100LL still contains around 0.56g/L of lead. Children bio-accumulate lead more easily than adults if absorbed via the stomach or airway.
If you've ever spilled AVGAS on your clothing or shoes and had to fly somewhere wearing those cloths I'm sure you'll quickly change your mind as to how aromatic AVGAS really is.
Inhalation of vapours or aerosols (mists, fumes), generated by the material during the course of normal handling, may produce toxic effects.
Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and
vertigo.
Limited evidence or practical experience suggests that the material may produce irritation of the respiratory system, in a significant number of individuals,
following inhalation. In contrast to most organs, the lung is able to respond to a chemical insult by first removing or neutralising the irritant and then repairing
the damage. The repair process, which initially evolved to protect mammalian lungs from foreign matter and antigens, may however, produce further lung
damage resulting in the impairment of gas exchange, the primary function of the lungs. Respiratory tract irritation often results in an inflammatory response
involving the recruitment and activation of many cell types, mainly derived from the vascular system.
High inhaled concentrations of mixed hydrocarbons may produce narcosis characterised by nausea, vomiting and lightheadedness. Inhalation of aerosols may
produce severe pulmonary oedema, pneumonitis and pulmonary haemorrhage. Inhalation of petroleum hydrocarbons consisting substantially of low molecular
weight species (typically C2-C12) may produce irritation of mucous membranes, incoordination, giddiness, nausea, vertigo, confusion, headache, appetite
loss, drowsiness, tremors and anaesthetic stupor. Massive exposures may produce central nervous system depression with sudden collapse and deep coma;
fatalities have been recorded. Irritation of the brain and/or apnoeic anoxia may produce convulsions. Although recovery following overexposure is generally
complete, cerebral micro-haemorrhage of focal post-inflammatory scarring may produce epileptiform seizures some months after the exposure. Pulmonary
episodes may include chemical pneumonitis with oedema and haemorrhage. The lighter hydrocarbons may produce kidney and neurotoxic effects. Pulmonary irritancy increases with carbon chain length for paraffins and olefins. Alkenes produce pulmonary oedema at high concentrations. Liquid paraffins may produce
anaesthesia and depressant actions leading to weakness, dizziness, slow and shallow respiration, unconsciousness, convulsions and death. C5-7 paraffins
may also produce polyneuropathy. Aromatic hydrocarbons accumulate in lipid rich tissues (typically the brain, spinal cord and peripheral nerves) and may
produce functional impairment manifested by nonspecific symptoms such as nausea, weakness, fatigue and vertigo; severe exposures may produce inebriation
or unconsciousness. Many of the petroleum hydrocarbons are cardiac sensitisers and may cause ventricular fibrillations.
Central nervous system (CNS) depression may include nonspecific discomfort, symptoms of giddiness, headache, dizziness, nausea, anaesthetic effects,
slowed reaction time, slurred speech and may progress to unconsciousness. Serious poisonings may result in respiratory depression and may be fatal.
The symptoms of exposure to high vapour concentrations of benzene include confusion, dizziness, tightening of the leg muscles and pressure over the
forehead followed by a period of excitement. If exposure continues, the casualty quickly becomes stupefied and lapses into a coma with narcosis. In non-fatal
cases, recovery is usual. Effects of inhalation may include nausea, vomiting, headache, dizziness, drowsiness, weakness, sometimes preceded by brief periods
of ataxia, staggering, weak and rapid pulse, chest pain and tightness with breathlessness, pallor, cyanosis of the lips and fingertips and tinnitus. Severe
exposures may produce blurred vision, shallow rapid breathing, delirium, cardiac arrhythmias, unconsciousness, deep anaesthesia, paralysis and coma
characterised by motor restlessness, tremors and hyperreflexia (occasionally preceded by convulsions). Polyneuritis and persistent nausea, anorexia, muscular
weakness, headache, drowsiness, insomnia and agitation may also occur. Two to three weeks after exposure, nervous irritability, breathlessness and unsteady
gait may still persist; cardiac distress and unusual discolouration of the skin may be evident for up to four weeks. Haemotoxicity is not usually a feature of acute
exposures although anaemia, thrombocytopenia, petechial haemorrhage, and spontaneous internal bleeding have been reported. Fatal exposures may result in
asphyxia, central nervous system depression, cardiac and respiratory failure and circulatory collapse; sudden ventricular fibrillation may also be fatal. Death
may be sudden or may be delayed for 24 hours. Central nervous system, respiratory or haemorrhagic complications may occur up to five days after exposure and
may be lethal; pathological findings include congestion, cerebral oedema, and lung haemorrhage, renal congestion, cerebral oedema and extensive petechial
haemorrhage in the brain, pleurae, pericardium, urinary tract, mucous membrane and skin. Exposure to toxic levels has also produced chromosomal damage