Poisoning dermal exposure

In a case study of a human male accidentally sprayed with acrylonitrile, recurring signs of cyanide poisoning were seen over a 3 day period (Vogel and Kirkendall 1984). This indicates that acrylonitrile is also metabolized to cyanide following predominantly dermal exposure. 

In animals, deaths from acrylonitrile have been reported in several species following inhalation, oral or dermal exposure. In most species, death appears to be related to cyanide poisoning. That the cyanide moiety is involved in human toxicity of acrylonitrile has been reported in a case study in which a human male was sprayed with acrylonitrile when a valve burst (Vogel and Kirkendall 1984). This individual suffered symptoms characteristic of cyanide poisoning, and treatments designed to reduce cyanide levels in the blood were required in order to save his life. 

Dermal exposure of rats and rabbits to endrin resulted in toxicity and death (Gaines 1960 Treon et al. 1955), indicating that percutaneous absorption of endrin occurs. It is likely that occupational poisonings reported by Hoogendam et al. (1962, 1965) also involved dermal absorption, but the extent and relative contribution of dermal exposure cannot be determined. Data describing the rate or extent of dermal absorption were not located. 

Persons with a history of convulsive disorders would be expected to be at increased risk from exposure to endrin. Children may be more sensitive than adults to the acute toxic effects of endrin. In an endrin poisoning episode in Pakistan, children 1-9 years old represented about 70% of the cases of convulsions (Rowley et al. 1987). The causative factor responsible for the outbreak was not identified, however, and the age distribution of cases could be explained by age-specific exposure situations. In general, following oral administration, female animals appear to be more susceptible to endrin toxicity than males (Gaines 1960 Treon et al. 1955). The difference may be due to the more rapid excretion of endrin by male versus female rats (Hutson et al. 1975 Klevay 1971 Korte et al. 1970). A sex-related difference in toxicity was not apparent following dermal exposure (Gaines 1960, 1969). No sex-based differences in endrin-related... 

Other Systemic Effects. Inhalation and/or dermal exposure to diesel fuel has been associated with edema in two individuals (Crisp et al. 1979 Reidenberg et al. 1964). In one of these cases, loin pains, thirst, and severe exhaustion were also reported (Crisp et al. 1979). Several case studies reported fever in children following acute ingestion of kerosene (Akamaguna and Odita 1983 Aldy et al. 1978 Dudin et al. 1991 Mahdi 1988 Majeed et al. 1981 Nouri and Al-Rahim 1970 Saksena 1969 St. John 1982 Subcommittee on Accidental Poisoning 1962). The effects of oral exposure to kerosene in children cannot be used to predict possible effects in adults or the effects of other fuel oils by this route without additional information. Similarly, it cannot be determined whether the effects of diesel fuel noted in humans would occur from exposure to other fuel oils or in the general population since limited information is available. 

There is no evidence that inhalation exposures in occupational settings cause the rapid progressive pulmonary fibrosis and injury to the heart, liver, and kidneys that occur after ingestion. Because of the low vapor pressure, there is little inhalation hazard. Spray droplets are usually too large to reach the alveoli. If exposure is excessive, droplets may be inhaled into the upper respiratory tract and cause nosebleed, sore throat, headache, and coughing from local irritant action. Rarely, dermal exposure to paraquat has resulted in systemic poisonings and deaths with renal and pulmonary... 

Parathion is not irritating to the skin but is rapidly absorbed through the intact skin. With dermal exposure in the occupational setting, onset of symptoms may be delayed for several hours up to as long as 12 hours. This delay in onset, which is unusual for other organophos-phate compounds, may occur even with poisonings that prove to be serious. ... 

Strychnine poisoning may also occur from dermal exposure. In one recent case report a women experienced marked pain in the lower limbs, dermal sensitivity, and stif iess in her jaw 24 hours after cleaning up a strychnine spill. Strychnine was confirmed in the plasma and urine by gas chromatography-mass spectrometry. ... 

Bioavailability from Environmental Media. Case reports of people who have experienced cresol poisoning following oral and dermal exposure indicate that all cresols can be absorbed by these routes (Cason 1959 Chan et al. 1971 Green 1975). However, no information is available regarding oral or dermal absorption of cresols located in water, soil, or plant material. Studies in animals have shown that cresols can be absorbed from contaminated air by inhalation but have not attempted to... 

With exposure to poisons by inhalation, the basic principle is to remove the patient to a well ventilated area. With dermal exposure, and skin contamination. 

Most of the information on the toxicity of white phosphorus in humans comes from case reports of individuals who intentionally or accidentally ingested a single dose of phosphorus that was a component of poison or fireworks. These case reports provide information on acute systemic effects, possible immunological effects, neurological effects, reproductive effects, and death in humans. In addition to these case reports of single exposures, there are several case reports of children ingesting white phosphorus for an intermediate duration these studies provide information on intermediate systemic effects and developmental effects. Information on chronic oral and dermal exposure in humans is limited to occupational exposure studies in which workers were exposed to white phosphorus via inhalation, oral, or dermal routes. Some limited information on chronic systemic effects is available from these studies. There is limited information on the toxicity of inhaled white phosphorus in humans. Several occupational exposure studies are available however, only a limited number of parameters were assessed in these studies. 

DNOC is rapidly absorbed by the respiratory tract in humans and animals. A serum DNOC concentration of 1,000 pg/mL was detected in a spray operator 24-36 hours after inhaling a dense DNOC mist for an acute duration (van Noort et al. 1960). The worker subsequently died. Because the spray operator had previous dermal exposure to DNOC, the acute inhalation of dense DNOC mist probably caused the serum DNOC level to spike to lethal levels. A blood DNOC concentration of 60 pg/g was detected in a spray operator who had periodically inhaled an unknown amount of DNOC for 5 weeks (Pollard and Filbee 1951). The blood sample was collected after a 2-day period of no exposure. In addition, a DNOC peak urinary level of 22 mg was detected on the third day after the patient was admitted to the hospital, and a total of 89.9 mg DNOC was eliminated in the urine over 20 days. While these data indicate absorption after inhalation exposure, there was also possible dermal absorption. In an occupational exposure study involving DNOC manufacturers, winter-washer sprayers, and cereal-crop sprayers, a correlation between blood DNOC levels and the symptoms and signs of poisoning was observed (Bidstrup et al. 1952). Blood DNOC levels <10-20 p g/g were not generally associated with signs of toxicity, while concentrations greater than 44 pg/g resulted in several illnesses. 

Recently, a 6-year-old child, acutely poisoned by sitting in a pool of parathion, was studied and found to be excreting PNP for 72 hours, suggesting that the prolonged excretion pattern is more a manifestation of dermal exposure and is in contrast to the shorter excretion pattern observed following accidental ingestion. 

Toxicity and health effects Benzidine is known to be acutely toxic to humans by ingestion. The symptoms of acute poisoning by ingestion include but are not restricted to cyanosis, headache, mental confusion, nausea, and vertigo. Dermal exposure may cause skin rashes and irritation. There is no information available on the acute effects of benzidine in humans via inhalation exposure. Animals exposed for a prolonged period of time developed effects on the blood, liver, kidney, and CNS. Chronic exposure caused bladder injury among workers. ... 

Strychnine is rapidly absorbed from the gastrointestinal tract, mucous membranes, and parenteral sites of injection (Thienes and Haley, 1972) and also from the oral cavity (LaDu et al, 1971). A nonfatal case of strychnine poisoning through dermal exposure is also described (Greene and Meatherall, 2001). Strychnine is transported by plasma and... 

SAFETY PROFILE Confirmed carcinogen. Mildly toxic by inhalation. Human systemic effects by inhalation cough, conjunctiva irritation, hallucinations or distorted perceptions. Repeated or prolonged dermal exposure causes dermatitis. Can cause blistering of skin. Inhalation or ingestion can cause central nervous system depression. Pulmon-aty aspiration can cause severe pneumonitis. Some addiction has been reported from inhalation of fumes. Even brief inhalations of high concentrations can cause a fatal pulmonary edema. The vapors are considered to be moderately poisonous. If its con-... 

SAFETY PROFILE Poison by intravenous route. May act as a simple asphjndant. See also ARGON for a description of simple asphyxiants. A narcotic in high concentration. Human dermal exposure to undiluted octane for five hours resulted in blister formation but no anesthesia exposure for one hour caused diffuse burning sensation. A ver) dangerous fire hazard and severe explosion hazard when exposed to heat, flame, or oxidizers. When heated to decomposition it emits acrid smoke and irritating fumes. See also ALKANES. 

Renal Effects. Rabbits, guinea pigs, rats, and mice dermally exposed to uranyl nitrate hexahydrate for 1 day showed proteinuria for up to 10 days, followed by recovery to control values. The degree of proteinuria did not correlate well with the applied dose of uranium. Rabbits had elevated blood NPN at doses over 270 mg U/kg. The animals that died from dermal exposure to uranium had microscopic renal damage typical of uranium poisoning. The kidneys of the animals that did not die were essentially normal, which may reflect repair of acute renal injury (Orcutt 1949). Chemically induced renal failure caused 100% mortality in male Wistar rats after 5 daily exposures to 237 or 1,928 mg U/kg/day as uranyl nitrate hexahydrate or ammonium uranyl tricarbonate, respectively, applied in a water-Vaseline emulsion (De Rey et al. 1983). Deaths from renal failure were also reported in this study for male Wistar rats that received daily apphcations of 1,965 mg U/kg as uranyl acetate dihydrate for 1-11 days. 

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