Environmental and occupational hazards are challenging for the clinician because of the intense concern expressed by many potentially exposed women and their families. Although it is true that some types of exposures can cause birth defects and other problems, in many cases there is little to no risk for the patient or the fetus, because the exposure dose is negligible. Establishing exposure levels can be challenging because many toxicants have no readily available assay to assess the dose absorbed into the body. Even if a blood or urine test is available, compounds may be rapidly metabolized, so that an exposure last week or last month cannot be detected by a test today. A careful environmental and occupational history can provide an estimate of exposure levels.

Another challenge is reducing exposures that are identified in the history. The clinician cannot ensure that the patient will be able to take appropriate exposure remediation steps. Environmental hazards may be unavoidable when contamination of air, water, or soil is widespread. For occupational exposures, the patient may wish to follow the clinician's advice, but the workplace may refuse to modify the patient's work duties. A work restriction may cause the woman to lose her job, especially in countries that have not enacted maternity protection legislation. This barrier to managing the patient can be overcome, in part, by judicial use of work restrictions.

The number of potential environmental and occupational exposures is enormous, so the clinician will need information resources. The reproductive and developmental effects of all agents cannot be described in a single textbook chapter. Caution should be exercised when reviewing the health information on the material safety data sheets that patients may bring to clinic. Several studies have demonstrated that the known adverse health effects of a compound may be missing from these sheets, particularly the reproductive effects.^1,2

To assess an agent for any associations with adverse health outcomes, a literature search should be conducted or an expert should be consulted. Information resources available by telephone in North America include the Organization of Teratology Information Services (http://www.otispregnancy.org) and Motherrisk (http://www.motherisk.org). The web pages of these organizations provide links to resources in other parts of the world. Reproductive toxicity data syntheses are available by subscription from services such as REPROTOX (http://www.reprotox.org/) or the Teratogen Information System, TERIS (http://depts.washington.edu/terisweb/teris/index.html). Poison control centers, medical school libraries, and hospital emergency departments may have subscriptions to these and other computerized databases that contain health information about hazardous agents.

Environmental pollutants can cause developmental effects at prenatal exposure levels that do not cause symptoms in the mother. Trace amounts of toxicants can be found in food, air, and water, but there are a number of laws and regulations in place in the United States to limit toxicants to levels that are unlikely to be harmful. There are circumstances, however, when environmental exposures can exceed recommended levels and the woman can take steps to lower her exposure.

Methylmercury is a contaminant that can be found in fish. Its toxic properties were noted during poisonings in Japan and Iraq and further confirmed by studies in laboratory animals.^3,4 In Japan, pregnant women consumed fish poisoned by methylmercury released as industrial waste into Minamata Bay. In Iraq, pregnant women consumed grain that had been treated with pesticides containing the compound. Their infants had microcephaly, learning deficits, abnormal gait, dysarthria, ataxia, visual problems, and deafness, whereas the mothers showed little to no toxic effects. Pregnant women in the Faeroe Islands had exposures from consuming pilot whale meat, and their children at age 7 had neuropsychologic dysfunction that included problems with language, attention, and memory.⁵

Because mercury is currently found in many fish species, a warning about fish consumption was issued in the United States during 2001 by the Environmental Protection Agency and the Food and Drug Administration.^6,7 The Food and Drug Administration recommended that women who may become pregnant and women who are pregnant or breastfeeding should not eat shark, swordfish, king mackerel, or tile fish. Avoidance of these fish was recommended because long-lived, large fish that feed on other fish accumulate methylmercury over their lifetimes. In addition, the women were advised to limit intake of all other fish to 12 ounces per week on average. The Environmental Protection Agency recommended a consumption limit of 6 ounces of cooked fish per week for the women and 2 ounces of cooked fish per week for young children. Sport fish that are smaller (within legal limits) contain fewer pollutants than larger, older fish. Blue gill, perch, stream trout and smelt that feed on insects and the like contain lower levels of pollutants than fish that feed on the bottoms of lakes and streams, such as catfish or carp. When cleaning and cooking fish, removal of the fat reduces pollutant levels.⁸

Tuna is one of the most consumed fish. Certain countries recommend that pregnant or nursing women or women who could become pregnant limit consumption of tuna steaks to once per week (United Kingdom)⁹ or once per month (Canada).¹⁰ Mercury levels are lower in canned tuna than in tuna steak, because canned tuna is prepared from smaller fish. In the United Kingdom, women who are pregnant, lactating, or could become pregnant have been advised to consume no more than two medium-size cans of canned tuna per week, amounting to a drained weight of 140 grams per can.⁹ This weekly intake is equivalent to 9.9 ounces, which is within the 12-ounce limit recommended by the United States Food and Drug Administration.

Another example of an environmental exposure that can affect pregnancy and fetal development is lead. Approximately 1 in 200 childbearing-aged women have blood lead levels exceeding the recommended level of 10 μg/dL (.483 micromols).¹¹ Women at greater risk for elevated blood levels include those whose children were found to have an elevated lead level during screening or those who live in a house built before 1960 that was recently renovated or currently has peeling or chipped paint. Other risk factors include engaging in hobbies involving lead or having a household member who works in a job with lead exposure, eating or chewing nonfood items, being a current smoker, or consuming more than nine servings of canned food per week. In a study of pregnant women, presence of at least one of these risk factors had a sensitivity of 89.2% and a positive predictive value of 96.4% for exceeding the recommended blood lead level.¹¹

Multiple new sources of information about terrorism and disasters are being developed to assist the clinician to manage patients. Some of the bulletins specifically address the needs of pregnant women. The Centers for Disease Control and Prevention provides many fact sheets and links to information about biologic, nuclear, and chemical terrorism at http://www.bt.cdc.gov.

Women who are considered at high risk for exposure to agents used for bioterrorism, especially smallpox and anthrax, can be counseled about vaccination and antibiotic prophylaxis based on published guidelines.^12,13,14 It is advisable to consult the most recent bulletins from the Centers for Disease Control and Prevention, the American College of Obstetricians and Gynecologists, and others. Immunization during pregnancy is further discussed in Chapter 52.

Smallpox vaccine should not be administered to women who are pregnant, and vaccinated women should avoid pregnancy for 4 weeks after vaccine administration. Smallpox vaccine should not be administered to anyone who has close physical contact with a pregnant woman, such as household members and sexual partners. To ascertain the magnitude of risk from smallpox vaccine exposure during pregnancy, new data are being assembled from a registry of pregnant women inadvertently exposed to smallpox vaccine. Breastfeeding is also a contraindication to receiving smallpox vaccine, although people who are in close contact with a breastfeeding woman may be vaccinated.¹⁵

Anthrax vaccine administration to pregnant women has been criticized because little research is available to confirm its safety during pregnancy.¹⁶ It is an inactivated bacterial vaccine and its use should be reserved for situations in which there is a risk for serious maternal illness or death if the vaccine is not administered. The American College of Obstetricians and Gynecologists has stated that the risk of teratogenicity from anthrax vaccine is theoretical and that vaccination of pregnant women is “not routinely recommended unless pregnant women work directly with B anthracis, imported animal hides, potentially infected animals in high incidence areas (not United States), or military personnel deployed to high-risk exposure areas.”¹⁷ Antibiotic prophylaxis of asymptomatic pregnant and lactating women should be limited to those exposed to a confirmed environmental contamination or high-risk source as determined by the local Department of Health.¹⁴ Ciprofloxacin 500 mg orally every 12 hours is recommended for 60 days, although if the bacteria is found to be penicillin-sensitive, the patient should use amoxicillin instead. For exposed pregnant women who are allergic to penicillin and ciprofloxacin, doxycycline should be administered or penicillin desensitization should be considered. Guidelines stress that benefits of therapy should outweigh risks. While human teratogenicity with fluoroquinolones has not been confirmed, some studies have shown irreversible drug-induced arthropathy in adolescent animals administered ciprofloxacin, and doxycycline can cause dental staining of the primary teeth and possibly decreased bone growth.¹⁴

Substantial environmental exposure to radiation could occur as a result of a disaster or terrorism incident, although small-scale releases may generate more fear than actual exposure. Some of the issues to discuss with patients after an environmental radiation release would be similar to those that arise in context of diagnostic tests (see Volume 2, Chapter 101). If the exposure was negligible, then the clinician will be able to reassure the patient that termination of pregnancy is not necessary and that no increase in adverse health consequences is anticipated.

When the nuclear plant at Chernobyl exploded, a huge amount of fallout was released that migrated to the surrounding regions. When the cloud reached Finland, radiation exposure was twice the background level.¹⁸ Although there was an increase in spontaneous abortions in Finland after the incident, reporting bias or confounding could not be ruled out. Studies of childhood leukemia incidence in the areas surrounding the plant were inconclusive, but a definite increase in thyroid cancer was found among children in Belarus who were exposed in utero or during infancy.¹⁹ The increase in childhood thyroid cancer occurred in the context of low-level iodine deficiency because iodinization of salt was not used in the former Soviet Union.²⁰ This finding emphasizes the importance of iodine prophylaxis among pregnant women if a nuclear incident occurs. Iodine reduces the risk for thyroid cancer by binding to receptors in the thyroid, which prevents uptake of radioactive iodine isotopes. The Centers for Disease Control and Prevention recommends that in the event of a nuclear disaster, pregnant and breastfeeding women should be administered the same dose of potassium iodide as other young adults.²¹

Any chemical could theoretically result in population exposures during a terrorist attack or disaster. Chemicals that are regarded as likely agents for terrorist attacks include sarin nerve gas, mustard gas, and the poisons ricin or VX. Very little information is available about caring for pregnant women exposed to these agents. The general principles of decontamination and supportive management would apply to pregnant women. A significant issue during an incident will be the high level of fear among pregnant women whose exposures are negligible. Education can help to address this fear. Psychiatric morbidity has been studied after natural disasters such as earthquakes.^22,23 These studies suggest that pregnant women who may need the most intensive psychosocial support include those who were injured, had a family member who was injured, or are earlier in gestation when the disaster occurs.

The occupational history can be used to assess whether the patient works with chemicals, biological agents, physical hazards such as noise and radiation, and ergonomic job demands, circadian rhythm disturbances from shift work, and any other hazards. In clinical practice, the woman is the patient and the history focuses on her health and her risk factors. The male partner's occupational exposures can also impact reproductive outcomes, so it is important to assess his history, also. Examples of associations between paternal exposures and pregnancy outcomes are provided below.

In addition to obtaining a complete list of the couple's occupational exposures, the history should also be used to estimate exposure levels. Working with an agent is not the same as being exposed to it internally. Chemical and biological agents in the workplace are typically absorbed into the body through inhalation, dermal absorption, or contamination of tobacco products or food or drinks that are ingested.

If an agent is heated or is or is agitated or sprayed (aerosolization), or if it is in the form of a fine powder, inhalation often increases. Agents that are agitated, sprayed, or poured may have more opportunities to contact the skin, increasing the risk for dermal absorption among those agents for which the skin is not an effective barrier, such as certain organic solvents and pesticides. If a large amount of the agent is used and the work task involving the chemical is frequently performed, the chance of internal exposure may be increased. If no gloves or protective clothing is used, dermal exposure risk is increased. All gloves are not equally impermeable, so the proper type of gloves must be worn for specific chemicals. Efficient workplace ventilation is preferable to use of a respirator. Pregnant women may wear most lightweight respirators for limited periods, and a properly designed respiratory protection program can minimize inhalational exposures. However, respirators do not prevent all exposures. Breaks in technique occur, leading to potentially significant exposures and a false sense of security.

Few data are available to estimate the noise threshold at which fetal hearing may be compromised by maternal noise exposure late in pregnancy, but extremely loud noise will be transferred through the abdominal wall. However, woman may be required to wear hearing protection for modestly elevated noise levels that are not thought to cause harm to the fetus. Employees with potential exposure to radiation often wear badges, and these data can be reviewed early in pregnancy to ascertain whether past exposures exceed recommended levels during pregnancy.

Examples of occupational and environmental exposures that have been linked with spontaneous abortion, congenital anomalies, fetal neurobehavioral effects, fetal growth retardation, preterm birth, and other adverse pregnancy effects are described below. Although the critical period for the development of birth defects of many organ systems is in the first trimester, the following examples demonstrate that it is important to control hazardous exposures in the preconception period and throughout the pregnancy. In addition, many hazardous chemicals to which a mother is exposed can be found in breast milk. If the mother's exposure level is low, then the toxicant level in breast milk is probably very low. The benefits of breastfeeding may outweigh any risk of exposure to the infant. Very few epidemiologic studies have assessed lactational exposures.

Spontaneous abortion can be related to toxicant exposures, although the rate is high among women with no known hazardous exposures. Many recent epidemiologic studies have been able to control for the main confounders and suggest that the clinician should be concerned when the patient's history reveals certain types of hazardous exposures. The biologic plausibility of findings from epidemiologic studies among women and men is supported by experimental studies among laboratory animals.

The critical period during which a parental exposure to a hazardous agent may increase the risk for spontaneous abortion probably includes not only the early weeks of pregnancy but also the preconception period. Paternal exposures in the preconception period may increase the risk for spontaneous abortion, and the mechanism by which this occurs may be genetic alterations in sperm, transfer of toxic exposures to the mother through soiled clothing, or other mechanisms. Spontaneous abortion and other types of fetal death have been increased in populations in which the father was exposed to organic solvents, lead, mercury, welding fumes or pesticides.^24,25,26,27

Among women, some preconception exposures take time to be cleared from the body (e.g., heavy metals and chlorinated pesticides), so prudent avoidance during the preconception period is warranted. During early pregnancy, many studies show that intensive exposure to organic solvents increases the risk for miscarriage. Some of the organic solvents causing miscarriage include carbon disulfide, dimethylformamide, methylene chloride, toluene, xylene, and formaldehyde. Maternal lead exposure, certain pesticides, disinfectants like formaldehyde, and other exposures increase the risk of spontaneous abortions.^28,29

Maternal exposures in health care workplaces that can increase the risk for miscarriage include certain medications, sterilants, waste anesthetic gases, and others.^30,31,32 Drugs of concern include antiviral agents like acyclovir and zidovine, antineoplastic agents, and others. Pharmaceuticals are further discussed in Volume 2, Chapter 6. A very large dose of ionizing radiation soon after conception may be embryolethal, causing a subclinical or clinical miscarriage. Ionizing radiation is further discussed in Volume 2, Chapter 101.

Hazardous exposures can cause birth defects, although a substantial proportion of congenital anomalies are unexplained. The critical period during which an exposure increases the risk for congenital anomalies may extend into the preconception period. Occupational exposure to pesticides has been shown to increase aneuploidy in sperm cells, suggesting a genetic mechanism by which paternal preconception exposures could cause birth defects.³³ Agents that have been associated in epidemiologic studies with birth defects in offspring after paternal exposure include pesticides, welding fumes, and possibly lead.^34,35,36,37

Because many women are not sure they are pregnant until organogenesis is well underway, reducing hazardous exposures is best accomplished in the preconception period. Metals such as methylmercury have induced birth defects. Several studies suggest that maternal lead exposure increases the risk for neural tube defects.^38,39 The mechanism by which this might occur is that lead exposure can lead to zinc deficiency, and this in turn impairs absorption of folic acid.³⁸

Organic solvent use at work increases risk for birth defects by approximately 64%.⁴⁰ Occupational exposure to glycol ethers occurred twice as frequently among mothers of infants with neural tube defects, cleft lip, or multiple anomalies in a large European study.⁴¹ When detailed occupational exposure histories are available, results suggest that exposure levels that are most worrisome are those that are high enough to cause sensory irritation,⁴² although with chronic exposure, sensory symptoms often attenuate.

Pesticides vary in their reproductive toxicity from relatively low (pyrethrins) to relatively high (dibromochloropropane). Many epidemiologic studies of pesticide contact during pregnancy are limited by inexact assessment of exposure. Birth defects have been associated with certain pesticides in studies of animals and in some studies of mothers who had occupational or environmental pesticide exposures.^43,44 In a registry study in Norway that involved 192,417 births, limb reduction defects were associated with grain farming.³⁵ Animal research has shown an increase in limb defects on exposure to certain fungicides.⁴⁵

Ionizing radiation exposure during pregnancy can cause microcephaly and other defects. The likelihood of malformation and the organs affected depends on the dose of radiation and the stage of development at which the radiation is received. Workplaces that follow the mandates of the Nuclear Regulatory Commission will keep exposures at a protective level of less than 50 mrem in any gestational month and 500 mrem throughout the pregnancy.

A potential genetic mechanism has been suggested by studies of paternal solvent exposure that have shown associations with fetal growth retardation or preterm birth.^46,47 Contamination of the home could partly explain why paternal lead exposure has been implicated. Studies have found that risk increased if the father's exposure level was high, of long duration, or combined with other toxicants.^46,48,49

Many epidemiologic studies have found that occupational risk factors for the conditions resulting in low birth weight include intensive physical demands such as standing more than 6 hours per shift, work days longer than 8 hours, work weeks longer than 40 hours, night-shift work, and frequently rotating shifts.^50,51,52,53 Some of the studies have been prospective, and a growing number have controlled for multiple other risk factors to assess the independent effect of physically heavy work. Although this information can be useful in counseling women about potential risks, whether all women should receive routine restrictions on job physical demands is debatable. There are no randomized trials to assess the benefits and consequences of various work restriction approaches among subgroups of women stratified by nonoccupational risk factors for preterm birth or fetal growth retardation.

The mechanism by which chemicals may increase the risk for preterm birth or fetal growth restriction is not well understood. Studies have noted associations for occupational exposure to ethylene oxide, nitrous oxide, lead, organic solvents, and environmental exposure to air pollution.^{31,54,55,56,57} Preterm delivery is sometimes indicated because of preeclampsia. Women who were exposed to solvents during pregnancy were shown in one study to have 3.9-times the frequency of preeclampsia as unexposed women.⁵⁸ Occupational exposure to solvents has been associated with increased risk of gestational hypertension.^59,60 A blood lead level of 6.9 μg/dL or greater significantly increased the risk of hypertension during pregnancy in one study.⁶¹

Hazardous exposures that result in fetal growth restriction could theoretically increase the risk for heart disease and diabetes later in life, because small-for-gestational-age infants are at increased risk for these conditions through a process that has been called fetal programming.⁶²

The fetal brain is vulnerable to neurotoxic exposures throughout pregnancy.⁶³ Children with low-level prenatal lead exposure may demonstrate cognitive deficits well into late childhood, even after adjustment for the most important confounders.⁶⁴ Similar effects have been seen for gestational exposure to polychlorinated biphenyls (PCBs) and from organic solvents in the mother's workplace.^65,66

Whether attention deficit hyperactivity disorder (ADHD) in children is related to pollution or hazardous occupational exposures of their parents is unclear. Many epidemiologic studies have shown that maternal smoking during pregnancy increases the risk of ADHD in offspring, as well as aggressive and oppositional behavior. The findings persisted in studies that controlled for parental ADHD, parental IQ, and socioeconomic status.^67,68 These studies show that a toxic mechanism could play a role, but the chemical exposure level from smoking is relatively high compared with exposure to environmental pollution.

Autism spectrum disorders are increasingly recognized, and this has led to a concern that environmental exposures may play a role in their etiology.⁶⁹ Autism is believed to be a disorder with multifactorial etiology in which gene–environment interaction may play a role. Early pregnancy when the brainstem forms is a critical period for exposure.⁷⁰ Other vulnerable periods may include later pregnancy when brain structures develop that are responsible for executive functions and the postnatal period when synaptic pruning occurs. Prenatal rubella infection and postnatal herpes encephalitis can cause autism, but prospective studies have shown no association with the measles, mumps, rubella vaccine.^69,71,72 Daily prenatal smoking increases the risk for autism by approximately 40%.⁷³ Drugs that can cause autistic disorders in humans include thalidomide and valproate, and the critical period for exposure is at neural tube closure (gestational days 20 to 24). Autism has a strong genetic component, with 66% concordance in monozygotic twins, compared with a background rate of approximately one per 1000 in the general population. Knockout mice lacking Hoxa-1 and Hoxb-1 genes have some of the same abnormalities as rats exposed prenatally to valproate and people with autism, notably brainstem abnormalities and a decrease in cerebellar Purkinje cells.^69,70,71 Clusters of autism have been investigated in communities with pollution concerns in New Jersey and Massachusetts, but retrospective maternal exposure assessments were imprecise and no definitive relationship with toxicants was established.^69,74 A large study of the determinants of autism was authorized in the Children's Health Act of 2000 (Public Law No. 106-310), which will provide an opportunity to assess prospectively the role of environmental exposures. In the interim, one should note that toxicant exposures may increase the risk for frank neural tube defects.^38,39,41 Because the initial window of vulnerability for autism may be at the time of neural tube closure, this further reinforces the importance of minimizing hazardous exposures in the periconceptual period.

The anatomic anomalies of the brain seen in schizophrenia suggest that neuronal migration and apoptosis did not occur normally during the second trimester of pregnancy.^75,76 This has led to hypotheses that the disorder may be caused by prenatal noxious exposures among genetically susceptible individuals. Conditions associated with fetal hypoxia have been linked to later schizophrenia by several groups of researchers.^77,78,79 Winter pregnancy (birth in February or March) is a well-established risk factor for schizophrenia, but only approximately 10% of cases could potentially be prevented by timing pregnancies to avoid these birth months.⁸⁰ Studies are conflicted about whether any specific infection (such as influenza) is the reason for the association between schizophrenia and season of birth.^81,82 No studies of parental exposures to environmental or workplace contaminants and later development of schizophrenia in offspring were located.

The fetal immune system can be affected by toxicants, including maternal smoking and possibly urban air pollution and other exposures.^83,84,85 These exposures may increase the risk for childhood asthma, atopy, and other conditions.

Transplacental carcinogenesis from prenatal diethylstilbestrol exposure is well known. In laboratory animals, hazardous chemicals administered to male and female animals in either the preconception period or the prenatal period can cause malignancies in offspring.⁸⁶ Although some results conflict and confounders were not always well controlled, epidemiologic studies have suggested that paternal preconception exposure to tobacco, certain metal compounds, or petroleum products may increase the risk of childhood cancer.^87,88 Studies of maternal employment, hobbies, and habits during pregnancy suggest that nuclear fallout or intensive exposure to organic solvents, tobacco smoke, and some other toxicants may increase the risk for childhood cancers.^89,90,91,92

Labor regulations and workplace health and safety law are the purview of a number of federal and state agencies in the United States, and expertise in all aspects is beyond the scope of clinical practice. Pregnant women should be advised to obtain information about the policies at their company for implementing these laws and regulations. Further information can be obtained from external sources such as the United States Department of Labor and the Occupational Safety and Health Administration (OSHA). Most workplaces are regulated by OSHA, which has promulgated several standards that explicitly aim to protect reproductive health. Like the enforcement of speed limit laws, however, OSHA enforcement is unable to ensure that all employers comply with all the standards all the time. In addition, some of the legally binding occupational exposure limits were set in the 1970s and have not kept pace with new research on reproductive and developmental hazards that occur at lower exposure levels. Because of this phenomenon, sometimes the patient and the clinician determine that a modification of duties is warranted to reduce reproductive risks.

In Canada, the European Union, and many other countries, a woman who needs time off from work because of pregnancy complications or hazardous exposures can receive temporary income support from a governmental program that is like the social security disability system in the United States. The United States has the Family and Medical Leave Act, which provides for 12 weeks of unpaid leave each year. There are certain exclusions from the Act, and it only applies to women who work in companies with 50 or more employees. Some employers may interpret the Act to mean that a medical complication has to have arisen in the pregnancy before the leave can be used, excluding its use for reducing risk.⁹³ The Americans with Disabilities Act explicitly excludes pregnancy because the Act only applies to permanent conditions.

The Pregnancy Discrimination Act has no provisions to require employers to provide more access for pregnant women to limited duty or medical leave than would be provided for other employees. Case law interpreting the Act in relation to hazardous exposures includes the Supreme Court decision commonly known as the Johnson Controls case.⁹³ The Court struck down the fetal protection policy used by the company, because the policy did not allow any women capable of bearing children to work with lead. The Court found that the policy was discriminatory in part because men are also susceptible to reproductive effects from lead. A better way to handle reproductive hazards is to reduce exposure levels for all workers and to provide supervisors with training to avoid discriminatory behavior against pregnant employees.⁹⁴ When an infant health problem may have been caused by work, workers' compensation does not apply because the fetus is not an employee. Civil and criminal suits may be brought against health care providers, employers, or manufacturers of products used in the workplace if harm occurs.⁹³

The goal of counseling is to educate patients about potential risks while keeping these risks in perspective. An ethical keystone of informed consent is patient autonomy, which includes the ability to have a say in managing risks to one's health. The approach to risk may appropriately vary depending on whether the issue at hand is avoidance of risk from a future exposure or assessment of the magnitude of risk from an exposure that has already occurred.

The history and any data from biologic or workplace monitoring can be used to assess whether internal exposure to hazardous agents is likely. A thorough evaluation may discover that a job that initially seemed hazardous actually entails negligible risk. Then reassurance can be provided and the woman can avoid the social and economic losses that may accompany unnecessarily restrictive medical recommendations. If an exposure to a reproductive toxicant at a significant dose has already occurred during the pregnancy, then counseling should include not only the potential risk but also the best estimate of the magnitude of risk. For example, it may help to explain that because birth defects are relatively uncommon, a 50% increase in risk means that most exposed pregnancies will not be affected by anomalies. The patient, her family, and the clinician may elect to follow-up the pregnancy closely rather than automatically elect voluntary termination.

If exposure has not already occurred, the best decision may be to make job changes to prevent future exposures, preferably before conception. Workers can often modify their technique to reduce future exposures, for instance, by fully complying with use of gloves and protective clothing. A written work restriction or a medical leave may be warranted in some cases. Many companies have generous programs to assist employees who need medically related work modifications or temporary medical leave. Even if the patient will experience economic hardship, in some cases it is better to recommend strongly that the patient avoid further exposures from an unsafe job. The patient should provide consent before the employer is contacted to obtain workplace exposure data or to recommend changes in job duties.

Occupational and environmental exposures can affect both men and women. When the male partner has intensive occupational exposure to certain pesticides, heavy metals, organic solvents, or other agents, pregnancy outcomes such as spontaneous abortion and birth defects may be increased. Among women, adverse effects of exposure include spontaneous abortion, congenital anomalies, fetal growth restriction, gestational hypertension, and preterm birth. When infants are followed-up into childhood, certain prenatal exposures are associated with neurobehavioral effects. Laboratory animal studies confirm the biologic plausibility of these associations and also have documented transplacental carcinogenesis and fetal immune system changes. Health effects from maternal exposure have been linked to certain heavy metals, organic solvents, pesticides, and pharmaceuticals such as antineoplastic and antiviral agents. Hazardous maternal exposures also include certain biologic agents, radiation, and ergonomic stressors such as prolonged standing, long working hours, and excessive shift work. The rate of adverse reproductive effects is dose-dependent. Clues from the occupational history that substantial internal exposure may be occurring include frequent use of large quantities of the agent, and work practices that promote inhalational or dermal exposure, as well as contamination of food or drink. Personal protective equipment may fail, giving a false sense of security. Counseling can assist the couple to ascertain the level of risk, put their risk from occupational and environmental exposures into perspective, and to find ways to reduce exposures when warranted.

1. Paul M, Kurtz S: Analysis of reproductive health hazard information on material safety data sheets for lead and the ethylene glycol ethers. Am J Ind Med 25:403, 1994

2. Frazier LM, Beasley BW, Sharma GK et al: Health information in material safety data sheets for a chemical that causes asthma. JGIM 16:89, 2001

3. Myers GJ, Davidson PW: Does methylmercury have a role in causing developmental disabilities in children. Environ Health Perspect 108:(S3):413, 2000

4. Satoh H: Occupational and environmental toxicology of mercury and its compounds. Ind Health 38:153, 2000

5. Grandjean P, Weihe P, White RF et al: Cognitive deficit in 7-year old children with prenatal exposure to methylmercury. Neurotoxicol Teratol 19:417, 1997

6. US Environmental Protection Agency: National advice on mercury in fish caught by family and friends: For women who are pregnant or may become pregnant, nursing mothers and young children. Office of Water, US Environmental Protection Agency, January 2001. Available at: http://www.epa.gov/waterscience/fishadvice/factsheet.html verified 6/19/03

7. US Food and Drug Administration: An important message for pregnant women and women of childbearing age who may become pregnant about the risks of mercury in Fish. Consumer Advisory, Center for Food Safety and Applied Nutrition, US Food and Drug Administration, March 2001. Available at: http://www.cfsan.fda.gov/ verified 6/19/03

8. US Environmental Protection Agency: A guide to healthy eating of the fish you catch. Office of Water, US Environmental Protection Agency, Publication No. EPA 823-F-02-005. April 2001

9. United Kingdom Food Standards Agency: Agency updates advice to pregnant and breastfeeding women on eating certain fish. Food Standards Agency, 17 February, 2003. Available at: http://www.foodstandards.gov.uk/news/pressreleases/tuna_mercury verified 7/12/03

10. Health Canada: Information on mercury levels in fish. Health Canada-Sante Canada, May 29, 2002. Available at: http://www.hc-sc.gc.ca/english/protection/warnings/2002/2002_41e.htm verified July 12, 2003

11. Stefanak MA, Bourguet CC, Benzies-Styka T: Use of the Centers for Disease Control and Prevention childhood lead poisoning risk questionnaire to predict blood lead elevations in pregnant women. Obstet Gynecol 87:209, 1996

12. Wharton M, Strikas RA, Harpaz R et al: Recommendations for using smallpox vaccine in a pre-event vaccination program. Supplemental recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Healthcare Infection Control Practices Advisory Committee (HICPAC) MMWR Morb Mortal Wkly Rep 52 (RR-7):1, 2003

13. Suarez VR, Hankins GD: Smallpox and pregnancy: From eradicated disease to bioterrorist threat. Obstet Gynecol 100:87, 2002

14. American College of Obstetricians and Gynecologists: ACOG Committee Opinion. Management of asymptomatic pregnant or lactating women exposed to anthrax. Obstet Gynecol 99:366, 2002

15. Centers for Disease Control and Prevention: Pregnancy and breastfeeding mean you should not get smallpox vaccine. Centers for Disease Control and Prevention, May 1, 2003. Available at: http://www.bt.cdc.gov/agent/smallpox/vaccination/preg-contra.asp, verified 7/12/03.

16. Nass M: The anthrax vaccine program: An analysis of the CDC's recommendations for vaccine use. Am J Public Health 92:715, 2002

17. American College of Obstetricians and Gynecologists: ACOG Committee Opinion. Immunization during pregnancy Obstet Gynecol 101:207, 2003

18. Auvinen A, Vahteristo M, Arvela H et al: Chernobyl fallout and outcome of pregnancy in Finland. Environ Health Perspect 109:179, 2001

19. Moysich KB, Menezes RJ, Michalek AM: Chernobyl-related ionising radiation exposure and cancer risk: An epidemiological review. Lancet Oncol 3:269, 2002

20. Jackson RJ, DeLozier DM, Gerasimov G et al: Chernobyl and iodine deficiency in the Russian Federation: An environmental disaster leading to a public health opportunity. J Public Health Policy 23:453, 2002

21. Centers for Disease Control and Prevention: Potassium Iodide. Public Health Emergency Preparedness and Response. 2003. Available at: http://www.bt.cdc.gov/radiation/ki.asp, verified July 2, 2003

22. Glynn LM, Wadhwa PD, Dunkel-Schetter D, et al: When stress happens matters: Effects of earthquake timing on stress responsivity in pregnancy. Am J Obstet Gynecol 184:637, 2001

23. Chang HL, Chang TC, Lin TY et al: Psychiatric morbidity and pregnancy outcome in a disaster area of Taiwan 921 earthquake. Psychiatry Clin Neurosci 56:139, 2002

24. Taskinen H, Anttila A, Lindbohm ML et al: Spontaneous abortions and congenital malformations among the wives of men occupationally exposed to organic solvents. Scand J Work Environ Health 15:345, 1989

25. Lindbohm ML, Sallmen M, Anttila A et al: Paternal occupational lead exposure and spontaneous abortion. Scand J Work Environ Health 17:95, 1991

26. Arbuckle TE, Savitz DA, Mery LS et al: Exposure to phenoxy herbicides and the risk of spontaneous abortion. Epidemiology 10:752, 1999

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