You need to write a book! I haven't seen a case of CJD since training... We are extremely cautious about it. However, the current evidence suggests it is not transmissible through most casual contact. You'd have to be exposed to contaminated brain tissue for the most part. But, uhh, remind me not to shake your hand if we ever meet in person!
As for the scleroderma... Horrible stuff... I tried out our medical AI Open Evidence on it... Lots of interesting exposures there which can trigger scleroderma!
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This is a fascinating historical question. A veteran of the
Battle of Verdun (1916) would have been exposed to several chemicals with potential relevance to
scleroderma, though direct evidence linking WWI battlefield exposures specifically to systemic sclerosis is limited.
Relevant Chemical Exposures at Verdun
The Battle of Verdun (February–December 1916) was one of the most intense engagements of WWI. Soldiers there faced multiple hazardous exposures:
- Phosgene (COCl₂) — The predominant chemical warfare agent used at Verdun in 1916. Phosgene was a choking agent causing severe pulmonary injury and was responsible for the majority of chemical warfare deaths in WWI. [1-2]
- Chlorine gas — Used earlier in the war (first deployed at Ypres in 1915) and continued in various combinations. Chlorine is a potent respiratory irritant. [1][3]
- Sulfur mustard — First deployed by Germany in July 1917 at Ypres (after the main Verdun battle), so exposure at Verdun itself is less likely unless the veteran served later in the war as well. Sulfur mustard is an alkylating agent that causes chronic skin, pulmonary, and ocular injury, and notably can produce a sclerodermoid histopathologic pattern in skin biopsies. Long-term survivors of sulfur mustard exposure show significantly elevated autoimmune markers (ANA, anti-dsDNA, RF), suggesting a possible autoimmune-triggering effect, though a large retrospective cohort study of Iranian veterans did not find a significantly increased risk of morphea, DLE, or SLE. [4-6]
- Arsenic — Arsenical shells were extensively used at Verdun, and post-war destruction of 1.5 million chemical shells near Verdun resulted in severe arsenic and heavy metal soil contamination (arsenic concentrations up to 175,907 mg/kg). Arsenic causes immune dysregulation and has been associated with carcinogenesis, though it is not among the heavy metals most strongly linked to SSc (antimony, cadmium, lead, and mercury have the strongest associations). [7-11]
- Heavy metals (lead, zinc, cadmium, copper) — Extremely high concentrations of lead (up to 26,398 mg/kg) and zinc (up to 133,237 mg/kg) were documented in Verdun battlefield soils from munitions residue. Lead and cadmium are among the heavy metals significantly associated with SSc in case-control studies. [7][9-10]
- Silica dust — Trench warfare involved prolonged exposure to soil dust from constant shelling and excavation. Crystalline silica, the strongest known environmental risk factor for SSc, could plausibly have been inhaled during the massive artillery bombardments at Verdun. [12-13]
Synthesis and Plausibility
While there is no direct epidemiological study linking WWI combat exposure to scleroderma, a Verdun veteran would have had biologically plausible exposures to multiple agents associated with SSc risk:
silica dust from trench warfare and artillery bombardment,
heavy metals (particularly lead and cadmium) from munitions, and potentially
organic chemical agents. Sulfur mustard, if encountered later in the war, can induce a sclerodermoid skin pattern and trigger autoimmune markers, though it has not been definitively linked to true SSc. [4-5] The combination of these exposures in a genetically susceptible individual could theoretically contribute to SSc development, consistent with the multifactorial model of SSc pathogenesis. [14-15]
It is worth noting that occupational exposure assessment in SSc patients should be systematic, as many exposures go unrecognized without structured evaluation. [9]
