Breathe clean air, not microplastics! Tyre wear – an underestimated source of air pollution that needs to be tackled

Plastic degradation in our environment is a global threat that affects our planet and our health. According to a new study published by Hull York Medical School (United Kingdom) in March 2022, for the first time, microplastic pollution has been discovered lodged deep in the lungs of living people. In the same month, microplastics were also detected in human blood for the first time, showing that microplastic particles can not only enter the body but travel around and possibly lodge themselves in people’s organs.

Made of synthetic polymers, microplastics are small pieces of plastics, usually smaller than 5 millimetres, which do not biodegrade and tend to accumulate once in the environment. Microplastic pollution is now ubiquitous across the planet, from the summits of the Himalayas to the bottom of world’s deepest ocean trench, and to the placentas of pregnant women. As a result, there is increasing concern regarding the impact of microplastics on the environment and human health.

Despite the huge problem that microplastics pose, there is currently no single European law that covers microplastic pollution in a comprehensive manner. The European Commission now wants to reduce the amount of unintentionally released microplastics in the environment, including those from automotive tyres. The Commission plans to publish its legislative initiative by the end of 2022 and needs feedback from key stakeholders, such as representatives of civil society and health experts. The public consultation is open for feedback until 17 May 2022.

EPHA has been working on tackling air pollution emitted by the road sector for a long time now. As part of its work on tackling the health impacts of non-exhaust road emissions, EPHA is focusing more on microplastics emissions from tyre abrasion. According to preliminary research led by the Commission, microplastics emissions from automotive tyres in the EU 27 equals approximately 450,000 tonnes per year.

As tyre and road wear particles (TRWP) are caused by the friction process between tyres and the road surface, the best solution to decrease tyre wear emissions is to tackle it at the source by reducing driving mileage. EPHA supports switching to active and shared mobility such as walking cycling and public transport, wherever possible. Promoting active mobility reduces the consumption of fossil fuels and consequently carbon emissions, whilst also improving health by increasing physical activity. It is also important to promote the shift of freight transport from the roads to more efficient and less polluting rail and waterways. Similarly, vehicle weight and tyre wear are correlated: as the load increases, the tyre wear emission also increases. Hence, decreasing the size and the mass of vehicles reduces TRWP as well as their CO2 emissions, life cycle ecological footprint, and road accident risks. EPHA is in favour of establishing a regulatory framework that precisely limits the mass, power, and speed of cars, as developed by the LISA (LIght and SAfe) car project. The current trend towards ever bigger and heavier SUVs cannot continue.

Another key solution that the European Commission must consider is improvements in tyre characteristics including banning tyres with high microplastic emissions from the market with a clear limit value for abrasion. In contrast to exhaust emissions, there are no tyre abrasion limits in the EU and no labelling of tyre’s based on their abrasion performance. As a result, poorly performing tyres are present on the EU market. These are not just bad for health and the environment but also hurt consumer pockets through poor durability. Nevertheless, the recently revised Tyre Labelling Regulation is expected to provide a standardised test method to determine the abrasion rate of tyres. This regulation will make it possible to test their abrasion performance and set a limit value to remove the worst performers from the market. The test method could also allow information on abrasion, lifespan and microplastic release to be included in the tyre energy label.

Finally, it is crucial that tyre manufacturers develop new tyres with less tyre wear emissions. To encourage manufactures to take action, the Extended Producer Responsibility (EPR) approach should be taken. EPR is a policy under which producers are given significant financial or physical responsibility for the treatment or disposal of post-consumer products. Assigning such responsibility to tyre manufacturers for microplastic pollution would incentivise prevention of microplastic pollution at the source and promote product design for the environment and health.

These actions will beyond doubt improve air quality across Europe.

For more information on the production, use and recycling of plastics their consequences for our health, read “Turning the Plastic Tide” by the Health and Environment Alliance (HEAL). 

Breathe clean air, not microplastics! Tyre wear – an underestimated source of air pollution that needs to be tackled – EPHA
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Air pollution exposure may cause heart attack within an hour

Exposure to air pollutants—even at levels below World Health Organization air quality guidelines—may trigger a heart attack within the hour, according to a new study from China that found the risks were highest among older people and when the weather was colder.

The study found exposure to any level of four common air pollutants could quickly trigger the onset of acute coronary syndrome. ACS is an umbrella term describing any situation in which blood supplied to the heart muscle is blocked, such as in a heart attack or unstable angina, chest pain caused by blood clots that temporarily block an artery. The strongest risk occurred within the first hour of exposure and diminished over the course of the day.

“The adverse cardiovascular effects of air pollution have been well documented. But we were still surprised at the very prompt effects,” said Haidong Kan, a professor in the School of Public Health at Fudan University in Shanghai. He led the study published Friday in the American Heart Association’s journal Circulation.

“Another surprise was the non-threshold effects of air pollution,” he said. “In other words, any concentrations of air pollutants (such as fine particulate matter, nitrogen dioxide, sulfur dioxide and carbon monoxide) recorded in the present study may have the potential to trigger the onset of a heart attack.”

Exposure to fine particulate matter—microscopic solids or liquid droplets that come from automobile emissions, power plants, construction sites and other sources of pollution—has been unequivocally linked to heart disease, stroke and other health issues, as well as 4.2 million premature deaths worldwide. These particles can be so small that when inhaled, they may go deep into the lungs or even the bloodstream.

In the new study, researchers analyzed medical data for nearly 1.3 million people treated for heart attacks and unstable angina at 2,239 hospitals in 318 Chinese cities between 2015 and 2020. They compared hourly onset times of heart events with concentrations of fine particulate matter, coarse particulate matter, nitrogen dioxide, sulfur dioxide, carbon monoxide and ozone.

Short-term exposure to any level of fine particulate matter, nitrogen dioxide, sulfur dioxide and carbon monoxide was associated with the onset of all types of acute coronary syndrome.

As levels of the studied pollutants rose, so did the risk for heart attacks. Exposure to nitrogen dioxide was most strongly associated, followed by fine particulate matter, and was most dangerous during the first hour following exposure. The link was strongest among adults age 65 and older with no history of smoking or other respiratory illnesses and for people exposed during the colder months.

“The cardiovascular effects of air pollution should be a serious concern for all, including policymakers, clinicians and individuals,” Kan said. “For policymakers, our findings underline the need of further tightening air quality standards, more stringent air pollution control and prompt public health response.”

The study is the first to establish a link between pollution exposure and heart attacks on an hourly basis, said Dr. Sanjay Rajagopalan, director of the Cardiovascular Research Institute at Case Western Reserve University in Cleveland. Rajagopalan was not involved in the study.

“The authors were able to show with a fair degree of certainty that air pollution levels at the hour of heart attack occurrence were strongly correlated with air pollution levels during that same hour,” he said. “This suggests that taking protective measures when air pollution levels are high could help prevent heart attacks.”

Rajagopalan co-authored an AHA scientific statement in 2020 about how to reduce exposure to air pollution. Strategies include closing windows and using portable air cleaners and built-in air conditioning filters, as well as personal air-purifying respirators that cover the nose and mouth for people at high risk.

Properly fitted masks, such as those used to prevent the spread of COVID-19, also can help, Rajagopalan said.

“One of the silver linings of COVID-19 is the widespread use of N95 masks,” he said. “These are very good at reducing particulate exposures. They will stop you from inhaling them.”

Though this study was done in China, which has some of the worst air quality in the world, the findings still are meaningful for other countries, Kan said.

The fact there was no threshold of pollution—no minimum that was safe—suggests the findings can be applied to countries with lower levels of air pollution, such as the U.S., he said. “However, the effects of specific air pollutants on ACS need to be replicated given the apparent differences of air pollution characteristics and population vulnerability.”

Air pollution exposure may cause heart attack within an hour
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Scientists Discover How Air Pollution Alters Lung Tissue, Increasing Cancer Susceptibility

Inhaled fine particulate matter (shown here in red) pulls strings of collagen to disturb the immune defense in mice with lung cancer cells. This activity delays the movement of cytotoxic T-cells (purple) as they migrate towards the cancer cells (green) to destroy them. Credit: Wang et al.

Research findings highlight a potential new target for preventing lung disease caused by air pollution.

According to a paper published in the journal eLife on April 19, 2022, scientists have uncovered a mechanism that explains how small air pollution particles may induce lung cancer.

The discovery could pave the way for novel techniques to prevent or treat the early lung alterations that lead to the disease.

Tiny, inhalable fine particulate matter (FPM) found in air pollutants has been recognized as a Group 1 carcinogen and a substantial threat to global health. However, the cancer-causing mechanism of FPM remains unclear.

“Despite its potential to cause mutations, recent research suggests that FPM does not directly promote – and may even inhibit – the growth of lung cancer cells,” explains first author Zhenzhen Wang, an associate researcher at Nanjing University (NJU), Nanjing, China, who carried out the study between labs at NJU and the University of Macau where she was sponsored by a University of Macau Fellowship. “This suggests that FPM might lead to cancer through indirect means that support tumor growth. For example, some studies suggest FPM can prevent immune cells from moving to where they are needed.”

To explore this possibility, Wang and the team collected FPM from seven locations in China and studied its effects on the main immune cells that defend against tumor growth – called cytotoxic T-cells (CTLs). In mice administered with lung cancer cells that were not exposed to FPM, CTLs were recruited to the lung to destroy the tumor cells. By contrast, in the mice whose lungs were exposed to FPM, the infiltration of CTLs was delayed – potentially allowing the tumor cells to establish in lung tissue.

To investigate why the CTLs did not enter the lung as quickly in the FPM-exposed lungs, the team studied both the CTLs themselves and the lung tissue structure. They found that CTLs exposed to FPM still retained their migratory ability, but that FPM exposure dramatically compressed the lung tissue structure and the spaces that immune cells move between. There were also much higher levels of collagen – a protein that provides biomechanical support for cells and tissues. When the team studied the movement of CTLs in the mice, in lung tissue exposed to FPM, CTLs struggled to move, whereas those in the untreated tissue were able to move freely.

Further analysis of the tissue showed that the structural changes were caused by increases in a collagen subtype called collagen IV, but the team still did not know how FPM triggered this. They found the answer when they looked more closely at the structural changes to collagen IV and the enzyme responsible for making them – called peroxidasin. This enzyme drives a specific type of cross-linking that exposure to FPM was found to cause and aggravate in the lung tissue.

“The most surprising find was the mechanism by which this process occurred,” Wang says. “The peroxidasin enzyme stuck to the FPM in the lung, which increased its activity. Taken together, this means that wherever FPM lands in the lung, increased peroxidasin activity leads to structural changes in the lung tissue that can keep immune cells out and away from growing tumor cells.”

“Our study reveals a completely new mechanism by which inhaled fine particles promote lung tumor development,” concludes senior author Lei Dong, Professor at the School of Life Sciences, Nanjing University. “We provide direct evidence that proteins that stick to fine particulate matter can cause a significant and adverse effect, giving rise to pathogenic activity. Our discovery that peroxidasin is the mediator of this effect in lung tissue identifies it as a specific and unexpected target for preventing lung disease caused by air pollution.”

Reference: “Air pollution particles hijack peroxidasin to disrupt immunosurveillance and promote lung cancer” by Zhenzhen Wang, Ziyu Zhai, Chunyu Chen, Xuejiao Tian, Zhen Xing, Panfei Xing, Yushun Yang, Junfeng Zhang, Chunming Wang and Lei Dong, 19 April 2022, eLife.DOI: 10.7554/eLife.75345

Scientists Discover How Air Pollution Alters Lung Tissue, Increasing Cancer Susceptibility
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Air pollution linked to higher risk of COVID-19 in young adults

Residential exposure to ambient air pollutants is linked to an elevated risk of SARS-CoV-2 infection, an observational study of young adults in Stockholm, Sweden shows. The study was conducted by researchers from Karolinska Institutet and is published in JAMA Network Open.

Since pollutants in outdoor air can increase the risk of respiratory infections such as influenza and SARS, the COVID-19 pandemic aroused fears that they could also contribute to the risk of SARS-CoV-2 infection. Studies have also shown that areas of poor air quality have more cases of COVID-19.

Researchers at Karolinska Institutet have now studied this more closely by examining the link between estimated exposure to air pollutants at home addresses and positive PCR tests for SARS-CoV-2 in young adults in Stockholm, Sweden.

The results show that exposure to certain traffic-related air pollutants is associated with a greater likelihood of testing positive.

“Our results add to the growing body of evidence that air pollution has a part to play in COVID-19 and support the potential benefit of improving air quality,” says Olena Gruzieva, associate professor at the Institute of Environmental Medicine at Karolinska Institutet and one of the study’s last authors.

The study draws on the population-based BAMSE project, which has regularly followed over 4,000 participants in Stockholm from birth. By linking these data to the national communicable disease registry (SmiNet), the researchers identified 425 individuals who had tested positive for SARS-CoV-2 (PCR test) between May 2020 and the end of March 2021. The average age of the participants was 26, and 54 per cent were women.

Daily outdoor concentrations of different air pollutants at the participants’ home addresses were estimated using dispersion models. The pollutants were particles with a diameter less than 10 micrometers (PM10) and 2.5 micrometers (PM2.5), black carbon and nitrogen oxides.

The researchers studied the associations between infection and exposure to air pollutants in the days before the positive PCR test, on the day of the test and on later control days. Each participant served as his or her own control on these different occasions.

The results show associations between infection risk and exposure to PM10 and PM2.5 two days before a positive test and exposure to black carbon one day before. They found no link between the risk of infection and nitrogen oxides.

The increase in risk was of an order of magnitude around seven per cent per particle exposure increase equivalent to the interquartile range, i.e. between the first quartile (25%) and the third quartile (75%) of the estimated particle concentrations.

“Seven per cent doesn’t sound much, but given that everyone is more or less exposed to air pollutants, the association may be of great significance to public health,” says Erik Melén, professor of paediatrics at the Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, BAMSE project leader and the study’s joint last author.

The observed association was not influenced by gender, smoking, overweight or asthma.

The researchers note that the results might be affected by the willingness to take a PCR test and the fact that many of the young adults were asymptomatic or had only mild symptoms following infection. The study can also not rule out the possibility that time-varying confounding factors also influenced the results.

The researchers are now examining the link between air pollutants and post-COVID symptoms in young adults.

The first author of the paper is Zhebin Yu, postdoctoral researcher in Olena Gruzieva’s group. The study was financed by Forte, the Swedish Research Council, the Swedish Heart-Lung Foundation and Region Stockholm. The authors have reported no conflicts of interest.

Air pollution linked to higher risk of COVID-19 in young adults — ScienceDaily
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Researchers map lung development after birth

How do the lungs develop after taking their first breaths outside the womb? What cellular events and changes early in life give rise to lung malfunction and disease? To help answer these questions, scientists have constructed the first single-cell atlas of postnatal lung development in humans and mice.

The research could help provide a more detailed understanding—at the level of individual cells—of which genetic and epigenetic factors affect lung health across the human lifespan, starting from birth. 

The work, recently published in Cell Genomics, was led by a team of researchers at the University of California San Diego and the University of North Carolina at Chapel Hill.

By analyzing lung tissue samples from newborn and young humans and mice, the researchers were able to gain insights on how certain cell types in the lung originate and change during childhood.

“These are unique samples that we’ve collected information on during a time in lung development that has not been well studied,” said first author Thu Elizabeth Duong, a physician-scientist in pediatric respiratory medicine at UC San Diego School of Medicine and pulmonologist at Rady Children’s Hospital-San Diego. “What’s exciting is being able to see, at single-cell resolution, what the lung cells are doing at this stage in development.”

The goal is to build a so-called “reference map” of the human lungs. Such a map would serve as a foundation to understand the cellular differences between healthy and diseased lungs. This work represents a small step toward building a reference for the pediatric population.

“Your respiratory health gets shaped by what happens during your early years of life. So when things go wrong, we can refer back to these early years to identify potential causes of disease,” said Duong.

“In cases of lung abnormality or disease, we can zoom in and examine what specific types of cells are different from their counterparts in the healthy references and what are the molecular pathways underlying these changes,” said Kun Zhang, professor and chair of bioengineering at UC San Diego who is a senior author of the study. “Diagnosis and treatment could then be developed based on differences from the reference map.”

The lungs are an important barrier in the body. They let in and maintain the balance of vital substances such as oxygen, while removing wastes such as carbon dioxide. And they filter the air that we breathe. The researchers hope that their findings here will lay the groundwork for more in-depth studies of how environmental factors such as exposure to air pollution and smoking influence lung health and disease throughout different stages of life.

To construct their map, the researchers analyzed post-mortem human lung tissues that were collected at different time points, starting from day one and up to 9 years after birth. The researchers also collected lung tissue samples from mice at matching time points between one day and nearly one month after birth.

The researchers used next-generation single-cell sequencing technologies developed in Zhang’s lab to analyze individual nuclei of more than 80,000 human and mouse lung cells combined.

With this analysis, the researchers could start to map developmental pathways for different lung cell types including alveolar epithelial type 1 cells. These cells are vital for the exchange of oxygen and carbon dioxide gases. The researchers gained clues as to how alveolar type 1 cells communicate with other cells such as myofibroblasts, and how this communication could play a role in alveolar cell development.

The study also revealed a unique population of fibroblast cells in the human lung that was not observed in mice. These fibroblasts are cells in connective tissue that play a role in how the lungs stretch. The researchers also found cell states in the human lung that are present in early life at birth but disappear by 9 years of age.

“These data are helping us piece together how key cell types in the lung come into existence,” said Duong. “We hope this will serve as a valuable resource for lung researchers moving forward.”

Paper: “A single-cell regulatory map of postnatal lung alveologenesis in humans and mice.” Co-authors include Yan Wu, Brandon Chin Sos, Weixiu Dong and Siddharth Limaye, UC San Diego; Lauraine H. Rivier, Greg Myers and James S. Hagood, University of North Carolina at Chapel Hill.

Researchers map lung development after birth | EurekAlert!
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Tropical city air pollution led to 470,000 premature deaths in 2018

Cities in the tropics are experiencing a growing air pollution problem, which is estimated to have led to a 62 per cent rise in premature deaths since 2005

Some 470,000 people in cities near the equator died prematurely in 2018 because of air pollution, an analysis suggests. As the cities are expected to grow rapidly this century, the problem could become worse without new measures to reduce the pollution.

Karn Vohra at University College London and his colleagues analysed the rise in fine particulate pollution in 46 tropical cities, including Mumbai, Dhaka and Lagos, each of which is expected to have more than 10 million inhabitants by 2100. The researchers looked at satellite data collected between 2005 and 2018 by NASA and the European Space Agency.

They were able to decipher the long-term trends in fine particulate pollution in the air above each city by looking at how sunlight was scattered by the particles. From this, they found there was a 1.5-to-fourfold increase in this pollution for 33 of the cities during the study period.

Vohra says this rise is probably caused by increases in road traffic, refuse burning and the household use of charcoal.

The team then put the data into a health risk model that links a rise in exposure to fine particulate pollution to premature mortality. The results suggested that more than 30 per cent of known premature deaths in Asia are partly caused by this pollution, according to Vohra.

“These [particles] penetrate deep into our lungs and have been shown to impact just about every organ in our body,” he says.

The research indicates that Dhaka, the capital of Bangladesh, had the largest increase in premature deaths from air pollution during the study period. Between 2005 and 2018, about 24,000 more people in the city may have died prematurely because of air pollution.

The problem is worsening, both because more pollution is being generated and because the cities are growing. The research suggests that, across the tropics, there has been a 62 per cent increase in the number of premature deaths due to air pollution exposure between 2005 and 2018.

Vohra says even more people will die prematurely unless solutions are found. “Even if air quality is unchanged, urban population is increasing in all cities in the tropics, so this will inevitably increase urban exposure,” he says.

“I think this study gives a good overview of recent air pollution trends in rapidly growing cities across Africa, South and South-East Asia,” says Miranda Loh at the Institute of Occupational Medicine.

“Satellite data and models – as used in the article – are useful for this type of global analysis, especially if there is a lack of ground monitoring data. But if we want to better track population exposures, it is important to improve ground-level monitoring worldwide,” she says.

Journal reference: Science Advances, DOI: 10.1126/sciadv.abm4435

Tropical city air pollution led to 470,000 premature deaths in 2018 | New Scientist
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Smog smothers Beirut at the start of Spring

Beirut’s air quality is a consistent problem, creating long-term health risks for its residents.

A heavy cloud of smog smothered Lebanon’s capital city of Beirut this week, with air pollutant levels reaching a high of 9.5 times the WHO recommended air quality index.

The smog is “seasonal” and a product of dust carried from deserts from neighbouring countries, Dr Najat Saliba, an atmospheric chemist and professor at the American University of Beirut, told The New Arab.

She added that Jordan and other regional neighbours were experiencing similar air pollution.

Beirut’s air pollution is a constant problem, and smog hanging over the mountain-fringed port city is visible year-round.

“Beirut has a more or less constant average of 30 micrograms of fine particulate matter per cubic meter… which is six times higher than the annual average recommended by the WHO,” Saliba said.

Poor air quality can have an immediate effect on those suffering from chronic respiratory diseases, such as asthma. Over the long term, persistent pollutants can lead to health concerns such as cancer and decreased lung capacity.

The main cause of Beirut’s worsening air quality is the widespread use of personal generators to power city residences, as well as the old age of vehicles in the city.

According to Dr Saliba, the average age of a car in Beirut is 19 years old – which is likely to persist given Lebanon’s economic crisis.

Lebanon has suffered from an acute energy crisis over the past two years, with the national power grid providing only two-three hours of electricity a day.

Households, businesses and public institutions have turned to privately owned generators for electricity, consuming tons of diesel a week and throwing up fumes across the country.

“Generators are loaded with small particles which contain heavy metals and carcinogens. Long-term exposure to this is definitely linked to cancer. We have been exposed to these fumes for over 10 years, and that’s very bad,” Dr Saliba said.

She added that a turn towards renewable energies, centralising power generation and creating more options for public transport are easily achievable and practical steps to lessen air pollution in Lebanon.

Despite continuing promises by the sitting Energy Minister that state power will increase soon, the national power company is continuing to be mired in inefficiency.

The national power company will reportedly struggle to keep the country’s lights on during the 15 May elections next month.

Smog smothers Beirut at the start of Spring

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Microplastics found deep in lungs of living people for first time

Particles discovered in tissue of 11 out of 13 patients undergoing surgery, with polypropylene and PET most common

Microplastic pollution has been discovered lodged deep in the lungs of living people for the first time. The particles were found in almost all the samples analysed.

The scientists said microplastic pollution was now ubiquitous across the planet, making human exposure unavoidable and meaning “there is an increasing concern regarding the hazards” to health.

Samples were taken from tissue removed from 13 patients undergoing surgery and microplastics were found in 11 cases. The most common particles were polypropylene, used in plastic packaging and pipes, and PET, used in bottles. Two previous studies had found microplastics at similarly high rates in lung tissue taken during autopsies.

People were already known to breathe in the tiny particles, as well as consuming them via food and water. Workers exposed to high levels of microplastics are also known to have developed disease.

Microplastics were detected in human blood for the first time in March, showing the particles can travel around the body and may lodge in organs. The impact on health is as yet unknown. But researchers are concerned as microplastics cause damage to human cells in the laboratory and air pollution particles are already known to enter the body and cause millions of early deaths a year.

“We did not expect to find the highest number of particles in the lower regions of the lungs, or particles of the sizes we found,” said Laura Sadofsky at Hull York medical school in the UK,a senior author of the study. “It is surprising as the airways are smaller in the lower parts of the lungs and we would have expected particles of these sizes to be filtered out or trapped before getting this deep.”

“This data provides an important advance in the field of air pollution, microplastics and human health,” she said. The information could be used to create realistic conditions for laboratory experiments to determine health impacts.

The research, which has been accepted for publication by the journal Science of the Total Environment, used samples of healthy lung tissue from next to the surgery targets. It analysed particles down to 0.003mm in size and used spectroscopy to identify the type of plastic. It also used control samples to account for the level of background contamination.

A 2021 study in Brazil on autopsy samples found microplastics in 13 of the 20 people analysed, whose average age was higher than those assessed by Sadofsky’s study. Polyethylene, used in plastic bags, was one of the most common particles. The researchers concluded: “Deleterious health outcomes may be related to … these contaminants in the respiratory system following inhalation.”

A US study of lung cancer patients in 1998 found plastic and plant fibres (such as cotton) in more than 100 samples. In cancerous tissue, 97% of samples contained the fibres and in non-cancerous samples, 83% were contaminated.

Huge amounts of plastic waste are dumped in the environment, and microplastics contaminate the entire planet, from the summit of Mount Everest to the deepest oceans. Microplastics have been found in the placentas of pregnant women, and in pregnant rats they pass rapidly through the lungs into the hearts, brains and other organs of the foetuses.

A recent review assessed cancer risk and concluded: “More detailed research on how micro- and nanoplastics affect the structures and processes of the human body, and whether and how they can transform cells and induce carcinogenesis, is urgently needed, particularly in light of the exponential increase in plastic production.”

Microplastics found deep in lungs of living people for first time | Plastics | The Guardian
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