As I said, it depend entirely on the products in question as well as the market. Aluminum is valuable enough to more than pay for salvaging costs for most products that contain a meaningful amount.

Glass meanwhile is currently not cost-effective because the value of salvaged glass has recently fallen below the salvaging cost, even though glass recycling was quite cost-effective in the past. The market is just as important as anything else here.

Solar panels are not cost effective at all to salvage as their components are not particularly valuable but are quite costly to salvage from the panels. Thus they are piling up in landfills wherever there are no regulations that require proper recycling.

You could ask this about most products with salvageable materials, but you'd be surprised how often the answer is that the former option is cheaper.

It's a matter of the cost of the salvaging process compared to the value of salvaged materials, versus the cost-value from fresh mining.

Lolwut? You think Philadelphia is less corrupt than Harrisburg?

It's is literally one of the most corrupt cities in the country, ranking #7 on the number of corruption convictions alone which is an objective metric.

https://www.forbes.com/sites/niallmccarthy/2019/02/15/where-corruption-is-rampant-in-american-cities-infographic/?sh=47429300118b

https://www.vice.com/en/article/jp3vak/is-philadelphia-the-most-corrupt-city-in-america

https://6abc.com/pennsylvania-news-philadelphia-politics-corruption-chaka-fattah/2164642/

Ah I see you're a man of culture as well. I usually add a little meat to my habanero sandwich for some protein though, and ghost pepper cheese. Dairy emulsifies the capsaicin nicely

Always happy to share my thoughts on neurobiology. Let me know if you learn anything interesting

Abstract:

>Neuroepithelial crosstalk is critical for gut physiology. However, the mechanisms by which sensory neurons communicate with epithelial cells to mediate gut barrier protection at homeostasis and during inflammation are not well understood. Here, we find that Nav1.8+CGRP+ nociceptor neurons are juxtaposed with and signal to intestinal goblet cells to drive mucus secretion and gut protection. Nociceptor ablation led to decreased mucus thickness and dysbiosis, while chemogenetic nociceptor activation or capsaicin treatment induced mucus growth. Mouse and human goblet cells expressed Ramp1, receptor for the neuropeptide CGRP. Nociceptors signal via the CGRP-Ramp1 pathway to induce rapid goblet cell emptying and mucus secretion. Notably, commensal microbes activated nociceptors to control homeostatic CGRP release. In the absence of nociceptors or epithelial Ramp1, mice showed increased epithelial stress and susceptibility to colitis. Conversely, CGRP administration protected nociceptor-ablated mice against colitis. Our findings demonstrate a neuron-goblet cell axis that orchestrates gut mucosal barrier protection.

Capsaicin produced the effect, though not directly on the TRPV1 (aka "capsaicin/vanilloid receptor"). But this suggests that TRPV1 is likely the "nociceptor" being described here, and CGRP is produced downstream which then mediates the rest of the effect (likely including pain)

CGRP is believed to be the major downstream mediator of migraines, as CGRP inhibitors (receptor antagonists) tend to provide faster relief of symptoms than 5-HT1B / 5-HT1D agonists like the tryprans which reduce CGRP production but don't block the already existing CGRP from their receptors. Whether or not CGRP from the gut can contribute to migraine would be an interesting subject for future study, as gut problems are known to be fairly comorbid with headaches