Where do we stand on our fight against cancer causing substances?

 

We keep adding a list of these carcinogens or toxins each year. We have produced and manufactured foods in the factory in greater quantities and have to rely on so many chemicals.  Educating the public about the hazards of these carcinogens is very slow and tricky.  We have seen an increase in number of women with hysterectomies and breast/ovarian cancers. And we also have seen an increase in autism and Alzheimer’s disease.

We have to educate the public to:

  1. Wash vegtables and fruits (pesticide laden) with salt water or diluted vinegar.
  2. Stay away from toxic substances at home, preserved and packaged foods, materials in our foods, chemicals in our environment and other hidden toxins.
  3. Eat more fiber in the hopes that fiber can encapsulate the fat, sugar and toxins out of our bodies.
  4. Use organic, whole foods and less preserved food and more in its natural form.
  5. Live in a city that is not polluted and with well controlled hazardous substances to man and the environment.
  6. Stay at normal weight, reduce excess fat and excessive use of medications or drugs, even cosmetics and hair dyes.
  7. Walk our talk at home and in the community we live. Educate others.

Most toxic substances are substances that are persistent, bioaccumulative and toxic. These are substances that do not easily break down, instead they build up in nature and in the fatty tissue of mammals, with a potential to cause serious and long-term irreversible effects. The more fat we have in our body, the more our body is susceptible to storing carcinogens.  We hope that the recent research on the number of gene expressions related to cancer can shed light to how our body or personalized medicine can combat cancer.

 

Today, many women have hysterectomies and other form of reproductive cancer.  From the P65 list (created from 1987 to present, updated yearly), a total of 867 substances are listed as carcinogenic for reproductive and developmental health of growing embryo with 546 of these chemicals as specific contributor to cancer.  In 2011, there are 26 added carcinogens from the P65 list.

Source: STATE OF CALIFORNIA, ENVIRONMENTAL PROTECTION AGENCY, OFFICE OF ENVIRONMENTAL HEALTH HAZARD ASSESSMENT, SAFE DRINKING WATER AND TOXIC ENFORCEMENT ACT OF 1986, CHEMICALS KNOWN TO THE STATE TO CAUSE CANCER OR REPRODUCTIVE TOXICITY Mar 16, 2012 Update.

The following are a short list of carcinogens or toxins to man and the environment.

Obesity and Autism

Women who are obese and/or have diabetes or high blood pressure during pregnancy may be about 60% more likely to have babies with autism, a new study suggests. While the new research points to an association between mom’s health during pregnancy and autism, it’s important to note that “we can’t really draw causal links,” says researcher Paula Krakowiak. She is a PhD candidate in epidemiology at the University of California, Davis.

Styroform

A 1988 survey published by the Foundation for Advancements in Science and Education also found styrene in human fatty tissue with a frequency of 100% at levels from 8 to 350 nanograms/gram (ng/g). The 350 ng/g level is one third of levels known to cause neurotoxic symptoms.[5] determined that Styrofoam drinking leach Styrofoam into the liquids they contain. The cups apparently lose weight during the time they are at use. The studies showed that tea with lemon produced the most marked change in the weight of the foam cup

Source:

“Are Styrene Food and Beverage Containers A Health Hazard?,” Institute for Local Self-Reliance, Washington, DC, August 15, 1990.
Brian Lipsett, “Areas of Expertise Pertaining to McDonald’s Corp..”
K. Figge, “Migration of Additives from Plastic Films into Edible Oils and Fat Stimulants,” Food Cosmet Toxicol, December 10, 1972, Vol. 6, pages 815 828.
B.J. Dowty, J.L. Laseter, and J. Storet, “Ther Transplacental Migration and Accumulation in Blood of Volatile Organic Constituents,” Pediatric Research, Vol. 10, pages 696-701, 1976.
“Polystyrene Fact Sheet,” Foundation for Advancements in Science and Education, Los Angeles, California.

According to a Foundation for Achievements in Science and Education fact sheet, long term exposure to small quantities of styrene can cause neurotoxic (fatigue, nervousness, difficulty sleeping), hematological (low platelet and hemoglobin values), cytogenetic (chromosomal and lymphatic abnormalities), and carcinogenic effects.[1,2] In 1987, the International Agency for Research on Cancer, Lyon, France, reclassified styrene from a Groups 3 (not classifiable as to its carcinogenicity) to a Group 2B substance (possibly carcinogenic to humans).

Although there is evidence that styrene causes cancer in animals, it has not yet been proven to cause cancer in humans. Styrene primarily exhibits its toxicity to humans as a neurotoxin by attacking the central and peripheral nervous systems. The accumulation of these highly lipid-soluble (fat-soluble) materials in the lipid-rich tissues of the brain, spinal cord, and peripheral nerves is correlated with acute or chronic functional impairment of the nervous system.

For example, women exposed to low concentrations of styrene vapors in the workplace are known to have a variety of neurotoxic and menstrual problems. A Russian study of 110 women exposed to styrene vapors at levels about 5 mg/m3 demonstrated menstrual disorders, particularly perturbations of the menstrual cycle and a hypermenorrhea (unusually heavy flow of menses during the menstrual cycle) syndrome. Styrene- exposed women often suffered from metabolic disturbances occurring during pregnancy.

The root cause of the build up of the toxin, styerene, is not the answer to our problem but the protection of our bodies against the onslaught of these toxins is far more important. Can a strong immune system help? What about lifestyle changes?

Dioxins

Dioxins are a group of chemicals that form as unwanted byproducts from incomplete burning of household and industrial waste. They also can be produced during bleaching of paper pulp and the manufacture of certain chlorinated chemicals like polychlorinated biphenyls (PCBs), chlorinated phenols, chlorinated benzene and certain pesticides. Exhaust from vehicles, forest fires, and burning wood also releases dioxins into the air. Very small amounts of dioxins, that are not considered harmful, are present in bleached paper products including facial or toilet tissue, paper towels, and disposable diapers.

Dioxin exposure can cause a severe skin condition called chloracne, which results in small, pale yellow skin lesions that may last from weeks to years. Dioxins can cause short-term liver effects without any visible symptoms. Studies of people exposed to high levels of dioxins through occupation, accidents or military service do not suggest that adverse health affects will occur at low levels in the environment. A large historical study suggested workers exposed to dioxins for many years had increased cancer rates. However, other environmental factors may be related to the cancer. Studies have shown that reproductive, immune and nervous systems of the developing fetus and children are more susceptible to dioxins.

In animal studies, dioxins have caused nerve damage, birth defects, increased rates of miscarriages and changes to the immune system. Although the U.S. Environmental Protection Agency has classified dioxins as a probablehuman carcinogen (cancer causing chemical), there is not sufficient evidence to prove that dioxins cause cancer from exposure to the low levels normally found in the environment. One dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is listed as a known human carcinogen and all the others as probable human carcinogens.

Source:  Illinois Department of Public Health
Division of Environmental Health
525 W. Jefferson St.
Springfield, IL 62761
217-782-5830
TTY (hearing impaired use only) 800-547-0466

PCBs

In 1999, the draft Fox River clean-up proposal included a local cancer risk assessment for recreational anglers and subsistence anglers due primarily to consumption of fish containing PCBs. Using fish concentration data from 1990 on (and Walleye data from 1989 in Green Bay), the cancer risks were as high as 1.1 in a 100 for recreational anglers, and 1 in 67 for subsistence anglers. These risks are more than 1,000 times greater than the standard 1-in-a-million cancer risk level used by Wisconsin to regulate hazardous waste sites. These risks are 23 times higher than the cancer risks from fish-eating from Lake Winnebago, which the DNR considers a background level for PCBs (though it’s clear that Lake Winnebago fish are also contaminated.)

Reference: ThermoRetec. Feb. 1999. “Draft Feasibility Study, Lower Fox River, Wisconsin, Summary of Baseline Human Health and Ecological Risk Assessment.” Section 3.2.1.

Hazardous House Cleaners

In 1990, more than 4,000 toddlers under age four were admitted to hospital emergency rooms as a result of household cleaner-related injuries. That same year, 18,000 pesticide-related hospital emergency room admissions were reported with almost three-fourths for children age fourteen and under.

Methylene chloride, the propellant used in many aerosol products, is carcinogenic. Some products containing methylene chloride have been pulled from the market, but the carcinogen continues to be found in many consumer products such as spray paint and stripper.

 

 

Cosmetic Toxins

Not a single cosmetic company warns consumers of the presence of carcinogens in its products – despite the fact that a number of common cosmetic ingredients are carcinogenic or carcinogenic precursors.

Some experts estimate that 20 percent of non-Hodgkin’s lymphoma cases among women are attributable to their use of hair dyes.

Source: Cancer Prevention Coalition c/o School of Public Health, M/C 922
University of Illinois at Chicago 2121 West Taylor Street  Chicago, IL 60612
(312) 996-2297, Fax: (312) 413-9898 Email: epstein@uic.edu

Tobacco and tobacco smoke

Tobacco smoke is a major source of human exposure to polycyclic aromatichydrocarbons (PAHs). The concentration of PAHs in lung tissue would reflect an individual’s dose, and its variation could perhaps reflect cancer risk. Eleven PAHs were measured in 70 lung tissue samples from cancer-free autopsy donors by gas chromatography-mass spectrometry. There were 37 smokers and 33 nonsmokers as estimated by serum cotinine concentration. The sum of PAH concentrations was higher in smokers (P = 0.01), and there was a dose-response relationship for greater smoking (P < 0.01).

Smoking increased the concentration of five PAHs including benzo(a)pyrene, which increased ∼2-fold. The risk for increasing carcinogenic PAHs (odds ratio, 8.20; 95% confidence interval, 2.39–28.09) was 3-fold compared with noncarcinogenic PAHs (odds ratio, 2.61; 95% confidence interval, 0.75–9.12). A higher concentration of PAHs was detected in the lung tissue of males, although the estimated smoking was similar in males and females. Race was not associated with PAH concentrations overall, but PAH concentrations appeared to be higher in African-American males than in any other group. Age was weakly correlated with an increase in fluoranthene and pyrene. The measurement of PAHs in human lung tissue can be used to estimate the actual dose to the target organ.

Source:  Cancer Res September 1, 2001 61; 6367

References

IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Vol. 38. Appendix 2, pp. 389–394. Lyon, France: IARC, 1986.

Doll R., Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today.. J. Natl. Cancer Inst., 66: 1191-1308, 1981.

Conney A. H. Induction of microsomal enzymes by foreign chemicals and carcinogenesis by polycyclic aromatic hydrocarbons: G. H. A. Clowes Memorial Lecture. Cancer Res., 42: 4875-4917, 1982.

Greenblatt M. S., Bennett W. P., Hollstein M., Harris C. C. Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis.. Cancer Res., 54: 4855-4878, 1994.

Denissenko M. F., Pao A., Tang M., Pfeifer G. P. Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in p53.. Science (Wash. DC), 274: 430-432, 1996.

Dipple A. DNA adducts of chemical carcinogens.. Carcinogenesis (Lond.), 16: 437-441, 1995.

Hollstein M., Sidransky D., Vogelstein B., Harris C. C. p53 mutations in human cancers.. Science (Wash. DC), 253: 49-53, 1991.

Perera F. P., Hemminki K., Gryzbowska E., Motkiewicz G., Michalska J., Santella R. M., Young T. L., Dickey C., Brandt-Rauf P., DeVivo I., Blaner W., Tsai W. Y., Chorazy M. Molecular and genetic damage in humans from environmental pollution in Poland.. Nature (Lond.), 360: 256-258, 1992.

Hoffmann D., Hoffmann I. The changing cigarette, 1950–1995.. J. Toxicol. Environ. Health, 50: 307-364, 1997.

Howard J. W., Fazio T. Analytical methodology and reported findings of polycyclic aromatic hydrocarbons in foods.. J. Assoc. Off. Anal. Chem., 63: 1077-1104, 1980.

Waldman J. M., Lioy P. J., Greenberg A., Butler J. P. Analysis of human exposure to benzo(a)pyrene via inhalation and food ingestion in the Total Human Environmental Exposure Study (THEES).. J. Expo. Anal. Environ. Epidemiol., 1: 193-225, 1991.

Beach J. B., Pellizzari E., Keever J. T., Ellis L. Determination of benzo[a]pyrene and other polycyclic aromatic hydrocarbons (PAHs) at trace levels in human tissues.. J. Anal. Toxicol., 24: 670-677, 2000.

Sepkovic D. W., Haley N. J. Biomedical applications of cotinine quantitation in smoking related research.. Am. J. Public Health, 75: 663-665, 1985.

Perez-Stable E. J., Marin G., Marin B. V., Benowitz N. L. Misclassification of smoking status by self-reported cigarette consumption.. Am. Rev. Respir. Dis., 145: 53-57, 1992.

Greizerstein H. B., Gigliotti P., Vena J., Freudenheim J., Kostyniak P. J. Standardization of a method for the routine analysis of polychlorinated biphenyl congeners and selected pesticides in human serum and milk.. J. Anal. Toxicol., 21: 558-566, 1997.

Lodovici M., Akpan V., Giovannini L., Migliani F., Dolara P. Benzo[a]pyrene diol-epoxide DNA adducts and levels of polycyclic aromatic hydrocarbons in autoptic samples from human lungs.. Chem. Biol. Interact., 116: 199-212, 1998.

Seto H., Ohkubo T., Kanoh T., Koike M., Nakamura K., Kawahara Y. Determination of polycyclic aromatic hydrocarbons in the lung.. Arch. Environ. Contam. Toxicol., 24: 498-503, 1993.

Tokiwa H., Sera N., Horikawa K., Nakanishi Y., Shigematu N. The presence of mutagens/carcinogens in the excised lung and analysis of lung cancer induction.. Carcinogenesis (Lond.), 14: 1933-1938, 1993.

Tomingas R., Pott F., Dehnen W. Polycyclic aromatic hydrocarbons in human bronchial carcinoma.. Cancer Lett., 1: 189-195, 1976.

Garfinkel L., Mushinski M. Cancer incidence, mortality and survival: trends in four leading sites.. Stat. Bull. Metrop. Life Insur. Co., 75: 19-27, 1994.

Carpenter C. L., Jarvik M. E., Morgenstern H., McCarthy W. J., London S. J. Mentholated cigarette smoking and lung-cancer risk.. Ann. Epidemiol., 9: 114-120, 1999.

Obana H., Hori S., Kashimoto T., Kunita N. Polycyclic aromatic hydrocarbons in human fat and liver.. Bull. Environ. Contam. Toxicol., 27: 23-27, 1981.

Schnellmann R. G., Putnam C. W., Sipes I. G. Metabolism of 2,2′,3,3′,6,6′-hexachlorobiphenyl and 2,2′,4,4′,5,5′-hexachlorobiphenyl by human hepatic microsomes.. Biochem. Pharmacol., 32: 3233-3239, 1983.

Harris C. C., Autrup H., Stoner G. D., Yang S. K., Leutz J. C., Gelboin H. V., Selkirk J. K., Connor R. J., Barrett L. A., Jones R. T., McDowell E. M., Trump B. F. Metabolism of benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene in cultured human bronchus and pancreatic duct.. Cancer Res., 37: 3349-3355, 1977.

More of us are relying on food containing endocrine disruptive chemicals such as synthetic hormones in meat, eggs and milk.

Sugar (High fructose corn syrup) and our Liver

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

Source: http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?pagewanted=all

However, further analysis within the Nurses’ Health Study indicates that there may be an association between consumption of sugar-sweetened beverages, other than fruit juices, and an increased risk of type 2 diabetes in women, possibly by providing excessive calories and large amounts of rapidly absorbable sugars (Schulze, 2004).

Reactive carbonyls also are elevated in the blood of individuals with diabetes and linked to the complications of that disease. Based on the study data, Ho estimates that a single can of soda contains about five times the concentration of reactive carbonyls than the concentration found in the blood of an adult person with diabetes.

Ho and his associates also found that adding tea components to drinks containing HFCS may help lower the levels of reactive carbonyls. The scientists found that adding epigallocatechin gallate (EGCG), a compound in tea, significantly reduced the levels of reactive carbonyl species in a dose-dependent manner when added to the carbonated soft drinks studied. In some cases, the levels of reactive carbonyls were reduced by half, the researchers say.

Source: This research was reported August 23 at the 234th national meeting of the American Chemical Society, during the symposium, “Food Bioactives and Nutraceuticals: Production, Chemistry, Analysis and Health Effects: Health Effects.” ScienceDaily (Aug. 23, 2007)

Endocrine-Disrupting Chemicals

There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health.

The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor γ, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models.

Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use.

We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness.

Source: Andrea C. Gore, Ph.D., The University of Texas at Austin, College of Pharmacy, 1 University Station, A1915, Austin, Texas 78712. E-mail: andrea.gore@mail.utexas.edu.

BHA, stabilizes the petroleum wax in food products, is also a carcinogen.

Source: http://ntp.niehs.nih.gov/

Asbestos

From the 53 list, let’s take a look at asbestos.  Asbestos has been classified as a known human carcinogen (a substance that causes cancer) by the U.S. Department of Health and Human Services, the EPA, and the International Agency for Research on Cancer (2, 3, 7, 8). Studies have shown that exposure to asbestos may increase the risk of lung cancer and mesothelioma (a relatively rare cancer of the thin membranes that line the chest and abdomen). Although rare, mesothelioma is the most common form of cancer associated with asbestos exposure. In addition to lung cancer and mesothelioma, some studies have suggested an association between asbestos exposure and gastrointestinal and colorectal cancers, as well as an elevated risk for cancers of the throat, kidney, esophagus, and gallbladder (3, 4). www.cancer.gov

The following are 53 carcinogens from the National Toxicology Program, Department of Health and Human Services Report on Carcinogens, Twelfth Edition (2011)
Source:  http://ntp.niehs.nih.gov/go/roc
Aflatoxins
Alcoholic Beverage Consumption………..
4-Aminobiphenyl…
Analgesic Mixtures Containing Phenacetin (see Phenacetin and Analgesic Mixtures Containing Phenacetin)………..
Aristolochic Acids
Arsenic and Inorganic Arsenic Compounds…..
Asbestos
Azathioprine…………..
Benzene
Benzidine (see Benzidine and Dyes Metabolized to Benzidine)….
Beryllium and Beryllium Compounds…
Bis(chloromethyl) Ether and Technical-Grade Chloromethyl Methyl Ether……
1,3-Butadiene………..
Cadmium and Cadmium Compounds..
Chlorambucil………..
1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (see Nitrosourea Chemotherapeutic Agents)…….
Chromium Hexavalent Compounds….
Coal Tars and Coal-Tar Pitches…………….
Coke-Oven Emissions…………..
Cyclophosphamide
Cyclosporin A………
Diethylstilbestrol..
Dyes Metabolized to Benzidine (Benzidine Dye Class) (see Benzidine and Dyes Metabolized to Benzidine)……………..
Erionite
Estrogens, Steroidal
Formaldehyde….
Hepatitis B Virus….
Hepatitis C Virus….
Human Papillomaviruses: Some Genital-Mucosal Types……………..
Melphalan……………
Methoxsalen with Ultraviolet A Therapy………
Mineral Oils: Untreated and Mildly Treated….
Mustard Gas………..
2-Naphthylamine.
Neutrons (see Ionizing Radiation)………
Nickel Compounds (see Nickel Compounds and Metallic Nickel)..
Radon (see Ionizing Radiation)…………..
Silica, Crystalline (Respirable Size)……..
Solar Radiation (see Ultraviolet Radiation Related Exposures)……
Soots…..
Strong Inorganic Acid Mists Containing Sulfuric Acid..
Sunlamps or Sunbeds, Exposure to (see Ultraviolet Radiation Related Exposures)…..
Tamoxifen…………….
2,3,7,8-Tetrachlorodibenzo-p-dioxin….
Thiotepa.
Thorium Dioxide (see Ionizing Radiation)…….
Tobacco Smoke, Environmental (see Tobacco-Related Exposures)
Tobacco Smoking (see Tobacco-Related Exposures)…..
Tobacco, Smokeless (see Tobacco-Related Exposures)
Ultraviolet Radiation, Broad-Spectrum (see Ultraviolet Radiation Related Exposures).
Vinyl Chloride (see Vinyl Halides [selected])…
Wood Dust…………..
X-Radiation and Gamma Radiation (see Ionizing Radiation)………

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