U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Environmental Toxins and Infertility

; .

Author Information and Affiliations

Last Update: June 7, 2023.

Continuing Education Activity

Environmental toxins can have a profound impact on reproductive health, including fertility. This activity reviews the appropriate fertility workup with targeted screening for environmental exposures, discusses toxins known to impact fertility, and outlines treatment and prevention tactics by an interprofessional team.


  • Describe the general workup for infertility, focusing on identifying environmental toxin exposure.
  • Identify environmental toxins known to affect male and female fertility.
  • Outline treatment and prevention recommendations, including at government and policy levels.
  • Review the case for environmental toxin exposure as a source of health disparity.
Access free multiple choice questions on this topic.


Infertility is defined as the inability to conceive following a year of regular unprotected intercourse or donor insemination. This definition is reduced to 6 months for women over 35 or with other known risk factors for infertility.[1] In the United States, 13.1% percent of women aged 15 to 49 have known infertility based on 2015 through 2017 national survey data.[2] Numerous etiologies for infertility exist, including ovulatory dysfunction, diminished ovarian reserve, tubal factor, male factor, multifactorial etiologies, and unexplained infertility.     

Environmental toxins are ubiquitous and sometimes implicated in infertility development, either through anatomical abnormalities or endocrinological dysfunction. Based on a National Health and Nutrition Survey from 2003 through 2004, pregnant women in the United States are exposed to 43 or more different potential chemical toxins.[3] Knowledge and experience in evaluating exposure to environmental toxins are critical for any reproductive endocrinology and infertility specialist. 

Environmental toxins affect individuals throughout the lifespan, including prenatally, and can have various effects, from increasing cancer risk to ovulatory dysfunction to altered semen quality. This article is a focused review on the specific toxins known to influence fertility and the recommended evaluation, treatment, and prognosis for these patients.

Issues of Concern

Environmental Toxins Associated with Infertility

Endocrine Disrupting Chemicals 

Endocrine Disrupting Chemicals (EDCs) are exogenous chemicals that, when exposed, specifically in utero or puberty, can contribute to both female and male infertility and predispose to the development of other diseases that affect fertility as obesity, diabetes, and endocrine cancers (Birnbaum). 

EDCs derive from various sources, including plant-derived phytoestrogens (such as soy products), industrial chemicals (such as flame retardants, pesticides, and lubricants), household consumables (such as bisphenol A [BPA] products, phthalates, tea, and lavender oils), and pharmaceutical products (such as diethylstilbestrol [DES] and estradiol).  

DES may be the most infamous of these compounds. DES was used primarily in the 1950s and 1960s in pregnant mothers for miscarriage prevention until DES exposure in utero was associated with developing vaginal clear cell adenocarcinoma (CCA) in female children. Exposure in offspring resulted in congenital anomalies in the reproductive tract and adverse pregnancy outcomes rendering affected women infertile or sub-fertile (Figure 1). Though most of these women are past reproductive age at this point, its historical use is still relevant for the increased risk for CCA and cervical cancer.[4][5]  

EDCs disrupt the human endocrine system by either increasing or decreasing the production of endogenous hormones or altering the peripheral distribution of endogenous hormones.[6] This may happen through several proposed molecular pathways, though the nuclear receptor pathway is the most established. In this pathway, EDCs bind to the hormone receptors for estrogens, progestins, androgens, and thyroid hormones, either disrupting or augmenting their cellular activity.[7] Other proposed mechanisms exist, including the likelihood of prenatal and early exposure leading to epigenetic effects, predisposing individuals to various disease processes such as rare cancers, obesity, and endocrine disorders such as diabetes.[8][9]

In terms of fertility concerns specifically, EDCs have been linked with reproductive development disorders, ovarian dysfunction, subfertility, and polycystic ovarian syndrome (PCOS) in women. As far as reproductive development, the most striking example is DES as above. However, animal models have suggested an association of BPA with ovarian cysts, uterine polyps, vaginal adenosis, and impaired implantation in in-vitro fertilization (IVF) patients.[10][11] 

Higher serum BPA concentrations were seen in women with PCOS, with increasing evidence of insulin resistance and hyperandrogenism associated with increasing BPA concentrations.[12] Other EDCs have also been associated with ovarian dysfunction and infertility as well. Exposure to polychlorinated biphenyls (PCBs), used in electrical equipment, has been associated with a more extended period of trying to conceive before achieving pregnancy and worse fertilization rates in those undergoing IVF.[13][14] Increased exposure to phthalates, commonly found in plastics, has been demonstrated to be associated with lower antral follicle counts and mature oocyte numbers in patients undergoing IVF.[15][16]

EDCs have also been associated with male infertility. Dichlorodiphenyltrichloroethane (DDT), for example, is a metabolite of a pesticide no longer used in the United States but still in use globally, has been shown to reduce sperm concentration, normal morphology, and motility in semen analyses.[17] Similarly, BPA exposure has been shown to negatively affect sperm quality in epidemiological studies.[18]  

Beyond reproductive organs, EDCs also affect other aspects of the endocrine system that also impact fertility, such as the thyroid, including abnormalities in metabolism and transport, resulting in an association with hypothyroidism.[19]

Heavy Metals 

Heavy metal exposure has also been implicated in infertility. Exposure can come from the natural environment and housing/work environments, as in the case of lead exposure through paint or mercury and arsenic exposure through food and water supply. Heavy metals that have been found to affect reproductive activity include lead, mercury, cadmium, and arsenic. 

Individuals can be exposed to lead from a variety of sources, including, but not limited to, lead paints, water from lead pipes, cosmetics, construction sites, and herbal supplements. In patients identified as high risk based on exposure, a venous blood level can be collected. A lead level >15.47 ppb is associated with a twofold infertility risk compared to individuals below that threshold.[20] Increased lead exposure has also been associated with an increased risk for spontaneous abortion and preterm birth.[21][22] Treatment of elevated blood leads levels during the preconception period either entails identifying and eliminating environmental exposures or chelation in severe cases. 

Mercury exposure usually comes from diet, primarily from predatory fish consumption. Mercury enters the seascape via industrial waste sources and accumulates in predatory fish. Other less common sources are women exposed to gold mining and some skin-lightening creams.[23] While mercury toxicity in pregnant women is usually linked with neurodevelopmental disorders in offspring, there is also an association with female infertility.[24][25] Treatment in the preconception period of elevated mercury levels again hinges on identifying and eliminating exposure and chelation only in cases of very high levels of mercury toxicity. 

Cadmium exposure can stem from rechargeable batteries and certain paints and plastics. It can enter the food supply through resorption in the soil, resulting in cadmium exposure in various foods, including rice, wheat, leafy vegetables, and shellfish.[26] Increased cadmium levels are also noted in cigarette smokers (discussed below). In a small prospective study of infertile couples undergoing IVF, decreased oocyte fertilization rates and implantation rates were noted in patients with increased cadmium levels, though further research is needed.[27][28] Treatment in the preconception period of elevated cadmium levels is again identification and elimination of exposure and chelation in cases of very high toxicity levels.  

Arsenic exposure usually comes from certain groundwater sources, though it can also stem from certain pesticides and industrial exposures. Arsenic is primarily associated with otherwise unexplained male factor infertility.[29] Treatment involves exposure elimination only, as it quickly clears from the bloodstream. 


Smoking is a known environmental exposure that is modifiable, that influences fertility. Cigarette smoking is an important environmental toxin to consider, as 17.8% of adults in the United States smoke.[30] Cigarette smoking is most frequently considered prenatally associated with various adverse pregnancy outcomes such as preterm birth and placental abruption. However, it has also been shown to affect fertility in a dose-dependent manner.[31] It is theorized that the accumulation of cadmium and cotinine (a major nicotine metabolite) in follicular fluid in the ovaries compromises oocyte quality, thus resulting in infertility. It is worth noting that even when the female herself is a nonsmoker but lives with a smoker, cotinine levels are still elevated.[32][33]

In smoking men, there is evidence of reduced sperm concentration and motility, as well as evidence in animal studies that smoking may reduce sperm’s ability to bind to the zona pellucida for fertilization.[34]

In a meta-analysis of seven studies, it was noteworthy that in patients undergoing assisted reproduction, such as IVF, smokers require twice as many IVF cycles before conception compared to nonsmokers.[35]

Clinical Significance

Understanding environmental toxins' effect on infertility is clinically significant, as it is preventable, and in some instances, modifiable once already exposed.

Treatment and Prevention

In certain cases, toxicity can be treated, such as in the case of heavy metal exposure. Additionally, with cigarette smoking, return to normal fecundity is noted with smoking cessation, making cessation counseling of utmost importance during an evaluation for infertility.[36] In other cases, such as exposure to EDCs, prevention is the primary aim. 

Prevention of environmental toxin exposure comes from individual action and community and policy level change. Reproductive health providers are especially poised for exposure prevention, as they can identify at-risk patients during pre-conception counseling and pregnancy, perhaps even preventing prenatal exposure. Providers can prevent exposure through appropriate reporting and patient education. If a patient is found to have an exposure-related illness or suspected exposure based on screening, the case should be referred to occupational medicine programs or an Environmental Health Specialty Unit.[37]

Patient education is extremely important and can be done easily through counseling and education pamphlets to prevent or minimize exposure. A specific example of this includes a research study that showed that transitioning a child's food consumption to an organic diet significantly reduces organophosphate pesticide metabolite concentration in the urine.[38] 

Another study found that avoiding sources of bisphenol A, such as canned food, reduced levels of bisphenol A in study participants.[39] Based on this literature, dietary recommendations for patients to reduce environmental toxin exposure primarily involve moving towards a diet dominated by fruit, vegetables, and whole grains, avoiding processed foods and fast foods, and avoiding products containing known EDCs like BPA. 

Large-scale prevention will ultimately involve policy change. Several academic societies, including the American Society of Reproductive Medicine and the Endocrine Society, have called for public policy change to regulate environmental toxin exposure. These statements urge the United States Environmental Protection Agency and other involved government agencies to analyze substances made available to the public for their effect on human health. 

Certain actions have already been taken to reduce specific exposures, such as banning certain EDCs like DES by the Food and Drug Administration. BPA has also been regulated by banning its presence in various early life products such as baby bottles and infant formula.[40]

Other Issues

It is important to consider environmental disparities in the process of identifying high-risk patients in a screening evaluation for exposure to environmental toxins. Studies in the United States have shown that the presence of various toxins such as air pollutants, lead, and pesticides are increased in communities with a lower socioeconomic status.[41] Additionally, socioeconomically disadvantaged populations, such as low-wage immigrants, are more likely to have occupational exposures, such as organophosphate pesticides.[42]

For patients identified as high risk based on their community, socioeconomic status, or occupation, it is necessary to include a comprehensive screening evaluation of environmental exposures when evaluating for etiologies of infertility if it is not already routine.[43]

Enhancing Healthcare Team Outcomes

Screening, treatment, and prevention of fertility-altering environmental toxins requires action amongst women’s health providers and reproductive infertility specialists and their ancillary staff and requires cooperation and active management by local government, environmental agencies, and public policymakers. By enacting treatment and change in environmental exposures from the individual to government level, the effects of environmental toxins on infertility can be minimized and ideally even be entirely prevented.[1]

Review Questions

Classic “T-shaped” uterus on hysterosalpingogram in a 28-year-old female with uterine factor infertility secondary to in utero DES exposure Used with permission of: Zafarani F, Ahmadi F, Shahrzad G


Classic “T-shaped” uterus on hysterosalpingogram in a 28-year-old female with uterine factor infertility secondary to in utero DES exposure Used with permission of: Zafarani F, Ahmadi F, Shahrzad G. Hysterosalpingography in The Assessment (more...)


Practice Committee of the American Society for Reproductive Medicine. Electronic address: asrm@asrm.org. Definitions of infertility and recurrent pregnancy loss: a committee opinion. Fertil Steril. 2020 Mar;113(3):533-535. [PubMed: 32115183]
Perez Capotosto M, Jurgens CY. Exploring Fertility Awareness Practices Among Women Seeking Pregnancy. Nurs Womens Health. 2020 Dec;24(6):413-420. [PubMed: 33157071]
Woodruff TJ, Zota AR, Schwartz JM. Environmental chemicals in pregnant women in the United States: NHANES 2003-2004. Environ Health Perspect. 2011 Jun;119(6):878-85. [PMC free article: PMC3114826] [PubMed: 21233055]
Herbst AL, Ulfelder H, Poskanzer DC. Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women. N Engl J Med. 1971 Apr 22;284(15):878-81. [PubMed: 5549830]
Troisi R, Hatch EE, Palmer JR, Titus L, Robboy SJ, Strohsnitter WC, Herbst AL, Adam E, Hyer M, Hoover RN. Prenatal diethylstilbestrol exposure and high-grade squamous cell neoplasia of the lower genital tract. Am J Obstet Gynecol. 2016 Sep;215(3):322.e1-8. [PMC free article: PMC5003722] [PubMed: 26979629]
Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AM, Zoeller RT, Gore AC. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev. 2009 Jun;30(4):293-342. [PMC free article: PMC2726844] [PubMed: 19502515]
Schug TT, Janesick A, Blumberg B, Heindel JJ. Endocrine disrupting chemicals and disease susceptibility. J Steroid Biochem Mol Biol. 2011 Nov;127(3-5):204-15. [PMC free article: PMC3220783] [PubMed: 21899826]
Gore AC, Chappell VA, Fenton SE, Flaws JA, Nadal A, Prins GS, Toppari J, Zoeller RT. EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr Rev. 2015 Dec;36(6):E1-E150. [PMC free article: PMC4702494] [PubMed: 26544531]
Stel J, Legler J. The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals. Endocrinology. 2015 Oct;156(10):3466-72. [PMC free article: PMC4588824] [PubMed: 26241072]
Newbold RR, Jefferson WN, Padilla-Banks E. Prenatal exposure to bisphenol a at environmentally relevant doses adversely affects the murine female reproductive tract later in life. Environ Health Perspect. 2009 Jun;117(6):879-85. [PMC free article: PMC2702400] [PubMed: 19590677]
Peretz J, Vrooman L, Ricke WA, Hunt PA, Ehrlich S, Hauser R, Padmanabhan V, Taylor HS, Swan SH, VandeVoort CA, Flaws JA. Bisphenol a and reproductive health: update of experimental and human evidence, 2007-2013. Environ Health Perspect. 2014 Aug;122(8):775-86. [PMC free article: PMC4123031] [PubMed: 24896072]
Kandaraki E, Chatzigeorgiou A, Livadas S, Palioura E, Economou F, Koutsilieris M, Palimeri S, Panidis D, Diamanti-Kandarakis E. Endocrine disruptors and polycystic ovary syndrome (PCOS): elevated serum levels of bisphenol A in women with PCOS. J Clin Endocrinol Metab. 2011 Mar;96(3):E480-4. [PubMed: 21193545]
Cooper GS, Klebanoff MA, Promislow J, Brock JW, Longnecker MP. Polychlorinated biphenyls and menstrual cycle characteristics. Epidemiology. 2005 Mar;16(2):191-200. [PubMed: 15703533]
Younglai EV, Foster WG, Hughes EG, Trim K, Jarrell JF. Levels of environmental contaminants in human follicular fluid, serum, and seminal plasma of couples undergoing in vitro fertilization. Arch Environ Contam Toxicol. 2002 Jul;43(1):121-6. [PubMed: 12045882]
Messerlian C, Souter I, Gaskins AJ, Williams PL, Ford JB, Chiu YH, Calafat AM, Hauser R., Earth Study Team. Urinary phthalate metabolites and ovarian reserve among women seeking infertility care. Hum Reprod. 2016 Jan;31(1):75-83. [PMC free article: PMC4677966] [PubMed: 26573529]
Hauser R, Gaskins AJ, Souter I, Smith KW, Dodge LE, Ehrlich S, Meeker JD, Calafat AM, Williams PL., EARTH Study Team. Urinary Phthalate Metabolite Concentrations and Reproductive Outcomes among Women Undergoing in Vitro Fertilization: Results from the EARTH Study. Environ Health Perspect. 2016 Jun;124(6):831-9. [PMC free article: PMC4892919] [PubMed: 26545148]
De Jager C, Farias P, Barraza-Villarreal A, Avila MH, Ayotte P, Dewailly E, Dombrowski C, Rousseau F, Sanchez VD, Bailey JL. Reduced seminal parameters associated with environmental DDT exposure and p,p'-DDE concentrations in men in Chiapas, Mexico: a cross-sectional study. J Androl. 2006 Jan-Feb;27(1):16-27. [PubMed: 16400073]
Li DK, Zhou Z, Miao M, He Y, Wang J, Ferber J, Herrinton LJ, Gao E, Yuan W. Urine bisphenol-A (BPA) level in relation to semen quality. Fertil Steril. 2011 Feb;95(2):625-30.e1-4. [PubMed: 21035116]
Oulhote Y, Chevrier J, Bouchard MF. Exposure to Polybrominated Diphenyl Ethers (PBDEs) and Hypothyroidism in Canadian Women. J Clin Endocrinol Metab. 2016 Feb;101(2):590-8. [PubMed: 26606679]
Lei HL, Wei HJ, Ho HY, Liao KW, Chien LC. Relationship between risk factors for infertility in women and lead, cadmium, and arsenic blood levels: a cross-sectional study from Taiwan. BMC Public Health. 2015 Dec 09;15:1220. [PMC free article: PMC4673771] [PubMed: 26653029]
Jelliffe-Pawlowski LL, Miles SQ, Courtney JG, Materna B, Charlton V. Effect of magnitude and timing of maternal pregnancy blood lead (Pb) levels on birth outcomes. J Perinatol. 2006 Mar;26(3):154-62. [PubMed: 16453008]
Borja-Aburto VH, Hertz-Picciotto I, Rojas Lopez M, Farias P, Rios C, Blanco J. Blood lead levels measured prospectively and risk of spontaneous abortion. Am J Epidemiol. 1999 Sep 15;150(6):590-7. [PubMed: 10489998]
Chan TY. Inorganic mercury poisoning associated with skin-lightening cosmetic products. Clin Toxicol (Phila). 2011 Dec;49(10):886-91. [PubMed: 22070559]
Grandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K, Murata K, Sørensen N, Dahl R, Jørgensen PJ. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol. 1997 Nov-Dec;19(6):417-28. [PubMed: 9392777]
Maeda E, Murata K, Kumazawa Y, Sato W, Shirasawa H, Iwasawa T, Izumo K, Tatsuta N, Sakamoto M, Terada Y. Associations of environmental exposures to methylmercury and selenium with female infertility: A case-control study. Environ Res. 2019 Jan;168:357-363. [PubMed: 30384229]
Järup L, Berglund M, Elinder CG, Nordberg G, Vahter M. Health effects of cadmium exposure--a review of the literature and a risk estimate. Scand J Work Environ Health. 1998;24 Suppl 1:1-51. [PubMed: 9569444]
Bloom MS, Parsons PJ, Steuerwald AJ, Schisterman EF, Browne RW, Kim K, Coccaro GA, Conti GC, Narayan N, Fujimoto VY. Toxic trace metals and human oocytes during in vitro fertilization (IVF). Reprod Toxicol. 2010 Jun;29(3):298-305. [PMC free article: PMC2882801] [PubMed: 20096775]
Bloom MS, Fujimoto VY, Steuerwald AJ, Cheng G, Browne RW, Parsons PJ. Background exposure to toxic metals in women adversely influences pregnancy during in vitro fertilization (IVF). Reprod Toxicol. 2012 Nov;34(3):471-81. [PubMed: 22732149]
Wang X, Zhang J, Xu W, Huang Q, Liu L, Tian M, Xia Y, Zhang W, Shen H. Low-level environmental arsenic exposure correlates with unexplained male infertility risk. Sci Total Environ. 2016 Nov 15;571:307-13. [PubMed: 27485131]
Jamal A, Agaku IT, O'Connor E, King BA, Kenemer JB, Neff L. Current cigarette smoking among adults--United States, 2005-2013. MMWR Morb Mortal Wkly Rep. 2014 Nov 28;63(47):1108-12. [PMC free article: PMC5779518] [PubMed: 25426653]
Baird DD, Wilcox AJ. Cigarette smoking associated with delayed conception. JAMA. 1985 May 24-31;253(20):2979-83. [PubMed: 3999259]
Zenzes MT, Krishnan S, Krishnan B, Zhang H, Casper RF. Cadmium accumulation in follicular fluid of women in in vitro fertilization-embryo transfer is higher in smokers. Fertil Steril. 1995 Sep;64(3):599-603. [PubMed: 7641916]
Zenzes MT, Reed TE, Wang P, Klein J. Cotinine, a major metabolite of nicotine, is detectable in follicular fluids of passive smokers in in vitro fertilization therapy. Fertil Steril. 1996 Oct;66(4):614-9. [PubMed: 8816626]
Pasqualotto FF, Umezu FM, Salvador M, Borges E, Sobreiro BP, Pasqualotto EB. Effect of cigarette smoking on antioxidant levels and presence of leukocytospermia in infertile men: a prospective study. Fertil Steril. 2008 Aug;90(2):278-83. [PubMed: 18462724]
Soares SR, Simon C, Remohí J, Pellicer A. Cigarette smoking affects uterine receptiveness. Hum Reprod. 2007 Feb;22(2):543-7. [PubMed: 17095517]
Howe G, Westhoff C, Vessey M, Yeates D. Effects of age, cigarette smoking, and other factors on fertility: findings in a large prospective study. Br Med J (Clin Res Ed). 1985 Jun 08;290(6483):1697-700. [PMC free article: PMC1416131] [PubMed: 3924219]
Sathyanarayana S, Focareta J, Dailey T, Buchanan S. Environmental exposures: how to counsel preconception and prenatal patients in the clinical setting. Am J Obstet Gynecol. 2012 Dec;207(6):463-70. [PubMed: 22440197]
Lu C, Toepel K, Irish R, Fenske RA, Barr DB, Bravo R. Organic diets significantly lower children's dietary exposure to organophosphorus pesticides. Environ Health Perspect. 2006 Feb;114(2):260-3. [PMC free article: PMC1367841] [PubMed: 16451864]
Rudel RA, Gray JM, Engel CL, Rawsthorne TW, Dodson RE, Ackerman JM, Rizzo J, Nudelman JL, Brody JG. Food packaging and bisphenol A and bis(2-ethyhexyl) phthalate exposure: findings from a dietary intervention. Environ Health Perspect. 2011 Jul;119(7):914-20. [PMC free article: PMC3223004] [PubMed: 21450549]
Erler C, Novak J. Bisphenol a exposure: human risk and health policy. J Pediatr Nurs. 2010 Oct;25(5):400-7. [PubMed: 20816563]
Adamkiewicz G, Zota AR, Fabian MP, Chahine T, Julien R, Spengler JD, Levy JI. Moving environmental justice indoors: understanding structural influences on residential exposure patterns in low-income communities. Am J Public Health. 2011 Dec;101 Suppl 1(Suppl 1):S238-45. [PMC free article: PMC3222513] [PubMed: 21836112]
Hines CJ, Nilsen Hopf NB, Deddens JA, Calafat AM, Silva MJ, Grote AA, Sammons DL. Urinary phthalate metabolite concentrations among workers in selected industries: a pilot biomonitoring study. Ann Occup Hyg. 2009 Jan;53(1):1-17. [PubMed: 18948546]
McCauley LA. Immigrant workers in the United States: recent trends, vulnerable populations, and challenges for occupational health. AAOHN J. 2005 Jul;53(7):313-9. [PubMed: 16097105]

Disclosure: Meaghan Jain declares no relevant financial relationships with ineligible companies.

Disclosure: Manvinder Singh declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK576379PMID: 35015404


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...