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Switzerland - Final Regulatory Action
Carbon tetrachloride CAS number:
Date circular:

Chemical name: Methane, tetrachloro-

Final regulatory action has been taken for the category: Pesticide, Industrial

Final regulatory action: The chemical is Banned

Use or uses prohibited by the final regulatory action:

All uses and formulations are prohibited
Ozone depleting substances shall not be use.
The following is prohibited:
a.the manufacture of ozone depleting substances; this prohibition shall not apply to the manufacture of ozone depleting substances by means of recycling used ozone depleting substances, if ozone depleting substances are not chemically changed by this process;
b.the import and export of ozone depleting substances; this prohibition shall not apply to imports from States and exports to States which adhere to the provisions of the Montreal Protocol of 16 September 1987 (SR 814.021) to phase out Ozone Depleting Substances (hereinafter Protocol), approved by Switzerland.
c.the import of products and articles containing ozone depleting substances; except for products and articles, which may be imported in accordance with the provisions of Annexes 4.9, 4.11, 4.14, 4.15 and 4.16;
d.the import of products and articles containing ozone depleting substances or manufactured using ozone depleting substances and listed in an appendix to the Protocol; subject to letter c this prohibition shall not apply to imports from States which adhere to the provisions of th Protocol approved by Switzerland.

Use or uses that remain allowed:

Exemptions exist for the following purposes: manufacture products or articles which may be supplied or imported in accordance with the provisions of Number 22 and Annexes 4.9, 4.11, 4.14, 4.15 and 4.16;
b.for use as intermediate products for further chemical conversion;
c.for research purposes;
d.pest control with a permit under Article 35 of the Ordinance on Toxic Substances of 19 September 1983 (SR 813.01)
The Federal Agency may authorise limited exemptions for other uses, provided that:
a.according to the state of the art, no replacement is available for ozone depleting substances or for the products and articles manufactured using ozone depleting substances, and more than the minimum amount of ozone depleting substances necessary for the desired purpose is used

The final regulatory action was based on a risk or hazard evaluation: Yes

Summary of the final regulatory action:

Carbon tetrachloride is listed as an ozone depleting substance in Annex 3.4, Number 1 of the Ordinance relating to Environmentally Hazardous Substances.
The use, production, import and export of ozone depleting substances (as well as simple mixtures and products containing ozone depleting substances if they are in containers used solely to transport or store these substances) is prohibited.
Exception: recycled ozone depleting substances which are not chemically changed by the process
Exception: manufacture of products or articles which may be supplied or imported in accordance with the provisions of Annexes 4.9 (compressed gas cylinders), 4.11 (plastics), 4.14 (solvents, 4.15(refrigerants), and 4.16 (extinguishing agents). This applies only to imports/exports from/to States which adhere to the provisions of the Montreal Protocol of 16 September 1987, and its amendments of 29 June 1990, 25 November 1992, 17 September 1997 and 3 December 1999.

The reasons for the final regulatory action were relevant to: Human health and environment

Summary of known hazards and risks to human health:

Mouse LD50(IP) 3350- 4676 mg/kg body weight.
Rat LD50 (oral) 10054 mg/kg body weight
Rat LD50 (IP) 3029 - 6603 mg/kg bodyweight
Rat 100% death rate after inhalation of 121600 mg/m3 for 2.2 h or 46700 mg/m3 for 8 h
Guinea pig and rabbit LD50 (dermal) >15 g/kg body weight
Carbon tetrachloride accumulates in fat, bone marrow, white matter of brain, spinal cord and nerves, liver, kidney, salivary glands, and gastrointestinal mucosa (mouse, inhalation); in liver, kidney, brain, muscle and blood (rat, oral); in brain, heart, liver and blood (Beagle dogs, inhalation).
Carbon tetrachloride is metabolized by CYP2E1 and CYP2B1/2B2 to a trichloromethyl radical, which may undergo reductive or oxidative biotransformation. The trichloromethyl radical may react with molecular oxygen, resulting in the formation of trichlorometylperoxyl radicals. This radical may react with lipids, causing lipid peroxidation along with the production of 4-hydroxyalkenals. It is also presumed that the trichloromethylperoxyl radical will react further to produce phosgene, which may further react with tissue macromolecules or with water, finally producing hydrochloric acid and carbon dioxide.
Major effects in mice resulting from carbon tetrachloride exposure by acute oral exposure are changes in liver enzyme levels and other liver effects such as decreases in protein, glucose, phospholipids, DNA, RNA concentrations, increases in triglycerides, glycogen and free and esterified cholesterol concentrations. Centrilobular necrosis was seen in the low-dose (32 mg/kg body weight, 13-327 h) and mild midzonal necrosis in the mid-(797 mg/kg bodyweight) and high-dose (2391 mg/kg bodyweight) group. Rats showed dose-related increases in liver and serum alanine transferase (ALAT), liver tyrosine transaminase and alkaline phosphatase activities after a single oral dose of 797-3188 mg/kg body weight. Centrilobular hepatocellular necrosis was observed in 2/4 monkeys 24 h after oral administration of a single dose of carbon tetrachloride.
Exposure by inhalation produced Clara cell lesions in mice (0.46 or 0.92 mmol/litre air for 1 h, 1.84 mmol/litre air for 12 min, and 3.68 mmol/litre air for 2 min) Rats showed increases in aspartate aminotransferase (ASAT), ALAT, sorbitol dehydrogenase (SDH) and glutamate dehydrogenase activities in the serum 24 h post-inhalation exposure at >3404 mg/m3 air for 4 h.
Long-term exposure (1.3 ml/kg bodyweight of 40% CCl4, SC) resulted in severe cirrhosis in Sprague-Dawley rats (they did not develop carcinomas) and hepatocellular carcinoma and hyperplastic nodules in 8/13 Osborne-Mendel rats and in 12/15 Japanese rats. BDF1 mice which were exposed up to 801-25 mg/m3 CCL4 (2 years, whole body) showed a significant decrease in survival, changes in haematology, blood biochemistry and urinalysis, changes in liver, kidney and spleen at >160.25 mg/m3 CCL4.
Carbon tetrachloride can be considered a reproductive toxicant; it is however not embryotoxic or teratogenic.
Findings from mutagenicity studies are equivocal; positive findings such as strand-breakage and aneuploidy may be the consequence of nuclear protein or DNA damage induced secondarily to CCL4 toxicity.
Carbon tetrachloride was shown to be immunotoxic in B6C3F1 female mice, resulting in a suppression of both humoral and cell-mediated immune functions. The T-cell dependent antibody formation against sheep red blood cell was shown to be a very sensitive parameter. CCl4 was toxic at all doses (25-5000 mg/kg bodyweight) tested, independent of the route (ip or oral). Rats showed no immunotoxic effects up to concentrations of 40 mg/kg bodyweight. T-cell dependent immune processes seem to be more sensitive than B-cells.
Controlled studies in humans showed no adverse effects of carbon tetrachloride. Cases of poisonings have resulted from accidental exposure, mainly of CCL4 vapours, or suicidal ingestion. In humans it seems to be toxic to liver and kidney. Concentration of 64.1 - 512.8 mg/m3 for 3-4 hours have no adverse effects, at higher concentrations nausea, headache, vomiting, rapid pulse, rapid respiration, sleepiness, dizziness, unconsciousness and immediate death occur. The lethal oral dose (1.5 to 355 ml CCL4) varies widely due to individual differences, actual doses are, however, often difficult to ascertain. Non-cancer epidemiology shows significant effects (ALAT; ASAT; alkaline phosphatase, gamma-GT, glutamate dehydrogenase and others) in workers exposed to air CCl4 concentrations of ?6.4 mg/m3. Cancer epidemiology has not established an association between CCl4 exposure and increased risk of mortality, neoplasia or liver disease.

Expected effect of the final regulatory action in relation to human health:

The reduction in carbon tetrachloride emission, together with the reduction in emissions of other ozone depleting substances, is expected to reduce the risk of increase of UV radiation due to depletion of stratospheric ozone ("ozone hole").

Summary of known hazards and risks to the environment:

Carbon tetrachloride of low to moderately toxic to bacteria (however: methanogenic bacteria IC50 6.4 mg/l), protozoa and algae.
Aquatic invertebrates: Daphnia magna acute LC50 (24/48 h, static) 28 - >770 mg/l, no effect on the development of sea urchins.
Aquatic vertebrates: Golden Orfe (Leuciscus idus melanotus) LC50 (48h) 13 to 472 mg/l; Dab (Limanda limanda) LC50 50 mg/l
Rainbow trout (Oncorhynchus mykiss) no effects at 1-80 mg/l for up to 336 h under semi-static renewal
Common bullfrog (Rana catesbiana) LC50 0.92 mg/l
CCl4 seems to be more toxic to embryo-larval stages of fish and amphibians that adults. O. mykiss LC50 (27d) 1.97 mg/l; most sensitive species R. catesbiana 1% incidence of teratic larvae at 60 g/l, 17% at 7.8 mg/l
Earthworms (Eisenia foetida) LC50 160 g/cm2 on filter paper in glass vials.
Ozone depletion
Carbon tetrachloride is subject to the UN Vienna Convention for the Protection of the Ozone Layer and Montreal Protocol on Substances that Deplete the Ozone Layer and is listed in Annex B Group II. This means that by January 1, 1996, Switzerland will have reduced its carbon tetrachloride production and consumption by 100% (with possible essential use exemptions). Global atmospheric emissions of carbon tetrachloride in 1996 were estimated as 41000 tonnes, of which some 26 000 tonnes originate from carbon tetrachloride production in Article 5(1) Parties (developing countries) and Countries with Economies in Transition. Emissions of carbon tetrachloride can be technically and economically reduced from both feed stock and process agent uses, although in some cases, alternatives to carbon tetrachloride use may not be available. Emissions from carbon tetrachloride used as a final product are estimated to be in the range of 11500 to 12400 metric tones. Doubts exist, however, as to the validity of the reported data. But it seems that industrialized countries have phased out production and consumption of carbon tetrachloride. In Article 5(1) countries and Countries with Economies in Transition there is significant trade, eg India imports 17000 to 20000 metric tonnes/year. The global lifetime of carbon tetrachloride is currently estimated to be 23 to 42 years. Global surface mixing ratios (tropospheric concentrations) have decreased since about 1990; mixing ratios in 2000 were between 95-100 ppt.
Health effects potential health effects of ozone depletion are the result of elevated levels of ambient UV-B radiation. UV-B radiation is a risk factor for certain types of cataract, squamous cell carcinoma, it contributes to the formation of basal cell carcinoma and cutaneous melanoma and possibly to immune suppression. Since the risk of increased UV-B radiation is largely dependent on human behaviour, it is difficult to quantify. Further complications stem from the emerging possibilities regarding interactions between ozone depletion and global climate change. A study in punta Arenas, chile, showed a relationship between episodes of ozone depletion, increased terrestrial UV-B radiation and sunburn during the spring months. The Antarctic "ozone hole" passes over Punta Arenas each spring and a rise in the number of sunburn cases after sudden ozone depletion, coinciding with Sunday outdoor recreational activities could be documented. In the skin UV-B radiation causes specific DNA damage, leads to the generation of reactive oxygen species, point mutations, DNA deletions and micronuclei. Basal cell carcinomas, squamous cell carcinoma, and cutaneous melanoma are all related to UV exposure. Concerning cutaneous melanoma, exposure in childhood seems to be a far higher risk factor than chronic exposure in adulthood. Solar UV radiation also seems to be a risk factor in the development on non-Hodgkin's Lymphoma and chronic lymphocytic leukaemia.
Environmental effects
Environmental damage to terrestrial or aquatic ecosystems due to increased UV-B radiation is difficult to observe or to quantify. With respect to terrestrial ecosystems, meta-analysis of >60 studies showed enhancement in some plant characteristics (plant height, leaf area, and shoot mass) while most studies reported decreases in these characteristics. There are also reports of studies where solar UV-B promoted plant growth. A potentially important phenomena is that small effects of UV-B radiation might accumulate to produce larger effects in subsequent years in perennial plants. This is, however, being discussed controversially since cumulative effects, eg in subarctic heath perennials, were apparent from some traits of some species but not for others. Furthermore cumulative effects disappeared over a longer period of time. High UV-B may also affect genetic stability of plants causing long-term heritable effects, with a high frequency of deleterious mutations, such as the activation of "mutator transposons" in maize. With respect to insect herbivory, enhanced UV-B radiation seems to lead to reduced herbivory and/or insect growth, mostly mediated through the host plant. Concerning aquatic ecosystems there is general consensus that solar UV negatively affects aquatic organisms. Reductions in productivity, impaired reproduction and development, and increased mutation rate have been shown for phytoplankton, macroalgae, fish eggs and larvae, zooplankton and primary and secondary consumers exposed to UV radiation. Decreases in biomass productivity due to enhanced UV-B radiation are relayed through all levels of the food web; quantitation of such effects is, however, difficult to perform. Species interactions and ecosystem dynamics are difficult to evaluate, model and predict. Feedback mechanisms between aquatic ecosystems, physical factors and atmospheric and oceanic circulation have significant impact on primary productivity and ecosystem integrity, but are not well understood and difficult to predict. Bacterioplankton does not seem to be very sensitive to enhanced UV-B radiation and cyanobacteria have been shown to be able to protect themselves with mycosporine-like amino acids, scytonemin, carotenoids, superoxide dismutase, and migration to habitats with reduced radiation. Phytoplankton communities have been shown to be quite sensitive to slar ambient UV. UV impairs photosynthesis, nitrogen metabolism, bleaces photosynthetic pigments and induces DNA damage. There are, however, efficient repair and protection mechanisms in phytoplanter, including the xanthophylls cycle in photosynthesis, screening pigment production, synthesis of antioxidants and DNA repair. Studies in Patagonia, Argentina, which is occasionally under the influence of the Arctic "ozone hole" showed that photosynthetic inhibition in phytoplankton varies considerably between different environments and depends on the optical depth of the water column. Macroalgae and seagrass are important biomass producers, are exploited commercially and form habitats for larval stages of fish, shrimp and other crustaceans. Both long-and short-term exposure to solar radiation inhibits growth in adult stages of several species of macroalgae. Susceptibility to UV is, however, highly variable among species which result in a specific depth distribution. UV exposure is considered to be a major stress factor for zooplankton, resulting in vertical migration into lower and darker water layers as well as the production of UV-protective pigments such as melanin and carotenoids and mycosporine-like amino acids. Both the Arctic and Antarctic ecosystems may be affected by increased ambient UV-B radiation. The effects of increased UV-B radiation may, however, be masked by other climatic effects. It has for example been shown that large spatial and temporal interannual variability in cloud cover maz augment or reduce increases in UV-B radiation. Arctic marine phytoplankton may be more sensitive to increased UV radiation than its Antarctic counterpart. In both ecosystems, however, a shift has been observed in species composition to diatom-dominated assemblages, which are capable of synthesizing UV screening compounds. Furthermore, results indicate that currently measured UV levels do not affect high Arctic macroalgal communities

Expected effect of the final regulatory action in relation to the environment:

The reduction in carbon tetrachloride emission, together with the reduction in emissions of other ozone depleting substances, is expected to reduce the risk of increase of UV radiation due to depletion of stratospheric ozone ("ozone hole").

Date of entry into force of the final regulatory action: 14/08/1991