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Old 05-14-2007, 03:19 PM   #1
Lani
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216 environmental chemicals which can cause breast cancer identified

Study identifies 216 chemicals that caused breast cancer in lab rats

A cancer-research group that compiled data from previous studies of carcinogens is reporting that more than 216 compounds, many of which people are exposed to on a regular basis, have caused breast cancer in lab rats.
According to an article to be published in Cancer, a scientific journal, the database shows that among the 216 compounds that cause breast tumors in animals:


73 have been present in consumer products or as contaminants in food
35 are air pollutants
25 have been associated with occupational exposures affecting more than 5,000 women a year
29 are produced in the United States in large amounts, often exceeding 1 million pounds per year.
The researchers say the list is incomplete because relatively few of the USA's 80,000 chemicals have been tested to see if they're carcinogenic.

"Almost all of the chemicals identified as mammary carcinogens were mutagenic (they damage DNA) and caused tumors in multiple organs and species; these characteristics are generally thought to indicate likely carcinogenicity in humans, even at lower exposure levels," a summary of their report says. "However, some aspects of the animal studies make them difficult to interpret, so future research to better understand relationships between animal and human breast cancers will be helpful."

The American Cancer Society reported in a press release today that the mammography rate has declined since 2000, with fewer women undergoin a simple test that can detect breast cancer.

SUMMARY: Chemicals causing mammary gland tumors in animals signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention [Silent Spring Institute]
Introduction
Testing chemicals in animal studies is currently the primary means of identifying chemicals that might cause cancer in humans. Animal studies are used to identify health risks from pollution in much the same way they are used to test drugs before they are tested on humans. All known human carcinogens that have been tested on animals have been found to cause cancer in animals as well. Scientists evaluate the strength of evidence from animal studies as an indication of how likely it is that the chemical will also cause cancer in humans.

Animal studies are a particularly important resource for understanding environmental pollutants and breast cancer, because there are only a limited number of human studies and those are hampered by difficulties in estimating relevant exposures, especially exposures years ago when a woman's cancer first began. Results: of animal studies can inform actions by individuals, government agencies, and industry to reduce exposure. They also suggest ideas for future human studies.

Sometimes, people question whether the relatively high doses of chemicals are relevant to typical human exposures. Scientists use high doses so they don't need to study a very large number of animals to find chemical risks of public health importance. In addition, research suggests that low levels of exposure to many chemicals also can have negative health effects.

Methodology

To make information on chemical mammary gland carcinogens readily accessible, we developed a database of exposure and carcinogenicity data. The database is the most comprehensive of its kind and is available at>

http://www.silentspring.org/sciencereview/

and at

http://www.komen.org/environment

The database includes chemicals identified as mammary gland carcinogens in at least one study reported in one of the following sources: Carcinogenic Potency Database (CPDB), International Agency for Research on Chemicals (IARC) Monographs summaries, National Toxicology Program (NTP) Technical Reports, NTP 11th Report on Carcinogens (11th ROC), and Chemical Carcinogenesis Research Information Service (CCRIS). In the absence of conflicting information, positive results in a single well-conducted study are generally considered sufficient to identify a chemical as a potential human carcinogen.

Results and Discussion

The study identified 216 chemicals that have been associated with increased mammary tumors in at least one animal study. Exposure is likely to be widespread, since 29 of the chemicals are produced in the US at rate of more than 1 million pounds/year, 35 are air pollutants, 25 have involved occupational exposures to greater than 5,000 women, 10 are food additives, and 73 are or have historically been present in consumer products or as contaminants of food. The identified chemicals include 36 industrial chemicals, 6 chlorinated solvents, 18 products of combustion, 10 pesticides, 18 dyes, four types of radiation, one drinking water disinfection byproduct, 47 pharmaceuticals, 17 hormones (some of which are pharmaceuticals), five natural products, and 54 unclassified chemicals.

Regulators have not paid much attention to potential mammary carcinogens. For example, US EPA uses animal tumor data to develop estimates of the potency of carcinogens so they can evaluate regulatory options for various exposure scenarios, but they have developed potency factors for only 20 of the 216 chemicals on the mammary carcinogens list. In addition, OSHA requires medical surveillance for workers exposed to 11 of the chemicals on our list, but does not require breast cancer screening.

The list of 216 chemicals is incomplete, because only a small fraction of the estimated 80,000 chemicals registered in the U.S. for commercial use have been tested to see if they cause cancer in animals.

Almost all of the chemicals identified as mammary carcinogens were mutagenic (they damage DNA) and caused tumors in multiple organs and species; these characteristics are generally thought to indicate likely carcinogenicity in humans, even at lower exposure levels. However, some aspects of the animal studies make them difficult to interpret, so future research to better understand relationships between animal and human breast cancers will be helpful.

Some of the mammary gland carcinogens with particularly widespread exposure include PAHs, present in auto and diesel exhaust; MX, a byproduct of chlorine disinfection of drinking water; and chlorinated solvents, which can be drinking water contaminants, gasoline additives, and in some consumer products such as paint strippers or spot removers. Human studies of chlorinated solvents and PAHs both suggest a possible association with breast cancer, while not enough research has been done to evaluate a potential association between drinking water chlorination and breast cancer. Despite these findings, major governmental reports on health effects of these common pollutants do not discuss potential associations with breast cancer.

Recommendations

Future human studies should target more of the chemicals associated with mammary tumors in animal studies. In the meantime, we need to rely on animal models for public health purposes such as developing regulations to limit chemical exposures or reformulating products to reduce use of these chemicals.

The results of research to date on mammary carcinogens warrants increased attention from regulators, manufacturers, and nonprofit organizations. Efforts should be made to develop better testing methods, test additional chemicals, make better use of testing information in setting health policies, and establish workplace and national monitoring of exposure to suspect chemicals.

EARLY VIEW: OPEN ACCESS: Chemicals causing mammary gland tumors in animals signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention [Cancer; Subscribe; Sample]
Identifying chemical carcinogens in animal studies is currently the primary means of anticipating cancer effects in humans. Animal studies to evaluate potential chemical carcinogenicity are particularly important for breast cancer because environmental and occupational epidemiologic research is sparse. Chemicals that increased mammary gland tumors in animal studies were compiled from the International Agency for Research on Cancer (IARC), the U.S. National Toxicology Program (NTP), and other sources. Summary assessments of the carcinogenic potential for each chemical and potentially exposed populations were also compiled. In all, 216 chemicals were identified that have been associated with increases in mammary gland tumors in at least 1 study. These include industrial chemicals, chlorinated solvents, products of combustion, pesticides, dyes, radiation, drinking water disinfection byproducts, pharmaceuticals and hormones, natural products, and research chemicals. Twenty-nine are produced in the U.S. at >1 million pounds/year; 35 are air pollutants, 25 have involved occupational exposures to >5000 women, and 73 have been present in consumer products or as contaminants of food. Thus, exposure is widespread. Nearly all of the chemicals were mutagenic and most caused tumors in multiple organs and species; these characteristics are generally believed to indicate likely carcinogenicity in humans. To our knowledge, this is the most comprehensive list developed of animal mammary gland carcinogens and, along with associated data, is publicly available at:
http://www.silentspring.org/sciencereview/

and at

http://www.komen.org/environment

Valuable information from cancer bioassays is not well utilized in risk assessment and regulatory processes, suggesting a need to strengthen chemicals testing and risk assessment as tools for breast cancer prevention.

EARLY VIEW: OPEN ACCESS: Environmental pollutants and breast cancer: Epidemiologic studies [Cancer; Subscribe; Sample]
Laboratory research has shown that numerous environmental pollutants cause mammary gland tumors in animals; are hormonally active, specifically mimicking estrogen, which is a breast cancer risk factor; or affect susceptibility of the mammary gland to carcinogenesis. An assessment of epidemiologic research on these pollutants identified in toxicologic studies can guide future research and exposure reduction aimed at prevention. The PubMed database was searched for relevant literature and systematic critical reviews were entered in a database available at URL:
http://www.silentspring.org/sciencereview/

and at

http://www.komen.org/environment

Based on a relatively small number of studies, the evidence to date generally supports an association between breast cancer and polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) in conjunction with certain genetic polymorphisms involved in carcinogen activation and steroid hormone metabolism. Evidence regarding dioxins and organic solvents is sparse and methodologically limited but suggestive of an association. Methodologic problems include inadequate exposure assessment, a lack of access to highly exposed and unexposed populations, and a lack of preclinical markers to identify associations that may be obscured by disease latency. Among chemicals identified in toxicologic research as relevant to breast cancer, many have not been investigated in humans. The development of better exposure assessment methods is needed to fill this gap. In the interim, weaknesses in the epidemiologic literature argue for greater reliance on toxicologic studies to develop national policies to reduce chemical exposures that may be associated with breast cancer. Substantial research progress in the last 5 years suggests that the investigation of environmental pollutants will lead to strategies to reduce breast cancer risk.

sorry for the repeats!
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Old 05-14-2007, 04:48 PM   #2
hutchibk
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Thanks Lani. Can't wait until I have time to read the whole thing... Good work!
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Brenda

NOV 2012 - 9 yr anniversary
JULY 2012 - 7 yr anniversary stage IV (of 50...)

Nov'03~ dX stage 2B
Dec'03~
Rt side mastectomy, Her2+, ER/PR+, 10 nodes out, one node positive
Jan'04~
Taxotere/Adria/Cytoxan x 6, NED, no Rads, Tamox. 1 year, Arimadex 3 mo., NED 14 mo.
Sept'05~
micro mets lungs/chest nodes/underarm node, Switched to Aromasin, T/C/H x 7, NED 6 months - Herceptin only
Aug'06~
micro mets chest nodes, & bone spot @ C3 neck, Added Taxol to Herceptin
Feb'07~ Genetic testing, BRCA 1&2 neg

Apr'07~
MRI - two 9mm brain mets & 5 punctates, new left chest met, & small increase of bone spot C3 neck, Stopped Aromasin
May'07~
Started Tykerb/Xeloda, no WBR for now
June'07~
MRI - stable brain mets, no new mets, 9mm spots less enhanced, CA15.3 down 45.5 to 9.3 in 10 wks, Ty/Xel working magic!
Aug'07~
MRI - brain mets shrunk half, NO NEW BRAIN METS!!, TMs stable @ 9.2
Oct'07~
PET/CT & MRI show NED
Apr'08~
scans still show NED in the head, small bone spot on right iliac crest (rear pelvic bone)
Sept'08~
MRI shows activity in brain mets, completed 5 fractions/5 consecutive days of IMRT to zap the pesky buggers
Oct'08~
dropped Xeloda, switched to tri-weekly Herceptin in combo with Tykerb, extend to tri-monthly Zometa infusion
Dec'08~
Brain MRI- 4 spots reduced to punctate size, large spot shrunk by 3mm, CT of torso clear/pelvis spot stable
June'09~
new 3-4mm left cerrebellar spot zapped with IMRT targeted rads
Sept'09~
new 6mm & 1 cm spots in pituitary/optic chiasm area. Rx= 25 days of 3D conformal fractionated targeted IMRT to the tumors.
Oct'09~
25 days of low dose 3D conformal fractionated targeted IMRT to the bone mets spot on rt. iliac crest that have been watching for 2 years. Added daily Aromasin back into treatment regimen.
Apr'10~ Brain MRI clear! But, see new small spot on adrenal gland. Change from Aromasin back to Tamoxifen.
June'10~ Tumor markers (CA15.3) dropped from 37 to 23 after one month on Tamoxifen. Continue to monitor adrenal gland spot. Remain on Tykerb/Herceptin/Tamoxifen.
Nov'10~ Radiate positive mediastinal node that was pressing on recurrent laryngeal nerve, causing paralyzed larynx and a funny voice.
Jan'11~ MRI shows possible activity or perhaps just scar tissue/necrotic increase on 3 previously treated brain spots and a pituitary spot. 5 days of IMRT on 4 spots.
Feb'11~ Enrolled in T-DM1 EAP in Denver, first treatment March 25, 2011.
Mar'11~ Finally started T-DM1 EAP in Denver at Rocky Mountain Cancer Center/Rose on Mar. 25... hallelujah.

"I would rather be anecdotally alive than statistically dead."
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