Potential dermal exposure

Wet wipe sampling is generally not recommended for carpet, upholstery and other fabric-covered or soft surfaces because the solvent may be absorbed into the surface being sampled. Wipes of soft surfaces also are less likely than wipes of hard surfaces to reflect the dermal exposure potential (Ness, 1994). However, Lu and Fenske (1999) recently reported the use of cotton gauze wetted by misting with distilled water to wipe carpets freshly treated with a chlorpyrifos formulation (Dursban L.O.) and found it to be 23 to 24 times more efficient than transfer to dry palm presses. 

Care must be exercised in handling carbon disulfide because of both health concerns and the danger of fire or explosions. Occupational exposure potentially may involve as many as 20,000 workers in the United States (136). Ingestion is rare, but a 10 mL dose can prove fatal (137). Contact usually occurs by inhalation of vapor. However, vapor and Hquid can be absorbed through intact skin and poisoning may occur by the dermal route (138). 

In addition, the use of chemical protective clothing was not supported by air or surface contamination monitoring to determine the potential for dermal exposure and the appropriate PPE. 

There are insufficient data to determine potential daily inhalation and dermal exposure levels. However, based on the information presented in Seetions 6.3 and 6.4, exposure levels for the general population are probably very low by these routes. Inhalation exposure is not important for the general population, with the possible exception of those individuals living near areas where methyl parathion is frequently sprayed. Since methyl parathion is readily adsorbed through the skin, dermal eontact may be the most relevant exposure pathway. Dermal eontaet is most likely to oeeur in people who are occupationally exposed. 

The calculation of potential total dermal exposure of mixer-loaders and re-entry workers using dosimetry data and calculation of the internal dose using biological monitoring data is complex but will be discussed briefly. 

No studies were located regarding interactions with other substances in humans or animals after exposure to diisopropyl methylphosphonate. However, the potential for multiple chemical interactions does exist. Diisopropyl methylphosphonate has been identified in the RMA in the presence of many other chemicals (such as endrin, dieldrin, dicyclopentadiene, bicycloheptdiene, diethyl benzene, and diethyl disulfide). The nervous system is a target of many of these compounds found at the RMA, including diisopropyl methylphosphonate. Therefore, there is potential for interaction, and studies examining multiple exposures would be useful in predicting risk to humans. Workers at the RMA reported skin irritation after dermal exposure to diisopropyl methylphosphonate at concentrations around 11.3 ppm in water. However, several other chemicals were also in the area (NIOSH 1981). Therefore, it is not clear if diisopropyl methylphosphonate contributed to the effects. 

The variances of potential dermal exposure are presented in Table 1. Very large "within-worker" variances of potential exposure of the hands resulted in insignificant differences between workers. For harvesters, a similar result was obtained for potential exposure of the body parts. For both applicators and harvesters, significant "between-worker" differences of total potential exposure were observed. 

Figure 1 Distribution of the potential dermal exposure of applicators (N = 3, n = 9) to propoxur and of harvesters (N = 6, n = 18).

For applicators, hand exposure was approximately 15% of the total potential dermal exposure. 

The design of a study by Davies et al. (1982) for mixers and applicators was similar to that of Nigg and Stamper (1983). "Between-days" variances of exposure were not given. Mean urinary metabolite concentrations were used to show reduction of internal exposure by protective clothing. The design of the study by van Rooij et al. (1993) was similar to our study (i.e., "within-worker" comparisons of internal exposure). Because no potential dermal exposure was assessed in this study, "within-worker" variances of potential exposure are not known. 

The total unprotected dermal exposure (TUDX) is the sum of the exposure on coveralls, socks, hands, gloves, hat, face, and neck. This represents the maximum potential exposure of the operator, and this value and provides... 

Potential dermal exposure (PDE) was the sum of the amount of chlorpyrifos retained by the dosimeter (socks, gloves, and union suit) during the 20-min exposure period. Absorbed daily dose (ADD) was the sum of chlorpyrifos equivalents measured in urine for days 2,3, and 4. Home-use biomonitoring data are expressed as chlorpyrifos equivalents per day, as exposure continued throughout the test period. 

The WBDs retained an average potential dermal exposure (PDE) of 13,757 pg chlorpyrifos. If clothing penetration is assumed to be 10% and dermal absorption 9.6% per 24 hr, then the absorbed dose would be 132 pg, and the absorbed dosage would be about 1.9 pg/kg. Biological monitoring of the 13 volunteers wearing cotton dosimeters indicated that the absorbed daily dose that penetrated the WBD and was absorbed was 2 pg chlorpyrifos equivalents/kg (Table 2). 

Krieger, R.I., Bernard, C.E., Dinoff, T.M., Fell, L., Osimitz, T. G., Ross, J.I., and Thongsinthusak, T. (2000) Biomonitoring and whole body cotton dosimetry to estimate potential human dermal exposure to semivolatile chemicals, /. Exposure Anal. Environ. Epidemiol., 10 50-57. 

The first pesticide exposure study was reported by Griffiths et al. (1951). Parathion was trapped on respirator filter discs during application to citrus trees. Batchelor and Walker (1954) expanded exposure monitoring to include the estimation of potential dermal exposure using pads attached to workers clothing. Durham and Wolfe (1962), in their classic review of worker exposure methodologies, also provided some experimental validation for the best available methods. 

The carcinogenic potential of hexachloroethane has not been evaluated following chronic inhalation or dermal exposure. Hexachloroethane increased the incidence of renal tumors in male rats (NTP 1989) following chronic oral exposure. However, these tumors were associated with renal hyaline droplets and, thus, are unique to male rats. Although kidney damage was present in female rats after lifetime exposures to 80 and 160 ppm hexachloroethane, there was no increase in renal tumors. Liver lesions and liver tumors were found in mice following long-term oral exposure (NTP 1977). 

Studies regarding the systemic effects that have been observed in humans and animals after dermal exposure to endrin are discussed below. With regard to potential dermal effects, no reports of irritative effects have appeared in the medical or industrial hygiene literature despite several decades of use by hundreds of workers. No reliable studies were located regarding respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, endocrine, dermal, ocular, or body weight effects in humans or animals after dermal exposure to endrin, endrin aldehyde, or endrin ketone. 

Intermediate-Duration Exposure.No studies are available on the adverse health effects from intermediate-duration exposure in humans by any route. Studies in animals indicate that exposure to endrin via inhalation can be lethal and causes effects on the nervous and respiratory systems, the liver, the brain, adrenals, and kidneys (Treon et al. 1955). Since systemic effects were observed at levels which caused death, data are not sufficient to derive an intermediate-duration inhalation MRL. Animal studies also demonstrate that oral intermediate-duration exposure can lead to death in several species (rat, mouse, hamster, rabbit, monkeys, cat) (Treon et al. 1955). Endrin was lethal in rabbits following dermal exposure (Treon et al. 1955). No other treatment-related disorders are known. Additional studies for oral and dermal routes using a range of exposure levels would be useful in identifying potential target tissues. 

Genotoxicity. No in vivo studies were found in humans or animals following inhalation, oral, or dermal exposure to endrin. Microbial assays and one mammalian cell assay have demonstrated that endrin does not have mutagenic potential with or without metabolic activation (Ames et al. 1975 Glatt et al. 

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