Nilika G Wijeratne1, James CG Doery1,2 A 20-YEAR AUDIT OF SCREENING FOR LEAD POISONING – CAN WE REDUCE THE COST? Nilika G Wijeratne1, James CG Doery1,2 1 Department of Pathology, Southern Health, Clayton Victoria; 2 Department of Medicine, Monash University, Clayton, Victoria Environmental lead exposure is now a rare occurrence due to the removal of lead from petrol and paint as well as stricter workplace and environmental policies. Nevertheless lead exposure and toxicity still occurs but usually from more exotic sources. METHOD We audited all the lead analyses from 1990-2010 to identify positive cases. Hematological features were reviewed to assess how well they correlated with the lead level. The causes of lead poisoning were also reviewed. DISCUSSION Screening for lead poisoning is usually contemplated as a ‘desperate’ investigation when clinicians are unable to make a firm diagnosis of neurological or GI symptoms. The yield, however, is extremely low. If lead investigations were reserved for patients with Hb<120 g/L, no symptomatic patients would have been missed over the past 20 years and approximately ‘80%’ of lead analyses would have been saved. Hb level would not be a reliable marker to detect asymptomatic lead exposure (0.48-2.4 umol/L) All our symptomatic patients had basophilic stippling at presentation. However, basophilic stippling would not be reliable to detect a symptomatic patient with lead level between 2.4 – 4.1 umol/L. All lead results RESULTS Approximately 640 patients were tested over 20 yrs. 12 individuals (1.9%) had lead levels >0.48 umol/L (above the target Goal for All Australians set by NHMRC) (Table 1) 7 individuals (1.1%) had symptomatic lead poisoning Their lead levels >2.4 umol/L and were candidates for chelation therapy (Figure A) Their Hb was <120 g/L (Figure B) Coarse basophilic stippling (Figure C) was seen in all with lead >4.1 umol/L but absent if lead ≤3 umol/L. (Figure D) Main source of symptomatic lead poisoning was Ayurvedic and herbal medicines. 20% of all individuals, however, had Hb <120 g/L irrespective of their lead levels. Figure A Presenting symptoms Initial Lead (umol/L) Initial Hb level (g/L) Source of lead UNRELATED PRESENTATIONS Unavailable 0.71 102 Uncertain Accidental ingestion of art glaze 1.9 Not available Accidental ingestion of art glaze containing lead silicate HCV infection, heroin addict 137 Sandblaster- ? Work related Submandibular abscess 1.92 140 Fracture left hand 1.98 SYMPTOMATIC PATIENTS Abdominal pain, constipation 4.14 108 Ayurvedic medicine Loss of weight, nausea, vomiting, abdominal pain 5.05 84 Herbal medicine Headache, cough, lethargy, blurred vision 5.4 100 Oxy cutting old railway ridges coated with lead paint Abdominal pain 5.79 90 Myalgia, arthralgia, nausea, lethargy 9.4 98 Use of copper kettle with lead solder Loss of weight, vomiting, abdominal pain 9.54 96 Ingestion of lead weight Tonic clonic seizures, loss of weight 13.0 88 Telecommunication work, pipe/ cable laying Figure B CONCLUSION Lead poisoning is a very uncommon cause for GI and neurological symptoms. It is very unlikely to have a symptomatic chronic lead poisoning with Hb >120 g/L. When lead poisoning is present, the sources of lead poisoning are generally exotic. Herbal remedies especially ayurevedic medicine is becoming a significant cause of concern. Basophilic stippling Figure C REFERENCES Blood lead levels for Australians. NHMRC information paper 2009. URL:http://www.nhmrc.gov.au/_files_nhmrc/file/publications/synopses/gp03-lead-pub-stmnt.pdf Lead poisoning, PPP. URL:http://www.lead.org.au/bblp/sld001.htm Figure D Table 1