Dioxin Causes Chloracne in West German Chemical Workers Summary

  • Last updated on November 10, 2022

An extremely toxic substance contaminating an industrial herbicide, dioxin was observed to cause chloracne in West German chemical plant workers, demonstrating the dangers it posed to people and the environment.

Summary of Event

In the 1940’s, the herbicides Herbicides 2,4-dichlorophenoxyacetic acid 2,4-dichlorophenoxyacetic acid[two four dichlorophenoxyacetic acid] (2,4-D) and 2,4,5-trichlorophenoxyacetic acid 2,4,5-trichlorophenoxyacetic acid[two four five trichlorophenoxyacetic acid] (2,4,5-T) were introduced into wide use as part of the effort to increase worldwide agricultural crop yields. These herbicides were initially regarded as both inexpensive and safe; 2,4-D was used as a killer of broad-leaf weeds and 2,4,5-T as a killer of underbrush and unwanted trees. Beginning in 1957, an outbreak of chloracne in West German chemical workers alerted the world to a potential danger associated with 2,4,5-T. The substance was banned in the United States in 1985, but between 1960 and 1970, fifty-four thousand tons of 2,4,5-T were manufactured and sprayed on the world’s farmland. In addition, millions of pounds of the 2,4,5-T-containing Agent Orange Agent Orange defoliant were used in the Vietnam War Vietnam War (1959-1975);Agent Orange , where it reportedly wreaked havoc on the Viet Cong and caused health problems, including chloracne, to the American military personnel who sprayed it on the countryside. Dioxin Chloracne Pollution;West Germany Hazardous materials Labor;workplace hazards Workplace hazards [kw]Dioxin Causes Chloracne in West German Chemical Workers (1957) [kw]Chloracne in West German Chemical Workers, Dioxin Causes (1957) [kw]West German Chemical Workers, Dioxin Causes Chloracne in (1957) [kw]Workers, Dioxin Causes Chloracne in West German Chemical (1957) Dioxin Chloracne Pollution;West Germany Hazardous materials Labor;workplace hazards Workplace hazards [g]Europe;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] [g]Germany;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] [g]West Germany;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] [c]Business and labor;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] [c]Health and medicine;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] [c]Social issues and reform;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] [c]Environmental issues;1957: Dioxin Causes Chloracne in West German Chemical Workers[05340] Schulz, Karl Sorge,George

Chloracne, first seen in the 1890’s, in Germany, was originally limited to workers in chemical plants. The disease—which resembles severe acne—often covers the face, neck, shoulders, chest, and back of the victim with large blackheads cysts, and oozing pustules. It was initially thought to be caused by exposure to a corrosive chlorine gas widely used in the chemical industry. Later, extensive medical exploration showed that chloracne was caused by chlorinated aromatic hydrocarbons.

The most dangerous causative agent for chloracne was demonstrated to be one of several related substances called dioxins, namely, 2,3,7,8-tetrachlorobenzo-p-dioxin (TCDD). At one time, TCDD was produced mostly as a contaminant of the production of 2,4,5-T, originating at the stage where one of the starting materials, trichlorophenol (TCP), was produced.

The evidence that a 2,4,5-T component caused chloracne was first obtained by Karl Schulz, a German dermatologist who observed chloracne in German chemical workers at a Boehringer Company Boehringer Company plant in 1957. Suspecting TCP of being the disease agent, Schulz tested its toxic action in rabbits by rubbing it into the shaved ear of an animal; although pure TCP was found to have no effect, impure samples of the substance caused the appearance of chloracne, which proved that the active toxic agent was not TCP but an impurity contaminating the TCP. Such impurities are common in the production of complex industrial chemicals, where they are tolerated as long as they do not interfere with the manufacturing process.

Schulz tested many of the chemicals that contaminate TCP preparations, substances supplied to him by Boehringer chemist George Sorge, but he was unable to identify a chloracne-causing agent. Purely by chance, a laboratory accident helped identify the culprit substance when an experimental wood preservative was found to cause the disease. From studies following this accident, the chloracne-causing agent in contaminated TCP and in the 2,4,5-T made from it was finally determined to be TCDD. Once it was found that lowering the temperature at which TCP was manufactured could nearly eliminate the production of TCDD, it became possible to manufacture much safer forms of 2,4,5-T.

A wide range of people were originally exposed to dangerous amounts of TCDD. At highest risk were workers involved in the production of TCP and those who serviced or repaired the plants that manufactured TCP. Their exposure resulted from small explosion-like accidents that occurred during its manufacture, producing large amounts of TCDD as vapor, hot liquid, and solid forms, and from frequent small leaks in the equipment.

Chemical workers involved in the manufacture of 2,4,5-T, and those who mixed 2,4,5-T with other substances to produce herbicide mixtures such as Agent Orange, were also exposed to dangerous levels of TCDD. These workers may have been at an especially high risk because the herbicide preparations often contained added substances to make them adhesive.

Also at risk of TCDD contamination were farmers and other workers who sprayed the herbicides on crops. Theirs, however, was a much lower risk than that of industrial workers, since they came into contact with pounds of 2,4,5-T at a time instead of with the tons of TCP or chlorophenoxy herbicides prepared in chemical plants. This risk group also included the military personnel who sprayed Agent Orange during the Vietnam War.

As a result of the heavy use of 2,4,5-T before 1985, hundreds of millions of people around the world were considered to be at risk of contacting dangerous amounts of TCDD from the environment around them. The farmland sprayed with 2,4,5-T was expected to remain contaminated for a great many years (though the individual risk here is much smaller because relatively small amounts of toxic TCDD are involved). Moreover, some risk to chemical plant workers probably continued to exist after 1985, because industrial TCDD production had not been completely eradicated.


2,4,5-T is a potent defoliant and killer of woody plants (such as trees). The compound herbicides produced by mixing 2,4,5-T and 2,4-D proved so useful in clearing land that the U.S. Armed Forces bought huge amounts of one such substance—which was shipped in bright orange drums and therefore called Agent Orange—for use as a jungle defoliant during the Vietnam War. The defoliation made it easier to find Viet Cong troop concentrations. The toxic TCDD contained in the Agent Orange has been accused of causing many health problems, including cancer, in the military personnel who sprayed Agent Orange or otherwise came into contact with it during the Vietnam War.

Many regard chloracne as being not only a symptom of dangerous TCDD exposure but also a possible precursor to cancer. Incidents of TCDD-caused chloracne have been observed in chemical plants around the world, including in Italy, Japan, the United States, and Czechoslovakia. Furthermore, the environmental hazards from improperly handled TCDD in waste dumps have been reported at sites such as Love Canal in Niagara Falls, New York, and in a number of chemical-plant explosions, such as the one in Seveso, Italy, in 1976.

TCDD is also suspected of being present in the emissions from fossil-fuel power plants and diesel engines, as well as in the fly ash and flue gas produced by the burning of municipal garbage in incinerators. Even more dangerous is incineration of chlorinated wastes such as chlorinated synthetic polymers, or plastics, and electrical transformers containing the polychlorinated biphenyls. As the dangers became more widely reported, the use or production of many such substances was phased out or banned, and efforts have been made to promote safer handling of potentially toxic materials of this type.

In the United States and other industrial nations, TCDD and related substances are made at much lower levels than in the past. Nevertheless, chemical-plant workers, firefighters, and incinerator attendants are still at high risk of TCDD contamination as a major occupational hazard. The general public, too, is still vulnerable to TCDD exposure from a number of sources, such as milk, meat, and seafood from animals that ingested materials containing TCDD left over from herbicides originally sprayed years previously.

The link between cancer and TCDD in humans is not clear. Cancer may take twenty to thirty years to develop in an individual, and the initial cause is difficult to pinpoint. TCDD is variably toxic to many animal species (especially the guinea pig), but evidence for corresponding toxicity in humans, while suspected, is not well established. Rhetoric abounds on both sides of the issue, with viewpoints ranging from the conviction that TCDD is among the most toxic substances known to the belief that it is relatively harmless. Caution in the handling of any potential TCDD source is the best course of action.

Opponents of the use of chlorinated herbicides suggest that their use should be banned. It is not clear what the results of such action would be on world agriculture and on society in general, but many fear that huge numbers of people would die of starvation if weeds could no longer be kept in check. Studies supporting this possibility include estimates that the use of chlorophenoxyacetic acid herbicides in the 1940’s may have saved as much as $5 billion worth of American crops. Dioxin Chloracne Pollution;West Germany Hazardous materials Labor;workplace hazards Workplace hazards

Further Reading
  • citation-type="booksimple"

    xlink:type="simple">Ashton, Floyd M., and Alden S. Crafts. Mode of Action of Herbicides. New York: Wiley-Interscience, 1973. A solid scientific treatise containing much information on the chemistry, use, and problems associated with herbicides. Also includes a section about 2,4-D, 2,4,5-T, and other chlorophenoxy compounds.
  • citation-type="booksimple"

    xlink:type="simple">Bender, David L., and Bruno Leone. The Environmental Crisis: Opposing Viewpoints. San Diego, Calif.: Greenhaven Press, 1991. A thoughtful, provocative book of essays on environmental topics from differing viewpoints. Several essays discuss pesticide and TCDD issues.
  • citation-type="booksimple"

    xlink:type="simple">“Dioxin Toxicity.” American Family Physician 47 (1993): 855-861. Written by the staff of the Agency for Toxic Substances and Disease Registry. Concise description of the production history and effects of TCDD and related chemicals; also describes the treatment of toxic manifestations. Includes some useful suggested readings.
  • citation-type="booksimple"

    xlink:type="simple">Environmental Protection Agency, National Center for Environmental Assessment. Database of Sources of Environmental Releases of Dioxin-Like Compounds in the United States. Washington, D.C.: Author, 2001. Governmental computer database listing sources of dioxins and similar compounds being released into the environment in the United States.
  • citation-type="booksimple"

    xlink:type="simple">Kamrin, Michael L., and Paul W. Rodgers. Dioxins in the Environment. Washington, D.C.: Hemisphere, 1985. Highly technical summary of an international workshop at Michigan State University. A thorough examination of the dioxins, describing TCDD testing, TCDD dynamics in the environment, and toxicology of the dioxins. Includes useful workshop summaries, and an extensive bibliography.
  • citation-type="booksimple"

    xlink:type="simple">Tamburro, C. H. “Chronic Liver Injury in Phenoxy Herbicide-Exposed Vietnam Veterans.” Environmental Research 59 (1992): 175-178. Examines reports of chronic liver injury in Vietnam veterans and concludes that the data point to viral and alcoholic causes, not herbicides such as Agent Orange and their TCDD contaminant.
  • citation-type="booksimple"

    xlink:type="simple">Wilcox, Fred A. Waiting for an Army to Die. New York: Vantage Books, 1983. Argues that the effects of dioxin in Agent Orange on Vietnam veterans and their children have been covered up by the government and the chemical industry.

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Categories: History