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EC number: 232-235-1 | CAS number: 7790-98-9
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
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- Density
- Particle size distribution (Granulometry)
- Vapour pressure
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- Storage stability and reactivity towards container material
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- Nanomaterial crystalline phase
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- Endpoint summary
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- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
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- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
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- Endocrine disrupter testing in aquatic vertebrates – in vivo
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- Toxicological Summary
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- Specific investigations
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- Additional toxicological data
Endpoint summary
Administrative data
Description of key information
Two occupational studies were run in the same ammonium perchlorate plant in the US, with chronic (mainly respiratory) exposure at 42h/week. In both studies, controls were imperfect (suspected tendency to hypothyroidism) so worker data were compared with normal limits, enabling robust conclusion. Both studies lacked histological data, impossible to gather in worker studies.
In Braverman 2005, among 29 male workers, no effect on T3, T4 and TSH, thyroid volume (as a surrogate for histological investigations), thyroglobulin and urinary iodine excretion occurred at a median absorbed dose of 0.167 mg perchlorate ion/kg/day (based on serum and urine perchlorate concentrations), over 5.9 years (median). Free T4 index was above normal limits in all groups but this is the opposite to the expected effect of perchlorate. Decreased radioiodine uptake and increased serum and urinary perchlorate levels were noted (non-adverse effects). Median exposure corresponded to 0.20 mg ammonium perchlorate/kg/day and was the NOAEL for 42h/week chronic exposure.
In Lamm 1999, among 35 male and 2 female workers, T3, T4, red and white blood cell and platelet counts, urine iodine, were all within normal limits at up to individual absorbed doses of 69 mg perchlorate/shift, for a 60th exposure percentile of 5 years (chronic exposure). TSH was above normal limits (up to 8.2 mUI/L) in about half of the 15 high-dose workers, but as the same observation (TSH up to 8.4 mUI/L) was made in controls, a causal relationship with perchlorate exposure seemed unlikely. Some parameters were not perfectly within normal limits in exposed groups but lacked dose-relationship (thyroid hormone binding ratio, free T4 index, thyroid peroxidase antibody titers). Non-adverse increases in blood and urine perchlorate levels were noted. The high-dose group's 25%tile of absorbed dose was 24.68 mg perchlorate/shift, equivalent to 0.21 mg Ammonium perchlorate/kg/day, retained as NOAEL for 42h/week chronic exposure.
Additional information
The vast majority of publications in workers, volunteers or general population generally did not evidence any adverse effect of perchlorate on toxicologically relevant thyroid function endpoints i.e. T3, T4, TSH and thyroid volume (at up to a median exposure of 0.20 mg ammonium perchlorate/kg/day: Braverman 2005) as well as on neonate thyroid endpoints and growth parameters (at up to 9.3 µg/kg/day: Amitai 2007). Not included as adverse effects, were inhibition of iodine uptake (RAIU) by the iodine transport protein (NIS) and elevation of serum or urinary concentrations of perchlorate, which were evidenced in all studies in which they were investigated.
The few exceptions with mention of possible adverse effects were of doubtful relevance:
o TSH values above the physiological limits in a few persons in a worker study (Lamm 1999), at individual exposure levels up to 0.60 mg AP/kg/day (exact range unknown). However similarly elevated values were noted in the sodium azide control group, carrying out similar tasks in the same plant, so that a causal relationship with perchlorate was unlikely. Furthermore the study enabled to derive a NOAEL from less exposed individuals, in a conservative approach: 0.21 mg Ammonium Perchlorate/kg/day.
o Moderate, non-significant statistical correlations between urinary perchlorate excretion and T4 (negative) and TSH (positive) levels, in women with low urinary iodine and thiocyanate levels (a possible antithyroid confounder; Steinmaus 2007 re-assessment of Blount 2006 study). These can not be used in risk assessment since perchlorate urinary levels could not be converted in mg/kg/day.
o TSH increases in neonates in a region with perchlorate-contaminated water (Brechner 2000). However the absence of reporting on contamination levels and estimated intake during pregnancy excludes any use of the study in risk assessment.
Two occupational studies were retained as being of optimal quality for risk assessment purposes, based on several quality criteria and also the fact that they involved relatively high exposure levels for chronic exposures: Lamm 1999 and Braverman 2005, both subject to specific Robust Study Summaries. They lead to similar repeat-dose toxicity NOAELs of 0.21 and 0.20 mg Ammonium Perchlorate/kg/day for chronic exposure. All other studies were not summarized as RSS due to their important limitations for risk assessment purposes.
The detailed process of assessment, covering the whole range of human data on perchlorate, is reported in attachment.
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