Does organophosphate exposure cause neuropathy?
Neuropathy is, put simply, a condition caused by some kind of damage or interference with the nerves. It can occur independently of any other health condition, or may occur concurrently with, or as a symptom of, another disease or disorder.There are 4 main kinds of neuropathy:
- Peripheral neuropathy - Most people are somewhat familiar with peripheral neuropathy, which occurs when the nerves that control movement and sensation in your limbs (like your arms, fingers, etc.) are affected. Changes in the ability to control and feel the hands and feet are most common, though other body parts can be affected also.
- Autonomic neuropathy - Autonomic neuropathy occurs when the nerves that direct the involuntary actions of the organs are damaged or otherwise impaired. So, this would alter the function of organs like the heart (by changing blood pressure or causing arrhythmias, for instance), the bladder (by causing incontinence, etc.), the intestines (by affecting bowel movements, nutrient absorption, etc.), and other organs. Autonomic neuropathy is closely associated with severe diabetes, kidney failure, cancer, and other systemic conditions. Read more about diabetes cures at this link. For our complete list of cancer cures, download our book series, The Cancer Cure Catalog (the first volume is available for free when you sign up for the Alive-N-Healthy newsletter).
- Proximal neuropathy - Proximal neuropathy primarily affects the nerves in the torso or in the limbs closest to the torso, such as the shoulders, upper arms, and thighs. In most cases, this type of neuropathy only affects one side of the body (meaning that it’s asymmetrical), or affects one side of the body significantly more than the other. The development of proximal neuropathy is linked to conditions like Guillain-Barre syndrome, some cancers, and chronic inflammatory demyelinating polyneuropathy. Learn about natural cures for Guillain-Barre Syndrome here. Read about Vitamin B12 supplementation for demyelination disease at this link.
- Focal neuropathy - Focal neuropathy is focused on one specific nerve or grouping of nerves. Compression of a nerve can sometimes cause this kind of neuropathy, as can infection or inflammation. Carpal tunnel syndrome, ulnar neuropathy, Bell’s palsy, and trigeminal neuralgia are all common examples of focal neuropathy. Read about natural cures for Bell’s palsy here.
The symptoms of neuropathy vary from person to person and between types of neuropathy, but most cases of peripheral, focal, and proximal neuropathy all involve symptoms such as a prickling sensation somewhere in the body (paresthesia), decreased tactile sensations, and debility/muscle weakness. Autonomic neuropathy has somewhat different symptoms, which can differ depending on the specific set of nerves that are affected, but may involve diarrhea/constipation, urinary incontinence, lightheadedness, changes in blood pressure, and flushing, and other symptoms.
Organophosphate-Induced Delayed Neuropathy (OPIDN) / Organophosphate-Induced Delayed Polyneuropathy (OPIDP)
Organophosphate-induced delayed neuropathy (OPIDN) is the generally accepted term that refers to neuropathy caused by organophosphate exposure. This is by far one of the most widely known and acknowledged expressions of acute organophosphate exposure in the conventional medical community, and supports the link between organophosphates and nervous system problems of all kinds.OPIDN causes neuropathy specifically by killing nerve cells in the central nervous system (CNS), such as in the spinal cord. The symptoms of OPIDN generally occur between 1-4 weeks after acute organophosphate exposure, or they may develop over time after chronic organophosphate exposure. Many organophosphates (and some other non-organophosphate insecticide chemicals, too) are connected to the development of this condition, including by chlorpyrifos, dichlorvos, phosphamidon/mevinphos, mipafox, trichlorfon, trichlornat, isofenphos, and methamidophos. Malathion, leptophos, metriphonate, paration, and tri-o-cresyl phosphate (TOCP) are also closely linked to the development of organophosphate-induced delayed neuropathy.
High-dose exposure to organophosphates initially (within the first 24 hours of ingestion) causes symptoms such as an abnormally fast or slow heart rate, diarrhea, vomiting, irritability, fatigue, decreased alertness, convulsions, sweating, or salivation. After this, about 20-50% of individuals will enter the “intermediate syndrome” phase of OPIDN within 2-4 days after organophosphate ingestion; this phase lasts about 5-18 days, and patients often experience muscle weakness as well as cerebral nerve palsies (which can cause drooping of eyelids, double vision, difficulty in moving the eyes, etc).
The third stage, which is formally classified as OPIDN, may cause symptoms of peripheral neuropathy such as leg cramps, paresthesias, jerkiness in the ankles, weakness in the hand muscles and hip/knee flexors, and difficulties with coordination and movement. This stage usually develops between 10 days to 3 weeks after organophosphate exposure. Some patients will recover completely, while others may have persistent symptoms for years afterwards. Lasting effects of OPIDN can include claw hand deformities, muscular atrophy, problems with speech and coordination, and foot drop.
It’s worth noting that Guillain-Barre syndrome and acute disseminated encephalomyelitis are considered to be differential diagnoses for OPIDN.
Learn more about cures for acute disseminated encephalomyelitis here.
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Long-Term Organophosphate Exposure and Neuropathy
Most conventional medical circles accept that short-term, high-level organophosphate exposure/ poisoning can cause symptoms of severe neuropathy. However, long-term exposure to lower levels of organophosphates can also lead to the development of neuropathy. This link is somewhat less explored, since identifying the link between long-term, low level organophosphate exposure and neuropathy is less obvious than that of neuropathy development in acute organophosphate poisoning symptoms, but there are still some studies that successfully make this connection.One study in Iran observed male farmers who had been exposed to low levels of organophosphate pesticides over the long-term. Among these farmers, a total of 55 out of 100 had systemic issues; out of the entire group of 100 individuals, 44% exhibited ophthalmologic symptoms (such as redness, itching, or burning of the eyes), 40% had dermatologic problems (like burning/itching sensations on the skin or hypersensitivity), and 32% had pulmonary symptoms like cough and difficulty breathing.
Some individuals also exhibited sensory problems, with a few exhibiting motor symptoms as well. 37 individuals exhibited paresthesias, 16 reported a diminished sense of pain or tactile temperature, and 2 exhibited weakness in one of the four limbs (note that a total of 40 individuals in the group of 100 exhibited these types of symptoms).
The farmers who experienced these neurological symptoms tended to have been exposed to organophosphate pesticides in their work for a notably longer period of time than the farmers who didn’t report any symptoms. The symptomatic farmers, on average, had been exposed to organophosphates between 4-7 years longer than their nonsymptomatic counterparts.
Other studies support these findings in many other countries, including in the US, the UK, Ireland, and others. In the US and UK, paresthesia symptoms have been reported in 2-31% of farmers who have been exposed to organophosphates over the long-term, while other studies have reported that long-term organophosphate exposure leads to impaired temperature sensations in up to 65% of cases.
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Related Posts:Resources:
- Vasconcellos, Luiz Felipe, et. al. (2002). Neuropatia tardia por organofosforado: relato de caso. Retrieved October 27, 2022 from: https://www.scielo.br/j/anp/a/Ftfc8hfqTxPT6dCWc7SrTWN/?lang=en