Proudfoot Alex T
National Poisons Information Service, City Hospital, Birmingham, UK.
Clin Toxicol (Phila). 2009 Feb;47(2):89-100. doi: 10.1080/15563650802520675.
Aluminium and zinc phosphides are highly effective insecticides and rodenticides and are used widely to protect grain in stores and during its transportation. Acute poisoning with these compounds may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine generated during their approved use.
Both forms of poisoning are mediated by phosphine which has been thought to be toxic because it inhibits cytochrome c oxidase. While phosphine does inhibit cytochrome C oxidase in vitro, the inhibition is much less in vivo. It has been shown recently in nematodes that phosphine rapidly perturbs mitochondrial morphology, inhibits oxidative respiration by 70%, and causes a severe drop in mitochondrial membrane potential. This failure of cellular respiration is likely to be due to a mechanism other than inhibition of cytochrome C oxidase. In addition, phosphine and hydrogen peroxide can interact to form the highly reactive hydroxyl radical and phosphine also inhibits catalase and peroxidase; both mechanisms result in hydroxyl radical associated damage such as lipid peroxidation. The major lethal consequence of phosphide ingestion, profound circulatory collapse, is secondary to factors including direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. In addition, phosphine and phosphides have corrosive actions.
There is usually only a short interval between ingestion of phosphides and the appearance of systemic toxicity. Phosphine-induced impairment of myocardial contractility and fluid loss leads to circulatory failure, and critically, pulmonary edema supervenes, though whether this is a cardiogenic or non-cardiogenic is not always clear. Metabolic acidosis, or mixed metabolic acidosis and respiratory alkalosis, and acute renal failure are frequent. Other features include disseminated intravascular coagulation, hepatic necrosis and renal failure. There is conflicting evidence on the occurrence of magnesium disturbances.
There is no antidote to phosphine or metal phosphide poisoning and many patients die despite intensive care. Supportive measures are all that can be offered and should be implemented as required.
磷化铝和磷化锌是高效杀虫剂和灭鼠剂，广泛用于储存和运输过程中的谷物保护。这些化合物的急性中毒可能是由于直接摄入盐类所致，也可能是在其批准使用过程中意外吸入产生的磷化氢间接导致的。
两种中毒形式均由磷化氢介导，人们一直认为磷化氢有毒，因为它会抑制细胞色素c氧化酶。虽然磷化氢在体外确实会抑制细胞色素C氧化酶，但在体内这种抑制作用要小得多。最近在线虫中发现，磷化氢会迅速扰乱线粒体形态，抑制70%的氧化呼吸，并导致线粒体膜电位严重下降。这种细胞呼吸的失败可能是由于细胞色素C氧化酶抑制以外的机制。此外，磷化氢和过氧化氢可以相互作用形成高活性的羟基自由基，磷化氢还会抑制过氧化氢酶和过氧化物酶；这两种机制都会导致与羟基自由基相关的损伤，如脂质过氧化。摄入磷化物的主要致命后果是严重的循环衰竭，这是由包括对心肌细胞的直接影响、液体流失和肾上腺损伤等因素继发的。此外，磷化氢和磷化物具有腐蚀作用。
摄入磷化物与全身毒性出现之间的间隔通常很短。磷化氢引起的心肌收缩力损害和液体流失导致循环衰竭，关键的是会并发肺水肿，不过其是心源性还是非心源性的并不总是很清楚。代谢性酸中毒，或混合性代谢性酸中毒和呼吸性碱中毒，以及急性肾衰竭很常见。其他特征包括弥散性血管内凝血、肝坏死和肾衰竭。关于镁紊乱的发生存在相互矛盾的证据。
对于磷化氢或金属磷化物中毒没有解毒剂，许多患者尽管接受了重症监护仍死亡。所能提供的只有支持性措施，应根据需要实施。
