science/unepSciQandA.pdf. Accessed February 9, 2005.
High Ozone Levels in the Troposphere Increase
the Risk of Premature Death
Ozone Limits
Maximum 8-hour standard of 80 parts per billion (ppb)
Study of 95 U.S. Cities (1987-2000)
Average daily ozone concentration: 26 ppb
Daily mortality increased .52% per 10 ppb
increase in surface ozone
Age 65–75 Years: daily mortality increased .70%
Sources: Bell ML, McDermott A, Zeger SL, Samet JM, Dominici F. Ozone and short-term mortality in 95 US urban communities, 1987-2000. JAMA. 2004;292:2372-2378.
US Environmental Protection Agency. National Ambient Air Quality Standards for ozone, final rule. Federal Register. 1997;62:38855-38896. Cited in Bell ML, McDermott A,
Zeger SL, Samet JM, Dominici F.
What Do We Now Know About Ozone
and Its Effects on Health?
Ozone in the upper atmosphere is GOOD
• Both are under human control
Ozone in the lower atmosphere is BAD
• Policy and regulations are needed
– to decrease use of ozone-harmful compounds
– to control release of hydrocarbons and
nitric oxides
Ammonia


General consideration

Soluble, colorless, pungent odor, irritant

Ammounium hydroxide with water reaction and necrosis
Exposure

Cleaning agents

Refrigeration equipment, plastic, explosive, fertilizer
Ammonia
clinical effects


Acute

Irritation of MM skin: , sever edema of the larynx; upper airway obstruction

Chemical bronchitis, bronchospasm, pul edema

Blindness and ….

Complete recovery to RADS, bronchopneumonia,bronchiectasis,air way stenosis,
bronchiolitis obliterans
Chronic

Reversible eye, nose, throat irritation
Ammonia
management

Observe for24 h

Airway patency

O2

Bronchodilator

Steroids??
Chlorine

Yellowish green gas, strong odor,sensory irritation,,

Usage & exposure: making paper, bleaching(janitorial cleaning),accidental in
transport and spill , sewage treatment
Chlorine
clinical effects

Acute


Minor mucosal to pulmonary irritation and edema and RADS
Chronic

Air flow obstruction
Chlorine
management

Observe for progressive airway and lung injury

Evaluation: PFT, ABG, CXR

TREATMENT: supportive.steroide??