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EC number: 233-032-0 | CAS number: 10024-97-2
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Toxicological Summary
- Administrative data
- Workers - Hazard via inhalation route
- Workers - Hazard via dermal route
- Workers - Hazard for the eyes
- Additional information - workers
- General Population - Hazard via inhalation route
- General Population - Hazard via dermal route
- General Population - Hazard via oral route
- General Population - Hazard for the eyes
- Additional information - General Population
Administrative data
Workers - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 183 mg/m³
DNEL related information
- DNEL derivation method:
- other: National OEL
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Workers - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Workers - Hazard for the eyes
Local effects
- Hazard assessment conclusion:
- no hazard identified
Additional information - workers
N2O – Rationale for determining DNELs
Whilst there is a plenty of animal data available for N2O, the extent of regulatory animal toxicology data for N2O are limited, with current national OELs set from old experimental data. There is extensive information on human volunteer studies at occupationally relevant N2O concentrations, these studies have provided a wealth of data from which OELs have been derived. A search of the literature has revealed that most animal toxicity studies have been done at high doses, usually using prolonged (continuous) exposures to characterise adverse effects of N2O and in some cases to investigate mechanisms of N2O toxicity. Few studies have been designed to define NOAELs for risk assessment purposes. DNELs could be derived from toxicology studies submitted in this dossier; however these would ignore the extensive human data. For example, the lowest dose level in developmental toxicity studies in rats (section 7.8.1) was 500 ppm for teratogenic effects. According to the guidance in Chapter R.8 the following assessment factors (AFs) would be appropriate:
Interspecies factor = 2.5 (no correction required for allometric scaling)
Intraspecies factor = 5 for workers
Exposure duration = 1 (24 hours exposure/day during days 1-19 of gestation, therefore no correction required)
Dose-response = 1
Quality of whole database = 1 (this factor could arguably be higher based on quality of the animal toxicity data)
Total AF = 12.5
DNEL = 500/12.5 =
40 ppm
This DNEL is comparable to the OEL set
for Belgium, Denmark and Spain, but 2.5 fold lower than other EU
countries. Lowering the
occupational limit to 40 ppm based on a DNEL from animal toxicity data
would clearly give an exposure which is much lower than the
concentrations reported in dental offices (400 to 1000 ppm). However,
OEL below 100 ppm are all based on the effects on performance observed
and reported by Bruceet al(1974, 1975). These
studies have been severely criticised and despite attempts the results
have not been reproduced.
In terms of
environmental exposure, N2O is ubiquitous in the
atmosphere because it is a product of biological processes in soil as
well as anthropogenic activities. It is not involved to any appreciable
extent in chemical reactions in the lower atmosphere, but it is an
active "greenhouse" gas. In the stratosphere N2O
forms NO by reaction with excited oxygen atoms, and this NO then acts to
deplete the stratospheric O3 concentration.
Occupational Exposure Limits
Due to N2O
being readily oxidised, elevated concentrations of N2O occur in numerous
settings, including those at work, at home or in the street. N2O
is not very toxic after acute or repeated exposures. Concentrations
of 300000 ppm and more have analgesic effects and 800000 ppm and more
have anaesthetic effects. A
NOEL of 100000 ppm has been identified for acute CNS distrubance
identified by psychometric testing under laboratory conditions (COT,
1995). Three kinds
of occupational exposure limits are currently utilized in a number of
countries. The most
common are: average permissible concentrations for a typical 8 hour
working day (time-weighted average, TWA); concentrations for short-term
exposures, generally of 15-min duration (short-term exposure limit,
STEL); and maximum permissible concentrations not to be exceeded
(ceiling limit). This discussion will centre round the justification for
a common OEL (TWA and STEL) to take forward for DNEL setting and risk
characterisation for the N2O chemical safety report.
Discussion of OELs below has been summarised from authoritative reviews of extensive, relevant published literature (EHC, 1997, EIGA, 2008, COT 1995), with a summary of available OELs taken directly from the IFA website.
Occupational exposure limits
Country |
Limit value – 8 h |
Limit value – short term |
||
ppm |
mg/m3 |
ppm |
mg/m3 |
|
Australia |
25 |
45 |
|
|
Austria |
100 |
180 |
400 |
720 |
Belgium |
50 |
91 |
|
|
Denmark |
50 |
90 |
100 |
180 |
EU |
|
|
|
|
France |
|
|
|
|
Germany |
100 |
180 |
200 |
360 |
Hungary |
|
180 |
|
720 |
Italy |
|
|
|
|
New Zealand |
|
|
|
|
Poland |
|
90 |
|
|
Singapore |
50 |
90 |
|
|
Spain |
50 |
92 |
|
|
Sweden |
100 |
180 |
500 |
900 |
Switzerland |
100 |
182 |
200 |
364 |
The Netherlands |
|
|
|
|
United Kingdom |
100 |
183 |
|
|
North America and US |
||||
Canada (Ontario) |
25 |
45 |
|
|
Canada (Québec) |
50 |
90 |
|
|
US – NIOSH |
25 |
46 |
|
|
Table has been adapted from the IFA Institut fur Arbeitsschutz der Deutschen Gesetzlichen Unfallversicherung (website details included under references)
The UK established the OEL at 100 ppm based on studies relating to developmental toxicity in experimental animals. In relation to this endpoint, the overall NOAEL in the rat was 500 ppm. The probable underlying mechanism for developmental toxicity is impairment of DNA synthesis resulting from inhibition of vitamin B12-dependent methionine synthase. Studies in humans, including limited investigations in dentists indicate consistent mechanism in rodents and humans. Given this toxicological picture, an OEL of 100 ppm (8 h TWA), a factor of 5-fold below the overall NOAEL for developmental toxicity in animals was established by the UK Committee on Toxicity (UK COT, 1995), with Austria, Germany, Sweden and Switzerland concluding the same OEL.
Whilst it is
recognised that OELs within some European countries and North
America / US are below 100 ppm this is based
on the effects on performance observed and reported by Bruceet al(1974,
1975). These studies
have been severely criticised and despite attempts the results have not
been reproduced.
The requirement to set a STEL in the UK was not deemed necessary due to the non-toxic nature of N2O.
Conclusions on DNEL setting
The use of animal toxicity data on N2O is not appropriate for deriving DNELs. The use of OELs from which to derive DNELs for N2O is considered to be scientifically justified since OELs have been set based on extensive human and animal data.
Therefore under
guidance from ECHA (2010), as national OELs have already been set by
several EU and Non-EU countries for daily inhalation exposure over 8
hours/working day and for acute / short term exposure (15 minutes);
relevant DNELs will be derived from these.
The proposed UK / Sweden / Germany / Austria OEL for the 8-hour working
limit of 100 ppm (180 mg/m3) are are selected as the DNELs
for occupational exposure. In
accordance with ECHA (2010), Chapter R.8 “a DNELfor acute toxicity
should be derived if an acute toxicity hazard (leading to C&L) has been
identified and there is a potential for high peak exposures.” N2O
is considered to be neither acutely toxic (i.e. absence of C&L for this
endpoint) and the intended uses will not result in high peak exposures,
therefore an acute DNEL is considered unnecessary. Following
a review of the latest available data there are no new studies which
would negatively impact upon the position that these values are
protective with regard to occupational exposure.
General Population - Hazard via inhalation route
Systemic effects
Acute/short term exposure
DNEL related information
Local effects
Acute/short term exposure
DNEL related information
General Population - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
General Population - Hazard via oral route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- no hazard identified
Acute/short term exposure
- Hazard assessment conclusion:
- no hazard identified
DNEL related information
General Population - Hazard for the eyes
Local effects
- Hazard assessment conclusion:
- no hazard identified
Additional information - General Population
In accordance with ECHA (2010), Chapter R.8 “a DNELfor acute toxicity should be derived if an acute toxicity hazard (leading to C&L) has been identified and there is a potential for high peak exposures.” N2O is considered to be neither acutely toxic (i.e. absence of C&L for this endpoint) and the intended uses will not result in high peak exposures, therefore an acute DNEL is considered unnecessary.
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