Disponibilidade De Antídotos No Município De Campinas, São Paulo

The lack of availability of antidotes in emergency services is a worldwide concern. The aim of the present study was to evaluate the availability of antidotes used for treating poisoning in Campinas (SP). DESIGN AND SETTING: This was a cross-sectional study of emergency services in Campinas, conducted in 2010-2012. METHODS: The availability, amount in stock, place of storage and access time for 26 antidotal treatments was investigated. In the hospitals, the availability of at least one complete treatment for a 70 kg adult over the first 24 hours of admission was evaluated based on stock and access recommendations contained in two international guidelines. RESULTS: 14 out of 17 functioning emergency services participated in the study, comprising pre-hospital services such as the public emergency ambulance service (SAMU; n = 1) and public emergency rooms for admissions lasting ≤ 24 hours (UPAs; n = 3), and 10 hospitals with emergency services. Six antidotes (atropine, sodium bicarbonate, diazepam, phytomenadione, flumazenil and calcium gluconate) were stocked in all the services, followed by 13 units that also stocked activated charcoal, naloxone and diphenhydramine or biperiden. No service stocked all of the recommended antidotes; only the regional Poison Control Center had stocks close to recommended (22/26 antidotal treatments). The 10 hospitals had almost half of the antidotes for starting treatments, but only one quarter of the antidotes was present with stocks sufficient for providing treatment for 24 hours. CONCLUSION: The stock of antidotes for attending poisoning emergencies in the municipality of Campinas is incomplete and needs to be improved. © 2017, Associacao Paulista de Medicina. All rights reserved.13511522FAPEAM, Fundação de Amparo à Pesquisa do Estado do Amazona

A Clinico-epidemiological Study Of Bites By Spiders Of The Genus Phoneutrla

From January, 1984 to December, 1996, 422 patients (ages 9 m-99 y, median 29 y) were admitted after being bitten by spiders which were brought and identified as Phoneutria spp. Most of the bites occurred at March and April months (29.2%), in the houses (54.5%), during the day (76.5%), and in the limbs (feet 40.9%, hands 34.3%). Upon hospital admission, most patients presented only local complaints, mainly pain (92.1%) and edema (33.1%) and were classified as presenting mild (89.8%), moderate (8.5%) and severe (0.5%) envenomation. Few patients (1.2%) did not present signs of envenomation. Severe accidents were only confirmed in two children (9 m, 3 y). Both developed acute pulmonary edema, and the older died 9 h after the accident. Patients more than 70 yearold had a significantly greater (p<0.05) frequency of moderate envenomations compared to the 10-70-year-old individuals. Proceedings to relief local pain were frequently performed (local anesthesia alone 32.0%, local anesthesia plus analgesics 20.6% and oral analgesics alone 25.1%). Only 2.3% of the patients (two cases classified as severe and eight as noderate, eight of them in children) were treated with i.v. antiarachnid antivenom. No antivenom early reaction was observed. In conclusion, accidents involving the genus Phoneutria are common in the region of Campinas, with the highest risk groups being children under 10 years of age and adults over 70 years of age. Cases of serious envenomation are rare (0.5%).4211721Antunes, E., Marangoni, R.A., Brain, S.D., De Nucci, G., Phoneutria nigriventer (armed spider) venom induces increased vascular permeability in rat and rabbit skin in vivo (1992) Toxlcon, 30, pp. 1011-1016Antunes, E., Marangoni, R.A., Borges, N.C.C.T., Effects of Phoneutria nigriventer venom on rabbit vascular smooth muscle (1993) Braz. J. Med. Biol. Res., 26, pp. 81-91Bucaretchi, F.-., (1990) Análise das Principais Diferenças Clinicas e Epidemiológicas Dos Acidentes Por Escorplões Das Espécies Tityus Serrulatus e Tityus Bahiensis, e Por Aranhas do Gẽnero Phoneutria, Atendidos no CCI-HC-UNICAMP, no Período de Janeiro de 1984 a Julho de 1988, , Campinas, Dissertação de Mestrado -Faculdade de Ciẽncias Médicas da Universidade Estadual de CampinasBucaretchi, F., Acidentes por Phoneutria (1992) Plantas Venenosas e Animals Peçonhentos, pp. 196-201. , SCHVARTSMAN, S., ed. Sãu Paulo, SarvierBucaretchi, F., Collares, E.F., Effect of Phoneutria nigriventer spider venom on gastric emptying in rats (1996) Braz. J. Med. Biol. Res., 29, pp. 205-211Bücherl, W., A "armadeira": A aranha mais perigosa do mundo! (1985) Acúleos Que Matam, pp. 35-45. , BÜCHERL. W., ed. Rio De Janeiro. KosmosCosta, S.K.P., Moreno, J.R.H., Brain, S.D., The effect of Phoneutria nigriventer (armed spider) venom on arterial blood pressure of anaesthetised rats (1996) Europ. J. Pharmacol., 298, pp. 113-120Cruz-Hofling, M.A., Love, S., Brook, G., Duchen, L.W., Effects of Phoneutria nigriveter spider venom on mouse peripheral nerve (1985) Quart. J, Exp. Physlol., 70, pp. 623-640Fontana, M.D., Vital-Brazil, O., Mode of action of Phoneutria nigriventer spider venom at the isolated phrenic nerve-diaphragm of the rat (1985) Braz. J. Med. Biol. Res., 18, pp. 557-565Lopes-Martins, R.A.B., Antune, S.E., Oliva, M.L.V., Pharmacological characterization of rabbit corpus cavernosum relaxation mediated by the tissue kallikrein-kinin system (1994) Brit. J. Pharmacol., 113, pp. 81-86Lucas, M.S., Spiders in Brazil (1988) Toxicon, 26, pp. 759-772Marangoni, R.A., Antunes, E., Brain, S.D., De-Nucci, G., Activation by Phoneutria nigriventer (armed spider) venom of the tissue kallikrein-kininogen-kinin system in rabbit skin in viva (1993) Brit. J. Pharmacol., 109, pp. 539-543Acidentes por Phoneutria (1998) Manual de Diagnóstico e Tratamento de Acidentes Por Animals Peçonhentos, pp. 54-56. , Brasflia, Ministério da Saúde/Fundação Nacional da SaúdeAraneísmo (1998) Manual de Diagnóstico e Tratamento de Acidentes Por Animals Peçonhentos, pp. 49-53. , Brasfia, Ministério da Saúde/Fundação Nacional da SaúdeRamos, E.F., Almeida, C.E., Gouvêa, E., Carmo-Silva, M., Considernções sobre a atividade de locomoção, preferência por ecótopos e aspectos territoriais de phoneutria nigriventer (Keiserling, 1891) (1998) Rev. Bras. Biol., 58, pp. 71-78. , Aranae. CtenidaeRego, E., Bento, A.C., Lopes-Martins, A.B., Isolation and partial characterization of a polypeptide from Phoneutria nigriventer spider venom that relaxes rabbit corpus cavernosum in vitro (1996) Toxicon, 34, pp. 1141-1147Rosenfeld, G., Animais peçonhentos e tóxicos do Brasil (1972) Introdução à Geografia Médica do Brasil, pp. 430-475. , LACAZ. C.S.: BARUZZI, R.G. & SIQUEIRA Jr., W., ed. São Paulo, EDUSPVellard, J., Les araignées vraies. Les ctènes (1936) Le Venin des Araignèes. Monographies de L'institut Pasteur, pp. 169-184. , VELLARD, J., ed. Paris. MassonVital-Brazil, Vellard, J., Contribuição ao estudo do veneno das aranhas. II. Mem. Inst (1926) Butantan, 2, pp. 3-77Vital-Brazil, O., Bernardo-Leite, G.B., Fontana, M., Modo de ação da peçonha da aranha armadeira, phoneutria nigriventer (Keiserling, 1891), nas aurífculas isoladas de cobain (1988) Ciênc. Cult., 40, pp. 181-18

Urinary Protein Excretion Profile: A Contribution For Subclinical Renal Damage Identification Among Environmental Heavy Metals Exposure In Southeast Brazil

In Southeast Brazil. Ribeira Valley region has been a major public health concern due to the environmental heavy metals contamination indexes of vegetation, rocks and aquifers, caused by local mining in the past. Human contamination by low levels of heavy metals doesn't cause acute intoxication but in chronic exposure, renal damage may occur with progressive tubulointerstitial changes evolving to glomerular lesion. In this study we investigated the relationship between the profile of urinary excreted proteins (glomerular or tubular origin) of arsenic and mercury and blood lead concentration in children and adults from highly exposed regions of the Ribeira Valley. The subjects were classified as GROUP 1 (G1; higher environmental risk, n=333) and GROUP 2 (G2; lower risk of contamination, n=104). In order to determine the urinary excretion of total protein, albumin (MA, glomerular marker) and alpha I microglobulin (A1M, tubular marker) and the blood lead concentrations, random urine and blood samples were obtained. Plasmatic lead levels were assessed by atomic absorption spectrometry with graphite furnace. Total protein concentration (PROT) was assessed on a biochemical analyzer (pyrogallol red method). MA and A1M were determined by nephelometric method. Group 1 showed a higher frequency of altered urinary excretion of PROT (G1=3.4%; G2=1.0%), MA (G1=9.0%; G2=5.1%) and A1M (G1=7.5%; G2=3.8%), without significant differences between both groups. Elevated arsenic levels were more prevalent among subjects from Group 1 (28.8%) and demonstrated a significant correlation with abnormal urinary excretion of albumin and alpha-1-microglobulin (p=0.019). Lead and mercury levels showed no difference among the groups and no correlation with MA and/or A1M. Our data suggests that abnormal urinary protein excretion is relatively frequent in this population independently of the plasmatic or urinary heavy metal levels. The early detection of possible renal damage become necessary for effective measures can be taken to prevent clinical nephropathies.107I513516Eysink, G.G.J., Avaliação da qualidade ambiental do Rio Ribeira do Iguape- Considerações preliminares, relatório técnico da CETESB (1991), p. 54. , CETESB, São PauloPaoliello, M.M.B., De Capitani, E.M., Cunha, F.G., Matsuo, T., Carvalho, M.F., Sakuma, A., Figueiredo, B.R., Exposure of children to lead and cadmium from a mining area of Brazil (2002) Environmental Research, 88, pp. 120-128Bennet, B.G., Exposure of man to environmental arsenic - an exposure commitment assessment (1981) Sci Total Environ, 20 (2), pp. 99-107Hewitt, D.J., Millner, G.C., Nye, A.C., Simmons, H.F., Investigation of arsenic exposure from soil at a superfund site (1995) Environ. Research, 68, pp. 73-81Goyer, R.A., Mechanisms of lead and cadmium nephrotoxicity (1989) Toxicol Lett., 46, pp. 153-162Chia, K.S., Jeyaratnam, J., Lee, J., Tan, C., Ong, H.Y., Ong, C.N., Lee, E., Lead-induced nephropathy: Relationship between various biological exposure indices and early markers of nephrotoxicity (1995) Am J Ind Med, 27 (6), pp. 883-895Kim, R., Rotnitsky, A., Sparrow, D., Weiss, S., Wager, C., Hu, H., A longitudinal study of low level lead exposure and impairment of renal function. The normative aging study (1996) JAMA, 275, pp. 1177-1181Cardenas, A., Roels, H., Bernard, A.M., Markers of early renal changes induced by industrial pollutants. II. Application to workers exposed to lead (1993) Br J Ind Med, 50, pp. 28-36Kusano, E., Suzuki, M., Asano, Y., Takagi, K., Tadashi, K., Human alfa-1-microglobulin and its relationship to renal function (1985) Nephron, 41, pp. 320-324Pergande, M., Jung, K., Precht, S., Fels, L.M., Herbort, C., Stolte, H., Changed excretion of urinary proteins and enzymes by chronic exposure to lead (1994) Nephrol Dial Transplant, 9 (6), pp. 613-618Preventing lead poisoning in young children: A statement by the centers for disease control (1991), Centers for Disease Control and Prevention-USDHHS- PHS, Washington, octoberPaschal, D.C., Trace metals in urine of United States residentes: Reference range concentrations (1998) Environ Research, 76, pp. 53-59not

Finger Burns Caused By Concentrated Hydrofluoric Acid, Treated With Intra-arterial Calcium Gluconate Infusion: Case Report [queimadura Digital Por ácido Fluorídrico Concentrado Tratada Com Infusão Intra-arterial De Gluconato De Cálcio: Relato De Caso]

Context: Hydrofluoric acid (HF) is widely used in industry and at home. Severe lesions can occur after contact with highly concentrated solutions, leading to tissue necrosis and bone destruction. Specific treatment is based on neutralization of fluoride ions with calcium or magnesium solutions. Case report: A 41-year-old male was seen at the emergency department 35 minutes after skin contact with 70% HF, showing whitened swollen lesions on the middle and fourth fingers of his right hand with severe pain starting immediately after contact. 2.5% calcium gluconate ointment was applied. Twenty-four hours later, the patient was still in severe pain and the lesions had worsened. Considering the high concentration of the solution, early start of severe pain, lesion characteristics and impossibility of administering calcium gluconate subcutaneously because of the lesion location, the radial artery was catheterized and 2% calcium gluconate was administered via infusion pump for 36 hours, until the pain subsided. No adverse effects were seen during the procedure. Ten days later, the lesions were stable, without bone abnormalities on X-rays. Six months later, a complete recovery was seen. Conclusions: Intra-arterial calcium gluconate might be considered for finger burns caused by concentrated HF. Complete recovery of wounded fingers can be achieved with this technique even if started 24 hours after the exposure. However, controlled clinical trials are needed to confirm the effectiveness and safety of this intervention.1276379381Anderson, W.J., Anderson, J.R., Hydrofluoric acid burns of the hand: Mechanism of injury and treatment (1988) J Hand Surg Am, 13 (1), pp. 52-57Sheridan, R.L., Ryan, C.M., Quinby Jr., W.C., Blair, J., Tompkins, R.G., Burke, J.F., Emergency management of major hydrofluoric acid exposures (1995) Burns, 21 (1), pp. 62-64Lin, T.M., Tsai, C.C., Lin, S.D., Lai, C.S., Continuous intra-arterial infusion therapy in hydrofluoric acid burns (2000) J Occup Environ Med, 42 (9), pp. 892-897Roblin, I., Urban, M., Flicoteau, D., Martin, C., Pradeau, D., Topical treatment of experimental hydrofluoric acid skin burns by 2.5% calcium gluconate (2006) J Burn Care Res, 27 (6), pp. 889-894Vance, M.V., Curry, S.C., Kunkel, D.B., Ryan, P.J., Ruggeri, S.B., Digital hydrofluoric acid burns: Treatment with intraarterial calcium infusion (1986) Ann Emerg Med, 15 (8), pp. 890-896Graudins, A., Burns, M.J., Aaron, C.K., Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity (1997) Ann Emerg Med, 30 (5), pp. 604-60

Volumetric Capnography For The Evaluation Of Chronic Airways Diseases

Background: Obstructive lung diseases of different etiologies present with progressive peripheral airway involvement. The peripheral airways, known as the silent lung zone, are not adequately evaluated with conventional function tests. The principle of gas washout has been used to detect pulmonary ventilation inhomogeneity and to estimate the location of the underlying disease process. Volumetric capnography (VC) analyzes the pattern of CO2elimination as a function of expired volume.Objective: To measure normalized phase 3 slopes with VC in patients with non-cystic fibrosis bronchiectasis (NCB) and in bronchitic patients with chronic obstructive pulmonary disease (COPD) in order to compare the slopes obtained for the groups.Methods: NCB and severe COPD were enrolled sequentially from an outpatient clinic (Hospital of the State University of Campinas). A control group was established for the NCB group, paired by sex and age. All subjects performed spirometry, VC, and the 6-Minute Walk Test (6MWT). Two comparisons were made: NCB group versus its control group, and NCB group versus COPD group. The project was approved by the ethical committee of the institution. Statistical tests used were Wilcoxon or Student’s t-test; P,0.05 was considered to be a statistically significant difference.Results: Concerning the NCB group (N=20) versus the control group (N=20), significant differences were found in body mass index and in several functional variables (spirometric, VC, 6MWT) with worse results observed in the NCB group. In the comparison between the COPD group (N=20) versus the NCB group, although patients with COPD had worse spirometric and 6MWT values, the capnographic variables mean phase 2 slope (Slp2), mean phase 3 slope normalized by the mean expiratory volume, or mean phase 3 slope normalized by the end-tidal CO2concentration were similar.Conclusion: These findings may indicate that the gas elimination curves are not sensitive enough to monitor the severity of structural abnormalities. The role of normalized phase 3 slope may be worth exploring as a more sensitive index of small airway disease, even though it may not be equally sensitive in discriminating the severity of the alterations.9983989Robinson, P.D., Goldman, M.D., Gustafsson, P.M., Inert gas washout: Theoretical background and clinical utility in respiratory disease (2009) Respiration, 78 (3), pp. 339-355Ribeiro, M., Silva, M.T., Ribeiro, J.D., Volumetric capnography as a tool to detect early peripheric lung obstruction in cystic fibrosis patients (2012) J Pediatr (Rio J), 88 (6), pp. 509-517Almeida, C.C., Almeida-Júnior, A.A., Ribeiro, M.A., Nolasco-Silva, M.T., Ribeiro, J.D., Volumetric capnography to detect ventilation inhomogeneity in children and adolescents with controlled persistent asthma (2011) J Pediatr (Rio J), 87 (2), pp. 163-168Veronez, L., Moreira, M.M., Soares, S.T., Volumetric capnography for the evaluation of pulmonary disease in adult patients with cystic fibrosis and noncystic fibrosis bronchiectasis (2010) Lung, 188 (3), pp. 263-268Moreira, M.M., Terzi, R.G., Carvalho, C.H., de Oliveira Neto, A.F., Pereira, M.C., Paschoal, I.A., Alveolar dead space and capnographic variables before and after thrombolysis in patients with acute pulmonary embolism (2009) Vasc Health Risk Manag, 5 (1), pp. 9-12Moreira, M.M., Terzi, R.G., Paschoal, I.A., Martins, L.C., Oliveira, E.P., Falcão, A.L., Thrombolysis in massive pulmonary embolism based on the volumetric capnography (2010) Arq Bras Cardiol, 95 (4), pp. e97-e99Pereira, D.J., Moreira, M.M., Paschoal, I.A., Martins, L.C., Metze, K., Moreno Junior, H., Near-fatal pulmonary embolism in an experimental model: Hemodynamic, gasometric and capnographic variables (2011) Rev Bras Cir Cardiovasc, 26 (3), pp. 462-468Schwardt, J.D., Gobran, S.R., Neufeld, G.R., Aukburg, S.J., Scherer, P.W., Sensitivity of CO2 washout to changes in acinar structure in a single-path model of lung airways (1991) Ann Biomed Eng, 19 (6), pp. 679-697Schreiner, M.S., Leksell, L.G., Gobran, S.R., Hoffman, E.A., Scherer, P.W., Neufeld, G.R., Microemboli reduce phase III slopes of CO2 and invert phase III slopes of infused SF6 (1993) Respir Physiol, 91 (2-3), pp. 137-154Vestbo, J., Hurd, S.S., Agustí, A.G., Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary (2013) Am J Respir Crit Care Med, 187 (4), pp. 347-365ATS statement: Guidelines for the six-minute walk test (2002) Am J Respir Crit Care Med, 166 (1), pp. 111-117. , ATS Committee on Proficiency Standards for Clinical Pulmonary Function LaboratoriesPréfaut, C., Durand, F., Mucci, P., Caillaud, C., Exercise-induced arterial hypoxaemia in athletes: A review (2000) Sports Med, 30 (1), pp. 47-61Pereira, C.A., Sato, T., Rodrigues, S.C., New reference values for forced spirometry in white adults in Brazil (2007) J Bras Pneumol, 33 (4), pp. 397-406Cosio, M., Ghezzo, H., Hogg, J.C., The relations between structural changes in small airways and pulmonary-function tests (1978) N Engl J Med, 298 (23), pp. 1277-1281Stănescu, D.C., Rodenstein, D.O., Hoeven, C., Robert A. “Sensitive tests” are poor predictors of the decline in forced expiratory volume in one second in middle-aged smokers (1987) Am Rev Respir Dis, 135 (3), pp. 585-590Buist, A.S., Vollmer, W.M., Johnson, L.R., McCamant, L.E., Does the single-breath N2 test identify the smoker who will develop chronic airflow limitation? (1988) Am Rev Respir Dis, 137 (2), pp. 293-301Verbanck, S., Schuermans, D., Meysman, M., Paiva, M., Vincken, W., Noninvasive assessment of airway alterations in smokers: The small airways revisited (2004) Am J Respir Crit Care Med, 170 (4), pp. 414-419Verbanck, S., Schuermans, D., Paiva, M., Vincken, W., Nonreversible conductive airway ventilation heterogeneity in mild asthma (2003) J Appl Physiol (1985), 94 (4), pp. 1380-1386Verbanck, S., Paiva, M., Schuermans, D., Malfroot, A., Vincken, W., Vanderhelst, E., Acinar and conductive ventilation heterogeneity in severe CF lung disease: Back to the model (2013) Respir Physiol Neurobiol, 188 (2), pp. 124-132Verbanck, S., Schuermans, D., Van Muylem, A., Conductive and acinar lung-zone contributions to ventilation inhomogeneity in COPD (1998) Am J Respir Crit Care Med, 157 (5), pp. 1573-1577Verbanck, S., Thompson, B.R., Schuermans, D., Ventilation heterogeneity in the acinar and conductive zones of the normal ageing lung (2012) Thorax, 67 (9), pp. 789-795Hogg, J.C., Timens, W., The pathology of chronic obstructive pulmonary disease (2009) Annu Rev Pathol, 4, pp. 435-459McDonough, J.E., Yuan, R., Suzuki, M., Small-airway obstruction and emphysema in chronic obstructive pulmonary disease (2011) N Engl J Med, 365 (17), pp. 1567-1575Tiddens, H.A., Donaldson, S.H., Rosenfeld, M., Paré, P.D., Cystic fibrosis lung disease starts in the small airways: Can we treat it more effectively? (2010) Pediatr Pulmonol, 45 (2), pp. 107-117Matsui, H., Grubb, B.R., Tarran, R., Evidence for periciliary liquid layer depletion, not abnormal ion composition, in the pathogenesis of cystic fibrosis airways disease (1998) Cell, 95 (7), pp. 1005-1015Boucher, R.C., Relationship of airway epithelial ion transport to chronic bronchitis (2004) Proc Am Thorac Soc, 1 (1), pp. 66-70Randell, S.H., Boucher, R.C., Effective mucus clearance is essential for respiratory health (2006) Am J Respir Cell Mol Biol, 35 (1), pp. 20-28. ,University of North Carolina Virtual Lung GroupSvartengren, K., Philipson, K., Svartengren, M., Nerbrink, O., Camner, P., Clearance in smaller airways of inhaled 6-microm particles in subjects with immotile-cilia syndrome (1995) Exp Lung Res, 21 (5), pp. 667-682Kang, E.Y., Miller, R.R., Müller, N.L., Bronchiectasis: Comparison of preoperative thin-section CT and pathologic findings in resected specimens (1995) Radiology, 195 (3), pp. 649-654Reid, L.M., Reduction in bronchial subdivision in bronchiectasis (1950) Thorax, 5 (3), pp. 233-247Dutrieue, B., Vanholsbeeck, F., Verbanck, S., Paiva, M., A human acinar structure for simulation of realistic alveolar plateau slopes (2000) J Appl Physiol (1985), 89 (5), pp. 1859-1867Gustafsson, P.M., De Jong, P.A., Tiddens, H.A., Lindblad, A., Multiple-breath inert gas washout and spirometry versus structural lung disease in cystic fibrosis (2008) Thorax, 63 (2), pp. 129-134Horsley, A., Lung clearance index in the assessment of airways disease (2009) Respir Med, 103 (6), pp. 793-799Verbanck, S., Paiva, M., Schuermans, D., Hanon, S., Vincken, W., Van Muylem, A., Relationships between the lung clearance index and conductive and acinar ventilation heterogeneity (2012) J Appl Physiol (1985), 112 (5), pp. 782-79

Transverse lattice calculation of the pion light-cone wavefunctions

We calculate the light-cone wavefunctions of the pion by solving the meson boundstate problem in a coarse transverse lattice gauge theory using DLCQ. A large-N_c approximation is made and the light-cone Hamiltonian expanded in massive dynamical fields at fixed lattice spacing. In contrast to earlier calculations, we include contributions from states containing many gluonic link-fields between the quarks.The Hamiltonian is renormalised by a combination of covariance conditions on boundstates and fitting the physical masses M_rho and M_pi, decay constant f_pi, and the string tension sigma. Good covariance is obtained for the lightest 0^{-+} state, which we identify with the pion. Many observables can be deduced from its light-cone wavefunctions.After perturbative evolution,the quark valence structure function is found to be consistent with the experimental structure function deduced from Drell-Yan pi-nucleon data in the valence region x > 0.5. In addition, the pion distribution amplitude is consistent with the experimental distribution deduced from the pi gamma^* gamma transition form factor and diffractive dissociation. A new observable we calculate is the probability for quark helicity correlation. We find a 45% probability that the valence-quark helicities are aligned in the pion.Comment: 27 pages, 9 figure

Transverse momentum spectra of charged particles in proton-proton collisions at s=900\sqrt{s} = 900 GeV with ALICE at the LHC

The inclusive charged particle transverse momentum distribution is measured in proton-proton collisions at $\sqrt{s} = 900$ GeV at the LHC using the ALICE detector. The measurement is performed in the central pseudorapidity region $(|\eta|<0.8)$ over the transverse momentum range $0.15<p_{\rm T}<10$ GeV/$c$. The correlation between transverse momentum and particle multiplicity is also studied. Results are presented for inelastic (INEL) and non-single-diffractive (NSD) events. The average transverse momentum for $|\eta|<0.8$ is $\left<p_{\rm T}\right>_{\rm INEL}=0.483\pm0.001$ (stat.) $\pm0.007$ (syst.) GeV/$c$ and \left_{\rm NSD}=0.489\pm0.001 (stat.) $\pm0.007$ (syst.) GeV/$c$, respectively. The data exhibit a slightly larger $\left<p_{\rm T}\right>$ than measurements in wider pseudorapidity intervals. The results are compared to simulations with the Monte Carlo event generators PYTHIA and PHOJET.Comment: 20 pages, 8 figures, 2 tables, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/390

Diagnosis And Treatment Of Lead Poisoning In Children And Adults [diagnóstico E Tratamento Da Intoxicação Por Chumbo Em Crianças E Adultos]

Diagnosis of lead intoxication must be based basically on signs and symptoms produced by the main affected target organs: brain, hemopoietic system, kidneys, and periphery nervous system. The critical organ is the brain, promoting signs and symptoms of encephalopathy more or less pronounced according to the dose and duration of exposure. Such a symptoms are: headache, memory loss, concentration and attention problems, humor changes, irritability, depression, insomnia, somnolence, stupor, convulsions and coma. Diagnosis can be confirmed by blood and urine lead measurement, or by dosage of any parameter of lead effect on hemoglobin formation, like delta aminulevulinic acid in blood or urine and blood erythrocyte protoporphirin. Treatment is performed using chelating agents. Considering costs and commercial availability Brazilian experience regarding chelating agents for lead intoxications is limited to the use of dimecaprol (BAL), calcium versenate (EDTACaNa2) and D-penicilamine. However, the most efficacious drugs are intravenous EDTACaNa2, and oral dimercapto succinic acid (DMSA). BAL can be used together with EDTACaNa2 in adults when encephalopathic signs are present, or in children using EDTACaNa2 even without CNS signs and symptoms because BAL can pass blood-brain barrier chelating lead in the brain and protecting children against lead mobilization from other tissues to the brain provoked by EDTACaNa2.423309319Paoliello MMB, De Capitani EM. Chumbo. In: Azevedo AA, M. CAA, eds. Metais - Gerenciamento da Toxicidade São Paulo: Atheneu-Intertox2003:353-98Dal Molin, F., Paoliello, M.M.B., De Capitani, E.M., A zincoprotoporfirina como indicador biológico na exposição ao chumbo: Uma revisão. (2006) Rev Bras Toxicol, 19, pp. 71-80Nadig, R.J., Treatment of lead poisoning (1990) Jama, 263, pp. 2181-2182de Madureira, P.R., De Capitani, E.M., Vieira, R.J., Lead poisoning after gunshot wound (2000) Sao Paulo Med J, 118, pp. 78-80Somervaille, L., Chettle, D., Scott, M., In vivo tibia lead measurement as an index of cumulative exposure in occupationally exposed subjects (1988) Br J Ind Med, 45, pp. 174-181Somervaille, L.J., Nilsson, U., Chettle, D.R., In vivo measurements of bone lead - a comparison of two x-ray fluorescence techniques used at three different bone sites (1989) Phys Med Biol, 34, pp. 1833-1845Ahlgren, L., Liden, K., Mattsson, S., Tejning, S., X-ray fluorescence analysis of lead in human skeleton in vivo (1976) Scand J Work Environ Health, 2, pp. 82-86Ahlgren, L., Haeger-Aronsen, B., Mattsson, S., Schutz, A., In-vivo determination of lead in the skeleton after occupational exposure to lead (1980) Br J Ind Med, 37, pp. 109-113Schutz A, Skerfving S, Christoffersson JO, Ahlgren L, Mattson S. Lead in vertebral bone biopsies from active and retired lead workers. Arch Environ Health. 1987;42:340-6CDC. Preventing lead poisoning in young children - a statement by the Centers for Disease Control - Oct 1991: USDHHS-PHS-CDCP1991CDC. Screening young children for lead poisoning: guidance for state and local public helath officials. In: Program. U-C-CIPP, ed. Atlanta1997Needleman, H.L., Gunnoe, C., Leviton, A., Deficits in psychologic and classroom performance of children with elevated dentine lead levels (1979) N Engl J Med, 300, pp. 689-695Needleman, H.L., Schell, A., Bellinger, D., Leviton, A., Allred, E.N., The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report (1990) N Engl J Med, 322, pp. 83-88Rogan, W.J., Dietrich, K.N., Ware, J.H., The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead (2001) N Engl J Med, 344, pp. 1421-1426Tong, S., Baghurst, P.A., Sawyer, M.G., Burns, J., McMichael, A.J., Declining blood lead levels and changes in cognitive function during childhood: The Port Pirie Cohort Study (1998) Jama, 280, pp. 1915-1919Stokes, L., Letz, R., Gerr, F., Neurotoxicity in young adults 20 years after childhood exposure to lead: The Bunker Hill experience (1998) Occup Environ Med, 55, pp. 507-516Porru, S., Alessio, L., The use of chelating agents in occupational lead poisoning (1996) Occup Med, 46, pp. 41-48. , LondMarkowitz, M.E., Rosen, J.F., Need for the lead mobilization test in children with lead poisoning (1991) J Pediatr, 119, pp. 305-310Lee, B.K., Schwartz, B.S., Stewart, W., Ahn, K.D., Provocative chelation with DMSA and EDTA: Evidence for differential access to lead storage sites (1995) Occup Environ Med, 52, pp. 13-19Markowitz, M.E., Rosen, J.F., Assessment of lead stores in children: Validation of an 8-hour CaNa2EDTA provocative test (1984) Pediatrics, 104, pp. 337-341Apostoli, P., Porru, S., Duca, P., Ferioli, A., Alessio, L., Significance and validity of a shortened lead chelation test (1990) J Occup Med, 32, pp. 1124-1129De Capitani EM, Paoliello MMB. Diagnóstico e Tratamento das Intoxicações. In: Azevedo AA, M. CAA, eds. Metais - Gerenciamento da Toxicidade. São Paulo: Atheneu-Intertox2003:415-50Klaassen, C.D., Heavy metals and heavy-metal antagonists (1996) Goodman & Gilman's The Pharmacological Basis of Therapeutis, p. 1905. , Hardman JG, Limbird LE, eds, 9th ed. New York: McGraw-Hill;Cardani, A., Farina, G., Profilassi del saturnismo mediante somministrazione di versene per via intramoscolare. (1970) Med Lav, 61, pp. 220-226Sachs, H.K., Blanksma, L.A., Murray, E.F., O'Connell, M.J., Ambulatory treatment of lead poisoning: Report of 1,155 cases (1970) Pediatrics, 46, pp. 389-396De Capitani, E.M., de Madureira, P.R., Moreira Filho, D.C., Estudo comparativo de tratamento quelante de pacientes intoxicados por chumbo inorgânico com EDTACaNa2 por duas vias de administraçã o. (2004) Rev Bras Med Trab, 2, pp. 185-190Cory-Slechta, D.A., Weiss, B., Cox, C., Mobilization and redistribution of lead over the course of calcium disodium ethylenediamine tetraacetate chelation therapy (1987) J Pharmacol Exp Ther, 243, pp. 804-813Graziano, J.H., 2,3-dimercaptosuccinic acid (DMSA, Succimer) (1994) Goldfrank's Toxicologic Emergencies, pp. 1045-1047. , Goldfrank LR, ed, 5th ed. 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Silicosis (still) Among Us [a Silicose (ainda) Entre Nós]

[No abstract available]326xxxiiixxxvFerreira, A., Moreira, V., Ricardo, H., Coutinho, R., Gabetto, J., Marchiori, E., Fibrose maciça progressiva em trabalhadores expostos à sílica - Achados na tomografia computadorizada de alta resolução (2006) J Bras Pneumol, 32 (6), pp. 523-528Saiyed HN, Sharma YK, Sadhu HG, Norboo T, Patel PD, Patel TS, et al. Non-occupational pneumoconiosis at high altitude villages in central Ladakh. Br J Ind Med. 1991;48(12):825-9. Comment in: Br J Ind Med. 1992;49(6):452-3Norboo T, Angchuk PT, Yahya M, Kamat SR, Pooley FD, Corrin B, et al. Silicosis in a Himalayan village population: role of environmental dust. Thorax. 199146(5): 341-3. Erratum in: Thorax. 1991;46(7):544Brasil. Ministério do Trabalho e Emprego. FUNDACENTRO. Programa Nacional de Eliminação da Silicose. PNES.[texto na Internet]. Brasília2003. [citado Jul 18]. Disponível em: http://www.fundacentro.gov.br/CTN/detalhesprograma.asp D=CTN&cod=13Algranti, E., De Capitani, E., Carneiro, A., Saldiva, P., Patologia respiratória relacionada com o trabalho (2003) Patologia do trabalho, pp. 1329-1398. , Mendes R, editor, 2α ed. São Paulo: Atheneu;Occupational Safety and Health. Guidelines for the use of the ILO International Classification of Radiographs of Pneumoconioses. 2000 ed. rev. Geneva: International Labour Organization2002Webb, W., Muller, N., Naidich, D., (2001) High-Resolution CT of the Lung, , 3rd ed. Philadelphia: Lippincott Williams & Wilkins;Antão, V.C., Pinheiro, G.A., Terra-Filho, M., Kavakama, J., Muller, N.L., High-resolution CT in silicosis: Correlation with radiographic findings and functional impairment (2005) J Comput Assist Tomogr, 29 (3), pp. 350-356Ooi, C.G., Khong, P.L., Cheng, R.S., Tan, B., Tsang, F., Lee, I., The relationship between mediastinal lymph node attenuation with parenchymal lung parameters in silicosis (2003) Int J Tuberc Lung Dis, 7 (12), pp. 1199-1206Begin, R., Ostiguy, G., Fillion, R., Colman, N., Computed tomography scan in the early detection of silicosis (1991) Am Rev Respir Dis, 144 (3), pp. 697-705Jacobsen, M., The international labour office classification: Use and misuse (1991) Ann N Y Acad Sci, 643 (1), pp. 100-107Kusaka, Y., Hering, K., Parker, J., (2005) International classification of HRCT for occupational and environmental respiratory diseases, , Tokyo: Springer-Verlag;Carneiro, A., (2006) A tomografia computadorizada de alta resolução de tórax em casos borderline de silicose: Quando indicála? [tese], , Belo Horizonte: Universidade Federal de Minas Gerais

Metabolism And Toxicity Of Lead In Children And Adults [meta Metabolismo Bolismo E To Toxicidade Xicidade Do Chumbo Humbo Na Criança E No Adulto]

Lead does not participate in any metabolic process in humans. Nevertheless, it is the most important non ferrous metal in industry since ancient times. This fact promoted a huge and extensive environmental contamination, allowing for an excessive input of lead by humans through ingestion and inhalation. In this review it is discussed aspects of kinetics and toxicity of lead in its inorganic form, being the most important chemical form presenting in occupational and general environment. As a metal, lead does not suffer biotransformation as other toxic substances. Its metabolism is limited to a complex kinetics of distribution and excretion which depends on its chemical speciation, determining the redox potential, rates of ionization and protein binding; crossing of blood brain and placental barriers; rates of tissue accumulation and renal excretion. Adults absorb 10% after lead ingestion, contrasting with children that can absorb 50%. Lead is distributed rapidly and easily through all tissues, including brain, crossing placental barrier and being secreted in maternal milk. Elimination half lifes can be very different according to the body compartment as follows: for blood = 15 to 30 days (in children under low doses of exposure = 10 to 12 months); soft tissues in general = 60 days; trabecular bone = 90 to 120 days; cortical bone with stable deposits = 25 to 30 years. Lead presents toxic action in the central and peripheral nervous system, renal and hemopoietic systems, by toxic mechanisms that are discussed in the paper.423268276Patterson, C., Ericson, J., Manea-Krichten, M., Shirahata, H., Natural skeletal levels of lead in Homo sapiens sapiens uncontaminated by technological lead (1991) Sci Total Environ, 107, pp. 205-236Paoliello MMB, De Capitani EM. Chumbo. In: Azevedo AA, M. CAA, eds. Metais - Gerenciamento da Toxicidade São Paulo: Atheneu-Intertox2003:353-98Leggett, R.W., An age-specific kinetic model of lead metabolism in humans (1993) Environ Health Perspect, 101, pp. 598-616Shäfer, S.G., Dawes, R.L.F., Elsenhans, B., Forth, W.K.S., Metals Toxicology, pp. 755-804. , Marquardt H, Schafer SG, McCellan R, Welsch F, eds, San Diego: Academic Press;Carrington, C.D., Bolger, P.M., An assessment of the hazards of lead in food (1992) Regul Toxicol Pharmacol, 16, pp. 265-272Toxicologic Profile for Lead - Update Statement (1999) Registry, p. 587. , ATSDR, USDoHHS-PHS-AfTSaD, ed. Atlanta;Davies, D.J., Thornton, I., Watt, J.M., Lead intake and blood lead in two-year-old U.K. urban children (1990) Sci Total Environ, 90, pp. 13-29Nadig, R.J., Treatment of lead poisoning (1990) Jama, 263, pp. 2181-2182Rabinowitz, M.B., Wetherill, G.W., Kopple, J.D., Kinetic analysis of lead metabolism in healthy humans (1976) J Clin Invest, 58, pp. 260-270Gulson, B.L., Jameson, C.W., Mahaffey, K.R., Mizon, K.J., Korsch, M.J., Vimpani, G., Pregnancy increases mobilization of lead from maternal skeleton (1997) J Lab Clin Med, 130, pp. 51-62Bellinger, D., Leviton, A., Waternaux, C., Needleman, H., Rabinowitz, M., Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development (1987) N Engl J Med, 316, pp. 1037-1043Silbergeld EK. Lead in bone: implications for toxicology during pregnancy and lactation. Environ Health Perspect 1991;91:63-70Ong, C.N., Phoon, W.O., Law, H.Y., Tye, C.Y., Lim, H.H., Concentrations of lead in maternal blood, cord blood, and breast milk (1985) Arch Dis Child, 60, pp. 756-759Gulson, B.L., Jameson, C.W., Mahaffey, K.R., Relationships of lead in breast milk to lead in blood, urine, and diet of the infant and mother (1998) Environ Health Perspect, 106, pp. 667-674Koyashiki, G.A.K., (2008) Níveis de chumbo em leite e sangue de doadores de banco de leite em município do Sul do Brasil, , Mestrado, Londrina: Universidade Estadual de Londrina;Barry, P.S., A comparison of concentrations of lead in human tissues (1975) Br J Ind Med, 32, pp. 119-139Kosnett, M., Becker, C., Osterloh, J., Kelly, T., Pasta, D., Factors influencing bone lead concentration in a suburban community assessed by noninvasive K X-ray fluorescence (1994) J Am Med Assoc, 271, pp. 197-203Smith, D.R., Osterloh, J.D., Flegal, A.R., Use of endogenous, stable lead isotopes to determine release of lead from the skeleton (1996) Environ Health Perspect, 104, pp. 60-66Kehoe, R.A., The metabolism of lead in man in health and disease. I. The normal metabolism of lead (1961) J R Inst Public Health, 24, pp. 81-97Alessio, L., Lead, F.V., (1983) Human biological monitoring of indutrial chemicals series, p. 188. , Alessio L, Berlin A, Roi R, Boni M, eds, Brussels, Luxembourg: Commission of The European Communities;Henretig FM. Lead. In: Goldfrank LR, ed. Goldfrank's Toxicologic Emergencies. New York: McGraw-Hill2002:1200-27Lauwerys, R., Buchet, J.P., Roels, H., Berlin, A., Smeets, J., Intercomparison program of lead, mercury, and cadmium analysis in blood, urine, and aqueous solutions (1975) Clin Chem, 21, pp. 551-557Holness, D., Nethercott, J., Acute lead intoxication in a group of demolition workers (1988) Appl Ind Hyg, 3, pp. 338-341Feldman, R.G., (1999) Occupational and Environmental Neurotoxicology, , Philadelphia: Lippincott-Raven;Matte, T., Figueroa, J., Burr, G., al e. Lead exposure among leadacid battery workers in Jamaica (1989) Am J Ind Med, 16, pp. 167-177Marino, P., Franzblau, A., Lilis, R., al e. Acute lead poisoning in construction workers: The failure of current protective standards (1989) Arch Environ Health, 44, pp. 140-145Lilis, R., Fischbein, A., Diamond, S., Lead effects among secondary lead smelter workers with blood lead levels below 80 mcg/100ml (1977) Arch Environ Health, pp. 256-266Dahlgren, J., Abdominal pain in lead workers (1978) Arch Environ Health, pp. 156-159Spivey, G., Brown, C., Baloh, R., Subclinical effects of chronic increased lead absorption: A prospective study (1979) J Occup Med, 21, pp. 423-429Cullen, M., Robins, J., Eskenazi, B., Adult inorganic lead intoxication: Presentation of 31 new cases and a review of recent advances in the literature (1983) Medicine, 62, pp. 221-247(1992) Oxford Textbook of Clinical Nephrology, , Cameron S, Davison AM, Grunfeld J-P, Kerr D, Ritz E, eds, Oxford: Oxford, Oxford University Press;Woods, J.S., Hematopoietic system (1995) Metal Toxicology, pp. 287-304. , Goyer RA, Klaassen C, Waalkes M, eds, San Diego: Academic Press;CDC. 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A meta-analysis of modern studies (1990) Jama, 263, pp. 673-678Haenninen, H., Hernberg, S., Mantere, P., Vesanto, R., Jalkanen, M., Psychological performance of subjects with low exposure to lead (1978) J Occup Med, 20, pp. 683-689Hogstedt, C., Hane, M., Agrell, A., Bodin, L., Neuropsychological test results and symptoms among workers with well-de fined long-term exposure to lead (1983) Br J Ind Med, 40, pp. 99-105Batuman, V., Maesaka, J.K., Haddad, B., Tepper, E., Landy, E., Wedeen, R.P., The role of lead in gout nephropathy (1981) N Engl J Med, 304, pp. 520-523Batuman, V., Lead nephropathy, gout, and hypertension (1993) Am J Med Sci, 305, pp. 241-247Emmerson, B.T., Chronic lead nephrompathy: The diagnostic use of calcium EDTA and the association with gout (1963) Aust Ann Med, 12, pp. 310-324Bennet, W., Lead nephropathy (1985) Kidney Int, 28, pp. 212-220Wedeen, R.P., Malik, D.K., Batuman, V., Detection and treatment of occupational lead nephropathy (1979) Arch Intern Med, 139, pp. 53-57Tuppurainen, M., Wagar, G., Kurppa, K., Thyroid function as assessed by routine laboratory tests of workers with longterm lead exposure (1988) Scand J Work Environ Health, 14, pp. 175-180Gennart, J.P., Buchet, J.P., Roels, H., Ghyselen, P., Ceulemans, E., Lauwerys, R., Fertility of male workers exposed to cadmium, lead, or manganese (1992) Am J Epidemiol, 135, pp. 1208-1219Siegel, M., Forsyth, B., Siegel, L., Cullen, M.R., The effect of lead on thyroid function in children (1989) Environ Res, 49, pp. 190-196Huseman, C.A., Varma, M.M., Angle, C.R., Neuroendocrine effects of toxic and low blood lead levels in children (1992) Pediatrics, 90, pp. 186-189Rosen, J.F., Chesney, R.W., Hamstra, A., DeLuca, H.F., Mahaffey, K.R., Reduction in 1,25-dihydroxyvitamin D in children with increased lead absorption (1980) N Engl J Med, 302, pp. 1128-1131Koo, W.W., Succop, P.A., Bornschein, R.L., Serum vitamin D metabolites and bone mineralization in young children with chronic low to moderate lead exposure (1991) Pediatrics, 87, pp. 680-687Alexander, B.H., Checkoway, H., van Netten, C., Semen quality of men employed at a lead smelter (1996) Occup Environ Med, 53, pp. 411-416Lin, S., Hwang, S.A., Marshall, E.G., Stone, R., Chen, J., Fertility rates among lead workers and professional bus drivers: A comparative study (1996) Ann Epidemiol, 6, pp. 201-208Telisman, S., Cvitkovic, P., Jurasovic, J., Pizent, A., Gavella, M., Rocic, B., Semen quality and reproductive endocrine function in relation to biomarkers of lead, cadmium, zinc, and copper in men (2000) Environ Health Perspect, 108, pp. 45-53Hu, H., Knowledge of diagnosis and reproductive history among survivors of childhood plumbism (1991) Am J Public Health, 81, pp. 1070-1072McMichael, A.J., Vimpani, G.V., Robertson, E.F., Baghurst, P.A., Clark, P.D., The Port Pirie cohort study: Maternal blood lead and pregnancy outcome (1986) J Epidemiol Community Health, 40, pp. 18-25Baghurst, P.A., Robertson, E.F., McMichael, A.J., Vimpani, G.V., Wigg, N.R., Roberts, R.R., The Port Pirie Cohort Study: Lead effects on pregnancy outcome and early childhood development (1987) Neurotoxicology, 8, pp. 395-401Ernhart, C.B., Wolf, A.W., Kennard, M.J., Erhard, P., Filipovich, H.F., Sokol, R.J., Intrauterine exposure to low levels of lead: The status of the neonate (1986) Arch Environ Health, 41, pp. 287-291Needleman, H.L., Rabinowitz, M., Leviton, A., Linn, S., Schoenbaum, S., The relationship between prenatal exposure to lead and congenital anomalies (1984) Jama, 251, pp. 2956-295