Lead is an abundantly distributed heavy metal in our environment which in higher concentrations is hazardous to the body [1]. Nervous system remains the most severely affected, effect being more pronounced on growing children [2]. Common sources are lead based paint, lead contaminated air, soil, dust, drinking water through lead soldered pipes, lead coated vessels used for cooking, traditional medications and certain cosmetics [1]. Absorbtion of lead varies depending on the chemical form and the mode of exposure (ingestion > inhalation >transdermal). The half life of lead in blood and soft tissues is 35 days as compared to bones being 5-20 years. Bone stores release lead to the blood which may add up to a toxicologically significant amount [3]. We report a boy with lead encephalopathy, who required repeated chelation therapy.

A 7-year-old boy, presented with refractory status epilepticus. He was the first born child of a non-consanguineous marriage from Nilgiris, Tamilnadu, with unremarkable neonatal period. He was developmentally and neurologically normal with no behavioural problems and immunized upto date as per national immunization schedule. There was no family history of seizures. The child was on traditional medicines for about a year for vitiligo over lips and face. He developed unilateral headache 10 days prior to the onset of seizures along with intermittent abdominal pain and vomiting for which symptomatic treatment was given. One such episode of vomiting was followed by right sided focal seizures. The child was given parental anti-convulsants. However, due to worsening of sensorium and uncontrolled seizures, he was put on mechanical ventilation and started on multiple anticonvulsants. Child was gradually stabilized and extubated.

Laboratory analysis showed leucocytosis with polymorphic preponderance and microcytic hypochromic anemia. Serum Iron was low - 21 mcg/dL [Normal 50-120 mcg/dL] though serum ferritin and total iron binding capacity were within normal range. Liver functions, renal functions and coagulation profile were normal. Cerebrospinal fluid analysis showed mild leucocytosis, with minimally elevated proteins. Cerebrospinal fluid Gene X pert for tuberculosis was negative. Neuro-imaging was normal. Heavy metal screening of blood showed high lead levels of 80.31 mcg/dL (acceptable upto 5 mcg/dL). Skeletal survey showed lead lines over lower end of femur (Fig. 1). Parents were screened and their blood lead levels (BLL) were within normal limits.

Fig. 1 X-ray left knee of the index patient showing lead lines (arrows) over lower end of femur and upper end of tibia.

He underwent lead chelation therapy with Dimercapto-succinic acid 30 mg/kg/day for 5 days followed by 20 mg/kg/day for 14 days. Other effective agents including Dimercaprol and Edetate disodium calcium (CaNa2EDTA) could not be procured at that time. Supplementation with Iron, vitamin D, zinc, vitamin C was done. He was stabilized, anticonvulsants were gradually weaned off. BLL dropped to 38.08 mcg/dL. On review after 2 months, BLL showed a rise to 56.38 mcg/dL. Child, however remained asymptomatic. Repeat chelation therapy was given and BLL dropped further to 32.9 mcg/dL only to rise to 62.9 mcg/dL in 2 months. He has undergone four doses of periodic chelation at the time of writing this report. He has been stable except for a few bouts of anger outbursts for which he is on follow up with child psychiatrist. He is on close follow-up and may require further chelation.

Lead is not known to serve any significant biological function and deposition does not spare any organ in the body [1]. It has high affinity for the skeleton and chronic exposure often sequesters large proportion in the bones followed by the kidneys [4]. After a period of initial exposure lead is redistributed to the soft tissues. If cessation of exposure occurs at this juncture, there is a decrease in the blood lead levels post the initial rise [5]. Bone, being a dynamic tissue, undergoes remodelling throughout life which is regulated by a wide range of hormones and local availability factors. Prolonged exposure also results in slow release of lead from the bone stores over a protracted period of time [4]. Children are at high risk of lead poisoning as they are in a state of constant growth and development. Moreover, the growing bones in children undergo perpetual remodelling which allows lead to be regularly re-introduced into the blood stream [6]. Chelation therapy brings down the blood lead levels acutely only to rebound within weeks to months after treatment. Often, repeated courses of chelation are required [5].

This case report emphasizes the need for long term follow-up with periodic monitoring of lead levels in children with chronic lead poisoning to assess the need for repeated chelation therapy. Blood lead concentration may rise to toxic levels even after removal of exposure due to constant re-distribution in a growing child.

1. Wani AL, Ara A, Usmani JA. Lead toxicity: A review. Interdiscip Toxicol. 2015;8:55-64.

2. Keosaian J, Venkatesh T, D’Amico S, Gardiner P, Saper R. Blood lead levels of children using traditional Indian medicine and cosmetics: A feasibility study. Glob Adv Health Med. 2019;8:1-6.

3. Krishnaswamy K, kumar BD. Lead toxicity. Indian Pediatr. 1998;35:209-16.

4. Pounds JG, Long GJ, Rosen JF. Cellular and molecular toxicity of lead in bone. Environ Health Perspect. 1991;91: 17-32.

5. Hu H, Pepper L, Goldman R. Effect of repeated occupational exposure to lead, cessation of exposure and chelation on levels of lead in bone. Am J Ind Med. 1991;20:723-35.

6. Barbosa Jr F, Tanus- Santos JE, Gerlach RF, Parsons PJ. A critical review of biomarkers used for monitoring human exposure to lead: Advantages, limitations, and future needs. Environ Health Perspect. 2005;113:1669-74.