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Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health
Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health
Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health
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Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health

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Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health focuses on the ways in which food, dietary supplements, and toxic agents, including alcohol and nicotine affect the reproductive health of both women and men.

Researchers in nutrition, diet, epidemiology, and endocrinology will find this comprehensive resource invaluable in their long-term goal of understanding and improving reproductive health.

This book brings together a broad range of experts researching the different aspects of foods and dietary supplements that promote or detract from reproductive health.

Section One contains several overview chapters on fertility, how it is assessed, and how it can be affected by different metabolic states, nutritional habits, dietary supplements, the action of antioxidants, and lifestyle choices. Sections Two and Three consider how male and female fertility are affected by obesity, metabolic syndrome, hormonal imbalance, and even bariatric surgery.

Section Four explores the ways diet, nutrition, and lifestyle support or retard the success of in vitro fertilization, while Section Five explores how alcohol and other drugs of abuse lower fertility in both women and men.

  • Explores how alcohol, nicotine, and other drugs of abuse disrupt and impair reproductive health
  • Reviews studies of common conditions such as obesity and metabolic syndrome and their effect on fertility and reproductive health
  • Investigates the components of foods and dietary supplements, in particular oxidative stress and antioxidants
  • Presents the nutritional effects of foods and dietary supplements and their benefits and risks relating to reproductive health
LanguageEnglish
Release dateApr 27, 2015
ISBN9780128009932
Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health

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    Handbook of Fertility - Ronald Ross Watson

    Handbook of Fertility

    Nutrition, Diet, Lifestyle and Reproductive Health

    Ronald Ross Watson

    University of Arizona, Arizona Health Sciences Center, Tucson, AZ, USA

    Table of Contents

    Cover

    Title page

    Copyright

    List of Contributors

    Preface

    Acknowledgments

    Section A: Overview on fertility

    Chapter 1: Perceptions of Environmental Risks to Fertility

    Abstract

    Introduction

    Conclusions

    Chapter 2: Paternal Smoking as a Cause for Transgenerational Damage in the Offspring

    Abstract

    Introduction

    Tobacco smoke

    Genetic, epigenetic, and other transmissible factors

    Quality control of paternal germ cells, post-fertilization repair of sperm DNA damage

    Conclusions

    Chapter 3: Impact of Cigarette Smoking During Pregnancy on Conception and Fetal Health through Serum Folate Levels

    Abstract

    Introduction

    General knowledge on folate

    Smoking and pregnancy

    Conclusion

    Chapter 4: The Effect of Maternal Metabolic Health and Diet on the Follicular Fluid Composition and Potential Consequences for Oocyte and Embryo Quality

    Abstract

    Introduction

    Metabolic health related composition of ovarian follicular fluid and its relation to oocyte and embryo quality parameters

    Fatty Acids in the Ovarian Follicular Fluid

    The effect of elevated NEFA concentrations on oocyte and embryo quality

    Conclusions

    Chapter 5: The Effect of Heavy Metals on Preterm Mortality and Morbidity

    Abstract

    Introduction

    Heavy metals and preterm mortality and morbidity

    Lead

    Mercury

    Cadmium

    Arsenic

    Conclusions

    Chapter 6: Nitrate, Nitrite, Nitrosatable Drugs, and Congenital Malformations

    Abstract

    Introduction

    Maternal exposures to nitrate, nitrite, and n-nitroso compounds

    Nitrosatable drugs and birth defects

    Nitrate in drinking water and birth defects

    Dietary intake of nitrates, nitrites, and nitrosamines in foods and birth defects

    Joint exposures of nitrosatable drugs and nitrate/nitrite and birth defects

    Vitamin C, prenatal nitrosatable drug use, and birth defects in offspring

    Conclusions, clinical implications, and suggestions for further research

    Chapter 7: The Application of Reproductive Techniques (ART): Worldwide Epidemiology Phenomenon and Treatment Outcomes

    Abstract

    Background

    Evaluation of ART procedures worldwide: the diverse ART data collection systems

    Reasons for different ART utilization

    ART application and availability

    ART application/number of treatment cycles

    ART principal outcomes

    Discussion

    Chapter 8: The Effects of Environmental Hormone Disrupters on Fertility, and a Strategy to Reverse their Impact

    Abstract

    Introduction

    Historic aspects

    Methodological aspect

    The estrogen receptor binding assay

    Application of the ERBA test to environmental samples

    Xenoestrogens in flemish surface waters

    Strategy to reduce environmental contamination

    Effect of reducing environmental contamination of sperm quality in flanders

    Effect of antiestrogen treatment on semen quality and male fertility

    Complementary treatment with a specific nutraceutical

    Female infertility

    Estrogen metabolism

    Conclusions

    Appendix

    Chapter 9: Embryo Losses During Nutritional Treatments in Animal Models: Lessons for Humans Embryo Losses and Nutrition in Mammals

    Abstract

    Human infertility and nutrition

    The sheep as a model

    Embryo development and maternal recognition of pregnancy

    Effect of undernutrition on embryo development

    Lessons for humans

    Section B: Bariatric surgery, obesity, and fertility

    Chapter 10: Fertility and Testosterone Improvement in Male Patients After Bariatric Surgery

    Abstract

    Male obesity and sex hormones

    Reproductive functions in obese men

    Bariatric surgery and its effect on male fertility

    Conclusions

    Chapter 11: Obesity and Reproductive Dysfunction in Men and Women

    Abstract

    Introduction

    Obesity impacts on female fertility

    Obesity impacts on male fertility

    Practical advice and implications

    Conclusions

    Chapter 12: Obesity and Gestational Outcomes

    Abstract

    Introduction: obesity in women of childbearing age

    Obesity and adverse maternal outcomes

    Obesity and adverse neonatal outcomes

    Mechanisms of adverse outcomes

    Obesity management: prepregnancy

    Management of obesity during pregnancy

    Conclusions

    Section C: Exercise and lifestyle in fertility

    Chapter 13: Lifestyle Factors and Reproductive Health

    Abstract

    Introduction

    Effects of lifestyle factors on fertility

    Other factors

    Conclusions and recommendations

    Chapter 14: Effect of Diet and Physical Activity of Farm Animals on their Health and Reproductive Performance

    Abstract

    Introduction

    Farm animal vigor and health status

    Reproductive performance of livestock species

    Influence of diet on the health and reproduction performance of livestock

    The effect of physical activity on health and reproduction of livestock species

    Conclusions

    Chapter 15: Prenatal Physical Activity and Gestational Weight Gain

    Abstract

    Introduction

    Gestational weight gain guidelines

    Health care provider advice on GWG

    Physical activity in pregnancy

    GWG interventions

    Achieving healthy GWG

    Chapter 16: Lifestyle Intervention for Resumption of Ovulation in Anovulatory Women with Obesity and Infertility

    Abstract

    Introduction

    Defining obesity and its contribution to anovulation

    The role of lifestyle intervention for resumption of ovulation

    Implementation of lifestyle intervention

    Conclusions

    Chapter 17: Effects of Lifestyle on Female Reproductive Features and Success: Lessons from Animal Models

    Abstract

    Introduction

    Animal models

    Effects of diet and lifestyle on puberty

    Effects of diet and lifestyle on fertility

    Effects of diet and lifestyle on pregnancy and offspring development

    Conclusions

    Acknowledgments

    Section D: Nutrition and reproduction

    Chapter 18: Green Leafy Vegetables: A Health Promoting Source

    Abstract

    Introduction

    Therapeutic value and health benefits of green leafy vegetables

    Effect of green leafy vegetables on mother and fetus health

    Conclusions

    Chapter 19: Nutrition, Lifestyle, and Obesity in Urology

    Abstract

    Obesity and benign urological disease

    Obesity and urological malignancy: possible mechanisms

    Protecting nutritional factors

    Physical exercise and weight loss

    Key points

    Chapter 20: Pregnancy with Multiple Micronutrients: Perinatal Mortality Reduction

    Abstract

    Introduction

    Methods

    Results

    Discussion

    Conclusions

    Chapter 21: Nutrition and Hormones: Role in Male Infertility

    Abstract

    Introduction

    Chapter 22: Nutrition and Developmental Programming of Central Nervous System (CNS)

    Abstract

    Introduction

    Developmental origins of adult disease

    Role of maternal nutrition in early life programming

    Nutritional deficiencies

    The developing nervous system

    Probable mechanism of action

    Nutritional inadequacies and their neurological consequences

    Nutritional deficiencies and psychiatric disorders

    Early life malnutrition and aging brain

    Nutritional intervention

    Chapter 23: Herbal Supplements in Pregnancy: Effects on Conceptions and Delivery

    Abstract

    Traditional medicine: Introduction

    Traditional Chinese medicine

    Herbal remedies and fertility

    Herbal remedies during pregnancy

    Chapter 24: Selenium in Fertility and Reproduction

    Abstract

    Selenium background

    Selenium and reproductive health

    Selenium and pregnancy

    Selenium and early childhood

    Conclusions

    Chapter 25: The Role of Oxidative Stress in Endometriosis

    Abstract

    Introduction

    Background of disease

    The origin of endometriosis

    Relationship between oxidative stress and endometriosis

    Oxidative stress markers in endometriosis

    Nitric oxide and endometriosis

    Role of iron

    Role of cytokines

    Treatment of endometriosis

    Conclusions

    Chapter 26: Oxidative Stress in Preeclampsia

    Abstract

    Introduction

    Definition of preeclampsia

    Pathophysiology of preeclampsia

    Risk factors for preeclampsia

    Effects on mother and baby

    Treatment of preeclampsia

    Preeclampsia-related oxidative stress

    Complications in the fetus and newborn

    Interventions to overcome oxidative stress in preeclampsia

    Future directions

    Conclusions

    Section E: Nutrition and lifestyle in in vitro fertilization

    Chapter 27: The Psychological Management of Infertility

    Abstract

    Introduction

    Stress and infertility

    The cycle of infertility

    The consequences of infertility

    Infertility and one’s relationship

    Psychoneuroimmunology

    Real and self-induced stress

    Time urgency perfectionism stress

    Adoption and the impact on infertility

    Identifying chronic stress

    Managing one’s stress

    Other stress management techniques in infertility

    Spousal involvement

    Conclusions

    Chapter 28: The Role of Body Mass Index on Assisted Reproductive Treatment Outcome

    Abstract

    Introduction: Obesity and fertility

    Maternal obesity and fertility

    Paternal obesity and fertility

    Conclusions

    Chapter 29: Health Outcomes of Children Conceived Through Assisted Reproductive Technology

    Abstract

    Introduction

    Congenital malformations

    Perinatal complications

    Imprinting disorders

    Cardiovascular and metabolic effects

    Malignancy

    Respiratory and allergy disorder: asthma, allergy, and atopy

    Endocrine

    Ophthalmological and auditory disorders

    Growth and pubertal development

    General health and well-being

    Testicular function

    Cerebral palsy

    Neuromotor development

    Cognitive function

    School performance

    Socio-emotional development and psychological disorders

    Autism

    Attention deficit disorder

    Conclusions

    Chapter 30: Influence of Male Hyperinsulinemia on IVF Outcome

    Abstract

    Introduction

    Semen parameters and functional assays in hyperinsulinemic patients

    Results

    IVF outcome of hyperinsulinemic sperm donors

    Influence of male hyperinsulinemia on IVF outcome

    The effect of metformin therapy and dietary supplements on semen parameters in hyperinsulinemic males

    Section F: Nutrition, lifestyle, and male fertility

    Chapter 31: Dietary Zinc Deficiency and Testicular Apoptosis

    Abstract

    Zinc biology

    Zinc absorption

    Zinc deficiency

    Zinc in male reproduction

    Apoptosis and apoptotic genes

    Zinc and apoptosis

    Spermatogenesis and germ cell apoptosis

    Chapter 32: Environmental Factors, Food Intake, and Social Habits in Male Patients and its Relationship to Intracytoplasmic Sperm Injection Outcomes

    Abstract

    Introduction

    Weight and exercise

    Recreational substances and illicit drugs

    Occupational and environmental factors

    Caffeine

    Food intake

    Conclusions

    Chapter 33: The Role of Over-the-Counter Supplements in Male Infertility

    Abstract

    Introduction

    Oxidative stress and male infertility

    Supplements

    Conclusions

    Chapter 34: Sperm Physiology and Assessment of Spermatogenesis Kinetics In Vivo

    Abstract

    Introduction

    The testis: structure and function

    The epididymis: structure and function

    Sperm function

    Assessment of spermatogenesis kinetics in vivo

    Conclusions

    Chapter 35: Antioxidant Treatment and Prevention of Human Sperm DNA Fragmentation: Role in Health and Fertility

    Abstract

    Introduction

    Antioxidants and general health

    Oxidative stress and DNA fragmentation prevention in infertile man

    Antioxidant treatment

    Conclusions

    Chapter 36: Epigenetics and its Role in Male Infertility

    Abstract

    Introduction

    Epigenetics of the male gamete

    DNA methylation

    Chromatin reorganization

    Histone modifications

    Sperm RNAs

    Male infertility

    Epigenetics and testicular cancer

    Nutrition and epigenetics

    The impact of environment on epigenetics

    Epigenetics and ART

    Current techniques for the assessment of spermatozoa epigenetics

    The future of epigenetics

    Index

    Copyright

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    List of Contributors

    José-Alfonso Abecia DVM, MSc, PhD,     Universidad de Zaragoza, Zaragoza, Spain

    Ashok Agarwal PhD,     Center for Reproductive Medicine, Cleveland Clinic, Cleveland, Ohio, USA

    Diana Anderson PhD,     University of Bradford, Medical Sciences, Bradford, West Yorkshire, UK

    Susana Astiz MVD, PhD, Dip ECBHM,     INIA, Madrid, Spain

    Adolf Baumgartner PhD,     University of Bradford, Medical Sciences, Bradford, West Yorkshire, UK

    Ranveer Singh Bedwal MSc, PhD,     Cell Biology Laboratory, Department of Zoology, University of Rajasthan, Jaipur, India

    Zulfiqar A. Bhutta PhD, MBBS, FRCPCH, FAAP,     Robert Harding Chair in Global Child Health and Policy, Centre for Global Child Health, Hospital for Sick Children, Toronto, Canada

    Edson Borges, Jr. MD, PhD,     Fertility – Assisted Fertilization Centre; Sapientiae Institute – Educational and Research Centre in Assisted Reproduction, São Paulo, SP – Brazil

    Edolene Bosman MSc,     TUPS Stress, Medfem Fertility Clinic, Bryanston, Johannesburg, South Africaa

    Jean D. Brender PhD, RN, FACE,     Texas A&M Health Science Center, College Station, Texas, USA

    Cynthia H. Chuang MD, MSc,     Penn State College of Medicine, Hershey, Pennsylvania, USA

    Frank H. Comhaire MD, PhD,     Fertility-Belgium Centre, Belgium

    Giovanni Corona MD, PhD,     University of Florence, Florence; Azienda Usl Bologna Maggiore-Bellaria Hospital, Bologna, Italy

    Giulia Dante MD,     Policlinico Hospital – University of Modena and Reggio-Emilia, Modena, Italy

    Wim A.E. Decleer MD,     Fertility-Belgium Centre, Belgium

    Michael C. Dennedy MD, PhD,     Galway Diabetes Research Centre; National University of Ireland, Galway, Ireland

    Sejal Doshi MD,     Northeastern Ohio Medical University, Rootstown, Ohio, USA; Center for Reproductive Medicine, Cleveland Clinic, Cleveland, Ohio, USA

    Damayanthi Durairajanayagam PhD,     Department of Physiology, Faculty of Medicine, MARA University of Technology, Selangor, Malaysia

    Aoife M. Egan MB, BCh, BAO,     Galway Diabetes Research Centre, Galway, Ireland

    Omer Erdeve MD,     Ankara University School of Medicine Children’s Hospital, Ankara, Turkey

    Aletta Dorothea Esterhuizen PhD,     TUPS Stress, Medfem Fertility Clinic, Bryanston, Johannesburg, South Africa

    Sandro C. Esteves MD, PhD,     ANDROFERT, Referral Center for Male Reproduction, Campinas, SP, Brazil

    Enrico Facchiano MD,     Azienda Sanitaria di Firenze, Santa Maria Nuova Hospital, Florence, Italy

    Fabio Facchinetti MD,     Policlinico Hospital – University of Modena and Reggio-Emilia, Modena, Italy

    Daniela Paes de Almeida Ferreira Braga DVM, MSc,     Fertility – Assisted Fertilization Centre; Sapientiae Institute – Educational and Research Centre in Assisted Reproduction, São Paulo, SP – Brazil

    J. Gual Frau MD Bs,     Urology Department, Corporació Sanitària Parc Taulí, Institut Universitari Parc Taulí, Sabadell, Spain

    Tod Fullston BSc (Hons), PhD,     University of Adelaide, South Australia, Australia

    C. Abad Gairín MD Bs,     Urology Department, Corporació Sanitària Parc Taulí, Institut Universitari Parc Taulí, Sabadell, Spain

    Kathryn Gebhardt PhD,     Repromed; University of Adelaide, Adelaide, South Australia, Australia

    Antonio Gonzalez-Bulnes MVD, PhD,     INIA, Madrid, Spain

    Jaime Gosalvez PhD,     Universidad Autonoma de Madrid, Madrid, Spain

    N. Hannaoui Hadi MD Bs,     Urology Department, Corporació Sanitària Parc Taulí, Institut Universitari Parc Taulí, Sabadell, Spain

    Batool A. Haider MD, MSc, ScD,     Harvard School of Public Health, Boston, Massachusetts, USA

    Roger Hart MD,     School of Women’s and Infants’ Health, University of Western Australia, King Edward Memorial Hospital, Perth, Western Australia, Australia; Fertility Specialists of Western Australia, Bethesda Hospital, Perth, Western Australia, Australia

    Annemieke Hoek MD, PhD,     Department of Obstetrics and Gynecology, University Medical Center Groningen, Groningen, The Netherlands

    Muhammad Sameem Javed BSc, MSc,     University of Agriculture, Faisalabad, Pakistan

    Ammar Ahmad Khan BSc, MSc,     University of Agriculture, Faisalabad, Pakistan

    Dariusz Kokoszyński PhD,     Department of Poultry Breeding and Animal Products Evaluation, University of Technology and Life Sciences, Bydgoszcz, Poland

    Jennifer L. Kraschnewski MD, MPH,     Penn State College of Medicine, Hershey, Pennsylvania, USA

    Walter K. Kuchenbecker MBChB,     Isala Fertility Center, Isala Clinics, Zwolle, The Netherlands

    Deepa Kumari MSc, PhD,     Cell Biology Laboratory, Department of Zoology, University of Rajasthan, Jaipur, India

    Lesia O. Kurlak PhD,     University of Nottingham, Nottingham, UK

    Abbie Laing MBChB,     King Edward Memorial Hospital, Perth, Western Australia, Australia

    Fiona Langdon MBBS,     King Edward Memorial Hospital, Perth, Western Australia, Australia

    J.L.M.R. Leroy MSc, PhD-student,     Gamete Research Centre, Veterinary Physiology and Biochemistry, Department of Veterinary Sciences, University of Antwerp, Belgium

    Marcello Lucchese MD,     Azienda Sanitaria di Firenze, Santa Maria Nuova Hospital, Florence, Italy

    Michaela Luconi PhD,     University of Florence, Florence, Italy

    Mario Maggi MD,     University of Florence, Florence, Italy

    Ana Meikle DVM, MSc, PhD,     Universidad de la República, Montevideo, Uruguay

    Hiten D. Mistry PhD,     University of Bern, Berne, Switzerland

    Ricardo Miyaoka MD, PhD,     University of Campinas, Campinas SP; ANDROFERT, Referral Center for Male Reproduction, Campinas SP; Sumaré State Hospital, Sumaré SP, Brazil

    Lisa J. Moran BSc (Hons), BND, PhD,     University of Adelaide, South Australia; Monash University, Victoria, Australia

    Aditi Mulgund MD,     Northeastern Ohio Medical University, Rootstown; Center for Reproductive Medicine, Cleveland Clinic, Cleveland, Ohio, USA

    Neena Nair MSc, PhD,     Cell Biology Laboratory, Department of Zoology, University of Rajasthan, Jaipur, India

    Isabella Neri MD,     Policlinico Hospital – University of Modena and Reggio-Emilia, Modena, Italy

    Mehmet Yekta Oncel MD,     Zekai Tahir Burak Maternity Teaching Hospital, Ankara, Turkey

    A. García Peiró PhD,     Centro de Infertilidad Masculina y Análisis de Barcelona (CIMAB), Edifici Eureka, Bellaterra, Spain

    Karen P. Phillips PhD,     Interdisciplinary School of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada

    Alan Scott Polackwich, Jr. MD,     Glickman Urological and Kidney Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA

    Sayali Chintamani Ranade PhD,     National Brain Research Centre, Manesar, Haryana, India

    Muhammad Atif Randhawa BSc, MSc, PhD,     University of Agriculture, Faisalabad, Pakistan

    Leonardo Reis MD, MSc, PhD,     University of Campinas; Pontifical Catholic University of Campinas, Campinas SP, Brazil

    Francisco Antonio Rodrigues MBBCh,     TUPS Stress, Medfem Fertility Clinic, Bryanston, Johannesburg, South Africa

    Mandy J. Rodrigues MA,     TUPS Stress, Medfem Fertility Clinic, Bryanston, Johannesburg, South Africa

    Edmund S. Sabanegh MD,     Glickman Urological and Kidney Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA

    Muhammad Wasim Sajid BSc, MSc,     University of Agriculture, Faisalabad, Pakistan

    Giulia Scaravelli MD, PhD,     National Health Institute, Rome, Italy

    Thomas Ernst Schmid PhD,     Klinikum rechts der Isar, Technische Universität München, Department of Radiooncology, Germany

    Cecilia Sosa DVM, MSc, PhD,     Universidad de Zaragoza, Zaragoza, Spain

    Roberta Spoletini PhD,     National Health Institute, Rome, Italy

    Lakshana Sreenivasan BSc,     The University of Arizona, Arizona, USA

    Helena J. Teede MBBS, PhD, FRACP,     Monash University; Diabetes and Vascular Medicine, Monash Health, Victoria, Australia

    Gülcan Türker MD,     Kocaeli University, Kocaeli, Turkey

    Eva Tvrda PhD,     Center for Reproductive Medicine, Cleveland Clinic, Cleveland, Ohio, USA; Department of Animal Physiology, Slovak University of Agriculture, Nitra, Slovakia

    S.D.M. Valckx PhD,     Gamete Research Centre, Veterinary Physiology and Biochemistry, Department of Veterinary Sciences, University of Antwerp, Belgium

    Carolina Viñoles DVM, MSc, PhD,     Instituto Nacional de Investigación Agropecuaria, Tacuarembó, Uruguay

    Anna Wilkanowska MSc,     Department of Agricultural, Environmental and Food Sciences, University of Molise, Campobasso, Italy

    Linda Wu BPharmSc, PhD,     University of Adelaide, South Australia, Australia

    Deirdre Zander-Fox PhD,     Repromed; University of Adelaide, Adelaide, South Australia, Australia

    Preface

    Many factors affect fertility, positively and negatively. Toxins and contaminants are important in cell functions and the growth of eggs.

    Section A. Overview on fertility

    Karen P. Phillips describes the public’s perception of environmental risks, especially those that affect the ability to conceive and carry to birth. Diana Anderson, Thomas Ernst Schmid, and Adolf Baumgartner focus on the well-known role of mothers who use tobacco. This leads to transgenerational damage in the offspring. Mehmet Y. Oncel and Omer Erdeve review the role of tobacco smoking on after conception and its damage on fetal health, and they describe a key mechanism – serum folate levels. S. D. M. Valckx and J. L. M. R. Leroy approach this issue in another way by evaluating the effects of maternal metabolic health. Then they evaluate the effects of maternal health as well as diet on follicular fluid composition. Finally, they review the consequences on the embryo as well as the oocyte. Gülcan Türker reviews heavy metals, such as mercury, which are well known major toxins. He describes their actions on preterm mortality and morbidity. Jean D. Brender reviews common materials on foods, like bacon, and known to cause cancer. They review nitrate and nitrite, which are metabolites of foods that mothers consume, and nitrosable drugs for their effects on congenital malformations. Giulia Scaravelli and Roberta Spoletini describe the application of reproductive techniques on worldwide epidemiology phenomenon and treatment outcomes. Frank H. Comhaire and W. A. E. Decleer discuss the effect of environmental hormone disrupters on infertility. Then the authors review strategies to reverse the effects of agents affecting hormones. Finally, Carolina Viñoles, Cecilia Sosa, Ana Meikle, and José-Alfonso Abecia review animal models where experimental studies can be done. They review damage to embryos during nutritional supplementation in animal models. Finally, they review human embryo losses and nutrition and nutritional deficiencies.

    Section B. Bariatric surgery, obesity, and fertility

    Humans are more frequently obese, which affects male and female fertility. In chapter Fertility and Testosterone Improvement in Male Patients After Bariatric Surgery written by Michaela Luconi, Giovanni Corona, Enrico Facchiano, Marcello Lucchese, and Mario Maggi shows that surgery to reduce weight has a positive effect in male fertility via improvements in hormone levels. Tod Fullston, Linda Wu, Helena J. Teede, and Lisa J. Moran broadly review the role of obesity in men as well as women in reproductive dysfunction. Michael Conall Dennedy reviews obesity per se and gestational outcomes.

    Section C. Exercise and lifestyle in fertility

    Ashok Agarwal and Damayanthi Durairajanayagam review lifestyle factors and reproductive health. Anna Wilkanowska and Dariusz Kokoszyński use animal models wherein animals are not purposely exercised. They review the normal activity of farm animals on their health and reproductive performance. Jennifer L. Kraschnewski describes the data and mechanism of the effects of physical activity on gestational weight gain. Clearly, exercise can change the growth and body mass. Walter K. Kuchenbecker and Annemieke Hoek review lifestyles to modulate ovulation. Lifestyle intervention was able to increase ovulation in anovulatory women, especially those with obesity or infertility. Finally, A. Gonzalez-Bulnes reviews reproduction learned from animal models.

    Section D. Nutrition and reproduction

    In chapter Green Leafy Vegetables: A Health Promoting Source written by Muhammad Atif Randhawa, A. Khan, Muhammad Sameem Javed, and Wasim Sajid begin the reviews of food, metabolism, and nutrition on fertility. They found that green leafy vegetables, as with most health situations, are very helpful for the promotion of infants’ health. Leonardo Reis and Ricardo Miyaoka found nutrition lifestyle and obesity in urology. Batool A. Haider and Zulfiqar A. Bhutta describe the role of multiple micronutrients in perinatal health and mortality reduction. Similarly, Lakshana Sreenivasan and Ronald R. Watson found that nutrition and hormones have a role in male infertility. S. C. Ranade found that nutrition had effects on the development and programming of neurological systems. Fabio Facchinetti, Giulia Dante, and Isabella Neri review herbs and their components in dietary supplements that affect delivery and conception. Nutrition supplements also affect pregnancy. Hiten D. Mistry and Lesia O. Kurlak review a key nutrient with the potential to provide toxicity with too much consumption. They found that selenium affects reproduction and fertility. It may function in part by antioxidant activity. Finally, Aditi Mulgund, Sejal Doshi, and Ashok Agarwal found a role for antioxidant stress in endometriosis, while Ashok Agarwal, Eva Tvrda, and Aditi Mulgund found that oxidative stress promotes preeclampsia.

    Section E. Nutrition and lifestyle in in vitro fertilization

    In vitro fertilization has been shown to be affected by nutrition and lifestyle. Mandy J. Rodrigues and Francisco Antonio Rodrigues review the regulation and management of the psychological effects of infertility. Kathryn Gebhardt and Deidre L. Zander-Fox found that the role of body mass index or obesity is associated with the success or failure on assisted reproductive treatment outcome. Fiona Langdon, Abbie Laing, and Roger Hart review the health outcomes of children conceived through assisted reproductive technology. Edolene Bosman, Aletta Dorothea Esterhuizen, and Francisco Antonio Rodrigues review chronic diseases and their influences on in vitro outcomes. They emphasize hyperinsulinemia on male regulation of in vitro fertilization.

    Section F. Nutrition, lifestyle, and male fertility

    Clearly, the needs of males for fertility are different from females. Deepa Kumari, Neena Nair, and R.S. Bedwal found that zinc deficiency changed testicular apoptosis. Inadequate cell division is a serious inhibition to sperm growth. Edson Borges Jr. and Daniela Braga found that environmental factors, food intake, and social habits modify male patients and their relationship to intracytoplasmic sperm injection outcomes. Alan Polackwich and Edmund S. Sabanegh Jr. review the role of over-the-counter supplements in male infertility as diet and medicines do not have to be new pharmaceutical drugs. Sandro C. Esteves and Ricardo Miyaoka review sperm physiology and assessment of spermatogenesis kinetics in vivo, which is critical for understanding the role of lifestyle and food in cell growth for male fertility. Carlos Abad, N. Hannaoui Hadi, and A García Peiró discuss antioxidant treatment and prevention of human sperm DNA fragmentation, specifically its role in health and fertility. Finally, Eva Tvrda, Jaime Gosalvez, and Ashok Agarwal review epigenetics and its role in male infertility.

    Acknowledgments

    The work of Dr. Watson’s editorial assistant, Bethany L. Stevens, in communicating with authors and working on the manuscripts was critical to the successful completion of the book. It is very much appreciated. The encouragement, advice, and support of Jeffrey Rossetti in Elsevier book preparation were very helpful. Support for Ms. Stevens and Dr. Watson was graciously provided by the Natural Health Research Institute (www.naturalhealthresearch.org), a nonprofit health promotion institute. Finally, the work of the librarian at the Arizona Health Science Library, Mari Stoddard, was vital and very helpful in identifying the key researchers who participated in the book.

    Section A

    Overview on fertility

    Chapter 1: Perceptions of Environmental Risks to Fertility

    Chapter 2: Paternal Smoking as a Cause for Transgenerational Damage in the Offspring

    Chapter 3: Impact of Cigarette Smoking During Pregnancy on Conception and Fetal Health through Serum Folate Levels

    Chapter 4: The Effect of Maternal Metabolic Health and Diet on the Follicular Fluid Composition and Potential Consequences for Oocyte and Embryo Quality

    Chapter 5: The Effect of Heavy Metals on Preterm Mortality and Morbidity

    Chapter 6: Nitrate, Nitrite, Nitrosatable Drugs, and Congenital Malformations

    Chapter 7: The Application of Reproductive Techniques (ART): Worldwide Epidemiology Phenomenon and Treatment Outcomes

    Chapter 8: The Effects of Environmental Hormone Disrupters on Fertility, and a Strategy to Reverse their Impact

    Chapter 9: Embryo Losses During Nutritional Treatments in Animal Models: Lessons for Humans Embryo Losses and Nutrition in Mammals

    Chapter 1

    Perceptions of Environmental Risks to Fertility

    Karen P. Phillips PhD    Interdisciplinary School of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada

    Abstract

    Environmental risks to fertility include lifestyle habits, sexually transmitted infections, and occupational/environmental exposures. Perception of reproductive risks is shaped by culture, individual factors, such as personal experience, gender, socioeconomic status, and race/ethnicity, and by the social discourse of risk. Awareness, identification, and risk perception of reproductive hazards are important prerequisites to lifestyle modifications and risk mitigation. As many fertility risk factors are also public health threats, a public health framework is proposed to promote fertility awareness, increase surveillance of infertility subtypes, provide enhanced screening for fertility risk factors among vulnerable populations, and enhance interdisciplinary collaborations to address reproductive health policy and management of infertility.

    Keywords

    environment

    lifestyle

    risk perception

    infertility

    framework

    public health

    Introduction

    Environmental risks, including lifestyle habits, infectious disease, and occupational exposures, are increasingly examined as modifiable infertility risk factors. This chapter will provide an overview of infertility risk factors and explain how risk perception is formed. Perceptions of fertility risks within specific populations will also be examined. Finally, a public health framework is proposed to enhance fertility-specific health promotion and enable mitigation of modifiable risks to fertility.

    Infertility – Definitions, Manifestations, and Risk Factors

    Infertility is generally defined as the absence of conception after 1 year of regular, unprotected intercourse. Prevalence of current infertility in North America ranges from 11.5% to 15.7% in Canada [1] and 15.5% among US women [2]. The pathophysiology of infertility may include genetic/chromosomal anomalies, congenital or infectious malformations of the reproductive tract, and endocrine disorders (hypogonadism, anovulation) in both men and women. Additionally, female infertility is caused by advanced age, endometriosis, polycystic ovarian syndrome, and diminished ovarian reserve [3]. Infertility manifests as ovulatory dysfunction, amenorrhea, implantation failure/spontaneous abortion, and diminished semen parameters [3]. For about 10–15% of infertile couples, infertility is unexplained, with minimal abnormal findings upon medical investigation [3].

    Most modifiable risk factors can be categorized under environment. Diet, lifestyle habits (cigarette smoking, alcohol use), history of sexually transmitted infections (STI), pharmaceutical/medical treatments, as well as environmental exposures to chemicals, radiation, air pollution, and heavy metals are identified as risk factors to fertility [4–6] (Box 1.1). Environmental exposures and lifestyle habits represent sex-specific risks to fertility based on differences in reproductive physiology and urogenital anatomy. Common lifestyle and environmental determinants of fertility and reproductive health are summarized next.

    Box 1.1

       Modifiable risks to infertility

    • BMI > 30 mg/kg²

    • BMI< 18 mg/kg²

    • Alcohol

    • Cigarette smoke

    • Recurrent sexually transmitted infections

    Less evidence for

    • Environmental contaminants (ambient exposure levels)

    • Caffeine

    Lifestyle and Infertility

    Body Weight

    Obesity (body mass index (BMI) ≥ 30 kg/m²) is increasingly described as a global phenomenon, contributing significantly to morbidity and mortality (cardiovascular disease, diabetes, mobility issues, etc.). For both men and women, obesity contributes to hypogonadism and other perturbations of the endocrine system that may contribute to infertility [7–10]. Obese women have generally poor outcomes with assisted reproductive technologies (ART) [11,12] including fewer metaphase II oocytes retrieved, oocyte spindle defects [13], more canceled cycles [14], decreased fertilization [15] and decreased live birth rates [12,16–18]. Similarly, obesity in the male partner may be associated with decreased clinical pregnancy [19,20] and live birth rates [10,20]. Obese women also face increased risks during pregnancy, such as gestational diabetes, hypertension, spontaneous abortion, large fetuses for gestational age, and concomitant delivery complications [21,22]. Poor ART outcomes, coupled with concerns of increased pregnancy complications in the obese mother, have prompted suggestions that ART be denied to women with BMI ≥ 30–35 kg/m² [22]. Critics of such policies argue that greater emphasis should be placed on weight–hip ratio as a predictor of reproductive risk, BMI limits are discriminatory and stigmatizing, and sustained weight loss is difficult to achieve for many individuals [22]. Over half of American men and women surveyed supported BMI limits for ART, citing risks of pregnancy complications in obese patients and possibility of health complications including obesity in offspring [23]. BMI ART treatment limits have not been proposed for obese male patients. As lifestyle modifications are difficult to achieve and sustain, support for weight management should be a component of preconception care [11,24].

    Underweight individuals also face fertility challenges and may be less responsive to ART [11,21]. Women with a BMI <18 mg/kg² are at increased risk for ovulatory dysfunction and pregnancy complications, such as preterm labor. General recommendations for fertility planning include maintenance of healthy body weight, nutritious diet, and moderate exercise [11,21,25].

    Tobacco

    Tobacco smoking is a leading cause of adverse health effects, including cancer, cardiovascular, and respiratory disease. Although cigarette smoking is declining, 18.1% of American adults [26] and 16% of Canadian adults [27] were smokers in 2012. Globally, tobacco use is increasing rapidly among young girls aged 13–15 years. Despite health promotion efforts, continued use of tobacco by these young girls may herald future increases in global rates of smoking among adult women [28]. Cigarette smoke represents a well-established mixture of reproductive toxicants for both men and women [29,30]. Reproductive pathology may result from vasoconstriction, generation of reactive oxygen species and concomitant oxidative stress, and alterations in endocrine signaling. Male smoking is associated with decreased sperm count, motility, seminal volume, and reduced ART outcomes [31,32] – manifested at a cellular level as sperm DNA damage (e.g., DNA fragmentation, formation of DNA adduct) and pathological changes to the acrosomal membrane and tail [25,33,34].

    For women, smoking is associated with earlier age at menopause, premature ovarian failure, infertility, and spontaneous abortion [35]. Female smokers respond poorly to ART gonadotropin stimulation, producing fewer oocytes with low developmental potential, and decreased live birth rates [18,36,37]. Cadmium, nicotine-metabolite cotinine, and polycyclic aromatic hydrocarbons, such as benzo[a]pyrene (B[a]P), are examples of some of the toxic compounds contained in cigarette smoke and have also been detected in follicular fluid [29,38,39]. Accumulation of toxicants in the follicular compartment has the potential to perturb oocyte growth, induce follicular atresia, and dysregulate necessary hormonal support for the initiation of meiotic resumption and ovulation [38,40,41].

    Side-stream or second-hand smoke exposure is also detrimental to fertility. Women exposed to side-stream smoke or mainstream smoke face compromised ART outcomes including reductions in implantation and pregnancy rates [39]. As described, obese women tend to respond poorly to ART; however, obese smokers may face even greater reproductive challenges [18]. Given the significant health risks posed by tobacco smoking, it is clearly evident that smoking cessation should be recommended prior to commencement of natural conception or ART for both men and women [42]. Encouragingly, the effects of smoking on oocyte/embryo developmental potential may be transient, as former smokers have an increased pregnancy rate compared with smokers [36].

    Alcohol

    Heavy alcohol consumption is generally associated with poor fertility outcomes in both men and women, along with significant pregnancy complications and adverse fetal development [21,35]. Both moderate (7–8 drinks/week) and low alcohol consumption (1 drink/week) may be associated with impaired fertility [21]. Alcohol’s reproductive toxicity may be due to impaired hypothalamic–pituitary–testicular signaling manifesting as decreased semen quality [35]. Female fertility may also be reduced by alcohol consumption with possible effects on the hypothalamus resulting in decreased luteinizing hormone secretion and anovulation [35]. Alcohol’s teratogenic effects on the developing embryo and fetus have prompted general advisements for women attempting to conceive to abstain from alcohol [21,35].

    Caffeine

    The literature examining effects of caffeine intake on fertility is limited by methodological issues (retrospective studies – recall bias of caffeine intake) and lack of consensus [11,21,25,35]. The effects of caffeine consumption on prolonged time-to-pregnancy may be confounded by other negative lifestyle habits such as smoking [11]. It is accepted that caffeine intake of <200–300 mg per day is unlikely to cause detrimental reproductive outcomes such as spontaneous abortion or fetal development [21]. Women who are trying to conceive or are pregnant are advised to limit caffeine intake to 100–200 mg per day [21].

    Sexually Transmitted Infections

    STI risk is particularly high in adolescents and young adults. Despite mandatory sexual health education in public schools in Canada [43], increased rates of infection with Chlamydia trachomatis and Neisseria gonorrhoeae have been reported [44]. In the United States, public school sexual health education varies by state [45] with regional, ethnic, and race disparities evident in STI prevalence [46]. Rates of chlamydial infections have continued to rise in many European countries despite implementation of screening programs [47]. Recurrent STI within high-risk groups, safe sex fatigue, high-risk sexual encounters facilitated by social media, and lack of awareness of long-term consequences of STI, such as cancer and infertility, may explain these trends [48].

    STI are caused by viruses, bacteria, and other pathogens. Although viral infections may pose risks for reproductive health, most studies have emphasized bacterial STI as risks to fertility. Although isolated infections of C. trachomatis or N. gonorrhoeae pose little risk to fertility or perinatal outcomes if promptly treated, for many men and women, STI may be asymptomatic, which may preclude medical interventions [47,49]. Women with a history of bacterial STI may experience inflammatory obstructions of the reproductive tract (pelvic inflammatory disease – PID), including scarring of the fallopian tubes – a major cause of female infertility and risk factor for ectopic pregnancy [50]. PID had been strongly associated with chlamydial and gonorrheal infections; however, rates of PID seem to be decreasing along with related complications such as tubal factor infertility and ectopic pregnancy [47,51–53]. A history of recurrent chlamydial or gonorrheal infections remains a significant risk factor for these reproductive tract pathologies [47,50]; however, improved screening and prompt treatment may be responsible for reducing the rates of these complications even in high-risk groups [52].

    The relationship between bacterial STI and male infertility is less clear [54]. Bacterial STI gain entry to the reproductive tract via urogenital passages, producing urethritis, or less commonly, prostatitis or epididymitis [49,55]. Men with chlamydial infections tend to exhibit diminished semen quality along with sperm DNA damage; however, it is unclear whether these deficits significantly impair fertility [56,57]. Further study is warranted regarding the history of recurrent STI and male infertility.

    Summary

    In addition to the described lifestyle risks (obesity, being underweight, alcohol, smoking, and STI), stress and anxiety prior to ART have also been proposed as infertility risk factors [30,58]. Men and women planning to conceive should optimize fertility by maintaining a healthy body weight, abstaining from excessive alcohol or caffeine intake, and be supported to quit smoking. Sexual health promotion strategies (education, screening, condom distribution) enable early detection and treatment of STI, thereby preventing later fertility issues.

    Environmental Disruption of Reproductive Health

    Reproductive and developmental health are adversely affected by ionizing radiation, heavy metals, lead, industrial chemicals/solvents, temperature, and contaminated food and water (biological/chemical) [4,6] (Fig. 1.1). It is also biologically plausible, though there is less evidence, that exposures to air pollution [6,59,60], electromagnetic or radiofrequency fields (WiFi [61], cell phones [62,63]), along with social environmental factors, particularly disparities in socioeconomic status (SES) and social stress [64–66], impair human reproduction and development. Endocrine disrupters are perhaps the most widely studied environmental modulators of fertility and reproductive health, with effects demonstrated in wildlife, laboratory animals, and humans [67,68]. Endocrine disrupters encompass a wide range of chemical species, mixtures, and compounds including phytoestrogens, pesticides, industrial chemicals, and by-products [67,69]. Endocrine disrupters have been linked to adverse health effects including infertility, abnormal prenatal and childhood development (spontaneous abortion, male reproductive tract abnormalities and other birth defects, sex ratios, precocious puberty), and reproductive cancers (prostate, breast, ovarian, endometrial, and testicular) [67,71]. It is hypothesized that global declines in men’s reproductive health characterized by poor semen quality, urogenital birth defects (cryptorchidism, hypospadias), and testicular cancer, collectively called testicular dysgenesis syndrome, are caused by exposures to endocrine disrupters [67,70,71].

    Figure 1.1   Environmental determinants of reproductive health.

    Reproductive health may be adversely affected prior to conception, during gestation and delivery, childhood development, or as adult-onset diseases. Lifestyle habits (smoking, alcohol, drugs, stress, obesity, STI) and environmental exposures (endocrine disrupters/contaminants, radiation, pollution, metals, solvents, temperatures, social stressors) have been identified as risk factors for infertility and other adverse reproductive health outcomes [11,21,30]. STI, sexually transmitted infections; SES, socioeconomic status.

    Endocrine disruption represents one of the most plausible mechanisms by which environmental chemical exposures may adversely affect reproductive capacity [67,69,71]. Molecular mechanisms of these contaminants may include endocrine receptor agonists, antagonists, enzyme inhibitors, and steroid hormone transport interference (Box 1.2). Perhaps the most widely studied endocrine disrupters are xenoestrogens or chemicals that mimic endogenous estrogens by binding to estrogen receptors and regulating gene expression [67]. Diethylstilbestrol (DES), the phytoestrogens genistein and coumestrol, certain polychlorinated biphenyls (PCBs), nonylphenol, the insecticides methoxychlor and chlordecone, and bisphenol A (BPA) are examples of xenoestrogens [72]. Some chemicals (e.g., the fungicide vinclozolin, dichlorodiphenyl trichloroethane (DDT)-metabolite dichlorodiphenyl dichloroethylene (p,p′-DDE)) exhibit antiandrogenic activity [67]. Other endocrine disrupters are aromatase inhibitors (fungicide fenarimol) and aryl hydrocarbon receptor agonists (dioxins, PCBs, polychlorinated dibenzofurans (PCDFs)), while other chemicals exhibit mixed mechanisms of action (diethylhexyl phthalate (DEHP), methoxychlor-antiandrogen, weak estrogen) [67]. By disrupting endogenous endocrine pathways, endocrine disrupters have the potential to dysregulate the growth and maturation of gametes, disrupt ovulation, embryo and fetal development, and labor and delivery.

    Box 1.2

       Environmental perturbation of fertility: molecular mechanisms

    • Endocrine disruption

    • Hormone receptor agonists

    • Hormone receptor antagonists

    • Enzyme inhibitors

    • Alterations in hormone synthesis, transport

    • Cell injury

    • Oxidative stress

    • Heat stress

    • Inflammation/scar tissue

    • DNA damage/alterations

    • Epigenesis

    • Carcinogenesis

    • Cell death

    • Apoptosis

    • Toxicity/necrosis

    • Gamete-specific damage

    • Oocyte spindle defects (congression failure)

    • Follicular atresia

    • Inhibited spermatogenesis

    • Sperm-defects (membrane, motility, DNA damage)

    Gene–environment interactions, such as epigenetic processes (methylation, histone modifications), represent additional pathways by which environmental chemicals may perturb reproductive function [73–75]. DNA methylation has been recognized as a key event in epigenetic silencing of genes involved in embryonic development, X-chromosome inactivation, genomic imprinting, and chromosome instability. Epigenetic processes may be triggered by stress, diet, or environmental exposures [74,75]. Germ line epigenetic alterations are associated with birth defects, spontaneous abortions, and abnormal fetal developmental programming [74,76,77]. Beyond the disruption of endocrine signaling, epigenetic transformations have the potential to modulate gene expression and contribute to infertility in later generations [78].

    Human Exposure

    The routes of human exposure to environmental contaminants typically include inhalation, oral (water, diet), and dermal. Ongoing monitoring of the arctic peoples and wildlife is necessitated by bioaccumulation of organic pollutants present in marine mammals and human lipid stores (e.g., adipose tissue, breast milk) [67]. Similarly, consumption of Great Lakes fish may pose a risk due to bioaccumulation of lake pollution [67]. Farm-workers, agricultural workers, and their families also represent populations typically exposed to greater levels of pesticides that are associated with increased risk of birth defects [79], spontaneous abortion [30,80], and prolonged time to pregnancy [81]. In the general public, biomonitoring data do indicate detectable levels of endocrine disrupters and other environmental contaminants in semen (reviewed) [82] and follicular and amniotic fluid [83–90]. The presence of contaminants in reproductive compartments provides biological plausibility for perturbation of gametes and embryo/fetal development; however, the extent to which exposures to environmental contaminants contribute to infertility and reproductive dysfunction remains unclear.

    Summary

    Environmental hazards, replete with complex scientific names and equivocal evidence of reproductive risks, have nonetheless become social issues, in part because of their putative threats to health and safety [91]. For most individuals, exposure to such hazards is at environmental levels; however, the science is unclear regarding the adverse health effects of these low-dose exposures [30,67–69,92]. Occupational exposures are recognized as significant health threats [5,6,30,31], necessitating health and safety workplace standards and education, use of personal protective equipment (PPE), and regulatory oversight. Individuals attempting to conceive should identify any environmental exposures obtained through leisure activities, diet, community, and workplace with their healthcare providers.

    Risk Perception

    Navigating often complex and conflicting environmental and lifestyle risk information is challenging for infertility patients. Which environmental exposures should be minimized? Which lifestyle choices should be adopted? How can lifestyle modifications improve the success of ART? Perceptions of risk may contribute to anxiety, worry, or stimulate behavior change to diminish risk [93]. Awareness, understanding, and ultimately mitigation of modifiable risks to fertility may enable some patients to regain a sense of control while undergoing treatment for infertility. Infertility prevention may also be optimized by knowledge, awareness, and understanding of infertility risk factors [68,94]. Risk mitigation requires both awareness of environmental determinants of reproductive health and the perception of these factors as potential hazards. Understanding how people perceive risk is fundamental to designing effective environmental health promotion strategies.

    Environmental Risk Perception

    Risk perception is suggested to be shaped by social context and culture [95], personal ability to influence risk, bias, familiarity with the hazard [91,96], and personal beliefs [97]. The public may appear more concerned about low-probability risks (e.g., nuclear power) than high-probability risks (speeding without seat belts), which has led to the characterization of the public as scientifically illiterate and unable to comprehend technical and scientific issues [91]. Most people have difficulties with interpretation of probabilities, are less concerned with inconsistencies in the scientific evidence, and are generally most concerned about public risks that would generate mass-scale death and disability [91]. Mental models or heuristics enable individuals to evaluate situations and form judgments based on prior experience, beliefs, and common knowledge. Although heuristics may assist in rapid problem solving and learning, they may also lead to erroneous conclusions, particularly with technical or scientific risk issues [91,98].

    The Social Amplification of Risk Framework [99] provides a model for heightened risk perception within the social context of communications from media, activist organizations, opinion leaders, peers, and public agencies (Fig. 1.2). The public is exposed to increasingly polarized social discourse regarding these often technical environment-related topics, with perceptions of environmental risks suggested to be amplified [98]. In spite of sometimes weak or inconclusive evidence linking environmental exposures to adverse human health effects, risk perceptions are influenced by media’s emphasis on health hazards [98]. It is highly evident that controversial health topics are dramatized by communication/information channels (e.g., media, Internet), which serve to amplify risk perceptions [96,99]. Controversial issues are repeated within media cycles such that repetitive risk messaging (volume), controversy, and dramatization of the risk collectively influence social amplification of a particular hazard [99]. Risks to populations symbolically portrayed as vulnerable (e.g., developing fetus, infants, and children) [100] and likewise information perceived to have symbolic connotations also contribute to amplification [99]. Models of risk perception enable a greater understanding of health risk information uptake by the public and the variables that ultimately shape the development of individual risk heuristics.

    Figure 1.2   Social amplification of risk framework.

    Perceptions of risk are shaped by personal beliefs, familiarity/experience with hazard, and personal sense of control [95]. Within the context of society and culture, certain risks may be amplified through repetitive social discourses, dramatizations of potential outcomes, and controversy [99].

    Gender and Risk Perception

    Men and women exhibit gendered preferences for occupations, lifestyle habits, leisure activities, and health behaviors; all of which may shape perceptions of environmental influences on fertility, pregnancy, and development. It is well established that men and women perceive risks differently [100–103]. Men and women worry about different types of risks: women express concerns with hazards associated with home and family, particularly hazards that may produce accidents, adverse health, or death, whereas men tend to be more concerned about risks to occupation or career [101]. Women report greater concern about environmental risks and infectious diseases, while men worry about health and safety including occupational accidents [101,104]. Studies also consistently demonstrate that men exhibit lower risk perception compared with women for a range of hazards [101,104]. Gender and race are consistent predictors of risk perception such that women and minorities are more likely to identify hazards as high risk compared with white men [103,105]. It is evident that sociopolitical status, sense of control, power, and economic freedom may collectively diminish concerns about environmental hazards [103,105].

    Reproductive health is a societal norm, such that the issue of infertility produces a social stigma, isolation, and altered perceptions of gender roles [93]. In particular, women’s social and cultural constructions of motherhood greatly influence their perceptions of risk. Infertile women are willing to assume greater risks than their male partners to conceive [93]. Their risk–benefit compromise will require infertile women to risk potential long-term effects of fertility drugs and ART complications, such as ovarian hyperstimulation syndrome and multiple births, in exchange for the benefit of having a baby [93]. Although women will assume personal risks to conceive, upon becoming a mother and caregiver, risk perception becomes heightened regarding home and family [102,103].

    Reproductive risks have been examined in many contexts including DES exposure in utero, reproductive risks in the workplace, risks of childbirth, and adverse pregnancy outcomes. Studies from social sciences examine how reproductive risks are perceived, constructed, and influenced by gender, race/ethnicity, culture [101], economics, and the law [106]. During the 1970s through 1990s, many US companies used discriminatory screening practices to exclude presumed fertile women from employment on the basis of reproductive risk due to occupational hazards [106]. Johnson Controls, Inc., a battery manufacturer, excluded fertile women from jobs working with lead, going so far as to require women to produce proof of sterilization [106]. Such fetal exclusion policies were perceived by employers to mitigate reproductive risk in the workplace and avoid media stigma and lawsuits. In addition to being discriminatory, such hiring practices implicitly negate reproductive and other health risks to nonfertile women and male workers [106]. Occupational reproductive risk assessments tend to be biased toward women’s health, often omitting screening and education for male employees [107]. For occupational exposures where the reproductive risk to men has been proven significant (e.g., the pesticide dibromochloropropane (DBCP)), rather than restrict opportunities for male workers, the pesticide itself was banned, suggesting a gender-biased approach to occupational risk assessment [107]. Ultimately, the Johnson Controls 1991 U.S. Supreme Court decision ruled that exclusion of fertile women from jobs involving toxic exposures was discriminatory [106], providing legal protection for equal employment opportunity. However, the concept of fetal protectionism remains pervasive within Western culture. Pregnant women who engage in behaviors perceived as reproductively risky, such as smoking, alcohol consumption, or use of unnecessary pharmaceuticals, are viewed as irresponsible or reckless [108]. Increasingly, the social discourse around pregnancy and environmental risk reduction, such as uptake of environmentally friendly foods and products, has become conflated with good mothering, representing additional social pressure for women to mitigate environmental risks to reproductive health [108].

    Race/Ethnicity and Risk Perception

    Individuals of low SES and belonging to racial/ethnic minority communities are disproportionately affected by environmental health risks [91,109]. Environmental health perspectives of minority and low-income communities have been assessed in urban US studies. Women living in Manhattan- and Boston-area minority communities express environmental concerns about neighborhood local pollution, lead exposure, garbage, pests (e.g., rodents, roaches), noise levels, and community safety [110,111]. Low SES and minority communities face barriers to health promotion messages due to reduced uptake/access local media and Internet [111]. In North America, influences of SES and race/ethnicity on environmental risk perception may be difficult to delineate. Examination of environmental risks to health in poor, minority communities may require consideration of multiple, interacting risks rather than a focus on single contaminants. This approach better reflects the experiences of many communities exposed to several types of hazards within substandard housing, occupational, and educational facilities [109]. The concept of environmental justice is used to reflect these disparities in home and work environments experienced by poor and minority members of society [109].

    Population-Based Environmental Risk Perception Studies

    Public risk perception has been a driving force for the development of environmental policy in Australia [100], Canada [112], and the United States [113]. Population-based environmental risk perception studies have been conducted in Canada in the past two decades [114,115], with cigarette smoking, obesity, and unprotected sex perceived as the top three health hazards [115]. Hazards that are exotic, unfamiliar, unfairly distributed, anthropomorphic (e.g., affecting pregnant women or children), or scientifically uncertain were perceived by Australians to pose significant risk [100]. Passive smoking, water scarcity, and sun exposure were identified as the top three environmental risks by Western Australians and rated as high risks to health [116]. A US ecological study did not emphasize health hazards, but did report that public ranking of ecological risks was influenced by values, beliefs, and worldviews [117]. Compared with risk professionals, US lay public perceives low-probability, high-consequence risks (e.g., hazardous waste sites, persistent organics, sewage, and radiation) to be of greatest concern [117]. These population studies also report that advanced age and lower SES were associated with higher environmental risk perception [100,115–117].

    Summary

    Men and women assess reproductive and environmental risks differently, which may ultimately produce gender-specific health behaviors and choices. Minority and low-income communities face significant environmental health challenges due to SES disparities, neighborhood-level hazards, and heightened risk perception. Understanding the many influences used by men and women to process and assess environmental health risk information is necessary to optimize reproductive-specific health promotion programs.

    Risk Perception of Environmental Risks to Fertility

    In addition to gender, personal experiences also shape risk perception. Dramatic life experiences may be conflated with hazard identification and produce heightened risk perception [99]. Personal experience with family planning, pregnancy, parenthood, and infertility may influence perception of environmental risks to fertility. Risk perceptions are examined within three specific populations: (1) adolescents and young adults, (2) general public, and (3) occupationally exposed workers.

    Preconception: Adolescents and Young Adults

    Fertility knowledge and awareness has been examined in university students from Sweden [118–120], Finland [121], Italy [122], the United States [123], the United Kingdom [124], Israel [125], and Canada [126,127], with the general consensus that young adults lack an understanding of the age-related decline in female fertility. University students, typically aged 18–25 years, are generally engaged in pregnancy prevention, with parenthood postponed upon completion of academic studies and achievement of career, economic, and relationship stability [118–120,128]. For most young adults, awareness and knowledge of fertility risk factors will come from health professionals, media, Internet, health promotion/education, and anecdotal information from social networks [129,130].

    Lifestyle habits, such as smoking, alcohol consumption, and STI, were identified as risks to female fertility in studies from the United Kingdom [124], Sweden [118], British Columbia, Canada [126], and Ottawa, Canada [127]. About a quarter of British Columbian female undergraduates perceived physical or emotional stress and exposure to cigarette smoke as higher risks to female fertility than age [126]. In a qualitative study, Ottawa male and female undergraduates described the modern culture of stress as contributing to infertility and adverse health outcomes in general [48]. Ottawa male and female undergraduates recognized that fertility risks due to lifestyle factors, such as alcohol and smoking, were related to timing of exposures, dose, and frequency [48]. Secondary school female adolescents from Toronto, Ontario, also exhibit awareness of infertility, with STI, smoking, being overweight or underweight, street drugs, and heavy alcohol consumption identified as risks to fertility [131]. Most female adolescents, but fewer males from low-income, predominantly African-American neighborhoods of San Francisco identified STI including chlamydia and gonorrhea as risk factors for female infertility [132]. These studies indicate that adolescents and young adults are generally aware of lifestyle risk factors for female infertility.

    Few studies have examined awareness and perceptions of risk factors for male infertility. Most Toronto high school boys asserted that their fertility was an important issue, and recognized lifestyle habits as risks for male infertility [131]. Although few were concerned about the possibility of infertility, most Ottawa men identified they wished to become fathers in the future [128]. Turkish male and female university students identified smoking, alcohol, and STIs as risk factors for both male and female infertility; however, these lifestyle risks were perceived to primarily affect women [133]. Male and female Ottawa undergraduates also described lifestyle risks to male fertility with more men than women believing that advanced paternal age was also a risk factor [127].

    Very few studies have examined university students’ perceptions of environmental hazards as risks to fertility. Environmental exposures (e.g., pollution, chemicals, radiation/X-rays) were considered risk factors for both male and female infertility by Turkish students [133]. Similarly, Ottawa undergraduates believed that environmental exposures to pollutants, pesticides, plastics, and BPA would increase risk of infertility [48]. Negative perceptions of environmental risks were influenced by media reports and anecdotal information, with Ottawa students generally asserting that industrial chemicals contribute to widespread public exposure and adverse health [48].

    There is a global emphasis on the promotion of a healthy lifestyle including smoking cessation, alcohol moderation, maintenance of healthy body weight, and HIV/STI risk reduction [134]. Although a healthy lifestyle may mitigate some modifiable fertility risk factors, it will not abrogate risks caused by maternal age, hormonal, genetic, or congenital abnormalities. Such confusion is evident in UK students who asserted that healthy lifestyle habits would actually increase female fertility [124]. Ottawa undergraduates similarly believed that adherence to a healthy lifestyle ensured overall good health, including fertility [48]. Despite the existence of knowledge gaps, particularly among boys and men, adolescents and young adults seem to be aware of lifestyle risk factors for infertility. It is also possible that any hazards to adverse health are also assumed to be risk factors for infertility, with little understanding of the mechanisms or fertility-specific risk factors such as maternal age.

    General Public: Childless Adults and Parents

    Studies examining reproductive risk perception in the general population have recruited participants within broad age ranges, typically with a mean age 28–33 years [135–140]. These slightly older participants will have completed the transition to adulthood with school/college/university matriculation, entrance to workforce, development of relationships, and contemplation of parenthood [141]. Very few studies have specifically examined public perceptions of environmental risks to fertility. Australians living in Queensland perceive pesticides, household chemicals, and animal-borne diseases to be harmful to human reproduction, with women more likely to perceive hazards as risky compared with men [140]. Lead exposure followed by stress was perceived as the most harmful hazard to either male or female reproduction [140]. Differences in environmental risk perception were apparent in older participants (45+ years) who perceived household chemicals/paint, radiation, and lead exposures as more significant hazards to reproductive health compared with participants aged 18–34 years [140]. Obesity and smoking were identified as fertility risks in a second study from Australia [135], and by childless Canadian women who also considered STI as risk factors [139]. Similarly, American women identified alcohol, smoking, history of STI, and being overweight or underweight as risks to female fertility [137]. Stress was perceived by more than 90% of American women as a risk factor for infertility [137]. Childless Canadian men [138], but not male Australians [135], identified smoking as a risk factor for male fertility; however, neither group recognized male obesity as a risk factor.

    The public has a general understanding of fertility risk factors; however, there is a pronounced gender gap. Awareness of risk factors for infertility is related to female gender, high human development index nationality, advanced education, employment, and medical consultation for infertility problems [135].

    Occupationally Exposed: Agricultural Workers

    US agricultural workers, including farmers, pesticide applicators, and workers involved in the manufacture of pesticides, are mostly immigrants from Mexico or Latin America with low SES, poor English proficiency and literacy, and limited access to healthcare [142–144]. Several studies have reported reproductive risk perceptions of workers and family members employed in California, Washington State, Florida, and North Carolina. Pesticides were perceived to be poisonous and dangerous, with risk signified by the strong chemical odor of the pesticide [142,145,146]. Both men and women believed that pesticides caused a range of health risks, including dermal irritation, respiratory conditions, and headaches, as well as adverse reproductive health such as infertility, miscarriage, and birth defects [142,144–148]. Female farmworkers and women in farmworker households conflated pesticide exposure with infection, believing that pesticides cause STI and blood contamination, which could be genetically transmitted by exposed men to the fetus [142,147]. Health and safety practices recommend the use of PPE, frequent hand-washing, and removal of contaminated clothing prior to family interactions to reduce the take-home exposure pathway [144]. Workers and family members perceived a lack of control over pesticide exposures and identify barriers to risk mitigation such as lack of workplace facilities, resources, time, and health and safety knowledge gaps [142,144,145].

    Summary

    Knowledge and awareness of environmental risks to fertility develops over the life-course as young adults transition from pregnancy prevention to family planning. In addition to US agriculture, many industries are associated with occupational contaminant exposures, representing potential risk for workers. Although the perception of reproductive risks may be heightened, workers and their families may lack the resources or voice to mitigate risks of occupational exposures. More risk perception studies are required focusing on male fertility and perceptions related to exposures to environmental contaminants, radiation, and other hazards.

    Mitigation of Environmental Risks to Fertility

    The evaluation of risk information, characterization of hazards, and assessment of public reaction to environmental health topics are collectively used to improve communication of related risk information [96]. Risk communication is an essential component of health promotion and health education; ultimately intended to influence health behaviors [96]. Health promotion and education remain the most important correlates of fertility knowledge rather than personal fertility or parenting experience [135]. Fertility-specific health promotion will enable the development of self-efficacy [68,94,149], such as lifestyle modifications and early recognition and treatment of fertility-related medical conditions [150]. Evidence-based infertility risk communication targeted at the general public should include information on prevalence, causes, signs and symptoms, consequences, and risk mitigation strategies [150]. Designing such reproductive risk communication programs is not simple. The 2001 American Society for Reproductive Medicine (ASRM) infertility prevention campaign received significant criticism for use of shock tactics, contributing to stigma against people with infertility and the individuals with the four target risk factors (smoking, weight problems, STIs, and advance maternal age) [151,152]. Emphasis on individual factors also fails to communicate the increased likelihood of infertility posed by multiple, interacting risk factors in both the male and female [152].

    FertiSTAT, a self-administered, multifactorial tool, provides women with a personalized fertility risk assessment and recommendations, and has the potential to provide effective risk communication [153]. This fertility-specific risk communication tool addresses two prerequisites for behavior modification: education and personalized risk [149,154]. Although FertiSTAT does not include environmental/occupational exposures, women may select individualized risk factors (e.g., age), reproductive factors (e.g., PID and STI), lifestyle factors (alcohol, illegal drugs, caffeine, smoking, stress, BMI > 25, unprotected sex with multiple partners), as well as indicators for male infertility (postpubertal mumps, undescended testicles) to achieve an infertility risk profile [153]. An Australian program – FAST (Fertility ASsessment and advice Targeting lifestyle choices and behaviors) provides infertility patients with individualized counseling and support, which has proved successful in a pilot study [155]. A similar Dutch lifestyle intervention incorporated fertility nurses in the provision of preconception care [156]. Characteristics of successful lifestyle interventions include structured approach, involvement of trained health-care professionals, and a patient-centered and motivational approach to help achieve behavior changes and optimize fertility [11,155,156].

    Barriers to Risk Mitigation

    Comprehensive sexual and reproductive health education, which includes signs and symptoms of reproductive health problems and consequences of STI, such as cancer and infertility, is essential for adolescents and adults, and yet rarely delivered [43,157]. Fundamental gaps in

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