front |1 |2 |3 |4 |5 |6 |7 |8 |9 |10 |11 |12 |13 |14 |15 |16 |17 |18 |19 |20 |21 |review |
Like the three
case studies selected in the last lecture, the three selected for illustration here are
all too familiar to many epidemiology or toxicology students. These are the ginger jake
paralysis epidemic, the London smog of 1952, and the multistage model of carcinogenesis. The ginger jake paralysis episode was a result of delayed neourotoxicity induced by tri-ortho-cresyl phosphate, which is one of the organophosphates generally recognized as having the ability to selectively inhibit the acetylcholinesterase enzyme activity in mammals and hence to cause fatal hyperactivity of their acetylcholine neurotransmitter. The London smog of 1952 was a predictable environmental disaster involving fatal respiratory stress caused by breathing heavily air pollutants each with their acute toxic effects already well studied. It was this 1952 incident that had brought the issue of air pollution to global attention. Carcinogenesis is the biochemical as well as mechanistic process that characterizes the transformation of normal cells to neoplastic cells and the further development of neoplastic cells into a tumor. The focus with this case is to demonstrate how epidemiologic information can be used to confirm the multistage development of certain forms of human cancer. Numerous toxicologic events occurred in history. The above three case studies were selected primarily because they represent a wide spectrum of use of epidemiologic studies, even though these cases all occurred within a period of three decades running from the 1930s to the 1950s. |