**1. Introduction**

Plasma concentration (>5 to >100 μg/dl) of lead can cause neurological, cardiovascular, hematological, reproductive, renal, immunological, and respiratory problems [1]. The reported lead concentrations of surface sample of soil was 23–35 mg/kg soil, whereas the concentration of the lead elute from soil was 0.6 mg/L, respectively [2]. Lead has the ability to penetrate brain having molecular weight of 207.28 g [3] and elimination half-life of 18 months. Highly contaminated soil could have the concentration of lead 3.03 times higher than the maximum limit for agricultural soil and 1.97 times higher than the value limit for fodder [4], suggesting that lead is very stable in soil and toxic to human [5]. However, soil concentration of lead (11.42 mg/L) could decrease during rainy season relative to dry season [6]. Lead exerts opposite effects on antibody response and phagocytosis [7]. Some plants such as *Cyamopsis tetragonoloba* and *Sesamum indicum* could tolerate lead concentration of up to 1000 mg/kg; hence, they could be used for bioremediation of soil heavily contaminated by lead [8]. The factors responsible for penetration of central nervous system acting agents are lipid solubility, pH, and molecular weight [9]. Hence, toxicological study of chemicals is necessary for the identification of potential toxicants [10]. Severe lead poisoning in young children and neonatal rats may cross microvessel endothelium of the brain. There is evidence that lead can cause brain damage, and lead uptake in the endothelium is reduced by calcium adenosine triphosphatase (ATPase) pump [11]. In view of this, transport of lead through brain capillary was mathematically assessed with a view to identifying pathogenesis of brain injury caused by lead in humans.
