Registration Dossier

Toxicological information

Exposure related observations in humans: other data

Currently viewing:

Administrative data

Endpoint:
exposure-related observations in humans: other data
Type of information:
other: MAK value
Adequacy of study:
weight of evidence
Rationale for reliability incl. deficiencies:
other: Maximum Concentration at the workplace (MAK value) of CO; established by the Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, DFG (Deutsche Forschungsgemeinschaft/German Research Association)

Data source

Referenceopen allclose all

Reference Type:
publication
Title:
Unnamed
Year:
1992
Reference Type:
publication
Title:
Unnamed
Year:
2001

Materials and methods

Test material

Reference
Name:
Unnamed
Type:
Constituent

Results and discussion

Any other information on results incl. tables

Effects of CO in Man

The symptoms of acute CO intoxication with increasing carboxyhaemoglobin (CO-Hb) levels in the blood include: mild headaches, respiratory distress during exercise, reddening of the skin (10-20 % CO-Hb), more severe headaches, frontal pulse, palpitations, dizziness, tinnitus, spots before the eyes, weakness (20 -30 % CO-Hb), exhaustion, nausea, vomiting, sometimes collapse (30 -40 % CO-Hb), increased respiration rate and pulse rate, collapse, unconsciousness (40 -50 % CO-Hb), coma, convulsions, Cheyne-Stokes' respiration (50-60 % CO-Hb), progressive failure of the cardiocirculatory system and respiration, death (60 -70 % CO-Hb) (Lindgren, 1961; Stewart et al., 1970).

Late sequelae of acute CO intoxications can take very different forms. The symptoms usually involve the central and peripheral nervous systems, less frequently the heart, vessels and internal organs. It is, however, likely that the nervous system symptoms result from vessel damage caused directly by CO.

Long-term continuous or intermittent CO exposure can result in symptoms like those seen in acute intoxications when the CO-Hb level exceeds about 10 %. At lower blood CO-Hb levels (2 -5 %), laboratory studies have revealed reduction in psychosensory and psychomotor abilities; the practical relevance of these findings is controversial (Groll-Knapp et al., 1972; Beard and Wertheim, 1967; Beard and Grandstaff, 1970). In addition, at CO-Hb levels above 5%, ischaemic changes in heart function have been demonstrated experimentally in persons with cardiac disease (Aronow et al., 1972; Anderson et al., 1973; Aronow and Isbell, 1973).

Some habituation to low CO-Hb levels has been demonstrated in heavy smokers and in gas works employees whose average CO-Hb level was 3.8 %. Occasional higher CO-Hb levels, 30-40 %, were not associated with the usual symptoms of intoxication in these workers. It was also possible to produce experimentally a certain resistance to elevated CO-Hb levels by repeated exposure of persons and experimental animals to low CO concentrations. It is not clear whether or not this resistance is simply a result of the increases in haematocrit, Hb and erythrocyte count produced by this treatment (Ray and Rockwell, 1967; Ehrich et al., 1944; Astrup et al., 1967; Wilks et al., 1959).

 

References:

Anderson EW, Andelman RJ, Strauch JM, Fortuin NJ and Knelson JH (1973). Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris. A study in ten patients with ischemic heart disease. Ann Intern Med 79: 46-50.

Aronow WS and Isbell MW (1973). Carbon monoxide effect on exercise-induced angina pectoris. Ann Intern Med 79: 392-395.

Aronow WS, Harris CN, Isbell MW, Rokaw SN, Imparato B (1972). Effect of freeway travel on angina pectoris. Ann intern Med 77: 669 -676.

Astrup P, Kjeldsen K and Wanstrup J (1967). Enhancing influence of carbon monoxide on the development of atheromatosis in cholesterol-fed rabbits. J Atheroscler Res 7: 343 -354.

Beard RR and Grandstaff N (1970). New York Academy of Science Conference on Biological Effects of Carbon Monoxide. New York City.

Beard RR and Wertheim GA (1967). Behavioral impairment associated with small doses of carbon monoxide. Am J public Health 57: 2012 -2022.

Ehrich WE, Bellet S and Lewey FH (1944). Cardiac changes from CO poisoning. Am J med Sci 208: 512 -523.

Groll-Knapp E, Wagner H, Hauck H and Haider M (1972). Effects of low carbon monoxide concentrations on vigilance and computer-analyzed brain potentials. Staub Reinhalt Luft 32: 64 -68.

Lindgren SA (1961). A study of the effect of protracted occupational exposure to carbon monoxide with special reference to the occurrence of so-called chronic carbon monoxide poisoning. Acta med scand 167 (Suppl. 356): 1 -135.

Ray AM and Rockwell TH (1967). Ohio State University, Dept. of Industrial Engineering Columbus, Ohio. Report Number IE-i.

Stewart RD, Peterson JE, Baretta ED, Bachand RT, Hosko MJ and Herrmann AA. (1970). Experimental human exposure to carbon monoxide. Arch Environ Health 21: 154 -164.

Wilks SS, Tomashefski JF and Clark RT (1959). Physiological effects of chronic exposure to carbon monoxide. J Appl Physiol 14: 305 -310.

Applicant's summary and conclusion

Executive summary:

A maximum (allowable) concentration at the workplace (MAK value) of 30 mL/m³ (35 mg/m³) was defined for CO (DFG, 1992). This value is based on data obtained with non-smokers and does not apply for pregnant women. With regard to short term-exposure to CO, a value of 30 mL/m³ was indicated (DFG, 2001).