The temporal relationship between behavioral and hematological effects of inhaled benzene

Dempster, Alice M.; Evans, Hugh L.; Snyder, Carroll A.

doi:10.1016/0041-008x(84)90042-5

Cited by 24 publications

(12 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Intermediate-duration inhalation and oral exposures to 100 ppm benzene reduced limb GS (Dempster et al, 1984). While our earlier studies demonstrated that VOCs mixture of high dose (VOCs are 100 times the IAQS in China) short-term (2 h/d, 10 d) inhalation did not affect GS of mice.…”

Section: Discussionmentioning

confidence: 67%

Potential mechanisms of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose VOCs

Fan¹,

Li²,

Liu³

et al. 2014

Inhalation Toxicology

View full text Add to dashboard Cite

To investigate effects of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose volatile organic compounds (VOCs) and the possible mechanism for these effects, 60 male Kunming mice were exposed in 5 similar static chambers, 0 (control) and 4 different doses of VOCs mixture (G1-4) for consecutively 90 d at 2 h/d. The concentrations of VOCs mixture were as follows: formaldehyde, benzene, toluene, and xylene 0.05 + 0.05 + 0.10 + 0.10 mg/m(3), 0.10 + 0.11 + 0.20 + 0.20 mg/m(3), 0.50 + 0.55 + 1.00 + 1.00 mg/m(3), 1.00 +1.10 + 2.00 + 2.00 mg/m(3), respectively, which corresponded to 1/2, 1, 5, and 10 times of indoor air quality standard in China. Morris water maze (MWM) and Grip strength (GS) test were performed in the last 7 weeks. One day following VOCs exposure, oxidative stress markers, neurotransmitters, and cholinergic system enzymes in brain were examined. In addition, the expressions of N-methyl-d-aspartate (NMDA) receptor in hippocampus were determined. VOCs exposure induced behavioral impairment of mice in MWM and GS test. The levels of reactive oxygen species (ROS), malondialdehyde (MDA) and glutamic acid (Glu) were significantly increased, while the acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and acetylcholine (ACh) levels, and the expression of NMDA receptor were significantly decreased in VOCs exposed groups. Results showed that sub-chronic exposure to low-dose VOCs induced damage on physique and motor function, as well as impairment on learning and memory capacity of mice. Oxidative damage, abnormal metabolism of neurotransmitters and cholinergic system enzymes, and the alternation of NMDA receptor expression may be the possible mechanism for VOCs-induced neurotoxicity.

show abstract

Section: Discussionmentioning

confidence: 67%

Potential mechanisms of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose VOCs

Fan¹,

Li²,

Liu³

et al. 2014

Inhalation Toxicology

View full text Add to dashboard Cite

show abstract

“…Studies in animals. Inhalation exposure of laboratory animals has resulted in depressed electrical activity in the brain (Frantik et al, 1994 ), loss of involuntary reflexes and narcosis (Carpenter et al, 1944;Evans et al, 1981 ), and decreases in hind -limb grip strength and tremor (Dempster et al, 1984 ).…”

Section: _20 Yearsmentioning

confidence: 99%

Agency for Toxic Substances and Disease Registry's 1997 priority list of hazardous substances. Latent effects—carcinogenesis, neurotoxicology, and developmental deficits in humans and animals

et al. 1999

View full text Add to dashboard Cite

In support of Superfund re-authorization legislation, the Division of Toxicology of the Agency for Toxic Substances and Disease Registry (ATSDR) prepared a chemical-specific consultation document for Congress that identified those chemicals with carcinogenic, neurological, or developmental adverse effects having a latency period longer than 6 years. The review was limited to the top 50 substances listed on ATSDR's 1997 Priority List of Hazardous Substances (Priority List). Among the top 50 chemicals, a review of the technical literature indicated that 38 (76%) were classified as "reasonably anticipated," "possibly," or "probably" capable of causing cancer in humans, based either on human and animal data. Eight chemicals (16%) had well-established cancer latency periods in humans of 6 years or more following exposure. Three substances (6%)--arsenic, creosote, and benzidine--had data indicating latency periods longer than 6 years. The technical literature review likewise confirmed the potential for neurological and developmental effects with a latency of 6 years. Twenty-seven (54%) of the top 50 substances caused acute and/or chronic neurotoxic effects; a number of these also caused neurological effects that persisted beyond 6 years (or the equivalent in animal studies) such as: behavioral problems, neurological deficiencies, reduced psychomotor development, cognitive deficiencies, and reduced IQ. Twenty-eight substances (56%) caused adverse developmental effects in offspring of exposed individuals or animals including increased fetal and infant mortality, decreased birth weights and litter sizes, and growth delays. Latency periods for related chemicals are expected to be similar due to structural and toxicological similarities.

show abstract

“…Subtle neurobehavioral effects in animals due to benzene exposure have been reported. Consistent and significant changes in mouse milk-licking responses have been reported after approximately 1 week of inhalation exposure to benzene at 300 ppm (27) A summary of the neurotoxic effects reported for benzene is shown in Table 3. The earliest indicators of effects due to benzene exposure in humans and animals is anemia and leukopenia.…”

Section: Benzenementioning

confidence: 61%

“…The primary effects associated with chronic benzene exposure in humans and animals are anemia and leukopenia (27). Neurotoxic effects in humans due to benzene exposure have not been reported.…”

Section: Benzenementioning

confidence: 99%

Neurotoxic effects of gasoline and gasoline constituents.

Burbacher

1993

Environ Health Perspect

View full text Add to dashboard Cite

This overview was developed as part of a symposium on noncancer end points of gasoline and key gasoline components. The specific components included are methyl tertiary butyl ether, ethyl tertiary butyl ether, tertiary amyl methyl ether, butadiene, benzene, xylene, toluene, methyl alcohol, and ethyl alcohol. The overview focuses on neurotoxic effects related to chronic low-level exposures. A few general conclusions and recommendations can be made based on the results of the studies to date. a) All the compounds reviewed are neuroactive and, as such, should be examined for their neurotoxicity. b) For most of the compounds, there is a substantial margin of safety between the current permissible exposure levels and levels that would be expected to cause overt signs of neurotoxicity in humans. This is not the case for xylene, toluene, and methanol, however, where neurologic effects are observed at or below the current Threshold Limit Value. c) For most of the compounds, the relationship between chronic low-level exposure and subtle neurotoxic effects has not been studied. Studies therefore should focus on examining the dose-response relationship between chronic low-level exposure and subtle changes in central nervous system function.

show abstract

The temporal relationship between behavioral and hematological effects of inhaled benzene

Cited by 24 publications

References 17 publications

Potential mechanisms of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose VOCs

Potential mechanisms of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose VOCs

Agency for Toxic Substances and Disease Registry's 1997 priority list of hazardous substances. Latent effects—carcinogenesis, neurotoxicology, and developmental deficits in humans and animals

Neurotoxic effects of gasoline and gasoline constituents.

Contact Info

Product

Resources

About