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  1. Workers now need concise very solid written guaranteed paperwork signed by a qualified industrial toxicologist to be given to each separate worker inside each location, specifying the safe duration and time that is is safe to continue to undergo work during the number of days, to months, that it is always safe, and to keep as evidence should any of the workers find they suffer any health effects after any elapsed time after this contract work time as you show here that the claim made by Skycity that it was safe was found to be untrue.

    Quote; “Despite claims by SkyCity that Worksafe “approved” their re-opening it’s clear that was untrue. A Worksafe staff member was asked to attend a briefing at SkyCity and no independent inspection, investigation, clearance or monitoring of any type was undertaken by them.”Workers need solid paperwork given to each worker that is is safe to work after this was found to be untrue.

    I wrote in the earlier discussion last week as the first discussion arose about workers exposure in this Skytower so let me refer again;

    As I was chemically damaged inside the construction of the Toronto building dubbed as a “sick building” that is called “the CBC Broadcast Centre” in 1992.

    That was similar workplace environment without adequate clean air provided became very sick along with 40 other workers then and are still permanently chronically ill, even today by the medical profession diagnosed 27yrs later, so paperwork is vital to workers proving their case of permanent injury in the workplace.

    Anyone worried about storing toxins in their bodies now should request now for a GCMS analysis -diagnosis of their fat (adipose) issues to find how much buildup of toxins are being stored inside their bodies, and it is a simple test by a painless extraction of a small sample of tissue, as this is now the gold standard abroad for water and food testing for chemical toxicity exposure to the human body of exposed workers and consumers of food and water.
    This first site was a solid case proven of a UK worker exposed to ‘toxic poisons from rat poison’ using GCMS analysis.
    https://people.ok.ubc.ca/robrien/BromethalinPoisoning.pdf

    Melissa A. Pasquale-Styles,1 M.D.; Mark A. Sochaski,2 Ph.D.; David C. Dorman,2 D.V.M., Ph.D.;
    Willane S. Krell,3 M.D.; Aashit K. Shah,4 M.D.; and Carl J. Schmidt,5 M.D.
    Fatal Bromethalin Poisoning
    ABSTRACT: Bromethalin is a neurotoxin found in some rodenticides. A delusional 21-year-old male presented to a hospital with altered mental status the day after ingesting a bromethalin-based rodenticide. He died 7 days after his self-reported exposure to c. 17 mg bromethalin (equivalent
    to 0.33 mg bromethalin/kg). His clinicopathologic course was characterized by altered mental status, obtundation, increased cerebrospinal fluid pressure, cerebral edema, death, and diffuse histologic vacuolization of the white matter in the central nervous system seen on microscopic
    examination at autopsy. The presence of a demethylated form of bromethalin in the patient’s liver and brain was confirmed by gas chromatography with mass spectrometry.

    Clinical signs and lesions observed in this patient are similar to those seen in animals poisoned with bromethalin. This case illustrates the potential for bromethalin ingestion to result in fatal human poisoning.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773935/

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834485/

    https://www.agilent.com/en/solutions/food-testing-agriculture/pesticides/gc-ms-pesticide-analysis

    https://caltestlabs.com/analytical-services/pyrethroids-fipronil-and-other-pesticides/

  2. In any smoke emitted from fires are containing toxic; quote; (POP’s) “persistent organic pollutants”- chemicals claim this study from; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569688/

    So inhalation of those “smoke particles” that contain (POP’s) are dangerous to human health.

    Firefighters the world around have suffered from inhalation of smoke from fires and are already dying from inhalation so workers inside a smoky smelling building will also be exposed until the buildings are rid of the coating that has stained the whole inside/outside of any building close to the fire.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569688/ GCMS analysis of toxins in human adipose tissue for toxins.
    • Environ Health Perspect
    • v.121(2); 2013 Feb
    • PMC3569688

    Environ Health Perspect. 2013 Feb; 121(2): 162–169.
    Published online 2012 Dec 5. doi: 10.1289/ehp.1205485
    PMCID: PMC3569688
    PMID: 23221922
    Review
    Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
    Michele La Merrill,1 Claude Emond,2,3 Min Ji Kim,4,5,6,7 Jean-Philippe Antignac,8 Bruno Le Bizec,8 Karine Clément,9,10,11,12 Linda S. Birnbaum,13,14 and Robert Barouki 4,5,6
    Author information Article notes Copyright and License information Disclaimer
    This article has been cited by other articles in PMC.
    Go to:
    Abstract
    Background: Adipose tissue (AT) is involved in several physiological functions, including metabolic regulation, energy storage, and endocrine functions.
    Objectives: In this review we examined the evidence that an additional function of AT is to modulate persistent organic pollutant (POP) toxicity through several mechanisms.
    Methods: We reviewed the literature on the interaction of AT with POPs to provide a comprehensive model for this additional function of AT.
    Discussion: As a storage compartment for lipophilic POPs, AT plays a critical role in the toxicokinetics of a variety of drugs and pollutants, in particular, POPs. By sequestering POPs, AT can protect other organs and tissues from POPs overload. However, this protective function could prove to be a threat in the long run. The accumulation of lipophilic POPs will increase total body burden. These accumulated POPs are slowly released into the bloodstream, and more so during weight loss. Thus, AT constitutes a continual source of internal exposure to POPs. In addition to its buffering function, AT is also a target of POPs and may mediate part of their metabolic effects. This is particularly relevant because many POPs induce obesogenic effects that may lead to quantitative and qualitative alterations of AT. Some POPs also induce a proinflammatory state in AT, which may lead to detrimental metabolic effects.
    Conclusion: AT appears to play diverse functions both as a modulator and as a target of POPs toxicity.
    Keywords: adipose tissue, aryl hydrocarbon receptor, development, diabetes, dioxin, inflammation, obesity, obesogens, polychlorinated biphenyls, toxicity, toxicokinetics
    Obesity is increasing in developed countries and is a commonly known risk for disorders such as impaired glucose tolerance, metabolic syndrome, diabetes mellitus, liver and cardiovascular disease (CVD), and cancer (Ludescher et al. 2009). Adipose tissue (AT) has historically been considered a simple storage tissue; however, its physiological functions have been appreciably reassessed over the last decade (Lafontan 2012), and evidence for metabolic and endocrine functions of AT has accumulated. More is known about the histological architecture of AT and the role of AT stroma, including immune cells. The pathological contribution of AT to obesity and metabolic disorders such as type 2 diabetes is gaining more attention. Recently, various interactions between AT and persistent organic pollutants (POPs) have been reported, suggesting that this tissue plays a significant role in the kinetics and the toxicity of POPs (Kim et al. 2011, 2012).
    On the basis of these studies, we propose that AT, in addition to its other metabolic and endocrine functions, has diverse toxicological functions: a) AT can store a variety of hydrophobic xenobiotic chemicals, in particular POPs; b) AT constitutes a low-grade internal source of stored POPs leading to continuous exposure of other tissues; and c) AT can be a target for the effects of a xenobiotic chemical that alters AT functions, increases AT inflammation, and/or modulates the differentiation of AT precursor cells. For instance, obesogens are exogenous chemicals (from a nutritional, pharmaceutical, or environmental origin) that directly or indirectly increase obesity through disruption of metabolic, hormonal, or developmental processes (Grun and Blumberg 2007; Schug et al. 2011). Conversely, several POPs are known to induce cachexia, particularly at high doses. In this review, we discuss these issues and present evidence that supports a complex, previously unsuspected role of AT in toxicology.

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