7 carcinogens added to the list

Seven new substances have been added to the U.S. Department of Health and Human Services’ list of cancer-causing agents.

Six of these substances are listed as “known” to cause cancer, while one is “reasonably anticipated to be a human carcinogen,” according to a statement today (Nov. 3) from the National Institutes of Health (NIH).

Five of the new substances on the list are viruses, and all of those are among the “known carcinogens,” the NIH says. The viruses include human T-cell lymphotropic virus type 1, Epstein-Barr virus, Kaposi sarcoma-associated herpesvirus, Merkel cell polyomavirus and human immunodeficiency virus type 1 (HIV-1). [10 Do’s and Don’ts to Reduce Your Risk of Cancer]

Together, the viruses have been linked to more than 20 different types of cancer, according to the NIH. For example, HIV-1, which is the virus that causes acquired immune deficiency syndrome, or AIDS, weakens the immune system and increases a person’s risk of infection from other cancer-causing viruses, the NIH says. There is “sufficient evidence” that HIV-1 can lead to cervical cancer, conjunctival eye cancer and non-melanoma skin cancer, among others, according to the NIH.

“Approximately 12 percent of human cancers worldwide may be attributed to viruses,” Linda Birnbaum, the director of the National Institute of Environmental Health Sciences and the National Toxicology Program, said in the statement. However, there are currently no vaccines available for the five viruses that have been added to list, Birnbaum said. Because of this, prevention strategies to avoid these viruses are “even more critical,” she said.

A chemical called trichloroethylene was also added to the list as a “known carcinogen,” according to the NIH. Trichloroethylene is an industrial solvent used to make hydrofluorocarbons, which are in a number of appliances and products. It’s also used by the military to degrease metal, the NIH says. Studies have shown a cause-and-effect link between the chemical and kidney cancer.

The other substance added to the list was the element cobalt. Cobalt is a naturally occurring metal, and can be found in rechargeable batteries and blue pigmented glass, tiles and ceramics, according to the NIH. It may also be used in some medical devices and solar panels.

Cobalt is “reasonably anticipated to be a human carcinogen,” the NIH says. This means that although studies have not shown a cause-and-effect link between cobalt and cancer in humans, the element has been shown to cause cancer in animals, and lab studies have demonstrated a possible mechanism for how this metal could cause cancer.

Cobalt is thought to be linked to cancer because it can release charged particles called ions in the body. These particles may damage a person’s DNA and lead to cancer, the NIH says.

Cobalt is also found in vitamin B12; however, this form of cobalt does not release ions and is therefore not considered to be linked to cancer, according to the NIH.

The NIH noted in the statement that inclusion in the report “does not by itself mean that a substance or a virus will cause cancer.” Many factors, including how susceptible a person is to the substance, how much of it they are exposed to and for how long also play a role, according to the statement.

The seven substances bring the total list of carcinogens on the list to 248, according to the NIH. This is the 14thtime the agency has issued its Report on Carcinogens.


MEDICATIONS TO AVOID that worse PD (Parkinson’s disease)

tramadol meds

Some medications can worsen movement symptoms of PD, including slowness, stiffness, tremor and dyskinesia. These drugs, listed below, are used to treat psychiatric problems such as hallucinations, confusion or gastrointestinal problems, such as nausea. The stress of your illness, hospital stay or new medicines can increase your risk of hallucinations while hospitalized. Common anti-hallucination medicines to be avoided are listed by generic or chemical name followed by the trade name.


Note: the anti-hallucination medicines Quetiapine (Seroquel) or Clozapine (Clozaril) can be used. The following should be avoided:

aripiprazole (Abilify), chlorpromazine (Thorazine), flufenazine (Prolixin), haloperidol (Haldol), molindone (Moban), perphenazine (Trilafon), perphenazine and amitriptyline (Triavil), risperidone (Risperdol), thioridazine (Mellaril), thiothixene (Navane)


metoclopramide (Reglan), phenothiazine (Compazine), promethazine (Phenergan)


Pain medicines – Meperidine (Demerol), Tramadol (Ultram),Antispasmodic medicine Flexeril , Dextromthorphan and St Johns Wort.

This is not a complete list of medicines to avoid. If you have questions about other medications, ask your pharmacist or doctor.

Any medication that blocks dopamine in the body can cause Parkinson’s symptoms.

By Louis Neipris, M.D., Staff Writer, myOptumHealth

You may have heard of Parkinson’s disease (PD), a movement disorder. Someone with it may have characteristic signs, such as a pill-rolling tremor in the fingers or a hunched forward posture. You may recognize someone with this disease from the faltering, tiny steps they take when they walk or by their rigidly emotionless face.

The cause of Parkinson’s disease is mostly unknown. Some people develop Parkinson’s-like symptoms after treatment with certain medications. This is called drug-induced parkinsonism (DIP) or secondary parkinsonism. Certain medications can also worsen symptoms in someone who already has Parkinson’s disease.

Any medication that blocks dopamine in the body can cause Parkinson’s symptoms. Dopamine is a brain chemical that helps control movement. Common dopamine-blocking drugs are antipsychotics. They are used to treat certain mental illnesses or severe nausea. Less commonly, certain types of calcium channel blockers cause drug-induced parkinsonism. These drugs may be used to treat chest pain and high blood pressure, or irregular heart rate.

Other types of medications that may cause drug-induced parkinsonism are:

* Some antidepressants
* Certain anti-nausea drugs
* Some drugs used to treat vertigo
* Certain drugs used to treat epilepsy
* Some anti-arrhythmics (used to treat irregular heart rhythm)

Not all drugs in these classes will cause symptoms of parkinsonism.

What’s the difference?

Drug-induced parkinsonism usually develops on both sides of the body, while typical Parkinson’s disease does not. Also, drug-induced parkinsonism usually does not progress like typical Parkinson’s.

Unlike Parkinson’s, drug-induced symptoms usually go away after the drug is stopped. It may take several months, though, for the symptoms to completely stop. If the symptoms remain, then it is possible that the drug may have “unmasked” underlying Parkinson’s disease.

Who is at risk?

  • Female: Women are twice as much at risk as men.
  • Elderly: Older people are more likely to be on multiple medications or to have underlying Parkinson’s disease.
  • Those with a family history of Parkinson’s disease.
  • People with AIDS.

What to do to prevent drug-induced parkinsonism?

The most common drugs linked to this condition are two used to treat schizophrenia or psychotic symptoms of dementia. They are haloperidol (Haldol) and perphenazine (Trilafon). Ask your doctor about parkinsonism if you or a loved one is concerned about a drug, especially these two drugs.

In general:

* Make sure you or a loved one are on the lowest effective dose.
* If you already have Parkinson’s disease, then tell your doctor if the symptoms appear to be getting worse since starting the drug.
* Never stop taking a drug on your own. Talk to your doctor about any concerns.


* Parkinson’s Disease Society. Drug-induced parkinsonism.
* Albin RL. Parkinson’s disease: background, diagnosis, and initial management. Clinics in Geriatric Medicine. 2006;22(4):735-751.
* Alvarez MV, Evidente VG. Understanding drug-induced parkinsonism Separating pearls from oysters. Neurology. 2008;70(8):e32-e34.



Connie’s notes: Neuro meds common side effects include dizziness,nausea,headache,vomitting and sleep disorders

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Antipsychotic drugs, called neuroleptics

Drug-induced parkinsonism is due primarily to drugs that block dopamine receptors, particularly the D2 receptors (Shin and Chung 2012). These drugs are most often the antipsychotic drugs, called neuroleptics, such as haloperidol, chlorpromazine, and trifluoperazine, but include metoclopramide, a gastrointestinal motility enhancer, and the antiemetics prochlorperazine and droperidol. In addition, medications that block synthesis of dopamine, such as alpha-methyl para-tyrosine and alpha-methyl dopa or deplete dopamine (such as tetrabenazine and reserpine, which block dopamine’s entry into the vesicles that are released into the synapse) also induce parkinsonism. In these cases the pathophysiology is presumably due to diminished dopamine receptor stimulation, resulting in a pharmacologic state closely resembling Parkinson disease.

However, the atypical antipsychotics also block D2 receptors. Yet there is no apparent correlation between the degree of this blockade and the risk for inducing parkinsonism. The explanation for this is uncertain. One current hypothesis is the “fast off” theory, postulating that the duration of the D2 blockade, rather than the percentage of receptors blocked, determines the likelihood of parkinsonism (Seeman 2002). A competing theory is that the ratio of 5 HT-2a receptor blockade versus the dopamine D2 receptor blockade is critical because of the interplay between the serotonin and dopamine systems in the brain. An older theory relating extrapyramidal side effects to anticholinergic activity is considered untenable because the concomitant use of anticholinergics does not eliminate the problem.

Cholinesterase inhibitors, widely used to treat dementia

Cholinesterase inhibitors, widely used to treat dementia, may cause worsened parkinsonism, primarily increased tremor (Anonymous 2007). Large double-blind trials of rivastigmine, a cholinesterase-inhibiting drug, in both dementia with Lewy bodies and Parkinson disease dementia have demonstrated that rivastigmine is well tolerated without significant worsening of motor function overall, although tremor may increase (Emre et al 2004). The other cholinesterase inhibitors have been less well studied but appear to have similar benefits and side effects.

Serotonin reuptake blocking antidepressants fluoxetine, sertraline, and paroxetine

Several other medications have been reported to cause drug-induced parkinsonism and to worsen parkinsonism in people with Parkinson disease, including the serotonin reuptake blocking antidepressants fluoxetine, sertraline, and paroxetine. Two calcium channel blockers available in Europe and South America (flunarizine and cinnarizine), which are piperazine derivatives, are thought to cause drug-induced parkinsonism by blocking dopamine receptors. Reports of parkinsonism induced by other drugs, such as lithium and amiodarone, are so rare that only after parkinsonism has developed should the possible drug effect be taken into account. Because lithium is not known to block dopamine receptors, another mechanism is likely. Some animal data implicate an effect of lithium on intercellular signalling via G-protein coupled receptors (Beaulieu et al 2008). One antidepressant, amoxapine, has dopamine receptor-blocking properties and, therefore, may induce parkinsonism. Parkinsonism as a transient (lasting days to weeks) side effect of alcohol withdrawal has been reported without later development of Parkinson disease, but it is unknown how common this is (Shandling et al 1992).

Valproic acid

Valproic acid has been reported to induce parkinsonism in the majority of patients whose serum levels are over 40 (Armon et al 1996). Although subsequent reports support the association between valproate and parkinsonism, the frequency appears to be uncommon in some reports (Hauben and Reich 2005; Masmoudi et al 2006) but affecting about 5% in others (Jamora et al 2007; Zadikoff et al 2007). The mean dose of patients with valproate-induced parkinsonism was 750 mg/day, and the syndrome was 5 times more common with valproic acid than the other anticonvulsants.

Tetrabenazine, approved for treatment of chorea in people with Huntington disease, is also widely used to treat tardive dyskinesia. Oftentimes, especially in elderly with tardive dyskinesia, one must choose between reduced dyskinesia or increased parkinsonism.

UFPs from 3D printers harmful to health, causing cardio-respiratory mortality

A new study by researchers at the Illinois Institute of Technology shows that commercially available desktop 3D printers can have substantial emissions of potentially harmful nano-sized particles in indoor air. The study, which was recently published in the journal Atmospheric Environment, is the first to measure airborne particle emissions from commercially available desktop 3D printers. Desktop 3D printers are now widely accessible for rapid prototyping and small-scale manufacturing in home and office settings. Many desktop 3D printers rely on a process where a thermoplastic feedstock is heated, extruded through a small nozzle, and deposited onto a surface to build 3D objects. Similar processes have been shown to have significant aerosol emissions in other studies using a range of plastic feedstocks, but mostly in industrial environments.

In this work, assistant professor Brent Stephens and graduate students in his Built Environment Research Group in the Department of Civil, Architectural and Environmental Engineering at Illinois Institute of Technology in Chicago, IL measured ultrafine particle concentrations resulting from the operation of a single type of popular commercially available desktop 3D printers inside an office space. Ultrafine particles (or UFPs) are small, nano-sized particles less than 100 nanometers in diameter. The printers were used to print small plastic figures during normal operation. The resulting concentration measurements were then used to estimate UFP emission rates from these printers.
Estimates of emission rates of total UFPs were high, ranging from about 20 billion particles per minute for a 3D printer utilizing a lower temperature polylactic acid (PLA) feedstock to about 200 billion particles per minute for the same type of 3D printer utilizing a higher temperature acrylonitrile butadiene styrene (ABS) feedstock.

The emission rates were similar to those measured in previous studies of several other devices and indoor activities, including cooking on a gas or electric stove, burning scented candles, operating laser printers, or even burning a cigarette.
Human inhalation of UFPs may be important from a health perspective. UFPs deposit efficiently in both the pulmonary and alveolar regions of the lung, as well as in head airways. Deposition in head airways can also lead to translocation to the brain via the olfactory nerve. The high surface areas associated with UFPs also lead to high concentrations of other adsorbed or condensed compounds. Several recent epidemiological studies have also shown that elevated UFP number concentrations are associated with adverse health effects, including total and cardio-respiratory mortality, hospital admissions for stroke, and asthma symptoms.

In addition to large differences in emission rates observed between PLA- and ABS-based 3D printers, there may also be differences in toxicity because of differences in chemical composition of the feed-stocks and UFP byproducts. Thermal decomposition products from ABS processing have been shown to have toxic effects in mice and rats in previous studies; however, PLA is actually known for its biocompatibility in humans. PLA nanoparticles are even widely used in drug delivery.

Because most of these devices are currently sold as standalone devices without any exhaust ventilation or filtration accessories, the researchers suggest caution should be used when operating in inadequately ventilated or unfiltered indoor environments. They also recommend that more controlled experiments be conducted to more fundamentally evaluate particle emissions from a wider range of desktop 3D printers.


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