1 Department of Pediatrics and the Steele Memorial Children's Research Center, University of Arizona College of Medicine, Tucson, Department of Pediatrics, Maricopa Medical Center, Phoenix, AZ
2 Department of Pediatrics and the Steele Memorial Children's Research Center, University of Arizona College of Medicine, Tucson, AZ
Objective. To determine if maternal toluene abuse produces any structural or developmental disabilities in the developing fetus, a cohort of toluene-exposed infants was ascertained and examined.
Methodology. Eighteen infants with a history of in utero toluene exposure were examined at birth. Nine of these infants were reexamined 3 to 36 months after their initial evaluations. The clinical findings in these patients were compared with those of similarly exposed children from the literature and with patients who had the fetal alcohol syndrome.
Results. Thirty-nine percent of all toluene-exposed infants described in this and other studies were born prematurely, and 9% died during the perinatal period. Fifty-four percent were small for gestational age, and 52% exhibited continued postnatal growth deficiency. A 33% incidence of prenatal microcephaly, a 67% incidence of postnatal microcephaly, and an 80% incidence of developmental delay were observed. Eighty-three percent of the patients had craniofacial features similar to the fetal alcohol syndrome, and 89% of these children had other minor anomalies.
Conclusions. Data from the patients herein described and the available scientific literature suggest that the mechanism of alcohol craniofacial teratogenesis may be nonspecific, with a variety of teratogens, including toluene, giving rise to phenotypic facial abnormalities similar to those of the fetal alcohol syndrome. We propose a common mechanism of craniofacial teratogenesis for toluene and alcohol, namely a deficiency of craniofacial neuroepithelium and mesodermal components due to increased embryonic cell death.
Submitted on August 27, 1992
This article has been cited by other articles:
![]() |
M.-H. Chan, Y.-C. Tang, T.-H. Chien, and H.-H. Chen Toluene Exposure during the Brain Growth Spurt Reduced Behavioral Responses to Nicotine in Young Adult Rats: A Potential Role for Nicotinic Acetylcholine Receptors in Fetal Solvent Syndrome Toxicol. Sci., February 1, 2008; 101(2): 286 - 293. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. F. Williams, M. Storck, and the Committee on Substance Abuse, and and Committee on Native American Child Health Inhalant Abuse Pediatrics, May 1, 2007; 119(5): 1009 - 1017. [Abstract] [Full Text] [PDF] |
||||
![]() |
C.-L. Liu, Y.-R. Lin, M.-H. Chan, and H.-H. Chen Effects of Toluene Exposure during Brain Growth Spurt on GABAA Receptor-Mediated Functions in Juvenile Rats Toxicol. Sci., February 1, 2007; 95(2): 443 - 451. [Abstract] [Full Text] [PDF] |
||||
![]() |
U Kini, N Adab, J Vinten, A Fryer, J Clayton-Smith, and on behalf of the Liverpool and Manchester Neurodev Dysmorphic features: an important clue to the diagnosis and severity of fetal anticonvulsant syndromes Arch. Dis. Child. Fetal Neonatal Ed., March 1, 2006; 91(2): F90 - F95. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Stromland and M. D. Pinazo-Duran OPHTHALMIC INVOLVEMENT IN THE FETAL ALCOHOL SYNDROME: CLINICAL AND ANIMAL MODEL STUDIES Alcohol Alcohol., January 1, 2002; 37(1): 2 - 8. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. L. Cruz, T. Mirshahi, B. Thomas, R. L. Balster, and J. J. Woodward Effects of the Abused Solvent Toluene on Recombinant N-Methyl-D-Aspartate and non-N-Methyl-D-Aspartate Receptors Expressed in Xenopus Oocytes J. Pharmacol. Exp. Ther., July 1, 1998; 286(1): 334 - 340. [Abstract] [Full Text] |
||||