Your Environment Your Fertility Is There a Link

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Shanna H. Swan Introduction

Fertility, the ability of people to produce offspring, was a concept formerly applied only to the female. Demographers traditionally defined the fertility rate as the average number of live-born children per woman of reproductive age. However, fertility is one of the few measures that reflect the joint health of two individuals, and we have only recently begun to appreciate the extent to which fertility depends on the health and environment of both the male and female partner, as well as the interaction between partners. Males appear to be solely responsible for infertility in about 20% of infertile couples and contribute to infertility in another 30-40%.

Using the demographic definition above, fertility declined 50% worldwide between 1950 and 2000. Between 1976 and 1998, the percent of women in the United States aged 35-39 who were childless increased from 10.5% to 19.8%. Moreover, the number of annual office visits for infertility increased from 600,000 to 2 million between 1968 and 1990. While these data indicate that fertility, at least by the demographers' definition, has declined, they do not answer the critical question; Are a woman and her partner who desire pregnancy less able to conceive today than a comparable couple of the same age 50 years ago? They also do not address causes of the decline and, in particular, the role of environmental factors, which is the focus of this discussion.

These trends undoubtedly reflect, at least in part, changes in nonenvironmental factors that affect a couple's ability and/or desire to conceive. Women and their partners may choose to delay childbearing, resulting in decreased fertility when their first pregnancy attempt occurs at an older age. Several nonenvironmental factors may also influence trends in fertility: increasing access to and acceptability of contraception and assisted reproduction, changes in attitudes towards voluntary pregnancy termination, rates of sexually transmitted diseases, and the education of women and their role in the workforce.

These factors vary geographically, temporally, and within ethnic/racial groups. Moreover, they are interrelated in complex ways. Several more useful measures of "fertility potential" are available. Fecundity (or fecundability) has been defined as, "the monthly probability of conception in the absence of contraception outside the gestation period and the temporary sterile period following the termination of a pregnancy". The National Center for Health Statistics uses a measure of decreased fecundity, "impaired fecundity", which they define as a woman's inability to conceive or bear a child to term. The number of cycles of unprotected intercourse with out conception, or "time-to-pregnancy" (TTP) is another useful measure and infertility is often diagnosed when TTP exceed 12 months (or cycles).

Changes in fecundity and impaired fecundity in the US have been examined by comparing responses to the National Survey for Family Growth (NSFG) in 1982, 1988 and 1995. This analysis found increases in impaired fecundity over that time period, and the authors suggested that this change was due to more couples voluntarily delaying child-bearing. We questioned that interpretation, however, since the greatest increase in impaired fecundity was seen in women under 25, precisely the age group in which subfecundity, because of delayed childbearing, would be least likely. These data suggest that, at least in the US, fecundity declined between 1982 and 1995. Limited data have recently become available from the sixth cycle of the NSFG. However, data on live birth rates between 1990 and 2000 suggest a reversal of the decline seen in previous reports. This reversal is seen across race/ethnic groups and for most age groups. Data on impaired fecundity, perhaps the most relevant statistics for assessing trends in involuntary subfertility, are not yet available but are expected later in 2006. On balance, the limited data available do not allow us to draw any conclusions about trends in fecundity.

Reproductive health is affected by the interaction of multiple factors, among them age, genetics, nutrition, lifestyle behaviors, reproductive tract infections, stress, and pharmaceutical use. In recent years, scientists have increasingly reported evidence that certain pollutants in the environment may also play an important role, contributing at least in some cases to underlying causes of fertility problems. A surprisingly wide range of compounds has been implicated, particularly in studies of laboratory animals and wildlife, although for the most part the data on the effects of these chemicals on human fertility is still inconclusive.

What is now clear is that environmental chemicals may impact fertility at multiple developmental stages, with differing effects. Many chemical exposures have been shown to impact human and/or animal fertility when exposure occurs during adulthood. These are summarized in Table 19.1. Adult exposures tend to cause changes that are transient; for example, men exposed to DBCP who were azoospermic recovered the ability to produce sperm once exposure had ceased. On the other hand, exposures during development, summarized in Table 19.2, cause changes that are permanent (such as DES-caused cervical and uterine abnormalities) and often cause effects at much lower levels than those needed to cause changes in adults. These tables are not intended to be exhaustive but rather to give examples of such exposures.

The Environment and Reproductive Factors in the Male

One action of environmental exposures on fertility is through their effect of semen quality. This question was first examined in the workplace, where exposures are usually far higher than those encountered environmentally. There is a large body of literature demonstrating strong relationships between work place exposures and decreases in semen quality and other factors that can affect a couples' fertility. For example, widespread concern was generated in the late 1970s following reports of sterility and decreased sperm counts in workers exposed to the agricultural nemato-cide DBCP. The chlorinated hydrocarbon pesticide chlordecone (kepone) was withdrawn because of its severe effects on semen quality. Ethylene dibromide (EDB) was an active component of approximately 100 pesticides. Its use was severely restricted in 1984 due to reduced sperm counts and semen quality. For a more complete treatment, see Schettler et al, Generations at Risk (1999).

More recently, adult exposure to several pollutants at low environmental levels has been linked to reduced semen quality. If these exposures have increased over time, these could, in principle, contribute to the reported declines in sperm concentration. For example, after we saw significantly poorer semen quality in men living in agricultural mid-Missouri compared to men living in urban centers, we examined pesticide metabolite levels in the men's urine. We found several (alachlor, atrazine and diazinon, particularly) to be linked to poor semen quality. A range of other low-level environmental exposures have been linked to impaired semen quality including phthalates, PCBs and DDT, maternal smoking, water chlorination by-products and air pollution.

Does it follow that men (or couples) exposed to these environmental chemicals have impaired fecundity? Among Danish couples attempting to conceive for the first time, men whose initial sperm concentration was less than 40 x 106/ml had significantly reduced fecundability and took longer to conceive. In mid-Missouri, sperm concentration of 35% of fertile men fell below 40 x 106/ml, a point below which fecundity decreases significantly. Among men living in central Minneapolis, only 19% fell below this cut-off. Since poor semen quality in these men was linked to pesticide exposure, it is plausible—though far from proven—that these chemicals can impair human fecundity.

We cannot, however, conclude that a decrease in sperm count directly implies a decrease in fecundity on a population level. Even if semen quality is declining, there may be no net decrease in couple fecundity. For example, if couples trying to conceive are better educated (such as through the use of home kits to detect ovulation), this will tend to increase conception success. Increased female fertility, for example, as a result of the declining incidence of sexually transmitted disease, which has occurred in the United States since 1980 (CDC 2000), will also increase couple fecundity.

The Environment and Reproductive Factors in the Female

Measures of female fertility are more difficult to quantify. For example, a measure analogous to sperm count, ovarian follicular number, is more difficult to ascertain, as it requires a vaginal ultrasound. Thus, this endpoint has been rarely studied. However, failure to conceive may be the reflection of a hidden increase in early pregnancy loss. Since a marker for early loss must be ascertained in urine samples collected soon after conception, this too is logistically difficult and few studies have related this endpoint to environmental exposures. Endometriosis is a fertility-related endpoint that has been examined with respect to some environmental exposures, notably dioxin; human data on this association are conflicting. Alterations in menstrual function, such as short follicular phase, may contribute to impaired fecundity. These studies are also quite difficult since they require prospective collection of daily urine samples and extensive hormonal analysis. For these reasons, there are far fewer studies of environmental causes of impaired female factors than male. However, many environmental agents that have been shown to adversely effect male fertility have also been related to impaired female reproductive function when that has been examined. Examples include; cigarette smoke, radiation, lead, ethylene glycol ethers and water chlorination by-products (total trihalomethane).

Table 19.1. Chemical exposures during adulthood that may alter fertility-related endpoints

Exposure

Sources and Uses

Bisphenol A (BPA)

Monomer used to make polycarbonate plastic, resins

Chlorinated hydrocarbons

Dioxins/furans, PCBs, some pesticides (organochlorines) and wood preservative (pentachlorophenol)

Disinfection by-products

Result of drinking water treatment

Ethylene oxide

Chemical sterilizer used in dental and medical practices

Heavy metals

Lead, mercury, manganese, cadmium

Pesticides

Includes insecticides, fungicides, herbicides, rodenticides, and fumigants

Reported Effects in Females

Chromosomal abnormalities, (A) Recurrent miscarriage (H)

Menstrual irregularities'1 (H, A) Hormonal changes (H, A) Reduced fertility* (A) Endometriosis (H, A) Fetal lossA (H, A)

Fetal lossA (H) Menstrual irregularities'1 (H)

Fetal lossA (H, A) Reduced fertility* (H) Hormonal changes (A) Menstrual irregularities'1 (H)

Menstrual irregularities'1 (H) Reduced fertility* (H, A) Fetal lossA (H, A)

Reported Effects in Males

Decreased semen quality* (A)

Decreased semen quality* (H) Hormonal changes (H, A)

Decreased semen quality* (H,A)

Decreased semen quality* (H) Fetal loss in female partner (H)

Decreased semen quality* (H) Reduced fertility* (H, A) Hormonal changes (H)

Decreased semen quality* (H, A) Reduced fertility* (H, A) Fetal loss in female partner (H) Sperm chromosome abnormalities (H) Hormonal changes (H)

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Exposure

Sources and Uses

Phthalates

Plasticizers added to soften plastics like PVC; also in cosmetics, toys, pharmaceuticals, and medical devices

Glycol ethers

Paints, varnishes, thinners, printing inks, semiconductor industry

Other solvents

Benzene, toluene, xylene, styrene, 1-bromopropane, 2-bromopropane, perchloroethylene, trichloroethylene, and others

Cigarette smoke

Active and/or passive smoking

Reported Effects in Females

Fetal lossA (A) Menstrual irregularities'1 (A) Reduced fertility* (A)

Fetal lossA (H) Reduced fertility* (H)

Reduced fertility* (H) Fetal lossA (H, A) Hormonal changes (H, A) Menstrual irregularities'1 (H)]

Reduced fertility* (H) Fetal loss (H) Early menopause (H) Hormonal changes (H)

Reported Effects in Males

Decreased semen quality* (H)

Decreased semen quality* (H)

Decreased semen quality* (H) Reduced fertility* (H) Fetal loss in female partner (H) Hormonal changes (H)

Reduced fertility* (H) Decreased semen quality (H) Hormonal changes (H)

(H) Data from human studies. (A) Data from human studies. *, Decreased semen quality may include decreased sperm concentration, sample volume, motility or percent normal morphology. *, Reduced fertility may include infertility, increased time to pregnancy (reduced fecundity), greater proportion with failure to conceive in 1 2 months. A, Menstrual irregularities may include altered cycle length, irregular cycles, abnormal bleeding, anovulation in humans, estrous cycle irregularities in animals. A, Fetal loss may include spontaneous abortion (clinical or sub-clinical and stillbirth). Table modified with permission from: Challenged Conceptions: Environmental Chemicals and Fertility. Carlson A, Eddy E, Giudice L et al, eds. A Report of the Fertility/Pregnancy Compromise Working Group of the Collaborative on Health and the Environment. 2005.

Table 19.2. In utero exposures that may alter fertility-related endpoints

Exposure

Sources and Uses

Bisphenol A (BPA)

Monomer used to make polycarbonate plastic, resins

Chlorinated hydrocarbons Dioxins/furans, PCBs

Organochlorine pesticides DDT/DDE, linuron, others

Pesticides

Includes insecticides, fungicides, herbicides, rodenticides, and fumigants

Reported Effects in Females

Altered puberty onset (A) Obesity (A)

Malformations of the reproductive tract* (A) Altered estrous cycle (A) Reduced fertility* (A) Hormonal changes (H, A) Altered sex ratio (H,A) Altered puberty onset (H) Delayed time to pregnancy (H)

Altered sex ratio (H,A) Altered puberty onset (A)

Cigarette smoke Maternal smoking

Diethylstilbestrol (DES)

Pharmaceutical thought (erroneously) to prevent recurrent or threatened spontaneous abortion

Malformations of reproductive tract* (H,A) Altered hormone response (A) Menstrual irregularities'1 (H,A) Reduced fertility* (H,A) Uterine fibroids (A) ] Fetal loss (H)

Reported Effects in Males

Altered prostate development (A) Decreased semen quality* (A) Hormonal changes (A)

Malformations of the reproductive tract* (H,A) Decreased semen quality* (H,A) Altered sex ratio (H,A) Altered puberty onset (H)

Malformations of reproductive tract^ (A)

Altered sex ratio (H,A) Altered puberty onset (A) Malformations of reproductive tract* (H,A) Reduced fertility (A) Decreased semen quality* (H)

Malformations of reproductive tract* (H,A) Altered hormone response (A)

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Exposure

Sources and Uses

Heavy metals

Lead, mercury, manganese, cadmium

Phthalates

Plasticizers added to soften plastics; also found in cosmetics, toys, pharmaceuticals, and medical devices

Perfluorinated compounds (PFOS, PFOA) Used to make fabrics stain-resistant/ water-repellant; in coating of cooking pans, floor polish, insecticides

Polybrominated diphenyl ethers (PBDEs) Flame retardants found infurniture foam, mattresses, textiles, and electronics

Octylphenol/nonylphenol Surfactants

Reported Effects in Females

Hormonal changes (A) Altered puberty onset (H)

Hormonal changes (A)

Hormonal changes (A) Altered puberty onset (A)

Reported Effects in Males

Shortened anogenital distance (H) Malformations of reproductive tract* (A) Hormonal changes (A) Decreased semen quality* (A)

Hormonal changes (A)

Decreased semen quality* (A)

Hormonal changes (A) Decreased semen quality*(A) Decreased testes size (A)

Decreased semen quality may include decreased sperm concentration, sample volume, motility or percent normal morphology. Reduced eive in 12 nr r . in9'c in animals. A, Fetal loss may include spontaneous abortion (clinical or sub-clinical and stillbirth). *, malformations of the reproductive tract: In fertility may include infertility, increased time to pregnancy (reduced fecundity), greater proportion with failure to conceive Menstrual irregularities may include altered cycle length, irregular cycles, abnormal bleedin months.

anovulation in humans, estrous cycle irregularities males, may include shortened anogenital distance, undescended testicles (cryptorchidism), and abnormalities of the testicles or epididymis. In females, may include hypoplastic ovaries, reduced number of follicles, and structural abnormalities of the oviducts, uterus, cervix, and/or vagina. Table modified with permission from: Challenged Conceptions: Environmental Chemicals and Fertility. Carlson A, Eddy E, Giudice L et al, eds. A Report of the Fertility/Pregnancy Compromise Working Group of the Collaborative on Health ana the Environment. 2005.

Factors That May Alter a Couples' Fertility

While we have focused here on environmental exposures, a wide range of environmental, infectious, endocrine, lifestyle and genetic factors may play a role in infertility. These factors may result in a range of clinical endpoints including fetal loss (both subclinical and clinical), menstrual dysfunction, endometriosis, uterine fibroids, and hormonal irregularities. Clearly, a full discussion of all factors and their influence on each of these endpoints is beyond the scope of this brief discussion. However, several general comments may be helpful.

Exposure to factors that can alter fertility may occur at any time from gestation to adulthood. Adults today carry an enormous body burden of chemicals of which we are likely unaware since these exposures are "invisible" except by examining levels in human samples (such as blood and urine). In a study led by Mount Sinai School of Medicine in New York, in collaboration with the Environmental Working Group and Commonweal, researchers at two major laboratories found an average of 91 industrial compounds, pollutants, and other chemicals in the blood and urine of nine volunteers, with a total of 167 chemicals found in the group (http:// www.ewg.org/reports/bodyburden/). Like most of us, the people tested do not work with chemicals on the job and do not live near an industrial facility.

While it is not possible to provide full toxicological profiles of the chemicals that are prevalent today, an overview of the contaminants found most frequently in the Mt. Sinai survey may be useful. PCBs, which were used as industrial insulators and lubricants prior to being banned in the US in 1976, persist for decades in the environment and accumulate up the food chain, to man. A recent study found PCBs to be associated with reduced semen quality. There are 210 different dioxins and furans, which are by-products of PVC production, industrial bleaching, and incineration. These chemicals can also persist for decades in the environment and are found in air, water, soil and food. Dioxins are developmental toxicants affecting the developing endocrine (hormone) system. For example, a significant deficit of male babies was reported among couples exposed to high levels of dioxin. Organochlorine pesticides (such as DDT and chlordane) also accumulate up the food chain to man and have been shown to cause cancer and numerous reproductive effects. There are a range of organophosphate insecticide metabolites, such as breakdown products of chlorpyrifos and malathion which are potent nervous system toxicants found most commonly as residues in food. Metals, including lead, mercury, arsenic and cadmium, have long been shown to cause lowered IQ, developmental delays, behavioral disorders and cancer at doses found in the environment. Most exposures to lead are from lead paint. Most exposures to mercury are from fish, particularly canned tuna. The main sources of arsenic exposures are from arsenic (CCA) treated lumber and contaminated drinking water. Sources of cadmium exposure include pigments and bakeware. Phthalates, plasti-cizers found in a wide range of cosmetic and personal care products, have recently been associated with reduced semen quality and in animal models cause birth defects of male reproductive organs.

Unfortunately, we cannot reduce our body burden of past exposures, most of which persist in the body for decades. Work place exposures, which may be avoidable, can be far higher, and it is in those settings that we have learned much of what we know about human reproductive risks. Workers, particularly those attempting

to conceive, should be provided with full information on the reproductive risks of the agents with which they are working. If economics permit, it would be prudent for those of reproductive age to avoid occupational exposure to reproductive toxins.

Setting aside fetal and childhood exposures and occupational setting exposures, we are left with exposure to currently used chemicals in the home and the surrounding environments. The routes of these exposures (i.e., water, air, food, skin) are limited. There are steps that one can take to limit exposure via each of these routes. There are several nongovernmental organizations that have produced excellent web-based facts sheets for consumers that provide practical information based on good science. These are provided below.

Key Points

Though data suggest causal links between environmental exposures and fertility-related endpoints, many uncertainties remain, particularly with respect to human fertility. Fertility and the related endpoint, impaired fecundity, can be caused by female, male, couple-dependent factors, or some combination of these. Identifying the role of environmental factors, on the clinical level, will seldom be possible, except for extreme examples, such as pharmaceuticals (e.g., DES), or some occupational exposures (such as DBCP). Nonetheless, environmental factors may well be having adverse effects on population fertility. An awareness of the emerging evidence can help clinicians educate their patients about potential exposures to avoid (pesticides, heavy metals, phthalates). Unraveling the extent of these effects, and the principal agents of concern, are the challenges now faced by researchers in this field.

Web-Based Resources

General Information on Fertility and the Environment

An excellent overview, used extensively in this review, Challenged Conceptions: Environmental Chemicals and Fertility, Carlson A, Eddy E, Giudice L et al, eds. A report of the Fertility/Pregnancy Compromise Working Group of the Collaborative on Health and the Environment, October 2005. Proceeding of February 2005 Vallombrosa Workshop Understanding Environmental Contaminants and Human Fertility Compromise: Science and Strategy (http://www.healthandenvironment.org/ working_groups/fertility).

The Collaborative for Health and the Environment (CHE) maintains a web page that provides accurate and timely information on the environment and fertility (http:/ /www.healthandenvironment.org/infertility) and more general information on environment and health http://www.healthandenvironment.org.

Infertility and Related Reproductive Disorders by Ted Schettler includes an excellent discussion of the role of the environment (http://www.healthandenvironment.org/ infertility/peer_reviewed).

Food

Food News, an affiliate of the Environmental Working Group (EWG) has compiled a Shoppers Guide for Pesticide in Produce. The report suggests substituting organic for conventional produce that is consistently contaminated with pesticides and, when organic products are not a choice, to consume fruits and vegetables with consistently low pesticide loads (http://www.foodnews.org/walletguide.php).

Water

The EWG has conducted an extensive survey of drinking water sources by state and compiled the Clean Water Report Card (that will help consumers evaluate the quality of their own drinking water (http://www.ewg.org/reports/reportcard/ home.html)

Personal Care Products

The EWG has conducted an extensive, chemical-by-chemical evaluation of personal care products called Skin Deep (http://www.ewg.org/reports/skindeep/).

Fish Consumption

A report with a pocket size shopping guide on contaminants in fish, Healthy Fish, Healthy Families has been compiled Physicians for Social Responsibility (http:/ /www.mercuryaction.org/fish/).

Suggested Reading

1. Bonde JP, Ernst E, Jensen TK et al. Relation between semen quality and fertility: A population-based study of430 first-pregnancy planners. Lancet 1998; 352:1172-1177.

2. Challenged Conceptions: Environmental Chemicals and Fertility. In: Carlson A, Eddy E, Giudice L et al, eds. A Report of the Fertility/Pregnancy Compromise Working Group of the Collaborative on Health and the Environment. 2005 (http:// www.healthandenvironment.org/working_groups/fertility)

3. Carlsen E, Giwercman A, Keiding N et al. Evidence for decreasing quality of semen during past 50 years. BMJ (Clinical Research Ed) 1992; 305:609-613.

4. Centers for Disease Control and Prevention. Tracking the Hidden Epidemics: Trends in STDs in the United States 2000. Atlanta: Centers for Disease Control and Prevention, 2001.

5. Chandra A, Stephen EH. Impaired fecundity in the United States: 1982-1995. Fam Plann Perspect 1998; 30:34-42.

6. Duty SM, Silva MJ, Barr DB et al. Phthalate exposure and human semen parameters. Epidemiology 2003; 14:269-277.

7. Evenson DP, Jost LK, Perreault SD et al. Application of the sperm chromatin structure assay to the Teplice Program semen studies: A new method for evaluating sperm nuclear chromatin damage. In: Sram RJ, ed. Teplice Program: Impact of Air Pollution on Human Health. Prague: Academia, 2001:167-180.

8. Faroon O, Kueberuwa S, Smith L et al. ATSDR evaluation of health effects of chemicals. II. Mirex and chlordecone: Health effects, toxicokinetics, human exposure, and environmental fate. Toxicol Ind Health 1995; 11:1-203.

9. Fenster L, Waller K, Windham G et al. Trihalomethane levels in home tap water and semen quality. Epidemiology 2003; 14:650-658.

10. Glebatis DM, Janerich DT. A statewide approach to diethylstilbestrol—the New York program. N Engl J Med 1981; 304:47-50.

11. Goldsmith JR. Dibromochloropropane: Epidemiological findings and current questions. Ann N Y Acad Sci 1997; 837:300-306.

12. Hauser R, Chen Z, Pothier L et al. The relationship between human semen parameters and environmental exposure to polychlorinated biphenyls and p,p'-DDE. Environ Health Perspect 2003; 111:1505-1511.

13. Jensen TK, Jorgensen N, Punab M et al. Association of in utero exposure to maternal smoking with reduced semen quality and testis size in adulthood: A cross-sectional study of 1,770 young men from the general population in five European countries. Am J Epidemiol 2004; 159:49-58.

14. Mocarelli P, Brambilla P, Gerthoux PM et al. Change in sex ratio with exposure to dioxin. Lancet 1996; 348:409.

15. Schettler T, Solomon G, Valenti M et al. Generations at risk: Reproductive Health and the Environment. Cambridge: MIT Press, 1999.

16. Schrader SM, Turner TW, Ratcliffe JM. The effects of ethylene dibromide on semen quality: A comparison of short-term and chronic exposure. Reproductive Toxicology 1988; 2:191-198.

17. Seibel MM. Infertility: A comprehensive text. In: Seibel MM, ed. Diagnostic Evaluation of an Infertile Couple. Stamford: Appleton and Lange, 1997:3-28.

18. Slutsky M, Levin JL, Levy BS. Azoospermia and oligospermia among a large cohort of DBCP applicators in 12 countries. Int J Occup Environ Health 1999; 5:116-122.

19. Swan SH, Elkin EP, Fenster L. Have sperm densities declined? A reanalysis of global trend data. Environ Health Perspect 1997; 105:1228-1232.

20. Swan SH, Hertz-Picciotto I. Reasons for infecundity. Fam Plann Perspect 1999; 31:156-157.

21. Swan SH, Kruse RL, Liu F et al. Semen quality in relation to biomarkers of pesticide exposure. Environ Health Perspect 2003a; 111:1478-1484.

22. Swan SH, Brazil C, Drobnis EZ et al. Geographic differences in semen quality of fertile U.S. males. Environ Health Perspect 2003b; 111:414-420.

23. United Nations Population Information Network (POPIN) dictionary of demographic and reproductive health terminology (1990). Retrieved 2002, (from http://www.un.org/ popin/).

24. Ventura SJ, Abma JC, Mosher WD et al. Estimated pregnancy rates for the United States, 1990-2000: An update. National Vital Statistics Report 2004; 52:1-9.

25. Whorton D. The effect of occupation on male reproductive function. In: Spira A, Jouannet P, eds. Human Fertility Factors. Paris: Editions INSERM, 1981:339-348.

Index

Acupuncture 100, 189, 190, 192 Adenoma 15, 32, 68, 70, 90-92, 136,

148, 149, 165, 171 Adhesiolysis 150, 154 Adrenarche 10, 12 Age 3, 10-15, 17, 20, 21, 23, 33, 48, 56, 57, 62, 65, 71, 82, 84, 88, 107, 108, 113, 115, 116, 118,

137, 138, 145, 149, 151, 153, 159, 163, 168, 179, 184-186, 191, 196, 201, 202, 209

Alternative/complementary treatment

100, 105, 110, 115 Amenorrhea 4, 17, 18, 20, 21, 23-25, 28, 29, 31-35, 39, 45, 47, 49, 50, 65, 68-70, 85, 92, 107, 110, 121, 124-126, 146, 147, 149, 162, 165

Androgen insensitivity syndrome (AIS)

16, 20, 31, 35, 121 Antifibrinolytic agent 44 Antral follicle count (AFC) 34, 129,

138, 181 Appetite suppressant 59 Aromatase inhibitor 15, 87, 166, 170 Ascorbic acid 191

Asherman's syndrome 29, 31, 35, 162 Asthenospermia 197, 198 Azoospermia 19, 184, 194, 196-198

Bariatric surgery 61, 62 Bisphosphonate 115 Body mass index (BMI) 10, 19, 51, 56, 57, 59-62, 146, 149, 179, 190

Breast cancer 19, 56, 70, 71, 75, 77, 80, 111, 114, 116, 117, 168

Calcium supplement 100, 105, 115 Cardiovascular disease 51, 56-59, 62,

71, 77, 108, 115, 116 Cervical factor 145, 146 Chaste berry 191 Chemicals 120, 196, 202-205, 207-210

Classification of endometriosis 84, 156

Clomiphene citrate (CC) 137, 149,

151, 166, 168-171, 176 Combined oral contraceptive (COC)

67, 70-75, 78-82 Contraception 7, 35, 44, 53, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 76, 77, 78, 79, 80, 81, 82, 145, 147, 201

Contraceptive vaginal ring 66, 68, 73, 74, 82, 109, 111, 112

Controlled ovarian hyperstimulation

(COH) 165, 167, 168, 176, 178 Craniopharyngioma 19, 32, 91

Delayed puberty 15-17, 21 Depo-Provera 76, 77, 82 Depressive disorder 97, 98, 100 Diet 54, 58-63, 96, 100, 101, 105,

111, 115, 191-193 Distal tubal occlusion 128, 156, 158 Dopamine 3, 19, 35, 59, 89, 90, 91, 92, 93, 94, 104, 111, 149, 166, 171, 172

Dysfunctional uterine bleeding (DUB)

Ectopic pregnancy 37, 38, 40, 68, 69,

125, 147, 158, 159, 182, 186 Emergency contraception (EC) 59,

72-75, 79-82 Endometrial ablation 44, 45 Endometrial cavity 7, 31, 84, 125,

126, 128-130, 135, 141, 150 Endometriosis 37, 45, 72, 76, 84-88,

128, 129, 139-141, 145-147, 149, 150, 152-156, 163, 165, 166, 176, 179, 181, 182, 203, 204, 208

Environment 6, 84, 112, 120, 137, 153, 180, 196, 201-203, 205, 207-209

Estrogen 3-6, 8-10, 13-16, 18-21, 23, 25, 27, 29, 32, 35, 38, 43, 53, 67, 70, 72, 75, 76, 82, 84-87, 90, 99, 108-118, 124, 146, 148, 149, 151, 161, 162, 165, 168-170, 172, 191, 195 Estrogen replacement therapy (ERT) 110, 111, 112, 115-118 Etiology 12, 13, 21, 25, 28, 89, 96,

99, 165, 166, 189, 191, 199 Eugonadal 25, 28, 29, 31 Extended use contraception 70

Fecundity 20, 145, 146, 151, 152, 165, 201-203, 205, 207, 209 Fertility 19, 20, 35, 43, 45, 76, 86, 108, 141, 146, 150, 152-154, 159, 165, 180, 182, 189, 190-192, 194, 196, 201-209 Fimbrioplasty 158 Follicular phase 4-8, 49, 97, 98, 103, 161, 181, 203

Galactorrhea 32, 90-92, 111, 149, 179

Gonadotropin 3-6, 8-11, 14-17, 19, 21, 28, 32-34, 38, 45, 86, 98, 99, 104, 107, 108, 125, 138, 146, 149-151, 155, 161, 165-168, 171-176, 179, 183, 186, 189-191 Gonadotropin therapy 151, 171, 172, 176

Gonadotropin releasing hormone

(GnRH) 3-14, 19, 21, 29, 32, 33, 45, 48, 85-88, 98, 99, 104, 141, 146, 155, 161, 165, 171, 173, 189, 190

analog 86, 88, 161 pulse generator 4, 8, 10, 12, 48, 189

Heavy menstrual bleeding 36 Herbal medicine 60, 100, 101, 105,

112, 191, 192, 196 Hormone replacement therapy (HRT) 39, 109, 110, 112, 116-119, 149 Hot flashes 68, 86, 98, 107-112, 170 Human chorionic gonadotropin (hCG) 8, 9, 14, 20, 38, 125, 167, 170-176, 185, 186 Hydrosalpinx 126, 128-130, 135, 150, 158

Hyperandrogenism 44, 48, 49, 121, 136, 183

Hypergonadotropic hypogonadism

17-19, 32-34 Hypogonadism 15-20, 23, 25, 27, 29, 30, 32-35, 86, 91-93, 146, 166, 171, 175, 176, 195, 197 Hypogonadotropic hypogonadism 17, 19, 20, 32, 33, 171, 175, 176, 195, 197

Hysterectomy 45, 87, 97, 116, 184 Hysterosalpingogram 41, 42, 126, 129, 141, 148, 151, 153, 162, 165, 181

Hysteroscopy 41-45, 129, 135, 150, 161, 162, 181

Impaired glucose tolerance 51 Implanon 75, 77 Implantable contraception 77 Implantation 3, 8, 9, 67, 79, 80, 126, 150, 151, 158, 159, 163, 178, 179, 184, 185, 190, 192 In vitro fertilization (IVF) 18, 19, 129, 135, 138, 140, 141, 149-154, 156, 158, 159, 162, 163, 165, 166, 169, 173, 176, 178, 179, 181-187, 190-192, 198

Infertility 8, 25, 28, 31, 39, 42, 56, 79, 82, 84, 88, 92, 93, 124, 126, 128, 135-139, 141, 145-154, 158, 161-163, 165-167, 176, 179-185, 187, 189-202, 205, 207-209

Infertility treatment 56, 138, 145,

176, 181, 182, 190-193 Inhibin 4, 5, 8, 11, 12, 107 Injectable hormonal contraception 74 Insemination 19, 129, 135, 149, 151, 162, 163, 166, 167, 174, 175, 183, 195 Insulin resistance 31, 35, 48, 51, 53-55, 180, 181, 183

Intracytoplasmic sperm injection

(ICSI) 19, 151, 178, 183, 185, 187, 198 Intrauterine contraception (IUC)

78-80, 82 Intrauterine device (IUD) 37, 44, 65, 66, 69, 78, 87, 147

Kallman syndrome 20, 32, 195, 197 Klinefelter syndrome 19, 180

L-arginine 192

Laparoscopic ovarian diathermy (LOD) 171, see also Ovarian drilling

Laparoscopic uterosacral nerve ablation

Laparoscopy 85-87, 128, 129,

Levonorgestrel-releasing intrauterine system (LNG-IUS) 44, 45, 78, 79, 81, 82 LH surge 6-8, 148, 149, 167,

170-173, 180 Luteal phase 4, 7-9, 96-98, 103-106, 148, 171, 180, 191

Luteal phase dosing of serotonin reuptake inhibitors 103, 104, 106

Male infertility 181, 194, 195, 198-200

McCune-Albright syndrome (MAS)

36, 39, 47, 49, 147 Menopause 3, 12, 36, 41, 45, 57, 85, 86, 99, 107-113, 115-118, 138, 165, 172, 178, 184, 205 Menorrhagia 36, 38-41, 72, 141 Menstrual irregularity 48, 50-53, 55,

93, 191, 204-207 Menstruation 4, 9, 11, 20, 31, 32, 38,

Metaplastic theory 84

170, 171, 176, 183 Metrorrhagia 36 Mifepristone 87 Mind/body technique 192 Mirena 44, 78, 82 Mullerian anomalies 20, 21, 35, 121, 122, 124, 125, 135, 136, 180, 184

Multiple gestation/pregnancy 125, 185-187

Nonsteroidal anti-inflammatory drug

(NSAID) 44 NuvaRing 73

117, 146, 195, 206 Oligospermia 194, 196-198 Oocyte donation 18, 149, 152, 165,

166, 187 Operative hysteroscopy 150, 162 Oral contraceptive 18, 21, 43, 53, 67, 70, 79, 81, 85, 88, 96, 104, 147 Ortho Evra 72

113-115, 119, 149, 168 Ovarian drilling 159, 161, see also

Laparoscopic ovarian diathermy

Ovarian failure 17, 18, 21, 29, 33-35, 50, 137, 146, 149, 152, 159,

Ovarian hyperstimulation syndrome

(OHSS) 152, 167, 168, 170, 173-176, 183, 186 Ovarian reserve 137, 138, 148, 151,

181, 184, 185 Overweight 54-57, 72, 76, 168 Ovulation 4-8, 18, 20, 21, 29, 35, 38, 40, 41, 43-45, 47, 54, 67, 70, 74, 76, 79, 86, 94, 107, 122, 146, 148-153, 159, 165-176,

179, 180, 183, 187, 190, 191, 194, 195, 203, 205, 207

Ovulation induction 18, 20, 21, 35, 44, 149, 150, 152, 159, 165-176, 183, 187, 190 Ovulatory dysfunction 39, 41, 47, 56, 146, 148, 152, 165, 185, 192

Pelvic inflammatory disease (PID) 66, 68, 69, 79, 80, 82, 125, 126, 130, 147, 149, 154, 156, 163, 179, 180, 187

Pelvic magnetic resonance imaging

(MRI) 41, 42 Pelvic ultrasound 49, 167 Perimenopause 98, 107, 108 Phytoestrogen 111, 191

Pituitary 3, 5, 9-12, 14, 17, 19-21, 25, 32, 48, 53, 86, 89-92, 94, 95, 107, 108, 136, 146, 148, 149, 151, 159, 165, 169-173, 189-191, 195-199 Polycystic ovary syndrome (PCOS) 12, 15, 21, 29, 31, 35, 40, 41, 47-55, 58, 136, 148, 149, 152, 159, 165, 167-171, 173, 174, 176, 180, 181, 183 Precocious puberty 12-15, 21 Pregnancy 5, 7-9, 16, 18, 19, 21, 25, 33-35, 37-41, 43-45, 52-54, 56, 62, 65, 68, 69, 72, 75-77, 79-82, 89, 90, 92-94, 121, 124, 125, 128, 129, 135, 138, 141, 145-147, 149-151, 153-156, 158, 159, 161-163, 167-176, 178, 179, 182-187, 190, 196, 198, 199, 201-203, 205-207, 209

Preimplantation genetic diagnosis

Premenstrual dysphoric disorder

(PMDD) 72, 96-106 Premenstrual syndrome (PMS) 68,

96-105 Presacral neurectomy 87 Primary amenorrhea 23, 29, 31, 32, 121, 124

Progesterone 3, 4, 7-9, 12, 13, 16, 18, 21, 25, 35, 38, 40, 41, 43, 49, 53, 74, 76, 86, 99, 104, 109, 110, 116, 117, 122, 146, 148, 167, 169, 172, 180, 181, 191 Progestin 16, 18, 19, 21, 25, 35, 43, 44, 52, 53, 66-68, 70, 72, 74-77, 79-82, 86, 110, 111, 115, 117, 165, 174

Progestin challenge test 16, 25, 165 Progestin only pill (POP) 66, 74, 75,

77, 79, 81, 82 Prolactin (PRL) 14, 15, 19, 21, 25, 32, 33, 49, 50, 89-95, 99, 136, 146, 148, 149, 165, 171, 181, 191, 195, 197-199 Prolactinoma 19, 29, 32, 34, 90-95 Proliferative phase 6, 8, 38, 130 Prospective daily rating 97 Psychotherapy 101

Retrograde menstruation 84

Saline sonohysterogram (SSH) 41, 42, 44, 45

Scrotal ultrasound 195, 199, 200 Secondary amenorrhea 23, 29, 34,

125, 126 Secretory phase 8, 9, 38, 43, 180 Selective estrogen receptor modulator

Selective serotonin reuptake inhibitor

(SSRI) 90, 101-106 Semen analysis 20, 147, 148, 153, 165, 181-183, 195, 197-200 Serotonin reuptake inhibitor (SRI) 90,

98, 99, 101, 104, 105, 110 Sonohysterogram 41, 42, 126, 129,

135, 141, 181 Spermatogenesis 20, 146, 180, 194 Spironolactone 52, 53, 104 Sterilization 69, 78, 82, 147, 156,

158, 159, 182 Surrogacy 178, 184, 187

Tanner stage 10, 11 Teratozospermia 198 Testosterone 11-15, 19, 20, 28, 31-34, 48-50, 52-54, 108-110, 118, 167, 181, 190, 194-196, 198, 199

Thelarche 10-12, 15, 21, 121 Transvaginal ultrasonography 42, 45, 181

Treatment 12, 14, 18-21, 34, 35, 38, 41, 43-45, 51-61, 64, 72, 79, 84-87, 92-96, 98-107, 109-112, 114-116, 119-122, 124, 129, 137-139, 141, 145, 146, 149-151, 153-156, 158, 159, 161-163, 165-172, 176, 178-184, 187, 189-193, 196, 198-200, 202, 204

Tubal catheterization 159

Tubal disease 42, 128, 149, 150, 158,

167, 181, 182, 186 Tubal infertility 79, 82 Turner's syndrome 33, 34, 180 Type 2 diabetes 51, 53, 57, 60

Ultrasound 12-14, 17, 28, 42, 43, 47, 49, 50, 85, 120-125, 130, 135-141, 152, 153, 158, 159, 162, 167, 169, 170, 174-176,

181, 186, 195, 197-200, 203 Unintended pregnancy 65, 77, 79, 80,

Vaginal maturation index 16, 21 Varicocele 180, 195, 197, 199 Vasectomy 180, 195 Vasomotor symptom 25, 45, 108,

111, 119

191-193, 196 von Willebrand disease (VWD) 37, 39-43

Waist circumference 48, 51, 57 WHO criteria 70, 71, 74, 75, 77, 80, 146, 165, 166, 171, 175, 176,

Women's Health Initiative (WHI)

112, 114-118

LANDES

BIOSCIENCE

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