Step 1: Identify the toxin and clinical picture. A cluster of people drinking contaminated (illicit) alcohol with abdominal pain, confusion and decreased vision, plus a measured methyl alcohol (methanol) level of 20 mg%, is methanol poisoning. The visual loss is the hallmark.
Step 2: Recall the metabolic pathway of methanol. Methanol is oxidised in the liver:
\[\text{Methanol} \xrightarrow{\text{alcohol dehydrogenase}} \text{Formaldehyde} \xrightarrow{\text{aldehyde dehydrogenase}} \text{Formic acid}\]
The toxic end-metabolite is formic acid (formate), which inhibits cytochrome oxidase, damages the optic nerve/retina and produces a severe high-anion-gap metabolic acidosis.
Step 3: Account for the second acid. The accumulating formate impairs mitochondrial respiration; tissue hypoxia and anaerobic glycolysis then generate lactic acid. So both formic acid and lactic acid build up and together drive the high-anion-gap acidosis seen in methanol poisoning. Hence the metabolites detected are formic acid and lactic acid.
Step 4: Eliminate the distractors. Glycolic acid and oxalic acid (B), oxalic acid and formic acid (C) and glyoxylic acid and formic acid (D) all involve glycolic/oxalic/glyoxylic acids - these are products of ETHYLENE GLYCOL metabolism, not methanol. Ethylene glycol is metabolised through glycolaldehyde → glycolic acid → glyoxylic acid → oxalic acid (causing calcium-oxalate crystals and renal failure). Since the toxin here is methanol, oxalic/glycolic/glyoxylic acids do not apply.
Final answer: A - Formic acid & lactic acid.