This article was originally published in The Conversation. For us as radicals, spraying pesticides is not only a horrible crime committed to our fellow beings, it is also unbelievable stupid to poison our own food chain. While all large-scale monoculture is destructive, a world wide ban of all pesticides would be a huge step forward towards harm reduction and a healthier landbase.
When you think of bees, a hive humming with activity probably comes to mind. But most of the world’s 20,000 bee species don’t call a hive home. These wild species lead solitary lives instead, and around 70% of them build nests underground where they raise their offspring on the nectar they gather from flowers.
Incredibly, almost all scientific understanding of how pesticides affect bees has came from testing domesticated honeybees, and, more recently, bumblebees. That’s largely because these species tend to be easier to work with in lab conditions. How non-social bees cope with these chemicals is largely understudied, despite them making up the vast majority of bee species worldwide.
Neonicotinoids are a family of pesticides which have been used in farming across the world. Their chemical structure resembles nicotine and they’re designed to kill crop pests by targeting the insect nervous system. Neonicotinoids can be sprayed on plants, but are most commonly used to coat seeds. Since their introduction in the late 1980s, robust scientific evidence has emerged to suggest these chemicals impair learning and memory, foraging behaviour, and pollination in bees. The EU banned neonicotinoids in 2019, and while the UK government pledged to follow suit, it granted a special exemption for sugar beet farmers to use the neonicotinoid thiamethoxam in January 2021. Thankfully, it wasn’t used.
Because honeybees don’t spend much time on the ground, environmental risk assessments for neonicotinoids often neglect to consider how exposure to these chemicals in the soil affects all pollinators. But in a landmark study published in Nature, researchers have shown how neonicotinoids affect bees not just by accumulating in the plants pollinators visit, but in the ground where most wild bees build their nests.
Down on the farm
Working over three years in Ontario, Canada, the researchers mimicked the conditions on a real farm by growing crops of squash plants in large polytunnels. Before planting, common neonicotinoid pesticides were applied to the seeds and later the leaves, while one chemical called imidacloprid was applied to the soil. This is used in Ontario to control the striped cucumber beetle.
Mated female bees were introduced when the crop came into bloom. They dug nests in the earth around the plants and began foraging for nectar from the large, yellow squash flowers, which they’d bring back to offspring tucked away in special chambers underground.
These were hoary squash bees – a ground-nesting species found on farmland throughout North America. Squash bees are uniquely suited to pollinating the flowers of squashes, pumpkins and cucumbers thanks to special leg hairs that fit the size and shape of their pollen grains. They tend to forage earlier in the day than most bees too, to match the early morning flowering of these plants.
The researchers studied nest building, foraging and reproduction in these bees and found imidacloprid in particular – one of the most widely used neonicotinoids worldwide – had a devastating effect on all aspects of squash bee life. Compared to insects living on untreated cropland, the hoary squash bees exposed to imidacloprid in the soil created 85% fewer nests, left 5.3 times more pollen unharvested and produced a staggering 89% fewer offspring.
Imidacloprid appeared to rob squash bees of their usual industrious attitude towards the laborious work of building nests, foraging for food and rearing young. These non-social bees lack the support of relatives in big hives, and must face these essential tasks alone. By reducing the amount of pollen they collect, the pesticide could leave squash bees and their offspring with less energy to do so.
But it’s not just bees which are in trouble. Pumpkins, squashes and gourds are entirely dependent on pollination by bees to set fruit. Without an influx of new bees or a recovery in their reproduction, farm productivity could suffer too.
Hoary squash bees, like many bee species, are specialists. Unlike generalist honeybees which are comfortable pollinating a wide range of plants, specialists co-evolved with their host plants and are uniquely adapted to pollinating them. Generalists can sometimes step in to do their work, but they’re unlikely to manage it with the same kind of skill.
Due to their wild nature, non-social insects are far harder to protect on farmland than domestic species. Honeybees hives can be moved around the countryside if an area is no longer able to support them. Squash bees and other non-social bees build small nests throughout the landscape, making it impossible to pinpoint and protect them all. Protecting honeybees from pesticides is already difficult. For wild bees which forage and nest among a wide variety of crops worldwide, it may be impossible.
Editors note: We are publishing this release because we support all movements against extractive industries. But we want to make clear that bypassing safety precautions is standard for the oil industry and extractive corporations around the planet, and that even when the best available technologies and precautions are used, these things still kill the planet by their very nature. For example, it’s not gas drilling “done irresponsibly” that is the problem. It’s gas drilling as a whole, and by extension the entire industrial economy.
Featured image: Okavango River by Dr. Thomas Wagner, CC BY-SA 3.0 via Wikimedia Commons
Media Release
ReconAfrica fails to place a leack proof lining system in the drilling fluid containment pond. Drill site 6-2 Kavango Namibia
ReconAfrica is a Vancouver based Canadian petroleum exploration company that has acquired an exploration licence for the PEL 73 area located in Kavango East and West in Namibia. Drilling of the first of two permitted exploration boreholes began in December 2020. The borehole, referenced BH 6-2 is situated approximately 600m from the ephemeral river Omatako Omarumba, and all earthworks required to facilitate the drill rig have been completed. This includes a below ground level drill fluid containment pond.
The pond is approximately 45m in length, 30m in width and some 3m in depth and capable of holding almost 4.2million liters of liquid waste It is not known if the capacity of the pond has been designed to contain at least 110% of the largest expected wastewater volume at any given stage as is standard practise. During the drilling process waterbased drilling fluids are used to provide lubrication to the drill bit and to stabilise the borehole amongst other reasons. The drilling fluids are circulated down the borehole and pumped back to the surface for storage in the containment pond.
As drilling progresses the borehole will initially intersect shallow ground water aquifers that typically occur at a depth of 10 to 30m below ground level, At greater depths, at the base of the Kalahari beds and beyond into the underlying Karoo formations, beyond an anticipated depth of about 900m, highly saline groundwater will be intersected. This was revealed in the Environmental Impact Report prepared by Risk Based Solutions. As drill fluids circulate they will bring rock cuttings and a quantity of groundwater back to the surface which is stored in the containment pond built for the purpose. Due to the proposed ultimate borehole depths of 2500m, hypersaline fluid brine will be intersected in the deep Karoo sediments. The return drill fluids that will be placed in the containment pond will therefore contain drilling mud and rock cuttings from the Karoo sediments that are known to contain natural occurring radioactive materials (NORMS), and hypersaline brine – a cocktail that must be treated as hazardous liquid waste.
An onsite visual assessment of the containment pond located adjacent to BH 6-2 has revealed that the containment pond has not been lined with an appropriate water proof barrier system. Although not explicitly stated as a requirement in the Environmental Management Programme prepared by Risk Based Solutions, the requirements for a liner are implied. The report makes it a requirement of ReconAfrica to “…Never allow any hazardous substance to soak into the soil”. Furthermore, the document also requires that upon completion of the drilling, ReconAfrica must “… allow the pollution control dam to evaporate completely, scrape all waste that has collected in the pond and dispose of these and the pond lining at a suitable site”
No lining or efforts to render the containment pond impervious have been made despite the implied requirement that there should be at least a single pond liner. As reported by National Geographic on 29th January 2021 a spokesperson for ReconAfrica indicated in a written reply in October 2020 that potentially toxic drill cuttings from the oil test wells “will be managed in lined pits, cleaned, and disposed of offsite as per company and regulatory requirements.”
Given the vulnerability of groundwater at this site, it would be expected that a double lining system would be required, coupled with monitoring of the pond lining, the interstitial pond fluid (i.e. the fluid between the two liners), the returned wastewater quality for selected parameters such as electrical conductivity (EC) and radioiactivity. Regular monitoring of the groundwater quality in the immediate vicinity of the site must also be implemented.
Management guideline for saline fluids for hydraulic fracturing published by the British Oil and Gas Commission in April 2019 provide detailed requirements for the impoundment of saline flowback such as anticipated in Kavango East and West. Among the many design requirements specified in Canada some include:
The primary synthetic liner must be a minimum of 60 mil (1.5 mm) thick, have hydraulic conductivity of 10-7cm/s or less and must have properties that are fit for the purpose intended and conditions and temperature extremes encountered.
The secondary synthetic liner must be a minimum of 60 mil (1.5 mm) thick, have hydraulic conductivity of 10-7cm/s or less.
The design must incorporate a leak detection system within the engineered seepage pathway leading to at least one leak detection well, vault, or port. This must allow for water sampling from the lowest point of the pond, positioned between the primary and secondary liners and be designed for accurate measurement of leakage rate.
The BC Oil and Gas Commission also provide guidelines for the management of containment ponds which include some of the following actions:
The pond must be constructed and bermed in a manner that does not allow surface runoff from the site to enter the pond. A minimum of 1.0 m freeboard must be maintained within the containment pond at all times. The primary containment liner be regularly inspected for evidence of leaks and damage and that records of issues related to inspections and corrective actions be maintained.
A groundwater monitoring program must be developed by a qualified professional to evaluate potential groundwater impacts that could be associated with the pond. Monitoring wells must be used to establish baseline conditions for groundwater levels and chemistry prior to use of the containment pond and the baseline monitoring. Samples from the leak detection system and sub-drain must be collected and analyzed on a weekly basis.
Visual evidence obtained from the site indicate that ReconAfrica are not in compliance with their own declarations made in October 2020, and do not comply with the requirements of the EMPR. They are therefore in violation of the Environmental Compliance Certificate issue by the Ministry of Environment and Tourism. In addition, ReconAfrica have chosen to ignore Canadian industry approved guidelines issued by the Oil and Gas Commission in British Columbia, the state in which the companies head offices are located.
Despite the fanfare and extensive publicity that ReconAfrica have generated over the drilling of water wells adjacent to each exploration borehole will be made available to the communities once the exploration holes are completed – there will be no benefit accrued if the groundwater is contaminated by drilling effluent. The conclusions and inferences that can be drawn from the cavalier attitude of Recon Africa is that there is a lack of respect for the rural indigenous people of Kavango East and West who’s livelyhoods are total dependent on access to clean groundwater.
This articles outlines scientific research regarding the harms from pesticides to bees. Originally published on The Conversation. Republished with permission.
Neonicotinoids, the most commonly used pesticides in the world, were banned in the EU in 2018. More than 99,000 people petitioned the UK government to support the ban amid a wealth of scientific evidence linking this group of chemicals to poor health in bees, from the reduced production of bumblebee queens to slashed sperm counts among male honeybees.
The UK government had pledged to keep the EU’s restrictions post-Brexit, but recently granted a special exemption to allow farmers to use the neonicotinoid thiamethoxam on sugarbeet throughout 2021, and possibly until 2023.
Dire Consequences
If this signals the government’s intention to roll back regulations on agricultural chemicals now that the UK has left the EU, the consequences for pollinating insects could be dire. Research into the effects of these pesticides on pollinators is still ongoing, but new harmful effects are discovered all the time.
In a new study, my colleagues and I have uncovered the most recent example. We looked into the effect of these pesticides on the body clock and sleep of flies and bumblebees. Just like us, insects need sleep. And, like us, they have an internal sense of time – more commonly known as a body clock – which helps them synchronise their activity and sleep patterns with the rest of the world. Your body clock might allow you to wake up just a few minutes before your alarm goes off. For insects, it ensures they’re able to forage in the day when flowers are open and sleep at night when it’s usually too dark to fly.
Using lab-based colonies of buff-tailed bumblebees, the most common British bumblebee species, we showed that a neonicotinoid pesticide called imidacloprid turns night into day for bees. Foraging bumblebees were fed concentrations of imidacloprid that were similar to what they might encounter in the wild (around ten parts per billion). After exposure, the dosed bees were more likely to try to forage at nighttime and sleep in the daytime, and they were more sluggish overall, going on far fewer foraging trips than normal.
At the same time as we were experimenting on bumblebees, we were also studying the response of fruit flies to neonicotinoids. Scientists often use fruit flies as a model to help understand other animals, as we have a deep understanding of their genes and the ability to edit them. In our study, we labelled the brain cells which set the pace of the fruit fly body clock with fluorescent dye, to see if the pesticides could be directly affecting them.
In a normal fly, these cells collect information from the eyes and other light-sensing organs. The cells then change shape between daytime and nighttime and release signals to other parts of the body to ensure that sleep and other activities happen at the right time of day. But neonicotinoids appeared to interfere with both of these processes, freezing the body clock cells in daytime mode. Given how similar these cells are between fruit flies and bees, this process may be behind the effects on sleep and foraging that we saw in bumblebees.
The environmental impact
If bees can’t synchronise their foraging with the dawn, when nectar and pollen are most abundant, this will limit the amount of food they can gather, stunting the colony’s ability to grow and produce more bees.
The body clock is also an important part of communication in bees. Honeybees have a dance language which lets them tell each other where the best flowers are. They use the position of the sun in the sky as a tool for navigation, which means that honeybees need to be able to keep track of the time of day within the darkness of the hive. If their body clock is disrupted, it could affect their ability to communicate vital information to each other and reduce their ability to forage and pollinate.
The changes to sleep that we saw in the buff-tailed bumblebees are also worrying. Sleep during the night helps bees form memories, and so if neonicotinoids are disrupting their sleep, it could cause problems with remembering important information, such as the route back to the hive. The correct timing of sleep is also really important for childcare in the colony. When bumblebees are looking after their young, they have to tend to them and feed them round the clock, taking little naps between feeds. If neonicotinoids change their sleep patterns in a way that they can’t control, adult bumblebees may struggle to properly care for the next generation. All of these effects could potentially prevent colonies from growing and reproducing properly, threatening their long-term survival.
Bumblebees, like honeybees and other bees, are important pollinators for 84% of crops and 80% of wild flowering plants in Europe. Neonicotinoids pose a real threat to not only the health of these pollinating insects, but the agriculture and ecosystems they support. As a scientist who studies the effects of these chemicals, I hope that the “emergency use” that was recently granted by the UK government isn’t a sign of worse things to come.
The first time I saw a coyote with mange my heart broke.
Most of her fur was gone. Her skin, covered with scabs and lesions, had a sickly pink pallor. Her tail seemed stuck between her legs. And, her movements, as she stumbled through a ditch next to a Colorado country road, were lethargic and listless. Just the sight of her made my own skin chafe and itch. As I hugged myself to ward away the horror, my fingernails dug into my own skin, scratching at the backs of my arms. The experience educated me in the realest ways about what the phrase “it made my skin crawl” truly means.
After witnessing this, I had to know more about what I had seen. I learned that this coyote was suffering from what scientists call sarcoptic mange, which is caused by mites who live in the skin of many wild canids. In burrowing into the animals’ skin to lay their eggs, these mites cause intense irritation and itchiness, scabbing, and hair loss. An animal affected by mange can develop secondary bacterial skin infections, too. Worst of all, mange can be fatal for animals if left untreated. With the loss of their fur, animals affected by mange often freeze to death. And, if the cold doesn’t kill them, those secondary bacterial skin infections exacerbated by excessive scratching will.
While mange does occur naturally,
recent research suggests that the widespread use of anticoagulant rodenticides – a type of rat poison – weakens the immune systems of animals and makes them more susceptible to mange. A 2017 study linked anticoagulant exposure to mange in bobcats, for example. Notoedric mange – which affects felines and is closely related to the sarcoptic mange that affects coyotes – ravaged the population of urban bobcats at Santa Monica Mountains National Recreation Area in southern California from 2002-2005. After mange was detected in 2001, the average annual survival of these bobcats plummeted by 49%. Mange-infected bobcats were necropsied and 98% of infected individuals had been exposed to anticoagulant rodenticides. These bobcats also had greater amounts of anticoagulant rodenticides than bobcats who did not die with mange.
After reading the results of the bobcat study, and against my better judgment, I was compelled to find images of bobcats with mange. I was met with the stares of blue-eyed bobcats, stripped of fur and looking like hairless, Sphynx cats. Unlike Sphynx cats, these bobcats weren’t bred selectively to be hairless. Their hair had been stripped and their skin ravaged by mites because they had eaten rodents who had eaten too many anticoagulant rodenticides.
What exactly are anticoagulant rodenticides?
Anticoagulant rodenticides are widely used as a cheap and effective means for killing rodents. These rodenticides disrupt coagulation and cause fatal hemorrhaging. In simple terms, rodenticides cause the creatures who eat them to bleed more easily. Similar to the way a minor wound to a human taking a blood-thinner can cause a human to bleed out, rodents who have ingested anticoagulant rodenticides bleed to death.
Rodents exposed to anticoagulant rodenticides don’t just bleed to death – they bleed to death slowly. Rodents are very intelligent. They are so intelligent, in fact, that the use of toxins that immediately harm a rodent have proven to be completely ineffective because rodents learn not to eat things that instantaneously kill their kin. Anticoagulant rodenticides are effective because they can be mixed with rodents’ favorite foods as bait and the 3-7 days it takes for exposure to kill rodents makes it very difficult for them to understand what is killing them.
Anticoagulant rodenticides have been in use since the late 1940s, and by the early 1980s, genetic resistance to what are now called “first-generation anticoagulant rodenticides” was reported in rats and mice around the world. These first-generation anticoagulant rodenticides include the chemicals diphacinone, warfarin, coumatetralyl, and chlorophacinone and they killed rodents only after prolonged or repeated exposure. Due to genetic resistance, second-generation anticoagulants developed. These chemicals – which include difenacuom, brodifacoum, bromadiolone, difethialone, and flocoumafen – are much more potent, have a longer half-life, and can kill rodents after only one feeding. This potency poses an increased risk of harm non-target species.
Inevitably, predators who eat rodents are exposed to the rodenticides ingested by their prey.
In one study, 70% of mammals tested in California were found to have been exposed to anticoagulants. Anticoagulant rodenticides were detected in 49% of the raptors tested in New York City, including in 81% of the great horned owls tested. A study of three species of owls in British Columbia and the Yukon detected anticoagulant rodenticides in 62% of barn owls, 92% of barred owls, and 70% of great horned owls. In sum, the Canadian researchers detected anticoagulant rodenticides in 70% of 164 owls. They also confirmed that rodenticides killed two barn owls, three barred owls, and one great horned owl.
As described above, rodents usually do not die for several days after consuming a lethal dose. This means they may continue to move through habitat shared with predators and they may continue to feed on poisoned bait. Additionally, rodents – exposed to anticoagulant rodenticides and who may be hemorrhaging internally – spend more time in open areas, stagger as they move, and sit motionless before death. All of this makes them easier prey for predators.
Coyotes, and especially urban coyotes, rely heavily on rodents for food.
It appears anticoagulant rodenticides are harming coyotes. Scientists in the Denver metropolitan area, for example, researching the effects of anticoagulant rodenticides on coyotes, found a dead juvenile male with no obvious external injuries or other signs of trauma. However, when they necropsied the young coyote, they “found free blood in the abdominal cavity” and “a puncture wound [that] was present on the left side of the body overlying the spleen but not penetrating the abdominal wall.” They determined that the coyote died from “acute severe hemorrhage, disproportionate to the amount of trauma observed.” The coyote’s liver tested positive for an anticoagulant rodenticide. In other words, it’s likely that the rodenticide in the coyote’s body turned a minor injury lethal.
These scientists found another young male coyote dead on a two-lane road “with minor evidence of skin tearing over the ventral neck and chest.” When they necropsied the coyote, they found that the coyote’s chest was filled with blood and they concluded that the coyoted was killed by “severe acute hemorrhage, disproportionate to the mild to moderate trauma received from being hit by a vehicle.” The scientists suspected rodenticide exposure. And, sure enough, the coyote’s liver tested positive for two types of anticoagulant rodenticides. Again, rodenticides turned a small injury into a coyote’s death.
There have been many more studies demonstrating the harmful effects anticoagulant rodenticides have on non-rodent species.
Some of these studies include harmful effects on buzzards, mountain lions, otters, endangered European mink, polecats, and, even, freshwater fish. Anticoagulants, in fact, act on all vertebrates – not just the rodents they’re intended for. Scientists have also discovered anticoagulant rodenticides in raw and treated wastewater, sewage sludge, estuarine sediments, and particulate matter suspended in the air.
For brevity’s sake, I’ll stop here. But, it bears mentioning that as I sifted through study after study describing the havoc anticoagulant rodenticides wreak on natural communities and felt my stomach grow increasingly sour, I learned the literal meaning of another phrase: ad nauseum. It is also important to remember that, despite the amount of studies being conducted on the effects of anticoagulant rodenticides on non-target wildlife, scientists caution us that most of this poisoning remains undetected because the necropsy and liver analysis required is labor and cost intensive. Similarly, unless an animal is being tracked through radiotelemetry, finding dead animals in a non-decomposed state, is difficult.
***
After learning about problems with anticoagulant rodenticides, the torturous manner in which these chemicals kill, and how they are making predators of rodents more susceptible to mange, most people want to know:
What can I do?
This is the wrong question. Don’t ask: What can I do? Ask: What needs to be done? What do bobcats – blue eyes unblinking despite the pain of internal hemorrhaging – need us to do? What do coyotes – scraping their inflamed skin against fence posts, the corners of concrete walls, and rough tree trunks – need us to do? What do rodents – intelligent, sociable, and bleeding to death – need us to do?
Rodents, and all those who eat them, need us to stop the manufacture and application of anticoagulant rodenticides. And, they need this to happen as quickly as possible. This is, of course, much easier said than done.
Individual home or other property owners, as opposed to government or business entities, account for a portion of total anticoagulant rodenticide use. If these individuals could be convinced to live and let rodents live, or to employ non-lethal, non-toxic measures such as blocking holes and other openings rodents use to access buildings, practicing better sanitation, or trapping rodents and removing them to better habitat, then the total use of anticoagulant rodenticides could be reduced.
There are barriers making it unlikely that individual property owners will forego the use of anticoagulant rodenticides:
First, fear of rodents is so pervasive in the dominant culture that there are multiple words to describe this fear including musophobia (fear of mice specifically), murophobia (fear of the taxonomic family Muridae, which includes mice and rats), and suriphobia (which comes from the French souris meaning “mouse”). Similarly, calling someone a “rat” is a grave insult.
Second, anticoagulant rodenticides are simply more economical. Sealing up holes in a house and live-trapping rodents can be costly and can require much more labor than using poison. In fact, a member of California’s Department of Consumer Affairs, Structural Pest Control Board recently estimated that pest control services employing only sanitation, exclusion of rodents, and removal of harborage can be 2-5 times more costly than using rodenticide due to labor and material costs.
I want to be clear here: I am not saying we shouldn’t try to convince everyone we can to stop using anticoagulant rodenticides. This is, of course, one reason I wrote this piece. I am saying, however, that coyotes, bobcats, other predators of rodents, and rodents, themselves, need us to do much more than to simply refuse to stop using anticoagulant rodenticides in our own homes.
Many people assume that if homeowners stopped using these rodenticides the problem would go away. Unfortunately, this is not the case. National and global anti-rodenticide market data are protected by business privacy laws as
“confidential business information.”
However, it’s safe to say that while individual, residential use of anticoagulant rodenticides accounts for a portion of global rodenticide use, governments and agricultural corporations are likely the biggest users of anticoagulant rodenticides.
Statistics from California tend to support this point. In 2012, California imposed stricter regulations on second-generation anticoagulant rodenticides including restricting sales of these chemicals to the general public. Then, in 2014, they imposed a new round of restrictions that were specifically intended to restrict the access of homeowners to second-generation anticoagulant rodenticides. But, using data from the California Department of Pesticide Regulation’s Pesticide Use Reporting database, it does not appear that the amount of second-generation anticoagulant rodenticides applied between 2012-2017 was significantly reduced despite the new regulations.
So, if homeowners are only part of the problem, and governments and corporations are the worst offenders, how do we stop governments and corporations from using anticoagulant rodenticides?
A common response is: change the law. It is highly unlikely, however, that governments will ever impose a true ban on anticoagulant rodenticides. The agricultural lobby is one of the most powerful political forces in American politics. Meanwhile, in the United States, rodents are responsible for an estimated $19 billion in economic damages annually through the consumption and contamination of stored grains. Rodents don’t just pose a threat to agricultural interests, either. A British study, which attempted to determine the cost of physical damage to the built environment caused by rodents, estimated that rodents cost the British economy £200 million per year.
An astute reader may be saying to herself: “Didn’t California recently ban anticoagulant rodenticides?” And, of course, despite the headlines, California did not ban anticoagulant rodenticides. To understand this, we must look to the actual text of the California Ecosystems Protection Act of 2020 (also known as Assembly Bill No. 1788). Courts applying law do not rely on newspaper headlines – they rely on what a piece of legislation actually says.
The pertinent section (12978.7(c)) reads:
“Except as provided in subdivision (e) or (f), the use of any second generation anticoagulant rodenticide is prohibited in this state until the director makes the certification described in subdivision (g).”
So, first, the prohibition only applies to second generation anticoagulant rodenticides and excludes the less potent but still deadly first generation anticoagulant rodenticides.
Second, if we scroll down to the exceptions provided in subdivisions (e) and (f), we see how hollow this “prohibition” really is. Subdivision (e) declares that the prohibition does not apply to governmental agency employees who use second generation anticoagulant rodenticides for public health activities or for protecting water supply infrastructure and facilities; to mosquito or vector control districts; to efforts to eradicate nonnative invasive species on offshore islands; to efforts to control an actual or potential rodent infestation associated with a public health need, as determined by a declaration from a public health officer; or for further research into the dangers posed by second generation anticoagulant rodenticides.
Subdivision (f) creates exceptions to the prohibition for medical waste generators and for “agricultural activities” conducted at warehouses used to store foods for human and animal consumption; slaughterhouses; canneries; factories; breweries; an agricultural production site housing water storage and conveyance facilities; and agricultural production sites housing rights-of-way and other transportation infrastructure.
The power of agricultural interests should be clear from these lists of exceptions to this so-called “prohibition” on second generation anticoagulant rodenticides.
It should also be clear that the California Ecosystems Protection Act of 2020 has not banned anticoagulant rodenticides. At best, the law simply prevents individual homeowners and property owners from using a subset of anticoagulant rodenticides while exempting those who likely use second generation rodenticides the most.
To repeat, it is unlikely that governments will ever truly ban anticoagulant rodenticides. This does not mean that we have no power to stop the manufacture and application of these poisons. It is true that we must raise awareness about the harms of anticoagulant rodenticides. And, anyone who reads this, please, please stop using these toxic chemicals. Similarly, pushing for legislation to limit the use of anticoagulant rodenticides can help. But, if we truly want to protect rodents, and the predators who eat them, from horrible deaths, and if we truly want to keep these poisons out of the natural communities we depend on for life, we will have to do it ourselves.
As with any truly effective tactic that impedes humans’ ability to destroy the natural world, stopping anticoagulant rodenticides will require exceptional bravery. To find that bravery, I return to the first mangy coyote I saw. If it was me, and my skin was covered in itchy sores and lesions, my organs were hemorrhaging blood, and my movements were growing ever slower, I’d likely give in, lay down, and let death take me.
But, that first mangy coyote I watched struggle to keep moving through a roadside ditch did not give up. She kept moving in an effort to fulfill her species’ ancient role as a trickster lesson-giver. She wanted us to see her. She wanted us to know what happened to her. And, she wanted us to stop those who hurt her.
Will Falk is a DGR member, lawyer for the natural world and is currently journeying in conversation with the Ohio River. You can read about Will’s journey with the Ohio River here.
This episode of the Green Flame podcast is a discussion based on the film “Ocean Poubelles.” We talk about nuclear waste, the nuclear waste industry, nuclear waste dumping, and the production of nuclear weapons, nuclear power, and nuclear medicine that results in this highly dangerous and long-lasting radioactive material.
Nuclear waste is a massive issue. It’s actually a much more serious danger in the nuclear industry than a meltdown or some Chernobyl type incident. Nuclear waste is something that is ubiquitous in the nuclear industry and nobody really knows what to do with it. There’s no safe way to store it. There’s nothing that can be done to safely “dispose” of materials that will be deadly for tens of thousands, hundreds of thousands, millions of years into the future. Our discussion this week is on this topic of nuclear waste, which in many ways is a fascinating insight into industrial civilization, how it functions, the mindset of the technocrats that run the largest corporations in the world, the militaries and so on.
The Green Flame is a Deep Green Resistance podcast offering revolutionary analysis, skill sharing, and inspiration for the movement to save the planet by any means necessary. Our hosts are Max Wilbert and Jennifer Murnan.
A new study has found microplastics present inside human placentas, which could potentially affect fetal health and development.
The microplastics probably entered the women’s bodies through ingestion and inhalation, and then translocated to the placentas, the study suggests.
While further research needs to be done on the subject, it is believed that these microplastics could disrupt immunity mechanisms in babies.
Plastic is everywhere — literally everywhere. A growing body of research shows that plastic is not only filling the world’s oceans and wilderness regions, it’s also invading our bodies through the air we breathe, the water we drink and the food we consume. And now, a new study has shown that microplastics — tiny plastic particles smaller than 5 millimeters but bigger than 1 micron — are even present inside human placentas, posing a potential risk to fetal health and development.
Published this month in Environmental International, the study examined six human placentas from women who experienced healthy pregnancies and births. During delivery, the obstetricians and midwives followed a “plastic-free protocol,” swapping plastic gloves for cotton ones, and not using any plastic equipment or supplies to avoid cross-contamination.
The researchers found a total of 12 microplastic fragments in four of the six placentas. Three of these pieces were recognized as polypropylene, a plastic commonly used in food containers and packaging. While the other pieces were harder to identify, they appeared to be plastic bits from “man-made coatings, paints, adhesives, plasters, finger paints, polymers and cosmetics and personal care products,” according to the study.
The effects of microplastics in the human body on health are still largely unknown, but the researchers said it was “a matter of great concern” due to the critical role the placenta plays in fetal development.
Lead author Antonio Ragusa, director of obstetrics and gynecology at the San Giovanni Calibita Fatebenefratelli hospital in Rome, said it’s likely that microplastics would be present in the babies themselves, although further research would need to confirm this.
“I cannot support it with scientific evidence, since ours is the first study in the world on this topic, [but] I think that if we could look for them we will also find microplastics in the organs of the newborn, because the placenta is a temporary fetal organ, and not a maternal organ,” Ragusa told Mongabay in an emailed statement. “Of course this is just a guess.”
While all of the babies were healthy at birth, Ragusa said that the microplastics in the placenta had the potential to “alter several cellular regulating pathways … such as immunity mechanisms.”
“The presence of MPs [microplastics] in the placenta tissue requires the reconsideration of the immunological mechanism of self-tolerance, a mechanism that may be perturbed by the presence of MPs,” Ragusa said. “In fact, it is reported that, once present in the human body, MPs may accumulate and exert localized toxicity by inducing and/or enhancing immune responses and, hence, potentially reducing the defense mechanisms against pathogens and altering the utilization of energy stores.”
The researchers say it’s likely that the microplastics entered the mothers’ bodies through food ingestion or through respiration, and then translocated into the placentas.
Steve Allen, a microplastics researcher from the University of Strathclyde in Glasgow, who was not involved in the study, said he wasn’t surprised by the findings: “I’d say with complete confidence that using the right tools, we will find it in every part of the human body.”
A similar study has shown that pregnant rats forced to inhale nanoplastics ended up having particles present in their placentas, as well as the fetal liver, lungs, heart, kidney and brain.
“Considering it can move through rats like that, I wouldn’t be surprised if it can do exactly the same thing to humans,” said Deonie Allen, also a microplastics researcher at the University of Strathclyde.
Ragusa says he and his colleagues will be doing further research on microplastics with regard to maternal and infant health.
“We now have to understand if microplastics are present in the newborn at birth and we will do it by taking the umbilical cord blood at birth,” he said. “Another important step will be to understand if microplastics are present in breast milk.”
Citations:
Fournier, S. B., D’Errico, J. N., Adler, D. S., Kollontzi, S., Goedken, M. J., Fabris, L., Yurkow, E. J. & Stapleton, P. A. (2020). Nanopolystyrene translocation and fetal deposition after acute lung exposure during late-stage pregnancy. Particle and Fibre Toxicology, 17(55). doi:10.21203/rs.3.rs-39676/v1
Ragusa, A., Svelato, A., Santacroce, C., Catalano, P., Notarstefano, V., Carnevali, O., Papa, F., Rongioletti, M. C. A., Baiocco, F., Draghi, S., D’Amore, E., Rinaldo, D., Matta, M., Giorgini, E. (2021). Plasticenta: First evidence of microplastics in human placenta. Environment International, 146, 106274. doi:10.1016/j.envint.2020.106274
Elizabeth Claire Alberts is a staff writer for Mongabay. Follow her on Twitter @ECAlberts.
