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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
Endpoint summary
Administrative data
Description of key information
Additional information
Currently, very
limited information is available in the literature concerning the N2O
concentration – dose response relationships in humans. The
concentration of N2O in the blood at any one time will depend
on several factors. The
blood/gas solubility coefficient of N2O is ~30x that of
nitrogen, therefore the number of N2O molecules given up by
the blood to air will exceed the number of nitrogen and oxygen molecules
absorbed by the blood. As
a result the pressure in confined spaces will increases, typically N2O
anaesthesia will increase intracranial pressure after air is introduced
into brain ventricles for pneumoencephalography (removal of CSF from
brain / spinal cord and replaced with oxygen to allow the brain to be
imaged more clearly). A
review and discussion of these health effects have been summarised below
from existing literature (Eger 1985; EIGA 2008; EHC 1997).
Central nervous system effects
Several studies
have examined the effects of trace concentrations of N2O on
perceptual, cognitive and motor skills. The
conclusions drawn from these studies are that impairment of mental
function is unlikely to result from inhalation of trace levels of N2O
encountered in operating rooms. When
this work was carried out the trace level of N2O in
un-scavenged operating rooms was estimated to be 130 ppm N2O
and with waste anaesthetic gases scavenged concentrations of N2O
were 50 ppm.
Reaction times on
a choice-decision test do not increase significantly until 10 to 20%
(100000 to 200000 ppm) N2O is breathed. Short
term memory performances decrease with 30% (300000 ppm) N2O. Tinnitus,
nausea, paresthesias and disorientation also occur at 20 and 30% (200000
to 300000 ppm) N2O. These
levels are 200 – 400x greater than the average levels reported in
non-scavenged operating rooms.
N2O
induced neuropathy is characterised by numbness of the distal
extremities, hypoactive reflexes and an “electric shock” sensation
travelling upward from the feet after flexion of the neck, psychomotor
symptoms, including impaired memory function, difficulties in thinking
clearly and depression. Most
of these symptoms disappear slowly when N2O inhalation is
stopped, but in some cases debilitating neurological symptoms remain.
Cardiovascular and respiratory effects
In normal patients, N2O slightly increases pulmonary vascular resistance. In patients with increased pulmonary vascular resistance, especially very young patients, N2O may increase resistance further and thus increases shunting and impair oxygenation. N2O has little effect on hypoxia-induced pulmonary vasoconstriction.
When inhaling N2O
tidal volume decreases with respiratory rate and minute ventilation
increasing whilst PaCO2remains normal. The
ventilatory response is depressed by N2O, resulting in
increased PaCO2. Like
other inhaled agents, N2O depresses the ventilatory response
to hypoxia profoundly. The
greater density of N2O produces slightly more airway
resistance than oxygen or air. Alveolar
collapse by absorption of gases in an obstructed lung segment may be
greater with N2O than with nitrogen. N2O
directly depresses human neutrophil chemotaxis and through this or other
actions may increase the incidence of postoperative respiratory
complications.
Fertility and developmental effects
Regular exposure
to N2O during pregnancy in the normal course of occupations
such as anaesthetist, dental staff and midwife has been of concern since
the first studies of N2O in pregnant animals demonstrated the
capacity to cause teratogenic effects. In
these animal studies the teratogenic effects are only caused by the most
extreme conditions of exposure, such continuous exposure during critical
stages of foetal development. Alternatively,
when the exposure is to a lower concentration or the duration is shorter
then such severe effects are not observed. Two
studies have shown higher levels of congenital abnormalities in the
offspring of women exposed to anaesthetics, these studies however have
serious flaws which would tend to lead to an overestimate of such risks.
Review of all other available human data has not identified any excess
of congenital abnormalities in the offspring of mothers exposed to N2O
under various circumstances.
While exposures
in excess of 10% N2O for various durations have shown some
evidence of effects on fertility this seems to be associated with
methionine synthase inactivation in that longer daily durations of
exposure seem to have the greatest effect. No study has shown any effect
on fertility in animals at daily exposures of 1000 ppm or below. This
would indicate that occupational exposure is unlikely to have any effect
on fertility and the limited clinical data available indicate no male
fertility effects. The
clinical data which claim to show an effect on female fertility are
based on very small numbers of participants and a questionnaire design
which almost certainly attracted participation by women who believed
that occupational exposure may have been the reason for their
infertility. In the
context of the available data on animal effects and mechanism there is
little likelihood that any effects seen in those studies are resultant
from occupational exposure to N2O.
Much of the uncertainty regarding the reproductive risks of N2O has come from poorly constructed retrospective clinical studies plus animal studies that were not designed to provide answers to the current questions. The evidence from mechanistic studies and some clinical studies provides reassurance that the risks are negligible.
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