Ocupational Poisoning By : Dr ASLANI

OCCUPATIONAL MEDICINE SPECIALIST1

Content

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• Definition• Etiology• Types of Toxicity• Lead• Mercury

Introduction

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Introduction

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HEAVY METALS

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CHEMICAL PESTICIDES

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ORGANIC SOLVENTS

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Gases and vapors

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Types of Toxicity

• Acute toxicity• Chronic toxicity• Irritation and corrosivity• Sensitization• Carcinogenicity• Reproductive toxicity

Types of toxicity continues

• Mechanisms of toxicity:

• Direct local toxicity to tissues first in contact with the substance

• Systemic effects due to the absorption of the substance

• Occupational toxicity deals with the chemicals found in the place of work.

• Persons working in various industries may be exposed to various agents during

the synthesis, or through their use during the occupation.

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Lead

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Lead metal

• Soft • Malleable• Corrosion resistance• Low melting point

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Some Sources of Lead Exposure

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Battery manufacturing Chemical industry

Gasoline additives production Foundry workers Welders

Jewelers Lead miners

Pigment manufacturing

Plastics industry Pottery workers

Radiator repair

Soldering of lead Rubber industry products

Occupational exposure

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Lead in the Environment Lead in the Environment

• Varies from place to place• Soil near roadways

• Elevated in soil, water, or air near lead mining or smelting facilities

• Near smaller businesses and industries that involve lead

Routes of Entry

• Lead gets into the body by the following routes of entry:

• Inhalation (breathing)

• Ingestion (swallowing)

• Skin absorption

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Inhalation

• Inhalation is the primary route of entry for lead. – Occurs when lead dust or fume is

released into the air and inhaled. • welding on steel coated with lead-based

paint• Approximately 40 to 50 percent of the lead

that is inhaled is absorbed into the body

Ingestion

• Lead-based paint was banned from residential because of lead poisoning in children.

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Skin absorption

• Certain lead compounds can be absorbed through the skin (TEL).

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Toxicology

Absorption Respiratory (30 to 40 % ):

Gastrointestinal systems: (10 to 15% )

adults < children Cutaneous

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Toxicology

Increased Absorption: Deficient in calcium

Iron Phosphorus

zinc

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Neurological Effects

Health effects of lead

Gastrointestinal Effects

Heme Synthesis

Renal Effects Reproductive Effects

Other

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Acute Inorganic Lead Toxicity

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Acute Inorganic Lead Toxicity: Excessive exposure in brief period Acute lead poisoning

syndrome. Classic clinical findings : Abdominal colic

Constipation Fatigue hemolytic anemia CNS dysfunction.

in profound case: Acute encephalopathy withComa

Convulsions papill edema

In milder exposures : headaches personality changes

Acute Inorganic Lead Toxicity

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Acute Inorganic Lead Toxicity: Abdominal colic (lead colic)

• it has sometimes been misdiagnosed as appendicitis, peptic ulcer, biliary colic,pancreatitis, pelvic inflammatory disease

Chronic Inorganic Lead Toxicity

Late effects : Chronic renal failure

Hypertension

Gout

Chronic encephalopathy

Classic abdominal colic of acute lead poisoning is absent.

Symptoms: Arthralgias Headache

Weakness Depression

Loss of libido

Impotence

Sperm count dec.

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Physical Exam

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Lead line

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Heath Effects vs Symptomology

• Some workers may experience symptoms at

lower blood lead levels while others may tolerate

very high levels without showing symptoms

Organs and Systems Affected by Lead

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Hematologic toxicity

Anemia induced by lead:

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Effects on the Nervous System

• Damage to the brain may also result in behavioral problems, i.e.,

• Poor memory• Reduced intelligence• Instability of mood(40-70µg/dl)• Visual disturbances• Confusion• Encephalopathy (a degenerative brain

disease) may occur.

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Effects on the Nervous System

• Peripheral neuropathy:– Weakness and/or paralysis of the hands or legs

can cause "wrist drop" or "foot drop".– Motor-sensory neuropathy – Asymmetry

NEWMonths to years of high dose leadexposure (eg, blood lead concentrations >80 μg/dL) may be associated with a

predominantly motor peripheral neuropathy32

Effects on the Kidneys

• Often damage is not detected until it’s too late

• Increase BUN and Cr. until 50-70%of the nephron destroyed.

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NEWMonths to years of high dose leadexposure (eg, blood lead concentrations >80 μg/dL) may be associated with a

predominantly nephropathycharacterized by interstitial fibrosis and

nephrosclerosis.

Lead and hypertension

• Increase mortality heart disease and stroke

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Effects on the Reproductive System

• Female Reproductive Health and Pregnancy:

– Reduces fertility

– Spontaneous abortion

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Organic lead

skin absorption Acute or sub acute CNS symptoms and signs (TEL):

Early symptoms: insomnia, anorexia, muscle irritability

severe poisoning: Agitated encephalopathy, delirium tremens , cerebellar

signs( tremor, ataxia), increased DTR.CSF examination usually is normal.

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LAB FINDING

• Whole blood lead concentration: is the most common and

useful laboratory test to confirm exposure

• Noninvasive K x-ray fluorescence measurement of lead in bone: a biomarker of long-term cumulative lead exposure, is used predominantly as a research tool.

• Measurement of lead in urine following a dose of a chelating agent (chelation challenge testing): correlates satisfactorily in most cases with blood lead test results, and is seldom indicated in clinical practice.

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LAB FINDING

An elevation in erythrocyte protoporphyrin (often measured as zinc protoporphyrin or ZPP):

reflects lead-induced inhibition of heme synthesis. Because there is a time lag of several weeks associated with lead-induced elevation in ZPP,

the finding of a blood lead of ≥30 μg/dL with no

concurrent increase in ZPP suggests that the lead exposure was of recent

onset.38

OSHA standard

o whole BLL :o 1.every 6 months if BLL <40 µg/dlo 2.every 2 months If BLL>40 µg/dl until 2times BLL <40 µg/dlo 3.monthly during removal

o Removal from exposure:o 1. worker BLL>60 µg/dlo 2. worker average BLL >50 µg/dlo 3. worker at risk of health impairment

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OSHA standard

NEW• Current OSHA lead standards that require medical

removal from elevated workplace lead exposure when blood lead levels exceed 50 or 60 μg/dL were enacted several decades ago and offer insufficient protection

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OSHA standard

NEW• An expert panel in 2007 recommended that

removal be initiated for a single blood lead level greater than 30 μg/dL, or when two successive blood lead levels measured over a 4-week interval are ≥20 μg/dL.

• • The longer-term goal should be

for workers to maintain blood lead levels <10 μg/ dL

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Primary Prevention of Lead Poisoning

Engineering controls Substitution of less hazardous material Isolation via containment structure Ventilation via local exhaust system Personal protective equipment Respirator utilization Work practices Personal hygiene practices Periodic inspection/maintenance of control equipment

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Mercury

Mercury

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Exposure

• elemental mercury:is a liquid at room temperature with

a substantial vapor pressure• Inorganic mercury salts:(mercuric sulphide (HgS),

mercuric oxide (HgO) and mercuric chloride (HgCl2))• organic mercury: short-chain alkyl: methyl mercury salts long-chain alkyl non-alkyl organic compounds: phenyl mercury

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General consideration

• Toxicity:

• Specific form and compounds• Route of exposure• Dose• Age

• Bind to sulfhydryl groups and interfere with numerous cellular enzyme systems.

Elemental mercury

• Heavy shiny silver-white metal • liquid or vapor at room temperature

Elemental mercury

• Occupational exposure:• Extraction of mercury & silver & gold• Burning fossil fuels (high- sulfur coal)• Maintenance work on furnaces, flues• Chloralkali production plants ( use of mercury in

the electrolysis of salt)• Dentist & dental technicians

Elemental mercury

• Absorption:• Inhalation is major route of exposure (pulmonary

retention is more than 80%)• Skin and gastrointestinal absorption are poor (0.1%)• Heating increase absorption

• Elimination : - urine

Elemental mercury

• Acute effect:• Primarily affects the respiratory system• ( MFF , bronchial irritation, chemical pneumonitis )• Gingivitis & stomatitis few weeks after recovery• Residual restrictive impairment & ↓ DLCO• ACD (rare)

Elemental mercury

• Chronic effects:• Elemental mercury concentrated in CNS & kidneys

• Classic mercurialism :Primary target organs are Nervous system , Oral cavity and Kidneys

Elemental mercury

• Classic mercurialism (neuropsychiatry): • Fine intention tremor of the extremities, tongue and lips

(early sign of neurotoxicity)

• Erythrism :psychological disturbances, Irritability, Shyness , Memory loss, Hallucination

• Peripheral polyneuropathy (sensor motor axonopathy) with distal paresthesias • DDx : Gilan- Barre

Exposure to Amalgam

Dental amalgam consists of ( by weight ):

50% mercury, 35% silver, 9% tin, 6% copper and a trace amount of zinc

Occupational exposure of dental personnel has been well documented.

Patients exposure to amalgam are small

Inorganic mercury

• More commonly found in nature• Sulphide , oxide, chloride

Inorganic mercury

• Occupational exposure:

• Paint & dyes

• Tannery worker

• Wood preservative

• Taxidermy

• Medicine (antiseptic, diuretic)

Inorganic mercury

Absorption: skin & GI tract (10%)

Acute clinical effects:

• GI: Ingestion of mercuric chloride (HgCl2) May be lethal

(suicide).Direct GI irritation with fluid loss and shock.

• Kidney: ARF, ATN

Organic mercury

• Non alkyl compounds (phenyl)• Long-chain alkyl compounds • Short-chain alkyl compounds

( methyl and dimethyl mercury )

Organic mercury

• Occupational exposure:

• Fungicides

• Bactericides

• Insecticides

• Farmer

• Wood preservatives

Organic mercury

• Absorption Alkyl Mercury Compounds:• Readily absorbed through all routes• skin, gastrointestinal (95%), inhalation• concentrated in RBC & CNS• SCA cross the placenta

Organic mercury

• Acute overdose: • Paresthesias• Ataxia• Generalized weakness• Visual & hearing impairment• Tremor• Muscle spasticity• Coma• Death

Renal effect

• The kidneys contain the highest concentration of mercury following exposure to inorganic salts of mercury and mercury vapor

• organic mercury has a greater affinity for the brain.

Biologic monitoring

• Exposure to elemental, inorganic or non S-C-A mercury compounds:• Periodic measurement of mercury in 24-hour

urine specimens. • Exposure to S-C-A mercury compounds:

• Periodic assessment of mercury in whole blood.

Air exposure Urine Level Action

>50 µg/m³ >100 µg/g cr Remove from exposure until <50 Medical examination if over 150 or if two consecutive levels exceed 100 Repeat measurement weekly

50 µg/m³ 75-100 µg/g cr Monitor weekly Perform hygiene assessment to limit exposure

25-50 µg/m³ 50-75 µg/g cr Monitor monthly

25 µg/m³ 35-50 µg/g cr Monitor quarterly

<25 µg/m³ <35 µg/g cr Monitor semiannually

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