LEAD Francine Lortie-Monette, MD, MSc, CSPQ, MBA Department of Epidemiology and Biostatistics University of Western Ontario 2003

LEAD (heme synthesis inhibitor) Concentrations increased substantially during the Industrial Era. But decreased with the removal of lead from gasoline, paint (interior paint: 50’s, exterior paint: 70’s) and soldered food cans.

Routes of Occupational Exposure Inhalation (e.g. due to abrasive blasting, sanding, removal with heat guns, grinding):  nearly 100% of inhaled lead enters the blood Ingestion (e.g. hand-mouth contact and eating-on-site in construction, battery and refinery workers):  more variable absorption

Lead-using industries / occupations Lead smelters and refineries Glassworks (crystal glass) Artisan trades (ceramics, although lead- containing glazes are becoming rare)

Lead-using industries / occupations (Cont’d) Printing, publishing, photocopiers and related industries Battery making and recycling Wireworks producing sheathing for wires and cables (although cables now mostly coated with plastic or metal sheathing)

Lead-using industries / occupations (Cont’d) Pest control (many insecticides formerly contained lead arsenate) Plastic industries (lead stabilizers) Radiation shielding (used in X-ray rooms and nuclear reactors) Building demolition and construction industries – especially where lead-paint is still used for non- corrosive metal coatings (e.g. on ships and bridges) The use of oxy-acetylene cutters for demolition on such structures can create hazardous lead fumes.

Around the House and Garden Houses built before 1950 are most likely to contain large amounts of lead in paint, plumbing pipes and fixtures, in soil around the base of the house, or near old porches and railings. Home renovations with removal of old paint are a very important cause of lead exposure. Houses built between 1950 and 1980 may have moderate amounts of lead in paint and plumbing, and in outdoor areas.

Around the House and Garden (Cont’d) Still: In 1997: 4.4% of children had elevated blood levels in the USA

Around the House and Garden (Cont’d) In Ontario:  the mean level in children decreased from 0.91 μmol/L (1972) to 0.29 μmol/L (1988) BUT: 4-8% of Canadian children have elevated blood levels  50% of children had elevated levels in a B.C. site near a lead / zinc smelter

Toxicity Lead absorption is not always associated with lead poisoning: Toxicity varies with: Solubility and particle size of the compound Conditions of use

Toxicity Examples: Lead arsenate: Lead carbonate, monoxide and sulphate: Lead chromate: - very toxic - more toxic than other lead compounds - Less toxic (low solubility)

Distribution of Absorbed LEAD Lead absorbed from the lung or from GI tract is distributed in 3 main compartments: i.Blood (blood lead levels reflects recent exposure (prior month)) ii.Soft tissues (kidney, bone marrow, liver, brain) iii.Bone/Teeth (the skeleton = the accumulating reservoir; X-ray fluorescence measurement of lead concentrations is an index of cumulative exposure)

Signs of LEAD Absorption Increased urinary excretion of lead Possibly increased lead blood levels Decreased hemoglobin levels

Health Effects  Acute / Severe  Chronic

Health Effects: Acute / Severe anaemia abdominal colic peripheral neuropathy (extensor weakness) “wrist/ankle drop” central neuropathy with toxic encephalopathy sterility

Health Effects: Chronic Blood Forming Organs: anemia increases the rate of erythrocyte destruction / interferes with heme synthesis pallor

Health Effects: Chronic (Cont’d) Peripheral nervous system (“paralysis”): decreased coordination slowing of nerve conduction Central nervous system (prefrontal cortex, hippocampus, cerebellum): decreased auditory sensitivity & visual motor performance behavioral changes (e.g. attention deficit & memory problems) sometimes (rare) encephalopathy

Health Effects: Chronic (Cont’d) Kidney / Reproductive: irreversible nephritis (glycosuria, proteinuria, chronic renal failure and hypertension risk of fetal damage and of miscarriage

Acute Poisoning Treatment decision based on: –current blood lead level –evidence of current adverse clinical effects –duration of excessive exposure and of symptoms Chelation if blood lead level rises to 80  g / dL, specially if associated with symptoms / signs of central or of peripheral nervous system dysfunction. Chelation rarely considered if blood level is below 60  g / dL.

Treatment In general, blood lead levels decrease by about 305  g / dL per week. Half-life in blood: (about) 25 days soft tissues: 40 days skeletal compartment: (over) 25 yrs

Physical Examination in Lead-Exposed Workers Blood pressure Pallor Appearance of chronic illness Lead (blue-black) lines on gums Abdominal tenderness Motor/sensory/cerebellar neurological deficits Tremor Cognitive function Mood and affect

Physical Examination in Lead-Exposed Workers (Cont’d) For individuals with fertility / reproductive concerns (to exclude other causes of impaired reproductive function): Degree of sexual maturation Testicular atrophy or enlargement Cryptorchidism Orchitis

Prevention Enclosure of the source; ventilation Respirators Personal hygiene/laundering of work clothes

Physical Examination in Lead-Exposed Workers (Cont’d) Ask also about: Home:  living near plant?  lead paint (old house)? In 2000, the Canada Mortgage & Housing Corp. estimated that 15% of houses built before  pre-1989 plumbing? Hobbies:  stained glass, furniture refinishing?

Sampling for Lead (residential) Home entry areas Laundry areas Sinks/bathrooms Vacuum systems Carpets/floors Automobile carpets

Case Scenario Patient who feels tired/lacks energy Blood work: anemia Elevated lead blood level Perhaps subtle signs of peripheral neuropathy

Lowest-effect levels for key lead- induced health effects in adults Lowest-observed effect level (PbB) 2 (  g/dL) Heme synthesis and hematological effects Neurological effectsEffects on the kidney Reproductive function effects Cardiovascular effects Encephalopathic signs and symptoms Chronic nephropathy 80Frank anemia 60 Female reproductive effects Altered testicular function 50 Reduced hemoglobin production Overt subencephalopathic neurological symptoms Peripheral nerve dysfunction (slowed nerve conduction) 40 Increased urinary ALA and elevated coproporphyrins 30 Elevated blood pressure (White males, aged 40-59)  ? Erythrocyte protoporphyrin (EP) elevation in males Erythrocyte protoporphyrin (EP) elevation in females ALA-D inhibition < 10

Lead Levels Traditional Unit of Measurement in blood: –  g/dL International System of Units (SI): –  mol/L (traditional unit X )

Blood Lead Levels (  mol/L)Onset of Effect < 0.5Usual background level Neurological development effects in infants & children. Inhibition of porphyrin enzymes 2.0Allowable occupational exposure > 2.0Altered RBC count Subclinical peripheral neuropathy Clinical peripheral neuropathy 4.0Encephalopathy (chronic exposure) 7.0Encephalopathy (acute exposure) 4.0Early GI symptoms 6.0Colic