Neurotoxic Effects from Butane Gas
Acute Intoxication
Because butane gas inhalants enter through the pulmonary system, they immediately enter into the blood supply and within seconds produce intoxication. The acute effects of inhalants include dizziness, hypertension (increased blood pressure), tachycardia (increased heart rate), impaired coordination, disorientation, temporal distortion, confusion, thick slurred speech, delirium, hallucinations, assaults and suicide attempts. Depending upon the inhalant, recovery may take minutes to hours or may not occur at all. Single episode use can be fatal because of oxygen displacement from red blood cells, hypoxia and asphyxiation. Victims of pulmonary effects are often found with a paper bag over the head.
Profound relaxation and deep sleep usually follow the initial euphoric phase.Unpleasant symptoms reported after the use of inhalants include agitation, seizures, ataxia, headache, and dizziness.
Chronic Effects
Chronic inhalant abuse destroys motor neurons that send commands from the brain to the hands and feet. As these motor neurons fail, varying degrees of motor impairment result, including a decreased ability to perform manual and mental tasks. For example, toluene vapors produce high levels of this lipid soluble chemical, particularly in the brain. Toluene abusers present symptoms of motor uncoordination, fatigue, mental impairment, and increasingly greater degrees of permanent central nervous system damage. Most inhalants produce some degree of hepatotoxicity (liver damage). Halogenated hydrocarbons, such as freon, cause severe hepatotoxicity.
Some inhalants change cardiac physiology and increase the risk for cardiac failure. For example,butane (from cigarette lighters), freon (from aerosol propellants) and toluene (from glues) hypersensitize cardiac cells to norepinephrine, the neurotransmitter that stimulates cardiac contractions. Inhalants interfere with the transport of oxygen by interfering with the binding or release of oxygen by red blood cells. The resulting hypoxia also causes cardiac cell hypersensitivity to norepinephrine. Norepinephrine sensitivity and hypoxia can cause cardiac muscles to defibrillate or begin contracting randomly. A syndrome called Sudden Sniffing Death (SSD) occurs without warning, and discontinuation of breathing the inhalant does not reverse the sequence of events. Victims of SSD often appear to sense that something is wrong, and run away from the source or site where they were inhaling, before collapsing and dying.
Neurotoxic Effects
Permanent cerebral and cerebellar neurological disability is the most well known toxic effect of chronic inhalant abuse. Long-term abusers are at significant risk for a neurological syndrome consisting of memory loss, cognitive impairment, sleep disturbance, depression, anxiety, and personality changes. Permanent cognitive disorders are also well described in patients who chronically sniff gasoline. Long term occupational chemical exposure (e.g., painters) may result in the development of cerebral atrophy and abnormal EEGs.
Chronic abuse of n-hexane and nitrous oxide are well known to cause peripheral neurological deficits including profound sensorimotor polyneuropathy (n-hexane) and a demyelinating polyneuropathy and extremity weakness (nitrous oxide), which appears to be related to the inactivation of vitamin B12, an important cofactor in many necessary biochemical reactions.
Inhalation of leaded gasoline increases the risk for neurological complications from organic lead poisoning. These include mental confusion, poor short-term memory, psychosis, and encephalopathy. Symptoms of inorganic lead poisoning (headache, abdominal pain, hepatic injury, renal damage) have also been reported in patients who chronically inhale gasoline.
Animal and human research shows that most inhalants are extremely toxic. Perhaps the most
significant toxic effect of chronic exposure to inhalants is widespread and long-lasting damage to
the brain and other parts of the nervous system. For example, both animal research and human
pathological studies indicate that chronic abuse of volatile solvents such as toluene damages the
protective sheath around certain nerve fibers in the brain and peripheral nervous system. This
extensive destruction of nerve fibers is clinically similar to that seen with neurological diseases
such as multiple sclerosis.
The neurotoxic effects of prolonged inhalant abuse include neurological syndromes that reflect
damage to parts of the brain involved in controlling cognition, movement, vision, and hearing.
Cognitive abnormalities can range from mild impairment to severe dementia. Other effects can
include difficulty coordinating movement, spasticity, and loss of feeling, hearing, and vision.
Inhalants also are highly toxic to other organs. Chronic exposure can produce significant damage
to the heart, lungs, liver, and kidneys. Although some inhalant-induced damage to the nervous
and other organ systems may be at least partially reversible when inhalant abuse is stopped,
many syndromes caused by repeated or prolonged abuse are irreversible.
Abuse of inhalants during pregnancy also may place infants and children at increased risk of
developmental harm. Animal studies designed to simulate human patterns of inhalant abuse
suggest that prenatal exposure to toluene or trichlorethylene (TCE) can result in reduced birth
weights, occasional skeletal abnormalities, and delayed neurobehavioral development. A number
of case reports note abnormalities in newborns of mothers who chronically abuse solvents, and
there is evidence of subsequent developmental impairment in some of these children. However,
no well-controlled, prospective study of the effects of prenatal exposure to inhalants in humans
has been conducted, and it is not possible to link prenatal exposure to a specific chemical to a
specific birth defect or developmental problem.
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