Nickel Carbonyl Inhibition of RNA Synthesis by a …

(CSDS, 1991) Uses Nickel carbonyl is an intermediate in the Mond process of nickel refining.

Nickel carbonyl inhibition of RNA synthesis by a …

Neither human nor animal data are available for deriving AEGL-1 values. Both human and animal data affirm the extreme toxicity of nickel carbonyl. Published accounts of human exposures indicate that symptoms of toxicity can occur in the absence of olfactory or other sensory detection. Severe pulmonary edema and hemorrhage can follow initial asymptomatic exposures by as much as 12 h after exposure. Therefore, AEGL-1 values are not recommended.

Efficacy of orally-administered chelating agents for nickel carbonyl toxicity in rats.

Use of nickel carbonyl in organic synthesis: G

EPA (U.S. Environmental Protection Agency). 1991c. Nickel Carbonyl (CASRN 13463-39-3): Carcenogenicity Assessment for Lifetime Exposure. Integrated Risk Information System (IRIS), U.S. Environmental Protection Agency [online]. Available: [accessed August 1, 2007].

CEC (Commission of the European Communities). 1990. Nickel tetracarbonyl. Pp. 49-52 in The Toxicology of Chemicals, Vol. II. Luxembourg: Commission of the European Communities.

Abstracts of Articles on Organic Synthesis

As previously noted, lethality data are available for several species but are limited to LC50 determinations. Kincaid et al. (1953) suggest that sensitivity to nickel carbonyl may be a function of body mass, and as a result, lethal exposures for humans have been estimated. Based on data from mice, rats, and cats, these investigators estimated that the lethality of nickel carbonyl was directly proportional to body weight to the 2/3 power. Human exposure reports suggest a wide range of nonlethal responses to acute exposure to nickel carbonyl as well as a characteristic latency period between initial exposure and subsequent, more serious effects.

Amine Structure & Synthesis

Exposure-response data over multiple time periods were unavailable for nickel carbonyl, and therefore empirical derivation of a scaling factor (n) was not possible. The concentration exposure-time relationship for many irritant and systemically acting vapors and gases may be described by Cn × t = k, where the exponent n ranges from 0.8 to 3.5. In the absence of an empirically derived exponent, and to obtain conservative and protective AEGL values, temporal scaling was performed using n = 3 when extrapolating to shorter time points and n = 1 when extrapolating to longer time points. A total uncertainty factor adjustment of 10 was applied. An uncertainty factor of 3 was applied to account for interspecies variability. The available lethality data, however, do suggest that the mouse represents a sensitive species. Based on available lethality data and the analysis conducted by Kincaid et al. (1953) indicating an inverse relationship between lethality and body size (see .), the interspecies uncertainty factor of 3 appears to be justified. Although intraspecies variability is difficult to assess based on available data, an uncertainty factor of 3 was applied with the assumption that neither the effects of nickel carbonyl on pulmonary tissues nor dosimetry would vary greatly among individuals. The occupational exposure data reported by Shi et al. (1994b) suggest that the AEGL-2 values are sufficiently protective. The overall dataset for nickel carbonyl is deficient regarding nonlethal effects of nickel carbonyl inhalation. Therefore, a modifying factor of 3 was applied in the development of the AEGL-2 values to account for these deficiencies and the possibility of developmental toxic effects reported by Sunderman and colleagues. The resulting AEGL-2 values are shown in and their derivations in .

Our last topic for today is the synthesis of amines

The development of the AEGL-2 values for nickel carbonyl is based on the toxic response of mice following 30-min inhalation exposures at seven concentrations: 2.17, 6.51, 7.84, 8.68, 9.80, 10.9, or 12.6 ppm (Kincaid et al. 1953). A concentration-dependent lethal response was observed for exposures to 6.51-12.6 ppm, but the lowest exposure (2.17 ppm) resulted in no deaths. Exposure to 6.51 ppm resulted in the deaths of two of 15 mice. A 30-min LC50 of ~9.4 ppm was estimated by the investigators. Although no histopathology examinations were performed on the mice in the 2.17-ppm group, Kincaid et al. (1953) and Barns and Denz (1951) reported findings of pleural effusion, severe pulmonary congestion, and pulmonary edema in rats that died following exposure to nickel carbonyl. Therefore, the 30-min exposure to 2.17 ppm was considered a reasonable estimate of an exposure that may cause pulmonary damage in the mouse (most sensitive species tested) but not result in irreversible adverse effects. As shown by the multiple-exposure studies of Kincaid et al. (1953), repeated exposures of mice to this or greater concentrations did not result in a lethal response. Pulmonary damage appears to a component in the continuum of the toxic response to nickel carbonyl and an appropriate critical effect for AEGL-2 development. The 30-min exposure to 2.17 ppm was considered a point-of-departure