People experienced less stress and anxiety while listening to nature soundscapes, but the addition of road traffic noise increased their stress and anxiety
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Manmade sounds such vehicle traffic can mask the positive impact of nature soundscapes on people’s stress and anxiety, according to a new study published November 27, 2024, in the open-access journal PLOS ONE by Paul Lintott of the University of the West of England, U.K., and Lia Gilmour of the Bat Conservation Trust, U.K.
Existing research shows that natural sounds, like birdsong, can lower blood pressure, heart, and respiratory rates, as well as self-reported stress and anxiety. Conversely, anthropogenic soundscapes, like traffic or aircraft noise, are hypothesized to have negative effects on human health and wellbeing in a variety of ways.
In the new study, 68 student volunteers listened to three 3-minute soundscapes: a nature soundscape recorded at sunrise in West Sussex, U.K., the same soundscape combined with 20 mile per hour road traffic sounds, and the same soundscape with 40 mile per hour traffic sounds. General mood and anxiety were assessed before and after the soundscapes using self-reported scales.
The study found that listening to a natural soundscape reduced self-reported stress and anxiety levels, and also enhanced mood recovery after a stressor. However, the benefits of improved mood associated with the natural soundscape was limited when traffic sounds were included. The natural soundscape alone was associated with the lowest levels of stress and anxiety, with the highest levels reported after the soundscape that included 40 mile per hour traffic.
The authors conclude that reducing traffic speed in urban areas might influence human health and wellbeing not only through its safety impacts, but also through its effect on natural soundscapes.
The authors add: “Our study shows that listening to natural soundscapes can reduce stress and anxiety, and that anthropogenic sounds such as traffic noise can mask potential positive impacts. Reducing traffic speeds in cities is therefore an important step towards more people experiencing the positive effects of nature on their health and wellbeing.”
A team of University of Utah chemists have found that carbon dioxide, well-known for being deadly at high concentrations, also has an important beneficial effect in preserving cell function. This is something not accounted for in most in vitro experiments of cell damage, and may have important consequences for understanding environments with high CO2 concentrations, like underground mines, submarines and spacecraft.
The cells in our bodies are like bustling cities, running on an iron-powered system that uses hydrogen peroxide (H₂O₂) not just for cleaning up messes but also for sending critical signals. Normally, this works fine, but under stress, such as inflammation or a burst of energy use, oxidative stress damages cells at the genetic level.
This is because iron and H₂O₂ react in what’s known as the Fenton reaction, producing hydroxyl radicals, destructive molecules that attack DNA and RNA indiscriminately. But there’s a catch. In the presence of carbon dioxide, our cells gain a secret weapon in the form of bicarbonate which helps keep pH levels balanced.
In this study, the researchers discovered that bicarbonate doesn’t just act as a pH buffer but also alters the Fenton reaction itself in cells. Instead of producing chaotic hydroxyl radicals, the reaction instead makes carbonate radicals, which affect DNA in a far less harmful way, according to Cynthia Burrows, a distinguished professor of chemistry and senior author of a study published this week in PNAS.
“So many diseases, so many conditions have oxidative stress as a component of disease. That would include many cancers, effectively all age-related diseases, a lot of neurological diseases,” Burrows said. “We’re trying to understand cells’ fundamental chemistry under oxidative stress. We have learned something about the protective effect of CO₂ that I think is really profound.”
Without bicarbonate or CO₂ present in experimental DNA oxidation reactions, the chemistry is also different. The free radical species generated, hydroxyl radical, is extremely reactive and hits DNA like a shotgun blast, causing damage everywhere, Burrows said.
In contrast, her team’s findings show that the presence of bicarbonate from dissolved CO₂ changes the reaction to make a milder radical striking only guanine, the G in our four-letter genetic code.
“Like throwing a dart at the bullseye where G is the center of the target,” Burrows said. “It turns out that bicarbonate is a major buffer inside your cells. Bicarbonate binds to iron, and it completely changes the Fenton reaction. You don’t make these super highly reactive radicals that everyone’s been studying for decades.”
What do these findings mean for science? Potentially a lot.
For starters, the team’s discovery shows cells are a lot smarter than previously imagined, which could reshape how we understand oxidative stress and its role in diseases like cancer or aging.
But it also raises the possibility that many scientists studying cell damage have been conducting laboratory experiments in ways that don’t reflect the real world, rendering their results suspect, Burrows said. Chemists and biologists everywhere grow cells in a tissue culture in an incubator set to 37°C. In these cultures, carbon dioxide levels are raised to 5%, or about 100 times more concentrated than what’s found in the atmosphere.
The elevated CO₂ recreates the environment the cells normally inhabit as they metabolise nutrients, however, it is lost when researchers start their experiments outside the incubator.
“Just like opening up a can of beer. You release the CO₂ when you take your cells out of the incubator. It’s like doing experiments with a day-old glass of beer. It’s pretty flat. It has lost the CO₂, its bicarbonate buffer,” Burrows said. “You no longer have the protection of CO₂ to modulate the iron-hydrogen peroxide reaction.”
She believes bicarbonate needs to be added to ensure reliable results from such experiments.
“Most people leave out bicarbonate/CO₂ when studying DNA oxidation because it is difficult to deal with the constant outgassing of CO₂,” Burrows said. “These studies suggest that to get an accurate picture of DNA damage that occurs from normal cellular processes like metabolism, researchers need to be careful to mimic the proper conditions of the cell and add bicarbonate, ie baking powder!”
Burrows anticipates her study could result in unintended outcomes that may someday benefit research in other areas. Her lab is seeking new funding from NASA, for example, to study the effect of CO₂ on people confined to enclosed spaces, such as inside of space capsules and submarines.
“You’ve got astronauts in a capsule living and breathing, and they are exhaling CO₂. The problem is how much CO₂ can they safely handle in their atmosphere? One of the things we found is that, at least in terms of tissue culture, CO₂ does have a protective effect from some of the radiation damage these astronauts might experience. So what you might want to do is push up that CO₂ level. You certainly don’t want to go very high, but having it slightly higher might actually have a protective effect against radiation, which generates hydroxyl radicals.”
Data from hundreds of thousands of U.S. adults suggests that each zip code increase of 10 µm/m3 in PM2.5 levels is associated with a doubling in eczema rates among residents
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People living in areas with higher levels of air pollution are more likely to have eczema, according to a new study published November 13, 2024 in the open-access journal PLOS ONEby Dr Jeffrey Cohen of Yale School of Medicine, USA.
The prevalence of eczema has increased globally with industrialisation, suggesting a possible contribution from environmental factors. In the new study, researchers used data from the U.S. National Institutes of Health All of Us Research Program, covering hundreds of thousands of U.S. adults. The current study included 286 862 people for whom there was available demographic, zip code and electronic health record data.
Overall, 12 695 participants (4.4%) were diagnosed with eczema. After controlling for demographics and smoking status, people with eczema were more likely to live in zip codes with high levels of fine particulate matter, or PM2.5, in the air. For every increase of 10 µm/m3 in average PM2.5 air pollution in their zip code, people were more than twice as likely to have eczema.
The authors conclude that increased air pollution, as measured by PM2.5, may influence the risk of developing eczema, likely through its effects on the immune system.
The authors add: “Showing that individuals in the United States who are exposed to particulate matter are more likely to have eczema deepens our understanding of the important health implications of ambient air pollution.”
US county-level data point to specific pesticides that may increase prostate cancer incidence and death.
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Researchers have identified 22 pesticides consistently associated with the incidence of prostate cancer in the United States, with four of the pesticides also linked with prostate cancer mortality. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.
To assess county-level associations of 295 pesticides with prostate cancer across counties in the United States, investigators conducted an environment-wide association study, using a lag period between exposure and prostate cancer incidence of 10–18 years to account for the slow-growing nature of most prostate cancers. The years 1997–2001 were assessed for pesticide use and 2011–2015 for prostate cancer outcomes. Similarly, 2002–2006 were analysed for pesticide use and 2016–2020 for outcomes.
Among the 22 pesticides showing consistent direct associations with prostate cancer incidence across both time-based analyses were three that had previously been linked to prostate cancer, including 2,4-D, one of the most frequently used pesticides in the United States. The 19 candidate pesticides not previously linked to prostate cancer included 10 herbicides, several fungicides and insecticides, and a soil fumigant.
Four pesticides that were linked to prostate cancer incidence were also associated with prostate cancer mortality: three herbicides (trifluralin, cloransulam-methyl, and diflufenzopyr) and one insecticide (thiamethoxam). Only trifluralin is classed by the Environmental Protection Agency as a “possible human carcinogen,” whereas the other three are considered “not likely to be carcinogenic” or have evidence of “non-carcinogenicity.”
“This research demonstrates the importance of studying environmental exposures, such as pesticide use, to potentially explain some of the geographic variation we observe in prostate cancer incidence and deaths across the United States,” said lead author Simon John Christoph Soerensen, MD, of Stanford University School of Medicine. “By building on these findings, we can advance our efforts to pinpoint risk factors for prostate cancer and work towards reducing the number of men affected by this disease.”
Some per- and polyfluoroalkyl substances (PFAS) are poorly degradable and are also known as “forever chemicals”. They adversely affect health and can lead to liver damage, obesity, hormonal disorders, and cancer. A research team from the Helmholtz Centre for Environmental Research (UFZ) has investigated the effects of PFAS on the brain.
Using a combination of modern molecular biology methods and the zebrafish model, the researchers revealed the mechanism of action and identified the genes involved, which are also present in humans. The test procedure developed at the UFZ could be used for the risk assessment of other neurotoxic chemicals. The study was recently published in Environmental Health Perspectives.
Because of their special properties – heat resistance, water and grease repellence, and high durability – PFAS are used in many everyday products (eg, cosmetics, outdoor clothing, and coated cookware). But it is precisely these properties that make them so problematic. “Because some PFAS are chemically stable, they accumulate in the environment and enter our bodies via air, drinking water, and food”, says UFZ toxicologist Prof Dr Tamara Tal. Even with careful consumption, it is nearly impossible to avoid this group of substances, which has been produced since the 1950s and now includes thousands of different compounds. “There is a great need for research, especially when it comes to developing fast, reliable, and cost-effective test systems for assessing the risks of PFAS exposure”, says Tal. So far, the environmental and health consequences have been difficult to assess.
In their current study, the researchers investigated how PFAS exposure affects brain development. To do this, they used the zebrafish model, which is frequently used in toxicology research. One advantage of this model is that around 70% of the genes found in zebrafish (Danio rerio) are also found in humans. The findings from the zebrafish model can therefore likely be transferred to humans. In their experiments, the researchers exposed zebrafish to two substances from the PFAS group (PFOS and PFHxS), which have a similar structure. The researchers then used molecular biological and bioinformatic methods to investigate which genes in the brains of the fish larvae exposed to PFAS were disrupted compared to the control fish, which were not exposed. “In the zebrafish exposed to PFAS, the peroxisome proliferator-activated receptor (ppar) gene group, which is also present in a slightly modified form in humans, was particularly active”, says Sebastian Gutsfeld, PhD student at the UFZ and first author of the study. “Toxicity studies have shown this to be the case as a result of exposure to PFAS – albeit in the liver. We have now also been able to demonstrate this for the brain”.
But what consequences does an altered activity of the ppar genes triggered by PFAS exposure have for brain development and behaviour of zebrafish larvae? The researchers investigated this in further studies using the zebrafish model. Using CRISPR/Cas9 ‘gene scissors’ the researchers were able to “selectively cut individual or several ppar genes and prevent them from functioning normally”, explains Gutsfeld. “We wanted to find out which ppar genes are directly linked to a change in larval behaviour triggered by PFAS exposure”. Proof of the underlying mechanism was directly provided. In contrast to genetically unaltered zebrafish, the knockdown fish in which the gene scissors were used should not show any behavioural changes after exposure to PFAS.
The two behavioural endpoints
In one series of experiments, the researchers continuously exposed zebrafish to PFOS or PFHxS during their early developmental phase between day one and day four and in another series of experiments only on day five. On the fifth day, the researchers then observed swimming behaviour. They used two different behavioural endpoints for this purpose. In one endpoint, swimming activity was measured during a prolonged dark phase. PFAS-exposed fish swam more than fish not exposed to PFAS, whether continuously exposed to PFAS during brain development or shortly before the behaviour test. Interestingly, hyperactivity was only present when the chemical was around. When the researchers removed PFOS or PFHxS, hyperactivity subsided. In the second endpoint, the startle response after a dark stimulus was measured. “In zebrafish exposed to PFOS for four days, we observed hyperactive swimming behaviour in response to the stimulus”, says Gutsfeld. In contrast, zebrafish only exposed to PFOS or PFHxS on the fifth day did not have a hyperactive startle response.
Based on these responses, the researchers conclude that PFOS exposure is associated with abnormal consequences – particularly during sensitive developmental phases of the brain. Using knockdown zebrafish, the researchers identified two genes from the ppar group that mediate the behaviour triggered by PFOS.
“Because these genes are also present in humans, it is possible that PFAS also have corresponding effects in humans”, concludes Tal. The scientists working with Tal want to investigate the neuroactive effects of other PFAS in future research projects and expand the method so that it can ultimately be used to assess the risk of chemicals in the environment, including PFAS.
In research published in Environmental Toxicology & Chemistry, investigators sampled water from 19 locations across the Hudson and East Rivers in 2021 and 2022 to identify and quantify the prescribed pharmaceuticals and drugs of abuse that are making their way into New York City’s rivers and to determine the source of these pollutants.
Metoprolol and atenolol (blood pressure medications), benzoylecgonine (the main metabolite of cocaine), methamphetamine (a stimulant), and methadone (an opioid) were the most prevalent drugs, present in more than 60% of water samples.
More drugs and higher concentrations were detected in water contaminated by Enterococci (bacteria that live in the intestinal tract) and after rainfall, indicating an impact from sewer overflow. However, the presence of drugs in clean water and during periods of dry weather indicated that wastewater treatment plant discharge may also contribute to the presence of drugs in rivers.
“This study shows how pharmaceuticals and drugs of abuse enter the New York City aquatic environment, highlighting the necessity of improving the current water management system,” said corresponding author Marta Concheiro-Guisan, PharmD, PhD, of the John Jay College of Criminal Justice.
Long term exposure to arsenic in water may increase cardiovascular disease and especially heart disease risk even at exposure levels below the US regulatory limit (10µg/L) according to a new study in Environmental Health Perspectives. This is the first study to describe exposure-response relationships at concentrations below the current regulatory limit and substantiates that prolonged exposure to arsenic in water contributes to the development of ischaemic heart disease.
The researchers, from Columbia University Mailman School of Public Health, compared various time windows of exposure, finding that the previous decade of water arsenic exposure up to the time of a cardiovascular disease event contributed the greatest risk.
“Our findings shed light on critical time windows of arsenic exposure that contribute to heart disease and inform the ongoing arsenic risk assessment by the EPA. It further reinforces the importance of considering non-cancer outcomes, and specifically cardiovascular disease, which is the number one cause of death in the US and globally,” said Danielle Medgyesi, a doctoral Fellow in the Department of Environmental Health Sciences at Columbia Mailman School. “This study offers resounding proof of the need for regulatory standards in protecting health and provides evidence in support of reducing the current limit to further eliminate significant risk.”
According to the American Heart Association and other leading health agencies, there is substantial evidence that arsenic exposure increases the risk of cardiovascular disease. This includes evidence of risk at high arsenic levels (> 100µg/L) in drinking water. The U.S. Environmental Protection Agency reduced the maximum contaminant level (MCL) for arsenic in community water supplies (CWS) from 50µg/L to 10µg/L beginning in 2006. Even so, drinking water remains an important source of arsenic exposure among CWS users. The natural occurrence of arsenic in groundwater is commonly observed in regions of New England, the upper Midwest, and the West, including California.
To evaluate the relationship between long-term arsenic exposure from CWS and cardiovascular disease, the researchers used statewide healthcare administrative and mortality records collected for the California Teachers Study cohort from enrollment through follow-up (1995-2018), identifying fatal and nonfatal cases of ischemic heart disease and cardiovascular disease. Working closely with collaborators at the California Office of Environmental Health Hazard Assessment (OEHHA), the team gathered water arsenic data from CWS for three decades (1990-2020).
The analysis included 98 250 participants, 6119 ischaemic heart disease cases and 9,936 CVD cases. Excluded were those 85 years of age or older and those with a history of CVD at enrolment. Similar to the proportion of California’s population that relies on CWS (over 90%), most participants resided in areas served by a CWS (92%). Leveraging the extensive years of arsenic data available, the team compared time windows of relatively short-term (3-years) to long-term (10-years to cumulative) average arsenic exposure. The study found decade-long arsenic exposure up to the time of a cardiovascular disease event was associated with the greatest risk, consistent with a study in Chile finding peak mortality of acute myocardial infarction around a decade after a period of very high arsenic exposure. This provides new insights into relevant exposure windows that are critical to the development of ischemic heart disease.
Nearly half (48%) of participants were exposed to an average arsenic concentration below California’s non-cancer public health goal < 1 µg/L. In comparison to this low-exposure group, those exposed to 1 to < 5 µg/L had modestly higher risk of ischaemic heart disease, with increases of 5 to 6%. Risk jumped to 20% among those in the exposure ranges of 5 to < 10 µg/L (or one-half to below the current regulatory limit), and more than doubled to 42% for those exposed to levels at and above the current EPA limit ≥ 10µg/L. The relationship was consistently stronger for ischemic heart disease compared to cardiovascular disease, and no evidence of risk for stroke was found, largely consistent with previous research and the conclusions of the current EPA risk assessment.
These results highlight the serious health consequences not only when community water systems do not meet the current EPA standard but also at levels below the current standard. The study found a substantial 20% risk at arsenic exposures ranging from 5 to < 10 µg/L which affected about 3.2% of participants, suggesting that stronger regulations would provide significant benefits to the population. In line with prior research, the study also found higher arsenic concentrations, including concentrations above the current standard, disproportionally affect Hispanic and Latina populations and residents of lower socioeconomic status neighbourhoods.
“Our results are novel and encourage a renewed discussion of current policy and regulatory standards,” said Tiffany Sanchez, senior author. “However, this also implies that much more research is needed to understand the risks associated with arsenic levels that CWS users currently experience. We believe that the data and methods developed in this study can be used to bolster and inform future studies and can be extended to evaluate other drinking water exposures and health outcomes.”
Chemicals are omnipresent today: they enter our bodies through food, air or the skin. But how do these complex mixtures of chemicals affect our health? In a study published in the journal Science, a research team from the Helmholtz Centre for Environmental Research (UFZ) has shown that chemicals that occur in complex mixtures and in concentration ratios as found in humans act together. Even if the concentrations of the individual substances were each below the effect threshold, the chemicals in the mixture showed a cumulative neurotoxic effect.
For their investigations, they used blood samples from pregnant women from the LiNA mother-child study (lifestyle and environmental factors and their influence on the newborn allergy risk), which has been running at the UFZ since 2006.
In our everyday lives, we are exposed to a wide variety of chemicals that are distributed and accumulate in our bodies. These are highly complex mixtures that can affect bodily functions and our health,” says Prof Beate Escher, Head of the UFZ Department of Cell Toxicology and Professor at the University of Tübingen. “It is known from environmental and water studies that the effects of chemicals add up when they occur in low concentrations in complex mixtures. Whether this is also the case in the human body has not yet been sufficiently investigated – this is precisely where our study comes in.”
The extensive research work was based on over 600 blood samples from pregnant women from the Leipzig mother-child cohort LiNA, which has been coordinated by the UFZ since 2006. The researchers first analysed the individual mixtures of chemicals present in these samples.
“We wanted to find out which chemicals were contained in the blood plasma and in what concentrations. We used a two-step extraction process to isolate as diverse chemical mixtures as possible,” says Georg Braun, postdoctoral researcher in Beate Escher’s working group and first author of the study. “Using mass spectrometry analyses, we searched for 1000 different chemicals that we knew could occur in the environment, could potentially be ingested by humans and could be relevant for adverse human health effects. Of these, we were able to quantify around 300 chemicals in several plasma samples.” This provided the researchers with information on the composition and concentration ratios of the chemical mixtures present in the 600 individual plasma samples.
The researchers used a prediction model to calculate the neurotoxic effects of the chemical mixtures. To test the predictions of the mixture effects experimentally, they used an established cellular bioassay based on human cells that indicates neurotoxic effects.
“We analysed individual chemicals as well as around 80 different, self-produced chemical mixtures in realistic concentration ratios. The extracts of the plasma samples were also tested,” says Georg Braun. The results were clear. “The laboratory experiments confirmed the predictions from the model: the effects of the chemicals add up in complex mixtures,” says environmental toxicologist Beate Escher. “Even if the individual concentrations of neurotoxic chemicals are so low that they are each below the effect threshold, there is still an effect on nerve-like cells in complex mixtures with many other chemicals.”
But what exactly do these results mean? “With our study, we were able to prove for the first time that what is known about the effects of chemical mixtures in the environment also applies to humans,” says Escher. “It is therefore imperative that we rethink risk assessment. Indicator substances alone are far from sufficient. In future, we must learn to think in terms of mixtures.” UFZ environmental immunologist and head of the LiNA study Dr Gunda Herberth adds: “It is becoming increasingly clear that many diseases such as allergies, immune system disorders, obesity or the development of the nervous system are linked to exposure to chemicals in the womb or in early childhood.”
The test method presented in this study – the extraction of chemical mixtures from human samples and their characterisation using chemical analysis combined with cell-based biotest systems – opens up new possibilities for researching the effects of complex chemical mixtures on human health. In future research projects, the scientists want to refine their test method and investigate the effects of chemical mixtures on other health-relevant endpoints such as immunotoxicity. In addition, they would like to uncover possible links between chemical exposure and the development of developmental disorders in children.
A new study documents how people in California are chronically being exposed to toxic airborne chemicals called plasticisers, including one banned from children’s items and beauty products.
Plasticizers are chemical compounds that make materials more flexible. They are used in a wide variety of products ranging from lunchboxes and shower curtains to garden hoses and upholstery.
“It’s not just for drinking straws and grocery bags,” said David Volz, environmental sciences professor at UC Riverside, and corresponding author of the study published in the journal Environmental Research.
Previous California monitoring programs focused on plasticisers called ortho-phthalates, some of which were phased out of manufacturing processes due to health and environmental concerns. Less research has focused on the health effects of their replacements, called non-ortho-phthalates. This study revealed the presence of both types of plasticisers in the air throughout Southern California.
“The levels of these compounds are through the roof,” Volz said. “We weren’t expecting that. As a result, we felt it was important for people to learn about this study.”
The National Institute of Environmental Health Sciences also wants to increase the visibility of this study, one of only a few to document the phthalates’ presence in the air of urban environments. The institute’s monthly newsletter, Environmental Factor, highlights the study in their October 2024 issue.
The researchers tracked two groups of UCR undergraduate students commuting from different parts of Southern California. Both groups wore silicone wristbands designed to collect data on chemical exposures in the air.
The first group wore their wristbands for five days in 2019, and the second group wore two different wristbands for five days each in 2020. Both groups wore the bands continuously, all day, as they went about their activities. At the end of the data collection period, the researchers chopped the wristbands into pieces, then analysed the chemicals they contained.
In a previous paper, the team focused on TDCIPP, a flame-retardant and known carcinogen, picked up in the wristbands. They saw that the longer a student’s commute, the higher their exposure to TDCIPP.
Unlike TDCIPP, which most likely migrates out of commuters’ car seats into dust, the team cannot pinpoint the origin of the plasticisers. Because they are airborne, rather than bound to dust, the wristbands could have picked them up anywhere, even outside the students’ cars.
For every gram of chopped-up wristband, the team found between 100 000 and 1 million nanograms of three phthalates, DiNP, DEHP, and DEHT. Ten total plasticizers were measured, but the levels of these three stood out.
Both DiNP and DEHP are included on California’s Proposition 65 list, which contains chemicals known to cause cancer, birth defects, or other reproductive harm. DEHT was introduced as an alternative, but its effects on human health have not been well studied.
This study suggests that introducing DEHT also has not done much to reduce the public’s level of exposure to DiNP or DEHP. Levels of all three chemicals found by Volz and his team were similar to those found by researchers in unrelated studies conducted on the East Coast.
Despite differences in climate, the air on both coasts is likely carrying similar levels of phthalates.
“No matter who you are, or where you are, your daily level of exposure to these plasticizer chemicals is high and persistent,” Volz said. “They are ubiquitous.”
To Volz, studies like this one amplify the need to find alternatives to plastic. As plastics degrade, these compounds and others like them are leaching out into the environment and into the body.
“The only way to decrease the concentration of plasticisers in the air is to decrease our production and consumption of materials containing plasticisers,” he said.
Girls exposed to certain endocrine-disrupting chemicals (EDCs) may be more likely to start puberty early, according to new research published in Endocrinology, the flagship basic science journal of the Endocrine Society. EDCs mimic, block or interfere with hormones in the body’s endocrine system.
There has been an alarming trend toward early puberty in girls, suggesting the influence of chemicals in our environment. Early puberty is associated with an increased risk of psychosocial problems, obesity, diabetes, cardiovascular disease, and breast cancer.
“We conducted a comprehensive screen of 10 000 environmental compounds with extensive follow-up studies using human brain cells that control the reproductive axis, and our team identified several substances that may contribute to early puberty in girls,” said study author Natalie Shaw, MD, MMSc, of the National Institute of Environmental Health Sciences (NIEHS).
Those substances include musk ambrette, which is a fragrance used in some detergents, perfumes, and personal care products, and a group of medications called cholinergic agonists.
“More research is needed to confirm our findings,” noted Shaw. “But the ability of these compounds to stimulate key receptors in the hypothalamus – the gonadotropin-releasing hormone receptor [GnRHR] and the kisspeptin receptor [KISS1R] – raises the possibility that exposure may prematurely activate the reproductive axis in children.”
According to the research team, musk ambrette is potentially concerning because it can be found in personal care products, and some rat studies have suggested it can cross the blood-brain barrier. Children are less likely to encounter cholinergic agonists in their daily lives.
Canadian and European regulations restrict musk ambrette use because of its potential toxicity, and the U.S. Food and Drug Administration removed the fragrance from its “generally recognized as safe” list. Yet it is still available on the market in some personal care products.
“This study suggests that, out of an abundance of caution, it is important for parents to only use personal care products for their children that are federally regulated,” Shaw said.
As part of the study, the research team screened a Tox21 10 000-compound library of licensed pharmaceuticals, environmental chemicals and dietary supplements against a human cell line overexpressing GnRHR or KISS1R. They conducted follow-up analysis using human hypothalamic neurons and zebrafish, finding that musk ambrette increased the number of GnRH neurons and GnRH expression.
“Using human hypothalamic neurons and zebrafish provides an effective model for identifying environmental substances that stimulate the KISS1R and GnRHR,” said co-author Menghang Xia, PhD, from the National Center for Advancing Translational Sciences (NCATS) “This study was a multidisciplinary team effort, and it showed that we can efficiently reduce the time and cost of assessing environmental chemicals for their potential effects on human health.”
