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Methanol was readily degraded in both inocula at all concentrations with average disappearance of methanol as follows: a) after 5 days, 76% bio-oxidation in fresh water and 69% in salt water; b) after 10 days, 88% bio-oxidation in fresh water and 84% in salt water; c) after 15 days, 91% bio-oxidation in fresh water and 85% in salt water and d) after 20 days, 95% bio-oxidation in fresh water and 97% in salt water.

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Those blood samples possessing metabolic activity (conjugators) were inactive in the assay, whereas those samples which were metabolically inactive (non- conjugators) produced significant increases in SCEs (see also section 6.3.1).

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Formate concentrations measured in the vitreous humour and retinas of methanol-intoxicated rats (Eells, 1991; Eells et al., 1996) were equivalent to or greater than corresponding blood formate concentrations.

Although methanol intoxication is known to disrupt brain function and severe intoxication results in coma and death, the most common permanent consequence of methanol intoxication is blindness (Röe, 1955).

(All destinations. All destinations applies to all Group 3 Items.)

8.6.1.5 DNA damage Concentrations of up to 16 mM methylene chloride failed to induce unscheduled DNA synthesis (UDS) in cultured rat hepatocyte, although some reduction in replicative DNA synthesis occurred at the higher doses (Andrae & Wolff, 1983).

The apparent selective vulnerability of the retina and optic nerve to the toxic actions of formate in methanol poisoning has been the subject of considerable speculation (Röe, 1955; Sharpe et al., 1982; Jacobsen & McMartin, 1986).

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  • Canadian Nuclear Safety Commission (CNSC) Note:

    2,6-DICHLORO-4-NITROANILINE | C6H4Cl2N2O2 - …

  • Group 3 does not control “software” which is either:

    C6 - Amines | Sigma-Aldrich

  • 3-1.1. does not control the following:

    Sigma-Aldrich Online Catalog Product List: C6 ..

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3-1.2 Special fissionable materials

The results were statistically significant only at the highest concentration (7%) and exposures of shorter duration (2, 4 or 6 h) were without effect (McCaroll et al., 1983).

3-1.2. does not control the following:

These findings provide direct evidence that formate acts as retinal mitochondrial toxin and suggest that one component of the retinotoxic actions of formate may be due to tissue-specific differences in mitochondrial transport mechanisms or in mitochondrial metabolism.

3-2.2 Non-nuclear materials for reactors;

These data suggest that the toxic actions of methanol on the visual system may be due to the selective accumulation of formate in the vitreous humour and the retina as compared with other regions of the central nervous system.

BEZ (ppm) = CF x concentration of element Z (in ppm);

A small increase in sister-chromatid exchanges (SCEs), without clear evidence of a dose-response relationship, was found in V79 cells when exposed to gaseous methylene chloride at concentrations up to 5% (Jongen et al., 1981 ).

CF is the conversion factor: (σZ x AB) divided by (σB x AZ);

In experiments using no exogenous activation systems, exposure of hamster V79 cells or human fibroblasts (AH cells) to methylene chloride concentrations of between 0.5 and 5% did not induce UDS (Jongen et al., 1981).

Note: In lieu of an abstract, this is the article's first page.

Comparative studies conducted in mitochondria isolated from bovine heart showed little or no inhibition of ATP synthesis at formate concentrations up to 50 mM.

Such equipment or systems of equipment may include, for example:

Chromosomni alterations (chromatid damage, chromosomni exchanges, but no increase in sister chromatid exchanges) were observed in CHO cells (Thilagar & Kumaroo, 1983), human lymphocytes and L5178Y cells (Thilagar et al., 1984a,b), both with and without metabolic activation.

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