From the Guidelines

Acetaminophen does not exhibit dose-dependent pharmacokinetics due to prolonged absorption or excretion.

The provided evidence does not support the notion that acetaminophen exhibits dose-dependent pharmacokinetics due to prolonged absorption or excretion 1.
Acetaminophen is a dose-related toxin, and most ingestions leading to acute liver failure (ALF) exceed 10 gm/day, but severe liver injury can occur rarely when doses as low as 3-4 gm/day are taken 1.
The standard acetaminophen toxicity nomogram may aid in determining the likelihood of serious liver damage, but cannot be used to exclude possible toxicity due to multiple doses over time, or altered metabolism in the alcoholic or fasting patient 1.
Observational studies have reported a dose–response relationship between paracetamol at standard analgesic doses and adverse events (AEs) such as mortality, cardiovascular, gastrointestinal (GI), and renal AEs in the general adult population 1.
However, the evidence for dose-dependent pharmacokinetics is limited, and the relationship between acetaminophen dose and pharmacokinetics is not well established in the provided studies.

The half-life of acetaminophen is increased several folds in patients with liver cirrhosis compared to that in healthy individuals 1.
A daily dose of 2–3 g of acetaminophen is generally recommended, as patients with liver cirrhosis are at risk of metabolic disorder and prolonged half-life of acetaminophen 1.
The dose of acetaminophen should be limited to ≤325 mg per dosage unit (tablet, capsule) in order to reduce liver damage induced by acetaminophen when other analgesics are added as a fixed dose combination 1.

From the FDA Drug Label

The FDA drug label does not answer the question.

The absorption of acetaminophen is rapid and complete, with a mean systemic availability of about 75% 2
The rate of absorption depends on the rate of gastric emptying, which can be affected by factors such as food, other medications, and surgery 3, 4
Acetaminophen is extensively metabolized, with a plasma half-life of 1.5-2.5 hours, and is excreted in the urine as glucuronide, sulphate, mercapturic acid, and cysteine conjugates 3, 2

The systemic bioavailability of acetaminophen is dose-dependent, ranging from 70 to 90% 3
Large doses of acetaminophen can cause saturation of sulphate conjugation, leading to an increase in the proportion of the dose excreted as mercapturic acid and cysteine conjugates 2
Prolonged absorption and delayed peak paracetamol concentration can occur with extended-release formulations, requiring extended treatment with intravenous N-acetylcysteine 5

Clinical factors such as diet, concomitant medication, surgery, pregnancy, and others can affect the absorption of acetaminophen or the rate of gastric emptying 4
The absorption of oral acetaminophen occurs primarily along the small intestine by passive diffusion, with the rate-limiting step being the rate of gastric emptying into the intestines 4