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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.”

COMMENTARY
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 (http://www.sti.nasa.gov/tto/Spinoff2007/ps_3.html).  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)
http://www.jhsph.edu/publichealthnews/press_releases/2009/breysse_indoor_asthma.html

Pollution at Home Often Lurks Unrecognized (12/26/2008, Reuters Health) by Amy Norton
http://www.reuters.com/article/2008/12/26/us-pollution-home-idUSTRE4BP1ZL20081226

Air Purifiers and Air Filters Can Help the Health of Allergy and Asthmas Sufferers (S. A. Smith)
http://ambafrance-do.org/alternative/11888.php

Indoor Air Pollution Fact Sheet (08/1999, American Lung Association)
http://www.lungusa.org/healthy-air/home/healthy-air-at-home/

An Introduction to Indoor Air Quality (Environmental Protection Agency)
http://www.epa.gov/iaq/ia-intro.html

References

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.

SUPPORTING ABSTRACTS
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.

Mold In Your Cellar?

water-damaged-basement-wallThere are wet clothes on the line downstairs. Last night’s rain storm left a few puddles on the floor near the cellar windows. It feels a few degrees warmer in the cellar than in the kitchen because it’s more humid. Situations like this create a breeding ground for mold, one of the fungus kingdom. Molds are everywhere, and are a common component of dust. Large quantities of mold can become a health hazard, causing allergic reactions and respiratory problems. Those few that produce mycotoxins can pose a serious risk to human health, and are the “toxic molds” of conversation. One of the most infamous is called Stachybotrys chartarum, more commonly found outside than in, but an occasional resident of flooded buildings. Molds can live on plants, foods, dry leaves, and other organic matter, but can also grow on hard surfaces.

Molds are produced by spores, which can be carried by air currents because they are tiny and lightweight. Fungi in general are necessary to the food chain as decomposers. But as molds inside your house they can cause a myriad of problems. For significant mold growth to happen there needs to be a source of dampness, a source of food, and a substrate capable of sustaining growth. Building supplies, including carpets, plywood, sheetrock, and other porous materials, are ideal places for molds to live and grow. Cellulose is one of their favorites. A single incident of water damage can encourage mold to live inside a wall, later to be resurrected from near dormancy by high humidity. Identifying the source of humidity is an important step in resolution. Even the steam from a stovetop or the shower, the watering of houseplants or the use of a central humidifier can exacerbate—or even initiate—a mold problem.

The health effects of mold exposure include allergic reactions, eye and respiratory irritation, infection, and toxicity. About five percent of individuals are predicted to have some airway symptom from molds over their lifetimes. Wherever and whenever mold infestation is identified it needs to be remediated.

If the cellar is where the kids play when the outdoors is uninviting, paying attention to the presence of mold is important. If enough is there, you’ll be able to smell it, even if you can’t see it. If the mold is growing in black streaks and looks slimy, it could be Stachybotrys chartarum, and is usually indicative of poor indoor air quality. If the texture is fuzzy or matte, it’s likely another strain, such as Aspergillus or Fusarium. Regardless of what it is, it is advisable not to touch it or to inhale deeply when you examine it.

Sometimes you’ll see condensation on your (cellar) windows or walls. This might mean there’s a combustion problem with an appliance. Is the dryer properly vented?  How about the furnace and water heater?  Too little air to the furnace can cause back drafting, which is also a carbon monoxide threat. Using a de-humidifier in the cellar, especially if it’s unheated, is sound practice. If your dryer is vented into a bucket of water to trap lint because outdoor venting is difficult or impossible, and if the cellar lacks heat, the damp air from the dryer can condense once it contacts the cold walls. Hence the rationale for a dehumidifier. A fan can desiccate the air enough to deny mold a happy home.

The dryness of indoor wintertime air can cause static electricity, shrinking and warping of furniture, skin irritation, and even bloody noses. At 40% humidity, most of us are reasonably comfortable. Increasing indoor humidity to prevent problems is O.K. as long as there is no condensation inside the living room windows. Cold air cannot hold much moisture, and a heater dries it out even more. Being overzealous with humidification can create conditions favorable to mold, which prefers temperatures between 77° F. and 85° F, but can survive anywhere between 32° and 95°.   Unless there are symptoms of mold sensitivity, testing is unnecessary. If it is done, it should be performed by a trained professional. In a baseline home, mold spore counts may range from 300 to 1200 spores per cubic meter. Counts above 1000 suggest a mold problem. (Rockwell, 2005)  On the other hand, there are no regulations that outline acceptable mold counts

Simple steps to remedy a small occurrence start with sunshine, improved ventilation, additional insulation in the walls, and dehumidification. But these do not get rid of what’s already present; they only make it non-viable. Simply killing mold is not enough. It has to be removed because the chemicals and proteins that evoke a reaction are still present in dead mold. Using bleach will only make it lighter in color and fail to kill the roots. Why?  Because bleach is mostly water, and water is what mold needs to thrive.  The active ingredient in bleach, often sodium hypochlorite, is weakened. A stronger product than what we get from a store is dangerous. Not only that, bleach will only work on non-porous surfaces, like tubs and tiles. It does not penetrate porous materials, even concrete, so it can’t get to the roots, and the mold will return. It does, however, change the color. Some people think that if they can’t see any mold, all is well.

Borax and straight white vinegar can kill mold, but you have to be patient. Borax has to be mixed with water, but is strong enough and safe enough to do the job. Neither product needs to be rinsed. If you don’t care about spending money, tea tree oil is a great antifungal, using a teaspoon per cup of water in a spray bottle. It’s safe to humans and animals, and is one of the best mold slayers. People use it on cuts and scrapes because it’s also antibacterial. Any residue will prevent recurrence of mold. A novel product in the fight against mold is grapefruit seed extract, used to fight bacterial, yeast and viral infections. The citric acid seems to be the active component. Ten drops of this go into a cup of water in a spray bottle. It’ll kill the mold down to its roots. If a mold problem is severe, get a professional to do the job, but make sure he’s qualified.

References

http://blackmold.awardspace.com/kill-remove-mold.html

Hardin BD, Kelman BJ, Saxon A.
Adverse human health effects associated with molds in the indoor environment.
J Occup Environ Med. 2003 May;45(5):470-8.

Koburger T, Below H, Dornquast T, Kramer A.
Decontamination of room air and adjoining wall surfaces by nebulizing hydrogen peroxide.
GMS Krankenhhyg Interdiszip. 2011;6(1):Doc09.

Kuhn DM, Ghannoum MA.
Indoor mold, toxigenic fungi, and Stachybotrys chartarum: infectious disease perspective.
Clin Microbiol Rev. 2003 Jan;16(1):144-72.

Mudarri D, Fisk WJ.
Public health and economic impact of dampness and mold.
Indoor Air. 2007 Jun;17(3):226-35.

Robbins CA, Swenson LJ, Nealley ML, Gots RE, Kelman BJ
Health effects of mycotoxins in indoor air: a critical review.
Appl Occup Environ Hyg. 2000 Oct;15(10):773-84.

Rockwell W.
Prompt remediation of water intrusion corrects the resultant mold contamination in a home.
Allergy Asthma Proc. 2005 Jul-Aug;26(4):316-8.

Terr AI.
Are indoor molds causing a new disease?
J Allergy Clin Immunol. 2004 Feb;113(2):221-6.

U.S. Environmental Protection Agency
“A Brief Guide to Mold. Moisture, and Your Home”
www.eps.gov/mold/whattowear.html

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

Reduce Inflammation through Weight Loss

acute-pain-in-a-woman-kneeSome of us know inflammation too well. When getting out of bed in the morning becomes an auditory event in your joints that rivals a flamenco dancer’s castanets, you know inflammation. What you may not know, or at least not realize, is that your weight has something to do with it. For many of us, the seeds of inflammation were planted years ago. Our genes, body weight, diet, lifestyle and fitness determine our states of wellness and non-wellness, some of which we cannot sense. Silent inflammation is probably worse than that we can feel from getting cut or hit by a baseball. If it hurts or is uncomfortable, we’ll take care of it right away. If it’s not noticeable, it can smolder for years, eventually exploding into a chronic illness.

Inflammation is the response of tissue to injury or insult, occasionally caused by an invading pathogen. Characteristics, which you can sense, include increased blood flow to the injured area, elevated temperature, redness, swelling and pain. Inflammatory responses to what should have been a harmless agent include allergies and autoimmune diseases, states where the response is either out of proportion to the threat it faces or is directed against an inappropriate target, such as self. In these cases, the response is worse than anything the agent itself could have generated, and is often insensate. The cascade of cellular and molecular signals that accompany inflammation can perpetuate it and make it chronic, in which case monocytes and macrophages take over the management. This may sound cool, but the chemicals they create inside the tissues wreak havoc. Macrophages begin to swallow everything that appears derelict, including senescent cells and whatever is deemed a pathogen, whether it truly is or not.

At some point in this chronology, chemical mediators are released, including things like Interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-a) and prostaglandins that keep the ball rolling…on and on. When the body tries to control all this nefarious activity it replaces damaged tissue with replacement cells of the same type, but occasionally fails and results in diseased states, such as asthma, rheumatoid arthritis, tendonitis, celiac and inflammatory bowel diseases.

Inflammation is recognized as causal to several chronic diseases and all-cause mortality, and is prevalent among those who have a body mass index above 30.0.  Biomarkers of inflammation are used to examine the relationship of inflammation to chronicity, with C-reactive protein (CRP), IL-6, TNF-a, and IL-8 as indicators. CRP probably is the first one your doctor will interpret, since it’s a prime marker of inflammation. It just doesn’t pinpoint the location. CRP is a native protein made by the liver in response to factors released by fat cells. In acute inflammation, such as from an infection, levels can rise in less than six hours and be hundreds of times higher than normal, which is lower than 10 mg per liter. With a severe bacterial infection, it can reach 200 or more. The absolutely perfect reading is 1.0. Levels above 2.4 are supposed to be associated with increased risk of cardiovascular events, but that’s debatable because the studies were done with people who had unstable angina (Pepys, 2003).

Human adipose tissue expresses and releases the pro-inflammatory artifacts, inducing low-grade systemic inflammation in people with too much body fat. Pediatricians in the Netherlands looked at overweight children in their country and saw higher levels of CRP than in normal-weight children (Visser, 2001), accompanied by higher white cell counts. In 2007, the Archives of Internal Medicine published an analysis of more than thirty separate studies, concluding that weight loss is a major factor in the reduction of CRP, adding that a loss of one kilogram (2.2 lbs) equates to a 0.13 mg/L drop in CRP (Selvin, 2007).

Many parents think that their kids will outgrow the chubby stage. Sometimes, yes; often, no. We now see 400-pound 20-year-olds who were obese at age eight, whose parents ignored admonitions to address the foreboded tragedy at the early age. That collection of fat that hangs over the belt, sometimes reaching the thighs, is called a panniculus, and is more than just a dormant spare tire. It secretes adipokines, or chemical signals, to other parts of the body, increasing risk of serious disease through disrupted homeostasis (Rosenow, 2010). If this describes someone you know, eventually you’ll likely see diabetes, heart disease, and maybe even some form of cancer (Ibid).

There are plenty of overweight seniors, some of whom achieve that senior designation at age 40, others above 70. Just by virtue of their age, they’re more likely to report joint pain, but obesity at any age is a predictor of low-grade chronic inflammatory state.  Whether by diet or exercise, or both, weight loss is extremely vital to maintaining one’s health. In comparisons, the low-carb folks lost more weight than the low-fat. Think about this.  The knee pain in the 50-year-old guy is so bad he can’t walk behind his lawnmower. The problem is that he’s carrying 375 pounds on a frame designed to carry 150-180, and his femur is squeezing the cushions at the tibia. Yes, it’s distinctly possible that thyroid issues are causative of the extra weight. There may be other factors that include lack of sleep, too much stress, certain medications, uncontrolled cortisol (kinda rare), and menopause in women. Some of these can be managed and can be worked out with the family physician and maybe a visit to a dietitian. However, looking more closely at his eating habits, we see carbohydrates as the main source of gustatory input, with beneficial fats and lean protein given the back seat. Self-inflicted obesity has no excuse. Inflammatory biomarkers can be attenuated with even a small reduction in weight (Miller, 2008) (You, 2006).  Now, get this. The physical movement required to mow the lawn might be just enough to reduce inflammation, despite the immediate discomfort, which will eventually taper off. (Ford, 2002) (Miller, 2008).

Obesity is a problem of epidemic proportions. Certain people are perceived as anathema, bête noir, pariah, and may pay for self-destructive behavior. If cigarette cessation clears the lungs, could weight reduction clear the blood? Yep. Dietary interventions will help both, but sticking a finger into the dike doesn’t quite do it.

References

Clément K, Viguerie N, Poitou C, Carette C, Pelloux V, Curat CA, Sicard A, Rome S, Benis A, Zucker JD, Vidal H, Laville M, Barsh GS, Basdevant A, Stich V, Cancello R, Langin D.
Weight loss regulates inflammation-related genes in white adipose tissue of obese subjects.
FASEB J. 2004 Nov;18(14):1657-69.

Mary Elizabeth Dallas
Losing Weight May Lower Cardiac Risks
Study finds both low-carb and low-fat diets help overweight people reduce inflammation
NIH, 5 Nov, 2012
MedlinePlus Trusted Health Information for You A service of the U.S. National Library of Medicine
From the National Institutes of HealthNational Institutes of Health
http://www.nlm.nih.gov/medlineplus/news/fullstory_131011.html

Esposito K, Pontillo A, Di Palo C, Giugliano G, Masella M, Marfella R, Giugliano D.
Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial.
JAMA. 2003 Apr 9;289(14):1799-804.

Ford, Earl S.
Does Exercise Reduce Inflammation? Physical Activity and C-Reactive Protein Among U.S. Adults
Epidemiology:. September 2002 – Volume 13 – Issue 5 – pp 561-568

Gilbert CA, Slingerland JM.
Cytokines, Obesity, and Cancer: New Insights on Mechanisms Linking Obesity to Cancer Risk and Progression.
Annu Rev Med. 2012 Oct 26. [Epub ahead of print]

Kawasaki N, Asada R, Saito A, Kanemoto S, Imaizumi K.
Obesity-induced endoplasmic reticulum stress causes chronic inflammation in adipose tissue.
Sci Rep. 2012;2:799. Epub 2012 Nov 12.

Stephen P Messier, Claudine Legault, Shannon Mihalko, Gary D Miller, Richard F Loeser, Paul DeVita, Mary Lyles, Felix Eckstein, David J Hunter, Jeff D Williamson and Barbara J Nicklas
The Intensive Diet and Exercise for Arthritis (IDEA) trial: design and rationale
BMC Musculoskeletal Disorders 2009, 10:93

Miller GD, Nicklas BJ, Loeser RF.
Inflammatory biomarkers and physical function in older, obese adults with knee pain and self-reported osteoarthritis after intensive weight-loss therapy.
J Am Geriatr Soc. 2008 Apr;56(4):644-51. Epub 2008 Feb 28.

Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS, Klein S, Coppack SW.
Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo.
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Navarro SL, Brasky TM, Schwarz Y, Song X, Wang CY, Kristal AR, Kratz M, White E, Lampe JW.
Reliability of serum biomarkers of inflammation from repeated measures in healthy individuals.
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Nicklas BJ, Ambrosius W, Messier SP, Miller GD, Penninx BW, Loeser RF, Palla S, Bleecker E, Pahor M.
Diet-induced weight loss, exercise, and chronic inflammation in older, obese adults: a randomized controlled clinical trial.
Am J Clin Nutr. 2004 Apr;79(4):544-51.

Pepys MB, Hirschfield GM.
C-reactive protein: a critical update.
J Clin Invest. 2003 Jun;111(12):1805-12.

Anja Rosenow, Tabiwang N. Arrey, Freek G. Bouwman, Jean-Paul Noben, Martin Wabitsch, Edwin C.M. Mariman, Michael Karas, and Johan Renes
Identification of Novel Human Adipocyte Secreted Proteins by Using SGBS Cells
J. Proteome Res., 2010, 9 (10), pp 5389–5401

Roth CL, Kratz M, Ralston MM, Reinehr T.
Changes in adipose-derived inflammatory cytokines and chemokines after successful lifestyle intervention in obese children.
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Elizabeth Selvin, PhD, MPH; Nina P. Paynter, MHS; Thomas P. Erlinger, MD, MPH
The Effect of Weight Loss on C-Reactive ProteinA Systematic Review
Arch Intern Med. 2007;167(1):31-39

Tam CS, Clément K, Baur LA, Tordjman J.
Obesity and low-grade inflammation: a paediatric perspective.
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André Tchernof, PhD; Amy Nolan, RD; Cynthia K. Sites, MD; Philip A. Ades, MD; Eric T. Poehlman, PhD
Weight Loss Reduces C-Reactive Protein Levels in Obese Postmenopausal Women
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You T, Nicklas BJ
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Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB.
Elevated C-reactive protein levels in overweight and obese adults.
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Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB.
Low-grade systemic inflammation in overweight children.
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Viviane Zorzanelli Rocha, M.D., Eduardo J. Folco, PhD, Galina Sukhova, PhD, Koichi Shimizu, M.D., Israel Gotsman, M.D., Ashley H. Vernon, M.D., and Peter Libby, M.D.
Interferon-gamma, a Th1 Cytokine, Regulates Fat Inflammation A Role for Adaptive Immunity in Obesity
Circ Res. 2008 August 29; 103(5): 467–476.

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

Seasonal Allergies – Autumn In New York

seasonal-allergiesAutumn in New York might be a great song, but that’s about as far as it goes for allergy sufferers. In a city made from concrete and glass, you’d think it was easy to escape an attack by natural allergens, like pollen and mold. Ragweed is the chief culprit that arouses immune cells to churn out antibodies to its pollen. The subsequent biochemical reactions flood the bloodstream with histamine, the chemical that gives rise to the familiar allergy symptoms. One ragweed plant can produce a billion grains of pollen in a season, and the grains are so light that they can travel hundreds of miles on the gentlest waft of air. That is why a city made of concrete and glass is not immune to a covert pollen attack. To make matters worse, you can’t just move to the mountains. The ragweed will follow you.

What used to be an allergy season running from mid-August to September is now on the calendar from the first of August to the middle of October. Rising temperatures and elevated carbon dioxide levels extend the season. Trees, grasses and molds are not dismissed as causes of seasonal misery. Damp leaves harbor molds that are kicked up when hit by the rake. In school, kids are assaulted by dust mites that have waited all summer for company.

It’s generally accepted that allergies are triggered by a protein. When a cruising lymphocyte identifies a threat it launches a countermeasure against it. In this complicated biochemical process antibodies are made. The particular antibody for allergic reactions is called immunoglobin E, or IgE, which attaches itself to mast cells and basophils, the cells that activate and release histamine. Histamine opens the flood gates of response, and blood vessels dilate, causing blood pressure to drop. The spaces surrounding cells fill with fluid and the symptoms begin—itching, hives, sneezing, wheezing, and more. In severe cases, anaphylactic shock may occur, a reaction that can be fatal if not handled immediately. The Epi-Pen addresses anaphylaxis. It contains epinephrine, a natural hormone that counteracts dangerous physiological changes that appear during allergic response.

Conventional treatments for allergies include steroid nasal sprays, antihistamines, decongestants, eye drops and shots. They’re used before, during and after symptoms occur. Rhinitis, characterized by irritated mucous membranes of the nose, is a common sign of seasonal allergy that responds to alternative measures, notably to butterbur. Butterbur rhizome extracts that are free of pyrrolizidine alkaloid hepatotoxic constituents have been found safe to use for up to four months (Schapowal, 2005), though many people use them longer. Pyrrolizidine alkaloids are produced by plants to protect them against insect herbivores, but are a danger to the liver, occluding small blood vessels and causing the organ to swell. Petasin, the active ingredient in butterbur, is an anti-inflammatory compound with relaxant properties (Ko, 2001), able also to inhibit histamine and leukotrienes, the latter being white blood cell components responsible for allergic and inflammatory reactions (Thomet, 2002).

Cetirizine is Zyrtec, the antihistamine that addresses the symptoms of allergic rhinitis. A quickened heartbeat, weakness or tremors, problems with urination, insomnia and dizziness are among its side effects. Butterbur, on the other hand, is generally well tolerated, although belching may occur, and those who are sensitive to some plant compounds may experience itching and mild rash. The fatigue and drowsiness common to cetirizine are absent. In a randomized study conducted in Switzerland, seasonal rhinitis patients receiving butterbur fared as well as those receiving cetirizine, without any of the sedative effects (Schapowal, 2002).

Nasal irrigation is the practice of using a fluid-filled vessel to flush excess mucus and debris from the nose and sinuses. Advocates insist that it promotes nasal and sinus health. The saline solution that is commonly employed may act as an antibacterial agent, as well. Being inexpensive and simple, the practice has gained considerable acceptance among Canadian and American medical practitioners, who agree that it could reduce reliance on antibiotics (Papsin, 2003) and antihistamines (Garavello, 2003). If it relieves symptoms, it’s a welcome ritual.

There is a plant chemical that acts simultaneously as a bronchodilator and an inhibitor of histamine and other allergic or pro-inflammatory chemicals in the body—quercetin, a compound common to apples, onions, dill, Hungarian peppers, capers and radishes. How’s that for diversity? Quercetin is a flavonoid, one of several substances known years ago as vitamin P, a designation that has fallen from favor. Flavonoids are noted for the coloration of many flowers designed to attract pollinators. In the higher plants, they act as chemical messengers, cell cycle inhibitors and directors of the total physiological machinery. Good for us is that these properties translate to humans, although they are slow to be recognized by the FDA and its European counterparts, primarily because absorption is an issue and clinical studies are few.

Where funding was available, outside the realm of pharmaceutical giants, quercetin and its comrades were found to demonstrate several pharmacological effects, including anti-viral, anti-microbial, anti-inflammatory and anti-allergic potential. These properties demonstrate a capability to down-regulate and to suppress certain of the many inflammatory pathways, including those involved in allergic inflammation and basophil enlistment (Chirumbolo, 2010). Of the flavonoids, quercetin is the most abundant, but has received the most attention because its effects on basophils are seen at billionth of mole concentrations, where studies in Italy learned that quercetin was able to sequester histamine release in activated cells (Chirumbolo, Marzotto, et al, 2010). Using mast cells sensitized with IgE, Japanese scientists learned that flavonoid varieties akin to quercetin display similar activity by inhibition of the calcium influx that signals the release of histamine and pro-inflammatory mediators (Kimata, 2000) (Kawai, 2007).

A regimen consisting of herbal interventions and dietary flavonoids (there are many to pick from) presents a complementary / alternative approach to the management of allergic misery with considerable effectiveness. Maybe it’s worth a try and you’ll save money on tissues.

References

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