Relationship between lead mining and blood lead levels in children

The authors studied blood lead levels of 226 randomly selected children, aged 6-92 mo, who lived in either a lead-mining area or a nonmining area, and 69 controls. The authors sought to determine to what extent mining activities contributed to blood lead levels in the children. The mean blood lead levels in the study and control groups were 6.52 microg/dl and 3.43 microg/dl, respectively. The corresponding proportions of children with elevated blood lead levels were 17% and 3%. Soil and dust lead levels were up to 10 times higher in the study than the control group. Elevated blood lead levels appeared to result from exposure to both lead-mining waste and lead-based paint. Mining waste was the cause of the higher prevalence of elevated blood lead levels in these children.     

Design, construction, implementation, and cost of a hospital pharmacy cleanroom

The authors sought to clarify in a cross-sectional study the possible associations between homeostatic regulators of calcium and occupational exposure to lead. Subjects were 146 industrial male employees, 56 with and 90 without occupational lead exposure. The main outcome measures were serum concentration of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D (calcitriol). The median values of blood lead were 40.5 microg/dl in the exposed group and 4.0 microg/dl in the controls. There were no differences between groups in dietary history and serum calcium levels. PTH and calcitriol levels were significantly higher in the exposed than in the nonexposed subjects (42.0+/-24.2 vs. 33.6+/-14.9 pg/ml, p <0.05; and 83.8+/-27.0 vs. 67.9+/-17.6 pmol/liter, p <0.001, respectively). Multivariate analyses showed that after controlling for possible confounders, occupational lead exposure (no/yes) was independently associated with PTH level (pg/ml) (beta = 7.81, 95% confidence interval (CI) 3.7-11.5) and with calcitriol (pmol/liter) (beta = 12.3, 95% CI 3.84-20.8). It is concluded that subjects occupationally exposed to lead show a substantial compensatory increase in PTH and calcitriol activities which keep serum calcium levels within normal range. This may be of clinical significance since a sustained increase in calcitropic hormones in susceptible subjects may eventually increase the risk of bone disorders.     

Paracrine stimulation of cell growth by cholecystokinin/gastrin through cholecystokinin-B receptor on GH3 cells in vitro

Self-reported reproductive histories of male employees of a lead-zinc smelter were related to pre-conception measures of lead exposure to examine associations between paternal occupational lead exposure and adverse pregnancy outcome. The participants reported 2,021 pregnancies which resulted in 1,684 normal live births, 12 stillbirths, 30 birth defects, 203 spontaneous abortions, and 92 "other" outcomes. Birth defects and stillbirths were combined for the analysis. The risk of a stillbirth or birth defect was elevated for pre-conception employment in a high-lead-exposure compared with a low-lead-exposure job (odds ratio = 2.7, 95% confidence interval = 0.7, 9.6). A similar risk was found for pre-conception blood lead levels of 25-39 μg/dL and >/= 40 μg/dL when compared with blood lead levels of < 25 μg/dL (OR = 2.9, 95% CI = 0.6, 13.3, and OR = 2.5, 95% CI = 0.5, 11.6, respectively). No association was found between pre-conception lead exposure and spontaneous abortion. A relatively low response rate to the questionnaire and potentially erroneous reporting of reproductive outcomes by male workers are limitations of the study.     

Lead exposure causes generation of reactive oxygen species and functional impairment in rat sperm

The relationships between blood lead, sperm lead, sperm reactive oxygen species (ROS) level, and sperm fertile capability were investigated to understand the effects of lead exposure on sperm function and the mechanism of these effects. Male Sprague-Dawley rats, 7 weeks old, were randomly divided into control group and lead-treated group. The controls and lead-treated animals received intraperitoneal injection of 10 mg sodium acetate and 10 mg lead acetate/kg body weight, respectively, weekly for 6 or 9 weeks. The blood lead and epididymal sperm lead were analyzed by graphite furnace atomic absorption spectrophotometer. Chemiluminescence was measured to evaluate the generation of sperm ROS. Sperm-oocyte penetration rate (SOPR) was measured to evaluate sperm function. After 6 weeks of lead exposure, the rats had average blood lead levels of 32 microg/dl, sperm lead levels of 0.67 +/- 0.11 microg/10(9) sperm, unchanged epididymal sperm counts, percent of motile sperms, and motile epididymal sperm counts compared with control animals. However, after 9 weeks of lead exposure, the rats had average blood lead levels of 48.0 +/- 4.3 microg/dl, sperm lead levels of 0.88 +/- 0.16 microg/10(9) sperm, statistically lower epididymal sperm counts, and lower motile epididymal sperm counts. There was a good correlation between the blood lead and sperm lead(r2 = 0.946, P < 0.001). The sperms of lead-exposed rats produced significantly higher counts ofchemiluminescence than did those from the control rats (P < 0.001). The chemiluminescence counts were positively associated with sperm lead level (r2 = 0.613, P < 0.001). Epididymal sperm counts, motility and motile epididymal sperm counts were negatively associated with sperm chemiluminescence (r2 = 0.255, 0.152, and 0.299; P < 0.01, 0.05, and 0.01, respectively). The SOPR were positively associated with epididymal sperm counts, motility and motile epididymal sperm counts (r2 = 0.136, 0.285, and 0.264; P < 0.05, 0.01, and 0.001, respectively). The sperm chemiluminescence was negatively associated with SOPR (r2 = 0.519, P < 0.001). It is concluded that lead exposure probably affected the sperm function by activating one of the pathways of ROS generation.     

Childhood lead poisoning in Asturias

We have determined the blood lead levels of 1,242 children, from newborn to 14 years old, and 79 young mothers in a period of 10 months in Asturias (Spain). All of them were selected at random among those who consulted one of the three main hospitals in Asturias, but none were diagnosed as lead poisoning. We have found a mean blood lead level of 22.11 micrograms/dl; 23.55% had high levels (= 25 micrograms/dl). Sex was not significantly associated with blood lead levels either in the whole sample or in different age groups. Blood lead level increases rapidly from birth (19.3 micrograms/dl) to the age of one year (23.3 gamma/dl), fluctuating around this level until the age of 7. Then it declines with age until adolescence (19.6 micrograms/dl). From October (25.5 micrograms/dl) to July (20.9 micrograms/dl) the decrease in lead blood level was statistically significant. No difference has been found between urban and rural population. The decree of urbanization has not been found significant. The mean blood lead level in the mothers was 20.5 micrograms/dl.     

One-week low-dose triple therapy is effective in treating Helicobacter pylori-infected patients with bleeding peptic ulcers

Although lead has been extensively studied in children, its sources and effects remain unclear in adolescents. This study examined the relation of blood and tibia bone lead levels to lead determinants. One hundred adolescents living in Mexico City and surrounding suburbs were studied. Blood lead was measured by atomic absorption spectroscopy, and tibia lead was measured by a K X-ray Fluorescence (KXRF) instrument. Blood lead ranged from 1.8 to 29.2 microgram/dl, with a mean of 7.4 microgram/dl. Bone lead ranged from <1 to 44.82 microgram Pb/g bone mineral, with a mean of 4.8 microgram Pb/g. Predictors of bone lead included higher traffic density near the home, mother's smoking history, and time spent outdoors. Predictors of log-transformed blood lead included bone lead levels, male sex, use of lead-glazed ceramics, and living in Mexico City. Bone lead remained a significant predictor of blood lead after adjusting for covariates in a final multivariate regression model. In our final model, a rise in bone lead from the middle of the lowest quintile to the middle of the highest quintile (a difference of 21.6 microgram Pb/g) was associated with an increase in blood lead of 1.2 microgram/dl. Our data suggest that in addition to current sources of environmental lead exposure, bone lead accumulated over time constitutes a moderate source of circulating lead during adolescence and may account for some of the adverse health effects documented in recent studies.     

Declining blood lead levels and changes in cognitive function during childhood: the Port Pirie Cohort Study

CONTEXT: Many studies have found a significant inverse association between early exposure to environmental lead and cognitive function in childhood. Whether these effects are reversible when exposure is reduced is not clear. OBJECTIVE: To assess the reversibility of the apparent effects of lead on cognitive abilities in early childhood by testing whether declines in blood lead concentrations beyond the age of 2 years are associated with improvements in cognition. SETTING: Urban and rural communities surrounding a large lead smelter in Port Pirie, South Australia. PARTICIPANTS: A total of 375 children followed up from birth to the age of 11 to 13 years. DESIGN: Long-term prospective cohort study. MAIN OUTCOME MEASURES: The Bayley Mental Development Index at age 2 years, the McCarthy General Cognitive Index at age 4 years, and IQs from the Wechsler Intelligence Scale (revised version) at ages 7 and 11 to 13 years. RESULTS: Mean blood lead concentrations in the children decreased from 1.02 pmol/L (21 .2 microg/dL) at age 2 years to 0.38 micromol/L (7.9 microg/dL) at age 1 1 to 13 years, but cognitive scores in children whose blood lead concentration declined most were generally not improved relative to the scores of children whose blood lead levels declined least. Changes in IQ and declines in blood lead levels that occurred between the ages of 7 and 11 to 13 years (r= 0.12, P= .09) suggested slightly better cognition among children whose blood lead levels declined most. CONCLUSION: The cognitive deficits associated with exposure to environmental lead in early childhood appear to be only partially reversed by a subsequent decline in blood lead level.     

Low-level lead exposure and children's intelligence from recent epidemiological studies in the U.S.A. and other countries to progress in reducing lead exposure and screening in the U.S.A

From the 1980s many well-designed epidemiological studies have confirmed that low-level, subclinical lead exposure in early life is associated with decrements in children's intelligence. Neurodevelopmental deficits from exposure to a low level of lead have been held to be not only an American problem, but also a worldwide issue in the past decade. Good epidemiological studies were reported from England, Scotland, Germany, Greece, Australia and New Zealand. Well-designed cross-sectional and prospective studies were carried out to quantify the magnitude of the relation between full scale IQ in children aged five years or more and the burden of lead (PbB or PbT) in early life of children. Of five cross-sectional studies of blood lead, two demonstrated a significant inverse association between lead and IQ even after adjustment for confounders. Two other studies, however, showed no firm evidence of inverse association after adjustment for confounders, and the remaining study demonstrated no significant inverse association of five cross-sectional studies of tooth lead, two indicated an inverse association between tooth lead and IQ, two others showed no significant inverse association after adjustment for confounders, and the remaining one manifested no association. Of four prospective studies, two revealed strong evidence of an inverse association between blood lead at the age of around two years and IQ. Another one, however, revealed an inverse association between mean postnatal blood level and IQ, while the remaining one demonstrated no significant inverse association between IQ and postnatal blood lead level after adjustment for confounders. In a comprehensive review of 26 epidemiological studies since 1979, including a meta-analysis, Pococok et al. indicated that doubling of the body lead burden (from 10 to 20 micrograms/dl) blood lead or (from 5 to 10 micrograms/g) tooth lead is typically associated with a mean deficit in full-scale IQ of around 1-2 IQ points. Lead in interior household dust, exterior surface soil, and old residential lead paint, which is deteriorated or removed, constitute the major sources of lead poisoning in children in the United States. Infants and children, who typically engage in hand to mouth activities, frequently come into contact with lead dust in soil and on the floor. Marked declines both in air lead and blood lead concentrations are evident parallel to the phase-down of lead in gasoline and soldered cans by U.S. food processors. The major source of lead in drinking water is from lead pipes used in household plumbing. The CDC revised its guidelines concerning childhood lead poisoning, stating that community prevention activities should be triggered when a large percentage of children in a community have blood lead levels of 10 micrograms/dl, the lowest level at which neurodevelopmental effects were believed to occur. For children with blood lead level concentrations between 10 and 14 micrograms/dl, more frequent rescreening may be needed. For concentrations between 15 and 19 micrograms/dl, in addition to more frequent screening, nutritional and educational advice should be given. In cases where these levels persist, there should be environmental investigation and intervention. All children with blood levels of 20 micrograms/dl or greater should receive environmental evaluation and medical examination. Such children may need pharmacological treatment.     

Neurotoxicity in young adults 20 years after childhood exposure to lead: the Bunker Hill experience

OBJECTIVES: An epidemiological study of young adults was conducted to determine whether environmental exposure to lead during childhood was associated with current adverse neurobehavioural effects. METHODS: The exposed group consisted of 281 young adults who had been exposed environmentally to lead as children and the unexposed referent group consisted of 287 age and sex frequency matched subjects. Information on demographics, past and current health, and past exposures to neurotoxicants, and responses to the Swedish Q16 questionnaire were collected by interview. Standard neurobehavioural and neurophysiological tests were administered by computer or trained technicians. K x ray fluorescence was used to estimate tibial bone lead concentrations among the exposed and unexposed groups. Associations were examined between the exposed group and referents and tibial bone lead concentration and the neurobehavioural and neurophysiological outcomes of interest. RESULTS: Among the measures of peripheral nerve function, after controlling for confounders, sural sensory nerve evoked response amplitude, peroneal motor nerve compound motor action potential amplitude, vibrotactile thresholds of fingers and toes, and standing steadiness were significantly associated with exposure group. Among the neurobehavioural tests, hand-eye coordination, simple reaction time latency, trails B latency, symbol digit latency, serial digit, and learning error score were also significantly associated with exposure group after controlling for confounders. Exposed subjects had significantly more neuropsychiatric symptoms than the referents. Associations between tibial bone lead concentration and scores for vocabulary, vibrotactile thresholds of the fingers, and vibrotactile thresholds of the toes approached significance. CONCLUSIONS: Significant adverse central and peripheral neurological effects were found in a group of young adults 20 years after childhood environmental exposure to lead when compared with non-exposed controls. The absence of a significant association between neurological outcomes and tibial bone lead concentration, and the presence of significant associations between neurological outcomes and exposure group may be due to either the magnitude of measurement uncertainty in K x ray films relative to the actual tibial bone lead concentration in these young non-occupationally exposed subjects, or uncontrolled confounding of the exposure group.     

Effects of lifetime lead exposure on spatial and temporal visual function in monkeys

Detailed characterization of several aspects of visual function was performed in two groups of monkeys (Macaca fascicularis) exposed to lead continuously from birth. One group of four monkeys was dosed from birth onward with 500 microg/kg/day of lead as lead acetate, while another group of six monkeys was dosed with 2000 microg/kg/day. Blood lead levels peaked in the former group at 50 microg/dl early in life; the latter group had peak blood lead concentrations averaging 115 microg/dl during infancy. Blood lead concentrations decreased before one year of age to stable levels of 25 or 35 microg/dl in the low and high dose groups respectively. Spatial and temporal visual function was assessed using a psychophysical procedure at 7-9 years of age. Six age-matched controls were tested concurrently. Two treated monkeys had severe hyperopia: one was assessed on temporal vision only and the other was not assessed. Spatial data from a third monkey were considered suspect and excluded. Six of the nine treated monkeys in which temporal vision was assessed had thresholds below control values at low and/or middle frequencies under high luminance conditions. Low-luminance temporal vision was not affected. There was no evidence of impairment of spatial visual function in lead-exposed monkeys with normal refractive status at either high or low luminance. This study suggests that temporal visual function may be preferentially impaired as a result of lifetime exposure to a moderate body burden of lead, although these results require replication before definitive conclusions may be drawn.     

Environmental urban lead exposure and blood lead levels in children of Mexico City

Lead contamination is now a leading public health problem in Mexico. However, there are few data on the lead content of various environmental sources, and little is known about the contribution of these sources to the total lead exposure in the population of children residing in Mexico City. We conducted a cross-sectional study in a random sample of 200 children younger than 5 years of age who lived in one of two areas of Mexico City. Environmental samples of floor, window, and street dust, paint, soil, water, and glazed ceramics were obtained from the participants' households, as well as blood samples and dirt from the hands of the children. Blood lead levels ranged from 1 to 31 micrograms/dl with a mean of 9.9 micrograms/dl (SD 5.8 micrograms/dl). Forty-four percent of the children 18 months of age or older had blood lead levels exceeding 10 micrograms/dl. The lead content of environmental samples was low, except in glazed ceramic. The major predictors of blood lead levels were the lead content of the glazed ceramics used to prepare children's food, exposure to airborne lead due to vehicular emission, and the lead content of the dirt from the children's hands. We conclude that the major sources of lead exposure in Mexico City could be controlled by adequate public health programs to reinforce the use of unleaded gasoline and to encourage production and use of unleaded cookware instead of lead-glazed ceramics.     

Increased lead absorption with anemia and slowed nerve conduction in children near a lead smelter

Studies to evaluate the prevalence, sources, and health consequences of lead absorption were conducted among children living near a primary lead smelter. Lead levels in air, soil, and dust were highest at the smelter and decreased with distance. Ninety-nine percent of one- to nine-year-old children living within 1.6 kilometers had blood lead levels greater than or equal 40 mug/dl, indicating increased absorption, and 22% had levels greater than or equal 80 mug/dl. The prevalence of lead levels greater than or equal 40 mug/dl decreased with distance; at 72 kilometers from the smelter it was 1%. Erythrocyte protoporphyrin levels increased with blood lead levels: 17% of children with lead levels of greater than or equal 80 mug/dl were anemic. There was no overt neurologic toxicity. Significant negative correlation was found in 202 five- to nine-year-old children between blood lead levels and motor nerve conduction velocity (r = 0.38, p less than 0.02).     

Assessment of lead exposure in schoolchildren from Jakarta

Children attending schools in urban areas with high traffic density are a high risk group for lead poisoning. We assessed the magnitude of lead exposure in schoolchildren from Jakarta by analyzing blood lead concentrations and biomarkers of heme biosynthesis. A total of 131 children from four public elementary schools in Jakarta (two in the southern district and two in the central district) were enrolled in the study. To evaluate lead pollution in each area, soil samples and tap water were collected. The mean blood lead concentration was higher in the central district than in the southern district (8.3 +/- 2.8 vs. 6.9 +/- 3.5 microg/100 ml; p<0.05); 26.7% of the children had lead levels greater than 10 microg/100 ml. In 24% of the children, zinc protoporphyrin concentrations were over 70 micromol/mol hemoglobin; in 17% of the samples, hemoglobin was less than 11 g/100 ml. All other values were within the physiological range. Blood lead concentration and hematological biomarkers were not correlated. Analyses of tap water revealed lead values under 0. 01 mg/l; lead contamination of soil ranged from 77 to 223 ppm. Our data indicate that Indonesian children living in urban areas are at increased risk for blood lead levels above the actual acceptable limit. Activities to reduce pollution (e.g., reduction of lead in gasoline) and continuous monitoring of lead exposure are strongly recommended.     

The influence of bone and blood lead on plasma lead levels in environmentally exposed adults

There is concern that previously accumulated bone lead stores may constitute an internal source of exposure, particularly during periods of increased bone mineral loss (e.g., pregnancy, lactation, and menopause). Furthermore, the contribution of lead mobilized from bone to plasma may not be adequately reflected by whole-blood lead levels. This possibility is especially alarming because plasma is the main circulatory compartment of lead that is available to cross cell membranes and deposit in soft tissues. We studied 26 residents of Mexico City who had no history of occupational lead exposure. Two samples of venous blood were collected from each individual. One sample was analyzed by inductively coupled plasma-magnetic sector mass spectrometry for whole-blood lead levels. The other sample was centrifuged to separate plasma, which was then isolated and analyzed for lead content by the same analytical technique. Bone lead levels in the tibia and patella were determined with a spot-source 109Cd K-X-ray fluorescence instrument. Mean lead concentrations were 0.54 microg/l in plasma, 119 microg/l in whole blood, and 23.27 and 11.71 microg/g bone mineral in the patella and tibia, respectively. The plasma-to-whole-blood lead concentration ratios ranged from 0.27% to 0.70%. Whole-blood lead level was highly correlated with plasma lead level and accounted for 95% of the variability of plasma lead concentrations. Patella and tibia lead levels were also highly correlated with plasma lead levels. The bivariate regression coefficients of patella and tibia on plasma lead were 0.034 (p<0. 001) and 0.053 (p<0.001), respectively. In a multivariate regression model of plasma lead levels that included whole-blood lead, patella lead level remained an independent predictor of plasma lead level (ss = 0.007, p<0.001). Our data suggest that although whole-blood lead levels are highly correlated with plasma lead levels, lead levels in bone (particularly trabecular bone) exert an additional independent influence on plasma lead levels. It will be important to determine whether the degree of this influence increases during times of heightened bone turnover (e.g., pregnancy and lactation).     

Cost-effectiveness of screening for asymptomatic carotid stenosis

Exposure to stress has previously been found to impair long-term potentiation (LTP) in the hippocampus. Exposure to stress has also been proposed to induce an LTP-like effect. We examined the effect of acute cold stress on synaptic transmission, neuronal excitability, and LTP induction in the medial perforant path-granule cell synapse of freely moving rats. After obtaining baseline recordings of evoked field potentials at room temperature (23 degrees C), rats were transferred to an environmental cage maintained at 4 degrees C (cold group) or 23 degrees C (control group) and, 90 min later, high-frequency stimulation (HFS) was applied to the medial perforant path. Serum corticosterone measured in trunk blood from rats without implanted electrodes was significantly elevated in cold exposed (28. 7 microg/dl) rats relative to control (6.6 microg/dl). Despite increased corticosterone levels indicative of stress activation, cold exposed rats exhibited LTP of the fEPSP slope and population spike of similar magnitude and time course as controls. In addition, there was no stress-specific effect on the fEPSP slope or population spike and no effect on paired-pulse plasticity. Surprisingly, despite extensive cage acclimation, transferring rats to the environmental cage was associated with a reduction in population spike amplitude and an enhancement in paired-pulse facilitation. The results show that acute cold stress leading to elevated serum corticosterone levels neither induces LTP-like increases in synaptic efficacy nor impairs tetanus-evoked LTP in the dentate gyrus of freely moving rats. Thus, impaired working memory during cold stress is not due to an inability of perforant path synapses to express LTP.     

Lead exposure of workers in the ceramics industry and relevant factors

To clarify lead exposure and factors relevant to it, an occupational health survey and air lead-concentration survey were conducted among 425 workers in the ceramics industry in the Seto region in Aichi Prefecture. As for biological monitoring, blood lead level was measured according to sex, job, product, factory size and duration of lead exposure. The following major findings were obtained in the present analysis. Workers making dolomite novelties showed higher blood lead levels than those making porcelain novelties, semi-porcelain novelties and tableware. The difference in blood lead level by job was statistically significant, but not that by factory size. In males, the highest blood lead level was found for spray painting work (28.7 micrograms/dl), followed by glazing work (28.0 micrograms/dl), kiln work (23.3 micrograms/dl) and painting work (22.3 micrograms/dl). In females, the blood lead level for painting work (13.5 micrograms/dl) was lower than those for glazing work (26.1 micrograms/dl) and kiln work (31.4 micrograms/dl). The blood lead level was significantly increased with the number of years of lead exposure in females (painting work). It was coincidentally clarified that the environmental lead concentration varied according to the job in which workers were engaged. As protective measures against lead exposure for workers in the ceramics industry, the development of nonlead paint and glaze and the introduction of more effective dust collectors at the workplace should be established.     

Lipofuscin product accumulation, insufficient antioxidant defence in erythrocytes and plasma and enhanced susceptibility to oxidative haemolysis after thermal trauma

The paper presents the results of the large-scale blood lead levels survey in pre-school urban children living in industrial area of Poland (Katowice Voivodship, Upper Silesian Industrial Zone-USIZ). The program, established in 1993, involves education, screening and medical care of case-children, as its major elements. Until December 1995 six thousand nine hundred sixty nine children aged 2-6 years have been examined in three towns (Chorzów, Kalowice, Sosnowiec). Geometric mean value of blood lead level (PbB) was slightly but not statistically significantly larger in boys (6.68 +/- 1.51 micrograms/dl) than in girls (6.58 +/- 1.54 micrograms/dl). In a multiple regression analysis the following variables explained variation in PbB: town (p = 0.0001), age (p = 0.005), floor on which apartment was located (p = 0.0001), number of siblings (p = 0.0001), apartment quality (p = 0.0001), carpet in a child's room (p = 0.0001), consumption of locally grown vegetables (p = 0.007), frequent trips outside the region (p = 0.0001). The results were verified with PbB as dichotomous variable. The occurrence of PbB above 10 micrograms/dl (frequency, 14.2%-17.2%) was associated with floor on which apartment was located, number of siblings, apartment's quality, the presence of carpet in child's room and frequent trips outside the region. The occurrence of PbB above 15 micrograms/dl (frequency: 2.5%-4.2% of children) was associated with the same variables and additionally, with the place of residence and intensity of vehicle traffic. The findings yield reliable population-based estimates of the risk of over-exposure of "non-hot-spot" urban children to environmental lead and highlight the important role of factors that could be classified as environmental and socio-economical determinants of blood lead level. Among environmental factors deposits of lead are still a problem in a densely populated industrial center of USIZ and the use of leaded gasoline adds to the magnitude of exposure.     

Development and test of an extendable endoprosthesis for bone reconstruction in the leg

Chemical contamination in the environment is affecting public health in increasing numbers of communities across the country. Although historically and theoretically well within the realm of nursing, methods for assessing and diagnosing threats to community environmental health are not being included in community health nurses' training. A community's environmental health is assessed by retrieving information from federal, state, and local sources. Developing the diagnosis involves four steps: identifying a community aggregate at highest risk of exposure, determining the potential or actual health response, citing related host and environmental factors, and correlating any existing epidemiologic data that may substantiate the nursing diagnosis. To illustrate these concepts, a systematic environmental health assessment was conducted for Douglas, Arizona. The results indicated elevated lead levels in residential soils and led to the community diagnosis, potential for injury: children in Douglas are at risk of developing adverse neurobehavioral health effects, and pregnant women in Douglas are at risk of developing adverse reproductive health effects related to several environmental and host factors, as evidenced by average blood lead level, in children exceeding the Centers for Disease Control recommended level of 10 micrograms/dl.     

delta-Aminolevulinic acid in plasma or whole blood as a sensitive indicator of lead effects, and its relation to the other heme-related parameters

To evaluate the subclinical effect of lead exposure, we determined delta-aminolevulinic acid (ALA) levels in plasma (ALA-P), blood (ALA-B), and urine (ALA-U) and the activity of delta-aminolevulinic acid dehydratase (ALAD) in lead workers. Almost all of the ALA molecules in blood were present in plasma and not in blood cells, irrespective of the blood lead concentration (Pb-B). ALA-P or ALA-B levels increased slowly at Pb-B levels below 40 micrograms/dl (slow phase) and rapidly at levels above 40 micrograms/dl (rapid phase). In both phases, ALA-P and ALA-B were well correlated with Pb-B and ALAD activity. The threshold value (no-effect level) of Pb-B for elevation of the ALA-P or ALA-B level was coincident with that for ALAD inhibition; the value was around 5 micrograms/dl. In the rapid phase, ALA-P increased continuously up to 100 micrograms/dl of Pb-B, while ALAD activity reached a plateau. Receiver operative characteristic (ROC) plot analyses indicated that ALA-P and ALAD activity [ALAD(u)] had a similar diagnostic value at Pb-B levels between 10 and 40 micrograms/dl, although ALAD(%), the remaining ALAD activity as a percentage of the whole activity restored by zinc and dithiothreitol, had the most powerful diagnostic efficiency at these Pb-B levels. By contrast, ALA-U and zinc protoporphyrin were less effective for the diagnosis of lead exposure than ALAD and ALA-P. These findings indicate that ALA-P is the best discriminators of lead exposure form baseline to high levels of exposure.     

Health risks of ionizing radiation

SETTING: Department of Paediatrics and Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India. OBJECTIVE: To assess the plasma zinc status in children with tuberculosis and to correlate it with nutritional status, activity and severity of disease in relation to antituberculosis therapy. DESIGN: The plasma zinc status of 50 children with different forms of tuberculosis was compared with 10 healthy and 10 malnourished children without tuberculosis at 0, 1, 2, 3 and 6 months of antituberculosis therapy. RESULT: The mean plasma zinc concentration in children with pulmonary tuberculosis (n = 20) was 68.65+/-2.50 microg/dl, central nervous system (CNS) tuberculosis (n = 10) was 64.20+/-3.82 microg/dl, tuberculous lymphadenitis (n = 10) was 63.2+/-3.77 microg/dl and disseminated tuberculosis (n = 10) was 59.0+/-2.75 microg/dl at 0 months. The mean plasma zinc level of healthy children was 129.10+/-3.01 microg/dl and in malnourished non-tuberculous children it was 108.40+/-3.16 microg/dl. Thus children with tuberculosis had significantly lower plasma zinc level than those without tuberculosis, irrespective of their nutritional status (P < 0.001). There was a significant rise in zinc level at the end of 6 months of antituberculosis therapy (P < 0.001). CONCLUSION: Plasma zinc status may prove to be a good objective marker for monitoring the severity of the disease and the response to therapy.