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Biomedical subjects

B Ballantyne

Publications and source records attributed to B Ballantyne.

At least 37 records · Page 2Linked to original sources
PubMed1995

Repeated exposure toxicity of 2-ethyl-1,3-hexanediol by cutaneous applications to the rat for 9 and 90 days.

2-Ethyl-1,3-hexanediol (EHD; CASRN 94-96-2), an industrial chemical and insect repellent, has a high potential for recurrent skin contact. Short-term (9 d) and subchronic (13 w) repeated epicutaneous contact studies were conducted to determine the potential for cumulative local skin irritation and systemic toxicity in Fischer 344 rats. Doses were 0.5, 2.0 or 4.0 ml/kg/d of undiluted EHD. There were no clinical signs and no treatment-related effects on hematology, clinical chemistry or histology of a large number of organs and tissues including the treated skin. The only effects where slight decreases in body weight gain for the high-dose males in the 9-d study and males and females of the high-dose group in the subchronic study; slight decreases in food consumption for females of all treatment groups in the subchronic study; and slight increases in relative liver weight for high-dose females in the 9-d study and high-dose males in the subchronic study, which is probably a compensatory hypertrophy for the metabolism of EHD. Thus, recurrent epicutaneous applications of undiluted EHD to the rat did not cause any local skin irritation or cumulative or organ-specific toxicity.

Administration, Cutaneous↗
PubMed1994

Evaluation of exposure to water aerosol or air by nose-only or whole-body inhalation procedures for CD-1 mice in developmental toxicity studies.

This study was performed to evaluate the effects of nose-only restraint versus whole-body exposure procedures in the absence of test chemical, and to determine the appropriate control environment (water aerosol or air) for subsequent developmental toxicity studies of test materials administered as aerosols. Timed-pregnant CD-1 mice, 30/group, were exposed to high concentrations of water aerosol or to air by whole-body or nose-only inhalation procedures on Gestational Days (GD) 6 through 15 for 6 hr per day. The group exposed to air by whole-body procedures was designated as the control group. Clinical observations and maternal body weights were recorded throughout gestation. At scheduled necropsy on GD 18, maternal animals were evaluated for body weight, gravid uterine weight, liver weight, number of ovarian corpora lutea, and status of uterine implantation sites. Fetuses were counted, weighed, and sexed and were examined for external, visceral (including craniofacial), and skeletal alterations. Indices of maternal toxicity were affected in both nose-only groups. Maternal body weights were reduced during and after the exposure period; maternal weight gain was reduced during the exposure period. Clinical signs observed, from animals struggling during restraint, were resolved by GD 18. At sacrifice on GD 18, maternal body weights and maternal gestational weight gains (both corrected for gravid uterine weights) and absolute liver weights were reduced in both nose-only groups. Four females died (13.3%, all pregnant) in the air nose-only group, and maternal liver weight (relative to body weight) was reduced in the aerosol nose-only group. Gestational parameters were unaffected by any of the treatments. There were no statistically significant differences in the incidences of any individual malformations or malformations by category (external, visceral, or skeletal) or of total malformations. However, exencephaly, low set ears, cleft palate and ventricular septal defect were observed only in both aerosol-exposed groups (whole-body and nose-only exposed). The incidences of individual external or visceral variations or of variations by category or of total variations were unaffected. The incidence of one skeletal variation, poorly ossified supraoccipital skull bone, was significantly increased in the aerosol nose-only group relative to the air whole-body controls. There were also increased incidences (not statistically significant) of extra (14th) ribs in both aerosol groups. Therefore, maternal restraint (in both nose-only groups) during organogenesis produced indications of maternal toxicity, but restraint did not appear to affect normal embryo/fetal morphologic development.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗
PubMed1994

Pulmonary alveolar phospholipoproteinosis induced by Orasol Navy Blue dust.

1. Orasol Navy Blue (ONB) is a water-insoluble nitroaromatic dye to which workers may be exposed to the dust. 2. Rats and guinea pigs exposed for 30 min to 173 mg m-3 did not show toxic signs or respiratory tract histopathology. 3. Rats, mice and guinea pigs were exposed 6 h a day for 20 or 100 days to 2.05 mg m-3 ONB dust (particle size, 33.6% < 5 microns). Except for decreased body weight of guinea pigs during the exposure period, no adverse signs were seen over a 1-year period from the first exposure. Respiratory tract histopathology was not seen in mice or guinea pigs. Rats showed scattered alveolar lesions characterized by aggregations of macrophages, PAS-positive debris, cholesterol, sudanophilia and birefringence, with preservation of the interstitum and no fibrogenic response. The number and size of these lesions was related to the duration of exposure. 4. The similarity of the lesions seen in the rat following exposure to ONB dust and those seen in humans from other exogenous causes of pulmonary alveolar phospholipoproteinosis suggests that overexposure of humans to a respirable dust of ONB may produce this lesion. 5. The rat is a convenient model to investigate pulmonary alveolar phospholipoproteinosis by exposure to respirable dusts.

Animals↗
PubMed1992

The acute toxicity, primary irritancy and skin sensitizing potential of glutaric anhydride.

Glutaric anhydride (GA), an industrial chemical, was found of moderate acute peroral lethal toxicity with LD50 values (95% confidence limits) in the rat of 1.41 (0.80-2.49) g/kg (males) and 0.54 (0.36-0.79) g/kg (females), with death being due in part to gastrointestinal irritancy. Dilution with water given by gavage after peroral dosing had no effect on lethal toxicity. Acute percutaneous LD50 values (rabbit) by 24-h occlusion were 6.25 (5.34-7.33) g/kg in males and 5.66 (3.21-9.95) g/kg in females; local skin effects included erythema, edema, necrosis and ulceration. A 6-h exposure to a statically generated saturated vapor atmosphere (rat) produced no signs of toxicity or irritancy. A 4-h, but not 1-h or 3-min occluded contact with 0.5 g of moistened GA (rabbit) produced erythema, edema and necrosis. Contamination of the eye (rabbit) with 10 mg GA produced conjunctivitis (hyperemia, chemosis and discharge) which persisted 7 to 14 d, mild iritis of 2 to 14 d duration, and mild to severe corneal injury which healed within 14 d. A maximization study in guinea pigs by the method of Magnusson and Kligman showed no potential for skin sensitization with GA. The major acute hazards of GA were by swallowing, eye contact and sustained skin contact.

Administration, Cutaneous↗
PubMed1991

Ophthalmic effects of oximes: a review.

Evidence from controlled clinical trials of oximes indicates that high doses given im or iv may cause transient disturbances of vision. Blurring of vision and diplopia present for up to an hour can occur. These are often accompanied by other side effects such as nausea, epigastric discomfort, drowsiness and dizziness. Visual effects have not been reported following high doses of oximes given po. Experimental studies provide evidence that some oximes given at high dosages may penetrate the blood-brain and blood-aqueous humor barriers. These suggest that the visual effects may be mediated through the CNS and/or by direct effects on the accommodation mechanisms of the eye. Although transient, the visual effects should be taken into account in clinical trials designed to assess the dosage necessary to achieve prophylaxis against OP antiChE poisoning in occupational situations.

Central Nervous System↗
PubMed1989

Dermal oncogenicity studies on two methoxysilanes and two ethoxysilanes in male C3H mice.

The dermal oncogenic potential of beta-(3,4-epoxycyclohexyl)ethyltrimethoxysilane (EEMS), gamma-glycidoxypropyltrimethoxysilane (GPMS), beta-(3,4-epoxycyclohexyl)ethyltriethoxysilane (EEES), and gamma-glycidoxypropyltriethoxysilane (GPES) was assessed by applying 25-microliters aliquots of acetone solutions to the skin of 40 male C3H/HeJ mice. The concentrations applied were 100, 25, 10, and 10% by volume for EEMS, GPMS, EEES, and GPES, respectively. Applications were made thrice weekly until the death of the animals. A negative control group received acetone (solvent) only. No treatment-related skin tumors were observed, nor was there evidence of increased incidence of any internal tumor in the groups that received GPMS, EEES, or GPES. In the group treated with EEMS, four mice were observed with squamous cell carcinomas of the treated skin and two mice had subcutaneous sarcomas outside of the treated area. No skin tumors were observed in the group treated with acetone, but two mice had subcutaneous sarcomas outside of the treated area. The mean survival times were 529, 482, 545, 492, and 502 days for the EEMS, GPMS, EEES, GPES, and acetone control groups, respectively. In no case was the mortality rate significantly different from that of the controls. The results indicate that only EEMS was oncogenic under the conditions of these studies.

Animals↗
PubMed1989

Evaluation of the developmental toxicity of ethylene glycol monohexyl ether vapor in Fischer 344 rats and New Zealand white rabbits.

Timed pregnant Fischer 344 rats and New Zealand White rabbits were exposed to vapor from ethylene glycol monohexyl ether (EGHE, CAS No. 112-25-4) for 6 hr/day on gestational days (gd) 6 through gd 15 (rats) or gd 6 through gd 18 (rabbits) at analytically measured concentrations (as means +/- SD) of 20.8 +/- 0.90, 41.1 +/- 1.77, or 79.2 +/- 10.8 ppm; control animals were exposed to air alone. Monitors for maternal toxicity were body weight, food and water consumption, clinical signs, and hematology. At sacrifice (gd 21 rats, gd 29 rabbits) maternal weight, liver weight, and gravid uterine weight were measured. Gestational parameters monitored were numbers of corpora lutea, preimplantation losses, viable implants, early and late resorptions, and dead fetuses. Live fetuses were sexed, weighed, and examined for external, visceral, and skeletal malformations and variations. Rabbit maternal toxicity occurred at 79.2 ppm as transient weight gain reduction during the exposure period. For maternal rats at 79.2 ppm, there were transient decrease in body weight and body weight gain during exposure, reduced food consumption, increased water consumption, and excess lacrimation. At 41.1 ppm, maternal body weight gain was reduced during the exposure period only. There were no treatment-related effects with respect to hematology, necropsy, or gestational parameters and no significant change in the incidence of malformations or variations (expressed as total, individual, external, visceral, or skeletal). Thus, exposure of rats and rabbits to EGHE vapor during the period of organogenesis produced maternal toxicity at near-saturation vapor concentrations (79.2 ppm), but no evidence for developmental toxicity or teratogenicity. The no-effect vapor concentrations for maternal toxicity were 41.1 ppm for rabbits and 20.8 ppm for rats.

Animals↗
PubMed1989

The acute toxicity of tris(dimethylamino)silane.

The acute handling hazards of tris(dimethylamino)silane [TDMAS] were investigated. The acute male rat peroral LD50 (with 95% confidence limits) was 0.71 (0.51-0.97) ml/kg, and the acute male rabbit percutaneous LD50 was 0.57 (0.35-0.92) ml/kg. The liquid was severely irritating to the rabbit eye and skin, and the vapor severely irritating to the rat eye. The dynamically generated saturated vapor Lt50 in female rats was 12 (9.7-15) min. The effect of varying the atmospheric concentration of vapor from TDMAS on acute inhalation toxicity was investigated by passing ordinary moist air countercurrent to liquid TDMAS metered into a slightly heated glass tube. Based on nominal concentrations, the 4 hr-LC50 for vapor from TDMAS was 734 (603-893) ppm in female rats by this procedure. Stoichiometrically, this accords with toxicity due to liberation of dimethylamine (DMA) from TDMAS. In a subsequent study designed to assess the influence of relative humidity on vapor toxicity, nitrogen was passed over heated liquid TDMAS and the resultant atmosphere was introduced into the air intake duct of the inhalation exposure chamber. Gas chromatographically measured TDMAS concentrations (+/- SD) were 395 +/- 111, 127 +/- 25, 62 +/- 8 and 23 +/- 21 ppm; the corresponding DMA vapor concentrations were 112 +/- 171, 31 +/- 43, 10 +/- 6 and 26 +/- 44 ppm. The 4-hr LC50 (males and females) was 38 (34-43) ppm TDMAS vapor. Thus, TDMAS is of moderate acute peroral and percutaneous toxicity, a severe primary skin and eye irritant, an aspiration hazard, and of high intrinsic acute inhalation toxicity, but in moist air conditions lethal toxicity may be reduced and in such circumstances DMA may be a significant factor in toxicity.

Administration, Inhalation↗
PubMed1989

Dominant lethal assay of 2,4-pentanedione vapor in Fischer 344 rats.

2,4-Pentanedione (2,4-PD: CAS No. 123-54-6) is a volatile industrial chemical of moderate acute toxicity, centrally neurotoxic by repeated exposure to high vapor concentrations, fetotoxic, and clastogenic. Its wide use and known toxicology indicated the conduct of a dominant lethal assay. Male Fischer 344 rats, 20 per group, were exposed to 2,4-PD vapor concentrations (mean +/- SD) of 0, 99.1 +/- 2.2, 412 +/- 12.6 and 694 +/- 9.1 ppm, for 6 hr/day for 5 consecutive days. The day following the final exposure they were bred to unexposed female Fischer 344 rats, 2 per week for 8 consecutive weeks. Weight loss occurred with males during 2,4-PD exposure for the 412 and 694 ppm groups, with compensatory increased weight at 694 ppm, for the first two weeks postexposure. No histopathological change was seen in brain, testes or thymus from high concentration males sacrificed after eight weeks of mating. Minor transient reproductive and gestational effects were present at 412 and 694 ppm. At week 2 there was a reduction, not statistically significant, in the number of corpora lutea and total and viable implants per dam at 694 ppm, and a slight increase in preimplantation loss. At week 3 the number of pregnant females was slightly reduced at 412 and 694 ppm, causing a lowered female fertility index. At week 4 there was a slight reduction in the number of total and viable implants per litter and a significant preimplantation loss at 694 ppm. The dominant lethal factor (FL%) was increased slightly at 694 ppm for weeks 2 and 4. Thus, the "no observable effect" level for dominant lethal effects was 99 ppm. The results, although not statistically significant, are dose-related and compatible with a transient slight dominant lethal effect at the spermatid stage of spermatogenesis.

Animals↗
PubMed1989

Acute vapour inhalation toxicity of acrolein and its influence as a trace contaminant in 2-methoxy-3,4-dihydro-2H-pyran.

1. The LC50 values for acrolein (AC) vapour to Sprague-Dawley rats (combined sexes) were determined to be 26 ppm (1 h) and 8.3 ppm (4 h). Signs of severe irritancy were present, and death was due to lung injury. 2. Exposure of rats to a 2-methoxy-3,4-dihydro-2H-pyran (MDP) saturated vapour atmosphere statistically generated from liquid MDP containing 0.037% AC, caused severe irritancy and death from accumulation of AC vapour. Sparging the impure material with nitrogen gas before atmosphere generation significantly reduced or abolished lethal toxicity. 3. Dynamically generated MDP vapour atmosphere produced transient respiratory and ocular irritancy, but no mortalities. The intrinsic acute vapour inhalation toxicity of MDP is low. 4. The presence of highly volatile toxic impurities in a material may confer a significant acute inhalation toxicity and hazard under conditions of low air movement. Assessment of potential inhalation hazards from liquid mixtures may require investigation by static and dynamic methods for vapour generation.

Acrolein↗
PubMed1988

In vitro and in vivo evaluation of the genotoxic potential of 2-ethyl-1,3-hexanediol.

2-Ethyl-1,3-hexanediol (EHD) has intentional human exposure because of its application to skin as an insect repellent and its use in various skin care products. Genotoxicity studies on EHD were conducted to determine mutagenic and clastogenic potential using in vitro and in vivo test systems. In vitro tests were conducted both with and without an Aroclor-induced, rat-liver S9 metabolic activation system and within a range of cytotoxic to non-cytotoxic doses. EHD did not produce dose-related positive increases in gene mutations in the Salmonella (Ames) test or in the CHO/HGPRT forward mutation test. No statistically significant or dose-related increases in sister chromatid exchanges indicative of DNA damage were produced by EHD in CHO cells. Small but statistically significant increases in chromosome aberrations were produced in CHO cells only in tests with S9 activation. However, no evidence of clastogenicity of EHD was obtained in vivo in a mouse peripheral blood micronucleus test or in 2 rat bone marrow chromosome aberration studies using single or repeated dosing procedures. The overall negative pattern of mutagenic and clastogenic results in the majority of tests conducted suggests that EHD is unlikely to pose significant hazard as a genotoxic agent or to possess carcinogenic initiating activity in animals.

Animals↗
PubMed1988

Evaluation of the developmental toxicity of beta-(3,4-epoxycyclohexyl)ethyltrimethoxysilane in Fischer 344 rats and New Zealand white rabbits.

beta-(3,4-epoxycyclohexyl)ethyltrimethoxysilane (ECEMS, CAS No. 3388-04-3) is mutagenic in vitro and weakly carcinogenic in mice after dermal application. Timed pregnant Fischer 344 rats and New Zealand white rabbits were dosed with ECEMS in corn oil by gavage on gestational days (gd) 6 through 15 at doses of 0.0, 0.25, 1.0, or 2.5 ml ECEMS/kg for rats and 0.0, 0.05, 0.25, or 0.75 ml ECEMS/kg for rabbits. At termination on gd 21 (rats) or gd 29 (rabbits), live fetuses were examined for external, visceral, and skeletal alterations. In rats, maternal toxicity was observed at 1.0 and 2.5 ml/kg, as evidenced by reduced weight gain and food consumption during treatment, clinical signs of toxicity, reduced body weight on gd 21 (corrected for gravid uterine weight), and increased relative liver weight. There were no significant differences among groups on pre- or postimplantation loss, fetal body weight/litter, or on the incidence of malformations. Minimal fetal toxicity, dilated lateral cerebral ventricles and reduced ossification in the forelimbs, was observed at 2.5 ml/kg. In rabbits, maternal mortality (2/20 does) and slightly (but statistically significantly) elevated maternal relative kidney weight were observed at 0.75 ml/kg. Clinical signs of toxicity were observed at 0.25 and 0.75 ml/kg. Pre- and postimplantation loss, fetal body weight/litter, and the incidence of malformations were all unaffected by treatment. Minimal fetal toxicity, extra (13th) ribs and reduced ossification in lumbar arch 4, was observed at 0.75 ml/kg ECEMS. Therefore, administration of ECEMS during organogenesis in rats and rabbits produced maternal toxicity at 1.0 and 2.5 ml/kg in rats and at 0.25 and 0.75 ml/kg in rabbits. Minimal fetal toxicity was observed at 2.5 ml/kg in rats and at 0.75 ml/kg in rabbits. No embryotoxicity or teratogenicity was observed in either species at any dosage. The "no observable effect level" (NOEL) for maternal toxicity was 0.25 ml/kg for rats and 0.05 ml/kg for rabbits; the NOEL for developmental toxicity was 1.0 ml/kg for rats and 0.25 ml/kg for rabbits.

Adhesives↗
PubMed1988

Toxicology and hazard evaluation of cyanide fumigation powders.

Studies were conducted to assess potential handling hazards from the pesticidal use of HCN-liberating "cyanide fumigation powders". Simulations were conducted in enclosed chambers on the release of HCN vapor from wetted powder containing 40% NaCN/60% kaolin at application rates of 1 g powder/m3 of space (usual rate) and 5 g/m3 (overuse condition). With the overuse situation, HCN vapor concentrations may be rapidly attained that produce serious or lethal toxicity; with the lower application rate minor signs and symptoms of HCN vapor exposure toxicity may develop. The acute peroral LD50 (rat and rabbit) of fumigant formulation is reduced in proportion to the kaolin content, but kaolin does not modify the inherent toxicity of NaCN. A typical cyanide hazard exists from swallowing cyanide fumigant powder formulations. Lethal systemic toxicity was produced by contamination of the eye (rabbit) with powder formulation, which also caused a rapid onset of moderately severe conjunctivitis and keratitis. Applied to dry intact skin (rabbit) neither NaCN nor its kaolin formulation produced systemic toxicity. However, on moistened intact skin lethal amounts of cyanide were absorbed; but the kaolin content reduced the hazard in comparison with NaCN-alone applied to moist skin. With abraded dry skin there was no difference in lethal toxicity between NaCN-alone and its formulation; also, the toxicity of the formulation on abraded skin was three times that on intact moist skin. These finds indicate that the use of cyanide fumigant powder formulations may be hazardous by contact of powder with moist or abraded skin, contamination of the eye, swallowing, and inhalation of evolved HCN. There is a clear need for respiratory, cutaneous, and ocular protection when handling cyanide fumigant powder formulations.

Administration, Cutaneous↗
PubMed1988

The acute toxicity and mutagenic potential of 3-methyl-2-benzothiazolinone hydrazone.

3-Methyl-2-benzothiazolinone hydrazone (MBTH), widely used in analytical laboratories, was investigated for potential handling hazards. Tested as the hydrochloride, it was found to be of moderately high acute peroral toxicity with LD50 values in rabbits of 177 mg/kg (males) and 268 mg/kg (females), and in the rat 308 mg/kg (males) and 149 mg/kg (females). The major signs of toxicity, seen at peroral doses of 125 mg/kg and above, were convulsions. Although of low acute lethal percutaneous toxicity in rats (LD50 greater than 16 g/kg), rabbits were more sensitive with one of five males dying at an applied dose of 16 g/kg, and females having an LD50 of 12.3 g/kg; convulsions were seen in rabbits having applied cutaneous doses of 4 g/kg and above. There was no evidence for cutaneous inflammation after a 4 hour occluded contact with MBTH in rabbits, although following 24 hour occlusive contact in the acute percutaneous toxicity study there was erythema, edema, desquamation and, in a few animals, local necrosis. Ocular studies in rabbits indicated that, depending on the degree of contamination, MBTH produced mild to moderate eye irritation. In keeping with its low vapor pressure, there were no adverse effects from a 6 hour exposure of rats to an atmosphere saturated with any vapor produced from solid MBTH at ambient temperature. MBTH was positive in an Ames bacterial mutagenicity assay, particularly in the absence of metabolic activation. These studies indicate MBTH to be of moderately high acute peroral toxicity, of moderate percutaneous toxicity, a mild primary skin irritant, a mild to moderate eye irritant, and produced mutations in Salmonella. There is a need for skin and eye protection, and avoidance of swallowing, when handling MBTH.

Animals↗
PubMed1988

The acute toxicity and primary irritancy of 1-propoxy-2-propanol.

1-Propoxy-2-propanol, a widely used industrial chemical, was found to have acute peroral LD50 values in the rat of 4.92 ml/kg (males) and 2.83 ml/kg (females), with the signs of systemic toxicity being principally related to narcosis. Acute percutaneous LD50 values in the rabbit (24-hr occluded) were 4.29 ml/kg (males) and 4.92 ml/kg (females); signs of systemic toxicity were related to narcosis, and local effects were severe inflammation and corrosion. There were signs of sensory irritation of the eye during a 6-hr exposure to a dynamically generated saturated vapor atmosphere, but no signs of toxicity during exposure or in a 14-hr day postexposure observation period. A 4-hr occluded cutaneous application with 0.5 ml PP in rabbits produced mild to moderate erythema and edema of about 3 days duration, but no signs of corrosion. Contamination of the eye (0.005 to 0.1 ml PP) produced moderate to severe conjunctivitis (hyperaemia and chemosis), with mild iritis and diffuse mild keratitis; spontaneously healing occurred within 3 days (0.005 ml) to 7 days (0.1 ml). The major acute hazards with PP are by swallowing, splash contamination of the eye, and sustained skin contact.

Administration, Inhalation↗
PubMed1987

Dimethylethanolamine: acute, 2-week, and 13-week inhalation toxicity studies in rats.

Dimethylethanolamine (DMEA) is a volatile, water-soluble amine that has applications in the chemical and pharmaceutical industries. These studies evaluated the acute and subchronic inhalation toxicity of DMEA. Acute (4-hr) exposures of Wistar rats to DMEA vapor resulted in an LC50 value (95% confidence limits) of 1641 (862-3125) ppm. Clinical signs of nasal and ocular irritation, respiratory distress, and body weight loss were observed in rats exposed to 1668 ppm DMEA and higher. In the 2-week study, F-344 rats exposed to 98, 288, or 586 ppm DMEA for 9 days (6 hr/day) during an 11-day period also exhibited signs of respiratory and ocular irritation (except the 98 ppm group). All animals of the 586 ppm group and 4 of 15 male rats of the 288 ppm group died. Body weight values for the 288 ppm group were reduced to about 75% of preexposure values, while the 98 ppm group gained 35% less weight than controls. Statistically significant differences in clinical pathology parameters (288 ppm group) and in organ weight values (288 and 98 ppm groups) probably resulted from the decreased food consumption and not from specific target organ toxicity. In the groups evaluated histologically (the 98 and 288 ppm groups) the eye and nasal mucosa were the primary target organs. In the 13-week subchronic study, F-344 rats were exposed to 0, 8, 24, or 76 ppm DMEA for 6 hr/day, 5 days/week for 13 weeks. The principal exposure-related changes were transient corneal opacity in the 24 and 76 ppm groups; decreased body weight gain for the 76 ppm group; and histopathologic lesions of the respiratory and olfactory epithelium of the anterior nasal cavity of the 76 ppm group and of the eye of several 76 ppm group females. Rats maintained for a 5-week recovery period only exhibited histological lesions of the nasal tissue, with the lesions being decreased in incidence and severity. DMEA acts primarily as an ocular and upper respiratory tract irritant and toxicant at vapor concentrations of 76 ppm, while 24 ppm or less produced no biologically significant toxicity in rats. Thus, 24 ppm was considered to be the no-observable-effect level.

Administration, Inhalation↗