Paraquat is a commercial herbicide effective in controlling weeds and grasses. Its high toxicity to humans has led to its classification as a “restricted-use” product in many countries, including the United States, where a license is required for its application. This control is a direct response to the severe health consequences that can arise from exposure.
Routes of Human Exposure
The most severe and often fatal cases of paraquat poisoning result from ingestion. Many poisoning incidents occur when the herbicide is transferred from its original packaging into unlabeled containers, such as beverage bottles, leading to accidental consumption. Intentional self-harm is another significant cause of ingestion-related fatalities.
Occupational exposure is another primary route, particularly for licensed agricultural workers. Inhalation of paraquat particles during spraying can lead to direct lung damage. Dermal exposure is also a concern; while intact skin provides a barrier, the risk of systemic toxicity increases if the chemical contacts damaged skin. Prolonged contact with clothing soaked with the herbicide can also lead to life-threatening absorption. The risk for the general public is lower but may exist for those living near agricultural areas where paraquat is applied.
Immediate Health Consequences of Poisoning
Upon ingestion, paraquat acts as a caustic agent, causing burning pain and swelling in the mouth and throat. This is often accompanied by gastrointestinal distress, including stomach pain, nausea, and vomiting, which may contain blood. The chemical’s rapid absorption begins to damage cells throughout multiple organ systems.
Within a few days, the poisoning progresses to cause severe organ damage. The kidneys and liver are particularly vulnerable, often leading to acute renal and hepatic failure. The primary target of paraquat is the lungs. The herbicide is actively transported into lung cells, where it accumulates and generates reactive oxygen species, leading to cellular damage and inflammation.
This process results in acute alveolitis, where the air sacs in the lungs become inflamed and can lead to collapse. The progressive lung damage culminates in pulmonary fibrosis, a scarring of the lung tissue that severely impairs breathing. This irreversible lung injury is the cause of death in most fatal cases, which can occur days or weeks after the initial exposure.
Long-Term Health Risks from Exposure
Scientific research has identified an association between paraquat exposure and an increased risk of developing Parkinson’s disease. The mechanism involves oxidative stress, where the chemical’s interaction produces unstable molecules that damage cells. Paraquat is believed to harm the dopamine-producing neurons in a region of the brain called the substantia nigra. The loss of these neurons is a hallmark of Parkinson’s disease, leading to motor symptoms like tremors, rigidity, and impaired balance.
This neurotoxic effect is not limited to high-dose, acute poisoning. Studies suggest that chronic, low-level exposure, such as that experienced by agricultural workers, may be sufficient to elevate the risk of developing the disorder over time. The onset of symptoms can occur many years after the initial exposure period.
For individuals who survive an acute poisoning event, the long-term consequences can be severe. The most common lasting effect is permanent lung scarring, a form of pulmonary fibrosis that leaves survivors with chronic breathing difficulties. Survivors may also face other irreversible health problems, including kidney failure that necessitates lifelong dialysis or esophageal damage that creates strictures, making it difficult to swallow.
Medical Management of Paraquat Poisoning
There is no specific antidote to reverse the effects of paraquat poisoning. Medical intervention is therefore focused on supportive care and limiting the body’s absorption of the toxin. Immediate treatment is centered on decontamination of the gastrointestinal tract. This is commonly achieved by administering activated charcoal or Fuller’s earth, which bind to paraquat in the stomach and prevent its absorption.
Once the poison has been absorbed, treatment shifts to managing organ damage. Therapies such as hemodialysis or hemoperfusion may be used to filter the poison from the blood, although their effectiveness in changing the clinical outcome is debated. Supportive care, including intravenous fluids and mechanical ventilation, is administered to manage symptoms like dehydration.
Some treatment protocols may include immunosuppressive drugs like cyclophosphamide and corticosteroids. The theory is to reduce the intense inflammatory response that paraquat triggers, particularly in the lungs, to inhibit fibrosis. Despite these interventions, the prognosis for patients who have ingested a significant amount of paraquat remains poor, and immediate medical care is necessary to offer any chance of survival.