They are produced by the dendritic, octopus-like melanocytes, seen between the epithelial cells situated closest to the epithelium/connective tissue border.In tobacco-users the melanocytes are stimulated to produce melanin granules and to distribute them out to the surrounding epithelial cells for further transport to the mucosal surface, like the mechanism in melanin-pigmented skin. Small amounts of melanin-like granules together with other electron-dense particles can also be seen within large melanosome complexes in the underlying connective tissue. If the granules derive from the epithelium,  a phenomenon known as melanin incontinence, is not known. In Caucasians these granules are not expected to influence on the clinically observed degree of smokers melanosis. Causes
Smoking or the use of nicotine-containing drugs is the cause to Smokers melanosis,. Also tar-components (benzopyrenes) are known to stimulate melanocytes to melanin production, and other unknown toxic agents in tobacco may also be the cause. These chemical agents have a polycyclic, chain-like structure. Environmental tobacco smoke from parents is causing smokers melanosis in their children    Swedish snuff causes a small elevation of oral melanin pigmented individuals from 3.0% to 4.7%. Nicotine tablets have shown to stimulate to melanin pigmentation of the oral mucosa. Treatment and prognosis
Lesions usually disappear between 3 months to 3 years for those who stop smoking. Smokers melanosis is a benign, normal physiological reaction, and does not develop into cancer. If it does not disappear, however, a biopsy can verify the diagnosis.
Symptoms
The most common symptoms of acquired and transient cortical blindness include:

A complete loss of visual sensation and of vision
Preservation/sparing of the abilities to perceive light and/or moving, but not static objects (Riddoch syndrome)
A lack of visual fixation and tracking 
Denial of visual loss (Anton–Babinski syndrome)
Visual hallucinations 
Macular sparing, in which vision in the fovea is spared from the blindness. Causes
The most common cause of cortical blindness is ischemia (oxygen deprivation) to the occipital lobes caused by blockage to one or both of the posterior cerebral arteries. However, other conditions have also been known to cause acquired and transient cortical blindness, including:

Congenital abnormalities of the occipital lobe
Head trauma to the occipital lobe of the brain
Bilateral lesions of the primary visual cortex
Infection
Creutzfeldt–Jakob disease (CJD), in association with a rapid onset of dementia
rarely Dissociative identity disorder (DID)
Side effect of some anti-epilepsy drugs (AEDs)
Hyperammonemia
Eclampsia and, rarely, pre-eclampsiaThe most common causes of congenital cortical blindness are:

Traumatic brain injury (TBI) to the occipital lobe of the brain
Congenital abnormalities of the occipital lobe
Perinatal ischemia
Encephalitis
Meningitis

Diagnosis
A patient with cortical blindness has no vision but the response of his/her pupil to light is intact (as the reflex does not involve the cortex). Therefore, one diagnostic test for cortical blindness is to first objectively verify the optic nerves and the non-cortical functions of the eyes are functioning normally. This involves confirming that patient can distinguish light/dark, and that his/her pupils dilate and contract with light exposure. Then, the patient is asked to describe something he/she would be able to recognize with normal vision.