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Children, accidental ingestion

Ingestion of contaminants is the primary exposure pathway for drinking-water. Dermal absorption and inhalation of contaminants during bathing are other common pathways. When contaminated surface waters serve as recreational areas for children, accidental ingestion (water or sediment) and dermal contact become additional pathways for exposure. Finally, aquatic organisms can bioaccumulate contaminants in surface waters, which can lead to dietary exposure through the food-chain. [Pg.152]

In young children, accidental ingestion leads to the rapid onset of drowsiness, hypotonia, dilated pupils, and coma. Fortunately, gradual recovery occurs spontaneously, barring accidents. Passive inhalation of marijuana in infants can have serious consequences. [Pg.482]

Mineral Oil Hydraulic Fluids. Lipoid pneumonia with marked interstitial pneumonitis and pulmonary fibrosis was observed in a child accidentally ingesting a lethal dose of automotive transmission fluid (Perrot and Palmer 1992). Although the exact composition of the hydraulic fluid was not reported, it is assumed to be a mineral oil hydraulic fluid because automotive transmission fluids typically contain... [Pg.110]

Mineral Oil Hydraulic Fluids. There is limited information on the toxicity of mineral oil hydraulic fluids in humans. A single case report of a child accidentally ingesting a single dose of automotive transmission fluid provides limited information on death and systemic effects. A case-control study provides some information on the carcinogenicity of mineral oil hydraulic fluids. The study population was exposed via inhalation and dermal routes. An occupational exposure study provides information on neurotoxicity following chronic dermal exposure. Information on the toxicity of mineral oil hydraulic fluids is limited to a series of inhalation, oral, and dermal acute-duration exposures. These studies provide information on death, systemic effects, and neurotoxicity by inhalation, oral, and dermal routes, and immunotoxicity following dermal exposure. [Pg.234]

Mineral Oil Hydraulic Fluids. There is limited information on the acute toxicity of mineral oil hydraulic fluids to humans. A single case report of a child accidentally ingesting automotive transmission fluid reported respiratory and gastrointestinal effects (Perrot and Palmer 1992). [Pg.238]

A two year old child accidentally ingested DDT/Kerosene mixture equivalent to 278 mg/Kg and died. Workers have experienced suhstantially higher concentrations without ill... [Pg.123]

Accidental ingestion of nickel sulfate crystals (15-20 grams) by 2.5 year-old female child Death in 4 h of heart failure blood had 7.5 mg Ni/kg, urine 50 mg/L, and liver 25 mg Ni/kg FW 6, 8... [Pg.503]

Even children are not immune from poisoning by PCP. Six cases were observed at the UCLA Medical Center, all 5 years old or younger. Presumably, most were poisoned by accidental ingestion of the drug, which was available in the house one child, only 11 days old, was presumably poisoned by passive inhalation of the smoke produced by the adults around him. The most common clinical manifestations in these youngsters was bizarre behavior, lethargy, ataxia, and nystagmus (48). [Pg.22]

Paradoxically, catnip fed to mice had stimulant effects, with increased rearing, locomotion, and stereotypical behavior, increased susceptibility to chemically induced (picrotoxin and strychnine) seizures, and decreased sleeping time after barbiturate administration (Massoco et al. 1995). The LD50 for nepetalactone in mice was reported to be quite high at 1300 mg/kg (Harney et al. 1978). In chicks, an a cohol extract of catnip had biphasic effects, where low to moderate doses (25-1800 mg/kg) produced sedative effects, while higher doses (>2 g/kg) had less sedative and perhaps stimulant effects (Sherry and Hunter 1979). Humans have reported sedative effects of catnip, and one accidental ingestion by a young child reportedly produced sedative effects (Osterhoudt et al. 1997). [Pg.243]

Numerous case studies have described death following the accidental ingestion of kerosene by children (usually under the age of 5 but as old 15 years). The deaths are usually attributed to lipoidal pneumonia (Morrison and Sprague 1976 Santhanakrishnan and Chithra 1978 Zucker et al. 1986) that was probably induced by the aspiration of the kerosene. Specific respiratory effects associated with death from kerosene ingestion include pneumothorax (Mahdi 1988 Zucker et al. 1986), emphysema (Mahdi 1988), and pneumonitis (Singh et al. 1981). Cardiac arrhythmia was reported as the cause of death in one child however, it was suspected that myocarditis and pulmonary edema may have been the cause of the rapid deterioration and death of the child (Dudin et al. 1991). [Pg.47]

Methadone, used as an analgesic, may be dispensed in any licensed pharmacy. Methadone dispersible tablets are for oral administration only. This preparation contains insoluble excipients and therefore must not be injected. It is recommended that methadone dispersible tablets, if dispensed, be packaged in child-resistant containers and kept out of the reach of children to prevent accidental ingestion. [Pg.839]

One human death following oral exposure to nickel was reported (Daldrup et al. 1983). Nickel sulfate crystals (rough estimate of 570 mg nickel/kg) were accidentally ingested by a 2-year-old child. Four hours after ingestion, cardiac arrest occurred, and the child died 8 hours after exposure. [Pg.66]

Cardiovascular Effects. A 2-year-old child died from cardiac arrest following accidental ingestion of nickel sulfate (Daldrup et al. 1983). No increases in numbers of deaths from cardiovascular diseases were reported in nickel workers (Cornell and Landis 1984 Cox et al. 1981 Cragle et al. 1984). [Pg.123]

Humans have been exposed to nickel in nickel mines and processing plants, and numerous epidemiology studies have been performed to assess the cause of death in these workers. Accidental ingestion of nickel also has been documented in a small child and in electroplating workers. Nickel dermatitis is the most prevalent effect of nickel in humans. [Pg.152]

Accidental ingestion ot nickel sultate crystals (15-20 grams) by 2.5 year-old temale child... [Pg.503]

An 11-kg, 1-year-old child developed agitation followed by prolonged lethargy after accidental ingestion of an unknown amount of olanzapine (260). [Pg.319]

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. [Pg.83]

Nisse P, Lhermitte M, Dherbecourt V, Fourier C, Leclerc F, Houdret N, Mathieu-Nolf M. Intoxication mortelle apres ingestion accidentelle de Xylocaine visqueuse a 2% chez une jeune enfant. [Fatal intoxication after accidental ingestion of viscous 2% lidocaine in a young child.] Acta Clin Belg Suppl 2002 (l) 51-3. [Pg.2060]

The human literature primarily consists of case reports. In the industrial environment, symptoms including headache, numbness, skin irritation and redness, eye irritation and redness, irritation and redness of the upper respiratory tract, bronchitis, dizziness, somnolence, loss of consciousness, hematopoietic effects, gastritis, hepatitis, and neuromuscular changes have been reported. Accidental ingestion of 5-10 ml of a cleaning agent containing chlorobenzene caused loss of consciousness, vascular paralysis, and heart failure in a child ( 2 years old). [Pg.558]

A comprehensive review estimated that child resistant closures on prescription medicines have prevented over 200,0(X) accidental ingestions during 1974-1978 and saved, on average, 26 children s lives a in the United States. The ingestion rate per thousand children has declined from 5.7 cases to 3.5 during the same period. Child resistant closures are now accepted and widely used in the USA [18]. [Pg.418]

C. The child is over 4-5 years old. Accidental ingestions are rare in older children, and ingestion may be a signal of abuse or neglect. [Pg.61]

It should be noted from Table XI that the iodine dose (5.2 rad) that can be received by accidental ingestion as defined in the previous paragraph is comparable in size to the iodine dose from inhalation (15.5 rads-Table IX). Figure 15 of Beattie and Bryant (39) shows that 10% of the iodine in milk dose could be received by the child within the first day. Therefore, for public areas close to and downwind of the reactor, the milk ban should be prompt if the ERL of 25 rads thyroid dose is not to be exceeded. More distant areas with lower levels of milk contamination can wait. Technically,... [Pg.43]


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See also in sourсe #XX -- [ Pg.38 ]




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