Double Standards - it's not okay to ingest this but fine if we inject it
Toxic Toiletries - The Problem With Formaldehyde, A Vaccine Ingredient
Extensive studies of two toxic chemicals found in children's bath and personal care products suggest that if they pose a health hazard, it is likely to be extremely small.
The two chemical compounds -- 1,4-dioxane and formaldehyde -- were found in trace quantities in children's shampoos, bath gels, lotions and wipes in a study conducted by the consumer group Campaign for Safe Cosmetics.
The Environmental Protection Agency, which evaluates the toxicity of chemical compounds, released a statement yesterday saying that it "is currently doing new human health risk assessments on both dioxane and formaldehyde."
It noted that previous studies had shown dioxane may cause cancer when inhaled, and formaldehyde may cause cancer when ingested, but that the agency has "not yet reached a determination pertaining to skin exposure."
The human health effects of formaldehyde have been studied extensively; those of 1,4-dioxane, less so.
Formaldehyde can cause two kinds of skin problems: allergic reactions in people sensitive to it; and garden-variety irritation in people chronically exposed, such as embalmers.
Studies suggest that 1 to 4 percent of the population is allergic to formaldehyde. However, allergic reactions are rare when the concentration is less than .025 percent, which is the equivalent of 250 parts per million. Thirteen out of the 23 products found to contain formaldehyde in the Campaign for Safe Cosmetics survey had levels over 250 parts per million (with the highest being 610).
There are no studies of mortality from skin exposure to formaldehyde. However, mice exposed repeatedly to 10 percent concentrations of the chemical did not have shorter lives than other mice.
Formaldehyde is also a "probable human carcinogen" in the EPA's eyes.
Lab animals chronically inhaling the compound have higher rates of cancer of the nasal passages. More than 40 human studies of occupational exposure -- in pathologists, funeral directors, garment workers, resin-makers -- overall demonstrate a slight increase in cancer of the lungs and the nose and throat.
Source: The Washington Post, by David Brown, 14 March 2009.
VAN UK'S Comment: They know all this about formaldehyde, cancer and 4% of being being allergic to it and they still put it in children's vaccines, while the safety of the product is still being studied? That is very wrong.
Formaldehyde Is A Cause Of More Common Cancers
New research raises additional concerns about the harmful effects of formaldehyde, a common chemical found in everything from plywood to nail polish, car exhaust and cigarette smoke.
Formaldehyde has long been linked to rare tumors of the nasopharynx, which includes the back of the throat, which affect about 2,000 Americans a year, according to the American Cancer Society.
KIDS: Formaldehyde found in 23 of 28 tested bath products
The new study — the largest to date on workplace exposures — provides further evidence linking formaldehyde with cancers of the blood and lymphatic system. These cancers are far more common, affecting nearly 140,000 Americans a year.
In the study, scientists from the National Cancer Institute followed 25,000 workers for a median of 42 years, estimating the amount of formaldehyde to which each person was exposed on the job. Among other things, scientists compared workers' "peak" exposures to formaldehyde, or the greatest single dose they might encounter at one time.
Workers with the highest peak exposures were 37% more likely to die from any blood or lymphatic cancer, and 78% more likely to die from myeloid leukemia — a cancer of the white blood cells — compared to those with lowest levels, according to the study, published online today in the Journal of the National Cancer Institute.
Highly exposed workers also were nearly four times more likely to die of Hodgkin lymphoma, which affects immune cells, the study shows. This study is the first to link a chemical with an increased risk of death from Hodgkin lymphoma, according to the NCI.
The overall risk of death from these cancers was relatively low, causing only 319 of the 14,000 deaths during the study, says author Laura Beane Freeman, an NCI scientist.
More than 2 million Americans are exposed to formaldehyde in the workplace, the study says.
Freeman says her study doesn't allow her to estimate the risk of formaldehyde exposure to the general public.
But the cancer society's Elizabeth Ward notes that exposure to formaldehyde, which can seep out of wood and other products to pollute indoor air, is "ubiquitous."
Dangerously high formaldehyde levels have been found in trailers provided by the Federal Emergency Management Agency to Gulf Coast residents displaced by Hurricane Katrina. A March report from the Campaign for Safe Cosmetics, an environmental advocacy group, also found formaldehyde in more than 80% of bath and shampoos tested.
The Environmental Protection Agency listed formaldehyde as a "probable human carcinogen" in 1987. In 2004, the International Agency for Research on Cancer went further, classifying formaldehyde as a "known human carcinogen" based partly on research suggesting a link to leukemia.
The study's authors acknowledge that they don't know the mechanism by which formaldehyde might cause leukemia. Authors do note, though, that people exposed to formaldehyde have higher rates of chromosome abnormalities in their lymphocytes, a type of white blood cell that fights infection.
Source: USA Today, 13th May 2009, by Liz Szabo.
National Cancer Institute Formaldehyde Fact Sheet
* Formaldehyde is a colorless, flammable, strong-smelling chemical that is used to manufacture building materials and to produce many household products (see Question 1).
* Formaldehyde sources in the home include pressed-wood products, cigarette smoke, and fuel-burning appliances (see Question 2).
* When exposed to formaldehyde, some individuals may experience various short-term health effects (see Question 3).
* Formaldehyde has been classified as a known human carcinogen (cancer-causing substance) by the International Agency for Research on Cancer and as a probable human carcinogen by the U.S. Environmental Protection Agency (see Question 4).
* Research studies of workers exposed to formaldehyde have suggested an association between formaldehyde exposure and cancers of the nasal sinuses, nasopharynx, and brain, and possibly leukemia (see Questions 4, and 5).
1. What is formaldehyde?
Formaldehyde is a colorless, flammable, strong-smelling chemical that is used to manufacture building materials and to produce many household products. It is used in pressed-wood products, such as particleboard, plywood, and fiberboard; glues and adhesives; permanent-press fabrics; paper product coatings; and certain insulation materials. In addition, formaldehyde is commonly used as an industrial fungicide, germicide, and disinfectant, and as a preservative in mortuaries and medical laboratories.
2. How is the general population exposed to formaldehyde?
According to a 1997 report by the U.S. Consumer Product Safety Commission, formaldehyde is normally present in both indoor and outdoor air at low levels, usually less than 0.03 parts of formaldehyde per million parts of air (ppm). Materials containing formaldehyde can release formaldehyde gas or vapor into the air. One example of formaldehyde exposure in the air is through automobile tailpipe emissions.
During the 1970s, urea-formaldehyde foam insulation (UFFI) was used in many homes. However, few homes are now insulated with UFFI. Homes in which UFFI was installed many years ago are not likely to have high formaldehyde levels now. Pressed-wood products containing formaldehyde resins are often a significant source of formaldehyde in homes. Other potential indoor sources of formaldehyde include cigarette smoke and the use of unvented fuel-burning appliances, such as gas stoves, wood-burning stoves, and kerosene heaters.
Industrial workers who produce formaldehyde or formaldehyde-containing products, laboratory technicians, health care professionals, and mortuary employees may be exposed to higher levels of formaldehyde than the general public. Exposure occurs primarily by inhaling formaldehyde gas or vapor from the air or by absorbing liquids containing formaldehyde through the skin.
3. What are the short-term health effects of formaldehyde exposure?
When formaldehyde is present in the air at levels exceeding 0.1 ppm, some individuals may experience health effects, such as watery eyes; burning sensations of the eyes, nose, and throat; coughing; wheezing; nausea; and skin irritation. Some people are very sensitive to formaldehyde, whereas others have no reaction to the same level of exposure.
4. Can formaldehyde cause cancer?
Although the short-term health effects of formaldehyde exposure are well known, less is known about its potential long-term health effects. In 1980, laboratory studies showed that exposure to formaldehyde could cause nasal cancer in rats. This finding raised the question of whether formaldehyde exposure could also cause cancer in humans. In 1987, the U.S. Environmental Protection Agency (EPA) classified formaldehyde as a probable human carcinogen under conditions of unusually high or prolonged exposure (1). Since that time, some studies of industrial workers have suggested that formaldehyde exposure is associated with nasal sinus cancer and nasopharyngeal cancer, and possibly with leukemia. In 1995, the International Agency for Research on Cancer (IARC) concluded that formaldehyde is a probable human carcinogen. In June 2004, after evaluating all existing data, the IARC reclassified formaldehyde as a known human carcinogen (2).
5. What have scientists learned about the relationship between formaldehyde and cancer?
Since the 1980s, the National Cancer Institute (NCI), a component of the National Institutes of Health, has conducted studies to determine whether there is an association between occupational exposure to formaldehyde and an increase in the risk of cancer. The results of this research have provided EPA and the Occupational Safety and Health Administration (OSHA) with information to evaluate the potential health effects of workplace exposure to formaldehyde.
Long-term effects of formaldehyde have been evaluated in epidemiologic studies (studies that attempt to uncover the patterns and causes of disease in groups of people). One type of epidemiologic study is called a cohort study. A cohort is a group of people who may vary in their exposure to a particular factor, such as formaldehyde, and are followed over time to see whether they develop a disease. Another kind of epidemiologic study is called a case-control study. Case-control studies begin with people who are diagnosed as having a disease (cases) and compare them to people without the disease (controls), trying to identify differences in factors, such as exposure to formaldehyde, that might explain why the cases developed the disease but the controls did not.
Several NCI studies have found that anatomists and embalmers, people who are potentially exposed to formaldehyde in their professions, are at an increased risk of leukemia and brain cancer compared with the general population. In 2003, a number of cohort studies were completed among workers exposed to formaldehyde. One study, conducted by NCI, looked at 25,619 workers in industries with the potential for occupational formaldehyde exposure and estimated each worker’s exposure to the chemical while at work (3). The results showed an increased risk of death due to leukemia, particularly myeloid leukemia, among workers exposed to formaldehyde. This risk was associated with increasing peak and average levels of exposure, as well as with the duration of exposure, but not with cumulative exposure. Using an additional 10 years of data, a follow-up study published in 2009 continued to show a possible link between formaldehyde exposure and cancers of the hematopoietic and lymphatic systems, particularly myeloid leukemia, as was previously reported (4). As in the previous study, the risk was highest earlier in the follow-up period and declined steadily over time, such that the cumulative excess risk of myeloid leukemia was no longer statistically significant. The researchers noted that similar patterns of risks over time had been seen for other agents known to cause leukemia.
A separate study of 11,039 textile workers performed by the National Institute for Occupational Safety and Health (NIOSH) also found an association between the duration of exposure to formaldehyde and leukemia deaths (5). However, the evidence remains mixed because a cohort study of 14,014 British industry workers found no association between cumulative formaldehyde exposure and leukemia deaths (6).
Formaldehyde undergoes rapid chemical changes immediately after absorption. Therefore, some scientists think that formaldehyde is unlikely to have effects at sites other than the upper respiratory tract. However, some laboratory studies suggest that formaldehyde may affect the lymphatic and hematopoietic systems. Based on both the epidemiologic data from cohort studies and the experimental data from laboratory research, NCI investigators have concluded that exposure to formaldehyde may cause leukemia, particularly myeloid leukemia, in humans. However, inconsistent results from other studies suggest that further research is needed before definite conclusions can be drawn.
Several case-control studies and cohort studies, including analysis of the large NCI cohort, have reported an association between formaldehyde exposure and nasopharyngeal cancer, although some other studies have not. Data from extended follow-up of the NCI study found that the excess of nasopharyngeal cancer observed in the earlier report persisted (7).
Earlier analysis of the NCI cohort found increased lung cancer deaths among industrial workers compared with the general U.S. population. However, the rate of lung cancer deaths did not increase with higher levels of formaldehyde exposure. This observation led the researchers to conclude that factors other than formaldehyde exposure might have caused the increased deaths. New data on lung cancer from the extended follow-up did not find any relationship between formaldehyde exposure and lung cancer mortality.
6. What has been done to protect workers from formaldehyde?
In 1987, OSHA established a Federal standard that reduced the amount of formaldehyde to which workers can be exposed over an 8-hour work day from 3 ppm to 1 ppm. In May 1992, the standard was amended, and the formaldehyde exposure limit was further reduced to 0.75 ppm.
7. How can people limit formaldehyde exposure in their homes?
The EPA recommends the use of “exterior-grade” pressed-wood products to limit formaldehyde exposure in the home. Before purchasing pressed-wood products, including building materials, cabinetry, and furniture, buyers should ask about the formaldehyde content of these products. Formaldehyde levels in homes can also be reduced by ensuring adequate ventilation, moderate temperatures, and reduced humidity levels through the use of air conditioners and dehumidifiers.
8. Where can people find more information about formaldehyde?
The following organizations can provide additional resources that readers may find helpful:
The U.S. Consumer Product Safety Commission (CPSC) has information about household products that contain formaldehyde. CPSC can be contacted at:
Address: U.S. Consumer Product Safety Commission
4330 East West Highway
Bethesda, MD 20814–4408
Telephone: 1–800–638–2772 (1–800–638–CPSC)
TTY: 1–800–638–8270
Web site: http://www.cpsc.gov
The U.S. Food and Drug Administration (FDA) maintains information about cosmetics and drugs that contain formaldehyde. FDA can be contacted at:
Address: U.S. Food and Drug Administration
10903 New Hampshire Avenue
Silver Spring, MD 20903
Telephone: 1–888–463–6332 (1–888–INFO–FDA)
Web site: http://www.fda.gov
The Federal Emergency Management Agency (FEMA) has information about formaldehyde exposure levels in mobile homes and trailers supplied by FEMA after Hurricane Katrina. FEMA can be contacted at:
Address: Federal Emergency Management Agency
Post Office Box 10055
Hyattsville, MD 20782–7055
Telephone: 1–800–621–3362 (1–800–621–FEMA)
Web site: FEMA-Correspondence-Unit@dhs.gov
Web site: http://www.fema.gov
The Occupational Safety and Health Administration (OSHA) has information about occupational exposure limits for formaldehyde. OSHA can be contacted at:
Address: U.S. Department of Labor
Occupational Safety and Health Administration
200 Constitution Avenue
Washington, DC 20210
Telephone: 1–800–321–6742 (1–800–321–OSHA)
Web site: http://www.osha.gov
Selected References
1. U.S. Environmental Protection Agency, Office of Air and Radiation. Report to Congress on Indoor Air Quality, Volume II: Assessment and Control of Indoor Air Pollution, 1989.
2. International Agency for Research on Cancer (June 2004). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans Volume 88 (2006): Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. Retrieved May 4, 2009, from: http://monographs.iarc.fr/ENG/Monographs/vol88/index.php.
3. Hauptmann M, Lubin JH, Stewart PA, Hayes RB, Blair A. Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries. Journal of the National Cancer Institute 2003; 95(21):1615–1623.
4. Beane Freeman L, Blair A, Lubin JH, et al. Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries: The National Cancer Institute cohort. Journal of the National Cancer Institute 2009; 101(10):751–761.
5. Pinkerton LE, Hein MJ, Stayner LT. Mortality among a cohort of garment workers exposed to formaldehyde: An update. Occupational Environmental Medicine 2004; 61:193–200.
6. Coggon D, Harris EC, Poole J, Palmer KT. Extended follow-up of a cohort of British chemical workers exposed to formaldehyde. Journal of the National Cancer Institute 2003; 95(21):1608–1615.
7. Hauptmann M, Lubin JH, Stewart PA, Hayes RB, Blair A. Mortality from solid cancers among workers in formaldehyde industries. American Journal of Epidemiology 2004; 159(12):1117–1130.
Source: National Cancer Institute, www.cancer.gov
Formaldehyde Causes Leukaemia
Formaldehyde, a carcinogen used in many sectors of industry, may increase the risk of developing leukaemia, reports an expert opinion given to an October meeting of the International Agency for Research on Cancer (IARC). Formaldehyde is classified as a known human carcinogen (Group 1) but so far mainly linked to nasopharyngeal and nasal sinus cancer.
In late November, a new study confirmed the association between formaldehyde and leukaemia. Long durations of exposure to formaldehyde used for embalming in the funeral industry were associated with an increased risk of death from myeloid leukemia, according to a study published online November 20 in the Journal of the National Cancer Institute.
Previous studies have shown excess mortality from lymphohematopoietic malignancies and brain cancer in anatomists, pathologists, and funeral industry workers, all of whom may have worked with formaldehyde.
For this study, researchers at the Division of Cancer Epidemiology and Genetics at the National Cancer Institute in Bethesda, Md., and colleagues investigated the relation of mortality to work practices and formaldehyde exposure levels among these professionals. In a case-control study among funeral industry workers who had died between 1960 and 1986, researchers compared those who died from lymphohematopoietic malignancies and brain tumors with those who died from other causes. Lifetime work practices and exposures to formaldehyde were obtained by interviews with next of kin and coworkers.
This study was the first epidemiological investigation, to the authors' knowledge, to relate cancer risk to duration of employment, work practices, and estimated formaldehyde exposure levels in the funeral industry.
The number of years of embalming practice and related formaldehyde exposures were associated with statistically significantly increased mortality from myeloid leukaemia, with the greatest risk among those who practiced embalming for more than 20 years. No associations were observed with other lymphohematopoietic malignancies; associations with brain cancer were unclear.
Source: Journal of the National Cancer Institute, Risks, via European Trade Union Institute, 30 November 2009.
Embryo toxicity and teratogenicity of formaldehyde
C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins.
Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. The following questions must be addressed: What adducts (e.g., N-methyl amino acids) are formed in the blood following formaldehyde inhalation? What role do N-methyl-amino adducts play in alkylation of nuclear and mitochondrial deoxyribonucleic acid, as well as mitochondrial peroxidation? The fact that the free formaldehyde pool in blood is not affected following exposure to the chemical does not mean that formaldehyde is not involved in altering cell and deoxyribonucleic acid characteristics beyond the nasal cavity. The teratogenic effect of formaldehyde in the English literature has been sought, beginning on the 6th day of pregnancy (i.e., rodents) (Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545-48; Martin WJ. Reprod Toxicol 1990, pp 237-39; Ulsamer AG, et al. Hazard Assessment of Chemicals; Academic Press, 1984, pp 337-400; and U.S. Department of Health and Human Services. Toxicological Profile of Formaldehyde; ATSDR, 1999 [references 1-4, respectively, herein]).
The exposure regimen is critical and may account for the differences in outcomes. Pregnant rats were exposed (a) prior to mating, (b) during mating, (c) or during the entire gestation period. These regimens (a) increased embryo mortality; (b) increased fetal anomalies (i.e., cryptochordism and aberrant ossification centers); (c) decreased concentrations of ascorbic acid; and (d) caused abnormalities in enzymes of mitochondria, lysosomes, and the endoplasmic reticulum. The alterations in enzymatic activity persisted 4 mo following birth. In addition, formaldehyde caused metabolic acidosis, which was augmented by iron deficiency. Furthermore, newborns exposed to formaldehyde in utero had abnormal performances in open-field tests. Disparities in teratogenic effects of toxic chemicals are not unusual. For example, chlorpyrifos has not produced teratogenic effects in rats when mothers are exposed on days 6-15 (Katakura Y, et al. Br J Ind Med 1993, pp 176-82 [reference 5 herein]) of gestation (Breslin WJ, et al. Fund Appl Toxicol 1996, pp 119-30; and Hanley TR, et al. Toxicol Sci 2000, pp 100-08 [references 6 and 7, respectively, herein]).
However, either changing the endpoints for measurement or exposing neonates during periods of neurogenesis (days 1-14 following birth) and during subsequent developmental periods produced adverse effects. These effects included neuroapoptosis, decreased deoxyribonucleic acid and ribonucleic acid synthesis, abnormalities in adenylyl cyclase cascade, and neurobehavioral effects (Johnson DE, et al. Brain Res Bull 1998, pp 143-47; Lassiter TL, et al. Toxicol Sci 1999, pp 92-100; Chakraborti TK, et al. Pharmacol Biochem Behav 1993, pp 219-24; Whitney KD, et al. Toxicol Appl Pharm 1995, pp 53-62; Chanda SM, et al. Pharmacol Biochem Behav 1996, pp 771-76; Dam K, et al. Devel Brain Res 1998, pp 39-45; Campbell CG, et al. Brain Res Bull 1997, pp 179-89; and Xong X, et al. Toxicol Appl Pharm 1997, pp 158-74 [references 8-15, respectively, herein]). Furthermore, the terata caused by thalidomide is a graphic human example in which the animal model and timing of exposure were key factors (Parman T, et al. Natl Med 1999, pp 582-85; and Brenner CA, et al. Mol Human Repro 1998, pp 887-92 [references 16 and 17, respectively, herein]). Thus, it appears that more sensitive endpoints (e.g., enzyme activity, generation of reactive oxygen species, timing of exposure) for the measurement of toxic effects of environmental agents on embryos, fetuses, and neonates are more coherent than are gross terata observations. The perinatal period from the end of organogenesis to the end of the neonatal period in humans approximates the 28th day of gestation to 4 wk postpartum. Therefore, researchers must investigate similar stages of development (e.g., neurogenesis occurs in the 3rd trimester in humans and neonatal days occur during days 1-14 in rats and mice, whereas guinea pigs behave more like humans). Finally, screening for teratogenic events should also include exposure of females before mating or shortly following mating. Such a regimen is fruitful inasmuch as environmental agents cause adverse effect.
Source: Arch Environ Health. 2001 Jul-Aug;56(4):300-11.
EPA Slashes Mercury from Gold Production
The U.S. Environmental Protection Agency (EPA) is proposing to cut emissions from gold ore processing and production facilities, the sixth largest source of mercury air emissions in the country. Today’s action is one of several steps EPA is taking to reduce mercury, which can damage children’s developing brains and nervous systems, even before they are born.
EPA’s proposal would reduce annual mercury emissions to about 1,390 pounds a year – a 73 percent reduction from 2007 levels. This action will build on reductions from Nevada’s successful program for controlling mercury emissions from precious metal mining.
“Taking mercury out of the air makes our communities safer for everyone,” said Gina McCarthy assistant administrator for EPA’s Office of Air and Radiation. “Our proposal will further progress that has already been made to limit mercury emissions from this industry.”
There are about 20 facilities in the United States that extract gold from ore that would be subject to the proposed rule. Some facilities in Nevada already are making significant progress toward the proposed reductions under that state’s program.
Mercury emitted to the air eventually settles in water, where it can change into methylmercury, which builds up in ocean and freshwater fish and can be highly toxic to humans who eat the fish– sometimes leading to fish consumption advisories to protect public health.
EPA will take public comment on the proposed rule for 30 days after it is published in the Federal Register.
Source: EPA News Release, 16 April 2010.
Thimerosal - Mercury Derivative. Information from Lilly Manufacturing Company
Primary Physical and Health Hazards: Skin Permeable. Toxic. Mutagen. Irritant (eyes).
Allergen. Nervous System and Reproductive Effects.
Caution Statement: Thimerosal may enter the body through the skin, is toxic, alters genetic material, may be irritating to the eyes, and causes allergic reactions. Effects of exposure may include numbness of extremities, fetal changes, decreased offspring survival, and lung tissue changes.
Routes of Entry: Inhalation and skin absorption.
Effects of Overexposure: Topical allergic dermatitis has been reported. Thimerosal contains
mercury. Mercury poisoning may occur and topical hypersensitivity reactions may be seen. Early signs of mercury poisoning in adults are nervous system effects, including narrowing of the visual field and numbness in the extremities. Exposure to mercury in utero and in children may cause mild to severe mental retardation and mild to severe motor coordination impairment. Based on animal data, may be irritating to the eyes.
Medical Conditions Aggravated by Exposure: Hypersensitivity to mercury.
Carcinogenicity: No carcinogenicity data found. Not listed by IARC, NTP, ACGIH, or OSHA.
Section 4 - First Aid Measures
Eyes: Hold eyelids open and flush with a steady, gentle stream of water for 15 minutes. See an
Thimerosal ophthalmologist (eye doctor) or other physician immediately.
Skin: This product is intended for topical application to the skin. However, in case of unintentional
exposure, especially to large areas of skin, wash with soap and water. If symptoms develop consult a physician.
Inhalation: Move individual to fresh air. Get medical attention if breathing difficulty occurs. If not breathing, provide artificial respiration assistance (mouth-to-mouth) and call a physician immediately.
Ingestion: Call a physician or poison control center. Drink one or two glasses of water and give 1-2 tablespoons syrup of ipecac to induce vomiting. Do not induce vomiting or give anything by mouth to an unconscious person. Use of chelating agents such as BAL may be needed to treat ingestion of mercury. Immediately transport to a medical care facility and see a physician.
Source: http://www.vaccine-tlc.org/docs/Thimerosal%20Material%20Safety%20Data%20Sheet.pdf
Formaldehyde induces neurotoxicity to PC12 cells involving inhibition of paraoxonase-1 expression and activity.
Abstract
Formaldehyde (FA) has been found to cause toxicity to neurons. However, its neurotoxic mechanisms have not yet been clarified. Increasing evidence demonstrated that oxidative damage is one of the most critical effects of formaldehyde exposure. Paraoxonase-1 (PON-1) is a pivotal endogenous antioxidant. Thus, we hypothesized that FA-mediated down-regulation of PON1 is associated with its neurotoxicity. In the present work, we used PC12 cells to study the neurotoxicity of FA and explore whether PON-1 is implicated FA-induced neurotoxicity. We found that FA has potent cytotoxic and apoptotic effects on PC12 cells. FA induces accumulation of intracellular reactive oxygen species along with down-regulation of Bcl-2 expression as well as increased cytochrome c release. FA significantly suppressed the expression and activity of PON-1 in PC12 cells. Furthermore, H(2) S, an endogenous antioxidant gas, antagonizes FA-induced cytotoxicity as well as 2-Hydroxyquinoline, a specific inhibitor of PON-1, also induces cytotoxicity to PC12 cells. The results of the present study provide, for the first time, evidence that the inhibitory effect on PON-1 expression and activity is involved in the neurotoxicity of FA and suggest a promising role of PON-1 as a novel therapeutic strategy for FA-mediated toxicity.
Source: Clin Exp Pharmacol Physiol. 2011 Jan 24. doi: 10.1111/j.1440-1681.2011.05485.x
Formaldehyde Ruled as a Carcinogen
Late last week, the Department of Health and Human Services classified formaldehyde as "a known carcinogen," adding its verdict to two similar reports released by key agencies since 2009.
But despite the growing scientific consensus about how formaldehyde can affect human health, it remains to be seen if the studies will lead to tighter U.S. formaldehyde regulations.
As we've previously reported, the Environmental Protection Agency has been trying to update its chemical risk assessment for formaldehyde since 1998, but has been stalled repeatedly by the chemical manufacturing industry.
EPA assessments are the country's gold standard for how dangerous a chemical is. The formaldehyde assessment would undoubtedly influence the stringency of a rule the EPA is developing on how much of the chemical can safely be released from construction materials that contain it
In 2009, Sen. David Vitter, R-La., maneuvered successfully to delay the assessment by putting a hold on the nomination of a key EPA appointee and forcing the agency to send its draft to the National Academy of Sciences for review.
Vitter has received substantial campaign contributions from the nation's largest formaldehyde manufacturers and users. After the EPA agreed to send its assessment to the NAS, a top industry lobbyist, Charles Grizzle, threw Vitter a fundraising party, requesting donations of $1,000 a plate.
The NAS finished reviewing the EPA assessment in April, sending back a long list of questions and advising the EPA not to finalize the document until it could show exactly how formaldehyde causes cancer, a biological mechanism known as the "mode of action."
Dr. Peter Infante, a former director of the Office of Carcinogen Identification and Classification at the Occupational Safety and Health Administration, called the NAS critique "arrogant" because "we don't know the mode of action for most things that cause cancer."
Christopher De Rosa, a former senior toxicologist for the Centers for Disease Control, said the HHS study might "galvanize the EPA's political will to go forward with the risk assessment because it represents a convergence of opinions worldwide in terms of formaldehyde being a known carcinogen."
A spokesperson for the EPA did not respond to questions about how the HHS report will affect the EPA's risk assessment.
The American Chemistry Council, a trade group that represents the chemical industry, said in a written statement that the HHS report flies in the face of the Obama administration's commitment to sound science.
"We are extremely concerned that politics may have hijacked the scientific process and believe this report by HHS is an egregious contradiction to what the president said early in his administration," said Chemistry Council Chief Executive Cal Dooley.
Source: Scientific American, 15th June 2011.
Aluminium Causes Cell Death
Aluminum-based adjuvants (aluminum salts or alum) are widely used in human vaccination, although their mechanisms of action are poorly understood. Here we report that, in mice, alum causes cell death and the subsequent release of host cell DNA, which acts as a potent endogenous immunostimulatory signal mediating alum adjuvant activity. Furthermore, we propose that host DNA signaling differentially regulates IgE and IgG1 production after alum-adjuvanted immunization. We suggest that, on the one hand, host DNA induces primary B cell responses, including IgG1 production, through interferon response factor 3 (Irf3)-independent mechanisms. On the other hand, we suggest that host DNA also stimulates 'canonical' T helper type 2 (TH2) responses, associated with IgE isotype switching and peripheral effector responses, through Irf3-dependent mechanisms. The finding that host DNA released from dying cells acts as a damage-associated molecular pattern that mediates alum adjuvant activity may increase our understanding of the mechanisms of action of current vaccines and help in the design of new adjuvants.
Source: Nature Medicine
Year published:
(2011)
DOI:
doi:10.1038/nm.2403
Patent for New Vaccine Lists Formaldehyde as a Carcinogen
Current methods used to inactivate living pathogens in vaccine production involve the use of chemical agents such as formaldehyde or betapropiolactone to chemically modify the genetic material of the pathogen. However, there is substantial evidence that both of these agents are human and animal carcinogens. For example, studies in rats exposed to formaldehyde by inhalation have shown that formaldehyde induces squamous-cell carcinoma of the nasal cavity. Additionally, formaldehyde has been shown to be genotoxic in vitro and in vivo. Both genotoxicity and cytotoxicity play an important role in the carcinogenicity of formaldehyde.
Although the concentration of formaldehyde in vaccines is typically low (below 0.02%), this represents up to 50-100 micrograms of formaldehyde per injected dose in many vaccines (for example, Anthrax vaccine produced by Bioport Corp. contains 100 microgram/ml formaldehyde as a preservative) and poses a potential hazard due to the number of vaccinations a person receives over the course of a lifetime. Particularly dangerous is the amount of formaldehyde that is injected into infants and small children during the course of multiple routine childhood vaccinations. While the amount of formaldehyde in each vaccine dose is low, the combined amount can become substantial.
Similarly, betapropiolactone, which is used in the inactivation of rabies virus, can produce an immune complex-reaction when combined with other components of the rabies vaccine. Additionally, it has been shown to produce squamous cell carcinomas, lymphomas and hepatomas in mice. Thus, there is a need to develop a low cost, nontoxic alternative to formaldehyde and betapropiolactone for the inactivation of live pathogens, such as viruses, bacteria and parasites. The methods disclosed herein address this need, and provide substantial benefits not previously described in the art.
Source:
Inactivating pathogens with oxidizing agents for vaccine production
United States Patent: 8,124,397.
http://www.pharmcast.com/Patents200/Yr2012/Feb2012/022812/8124397_Pathogens022812.htm?utm_source=January+28%2C+2013+Newsletter&utm_campaign=Jan+28%2C2013+newsletter&utm_medium=email
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