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No “Bones” About It…

Essential Fatty Acids and BonesEssential Fatty Acids may be a key ingredient in supporting bone health.

Essential fatty acids (EFAs) do not come to mind as the first thought in searching for nutritional answers regarding bone health.  “Recent evidence-based research, however, supports intervention with adequate amounts of specific nutrients including vitamin D, strontium, vitamin K, and essential fatty acids in the prevention and primary management of osteoporosis” (Genius, Clin Nutr. 2007).  Osteoporosis has become an epidemic in the Western World in recent years.  How do EFAs fit into this problem that plagues us especially as we get older?

When we think about osteoperosis, we think calcium.  Calcium and bone go together like salt and pepper.  Add in some vitamin D and that’s about it.  However, looking into it deeper we came up with a number of studies that say that EFAs should be right up front and strongly considered in our first line of bone defense.

Essential fatty acids are necessary to human survival, and are called essential because they must come from the diet; they cannot be made by the body.  The omega-6 and omega-3 fatty acids are the best known.  Learning that they are also important for bone health is something we need to know.

In vivo studies (that means in a living animal) have shown that supplementation with long chain n-6 poly-unsaturated fatty acids (PUFAs) in rats causes increases in intestinal Calcium absorption (Haag 2001).  Haag and his colleagues reported a higher total calcium balance and bone calcium content just by adding in either sunflower or safflower oil in their diet.

In another study pregnant female rats were made diabetic. They use a chemical called streptozotocin to duplicate the disorder in the animals.  They were then fed evening primrose oil (GLA) at 500 mg/kg/d throughout their pregnancy and found an almost complete restoration of bone ossification (process of laying down new bone) occurred just by adding in the primrose oils (Braddock, Pediatr Res. 2002).

Claassen et al, Prostaglandins 1995, found that the supplementation of essential fatty acids (EFAs) leads to increased intestinal calcium absorption and calcium balance. The main dietary EFAs they used were linoleic acid (LA) from sunflower oil and alpha-linolenic acid (ALA) from flax seed oil.  They were administered in a ratio of 3:1 which is very close to our 4:1 BodyBio Balanced oil.  The calcium balance (mg/24 h) and bone calcium (mg/g bone ash) increased significantly in the group that were on the EFAs as compared to the animals that were not given the oils.

Schlemmer et al, Prostaglandins 1999, found that if you make animal’s essential fatty acid deficient they flat out develop osteoporosis.  He then added in evening primrose oil (GLA) and completely reversed the loss of bone and reported positive effects on bone metabolism in both the growing male and female rat.

It certainly goes against what you might think.  Oils are thin, some of them even squishy, while bone is completely hard as a rock.  But leaning on our visual senses doesn’t work with body chemistry, obviously.

Bone remodeling is a life-long process where mature bone tissue is removed from the skeleton and is called resorption, while new bone tissue is formed.  It’s a process called ossification or new bone formation. These processes go on all the time and are managed by special cells that crawl along our bones and chew up excess bone growth, osteoclast.  There is another cell osteoblast, that busily does the opposite, laying down new growth where it’s needed.

In the first year of life, almost 100% of the skeleton is replaced.  In adults, remodeling proceeds at about 10% per year (Wheeless).  That means that in a span of 10 years our skeleton is brand new,  If the process is continuous those cells that do the work must be directly influenced by essential fatty acids, and if EFAs are needed to get the job done, well…

References

Genuis SJ, Schwalfenberg GK. Picking a bone with contemporary osteoporosis management: Nutrient strategies to enhance skeletal integrity. Clin Nutr. 2007 Apr;26(2):193-207

Haag M, Kearns SD, Magada ON, Mphata PR, Claassen N, Kruger MC. Effect of arachidonic acid on duodenal enterocyte ATPases. Prostaglandins Other Lipid Mediat. 2001 Aug;66(1):53-63

Braddock R, Siman CM, Hamilton K, Garland HO, Sibley CPGamma-linoleic acid and ascorbate improves skeletal ossification in offspring of diabetic rats. Pediatr Res. 2002 May;51(5):647-52.

Claassen N, Coetzer H, Steinmann CM, Kruger MC. The effect of different n-6/n-3 essential fatty acid ratios on calcium balance and bone in rats. Prostaglandins Leukot Essent Fatty Acids. 1995 Jul;53(1):13-9.

Schlemmer CK, Coetzer H, Claassen N, Kruger MC. Oestrogen and essential fatty acid supplementation corrects bone loss due to ovariectomy in the female Sprague Dawley rat. Prostaglandins Leukot Essent Fatty Acids. 1999 Dec;61(6):381-90

Wheeless Textbook of Orthopedics, Clifford R. Wheeless, III, MD.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Food Safety: Packed Lunch

Food Safety and Packed LunchThe featured abstract, from the respected journal, Pediatrics, explores the condition of packed lunches at a pre-school.  There is no reason to think that other school environments are any different.  Despite a parent’s best efforts at keeping a child’s lunch from spoiling and causing food-related illnesses, such incidents still occur because of inattentive food handling at school.  Malevolence is not usually a factor.

The University of Texas initiated a study into the conditions at schools that can lead to food-borne pathogenic illnesses, and found that temperature control is the prime concern.  Ninety percent of kids’ packed lunches reach unsafe zones. Even with multiple ice packs, “…the majority of lunch items…were at unsafe temperatures.”  As is the case with all health-related measures, “Education of parents and the public must be focused on methods of packing lunches that allow the food to remain in the safe temperature zone to prevent foodborne illnesses.”
(Almansour. 2011)

The “danger zone” for foods lies between 40° F. and 140° F.  Therefore, foods kept outside the “zone” are subject to the growth of pathogenic micro-organisms, whether at school, on a picnic, in the backyard, or in the kitchen.  A mantra that has been embraced long ago is that food should not be kept out of refrigeration longer than two hours.  Luncheon meats, smoked meats, and other cured comestibles are not an exception.  If the ambient temperature is higher than 90° F., the limit is one hour.  Unless the classroom has a refrigerator, this is practically impossible to do at school.  Note that the insulated bags we use to pack our kids’ lunches can rebound inside a refrigerator and prevent the cold from getting to the food.

Of course, Mom or Dad has to start with clean ingredients prepared on a clean surface, using clean hands and clean implements.  The CDC holds that only 3% of food contamination can be attributed to the farm.  The other 97% occurs between there and the kitchen.  (Alliance for Food and Farmng.  2010)  Including an ice source is imperative if you know the lunch will be kept at room temperature, such as within a middle-school locker, where teachers have found last month’s French fries after the mephitis rendered the neighboring crowd semi-conscious.  If the timing can be figured out, it’s O.K. to freeze those items that can be frozen without compromising their sensory quality.  Dressings like mayonnaise, and delicate items like tomatoes, are not in this group.  Peanut butter and jelly, and whole fruits and vegetables need not be cold.

If salad ingredients are part of the repast, especially lettuce, it’s vital that they be kept below 39° F. or so, lest they start to show a significant decline in visual quality as well as in safety.  However, even if it looks good, lettuce can harbor and encourage proliferation of E. coli, a dastardly micro-organism with a reputation worse than Blackbeard’s. By the way, this bacterium can thrive even on the pre-washed, ready-to-eat greens you bring directly home from the supermarket.  (Luo. 2010)  Wash them anyway. Plain water works, but a 50-50 mix with hydrogen peroxide can set the mind at ease. Peroxide reverts to plain water after exposure to light and air. That’s why it comes in an opaque brown bottle.

Smaller amounts of food in shallow containers are easiest to handle. You really don’t want to be sorting leftovers after they’ve been on the bus ride home.  Getting the containers back is another story.

References

Pediatrics 2011; 128; peds.2010-2885
Published online August 8, 2011 (doi: 10.1542/peds.2010-2885)
Temperature of Foods Sent by Parents of Preschool-aged Children
Fawaz D. Almansour, MS, Sara J. Sweitzer, PhD, RD, LD, Allison A. Magness, BS, Eric E. Calloway, BS, Michael R. McAllaster, BS, Cynthia R. Roberts-Gray, PhD, Deanna M. Hoelscher, PhD, RD, LD, CNS, Margaret E. Briley, PhD, RD, LD

J Food Sci. 2010 Sep;75(7):M390-7.
Effect of storage temperature and duration on the behavior of Escherichia coli O157:H7 on packaged fresh-cut salad containing romaine and iceberg lettuce.
Luo Y, He Q, McEvoy JL.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Child Athletes Nutrition

children-sportsA child is not a miniature adult. His or her nutrition and hydration needs are not exactly the same, especially in sports participation.  With the growth and availability of sports opportunities, you’d think that related nutrition needs would be a concern. To the contrary, sports nutrition for youngsters receives less attention than it deserves.

“Most children and adolescents who are strongly committed to sports are not concerned about nutrition as it relates to energy balance and obesity,” states a report from a 2004 issue of Nutrition.  The interactions among nutrition, growth, and development deserve attention if a participant expects to achieve optimal performance and to avoid the injuries and problems that stem from nutritional deficiencies.   Daily fluid turnover in adult athletes has received intense study, but that for children and adolescents hasn’t.  That of adults may be two to three liters a day, but in youngsters has only been estimated at half that—and that has been based on sedentary youth.  Although “sweating capacity is typically reported to be lower in children,” there is an increase in sweat rate when adjusted for body surface area.  Besides the energy needed for normal growth and development, children athletes need to accommodate the greater expenditure from physical activity.  That can vary from one sport to another.  (Petrie. 2004).

Besides the fun, kids participate in sports to hone their skills, to experience the excitement of competition, to be part of a team, and to stay in shape, among other reasons.  But they pay little or no attention to fuel and hydration needs.  Parents and coaches, on the other hand, do.  At least they should.  Hectic schedules, availability of foods, limited time and extended days interfere with choices and timing.

Even though the number of kids playing organized sports is on the rise, fitness levels are on the decline, and are much lower than in previous decades.  This partially explains the spate of sports-related injuries.  (Cordelia. 2011).  Targeted intervention strategies include ample hydration and nutrition.  Because of maturation differences, kids need more protein to support growth, more calcium to support bone, and more attention to the prevention of hypohydration.  (Bar-Or. 2001).

Sweat helps to cool the body, and what comes out has to be replaced, otherwise performance suffers and health is at risk.  To prevent the dizziness, fatigue, nausea, and cramps that characterize dehydration, the young athlete should drink one or two cups of water or electrolyte within four hours of an event.  If no urine has been passed, or if urine is bright yellow and minimal, another 1 ½ cups is suggested within two hours of the game.  During the event, try to replace fluids as they are lost to sweat, about a cup every fifteen or twenty minutes if possible.  Plain water will do, but if the event is longer than an hour, use an electrolyte replacement.  Recovery is just as important to a preteen or teen as it is to an adult.  The best way to determine post-exercise hydration needs is to weigh the child to compute weight loss, and to replace fluid at one and a half times the volume lost to sweat.  One ounce of water (sweat) weighs one ounce, so the math is simple.  A kid’s thirst mechanism is not well-developed, so you’ll almost have to force him to drink…but do it.

The nutrients in which young athletes are most deficient include carbohydrates, calcium, vitamin B6, folate and iron, the last being especially important to girls.  Carbohydrate inadequacy leads to shortened glycogen stores and premature fatigue, especially if the game is sixty minutes or longer.  Once glycogen is gone, fat gets mobilized and the child will “bonk.”  The last thing you want is for the young athlete to burn protein for fuel. An active child will need as many as 500 to 1500 more calories a day than his inert peers.

Two to three hours before an event, give your athlete a light, carb-rich meal:  carrot sticks and a piece of cheese; a little pasta; a small sandwich.  Have him exert himself on a slightly empty stomach to avoid cramping, even fatigue.  Chips, cakes or cookies, and candy are out.  The protein your child needs will not build bulk.  That comes with age.  Normal muscle development will require as much as one and a half grams of protein for each kilogram of body weight, but need not be much more than fifteen to twenty percent of daily calorie intake.  Reduce that during the off season. Thirty percent fat in the daily intake will help to supply needed calories.  Reduce that off-season, too, lest you greet Tweedledee one morning.

The matter of iron deficiency is a particular concern for girls, especially after the onset of menarche, which can be a couple of years late for an iron-fisted ball player.  Iron-deficiency anemia is a real threat for female athletes.  Besides affecting performance and recovery, low iron stores impair immune function and may initiate other physiological problems.  Supplementation is not intended to replace food as a source of nutrients, but in the case of iron deficit, it may be recommended.  (Beard. 2000).  There’s no need for your daughter to join the 50% of the world population who are deficient in iron.  (Ahmadi. 2010).  Raw meat probably won’t help, but getting 15 mg a day from supervised supplementation will.

Youngsters are often grossly misinformed about what they need and don’t need.  Their peers and the internet are not always reliable sources of information.  Some young athletes need only a minor tweak to their diets; others need a complete overhaul.  If you feel inadequate, don’t be embarrassed.  There are dietitians and sports nutritionists who can help.

References

Petrie HJ, Stover EA, Horswill CA.
Nutritional concerns for the child and adolescent competitor.
Nutrition. 2004 Jul-Aug;20(7-8):620-31.

Cordelia W Carter, Lyle J Micheli
Training the child athlete: physical fitness, health and injury
Br J Sports Med 2011;45:880-885

Bar-Or O.
Nutritional considerations for the child athlete
Can J Appl Physiol. 2001;26 Suppl:S186-91.

Beard J, Tobin B.
Iron status and exercise.
Am J Clin Nutr. 2000 Aug;72(2 Suppl):594S-7S.

Ahmadi A, Enayatizadeh N, Akbarzadeh M, Asadi S, Tabatabaee SH.
Iron status in female athletes participating in team ball-sports.
Pak J Biol Sci. 2010 Jan 15;13(2):93-6.

Koehler K, Braun H, Achtzehn S, Hildebrand U, Predel HG, Mester J, Schänzer W.
Eur J Appl Physiol. 2011 May 19. [Epub ahead of print]
Iron status in elite young athletes: gender-dependent influences of diet and exercise.

Committee on Sports Medicine and Fitness
AMERICAN ACADEMY OF PEDIATRICS
Intensive Training and Sports Specialization in Young Athletes
Pediatrics Vol. 106 No. 1 July 1, 2000 : pp. 154 -157

Martinez LR, Haymes EM.
Substrate utilization during treadmill running in prepubertal girls and women.
Med Sci Sports Exerc. 1992 Sep;24(9):975-83.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Enhancing The Worst

burger-on-trayIt’s bad enough when the junk in (or on) your food harms you—you know, the preservatives, the agricultural sprays, the stuff in there that you can’t begin to pronounce, the coloring agents, and whatever—but this is getting ridiculous.  It’s not necessarily the food you prepare at home from scratch that we’re talking about.  It’s not even the Boiled Water Helper that some “cooks” need to put something mostly edible in front of you.  It’s the wrapper, especially the one making cozy with your fast food burger.  And so we moan, “Now, what is it?”

If you’re ready, we’ll give you the list.  Even if you’re not, here it comes:  perfluoroalkyls, polyfluoroalkyl phosphate esters (PAP’s), polyfluorinated carboxylic acids (PFCA’s), and everyone’s favorite, perfluorooctanoic acid (PFOA).  You don’t have to remember these, but note that fluorine is a central player in the cast.  Yep, the same stuff in your toothpaste, the label of which tells you not to swallow too much.

Fluorine belongs to a group of chemical elements called halogens, along with chlorine, bromine, iodine, and astatine, the last of which is essentially unavailable in nature and is radioactive.   The halogens are the only group that contains elements in all three states of matter—fluorine and chlorine are gases, iodine is a solid, and bromine is a liquid.  All are non-metals.  Because they are highly reactive, they’re found in the environment only as compounds.  Iodine is the heaviest element needed by living creatures, and its appropriateness to thyroid health is well-known.  But it’s less reactive than its fellows, so it’s easily displaced.  That means that fluorine and bromine, which is used to bleach flour, can push it aside and take its place in your thyroid gland.   Hypothyroidism, anyone?

Fluorides are moderately toxic and, if conditions are right, can attack intracellular calcium.  It’s readily absorbed and forms an acid that binds with calcium and interferes with several enzymes.  Too much fluoride leads to skeletal fluorosis and mottled teeth.  (Reddy, 2009)  It might be all right to use on the teeth from the outside, but certainly not from inside the body.

What’s this got to do with food wrappers?  The compounds named in the second paragraph are stable synthetic chemicals that repel grease, oil, and water.  If you ever saw the television commercial that boasted of stain-repellent and water-repellent clothing, you’ve seen these chemicals at work.  Though still popular on carpets, they pretty much have been removed from materials that touch the skin.  Hmmm.  However, they are used to make paper and cardboard packaging.  These would be the PFCA’s, which break down into PAP’s, and they wrap your burger so you can eat it while you drive and stay relatively grease free.  Do you microwave popcorn?  Guess what coats the inside of the bag.

Human exposure to PFCA’s is worldwide.  These chemicals are environmentally persistent, as well, and have generated considerable scientific and regulatory interest on a global scale.  (Andersen, 2008)  Research at the University of Toronto found that the PAP in food contact applications does affect blood chemistry in humans, causing changes in sex hormones and cholesterol.  In laboratory animals, which are obviously smaller than people, premature death and developmental delay have been observed.  Some of the effects on rats—tumor growth, for example—may not be applicable to humans.  (D’eon, 2011)  But who knows?  We mentioned that these fluorinated substances are environmentally persistent.  They also persist in the blood stream.  Think of what happens to people who eat fast food every day.

PFOA has been detected in a high percentage of human blood samples and house dust taken from homes in Massachusetts, Maine, New York, Oregon, and California, and it has contaminated drinking water in West Virginia and Minnesota.  Two companies that manufacture the chemicals, DuPont and 3M, were allegedly aware of the potentially harmful effects on humans, but sequestered the data and never told the U.S. Environmental Protection Agency of the adverse effects information, as required under the Toxic Substances Control Act.  They got banged for a minimum of thirteen million dollars in fines, with the potential to reach three hundred million.  DuPont settled a class action suit with West Virginia in 2004.  The courts added that the ante will be upped if a definitive link is found between the chemicals and human misery.  This could exceed three hundred million dollars.  Ouch. (http://www.defendingscience.org/case_studies/perfluorooctanoic-acid.cfm)

The Office of Research and Development of the EPA issued a paper in March, 2009, that listed a hundred sixteen “articles of commerce” that contain perfluorocarboxylic acid (aka PFCA).  How come we never heard about any of this?  Of course, typical of many authorities, is the hedge that additional study is warranted before anything definite can be proposed.  The list covers commodities from household liquids to textiles, from Teflon cookware to food contact paper, and even…gets this…dental floss.  Dental floss???  You can check it out at www.oecd.org/dataoecd/47/50/48125746.pdf
Makes you proud, doesn’t it?

It appears that interest in this matter was contagious in the first decade of the new century.  The FDA learned that fluorochemical paper additives migrate into food, after it examined coconut and other oils, butter, water, vinegar, and alcohol.  Buttered microwave popcorn was a star.  (Begley, 2008)  The persistence of the fluorinated entities was supported by Canadian research the following year.  (Benskin, 2009)  Even the State of New Jersey got into the act and looked at drinking water in selected areas, finding detectable levels of PFOA in a variety of sources, but adding that levels are not regulated under State requirements.  That means everything is fine and dandy, right?  Of all the samples tested, 78% were positive for fluoride contamination.  This site http://www.nj.gov/dep/watersupply/pfoa.htm will give you the dope.

This stuff interferes with immunity in humans and wildlife (Dewitt, 2011), could possibly be associated with longer time to pregnancy (Vestergaard, 2012), and might affect your liver (Naile, 2012) and thyroid (Boas, 2011).  We need to call our favorite fast food emporiums and ask a few questions.  Does it matter to you?

References

Andersen ME, Butenhoff JL, Chang SC, Farrar DG, Kennedy GL Jr, Lau C, Olsen GW, Seed J, Wallace KB.
Perfluoroalkyl acids and related chemistries–toxicokinetics and modes of action.
Toxicol Sci. 2008 Mar;102(1):3-14.

Begley TH, Hsu W, Noonan G, Diachenko G.
Migration of fluorochemical paper additives from food-contact paper into foods and food simulants.
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Mar;25(3):384-90.

Benskin JP, De Silva AO, Martin LJ, Arsenault G, McCrindle R, Riddell N, Mabury SA, Martin JW.
Disposition of perfluorinated acid isomers in Sprague-Dawley rats; part 1: single dose.
Environ Toxicol Chem. 2009 Mar;28(3):542-54.

Boas M, Feldt-Rasmussen U, Main KM.
Thyroid effects of endocrine disrupting chemicals.
Mol Cell Endocrinol. 2011 Sep 10.

Cheng X, Klaassen CD.
Perfluorocarboxylic acids induce cytochrome P450 enzymes in mouse liver through activation of PPAR-alpha and CAR transcription factors.
Toxicol Sci. 2008 Nov;106(1):29-36.

Defending Science
Perfluorooctanoic Acid
http://www.defendingscience.org/case_studies/perfluorooctanoic-acid.cfm

D’Eon JC, Mabury SA.
Production of perfluorinated carboxylic acids (PFCAs) from the biotransformation of polyfluoroalkyl phosphate surfactants (PAPS): exploring routes of human contamination.
Environ Sci Technol. 2007 Jul 1;41(13):4799-805.

D’eon JC, Mabury SA.
Exploring indirect sources of human exposure to perfluoroalkyl carboxylates (PFCAs): evaluating uptake, elimination, and biotransformation of polyfluoroalkyl phosphate esters (PAPs) in the rat.
Environ Health Perspect. 2011 Mar;119(3):344-50. Epub 2010 Oct 29.

Dewitt JC, Peden-Adams MM, Keller JM, Germolec DR.
Immunotoxicity of Perfluorinated Compounds: Recent Developments.
Toxicol Pathol. 2011 Nov 22. [Epub ahead of print]

Fromme H, Schlummer M, Möller A, Gruber L, Wolz G, Ungewiss J, Böhmer S, Dekant W, Mayer R, Liebl B, Twardella D.
Exposure of an adult population to perfluorinated substances using duplicate diet portions and biomonitoring data.
Environ Sci Technol. 2007 Nov 15;41(22):7928-33.

Naile JE, Wiseman S, Bachtold K, Jones PD, Giesy JP.
Transcriptional effects of perfluorinated compounds in rat hepatoma cells.
Chemosphere. 2012 Jan;86(3):270-7.

NJ Department of Environmental Protection
Determination of Perfluorooctanoic Acid (PFOA) in Aqueous Samples
January, 2007
http://www.nj.gov/dep/watersupply/pfoa.htm

J Ostertag SK, Chan HM, Moisey J, Dabeka R, Tittlemier SA.
Historic dietary exposure to perfluorooctane sulfonate, perfluorinated carboxylates, and fluorotelomer unsaturated carboxylates from the consumption of store-bought and restaurant foods for the Canadian population.
Agric Food Chem. 2009 Sep 23;57(18):8534-44.

Reddy DR.
Neurology of endemic skeletal fluorosis.
Neurol India. 2009 Jan-Feb;57(1):7-12.

U.S. EPA , March 2009
PERFLUOROCARBOXYLIC ACID CONTENT IN 116 ARTICLES OF COMMERCE
www.oecd.org/dataoecd/47/50/48125746.pdf

Vestergaard S, Nielsen F, Andersson AM, Hjøllund NH, Grandjean P, Andersen HR, Jensen TK.
Association between perfluorinated compounds and time to pregnancy in a prospective cohort of Danish couples attempting to conceive.
Hum Reprod. 2012 Jan 13. [Epub ahead of print]

 Yamashita N, Kannan K, Taniyasu S, Horii Y, Petrick G, Gamo T.
A global survey of perfluorinated acids in oceans.
Mar Pollut Bull. 2005;51(8-12):658-68.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Solvents In The Home And Workplace

kitchen-cleanersThere are too many things we take for granted.  When it comes to health, if it doesn’t hurt, we don’t pay attention to it.  This is the case with the solvents we use around the house, including the apparently harmless cleaners and the more aggressive degreasers and thinners.  The solvents used at the workplace are considerably more powerful.  In general, quite a few of the products we use at home fit the definition of toxic.

The term solvent refers to liquid (usually organic) chemicals used to dissolve solids.  Some, like turpentine and the citrus solvents, are naturally derived.  Others are made from petroleum or other synthetic sources.  None is “safe,” although there are degrees of “un-safeness.”   (CDC. 2010)  Skin contact and inhalation are both means of entry into the body, and may be categorized by duration as long or short, and by intensity as low or high.  Acute effects occur after short-term exposure; chronic effects after a longer period of time.  Health consequences may be subclinical, meaning that symptoms are not yet manifest.

Some solvents—this includes pesticides—are fat-soluble and allow metabolites access to the central and peripheral nervous systems (CNS and PNS).  While narcosis (stupor) may be reversible, demyelination and cell death often are not.  Researchers in France looked at the relation between Parkinson’s disease and exposure to pesticides in a population whose exposure to these chemicals is prevalent (exterminators), and found that relation to be positive, especially for organochlorine insecticides.  (Elbaz. 2009)  Prior studies on the epidemiology of Parkinson’s by the same team came to a similar conclusion.  (Elbaz. 2008)

All solvents can dissolve the skin’s protective barrier of oils, causing the skin to dry and chap and leading to some form of dermatitis.  Some of the natural ones, like turpentine, may cause allergic reactions.  Some cause no overt damage but penetrate the skin, enter the bloodstream, and damage other organs, particularly the liver.  (Nachman. 2002)  Most of us connect toxicity to physical contact, never thinking that the vapors alone can cause damage, but scientists in Messina, Italy found depletion of reduced glutathione, decreased antioxidant activity, and oxidative damage in subjects exposed to the vapors of organic solvents.  (Costa. 2006)  All studies agree that early detection of toxicity is important to resolution.

The effects of solvent exposure upon the eyes and respiratory tract are realized quickly if concentrations are high enough, but workers are commonly unaware of a solvent’s effects at low concentrations.  Often the only indication of exposure is an increased frequency of colds and respiratory infections.  Over time, chronic bronchitis may develop.   However, the instigating factor(s) may be out of mind and the relationship is never made.  The ubiquity of certain solvents, especially formaldehyde, takes a toll on unsuspecting consumers.  (Schenker. 1996)   Wall finishes, carpeting, cabinetry, plywood, insulation, timber paneling, and even some shampoos, lotions, baby wipes, and body washes may contain formaldehyde.  Some manufacturers will use unfamiliar synonyms to mask the presence of this proven carcinogen.  Formalin, methanol, urea, methylaldehyde, and formic aldehyde are but a few.  Tightness in the chest, breathing difficulty, unexplained rash, and swelling of the mouth and tongue are the more-common signs of exposure to formaldehyde.  Changes in heart rate are not uncommon with over-exposure to any organic solvent, with “over-exposure” being the key modifier, however subjective that may be.  (Morrowa.  1995)

An area lacking in study is reproductive health, but the little research already done points to solvents’ culpability.   Small studies indicate that subjection to solvents that are particular to specific industries may induce decline in sperm motility.  The painting and sheet metal trades and others that use naphtha, methyl ethyl ketone, xylene, toluene and the like are most likely to experience detrimental reproductive consequences.  (Lemasters.  1999)   Although tests in females are not nearly so definitive, infertility, spontaneous abortion, and reproductive cancers have been reported in some studies after chemical exposures.  The ambiguity of testing in females may be due to multiple confounders that include poor methodology and small sample size.  (Sharara. 1998)

Alternatives to harmful solvents are available, but, because they might demand more physical labor, are not the most popular items on the shelf.  Baking soda can kill foul odors.  Vinegar in water or cream of tartar in water can clean aluminum.  Borax cleans the bathroom, and bleach + water will remove mildew from grout.  TSP and water can clean almost anything.  Dismissing solvents is not only a matter of “going green,” but also a matter of personal and family health.  Thinking that your hobby is great fun, you might be surprised to hear that exposure to the solvents used in building models and in artwork during the year preceding childbirth has been associated with elevated risk of childhood leukemia.  (Freedman.  2001)

References

CDC, 2010
Workplace Safety & Health Topics
ORGANIC SOLVENTS
Page last updated:July 20,2010
http://www.cdc.gov/niosh/topics/organsolv/

Elbaz A, Clavel J, Rathouz PJ, Moisan F, Galanaud JP, Delemotte B, Alpérovitch A, Tzourio C.
Professional exposure to pesticides and Parkinson disease.
Ann Neurol. 2009 Oct;66(4):494-504.

Elbaz A, Moisan F.
Update in the epidemiology of Parkinson’s disease.
Curr Opin Neurol. 2008 Aug;21(4):454-60.

Nachman Brautbar, John Williams II
Industrial solvents and liver toxicity: Risk assessment, risk factors and mechanisms
International Journal of Hygiene and Environmental Health. Vol 205, Iss 6, 2002, Pp 479-491

Chiara Costa, Rita De Pasquale, Virginia Silvari, Mario Barbaro, Stefania Catania
In vitro evaluation of oxidative damage from organic solvent vapours on human skin
Toxicology in Vitro  Volume 20, Issue 3, April 2006, Pages 324-331

M.B. Schenker , J.A. Jacobs
Respiratory effects of organic solvent exposure
Tubercle and Lung Disease. Volume 77, Issue 1, February 1996, Pages 4-18

Lisa A. Morrowa, , Stuart R. Steinhauerb
Alterations in heart rate and pupillary response in persons with organic solvent exposure
Biological Psychiatry.  Volume 37, Issue 10, 15 May 1995, Pages 721-730

Grace Kawas Lemasters, Donna M Olsen, James H Yiin, James E Lockey, Rakesh Shukla, et al
Male reproductive effects of solvent and fuel exposure during aircraft maintenance
Reproductive Toxicology.  Volume 13, Issue 3, May-June 1999, Pages 155-166

Fady I Sharara M.D., David B Seifer M.D., Jodi A Flaws Ph.D.
Environmental toxicants and female reproduction
Fertility and Sterility.  Volume 70, Issue 4, October 1998, Pages 613-622

D M Freedman, P Stewart, R A Kleinerman, S Wacholder, E E Hatch, R E Tarone, L L Robison, and M S Linet
Household solvent exposures and childhood acute lymphoblastic leukemia
Am J Public Health. 2001 April; 91(4): 564–567.

Seaton A, Jellinek EH, Kennedy P.
Major neurological disease and occupational exposure to organic solvents.
Q J Med. 1992 Sep;84(305):707-12.

Ng TP, Lim LC, Win KK.
An investigation of solvent-induced neuro-psychiatric disorders in spray painters.
Ann Acad Med Singapore. 1992 Nov;21(6):797-803.

Y. Lolin
Chronic Neurological Toxicity Associated with Exposure to Volatile Substances
Hum Exp Toxicol July 1989 vol. 8 no. 4 293-300

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Brain Fog On Your Mind?

brain-ringCharity begins at home, and the brain is no stranger to this maxim. The brain is not only immunologically active on its own behalf, but also plays a role in protecting the rest of the body. The brain directs cell-to-cell communications, but those messages do not always host good news. Sometimes they carry the black cloud of inflammation, which is supposed to be a protective response to an insult, injury, or destruction of tissue, but it also may lead to loss of some kinds of function, including thought.  The chemicals that coordinate the inflammatory process are called cytokines, and they amplify immunological activity.

Given the role of cytokines in the neuroimmune process, it has been suggested that these molecules influence cognitions—the mental processes of knowing, which is an exercise that includes awareness, perception, reasoning and judgment.  Investigators at the St. Vincent Hospital, in Indianapolis, studied the relationship between inflammation and cognition and found that, “There is abundant evidence that inflammatory mechanisms within the central nervous system contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells,” adding that there is a growing awareness of the role of cytokines in “…the inflammatory processes in neurodegenerative diseases…”  (Wilson. 2002)  A considerable volume of such activity results from stress and its effect on immunity.

A dab of semantic guidance might be appropriate.  First, glial cells are a kind of scaffolding that supports and surrounds nerve cells.  Each neuron is surrounded by several.  In the brain, glia account for about forty percent of brain volume.  They’re smaller than neurons, maintaining the capacity to divide and form part of the blood-brain barrier that is designed to regulate the passage of matter between the blood and the central nervous system.  Second, cytokines have multiple tasks, including blood clotting, growth and development, and, of course, immunity.  They comprise several groups.  There are those that regulate T-cells and B-cells in the immune system, called interleukins; those that block pathogens such as viruses, called interferons; and those that promote cell proliferation, called transforming growth factors, among others.

Cytokines can get excited by physical, mental, spiritual, biochemical, and psychological stress.  That runs the gamut from strenuous activity to poor diet to arguing with the kids to sickness or disease, all of which can lead to lack of mental clarity, confusion, tiredness, difficulty in concentrating, and forgetfulness—brain fog.   The cytokines can interfere with complex cognitive processes at the molecular level, where the regulation of neurotransmitters is disturbed and memory is distorted.  (McAfoose. 2009)   Recent studies in the Netherlands found that women are more prone to cognitive deficiencies caused by inflammation than men.  (Trollor. 2011)

When markers of inflammation are elevated they offer an explanation for the subsequent brain fog.  Of the several markers, C-reactive protein (CRP) is one of the most commonly measured.  Its elevation denotes the presence of inflammation somewhere in the body.  Not all inflammation is as painful as that from an ingrown toenail with its accompanying redness, swelling and pain.  But high CRP may account for, and even predict, memory impairment.  (Noble. 2010)  The diseases that are attributed to old age, such as arthritis, and the recruitment of the immune system, such as during a viral or bacterial attack, will increase circulating interleukins as well as CRP, both of which affect memory, attention, abstract thinking, the initiation and inhibition of appropriate actions, and planning.  (Hoth. 2008)

The factors that cause brain fog have a more profound effect as we age. If, however, we learn to control those factors now, it makes geriatric life a breeze. Removing dietary insults is one step.  The hardest slap comes from sugar and refined carbohydrates.  Supplementation with the B vitamins, the stress fighters, helps to maintain nerve integrity and function.  Sleep, a little exercise, counseling, and meditating on those things that are just, pure, lovely and of good report can ameliorate those little irritations that accumulate into seemingly insurmountable roadblocks to peace and the mental clarity that ensues.  By the way, keeping your teeth in good shape can help. (Kamer. 2011)

References

Wilson CJ, Finch CE, Cohen HJ.
Cytokines and cognition–the case for a head-to-toe inflammatory paradigm.
J Am Geriatr Soc. 2002 Dec;50(12):2041-56.

Neurosci Biobehav Rev. 2009 Mar;33(3):355-66. Epub 2008 Oct 18.
Evidence for a cytokine model of cognitive function.
McAfoose J, Baune BT.

Julian N Trollor, Evelyn Smith, Emmeline Agars, Stacey A Kuan, Bernhard T Baune
The association between systemic inflammation and cognitive performance in the elderly: the Sydney Memory and Ageing Study.
Age Dordrecht Netherlands (2011) Issue: 95, Pages: 1-10

Noble JM, Manly JJ, Schupf N, Tang MX, Mayeux R, Luchsinger JA.
Association of C-reactive protein with cognitive impairment.
Arch Neurol. 2010 Jan;67(1):87-92.

Karin F. Hoth, PhD, Andreana P. Haley, PhD, John Gunstad, PhD, et al
Elevated C-Reactive Protein Is Related to Cognitive Decline in Older Adults with Cardiovascular Disease
J Am Geriatr Soc. 2008 October; 56(10): 1898–1903.

Kamer AR, Morse DE, Holm-Pedersen P, Mortensen EL, Avlund K
Periodontal Inflammation in Relation to Cognitive Function in an Older Adult Danish Population.
J Alzheimers Dis. 2011 Nov 1. [Epub ahead of print]

Grassi-Oliveira R, Bauer ME, Pezzi JC, Teixeira AL, Brietzke E.
Interleukin-6 and verbal memory in recurrent major depressive disorder.
Neuro Endocrinol Lett. 2011;32(4):540-4.

Ridker PM, Hennekens CH, Buring JE, Rifai N.
C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women.
N Engl J Med. 2000 Mar 23;342(12):836-43.

Marioni, Riccardo Emilio
Inflammation and cognition : the association between biomarker levels, their genetic determinants, and age-related cognitive decline.
The University of Edinburgh. 2010
http://hdl.handle.net/1842/4436

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

BHT In My Cereal?

cereal-bagCan there be too much of a good thing? Drinking too much water can dilute the electrolytes in the body and short circuit the wiring.  It’s called water intoxication, and can lead to death.  Though eating too much candy might not cause a person to die, the resultant stomach distress might bring on the wish to expire early.  If there can be too much of a good thing, can there also be too little of a bad thing, meaning how much of a toxin can I consume before the symptoms show up or I keel over? Such is the case with some food additives. If enough people pronounce a falsehood as fact, does that make it true merely by the sheer number of proponents? Let’s talk about BHT and you decide whether it’s good or bad.

Butylated Hydroxytoluene is a horrendous sounding name.  Its presence lets us to keep a box of cereal in the cabinet for weeks at a time, and allows the product to withstand its protracted journey from maker to kitchen.  Its absence, on the other hand, yields a noxious aroma akin to a week-old dishrag that really needs a bath.  The culprit?  Rancid fats.  But what does BHT do to people?

BHT and its relative, BHA, have been used extensively as antioxidants for decades.  BHT was patented in 1947.  Since then it has become the most prevalent and approved antioxidant in the world.  The FDA, disbelieved by many consumers, approved BHT as an additive to foods and food packaging in 1954.  BHT is a phenol derivative that slows the rate of oxidation.  Oxygen prefers BHT to the fats in our foods.  The public gets upset when it learns that a material used to make non-foods appears in their victuals.  Yes, it is true that BHT is used in the manufacture of tires, some plastics and diesel fuel.   But it does what it is supposed to do without adverse effects.  It’s even been certified Kosher by the Union of Orthodox Jewish Congregations of America, and also certified Halal by the Islamic Food Nutrition Council of America.

Toxicology studies that added BHT to animal feed found that adverse effects were dose-dependent.  Amounts of BHT in excess of 526 mg/kg/day resulted in pleural and peritoneal hemorrhage in laboratory rats. (Takahashi.  1978) A human consumes in the neighborhood of 0.1 mg/kg/day of BHT.  Research shows that 500 times this amount yields no injurious effects.  (Branen.  1975)  This study added that 7 ounces of BHT per pound of body weight would result in pathological, enzyme, and lipid alterations that may be causative of certain cancers.  (Ibid.)

Some scientific research deals with topics and events that are way out there, seeming to have no bearing on real health issues.  (Gee, if I swallow a handful of number eight woodscrews and drink a cup of WD-40, will the screws still rust?)  There’s a similarly inane study in which lab animals were given more than four ounces of BHT per pound of body weight a day for three days, combined with a healthy dose of E.coli bacteria to learn of adverse effects on the liver.  What do you think happened?  The conclusion was that there is risk of liver damage with high-dose BHT in the presence of pathogenic bacteria.  (Engin. 2011)  This makes you wonder whose dime is in the phone booth.

The World Health Organization (WHO) asked its expert committee on food additives to evaluate the intake of BHT in ten participating countries in 1999.  After identifying certain foods as major contributors to overall intake, the committee agreed that 0.3 mg/kg of body weight a day is tolerable. (WHO, Geneva. 1999)  It is interesting to note that more BHT is allowable in the United States than in the other countries.  This might be explained by the fact that packaging materials are also treated with BHT, and that these plastics and waxed papers may carry as much as 7.8 mg/kg.  (Xiong. 2011)

That BHT has antioxidant properties was acknowledged by Korean researchers when they determined that, according to the National Health and Nutrition Survey, first conducted in 1971 and regularly afterward, one hundred thirty-three foods in twelve categories actually held significantly less BHT than the maximum limits. (Suh. 2005)  For most of these foods, less than 0.008 mg/kg was consumed.  Not to be outdone, Dutch scientists sought a connection between BHT intake and gastric cancers, studying a group of more than 120 thousand individuals, starting in 1986.  This longitudinal study examined BHT foods that included mayonnaise, cooking fats and oils, creamy salad dressings, and dried soups.  Via food frequency questionnaire, it was ascertained that the average intake of BHT was 351 micrograms a day total, not per pound or kilogram.  No association with gastric cancer was observed.  Oddly, an inverse association was found.  (Botterweck. 2000)

Around the time Christopher Columbus was floating in the Atlantic and Caribbean, a Swiss physician named Paracelsus, the first guy to call zinc, zinc, who is also known as the father of toxicology, was attributed with the dictum, “The dose makes the poison.”  His intended meaning was that a substance considered toxic may be harmless in small doses and that, conversely, an ordinarily harmless substance may be toxic in large doses—like water.  Such may be the case with BHT.

BHT was lauded as being protective against atherosclerosis in work performed in Sweden in the early 1990’s, where BHT was added to a 1% cholesterol diet in rabbits, whose digestive prowess parallels humans’.  Although lipid profiles were elevated, atherosclerotic involvement was considerably lower in the BHT rabbits than in those not receiving the substance in the same diet.  These investigators concluded that the antioxidant character of BHT prevented unwelcomed cardiac influences, although modulation of monocyte adhesion may be a factor.  (Björkhem. 1991)  Further study along this line, using a similar dietary protocol, discovered that LDL from other BHT-fed rabbits was less sensitive to oxidation than LDL from rabbits whose diets lacked BHT.
(Freyschuss. 2001)  It is accepted that oxidized LDL is the cause of ischemic heart disease.

What about cancer?  Pathologists at New York Medical College assessed BHT as a food additive in meta-analyses that inferred no cancer hazard at levels commonly used in food processing and manufacturing.  (Williams. 1999)  Laboratory animals that were purposely exposed to carcinogenic substances, notably aflatoxins that cause liver cancer, were spared from disease when administered BHT at doses of 1.5 mg/kg total over a period of twenty weeks (about 25 micrograms/kg, 3 x a week).  (Williams. 1986)  Other substances used to model liver carcinogenesis were almost completely neutralized in the presence of BHT, as reported in a study performed more than three decades ago.  (Ulland. 1973)

The dermatological use of BHT, as in cosmetics and other topically administered products, tells a somewhat different story in laboratory animals, since BHT is absorbed through the skin.  Stomach acid and digestive fluids appear to attenuate any pathogenic activity of the chemical.  Although the mechanism has not been completely explained, acute doses of BHT, as much as 1.0 g/kg, have caused some renal and hepatic damage in lab rats.  That is not to say that the same thing will happen to a human, since people are not likely to have exposure to such concentrated amounts.  (Lanigan. 2002)

For the time being, it looks like your cereal is off the hook.  There is one lingering question, though.  If natural vitamin E, as d-alpha-tocopherol, can do the same thing as BHT, why isn’t it being used?  It must be the money.

References

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    O. Takahashi, K. Hiraga
    Dose-response study of hemorrhagic death by dietary butylated hydroxytoluene (BHT) in male rats
    Toxicology and Applied Pharmacology.  Volume 43, Issue 2, February 1978, Pages 399-406

    A.L. Branen
    Toxicology and biochemistry of Butylated Hydroxyanisole and  Butylated Hydroxytoluene
    J Am Oil Chem Soc. 1975, Feb.; 52(2): 59-63

    Engin AB, Bukan N, Kurukahvecioglu O, Memis L, Engin A.
    Effect of butylated hydroxytoluene (E321) pretreatment versus l-arginine on liver injury after sub-lethal dose of endotoxin administration.
    Environ Toxicol Pharmacol. 2011 Nov;32(3):457-64. Epub 2011 Sep 10.

    WORLD HEALTH ORGANIZATION
    INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

    World Health Organization, Geneva, 1999
    IPCS - International Programme on Chemical Safety
    EVALUATION OF NATIONAL INTAKE ASSESSMENTS OF
     BUTYLATED HYDROXYTOLUENE (BHT)
    http://www.inchem.org/documents/jecfa/jecmono/v042je24.htm 
      Xiong Z, Wang L, Li N, Yu Y, Jia X
    Determination of antioxidant residues in polymer food package using gas chromatography.
    Se Pu. 2011 Mar;29(3):273-6.

    Suh HJ, Chung MS, Cho YH, Kim JW, Kim DH, Han KW, Kim CJ.
    Estimated daily intakes of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT) and tert-butyl hydroquinone (TBHQ) antioxidants in Korea.
    Food Addit Contam. 2005 Dec;22(12):1176-88

    Botterweck AA, Verhagen H, Goldbohm RA, Kleinjans J, van den Brandt PA.
    Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study.
    Food Chem Toxicol. 2000 Jul;38(7):599-605.

    Björkhem I, Henriksson-Freyschuss A, Breuer O, Diczfalusy U, Berglund L, Henriksson P.
    The antioxidant butylated hydroxytoluene protects against atherosclerosis.
    Arterioscler Thromb. 1991 Jan-Feb;11(1):15-22.

    Freyschuss A, Al-Schurbaji A, Björkhem I, Babiker A, Diczfalusy U, Berglund L, Henriksson P.
    On the anti-atherogenic effect of the antioxidant BHT in cholesterol-fed rabbits: inverse relation between serum triglycerides and atheromatous lesions.
    Biochim Biophys Acta. 2001 Dec 30;1534(2-3):129-38.

    G.M Williams, M.J Iatropoulos, J Whysner
    Safety Assessment of Butylated Hydroxyanisole and Butylated Hydroxytoluene as Antioxidant Food Additives
    Food and Chemical Toxicology.  Vol 37, Iss 9-10, Sep-Oct 1999, Pages 1027-1038

    Williams GM, Tanaka T, Maeura Y.
    Dose-related inhibition of aflatoxin B1 induced hepatocarcinogenesis by the phenolic antioxidants, butylated hydroxyanisole and butylated hydroxytoluene.
    Carcinogenesis. 1986 Jul;7(7):1043-50.

    B.M. Ulland, J.H. Weisburger†, R.S. Yamamoto, Elizabeth K. Weisburger
    Antioxidants and carcinogenesis: butylated hydroxytoluene, but not diphenyl-p-phenylenediamine, inhibits cancer induction by N-2-fluorenylacetamide and by N-hydroxy-N-2-fluorenylacetamide in rats*
    Food and Cosmetics Toxicology.  Volume 11, Issue 2, 1973, Pages 199-207

    Lanigan RS, Yamarik TA.
    Int J Toxicol. 2002;21 Suppl 2:19-94.
    Final report on the safety assessment of BHT(1).

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Exposure To Motor Lubricants & Solvents

car-engineMuscle car plus motor head does not equal muscle head, although it could. The first pair evokes positive images for those who remember Holley carburetors, dual exhausts, Hurst shifters and four on the floor (gears, that is). The muscle cars of the 60’s were exciting to drive and fun to work on. That was an era when there was enough room in the engine compartment to swing a socket wrench. Of course, without air conditioning there was plenty of space to climb inside and yank a Champion or two. Considering that engine oil is to a car what blood is to the human body, you can bet that oil changes were dutifully timed events. Unlike blood, oil has changed over the years. Modern engine oils have viscosity-index improvers, antioxidants, dispersants, corrosion and foam inhibitors, and anti-wear agents that were absent half a century ago. Also some oil formulations vary from state to state. In the past, wearing oil and grease on hands and clothes was a badge of honor, an announcement that proclaimed mastery over a demanding technology. Today, protective gloves need to be the order of the day.

Mechanics and other auto workers who are exposed to used crankcase oil have experienced skin rashes, blood effects similar to anemia, headaches and tremors. Along with used oil, they are exposed to other chemicals/toxins common to the auto industry, including fluids, metal particles and fumes. Used oil may contain chemical constituents that result from the internal combustion process, such as the polycyclic aromatic hydrocarbons (PAH) associated with benzene and related suspect carcinogenic compounds. Systemic effects of exposure to used oils and automotive fluids may include elevated blood pressure, aberrant red blood cell values (caused by lead exposure), stress to the liver (as indicated by irregularities in enzyme markers), and skin rashes (Clausen and Rastogi, 1977). In mechanics who work with new cars, interior cabin materials present no less a threat to health. Exposures to high concentrations of the aliphatic hydrocarbons that render the appealing “new car smell” are found to accumulate in the body (Yoshida, Jan 2010 and Aug 2010).

What’s the big deal?

There is more than one route to internal toxicity. You can swallow almost anything, inhale too many other things, and absorb more than a handful of the remaining damaging substances available to the environment. Compounds that contain only hydrogen and carbon are called hydrocarbons. The number of atoms of either element can change to make a different substance, one of the simplest being CH4, known as methane. During the refining of petroleum, one kind of hydrocarbon can be converted to another, giving us gasoline, naphtha, kerosene, lubricating oils and more. Adding chlorine to the C-H backbone reduces flammability and increases stability, resulting in chlorinated hydrocarbon solvents that can be used to clean, degrease and thin almost anything. At high temperatures that vary according to the compound, they give off seriously toxic gases and can enter the body through the skin.

Most foreign substances are unable to penetrate skin, the outer layer of which is an effective barrier to most inorganic particles. But damage to the stratum corneum, whether by abrasion, exposure to U-V light, or by chemical insult, can allow penetration. Lubricating oils, some waxes, and greases can induce primary irritations and photosensitivity to skin. The severity depends on the nature of the oil, the integrity of the skin, the frequency and length of contact, and individual susceptibility. Certain size molecules of chlorinated and simpler hydrocarbons, and of those with a greater number of carbon atoms than hydrogens, are more apt to enter skin than others (Riihimaki and Pfaffli, 1978) (Babu et al, 2004).

Among the riskier materials are automotive and industrial solvents made with trichloroethylene or tetrachloroethylene, known to penetrate the skin and suspected of being carcinogenic. Up to the 1970’s, trichloroethylene was used directly on humans as a general anesthetic and as a wound disinfectant. Believe it or not, it was also used as a flavoring agent for coffee. This nonsense was halted in 1977. Today it’s being used as a degreaser, as a cleaner for textiles, as an additive to inks and paints, and as an ingredient in PVC (the polyvinyl chloride in plastic plumbing). At least it won’t catch fire. Strangely, the metabolites of trichloroethylene are identical to those that follow the chlorination of municipal water supplies, namely chloral, chloral hydrate, monochloroacetic acid, and di- and trichloroacetic acids (Simon, 2005).

Tetrachloroethylene is also known as perchloroethylene, most commonly used in dry cleaning.  Exposure, either respiratory or dermal, may cause depression of the CNS, liver and kidney damage, impaired memory and headaches (DHHS, 1991). Like trichloroethylene, it is non-flammable and stable. Earlier in its history it was used in commercial refrigerants and auto air conditioners. But it’s an excellent solvent for organic materials such as the greases and lubricants used in the automotive industry…and it dissolves fats from skin, resulting in skin irritation.

Does It Hurt?

Once in the body, either through the skin or the nose, these hydrocarbons attack the cell membrane and the proteins that prevent entry of toxic compounds. A bodyguard enzyme called ATP-ase directs cell traffic by letting food and energy in, and by escorting wastes and toxins to the door. Another of its jobs is to control the balance of sodium and potassium. Sodium tells a cell to contract so you can pick up a tool, and potassium tells it to relax so you can put it down again. Chlorinated solvents, though, attack the fats from which the membrane is made and cause it to lose its shape and to resemble a half deflated basketball. Now, it can’t do its job and you get tired quickly and your thinking becomes foggy. Once ATP-ase gets dissolved by chlorinated hydrocarbons, any work that requires muscle power becomes more and more difficult. There are no alternatives to crankcase oil, but there are optional solvents and degreasers. Read the labels, wear gloves, and protect your eyes. No matter how thick-skinned we think we are, we really aren’t.

References

Armstrong SR, Green LC.
Chlorinated hydrocarbon solvents.
Clin Occup Environ Med. 2004 Aug;4(3):481-96


Babu RJ, Chatterjee A, Ahaghotu E, Singh M.
Percutaneous absorption and skin irritation upon low-level prolonged dermal exposure to nonane, dodecane and tetradecane in hairless rats.
Toxicol Ind Health. 2004 Sep;20(6-10):109-18.


Clausen J, Rastogi S.
Heavy metal pollution among autoworkers:I Lead.
Br J Ind Med. 1977; 34(3):208-215.


Clayton GD, Clayton FE, eds. 1981.
Patty’s industrial hygiene and toxicology. Volume 2B: Toxicology. 3rd ed.
New York, NY: John Wiley and Sons, 3373, 3397-3398.


Clonfero E, Zordan M, Cottica D, et al.
Mutagenic activity and polycyclic aromatic hydrocarbon levels in urine of humans exposed to therapeutic coal tar. Carcinogenesis. 1986; 7:819-823.


DHHS 1991.  (NIOSH) Publication Number 97-155
Control of Exposure to Perchloroethylene in Commercial Dry Cleaning
http://www.cdc.gov/niosh/docs/hazardcontrol/hc17.html


Duprat P, Gradiski D.
Percutaneous toxicity of hexachlorobutadiene.
Acta Pharmacol Toxicol (Copenh). 1978 Nov;43(5):346-53.


Edelfors S, Ravn-Jonsen A.
Effect of organic solvents on nervous cell membrane as measured by changes in the (Ca2+/Mg2+) ATPase activity and fluidity of synaptosomal membrane.
Pharmacol Toxicol. 1992 Mar;70(3):181-7.


Filon FL, Boeniger M, Maina G, Adami G, Spinelli P, Damian A.
Skin absorption of inorganic lead (PbO) and the effect of skin cleansers.
J Occup Environ Med. 2006 Jul;48(7):692-9.


Jorgensen PL, Hakansson KO, Karlish SJ.
Structure and mechanism of Na,K-ATPase: functional sites and their interactions.
Annu Rev Physiol. 2003;65:817-49. Epub 2002 May 1.


Korpela M, Tähti H.
Effects of industrial organic solvents on human erythrocyte membrane adenosine triphosphatase activities in vitro.
Scand J Work Environ Health. 1987 Dec;13(6):513-7.


Francis J. Koschier
Toxicity of Middle Distillates from Dermal Exposure
Drug and Chemical Toxicology. 1999, Vol. 22, No. 1 , Pages 155-164


McDougal JN, Pollard DL, Weisman W, Garrett CM, Miller TE.
Assessment of skin absorption and penetration of JP-8 jet fuel and its components.
Toxicol Sci. 2000 Jun;55(2):247-55.


Monteiro-Riviere NA, Inman AO, Riviere JE.
Skin toxicity of jet fuels: ultrastructural studies and the effects of substance P.
Toxicol Appl Pharmacol. 2004 Mar 15;195(3):339-47.


Naskali L, Oksanen H, Tähti H.
Astrocytes as targets for CNS effects of organic solvents in vitro.
Neurotoxicology. 1994 Fall;15(3):609-12.


E Reese and R D Kimbrough
Acute toxicity of gasoline and some additives.
Environ Health Perspect. 1993 December; 101(Suppl 6): 115–131.


Riihimäki V, Pfäffli P.
Percutaneous absorption of solvent vapors in man.
Scand J Work Environ Health. 1978 Mar;4(1):73-85.


Skou JC, Esmann M.
The Na,K-ATPase.
J Bioenerg Biomembr. 1992 Jun;24(3):249-61.


Suzanne E. Simon
Editor’s perspective: The prevalence of trichloroethylene metabolites in public drinking-water supplies
Remediation Journal. Summer 2005; 15(3): 1-4


Vaalavirta L, Tähti H.
Astrocyte membrane Na+, K(+)-ATPase and Mg(2+)-ATPase as targets of organic solvent impact.
Life Sci. 1995;57(24):2223-30.


Vaalavirta L, Tähti H.
Effects of selected organic solvents on the astrocyte membrane ATPase in vitro.
Clin Exp Pharmacol Physiol. 1995 Apr;22(4):293-4.


Yoshida T.
Approach to estimation of absorption of aliphatic hydrocarbons diffusing from interior materials in an automobile cabin by inhalation toxicokinetic analysis in rats.
J Appl Toxicol. 2010 Jan;30(1):42-52.


Yoshida T.
Estimation of absorption of aromatic hydrocarbons diffusing from interior materials in automobile cabins by inhalation toxicokinetic analysis in rats.
J Appl Toxicol. 2010 Aug;30(6):525-35.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Electromagnetic Headaches

emf-headachesWhen it blows in the wind, we try to find out where it’s coming from. Once in a while, though, there’s so much stench we can’t identify the source. Such is the case with electromagnetic fields—EMF’s— and related wavy things. There’s so much hullabaloo about the good and the bad that we can’t decide if EMF’s are, well, good or bad. They’ve been around forever, so exposure to them is nothing new. Man-made EMF’s, from the generation of electricity, household appliances, industrial equipment and, of course, telecommunications and broadcasting, add to the apparent physiological burden already begun by the simplicity of human metabolism and Earth’s magnetic properties. Is it really a big deal?

Tiny electric currents exist in the body because of the chemistry that allows it to work, even in the absence of external electrical fields. Nerves, for example, send signals by transmitting electrical impulses. All our biochemical reactions follow the rearrangement of charged particles. Your heart responds to an electrocardiogram, right? The concern is that low-frequency electrical fields affect the human body just as they affect anything else made from charged particles. These exogenous fields, if large enough, can cause changes inside the body by stimulating nerves or muscles…or organs. Lucky for us, most exogenous currents are too small to have any ill effect, even directly beneath a high voltage transmission line. On the other hand, the biological effect of radiofrequency fields is heating, and this is the reason for scientific intervention in the placement of sources, such as phone towers.

Biological effects are measurable responses to a stimulus or to a change in the environment. Most of these are harmless, like listening to music or exercising. Changes that are irreversible or that persist for a long time might not be harmless. Electromagnetic fields above a certain level present a concern. That is understandable, and measures are taken to limit exposure, even internationally. Lower levels, over the long term, are suspected of causing unwanted biological responses, including headaches, to which some people are more or less sensitive. Cases of hypersensitivity to EMF’s have been reported for a few decades. Some researchers group them with the condition known as multiple chemical sensitivity illness. Oddly, a plethora of those reporting such sensitivity seem to fall into categories that defy characterization (Levallois, 2002). In polls and surveys, people will express a concern about the ill effects of EMF’s in the absence of personal symptoms, worrying that their cell phones may eventually cause sleep disturbances and headaches (Schreier, 2006) (Hillert, 2002).

Cell phones emit waves as long as they’re turned on and are looking for a signal from the tower. Wi-Fi, not necessarily related to wireless fidelity, contains that technology which connects electronic devices to each other and to the internet using radio waves. Some investigators claim that both can interfere with a child’s ability to learn and remember, while others feel that autistic spectrum conditions are likewise related (Herbert, 2013, parts 1 and 2). If the pharmaceutical powers control a considerable part of the economy, they deserve credit for telling us in their TV spiels that the side effects of their products are worse than the diseases they purport to treat. Powerful industrial entities have an interest in leading the unsuspecting public to believe their EMF’s are completely harmless, since they cannot be perceived by the senses, including pain receptors. If, as suspected, DNA damage actually results from EMF-induced oxidative stress, physiologic consequences can be expected and headaches to be the presentation (Wolf, 2005). Children are exposed to EMF’s at home, on the school bus, in the classroom, at the doctor’s office, and probably everywhere else, with few exceptions, if any. Cell phone standards, by the way, were established years ago and have not been revisited. We are unsure of their effects on developing brains, but, by looking at students’ academic orientation, we can guess. Most European nations forbid the sale of cell phones to those under eighteen.

Cause-effect situations are more definitive than associations or relations. Pathologies that may be associated with EMF’s are not definitely caused by them. Therefore, compared to other disease vectors, little is being done to address possibilities of EMF involvement. Some reports indicate the blood-brain barrier to become more permeable after exposure to EMF’s (Leszczynski, 2002), even from fellow riders in a public conveyance (Kato, 2012). That we are constantly bombarded with radiation is a concern of WHO and the children’s health expert panel (WHO, 2011) (ICNIRP, 2009), (IEEE, 2005). But that concern is magnified because mobile phones work close to the head, causing the distribution of energy to be direct. This raises the question of relationships/associations to glioma and neuroma (Hours, 2007) (Schüz, 2006) naturally requiring closer inspection. Because of subjectivity, no determination is possible (Cardis, 2010), although hints are numerous (Cardis, 2011).

Cancer aside, the headache issue is a global topic. In many countries, about a fourth of cell phone users polled associate headache with EMF (Thamire, 2004) (Meg, 2005) (Al-Khlaiwi, 2004) (Genius, 2012) (Kato, 2012) (Schreier, 2006). Yet, until asked, none relates the two. Talking on a mobile phone for one hour a day incurs the cumulative effect that upsets homeostasis, allowing for exposure to ten thousand watts of accrued radiation. A microwave oven emits only 2 milliwatts at two inches distance; a hundredth of that at twenty inches (FDA, 2011).

We all know that lifestyle can’t be dictated. Smokers smoke and drinkers drink.Second-hand smoke is a health matter. There is no such thing as second-hand drinkingexcept to a fetus. But there is such a thing as second-hand radiation. We seemto prefer first-hand.

References

Al-Khlaiwi T, Meo SA.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population.
Saudi Med J. 2004 Jun;25(6):732-6.

Augner C, Hacker GW.
Are people living next to mobile phone base stations more strained? Relationship of health concerns, self-estimated distance to base station, and psychological parameters.
Indian J Occup Environ Med. 2009 Dec;13(3):141-5.

Belyaev IY, Hillert L, Protopopova M, Tamm C, Malmgren LO, Persson BR, Selivanova G, Harms-Ringdahl M.
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy persons.
Bioelectromagnetics. 26(3):173-184, 2005.

Belyaev IY, Markovà E, Hillert L, Malmgren LO, Persson BR.
Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-H2AX DNA repair foci in human lymphocytes.
Bioelectromagnetics. 2008 Oct 6. [Epub ahead of print]

Cardis E, Deltour I, Vrijheid M, Combalot E, Moissonnier M, Tardy H, Armstrong B, et al
INTERPHONE Study Group.
Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study.
Int J Epidemiol. 2010 Jun;39(3):675-94.

Cardis E, Armstrong BK, Bowman JD, Giles GG, Hours M, Krewski D, McBride M, Parent ME, et al
Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five Interphone countries.
Occup Environ Med. 2011 Sep;68(9):631-40.

Dahmen N, Ghezel-Ahmadi D, Engel A.
Blood laboratory findings in patients suffering from self-perceived electromagnetic hypersensitivity (EHS). Bioelectromagnetics. 30(4):299-306, 2009.

Eltiti S, Wallace D, Ridgewell A, Zougkou K, Russo R, Sepulveda F, Mirshekar-Syahkal D, Rasor P, Deeble R, Fox E.
Does short-term exposure to mobile phone base station signals increase symptoms in individuals who report sensitivity to electromagnetic fields? A double-blind randomized provocation study.
Environ Health Perspect. 2007 Nov;115(11):1603-8.

FDA. 2011
Microwave Oven Radiation
http://www.fda.gov/radiation-emittingproducts/resourcesforyouradiationemittingproducts/ucm252762.htm

Furubayashi T, Ushiyama A, Terao Y, Mizuno Y, Shirasawa K, Pongpaibool P, Simba AY, et al.
Effects of short-term W-CDMA mobile phone base station exposure on women with or without mobile phone related symptoms.
Bioelectromagnetics. 30(2):100-113, 2009.

Genuis SJ, Lipp CT.
Electromagnetic hypersensitivity: fact or fiction?
Sci Total Environ. 2012 Jan 1;414:103-12.

Herbert MR, Sage C.
Autism and EMF? Plausibility of a pathophysiological link – Part I.
Pathophysiology. 2013 Jun;20(3):191-209.

Herbert MR, Sage C
Autism and EMF? Plausibility of a pathophysiological link part II.
Pathophysiology. 2013 Jun;20(3):211-34.

Hietanen M, Hämäläinen A-M, Husman T.
Hypersensitivity symptoms associated with exposure to cellular telephones: No causal link. Bioelectromagnetics 23:264-270, 2002.

Hillert L, Berglind N, Arnetz BB, Bellander T.
Prevalence of self-reported hypersensitivity to electric or magnetic fields in a population-based questionnaire survey.
Scand J Work Environ Health. 2002 Feb;28(1):33-41.

Hours M, Bernard M, Montestrucq L, Arslan M, Bergeret A, Deltour I, Cardis E.
Cell Phones and Risk of brain and acoustic nerve tumours: the French INTERPHONE case-control study.
Rev Epidemiol Sante Publique. 2007 Oct;55(5):321-32.

Institute of Electrical and Electronics Engineers (IEEE).
IEEE standard for safety levels with respect to human exposure to radio frequency electromagnetic fields, 3 kHz to 300 GHz, IEEE Std C95.1, 2005.

International Commission on Non-Ionizing Radiation Protection (ICNIRP).
Statement on the “Guidelines for limiting exposure to time-varying electric, magnetic and electromagetic fields (up to 300 GHz)”, 2009.

Johansson A, Nordin S, Heiden M, Sandström M.
Symptoms, personality traits, and stress in people with mobile phone-related symptoms and electromagnetic hypersensitivity.
J Psychosom Res. 68(1):37-45, 2010.

Kato Y, Johansson O.
Reported functional impairments of electrohypersensitive Japanese: A questionnaire survey.
Pathophysiology. 2012 Apr;19(2):95-100.

Kim DW, Lee JH, Ji HC, Kim SC, Nam KC, Cha EJ.
Physiological effects of RF exposure on hypersensitive people by a cell phone.
Conf Proc IEEE Eng Med Biol Soc. 2008;1:2322-2325.

Landgrebe M, Hauser S, Langguth B, Frick U, Hajak G, Eichhammer P.
Altered cortical excitability in subjectively electrosensitive patients: results of a pilot study.
J Psychosom Res. 62(3):283-288, 2007.

Landgrebe M, Frick U, Hauser S, Langguth B, Rosner R, Hajak G, Eichhammer P.
Cognitive and neurobiological alterations in electromagnetic hypersensitive patients: results of a case-control study.
Psychol Med. 38(12):1781-1791, 2008.

Dariusz Leszczynski
EFFECT OF GSM MOBILE PHONE RADIATION ON BLOOD-BRAIN BARRIER (2002)
http://www.ursi.org/Proceedings/ProcGA02/papers/p1043.pdf

Levallois P, Neutra R, Lee G, Hristova L.
Study of self-reported hypersensitivity to electromagnetic fields in California.
Environ Health Perspect. 2002 Aug;110 Suppl 4:619-23.

Markova E, Hillert L, Malmgren L, Persson BR, Belyaev IY.
Microwaves from GSM Mobile Telephones Affect 53BP1 and gamma-H2AX Foci in Human Lymphocytes from Hypersensitive and Healthy Persons.
Environ Health Perspect. 113(9):1172-1177, 2005.

McCarty DE, Carrubba S, Chesson AL, Frilot C, Gonzalez-Toledo E, Marino AA.
Electromagnetic hypersensitivity: evidence for a novel neurological syndrome.
Int J Neurosci. 2011 Dec;121(12):670-6.

Meo SA, Al-Drees AM.
Mobile phone related-hazards and subjective hearing and vision symptoms in the Saudi population.
Int J Occup Med Environ Health. 2005;18(1):53-7.

Nieto-Hernandez R, Rubin GJ, Cleare AJ, Weinman JA, Wessely S.
Can evidence change belief? Reported mobile phone sensitivity following individual feedback of an inability to discriminate active from sham signals.
J Psychosom Res. 65(5):453-460, 2008.

Schreier N, Huss A, Röösli M.
The prevalence of symptoms attributed to electromagnetic field exposure: a cross-sectional representative survey in Switzerland.
Soz Praventivmed. 2006;51(4):202-9.

Schuz J, Böhler E, Berg G, Schlehofer B, Hettinger I, Schlaefer K, Wahrendorf J, Kunna-Grass K, Blettner M.
Cellular phones, cordless phones, and the risks of glioma and meningioma (Interphone Study Group, Germany).
Am J Epidemiol. 2006 Mar 15;163(6):512-20.

Simkó M, Mattsson MO.
Extremely low frequency electromagnetic fields as effectors of cellular responses in vitro: possible immune cell activation.
J Cell Biochem. 2004 Sep 1;93(1):83-92.

Thamire  Al-Khlaiwit,  Sultane A Meoos
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population
Saudi Medical Journal 2004; Vol. (6): 732-736

WHO
Electromagnetic fields and public health: mobile phones
Fact sheet N°193. June 2011
http://www.who.int/mediacentre/factsheets/fs193/en/

Wolf FI, Torsello A, Tedesco B, Fasanella S, Boninsegna A, D’Ascenzo M, Grassi C, Azzena GB, Cittadini A.
50-Hz extremely low frequency electromagnetic fields enhance cell proliferation and DNA damage: possible involvement of a redox mechanism.
Biochim Biophys Acta. 2005 Mar 22;1743(1-2):120-9.

Yokus B, Cakir DU, Akdag MZ, Sert C, Mete N.
Oxidative DNA damage in rats exposed to extremely low frequency electro magnetic fields.
Free Radic Res. 2005 Mar;39(3):317-23.

*These statements have not been evaluated by the FDA.
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