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Planning and Designing SharePoint Server 2007 Design Life Cycle Major Milestone 1 Design Phase Major Milestone 2 Build Readiness Major Milestone 3 Operational Readiness Major Milestone 4 Operation and Supporting Summary Planning and Designing Designing Business Requirements Business Requirements Planning and Designing Project Plans for a SharePoint Server 2007 Deployment Understanding Microsoft s SharePoint Server 2007 Development Plan The Envisioning State The Planning Stage Deployment, Implementation, and ConfigurationManagement Post-Implementation Operations, Optimization, and Business Review Building Document Management Building Enterprise Content Management Building Business Processes and Workflows Building Branding and Customization Building Web Parts, Features, and Solutions Management Building Creating and Managing Publishing Sites Building Understanding and Implementing Microsoft Search Server 2008
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CHAPTER XXXVI UP CHAPTER XXXVIII CHAPTER XXXVII The Reaper Whose Name Is Death 「The Reaper Whose Name Is Death」松本訳注第37章(1) p. 531参照 第37章 死という命の刈りとり（松本訳） "Matthew--Matthew--what is the matter? Matthew, are you sick?" It was Marilla who spoke, alarm in every jerky word. Anne came through the hall, her hands full of white narcissus,--it was long before Anne could love the sight or odor of white narcissus again,--in time to hear her and to see Matthew standing in the porch doorway, a folded paper in his hand, and his face strangely drawn and gray. Anne dropped her flowers and sprang across the kitchen to him at the same moment as Marilla. 「sprang」 They were both too late; before they could reach him Matthew had fallen across the threshold. "He s fainted," gasped Marilla. "Anne, run for Martin-- quick, quick! He s at the barn." Martin, the hired man, who had just driven home from the post office, started at once for the doctor, calling at Orchard Slope on his way to send Mr. and Mrs. Barry over. Mrs. Lynde, who was there on an errand, came too. They found Anne and Marilla distractedly trying to restore Matthew to consciousness. Mrs. Lynde pushed them gently aside, tried his pulse, and then laid her ear over his heart. She looked at their anxious faces sorrowfully and the tears came into her eyes. "Oh, Marilla," she said gravely. "I don t think--we can do anything for him." "Mrs. Lynde, you don t think--you can t think Matthew is-- is--" Anne could not say the dreadful word; she turned sick and pallid. "Child, 「Child」この話し掛け方は……、特別な意味はないんでしょうね、たぶん yes, I m afraid of it. Look at his face. When you ve seen that look as often as I have you ll know what it means." Anne looked at the still face and there beheld the seal of the Great Presence. 「the seal of the Great Presence」重々しく、かつ、間接的な表現は……、どうなんでしょう。アンの気持ちを表すのに適切？ When the doctor came he said that death had been instantaneous and probably painless, caused in all likelihood by some sudden shock. The secret of the shock was discovered to be in the paper Matthew had held and which Martin had brought from the office that morning. It contained an account of the failure of the Abbey Bank. 「an account of the failure of the Abbey Bank」この account は、記事、の意味ととるべきでしょう。しかし、もちろん、銀行の口座も account なので、モードは掛け言葉のように、記事、口座のどちらの意味もある単語を使ったのに違いありません 「the failure of the Abbey Bank」松本訳注第37章(2) p. 531参照 The news spread quickly through Avonlea, and all day friends and neighbors thronged Green Gables and came and went on errands of kindness for the dead and living. For the first time shy, quiet Matthew Cuthbert was a person of central importance; the white majesty of death had fallen on him and set him apart as one crowned. When the calm night came softly down over Green Gables the old house was hushed and tranquil. In the parlor lay Matthew Cuthbert in his coffin, his long gray hair framing his placid face on which there was a little kindly smile as if he but slept, dreaming pleasant dreams. There were flowers about him--sweet old-fashioned flowers which his mother had planted in the homestead garden in her bridal days 「in her bridal days」グリーンゲイブルズを建てる前から、同じ場所に植えてあったのでしょう。グリーンゲイブルズが建ったときには、マシューもマリラも子供ではなかったのですから。It seems uncanny to think of a child at Green Gables somehow; there s never been one there, for Matthew and Marilla were grown up when the new house was built （CHAPTER I with impressionMrs. Rachel Lynde is Surprised ） and for which Matthew had always had a secret, wordless love. Anne had gathered them and brought them to him, her anguished, tearless eyes burning in her white face. It was the last thing she could do for him. The Barrys and Mrs. Lynde stayed with them that night. Diana, going to the east gable, where Anne was standing at her window, said gently "Anne dear, would you like to have me sleep with you tonight?" "Thank you, Diana." Anne looked earnestly into her friend s face. "I think you won t misunderstand me when I say I want to be alone. I m not afraid. I haven t been alone one minute since it happened-- and I want to be. I want to be quite silent and quiet and try to realize it. I can t realize it. Half the time it seems to me that Matthew can t be dead; and the other half it seems as if he must have been dead for a long time and I ve had this horrible dull ache ever since." Diana did not quite understand. Marilla s impassioned grief, breaking all the bounds of natural reserve and lifelong habit in its stormy rush, she could comprehend better than Anne s tearless agony. 倒置。ふつうの順にすれば、She could comprehend Marilla s impassioned grief, breaking all the bounds of natural reserve and lifelong habit in its stormy rush, better than Anne s tearless agony. 「Marilla s」は所有格。昼間、弔問客の来ているとき、マリラは大泣きをしていたが、アンは涙を流さなかった。そして、その上、ひとりにしてほしい、と言ったことも含め、ダイアナにはアンがよくは理解できなかった。この文は、そういうことでしょう But she went away kindly, leaving Anne alone to keep her first vigil with sorrow. Anne hoped that the tears would come in solitude. It seemed to her a terrible thing that she could not shed a tear for Matthew, whom she had loved so much and who had been so kind to her, Matthew who had walked with her last evening at sunset and was now lying in the dim room below with that awful peace on his brow. But no tears came at first, even when she knelt by her window in the darkness and prayed, looking up to the stars beyond the hills--no tears, only the same horrible dull ache of misery that kept on aching until she fell asleep, worn out with the day s pain and excitement. In the night she awakened, with the stillness and the darkness about her, and the recollection of the day came over her like a wave of sorrow. She could see Matthew s face smiling at her as he had smiled when they parted at the gate that last evening--she could hear his voice saying, "My girl--my girl that I m proud of." Then the tears came and Anne wept her heart out. Marilla heard her and crept in to comfort her. "There--there--don t cry so, dearie. It can t bring him back. It--it--isn t right to cry so. I knew that today, but I couldn t help it then. He d always been such a good, kind brother to me--but God knows best." "Oh, just let me cry, Marilla," sobbed Anne. "The tears don t hurt me like that ache did. Stay here for a little while with me and keep your arm round me--so. I couldn t have Diana stay, she s good and kind and sweet--but it s not her sorrow--she s outside of it and she couldn t come close enough to my heart to help me. It s our sorrow-- yours and mine. 「yours and mine」アンの home はふたりだけになってしまった Oh, Marilla, what will we do without him?" "We ve got each other, Anne. 「We ve got each other」いまひとつ、わかりづらい。have got は、have とほぼ同じだから……。日本語だと、「いる」と思うけれども、英語だと「持つ」という表現の違いか。なるほど。兄（弟）がいます、が、I have a brother になるように。「わたしたちにはお互いがいる」 I don t know what I d do if you weren t here--if you d never come. 仮定法 Oh, Anne, I know I ve been kind of strict and harsh with you maybe-- but you mustn t think I didn t love you as well as Matthew did, for all that. I want to tell you now when I can. It s never been easy for me to say things out of my heart, but at times like this it s easier. I love you as dear as if you were my own flesh and blood and you ve been my joy and comfort ever since you came to Green Gables." Two days afterwards they carried Matthew Cuthbert over his homestead threshold and away from the fields he had tilled and the orchards he had loved and the trees he had planted; and then Avonlea settled back to its usual placidity and even at Green Gables affairs slipped into their old groove and work was done and duties fulfilled with regularity as before, although always with the aching sense of "loss in all familiar things." 「"loss in all familiar things"」松本訳注第37章(3) p. 532参照 Anne, new to grief, thought it almost sad that it could be so--that they COULD go on in the old way without Matthew. She felt something like shame and remorse when she discovered 「that」アンが discover したことは文末までに４つ示されていて、それぞれ that節になっている。こういうのは話し言葉ではあまりないのではないいでしょうか that the sunrises behind the firs and the pale pink buds opening in the garden gave her the old inrush of gladness when she saw them--that Diana s visits were pleasant to her and that Diana s merry words and ways moved her to laughter and smiles--that, in brief, the beautiful world of blossom and love and friendship had lost none of its power to please her fancy and thrill her heart, that life still called to her with many insistent voices. "It seems like disloyalty to Matthew, somehow, to find pleasure in these things now that he has gone," she said wistfully to Mrs. Allan one evening when they were together in the manse garden. "I miss him so much--all the time-- and yet, Mrs. Allan, the world and life seem very beautiful and interesting to me for all. Today Diana said something funny and I found myself laughing. I thought when it happened I could never laugh again. And it somehow seems as if I oughtn t to." "When Matthew was here he liked to hear you laugh and he liked to know that you found pleasure in the pleasant things around you," said Mrs. Allan gently. "He is just away now; 「He is just away now」松本訳注第37章(4) p. 532参照 and he likes to know it just the same. I am sure we should not shut our hearts against the healing influences that nature offers us. But I can understand your feeling. I think we all experience the same thing. We resent the thought that anything can please us when someone we love is no longer here to share the pleasure with us, and we almost feel as if we were unfaithful to our sorrow when we find our interest in life returning to us." "I was down to the graveyard to plant a rosebush on Matthew s grave this afternoon," said Anne dreamily. "I took a slip of the little white Scotch rosebush his mother brought out from Scotland long ago; 「I took a slip of the little white Scotch rosebush」白い小さなスコッチローズから挿し木にする枝を取った。少し上のほうに even at Green Gables affairs slipped into their old groove グリーンゲイブルズでも、いろいろなことは元の習慣に戻った、とあるところにも、slip が使われているのですが、関連させていると思うのは考えすぎでしょうか 「from Scotland」マシューのお母さんはスコットランドからの移民。結婚して、夫婦でプリンスエドワード島に来たんでしょうね、きっと。単身もありえなくはないでしょうけども。または、両親とともにカナダにやってきて、そのときにバラも持ってきていて、結婚後、植えたか Matthew always liked those roses the best--they were so small and sweet on their thorny stems. It made me feel glad that I could plant it by his grave--as if I were doing something that must please him in taking it there to be near him. I hope he has roses like them in heaven. Perhaps the souls of all those little white roses that he has loved so many summers were all there to meet him. I must go home now. Marilla is all alone and she gets lonely at twilight." "She will be lonelier still, I fear, when you go away again to college," said Mrs. Allan. このアラン夫人の言葉は、転換点のひとつに相当 Anne did not reply; she said good night and went slowly back to green Gables. 「slowly」すぐ前では、もうおいとましなくては I must go home now. とアラン夫人にアンは言っているにも拘らず、歩みは遅い。アラン夫人の言葉を受けて、歩みが遅くなったわけですが、このアラン夫人の言葉が転換点であったのかは、すぐ後の文（グリーンゲイブルズの描写やマリラとの会話）からはわからないような構成になっている。しかも、その転換がどうだったのか、つまり、アンがどう考え、どう行動し、そして、周りの人がどんな風に協力、対応したかは、次章で明らかになる。転換点をあまり転換点らしく表現していないのは、たぶん、小説の技法としてはいいことなんでしょう。「Anne did not reply」があるので、転換点を強調してはいますが Marilla was sitting on the front door-steps and Anne sat down beside her. The door was open behind them, held back by a big pink conch shell with hints of sea sunsets in its smooth inner convolutions. Anne gathered some sprays of pale-yellow honeysuckle and put them in her hair. She liked the delicious hint of fragrance, as some aerial benediction, above her every time she moved. "Doctor Spencer was here while you were away," Marilla said. "He says that the specialist will be in town tomorrow and he insists that I must go in and have my eyes examined. I suppose I d better go and have it over. I ll be more than thankful if the man can give me the right kind of glasses to suit my eyes. 「the man」やはり、眼科医は男性であったか You won t mind staying here alone while I m away, will you? Martin will have to drive me in and there s ironing and baking to do." "I shall be all right. Diana will come over for company for me. I shall attend to the ironing and baking beautifully-- you needn t fear that I ll starch the handkerchiefs or flavor the cake with liniment." もちろん、これは、CHAPTER XX with impression? A Good Imagination Gone Wrong と CHAPTER XXI with impression? A New Departure in Flavorings のお話。ちょうど４年前、アン12歳 Marilla laughed. "What a girl you were for making mistakes in them days, Anne. 「in them days」これは、ふつうなら in those days ではないかしら You were always getting into scrapes. I did use to think you were possessed. Do you mind the time you dyed your hair?" もちろん、これは、CHAPTER XXVII with impression Vanity and Vexation of Spiritのお話。３年と少し前、アン13歳 "Yes, indeed. I shall never forget it," smiled Anne, touching the heavy braid of hair that was wound about her shapely head. 「the heavy braid of hair」３年経てば、髪もそれなりに十分伸びたでしょう。でも、小さいころのように編み下げにはしていないようですが。まだあまり長くはないでしょうし "I laugh a little now sometimes when I think what a worry my hair used to be to me--but I don t laugh MUCH, because it was a very real trouble then. I did suffer terribly over my hair and my freckles. My freckles are really gone; and people are nice enough to tell me my hair is auburn now--all but Josie Pye. She informed me yesterday that she really thought it was redder than ever, or at least my black dress made it look redder, 「black dress」松本訳注第37章(5) p. 532参照 and she asked me if people who had red hair ever got used to having it. Marilla, I ve almost decided to give up trying to like Josie Pye. I ve made what I would once have called a heroic effort to like her, but Josie Pye won t BE liked." "Josie is a Pye," said Marilla sharply, "so she can t help being disagreeable. I suppose people of that kind serve some useful purpose in society, but I must say I don t know what it is any more than I know the use of thistles. 「thistle」アザミ：スコットランドの国花。Pye 家も（Cuthbert 家や モンゴメリ家のように）スコットランドからの移民なのかしら Is Josie going to teach?" "No, she is going back to Queen s next year. First class licence が得られるはず So are Moody Spurgeon and Charlie Sloane. Jane and Ruby are going to teach and they have both got schools--Jane at Newbridge and Ruby at some place up west." "Gilbert Blythe is going to teach too, isn t he?" "Yes"--briefly. "What a nice-looking fellow he is," 「a nice-looking fellow」boyではなく、fellowだ！ Puffin Books 版では、a nice-looking young fellow said Marilla absently. 「absently」これは Gilbert の中に John を見ているからでしょう "I saw him in church last Sunday and he seemed so tall and manly. 「so tall and manly」お～、ほめてるほめてる He looks a lot like his father did at the same age. John Blythe was a nice boy. 「a nice boy」ここでは、boy となっている。little girl 同様、boy も英語では難しい We used to be real good friends, he and I. People called him my beau." Anne looked up with swift interest. "Oh, Marilla--and what happened?--why didn t you--" "We had a quarrel. I wouldn t forgive him when he asked me to. I meant to, after awhile--but I was sulky and angry and I wanted to punish him first. He never came back--the Blythes were all mighty independent. 「the Blythes」さっきは、Pye 家の話でしたが、家柄を強調するあたり、少々古い小説と感じてしまう。もちろん古いのですが But I always felt--rather sorry. I ve always kind of wished I d forgiven him when I had the chance." "So you ve had a bit of romance in your life, too," said Anne softly. "Yes, I suppose you might call it that. You wouldn t think so to look at me, would you? But you never can tell about people from their outsides. Everybody has forgot about me and John. I d forgotten myself. But it all came back to me when I saw Gilbert last Sunday." CHAPTER XXXVI UP CHAPTER XXXVIII 12 August 2007 今日 - | 昨日 - | Total - since 12 August 2007 last update 2007-08-12 21 35 11 (Sun)
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position-flag? その位置の位置フラグの値（「true」または「false」）を確認します。 (position-flag? flag-name ) その位置の位置フラグ flag-name の値が「true」かどうかを確認します。 (position-flag? flag-name position ) ある位置 position の位置フラグ flag-name の値が「true」かどうかを確認します。 (position-flag? flag-name direction ) ある方向 direction の位置フラグ flag-name の値が「true」かどうかを確認します。 (not-position-flag? flag-name ) その位置の位置フラグ flag-name の値が「false」かどうかを確認します。 (not-position-flag? flag-name position ) ある位置 position の位置フラグ flag-name の値が「false」かどうかを確認します。 (not-position-flag? flag-name direction ) ある方向 direction の位置フラグ flag-name の値が「false」かどうかを確認します。 指定された位置における指定された位置フラグの値を返します。 位置フラグは、「set-position-flag」を使用して設定できます。 (verify (position-flag? my-flag)) 位置フラグ my-flag が「true」の場合に実行します。 Ultimaの使用例 コーディネーターは、コーディネーターの移動先と同じランクまたはファイルにあり、かつ味方のキングと同じランクまたはファイルにある全ての駒をキャプチャする駒です。 つまり、コーディネーターは盤上でキングとともに矩形を形成し、矩形の他の2つの頂点にある駒がキャプチャされます。 次のマクロでは、方向$1の直線上の全てのマスに位置フラグ king-line を「true」設定します。 (define make-king-line (while (on-board? $1) $1 (set-position-flag king-line true) ) ) 次のマクロは、直線上に延長して、位置フラグ king-line が「true」に設定されているマスにいる全ての敵の駒をキャプチャします。 (define coordinate (while (on-board? $1) $1 (if (and enemy? (position-flag? king-line)) capture) ) (go to) ) コーディネーターの移動の開始時に、キングと同じランクまたはファイルの全てのマスに、位置フラグ king-line が設定されます。 キング位置から始めて、上下左右に (make-king-line n) back (make-king-line e) back (make-king-line s) back (make-king-line w) コーディネーターの移動が「add」される前に、全ての直交方向でキャプチャが検索されます。 (if (not-position-flag? king-line) (coordinate n) (coordinate e) (coordinate s) (coordinate w) ) add 解説：flag関係 解説：set-position-flag 解説：flag 解説：set-flag 解説：attribute 解説：set-attribute
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TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS -index ▼2 HEALTH EFFECTS ▼▼2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 2.2.2 Oral Exposure -2 2.2.2 Oral Exposure(2.2.2.0 preface) 2.2.2.1 Death 2.2.2 Oral Exposure -22.2.2.2 Systemic Effects(preface) Respiratory Effects. Cardiovascular Effects. Gastrointestinal Effects. Hematological Effects. Musculoskeletal Effects. Hepatic Effects. Renal Effects. Dermal Effects. Other Systemic Effects. 2.2.2 Oral Exposure -32.2.2.3 Immunological and Lymphoreticular Effects 2.2.2.4 Neurological Effects 2.2.2.5 Reproductive Effects 2.2.2.6 Developmental Effects 2.2.2.7 Genotoxic Effects 2.2.2.8 Cancer 2.2.2.2 Systemic Effects (preface) Systemic effects of white phosphorus in humans and animals after oral exposure are discussed below. The highest NOAEL value and all reliable LOAEL values from each reliable study for systemic effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. No studies were located regarding ocular effects in humans or animals after oral exposure to white phosphorus. Respiratory Effects. Studies on respiratory effects following acute oral exposure of humans to white phosphorus were limited to case reports of intentional or accidental consumption of materials containing white phosphorus. Although intake of phosphorus was often reported, dose could be estimated for only one study (Hann and Veale 1910), because vomiting and/or gastric lavage nearly always occurred soon after poisoning, expelling much of the ingested phosphorus from the body. Tachypnea (increased respiratory rate; 48 breaths/minute) was observed in a woman consuming rat poison containing 4% white phosphorus (Hann and Veale 1910); the woman apparently did not vomit until the second day, and the vomitus was clear. The estimated dose was 2 mg/kg. Four days after ingesting the rat poison, the woman died, apparently from liver failure. Autopsy showed that the pleural cavity was filled with a dark fluid, but no histological abnormalities were observed in the lungs (Hann and Veale 1910). In the following studies, no doses could be estimated for respiratory effects because of vomiting and/or gastric lavage. In a case report involving ingestion of rat poison containing white phosphorus, the patient arrived at a hospital in a coma and displayed Cheyne-Stokes respirations and rales (Wechsler and Wechsler 1951). The Cheyne-Stokes respirations increased to an extreme degree, and the patient died. Autopsy revealed pulmonary congestion and edema throughout the stroma. Increased respiratory rate (56 breaths/minute) and rales also were observed in an infant ingesting rat poison containing white phosphorus (Rao and Brown 1974). The child died, and autopsy revealed evidence of pulmonary edema. Rales were observed in a child ingesting a fatal dose of white phosphorus in fireworks; autopsy indicated that the lungs were normal except for some fibrous adhesions (Dwyer and Helwig 1925). Hemorrhagic bronchopneumonia was observed following autopsy of a man ingesting a fatal dose of rat poison containing white phosphorus (Winek et al. 1973). Autopsy of a child who died following ingestion of a firecracker revealed fatty deposition in parenchyma, bronchial epithelium, and tracheal epithelium and cartilage (Humphreys and Halpert 1931). Death from cardiopulmonary failure was reported for a 63-year-old woman (Winek et al. 1973), a 2-year-old boy (Simon and Pickering 1976), and a 3-year-old girl (Simon and Pickering 1976) following ingestion of white phosphorus in rat poison; a respiratory rate of 44 breaths/minute was initially observed in the girl (Simon and Pickering 1976). Increased respiratory rate was observed prior to death in two case reports involving ingestion of rat poison (Talley et al. 1972; Winek et al. 1973). Shallow respirations and cyanosis were observed prior to death in an adult female following ingestion of rat/roach poison containing white phosphorus (Rubitsky and Myerson 1949). Rales were observed 1 day after intentional ingestion of rat poison by a 30-year-old man; 2 days later the patient went into shock but survived the poisoning and eventually recovered (Pietras et al. 1968). No treatment-related respiratory effects were reported in children treated with white phosphorus for intermediate durations. No treatment-related microscopic changes were observed in the lungs of rats exposed to 0.2 mg/kg/day white phosphorus in the diet for a chronic duration (Fleming et al. 1942) or 0.075 mg/kg/day phosphorus by gavage for an intermediate duration (LRDC 1985). Heavy breathing and apnea were reported following ingestion of a fatal quantity of white phosphorus by a cat (Frye and Cucuell969). Necropsy revealed hyperemia, hemorrhage and edema in the lungs. Cardiovascular Effects. Alterations in electrocardiograms, such as altered or inverted T waves and changes in the QRS complex, and other cardiac changes, such as tachycardia, arrhythmias, atrial fibrillation, and decreased ventricular contractility, have been observed in individuals accidentally or intentionally ingesting a single dose of white phosphorus (Dathe and Nathan 1946; Diaz-Rivera et al. 1950, 1961; Dwyer and Helwig 1925; Ehrentheil 1957; Matsumoto et al. 1972; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968; Rao and Brown 1974; Simon and Pickering 1976; Talley et al. 1972). Damage to the myocardium was verified by a number of cases in which histological examination of the heart was performed. Prominent cross striations in the myocardium (Dwyer and Helwig 1925), fatty infiltration of muscle (Diaz-Rivera et al. 1961; Humphreys and Halpert 1931; Wertham 1932), necrosis of myocardium (Wechsler and Wechsler 1951), markedly dilated cardiac chamber (Rao and Brown 1974), and interstitial edema of the myocardium and vacuolation of cells (Talley et al. 1972) have been observed. Because of vomiting and gastric lavage, doses cannot be calculated from the human studies. No cardiac effects were reported in longer term human studies. In addition to the effects on the heart, a number of vascular effects have been observed in humans acutely exposed to white phosphorus. A markedly decreased or undetectable blood pressure (Caley and Kellock 1955; Dathe and Nathan 1946; McCarron et al. 1981; Rubitsky and Myerson 1949; Simon and Pickering 1976; Wechsler and Wechsler 1951), vascular collapse (Diaz-Rivera et al. 1950, 1961), undetectable or decreased pulse (Dwyer and Helwig 1925; Rubitsky and Myerson 1949), and increased pulse (Dathe and Nathan 1946; Hann and Veale 1910; McCarron et al. 1981; Wechsler and Wechsler 1951) have been observed. In addition, individuals have died following cardiopulmonary arrest (Simon and Pickering 1976; Winek et al. 1973), which may be due to effects on the heart or vascular system. A dose of 2 mg/kg/day for vascular effects was identified from the Hann and Veale (1910) report of a woman ingesting a single dose of white phosphorus. Dose levels cannot be estimated for the other case reports. Hemorrhaging in internal organs, as well as the appearance of petechial hemorrhages on the skin, have been reported in a number of acute human exposure cases (Hann and Veale 1910; Humphreys and Halpert 1931; Winek et al. 1973). It is not known whether these effects are due to impairment of the integrity of the blood vessels or due to damage of the affected organ (e.g., liver, stomach) itself. In rats administered 0.075 mg/kg/day white phosphorus for an intermediate duration, no histological alterations were observed in the heart (Bio/dynamics 1991; IRDC 1985). In rats exposed for an intermediate duration to an unknown concentration of airborne white phosphorus from the furnace room of a phosphorus factory, an increase in permeability of capillary walls, lesions in the walls of blood vessels and evidence of impaired microcirculation were observed in the mouth (Ruzuddinov and Rys-Uly 1986). These effects probably resulted from the local action of white phosphorus on the oral cavity. Gastrointestinal Effects. Most of the human case reports listed vomiting as an early effect following ingestion of a single high dose of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Dwyer and Helwig 1925; Ehrentheil 1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Hann and Veale 1910; Humphreys and Halpert 193 1; Matsumoto et al. 1972; McCarron et al. 1981; McIntosh 1927; Newburger et al. 1948; Pietras et al. 1968; Rubitsky and Myerson 1949; Simon and Pickering 1976; Wechsler and Wechsler 1951; Winek et al. 1973). The doses that induced vomiting ranged from 2 to 23 mg/kg (Caley and Kellock 1955; Ehrentheil 1957; Fletcher and Galambos 1963; Harm and Veale 1910; Matsumoto et al. 1972; McCarron et al. 1981; Newburger et al. 1948; Rubitsky and Myerson 1949). Vomiting generally started within hours after ingesting the white phosphorus, and sometimes continued for many days. Other gastrointestinal effects included abdominal cramps or pain (often severe) (Dwyer and Helwig 1925; Ehrentheil1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Humphreys and Halpert 1931; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968), vomiting blood and/or pieces of the gastric mucosa (Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Rubitsky and Myerson 1949), necrosis and erosion of mucosa in the esophagus, stomach, duodenum, and jejunum (Wechsler and Wechsler 1951), and gastrointestinal hemorrhage (Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; Wertham 1932, Winek et al. 1973). These effects, with the exception of necrosis, were probably due to the irritating effects of white phosphorus on the mucosa of the gastrointestinal tract. Vomitus often contained white phosphorus, indicating that vomiting generally occurred before all white phosphorus and/or its oxidation products had been absorbed. No gastrointestinal effects were reported in children receiving treatment with 0.026-0.158 mg/kg/day white phosphorus for as much as 26 months (Phemister 1918; Compere 1930a). An infant became seriously ill during treatment with 0.083 mg/kg/day white phosphorus (6-month time-weighted average dose), but recovered entirely following discontinuation of the treatment (Sontag 1938). No vomiting or diarrhea was observed during the treatment period. Gastrointestinal effects were not reported in studies examining longer term occupational exposure to white phosphorus (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928). Erosion and hemorrhages in tissue in the esophagus and stomach were observed following ingestion of a fatal unknown quantity of white phosphorus by a cat (Frye and Cucuel 1969). Vomiting was observed in 6 of 21 dogs treated by gavage with an unknown quantity of white phosphorus from firecrackers (Dwyer and Helwig 1925). No gross or microscopic alterations were observed in the gastrointestinal tract of rats treated by gavage with 0.075 mg/kg/day for 204 days (IRDC 1985). Hematological Effects. Hematological effects have been reported in a number of case histories of individuals accidentally or intentionally ingesting a single dose of white phosphorus contained in rat (and cockroach) poisons or fireworks. Because most of the individuals vomited or received gastric lavage shortly after ingestion, the amount of white phosphorus available for absorption is not known. Increases in erythrocyte levels (Diaz-Rivera et al. 1950) and hemoglobin levels (Diaz-Rivera et al. 1950; McIntosh 1927); decreases in erythrocyte levels (Dwyer and Helwig 1925) and hemoglobin and/or hematocrit levels (Simon and Pickering 1973); and anemia (Caley and Kellock 1955) have been observed in some of these individuals. A number of individuals had no change in erythrocyte parameters (Ehrentheil 1957; Fletcher and Galambos 1963; Newburger et al. 1948; Simon and Pickering 1976). The decreases in erythrocyte parameters may be a reflection of the hemorrhages observed in specific tissues (e.g., gastrointestinal tract, liver, skin) (Dathe and Nathan 1946; Hann and Veale 1910; Humphreys and Halpert 1931; Wechsler and Wechsler 1951; Winek et al. 1973). In addition to these changes in erythrocyte parameters, changes in total or differential leukocyte levels were reported in a number of individuals acutely exposed to white phosphorus. Decreases in total leukocyte levels (Diaz-Rivera et al. 1950; Ehrentbeil 1957; Fletcher and Galambos 1963; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968) and decreases or increases in the percentage of polymorphonuclear leukocytes (neutrophils) have been reported (Ehrentheil 1957; McCarron et al. 1981; Pietras et al. 1968). No changes in leukocyte parameters were observed in a number of individuals (Fletcher and Galambos 1963; Newburger et al. 1948; Simon and Pickering 1976). Abnormally low protbrombin times or levels (hypo-prothrombinemia) and a moderate decrease in platelets were observed in a number of individuals ingesting single doses of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Ehrentheil 1957; Fletcher and Galambos 1963; McCarron et al 1981). Most of the patients developed hypoprothrombinemia within 4-8 days (McCarron et al. 1981). This is probably secondary to the liver damage rather than a direct effect on platelets. No changes in hematological parameters were observed in a child ingesting phosphorized cod liver oil (0.083 mg/kg/day phosphorus) for 184 days (Sontag 1938). Anemia and leukopenia were observed in individuals occupationally exposed to white phosphorus chronically (Ward 1928). It is likely that workers were exposed by the inhalation, oral, and dermal routes. Because there is very little consistency regarding the length of time that elapsed between ingestion and measurement of hematological parameters and the doses cannot be calculated, it is difficult to compare the results of different studies. There is insufficient information to determine whether white phosphorus has a direct effect on erythrocytes and/or leukocytes. The effects observed may be secondary effects. The decrease in erythrocyte, hemoglobin, hematocrit and leukocyte levels may be secondary to hemorrhaging or hematoemesis (Diaz-Rivera et al. 1950; Rubitsky and Myerson 1949) and the increase in erythrocytes and hemoglobin may be a compensatory mechanism due to tissue anoxia. However, since red blood cell synthesis takes 3-5 days, the observed effects may be direct if they are occurring within l-2 days. A slight decrease in hemoglobin levels and increase in eosinophil levels were observed in a 30-year-old man who performed magic shows that involved placing white phosphorus pellets in the mucobuccal folds of his mouth for 15 years. He had no other personal habits that might adversely affect his health except for occasional bidi smoking for about 8 years (Jakhi et al. 1983). Information on hematological effects in animals is limited to one study in which a marked increase in total leukocyte levels and the percentage of monocytes were observed in a guinea pig acutely exposed to 0.9-2.4 mg/kg/day of white phosphorus in a complex dosing regimen (Lawrence and Huffman 1929). The study authors did not specify at which doses the effects occurred. Musculoskeletal Effects. Following ingestion of a fatal dose of rat poison containing white phosphorus by a woman, autopsy revealed fatty infiltration of essentially all tissues, including the musculature (Wertham 1932). Similar effects were reported following the death of a male child who accidentally ingested a firecracker containing white phosphorus; autopsy revealed fatty deposition in many tissues, included the diaphragmic muscle (Humphreys and Halpert 1931). Humans occupationally exposed to white phosphorus probably ingested some airborne white phosphorus. In a study of 71 humans occupationally exposed to white phosphorus, oral exposure to white phosphorus via hand-to-mouth activity was likely because the workers constantly handled a paste containing 4-6% white phosphorus and washroom facilities were inadequate (Ward 1928). In workers exposed to white phosphorus for intermediate durations, 2 of 44 developed phossy jaw, described as slight necrosis in the lower jaw. In workers exposed to white phosphorus for chronic durations, 12 of 27 developed phossy jaw, with necrosis ranging from slight to severe; 2 of the 12 workers developing phossy jaw died from complications related to the necrosis. The progression of the disease was similar in the cases described, usually beginning with the extraction of one or more teeth, poor healing of the socket, followed by necrosis of tissue in the jaw with severe pain and infection. Treatment consisted of repeated removal of destroyed bone tissue and teeth, draining of abscesses, and reconstructive surgery. In severe cases, extensive removal of necrotic bone tissue led to permanent disfigurement. However, exposure levels of white phosphorus were not reported (Ward 1928). Case reports of development of phossy jaw following intermediate or chronic occupational exposure to unreported levels of white phosphorus and phosphorus compounds describe a similar progression of symptoms, with similar results; even in cases of early diagnosis and prompt, intensive treatment of phossy jaw, recovery often took several years (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944). It is likely that the effect of white phosphorus in the oral cavity is local, resulting from contact of “inhaled”white phosphorus particles with tissue in the mouth. White phosphorus may affect the oral mucosa. Dull, red spots in the oral mucosa, an early sign of phossy jaw, have been reported to precede its development in occupationally exposed workers (Kennon and Hallam 1944). The oral mucosa of workers exposed to white phosphorus has been described as having a dull, red, unhealthy appearance (Hughes et al. 1962). Exposed bones may be especially susceptible to the irritating affects of white phosphorus. It is not known whether white phosphorus ingested and absorbed into the systemic circulation contributed to the development of phossy jaw. Not all workers exposed to white phosphorus for longer-term durations developed phossy jaw. In a study of 71 workers exposed to airborne white phosphorus for intermediate or chronic durations, 4.5% and 44%, respectively, developed phossy jaw (Ward 1928). Forty-eight male workers with exposure to white phosphorus ranging from 1 to 17 years were found to be normal and healthy with regards to many parameters, including serum levels of calcium and phosphorus, and bone density; none of the men developed phossy jaw (Hughes et al. 1962). Tooth loss often precedes and accompanies the progression of development of phossy jaw (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928). Tooth loss during the later stages of phossy jaw clearly results from destruction of the-bone structure supporting the teeth (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Legge 1920; Ward 1928). It is not known if tooth loss prior to diagnosis of phossy jaw or early in the development of the condition is related to the white phosphorus exposure. Poor dental hygiene alone can result in tooth loss, and in several case reports some of the workers were described as having poor dental hygiene (Kennon and Hallam 1944). Tooth loss followed by poor healing of the socket often precedes development of the necrosis (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928), suggesting that poor dental hygiene and exposure to white phosphorus may both be contributing factors to the development of phossy jaw. In a case report, five men developed “precursor signs” (delayed healing of extracted tooth sites and residual sepsis) of phossy jaw developed following tooth extraction and occupational exposure to white phosphorus (Hughes et al. 1962). However, the condition did not develop into “classical” phossy jaw. A man was repeatedly exposed to white phosphorus pellets, placed in the right mucobuccal cavity for magic shows, for . 15 years (Jakhi et al. 1983). After . 14.5 years of this type of exposure to white phosphorus, right maxillary molars became loose, and were subsequently lost. This was followed by a lack of healing and development of fistulae in the sockets of the right maxillary molars. White phosphorus necrosis of the jaw developed, with massive necrosis of the maxilla and floor of the antrum on the right side of the mouth; perforations were present through which the maxillary sinus and nasal cavity were visible. No effects were observed on the left side of the maxilla or on the mandible. Radiographs revealed no evidence of pathology in the chest and long bones. The damage to the jaw was probably caused by direct local contact of phosphorus with the soft tissue and bone in the oral cavity. No microscopic or histological abnormalities were observed in the bone of rats treated by gavage with 0.075 mg/kg/day for 204 days (IRDC 1985). Rats exposed for a chronic duration to 0.2 mg/kg/day white phosphorus in the diet had epiphyseal line thickening and greater extension of trabeculae into the diaphysis of unspecified bones, compared to a control group (Fleming et al. 1942). This study is limited by the failure to specify incidences of effects at interval during dosing and by the failure to state the dosing duration explicitly. Bone effects were observed in children (Compere 1930a; Phemister 1918; Sontag 1938) and young animals (Adams 1938a, 1938b; Adams and Sarnat 1940; Whalen et al. 1973) following acute and intermediate oral exposure to white phosphorus. Because white phosphorus-related effects were observed in growing bones, these effects were considered developmental effects, and are discussed in. Section 2.2.2.6. Hepatic Effects. Hepatic effects have been observed in most individuals accidentally or intentionally ingesting a single dose of white phosphorus. These effects include jaundice (Caley and Kellock 1955; Diaz-Rivera et al. 1950, 1961; Ehrentheil 1957; Greenberger et al. 1964; Humphreys and Halpert 1931; McCarron et al. 1981), hepatomegaly (Diaz-Rivera et al. 1950; Fletcher and Galambos 1963; Humphreys and Halpert 1931; Rao and Brown 1974; Simon and Pickering 1976; Wechsler and Wechsler 1951), increased levels of serum bilirubin (Caley and Kellock 1955; Fletcher and Galambos 1963; McCarron et al. 1981; Pietras et al. 1968), impaired liver function test results (Fletcher and Galambos 1963; Newburger et al. 1948; Pietras et al. 1968; Rubitsky and Myerson 1949), and increases in AST, ALT, and/or lactate dehydrogenase (Ehrentheil 1957; Matsumoto et al. 1972; McCarron et al. 1981; Pietras et al. 1968). In addition to these effects, autopsies or liver biopsies have revealed a number of histological alterations in these individuals. Necrosis (Fletcher and Galambos 1963; Rao and Brown 1974; Wechsler and Wechsler 1951), degeneration (Dwyer and Helwig 1925; Greenberger et al. 1964; Wechsler and Wechsler 1951), fibrosis (Greenberger et al. 1964), hemorrhages (Wechsler and Wechsler 1951), and fatty infiltration (Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; Wertham 1932) have been observed in the liver. In addition to these effects, altered prothrombin time or level has been observed in a number of individuals ingesting a single dose of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Ehrentheill957; Fletcher and Galambos 1963; McCarron et al. 1981). Prothrombin and other plasma proteins that are required for the efficient progression and regulation of blood coagulation are primarily synthesized in the liver. A deficiency of these proteins is often observed in individuals with severe liver disease. A prolongation of prothrombin time is in part due to this impaired synthesis. Liver function tests were normal in workers chronically exposed to unreported levels of airborne phosphorus (Hughes et al. 1962). Similar hepatic alterations have been observed in animals acutely exposed to white phosphorus. Increases in AST and ALT levels (Paradisi et al. 1984), impaired liver function tests (Ghoshal et al. 1969; Hurwitz 1972; Sigal et al. 1954) increased liver weight (Ghoshal et al. 1969; Seakins and Robinson 1964), increased hepatic triglyceride levels (Ghoshal et al. 1969; Pani et al. 1972; Paradisi et al. 1984; Seakins and Robinson 1964), decreased protein synthesis (Barker et al. 1963; Seakins and Robinson 1964), disaggregation of polyribosomes (Pani et al. 1972), fatty degeneration (Ghoshal et al. 1969) and necrosis (Ghoshal et al. 1969) have been observed. No NOAEL values for hepatic effects following acute animal exposure were identified. In rats, the LOAEL value for liver effects was 6 mg/kg (Barker et al. 1963); in mice it was 5 mgkglday (Hurwitz 1972); and in dogs it was 0.2 mg/kg/day (Sigal et al. 1954). The liver effects occurred shortly after dosing; 3 hours after dosing, a significant decrease in protein synthesis was observed in the liver (Barker et al. 1963), minimal hepatocytic fatty changes were observed after 4 hours (Ghoshal et al. 1969), and severe hepatocytic fatty changes were observed after 12 hours (Ghoshal et al. 1969). The following hepatic effects have been observed in animals orally exposed for an intermediate duration fatty infiltration in guinea pigs exposed to 0.75 mg/kg/day (Ashbum et al. 1948), presence of eosinophilic granules at 0.25 mg/kg/day and cirrhosis at 0.66 mg/kg/day in rabbits and guinea pigs (Mallory 1933), and fibrosis and cirrhosis in pigs exposed to 0.6 mg/kg for 5 days/week (Peterson et al. 1991). In the Peterson et al. (1991) study, no liver effects were observed after 4 weeks of exposure; after 8 weeks, there were early signs of fibrosis, and after 12 weeks, extensive fibrosis was observed. Exposure to 0.075 mg/kg/day for an intermediate duration resulted in slight-to-moderate liver necrosis in dying pregnant rats (Bio/dynamics 1991), but no hepatic effects in the surviving pregnant rats or in male rats (Bio/dynamics 1991). In another reproduction study, liver effects were not observed in dying pregnant rats exposed to 0.075 mg/kg/day (IRDC 1985). Both studies used similar exposure protocols and similar vehicles; the difference in the occurrence of liver damage between the studies cannot be explained. Renal Effects. Evidence of severe renal effects have been observed in a number of individuals intentionally or accidentally ingesting a single dose of white phosphorus contained in rat (or roach) poison or fireworks. Proteinuria (Matsumoto et al. 1972; Pietras et al. 1968; Rao and Brown 1974), albuminuria (Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Dwyer and Helwig 1925; Fletcher and Galambos 1963; McCarron et al. 1981; Rubitsky and Myerson 1949), acetonuria (Pietras et al. 1968), increased urobilinogen (Matsumoto et al. 1972), oliguria (Dathe and Nathan 1946; McCarron et al. 1981; Rao and Brown 1974), increased blood levels of urea and/or nitrogen (Diaz-Rivera et al. 1950, 1961; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968; Rao and Brown 1974; Rubitsky and Myerson 1949), and increased blood creatinine levels (Dathe and Nathan 1946; McCarron et al. 1981) have been observed in these individuals. Renal insufficiency may be due to a direct toxic effect of phosphorus on the kidneys or to acute renal tubular necrosis from fluid loss and shock. Patients in shock may have a peculiar pallor and cyanosis. These probably reflect extensive cellular damage with poor perfusion of the capillary beds, and are a prognostic sign of serious health effects (Melamon et al. 1981). Several case reports have reported no alterations in kidney function (Ehrentheil 1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Simon and Pickering 1976). Histological alterations have also been observed in a number of humans ingesting a single dose of white phosphorus. Fatty changes in the tubules and loop of Henle (Dwyer and Helwig 1925; Humphreys and Halpert 1931; Wertham 1932) and engorged glomeruli and intratubular capillaries (Wechsler and Wechsler 1951) have been observed. Because most individuals vomited shortly after ingesting the white phosphorus or were lavaged, accurate doses cannot be calculated except for one study (Harm and Veale 1910). Histological alterations in the kidney were observed in an individual ingesting 2 mg/kg/day, but the lesion was not described. Creatinine levels were similar among unexposed workers and workers exposed to white phosphorus for chronic durations (Hughes et al. 1962). In animals, fatty infiltration in the nephron and subcapsular hemorrhages were observed in dogs acutely exposed to an unspecified amount of white phosphorus (Dwyer and Helwig 1925). No renal effects were observed in rats exposed to 0.075 mg/kg/day for an intermediate duration (Bio/dynamics 1991; IRDC 1985). No chronic exposure animal studies examining renal effects were located. Dermal Effects. Transient toxic dermatitis (described as a scalartiniform rash) developed 9 days after a man ingested a near-fatal dose of rat poison (Dathe and Nathan 1946). Edema of eyelids was reported in a 13-month-old child after ingestion of a fatal dose of white phosphorus (Rao and Brown 1974). Subcutaneous hemorrhages were visible in the left foot in a woman after consumption of 3.9 g of rat poison containing 4% phosphorus (Hann and Veale 1910). The woman died 4 days after the initial poisoning. At this time, an enormous subcutaneous hemorrhage was visible below the waist line. In this case report, the woman apparently did not expel (via vomiting) any of the ingested dose. Thus, it is likely that the ingested dose (2 mg/kg) was representative of the effective dose. Scattered blue-green petechiae were observed on the abdomen of a male child following accidental ingestion of a fatal dose of white phosphorus mixed with other ingredients from a firecracker (Humphreys and Halpert 1931). The dose level in this study could not be determined; the firecracker was a red composition of phosphorus mixed with other ingredients and was thought to contain about 10% phosphorus (Humphreys and Halpert 1931). No studies were located regarding dermal effects in animals after oral exposure to white phosphorus. Other Systemic Effects. A number of other systemic effects have been observed in humans ingesting a single dose of white phosphorus. The effects that are observed most consistently are hypoglycemia (Diaz-Rivera et al. 1950; McCarron et al. 1981; McIntosh 1927; Wechsler and Wechsler 1951), an increase in body temperature (mild pyrexia or fever) (Dathe and Nathan 1946; McIntosh 1927), and a decrease in plasma calcium, potassium, and/or sodium levels (Caley and Kellock 1955; McCarron et al. 1981; Rao and Brown 1974). It is unclear whether the fever seen is a symptom of phosphorus poisoning or a result of the treatment involved. In addition to these effects, metabolic acidosis (Rao and Brown 1974), hypothermia (Simon and Pickering 1976), damage to the spleen (Greenberger et al. 1964), ascites (Fletcher and Galambos 1963), fatty infiltration of the pancreas (Humphreys and Halpert 193 l), and necrosis of the adrenal medulla and cortex (Wechsler and Wechsler 1951) have been observed. In a child ingesting 0.083 mg/kg/day white phosphorus for an intermediate duration, decreased appetite, impaired body weight gain, and poor turgor (fullness or tension produced by the fluid content of blood vessels, capillaries, and cells) were observed (Sontag 1938). Serum glucose levels were decreased in workers occupationally exposed to white phosphorus for a chronic duration. It is likely that the workers were exposed by the inhalation, oral, and dermal routes (Ward 1928). In dogs acutely exposed to an unspecified amount of white phosphorus, hypoglycemia was observed (Williamson and Mann 1923). Rats received intermittent exposure to the atmosphere in the furnace room of a phosphorus factory for 14 months (Ruzuddinov and Rys-Uly 1986). Histology of rats killed monthly revealed progressive morphological degeneration of the tongue and oral mucosa of the cheek, gum, and hard palate. Epithelium and connective tissue from different parts of the oral cavity responded similarly to the treatment. Changes in the epithelial layer, observed after only 1 month of exposure, included increases in keratinization and numbers of cell layers, resulting in thickening and hyperkeratosis in the epithelium of the mucosa. Over time, the thickening and hyperkeratosis in the epithelium increased and histological changes were observed in the subepithelial connective tissue base. Eventually, the oral cavity contained areas of thickening of the mucosa from hyperkeratosis and increased epithelial cell layers interspersed with areas of decreased thickness of the epithelial layer due to atrophy, dystrophy, and cellular necrosis. At this time, adverse changes in the subepithelial connective tissue were considered pronounced. These effects occurred in most of the animals exposed to the atmosphere. It is likely that the observed effects of phosphorus on the oral cavity were local rather than systemic, resulting from direct contact of white phosphorus with tissues in the mouth. The study presented essentially no quantitative data, and the types and exposure levels of chemicals in the atmosphere (thought to contain elementary phosphorus and its inorganic compounds) were not reported (Ruzuddinov and Rys-Uly 1986). 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
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