Transcript Lead metal

Ocupational Poisoning
By : Dr ASLANI
OCCUPATIONAL MEDICINE SPECIALIST
1
Content
•
•
•
•
•
Definition
Etiology
Types of Toxicity
Lead
Mercury
2
Introduction
3
Introduction
4
HEAVY METALS
5
CHEMICAL PESTICIDES
6
ORGANIC SOLVENTS
7
Gases and vapors
8
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.
11
Lead
12
Lead metal
•
•
•
•
Soft
Malleable
Corrosion resistance
Low melting point
13
Some Sources of
Lead Exposure
14
Battery manufacturing
Chemical industry
Gasoline additives production
Foundry workers
Welders
Jewelers
Occupational exposure
Lead miners
Pigment manufacturing
Plastics industry
Pottery workers
Radiator repair
Soldering of lead
Rubber industry products
15
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
17
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
18
Ingestion
• Lead-based paint was banned
from residential because of lead
poisoning in children.
19
Skin absorption
• Certain lead compounds can
be absorbed through the skin
(TEL).
20
Toxicology
Absorption
 Respiratory (30 to 40 % ):
 Gastrointestinal systems: (10 to 15% )
adults
< children
 Cutaneous
21
Toxicology
Increased Absorption:
Deficient in calcium
Iron
Phosphorus
zinc
22
Gastrointestinal Effects
Neurological Effects
Heme Synthesis
Renal Effects
Health effects
of lead
Other
Reproductive Effects
23
Acute Inorganic Lead Toxicity
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 with
Coma
Convulsions
papill edema
In milder exposures : headaches
personality changes
24
Acute Inorganic Lead Toxicity
Acute Inorganic Lead Toxicity:
Abdominal colic (lead colic)
it has sometimes been misdiagnosed as
appendicitis,
 peptic ulcer,
 biliary colic,
pancreatitis,
pelvic inflammatory disease
•
25
Chronic Inorganic Lead Toxicity
Symptoms:
Arthralgias
Headache
Weakness
Depression
Late effects : Chronic renal failure
Hypertension
Gout
Chronic encephalopathy
Loss of libido
Impotence
Sperm count dec.
Classic abdominal colic of acute
lead poisoning is absent.
26
Physical Exam
Lead line
27
Heath Effects vs Symptomology
• Some workers may experience symptoms at
lower blood lead levels while others may tolerate
very high levels without showing symptoms
28
Organs and Systems
Affected by Lead
29
Hematologic toxicity
Anemia induced by lead:
30
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.
31
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
NEW
Months to years of high dose lead
exposure (eg, blood lead concentrations >80 μg/dL)
may be associated with a
predominantly motor peripheral neuropathy
32
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.
NEW
Months to years of high dose lead
exposure (eg, blood lead concentrations >80 μg/dL)
may be associated with a
predominantly nephropathy
characterized by interstitial fibrosis and
nephrosclerosis.
33
Lead and hypertension
• Increase mortality heart disease and stroke
34
Effects on the Reproductive System
• Female Reproductive Health and Pregnancy:
– Reduces fertility
– Spontaneous abortion
35
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.
36
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.
37
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/dl
o 2.every 2 months If BLL>40 µg/dl until 2times BLL <40 µg/dl
o 3.monthly during removal
o Removal from exposure:
o 1. worker BLL>60 µg/dl
o 2. worker average BLL >50 µg/dl
o 3. worker at risk of health impairment
39
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
40
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
41
42
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
43
Mercury
Mercury
45
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
46
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
 Remove from exposure until <50
 Medical examination if over 150 or if
two consecutive levels exceed 100
 Repeat measurement weekly
 Monitor weekly
 Perform hygiene assessment to limit
exposure
>50 µg/m³
>100 µg/g cr
50 µg/m³
75-100 µg/g cr
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
65