Profile of Patients with Chemical Injury & Sensitivity

Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardised questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychological origin of chemical sensitivity.

Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research.

Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals).

Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitisation (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation

Please read full report below.

Grace Ziem – Occupational and Environmental Medicine, Baltimore, Maryland, USA. James McTamney – Clinical Psychologist, Lutherville, Maryland, USA

2 thoughts on “Profile of Patients with Chemical Injury & Sensitivity”

  1. Grace Ziem’s research has been systematically supressed. In a personal correspondence with Professor Steven Rochlitz, a kinesiologist, I learned that Grace Ziem was threatened and she never published a word about porphyrin metabolism, haem/ US heme or porphyria, acquired porphyria, porphyrinopathies etc. Rochlitz is the author of “Porphyria, the Ultimate cause of chronic and environmental illnesses”.
    The porphyria research is hidden in the free radical research. Nitric oxide becomes a free radical, leading to formation of peroxinitrite – but nitric oxide synthase, the enzyme that produces nitric oxide is a haem enzyme. Lack of haem or too high levels of free haem wreak havoc in the metabolism.

    One other blood disease, deficiency in glucose-6- phosphate dehydrogenase, has been mainly overlooked in research into chemical sensitivity. G6PD is an enzyme that is necessary of the synthesis of the antioxidant glutathione and also for NADPH, that is essential for proper functioning of mitochondria, the energy centres of cells.
    The Irish have higher rates of porphyria than other European nations.
    Already the Scythians had high rates of porphyria. They are a race the Celts are either descended from or at least freely intermingled with.
    G6PD deficiency – in actual fact, the most frequent enzyme deficiency in mankind – is found more frequently in areas with malaria e.g. the Mediterranean and Africa. The highest rate have the Kurds.
    Great Britain, as well as huge parts of Germany, Austria and France, was part of the Roman Empire.
    Sweden, Norway and Finland have the highest rate of porphyria in the world. Vikings genes added to the gene pool, the Normans invasion brought more porphyria. The Normans were Scandinavians who settled in Normandy, northern France.

    A quick search ” trichloroethylene, heme, porphyrin” gave this result:

    The enzyme δ -aminolevulinic acid dehydratase (ALAD), which catalyzes
    the second step of heme synthesis, can be inhibited by several
    chemicals, including lead, a potential risk factor for brain tumors,
    particularly meningioma.

    Although ALAD can be inhibited by a variety of chemicals, including
    lead, trichloroethylene, bromobenzene, and styrene (Fujita et al.
    2002), polymorphic differences in enzyme binding or chemical uptake
    have been examined most extensively for lead

    Tohoku J Exp Med. 2002 Feb;196(2):53-64.
    Lead, chemical porphyria, and heme as a biological mediator.
    Fujita H1, Nishitani C, Ogawa K.
    Author information
    Laboratory of Environmental Biology, Hokkaido University School of
    Medicine, Sapporo 060-8638, Japan.
    One of the most well-characterized symptoms of lead poisoning is
    porphyria. The biochemical signs of lead intoxication related to
    porphyria are delta-aminolevulinic aciduria, coproporphyrinuria, and
    accumulation of free and zinc protoporphyrin in erythrocytes. From the
    1970s to the early 80s, almost all of the enzymes in the heme pathway
    had been purified and characterized, and it was demonstrated that
    delta-aminolevulinic aciduria is due to inhibition of
    delta-aminolevulinate dehydratase by lead. Lead also inhibits purified
    ferrochelatase; however, the magnitude of inhibition was essentially
    nil even under pathological conditions. Further study proved the
    disturbance of iron-reducing activity by moderate lead exposure. Far
    different from these two enzymes, lead failed to inhibit purified
    coproporphyrinogen oxidase, i.e., the mechanism of coproporphyrinuria
    has not yet been understood. During the 80s to the 90s, the effects of
    environmental hazards including lead were elucidated through stress
    proteins, indicating the induction of some heme pathway enzymes as
    stress proteins. At that time, gene environment interaction was
    another focus of toxicology, since gene carriers of porphyrias are
    considered to be a high-risk group to chemical pollutants.
    Toxicological studies from the 70s to the 90s focused on the direct
    effect of hazards on biological molecules, such as the heme pathway
    enzymes, and many environmental pollutants were proved to affect
    cytosolic heme. Recently, we demonstrated the mechanism of the
    heme-controlled transcription system, which suggests that the indirect
    effects of environmental hazards are also important for elucidating
    toxicity, i.e., the hazards can affect cell functions through such
    biological mediators as regulatory heme. It is, therefore, probable
    that toxicology in the future will focus on biological systems such as
    gene regulation and signal transduction systems.
    PMID: 12498316
    [Indexed for MEDLINE]
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