As we watched each of our five grandchildren and their friends enter this world and begin their life’s journey, it became more and more clear that something is amiss with this generation.  How are your children and your friend’s children doing?

In the United States, one of three of the children in this generation suffers from a chronic illness.  Perhaps it’s cancer, or birth defects, perhaps asthma, or a problem that affects the child’s mind and behavior, such as Downs Syndrome, learning disorders, ADHD or autism.  Though one in three may sound exaggerated, unbelievable, the figures are there amidst various government files.

This generation is different.  Childhood cancer, once a medical rarity, has grown 67 percent since 1950.  Asthma has increased 140 percent in the last twenty years and autism rates without a doubt have increased at least 200 percent.  Miscarriages and premature births are also on the rise, while the ratio of male babies dwindles and girls face endometriosis even in teenage.

The generations born from 1970 on are the first to be raised in a truly toxified world.  Even before conception and on into adulthood, the assault is everywhere: heavy metals and carcinogenic particles in air pollution; industrial solvents, household detergents, prozac and radioactive wastes in drinking water; pesticides in flea collars; artificial growth hormones in beef, arsenic in chicken; synthetic hormones in bottles, teething rings and medical devices; formaldehyde in cribs and nail polish, and even rocket fuel in lettuce.   Pacifiers are now manufactured with nanoparticles from silver, to be sold as “antibacterial.”  What’s wrong with rinsing a pacifier in soapy water?

Despite naysayers (who pays them to say nay? ”that’s a whole story in itself), it’s clear there is both an association and a causative connection between the vast explosion of poisons in our everyday lives and our children’s “issues.”  Over 80,000 industrial chemicals (tested only by the manufacturer) are in commerce in this country, produced or imported at 15 trillion pounds a year.   Pesticide use has leapt from the troubling 400 million pounds Rachel Carson wrote about in the 1960s to the mind-boggling 4.4 billion pounds in use today.   Nuclear power plants, aging and under-maintained, increasingly leak wastes, often without notifying their community.

What could be more elemental than our desire to protect our children.  Children and fetuses, because of their undeveloped defense systems, are ten to sixty-five times more susceptible to specific toxics than adults.  These toxics diminish the capacities of our children…the future of our families, our communities, our nation, and yours.

Illness does not necessarily show up in childhood.  Environmental exposures, from conception to early life, can set a person´s cellular code for life and can cause disease at any time, through old age. This accounts for the rise in Parkinson´s and Alzheimer´s diseases, prostate and breast cancer.

Yet this is not the dispiriting “Bad News” it might seem.  It is, actually, a message of hope and optimism.  We are fearful only when we are ignorant and powerless.  Now that we know what is happening, we can determine not to let it happen further.

These poisons are manmade; manufacturers can take them out of our children´s lives and make profits from safe products.  “Green chemistry” can replace toxic molecules with harmless ones.  We can connect global climate change actions to environmental health strategies.  If we replace coal-fired power, in the process we reduce not only carbon but also emissions of the tons of lead, mercury, hydrochloric acid, chromium, arsenic, sulfur and nitrogen oxides that cause autism, Alzheimer’s and other public health menaces.

We cannot bury our heads and hope it will all go away.  We cannot leave the job to someone else.  Some may feel the problem is so massive, it’s best to pretend it doesn’t exist.  But it isn’t more massive than we allow it to be.  It’s totally within our reach.

Here America, we look to Europe for ideas and strategies you have used, for the research coming out of your universities, for an understanding of the politics that enable your governments to pass strong environmental health laws.  The weed killer named atrazine in the U.S., made by Syngenta, a Swiss company, has never been approved for use in Europe.  But in the U.S., it is used on tens of millions of acres of farmland, on our lawns, gardens, parks, and golf courses.   Why?  And why has Europe begun screening chemicals under the REACH program, while industry in the U.S. has successfully opposed it?

Learning from each other, we can make each other smarter and stronger.  It is in our power to learn about what harms our children, to share our knowledge, and to demand action.

Author: Alice Shabecoff for CSN – Chemical Sensitivity Network, September 14, 2009

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Alice Shabecoff is the co-author with her husband Philip of Poisoned Profits: The Toxic Assault on our Children, published by Random House last year.  See their website, www.poisonedprofits.com.

Research by UC Riverside scientists is first to link passive smoking to nonalcoholic fatty liver disease

A team of scientists at the University of California, Riverside has found that even second-hand tobacco smoke exposure can result in nonalcoholic fatty liver disease (NAFLD), a common disease and rising cause of chronic liver injury in which fat accumulates in the liver of people who drink little or no alcohol. 

The researchers found fat accumulated in liver cells of mice exposed to second-hand cigarette smoke for a year in the lab. Such fat buildup is a sign of NAFLD, leading eventually to liver dysfunction. 

In their study, the researchers focused on two key regulators of lipid (fat) metabolism that are found in many human cells as well: SREBP (sterol regulatory element-binding protein) that stimulates synthesis of fatty acids in the liver, and AMPK (adenosine monophosphate kinase) that turns SREBP on and off. 

They found that second-hand smoke exposure inhibits AMPK activity, which, in turn, causes an increase in activity of SREBP. When SREBP is more active, more fatty acids get synthesized. The result is NAFLD induced by second-hand smoke. 

“Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development,” said Manuela Martins-Green, a professor of cell biology, who led the study. “Our work points to SREBP and AMPK as new molecular targets for drug therapy that can reverse NAFLD development resulting from second-hand smoke. Drugs could now be developed that stimulate AMPK activity, and thereby inhibit SREBP, leading to reduced fatty acid production in the liver.” 

Results of the study appear in the September issue of the Journal of Hepatology. 

The study emphasizes that discouraging cigarette smoking helps prevent not only cardiovascular disease, pulmonary disease and cancer, but now also liver disease. 

Second-hand smoke is the combination of smoke exhaled by a smoker and smoke given off by the burning end of a tobacco product. Lingering in the air long after tobacco products have been extinguished, it is involuntarily inhaled by nonsmokers in the vicinity. 

Second-hand smoke is a major toxicant that affects children, the elderly and nonsmokers living in the household of adults who smoke. Many state and local governments have passed laws prohibiting smoking in public facilities. Diseases associated with second-hand smoking include cancer, heart disease, atherosclerosis, pneumonia, bronchitis and severe asthma. 

Despite the large body of scientific evidence documenting the effects of passive or active smoking on the heart and lungs, reports investigating how smoking causes liver injury are scant. 

“Until our study, second-hand smoking had not been linked to NAFLD development,” Martins-Green said. 

She was joined in the study by her graduate student Hongwei Yuan (first author of the research paper and now a postdoctoral researcher in her lab) and UC Riverside’s John Shyy, a professor of biomedical sciences. Next, the team plans to investigate the clinical relevance of their findings. A grant to Martins-Green from Philip Morris USA, Inc., supported the research. 

Reference: University of California, Second-hand smoking results in liver disease, study finds, RIVERSIDE, Calif., September 10, 2009

Picture: Martins-Green lab, UC Riverside

Scientists here are the first to demonstrate that the link between diesel fume exposure and cancer lies in the ability of diesel exhaust to induce the growth of new blood vessels that serve as a food supply for solid tumors. 

The researchers found that in both healthy and diseased animals, more new blood vessels sprouted in mice exposed to diesel exhaust than did in mice exposed to clean, filtered air. This suggests that previous illness isn’t required to make humans susceptible to the damaging effects of the diesel exhaust. 

The tiny size of inhaled diesel particles, most less than 0.1 microns in diameter, potentially enables them to penetrate the human circulatory system, organs and tissues, meaning they can do this damage just about anywhere in the body. A micron is one millionth of a meter. 

Diesel exhaust exposure levels in the study were designed to mimic the exposure people might experience while living in urban areas and commuting in heavy traffic. The levels were lower than or similar to those typically experienced by workers who use diesel-powered equipment, who tend to work in mines, on bridges and tunnels, along railroads, at loading docks, on farms and in vehicle maintenance garages, according to the U.S. Department of Labor. 

“The message from our study is that exposure to diesel exhaust for just a short time period of two months could give even normal tissue the potential to develop a tumor,” said Qinghua Sun, senior author of the study and an assistant professor of environmental health sciences at Ohio State University. 

“We need to raise public awareness so people give more thought to how they drive and how they live so they can pursue ways to protect themselves and improve their health. And we still have a lot of work to do to improve diesel engines so they generate fewer particles and exhaust that can be released into the ambient air.”

The research appears online and is scheduled for later print publication in the journal Toxicology Letters. 

The researchers experimented with mice that resembled two conditions that could be present in a human body. In one, the scientists implanted a small platform seeded with normal endothelial cells, the cells that line blood vessels, under the skin of the mice. This was designed to mimic relatively normal conditions in human bodies for cell growth. 

In the other, the researchers created an environment that would follow a significant loss of blood flow to a section of a vessel, called ischemia, in the hind limbs of the mice. This generated severe hypoxia, an area with low or no oxygen, a condition that is present in certain diseases. 

Both types of mice were then exposed to either whole diesel exhaust containing particles at a concentration of about 1 milligram per cubic meter, or to filtered outdoor air, for six hours per day five days a week. The rest of the time they breathed filtered air in their cages. Effects of the exposure were measured after two weeks, five weeks and eight weeks of the exposures.  

Though some blood vessel growth and chemical changes could be seen in the mice after two weeks of exposure, “generally, the longer the exposure, the more effects we could see,” said Sun, also an investigator in Ohio State’s Davis Heart and Lung Research Institute. “It’s difficult to translate outcomes from an animal study directly to the human experience, but the bottom line is, the shorter the exposure to diesel exhaust, the better.” 

The exposure to diesel exhaust caused a six-fold increase in new blood vessel formation in the ischemic hind limbs after eight weeks and a four-fold increase in vessel sprouting in the normal hind limbs of the mice in the same amount of time, compared to mice breathing filtered air.  

The researchers also saw significantly more blood vessel growth in the implanted cells and in rings of tissue taken from the aortas of mice exposed to the exhaust compared to the control mice exposed to clean air. In fact, the researchers found that three types of blood vessel development occurred in these areas after exposure to the diesel exhaust: angiogenesis, the development of new capillaries; arteriogenesis, the maturation or re-started growth of existing vessels; and vasculogenesis, the formation of new blood vessels. 

All of these processes are associated with tumor growth, but unprogrammed angiogenesis in particular can wreak havoc in the human body, Sun said. 

“Whenever you talk about a solid tumor, angiogenesis is one of the fundamental mechanisms behind its development. Angiogenesis provides the means for tumor cells to grow because they have to have a blood supply. Without a blood supply, solid tumors will not grow,” he said. 

“We want our bodies to generate new blood vessels only when we need them. And then stop producing them when we need them to stop.” 

Though the researchers have not defined every mechanism behind these processes, they sought to explain at least a few ways in which blood vessels are able to sprout or mature after exposure to diesel exhaust.  

They observed that diesel exhaust exposure activated a chemical signal, vascular endothelial growth factor, which has long been associated with new blood vessel development. The exposure also increased levels of a protein, hypoxia-inducible factor 1, that is essential to blood vessel development when oxygen levels are low. At the same time, the presence of the exhaust lowered the activity of an enzyme that has a role in producing substances that can suppress tumor growth. 

The scientists also tracked low-grade inflammation in tissues exposed to the exhaust, which is often associated with tumor development. 

Though the tiny size of diesel exhaust particles may contribute to their ability to penetrate all areas of the body, Sun noted that their complex chemical composition, and the way in which those chemicals are released once particles enter the body, also influence how they react with human cells.  

Gasoline exhaust particles are larger than diesel fume particles, but it’s premature to suggest that they are any less dangerous to humans, Sun said. 

“The bigger particles are known to be harmful primarily for upper respiratory tract illnesses. Larger particles also can’t travel long distances – they tend to fall to the ground,” he said. “Smaller particles hover in the air for a long time and can have long-term impact on humans when inhaled.”

Sun and colleagues are now conducting a study testing whether the exhaust particles promote tumor development and metastasis. 

This work is supported by Health Effects Institute awards and grants from the National Institutes of Health.  

Reference:    Ohio State University, Diesel Exhaust is linked to Cancer Developement via new Blood Vessel Growth, Columbus, Ohio, September 2, 2009

New study suggests possible genetic links between environmental toxins and multiple myeloma

The International Myeloma Foundation (IMF) – supporting research and providing education, advocacy and support for myeloma patients, families, researchers and physicians – today said newly published data may provide a possible genetic link between environmental toxins and bone disease in multiple myeloma. Myeloma, also called multiple myeloma, is a cancer of cells in the bone marrow that affect production of blood cells and can damage bone. Once considered a “rare disease of the elderly,” it is increasingly being diagnosed in patients under 45 years old, including some of the early responders to the 9/11 World Trade Center site. Now a study published this week may help explain why.

The study from researchers with the IMF gene bank identified several changes in DNA sequences called SNPs (single nucleotide polymorphisms) that are associated with a risk of bone disease in myeloma. Further analyses showed that many of these DNA changes may be involved with the way the human body responds to certain environmental toxins, providing a possible link between myeloma and the environment. The findings were published in the latest issue of the journal Leukemia*.

Brian G.M. Durie, M.D., lead author of the study and Chairman of the IMF said: “This is a hypothesis-generating study. While the functional role of many SNPs is still uncertain, this study is supportive of the notion that genetic factors affecting toxin breakdown may be related to the development of myeloma. This gives us an important starting point for further studies.”

The findings may help explain a widely reported study this week in the Journal of Occupational and Environmental Medicine, that found more cases of myeloma among younger responders to the 9/11 World Trade Center site than would normally be expected. The findings are also supportive of a study published earlier this year that suggests a link between certain pesticide exposures in agricultural workers and a precursor to multiple myeloma. Previous studies have also shown an increased risk for myeloma among firefighters, and the IMF has issued guidelines for firefighters for the prevention and treatment of this disease.

“Multiple myeloma is not a familiar cancer to patients or even to many doctors, but taken together, these studies say it should not be overlooked,” said Susie Novis, President and Co-founder of the IMF. “While multiple myeloma cannot be cured, it can be treated with new, targeted therapies. These studies tell us it is critically important for medical practitioners to know the possible risk factors for myeloma along with the early warning signs so they will be alerted to test for it.”

Myeloma affects an estimated 750,000 people worldwide, and in industrialized countries it is being diagnosed in growing numbers and in increasingly younger people.

Reference: International Myeloma Foundation gene bank, Bank on a Cure North Hollywood, CA, New study suggests possible genetic links between environmental toxins and multiple myeloma, Eureka, August 13, 2009

International Journal of Occupational and Environmental Health Features Discovery of Asbestos-Related Pain Origin from Scientists at the Karmanos Cancer Institute in Detroit 

Scientists at the Barbara Ann Karmanos Cancer Institute’s National Center for Vermiculite and Asbestos-Related Cancers (NCVAC) have discovered a probable reason for the unrelenting chest pain experienced in certain patients with asbestos-related diseases and cancers. The findings, featured in the July 20, 2009 edition of the International Journal of Occupational and Environmental Health, were published in an academic peer-reviewed manuscript by principal author Michael Harbut, M.D., MPH, co-director of the NCVAC and chief of the Center for Occupational and Environmental Medicine, affiliated with Wayne State University.  

Harbut reported the findings after studying a patient who was exposed to taconite dust as a child.  

Using a new radiography approach developed by Carmen Endress, M.D., FACR, associate professor of Radiology, Wayne State University School of Medicine and radiologist at the NCVAC, there was a documented increase in pleural plaques, causing erosion on the interior wall of the ribs. 

“This action of the pleural plaque against the covering of the bone and the bone itself is a biologically plausible and an anatomically logical explanation of the unrelenting pain which some patients experience,” said Dr. Harbut.

This new imaging approach involves enhancing images obtained on the 64-slice high resolution CT scan using the Vitrea(R) imaging software program by Vital Images. By using this imaging approach, Dr. Harbut was able to demonstrate that: 

Evidence based on the CT findings, the physical examination, pulmonary function studies, epidemiology and history of the patient’s intractable pleural pain meets the criteria for diagnosis of asbestosis. Combined with the known science of taconite dust, a link between the mine where the patient’s father worked and the patient’s disease was established.  

Due to the clarity and definition of this new imaging approach, it is more likely to detect asbestos-related diseases and cancer at an earlier stage.  

Earlier detection will allow the possibility for additional treatment options to manage the pain caused by pleural plaque beyond the narcotics often prescribed for patients with advanced stages of asbestos disease. This includes exploring other forms of traditional and nontraditional methods to control pain.  

The patient, studied since 2004 and currently 55 years of age, was exposed as a child to taconite dust unknowingly by her father, a taconite miner from 1962 – 1969, who carried the taconite dust on his work clothes. Taconite is used in the production of steel and road-patching material. It has been mined in Michigan and Minnesota. 

The patient has experienced increasing pain on her right side for the past 31 years, a persistent cough and wheezing. As the pain increased so did her medication. Using the new imaging approach, Dr. Harbut was able to show the progression of the patient’s pleural plaque over a three year period, from 2005 – 2008. The patient’s pleuritic pain, as well as the findings of her pulmonary function, physical exam and symptomology are consistent with those diagnosed with asbestosis and pleural plaques, as established by the American Thoracic Society.  

These findings also support earlier human and animal reports that dusts produced by taconite mining can evoke the same biological responses as do other fibers already defined as asbestos or asbestiform materials. 

Harbut added, “Patients often require a lifetime of narcotics to allow functioning, but we are hopeful that with this new imaging technology, more selective pain management approaches with fewer side effects can be instituted resulting in a better quality of life.”

Finally, the report supports the identification of taconite, which has not yet been categorized as asbestos but causes a disease consistent with asbestosis, and recommends a reevaluation of the definition of asbestos. This is especially important within the context of legislative efforts to prohibit the use of asbestos. 

Karmanos scientists are continuing their series of patient studies and will submit similar findings for peer review later this summer.  

In addition to Dr. Harbut, co-authors of the report include Carmen Endress, M.D., FACR; John J. Graff, Ph.D., MS, assistant professor, Wayne State University School of Medicine, and chief, Cancer Surveillance Research at the Barbara Ann Karmanos Cancer Institute; Christopher Weis, Ph.D., National Enforcement Investigations Center, United States Environmental Protection Agency; and Harvey Pass, M.D., director, New York University’s Division of Thoracic Surgery.  

About the National Center for Vermiculite and Asbestos-Related Cancers (NCVAC at Karmanos)  

In response to the United States Environmental Protection Agency’s (EPA) identification of major sources of public asbestos exposure in Michigan, and to address the need for early diagnosis and aggressive treatment of asbestos-related diseases, the Barbara Ann Karmanos Cancer Institute and the Center for Occupational and Environmental Medicine (COEM) affiliated with Wayne State University established Karmanos’ National Center for Vermiculite and Asbestos-Related Cancers. The NCVAC is co-directed by Michael Harbut, M.D., MPH, Karmanos Cancer Institute and Chief of the Center for Occupational and Environmental Medicine; and John J. Graff, Ph.D. MS, chief of Cancer Surveillance Research, Karmanos Cancer Institute and assistant professor, Department of Family Medicine and Public Health Sciences, Wayne State University School of Medicine. 

Reference: Barbara Ann Karmanos Cancer Institute, International Journal of Occupational and Environmental Health Features Discovery of Asbestos-Related Pain Origin from Scientists at the Karmanos Cancer Institute in Detroit , US Newswire, DETROIT, July 20, 2009.