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Gas chromatography was used to quantitate CO in air and also as an indirect means of determining %COHb in blood. The blood was then used to calibrate four CO-Oximeters used in a survey to determine average COHb levels in various segments of the U.S. population. Mean differences, both between the two methods of analysis and between pairs of CO-Oximeters were less than 0.1% COHb saturation. COHb values obtained on consecutive days using one CO-Oximeter were repeatable within a S.D. +/- 0.13% COHb.

Six healthy male human volunteers were exposed to seven high carbon monoxide (CO) concentrations ranging from 1,000 ppm for ten minutes to 35,600 ppm for 45 seconds. Carbon monoxide was rapidly absorbed and the increase in percent carboxyhemoglobin (COHb) saturation in venous blood per liter of CO mixture inhaled could be accurately predicted by the equation, log (Δ% carboxyhemoglobsn/liter) = 1.036 log (ppm CO inhaled) -4.4793. The abrupt increase in carboxyhemoglobin concentration of 11.6% and 9.1% saturation in two subjects produced the immediate onset of mild frontal headache. The subject exposed to 35,600 ppm demonstrated slight sagging of the ST-segsnent of lead II. This occurred 20 seconds after the exposure had started and persisted for ten minutes after exposure. Neither the spontaneous nor the evoked electrical activity of the brain exhibited significant changes which could be attributed to CO exposure over the range studied.

Acute exposures to isobutane, propane, F-12, and F-11 in concentrations of 250, 500, or 1000 ppm for periods of 1 min to 8 hr did not produce any untoward physiological effects as determined by the methods employed which included serial EKG's and continuous monitoring of modified V5 by telemetry during exposure. Repetitive exposures to these four propellants were also without measurable untoward physiological effect with the exception of the eight male subjects repetitively exposed to 1000 ppm, F-11, who did show minor decrements in several of the cognitive tests. Of particular importance is the observation that none of the subjects showed any decrement in pulmonary function or alteration in cardiac rhythm as the result of exposure to concentrations of the gases or vapors far greater than encountered in the normal use of aerosol products in the home.

Short-term 20-second exposure to hair sprays A and B failed to show significant decreases in maximum expiratory flow rates at low pulmonary volumes in normal subjects; however, significant decreases were observed with hair spray B in eight subjects with hyperreactive airways (abnormal response to inhalation of methacholine). On the partial flow-volume curves, flows at 40 percent and 25 percent of forced vital capacity decreased 8.9 to 10.3 percent and 14 to 18.7 percent, respectively. The hair sprays differed in their content of perfume and plasticizer, and since the latter is generally considered nontoxic at room temperature, the perfume may be the responsible agent It would appear from this study that normal healthy individuals are at little risk, at least from brief exposure to hair spray; however, in the presence of hyperreactive airways, as seen in asthmatic subjects and in some people with allergic rhinitis and viral respiratory infections, an immediate response of the airways may result from exposure to some hair sprays.

Eight adult volunteers of both sexes were exposed to isobutane in a controlled-environment chamber for the purpose of monitoring their physiological responses to a series of gas concentrations ranging from 250 to 1,000 ppm. First, the response to exposure periods of 1 min, 2 min, 1 h, 2 h, and 8 h were studied. There being no untoward responses to these acute exposures, the eight volunteers were exposed repetitively to isobutane at concentrations of 500 ppm, 1, 2 or 8 h per day, five days per week for two weeks. Then exposures to two mixtures of isobutane and propane for 1, 2 or 8 h per day for two days were studied. During the investigation all subjects were kept under comprehensive medical surveillance. No untoward subjective responses or abnormal physiological responses occurred during or following these exposures. Special emphasis was placed on evaluating the cardiac and pulmonary response to these exposures through the use of continuous ECG telemetry and serial computerized spirometric measurements. The following serial laboratory studies were unaltered by the exposures: complete blood count, urinalysis, serum alkaline phosphatase, SGOT, LDH, serum bilirubin, blood sugar, serum calcium, serum phosphorus, BUN, spontaneous electroencephalogram, visual evoked response, a battery of cognitive tests, and an ACTH stimulation test.

An environmental survey was conducted to determine the time-weighted average exposure (TWA) of a group of chemical plant workers to vinyl chloride (VCl) vapor. This survey featured continuous multipoint air sampling and analysis using an infrared spectrophotometer. The inhalation exposure data were digitized and recorded on paper tape for subsequent computer analysis and derivation of daily TWA values for each worker. A breath sampling program was conducted concurrently with the environmental survey, and a series of breath decay curves relating post exposure breath concentration to vapor exposure were derived from the data. To validate the breath curves derived from on-the-job data, post exposure breath curves were also constructed from breath data obtained following experimental human exposures to carefully controlled concentrations of VCl vapor. The close agreement between post exposure breath concentrations at the corresponding TWA's obtained by each of the methods suggests that either continu...

Inhalation of dichloromethane vapor in concentrations of 500 to 1000 parts per million for 1 to 2 hours promptly initiated the formation of significant quantities of carbon monoxide in human subjects. The evidence suggests that carbon monoxide may be a metabolite of dichloromethane and, that exposure to concentrations of dichloromethane below the industrial threshold limit values may result in the formation of carbon monoxide in amounts that exceed the allowable limits.

Human volunteers were exposed to carbon monoxide at concentrations of < 1, 25, 50, 100, 200, 500, and 1,000 ppm for periods of one-half to 24 hours. No untoward effects were observed in sedentary males exposed to 100 ppm for eight hours. Exposures producing carboxyhemoglobin saturations greater than 15% to 20% resulted in delayed headaches, changes in the visual evoked response, and impairment of manual coordination.

Inhalation of methylene chloride vapor In concentrations of 500 to 1,000 ppm for one to two hours was followed promptly by a sustained elevation of carboxyhemoglobin level in all 11 subjects studied. The evidence suggests that carbon monoxide may fee a metabolite of methylene chloride and that exposure to concentrations of methylene chloride that do not exceed the Industrial Threshold Limit Value for that solvent may result in a carboxyhemoglobin saturation level in excess of that allowable from carbon monoxide itself. In addition, methylene chloride produced signs and symptoms of central nervous system depression in subjects exposed to vapor concentrations of 1,000 ppm.