Lead poisoning and Burton’s line

Jayne E Camuglia, George Grigoriadis and Christopher P Gilfillan
Med J Aust 2008; 189 (6): 339. || doi: 10.5694/j.1326-5377.2008.tb02057.x
Published online: 15 September 2008

A 66-year-old, previously well man presented with colicky abdominal pain and vomiting. He was a cigarette smoker and consumed homemade spirits daily. On physical examination, the patient had poor dentition, a bluish pigment along the gingival line (Figure, arrow), and generalised abdominal tenderness with no peritonism; he was afebrile with a heart rate of 68 beats/min, blood pressure of 190/90 mmHg with no postural drop, and oxygen saturation of 99% in room air; and all other results were normal. Full blood examination revealed normocytic anaemia (haemoglobin, 90 g/L; reference range, 130–180 g/L) and basophilic stippling. The patient’s blood lead level was elevated at 7.10 μmol/L (reference range, < 0.48 μmol/L), but fell to 2.28 μmol/L after 3 weeks of treatment with the chelating agent 2,3-dimercaptosuccinic acid (DMSA).

Burton’s lead line indicates lead poisoning and occurs due to deposition of lead sulfide, the result of a reaction between sulfur produced by oral flora and lead.1,2 The source of this patient’s lead exposure is unknown. Distilling equipment, especially for spirits, can be a source of lead exposure,3 but testing of this patient’s equipment ruled it out as a source.

  • Jayne E Camuglia1
  • George Grigoriadis1
  • Christopher P Gilfillan2

  • 1 The Alfred Hospital, Melbourne, VIC.
  • 2 Eastern Health, Melbourne, VIC.


  • 1. Pearce J. Burton’s line in lead poisoning. Eur Neurol 2007; 57: 118-119.
  • 2. Nogue S, Culla A. Burton’s line. N Engl J Med 2006; 354: e21.
  • 3. Holstege CP, Ferguson JD, Wolf CE, et al. Analysis of moonshine for contaminants. J Toxicol Clin Toxicol 2004; 42: 597-601.


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