PART XI — HUMAN ADAPTATION TO ENVIRONMENTAL STRESS 



Figure XI-7 — POSSIBLE EPIDEMIOLOGICAL AND PATHOPHYSIOLOGICAL 



MECHANISMS RELATING CARBON MONOXIDE 



AND MYOCARDIAL INFARCTION 



Cigarette Smoking 



Domestic 

 (?Seasonal)" 



Ambient Pollution 



_. CARBON MONOXIDE . 

 "* EXPOSURE 



-Occupation 



■ Emphysema - 



->(Pulmonary Diffusion) 



I j ^ Carboxyhemoglobin 



>0xygen Delivery Rate ♦ 



Y„ Y 2 , . . Y„ 



-> Hematopoesis 



Blood Viscosity 



Heme Catabolism 

 '(Hgb, Catalase, etc.) 



Carboxymyoglobin 



Oxyhemoglobin 

 Dissociation 



Myocardial 

 Atherosclerosis Metabolism 



Cardiac Work 



X,, X„ . . X„ 



Thrombo-embolism 



Myocardial Infarction ^_ 



Fatal Myocardial Infarction 



The figure shows, on the right-hand side, possible biochemical and physiological 

 mechanisms and, on the left-hand side, possible epidemiological associations. 

 Solid arrows indicate an increase; open arrows, a decrease or impairment of the 

 mechanism. This scheme is qualitative and some of the reactions shown may be 

 of insignificant magnitude. 



Testable hypotheses relating carbon monoxide and myocardial infarction from a 

 clinical and mechanistic view are numerous, but testable hypotheses relevant to 

 the epidemiological approach are few. And yet an investigation of the epidemio- 

 logical approach would produce observations on biological and physiological 

 processes as well as studies of disease frequency. 



Scientific opinion increasingly tends 

 to the view that air-pollutant expo- 

 sures, whether smog or carbon mon- 

 oxide, do not generally cause a specific 

 disease, but rather that they contrib- 

 ute to the aggravation, and possibly 

 to the causes, of several possible dis- 

 eases. In an excessively simplistic 

 way, the main target organ for smog 



is the respiratory system. The main 

 target organ for carbon monoxide is 

 the circulatory system, with the cen- 

 tral nervous system being a secondary 

 target. 



The human processes of adapting 

 to these agents produce alterations in 

 function and may also be the same 



mechanisms that lead to their con- 

 tributions to chronic disease and dis- 

 ability. Should this suspicion be 

 borne out by research over the next 

 five to ten years, the likelihood of 

 a substantial reduction in two very 

 common classes of chronic disease 

 would be greatly advanced. Since 

 heart disease accounts for about 20 

 percent and chronic respiratory dis- 

 ease for about 2.5 percent of all 

 deaths in California from 1965 

 through 1967, even a small diminu- 

 tion in the burden attributable to 

 them from adaptive reactions would 

 be well worthwhile. 



Present Scientific Data Base 



One major piece of evidence re- 

 lating the finding of symptoms of 

 persistent cough and sputum and 

 impairment of respiratory function 

 with the likelihood of developing 

 chronic respiratory disease is a study 

 by Gregg, a general practitioner, of 

 patients in a relatively unpolluted 

 sector of London. Cigarette smokers 

 in his practice who had persistent 

 cough and sputum when first ex- 

 amined had a more rapid deteriora- 

 tion of pulmonary function during 

 the ensuing five years and also a 

 lower initial function than persons 

 with a similar smoking history but 

 no symptoms. In the case of carbon 

 monoxide exposures, the much higher 

 frequencies of coronary heart disease 

 among cigarette smokers suggest a re- 

 lationship between carbon monoxide 

 exposures and the chronic diseases 

 associated with lipid deposition in 

 the main blood vessels. So, too, does 

 the demonstration by Astrup in Den- 

 mark that, among persons with well- 

 advanced atherosclerotic disease who 

 were smokers, there were much 

 higher levels of carboxyhemoglobin 

 than among those with similar smok- 

 ing histories but who did not have 

 atherosclerosis. 



Recent findings may help to iden- 

 tify those individuals in a population 

 who are susceptible to the chronic 

 diseases associated with maladapta- 

 tion to inhaled pollutants. These in- 



386 



