Toxicity threats
FOCUS
Figure 1
Asphyxiant and irritant gases Smoke contains asphyxiant gases (which prevent O uptake by the body, with loss of consciousness and ultimately death) and irritant gases (which cause immediate incapacitation, mainly by effects on the eyes and upper respiratory tract, and longer term damage deeper in the lung). The effect of asphyxiants and deep lung irritants depends on the accumulated doses – the sum of each of the instantaneous concentrations multiplied by the exposure time – for each product; upper respiratory tract irritation depends on the concentration alone. The most common acutely toxic components
in fire effluents are presented in the table in Figure 2. Since every fire can be considered a unique chemical reactor, producing a mixture of known and unknown products, other components may make a greater contribution to the toxicity in a particular fire. However, the presence of other acute toxicants, which have yet to be characterised, is less likely than for longer term toxicants and carcinogens.
Oxygen and carbon dioxide Fire effluents are O depleted, which causes impairment at around 15% O and lethality below 6%. However, in a fire effluent, the harm from other toxicants such as CO and HCN will be greater. CO2
increases breathing rate, resulting in increased uptake of O and of toxic gases.
Carbon monoxide CO binds to the haemoglobin in red blood cells, impeding the transport of O within the body.
Asphyxiant gases
Carbon monoxide (CO)
Hydrogen cyanide (HCN)
Figure 2
www.frmjournal.com MARCH 2020 31 Irritant gases
Hydrogen fluoride (HF) Hydrogen chloride (HCl) Hydrogen bromide (HBr) Nitrogen dioxide (NO2 Sulphur dioxide (SO2
) ) Organo irritants (OI)
Toxicity related components
Oxygen (O2 )
Carbon dioxide (CO2
)
It impairs an individual’s ability to escape, causing at ten parts per million (ppm) impairment of judgement and visual perception; at 100ppm dizziness, headache and weariness; at 250ppm loss of consciousness; and at 1000ppm rapid death.
Hydrogen cyanide HCN is approximately 25 times more toxic than CO. Inhaled cyanide is distributed throughout the extra cellular fluid of tissues and organs, where it inhibits the enzyme cytochrome oxidase, preventing the utilisation of O by the cells. The O deprivation caused by cyanide also increases the breathing rate in humans and primates, resulting in a factor of four increase in uptake of cyanide and other toxicants. Concentrations of 150ppm HCN cause collapse and loss of consciousness within a few minutes. In most cases, the unconscious victim will continue to breathe smoke until death occurs.
is usually present at around 1 to 5% in smoke. Inhalation of CO2
Irritant gases Incapacitating irritants and smoke can prevent escape from fire by causing severe pain to the eyes, nose, throat and upper respiratory tract. The effects range from tears and reflex blinking of the eyes; pain in the nose, throat and chest; breath holding; coughing; and excessive secretion of mucus, to bronchoconstriction and laryngeal spasms. At sufficiently high concentrations – or when attached to micrometre sized particles such as soot – most irritants can penetrate deeper into the lungs, causing pulmonary irritation which may result in post exposure respiratory distress and death, generally occurring from a few hours to several days after exposure due to pulmonary oedema (flooding of the lungs). This may trap the victim, allowing their uptake of other toxicants to continue. Victims trapped by irritant gases are likely to be found with elevated levels of CO in their blood, which will be reported as the cause of death.
Estimating acute smoke toxicity In order to estimate the effects of the toxicant yields on an exposed human population, it is
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