過塩素酸リチウム

In case of oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mol) of water or milk. Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in Trendelenburg and left lateral decubitus position or by endotracheal intubation. Control any seizures first. Maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Following inhalation, Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of acute lung injury, maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (T36)

Adverse effects on a wide variety of organ systems can result from disruption in the availability of T3 to target tissues. Organ systems affected by disturbances in T3 levels include the skin, cardiovascular system, pulmonary system, kidneys, gastrointestinal tract, liver, blood, neuromuscular system, central nervous system, skeleton, male and female reproductive systems, and numerous endocrine organs, including the pituitary and adrenal glands. Such an array of secondary potential targets underscores the need to maintain an adequate level of circulating thyroid hormones. Perchlorate, an environmental contaminant, is known to disturb the hypothalamus-pituitary-thyroid (HPT) axis by blocking iodide accumulation in the thyroid. Iodide deficiency can lead to hypothyroidism and goiter (L894, A267).

The primary and most sensitive target of the perchlorate anion (perchlorate) is the thyroid gland. Perchlorate inhibits the transport of iodide (I-) from the blood into the thyroid follicle cells. The inhibition is thought to be accomplished by perchlorate competitively blocking iodide binding to a carrier, or sodium/iodide symporter (NIS), which catalyzes the simultaneous transfer of Na+ and I-across the basolateral membrane of thyroid follicle cells. Perchlorate inhibition of the NIS can limit the availability of iodide needed for the production of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), which in turn, may affect the circulating levels of T4 and T3. All known effects of perchlorate on the thyroid hormone system derive directly or secondarily from the inhibition of the NIS. T3 is essential for normal development of the nervous system and for the regulation of metabolism of cells in nearly all tissues of the body. Disruption in the availability of T3 in target tissues can result in adverse effects on a wide variety of organs and systems (L894).

0.0007

IRIS Current

5.50e+01

8.20e+02

1.40e+01

4.00e-03

7.00e-04

Volatile

1.60e+02

2.50e+03

4.20e+01

4.00e-03

7.00e-04

Volatile