Biomedical subjects

P B Hammond

Publications and source records attributed to P B Hammond.

16 recordsLinked to original sources

PubMed1991

Lead exposure and growth in the early preschool child: a follow-up report from the Cincinnati Lead Study.

This report is a follow-up of an earlier study of the effects of low to moderate prenatal and postnatal lead exposure on children's growth in stature. Two hundred thirty-five subjects were assessed every 3 months for lead exposure (blood lead level) and stature (recumbent length) up to 33 months of age. Fetal lead exposure was indexed by maternal blood lead level during pregnancy. The adverse effects of lead on growth during the first year of life were reported previously. This analysis covers essentially the second and third years of life. The results indicate that mean blood lead level during this period was negatively associated with attained height at 33 months of age (P = .002). This association was, however, evidenced only among those children who had mean blood lead levels greater than the cohort median (greater than or equal to 10.77 micrograms/dL) during the 3- to 15-month interval. The results also suggest that the effect of lead exposure (both in utero as well as during the first year of life) are transient provided that subsequent exposure to lead is not excessive. It appears that maintaining an average blood lead level of 25 micrograms/dL or more during the second and third year of life was detrimental to the child's attained stature at 33 months of age. Approximately 15% of this cohort experienced these levels of lead exposure. Continued follow-up of this cohort will reveal whether these lead-related deficits persist and whether they continue to be dependent on the level of exposure in an earlier period.

Body Height↗

PubMed1990

Lead exposure in early life: health consequences.

Until very recently it has been considered that of the many manifestations of lead toxicity, those involving the elaboration and function of hemoproteins occur at lower levels of lead exposure than any others. The critical target seems to be the enzyme heme synthetase, which is essential for the insertion of iron into the precursor, protoporphyrin IX. The major consequences of this effect, which have been evaluated in both adults and children, are reduction of circulating levels of hemoglobin and cytochrome P-450-dependent Phase I drug metabolism. Lead clearly inhibits normal hemoprotein function in both respects. The threshold level of lead exposure for these effects seems to be at a circulating lead concentration (PbB) of approximately 30 to 40 micrograms/dL. A growing body of evidence suggests, however, that the functional integrity of the central nervous system is compromised at substantially lower levels of lead exposure, particularly in the human fetus and young child. Early postnatal neurobehavioral development is compromised at maternal or cord PbB of somewhat less than approximately 10 micrograms/dL, a level of lead exposure not uncommon in the general population. Results of more recent cross-sectional and prospective studies indicate that postnatal lead exposure resulting in PbBs as low as 25 micrograms/dL, and probably lower, also are associated with deficits in intellectual attainment, achievement, and behavior. The long-term consequences of these effects remain to be fully evaluated. Little is known concerning basic mechanisms that are responsible for these effects. They may be manifestations of a more basic common effect of lead on cell proliferation and differentiation.

Adult↗

PubMed1990

Lead exposure lowers the set point for food consumption and growth in weanling rats.

Lead (Pb) depresses growth in infants and young children. Our earlier studies using a weanling rat model of Pb exposure suggest that this Pb effect is due to depression of appetite. In the present study we examined whether this depression of appetite is consistent with a down-regulation of the appetite "set point" as described using dietary manipulations following either lesions of certain hypothalamic regions or 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure. Two types of dietary manipulations were employed: (a) consumatory response to hyperalimentation (force-feeding), and (b) consumatory and growth response during the catch-up period following food restriction. In the hyperalimentation experiments, food intake was determined (a) with and without force-feeding, and (b) without Pb and with Pb administered either orally or systemically. Pb exposure reduced food consumption compared to controls. Force-feeding of a liquid diet further reduced food consumption, but only to the level that maintained total caloric intake at, or close to, the level of Pb animals not force-fed. In the food-restriction experiments, weanling rats had their food intake restricted for 4 days and then were provided free access to food, at which time one subgroup of these animals was exposed to Pb. Catch-up of previously food-restricted animals, in terms of food consumption and growth, was the same in the first 2 days, regardless of whether Pb was administered. During the next 10 days, the food intake and growth of the non-Pb-exposed, food-restricted animals gradually converged on the previously free-fed, non-Pb-exposed animals, whereas the food-restricted. Pb-exposed animals converged on the growth-depressed, previously free-fed Pb-exposed animals. All these responses to dietary manipulations are consistent with a reduced set point for appetite rather than with a nonspecific effect of Pb, e.g., aversion to food or general malaise.

Animals↗

PubMed1990

Lead exposure and neurobehavioral development in later infancy.

A prospective methodology was used to assess the neurobehavioral effects of fetal and postnatal lead exposure during the first 2 years of life. Lead was measured in whole blood prenatally in mothers and at quarterly intervals in the infant. Prenatal blood lead levels were low (mean = 8.0 micrograms/dL). However, approximately 25% of the study infants had at least one serial blood lead level of 25 micrograms/dL or higher during the second year of life. Multiple regression and structural equation analyses revealed statistically significant relationships between prenatal and neonatal blood lead level and 3- and 6-month Bayley Mental and/or Psychomotor Development Index. However, by 2 years of age, no statistically significant effects of prenatal or postnatal lead exposure on neurobehavioral development could be detected. Data consistent with the hypothesis that a postnatal neurobehavioral growth catch-up occurred in infants exposed fetally to higher levels of lead are presented.

Child Behavior↗

PubMed1989

Mechanisms by which lead depresses linear and ponderal growth in weanling rats.

Lead is known to reduce linear and ponderal growth in children, even at levels of exposure common in the general population. The mechanism involved is not known. The present study was conducted in order to establish the role of food consumption and insulin-like growth factor (IGFI), also commonly known as somatomedin C (SmC), in lead-induced reduction in growth in weanling rats. A further purpose was to test the hypothesis that depressed growth could be prevented by administration of growth hormone and thyroxine, a procedure which prevents arrested growth due to hypophysectomy. Treatment with growth hormone in combination with thyroxine had no effect on depressed growth or food consumption. The reduction in linear and ponderal growth due to lead (approximately 17%) could be largely though not completely accounted for on the basis of reduced food consumption, apparently by a mechanism not involving growth hormone or thyroxine (see above). Plasma SmC was reduced in proportion to reduced food intake, regardless of whether due to Pb or to restriction of food intake in a pair-feeding experiment thereby ruling out an effect of lead on SmC synthesis or activity other than through reduced food consumption. The experiments leading to these conclusions all involved administration of lead in the drinking water, suggesting the possibility that reduced food consumption was peripherally mediated as a result of contact of lead with appetite-depressant receptors in the gastrointestinal tract, e.g., taste receptors. An additional experiment therefore was conducted comparing food consumption and growth resulting from oral lead administration to subcutaneous administration. Similar depressant effects on food consumption and growth resulted at similar concentrations of lead and zinc protoporphyrin in blood. These effects were significantly greater following oral administration, however, suggesting that lead depresses appetite by both a systemic mechanism and one operating at the level of the gastrointestinal tract.

Animals↗

PubMed1989

Fetal and infant lead exposure: effects on growth in stature.

The growth of a cohort of 260 infants was prospectively followed up from birth. Blood lead and stature measurements were obtained every 3 months until 15 months of age. Fetal lead exposure was indexed by measuring lead in maternal blood during pregnancy. A longitudinal analysis revealed that covariate adjusted growth rates in stature were negatively related to the infants' postnatal blood lead concentration, as indexed by increase in average blood lead values from 3 to 15 months. However, this relationship between growth rate and change in blood lead concentration was evidenced only among those infants whose mothers had prenatal blood lead levels greater than the maternal cohort median of 7.7 micrograms/dL is about 2 cm shorter at 15 months of age if, postnatally, the infant incurred a 10-micrograms/dL blood lead increase during the 3- to 15-month interval of life, compared with an infant who has no increase.

Cohort Studies↗

PubMed1988

Anodic stripping voltammetry procedure modified for improved accuracy of blood lead analysis.

In evaluating the accuracy and reliability of blood lead (PbB) measurements with the Environmental Science Associates Model 3010A Trace Metal Analyzer, intralaboratory comparison demonstrated that use of the operating conditions recommended by the manufacturer resulted in consistently underestimated PbB concentrations less than 400 micrograms/L and overestimated PbB values greater than 400 micrograms/L. At PbB concentrations less than 50 micrograms/L, measured concentrations were often registered as negative results. However, these negative values could be replicated to within +/- 10 micrograms/L, indicating good precision of the method, but obviously not good accuracy. In addition, lower-than-expected lead (Pb) values were measured in samples containing increased concentrations of copper (Cu), such as may occur in pregnant women. We modified the procedure to eliminate these inaccuracies by substituting manual peak-height measurements for reliance on the integrator and digital display of the instrument. We established the accuracy of the modified procedure by using calibration standards previously quantified by isotope dilution-mass spectroscopy. A quality-control program for monitoring PbB analysis is also described.

Copper↗

PubMed1987

Low-level fetal lead exposure effect on neurobehavioral development in early infancy.

A prospective method was used in this study to assess the effects of fetal lead exposure on neurodevelopmental status in 3- and 6-month old infants. At their first prenatal medical appointments, 305 lower socioeconomic status women residing in predesignated lead-hazardous areas of Cincinnati were recruited. Lead was measured in whole blood in both the mother and fetal-placental unit (prenatal and cord) and the neonate (ten days and 3 months). All blood lead levels were less than 30 micrograms/dL. Infant development was assessed with the Bayley scales at 3 and 6 months of age. Multiple regression analyses which treated perinatal health factors such as birth weight and gestation as confounders indicated an independent, inverse relationship between both prenatal and neonatal blood lead levels and performance on the Bayley Mental Developmental Index at both ages. Male infants and infants from the poorest families appeared to be especially sensitive to these psychoteratogenic influences. Further study using a structural equations approach indicated that neurobehavioral deficits were partly mediated by lead-related reductions in birth weight and gestation.

Age Factors↗

PubMed1986

Resistance of the rat to development of lead-induced renal functional deficits.

Lead nephropathy, characterized functionally by depression of effective renal plasma flow (ERPF), glomerular filtration rate (GFR), and maximum glucose reabsorption rate, is associated with prolonged occupational exposure to lead. Production of comparable lead-related renal functional deficits in rats has been difficult to achieve. We have examined in rats some of the factors that might be expected to influence the development of lead-induced renal functional damage, using GFR (as inulin clearance), ERPF (as para-aminohippurate clearance), and maximum glucose reabsorption rate as indices of renal functional competence. Although lead produces a significant weight loss, this can be accounted for by reduced food intake and is not associated with reduction in renal function. Even exposure to large amounts of lead in conjunction with other factors, such as controlled diet (NIH-07 and AIN-76) and early age of initial exposure, that might have been expected to increase the rats' susceptibility has not resulted in the development of renal functional deficits. It is unlikely that the rat can be successfully exploited as an animal model of human lead nephropathy with accompanying functional deficits.

Animals↗

PubMed1979

Trends in university environmental health research and training.

A survey of 157 college and university programs in the United States indicates that, during the ten-year period from 1967 through 1976, the number of people completing graduate programs in environmental health specialties at the master's, doctoral, and post-doctoral levels doubled. In 1974-75, 75 per cent of those completing master's degree programs were in the specialty areas of water pollution, air pollution, and occupational health; 76 per cent of those completing doctoral programs were in water pollution, toxicology, radiation protection, air pollution, and cancer research; and 61 per cent of those completing post-doctoral programs were in cancer research and toxicology. Including those whose current positions could not be ascertained, less than 10 per cent of all graduates accepted employment outside the field of environmental health. Funding for university environmental health research continued to increase throughout this ten-year period. The sources of this funding, however, changed dramatically, with the relative contributions from the U.S. Department of Health, Education, and Welfare decreasing significantly, while those from industry and other federal agencies increased. In contrast, funding for university environmental health training increased significantly between 1966 and 1971, but showed no increase from 1971 to 1975. During this latter period, training support provided by HEW remained essentially constant, that by the Environmental Protection Agency decreased to less than half, while that from the universities approximately tripled. (Am. J. Public Health 69:125-129,1979.)

Education, Graduate↗

PubMed1977