
<b>OCCUPATIONAL and ENVIRONMENTAL EXPOSURES</b>

Considerable evidence supports a relationship between occupational chemicals as <b>vinyl chloride, phenoxyacetic acid herbicides, chlorphenols, dioxin, arsenical pesticides and medications, medicinal measures as Thorotrast exposure , immunosuppressive drugs, alkylating agents, androgen-anabolic steroids,</b> and cutting oil exposure , and the development of soft tissue sarcoma. 
Statistical models identified different odds ratios across sarcoma subtypes for plywood exposure and exposure to wood and saw dust. Although exploratory, this analysis suggests that occupational risk factors for sarcoma are not uniform across subtypes.
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Although bone and soft tissue sarcomas are not common, a significant number of patients who develop these tumors will die with metastatic disease. Part of the reason is that many of the patients have advanced disease at diagnosis. Identification of an etiologic agent should allow for diagnosis at an earlier stage. ... The role of various chemical agents in the development of sarcomas needs further definition, as the literature is replete with conflicting reports. Problems exist in that we are dealing with a variety of agents with different levels of exposure, possibly resulting in different types of neoplasms. Additionally, many of the agents in question are not pure substances, but frequently are contaminated with other potentially carcinogenic agents. Finally, the majority of studies reported are from different countries. Thus, there may be unidentified operative genetic and environmental factors...
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<b>PREVENTION AND ENVIRONMENTAL EXPOSURE</b>
Environmental causes probably account for well over half of all cancer cases. Most environmental risks are determined by lifestyle choices (smoking, diet, etc.), while the rest arise in community and workplace settings. The degree of cancer hazard posed by these voluntary and involuntary risks depends on the concentration or intensity of the carcinogen and the exposure dose a person received. In situations where high levels of carcinogens are present and where exposures are extensive, significant hazards may exist, but where concentrations are low and exposures limited, hazards are often negligible. When low-dose exposures persist over time they can represent significant public health hazards (for example, exposure to secondhand tobacco smoke). 

Various chemicals (for example, benzene, asbestos, vinyl chloride, arsenic, aflatoxin) show definite evidence of human carcinogenicity; others are considered probable human carcinogens based on evidence from animal experiments (for example, chloroform, dichlorodiphenyl-trichloroethane [DDT], formaldehyde, polychlorinated biphenyls [PCBs], polycyclic aromatic hydrocarbons). Often in the past, direct evidence of human carcinogenicity has come from studies of workplace conditions involving sustained, high-dose exposures. Risks can be increased when particular exposures occur together (for example, asbestos exposure and cigarette smoking).
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<b>Occupational Cancer </b>

Based on well-documented associations between occupational exposures and cancer, it is estimated that approximately 20,000 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.  
Millions of U.S. workers are exposed to substances that have tested as carcinogens in animal studies.
Less than 2% of chemicals in commerce have been tested for carcinogenicity.

Cancer is a group of different diseases that have the same feature, the uncontrolled growth and spread of abnormal cells. Each different type of cancer may have its own set of causes. Many factors play a role in the development of cancer. The importance of these factors is different for different types of cancer. A person's risk of developing a particular cancer is influenced by a combination of factors that interact in ways that are not fully understood. Some of the factors include:

personal characteristics such as age, sex, and race 
family history of cancer 
diet and personal habits such as cigarette smoking and alcohol consumption, 
the presence of certain medical conditions, 
exposure to cancer-causing agents in the environment, and 
exposure to cancer-causing agents in the workplace. 
In many cases, these factors may act together or in sequence to cause cancer.

NIOSH  National Istitute of Occupational Safety and Health
The NIOSH Web site features many different types of databases and information resources. They are categorized here by Chemical; Injury, Illness & Hazards Data and Information; Publications; Respirators and other Personal Protective Equipment; Agriculture; and Construction. The most popular databases include the International Chemical Safety Cards, NIOSH Pocket Guide to Chemical Hazards, and NIOSHTIC-2.
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 <b>National Institute for Occupational Safety and Health</b>
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<b>US Dept of Labour  OSHA site
Occupational Safety and Health Administration</b>
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<b>Occupational and Environmental Epidemiology Branch,</b>
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<b>Cancer Causes and Risks,from cancer.gov </b>
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<b>Artificial implants and soft tissue sarcomas.</b>

The carcinogenic potential of artificial implants has been of concern in recent years.  ... This paper examines a possible association between artificial implants and soft tissue sarcomas.  J Clin Epidemiol. 1995
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<b>DIOXIN</b>

<b>Exposure to Agent Orange and occurrence of soft-tissue sarcomas </b>

Agent Orange was the most common herbicide used in the Second Indochina War in the course of military operations in the former South Vietnam. Agent Orange is contaminated by the carcinogen 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD) in mean concentrations of 2 mg/kg. After much dispute of a causal association between exposure to herbicides containing TCDD and occurrence of soft-tissue sarcoma ... two simultaneous case-control studies were set up in Vietnam to examine possible relationships. ..
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<b>An evaluation of dioxin/phenoxy herbicides/chlorophenols exposure and soft tissue sarcoma </b>

A review of employment records and tissue specimens of seven workers, reported previously as having occupational dioxin exposure and soft tissue sarcomas, confirms that ... Methodological problems are discussed which must be addressed in the epidemiologic evaluation of the outcome of soft tissue sarcoma.
Other studies cited as well.
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<b>Risk of soft tissue sarcomas and residence near incinerator of industrial wastes.</b>

To investigate the association between occurrence of soft tissue sarcomas (STS) in Mantua and residence near an incinerator of industrial wastes. 
.. CONCLUSION: The study shows a significant increase in risk of STS associated with residence within 2 km of an industrial waste incinerator; an aetiological role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be hypothesised.  Occup Environ Med. 2003
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<b>dioxin and sarcoma</b>
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<b>VINYL CHLORIDE and POLYMERIC MATERIALS</b>
 
<b>Exposure to polymeric materials in vascular soft-tissue sarcomas.</b>

..Since 1974, several reports have appeared on a distinct relationship between the exposure to vinyl chloride monomers and angiosarcomas of the liver. ...
..Among 21 adult cases of vascular sarcomas there were 4 patients with occupational exposure to vinyl chloride (VC) either alone or together with other artificial polymers. Seven other patients showed exposure to several plastics or resins other than VC. Altogether, 11 of 21 (52%) of the explored patients were found to have been exposed to artificial polymeric materials over a mean period of 18 years. ...

This study offers new evidence of the occurrence of vinyl-chloride-induced angiosarcomas outside the liver and confirms observations that have previously been published in case reports. Moreover, it may be suspected from this analysis that polyvinyl chloride and its monomers are not the only polymeric materials that may contribute to an induction of angiosarcomas in humans. Repeated occupational histories have to be taken from the patients to achieve data of the greatest value, since there are many professional activities that do not primarily lead to the assumption of specific exposure to polymeric materials.  
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<b>Vinyl chloride-specific mutations in humans and animals.</b>

Vinyl chloride is a potent hepatocarcinogen which reacts with DNA to generate etheno bases. In order to determine whether mutational patterns in target genes in vivo are characteristic of vinyl chloride ... Two alterations were found which could be attributed to a direct effect of vinyl chloride: ... in human liver angiosarcomas, and lesions ...which lead to mutations in the p53 gene in human ...
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<b>[The carcinogenic potential of biomaterials in hernia surgery]</b>

... In conclusion, there are no data so far indicating a real risk for humans to develop malignant tumors due to implanted meshes. Therefore we further propagate the implantation of meshes in hernia repair in adult patients.
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<b>EPA site for radiation exposure
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Exposure to Tobacco Smoke
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Environmental Exposures and Cancer

cancer.gov
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Majority of Cancers are Linked to the Environment
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Breast Cancer and the Environment Studies 
supported by NCI
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<b>HEAVY METAL EXPOSURE</b>   
Heavy metals are metals like lead, arsenic, cadmium.  Lead is present in old paint, in some painted bowls, in leaded gasoline exposure.
 
<b>Enhanced invasiveness of tumour cells after host exposure to heavy metals.</b>

The invasiveness of tumour cells to heavy metal-exposed host cells or tissues was investigated....The results suggest that heavy metal-induced metallothioneins serve as a host-derived factor in malignant disease and closely relate to metastasis.
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<b>Implanted depleted uranium fragments cause soft tissue sarcomas in the muscles of rats.</b>

In this study, we determined the carcinogenicity of depleted uranium (DU) metal fragments containing 0.75% titanium in muscle tissues of rats. The results have important implications for the medical management of Gulf War veterans who were wounded with DU fragments and who retain fragments in their soft tissues.
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..After lifetime observation, the incidence of soft tissue sarcomas increased significantly ... These results indicate that DU fragments of sufficient size cause localized proliferative reactions and soft tissue sarcomas that can be detected with radiography in the muscles of rats. 
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<b>Arsenic exposure and carcinogenesis.</b>

Arsenic is well established as a human carcinogen,... Arsenic ...may act as a carcinogen through inhibition of DNA repair mechanisms, leading indirectly to increased mutations from other DNA damaging agents. 

.. Although our findings need verification in a larger study group, they are consistent with the hypothesis that inhibition of DNA repair capacity is a potential mechanism for the co-carcinogenic activity of arsenic. 
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<b>Occupational exposure to heavy metals: </b>

DNA damage induction and DNA repair inhibition prove co-exposures to cadmium, cobalt and lead as more dangerous than hitherto expected 

Co-exposure to cadmium, cobalt, lead and other heavy metals occurs in many occupational settings, such as pigment and batteries production, galvanization and recycling of electric tools. However, little is known about interactions between several heavy metals. ...

.. In conclusion, the hazard due to cobalt exposure ... seems to be underestimated, especially when individuals are co-exposed to cadmium or lead. Co-exposure may cause genotoxic effects, even if the concentrations of individual heavy metals do not exceed TRK-values. 
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<b>Molecular and cellular mechanisms of cadmium carcinogenesis</b>.

Cadmium is a heavy metal, which is widely used in industry, affecting human health through occupational and environmental exposure. In mammals, it exerts multiple toxic effects and has been classified as a human carcinogen by the International Agency for Research on Cancer. 

Cadmium affects cell proliferation, differentiation, apoptosis and other cellular activities. ... indirect mechanisms are implicated in the carcinogenicity of cadmium. In this review multiple mechanisms are discussed, ... The inhibition of DNA repair processes by cadmium represents a mechanism by which cadmium enhances the genotoxicity of other agents and may contribute to the tumor initiation by this metal. The disruption of E-cadherin-mediated cell-cell adhesion by cadmium probably further stimulates the development of tumors. It becomes clear that there exist multiple mechanisms which contribute to the carcinogenicity of cadmium, ...
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<b>Hepatic angiosarcoma and heavy metal exposures</b>

Hepatic angiosarcoma .... One fourth of the cases have demonstrated a relation with chemical carcinogens with the most frequent being thorium dioxide (thorotrast) and vinyl chloride. The case of an hepatic angiosarcoma which presented as an intraperitoneal hemorrhage in a patient who had undergone treatment with Neosalvarsan (dioxidiaminoarsenobenzol) 46 years beforehand is reported. The previous published reports include 6 cases of hepatic angiosarcoma related with treatment with arsenic salts and 4 cases in whom exposure was environmental.
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<b>Corrosion products and their role in malignancy</b>

We report a case of malignant fibrous histiocytoma of the bone that developed 20 years after a femoral fracture treated by plate-screw fixation. 

Similar cases reported over the past fifteen years in the literature suggest the possible mechanisms of sarcomatous degeneration. 

The possible carcinogenic effect of corrosion products is emphasized. ..[Analysis] of the tumor demonstrated the presence of chromium, iron and nickel at different concentrations. The association with other elements clearly demonstrates that the corrosion products were metabolized. The presence of metallic components in tumoral cells suggests a possible relationship between metallic implants and malignancy. 

These observations emphasize the importance of creating a national, or even international, registry of malignant tumors that develop in contact with metallic implants in order to search for a possible cause and effect relationship.
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<b>Cancer burden from arsenic in drinking water in Bangladesh.</b>
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<b>Tissue studies of persons with intakes of the actinide elements: the U.S. Transuranium and Uranium Registries.</b>

For more than three decades, the United States Transuranium and Uranium Registries (USTUR) have studied the biokinetics, dosimetry, and biological effects of plutonium, uranium, and americium through voluntary postmortem tissues from persons with known intakes. Radiochemical analyses of tissue obtained at autopsy have shown that plutonium and americium have different biokinetics and an appreciable deposition in the soft tissues of the body as well as the known depots in skeleton and liver. Studies of whole-body Thorotrast donors to the USTUR indicate that commonly accepted risk coefficients for alpha induction of bone sarcoma may be too high while those for leukemia are a factor of six too low. ,,,
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<b>Risk of esophageal, ovarian, testicular, kidney and bladder cancers and leukemia among Finnish workers exposed to diesel or gasoline engine exhaust</b>.
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<b>Risk analysis of drinking water microbial contamination versus
disinfection by-products (DBPs)</b>.
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<b>Formaldehyde and Cancer</b>
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<b>Thorotrast</b>

 is an alpha-particle-emitting radiological contrast medium that caused chronic exposure to internal alpha-particle radiation when it was administered systemically. Cancer incidence in 432 Swedish patients exposed to Thorotrast was evaluated by computerized linkage of the cohort with the Swedish Cancer Register. Standardized incidence ratios (SIRs) were calculated as the ratio of observed cases in the cohort to expected cases in the general population. A total of 170 cancers occurring in 152 individuals were reported, whereas only 57 cases were expected. The SIR was significantly increased for cancer at all sites (3.0), with the largest excesses noted for primary liver and gallbladder cancer (SIR = 39.2). Other significantly elevated risks were observed for liver cancer not specified as primary, small intestine cancer, stomach cancer, leukemia, kidney cancer, CNS tumors, and pancreatic cancer. Among women, there was a significantly increased risk for lung cancer, based on a small number. Our results show that cumulative radiation exposure is directly related to carcinogenesis in the liver and gallbladder, which is consistent with earlier findings. In addition, there may be a relationship between radiation exposure and the development of other solid tumors
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<b>Active Smoking</b>

 Our study provides evidence that active smoking may play a
role in breast cancer etiology and suggests that further research into
the connection is warranted, especially with respect to genetic
susceptibilities...
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<b>Nickel-induced cancerous transformation </b>...

Nickel (Ni) compounds are potent carcinogens and can induce malignant transformation of rodent and human cells...
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<b>Angiosarcoma associated with foreign body material. A report of three cases.</b>

The production of tumors through solid-state mechanisms has been demonstrated in experimental animals, but foreign body tumorigenesis has not been proven definitively in man. The authors report three patients with angiosarcoma that occurred in intimate association with foreign material retained for prolonged periods. ... Review of the literature disclosed six cases of angiosarcoma and 40 cases of sarcomas of other histologic types associated with foreign material, with latency periods of from 4 months to 63 years. Implanted foreign material thus should be considered capable of inducing virtually any form of sarcoma in humans.
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<b>Neoplastic transformation of human cell lines by heavy metal-tungsten alloy particles</b>.

                Heavy metal-tungsten alloys (HMTAs) are dense heavy metal composite materials used primarily in military applications. HMTAs are composed of a mixture of tungsten (91-93%), nickel (3-5%) and either cobalt (2-4%) or iron (2-4%) particles. ...
Like the heavy metal depleted uranium (DU), the use of HMTAs in military munitions could result in their internalization in humans. Limited data exist, however, regarding the long-term health effects of internalized HMTAs in humans. ...This is the first report showing that HMTA mixtures of W, Ni and Co or Fe cause human cell transformation to the neoplastic phenotype. While additional studies are needed to determine if protracted HMTA exposure produces tumors in vivo, the implication from these ... results is that the risk of cancer ...from internalized HMTAs exposure may be comparable with the risk from other biologically reactive and insoluble carcinogenic heavy metal compounds (e.g. nickel subsulfide and nickel oxide).
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<b>Increase in neoplasia in mice offspring after preconception exposure of parents to urethane or chromium(III)</b>

 ...The present study examined the hypothesis that preconception carcinogenesis involves an increase in the rate of occurrence of neoplasms ...
.. Offspring (48-78/sex/group) were examined for all grossly apparent changes when moribund or at natural death, followed by histopathological diagnosis and statistical analysis. 
Significant exposure-related changes occurred in multiple organs. Ten to 20 percent of offspring showed changes related to paternal exposure, including at least one sired by most treated males. ...
[list of lesions. ]   Thus, preconception exposure of fathers to toxicants had a significant impact on both neoplastic and non-neoplastic changes in almost all tissues in which these lesions often occur naturally during the aging process. .
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