Reproductive toxicity herbicides

The triazine herbicides, with the exception of cyanazine, did not produce developmental or reproductive effects at maximally tolerated doses. Cyanazine produced developmental effects in rats and rabbits at the highest doses tested. Effects noted at doses that were toxic to the mothers were cyclopia and diaphragmatic hernia in rabbits and an apparent increase in the incidence of skeletal variations (i.e., anomalies) in rats (USEPA, 1994). 

The extreme toxicities of the nitrophenolic herbicides probably accounts for the paucity of teratogenic studies in this class of herbicides. Rat studies of the related hair dyes 1,2- and 1,4-diaminonitrobenzenes revealed extensive reproductive anomalies. 

SAFETY PROFILE Moderately toxic by ingestion. Experimental reproductive effects. An eye irritant. Mutation data reported. An herbicide. When heated to decomposition it emits very toxic fumes of NOx and SOx. See also MERCAPTANS. 

OSHA PEL TWA 0.5 mg(As)/m3 ACGIH TLV BEI 35 (As)/L inorganic arsenic and methylated metabolites in urine DOT CLASSIFICATION 6.1 Label Poison SAFETY PROFILE Poison by an unspecified route. Moderately toxic by ingestion and intraperitoneal routes. Experimental teratogenic and reproductive effects. A skin and eye irritant. Questionable carcinogen with experimental tumorigenic data. Mutation data reported. Used as an herbicide, defoliant, and silvicide. Hazardous when water solution is in contact with active metals, e.g., Fe, Al, Zn. When heated to decomposition it emits toxic fumes of As. 

Chronic exposure to maneb has been related to reproductive, embryotoxic teratogenic, and neurotoxic effects. Although the toxicity associated with maneb exposure is low, it has been shown that in combination with other toxicants such as metals, other fungicides and herbicides the effects of maneb may be more pronounced, leading to more severe deficits. 

Most of what is known about the toxicity of dioxins in the human comes from individuals exposed incidentally or chronically to higher levels (e.g., industrial accidents or presence in areas sprayed with Agent Orange or other herbicides contaminated with dioxins.). The lowest dose effects are probably associated with thymic atrophy and decreased immune response, chloracne and related skin lesions, and neoplasia (cancer). Dioxins can cross into the placenta to cause developmental and reproductive effects, decreased prenatal growth, and prenatal mortality. 

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. 

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