Male reproductive disorders that are of interest from an environmental point of view include sexual dysfunction, infertility, cryptorchidism, hypospadias and testicular cancer.

Several reports suggest declining sperm counts and increase of these reproductive disorders in some areas during some time periods past 50 years. Except for testicular cancer this evidence is circumstantial and needs cautious interpretation. However, the male germ line is one of the most sensitive tissues to the damaging effects of ionizing radiation, radiant heat and a number of known toxicants.

So far occupational hazards are the best documented risk factors for impaired male reproductive function and include physical exposures (radiant heat, ionizing radiation, high frequency electromagnetic radiation), chemical exposures (some solvents as carbon disulfide and ethylene glycol ethers, some pesticides as dibromochloropropane, ethylendibromide and DDT/DDE, some heavy metals as inorganic lead and mercury) and work processes such as metal welding. Improved working conditions in affluent countries have dramatically decreased known hazardous workplace exposures, but millions of workers in less affluent countries are at risk from reproductive toxicants. New data show that environmental low-level exposure to biopersistent pollutants in the diet may pose a risk to people in all parts of the world.

For other noxicants the evidence is only suggestive and further evaluation is needed before conclusions can be drawn. Whether compounds as phthalates, bisphenol A and boron that are present in a large number of industrial and consumer products entails a risk remains to be established. The same applies to psychosocial stressors and use of mobile phones.

Finally, there are data indicating a particular vulnerability of the fetal testis to toxicants – for instance maternal tobacco smoking. Time has come where male reproductive toxicity should be addressed form entirely new angles including exposures very early in life.

Literatur:
Bonde JP., Male reproductive organs are at risk from environmental hazards, Department of Occupational and Environmental Medicine, Bispebjerg University Hospital, Copenhagen, Denmark, Asian J Androl. 2009 Dec 7.

High levels of persistent environmental chemicals found in breast milk in a population with many male reproductive problems 

A comparison of breast milk samples from Denmark and Finland revealed a significant difference in environmental chemicals which have previously been implicated in testicular cancer or in adversely affecting development of the fetal testis in humans and animals. This finding is published today in the International Journal of Andrology. 

In recent years a worldwide increase in testicular cancer has been noticed, but the cause remains unknown. In some countries, such as Denmark the prevalence of this disease and other male reproductive disorders, including poor semen quality and congenital genital abnormalities is conspicuously high; while in Finland, a similarly industrialized Nordic country, the incidences of these disorders are markedly lower. In the UK, almost 2,000 men are diagnosed with testicular cancer every year, and in the US this number is over 8,000. There is a wide variation in incidence rates of testicular cancer around the globe, and the reasons behind the observed trends are unexplained. 

Environmental endocrine disrupting chemicals (EDCs) are commonly found in fatty foods, paints, plasticizers, pesticides, and the byproducts of industrial processes, and in recent studies an association has been shown between some of these agents and male reproductive problems. To investigate whether EDCs could be related to such great differences in reproductive disorders between closely related countries, Konrad Krysiak-Baltyn and colleagues from Denmark, Finland, and Germany measured levels of 121 chemicals in 68 breast milk samples from Denmark and Finland to compare exposure of mothers to EDCs. 

With so many chemicals, they used sophisticated, bioinformatics tools to interpret the complex data, and the results showed a clear distinction between the countries. 

“We were very surprised to find that some EDC levels, including some dioxins, PCBs and some pesticides, were significantly higher in Denmark than in Finland,” said Professor Niels Skakkebaek, a senior member of the research team, based at the University Department of Growth and Reproduction, Rigshospitalet, Denmark. “Our findings reinforce the view that environmental exposure to EDCs may explain some of the temporal and between-country differences in incidence of male reproductive disorders.”

“In spite of the findings, I would strongly urge women, including Danish mothers, to continue with breast feeding, which has many beneficial effects for the child,” added Skakkebaek. 

Reference: Wiley-Blackwell, Environmental chemicals found in breast milk and high incidence of testicular cancer, September 24, 2009

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