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EC number: 240-973-0 | CAS number: 16919-58-7
- 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
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- Nanomaterial pour density
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- 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
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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:
- high hazard (no threshold derived)
- Most sensitive endpoint:
- sensitisation (respiratory tract)
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- acute toxicity
- Route of original study:
- Oral
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- high hazard (no threshold derived)
- Most sensitive endpoint:
- sensitisation (respiratory tract)
Acute/short term exposure
- Hazard assessment conclusion:
- high hazard (no threshold derived)
- Most sensitive endpoint:
- sensitisation (respiratory tract)
DNEL related information
Workers - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- high hazard (no threshold derived)
- Most sensitive endpoint:
- sensitisation (respiratory tract)
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- acute toxicity
- Route of original study:
- Oral
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- sensitisation (skin)
Acute/short term exposure
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
- Most sensitive endpoint:
- sensitisation (skin)
Workers - Hazard for the eyes
Local effects
- Hazard assessment conclusion:
- medium hazard (no threshold derived)
Additional information - workers
Hazard via inhalation route: systemic effects following long-term exposure
As no relevant data on effects of repeated inhalation exposure to diammonium hexachloroplatinate in laboratory animals are available, route-to-route extrapolation to calculate an inhalation DNEL from a reliable repeated-dose oral toxicity study was considered a suitable alternative (particularly as first pass effects are not expected to be significant for an inorganic compound). Further reassurance was gained from a reliable oral reproductive/developmental toxicity screening study, also on diammonium hexachloroplatinate.
In a guideline (OECD TG 407) 28-day gavage toxicity study, conducted according to GLP, rats (5/sex/dose) were administered diammonium hexachloroplatinate doses of 0, 10, 30 or 100 mg/kg bw/day. Males in the mid-dose group had reduced body weight and body weight gain (likely a consequence of reduced food consumption, possibly due to the local effects on the stomach), compared to controls, and mid-dose males and females were found to have lesions in the kidneys and stomach. In the high-dose group, body weights and body weight gain were affected in males and females, and lesions of the kidneys and stomach - additional to those also present in mid-dose animals - were reported. Accordingly, the NOAEL was established as 10 mg/kg bw/day (Hansen, 2015a).
In a guideline reproductive/developmental screening study (OECD TG 421), using the same gavage dose groups, high-dose parental animals displayed similar stomach and kidney lesions as those seen in the 28-day toxicity study. In this study, the NOAEL for general toxicity was set as 30 mg/kg bw/day. Females in the high-dose group also displayed slightly increased post-implantation loss and decreased birth index, although this was attributed to a single female with all dead implantations and 2 other females with high post-implantation losses. The NOAEL for fertility effects was, nevertheless, set at 30 mg/kg bw/day. There were no developmental effects seen at any dose (developmental NOAEL 100 mg/kg bw/day)(Hansen, 2015b).
Overall, the systemic NOAEL of 10 mg/kg bw/day (equivalent to 4.39 mg/kg bw/day for elemental platinum based on MWt ratios[1]) from the repeated-dose oral toxicity study was taken as the critical point of departure for calculating the long-term systemic DNEL.
Laboratory studies provide only very limited insights into the extent of absorption of platinum compounds following inhalation. When two volunteers inhaled mainly diammonium hexachloroplatinate at calculated mean air concentrations of 1.7 and 0.15 µg Pt/m3, respectively, urinary Pt concentrations peaked (15-100-fold increases were seen) about 10 hr later. The results indicated rapid absorption and urinary excretion, but gave no quantitative insights into the extent of absorption (Schierl et al., 1998). Urinary Pt measurements in rats following an acute inhalation of radiolabelled Pt, PtO2, PtCl4 or Pt(SO4)2 (particle diameter around 1 µm) indicated only small fractions of the administered dose were absorbed, even for the two soluble salts. Most of the radiolabel appeared in the faeces, presumably reflecting mucociliary clearance and a lack of significant absorption from the gastrointestinal tract (Moore et al., 1975a).
Available data indicate that absorption of soluble Pt compounds is also very low following oral exposure. In rats, less than 0.5% of an oral dose of radiolabelled PtCl4 was absorbed (Moore et al., 1975b,c). Similar results were obtained when Pt(SO4)2 was administered orally to mice (Lown et al., 1980). Following REACH guidance, the worst-case (and, therefore, most health-precautionary) scenario for DNEL calculation is obtained by considering the minimum absorption by the ‘starting’ route. Therefore, for this oral-to-inhalation extrapolation, a figure of 0.5% oral absorption has been used, taken from the laboratory study in rats. In line with the guidance, the worst-case of 100% absorption after inhalation has still been assumed for the ‘end’ route (which is clearly significantly higher than the available, albeit limited, data indicates, and thus almost certainly over-precautionary).
Corrected inhalatory NOAEC (worker, 8 h exposure/day) = oral NOAEL*(1/sRv[rat])*(ABS[oral-rat]/ABS[inh-human]) *(sRV[human]/wRV) = 10 mg/kg bw/day*(1/0.38 m3/kg bw/day)*(0.5/100)*(6.7 m3 [8h]/10 m3 [8h]) = 0.088 mg/m3
It is noted that the standard respiratory rate conversion figure (0.38 m3/kg bw/day) already incorporates a factor of 4 for allometric scaling from rat to human. An assessment factor (AF) for allometric scaling is not considered to be justified in this scenario, given that the metabolism of inorganic metal cations is conventionally assumed not to occur to any relevant extent. Moreover, ECHA guidance notes that “allometric scaling is an empirical approach for interspecies extrapolation of various kinetic processes generally applicable to substances which are renally excreted, but not to substances which are highly extracted by the liver and excreted in the bile. It appears that species differences in biliary excretion and glucuronidation are independent of caloric demand (Walton et al. 2001)” (ECHA, 2012a). Oral toxicokinetic studies have demonstrated that, while gastrointestinal absorption of platinum is very low, the absorbed fraction is excreted predominantly via the faecal route (Moore et al., 1975b). It is therefore considered appropriate to increase the corrected inhalatory NOAEC by a factor of 4.
Dose descriptor starting point (after route to route extrapolation) = Corrected inhalatory NOAEC (worker, 8 h exposure/day)*4 = 0.088*4 = 0.35 mg/m3
Application of the appropriate assessment factors (overall AF 75, described above) to this corrected inhaled NOAEC gives a systemic long-term inhalation DNEL for diammonium hexachloroplatinate of 0.0047 mg/m3 [4.7 μg/m3]. This equates to an elemental platinum exposure of 0.0021 mg/m3 [2.07 μg/m3].
Recent epidemiological studies (including Heederik et al., 2016, a retrospective cohort study of about 1040 platinum refinery workers) have provided some evidence that platinum salt sensitisation can be induced at airborne soluble platinum concentrations below 2 μg/m3. In addition, a non-guideline study demonstrated that a single respiratory challenge to mice topically sensitised to ammonium hexachloroplatinate can induce dose-dependent changes in pulmonary function indicative of an allergic lung response (Williams et al., 2015). This suggests that both dermal and inhalation exposure to chloroplatinates may play a role in occupational respiratory sensitisation/asthma. Consequently, the most appropriate and health precautionary approach was deemed to be to formulate a qualitative assessment (with ‘high hazard’ banding and recommended RMMs/OCs in Table E.3-1 of ECHA, 2012b) for systemic exposure to workers by inhalation. [For further discussion of the potential respiratory sensitisation and irritation, including that reported in recent epidemiological studies, please see the ‘Hazard via inhalation route: local effects following long-term or acute exposure’ section, below]. (It is anticipated that this qualitative approach with its associated stringent RMMs/OC requirements will also be protective for general systemic toxic effects (with due consideration of the DNEL that would be applied to the latter).
Hazard via inhalation or dermal route: systemic effects following acute exposure
DNELs for acute toxicity should be calculated if an acute toxicity hazard, leading to classification and labelling (i.e. under EU CLP regulations) has been identified and there is a potential for high peak exposures (this is only usually relevant for inhalation exposures).
There are no data in relation to acute inhalation or dermal exposure to diammonium hexachloroplatinate (or closely-related compounds). In an acute oral toxicity study in rats, an LD50 value of around 200 mg/kg bw was reported. In a range-finding phase, both rats administered 2000 mg/kg bw died, but there were no deaths at 500 mg/kg bw or below. However, when a larger group (10/sex) of animals were administered single gavage doses of 500 mg/kg bw, 4 males and 4 females died within 3 days. A subsequent group was administered 200 mg/kg bw; 4 females died from this treatment, but the remaining female and all 5 tested males survived (Middleton, 1978). On this basis, diammonium hexachloroplatinate was classified for its acute oral toxicity in category 3, according to EU CLP criteria (EC 1272/2008).
“A qualitative risk characterisation for this endpoint could be performed for substances of very high or high acute toxicity classified in Category 1, 2 and 3 according to CLP… when the data are not sufficiently robust to allow the derivation of a DNEL” (ECHA, 2012b). It is, therefore, considered suitably health precautionary to adopt the “moderate” hazard banding, and to consider the recommended RMMs/OCs in Table E.3-1 of ECHA (2012b).
Hazard via inhalation route: local effects following long-term or acute exposure
The development of allergic sensitisation following exposure to halogenated platinum compounds via the inhalation route is a well-established human health hazard associated with occupational exposure, and has been the subject of a number of comprehensive expert reviews (HCN, 2008; IPCS, 1991; Ravindraet al., 2004; SCOEL, 2011; US EPA, 2009; WHO, 2000, 2012). There is extensive epidemiological evidence (from cohort studies and case reports) that halogenated platinum salts, in particular chloroplatinates, can act as respiratory sensitisers, with exposed workers developing symptoms if the occupational levels are sufficiently high. Asymptomatic respiratory sensitisation (detected by skin prick testing; SPT) can proceed to occupational asthma and rhinitis if exposure is continued, and such symptoms may be severe.
In most occupational studies, the individual platinum compounds involved cannot be identified because workers are unlikely to be exposed to a single platinum compound. Work by Cristaudo et al. (2005), and Linnett and Hughes (1999) indicated that the allergenic potential may be related to the degree of chlorination. Results from laboratory animal studies provide data supporting a relationship between allergenic potential and the degree of chlorination (Murdoch and Pepys, 1986, 1985, 1984a,b; Schuppe et al., 1992, 1997; WHO, 2012), and some data suggest that there is a correlation between activity and the degree of chlorination between the series of hexachloroplatinate and tetrachloroplatinate salts.
A recently-published retrospective cohort study designed to investigate platinum salt sensitisation (PSS) found a clear exposure-response relationship between chloroplatinate salts and respiratory sensitisation in workers. The study involved about 1040 refinery workers who newly joined one of five refineries during an 11-year period (1 January 2000 to 31 December 2010), and for whom a total of around 1760 personal time weighted average exposure measurements (to soluble platinum; used as a surrogate for the various chloroplatinate intermediates in particulate and liquid aerosol forms) were available. Only personal time-weighted average measurements based on the inhalable or total dust fraction, and approximating to 8-hour workshift values were included in the exposure database. Sensitisation cases were detected by SPT using a hexachloroplatinate salt, which is a method with high sensitivity and predictivity. The relationship was strongest for current (recent) and average exposure, and weaker for cumulative exposure. For current exposure categories of ≤49, >49‑≤100, >100-≤252 and >252 ng/m3, Risk Ratios (RRs) were 1 (reference), 1.4, 2.2 and 3.2, respectively, the latter two values being statistically significant (p<0.005 or better). For average exposure, RRs were 1, 1.8, 4.2 and 3.0, respectively, for the ≤51.1, >51.1-≤105, >105-≤250 and >250 ng/m3 categories (all statistically significant at p<0.05 or better). The investigators concluded that “the exposure-relation for current exposure is characterized by an initial steep increase in risk starting at low exposure levels and levelling off at levels of greater than 200 ng/m3” (Heederik et al., 2016).
This recent, high-quality study is consistent with other epidemiology studies in demonstrating that PSS can be induced at estimated airborne soluble platinum concentrations (as a chloroplatinate surrogate measure) of less than 2 µg/m3 (2000 ng/m3) as an 8-hour time-weighted average value. Although the study possessed higher statistical power than any previous epidemiology investigation of PSS, due to some limitations in the low-end exposure dataset it was not possible to define a robust induction threshold (airborne critical concentration) for respiratory sensitisation to chloroplatinates.
Given the frequency of occurrence of respiratory sensitisation in workers exposed to sufficiently high occupational levels of chloroplatinates, and the severity of the symptoms that may develop, particularly if exposure is continued, the available data indicate that it is appropriate to classify diammonium hexachloroplatinate as a respiratory sensitiser, in sub-category 1A, according to EU CLP criteria. The available epidemiology data has not yet permitted delineation of an induction threshold for PSS in workplace exposure scenarios. In a recent non-guideline study, it was demonstrated that a single respiratory challenge to mice topically sensitised to ammonium hexachloroplatinate can induce dose-dependent changes in pulmonary function indicative of an allergic lung response (Williams et al., 2015). This suggests that both dermal and inhalation exposure to chloroplatinates may play a role in occupational respiratory sensitisation/asthma, further supporting the decision to formulate a qualitative assessment approach as most appropriate and health precautionary for the local effects to the respiratory tract.
It is, therefore, considered suitably health precautionary to adopt the “high” hazard banding, and to consider the recommended RMMs/OCs in Table E.3-1 of ECHA (2012b).
Hazard via dermal route: systemic effects following long-term exposure
As no relevant data on effects of repeated dermal exposure to diammonium hexachloroplatinate in humans or laboratory animals are available, route-to-route extrapolation to calculate a dermal DNEL from a reliable repeated-dose oral toxicity was considered a suitable alternative (particularly as first pass effects are not expected to be significant for an inorganic compound). Further reassurance was gained from a reliable oral reproductive/developmental toxicity screening study, also on diammonium hexachloroplatinate. These two studies have been described in detail above [“Hazard via inhalation route: systemic effects following long-term exposure”] (Hansen, 2015a,b).
The oral NOAEL of 10 mg/kg bw/day for repeated dose effects seen in the Hansen (2015a) study was taken as the health-precautionary critical point of departure for calculating the long-term systemic dermal DNEL for diammonium hexachloroplatinate. This equates to a NOAEL of 4.39 mg/kg bw/day for elemental platinum (based on MWt ratios). This point of departure is also expected to be sufficiently protective against fertility or developmental effects.
This derivation has utilised REACH guidance. In order to make the most health-precautionary derivation, the worst-case scenario is obtained by the minimum absorption by the ‘starting’ route. Therefore, for this oral-to-dermal extrapolation, a figure of 0.5% oral absorption has been used based on experimental data in rats (Moore, 1975b,c). The default assumption in the REACH guidance is that dermal absorption will not be higher than by the oral route (ECHA, 2012a).
However, two in vitro permeation studies on a chloroplatinate analogue, dipotassium tetrachloroplatinate, indicated a greater degree of dermal absorption [about 5-8%] than this default process would assume. Using a K2PtCl4 solution (0.3 mg Pt/ml in synthetic sweat) and full thickness skin from six donors (three African and three Caucasian), 4.8 and 2.3%, respectively (as mean values), diffused into the skin in 24 hr; the receptor solutions contained a further 3.4 and 0.5%, respectively (Franken et al., 2015). A slightly earlier publication reported mean skin diffusion and receptor solution percentages of 2.2% and 2.3%, respectively, in similar studies on full thickness skin from four Caucasian females (Franken et al., 2014). Apart from these studies, very little information appears to be available regarding dermal absorption of platinum compounds.
Furthermore, evidence of skin irritation was seen in a non-guideline patch test (Middleton, 1978), and in a skin sensitisation study (Middleton, 1977), both carried out on diammonium hexachloroplatinate. Irritation, manifesting as swelling of the ear, was also seen in a skin sensitisation test (using the mouse ear swelling test method) conducted on disodium hexachloroplatinate, a member of the “hexachloroplatinate(IV) compounds” category (Schuppe et al., 1997b). In addition, diammonium hexachloroplatinate was found to be immediately corrosive when instilled into the eyes of rabbits (Berthold, 1994), and is corrosive to metals (Harlan, 2011). As such, the possibility that diammonium hexachloroplatinate has the potential to disrupt the skin barrier (potentially facilitating dermal uptake) cannot be ruled out (despite it not being classified for skin irritation).
A high dermal bioavailability is unlikely, notably based on its high water solubility as well as experimental dermal penetration data (human in vitro studies) for a closely-related surrogate [indicating about 5-8% dermal absorption]. However, the potential of diammonium hexachloroplatinate to disrupt skin barrier function, facilitating increased dermal penetration, cannot be excluded, especially considering its known corrosivity to metals and to the eyes of rabbits. A value of 20% absorption is, therefore, proposed.
Dose descriptor starting point (after route to route extrapolation) = NOAEL*(ABS[oral-rat]/ABS[der-human]) = 10 mg/kg bw/day*(0.5%/20%) = 0.25 mg/kg bw/day.
Application of the appropriate assessment factors (overall AF 75, described above) to this corrected dermal NOAEL gives a systemic long-term dermal DNEL for diammonium hexachloroplatinate of 3.33 μg/kg bw/day, which equates to an elemental platinum exposure of 1.46 μg/kg bw/day.
However, in a recent non-guideline study, it was demonstrated that a single respiratory challenge to mice topically sensitised to ammonium hexachloroplatinate can induce dose-dependent changes in pulmonary function indicative of an allergic lung response (Williams et al., 2015). This suggests that both dermal and inhalation exposure to chloroplatinates may play a role in occupational respiratory sensitisation/asthma. As such, the most appropriate and health precautionary approach was deemed to be to formulate a qualitative assessment (with ‘high hazard’ banding and recommended RMMs/OCs in Table E.3-1 of ECHA, 2012b) for systemic exposure to workers by the dermal route. [For further discussion of the potential respiratory sensitisation and irritation, including that reported in recent epidemiological studies, please see the ‘Hazard via inhalation route: local effects following long-term or acute exposure’ section, above].
Hazard via dermal route: local effects following long-term or acute exposure
No convincing evidence of skin sensitisation was found in the only study accepted as specifically investigating this endpoint, a Guinea Pig Maximisation Test (GPMT) following a protocol considered equivalent to OECD Test Guideline 406. In the induction phase, ten females were given an intradermal injection of a saturated solution of diammonium hexachloroplatinate, followed a week later by a topical application of 50% w/w test material in petroleum jelly. Two weeks after this, a challenge topical application of 10% w/w in petroleum jelly was administered. Eight out of ten animals showed reactions 24 hours after challenge administration, but only 2/10 reactions were still observable a further 24 hours later. No reactions were seen when the animals were re-challenged a week later with lower concentrations (1 and 5%) of the test material. The study authors considered that the reactions were the result of irritation, and concluded that diammonium hexachloroplatinate was not a skin sensitiser (Middleton, 1977).
Three other available studies are relevant but might not clearly differentiate between respiratory and skin sensitisers. The first used an adaptation of the murine Local Lymph Node Assay (LLNA) method and found that cytokine levels in the lymph nodes after application of diammonium hexachloroplatinate (0.25, 0.5 or 1% in DMSO) to the ears of female mice (5/group) were comparable to those seen following testing with known respiratory (trimellitic anhydride) and skin (2,4-dinitrochlorobenzene) sensitisers (Dearman et al., 1998).
The other two studies were carried out on the structurally-related disodium hexachloroplatinate. The first used a similar protocol to the LLNA and found a 23-fold increase in the number of proliferating auricular lymph node (ALN) cells, 48 hours after application of a 5% solution in acetone to the ears of five female mice on 4 consecutive days. The response was said to be similar to that induced by the known skin sensitiser, oxazolone (Schuppe et al., 1997a). The same investigators also carried out a ‘mouse ear swelling test’ (MEST), a scientifically-acceptable study despite not following a harmonised guideline. In this study, a 5% solution of disodium hexachloroplatinate in acetone was applied to the right ear of 4-5 female mice. Challenges were applied to the left ear of the treated animals using 0.5 or 2% solutions, 6 days and 4, 8, and 20 weeks after induction. Significant increases in left ear thickness were seen in animals challenged with 2% disodium hexachloroplatinate, and the study authors concluded that the test substance was a skin sensitiser (Schuppe et al., 1997b).
The proliferative responses reported in the studies described above can be indicative of a skin or respiratory sensitisation effect. Given that reports of skin sensitisation in humans after exposure to chloroplatinate compounds (including diammonium hexachloroplatinate) are uncommon, and considering the well-documented potential for this class of compounds to cause respiratory sensitisation, it is considered that the critical hazard following exposure by the dermal route is respiratory sensitisation. Pending further investigations, it is considered suitably health-precautionary to retain the classification of diammonium hexachloroplatinate as a skin sensitiser, in sub-category 1B, according to EU CLP criteria.
According to ECHA (2012b) guidance “moderate skin sensitisers (classified in Sub-category 1B in CLP) are allocated to the moderate hazard category band on the basis that exposure to these moderate skin sensitising substances should be well-controlled”. Therefore, consider recommended RMMs/OCs in Table E.3-1 of ECHA (2012b). It should be noted that control of potential respiratory sensitisation risk via skin exposure is the predominating concern, but that the RMMs/OCs associated with the “high hazard” banding for respiratory sensitisation (as discussed in more detail, above) are considered to be sufficiently protective.
Hazard for the eyes
In a GLP study conducted according to OECD Test Guideline 405, the eye irritancy potential of diammonium hexachloroplatinate was assessed. About 90 mg (volume of about 0.1 mL) of the solid test material was instilled into the conjunctival sac of the right eye of three New Zealand white rabbits and the ocular response assessed. The severity of the corrosive effects observed caused the study investigators to sacrifice 2/3 animals after 7 days’ observation, and consequently a score for irritation index could not be calculated. In the surviving animal, marked (but reversible) irritation was seen (Berthold, 1994).
On this basis, diammonium hexachloroplatinate has been classified as causing serious eye damage (category 1), and has been allocated to the “moderate” hazard band. Therefore, consider recommended RMMs/OCs in Table E.3-1 of ECHA (2012b).
[1]MWts: Pt metal, 195.08 g mol-1; Diammonium hexachloroplatinate, 443.87 g mol-1
General Population - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
Acute/short term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
Acute/short term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
DNEL related information
General Population - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
Acute/short term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
Acute/short term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
General Population - Hazard via oral route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
Acute/short term exposure
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
DNEL related information
General Population - Hazard for the eyes
Local effects
- Hazard assessment conclusion:
- hazard unknown but no further hazard information necessary as no exposure expected
Additional information - General Population
DNELs have been derived only for workers, not for consumers/general population. No uses have been identified in which consumers are exposed to diammonium hexachloroplatinate. In all uses with potential consumer exposure due to service life of articles, diammonium hexachloroplatinate is chemically transformed into another substance before reaching the consumers, and the subsequent lifecycle steps after this transformation are included in the assessment of the newly-formed substance. Regarding the general population, and following the criteria outlined in ECHA guidance R16 (2016), an assessment of indirect exposure of humans via the environment for diammonium hexachloroplatinate has not been performed as the registered substance is manufactured/imported/marketed at <100 tpa and is not classified as CMR.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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