ADAPTATION TO SMOG AND CARBON MONOXIDE 



Figure XI-9 — HEMODYNAMIC AND RESPIRATORY RESPONSES OF FIVE 

 NORMAL SUBJECTS TO CARBOXYHEMOGLOBIN (COH. ) 



The table shows that the oxygen tensions of arterial and mixed-venous bloods 

 decreased between 7.3 and 13.3 percent, respectively, when the carboxy- 

 hemoglobin rose to between 4.95 and 9.69 percent of saturation. Cardiac output, 

 oxygen consumption, and body-surface ventilation per minute did not change 

 consistently, but the difference in arterial and venous blood, reflecting extraction 

 of oxygen by tissue increased in all five subjects. In the one patient who received 

 the greatest amount of carbon monoxide, left arterial pressure rose and cardiac 

 output fell, indicating abnormal left ventricular function. These studies show that 

 small amounts of carboxyhemoglobin do indeed decrease oxygen tension in the 

 blood which in turn may cause other problems related to the supply of blood 

 throughout the body. 



The first line of each set of data shows value before breathing CO at 0.4 percent in 

 air; the second after breathing. Abbreviations are: sat, saturation; LA, left atrium; 

 PA, pulmonary artery; AR, arterial; t,, , oxygen tension; Ven, mixed venous; Ar-ven 



diff, arterial-venous difference; Vent, ventilation per square meter of body-surface 

 area per minute; t co , carbon-dioxide tension. 



of metabolism. Such individuals can- 

 not adapt efficiently to carbon mon- 

 oxide exposures. 



r'ermutt and Farhi have worked out 

 a theoretical example of the compen- 

 sations needed to maintain tissue 

 oxygenation in the presence of 9 

 percent carboxyhemoglobin, which 

 would correspond to a continuous 

 exposure of a normal subject at sea 

 level for several hours to carbon 

 monoxide (CO) at 70 parts per mil- 

 lion. Such a CO hemoglobin satura- 

 tion would have an effect equivalent 

 to that found with a 23 to 46 percent 

 decrease in the oxygen pressure 

 available for supplying the needs of 



the body, and a 13 to 37 percent 

 decrease in blood flow or decrease 

 in the amount of circulating hemo- 

 globin. In order to compensate for 

 this amount of COHb, an increase 

 of from 19 to 39 percent in blood 

 flow would be required. This analysis 

 has forcefully driven home the high 

 physiologic cost of adapting to car- 

 bon monoxide. 



The Risks of Long-Term Expo- 

 sures — Long-term exposures of an- 

 imals, particularly small rodents, have 

 shown that ozone will increase pul- 

 monary fibrosis, just as long-term 

 exposure of other animals will in- 

 crease pulmonary emphysema. It has 



also been shown by Stokinger and 

 his colleagues that the exposure of 

 experimental animals to brief, low 

 levels of ozone protects them from 

 subsequent high-level exposure which 

 would otherwise be fatal. This is 

 doubtless a useful adaptive mech- 

 anism, but its cost may be to increase 

 the risk of chronic respiratory dis- 

 ease. Stokinger and his group have 

 also shown cross-tolerance between 

 ozone and other oxidants. However, 

 tolerance in man has not been dem- 

 onstrated. 



Bennett has reported on long-term 

 exposures of small numbers of hu- 

 man subjects to 0.5 parts per million 



389 



