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The World Resources Institute, Washington, D.C. reports that cancer mortality is increasing with little explanation of the cause. The first step in preventing cancer is identifying known carcinogens, many of which readily are found in the workplace. The second step is empowering our system of civil justice to hold accountable the manufacturers and distributors of these carcinogens. The plaintiffs’ bar knows that cancer prevention will become the watchword of American business when it is no longer profitable to use or manufacture products, pesticides and preservatives that contain cause cancer.

The following chemicals are commonly found in construction and industrial settings. They should never be used without protective clothing and breathing protection. To easily learn how dangerous the following chemicals are ask your local dump operator how to legally dispose of them.


Benzene causes leukemia. It is commonly found in construction solvents, as well as paints, inks, adhesives, rubbers, glues, stain removers, and furniture wax. It has been used as an antiknock additive in gasoline. Rubber workers exposed to benzene had a tenfold increase in leukemia. The National Institute for Occupational Safety and Health recommends workers should not be exposed to 1 parts per ten million. Gasoline fumes have 1,000 times the concentration recommended by NIOSH.

Polyvinyl Chloride

Polyvinyl chloride, a plastic used in pipe, electrical wire and cable, home furnishings, toys, packaging, upholstery and auto parts, is made from vinyl chloride. It causes liver cancer, with a latency period is 15 to 40 years. Never inhale smoke from burning foam or plastic, such as in a car fire, and never dispose of these materials in a scrap fire or fireplace.

Methylene Chloride

Methylene chloride is a popular solvent for resins, fats, and waxes and is used in paint, thinners, removers, adhesives, film, plastics, inks, foams, hairsprays, air fresheners, and printed circuit boards. Exposed workers have an increased incidence of pancreatic and liver cancer deaths. It produces malignant liver and lung neoplasms in animals. EPA considers it a probable human carcinogen.


Trichloroethylene (TCE) is used for degreasing metal parts. It has been found in typewriter correction fluids, paint removers and strippers, adhesives, and spot removers. TCE in mice produces liver and lung tumors, kidney cancers, testicular tumors and leukemia in rats. Exposed workers have a high incidence of bladder cancer and lymphomas. It is probably a human carcinogen.


Tetrachloroethylene and perchloroethylene have been used in dry cleaning, degreasing metal, suede protectors, paint removers, water repellents, silicone lubricants, adhesives, spot removers, wood cleaners and many products used by hobbyists. In studies of rats and mice, liver and kidney cancers and leukemia have been produced at a sufficient level to cause EPA to classify it as an animal carcinogen and a probable human carcinogen. Old cans of spot remover contain this material.

Polychlorinated Biphenyls

Polychlorinated biphenyls (PCBs) include 209 related chemicals and are found in transformers manufactured before 1977, older welding equipment, x-ray machines, refrigerators and in fluorescent light fixtures. In laboratory tests PCBs cause liver, pituitary, and gastrointestinal tumors, as well as leukemia and lymphomas. EPA considers PCBs probable human carcinogens.

Methyl Ethyl Ketone

MEK is a colorless, volatile, organic solvent with a pleasant pungent odor akin to lacquer thinner. It is commonly used as a cleaning solvent in construction. Chronic inhalation of MEK vapors at concentrations in the range of 100-300 PPM and higher is toxic to the adult central nervous system. Headache, dizziness, and mental confusion are common early signs of MEK’s neurotoxic potential. MEK also has the peculiar property of potentiating the neurotoxicity of other organic solvents. MEK has a remarkable ability to enter the body through intact human skin. Animal developmental toxicology studies on MEK in peer-reviewed literature show it is fetotoxic; it has the capacity to interfere with normal fetal growth and development. If this occurs throughout gestation can actually cause much more devastating and irreparable harm, especially if the affected system is the developing central nervous system.

MEK’s fetotoxic ability is dose-dependent, with the nature and extent of fetal harm increasing as the daily dose and the duration of exposure increases. The animal toxicology studies on MEK are all large, well-designed studies and all demonstrate significant dose-related fetotoxicity, namely intra-uterine growth retardation. As a result, the U.S. EPA set a “reference dose” of .3 PPM for human inhalation exposure to MEK. The dose of MEK absorbed into the bloodstream of a pregnant woman is approximately the dose delivered through the placenta to her fetus. As a result, if a pregnant woman is routinely breathing air containing significantly more than .3 PPM of MEK, her fetus will be receiving a fetotoxic dose of MEK. Daily doses of MEK in common workplace settings, where MEK is used as a solvent without positive ventilation or protective equipment, result in air concentrations several hundred times greater than the so-called “safe harbor” reference dose.

Chlorinated Hydrocarbons: Dioxins and Furans

Dioxins and furans are found in chlorinated organic solvents, pesticides, weed killers, wood preservatives, such as pentachlorophenol, and charcoal starter. Although no longer manufactured in the U.S., they can still be found in the herbicide 2,4-D and 2,4,5-T. EPA considers dioxin to be a “cancer promoter” and classifies it as a probable human carcinogen responsible for leukemia, lymphoma, Non-Hodgkins Lymphoma and soft-tissue sarcoma’s which have latency periods of 20+ years. Unfortunately today’s treating physician rarely inquires concerning potential causation when the immediate need is to provide care, but all such cancers should be closely scrutinized to determine a toxic starting point.

Proving Dioxin Exposure

Long latency periods are a significant, but not insurmountable, challenge in proving toxic chemical exposure cases. In 1995 our firm represented Long latency periods are a Joe Pickering who died from a soft tissue sarcoma – very rare in a 40 year old – as a result of being exposed to dioxin laden “Weed B Gon” manufactured by Chevron under its Ortho line of products. Joe was exposed to silvex during the early 1970s when we worked on a bottling line in Martinez, California. During that time, silvex [2,,4,5 TP] was the prime component of Weed B Gon and although we litigated this case in 1994-95, we located and tested cans of Weed B Gon found in garages in South San Francisco Bay’s Santa Clara County where they had been sitting for 20 years. We were able to time date the products based on Chevron’s label numbers. The products we tested which had been bottled in 1972-74, contained 2, 4 D and 2, 4, 5 TP [silvex] that were loaded with dioxins. Because of that testing we were able to successfully conclude that legal claim for Joe Pickering.

This is not the first case in which we have found “archive” samples of chemical carcinogens sitting on garage shelves. We successfully followed the same protocol in a leukemia cluster in Northern California where we proved that dioxin laced pentachlorophenol was the cause of four leukemias in employees of a small lumber mill operated by the Simpson Lumber Company in Arcata, California. In that case the offending product was Woodlife which contained pentachlorophenol heavily contaminated with dioxins and furans. In fact, a twenty -year old bucket of Woodlife found in a former employee’s garage, when subjected to mass spectroscopy, showed a pattern of dioxins that correlated with the pattern of dioxins found in our client’s body fat. The match was not perfect, but after 20 years we were still able to prove a correlation factor of 80% and end any doubt to the validity of our claim that exposure to Woodlife was the cause of these leukemias.

Construction laborers and landscaping crews who regularly used Weed B Gon and who have suffered a chronic exposure are progressing towards a time when soft tissue sarcomas, leukemias, and Non-Hodgkins Lymphomas, among others, may be presenting, twenty years after the fact. That’s what we learned from Seveso dioxin explosion and which has been confirmed in our own cases. The sad fact is that many who will are diagnosed with these diseases may never learned that they are suffering because of workplace exposures that occurred years ago.


Corning Fiberglas Company was formed in 1938, and only three years later, in 1941, evidence of pulmonary disease was reported by Walter J. Siebert, who investigated the health of workers with the cooperation of Owens Corning.

Fiber glass is now used for thermal insulation of industrial buildings and homes, as acoustic insulation, for fireproofing, as a reinforcing material in plastics, cement, and textiles, in automotive components, in gaskets and seals, in filters for air and fluids, and for many other miscellaneous uses. More than 30,000 commercial products now contain fiber glass.

As asbestos has been phased out because of health concerns, fiber glass production in the U.S. has been rising. In 1975, U.S. production of fiber glass was 247.88 million kilograms (545.3 million pounds); by 1984 it had risen to 632.88 million kilograms (1392.3 million pounds). If that rate of growth (10.4% per year) held steady, then production of fiber glass in the U.S. in 1995 would be 4365 million pounds.

Dr. Mearl F. Stanton of the National Cancer Institute found that glass fibers less then 3 microns in diameter and greater than 20 microns in length are “potent carcinogens” in rats; and, he said in 1974, “it is unlikely that different mechanisms are operative in man.” A micron is a millionth of a meter (and a meter is about three feet). Fibers of this size not only cause cancer in laboratory animals, but also cause changes in the activity and chemical composition of cells, leading to changes in the genetic structure in the cellular immune system.

In 1970, Dr. Stanton announced that “it is certain that in the pleura of the rat, fibrous glass of small diameter is a potent carcinogen.” The pleura is the outer casing of the lungs; cancer of the pleura in humans is called mesothelioma and it is caused by asbestos fibers. Stanton’s research shows that when glass fibers are manufactured as small as asbestos fibers, glass causes cancer in laboratory animals just as asbestos does.

The International Agency for Research on Cancer (IARC), of the World Health Organization, listed fiber glass as a “probable [human] carcinogen” in 1987. In 1990, the members of the U.S. National Toxicology Program (NTP)‹representatives of 10 federal health agencies‹concluded unanimously that fiber glass “may reasonably be anticipated to be a carcinogen” in humans. In 1994, the U.S.Department of Health and Human Services reported to Congress that fiber glass is “reasonably anticipated to be a carcinogen.” In the U.S., fiber glass must now be labeled a carcinogen.

It has been 25 years since researchers at the National Cancer Institute concluded that fiber glass is a potent carcinogen in experimental animals. Since then science has well documented the hazard. Ninety percent of American homes now contain fiber glass insulation. All of this fiber glass will eventually be released into the environment and cause significant health hazards.

Special thanks to Rachel’s Environment and Health Weekly, June 1, 1995, published by the Environmental Research Foundation which provided the material on fiberglass. The ERF deserves broad base support for its commitment to a national environmental policy which makes health risks to people a national priority and for its commitment to public education. The ERF not only allows the re-distribution of its research and articles, but encourages it. ERF deserves the highest praise. Anyone interested in toxic tort litigation should subscribe to Rachel’s Weekly by calling 410.263.1584.

For more information on the health effects of fiberglass: Philip J. Landrigan, “Commentary: Environmental Disease: A Preventable Epidemic,” American Journal of Public Health Vol. 82 (July 1992), pg. 941. Peter F. Infante and others, “Fibrous Glass and Cancer,” American Journal of Industrial Medicine Vol. 26 (1994), pgs. 559-584, which reviews the following studies, among others: L. Simonato and others, “The International Agency for Research on Cancer Historical Cohort of MMMF Production Workers in Seven European Countries Extension of the Follow-Up,” Annals of Occupational Hygiene Vol. 31, No. 4B (1987), pgs. 603-623; Philip E. Enterline and others, “Mortality Update of a Cohort of U.S. Man Made Mineral Fibre Workers,” Annals of Occupational Hygiene Vol. 31, No. 4B (1987), pgs. 625-656; Harry S. Shannon and Others, “Mortality Experience of Ontario Glass Fibre Workers‹Extended Follow-UP,” Annals of Occupational Hygiene Vol. 31, No. 4B (1987), pgs. 657-662; and John R. Goldsmith, “Comparative Epidemiology.

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