Carbon monoxide (CO) is a nonirritating, colorless, tasteless, odorless gas. It is produced by the incomplete oxidation of carbonaceous materials. Its sources include automotive engines, industries using fossil fuels, home oil burners, and cigarette smoke. The low levels often found in ambient air may contribute to impaired respiratory function but usually are not life threatening. However, persons working in confined environments with high exposure to fumes, such as tunnel and underground garage workers, may develop chronic poisoning. CO is included here as an air pollutant, but it also is an important cause of accidental and suicidal death. In a small, closed garage, exhaust from a running car engine can induce a lethal coma within 5 minutes. CO is a systemic asphyxiant that kills by binding to hemoglobin and preventing oxygen transport. Hemoglobin has a 200-fold greater affinity for CO than for O2. The carboxyhemoglobin, that is formed by binding of CO is incapable of carrying oxygen. Hypoxia leads to central nervous system (CNS) depression, which develops so insidiously that victims often are unaware of their plight and are unable to help themselves. Systemic hypoxia appears when the hemoglobin is 20% to 30% saturated with CO, and unconsciousness and death are probable with 60% to 70% saturation. The diagnosis of CO poisoning is based on detection of high levels of carboxyhemoglobin in the blood.
MORPHOLOGYChronic poisoning byCOdevelopsbecausecarboxyhemoglobin,onceformed,isremarkablystable.Asaresult,withlow-levelpersistentexposuretoCO,carboxyhemoglobinmayaccumulatetoalife-threateningconcentrationintheblood.Theslowlydevelopinghypoxiacanevokewidespreadischemicchangesinthebrain,particularlyinthebasalgangliaandlenticularnuclei.WithcessationofexposuretoCO,thepatientusuallyrecovers,buttheremaybepermanentneurologicdamage.
Acute poisoning byCOgenerallyisaconsequenceofaccidentalexposureorsuicideattempt.Inlight-skinnedpeople,itismarkedbyacharacteristicgeneralized cherry-red color of the skin and mucous membranes, acolorimpartedbycarboxyhemoglobin.Ifdeathoccursrapidly,morphologicchangesmaynotbepresent;withlongersurvival,thebrainmaybeslightlyedematousandexhibitpunctatehemorrhagesandhypoxia-inducedneuronalchanges.Thesechangesarenotspecific;theysimplyimplysystemichypoxia(Chapter23).InvictimswhosurviveCOpoisoning,completerecoveryispossible;however,impairmentsofmemory,vision,hearing,andspeechsometimesremain.
As modern homes are increasingly “buttoned up” to exclude the environment, the potential for pollution of the indoor air increases. The most common pollutant is tobacco smoke (discussed later), but additional offenders are CO, nitrogen dioxide (already mentioned as outdoor pollutants), and asbestos (discussed in Chapter 13). A few comments about some other agents are presented here.
Smoke from burning of organic materials, containing various oxides of nitrogen and carbon particulates, is an irritant that predisposes exposed persons to lung infections and may contain carcinogenic polycyclic hydrocarbons. It is estimated that one-third of the world, mainly in developing areas, burn carbon-containing material such as wood, dung, or charcoal in their homes for cooking, heating, and light.
Radon, a radioactive gas derived from uranium, is widely present in soil and in homes. Although radon exposure can cause lung cancer in uranium miners (particularly in those who smoke), it does not appear that low-level chronic exposures in the home increase lung cancer risk, at least for nonsmokers.