Iron Is the New Cholesterol


Cheerios are the best-selling breakfast cereal in America. The multi-grain version contains 18 milligrams of iron per serving, according to the label. Like almost any refined food made with wheat flour, it is fortified with iron. As it happens, there’s not a ton of oversight in the fortification process. One study measured the actual iron content of 29 breakfast cereals, and found that 21 contained 20 percent1 more than the label value, and 8 contained 50 percent more.1 One contained nearly 200 percent of the label value.

If your bowl of cereal actually contains 120 percent more iron than advertised, that’s about 22 mg. A safe assumption is that people tend to consume at least two serving sizes at a time.1 That gets us to 44 mg. The recommended daily allowance of iron is 8 mg for men and 18 mg for pre-menopausal women. The tolerable upper intake—which is the maximum daily intake thought to be safe by the National Institutes of Health—is 45 mg for adults.

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It is entirely feasible that an average citizen could get awfully close to exceeding the maximum daily iron intake regarded as safe with a single bowl of what is supposed to be a pretty healthy whole-grain breakfast option.

And that’s just breakfast.

At the same time that our iron consumption has grown to the borders of safety, we are beginning to understand that elevated iron levels are associated with everything from cancer to heart disease. Christina Ellervik, a research scientist at Boston Children’s Hospital who studies the connection between iron and diabetes, puts it this way: “Where we are with iron now is like where we were with cholesterol 40 years ago.”

The story of energy metabolism—the basic engine of life at the cellular level—is one of electrons flowing much like water flows from mountains to the sea. Our cells can make use of this flow by regulating how these electrons travel, and by harvesting energy from them as they do so. The whole set-up is really not so unlike a hydroelectric dam.

The sea toward which these electrons flow is oxygen, and for most of life on earth, iron is the river. (Octopuses are strange outliers here—they use copper instead of iron, which makes their blood greenish-blue rather than red). Oxygen is hungry for electrons, making it an ideal destination. The proteins that facilitate the delivery contain tiny cores of iron, which manage the handling of the electrons as they are shuttled toward oxygen.

This is why iron and oxygen are both essential for life. There is a dark side to this cellular idyll, though.

Oxygen and iron are essential for the production of energy, but may also conspire to destroy the delicate order of our cells.

Normal energy metabolism in cells produces low levels of toxic byproducts. One of these byproducts is a derivative of oxygen called superoxide. Luckily, cells contain several enzymes that clean up most of this leaked superoxide almost immediately. They do so by converting it into another intermediary called hydrogen peroxide, which you might have in your medicine cabinet for treating nicks and scrapes. The hydrogen peroxide is then detoxified into water and oxygen.

Things can go awry if either superoxide or hydrogen peroxide happen to meet some iron on the way to detoxification. What then happens is a set of chemical reactions (described by Haber-Weiss chemistry and Fenton chemistry) that produce a potent and reactive oxygen derivative known as the hydroxyl radical. This radical—also called a free radical—wreaks havoc on biological molecules everywhere. As the chemists Barry Halliwell and John Gutteridge—who wrote the book on iron biochemistry—put it, “the reactivity of the hydroxyl radicals is so great that, if they are formed in living systems, they will react immediately with whatever biological molecule is in their vicinity, producing secondary radicals of variable reactivity.”2

Such is the Faustian bargain that has been struck by life on this planet. Oxygen and iron are essential for the production of energy, but may also conspire to destroy the delicate order of our cells. As the neuroscientist J.R. Connor has said, “life was designed to exist at the very interface between iron sufficiency and deficiency.”3

Hemoglobin, ferritin, and transferrin

At the end of the 20th century, the metabolism of iron in the human body was still a bit of a mystery. Scientists knew of only two ways that the body could excrete iron—bleeding, and the routine sloughing of skin and gastrointestinal cells. But these processes amount to only a few milligrams per day. That meant that the body must have some way to tightly regulate iron absorption from the diet. In 2000 a major breakthrough was announced—a protein was found that functioned as the master regulator for iron. The system, as so many biological systems are, is perfectly elegant. When iron levels are sufficient, the protein, called hepcidin, is secreted into the blood by the liver. It then signals to gastrointestinal cells to decrease their absorption of iron, and for other cells around the body to sequester their iron into ferritin, a protein that stores iron. When iron levels are low, blood levels of hepcidin fall, and intestinal cells begin absorbing iron again. Hepcidin has since become recognized as the principal governor of iron homeostasis in the human body.

But if hepcidin so masterfully regulates absorption of iron from the diet to match the body’s needs, is it possible for anyone to absorb too much iron?

In 1996, a team of scientists announced that they had discovered the gene responsible for hereditary hemochromatosis, a disorder causing the body to absorb too much iron. They called it HFE. Subsequent work revealed that the product of the HFE gene was instrumental in regulating hepcidin. People with a heritable mutation in this gene effectively have a gross handicap in the entire regulatory apparatus that hepcidin coordinates.

This, then, leaves open the possibility that some of us could in fact take in more iron than the body is able to handle. But how common are these mutations? Common enough to matter for even a minority of people reading these words?

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Surprisingly, the answer is yes. The prevalence of hereditary hemochromatosis, in which two defective copies of the HFE gene are present and there are clinical signs of iron overload, is actually pretty high—as many as 1 in 200 in the United States. And perhaps 1 in 40 may have two defective HFE genes without overt hemochromatosis.4 That’s more than 8 million Americans who could have a significant short-circuit in their ability to regulate iron absorption and metabolism.

What if you have only one defective HFE gene, and one perfectly normal gene? This is called heterozygosity. We would expect to find more people in this situation than the homozygotes, or those with two bad copies of the gene. And in fact we do. Current estimates suggest that more than 30 percent of the U.S. population could be heterozygotes with one dysfunctional HFE gene.4 That’s pretty close to 100 million people.

Does this matter? Or is one good gene enough? There isn’t much research, but so far the evidence suggests that some heterozygotes do have impaired iron metabolism. Studies have shown that HFE heterozygotes seem to have modest elevations of ferritin as well as transferrin, a protein which chaperones iron through the blood, which would indicate elevated levels of iron.5,6 And a study published in 2001 concluded that HFE heterozygotes may have up to a fourfold increased risk of developing iron overload.4

A host of research articles have supported an association between iron and cancer.

Perhaps more concerning is that these heterozygotes have also been shown to be at increased risk for several chronic diseases, like heart disease and stroke. One study found that heterozygotes who smoked had a 3.5 times greater risk of cardiovascular disease than controls, while another found that heterozygosity alone significantly increased the risk of heart attack and stroke.7,8 A third study found that heterozygosity increased nearly sixfold the risk of cardiomyopathy, which can lead to heart failure.9

The connection between excessive iron and cardiovascular disease may extend beyond HFE heterozygotes. A recent meta-analysis identified 55 studies of this connection that were rigorous enough to meet their inclusion criteria. Out of 55 studies, 27 supported a positive relationship between iron and cardiovascular disease (more iron equals more disease), 20 found no significant relationship, and 8 found a negative relationship (more iron equals less disease).10

A few highlights: a Scandinavian study compared men who suffered a heart attack to men who didn’t, and found that elevated ferritin levels conferred a two- to threefold increase in heart attack risk. Another found that having a high ferritin level made a heart attack five times more likely than having a normal level. A larger study of 2,000 Finnish men found that an elevated ferritin level increased the risk of heart attack twofold, and that every 1 percent increase in ferritin level conferred a further 4 percent increase in that risk. The only other risk factor found to be stronger than ferritin in this study was smoking.

Ferritin isn’t a perfect marker of iron status, though, because it can also be affected by anything that causes inflammation. To address this problem a team of Canadian researchers directly compared blood iron levels to heart attack risk, and found that higher levels conferred a twofold increased risk in men and a fivefold increased risk in women.

If cardiovascular disease is one point in iron’s web of disease, diabetes may be another. The first hint of a relationship between iron and diabetes came in the late 1980s, when researchers discovered that patients receiving regular blood transfusions (which contain quite a bit of iron) were at significantly increased risk of diabetes. In hemochromatosis, there had been no way to know if the associated disturbance in glucose metabolism was due to the accumulation of iron itself, or to the underlying genetic defect. This new link between frequent transfusions and diabetes was indirect evidence that the iron itself may be the cause.

The next step was to mine existing data for associations between markers of iron status and diabetes. The first study to do so came out of Finland in 1997: Among 1,000 randomly selected Scandinavian men, ferritin emerged as a strong predictor of dysfunctional glucose metabolism, second only to body mass index as a risk factor.11 In 1999, researchers found that an elevated ferritin level increased the odds of having diabetes fivefold in men and nearly fourfold in women—similar in magnitude to the association between obesity and diabetes.12 Five years later, another study found that elevated ferritin roughly doubled the risk for metabolic syndrome, a condition that often leads to diabetes, hypertension, liver disease, and cardiovascular disease.13

Christina Ellervik’s first contribution to the field came in 2011, with a study investigating the association between increased transferrin saturation—a measure of how much iron is loaded onto the transferrin protein, which moves iron through the blood—and diabetes risk.14 Ellervik found that within a sample of nearly 35,000 Danes, transferrin saturation greater than 50 percent conferred a two- to threefold increased risk of diabetes. She also identified an increase in mortality rates with transferrin saturation greater than 50 percent.

In 2015, she led another study that found that, among a sample of 6,000 people, those whose ferritin levels were in the highest 20 percent had 4 times greater odds of diabetes than those with ferritin levels in the lowest 20 percent.15 Blood glucose levels, blood insulin levels, and insulin sensitivity all were raised with higher ferritin levels.

“It’s incredible that there is so much promising literature, and nobody—nobody—is doing the clinical trials.”

There’s a problem here, though. All of these studies show associations. They show that two things tend to happen together. But they don’t tell us anything about causality. To learn something about causality, you need an intervention. In the case of iron, you’d need to lower the iron and then watch what happens. Fortunately, there’s a very easy and very safe intervention to lower iron levels that’s performed millions of times every year—phlebotomy, also known as blood donation.

One of the first studies to use phlebotomy to examine the relationship between iron and diabetes was published in 1998.16 The authors found that among both healthy and diabetic subjects, phlebotomy improved insulin sensitivity and glucose metabolism. A 2005 study found that regular blood donors exhibited lower iron stores and significantly greater insulin sensitivity than non-donors.17 In 2012, researchers phlebotomized pre-diabetic volunteers until their ferritin levels dropped significantly, and found a marked subsequent improvement in their insulin sensitivity.18 In that same year, a different group of scientists studied the effect of phlebotomy on several elements of metabolic syndrome, including glucose metabolism. They found that a single phlebotomy session was associated with improvement in blood pressure, fasting glucose, hemoglobin A1C (a marker for average glucose levels), and blood cholesterol six weeks later.19

Many caveats apply to this evidence—the line between correlation and causation remains unclear, some of the studies used relatively small sample sizes, and phlebotomy may cause other changes in addition to lowering iron. But taken together, the data lends weight to the idea that iron plays a significant role in the tortuous pathophysiology of diabetes.

As more published data began to suggest a relationship between iron, cardiovascular disease, and diabetes, researchers started casting broader nets.

Next up was cancer.

It had been known since the late 1950s that injecting large doses of iron into lab animals could cause malignant tumors, but it wasn’t until the 1980s that scientists began looking for associations between iron and cancer in humans. In 1985, Ernest Graf and John Eton proposed that differences in colon cancer rates among countries could be accounted for by the variation in the fiber content of local diets, which can in turn affect iron absorption.20

The following year, Richard Stevens found that elevated ferritin was associated with triple the risk of death from cancer among a group of 20,000 Chinese men.21 Two years later Stevens showed that American men who developed cancer had higher transferrin saturation and serum iron than men who didn’t.22 In 1990, a large study of Swedish blood donors found that they were 20 percent less likely to get cancer than non-donor controls.23 Four years later, a group of Finnish researchers found that elevated transferrin saturation among 40,000 Scandinavians conferred a threefold increase risk for colorectal cancer, and a 1.5-fold increased risk for lung cancer.24

A host of research articles have been published since Graf and Eton’s first paper, and most have supported an association between iron and cancer—particularly colorectal cancer. In 2001, a review of 33 publications investigating the link between iron and colorectal cancer found that more than 75 percent of them supported the relationship.25 A 2004 study found an increased risk of death from cancer with rising serum iron and transferrin saturation. People with the highest levels were twice as likely to die from cancer than those with the lowest levels.26 And in 2008, another study confirmed that Swedish blood donors had about a 30 percent decrease in cancer risk.27

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There are a few other lines of evidence that support the association between iron and cancer. People with an HFE mutation have an increased risk of developing colon and blood cancers.28 Conversely, people diagnosed with breast, blood, and colorectal cancers are more than twice as likely to be HFE heterozygotes than are healthy controls.29

There are also a handful of interventional trials investigating the relationship between iron and cancer. The first was published in 2007 by a group of Japanese scientists who had previously found that iron reduction via phlebotomy essentially normalized markers of liver injury in patients with hepatitis C. Hepatocellular carcinoma (HCC) is a feared consequence of hepatitis C and cirrhosis, and they hypothesized that phlebotomy might also reduce the risk of developing this cancer. The results were remarkable—at five years only 5.7 percent of patients in the phlebotomy group had developed HCC compared to 17.5 percent of controls. At 10 years the results were even more striking, with 8.6 percent of phlebotomized patients developing HCC compared to an astonishing 39 percent of controls.30

The second study to investigate the effects of phlebotomy on cancer risk was published the following year by Leo Zacharski, a colorful emeritus professor at Dartmouth. In a multi-center, randomized study originally designed to look at the effects of phlebotomy on vascular disease, patients allocated to the iron-reduction group were about 35 percent less likely to develop cancer after 4.5 years than controls. And among all patients who did develop cancer, those in the phlebotomy group were about 60 percent less likely to have died from it at the end of the follow-up period.31

The brain is a hungry organ. Though only 2 to 3 percent of body mass, it burns 20 percent of the body’s total oxygen requirement. With a metabolism that hot, it’s inevitable that the brain will also produce more free radicals as it churns through all that oxygen. Surprisingly, it’s been shown that the brain appears to have less antioxidant capacity than other tissues in the body, which could make it more susceptible to oxidative stress.32 The balance between normal cellular energy metabolism and damage from reactive oxygen species may be even more delicate in the brain than elsewhere in the body. This, in turn, points to a sensitivity to iron.

It’s been known since the 1920s that neurodegenerative disease—illnesses like Alzheimer’s and Parkinson’s—is associated with increased iron deposition in the brain. In 1924, a towering Parisian neurologist named Jean Lhermitte was among the first to show that certain regions of the brain become congested with abnormal amounts of iron in advanced Parkinson’s disease.33 Thirty years later, in 1953, a physician named Louis Goodman demonstrated that the brains of patients with Alzheimer’s disease had markedly abnormal levels of iron deposited in the same regions as the famed plaques and tangles that define the illness.34 Goodman’s work was largely forgotten for several decades, until a 1992 paper resurrected and confirmed his findings and kindled new interest. Two years later an exciting new technology called MRI was deployed to probe the association between iron and disease in living patients, confirming earlier autopsy findings that Alzheimer brains demonstrated significant aberrations in tissue iron.35

Zacharski is convinced that iron overload is a huge common fulcrum underlying much of the chronic metabolic disease that is sweeping Western countries.

By the mid 1990s, there was compelling evidence that Alzheimer’s and Parkinson’s disease involved some dysregulation of iron metabolism in the brain, but no one knew whether the relationship was cause or consequence of the disease process. Hints began trickling in at around the same time the MRI findings were being published. A 1993 paper reported that iron promoted aggregation of amyloid-b, the major constituent of Alzheimer’s plaques.36 In 1997, researchers found that the aberrant iron associated with Alzheimer’s plaques was highly reactive and able to freely generate toxic oxygen radicals.37 By 2010, it had been shown that oxidative damage was one of the earliest detectable changes associated with Alzheimer’s, and that reactive iron was present in the earliest stages of the disease.38,39 And in 2015, a seven-year longitudinal study showed that cerebrospinal fluid ferritin levels were a strong predictor of cognitive decline and development of Alzheimer’s dementia.40

Perhaps most surprising was the discovery in 1999 that the pre-cursor to amyloid-b was under direct control by cellular iron levels—the more iron around, the more amyloid was produced.41 This raised the tantalizing possibility that amyloid plaques might actually represent an adaptive response rather than a cause, an idea that has been indirectly supported by the spectacular failure of essentially all efforts to directly target amyloid protein as treatment for the disease.

Together, these findings suggest that abnormal iron metabolism in the brain could be a causative factor in Alzheimer’s and other neurodegenerative diseases. If that’s true, then we might expect people who are genetically predisposed to an aberrant iron metabolism would be at higher risk of dementing diseases than others. And so they are.

In the early 2000s, it was discovered that patients with familial Alzheimer’s were more likely to possess one of the HFE genes than healthy controls.42 Another study found that these genotypes were associated with earlier onset of the disease compared to controls, and that there was an even more powerful effect in people who an HFE as well as an ApoE4 gene, the primary genetic risk factor for Alzheimer’s disease.43 A 2004 study showed that the co-occurrence of the HFE gene with a known variant in the transferrin gene conferred a fivefold increased risk of Alzheimer’s.44 Two years later a team of Portuguese scientists found that the HFE variants were associated with increased risk of Parkinson’s as well.45

What about interventional trials? For neurodegenerative disease, there has been exactly one. In 1991, a team of Canadian scientists published the results of a two-year randomized trial of the iron chelator desferrioxamine in 48 patients with Alzheimer’s disease.46 Chelators are a class of medication that bind metal cations like iron, sequester them, and facilitate their excretion from the body. Patients were randomly allocated to receive desferrioxamine, placebo, or no treatment. The results were impressive—at two years, iron reduction had cut the rate of cognitive decline in half.

The study was published in The Lancet, one of the world’s most prestigious medical journals, but seems to have been forgotten in the 20-odd year interim. Not a single interventional study testing the role of iron in Alzheimer’s disease has been published since.

If so many studies seem to show a consistent association between iron levels and chronic disease, why isn’t more work being done to clarify the risk?

“It’s incredible that there is so much promising literature, and nobody—nobody—is doing the clinical trials,” Dartmouth’s Zacharski said to me. “If people would just take up the gauntlet and do well-designed, insightful studies of the iron hypothesis, we would have a much firmer understanding of this. Just imagine if it turns out to be verified!”

His perspective on why more trials haven’t been done is fascinating, and paralleled much of what other experts in the field said. “Sexiness,” believe it or not, came up in multiple conversations—molecular biology and targeted pharmaceuticals are hot (and lucrative), and iron is definitively not. “Maybe it’s not sexy enough, too passé, too old school,” said one researcher I spoke to. Zacharski echoed this in our conversation, and pointed out that many modern trials are funded by the pharmaceutical industry, which is keen to develop the next billion-dollar drug. Government agencies like the NIH can step in to fill gaps left by the for-profit research industry, but publically funded scientists are subject to the same sexiness bias as everyone else. As one senior university scientist told me, “NIH goes for fashion.”

Zacharski is convinced that iron overload is a huge common fulcrum underlying much of the chronic metabolic disease that is sweeping Western countries. He thinks that even subtly elevated iron levels can result in free radical formation, which then contribute to chronic inflammation. And chronic inflammation, we know, is strongly linked to everything from heart disease to diabetes, cancer to Alzheimer’s.

“If this doesn’t deserve randomized trials,” he told me, “then I don’t know what does.”

Until those randomized trials arrive—I’ll see you at the blood bank.

Clayton Dalton is an emergency medicine resident at Massachusetts General Hospital in Boston. He has published stories and essays with NPR, Aeon, and The Los Angeles Review.

Lead image: Liliya Kandrashevich / Shuttterstock

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2. Halliwell, B. & Gutteridge, J.M. Oxygen toxicity, oxygen radicals, transition metals and disease. Biochemical Journal 219, 1-14 (1984).

3. Connor, J.R. & Ghio, A.J. The impact of host iron homeostasis on disease. Preface. Biochimica et Biophysica Acta 1790, 581-582 (2009).

4. Hanson, E.H., Imperatore, G., & Burke, W. HFE gene and hereditary hemochromatosis: a HuGE review. Human Genome Epidemiology. American Journal of Epidemiology 154, 193-206 (2001).

5. Beutler, E., Felitti, V.J., Koziol, J.A., Ho, N.J., & Gelbart, T. Penetrance of 845G—> A (C282Y) HFE hereditary haemochromatosis mutation in the USA. The Lancet 359, 211-218 (2002).

6. Rossi, E., et al. Effect of hemochromatosis genotype and lifestyle factors on iron and red cell indices in a community population. Clinical Chemistry 47, 202-208 (2001).

7. Roest, M., et al. Heterozygosity for a hereditary hemochromatosis gene is associated with cardiovascular death in women. Circulation 100, 1268-1273 (1999).

8. Tuomainen, T.P., et al. Increased risk of acute myocardial infarction in carriers of the hemochromatosis gene Cys282Tyr mutation: A prospective cohort study in men in eastern Finland. Circulation 100, 1274-1279 (1999).

9. Pereira, A.C., et al. Hemochromatosis gene variants in patients with cardiomyopathy. American Journal of Cardiology 88, 388-391 (2001).

10. Muñoz-bravo, C., Gutiérrez-bedmar, M., Gómez-aracena, J., García-rodríguez, A., & Navajas, J.F. Iron: protector or risk factor for cardiovascular disease? Still controversial. Nutrients 5, 2384-2404 (2013).

11. Tuomainen, T.P., et al. Body iron stores are associated with serum insulin and blood glucose concentrations. Population study in 1,013 eastern Finnish men. Diabetes Care 20, 426-428 (1997).

12. Ford, E.S. & Cogswell, M.E. Diabetes and serum ferritin concentration among U.S. adults. Diabetes Care 22, 1978-1983 (1999).

13. Jehn, M., Clark, J.M., & Guallar, E. Serum ferritin and risk of the metabolic syndrome in U.S. adults. Diabetes Care 27, 2422-2428 (2004).

14. Ellervik, C., et al. Elevated transferrin saturation and risk of diabetes: three population-based studies. Diabetes Care 34, 2256-2258 (2011).

15. Bonfils, L., et al. Fasting serum levels of ferritin are associated with impaired pancreatic beta cell function and decreased insulin sensitivity: a population-based study. Diabetologia 58, 523-533 (2015).

16. Facchini, F.S. Effect of phlebotomy on plasma glucose and insulin concentrations. Diabetes Care 21, 2190 (1998).

17. Fernández-real, J.M., López-bermejo, A., & Ricart, W. Iron stores, blood donation, and insulin sensitivity and secretion. Clinical Chemistry 51, 1201-1205 (2005).

18. Gabrielsen, J.S., et al. Adipocyte iron regulates adiponectin and insulin sensitivity. Journal of Clinical Investigation 122, 3529-3540 (2012).

19. Houschyar, K.S., et al. Effects of phlebotomy-induced reduction of body iron stores on metabolic syndrome: results from a randomized clinical trial. BMC Medicine 10:54 (2012).

20. Graf, E. & Eaton, J.W. Dietary suppression of colonic cancer. Fiber or phytate?. Cancer 56, 717-718 (1985).

21. Stevens, R.G., Beasley, R.P., & Blumberg, B.S. Iron-binding proteins and risk of cancer in Taiwan. Journal of the National Cancer Institute 76, 605-610 (1986).

22. Stevens, R.G., Jones, D.Y., Micozzi, M.S., & Taylor, P.R. Body iron stores and the risk of cancer. New England Journal of Medicine 319, 1047-1052 (1988).

23. Merk, K., et al. The incidence of cancer among blood donors. International Journal of Epidemiology 19, 505-509 (1990).

24. Knekt, P., et al. Body iron stores and risk of cancer. International Journal of Cancer 56, 379-382 (1994).

25. Nelson, R.L. Iron and colorectal cancer risk: human studies. Nutrition Review 59, 140-148 (2001).

26. Wu, T., Sempos, C.T., Freudenheim, J.L., Muti, P., & Smit, E. Serum iron, copper and zinc concentrations and risk of cancer mortality in US adults. Annals of Epidemiology 14, 195-201 (2004).

27. Edgren, G., et al. Donation frequency, iron loss, and risk of cancer among blood donors. Journal of the National Cancer Institute 100, 572-579 (2008).

28. Nelson, R.L., Davis, F.G., Persky, V., & Becker, E. Risk of neoplastic and other diseases among people with heterozygosity for hereditary hemochromatosis. Cancer 76, 875-879 (1995).

29. Weinberg, E.D. & Miklossy, J. Iron withholding: a defense against disease. Journal of Alzheimer’s Disease 13, 451-463 (2008).

30. Kato, J., et al. Long-term phlebotomy with low-iron diet therapy lowers risk of development of hepatocellular carcinoma from chronic hepatitis C. Journal of Gastroenterology 42, 830-836 (2007).

31. Zacharski, L.R., et al. Decreased cancer risk after iron reduction in patients with peripheral arterial disease: results from a randomized trial. Journal of the National Cancer Institute 100, 996-1002 (2008).

32. Lee, H.G., et al. Amyloid-beta in Alzheimer disease: the null versus the alternate hypotheses. Journal of Pharmacology and Experimental Therapeutics 321, 823-829 (2007).

33. Lhermitte, J., Kraus, W.M., & Mcalpine, D. Original Papers: On the occurrence of abnormal deposits of iron in the brain in Parkinsonism with special reference to its localisation. Journal of Neurology and Psychopathology 5, 195-208 (1924).

34. Goodman, L. Alzheimer’s disease; a clinico-pathologic analysis of twenty-three cases with a theory on pathogenesis. The Journal of Nervous and Mental Disease 118, 97-130 (1953).

35. Bartzokis, G., et al. In vivo evaluation of brain iron in Alzheimer’s disease and normal subjects using MRI. Biological Psychiatry 35, 480-487 (1994).

36. Mantyh, P.W., et al. Aluminum, iron, and zinc ions promote aggregation of physiological concentrations of beta-amyloid peptide. Journal of Neurochemistry 61, 1171-1174 (1993).

37. Smith, M.A., Harris, P.L., Sayre, L.M., & Perry, G. Iron accumulation in Alzheimer disease is a source of redox-generated free radicals. Proceedings of the National Academy of Sciences 94, 9866-9868 (1997).

38. Nunomura, A., et al. Oxidative damage is the earliest event in Alzheimer disease. Journal of Neuropathology and Experimental Neurology 60, 759-767 (2001).

39. Smith, M.A., et al. Increased iron and free radical generation in preclinical Alzheimer disease and mild cognitive impairment. Journal of Alzheimer’s Disease 19, 363-372 (2010).

40. Ayton, S., Faux, N.G., & Bush, A.I. Ferritin levels in the cerebrospinal fluid predict Alzheimer’s disease outcomes and are regulated by APOE. Nature Communications 6:6760 (2015).

41. Rogers, J.T., et al. Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5’-untranslated region sequences. Journal of Biological Chemistry 274, 6421-6431 (1999).

42. Moalem, S., et al. Are hereditary hemochromatosis mutations involved in Alzheimer disease? American Journal of Medical Genetics 93, 58-66 (2000).

43. Combarros, O., et al. Interaction of the H63D mutation in the hemochromatosis gene with the apolipoprotein E epsilon 4 allele modulates age at onset of Alzheimer’s disease. Dementia and Geriatric Cognitive Disorders 15, 151-154 (2003).

44. Robson, K.J., et al. Synergy between the C2 allele of transferrin and the C282Y allele of the haemochromatosis gene (HFE) as risk factors for developing Alzheimer’s disease. Journal of Medical Genetics 41, 261-265 (2004).

45. Pulliam, J.F., et al. Association of HFE mutations with neurodegeneration and oxidative stress in Alzheimer’s disease and correlation with APOE. American Journal of Medical Genetics; Part B 119B, 48-53 (2003).

46. Crapper-McLachlan, D.R., et al. Intramuscular desferrioxamine in patients with Alzheimer’s disease. The Lancet 337, 1304-1308 (1991).

Two Lawmakers Question EPA on Asbestos After Reuters Report


Two Democratic U.S. lawmakers have called on the Environmental Protection Agency to answer questions about asbestos exposure after Reuters reported that documents showed Johnson & Johnson knew for decades of the mineral’s presence in its popular baby powder.

Whether asbestos in the talc supply in Johnson & Johnson’s Baby Powder caused cancer has been the subject of litigation for years.

The lawmakers, Senator Jeff Merkley and Representative Suzanne Bonamici, did not mention Johnson & Johnson by name but expressed “deep concern” about Friday’s Reuters report, according to a copy of their letter dated Dec. 19 and reviewed by Reuters.

In their letter, the two lawmakers asked the EPA how it was regulating potentially unsafe asbestos-containing products.

J&J has disputed the Reuters report, calling it a “misrepresentation.” The company says its talc is safe and has never contained asbestos, adding that decades of studies and regulatory assessments confirm the safety of its product.

Representatives for the EPA did not be respond to an email or a telephone call seeking comment on the congressional letter.

Asked about the lawmakers’ letter, J&J spokesman Ernie Knewitz declined to comment but said the Reuters report was “one-sided, false and inflammatory.”

According to the Reuters report, documents as well as deposition and trial testimony showed that from at least 1971 to the early 2000s the company’s raw talc and finished powders sometimes tested positive for small amounts of asbestos.

Most internal J&J asbestos test reports Reuters reviewed did not find asbestos.

The company has defended its products in recent days with a series of full-page newspaper advertisements and a television interview with its chief executive. Shares of the company have fallen about 12.5 percent since the Reuters report on Friday.

Merkley and Bonamici also asked the EPA to detail what steps it was taking to help prevent vulnerable populations such as pregnant women and infants from being exposed to products containing asbestos, including other products with talc, a mineral.

Although baby powder is subject to regulation under the Federal Food, Drug, and Cosmetic Act, other talc products sold to consumers would be within the purview of the Toxic Substances Control Act (TSCA) and thus the responsibility of the EPA, they wrote in the letter.

Democratic U.S. Senator Edward Markey separately called on the FDA to investigate the findings in the Reuters report in a letter on Friday. The FDA could not immediately be reached for comment.

“Asbestos is a known carcinogen, and one for which there is no controlled use or safe level of exposure,” Merkley and Bonamici wrote. “Fifty-five countries have already banned asbestos. Unfortunately, the United States still permits the use of asbestos.”

Scientists Discover Fungicide and Pesticide are Killing Bees―and It’s Worse Than You Thought.


Story at-a-glance

  • Researchers analyzed pollen from bee hives and found 35 different pesticides along with high fungicide loads.
  • Each sample contained, on average, nine different pesticides and fungicides, although one contained 21 different chemicals.
  • While previously assumed to be safe for bees, bees fed pollen contaminated with high levels of fungicides had a significant decline in the ability to resist infection with the Nosema ceranae parasite, which has been implicated in Colony Collapse Disorder (CCD)
  • In the US, the “Save America’s Pollinators Act” has been introduced; if passed, this bill, HR 2692, would require the EPA to pull neonicotinoid pesticides, also implicated in bee die-offs, from the market until their safety is proven.
  • killing-bees

Bee populations are dwindling across the globe, putting one in three food crops like apples and almonds, which depend on pollination from bees, at serious risk.

In the US, beekeepers have reported annual losses of about 33 percent of their hives each year, a level of loss that the Agricultural Research Services reports could threaten the economic viability of the bee pollination industry if it continues1(and some beekeepers report much higher losses than this at upwards of 70 or, in some cases, 100 percent).

Despite the growing losses, the causes of the massive bee die-offs have yet to be firmly defined, although accumulating research is pointing to a cocktail of agricultural chemicals as a likely primary culprit.

New Study: Fungicides May Be Killing Bees

Systemic neonicotinoid pesticides have been increasingly blamed for bee deaths (and were implicated in a recent mass bee die-off of 25,000 bumblebees along with millions of bee deaths in Canada), prompting the European Union (EU) to ban them for two years.

Now, it appears measures that target single classes of pesticides, though a move in the right direction, may be falling short. In a first-of-its-kind study, researchers analyzed pollen from bee hives in seven major crops and found 35 different pesticides along with high fungicide loads.2 Each sample contained, on average, nine different pesticides and fungicides, although one contained 21 different chemicals.

Furthermore, when the pollen was fed to healthy bees, they had a significant decline in the ability to resist infection with the Nosema ceranae parasite, which has been implicated in Colony Collapse Disorder (CCD).

What makes the research particularly unique is the concerning data on fungicides, which has so far been assumed to be safe for bees. While farmers are advised to avoid spraying pesticides when bees are present, for instance, fungicides contain no such warnings.

The researchers explained:

“While fungicides are typically seen as fairly safe for honey bees, we found an increased probability of Nosema infection in bees that consumed pollen with a higher fungicide load. Our results highlight a need for research on sub-lethal effects of fungicides and other chemicals that bees placed in an agricultural setting are exposed to.”

Also concerning, the researchers found that the bees in the study collected pollen almost exclusively from weeds and wildflowers, and this, too, was contaminated with pesticides even though they were not directly sprayed.

“It’s not clear whether the pesticides are drifting over to those plants but we need take a new look at agricultural spraying practices,” the study’s lead author told Quartz.3

US Bill Introduced to Take Neonicotinoids Off the Market

Following the June incident that killed 25,000 bumblebees, the Oregon Department of Agriculture (ODA) announced that they were restricting the use of 18 pesticide products containing dinotefuran, a type of neonicotinoid.

These chemicals are typically applied to seeds before planting, allowing the pesticide to be taken up through the plant’s vascular system as it grows. As a result, the chemical is expressed in the pollen and nectar of the plant, and hence the danger to bees and other pollinating insects.

As mentioned, the EU has also banned these pesticides, beginning December 1, 2013, to study their involvement with large bee kills they, too, are experiencing.

To date, however, the US Environmental Protection Agency (EPA) has failed to take action and has already been sued once by beekeepers and environmental groups for failing to protect bees from neonicotinoid pesticides. 

They have also green-lighted another pesticide that is a close cousin to these toxic chemicals (sulfoxaflor) and, as a result, several beekeeping organizations and beekeepers have filed a legal action against the EPA for approving sulfoxaflor, which is considered by many to be a “fourth-generation neonicotinoid.

In the US, the tide may be turning, however, as just last month the “Save America’s Pollinators Act” was introduced. If passed, this bill, HR 2692, would require the EPA to pull neonicotinoid pesticides from the market until their safety is proven. Please contact your representative today to voice your support for this incredibly important issue.

US Almond Crops Are Already At Risk

We’re beginning to get a taste of what the world would be like without bees. This year, many of the 6,000 almond orchard owners in California simply could not find enough bees to pollinate their almond trees, at any price. This is alarming, considering that 80 percent of the world’s almonds come from California’s central valley, an 800,000-acre area of almond orchards that are 100 percent dependent on bees pollinating the trees. Surprisingly, almonds are the number one agricultural product in California.

Fortunately, unsurpassed efforts that included persuading beekeepers as far away as Florida to ship their bees cross country, delayed bloom, and unseasonably good weather thereafter allowed almond growers to dodge the bullet – this year – despite having fewer and weaker-than-ever hives…

This narrowly achieved success may lead some to reach the mistaken conclusion that beekeepers’ concerns are overblown, but don’t be fooled. One beekeeper went so far as to say he believes the beekeeper industry is doomed and cannot survive for more than another two to three years unless drastic changes are implemented immediately…

What Are Some of the Top Theories for Bee Die-Offs?

Environmental chemicals are a forerunner for what’s causing so many bees to die, but it’s likely that there are multiple factors at play here. Among the top proposed culprits include:

·         Pesticides, insecticides and fungicides – Neonicotinoids, such as Imidacloprid and Clothianidin, kills insects by attacking their nervous systems. These are known to get into pollen and nectar, and can damage beneficial insects such as bees.

·         Malnutrition/Nutritional deficiencies – Many beekeepers place the hives near fields of identical crops, which may result in malnutrition as the bees are only getting one type of nectar. Essentially, this theory is identical to that of human nutrition; we need a wide variety of nutrients from different foods.

If you keep eating the same limited range of foods, you can easily end up suffering from nutritional deficiencies. Poor nutrition suppresses immune function, making the bees far more susceptible to toxins from pesticides, viruses, fungi, or a combination of factors that ultimately kill them.

·         Viruses and fungi – There’s even the possibility that some new form of “AIDS-like” viral infection is affecting the bees.

·         Electromagnetic fields (EMFs) – Researchers have discovered that when a cellular phone is placed near a hive, the radiation generated by it (900-1,800 MHz) is enough to prevent bees from returning to them, according to a study conducted at Landau University several years ago.4

More recently, a study published in 2011 found that the presence of microwaves from cell phones have a dramatic effect on bees, causing them to become quite disturbed.5

·         Lack of natural foraging areas – Mass conversions of grasslands to corn and soy in the Midwest has dramatically reduced bees’ natural foraging areas.

·         Genetically modified (GM) crops – In 2007, a German study demonstrated that horizontal gene transfer appears to take place between the GM crop and the bees that feed on it.6 When bees were released in a field of genetically modified rapeseed, and then fed the pollen to younger bees, the scientists discovered the bacteria in the guts of the young ones mirrored the same genetic traits as ones found in the GM crop.

You Can Start Helping Bees Right in Your Own Backyard

The Pollinator Partnership has revealed many ways you can help the urgent issue of declining pollinator populations.7 Clearly major steps need to be taken on a national level to protect pollinators from toxic chemicals and other threats, and you can help in this regard by supporting the Save America’s Pollinators Act. Friends of the Earth has also launched the Bee-Action Campaign to tell stores to take bee-killing pesticides like neonicotinoids off of their shelves, and you can help by signing their petition now.

That said, you can even make a difference right in your own backyard:

·         Reduce or eliminate your use of pesticides

·         Plant a pollinator-friendly garden by choosing a variety of plants that will continue flowering from spring through fall; check out the Bee Smart Pollinator App for a database of nearly 1,000 pollinator-friendly plants

·         Choose plants native to your region and stick with old-fashioned varieties, which have the best blooms, fragrance and nectar/pollen for attracting and feeding pollinators

·         Install a bee house

Finally, if you would like to learn even more about the economic, political and ecological implications of the worldwide disappearance of the honeybee, check out the extremely informative documentary film Vanishing of the Bees.

Study Finds Link Between Herbicide Exposure and Depression.


Knowing that herbicides are poisoning ecosystems and degrading human health is enough to get you down. Hold on, though. Recent research has found a significant link between herbicide exposure and depression. Findings were reported in the American Journal of Epidemiology.
A study of more than 700 French farmers found that those who used herbicides were 2.5 times more likely to develop depression than those who did not. Further, the higher the exposure to herbicides, the greater the chance of being treated for depression.

The authors go on to say: “If true, our findings have important public health implications for agricultural workers given the tremendous public health burden of depression and the fact that herbicides are widely used in agriculture and landscape management.”

As REALfarmacy reported previously, the EPA has raised the allowable level of glyphosate  in our food. This comes on the heels of a tremendous rise in the use of glyphosate after Monsanto unleashed its RoundUp Ready crops that are engineered to be drenched in the herbicide. The hbiotech industry is working on new GMO crops that can withstand other, more toxic herbicides like 2,4-D and dicamba.

Although the mechanism behind this disturbing relationship of herbicide use and depression is not yet known, it adds to the growing scientific evidence that herbicide exposure is a health hazard. Studies are finding possible links between Parkinson’s disease, infertility, cancer, and birth defects. Now we find out that herbicides can have psychological effects too.

Herbicide use by homeowners is certainly common. And it’s no wonder, as a visit to the big box home improvement stores inundates a person with ads for manufactured poisons. The biggest herbicide use, however, exists in the agricultural sectorAccording to EPA reports from 2007, 80% of pesticide use (including herbicides) was in agriculture.

Herbicide use is bound to continue rising as long as industrial agriculture and GMO companies control the food system. In fact, this is a market strategy considering that herbicide-resistant crops are central to their plans for the future. Can we expect a concomitant rise in cases of depression?

Source: http://www.realfarmacy.com/

 

Surprising Source of Arsenic in Your Drinking Water—Will EPA Take Steps to Protect Your Health?


Story at-a-glance

  • While naturally-occurring arsenic in groundwater is one of the most common sources of exposure, hydrofluorosilicic acid (fluoride) added to drinking water is commonly contaminated with toxic arsenic
  • According to recent research, diluted fluorosilic acid adds, on average, about 0.08 ppb of arsenic to your drinking water
  • Low-level chronic exposure to arsenic can lead to a wide variety of health problems, including chronic fatigue, reproductive problems, reduced IQ and other neurological problems, and various cancers
  • As petition urges the EPA to change the source of fluoride in US drinking water, as the most commonly used form, hydrofluorosilicic acid, increases lung and bladder cancer risk
  • Switching from hydrofluorosilicic acid to pharmaceutical-grade fluoride could save the US $1-6 billion annually and prevent an estimated 1,800 cases of lung and bladder cancer

Pure water is one of the most important foundations for optimal health.Unfortunately, most tap water is far from pure, containing a vast array ofdisinfection byproducts, chemicals, heavy metals and even pharmaceutical drugs.Fluoride and arsenic are two prime examples of hazardous water contaminants.

Image

Not only is the level of arsenic in US tap water high due to natural groundwater contamination,1 the most commonly used form of fluoride added to water supplies also tends to be contaminated with arsenic. As reported by the featured article:2

“In early August, the Environmental Protection Agency is set to decide on a petition to change the source of fluoride in US drinking water.

Currently, the source of fluoride in most public water supplies isfluorosilicic acid, according to government records. The petition calls for the EPA to instead require the use of pharmaceutical-grade sodium fluoride in water fluoridation, which is the addition of fluoride to drinking water for the purpose of preventing cavities.

Fluorosilicic acid is often contaminated with arsenic, and recent research has linked the arsenic from fluorosilicic acid in drinking water to as many as 1,800 extra cases of cancer yearly in the United States…”

The petition3 was submitted by William Hirzy, a chemistry researcher at the American University in Washington, D.C. Hirzy previously worked at the EPA for 27 years.

His team recently published a study entitled: Comparison of hydrofluorosilicic acid and pharmaceutical sodium fluoride as fluoridating agents – a cost-benefit analysis, in the journal Environmental Science & Policy.4

According to their estimation, switching the type of fluoride used to pharmaceutical-grade sodium fluoride would reduce the amount of inorganic arsenic contamination in drinking water by 99 percent!

The Health Dangers of Inorganic Arsenic

Inorganic arsenic is a powerful carcinogen that has been linked to an increased risk of several types of cancer. In 2001 the Environmental Protection Agency(EPA) lowered the maximum level of arsenic permitted in drinking water from 50 ug/L to 10 ug/L (or 10 parts per billion (ppb)) due to the established cancer risk.

The Natural Resources Defense Council5 estimates that as many as 56 million Americans living in 25 states drink water with arsenic at unsafe levels. According to the EPA:6

“Chronic inorganic arsenic exposure is known to be associated with adverse health effects on several systems of the body, but is most known for causing specific types of skin lesions (sores, hyperpigmentation, and other lesions) and increased risks of cancer of the lungs and skin.”

Other impacts of chronic arsenic exposure include, according to the EPA:

Kidney damage and failure Anemia Low blood pressure
Shock Headaches Weakness
Delirium Increased risk of diabetes Adverse liver and respiratory effects, including irritation of mucous membranes
During development, increased incidence of preterm delivery, miscarriage, stillbirths, low birth weight, and infant mortality During childhood, decreased performance in tests of intelligence and long-term memory Skin lesions

Water Fluoridation Chemicals Are NOT Pharmaceutical Grade

While naturally-occurring arsenic in groundwater is one of the most common sources of exposure, hydrofluorosilicic acid—the most commonly used form of fluoride added to water supplies—is a toxic waste product from the phosphate fertilizer industry that is commonly contaminated with arsenic, radionucleotides, aluminum and other industrial contaminants.

According to the featured research, diluted fluorosilic acid adds, on average, about 0.08 ppb of arsenic to your drinking water.

Most people are shocked when they realize that the fluoride added to their water supply is actually a toxic byproduct from the fertilizer industry, opposed to a pharmaceutical-grade chemical. The source of most water fluoridation chemicals is explained by Michael Miller, a minerals commodity specialist for the US Geological Survey, in the featured article:7

“During the production of phosphate fertilizer, phosphate ore is reacted with sulfuric acid to produce toxic gases. These are taken out of the air after being sprayed with water, which produces fluorosilicic acid… The solution is sold to water systems nation-wide, where it is diluted and put into drinking water. Occasionally, it is treated to create sodium fluorosilicate. Together, these compounds (called silicofluorides) provide fluoride to 90 percent of U.S. drinking water systems that are fluoridated…”

Water Fluoridation May Be Placing Infants at Great Risk

Not only is there mounting evidence that fluoride poses grave health risks to infants and children—including reductions in IQ—arsenic exposure in utero and during early childhood is also particularly problematic, as it can cause lasting harm to children’s developing brains, and endocrine- and immune systems.

For example:

  • A 2006 study8 found that Chileans exposed to high levels (peaking at 1,000 ppb) of naturally-occurring arsenic in drinking water in utero and during early childhood had a six times higher lung cancer death rate compared to Chileans living in areas with lower levels of arsenic in their water. And their mortality rate in their 30s and 40s from another form of lung disease was almost 50 times higher than for people without that arsenic exposure.
  • A 2004 study9 showed children exposed to arsenic in drinking water at levels above 5 ppb had lower IQ scores. Earlier studies have linked chronic arsenic exposure to a range of cognitive dysfunctions, including learning disabilities, memory problems, poor concentration, and peripheral and central neuropathies.
  • A study10 published in 2011 examined the long-term effects of low-level exposure on more than 300 rural Texans whose groundwater was estimated to have arsenic at median levels below the federal drinking-water standard. It also found that exposure was related to poor scores in language, memory, and other brain functions.

Is It Worth Increasing Cancer Risk for Minimal, if Any, Benefit to Teeth?

Some proponents of fluoridation believe that the large dilution of these fluoridating chemicals that takes place when they are added at the public water works ameliorates concerns about the known contaminants. However, arsenic is a known human carcinogen, for which there is no safe level.

Inevitably, the addition of contaminated hexafluorosilicic acid to the water supply by definition must increase the cancer rate in the US because of the arsenic it contains, and this is exactly what Hirzy’s research shows. Why would any rational government do that to reduce – at best – a miniscule amount of tooth decay? According to Hirzy:11

“We found that the United States as a society is spending, conservatively speaking, $1 billion to $6 billion treating the excess bladder and lung cancers caused by arsenic in the most commonly used fluoridation chemical, fluorosilicic acid… The switch [to pharmaceutical-grade sodium fluoride] would cost $100 million, but would save billions in reduced cancer costs.”

For people living in areas with fluoridated tap water, fluoride is a part of every glass of water, every bath and shower, and every meal cooked using that water. This makes absolutely no sense considering the carcinogenic nature of arsenic—especially in light of the epidemic of cancer.

Hirzy’s study is actually the first risk assessment of arsenic-contaminated fluoride in drinking water. This is particularly shocking considering the fact that fluorosilicic acids have been used since the early 1950’s12 (prior to that, sodium fluoride, a byproduct of the aluminum industry, was typically used). Incredibly, while the EPA performs risk assessments for most drinking water contaminants, the agency does NOT oversee the addition of fluoridation chemicals. As stated in the featured article, this policy makes no sense whatsoever.

“Under the Toxic Substances Control Act, the EPA has the authority to regulate or ban almost any substance — including fluorosilicic acid — that poses an ‘unreasonable risk’ to public health, [Hirzy] said.”

Appropriations Bill Would Prohibit EPA’s Phase-Out of Sulfuryl Fluoride

While we’re on the topic of fluoride, a related news item13 is worthy of note. Drinking water is not the only source of fluoride, as I’ve discussed previously. Fluoride also enters the human food chain via fluoridated pesticides. According to a recent report, the House of Representatives Appropriations Interior and Environmental subcommittee has voted to approve an appropriations bill that cuts the EPA’s budget by nearly one-third.

What’s worse, the bill specifically prevents the EPA from enforcing its decision to phase out sulfuryl fluoride—a neurotoxic fumigant that has been linked to cancer and neurological-, developmental-, and reproductive damage. If it passes once markups by the Appropriations Committee are completed, it will move to a House vote. According to the news report:

“This is an outrageous attempt to circumvent a basic risk assessment calculation that EPA acknowledges puts the public at risk, given current exposure patterns, to a chemical that is especially hazardous to children.”

In response, Beyond Pesticides, the Environmental Working Group (EWG), and the Fluoride Action Network (FAN) submitted a letter14 to the House Appropriation Committee Chairman and Ranking members, urging them to remove the section in question (section 449) from the bill. You can help by writing or calling your state Representative, asking him or her to uphold the EPA’s ability to protect the health of all Americans by removing this hazardous pesticide from our food production. There’s no need for it, as there are many other viable alternatives, including:

  • Temperature manipulation (heating and cooling)
  • Atmospheric controls (low oxygen and fumigation with carbon dioxide)
  • Biological controls (pheromones, viruses and nematodes)
  • Less toxic chemical controls, such as diatomaceous earth

Water Filtration – A Must for Clean Pure Water…

If you have well water, it would be prudent to have your water tested for arsenic and other contaminants. If you have public water, you can get local drinking water quality reports from the EPA.15

In general, most water supplies contain a number of potentially hazardous contaminants, from fluoride, to drugs and disinfection byproducts (DBP’s), just to name a few. You can get a good idea of what types of contaminants could be in your drinking water right now by viewing this awesome graphic from GOOD Environment16 (reprinted with permission.) It gives you a look at the five most and least polluted water systems in America (in cities with more than 100,000 population), including pointing out the pollutants of largest concern.

I strongly recommend using a high quality water filtration system unless you can verify the purity of your water. To be absolutely certain you are getting the purest water you can, you’ll want to filter the water both at the point of entry and at the point of use. This means filtering all the water that comes into the house, and then filtering again at the kitchen sink. I currently use a whole house carbon-based water filtration system, and prior to this I used reverse osmosis (RO) to purify my water.

You can read more about water filtration in this previous article to help you make a decision about what type of water filtration system will be best for you and your family. Since most water sources are now severely polluted, the issue of water filtration and purification couldn’t be more important.

Ideal Water Sources

Besides purification, I also believe it’s critical to drink living water. I recently interviewed Dr. Gerald Pollack about his book, The Fourth Phase of Water: Beyond Solid, Liquid, and Vapor. This fourth phase of water is referred to as “structured water” and is the type of water found in all of your cells. This water has healing properties, and is naturally created in a variety of ways.

Water from a deep spring is one excellent source of structured water. The deeper the better, as structured water is created under pressure. There’s a great website called FindaSpring.com17 where you can find a natural spring in your area.

But you can also promote structured water through vortexing. I personally drink vortexed water nearly exclusively as I became a big fan of Viktor Schauberger who did much pioneering work on vortexing about a century ago. Dr. Pollack found that by creating a vortex in a glass of water, you’re putting more energy into it, thereby increasing the structure of the water. According to Dr. Pollack, virtually ANY energy put into the water seems to create or build structured water.

My own R&D team is working on a careful study in which we use vortexed water to grow sprouts, to evaluate the vitality and effectiveness of the water. We are conducting extensive internal research to develop the best vortex machine on the market, because we believe an ideal vortexer could be one of the simplest ways to improve people’s health.

Water Fluoridation Is Anything But Safe…

According to Bill Hirzy, water fluoridation remains a government policy because of “institutional inertia [and] embarrassment among government agencies that have been promoting this stuff as safe.” This is probably true, yet it’s shameful that the practice is allowed to continue in the face of overwhelming evidence showing the health hazards of not just fluoride itself, but also of related contaminants such as arsenic.

Clean pure water is a prerequisite to optimal health. Industrial chemicals, drugs and other toxic additives really have no place in our water supplies.

Source: mercola.com

The Soap You Should Never Use — But 75% of Households Do


Story at-a-glance

  • Triclosan, a high production volume ingredient used as a bactericide in personal care products such as toothpaste and deodorant, has been linked to heart disease and heart failure in a new study
  • After mice were exposed to one dose of triclosan, heart muscle function was reduced by 25 percent, and grip strength was reduced by 18 percent
  • Researchers also exposed individual human muscle cells (from heart and skeletal muscles) to a triclosan dose similar to everyday-life exposure, and this, too, disrupted muscle function and caused both heart and skeletal muscles to fail
  • Triclosan has also been linked to disruption of hormone function
  • Triclosan is listed on product ingredient labels, so you can easily check to see if it is there before deciding on a purchase.

Triclosan, a high production volume ingredient used as a bactericide in personal care products such as toothpaste, deodorant, and antibacterial soap, has been linked to heart disease and heart failure in a new study.

Yet the U.S. Food and Drug Administration (FDA) states that “Triclosan is not currently known to be hazardous to humans.”1

What this means is that until action is taken to get this common additive out of your toiletries, you could be applying a chemical with proven toxicity to your body multiple times a day …

Triclosan Interferes With Muscle Function

Tricolsan impairs muscle function and skeletal muscle contractility, researchers report in a new study done at the University of California Davis. Although the study was done in mice, researchers said the effects of the chemical on cardiac function were “really dramatic.”

After mice were exposed to one dose of triclosan, heart muscle function was reduced by 25 percent, and grip strength was reduced by 18 percent. Fish were also exposed to triclosan – about the equivalent dose as would be accumulated in a week in the wild – and this led to poorer swimming performance. Researchers also exposed individual human muscle cells (from heart and skeletal muscles) to a triclosan dose similar to everyday-life exposure, and this, too, disrupted muscle function and caused both heart and skeletal muscles to fail.

The study’s lead author noted:2

“Triclosan is found in virtually everyone’s home and is pervasive in the environment. These findings provide strong evidence that the chemical is of concern to both human and environmental health.”

Triclosan May Also Alter Hormone Regulation

This ubiquitous chemical is a chlorinated aromatic compound and is used to help reduce or prevent bacterial contamination. It’s commonly added to many antibacterial soaps and body washes, toothpastes and certain cosmetics, as well as furniture, kitchenware, clothing and toys.

It would be wise to seriously question purchasing ANY product that contains triclosan as an ingredient on the label, not only because of the new muscle function finding discussed above, but also because of its potential impact on hormones.

Toxicological Sciences study found that triclosan affected estrogen-mediated responses, and many chemicals that imitate estrogen are known to increase breast cancer risk.3 Triclosan also suppressed thyroid hormone in rats, and this is only one study in an accumulating body of research showing this chemical to be a potent endocrine disrupter.

Past research has also shown:

  • Exposure to triclosan disrupts thyroid hormone-associated gene expression in frogs, even at low levels (triclosan exposure at 0.15 parts per billion was enough to disrupt a hormone-signaling system in frogs)4
  • Triclosan decreases circulating concentrations of the thyroid hormone thyroxine (T4) in rats5

Even the FDA states that “animal studies have shown that triclosan alters hormone regulation” and that “other studies in bacteria have raised the possibility that triclosan contributes to making bacteria resistant to antibiotics.”6 Although they still maintain that triclosan is not known to be hazardous to humans, they are conducting a review of the chemical, the results of which they expect to release to the public in the winter of 2012.

The U.S. Environmental Protection Agency (EPA), which regulates triclosan as a pesticide, has also announced it will undertake a comprehensive review of triclosan beginning in 2013, and notes they will “pay close attention to the ongoing endocrine research and will amend the regulatory decision if the science supports such a change.” Unfortunately, what this means for you for now is that essentially nothing is being done right now to get this chemical out of your hand soap, body wash and toothpaste.

Triclosan Was First Registered as a Pesticide

If you need more indication that triclosan is probably not the best ingredient to be brushing your teeth with or rubbing onto your underarms, consider that it was first registered with the EPA in 1969 … as a pesticide.

Today it is still registered as a pesticide, although aside from this and its uses in personal care products, it’s also widely used for industrial uses, for instance it is incorporated in conveyor belts, fire hoses, dye bath vats, or ice-making equipment as an antimicrobial pesticide, as well as added to adhesives, fabrics, vinyl, plastics (toys, toothbrushes), polyethylene, polyurethane, polypropylene, floor wax emulsions, textiles (footwear, clothing), caulking compounds, sealants, rubber, carpeting, and a wide variety of other products.7

Triclosan is Already Found in 75% of Americans

As it stands, this chemical has already been detected in the urine of three-quarters of the U.S. population,8 which means urgent action is clearly needed. Last year, House Rules Committee Chairwoman Louise M. Slaughter and two colleagues called on the FDA to enact a ban on triclosan, noting that “triclosan is clearly a threat to our health” and citing the following reasons for the proposed ban:9

  • “The presence of triclosan in the human body and its impact on our ‘body burden’
  • Bacterial resistance to antibiotic medications and antibacterial cleaners
  • The potential for endocrine disruption as a result of triclosan bioaccumulation in the body
  • Wastewater contamination
  • The threat of destroying ecological balance
  • The fact that triclosan is no more effective than soap and water”

This last point is an important one, as the “benefit” of adding an antimicrobial product like triclosan to your hand soap is that it should kill off more germs, and theoretically keep you healthier. On the contrary, there is little or no evidence that these triclosan-containing antibacterial products outperform the good-old-fashioned techniques like washing with soap and water. There is, however, evidence that plain soap is more effective than its antibacterial counterparts. Researchers noted:10

“The lack of an additional health benefit associated with the use of triclosan-containing consumer soaps over regular soap, coupled with laboratory data demonstrating a potential risk of selecting for drug resistance, warrants further evaluation by governmental regulators regarding antibacterial product claims and advertising.”

It’s Easy to Opt Out of Triclosan-Containing Products

The decision to stop using products that contain triclosan is an easy way to positively impact your and your family’s health. There is simply no reason to ever purchase any product with triclosan in it. Triclosan is clearly listed on product ingredient labels, so you can easily check to see if it’s there before deciding on a purchase. Remember, this chemical is not only in soaps but also body washes, toothpaste, shampoo, and 140+ other personal care and home products. Unfortunately, triclosan is now also contaminating rivers, streams and sewage sludge that is applied to agricultural fields, so there is a chance you’re getting exposed from environmental sources as well.11

Aside from reading labels, if a product claims to be “antibacterial,” there’s a good chance it contains triclosan, so this can be used as a warning label of sorts if you’re looking to avoid this chemical.

Source: mercola.com

Roundup and Glyphosate Toxicity Have Been Grossly Underestimated..


Story at-a-glance

  • Research shows glyphosate is toxic to water fleas at extraordinarily low levels, well within the levels expected to be found in the environment. These findings throw serious doubt on glyphosate’s safety
  • Previous research has shown that Roundup is toxic to human DNA even when diluted to concentrations 450-fold lower than used in agricultural applications
  • “Inactive” ingredients such as solvents, preservatives, and surfactants contribute to toxicity in a synergistic manner, and ethoxylated adjuvants in glyphosate-based herbicides have been found to be “active principles of human cell toxicity”
  • Cell damage and even cell death can occur at the residual levels found on Roundup-treated food crops, as well as lawns and gardens where Roundup is applied for weed control
  • Liver, embryonic and placental cell lines are adversely affected by glyphosate at doses as low as 1 ppm. GM corn can contain as much as 13 ppm of glyphosate, and Americans eat an average of 193 lbs of GM foods annually.
  • glyphosate

 

The true toxicity of glyphosate—the active ingredient in Monsanto’s broad-spectrum herbicide Roundup—is becoming increasingly clear as study after study is published demonstrating its devastating effects. In June, groundbreaking research was published detailing a newfound mechanism of harm for Roundup.

This was immediately followed by tests showing that people in 18 countries across Europe have glyphosate in their bodies,1 while yet another study revealed that the chemical has estrogenic properties and drives breast cancer proliferation in the parts-per-trillion range.2

This finding might help explain why rats fed Monsanto’s maize developed massive breast tumors in the first-ever lifetime feeding study published last year. Other recently published studies demonstrate glyphosate’s toxicity to cell lines, aquatic life, food animals, and humans.

Glyphosate Toxicity Underestimated, Study Concludes

One such study, published in the journal Ecotoxicology,3 found that glyphosate is toxic to water fleas (Daphnia magna) at minuscule levels that are well within the levels expected to be found in the environment.

According to regulators, glyphosate is thought to be practically nontoxic to aquatic invertebrates. The water flea is a widely accepted model for environmental toxicity, so this study throws serious doubt on glyphosate’s classification as environmentally safe. According to the study:

“To test the acute effects of both glyphosate and a commercial formulation of Roundup (hereafter Roundup), we conducted a series of exposure experiments with different clones and age-classes of D. magna…. Roundup showed slightly lower acute toxicity than glyphosate IPA alone… However, in chronic toxicity tests spanning the whole life-cycle, Roundup was more toxic.

…Significant reduction of juvenile size was observed even in the lowest test concentrations of 0.05 mg a.i./l, for both glyphosate and Roundup. At 0.45 mg a.i./l, growth, fecundity and abortion rate was affected, but only in animals exposed to Roundup.

At 1.35 and 4.05 mg a.i./l of both glyphosate and Roundup, significant negative effects were seen on most tested parameters, including mortality. D. magna was adversely affected by a near 100% abortion rate of eggs and embryonic stages at 1.35 mg a.i./l of Roundup.

The results indicate that aquatic invertebrate ecology can be adversely affected by relevant ambient concentrations of this major herbicide. We conclude that glyphosate and Roundup toxicity to aquatic invertebrates have been underestimated and that current European Commission and US EPA toxicity classification of these chemicals need to be revised.”

Herbicide Formulations Far More Toxic Than Glyphosate Alone

An article published on Greenmedinfo.com4 last year reviewed several interesting studies relating to the profound toxicity of Monsanto’s herbicide Roundup:

“Back in Feb. of 2012, the journal Archives of Toxicology5 published a shocking study showing that Roundup is toxic to human DNA even when diluted to concentrations 450-fold lower than used in agricultural applications.

This effect could not have been anticipated from the known toxicological effects of glyphosate alone. The likely explanation is that the surfactant polyoxyethyleneamine within Roundup dramatically enhances the absorption of glyphosate into exposed human cells and tissue,” Sayer Ji writes.

“If this is true, it speaks to a fundamental problem associated with toxicological risk assessments of agrichemicals (and novel manmade chemicals in general), namely, these assessments do not take into account the reality of synergistic toxicologies, i.e. the amplification of harm associated with multiple chemical exposures occurring simultaneously.”

‘Inert’ Ingredients Does NOT Mean They Are Inactive…

Similarly, another study published that year in the journal Toxicology6, 7 revealed that inert ingredients such as solvents, preservatives, surfactants and other added substances are anything but “inactive.” They in fact contribute to toxicity in a synergistic manner, and ethoxylated adjuvants in glyphosate-based herbicides were found to be “active principles of human cell toxicity.”

(On a side note, an “ethoxylated” compound is a chemical that has been produced using the carcinogen ethylene oxide.8 The ethoxylation process also produces the carcinogenic byproduct 1,4-dioxane. It’s also worth noting here that the term “inert ingredient” does NOT actually mean that it is biologically or toxicologically harmless! When you see “inert” or “inactive ingredients” listed on the label of a pesticide or herbicide, it only means that those ingredients will not harm pests or weeds. This is how federal law classifies “inert” pesticide ingredients.)9

The study found that liver, embryonic and placental cell lines exposed to various herbicide formulations for 24 hours at doses as low as 1 part per million (ppm), had adverse effects.10 According to the authors:11

“Here we demonstrate that all formulations are more toxic than glyphosate, and we separated experimentally three groups of formulations differentially toxic according to their concentrations in ethoxylated adjuvants. Among them, POE-15 clearly appears to be the most toxic principle against human cells, even if others are not excluded. It begins to be active with negative dose-dependent effects on cellular respiration and membrane integrity between 1 and 3ppm, at environmental/occupational doses. We demonstrate in addition that POE-15 induces necrosis when its first micellization process occurs, by contrast to glyphosate which is known to promote endocrine disrupting effects after entering cells.

Altogether, these results challenge the establishment of guidance values such as the acceptable daily intake of glyphosate, when these are mostly based on a long term in vivo test of glyphosate alone. Since pesticides are always used with adjuvants that could change their toxicity, the necessity to assess their whole formulations as mixtures becomes obvious. This challenges the concept of active principle of pesticides for non-target species.” [Emphasis mine]

Perhaps most disturbing of all, the researchers claim that cell damage and even cell death can occur at the residual levels found on Roundup-treated crops, as well as lawns and gardens where Roundup is applied for weed control. They also suspect that:12

“Roundup might cause pregnancy problems by interfering with hormone production, possibly leading to abnormal fetal development, low birth weights or miscarriages.”

Birth Malformation Skyrocketing in Agricultural Centers of Argentina

Indeed, miscarriages, fertility problems and abnormal fetal development are all problems that are skyrocketing in Argentina, where many are exposed to massive spraying of herbicides. More than 18 million hectares in Argentina are covered by genetically engineered soy, on which more than 300 million liters of pesticides are sprayed. In the village of Malvinas Argentinas, which is surrounded by soy plantations, the rate of miscarriage is 100 times the national average, courtesy of glyphosate.

According to Dr. Medardo Vasquez, a neonatal specialist at the Children’s Hospital in Cordoba, featured in the documentary film People and Power — Argentina: The Bad Seeds:

“I see new-born infants, many of whom are malformed. I have to tell parents that their children are dying because of these agricultural methods. In some areas in Argentina the primary cause of death for children less than one year old is malformations.”

But even if you don’t live in an agricultural area where you might be exposed to Roundup directly, you’re still getting it through your diet if you’re eating non-organic foods. A report given to MomsAcrossAmerica13 by an employee of De Dell Seed Company (Canada’s only non-GM corn seed company) shows that GM corn contains as much as 13 ppm of glyphosate, compared to zero in non-GM corn.

The EPA standard for glyphosate in American water supplies is 0.7 ppm. In Europe, the maximum allowable level in water is 0.2 ppm. Organ damage in animals has occurred at levels as low as 0.1 ppm, and in the study on cell lines discussed above, liver, embryonic and placental cell lines were adversely affected at doses as low as 1 ppm. The fact that genetically modified corn can contain as much as 13 ppm of glyphosate has staggering implications for Americans who eat an average of 193 pounds of genetically engineered foods each year!14

Glyphosate Predisposes Cattle to Botulism

A German study15 published earlier this year looked at glyphosate’s role in the rise of toxic botulism in cattle. This used to be extremely rare, but the incidence has become increasingly common over the past 10-15 years. Normal intestinal microflora is essential for keeping Clostridium botulinum and other pathogens in check, and researchers are now finding that the beneficial gut bacteria in both animals and humans is very sensitive to residual glyphosate levels. This has been discussed previously by both Dr. Don Huber and Dr. Stephanie Seneff.

In this study, the researchers explain that certain intestinal bacteria produce bacteriocines that are specifically directed against C. botulinum, as well as other dangerous pathogens. According to the authors, lactic acid producing bacteria that help defend against Clostridium pathogens are destroyed by glyphosate, suggesting that the rise in C. botulinum associated diseases may be due to glyphosate-tainted animal feed.

The Overlooked Component of Toxicity in Humans

As for its effects on humans, the Samsel – Seneff study published in June suggests that glyphosate may actually be the most important factor in the development of a wide variety of chronic diseases, specifically because your gut bacteria are a key component of glyphosate’s mechanism of harm. Monsanto has steadfastly claimed that Roundup is harmless to animals and humans because the mechanism of action it uses (which allows it to kill weeds), called the shikimate pathway, is absent in all animals. However, the shikimate pathway IS present in bacteria, and that’s the key to understanding how it causes such widespread systemic harm in both humans and animals.

The bacteria in your body outnumber your cells by 10 to 1. For every cell in your body, you have 10 microbes of various kinds, and all of them have the shikimate pathway, so they will all respond to the presence of glyphosate!

Glyphosate causes extreme disruption of the microbe’s function and lifecycle. What’s worse, glyphosate preferentially affectsbeneficial bacteria, allowing pathogens to overgrow and take over. At that point, your body also has to contend with the toxins produced by the pathogens. Once the chronic inflammation sets in, you’re well on your way toward chronic and potentially debilitating disease…

The answer, of course, is to avoid processed foods of all kinds, as they’re virtually guaranteed to contain genetically engineered ingredients, and center your diet around whole, organic foods as toxic pesticides are not permitted in organic farming. Supporting GMO labeling is also important if you value your health, and that of your family and friends, in order to be able to make informed shopping decisions.

Source: mercola.com

Air pollution killing over two million annually, study says.


More than two million people are dying every year from the effects of outdoor air pollution, according to a new study.

An estimated 2.1 million deaths are caused by anthropogenic increases of fine particulate matter (PM2.5) while a further 470,000 are killed annually as a result of human-caused increases in ozone pollution.

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Jason West, co-author of the study published in the journal of Environmental Research Letters said: “Outdoorair pollution is an important problem and among the most important environmental risk factors for health.”

East Asia is the worst affected area with researchers estimating more than a million people dying prematurely every year from PM2.5 pollution and 203,000 from ozone pollution.

India has the second highest air pollution mortality rates with an estimated 397,000 deaths from fine particulates and ozone accounting for, on average, 118,000.

Next comes Southeast Asia which has estimated average of 158,000 deaths from PM2.5 and 33,300 attributed to ozone.

Europe has fractionally less PM2.5 deaths (154,000, on average) and 32,800 premature deaths related to ozone while in North America there were an average of 43,000 deaths from fine particulates and 34,400 related to ozone.

West et al used an ensemble of global atmospheric chemistry climate models to estimate concentrations of PM2.5 and ozone pollutants.

Outdoor air pollution is an important problem and among the most important environmental risk factors for health

 

Fine particulate matter (dust, soot, smoke and liquid droplets) is classified as less than 2.5 micrometers in diameter. It is particularly dangerous to human health because it can lodge deep in the lungs causing cancer and other respiratory disease, according to the U.S. Environmental Protection Agency.

Ground level ozone is created by chemical reactions between oxides of nitrogen and volatile organic compounds (VOC) in the presence of sunlight, say the EPA.

The study also investigated the effects of climate change on worsening air pollution, comparing climate models from the year 2000 with pre-industrial times (1850).

“Very few studies have attempted to estimate the effects of past climate change on air quality and health. We found that the effects of past climate change are likely to be a very small component of the overall effect of air pollution,” said West, assistant professor in the Department of Environmental Sciences and Engineering at the University of North Carolina at Chapel Hill.

“Going forward into the future, climate change will get more severe and that could have greater effects on air pollution.”

The research adds to a growing body of evidence revealing both the human and economic impacts of air pollution around the world.

A recent report published in the British medical journal, The Lancet found that the incidence of heart failure rises when air pollution is higher. The research, funded by the British Heart Foundation, concluded that a reduction of PM2.5 could reduce hospitalizations due to heart failure in the U.S. saving a third of a billion dollars per year.

Going forward into the future, climate change will get more severe and that could have greater effects on air pollution
Jason West, co-author of study

Another recent study published in the Proceedings of National Academy of Sciences highlighted air pollution problems in Northern China, suggesting life expectancy could have been lowered by five-and-a-half years.

Even in the European Union, air pollution takes a sizable 8.6-month chunk off life expectancy according to theWorld Health Organization.

But technology to monitor air pollution is improving all the time, says Roland Leigh, an air quality scientist from theUK’s University of Leicester.

“Historically, air quality is something very much we’ve tried to measure and manage spatially — considering over a total city what the average air quality is. What we are getting to now is systems that let us manage the distribution of air quality with knowledge of where people are and what people are doing,” Leigh told CNN.

Improved data can help manage the exposure of sensitized individuals (the young, asthma sufferers, the elderly), he says. But he concedes that the road to improved air quality might be a long one.

“We have come to terms with the fact that in the urban environment we get exposed to emissions by our transport systems. That transport system is essential and at the moment there is no economically viable way of not emitting pollution at the point of use.

“Either we have to manage those emissions and exposure more intelligently or technologies need to change in our cars.”

 

Source: CNN

Studies on radon concentration in aqueous samples at Mysore city, India.


 

Abstract

Context: Natural radionuclides are wide spread in air, water, soil, plants and in consequence in the human diet. 222 Ra is the daughter product of 226 Ra which belongs to 238 U radioactive seriesAims: Radon enters the human body through ingestion of water and inhalation. Since alpha emitters are the most dangerous, studies on water containing dissolved radon are very important. Materials and Methods: The activity concentration of 222 Ra has been analyzed in water samples collected from lakes, open wells, drilled wells, taps and rivers in and around Mysore city, Karnataka State, India using radon emanometric technique. Results: The present study shows a wide range of radon concentration in water, which varies from below detection limit to 643.9 BqL -1 with a median of 15.8 BqL -1. An annual effective dose with a median of 0.043 μSv y-1 was estimated from the ingestion of 222 Ra through water. Conclusions: 222 Rn concentration in 80% of bore-well water samples are higher than the maximum acceptable contaminant level of 11.1 BqL -1 as prescribed by the environmental protection agency.

Conclusion

The 222 Rn concentrations in 80% of the bore well water samples are higher than the 11.1 BqL -1 prescribed by the EPA. But radon concentration is found to be less in surface water and tap water. Radon concentration in 40% of the bore well water samples are in the range of 4-40 BqL -1 . Consequently, the ingestion dose to the children, adult and the effective dose was found to be with a mean of 0.026, 0.01 and 0.162 μSvy-1 respectively, which is less than the 100 μSvy-1 as recommended by WHO..

 

 

Prenatal Exposure to Air Pollution Associated with Autism.


Prenatal exposure to air pollution is associated with increased risk for autism spectrum disorders in childhood, according to a case-control study in Environmental Health Perspectives.

Using data from the Nurses’ Health Study II, researchers matched 325 children with autism to 22,000 control children without autism. Contemporary EPA-modeled air pollution concentrations were identified for the children’s addresses at birth.

After adjustment for socioeconomic status and other potential confounders, the highest quintile of exposures to diesel, lead, manganese, mercury, methylene chloride, and overall metals was associated with increased risk for autism spectrum disorders, compared with the lowest quintile (odds ratios, 1.5 to 2.0). The associations were stronger among boys than girls, but that may be related to the low number of girls with autism in the study, the authors note.

They conclude that the results “strongly support previous evidence of associations” between air pollution and autism spectrum disorders.

Source: Environmental Health Perspectives