Lindane in soil can leach to surface and even ground water, and can bioaccumulate in the food chain. However, biotransformation and elimination are relatively rapid when exposure is discontinued. Most exposure of the general population to lindane has resulted from agricultural uses and the intake of foods, such as produce, meats, and milk, produced from treated agricultural commodities. Human exposure has decreased significantly since the cancellation of agricultural uses in 2006. Even so, the CDC published in 2005 its Third National Report on Human Exposures to Environmental Chemicals, which found no detectable amounts of lindane in human blood taken from a random sampling of about 5,000 people in the US as part of the NHANES study (National Health and Nutrition Examination Survey at: https://www.cdc.gov/nchs/nhanes/about_nhanes.htm). The lack of detection of lindane in this large human "biomonitoring" study likely reflects the increasingly limited agricultural uses of lindane over the last two decades. The cancellation of agricultural uses in the United States will further reduce the amount of lindane introduced into the environment by more than 99%.Over time, lindane is broken down in soil, sediment, and water into less harmful substances by algae, fungi, and bacteria; however, the process is relatively slow and dependent on ambient environmental conditions. Lindane residues in honey and beeswax are reported to be the highest of any historical or current pesticide and to continue to pose a threat to honeybee health. The ecological impact of lindanes environmental persistence continues to be debated.
Injury to the brain occurs when neurons that require high amounts of energy from thiamine dependent enzymes are not supplied with enough energy and die.Brain atrophy associated with WKS occurs in the following regions of the brain: 

the mammillary bodies,
the thalamus,
the periaqueductal grey,
the walls of the 3rd ventricle,
the floor of the 4th ventricle,
the cerebellum, and
the frontal lobe.In addition to the damage seen in these areas there have been reports of damage to cortex, although it was noted that this may be due to the direct toxic effects of alcohol as opposed to thiamine deficiency that has been attributed as the underlying cause of Wernicke-Korsakoff Syndrome.The amnesia that is associated with this syndrome is a result of the atrophy in the structures of the diencephalon (the thalamus, hypothalamus and mammillary bodies), and is similar to amnesia that is presented as a result of other cases of damage to the medial temporal lobe. It has been argued that the memory impairments can occur as a result of damage along any part of the mammillo-thalamic tract, which explains how WKS can develop in patients with damage exclusively to either the thalamus or the mammillary bodies. Diagnosis
Diagnosis of Wernicke–Korsakoff syndrome is by clinical impression and can sometimes be confirmed by a formal neuropsychological assessment. Wernicke encephalopathy typically presents with ataxia and nystagmus, and Korsakoffs psychosis with anterograde and retrograde amnesia and confabulation upon relevant lines of questioning.Frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in Wernicke encephalopathy, patients will have marked degeneration of the mammillary bodies.