A bike ride a day…. might not keep the doctor away?

An abbreviated version of this post was originally published in The Crosscut with the title “Is biking a Catch-22 situation?

My friends think that I’m slightly obsessed. I prefer to think of myself as extremely passionate.

I’m getting my PhD in toxicology, but my interests don’t stop when I leave campus. I live and breathe this stuff: I love reading, learning, and writing about all things environmental health.

So, naturally, I’m worried about my own exposures to the overwhelming number of pollutants that we’re surrounded by. Though much is out of my control, I do what I can to minimize my exposures by buying organic (even on a student budget, and sometimes to an extreme that annoys my friends and family), avoiding processed and packaged foods, minimizing my use of plastics, choosing fragrance-free products, obsessively searching for flameretardant free furniture, etc. The list goes on. My environmental health knowledge and concern for my health (as well as the health of my potential future children?) drive my lifestyle and purchasing decisions.

Yet, there’s one lifestyle choice that I’m not willing to give up, especially while living in Seattle: biking. I bike commute to school almost every day of the year. (I only missed 2 days this winter, when the roads were icy). I love riding to campus; it’s my morning and evening meditation/reflection time and my exercise.

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Heading home from school on my bike. Photo credit: Alex Kritchevsky

While I do ride on the BurkeGilman trail for most of the way, with gorgeous views of the water, mountains and city skyline, there are also several segments on roads. Obviously, biking on busy, car-filled streets presents immediate physical dangers, like car-bike collisions (my housemate has been hit twice in 6 months) and getting doored (ouch! Looks so painful). But, there’s also all that disgusting air pollution I inhale as take deep breaths alongside the ever-steady stream of cars. Luckily, at least for now, I’m not affected by asthma or other respiratory conditions. Yet, air pollution has been linked to many health problems, including cardiovascular disease and dementia (the latter is the subject of my PhD dissertation); I can’t help but think about those dangers on my daily rides.

Am I causing more harm than good to myself by commuting by bike? Why am I willing to impose such strict controls on other parts of my life (ie: purchasing decisions), but I allow myself to take deep breaths of noxious miasma every single day? Sure, exercise is good for me – for both my physical health and my brain health. But, do the negatives (pollution, collisions) outweigh the positives (physical and emotional health)?

What am I exposed to?

The short answer is: a toxic brew of traffic-related air pollution, at higher levels when biking on busier roads, and probably in higher doses than while driving in a car.

This report (prepared for the National Institute for Transportation and Communities) has a good summary of the research (as of 2014) about traffic-related air pollution exposure to bicyclists. Since then, more studies (for example, in Salt Lake City, Utah; Minneapolis, Minnesota; and Montreal, Canada (here and here)) have also quantified exposures to city cyclists; others (like this one in New York City) are in process now. All of these assessments are specific to each city, season, time, and route. It will take much more research to develop a body of information that reflects the average and range of possible exposures to cyclists.

Such research with individual level measurements is crucial. We routinely track ambient air pollution across the country with a surprisingly few number of monitors (check out this interactive map to explore your area). These devices, which are often located away from major roadways or pollution sources, would definitely underestimate my own exposure, especially when I’m biking right behind a bus.

Exact quantification pending, what am I breathing in on my morning and evening commutes?

  • Particulate matter (PM): PM is a mix of dust, dirt, and soot particles. Sources of PM (and gases that trigger formation of PM) include wood stoves, fires, power plants, vehicles, industrial facilities, and construction sites, among others. PM can also include heavy metals (such as lead, cadmium, copper, and zinc) from tires, brake wear, and diesel exhaust, as well as black carbon. Smaller particles, such as PM2.5 (≤2.5 micrometers) and ultrafine (UF) PM (≤100 nanometers), can penetrate more deeply into our bodies (and are thus likely more dangerous) than PM10 (≤10 micrometers). PM has been linked to adverse respiratory, cardiovascular, cognitive (neurodevelopmental and neurodegenerative), and reproductive outcomes.
  • Nitrogen oxides (NOx): Nitrogen oxides, reactive gases emitted from vehicles and power plants, are highly irritating to the respiratory system.
  • Volatile organic compounds (VOCs): Released from fuels and vehicle exhaust, this large class of compounds contributes to ozone formation. Many have also been classified as “hazardous air pollutants” by the US EPA because of their link to cancer, reproductive, or adverse environmental effects.
  • Ozone (O3): Ozone is formed through chemical reactions of NOx and VOCs in the presence of sunlight and triggers respiratory health effects, like reduced lung function and asthma attacks.
  • Carbon monoxide (CO): Colorless and odorless, carbon monoxide is produced through incomplete combustion from cars, trucks, and machinery. While the major concern with CO exposure at high levels indoors is its potential to interfere with transport of oxygen in the body and cause acute neurological and cardiac effects, the likely consequences of lower level outdoor exposures are more subtle effects on the heart and brain.
  • Sulfur dioxide (SO2): Sulfur dioxide is released from industrial facilities and vehicles burning fuel with high sulfur content. It is linked to respiratory problems (like asthma attacks and airway irritation) and can contribute to formation of PM.


Of course, we are all exposed to these air pollutants when we walk outside (and while driving in cars). But, during vigorous exercise, like biking up Seattle’s killer hills, we breathe in at 2-5x higher rates, and also more deeply, than at rest. So, I’m inhaling much more of all this bad stuff when I bike – in traffic – each day.

What are the consequences?

Research on the effects of air pollution exposure during exercise and active transportation (ie: walking and cycling) is beginning to emerge. According to one recent study, walking along busy streets reduced the short term cardiovascular benefits of the exercise compared to walking in a park. In studies of cyclists, researchers have found that biking in traffic is associated with various physiological changes, such as increases in certain inflammatory blood cells, alterations in heart rate variability (see here, here, and here) and other cardiovascular measures, and decreases in lung function. The implications of these changes are still unclear, however.  As usual, we need more research on the short- and long-term health effects of cycling in traffic.

Several studies (see selected examples from 2017, 2016, 2015, 2014, and 2010) have tried to examine the overall health trade-offs of cycling in cities. The general conclusion is that the long-term benefits of active transportation (ie: namely, physical activity) outweigh the potential risks from traffic accidents and air pollution. However, I think these assessments are limited in several ways:

  • Most focus on the impact on mortality only, rather than the other myriad of health effects from air pollution that could lead to decreased quality of life and then, indirectly, mortality.
  • Most only consider the effects of a single pollutant (usually PM2.5) rather than the effects of combined exposures to multiple traffic-related air pollutants (ie: what happens in the real world).
  • On a more technical level, they assume a linear dose-response (solid line, below), where the relationship between exposure and outcome is the same across all levels of exposure. However, some evidence suggests that this may not actually be the case for PM2.5. Instead, the curve might be supralinear (dashed line, below), where the risk increases more steeply at lower levels of exposure. In this scenario, there might be greater benefits to health per unit decrease in exposure at lower ends of the spectrum, which would alter the modeling calculations.
Linear (solid line) vs. supralinear cure (dashed line). Image from: Goodkind, Andrew L., et al. “A Spatial Model of Air Pollution: The Impact of the Concentration-Response Function.” Journal of the Association of Environmental and Resource Economists, vol. 1, no. 4, 2014, pp. 451–479. JSTOR, JSTOR, http://www.jstor.org/stable/10.1086/678985.
  • The alternative scenario (in epidemiology speak, the “counterfactual”) used in these cost-benefit assessments is decreased physical exercise. In other words, they are roughly comparing: [exercise + pollution] vs. [no exercise + pollution]. Because the benefits of physical activity are so enormous, this equation tips towards the [exercise + pollution] side. However, if I didn’t commute by bike, I would replace this exercise with alternative activities (with less exposure to air pollution, presumably). If my equation is instead [exercise + pollution] vs. [exercise + less pollution], it would likely tip in the other direction.

So, in summary, we don’t fully understand all of the physiological impacts of biking in traffic-related air pollution, and I think that the current cost-benefit analyses may actually underestimate the long-term costs to my health.

Hmmm…. Should I re-evaluate my decision?


            Last summer, I bought myself an air pollution mask to wear while biking. But, while I hate to admit it, I don’t use it every day. (It often causes my sunglasses to fog up!). I really should use it – assuming it is as effective as it claims?

Even though Seattle has the reputation of having fairly good air quality, the 2018 American Lung Association State of the Air Report indicates that there is still enormous room for improvement. (And, as I noted above, this city-level ranking, based on ambient air monitors, likely definitely underestimates my exposure while biking).

Everyone makes risk-related choices differently, based on their own calculations and priorities; risk perception and decision-making is complex and not entirely rational. But, in general, people are more likely to accept risks that they perceive as controllable, familiar and natural compared to those they perceive as imposed by others, uncontrollable, and unfamiliar (see image, below).

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Risk Space & Public Perception. Morgan, M. Granger. “Risk Analysis and Management.” Scientific American, vol. 269, no. 1, 1993, pp. 32–41. JSTOR, JSTOR, http://www.jstor.org/stable/24941545.

I’m still trying to understand the calculations that led me to my decision to expose myself to substantial pollution every day. Maybe it is related to the fact that I have control in this situation, since it is my choice to bike? Maybe it is because Seattle appears to have relatively clean air, compared to other places I’ve lived, like Atlanta and Bangkok, where the pollution is more directly visible?

Maybe… maybe… I just love biking too much, and this is where I draw my personal line. While it is definitely important to me to minimize harmful exposures and prioritize my health, I cannot and do not want to live in a complete bubble (though sometimes it seems to others that I already do). Life involves risk, and I’ve somehow decided that this is one I’m willing to take. Biking every day brings me too much happiness to give up (at least for now). Plus, cars are no safe haven; there’s plenty of dirty air inside from both internal and external sources.

Consolatory actions

While I take this risk, which is perhaps ironic given my PhD research on air pollution and dementia, there are some things I can do to mitigate my exposures. In addition to wearing my mask more consistently, I can check local air quality (like through this pollution app) and avoid riding on particularly bad days (like last summer, when Seattle was choked by horrific wildfire smoke). When bike paths are not available, I can do a better job of altering my route to prioritize low traffic roads, where I will be less exposed than on busier routes.

However, like for all pollutants, individuals only have limited abilities to control their own exposures. In the end, we need systemic, societal changes to make cities safer and healthier for people: stricter controls of vehicle emissions, increased utilization of electric cars and buses, improved public transportation, better bicycling infrastructure (eg: off-street bike paths), more greenspace, etc. The intersection of urban planning and public health definitely intrigues me (my next PhD? No, just kidding).

Ultimately, I hope that my own research can demonstrate the importance of strengthening air quality regulations and help motivate policies to reduce exposures across the population.

As you can see, it’s personal now.



Towards a CRISPR understanding of toxicology

[This post was originally published on Envirobites.org]

Scientists create yellow, three-eyed, wingless mosquitoes by using gene editing tool

Plant geneticists develop a new application of CRISPR to break yield barriers in crops

Gene-Editing: New technique stops progression of muscular dystrophy in mice

You don’t have to search long to find eye-catching headlines about CRISPR/Cas9, a technique that allows scientists to more easily edit specific parts of the genome. It’s particularly exciting for the same reason that it’s particularly concerning: it opens up a whole new world of possibilities for gene manipulation in humans, animals, and plants. The technology offers hope for real scientific, societal and medical advances, from engineering oranges to be resistant to citrus greening and controlling mosquito populations by making them infertile to removing genetic mutations that cause disease in humans (as demonstrated on a mutation that causes heart muscle to thicken dangerously).

However, since I’m a PhD student in Toxicology, I investigate the role of environmental exposures on human health. What happens in your body when you inhale polluted air or drink contaminated water, and how does this ultimately affect your risk for certain health effects?

So, while I had casually followed the news about CRISPR/Cas9 over the years, I had not seriously considered its application to my field until listening to the recent National Academies of Sciences workshop, The Promise of Genome Editing Tools of Advance Environmental Health Research. This workshop brought together experts from across the disciplines of environmental health to understand how these technologies can improve our understanding of the impacts of exposures.

It turns out, there’s a lot to be excited about. Here’s a snapshot of where they saw potential.

Identifying affected biological pathways

Much of the work of toxicologists is focused on understanding the specific biological mechanism, or “adverse outcome pathway,” that is affected by a pollutant when it enters the body. If the pollutant changes the normal signaling for a gene or protein, it could set off a domino effect of problems (like when bisphenol-A (BPA), an estrogen mimic, prompts inappropriate estrogen signaling in the body). CRISPR/Cas9 technology could allow researchers to alter different genes in different adverse outcome pathways of their model systems (either in vitro, cell-based, or in vivo, with whole animals) and then see how response to the exposure changes. If changing a specific gene leads to a change in biological response, it would provide insight to how the chemical exerts its effects.


For example, imagine that a pollutant activates a certain receptor by fitting into it perfectly, like a lock and key. Researchers could use CRISPR/Cas9 to alter the gene that determines the shape of the receptor so that the pollutant no longer fits – and thus could not activate the receptor and prompt associated changes in the cell. If, after this genetic modification, the pollutant does not trigger a response, we would know that it acts through the pathway that includes that specific receptor.


Incorporating and understanding human variability

Current toxicity testing approaches are usually based on genetically identical model systems, like mice, that do not represent the genetic diversity in humans. So, unsurprisingly, results from the lab do not reflect the full spectrum of effects that would be expected in the actual population. To remedy this issue, researchers could use CRISPR/Cas9 to introduce relevant human genetic variation into their models and then see how response to the exposure changes accordingly.

Information about which genetic variants are more vulnerable to specific exposures can be used to improve risk assessment. And, policy-makers could set regulations to protect even those individuals with highly sensitive genetic variants from harmful health effects. (This situation has come up with occupational beryllium exposure limits, since we know about a specific mutation that makes people much more likely to get chronic beryllium disease)

Elucidating effects of epigenetic changes

In recent years, toxicologists have become increasingly concerned about the potential for pollutants to make subtle changes in how genes are expressed without actually changing the genes themselves. This field of research is called “epigenetics” and is particularly relevant to the effects of early-life exposures. However, in many cases, we don’t fully understand the long-term implications of these changes. CRISPR/Cas9 could allow researchers to artificially induce epigenetic alterations of interest in the lab and then carefully track the consequences over time.

A slow start, but lots of potential

The applications described above, among others, clearly indicate that CRISPR/Cas9 gene editing technologies could hold great promise for advancing our understanding of the effects of environmental exposures across the population. While there are some studies that have already utilized this approach (for example, a 2016 study about the effects of the antimicrobial triclosan on human liver cells), its use across toxicology have been limited so far. Hopefully, the discussions and excitement following this workshop can prompt further widespread adoption.

Yet, tricky ethical questions also exist for CRISPR/Cas9’s potential environmental health applications. If we have the ability to eliminate a gene that makes someone susceptible to an environmental exposure, should we act to remove it from future generations? Once we start, where do we draw the line? Undoubtedly, these issues will be debated over the coming years. Nevertheless, when used for basic and translational toxicological research in the short term, CRISPR/Cas9 should be seen as an important tool to help us address the huge gaps in our understanding about the chemicals that we are exposed to on a daily basis.

The Minamata Convention: Can We Make Mercury History?

This post was originally published on Envirobites.org

Last month, the Lancet Commission on Pollution and Health released a striking report estimating that pollution caused 9 million deaths worldwide in 2015 – 3 times more deaths than caused by AIDS, tuberculosis, and malaria combined. Air pollution was responsible for the vast majority of these deaths, but water and chemical pollution also contributed substantial burdens.

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Global estimated deaths by major risk factor and cause, 2015; The Lancet Commission on Pollution and Health (2017)

One of the chemical pollutants highlighted by the Lancet Commission is mercury, a known neurotoxicant. The report discusses the dangers of mercury when used specifically in small-scale gold mining in low-income countries, yet populations across the world can also be exposed through fish consumption or consumer products, among other sources.

Well before the new Lancet report was released, the international community had recognized the dangers of mercury and had been working to develop policies to minimize exposure to this pollutant. In fact, on August 16, 2017, after sixteen years of work and negotiations, the Minamata Convention on Mercury entered into force.

This global treaty aims to protect human health and the environment from the toxic effects of mercury through restriction of mercury products and processes. It is the first new international convention in almost 10 years focused specifically on health and the environment. (Other previous treaties include the Basel Convention for hazardous waste, the Rotterdam Convention for pesticides and industrial chemicals, and the Stockholm Convention for highly persistent global pollutants).

The convention is named after the decades-long environmental health tragedy in Minamata, Japan. Residents and animals in this area developed severe neurological syndromes after eating seafood that had been highly contaminated with mercury from industrial pollution.


Why Mercury?

Mercury is a naturally occurring metal, and certain chemical forms (specifically, methylmercury and metallic mercury vapor) are highly toxic. According to the World Health Organization (WHO), mercury is one of the top ten chemicals of public health concern. The nervous system – and in particular, the developing brain – is highly vulnerable to mercury. Exposure can result in permanent neurological damage. (Remember the Mad Hatter from Alice In Wonderland?) Other organ systems, such as the lungs, kidneys, and immune systems, may also be affected. The United Nations Environment Programme (UNEP) has stated that there is no safe level of mercury exposure.

How Are We Exposed Today?

Mercury is emitted through both natural and industrial processes. Examples of natural processes that release mercury include rock weathering, forest fires, and volcanic eruptions.

However, this global treaty targets mercury from industrial and human processes. These include coal burning, waste incineration, consumer products, and small-scale gold mining. Because mercury emissions travel through air and water without regard to political borders, only an international treaty could truly be effective in addressing this pollutant.

Human exposure to mercury occurs through several possible routes, including consumption of contaminated fish, inhalation of mercury vapors from the air, or even from the use of mercury in dental fillings.

Convention Commitments

The 84 countries that have already ratified the treaty (and the many other countries anticipated to fully join in the near future) will be required to take the following steps by 2020:

  • Phase-out or reduce mercury from products such as batteries, certain light bulbs, cosmetics, and pesticides
  • Control mercury air emissions from coal-fired power plants, waste incineration, and related industrial processes
  • Reduce or eliminate the use of mercury in small-scale gold mining
  • Reduce or eliminate the use of mercury in chemical manufacturing processes

The convention also provides guidance for safe storage of mercury, waste disposal, and contaminated sites.

Threats to U.S. Progress and Compliance

The U.S. Environmental Protection Agency (EPA) aims to address mercury pollution through numerous programs and regulations. But now, some of those efforts are under attack or subject to delay – threatening our prospects for reducing mercury exposure and complying with the convention.

For example, the Mercury and Air Toxics Standards (MATS) rule, passed under the Obama administration, limits the amount of mercury released from coal-fired power plants. The D.C. Circuit Court of Appeals had planned to review the cost-benefit analysis for this regulation but recently decided to delay the case instead. The Trump administration may actually decide to repeal the regulation altogether rather than defend the rule in court.

The administration’s vocal support for revitalizing the coal industry and the proposed repeal of the Clean Power Plan would further reverse progress that we have made in reducing mercury emissions. Recent shifts away from coal in this country have led to decreased mercury emissions and declining mercury contamination in tuna – historically, a significant exposure route for the population.

The current administration may also review a 2015 rule that set standards for disposal of coal ash, a byproduct of coal combustion. Improper disposal of coal ash in landfills can result in release of mercury, among other toxic chemicals.

These steps are hugely disappointing. Tackling this global pollution problem requires global action, and therefore the U.S. must continue to take strong steps to reduce mercury use and releases.

During these tumultuous times in particular, the ratification of this global treaty is an important victory for human health and the environment – and a reminder that we can still come together to make progress towards global health and sustainability. But, the realization of these goals requires political will and cooperation from all parties, and only time will tell if they can follow through on these targets.

Getting the lead out of our skies


This article was written in collaboration with Dr. Steven Gilbert and originally posted in Environmental Health News. 

The excitement of watching sea planes take off and land from Lake Union, Seattle belies their hidden danger: leaded gasoline.

While lead was removed from automobile and other transportation gasoline more than two decades ago, it’s still used in aviation gasoline, or “avgas,” to prevent knocking in over 167,000 piston-engine aircrafts around the country. According to the U.S. Environmental Protection Agency (EPA), avgas is the single largest source of lead emissions in the country. Avgas released during flight has the potential to disperse lead widely in the environment, contaminating water bodies, soil near the air fields, and farms.

Lead is a well-known neurotoxicant, and children are particularly vulnerable to its devastating and irreversible impacts. The U.S. Centers for Disease Control and Prevention (CDC) says there is no safe level of blood lead in children. The EPA estimates that approximately 16 million people, including 3 million children, live or attend school within one mile of airports using leaded avgas. Researchers have found that children living close to airports with planes using avgas have higher blood lead levels than children living farther from those airports. Workers who service or refuel the aircrafts may also be exposed.

There are alternatives to avgas, and it is estimated that about 80 percent of the current piston fleet across the country could operate safely on these fuels without retrofitting. Europe already implemented policies to promote the use of unleaded alternatives. Yet, without regulatory updates in the U.S., there is little incentive for industries to change or for airports to provide alternatives.

What is the roadblock to these policy changes? To regulate lead under the Clean Air Act, the EPA must make an “endangerment finding” that documents the hazard of lead released from aviation gasoline. Despite petitions from multiple advocacy groups, however, the EPA has declined to make this determination and has insisted on the need for more data.

In the meantime, the Federal Aviation Administration (FAA) formed the Piston Aviation Fuel Initiative, a collaboration between FAA and industry to spur the development of additional avgas substitutes by 2018. Whether this effort delivers on its promise remains to be seen. And even if a replacement is “certified,” the FAA estimated that a complete phase out of leaded fuel could take 11 years.

To spur changes in the absence of efficient federal progress, action at the state and local levels is needed. For example, requiring airports to provide unleaded gasoline or adopting taxes on leaded gasoline to promote use of alternatives. Revenue generated could be used for soil lead testing or remediation at homes, schools, and parks near airports using leaded gasoline. We urge local policymakers to consider such initiatives in the coming legislative sessions.

recent report from the Pew Charitable Trusts calculated that removing lead from aviation fuel would prevent a 5.7 percent increase in child blood lead across the country and result in $262 million in gross future benefits.

Given the known hazards of lead exposure and the existence of alternative aviation fuels, we have an ethical responsibility to eliminate the use of avgas and protect our population from such a significant source of lead pollution.

High Impact Report on Low-Dose Toxicity

A condensed version of this post was originally published on The Conversation with the title “Can low doses of chemicals affect your health? A new report weighs the evidence.

Toxicology’s founding father, Paracelsus (1493-1541), is famous for his paraphrased proclamation: “the dose makes the poison.” This phrase represents a pillar of traditional toxicology: Essentially, chemicals are harmful only at high enough doses.

But, increasing evidence suggests that even low levels of “endocrine disrupting chemicals (EDCs)” can interfere with hormonal signals in the body in potentially harmful ways.

Standard toxicity tests don’t always detect the effects that chemicals can have at lower levels. There are many reasons for this shortcoming, including a focus on high dose animal testing as well as failure to include endpoints relevant to low dose disruption. And, even when the data do suggest such effects, scientists and policymakers may not act upon this information in a timely manner.

Recognizing these challenges, the U.S. Environmental Protection Agency (EPA) asked the National Academy of Sciences convene a committee to study the issue in detail. How can we better identify whether chemicals have effects at low doses? And how can we act on this information to protect public health?

After several years of work, the committee’s report was released in July. This landmark report provides the EPA with a strategy to identify and systematically analyze data about low-dose health effects, as well as two case study examples. It is an evidence-based call to action, and scientists and policymakers should take notice.

Delving into definitions

Before discussing the report, let’s review some definitions…

We know that animal experiments usually use high doses, but in comparison, what is a “low dose?”

This issue was a matter of considerable debate, but ultimately, the committee decided to proceed with a fairly general definition of low dose as “external or internal exposure that falls with the range estimated to occur in humans.” Therefore, any dose that we would encounter in our daily lives could be included, as well as doses that would be experienced in the workplace.

The committee also clarified the meaning of “adverse effects.” When a chemical produces a visible malformation, it is easy to conclude that it is adverse. But, when a chemical causes a small change in hormone levels, it is more difficult to conclusively state that the change is adverse. Are all hormone changes adverse? If not, what is the threshold of change that should be considered adverse?

In this context, an adverse effect was defined as “a biological change in an organism that results in an impairment of functional capacity, a decrease in the capacity to compensate for stress, or an increase in susceptibility to other influences.”

A strategy to identify low dose toxicity

With these semantics settled, the committee developed a 3-part strategy to help with timely identification, analysis, and action on low-dose toxicity information:

(1) Surveillance: Active monitoring of varied data sources and solicitation of stakeholder input can provide information on low dose effects of specific chemicals, especially since EPA’s standard regulatory testing framework may not always identify such effects. Human exposure and biomonitoring data should also be collected to help define relevant exposure levels of concern across the population.

(2) Investigation & Analysis: Systematic review and related evidence integration methods can be used to conduct targeted analysis of the human, animal, and in vitro studies identified in the surveillance step. Each of these approaches has different strengths and weaknesses, so examining the evidence together offers insight that a single approach could not provide.

(3) Actions: New evidence can be incorporated into risk assessments or utilized to improve toxicity testing. For example, protocols could be updated to include newly identified outcomes relevant to endocrine disruption.

Leading by example: systematic review case studies

To put their strategy into practice, the committee conducted two systematic reviews of low dose EDC effects.

The first case study looked at phthalates, chemicals that increase the flexibility of plastic products such as shower curtains and food wrapping.

The committee found that diethylhexyl phthalate and other selected phthalates are associated with changes in male reproductive and hormonal health. Overall, the data were strong enough to classify diethylhexyl phthalate as a “presumed reproductive hazard” in humans.

The second case study focused on polybrominated diphenyl ethers (PBDEs), flame retardants used for over 30 years. Though they are now being phased out, these chemicals remain a concern for humans. They are still present in older products and can persist in the environment for many years.

Based on data showing the impact of these chemicals on learning and IQ, the panel concluded that developmental exposure is “presumed to pose a hazard to intelligence in humans.”

Questions and challenges for the future

During its review, the committee encountered a variety of barriers that could impede similar investigations into specific chemicals.

First, when reviewing evidence, it’s important to assess any systematic errors – also known as biases – that might have led to incorrect results. These errors can arise from study design flaws, such as failure to properly blind the researchers during analysis.

Some journals have strict guidelines for reporting details related to bias, but many do not. Better adherence to reporting guidelines would improve scientists’ ability to assess the quality of evidence.

Second, the committee noted a discrepancy between the concept of doses used in human and animal studies, which made it difficult to compare data from different sources.

For example, most toxicologists simply report the dose that they delivered to animals. But some of that administered dose might not actually be absorbed. The actual internal dose of chemical circulating in the body and causing harm may differ from the amount that was administered. By contrast, epidemiologists usually think about dose as the level of chemical they detect in the body, but they may not know how much of the chemical an individual was actually exposed to.

Biological modeling techniques can help scientists draw the connection between administered and internal doses and more closely compare results from animal and human studies.

Finally, many toxicology studies focus on only a single chemical. This is a valuable way to identify how one chemical affects the body. However, given that we are all exposed to chemical mixtures, these procedures may be of limited use in the real world.

The committee suggested that toxicologists incorporate real-world mixtures into their studies, to provide more relevant information about the risk to human health.

Leveraging toxicity testing for answers about low dose effects

This report demonstrates one of the challenges facing the field of toxicology and environmental health: How well can existing and emerging laboratory techniques predict adverse outcomes in humans? (If you’ve read some of my previous posts, you know that this issue is of particular interest to me.)

Traditional animal experiments usually use high doses, which don’t necessarily reflect the real world. These studies can be an important first step in identifying health hazards, but they cannot accurately predict how or at what levels the chemicals affect humans. The committee noted that more relevant doses and better modeling could help mitigate this problem.

Emerging high-throughput testing techniques use cell-based methods to detect how a chemical changes specific molecular or cellular activities. These newer methods are increasingly used in toxicology testing. They have the potential to quickly identify harmful chemicals, but have yet to be fully accepted or validated by the scientific community.

For these two case studies, the committee noted that high-throughput tests were not particularly helpful in drawing conclusions about health effects. Many of these studies are narrowly focused – looking at, for example, just a single signaling pathway, without indicating a chemical’s overall influence on an organism. Nevertheless, these methods could be used to prioritize chemicals for further in-depth testing, since activity in one pathway may predict a chemical’s capacity to cause harm.

Putting the report into action

Despite the imperfections of our testing methods, there’s already ample evidence about low-dose effects from many chemicals (including the two cases studies from the committee). The EPA should implement this new strategy to efficiently identify and act on problematic endocrine-disrupting chemicals. Only through such strong, science-based efforts can we prevent adverse effects from chemical exposures – and allow everyone to live the healthy lives that they deserve.

Lessons from A Toxicology Detective Story: Use Caution with Controls

This article was originally posted on the Massive Science Consortium website, with the title “An Unexplained Result Shows Why Studying the Effects of Chemicals is so Tricky

Toxicologists are no strangers to mysteries. In fact, understanding unexpected results caused by unintentional chemical contamination in the laboratory has a storied history in the environmental health field.

In the late 1980’s, researchers at Tufts University accidentally discovered that certain plastic components caused their estrogen-responsive cells to grow uncontrollably. Their findings spurred extensive work on endocrine disrupting chemicals (EDCs), which can interfere with normal hormonal activity in the body. Bisphenol-A (BPA), found in many plastic products, is a common example of an EDC.

Following in this tradition, researchers at the University of Massachusetts (UMass) Amherst recently conducted some important toxicology detective work after they noticed that mammary glands of adult male mice raised in a commercial laboratory (that supplies mice for scientists) were larger and more developed than the mammary glands of the same type of mice raised in their own laboratory.

Scientists use rodent mammary glands as models of human breasts, which allow them to better understand growth and development as well as risk factors and treatments for diseases like breast cancer. Toxicologists have paid particular attention to how mammary glands change after exposure to EDCs, since the chemicals can interfere with hormonal activity and mammary glands are especially responsive to hormonal signals.

So, when the UMass Amherst researchers noticed a difference in the mammary glands between the two groups of theoretically similar mice, it set off some alarm bells. Could an unidentified EDC exposure in the commercial lab be the culprit? And if so, could this potential EDC exposure impact the ability of scientists and policy-makers to draw conclusions from toxicological experiments?

Comparing Gland Growth

To find out, the researchers carefully compared the mammary glands and blood hormones between the two groups of mice. One group was ordered directly from a commercial supplier. The other group was ordered from the same commercial supplier and then bred for two generations to produce offspring that were raised in their own lab under controlled conditions to minimize exposure to EDCs.

The findings supported their preliminary observations: the mammary glands in the male mice raised in the commercial lab were larger and more developed than those of male mice raised in their own lab. The researchers noted that the commercially-raised mouse mammary glands actually mirrored those of mice from different experiments that had been intentionally exposed to BPA during early development.

By contrast, female mice had smaller and less developed mammary glands at puberty. While this difference in response may at first seem counter-intuitive, endocrine disruptors are complicated. Because they interfere with hormones, which are gender-specific, EDCs have the potential to affect males and females in different ways.

Contemplating the Culprit

Although the researchers found differences between the two sets of mice, they didn’t immediately know why. A simple explanation would have been that different amounts of circulating hormones at the time they examined the mice might have influenced their body composition. Yet, they detected no significant differences in estrogen, the primary hormone that drives mammary gland development, between the two groups.

It is also unlikely that genetic differences could have contributed to the distinct mammary gland growth, given that the non-commercially raised animals were actually only two generations removed from the original commercial strain. Such drastic genetic changes do not usually occur over such short cycles.

Therefore, the researchers hypothesized that the difference was more likely due to the effects of EDC exposures during their early life in the commercial laboratory. (However, they were not able to confirm this theory through specific tests.) Exposures to EDCs, among other chemicals, during sensitive windows of development in early life have the potential to cause long-lasting changes, including in the mammary gland.

Considering the Consequences

These findings, which suggest that animals raised in commercial labs may be exposed to EDCs, could impact how we interpret toxicological studies.

One main reason is what researchers call the “two-hit” model, which suggests that an exposure in early life makes an individual more sensitive to the effects of a second exposure later in life. In this context, early exposures to EDCs might prime laboratory animals for more pronounced responses when treated with a test chemical in an experiment later in life. In other words, some laboratory experiments may be erroneously linking the test chemical to an outcome that is actually due to a combination of the test chemical and being exposed to EDCs earlier in life.

This study only evaluated animals from one commercial lab, and conditions may differ in other labs. The possibility that animals could be subject to different unintentional exposures may affect our ability to compare studies and pool data from diverse labs to make science-based policies. This issue may also partially explain why research and policy on EDCs has been so highly controversial, with distinct labs generating very different results about the same chemicals.

These differences also have implications for a controversial practice in the field of toxicology: the use of “historical controls.” Sometimes, scientists compare the changes in treated animals from one study to a database of untreated animals from a collection of previous studies. This practice can provide researchers with a better sense of whether the treated animals they are studying are truly different from normal. Yet, this study suggests that control animals raised in some laboratories may be exposed to EDCs, and therefore it would not be appropriate to compare them to treated animals raised in different environments. The presence of too many differing variables would make it difficult to make an accurate comparison.

Taken together, these findings suggest that both scientists and the public should be cautious when interpreting certain studies. While the researchers did not conclusively confirm the linkage to early life EDC exposure, this highly likely explanation illustrates that, at least in some cases, there may be factors behind the scenes that could be influencing the results of toxicology experiments.

How should the scientific community address the implications of this study? While researchers could try to mitigate the impact of these exposures on their subsequent toxicological experiments by screening animals prior to beginning their work, a better approach would be to improve handling of animals in commercial facilities through strict standards. Exposures to EDCs, among other chemicals, should be minimized. If such exposures continue, it may be hard to trust the results of these toxicological studies, which could impede the development of appropriate, evidence-based environmental health policies and protections for the population.

Developing Data on the “Developmental Origins of Health and Disease”

The Developmental Origins of Health and Disease (DOHaD) paradigm suggests that there are specific windows of development that are highly susceptible to disruption from environmental exposures and that these early life exposures can lead to adverse outcomes later in life. The British epidemiologist David Barker is credited with pioneering this field in the 1980’s, with his research on the link between prenatal nutrition and adult coronary heart disease.

Last month, researchers published a review of the environmental epidemiological literature on DOHaD in a special “Developmental Origins of Disease” issue of Reproductive Toxicology. This review paper, which summarizes 425 articles published between 1988-2014, provides a helpful overview of the state of the science and identifies key areas for future study.

Chemical Culprits

Across these hundreds of publications, which chemicals emerged as the most commonly examined culprits?

Figure 3 from their review, below, displays this information. Polychlorinated biphenyls (PCBs), organochlorine pesticides (such as DDT), metals (such as mercury and lead), and air pollutants (including polycyclic aromatic hydrocarbons and particulate matter) were the most frequently studied across the literature.

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Chemical exposures examined in DOHaD epidemiology studies (1988-2014)

Just because these chemicals are the most highly studied does not necessarily mean that they are the most harmful, however. This research could be subject to observational bias from the “streetlight effect,” and investigators may be overlooking other chemicals that also disrupt early life processes.

Concerning Outcomes

The vast majority of DOHaD work to date has examined neurobehavioral and neurodevelopmental outcomes, such as changes in IQ and executive function. The authors hypothesize that one of the reasons that these outcomes have received the most attention is that there are multiple relevant assessments that can be performed in early life. By contrast, outcomes with longer latency periods or fewer clear assessment methods may pose challenges for researchers.

Less frequently studied DOHaD outcomes included cancer as well as adverse impacts on the respiratory, reproductive, immune, and metabolic systems. [Note: companion publications in this journal issue provide reviews of the developmental origins of reproductive disorders and metabolic disorders.] Very few studies have focused on the cardiovascular system, thyroid regulation, and gastrointestinal system, among others.

Key Areas for Future Research

Additional Exposure Periods

Most DOHaD studies have focused on environmental exposures that occur in utero. Research on this vulnerable period is extremely important, yet exposures during other periods of life can be problematic as well.

For example, emerging evidence suggests that even preconception exposures in the mother and father – particularly to persistent pollutants or to chemicals and experiences that alter epigenetic marks– may impact child health outcomes.

Additionally, because of the substantial brain changes that take place between the last trimester of pregnancy and two years of age, the “first 1000 days of life” movement has highlighted the importance of optimal nutrition during the prenatal and postnatal period. If the young brain can be affected by nutrition, it can also be altered by environmental pollutants – and thus studies that capture this timeframe are crucial.

Additional Outcomes

As mentioned above, much of the research in the field of DOHaD has focused on the neurodevelopmental consequences of early life exposures. In the coming years, researchers should also expand their work to other organ systems and processes, such as the cardiovascular, immune and gastrointestinal systems.

Moreover, while challenging, researchers should attempt to address the possibility that exposures may impact multiple biological processes through related pathways. For example, given the central role of hormonal signaling in the body, it is highly plausible that disruption of these processes could lead to adverse effects on the reproductive system, neurological system, and metabolic system, among others.

Additional Chemical Exposures

Persistent pollutants and metals have dominated the DOHaD field, perhaps because exposure information is more easily obtainable. More recent efforts have utilized advanced methods to examine additional chemicals, and future research should continue to assess a broadened group of exposures. Even chemicals that are non-persistent (short-lived) in the body may be problematic, particularly if their ubiquitous presence in our society ensures near constant exposures.

In addition, given that 1) combinations of chemicals may act differently than single chemicals, and 2) we are all exposed to numerous chemicals at the same time, it will be important to examine the effects of early life exposures to complex mixtures.

Later Life Assessment of Adverse Health Outcomes

The authors note that of the 425 publications reviewed, only 43 examined adverse outcomes in individuals over the age of 18. Thus, the environmental health field lacks the long-term follow-up that would provide evidence comparable to Barker’s early work on adult cardiovascular outcomes.

Such studies are challenging and costly; yet, they are crucial for elucidating the implications of exposures over the life course. Continued funding of longitudinal cohorts over extended periods of time will ensure that these data are generated.

Systematic Review

The purpose of this work was not to draw conclusions about the strength of the evidence of links between certain chemicals and outcomes. The authors did, however, suggest that the most commonly studied chemical/outcome combinations may be ready for systematic reviews, including:

  • Pesticides and cancer
  • Air pollution and respiratory effects
  • Organochlorine pesticides and respiratory effects
  • Polyfluoroalkyl substances (PFAS) and immune outcomes

My Take on the Bottom Line: Science & Ethics

This summary of DOHaD literature from an environmental health perspective can direct researchers to focus their future work on key areas that need further attention, as noted above. Continued epidemiological research, in conjunction with toxicological studies that can elucidate mechanistic pathways, will help advance our understanding of the implications of early life exposures.

Yet for many chemicals, such as lead, there is already ample evidence of harm from early life exposures. In this situation – and as data continue to be generated for other chemicals in the coming years – the essential next step is to take action to protect children during vulnerable periods of development.

As described in “Science and Social Responsibility in Public health,” “…environmental health researchers have a joint responsibility to acquire scientific knowledge that matters to public health and to apply the knowledge gained in public health practice.”

This responsibility not only to conduct strong research but also to ensure implementation of science-based policies is our ethical duty – and the health of the next generation depends on it.

How the U.S. is taking the lead to prevent lead poisoning

This piece was first published on the Interdisciplinary Association for Population Health Science (IAPHS) blog. You can see the original posting here.  

The crisis in Flint, Michigan, returned our attention to a problem that we would have preferred to believe was behind us: lead poisoning. This incident highlighted the dangers of lead-lined water pipes; but, unfortunately, there are numerous other sources of lead exposure throughout the United States. I’ve written previously about risks from contact with contaminated soil or through the workplace. Lead-based paint, outdoor air, and manufactured products also pose risks. Because of these diverse sources, eliminating lead poisoning is challenging and requires coordination across multiple programs and policies.

Understanding this complex need—and perhaps sensing the increased public concern regarding lead in the United States—the President’s Task Force on Environmental Health Risks and Safety Risks to Children recently released a report entitled “Key Federal Programs to Reduce Childhood Lead Exposures and Eliminate Associated Health Impacts.” This report describes the dozens of federal regulations and programs that have been established to address lead exposures in children. It also marks progress towards the development of an enhanced lead strategy that will address existing policy gaps.

The report is worth a read; you may be surprised by the number of existing policies and efforts aimed at mitigating lead exposure. There are almost 60 programs and activities administered by nine agencies and close to 30 specific regulations that address lead exposures, directly or indirectly, in children. Some of these programs and regulations include:

Together, all of these efforts have contributed to the impressive decline in blood lead levels in this country, as illustrated in the figure below.


Despite this progress, significant challenges remain. Exposure to lead occurs disproportionately in minority and low-income families, and future work should focus on mitigating this disparity. As prescribed by Executive Order 12898, environmental justice must be a core component of agency activities.

To meet these environmental justice goals and continue to reduce lead exposure across the country, continued funding of these programs is essential. This report demonstrates that eliminating lead hazards requires parallel efforts and synergies between nine different government agencies—from the EPA to HUD, and the Department of Education to the Department of Transportation. Therefore, in the coming years, we must ensure that these agencies continue to receive the resources to be able to adequately address this critical public health issue. Call or write your representatives to voice your thoughts on the importance of protecting funding for public health agencies.

We have come so far in addressing lead in this country; let’s make sure we can finish the job completely.

A Decade into the “Vision,” Environmental Health gets a Progress Report

This year represents an important 10-year milestone for science and society.

No, I’m not referring to the 10th anniversary of the Apple iPhone, though that has undoubtedly changed all of our lives. Rather, 2017 marks ten years since the National Academy of Sciences (NAS) released its seminal report, Toxicity Testing in the 21st Century: A Vision and a Strategy.

In that report, the NAS laid out a vision for a new approach to toxicology that incorporates emerging cell-based testing techniques, rather than costly and time-intensive whole animal models, and utilizes early biological pathway perturbations as indications of adverse events, rather than relying on evaluations of end disease states. Tox21 and ToxCast, two federal programs focused on using alternative assays to predict adverse effects in humans, were initiated as first steps in this strategy. In the years since its release, the report has profoundly shaped the direction of environmental health sciences, particularly toxicology. (An analogous exposure sciences report, Exposure Science in the 21st Century: A Vision and a Strategy, was published in 2012.)

Now, one decade later, the NAS has reviewed progress on these efforts in its recently released report, Using 21st Century Science in Risk-Based Evaluations.

How are we doing, and what are next steps?

Overall, the committee supports efforts to use data from new tools, such as biological pathway evaluations, in risk assessment and decision-making. (Of course, limitations should be clearly communicated, and tools should be validated for their specific purposes.) Several case studies are described as examples of situations where emerging tools can be useful, such as quickly prioritizing chemicals of concern or evaluating risks from chemical mixtures at a contaminated site.

This report also documents advancements and challenges for each of the three interconnected fields of environmental health sciences: toxicology, exposure science, and epidemiology. I’ve summarized some of these key points in the chart below, and additional (digestible) information is available in the NAS report summary.



Recent Advancements

Key Challenges


  • Incorporate metabolic capacity in in vitro assays
  • Understand applicability & limitations of in vitro assays
  • Improve biological coverage
  • Address human variability & diversity in response

Exposure Science

  • Coordination of exposure science data (ex: databases)
  • Integration of exposure data of multiple chemicals obtained through varied methods


  • Improved data management & data sharing
  • Improved methods for estimation of exposures

I won’t go into detail on all of these points, but I do want to highlight some of the key challenges that the field of toxicology will need to continue to address in the coming years, such as:

  • Improving metabolic capacity of in vitro assays: Cell-based assays hold promise for predicting biological responses of whole animals, but it is critical to remember that these new tools rarely reflect human metabolic capacity. For example, if a chemical is activated or detoxified by an enzyme in our bodies, reductionist assays would not adequately reflect these changes – and thus their prediction would not be fully relevant to human health. We need continued work to incorporate metabolic capacity into such assays.
  • Improving biological coverage: An analogy that I’ve often heard in relation to the limitations of these new tools is that they are only “looking under the biological lamp post.” Essentially, we can only detect effects that the assays are designed to evaluate. So, we need further development of assays that capture the wide array of possible adverse outcomes. And we cannot assume that there is no hazard for endpoints that have not been evaluated.

New models of disease causation

Not only is the environmental health science ‘toolkit’ changing but also our understanding of disease causation. As discussed in the report, 21st century risk assessment must acknowledge that disease is “multifactorial” (multiple different exposures can contribute to a single disease) and “nonspecific” (a single exposure can lead to multiple different adverse outcomes). This advanced understanding of causality will pose challenges for interpreting data and making decisions about risk, and we will need to incorporate new practices and methods to address these complexities.

For example, we can no longer just investigate whether a certain exposure triggering a certain pathway causes disease in isolation, but also whether it may increase risk of disease when combined with other potential exposures. It gets even more complicated when we consider the fact that individuals may respond to the same exposures in different ways, based on their genetics or pre-existing medical conditions.

The Academy suggests borrowing a tool from epidemiology to aid in these efforts. The sufficient-component-cause model provides a framework for thinking about a collection of events or exposures that, together, could lead to an outcome.


Sufficient-component-cause model. Three disease mechanisms (I, II, III), each with different component causes. Image from NAS Report, Using 21st Century Science to Improve Risk Related Evaluations


Briefly, each disease has multiple component causes that fit together to complete the causal pie. These components may be necessary (present in every disease pie) or sufficient (able to cause disease alone), and different combinations of component causes can produce the same disease. Using this model may promote a transition away from a focus on finding a single pathway of disease to a broadened evaluation of causation that better incorporates the complexities of reality. (I’ve blogged previously about the pitfalls of a tunnel-vision, single pathway approach in relation to cancer causation.)

Integration of information, and the importance of interdisciplinary training

As the fields of toxicology, exposure science, and epidemiology continue to contribute data towards this updated causal framework, a related challenge will be the integration of these diverse data streams for risk assessment and decision-making. How should we weigh different types of data in drawing conclusions about causation and risk? For example, what if the in vitro toxicology studies provide results that are different than the epidemiology studies?

The committee notes that we will need to rely on “expert judgment” in this process, at least in the short term until standardized methods are developed. And they discuss the need for more interaction between individuals from different disciplines, so that knowledge can be shared and applied towards making these difficult decisions.

One issue that was not discussed, however, is the importance of training the next generation of scientists to address these complex challenges. Given the inevitable need to integrate multiple sources of data, I believe it is critical that the students in these fields (like me!) receive crosscutting training as well as early practice with examples of these multi-faceted assessments. Some programs offer more opportunities in this area than others, but this should be a priority for all departments in the coming years. Otherwise, how can we be prepared to step up to the challenges of 21st century environmental health sciences?

Looking forward

Speaking of challenges, we certainly have our next decade of work cut out for us. It is amazing to think about how much progress we have made over the last ten years to develop new technologies, particularly in toxicology and exposure sciences. Now we must: refine and enhance these methods so they provide more accurate information about hazard and exposure; address the complexities of multifactorial disease causation and inter-individual susceptibility; and work across disciplines to make decisions that are better protective of public health and the environment.

Election Reflections: Women in Science

It goes without saying that the outcome of the recent U.S. presidential election was a shock. I will avoid a long-winded discussion of the associated consequences and just acknowledge that we came painfully close to electing the first female president of the country.

In the weeks leading up to the election, I had felt a contagious energy among my female friends – a great hope that we could have a role model in the highest office of the country.

I don’t have presidential aspirations, however. So, upon further reflection, I realized that much more important to my own growth and ambitions has been the presence of female role models in my field of environmental health sciences. Unlike for my mother, who had few women role models in her early days in public health, I feel fortunate to have numerous, highly successful female scientists to look up to. Because of these inspiring women (including my mother!), I have never doubted the possibility that I can achieve my professional goals.

Perhaps my earliest model of a female scientist and change-maker was Rachel Carson, whose pioneering environmental work I learned about during elementary school. While I probably did not understand the full scope of her impact at that young age, I was evidently motivated enough by her story to dress up as Carson during career day.

Years later, during college, I read Our Stolen Future, an eye-opening book that Al Gore has referred to as a sequel to Carson’s Silent Spring. Who better to learn from about endocrine disruption than the late Theo Colborn, co-author of this book and a visionary leader who is often called the “mother of endocrine disruption?” Reading this work provided immediate clarity and direction to my undergraduate studies. After college, as I began to further immerse myself in the world of environmental health at Environmental Defense Fund, I became increasingly inspired by the work of Colborn and the many other contemporary female scientists who are shaping the field.

Women are leading some of today’s most important science policy and advocacy efforts, and I have had the privilege to interact with several of these amazing individuals. I greatly admire Sarah Vogel (Environmental Defense Fund) Ruthann Rudel (Silent Spring Institute), Jennifer Sass (Natural Resources Defense Council), and Molly Rauch (Moms Clean Air Force), among others, for their efforts to promote the translation of strong science into health protective policies.

All science is a team effort, of course, but female scientists across the country have led many of the studies that these and other organizations draw upon in their public health work.

  • Ruthann and her team at Silent Spring Institute have conducted important and innovative work related to endocrine-active chemicals and breast cancer risk.
  • North Carolina has the preeminent Heather Duo: Heather Stapleton at Duke University, who researches routes of exposure to flame retardants, and Heather Patisaul, at North Carolina State University, who is examining the effects of chemical exposures on the neuroendocrine (brain & hormonal) system.
  • Dana Dolinoy, at the University of Michigan, is a leading expert in epigenetics (changes in how a gene is expressed rather than a change in the genetic code itself).
  • Tracey Woodruff and her team at the UCSF Program on Reproductive Health and the Environment have done extensive work in diverse areas, ranging from advancing methods for systematic review to assessing prenatal chemical exposures.
  • Frederica Perera, at Columbia University, pioneered the field of molecular epidemiology (using specific biomarkers to understand the link between environmental exposures and disease).
  • Irva Hertz-Picciotto, at the University of California, Davis is a top environmental epidemiologist with a particular focus on the environmental factors that contribute to autism. (She recently co-founded Project TEDNR, a collaborative initiative involving scientists, policy-makers, and advocates that aims to reduce exposures to neurotoxicants.)

I could go on and on (and on), but you get the idea. Women are making waves in environmental health sciences through their robust, cutting-edge research.

Government is no exception. I am excited by the work of early career scientists, such as Tamara Tal, who is conducting innovative toxicological studies in zebrafish at the Environmental Protection Agency (EPA), and Kelly Ferguson, an environmental epidemiologist at the National Institute of Environmental Health Sciences (NIEHS) who studies how chemical exposures during pregnancy impact child health and development. And, I am inspired by the many women who are leaders within these agencies, such as Elaine Cohen-Hubal (Integrated Systems Toxicology Division, EPA), Kristina Thayer (Office of Health Assessment and Translation, NIEHS) Dale Sandler (Chronic Disease Epidemiology, NIEHS), and Nicole Kleinstreuer (National Toxicology Program Interagency Center for the Evaluation of Alternative Toxicological Methods, NIEHS).

We also have two phenomenal and highly accomplished women leading our environmental and public health agencies: Gina McCarthy (EPA) and Linda Birnbaum (NIEHS).

These are all women who I look up to tremendously and whose work I follow closely. But, on a more personal level, I have been fortunate to work directly with several amazing female scientists during my training so far. Pamela Lein (University of California, Davis) Stephanie Padilla (EPA), Elaine Faustman (University of Washington, Seattle), Sheela Sathyanarayana (University of Washington, Seattle), and Lianne Sheppard (University of Washington, Seattle) have all provided valuable mentorship and guidance to me.

So, while we do not yet have our first female president, this post is my way of acknowledging all of the incredible female scientists who have impacted my life through their work in environmental health sciences. Because of these inspiring, accomplished women (and the numerous others who I have not mentioned for the sake of brevity), I do not feel limited when I imagine my future. I have confidence that, with hard work and dedication, I can achieve what I set my mind to.

Thank you for being role models to me and the many other aspiring environmental health scientists of my generation!

Me, in elementary school, already aspiring to follow in Rachel Carson’s footsteps