Herbicide exposures poisoning

At very high doses, such as experienced by a few chemical workers and attempted suicides, herbicides can cause symptoms of acute chemical poisoning. Environmental exposures do not cause such effects, and none was reported in the Ranch Hands. 

Trichlorophenols are generally poisons and may be carcinogens. They may contain 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a contaminant. Some trichlorophenols are used as herbicides (e.g., 2,4,5-T and silvex). Human exposure may cause chloracne, liver dysfuncdon, muscle weakness, and prophyria. 

Dieldrin has caused numerous cases of chronic poisoning to workers who have sprayed the compound for several months. Characteristically there is headache, dizziness, and involuntary muscular movements. In severe cases there are epileptic convulsions with loss of consciousness. The only ocular disturbance so far noted in human beings has been blurred vision of undetermined cause, and nystagmus accompanying incoordination and tremor. In a study of five male farm workers exposed to a mixture of herbicides and pesticides including dieldrin, four were found to have suffered impotence after chronic exposure sexual function recovered after termination of exposure. 

Paraquat. Paraquat is a widely used herbicide in cotton and potato culture, on orchard floors, and in landscape maintenance. There have been persistent reports of paraquat poisoning, mostly from ingestion both intentional and accidental, but also from dermal contact. There have also been reports linking paraquat to chronic intoxication, particularly in pulmonary disease from inhaling paraquat aerosols. In addition to food residue analysis in support of tolerance, worker exposure samples and ambient environmental samples are also of great interest. 

TCDD, the most toxic of the 75 dioxin isomers and possibly the most toxic manufactured chemical, contaminates phenoxy herbicides during the production process (Demers and Perrin 1995 Klaassen 1985). Conflicting literature addresses TCDD lethality in humans. Some reviews deny that human deaths result from systemic effects of TCDD (Demers and Perrin 1995). Others describe successful suicides with phenoxy herbicides (Nielsen et al. 1965). Despite extensive reports of numerous medical conditions from TCDD, the literature confirms only chloracne and transient mild hepatotoxicity in humans. Table 1-6 lists the various, but unconfirmed, signs and symptoms associated with human poisonings. Table 1-7 lists the unconfirmed psychiatric symptoms attributed to TCDD exposure. 

Expensive biological measures, including blood and adipose levels of TCDD, do not correlate with clinical symptoms (Demers and Perrin 1995). Elevated liver function tests in the presence of chloracne indicate exposure. Dioxin has no antidote, and most symptoms require supportive management. No specific literature addresses psychiatric treatment issues of dioxin poisoning. In most exposures to an unknown herbicide, fumigant, or pesticide, the clinical evaluation should proceed as described in Chapter 4. 

Industrial and environmental sources cause most modern cases of arsenic poisoning. A National Institute for Occupational Safety and Health study in 1975 estimated that 1.5 million workers had potential exposure to arsenic (Hartman 1988). Poisonings have resulted from veterinary compounds, paints, herbicides, pesticides, rodenti-cides, treated lumber, and Chinese herbal products (Garvey et al. 2001 Gosselin et al. 1984 Peters et al. 1983). Table 7-1 lists occupations with the greatest risk of exposure to arsenic. 

Like most other classes of pesticides and herbicides, the degree of toxicity of triazines has been found to vary with compounds. Thus, the toxicity may not be solely attributed to the triazine ring. For example, while substances such as atrazine, metribuzin, and cyanazine are moderately toxic by all routes of exposure, compounds such as prometryn and propazine have a very low order of toxicity. However, no cases of human poisonings have been reported. A few selected triazine herbicides are discussed individually in the following sections. 

HUMANS EXPOSED TO MATERIALS REPORTED TO BE CONTAMINATED WITH TCDD HAVE DEVELOPED CHLORACNE AND OTHER SIGNS OF SYSTEMIC POISONING. SOFT TISSUE SARCOMA HAS BEEN OBSERVED IN EXCESS AMONG WORKERS EXPOSED TO PHENOXY HERBICIDES. THESE DATA ARE INCONCLUSIVE REGARDING TCDD TOXICITY IN HUMANS BECAUSE THE POPULATIONS STUDIED HAD MIXED EXPOSURES MAKING CAUSAL RELATIONSHIPS BETWEEN EXPOSURE AND EFFECT UNCLEAR. THE DATA ARE, HOWEVER, SUGGESTIVE OF AN ASSOCIATION BETWEEN EXPOSURE TO PHENOXYACETIC HERBICIDES CONTAMINATED WITH TCDD AND EXCESS LYMPHOMA AND STOMACH CANCER. ATTEMPTS TO ASSOCIATE REPRODUCTIVE EFFECTS WITH TCDD EXPOSURE ARE INCONCLUSIVE BECAUSE OF THE INADEQUATELY DEFINED POPULATIONS STUDIED AND THE DIFFICULTIES OF DEFINING EXPOSURE. 

In Europe, in the 1970s one major chemical accident in particular prompted the adaption of legislation aimed at the prevention and control of major accidents in the chemical process industry. The Seveso accident in northern Italy in 1976 occurred at a chemical plant manufacturing pesticides and herbicides. A dense vapor cloud containing dioxin was released due to an uncontrolled exothermic reaction. The poisonous and carcinogenic dioxin is lethal in microgram quantities and contaminated ten square miles, and more than 2,000 people were treated for exposure. Luckly, there were no immediate fatalities. 

Contact reactions to plants in farm workers cover a wide spectrum. Reactions occur to poison ivy, oak and sumac [145] which are often not reported. Exposure can occur when clearing fence rows and sometimes when handling domestic animals. These plants are not usually found with the crops, where herbicides are used for weed control, but are more often seen on fence rows. Sometimes contaminated hair of farm animals is the source. The details of Toxicodendron dermatitis were given in the previous section. 

In the practical experience of manufacturers and applicators, herbicidal 5-triazines have proved to be virtually nontoxic. Consistent evidence of toxic effects has not been reported (Deutsche Forschungsgemeinschaft 1986 Loosli 1994 Velvart 1993). It is particularly pertinent that the health files of major manufacturing plants have no record of triazine poisoning, although safety precautions in the early years of production prevented worker exposure to a limited extent only (Ciba-Geigy 1993, personal communication). 

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