Postnatal blood lead levels

Analysis of the unadjusted data showed that all postnatal blood lead levels were inversely associated with Full Scale IQ measured at age 10 however, only the associations involving PbB level at ages 10 years,... 

Schnaas, L., Rothenberg, S.J., Perroni, E., Martinez, S., Hernandez, C Hernandez, R.M., 2000. Temporal pattern in the effect of postnatal blood lead level on intellectual development of young children. NeurotoxicoL Teratol. 22, 805—810. 

This birth cohort is being followed until all children are aged seven years in order (1) to examine prospectively the relationship between cumulative lead burdens and other possible genetic and sociodemographic influences on developmental outcome at ages 2, 4 and 7 years and (2) to examine longitudinal trends in mother-child lead parameters, and the relationship between antenatal and postnatal blood lead levels and tooth lead. 

To assess the association between prenatal/early postnatal lead exposure and development, we followed a group of urban US infants from birth to 2 years of age. Estimates of the association between lead and Bayley Mental Development Index (MDI) scores at ages 6, 12, 18, and 24 months were obtained using several regression options. In all multivariate models examined, MDI scores were associated with umbilical cord blood lead levels, but not with postnatal blood lead levels. Infants with high cord blood lead levels (10-25 jUg/dl) consistently scored 4 to 8 points lower than infants with low cord blood lead levels (< 3 jUg/dl). Infants vulnerability to lead s developmental toxicity appears to be greatest during the fetal period. 

After birth the sharp distinctions among groups in terms of blood lead levels were lost. In the sample as a whole, mean postnatal blood lead level did not exceed 8 fig/dl at any age and, on most occasions, postnatal levels were not associated with infants cord blood lead classifications. In contrast to the trimodal distribution of cord blood lead levels created by our sampling strategy, the distribution of postnatal blood lead levels more closely approached normality (Rabinowitz et al, 1984). Because extreme postnatal values are much less frequent in our sample than are extreme cord blood values, we can evaluate the hypothesis of an association between infant development and prenatal lead exposure more efficiently than the hypothesis of an association between infant development and postnatal exposure. Moreover, the weak correlations between infants cord blood lead levels and their postnatal lead levels (Rabinowitz et al, 1984) mean that any cord blood lead level-outcome relationship is not likely to be confounded by infants postnatal lead exposures. 

Most of our subjects are middle to upper-middle class white infants, for whom socioeconomic status and quality of caregiving are at most only weakly associated with prenatal or postnatal blood lead levels (Bellinger et al, 1985b, 1986b). They do not display the typical association between demographic/ economic risk factors and increased lead exposure seen in most samples. As a consequence, the likelihood of observing a spurious association between elevated lead exposure and poor outcome is lower in this sample than it is in most samples recruited to study the developmental impact of lead. 

Postnatal blood lead levels compared in pups exposed to lead from conception and... 

Impairment has also been reported at low blood lead levels in other types of behavior/leaming studies in rats. In a test of spatial discrimination, rats were exposed to lead acetate at 745 mg lead/kg/day in the diet indirectly via administration to their dams through gestation and lactation and then directly until testing (at 100 and 200 days of age) (Winneke et al. 1977). The lead-exposed rats were slower to leam the discrimination than were controls. Their PbB levels at postnatal day 16 averaged 26.6 pg/dL and the levels at 190 days averaged 28.5 pg/dL. 

In contrast to the animal studies for prenatal exposure, animal studies for postnatal exposure report effects at blood lead levels similar to those associated with effects in humans. 

Wang, H-L., Chen, X-T., Yang, B., Ma, F. L., Wang, S., Tang, M. L., Hao, M. G., Ruan, D. Y. (2008). Case-Control Study of Blood Lead Levels and Attention-Deficit Hyperactivity Disorder in Chinese Children. Environ. Health Perspect. 116 1401—1406. Wang, L. Pinkerton, K. E. (2007). Air pollutant effects on fetal and early postnatal development. Birth Defects Res. C Embryo Today. 81 144—154. 

Al-Saleh, I., N. Shinwari, M. Nester, A. Mashhour, L. Moncari, G. El Din Mohamed, and A. Rabah. 2008b. Longitudinal study of prenatal and postnatal lead exposure and early cognitive development in Al-Khaij, Saudi Arabia Preliminary results of cord blood lead levels. J. Trop. Pediatr. 54(5) 300-307. 

Support for this idea comes from Rafales et al. (1981). Their study reported no change in activity in rats dosed with 109 ppm Pb postnatally. The possibility of observable general toxicity at this dose is extremely unlikely and blood lead levels were reported in the normal human range (20-30/tg Pb/lOOml). However, amphetamine administration to male rats caused a significant (21 %) increase in locomotor activity over that of controls. 

Ramsay, P. B., Krigman, M. R. and Morrell, P. (1980). Developmental studies of the uptake of choline, gaba and dopamine by crude synapsomal preparations after in vivo or in vitro lead treatment. Brain Res., 187, 383 Ratcliffe, J. M. (1977). Developmental and behavioural functions in young children with elevated blood lead levels. Br. J. Preventive Social Med., 31, 258 Reiter, L. W. (1977). Behavioral toxicology effects of early postnatal exposure to neurotoxins on development of locomotor activity in the rat. J. Occupational Med., 19, 201... 

Gump, B.B., Stewart, P., Reihman, J., Lonky, E., DarviU, T., Parsons, P.J., 2008. Lx)w-level prenatal and postnatal blood lead exposure and adrenocortical responses to acute stress in children. Environ. Health Perspect. 116, 249—255. 

Rhesus monkeys were pre- and postnatally e q)osed to 0, 350, or 600 ppm (parts per million) of lead acetate in the diet over 9 years. These doses resuhed in an averaged daily oral intake of 0, 42, or 70 mg lead calculated for an adult animal. The doses were sub-to dc, and neither the body weight nor the haematological parameters were influenced by lead exposure. Blood lead levels during this period are own in Figure lA. 

Figure 1. The graphs show blood lead levels in control animals and in those exposed to 350 ppm or 600 ppm lead acetate during the first nine years of postnatal development (A) and blood lead levels during the following 32 month of lead free diet (B). Means are given and the standard deviations are included.

Using these procedures, the postnatal blood levels of pups from dams exposed to lead at time of conception were found to be markedly elevated (45 fig lead/dl blood) between postnatal days 4-8 (Table 2). This corresponds with periods of extensive cell acquisition, particularly in the cerebellum which is completely formed postnatally (Jacobson, 1978). Subsequently the blood lead levels dramatically declined to 20jUg/dl by day 12 and then slowly increased to 40 jUg/dl at time of weaning (day 20). 

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