Development through the lifespan

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Abstract

Prenatal exposure to tobacco smoke and alcohol are two the most preventable causes birth deficits, such as mental retardation and low birth weight, in the United States. Numerous studies have concluded that social consumption of teratogens, such as cigarettes and alcohol, can produce detrimental effects on an unborn child. Some birth deficits, such as fetal alcohol syndrome (FAS), have lifelong effects such as learning disabilities and behavioral issues. Cigarette smoke alone contains over 4000 various chemicals including known carcinogens. This overview concluded that there is evidence of a safe level of consumption of known teratogens such as alcohol and tobacco smoke during pregnancy.

Effects of Social Alcohol and Cigarette Smoke Exposure on Human Development

Exposure to cigarette smoke and alcohol has severe adverse effect on human development (Rogers, 2009). Although there is documentation of distinct relationships between increased use of substances, such as alcohol and tobacco, and pre and postnatal complications, the number of children born with related birth defects is still significant in the U.S. (Berk, 2007).

Maternal tobacco use is one of the most preventable causes of pregnancy associated death in the United States (Dempsey, 2001). Recent studies on small mammals indicate that fetal exposure to nicotine can lead to sudden infant syndrome, uteroplacental insufficiency, pre-tem births, low birth weight, and learning problems (Dempsey, 2001; Coleman et al., 2007; Rogers, 2009; Lobel et al., 2008). Studies of children who were exposed to smoke in utro, illustrated behavioral abnormalities, decreased attention to sound, and health complications in their later years (Gruslin et al., 2009; Berk, 2007).

An article by J. M. Rogers, entitled Tobacco and Pregnancy, stated the severe and long term effects tobacco used can have on a fetus. Rogers identified that cigarettes are not the only adverse type of tobacco exposure a mother can have; this includes tobacco smoke, smokeless tobaccos, nicotine from nicotine replacement therapy, cigarettes and secondhand smoke from the environment. Cigarette smoke can contain thousands of chemical constituents, reproductive toxins, and carcinogens, which can lead to a number of abnormalities during development (Rogers, 2009; Dempsey, 2001).

According to A. Niccols, author of Fetal Alcohol Syndrome and the Developing Socio-Emotional Brain, fetal alcohol syndrome (FAS) is the most common known cause of mental retardation, affecting 0.01 to 0.07% of conceived infants (as cited by Niccols, 2007). Any consumption of alcohol by maternal women places infants at significant risk for complications during pregnancy (Gauthier et al., 2010). L. E. Berk states in her book, Development Through the Lifespan, that even mild drinking can be associated with fetal alcohol syndrome, thus concluding that no amount of alcohol during conception or pregnancy is safe. Prenatal exposure can cause birth defects, insufficiency in learning, memory, executive functioning, neurodevelopmental disorders, , hyperactivity, impulsivity, reduced head size, and low mental scores (Wedding et al., 2007; Berk, 2007; Niccols, 2007; Gauthier et al., 2010)

Maternal use of alcohol and tobacco during pregnancy is a major risk factor for infant deficits. Although some women believe social drinking and smoking is not detrimental to a fetus, there is no evidence that supports any use of such substances.

References

  • Berk, L. E. (2007). Development Through the Lifespan (4th Edition). Boston, MA: Pearson Education, Inc.
  • Coleman, T., Thornton, J., Britton, J., Lewis, S., Watts, K., Coughtrie, M., et al. (2007). Protocol for the Smoking, Nicotine and Pregnancy (SNAP) trial: double-blind, placebo-randomised, controlled trial of nicotine replacement therapy in pregnancy. BMC Health Services Research, 7, 1-15.
  • Day, N., Leach, S L., Richardson, G A., Cornelius, M D., Robles, N., Larkby, C. (2002). Prenatal alcohol exposure predicts continued deficits in offspring size at 14 years of age. Alchololism: Clinical and Experimental Research, 26, 1584-1591.
  • Dempsey, D.A, .Benowitz, N.L. (2001). Risks and Benefits of Nicotine to Aid Smoking Cessation in Pregnancy. Drug Safety, 24(4), 227-322.
  • Floyd, R. L., Weber, M. K., Denny, C., O'Connor, M. J. (2009). Prevention of fetal alcohol spectrum disorders. Developmental Disabilities Research Reviews, 15(3), 193-199.
  • Gauthier, T. W., Kable, J. A., Burwell, L., Coles, C. D., Brown, L. A. S. (2010). Maternal Alcohol Use During Pregnancy Causes Systemic Oxidation of the Glutathione Redox System. Alcoholism: Clinical & Experimental Research 34(1), 123-130.
  • Gruslin, A., Cesta, C. E., Bell, M., Qing Q., Petre, M. A., Holloway, A. C. (2009). Effect of Nicotine Exposure During Pregnancy and Lactation on Maternal, Fetal, and Postnatal Rat IGF-II Profile. Reprodictive Sciences 16(9), 875-882.
  • Harrison, P. A., Sidebottom, A. C. (2009). Alcohol and Drug Use Before and During Pregnancy: An Examination of Use Patterns and Predictors of Cessation. Maternal & Child Health Journal 13(3), 386-394.
  • Jacabson, S W., Jacobson J L., Sokol, R J., Chiodo, L M., Corobana, R. (2004). Maternal age, alcohol abuse history, and equality of parenting as moderators of the effects of prenatal alcohol exposure on 7.5 year intellectual function. Alcoholism: Clinical and Experimental Research 28, 1732-1745.
  • Lobel, M., Cannella, D. L., Graham, J. E., DeVincent, C., Schneider, J., Meyer, B. A. (2008). Pregnancy-specific stress, prenatal health behaviors, and birth outcomes. Health Psychology, 27(5), 604-615.
  • Niccols, A. (2007). Fetal alcohol syndrome and the developing socio-emotional brain. Brain and Cognition 65(1), 135-142.
  • Rogers, J. M. (2009). Tobacco and pregnancy. Reproductive Taxicology 28(2), 152-160.
  • Wedding, D., Kohout, J., Mengel, M. B., Ohlemiller, M., Ulione, M., Cook, K., et al. (2007). Psychologists' knowledge and attitudes about fetal alcohol syndrome, fetal alcohol spectrum disorders, and alcohol use during pregnancy. Professional Psychology: Research and Practice 38(2), 208-213.

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