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https://w.atwiki.jp/thecockrockshockpop/pages/1523.html
http //www.halofriendlies.com/ http //www.myspace.com/thehalofriendlies member Get Real Get Real 2002年07月29日 ( HD ) 1. Sellout / 2. Over It / 3. I m All Eyes / 4. Just Like You / 5. Anything For You / 6. Milwaukee / 7. Run Away / 8. Nice Guys / 9. Don t Let Me Down / 10. Disappear / 11. Selfish / 12. Unsaid Goodbyes
https://w.atwiki.jp/exp8606f/pages/12.html
人気商品一覧 @wikiのwikiモードでは #price_list(カテゴリ名) と入力することで、あるカテゴリの売れ筋商品のリストを表示することができます。 カテゴリには以下のキーワードがご利用できます。 キーワード 表示される内容 ps3 PlayStation3 ps2 PlayStation3 psp PSP wii Wii xbox XBOX nds Nintendo DS desctop-pc デスクトップパソコン note-pc ノートパソコン mp3player デジタルオーディオプレイヤー kaden 家電 aircon エアコン camera カメラ game-toy ゲーム・おもちゃ全般 all 指定無し 空白の場合はランダムな商品が表示されます。 ※このプラグインは価格比較サイト@PRICEのデータを利用しています。 たとえば、 #price_list(game-toy) と入力すると以下のように表示されます。 ゲーム・おもちゃ全般の売れ筋商品 #price_list ノートパソコンの売れ筋商品 #price_list 人気商品リスト #price_list
https://w.atwiki.jp/wiki7_hetare/pages/10.html
零～zero～ 零～紅い蝶～ 零～刺青の聲～ SIREN バイオハザード4（中途半端にハンドガン縛り） 龍が如く かまいたちの夜 学校であった怖い話(1週のみ) LIVE A LIVE ロックマン2 ロックマン3 サイレントヒル（ＢＡＤ－） SIREN2 忍道戒 ドラえもん のび太の BIOHAZARD(全員生還,ランクC) アソパソクエスト(隠しダンジョン含む) ロックマン4 マリオ2 ハングリーゴースト(ランクN) 蚊 オペレーターズサイド SILENT HILL2 最期の詩(leave END) THE 地球防衛軍(normalのみ) かまいたちの夜2 監獄島のわらべ唄 かまいたちの夜×3 BLACK ゴッドハンド コンデムド プロジェクト シルフィード デッドライジング(日本語版) eM -eNCHANTarM- クロムハウンズ カルドセプト ロストプラネット Gears of War クロックタワー3 零 月蝕の仮面 Halo3 ODST? FIRE その他 皆で遊ぶゲーム
https://w.atwiki.jp/retrogamewiki/pages/4365.html
今日 - 合計 - HALO ヒストリーパックの攻略ページ 目次 基本情報 [部分編集] ストーリー [部分編集] 攻略情報 [部分編集] Tips [部分編集] プチ情報 [部分編集] 関連動画 [部分編集] 参考文献、参考サイト [部分編集] 感想・レビュー 基本情報 [部分編集] ストーリー [部分編集] 攻略情報 [部分編集] Tips [部分編集] プチ情報 [部分編集] 関連動画 [部分編集] 参考文献、参考サイト [部分編集] 感想・レビュー 名前 コメント 選択肢 投票 役に立った (0) 2012年10月09日 (火) 15時28分00秒 [部分編集] ページごとのメニューの編集はこちらの部分編集から行ってください [部分編集] 編集に関して
https://w.atwiki.jp/callofduty4pc/pages/97.html
Challenge Challengeのアンロック内容，必要ポイントなど。カッコ内は必要ポイント。 対戦中、画面下に表示される黄色いバーは取得EXPを表す。ゲージが右端まで溜まるとレベルアップする。 ちなみに、チャレンジの解除音はLv55止まりの状態でもしっかり鳴る。聞くためにプレステする必要はない。 Assault SMG LMG Shotgun Sniper Boot Camp ブートキャンプ Operations オペレーション Killer キラー Humiliation 屈辱 Elite エリート Assault Challenge名 Ⅰ Ⅱ Ⅲ 条件 M16 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 M16 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 AK47 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 AK47 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 G3 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 G3 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 M4 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 M4 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 M14 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 M14 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 G36c Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 G36c Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 MP44 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 Assault共通 Ⅰ Ⅱ Ⅲ XP 100 500 1000 ▲上へ SMG Challenge名 Ⅰ Ⅱ Ⅲ 条件 MP5 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 MP5 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 Scopion Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 Scopion Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 Mini-UZI Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 Mini-UZI Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 AK-74u Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 AK-74u Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 P90 Marksman Dot sight(25) サイレンサー(75) ACOG Scope(150) 殺害人数 P90 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 SMG共通 Ⅰ Ⅱ Ⅲ XP 100 500 1000 ▲上へ LMG Challenge名 Ⅰ Ⅱ Ⅲ 条件 M249 MINIMI Marksman Dot sight(25) Grip(75) ACOG Scope(150) 殺害人数 M249 MINIMI Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 RPD Marksman Dot sight(25) Grip(75) ACOG Scope(150) 殺害人数 RPD Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 M60E4 Marksman Dot sight(25) Grip(75) ACOG Scope(150) 殺害人数 M60E4 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 LMG共通 Ⅰ Ⅱ Ⅲ XP 100 500 1000 ▲上へ Shotgun Challenge名 Ⅰ Ⅱ Ⅲ 条件 W1200 Marksman Dot sight(25) Grip(50) × 殺害人数 W1200 Expert Digitalカモ(25) Blue Tigerカモ(50) Red Tigerカモ(100) ヘッドショット数 M1014 Marksman Dot sight(25) Grip(50) × 殺害人数 M1014 Expert Digitalカモ(25) Blue Tigerカモ(50) Red Tigerカモ(100) ヘッドショット数 Shotgun共通 Ⅰ Ⅱ Ⅲ XP 100 500 1000 ▲上へ Sniper Challenge名 Ⅰ Ⅱ Ⅲ 条件 M40A3 Marksman ACOG Scope(100) × × 殺害人数 M40A3 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 M21 Marksman ACOG Scope(100) × × 殺害人数 M21 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 DragunovSVD Marksman ACOG Scope(100) × × 殺害人数 DragunovSVD Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 R700 Marksman ACOG Scope(100) × × 殺害人数 R700 Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 Barrett.50cal Marksman ACOG Scope(100) × × 殺害人数 Barrett.50cal Expert Digitalカモ(25) Blue Tigerカモ(75) Red Tigerカモ(150) ヘッドショット数 Sniper Marksman共通 XP 500 Sniper Expert共通 Ⅰ Ⅱ Ⅲ XP 100 500 1000 ▲上へ Boot Camp ブートキャンプ Challenge名 日本版名 条件 XP Ⅰ Ⅱ Ⅲ Radar Inbound レーダー・インバウンド UAV起動 50 × × Airstrike Inbound エアストライクインバウンド 空爆要請 50 × × Chopper Inbound チョッパーインバウンド ヘリ要請 50 × × Flyswatter ハエたたき 敵のヘリ撃墜 250 × × Marathon マラソン 26マイル(約42km)走る 250 × × Goodbye グッバイ 30ft (約9ｍ)以上の高さから落ちて死ぬ 250 × × Base Jump ベースジャンプ 15ft (約4.5ｍ)以上の高さから落ちて生き延びる 250 × × Crouch Shot クラウチショット しゃがみ撃ち状態での殺害人数 50 100 250 Prone Shot プローンショット ほふく撃ち状態での殺害人数 50 100 250 Grenade Kill グレネードキル グレネードによる殺害人数 50 100 250 Point Guard ポイントガード アシスト回数 50 100 250 X-Ray Vision X線ビジョン 壁抜きによる殺害人数 50 100 250 Vandalism ヴァンダリズム 破壊した車の数 50 100 250 Exposed 露出 UAVを呼んだ回数 50 100 250 Backdraft バックドラフト 敵の爆発物（クレイモア等）の破壊数 50 100 250 Knife Veteran ナイフベテラン ナイフによる殺害人数 50 100 250 グッバイ Countdownのミサイルサイロにグッバイするのが一番手っ取り早い。 ベースジャンプ 実は落ちなくてもハシゴを降りても成立。 ▲上へ Operations オペレーション 勝利数等は途中参加ではカウントされない。 Challenge名 日本版名 条件 XP Ⅰ Ⅱ Ⅲ Free-for-all Victor フリー・フォー・オール勝者 Free-for-allで３位以内に入った回数 50 100 250 Team Player チームプレイヤー Team Deathmatchでの勝利数 50 100 250 Search and Destroy Victor サーチ・アンド・デストロイ勝者 Search and Destroyでの勝利数 50 100 250 MVP Team Deathmatch MVPチームデスマッチ Team Deathmatchで全プレイヤー中最高得点を獲得 250 × × Hardcore Team Player ハードコアチームプレイヤー Team Hardcoreでの勝利数 50 100 250 Sabotage Victor サボタージュ勝者 Sabotageでの勝利数 50 100 250 MVP Team Hardcore MVPチームハードコア Team Hardcoreで全プレイヤー中最高得点を獲得し勝利 50 × × Bomb Down ボムダウン SabotageかSearch and Destroyで爆弾を持っている敵を殺害 250 × × Bomb Defender ボムディフェンダー SabotageかSearch and Destroyで爆弾を解除している敵を殺害 250 × × Bomb Planter ボムプランター SabotageかSearch and Destroyで爆弾を仕掛けている敵を殺害 250 × × Hero ヒーロー SabotageかSearch and Destroyで仕掛けられた爆弾を解除 250 × × Last Man Standing ラストマンスタンディング Search and Destroyで最後の一人になる 250 × × ▲上へ Killer キラー Challenge名 日本版名 条件 XP Ⅰ Ⅱ Ⅲ Claymore Shot クレイモアショット クレイモアで５人殺害 250 × × Assault Expert アサルトエキスパート アサルトライフルでのヘッドショットによる殺害人数 50 100 250 SMG Expert SMGエキスパート サブマシンガンでのヘッドショットによる殺害人数 50 100 250 LMG Expert 軽機関銃エキスパート ライトマシンガンでのヘッドショットによる殺害人数 50 100 250 Last Stand Veteran ラストスタンドベテラン Last Stand中の殺害人数 50 100 250 Master Chef マスターシェフ 投げたグレネードによる殺害人数 50 100 250 Airstrike Veteran エアストライクベテラン 援護空爆による殺害人数 50 100 250 Chopper Veteran チョッパーベテラン 援護ヘリによる殺害人数 50 100 250 Stun Veteran スタンベテラン スタングレネードで無力化した敵の殺害人数 50 100 250 Multi-RPG マルチ-RPG １発のRPGで２人以上殺害 250 × × Martydom Veteran 殉教ベテラン Martydomで落としたグレネードによる殺害人数 50 100 250 Clay More クレイモア 一つのクレイモアで２人以上殺害 250 × × Stealth ステルス サイレンサー付の武器による殺害人数 50 100 250 Invisible インビジブル 伏せた状態でのスナイパーライフルによる殺害人数 50 100 250 Counter-Claymore カウンタークレイモア クレイモアを撃って爆発させることによる殺害人数 50 100 250 Counter-C4 カウンターC4 C4を撃って爆発させることによる殺害人数 50 100 250 マスターシェフ ただフラグを投げて倒すだけではダメ。日本語版の説明では誤解しがち。 ボタン長押しで2つほど数えてから投げよう。 マルチ-RPG Perk2にSonic Boom（ソニックブーム）を付けると良い。 狙いやすいマップはWet WorkかVacant。 ▲上へ Humiliation 屈辱 Challenge名 日本版名 条件 XP Ⅰ Ⅱ Ⅲ Airborne エアボーン 空中で撃った弾による２連続キル 250 × × Multi-Frag マルチ-破片 一つのグレネードで２人以上殺害 250 × × Carpet Bomb 絨毯爆撃 一回の空爆で５人殺害 250 × × MG Master MGマスター 備え付けのMGで５連続キル 250 × × Slasher スラッシャー ナイフで３連続キル 250 × × Multi-C4 マルチ-C4 一つのC4で２人以上殺害 250 × × Hot Potato ホットポテト 投げ返したグレネードによる殺害人数 50 100 250 Car Bomb 車両爆弾 車を破壊して傍にいる敵を殺害 250 × × Backstabber バックスタバー 敵を背後からナイフで暗殺 250 × × Slow But Sure スロウ・バット・シュア 自分がスタングレネードで遅くなっている時に敵を殺害 250 × × Flashbang Veteran 閃光弾ベテラン フラッシュグレネードで無力化した敵の殺害人数 50 100 250 Misery Loves Company ミザリーラブズカンパニー グレネードを自分の手に持ったまま爆発させ、自分と敵を同時に殺害した回数 50 100 250 Ouch アウチ ライフルグレネードを爆発させないで直接当てることによる殺害人数 50 100 250 Rival ライバル 一試合中に同じ敵を５回殺害 250 × × Cruely 残虐行為 殺害した敵の武器を使用して同じ敵を殺害 250 × × Think Fast シンクファスト グレネードを直接敵に当てて殺害 250 × × Think Fast Stun シンクファストスタン スタングレネードを直接敵に当てて殺害 250 × × Think Fast Flash シンクファストフラッシュ フラッシュグレネードを直接敵に当てて殺害 250 × × Return To Sender リターン・トゥ・センダー C4を撃って爆発させ、そのC4を仕掛けた本人を殺害 250 × × Blindfire ブラインドファイア 自分がフラッシュグレネードで視界を奪われている時に敵を殺害 250 × × シンクファスト関連 ラストスタンド中の敵にフラグ等ぶつけると簡単。 ▲上へ Elite エリート Challenge名 日本版名 条件 XP Ⅰ Ⅱ Ⅲ The Brink ザ・ブリンク 瀕死（画面が赤い）状態で３連続キル 250 × × Collateral Damage コラテラルダメージ 一発のスナイパーライフルの弾丸で２人以上殺害 250 × × The Edge ザ・エッジ 自分のキルがその試合最後のキルとなった回数 50 100 250 Flawless 無傷 最初から参加した試合を一度も死ぬことなく終える 250 × × Tango Down タンゴダウン 最低４人以上の敵チーム全員を殺害 250 × × Hard Landing ハードランディング 空中にいる敵を殺害 250 × × Extreme Cruelty 過度の残虐行為 自分が死ぬことなく最低４人以上の敵チーム全員を殺害 250 × × Fast Swap ファストスワップ メイン武器でダメージを与えた敵をピストルで殺害 250 × × Star Player スタープレイヤー 最初から参加した試合を５以上のキル/デス・レシオで終える 250 × × How The ? いったい？ 壁抜きで爆発物を撃ち、爆発させて敵を殺害 250 × × Dominos ドミノ 爆発物を撃ち、爆発を連鎖させて敵を殺害 250 × × No Secrets シークレットなし 一試合中に三度UAVを召喚 250 × × Afterburner アフターバーナー 一試合中に二度空爆を要請 250 × × Air Superiority 航空優勢 一試合中に二度ヘリを召喚 250 × × Fearless 恐れ知らず 自分が死ぬことなく１０人の敵を殺害 250 × × Counter-MVP カウンターMVP 一試合中に敵チーム一位のプレイヤーを１０回殺害 250 × × invincivle インビンシブル 自分が死ぬことなく「ダメージを食らう→回復」を５回繰り返す 250 × × Survivalist サバイバリスト 自分が死ぬことなく試合に５分間参加する 250 × × ザ・ブリンク 1回の瀕死中に3連殺・・・ではなく「瀕死中にキル→回復、瀕死中にキル→回復、瀕死中にキル→回復」でいい ザ・エッジ 空爆やヘリのキルではカウントされないようだ。 ハードランディング 敵がジャンプ中の時や、ハシゴの上り下りの途中に倒しても「空中」と見なされる模様。 相手が倒れる瞬間にジャンプしていると、予期せぬ達成なんてことも。 ファストスワップ Perk3のラストスタンドを使っても達成可。 撃ち合いで負けた時、倒れた後に自動で置き換わるハンドガンで倒せばおｋ。 スタープレイヤー 条件 （最初から参加、５以上のキル/デス レシオ）を満たしていれば、ホストがゲームを中断しても達成になる。 ▲上へ
https://w.atwiki.jp/eeic08exp19/pages/4.html
ニュース @wikiのwikiモードでは #news(興味のある単語) と入力することで、あるキーワードに関連するニュース一覧を表示することができます 詳しくはこちらをご覧ください。 ＝＞http //atwiki.jp/guide/17_174_ja.html たとえば、#news(wiki)と入力すると以下のように表示されます。 【グランサガ】リセマラ当たりランキング - グランサガ攻略wiki - Gamerch(ゲーマチ) 【まおりゅう】八星之紋章交換のおすすめ交換キャラ - AppMedia(アップメディア) Among Us攻略Wiki【アマングアス・アモングアス】 - Gamerch(ゲーマチ) マニュアル作成に便利な「画像編集」機能を提供開始！ - ナレッジ共有・社内wikiツール「NotePM」：時事ドットコム - 時事通信 マニュアル作成に便利な「画像編集」機能を提供開始！ - ナレッジ共有・社内wikiツール「NotePM」 - PR TIMES 【Apex Legends】ヴァルキリーの能力と評価【エーペックス】 - Gamerch(ゲーマチ) モンハンライズ攻略Wiki｜MHRise - AppMedia(アップメディア) 【ウインドボーイズ】リセマラ当たりランキング（最新版） - ウインドボーイズ攻略Wiki - Gamerch(ゲーマチ) ポケモンBDSP(ダイパリメイク)攻略wiki - AppMedia(アップメディア) 【テイルズオブルミナリア】リセマラ当たりランキング - TOルミナリア攻略Wiki - Gamerch(ゲーマチ) SlackからWikiへ！シームレスな文章作成・共有が可能な「GROWIBot」リリース - アットプレス（プレスリリース） ドラゴンクエストけしケシ攻略Wiki - Gamerch(ゲーマチ) 【ウマ娘】チャンピオンズミーティングの攻略まとめ - Gamerch(ゲーマチ) 【ウマ娘】ナリタブライアンの育成論｜URAシナリオ - Gamerch(ゲーマチ) 【ウマ娘】フジキセキの育成論｜URAシナリオ - Gamerch(ゲーマチ) サモンズボード攻略wiki - GameWith 【スタオケ】カード一覧【金色のコルダスターライトオーケストラ】 - Gamerch(ゲーマチ) 【スマブラSP】ソラのコンボと評価【スマブラスペシャル】 - 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https://w.atwiki.jp/cohstatsjp/pages/290.html
Vehicle Infantry Halftrack Contents 1 Infantry Halftrack Veterancy 2 Tactics 3 History 4 Built From 4.1 Kampfgruppe Kompanie 5 Vehicle Abilities 5.1 Vehicle Cover 6 Vehicle Weapons 6.1 MG42 Infantry Halftrack Infantry Halftrack Health 300 Max Speed 6.5 Sight 35 Cost 24020 Acceleration 4.5 Detection 0/0 Time 45 Deceleration 3 Hotkey H Population 4 Rotation 50 Target Type vehicle_22x Upkeep 4.032 Crush Human Critical Type vehicle_halftrack Crush Mode Rear Damage Enabled false Infantry Halftrack Veterancy [Expand][Hide] Received Damage Received Accuracy Maximum Speed Maximum Health 0.9 0.9 1.15 1.15 Accuracy Reload Cooldown Penetration 1.15 0.9 0.9 1.15 8 Vet-Exp Received Damage Received Accuracy Maximum Speed Maximum Health 0.95 0.95 1.05 1.15 Accuracy Reload Cooldown Penetration 1.15 0.9 0.9 1.15 22 Vet-Exp Received Damage Received Accuracy Maximum Speed Maximum Health 0.95 0.95 1.05 1.15 Accuracy Reload Cooldown Penetration 1.15 0.9 0.9 1.15 38 Vet-Exp Tactics Infantry squads that are nearby can reinforce at an Infantry Halftrack. Infantry can fire from the Halftrack when inside. To increase the anti-tank effectiveness or your shreck d Gren squads choose the Double AT-Effort ability from the Tank-Hunter CP-Tree. Place a Gren squad upgraded with shrecks inside the halftrack. This allows the Halftrack to become useful against enemy tanks. With its speed it can easily outflank unguarded heavy tanks. In the early game, support garrisoned Gewehr 43 Panzer Grenadiers with MP44 Panzer Grenadiers inside the Halftrack. They can provide deadly close range damage, and can be covered by the Gewehr 43 s in case the Halftrack s health runs low. Upgrade the building that has your garrison of Gewehr 43 P. Grenadiers into a Reinforce point (It must be in territory though), and research Defensive Operations at your HQ. This allows squads in and around the Reinforce point to reinforce and heal, gaining almost invulnerability through a small skirmish. Constantly harass your opponents to prevent artillery from reaching, or a large enough army that can penetrate your defensive line. History The SdKfz 250 halftrack was a lighter design than the standard SdKfz 251 halftrack that was used for troop transport. Its carrying capacity was only six men (including both the driver and gunner) so infantry squads normally required two of them to transport the whole squad. It was primarily used by Panzeraufklärungsabteilung (Mechanized Reconnaissance Battalions) in Panzer, and Panzergrenadier divisions. Built From Kampfgruppe Kompanie [Expand][Hide] Health 1000 Target Type building Cost 22020 Critical Type building Time 115 Hotkey K Effects Makes available the Infantry Halftrack, Mortar Halftrack, and Tank Buster Squads. Available upgrades can increase territory capture rate of Infantry squads and improve their repair skills. ESee Structure Kampfgruppe Kompanie for details. Vehicle Abilities Vehicle Cover [Expand][Hide] Cost Activation always_on Duration _ Target tp_any Recharge 0 Hotkey Effects $0 no key ESee Ability Vehicle Cover for details. Vehicle Weapons MG42 Infantry Halftrack [Expand][Hide] Weapon MG42 Infantry Halftrack See Weapon MG42 Infantry Halftrack for details. Retrieved from http //coh-stats.com/Vehicle Infantry_Halftrack
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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