Why More and More Girls Are Hitting Puberty Early

Megan Gray was eight years old when she got her first period. She was playing hide-and-seek with her older sister and a friend at their friend’s house in suburban Sacramento. She was wearing pink jeans, which she had saved up for a long time to buy. She tied a sweatshirt around her waist to hide the bloodstain, and, later, threw the ruined pink jeans away; when her mother asked where they’d gone, she threw a tantrum to deflect the question.

Gray had a close relationship with her mom, but she was so young that they’d had no conversations about puberty; her older sister had not yet gotten her period. “There was nothing, no context for understanding,” Gray told me. “I knew what a period was—I didn’t think I was dying or anything. But still, I didn’t tell anyone for months. I just used wadded-up toilet paper. It felt so awkward and shameful.” She did eventually talk with her mom about it. But this was the nineteen-eighties.

“It wasn’t some big informational session. It was very Gen X—you just dealt with things by yourself and got on with it.” Gray was taller than her peers and wore layers of tops to conceal her developing breasts. She estimates that she was a C-cup by fifth grade. “There were assumptions about me because I had boobs. And I had never even kissed anyone. I was lucky, because nothing traumatic occurred. Yet I do think that there is a trauma in being sexualized.”

Maritza Gualy got her first period when she was eight going on nine, at the end of the eighties. Her mom showed her how to use a thick Kotex pad. Eventually, her older sister introduced her to o.b. tampons—the ones with no applicator; they were small and easier to hide. The sisters, whose parents were Colombian immigrants, attended a majority-white Catholic school in Nashville.

Her school uniform had no pockets, so whenever Gualy had her period, she had to hide tampons in her bra or in the waistband of her skirt. One day, an o.b. fell out of her skirt when she and her classmates were sitting on the rug together. Later, when they were back at their desks for a spelling test, Gualy recalled, “the teacher went around from kid to kid with the tampon. ‘Is this yours?’ ‘Is this yours?’ Except she was only asking the more well-developed girls! I knew I wasn’t going to admit to it.”

In fifth grade, Gualy’s best friend got her period, and she was upset to learn that Gualy had started hers more than a year earlier and hadn’t mentioned anything. “But I already felt so othered,” Gualy said, “and I didn’t want to add to that.” When Gray and Gualy were kids, pediatricians thought that the average age of onset of puberty in girls—defined in most medical literature as thelarche, when breast tissue begins to develop—was about eleven years old. Menarche, or first period, was thought to happen around age thirteen.

Only a small percentage of girls had started puberty by the age of eight, much less started menstruating.  But, by the two-thousands, new research had found that eighteen per cent of white girls, thirty-one per cent of Hispanic girls, and forty-three per cent of Black girls had entered thelarche by age eight, according to a study published in 2010.

Often, these girls were taller than most of their peers and showed other signs of accelerated physical maturation, such as pubic hair and underarm odor. Thelarche typically presages the onset of menstruation by two to three years, meaning that some of these girls would have to deal with the mess and discomfort of a monthly period before they’d finished elementary school.

Researchers and physicians hypothesized about possible causes for the increase in early puberty, such as increasing rates of obesity; greater exposure to endocrine-disrupting chemicals found in food, plastics, and personal-care products; and stressful or abusive home environments. Then, during the coronavirus pandemic, pediatric endocrinologists saw a new surge of referrals for girls with early puberty.

Recent retrospective studies from Germany and Turkey show that the number of these referrals doubled or even tripled during the lockdown periods of 2020 (this at a time when many families may have been avoiding non-emergency doctor’s visits for fear of COVID-19). A paper published in August in the journal Frontiers in Pediatrics, which analyzed data from South Korea’s national statistics portal, found that the number of children diagnosed with precocious puberty almost doubled between 2016 and 2021, with a sharp post-2020 spike.

The rise in early puberty “is a phenomenon that is occurring all over the world,” Frank M. Biro, the former director of the adolescent-medicine division at Cincinnati Children’s Hospital Medical Center, told me. (Although there has also been a rise among boys, girls experiencing early puberty still vastly outnumber them.)

The new data may offer some safety in numbers to early-developing girls—if Gray and Gualy were growing up today, they might have found a friend or two on the same accelerated track. But early puberty is associated with a daunting list of adverse physical and psychological outcomes: various studies have suggested that early-maturing girls are at greater risk for developing obesity, breast cancer, eating disorders, depression, and a range of behavioral issues.

Especially in the midst of what is increasingly understood to be a post-COVID youth mental-health crisis, the startling new uptick in early puberty is troubling to some physicians and parents. But, because the spike appears to have been triggered within a compressed, well-defined timeframe, it also offers rich terrain for better understanding the condition’s causes and effects.

It also provides a chance to rethink puberty: to see it not as a gateway into adulthood but as another stage of childhood—one that is highly variable from kid to kid and need not be cause for alarm. “We are in a great natural experiment at the moment, and we might not know the results of it for another ten years or more,” Louise Greenspan, a pediatric endocrinologist at Kaiser Permanente, San Francisco, said.

“I do wonder if this is going to be a cohort of kids whose puberty was more rapid because they were in a critical window of susceptibility during a time of great social upheaval.” For generations, pediatricians have referred to a table of pubertal development known as Tanner stages, named for the pediatric endocrinologist James Tanner, one of the lead investigators of the landmark Harpenden Growth Study, conducted from 1949 to 1971 at a charity home for orphaned and neglected children in a suburb of London.

There, hundreds of boys and girls were photographed naked at three-month intervals. Although the data for the Tanner scale were gathered from kids of a narrow demographic—white, thin, and bearing the internal scars of trauma or adversity in their formative years—it established, in a pair of papers published in 1969, our modern benchmarks of puberty: five distinct stages, ranging from prepubertal to fully developed.

On average, the girls in the study began showing breast buds—the “Tanner II” stage—at age eleven or so, and began menstruating between thirteen and fourteen. Early puberty is identified through physical examination, blood tests to measure levels of sex hormones, and a bone X-ray to estimate “bone age”—how close a child’s skeletal system is to reaching maturation.

Puberty typically begins in girls when the pituitary gland starts secreting hormones known as gonadotropins; these hormones cause the ovaries to grow and to produce estrogen, the sex hormone that triggers the development of secondary sex characteristics…Read more

Source: Why More and More Girls Are Hitting Puberty Early | The New Yorker

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Can Processed Meat Ever Be Healthy And How Much Is OK To Eat?

We know that cigarettes cause cancer, and as a result, they are becoming increasing difficult and expensive to buy. We know that alcohol consumption is too associated with an increased risk of developing several types of cancer, and as such there are clear guidelines on the maximum amount of alcohol the average adult should consume each week.

So, given that the World Health Organisation (WHO) has classified processed meat including ham as a group 1 (known to cause cancer) carcinogen, why are processed meats including ham, salami and bacon still sold freely in supermarkets (minus any public health warning)?

Processed meat including salami and bacon are foods that have been enjoyed in many cultures for thousands of years, and are meats that have been treated via processing techniques such as curing, fermenting, smoking or salting to extend the shelf life and add taste and texture.

Delve into the science

The key health concern relating to processed meat is that it can contain compounds called N-nitroso chemicals that can damage cells in the wall of the bowel, which can cause bowel cancer. In addition, the nitrate-based preservatives used to make processed meat also produce these same N-nitroso chemicals

It is important to remember that the amount of processed meat we eat can add up across the week.  Clare Hughes

While this science has been known for some time, and the public health position to limit the consumption of processed meat endorsed by a number of key public health organisations including Cancer Council Australia, the American Heart Association, the American Cancer Society and the Harvard School of Public Health, the question remains, if this food is so potentially dangerous for us, why does it remain freely available for human consumption?

Indeed, this is a question raised indirectly recently when a group of health researchers published a paper in the Journal of Internal Medicine, which concluded that based on a summary of current data available, there was no need for adults to reduce their current consumption of processed meat.

The review of 61 scientific studies, and over 4 million people led the investigators to conclude that the “strong anti-meat” dietary recommendations are not justified.

Health recommendations

Current recommendations are for Australians to consume no more than 455 grams of cooked lean meat each week and avoid processed meats such as ham entirely.

There are no specific recommendations for children, which leaves parents in no man’s land, with many families relying on budget-friendly processed meats such as ham as cost-effective sandwich fillings.

It also fails to take into account leaner varieties of processed meat, and the newer varieties that do not contain added nitrates, and whether these are “safer” options that can be enjoyed more freely.

Clare Hughes, the nutrition unit manager from the Cancer Council, is aware that this is complicated area.

“Nitrate-free varieties of processed meat are relatively new and as such the evidence available does not distinguish between processed meat that is nitrate-free or not, so we recommend people limit their intake regardless,” she says.

“It is important to remember that the amount of processed meat we eat can add up across the week. It could be a bacon and egg breakfast on weekends, then ham sandwiches for lunch as well as salami on a pizza weekly, in addition to mixed meats on weekend grazing platters. Here processed meat is being consumed on more days than not.

“Once a week on a pizza or in a cooked breakfast at the weekend is probably fine but if it’s something that you’re finding you are eating every day or most days during the week, it is a good idea to look for ways you can cut back and include other alternatives such as unprocessed meats, seafood, eggs, legumes and vegetables, especially if there is a family history of bowel cancer,” Hughes says.

Balance is key

The other key point to consider is what other nutrient-rich foods are being consumed by the family.Individual foods do not cause cancer in isolation, but rather dietary patterns over time. In other words, the overall nutrient balance is the most important thing when it comes to health and disease risk.

This means that a diet full of whole grains, fresh fruits and vegetables with only the occasional processed meat (once or twice each week), is much better than a diet that includes little fresh food, and a ham sandwich on white bread each day for lunch.

This may partially explain while some cultures, such as in Greece or Italy, may consume processed meats more liberally, yet do not have a greater incidence of bowel cancer that presents here in Australia.

Perhaps most importantly is an understanding of how the risk of eating processed meat regularly compares to other carcinogens such as cigarettes. It has been shown that individuals who eat 50 grams of processed meat per day have 1.18 times higher risk of developing bowel cancer than those who don’t eat processed meat at all.

By comparison, the worst-case increase in risk of bowel cancer linked to eating processed meat is less than two times the risk compared to lifetime smoking, which increases the risk of developing lung cancer by 50.

This means it may simply come down to choosing the leanest processed meats you can find (free of added nitrates where possible), and enjoying it at most once or twice each week as a special breakfast addition, or on your favourite pizza, rather than your daily sandwich filler.

By: Susie Burrell

Susie Burrell is an accredited practising dietitian and nutritionist and holds a master in coaching psychology.

Source: Can processed meat ever be healthy – and how much is OK to eat?

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Critics by Jillian Kubala

Nearly all foods are processed, at least to some extent. For example, manufacturers process dried beans to make them shelf-stable. This does not make them less healthy. So, before we get into what makes a food highly processed, it’s important to understand that foods aren’t “unhealthy” just because they’re processed in some way.

To make it easier to understand food processing, researchers have separated foods into four categories based on the extent of processing. To do this, they used NOVA, a food classification system developed by researchers at the University of Sao Paulo, Brazil (1, 2Trusted Source, 3):

  • NOVA Group 1. Minimally processed and unprocessed foods. Vegetables, fruits, grains, beans, and nuts fall into this category. These foods may have gone through roasting, boiling, or pasteurization to increase shelf life or make them safe to eat.
  • NOVA Group 2. Processed culinary ingredients obtained directly from group 1 foods or from nature. This can include foods such as olive oil, maple syrup, and salt. Group 2 foods are mainly used in preparation and cooking of group 1 foods.
  • NOVA Group 3. Processed foods, including items made by adding ingredients like salt, sugar, or other substances from group 2 to group 1 foods. Examples include fresh bread, fruits in syrup, and cheese.
  • NOVA Group 4. Ultra-processed foods. These contain little, if any, of the foods or ingredients from group 1. These items are meant to be convenient, hyper-palatable, and low cost and are typically high in sugars, refined grains, fats, preservatives, and salt.

Ultra-processed, or highly processed, foods typically contain substances you wouldn’t use in food preparation at home, such as (4Trusted Source):

  • hydrolyzed proteins
  • modified starches
  • hydrogenated oils
  • colorants
  • flavorings
  • high fructose corn syrup
  • artificial sweeteners
  • bulking agents

These definitions aren’t perfect or 100% accurate for classifying foods, and experts admit that there’s considerable variability when it comes to listing foods as “highly processed” in research studies (4Trusted Source). For example, breakfast cereals are considered highly processed in many studies. However, healthcare experts do not consider some cereals highly processed if they contain no added sugar and have undergone minimal processing.

That said, this classification system is simply meant to provide a general idea of what makes a food highly processed based on its manufacturing and ingredients.

Examples of highly processed foods

Now that you have a general idea of what makes a food highly processed, you’re probably wondering which foods and beverages fall into this category.

Here are some common examples of ultra-processed foods (2Trusted Source):

  • sugary beverages such as carbonated soft drinks, sugary coffee drinks, energy drinks, and fruit punch
  • sweet or savory packaged snacks such as chips and cookies
  • sweetened breakfast cereals such as Froot Loops, Trix, Cinnamon Toast Crunch, and sweetened oatmeals
  • baking mixes such as stuffing, cake, brownie, and cookie mixes
  • reconstituted meat products such as hot dogs and fish sticks
  • frozen meals such as pizza and TV dinners
  • powdered and packaged instant soups
  • candies and other confectionery
  • packaged breads and buns
  • energy and protein bars and shakes
  • meal replacement shakes and powders meant for weight loss
  • boxed pasta products
  • ice cream, sweetened yogurt, and cocoa mixes
  • margarine and other ultra-processed spreads such as sweetened cream cheese

Keep in mind that this list is not exhaustive. Many other foods and ingredients are also considered ultra-processed. It’s not always immediately clear whether a food is highly processed, which could make it difficult for consumers to minimize these products in their diet.

The most reliable way to identify highly processed foods is to read the ingredient labels. Ultra-processed foods have ingredients like (2Trusted Source):

  • artificial colorings and flavorings
  • thickeners and preservatives
  • hydrolyzed proteins
  • sweeteners such as fructose, high fructose corn syrup, invert sugar, and maltodextrin
  • hydrogenated or interesterified oils
  • bulking, foaming, and gelling agents
  • flavor enhancers such as monosodium glutamate (MSG)

The world of food additives can be overwhelming and confusing, and you might find it difficult to identify everything on ingredient lists. If you’re interested in learning more about food additives and which additives manufacturers commonly include in ultra-processed foods, check out the United Nations Codex Alimentarius, which keeps an updated list of food additives.

Related contents:

Liver King and Dr. Saladino Discuss Dangers of Processed Food and Seed Oils: ‘Stop Feeding Your Children Garbage’ FitnessVolt

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PFAS Forever Chemicals Linked To Liver Cancer In First of Its Kind Study

New research has reported a link between elevated blood levels of perfluooctane sulfate (PFOS) and increased risk of liver cancer. The study is the first to directly associate exposure from this “forever chemical” to liver cancer in humans.There are thousands of different chemicals under the umbrella of per- and polyfluoroalkyl substances, or PFAS. These substances are often informally referred to as “forever chemicals” because they can persist in the environment for decades.

For much of the 20th century PFAS chemicals were used in a broad variety of manufacturing contexts. However, over the past 20 years an increasing body of evidence has revealed exposure to PFAS can contribute to a number of deleterious health effects, from low birth weight to hypothyroidism.

Following on from animal and lab-based studies suggesting PFAS exposure is potentially damaging to liver cells, this new research offers the first robust investigation into the relationship between the chemicals and liver cancer in humans.

The power of this new research is in its leveraging of data from a multi-decade health study following more than 200,000 people since the early 1990s. This allowed the researchers to look at historic blood levels of PFAS in subjects years before they presented with cancer.“Part of the reason there has been few human studies is because you need the right samples,” explained Veronica Wendy Setiawan, an author on the new study. “When you are looking at an environmental exposure, you need samples from well before a diagnosis because it takes time for cancer to develop.”

Several types of PFAS were found in blood samples from subjects who ultimately went on to develop liver cancer. But one particular chemical stood out, perfluooctane sulfate (also known as PFOS). Those subjects with the highest blood levels of PFOS were 4.5 times more likely to develop liver cancer compared to the group with the lowest PFOS blood levels.

The study also homed in on some potential mechanisms by which PFOS exposure could be causing liver cancer. Four particular metabolites were found to link PFOS levels with liver cancer: “glucose, butyric acid (a short chain fatty acid), α-Ketoisovaleric acid (a branched-chain α-keto acid), and 7α-Hydroxy-3-oxo-4-cholestenoate (a bile acid).”

“We believe our work is providing important insights into the long-term health effects that these chemicals have on human health, especially with respect to how they can damage normal liver function,” explained lead researcher on the project Leda Chatzi. “This study fills an important gap in our understanding of the true consequences of exposure to these chemicals.”

The new findings come just days after another study found levels of PFAS in rainwater often exceed new safety limits set by the Environmental Protection Authority (EPA). That research called for a global phase-out of PFAS from all manufacturing contexts as soon as possible. An expert committee formed by the United Nations to review persistent pollutants in 2019 also called for the elimination of all use of PFAS chemicals to, “protect human health and the environment from its harmful impacts.”

Source: PFAS “forever chemicals” linked to liver cancer in first-of-its-kind study

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How Do Painkillers Kill Pain? It’s About Meeting The pain Where It’s At

Without the ability to feel pain, life is more dangerous. To avoid injury, pain tells us to use a hammer more gently, wait for the soup to cool or put on gloves in a snowball fight. Those with rare inherited disorders that leave them without the ability to feel pain are unable to protect themselves from environmental threats, leading to broken bones, damaged skin, infections, and ultimately a shorter life span.

In these contexts, pain is much more than a sensation: It is a protective call to action. But pain that is too intense or long-lasting can be debilitating. So how does modern medicine soften the call?

As a neurobiologist and an anesthesiologist who study pain, this is a question we and other researchers have tried to answer. Science’s understanding of how the body senses tissue damage and perceives it as pain has progressed tremendously over the past several years. It has become clear that there are multiple pathways that signal tissue damage to the brain and sound the pain alarm bell.

Interestingly, while the brain uses different pain signaling pathways depending on the type of damage, there is also redundancy to these pathways. Even more intriguing, these neural pathways morph and amplify signals in the case of chronic pain and pain caused by conditions affecting nerves themselves, even though the protective function of pain is no longer needed.

Painkillers work by tackling different parts of these pathways. Not every painkiller works for every type of pain, however. Because of the multitude and redundancy of pain pathways, a perfect painkiller is elusive. But in the meantime, understanding how existing painkillers work helps medical providers and patients use them for the best results.

Anti-inflammatory painkillers

A bruise, sprain, or broken bone from an injury all lead to tissue inflammation, an immune response that can lead to swelling and redness as the body tries to heal. Specialized nerve cells in the area of the injury called nociceptors sense the inflammatory chemicals the body produces and send pain signals to the brain.

Common over-the-counter anti-inflammatory painkillers work by decreasing inflammation in the injured area. These are particularly useful for musculoskeletal injuries or other pain problems caused by inflammation such as arthritis.

Nonsteroidal anti-inflammatories like ibuprofen (Advil, Motrin), naproxen (Aleve), and aspirin do this by blocking an enzyme called COX that plays a key role in a biochemical cascade that produces inflammatory chemicals. Blocking the cascade decreases the amount of inflammatory chemicals, and thereby reduces the pain signals sent to the brain. While acetaminophen (Tylenol), also known as paracetamol, doesn’t reduce inflammation as NSAIDs do, it also inhibits COX enzymes and has similar pain-reducing effects.

Prescription anti-inflammatory painkillers include other COX inhibitors, corticosteroids, and, more recently, drugs that target and inactivate the inflammatory chemicals themselves.

Because inflammatory chemicals are involved in other important physiological functions beyond just sounding the pain alarm, medications that block them will have side effects and potential health risks, including irritating the stomach lining and affecting kidney function. Over-the-counter medications are generally safe if the directions on the bottle are followed strictly.

Corticosteroids like prednisone block the inflammatory cascade early on in the process, which is probably why they are so potent in reducing inflammation. However, because all the chemicals in the cascade are present in nearly every organ system, long-term use of steroids can pose many health risks that need to be discussed with a physician before starting a treatment plan.

Topical medications

Many topical medications target nociceptors, the specialized nerves that detect tissue damage. Local anesthetics, like lidocaine, prevent these nerves from sending electrical signals to the brain.

The protein sensors on the tips of other sensory neurons in the skin are also targets for topical painkillers. Activating these proteins can elicit particular sensations that can lessen the pain by reducing the activity of the damage-sensing nerves, like the cooling sensation of menthol or the burning sensation of capsaicin.

Because these topical medications work on the tiny nerves in the skin, they are best used for pain directly affecting the skin. For example, a shingles infection can damage the nerves in the skin, causing them to become overactive and send persistent pain signals to the brain. Silencing those nerves with topical lidocaine or an overwhelming dose of capsaicin can reduce these pain signals.

Nerve injury medications

Nerve injuries, most commonly from arthritis and diabetes, can cause the pain-sensing part of the nervous system to become overactive. These injuries sound the pain alarm even in the absence of tissue damage. The best painkillers in these conditions are those that dampen that alarm.

Antiepileptic drugs, such as gabapentin (Neurontin), suppress the pain-sensing system by blocking electrical signaling in the nerves. However, gabapentin can also reduce nerve activity in other parts of the nervous system, potentially leading to sleepiness and confusion.

Antidepressants, such as duloxetine and nortriptyline, are thought to work by increasing certain neurotransmitters in the spinal cord and brain involved in regulating pain pathways. But they may also alter chemical signaling in the gastrointestinal tract, leading to an upset stomach.

All these medications are prescribed by doctors.

Opioids

Opioids are chemicals found or derived from the opium poppy. One of the earliest opioids, morphine, was purified in the 1800s. Since then, medical use of opioids has expanded to include many natural and synthetic derivatives of morphine with varying potency and duration. Some common examples include codeine, tramadol, hydrocodone, oxycodone, buprenorphine and fentanyl.

Opioids decrease pain by activating the body’s endorphin system. Endorphins are a type of opioid your body naturally produces that decreases incoming signals of injury and produces feelings of euphoria—the so-called “runner’s high.” Opioids simulate the effects of endorphins by acting on similar targets in the body. Although opioids can decrease some types of acute pain, such as after surgery, musculoskeletal injuries like a broken leg, or cancer pain, they are often ineffective for neuropathic injuries and chronic pain.

Because the body uses opioid receptors in other organ systems like the gastrointestinal tract and the lungs, side effects and risks include constipation and potentially fatal suppression of breathing. Prolonged use of opioids may also lead to tolerance, where more drug is required to get the same painkilling effect. This is why opioids can be addictive and are not intended for long-term use. All opioids are controlled substances and are carefully prescribed by doctors because of these side effects and risks.

Cannabinoids

Although cannabis has received a lot of attention for its potential medical uses, there isn’t sufficient evidence available to conclude that it can effectively treat pain. Since the use of cannabis is illegal at the federal level in the US, high-quality clinical research funded by the federal government has been lacking.

Researchers do know that the body naturally produces endocannabinoids, a form of the chemicals in cannabis, to decrease pain perception. Cannabinoids may also reduce inflammation. Given the lack of strong clinical evidence, physicians typically don’t recommend them over FDA-approved medications.

Matching pain to drug

While sounding the pain alarm is important for survival, dampening the klaxon when it’s too loud or unhelpful is sometimes necessary.

No existing medication can perfectly treat pain. Matching specific types of pain to drugs that target specific pathways can improve pain relief, but even then, medications can fail to work even for people with the same condition. More research that deepens the medical field’s understanding of the pain pathways and targets in the body can help lead to more effective treatments and improved pain management.

Source: How do painkillers kill pain? It’s about meeting the pain where it’s at | Ars Technica

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This Is Where We’re Most at Risk From Toxic Microplastics

Australians are eating and inhaling significant numbers of tiny plastics at home, our new research shows. These “microplastics”, which are derived from petrochemicals extracted from oil and gas products, are settling in dust around the house. Some of these particles are toxic to humans — they can carry carcinogenic or mutagenic chemicals, meaning they potentially cause cancer and/or damage our DNA.

We still don’t know the true impact of these microplastics on human health. But the good news is, having hard floors, using more natural fibres in clothing, furnishings and homewares, along with vacuuming at least weekly can reduce your exposure.

What are microplastics?

Microplastics are plastic particles less than five millimetres across. They come from a range of household and everyday items such as the clothes we wear, home furnishings, and food and beverage packaging. We know microplastics are pervasive outdoors, reaching remote and inaccessible locations such as the Arctic, the Mariana Trench (the world’s deepest ocean trench), and the Italian Alps. Our study demonstrates it’s an inescapable reality that we’re living in a sea of microplastics — they’re in our food and drinks, our oceans, and our homes.

What we did and what we found

While research has focused mainly on microplastics in the natural environment, a handful of studies have looked at how much we’re exposed to indoors. People spend up to 90% of their time indoors and therefore the greatest risk of exposure to microplastics is in the home. Our study is the first to examine how much microplastic we’re exposed to in Australian homes. We analysed dust deposited from indoor air in 32 homes across Sydney over a one-month period in 2019.

We asked members of the public to collect dust in specially prepared glass dishes, which we then analysed. We found 39% of the deposited dust particles were microplastics; 42% were natural fibres such as cotton, hair and wool; and 18% were transformed natural-based fibres such as viscose and cellophane. The remaining 1% were film and fragments consisting of various materials. Between 22 and 6,169 microfibres were deposited as dust per square metre, each day.

Homes with carpet as the main floor covering had nearly double the number of petrochemical-based fibres (including polyethylene, polyamide and polyacrylic) than homes without carpeted floors. Conversely, polyvinyl fibres (synthetic fibres made of vinyl chloride) were two times more prevalent in homes without carpet. This is because the coating applied to hard flooring degrades over time, producing polyvinyl fibres in house dust.

Microplastics can be ingested by various animals, ranging in size from tiny creatures like zooplankton to sharks and whales. The likelihood of microplastics being eaten is influenced by the amount in the environment and how closely they resemble food. Laboratory studies indicate that microplastics can potentially transfer through the food web when marine, terrestrial and freshwater species that have previously ingested microplastics are preyed on by other animals.

Microplastics eaten by larger marine animals will generally pass through their bodies. However, research does show that microplastics can be retained in the gut for extended periods where they may cause abrasion and damage to internal tissues. Nanoplastics can pass through the gut wall and travel to different parts of the body, such as the lungs and liver, where they can cause damage. Further research is required to understand the potential health implications from ingesting microplastics.

Microplastics can be toxic

Microplastics can carry a range of contaminants such as trace metals and some potentially harmful organic chemicals. These chemicals can leach from the plastic surface once in the body, increasing the potential for toxic effects. Microplastics can have carcinogenic properties, meaning they potentially cause cancer. They can also be mutagenic, meaning they can damage DNA.

However, even though some of the microplastics measured in our study are composed of potentially carcinogenic and/or mutagenic compounds, the actual risk to human health is unclear. Given the pervasiveness of microplastics not only in homes but in food and beverages, the crucial next step in this research area is to establish what, if any, are safe levels of exposure.

How much are we exposed to? And can this be minimised?

Roughly a quarter of all of the fibres we recorded were less than 250 micrometres in size, meaning they can be inhaled. This means we can be internally exposed to these microplastics and any contaminants attached to them.

Using human exposure models, we calculated that inhalation and ingestion rates were greatest in children under six years old. This is due to their lower relative body weight, smaller size, and higher breathing rate than adults. What’s more, young children typically have more contact with the floor, and tend to put their hands in their mouths more often than adults.

What is the World Economic Forum doing about plastic pollution?

More than 90% of plastic is never recycled, and a whopping 8 million metric tons of plastic waste are dumped into the oceans annually. At this rate, there will be more plastic than fish in the world’s oceans by 2050. The Global Plastic Action Partnership (GPAP) is a collaboration between businesses, international donors, national and local governments, community groups and world-class experts seeking meaningful actions to beat plastic pollution.

In Ghana, for example, GPAP is working with technology giant SAP to create a group of more than 2,000 waste pickers and measuring the quantities and types of plastic that they collect. This data is then analysed alongside the prices that are paid throughout the value chain by buyers in Ghana and internationally. It aims to show how businesses, communities and governments can redesign the global “take-make-dispose” economy as a circular one in which products and materials are redesigned, recovered and reused to reduce environmental impacts.

Children under six inhale around three times more microplastics than the average — 18,000 fibres, or 0.3 milligrams per kilogram of body weight per year. They would also ingest on average 6.1 milligrams of microplastics in dust per kg of body weight per year. For a five-year-old, this would be equivalent to eating a garden pea’s worth of microplastics over the course of a year. But for many of these plastics there is no established safe level of exposure. Our study indicated there are effective ways to minimise exposure.

First is the choice of flooring, with hard surfaces, including polished wood floors, likely to have fewer microplastics than carpeted floors. Also, how often you clean makes a difference. Vacuuming floors at least weekly was associated with less microplastics in dust than those that were less frequently cleaned. So get cleaning! Some pollutants and heavy metals can also adsorb or stick to plastic surfaces. As a result, plastics can act like sponges in the environment, passively collecting chemicals onto their surfaces.

While plastics can remove some persistent organic pollutants (POPs) from the surrounding water, there is concern about what happens when plastics containing these adsorbed pollutants are ingested by animals. The ability of some POPs to bind to plastics is particularly concerning due to their toxicity at low doses. These toxic and persistent chemicals are widely distributed in the marine environment and are readily concentrated onto plastic surfaces at up to 1 million times the concentration than in the surrounding water.

Studies have shown that these chemicals can transfer from ingested plastics to animal tissue where they can become concentrated within the animal and transfer through the food chain. Plastics are beneficial to human health through their use in medical applications and for protecting our food and beverages. Plastics have revolutionized healthcare through improving sterility by the use of disposable syringes, gloves, IV tubes and catheters and providing increased comfort with hypoallergenic medical devices, heart valves, and flexible prosthetics (artificial body parts).

Plastic bottles and containers provide a way of distributing water that is safe to drink in locations where there are major issues of water contamination. Plastic packaging limits food and beverage spoilage through microbial contamination. It is likely that we are ingesting some level of plastics in our diet. A rapidly growing body of research is showing that ongoing accumulation of toxins associated with plastics poses a risk to our food safety and public health. However, the levels of plastics and associated chemicals we are exposed to in our diet compared with other everyday activities has not been assessed.

Source: This is where we’re most at risk from toxic microplastics | World Economic Forum

More contents:

Microplastic Ingestion by Zooplankton”

Where Does Marine Litter Come From?”

Chemical mapping of tire and road wear particles for single particle analysis”.

“Plastic free July: How to stop accidentally consuming plastic particles from packaging”

Development solutions: Building a better

“Proceedings of the International Research Workshop on the Occurrence, Effects and Fate of Microplastic Marine Debris”

Annual variation in neustonic micro- and meso-plastic particles and zooplankton in the Bay of Calvi (Mediterranean–Corsica)”

Restricting the use of intentionally added microplastic particles to consumer or professional use products of any kind”.

Microplastics have spread right to the sea bed, study finds 

90% of table salt is contaminated with microplastics, according to a new report

The water where baby fish are outnumbered 7 to 1 by plastic

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