The UK has the highest incidence in the world of poisonings caused by the toxins produced by E.coli O157:H7. It killed 17 people in the outbreak centred on Wishaw in central Scotland in 1996, still a world record for lethality. My involvement in attempts to stop a repeat led to an invitation to visit the Defence Science and Technology Laboratory at Porton Down. Security was impressive. The heavily armed welcome at the gate left an abiding memory. It is reasonable to guess that the Russian chemical warfare facility at Shikhany is as well guarded. The notion that nasty substances of high purity could leave it without some kind of authorisation seems highly unlikely.

The precise chemical name of the agent that was used in Salisbury on 4 March hasn’t yet been publicly disclosed. Without doubt the initial symptoms and laboratory test results on the victims gave very strong clues about its nature, and techniques such as mass spectroscopy went on to give a precise identification. The Organisation for the Prohibition of Chemical Weapons yesterday confirmed Porton Down’s findings.

The OPCW note mentions receiving information about the acetylcholinesterase status of the three affected individuals. Acetylcholinesterase plays an essential role in the control of muscles by nerves. Its action is blocked by classical nerve agents of the sarin, tabun and VX family. It seems likely that the poison deployed in Salisbury was related to these, possibly developed as a tool for assassins rather than for military use – a murder weapon as novel as the ricin in the pellet shot from an umbrella on Waterloo Bridge into Georgi Markov in 1978, or the polonium that was put in Alexander Litvinenko’s tea in 2006.

The Skripals are on the mend. This is not unprecedented. A person in Malaysia with puffer fish poisoning who developed fixed dilated pupils and brain stem areflexia – the cardinal features of brain death – made a complete recovery after being mechanically ventilated. The puffer fish toxin is tetrodotoxin, one of the most potent non-protein poisons known. It attacks nerves and the heart by blocking sodium ion channels. Recovery depends on growing new ones. Recovery from classical nerve agent poisoning is similar; it happens when the victim makes new acetylcholinesterase molecules to replace the ones to which the nerve agent has irreversibly attached itself.

I recently spoke at a food science conference in Chile. I walked every day to the Santiago Metro past the Escuela Militar del Libertador Bernardo O’Higgins. The Pinochet junta was sworn in there. The junta soon established its secret police – the Dirección de Inteligencia Nacional – which not only ran the notorious Villa Grimaldi torture centre, but organised the assassination of exiles abroad: General Carlos Prats (Pinochet’s predecessor as army commander in chief) and his wife, killed by a car bomb in Buenos Aires; the Christian Democrat politician Bernardo Leighton, shot in Rome (he survived); Orlando Letelier, killed by a car bomb outside the Chilean embassy in Washington DC, where he had been ambassador in the Allende era.

It seems highly unlikely that Sergei Skripal was considered to be a personal threat to the continued existence of the Russian regime. But it could have been a mistake on his part to live in Salisbury. The city’s proximity to Porton may well have pointed to the kind of poison to use against him. And in case of failure it would provide a useful way to muddy the waters. It is reasonable to speculate that the assassination attempt was designed to kill Skripal very quickly; the sudden death of a 66-year-old diabetic who had spent four years in a Russian prison would not be medically suspicious. But the attempt was botched. The method of delivery of the poison, environmental contamination, delivered only a sub-lethal dose.