2. Occupational poisoning
By:
Sotoudeh-manesh MD
Occupational medicine specialist

3. Introduction Poison: Poisoning: Toxic:
– Any substance that, when administered to a living organism, causes a harmful effect.
Poisoning:
– The morbid condition produced by a poison. – Systemic effects of toxic materials
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)

4. Introduction Gases, vapours and particulates Heavy metals Pesticides
• Common occupational toxic substances can be divided into 4 groups:
Gases, vapours and particulates
Heavy metals
Pesticides
Organic solvents

5. 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.

6. Classification of particles by size:
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
– Dissoluble particles are hazardous (e.g. lead fume)
3. Respirable particle (alveolar region)
– Smaller than 10 μm (0.01mm)
– Deposition in alveolar area (e.g. pneumoconiosis)

9. Particle size Lung parenchyma Water Solubility gases Example
Site of injury
High
Ammonia,formaldehyde
Upper airway
Moderate
Chlorine,sulfur dioxide
Lower airway
Low
NOx ,phosgene
Lung parenchyma
Particle size
>10μm
Dust
2.5 – 6μm
Fire smoke particle
< 2.5μm
Fume ,asbestos fibers

10. Toxic gas
General consideration
Odors
Asphyxiant
solubility

11. Factors affecting the dose of inorganic gas delivered to the respiratory system
Physicochemiacal factors
Concentration
Duration of exposure
Minute ventilation

12. Toxicity of Gases and vapours
• Asphyxiation:
simple asphyxiants
– 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
• Sensitization – asthma

13. 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.
OHxشغل نجار و كار بر روي محصولات روكش داربه مدت 6 ماه.10نفر همكار ديگر هم دارد.فضاي کارگاه 25*100 مترمي باشد.در داخل كارگاه يك اتاقك كوچك باز جهت اسپري كردن و استفاده از مواد جلا دهنده با تهويه و يك بخاري گازي وجود دارد.درب كارگاه در فصل زمستان كاملا بسته مي شود.
Task:استفاده از مواد جلا دهنده
MSDS: حدود 70% متيلن كلرايد،تولوئن،متيل اتيل كتون،ايزوپروپيل الكل،اتيل استات

14. 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

15. CO poisoning Exposure setting
Incomplete combustion
Smoking:400ppm(0.04%)
PEL:50 ppm
CoHb:3-8% occasionally up to 15%
Inadequate ventilation
Methylene chloride

16. CO poisoning Environmental measurement
Colorimetric device(in home)
Electronic short testing devices(in home)
CO2 measurement
Indicator tubes

17. CO poisoning Biologic monitoring
CoHb
COHb=[Co]air*KT
220 times affinity co for Hb as O2
Half time=320min

18. CO poisoning pathophysiology
Reduce the oxygen-carrying
Alter arterial oxygen tension and hemoglobin saturation
Cytochrome effect
Reoxygenation and demyelination

19. CO poisoning Acute clinical effect
Non-specific =viral infection
COHb 5%:visual perception ,CNS+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

22. 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

23. CO poisoning Chronic effects
Erythrocytosis
Angina
Atherosclerosis???

24. 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 % 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

25. Cherry red skin color is not always present and, when present, is often a late finding.
Signs and Symptoms
Severity
CO-Hb Level
Signs & Symptoms
Mild
< %
Headache, nausea, vomiting, dizziness, blurred vision.
Moderate %
Confusion, syncope, chest pain, dyspnea, weakness, tachycardia, tachypnea, rhabdomyolysis.
Severe %
Palpitations, dysrhythmias, hypotension, myocardial ischemia, cardiac arrest, respiratory arrest, pulmonary edema, seizures, coma.
Fatal
> 60%
Death
COHb levels do not always correlate with symptoms nor predict sequelae.

26. CO poisoning Clinical evaluation
Clinical suspicion
COHb measurement or CO measurement in exhaled air
Neurology neuropsychology evaluation

27. 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

28. case2
آقاي 40ساله با شرح حال تماس با پودر و مواد جواهرسازی توسط همكاران به اورژانس آورده مي شود.وي داراي يك مغازه طلاسازي و پرداخت كننده طلا مي باشد.در روز حادثه در هنگام كار با مواد صيقل دهنده fanبالاي سرش را روشن مي كند و پودر در داخل مغازه پراكنده مي شود.بلافاصله 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=80 و BP=100/60.معاينه شكم و ريه نرمال است.4 مرتبه LOOSE STOOL داشته است .سرگيجه تنگي نفس و خونريزي و تشنج نداشت.بعد از 2 ساعت BPكاهش مي يابد. ABG 79= pH 7.30, pO2 50, pCO2 23, HCO3=11.6, SO2 بود. اقدامات ساپرتيو موثر نبود و فرد در نهايت فوت نمود

29. Hydrogen cyanide is a colorless or pale blue liquid or gas with a faint bitter almond like odor

30. 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.

31. Cyanide Usage PEL:10PPM, IDHI:50PPM Insecticides & rodenticide
Electroplating
Nylon
Metal cleaning
PEL:10PPM,
IDHI:50PPM

32. Cyanide measurement
Difficult
BM:thiocyanate level in blood or urine

33. Cyanide pathophysiology
Cytochrome oxidase enzyme

34. 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

35. Cyanide chronic clinical effects
Skin and MM irritation and ulcer
Thyroid gland enlargement
Rash, bitter almond ,headache
Smokers amblyopia

37. 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

38. Case3
آقاي 27 ساله –كارگر دامپروري -به منظور تميز كردن پمپ داخل گودالي از كود به عمق 6 متر مي شود.پس از پايين رفتن در حدود 3 متر داخل گودال سقوط مي كند.همكار فرد داخل گودال مي شود تا وي را نجات دهد كه او نيز به داخل گودال سقوط مي كند.20دقيقه بعد نيروي امداد مي رسد و با كمك آپارات هردو را خارج مي كند ولي هردو نفر در مسير بيمارستان فوت مي كنند

40. 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

41. Hydrogen sulfide exposure
Decay of organic sulfur-containing material: sewer gas
Petroleum process
Underground coal mines
Livestock raising
Nuclear reactors
Sour gas
TLV:20PPM
IDHL:100PPM
سنگین تر از هوا

42. 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

43. Hydrogen sulfide chronic clinical effects
Irritation
Loss of odor sensation
Cognitive and personality

44. H2S Awareness Concentration Health Effects 10 ppm
Beginning eye irritation
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 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
ppm
Severe respiratory tract irritation after 1 hour of exposure. Possible pulmonary edema (fluid in the lungs).
ppm
Loss of consciousness and possibly death in 30 minutes to 1 hour.
700-1,000 ppm
Rapid unconsciousness, loss of respiration, and death after 1-3 minutes.
1,000-2,000ppm
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.

45. Hydrogen sulfide clinical evaluation
Awareness of the circumstances: patients breath , clothing
Urinary thiosulfate??

46. Hydrogen sulfide management
Sodium nitrate 300mg,iv for2-4min

47. Ozone’s Effects on Health: A Story of Good and Bad
Where Healthcare Meets Policy

48. 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
(Title Appears) Ozone is a very small part of our atmosphere, but its presence has significant effects – good and bad – on our health. To understand this concept, one first needs to understand ozone itself. (1st Text Line Appears) Ozone was first discovered in a laboratory experiment in the mid-1800s. (2nd Text Line Appears) The word ozone comes from the Greek word ozein, meaning “to smell”. (1st Text Box Appears) Ozone is a pungent blue gas, detectable in small amounts. (3rd Text Line Appears) It is composed of three oxygen atoms linked together and is signified chemically as 03.1
(2nd Text Box Appears) Ozone is highly reactive with many chemicals. Its reactivity is part of what makes ozone both good and bad.
Highly reactive with many chemicals
Source: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: Accessed February 9, 2005.

49. 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
(Title, 1st Text Box, and 1st Upper Bullet Appear) Ninety percent of ozone exists in the “ozone layer” in the stratosphere. (1st Upper Sub-Bullet Appears) This ozone is naturally formed in chemical reactions involving ultraviolet sunlight and oxygen molecules, which make up 21 percent of the atmosphere. . (2nd Upper Sub-Bullet Appears) That said, ozone is relatively uncommon in the atmosphere, with only 12,000 molecules per billion air molecules in the stratosphere, (2nd Text Box and 1st Lower Bullet Appears) and only 20 to 100 molecules per billion air molecules in the troposphere.1 While most of the ozone that is present in the upper atmosphere is naturally occurring, (2nd Lower Bullet Appears) most ozone in the lower atmosphere is the result of human pollution. . (3rd Upper Sub-Bullet Appears) Ozone above shields humans from the harmful effects of ultraviolet radiation and stabilizes global weather. (1st Lower Sub-Bullet Appears) Ozone below irritates the heart and lungs and traps heat, which contributes to global warming.1,3
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: Accessed February 9, 2005.
Bell ML, McDermott A, Zeger SL, Samet JM, Dominici F. Ozone and short-term mortality in 95 US urban communities, JAMA. 2004;292:

50. Some Human-Produced Chemicals Can Destroy Stratospheric Ozone
Refrigerants
Air conditioning
Foam blowing
Industrial cleaning
 UV protection
 Weather stabilization
Deplete ozone
Chlorofluorocarbons (CFCs)
(Stable in troposphere)
(Title Appears) In the mid-1970s, it was discovered that some human-produced chemicals can destroy ozone. (1st and 2nd Text and first arrow in Cycle Appears) Chlorine-containing compounds like chlorofluorocarbons (CFCs), which are very stable in the troposphere, (2nd Arrow and 3rd Text in Cycle Appear) are readily broken down by ultraviolet radiation in the stratosphere. Such compounds were commonly used in refrigeration, air conditioning, foam blowing, and industrial cleaning. (3rd Arrow and 4th Text in Cycle Appear) The released chlorine atoms (4th Arrow and 5th Text in Cycle Appear) break the ozone molecule apart, (5th Arrow and 6th Text in Cycle Appear) decreasing human protection from cancer-causing ultraviolet radiation and disrupting normal weather patterns.1,2 (Bottom Right Text Box Appears) And bromine-containing compounds, like halon, have proved to be even more destructive.
Release chlorine
Bromine-containing compounds are even more destructive
Stratosphere CFCs Broken Down by UV Rays
Sources: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: Accessed February 9, 2005.
US Environmental Protection Agency. Ozone Depletion Glossary. Available at: Accessed February 9, 2005.

51. Pollution Produces Bad Ozone in the Troposphere
Fossil fuel combustion
Naturally degraded by chemicals, soils, plants
Hydrocarbons + Nitric Oxides +
Sunlight
Little escape to stratosphere
(Title Appears) In the lower atmosphere, the problem is different. (1st Text in Cycle Appears) Here, fossil fuel combustion leads to (1st Arrow and 2nd Text in Cycle Appear) the release of hydrocarbons and nitric oxides. (2nd Arrow and 3rd Text in Cycle Appear) When these are exposed to sunlight, ozone is produced. (Bottom 3rd Arrow and 4th Text in Cycle Appear) Exposure to ozone at high levels is known to be associated with increased rates of hospitalization, increased emergency department visits, exacerbation of chronic respiratory disease, decreased lung function, and increased death rates. (Middle 3rd Arrow and 5th Text in Cycle Appear) Little good comes of this ozone, identical chemically to its naturally occurring stratosphere cousin, because it exists in very small quantities and has difficulty rising to that level. (Upper 3rd Arrow and 6th Text in Cycle Appear) On the surface, it is naturally degraded by other chemicals, soil, and plants.1
 Hospitalization
Emergency room visits
Respiratory disease
Lung function
 Death rates
Ozone
Source: Fahey DW. Twenty Questions and Answers About the Ozone Layer. Available at: Accessed February 9, 2005.

52. 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 ( )
Average daily ozone concentration: 26 ppb
(Title Appears) High ozone levels in the troposphere, independent of other variables such as temperature or particulate matter, are now known to increase premature death.3 (1st Text Box Appears) The current ozone limit set by the U.S. government is (1st text line Appears) a daily maximum eight-hour standard of 80 parts per billion (ppb).4 (2nd Text Box Appears) A study of 95 U.S. cities from 1987 to 2000 (2nd text line appears) showed an average daily ozone concentration of 26 ppb. Tracking death rates several days before and after ozone spikes uncovered that (third Text Lines Appear) daily mortality increased by .52 percent for every 10 ppb increase in surface ozone. (4th Text Line Appears) The risk increased to .7 percent for those age 65 to 75.3
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, JAMA. 2004;292:
US Environmental Protection Agency. National Ambient Air Quality Standards for ozone, final rule. Federal Register. 1997;62: Cited in Bell ML, McDermott A, Zeger SL, Samet JM, Dominici F.

53. 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
(Title Appears) What do we now know about ozone and its effects on health? (1st Text Box Appears) Ozone in the upper atmosphere is good. (2nd Text Box Appears) Ozone in the lower atmosphere is bad. (1st Bullet Appears) And both are under human control. (2nd Bullet Appears) Enlightened policy and regulation can (1st Sub-Bullet Appears) decrease the invasion of the stratosphere by unstable bromine- and chlorine-containing compounds that are destroying its protective layer. (2nd Sub-Bullet Appears) Sound government policy can also control the release of primarily auto-emitted hydrocarbons and nitric oxides that create a deadly ozone brew for humans when exposed to surface sunlight.
to decrease use of ozone-harmful compounds
to control release of hydrocarbons and nitric oxides

54. آقای 49ساله تکنسین تعمیرات یخچال با اشکریزش و سوزش در حلق و گلو و بدنبال دیسپنه و سرفه .خس خس سینه و درد قفسه سینه و تپش قلب مراجعه کرده است
در معاینه دیسپنیک .ضربان قلب 140در دقیقه فشار خون 110/60و o2 sat=98%بود سمع ریه پاک است. آبریزش و اشکریزش دارد.معاینه نبضها غیر منظم است.سایر موارد نرمال است
آزمایشات خون و بیوشیمی خون طبیعی است
An arterial blood gas revealed a pH of 7.39, pCO2 of 36 mmHg, and pO2 of 92 mmHg
CXRنرمال است
نوار قلب:Afبا ریت 140

55. Phosgene general consideration
Synonyms: carbonic acid dichloride ,carbonyl chloride,chloroformyl chloride, carbon oxychloride
Colorless ,low solubility, oxidant gas, odor rotting vegetables
یکی از شایعترین گازهای توکسیک صنعت
فقدان علایم هخطار

56. Phosgene exposure
Usages: isocyanate ,coal tar, dyes, pharmaceuticals ,insecticides
Chlorinated hydrocarbon are heated: welding of metals degreased with solvent(trichloroethylene &trichloroethane) or carbone teracholoride as a fire fighting

57. Phosgene measurement IR spectrophotometry , GC,
phosgene indicator badges

58. Phosgene clinical effects
acute
Irritation of MM,
Alveolar injury: acute pneumonitis , pul edema
Delay??
Chronic
PFT abnormalities
شدت علایم با شدت مسمومیت ارتباط ندارد

59. Phosgene managements Observe at least for 24h Patent of airway O2
Positive pressure ventilation
Corticosteroids
Supportive: theophylline, salbutamol

60. Thanks