Tiny air pollution particles may lead to reduced sperm production

Particulate air pollution linked with reduced sperm production in mice, 2019

New Orleans, LA – Exposure to tiny air pollution particles may lead to reduced sperm production, suggests new research in mice, presented Monday, March 25 at ENDO 2019, the Endocrine Society’s annual meeting.

“Infertility rates are increasing around the world, and air pollution may be one of the main factors,”

said lead researcher Elaine Maria Frade Costa, M.D., Ph.D., of Sao Paulo University in Sao Paulo, Brazil.

The World Health Organization (WHO) estimates that approximately 15 percent of the global population has difficulty with fertility, and male infertility accounts for about half of those problems.

The study looked at the effect of particulate matter (PM) on sperm production. PM is a mixture of solid particles and liquid droplets found in the air. PM2.5 is a fine inhalable particle with diameters that are 2.5 micrometers or smaller. The average human hair is about 70 micrometers in diameters, making it 30 times larger than the biggest fine particle. PM2.5 is known to disrupt the endocrine system in humans and animals. The endocrine system is involved in reproduction, including the production of sperm.

The study included four groups of mice. One was exposed to PM2.5 from Sao Paolo before and after birth, from the day they were weaned from their mother’s milk until adulthood. The second group was exposed only during gestation. The third group was exposed after birth from weaning until adulthood; and the fourth group was exposed only to filtered air during gestation and from the time they were weaned until adulthood.

The researchers analyzed the testes of the mice and their production of sperm. DNA tests were used to evaluate gene expression, the process by which genes in DNA provide instructions for proteins.

The tubes in the testes that produce sperm of all the exposed mice showed signs of deterioration. In comparison with the mice not exposed to PM2.5, the sperm of the first group, which was exposed before and after birth, was of significantly worse quality.

The exposure to PM2.5 led to changes in the levels of genes related to testicular cell function. Exposure to PM2.5 after birth seemed to be the most harmful to testicular function, the study found.

Costa said these changes are epigenetic, which means they are not caused by changes in the DNA sequence. Epigenetic changes can switch genes on or off and determine which proteins a gene expresses.

The research demonstrates for the first time that exposure to air pollution of a large city impairs production of sperm through epigenetics, mainly in exposure after birth, Costa said.

“These findings provide more evidence that governments need to implement public policies to control air pollution in big cities,”

she said. Reference. Featured image.

Impact of male factor infertility on offspring health and development

Long-term health and developmental outcomes in children conceived with intracytoplasmic sperm injection

2019 Study Abstract

Monitoring the safety of intracytoplasmic sperm injection (ICSI) has been impeded by uncertainties regarding the extent to which offspring health is influenced by paternal characteristics linked to male infertility or the processes that ICSI treatment entails.

Few studies examining long-term health and developmental outcomes in children conceived with ICSI have considered the influence of paternal infertility adequately.

In the available literature, large population-based studies suggest underlying male factors, and the severity of male factor infertility, increase the risk of mental retardation and autism in offspring, as does the ICSI procedure itself, but these findings have not been replicated consistently.

Robust evidence of the influence of male factors on other health outcomes is lacking, with many studies limited by sample size.

Nevertheless, emerging evidence suggests children conceived with ICSI have increased adiposity, particularly girls.

Further, young men conceived with ICSI may have impaired spermatogenesis; the mechanisms underlying this remain unclear, with inconclusive evidence of inheritance of Y chromosome microdeletions.

The current inconsistent and often sparse literature concerning the long-term health of children conceived with ICSI, and the specific influence of male infertility factors, underscore the need for concerted monitoring of children conceived with this technique across the lifespan.

With the rapid expansion of use of ICSI for non-male factors, sufficiently large studies that compare outcomes between groups conceived with this technique for male factors versus non-male factors will provide critical evidence to elucidate the intergenerational impact of male infertility.

Reference. Image credit fertilitysmarts.

Why are ObGyns Talking Toxins ?

Let’s make environmental health part of health care

Doctors from 125 countries want policies to prevent exposure to toxic chemicals

Produced for PRHE by Susan Lamontagne, Public Interest Media Group, for the International Federation of Gynecology and Obstetrics (FIGO) XXI World Congress on September 30, 2015.

Why are Doctors Talking Toxins ?

And how to reduce exposure to toxic chemicals worldwide ?

It’s time to shift the burden of proof, from scientists, back to the chemical industry

Video published on 5 June 2019, by UCSF Program on Reproductive Health and the Environment.

PFCs chemicals impact young men fertility, Endocrine Society reports

Endocrine Disruption of Androgenic Activity by Perfluoroalkyl Substances: Clinical and Experimental Evidence, 2019

Perfluoroalkyl compounds (PFCs) are a class of organic molecules that are used in many everyday products such as oil and water repellents, coatings for cookware, carpets, and textiles.

The crucial emerging role of PFCs as pollutants of water, soil, and air and their persistent level in males warrant for more investigation on the mechanisms of PFC toxicity in humans.

There is a new reason to be concerned about toxic chemicals used in nonstick pans, waterproof products, and firefighting foam: PFCs impair male reproductive health, according to a recent study, the intercept reports.


Considerable attention has been paid to perfluoroalkyl compounds (PFCs) because of their worldwide presence in humans, wildlife, and environment. A wide variety of toxicological effects is well supported in animals, including testicular toxicity and male infertility. For these reasons, the understanding of epidemiological associations and of the molecular mechanisms involved in the endocrine-disrupting properties of PFCs on human reproductive health is a major concern.

To investigate the relationship between PFC exposure and male reproductive health.

This study was performed within a screening protocol to evaluate male reproductive health in high schools.

This is a cross-sectional study on 212 exposed males from the Veneto region, one of the four areas worldwide heavily polluted with PFCs, and 171 nonexposed controls.

Main Outcome Measures
Anthropometrics, seminal parameters, and sex hormones were measured in young males from exposed areas compared with age-matched controls. We also performed biochemical studies in established experimental models.

We found that increased levels of PFCs in plasma and seminal fluid positively correlate with circulating testosterone (T) and with a reduction of semen quality, testicular volume, penile length, and anogenital distance. Experimental evidence points toward an antagonistic action of perfluorooctanoic acid on the binding of T to androgen receptor (AR) in a gene reporter assay, a competition assay on an AR-coated surface plasmon resonance chip, and an AR nuclear translocation assay.

This study documents that PFCs have a substantial impact on human health as they interfere with hormonal pathways, potentially leading to male infertility.

Effect of environmental and pharmaceutical exposures on fetal testis development and function

A systematic review of human experimental data, 2019


Overall, the incidence of male reproductive disorders has increased in recent decades. Testicular development during fetal life is crucial for subsequent male reproductive function. Non-genomic factors such as environmental chemicals, pharmaceuticals and lifestyle have been proposed to impact on human fetal testicular development resulting in subsequent effects on male reproductive health. Whilst experimental studies using animal models have provided support for this hypothesis, more recently a number of experimental studies using human tissues and cells have begun to translate these findings to determine direct human relevance.

The objective of this systematic review was to provide a comprehensive description of the evidence for effects of prenatal exposure(s) on human fetal testis development and function. We present the effects of environmental, pharmaceutical and lifestyle factors in experimental systems involving exposure of human fetal testis tissues and cells. Comparison is made with existing epidemiological data primarily derived from a recent meta-analysis.

For identification of experimental studies, PubMed and EMBASE were searched for articles published in English between 01/01/1966 and 13/07/2018 using search terms including ‘endocrine disruptor’, ‘human’, ‘fetal’, ‘testis’, ‘germ cells’, ‘testosterone’ and related search terms. Abstracts were screened for selection of full-text articles for further interrogation. Epidemiological studies involving exposure to the same agents were extracted from a recent systematic review and meta-analysis. Additional studies were identified through screening of bibliographies of full-texts of articles identified through the initial searches.

A total of 25 experimental studies and 44 epidemiological studies were included. Consistent effects of analgesic and phthalate exposure on human fetal germ cell development are demonstrated in experimental models, correlating with evidence from epidemiological studies and animal models. Furthermore, analgesic-induced reduction in fetal testosterone production, which predisposes to the development of male reproductive disorders, has been reported in studies involving human tissues, which also supports data from animal and epidemiological studies. However, whilst reduced testosterone production has been demonstrated in animal studies following exposure(s) to a variety of environmental chemicals including phthalates and bisphenol A, these effects are not reproduced in experimental approaches using human fetal testis tissues. Image credit academic.oup.

Direct experimental evidence for effects of prenatal exposure(s) on human fetal testis development and function exists. However, for many exposures the data is limited. The increasing use of human-relevant models systems in which to determine the effects of environmental exposure(s) (including mixed exposures) on development and function of human tissues should form an important part of the process for assessment of such exposures by regulatory bodies to take account of animal-human differences in susceptibility.

The negative impact of the environment on methylation/epigenetic marking in gametes and embryos

A plea for action to protect the fertility of future generations, 17 January 2019


Life expectancy has increased since World War II and this may be attributed to several aspects of modern lifestyles. However, now we are faced with a downturn, which seems to be the result of environmental issues. This paradigm is paralleled with a reduction in human fertility: decreased sperm quality and increased premature ovarian failure and diminished ovarian reserve syndromes.

Endocrine Disruptor Compounds (EDCs) and other toxic chemicals: herbicides, pesticides, plasticizers, to mention a few, are a rising concern in today environment. Some of these are commonly used in the domestic setting: cleaning material and cosmetics and they have a known impact on epigenesis and imprinting via perturbation of methylation processes. Pollution from Poly Aromatic Hydrocarbons (PAH), particulate matter (PM), <10 and <2.5 μm and ozone, released into the air all affect fertility. Poor food processing management is a source DNA adducts formation, impairing gametes quality. An important question to be answered is that of nanoparticles (NPs) that are present in food and which are thought to induce oxidative stress. Now is the time to take a step backwards. Global management of the environment and food production is required urgently in order to protect the fertility of future generations.


DES and the GENES

Impact of endocrine disrupting chemicals exposure on fecundity as measured by time to pregnancy

A systematic review;, Environmental research, 2018 Dec


Emerging scientific evidence suggests that exposure to environmental pollutants is associated with negative effects on fecundity as measured by time to pregnancy (TTP).

To conduct a systematic review of the literature on the association between selected endocrine disrupting chemicals (EDCs), and fecundity as measured by TTP in humans. Compounds included in this review are: brominated flame retardants (BFRs) such as hexabromocyclododecane, tetrabromobiphenol A and polybrominated diphenyl ethers; organophosphates flame retardants (OPFRs); and phthalates.

Scopus, MEDLINE via Ebscohost and EMBASE databases were searched for articles exploring the relationships between selected EDCs and fecundity as measured by time to pregnancy. We assessed the quality of included studies and evidence for causality was graded using the criteria developed by the World Cancer Research Fund.

14 studies of 191 full-text articles assessed for eligibility were included for qualitative synthesis. Five studies examined BFRs and 10 studies examined phthalates. Among the fourteen, one study assessed both BFRs and phthalates. There were no studies which investigated fecundity as measured by TTP on HBCD, TBBPA, or OPFRs. We recorded plausible fecundity outcomes as measured by TTP related to some of these EDCs. BFRs or phthalates increased TTP. However, results were inconsistent.

We recorded mostly weak associations between exposure to selected EDCs and fecundity. However, evidence was considered limited to conclude a causal relationship due to inconsistency of results. The health risks posed by these chemicals in exposed populations are only beginning to be recognized and prospective measurement of the environmental effects of the chemicals in large cohort studies are urgently needed to confirm these relationships and inform policies aimed at exposure prevention

Childhood obesity before 12 years of age appears to increase the risk of female infertility in later life

Association of childhood obesity with female infertility in adulthood: a 25-year follow-up study

2018 Study Abstract

To evaluate whether childhood obesity is associated with infertility in women’s reproductive-aged life.

Prospective longitudinal study.

Not applicable.


A total of 1,544 girls, aged 7–15 years in 1985, and who completed questionnaires at follow-up in 2004-2006 and/or 2009-2011.

Main Outcome Measure(s)
Infertility was defined as having difficulty conceiving (had tried for ≥12 months to become pregnant without succeeding) or having seen a doctor because of trouble becoming pregnant.

At ages from 7–11 years, girls at both the lower and upper end of the body mass index (BMI) z score had increased risk of infertility. Compared with normal weight girls, those with obesity at ages 7–11 years were more likely in adulthood to report infertility (adjusted relative risk [aRR] = 2.94, 95% confidence interval [CI] 1.48–5.84), difficulty conceiving (aRR = 3.89, 95% CI 1.95–7.77), or having seen a doctor because of trouble becoming pregnant (aRR = 3.65, 95% CI 1.90–7.02) after adjusting for childhood age, follow-up length, highest parental education, and marital status.

Childhood obesity before 12 years of age appears to increase the risk of female infertility in later life.

Le lien entre la prise de distilbène de la (grand-)mère et la stérilité de la descendance

Toute une histoire, vidéo publiée le 5 octobre 2015

Le distilbene est un “modèle” des perturbateurs endocriniens.

Le Distilbène DES, en savoir plus