Abstract  Triethyllead and the total lead were determind in the tissues in three acute fatal cases of tetraethyllead poisoning. In each case high concentrations of triethyllead were found (2.0–22.0 mgrg/g) being of the same range as the total lead content. The triethyllead content of the tissues showed a slightly decreasing trend with the length of the surviving period. High levels of the total lead were also found in blood (3.3–4.0 mgrg/ml), and urine (0.4–8.0 mgrg/ml), the highest values being observed after EDTA treatment. The triethyllead content in blood and urine was much lower.

Abstract  The biotic ligand model (BLM) is a mechanistic approach that greatly improves our ability to generate site-specific ambient water quality criteria (AWQC) for metals in the natural environment relative to conventional relationships based only on hardness. The model is flexible; all aspects of water chemistry that affect toxicity can be included, so the BLM integrates the concept of bioavailability into AWQC-in essence the computational equivalent of water effect ratio (WER) testing. The theory of the BLM evolved from the gill surface interaction model (GSIM) and the free ion activity model (FIAM). Using an equilibrium geochemical modeling framework, the BLM incorporates the competition of the free metal ion with other naturally occurring cations (e.g., Ca2+, Na+, Mg2+, H+), together with complexation by abiotic ligands [e.g., DOM (dissolved organic matter), chloride, carbonates, sulfide] for binding with the biotic ligand, the site of toxic action on the organism. On the basis of fish gill research, the biotic ligands appear to be active ion uptake pathways (e.g., Na+ transporters for copper and silver, Ca2+ transporters for zinc, cadmium, lead, and cobalt), whose geochemical characteristics (affinity = log K, capacity = Bmax) can be quantified in short-term (3-24 h) in vivo gill binding tests. In general, the greater the toxicity of a particular metal, the higher the log K. The BLM quantitatively relates short-term binding to acute toxicity, with the LA50 (lethal accumulation) being predictive of the LC50 (generally 96 h for fish, 48 h for daphnids). We critically evaluate currently available BLMs for copper, silver, zinc, and nickel and gill binding approaches for cadmium, lead, and cobalt on which BLMs could be based. Most BLMs originate from tests with fish and have been recalibrated for more sensitive daphnids by adjustment of LA50 so as to fit the results of toxicity testing. Issues of concern include the arbitrary nature of LA50 adjustments; possible mechanistic differences between daphnids and fish that may alter log K values, particularly for hardness cations (Ca2+, Mg2+); assumption of fixed biotic ligand characteristics in the face of evidence that they may change in response to acclimation and diet; difficulties in dealing with DOM and incorporating its heterogeneity into the modeling framework; and the paucity of validation exercises on natural water data sets. Important needs include characterization of biotic ligand properties at the molecular level; development of in vitro BLMs, extension of the BLM approach to a wider range of organisms, to the estuarine and marine environment, and to deal with metal mixtures; and further development of BLM frameworks to predict chronic toxicity and thereby generate chronic AWQC.

Abstract  The toxicity of all atomically stable metals in the periodic table, excluding Na, Mg, K, and Ca, was measured in one-week exposures using the freshwater amphipod Hyalella azteca in both Lake Ontario, Canada, and soft water (10% Lake Ontario). Metals were added as atomic absorption standards (63 metals), and also as anion salts for 10 metals. Lethal concentrations resulting in 50% mortality (LC50s) were obtained for 48 of the metals tested; the rest were not toxic at 1,000 Ág/L. The most toxic metals on a molar basis were Cd, Ag, Pb, Hg, Cr (anion), and Tl, with nominal LC50s ranging from 5 to 58 nmol/L (1 to 58 nmol/L measured). These metals were followed by U, Co, Os, Se (anion), Pt, Lu, Cu, Ce, Zn, Pr, Ni, and Yb with nominal LC50s ranging from 225 to 1,500 nmol/L (88û1,300 nmol/L measured). Most metals were similarly or slightly more toxic in soft water, but Al, Cr, Ge, Pb, and U were >17-fold more toxic in soft water; Pd was less toxic in soft water. Atomic absorption (AA) standards of As and Se in acid had similar toxicity as anions, Sb was more toxic as the AA standard, and Cr and Mn were more toxic as anions. One-week LC50s for H. azteca correlate strongly with three-week LC50s and three-week effect concentrations resulting in 50% reduction in reproduction (EC50s) in Daphnia magna.

Abstract  Metallothionein, a protein of small molecular weight, isolated from equine renal cortex contains 2.9% of cadmium, 0.6% of zinc, and 4% of sulfur. The protein, homogeneous on ultracentrifugation, but containing minor impurities on electrophoresis, does not absorb radiation at and near 280 m'mu', corresponding to a very low content of aromatic amino acids. A large number of cysteine residues account for the high sulfur content. The stoichiometry between titratable --SH groups and metal atoms, the displacement of the metals by --SH specific agents, and the selective removal of zinc and cadmium by hydrogen ions, all suggest isomorphous binding of the two metals to the protein through mercaptide linkages. Although the biological function of metallothionein is not known thus far, the specific association of cadmium with this macromolecule suggests a biological role of this cadmium-containing protein.

Abstract  Aims: Chronic exposure to lead results in sustained hypertension in humans and experimental animals. We investigated the possible role of reactive oxygen species (ROS) and their impact on DNA damage in lead-induced hypertension. Further the effect of short-term supplementation of vitamin C is also demonstrated. Methods: Male Wistar rats were treated with either lead acetate (100 ppm) alone or lead acetate plus vitamin C (20 mg/rat/day). The control rats were fed regular rat chow. Blood pressure, antioxidants, total antioxidant status as measured by ferric-reducing antioxidant power, nitric oxide (NO) metabolites, malondialdehyde (MDA) and 8-hydroxy 2-deoxyguanosine were determined after 0, 1, 2 and 3 months. Results: The lead-exposed group showed a significant rise in blood pressure, lipid peroxidation (MDA) and a substantial oxidative damage to the DNA. A significant fall in NO metabolites, total antioxidant levels and ferric-reducing antioxidant power was also observed in this group. Concomitant administration of vitamin C ameliorated hypertension, normalized NO levels and abrogated lipid peroxidation. Also, it completely prevented oxidative damage to the DNA. Conclusions: These findings point to enhanced ROS-mediated inactivation and sequestration of NO which can potentially contribute to hypertension, lipid peroxidation, reduced antioxidant status and oxidative DNA damage. The beneficial effects of vitamin C on these parameters support the role of increased ROS activity in the pathogenesis of these abnormalities in this model.

Abstract  The pattern of blood lead during pregnancy was investigated in a cohort of 195 women who, between October 1992 and February 1995, entered prenatal care at Magee-Womens Hospital in Pittsburgh, Pennsylvania, by week 13 of pregnancy. Blood was drawn as many as five times, once in each of the first two trimesters and a maximum of three times in the third trimester. Blood lead determinations were made by atomic absorption spectrophotometry. Potential sources or modifiers of lead exposure were collected by interviews, including sociodemographic, pregnancy history, occupational, and lifestyle data. Results confirmed a previously reported U-shaped curve in blood lead concentration during pregnancy as well as findings that blood lead levels increase with age, smoking, lower educational level, and African-American race and decrease with history of breastfeeding and higher intake of calcium. Additionally, interactions were found between time since last menstrual period and both maternal age and calcium. Specifically, older mothers showed steeper increases in blood lead concentrations during the latter half of pregnancy than did younger mothers, and intake of calcium had a protective effect only in the latter half of pregnancy, an effect that became stronger as pregnancy progressed. These findings provide further evidence that lead is mobilized from bone during the latter half of pregnancy and that calcium intake may prevent bone demineralization.

Abstract  BACKGROUND: Serum creatinine concentration is widely used as an index of renal function, but this concentration is affected by factors other than glomerular filtration rate (GFR). OBJECTIVE: To develop an equation to predict GFR from serum creatinine concentration and other factors. DESIGN: Cross-sectional study of GFR, creatinine clearance, serum creatinine concentration, and demographic and clinical characteristics in patients with chronic renal disease. PATIENTS: 1628 patients enrolled in the baseline period of the Modification of Diet in Renal Disease (MDRD) Study, of whom 1070 were randomly selected as the training sample; the remaining 558 patients constituted the validation sample. METHODS: The prediction equation was developed by stepwise regression applied to the training sample. The equation was then tested and compared with other prediction equations in the validation sample. RESULTS: To simplify prediction of GFR, the equation included only demographic and serum variables. Independent factors associated with a lower GFR included a higher serum creatinine concentration, older age, female sex, nonblack ethnicity, higher serum urea nitrogen levels, and lower serum albumin levels (P < 0.001 for all factors). The multiple regression model explained 90.3% of the variance in the logarithm of GFR in the validation sample. Measured creatinine clearance overestimated GFR by 19%, and creatinine clearance predicted by the Cockcroft-Gault formula overestimated GFR by 16%. After adjustment for this overestimation, the percentage of variance of the logarithm of GFR predicted by measured creatinine clearance or the Cockcroft-Gault formula was 86.6% and 84.2%, respectively. CONCLUSION: The equation developed from the MDRD Study provided a more accurate estimate of GFR in our study group than measured creatinine clearance or other commonly used equations.

Abstract  We report 208Pb/207Pb and 206Pb/207Pb ratios for 1001 duplicate diets collected from mothers and children, 1304 samples of house dust and hand wipes, and 64 samples of aerosols that were taken in Omaha, Nebraska, during the period from 1990 to 1997. A plot of 208Pb/207Pb versus 206Pb/207Pb for the dust and hand wipes indicates that they contain lead from ores mined in Idaho, Missouri, and Mexico. The absence of lead from Utah suggests that this mixture is not representative of the whole country. The lead in the aerosols has a narrower range of isotope ratios and resembles aerosols collected elsewhere in the United States. Most dietary collections contain a large component of house dust. Some, especially those from infants, are dominated by uranogenic lead with high 206Pb/207Pb ratios. Its source is taken to be calcium-supplemented food where the calcium is derived from limestone. Another source of lead is thorogenic and is ascribed to lead in tin coatings. Agricultural lead, whether from soil (estimated from recently published analyses of sedimentary materials), fertilizer, or agricultural lime, could not be unambiguously identified in the diets. Lead derived from aerosols, if present at all, is insignificant.

Abstract  Lead (Pb) affects elements of humoral and cell-mediated immunity, and diminishes host resistance to infectious disease. Evidence is presented supporting a hypothesis of Pb-induced immunosuppression stemming from altered fatty acid metabolism, and mediated by eicosanoids and macrophages (M0). Chronic Pb exposure increases the proportion of arachidonate (ArA) among fatty acids in lipid from avian tissues, and this change provides precursors for eicosanoids, the oxygenated derivatives of ArA that mediate M0 acute inflammatory response. In the current study, we showed that the concentration of ArA in phospholipids of M0 elicited from turkey poults fed 100 ppm dietary Pb acetate was twice that of controls. In vitro production of eicosanoids by these M0 was substantially increased, and this effect was most pronounced following lipopolysaccharide stimulation: prostaglandin F2alpha was increased 11-fold, thromboxane B2 increased threefold, and prostaglandin E2 increased by 1.5 times. In vitro phagocytic potential of these M0 was suppressed, such that the percentage of M0 engulfing sheep red blood cell (RBC) targets was reduced to half that of control M0. In vivo susceptibility of Pb-treated and control birds to Gram-negative bacteria challenge was also evaluated. The morbidity of chicks inoculated with Salmonella gallinarum and fed either control or 200 ppm Pb acetate-supplemented diets was similar, except early in the course of the disease when mortality among Pb-treated birds was marginally greater. In these studies, effects of Pb that could influence immunological homeostasis were demonstrated for M0 metabolism of ArA, for production of eicosanoids, and for phagocytosis. There was also the suggestion that these in vitro indices of immune function are related to in vivo disease resistance.

Abstract  Lead, a ubiquitous environmental contaminant, has been shown to modulate various functions of the immune system and decrease host resistance to infectious disease. However, limited information is available concerning the direct effects of lead on the host immune response to an infectious agent after developmental exposure. The current study utilized chickens to examine the effect of embryonic lead exposure on immune and cellular responses during viral challenge. Sublethal doses of lead were introduced into fertilized Cornell K Strain White Leghorn chicken eggs via the air sac at day 5 or day 12 of embryonic development (designated as E5 and E12, respectively). Four-week-old female chickens were inoculated with infectious bronchitis virus (IBV) strain M41. Antibody titer to IBV, delayed-type hypersensitivity (DTH) response against bovine serum albumin (BSA), the absolute number and percentage of leukocyte subpopulations, and interferon-? (IFN-?)-like cytokine production by splenocytes were evaluated at 5û6 weeks of age. While antibody response to IBV in juvenile chicks was unaffected by the in ovo lead exposure, IFN-?-like cytokine production by splenocytes was significantly depressed following lead exposure at both developmental stages. In contrast with this pattern, the DTH response against BSA was unaffected following E5 exposure, but was significantly decreased after E12 exposure to lead. These changes were similar to those previously reported in chickens not exposed to IBV. While lead exposure at E5 induced significant changes in the percentage of circulating heterophils at 1 day postinfection (dpi), lead did not cause any change in relative leukocyte counts after E12 exposure. At 7 dpi, E5 lead exposure resulted in decreased absolute number and percentage of circulating lymphocytes, while total leukocyte counts, and the absolute number and percentage of circulating monocytes and heterophils were significantly reduced in E12 lead-exposed chickens. These results suggest that low-level exposure to lead has a direct effect on the developing chicken immune system, which is evident even during a postnatal infection. Furthermore, some of the changes were observed only when chicks were stressed by the viral infection. It appears that lead exposure during different stages of embryonic development is likely to result in different immunotoxic outcomes in juveniles.

Abstract  Average concentration of Pb in atmospheric air particulates in different suburbs of Mumbai was studied for almost a decade and its spatial and temporal profiles are discussed in relation to emission sources. In general the concentration of Pb in all the residential suburban atmosphere is well below the Central Pollution Control Board (CPCB, 1994) prescribed limit of 1.5 microg m(-3) barring a few exceptions for some residential/industrial sites, such as those of Thane and Kurla scrap yards. The correlation between blood lead of children and air lead reveals that the blood Pb level in children could increase by 3.6 microg dl(-1) for an incremental rise of 1.0 microg Pb m(-3) of air. The temporal profile of air Pb values indicates a decreasing trend in residential suburbs (Khar: 1984, 0.39 microg m(-3); 1996, 0.17 microg m(-3)) as well as in suburban residential areas with low traffic (Goregaon: 1984, 0.53 microg m(-3); 1996, 0.30 microg m(-3)).

Abstract  An oligoclonal utilization of V"beta" 's has been reported for pathogenesis of several autoimmune diseases, anti-tumorigenic activity, and superantigen-regulation of thymic T cell development. Altered ratios of Th1 and Th2 cells also are observed in immunodysregulations, leading to impaired cell-mediated immunity with an increased incidence of infectious disease or cancer and/or aberrant immunity that could culminate with an autoimmune disease. Lead (Pb) and mercury (Hg) are known pollutants with immunodisrupting activities; Hg is known to cause autoimmune glomerulonephritis. Both metals are known to suppress host resistance to pathogens. To further evaluate the manner by which these metals causein vivoimmunomodulation, theirin vivoeffects on V"beta" expression were evaluated along with the Th1 and Th2 frequency. Exposure of BALB/c mice to PbCl2or HgCl2induced an oligoclonal response with increases of V"beta" 5+, V"beta" 7+, and V"beta" 13+CD4+splenic, but not thymic, T cells. A significantly skewed frequency of Pb-induced splenic Th2 cells expressing V"beta" 7 or V"beta" 13 over Th1 cells was determined by limiting dilution analysis, but this Th2 predominance was not observed with CD4+T cells expressing V"beta" 8. DO11.10 transgenic mouse exposed to Pb and antigen also demonstrated a skewed type-2 response evidenced by significantly increased IgE levels, lowered IFN-"gamma" levels, and increased IgG1 and lowered IgG2a anti-OVA levels. Even in the absence of specific T cell responses to a Pb-induced antigen, due to the restricted T cell specificity in the transgenic mouse model, Pb still was able to skew the response toward type-2 reactivity. However, this skewing occurred only in the presence of antigen. Therefore, the Pb-induced oligoclonal T cell response in BALB/c mice which must be initiated by self-antigens and was predominately type-2 may be responsible for autoantibody production and the detrimental health effects associated with Pb exposure.

Abstract  It has been repeatedly shown that the heavy metal mercury can induce or exacerbate lupus like autoimmunity in susceptible strains of rats and mice. A hallmark of such autoimmune induction is the accompaniment of an immune shift, in which there is usually an initial skewing toward a Th2-like immune environment. Another heavy metal, lead (Pb), has also been found to induce a Th2 shift in mice. However, exposure of normal mouse strains to Pb does not appear to induce autoimmunity. In order to investigate whether mice genetically predisposed to murine systemic lupus erythematosus (SLE) are susceptible to a Pb-induced exacerbation of lupus, males and females of four New Zealand mixed (NZM) mouse strains, along with BALB/c and C57Bl/6 controls, were administered three 100-microliter intraperitoneal injections of either 1.31 mM lead or sodium acetate per week for 3 wk. The four NZM strains chosen, NZM391, NZM2328, NZM88, and NZM2758, have differential genetic penetrance for SLE with variances in certain manifestations of the disease, but all of these strains naturally develop glomerulonephritis and produce high titers of anti-nuclear autoantibodies. The mice were prebled for baseline values and were bled directly after the injection period (d 1) and monthly thereafter for 5 mo. Sera were assessed for anti-double-stranded DNA titers, urea nitrogen levels, and creatine kinase activity, as well as four total immunoglobulin (Ig) G2a and IgG1 levels. Mortality and morbidity of the mice were also recorded. All NZM strains showed an acute, non-gender-based, susceptibility to Pb at d 1, but the control strains were unaffected. Over time, it became apparent that the strains diverged: The NZM391 strain showed gender-independent susceptibility to Pb enhancement of lupus manifestations and mortality; the NZM2328 strain exhibited gender-independent Pb susceptibility to manifestations, although only females had increased mortality; the NZM2758 strain exhibited non-gender-based elevations in urea nitrogen and creatine kinase activity levels; and the NZM88 strain displayed male susceptibility to anti-DNA and life span. Surprisingly, Pb increased the longevity of NZM88 and NZM2758 females. These results indicate that Pb indeed can exacerbate SLE in lupus-prone mice; however, even among lupus-prone strains, genetic differences determine the degree of exacerbation. Using the known phenotype and genetic differences, one can identify and characterize possible traits and loci associated with Pb susceptibility.

Abstract  The effect of oral administration of lead, as Pb-acetate, via the drinking water on the murine delayed type hypersensitivity (DTH) response was investigated. The DTH response of BALB/c mice sensitized intraveneously with sheep red blood cells (SRBC) was found to be suppressed markedly in lead-intoxicated mice. Suppression of the DTH correlated with increasing blood Pb concentration. Suppression of the DTH response by Pb intoxication depended on the route of administration of the sensitizing antigen, as Pb intoxication did not impair the DTH reaction when mice were sensitized to SRBC via intraperitoneal injection. Since DTH reactions are regulated in large part by Th1 cells, these data establish an in vivo model system based on a rational route of Pb exposure in which to study further the modulation of Th1-mediated immune effector function by Pb.

Abstract  Lead is known to impede the male reproductive function, however, the mechanisms through which the adverse effects are mediated are not clearly elucidated. In order to get insight into those mechanisms, we have examined the effects of lead on the biosynthesis of steroid hormones by Leydig cells in the rat. To determine whether lead has a direct action on Leydig cells, we have compared the concentrations of testosterone secreted by Leydig cells in ex vivo experiments after animals had been injected with high doses of lead and in vitro experiments with Leydig cells from normal rats maintained in culture in presence or absence of lead. In ex vivo experiments male Sprague-Dawley rats were injected i.p. with lead acetate (8 mg lead/kg/day, 5 days a week for S weeks) or with sodium acetate. Testosterone production by Leydig cells isolated and maintained in culture for 48 h was then assessed under basal conditions or after stimulation by human chorionic gonadotrophin (hCG). Both basal and hCG-stimulated testosterone production dropped by 59% and 37%, respectively, with Leydig cells from lead-exposed rats. For in vitro experiments, cultures of Leydig cells from control rats were exposed to various concentrations of lead acetate for different periods. Dose and time-dependent reductions of testosterone level were observed in the culture medium. The effective doses of hCG for maximal and half-maximal testosterone production did not change, indicating that the sensitivity of Leydig cells to hCG was not impaired by exposure to lead in vitro. Progesterone production was also decreased after this exposure. The negative effect of lead on testosterone and progesterone production was correlated with the lower expression of the enzymes cytochromes P450scc (CYP11 A1) and P450c17 (CYP17) and 3"Beta"-hydroxysteroid dehydrogenase (3"Beta"-HSD) involved in steroid hormone biosynthesis, as shown by immunohistochemistry. Ultrastructural alterations of the smooth endoplasmic reticulum observed after lead administration might be correlated with the lower expression of the microsomal enzymes P450cl7 and 3"Beta"-HSD. Our results indicate that lead can adversely affect the Leydig cell function by impairing directly steroidogenesis.

Abstract  Female BDF1 mice were exposed to lead in the drinking water at concentrations ranging from 0 to 1000 ppm lead for 3 weeks. Immunological studies demonstrated that lead suppressed macrophage-dependent immune responses. The functional activity of the macrophage was evaluated by the Mishell-Dutton, in vitro, antibody production technique. Lead suppressed the immune response when the macrophage-dependent antigens, sheep red blood cells or dinitrophenyl-Ficoll, were utilized, but the response to the macrophage-independent antigen, Escherichia coli lipopolysaccharide, was not suppressed. The macrophage substitute, 2-mercaptoethanol, caused restoration of the lead-suppressed immune response. The immune responses seen in the four combinations of adherent/nonadherent and lead-exposed/non-lead-exposed cell cultures, were suppressed only in cultures containing lead-exposed adherent cells. The immunosuppressive effects of lead were produced at relatively low lead exposures as indicated by the blood lead concentrations. Weight gains and water consumption were not affected by these lead exposures. The low level lead exposure effects manifested by immunosuppression indicate that immune dysfunction is a sensitive indicator of lead exposure.

Abstract  A field campaign on aerosol chemical properties and trace gases measurements was carried out along the Delhi-Hyderabad-Delhi road corridor (spanning about 3,200 km) in India, during February 1-29, 2004. Aerosol particles were collected on quartz and cellulose filters using high volume (PM(10)) sampler at various locations along the route (i.e., urban, semi-urban, rural, and forest areas) and have been characterized for major cations (Na(+), Ca(2+), Mg(2+), K(+), and NH (4) (+) ), anions (Cl(-), NO (3) (-) , and SO (4) (2-) ), and heavy metals (Cu, Cd, Fe, Zn, Mn, and Pb). Simultaneously, we measured NO(2) and SO(2) gases. These species show large spatial and temporal variations. The ambient PM(10) concentration has been observed to be the highest (55 ± 4 μg m(-3)) near semi-urban areas followed by forest areas (48 ± 2 μg m(-3)) and in rural areas (44 ± 22 μg m(-3)). The concentrations of NO( x ) (NO(2)+NO) and SO(2) ranged from 16 to 69 μg m(-3) and 4 to 11 μg m(-3), respectively. Among anions, NO(3) (-) and SO(4) (2-) are the major constituents of PM(10). The urban and semi-urban sites showed enhanced concentrations of Fe, Zn, Mn, Cd, and Pb. This study provide information about atmospheric concentrations of various species in the northern to central India, which may be important for policy makers to better understand the air quality of the region.

Abstract  The activity of (210)Po and (210)Pb was determined in mussels of the same size (3.5-4.0 cm shell length) sampled monthly over a 17-month period at the Atlantic coast of Portugal. Average radionuclide concentration values in mussels were 759±277 Bq kg(-1) for (210)Po (range 460-1470 Bq kg(-1) dry weight), and 45±19 Bq kg(-1) for (210)Pb (range 23-96 Bq kg(-1) dry weight). Environmental parameters and mussel biometric parameters were monitored during the same period. Although there was no seasonal variation of radionuclide concentrations in sea water during the study period, the concentration of radionuclide activity in mussels varied seasonally displaying peaks of high concentrations in winter and low concentrations in summer. Analysis of radionuclide data in relation to the physiological Condition Index of mussels revealed that (210)Po and (210)Pb activities in the mussel (average activity per individual) remained nearly constant during the investigation period, while mussel body weight fluctuated due to fat storage/expenditure in the soft tissues. Similar variation of radionuclide concentrations was observed in mussels transplanted from the sea coast into the Tejo Estuary. However, under estuarine environmental conditions and with higher food availability throughout the year, transplanted mussel Condition Index was higher than in coastal mussels and average radionuclide concentrations were 210±75 Bq kg(-1) (dry weight) for (210)Po and 10±4 Bq kg(-1) (dry weight) for (210)Pb, therefore lower than in coastal mussels with similar shell length. It is concluded that the apparent seasonal fluctuation and inter-site difference of radionuclide concentrations were mostly caused by mussel body weight fluctuation and not by radionuclide body burden fluctuation. This interpretation can be extended to the apparent seasonal fluctuation in concentrations of lipophilic and lipophobic contaminants in mussels, and provides an explanation for occasional high concentrations of (210)Po and man-made contaminants measured in mussels far from pollution sources.

Abstract  The research was carried out around dumps made at the beginning of twentieth century linked to Zn–Pb ore mining of deposits of Mississippi Valley type in Southern Poland. Soil algae communities were investigated near spoil dumps rich in Zn, Pb, Fe, Cd, and Tl. In algal crusts, Chlorophyta and Cyanophyta occur in filament forms such as Stichococcus bacillaris, Stichococcus chlorelloides, S. cf. fragilis, and Cylindrocapsa sp. The algal crusts form aggregates containing metal-bearing minerals and algal organic material. The development of the crusts occur on sandy-clayey soils poor in water and highly enriched in heavy metals (up to 68,800 mg kg−1 for Zn, 85,060 mg kg−1 for Pb, 369 mg kg−1 for Cd and 355 mg kg−1 for Tl). Algal-crust formation is an important initial stage which facilitates vascular plant succession and topsoil formation. The results of investigation of algal material with ESEM are presented and the mineral phases in the top soil layer based on the XRD and EDS are described. The results indicate the presence of secondary labile minerals of lead, e.g., anglesite and plumbojarosite and minerals of Zn, e.g., smithsonite and minrecordite.

Abstract  Reactive oxygen species (ROS) serve as cell signaling molecules for normal biologic processes. However, the generation of ROS can also provoke damage to multiple cellular organelles and processes, which can ultimately disrupt normal physiology. An imbalance between the production of ROS and the antioxidant defenses that protect cells has been implicated in the pathogenesis of a variety of diseases, such as cancer, asthma, pulmonary hypertension, and retinopathy. The nature of the injury will ultimately depend on specific molecular interactions, cellular locations, and timing of the insult. This review will outline the origins of endogenous and exogenously generated ROS. The molecular, cellular, pathologic, and physiologic targets will then be discussed with a particular emphasis on aspects relevant to child development. Finally, antioxidant defenses that scavenge ROS and mitigate associated toxicities will be presented, with a discussion of potential therapeutic approaches for the prevention and/or treatment of human diseases using enzymatic and nonenzymatic antioxidants.

Abstract  Previous studies have shown that fasting increases lead absorption in the gastrointestinal tract of adults. Regular meals/snacks are recommended as a nutritional intervention for lead poisoning in children, but epidemiological evidence of links between fasting and blood lead levels (B-Pb) is rare. The purpose of this study was to examine the association between eating a regular breakfast and B-Pb among children using data from the China Jintan Child Cohort Study.

Parents completed a questionnaire regarding children's breakfast-eating habit (regular or not), demographics, and food frequency. Whole blood samples were collected from 1,344 children for the measurements of B-Pb and micronutrients (iron, copper, zinc, calcium, and magnesium). B-Pb and other measures were compared between children with and without regular breakfast. Linear regression modeling was used to evaluate the association between regular breakfast and log-transformed B-Pb. The association between regular breakfast and risk of lead poisoning (B-Pb≥10 μg/dL) was examined using logistic regression modeling.

Median B-Pb among children who ate breakfast regularly and those who did not eat breakfast regularly were 6.1 μg/dL and 7.2 μg/dL, respectively. Eating breakfast was also associated with greater zinc blood levels. Adjusting for other relevant factors, the linear regression model revealed that eating breakfast regularly was significantly associated with lower B-Pb (beta = -0.10 units of log-transformed B-Pb compared with children who did not eat breakfast regularly, p = 0.02).

The present study provides some initial human data supporting the notion that eating a regular breakfast might reduce B-Pb in young children. To our knowledge, this is the first human study exploring the association between breakfast frequency and B-Pb in young children.