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Microplastics featured article

Introduction

Microplastics are everywhere: in the food we eat, the water we drink, and even the air we breathe. Imagine consuming the equivalent of a credit card’s worth of plastic every week—just by going about your daily routine. As startling as it may seem, this is the reality we face, exposing our bodies to a hidden threat that’s growing by the day.

What are microplastics? They're tiny pieces of plastic or other polymer-based materials, ranging from 5 millimeters (~0.2 inches) to as small as 100 nanometers, often called nanoplastics. These tiny particles contain a variety of chemicals that are harmful to humans, including polyethylene terephthalate (commonly called PET), polyethylene, polypropylene, polyvinyl chloride, polystyrene, polyester, polyurethane, polyamide, styrene acrylate, and polymethyl-methacrylate.

Roughly 70% to 80% of micro- and nanoplastics come from the breakdown of larger plastic pieces, either through oxidation or other degradation processes. The...

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In this clip, Dr. Rhonda Patrick discusses a new study revealing that living near a golf course can increase your risk of...

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In this clip, Drs. Andy Galpin and Rhonda Patrick discuss how bedroom CO₂ and nasal allergies disrupt sleep, and share science-based tips for...

Topic Pages

  • Microplastics

    Environmental physicochemical and biological processes drive microplastic generation, dispersal, chemical aging, pollutant sorption, and trophic transfer.

News & Publications

  • Young children spend a large portion of the day asleep, making their sleeping environment an important but often overlooked source of potentially harmful indoor pollutants. To address this, researchers investigated how much exposure occurs during sleep and which sources drive it.

    Parents placed three small silicone sheets in their child's bedroom for seven days: one hung on a metal stand to monitor room air, one on the mattress under the bedsheet, and one on the mattress with its top covered to isolate chemicals from the mattress. The researchers screened for 51 semivolatile organic compounds, which are chemicals that slowly escape from materials into air and dust: phthalates (plastic softeners), organophosphate esters (often used as flame retardants), and UV filters used to protect materials from sunlight.

    • Chemicals were found in all tested locations, but the air around the child's bed contained more detected compounds and often higher concentrations than the general bedroom air. A total of 28 chemicals were detected in the room air, 31 in the bed area, and 30 from mattresses.
    • Several plastic softeners and flame retardants were more concentrated in the samples capturing emissions from the mattresses, indicating that mattresses can be an important source of these chemicals.
    • One compound (tris(2-butoxyethyl) phosphate) was found at higher levels in the bed area than in mattress-only samples, suggesting that for some chemicals the bedding or other textiles may be more important sources than the mattress itself.
    • Older mattresses were associated with higher levels of certain phthalates, consistent with material breakdown and changes in manufacturing practices over time.

    These findings indicate that a child's bed is not just part of the normal indoor environment but forms a distinct sleeping microenvironment shaped by both the mattress and surrounding items. Because young children spend many hours in close contact with these materials, the measured emissions could contribute meaningfully to their overall exposure.

    Although the study was relatively small and did not assess how much of these substances were actually taken up by the children, it highlights the importance of the sleep environment. Selecting products tested for chemical emissions and maintaining adequate ventilation may help reduce potential exposure. In this clip, Dr. Andy Galpin explains how elevated bedroom CO₂ levels can disrupt sleep and outlines proven strategies to reduce them.

  • Silicone bakeware has become a kitchen staple for its flexibility and nonstick surface, yet little is known about how much of its chemical ingredients migrate into food or the air when heated. Scientists at Health Canada set out to fill that gap by measuring how cyclic siloxanes, chemical compounds that can remain as residual substances in silicone baking forms after the manufacturing process, behave during typical baking conditions.

    The team tested 25 new silicone baking products bought in Canada, including cupcake molds, loaf containers, and cookie sheets. Each was baked at 177°C (338°F) for one hour inside a small, ventilated room, using a mixture of oil and sand to mimic food with a moderate fat content. Air samples were taken before, during, and after baking to track volatile chemicals, while the simulated food was analyzed to quantify the migration of different cyclic siloxanes into it. Using the measured concentrations together with age-specific breathing rates, food intake, and body weights, the researchers also modeled potential exposures for different age groups.

    The results revealed that new silicone bakeware can emit and transfer measurable amounts of cyclic siloxanes during baking:

    • Every product contained cyclic siloxanes, with twenty-five types (D3–D27) identified and quantifiable forms (D4–D16) totaling about 680 to 4,300 micrograms per gram of silicone.
    • After one bake, the simulated food contained an average of around 105 micrograms per gram of siloxanes, and molds with larger contact area released the most.
    • Indoor air samples collected during baking showed sharp spikes in siloxane levels, averaging about 646 micrograms per cubic meter during the hour of heating, and returned close to background levels once baking ended.
    • Heavier forms of siloxanes were the main contributors to food-based exposure (D11–D16) and also to air concentrations (D7–D9).
    • When a cupcake mold was reused nine times, emissions to air and migration into food had already dropped by about 95 percent after the third cycle, suggesting that most releasable material is lost early on.
    • Based on the exposure modeling, a one‑year‑old child would have the highest exposure per kilogram of body weight on baking days for inhalation, while children aged 4–8 years would have the highest dietary intake.

    Lighter siloxanes such as D4–D6 are relatively well characterized and can affect the liver and lungs at high exposures. In contrast, the heavier forms remain largely untested for toxicity, making them a greater uncertainty.

    High-quality, food-grade silicone is manufactured in a way that minimizes cyclic siloxane residuals, yet even high-quality products can release small amounts during initial use. A noticeable chemical or "plastic" odor signals the release of cyclic siloxanes and other volatiles. Because emissions and migration dropped sharply during the first few baking cycles in the study, preheating or using new bakeware several times in a well-ventilated room before using them with food can substantially reduce exposure.

    The study used a single temperature and baking duration and relied on an oily food simulant rather than real foods, which limits how closely these results reflect typical household baking. Still, it highlights the importance of careful choice and use of everyday products to reduce exposure to potentially harmful chemicals. To learn more about everyday sources of invisible pollutants and practical ways to reduce exposure, listen to my episode on microplastics.

  • Pollution from microplastics and heavy metals has increased markedly in aquatic ecosystems in recent years, especially in industrial wastewater and municipal sewage, where these contaminants often coexist at high levels. As plastics break down into microplastics, they release organic compounds that behave differently from natural materials, especially when interacting with heavy metals. A recent study found that microplastic-derived organic matter, which makes up about 10% of surface ocean material in some regions, reacts with heavy metals in ways that could worsen environmental contamination.

    Researchers compared natural organic matter from soil and water with organic matter released by degraded plastics like polyethylene, polypropylene, and polyvinyl chloride. They analyzed how these substances interact with cadmium, chromium, copper, and lead to understand differences in their chemical behavior and transformations.

    They found that natural organic matter forms stable bonds with metals, whereas microplastic-derived compounds form unstable complexes. These complexes are highly reactive, especially with chromium, which explicitly targets compounds in microplastic-derived matter, causing it to break down into smaller, hazardous molecules like benzene and phenol. Notably, microplastic-derived compounds had almost 30% more condensed aromatics, a type of chemical structure that makes them more vulnerable to breaking down when exposed to oxygen.

    These findings suggest that plastic pollution worsens heavy metal contamination not only by adding pollutants but by changing how metal-organic complexes behave and move in the environment. Learn more about microplastics in our overview article.

  • Airborne microplastics are pervasive indoor contaminants that may pose considerable risks to respiratory health. Although previous studies have primarily focused on large microplastic particles, smaller particles capable of penetrating deep into the respiratory system are now under scrutiny. A recent study found that adults may inhale up to 68,000 microplastic particles per day in the 1 to 10 micrometer range—100 times more than prior estimates based on larger particle sizes.

    Researchers used spectroscopy to identify and quantify airborne suspended microplastics in homes and car cabin environments. This method allowed them to detect microplastic particles within the 1 to 10 micrometer size range, small enough to reach the lower lungs.

    They found that indoor microplastic concentrations were substantially higher in car cabins, with a median of 2,238 particles per cubic meter, compared to 528 particles per cubic meter in homes. Across both environments, 94% of particles measured fell within the 1 to 10 micrometer range. Most particles were irregular fragments, with polyethylene dominating in residential spaces and polyamide in car interiors. The data showed that smaller microplastic particles were far more common, and their numbers increased sharply as size decreased.

    These findings suggest that inhalation exposure to indoor microplastics—particularly within the 1 to 10 micrometer range—has been grossly underestimated. Learn ways to limit your microplastic exposure in this clip featuring Dr. Rhonda Patrick.

  • Plastics may be a hidden contributor to heart disease: chemical additives that disrupt hormone function and damage blood vessels. Evidence indicates that di-2-ethylhexylphthalate (DEHP)—a phthalate used to soften plastics—drives oxidative stress, metabolic dysfunction, and cardiovascular disease. A recent study found that this plastic additive may have contributed to more than 350,000 cardiovascular deaths worldwide in 2018.

    To estimate the global burden of cardiovascular disease linked to DEHP exposure, researchers combined country-level cardiovascular death rates with regional exposure estimates. They calculated the number of deaths and years of life lost that were likely due to the chemical, drawing on published hazard ratios and biomonitoring data.

    They found that DEHP exposure contributed to 356,000 cardiovascular deaths in 2018—around 13% of heart-related deaths among adults aged 55 to 64. Exposure varied widely by region. The Middle East and South Asia had the highest levels of several DEHP metabolites, including mono (2-ethylhexyl) phthalate at 19.460 micromoles per liter—six times higher than levels in Europe. Africa also showed high concentrations, including the highest recorded level of mono (2-ethyl-5-carboxypentyl) phthalate at 65.452 micromoles per liter. The Middle East, South Asia, and Africa bore the greatest exposure burden, while Europe had the lowest.

    These findings suggest that chemical additives in plastics pose a serious threat to cardiovascular health, especially in regions with growing plastic production or weaker environmental protections. As plastic products break down, they shed tiny fragments known as microplastics, which carry considerable health risks. Learn more in this episode featuring Dr. Rhonda Patrick.

  • While genes play a role in aging, lifestyle and environmental exposures—collectively called the exposome—may have a more robust effect on aging and longevity. A recent study found that the exposome contributes far more to premature death and age-related diseases than genetic risk alone.

    Researchers analyzed data from nearly 500,000 people enrolled in the UK Biobank to measure the exposome’s role in aging. They identified environmental exposures linked to early death and biological aging, then used a proteomic age clock—a tool that tracks molecular signs of aging—to confirm which exposures accelerate the aging process. Finally, they compared the exposome’s influence on disease risk to that of genetic predisposition.

    The exposome explained 17 percentage points more of the variation in mortality than genetic risk, which accounted for less than two percentage points. It was more strongly connected to lung, heart, and liver diseases, while genetic factors were more closely associated with certain cancers and dementias. The analysis identified three disease states and 22 biomarkers related to liver and kidney function, cardiovascular and metabolic health, inflammation, longevity, genetics, and vitamin and mineral status that independently drive biological aging and disease risk.

    These findings suggest that the exposome is critical in shaping health and longevity. While genes contribute to some diseases, environmental exposures throughout life greatly influence aging and survival. Air pollution is an exposome element contributing to disease and early death. Learn how wearable devices measure the air pollution exposome in this episode featuring Dr. Michael Snyder.

  • The environment plays a decisive role in heart health, with factors like air pollution, diet, and chemical exposures influencing cardiovascular disease risk. As plastic production and waste continue to rise, concerns about its effects on human health are increasing. A recent study found that frequent exposure to plastics, including those from disposable takeout containers, is associated with a 13% higher likelihood of developing cardiovascular disease.

    Researchers surveyed more than 3,000 people about their plastic exposure and heart health. They also provided rats with water that had been in contact with disposable plastic takeout containers at high temperatures for varying lengths of time. After three months, they analyzed the rats' heart tissue, blood markers, and gut bacteria to assess changes.

    They found that people with high plastic exposure had a 13% greater risk of congestive heart failure than those with lower exposure. In the rats, plastic exposure altered gut bacteria and increased markers of oxidative stress and inflammation in the heart. The structural changes observed in heart tissue suggest potential long-term damage.

    These findings suggest that plastic exposure increases the risk of heart disease and highlight the need to reduce exposure. Learn how to reduce your exposure to plastics and microplastics in this episode featuring Dr. Rhonda Patrick.

  • The risks of everyday plastics may go beyond environmental concerns, affecting our reproductive health on a cellular level. Benzyl butyl phthalate (BBP), a common plastic additive found in toys, cleaning products, food packaging, and cosmetics, has been linked to reproductive and developmental impairments. A recent study in worms found that BPP induced abnormalities in chromosome segregation and increased cell death in reproductive cells.

    Researchers exposed C. elegans, a type of roundworm, to four different concentrations of BBP: 1, 10, 100, and 500 micromolar. Then, they measured the chemical’s effects on the worms' chromosomes and cell structure while tracking its metabolism into two primary byproducts: monobutyl phthalate and monobenzyl phthalate.

    They found that exposure to 10 micromolar BBP induced considerable cellular disruption, increasing germ cell apoptosis, abnormalities in chromosome structure, and elevated levels of DNA damage throughout the reproductive tissues. The compound also triggered increased oxidative stress and affected critical genes involved in cell cycle progression and oxidative metabolism.

    These findings suggest that BBP exposure profoundly affects reproductive health by impairing the cellular processes necessary for healthy chromosome segregation and genomic stability. A person’s phthalate burden may contribute to poor metabolic function, inflammation, and cognitive dysfunction. Learn how sauna use induces substantial sweat losses, promoting the excretion of toxic compounds like BBP.

  • Melamine cleaning sponges are composed of hard, plastic strands assembled into a soft, lightweight foam. Commonly known as “magic erasers,” they are immensely popular due to their highly abrasive qualities. A recent study found that the global microplastic burden from melamine cleaning sponges may exceed 4.9 trillion particles, based on current sales.

    Researchers assessed microplastic release from melamine cleaning sponges under different scrubbing conditions, focusing on the shape, makeup, and number of fibers created. Then they quantified annual accumulation based on typical melamine sponge sales from two popular online retailers.

    They found that melamine sponges released straight and branched microplastic fibers made of poly(melamine-formaldehyde) polymer, ranging from 10 to 405 micrometers long. These fibers formed as the sponge’s structure broke down due to friction; consequently, the rougher the surface and denser the sponge, the more fibers produced. They estimated that sponge wear could release up to 6.5 million fibers per gram of sponge, potentially contributing up to 4.9 trillion fibers to aquatic environments globally.

    These findings suggest that melamine cleaning sponges are major contributors to the global microplastic burden. Human exposure to microplastics occurs through ingestion, inhalation, and skin contact. Evidence indicates that these particles accumulate in various body fluids and tissues and may increase the risk for metabolic dysfunction, neurotoxicity, and some cancers.

    Coming soon: A comprehensive overview article about microplastics and their putative effects on human health.

  • Perfluoroalkyl substances, or PFAS, are synthetic compounds found in food packaging, household products, and plastic bottles. These “forever chemicals” persist in the body for indefinite periods, posing significant health risks such as cancer, liver damage, and immune system dysfunction. To address these concerns, chemical companies have introduced shorter-chain PFAS alternatives, which break down more quickly in the environment. However, a recent study found that these alternatives readily penetrate the skin, potentially increasing the health risks associated with PFAS exposure.

    Researchers designed a three-dimensional model that mimicked the qualities of human skin. They applied various PFAS to the model skin, including perfluoroalkyl carboxylic acids (used on/in non-stick cookware, water and stain repellents, and food packaging) and perfluoroalkane sulfonic acids (used on/in carpets, clothing, paper products, and cleaning agents) and assessed whether the compounds were absorbed (consequently taken up into the bloodstream), unabsorbed, or retained within skin tissue.

    The researchers found that the skin absorbed as much as 58.9% of short-chain PFAS, and the absorption rate decreased as the carbon chain length increased. Interestingly, they found that large quantities of longer-chain PFAS (as much as 68.3%) were retained in the skin instead of being absorbed.

    These findings suggest that PFAS, especially shorter-chain forms, readily penetrate human skin and can gain access to the bloodstream. They also underscore the potential health risks of PFAS exposure and the need for further research and regulation.

  • Blood clots that form in the heart, arteries, and veins – called thrombi – are a major risk factor for heart attack, stroke, and respiratory problems. Evidence suggests that environmental factors contribute to thrombi formation. A recent study identified microplastics in 80 percent of surgically removed thrombi.

    Researchers surgically removed thrombi from patients scheduled for arterial or venous thrombectomy in the brain, heart, or legs using plastic-free surgical implements and storage techniques. Using mass spectrometry, they assessed the thrombi for microplastic particle content and determined the particles' sizes, shapes, and numbers.

    They found that 80 percent of the thrombi contained microplastics, including polyamide 66, polyvinyl chloride, and polyethylene. Higher concentrations of microplastics were associated with greater disease severity.

    This study was small, but its findings suggest microplastics are present in human thrombi and further increase disease risk. Microplastics are pervasive environmental contaminants present in land, water, and air. They have also been detected throughout the human body, including the sputum, lungs, heart, liver, blood, endometrium, testis, amniotic fluid, and placenta. Recent research found that microplastics in human arterial plaques increase the risk for cardiovascular disease-related events nearly fivefold.

  • Polyfluoroalkyl substances, or PFAS, are synthetic compounds used in food packaging, household products, and drinking water. PFAS aren’t excreted in bodily fluids like sweat or urine; instead, they persist in the body indefinitely and are often referred to as “forever chemicals.” A recent study found that seafood – including fish and shellfish – contains high PFAS levels.

    Researchers asked more than 1,800 people living in the northeastern U.S. about the amount and types of seafood they ate. Then, they measured PFAS levels in fish, lobster, shrimp, and scallops purchased from a market in that area.

    They found that the participants were regular seafood consumers, with adults consuming approximately 34 grams daily and children consuming 5 grams – slightly higher than national averages. They also found that the fish contained less than 1 nanogram per gram (ng/g) of PFAS; the shrimp contained 1.74 ng/g, and the lobster contained 3.30 ng/g. These levels may pose health concerns among high seafood consumers.

    These findings suggest that seafood is an abundant source of PFAS. Future research may illuminate the benefits and risks of consuming seafood. Exposure to PFAS has been linked to various health issues, including increased cholesterol levels, changes in liver function, and impaired immune function. Some studies suggest a potential association between PFAS exposure and increased risks of certain cancers and reproductive problems

  • Many hair care products contain siloxanes – a broad class of silicone-based compounds – that can become airborne during hair drying and styling. Evidence suggests siloxanes persist in the environment and cause liver or lung damage in rodents. A recent study found that a person can inhale up to 17 milligrams of siloxanes in a single home haircare session.

    Researchers conducted multiple experiments that replicated typical home haircare sessions using hair dryers, styling equipment, and products. Then, they measured the amount of chemicals emitted during the sessions using mass spectrometry.

    They found that the number of airborne chemicals emitted during haircare sessions, including monoterpenes, monoterpenoids, and propylene glycol, increased considerably indoors, especially when the various haircare products were heated. The most abundant chemical was a siloxane compound called D5, with participants inhaling up to 17 milligrams of siloxane in a single session.

    Using an exhaust fan reduced the amount of inhalable D5 by roughly half; however, the quantities of the exhausted compound increased outdoors. The researchers estimated that the emission of D5 from indoor to outdoor environments in the U.S. could be as high as six metric tons yearly.

    These findings suggest that people who use widely available haircare products in indoor environments are exposed to large quantities of inhalable, harmful compounds. These compounds can then be transmitted to the outdoor environment, where they persist, potentially posing considerable health threats.

  • People who live in large cities or near industrial areas are often exposed to high levels of particulate matter – a mixture of solid particles and liquid droplets in air pollution that forms fine inhalable particles with diameters typically 2.5 micrograms (PM2.5) or less. A recent study found that high exposure to PM2.5 increases the risk of developing Parkinson’s disease by nearly 20 percent.

    Researchers conducted a population-based study of more than 21 million older adults living in the US. They assessed their exposure to particulate matter based on their geographical location and ascertained whether they had Parkinson’s disease based on Medicare records.

    They found that people exposed to the median PM2.5 level were 56 percent more likely to develop Parkinson’s than those with the lowest PM2.5 exposures. For every additional microgram per cubic meter of PM2.5 exposure, risk increased by 4.2 percent. In the Mississippi-Ohio River Valley, where particulate matter levels are high, the risk of developing Parkinson’s disease was 19 percent greater than in the rest of the country.

    These findings suggest that exposure to particulate matter markedly increases a person’s risk of developing Parkinson’s disease, aligning with other evidence pointing to the disease’s environmental origins. Parkinson’s disease is a neurodegenerative disorder that affects the central nervous system. Caused by the destruction of nerve cells in the part of the brain called the substantia nigra, it typically manifests later in life and is characterized by tremors and a shuffling gait. Learn more about Parkinson’s disease and therapies in this episode featuring Dr. Giselle Petzinger.

  • Aging is the collective physiological, functional, and mental changes that accrue in a biological organism over time. However, people age at different rates, a consequence of both genetic and environmental factors. A recent study found that people whose biological age is five years older than their chronological age are roughly 40 percent more likely to develop vascular dementia or experience a stroke than those whose biological and chronological ages align.

    Using 18 routinely measured clinical biomarkers, researchers calculated the biological ages of more than 325,000 people enrolled in the UK Biobank study. Then, they evaluated how older biological age influenced the occurrence of neurological conditions, including dementia of all types, stroke, Parkinson’s disease, and motor neuron disease, over a nine-year follow-up period.

    They found that nearly 1,400 participants developed dementia, and more than 2,500 experienced a stroke. Having an older biological age that was five years older than chronological age increased the participants' risk of dementia by 26 percent, vascular dementia by 41 percent, and stroke by 39 percent. The findings were consistent even after considering various disease-specific risk factors.

    These findings suggest that accelerated biological aging markedly increases the risk of dementia and stroke. Age acceleration can result from intrinsic factors, such as normal metabolism and genetics, or extrinsic factors, such as diet, smoking, and exercise. Learn how epigenetic changes influence biological aging in our overview article.

  • Exposure to plastic particles alters sex hormones and promotes inflammation in rats, a new study shows. Estrogen levels in female rats that inhaled tiny particles of polyamide – commonly known as nylon – decreased and inflammatory cytokines increased.

    Researchers exposed female rats in heat to aerosolized polyamide particles for an average of 4.5 hours. Then they assessed the animals' overall health and measured their cytokine and reproductive hormone levels. They found that after a single exposure to the polyamide particles, the animals' blood pressure increased, estradiol (a form of estrogen) decreased, and pro-inflammatory cytokine interleukin-6 increased.

    Small plastic particles, often referred to as microplastics (ranging between 5 millimeters and 100 nanometers) or nanoplastics (less than 100 nanometers), are ubiquitous environmental pollutants. They have been identified in food (especially seafood), soil, drinking water, fresh- and saltwater bodies, and air.

    Exposure to microplastics is associated with a wide range of negative health outcomes in humans. For example, a comprehensive review of the effects of microplastics revealed that the pollutants induce oxidative stress and increase the risk for metabolic dysfunction, neurotoxicity, and some cancers. Some of these effects may be due to compounds commonly associated with plastic manufacturing, such as bisphenol A, or BPA, phthalates, and heavy metals, that are present in and on microplastics.

    This study demonstrates that even brief exposure to plastic particles is sufficient to alter sex hormones and promote inflammation in female rats.

  • From the publication:

    Per- and polyfluoroalkyl substances (PFAS), previously referred to as “perfluorinated compounds”, are a class of manufactured chemicals that have been detected in nearly all sampling of geographic locations and environmental matrices worldwide, including sites that had no nearby manufacture or use of PFAS. PFAS are used in hundreds of industrial and consumer products including food packaging and waterproof/stain resistant fabrics. Their strong carbon-fluorine bonds provide both hydrophobic and oleophobic properties, which make these chemicals extremely persistent in the environment. The class of PFAS includes tens of thousands of potential environmental contaminants including over one thousand chemicals previously or currently approved for use in the U.S..

    For PFAS measured at concentrations already found in the general population, exposure may suppress the immune system. Additionally, exposure to PFAS, with most studies on PFOA and PFOS, has been associated with many health harms, including an increased risk of cancer, high cholesterol, thyroid disease, and reproductive and developmental harms.

    The median level of total targeted PFAS in fish fillets from rivers and streams across the United States was 9,500 ng/kg, with a median level of 11,800 ng/kg in the Great Lakes. PFOS was the largest contributor to total PFAS levels, averaging 74% of the total. The median levels of total detected PFAS in freshwater fish across the United States were 278 times higher than levels in commercially relevant fish tested by the U.S. Food and Drug Administration in 2019–2022. Exposure assessment suggests that a single serving of freshwater fish per year with the median level of PFAS as detected by the U.S. EPA monitoring programs translates into a significant increase of PFOS levels in blood serum.

    Additional information:

    In June 2018, the Agency for Toxic Substances and Disease Registry (ATSDR) released a draft Toxicological Profile that derived minimal risk levels (MRLs), which are similar to RfDs, for intermediate duration exposure (15–364 days) of four PFAS routinely measured in NHANES [28]. The MRL [minimal risk levels] values for PFOA (3 ng/kg/day) and PFOS (2 ng/kg/day) are 6.7 and 10 times lower than the RfDs EPA used to develop its 2016 HAs and similar to those developed by New Jersey, though they are based on different studies and endpoints. View full publication

  • From the article:

    The study found that Bangladeshi men who grew up and lived as adults in the UK had significantly higher levels of testosterone compared to relatively well-off men who grew up and lived in Bangladesh as adults. Bangladeshis in Britain also reached puberty at a younger age and were taller than men who lived in Bangladesh throughout their childhood.

    The researchers say the differences are linked to energy investment as it may only be possible to have high testosterone levels if there are not many other demands placed on the body such as fighting off infections. In environments where people are more exposed to disease or poor nutrition, developing males direct energy towards survival at the cost of testosterone.

    The researchers collected data from 359 men on height, weight, age of puberty and other health information along with saliva samples to examine their testosterone levels. They compared the following groups: men born and still resident in Bangladesh; Bangladeshi men who moved to the UK (London) as children; Bangladeshi men who moved to the UK as adults; second-generation, UK-born men whose parents were Bangladeshi migrants; and UK-born ethnic Europeans.

    Men with higher levels of testosterone are at greater risk of potentially adverse effects of this hormone on health and ageing. Very high levels can mean increased muscle mass, increased risk of prostate diseases and have been linked to higher aggression. Very low testosterone levels in men can include lack of energy, loss of libido and erectile dysfunction. The testosterone levels of the men in the study were, however, all in a range that would unlikely have an impact on their fertility.

    View full publication

  • From the article:

    Animal and cellular studies have found that some phthalates block the effects of testosterone on the body’s organs and tissues. Researchers set out to examine whether these chemicals, which are widely used in flexible PVC plastics and personal care products, had a similar effect in humans.

    “We found evidence reduced levels of circulating testosterone were associated with increased phthalate exposure in several key populations, including boys ages 6-12, and men and women ages 40-60

    […]

    Researchers found an inverse relationship between phthalate exposure and testosterone levels at various life stages. In women ages 40-60, for example, increased phthalate concentrations were associated with a 10.8 to 24 percent decline in testosterone levels. Among boys ages 6-12, increased concentrations of metabolites of a phthalate called di-(2-ethylhexyl) phthalate, or DEHP, was linked to a 24 to 34.1 percent drop in testosterone levels.

    View full publication

  • Melamine, its derivatives, and other nitrogen-containing compounds are ubiquitous in the environment. Despite their known toxicity, these compounds are used in a variety of household products, including dishware, cleaning products, cosmetics, tattoo ink, and many others. Findings from a recent study suggest that pregnant females are exposed to a wide variety of these compounds via common household products.

    Toxic environmental exposures can have serious, harmful effects on pregnant females and developing fetuses. Evidence suggests that these toxic exposures are associated with an increased risk for infertility, miscarriage, preterm birth, low birth weight, neurodevelopmental disorders (such as autism and attention deficit hyperactivity disorder), and adult and childhood cancer.

    The study involved an ethnically diverse group of 171 pregnant females living in various parts of the United States. The investigators measured melamine, melamine derivatives, and other nitrogen-containing compounds (including cotinine, a byproduct of nicotine metabolism) in the participants' urine. Participants provided demographic information regarding their age, race/ethnicity, and marital status.

    The investigators found melamine and cyanuric acid (a melamine derivative) in nearly all the participants' urine samples. Levels were highest in Black and Hispanic females and those with greater exposure to tobacco. In addition, nearly all the samples contained nitrogen-containing compounds called aromatic amines, which are commonly used in products containing dyes and pigments, such as hair dyes and cosmetics.

    These findings suggest that pregnant females are exposed to a wide variety of toxic nitrogen-containing compounds, such as melamine, its derivatives, and aromatic amines. These exposures disproportionally affect Black and Hispanic females and those exposed to tobacco.

  • From the article:

    During the past few decades, the genetic makeup has been regarded as playing a significant role in the development of SAH [subarachnoid haemorrhage]. Contrary to this belief, however, a twin study recently published in the journal Stroke showed that environmental factors account for most of the susceptibility to develop SAH Conducted in Finland, Sweden and Denmark, the study is the largest population level twin study in the world.

    This means that instead of screening the close family members of SAH patients, the focus of preventive treatment may now be increasingly shifted to the efficient management of hypertension and smoking cessation intervention. This is what we do with other cardiovascular diseases as well."

    The Nordic study combined data on almost 80,000 pairs of twins over several decades. All in all, the follow-up time of all of the twin pairs corresponds to a staggering 6 million person-years.

    The researchers nevertheless emphasize that there are rare cases of families among whose members SAH is significantly more common than in the overall population. In these cases genetic factors are the principal cause underlying the development of the disease.

    View publication

  • Air pollution contains many toxic substances, including chemicals, gases, and particulate matter. Exposure to air pollutants is associated with poor health outcomes and increased risk of disease. Findings from a new study suggest that exposure to air pollutants, especially nitrogen dioxide, increases the risk of death due to COVID-19.

    Nitrogen dioxide is a gaseous air pollutant composed of nitrogen and oxygen. Commonly measured in air in terms of parts per billion, nitrogen dioxide is often present in air in urban areas with heavy automobile traffic. Exposure to nitrogen dioxide is associated with increased susceptibility to respiratory infections.

    To understand the relationship between exposure to key urban air pollutants (especially PM2.5, nitrogen dioxide, and ozone) and COVID-19 outcome, the authors of the study considered the case-fatality rate and the mortality rate – two major death outcomes associated with COVID-19. The case-fatality rate refers to how many of those with a confirmed diagnosis of COVID-19 die as a result of the disease. The mortality rate refers to the total number of COVID-19 deaths in the population.

    They found that exposure to urban air pollutants increased risk of poor outcome in COVID-19 in a dose-dependent manner. For every 4.6 parts per billion increase of nitrogen dioxide in the air, the case-fatality rate increased more than 11 percent and the mortality rate increased more than 16 percent. The authors' analysis also revealed that reducing nitrogen dioxide exposure could have prevented nearly 15,000 deaths among those who tested positive for COVID-19.

    These findings suggest that people living in urban areas where air pollution levels are high are at great risk of poor outcomes associated with COVID-19. They also support current efforts to reduce exposure to air pollutants in urban areas in the United States.

    Another prominent component of air pollution is benzene. Research indicates that sulforaphane, a phytochemical derived from broccoli sprouts, promotes excretion of benzene. Watch this clip featuring Dr. Jed Fahey to learn more.

  • The average person living in a temperate climate requires approximately two liters of water each day for optimal metabolic function. Many people meet their water needs with bottled water. As a result, the bottled water industry in the United States is robust, with consumers spending more than $30 billion per year on water products. Findings from a recent Consumer Reports study indicate that some bottled water products contain heavy metals and harmful compounds called PFAS.

    Heavy metals are naturally occurring metallic elements that adversely affect human health. They enter the environment by natural means and through human activities. In very low concentrations, heavy metals maintain various biochemical and physiological functions, but at higher concentrations are often toxic. The most commonly found heavy metals in the environment include arsenic, cadmium, chromium, copper, lead, nickel, and zinc. The FDA sets standards for acceptable levels of heavy metals in foods and beverages.

    PFAS, short for per- and polyfluoroalkyl substances, are man-made chemicals used in a variety of applications, including food packaging, household products, and drinking water, among others. Exposure to PFAS is linked to low birth weight, altered immune function, and cancer. Unlike some harmful synthetic compounds, PFAS are not excreted in bodily fluids like sweat or urine; rather, they persist in the body for indefinite periods and are often referred to as “forever chemicals.” The federal government and industry groups have set widely differing standards for acceptable levels of PFAS in water.

    The authors of the study tested two to four samples of 47 bottled waters (35 noncarbonated and 12 carbonated) for the presence of heavy metals (arsenic, cadmium, lead, and mercury). They also tested the products for the presence of 30 PFAS.

    They found that all but one of the noncarbonated water products had heavy metal levels well below federal safety limits, but nearly all of the products showed measurable levels of PFAS. The carbonated water products also had heavy metal levels that were below federal safety limits, but many of the products showed measurable levels of PFAS.

    These findings suggest that carbonated water products are sources of exposure to PFAS and underscore the importance of establishing federally mandated limits for PFAS in bottled drinking water products.

  • Perchlorate, a chemical used to propel rockets and airbags, accumulates in the environment as a pollutant. A new study suggests that perchlorate can enter the water supply and might be more detrimental to human health than previously thought.

    Perchlorate is transported from the blood into the thyroid gland by the sodium/iodide symporter, or NIS, which usually transports iodide and sodium. Iodide, the negatively charged form of iodine, is involved in producing thyroid hormone, which plays an important role in metabolism and development.

    Previous research has demonstrated that sodium and iodide are co-transported by the NIS symporter in a two to one ratio in an energetically favorable reaction. The current study investigated the mechanism by which perchlorate affects the function of this transporter.

    The authors of this cell culture study used radioactive iodine to determine how perchlorate influenced iodide transport across the NIS symporter. Using varying concentrations of perchlorate, they measured how much iodide was transported compared to sodium.

    The authors found that perchlorate inhibited the transport of iodide in two ways. First, it competed with iodide for a receptor site. In a second mechanism, perchlorate altered the shape of the transporter by blocking one of the two sodium binding sites. Normally, iodide is co-transported into thyroid cells with two sodium ions, providing the energy required to drive iodide into the cell. When perchlorate blocks one of the sodium binding sites, a single sodium ion is transported with iodide in a less energetic reaction. This slower iodide transport means that less iodide reaches the thyroid gland leading to lower thyroid hormone production.

    These findings suggest that perchlorate in the environment, even at low levels, can decrease the amount of iodide taken up by the thyroid gland. The resulting reduction in thyroid hormone production can be harmful to health, particularly to sensitive populations, including pregnant women, fetuses, and nursing infants.

  • Ozone air pollution was associated with a significant increase in emphysema. Lung scans of more than 7,000 participants were compared across 6 metropolitan regions in the US and air pollution levels were measured at the homes of study participants.

    This was a big study with analysis of more than 15,000 CT scans repeated on thousands of people over 18 years.

    The study also found that if the ambient ozone level was 3 parts per billion higher where you live compared to another location over 10 years, that was associated with an increase in emphysema roughly the equivalent of smoking a pack of cigarettes a day for 29 years.

    This study was a large prospective study so causation cannot be established. However, the authors developed novel and accurate exposure assessment methods for air pollution levels at the homes of study participants, collecting detailed measurement of exposures over years in these metropolitan regions, and measurements at the homes of many of the participants which strengthen the data.

  • Objective: We hypothesize that different sources of lung irritation may contribute to elicit an immune reaction in the lungs and subsequently lead to multiple sclerosis (MS) in people with a genetic susceptibility to the disease. We aimed to investigate the influence of exposure to organic solvents on MS risk, and a potential interaction between organic solvents and MS risk human leukocyte antigen (HLA) genes.

    Methods Using a Swedish population-based case-control study (2,042 incident cases of MS and 2,947 controls), participants with different genotypes, smoking habits, and exposures to organic solvents were compared regarding occurrence of MS, by calculating odds ratios with 95% confidence intervals using logistic regression. A potential interaction between exposure to organic solvents and MS risk HLA genes was evaluated by calculating the attributable proportion due to interaction.

    Results: Overall, exposure to organic solvents increased the risk of MS (odds ratio 1.5, 95% confidence interval 1.2–1.8, p = 0.0004). Among both ever and never smokers, an interaction between organic solvents, carriage of HLA-DRB115, and absence of HLA-A02 was observed with regard to MS risk, similar to the previously reported gene-environment interaction involving the same MS risk HLA genes and smoke exposure.

    Conclusion The mechanism linking both smoking and exposure to organic solvents to MS risk may involve lung inflammation with a proinflammatory profile. Their interaction with MS risk HLA genes argues for an action of these environmental factors on adaptive immunity, perhaps through activation of autoaggressive cells resident in the lungs subsequently attacking the CNS.

    http://n.neurology.org/content/neurology/early/2018/07/03/WNL.0000000000005906.full.pdf

  • [Abstract] Uncovering the interaction between genomes and the environment is a principal challenge of modern genomics and preventive medicine. While theoretical models are well defined, little is known of the G × E interactions in humans. We used an integrative approach to comprehensively assess the interactions between 1.6 million data points, encompassing a range of environmental exposures, health, and gene expression levels, coupled with whole-genome genetic variation. From ∼1000 individuals of a founder population in Quebec, we reveal a substantial impact of the environment on the transcriptome and clinical endophenotypes, overpowering that of genetic ancestry. Air pollution impacts gene expression and pathways affecting cardio-metabolic and respiratory traits, when controlling for genetic ancestry. Finally, we capture four expression quantitative trait loci that interact with the environment (air pollution). Our findings demonstrate how the local environment directly affects disease risk phenotypes and that genetic variation, including less common variants, can modulate individual’s response to environmental challenges.

  • This study shows some pretty interesting things in terms of a dramatic ability to (apparently) decrease lead status in the blood and seems to also really improve memory performance and reduce oxidative stress (from the lead) in the brain. It’s really pretty impressive, especially in light of the fact that, according to this paper, the neurotoxic effects are associated with amyloid beta production. This makes it plausibly relevant in the context of Alzheimer’s.

    FTA:

    “Compared with the normal saline and [corn oil-treated] groups, the lead level in the blood of sulforaphane and SFN + Vitamin E group had a significant decrease. In water maze test, the mice treated with sulforaphane or/and Vitamin E performed better than mice of the normal saline and corn oil groups. In addition, a remarkable decrease in MDA (malondialdehyde) level was found in mice treated with sulforaphane or/and vitamin E than those in normal saline and corn oil groups.”

    Not stated explicitly so far as I could tell in the article, but the figure 2 makes it look like lead content in the blood is reduced by almost 2/3rds. According to figure 6, MDA in the hippocampus, a marker for oxidative status, rises by approximately half of what the lead-exposed non-SFN group did (normal saline). In other words: more oxidative stress than control in the hippocampus, but not as much as lead without sulforaphane. It’s almost like they got half the lead exposure, if the dose-response was linear. Similarly, actual memory function was dramatically improved (measured by maze task) relative to non-sulforaphane group… but still lagged control by a little bit.

    Altogether interesting study!

  • FTA:

    Vinclozolin is a fungicide commonly used by farmers to treat fruits and vegetables.

    To test the effects of stress on rats, the researchers confined some of them to soft, warm cylinders for six hours a day for three weeks. This was done during adolescence, a developmentally sensitive time of life for rats, just as for humans. Months later, the researchers tested the brain chemistry, brain function, gene expression and behavior of the rats as adults.

    They discovered that for female rats, ancestral exposure to vinclozolin alone or stress during the animal’s adolescence alone had negligible effects on the rats' hormonal balance and behavior. However, the combination of ancestral exposure and stress caused the female rats to have dramatically higher levels of corticosterone (a stress hormone similar to cortisol in humans), higher expression of genes associated with anxiety and more anxious behaviors.