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1.  Measurement of the charge asymmetry in top quark pair production in pp collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s}=7\ \mathrm{TeV}$\end{document} using the ATLAS detector 
Aad, G. | Abbott, B. | Abdallah, J. | Abdelalim, A. A. | Abdesselam, A. | Abdinov, O. | Abi, B. | Abolins, M. | AbouZeid, O. S. | Abramowicz, H. | Abreu, H. | Acerbi, E. | Acharya, B. S. | Adamczyk, L. | Adams, D. L. | Addy, T. N. | Adelman, J. | Aderholz, M. | Adomeit, S. | Adragna, P. | Adye, T. | Aefsky, S. | Aguilar-Saavedra, J. A. | Aharrouche, M. | Ahlen, S. P. | Ahles, F. | Ahmad, A. | Ahsan, M. | Aielli, G. | Akdogan, T. | Åkesson, T. P. A. | Akimoto, G. | Akimov, A. V. | Akiyama, A. | Alam, M. S. | Alam, M. A. | Albert, J. | Albrand, S. | Aleksa, M. | Aleksandrov, I. N. | Alessandria, F. | Alexa, C. | Alexander, G. | Alexandre, G. | Alexopoulos, T. | Alhroob, M. | Aliev, M. | Alimonti, G. | Alison, J. | Aliyev, M. | Allport, P. P. | Allwood-Spiers, S. E. | Almond, J. | Aloisio, A. | Alon, R. | Alonso, A. | Alvarez Gonzalez, B. | Alviggi, M. G. | Amako, K. | Amaral, P. | Amelung, C. | Ammosov, V. V. | Amorim, A. | Amorós, G. | Amram, N. | Anastopoulos, C. | Ancu, L. S. | Andari, N. | Andeen, T. | Anders, C. F. | Anders, G. | Anderson, K. J. | Andreazza, A. | Andrei, V. | Andrieux, M-L. | Anduaga, X. S. | Angerami, A. | Anghinolfi, F. | Anisenkov, A. | Anjos, N. | Annovi, A. | Antonaki, A. | Antonelli, M. | Antonov, A. | Antos, J. | Anulli, F. | Aoun, S. | Aperio Bella, L. | Apolle, R. | Arabidze, G. | Aracena, I. | Arai, Y. | Arce, A. T. H. | Archambault, J. P. | Arfaoui, S. | Arguin, J-F. | Arik, E. | Arik, M. | Armbruster, A. J. | Arnaez, O. | Arnault, C. | Artamonov, A. | Artoni, G. | Arutinov, D. | Asai, S. | Asfandiyarov, R. | Ask, S. | Åsman, B. | Asquith, L. | Assamagan, K. | Astbury, A. | Astvatsatourov, A. | Aubert, B. | Auge, E. | Augsten, K. | Aurousseau, M. | Avolio, G. | Avramidou, R. | Axen, D. | Ay, C. | Azuelos, G. | Azuma, Y. | Baak, M. A. | Baccaglioni, G. | Bacci, C. | Bach, A. M. | Bachacou, H. | Bachas, K. | Bachy, G. | Backes, M. | Backhaus, M. | Badescu, E. | Bagnaia, P. | Bahinipati, S. | Bai, Y. | Bailey, D. C. | Bain, T. | Baines, J. T. | Baker, O. K. | Baker, M. D. | Baker, S. | Banas, E. | Banerjee, P. | Banerjee, Sw. | Banfi, D. | Bangert, A. | Bansal, V. | Bansil, H. S. | Barak, L. | Baranov, S. P. | Barashkou, A. | Barbaro Galtieri, A. | Barber, T. | Barberio, E. L. | Barberis, D. | Barbero, M. | Bardin, D. Y. | Barillari, T. | Barisonzi, M. | Barklow, T. | Barlow, N. | Barnett, B. M. | Barnett, R. M. | Baroncelli, A. | Barone, G. | Barr, A. J. | Barreiro, F. | Barreiro Guimarães da Costa, J. | Barrillon, P. | Bartoldus, R. | Barton, A. E. | Bartsch, V. | Bates, R. L. | Batkova, L. | Batley, J. R. | Battaglia, A. | Battistin, M. | Bauer, F. | Bawa, H. S. | Beale, S. | Beare, B. | Beau, T. | Beauchemin, P. H. | Beccherle, R. | Bechtle, P. | Beck, H. P. | Becker, S. | Beckingham, M. | Becks, K. H. | Beddall, A. J. | Beddall, A. | Bedikian, S. | Bednyakov, V. A. | Bee, C. P. | Begel, M. | Behar Harpaz, S. | Behera, P. K. | Beimforde, M. | Belanger-Champagne, C. | Bell, P. J. | Bell, W. H. | Bella, G. | Bellagamba, L. | Bellina, F. | Bellomo, M. | Belloni, A. | Beloborodova, O. | Belotskiy, K. | Beltramello, O. | Ben Ami, S. | Benary, O. | Benchekroun, D. | Benchouk, C. | Bendel, M. | Benekos, N. | Benhammou, Y. | Benhar Noccioli, E. | Benitez Garcia, J. A. | Benjamin, D. P. | Benoit, M. | Bensinger, J. R. | Benslama, K. | Bentvelsen, S. | Berge, D. | Bergeaas Kuutmann, E. | Berger, N. | Berghaus, F. | Berglund, E. | Beringer, J. | Bernat, P. | Bernhard, R. | Bernius, C. | Berry, T. | Bertella, C. | Bertin, A. | Bertinelli, F. | Bertolucci, F. | Besana, M. I. | Besson, N. | Bethke, S. | Bhimji, W. | Bianchi, R. M. | Bianco, M. | Biebel, O. | Bieniek, S. P. | Bierwagen, K. | Biesiada, J. | Biglietti, M. | Bilokon, H. | Bindi, M. | Binet, S. | Bingul, A. | Bini, C. | Biscarat, C. | Bitenc, U. | Black, K. M. | Blair, R. E. | Blanchard, J.-B. | Blanchot, G. | Blazek, T. | Blocker, C. | Blocki, J. | Blondel, A. | Blum, W. | Blumenschein, U. | Bobbink, G. J. | Bobrovnikov, V. B. | Bocchetta, S. S. | Bocci, A. | Boddy, C. R. | Boehler, M. | Boek, J. | Boelaert, N. | Böser, S. | Bogaerts, J. A. | Bogdanchikov, A. | Bogouch, A. | Bohm, C. | Boisvert, V. | Bold, T. | Boldea, V. | Bolnet, N. M. | Bona, M. | Bondarenko, V. G. | Bondioli, M. | Boonekamp, M. | Boorman, G. | Booth, C. N. | Bordoni, S. | Borer, C. | Borisov, A. | Borissov, G. | Borjanovic, I. | Borri, M. | Borroni, S. | Bos, K. | Boscherini, D. | Bosman, M. | Boterenbrood, H. | Botterill, D. | Bouchami, J. | Boudreau, J. | Bouhova-Thacker, E. V. | Boumediene, D. | Bourdarios, C. | Bousson, N. | Boveia, A. | Boyd, J. | Boyko, I. R. | Bozhko, N. I. | Bozovic-Jelisavcic, I. | Bracinik, J. | Braem, A. | Branchini, P. | Brandenburg, G. W. | Brandt, A. | Brandt, G. | Brandt, O. | Bratzler, U. | Brau, B. | Brau, J. E. | Braun, H. M. | Brelier, B. | Bremer, J. | Brenner, R. | Bressler, S. | Breton, D. | Britton, D. | Brochu, F. M. | Brock, I. | Brock, R. | Brodbeck, T. J. | Brodet, E. | Broggi, F. | Bromberg, C. | Bronner, J. | Brooijmans, G. | Brooks, W. K. | Brown, G. | Brown, H. | Bruckman de Renstrom, P. A. | Bruncko, D. | Bruneliere, R. | Brunet, S. | Bruni, A. | Bruni, G. | Bruschi, M. | Buanes, T. | Buat, Q. | Bucci, F. | Buchanan, J. | Buchanan, N. J. | Buchholz, P. | Buckingham, R. M. | Buckley, A. G. | Buda, S. I. | Budagov, I. A. | Budick, B. | Büscher, V. | Bugge, L. | Bulekov, O. | Bunse, M. | Buran, T. | Burckhart, H. | Burdin, S. | Burgess, T. | Burke, S. | Busato, E. | Bussey, P. | Buszello, C. P. | Butin, F. | Butler, B. | Butler, J. M. | Buttar, C. M. | Butterworth, J. M. | Buttinger, W. | Cabrera Urbán, S. | Caforio, D. | Cakir, O. | Calafiura, P. | Calderini, G. | Calfayan, P. | Calkins, R. | Caloba, L. P. | Caloi, R. | Calvet, D. | Calvet, S. | Camacho Toro, R. | Camarri, P. | Cambiaghi, M. | Cameron, D. | Caminada, L. M. | Campana, S. | Campanelli, M. | Canale, V. | Canelli, F. | Canepa, A. | Cantero, J. | Capasso, L. | Capeans Garrido, M. D. M. | Caprini, I. | Caprini, M. | Capriotti, D. | Capua, M. | Caputo, R. | Caramarcu, C. | Cardarelli, R. | Carli, T. | Carlino, G. | Carminati, L. | Caron, B. | Caron, S. | Carrillo Montoya, G. D. | Carter, A. A. | Carter, J. R. | Carvalho, J. | Casadei, D. | Casado, M. P. | Cascella, M. | Caso, C. | Castaneda Hernandez, A. M. | Castaneda-Miranda, E. | Castillo Gimenez, V. | Castro, N. F. | Cataldi, G. | Cataneo, F. | Catinaccio, A. | Catmore, J. R. | Cattai, A. | Cattani, G. | Caughron, S. | Cauz, D. | Cavalleri, P. | Cavalli, D. | Cavalli-Sforza, M. | Cavasinni, V. | Ceradini, F. | Cerqueira, A. S. | Cerri, A. | Cerrito, L. | Cerutti, F. | Cetin, S. A. | Cevenini, F. | Chafaq, A. | Chakraborty, D. | Chan, K. | Chapleau, B. | Chapman, J. D. | Chapman, J. W. | Chareyre, E. | Charlton, D. G. | Chavda, V. | Chavez Barajas, C. A. | Cheatham, S. | Chekanov, S. | Chekulaev, S. V. | Chelkov, G. A. | Chelstowska, M. A. | Chen, C. | Chen, H. | Chen, S. | Chen, T. | Chen, X. | Cheng, S. | Cheplakov, A. | Chepurnov, V. F. | Cherkaoui El Moursli, R. | Chernyatin, V. | Cheu, E. | Cheung, S. L. | Chevalier, L. | Chiefari, G. | Chikovani, L. | Childers, J. T. | Chilingarov, A. | Chiodini, G. | Chizhov, M. V. | Choudalakis, G. | Chouridou, S. | Christidi, I. A. | Christov, A. | Chromek-Burckhart, D. | Chu, M. L. | Chudoba, J. | Ciapetti, G. | Ciba, K. | Ciftci, A. K. | Ciftci, R. | Cinca, D. | Cindro, V. | Ciobotaru, M. D. | Ciocca, C. | Ciocio, A. | Cirilli, M. | Citterio, M. | Ciubancan, M. | Clark, A. | Clark, P. J. | Cleland, W. | Clemens, J. C. | Clement, B. | Clement, C. | Clifft, R. W. | Coadou, Y. | Cobal, M. | Coccaro, A. | Cochran, J. | Coe, P. | Cogan, J. G. | Coggeshall, J. | Cogneras, E. | Colas, J. | Colijn, A. P. | Collins, N. J. | Collins-Tooth, C. | Collot, J. | Colon, G. | Conde Muiño, P. | Coniavitis, E. | Conidi, M. C. | Consonni, M. | Consorti, V. | Constantinescu, S. | Conta, C. | Conventi, F. | Cook, J. | Cooke, M. | Cooper, B. D. | Cooper-Sarkar, A. M. | Copic, K. | Cornelissen, T. | Corradi, M. | Corriveau, F. | Cortes-Gonzalez, A. | Cortiana, G. | Costa, G. | Costa, M. J. | Costanzo, D. | Costin, T. | Côté, D. | Coura Torres, R. | Courneyea, L. | Cowan, G. | Cowden, C. | Cox, B. E. | Cranmer, K. | Crescioli, F. | Cristinziani, M. | Crosetti, G. | Crupi, R. | Crépé-Renaudin, S. | Cuciuc, C.-M. | Cuenca Almenar, C. | Cuhadar Donszelmann, T. | Curatolo, M. | Curtis, C. J. | Cuthbert, C. | Cwetanski, P. | Czirr, H. | Czodrowski, P. | Czyczula, Z. | D’Auria, S. | D’Onofrio, M. | D’Orazio, A. | Da Silva, P. V. M. | Da Via, C. | Dabrowski, W. | Dai, T. | Dallapiccola, C. | Dam, M. | Dameri, M. | Damiani, D. S. | Danielsson, H. O. | Dannheim, D. | Dao, V. | Darbo, G. | Darlea, G. L. | Daum, C. | Davey, W. | Davidek, T. | Davidson, N. | Davidson, R. | Davies, E. | Davies, M. | Davison, A. R. | Davygora, Y. | Dawe, E. | Dawson, I. | Dawson, J. W. | Daya-Ishmukhametova, R. K. | De, K. | de Asmundis, R. | De Castro, S. | De Castro Faria Salgado, P. E. | De Cecco, S. | de Graat, J. | De Groot, N. | de Jong, P. | De La Taille, C. | De la Torre, H. | De Lotto, B. | de Mora, L. | De Nooij, L. | De Pedis, D. | De Salvo, A. | De Sanctis, U. | De Santo, A. | De Vivie De Regie, J. B. | Dean, S. | Dearnaley, W. J. | Debbe, R. | Debenedetti, C. | Dedovich, D. V. | Degenhardt, J. | Dehchar, M. | Del Papa, C. | Del Peso, J. | Del Prete, T. | Delemontex, T. | Deliyergiyev, M. | Dell’Acqua, A. | Dell’Asta, L. | Della Pietra, M. | della Volpe, D. | Delmastro, M. | Delruelle, N. | Delsart, P. A. | Deluca, C. | Demers, S. | Demichev, M. | Demirkoz, B. | Deng, J. | Denisov, S. P. | Derendarz, D. | Derkaoui, J. E. | Derue, F. | Dervan, P. | Desch, K. | Devetak, E. | Deviveiros, P. O. | Dewhurst, A. | DeWilde, B. | Dhaliwal, S. | Dhullipudi, R. | Di Ciaccio, A. | Di Ciaccio, L. | Di Girolamo, A. | Di Girolamo, B. | Di Luise, S. | Di Mattia, A. | Di Micco, B. | Di Nardo, R. | Di Simone, A. | Di Sipio, R. | Diaz, M. A. | Diblen, F. | Diehl, E. B. | Dietrich, J. | Dietzsch, T. A. | Diglio, S. | Dindar Yagci, K. | Dingfelder, J. | Dionisi, C. | Dita, P. | Dita, S. | Dittus, F. | Djama, F. | Djobava, T. | do Vale, M. A. B. | Do Valle Wemans, A. | Doan, T. K. O. | Dobbs, M. | Dobinson, R. | Dobos, D. | Dobson, E. | Dodd, J. | Doglioni, C. | Doherty, T. | Doi, Y. | Dolejsi, J. | Dolenc, I. | Dolezal, Z. | Dolgoshein, B. A. | Dohmae, T. | Donadelli, M. | Donega, M. | Donini, J. | Dopke, J. | Doria, A. | Dos Anjos, A. | Dosil, M. | Dotti, A. | Dova, M. T. | Dowell, J. D. | Doxiadis, A. D. | Doyle, A. 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A measurement of the top-antitop production charge asymmetry AC is presented using data corresponding to an integrated luminosity of 1.04 fb−1 of pp collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s} = 7$\end{document} TeV collected by the ATLAS detector at the LHC. Events are selected with a single lepton (electron or muon), missing transverse momentum and at least four jets of which at least one jet is identified as coming from a b-quark. A kinematic fit is used to reconstruct the \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$t\bar{t}$\end{document} event topology. After background subtraction, a Bayesian unfolding procedure is performed to correct for acceptance and detector effects. The measured value of AC is \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$A_{C}= -0.019 \pm0.028 \ (\mathrm{stat}.) \pm0.024 \ (\mathrm{syst.})$\end{document}, consistent with the prediction from the MC@NLO Monte Carlo generator of AC=0.006±0.002. Measurements of AC in two ranges of invariant mass of the top-antitop pair are also shown.
doi:10.1140/epjc/s10052-012-2039-5
PMCID: PMC4370878  PMID: 25814837
2.  Search for lepton flavour violation in the eμ continuum with the ATLAS detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s} = 7~\mbox{TeV}$\end{document}pp collisions at the LHC 
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This paper presents a search for the t-channel exchange of an R-parity violating scalar top quark (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\tilde{t}$\end{document}) in the e±μ∓ continuum using 2.1 fb−1 of data collected by the ATLAS detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s}=7~\mbox{TeV}$\end{document}pp collisions at the Large Hadron Collider. Data are found to be consistent with the expectation from the Standard Model backgrounds. Limits on R-parity-violating couplings at 95 % C.L. are calculated as a function of the scalar top mass (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}$\end{document}). The upper limits on the production cross section for pp→eμX, through the t-channel exchange of a scalar top quark, ranges from 170 fb for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}=95~\mbox{GeV}$\end{document} to 30 fb for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}=1000~\mbox{GeV}$\end{document}.
doi:10.1140/epjc/s10052-012-2040-z
PMCID: PMC4370899  PMID: 25814838
3.  Drinking water disinfection byproducts: review and approach to toxicity evaluation. 
Environmental Health Perspectives  1999;107(Suppl 1):207-217.
There is widespread potential for human exposure to disinfection byproducts (DBPs) in drinking water because everyone drinks, bathes, cooks, and cleans with water. The need for clean and safe water led the U.S. Congress to pass the Safe Drinking Water Act more than 20 years ago in 1974. In 1976, chloroform, a trihalomethane (THM) and a principal DBP, was shown to be carcinogenic in rodents. This prompted the U.S. Environmental Protection Agency (U.S. EPA) in 1979 to develop a drinking water rule that would provide guidance on the levels of THMs allowed in drinking water. Further concern was raised by epidemiology studies suggesting a weak association between the consumption of chlorinated drinking water and the occurrence of bladder, colon, and rectal cancer. In 1992 the U.S. EPA initiated a negotiated rulemaking to evaluate the need for additional controls for microbial pathogens and DBPs. The goal was to develop an approach that would reduce the level of exposure from disinfectants and DBPs without undermining the control of microbial pathogens. The product of these deliberations was a proposed stage 1 DBP rule. It was agreed that additional information was necessary on how to optimize the use of disinfectants while maintaining control of pathogens before further controls to reduce exposure beyond stage 1 were warranted. In response to this need, the U.S. EPA developed a 5-year research plan to support the development of the longer term rules to control microbial pathogens and DBPs. A considerable body of toxicologic data has been developed on DBPs that occur in the drinking water, but the main emphasis has been on THMs. Given the complexity of the problem and the need for additional data to support the drinking water DBP rules, the U.S. EPA, the National Institute of Environmental Health Sciences, and the U.S. Army are working together to develop a comprehensive biologic and mechanistic DBP database. Selected DBPs will be tested using 2-year toxicity and carcinogenicity studies in standard rodent models; transgenic mouse models and small fish models; in vitro mechanistic and toxicokinetic studies; and reproductive, immunotoxicity, and developmental studies. The goal is to create a toxicity database that reflects a wide range of DBPs resulting from different disinfection practices. This paper describes the approach developed by these agencies to provide the information needed to make scientifically based regulatory decisions.
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PMCID: PMC1566350  PMID: 10229719
4.  EMF working group. 
PMCID: PMC1533239  PMID: 10048946
7.  Modulation of the soleus H-reflex during pedalling in normal humans and in patients with spinal spasticity. 
Soleus H-reflexes were recorded in 10 normal subjects and seven patients with spasticity caused by incomplete spinal cord injury while they pedalled on a stationary bicycle which had been modified to trigger electrical stimuli to the tibial nerve at eight precise points in the pedal cycle. Stimulus strength was adjusted to yield M-waves of constant amplitude at each pedal position. During active pedalling, all normal subjects showed modulation of the H-reflex with the amplitude being increased during the downstroke portion of the pedal cycle and the reflex suppressed or absent during the upstroke. This modulation was not present during passive pedalling, with the experimenter cranking the pedals by hand, or when the pedals were locked at each of the eight positions. In five of the seven patients with spasticity, there was reduced or absent modulation of the H-reflex during active pedalling and the reflex remained large during pedal upstroke. It is concluded that descending motor commands that produce patterned voluntary activity during pedalling normally cause cyclical gating of spinal reflexes by either presynaptic or postsynaptic inhibitory mechanisms. Loss of supraspinal control over these spinal inhibitory systems could result in failure to produce appropriate suppression of reflexes during patterned voluntary movements such as pedalling or walking, and may be an important factor contributing to the functional disability in spasticity.
PMCID: PMC1015331  PMID: 1479394
8.  Morphology of neoplastic lesions induced by 1,3-butadiene in B6C3F1 mice. 
1,3-Butadiene (CAS No. 106-99-0) was studied for potential carcinogenicity and chronic toxicity by inhalation in B6C3F1 mice. Groups of 50 mice of each sex were exposed to 0, 625, or 1250 ppm 1,3-butadiene for 6 hr/day, 5 days/week for 60 weeks (male) or 61 weeks (female). The study was scheduled for 104 weeks of exposure but was terminated early because of reduced survival related to induction of a variety of tumors in 1,3-butadiene-exposed mice. A second chronic inhalation study was conducted in which male and female mice were exposed to 0, 6.25, 20, 62.5, 200, or 625 ppm for up to 2 years. Additional groups of 50 male mice were exposed to 625 ppm for 13 or 26 weeks, 312 ppm for 52 weeks, or 200 ppm for 40 weeks, then held without exposure until scheduled sacrifice 104 weeks after initial exposure. 1,3-Butadiene-exposed mice from both studies had increased incidences of malignant lymphomas that were observed as early as week 20 in the first study and week 23 in the second study. The lymphomas were primarily lymphocytic and originated in the thymus, although generalized lymphoma was often present. Exposed mice in both studies developed cardiac hemangiosarcomas that were observed as early as week 32 in the first study and week 41 in the second study. Also present were foci of endothelial hyperplasia in the myocardium that were regarded as early evidence of developing hemangiosarcoma. Alveolar epithelial hyperplasia, alveolar/bronchiolar adenomas and alveolar/bronchiolar carcinomas represented the spectrum of proliferative lung lesions induced by exposure to 1,3-butadiene in both studies. Exposure-related proliferative forestomach lesions observed in both studies included epithelial hyperplasia, squamous cell papillomas, and squamous cell carcinomas. 1,3-Butadiene-exposed female mice in both studies developed mammary gland neoplasms at increased incidences. Most of the mammary tumors were pleomorphic adenocarcinomas, but several adenoacanthomas were also seen. Granulosa cell tumors of the ovary were exposure-related neoplasms in both studies. Occasionally the granulosa cell tumors were malignant as evidenced by vascular invasion or pulmonary metastasis. Although there was an increased incidence of hepatocellular neoplasms in exposed females in the first study, by week 65 of the second study there was not evidence of a clear response of liver neoplasms. The preliminary results of the second study indicate there was induction of tumors similar to those seen in the first study but occurring in response to lower concentrations of 1,3-butadiene.
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PMCID: PMC1567728  PMID: 2401271
9.  Two-hour methyl isocyanate inhalation exposure and 91-day recovery: a preliminary description of pathologic changes in F344 rats. 
The accidental release of methyl isocyanate (MIC) in Bhopal, India, was reportedly responsible for the deaths of more than 2,000 people. To study the pathology of acute inhalation exposure to MIC, the tissues of male and female Fischer 344 rats were evaluated immediately after a single 2-hr exposure to 0, 3, 10, or 30 ppm MIC, and through day 91. Early gross pathologic changes in the 30 ppm-exposed rats included a reddish white encrustation around the mouth and nose, a small thymus, and distension of the gastrointestinal tract with gas. Lungs (middle and median lobes) showed consolidation and hemorrhage and failed to deflate when the chest cavity was opened. Microscopic changes in the upper respiratory tract 3 hr after exposure included marked erosion and separation of olfactory and respiratory epithelia from the basement membrane with accumulation of serofibrinous fluid. On day 1, acute inflammation and fibrinopurulent exudate partially blocked the nasal passages. Epithelial cells had sloughed from the nasopharynx, trachea, bronchi, and major bronchioles, leaving the basement membrane covered with fibrin and exudate. Granulomatous inflammation and intraluminal fibrosis of the airways were observed by day 3, with increased intraluminal fibrosis by day 7. Lower airways became blocked by exfoliated cells, mucous plugs, and/or intraluminal fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
PMCID: PMC1474667  PMID: 3622446
10.  Ultrastructural changes in the nasal mucosa of Fischer 344 rats and B6C3F1 mice following an acute exposure to methyl isocyanate. 
Male rats and male mice received a single 2-hr exposure to 0 (control), 10, or 30 ppm of methyl isocyanate and were sacrificed after 1, 3, 14, or 90 days to assess the ultrastructural changes in the nasal mucosa by transmission electron microscopy. One day after exposure to methyl isocyanate, there were widespread areas of necrosis and degeneration of the respiratory and olfactory epithelium of rats and mice in the 10 ppm and 30 ppm groups. Qualitatively the ultrastructural findings were similar for both exposure groups and species. Degeneration followed by rapid regeneration was observed for both respiratory and olfactory epithelia but was most striking for olfactory epithelium in the dorsal meatus. Three days after the exposure, the olfactory epithelium was two to three cell layers thick due to a loss of supporting cells, olfactory neurons, and basal cells. By 14 days after exposure, the olfactory epithelium was composed of a heterogeneous cell population three to five cell layers thick. At 90 days following exposure, the epithelium was of normal thickness (eight to ten cell layers), with normal architectural arrangement, and composed of well-differentiated cells that appeared similar to those of controls. There were several findings that suggested the epithelial cells of Bowman's glands were the progenitor for the regenerating supporting cells of the olfactory epithelium. This study demonstrated that the respiratory and olfactory epithelium is capable of complete structural regeneration after an acute destruction by methyl isocyanate.
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PMCID: PMC1474640  PMID: 3622447
11.  Two-hour methyl isocyanate inhalation and 90-day recovery study in B6C3F1 mice. 
B6C3F1 mice were exposed by inhalation to 0, 3, 10, and 30 ppm methyl isocyanate for 2 hr followed by a 90-day recovery period. Sixteen of eighty (20%) male mice in the 30 ppm group died following exposure. There were no other unscheduled deaths in the mice. Five mice/sex/group were examined at 2 hr or at 1, 3, 7, 14, 28, 49, or 91 days following exposure. Chemical-related changes were restricted to the respiratory system. At 30 ppm there were extensive necrosis and erosion of the respiratory and olfactory epithelium in the nasal cavity. Severe necrosis and epithelial erosion were also found in the trachea and main bronchi. Regeneration of the mucosal epithelium occurred rapidly in the nasal cavity and airways. In the turbinates, mild incomplete olfactory epithelial regeneration persisted to day 91 in the male mice. Intraluminal fibrotic projections covered by respiratory epithelium and bronchial fibrosis were found in the major airways of the 30 ppm male and female mice by day 7. The intraluminal fibrosis persisted to day 91. In males with severe bronchial fibrosis, chronic alveolitis and atelectasis were found. In mice exposed to 3 or 10 ppm, persistent pulmonary changes were not found. These studies indicate that methyl isocyanate inhalation at or near lethal concentrations can cause persistent fibrosis of the major bronchi in mice.
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PMCID: PMC1474648  PMID: 3622445
12.  Myelotoxicity induced in female B6C3F1 mice by inhalation of methyl isocyanate. 
The effects of a 4-day inhalation exposure (6 hr/day) to 0, 1, and 3 ppm methyl isocyanate (MIC) on bone marrow parameters in female mice were examined at 5, 8, and 21 days following exposure. The MIC exposure was associated with myelotoxicity as evidenced by hypocellularity, suppression of pluripotent stem cells (CFU-S), granulocyte-macrophage progenitors (CFU-GM) and erythroid precursors (CFU-E) in both dose groups. Hematopoietic parameters returned to normal by 21 days in the 1 ppm dose group, but not in the 3 ppm dose group. This indicates that the alterations in the bone marrow parameters persist for a relatively long period at dose levels where there are little or no changes in body weight, clinical pathology, or immunological parameters, suggesting that the bone marrow may be a sensitive endpoint for MIC exposure in mice. MIC is a highly reactive chemical that appears to exert its effect directly on the lining epithelium of the nasal cavity and major airways; there was no histological evidence of a systemic effect. The pathogenesis of the bone marrow depression is unknown; however, there were chronic bronchitis and bronchial fibrosis in the 3 ppm dose group. One possible explanation is that the cell injury induced in the lung is associated with the release of inhibitory factors for hematopoiesis, as the rodent lung is a potent source of both stimulatory and inhibitory growth factors for bone marrow progenitor cells. A second possibility is that the thymic atrophy found in MIC-exposed mice might be related to myelotoxicity. The pathogenesis of myelotoxicity in MIC exposure and its relationship with pulmonary injury require further study.
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PMCID: PMC1474659  PMID: 3622428
13.  Proliferative lesions of the exocrine pancreas in male F344/N rats. 
While the rat pancreas is susceptible to experimental cancer induction, the spontaneous incidence of pancreatic cancer in this species is reported to be very low. However, we observed unusually high incidences of focal acinar hyperplasia and acinar adenoma in vehicle control male F344/N rats of some NCI/NTP 2-year toxicological studies. The vehicle in these studies was corn oil given by gavage. Focal acinar hyperplasia, acinar adenoma, and acinar carcinoma (found rarely) represent a continuous spectrum of proliferative lesions of the exocrine pancreas. While the carcinomas have clear morphological indications of malignancy, the biological behavior of focal acinar hyperplasia and acinar adenoma is not known. Although induction of acinar carcinomas is considered clear evidence of carcinogenicity of a test chemical, significantly increased incidences in treated rats of acinar adenomas but not carcinomas provides some evidence of carcinogenicity. The association of acinar hyperplasia and adenoma with vegetable oil gavage complicates the interpretation when marginally elevated incidences of these lesions are observed in rats administered the test chemical in vegetable oil vehicle. Studies of the biological behavior of exocrine pancreatic lesions in male rats would be helpful in assessing the significance of their presence when found after test compound administration.
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PMCID: PMC1568212  PMID: 6434300
14.  Cell-mediated immunity and its application in toxicology. 
A variety of in vivo and more recently in vitro assays have been described to assess cell mediated immunity (CMI). Two methods routinely employed in our laboratory to assess CMI following exposure to chemicals in rodents include delayed hypersensitivity and in vitro lymphoproliferation. Preliminary studies indicate that depressed delayed hypersensitivity responses, as performed by a radiometric assay, correlates with altered susceptibility to infectious agents and tumor cell challenge following exposure to immunotoxic chemicals. Furthermore, suppression of T-cell lymphoproliferative responses to at least 50% below control values correlated with depressed delayed hypersensitivity responses and altered host susceptibility. On the other hand, when suppression of T-cell lymphoproliferative responses are within 50% of control values, delayed hypersensitivity and host susceptibility parameters are not affected. Assuming adequate technical expertise and accurate data interpretation, CMI assays of these types can provide a valuable data base for toxicology studies and immunotoxicity assessment.
PMCID: PMC1568880  PMID: 7037387
15.  Methods and approaches for assessing immunotoxicity: an overview. 
The goals of the National Toxicology Program as they relate to immunological evaluation in toxicity assessment are discussed. The advantages of immune function assays for defining cellular injury as subtoxic levels following exposure to general or immunocyte specific chemical toxicants are proposed. A comprehensive screening panel of immune function and host resistance assays is presented in the context of an NIEHS approach for immunotoxicity assessment and methods selection. A second panel for defining the mechanism underlying immunological injury was also described. Studies utilizing these methods and approaches are described in companion papers by our group.
PMCID: PMC1568892  PMID: 7060546
16.  Assessment of myelotoxicity caused by environmental chemicals. 
Potential antineoplastic agents must be screened for the delayed toxicity that occurs in many cases of drug-induced bone marrow aplasia. In vitro clonal assays for hematopoietic progenitor cells have been developed to assess the degree of myelotoxicity. This adverse side effect is often the limiting factor in the development of new cancer chemotherapeutics. In addition, many environmental chemicals are cytotoxic to rapidly proliferating cells, but a systematic assessment of their myelotoxicity has not been performed. We have used clonal marrow assays to investigate a panel of chemicals including 2,3,7,8-tetrachlorodibenzo-p-dioxin, polybrominated biphenyls, diethylstilbestrol, benzo(a)pyrene and indomethacin. All were immunotoxic, some to pleuripotent hemopoetic stem cells and other to granulocyte-macrophage progenitors, and at concentrations below those causing other toxic manifestations. This shows that these bone marrow clonal assays, and hopefully future one for erythroid, B- and T-lymphocytes, and megakaryocytes, will provide the specificity and sensitivity necessary to delineate the myelotoxicity of a broad spectrum of environmental chemicals.
PMCID: PMC1568900  PMID: 6277616

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