The ‘Outside’ We’ve Made for Ourselves

A couple of summers ago, I visited the University of Arizona for a conference. I’ll spare you the details of why I was there, but what I can’t forget about that campus was the “Mall”, which is basically a giant stretch of sidewalk, grass, statues and beautiful campus buildings. If you live in or around the Twin Cities, imagine the Mall at Minnesota, but take that times about ten. I remember thinking, “I can’t imagine motivating myself to go to class if I went here—this place is amazing!”

Bringing it back closer to home at St. Thomas, I love walking or running through our campus when the grass is green, the sky is clear, and the sun it shining. People are playing football or Frisbee, or they’re reading, eating or talking on the grass or on a blanket.  I would wager this scene lives in one form or another across college and university campuses nationwide, even worldwide. What’s interesting is that I doubt most of these students consider themselves naturalists, environmentalists, or even ‘outdoorsy.’ They don’t have to. Most of us are guided by the thought, “It’s nice out. I should go find some friends and a green area with some sun.” If you live in an urban area like 80% of the U.S. population13, you’re likely seeking out a quad, or a backyard, or a local park. These aren’t ideal natural settings, but they beat hanging out inside, right? And they certainly can’t hurt us.

Though I’d have to agree that time spent outdoors is better for us than whatever it is we do inside for hours on end, I think there’s plenty of evidence that the kind of outdoors that we’ve limited ourselves to really can hurt us. Damn it, I love how pretty the grass, the flowers and the trees are on campus, and the same goes for the lawns and schoolyards where I see kids playing on Summit Avenue. But it’s like there’s something wrong with me: I can’t enjoy it all because I know these green areas are teeming with pesticides.

Though pesticides are useful for when we want to make lots of food and control for diseases carried by rodents and bugs, they are often quite literally designed to be toxic to organisms with physiologies similar in ways relevant to our own2. Pesticides and many other substances can act as persistent bioaccumulative and toxic pollutants (PBTs15,6). They’re persistent because they can sit around for years without breaking down or degrading in potency. They can accumulate in the soil, the water, the plants and the animals that occupy the food chain we tend to sit on top of, so we can consume these PBTs in higher concentrations when we put food in our mouths. They are stored in our fat cells, and they stack up in our bodies with continual exposure. Basically, we eat them, or we roll around in them, and they stay there in our bodies. So what?

Well for starters, PBTs can act as neurotoxins and damage or kill our brain cells, called neurons. They can damage the axon directly, or they can degrade the myelin sheath (fatty tissues insulating the axon); either would affect normal action potentials, the electrical transmission of information between neurons. They can also hinder chemical transmission (neurotransmitters) between neurons6,2. For the purposes of my ‘brainy theme’, I want to filter my discussion to the above effects. But, for your information, PBTs can also affect our endocrine system by acting as hormone disrupters or hormone mimics; they can serve to suppress our immune systems, and they can mutate our cells as carcinogens.

So because the United States has lots of people who like lots of “cheap” food, we have this (less than) awesome food industry that provides all that food through really, really big farms that “need” lots of pesticides to keep churning out all those crops used to make the food (among other things). So, there are over 1,055 active compounds registered with the Environmental Protection Agency (EPA), and they are used to make around 16,000 pesticide products in the U.S9. About 80% of those are used in the agricultural sector14, but about 75% of U.S. households use some sort of pesticide14. If you’re wondering, yes, St. Thomas uses pesticides*

I can’t go into detail about every pesticide, but I can try to cover the main ones: organophosphates, organochlorines, pyrethroids, and pyrethrins. First, organophosphates work mainly at the synapse, basically a gap where information is transferred between neurons. They act as inhibitors to acetylcholinesterase, which breaks down acetylcholine5. Acetylcholine accumulates in the synapse, and nerve impulses to the muscles never stop. Organochlorine, on the other hand, disrupts ion transfer across cell membranes. Though the mechanism of action isn’t perfectly understood, sodium and potassium transfer is altered at or around the axon membrane, and the result is an increased negative action potential, proceeded by prolonged action potentials5. Next, pyrethroids also alter ion transfer across cell membranes by slowing the opening and closing of sodium channels, increasing excitation. In addition, they might also alter intracellular concentrations of calcium, or bind to GABA-gated chlorine receptors5. Finally, pyrethrins affect voltage-dependent chlorine channels5.

Often when we think about what in our world is hurting us, we first turn to, of course, the children. If it isn’t obvious, neurotoxins can adversely affect the development of young brains. The developing nervous system goes through very strict, ordered chemical and anatomical stages. Neurons divide in the fetus, they migrate to specified areas in the brain, differentiate into various types of cells, and they form a network of synapses with other cells in a very directed way. This is just basic prenatal development; neurons keep moving around into the first few years of life, and myelination of axons and the networking of synapses continue throughout adolescence6. As you might guess, the chemical interference of pesticides can aggravate any point in this punctilious process. If baby wasn’t exposed to PBTs when he/she was hooked up to mom’s bloodstream in the womb, then exposure through breastfeeding** or crawling around on the ground (which kids do a lot of) are easy paths to get one’s fill16,6.

I’ll share with you a short list of depressing effects that are associated with childhood exposure to pesticides. When I say associated, I most certainly don’t mean “proven to cause” or “linked one-to-one, effectively establishing that exposure to pesticide X divines the development of symptom Y.” Obviously, problems with our bodies and our minds are always complicated with a multitude of contributing variables. First, prenatal exposure can cause brain atrophy and mental retardation1,6. Prenatal exposure is also linked to children with slowed reflexes18,6, impaired motor skills and social interactions4,6, long-term psychological impairment, and impaired visual-motor integration1,6. Additionally, some sad, sad cognitive deficits have been observed in Mexican Yaqui Indian children exposed to pesticides4,6. Rural children in frequent contact with pesticides are more likely to present with poorer balance, hand-eye coordination and reaction time1,3,6. Mothers living in agricultural regions where they apply pesticides tend to have more children with autism10,6. And one kind of pesticide exposure was correlated with more impulsiveness, anger and other interpersonal problems in children11,6.

Representative drawings of a person by 5-year-old Yaqui children from the valley and foothills of Sonora, Mexico (4,6).

Now, do we care about adults? Sure we do. From the get go, exposure to pesticides almost certainly aid in the development of Parkinson’s Disease. If you’ve ever heard of Michael J. Fox, Parkinson’s is bigger than him. If you’re over 65, there’s a 1% chance you have Parkinson’s7,8,6. There are about 39 million people in the U.S. who fit this profile (http://bit.ly/IUp8MB)—times 1%. So, BIG. Symptoms generally include trouble starting movements, tremors, impairment in cognition and memory, and shifts in mood12,6. Mechanistically, pesticide exposure may increase risk of Parkinson’s if an individual lacks enzymes to break down pesticides8,6. Long-term exposure, even at low levels could contribute to the disease even in people with such enzymes17,6.

So at the end of the day, we should probably just go outside. Yes, be aware and at least a little troubled about the presence of nasty chemicals on the ground you and your loved ones are standing on. Don’t let it ruin your outside time, but let it give you pause when you’re caring for our own lawn, or when you’re making food choices. Also, since “pesticides hurt brains” is politically transparent, I have no pause of my own in nudging you to vote and be active about the issue, locally and nationally. Although, “I can’t fix it by myself,” is an understandable way to cope with an overwhelming problem, we ought to constantly ask ourselves, “then, who can?” Going outside is important. So are our brains. Fight for them.

Notes

*ugh, don’t quote me…

**Breastfeeding still outweighs the cost of pesticide exposure.

References

  1. Bellinger, D.C., & Adams, H.F. (2001). Environmental pollutant exposures and childrens’ cognitive abilities. In R.J. Sternberg & E.L. Grigorenko (Eds.), Environmental effects of cognitive abilities (pp.157-188). Mahway, NJ: Erlbaum.
  2. Gilbert, S.G. (2004) A small dose of toxicology: The health effects of common chemicals. Boca Raton, FL: CRC press.
  3. Grandjean, P., & Landrigan, P. (2006). Developmental neurotoxicity of industrial chemicals. The Lancet, 368(9553), 2167-2178. doi:10.1016/S0140-6736(06)69665-7
  4. Guillette, E. A., Meza, M. M., Aquilar, M. G., Soto, A. D., & Garcia, I. E. (1998). An anthropological approach to the evaluation of preschool children exposed to pesticides in mexico. Environmental Health Perspectives, 106(6), 347-353. doi:10.1289/ehp.98106347
  5. Gupta, R. C. (2007). Veterinary toxicology: basic and clinical principles(1. ed.). Amsterdam [U.A.: Elsevier.
  6. Koger, S. M., & Winter, D. D. (2010).The psychology of environmental problems: psychology for sustainability (3rd ed.). New York: Psychology Press
  7. Landrigan, P. J., Sonawane, B., Butler, R. N., Trasande, L., Callan, R., & Droller, D. (2005). Early environmental origins of neurodegenerative disease in later life. Environmental Health Perspectives, 113(9), 1230-1233. doi:10.1289/ehp.7571
  8. Le Couteur, D. G., McLean, A. J., Taylor, M. C., Woodham, B. L., & Board, P. G. (1999). Pesticides and parkinson’s disease. Biomedicine & Pharmacotherapy, 53(3), 122-130. doi:10.1016/S0753-3322(99)80077-8
  9. National Institute for Occupational Safety and Health (2011). Pesticide Illness & Injury Surveillance. Retrieved from http://www.cdc.gov/niosh/topics/pesticides/
  10. 10. Roberts, E. M., English, P. B., Grether, J. K., Windham, G. C., & Wolff, C. (2007). Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the california central valley. Environmental Health Perspectives, 115(10), 1482-1489. doi:10.1289/ehp.10168
  11. 11. Ruckart, P. Z., Kakolewski, K., Bove, F. J., & Kaye, W. E. (2004). Long-term neurobehavioral health effects of methyl parathion exposure in children in mississippi and ohio. Environmental Health Perspectives, 112(1), 46-51. doi:10.1289/ehp.6430
  12. 12. Strange, P. G. (1992). Brain biochemistry and brain disorders. Oxford: Oxford University Press.
  13. 13. U.S. Census Bureau, Geography Division. (2010). Urban, Urbanized Area, Urban Cluster, and Rural Population, 2010 and 2000: United States. Retrieved from http://www.census.gov/geo/www/ua/2010urbanruralclass.html
  14. 14. U.S. Environmental Protection Agency (2007). Pesticide Industry Sales and Usage. Retrieved from http://www.epa.gov/opp00001/pestsales/07pestsales/market_estimates2007.pdf
  15. 15. U.S. Environmental Protection Agency (2011). Persistent Bioaccumulative and Toxic (PBT) Chemical program. Retrieved from http://www.epa.gov/pbt/
  16. 16. Weiss, B. (2000). Vulnerability of children and the developing brain to neurotoxic hazards. Environmental Health Perspectives, 108 (3), 375-381.
  17. 17. Weiss, B., Clarkson, T. W., & Simon, W. (2002). Silent latency periods in methylmercury poisoning and in neurodegenerative disease. Environmental Health Perspectives, 110 Suppl 5(Suppl 5), 851-854.
  18. 18. Young, J. G., Eskenazi, B., Gladstone, E. A., Bradman, A., Pedersen, L., Johnson, C., . . . Holland, N. T. (2005). Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Neurotoxicology, 26(2), 199-209. doi:10.1016/j.neuro.2004.10.004
Advertisements

One thought on “The ‘Outside’ We’ve Made for Ourselves

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s