The Bureau of Industrial Hygiene is at the present time embarking on a rather comprehensive study of the carbon monoxide hazard in the State of New York. In doing so, it is continuing a preliminary investigation begun some time ago by Dr. Ciampolini, Medical Inspector for the Bureau, who made a study of 31 public garages. Of these, 24, or 77.4 per cent., showed the presence of carbon monoxide in the air, and 17, or 54.8 per cent., showed a concentration of this gas which was in excess of the 0.1 per cent. regarded by authorities as the danger limit.
Of the 42 workers examined at the time, 29, or 69 per cent., showed definite evidence of carbon monoxide in their blood, and a number presented clinical symptoms of carbon monoxide poisoning. A study of the steam laundry industry, made by the Bureau at about the same time, brought to the light the fact that workers at gas-heated ironing machines had carbon monoxide in their blood in quantities ranging from 10-23 per cent. saturation.
While Carbon monoxide is, on the whole, more frequently found in high concentrations in public garages (the so-called “service stations”), and around blast furnaces, it may be looked for wherever gas is used as a source of heat; wherever the internal combustion engine is used as a source of power; indeed, wherever any organic substance is oxidized. It is not surprising, therefore, that there is every reason to believe that the carbon monoxide hazard is very definitely on the increase throughout the industrial world, as a result of the increasing use of gas as a fuel.
Watkins points out that this is particularly true of the steel industry where gas is now being used as a fuel to replace steam in open hearth furnaces; and he further states that the demand for many new grades and qualities of steel has led to the use of new and specially designed gas furnaces in that industry. Dr. Winslow in his recent book on “Ventilation” takes the position that carbon monoxide ranks first, and lead second among the industrial poisons.
Carbon monoxide is of especial interest to the Department of Labor, not merely because it is so universally present in industry, but also because of its peculiarly insidious action on those who are exposed to it. A colorless and odorless gas, it may prove suddenly fatal even in minute concentrations without necessarily giving any warning of its presence to those exposed. Blindness, paralysis, and even mental deterioration and insanity have in certain cases followed exposure to this gas – these conditions sometimes coming on days and even weeks after complete recovery had apparently taken place.
In its milder forms, the only clinical manifestations may be dizziness, smarting of the eyes, drowsiness, grogginess and lack of proper muscular co- ordination, followed after a time, as a general thing, by a most intense frontal or basal headache which may last for many hours and even days after exposure to fresh air. That any or all of these effects result in decreased efficiency on the part of the worker, and greatly predispose to accidents, is quite obvious. It has been shown that exposure of a pregnant woman to carbon monoxide gas may result in the death of the fetus in utero with subsequent miscarriage.
It might be well to review very briefly the action of carbon monoxide in the body. As is well known, the tissues of the body derive their oxygen from the oxyhemoglobin of the red blood corpuscles. The combination of hemoglobin with oxygen, however, is less stable than is the combination of hemoglobin with carbon monoxide. And the affinity of carbon monoxide for hemoglobin is approximately 300 times as great as is the affinity of oxygen for hemoglobin. Consequently, in the presence of carbon monoxide, the oxyhemoglobin molecule tends to become dissociated, and in its place carbon monoxide hemoglobin is formed.
When the hemoglobin has thus been deprived of its oxygen, it can no longer nourish the tissues and they become asphyxiated. When carbon monoxide displaces oxygen from the hemoglobin molecule it does so molecule for molecule – that is to say, one molecule of carbon monoxide displaces one molecule of oxygen. The extent to which the hemoglobin will combine with the two gases depends upon their relative concentrations in the air; their affinity for hemoglobin; and the amount of hemoglobin which is present in the blood at the time of exposure.
The whole reaction is in the nature of a reversible mass action, dependent for its direction upon the relative tensions of the two gases. About one-half the equilibrium is reached in the first hour, and about three- quarters in the first two hours. On breathing fresh air, carbon monoxide is eliminated from the body at the rate of 30-60 per cent. reduction of blood concentration per hour.
It has been shown by Sayers that with a subject at rest, exposure to low concentrations of carbon monoxide requires many hours for an equilibrium to be established. Strenuous exercise, however, results in a more rapid combination of carbon monoxide with hemoglobin due to the increased respiratory exchange. At high temperatures and humidities the combination of carbon monoxide with hemoglobin is likewise accelerated.
Physiologically, the principal action of carbon monoxide is thought to be its power to displace oxygen from the hemoglobin molecule, and cause asphyxia of the tissues. Haldane, Henderson and their followers believe that this is its sole action in the body, and that in every other respect it is a harmless, and physiologically inert gas.
They believe that all of the clinical manifestations, both primary and secondary – even coma which is prolonged for days after all carbon monoxide has been removed from the blood – can be explained on the basis of original damage done by oxygen privation at the time the individual was breathing the carbon monoxide gas. Opponents of this theory believe that carbon monoxide, in addition to causing tissue asphyxia due to anoxemia, has a direct toxic action which is specific for nerve cells.
Matthews believes that the carbon monoxide combines with other oxygen receptors, as well as with hemoglobin, and thus acts directly upon the cells. Glaister argues that since the respiratory centres do not respond in the usual manner to lack of oxygen in the body – that is to say, by the marked hyperapnoea ordinarily associated with air hunger in other conditions of oxygen in the body – that is to say, by the marked hyperapnoea ordinarily associated with air hunger in other conditions of oxygen privation – that it is proper to infer that carbon monoxide has a peculiar specific action on the nerve centres and the nerve cells.
Animal experimentation has been cited in support of both sides. Some very recent work of Stadie has thrown still another light on the controversy. As a result of animal experimentation, he has advanced the theory that the primary effect of carbon monoxide inhalation is its profound alteration of the normal oxygen dissociation curve, rather than the mere loss of functioning hemoglobin. This alteration, he believes, is caused by the fact that due to the presence of the carbon monoxide in the alveolar air, the partial pressure of oxygen there is markedly reduced, so that the same volume of oxygen carried in the capillaries would still not be equally available to tissues.
Staid has also brought out the point that due to the acid-base relation between hemoglobin and oxy- hemoglobin, the rate of the elimination of carbon monoxide from the blood stream is increased by any agent which would tend to increase the activity within the cell. This he believes to be one of the beneficial effects of carbon monoxide was obtained by him in his experiments, by the administration of hydrochloric acid by mouth. The question of the entire cause for the profound and prolonged nervous manifestations following exposure to carbon monoxide cannot be considered closed at the present time.
Pathologically, many changes have been reported in victims of carbon monoxide poisoning, which may be very briefly listed as follows: Dilatation of the blood vessels of the brain; hyperemia and edema of the brain and brain membranes; fatty and hyaline degeneration of the walls of the blood vessels with hypertrophy of the intima; extensive and universal capillary haemorrhages in the brain, the bronchial mucosa and elsewhere; blood pictures resembling pernicious anemia, normal blood pictures as well as those showing what is interpreted as a compensatory increase both in red blood cells and hemoglobin for purposes of maintaining an oxygen-carrying capacity more or less approaching normal requirements; eosinophilia; enlargement of the spleen; dilatation of the heart; myocardial degeneration; heart block increase in protein destruction with markedly increased nitrogen excretion; and increased urinary excretion of lactic acid. These are only some of the pathological changes which have been reported.
The extent and the seriousness of the carbon monoxide hazard in industry can readily be seen. It is the purpose of the present investigation conducted by the Bureau of Industrial Hygiene not only to discover the extent of carbon monoxide hazard in the State of New York with a view to eliminating this gas insofar as possible from the workrooms of the State, but to determine the physiological effects of chronic exposure to relatively small concentrations of this gas in order that some means may be developed for more adequately protecting the health and efficiency of the workers until such times as the hazard has been eliminated.
