Environmental Justice: Cancer Alley

Need a bit of inspiration to face our uncertain future? Look no further than the community organizers of Cancer Alley. Since the 1970’s these phenomenal people have stood up to multi-billion-dollar petrochemical companies. These companies, empowered by municipal planning boards and powerful politicians, release tons of carcinogenic and endocrine disrupting chemicals in the air and water, thereby sacrificing the health and lives of the good people who happen to live in nearby communities. In this post, based on research done by Lehigh student, Reese Keveanos, you’ll be introduced to activists and community organizers like Sharon Lavigne, a grandma and former special ed teacher who was awarded the prestigious Goldman Environmental Prize. She founded the Rise St. James organization, and so far, she and her allies have been able to delay construction of the several billion-dollar Formosa plastics complex, thereby preventing it from further polluting her Louisiana neighborhood.

Be sure to read through this post to find concrete ways you can help!

One Oppressive Economy Begets Another

Cancer Alley, also known as the Mississippi River Chemical Corridor, is an 85 mile strip of land that snakes from New Orleans to Baton Rouge. After the civil war, the former sugarcane plantations along the Mississippi River sprouted all manner of communities along The Great River Road. Families in these tight-knit communities enjoyed a seemingly endless supply of local fish, crawfish, and shrimp. Most families were not rich, but many enjoyed productive gardens and good health. The townships are still called parishes just as they were when the regions were first colonized by Roman Catholics from Spain and France. The parishes are named after the Biblical saints, e.g., Gabriel, Charles, John the Baptist, and James. The largest parts of these parishes are now home to over 200 chemical companies and refineries. The fish, crawfish, and shrimp are all gone, and little if anything grows in the poisoned soil and polluted air. Each year, chemical industrial development further encroaches on the majority-Black communities located near the petrochemical complexes. Rates of cancer are documented to be higher than the national average, especially in the African-American communities. Meanwhile, there is virtually no benefit to those communities; jobs in the petrochemical plants are held disproportionately by white residents. Barbara Allen, a professor of science, technology, and society at Virginia Tech puts it this way, “One oppressive economy begets another. The Great River Road was built on the bodies of enslaved Black people. The chemical corridor is responsible for the body burden of their descendants.”

The Heroes of Cancer Alley

Robert Bobby Taylor is a life-time resident of the St. John the Baptist Parish. He told Rebecca Hersher from NPR that he is flabbergasted to be alive today after living 77 years within the borders of the deadly corridor, “‘My mother succumbed to bone cancer. My brother had lung cancer,’ he ticks them off on his fingers. ‘My sister, I think it was cervical cancer. My nephew lung cancer. A favorite cousin. That cousin’s son. Both neighbors on one side, one neighbor on the other. And here I am. I don’t understand how it decides who to take,’” The St. John the Baptist Parish lies adjacent to the Denka neoprene plant (formerly owned by Dupont), which manufactures chloroprene, classified as a “suspected human carcinogen” by the Environmental Protection Agency (EPA). The Denka plant also emits ethylene oxide, a known human carcinogen. The plant is within 1,500 feet of an elementary school. Those who live within a mile of the plant have the highest cancer risk in the country — more than 700 times the national average in one part of St. John the Baptist Parish, according to EPA estimates. Instead of moving away from his home town, or simply accepting his fate, Bobby Taylor founded a community organization, Concerned Citizens of St. John the Baptist Parish. They are well known for their bright red t-shirts that spell out “Only 0.2 will Do,” referring to the EPA safety limit (in micrograms per cubic meter) for long-term exposure to chloroprene. Concerned Citizens of St. John the Baptist Parish picketed the Denko plant, and Taylor himself became the lead plaintiff in a lawsuit seeking to reduce pollution by Denka. EPA monitoring found levels of chloropene far above the safety limit all over St. John the Baptist Parish. Nevertheless, the lawsuit was thrown out by a federal judge citing failure to file by the deadline. The community continues to gain attention and allies. Most recently, the EPA Administrator, Michael Regan, under the Biden Administration, announced the agency will spend $600,000 to buy “mobile air pollution monitoring equipment” to deploy mainly near St. John the Baptist Parish to measure pollution accurately. St. John the Baptist Parish will need continued help to raise awareness.

To help the communities in St. John the Baptist Parish go to this link, but please read on to better understand our role in contributing to the problem, other victories and heroes, and more ways you can help.

Taylor is not the only one whose family suffered. Up the river, Sharon Lavigne of St. James’ Parish got so sick of burying her friends, neighbors, and family members that she founded the faith-based organization, Rise St. James. Please go to the link to help this tireless group fighting relentlessly for justice for parish residents. As you will read below, they are teaming up with other organizations to prevent yet another petrochemical company, Formosa Plastics, from moving into St. James Parish.

Why Plastics?

In case you wonder why industrial leaders including Russia, are investing in plastic, here is the story in a nutshell: The ingredients that make up plastic come from oil and gas. Plastic manufacturers turn by-products of oil and gas into millions of tons of tiny pellets, called nurdles, and plastic powder, a raw form of vinyl. These are shipped all over the world to make everything from baby bottles to yogurt containers. With the inevitable shift to renewable energy for heating and transportation, the fossil fuel industry will need a different market for selling fossil fuels. Their plan is the creation of a fake market for petroleum-based plastics. In fact, the plastics are already being made, and production is ramping up. Whether we need or or want it, the fossil fuel industry plans to increase plastic production to the point where 35% of all fossil fuel used will be in service of making plastic by the year 2025. You can learn more and help at this link.


As a part of this goal to expand the plastic industry (since burning fossil fuels for homes and cars is no longer tenable), Formosa Plastics proposed constructing a new 2,300 acre petrochemical complex in St. James Parish, in additional to their original complex in Baton Rouge. Formosa’s proposed complex would cost 9.4 billion dollars to complete and would include two ethane crackers as well as fourteen attached petrochemical facilities. Formosa is based in Taiwan, and their massive new complex is slated to be built in Northwestern St. James Parish across from already existing facilities. It would be squeezed into the borders of Cancer Alley with absolutely no regard for the health of the residents of the St.James Parish.

The Definition of Environmental Racism

How can they do that? The answer to that questions illustrates the concept of environmental racism, i.e., a form of systemic racism defined as the disproportionate exposure that Indigenous, Black and other racialized communities have to environmental hazards as a result of institutional policies and practices. Formosa did it with help from the local planning commission and parish council. The land owned by Formosa in St. James Parish was re-zoned “residential/industrial” in 2014 by the planning commission and parish council. According to Anne Rolfes of the Louisiana Bucket Brigade, the re-zoning “concentrates all industry in the two highest majority Black districts in the parish.” This fits the definition of environmental racism perfectly. There is no doubt that a new Formosa facility would be devastating, since their existing facility generates waste exceeding more than 800 tons of toxic liquid chemicals, almost 6,500 tons of volatile pollutants that have been linked to respiratory illness, 95 tons of carcinogenic compounds, and over 13.6 million tons of greenhouse gas emission per year. These emission statistics make Formosa one of the largest pollution-causing plants in the entire world. Currently, there is a Formosa plant operating in Baton Rouge from which the data are clear: the effects of having two facilities would more than double the problem. Air pollution would skyrocket and the pollutants would include nitrogen oxides, carbon monoxide, ozone, sulfur dioxide, and particulate matter. Nitrogen oxides can lead to new or worsening respiratory conditions and exaggerate pre-existing cardiac conditions. Carbon monoxide can aggravate cardiac symptoms and conditions, potentially leading to premature death. Ozone, or as it is often referred to, smog, can lead to new or worsening respiratory illness. Sulfur dioxide can lead to respiratory conditions and other ailments. Particulate matter can cause premature death in individuals with pre-existing respiratory and cardiac conditions.

In addition to these pollutants leading to ailments within communities, if Formosa Plastics Corporations were to expand into St.James, the residents would be more likely to develop multiple kinds of cancer. According to the Stop Formosa Organization, air pollution from this plastics plant would include ethylene oxide (a carcinogen that is known to cause breast cancer, non-Hodgkin lymphoma, and lymphocytic leukemia), benzene (carcinogen), vinyl chloride (hepatic angiosarcoma, leukemia, lymphoma, brain, and lung cancers), formaldehyde is (myeloid leukemia and other rare cancers), acetaldehyde (probable carcinogen). All of these pollutants are causing substantial harm to the environment (plants and animals are disappearing), and the people who live there are experiencing illness and premature death.

Considering these emissions, it is not surprising that the COVID-19 pandemic has hit Cancer Alley harder than most areas. Since these pollutants often lead to respiratory weakness and disease, higher COVID death rates follow. Areas such as St. John, Louisiana, which has the highest concentration of particulate matter, as well as the highest rate of COVID deaths, is an example of how these pollutants not only cause harm on their own but also interact with other diseases.


The struggle of Sharon Lavigne and Rise St. James was no picnic. Formosa plastics denied that any illness or death in St. James Parish was directly related to plastics production (they conducted their own studies to bolster their defense), and the company used a number of strategies to silence the St. James community. Lavigne says that many of her neighbors were afraid to speak up, and some who lacked an alternative means of livelihood were afraid to lose their jobs with Formosa. During the COVID pandemic, it was difficult to meet and carry out their plans. The odds continued to stack up against Rise St. James when the state legislature passed a bill requiring judges to impose a mandatory three-year minimum prison sentence with hard labor on protesters convicted of trespassing on industrial property or infrastructure. “Industrial property” was defined as “anywhere in a state with 125,000 miles of oil and gas pipelines,” which basically includes all of St. James Parish. It is beyond inspiring that Lavigne and Rise St. James persisted in the face of these obstacles.

Eventually, however, the bill to squelch St. James protests was vetoed by the governor. On April 8, 2021, the New Orleans City Council voted unanimously to declare its opposition. Unlike the city council, the Biden administration’s commitments are more than symbolic, and the Formosa project has been forestalled, at least for now. The victories were thanks to Sharon Lavigne, members of the St. James community, hard-working organizations like Rise St. James, the Biden administration, and the United Nations. The United States Army Corps of Engineers is the agency that grants construction permits per the Clean Water Act and the primary federal enforcers of regulations regarding water pollution. In August 2021, it announced that they would commission a full environmental impact statement, and this process will put a halt to future construction of the Formosa Plastics complex in St. James Parish for a number of years. Most recently, Formosa has been put on notice by Standard & Poor’s that the delays have actually helped its credit rating compared to its credit rating when the project was first announced. This implies that cancelling the project would be more profitable for the company than building the plant in St. James Parish. This is good news for St. James Parish, and vividly illustrates that industrial leaders pay attention to profits, not people. Sharon Lavigne shows us how to move forward even against all odds. Her strategy is one of perspective; she sees this development as a period of momentum in the trajectory of the environmental justice movement. Lavigne says, “Nobody took it upon themselves to speak for St James Parish until we started working to stop Formosa Plastics. Now the world is watching this important victory for environmental justice.”

WAYS YOU CAN HELP: Plastic Pollution Coalition

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Endocrine Disruptors, Environmental Justice, and the Ivory Tower

In this video, Professor Tyrone Hayes explains his research showing that Atrazine is an endocrine disruptor that increases the incidence of cancer and alters the development of reproductive organs. He raises the critical questions, “Who is most affected by endocrine disruptors?” and “How is knowledge about endocrine disruptors sequestered in the ivory tower by academic and publishing institutions?” and “Why is it never enough to simply ‘let the science speak for itself?'”

Professor Tyrone Hayes is professor of integrative biology at the University of California at Berkeley and a member of the American Academy of Arts and Sciences.

Tyrone B. Hayes, Vicky Khoury, Anne Narayan, Mariam Nazir, Andrew Park, Travis Brown, Lillian Adame, Elton Chan, Daniel Buchholz, Theresa Stueve, and Sherrie Gallipeau, Atrazine Induces Complete Feminization and Chemical Castration in male African clawed frogs, PNAS, 107:4612, 2010.

And finally, Professor Hayes throws down the Atrazine Rap: “your son or daughter will develop in water just like my tadpoles do”

And please check out a more recent update on the Tyrone Hayes-atrazine saga.

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Plastic = Endocrine Disruption: An Urgent Message from Jeff Bridges and the Plastic Pollution Coalition

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Too Hot for Endocrine Disruptors


Climate change and endocrine disruptors share two things in common. They are both real and they are both bringing species dangerously close to extinction. Here, Lehigh University undergrad, Nadine Boukhari, explains how they work together to exaggerate the problem. We miss things when we look at the geophysical planet separate from the biological beings that are living on the planet. This planet is its biology and the biology is its planet. They inter-are.

Despite the media depiction of “controversy” around the topic of climate change, 99% of climate scientists agree (Lynas et al., 2021) that: the planet is warming at unprecedented rates and the reason is human-made greenhouse gas emissions that come from burning fossil fuels (IPCC, 2021). Since the beginning of the industrial revolution, increases in the levels of human-made greenhouse gas emissions have warmed the planet at unprecedented rates, and this rate of change is far faster than the rate of evolutionary adaptation (Quintero and Wiens, 2013). For species examined by Quintero and Wiens (2013), they would have to evolve 10,000 times faster than their normal rates to adapt to current rates of global warming. If carbon emissions are not cut in half to prevent the Earth’s average temperature from rising 1.5oC above the temperature of the pre-industrial era, numerous species will suffer and die in great numbers due to the resulting climatic changes, specifically, heat waves, drought, sea level rise, floods, intensified storms, and ocean acidification (IPCC, 2021). Thousands of years of evolution have led to adaptations that allow populations to survive and reproduce in certain environments, but global warming and the resulting climate change creates a mismatch between those hard-wired adaptations and the current environments. Each species will be affected in different ways at different times, and some might reach the tipping point (the point of no return) sooner than others. How soon each species reaches the tipping point will depend on other environmental factors, one of which is the presence of endocrine disruptors.

Many people have never heard of endocrine disruptors, so they do not understand the severe threat they pose to the world. Endocrine disruptors are chemicals that mimic, block, or interfere with any part of the endocrine system, and the mechanisms include but are not limited to altering hormone synthesis and secretion and altering receptor binding and distribution (Colburn et al.,, 1993). They have been decimating the animal population worldwide (Vos et al., 2000). The human race has created chemicals that have begun to change animals on a biological level. Furthermore, endocrine disrupting chemicals appear to have caused animals to appear as though they have “lost their instincts,” which have been honed by thousands of years of natural selection and other evolutionary forces. In addition to simple instinct-like behaviors, some adaptations involve the ability to learn, which involves neural plasticity. For example, some species have evolved the ability to navigate, learn the location of prey, cache and then relocate food, and solve difficult puzzles to find and attract mating partners and protect offspring. Endocrine disrupting compounds can interfere with hormone-brain relations that underlie these cognitive functions.

            Jenssen (2006) in the article entitled “Endocrine-Disrupting Chemicals and Climate Change: A Worst-Case Combination for Arctic Marine Mammals and Seabirds?”  states, “Climate change and exposure to endocrine-disrupting chemicals (EDCs) are currently regarded as two of the most serious anthropogenic threats to biodiversity and ecosystems. We should, therefore, be especially concerned about the possible effects of EDCs on the ability of Arctic marine mammals and seabirds to adapt to environmental alterations caused by climate change.”

            He illustrates the impact of endocrine disruptors with an example of persistent organic pollutants (POPs): “endocrine-disrupting chemicals are chemicals that are resistant to physical, chemical, and biochemical degradation and, therefore, remain available for uptake and bioaccumulation for a long period of time. Thus, they have a potential for long-range environmental transport, and they have adverse effects. Examples of POPs found in Arctic marine mammals and seabirds are industrial organochlorines (OCs) such as polychlorinated biphenyls (PCBs), hexachlorobenzene (HCB), polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), and polychlorinated naphthalenes (PCNs), as well as OC pesticides such as dichlorophenyl-trichloroethane (DDT) and its metabolites, chlordane, heptachlor, dieldrin, endrin, and mirex (Arctic Monitoring and Assessment Programme 2004)”

Glaucus Gulls

Glaucus Gull

            One species that is directly affected by POPs and climate change is the Glaucous gull. In the Arctic food web, the gull is one of the top predators. They are exposed to extremely high levels of POPs, and their northern latitude habitat is warming at a rate that far exceeds that of temperate and equatorial regions. Studies of gulls from Bear Island (Bustnes et al. 2002; 2003) found a negative correlation between concentrations of POPs (both OCs and PCBs) and thyroid function, coupled with the fact that the gulls would leave the nest for longer periods of time, possibly because they were impaired in their ability to find food. The higher the level of PCBs in their system, the longer they would be from the nest. It is suspected that the PCBs had neurological effects in the gulls. In the case of the male gulls, they needed more time to gather food. The gulls are biparental and baby gulls need both mom and dad to keep them fed. When the dads took too long to find food, this caused many of the dependent offspring to starve. While in the case of female gulls, the endocrine disruptors caused them to produce nonviable offspring. Furthermore, the endocrine disruptors affect the thyroid hormones that regulate the molting and replacement of feathers. Hexachlorobenzene (HCB) and oxychlordane were the primary disruptors that hindered the thyroid hormones and stunted the growth and development of the gulls’ feathers and wings, which might be expected to affect the ability to migrate and find food. The study concluded that “adult yearly survival rate was also reported to have a significant negative relationship to blood concentrations of DDE, persistent PCB, HCB, and especially to oxychlordane. In the years following the creation of chemicals such as DDE the gull population dropped drastically.” As climate change and warming alters the availability of food, endocrine disruptor effects on food-finding ability, parental behavior, and migration might further endanger the Glaucus gull. More work is needed to determine the role of endocrine disruptors on hormone action and behavior and its interaction with climate.

Polar Bears

Help polar bears at this link: WWF

            A similar effect may be contributing to decreasing polar bear populations in certain areas. The polar bear is the top apex predator in the Arctic, increasingly full of endocrine disrupting compounds, and the poster child of climate change. Although polar bears are one of the few animals that “has a relatively well-developed capacity for metabolizing and excreting  persistent organic pollutants” (Jenssen, 2006), the large amount of the pollutants they are consuming are too great for them to process. Most of the chemicals are consumed through bioaccumulation in their adipose tissue. Furthermore, the prey of the polar bear mostly consists of large amounts of seal blubber, a major site of bioaccumulation of POPs (Derocher et al. 2002). Today’s seal blubber contains an alarming amount of these pollutants, including two classes, the OCs and the PCBs. The seals live in water that has been heavily polluted with these chemicals because big corporations are mass dumping the waste in the oceans. A number of studies have documented an overall negative association between the high levels of POP s and the levels of thyroid hormones. This is significant because thyroid hormones are important for metabolism and neural development, which both underlie cognitive function (Zoeller et al., 2002). Impaired learning and memory, navigation, and problem-solving might exaggerate the challenges posed by melting and receding ice shelves that normally are required for breeding and hunting. In addition, endocrine disruption can cause chronically elevated stress responses, which can weaken the immune system. Adaptation to changing climate would require increased reproductive success of some portion of the population, but elevated levels of the gonadal hormone progesterone are found, and this would be expected to inhibit fertility. Because their habitat is now considerably warmer, polar bears are also hibernating for shorter periods of time, which is reducing the seal population upon which they depend because of the increase of hunting year round. Furthermore, seals also use the ice caps for breeding, but with less space, the seal species’ birth rates are plummeting. These are only some of the ways that polar bears might be subjected to interactions among factors related to climate change and endocrine disrupting compounds.

You can help polar bears by donating to the WWF

Migratory Species

            As Jenssen (2006) points out, climate change is nothing new, but it has worsened in recent years. Since 1976, the warming has been at its highest in the past 1000 years. The earth has warmed already 0.6 degrees since the 1960s. Although this might not seem drastic given the seasonal weather changes we experience, the current rate of warming of the average global temperature will have a devastating effects on the ecosystem, including but not limited to melting glaciers, sea level rise, extreme weather events, as well as changes in the availability of prey and other food sources. Animals worldwide have evolved to reproduce in certain temperature ranges at particular latitudes, and even the slightest change will require population changes in gene frequency that are unlikely to accumulate in time to save those species. Whereas as rapid changes in gene frequency have been observed over a few generations in some species, these are not thought to be common (Quintero and Wiens, 2013). A major disruption that has been observed and well-documented worldwide is the migratory pattern of birds. The change in global temperature has affected the reproduction grounds of krill. Whereas they are tiny and therefore might seem insignificant to us, they are the main source of food for seabirds, fish, and some aquatic mammalian species. When temperatures increase, the hatching dates for birds and the breeding season of krill no longer align, and birds begin to migrate early in the pursuit of food. This can cause an abundance of krill in one area where birds are not hatching, and a lack of krill in other areas where birds have come to expect a feast. This change causes overpopulation of krill and underpopulation of seabirds. Meanwhile, endocrine disruptors cause neurodegenerative effects that diminish the birds’ cognitive flexibility in finding resources and mating partners and protecting offspring.

In summary, the temporal changes in the food chain caused by global warming combined with endocrine disruptors might wreck the underlying neuroendocrine systems for adaptive behaviors, including parental behavior, foraging, hunting, and breeding. This also goes hand-in-hand with the climate-induced change in the prey population. That is, some geographic areas will have a higher demand for food, but because of the warming, many of the prey will not have been conceived or born in time. Even though these studies were done exclusively in the Arctic, endocrine disruptors and climate change have altered dozens of ecosystems across the globe. The situation will continue unless people (1) realize the importance of these ecosystems, (2) begin to make drastic changes to their lifestyles, and (3) begin holding the fossil fuel and other polluting companies accountable for their role in the degradation of world climate and the local environment.

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The A,B, Cs of PCBs

Well, welcome to another class of chemicals that someone thought was a great idea at the time, but turned out to be a very bad idea. First-year Lehigh student Hanna Aldrich brings us the A, B, Cs of PCBs.

            The polychlorinated biphenyls, otherwise known as the PCBs, are human-made organic chlorine compounds with the formula C₁₂H10−ₓClₓ. After being produced in million-ton quantities, evidence accumulated that many of the PCBs are A) toxins, B) endocrine disruptors (EDs), and C) persistent organic pollutants (POPs). Plus, some are probably carcinogens. These categories overlap. EDs interfere with the endocrine system and some do this in ways that increase the likelihood of getting cancer (so they are carcinogenic EDs), and EDs that are POPs stay around in the environment for many years (10-18 years in the case of PCBs). In addition, many individual PCBs are classified as “dioxin-like” because their toxic effects and chemical structure are similar to another class of toxic POPs, the dioxins. PCBs were first synthesized in the early 1880s by Schmidt and Schultz. Shortly after in 1889, it was found that workers and researchers who came in contact with PCBs developed chloracne, a painful disfiguring skin disease.

Yet, PCBs were adopted for commercial use in 1929. PCBs were first valued for chemical stability and fire resistance, and “150 million pounds of PCBs are dispersed throughout the environment, including air and water supplies; an additional 290 million pounds are located in landfills.” PCBs were used in making a wide array of products such as lubricants, adhesives, plasticizers, insulating fluids, and coolants in electrical equipment (e.g., transformers and capacitors in TVs, radios, stereos, amplifiers, power substations and other machinery) from 1929-1977. In addition, beginning around 1970, PCBs were used to make carbonless copy paper (Erickson and Kaley 2011), used widely in schools and businesses all over the world. Later that decade, it was demonstrated that PCBs are readily absorbed through the skin or the latex gloves of those who handled the copy paper (Carpenter 2006). In 1973 a study in nonhuman primates showed that three months of dietary exposure to PCBs caused “liver enlargement, facial swelling, hair loss, and gastritis of the type associated with cancer.” PCBs were banned for most uses in the United States in 1979 by the Toxic Substances Control Act (TSCA).

A lot of TVs and radios

It wasn’t until after the ban on PCBs that many effects on the body were documented, and because they are POPs, we are stuck with them. Like the other EDs we encounter in our Lehigh course, “Endocrine Disruptors,” PCBs bioaccumulate (being fat soluable, they are taken up by the tissues of organisms, especially body fat), and they biomagnify (they are found in greater concentrations the higher they get in the food chain). They are found in our food, water, air, and soil. Much of the possible exposure comes from our food, being an average of about 96%, while the next highest possible exposure comes from the air, which is less than 3%. PCBs accumulate in leaves of trees, grasses, and weeds, and in the above-ground parts of plants and food crops. These are eaten by wildlife, meat and dairy animals, and humans. PCBs are known to be easily absorbed in fat tissue and are not eliminated by the body very well, thus making them accumulate in larger and larger quantities in the bodies of predators at the top of the food chain. For example, fish eat various plants and algae that contain PCBs. From the water and digestve tract, the fish take up (bioaccumulate) the PCBs, which biomagnifies in the fishes body fat with each meal that the fish eats. As a result, if we eat those fish, we are exposed to PCBs that have bioaccumulated and biomagnified in the fish. We might get even more PCBs from eating beef, pork, and poultry that have been fed corn or grains that contain PCBs. PCBs are so prevalent in the environment because they were released improperly from hazardous waste sites, from leaks in old electrical transformers, or during the burning of garbage in incinerators. They also have very long half lives, around 10-18 years, making them prevalent all over the environment and in animal and human bodies.

            PCBs have a wide array of impacts on the body, including immune, endocrine, reproductive, and neurological effects. They are also considered probable carcinogens by the EPA. It has long been known that prenatal exposures to PCBs cause irreversible brain damage in the fetus (Jacobson and Jacobson 1997). When exposed to PCBs, the immune system of primates takes a big hit (we are primates). Individuals with high levels in the blood, show decreases in the size of the thymus gland which is critical to the immune system. The effects are particularly serious in infants exposed prenatally to PCBs. A recent study on humans found that individuals infected with Epstein-Barr virus had a decreased resistance to the disease if exposed to PCBs, plus, they found a strong doseresponse relationship between serum PCB levels and non-Hodgkin lymphoma, a cancer of the lymphatic system. PCB exposure increased the risk of non-Hodgkin’s lymphoma along with viral infection, implicating the PCBs’ immune-depressive effects in the increased cancer risk. This finding in humans matches up with increases in Epstein Barr in PCB-exposed lab animals (EPA, 2021). These recent studies make a strong case for the effects of PCBs on the immune system, but this is only a small part of the effects of PCBs.

The endocrine disrupting properties of PCBs often involve the hypothalamic-pituitary-thyroid system. Thyroid hormone levels are critical for normal growth and development, and alterations in thyroid hormone levels may have significant implications for the developing brain. PCBs may interfere with the hormone signaling solely by reducing circulating levels of thyroid hormone and thereby elevating thyroid stimulating hormone secretion from the pituitary, or they may exert direct effects on thyroid hormone receptors. The effects of PCBs on the thyroid hormone are significantly stronger in women and older adults (National Center for Biotechnology Information (NCBI) in 2007). In addition, PCBs have been shown to exert estrogenic and antiestrogenic activity, impact various receptors, and modulate steroidogenesis, which is the formation of steroids, as by the adrenal cortex, testes, and ovaries. Perhaps most disturbing, impaired reproductive physiology has been identified as an inter- and transgenerational effect of PCBs in rodents. They may act epigenetically via Wnt7a signaling, as it has been demonstrated that PCB (Aclor) exposure decreases expression of the Wnt7a regulatory gene and disrupts uterine development.

Overall, it is important to perceive the recurring pattern: chemicals are invented for a particular use, but then later turn out to be making us get sick and die. A thing we at first love turns out to have been toxic the whole time. These endocrine disrupting chemicals from the environment are hard to avoid, especially because they were so widely dispersed and they are so persistent. In her 1962 best seller, Silent Spring, Rachel Carson asked two critical questions:

Should chemicals like DDT and PCBs be showered on the environment prior to understanding their effects? Should humans, pets, and wildlife have the right to refuse being showered with these chemicals? Good questions.

Well, here’s to finding out things we love are toxic…

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Endocrine Disrupting Effects in Grandchildren of Women Who Used DES

In a previous post, we learned about the history of DES daughters, the offspring of women who unwittingly took the carcinogen, DES in the 1940’s-1970’s, hoping to prevent miscarriage. In this follow-up post, first year Lehigh student, Brooke Lee, explains why the effects of DES persist today, even in DES granddaughters.

Diethylstilbestrol (DES) is a carcinogen (causes cancer), mutagen (causes mutations), and teratogen (malforms embryos), yet it was prescribed by doctors to menopausal women, and later, to pregnant women. It was touted as a healthy way to prevent miscarriages, premature labor, and other pregnancy-related complications. DES was estimated to be prescribed to about five-ten million women worldwide and approximately four million of those women were from the US before it was banned in 1971 by the FDA. These women would take DES in various ways such as orally with pills, DES injections, or DES suppositories, but all forms of DES have been proven incredibly dangerous and harmful to the women who took it, their offspring, and even later generations. For a detailed account of how DES was discovered and prescribed, check out the post on this blog by Katie Bashus. Not many people have heard about DES or know about its lasting side effects, however, a lot of people (whether they are aware of it or not) are negatively affected by DES. So, what do the effects of DES look like in the generations leading up to today? And what can be predicted about the future generations of those whose parents and grandparents were exposed to DES? Let’s find out.

Zamora-Leon, 2021

DES is an endocrine disruptor, that is it interferes with some aspect of the endocrine system. DES is nearly five times stronger than the body’s natural supply of estrogen, and it can bind more quickly and with greater affinity to the body’s estrogen receptors (ERs). For the offspring of women who take DES, exposure to DES causes about a 40% increase in risk for developing breast cancer. For the granddaughters of women who take DES they have an increased risk of irregular menstrual cycles, amenorrhea, and preterm delivery.

DES Daughters and Sons

Countless health issues have plagued the offspring of those who were exposed to DES in utero. To start, there is more known about the effects of DES on daughters than sons. In some studies, DES sons are reported to have higher rates of genital malformation if their mother took DES while pregnant with them, however, the data for the rate of genital malformation on male offspring of DES mothers varies greatly from study to study. While some researchers estimate that up to 15% of sons could experience genital malformation, other studies estimate that the fraction of sons who experience genital malformation may be under 5%. A large reason why some of these data are so inconclusive is that these studies don’t have large sample sizes. DES daughters on the other hand, according to a Herbst and Scully study in 1970, are significantly, almost 40%, more susceptible to developing a very rare cancer called clear cell adenocarcinoma. Usually, this form of cancer affects people over the age of 45, but DES daughters are at risk starting between the ages of 15-22 years old. DES daughters are also 2.5 times more prone to breast cancer after the age of 40 than women who weren’t exposed to DES. DES daughters go through menopause earlier on the average and this might be related to their susceptibility to some kinds of cancer. Additionally, DES can cause the malformation of the reproductive tract in women. Specifically, they can have partially developed internal and/or external genitalia (e.g. uterus, cervix, fallopian tubes, vaginal labia, and/or clitoris). They show higher rates of infertility or pregnancy issues. Some of these issues are potentially related to the malformation of their reproductive organs, but not all of these issues. Below is a table from a study conducted by Hoover and Fraumeni that compares data from women exposed to DES in utero and women who weren’t to show that those exposed to DES have higher rates of health issues. Fraumeni has a large number of participants in his study and uses rigorous data analysis to compare the health defects of women exposed vs. unexposed to DES. The data clearly suggests that women exposed to DES in utero experience a higher rate of health issues.

DES Grandchildren

The third generation, or F2 generation, has also been shown to have significant health issues. DES grandsons are at an increased rate of developing hypospadias, a birth defect where the urethra is not located at the tip of the penis. Scientists suspect that this defect may have been caused by the mutated DNA from their mothers/grandmothers or a hormonal imbalance that lead to this malformation. DES granddaughters are at risk for poor menstrual regulation and potential fertility issues.

Additionally, according to a 2016 study done by Réseau DES France, out of about 4409 DES grandchildren, 1⁄4 were born prematurely. Premature birth exposes “neonates to serious neonatal complications, including neurosensory disorders, disabilities, and increased neonatal mortality.” In other words, because DES babies are much more likely to be born prematurely, they are more at risk for health complications after birth. Additionally, the Réseau DES France study found that, in DES grandchildren, rates of cerebral palsy were much higher: “59/10,000, versus 6/10,000 in the control group.” An additional study conducted in the US also suggests that DES grandchildren were 8 times more at risk for infant death syndrome, and stillbirth was almost two times more likely. So, DES poses great health risks especially on the health of the infant offspring of DES children.

Further, not only does DES have physical effects in future generations, but many scientists hypothesize that DES can cause neurodevelopmental disorders, such as ADHD, and other mental health issues. Children and grandchildren of DES mothers are potentially at a higher risk for developing ADHD. Findings from a US study that took data from 47,540 women (861 were DES mothers) found that “7.7 percent of the grandchildren of women who used DES during pregnancy were diagnosed with ADHD, compared with 5.2 percent of other grandchildren in the study.” This study indicates that there is a potential connection between neurodevelopmental issues and DES exposure. These data, however, are strictly correlational and cannot be used as strong evidence for a causal relation between DES and ADHD. In addition to ADHD, some studies suggest that DES exposure might cause increased rates of depression in third-generation individuals as well. The DES Cohort Study conducted in 2011, found that, out of the 6093 (4244 exposed and 1849 unexposed) women and 2989 (1472 exposed, 1517 unexposed) men, 1398 women (993 exposed, 405 unexposed) were diagnosed with depression, and 358 men (177 exposed, 181 unexposed) were diagnosed with depression. These data suggest that descendants of DES users experience higher rates of depression. One limitation of this study is its full reliance on the survey answers sent by the participants. The connection between DES and mental health requires more study. One problem is that humans have a relatively long generation time. This means that the multigenerational effects of DES take many years to collect. Sample sizes are small and it can be difficult to locate DES granddaughters. If they are prone to cancer, it may not be discovered until more time has passed.

In contrast to studies using human subjects, there are a number of controlled studies using rodents, such as mice. The mouse reproductive system shares most traits in common with primates, including women, but the mouse generation time is much shorter, only a few months, not decades. DES-exposed mice have reduced rates of fertility and lower success in reproducing. In the F2 generation of DES mice, fertility is not impaired, but there is a significantly increased incidence of malignant reproductive tract tumors, including uterine adenocarcinoma. The range and prevalence of tumors increases with age (Newbold et al, 1998). Studies in mice also give some clues as to how the effects of DES can be passed to future generations. In contrast to mutagenic effects, epigenetic effects are those that are heritable without a change in the sequence of DNA. Rather, the unaltered gene sequences are prevented from being expressed by a number of processes. One such process is DNA methylation. DES treatment of mouse embryos alters the methylation of a particular gene known as the the Hoxa10 gene, and the resulting decrease in Hoxa10 expression adversely affects development of reproductive tissues. DNA methylation is promoted by DNA methyltransferases, and the data show that DES treatment up-regulates these DNA methyltransferases, thereby decreasing expression of the Hoxa10 gene. These experiments in mice show one possible way that DES might cause cancer in daughters and granddaughters without changing the DNA sequence, but rather by changing the expression of genes (Bromer et al, 2009). This line of research might lead to a treatment that could alter DNA methylation caused by DES exposure in past generations.

Reed and Fenton, 2013 (from IBCERCC Report)

People who are directly exposed to DES and those whose ancestors were exposed to DES are all at higher risk for serious health and reproductive issues. Because DES is an endocrine disruptor, a known carcinogen, and because its has known epigenetic effects, the full spectrum of potential health abnormalities will be hard to determine. Third and fourth generation offspring of DES grandmothers might not even know they have a relative who took DES. Work in progress using both humans and rodents is unraveling the changes that are passed from generation to generation. There is hope that scientists may be able to more accurately understand the true magnitude of the effects of DES and come up with a way to proactively support or treat affected individuals. Last, for those who know they have been exposed to DES, doctors recommend (especially for women) more frequent checkups/doctors appointments. Especially because DES is known to cause higher rates of cervical and breast cancer (among other forms of cancer), catching these cancers early could lead to more successful rates of treatment. DES has caused a wide array of malformations, disease, and hardships for many individuals, but it is possible that research can lead to methods to correct the epigenetic and germline changes that all originated from an understudied and oversupplied synthetic chemical from the 1950’s.

It’s hard to imagine what life has been like for women who were the early victims of the medical, industrial, and government greed and hubris that led to millions of prescriptions of DES. We dedicate this post to the DES grandmas.

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DES: An Endocrine Disruptor With Tragic Effects on Mothers and Daughters

Similar to the thalidomide tragedy of the 1950’s, the story of DES exemplifies the suffering caused by a mix of profit-motivated medicine, lack of scientific evidence, and oversimplified assumptions about women and their bodies. First-year Lehigh student, Katie Bashus, weaves the history of DES with the history of ignoring women’s perspectives.

An early ad for estrogen replacement that promotes an alarming view of menopause

The person who discovered DES did so in the course of studying the carcinogenic effects of various steroid molecules, so it shouldn’t be a surprise that DES was later found to be carcinogenic, after having been prescribed to women for many years. DES stands for diethylstilbestrol. Its formula is C18H20O2, and it has a structure that allows it to mimic, at least in some ways, the action of the naturally-occurring steroid hormone, estradiol. DES has a long and sordid history, having been prescribed to women for over 30 years, and then later found to be carcinogenic (causes cancer), mutagenic (causes genetic mutations) and teratogenic (malforms embryos). DES has had devastating physical and mental impacts on mothers as well as on their children. These effects of DES include clear cell adenocarcinoma (a type of cancer most common in elderly women) in girls and young women. How did DES, at the time a suspected carcinogen, infiltrate the medical world and the world of thousands of mothers and their families?

Menopause as a Disease

Doctors of the mid 20th century, the vast majority of them male, noted that at the end of their reproductive years, females experience a decrease in circulating ovarian hormones, especially the class of ovarian steroids known as estrogens, which include estradiol and estrone. Many saw this drop in ovarian steroids as a disease or medical problem, and their records indicate that their main focus was the lack of “femininity” they saw in women over the age of 40. Based on the fall in ovarian steroids and subsequent loss of femininity they conjectured that the “treatment” for the “disease” of menopause would be to increase estrogen levels by some sort of pharmaceutical prescription. At the time, a cost-effective, painless way of providing real estradiol had not yet been invented, so some scientists looked for a cost-effective alternative to real estradiol.

DES As A “Cure” for Menopause

Sir Edward Charles Dodds thought he had found the estrogen alternative that the pharmaceutical industry was seeking. Dr. Dodd was a researcher studying carcinogens and the link “between estrone and a group of carcinogens known as the phenanthrene group.” In 1938 he discovered an estrogenic chemical, DES, that could be synthesized very cheaply from coal-tar derivatives. Dr. Dodd never patented his discovery, and since distributors didn’t have to pay any royalties, this made it an attractive alternative to replacement estrogen.

DES is a type of endocrine disruptor that blocks the action of hormones that already exist in the body. Normally, hormones control processes in the body, including “development, growth, reproduction, metabolism, immunity and behavior.” They are secreted in precise time patterns and amounts that allow organisms to synchronize their bodily systems with the day-night cycle, meals, times of year, and phases of their life history. Endocrine disruptors interfere with these processes. Nuclear receptors are the main target of both endocrine disruptors and natural hormones. Normal steroid hormone-receptor complexes form, travel into the nucleus, and interact with DNA, acting as transcription factors. Endocrine disruptors typically come from outside the organism, and many either mimic or block the action of steroid hormones. Rather than rewriting the DNA sequence, endocrine disruptors such as DES have epigenetic effects that alter the timing of DNA expression. Such effects can be as serious as a genetic mutation and be passed to future generations. Even after exposure is over, endocrine disruptors’ health effects linger, having set in motion developmental chain reactions that cannot be undone.

Ignoring the Animal Studies

As explained in the book Toxic Bodies written by Nancy Langston, there were early indications that DES could have significant effects on mothers and their offspring. In one study, researchers gave DES to pregnant rats, mice, and chickens. The offspring exposed to DES were found to have changes in traditional sexual differentiation (females were masculinized), but problems were only seen when the treated animals reached sexual maturity. Another study found this similar exposure made the adult offspring of DES-exposed mice act more aggressively. Dr. Dodd’s research group found DES led to atrophy in reproductive organs. Some research scientists saw the red flags, but only those who understood that the reproductive systems of laboratory rodents share many important similarities with those of primates. Humans are a species of primate.

Then how was DES distributed to thousands of women even though animal studies indicated numerous problems? Some doctors thought DES would be safe because women already have estrogen in their bodies, so the post menopausal woman should be fine. Contrary to this belief, many biologists believed that the results of experiments on mice provided cautionary evidence. Physicians discredited this idea. They claimed that humans are different from animals, and women would not develop cancer from having extra estrogen. Their point of view was bolstered by the fact that cancer can take years to manifest. In other words, a lack of evidence of damage was seen as evidence of safety. Did all or even a majority of women want to “cure” menopause? Another point to consider is that most physicians at the time were men, and one wonders whether they valued or even solicited the opinions of females. Remember that at this time, the physicians expressed concerns about the femininity of older women, not their health.

The FDA Under Pressure from Industry

Initially, the FDA rejected DES to be used medicinally for menopausal women because of the carcinogenic and toxic effects. Their spinal cords crumbled, however, after pushback from the pharmaceutical industry and a court case. The FDA was brand new and members didn’t want to be seen as an enemy to drug companies for fear of losing their standing. The FDA therefore approved DES to cure menopause as long as information was provided on the possible adverse side effects and if it was only available by prescription. DES became the first medication deemed dangerous enough to warrant a prescription and became the first prescription drug in the US in 1941. Unfortunately, the information about DES’ toxicity was not given to physicians. The information was not even on the bottle; doctors had to write to the manufacturer to obtain that information. Most physicians did not seek to acquire the extra information. Their patients trusted DES because they trusted doctors. So a combination of mistrust of animal testing, no signs of immediate harmful effects in humans, a misogynistic mindset, and an inexperienced FDA led to the approval of DES to treat menopause.

DES To Prevent Miscarriage (not)

The use of DES as a treatment for menopause was short-lived, and an alternative market was quickly sought and discovered. After a while, a newer medication with fewer side effects called Premarin (isolated from the urine of pregnant horses) became the primary choice for menopausal women, so the pharmaceutical companies manufacturing DES had to switch gears and find a new market. Two Harvard researchers postulated that DES could help pregnant women. They reasoned that, since elevated estrogen levels during pregnancy usually stimulate the hormone progesterone, which the uterus needs to sustain pregnancy, increasing estrogen action by giving DES would prevent miscarriage. Their evidence was so thin as to be nonexistant, and we know now that their decision was dead wrong. One “study” examined diabetic women because they were considered to be at a high risk for miscarriage. The study consisted of six pregnant diabetic women, all given DES. That’s it. First of all, this sample size is ridiculously low. Second, there was no control group of diabetic women given placebo and no group of nondiabetic women to ascertain the rate of miscarriage. Of the six babies from diabetic mothers treated with DES, five carried their babies to term. From this they concluded that DES successfully prevented miscarriages. Nevertheless, DES found its place as a drug for diabetic women claiming to ensure healthy pregnancy without miscarriage, and gained approval in 1947. This distribution limitation (to diabetics) on the medication was not enforced as time went on, so eventually, many non-diabetic women were taking it during pregnancies as a supplement. In fact, DES was prescribed willy nilly for a number of loosely related uses. It was prescribed to prevent premature births and miscarriages, treat infertility of gynecological disorders, and inhibit milk flow after childbirth. The philosophy seemed to be “why not?” The belief at this time was that the placental barrier between baby and mother was impermeable so that nothing could get through from mother to child. This was later refuted and was a part of the reason that babies and not just the mothers were affected by DES. The expansion of DES usage was allowed by invalid assumptions, poor experimental methods, and disregard for the limitations on its prescription.

Scientific studies performed years after DES became a common pregnancy supplement showed that it was not beneficial to women. It did not prevent miscarriages and could do great harm to the daughters of DES mothers. In 1953, a study showed DES was ineffective at sustaining a pregnancy – 840 pregnant women on DES, 804 in the control group, and no discernible difference in the pregnancy outcome.

Despite this, DES continued to be prescribed for decades. The first red flag that DES was harmful was when an extremely rare cancer of the cervix was found in DES daughters in 1971. It occurred in their teens or early 20s, while this cancer typically happens much later in life. Clear cell adenocarcinoma, CCAC, was present in 1 in 1000 DES daughters. Shortly after that study, DES usage was stopped in the United States, but DES usage in Europe did not stop until around 1979. The increased risk of cancer from DES, though, was just the tip of the iceberg.

Other physical issues caused by DES were found in many later studies. The mothers who used DES had a 40% increase in the likelihood of getting breast cancer later in life. The primary victims of the DES exposure, however, were the children, both male and female. Cell alterations, cancer, and cysts were on the list of effects on the children of DES mothers, and there was also harm to fertility. Male genital anomalies were 200% higher than the general population. Some 95% of DES daughters had one or more reproductive issues. There were increased risks for infertility, miscarriages, ectopic pregnancies, and premature births. Infertility went up 30%, miscarriages went up 90%, and premature births increased 180%.

The reproductive issues in the offspring were often traced to malformation of the Müllerian ducts. With the right hormonal environment, Müllerian ducts in the fetus develop into fallopian tubes in females and completely disappear in males. These studies often saw that the fallopian tubes were not properly developed, and some Müllerian duct remained in men, which caused feminization. The abnormally T-shaped uterus became diagnostic for DES exposure. The presence of DES during development seemed to have affected the tubes’ proper development.

The effects of DES on offspring were not limited to the physical; a higher incidence of psychiatric disorders has also been discovered. A study conducted in France sent a questionnaire to women who took DES and had children between 1946 and 1995. Some 1182 children were reported on, including DES exposure, medical history, and occurrence of any psychiatric issues. The children were separated into three groups: children born before their mother took DES, children exposed to DES while in the womb, and children born after the mother stopped taking DES. The data shows a considerable increase in mental health diagnoses after DES was introduced into the mother’s system versus that of the general population. A surprising result is that children born post-DES showed a higher likelihood of mental illness than the general population. This suggests that DES was stored in the mother’s body after she stopped taking it and was later released. The increased occurrence of psychiatric disorders in the DES-exposed children, summarized in the chart below, shows the dangers to the brain and its development.

Soyer-Gobillard, Marie-Odile, et al. “Association between Fetal DES-Exposure and Psychiatric Disorders in Adolescence/Adulthood: Evidence from a French Cohort of 1002 Prenatally Exposed Children.” Gynecological Endocrinology, vol. 32, no. 1, 2015, pp. 25–29.

Why might these issues be occurring in DES offspring? Well, some evidence supports the idea that because the HOX genes are involved in the structural differentiation of the reproductive anatomy, DES delays the expression of these genes, causing the misprogramming of the molecules themselves, which can result in different anatomies or tumors. Also, demethylation, removal of CH3 from a molecule, “of the estrogen-responsive gene LF in the mouse uterus” was shown and could be another reason for issues with sexual differentiation in offspring. The ADAM TS9 gene is involved in controlling the development of the shape of reproductive organs and the development of the central nervous system. DES has been shown to alter the expression of the ZFP 57 gene on chromosome 6, affecting neurodevelopment and neuroplasticity. These epigenetic effects are just as scary as direct DNA altering, that is, genetic mutations.

DES use has been well investigated, and all evidence shows that DES is a dangerous endocrine disruptor. After being prescribed for menopausal women and then pregnant women, it was shown to be a threat to the physical and mental health of not only said women but also their offspring. Even after clear evidence of zero protection against miscarriage and harmful effects on mothers and offspring, DES was prescribed for decades. It is no coincidence that any and all benefits were accrued by the pharmaceutical industry. The continued sale of DES was aided by doctors’ failure to keep up with and heed the data supplied by the scientific experiments. Knowledge of this history is important because it reminds us that flawed decisions result from sexism and putting profits ahead of the health of women. Thousands of women were unknowingly taking toxic chemicals that would affect their children. The history of the approval of DES demonstrates the dangers of misguided assumptions, inadequate testing, and an FDA too willing to ignore the science to please the pharmaceutical industry. I think that the evidence in these articles is powerful and provides adequate proof of the dangers of DES. This research could still go on into the future because the full, long-term effects are not yet known in humans. Studies on DES grandchildren are still in progress, and we don’t yet know how far in the future DES will affect subsequent generations.

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DDT: The First Known Endocrine Disruptor

According to experts, Heather Patisaul and Heather Adewale, the first-known endocrine disruptor was DDT. Since DDT is best known as a biocide, a killer of biological organisms of all kinds, including bald eagles, it’s fascinating that Paul Hermann Müller actually won the Nobel Peace Prize for the discovery of DDT’s insecticidal properties! In the following post, first year Lehigh student, Sofia Weaver, provides the tumultuous history of DDT, a double-edged sword from the era of “better living through chemistry.”

According to the EPA, 1,350,000,000 pounds of DDT were used domestically in the 30 years before its ban in the US. Dichloro-diphenyl-trichloroethane, also known as 1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane, and most commonly as DDT, is a synthetic insecticide in the organo halogens family. DDT is created by condensing chloral hydrate with chlorobenzene in concentrated sulfuric acid.

We might think of DDT as a product of the flat-topped, white lab coat-wearing chemists of the 1950’s, but DDT was initially discovered in 1873 by Othmar Zeidler, a chemistry student at the University of Strasbourg.  

DDT was subequently resynthesized by Swiss chemist Paul Hermann Müller (shown at left).

Müller was the one to discover its insecticidal properties and received the Nobel Prize in Physiology or Medicine in 1948 for the discovery of DDT and its high efficiency as a contact poison against several arthropods in the control of vector diseases. In its earliest uses, DDT protected World War II soldiers against various vector diseases such as malaria, typhus, and yellow fever. Navy training videos show this philosophy and practice, wherein the disease-carrying insects were seen as part of the enemy axis. In fact, DDT was very effective. Malaria cases fell from 400,000 in 1946 to virtually zero in 1950 (Vandenberg et al. 2020). DDT was then used back at home against lice and agricultural/household pests before eventually being banned in 1972. The ban has been attributed to an environmental movement at least partially propelled by Rachel Carson’s Silent Spring, a book that directly challenged the indiscriminate use of DDT because of its adverse effects on wildlife and humans and because its efficacy waned as successive generations of insects became increasingly resistant to the chemical.

According to the National Institutes of Health (NIH), endocrine-disrupting chemicals (EDCs) are environmental agents, in this case synthetic chemicals, that interfere and inhibit hormone action by modifying normal hormone levels, mimicking hormones, or altering hormone production entirely, resulting in the increase of various health risks such as cancer, reproductive impairment, obesity, and cognitive impairment. Many EDCs, natural and synthetic, act on the estrogen receptors (ER), either mimicking the action of estradiol or other estrogens, or blocking estrogenic hormone action by binding to ER.  Currently, few if any environmental chemicals have been found to function as androgen mimics (agonists to the androgen receptor). However, numerous insecticides, including DDT, have been recognized as androgen antagonists, blocking androgens’ binding to the androgen receptor (AR). In fact, DDT, alongside various other chlorinated hydrocarbons, are estrogenic in both in vivo and in vitro models and assays and have been seen to bind to and activate the human ER (Bretveld et. al., 2006). Although DDT is seen to have an estrogenic affect, it has also been seen to bind to AR, and there is evidence that both DDT and its metabolite DDE compete with androgens for their receptors. Some phenotypes are expressed according to the overall ratio of estrogens to androgens, and some endocrinologists have suggested that the presence of these androgen-antagonist EDCs have overall estrogenic effects. DDT also has effects that are independent of steroid receptors, e.g., DDT can activate the transcription factor, Activator Protein 1 (AP-1), known to regulate gene expression in endometrial and kidney cells (Frigo et al., 2002).

DDT was the first known endocrine disruptor. It was first speculated that DDT was interfering with the endocrine system in the early 1930s by wildlife biologist Charles Broley after he observed rapid declines in populations, abnormal courtship behavior, and reduced nesting behavior in numerous species of birds across the US and Canada (Pautisal and Adewale, 2009). Broley hypothesized that fish contaminated with DDT were being consumed by the birds and DDT was sterilizing the birds. Birders, ornithologists, and wildlife officials were reporting massive die-off of many bird species, including raptors, such as eagles, ospreys, hawks, and falcons. Studies of peregrine falcons in the UK noted that less than one-fifth of the mated pairs in 1961 and 1962 successfully raised young. After numerous studies, it was concluded that DDT and its metabolites were not exactly “sterilizing” the birds, but rather, feminizing the male embryos, weakening and thinning eggshells, and interfering with reproductive behavior to such an extent that it was “decimating” bird populations. This was especially true in bald eagles. At one time, the bald eagle population was decreasing to the level that US officials were considering a new national bird in fear that the bald eagle was going to go extinct. Many of Broley’s 1930’s ideas were born out by data. It would be interesting to hear what Broley had to say when Paul Hermann Müller received the Nobel Peace Prize in 1948 for his role in the widespread use of DDT.  

Initially, DDT was passed off as innocuous by industry and government, because in addition to other various insecticides, it was created to target biological aspects believed (hoped? imagined?) to be unique to insects (e.g., metamorphosis). Although these biological aspects depend on hormones in insects, studies have shown physiological and structural similarities in similar hormones and their receptors in birds, crustaceans, and mammals, including humans (Vandenberg et al., 2020). These similarities resulted in numerous negative effects in non-target species due. In addition, DDT kills insects by interfering with neural transmission, i.e., by causing sodium channels to open, preventing action potentials, and causing death. However, sodium channels and action potentials are fundamental characteristics of the nervous system in all species that have a nervous system, and it became clear that DDT application killed everything from earthworms, to insects, fish, amphibians, reptiles, avian reptiles (birds), and mammals. The now released Navy training videos make it clear that the effects of DDT on the insect nervous system were well known.

One of the more alarming effects of DDT exposure is that it can be metabolized to other more deadly endocrine disruptors, such as DDE, which are fatal and much lower doses. Unfortunately, negative effects in non-target species are not rare and quite detrimental. Exposure to DDT, and its metabolite DDE, has been known to cause gynecomastia, oligospermia, impotence, hypogonadism, decreased libido, reduced motility, and menstrual cycle irregularities in humans (McLachlan, 2001). In Japanese Quail: abnormal reproductive behavior, hematology, and feather morphology. In gulls: abnormal development of ovarian tissue and oviducts in male embryos, and feminization in ovo. In alligators: abnormal gonads, decreased phallus size, and altered sex hormone levels. In numerous species of birds: thinning of eggshells, developmental abnormalities, growth retardation, and even mortality. In humans: DDT has been classified as a type 2A carcinogen, meaning there has been sufficient evidence that suggests that DDT causes cancer in humans (EPA). And this does not even scrape the surface of the various negative estrogenic effects DDT and its metabolites. Avoiding exposure is either virtually impossible, or completely out of the hands of the organism.

DDT bioaccumulates and biomagnifies, as shown on the left.

In addition to biomagnification, DDT bioaccumulates in lipids, so although a habitat (like a body of water) may be deemed DDT free, DDT is still found in the body fat of organisms that inhabit that environment. These chemicals also have a long half-life in the body: about 10 years in human blood, 4.2-5.6 years in adipose tissue, and most likely much longer for DDE. One of the more horrific effects of DDT was brought to light in Rachel Carson’s Silent Spring: Since DDT is a lipophilic chemical it accumulates in adipose tissue cells, increasing in total amount with each successive exposure. Later, any kind of mobilization of energy from fat stores, like the breakdown of triglycerides to free fatty acids and glycerol (lipolysis) that occurs when dieting or lactating releases DDT into the blood at a far greater amounts than the organism has previously experienced in the gradual accumulation process. Thus, a “small” application of DDT in the garden each spring, through bioaccumulation in tissues and later release during lipolysis, can become a deadly dose years later whenever the individual loses body weight. What’s more, DDT released during lipolysis can later be excreted through urination, defecation, and even lactation. This can result in nursing infants being exposed to high doses of DDT through their mothers, which is one of the reasons why we continue to see concentrations of DDT in humans. Human exposure to DDT has been documented for several decades by the US National Health and Nutrition Examination Survey (NHANES). In the second survey taken between 1976 and 1980, DDT was detected in 37.9% of samples, and DDE was detected in 99.5% of them. In the fourth survey taken between 1999 and 2004, DDT was detected in 73.8% of those 12 and older and DDE was detected in 99.7% of the same age range (CDC). However, although the concentration of DDT present in the individual samples decreased between the two surveys, more individuals were found to be exposed to DDT.

DDT and DDE are still very apparent in our environment and populations, and despite being banned in the US, DDT is still being used around the world. In 2014, the average global production and use of DDT was 3145 tons (Van Den Burg et al., 2017). It is estimated that DDT can last in humans for up to three generations. Its half-life in soil can be anywhere from 2-15 years (CDC). DDT is a biocide, not just an insecticide, and humans will continue to pay the price for our irresponsible use of it (shown in this video below).

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Of Dioxins and DDT

First year Lehigh student, Alisa Vukovic, finds some interesting similarities between the histories of DDT and dioxins:

            Think something is too good to be true? It probably is, especially if it’s manufactured and marketed by industry. For example, industry scientists convinced government agencies that the pesticide, DDT, was so safe and so effective that it was sprayed indiscriminately on crops, wildlife, and people. It turned out that DDT damage was not limited to insects but to species at all levels of the ecosystem from worms to humans. Do you think burning that pizza box is safe? It is not. When incinerated, cardboards emit a variety of toxic chemicals, depending on the various inks and other ingredients used in their manufacture. Many of these chemicals are well-known endocrine disruptors (ED’s, chemicals that disrupt hormone synthesis or action) and persistent organic pollutants (POP’s, carbon compounds that take 3-15 years to break down). The good news is that the more studies that are done, the more scientists can understand the long-term effects of how ED’s and POP’s affect our ecosystem and people. These studies educate us so we can learn to reduce our exposure to certain chemicals and demand that they be banned so we can protect ourselves and the ecosystem.


            Dichloro-Diphenyl-trichloroethane, also known as DDT, is the infamous organochlorine agent that was initially used as an insecticide, until it was discovered that its effects on the insect nervous system generalize to higher organisms, including people. The original outcome of DDT application was a dramatic drop in the incidence of insect-borne illness, including malaria, lice, and typhus in civilians and military personnel during WWII. This news made people believe it was safe for other uses, but the long-term effects were not studied prior to wide-spread use. Rachel Carson’s nonfiction best seller, Silent Spring, brought awareness of DDT’s dangers to the public. The chemical at the time was not regulated and was easily spread around via truck mounted hoses and crop dusting planes. In fact, the government would spray DDT over farms, cities, and towns. After Rachel Carson’s book was published and became an award-winning best seller, it drew the attention of the media and even the president of United States, who called for more research on DDT. The research eventually compelled the EPA to ban the use of DDT. The results showed, among other things, that “​​some animals exposed to DDT in studies developed liver tumors” and “in certain birds of prey caused their eggshells to thin so dramatically they could not produce life.” Carcinogenic effects were predicted to most likely be happening in humans as well. The CDC fact sheet also confirms that in response to high levels of DDT, “human symptoms can include vomiting, tremors or shakiness, and seizures,” another reason that is toxic to our health and ecosystem. With all of this evidence, the EPA and CDC have labeled it as a “possible human carcinogen,”  possible because of the inconsistency of evidence. Since the publication of Silent Spring, we have known that individuals differ in their reaction to DDT, depending on genetics, other environmental exposures, diet, and other factors. The severity of adverse effects depends on how often an individual is exposed to the toxin. DDT is classified as a Persistent Organic Pollutant (POPs) because it takes approximately 3-15 years to break down. Furthermore, it bioaccumulates (is taken up in tissues of animals), and it biomagnifies, i.e., it becomes more and more concentrated in animals higher in the food chain. The detrimental effect of DDT cannot be refuted. Yet, some have argued that the primary reason DDT was banned was because it eventually ceased to work as a pesticide.  “DDT’s quick success as a pesticide and broad use in the United States and other countries led to the development of resistance by many insect pest species.” In other words, over generations, populations of insect pests evolved to thrive and reproduce in greater and greater numbers in the presence of DDT, even as the doses of DDT being used increased and became more and more deadly to animals including humans.  


            Plastics, cardboard, and particle board seemed like great ideas at the time, but when incinerated, they release a class of chemicals known as dioxins. The dioxins are another class of POP even more toxic than DDT. Dioxins include the  polychlorinated dibenzo-para-dioxins (PCDD) and dibenzofurans (PCDF). TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is the most toxic of the dioxins and causes developmental problems, cardiovascular disease, and infertility along with increasing the incidence of cancer. TCDD exposure comes primarily from cigarette smoke, industrial bleaching, and burning garbage, and these sources in turn contaminate the water supply. The evidence for the toll of TCDD on human health is for the most part correlational, that is, the incidences of cancer and heart disease are higher in those with higher exposure to TCDD. Work in laboratory animals however, provides unequivocal evidence that the abnormalities are a direct result of the TCDD, and reveal the mechanism. What makes TCDD so dangerous is the way it affects the Aryl hydrocarbon receptor (Ah receptor). The Ah receptor is “a protein best known for its role in mediating toxicity” (Murray et al., 2014) so it is impacted by environmental exposure. Our knowledge of the mechanisms whereby toxins affect human health rely on studies in laboratory animals, wherein TCDD exposure and interacting variables can be manipulated with precision and the cardiovascular outcomes of these manipulations can be quantified with accuracy.  For example, two studies at Rutgers University-New Brunswick Medical School focused on the effects of TCDD exposure in pregnant mice and their offspring. The first paper documented effects of TCDD on gene expression in the fetal heart (Carreira et al, 2015). The second study shows that the effects of fetal exposure last into adulthood, even though the toxin was no longer present after fetal development (Carreira et al., 2015). In other words, the fetal exposure permanently changed the organization of the fetal heart in a way that could not be reversed after the TCDD exposure ended. The heart remained damaged in the adult. The effects of TCDD exposure were compared to the effects of total ablation of the Ahr receptor. Would exposure to TCDD mimic the effects of having no Ahr receptor on the heart? Mice with normal Ahr receptors were designated Ahr+/+ and mice with the gene for the Ahr receptor knocked out were designated Ahr-/-.  You can see in the figure below that ablation of the Ahr receptor decreases exercise endurance (green lines), especially in adult male mice, and this effect was mimicked by a high dose of TCDD during fetal development in mice with normal Ahr+/+ (red lines).

            Also, in female but not male mice, high levels of TCDD exposure during fetal development leads to heart abnormalities in the adult Ahr+/+ mice, and the effects are in the same direction as total ablation of the Ahr gene (Ahr-/-). In female but not male mice, both ablation of the Ahr receptor and treatment with high doses of TCDD significantly increased heart weight (cardiac hypertrophy), myofiber area, and fibrosis (below).

Like mice, humans also are vulnerable to dioxin exposure during pregnancy and adulthood. In one study that measured the levels of dioxins in the blood and adipose tissue of over 1,000 workers in a factory that produces herbicides, they found that mortality due to ischemic heart diseases showed a dose-dependent relation with the amount of TCDD in the blood (Flesch-Janys et al., 1995). Heart disease is only a small part of the documented effects of dioxin exposure. The Minnesota Department of Health says that  “health effects include changes in liver function, thyroid hormone levels, immune cell levels, and decreased performance in tests of learning and intelligence. “Humans don’t have to work herbicide factories or incinerator facilities to be exposed to dioxins. Aquatic animals are also heavily affected by TCDD because it is a POP. It does not easily dissolve in water, which means it lingers and sticks to plants and algae underwater. Many fish, amphibians, reptiles, and birds consume these dioxin-laden plants and algae. This is another similarity to DDT, which accumulates in earth worms and ends up in the flesh of birds, including the bald eagle. This bioaccumulation and biomagnification of dioxins occurs because each local ecosystem contains a food chain in which larger animals eat smaller animals. Dioxins from the smallest animals accumulated in the tissues of larger animals, which are eaten by larger animals. Even the dairy and meat animals that we eat can be eating food that is contaminated with dioxins (Hoogenboom, 2012).  Humans can be poisoned with dioxins from contaminated water, meats (beef, pork, foul, and fish), and airborn dust.

As with the dangers of DDT, we have not been informed or given a choice about whether or not we are exposed to dioxins. We can avoid smoking cigarettes, burning household trash, and buying herbicides and pesticides. Still, we need to gain control over DDT-like chemicals that are still in use outside the US and dioxins still in use in the US in agriculture, municiple incinerators, cement kilns, and golf courses. Dioxins are sprayed on roads and dioxins spew from incinerators. Ask the residents of The Ironbound district of Newark, New Jersey, exposed to smoke from incinerators that burn the garbage trucked in from the rest of the state. Ask the residents of the Superfund Site, Times Beach, Missouri, where roads were sprayed with a mix of dioxin and waste oil to “suppress dust.” When nearby waterways flooded, the dioxin from the roads was carried all through Times Beach, resulting in local dioxin levels over 300 times safe levels. As of now, it is up to the individual to somehow find the information they need to avoid exposure. Even soldiers in the middle east are not informed about the dioxin exposure from burn pits (garbage dumps filled with food waste, human excrement and other refuse, saturated in jet fuel, and then set ablaze), nor are they compensated when exposure to dioxins and other ED’s leads to chronic illness. Silent Spring warned us that we need to be the stewards of our environment and is often credited with inspiring events that led to the formation of our environmental regulatory agencies. Somehow even though we have the EPA, CDC, and FDA, it’s up to us to educated ourselves, other citizens, the media, and legislators to ban the use of these chemicals and the practices that release these chemicals into the air we breathe.

Thank you to Son Volt for speaking up with this haunting song about dioxin in Times Beach, Missouri.



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The Joke’s on You: Gender Bias in How Humor is Perceived

Wow! Fantastic post by Dr. Nancy Wayne on a recent study documenting how humor enhances the status of funny men while diminishing the status of humorous women. I’ve always been vaguely bewildered about how my jokes are perceived, but it’s absolutely mind blowing to see the data!

Dr. Nancy Wayne

I think of myself as having a good sense of humor. I like to laugh, and I often use humor as a way of connecting with people during work and play. I use humor and storytelling a lot when teaching—I thought it was an effective way of engaging students and enhancing their ability to understand and remember complex physiological concepts. And with some exceptions, student evaluations supported that notion. I use humor a lot when interacting with my colleagues as a way of connecting with them and diffusing tensions during difficult conversations—I thought it was an effective way of communicating, until I received a “360 feedback evaluation” in which about half the evaluators said otherwise (see Bringing Your Authentic Self to Work). 

There has been a lot written about the power of using humor during business transactions and in the classroom, including research studies supporting the use of positive…

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