The Tale of an Unusually Hazardous Pesticide
Dr. Allan S. Felsot, Environmental Toxicologist, WSU
Any astute student of biology who has had the fortitude to weather a biochemistry class can recite line and verse how a chemical known as dinitrophenol can adversely affect the energy generating reaction in a cell. No cell will live very long under the influence of high concentrations of dinitrophenol. Reduce the dose enough, however, and dinitrophenol can cause a body to burn enough energy to result in weight loss. And so it was during the 1930's that physicians unwittingly prescribed certain types of dinitrophenols as diet pills.
But these chemicals also had uses as pesticides. One chemical form known as DNOC had been discovered and patented in Germany in 1892 as an insecticide. By 1925 it was used as a herbicide and soon fungicidal properties were discovered. Dow Chemical changed the basic structure of dinitrophenol slightly to produce dinoseb, which was marketed in 1948. Dinoseb was widely used as a contact herbicide against broadleaf weeds with many registered uses in numerous minor crops.
Dinitrophenol pesticides cause toxicity the same way in plants, animals, and fungi because all cells contain very similar biochemical pathways for creating energy from the breakdown of sugars. Furthermore, photosynthesis in plants relies on an energy transfer system that is also inhibited by dinitrophenols.
Unfortunately for humans, DNOC and dinoseb have a propensity to be easily absorbed by the skin. Consequently, not only is it considered hazardous following ingestion, its toxicity is equally high from dermal exposure. Indeed, both herbicides are Category I poisons, a class reserved for chemicals with an oral LD50 (lethal dose to 50% of test animals) in the neighborhood of 50 milligrams per kilogram of body weight (mg/kg), and a dermal LD50 of 200 mg/kg or less. Cases of worker poisoning and deaths have been attributed to the dinitrophenol herbicides. It is rare for chemicals used as herbicides or fungicides to be that acutely toxic.
Given the high toxicity of dinoseb and related dinitrophenols, perhaps the EPA had good reason to ban it in 1986. But acute toxicity alone rarely causes regulatory action to suspend a pesticide. One notable exception was the organophosphate (OP) insecticide Phosdrin, whose registration was suspended following poisoning incidents in Washington State during 1993. Nevertheless, many OP insecticides are considered Category I poisons and are still widely used. The straw that broke the camel's back on dinoseb came in the mid 1980's from studies reporting birth defects in rabbits and rats born to females fed comparatively low doses (10 mg/kg/day) between day 6 and 18 of pregnancy. Other chronic toxicological effects at low doses could be described as endocrine disrupting-abnormal sperm and decreased weight of thyroid gland.
EPA concluded that the doses causing the birth defects and the endocrine disrupting effects were close to worker exposure levels. Thus, under emergency order issued in October of 1986, EPA suspended dinoseb with an intent to cancel its registration. Dinoseb was not associated with cancer nor was it found to cause gene mutations.
Any time a pesticide, banned or not, is found at levels of hundreds of parts per billion (ppb) in wells, a potential health hazard exists that demands immediate attention. Thus, the finding of two wells in the Yakima Valley with dinoseb levels between 100-500 ppb resulted in great concern among the hundreds of homeowners in the vicinity of those wells. Fortunately, dinoseb contamination has been limited to those two wells, but questions were raised of possible effects if dinoseb-contaminated water had been used, even though it was not found at the time of sampling. Obviously, pregnant women should not be exposed to those high levels of dinoseb, but what hazards would others face?
The silver lining in the cloud for dinoseb is that cancer is not considered a hazard. EPA considered the toxic effects of dinoseb to have a threshold, and the agency calculated a "safe" exposure level that depended on the length of time of exposure. Known as health advisory levels, these safety standards range from 300 ppb for a ten-day exposure to a 22-pound child to 10 ppb for a 7-year exposure. For a lifetime exposure, the regulatory level was set to 7 ppb. Thus, exposure to 7 ppb over an average 70-year lifespan would not be expected to produce adverse effects.
Fortunately, no one seems to have been drinking the contaminated water for very long. A public health crisis seems to have subsided, but monitoring of the contaminated wells will have to continue.
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