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The key cation-sites M3 and A1 (and, in principle, M2) determine the root name. In both clinozoisite and allanite subgroups no prefix is added to the root name if M1 = Al. The prefixes ferri, mangani, chromo, and vanado indicate dominant Fe 3+ , Mn 3+ , Cr 3+ , and V 3+ on M1, respectively. In the dollaseite subgroup no prefix is added to the root name if M1 = Mg. Otherwise a proper prefix must be attached; the prefixes ferro and mangano indicate dominant Fe 2+ and Mn 2+ at M1, respectively. The dominant cation on A2 (other than Ca) is treated according to the Extended Levinson suffix designation. This simple nomenclature requires renaming of the following approved species: Niigataite (old) = clinozoisite-(Sr) (new), hancockite (old) = epidote-(Pb) (new), tweddillite (old) = manganipiemontite-(Sr) (new). Minor modifications are necessary for the following species: Strontiopiemontite (old) = piemontite-(Sr) (new), androsite-(La) (old) = manganiandrosite-(La) (new). Before a mineral name can be assigned, the proper subgroup has to be determined. The determination of a proper subgroup is made by the dominating valence at M3, M1, and A2 expressed as M 2+ and or M 3+ , not by a single, dominant ion (i.e., Fe 2+ , or Mg, or Al). In addition, the dominant valence on O4: X -or X 2-must be ascertained. The dominant trivalent cation on M3 determines the name, whereas the A2 cation appearing in the suffix has to be selected from among the divalent cations. (2) Allanite and dollaseite subgroups: For the sites involved in the charge compensation of a heterovalent substitution in A2 and O4 (i.e. M3 in the allanite subgroup; M3 and M1 in the dollaseite subgroup), identification of the relevant end-member formula must take into account the dominant divalent charge-compensating octahedral cation (M 2+ ) and not the dominant cation in these sites.Formal guidelines and examples are provided in order to determine a mineral "working name" from electron-microprobe analytical data.

Airborne particulate matter (PM) of varying size and composition is known to cause health problems in humans. The iron oxide Fe(3)O(4) (magnetite) may be a major anthropogenic component in ambient PM and is derived mainly from industrial sources. In the present study, we have investigated the effects of four different size fractions of magnetite on signaling pathways, free radical generation, cytotoxicity, and genotoxicity in human alveolar epithelial-like type-II cells (A549). The magnetite particles used in the exposure experiments were characterized by mineralogical and chemical techniques. Four size fractions were investigated: bulk magnetite (0.2-10 μm), respirable fraction (2-3 μm), alveolar fraction (0.5-1.0 μm), and nanoparticles (20-60 nm). After 24 h of exposure, the A549 cells were investigated by transmission electron microscopy (TEM) to study particle uptake. TEM images showed an incorporation of magnetite particles in A549 cells by endocytosis. Particles were found as agglomerates in cytoplasm-bound vesicles, and few particles were detected in the cytoplasm but none in the nucleus. Increased production of reactive oxygen species (ROS), as determined by the 2',7'-dichlorfluorescein-diacetate assay (DCFH-DA), as well as genotoxic effects, as measured by the cytokinesis block-micronucleus test and the Comet assay, were observed for all of the studied fractions after 24 h of exposure. Moreover, activation of c-Jun N-terminal kinases (JNK) without increased nuclear factor kappa-B (NF-κB)-binding activity but delayed IκB-degradation was observed. Interestingly, pretreatment of cells with magnetite and subsequent stimulation with the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) led to a reduction of NF-κB DNA binding compared to that in stimulation with TNFα alone. Altogether, these experiments suggest that ROS formation may play an important role in the genotoxicity of magnetite in A549 cells but that activation of JNK seems to be ROS-independent.

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