Toxicity respiratory distress

Since chloroacetyl chloride can react with water in the skin or eyes to form chloroacetic acid, its toxicity parallels that of the parent acid. Chloroacetyl chloride can be absorbed through the skin in lethal amounts. The oral LD q for rats is between 120 and 250 mg/kg. Inhalation of 4 ppm causes respiratory distress. ATLV of 0.05 ppm is recommended (28,41). 

Menthol and camphor have caused respiratory distress in infants and should not be used in children under 2 years of age. Despite limits on the concentration of available products, camphor can be toxic to children even in small amounts.45 Patients should be advised to keep the products out of the reach of children. 

The comparative toxicity of hydrazine, and the symmetrical and asymmetrical isomers of dimethylhydrazine were reported by Jacobson et al. (1955). Rats and mice exposed to hydrazine, and rats exposed to symmetrical dimethylhydrazine exhibited restlessness, dyspnea, and convulsions with exophthalmos. Excessive salivation, vomiting, respiratory distress, and convulsions were reported for dogs exposed to asymmetrical dimethylhydrazine as well as monomethylhydrazine. Fourteen-day mortality in three groups of dogs (three dogs per group) exposed for 4 h to asymmetrical dimethylhydrazine at concentrations of 24, 52, or 111 ppm were 0/3, 1/3, and 3/3, respectively. For rodents, estimated LC50 values for hydrazine, asymmetrical dimethylhydrazine, and symmetrical dimethylhydrazine are shown in Table 3-8. 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to carbon monoxide diabetic ketoacidosis, hypothyroidism and myxedema coma, labyrinthitis, and lactic acidosis toxic exposures resulting in methemoglobinemia ingestion of alcohols or narcotics and diseases that cause gastroenteritis, encephalitis, meningitis, and acute respiratory distress syndrome. 

Human toxicity values have not been established or have not been published. However, concentrations above 1500 ppm cause gasping, refusal to breathe, coughing, substernal pain, and extreme respiratory distress. 

Suggested Alternatives for Differential Diagnosis Acute respiratory distress syndrome, congestive heart failure, pulmonary edema, AIDS, pneumonia, cardiogenic shock, septic shock, phosgene toxicity, phosphine toxicity, salicylate toxicity with pulmonary edema, influenza, plague, tularemia, and anthrax. 

The plant produced pesticides. An intermediate compound in this process is methyl isocyanate (MIC). MIC is an extremely dangerous compound. It is reactive, toxic, volatile, and flammable. The maximum exposure concentration of MIC for workers over an 8-hour period is 0.02 ppm (parts per million). Individuals exposed to concentrations of MIC vapors above 21 ppm experience severe irritation of the nose and throat. Death at large concentrations of vapor is due to respiratory distress. 

Effects Noted in Study and Corresponding Doses Doses of 0.20 mg/kg/day and greater resulted in neurotoxicity evidenced by convulsions, tremors, and degenerative lesions in the brain and systemic toxicity which included renal tubular necrosis, respiratory distress and pulmonary edema, and diffuse degenerative lesions of the heart. One animal administered diet corresponding to 0.20-0.27 mg/kg/day died after 47 days of feeding. 

Mouse Bioassay. When administered at 5 mg per mouse in 0.5 ml dose during the initial screening, the WSAP from G. toxicus caused death in all test mice within 120 minutes. The toxin had a latency period of approximately 30 minutes after which signs of toxicity were noticeable, and included in order of occurrance inactivity and piloerection followed by cyanosis of the tail and feet with concurrent hypothermia, vasodilation in the ears ( scarlet ears ), lacrimation, ptosis of the eye lid on the side of injection, ptosis of the abdomen (loss of muscular tone), asthenia, impairment of hind limb motor ability followed shortly by complete paralysis with the hind limbs extended posteriorly (complete prostration), and dyspnea (respiratory distress). Death occurred without convulsions and the eyes became cataracted just prior to or after death. 

The LCso in mice was 450 ppm for a 4-hour exposure in rats, the LCso for 8 hours was 580 ppm labored breathing, lacrimation, salivation, and nasal discharge were seen, and pneumonitis was observed at autopsy Rats repeatedly exposed to 400 ppm showed only slight eye irritation and mild respiratory distress, with no evidence of systemic toxicity. 

Studies indicate that isopropyl alcohol may be substantially better absorbed by the dermal route than had previously been believed, although significant toxicity by this route would require prolonged exposure. Delayed dermal absorption rather than inhalation may account for a number of pediatric poisonings that have occurred after repeated or prolonged sponged bathing with isopropyl alcohol to reduce fever. In several cases symptoms have included respiratory distress, stupor, and coma. Recovery was complete within 36 hours. Hypersensitivity characterized by delayed eczematous reactions have occasionally been observed after dermal contact with isopropyl alcohol. ... 

Musculoskeletal/Cardiac effects When serum sodium or calcium concentration is reduced, moderate elevation of serum potassium may cause toxic effects on the heart and skeletal muscle. Weakness and later paralysis of voluntary muscles, with consequent respiratory distress and dysphagia, are generally late signs, sometimes significantly preceding dangerous or fatal cardiac toxicity. 

Toxicity Toxicity is characterized by an exaggeration of parasympathomimetic effects which may include the following Headache visual disturbance lacrimation sweating respiratory distress Gl spasm nausea vomiting diarrhea AV block tachycardia bradycardia hypotension hypertension shock mental confusion cardiac arrhythmia tremors. 

Mercury was used to cure the felt used in hats, and workers developed the characteristic signs of mercury vapor toxicity. Acute exposure to high concentrations of mercury vapor causes respiratory distress, which can be fatal. The symptoms of chronic exposure to mercury vapor include personality changes such as excitability, depression, memory loss, fine motor tremor that can become progressively worse, gingivitis, and hallucination. There is some mercury inhalation exposure from dental amalgam, but for most people there are no health-related effects. Metallic mercury is very poorly absorbed from the intestine, thus it is much better to swallow the mercury from a thermometer than inhale it (see chapter on mercury). 

Animal studies also indicate that the respiratory system is a major target of toxicity following inhalation exposure to chlorine dioxide. Dalhamn (1957) reported the results of several inhalation studies in laboratory animals. In one study, a single 2-hour inhalation exposure of four rats to a chlorine dioxide concentration of 260 ppm (728 mg/m ) resulted in pulmonary edema and nasal bleeding. Respiratory distress was reported in three other rats subjected to 3 weekly 3-minute exposures to decreasing concentrations of airborne chlorine dioxide from 3,400 to 800 ppm (from 9,520 to 2,240 mg/m ) bronchopneumonia was observed in two of these rats. In a third rat study, repeated exposure to approximately 10 ppm (28 mg/m ) of chlorine dioxide (4 hours/day for 9 days in a 13-day period) resulted in rhinonhea, altered respiration, and respiratory infection. No indications of adverse effects were seen in rats exposed to approximately 0.1 ppm (0.28 mg/m ) of chlorine dioxide 5 hours /day for 10 weeks. 

Delayed respiratory distress, fibrosis, and atelectasis Gastrointestinal, liver, and kidney toxicity Formation of reactive oxygen species Block tricarboxylic acid cycle (fluoroacetates)... 

Serious, potentially fatal pulmonary toxicity (alveolitis, pulmonary fibrosis, pneumonitis, acute respiratory distress syndrome) may begin with progressive dyspnea and cough with crackles, decreased breath sounds, pleurisy, CH F, or hepatotoxicity. 

Nerve agents Highly toxic and potentially lethal chemical agents that affect the human nervous system by inhibiting the enzyme that aids the transmission of nerve impulses. Causes blurred vision, weeping, nausea, vomiting, urinary incontinence, respiratory distress, and reduced mental capability by attacking the nervous system. 

Deferoxamine (see also Chapters 58 and 59) Chelates excess iron Reduces the toxicity associated with acute or chronic iron overload Treatment of acute iron poisoning and for inherited or acquired hemochromatosis that is not adequately treated by phlebotomy Preferred route of administration is IM or SC Toxicity Rapid IV administration may cause hypotension acute respiratory distress has been observed with long infusions neurotoxicity and increased susceptibility to certain infections has occurred with longterm use... 

---