Cigarette smoking has been shown to be harmful to the viability of pregnancy. It can lead to increased spontaneous abortion in the first trimester. In addition, the mother and fetus are at increased risk for premature placenta abruption, preterm delivery, decreased birthweight, and sudden infant death syndrome (1). Infants who are born to women who smoke during pregnancy weigh, on average, are 150 to 300 g less than those children born to nonsmokers. In addition, smoking mothers are twice as likely to have small for gestational age (SGA) babies as mothers who do not smoke (2). The effects that smoking has on fetal growth and preterm delivery increase with increasing age of the mother (3). The older the mother is, the greater the risk to the fetus is her smoking.

Cigarette smoke is known to contain carbon monoxide and nicotine (see above). These components of cigarettes seem to affect birthweight and shorten the term of the pregnancy. The chemical bonding of carbon monoxide to hemoglobin produces carboxyhemoglobin and this creates fetal hypoxia. Fetal hypoxia is associated with sudden infant death syndrome (SIDS) (4). In addition, nicotine and carbon monoxide are strong vasoconstrictors and, therefore, will cause decreased blood flow to the fetus and increase maternal blood pressure and heart rate. Cigarette smoking decreases the appetite and, therefore, can decrease the amount of nutrients consumed by the pregnant woman. Cigarette smokers are less likely to consume micronutrient supplementation and more likely to consume alcohol and other substances that negatively interact with metabolism. Many other components of cigarette smoke (e.g., lead and cadmium) could cause damage to the fetus, but the effects of these are not known.

The worst case scenario of fetal exposure to alcohol is fetal death. If the fetus does survive the alcohol consumption by the mother, especially if it occurs early in the pregnancy, the child is, however, at high risk for fetal alcohol syndrome (FAS). FAS is a very significant developmental problem. The changes produced by fetal exposure to alcohol are permanent and irreversible. FAS babies are always retarded and display
a myriad of physical and neurologic anomalies. Of all the causes of mental retardation, this is the most preventable form. No direct relationship exists between how much alcohol the pregnant woman consumes and the expression of FAS, but all FAS babies are born to mothers who have consumed significant amounts of alcohol during the pregnancy. It is estimated that approximately 50% of U.S. women drink socially and about half of all U.S. pregnancies are unplanned and, therefore, about 25% of all newborns have been exposed to some alcohol in early gestation (5). FAS in its full-blown form includes physical abnormalities of structure and size and mental retardation. The characteristics manifest in the FAS child depend on during which trimesters of pregnancy the alcohol abuse takes place. If the drinking is during all three trimesters, the expression affects the physical appearance, the physical size, and mental function. If the drinking starts in the second trimester, it usually affects only physical size and mental function with no abnormal physical features. And if the drinking is only during the third trimester, neither physical appearance nor size is affected but the mental function is. The physical findings most characteristic of babies with FAS include growth retardation for height and weight, which persists after birth by at least two standard deviations; central nervous system (CNS) dysfunction, including mental retardation, microcephaly, and hyperactivity (6). The Mayo Clinic’s web page (7) reports that drinking alcohol during any part of the pregnancy will expose the fetus to risk, but the most critical period and one in which the fetus is most susceptible is the first trimester. It is known that if the mother drinks, the alcohol crosses the placenta to the fetus. Therefore, if the mother drinks, the fetus drinks. The Centers for Disease Control (8) defines FAS as the severe end of a spectrum of effects that can occur when the fetus is exposed to alcohol in utero. As mentioned, fetal death is the most extreme expression of this developmental anomaly. FAS is characterized by abnormal facial features, and growth and CNS problems. Stromland (9) describes FAS to include possible vision impairment and ocular anomalies affecting all parts of the eye, including optic nerve hypoplasia, coloboma of the iris, and choroid, microcornea, cataract, and others. The expression on the physical features of the face characteristic of the child with FAS include telecanthus with shortened palpebral fissures, flat philtrum, short upturned nose, epicanthal folds, and ptosis (6). These children have very significant visual anomalies. FAS, however, is now considered a spectrum disorder and great variability is seen among the signs in different children. Two other terminologies used to describe children with problems relating to prenatal alcohol exposure and are alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD), which can include problems involving kidneys, heart, bones and hearing. Children with FAS and ARND can exhibit the following: poor coordination, hyperactivity, learning disabilities, developmental disabilities (e.g., speech and language delays), mental retardation or low IQ, and poor reasoning and judgment skills.

Rubella, more commonly known as German measles, is a mild childhood viral illness that can be devastating to the fetus if the mother is infected within the first trimester. Rubella was a much more serious threat in the past because no immunization was available. Since 1969, children started receiving immunization for rubella and, since that time, no major outbreak of rubella has occurred in the United States. Cases of congenital rubella syndrome (CRS) still present clinically, however. The designation of CRS indicates significant impairment in the child, usually described as a triad including, but not limited to, congenital cataracts, deafness, and mental retardation. If the mother is infected later in the pregnancy the risk significantly decreases.

Relatively mild childhood viral illnesses that can harm the fetus in a pregnant woman who becomes infected include chickenpox (varicella) and fifth disease (parovirus B19). If the fetus becomes infected, it can be born with congenital varicella syndrome, which can include blindness, seizures, mental retardation, paralyzed limbs, and so on. The March of Dimes website (10) states that “a susceptible pregnant woman who is exposed to an infected household member is at about 90% risk of contracting chickenpox.” They also state, however, that only about 2% of infected mothers have babies with defects caused by the virus. As with other infectious conditions, the timing of the infection is important. Women who contract the varicella virus in the first half (20 weeks) of the pregnancy face a meaningful risk of having a child with a birth defect.

Fifth disease has a similar pattern of infection and defect. Fifth disease is the fifth in a series of rash-associated childhood illness including measles, scarlet fever, rubella, and fourth disease (origin of infection is unknown). Fifth disease is caused by parvovirus B19, which can cause serious anomalies to the fetus. The most serious of these is anemia, which can be sufficiently severe to abort the pregnancy. Again, the risks are much greater if infection is in the first 20 weeks of the pregnancy and then almost no risk thereafter.

Cytomegalovirus is a very common viral infection in the United States. Most people do not know they have it because no or very mild symptoms are present. It is estimated that by age 30 years, about 50% of all adults in the United States have been infected. If a pregnant woman becomes infected, she will almost always pass it on to the fetus. In some cases, this can result in very serious, possibly even life-threatening repercussions in the fetus (11,12). The range of manifestation of the cytomegaloviral infection in utero to the fetus can range from no involvement to death. The infected fetus may demonstrate low birthweight and deliver prematurely; neurologic involvement (seizures, microcephaly, hydrocephaly, mental retardation, developmental delay, learning disabilities) is frequently seen. Ocular findings are characteristically chorioretinal lesions, which obviously would affect visual function, dependent on the location of the lesions. The rate of intrauterine transmission of the CMV is directly related to gestational age of the fetus, with the rate of transmission increasing with increasing gestational age. Infected neonates can be born symptom-free and then develop some of the anomalies during the first 2 years.

No apparent defects are caused to the fetus of a mother who is human immunodeficiency virus positive (HIV+). A high transmission rate is seen of the virus to the infant perinatally (during delivery). Drug therapy regimens may be used to decrease rates of perinatal transmission, which can cause problems to the fetus. In the middle 1990s, zidovudine was used in cases of pregnant HIV+ mothers and the transmission rate fell from 30% to 8%. The drug is, however, known to cause significant birth defects (13).

Toxoplasma gondii is a one-celled parasite that can sometimes cause devastating effects on the fetus if the mother becomes infected for the first time during the pregnancy. Toxoplasmosis, the disease caused by the parasite, can infect the developing fetus. It is one of a group of infections, contracted in utero that comprises the Torch Syndrome. TORCH is an acronym for toxoplasmosis, other agents, rubella, cytomegalovirus, and herpes simplex.

The severity of the involvement to the fetus is related to the timing of the maternal infection occurs. The earlier in the pregnancy the infection occurs, the more severe the expression of the infection (14). Toxoplasmosis can cause widespread damage to body organs such as the brain, liver, and spleen. Ocular findings include chorioretinal lesions, optic atrophy, cataract, and strabismus. The infecting agent forms cysts inside its host. These cysts remain in the host for a lifetime. Whenever the cysts rupture, a flare-up occurs.