Carbon monoxide occupational exposure

Criteriafor a Recommended Standard Occupational Exposure to Carbon Monoxide, NIOSH-TR-007-72, National Technical Information Service, Spriugfield, Va., 1972. 

Hugod, C. 1979. Effect of exposure to 0.5 ppm hydrogen cyanide singly or combined with 200 ppm carbon monoxide and/or 5 ppm nitric oxide on coronary arteries, aorta, pulmonary artery, and lungs in the rabbit. Int. Arch. Occup. Environ. Health 44 13-23. 

One of the most carefully worked out dose-response relationships is that for carbon monoxide poisoning. Based on controlled studies of exposure in humans at low levels and on observations in humans who have suffered high level exposures because of their occupation or because of accidents or suicide attempts, the relationship between blood levels of carboxyhemoglobin (COHb) and toxicity is understood as follows ... 

Although a number of methods have been proposed for the biological monitoring of occupational methylene chloride exposure, measurement of urinary methylene chloride levels may be the most suitable. The measurement of urinary methylene chloride is nonin-vasive, not influenced by smoking as are COHb or carbon monoxide levels in alveolar air, and may reflect cumulative exposures more accurately "... 

However, the mathematics describes an idealized situation, and the real situation in vivo may not be so straightforward. For example, with carbon monoxide, as already indicated, the toxicity involves a reversible interaction with a receptor, the protein molecule hemoglobin (see chap. 7 for further details of this example). This interaction will certainly be proportional to the concentration of carbon monoxide in the red blood cell. However, in vivo about 50% occupancy or 50% carboxyhemoglobin may be sufficient for the final toxic effect, which is cellular hypoxia and lethality. Duration of exposure is also a factor here because hypoxic cell death is not an instantaneous response. This time-exposure index is also very important in considerations of chemical carcinogenesis. 

Viau, C., G. Hakizimana, and M. Bouchard. 2000. Indoor exposure to polycyclic aromatic hydrocarbons and carbon monoxide in traditional houses in Burundi. Int. Arch. Occup. Environ. Health 73(5) 331-338. 

Davies, D.M., E.J.Jolly, RJ.Pethybridge, and W.P.Colquhoun. 1981. The effects of continuous exposure to carbon monoxide on auditory vigilance in man. Int. Arch. Occup. Environ. Health 48(1) 25—34. 

Ernst, A., and J.D.Zibrak. 1998. Carbon monoxide poisoning. N. Engl. J. Med. 339(22) 1603-1608. Ettema, J.H., R.L.Zielhuis, E.Burer, H.A.Meier, L.Kleerekoper, and M.A.de Graaf. 1975. Effects of alcohol, carbon monoxide and trichloroethylene exposure on mental capacity. Int. Arch. Occup. Environ. Health 35(2) 117—132. 

Mihevic, P.M., J.A.Gliner. and S.M.Horvath. 1983. Carbon monoxide exposure and information processing during perceptual-motor performance. Int. Arch. Occup. Environ. Health 51 (4) 355—363. 

Atkins, E.H., Baker, E.L. (1985). Exacerbation of coronary artery disease by occupational carbon monoxide exposure a report of two fatalities and a review of literature. Am. J. Ind. Med. 7 73-9. 

A gas leak has led to the presence of 1.00 mole% carbon monoxide in a 350-m laboratory. The leak was discovered and sealed, and the laboratory is to be purged with clean air lo a point at which the air contains less than the OSHA (Occupational Safely and Health Administration)-specified Permissible Exposure Level (PEL) of 35 ppm (molar basis). Assume that the clean air and the air in the laboratory are at the same temperature and pressure and that the laboratory air is perfectly mixed throughout the purging process. 

Kerosene may enter the water or soil environment as a result of regular use (e.g., evaporation of pesticide solvent), from spills during use or transportation, or from leaking storage facilities. The relatively low vapor pressure of kerosene makes inhalation exposure unlikely under ordinary occupational conditions unless conditions of poor ventilation exist. The combustion product of burned kerosene, carbon monoxide, is of real concern when kerosene heaters are not vented. Exposure to kerosene mist can occur as kerosene is often applied in the form of a spray. Eye and skin contact with kerosene and kerosene mists and vapors can occur. The exposure pathway usually of... 

The USEPA standards for 24-h PM, and PM2.5 concentrations in ambient environments are 150 and 65 pg/m , respectively. Indeed in some settings the levels exceed what is considered acceptable for even occupational exposures. The threshold limit value adopted by the American Conference of Governmental Industrial Hygienists for respirable dusts is 5,000 pg/m and for carbon monoxide is 29 mg/m The comparison with these health-based standards (although currently available for settings other than indoor household environments) indicates the potential for significant health risks. 

Barrowcliff DF, Knell AJ Cerebral damage due to endogenous chronic carbon monoxide poisoning caused by exposure to methylene chloride. Journal of Social and Occupational Medicine 29 12-14, 1979... 

Carbon monoxide at high levels can cause myocardial infarction in otherwise healthy individuals and, at lower levels, can aggravate ischemia in the face of established atherosclerotic heart disease (ASHD). Chronic exposure to carbon monoxide may also be associated with ASHD. Many jurisdictions automatically grant workers compensation to firemen or policemen with ASHD, regarding it as a stress-related occupational disease. This is related to social policy rather than established epidemiologic risk. 

In some occupations, it is difficult to avoid long-term exposure to carbon monoxide. 

In the open literature, when effects have been observed in individual workers or in occupational populations as a result of quantifiable pollutant exposure, these can often be used to establish an effects baseline. This baseline ranges from a no observable effects exposure concentration, to a dosage level which results in death. A sample effects chart for carbon monoxide is shown in Fig. 4. Following... 

C) A statement that the employee has been informed by the physician or other licensed health care professional that MC is a potential occupational carcinogen, of risk factors for heart disease, and the potential for exacerbation of underlying heart disease by exposure to MC through its metabolism to carbon monoxide and... 

Table 5A of the Elements Handbook (Appendix A) contains carbon monoxide concentration data expressed as parts per million (ppm). The OSHA (Occupational Safety and Health Administration) limit for worker exposure to CO is 200 ppm for an eight-hour period. 

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