Once alcohol substances (e. g. ethanol, 1-butanol, 1-octanol, etc. ) antagonizes the cellular adhesion process necessary to the development of fetal body parts, dependent fetal abnormalities result bringing in the fetal teratogenic process. On the other hand, alcohol use has always been linked with tobacco smoking, especially during the first trimester of pregnancy (n=26% of 1134 samples) as determined by the study of Lorente, Cordier and Goujard et al. (2001).
Regardless of actual tobacco smoking habit, inhalation of tobacco smoke without direct use of tobacco (passive smoker) has been found to increase the risk of still birth (odds ratio: 1 out 4 pregnancies) and fetal death during the first year of life (odds ratio: 1 out 3 pregnancies) (Wisborg, Kesmodel and Henriksen et al. , 2001). According to the study of Milunsky, Carmella and Ye (2000), tobacco and its smoke consists of fetus specific carcinogen (absorption: 52.4% for active smokers; 6. 7% non-smokers) derived from nitrosamines and glucosiduronic acid –NNAL Gluc – that is capable of inducing fetal abnormalities, such as mental retardation, stunted growth and facial disfigurations (e. g. clef palate, etc. ).
a. Teratology of Tobacco and Alcohol In terms of alcohol consumption, commonly occurring teratogenic effects include low birth weight, microcephaly, craniofacial abnormalities (e. g. clef lip or palate, etc. ), and mental retardation. The mentioned clusters of physical and mental findings are categorized as syndrome conditions known as Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Spectrum Disorder (FASD) (Stoler and Holmes, 2000). According to United States epidemiological statistics, FAS affects 1 to 3 per 1000 live births, while FASD has been reported to occur among 9. 1 per 1000 live births annually (Chudley, Conry and Cook et al. , 2005).
In the study of Stoler and Holmes (2000), mothers reported using alcohol (n=18) have given birth to infants with small-for-gestational-age status (n=11), FAS (n=2), microcephaly (n=8) and facial disfiguration (n=3). In tobacco smoking, the most commonly observed teratogenic effects occurring among clinically tested infants include low birth weight, pre-term gestation, stunted growth and neurologic abnormalities (e. g. poor auditory orientation, autonomic regulation, tremors, etc) (Cornelius and Day, 2000).
In study of England, Kendrick and Gargiullo et al. (2001), sample findings from the Smoking Cessation in Pregnancy project (n=3,395; record reviews from 1987 to 1991) have proven the parallel relationship between the severity of tobacco smoking and birth weight deficiencies. According to the study of Wisborg, Kesmodel and Henriksen et al. (2001), approximately 25% of all stillbirths and 20% of all infant deaths in the sample studied (n=25,102 fetus; approximately 30% of total maternal population are active smokers) are generally (approximately 70% of sample population) brought by passive smoking of more than 16th week of gestation.
Meanwhile, infants of smokers are 150 to 250 grams lighter compared to infants of non-smokers (Cornelius and Day, 2000). Nicotine and nitrosamines present in tobacco are found to contribute in fetal hypoxia and cerebral impairments (e. g. neurohormonal decreases in hippocampal systems, lower dopamine and serotonin turnovers, etc. ) predisposing conditions, such as poor autonomic regulation, poor auditory orientation, inattention, impulsivity and stunted growth (Cornelius and Day, 2000).