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PubMed2000

Successful treatments of lung injury and skin burn due to hydrofluoric acid exposure.

Recent growth in the electronics and chemical industries has brought about a progressive increase in the use of hydrofluoric acid (HF), along with the concomitant risk of acute poisoning among HF workers. We report severe cases of inhalation exposure and skin injury which were successfully treated by administering a 5% calcium gluconate solution with a nebulizer and applying 2.5% calcium gluconate jelly, respectively. Case 1: A 52-year old worker used HF for surface treatment after welding stainless steel, and was hospitalized with rapid onset of severe dyspnea. On admission to the critical care medical center he had widespread wheezing and crackles in his lungs. Chest radiograph showed a fine diffuse veiling over both lower pulmonary fields. Severe hypocalcemia with high concentrations of F in serum and urine were disclosed. He was immediately given 5% calcium gluconate solution by intermittent positive-pressure breathing (IPPB), utilizing a nebulizer. On the 21st hospital day, chest film and CT scan did not demonstrate any abnormality. He was discharged very much improved on the 22nd hospital day. Case 2: A 35-year old worker at an electronics factory was admitted to his local hospital with severe skin burn on his face and neck after exposure to 100% HF. Treatment began with immediate copious washing with water for 20 min. Calcium gluconate 2.5% gel (HF burn jelly) was applied to the area as a first-aid measure. Persistent high concentrations of serum and urinary F were disclosed for 2 weeks. After treatment with applications of HF burn jelly, he was confirmed as being completely recovered. The present cases and a review of published data suggest that an adequate method of emergency treatment for accidental HF poisoning is necessary.

Administration, Topical↗
PubMed2001

Inhalation studies with the Göttingen minipig.

A method for inhalative exposure of minipigs to aerosols and gases has been developed. Minipigs are exposed via mask inhalation to the test substance using a computer-controlled exposure system that permits simultaneous exposure of groups of four animals in parallel to different controlled dose levels. We studied inhalation treatment of verapamil, a cardiovascular drug, and show good absorption and favorable pharmacokinetics when compared with iv drug application. The results shown in this study encourage inhalation studies with the Göttingen minipig.

Aerosols↗
PubMedDate not supplied

Chlorine gas exposure and the lung: a review.

We conducted a review of the literature detailing the respiratory effects of chlorine, an extremely important but toxic halogen. Historically, the heaviest mass inhalational exposures to chlorine resulted from World War I gassing. Currently potential human exposure to chlorine inhalation occurs in a variety of settings in the workplace, as a result of inadvertent environmental releases, and even in the home due to household cleaning mishaps. Chlorine species are highly reactive; tissue injury results from exposure to chlorine, hydrochloric acid, hypochlorous acid, or chloramines. Acute, high level exposure to chlorine gas in occupational or environmental settings results in a variety of dose-related lung effects ranging from respiratory mucus membrane irritation to pulmonary edema. Pulmonary function testing can reveal either obstructive or restrictive deficits immediately following exposure, with resolution over time in the majority of cases. However, some of those exposed may demonstrate long-term persistent obstructive or restrictive pulmonary deficits or increased nonspecific airway reactivity after high level exposure to chlorine gas. Symptoms and signs following inhalation of mixtures of chlorine-containing cleaners in the home are similar to those after occupational exposures and environmental releases. Although generally less severe, these events may be extremely common. Controlled human exposure data suggest that some subjects may be more responsive to the effects of chlorine gas; epidemiologic data also indicate that certain subpopulations (e.g., smokers) may be at greater risk of adverse outcome after chlorine inhalation. Although these findings are intriguing, additional study is needed to better delineate the risk factors that predispose toward the development of long-term pulmonary sequelae following chlorine gas exposure.

Animals↗
PubMed2005

Evaluation and further development of EASE model 2.0.

EASE (Estimation and Assessment of Substance Exposure) is a general model that may be used to predict workplace exposure to a wide range of substances hazardous to health. First developed in the early 1990s, it is now in its second Windows version. This paper provides a critical assessment of the utility and performance of the EASE model, and on the basis of this review, recommendations for the structure of a revised model are outlined. Twenty-seven stakeholders were interviewed about their previous use of EASE, perceived advantages and limitations of the model and suggestions for improvement. A subset of stakeholders was contacted on a second occasion to determine their views on the preferred outputs for an ideal exposure assessment model. Overall, stakeholders felt that the model should be updated to provide more accurate and precise exposure assessments. However, users also expressed the view that the simplicity and usability of the software model should not be compromised. Six studies investigating the validity of the inhalation exposure assessment section of EASE were identified. These showed that the model generally either predicted close to the measured exposures or overestimated exposure; though performance was highly variable. Two studies investigated the validity of the dermal exposure assessment and found that EASE produced considerable overestimates of actual dermal exposure (the amount of a substance that actually lands on the skin). A conceptual model of exposure was developed to investigate whether the structure of the EASE model is appropriate. Although EASE has a number of characteristics that describe exposure, it is a greatly simplified model and does not include all the important exposure determinants. More importantly, EASE can produce estimates of exposure that are ambiguous or incomplete. Our conceptual model may provide a rational basis for developing an improved version of EASE but further consultation is needed to decide the purpose and intended use of any successor to EASE.

Air Pollutants, Occupational↗
PubMed2003

Estimating methyl bromide exposure due to offgassing from fumigated commodities.

Methyl bromide (MB) is used to fumigate diverse commodities. During fumigation, the commodity can sorb a substantial mass of MB, which does not chemically react and is termed a residue. During subsequent commodity handling, the residue offgasses and can lead to MB inhalation exposure among processing workers. Although MB has a low 1 ppm 8-hr TLV-TWA as recommended by the American Conference of Governmental Industrial Hygienists (ACGIH(R)) and is considered a potential occupational carcinogen by the National Institute for Occupational Safety and Health, the recent industrial hygiene literature contains no pertinent exposure data. Limited measurements made in 1992 by the California Department of Pesticide Regulation are summarized here, but associated information on exposure determinants is lacking. In this article, mathematical models are used to integrate data on MB residue offgassing with several processing scenarios to estimate potential exposure levels. The main finding is that if a large volume of commodity rapidly offgasses MB and is handled under conditions of low ventilation, the potential exists for MB exposures above the 1 ppm TLV-TWA value. However, the combination of handling a smaller commodity volume and less rapid offgassing may be the more typical scenario. It is recommended that a pilot study be conducted to measure current MB exposure levels, test the validity of the mathematical models, and collect industry-wide data on exposure determinants. By using the latter data as inputs for validated models, public health scientists could estimate the distribution of MB exposure levels across the commodity processing industry.

Agrochemicals↗
PubMed1993

Styrene and styrene oxide: results of studies on carcinogenicity in experimental animals.

Fourteen long-term toxicity studies were reviewed in an effort to evaluate the potential carcinogenic activity of styrene and styrene oxide in animals. Each study was reviewed and evaluated for detail and adequacy of design, adequacy of reported data and interpretation. The results of the review are: 1. There is no convincing evidence for a carcinogenic action of styrene in animals, even though it has been studied in several species and by several routes of exposure: inhalation, gavage, in the drinking-water and by intraperitoneal and subcutaneous injection. Most of the studies of styrene, however, have deficiencies in design and/or conduct. 2. Styrene oxide was carcinogenic to the forestomach of rats and mice of each sex after exposure by gavage at all doses tested, including one as low as 50 mg/kg per day. An increase in the incidence of liver neoplasms was observed in male mice in one study. No carcinogenic activity was observed in mice exposed by skin painting. The relevance to humans of the studies in which exposure was by gavage is limited because: (i) the route is less than ideal for extrapolating to human risk from exposure by inhalation or dermally; (ii) xenobiotics often cause neoplasms at this site when given at high concentrations; and (iii) neoplasms at sites distant from the site of exposure were found in only one sex of one species. 3. None of the studies of styrene or styrene oxide reported here is well suited for extrapolating to potential carcinogenic activity in humans, because all have deficiencies in design, conduct and/or interpretation. An up-to-date chronic inhalation study would have to be conducted in order to evaluate this aspect of hazard assessment.

Animals↗
PubMed2002

Assessment of long-term neurotoxic effects of exposure to mesitylene (1,3,5-trimethylbenzene) based on the analysis of selected behavioral responses.

Trimetylbenzene isomers: pseudocumene, hemimellitene and mesitylene, are major components of numerous commercial solvents and high-grade fuels. In our earlier research on rats we have proved that inhalation exposure to pseudocumene or hemimellitene at concentrations close to the MAC value results in behavioral changes detectable many weeks after cessation of the exposure. The aim of our present study is to determine whether exposure to mesitylene causes effects similar to those observed for pseudocumene and hemimellitene. Male rats were used in the experiment. The animals were exposed in the inhalation chambers to mesitylene vapors at the following concentrations: 0 ppm--group MES0; 25 ppm (125 mg/m3)--group MES25; 100 ppm (500 mg/m3)--group MES100 and 250 ppm (1,250 mg/m3)--group MES250 for 4 weeks (6 h/day, 5 days/week). The following behaviors were tested: 1) ability to find water in a radial maze (14-19 days after the exposure); 2) open field locomotor activity (25 days after the exposure); 3) acquiring the conditioned reaction of active avoidance (35-45 days after the exposure); 4) sensitivity to pain and stress-induced changes of pain sensitivity (50-51 days after the exposure); and 5) acquiring the conditioned reaction of two-way active avoidance (54-60 days after the exposure). Significant between-group differences were noted in passive and active avoidance tests and sensitivity to pain. In the MES25, MES100 and MES250 rats, the persistence of the passive avoidance reaction was shorter, and more trials were required to produce the active avoidance reaction than in controls (group MES0), the MES100 group appeared to be more fearful on the second day of testing on the hot plate. The exposed groups did not differ in the magnitudes of the detected changes (no concentration-effect relationship). These results indicate that inhalation exposure to mesitylene, like that to pseudocumene and hemimellitene, at concentrations close to the current hygiene standard value for trimethylbenzene, may produce long-term functional changes in the rat central nervous system.

Administration, Inhalation↗
PubMed1980

Acute exposure of laboratory mice to manganese oxide.

An acute inhalation exposure of laboratory mice to respirable Mn3O4 aerosols is described. The generation system consisted of a Wright dust generator which produced 1.40 micrometer aerosols. A non-linear loss of deposited manganese from mouse lungs over the inital 24-hour post-exposure period was observed. Systemic distribution of the manganese was observed in various tissues following exposure.

Air Pollutants↗
PubMed1985

[Rhythm of lung function during the period of a week, with and without exposure to respiratory tract irritants].

In 10 subjects without inhalative exposure FVC, FEV-1 and Ros were measured at the same day-time over three weeks. Influence of the week course on lung function could not be proved statistically. On the other hand significant differences of FVC and FEV-1 between week-days depending on working conditions could be shown in 9 workers exposed to heated polyester materials. Likewise lung function values measured during the shift departed from the expected circadian rhythm.

Environmental Exposure↗
PubMedDate not supplied

Hexavalent chromium exposures during full-aircraft corrosion control.

Aluminum alloys used in the construction of modern aircraft are subject to corrosion. The principal means of controlling this corrosion in the U.S. Air Force are organic coatings. The organic coating system consists of a chromate conversion coat, epoxy resin primer, and polyurethane enamel topcoat. Hexavalent chromium (CrVI) is present in the conversion coat in the form of chromic acid and in the primer in the form of strontium chromate. CrVI inhalation exposures can occur when workers spray conversion coat onto bare metal and apply primer to the treated metal surface. In addition, mechanical abrasion of aircraft surfaces can generate particulates that contain chromates from previously applied primers and conversion coats. This study measured CrVI exposures during these corrosion control procedures. Mean time-weighted average (TWA) exposure to chromic acid during conversion coat treatment was 0.48 microg/m(3), below the current American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value (TLV(R)) TWA of 50 microg/m(3) for water-soluble CrVI compounds. Mean TWA exposures to strontium chromate were 5.33 microg/m(3) during mechanical abrasion and 83.8 microg/m(3) during primer application. These levels are in excess of the current ACGIH TLV-TWA of 0.5 microg/m(3) for strontium chromate. In the absence of a change from chromated to nonchromated conversion coats and primers, additional control measures are needed to reduce these exposures.

Aircraft↗
PubMed1999

Two-week inhalation toxicity of polymeric diphenylmethane-4, 4'-diisocyanate (PMDI) in rats: analysis of biochemical and morphological markers of early pulmonary response.

The pulmonary response of Wistar rats to respirable polymeric diphenylmethane-4,4'-diisocyanate (PMDI) aerosol was examined in a 2-wk repeated nose-only inhalation exposure study. Exposure concentrations were 1.1, 3.3, and 13.7 mg PMDI/m(3) (6 h/day, 15 exposures). The level of 13.7 mg/m(3) was actually a combination of an initial target concentration of 10 mg/m(3) in wk 1, which was raised to 16 mg/m(3) in wk 2, due to a lack of signs suggestive of pulmonary irritation. An acute sensory irritation study on rats served as basis for selection of these concentrations. Shortly after the 2-wk exposure period, rats were subjected to pulmonary function and arterial blood gas measurements. Lungs were examined by light and transmission electron microscopy, and labeling indices in terminal bronchioles were measured. Bronchoalveolar lavage (BAL) was performed to assess various indicators of pulmonary inflammation, including neutrophil and macrophage numbers, protein, lactate dehydrogenase (LDH), gamma-glutamyltranspeptidase (gamma-GT), alkaline phosphatase (APh), acid phosphatase (ACPh), and beta-N-acetylglucosaminidase (beta-NAG). Phosphatidylcholine in BAL fluid and BAL cells was determined as aggregated endpoint suggestive of changes in pulmonary surfactant. Rats exposed to 3.3 and 13.7 mg/m(3) experienced concentration-dependent signs of respiratory tract irritation. Determination of arterial blood gases, lung mechanics, and carbon monoxide diffusing capacity did not demonstrate specific effects. Analysis of BAL fluid and BAL cells revealed changes indicative of marked inflammatory response and/or cytotoxicity in rats exposed to 13.7 mg/m(3), and the changes were characterized by statistically significantly increased activities of LDH, beta-NAG, and protein. Phospholipid concentrations were increased in rats exposed to 1.1 mg/m(3) and above (elevated levels of lipid material in alveolar macrophages demonstrated by polychrome stain) and 3.3 mg/m(3) and above (increased intracellular ACPh activity and intracellular phospholipids). In these groups, gamma-GT was statistically significantly increased. These findings suggest that changes in phospholipid homeostasis appear to occur at lower levels than those eliciting inflammation and cytotoxicity. Light and transmission electron microscopy suggest that exposure to 3.3 and 13. 7 mg/m(3) resulted in focal inflammatory lesions and an accumulation of refractile, yellowish-brownish material in alveolar macrophages with concomitant activation of type II pneumocytes. In the terminal bronchioles a concentration-dependent increase of bromodeoxyuridine (BrdU)-labeled epithelial cells was observed in all PMDI exposure groups. In summary, it appears that respirable PMDI aerosol interacts with pulmonary surfactant, which, in turn, may stimulate type II pneumocytes to increase their production of surfactant and to proliferate.

Allergens↗
PubMed1999

Physiological modeling of the toxicokinetic interactions in a quaternary mixture of aromatic hydrocarbons.

The available data on binary interactions are yet to be considered within the context of mixture risk assessments because of our inability to predict the effect of a third or fourth chemical in the mixture on the interacting binary pairs. Physiologically based toxicokinetic (PBTK) models represent a framework that can be potentially used for predicting the impact of multiple interactions on component kinetics at any level of complexity. The objective of this study was to develop and validate an interaction-based PBTK model for simulating the toxicokinetics of the components of a quaternary mixture of aromatic hydrocarbons [benzene (B), toluene (T), ethylbenzene (E), m-xylene (X)] in the rat. The methodology consisted of: (1) obtaining and refining the validated individual chemical PBTK models from the literature, (2) interconnecting all individual chemical PBTK models at the level of liver on the basis of the mechanism of binary chemical interactions (e.g., competitive, noncompetitive, or uncompetitive metabolic inhibition), and (3) comparing the a priori predictions of the interaction-based model to corresponding experimental data on venous blood concentrations of B, T, E, and X during mixture exposures. The analysis of blood kinetics data from inhalation exposures (4 h, 50-200 ppm each) of rats to all binary combinations of B, T, E, and X was suggestive of competitive metabolic inhibition as the plausible interaction mechanism. The metabolic inhibition constant (K(i)) for each binary combination was quantified and incorporated within the mixture PBTK model. The binary interaction-based PBTK model predicted adequately the inhalation toxicokinetics of all four components in rats following exposure to mixtures of BTEX (50 ppm each of B, T, E, and X, 4 h; 100 ppm each of B, T, E and X, 4 h; 100 ppm B + 50 ppm each of T, E, and X, 4 h). The results of the present study suggest that data on interactions at the binary level alone are required and sufficient for predicting the kinetics of components in complex mixtures.

Administration, Inhalation↗
PubMed1998

Toxicologic profile of acrylonitrile.

Acrylonitrile is a monomer used extensively as a raw material in the manufacturing of acrylic fibers, plastics, synthetic rubbers, and acrylamide. It has been classified as a probable human carcinogen according to the results of numerous chronic rat bioassays. The present report summarizes the toxicity data on acrylonitrile and reviews available data concerning the mechanism (genetic versus epigenetic) by which acrylonitrile is carcinogenic in rats. From the evaluation of the relevant toxicity data, it can be concluded that acrylonitrile is indeed carcinogenic to rats after either oral or inhalational exposure. However, information on other mammalian species is lacking, and, moreover, the exact mechanism of the carcinogenic process is unclear. Therefore, it is recommended to conduct an additional long-term inhalation carcinogenicity study with acrylonitrile in mice, as well as studies into the mechanism by which acrylonitrile induces (brain) tumors in rats (genetic versus epigenetic).

Acrylonitrile↗
PubMed2002

Levels and risk assessment for humans and ecosystems of platinum-group elements in the airborne particles and road dust of some European cities.

Traffic is the main source of platinum-group element (PGE) contamination in populated urban areas. There is increasing concern about the hazardous effects of these new pollutants for people and for other living organisms in these areas. Airborne and road dusts, as well as tree bark and grass samples were collected at locations in the European cities of Göteborg (Sweden), Madrid (Spain), Rome (Italy), Munich (Germany), Sheffield and London (UK). Today, in spite of the large number of parameters that can influence the airborne PGE content, the results obtained so far indicate significantly higher PGE levels at traffic sites compared with the rural or non-polluted zones that have been investigated (background levels). The average Pt content in airborne particles found in downtown Madrid, Göteborg and Rome is in the range 7.3-13.1 pg m(-3). The ring roads of these cities have values in the range 4.1-17.7 pg m(-3). In Munich, a lower Pt content was found in airborne particles (4.1 pg m(-3)). The same tendency has been noted for downtown Rh, with contents in the range 2.2-2.8 pg m(-3), and in the range 0.8-3.0 and 0.3 pg m(-3) for motorway margins in Munich. The combined results obtained using a wide-range airborne classifier (WRAC) collector and a PM-10 or virtual impactor show that Pt is associated with particles for a wide range of diameters. The smaller the particle size, the lower the Pt concentration. However, in particles <PM-10, some of the highest values correspond to the fraction <0.39 microm. Considering an average Pt content in all particles of approximately 15 pg m(-3), which is representative for all countries and environmental conditions, the tracheobronchial fraction represents approximately 10% and the alveolar fraction approximately 8% of the total particles suspended in air. However, from the environmental risk point of view, an exposure to PGEs in traffic-related ambient air is at least three orders of magnitude below the levels for which adverse health effects might theoretically occur (of approx. 100 ng m(-3)). Therefore, today inhalation exposure to PGEs from automotive catalysts does not seem to pose a direct health risk to the general population. Even though the data available today indicate no obvious health effects, there are still a number of aspects related to PGEs and catalysts that justify further research. First, continual monitoring of changes in PGE levels in air and road dust is warranted, to make sure that there is no dramatic increase from today's levels. Secondly, more detailed information on the chemical composition of the PGE-containing substances or complexes leaving the catalyst surface and the size distribution of the PGE-containing particles released during driving will facilitate a more in-depth human risk assessment.

Air Pollutants↗
PubMed2006

TENORM aerosols in the Florida phosphate industry--assessment of lung fluid solubility and annual effective dose to workers.

Inhalation exposure to workers in the Florida phosphate industry due to TENORM aerosols has not been adequately addressed owing to lack of aerosol information. One of the more critical factors is the absorption rate of inhaled radionuclides into blood. In this study, this parameter was characterised using an in vitro dissolution test. The solubility data and other aerosol information were then used for individualised dose assessments at six different Florida phosphate facilities. The solubility data support the selections of ICRP Publication 66 Type M for uranium and lead isotopes and Type S for thorium isotopes. Total annual effective doses are 0.34 +/- 0.12 mSv at granulator areas, 0.30 +/- 0.10 mSv at storage areas and 0.23 +/- 0.02 mSv at shipping areas. These findings are considerably lower than originally postulated in previous studies where no site-specific information on particle size and lung fluid solubility had been available.

Aerosols↗
PubMed2006

Carcinogenicity and chronic toxicity in rats and mice exposed by inhalation to 1,2-dichloroethane for two years.

Carcinogenicity and chronic toxicity of 1,2-dichloroethane (DCE) were examined by inhalation exposure of groups of 50 F344 rats and 50 BDF1 mice of both sexes to DCE vapor or clean air as control for 6 h/d, 5 d/wk and 104 wk. The rats were exposed to 10, 40 or 160 ppm (v/v) DCE, while the mice were exposed to 10, 30 or 90 ppm. The 2-yr exposure to DCE produced a dose-dependent increase in incidences of benign and malignant tumors, including subcutaneous fibroma, mammary gland fibroadenoma and peritoneal mesothelioma in male rats; subcutaneous fibroma and mammary gland adenoma, fibroadenoma and adenocarcinoma in female rats; and bronchiolo-alveolar adenoma and carcinoma, endometrial stromal polyp, mammary gland adenocarcinoma and hepatocellular adenoma in female mice. No exposure-related change in the incidence of non-neoplastic lesions or in any hematological, blood biochemical or urinary parameter occurred in any DCE-exposed rat or mouse group. The types of tumors and their target organs found in this study were consistent with those observed in rats and mice administered DCE by gavage in a NCI study. Selection of the exposure concentrations was considered appropriate with reference to the maximum tolerated dose for the highest doses and an occupational exposure limit of DCE for the lowest dose. The present findings suggest that those carcinogenic responses be primarily considered for standard setting of occupational and environmental exposure to DCE.

Animals↗
PubMedDate not supplied

Toxicokinetics of human exposure to methyl tertiary-butyl ether (MTBE) following short-term controlled exposures.

Methyl tertiary-butyl ether (MTBE) is an oxygenated compound added to gasoline to improve air quality as part of the US Federal Clean Air Act. Due to the increasing and widespread use of MTBE and suspected health effects, a controlled, short-term MTBE inhalation exposure kinetics study was conducted using breath and blood analyses to evaluate the metabolic kinetics of MTBE and its metabolite, tertiary-butyl alcohol (TBA), in the human body. In order to simulate common exposure situations such as gasoline pumping, subjects were exposed to vapors from MTBE in gasoline rather than pure MTBE. Six subjects (three females, three males) were exposed to 1.7 ppm of MTBE generated by vaporizing 15 LV% MTBE gasoline mixture for 15 min. The mean percentage of MTBE absorbed was 65.8 +/- 5.6% following exposures to MTBE. The mean accumulated percentages expired through inhalation for 1 and 8 h after exposure for all subjects were 40.1% and 69.4%, respectively. The three elimination half-lives of the triphasic exponential breath decay curves for the first compartment was 1-4 min, for the second compartment 9-53 min, and for the third compartment 2-8 h. The half-lives data set for the breath second and blood first compartments suggested that the second breath compartment rather than the first breath compartment is associated with a blood compartment. Possible locations for the very short breath half-life observed are in the lungs or mucous membranes. The third compartment calculated for the blood data represent the vessel poor tissues or adipose tissues. A strong correlation between blood MTBE and breath MTBE was found with mean blood-to-breath ratio of 23.5. The peak blood TBA levels occurred after the MTBE peak concentration and reached the highest levels around 2-4 h after exposures. Following the exposures, immediate increases in MTBE urinary excretion rates were observed with lags in the TBA excretion rate. The TBA concentrations reached their highest levels around 6-8 h, and then gradually returned to background levels around 20 h after exposure. Approximately 0.7-1.5% of the inhaled MTBE dose was excreted as unchange urinary MTBE, and 1-3% was excreted as unconjugated urinary TBA within 24 h after exposure.

Adult↗
PubMed2004

Acute toxicity and cancer risk assessment values for tert-butyl acetate.

tert-Butyl acetate (TBAc) is an industrial chemical with potential uses as a degreaser and in architectural coatings. Limited chronic toxicity data exist for TBAc. However, acute inhalation exposure data are available for TBAc. Additionally, TBAc has been demonstrated to be substantially metabolized to tert-butanol (TBA) in rats, and a positive TBA genotoxicity study suggests that TBA may cause oxidative DNA damage. TBA has been shown to induce tumors in both rats and mice, and the Office of Environmental Health Hazard Assessment has calculated an oral cancer potency factor (CSF) for TBA of 3 x 10(-3)(mg/kg-day)(-1). Therefore, TBAc should be considered to pose a potential cancer risk to humans because of the metabolic conversion to TBA. An acute 1-h reference exposure level of 1 mg/m3 can be calculated from the extrapolated no observed adverse effect level of 50 mg/m3. A CSF of 0.002(mg/kg-day)(-1) can be derived for TBAc, assuming 100% metabolism of TBAc to TBA. An inhalation unit risk value for TBAc of 4 x 10(-7)(microg/m(3))(-1) can then be derived from the CSF value for TBAc by assuming a human breathing rate of 20 m3/day, 70% fractional absorption, and an average human body weight of 70 kg.

Acetates↗