Lead poisoning

Three decades ago, plumbism was a major health hazard in North America, particularly in American urban centres and especially for children living in low socioeconomic conditions, in old homes that contained lead-based paint. In addition, children living in proximity to car battery plants and along major highways were at increased risk of lead poisoning because of the use of lead in batteries and the emissions from lead-based gasoline. The prevalence of plumbism has decreased considerably during the last 30 years, but the toxic effect of lead on the developing central nervous system (CNS) remains a significant problem. What lessons have been learned from plumbism and what are the challenges for the future?

Lead is a metal that has no biological function in humans. It may be absorbed from the gastrointestinal tract (children with pica are especially vulnerable) or through the respiratory system. It is transported through blood and causes injury to several organs, including the kidney (renal failure, hypertension), bone marrow (anemia) and, especially, the CNS. The mechanism of injury to the brain includes disruption of the blood brain barrier, reduction of N-acetylaspartate/creatine and phosphocreatine ratios in frontal lobe gray matter (1), and in animal studies, disruption of N-methyl-D-aspartate receptor units in the hippocampus causing deficits in memory and spatial learning (2).

Before legislation that prohibited the use of lead-based paint in the interior of homes, the ingestion of chips of paint from dilapidated walls was the most common cause of lead poisoning in children. The ingestion of a ‘lead chip’ the size of a 25 cent piece was sufficient to cause lead encephalopathy and death. Old homes remain the greatest hazard today for lead poisoning in children. In most Canadian and American cities there are significant numbers of houses constructed before 1950 that may still contain lead-based paint. Of equal concern is the dissemination of lead ‘dust’ during the renovation process in old homes. Unless precautions are followed, the contaminated dust may be inhaled and cause plumbism, particularly in children.

Lead poisoning is difficult to diagnose unless the physician has a high index of suspicion. The symptoms and signs of plumbism reflect the blood lead levels (BLL). Gastrointestinal symptoms including abdominal cramps, constipation and vomiting are associated with BLL in excess of 20 ug/dL (0.966 mmol/L). Lead encephalopathy is more common in children than adults and is characterized by lethargy, headache, seizures and other signs of cerebral edema, including status epilepticus and coma. BLL found in children with encephalopathy range from 100 ug/dL to 300 ug/dL (4.83 mmol/L to 14.49 mmol/L). Unfortunately, in the past, many of these children died. Those that survived had a high incidence of epilepsy, cognitive impairment, poor memory and learning problems. Radiographs of the long bones often showed ‘lead lines’ in the metaphysis, and occasionally, basophilic stippling of red blood cells was evident. Most of these children were investigated for seizure disorders or brain tumours until the correct diagnosis was contemplated and established. Paediatric residents training in areas where plumbism was endemic soon learned to screen for lead poisoning in children by completing a urine coproporphyrin test at the bedside. Glacial acetic acid was added to a sample of urine, followed by the addition of ether and 1.5 N hydrochloric acid. An orange fluorescence of the urine sample by illumination with a Wood’s light indicated a positive test and led to the immediate determination of the BLL. The management of lead poisoning then and now is based on the use of chelating agents that include 99mTc-dimercaptosuccinic acid (succimer), ethylenediaminetetraacetic acid (versanate), British anti-Lewisite (dimercaprol) and penicillamine. The severity of the lead poisoning dictates the choice of chelating agent.

The dramatic decrease in the severity of lead poisoning in children living in North America during the past three decades is the result of laws that restrict the use of lead-based paint, the removal of lead from gasoline and surveillance of children at risk for plumbism. However, what has been learned is that blood levels previously thought to be safe and without biological consequence are now known to cause significant long term sequelae to the CNS. It is now established that even small amounts of lead may cause irreparable injury to the developing brain. Recent studies in Canada and the United States show that 4% to 5% of children have elevated BLL (3,4). An important study reported by Canfield et al (5) showed that BLL concentrations were inversely associated with intelligence quotient scores in children, even when the lead levels were below 0.483 mmol/L. These data suggest that greater attention must be given to prevention and that physicians should be diligent in assessing children at risk for lead poisoning.

Children at risk for lead poisoning include those living in impoverished and overcrowded homes, inhabitants of large urban cities and recent immigrants from countries that have not enacted measures to decrease lead exposure among children. Primary prevention strategies have been developed to identify at-risk toddlers and children. The American Academy of Pediatrics recommends that at every visit parents be asked the following questions to determine if further testing is required:

• does your child live in or regularly visit a house or child care facility built before 1950;

• does your child live in or regularly visit a house or child care facility built before 1978 that is being or has been renovated or remodeled within the past six months;

• does your child have a sibling or playmate who has or did have lead poisoning; and

• have you seen your child eat paint chips (6).

In most cases, the detection and management of lead poisoning comes too late, as the child will inevitably be left with significant neurologic sequelae. The challenge for the future is to eliminate lead from the environment while utilizing primary prevention strategies to identify children at risk.