Aldrin is a solid or liquid that can be white or dark brown and has a faint chemical odor. Typically, it is employed as an insecticide. Aldrin can be breathed in and absorbed through the skin; however, it is most frequently exposed by consuming contaminated foods like fish and shellfish.
Aldrin and dieldrin are two pesticides with comparable chemical compositions. Because aldrin converts to dieldrin very quickly in the body and the environment, they are described together in this fact sheet.
Pure aldrin and dieldrin resemble white powders with a light chemical odor.
Tan is the hue of commercial powders that are less pure. Neither chemical is found in the environment naturally. Aldrin and dieldrin were commonly used insecticides for crops, including corn and cotton, from the 1950s until 1970.
In 1974, the EPA outlawed aldrin and dieldrin for any purpose other than termite control due to concerns over potential environmental and human health harm. The EPA outlawed all usage in 1987.
Risks
Aldrin exposure over a brief period might cause headaches, lightheadedness, nausea, and vomiting. The skin and eyes may itch as a result of physical touch. Decreased fertility and liver damage may be the results of prolonged exposure.
Neurotoxicity
Neurotoxicity is one of the side effects that come with aldrin intoxication. Aldrin stimulates the central nervous system (CNS), which has been established in studies and may result in hyperexcitability and seizures.
There are two main ways that this phenomenon works.
Aldrin’s capacity to prevent the activity of brain calcium ATPases is one of the mechanisms. These ion pumps aggressively pump calcium out of the nerve terminal, relieving it of its burden. However, intracellular calcium levels increase when aldrin inhibits these pumps. A greater release of neurotransmitters happens as a result.
Aldrin’s capacity to inhibit gamma-aminobutyric acid (GABA) activity is used in the second mechanism.
The central nervous system’s main inhibitory neurotransmitter is GABA. Aldrin causes neurotoxic effects by obstructing the GABAA receptor and chloride channel combination.
Chloride cannot enter the synapse when this receptor is blocked, which prevents neural synapses from becoming hyperpolarized. As a result, action potentials are more likely to be produced at synapses.
Metabolism
Human studies on the metabolism of oral aldrin exposure are lacking. Animal studies, however, can give a thorough picture of the metabolism of aldrin. Humans and this data are related.
Epoxidation of aldrin by mixed-function oxidases (CYP-450) is the first step in the biotransformation of aldrin, which results in the creation of dieldrin. The liver is where this conversion primarily occurs. Tissues utilize the prostaglandin-endoperoxide synthase (PES) with low CYP-450 expression.
Effects and Effectiveness
The effectiveness of the substance has been assessed by taking into account the toxicokinetics of aldrin in the environment. Additionally, the negative effects of aldrin exposure are shown, demonstrating the compound’s risk.
Efficacy
Its effectiveness in controlling termites is investigated to ascertain the aldrin’s maximal application response. In 1953, US researchers tried aldrin and dieldrin at a rate of 2.25 pounds per acre on grounds where rodents were known to transport chiggers. Rats exposed to
Dieldrin-treated ground had 75 times fewer chiggers than untreated terrain, whereas rats exposed to Aldrin-treated territory had 25 times fewer chiggers. The Aldrin treatment shows a high level of productivity, especially when compared to other insecticides like DDT, sulfur, or BHC.
Adverse Effects
When aldrin is exposed to the environment, the chemical complex becomes localized in the air, soil, and water.
Aldrin concentrations in the environment at the primary exposure site and in plants are explained by the rapid conversion of aldrin to dieldrin and the delayed degradation of that compound.
Animals that consume poisoned plants or live in contaminated water can also contain these quantities. High amounts of their fat may result from this biomagnification.
After frequent exposures to dieldrin, several cases of employees developing anemia have been documented. However, Aldrin and Dieldrin’s primary side effect is on the central nervous system. It was thought that the body’s buildup of dieldrin caused convulsions.
In addition, various symptoms such as headaches, nausea, vomiting, anorexia, muscle twitching, myoclonic jerking, and EEG abnormalities were also described. All of these cases saw quick recoveries after the source of the aldrin/dieldrin exposure was eliminated.
Toxicity
The outcomes of numerous animal investigations are used to establish the toxicity of aldrin and dieldrin.
Although anemia-related deaths have been observed in rare cases following multiple exposures to aldrin, there have been no reports of a major rise in worker fatalities related to the substance.
In those instances, immunological testing connected an antigenic response to erythrocytes coated in dieldrin. Death caused directly by dose-response relationships has not yet been investigated.
The NOAEL determined from rat experiments was as follows:
- At acute oral exposure to aldrin, the lowest acceptable risk threshold is 0.002 mg/kg/day.
- Dieldrin’s minimal danger concentration for moderate exposure is 0.0001 mg/kg/day.
- The lowest acceptable risk level for chronic Aldrin exposure is 0.00003 mg/kg/day.
- Dieldrin chronic exposure has a minimal risk level of 0.00005 mg/kg/day.
In addition to these results, research on the risk of developing breast cancer showed a noticeably higher risk. When comparing the highest quartile range in the study to the lower quartile range, a 5-fold increased risk of death was found.
This was done by comparing blood concentrations to the number of lymph nodes and tumor size. The medication can also cause severe widespread convulsions in young children.
Animal Effects
Rats were employed in the majority of aldrin and dieldrin animal research. In many rat experiments, high dosages of aldrin and dieldrin indicated neurotoxicity, but they also revealed a special susceptibility of the mouse liver to dieldrin-induced hepatocarcinogenicity.
Additionally, Aldrin-treated rats showed an increase in post-natal mortality, and adults were more susceptible to the chemicals than youngsters were.
Effects on the Environment and Regulations
Aldrin is a highly lipophilic insecticide, similar to other polychlorinated pesticides. Its low solubility in water (0.027 mg/L) further contributes to its environmental durability. The Stockholm Convention on Persistent Organic Pollutants forbade it. Aldrin was canceled in the United States in 1974.
The EU forbids the substance’s usage in plant protection.
Issues of Environmental and Safety
Aldrin has a 39 to 60 mg/kg rat LD50 (oral in rats). However, fishing is exceedingly hazardous, with an LC50 for trout and bluegill being between 0.006 and 0.01.
The Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health in the US have set an occupational exposure limit for dermal exposures at 0.25 mg/m3 over an eight-hour time-weighted average.
Aldrin is recognized as a potential occupational carcinogen. In addition, an IDLH limit of 25 mg/m3 has been established based on acute toxicity findings in people, wherein subjects had convulsions within 20 minutes of exposure.
According to Section 302 of the U.S. Emergency Planning and Community Right-to-Know Act (42 U.S.C. 11002), it is categorized as an extremely hazardous substance in the United States and is subject to stringent reporting requirements by facilities that produce, store, or use it in significant quantities.
Should I Get in Touch with a Lawyer?
If Aldrin exposure has made you or a loved one ill, you might think about a class action lawyer. You can find out who caused your exposure to Aldrin and seek the right amount of compensation for your injuries with the assistance of an experienced class-action lawyer.
