Nearly 300 studies link the common pesticide chlorpyrifos to multi-organ damage, DNA disruption, and chronic disease 

Scientists tie chlorpyrifos to brain, liver, endocrine, and genetic damage, including at doses below current safety standards

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A small child eating canned peaches

Key findings:

For decades, regulators viewed chlorpyrifos — a pesticide widely used in the U.S. and around the world — primarily as a neurotoxin that disrupts signaling in the brain and nervous system. But as the EPA reconsiders whether to continue to allow its use on foods like apples and soybeans, a new review indicates other, more insidious harms.

Published in April [2026] in the International Journal of Molecular Sciences, the review synthesizes findings from nearly 300 studies worldwide published up to this year. These include laboratory experiments, animal studies, epidemiological research, regulatory documents, and risk assessments.

Growing evidence suggests chlorpyrifos may damage the brain, hormones, liver, gut microbiome, muscles, reproductive organs, and bones. Studies also link the pesticide to DNA damage and lasting changes in gene activity that may increase the risk of chronic disease.

Together, the findings portray chlorpyrifos as what the reviewers call a “multi-system toxicant” that poses a more significant threat to public health than previously understood. It suggests the pesticide acts on the body in ways far beyond disrupted nerve signaling or obvious poisoning. Pregnancy and early childhood are especially sensitive periods for chemical exposure.

“What has genuinely evolved over time is our understanding that chlorpyrifos causes harm in ways that go beyond its effects on the nervous system including damage to DNA, changes in how genes are switched on or off, interference with hormones, and disruption of the healthy bacteria that live in the gut,” said Dr. Dana Boyd Barr, a professor at Emory University’s Rollins School of Public Health and past president of the International Society of Exposure Science.

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The authors warn that current regulatory systems may not fully capture the complexity of chlorpyrifos’ dangers to the body. Many occur at levels too low to be detected by current safety testing, which looks for the disruption of an enzyme involved in nerve cell communication. 

The review links chlorpyrifos exposure to:

Industry pushback despite reported harms

The review comes as the EPA reassesses whether the pesticide’s remaining uses meet the statutory standard of “no unreasonable adverse effects.” The action follows years of official stalling, prior bans, policy reversals, and legal challenges. 

Meanwhile, agrichemical companies are lobbying federal and state lawmakers to shield pesticide manufacturers, including Bayer and its subsidiary Monsanto, from some lawsuits involving Roundup weedkiller. The suits allege their products cause non-Hodgkin lymphoma (NHL), among other cancers.  

In February 2020, Corteva Agriscience—then the world’s largest producer of chlorpyrifos — announced it would stop production, citing declining demand. But existing stocks continued to be used. The chemical remains approved for several major crops in the U.S., including apples, strawberries, soybeans, citrus, wheat and peaches.

Health concerns trigger restrictions and bans 

Chlorpyrifos — the active ingredient in Dursban® and Lorsban® — belongs to a class of chemicals known as organophosphates. Introduced in the U.S. in 1965, chlorpyrifos became one of the world’s most heavily used insecticides by the 1990s. 

Farmers use chlorpyrifos to control ticks on cattle and pests on crops. It is used on golf courses, in greenhouses, on wood products such as telephone poles, and in residential areas.

Chlorpyrifos poses a significant neurotoxic risk to humans, with developing fetuses and children being particularly vulnerable.

U.S. regulators banned chlorpyrifos for household use in 2001. The ban came after mounting evidence, including a prominent study by Columbia University, linked exposure to developmental brain harms in children.

Evidence that chlorpyrifos damages children’s brains later prompted bans or restrictions in more than 40 countries, including the European Union. The European Food Safety Authority concluded there was no safe exposure level, but it is still widely used elsewhere in the world. Several U.S. states, including California, New York, Hawaii, Oregon and Maryland, currently maintain restrictions or bans.

Yet chlorpyrifos persists in food (including fruits, cereals, and vegetables), the environment, and human tissue. The compound dissolves easily in fats and crosses cell membranes, allowing it to accumulate in tissues over time.

It can also travel long distances — in some cases more than 600 miles — from where it was applied. Researchers have detected residues in food, drinking water, soil, rain, snow, and wildlife. Samples range from the Mississippi River to remote Antarctica.

Children, pregnant women, farm workers face the highest risks

Health effects of chlorpyrifos depend on dose, duration, and route of exposure, the reviewers say. Genetic differences may also influence vulnerability.

For most people, exposure occurs through contaminated food, water, and air. Farmworkers often face the highest exposure levels. But researchers say chronic low-level exposure during pregnancy and childhood may also carry risks.

Infants and children remain especially vulnerable because their detoxification systems are still developing. They also consume more food relative to body weight and frequently put their hands in their mouths.

Chlorpyrifos risks extend beyond nerve damage

For years, scientists and regulators focused on one primary mechanism of harm. Chlorpyrifos becomes more toxic after the body converts it into a compound called chlorpyrifos-oxon. This blocks acetylcholinesterase (AChE), the enzyme that breaks down acetylcholine in the nervous system.

Acetylcholine is a neurotransmitter essential for communication between nerve cells. It also helps regulate attention, learning, memory, movement, breathing, and heart rate.

Without acetylcholinesterase, nerves fire uncontrollably. In insects, the effect causes paralysis and death. In humans, severe poisoning can cause seizures, respiratory failure, or death.

That effect on the single enzyme still matters. But the review argues it no longer explains the full scope of chlorpyrifos toxicity.

Chlorpyrifos affects the nervous system not only by blocking AChE activity, its well-known toxic mechanism, but also by disrupting fat balance in cells and interfering with other cell signaling pathways. These additional effects may worsen its harmful impacts on the brain and nervous system.

Chlorpyrifos is linked to cell damage throughout the body

Instead, researchers describe evidence that the pesticide may trigger widespread biological stress across organs and tissues. Studies point to several possible mechanisms, including inflammation and oxidative stress, when highly reactive oxygen-containing molecules build up, damage cells, and weaken the body’s defenses. Other ways include hormone disruption and altered gene regulation.

Chlorpyrifos may be especially harmful to mitochondria, the structures inside cells that produce most of the body’s energy. Damaged mitochondria can leak harmful, highly reactive molecules (mtROS) that can damage DNA, proteins, and cell structures.

The review also highlights how chlorpyrifos may cause genes to switch on and off. Scientists increasingly believe these changes may help explain how environmental exposures contribute to chronic disease years after exposure occurs.

“While traditionally characterized by its potent acetylcholinesterase-inhibitory properties, accumulating evidence now shows that chlorpyrifos and its bioactive metabolite, chlorpyrifos-oxon (CPO), exert far broader toxic effects, including the induction of oxidative stress, enhancement of neuroinflammatory processes, and the triggering of persistent epigenetic alterations,” the authors wrote.

Babies and children are more susceptible to chlorpyrifos harms

The American Academy of Pediatrics warns that chlorpyrifos exposure poses risks to fetuses, infants, children, and pregnant women. Chlorpyrifos crosses the placenta and injures the developing nervous system before birth.

“Chlorpyrifos poses a significant neurotoxic risk to humans, with developing fetuses and children being particularly vulnerable,” they wrote. “Neurotoxic effects of the pesticide have been observed even at low doses.”

The body’s defenses against chlorpyrifos also depend heavily on an enzyme called paraoxonase-1 (PON1) that helps break it down. But PON1 activity varies widely among individuals due to genetics and age.

Infants and young children naturally have lower levels. This may also increase their susceptibility to toxicity, the authors say.

Prenatal exposure linked to lasting brain damage and lower IQ

Human studies link prenatal chlorpyrifos exposure to:

For instance, an August 2025 study of New York City children found that prenatal exposure to chlorpyrifos was linked to widespread brain abnormalities and weaker motor skills years later. The researchers concluded prenatal exposure may cause lasting brain disruptions. The effects appeared to worsen with higher exposure.

What emerges is a troubling picture: the developing brain is being shaped by a toxic soup of chemicals acting on the same parts of the brain.

Meanwhile, animal studies show that chlorpyrifos disrupts nerve cell growth and alters brain signaling tied to learning and memory. It also damages connections between neurons during critical developmental periods, studies suggest. 

Perhaps most striking, chlorpyrifos appears in these studies to suppress brain-derived neurotrophic factor (BDNF). BPA, flame retardants, and other toxic chemicals also disrupt BDNF, which Dr. Bruce Lanphear describes as “fertilizer for the brain.” 

Brain-derived neurotrophic factor helps neurons survive and form synapses. It also helps them strengthen learning pathways and recover from injury.

“What emerges is a troubling picture: the developing brain is being shaped by a toxic soup of chemicals acting on the same parts of the brain,” said Lanphear, a preventive medicine physician and professor at Vancouver’s Simon Fraser University who studies how toxic chemicals impact human health. “Yet when the EPA evaluates chlorpyrifos, it largely considers the pesticide on its own—not alongside other chemicals that disrupt the same brain pathways.”

The ways chlorpyrifos affects the body may contribute to the growth and rate of liver, breast, and ovarian tumors, studies indicate. One large 2015 study of more than 30,000 women—spouses of pesticide applicators—linked chlorpyrifos exposure to elevated breast cancer risk. While human evidence remains limited and inconsistent, the reviewers say, the combination of effects warrants closer investigation.

Additionally, 3D laboratory models suggest that chlorpyrifos may cause breast cancer cells to invade nearby tissues more actively. Epidemiological studies also report associations with hormone-related cancers, particularly more aggressive forms of hormone receptor-negative breast cancer. 

Animal studies done in living organisms also indicate that long-term, low-dose exposure to chlorpyrifos increases the risk of breast cancer, the reviewers say. The pesticide can make tumors appear sooner and increase their number, likely due to hormone disruption.

Parkinson’s, memory loss and other neurological impacts

The review cites evidence linking chlorpyrifos exposure to movement problems, memory impairment, anxiety-like behaviors, and damage to brain regions involved in emotion and cognition. One recent study reports that chlorpyrifos exposure may be associated with more than double the risk of Parkinson’s disease.

Researchers say chlorpyrifos-oxon (CPO) — produced when the body breaks down chlorpyrifos — may be especially dangerous. According to federal researchers, chlorpyrifos-oxon is about 1,000 times more toxic than chlorpyrifos itself.

Laboratory research indicates CPO may disrupt pathways tied to learning, memory, inflammation, and nerve cell survival. Studies also suggest that chlorpyrifos-oxon damages a structural protein called tubulin, potentially disrupting brain development. Tubulin helps nerve cells grow and form connections.

“Overall, the ability of CPO to interfere with normal developmental processes in the nervous system far exceeds that of its parent compound,” the authors wrote.

Hormone disruption linked to fertility and metabolic problems

The review finds substantial evidence that chlorpyrifos may interfere with multiple hormone systems (endocrine disruption) throughout the body. These include thyroid, estrogen, and testosterone pathways.

Research links exposure to abnormal reproductive cycles and tissue development, lower sperm counts, and reduced sperm quality. Some studies suggest it causes reduced prostate weight and disrupted hormone signaling in placental cells. Chlorpyrifos may also contribute to obesity, insulin resistance, and blood sugar problems, the review shows. 

Gut bacteria changes may fuel inflammation and disease

The review also tracks harms involving the gut microbiome — the ecosystem of microbes that supports digestion, metabolism, and immune function. Experimental studies indicate reductions in beneficial bacteria alongside increases in potentially harmful microbes after chlorpyrifos exposure. 

These changes may be tied to leaky gut syndrome, when bacterial toxins enter the bloodstream and trigger inflammation throughout the body. This type of gut-liver axis disruption may contribute to systemic inflammation and metabolic disease, the reviewers say.

The liver itself emerges as a major target of chlorpyrifos, experimental studies show. Researchers describe potential ties between chlorpyrifos and:

The review also links chlorpyrifos to musculoskeletal damage, including weaker bone formation, reduced bone density, and increased bone breakdown. Some bone changes occurred alongside neurological problems, suggesting broader developmental damage.

Studies show structural and functional changes involving both “slow-twitch” endurance muscles and “fast-twitch” muscles used for rapid movement. Some suggest chlorpyrifos may damage the diaphragm.

Chlorpyrifos DNA damage and altered gene activity raise alarm

The review highlights growing evidence that chlorpyrifos may damage DNA. Researchers describe chromosome damage and broken DNA strands. 

Studies also point to disruption of microRNAs, molecules that help regulate processes such as brain development, inflammation, and cell growth. And they suggest chlorpyrifos alters gene regulation in ways linked to neurodevelopmental disorders, metabolic disease, inflammation, and cancer.

“Collectively, the studies discussed above indicate that chlorpyrifos is a multifaceted genotoxic agent whose harmful effects extend far beyond acetylcholinesterase inhibition to include direct DNA strand breaks, chromosomal instability, and epigenetic reprogramming in various cell types, tissues, and species, detectable even at environmentally and clinically relevant concentrations,” they wrote.

The ways chlorpyrifos affects the body may contribute to liver, breast, and ovarian tumors, studies indicate. These include changes in DNA damage and repair, cell growth control, and gene expression. 

Experimental studies in liver and breast cells found abnormal cell growth and altered tumor progression. Some epidemiological studies report associations with hormone-related cancers, particularly more aggressive forms of hormone receptor-negative breast cancer.

One large 2015 study of more than 30,000 women—spouses of pesticide applicators—linked chlorpyrifos exposure to elevated breast cancer risk. While human evidence remains limited and inconsistent, the reviewers say, the combination of effects warrants closer investigation.

Current safety standards fail to protect public health

Underlying the review is a larger challenge to how regulators evaluate the safety of chlorpyrifos and other pesticides. Current approaches, the authors say, do not adequately account for their effects, especially during fetal development and early childhood.

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“The regulatory system was designed to prevent obvious poisoning, but many pesticide-related diseases do not appear immediately. Exposures too low to cause symptoms today may impair fetal brain development or contribute to Parkinson’s disease decades later,” Lanphear added. “The science has moved ahead of the regulatory framework. That is the gap this review highlights.”

Epidemiological studies suggest that prenatal and early-life exposure, even at relatively low environmental levels, may be linked to impaired neurodevelopment and cognitive function. That means both the way exposure occurs and the amount of exposure should be considered important factors that influence toxic effects when evaluating health risks, they say.

They also revisit longstanding criticism of industry-funded chlorpyrifos studies that have been used to shape federal exposure limits for decades. They cite the so-called “Coulston study,” a 1972 safety evaluation funded by Dow Chemical. 

Later researchers questioned parts of the study, arguing that it was not peer-reviewed. They also found that some baseline data was excluded from the original analysis, understating the pesticide’s toxicity.

The review calls for an independent reassessment of industry-sponsored toxicology studies used in past safety evaluations. It also calls for stronger protections for children and pregnant women, expanded biomonitoring programs, and safer pesticide alternatives, the authors say.

They argue that academic research should play a larger role in regulatory decisions to provide a fuller picture of chlorpyrifos harms. Independent research indicates a potentially higher threat to human health, particularly for children, due to exposure to this pesticide, they say.

“The societal costs associated with these risks are substantial, highlighting the urgent need for stricter regulations on chlorpyrifos use,” the authors wrote.

Reference

Kalenik S, Zaczek A, Rodacka A. Chlorpyrifos and Chlorpyrifos-Oxon: A Widening Spectrum of Toxicity. International Journal of Molecular Sciences. 2026; 27(9):3909. https://doi.org/10.3390/ijms27093909