Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Inhalation Exposure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMedDate not supplied

Evaluation of a multitiered inhalation exposure chamber.

A multitiered inhalation exposure chamber was evaluated for use in aerosol toxicity studies by determining the uniformity of pulmonary deposition in 144 rats simultaneously exposed to 99mTc-CsCl aerosols. The activity median aerodynamic diameter and geometric standard deviation were 1.7-2.1 micron and 1.8 respectively. In one experiment, lung deposition of 99mTc in male and female rats was 728 and 544 nCi, respectively, after 130 min exposure to an aerosol concentration of 173 nCi/L. Analysis of variance revealed a significant effect of several factors on lung deposition. Animals housed on one side of the chamber had lung burdens 8-11% greater than those on the opposite side. Because an animal's location within the chamber had a slight effect on its lung burden of inhaled aerosol we recommend the rotation of animals among the chamber's six tiers during chronic aerosol toxicity studies. The overall coefficient of variation in lung burden was only 21% which is less than the variability reported in small rodents given a nose-only aerosol exposure.

Aerosols↗
PubMed1980

Inhalation exposure of cadmium workers: effects of respirator usage.

The objective of this study was to determine the average reduction in inhalation exposures produced by intermittent use of filter cartridge respirators by cadmium workers. Inhalation exposure was estimated by measuring the cadmium concentration inside the respirator while it was worn or hanging around the worker's neck. Air concentrations of cadmium were measured simultaneously inside the respirator and at the worker's lapel with a dual sampling system. Each of nine workers were measured on three consecutive days for a full work shift. The average inhalation exposures ranged from 3 to 67 micrograms/m3 while the TWA lapel concentrations ranged from 19 to 3600 micrograms/m3; respirator use produced a substantial reduction in inhalation exposures when lapel concentrations were above 100 micrograms/m3. On the average, the inhalation exposure was 26% of the lapel concentration, but the effective protection varied widely between individuals and from day to day. If used cautiously, this relationship may be useful for estimating the approximate average inhalation exposure of a group of workers routinely using half mask respirators.

Air Pollutants↗
PubMed2000

Inhalation exposure to THMs from drinking water in south Taiwan.

Trihalomethanes (THMs) are important disinfection byproducts (DBPs) in drinking water. To understand the magnitude of exposure to THMs for the people in southern Taiwan, models are used to estimate the inhalation exposure associated with drinking water based on raw water quality. Two parts of models are used in this study, one for estimating THM concentration from raw water quality, and one for estimating inhalation exposure to people. Important raw water quality and operational parameters, including TOC, UV254, pH, temperature, chlorine dosage, and water residence time of a major water treatment plant in south Taiwan were collected. An empirical THM formation model was then employed to predict the THM concentration at consumers' dwellings based on the parameters collected. Differences between the predicted results and experimental data were found to be small, indicating that the model is appropriate. The predicted THM concentration distribution was served as input parameters for the exposure models. Three major scenarios associated with probable inhalation exposure of THMs, including shower, pre- and post-cooking activities, and cooking processes, were considered in the exposure models. The model results show that the mean inhalation exposure of THMs for shower, pre- and post-cooking activities, and cooking processes are 26.4, 1.56, 3.29 micrograms/day, respectively. The total inhalation exposure (summation of the three scenarios) was found to be comparable with that for direct ingestion, indicating that inhalation is an important pathway for THM exposure from drinking water.

Activities of Daily Living↗
PubMedDate not supplied

Assessment of human inhalation exposure to polycyclic aromatic hydrocarbons.

The aim of the investigation was to find a suitable approach for assessing inhalation exposure of urban inhabitants to polycyclic aromatic hydrocarbons (PAHs) in air. Personal exposure to PAHs of fifteen subjects, Zagreb inhabitants, was measured over a week in summer and again in winter. All subjects kept a diary of motion and activities and filled in a questionnaire on the characteristics of their fiat and household members. PAHs concentrations inside and outside subject's homes were simultaneously measured as were those in the working environment and in transport. Using an exposure model which takes into account the time spent by the subjects in each microenvironment and the respective concentrations measured, the inhalation exposure of each subject was calculated and compared with the directly measured personal exposure for the winter season only the summer concentrations being negligible. For a few subjects the calculated inhalation exposure deviated considerably from the one measured directly. This could be attributed to the fact that the subject spent some time in a microenvironment with significantly different PAH levels which were not included in the calculation. However, if the average results for the whole group are considered, there was no statistically significant difference between the directly measured and calculated PAH inhalation exposures. Therefore the described approach could be used for calculating average inhalation exposure to PAHs of population groups with common characteristics.

Air Pollution↗
PubMed2001

Inhalation exposure in secondary aluminium smelting.

Inhalation exposure at seven UK secondary aluminium smelters was investigated to quantify the main exposures and identify their sources. The substances monitored were gases (carbon monoxide, hydrogen sulphide and nitrogen dioxide), total inhalable dust, metals, ammonia, polycyclic aromatic hydrocarbons (PAHs), particulate fluoride salts and acids. The results showed that people were exposed to a range of workplace air pollutants. Personal exposure results for total inhalable dust were between 700 and 5600 microg x m(-3) and the maximum personal exposure result for particulate fluoride salts was 690 microg x m(-3) (as F). The maximum aluminium, total PAH and lead personal exposure results were 900, 19 and 18 microg x m(-3) respectively. The average proportion of aluminium in total inhalable dust samples was 13% and rotary furnace processes generated the most dust. Particulate fluoride salt exposure was more widespread than hydrofluoric acid exposure. The source of the salt exposure was fluoride containing fluxes. The lead exposure source was lead solder contamination in the furnace charge.

Air Pollutants, Occupational↗
PubMed2001

Occupational inhalant exposure and respiratory disorders among never-smokers referred to a hospital pulmonary function laboratory.

BACKGROUND: Multiple reports have described associations between occupational inhalant exposure and lung disease. Previous occupational lung disease investigations have studied populations consisting of both smokers and nonsmokers. Smoking complicates interpretation of toxicant exposure-response relationships. The objective of this study was to determine whether, among never-smokers, occupational exposure to gases, dusts, or fumes is associated with a history of respiratory disorders and pulmonary function test defined obstructive lung disease. METHODS: We performed a retrospective analysis of 517 never-smoker patients who underwent pulmonary function testing in our clinical laboratory between 1986 and 1999. We calculated the relative risks of developing adverse respiratory health outcomes given a history of exposure to occupational inhalants. RESULTS: Compared with persons with a negative occupational exposure history, exposed persons had an increased risk of reporting a history of bronchitis [relative risk (RR), 1.59; 95% confidence interval (CI), 1.20-2.12], recurrent lung infections (RR, 2.09; 95% CI, 1.14-3.82), and bronchodilator use (RR, 1.61; 95% CI, 1.26-2.06). There was also a statistically significant association between a history of inhalant exposure and the finding of an obstructive ventilatory defect on pulmonary function testing (RR, 1.79; 95% CI, 1.12-2.85). A history of inhalant exposure was not associated with self-reported asthma (RR, 1.08; 95% CI, 0.83-1.41). The population attributable risk estimates for respiratory disorders due to inhalant exposure were: bronchitis, 23.6%; recurrent lung infection, 36.3%; bronchodilator use, 24.3%; and obstructive lung disease, 29.6%. CONCLUSIONS: Occupational inhalant exposure is a strong risk factor for lung disease in this population of never smokers. A significant burden of respiratory disease in this population may be attributable to occupational inhalant exposure.

Adolescent↗
PubMed2005

Ratios of N-(2,3,4-trihydroxybutyl) valine and N-(2-hydroxy-3-butenyl) valine formed hemoglobin adducts in female mice inhalation exposure with 1,3-butadiene.

1,3-Butadiene (BD) is a known rodent and probable human carcinogen (IARC, group 2A) or 'known to be a human carcinogen' (Department of Health and Human Services, 2000). Exposure to BD can occur either via petrochemical products or through the general environment. Adducts can be used as biomarkers for biological monitoring of carcinogen exposure. This study investigated the hemoglobin adducts in blood after inhalation exposure to BD in ICR female mice for three weeks (5 h/day x 5 days/week). During the inhalation exposure, the body weights of mice were significantly lower from day 9 onward for the 500 ppm BD group and from day 4 onward for the 1000 ppm BD group. On the 1st, 2nd and 3rd weeks after inhalation exposure, the concentrations of HB Val adducts were 1.8, 3.7 and 6.2 pmol/mg globin for the 500 ppm BD group, and 5.7, 7.4 and 16.0 pmol/mg globin for the 1000 ppm BD group. The concentrations of THB Val adducts were 32.0, 42.0 and 55.0 pmol/mg globin for the 500 ppm BD group, and 67.8, 72.7 and 83.5 pmol/mg globin for the 1000 ppm BD group. Their defined ratios were higher at the earlier exposure period and at the lower concentration. They were 17.8, 11.4 and 8.87 for the 500 ppm BD group, and 11.9, 9.8 and 5.2 for the 1000 ppm BD group, on the 1st, 2nd and 3rd weeks after inhalation exposure. THB Val and HB Val adducts appear to be the important hemoglobin adducts for monitoring BD exposure, with the latter being a more predictable biomarker than the former.

Administration, Inhalation↗
PubMed2003

Inhalation exposure to haloacetic acids and haloketones during showering.

Inhalation exposure to haloacetic acids (HAAs) and haloketones (HKs) in contaminated drinking water occurs during showering. The size distribution of the aerosols generated by a shower was determined using an eight size-range particle counter, which measured particles from 0.1 to >2 microm. An exponential increase in aerosol numbers was observed while the shower water was on, while the aerosol numbers declined exponentially once the water was turned off. The half-lives of the shower aerosols were longer than 5 min after the shower water was turned off. Although the majority of the shower-generated aerosols were smaller than 0.3 microm, these aerosols only contributed approximately 2% to the measured total aerosol mass. The total shower-generated particulate HAA and HK concentrations collected on an open face filter were approximately 6.3 and 0.13 microg/m3, respectively, for shower water HAA and HK concentrations of 250 and 25 microg/L, respectively. The vapor-phase HK concentrations were 25-50 microg/m3. The estimate of the dose from inhalation exposure of disinfection byproducts (DBPs) in the particulate phase indicate that they represent less than 1% of the ingestion dose, so inhalation is not expected to be an important exposure route to nonvolatile water contaminants or the portion of volatile DBPs that stay in the particulate phase, unless the lung is the target organ. The vapor-phase levels of volatile HKs, though, are significantly higher and can contribute greater than 10% of the ingestion dose during a shower. Thus, risk assessment to the these DBPs needs to consider the inhalation route.

Acetates↗
PubMed1987

Biological effects of short-term, high-concentration exposure to methyl isocyanate. I. Study objectives and inhalation exposure design.

Early reports from India indicated that humans were dying within minutes to a few hours from exposure to methyl isocyanate (MIC). Attempts to explain the cause(s) of these rapid mortalities is where Union Carbide Corporation concentrated its post-Bhopal toxicologic investigations. The MIC studies involving rats and guinea pigs focused primarily on the consequences of acute pulmonary damage. All MIC inhalation exposures were acute, of short duration (mainly 15 min), and high in concentration (ranging from 25-3506 ppm). MIC vapors were statically generated in a double chamber exposure design. Precautionary measures taken during exposures are discussed. Guinea pigs were more susceptible than rats to MIC exposure-related early mortality. A greater than one order of magnitude difference was observed between an MIC concentration that caused no early mortality in rats (3506 ppm) and an MIC concentration that caused partial (6%) early mortality in guinea pigs (225 ppm) for exposures of 10 to 15 min duration. For both species, the most noteworthy clinical signs during exposure were lacrimation, blepharospasm, and mouth breathing. Fifteen minute LC50 tests with 14-day postexposure follow-up were conducted, and the LC50 (95% confidence limit) values were 171 (114-256) ppm for rats and 112 (61-204) ppm for guinea pigs. Target exposure concentrations for the toxicologic investigations of MIC-induced early mortality were established. A short summary of pertinent results of Union Carbide Corporation's post-Bhopal toxicologic investigations is presented.

Animals↗
PubMed1989

Talc deposition and effects after 20 days of repeated inhalation exposure of rats and mice to talc.

The relationship between the inhalation exposure concentration of talc and the resulting lung burdens and histologic lesions was studied using groups of 20 F344/Crl rats and 20 B6C3F mice (10 male and 10 female) exposed to one of three concentrations of asbestos-free talc for 6 hr/day, 5 days/week for 4 weeks. Controls were exposed to filtered air using the same schedule. The pulmonary retention of talc and the development of pulmonary pathology were evaluated. The mass median aerodynamic diameter (MMAD) of the talc aerosol was 3.0 microns with a geometric standard deviation (sigma g) of 1.9. The mean exposure concentrations for rats were 0, 2.3, 4.3, and 17 mg talc/m3. Lung burdens in rats averaged 0, 0.07, 0.17, and 0.72 mg talc/g lung after the 20-day inhalation exposure; thus, the amount retained in the lung per unit of exposure concentration increased with increasing concentration. Mean exposure concentrations for the mice were 0, 2.2, 5.7, and 20.4 mg of talc/m3, which resulted in lung burdens of 0, 0.10, 0.29, and 1.0 mg talc/g lung; thus, the relationship between exposure concentration and the amount retained in the lung was approximately constant. Lung burdens from this study were used to project lung burdens that would result from longer exposures of rodents and man. No clinical signs were observed in the rats or mice prior to sacrifice 24 hr after the last exposure day. Histologic alterations in lung tissue consisted of only a modest, diffuse increase of talc-containing, free macrophages within alveolar spaces in both rat and mouse groups exposed to the highest level of talc for 20 days. A model simulating chronic talc inhalation exposure of rats and mice predicted lung burdens of 2-3 mg talc/g lung (wet wt) if animals were exposed to 17 mg talc/m3 for 2 years, and deposition and clearance of talc were unchanged by continued exposure. A potential limitation in this modeling is that if clearance of talc is delayed by continued exposure, the accumulated talc lung burdens would be higher than those projected by the simulation model. Humans exposed to aerosols of respirable talc are projected to accumulate much higher lung burdens than would occur in rodents exposed to the same aerosol, because humans have a higher estimated deposition fraction and slower estimated clearance of the deposited talc dust. Equilibrium lung burdens of greater than or equal to 2 mg talc/g lung were predicted for human exposures at or near the TLV for talc.

Aerosols↗
PubMed2004

Production of macrophage IL-1beta was inhibited both at the levels of transcription and maturation by caspase-1 following inhalation exposure to isobutyl nitrite.

Epidemiological studies have identified abuse of nitrite inhalants as an independent co-factor in HIV infection and in Kaposi's sarcoma (KS) in AIDS patients. In the present study we investigated the ability of macrophages from mice exposed to isobutyl nitrite to produce the inflammatory cytokine IL-1beta, upon stimulation with IFN-gamma and LPS. The production of IL-1beta was inhibited up to 55%. IL-1beta mRNA transcription was reduced by 35% following nitrite inhalant exposure, consistent with inhibition of activation-induced phosphorylation of macrophage mitogen-activated protein kinase p38. However, synthesis of the 31 kDa IL-1beta precursor protein was only marginally inhibited. Caspase-1, which cleaves the precursor IL-1beta into mature 17 kDa IL-1beta, was examined. Nitrite inhalant exposure blocked activation-induced increases in caspase-1 activity, consistent with a 50% reduction in 17 kDa IL-1beta shown in Western blots. Thus, exposure to nitrite inhalants reduced macrophage production of IL-1beta by reducing transcription, as well as post-translational processing mediated by caspase-1.

Acquired Immunodeficiency Syndrome↗
PubMed2004

The alteration of immune reactions in inbred BALB/c mice following low-level sarin inhalation exposure.

To study the influence of low-level sarin inhalation exposure on immune functions, inbred BALB/c mice were exposed to low concentrations of sarin for 60 min in the inhalation chamber. The evaluation of immune functions was carried out using phenotyping of CD3 (T lymphocytes), CD4 (helper T lymphocytes), CD8 (cytotoxic T lymphocytes), and CD19 cells (B lymphocytes) in the lungs, blood, and spleen, lymphoproliferation of spleen cells stimulated in vitro by various mitogens (concanavalin A, lipopolysaccharides), phagocyte activity of peritoneal and alveolar macrophages, production of N-oxides by peritoneal macrophages, and the measurement of the natural killer cell activity at 1 wk following sarin exposure. The results were compared to the values obtained from control mice exposed to pure air instead of sarin. The results indicate that low doses of sarin are able to alter the reaction of immune system at one week following exposure to sarin. While the numbers of CD3 cells in the lungs, blood, and spleen were slightly decreased, an increase in CD19 cells was observed, especially in the lungs and blood. The reduced proportion of T lymphocytes is caused by decay of CD4-positive T cells. Lymphoproliferation was significantly decreased regardless of the mitogen and sarin concentration used. The production of N-oxides by peritoneal macrophages was stimulated after exposure to the highest dose of sarin, whereas their ability to phagocytize the microbes was increased after exposure to the lowest dose of sarin. The natural killer cell activity was significantly higher in the case of inhalation exposure of mice to the highest level of sarin. Thus, not only organophosphorus insecticides but also nerve agents such as sarin are able to alter immune functions even at a dose that does not cause clinically manifested disruption of cholinergic nervous system in the case of inhalation exposure. Nevertheless, the alteration of immune functions following the inhalation exposure to a symptomatic concentration of sarin seems to be more pronounced.

Administration, Inhalation↗
PubMed1991

Disposition and metabolism of [14C]1,2-dichloropropane following oral and inhalation exposure in Fischer 344 rats.

The objective of this study was to compare the disposition and metabolism of [14C]1,2-dichloropropane [( 14C]DCP) following oral and inhalation exposure since these two routes are of interest with regards to occupational and accidental exposure. [14C]DCP was administered orally to groups of four rats of each sex as a single dose of 1 or 100 mg/kg and as a multiple 1 mg/kg nonradiolabeled dose for 7 days followed by a single 1 mg [14C]DCP/kg dose on day 8. In addition, four rats of each sex were exposed to [14C]DCP vapors for a 6-h period in a head-only inhalation chamber at target concentrations of 5, 50 and 100 ppm. [14C]DCP was readily absorbed, metabolized and excreted after oral or inhalation exposure. For all treatment groups the principal routes of elimination were via the urine (37-65%) and expired air (18-40%). The tissues, carcass, feces and cage wash contained less than 11, 9.7 and 3.8% of the dose, respectively. The major urinary metabolites, as a group, from the oral and inhalation exposures were identified as three N-acetylcysteine conjugates of DCP, N-acetyl-S-(2-hydroxypropyl)-L-cysteine, N-acetyl-S-(2-oxopropyl)-L-cysteine and N-acetyl-S-(1-carboxyethyl)-L-cysteine. The majority (61-87%) of the expired volatile organic material was found to be parent DCP in all samples analyzed. Increasing the dose/concentration of [14C]DCP resulted in an increase in the amount of exhaled [14C]-volatile organics. The peak DCP blood concentrations (inhalation exposure) were not proportional to dose, indicating a dose-dependency in the blood clearance of DCP. Nonetheless, upon termination of exposure, DCP was rapidly eliminated from the blood. In all treatment groups, following oral and inhalation exposure the majority of the radioactivity was eliminated by 24 h postdosing and no differences were noted between sexes. Therefore, it can be concluded that in the rat the pharmacokinetics and metabolism of [14C]DCP are similar regardless of route of exposure or sex.

Administration, Inhalation↗
PubMed1998

Breath, urine, and blood measurements as biological exposure indices of short-term inhalation exposure to methanol.

Due to their transient nature, short-term exposures can be difficult to detect and quantify using conventional monitoring techniques. Biological monitoring may be capable of registering such exposures and may also be used to estimate important toxicological parameters. This paper investigates relationships between methanol concentrations in the blood, urine, and breath of volunteers exposed to methanol vapor at 800 ppm for periods of 0.5, 1, 2, and 8 h. The results indicate factors that must be considered for interpretation of the results of biological monitoring. For methanol, concentrations are not proportional to the exposure duration due to metabolic and other elimination processes that occur concurrently with the exposure. First-order clearance models can be used with blood, breath, or urine concentrations to estimate exposures if the time that has elapsed since the exposure and the model parameters are known. The 0.5 to 2-h periods of exposure were used to estimate the half-life of methanol. Blood data gave a half-life of 1.44+/-0.33 h. Comparable but slightly more variable results were obtained using urine data corrected for voiding time (1.55+/-0.67h) and breath data corrected for mucous membrane desorption (1.40+/-0.38 h). Methanol concentrations in blood lagged some 15-30 min behind the termination of exposure, and concentrations in urine were further delayed. Although breath sampling may be convenient, breath concentrations reflect end-expired or alveolar air only if subjects are in a methanol-free environment for 30 min or more after the exposure. At earlier times, breath concentrations included contributions from airway desorption or diffusion processes. As based on multicompartmental models, the desorption processes have half-lives ranging between 0.6 and 5 min. Preliminary estimates of the mucous membrane reservoir indicate contributions of under 10% for a 0.5-h exposure and smaller effects for longer periods of exposure.

Adult↗
PubMed2005

Air pollution and young children's inhalation exposure to organophosphorus pesticide in an agricultural community in Japan.

Assessment of airborne organophosphorus pesticides in houses of young children (1-6 years old) and childcare facilities was conducted following pesticide applications in an agricultural community in Japan. Trichlorfon and fenitrothion, applied in two separate periods, were frequently detected from outdoor and indoor air. Dichlorvos, the primary degradation product of trichlorfon, was also detected after the application of trichlorfon. Both the outdoors and indoor concentration of applied pesticide were shown to increase with decreasing distance from the pesticide-applied farm. Indoor concentration of these pesticides significantly correlated with outdoor concentration (p=0.001 for trichlorfon and p=0.001 for fenitrothion), indicating infiltration of applied pesticide inside. Ratio of indoor to outdoor concentration (I/O ratio) of fenitrothion was higher for houses with windows open during the application than those with closed windows (median value: 0.74 vs. 0.16, p=0.003). However, a similar trend was not observed for trichlorfon as well as dichlorvos in the first period. Dichlorvos was found to have a higher I/O ratio than trichlorfon during the period, and clear correlation between indoor concentrations of dichlorvos and those of trichlorfon suggested increased decomposition of trichlorfon in the indoor environment. Daily inhalation exposure estimated by using the fixed measurement data and time-activity questionnaire ranged from 0 to 35 ng/kg/day for trichlorfon, from 0 to 26 ng/kg/day for dichlorvos, and from 0 to 44 ng/kg/day for fenitrothion. Median inhalation exposure from indoor air accounted for 74%, 86.3%, and 45% of the daily inhalation exposure, respectively. For kindergarteners or nursery school children, inhalation exposure at childcare facilities was comparable with or more than that at home, indicating that pollution level at childcare facilities had potential of high impact on children's exposure. Estimated daily inhalation exposures were inversely correlated to the proximity of their activity location to the pesticide-applied farm.

Air Pollution, Indoor↗
PubMed1986

A comparative study of the pharmacokinetics of carbon tetrachloride in the rat following repeated inhalation exposures of 8 and 11.5 hr/day.

To evaluate whether exposure to inhaled vapors for periods longer than 8 hr/day could affect the rates and routes of elimination, male Sprague-Dawley rats were repeatedly exposed to 100 ppm of radiolabeled carbon tetrachloride (14CCl4) in a closed-loop chamber. One group was exposed for 8 hr/day for 5 days and another group for 11.5 hr/day for 4 days. Two other groups were exposed for either 8 hr/day for 10 of 12 consecutive days or 11.5 hr/day for 7 of 10 days. The elimination of 14C activity was measured in the expired air, urine, and feces for up to 100 hr following exposure and the pharmacokinetic parameters were determined. Following 2 weeks of exposure to the 8-hr/day schedule, 14CCl4 in the breath and 14C activity in the feces comprised 45 and 48% of the total 14C excreted, respectively. Following 2 weeks of exposure to the 11.5-hr/day schedule, the values were 32 and 62%, respectively, indicating that repeated exposure to the longer schedule altered the route of elimination of CCl4. Regardless of the period of exposure, less than 8% of the inhaled 14CCl4 was excreted in the urine and less than 2% was exhaled in the breath as the 14CO2 metabolite. Approximately 97-98% of the 14C activity in the expired air was 14CCl4. The quantities of 14C noted in the feces and urine suggest that more than 60% of the inhaled CCl4 was metabolized. Elimination of 14CCl4 and 14CO2 in the breath followed a two-compartment, first-order pharmacokinetic model (r2 = 0.98). For rats exposed 8 hr/day and 11.5 hr/day for 2 weeks, the average half-lives for elimination of 14CCl4 in the breath for the fast (alpha) and slow (beta) phases averaged 96 and 455 min, and 89 and 568 min, respectively. The average alpha and beta half-lives for elimination of 14CO2 in the breath of rats exposed to the 11.5-hr/day schedule were 455 and 1824 min, and these were significantly longer than for the 8-hr/day groups, 305 and 829 min. The longer half-lives of elimination for 14CO2 and 14CCl4 which were observed for the groups exposed to the 11.5-hr/day schedule suggest that the 3.5 additional hr of daily exposure places a relatively greater percentage of the absorbed dose into poorly perfused lipophilic depots such as the fat.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

Characteristics of peaks of inhalation exposure to organic solvents.

OBJECTIVES: To determine which exposure metrics are sufficient to characterize 'peak' inhalation exposure to organic solvents (OS) during spraying operations. METHODS: Personal exposure measurements (n=27; duration 5-159 min) were collected during application of paints, primers, resins and glues in 15 companies. A MiniRAE Photo-Ionization Detector measured OS concentrations every second. These readings were adjusted for OS composition, which was determined by charcoal tubes. A peak was defined as a period during which exposure exceeded the time-weighted average (TWA) exposure. Five second and 1 and 15 min moving average times were considered in defining a peak. The number of peaks per hour, the duration of a peak, the maximum concentration within a peak, the average concentration within a peak, the ratio between maximum and average concentration within a peak and the average time between two peaks were recorded for each sample. Data were analyzed using factor analysis on 13 variables for the 27 samples: TWA concentration of the task and the six peak characteristics based on the 5 s and 1 min moving averaging time. RESULTS: There were three statistically independent sources of correlation among metrics of peak exposure, explaining 87% of the multiple correlation. The first factor reflected the intensity of peak exposure; it was also associated with the TWA. The second and third factors were related to measures of variability (in frequency and intensity) and duration of peaks, respectively. CONCLUSIONS: We present a method for describing peak profiles for inhalation exposure in terms of various distinguishable and independent parameters. Pending development of toxicologically justified peak exposure metrics, such investigations can be of value in identifying exposure metrics for which non-confounded risk estimates can be obtained in epidemiological studies.

Environmental Monitoring↗