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A few posts back, I noted the irony of growing up in Belgium, discovering horror for the first time, and reading Stephen King’s short story “The Mist” in a country where the fog is so thick, it’s infamous, requiering legislatively mandated special lights for both cars and roads. There was also tales of a toxic fog that, throughout history, would hit Belgium. The 1930 time article I cited also stated, that:

Experts of the French Army were busy last week at Lille (80 mi. from the stricken Meuse Valley) producing enormous clouds of what they called “a cheap, harmless artificial fog made from chalk, sulphuric acid and tar products which will be extremely useful to hide the movements of troops in war time.”

Well, there’s a technical paper out there that sort of builds on the idea of mass chemical poisoning, but doesn’t necessarily blame the French:

There is no doubt as to the connection between the activity of the factories and the disaster. If I draw attention to this somewhat unusual matter, it is because today we know more about a certain intoxication than was known in 1930. Naturally, it is not possible to give an explanation of the disaster, which is beyond discussion. The event is a thing of the past, and there is no chance of making direct observations. To me, however, it is quite probable that the affection from which these people suffered was an acute intoxication by gaseous fluorine compounds emanating from certain factories in the region concerned. That idea has been advanced before, by Storm van Leeuwen (4), Gram (5) and Fenner (6, 7), but without sufficient grounds to make it acceptable or even generally known. The Commission of Investigation also looked into the question of fluorine intoxication, but without crediting it with more than secondary and at the most doubtful importance. I am in a position, however, to put on record a number of new or hitherto neglected factors.

The author goes into great length about the history of the “outbreak” (for lack of a better term), and then goes onto to get into the specifics about flouride poisoning:

The symptoms of intoxication are partly local from the gastro-intestinal tract (vomiting, often sanguinolent, abdominal pains, diarrhea), partly due to absorption: alternate painful spasms and pareses, weakness, thirst, excessive salivation and perspiration. Death usually occurs in a few hours with increasing dyspnea and failing pulse. The face may be pale or cyanotic. Apart from corrosion in the gastro-intestinal tract, the post mortem findings are often small. Microscopic examination may reveal more or less pronounced degeneration phenomena in the parenchymatous organs (particularly liver and kidneys).

Perhaps another interesting note is a historical paralell the author notes:

Where plants in the neighborhood of a factory are corroded by fluoric gases, it happens that secondary, osteomalacia-like diseases occur among herbivorants grazing there. The symptoms are emaciation until cachexia sets in, stiff, laborious gait, possibly muscular restlessness and spasms, nodose thickenings of the extremity bones especially, and frequent spontaneous fractures. In the following instances this secondary, chronic fluorine intoxication of cattle has been involved, only the first case being a little doubtful:

1878 Germany, zinc works (38),
1912 Italy, superphosphate works (39),
1911-18 Switzerland, aluminium factory (32),
1928 France, superphosphate works (40),
1931 Germany, chemical works (31),
1931 Germany, superphosphate works (31),
1934 Norway, aluminium factory (27), and
1935 Italy, aluminiuin. factory (33)

A very similar disease may break out after volcanic eruptions.

But, ultimately, there’s the author’s conclusions to consider:

In the signs of intoxication there is no indication that it may not have been an acute fluorine intoxication, but much in favor of that assumption.

And then, the author moves on to other possibilities, but reinforces the fluorine plausibility in the final summary:

After a survey of acute and chronic fluorine intoxication, an analysis of the details of the disaster gives circumstantial evidence that the malady was acute fluorine intoxication. Of the 27 factories in the region, fifteen are industrial branches which either use raw products containing fluorine (superphosphate works, zinc works) or add fluorine compounds to the raw materials (steel works, iron foundries, glass works), involving the possibility of passing gasseous fluorine compounds (SiF4, HF) into the chimney smoke. Special climatic and topographic conditions played an important role in the development of the disaster. The toxicity of fluorine compounds is considerable, and little known in industry. Factories giving off gaseous fluorine compounds should be required to take measures for their effective removal from chimney smoke.


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