過塩素酸アンモニウム

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep drums, etc., cool by spraying with water. Combat fire from a sheltered position.

Fresh air, rest.

First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give one or two glasses of water to drink.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· Keep combustibles (wood, paper, oil, etc.) away from spilled material.

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

General First Aid:

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Use water spray to cool unopened containers.

If material on fire or involved in fire: Do not fight fires in a cargo of explosives. Evacuate area and let it burn. /Ammonium perchlorate explosives/

For more Fire Fighting Procedures (Complete) data for Ammonium perchlorate (6 total), please visit the HSDB record page.

Keep container tightly closed in a dry and well-ventilated place. Storage class (TRGS 510): Strongly oxidizing hazardous materials.

Separate from acids, alkalies, reducing agents, combustible materials. Store in cool, dry, well-ventilated location.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Sweep up and shovel. Contain spillage, and then collect with an electrically protected vacuum cleaner or by wetbrushing and place in container for disposal according to local regulations. Keep in suitable, closed containers for disposal.

Wear full protective clothing and positive pressure self-contained breathing apparatus. Prompt cleanup and removal are necessary in order to prevent contamination with combustible materials.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D003, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Product: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product.

...Perchlorate in 47 dairy milk samples from 11 states and in 36 human milk samples from 18 states were measured. Perchlorate was detectable in 81 of 82 samples. The dairy and breast milk means were, respectively, 2.0 and 10.5 ug/L with the corresponding maximum values of 11 and 92 ug/L. Perchlorate is present in virtually all milk samples, the average concentration in breast milk is five times higher than in dairy milk. Although the number of available measurements are few at this point, for breast milk samples with a perchlorate content greater than 10 ug/L, the iodide content is linearly correlated with the inverse of the perchlorate concentration with a r2 of >0.9 (n = 6). ... /Perchlorate/

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)

Radioactive iodide ((131)I-) protection studies have focused primarily on the thyroid gland and disturbances in the hypothalamic-pituitary-thyroid axis. The objective of the current study was to establish (131)I- urinary excretion profiles for saline, and the thyroid protectants, potassium iodide (KI) and ammonium perchlorate over a 75 hour time-course. Rats were administered (131)I- and 3 hours later dosed with either saline, 30 mg/kg of NH(4)ClO(4) or 30 mg/kg of KI. Urinalysis of the first 36 hours of the time-course revealed that NH(4)ClO(4) treated animals excreted significantly more (131)I- compared with KI and saline treatments. A second study followed the same protocol, but thyroxine (T(4)) was administered daily over a 3 day period. During the first 6-12 hour after (131)I- dosing, rats administered NH(4)ClO(4) excreted significantly more (131)I- than the other treatment groups. T(4) treatment resulted in increased retention of radioiodide in the thyroid gland 75 hour after (131)I- administration. We speculate that the T(4) treatment related reduction in serum TSH caused a decrease synthesis and secretion of thyroid hormones resulting in greater residual radioiodide in the thyroid gland. Our findings suggest that ammonium perchlorate treatment accelerates the elimination rate of radioiodide within the first 24 to 36 hours and thus may be more effective at reducing harmful exposure to (131)I- compared to KI treatment for repeated dosing situations. Repeated dosing studies are needed to compare the effectiveness of these treatments to reduce the radioactive iodide burden of the thyroid gland.

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).

LC50; Species: Daphnia magna (Water flea) age <24 hr neonate, clone K6; Conditions: freshwater, static, 20 °C; Concentration: 652060 ug/L for 24 hr

LC50; Species: Daphnia magna (Water flea) age <24 hr neonate, clone K6; Conditions: freshwater, static, 20 °C; Concentration: 396210 ug/L for 48 hr

TERRESTRIAL FATE: Ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). The perchlorate ion is only weakly absorbed to mineral surfaces of moderate ionic strength(1). Perchlorate ion also exhibits a high aqueous solubility; together these properties contribute to its ability to readily migrate in groundwater systems(2).

AQUATIC FATE: When released to water, ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). Perchlorates are readily soluble in water. In dilute aqueous solutions, the ion is very stable and inert and therefore may persist for decades under normal conditions in groundwater and surface water systems(2). Hydrolysis does not occur for inorganic salts such as ammonium perchlorate that ionize in aqueous solution(1). Perchlorates are not expected to undergo direct photolysis in water(1).

ATMOSPHERIC FATE: Perchlorate salts such as ammonium perchlorate are expected to exist as a solid aerosol or be absorbed to suspended particulate matter(1). Therefore removal from the atmosphere is expected to occur by both wet and dry depostion(1). Perchlorates are not expected to undergo direct photolysis in air(1).

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

Inhalation (L894) ; oral (L894) ; dermal (L894) ; eye contact (L894).

Perchlorate was unambiguously detected by ion chromatography-suppressed conductivity (IC-CD) and/or ion chromatography-electrospray mass spectrometry (IC-MS) in seven of seven supermarket milk samples bought randomly in Lubbock, TX. Quantitation by IC-MS and IC-suppressed conductivity detection in conjunction with a preconcentration-preelution method provided comparable results. With a sample cleanup procedure that involved protein removal by ethanol and sequential passage though activated alumina and C-18 silica, the limit of detection for perchlorate in milk was 0.5 ug/L. The levels found ranged from 1.7 to 6.4 ug/L. An evaporated milk sample contained perchlorate at 1.1 +/- 0.6 ug/L level, while we did not find detectable levels in a reconstituted powdered milk sample. /Perchlorate/

...Perchlorate in 47 dairy milk samples from 11 states and in 36 human milk samples from 18 states were measured. Perchlorate was detectable in 81 of 82 samples. The dairy and breast milk means were, respectively, 2.0 and 10.5 ug/L with the corresponding maximum values of 11 and 92 ug/L. Perchlorate is present in virtually all milk samples, the average concentration in breast milk is five times higher than in dairy milk. Although the number of available measurements are few at this point, for breast milk samples with a perchlorate content greater than 10 ug/L, the iodide content is linearly correlated with the inverse of the perchlorate concentration with a r2 of >0.9 (n = 6). ... /Perchlorate/

IDENTIFICATION AND USE: Ammonium perchlorate is a colorless, crystalline compound. The most common uses for ammonium perchlorate are in explosives and rocket propellants, which have been widely used in military munitions items, such as mortars, grenades and flares and solid fuel rocket. It is also used in analytical chemistry, and as etching and engraving agent. It has been tested as an experimental medication in (131)I exposure. HUMAN STUDIES: No perchlorate-attributable effects on thyroid, bone marrow, kidney, or liver function were detected in employees at an ammonium perchlorate production facility in Nevada. The study of workers in China also found no effect on thyroid function from long term, low-level documented exposure to ammonium perchlorate. However, epidemiological study of population drinking ammonium perchlorate contaminated water demonstrated statistically significant association between perchlorate exposure and newborn thyroid-stimulating hormone levels. ANIMAL STUDIES: In rats, exposure to ammonium perchlorate in drinking water resulted in statistically significant changes in thyroid stimulating hormone and other thyroid hormones. In developmental experiments in rats, changes in maternal and neonatal thyroid histopathology were detectable at 1.0 mg/kg-day exposure. Behavioral testing in rats suggested that prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups. Exposure of embryonic and larval Xenopus laevis to high concentrations of ammonium perchlorate salt produced a feminizing effect, resulting in a skewed sex ratio. Ammonium perchlorate (100-10,000 ug/plate) was neither toxic nor mutagenic in S. typhimurium TA98, TA100, TA102, TA104, TA1535, or TA1537 with or without metabolic activation. ECOTOXICITY STUDIES: Ammonium perchlorate exposure caused hypothyroidism in young Japanese quail and affected the expression of thyroid-responsive genes during early posthatch development. Furthermore, in Japanese quail maternal perchlorate exposure led to embryonic hypothyroidism and may have interfered with embryonic development. In X. laevis, ammonium perchlorate inhibited metamorphosis in a concentration-dependent manner as evident from effects on forelimb emergence, tail resorption, and hindlimb growth. It was also inhibiting thyroid activity and altered gonadal differentiation in developing X. laevis.

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).

/BIRDS and MAMMALS/ The effects of a wide range of ammonium perchlorate (AP) concentrations in drinking water on thyroid function in bobwhite quail chicks was investigated at 2, 4, and 8 weeks of exposure. ...Plasma thyroid hormones (THs) /were measured/ to evaluate organismal thyroid status, thyroid weights to evaluate hypothalamic-pituitary-thyroid (HPT) axis activation, and thyroidal TH content to assess TH stores. At the highest AP exposures plasma THs were decreased, thyroid glands were hypertrophied, and thyroidal TH content was decreased. As in ...previous studies, thyroidal thyroxine (T(4)) content was the most sensitive indicator of decreased thyroid function; plasma T(4) and thyroid weight were much less sensitive. The lack of sensitivity of these variables appears to result from cyclic patterns of thyroid responses involving the HPT axis and intermittent release of stored THs from the thyroid gland. With sustained AP exposure (8 weeks), at the lowest range of AP concentrations used, chicks showed adaptation in thyroid function that fully compensated for the initial (2 week) effects of AP. At the intermediate AP concentrations there was partial compensation for the initial AP effects. At the highest AP exposures used, thyroid function was very low throughout the study, with no indication of compensatory responses. The capability of chicks to increase some aspects of their thyroid function adaptively in response to some levels of sustained AP exposure is contrary to the common generalization that developing animals are most vulnerable to environmental contaminants.

/BIRDS and MAMMALS/ Ground-dwelling birds in perchlorate-contaminated areas are exposed to perchlorate ion, a known thyroid disruptor, and might be vulnerable to the developmental effects of perchlorate-induced hypothyroidism. ...Perchlorate-induced hypothyroidism would alter the expression of thyroid-responsive genes involved in thyroid hormone (TH) regulation and in the development of target organ function. Japanese quail chicks were exposed to 2000 mg/L ammonium perchlorate in drinking water for 7.5 weeks beginning on day 5 posthatch. Hypothyroidism was evident after 2 weeks of exposure as lower plasma THs and lower TH content in exposed chicks than in controls. The degree of hypothyroidism was increased at 7.5 weeks, as indicated by significant thyroid gland hypertrophy and sustained changes in thyroid function. After 2 weeks of exposure, hypothyroidism increased type 2 5'-deiodinase (D2) mRNA level and decreased Spot 14 (SP14) mRNA level in the liver, whereas D2 mRNA and RC3 mRNA levels in brain were not affected. After 7.5 weeks of exposure, mRNA levels in the exposed group did not differ from those in controls in either the liver or brain, suggesting the responsiveness of these genes to THs decreased during development. These results suggest that the brain, but not the liver, was protected from the effects of hypothyroidism, probably by changes in D2 activity at the protein level and/or regulation of TH entry and exit from the brain. ...Perchlorate exposure caused hypothyroidism in young Japanese quail and affected the expression of thyroid-responsive genes during early posthatch development.

(CA) CALIFORNIA 6 ug/L /Perchlorate ion/

(MA) MASSACHUSETTS 2 ug/L /Perchlorate ion/

Ammonium perchlorate

A Commercial Grade

5000

A Commercial Grade

400

Explosive chemical that can be released at a facility.

(CA) CALIFORNIA 6 ug/L /Perchlorate ion/

(ME) MAINE 1 ug/L /Perchlorate ion/