Indoor Air Pollution

indoor air pollutionIndoor air pollution is one of the most overlooked threats to human health. Households in developing countries might be the hardest hit. Because children spend almost eighty percent of their time indoors, they are the most likely victims. In the past several years it has been determined that conditions ranging from asthma, headaches and fatigue to allergic reactions, hormone imbalances and central nervous damage may be attributed to indoor air quality—or, rather, the lack of it. Most of us realize that outdoor air quality can affect health, but few pay attention to the indoor air…unless it smells bad.

In a paper supported by the University of Medicine and Dentistry of New Jersey and printed in the British Medical Bulletin in the early 2000’s, Junfeng (Jim) Zhang and Kirk Smith allowed that the ubiquitous character of indoor air pollution “…may contribute to increasing prevalence of asthma, autism, childhood cancer, medically unexplained symptoms, and perhaps other illnesses.”   Because the sources of indoor pollution are not expected to abate in the near future, particularly those associated with tobacco use, we can expect to voice concerns for a long time. The authors add that “…risks associated with solid fuel combustion coincide with risk associated with modern buildings.”

It is absurd that indoor air quality should be so poor that it causes sickness and disease, yet that appears to be more the rule than the exception in modern times.  Nobody would think of running a tractor-trailer or a tour bus in the living room, but the pollution effect is the same.  Most of us are unaware of the problem because a single major source of indoor pollution can’t be fingered. Despite this unrecognized threat, indoor pollution is twice as bad as outdoor, according to studies performed by the Bloomberg School of Public Health at Johns Hopkins.  Others put the rate at five times. There are so many sources of indoor pollution that have become part of our daily lives that we never question them. Have you thought about the unpronounceable ingredients in your cleaning products and other household chemicals, like the pesticides you use in the yard? How about your cosmetics and the smelly things you plug into the wall to hide other smelly things?  Got new carpet or upholstery? Oh, yeah, there are more, such as the aroma of hot tar being applied to the new roof at your children’s school…while school’s in session. The activity may be outdoors, but the sickening smell is certainly indoors.

The influx of biological pollutants is hard to manage.  Molds, bacteria, viruses, animal dander, skin particles (yes, even human), pollen and dust mites are everywhere.  You can see airborne particles in that beam of sunshine coming through the window, but you can’t identify any of them.  Some can breed in the stagnant water that sits in your humidifier, or where water has collected in your ceiling tiles, insulation or carpet.  These things can cause fever, chills, cough, and chest tightness, among other symptoms.  Even when we do what we think is good for the family, we may do the opposite.  Burning the woodstove or fireplace might save money on the heating bill (though the fireplace is suspect), but how about the junk it puts into the air?  You can’t win, eh?

In our attempts to conserve energy, we have sealed our houses so tightly that nothing can get in and less can get out.  Once we change the air pressure dynamics of our houses, we have allowed intruders to enter.  Radon and soil gases are most common, and they creep through the cellar floor.  Mechanical ventilation can help to get the junk out and bring at least some fresher air in.  Not only does insulation contribute to the tightness of our homes, but also it brings problems of its own in the form of irritating chemicals.

Increasing ventilation is one of the easiest steps to improving indoor air quality.  Even in the dead of winter it’s a good idea to open the front and back doors simultaneously once a day to let fresh cold air in and the stale reheated air out.  Pathogens grow in an environment that is warm, dark and damp.  Your hot-air heater is a prime breeding ground for colds and the like.  The American Lung Association and the Mayo Clinic have recognized air filters as being sufficiently effective to allay at least some of the problem.   Using a vacuum with a HEPA filter is another prudent intervention.

Concerning household cleaners, we all know that anything natural costs more than anything man-made, and that mindset is hard to figure out.  Why do we have to pay for things that are left out?  In the mean time, note that vinegar-water concoctions are just as good as many commercial products at cleaning our homes—even the commode.  Who cares if it smells like salad?

But what might just be the best air cleaner on the planet is a collection of house plants.  Formaldehyde is a major contaminant of indoor air, originating from particle board, carpets, window coverings, paper products, tobacco smoke, and other sources.  These can contribute to what has been called “sick building syndrome.”  The use of green plants to clean indoor air has been known for years.  This phytoremediation has been studied with great intensity in a few laboratories across the globe, where it was learned that ferns have the greatest capability of absorbing toxins.  (Kim, Kays. 2010)  As is the case with many endeavors, there is a hierarchy of plants that does the job.  After the ferns, the common spider plant (Chlorophytum comosum) was found best at removing gaseous pollutants, including formaldehyde.  Way back in 1984 NASA released information about how good the spider plant is at swallowing up indoor air pollution.  The heartleaf philodendron partners well with Chlorophytum.  Dr. Bill Wolverton, retired from NASA, has a list (  Areca and lady palms, Boston fern, golden pothos and the dracaenas are at the top.  Plants with fuzzy leaves are best at removing particulates from smoke and grease, and some are even maintenance-free (almost), including the aloes, cacti, and the aforementioned spider plants, pothos and dracaenas, the last sometimes called the corn plant.

For more information, try these resources:

Indoor Air Pollution Increases Asthma Symptoms (Johns Hopkins Bloomberg School of Public Health)

Pollution at Home Often Lurks Unrecognized (12/26/2008, Reuters Health) by Amy Norton

Air Purifiers and Air Filters Can Help the Health of Allergy and Asthmas Sufferers (S. A. Smith)

Indoor Air Pollution Fact Sheet (08/1999, American Lung Association)

An Introduction to Indoor Air Quality (Environmental Protection Agency)


Br Med Bull (2003) 68 (1): 209-225.
Indoor air pollution: a global health concern
Junfeng (Jim) Zhang and Kirk R Smith

Environmental and Occupational Health Sciences Institute & School of Public Health, University of Medicine and Dentistry of New Jersey, NJ

Indoor air pollution is ubiquitous, and takes many forms, ranging from smoke emitted from solid fuel combustion, especially in households in developing countries, to complex mixtures of volatile and semi-volatile organic compounds present in modern buildings. This paper reviews sources of, and health risks associated with, various indoor chemical pollutants, from a historical and global perspective. Health effects are presented for individual compounds or pollutant mixtures based on real-world exposure situations. Health risks from indoor air pollution are likely to be greatest in cities in developing countries, especially where risks associated with solid fuel combustion coincide with risk associated with modern buildings. Everyday exposure to multiple chemicals, most of which are present indoors, may contribute to increasing prevalence of asthma, autism, childhood cancer, medically unexplained symptoms, and perhaps other illnesses. Given that tobacco consumption and synthetic chemical usage will not be declining at least in the near future, concerns about indoor air pollution may be expected to remain.

Nippon Eiseigaku Zasshi. 2009 May;64(3):683-8.
[Indoor air pollution of volatile organic compounds: indoor/outdoor concentrations, sources and exposures]. [Article in Japanese]
Chikara H, Iwamoto S, Yoshimura T.
Fukuoka Institute of Health and Environmental Sciences, Mukaizano, Dazaifu, Fukuoka 818-0135, Japan. [email protected]

In this review, we discussed about volatile organic compounds (VOC) concentrations, sources of VOC, exposures, and effects of VOC in indoor air on health in Japan. Because the ratios of indoor concentration (I) to outdoor concentration (O) (I/O ratios) were larger than 1 for nearly all compounds, it is clear that indoor contaminations occur in Japan. However, the concentrations of basic compounds such as formaldehyde and toluene were decreased by regulation of guideline indoor values. Moreover, when the sources of indoor contaminations were investigated, we found that the sources were strongly affected by to outdoor air pollutions such as automobile exhaust gas. Since people live different lifestyles, individual exposures have been investigated in several studies. Individual exposures strongly depended on indoor concentrations in houses. However, outdoor air pollution cannot be disregarded as the sources of VOC. As an example of the effect of VOC on health, it has been indicated that there is a possibility of exceeding a permissible cancer risk level owing to exposure to VOC over a lifetime.

Environ Sci Technol. 2009 Nov 1;43(21):8338-43.
Uptake of aldehydes and ketones at typical indoor concentrations by houseplants.
Tani A, Hewitt CN.
Institute for Environmental Sciences, University of Shizuoka, Shizuoka 422-8526, Japan. [email protected]

The uptake rates of low-molecular weight aldehydes and ketones by peace lily (Spathiphyllum clevelandii) and golden pothos (Epipremnum aureum) leaves at typical indoor ambient concentrations (10(1)-10(2) ppbv) were determined. The C3-C6 aldehydes and C4-C6 ketones were taken up by the plant leaves, but the C3 ketone acetone was not. The uptake rate normalized to the ambient concentration C(a) ranged from 7 to 19 mmol m(-2) s(-1) and from 2 to 7 mmol m(-2) s(-1) for the aldehydes and ketones, respectively. Longer-term fumigation results revealed that the total uptake amounts were 30-100 times as much as the amounts dissolved in the leaf, suggesting that volatile organic carbons are metabolized in the leaf and/or translocated through the petiole. The ratio of the intercellular concentration to the external (ambient) concentration (C(i)/C(a)) was significantly lower for most aldehydes than for most ketones. In particular, a linear unsaturated aldehyde, crotonaldehyde, had a C(i)/C(a) ratio of approximately 0, probably because of its highest solubility in water.

Proc Am Thorac Soc. 2010 May;7(2):102-6.
Indoor air pollution and asthma in children.
Breysse PN, Diette GB, Matsui EC, Butz AM, Hansel NN, McCormack MC.
Department of Environmental Heath Sciences, Johns Hopkins University Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD 21205, USA. [email protected]

The purpose of this article is to review indoor air pollution factors that can modify asthma severity, particularly in inner-city environments. While there is a large literature linking ambient air pollution and asthma morbidity, less is known about the impact of indoor air pollution on asthma. Concentrating on the indoor environments is particularly important for children, since they can spend as much as 90% of their time indoors. This review focuses on studies conducted by the Johns Hopkins Center for Childhood Asthma in the Urban Environment as well as other relevant epidemiologic studies. Analysis of exposure outcome relationships in the published literature demonstrates the importance of evaluating indoor home environmental air pollution sources as risk factors for asthma morbidity. Important indoor air pollution determinants of asthma morbidity in urban environments include particulate matter (particularly the coarse fraction), nitrogen dioxide, and airborne mouse allergen exposure. Avoidance of harmful environmental exposures is a key component of national and international guideline recommendations for management of asthma. This literature suggests that modifying the indoor environment to reduce particulate matter, NO(2), and mouse allergen may be an important asthma management strategy. More research documenting effectiveness of interventions to reduce those exposures and improve asthma outcomes is needed.

HortScience 45: 1489-1495 (2010)
Variation in Formaldehyde Removal Efficiency among Indoor Plant Species
Kwang Jin Kim1, Myeong Il Jeong, Dong Woo Lee, Jeong Seob Song, Hyoung Deug Kim, Eun Ha Yoo, Sun Jin Jeong and Seung Won Han

The efficiency of volatile formaldehyde removal was assessed in 86 species of plants representing five general classes (ferns, woody foliage plants, herbaceous foliage plants, Korean native plants, and herbs). Phytoremediation potential was assessed by exposing the plants to gaseous formaldehyde (2.0 µL·L–1) in airtight chambers (1.0 m3) constructed of inert materials and measuring the rate of removal. Osmunda japonica, Selaginella tamariscina, Davallia mariesii, Polypodium formosanum, Psidium guajava, Lavandula spp., Pteris dispar, Pteris multifida, and Pelargonium spp. were the most effective species tested, removing more than 1.87 µg·m–3·cm–2 over 5 h. Ferns had the highest formaldehyde removal efficiency of the classes of plants tested with O. japonica the most effective of the 86 species (i.e., 6.64 µg·m–3·cm–2 leaf area over 5 h). The most effective species in individual classes were: ferns—Osmunda japonica, Selaginella tamariscina, and Davallia mariesii; woody foliage plants—Psidium guajava, Rhapis excels, and Zamia pumila; herbaceous foliage plants—Chlorophytum bichetii, Dieffenbachia ‘Marianne’, Tillandsia cyanea, and Anthurium andraeanum; Korean native plants—Nandina domestica; and herbs—Lavandula spp., Pelargonium spp., and Rosmarinus officinalis. The species were separated into three general groups based on their formaldehyde removal efficiency: excellent (greater than 1.2 µg·m–3 formaldehyde per cm2 of leaf area over 5 h), intermediate (1.2 or less to 0.6), and poor (less than 0.6). Species classified as excellent are considered viable phytoremediation candidates for homes and offices where volatile formaldehyde is a concern.

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

Do You Wash Your Produce? Why?

washing produce, e. coliIn his June 11, 2011 column for Newsmax Health (, Dr. Russell Blaylock, noted neurosurgeon and lecturer, admonished his readers to pay careful attention to the washing of their produce, especially in light of the recent outbreak of deadly E.coli in Europe, where more than 4,000 people were afflicted, and more than a few dozen died. None of us can tell where our food has been before it hit the home refrigerator. Not only E. coli, but also other strains of pathogenic bacteria can lurk in our foods. The steps we take to ensure food safety after we get it home from the store or the garden market makes all the difference in the world.

Dr. Blaylock states that, “Eating raw, contaminated food appears to be the culprit in the recent outbreak in Europe.” He cites two main reasons: the use of human waste as fertilizer and the failure of people to wash their produce before eating. He adds that the problem is rampant because, “People assume…that the government is looking out for their safety.” Although the FDA website reminds people to wash biocides off their produce, there are no public reminders of the biological menaces that might accompany those chemicals. Because kidney failure is one of the dangers of E.coli poisoning, Dr. Blaylock tells of using magnesium as a counter measure in his own case of food poisoning, keeping in mind that “magnesium protects the kidneys and can protect against vascular collapse associated with gram-negative bacteria such as E. coli.”

How many times has that lemon slice in the water your waiter brought you fallen to the floor?  How many people touched it before you got it?  Who handled it from orchard to the packing house to the grocery store to the restaurant?  Listeria, Salmonella, and E. coli could have come from any pair of dirty hands, whether organically or conventionally grown. We need the produce, but not the bacteria, pesticides and bugs that might be attached.

E. coli normally inhabits the intestines of humans and animals. There are a few different strains, but some are dangerous.  Bloody diarrhea, severe abdominal pain and vomiting are some of the symptoms of food poisoning. But some are worse. Among them is hemolytic uremic syndrome, where blood cells shrivel and die and kidneys fail to function in severe cases, usually among the old and the very young.

Washing produce is not really a big production. Start by keeping all work surfaces and cutting tools clean. Wash hands before preparing produce and meats, and always after handling animal products. Keep all fruits and vegetables away from raw meat to avoid cross-contamination.  If you wash produce too far ahead of the meal and keep it in the fridge too long, it might spoil before you get to eat it.  Foods with rinds or peels can harbor bacteria. Before you cut the cantaloupe or orange, and before you peel the banana, wash it. If you feel better about using a cleaning agent, try mixing hydrogen peroxide 50-50 with water, although 30-70 will probably suffice. In truth, those commercial preparations are no better than this, and are not much better than plain water.  Dump the outer leaves of lettuces and cabbages, and rinse the rest.  Get a salad spinner to dry leaves so the dressing will adhere.  Firm produce, like potatoes and apples, can withstand a brushing under running water.

When it comes to chemical contamination, some foods are worse than others, according to the Environmental Working Group.  The most heavily sprayed foods include apples, celery, strawberries, peaches, spinach, imported nectarines and grapes, bell peppers, potatoes, blueberries, lettuce, and kale and collards.  The least are onions, corn, pineapples, avocadoes, asparagus, peas, mangoes, eggplants, cantaloupes, kiwi, cabbages, watermelons, sweet potatoes, grapefruit, and mushrooms.

They might look gorgeous on the outside, but who knows what they’re really like…just as with people.

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

Laundry: A Toxic Venture

laundry productsWe like to think of ourselves as clean and fresh-smelling.  But at what price?  Although suspect for several years, the gentle aromas wafting from our laundry appliances are giving us more than we asked for—pollution.  Venting the dryer outside contributes to the air many of the same chemicals emanating from vehicle and industrial exhausts, but better-smelling.  If the dryer is vented indoors into a bucket of water for lack of a suitable alternative, the effect is concentrated to a much smaller environment.  Although dozens of potentially harmful compounds have been identified in laundry fragrances, from soap to dryer sheets, none, by law, needs to be listed on the product label.  We don’t know what we’re getting for our money, but you can bet it’s more than we bargained for.

The emissions from a dryer are not regulated or monitored.  “If they’re coming out of a smokestack or tailpipe, they’re regulated…” says the lead author of a study performed at the University of Washington.  Reporting in the 2011 online edition of Air Quality, Atmosphere and Health, Anne Steinemann, an environmental engineering professor at the university, found more than two dozen volatile organic compounds emitted through laundry vents.  Of these, seven are named as hazardous air pollutants, two of which are known carcinogens described by the EPA.  Acetaldehyde and benzene enjoy zero safe exposure level.  “These products can affect not only personal health, but also public and environmental health.  The chemicals can go into the air, down the drain and into water bodies,” Steinemann added.   To get a clearer picture of the problem, the aldehydes emitted by using a particular, though unnamed, brand of detergent represents three percent of that emitted by automobiles in the study area (King County, WA).  If combined, the top five brands of laundry products would account for six percent of vehicular aldehyde emissions.  (Steinemann. 2011)

Let’s start with the aldehydes and benzenes.  Acetaldehyde occurs naturally in coffee, breads and ripe fruits, and arises from normal plant metabolism.  It’s produced by the oxidation of alcohol, and is blamed for hangovers.  The liver converts ethanol to acetaldehyde through enzymatic activity.  Occurring also in tobacco smoke, acetaldehyde enhances the addictive effect of nicotine.  It is a probable carcinogen in humans.  (U.S. EPA. 1994)

Benzene is an important industrial solvent, once used as an additive to gasoline to increase octane ratings and to eliminate knocking, but still used to manufacture plastics and synthetic rubber, and, occasionally, some drugs.  Its carcinogenic property is well-established.  It can be formed wherever incomplete combustion of a carbon-rich substance occurs, as in forest fires and volcanoes, and in vehicle exhausts.  Its use in the United States is now limited, although it is making a minimal comeback since tetraethyl lead has been eliminated from vehicular fuel.   (Federal Register. 2006)

Although they can make your clothes soft and cuddly, fabric softeners are some of the most toxic substances around.  Because there are limited alternatives to these handy chemicals, few people are willing to give them up, and even fewer are likely to relate health problems with their use.  If you say they’re made from natural ingredients, remember that arsenic is all natural.  The chemicals in softeners in particular are designed to stay on the clothes for a while, and are absorbed through the skin as well as inhaled.  Because the dryer sheets are heated, they emit their chemicals into the vented air, either outside, inside, or both.  The chemicals that create the softening effect are strong smelling and pungent, so need to be masked with fragrances that are chemically just as bad.

What are some other noxious / toxic ingredients in laundry and other household products and their after effects?  Benzyl acetate in softeners causes pancreatic disease.  Camphor and ethanol affect the central nervous system.  Ethyl acetate affects the kidneys and skin.  Limonene is a sensitizer that is not to be inhaled, although we do anyway, but not on purpose.  The list goes on.  More than ninety-five percent are made from petrochemicals, and may present as neurological maladies, allergic reactions, birth defects, and cancer, not to mention sinusitis and asthma.

What to do?  Look for detergents that have no scent.  If they can’t be found in the supermarket, try a health food store or look online.  There are at least two multi-level marketing firms that offer them; one starts with an “S” and the other with an “A.”  To soften clothes, add a quarter cup of baking soda to the wash water.  The same amount of white vinegar can prevent static cling and still soften fabric…and won’t smell like a salad.

Those aromatic thingies you plug into an outlet?  Chuck ‘em.  Got petroleum-based candles that hide the mackerel miasma?  Dump ‘em.  Find out what’s in your underarm deodorant / anti-perspirants, the furniture polish, the toilet bowl cleaner, shampoo, and even toothpaste.  What makes your trousers wrinkle-free and stain-free, or your baby’s clothes fireproof, or the new sofa stain-resistant?  Nobody would have thought that “April Fresh,” “Ocean Mist,” and “Orange Honey” could be so dangerous.  We might be able to answer a few questions if we keep track of who gets sick and the materials to which they are exposed.  Manufacturers are not required to list ingredients in fragrances, so consumers are at the mercy of the establishment.


Anne C. Steinemann, Lisa G. Gallagher, Amy L. Davis and Ian C. MacGregor
Chemical emissions from residential dryer vents during use of fragranced laundry products
Air Quality, Atmosphere & Health   DOI: 10.1007/s11869-011-0156-1Online First™

University of Washington (2008, July 24).
Toxic Chemicals Found In Common Scented Laundry Products, Air Fresheners.

August 1994

“Control of Hazardous Air Pollutants From Mobile Sources”.
U.S. Environmental Protection Agency. 2006-03-29. p. 15853. Retrieved 2008-06-27.

International Agency for Rescarch on Cancer, World Health Organization. (1988).
Alcohol drinking.
Lyon: World Health Organization, International Agency for Research on Cancer. ISBN 92-832-1244-4. p3

Aberle NS 2nd, Burd L, Zhao BH, Ren J.
Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12.
Alcohol Alcohol. 2004 Sep-Oct;39(5):450-4.

Heisterberg MV, Menné T, Andersen KE, Avnstorp C, Kristensen B, Kristensen O, Kaaber K, Laurberg G, Henrik Nielsen N, Sommerlund M, Thormann J, Veien NK, Vissing S, Johansen JD.
Deodorants are the leading cause of allergic contact dermatitis to fragrance ingredients.
Contact Dermatitis. 2011 May;64(5):258-64.

Jacob SE, Castanedo-Tardan MP.
Alternatives for fragrance-allergic children.
Pediatr Ann. 2008 Feb;37(2):102-3.

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

Herbicides And Birth Defects

Herbicides & Birth DefectsAfter years of acceptance as a safe and effective weed killer, a popular herbicide is facing the guillotine as teratogenic—it causes malformations in an embryo or fetus. Initial investigations (in the 1970’s) into the safety record of the chemical, glyphosate, indicated that its safety to humans was guaranteed.  An organization called Earth Open Source has now indicted the chemical as a serious risk to public health while accusing the herbicide industry of hiding the truth for decades.

“Reports of neural defects and craniofacial malformations from regions where glyphosate-based herbicides (GBH) are used led us to undertake an embryological approach to explore the effects of low doses of glyphosate in development,” said researchers from the University of Buenos Aires, in Argentina (Paganelli 2010).  But even prior to this, sequestered research from 2007 showed that glyphosate induced fetal malformations in lab animals and “adverse reproductive effects in the male offspring of a certain kind of rat.” (Huffington Post 2011)  The basis for such concern is the interruption of retinoic acid signaling in the development of vertebrate embryos, where Pagnelli et al found that embryos of selected amphibians and chickens demonstrated “…a gradual loss of rhombomere domains, reduction of the optic vesicles, and microcephaly.”

First of all, the terms need description.  Rhombomeres are tiny parts of the neural tube that will become the central nervous system.  Optic vesicles are tiny sacs from which will develop the parts of the eye that actually see things.  Microcephaly is abnormal smallness of the head.  Now that we understand that these characteristics may befall an amphibian or a chicken, must we be concerned that the same could happen to a human embryo?  Could it happen to you or to one of your family from long-term exposure to glyphosate or a related substance?

One of the troublesome things about laboratory experiments is the deliberate exposure of lab animals to doses of chemicals at levels that are unlikely to contact a human.  However, it is a springboard for prudent conjecture, for it introduces the potential “what ifs” of the process.  Related animal testing in Brazil showed that exposure to large amounts of glyphosate caused death in half the study population (Dallegrave 2003), accompanied by severe developmental retardation of fetal skeletons.  A sensible question asks why this data has been kept under wraps for nearly a decade.  The sensible answer is that the chemical industry didn’t want this info to go public for fear of boycott and reprisal that would inflict fiduciary pain.  The industry response is to say that the test results remain unclear, but that might just depend on whose spectacles are covered with petroleum jelly.  After all, testing poisons directly on humans is not, well, um, human.

The EPA, a watchdog that some say wears an eye patch, evaluates biocides every fifteen years in a process called registration review.  Lots can happen in that time.  Glyphosate works on weeds and other plants that are not genetically modified to tolerate it.   That tells the consumer that wherever it is used, the food it protects against weed infiltration is probably a GMO, the long-term effects of which are yet unknown.  When the Argentine government pulled that nation out of recession in the 1990’s it relied on GMO soy to help.  Shortly thereafter, residents near those soy farms—where glyphosate was used—experienced adverse health they had not experienced before.  High rates of birth defects and cancer were among them.  But also, there was destruction of non-tolerant crops and livestock from drifting of the overspray.  Argentine officials were implored by a group of environmental lawyers to ban the glyphosate spray, but the ban was never adopted nation-wide, although several provinces restricted spraying near populated areas.

There is speculation that plants immune to glyphosate develop bacterial infections novel to their species, and that these bacteria pose a threat to animal husbandry by initiating miscarriages.  Corn and soy, the two most heavily genetically modified crops, suffer the most bacterial rampage.  There is a possibility that humans could be affected.  Don Huber, a retired plant pathologist from Purdue, told the agriculture department of these concerns early in 2011, but was offered no comment from the government, while being summarily dismissed by the maker of glyphosate in the United States.  Over a hundred glyphosate formulations are on the market, many made in Asia.  The glyphosate industry labels independent studies as bogus, incomplete, and short-sighted.  They do, however, offer their own research as alternatives.

So, what does retinoic acid have to do with this?  Retinoic acid is the metabolite of Vitamin A that controls growth and development.  If stymied, as happens in the presence of glyphosate, reproductive chaos ensues as hypogonadism and infertility.  We should feel comforted knowing that the glyphosate industry has everything under control.

Chem Res Toxicol. 2010 Aug 9. [Epub ahead of print]
Glyphosate-Based Herbicides Produce Teratogenic Effects on Vertebrates by Impairing Retinoic Acid Signaling.
Paganelli A, Gnazzo V, Acosta H, López SL, Carrasco AE.
Laboratorio de Embriologia Molecular, CONICET-UBA, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 3 degrees piso (1121), Ciudad Autonoma de Buenos Aires, Argentina.

Toxicol Lett. 2003 Apr 30;142(1-2):45-52.
The teratogenic potential of the herbicide glyphosate-Roundup in Wistar rats.
Dallegrave E, Mantese FD, Coelho RS, Pereira JD, Dalsenter PR, Langeloh A.
Department of Pharmacology, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul (UFRGS), Rua Sarmento Leite 500 sala 202, 90046-900 Porto Alegre, RS, Brazil. [email protected]

Environ Mol Mutagen. 1998;31(1):55-9.
32P-postlabeling detection of DNA adducts in mice treated with the herbicide Roundup.
Peluso M, Munnia A, Bolognesi C, Parodi S.

Environ Health Perspect. 2005 Jun;113(6):716-20.
Differential effects of glyphosate and roundup on human placental cells and aromatase.
Richard S, Moslemi S, Sipahutar H, Benachour N, Seralini GE.
Laboratoire de Biochimie et Biologie Moleculaire, USC-INCRA, Université de Caen, Caen, France

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

Phthalate Exposure

colorful-car-toyPhthalates are endocrine disrupters, widely present in the environment and able to impede mental and motor development in children by causing changes in the nascent brain. These chemicals are found in many consumer products, from shower curtains to plastic toys to shampoo and hair spray. Their ubiquity has led scientists to look more closely into the risks associated with exposure to phthalates during pregnancy. What they found was sufficiently disconcerting to make you scrutinize the products you buy if you are pregnant or contemplating being so.

Dr. Robyn Whyatt, from Columbia University’s Mailman School of Public Health, reported in September, 2011, that prenatal exposure to metabolites of four different types of phthalates significantly increases the chances of physical and mental delay, indicating the potential for future problems with gross and fine motor coordination.  “Our results suggest that prenatal exposure to these phthalates adversely affects child mental, motor and behavioral development during the preschool years,” commented Dr. Whyatt, adding that, “The results add to a growing public health concern about the widespread use of phthalates in consumer products.”  (Whyatt.  2011)  Although the actual mechanisms by which phthalates wreak their malevolence are still being examined, their endocrine disruption has been specifically linked to thyroid hormone and testosterone production.  Partner to the study, Dr. Pam Factor-Litvak explained that, “The results are concerning since increasing exposures from the lowest 25% to the highest 25% among the women in our study was associated with a doubling or tripling in the odds of motor and/or behavioral problems in the children.”

If you’re a baby boomer, you associate plastic with the cheap imported toys of the 50’s and 60’s, stuff that would snap in an instant.  Plastics—plasticizers in the case of phthalates–actually are materials that make other materials easier to handle, more flexible and pliable, and less brittle.  They work best if their molecules are both polar and non-polar, where the former help the plasticizer be retained in the system, and the latter decrease the attraction force between molecules to maintain flexibility.  This is how hair spray works; it’s flexible.  Otherwise, you’d be wearing a transparent motorcycle helmet.

Of the more than five hundred plasticizers available, fewer than a hundred are commonly used, phthalate esters being predominant, especially in PVC.  The real name for the most often used of these chemicals is orthophthalates.  It’s necessary to know that phthalates are not limited to the manufacture of containers, which is a common thought.  They are also ingredients in cosmetics, shower curtains, teething rings and toys, primarily because they afford flexibility.  However, they have the contemptible distinction of mimicking female hormones, resulting in the feminization of boys.  It’s one thing to have swapped paternal inheritance for creeping momism as a social misfeasance, which is rectifiable, but this physical assault is unforgiveable.

There is more than one type of phthalate to which a fetus might respond, some being termed less dangerous than others.  This is equivalent to saying that a person who is legitimately allergic to tree nuts will succumb more slowly to one type of nut than another.  In both cases the outcome is undesirable.  Delay of ossification in the skeleton with resultant deformities, cleft palates, eye deformation, and decreased fetal weight are but a few of the other abnormalities offered by phthalate plasticizers.  These are dose-dependent anomalies, but determining how much is too much is subjective. (Saillenfait. 2009)  The limit for phthalate exposure is set at 5 mg/kg of body weight a day…in rats.  .  (Grande. 2006)  People are not likely to get anything close to that dose unless they eat the plastic.

To assuage any fears, know that the PETE, polyethylene terephthalate, used for peanut butter jars, bottled water and juices, and salad dressings is not chemically similar to the phthalates we address here.  Phthalates are additives, not plastics.  PETE (aka PET) is not an orthophthalate.  If the dangers come from prenatal exposure to phthalates, it pays for the new mom to read labels.  Since 2002, safe alternatives are available for the manufacture of plastic wraps, food containers, toys, PVC pipe, medical devices, and health and beauty aids.  Citric acid esters are one of them.  To find out if your product is safe, check the ingredients.  If there is no label, as perhaps with a teething ring, either call the maker or leave it on the shelf.

Prenatal Exposure to Phthalates Linked to Decreased Mental and Motor Development and Increased Behavioral Problems at Age Three

Robin M. Whyatt, Xinhua Liu, Virginia A. Rauh, Antonia M. Calafat, Allan C. Just, Lori Hoepner, Diurka Diaz, James Quinn, Jennifer Adibi, Frederica P. Perera, Pam Factor-Litvak
Maternal Prenatal Urinary Phthalate Metabolite Concentrations and Child Mental, Psychomotor and Behavioral Development at Age Three Years
Environ Health Perspect. 2011.  doi:10.1289/ehp.1103705 [Online Ahead of Print]

Saillenfait AM, Gallissot F, Sabaté JP.
Differential developmental toxicities of di-n-hexyl phthalate and dicyclohexyl phthalate administered orally to rats.
J Appl Toxicol. 2009 Aug;29(6):510-21.

Grande SW, Andrade AJ, Talsness CE, Grote K, Chahoud I.
A dose-response study following in utero and lactational exposure to di(2-ethylhexyl)phthalate: effects on female rat reproductive development.
Toxicol Sci. 2006 May;91(1):247-54. Epub 2006 Feb 13.

Barbara Kolarika, Carl-Gustaf Bornehaga, Kiril Naydenove, et al
The concentrations of phthalates in settled dust in Bulgarian homes in relation to building characteristic and cleaning habits in the family
Atmospheric Environment. 42(37); Dec 2008: 8553-8559

Lyche JL, Gutleb AC, Bergman A, Eriksen GS, Murk AJ, Ropstad E, Saunders M, Skaare JU.
Reproductive and developmental toxicity of phthalates.
J Toxicol Environ Health B Crit Rev. 2009 Apr;12(4):225-49.

Deblonde T, Cossu-Leguille C, Hartemann P.
Emerging pollutants in wastewater: A review of the literature.
Int J Hyg Environ Health. 2011 Aug 30. [Epub ahead of print]

Yolton K, Xu Y, Strauss D, Altaye M, Calafat AM, Khoury J.
Prenatal exposure to bisphenol A and phthalates and infant neurobehavior.
Neurotoxicol Teratol. 2011 Aug 10. [Epub ahead of print]

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

Arthritis and Common Chemicals

arthritisMerely because something is hereditary doesn’t mean it has to be inherited unless it’s a defined, overt physical characteristic, such as eye color or hairline. Disease or propensity for disease does not have to telegraph itself through gene expression. In the belief that genetic activity can be turned on and off, more than a handful of scientists are convinced that arthritis, in this case, does not have to pass from seed to seed along the family tree. Arthritis, the osteo- kind, can be spawned from unseen environmental assaults, namely perfluorinated chemicals, which are fluorocarbon derivatives. You remember fluorocarbons. They’re part of the chlorofluorocarbons (CFC’s) once used as propellants in spray cans and in refrigerant fluids. Although they aren’t used for aerosol sprays any more, they’re still in the marketplace. When released into the atmosphere, CFC’s affect stratospheric ozone, the depletion of which is implicated in the rise of skin diseases and climate change, not to mention depressed growth in plants and interrupted photosynthesis. Photosynthesis is important only to those of us who need to eat. Fluorocarbons are bioaccumulative—they are stored in the body.

Of special concern are perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS). (Aren’t abbreviations great?) What in the world are these things used for? If what you own resists stains and water, it probably contains one of these. Ever hear of Scotchgard? How about stone or tile sealers? Got your new sofa treated against kids’ spillage? Fast food wrappers don’t leak grease, do they? Gunk doesn’t stick to dental floss, does it? Ever do any plumbing and use Teflon tape to help seal a joint? Oh, yeah, got Teflon? The oxygen atoms on these chemicals help them to bind proteins to fatty acids or hormone substrates such as albumin, and to nuclear receptors that regulate genes, such as PPAR’s (Anitole, 2007) (Cheng, 2008). Their half-life is about three years. Production of these nifty chemicals has declined for safety reasons, ahem, but exposure remains widespread.

PFOA, especially, is associated with infertility (Fei, 2009) (Joensen, 2009) and ADD/ADHD in young adolescents (Hoffman, 2010). But its association with osteoarthritis concerns us at this time. Fluorine (chemical symbol F) is a corrosive gas that reacts with practically everything else in the periodic table except the noble gases, which happen to be so noble that they don’t mix with anything. If fluorine mixes with something else, it’s now a fluoride. On teeth, from the outside, fluoride is O.K. From inside the body, it’s not. That’s why the toothpaste label says not to swallow it. Fluoride usually enters the body either by inhalation or ingestion. (Did you know that tea contains fluoride? We’ll get to that in a minute.)

F reacts with hydrochloric acid in the stomach to form hydrofluoric acid (HF), which just so happens to be the precursor to Prozac. This acid passes to the liver, but evades phase 1 detoxification, where the liver uses O2 and enzymes to oxidize toxins to make them water-soluble. This short circuit occurs because fluorine is the strongest oxidizer currently known. At this point, hydrofluoric acid passes into the bloodstream and is distributed to all body parts, including bones. Now, bones are made from calcium compounds, particularly carbonated hydroxyapatite. When an acid and a base combine, they form a salt. Hydrofluoric acid mixes with the calcium (alkaline) to form CaF2, an insoluble salt. That increases density of bone, but lowers strength. The bone is less elastic and more prone to fractures. As bone thickens, it restricts mobility. To compound matters, factors that acidify the urine increase the retention of fluoride. However, happily, the opposite is also true. Absorption of fluoride is reduced by calcium (Whitford, 1994).

Tea may pose problems for heavy tea drinkers. Being labeled a heavy tea drinker is not common in the United States unless you earn membership in the gallon-a-day club. Tea plants readily absorb fluoride—and aluminum—from soil. Therefore, the beverage will contain various levels of fluoride, depending on soil levels. Brewed black tea in the States contains about 3 to 4 parts per million (which is practically identical to milligrams per liter); commercial iced tea has between 1 and 4 (Whyte, 2006) (Whitford, 1994) (Izuora, 2011). The number of skeletal fluorosis reports has grown in recent years, but that has been seen mostly in people who consumed 20 milligrams of fluoride a day for decades. In the mean time, 5 milligrams a day (That would be about a quart a day.) can present preclinical stages of fluorosis, so what has been diagnosed as arthritis may actually be skeletal fluorosis. Though this problem is more extensive in the tea cultures of Asia, it’s still a good idea to drink tea in moderation.

Getting back to PFOA and PFOS, levels in humans vary widely. Certain occupations can increase exposure thousands of times, especially for those working in chemical, metal refining and power plants. Drinking water contaminated with these chemicals contributes to human misery as much as direct exposure. Some American states have ground water that contains either naturally occurring fluoride compounds or the wastes from industrial sources. Ohio and West Virginia are two. In areas such as these, osteoarthritis prevalence exceeds that in other regions. Though a terrible affliction for anyone, women seem to be affected more than men. Cartilage damage and inflammatory responses are part of the spectrum (Uhl, 2013).

If you start to feel aches and pains that are new to you, take a look at what you’re been wearing, where you’ve been, and what you ate and drank. Stain resistant trousers and shirts, high intake of black and green teas, and the wrappers from the fast-food joint might be the cause. (See  Global production of these substances has been on the wane, but leftovers still occupy the environment. Substitute compounds are no doubt in the future, but now we have to be concerned about their long-term effects. Although research is sketchy, iodine, calcium, magnesium and boron are being studied as antidotes to fluoride toxicity (Kao, 2004) (Heard, 2001).


Cao J, Bai X, Zhao Y, Liu J, Zhou D, Fang S, Jia M, Wu J.
The relationship of fluorosis and brick tea drinking in Chinese Tibetans.
Environ Health Perspect. 1996 Dec;104(12):1340-3.

Cao J, Zhao Y, Liu J, Xirao R.
[Brick-tea type adult bone fluorosis].
Wei Sheng Yan Jiu. 2003 Mar;32(2):141-3.

Cao J, Zhao Y, Liu J, Xirao R, Danzeng S, Daji D, Yan Y.
Brick tea fluoride as a main source of adult fluorosis.
Food Chem Toxicol. 2003 Apr;41(4):535-42.

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.

Czerwinski E, Nowak J, Dabrowska D, Skolarczyk A, Kita B, Ksiezyk M.
Bone and joint pathology in fluoride-exposed workers.
Arch Environ Health. 1988 Sep-Oct;43(5):340-3.

Fei C, McLaughlin JK, Lipworth L, Olsen J.
Maternal levels of perfluorinated chemicals and subfecundity
Hum Reprod. 2009 May;24(5):1200-5.

Grandjean P, Thomsen G.
Reversibility of skeletal fluorosis.
Br J Ind Med. 1983 Nov;40(4):456-61.

Hayacibara MF, Queiroz CS, Tabchoury CP, Cury JA.
Fluoride and aluminum in teas and tea-based beverages.
Rev Saude Publica. 2004 Feb;38(1):100-5.

Heard K, Hill RE, Cairns CB, Dart RC.
Calcium neutralizes fluoride bioavailability in a lethal model of fluoride poisoning.
J Toxicol Clin Toxicol. 2001;39(4):349-53.

Hoffman K, Webster TF, Weisskopf MG, Weinberg J, Vieira VM.
Exposure to polyfluoroalkyl chemicals and attention deficit/hyperactivity disorder in U.S. children 12-15 years of age
Environ Health Perspect. 2010 Dec;118(12):1762-7.

Izuora K, Twombly JG, Whitford GM, Demertzis J, Pacifici R, Whyte MP.
Skeletal fluorosis from brewed tea.
J Clin Endocrinol Metab. 2011 Aug;96(8):2318-24.

Joensen UN, Bossi R, Leffers H, Jensen AA, Skakkebaek NE, Jørgensen N.
Do perfluoroalkyl compounds impair human semen quality?
Environ Health Perspect. 2009 Jun;117(6):923-7.

Kao WF, Deng JF, Chiang SC, Heard K, Yen DH, Lu MC, Kuo BI, Kuo CC, Liu TY, Lee CH.
A simple, safe, and efficient way to treat severe fluoride poisoning–oral calcium or magnesium.
J Toxicol Clin Toxicol. 2004;42(1):33-40.

Kavanagh D, Renehan J.
Fluoride in tea–its dental significance: a review.
J Ir Dent Assoc. 1998;44(4):100-5.

Kurland ES, Schulman RC, Zerwekh JE, Reinus WR, Dempster DW, Whyte MP.
Recovery from skeletal fluorosis (an enigmatic, American case).
J Bone Miner Res. 2007 Jan;22(1):163-70.

Lau C, Anitole K, Hodes C, Lai D, Pfahles-Hutchens A, Seed J.
Perfluoroalkyl acids: a review of monitoring and toxicological findings.
Toxicol Sci. 2007 Oct;99(2):366-94.

Luo Rui, Liu Ri-guang1, Ye Chuan, Yu Yan-ni, Guan Zhi-zhong
Total knee arthroplasty for the treatment of knee osteoarthritis caused by endemic skeletal fluorosis
Chinese Journal of Tissue Engineering Research. Feb 26, 2012; 16 (9): 1555-1558

Petrone P, Giordano M, Giustino S, Guarino FM.
Enduring fluoride health hazard for the Vesuvius area population: the case of AD 79 Herculaneum.
PLoS One. 2011;6(6):e21085.

Savas S, Cetin M, Akdoğan M, Heybeli N.
Endemic fluorosis in Turkish patients: relationship with knee osteoarthritis.
Rheumatol Int. 2001 Sep;21(1):30-5.

Howard Thomas
Some Non-essential Aerosol Propellant Uses Finally Banned
Federal Regulations:  43 F. R. 11301 (1978)

Sarah A. Uhl, Tamarra James-Todd, and Michelle L. Bell
Association of Osteoarthritis with Perfluorooctanoate and Perfluorooctane Sulfonate in NHANES 2003–2008
Environ Health Perspect. February 14, 2013

Whitford GM.
Intake and metabolism of fluoride.
Adv Dent Res. 1994 Jun;8(1):5-14.

Whitford GM.
Fluoride metabolism and excretion in children.
J Public Health Dent. 1999 Fall;59(4):224-8.

Whyte MP.
Fluoride levels in bottled teas.
Am J Med. 2006 Feb;119(2):189-90.

Wong MH, Fung KF, Carr HP.
Aluminium and fluoride contents of tea, with emphasis on brick tea and their health implications.
Toxicol Lett. 2003 Jan 31;137(1-2):111-20.

Xiangjin Ge, Yuting Jiang, Guohua Tang, Meilie Zhang, Yurong Zhao
Investigations on the Occurrence of Osteoarthritis in Middle-aged and Elderly Persons in Fluorosis Afflicted Regions of Gaomi City with High Fluoride Concentration in Drinking Water
Preventive Medicine Tribune. Volume 12, No. 1;  January 2006:  pp. 57-58 ·57·

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

Toxins In Baby Wipes

baby-wipes-boxThe populace has become so self-assured that it trusts people and products to be what they want them to be, which could genuinely be opposite of their expectations. In the case of personal hygiene products, we are satisfied if they remove the smudge, erase the stain and kill the germ. Few consider the trade-off. Well, folks, it’s about time we did…consider the trade-offs, that is. As is the case with our food, if you can’t pronounce the name of the ingredient, it doesn’t belong in or on your body. We’re told that we consume too little of this or that chemical to be concerned about cancer but have you wondered if a little bit here and there adds up to a lot? Such it is with baby wipes.

Methylisothiazolinone (MIT) is one of those barely pronounceable words that may or may not find its way to the label of your baby wipes. It’s sort of like MSG, which has so many aliases you can’t tell if it’s in a food or not. Autolyzed this or that and hydrolyzed that or this are but two examples of MSG stage names. However, cosmetics and baby products do NOT fall under FDA regulations. A few things, such as soaps, require no label at all, but some makers include one to protect themselves legally. At the same time, proprietary ingredients can be secret and need not be listed at all. You see, if a product does not claim to have medicinal properties, its label can be vacant. MIT is a powerful biocide used in personal care products because it works well in solutions that contain water, which is a medium in which bacteria like to grow. Human occupational exposure to this chemical has resulted in contact dermatitis, chemical burns and allergic sensitization (Goncalo, 2013) (Urwin, 2013). Inhalation is also a common route of exposure (Aerts, 2013).  That means your baby gets a double whammy during a diaper change. The danger?  Neurotoxicity. Even brief exposure damages nerve cells (Du, 2002). One drop in a 55-gallon drum of water is all it takes. And that’s considered a safe level. Isn’t contact dermatitis enough insult (Lundov, 2011) (Monroe, 2010)?

A preservative originally meant for the paint industry has found its way into personal care products, including baby wipes. Iodopropynyl butylcarbamate (IPBC) is a biocide whose use is restricted in some countries, but not in the U.S.  Initially deemed safe, IPBC has been reported to be a potent contact allergen (Badreshia, 2002) (Bryld, 1997). Some things are put on the market without ever being checked out for safety. And that means long-term safety, not just for this week. Carbamate biocides inhibit acetylcholine at nerve synapses and neuromuscular junctions. Fortunately, this is reversible, but it might take a few weeks. Not all babies will react to all things in like manner, but there are signs to watch for. Hypersalivation, hypermotility of the GI system (stuff moves faster through the gut than normal), constriction of the pupil of the eye, vomiting, diarrhea, sweating, cyanosis, respiratory distress, muscle twitching and weakness, and convulsions are major reactions to carbamates (Merck Manual, 2013). This chemical has such potential for harm that the healthcare profession is prepared to handle its deployment as a terrorist weapon of mass casualties (Rosman, 2009). Sounds safe, eh?  If you don’t see it on the label, you have to call and ask…unless you have a guaranteed baby-safe product in your hand. This is serious business.

We’re not done yet. There’s one more. Actually, there are a few more, but time and space prevent their inclusion right now. If a disposable wipe is made from paper, it probably contains dioxins, which are not intentionally produced, but which are the by-products of several industrial processes, including bleaching of paper pulp, chemical and pesticide manufacture, and combustion activity. If there is waste incineration or a forest fire, there is combustion (Shibamoto, 2007) (Environment Australia, 1999). Anything termed “polychlorinated” is in the dioxin family. Notice that chlorine, a bleaching agent, is in the term. The toxicity of the various dioxin compounds varies, but it’s still there. Endocrine disruption is one action; altered gene expression is another. Reproduction problems, developmental delay, hormone dysfunction and immune damage add to the array. A more pressing matter with dioxins is their use in disposable diapers, where baby’ skin is exposed for a large part of the day.

Dioxins are persistent organic pollutants (POP’s) that exist ubiquitously—they’re everywhere, including the food supply, though because of strict emission controls are now on the wane. Because they accumulate in body fat, effects may not be realized for a long time, making it hard to pinpoint the blame for changes in liver function, heme metabolism, thyroid function and even diabetes and immunological disorders (Sweeney, 2000). Disturbances in tooth and sexual development have been observed (Alaluusua, 2004) (Mocarelli, 2000, 2008), as well as in bone resorption and formation (Koskela, 2012), where interference with the differentiation of osteoblasts and osteoclasts is a targeted effect (Korkalainen, 2009).

It’s important to purchase baby products that are safe. Adult products are no less contaminated with unpronounceable materials. Wipes made with organic fruit and vegetable extracts are much preferred, though paper may still be the substrate, in which case you night opt for cotton or flannel, which may be flushable, as hemorrhoid pads are. Considering the size of a baby’s gluteus, how big does a wipe need to be?  By the way, breast milk will contain dioxins that the mother has ingested from meats, poultry and fish that absorbed them from aerial transport of the chemical and consequent deposition on vegetables, pastures and roughages. Trimming fat from meat is the best first step to avoidance.


Aerts O, Cattaert N, Lambert J, Goossens A.
Airborne and systemic dermatitis, mimicking atopic dermatitis, caused by methylisothiazolinone in a young child.
Contact Dermatitis. 2013 Apr;68(4):250-1.

Alaluusua S, Calderara P, Gerthoux PM, Lukinmaa PL, Kovero O, Needham L, Patterson DG Jr, et al
Developmental dental aberrations after the dioxin accident in Seveso.
Environ Health Perspect. 2004 Sep;112(13):1313-8.

Badreshia S, Marks JG Jr.
Iodopropynyl butylcarbamate.
Am J Contact Dermat. 2002 Jun;13(2):77-9.

Bryld LE, Agner T, Rastogi SC, Menné T.
Iodopropynyl butylcarbamate: a new contact allergen.
Contact Dermatitis. 1997 Mar;36(3):156-8.

Castanedo-Tardana MP, Zug KA.
Dermatitis. 2013 Jan-Feb;24(1):2-6.

Coloe J, Zirwas MJ.
Allergens in corticosteroid vehicles.
Dermatitis. 2008 Jan-Feb;19(1):38-42.

Davies RF, Johnston GA.
New and emerging cosmetic allergens.
Clin Dermatol. 2011 May-Jun;29(3):311-5.

Du S, McLaughlin B, Pal S, Aizenman E.
In vitro neurotoxicity of methylisothiazolinone, a commonly used industrial and household biocide, proceeds via a zinc and extracellular signal-regulated kinase mitogen-activated protein kinase-dependent pathway.
J Neurosci. 2002 Sep 1;22(17):7408-16.

Environment Australia (1999),
Incineration and Dioxins: Review of Formation Processes
Department of the Environment and Heritage, Canberra.

Environmental Protection Agency
Mechanism of Formation of Dioxin-Like Compounds During combustion of Organic Materials
March, 4, 2005

European Commission
Brussels, 20 July 2001
Fact Sheet on dioxin in feed and food

Fewings J, Menné T.
An update of the risk assessment for methylchloroisothiazolinone/methylisothiazolinone (MCI/MI) with focus on rinse-off products.
Contact Dermatitis. 1999 Jul;41(1):1-13.

Gonçalo M, Goossens A.
Whilst rome burns: the epidemic of contact allergy to methylisothiazolinone.
Contact Dermatitis. 2013 May;68(5):257-8.

Korkalainen M, Kallio E, Olkku A, Nelo K, Ilvesaro J, Tuukkanen J, Mahonen A, Viluksela M.
Dioxins interfere with differentiation of osteoblasts and osteoclasts.
Bone. 2009 Jun;44(6):1134-42.

Koskela A, Viluksela M, Keinänen M, Tuukkanen J, Korkalainen M.
Synergistic effects of tributyltin and 2,3,7,8-tetrachlorodibenzo-p-dioxin on differentiating osteoblasts and osteoclasts.
Toxicol Appl Pharmacol. 2012 Sep 1;263(2):210-7.

Lundov MD, Krongaard T, Menné TL, Johansen JD.
Methylisothiazolinone contact allergy: a review.
Br J Dermatol. 2011 Dec;165(6):1178-82

Lundov MD, Zachariae C, Menné T, Johansen JD.
Airborne exposure to preservative methylisothiazolinone causes severe allergic reactions.
BMJ. 2012 Dec 4;345:e8221.

Macias VC, Fernandes S, Amaro C, Santos R, Cardoso J.
Sensitization to methylisothiazolinone in a group of methylchloroisothiazolinone/methylisothiazolinone allergic patients.
Cutan Ocul Toxicol. 2013 Jun;32(2):99-101.

Merck Manual. Feb 2013
Organophosphate and Carbamate Poisoning
Reviewed by Gerald O’Malley, DO and Rika O’Malley MD

Mocarelli P, Gerthoux PM, Ferrari E, Patterson DG Jr, Kieszak SM, Brambilla P, et al
Paternal concentrations of dioxin and sex ratio of offspring.
Lancet. 2000 May 27;355(9218):1858-63.
Mocarelli P, Gerthoux PM, Patterson DG Jr, Milani S, Limonta G, Bertona M, Signorini S, et al
Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality
Environ Health Perspect. 2008 Jan;116(1):70-7.

Monroe HR, Hu JC, Chiu MW.
Methylchloroisothiazolinone / methylisothiazolinone and moist wipe dermatitis.
Dermatol Online J. 2010 May 15;16(5):14.

National Library of Medicine
Toxicology Data Network

Natkunarajah J, Osborne V, Holden C.
Allergic contact dermatitis to iodopropynyl butylcarbamate found in a cosmetic cleansing wipe.
Contact Dermatitis. 2008 May;58(5):316-7.

Rosman Y, Makarovsky I, Bentur Y, Shrot S, Dushnistky T, Krivoy A.
Carbamate poisoning: treatment recommendations in the setting of a mass casualties event.
Am J Emerg Med. 2009 Nov;27(9):1117-24.

Sato S, Shirakawa H, Tomita S, Ohsaki Y, Haketa K, Tooi O, Santo N, Tohkin M, Furukawa Y, Gonzalez FJ, Komai M.
Low-dose dioxins alter gene expression related to cholesterol biosynthesis, lipogenesis, and glucose metabolism through the aryl hydrocarbon receptor-mediated pathway in mouse liver.
Toxicol Appl Pharmacol. 2008 May 15;229(1):10-9.

Schöllnast R, Kränke B, Aberer W.
Anal and palmar contact dermatitis caused by iodopropynyl butylcarbamate in moist sanitary wipes
Hautarzt. 2003 Oct;54(10):970-4.

Shibamoto T, Yasuhara A, Katami T.
Dioxin formation from waste incineration.
Rev Environ Contam Toxicol. 2007;190:1-41.

Siebert J.
The sensitizing potential of iodopropynyl butylcarbamate in the local lymph node assay.
Contact Dermatitis. 2004 Nov-Dec;51(5-6):318-9.

M.H. Sweeney, P. Mocarelli
Human health effects after exposure to 2,3,7,8- TCDD,
Food Addit. Contam. 17 (2000) 303–316.

U.S. Department of Health and Human Services
Household Products Database
Health and Safety Information on Household Products

Urwin R, Wilkinson M.
Methylchloroisothiazolinone and methylisothiazolinone contact allergy: a new ‘epidemic’.
Contact Dermatitis. 2013 Apr;68(4):253-5. doi: 10.1111/cod.12064.

Uter W, Gefeller O, Geier J, Schnuch A.
Methylchloroisothiazolinone/methylisothiazolinone contact sensitization: diverging trends in subgroups of IVDK patients in a period of 19 years.
Contact Dermatitis. 2012 Sep;67(3):125-9.

Warshaw EM, Belsito DV, Taylor JS, Sasseville D, DeKoven JG, Zirwas MJ, Fransway AF, Mathias CG, Zug KA, DeLeo VA, Fowler JF Jr, Marks JG, Pratt MD, Storrs FJ, Maibach HI.
North American Contact Dermatitis Group patch test results: 2009 to 2010.
Dermatitis. 2013 Mar-Apr;24(2):50-9.

Zirwas M, Moennich J.
Dermatitis. 2009 Mar-Apr;20(2):106-10.

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