DES (diethylstilbestrol) is a drug that mimics estrogen, a female hormone. From 1938 until 1971 doctors prescribed this drug to help some pregnant women who had had miscarriages or premature deliveries on the theory that miscarriages and premature births occurred because some pregnant women did not produce enough estrogen naturally to sustain the pregnancy for full term . An estimated 5-10 million pregnant women and the children born during this period were exposed to DES. Currently, DES is known to increase the risk of breast cancer, and cause a variety of birth-related adverse outcomes exposed female offsprings such as spontaneous abortion, second-trimester pregnancy loss, preterm delivery, stillbirth, neonatal death, sub/infertility and cancer of reproductive tissues . DES is an important developmental toxicant which links the fetal basis of adult disease.

Methylmercury and inorganic mercury is excreted in human breast milk and infants are particularly susceptible to toxicity due to this compound. The fetus and infant are especially vulnerable to mercury exposures with special interest in the development of the CNS since it can easily cross across the placental barrier, accumulate within the placenta and fetus as the fetus cannot eliminate mercury and have a negative effect on the fetus even if the mother does not show symptoms. Mercury causes damage to the nervous system resulting from prenatal or early postnatal exposure and is very likely to be permanent.

In the United States, intrauterine hypoxia and birth asphyxia were listed together as the tenth leading cause of neonatal death.

Substances whose toxicity can cause congenital disorders are called "teratogens", and include certain pharmaceutical and recreational drugs in pregnancy as well as many environmental toxins in pregnancy.

A review published in 2010 identified 6 main teratogenic mechanisms associated with medication use: folate antagonism, neural crest cell disruption, endocrine disruption, oxidative stress, vascular disruption and specific receptor- or enzyme-mediated teratogenesis.

It is estimated that 10% of all birth defects are caused by prenatal exposure to a teratogenic agent. These exposures include, but are not limited to, medication or drug exposures, maternal infections and diseases, and environmental and occupational exposures. Paternal smoking use has also been linked to an increased risk of birth defects and childhood cancer for the offspring, where the paternal germline undergoes oxidative damage due to cigarette use. Teratogen-caused birth defects are potentially preventable. Studies have shown that nearly 50% of pregnant women have been exposed to at least one medication during gestation. During pregnancy, a female can also be exposed to teratogens from the contaminated clothing or toxins within the seminal fluid of a partner. An additional study found that of 200 individuals referred for genetic counseling for a teratogenic exposure, 52% were exposed to more than one potential teratogen.

The mother's consumption of alcohol during pregnancy can cause a continuum of various permanent birth defects : cranofacial abnormalities, brain damage, intellectual disability, heart disease, kidney abnormality, skeletal anomalies, ocular abnormalities.

The prevalence of children affected is estimated at least 1 percent in U.S. as well in Canada.

Very few studies have investigated the links between paternal alcohol use and offspring health.

However, recent animal research has shown a correlation between paternal alcohol exposure and decreased offspring birth weight. Behavioral and cognitive disorders, including difficulties with learning and memory, hyperactivity, and lowered stress tolerance have been linked to paternal alcohol ingestion. The compromised stress management skills of animals whose male parent was exposed to alcohol are similar to the exaggerated responses to stress that children with Fetal Alcohol Syndrome display because of maternal alcohol use. These birth defects and behavioral disorders were found in cases of both long- and short-term paternal alcohol ingestion. In the same animal study, paternal alcohol exposure was correlated with a significant difference in organ size and the increased risk of the offspring displaying ventricular septal defects (VSD) at birth.

Sudden infant death syndrome (SIDS) is the sudden death of an infant that is unexplainable by the infant's history. The death also remains unexplainable upon autopsy. Infants exposed to smoke, both during pregnancy and after birth, are found to be more at risk of SIDS due to the increased levels of nicotine often found in SIDS cases. Infants exposed to smoke during pregnancy are up to three times more likely to die of SIDS that children born to non-smoking mothers.

Passive smoking is associated with many risks to children, including, sudden infant death syndrome (SIDS), asthma, lung infections, impaired respiratory function and slowed lung growth, Crohn's disease, learning difficulties and neurobehavioral effects, an increase in tooth decay, and an increased risk of middle ear infections.

IH/BA is also a causitive factor in cardiac and circulatory birth defects the sixth most expensive condition, as well as premature birth and low birth weight the second most expensive and it is one of the contributing factors to infant respiratory distress syndrome (RDS) also known as hyaline membrane disease, the most expensive medical condition to treat and the number one cause of infant mortality.

Hypercoagulability in pregnancy is the propensity of pregnant women to develop thrombosis (blood clots). Pregnancy itself is a factor of hypercoagulability (pregnancy-induced hypercoagulability), as a physiologically adaptive mechanism to prevent "post partum" bleeding. However, when combined with an additional underlying hypercoagulable states, the risk of thrombosis or embolism may become substantial.

Being pregnant decreases the risk of relapse in multiple sclerosis; however, during the first months after delivery the risk increases. Overall, pregnancy does not seem to influence long-term disability. Multiple sclerosis does not increase the risk of congenital abnormality or miscarriage.

Genetic

- Inborn errors of metabolism

1. Congenital disorder of glycosylation

2. Mitochondrial disorders

3. Peroxisomal disorder

4. Glucose transporter defect

5. Menkes disease

6. Congenital disorders of amino acid metabolism

7. Organic acidemia

Syndromes

- Contiguous gene deletion

1. 17p13.3 deletion (Miller–Dieker syndrome)

- Single gene defects

1. Rett syndrome (primarily girls)

2. Nijmegen breakage syndrome

3. X-linked lissencephaly with abnormal genitalia

4. Aicardi–Goutières syndrome

5. Ataxia telangiectasia

6. Cohen syndrome

7. Cockayne syndrome

Acquired

- Disruptive injuries

1. Traumatic brain injury

2. Hypoxic-ischemic encephalopathy

3. Ischemic stroke

4. Hemorrhagic stroke

- Infections

1. Congenital HIV encephalopathy

2. Meningitis

3. Encephalitis

- Toxins

1. Lead poisoning

2. Chronic renal failure

- Deprivation

1. Hypothyroidism

2. Anemia

3. Congenital heart disease

4. Malnutrition

Genetic factors may play a role in causing some cases of microcephaly. Relationships have been found between autism, duplications of chromosomes, and macrocephaly on one side. On the other side, a relationship has been found between schizophrenia, deletions of chromosomes, and microcephaly. Moreover, an association has been established between common genetic variants within known microcephaly genes ("MCPH1, CDK5RAP2") and normal variation in brain structure as measured with magnetic resonance imaging (MRI)i.e., primarily brain cortical surface area and total brain volume.

The spread of Aedes mosquito-borne Zika virus has been implicated in increasing levels of congenital microcephaly by the International Society for Infectious Diseases and the US Centers for Disease Control and Prevention. Zika can spread from a pregnant woman to her fetus. This can result in other severe brain malformations and birth defects. A study published in The New England Journal of Medicine has documented a case in which they found evidence of the Zika virus in the brain of a fetus that displayed the morphology of microcephaly.

A deficiency of folate itself does not cause neural tube defects. The association seen between reduced neural tube defects and folic acid supplementation is due to a gene-environment interaction such as vulnerability caused by the C677T Methylenetetrahydrofolate reductase (MTHFR) variant. Supplementing folic acid during pregnancy reduces the prevalence of NTDs by not exposing this otherwise sub-clinical mutation to aggravating conditions. Other potential causes can include folate antimetabolites (such as methotrexate), mycotoxins in contaminated corn meal, arsenic, hyperthermia in early development, and radiation. Maternal obesity has also been found to be a risk factor for NTDs. Studies have shown that both maternal cigarette smoking and maternal exposure to secondhand smoke increased the risk for neural tube defects in offspring. A mechanism by which maternal exposure to cigarette smoke could increase NTD risk in offspring is suggested by several studies that show an association between cigarette smoking and elevations of homocysteine levels. Cigarette smoke during pregnancy, including secondhand exposure, can increase the risk of neural tube defects. All of the above may act by interference with some aspect of normal folic acid metabolism and folate linked methylation related cellular processes as there are multiple genes of this type associated with neural tube defects.

After the dropping of atomic bombs "Little Boy" on Hiroshima and "Fat Man" on Nagasaki, several women close to ground zero who had been pregnant at the time gave birth to children with microcephaly. Microcephaly prevalence was seven of a group of 11 pregnant women at 11–17 weeks of gestation who survived the blast at less than from ground zero. Due to their proximity to the bomb, the pregnant women's "in utero" children received a biologically significant radiation dose that was relatively high due to the massive neutron output of the lower explosive-yielding Little Boy. Microcephaly is the only proven malformation, or congenital abnormality, found in the children of Hiroshima and Nagasaki.

Folic acid supplementation reduces the prevalence of neural tube defects by approximately 70% of neural tube defects indicating that 30% are not folate-dependent and are due to some cause other than alterations of methylation patterns. Multiple other genes related to neural tube defects exist which are candidates for folate insensitive neural tube defects. There are also several syndromes such as Meckel syndrome, and Triploid Syndrome which are frequently accompanied by neural tube defects that are assumed to be unrelated to folate metabolism

Prognosis is poor if this condition is not aggressively treated. In the 1970s, mortality was greater than 80%; with the current management, however, mortality is now less than 5%.

Patients with abnormal cardiac and kidney function may be more at risk for hemolytic uremic syndrome

Those working in industry, in the military, or as first responders may be required to wear personal protective equipment (PPE) against hazards such as chemical agents, gases, fire, small arms and even Improvised Explosive Devices (IEDs). PPE includes a range of hazmat suits, firefighting turnout gear, body armor and bomb suits, among others. Depending on design, the wearer may be encapsulated in a microclimate, due to an increase in thermal resistance and decrease in vapor permeability. As physical work is performed, the body’s natural thermoregulation (i.e., sweating) becomes ineffective. This is compounded by increased work rates, high ambient temperature and humidity levels, and direct exposure to the sun. The net effect is that desired protection from some environmental threats inadvertently increases the threat of heat stress.

The effect of PPE on hyperthermia has been noted in fighting the 2014 Ebola virus epidemic in Western Africa. Doctors and healthcare workers were only able to work 40 minutes at a stretch in their protective suits, fearing heat strokes.

Some drugs cause excessive internal heat production. The rate of drug-induced hyperthermia is higher where use of these drugs is higher.

- Many psychotropic medications, such as selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants, can cause hyperthermia. Serotonin syndrome is a rare adverse reaction to overdose of these medications or the use of several simultaneously. Similarly, neuroleptic malignant syndrome is an uncommon reaction to neuroleptic agents. These syndromes are differentiated by other associated symptoms, such as tremor in serotonin syndrome and "lead-pipe" muscle rigidity in neuroleptic malignant syndrome.

- Various stimulant drugs, including amphetamines and cocaine, and hallucinogenic drugs, including PCP, LSD, and MDMA can produce hyperthermia as an adverse effect.

- Malignant hyperthermia is a rare reaction to common anesthetic agents (such as halothane) or the paralytic agent succinylcholine. Those who have this reaction, which is potentially fatal, have a genetic predisposition.

- The use of anticholinergics, more specifically muscarinic antagonists are thought to cause mild hyperthermic episodes due to its parasympatholytic effects. The sympathetic nervous system a.k.a. the "Fight or Flight Response" dominates by raising catecholamine levels by the blocked action of the Rest and Digest System.

- Drugs that decouple oxidative phosphorylation may also cause hyperthermia. From this group of drugs the most well known is 2,4-Dinitrophenol which was used as a weight loss drug until dangers from its use became apparent.

It occurs in between 1:5,000 and 1:100,000 in procedures involving general anaesthesia. This disorder occurs worldwide and affects all racial groups. Most cases, however, occur in children and young adults, which might be related to the fact many older people will have already had surgeries and thus would know about and be able to avoid this condition.

The incidence of VACTERL association is estimated to be approximately 1 in 10,000 to 1 in 40,000 live-born infants. It is seen more frequently in infants born to diabetic mothers. While most cases are sporadic, there are clearly families who present with multiple involved members.

By 1990, 65 patients had been reported in the literature, with no sex or ethnic preference notable. Some individuals present with minimal malformation; rarely patients have died during infancy as a result of severe central nervous system involvement or respiratory complications. Several syndromes are related to the Freeman–Sheldon syndrome spectrum, but more information is required before undertaking such nosological delineation.

There are little data on prognosis. Rarely, some patients have died in infancy from respiratory failure; otherwise, life expectancy is considered to be normal.

Although it is very uncommon, women undergoing surgical abortion after 18 weeks gestation sometimes give birth to a fetus that may survive briefly. Longer term survival is possible after 22 weeks.

If medical staff observe signs of life, they may be required to provide care: emergency medical care if the child has a good chance of survival and palliative care if not. Induced fetal demise before termination of pregnancy after 20–21 weeks gestation is recommended to avoid this.

Death following live birth caused by abortion is given the ; data are identified as either fetus or newborn. Between 1999 and 2013, in the U.S., the CDC recorded 531 such deaths for newborns, approximately 4 per 100,000 abortions.

Aglossia (aglossia congenita) is a congenital defect resulting in a partial development or complete absence of a tongue.

Aglossiais commonly associated with craniofacial and limb defects (Adactylia syndrome) and is thought to belong to a family of oromandibular limb hypogenesis syndrome or OLHS. It is believed to be caused by heat-induced vascular disruption near the fourth week of embryonic development.

The first known case was reported in the early 18th century by a member of the prominent De Jussieu family in France and cases to this day remain rare.

The rate of cancer during pregnancy is 0.02–1%, and in many cases, cancer of the mother leads to consideration of abortion to protect the life of the mother, or in response to the potential damage that may occur to the fetus during treatment. This is particularly true for cervical cancer, the most common type of which occurs in 1 of every 2,000–13,000 pregnancies, for which initiation of treatment "cannot co-exist with preservation of fetal life (unless neoadjuvant chemotherapy is chosen)". Very early stage cervical cancers (I and IIa) may be treated by radical hysterectomy and pelvic lymph node dissection, radiation therapy, or both, while later stages are treated by radiotherapy. Chemotherapy may be used simultaneously. Treatment of breast cancer during pregnancy also involves fetal considerations, because lumpectomy is discouraged in favor of modified radical mastectomy unless late-term pregnancy allows follow-up radiation therapy to be administered after the birth.

Exposure to a single chemotherapy drug is estimated to cause a 7.5–17% risk of teratogenic effects on the fetus, with higher risks for multiple drug treatments. Treatment with more than 40 Gy of radiation usually causes spontaneous abortion. Exposure to much lower doses during the first trimester, especially 8 to 15 weeks of development, can cause intellectual disability or microcephaly, and exposure at this or subsequent stages can cause reduced intrauterine growth and birth weight. Exposures above 0.005–0.025 Gy cause a dose-dependent reduction in IQ. It is possible to greatly reduce exposure to radiation with abdominal shielding, depending on how far the area to be irradiated is from the fetus.

The process of birth itself may also put the mother at risk. "Vaginal delivery may result in dissemination of neoplastic cells into lymphovascular channels, haemorrhage, cervical laceration and implantation of malignant cells in the episiotomy site, while abdominal delivery may delay the initiation of non-surgical treatment."