88 research outputs found

    Correction: Distributions of Autocorrelated First-Order Kinetic Outcomes: Illness Severity

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    [This corrects the article DOI: 10.1371/journal.pone.0129042.]

    Pollution prevention technologies: A review and classification

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    Waste minimization practices, reported in the literature for major industries using or generating hazardous materials, were reviewed. Technologies are summarized briefly in this paper. The information was reorganized according to the function served by the material industrially, and the gene- ral chemical nature of the material. Ten basic functions were identified, as binding, pigmentation, reactants, reaction inhibition, catalysis, bleaching, mass deposition, mass removal, by-products, and end-products. The resulting perspective of this review is general with respect to industry, and with respect to waste phase, and considers productivity benefits along with prevention of risks associated with pollution. Simi- larities in waste reduction opportunities are evident between processes where hazardous materials perform similar functions, suggesting general approaches to industrial hazardous waste reduction

    Correction: Distributions of Autocorrelated First-Order Kinetic Outcomes: Illness Severity.

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    [This corrects the article DOI: 10.1371/journal.pone.0129042.]

    Estimating uncertain benefits and costs of pollution prevention

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    Distributions of Autocorrelated First-Order Kinetic Outcomes: Illness Severity

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    <div><p>Many complex systems produce outcomes having recurring, power law-like distributions over wide ranges. However, the form necessarily breaks down at extremes, whereas the Weibull distribution has been demonstrated over the full observed range. Here the Weibull distribution is derived as the asymptotic distribution of generalized first-order kinetic processes, with convergence driven by autocorrelation, and entropy maximization subject to finite positive mean, of the incremental compounding rates. Process increments represent multiplicative causes. In particular, illness severities are modeled as such, occurring in proportion to products of, e.g., chronic toxicant fractions passed by organs along a pathway, or rates of interacting oncogenic mutations. The Weibull form is also argued theoretically and by simulation to be robust to the onset of saturation kinetics. The Weibull exponential parameter is shown to indicate the number and widths of the first-order compounding increments, the extent of rate autocorrelation, and the degree to which process increments are distributed exponential. In contrast with the Gaussian result in linear independent systems, the form is driven not by independence and multiplicity of process increments, but by increment autocorrelation and entropy. In some physical systems the form may be attracting, due to multiplicative evolution of outcome magnitudes towards extreme values potentially much larger and smaller than control mechanisms can contain. The Weibull distribution is demonstrated in preference to the lognormal and Pareto I for illness severities versus (a) toxicokinetic models, (b) biologically-based network models, (c) scholastic and psychological test score data for children with prenatal mercury exposure, and (d) time-to-tumor data of the ED<sub>01</sub> study.</p></div

    Simulated (o) and fitted Weibull (––) and lognormal (—) distributions of illness severity.

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    <p>Severities were simulated as (a) the results of the multiplicative model of illness severities of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0129042#pone.0129042.e029" target="_blank">Eq 12</a>, and (b) the results of the simplified multiplicative model of illness severities of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0129042#pone.0129042.e030" target="_blank">Eq 13</a>. [Conditions: all fractions, <i>f</i><sub><i>X</i></sub>, distributed standard exponential, <i>N</i> = 100,000; subsequent fractions correlated by copula; MLE parameter fits]</p

    Definition diagram for a generalized, physiologically-based, first-order model of a liver-mediated toxicological pathway, including a terminal series of three generalized pharmacodynamic steps.

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    <p>Definition diagram for a generalized, physiologically-based, first-order model of a liver-mediated toxicological pathway, including a terminal series of three generalized pharmacodynamic steps.</p
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