Pesticides exposure pathways

Simcox NJ, Fenske RA, Wolz SA, et al. 1995. Pesticides in household dust and soil Exposure pathways for children of agricultural families. Environ Health Perspect 103 1126-1134. 

Children can be exposed to endosulfan by eating food contaminated with the pesticide, by accidentally ingesting the pesticide if it is stored around the house, or by breathing air contaminated with the pesticide if it is sprayed on nearby fields. There are no known unique exposure pathways for children. We do not know if children s intake of endosulfan per kilogram of body weight is different than that of adults. 

The committee recommends the inclusion of a detailed and accurate exposure analysis for a subset of the biomonitored population in large-scale biomonitoring studies that includes analyses of environmental media in the residence and uses a survey instrument to obtain information on diet, consumer product use, occupational exposures, and other factors relevant to the chemical exposure pathways that are being examined. The exposure assessment can be patterned on protocols used in other exposure analyses, such as the National Human Exposure Assessment Survey (NHEXAS), the Minnesota Children s Pesticide Exposure Study, and Children s Total Exposure to Pesticides and Other Persistent Organic Pollutants. 

Soils are the main and ultimate culprit of many different human exposure pathways to pollutants through the food chain, partly because lipophilic compounds that reside mainly in soils dissolve pesticides, herbicides, and the like. 

Lu, C., R.A. Fenske, N.J. Simcox and D. Kalman (2000). Pesticide exposure of children in an agricultural community evidence of household proximity to farmland and take home exposure pathways. Environ. Res., 84, 290-302. 

Exposure pathway The physical course a chemical or pollutant takes Pom the source to the organism exposed (USEPA, 1992a,b, 1997b,c REAP, 1995 AlHA, 2000). Some examples of exposure pathways are drinking water ingestion, dietary consumption, pesticide handling, contact with an exposure media, or an activity that brings an individual into contact with an exposure media (Sielken, Ch. 8). 

Kerosene may enter the water or soil environment as a result of regular use (e.g., evaporation of pesticide solvent), from spills during use or transportation, or from leaking storage facilities. The relatively low vapor pressure of kerosene makes inhalation exposure unlikely under ordinary occupational conditions unless conditions of poor ventilation exist. The combustion product of burned kerosene, carbon monoxide, is of real concern when kerosene heaters are not vented. Exposure to kerosene mist can occur as kerosene is often applied in the form of a spray. Eye and skin contact with kerosene and kerosene mists and vapors can occur. The exposure pathway usually of... 

Contradictory results for associations between pesticide levels indoors (air, dust) and results form human biomonitoring may be due to different volatilities of the pesticides and may be determined by the magnitude in contamination levels. For semivolatile pesticides it may be easier to detect an association, as indoor air and house dust may serve for exposure in contrast to particle-bound pesticides with house dust as the only exposure path. Furthermore high contamination levels make it easier to detect an association, as with low indoor contamination levels associations may be hidden by the ubiquitous presence of pesticides in indoor environments and by nonindoor exposure pathways like dietary intake. 

For inorganic manganese compounds, dermal exposure is not a typical pathway of exposure because manganese does not penetrate the skin readily. For organic manganese, dermal exposure is a possibility with all compounds discussed in this profile. This exposure pathway is most likely, however, with MMT, maneb and mancozeb, where occupational workers (mechanics, workers in the gasoline industry, pesticide manufacturers and sprayers) are likely to handle large quantities of these compounds. 

Maneb at aqueous concentrations of 5 ppm resulted in delayed development of amputated forearms in male and female newts, with reduced melanogenesis and malformations of regenerating limbs (Arias and Zavanella 1979 Zavanella et al. 1984). However, in light of the relevant pathways of pesticide exposure in humans, the relevance of this model system to human development is not clear. 

Fate and transport modeling was nsed to estimate the concentration of the insecticide in insect tissne consnmed by birds. The details of this modeling effort, which we omit here, are rather complex and involve characteristics of the field application of the insecticide, local weather, mnltiple pathways of exposure to insects, sequestration of insecticide by mortality of insects, and integration over 0- to 20-g pools of insect tissne that wonld compose a bird s daily diet. The model of the pesticide s fate and transport made a prediction abont the concentration variable, which is characterized by the p-box shown in the lower left graph of Figure 6.14. This p-box synthesizes all of the knowledge and nncertainty captured in the modeling effort. The model predicts the distribntion fnnction for concentrations, whatever it is, snrely lies within the bonnds shown. 

The routes of exposure to POPs for human beings include inhalation, dermal exposure, and ingestion of water or food contaminated by POPs. Cases of occupational or accidental exposure to POPs have been recorded, particularly during the application of pesticides (Vallack et al., 1998). However, food consumption is one of the most important pathways of exposure for the general population (Dougherty et al., 2000 Stefanelli et al., 2004). 

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