Non-linear development of postural control and strategy use in young children: a longitudinal study.

This longitudinal analysis confirmed a non-monotonic pattern of postural control development in children from age 5 to 8 years suggested by previous cross-sectional studies. Postural control was considered in terms of control strategy and its variability operationalized by mean and standard deviation of center of pressure (COP) velocity; and of effectiveness and its variability operationalized by mean and standard deviation of COP anteroposterior (a-p) excursion. Periods of significant variability were used to indicate behavioral transitions. Seventeen healthy children (nine males, eight females) aged 5-6 years (61.5-75 months) were tested at 3- to 4-month intervals up to age 8 years (83-97 months) in eyes-open quiet stance on a force platform for 30 s in each of ten trials. Data were reorganized into six developmental categories based on adjacent test dates prior to (-1) and after (+1, +2, +3, +4) a subject's trial with the lowest COP velocity (0). Developmental category is proposed to represent level of sensorimotor integrative skill. Within-subject ANCOVAs revealed a significant effect (P<0.0001) for developmental category with covariance due to height, weight and actual age removed. Post hoc tests showed a significant effect (P<0.0001) on measures of strategy. However, differences in COP velocity (type of strategy used) and differences in its variability (denoting a transition between strategies) were not always coincident. Performance outcome (COP a-p excursion) changed near linearly across categories. It was concluded that a non-monotonic change in control strategy as indicated by COP velocity describes the development of quiet stance equilibrium. A transition occurs from a primarily open-loop to incorporation of open- and closed-loop components of control. Honing of strategy used precedes and follows transitions. Constriction of velocity and excursion may typify the early stages of bimodal strategy. Developmental categories describe affiliation with the strategy employed and may represent differentiable levels of sensorimotor integrative skill. They may be more useful in assessing progression of equilibrium control than consecutive age in years.

Mutagenicity tests of 4-phenyl-1,3-dithia-2-thioxo-cyclopent-4-ene.

The mutagenicity of 4-phenyl-1,3-dithia-2-thioxo-cyclopent-4-ene (DT827B) was examined in reverse mutation tests using Salmonella typhimurium and Escherichia coli, in the chromosomal aberration test with Chinese hamster ovary (CHO) cells, and in the micronucleus test using mice bone-marrow. In reverse mutation assay on DT827B according to Ames' method, DT827B was not mutagenic to S. typhimurium or E. coli when tested in dimethylsulfoxide to the limit of its solubility where precipitation occurred. In chromosomal aberration assay using CHO cells, DT827B was not clastogenic to induce structural chromosomal aberration but capable of inducing polyploidy. In micronucleus test, DT827B did not show micronucleus-inducing potential at the maximum dose. In conclusion of the three mutagenicity studies, DT827B was considered to cause no mutagenicity under the conditions used in the present experiments except the increase in polyploidy, which probably is due to a toxic effect of the compound.

Postural stability measures: what to measure and for how long.

This paper assesses the repeatability of force plate postural stability measurements. The common parameters were investigated for five test durations, two vision conditions, and two stance conditions. All parameters were found to be reliable measures. Optimum test retest reliability was obtained at 20-s and 30-s trial periods. Centre of pressure measures increased with increased test duration while ground reaction forces and velocity decrease slightly. RELEVANCE:--The results indicate that measures of centre of pressure excursion and ground reaction forces can differentiate between various mechanical and sensory conditions and thus are clinically useful for detecting and quantifying both mechanical and sensorimotor postural deficiencies. It is also demonstrated that the test duration is important in the reliability and validity of stability measures.

Mutagenic responses of L5178Y mouse cells at the tk and hprt loci.

The expression of multiple recessive genes by aberrant mitotic lesions plays a major part in carcinogenesis. These lesions include intragenic mutations as well as chromosomal lesions. An in vitro model for studying carcinogenesis should respond to all these lesions. Mutagenesis studies that target hemizygous loci may not be useful in studying chromosomal mechanisms because lesions incorporating essential genes already missing on the inactive, homologous chromosome may be lethal to the cell. Cells heterozygous at the selectable gene may survive. Using L5178Y mouse cells, we compared the mutagenic responses at the heterozygous tk and hemizygous hprt loci to four chemicals-benzidine dihydrochloride, diglycidylresorcinol ether, nitrofen and p-benzoquinone dioxime. None of the compounds induced clear positive responses at the hprt locus. In contrast, all the compounds induced clear or marginal mutagenic responses at the tk locus. These data are consistent with the expectation that heterozygous loci can detect lesions that are refractory to hemizygous loci.

Frequency characteristics of postural control of children with and without visual impairment.

During quiet standing on a force platform, centre of pressure frequency characteristics of normal and visually impaired children were investigated under four conditions: normal surface, eyes open and closed; foam surface, eyes open and closed. Total power was calculated between 0 and 4Hz. Slopes of logarithmically transformed data were used to compare relative power at high and low frequencies. Younger children had greater total power and relatively more high frequency power. The results suggest that young children (four to six years) do not normally use immediate vision in postural control. Visually impaired children have greater instability than sighted children, with greatest differences between the two groups at 10 to 12 years.

Changes in centre of pressure of ground reaction forces prior to rapid arm movement in normal subjects and patients with cerebellar ataxia.

This study was designed to investigate the biomechanics of anticipatory postural responses. In particular the aim was to determine whether the centre of pressure of ground reaction forces moves in anticipation of an expected upper limb movement, and if so to determine the pattern (s) of centre of pressure change in normal subjects, and patients with cerebellar ataxia. Twenty-eight healthy, normal subjects (aged 30-64 years) and ten cerebellar ataxic patients (aged 30-80 years) each stood with feet parallel and 6 cm apart on a force platform. The subjects elevated their right arm to the horizontal as quickly as possible in response to a visual stimulus. The centre of pressure of ground reaction forces was recorded for 1 s: 600 ms before and 400 ms after initiation of arm movement. In 96% of normal subjects there were consistent patterns of change in the location of centre of pressure prior to the beginning of the rapid self-initiated arm movement. In 79% of subjects, there was a posterior shift of centre of pressure prior to arm movement. Ninety-six per cent of subjects exhibited a preparatory shift in centre of pressure in the lateral direction, most frequently to the left (75%). These patterns were repeatable both within and between subjects. There was a bimodal distribution in the onset time of the preparatory centre of pressure excursions, with initiation occurring at ⩽ 150 ms and ⩾ 300 ms prior to arm acceleration. Cerebellar ataxic subjects exhibited marked between-subject and within-subject variability in the patterns of centre of pressure excursion, including absence of preparatory excursions (in three subjects).

Responses of the L5178Y mouse lymphoma forward mutation assay: V. Gases and vapors.

A new protocol for testing vapors and gases in the L5178Y mouse lymphoma assay is presented. Four chemicals, propylene, 1,2-propylene oxide, 1,3-butadiene, and vinylidene chloride, were tested for their mutagenic potential. Cultures were exposed to the chemicals, which were delivered as vapors or gases, for 4 hr, then cultured for 2 days before plating in soft agar with or without trifluorothymidine (TFT), 3 microgram/ml. Each chemical was tested at least twice. Significant responses were obtained with 1,2-propylene oxide and vinylidene chloride, but neither cytotoxicity nor mutagenicity was induced by 1,3-butadiene; propylene could not be classified as either mutagenic or non-mutagenic in the assay. Rat liver S9 mix was not a requirement for the mutagenic activity of 1,2-propylene oxide, whereas the liver preparation markedly enhanced both the cytotoxicity and mutagenicity of vinylidene chloride.

Responses of the L5178Y mouse Lymphoma cell forward mutation assay. V: 27 coded chemicals.

Twenty-seven chemicals were tested for their mutagenic potential in the L5178Y tk+/tk- mouse lymphoma cell forward mutation assay using procedures based upon those described by McGregor et al. (McGregor DB, Martin R, Cattanach P, Edwards I, McBride D, Caspary WJ (1987): Environ Mol Mutagen 9:143-160). Cultures were exposed to the chemicals for 4 hr, then cultured for 2 days before plating in soft agar with or without trifluorothymidine (TFT), 3 micrograms/ml. The chemicals were tested at least twice. Statistically significant responses were obtained with acid orange 10, aniline, benzaldehyde, o-chloroaniline, chlorodibromomethane, cytembena, 1,2-dibromo-4-(1,2-dibromomethyl) cyclohexane, dieldrin, lithocholic acid, oxytetracycline, phenazopyridine HCl, 1-phenyl-3-methyl-5-pyrazolone, sodium diethyldithiocarbamate, solvent yellow 14, tetraethylthiuram disulfide (disulfiram), 2,4-toluene diisocyanate, and 2,6-toluene diisocyanate. Apart from phenazopyridine HCl, acid orange 10, and solvent yellow 14, rat liver S9 mix was not a requirement for the mutagenic activity of these compounds. Chemical not identified as mutagens were N-4-acetylaminofluorene, chlorpheniramine maleate, chloropropamide, 1,4-dioxane, endrin, ethylene glycol, iron dextran, methapyrilene, sodium(2-ethylhexyl)alcohol

Anticipatory postural control in children.

Postural responses, triggered by sensory feedback, are present very early in a child's development. The purpose of the present study was to investigate the ability of children to anticipate postural disturbances caused by self-initiated movements and their ability to coordinate anticipatory postural adjustments with movement execution. Children (N = 32) aged 4 to 14 years were asked to stand quietly on a stable force plate and to raise their right arm forward (or backward) to the horizontal position after a visual stimulus. Changes in the center of pressure beneath the feet were recorded before and during the arm raise. The anticipatory (feedforward) postural patterns seen before the arm movement, and noted in a previous study of adults, were present in the youngest of the children (4 years, 2 months). Longer reaction times and inconsistent postural responses (in the anteroposterior direction) suggest that children are less capable than adults of coordinating the anticipated postural adjustment with the forthcoming limb movement, however. In the lateral plane, anticipatory postural responses were initiated more consistently.

Studies on the activities of benzo[a]pyrene, benzidine and ethyl methanesulphonate in the L5178Y TK +/- mouse lymphoma mutagenicity assay using standardized and non-standardized protocols.

As part of the third UKEMS collaborative trial, ethylmethane sulphonate (EMS), benzo[a]pyrene (B[a]P) and benzidine (BZD) were assayed for mutagenicity using the L5178Y mouse lymphoma TK +/- forward mutation system. Exogenous metabolic activation was achieved with two different sources of rat liver S9 which were used under optimized conditions for B[a]P and BZD, the latter being tested also without S9. EMS was assayed in the absence of S9 only. Mutants were selected for trifluorothymidine (TFT) resistance after 48 and 72 h expression time. Mutant frequency (MF) data were subjected to ANOVA analysis and t-tests for differences between replicate cultures, linear trend and differences from solvent controls. Large TFT resistant colonies are believed to be due to induction of small amounts of genetic damage (point mutations, small deletions) at the tk locus, whilst small colonies are thought to be a result of larger effects. The relative proportions of the two colony types were determined in some experiments. All three compounds induced dose-related increases in MF under all conditions. B[a]P induced equal proportions of large and small colonies at all doses. EMS induced predominantly large colonies at all doses. The effect of BZD on colony size was variable. The source of S9 did not exert any consistent effect on toxicity, mutagenicity or mutant colony size. Maximum MF values occurred at 72 h for B[a]P and BZD but the results with EMS were variable. No consistent differences were apparent between estimates of toxicities made either by cloning immediately after treatment (day 0 cloning) or by estimating the relative total growth (RTG) at expression time.

L5178Y mouse lymphoma cell mutation assay results with 41 compounds.

Forty-one chemicals were tested for their abilities to induce trifluorothymidine resistance in L5178Y mouse lymphoma (MOLY) cells. These chemicals were included in the National Toxicology Program's evaluation of four in vitro short-term toxicity assays for predicting carcinogenicity in the rodent bioassay. Of the 41 chemicals examined for this report, 8 were equivocal in the rodent bioassay, and 7 were questionable in- the MOLY assay. If these chemicals are eliminated from an analysis of concordance, the remaining 26 chemicals lead to a concordance of 69% with a sensitivity of 71%. The specificity could not be determined because only two non-carcinogens were detected.

TFT and 6TG resistance of mouse lymphoma cells to analogs of azacytidine.

5-Azacytidine (5-aza-CR) and six of its analogs were examined for their ability to induce trifluorothymidine (TFT) and/or 6-thioguanine (6TG) resistance in L5178Y mouse lymphoma cells. These analogs were 5-aza-2'-deoxycytidine (5-aza-CdR), 5-fluoro-2'-deoxycytidine (5-FCdR), 5,6-dihydro-5-azacytidine (dH-aza-CR), 6-azacytidine (6-aza-CR), cytidine (CR) and 1-b-D-arabinofuranosylcytosine (ara-C). 5-Aza-CR and 6-aza-CR were examined for their ability to induce 6TG-resistant colonies and results demonstrated no effect. At least a 5-fold increase in TFT resistance was observed for 5-aza-CR, 5-aza-CdR, 5-FCdR, dH-aza-CR and ara-C. The concentration at which these compounds induced TFT resistance correlated well with the potential of the nucleoside analogs to induce differentiation in C3H10T1/2 cells as determined by Constantinides et al. (Nature, 267, 364-366, 1977). In L5178Y mouse lymphoma (MOLY) cells, 5-aza-CR induced TFT resistance and produced both small and large colonies. Previous studies using mammalian cells showed the absence of mutagenic activity with 5-aza-CR and some of its analogs at the ATPase and hgprt loci. However, the different spectrum of DNA lesions detected at the tk locus may be responsible for the response of MOLY cells to 5-aza-CR.

Visual fixation and postural sway in children.

Adults are able to use a visual target to reduce quiet-standing postural sway (Lee & Lishman, 1975). The present study was designed to determine whether children, under varying postural conditions, are also able to use a visual target to reduce postural sway. A second purpose was to determine the ability of children to visually fixate under different postural conditions. An inability to visually fixate may limit the usefulness of a visual target. The results indicate that, like adults, children are able to reduce sway in the presence of a visual target. Young children are less able than older children and adults to visually fixate. In addition, children show more spontaneous visual saccades in the no-target condition than in the target condition and more saccades in the Romberg stance than in a feet-together stance. The fact that saccades decrease with increasing age, even in the seated, head-stabilized condition, precludes the possibility that increased instability of the young children is the only cause of increased number of saccades.

Studies of an S9-based metabolic activation system used in the mouse lymphoma L5178Y cell mutation assay.

The purpose of this work was to define, in this laboratory, the conditions of most general utility for the metabolic activation of chemicals to mutagens in the mouse lymphoma L5178Y cell tk+tk- ----tk-tk- assay. The approach used was to optimize the generation of non-toxic concentrations of NADPH from NADP glucose-6-phosphate (G6P) and G6P dehydrogenase, then use that system to examine the effects of increasing concentrations of Aroclor-1254-induced Fischer 344 male rat liver post-mitochondrial supernatant fluid (S9) upon the mutagenicity of chemicals. The promutagens were 2-acetylaminofluorene, cyclophosphamide, dimethylnitrosamine, methanol, 3-methylcholanthrene and procarbazine. It was determined that: (i) cell population growth was reduced at NADPH concentrations of greater than or equal to 1 mM; (ii) to ensure a maximum conversion of NADP to NADPH the G6P/NADP ratio should be two or greater; (iii) excess G6P (2.5 mM) is not harmful to the cells; (iv) toxicity due to S9 was observed at 12.5 mg whole liver equivalents (WLE)/ml (i.e. 50 microliters of a 25% liver S9 preparation per ml); (v) concentrations of S9 between 2.5 and 7.5 mg WLE/ml appeared to be adequate for the activation of the six promutagens to demonstrably mutagenic products.

Responses of the L5178Y tk+/tk- mouse lymphoma cell forward mutation assay: III. 72 coded chemicals.

Seventy-two chemicals were tested for their mutagenic potential in the L5178Y tk+/- mouse lymphoma cell forward mutation assay, using procedures based upon those described by Clive and Spector (Mutat Res 44:269-278, 1975) and Clive et al. (Mutat Res 59:61-108, 1979). Cultures were exposed to the chemicals for 4 hr, then cultured for 2 days before plating in soft agar with or without trifluorothymidine (TFT), 3 micrograms/ml. The chemicals were tested at least twice. Significant responses were obtained with allyl isothiocyanate, p-benzoquinone dioxime, benzyl acetate, 2-biphenylamine HCl, bis(2-chloro-1-methylethyl)ether, cadmium chloride, chlordane, chlorobenzene, chlorobenzilate, 2-chloroethanol, chlorothalonil, cytarabine.HCl, p,p'-DDE, diazinon, 2,6-dichloro-p-phenylenediamine, N,N-diethylthiourea, diglycidylresorcinol ether, 2,4-dimethoxy aniline.HCl, disperse yellow 3, endosulfan, 1,2-epoxyhexadecane, ethyl acrylate, ethyl benzene, ethylene thiourea, F D and C yellow Number 6, furan, heptachlor, isophorone, mercuric chloride, 4,4'-methylenedianiline.2 HCl, methyl viologen, nickel sulfate.6H2O, 4,4'-oxydianiline, pentachloroethane, piperonyl butoxide, propyl gallate, quinoline, rotenone, 2,4,5,6-tetrachloro-4-nitro-anisole, 1,1,1,2-tetrachloroethane, trichlorfon, 2,4,6-trichlorophenol, 2,4,5-trimethoxybenzaldehyde, 1,1,3-trimethyl-2-thiourea, 1-vinyl-3-cyclopetene dioxide, vinyl toluene, and ziram. Apart from 2-biphenylamine.HCl, 2-chloroethanol, disperse yellow 3, ethylene thiourea, FD and C yellow number 6, phenol, and 1,1,2-tetrachloroethane, rat liver S9 mix was not a requirement for these compounds. Chemicals not identified as mutagens were acid red, 11-aminoudecanoic acid, boric acid, 5-chloro-o-toluidine, coumaphos, cyclohexanone, decabromodiphenyl oxide, di(2-ethylhexyl)adipate, ferric chloride, fluometuron, melamine, monuron, phenesterin, phthalimide, reserpine, sodium dodecyl sulfate, 4,4-sulfonyldianiline, tetrachloroethylene, and zearalenone. The assay was incapable of providing a clear indication of whether some chemicals were mutagens; these were benzyl alcohol, 1,4-dichlorobenzene, phenol, succinic acid-2,2-dimethyl hydrazide, and toluene.

Reactivity of catecholamines and related substances in the mouse lymphoma L5178Y cell assay for mutagens.

Using the L5178Y mouse lymphoma cell thymidine kinase locus and the Salmonella his locus assays, the mutagenic potentials of several catecholamines and related compounds were examined. No supplementary metabolic activation systems were used. In the mouse lymphoma assay, the dihydroxybenzenes catechol and hydroquinone had similar and appreciable mutagenic potentials, whereas resorcinol was less active. Derivatives of catechol, such as dopamine and epinephrine, were mutagenic, whereas the related monohydroxylated compounds tyramine and synephrine were inactive. The primary amine, arterenol, and the corresponding secondary amine, epinephrine, induced similar mutagenic responses. Carboxylation of the side chain of dopamine, giving L-dopa, reduced the maximum mutagenic response. The introduction of charged groups directly on to the aromatic ring also reduced mutagenic activity, while an intervening methylene reversed this effect. Thus, 3,4-dihydroxyhydrocinnamic acid was more active than 3,4-dihydroxybenzoic acid. The compound active at the lowest doses was 4-tert-butyl catechol. The activities of these compounds are highly dependent upon substituent groups. Experiments with superoxide dismutase gave circumstantial evidence for some of the mutagenic activity being due to superoxide anion. Active oxygen species might be responsible for some of the observed effects, but this cannot be concluded from the superoxide dismutase experiments. Mutagenic responses in Salmonella were very low but were significant for L-dopa in three strains and for epinephrine and arterenol in one strain. Limited DNA association studies of 14C-dopamine suggest interactions in L5178Y and Salmonella cells and in mouse liver. The mutagenicity of dopamine in L5178Y is reduced by high serum concentrations during the exposure period, while the apparent association with DNA is unaffected.

Maturation of postural sway in young children.

The postural sway of 76 healthy young children aged from two to 14 years was investigated to identify age-related changes in the extent of sway, the effects of eye-closure, and the spectral composition of sway. Postural sway was measured from the excursions of the centre of pressure of ground reaction forces, and was analysed for both time and frequency. Within the age-range of the children tested, postural sway decreased linearly with age. Boys tended to become more stable at a faster rate than girls, but started from an initially greater level of instability. The children's Romberg quotients, which provide an index of the influence of eye-closure on sway magnitude, were remarkably low in comparison with adult values. Power spectral analysis of the postural sway showed that the principal energy was contained below 0.7 Hz for both lateral and antero-posterior sway, but that very young children had some power in the 0.8 to 2.0 Hz range. Taken together, these results confirm and extend the previously established view that children use visual information to control balance in a manner different from that of adults, and that it is not until after the age of seven years that adult-like balance-control strategies begin to appear. Also, in contrast to adults, the appearance of sway at high frequencies in children is not necessarily associated with any pathology.

Mutagenic activity of fluorides in mouse lymphoma cells.

The L5178Y mouse lymphoma cell forward-mutation assay was used to test for the mutagenic activity of sodium and potassium fluoride at the thymidine kinase locus. Mutants were detected by colony formation in soft agar in the presence of trifluorothymidine. Mutagenic and toxic responses were observed in the concentration range of 300-600 micrograms/ml with both sodium and potassium fluoride. Approximately 3-fold increases in mutant frequency were observed for concentrations in the 500-700 micrograms/ml range that reduced the relative total growth to approximately 10% in the absence or presence of a rat-liver S9 activation system. A sample of 30% sodium fluoride-70% sodium bifluoride (NaHF2) induced a similar mutagenic response but was more toxic with respect to the fluoride concentration. A specificity for fluoride ions in causing mutagenesis was indicated by the fast that much higher concentrations of sodium or potassium chloride were necessary to cause toxicity and increases in the mutant frequency. The possible involvement of chromosomal changes was signaled by the predominant increase in the small colony class of mutants.

An electromyographic study of weight-bearing at the elbow joint.

The purpose of this study was to investigate the roles of specific muscles in supporting the elbow joint in full extension during a static weighted situation. Various forearm positions from pronation through supination were used to determine carrying efficiency by monitoring muscle activity. Fine-wire electrodes were inserted into the biceps brachii, brachialis, brachioradialis, and medial head of the triceps in order to record the action potentials of these muscles. The forearm was studied in four different positions: (1) prone, (2) relaxed or natural, (3) semiprone, and (4) supine. These positions were monitored by an elgon potentiometer. The loads for the subjects were from 2-20 kilograms. Reliability coefficients of repeated trials were significantly positive. It was concluded that the muscles played an important role in supporting the elbow in full extension during a detracting force and that there was no significant difference between the muscular activity of males and females. Of the four positions studied, the supine position required the most activity suggesting an inefficient carrying position. The triceps was significantly more active when the arm was in the prone position. The roles of muscle groups in supporting the fully extended elbow joint during a detracting force changed as the forearm moved between supination and pronation. The elbow flexors were most active in the supine position, while the elbow extensor muscle was most active in the prone position.

Genotoxic activity in microorganisms of tetryl, 1,3-dinitrobenzene and 1,3,5-trinitrobenzene.

N-Methyl-N,2,4,6-tetranitroaniline (tetryl), 1,3-dinitrobenzene, and 1,3,5-trinitrobenzene were subjected to DNA repair assays using the Escherichia coli W3110/polA+, p3478/polA- system, reverse mutation assays with His-Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98, and TA100, and mitotic recombinogenic tests with the yeast Saccharomyces cerevisiae D5. Tests were carried out in the absence of an exogenous activation system and in tissue homogenate-mediated assays using Aroclor 1254-induced, male rat-liver-derived S9 mix. Mutagenic activity of tetryl was demonstrated with S typhimurium strains TA1537, TA1538, TA98, and TA100. The responses were particularly strong in the absence of S9 mix. Tetryl also induced increases in recombinant numbers and frequencies in the S cerevisiae test without the S9 mix, but not in its presence. 1,3-Dinitrobenzene was demonstrated to be mutagen with S typhimurium strains TA1538, TA98, and TA100. Slight activity was also seen with TA1537. The S9 mix reduced the magnitude of the responses. 1,3,5-Trinitrobenzene was also demonstrated to be mutagenic with S typhimurium strains TA1535, TA1537, TA1538, TA98, and TA100. Again, the S9 mix reduced the magnitude of the responses. In this segment of a programme initiated by military authorities, the genotoxic potential of three nitroaromatic compounds, which have found significant use in explosive preparations, has been demonstrated. Twelve other compounds used in ordnance were not active in any of the test systems. These were octahydro-1-acetyl-3,5,7-trinitro-S-tetramine (SEX), hexahydro-1,3-dinitro-5-acetyl-S-triamine (TAX), ethyl centralite, 2-nitrodiphenylamine, N-nitrosodiphenylamine, diphenylamine, diethyleneglycoldinitrate, nitroguanidine, lead salicylate, lead resorcylate, red phosphorus, and zinc chloride.