Dermal exposure decrease

Abou-Donia et al. (2001b) Rat DEET, permethrin Combined dermal exposures decreased blood-brain barrier permeability in cerebral cortex and produced impaired sensorimotor performance... 

There is limited information available regarding the distribution of methyl parathion after dermal exposure in humans. Two subjects, dermally exposed to methyl parathion, had 2.74 and 1.23 mg on their hands. Twenty-four hours after exposure, the serum levels were 0.027 and 0.032 mg/L, respectively (Ware et al. 1973). Twelve hours after cotton fields were sprayed, five men entered the treated fields for 5 hours. An average of 1.7 mg methyl parathion was detected on their hands. Serum concentrations averaged 0.156 mg/L in these subjects after 3 hours of exposure. Levels decreased to 0.1 and 0.002 mg/L at 2 and 24 hours postexposure, respectively (Ware et al. 1975). Although 0.5 mg methyl parathion was detected on the hands of four subjects, none was found in the serum (Ware et al. 1974). No information on the tissue distribution of methyl parathion in humans was found. 

Central nervous system stimulation similar to that reported for occupational exposure is seen following acute dermal exposure to endosulfan in experimental animals. The spectrum of effects includes hyperexcitability, tremors, decreased respiration, tonic-clonic convulsions, and ultimately death (Gupta and Chandra 1975 Hoechst 1989b Nicholson and Cooper 1977). In rats, the lowest doses associated with these effects were 16 mg/kg/day in females and 250 mg/kg/day in males during a 6-hour/day, 5-day exposure regimen (Hoechst 1989b). 

No studies were located regarding reproductive effects in humans after dermal exposure to mirex. The available data in humans indicate that chlordecone causes male reproductive effects. Occupational exposure to chlordecone for up to 1.5 years caused oligospermia and decreased sperm motility in male workers. However, there were no reported infertility in these male subjects despite loss of sperm motility in some workers (refer to Section 2.2.1.5 for further details). 

Reproductive Effects. No studies were located regarding reproductive effects in humans or animals following inhalation or dermal exposure to di-ra-octylphthalate. No studies were located in humans following oral exposure to this compound. However, di-ra-octylphthalate has been shown to cause significant decreases in human sperm motility in vitro (Fredricsson et al. 1993). 

Reproductive Toxicity. No studies were located regarding reproductive effects in humans or animals following inhalation or dermal exposure to di-ft-octylphthalate. No studies were located in humans following oral exposure to this compound. Di-u-octylphthalate caused significant decreases in human sperm motility in vitro (Fredricsson et al. 1993). The results of several acute- and intermediate-duration oral studies in rodents indicate that the potential of di-w-octylphthalate to cause adverse reproductive effects is low. Unlike other phthalate esters such as di(2-ethylhexyl)phthalate, di-w-octylphthalate does not appear to adversely affect testicular function or morphology (Foster et al. 1980 Gray and Butterworth 1980 Heindel et al. 

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