Lead compounds were used in paint in households in at least the 19th century in the UK, and may be exposed by sanding and other decorating or construction work. Children have absorbed sufficient lead from such surfaces to be poisoned. Another such source is face painting. Cases have also been described due to lead in colourful glasses in mugs. Elemental lead should not be confused with 'lead' in pencils which is made from carbon (graphite).
Tetra-ethyl lead, a neurotoxin, was an early additive to petrol, reducing pre-ignition. This was widely abandoned in the latter years of the 20th century but still may cause exposure in some third world countries or from aviation sources. A significant amount of lead itself entered the environment around roads from this source.
Late in 2015 it was discovered that a 2014 change in water supply in Flint, Michigan poisoned around 100,000 people. This is a potential problem anywhere where lead might have been used as a component in the metal in water supply pipes historically.
- Abdominal pain due to lead colic, constipation, colonic pseudo-obstruction
- Cognitive changes
- As above but may be more vague
- Lead lines (bluish pigmentation at the gum–tooth line) in sub acute poisoning
- Neuropsychiatric effects
- Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
- Microcytic anaemia (with normal total iron binding capacity, basophilic stippling on blood film and a haemolytic component (raised reticulocytes)
- Hypophosphataemia(which may be due to renal phosphate wasting)
Haeme synthesis is impaired when 5-aminolevulinic acid dehydratase is 80 to 90% inhibited which occurs at a blood lead level of approximately 5.5 μg/mL. Features are similar to those of patients with acute porphyria, indeed plumboporphyria, due to a deficiency of ALA dehydratase is named by this analogy (plumbum:Latin:lead). Lead inhibits other enzymes active in the haeme biosynthetic pathway, including coproporphyrinogen oxidase, and ferrochelatase. This leads to more incorporation of zinc instead of iron into protoporphyrin IX (the immediate precursor of haeme). Lead inhibits erythrocyte pyrimidine 5'-nucleotidase and this results in a chronic haemolytic anaemia.
Blood lead level, in an EDTA venous sample, is probably best. A level of 1 μg/mL or higher is considered elevated in adults. Levels of over 100 μg/dL (10 µg/mL) may be seen in acute lead poisoning. Zinc protoporphyrin (ZPP) has also been measured but may be less reliable although it has been suggested to correlate to total lead burden. Free erythrocyte protoporphyrin and zinc protoporphyrin correlate best with 3 month exposure to lead. There is no elevation of porphobilinogen level in lead poisoning unlike in porphyria. Lead is stored in the bones (this can be seen on X-ray imaging), but this can also cause prolonged toxicity, even after removal of the source of exposure.
With severe symptoms chelation treatment:
- Calcium disodium EDTA
- 2,3-dimercaptosuccinic acid (succimer)
- ↑ Friedman LS, Simmons LH, Goldman RH, Sohani AR. Case records of the Massachusetts General Hospital. Case 12-2014. A 59-year-old man with fatigue, abdominal pain, anemia, and abnormal liver function. The New England journal of medicine. 2014 Apr 17; 370(16):1542-50.(Link to article – subscription may be required.)
- ↑ Miranda ML, Anthopolos R, Hastings D. A geospatial analysis of the effects of aviation gasoline on childhood blood lead levels. Environmental health perspectives. 2011 Oct; 119(10):1513-6.(Link to article – subscription may be required.)
- ↑ Hanna-Attisha M, LaChance J, Sadler RC, Champney Schnepp A. Elevated Blood Lead Levels in Children Associated With the Flint Drinking Water Crisis: A Spatial Analysis of Risk and Public Health Response. American journal of public health. 2015 Dec 21; :e1-e8.(Epub ahead of print) (Link to article – subscription may be required.)