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By Elizabeth Gribkoff

Around the world, regulators have long relied on one compound to assess a community's lung cancer risk from a class of chemicals that we're exposed to while grilling burgers, waiting in traffic, and breathing in wood smoke from a fire.

That compound—benzo(a)pyrene, a polycyclic aromatic hydrocarbon (PAH)—however, only accounts for 11% of lung cancer risk associated with PAHs, MIT researchers found in a study published earlier this month in GeoHealth. Meanwhile, 17% of the PAH-linked cancer risk in the study came from the largely unregulated and under-studied breakdown products.


People can be exposed to PAHs in a variety of ways, from smoking to eating grilled food to breathing in tailpipe or wildfire emissions. Workers in coal plants, or those who use coal products, are considered especially at-risk to PAH exposure.

When people inhale PAH particles, the particles can travel deep into the lungs, causing cell mutations that can lead to lung cancer. Scientists are also concerned about exposure to PAHs through food and drinking water, as ingestion has been linked to birth defects and higher prevalence of developing breast, pancreatic, and colon cancers.

Experts say this study provides further evidence that both regulators and scientists need to factor in a broader range of PAH compounds when assessing a community's cancer risks — and determining what pollution reduction projects to fund.

"The big challenge in regulating air pollutants is: What are the most important sources and locations to prioritize?" Noelle Selin, director of MIT's Technology and Policy Program and a co-author of the paper, told EHN. "If you're using just a model of benzo(a) pyrene, you might not actually end up with the best answer in terms of the most beneficial reductions."

Toxic Breakdown Products

In the 1970s, the U.S. Environmental Protection Agency (EPA) identified 16 of the more than 10,000 PAH compounds as pollutants of concern, and since then, that group of chemicals has been widely monitored around the world. One of those—benzo(a)pyrene—is still used as the toxicity benchmark for polycyclic aromatic hydrocarbons in epidemiological studies, in large part because it's the best-studied PAH.

But in recent years, researchers have been questioning whether that narrow focus makes sense. In particular, researchers have been challenging the assumption that once PAH compounds break down in the atmosphere, they're no longer carcinogenic. "It turns out that some of the products that they can react to are even more toxic than what's initially emitted," said Selin.

As part of their work on a Superfund site in Maine, the MIT researchers examined global lung cancer risk from 16 PAH compounds and their degradation products — 48 altogether.

Once they had developed a global atmospheric model for PAH concentrations and fine-tuned it against real-world pollutant measurements, the researchers used animal studies to assess the associated lung cancer risk from different PAH compounds. They also estimated lung cancer risks based on epidemiological studies that use benzo(a)pyrene as a proxy for overall PAH cancer risk.

While they found that industrial regions in China, India, and Eastern Europe had the highest levels of lung cancer risk in both methods, animal experiments showed that changing benzo(a)pyrene emissions did not have a linear correlation with overall lung cancer risk from PAHs. For example, although simulated benzo(a)pyrene emissions were 3.5 times higher in Hong Kong than in India, the animal-based method predicted that Hong Kong residents are 12 times more likely to develop lung cancer, according to the paper.

While it's difficult to scale up the animal studies to human outcomes, that data provides researchers with a window into the "relative importance" of different PAH compounds in overall cancer risk, said Selin. The study also showed the importance of monitoring the sub-compounds that PAHs can break down into.

Toxic Mixtures

Staci Simonich, an environmental toxicology professor at Oregon State University who also researches PAHs but was not involved in this study, told EHN that the new paper likely under-estimated the cancer risk as the researchers did not include the class of heavier-weight PAH compounds described in her 2011 study as a significant contributor to cancer risk. Selin said that her group had not included those and other PAH compounds due to limitations in global monitoring data — including having almost no measurements from Africa.

Both Selin and Simonich stressed the need for future studies that assess the risk of PAH mixtures, noting that the total toxicity might not always be as simple as just adding up the toxicity of the individual compounds.

"I think regulators, whether it's in air, soil or sediment, are getting the message … in Europe and the U.S. that you really have to take a much broader look at PAHs in terms of exposure and risk," said Simonich.

Reposted with permission from the Environmental Health News.

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Everyday cleaning products can emit harmful air pollution. SolStock / E+ / Getty Images

By Krystal Vasquez

A specific component of air particle pollution found in some common household products could be responsible for up to 900,000 premature deaths every year — 10 times greater than previous estimates, according to new research published in Atmospheric Chemistry and Physics.


While the majority of these components, referred to as anthropogenic secondary organic aerosols (ASOAs), are produced during the combustion of fossil fuels, some come from everyday use products, such as cleaning supplies, pesticides, or household paint.

"All those different smells you're getting from paint are different [volatile organic compounds] that are being emitted" into the air, Benjamin Nault, a research scientist at Aerodyne Research, Inc. and lead author of the study, told EHN. Once released, these gases, also known as VOCs, can transform into a new subset of stickier chemicals which clump together to form ASOAs.

Even though the majority of these compounds are produced indoors — and can play a role in creating poor indoor air quality — they will eventually escape outside through open windows or miniscule cracks in the foundation. In urban areas, ASOAs can make up a significant portion of the more commonly known pollutant, fine particulate matter (PM2.5).

"There's more people living in urban areas," Nault explains — more than 50% of the world's population, to be exact. With more people, "you need more of these everyday use products to paint all the apartments and townhouses, to put the asphalt down, [and] to clean everything up," said Nault. Urban populations are expected to increase by 150% by 2045.

Inhaling any type of particle — but especially PM 2.5 — can be detrimental to human health. According to the American Lung Association, potential health effects caused by prolonged exposure to PM 2.5 could include reduced lung function, the development of lung cancer, and an increased risk of death from cardiovascular disease. Because of this, many countries have developed laws that restrict the amount of particle-forming VOCs that can be released into the air. In the U.S., the creation of these regulations — especially those that have targeted transportation — have led to a nation-wide improvement in air quality.

Unfortunately, the same can't be said for the pollution created from these everyday consumer items, which are also referred to as volatile chemical products (VCPs). In contrast to the success seen in the transportation sector, emissions from VCPs are "remaining relatively flat or going up," said Nault, because they're "less regulated and more directly tied to everyday use and population."

VCPs are also more difficult to regulate as a whole since there are thousands of compounds emitted by a diverse range of sources that span from deodorant to asphalt to outdoor barbecues. Plus, the stickiness that makes them so efficient at forming ASOAs also makes them difficult to measure.

This "makes it really hard to say, 'these are the emissions that need to be regulated'... to improve public health," said Nault.

Air Pollution and Premature Deaths

Volatile chemical products are difficult to regulate as a whole since there are thousands of compounds emitted by a diverse range of sources that span from deodorant to asphalt to outdoor barbecues.

The new study builds upon previous work, led by the Cooperative Institute for Research in Environmental Sciences, that showed that VCP emissions are contributing to a large fraction of the PM 2.5 formed in Los Angeles. Even before that, however, the U.S. Environmental Protection Agency (EPA) has "long accounted for emissions from volatile chemical products in the National Emissions Inventory (NEI)," a spokesperson told EHN through email, and has been assessing their impact on air quality since at least 1995.

But many of these findings have been limited to the U.S., which is why Nault and his international team of researchers expanded the scope of research and incorporated air quality data collected across several continents. They found that 37% of ASOAs, on average, were derived from VCPs in cities located in North America, Europe, and Asia. "Other places around the world have both emissions from tailpipes, but also from these everyday use products," said Nault. "This is a global thing."

They then used models to correlate concentrations of ASOA to premature mortality and compared their values to previous estimates. Nault and his team suspect between 340,000 to 900,000 premature deaths are caused by ASOAs.

"There weren't very many estimates of [ASOA-related] premature deaths in literature prior to this," said Nault, but the ones that existed significantly underestimated the number of deaths ASOA contributed to.

It's likely this percentage of VCP-derived pollution could grow in the future as transportation emissions continue to decrease and city populations continue to grow. That's why, in the U.S., the National Volatile Organic Compound Emission Standard requires manufacturers to reduce the amount of VOCs emitted by consumer products to prevent formation of ozone, another dangerous pollutant. However, when swapping out these compounds in accordance with the rules, it's possible companies may inadvertently add others that are better equipped to create ASOAs.

"One of the big things that we really need is to really look at these products that we use every day and look at what is actually in them, and what is coming out of them," said Nault.

Consumer Products Regulation

Proper regulation of both VCPs and transportation emissions is paramount if we want to prevent premature deaths caused by ASOAs, especially considering that these numbers could be an underestimation. "We think that there's differences within the stuff in the [aerosols] that could lead to very different differences in health and mortality," said Nault.

Research led by the Gwangju Institute of Science and Technology (GIST) in South Korea backs this up. "Right now, it is assumed that the toxicity is the same for all types of particles," Kihong Park, a professor at GIST, told EHN. However, upon exposing human and animal cells to different types of particles, he concluded that's likely not the case.

"Typically, chemical components such salt species, sulfates, and nitrates have less toxicity than [polycyclic aromatic hydrocarbons], heavy metals, and organic compounds which are abundant in combustion-generated particles," Park explained. While he didn't assess the toxicity of VCP-derived particles in his original study, Park suspects that they might be comparable to aerosols that contain benzene or toluene, which elicited some of the highest toxicity scores in his study.

"In the future, we have to consider the differential toxicity of PM2.5, in addition to the amount of PM2.5, to better understand the effects of the PM2.5 on human health," said Park. "If the specific source for PM2.5 is more dangerous than others, we have to put more priority on the control of that source."

The U.S. has made great strides when it comes to improving our air quality. Much of this success has come from reducing transportation emissions. But we only focused on transportation because it "was very easy to recognize and say, 'this is where most of the pollution is coming from,'" said Nault.

Now, however, it's time to also turn our attention towards VCPs, he said.

The EPA spokesperson mentioned that the agency plans to "adopt new methods for quantifying emissions from volatile chemical products... as well as improve the representation of these emissions in air quality modeling efforts to better understand the relationship of volatile chemical products and criteria pollutants."

Still, more research needs to be done. "It's really tricky to try to track all those different [compounds]," explained Nault. Many ingredient lists are considered proprietary information and scientific equipment often struggles to measure all the compounds emitted from VCPs.

But "once we know what [these compounds] are and [which ones] contribute more to this PM 2.5," explained Nault, "then we can work on replacing those compounds with other ones" that might not produce as much pollution.

Reposted with permission from Environmental Health News.

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Anglers on Lake Ontario. Ian Muttoo / Flickr

By Andrew Blok

A record-setting fish was pulled from Hamilton Harbor at the western tip of Lake Ontario in 2015 and the world is learning about it just now.

The fish, a brown bullhead, contained 915 particles—a mix of microplastics, synthetic materials containing flame retardants or plasticizers, dyed cellulose fibers, and more—in its body. It was the most particles ever recorded in a fish.


"In 2015 we knew a lot less about microplastics and contamination in fish. I was expecting to see no particles in most fish," Keenan Munno, then a graduate student at the University of Toronto, told EHN. Every sampled fish had ingested some particles. Munno's 2015 master's work has spun out into six years' worth of research, including the new Conservation Biology paper that reports these findings.

The findings point to the ubiquity of microplastics and other harmful human-made particles in the Great Lakes and the extreme exposure some fish experience—especially those living in urban-adjacent waters. While direct links between microplastics and fish and human health are still an issue of emerging science, finding plastics within fish at such high amounts is concerning.

Great Lakes Plastics Problem

Researchers collected fish from three locations in both Lake Superior, Lake Ontario and the Humber River (a tributary of Lake Ontario). In all they gathered 212 fish and 12,442 particles.

In Lake Ontario, besides the record-setting bullhead, white suckers from Humber Bay and Toronto Harbor had 519 and 510 particles, respectively. A longnose sucker from Mountain Bay in Lake Superior had 790 particles. In the Humber River even common shiners, minnows which rarely get to eight inches long, had up to 68 particles.

"It was obviously concerning," said Munno, now a research assistant at University of Toronto. She extracted and counted all the microplastics and other particles from the fish's digestive tracts by hand. That includes all 915 record-setting particles.

"You feel bad for the fish that's eaten that much plastic," Munno said.

Of the human-made particles found in the group of fish, 59% were plastics in Lake Ontario, 54% in Humber River, and 35% in Lake Superior.

This new study is part of a growing and concerning body of research on plastics in the Great Lakes.

In a 2013 study, researchers sampled Great Lakes surface water and found an average of 43,000 microplastic particles per square kilometer. Near major cities they measured concentrations of 466,000 microplastics per square kilometer.

Recent research estimated that Great Lakes algae could be tangling with one trillion microplastics.

"Globally, 19-21 million tonnes of plastic waste were estimated to enter aquatic ecosystems in 2016," the study's authors wrote. That number is expected to double by 2030.

Microplastics' Impacts on Humans

Beach plastic litter

Beach plastic litter in Norway. Bo Eide / Flickr

"I've been studying microplastics for a long time and this is the study that blew me away," Chelsea Rochman, a coauthor on the study and University of Toronto professor of ecology and evolutionary biology, told EHN.

Rochman began her microplastics research in the trash gyres in the ocean. There she'd find microplastics in one out of 11 fish and usually only a couple of pieces in a single fish. While the findings were concerning, some people said the threat to animals was well into the future.

"We're finding that there are concentrations of microplastic in certain areas in the environment where the concentrations are so high that the animals might be at risk today," Rochman said.

Still unpublished research from Rochman's lab by a colleague of Munno's will show that microplastics can travel from the digestive tract to the fillets of the fish.

Microplastics in fish fillets could be one way they get to humans.

While research hasn't drawn robust links between microplastics and specific health problems in humans, they've been connected to neurotoxicity, metabolism and immunity disruption, and cancer in other laboratory tests, Atanu Sarkar, a professor of environmental and occupational health at Memorial University of Newfoundland, told EHN. Microplastics accumulate in the organs of mice exposed to them.

Even if they're not eaten by people, fish used as fertilizer or pet food can spread microplastics throughout the environment far from aquatic ecosystems, he said.

Rochman has worked to mitigate plastic pollution in Lake Ontario with the U of T Trash Team. The Trash Team and its partners have installed filters on washing machines to capture plastic microfibers and sea bins, which capture microplastics in the lake.

"In one sea bin sample—a 24-hour sample, one bin—we find hundreds of microplastics," Rochman said. The laundry filters likely capture one million in a month.

While microplastics continue to flood the Great Lakes, each one caught and removed is a small step in the right direction.

Reposted with permission from Environmental Health News.

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