top of page

A Silent Injustice: Lead’s Poison Agenda

by Laura Mittelman

art by Nava Himelhoch

In the heart of Baltimore, a resilient city that beats with a history of injustice and inequality, lies an issue so insidious that its detrimental effects often escape notice until they’ve already inflicted significant harm. Lead exposure, a peril entangled in the crossroads of historical redlining and a deteriorating housing market, places a disproportionate burden on Baltimore’s youth population because of its intrinsic neurotoxic mechanisms. Emblematic of systemic racism’s lasting impact, children growing up in historically segregated Black neighborhoods, in homes coated with lead paint, are at the mercy of this devastating crisis.

Lead (Pb2+) is a naturally occurring toxic heavy metal that possesses a particular proclivity for the central nervous system, which consists of the brain and spinal cord, rendering it a serious threat to the healthy neurodevelopment of children [1]. In fact, its toxicity is so vicious that it ranks among the most dire public health threats worldwide, and has harnessed the attention of researchers, media, and the World Health Organization alike [2, 3]. Children's heightened vulnerability to lead exposure stems from a triad of factors: their immature blood-brain barrier (which typically serves as a protective filter against harmful toxins), higher rates of gastrointestinal and respiratory absorption, and increased hand-to-mouth behavior at young ages [4, 5]. Childhood exposure to the neurotoxin, even at low levels, can have pervasive effects that persist into adolescence, including delayed developmental milestones, impaired cognitive function, and diminished academic performance [4]. The risk for lead exposure can even begin in utero, resulting in significantly reduced infantile growth and proper neurodevelopment, subjecting fetuses to the structural barriers of health inequality before even being born [4, 6]. Adding to the adversity, comorbidities such as anemia (iron deficiency) and vitamin deficiency can enhance the rate of lead absorption and place children with malnutrition at a heightened risk for lead neurotoxicity [7–9]. Access to nutritious meals is typically more limited in the city's segregated and low-income communities, leading to disproportionately higher rates of malnutrition among Black children [7, 10]. This underscores the critical role of social determinants of health in shaping children’s susceptibility to lead neurotoxicity and its consequential harm.

Altogether, these complex lead-risk adversities that children of systemically segregated households in Baltimore face shed light on the reciprocity between neurological health disparities and the much-larger perpetuation of socioeconomic and racial injustices.

The Primary Layers: Lead’s History

In 2021, the Maryland Department of the Environment reported that 78% of all potential sources of lead exposure were accounted for by lead-based paint – the same paint that coats the walls of families’ homes throughout Baltimore. Many of these homes are situated within the confines of historical redlines, which have partitioned Black Baltimorians to neighborhoods with limited opportunities for housing and economic prosperity [11]. In this regard, these racially discriminatory geographical confines effectively planted a seed that would grow into years of sustained disinvestment and discrimination against minority families across the city [11–13]. Present-day, disparate residential segregation persists, placing Black and low-income children powerless before an out-of-date and declining housing stock, where 90% of residential buildings were built during the height of lead-based paint usage [14].

Throughout the first half of the 20th century, the lead paint industry was booming with business, as nearly all historical paint colors contained the heavy metal and served as the principal pigment in homes across Baltimore [15]. The paint’s use on interior and exterior residential structures was unregulated, and despite the emergence of a mounting lead toxicity crisis beginning in the 1950s, continued through the 1970s [16]. In fact, in the book “Lead Wars,” David Rosner and Gerard Markowitx, professors specializing in the history of public health at Columbia University and City University of New York, respectively, argued that the federal government possessed knowledge of the numerous hazards of lead – but yielding to industry pressure, permitted its exposure to millions of children through use in publicly funded residential constructions [16]. Eventually, in 1978, lead paint was banned by federal legislation, but by then it was too late. Baltimore was already infiltrated with lead-painted homes and, in light of the city’s mounting economic decline, children all over the city were left at risk for lead poisoning without a viable solution. Fast forward to the present, Baltimore stands as one of the most hypersegregated cities in the country, and lead-based paint accounts for 78% of all potential sources of lead exposure city-wide, with a disproportionate number of Black children bearing the burden of the crisis [13, 15].

As a result, both local and state governments have initiated more serious steps to mitigate childhood lead exposure in homes, as seen in the 1994 Maryland Reduction of Lead Risk in Housing Law, which required landlords of rental properties built pre-1978 to take steps in reducing and reporting lead paint. In addition, healthcare providers practicing in Baltimore are required to perform lead tests on pediatric patients under the age of two [17]. Ongoing educational outreach programs are also continuing to help parents in high-risk neighborhoods identify lead hazards [13, 14]. However, despite these efforts, the persisting data shows a correlation between primarily Black communities and heightened average annual lead paint violations per 10,000 households in Baltimore, with the highest percentage of positive lead poisoning tests among children ages 0-6 [12]. The lack of direct eradication of residential lead hazards overtly discriminates against those who live in poverty or have been suppressed by historical racial agendas, placing their youth at greater risk for impaired neurodevelopment and cognitive deficits.

Mechanisms of Lead Absorption: From Blood to Brain

Now, you might be wondering how lead from paint on the walls, or even on toys, can access children’s nervous systems and exert its neurotoxic effects. For children, including those in Baltimore, the most common mechanism of exposure is the inhalation of lead-contaminated dust and flaking paint particles. Other methods include absorption through the gastrointestinal tract (digestive system) following ingestion of contaminated food or water, or even via hand-to-mouth contact after touching a lead-coated surface [18]. Children are particularly susceptible to this exposure because their immature biological systems absorb the heavy metal more readily compared to their adult counterparts [19]. Following absorption into the bloodstream, lead (Pb2+) travels throughout the circulatory system, disguising itself as other essential ions, such as zinc (Zn2+) and calcium (Ca2+) [1]. This ability for lead to cloak itself stems from its +2 charge, making its chemical identity similar enough to that of zinc and calcium that it can substitute their presence across various neurobiological pathways [1]. For example, you may have heard that the blood-brain barrier (BBB) is like a security system for the brain, acting as a blockade and protecting the brain from a plethora of potentially harmful substances. If this is true, then how is lead able to pass the ever-so-vigilant BBB? Lead is readily transported across the barrier in large part due to its ability to substitute for calcium ions (Ca2+) in a calcium-specific pump, which can be thought of as a gate-keeping protein that only opens for Ca2+ ions to flow into the brain [1, 20].

Upon entering the brain, lead accumulates in astrocytes – the most prevalent type of glial cells (non-neuronal brain cell) – via lead-binding proteins on their outer membrane, which facilitate the uptake of lead in their cytoplasm (cell interior) [21]. Astrocytes make up a significant portion of the BBB by wrapping their cellular extensions around blood vessels to form a physical barrier of tight junctions that serve as leak-proof seals for controlling the passage of substances into the brain [22]. Thus, astrocytic accumulation of lead initially serves as a protective mechanism against the metal’s toxic effects, mitigating the brain’s exposure to lead ions in adults [21]. However, in children, there is a caveat: their immature astrocytes have remarkably fewer lead-binding proteins, decreasing the cells’ ability to accumulate lead and rendering children more susceptible to lead neurotoxicity, even at lower concentrations [20]. Furthermore, the immature astrocytes themselves are more easily damaged by lead, which in turn obstructs the formation of the BBB, weakening the barrier, and further exacerbating children’s defenselessness against the metal [21]. Framing this in context, when children under the age of six living in segregated and resource-constrained communities throughout Baltimore are exposed, the effects of lead neurotoxicity are more pronounced given the rapid pace of critical neurodevelopment occurring at this age [1].

Brushing Against Danger: In Utero Lead Exposure

Although school-aged children across Baltimore are the most distinguished population at risk for lead poisoning, pregnant women and their fetuses are also vulnerable [6]. Given the pervasiveness of lead-based paint in Baltimore’s historically segregated neighborhoods, Black women of childbearing age are susceptible to cumulative lead exposure across their lifetime. In turn, increased maternal blood lead levels impart neurodevelopmental risks onto

fetuses and infants by transmitting Pb2+ ions across the placental barrier or via breastfeeding [23]. Even at low blood-lead levels, the effects of fetal or infantile encounters with lead persist into early childhood and are associated with a decline in IQ scores and ADHD-like symptoms [23]. This intergenerational transmission of lead exposure represents a cumulative effect of ongoing environmental injustices suffered by Black children across Baltimore.

The placenta is a temporary organ developed during pregnancy that influences the healthy neurodevelopment of the fetus in various ways [24]. Several studies indicate that lead transport across the placental barrier occurs via simple diffusion, a process whereby the metal can freely move from areas of higher concentration (maternal blood circulation) to areas of lower concentration (fetal blood circulation) [6]. In addition, the underdeveloped fetal BBB, which includes immature astrocytes, facilitates lead’s easy access to the CNS, where lead accumulation interferes with neural processes critical to the early stages of brain development [6]. Due to the fetus’s exceptional vulnerability to lead, measurable exposures during gestation (prenatal duration) have often been associated with behavioral impairments and learning difficulties [25]. Additionally, researchers have found that high placenta-lead levels were correlated with low APGAR scores, a rapid assessment that evaluates neonates appearance, pulse, grimace (reflexive response), activity, and respiration immediately after birth [26]. Low APGAR scores are associated with an increased need for medical attention; however, they are not direct indicators of adverse health outcomes in most infants. Rather, lower scores over time within a specific population can increase that population’s risk for poor neurological outcomes, a risk that Baltimore faces [27].

While lead primarily targets the underdeveloped fetal brain and its cells, various other tissues are vulnerable to prenatal lead exposure. As a result, a range of adverse pregnancy outcomes (APOs) can ensue, including premature birth, low birth weight, multi-organ malformations, and in-utero encephalopathy (an umbrella term for brain injuries that occur during pregnancy) [28, 29]. Gestational lead exposure and its associated APOs subject newborns to impaired cognitive development throughout early childhood [6]. Overall, lead’s ability to readily cross the placental barrier and reach the fragile, developing nervous system poses a significant environmental threat to Black and low-income pregnant mothers and their children.

Painting a Picture: Unveiling the Toxicokinetics of Lead

Exploring the intricate world of lead in the brain reveals a tapestry of cellular and molecular mechanisms underlying the heavy metal’s neurotoxicity. Unraveling these complexities is key to understanding the potential impacts lead exposure can have on neurodevelopmental outcomes in children burdened with lead exposure risks, such as those in Baltimore.

Specifically, prolonged exposure to lead, in any amount and at any stage of development, can lead to various neurocognitive deficits, including, but not limited to, impaired executive function, processing speed, and visual and verbal memory, as well as reduced cognitive function and academic achievement [4]. To fully understand the mechanisms behind childhood lead neurotoxicity, we must dive deeper into the toxicokinetics of lead. That is, the ways in which the inorganic metal traverses bodily systems and integrates itself into the central nervous system (CNS) via two fundamental processes: neuronal signaling and cellular deterioration [1].

Canvas A: Neural Signaling

When lead interferes with neurochemical signaling during the early stages of brain development, the functional basis for how neurons communicate with each other becomes disrupted [26]. Neurotransmitters, specific types of chemical messengers sent and received by neighboring neurons, make up the language that our brain uses to communicate and represent the foundation of neurochemical signaling. These little information-carrying messengers each have a specific job, much like different words in a language have a specific meaning. Glutamate, a neurotransmitter responsible for excitatory signaling, lies at the crossroads of neurological networks involved in learning and memory, holding a vital role in brain development throughout the neonatal period and into adolescence [30]. A notable mechanism of lead neurotoxicity is the disruption of proper glutamate signaling; glutamate transmits signals by binding to its receptor proteins situated on the membrane of recipient neurons [2]. Of note is the NMDA (N-methyl-D-aspartic acid) receptor, a glutamate-gated ion channel whose requirements for opening include the presence of glutamate binding. The resulting net influx of positive ions into the recipient cell is the neural basis for brain communication and neural network formation, a delicate process easily disrupted by lead [26].

A large body of evidence shows that lead interferes with glutamate transmission in the brain via two primary mechanisms: (1) inhibiting the effect of glutamate on signal transmission and (2) interfering with the brain’s ability to adapt, rewire, and form new connections (termed neuroplasticity, an important mechanism underlying learning and memory, especially across the early years of life) [26, 31, 32]. One mechanism of glutamatergic signaling occurs upon glutamate binding to the NMDA receptor, causing the channel to open and allowing an inward current of ions into the recipient neuron – a molecular process that excites neurons and is essential for neuroplasticity [33]. Lead interferes with this process by preventing glutamate from binding its NMDA receptor, which subsequently inhibits the opening of the receptor’s ion channel [34, 35]. Again, it is lead’s ability to disguise itself as zinc (Zn2+) that induces this disruption of signal transmission. In healthy neurophysiology, Zn2+ binds to the NMDA receptor to regulate glutamate signaling [2]. Lead binds the NMDA receptor at the Zn2+ binding site, which can alter the receptor's function and effectively inhibit glutamate signaling [2, 26]. This impairment of excitatory glutamate transmission diminishes the induction of long-term potentiation (LTP), which is the persistent strengthening of neural connections and the biological basis of neuroplasticity [2].

In addition to blocking NMDA receptor-based signal transduction, research also demonstrates that lead reduces the expression of NMDA receptor subunit NR2A [26]. The NMDA receptor is composed of various protein subunits; expression of the NR2A subunit is particularly important for neuroplasticity and brain maturation throughout infancy [26]. When this process occurs in the hippocampus, a complex brain region embedded deep in the center of our brains that plays a vital role in learning and memory, this molecular mechanism of lead interference prevents the typical increase in NR2A expression with age. As a result, the formation of important brain connections between developing hippocampal neurons is disrupted [26].

Lead also impairs neuroplasticity via a second mechanism: Pb2+ substitutes for Zn2+ on proteins that regulate gene expression. In doing this, lead alters gene expression necessary for the strengthening and growth of new brain connections [2]. This substitution occurs primarily in the hippocampus, thereby disrupting learning and memory, core components of healthy neurodevelopment, in fetuses, infants, and school-aged children alike [2, 26]. Combined, these factors contribute to children’s profound susceptibility to lead neurotoxicity and the disorders of higher brain function that follow [26, 36].

Canvas B: Reactive Oxygen Species

Another avenue of lead neurotoxicity is oxidative stress, a consequence of neuronal exposure to excessive harmful molecules, known as reactive oxygen species (ROS). ROS is a term generally used to describe free radicals, which are highly unstable compounds derived from oxygen (O2) [37]. They cause wear and tear on our cells, much like the rust build-up on a bicycle that causes its parts to deteriorate over time [37]. Our biological systems are equipped with the mechanisms needed to maintain a balance between free radicals and the ability to readily detoxify them; lead disturbs this balance in a process known as oxidative stress [21]. The development of ROS, such as hydroperoxide free radicals (HO2•), can result in lipid peroxidation, a process by which free radicals disrupt the integrity of neuronal plasma membranes [37]. This disruption causes neuronal apoptosis, or programmed cell death, leading to the aberrant destruction of otherwise healthy neurons [37]. Therefore, oxidative stress has the potential to induce brain damage, negatively impact healthy cognitive functions, and impair normal brain development, as evidenced by children across Baltimore [38]. Moreover, fetal exposure to ROS and subsequent oxidative stress can

lead to neonatal brain injury, a condition hallmarked by abnormal growth and loss of hippocampal interneurons. Hippocampal interneurons are known to be critical for functional plasticity, making it reasonable to infer that lead-inflicted damage to these neurons can hinder memory and learning [39, 40]. Such pathologies implicate the hippocampus as an especially sensitive brain region to lead-induced oxidative stress during the early years of development [39].

However, stressed cells typically have a potential lifeline: antioxidants. Antioxidants are important fighters against generated ROS and help maintain the body’s ability to readily detoxify and repair damage [21]. Their ability to chemically oppose free radicals manifests in two crucial ways: (1) by preventing the formation of ROS by chelating (metal trapping) lead in its molecular structure and (2) inactivating generated ROS, which prevents lead-induced oxidative stress and subsequent cellular damage. Some common antioxidants include vitamins, particularly B, C, and E, which have been found to be powerful fighters against toxicological outcomes of lead poisoning [21]. These vitamins have the magnificent ability to restore prooxidant-antioxidant homeostasis (balance against cell damage) in the brain, effectively decreasing oxidative stress. They can do this because of their ability to cross the blood-brain barrier through transport mechanisms, a unique feat that few large molecules can achieve [41–43].

The Final Layers of Lead

While we have traversed some of the most extensively studied mechanisms of lead poisoning, its neurotoxic effects extend beyond signaling disruption and oxidative stress [21]. This article sets forth a mere piece to a much larger puzzle that encompasses a variety of lead-induced neurotoxic pathways. Although the developing brain is the core target for lead in exposed children across Baltimore, once the heavy metal is absorbed and begins circulating throughout the body, it can have numerous effects on other biological systems, including the hematopoietic (blood production), renal (kidney), and cardiovascular systems [21]. Ultimately, these various modalities of lead poisoning serve as yet another setback within the overarching cycle of adversity and health inequality faced by Black newborns, children, and families living in historically segregated neighborhoods with homes coated in lead paint [44].

Lead neurotoxicity, an issue steeped in a history of racial injustice, inflicts silent harm on Baltimore’s Black and low-income youth populations by placing them at a heightened risk for worsened neurological health outcomes. Even at relatively low amounts, lead enters the brain, inducing oxidative stress and disrupting the neurochemical landscape [1, 21]. Lead contamination–in any amount–can result in cognitive deficits such as impaired learning and memory, difficulties concentrating, and lower IQ scores [26], which in turn can diminish academic performance. Such a significant setback for students who already face a scarcity of academic resources, such as fewer educational and career development opportunities, exacerbates the intertwined relationship between neurological health disparities and the broader perpetuation of socioeconomic and racial injustices [45]. All in all, these alarming disparities call for more proactive initiatives to dismantle the cycle of systemic racism and foster a healthier future for Baltimore’s marginalized youth.


1. Sanders, T., Liu, Y., Buchner, V., & Tchounwou, P. B. (2009). Neurotoxic Effects and Biomarkers of Lead Exposure: A Review. Reviews on environmental health, 24(1), 15–45.

2. Carmona, A., Roudeau, S., & Ortega, R. (2021). Molecular Mechanisms of Environmental Metal Neurotoxicity: A Focus on the Interactions of Metals with Synapse Structure and Function. Toxics, 9(9), 198.

3. Cory-Slechta, D. A. (1996). Legacy of Lead Exposure: Consequences for the Central Nervous System. Otolaryngology–Head and Neck Surgery, 114(2), 224–226.

4. Naranjo, V. I., Hendricks, M., & Jones, K. S. (2020). Lead Toxicity in Children: An Unremitting Public Health Problem. Pediatric Neurology, 113, 51–55.

5. Populations, N. R. C. (US) C. on M. L. in C. (1993). Biologic Markers of Lead Toxicity. In Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations. National Academies Press (US). Retrieved from

6. RÍsovÁ, V. (2019). The pathway of lead through the mother’s body to the child. Interdisciplinary Toxicology, 12(1), 1–6.

7. Perman, J. A. (n.d.). The Greatest Gap: Health Inequity in Baltimore.

8. Vilar-Compte, M., Burrola-Méndez, S., Lozano-Marrufo, A., Ferré-Eguiluz, I., Flores, D., Gaitán-Rossi, P., … Pérez-Escamilla, R. (2021). Urban poverty and nutrition challenges associated with accessibility to a healthy diet: a global systematic literature review. International Journal for Equity in Health, 20(1), 40.

9. Yu, X., Xiong, L., Zhao, S., Li, Z., Xiang, S., Cao, Y., … Qiu, J. (2023). Effect of lead, calcium, iron, zinc, copper and magnesium on anemia in children with BLLs ≥ 100 μg/L. Journal of Trace Elements in Medicine and Biology, 78, 127192.

10. Social Determinants of Health. (2018, August 26). Behavioral Health System Baltimore, Inc. Retrieved from

11. Huang, S. J., & Sehgal, N. J. (2022). Association of historic redlining and present-day health in Baltimore. PLoS ONE, 17(1), e0261028.

12. Center, C. (2021, December 3). Housing and Lead. ArcGIS StoryMaps. Retrieved October 20, 2023, from

13. Scrivener, L. (2022). Evaluating the Cost of Lead Hazard Control and Abatement in Baltimore City.

14. Baltimore, MD Program Information Lead | NCEH | CDC. (2023, June 7). Retrieved October 20, 2023, from

15. Barry-Jester, A. M. (2015, May 7). Baltimore’s Toxic Legacy Of Lead Paint. FiveThirtyEight. Retrieved from

16. Markowitz, G., & Rosner, D. (2013). Lead Wars: The Politics of Science and the Fate of America’s Children (1st ed.). University of California Press. Retrieved from

17. Overview of Childhood Lead Poisoning Prevention | Lead | CDC. (2023, January 19). Retrieved October 16, 2023, from

18. Gasana, J., Hlaing, W. M., Siegel, K. A., Chamorro, A., & Niyonsenga, T. (2006). Blood Lead Levels in Children and Environmental Lead Contamination in Miami Inner City, Florida. International Journal of Environmental Research and Public Health, 3(3), 228–234.

19. Rădulescu, A., & Lundgren, S. (2019). A pharmacokinetic model of lead absorption and calcium competitive dynamics. Scientific Reports, 9(1), 14225.

20. Lidsky, T. I., & Schneider, J. S. (2003). Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain, 126(1), 5–19.

21. Flora, G., Gupta, D., & Tiwari, A. (2012). Toxicity of lead: A review with recent updates. Interdisciplinary Toxicology, 5(2), 47–58.

22. Lawrence, J. M., Schardien, K., Wigdahl, B., & Nonnemacher, M. R. (2023). Roles of neuropathology-associated reactive astrocytes: a systematic review. Acta Neuropathologica Communications, 11, 42.

23. Yeter, D., Banks, E. C., & Aschner, M. (2020). Disparity in Risk Factor Severity for Early Childhood Blood Lead among Predominantly African-American Black Children: The 1999 to 2010 US NHANES. International Journal of Environmental Research and Public Health, 17(5), 1552.

24. Shallie, P. D., & Naicker, T. (2019). The placenta as a window to the brain: A review on the role of placental markers in prenatal programming of neurodevelopment. International Journal of Developmental Neuroscience, 73(1), 41–49.

25. Guilarte, T. R., & McGlothan, J. L. (1998). Hippocampal NMDA receptor mRNA undergoes subunit specific changes during developmental lead exposure. Brain Research, 790(1–2), 98–107.

26. Baranowska-Bosiacka, I., Gutowska, I., Rybicka, M., Nowacki, P., & Chlubek, D. (2012). Neurotoxicity of lead. Hypothetical molecular mechanisms of synaptic function disorders. Neurologia i Neurochirurgia Polska, 46(6), 569–578.

27. Simon, L. V., Hashmi, M. F., & Bragg, B. N. (2023). APGAR Score. In StatPearls. Treasure Island (FL): StatPearls Publishing. Retrieved from

28. Davis, J. M., & Svendsgaard, D. J. (1987). Lead and child development. Nature, 329(6137), 297–300.

29. Fahim, M. S., Fahim, Z., & Hall, D. G. (1976). Effects of subtoxic lead levels on pregnant women in the state of Missouri. Research Communications in Chemical Pathology and Pharmacology, 13(2), 309–331.

30. Basu, S. K., Pradhan, S., du Plessis, A. J., Ben-Ari, Y., & Limperopoulos, C. (2021). GABA and glutamate in the preterm neonatal brain: In-vivo measurement by magnetic resonance spectroscopy. NeuroImage, 238, 118215.

31. Miguel, P. M., Pereira, L. O., Silveira, P. P., & Meaney, M. J. (2019). Early environmental influences on the development of children’s brain structure and function. Developmental Medicine & Child Neurology, 61(10), 1127–1133.

32. Pal, M. M. (2021). Glutamate: The Master Neurotransmitter and Its Implications in Chronic Stress and Mood Disorders. Frontiers in Human Neuroscience, 15, 722323.

33. Jewett, C. (2023, January 26). How Do Heavy Metals Like Lead Get in Baby Food? The New York Times. Retrieved from

34. Büsselberg, D., Michael, D., & Platt, B. (1994). Pb2+ reduces voltage- and N-methyl-D-aspartate (NMDA)-activated calcium channel currents. Cellular and Molecular Neurobiology, 14(6), 711–722.

35. Guilarte, T. R., Miceli, R. C., & Jett, D. A. (1995). Biochemical evidence of an interaction of lead at the zinc allosteric sites of the NMDA receptor complex: effects of neuronal development. Neurotoxicology, 16(1), 63–71.

36. Cui, Z., Feng, R., Jacobs, S., Duan, Y., Wang, H., Cao, X., & Tsien, J. Z. (2013). Increased NR2A:NR2B ratio compresses long-term depression range and constrains long-term memory. Scientific Reports, 3(1), 1036.

37. Lopes, A. C. B. A., Peixe, T. S., Mesas, A. E., & Paoliello, M. M. B. (2016). Lead Exposure and Oxidative Stress: A Systematic Review. Reviews of Environmental Contamination and Toxicology, 236, 193–238.

38. Salim, S. (2017). Oxidative Stress and the Central Nervous System. The Journal of Pharmacology and Experimental Therapeutics, 360(1), 201–205.

39. Abbah, J., Vacher, C.-M., Goldstein, E. Z., Li, Z., Kundu, S., Talbot, B., … Gallo, V. (2022). Oxidative Stress-Induced Damage to the Developing Hippocampus Is Mediated by GSK3β. The Journal of Neuroscience, 42(24), 4812–4827.

40. Liguz-Lecznar, M., Urban-Ciecko, J., & Kossut, M. (2016). Somatostatin and Somatostatin-Containing Neurons in Shaping Neuronal Activity and Plasticity. Frontiers in Neural Circuits, 10, 48.

41. Aragón-González, A., Shaw, P. J., & Ferraiuolo, L. (2022). Blood–Brain Barrier Disruption and Its Involvement in Neurodevelopmental and Neurodegenerative Disorders. International Journal of Molecular Sciences, 23(23), 15271.

42. Banks, W. A. (2009). Characteristics of compounds that cross the blood-brain barrier. BMC Neurology, 9(1), S3.

43. Lee, P., & Ulatowski, L. M. (2019). Vitamin E: Mechanism of transport and regulation in the CNS. IUBMB life, 71(4), 424–429.

44. Racial segregation makes consequences of lead exposure worse. (2022, August 30). National Institutes of Health (NIH). Retrieved November 19, 2023, from

45. Noguera, P. A. (2017). Introduction to “Racial Inequality and Education: Patterns and Prospects for the Future.” The Educational Forum, 81(2), 129–135.

32 views0 comments

Recent Posts

See All


bottom of page