Overexposed: The role of environmental toxicants on your brain

By Carlie Hoffman

It is often said that we are products of our environment: who we are is shaped by the things, people, and situations with which we surround ourselves. However, whatever we may like to think, we are not in control of every facet of our environment. In fact, we are unknowingly and involuntarily exposed to dozens of man-made environmental chemicals, called toxicants, each day that can negatively alter our bodies and even our very brain matter. In essence, we are becoming literal products of our environment.

Synthetic chemicals and toxicants are ubiquitous within our surroundings. While some toxicants come from obvious sources, like cigarette smoke and car exhaust, other sources of exposure are more subtle. For instance, electrical equipment (like computers and cell phones), beauty products (like makeup and shampoo), mattresses, and furniture all contain flame retardants, chemicals used to reduce flammability [3, 13]. Bisphenol A (BPA) and phthalates, chemicals used to harden plastics, can also be found in dental sealants, cigarette filters, soda bottles, and the linings of canned foods [4, 8, 12]. Additionally, dichlorodiphenyltrichloroethane (DDT), a pesticide commonly used in the mid-1900s to combat outbreaks of pests, malaria, and lice, was banned in 1972 in the US and yet is still currently present within both the environment and human tissues [12].

Pesticides not only harm insects, but certain doses can also have harmful effects on the human body.

The presence of chemicals within almost every facet of our society means we are subjected to varying levels of environmental exposure throughout our lives– from the womb to the grave. A growing desire to characterize the effects of this lifetime of exposure resulted in the creation of a new concept: the “exposome.” Defined in 2005 by Dr. Christopher Wild as “every exposure to which an individual is subjected from conception to death,” this definition was expanded by Dr. Gary Miller and Dr. Dean Jones in 2014 to be “the cumulative measure of environmental influences and associated biological responses throughout the lifespan, including exposures from the environment, diet, behavior, and endogenous processes” [9, 14, 15]. Indeed, some say the exposome profile may tell a narrative about our individual lives with astounding accuracy– including where we’ve traveled, what we’ve eaten, and trends in our overall behavior.

As Dr. Wild stated, our environmental exposures, and our lives, begin in the womb. After this point, the developing fetus is subject to many of the environmental chemicals and toxicants to which the mother is (knowingly or unknowingly) exposed. A study described by CNN illustrated this point and found that pregnant mothers were exposed to pesticides and air pollutants while engaging in everyday activities.  Some of these chemicals were also able to pass through the umbilical cord and enter into the bloodstream of the fetus, resulting in an average of 232 chemicals being found in the cord blood of 10 babies born over the course of the study.  Pregnant mothers were also exposed to chemicals from unexpected sources, like taking a shower, cleaning the house, and putting on makeup.  Some of these chemicals also made it into the fetus and were found in the fetal cord blood.  However, it is important to note that the mere presence of such chemicals within the blood is not necessarily harmful to human health. Instead, toxicity is dependent upon the concentration and duration of exposure a person, or fetus, is subjected to– meaning the presence of exposure does not always lead to the occurrence of detrimental health effects.

That being said, certain types of environmental exposure can result in numerous negative consequences for the brain. For instance, exposure to certain amounts of air pollutants and pesticides during development has been associated with a reduction in white matter volume in the brain, slower information processing speed, behavioral problems, attention deficit/hyperactivity disorder (ADHD) symptoms, and an alteration in mental and psychomotor development [7, 10]. One study retrospectively examined a group of adults in Cape Cod, Massachusetts who experienced prenatal and early childhood exposure to drinking water contaminated with tetrachloroethylene, a chemical solvent used in dry cleaning, and found that early exposure was associated with impaired vision, increased reports of impulsive behavior, and increased risks of developing bipolar disorder and post-traumatic stress disorder (PTSD) in adulthood [1, 2, 6]. In addition, excessive prenatal exposure to BPA and phthalates has been found to alter sexually dimorphic development of the brain and can also lead to alterations in anxiety, hyperactivity, and emotional control [4, 8, 12].  Thus, exposure to environmental chemicals can influence how our brains function, affect our mental health, and alter how we interact with the world around us.

Given these documented detrimental health effects, we should seek to avoid excessive environmental exposures. However, while we can limit our interaction with known sources of environmental chemicals, such as by avoiding areas that have recently been sprayed with pesticides or not living in areas subjected to large amounts of car exhaust, how do we protect ourselves from environmental toxicants coming from largely unknown and unavoidable sources?  And why are chemicals are being added to commonly-used household items in the first place when such substances have the potential to negatively alter our brains and neurodevelopment?

The answer to this latter question can be traced to the years surrounding the Great Depression and World War II. In this era, the fields of human industry and farming began to employ synthetic chemicals for numerous beneficial purposes, like controlling pest populations, reducing flammability, and acting as additives in paints and wood finishes. These potential useful applications led to the quick introduction of such compounds to widespread use without thorough examination of their possible negative impacts on human health. The reason for rapidly adding these chemicals was described in the 1930s by the president of the Halowax Corporation: “The problem so far as the chemical manufacturer is concerned is a question of timing… should we take a product of which you have developed, say, 5 or 10g and spend $50,000 on research to determine whether or not it is toxic, or should you wait until you have determined whether you have a market for it?...You can see that would run into box car numbers in the way of dollars and cents until you ever sold any” [12]. Essentially, adequate chemical testing was not performed because it was not cost-effective, resulting in the public remaining largely unaware of the adverse health effects that could arise from excessive exposure to these added chemicals.

Unfortunately, this cost-driven lack of investigation still describes how chemical research is performed today.  An article in The New England Journal of Medicine stated that only 200 of the 80,000 chemicals added to products sold within the US in 2011 were sufficiently tested for carcinogenicity, not to mention the number of chemicals that were inadequately tested for other, non-cancer-related negative outcomes arising from excessive exposure [5].

This mass-production of chemicals without adequate toxicity testing continues in part because of the vague chemical testing regulations that govern chemical companies in the United States. According to the Environmental Protection Agency’s (EPA) chemical testing policy, chemical companies are responsible for determining whether their substances “may present an unreasonable risk of injury to health or the environment.” The nebulous wording of this regulation, the lack of a precise definition of “unreasonable risk,” and the increased cost associated with increased research has resulted in many chemical companies simply testing their chemicals for acute toxicity (which involves giving experimental animals large doses of a chemical and checking for a decrease in lifespan or the presence of illness), instead of performing long-term testing (which involves giving experimental animals small doses of a chemical over a long period of time). Thus, the effects of gradual exposure, as would be experienced through daily contact with a chemical over the course of a lifetime, are not examined and the effects of such gradual exposure are only determined as people are exposed to these chemicals for many years.

Thankfully, this problem of non-consensual daily exposure to toxic chemicals is not one without a solution– though working toward this solution will not be easy. One of the first steps toward a less-polluted and more hospitable future is to continue characterizing the human exposome. Several organizations within the United States and Europe, including the HERCULES exposome research center at Emory University, operate under this goal. These organizations seek to develop a better understanding of the role of the environment on brain disease onset and progression, to discover chemicals that cause disease, and to remove or diminish exposures to such chemicals [11]. More stringent regulations on chemical testing and increased collaboration between chemical companies and neuroscientists will also move chemical testing in the right direction, helping to elucidate the long-term effects of environmental chemicals on the brain and leading to more detailed chemical toxicity characterization. Unfortunately, increased chemical testing is often viewed as an unnecessary hindrance and is perceived as being less cost-effective than rapidly mass-producing a chemical. However, more thorough testing and increased chemical regulation will result in an improved quality of life, better brain development, and an increase in human liberties for individuals throughout our society and the world– and that is priceless.

Works Cited

1. Aschengrau, A, Weinberg, JM, Janulewicz, PA, Romano, ME, Gallagher, LG, Winter, MR, Martin, BR, Vieira, VM, Webster, TF, White, RF, & Ozonoff, DM (2011) Affinity for risky behaviors following prenatal and early childhood exposure to tetrachloroethylene (PCE)-contaminated drinking water: a retrospective cohort study. Environ Health 10: 102. doi: 10.1186/1476-069x-10-102

2. Aschengrau, A, Weinberg, JM, Janulewicz, PA, Romano, ME, Gallagher, LG, Winter, MR, Martin, BR, Vieira, VM, Webster, TF, White, RF, & Ozonoff, DM (2012) Occurrence of mental illness following prenatal and early childhood exposure to tetrachloroethylene (PCE)-contaminated drinking water: a retrospective cohort study. Environ Health 11: 2. doi: 10.1186/1476-069x-11-2

3. Ballesteros-Gomez, A, de Boer, J, & Leonards, PE (2014) A novel brominated triazine-based flame retardant (TTBP-TAZ) in plastic consumer products and indoor dust. Environ Sci Technol 48: 4468-4474. doi: 10.1021/es4057032

4. Braun, JM, Kalkbrenner, AE, Calafat, AM, Yolton, K, Ye, X, Dietrich, KN, & Lanphear, BP (2011) Impact of early-life bisphenol A exposure on behavior and executive function in children. Pediatrics 128: 873-882. doi: 10.1542/peds.2011-1335

5. Christiani, DC (2011) Combating environmental causes of cancer. N Engl J Med 364: 791-793. doi: 10.1056/NEJMp1006634

6. Getz, KD, Janulewicz, PA, Rowe, S, Weinberg, JM, Winter, MR, Martin, BR, Vieira, VM, White, RF, & Aschengrau, A (2012) Prenatal and early childhood exposure to tetrachloroethylene and adult vision. Environ Health Perspect 120: 1327-1332. doi: 10.1289/ehp.1103996

7. Gonzalez-Alzaga, B, Lacasana, M, Aguilar-Garduno, C, Rodriguez-Barranco, M, Ballester, F, Rebagliato, M, & Hernandez, AF (2014) A systematic review of neurodevelopmental effects of prenatal and postnatal organophosphate pesticide exposure. Toxicol Lett 230: 104-121. doi: 10.1016/j.toxlet.2013.11.019

8. Lin, CY, Shen, FY, Lian, GW, Chien, KL, Sung, FC, Chen, PC, & Su, TC (2015) Association between levels of serum bisphenol A, a potentially harmful chemical in plastic containers, and carotid artery intima-media thickness in adolescents and young adults. Atherosclerosis 241: 657-663. doi: 10.1016/j.atherosclerosis.2015.06.038

9. Miller, GW, & Jones, DP (2014) The nature of nurture: refining the definition of the exposome. Toxicol Sci 137: 1-2. doi: 10.1093/toxsci/kft251

10. Peterson, BS, Rauh, VA, Bansal, R, Hao, X, Toth, Z, Nati, G, Walsh, K, Miller, RL, Arias, F, Semanek, D, & Perera, F (2015) Effects of prenatal exposure to air pollutants (polycyclic aromatic hydrocarbons) on the development of brain white matter, cognition, and behavior in later childhood. JAMA Psychiatry 72: 531-540. doi: 10.1001/jamapsychiatry.2015.57

11. Rappaport, SM, Barupal, DK, Wishart, D, Vineis, P, & Scalbert, A (2014) The blood exposome and its role in discovering causes of disease. Environ Health Perspect 122: 769-774. doi: 10.1289/ehp.1308015

12. Rosner, D, & Markowitz, G (2013) Persistent pollutants: a brief history of the discovery of the widespread toxicity of chlorinated hydrocarbons. Environ Res 120: 126-133. doi: 10.1016/j.envres.2012.08.011

13. Venier, M, Salamova, A, & Hites, RA (2015) Halogenated Flame Retardants in the Great Lakes Environment. Acc Chem Res. doi: 10.1021/acs.accounts.5b00180

14. Wild, CP (2005) Complementing the genome with an "exposome": the outstanding challenge of environmental exposure measurement in molecular epidemiology. Cancer Epidemiol Biomarkers Prev 14: 1847-1850. doi: 10.1158/1055-9965.epi-05-0456

15. Wild, CP (2012) The exposome: from concept to utility. Int J Epidemiol 41: 24-32. doi: 10.1093/ije/dyr236

Want to cite this post?

Hoffman, C. (2015). Overexposed: The role of environmental toxicants on your brain. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2015/09/overexposed-role-of-environmental.html

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