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Toluene embryopathy: delineation of the phenotype and comparison with fetal alcohol syndrome
M A Pearson1, H E Hoyme, L H Seaver
1Department of Pediatrics, University of Arizona College of Medicine, Tucson.
Insights
Maternal toluene abuse can cause significant developmental and structural disabilities in infants, including microcephaly and growth deficiencies. These findings suggest toluene exposure leads to craniofacial abnormalities similar to fetal alcohol syndrome.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Maternal substance abuse is a significant concern in prenatal development.
- Toluene exposure during pregnancy is linked to potential adverse fetal outcomes.
Purpose of the Study:
- To investigate the structural and developmental effects of in utero toluene exposure on infants.
- To compare the outcomes of toluene-exposed infants with those of fetal alcohol syndrome patients.
Main Methods:
- Examined 18 infants with known in utero toluene exposure at birth.
- Re-examined 9 infants between 3 and 36 months of age.
- Compared clinical findings with literature data and fetal alcohol syndrome cases.
Main Results:
- High rates of prematurity (39%), perinatal death (9%), and small for gestational age (54%) were observed.
- Significant incidences of prenatal (33%) and postnatal (67%) microcephaly, and developmental delay (80%) were noted.
- Craniofacial features resembled fetal alcohol syndrome in 83% of patients, with 89% exhibiting other anomalies.
Conclusions:
- Toluene exposure during pregnancy can lead to severe structural and developmental disabilities in infants.
- Phenotypic facial abnormalities in toluene-exposed infants are similar to fetal alcohol syndrome.
- A common teratogenic mechanism involving neuroepithelium and mesodermal deficiency is proposed for both toluene and alcohol.
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.