Organochlorine Pesticide Toxicity 

  • Author: Jennifer Vyse Pope, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: May 11, 2010
 

Background

Chlorinated hydrocarbon (organochlorine) insecticides, solvents, and fumigants are widely used around the world. This class comprises a variety of compounds containing carbon, hydrogen, and chlorine. These compounds can be highly toxic, and some agents, such as DDT, have been banned in the United States because of their unacceptably slow degradation and subsequent bioaccumulation.

The toxicity of these agents varies according to their molecular size, volatility, and effects on the CNS. In general, they cause either CNS depression or stimulation, depending upon the agent and dose.[1]

These compounds can be separated into 5 groups, as follows:

  1. Dichlorodiphenyltrichloroethane (DDT) and analogues (eg, dicofol, methoxychlor)
  2. Hexachlorocyclohexane (ie, benzene hexachloride) and isomers (eg, lindane, gamma-hexachlorocyclohexane)
  3. Cyclodienes (eg, chlordane, heptachlor, aldrin, dieldrin, endrin, endosulfan, isobenzan)
  4. Chlordecone, kelevan, and mirex
  5. Toxaphene
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Pathophysiology

Absorption and metabolism

Organochlorines are well absorbed orally and by inhalation. Transdermal absorption is variable. For example, DDT is poorly absorbed transdermally, whereas cyclodienes have significant transdermal absorption rates.[2] Cyclodienes have high absorption levels when taken orally as in the case of food contamination with these pesticides.[3] Lindane is also absorbed after topical application. Studies have shown that the young, malnourished, and those with frequent application are at increased risk for toxicity.[4]

Organic chlorines are strongly lipid soluble and sequestered in body tissues with high lipid content, such as the brain and liver. Consequently, blood levels tend to be much lower than fatty tissue levels.[2] The lipophilic tendency of organochlorines accounts for prolonged systemic effects in overdose. The half-life of DDT has been measured in months or years, whereas other organic chlorines are metabolized faster, like lindane, with a half-life of 21 hours.[5]

Mechanism of toxicity

Toxicity in humans is largely due to stimulation of the central nervous system. The organochlorines disturb the neuronal membrane causing hyperexcitability of the nervous system. Specifically, cyclodienes, hexachlorocyclohexanes, and toxaphene organochlorines inhibit GABA-mediated chloride influx in the CNS, while DDT affects potassium and voltage-dependent sodium channels. These changes can result in agitation, confusion, and seizures. Cardiac effects have been attributed to sensitization of the myocardium to circulating catecholamines.

Some of the more volatile organochlorines can be inhaled while in vapor form or swallowed while in liquid form. Inhalation of toxic vapors or aspiration of liquid after ingestion may lead to atelectasis, bronchospasm, hypoxia, and a chemical pneumonitis. In severe cases, this can lead to acute lung injury (ALI), hemorrhage, and necrosis of lung tissue. In liquid form, they are easily absorbed through the skin and GI tract.

  • Highly toxic organochlorines
    • Aldrin
    • Dieldrin[6]
    • Endrin[7] (banned by the US Environmental Protection Agency [EPA])
    • Endosulfan[8]
  • Moderately toxic organochlorines
    • Chlordane
    • DDT (banned by the EPA)
    • Heptachlor
    • Kepone
    • Lindane
    • Mirex
    • Toxaphene
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Epidemiology

Frequency

United States

Organochlorine pesticides are now only rarely used in the developed world, and domestic poisonings have become correspondingly more rare. Lindane is still used as a second-line topical prescription treatment for head lice and scabies.

In the United States, approximately 42,000 cases of pesticide poisoning occur annually. In 2007, the Annual Report of the American Association of Poison Control Centers' National Poison Data System reported pesticide exposure as the ninth most common substance frequently involved in human exposures.[9] In 2007, 16 pesticide poisoning fatalities were reported. None of these were due to organochlorine pesticides.[9]

International

An estimated 3 million cases of severe pesticide poisoning and 220,000 deaths occur each year worldwide. Organochlorine poisoning accounts for only a small fraction of pesticide poisoning. Approximately 95% of fatal pesticide poisonings occur in developing countries.

Mortality/Morbidity

Toxic doses are variable, and reports of poisonings are limited.

Age

Adults are most likely to have serious intentional poisonings, and children are most likely to have unintentional poisonings.

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Contributor Information and Disclosures
Author

Jennifer Vyse Pope, MD  Staff Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center

Jennifer Vyse Pope, MD is a member of the following medical societies: Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Morgan Skurky-Thomas, MD  Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School

Morgan Skurky-Thomas, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Carlo L Rosen, MD  Associate Professor of Medicine, Harvard Medical School; Program Director, Vice Chair for Education, Department of Emergency Medicine, Beth Israel Deaconess Medical Center/Harvard Affiliated Emergency Medicine Residency program

Carlo L Rosen, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

David C Lee, MD  Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References

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  21. Mutter LC, Blanke RV, Jandacek RJ, Guzelian PS. Reduction in the body content of DDE in the Mongolian gerbil treated with sucrose polyester and caloric restriction. Toxicol Appl Pharmacol. Mar 15 1988;92(3):428-35. [Medline].

  22. Narahashi T, Frey JM, Ginsburg KS, Roy ML. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Toxicol Lett. Dec 1992;64-65 Spec No:429-36. [Medline].

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