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.

Strong associations between exposure to outdoor air contaminants and pediatric asthma in urban areas

Air Pollution and Pediatric Asthma, Collaborative on Health and the Environment, 2019

Listen to Dr. Michael Brauer and Dr. Erika Garcia giving an overview of their recent studies, which both demonstrated strong associations between exposure to outdoor air contaminants and pediatric asthma in urban areas. Reference.

Air pollution has been linked to the increased prevalence of pediatric asthma and reduced lung function growth in children. Children are more vulnerable to environmental contaminants including air pollution. They breathe more air per body weight than adults and their lungs and immune system are still developing. A number of studies have also shown that in utero exposure may be associated with the later development of pediatric asthma.

Farming causes harm to rural air quality, recent review says

A systematic review of the public health risks of bioaerosols from intensive farming

A recent review by he found evidence of respiratory problems in farm workers and raised concerns about exposure for people living close to intensive livestock farms, including some evidence of increased asthma in children, The Guardian reports.

Abstract

Background
Population growth, increasing food demands, and economic efficiency have been major driving forces behind farming intensification over recent decades. However, biological emissions (bioaerosols) from intensified livestock farming may have the potential to impact human health. Bioaerosols from intensive livestock farming have been reported to cause symptoms and/or illnesses in occupational-settings and there is concern about the potential health effects on people who live near the intensive farms. As well as adverse health effects, some potential beneficial effects have been attributed to farm exposures in early life. The aim of the study was to undertake a systematic review to evaluate potential for adverse health outcomes in populations living near intensive livestock farms.

Material and methods
Two electronic databases (PubMed and Scopus) and bibliographies were searched for studies reporting associations between health outcomes and bioaerosol emissions related to intensive farming published between January 1960 and April 2017, including both occupational and community studies. Two authors independently assessed studies for inclusion and extracted data. Risk of bias was assessed using a customized score.

Results
38 health studies met the inclusion criteria (21 occupational and 1 community study measured bioaerosol concentrations, 16 community studies using a proxy measure for exposure). The majority of occupational studies found a negative impact on respiratory health outcomes and increases in inflammatory biomarkers among farm workers exposed to bioaerosols. Studies investigating the health of communities living near intensive farms had mixed findings. All four studies of asthma in children found increased reported asthma prevalence among children living or attending schools near an intensive farm. Papers principally investigated respiratory and immune system outcomes.

Conclusions
The review indicated a potential impact of intensive farming on childhood respiratory health, based on a small number of studies using self-reported outcomes, but supported by findings from occupational studies. Further research is needed to measure and monitor exposure in community settings and relate this to objectively measured health outcomes.

First evidence of human exposure to microplastic through breathing indoor air

Simulating human exposure to indoor airborne microplastics using a Breathing Thermal Manikin

Researcher Alvise Vianello’s scientific report suggests that when we spend time indoors we are probably filling up our lungs with tiny plastic particles shed by all the plastic stuff filling our apartments, vice reports. Image credit Erica Cirino.

2019 Study Abstract

Humans are potentially exposed to microplastics through food, drink, and air. The first two pathways have received quite some scientific attention, while little is known about the latter. We address the exposure of humans to indoor airborne microplastics using a Breathing Thermal Manikin. Three apartments were investigated, and samples analysed through FPA-µFTIR-Imaging spectroscopy followed by automatic analyses down to 11 µm particle size. All samples were contaminated with microplastics, with concentrations between 1.7 and 16.2 particles m−3. Synthetic fragments and fibres accounted, on average, for 4% of the total identified particles, while nonsynthetic particles of protein and cellulose constituted 91% and 4%, respectively. Polyester was the predominant synthetic polymer in all samples (81%), followed by polyethylene (5%), and nylon (3%). Microplastics were typically of smaller size than nonsynthetic particles. As the identified microplastics can be inhaled, these results highlight the potential direct human exposure to microplastic contamination via indoor air.

Environmental Chemicals and Autism

A Scoping Review of the Human and Animal Research, 2019

The Endocrine Disruption Exchange newest scoping review finds that 152 environmental chemicals have been investigated in humans or animals for their association with autism. TEDX highlight the need for systematic review of lead, PCBs, and chlorpyrifos.

Abstract

Background
Estimates of autism prevalence have increased dramatically over the past two decades. Evidence suggests environmental factors may contribute to the etiology of the disorder.

Objectives
This scoping review aimed to identify and categorize primary research and reviews on the association between prenatal and early postnatal exposure to environmental chemicals and the development of autism in epidemiological studies and rodent models of autism.

Methods
PubMed was searched through 8 February 2018. Included studies assessed exposure to environmental chemicals prior to 2 months of age in humans or 14 d in rodents. Rodent studies were considered relevant if they included at least one measurement of reciprocal social communicative behavior or repetitive and stereotyped behavior. Study details are presented in interactive displays using Tableau Public.

Results
The search returned 21,603 unique studies, of which 54 epidemiological studies, 46 experimental rodent studies, and 50 reviews were deemed relevant, covering 152 chemical exposures. The most frequently studied exposures in humans were particulate matter (n=14), mercury (n=14), nonspecific air pollution (n=10), and lead (n=10). In rodent studies, the most frequently studied exposures were chlorpyrifos (n=9), mercury (n=6), and lead (n=4).

Discussion
Although research is growing rapidly, wide variability exists in study design and conduct, exposures investigated, and outcomes assessed. Conclusions focus on recommendations to guide development of best practices in epidemiology and toxicology, including greater harmonization across these fields of research to more quickly and efficiently identify chemicals of concern. In particular, we recommend chlorpyrifos, lead, and polychlorinated biphenyls (PCBs) be systematically reviewed in order to assess their relationship with the development of autism. There is a pressing need to move forward quickly and efficiently to understand environmental influences on autism in order to answer current regulatory questions and inform treatment and prevention efforts.

60 MiNueTs Toxic

UCSF Program on Reproductive Health and the Environment, 2017

Video published on 18 Apr 2019 by the UCSF Program on Reproductive Health and the Environment.

The University of California San Francisco (UCSF) Program on Reproductive Health and the Environment (PRHE)’s mission is to create a healthier environment for human reproduction and development through advancing scientific inquiry, clinical care and health policies that prevent exposures to harmful chemicals in our environment.

More Information

Adult and Prenatal Chemical Exposures

Breast Cancer Prevention Partners, with Tracey Woodruff, Ph.D., Mar 2019

  • How am I exposed to chemicals?
  • What are prenatal exposures?
  • How can I reduce my own personal exposures?
  • What more can I do to help make a change?

Featuring BCPP Science Advisory Panel member Tracey Woodruff, Ph.D., Director of the Program on Reproductive Health and the Environment, University of California, San Francisco, Professor in the Department of Obstetrics, Gynecology, and Reproductive Sciences and Philip R. Lee Institute for Health Policy Studies at UCSF

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.

Air pollution associated to psychotic experiences in young people

Association of Air Pollution Exposure With Psychotic Experiences During Adolescence

A new study finds that teens living in dirty air 70% more likely to have symptoms such as paranoia, the guardian reports. Image Duke University.

2019 Study Key Points

Question
Is exposure to air pollution associated with adolescent psychotic experiences?

Findings
In this nationally representative cohort study of 2232 UK-born children, significant associations were found between outdoor exposure to nitrogen dioxide, nitrogen oxides, and particulate matter and reports of psychotic experiences during adolescence. Moreover, nitrogen dioxide and nitrogen oxides together explained 60% of the association between urban residency and adolescent psychotic experiences.

Meaning
The association between urban residency and adolescent psychotic experiences is partly explained by the higher levels of outdoor air pollution in urban settings.

Abstract

Importance
Urbanicity is a well-established risk factor for clinical (eg, schizophrenia) and subclinical (eg, hearing voices and paranoia) expressions of psychosis. To our knowledge, no studies have examined the association of air pollution with adolescent psychotic experiences, despite air pollution being a major environmental problem in cities.

Objectives
To examine the association between exposure to air pollution and adolescent psychotic experiences and test whether exposure mediates the association between urban residency and adolescent psychotic experiences.

Design, Setting, and Participants
The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born during the period from January 1, 1994, through December 4, 1995, in England and Wales and followed up from birth through 18 years of age. The cohort represents the geographic and socioeconomic composition of UK households. Of the original cohort, 2066 (92.6%) participated in assessments at 18 years of age, of whom 2063 (99.9%) provided data on psychotic experiences. Generation of the pollution data was completed on October 4, 2017, and data were analyzed from May 4 to November 21, 2018.

Exposures
High-resolution annualized estimates of exposure to 4 air pollutants—nitrogen dioxide (NO2), nitrogen oxides (NOx), and particulate matter with aerodynamic diameters of less than 2.5 (PM2.5) and less than 10 μm (PM10)—were modeled for 2012 and linked to the home addresses of the sample plus 2 commonly visited locations when the participants were 18 years old.

Main Outcomes and Measures
At 18 years of age, participants were privately interviewed regarding adolescent psychotic experiences. Urbanicity was estimated using 2011 census data.

Results
Among the 2063 participants who provided data on psychotic experiences, sex was evenly distributed (52.5% female). Six hundred twenty-three participants (30.2%) had at least 1 psychotic experience from 12 to 18 years of age. Psychotic experiences were significantly more common among adolescents with the highest (top quartile) level of annual exposure to NO2 (odds ratio [OR], 1.71; 95% CI, 1.28-2.28), NOx (OR, 1.72; 95% CI, 1.30-2.29), and PM2.5 (OR, 1.45; 95% CI, 1.11-1.90). Together NO2 and NOx statistically explained 60% of the association between urbanicity and adolescent psychotic experiences. No evidence of confounding by family socioeconomic status, family psychiatric history, maternal psychosis, childhood psychotic symptoms, adolescent smoking and substance dependence, or neighborhood socioeconomic status, crime, and social conditions occurred.

Conclusions and Relevance
In this study, air pollution exposure—particularly NO2 and NOx—was associated with increased odds of adolescent psychotic experiences, which partly explained the association between urban residency and adolescent psychotic experiences. Biological (eg, neuroinflammation) and psychosocial (eg, stress) mechanisms are plausible.