Lead Exposure

A common misconception is that lead toxicity is a problem of the distant past, a problem confined only to areas of urban blight, or a problem only for children exposed to high levels of the toxin. Low-dose exposures still occurs and has a profound impact on childhood development. Identifying lead exposure can help protect the health of your child and may be a pathway for treating learning or behavioral disabilities without the use of powerful stimulant medications.

​

LEAD AND THE DEVELOPING NERVOUS SYSTEM:

​

Lead accumulates inside the body. Because of their size and developing nervous system, children are much more vulnerable to the effects of long-term, low-dose lead exposure. Growing children not only absorb lead more rapidly but also have not developed as effective toxic clearance mechanisms as adults.

​

“We are particularly concerned with lead toxicity at extremely low levels because the metabolism of neurotoxins may be insidiously slow in young organism(s),” observes researcher Donald A. Patillo, M.D., and his colleagues, who recently explored the relationship between maternal blood levels and fetal neuromotor development. They found that prenatal exposure to lead levels previously thought “unimportant” or “benign ” were associated with striking neurobehavioral deficits, including poorer motor control, reduced attention span and “nervous system irritability.”‘

​

IMPACT ON LEARNING AND BEHAVIOR:

​

Low-dose lead exposure has a profound impact on brain development. Lead interferes with cellular growth and reduces the brain’s ability to transmit neural impulses. Lead can also damage developing cells in the cerebral cortex and frontal lobes of the brain; these regions are linked to motor control and are particularly sensitive to lead toxicity.

​

In animal studies, lead blocks brain chemical reactions (mediated by norepinephrine) that stimulate emotional inhibition, possibly triggering impulsive reactions. Lead may also trigger overresponsiveness in children by interfering with the normal process of “neuronal pruning” that takes place at young ages. (1)

​

These insidious neurobehavioral effects can occur at very low doses. A recent study in Pediatrics reports that even low-level lead exposure has a severe impact on toddlers, significantly increasing patterns of impulsive, hyperactive, and easily frustrated behaviors. (3)

​

Dr. Robert Tuthill of the University of Massachusetts School of Public Health evaluated lead levels in the hair of 277 first graders and found “a striking dose-response relationship between levels of lead and negative teacher ratings.“ (4)

​

Unfortunately, the detrimental impact of early lead exposure on learning and behavior often carries over into later years, leading to increased risk of academic failure, aggressive/antisocial behavior, delinquency, depression, and anxiety. (2, 5)

​

In a cross-sectional study involving 877 children (aged 6 months to 5 years) participating in the Quality Improvement Demonstration Study, results indicate that folate supplementation may have a protective role in mitigating the negative association observed between blood lead levels and cognitive functioning. After adjusting for confounders, a 1 microg/dL increase in blood lead levels was associated with a 3.32 point decline in cognitive functioning in children aged 6 months to 3 years and a 2.47 point decline in children aged 3 to 5 years. Additionally, blood lead level was inversely associated with hemoglobin and folate levels. Furthermore, higher folate level was found to lessen the negative association between blood lead level and cognitive functioning. Thus, the authors of this study conclude, “These population-based data suggest greater lead toxicity on cognitive function than previously reported. Our findings also suggest that folate and iron deficient children a re more susceptible to the negative cognitive effects of lead. Folate supplementation may offer some protective effects against lead exposure.” (10)

​

SOURCES OF LEAD:

​

A common myth is that since lead has been taken out of gasoline in the U.S. and is rarely used in indoor house paint in new homes, the chances of being exposed are now very slim. Unfortunately this is not the case. Once released, lead is extremely resistant to break down in the environment. Exposure today still occurs from contaminated air, water, and soil.

​

Lead in drinking water is estimated to constitute about 10-20% of total lead exposure in children; in infants fed with baby formulas using tap water, this proportion rises to 40-60%. (6)

​

Lead can readily contaminate drinking water through pipe corrosion or through lead soldering, but also through new brass faucets and fittings which leach lead. While old homes with outdated piping systems constitute a high risk, according to the EPA, the newer the home, the greater the risk of lead contamination [in drinking water]. (6) Lead has no taste or smell or color, so high levels cannot be detected.

​

Lead sticks to soil and – as every parent knows-soil sticks to kids. Because leaded gasoline emissions in previous decades (as well as lead from current industrial releases and fossil fuel-burning sources) has accumulated in soil, toxicologists warn that lead-contaminated soil is now the main source of blood lead levels in children, representing an equal or greater exposure threat than lead paint.

​

Lead paint is still very much around. According to the EPA, 83% of all homes built before 1978 still contain some lead based paint at concentrations of at least one mg/cm. (7) Houses built before 1950 pose the greatest risk for of lead exposure for children, say the Centers for Disease Control. These dwellings still represent over 40% of all housing units in some states. (8) Here in Orange County, California this is not as much an issue.

​

OTHER FACTORS:

​

Iron and calcium deficiencies increase a child’s risk of suffering lead poisoning. Simple methods for reducing contamination risk in children include washing a child’s hands often. (9)

​

ASSESSMENT:

​

Children showing any of the following early symptoms of low-level lead exposure should be evaluated for heavy metal toxicity:

​

• slower reaction times

• behavior problems

• developmental delay growth problems

• diminished intellectual ability

• attention deficit

• poor balance

• hearing loss

• a sibling or other close family member with lead exposure

​

ASSESSING EXPOSURE:

​

Hair stores minerals, including lead and thus hair mineral analysis is a practical, noninvasive clinical means of evaluating long-term overall body burden/tissue stores of lead exposure. Evidence suggests that hair lead levels may correlate more closely with physician-diagnosed ADHD symptoms than whole teeth or blood lead levels. (4)

​

Urine shows clearance of toxins from the body, and allows clinicians to assess current or very recent exposure to toxic elements. May be used by practitioners to check for long-term heavy metal toxicity via the use of a provocative challenge agent, e.g., EDTA, DMSA, or our own NDF Mier Chelating Drops. These agents target and attach to specific metals and minerals, pulling them out of tissues and carrying them out in the urine.

​

Red blood cell levels provide information about the impact of toxicity and nutrient imbalances within the cell. Reveals current or recent exposure (hours to days, in some cases weeks) largely independent of tissue stores. RBC assessment is useful for confirming results of hair mineral analysis.

​

REFERENCES:

​

1. American Journal of Obstetrics Gynecology 1999;181: S2-S11

2. JAMA 1996; 26 (5): 363-9

3. Pediatrics 1998; 101 (3): E10

4. Archive Environmental Health 1996; 51 (3): 214-20

5. American J Epidemiology 1999; 149 (8): 740-9

6. www.epa.gov/safewater/pubs/lead1.html

7. Environmental Health Perspectives 1998; 106: 217-9

8. www.cdc.gov/nceh/programs/lead/guide/1997/pdf/chapter1.pdf

9. Archives Pediatric Adolescent Medicine 1998; 152: 1213-8

10. “Associations between cognitive function, blood lead concentration, and nutrition among children in the central Philippines,” Solon O, Riddell TJ, et al, J Pediatr, 2008; 152(2): 237-43.