Abstract:
Carbon monoxide (CO) is the ultimate environmental health hazard. It is odorless, colorless, and lacks warning properties other than the insidious onset of non-specific symptoms such as headache and nausea. Many survivors of CO exposure brushed off symptoms because they thought they were getting the flu. In concentrations that are easily produced by combustion with inadequate oxygen in the home, community, and workplace, CO can be very rapidly fatal. Ever since humans first took up shelter in caves heated by log fires, CO has caused a great many deaths. The earliest apparent reference to CO toxicity was from Aristotle (384 - 322 B.C.), who described how coal fumes lead to a heavy head and death (Lewin, 1920 and Pankow, 2000). Writings from the Byzantine era reveal that the practice of burning coal in braziers apparently caused the CO poisoning of one emperor and the death of another (Lascaratos and Marketos, 1998). The physician Marcellus Donato described in 1588 symptoms typical of CO exposure following exposure to coal fumes (Pankow, 2000). Bernardino Ramazzini, the father of occupational medicine, advised that artists and craftsmen could suffer disease or death from exposure to the fumes of burning charcoal or mineral coal (Pankow, 2000 and Weichardt, 1988). During the 18th century, chemists such as Lassone, Priestley, Dalton, and Henry described the properties and structure oc CO, followed by LeBlanc's identification of CO as the toxic component of coal fumes in 1842 (Lewin, 1920 and Pankow, 2000). Bernard and Hoppe independently discovered the binding of CO to hemoglobin in 1857 and both concluded that such a mechanism accounted for CO-related hypoxia (Bernard, 1857 and Hoppe, 1857). This view prevailed for most of the next 150 years until recent studies implicated CO's role as a cytochrome poison to be the most likely mechanism of human toxicity (Goldbaum, 1975 and Raub, 2000).
Taken from the beginning of thesis.