When hydrocarbon fuels are burnt in a supply of clean air, water and carbon dioxide are formed, CH4 + O2 → CO2 + H2O. Conversely if there is a restriction to the air source and the supply of oxygen is reduced, carbon monoxide is formed, CH4 +O2 → CO + H2O. Carbon monoxide is a colourless, tasteless, flammable, explosive and potentially deadly gas that gives no signs of its existence. Carbon monoxide is the result of an imperfect combustion of hydrocarbon fuels, or, when a hydrocarbon burning device is used in a room with inadequate ventilation (Baird p.59 2006). The intention of this essay is to discuss and evaluate the hazards of Carbon monoxide (CO) and its effect on health.

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Carbon monoxide was first identified in the early eighteenth century through the research of English clergyman chemist John Priestley. The properties of carbon monoxide and its relationship to the human anatomy were further researched during the mid-nineteenth century, by the French physiologist Claude Bernard.  Bernard explored the effects and relationships of carbon monoxide on the blood system, concluding that inhaled carbon monoxide connected with the haemoglobin in the blood to form deadly carboxyhaemoglobins, Hb(aq) + CO(g) → HbCO(aq) (Bernard 1865 p. 85-92). Carboxyhaemoglobins (COHb or HbCO) disrupts the transport of oxygen from the lungs to the bodies tissues. When there is too much carbon monoxide in the air the body starts to replace the oxygen in its red blood cells with the excess carbon monoxide, resulting in carboxyhaemoglobin. Carbon monoxide is highly toxic because it is around two hundred times more efficient at binding to haemoglobin than oxygen. Even when the amount of oxygen is greater than that of carbon monoxide, it is still more likely that the carbon monoxide will bond to the haemoglobin to create carboxyhaemoglobin.

Reports from the National Health Service (NHS) for England and Wales disclose that there are twenty-five fatalities each year that can attributed to carbon monoxide poisoning (www.nhs.uk). This figure is disputed by The Office of National Statistics (ONS) who put the number at fifty-three, more than double the NHS figure. Other statistics show that in Wales and England, annually, there are over two hundred carbon monoxide related hospital admissions and over four thousand accident and emergency attendees (www.ons.gov.uk). The health and Safety Executive (HSE) Gas and Carbon Monoxide awareness paper, reflects that statistics relating to the numbers of non-fatal incidents of carbon monoxide poisonings are uncertain, “with reported figures of CO poisoning in England and Wales each year likely to be a significant under-estimate” (HSE 2018). Carbon monoxide contamination frequently gets mis-diagnosed or undiagnosed because the symptoms of carbon monoxide poisoning are not always obvious. Symptoms, particularly when exposure is small, can mimic those of food poisoning or flu, however, unlike flu, there is no change in body temperature. Carbon monoxide poisoning is verified by measuring the amount of carboxyhaemoglobin in a thinned blood sample that has taken from oxygenated blood that is found in the pulmonary vein. A normal, non-smokers carboxyhaemoglobin level will average around 1%, whereas it can rise to 15% in a heavy smoker (Blumenthal 2001).

There are fundamentally two classes of carbon monoxide poisoning, Acute carbon monoxide poisoning and Chronic carbon monoxide poisoning. Acute carbon monoxide poisoning is the result of inhaling elevated levels of carbon monoxide over a brief period. These cases of poisoning normally come to the attention of a medical practitioner immediately after exposure, hence, most medical and scientific knowledge has been grounded on the research into Acute carbon monoxide poisoning. Chronic carbon monoxide poisoning occurs when the exposure to carbon monoxide is of a lower, but just as toxic level, over a more prolonged period (Battersby. p. 205, 2011). The terminology used for carbon monoxide poisoning that has not been medically reported or has been mis-diagnosed is Occult carbon monoxide poisoning.

The symptoms of acute carbon monoxide poisoning vary and depend on the severity of inhalation. Mild symptoms can include headaches, nausea and vomiting. Moderate symptoms can lead to neurological problems, with feelings of weariness, vertigo. disruption in concentration, confusion and drowsiness. The more obvious symptoms are raspatory problems and chest pains (www.nhs.uk). Symptoms of poisoning usually begin when the saturation of carbon monoxide rises above 10%. In general, levels below 40% are not connected to coma or death, however, when the exposure carbon monoxide is severe, the onset effects can be rapid. Seizures, coma and death can result. The organs and tissues most susceptible to severe exposure are the brain, circulatory system, skeletal muscle and the foetus. (www.headway.org.uk).

Unlike the studies of acute carbon monoxide poisoning, research into the effects of chronic carbon monoxide poisoning have been limited. However, there are strong indications that this type of exposure to carbon monoxide is responsible for extensive and substantial ill health. The medical conditions that arise are often overlooked due to of the range of indistinct symptoms, and the lack of awareness of the problem (Myers et al. 1998). Tests carried out in the USA proved that slight changes in ambient levels of carbon monoxide increased attendance at medical clinics with a range of conditions (Morris 1998). “This raises the possibility that large numbers of patients may be seen in UK emergency departments with symptoms caused by, or disease states worsened by, exposure to CO without staff being aware of the fact” (Henry.1999). Awareness of carbon monoxide, often termed to as “the silent killer”, is hampered by the compounds invisible make up. It is therefore essential to recognise the potential sources of carbon monoxide poisoning, especially when the domestic environment accounts for seventy two percent of carbon monoxide fatalities (www.co-gassafety.co.uk 2018).

The presence of carbon monoxide in the domestic home is mainly due to the inefficient burning of heating fuels such as gas, oil, coal and wood. These carbon fuels are used in boilers, central heating systems, cookers, gas and open-hearth fires. The exposure to carbon monoxide is generally caused by the deficient installation or maintenance of an appliance along with inadequate ventilation. The HSE Gas Safety (Installation and Use) Regulations (GSIUR) and The Approved Code of Practice (ACOP) reflect that “No person shall carry out any work in relation to a gas fitting or gas storage vessel unless he is competent to do so” (GSIUR and ACOP 2018). The regulation also stipulates that the installer or maintenance person must have successfully completed an industry-recognised training course and be assessed in competence.

There is legislation in place to aid the detection of carbon monoxide in the domestic dwelling. The government’s Building Regulations 2010 Combustion Appliances and Fuel Storage Systems Document J, requires that as from 2010, carbon monoxide alarms are to be fitted when solid fuel burning appliances are installed. In 2015 the government amended the regulations, stipulating that private rented sector landlords in England and Wales were to install a BS EN 50291 Kitemarked carbon monoxide alarm in every room used as living accommodation where solid fuel was to be used (www.gov.uk). Northern Ireland broadens the regulation by specifying that all combustible appliances should be monitored, “Where a combustion appliance is installed in a dwelling, reasonable provision shall be made to detect and give warning of the presence of carbon monoxide gas at levels harmful to people” (The Building Regulations (Northern Ireland) 2012). “Combustible appliance” includes gas stoves and gas fires.

 Carbon monoxide in the air is measured as parts per million, abbreviated as ppm. 1 ppm = 1.145 mg/m3. The United States Environmental Protection Agency’s (EPA) recommendation for permissible occupational exposure to carbon monoxide over an eight-hour time-weighted average (TWA) depends on the health and safety authority. The Occupational Safety and Health Administration (OSHA) deems that a carbon monoxide exposure of 50 ppm over an eight-hour TWA is acceptable. However, the American Conference of Government Industrial Hygienists (ACGIH) recommends a lower value of 25 ppm as a TWA over eight-hours (EPA 2017).  Carbon monoxide occupational concentration guidelines set out for the United Kingdom in the HSE paper Workplace Exposure Limits EH40/2005 suggests exposure limited to 20 ppm over an eight-hour period (HSE 2018).

The tolerable domestic exposure in the UK as recommended by the HSE is 50 ppm with a TWA of 30minutes, however, carbon monoxide alarms do not sound off until they detect 50 ppm with a TWA of eight hours (www.kidde.com).  This suggests that a person in a domestic environment can, over an eight-hour period, be subjected to carbon monoxide contamination of one hundred and fifty percent above the figure that is recommended in the HSE occupational guideline. The most vulnerable domestic group affected by carbon monoxide poisoning are the 71 to 80-year old group. This age group accounts for just 7% of the UK population, however it accounts for 17.1% of carbon monoxide fatalities. There are more fatalities for this age group during the coldest months of November to the end of January than the total for the rest of the year (www.co-gassafety.co.uk 2018). Unborn children are also high on the poisoning vulnerability list, the foetus can be affected by very low levels of carbon monoxide.

The foetus’s levels of carboxyhaemoglobins are influenced by the mother’s intake of carbon monoxide. The haemoglobin of a foetus will absorb the carbon monoxide directly from its mother’s blood. The carboxyhaemoglobins can then build up and poisoning transpires. Often going unnoticed, the mother can check negative, even though the foetus is contaminated. A child that has been subjected to carbon monoxide poisoning in the womb can display mental development problems later in life.  “A foetus that is exposed to elevated levels in the womb often display mental development issues later. Some foetuses can even die in the womb if their blood levels of COHb get too high and untreated” (Venditti et al, 2011). The risk can be magnified by smoking during pregnancy. The risk is at its critical point during the first months of infancy as this is when the foetal haemoglobin levels remain elevated. People with sickle cell anaemia and thalassaemia who have a raised foetal haemoglobin are likewise at excess risk. It was noted by the GST that there is no automatic post mortem test for carbon monoxide, once again questioning that the figures for carbon monoxide fatalities could be much higher.

The 2017 The All Party Parliamentary Carbon Monoxide Group (APPCOG) produced a report that listed the recommendations of health professionals. Recommendations concentrate on medical awareness, training, research and incident reporting. However, Amongst the recommendations is a call for all coroners’ post mortems to routinely check for carboxyhaemoglobin levels and to record death from carbon monoxide as a distinct category (APPCOG 2017). Another highlight of the APPCOG report is carbon monoxide poisoning during recreational pursuits. In recent years there have been several carbon monoxide related deaths on boats and at camping sites. This has prompted The Royal Society for the Prevention of Accidents (ROSPA) to issue advice regarding combustible equipment. Under the heading, “Anything that burns can give off invisible and dangerous CO gas”, ROSPA has recommended that stoves, fires and barbecues for cooking or for warmth should never be used in an indoor space with poor ventilation, for example, camper vans, tents and boats. People are often unaware that a smouldering barbeque brought into a confined area for warmth can still emit the deadly compound (www.rospa.com). The Gas Safety Trust (GST) statistics associated with carbon monoxide fatalities in tents, caravans and boats for the period between September 1995 and August 2017 show that carbon monoxide poisoning accounted for twelve percent of total UK carbon monoxide fatalities (GST 2017).

 The Department for Environment Food and Rural Affairs (DEFRA 2017) concludes that the largest source of carbon monoxide pollution is transport, although, industry does make a considerable contribution. Since the late 1990s UK carbon emissions have steadily declined, with the atmospheric concentrations of carbon monoxide falling well within the European Kyoto protocol guidelines. The National Atmospheric Emissions Inventory (NAEI) accredits the steady fall of carbon monoxide atmospheric pollution to, “significant reductions in emissions from road transport, iron and steel production and the domestic sector” (NAEI 2016). Emissions from road transport have been drastically reduced since the introduction of catalytic converters. The equipment is integrated into the exhaust system of motor vehicles. It contains a catalyst, normally palladium, that coverts any carbon monoxide or hydrocarbons that are produced during combustion into carbon dioxide and water.

Reduction of carbon monoxide contamination has been positive, however, there are still too many fatalities and incidents.

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