Many parents with infant children living in urban areas of New York are unaware of how lead poisoning can effect the growth of their child.  Elevated lead levels in an infant’s blood can cause serious problems in their brain development.  Moreover, many parents who have children diagnosed with elevated lead levels are unaware of how this poisoning occurs.  The following is a brief scientific overview of the common causes of lead poisoning and how it effects a developing infant.                   

The infant brain is undoubtedly sensitive to lead. The rapid of post-natal central nervous system development coincides with a time when infants are engaging in a high degree of hand-to-mouth activity.  Thus, young children living in environments where there are lead hazards can ingest significant amounts of lead dust at a time when their brains are most sensitive to the toxicant’s effects.

Exposure to a lead-contaminated environment can cause injury to an infant even when blood lead levels do not rise above the level defined as lead poisoning by the governmental agencies charged with setting the level that constitutes “poisoning”.

Lead ingestion and resulting injury frequently exists without external manifestations or subjective complaints, that is, without any overt signs or symptoms. For this reason, lead poisoning has sometimes been referred to as a silent epidemic.  Injury in the form of impairment of heme synthesis is an important concept in understating the mechanisms with by ingested lead particles first injure the body.

Injury resulting from lead exposure and ingestion of lead-based paint initially takes the form of an impairment of heme synthesis, that is, the body’s ability to synthesize new red blood cells and heme proteins throughout all the organs in the human body.

When a child begins to crawl and move around in a lead contaminated environment containing lead based paint chips, dust and peeling paint hazards, exposure and ingestion are inexorably contemporaneous.

In such an environment, very small particles of lead-based paint that cannot be seen by the naked eye unavoidably get into the household dust. This dust can come not only from areas of chipping, peeling, cracking paint in an apartment, but also from friction surfaces, such as window sills and doors being opened and shut.  Particles of this size and nature are the general cause of childhood lead poisoning because they totally pervade a child’s living environment and can remain in the environment for months despite normal cleaning routines.

Due to normal hand-to-mouth activities as the infant moves about in a lead-contaminated environment, the ingestion of microscopic lead particles is inevitable and unavoidable. In the case at hand, the infant was observed actually ingesting paint particles.

The primary route of lead absorption is ingestion. Absorbed lead is cleared by the kidneys in the urine and unabsorbed lead is eliminated in the feces.  Absorbed lead is carried throughout the body by the blood within the major burden (+95%) is carried by erythrocytes and the remainder, that most accessible to other tissues, in the plasma.

Lead’s impairment in heme production in a child’s body who is excessively exposed to lead is described in the following excerpt from the 1993 National Academy of Sciences publication:

The aspect of heme-synthesis disturbances by lead that has been most widely exploited as a biologic marker of early effect has been the accumulation of the heme precursor erythrocyte protoporphyrin IX or zinc protoporphyrin (EP or ZPP) in blood of children and in some adult populations.  EP accumulates in response to lead-related inhibition of the activity of the intramitochondrial enzyme ferrochelatase or lead-related impairment of intramitochondrial iron transport [Citations omitted] EP increase therefore indicates a generalized mitochondrial toxic response.

Heme synthesis impairment is a bodily injury by any definition and impairment of heme synthesis can be present without elevation in blood levels.