Dermal limit

Aldrin (CAS 309-00-2) Chlorinated insecticide (see p 161). Minor skin irritant. Convulsant. Hepatotoxin. Well absorbed dermally. Limited evidence for carcinogenicity in test animals (lARC 3). 0.25 mg/m S,A3 NIOSH CA 25 mg/m Tan to dark brown solid. A mild chemical odor. Vapor pressure is 0.000006 mm Hg at 20°C (68°F). Not flammable but breaks down, yielding hydrogen chloride gas. Most uses have been banned in US. 

Diazinon (0,0-diethyl 0-2-isopropyl-4-melhyl-6-pyiimidinylthio-phosphate [CAS 333-41-5]) An organophosphate-type cholinesterase inhibitor (see p 291). Well absorbed dermally. Limited evidence for adverse effects on male reproduction and fetal development in test animals at high doses. 0.1 mg/m , S Commercial grades are yellow to brown liquids with a faint odor. Vapor pressure is 0.00014 mm Hg at 20 C (68 F). Themnal-breakdown products include oxides of nitrogen and sulfur. 

Health and Safety Factors. See "General Health and Safety Eactors." The following toxicides for adiponitrile have been reported oral LD q (rats), 300 mg/kg dermal LD q (rabbits), 2,134 mg/kg and inhalation 4-h LC q (i ts), 1.7 mg. NIOSH has proposed an exposure limit of 4 ppm as a TWA (68). 

Hydraziae is toxic and readily absorbed by oral, dermal, or inhalation routes of exposure. Contact with hydraziae irritates the skin, eyes, and respiratory tract. Liquid splashed iato the eyes may cause permanent damage to the cornea. At high doses it can cause convulsions, but even low doses may result ia ceatral aervous system depressioa. Death from acute exposure results from coavulsioas, respiratory arrest, and cardiovascular coUapse. Repeated exposure may affect the lungs, Hver, and kidneys. Of the hydraziae derivatives studied, 1,1-dimethylhydrazine (UDMH) appears to be the least hepatotoxic monomethyl-hydrazine (MMH) seems to be more toxic to the kidneys. Evidence is limited as to the effect of hydraziae oa reproductioa and/or development however, animal studies demonstrate that only doses that produce toxicity ia pregaant rats result ia embryotoxicity (164). 

Although there is Httle toxicity information pubHshed on hydrides, a threshold limit value (TLV) for lithium hydride in air of 25 fig/has been established (52). More extensive data are available (53) for sodium borohydride in the powder and solution forms. The acute oral LD q of NaBH is 50-100 mg/kg for NaBH and 50-1000 mg/kg for the solution. The acute dermal LD q (on dry skin) is 4-8 g/kg for NaBH and 100-500 mg/kg for the solution. The reaction or decomposition by-product sodium metaborate is slightly toxic orally (LD q is 2000-4000 mg/kg) and nontoxic dermally. 

The hazards with glutaraldehyde are those of irritation to the skin, eyes, throat, and lungs. It can cause dermal and respiratory sensitization, resulting in rhinitis and conjunctivitis or asthma. In the UK the Maximum Exposure Limit is just 0.05 ppm (8 hr TWA limit) and 0.05 ppm (15 min STEL) with a Sen notation (p. 93). 

In a case-control study of pesticide factory workers in Brazil exposed to methyl parathion and formulating solvents, the incidence of chromosomal aberrations in lymphocytes was investigated (De Cassia Stocco et al. 1982). Though dichlorodiphenyltrichloroethane (DDT) was coformulated with methyl parathion, blood DDT levels in the methyl parathion-examined workers and "nonexposed" workers were not significantly different. These workers were presumably exposed to methyl parathion via both inhalation and dermal routes however, a dose level was not reported. The exposed workers showed blood cholinesterase depressions between 50 and 75%. However, the baseline blood cholinesterase levels in nonexposed workers were not reported. No increases in the percentage of lymphocytes with chromosome breaks were found in 15 of these workers who were exposed to methyl parathion from 1 week to up to 7 years as compared with controls. The controls consisted of 13 men who had not been occupationally exposed to any chemical and were of comparable age and socioeconomic level. This study is limited because of concomitant exposure to formulating solvents, the recent history of exposure for the workers was not reported, the selection of the control group was not described adequately, and the sample size was limited. 

Chromosome aberrations were detected in lymphocytes of individuals acutely intoxicated by methyl parathion by the inhalation route (Van Bao et al. 1974). Blood samples were taken 3-6 days after exposure and again at 30 and 380 days. A temporary but significant (p<0.05) increase was noted in the frequency of stable chromosomal aberrations in the exposed individuals. The study limitations include small sample size, absence of a control group, lack of quantification of exposure levels, and a possible concomitant exposure to other substances via the dermal route. 

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. 

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl parathion in humans and animals by various routes of exposure. The available literature reviewed concerning the health effects of methyl parathion in humans described case reports of longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The occupational exposure is believed to be via the dermal and inhalation routes. The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be quantified. 

The database for the health effects of methyl parathion after ingestion in experimental animals is substantial. However, as can be seen in Figure 3-5, only limited information is available on the effects of inhalation and dermal exposure to methyl parathion in animals. Furthermore, the health effects such as death and neurotoxicity resulting from acute exposure in animals are more fully studied than systemic and immunotoxic effects associated with acute exposure. 

No studies were located regarding excretion of methyl parathion in humans following inhalation exposure. The limited information available from human case studies indicates that the chemical s metabolites are rapidly excreted primarily in the urine in humans following oral (Morgan et al. 1977) or dermal (Ware et al. 1974, 1975) exposure and in animals following oral (Hollingworth et al. 1973) or dermal (Abu-Qare et al. 2000) exposure. 

Limited information is available regarding the effects of endosulfan in humans and animals after inhalation exposure. The reports of effects in humans are limited to case reports of adverse effects noted in workers exposed to large quantities of endosulfan during its manufacture. Exposures in these reports are likely to be a combination of inhalahon and dermal exposures. Therefore, the findings from these case reports are also presented in the section on dermal exposures (Section 2.2.3). 

The data in animals are insufficient to derive an acute inhalation MRL because serious effects were observed at the lowest dose tested (Hoechst 1983a). No acute oral MRL was derived for the same reason. The available toxicokinetic data are not adequate to predict the behavior of endosulfan across routes of exposure. However, the limited toxicity information available does indicate that similar effects are observed (i.e., death, neurotoxicity) in both animals and humans across all routes of exposure, but the concentrations that cause these effects may not be predictable for all routes. Most of the acute effects of endosulfan have been well characterized following exposure via the inhalation, oral, and dermal routes in experimental animals, and additional information on the acute effects of endosulfan does not appear necessary. However, further well conducted developmental studies may clarify whether this chemical causes adverse developmental effects. 

Since the limited information available on the effects of dermally administered endosulfan suggests that this chemical behaves similarly across both routes of exposure and that adverse effects on immune function end points have also been observed in vitro, there is no reason to suspect that the immunotoxic effects observed following oral exposure are route-specific. Tests of immunologic function in exposed human populations would provide information as to whether immunosuppression also occurs in humans... 

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