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磷化铝 | 20859-73-8

中文名称
磷化铝
中文别名
好达胜;磷毒
英文名称
alumanylidynephosphane
英文别名
Aluminum phosphide
磷化铝化学式
CAS
20859-73-8
化学式
AlP
mdl
——
分子量
57.9553
InChiKey
PPNXXZIBFHTHDM-UHFFFAOYSA-N
BEILSTEIN
——
EINECS
——
  • 物化性质
  • 计算性质
  • ADMET
  • 安全信息
  • SDS
  • 制备方法与用途
  • 上下游信息
  • 反应信息
  • 文献信息
  • 表征谱图
  • 同类化合物
  • 相关功能分类
  • 相关结构分类

物化性质

  • 熔点:
    2000℃
  • 密度:
    2.42
  • 溶解度:
    与H2O反应
  • 物理描述:
    Aluminum phosphide is a dark gray or dry, yellow, crystalline solid. It reacts with moisture to give phosphine, a flammable and poisonous gas. Normally, phosphine will spontaneously ignite upon contact with air. If there is an excess of water, the phosphine fire will not normally ignite any surrounding combustible material.
  • 颜色/状态:
    Dark gray or dark yellow crystals. Cubic zinc blende structure.
  • 气味:
    Garlic odor
  • 蒸汽压力:
    Very low, even at 1000 °C
  • 稳定性/保质期:
    1. 磷化铝是一种高毒杀虫剂。在干燥条件下,磷化铝对人畜相对安全。但其遇水或吸潮会自行分解释放出磷化氢气体,而磷化氢有毒性。当空气中含量达到0.01mg/L时,人体会感到危险;含量增至0.14mg/L时可能导致呼吸困难乃至死亡。德国规定最大允许浓度为0.1mg/m³,美国则为0.3mg/m³。吸入磷化氢气体可引起头晕、头痛、恶心、乏力等症状,并可能进一步导致中毒性精神症状、脑水肿、肺水肿以及肝、肾和心肌损害等严重后果。口服磷化铝同样会产生磷化氢中毒。 2. 磷化铝的稳定性较好。 3. 磷化铝应避免与氧化剂及酸类物质接触,以防发生危险反应。 4. 避免将磷化铝暴露在潮湿空气中。 5. 磷化铝不会发生聚合反应。
  • 分解:
    When heated to decomposition it emits toxic /phosphorus oxides/.

计算性质

  • 辛醇/水分配系数(LogP):
    0.48
  • 重原子数:
    2
  • 可旋转键数:
    0
  • 环数:
    0.0
  • sp3杂化的碳原子比例:
    0.0
  • 拓扑面积:
    0
  • 氢给体数:
    0
  • 氢受体数:
    0

ADMET

代谢
铝通过口服或吸入暴露的吸收情况很差,并且基本上不会通过皮肤吸收。铝的生物利用度受到铝化合物和饮食成分的强烈影响,这些成分可以与铝形成复合物,增强或抑制其吸收。铝在血液中与各种配体结合并分布到每个器官,其中在骨骼和肺组织中的浓度最高。在生物体内,铝被认为存在四种不同的形式:作为自由离子,作为低分子量复合物,作为物理结合的大分子复合物,以及作为共价结合的大分子复合物。吸收的铝主要通过尿液排出,其次是在胆汁中,而未吸收的铝则通过粪便排出。磷化氢和金属磷化物可能在摄入或吸入后被吸收,然后分布到神经系统、肝脏和肾脏。在体内,金属磷化物被水解为磷化氢,磷化氢被氧化为次磷酸盐和磷酸盐。代谢物通过尿液排出,而未改变的磷化氢则通过呼吸排出。(L982, L739)
Aluminum is poorly absorbed following either oral or inhalation exposure and is essentially not absorbed dermally. The bioavailability of aluminum is strongly influenced by the aluminum compound and the presence of dietary constituents which can complex with aluminum and enhance or inhibit its absorption. Aluminum binds to various ligands in the blood and distributes to every organ, with highest concentrations found in bone and lung tissues. In living organisms, aluminum is believed to exist in four different forms: as free ions, as low-molecular-weight complexes, as physically bound macromolecular complexes, and as covalently bound macromolecular complexes. Absorbed aluminum is excreted principally in the urine and, to a lesser extent, in the bile, while unabsorbed aluminum is excreted in the faeces. Phosphine and metal phosphides may be absorbed following ingestion or inhalation, then distribute to the nervous system, liver, and kidney. In the body, metal phosphides are hydrolysed to phosphine, and phosphine is oxidized to hypophosphite and phosphite. Metabolites are excreted in the urine, while unchanged phosphine is exhaled. (L982, L739)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
  • 毒性总结
识别和使用:磷化铝形成绿色或黄色立方晶体,具有大蒜气味。它被用作储粮的熏蒸剂、杀鼠剂和杀虫剂;用于控制挖掘啮齿动物的熏蒸剂。人体研究:195名摄入磷化铝的患者被送往医院。在195名患者中,有115人死亡。非幸存者的低血压和代谢性酸中毒比幸存者更严重,幸存者呕吐更严重。对115名受试者进行的尸检显示肝脏、脾脏、肾脏、肾上腺、胃肠和大脑充血,这与低血压的严重程度相关。摄入磷化铝极具毒性,致死剂量低至1.5克。主要临床特征是对多巴胺无反应的严重低血压。与轻度至中度毒性的患者相比,重度毒性患者的血清镁显著升高。在代谢激活剂存在的情况下,磷化铝在培养的人血液细胞中诱导了遗传毒性效应,如姐妹染色单体交换(SCE)和染色体畸变(CA)。动物研究:广泛用作熏蒸剂和杀鼠剂的磷化铝,如果摄入,会导致高死亡率。其毒性是由于与水分接触时释放的磷化氢。大鼠的毒性似乎是由于能量不足和氧化应激的共同结果,可能与组织细胞色素的优先相互作用。在大鼠中,磷化铝对心脏的有害作用是通过心肌细胞代谢下降以及心肌组织的坏死导致活性氧中间体的释放来介导的。在一项为期两年的大鼠喂养研究中没有看到致癌性的证据。磷化铝在大鼠中诱导了遗传和氧化损伤。染色体的畸变(CAs)和微核(MN)试验用于监测遗传毒性损伤。磷化铝增加了CA和MN试验的速率。生态毒性研究:铝和镁磷化物的一种使用模式,作为洞穴熏蒸剂,对受威胁和濒危的哺乳动物和爬行动物构成了风险。如果这些物种在熏蒸的洞穴中被发现,它们将面临风险。由于磷化氢气体的高度毒性,处理过的洞穴中的所有动物都将被杀死。1981年,美国鱼类和野生动物服务确定,使用铝和镁磷化物作为洞穴熏蒸剂可能会危及黑足鼬、犹他草原犬、圣华金山狐、扁平鼻豹蜥、东部靛蓝蛇和沙漠龟。
IDENTIFICATION AND USE: Aluminum phosphide forms green or yellow cubic crystals with a garlic odor. It is used as fumigant, rodenticide, and insecticide for stored cereal grains; fumigant for control of burrowing rodents. HUMAN STUDIES: 195 patients with aluminum phosphide ingestion were admitted to hospital. Of 195 patients, 115 died. The nonsurvivors had more severe hypotension and metabolic acidosis than the survivors who had more severe vomiting. Autopsies conducted in 115 subjects revealed congestion of liver, spleen, kidneys, adrenals, gastrointestinal tract and brain that correlated with the severity of hypotension. Aluminum phosphide when ingested is highly toxic with fatal dose as low as 1.5 g. The dominant clinical feature is severe hypotension refractory to dopamine. There was a significantly greater rise in serum magnesium in patients with severe toxicity compared to patients with mild to moderate toxicity. Aluminum phosphide induced genotoxic effects such as sister chromatid exchange (SCE) and chromosome aberration (CA) in cultured human blood cells in the presence of a metabolic activator. ANIMAL STUDIES: Aluminum phosphide, a widely used fumigant and rodenticide leads to high mortality if ingested. Its toxicity is due to phosphine liberated when it comes in contact with moisture. Toxicity in rats appears to result as a consequence of both-energy insufficiency and oxidative stress, with a possible and preferential interaction with the tissue cytochromes. In rats, the deleterious effect of aluminum phosphide on heart is mediated by both declined cellular metabolism of the myocardium as well as by necrosis of the cardiac tissue resulting in the release of reactive oxygen intermediates. In a two-year rat feeding study no evidence of carcinogenicity was seen. Aluminum phosphide induced genetic and oxidative damages in rats. Chromosomal aberrations (CAs) and micronucleus (MN) assay were used for monitoring genotoxic damage. Aluminium phosphide caused increase in CA and MN assay rates. ECOTOXICITY STUDIES: One use pattern of aluminum and magnesium phosphide, as a burrow fumigant, poses a risk to threatened and endangered species of mammals and reptiles. The risks posed to these species occur if they are found in a burrow that is fumigated. Because of the high degree of toxicity of phosphine gas, all animals in a treated burrow will be killed. In 1981, the United States Fish and Wildlife Service determined that use of aluminum and magnesium phosphide as a burrow fumigant may jeopardize the black-footed ferret, the Utah prairie dog, the San Joaquin kit fox, the blunt-nosed leopard lizard, the eastern indigo snake, and the desert tortoise.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 毒性总结
铝的主要靶器官是中枢神经系统和骨骼。铝与饮食中的磷结合,并影响胃肠道对磷的吸收。体内磷负荷的降低会导致骨软化(由于骨骼矿化缺陷导致的骨质疏松)和佝偻病。铝的神经毒性被认为涉及多种机制。细胞骨架蛋白功能的改变,如磷酸化、蛋白水解、运输和合成的改变,被认为是其中一个原因。铝可能通过影响血脑屏障的通透性、胆碱能活性、信号转导途径、脂质过氧化以及损害神经元谷氨酸一氧化氮-环磷酸鸟苷酸途径,以及由于类似的配位化学性质和随后的竞争性相互作用而干扰必需微量元素的代谢,从而诱导神经行为效应。有人提出铝与雌激素受体的相互作用增加了雌激素相关基因的表达,从而促进了乳腺癌的进展(A235),但研究未能建立铝与乳腺癌风险增加之间的明确联系(A15468)。某些铝盐通过激活炎症小体来诱导免疫反应。磷化氢抑制细胞色素c氧化酶,阻止线粒体的氧化磷酸化。这种非竞争性抑制阻止了细胞呼吸,导致多器官功能障碍。磷化氢还可以与过氧化氢反应形成高度反应性的羟基自由基,这可能导致脂质过氧化。(A291、A292、L739、A235、A236)
The main target organs of aluminum are the central nervous system and bone. Aluminum binds with dietary phosphorus and impairs gastrointestinal absorption of phosphorus. The decreased phosphate body burden results in osteomalacia (softening of the bones due to defective bone mineralization) and rickets. Aluminum's neurotoxicity is believed to involve several mechanisms. Changes in cytoskeletal protein functions as a results of altered phosphorylation, proteolysis, transport, and synthesis are believed to be one cause. Aluminum may induce neurobehavioral effects by affecting permeability of the blood-brain barrier, cholinergic activity, signal transduction pathways, lipid peroxidation, and impair neuronal glutamate nitric oxide-cyclic GMP pathway, as well as interfere with metabolism of essential trace elements because of similar coordination chemistries and consequent competitive interactions. It has been suggested that aluminum's interaction with estrogen receptors increases the expression of estrogen-related genes and thereby contributes to the progression of breast cancer (A235), but studies have not been able to establish a clear link between aluminum and increased risk of breast cancer (A15468). Certain aluminum salts induce immune responses by activating inflammasomes. Phosphine inhibits cytochrome c oxidase, preventing mitochondrial oxidative phosphorylation. This non-competitive inhibition prevents cellular respiration and leads to multi-organ dysfunction. Phosphine can also react with hydrogen peroxide to form the highly reactive hydroxyl radical, which can cause lipid peroxidation. (A291, A292, L739, A235, A236)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
  • 致癌性证据
A4;不可归类为人类致癌物。/铝金属和难溶化合物/
A4; Not classifiable as a human carcinogen. /Aluminum metal and insoluble compounds/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌物分类
未列入国际癌症研究机构(IARC)名录。国际癌症研究机构将铝生产归类为对人类致癌(第1组),但并未将铝本身视为人类致癌物。(L135)有人提出铝制止汗剂的使用与乳腺癌风险增加之间存在关联(A235),但研究并未能确立明确的联系(A15468)。
Not listed by IARC. IARC classified aluminum production as carcinogenic to humans (Group 1), but did not implicate aluminum itself as a human carcinogen. (L135) A link between use of aluminum-containing antiperspirants and increased risk of breast cancer has been proposed (A235), but studies have not been able to establish a clear link (A15468).
来源:Toxin and Toxin Target Database (T3DB)
毒理性
  • 健康影响
铝针对神经系统,导致神经系统性能下降,并与血脑屏障功能改变有关。体内铝的积累可能导致骨骼或脑部疾病。高水平的铝与阿尔茨海默病有关。少数人对铝过敏,接触或摄入含铝产品后会出现接触性皮炎、消化系统紊乱、呕吐或其他症状。吸入磷化氢可能导致严重的肺部刺激,进而引起急性肺水肿、心血管功能障碍、中枢神经系统兴奋、昏迷和死亡。还可能出现胃肠道紊乱、肾脏损害和白细胞减少。长期暴露于磷化氢可能导致贫血、支气管炎、胃肠道影响以及视觉、言语和运动问题。
Aluminum targets the nervous system and causes decreased nervous system performance and is associated with altered function of the blood-brain barrier. The accumulation of aluminum in the body may cause bone or brain diseases. High levels of aluminum have been linked to Alzheimer's disease. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. Inhalation of phosphine may cause severe pulmonary irritation leading to acute pulmonary oedema, cardiovascular dysfunction, CNS excitation, coma and death. Gastrointestinal disorders, renal damage and leukopenia may also occur. Chronic exposure to phosphine can result in anemia, bronchitis, gastrointestinal effects, and visual, speech and motor problems. (L980, L982, L739, L740)
来源:Toxin and Toxin Target Database (T3DB)
吸收、分配和排泄
实验中,它的水解产物一致地导致了严重的系统性中毒,这是由于在胃酸和/或呼吸湿气中水解成磷化氢后形成磷化氢的结果。
Experimentally, its hydrolysis product has consistently produced severe systemic intoxications as a consequence of phosphine formation subsequent to hydrolysis to phosphine in gastric acid an/or respiratory moisture.
来源:Hazardous Substances Data Bank (HSDB)

安全信息

  • 危险等级:
    4.3
  • 危险品标志:
    T+,F,N
  • 安全说明:
    S3/9/14,S30,S36/37,S45,S61
  • 危险类别码:
    R15/29
  • 危险品运输编号:
    1397
  • RTECS号:
    BD1400000
  • 海关编码:
    2848000010
  • 包装等级:
    I
  • 危险类别:
    4.3
  • 储存条件:
    储存时应注意以下事项:存放在阴凉、干燥且通风良好的专用库房内,库温不超过32℃,相对湿度控制在75%以内。远离火源和热源。包装需密封,避免与空气接触。应将储存物与其他氧化剂、酸类及食用化学品分开存放,禁止混合储存。储区应配备适当的材料以收集泄漏物品。

SDS

SDS:be93fe94a8a09d6f4523aa987f004955
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第一部分:化学品名称

制备方法与用途

磷化铝是一种常用的熏蒸杀虫剂,广泛用于粮食和仓库害虫的防治。以下是关于磷化铝的一些关键信息:

主要特点
  • 用途:主要用于粮仓、仓库等场所的熏蒸杀虫。
  • 毒性分级:剧毒。
化学性质与生产方法
  • 化学性质
    • 浅黄色或灰绿色正方结晶粉末,无气味。
    • 微溶于冷水,溶于乙醇和乙醚。
  • 生产方法
    • 合成法:将赤磷和铝粉按配料比均匀混合后点火燃烧,反应生成磷化铝。反应物经粉碎后加入缓释剂氨基甲酸铵和黏结剂,混合后压片。
化学反应方程式

[ \text{Pa} + 4\text{Al} \rightarrow 4\text{AlP} ]

主要用途
  • 粮食熏蒸:用量为10~30 g/t粮。
  • 仓库熏蒸:一般用量为1~4片/m³。
安全注意事项
  • 生产过程需完全密闭,通风良好。
  • 使用时佩戴防毒面具、橡胶手套等个人防护装备。
  • 避免与酸接触,库房应通风低温干燥并分开存放。
  • 库内施药后需密封3~5天。
中毒治疗

中毒者入院后,立即清洗全身皮肤、更换衣服,并吸氧。忌用解磷定、氯磷定治疗。

毒性

毒性极高,吸入或口服均可导致严重中毒症状如胸骨后疼痛、上腹部痛、全身发热烧灼感等。

急性毒性
  • 人:TDL0: 21毫克/公斤
  • 大鼠:TDL0: 10毫克/公斤
灭火剂与职业标准
  • 灭火剂:干砂、干粉。
  • 职业暴露限值:TLV-TWA 2 毫克/立方米;TWA 2 毫克/立方米。
注意事项
  • 气温在12℃~15℃时,应密闭5天;
  • 16℃~20℃时,应密闭4天;
  • 20℃以上时应密闭3天。
  • 开启盛装磷化铝药片的铁筒最好在室外通风处进行,并要戴防毒面具或防毒口罩和橡皮手套。

反应信息

  • 作为产物:
    描述:
    2-己酮 、 ammonium acetate 、 苯甲醛溶剂黄146 作用下, 生成 磷化铝
    参考文献:
    名称:
    Baliah; Govindarajan, Current Science, 1954, vol. 23, p. 91
    摘要:
    DOI:
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文献信息

  • Baliah; Govindarajan, Current Science, 1954, vol. 23, p. 91
    作者:Baliah、Govindarajan
    DOI:——
    日期:——
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