The detrimental effects of lead on early childhood development have been recognized by scientists, industry leaders, and government officials for over sixty years. However, only recently have researchers and activists begun to contextualize toxic lead exposure within the framework of environmental racism. As the water crisis in Flint, MI demonstrated, the impact of childhood lead exposure is not merely cognitive and psychological, but economic and racialized as well. Established studies on lead poisoning are reinforced by an environmental racism framework, expanding the possibilities for clinical response.
No level of lead is healthy, but the level of lead that is tolerable by public health standards has trended downwards. Today, the Center for Disease Control identifies 50 mcg/L as the upper limit for acceptable blood levels of lead, down from 600 mcg/L in the 1960s. Research shows that lead levels which reflect accumulation in the body over time are the most detrimental to the nervous system (Hou 2013). Infants and children are at most risk of adverse health effects due to a more permeable blood brain barrier and higher gut absorption of lead as compared to adults (Heath 2003).
The consequences of lead exposure in children are broad and persistent. Lead exposure has consistently been linked with lower IQ scores (Needham, 1990; Chen, 2003). Recent studies by Hou et. al have shown negative association between lead exposure to children ages 1-5 and gross motor performance, fine motor performance, language development, and aggression. A study by Miranda et. al revealed that even low levels of lead (20-50 mcg/l) in children negatively impacted later-life reading and math levels; Mendola et. al found correlations between childhood lead exposure and decreased attention span.
While epidemiologists have generated significant data on lead’s relationship to learning, attention, and IQ, molecular and neurobiologists are just beginning to uncover lead’s mechanism of action on the nervous system. Researchers have determined that lead acts primarily on glutamate receptors (Guilarte, 1997, Regunathan and Sundaresan, 1985 and Savolainen et al. 1995). The glutamate receptors are classified into both ionotropic and metabolic subtypes, depending on whether they are ion channel or G-protein coupled receptors. Two glutamate receptors involved in lead-based neurotoxicity are the NMDAR ionotropic receptor and the metabolic glutamate receptor 5 (mGluR5), both found in the hippocampus. These receptors seem to play a role in hippocampal based learning and memory (Xu, 2009). However, lead’s mechanism of action on these receptors is still unclear, and further research is needed to determine whether these are truly the key elements involved in lead-based neurotoxicity.
As the scientific evidence of lead’s toxicity accumulated, regulations mounted and its use dwindled. Lead has historically been used in a wide array of industrial products, including gasoline, paint, and water piping. The legal process of removing lead from gasoline began in 1965 and culminated in 1996. Lead was banned from paint in 1978, although it can still be found on the walls of many older buildings and houses. Similarly, although lead pipes were banned from use in plumbing systems in 1986, much of the country’s public water infrastructure predates the ban, leaving millions of feet of lead piping intact (Gilbert, 2006).
For many, Flint, Michigan epitomizes the modern dangers of lead and the public health risks latent within America’s corroded infrastructure. After Flint’s public water source was diverted from treated Detroit municipal water to Flint River water in 2014, residents were exposed to high levels of lead in their tap water. Residents and officials still raise concerns today about the safety of Flint’s water supply; the city anticipates that all lead pipes will be replaced by 2021, seven years of litigation and neurodevelopmental damage later.
The water crisis in Flint, a majority black and working class community, is a clear example of environmental racism. The concept of environmental racism has its origins in the Civil Rights Movement, and refers to institutional racial discrimination which exposes black and brown people to disproportionately higher rates of toxic and hazardous environments and materials. Data illustrates the prevalence and seriousness of this phenomenon. In 2013 the CDC published a study showing that, from 2007 to 2010, black children (1-5 years old) had twice the rate of lead poisoning than white children nationally.
Research conducted by the Connecticut Department of Health in 2013 has mirrored national data, confirming that black children in Connecticut are more than twice as likely to be exposed to lead levels above 50 mcg/L (Hung, 2014). The study also shows lead exposure by town across Connecticut. When comparing the map of lead poisonings to the demographic map, it is evident that the areas of highest lead exposure are most densely populated by African Americans (Hung, 2014).
The lasting, racialized, cognitive and psychological effects of lead exposure necessitate that mental health workers be engaged in ongoing environmental justice work. At base, mental health workers must be aware of their clients’ living environment, and the health implications and risks therein. Water quality, air quality, sound levels, and presence of toxins vary widely among communities even within a small geographic area. An environmental justice framework incorporates this knowledge into clinical practice.
Mental health practitioners occupy an important role in advocating for communities that are most impacted by lead exposure. By educating the public about the repercussions of lead exposure and developing programs to support children already impacted, mental health practitioners can build community resilience. They can work with clinics to distribute water filters to patients and community members and lobby local politicians to demand legal protections and accountability measures.
Mental health practitioners have a responsibility to document the effects of environmental racism on their patients by accurately diagnosing the results of toxic exposure instead of attributing symptoms to individual biological processes. In the case of lead exposure, mental health practitioners should obtain lead levels from patients exhibiting characteristics of ADHD, aggression, and/or intellectual disability at a young age.
Engaging in environmental justice work means providing mental health care within a political context. By taking advantage of this diagnostic lens, more relevant and effective interventions can take place on the level of the individual, and more meaningful prevention work on the level of the community.
Resources on lead and environmental justice:
The National Institute of Environmental Health Sciences: Lead
Connecticut Law for Lead Abatement
The Principles of Environmental Justice
References:
Frostenson, Sarah. America's lead poisoning problem isn't just in flint. It’s everywhere. – vox. January 21, 2016. Retrieved from http://www.vox.com/2016/1/21/10811004/lead-poisoning-cities-us
Centers for Disease Control and Prevention. Blood lead levels in children aged 1–5 years — united states, 1999–2010. Morbidity and Mortality Weekly Report (MMWR): April 5, 2013 / 62(13);245-248 Retrieved from http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6213a3.htm
Chen A, Dietrich KN, Ware JH, Radcliffe J, Roqan WJ: IQ and blood Lead from 2 to 7 years of age: are the effects in older children the residual of high blood Lead concentrations in 2-year-olds?. Environ Health Perspect. 2005, 113 (5): 597-601. 10.1289/ehp.7625.
Even A bit of lead is bad for kids' psychological development. American Psychological Association, February 2014. Retrieved from http://www.apa.org/action/resources/research-in-action/lead.aspx
Gilbert, S. G., & Weiss, B. (2006). A rationale for lowering the blood lead action level from 10 to 2 μg/dL. Neurotoxicology, 27(5), 693-701. doi:http://dx.doi.org/10.1016/j.neuro.2006.06.008
Heath LM, Soole KL, McLaughlin ML, McEwan GT, Edwards JW: Toxicity of environmental Lead and the influence of intestinal absorption in children. Rev Environ Health. 2003, 18 (4): 231-50.
Hung, T 2014. CT Department of Public Health Annual Disease Surveillance Report on Childhood Lead Poisoning, based on 2012 data. Hartford, CT: Connecticut Department of Public Health.
K.M. Savolainen, J. Loikkanen, J. Naarala Amplification of glutamate-induced oxidative stress Toxicol. Lett., 82–83 (1995), pp. 399–405
Miranda, M. L., Kim, D., Galeano, M. A. O., Paul, C. J., Hull, A. P., & Morgan, S. P. (2007). The Relationship between Early Childhood Blood Lead Levels and Performance on End-of-Grade Tests. Environmental Health Perspectives,115(8), 1242–1247. http://doi.org/10.1289/ehp.9994
Needleman HL, Gatsonis CA. Low-Level Lead Exposure and the IQ of Children: A Meta-analysis of Modern Studies. JAMA.1990;263(5):673-678. doi:10.1001/jama.1990.03440050067035.
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S. Regunathan, R. Sundaresan Effects of organic and inorganic lead on synaptosomal uptake, release, and receptor binding of glutamate in young rats J. Neurochem., 44 (1985), pp. 1642–1646
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Xu, J., Yan, C., Yang, B., Xie, H., Zou, X., Zhong, L., Shen, X. (2009). The role of metabotropic glutamate receptor 5 in developmental lead neurotoxicity. Toxicology Letters, 191(2–3), 223-230. doi:http://dx.doi.org/10.1016/j.toxlet.2009.09.001