Susceptibility to sunburns on high n-6 diets:

"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions."
Why is epidermis rich in LA that is unstable and inflammatory under UVB?

How does diet influence lipid composition of skin?
Experience with resistance to sunburns after switching to low n-6 diet is very often, at least in my social bubble. Illustrative story:

http://yelling-stop.blogspot.com/2010/12/my-vitamin-d-experiment.html
Note to self (from previous paper): "Linoleic acid is one of the essential ω-6 fatty acids, which leads to formation of the smooth, non-dry outer epidermal barrier upon dietary intake (Hansen et al., 1958; Gill and Valivety, 1997; Nakamura and Nara, 2003; Ramsden et al., 2017)."
It makes sense to me that upstream metabolites of toxic compounds were evolutionary selected as messengers for pain and inflammation.

https://www.frontiersin.org/files/Articles/473908/fphar-10-01147-HTML/image_m/fphar-10-01147-t001b.jpg
OXLAMs and psoriasis:

Bioactive Lipid Mediator Profiles in Human Psoriasis Skin and Blood

https://pubmed.ncbi.nlm.nih.gov/29454560/ 
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