Pancreatic smoking dose-response

Tobacco exposure raises pancreatic-cancer risk monotonically in pack-years, anchored to RR≈1.91 at 50 pack-years. The same barrier-lowering kernel, with one calibrated slope, reproduces RR rising from 1.00 to 1.30 at twenty and 1.91 at fifty pack-years, passing through the current-smoker range near thirty. The anchor is cited [L]; shape verified [V]; absolute incidence open [O].

Tobacco nitrosamines and PAHs bias the pancreatic-cell fate switch. One calibrated slope reproduces RR from 1.00 to 1.91 across 0–50 pack-years, with RR near 1.48 at 30 pack-years consistent with cited current-smoker estimates (~1.74). Anchor [L], shape [V], absolute incidence [O].

Tobacco exposure raises pancreatic-cancer risk monotonically in pack-years, anchored to RR ≈ 1.91 at 50 pack-years (Multiethnic Cohort). The same barrier-lowering kernel, with one calibrated slope, reproduces the full curve and passes through the current-smoker range near thirty pack-years.

Tobacco nitrosamines and polycyclic aromatic hydrocarbons supply the sustained bias on the pancreatic-cell fate switch. At 30 pack-years the kernel gives RR = 1.48, consistent with the cited current-smoker estimates (~1.74, Iodice 2008).

The anchor is cited [L]; the shape is verified [V]; absolute incidence is open [O]. The monotone rise from 1.00 to 1.91 uses a single slope calibrated to one anchor, so the intermediate pack-year risks are predictions rather than fitted points.