The Flint Water Crisis

Writer: Mihir Sekhar

Introduction

On April 25, 2014, the city of Flint, Michigan decided to switch their municipal water supply from Detroit’s Lake Huron to the Flint River [1]. Intended as a bold cost-saving measure to ease Flint’s financial struggles, this decision instead triggered one of the most devastating public health disasters of the 21st century.

History: Financial Hardships and the Water Switch

The tale of Flint, Michigan starts in the 1900s. As the birthplace of General Motors, the city quickly developed to meet the growing expectations and demands of the automobile boom [2]. Over a span of 80 years, the city experienced a long period of prosperity, growing to a population of over 200,000.

Flint’s prosperity, however, began to unravel as the automobile industry declined. As a result of rising oil prices and imports, workers experienced mass layoffs – decreasing the city’s population to 100,000, with ⅓ of Flint residents living below the poverty line [3]. By the 2000s, the city’s shrinking tax base and deepening poverty pushed local leaders to seek desperate financial solutions – one of which would change the city forever.

In 2011, Flint fell under state control. In 2014, to combat the financial crisis, a state-appointed emergency manager made the decision to switch Flint’s drinking water source to the Flint River, with the goal of saving the city $5 million over 2 years until a newly constructed, cost-saving pipeline was built [4]. The problem: Flint River water was highly contaminated and corrosive, and required proper treatment before distribution [5]. City officials had failed to add anti-corrosive chemicals into the water supply. This failure triggered a public health disaster as lead from aging pipes leached into the city’s drinking water.

Water Crisis: Overlapping Contamination Crises

The change in water quality was noticed almost immediately: residents reported foul tasting, discolored water to city officials. However, despite repeated concerns over the water, officials continued to maintain that the water was safe. Between April 2014 and October 2015, thousands of Flint residents were exposed to dangerous lead levels in their drinking water, with kids being the most at risk for sickness and adverse health effects [6].

Without proper corrosion control, the Flint River water stripped away layers from the old pipes, allowing toxic metals to leach into the drinking water [7]. A study conducted by researchers at Virginia Tech analyzed water samples collected from 252 homes. They found that roughly 17 percent of samples registered above the EPA’s accepted standards of 15 parts per billion (ppb), with over 40 percent of samples measuring above 5 ppb, which the researchers considered indicative of a major health problem [8].

Another study by Dr. Mona Hanna-Attisha, a Flint pediatrician, found that the number of children with elevated blood-lead levels had doubled since the switch to the Flint River water supply [9]. The health harms were significant: lead is highly dangerous to children, causing development delays, intellectual disabilities, and behavioral problems [10].

Compounding this crisis, low chlorine levels in the water supply resulted in an outbreak of Legionnaire's disease (a severe form of pneumonia), killing 12 residents and sickening over 87 people – the 3rd-largest outbreak of the disease in US history [11]. In response, officials increased the use of chlorine for water treatment, creating a new problem: high levels of total trihalomethanes (TTHMs) – chemical byproducts of chlorine that can cause cancer with prolonged exposure. Flint was now facing multiple overlapping contamination crises.

Impacts: State of Emergency and the Flint Recovery Plan

On January 5, 2016, Michigan Governor Rick Snyder declared a state of emergency in Flint [12]. President Barack Obama quickly followed up, declaring a federal emergency and allowing federal agencies to step in to supplement local and state efforts.

In response to the Flint Water Crisis, the federal government launched a comprehensive recovery plan comprising four key areas: safe water access, public health, infrastructure repair, and economic recovery. The Federal Emergency Management Agency (FEMA) distributed safe drinking water (bottled water, water filters), working in tandem with the US Department of Housing and Urban Development (HUD) which installed and maintained filters in public housing. The Department of Health and Human Services (HHS) expanded Medicaid coverage for children and pregnant women, funded local clinics, and coordinated lead testing for affected families. The Environmental Protection Agency (EPA) led long-term restoration efforts, conducting extensive testing and awarding over $100 million in grants to upgrade Flint’s water infrastructure. Other federal agencies offered nutritional assistance and social services to help decrease the effects of lead exposure and support residents during recovery [13].

On May 19, 2025, 9 years after issuing a state of emergency, the EPA lifted the Safe Drinking Water Act emergency order, marking an end to the water crisis [14].

Conclusion

The story of Flint, Michigan is powerful. It shows how financial struggles and governmental oversight led to one of the most devastating public health disasters of this century. The crisis exposed thousands of residents to toxic lead, along with countless other health harms resulting from drinking water contamination. Although progress has been made and Flint’s water system is now considered safe, the lasting effects on residents’ health and trust in government remain.

References:

[1] Centers for Disease Control and Prevention. Story: Flint water crisis. https://www.cdc.gov/casper/php/publications-links/flint-water-crisis.html

[2] A 20-year review of Flint finances shows consequences of lack of investment. https://fordschool.umich.edu/news/2022/20-year-review-flint-finances-shows-consequences-lack-investment

[3]Flint water crisis: Everything you need to know.https://www.nrdc.org/stories/flint-water-crisis-everything-you-need-know

[4] Board, D. F. P. E. (2024). 10 years after Flint water crisis began, emergency manager law must change. Detroit Free Press. https://www.freep.com/story/opinion/editorials/2024/04/25/flint-water-crisis-anniversary-michigan-emergency-manager-law/73423174007/

[5] Joy Crelin. Flint water crisis: Overview. EBSCO. https://www.ebsco.com/research-starters/environmental-sciences/flint-water-crisis-overview

[6] Runwal, P. (2025). 10 years on, Flint still faces consequences from the water crisis. Chemical & Engineering News. https://cen.acs.org/environment/water/10-years-Flint-Michigan-still-faces-consequences/102/i14

[7] Pieper, K. J., Tang, M., & Edwards, M. A. (2017). Flint Water Crisis Caused By Interrupted Corrosion Control. ACS Publications. https://pubs.acs.org/doi/10.1021/acs.est.6b04034

[8] Kennedy, M. (2016). Lead-laced water in Flint: A step-by-step look at the makings of a crisis. NPR. https://www.npr.org/sections/thetwo-way/2016/04/20/465545378/lead-laced-water-in-flint-a-step-by-step-look-at-the-makings-of-a-crisis

[9] U.S. Department of Health and Human Services. (2021). Pediatrician who uncovered Flint water crisis recounts experience. NIH. https://nihrecord.nih.gov/2021/04/30/pediatrician-who-uncovered-flint-water-crisis-recounts-experience

[10] World Health Organization. Lead poisoning.https://www.who.int/news-room/fact-sheets/detail/lead-poisoning-and-health

[11]Was Flint’s deadly Legionnaires’ epidemic caused by low chlorine levels in the water supply? AAAS. https://www.science.org/content/article/was-flint-s-deadly-legionnaires-epidemic-caused-low-chlorine-levels-water-supply

[12] Gov. Snyder declares emergency for Genesee County. State of Michigan. https://www.michigan.gov/formergovernors/recent/snyder/press-releases/2016/01/05/gov-snyder-declares-emergency-for-genesee-county

[13] National Archives and Records Administration. Fact sheet: Federal support for the Flint Water Crisis Response and Recovery.https://obamawhitehouse.archives.gov/the-press-office/2016/05/03/fact-sheet-federal-support-Flint-water-crisis-response-and-recovery

[14] Environmental Protection Agency. EPA lifts 2016 emergency order on drinking water in Flint, Michigan.https://www.epa.gov/newsreleases/epa-lifts-2016-emergency-order-drinking-water-flint-michigan

Cut, Paste, Prompt: How AI Can Help Rewrite Life Itself

Writer: Sandra Alb

Can a robot write a symphony? Can a robot turn a canvas into a beautiful masterpiece?” Will Smith’s character asks an artificial intelligence (AI)-powered robot in the movie I, Robot. The answer might still be no for now, but as of July 2025, AI can rewrite our genome. Dr. Le Cong’s team at Stanford Medicine has published a new large language model (LLM) called CRISPR-GPT, which is designed to aid in planning and executing CRISPR-Cas9 genome editing experiments.

This technology is very similar to the more familiar ChatGPT, using the same “chat” prompting format to allow for human-AI collaboration in three modes: beginner, expert, and Q&A [1]. According to Cong, the goals of this technology are to reduce the trial and error associated with CRISPR-Cas9 gene editing and to minimize any adverse effects that may occur due to genomic manipulation. CRISPR-Cas9 makes genomic edits by using an RNA guide (gRNA) that matches a specific DNA sequence as a GPS signal to lead the Cas9 enzyme to the exact spot in the genome. Cas9 then cuts both strands of the DNA (forming double-stranded breaks, or DSBs), causing the cell’s natural repair machinery to kick in. It either patches up the break with insertion/deletion or adds a supplied template to make precise edits. This system allows scientists to remove, add, or change stretches of DNA in a controlled way [3]. AI deep learning models like inDelphi have already been used to ensure that DSB repair mechanisms proceed without error but CRISPR-GPT takes a much more AI-involved role in prompted gene editing. CRISPR-GPT is only a part of a larger shift toward using AI for precision in gene editing. Deep learning models can predict gRNA efficiency and editing outcomes, though inconsistent datasets and the lack of standard evaluation methods still limit progress [4].

While this new form of gene editing is exciting and holds the promise of curing countless diseases such as hereditary diseases, genetic disorders, potentially cancers and more, it also raises profound ethical questions. An AI companion like CRISPR-GPT would not only assist researchers in editing genes but could also, in theory, design and execute experiments far beyond human oversight. To address risks of AI misuse, Dr. Le Cong and his team have built safeguards into the system [2]. If CRISPR-GPT is prompted to engage in unethical activities, such as editing human embryos or enhancing viruses, it is programmed to issue a warning and respond with an error message, halting the interaction [2]. However, these measures introduce a deeper dilemma: what happens if someone alters the AI’s parameters or bypasses its restrictions? And more importantly, who gets to decide what counts as “ethical” in the first place? As AI systems become more autonomous and integrated into biological research, the line between innovation and interference grows thinner. Moving forward, a considerable challenge will be to ensure that technologies like CRISPR-GPT remain tools for healing, not harming, and that our ethical frameworks evolve as fast as the algorithms guiding them.

CRISPR-GPT is a powerful fusion of AI and biotechnology that could redefine how we approach genetic medicine. With such power comes an equally great responsibility to ensure these tools are guided by rigorous ethics. Now, as we stand at the intersection of code and creation, the question is no longer what AI can do, but what we should allow it to do.

References:

[1] Qu Y, Huang K, Yin M, et al. CRISPR-GPT for agentic automation of gene-editing experiments. Nat Biomed Eng. 2025. doi:10.1038/s41551-025-01463-Z
[2] Kay C. AI-powered CRISPR could lead to faster gene therapies, Stanford Medicine study finds. Stanford Medicine. September 16, 2025. Accessed October 17, 2025. https://med.stanford.edu/news/all-news/2025/09/ai-crispr-gene-therapy.html
[3] Asmamaw M, Zawdie B. Mechanism and applications of CRISPR/Cas-9-mediated genome editing. Biologics (Targets & Therapy). 2021;15:353–361. doi:10.2147/BTT.S326422
[4] Naert T, Yamamoto T, Han S, et al. Precise, predictable genome integrations by deep-learning-assisted design of microhomology-based templates. Nat Biotechnol. 2025. doi:10.1038/s41587-025-02771-0

The Double-Edged Nature of Prions

One of the most gut-wrenching yet addictingly intriguing games I played growing up was Mafia. Sitting around a circle, discussing and debating the culprit…only for it to be the one person you thought was the healer!

The stealth and deception involved across the game reflect much more. Within our bodies, we see this play at a much larger scale across the immune system, manifesting as fevers, allergies, and other diseases. One prominent disease that often slips past our immune defenders, however, is prions. Our most secretive yet deadly macromolecules, prions, have the potential for immense harm but also surprising benefit.

But what exactly are they? Prions are a series of proteins that have become misfolded in a way that allows them to self-replicate, becoming independent of the cells in which they reside. They can be classified into three forms: prion proteins, responsible for forming prions, transcellular prionoids, misfolded proteins that aggregate through cell-cell interactions, and quasi-prions, anomalies in between prions and transcellular prionoids¹. Unlike viruses, bacteria, or even cells, prions are devoid of genetic material within their structure, with a mechanism of replication that varies based on how they have been misfolded. For instance, research on prions within the brain has shown that changes in electric charge may cause prion fibril elongation, leading the proteins to propagate and aggregate².

This aggregation mechanism often goes unnoticed by the immune system. As a biologically derived molecule, the prions are not viewed as foreign or antigenic by most immune cells. The most deadly is the neurodegenerative Creutzfeldt-Jakob disease (CJD), caused by overproduction of the prion protein, encompassing 85% of prion-disease forms in humans³. Variants of CJD spread dramatically due to mutation heritability and exposure to diseased tissue. In 1986, mad cow disease, a CJD that originated in cattle, spread to humans that ingested the meat, and was only controlled once infected herds were no longer consumed⁴. At a molecular level, it appeared that the abnormal prions in cattle were somehow modifying human prion development, indicating conserved mechanisms across species.

Prion disease manifestation can vary from person to person. CJD, for example, exhibits symptoms similar to many prevalent neurodegenerative diseases, making it hard to trace. Causing severe symptoms from confusion and dementia or hallucinations, the severe ailments that follow CJD still have very few treatment options⁵. Recent efforts have utilized a biotechnological approach to treating the disease, using tools such as gene editing with CRISPR-based tools, synthetic molecules and antibodies, and disinfectants⁶.

Like all biological phenomena, prions may have evolved to have unexpected positive effects. Due to their heritable nature, prions have the potential to pass on beneficial traits. A 2016 study at Stanford University found 46 prions in yeast cells that could improve the cell’s resistance to antifungals and heat⁷. With looser formations than their disease-causing counterparts, as well as a better affinity to DNA, these prions are more adaptable, ensuring better fitness of the cells containing these prions. Others like the CPEB prion-like proteins in the common fruit fly, Drosophila, have also shown potential to improve memory⁸.

For now, the legacy of prions in humans remains bleak. But could there be benefits to their existence? And, if we understand more prion-growth mechanisms, we might just alter our fundamental understanding of biology. This game of Mafia has just begun!

References

1. Harbi D, Harrison PM. ­Classifying prion and prion-like phenomena. Prion. 2014;8(2):161-165. doi:10.4161/pri.27960

2. UCL. Study reveals new detail on how prions replicate in neuronal cells. Brain Sciences. December 20, 2023. Accessed March 3, 2025. https://www.ucl.ac.uk/brain-sciences/news/2023/dec/study-reveals-new-detail-how-prions-replicate-neuronal-cells

3. Ritchie DL, Peden AH, Barria MA. Variant CJD: Reflections a Quarter of a Century on. Pathogens. 2021;10(11):1413. doi:10.3390/pathogens10111413

4. CDC. Bovine Spongiform Encephalopathy (BSE). Bovine Spongiform Encephalopathy (BSE). May 10, 2024. Accessed March 3, 2025. https://www.cdc.gov/mad-cow/php/animal-health/index.html

5. Prion Diseases. February 28, 2025. Accessed March 3, 2025. https://www.hopkinsmedicine.org/health/conditions-and-diseases/prion-diseases

6. Therapeutic Approaches for Prion Diseases | NIAID: National Institute of Allergy and Infectious Diseases. October 21, 2019. Accessed March 3, 2025. https://www.niaid.nih.gov/diseases-conditions/prion-therapeutic-approaches

7. Prions can pass on beneficial traits, study finds. News Center. Accessed March 3, 2025. https://med.stanford.edu/news/all-news/2016/10/prions-can-pass-on-beneficial-traits-study-finds.html

8.Prions: What Are They Good For? | Annual Reviews. Accessed March 3, 2025. https://www-annualreviews-org.ezproxy.rice.edu/content/journals/10.1146/annurev-cellbio-100913-013409#right-ref-B101

From Lizards to Mammals: Unraveling the Science Behind Cell Regeneration

Have you ever seen a lizard regrow its tail? What if people had this ability to regrow a lost limb or organ? In the animal kingdom, anamniotes—fish and amphibians that lay eggs in aquatic environments—such as salamanders and zebrafish, have extensive regenerative properties. The axolotl is the first model for regenerative studies and has been studied since the 1860s for its ability to restore limbs, tails, eyes, and hearts [1]. Zebrafish are even capable of regenerating their brains. Lizards, on the other hand, are part of a vertebrate group known as amniotes. Amniotes include reptiles, birds, and mammals that reproduce on dryland. Surprisingly, lizards are the only amniotes capable of cell regeneration and are the closest relatives of humans that can regrow tissue [5]. They regrow their tails through autonomy, an anti-predation strategy that utilizes cell regeneration to restore damaged and lost tissue [2]. Understanding this regenerative process could be essential for regenerative medicine and treating neurological disorders.

How is regeneration possible? Neurogenesis is a process integral to tail regeneration. Neurons are generated from neural stem cells in the adult brain to add to or replace neurons in pre-existing circuits [3]. It occurs in the telencephalon, the part of the brain responsible for higher-level functions such as thinking, memory, and processing sensory information. Adult neurogenesis occurs in all vertebrate groups, including humans, but has more extensive effects in non-mammalian groups [3]. For example, neurogenesis in lizards produces more neurons and impacts more parts of the brain. In mammals, it is restricted to olfactory bulbs and the hippocampal dentate gyrus, the regions of the brain responsible for sense of smell and processing sensory information. This limitation means that while neurons are replaced in these areas, other parts of the brain are still susceptible to damage and deterioration.

Current hypotheses suggest that regeneration is a trait that occurred early in evolution, as it is most commonly found in lower-level organisms. Higher-level organisms, like humans and other mammals, evolved to have more robust immune systems with defensive macrophages— white blood cells responsible for detecting and breaking down viruses and bacteria—at the expense of regenerative capabilities [1]. These strong immune systems dispose of viral and bacterial tissue, whereas lizards and anamniotes rely on non-immune mechanisms to avoid infection [5]. Baffling to researchers, although macrophages regulate the regeneration process, macrophage depletion in salamanders and zebrafish leads to delayed or altogether halted regeneration [5].

Harnessing this ability in humans would revolutionize research and healthcare. Researchers are working to leverage the unique regenerative capabilities of lizards as a model to transform the field of regenerative medicine. They use the lizard model to reprogram somatic cells—cells found in mammals that repair or replace damaged or aging tissue—toward a multipotent state, in which they become specialized for various tissues and functions [1]. This would mean that, on a small scale, humans could restore damaged or lost tissue. Advancements in studying neurogenesis could significantly impact regenerative medicine, neuroscience, and the treatment of neurological disorders. This progress would revolutionize the future of medicine, changing the landscape for disease and disorder treatment.

References

Daponte, V., Tylzanowski, P., & Forlino, A. (2021). Appendage Regeneration in Vertebrates: What Makes This Possible? Cells, 10(2), 242. https://doi.org/10.3390/cells10020242. Most helpful connection to biomedicine.

Donato, S. V., & Vickaryous, M. K. (2022). Radial Glia and Neuronal-like Ependymal Cells Are Present within the Spinal Cord of the Trunk (Body) in the Leopard Gecko (Eublepharis macularius). Journal of Developmental Biology, 10(2), 21. https://doi.org/10.3390/jdb10020021

González-Granero, S., Font, E., Desfilis, E., Herranz-Pérez, V., & José Manuel García‐Verdugo. (2023). Adult neurogenesis in the telencephalon of the lizard Podarcis liolepis. Frontiers in Neuroscience, 17. https://doi.org/10.3389/fnins.2023.1125999

Hye Ryeong Kim, Choi, H., Soon Yong Park, Song, Y., Kim, J.-H., Shim, S.-I., Jun, W., Kim, K., Han, J., Chi, S., Sun‐Hee Leem, & Jin Woong Chung. (2022). Endoplasmin regulates differentiation of tonsil-derived mesenchymal stem cells into chondrocytes through ERK signaling. Journal of Biochemistry and Molecular Biology, 55(5), 226–231. https://doi.org/10.5483/bmbrep.2022.55.5.173

Londono, R., Tighe, S., Milnes, B., DeMoya, C., Quijano, L. M., Hudnall, M. L., Nguyen, J., Tran, E., Badylak, S., & Lozito, T. P. (2020). Single cell sequencing analysis of lizard phagocytic cell populations and their role in tail regeneration. Journal of Immunology and Regenerative Medicine, 8, 100029. https://doi.org/10.1016/j.regen.2020.100029

Epigenetics: The Hidden Key To Development

Have you ever wondered why your parents have different colored eyes than you, or why you and your sibling don’t look alike? The answer may lie in one simple yet complicated term: epigenetics. Epigenetics is defined as the “study of heritable changes in gene expression that do not involve modification to the underlying DNA sequence” [1]. To put it in simpler terms, it’s how certain molecular modifications alter the way genes, such as those determining eye color, are expressed. There are a multitude of factors that determine how certain genes are expressed, but these epigenetic patterns begin in fetuses during pregnancy. 

To understand the factors that affect a fetus, we need to first understand the mechanism behind epigenetics. Firstly, gene expression is regulated by the modification of nucleosomes. A nucleosome is essentially elongated and uncoiled DNA that is wrapped around a set of proteins called histones [2]. While DNA carries a negative charge, histones generally carry a positive charge; like magnets, the negatively charged DNA molecules are attracted to the positively charged histones, and the degree of attraction regulates gene expressions. Modifications often affect how tight the DNA is wrapped around the histones [2]. One common modification is DNA methylation, in which a special molecule called methyl is added to the histones, which affects how tightly DNA is wrapped around the histones [2]. The increased attraction causes DNA to tightly coil around the histones, creating heterochromatin – tightly packed DNA — which prevents gene expression [2].   

Now, let's take a look at how these molecular processes apply to pregnancy. According to a study by Andrawus and peers, the patterns for DNA methylation in a fetus are established during pregnancy [3]. Furthermore, environmental factors during a pregnancy also play a role in epigenetics [3]. Two notable environmental factors that affect gene expression are pollution and nutrition. Pregnant mothers living in areas with increased air pollution “have been reported to show decreased DNA methylation” in a gene called LINE-1 [4]. Studies have shown that decreased methylation of LINE-1 is a common contributor to cancer and its development [5]. Furthermore, changes to maternal nutrition can lead to physical and mental changes in development [1]. According to Zuccarello and peers, vitamin B12 intake during pregnancy affects the methylation of DNA, and“high levels of vitamin B12 in maternal blood was correlated with the reduction” of DNA methylation of the fetus [1]. Such high levels of vitamin B12, and the corresponding decrease in DNA methylation levels, can result in potential intrauterine growth, which means that the fetus does not grow to a healthy weight as expected [1].

Overall, epigenetic expression during pregnancy plays an important role in our physical traits, as well as our overall well being. Both pollution and nutrition play a role in affecting DNA methylation patterns throughout development, which can affect the health of the child. Ensuring that pregnant women are in clean environments with access to correct nutrition allows them to sustain a healthy pregnancy and birth a healthy child.

References:

Zuccarello, D., Sorrentino, U., Brasson, V., Marin, L., Piccolo, C., Capalbo, A., Andrisani, A., & Cassina, M. (2022). Epigenetics of pregnancy: Looking beyond the DNA code. Journal of Assisted Reproduction and Genetics, 39(4), 801–816. https://doi.org/10.1007/s10815-022-02451-x

Al Aboud, N. M., Tupper, C., & Jialal, I. (2023). Genetics, Epigenetic Mechanism. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK532999/

Andrawus, M., Sharvit, L., & Atzmon, G. (2022). Epigenetics and Pregnancy: Conditional Snapshot or Rolling Event. International Journal of Molecular Sciences, 23(20), 12698. https://doi.org/10.3390/ijms232012698

Li, S., Chen, M., Li, Y., & Tollefsbol, T. O. (2019). Prenatal epigenetics diets play protective roles against environmental pollution. Clinical Epigenetics, 11(1), 82. https://doi.org/10.1186/s13148-019-0659-4

Phokaew, C., Kowudtitham, S., Subbalekha, K., Shuangshoti, S., & Mutirangura, A. (2008). LINE-1 methylation patterns of different loci in normal and cancerous cells. Nucleic Acids Research, 36(17), 5704–5712. https://doi.org/10.1093/nar/gkn571