Propylparaben is widespread, authors fear no way to avoid exposure
Low doses of propylparaben – a chemical preservative found in food, drugs and cosmetics – can alter pregnancy-related changes in the breast in ways that may lessen the protection against breast cancer that pregnancy hormones normally convey, according to a new study published by researchers at University of Massachusetts Amherst.
The findings, published March 16 in the journal Endocrinology, suggest that propylparaben is an endocrine-disrupting chemical that interferes with the actions of hormones, says environmental health scientist Laura Vandenberg, the study’s senior author. Endocrine disruptors can affect organs sensitive to hormones, including the mammary gland in the breast that produces milk.
“We found that propylparaben disrupts the mammary gland of mice at exposure levels that have previously been considered safe based on results from industry-sponsored studies. We also saw effects of propylparaben after doses many times lower, which are more reflective of human intake,” Vandenberg says. “Although our study did not evaluate breast cancer risk, these changes in the mammary tissue are involved in mitigating cancer risk in women.”
Hormones produced during pregnancy not only allow breast tissue to produce milk for the infant, but also are partly responsible for a reduced risk of breast cancer in women who give birth at a younger age.
The researchers, including co-lead author Joshua Mogus, a Ph.D. student in Vandenberg’s lab, tested whether propylparaben exposure during the vulnerable period of pregnancy and breastfeeding adversely alters the reorganization of the mammary gland. They examined the mothers’ mammary glands five weeks after they exposed the female mice to environmentally doses of propylparaben during pregnancy and breastfeeding.
Compared with pregnant mice that had not received propylparaben, the exposed mice had mammary gland changes not typical of pregnancy, the researchers report. These mice had increased rates of cell proliferation, which Vandenberg says is a possible risk factor for breast cancer. They also had less-dense epithelial structures, fewer immune cell types and thinner periductal collagen, the connective tissue in the mammary gland.
“Some of these changes may be consistent with a loss of the protective effects that are typically associated with pregnancy,” says Mogus, who was chosen to present the research, deemed “particularly newsworthy” by the Endocrine Society, at the international group’s virtual annual meeting, ENDO 2021, beginning March 20.
Mogus says future studies should address whether pregnant females exposed to propylparaben are actually more susceptible to breast cancer. “Because pregnant women are exposed to propylparaben in many personal care products and foods, it is possible that they are at risk,” Mogus says, adding that pregnant and breastfeeding women should try to avoid using products containing propylparaben and other parabens.
“This chemical is so widely used, it may be impossible to avoid entirely,” Mogus adds. “It is critical that relevant public health agencies address endocrine-disrupting chemicals as a matter of policy.”
New tool finds and fingerprints previously undetected PFAS compounds in watersheds on Cape Cod
Researchers from the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS) found large quantities of previously undetectable compounds from the family of chemicals known as PFAS in six watersheds on Cape Cod using a new method to quantify and identify PFAS compounds. Exposures to some PFAS, widely used for their ability to repel heat, water, and oil, are linked to a range of health risks including cancer, immune suppression, diabetes, and low infant birth weight.
The new testing method revealed large quantities of previously undetected PFAS from fire-retardant foams and other unknown sources. Total concentrations of PFAS present in these watersheds were above state maximum contaminant levels (MCLs) for drinking water safety.
“We developed a method to fully capture and characterize all PFAS from fire-retardant foams, which are a major source of PFAS to downstream drinking water and ecosystems, but we also found large amounts of unidentified PFAS that couldn’t have originated from these foams,” said Bridger Ruyle, a graduate student at SEAS and first author of the study. “Traditional testing methods are completely missing these unknown PFAS.”
PFAS — per- and polyfluoroalkyl substances — are present in products ranging from fire retardant foams to non-stick pans. Nicknamed “forever chemicals” due to their long lifespan, PFAS have been building up in the environment since they were first used in the 1950s.
Despite the associated health risks, there are no legally enforceable federal limits for PFAS chemicals in drinking water. The Environmental Protection Agency’s provisional health guidelines for public water supplies only cover PFOS and PFOA, two common types of PFAS. Massachusetts, along with a few other states, has gone further by including six PFAS in their new MCLs in drinking water. But there are thousands of PFAS chemical structures known to exist, several hundred of which have already been detected in the environment.
We’re simply not testing for most PFAS compounds, so we have no idea what our total exposure is to these chemicals and health data associated with such exposures are still lacking.
ELSIE SUNDERLANDGORDON MCKAY PROFESSOR OF ENVIRONMENTAL CHEMISTRY
“We’re simply not testing for most PFAS compounds, so we have no idea what our total exposure is to these chemicals and health data associated with such exposures are still lacking,” said Elsie Sunderland, the Gordon McKay Professor of Environmental Chemistry at SEAS and senior author of the paper.
The standard testing methods used by the EPA and state regulatory agencies only test for 25 or fewer known compounds. The problem is the overwhelming majority of PFAS compounds are proprietary and regulatory agencies can’t find what they don’t know exist.
The new method developed by Sunderland and her team can overcome that barrier and account for all PFAS in a sample.
PFAS are made by combining carbons and fluorine atoms to form one of the strongest bonds in organic chemistry. Fluorine is one of the most abundant elements on earth but naturally occurring organic fluorine is exceedingly rare — produced only by a few poisonous plants in the Amazon and Australia. Therefore, any amount of organofluorine detected in the environment is sure to be human made.
PFAS compounds found in the environment come in two forms: a precursor form and a terminal form. Most of the monitored PFAS compounds, including PFOS and PFOA, are terminal compounds, meaning they will not degrade under normal environmental conditions. But precursor compounds, which often make up the majority of PFAS chemicals in a sample, can be transformed through biological or environmental processes into terminal forms. So, while the EPA or state agencies may monitor PFAS concentrations, they still are not detecting much of the huge pool of PFAS precursors.
That’s where this new method comes in.
The researchers first measure all the organofluorine in a sample. Then, using another technique, they oxidize the precursors in that sample and transform them into their terminal forms, which they can then measure. From there, the team developed a method of statistical analysis to reconstruct the original precursors, fingerprint their manufacturing origin, and measure their concentration within the sample.
“We’re essentially doing chemical forensics,” said Sunderland.
Using this method, Sunderland and her team tested six watersheds on Cape Cod as part of a collaboration with the United States Geological Survey and a research center funded by the National Institutes of Health and led by the University of Rhode Island that focuses on the sources, transport, exposure and effects of PFAS.
The team focused on identifying PFAS from the use of fire-retardant foams. These foams, which are used extensively at military bases, civilian airports, and local fire departments, are a major source of PFAS and have contaminated hundreds of public water supplies across the US.
The research team applied their forensic methods to samples collected between August 2017 and July 2019 from the Childs, Quashnet, Mill Creek, Marstons Mills, Mashpee and Santuit watersheds on Cape Cod. During the collection process, the team members had to be careful what they wore, since waterproof gear is treated with PFAS. The team ended up in decades-old waders to prevent contamination.
The sampling sites in the Childs, Quashnet and Mill Creek watersheds are downstream from a source of PFAS from fire retardant foams — the Quashnet and Childs from The Joint Base Cape Cod military facility and Mill Creek from Barnstable County Fire Training Academy.
Current tests can only identify about 50 percent of PFAS from historical foams — products that were discontinued in 2001 due to high levels of PFOS and PFOA — and less than 1 percent of PFAS from modern foams.
Using their new method, Sunderland and her team were able to identify 100 percent of all PFAS compounds in the types of fire-retardant foams that were used for decades at Joint Base Cape Cod and Barnstable County Fire Training Academy.
“Our testing method was able to find these missing compounds that have been used by the chemical industry for more than 40 years,” said Sunderland.
The tests also revealed huge quantities of PFAS from unknown sources.
This has huge ramifications for not only our understanding of human exposure but also for how much PFAS is discharging into the ocean and accumulating in marine life.
BRIDGER RUYLEGRADUATE STUDENT, SEAS
“Our accounting of PFAS from firefighting foams could not explain 37 to 77 percent of the organofluorine that we measured,” said Ruyle. “This has huge ramifications for not only our understanding of human exposure but also for how much PFAS is discharging into the ocean and accumulating in marine life.”
To follow up on these findings, Ruyle is currently working with NIH to identify some of the health impacts of PFAS from contemporary firefighting foams using toxicology studies. Sunderland’s team is continuing to study the unknown PFAS to better identify their sources and potential for accumulation in abundant marine food webs on Cape Cod.
First of its kind study reveals evidence that early exposure to dirty air alters genes in a way that could lead to adult heart disease, among other ailments. The findings could change the way medical experts and parents think about the air children breathe and inform clinical interventions.
Children exposed to air pollution, such as wildfire smoke and car exhaust, for as little as one day may be doomed to higher rates of heart disease and other ailments in adulthood, according to a new Stanford-led study. The analysis, published in Nature Scientific Reports, is the first of its kind to investigate air pollution’s effects at the single cell level and to simultaneously focus on both the cardiovascular and immune systems in children. It confirms previous research that bad air can alter gene regulation in a way that may impact long-term health – a finding that could change the way medical experts and parents think about the air children breathe, and inform clinical interventions for those exposed to chronic elevated air pollution.
View from above Fresno, California, an area with some of the country’s highest air pollution levels. (Image credit: Vadim Manuylov / Wikimedia Commons)
“I think this is compelling enough for a pediatrician to say that we have evidence air pollution causes changes in the immune and cardiovascular system associated not only with asthma and respiratory diseases, as has been shown before,” said study lead author Mary Prunicki, director of air pollution and health research at Stanford’s Sean N. Parker Center for Allergy & Asthma Research. “It looks like even brief air pollution exposure can actually change the regulation and expression of children’s genes and perhaps alter blood pressure, potentially laying the foundation for increased risk of disease later in life.”
The researchers studied a predominantly Hispanic group of children ages 6-8 in Fresno, California, a city beset with some of the country’s highest air pollution levels due to industrial agriculture and wildfires, among other sources. Using a combination of continuous daily pollutant concentrations measured at central air monitoring stations in Fresno, daily concentrations from periodic spatial sampling and meteorological and geophysical data, the study team estimated average air pollution exposures for 1 day, 1 week and 1, 3, 6 and 12 months prior to each participant visit. When combined with health and demographics questionnaires, blood pressure readings and blood samples, the data began to paint a troubling picture.
The researchers used a form of mass spectrometry to analyze immune system cells for the first time in a pollution study. The approach allowed for more sensitive measurements of up to 40 cell markers simultaneously, providing a more in-depth analysis of pollution exposure impacts than previously possible.
Among their findings: Exposure to fine particulate known as PM2.5, carbon monoxide and ozone over time is linked to increased methylation, an alteration of DNA molecules that can change their activity without changing their sequence. This change in gene expression may be passed down to future generations. The researchers also found that air pollution exposure correlates with an increase in monocytes, white blood cells that play a key role in the buildup of plaques in arteries, and could possibly predispose children to heart disease in adulthood. Future studies are needed to verify the long-term implications.
Hispanic children bear an unequal burden of health ailments, especially in California, where they are exposed to higher traffic-related pollution levels than non-Hispanic children. Among Hispanic adults, prevalence for uncontrolled hypertension is greater compared with other races and ethnicities in the U.S., making it all the more important to determine how air pollution will affect long-term health risks for Hispanic children.
Overall, respiratory diseases are killing more Americans each year, and rank as the second most common cause of deaths globally.
“This is everyone’s problem,” said study senior author Kari Nadeau, director of the Parker Center. “Nearly half of Americans and the vast majority of people around the world live in places with unhealthy air. Understanding and mitigating the impacts could save a lot of lives.”