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Biomedical subjects

J D Prah

Publications and source records attributed to J D Prah.

13 recordsLinked to original sources
PubMed1998

1998 equivalence of sensory responses to single and mixed volatile organic compounds at equimolar concentrations.

Exposure to low levels of chemicals indoors is often to a mixture of volatile organic compounds (VOCs). It is of interest to determine if the symptomatic and sensory responses can be attributed to a single chemical or to a mixture of chemicals. To determine if sensory or symptomatic responses differ with exposure to single or mixed VOCs, 100 female subjects participated in a 6-hr exposure study. Subjects were exposed to one of six equimolar concentrations equivalent to 24 mg/m3 toluene, control, m-xylene, n-butyl acetate, m-xylene plus n-butyl acetate, a mixture of 21 chemicals including n-butyl acetate and m-xylene, and to the same mixture of chemicals without n-butyl acetate and m-xylene (19 chemicals). The results indicated that there was no difference in reporting of symptoms or sensory responses between the exposures. When the control group was added, some variables, primarily odor intensity and nasal irritation, attained significance.

Acetates↗
PubMed1997

Body burden measurements and models to assess inhalation exposure to methyl tertiary butyl ether (MTBE).

Biomarkers of methyl tertiary butyl either (MTBE) exposure and the partitioning of inhaled MTBE into the body were investigated in a human chamber study. Two subjects were exposed to an environmentally relevant nominal 5,011 micrograms/m3 (1.39 ppm) MTBE for 1 hour, followed by clean-air exposure for 7 hours. Breath and blood were simultaneously sampled, while total urine was collected at prescribed times before, during, and after the exposure. Mass-balance and toxicokinetic analyses were conducted based upon the time series measurement of multiple body-burden endpoints, including MTBE in alveolar breath, and MTBE and tertiary butyl alcohol (TBA) in venous blood and urine. The decay of MTBE in the blood was assessed by fitting the post-exposure data to a 2- or 3-exponential model that yielded residence times(tau) of 2-3 min, 15-50 min, and 3-13 h as measured by alveolar breath, and 5 min, 60 min, and 32 h as evaluated from venous blood measurements. Based on observations of lower than expected blood and breath MTBE during uptake and a decreasing blood-to-breath ratio during the post-exposure decay period, we hypothesize that the respiratory mucous membranes were serving as a reservoir for the retention of MTBE. The decay data suggest that 6-9% of the MTBE intake may be retained by this non-blood reservoir. The compartmental modeling was further used to estimate important parameters that define the uptake of inhaled MTBE. The first of these parameters is f, the fraction of C(air) exhaled at equilibrium, estimated as 0.60 and 0.46 for the female and male subject, respectively. The second parameter is the blood-to-breath partition coefficient (P) estimated as approximately 18. The product of these parameters provides an estimate of the blood concentration at equilibrium as 8-11 times the air concentration. Blood TBA lagged MTBE levels and decayed more slowly (tau = 1.5-3 h), providing a more stable indication of longer term integrated exposure. The concentration ranges of MTBE and TBA in urine were similar to that of the blood, ranging from 0.37 to 15 micrograms/L and 2 to 15 micrograms/L, respectively. In urine, MTBE and TBA by themselves bore little relationship to the exposure. However, the MTBE:TBA ratio followed the pattern of exposure, with peak values occurring at the end of the exposure (20- and 60-fold greater than pre-exposure values) before decaying back to pre-exposure levels by the end of the 7-h decay period. Urinary elimination accounted for a very small fraction of total MTBE elimination (< 1%).

Administration, Inhalation↗
PubMed1991

Functional deficits produced by 3-methylindole-induced olfactory mucosal damage revealed by a simple olfactory learning task.

Methods for assessing functional consequences of olfactory mucosal damage were examined in rats exposed to 3-methylindole (3-MI). Treatment with 3-MI (400 mg/kg) induced severe degeneration of olfactory sensory epithelium followed by regeneration, fibrous adhesions, and osseous remodeling of the nasal passages. At 100 mg/kg, there was mild Bowman's gland hypertrophy while the sensory epithelium remained intact. Rats receiving 3-MI demonstrated a treatment-related deficit in acquiring an olfactory learning task which was not due to altered cognitive abilities, as determined by subsequent testing in a step-through passive avoidance task. The results confirm the conclusion that alterations in functional indices resulted from 3-MI-induced anosmia and demonstrate the utility of simple learning tasks in assessing functional capacity following olfactory epithelial damage in rats.

Animals↗
PubMed1982

Olfaction: anatomy, physiology and behavior.

The anatomy, physiology and function of the olfactory system are reviewed, as are the normal effects of olfactory stimulation. It is speculated that olfaction may have important but unobtrusive effects on human behavior.

Animals↗
PubMed1979

Decrements in olfactory sensitivity due to ozone exposure.

Approximate olfactory thresholds were determined in an exploratory study in which subjects were exposed to ozone (O3). The odorants were butyl alcohol (BA) and acetic acid (AA). Preliminary data suggest (1) temporary increases in thresholds due to O3 exposure, (2) diminution of O3 effects with repeated exposures, and (3) greater and more reliable effects for BA than for AA.

Adult↗
PubMed1979

Carbon monoxide and human time discrimination: failure to replicate Beard-Wertheim experiments.

Beard and Wertheium described a dose-related deficit in human time perception during low level CO exposure. Two other laboratories were unable to replicate this finding, although methodological differences could explain these failures. This study more precisely repeated the original experiment, but failed again to obtain any CO-related deficit. The bulk of evidence, therefore, does not indicate any adverse effect of low level CO exposure on time perception in healthy young adults.

Acoustic Stimulation↗
PubMed1977

Lack of effects of carbon monoxide on human vigilance.

Previous publications on the effects of low levels of carbon monoxide (CO) on human vigilance performance have found conflicting results. While several studies have found statistically reliable effects, none have gone unchallenged. This article presents a critical review of the literature and the results of a study employing 52 human male subjects performing a numeric monitoring task. CO levels were 0, 100, and 200 ppm which produced mean carboxyhemoglobin levels 0.01, 4.61 and 12.62 percent respectively. No CO-exposure levels produced any effect on vigilance performance. The power of the statistical test for CO effects was shown to be quite high, even for fairly trivial possible decrements of performance.

Adult↗
PubMedDate not supplied

Effect of low level carbon monoxide on compensatory tracking and event monitoring.

Experiments by Putz et al. concerning the effect of carbon monoxide (CO) exposure on compensatory tracking and monitoring in healthy young men were replicated. Task and procedural variables were reproduced as closely as practical. Subjects were exposed to either room air or 100 ppm CO. Mean carboxyhemoglobin (COHb) levels in the high CO exposure groups were 5.1% for Putz et al. (70 ppm exposure), and 8.24% for the present study (100 ppm exposure). In both studies elevated COHb produced a statistically significant increase over time in log mean absolute deviation scores (tracking error) with respect to control groups. The magnitude of the effect was smaller in the present study, perhaps because of subtle methodological or training differences between studies. The relationship between task difficulty and magnitude of CO-induced dysfunction remains unresolved. In contrast to Putz et al., no statistically significant effect of COHb in monitoring behavior was found. The failure to replicate this feature of may reflect the large differences in baseline performance, and higher variance in the present study.

Adult↗
PubMedDate not supplied

Compensatory tracking in humans with elevated carboxyhemoglobin.

A total of seventy-four men divided into five groups performed a compensatory tracking task for 4 hr with group mean carboxyhemoglobin (COHb) levels of 0.9, 5.6, 6.1, 11.4 or 16.6%. In all but one group, COHb was formed in approximately 5 min by having the subject breathe a high concentration of carbon monoxide (CO) from a Douglas bag. An appropriate low level of CO in the exposure/test chamber maintained the elevated COHb for the 4-hr duration of the experiment. A slow COHb formation group, not exposed to CO during bag breathing, which was only exposed to low-level CO in the exposure/testing chamber, served as a positive control. Even though mean tracking error scores increased in a nearly monotone manner as a function of COHb, the effects were not statistically significant. Even at the highest dose, the increase in tracking error was small. The increased mean error score due to rapid formation was virtually the same as that due to slow formation.

Adult↗
PubMedDate not supplied

Carboxyhemoglobin and brain blood flow in humans.

It has been shown that with increased carboxyhemoglobin (COHb) and associated decrease in blood oxygen-carrying capacity, a compensatory increase in brain-blood flow (BBF) develops. The BBF response in humans has been shown to be quite variable. Two experiments were conducted in which humans were exposed to sufficient carbon monoxide (CO) to produce COHb levels up to 18.4%. BBF was measured by the method of impedance plethysmography. The first was a pilot study in which BBF in 14 men was studied after transient exposure to various concentrations of CO in air. BBF increased as a function of COHb but not to the same extent (or at all) in some subjects. In a confirmatory experiment with 12 men, BBF was measured once per h during a 4-h experiment. All 12 subjects received CO. The variation of the BBF response among subjects was large and statistically significant whereas the variation over time was not significant. Thus it appears that the magnitude of the BBF response is unique for a given subject and differs across subjects. These results may help predict CO-induced behavioral decrements in future studies if subjects whose BBF response to COHb is small or absent are also more susceptible to impairment by acute CO exposure.

Carbon Monoxide↗
PubMedDate not supplied

Time dependence of blood concentrations during and after exposure to a mixture of volatile organic compounds.

Volatile organic compounds constitute a group of important environmental pollutants that have been associated with the constellation of symptoms known as sick building syndrome. An understanding of the kinetics of uptake and elimination of volatile organic compounds is important for the proper interpretation of the internal dose concentrations of people exposed to these compounds. Blood concentrations measured before, during, and after exposure of five individuals to a mixture of volatile organic compounds in a controlled chamber are described. Blood concentrations were related directly to air exposure concentrations and appeared to be a function of the blood/air partition coefficient. The half-lives of the internal dose of the volatile organic compounds measured were less than 1/2 h, but the elimination time courses were multiexponential. The complexity of the elimination curve suggested the existence of multiple storage sites within the body. The presence of a long-term exponential in the blood elimination curve suggested that, with repeated exposure, bioaccumulation may occur in humans.

Adult↗