An analysis of maternal and fetal hair lead levels

Authors


* Dr S. Lindow, Department of Obstetrics and Gynaecology, Hull Maternity Hospital, Hedon Road, Hull HU9 5LX, UK.

Abstract

Lead contamination of the environment is an important public health consideration. There is evidence of declining blood lead levels in Britain, however, there is still concern about chronic exposure of the fetus and young children to low levels of lead and the effect that this has on neurodevelopment. Hair lead levels have been found to correlate well with body lead contamination. This study is the first to document the level of hair lead in pregnant women and their babies from an urban British population. There was no evidence of toxic maternal lead levels and the fetus is protected by the placental barrier.

Introduction

The increasing use of lead in industry, particularly automotive fuel, has led to recognition of the toxicity of chronic lead exposure. The most important chronic effect is neurotoxicity with the impairment of neurological development in children with high lead levels1,2. Developmental delay has also been found in infants with evidence of high lead levels in maternal and fetal blood3. A long term prospective study has demonstrated that this impairment occurs as a result of cumulative exposure to lead4. Importantly, there is evidence that this neurodevelopmental impairment is reversible if the child's lead exposure is reduced5.

Pregnancy has been targeted as a key area because of the vulnerability of the fetal nervous system during its development. Studies of maternal and fetal blood lead levels have shown high correlation with fetal levels between 55% and 92% of maternal levels1,6. In addition, it is known that 95% of lead stored in humans is in the skeleton. There was indirect evidence that lead could be substituted for calcium and thus would be mobilised in episodes of calcium stress, such as during pregnancy, shown through the use of lead isotope studies in migrant women7.

As it is the chronic exposure to lead and its accumulation in the soft tissues that are important in its toxicity, single measurements of blood lead may not be the best indicator of risk. It has been shown that lead is taken up into hair and incorporated into hair protein, where it remains very stable and gives an estimation of long term exposure2.

In this study, it is intended to investigate the relationship between maternal and fetal hair lead and document the normal range in an urban UK population.

Methods

This study was approved by the local ethics and research committee. Seventy-three women who had had delivery of a healthy infant at term (37–42 weeks of gestation) were approached and samples of the mother and baby's hair were taken. Maternal hair samples were all taken in an identical manner from the fine hairs at the nape of the neck. Steel scissors were used to cut the hair and it was marked with thread so that the cut ends were identified. Fetal hair specimens were all taken in an identical manner by cutting the hair on the back of the baby's head with steel scissors.

The laboratory analysis was performed using a previously described method8. After weighing, the hair samples underwent digestion by nitric acid/microwave and were then diluted to a standard volume. Analysis of lead was then performed using a thermoelemental inductively coupled plasma mass spectrometry. The limit of detection was 2.149 ppb of lead in the solution.

Results

Seventy-three mother/infant pairs had results for analysis. Two fetal levels were contaminated during analysis and both mother/fetal pairs were excluded from further analysis.

Of the 71 maternal specimens, 29 had undetectable lead levels. Of the 71 fetal specimens, 69 had undetectable lead levels. The median hair lead levels for detectable and undetectable groups for maternal and fetal samples are presented in Table 1. Demographic data for the mothers with detectable and undetectable hair lead were compared (Table 2). There were no significant differences between the two groups in age, height, weight and number of pregnancies or live births.

Table 1.  Hair lead levels for maternal and fetal samples. Values are median [range] or number (%).
Sample groupHair lead (μg/g)
Total maternal lead (n= 71)0.55 [0–12.07]
Number (%) with undetectable maternal lead29 (41)
Detectable maternal lead (n= 42)1.43 [0.31–12.07]
Number (%) with undetectable fetal lead69 (97)
Detectable fetal lead (n= 2)5.81 [2.08–9.55]
Table 2.  Comparison of demographic details and maternal hair lead for those with detectable and undetectable hair lead. Values are mean (SD) or median [range].
 Maternal detect able hair lead (n= 42)Maternal undetectable hair lead (n= 29)P
  1. *Unpaired t test.

  2. **Mann–Whitney U test.

Age (years)24.9 (4.38)26.4 (6.53)NS*
Height (cm)160.2 (26.1)157.7 (31.1)NS*
Weight (kg)68.8 (12.6)68.7(18.4)NS*
Gravida1.5 [1.0–5.0]2.0 [1.0–6.0]NS**
Parity1.0 [1.0–5.0]1.0 [1.0–5.0]NS**

There was one mother with a hair lead concentration of 12.07 μg/g and another fetus with a hair lead concentration of 9.55 μg/g. The mother with the high lead level had a fetus with an undetectable level of lead and the fetus with a high level had a mother with an undetectable lead level.

The mean maternal hair sample weight was 0.0284 g, and the mean fetal hair sample weight was 0.00897 g. The limit of detection of this method was calculated from the solution and the mean maternal hair specimen must have hair lead less than 0.3783 μg/g to be undetectable, and the mean fetal hair specimen must have hair lead less than 1.1979 μg/g to be undetectable.

Discussion

These results show that hair lead levels in pregnant women are low in this urban British population. This is expected given that the recognition of the acute and chronic effects of lead have led to increasing efforts to remove lead from the environment over the last 20 years. Exposure to lead occurs through diet, the atmosphere and water. Unleaded automotive fuel was introduced in many countries in 1985 and was in widespread use in the UK by 1988. In the UK, there was an attempt to remove older lead containing pipes in the 1980s9. In response to these and other initiatives, there has been a gradual fall in mean blood lead levels from ∼16 μg/dL in the 1970s to 3.9 μg/dL in the 1990s in the UK9. Over this same period, there has also been a decrease in the accepted safe levels of blood lead, in recognition of the fact that there probably is no completely safe level of lead in the body. The current recommended limit is <10 μg/dL1.

Undetectable fetal levels in this study reflect the capability to detect a lead level of 1.1979 μg/g in this size of fetal hair specimen. This shows that lead levels in fetal hair in this population are lower than children's hair lead levels reported in Czechoslovakia10. There it was found that median hair lead concentration in children aged 8–10 was 3.07 μg/g with a range of 0.50–9.72 μg/g for the 2.5 to 97.5 centiles. Blood levels measured simultaneously showed a mean blood lead concentration of 4.42 μg/dL in these children. This is comparable with the reported levels in British populations as discussed above.

Animal studies have confirmed that hair is a suitable medium to evaluate lead exposure. However, it is relevant that lead uptake varies through the hair cycle11. The amount of lead in hair increases with increasing distance from the scalp, indicating that lead is taken up from the atmosphere2. The reported range of lead concentration in hair has varied from 2 to 284 μg/g2 although the higher values are from occupationally exposed populations. Thus, hair lead concentration may represent a better indicator of chronic lead exposure, particularly fetal hair that is all actively growing hair that has not been exposed to the atmosphere.

The results of this study suggest that maternal and fetal hair lead levels are low in an urban British population. This is the first report of fetal hair lead levels and a further study to verify these results and correlate hair lead with blood lead would provide support for this finding.

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