Msds Hydrogen Peroxide

Msds Hydrogen Peroxide tài liệu, giáo án, bài giảng , luận văn, luận án, đồ án, bài tập lớn về tất cả các lĩnh vực kinh...

Decolorization of Dye with Iron Oxide Catalysed Decomposition of Hydrogen Peroxide Joonseon Jeong, Jeyong Yoon School of Chemical Engineering, College of Engineering, Seoul National University, San 56-1, Shilim-Dong, Kwanak-Goo, Seoul, Korea (151-742) ABSTRACT This study describes the dye removal under the iron oxide(FeOOH) catalysed decomposition of hydrogen peroxide. FeOOH was selected as iron oxide. The effect of FeOOH concentration, H 2 O 2 concentration, the presence of radical scavenger, and pH on the dye removal and the decomposition of hydrogen peroxide was investigated. The rate of H 2 O 2 decomposition was obtained as a pseudo-first-order kinetics relative to FeOOH concentration. However, despite of the increased H 2 O 2 decomposition rate, the dye removal rate was not proportional to FeOOH concentration because FeOOH surface plays a role of scavenging OH radical. The H 2 O 2 decomposition by FeOOH at pH 7 was more significant than that at pH 3, suggesting the possibility for overcoming limitations of homogeneous Fenton reaction which occurs only in acidic condition. The mechanism for the dye removal under the iron oxide catalysed decomposition of hydrogen peroxide was suggested, based on the experimental results obtained in this study. KEYWORDS FeOOH, hydrogen peroxide, dye, hydroxyl radical, decolorization INTRODUCTION AOPs (Advanced Oxidation Processes) which generate hydroxyl radical (OH•) have been introduced to water treatments recently. AOPs comprise various types such as O 3 /H 2 O 2 , Fe 2+ /Fe 3+ /H 2 O 2 , UV/H 2 O 2 , and UV/TiO 2 , depending on the how to produce OH•. Among these types, Fenton’s reagent, a mixture of ferrous iron and hydrogen peroxide, has been applied to treat a various wastewater and contaminated soils (Venkatadri and Peters, 1993). But it is effective only in acidic pH. In addition, the process generates a lot of iron sludge which need further treatment. Alternatively, a number of researchers investigated about hydrogen peroxide decomposition and contaminant degradation by iron oxide catalysed reaction (Valentine et al., 1998; Watts et al., 1993; Abbot et al., 1990). Iron oxides are abundant in natural water and known to effectively decompose hydrogen peroxide for generating hydroxyl radicals. Especially, it has the advantage which can operate in neutral pH condition. We selected dye as a model compound in this study. The treatment of dye wastewater is one of the most urgent subjects in pollution control because of its resistance to biodegradation (Ganesh et al., 1994). This study reports the mechanisms for the oxidation of commercial dye and H 2 O 2 decomposition in H 2 O 2 /iron oxide system. MATERIALS AND METHODS All solutions were prepared with deionised/distilled water, treated with a Barnstead NANO pure system, and analytical reagent grade chemicals. Hydrogen peroxide (30.0-35.5%) was obtained from the Junsei Chemical Co., Ltd. The α-FeOOH (30-50 mesh), Fe 3 O 4 , Fe 2 O 3 and tert-butanol (99.5+%) were purchased from Aldrich Chemical Company. Reactive Red 6 was obtained from Imperial Chemical Industries. All solutions used in experiment were prepared from dilution of the stock solution. The experiments were conducted in open batch reactor with mechanical mixing. The initial pH was controlled with solutions of 0.1N NaOH or 0.1N HClO 4 and pH was not further adjusted. The pH variation during the reaction was <±0.1 pH unit. The reactions were PHIẾU AN TOÀN HÓA CHẤT Phiếu an toàn hóa chất HYDROGEN PEROXIDE Số CAS: 7722-84-1 Số UN: 2014 Số đăng ký EC: 231-765-0 Số thị nguy hiểm tổ chức xếp loại (nếu có): Số đăng ký danh mục quốc gia khác (nếu có) I NHẬN DẠNG HÓA CHẤT - Tên thường gọi chất: Hydrogen Peroxide Mã sản phẩm (nếu có) - Tên thương mại: Hydrogen Peroxide - Tên khác (không tên khoa học): Nước oxy già - Tên nhà cung cấp nhập khẩu, địa chỉ: : Địa liên hệ trường hợp khẩn cấp: Trung tâm Dữ liệu Hỗ trợ úng phó cố hóa chất - Tên nhà sản xuất địa chỉ: Địa chỉ: Tầng 14, 655 Phạm Văn Đồng, phường Cổ Nhuế, quận Bắc Từ Liêm, Hà Nội - Mục đích sử dụng: Dùng công nghiệp, thí nghiệm, y tế Số điện thoại: 04.39362506 Email: nqkhanh1987@gmail.com Hotline: 0904773312 II THÔNG TIN VỀ THÀNH PHẦN HÓA CHẤT Tên thành phần nguy hiểm Số CAS Công thức hóa học Hàm lượng (%theo trọng lượng) Hydrogen Peroxide 7722-84-1 H2O2 30 – 50% Nước 7732-18-5 H2O 50 – 70% III NHẬN DẠNG ĐẶT TÍNH NGUY HIỂM CỦA HÓA CHẤT Mức xếp loại nguy hiểm Phân loại theo hệ thống hài hòa toàn cầu GHS: - Độc cấp tính, đường miệng (loại 4) - Gây tổn thương mắt nghiêm trọng (loại 1) Theo HMIS (Mỹ) : - Sức khỏe: - Dễ cháy: - Phản ứng: - Vật liệu có tính ôxy hóa loại C - Chất lỏng ăn mòn loại E - Vật liệu có phản ứng nguy hiểm loại F Cảnh báo nguy hiểm - Hình đồ cảnh báo: - Từ cảnh báo: Nguy hiểm - Cảnh báo nguy hiểm: - Rất nguy hiểm trường hợp tiếp xúc với da mắt (gây kích ứng), uống hít phải - Độc hại tiếp xúc với da mắt (ăn mòn) - Chất lỏng phun sương gây tổn thương mô, đặc biệt niêm mạc mắt, miệng đường hô hấp - Tiếp xúc da gây bỏng Lâu dài gây loét - Hơi sương gây kích thích đường hô hấp nghiêm trọng Ngăn ngừa - Không để nơi nhiệt độ cao/ gần nguồn lửa trần/ gần nơi có tia lửa / bề mặt nóng - Không hút thuốc - Thùng chứa đóng chặt - Nối dây tiếp đất cho công te nơ thiết bị tiếp nhận - Chỉ sử dụng thiết bị điện/ thiết bị thông gió/ thiết bị chiếu sáng không phát tia lửa điện - Chỉ sử dụng dụng cụ không phát tia lửa - Áp dụng biện pháp chống tượng phóng tĩnh điện - Tránh vào môi trường có bụi hoá chất - Rửa tay thật kỹ sau sử dụng, mang vác, tiếp xúc với hoá chất - Chỉ sử dụng trời nơi thông thoáng - Dùng găng tay, quần áo, kính, mạng che mặt phù hợp tiếp xúc với hoá chất Lưu trữ: - Lưu trữ môi trường thông thoáng, mát mẻ - Đóng chặt thùng chứa - Khóa kho cẩn thận Thải bỏ - Sản phẩm thải loại phương tiện chứa phải tồn chứa nơi thích hợp thu hồi/ tái chế theo quy định nhà nước Các đường tiếp xúc triệu chứng Đường mắt - Các dấu hiệu triệu chứng kích ứng mắt bao gồm cảm giác bỏng rát, đỏ mắt phồng rộp, và/ mờ mắt Đường hô hấp - Hít phải khí có nồng độ cao làm cho hệ thần kinh trung ương (CNS) bị tê liệt dẫn đến chóng mặt, choáng, đau đầu nôn ói Các dấu hiệu triệu chứng khác suy yếu hệ thần kinh trung ương (CNS) bao gồm đau đầu, buồn nôn khả điều khiển thể Tiếp tục hít dẫn đến hôn mê tử vong Đường da - Các dấu hiệu viêm da triệu chứng bao gồm cảm giác bỏng rát và/ da khô/ nứt nẻ Đường tiêu hóa - Nếu vật liệu vào phổi, dấu hiệu triệu chứng bao gồm ho, ngạt thở, thở khò khè, khó thở, tức ngực, hụt và/ sốt Các dấu hiệu triệu chứng kích ứng hô hấp bao gồm cảm giác bỏng tạm thời mũi họng, ho và/ khó thở IV BIỆN PHÁP SƠ CỨU VỀ Y TẾ Trường hợp tay nạn tiếp xúc theo đường mắt ( bị văng, dây vào mắt) - Thận trọng rửa mắt nước Tháo bỏ kính áp tròng đeo thấy dễ dàng Sau tiếp tục rửa mắt nước 15 phút giữ cho mí mắt hở Chuyển nạn nhân đến sở y tế gần để có chăm sóc Trường hợp tai nạn tiếp xúc da (bị dây vào da) - Cởi bỏ quần áo bị dính sản phẩm Rửa phận bị dính bẩn với nước sạc (và xà phòng có thể) Trường hợp tay nạn tiếp xúc theo đường hô hấp (hít thuở phải hóa chất nguy hiểm dạng hơi, khí) - Chuyển nạn nhân nơi thoáng khí Nếu không hồi phục nhanh chóng, chuyển nạnnhân đến sở y tế gần để có điều trị Giữ ngực nạn nhân tư thếthuận lợi cho hô hấp Trường hợp tay nạn theo đường tiêu hóa (ăn uống nuốt nhầm hóa chất) - Ngay gọi trung tâm cấp cứu gọi bác sĩ Không kích ứng gây nôn Nếu nạn nhân nôn ói, giữ cho đầu thấp hông để tránh hít vào V BIỆN PHÁP SỬ LÝ KHI CÓ HỎA HOẠN Xếp loại tính cháy: Không cháy Các mối nguy hại cụ thể phát sinh từ hóa chất: Dễ cháy tiếp xúc với cellulose vật liệu dễ cháy khác Phosphine, hydrogen sulfide, selenua cháy gặp axit nitric dạng khí gas Sản phẩm tạo bị cháy: Không phù hợp Các tác nhân gây cháy, nổ: Sự phóng tĩnh điện; lửa trần; tia lửa Các chất dập cháy thích hợp hướng dẫn biện pháp chữa cháy, biện pháp kết hợp khác : - Bọt chống cháy, phun nước hay sương Chỉ sử dụng bột hóa chất khô, cacbon dioxit, cát hay đất cho vụ hỏa hoạn nhỏ Không sử dụng vòi phun nước có áp lực để dập lửa Giải tán người nhiệm vụ khỏi khu vực có hỏa hoạn Phương tiện, trang phục bảo hộ cần thiết chữa cháy: - Mang đầy đủ quần áo bảo vệ dụng cụ thở có ôxy Khi chữa cháy không gian kín phải dùng thiết bị bảo hộ thích hợp, bao gồm mặt nạ phòng độc Các lưu ý dặc biệt cháy, nổ: Được coi chất không cháy tác nhân môi trường xung quanh chất cenllulose, hydrogen sulfite, cháy gặp acid nitric Vì tất khu vực cất chứa phải trang ...Production and utilization of hydrogen peroxide associated with melanogenesis and tyrosinase-mediated oxidations of DOPA and dopamine Maristella Mastore 1 , Lara Kohler 2 and Anthony J. Nappi 2 1 Universita ` degli Studi dell’Insubria, Dipartimento di Biologia Strutturale e Funzionale, Laboratorio di Immunologia Comparata, Varese, Italy 2 Animal Heath and Biomedical Sciences, University of Wisconsin-Madison, Madison, WI, USA Human melanins are heteropolymers synthesized by such diverse cells as those comprising portions of the skin, hair, inner ear, brain and retinal epithelium. These multifunctional pigments are derived from a complex series of enzymatic and nonenzymatic reac- tions initiated by the hydroxylation of l-phenylalanine to l-tyrosine. This reaction is mediated by the enzyme phenylalanine hydroxylase (EC 1.14.16.1), an iron-containing protein that requires the presence of the cofactor (6R)-l-erythro-5,6,7,8-tetrahydrobiopterin. A critical two-step reaction sequence follows involving the hydroxylation of tyrosine to DOPA (monopheno- lase activity), and the ensuing oxidation of the o-diphe- nol (diphenolase activity) to o-quinone (dopaquinone). Subsequent oxidative polymerizations of indolequinones yield brown to black eumelanins, whereas similar reac- tions involving cysteine and glutathione conjugates of dopaquinone form reddish-brown pheomelanins (Fig. 1). Neuromelanin, which is also a brown-black pigment, apparently is restricted to the substantia nigra pars compacta and certain other regions of the mamma- lian brain. The pigment is derived in large part from the oxidation of dopamine (i.e. the decarboxylated deriv- ative of DOPA) with a variety of nucleophiles, including thiols derived from glutathione [1–3]. Some of the numerous factors influencing pigment biogenesis in mammalian systems include substrate availability, the presence and concentrations of O 2 , metal ions, thiol Keywords hydrogen peroxide; melanogenesis; reactive intermediates of oxygen; tyrosinase Correspondence A. J. Nappi, Animal Heath and Biomedical Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA Fax: +1 608 2627420 Tel: +1 608 2622618 E-mail: anappi@svm.vetmed.wisc.edu (Received 10 December 2004, revised 3 February 2005, accepted 11 March 2005) doi:10.1111/j.1742-4658.2005.04661.x The synthesis and involvement of H 2 O 2 during the early stages of melano- genesis involving the oxidations of DOPA and dopamine (diphenolase activity) were established by two sensitive and specific electrochemical detection systems. Catalase-treated reaction mixtures showed diminished rates of H 2 O 2 production during the autoxidation and tyrosinase-mediated oxidation of both diphenols. Inhibition studies with the radical scavenger resveratrol revealed the involvement in these reactions of additional react- ive intermediate of oxygen (ROI), one of which appears to be superoxide anion. There was no evidence to suggest that H 2 O 2 or any other ROI was produced during the tyrosinase-mediated conversion of tyrosine to DOPA (monophenolase activity). Establishing by electrochemical methods the endogenous production H 2 O 2 in real time confirms recent reports, based in large part on the use of exogenous H 2 O 2 , that tyrosinase can manifest both catalase and peroxidase activities. The detection of ROI in tyrosinase-medi- ated in vitro reactions provides evidence for sequential univalent reductions of O 2 , most likely occurring at the enzyme active site copper. Collectively, these observations focus attention on the possible involvement of Glucose oxidase prevents programmed cell death of the silkworm anterior silk gland through hydrogen peroxide production Hiroto Matsui 1 , Motonori Kakei 2 , Masafumi Iwami 1,2 and Sho Sakurai 1,2 1 Division of Biological Sciences, Graduate School of Natural Science and Technology, Kanazawa University, Japan 2 Division of Life Sciences, Graduate School of Natural Science and Technology, Kanazawa University, Japan Introduction Programmed cell death (PCD) plays an important role in the elimination of cells and tissues as part of the progression of animal development. In insects, larval- specific tissues degenerate during metamorphosis in response to 20-hydroxyecdysone (20E), an active form of ecdysteroid. The induction of PCD by 20E has been extensively studied in the salivary glands of Drosoph- ila melanogaster [1], the intersegmental muscles [2] and prothoracic glands of Manduca sexta [3], and the ante- rior silk glands (ASGs) of Bombyx mori [4,5]. The B. mori ASG is a tubular organ consisting of a single layer of cells, and acts as a spinning apparatus for secreting silk thread, which is composed of two dif- ferent proteins produced in the middle and posterior silk glands. The ASG is eliminated at the end of the larval stage through PCD in response to the meta- morphic rise in the 20E concentration [4]. The ASG becomes competent to respond to 20E undergoing PCD late on day 5 of the fifth (last) instar stage, and exhibits full competence after the onset of spinning on day 6, but ASGs before the middle of day 5 do not respond to 20E [6]. Lepidopteran larval epidermis and wing disks lose their sensitivity to juvenile hormone after the change Keywords glucose oxidase; hydrogen peroxide; insect; programmed cell death; silk gland Correspondence S. Sakurai, Division of Life Sciences, Graduate School of Natural Science and Technology, Kanazawa University, Kanazawa 920-1192, Japan Fax: +81 76 264 6215 Tel: +81 76 264 6250 E-mail: ssakurai@kenroku.kanazawa-u.ac.jp (Received 15 November 2010, revised 16 December 2010, accepted 21 December 2010) doi:10.1111/j.1742-4658.2010.07996.x During pupal metamorphosis, the anterior silk glands (ASGs) of the silk- worm Bombyx mori degenerate through programmed cell death (PCD), which is triggered by 20-hydroxyecdysone (20E). 20E triggers the PCD of the ASGs of day 7 fifth instar (V7) larvae but not that of V5 larvae. When V7 ASGs were cocultured with V5 ASGs in the presence of 20E, neither culture of ASGs underwent PCD. The 20E-induced PCD of V7 ASGs was also inhibited when they were incubated in conditioned medium that was prepared by incubating V5 ASGs for 48 h, an indication that V5 ASGs released an inhibitor of 20E-induced PCD during incubation. The inhibitor was purified from conditioned medium and identified as glucose oxidase (GOD). GOD catalyzes the oxidation of glucose to gluconolactone, and generates hydrogen peroxide as a byproduct. We found that hydrogen per- oxide is the molecule that directly inhibits the action of 20E and may act to protect the ASGs from early execution of PCD during the feeding stage. GOD was localized in the inner cavity of the gland, and was discharged to the outside of the ASGs with the silk thread at the onset of spinning. Thus, the spinning behavior, occurring at the beginning of the Applied Catalysis B: Environmental 50 (2004) 259–269 Effect of hydrogen peroxide on the destruction of organic contaminants-synergism and inhibition in a continuous-mode photocatalytic reactor Dionysios D. Dionysiou a,∗ , Makram T. Suidan a , Isabelle Baudin b , Jean-Michel La ˆ ıné b a Department of Civil and Environmental Engineering, Drinking Water, Water Supply, Quality and Treatment Laboratories, University of Cincinnati, 765 Baldwin Hall, Mail Stop #0071, Cincinnati, OH 45221-0071, USA b Centre International de Recherche Sur l’Eau et l’Environnement, CIRSEE, ONDEO Services, 38 rue du President Wilson, 78230 Le Pecq, France Received 18 September 2003; received in revised form 16 January 2004; accepted 27 January 2004 Available online 2 April 2004 Abstract The effect of hydrogen peroxide on the photocatalytic degradation of organic contaminants in water was investigated using a TiO 2 -rotating disk photocatalytic reactor (RDPR) operated in a continuous-mode and at steady state. The experiments were performed at pH 3.0, in the presence of near-UV radiation, and using 4-chlorobenzoic acid (4-CBA) as a model non-volatile organic contaminant at influent concentration of 300 ␮mol l −1 . Experiments were performed at concentrations of hydrogen peroxide in the range 0–10.74 mmol l −1 . Addition of hydrogen peroxide at small concentrations (<2 mmoll −1 ) had a synergistic effect and increased considerably the rates of photocatalytic reactions. An optimum influent hydrogen peroxide concentration wasobserved at 1.6mmoll −1 , which caused an increased in the ratesof4-CBAdegradation and total organic carbon (TOC) mineralization by 1.72 and 2.13 times, respectively. This corresponded to an optimum oxidant to contaminant molar ratio of 5.33. At higher concentrations, hydrogen peroxide was found to cause an inhibiting effect on the photocatalytic reactions. The synergistic and inhibiting effects of hydrogen peroxide were rationalized based on the reaction rate constants between relevant radical species. © 2004 Elsevier B.V. All rights reserved. Keywords: TiO 2 ; Photocatalysis; Photocatalytic; Hydrogen peroxide; H 2 O 2 ; Radicals; Hydroxyl; Superoxide; Perhydroxyl; Reaction rate constants; Water treatment; Detoxification; Destruction; Organic; Contaminants; Rotating disk; Reactor; Continuous; Chlorobenzoic acid; Green engineering 1. Introduction Considering the chemical components of various tech- nologies for water treatment, including the so-called ad- vanced oxidation technologies (AOTs), TiO 2 photocatalysis can be viewed as a “green” technology. It is becoming more popular as a detoxification technology because of several reasons. First, TiO 2 photocatalytic systems that incorporate the catalyst immobilized require only the addition of UV radiation for the generation of the primary reactive species (i.e., electrons and holes) and subsequently the hydroxyl radicals, which are the primary oxidizing species in the process. Second, TiO 2 photocatalysis can result in the com- plete destruction of virtually all organic contaminants (i.e., mineralization) when the reactor set-up is optimized [1–12]. Third, TiO 2 catalyst is non-toxic, insoluble in water, photo- ∗ Corresponding author. Tel.: +1-513-556-0724; fax: +1-513-556-2599. E-mail address: dionysios.d.dionysiou@uc.edu (D.D. Dionysiou). stable, and relatively Mammalian 105 kDa heat shock family proteins suppress hydrogen peroxide-induced apoptosis through a p38 MAPK-dependent mitochondrial pathway in HeLa cells Nobuyuki Yamagishi, Youhei Saito and Takumi Hatayama Department of Biochemistry, Division of Biological Sciences, Kyoto Pharmaceutical University, Japan Heat shock proteins (Hsps) are a set of highly conserved proteins produced in response to physiologi- cal and environmental stress that serve to protect cells from stress-induced damage by preventing protein denaturation and ⁄ or repairing such damage [1]. Mam- malian Hsps are classified into several families on the basis of their apparent molecular weight and function, such as the HSP105 ⁄ 110, HSP90, HSP70, HSP60, HSP40, and HSP27 families. The HSP70 family is a major and well-characterized group of Hsps. Several species of HSP70 family proteins are present in the various compartments of eukaryotic cells. These pro- teins play important roles as molecular chaperones that prevent the irreversible aggregation of denatured proteins and assist the folding, assembly and transloca- tion across membranes of cellular proteins [2,3]. In addition, Hsp70 protects against apoptosis caused by a variety of stressors such as heat shock, oxidative stress and chemotherapeutic agents [4–6], and recent studies have demonstrated that Hsp70 can modulate the func- tions of several major components in the apoptotic process, including the caspase cascade and the c-Jun N-terminal kinase (JNK) signaling pathway [7–12]. Hsp105a and Hsp105b are mammalian members of the HSP105 ⁄ 110 family, a subgroup of the HSP70 family. Hsp105a is expressed constitutively and in response to various forms of stress, while Hsp105b is an alternatively spliced form of Hsp105a that is Keywords apoptosis; H 2 O 2; Hsp105; JNK; p38 MAPK Correspondence T. Hatayama, Department of Biochemistry, Division of Biological Sciences, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyoto 607-8414, Japan Fax: +81 75 595 4758 Tel: +81 75 595 4653 E-mail: hatayama@mb.kyoto-phu.ac.jp (Received 28 April 2008, revised 23 June 2008, accepted 15 July 2008) doi:10.1111/j.1742-4658.2008.06598.x Hsp105a and Hsp105b are major heat shock proteins in mammalian cells that belong to a subgroup of the HSP70 family, HSP105 ⁄ 110. Previously, we have shown that Hsp105a has opposite effects on stress-induced apop- tosis depending on the cell type. However, it is not fully understood how Hsp105 regulates stress-induced apoptosis. In this study, we examined how Hsp105a and Hsp105b regulate H 2 O 2 -induced apoptosis by using HeLa cells in which expression of Hsp105a or Hsp105b was regulated using doxycycline. Overexpression of Hsp105a and Hsp105b suppressed the acti- vation of caspase-3 and caspase-9 by preventing the release of cyto- chrome c from mitochondria in H 2 O 2 -treated cells. Furthermore, both c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) were activated by treatment with H 2 O 2 , and the activation of both kinases was suppressed by overexpression of Hsp105a and Hsp105b. However, H 2 O 2 -induced apoptosis was suppressed by treatment with a potent inhibitor of p38 MAPK, SB202190, but not a JNK inhibitor, SP600125. These findings suggest that Hsp105a and Hsp105b suppress H 2 O 2 -induced apoptosis by suppression of p38 MAPK signaling, one of the essential pathways for apoptosis. Abbreviations DOX, doxycycline; G3DPH, glyceraldehyde 3-phosphate dehydrogenase; Hsps, Heat shock proteins; JNK, c-Jun N-terminal kinase; p38 MAPK, p38 mitogen-activated protein kinase; PARP, ... PHẦN HÓA CHẤT Tên thành phần nguy hiểm Số CAS Công thức hóa học Hàm lượng (%theo trọng lượng) Hydrogen Peroxide 7722-84-1 H2O2 30 – 50% Nước 7732-18-5 H2O 50 – 70% III NHẬN DẠNG ĐẶT TÍNH NGUY HIỂM... TÁC ĐỘNG LÊN NGƯỜI VÀ YÊU CẦU VỀ THIẾT BỊ BẢO VỆ CÁ NHÂN Các giới hạn tiếp xúc Tên thành phần Hydrogen Peroxide Nguồn Loại Ppm ACGIH TWA STEL Mg/m3 Chú giải NIOSH TWA 1,4 Các biện pháp hạn chế tiếp... nguy hiểm: XI THÔNG TIN VỀ ĐỘC TÍNH Tên thành phần Loại ngưỡng Kêt Đường tiếp xúc Sinh vật thử Hydrogen Peroxide LD50 6667ppm Miệng Chuột Các ảnh hưởng mãn tính với người: Khả gây ung thư: Không