Air Pollution Toxicity
Air Pollution Toxicity
The body's primary defense against air pollutants is the respiratory system. When deposited on the lung epithelium, particulate pollutants are either cleared from the lungs by coughing and ciliary action, or ingested by alveolar macrophages. Because of their small molecular size, most gaseous pollutants bypass the pulmonary immune defenses and are absorbed directly into the blood stream.
The damage produced is dependent on the nature of the pollutant. In the case of a particulate pollutant, such as tobacco smoke or asbestos, the alveolar macrophages, which ingest the particles, eventually serve as localized sites of inflammation or cancer of the lung. Because gaseous pollutants usually enter the blood circulation, damage occurs throughout the body. Refer to the "Causes" section of this Health Condition for health effects of some of the most common air pollutants.
It has been difficult to establish a relationship between specific air pollutants and cancers. It is hard to determine the level and frequency of exposure to environmental toxins. Environmental chemicals are never encountered singly, but in combinations which may negate, or even promote, the cancer-causing potential of the individual pollutants.
People vary in their sensitivity and susceptibility to cancer. A person's nutritional status may have a protective effect against cancer, such as has been hypothesized for cadmium, zinc and prostate cancer. The presence of other risk factors, ie. tobacco smoking, or occupational exposure to high-levels of carcinogens, also influence the outcome.
The formation of smog
Air pollution comes from many natural (pollen grains, fungal spores, forest fires and volcanic eruptions) and manmade (vehicles exhaust, incinerators, tobacco smoking, mining and smelting) sources.
Gaseous pollutants include substance which are gaseous at normal temperatures and pressures, as well as vapors of substances that are liquid or solid at normal temperature and pressures. Gaseous pollutants include: carbon monoxide, hydrocarbons, nitrogen oxides, ozone, hydrogen sulfides and sulfur oxides. Particulate pollutants include: dust, fumes (such as lead or zinc oxides), mists, sprays or smoke.
Primary pollutants are those emitted into the air. Secondary pollutants are those formed in the atmosphere, such as ozone and photochemical smog. Nitrous oxides and hydrocarbons from the combustion of fuel react with the ultraviolet waves in sunlight in the atmosphere to produce ozone.
The production of ozone and smog is light-dependent. Levels are at their lowest at night, increase through the morning, peak at mid-day, decrease through the afternoon, only to mildly increase during the evening rush when there are more cars on the road. Pollution levels then drop to a minimum overnight.
Smog can build to unhealthful levels when a meteorological condition called an "inversion layer" occurs. This layer of warm air prevents pollutants from escaping vertically, and is usually accompanied by low surface winds which prevent horizontal dilution of the irritants. The smog thus accumulates over an area until a change in weather condition occurs.
Monitoring air pollution and smog levels
Environmental monitoring of air pollution and toxic chemical exposure can be measured through biological indicators. Blood and urine specimens can be used to measure the exposure to at least 100 different chemicals. Hair analysis is a reliable indicator of exposure to arsenic, mercury, cadmium, antimony, manganese, nickel and cobalt. Environmental pollution studies should sample groups of 10-year olds, because they are generally non-smokers, who have had no occupational exposure to the toxic chemicals in question.
Smog and vehicles
Vehicles are the major sources of toxic and carcinogenic air pollutants. Gaseous pollutants, such as carbon monoxide, nitrogen oxide and hydrocarbons, and particulate matter, such as smoke and lead, are released in exhaust from automotive engines. Diesel engines from trucks, buses, and some cars, emit carcinogenic carbon compounds, odors and visible smoke.
The air is now cleaner above metropolitan areas, such as New York City, Los Angeles, and Phoenix, Arizona, than it was 20 years ago. The cleaner air is due in part to modifications in the design of the automobile.
The switch to catalytic converters and fuel injection systems has resulted in a decrease of nitrous oxide, and carbon monoxide emissions. The unleaded gasoline required by newer cars has resulted in less atmospheric lead. However, catalytic converters, and the fuel additives in unleaded gasoline release manganese, a trace metal which accumulates in tissues, displaces zinc and can be toxic at high concentrations.
Characteristic: one of the rarer elements in nature. It competes with zinc for binding sites in the body.
Sources: 90% of emissions into the atmosphere are from smelting ores, and the manufacture and processing of metallic alloys. The rest is from incineration, automobile tire wear, burning of car motor oils, tobacco smoke and other industrial processes. Exposure in urban areas with no cadmium-emitting industries is low. Cadmium levels in the liver and kidneys of smokers are twice those of non-smokers. Non-smoking individuals, who are not employed in cadmium-related industries, take in most of their cadmium through food.
Effects: Ingestion of low-levels of cadmium have been shown to cause emphysema and reduced lung function in male rats. Cadmium absorbed through the lungs is first stored in the liver, then slowly released to the kidneys and the endocrine glands. Chronic occupational (that is, heavy) exposure to cadmium can produce glomerular and tubular kidney dysfunction. Chronic occupational exposure to cadmium may also promote development of cancer of the prostate, by disruption of the zinc-hormonal balance in the organ. The researcher cautioned against extrapolating these findings to low-level cadmium exposure.
Characteristics: A dense, soft, grayish and extremely toxic metal; one of the most common particulate pollutants.
Sources: Combustion of tetraethyl lead in leaded gasoline. Lead smelters and paint. Contaminated dust, soil and foods grown in urban environments. Because of curbs placed on environmental lead pollution, urban blood lead levels have dropped 37% between l976 and l980.
Effects: Interferes with development and maturation of red blood cells. Chronic exposure damages the kidneys, reproductive organs and the central nervous system. Symptoms include: stippled red blood cells, fatigue, apathy, drowsiness, insomnia, irritability, behavior disorders, vomiting and constipation.
Characteristics: A soft, silvery or reddish-gray metal. It is used in the alloy steel industry for deoxidation, for hardening and strengthening steel.
Sources: The combustion of fossil fuels containing thylcyclopentadienyltricarbonyl manganese anti-knock additives, and the catalyst in automotive catalytic converters.
Effects: Manganic pneumonia may result from low-level environmental air pollution. Manganese accumulates in body organs that are rich in mitochondria, especially the liver. Excessive exposure results in disorders of the lung, and liver, as well as the central nervous, gastrointestinal and genitourinary systems. Occupationally-related manganese poisoning is manifested by headaches, insomnia, dermatitis, itching and decreased libido. Manganese accumulates in the brain; chronic toxicity produces Parkinson-like symptoms: tremors, spastic muscle movements, and slow, slurred speech.
Sources: Gasoline incompletely burned in auto engines or evaporates from tanks or fuel lines. Industries using solvents. Paints and dry-cleaning fluids.
Effects: Form photochemical smog in a reaction with ozone. Photochemical smog causes eye irritation and reduced visibility.
Characteristics: A colorless gas with a pungent odor. It is corrosive to metal.
Source: A by-product of the combustion of coal and oils for heat and power; acid and paper manufacturing; petroleum refineries.
Effects: In the respiratory tract, it combines with water to form the irritant, sulfuric acid. It constricts bronchi, and slows down the beating and clearing action of the respiratory tract's cilia. Symptoms include throat and lung irritation, decreased lung function, increased susceptibility to respiratory infection, and exacerbation of cardiac and pulmonary diseases.
Characteristics: an odorless, colorless, and tasteless gas.
Source: Incomplete combustion of carbon-containing fuel. Motor vehicles.
Effects: This gas produces its damage by combining preferentially with hemoglobin, to the exclusion of oxygen. Symptoms include: giddiness, throbbing headaches, weakness, dizziness, nausea, vomiting, irritability, proceeding to collapse, convulsions, coma and even death. Carbon monoxide can exacerbate coronary heart disease and even precipitate attacks of angina pectoris. Four thousand premature deaths occur from cardiovascular disease each year in the United States due to automobile exhaust.
Characteristics: A yellow-brown gas with a disagreeable pungent odor.
Source: A product of high temperature combustion. It is a product or by-product of metal-cleaning, fertilizer, explosive or nitric acid manufacturing industries.
Effects: Produces the orange to reddish brown haze that clouds the view in certain cities. It is a primary component in formation of photochemical smog. In the respiratory tract, it combines with the moisture to form the irritant, nitric acid. Symptoms of exposure include: shortness of breath and pulmonary edema. Nitric oxide poisoning is signalled by chest pain, bloody sputum, chills, fever, coughing, nausea and vomiting.
Characteristics: A colorless gas of intensely irritating action.
Source: Lightning storms, produced in smog by the interaction of nitrous oxides and ultraviolet light from the sun.
Effects: Cracks rubber. Low-level exposure increases susceptibility to respiratory infections by promoting alveolar macrophage (AM) dysfunction, and inactivation of (AM) proteolytic enzymes. Symptoms include: dry throat, headache, disorientation, altered breathing patterns and a chronic or recurrent productive cough.
Signs & Symptoms
Shortness of breath
Irritated mucosal membranes in the throat and respiratory system
Eye irritation and loss of visual acuity
Decreased pulmonary function
Decreased muscular coordination
Structure & Function: Antioxidants
Selenium Vitamin A Vitamin C Vitamin E Zinc
Please refer to the respective topic for specific nutrient amounts.
One source of complete nutrition is often recommended to defend us against against our environmental pollution: spirulina. Other single nutrients are discussed:
From animal studies, there is the suggestion that methionine and cysteine supplementation may be effective against environmental pollutants, such as cigarette and marijuana smoke, and against hepatic toxins, such as carbon tetrachloride. However, there is need for such studies in humans.
Dietary deficiencies of calcium have been reported to enhance the absorption and accumulation of lead and cadmium in the body.
Although doses up to 4 times the normal level of calcium had a protective effect against cadmium and lead, caution should be exercised because therapeutic doses of calcium may be harmful in cases of insufficient dietary magnesium, and because inordinate amounts of dietary calcium may promote the formation of kidney stones.
Selenium has gained the reputation of being a general detoxifying agent. In rats and mice, selenium diminishes the toxicity and carcinogenicity of various environmental pollutants including: cadmium, lead, mercury, silver, benzene, carbon tetrachloride and ozone. Selenium can be toxic at higher concentrations, and there are few conclusive epidemiologic or clinical studies to verify this detoxifying effect in humans.
In experimental animals, Vitamin A has been shown to have a protective effect against the development of epithelial cancer induced by exposure to hydrocarbon carcinogens.
Supplementation with Vitamin B Complex reduces the toxicity of several environmental pollutants, such as cyanide and cadmium.
The effect of Vitamin C on toxicity due to environmental pollutants is still uncertain. Although Vitamin C protects against the adverse effects of some toxins, it also enhances the intestinal absorption and toxicity of environmental toxins such as mercury and lead. Further research is warranted.
Vitamin E, an antioxidant, has been shown to be protective against ozone and nitrogen oxide.
Zinc and cadmium are antagonistic for binding sites on metallothionein in target organs for cadmium toxicity. Dietary zinc deficiencies enhance the accumulation of cadmium in tissue.
Zinc deficiencies also lead to impairment of cell-mediated immunity which is responsible for protection against tumors. Prophylactic zinc is hypothesized to have a protective effect against lead intoxication, and renal damage and prostatic cancer due to cadmium accumulation.
Although zinc is an essential nutrient, zinc intoxication can occur at high doses. More research is needed in this area.
All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
The diet should include foods high in Vitamin A, members of the Vitamin B-complex, Vitamin E, selenium, zinc, calcium, amino acids, methionine and cysteine. Although there is a debate as to how effective Vitamin C is against pollutants, the diet should at the minimum contain foods which provide Vitamin C at the recommended dietary levels.
During periods of increased smog, plenty of water and fruit juices should be ingested to liquefy mucus. This enables the respiratory cilia to beat more efficiently and to clear particulate matter from the respiratory passages more easily.
Lead absorption may be diet-dependent. Monkeys were fed alternating diets of either infant formula alone, primate chow and water, or combinations of the two, and dosed daily with injections of lead acetate. Higher blood lead concentrations were measured when the monkeys were fed the infant formula diet, than when the monkeys were fed the primate chow. This was thought to be due to the phytic acid content of the chow, because blood lead levels were dramatically decreased when the milk only diet was supplemented with phytic acid. Phytic acid is a normal component of many grains and is known to bind with several trace elements.
Although there are no diets which specifically protect against the effects of smog, the Soviets have devised prophylactic diets for workers routinely exposed to high levels of common air pollutants in the workplace.
Protection against exposure to lead compounds is gained from a diet of 16% protein, 26% fat, 55% carbohydrates and 1364 kcal. per meal. Protection against chlorinated hydrocarbons, benzene, and arsenical compounds, is acquired from a diet composed of 18% proteins, 28% fat, 51% carbohydrates, and 1428 kcal. per meal. A prophylactic diet of 16% protein, 33% fat, 48% carbohydrates and 1428 kcal. per meal is indicated in the case of exposure to inorganic compounds of mercury, magnesium, and barium.
Daily supplementation with 4 mg thiamine, either mixed in the food or administered as an aqueous solution, is recommended for all three dietary regimens. Critics contend these dietary formulations are not supported by adequate experimental evidence.
1. Acidum nitricum - 6X to 15C
2.* Pollution nosode tinct. (Bioactive Nutritional)
3. Phytolacca decandra - 15 to 30C
4. Rhamnus californica - tincture, 15 - 20 drops 6 times/day or to 6X
Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.
X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.
Boericke, D.E., 1988. Homeopathic Materia Medica.
Coulter, C.R., 1986. Portraits of Homeopathic Medicines.
Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.
Koehler, G., 1989. Handbook of Homeopathy.
Shingale, J.N., 1992. Bedside Prescriber.
Smith, Trevor, 1989. Homeopathic Medicine.
Ullman, Dana, 1991. The One Minute (or so) Healer.
Algin (from kelp)
Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.
Algin and kelp
Brown Kelp is the only source of Algin. Algin and kelp offer incredibly good protection from many kinds of modern day pollutants, carcinogens and toxins. Researchers have found algin, although undigestible, can prevent living tissue from absorbing barium, mercury, zinc, tin, cadmium and manganese.
Ways Kelp could prevent cancer and reduce the risk of poisoning from many sources of environmental pollution can be listed as follows:
1. By providing a source of undigestible fiber it increases fecal bulk. For example, alginate powder has been used successfully, without irritation or side-effects, to treat constipation.
2. By reducing cholesterol levels through the inhibition of bile acid absorption, it may prevent cancer caused by faulty metabolism of bile acids, sterols and steroid hormones.
3. By altering the nature of fecal flora, it may render harmless the colonic bacteria that could be carcinogenic.
4. By a direct cytotoxic effect, it may mediate the enhancement of the immune response system.
Bran and pectin
Bran and Pectin, as obtained from dietary sources, have been experimentally shown to protect blood and tissue against various environmental toxins (and carcinogens) by ensuring regular cleansing of the bowel, and by complexing with certain air and waterborne pollutants. For example, according to Soviet investigators, heavy metals, such as lead and mercury, are excreted harmlessly from the body much more efficiently when Pectin is included in the diet.
See Fiber for more discussion on its role in gut clearance, serum cholesterol levels, and the possible protection against cancer.
Alfalfa contains at least one protein with known anti-tumor activity. Alfalfa is also a fiber. As such it has been shown, along with Bran and Pectin, to bind and neutralize various types of agents carcinogenic to the colon. Finally, some work suggests alfalfa induces activity in a complex chemical system that inactivates dietary chemical carcinogens in the liver and small intestine before they have the chance to do the body harm.
Aromatherapy - Essential Oils
Selection depends upon several factors e.g. presenting symptoms, acute or chronic stage etc.
If the source can be identified: chemicals, pollen etc.
Aniseed Essence, Cajeput Essence, Eucalyptus Essence, Garlic Essence, Hyssop Essence, Lavender Essence, Lemon Essence, Marjoram Essence, Niaouli Essence, Onion Essence, Peppermint Essence, Pine Essence, Rosemary Essence, Sage Essence, Savory Essence, Thyme Essence.
Related Health ConditionsAbstracts
Aitio, A. & J. Jarvisalo. l985. Biological monitoring of occupational exposure to toxic chemicals. Ann Clin Lab Sci 15:121-139.
Annest, J. L.et al., 1983. Chronological trend in blood lead levels between l976 and l980. New Engl. J. Med. 308:1373-1377.
Aronow, W. S. & N. W. Isbell. 1973. Carbon monoxide effect on exercise induced Angina Pectoris. Ann. Intern. Med. 79:392-395.
Bencko, V., & M. Cikrt. l984. Manganese: A review of occupational and environmental toxicology. J. Hyg. Epid. Microbiol. Immun. 28:139-148.
Benc ko, V., T. Geist, D. Arbetova, D. M. Dharmadikari, & E. Svandova. l986. Biological monitoring of environmental pollution and human exposure to some trace elements. J Hyg Epid Micro Immun. 30:1-25.
Blackstone, S.,et al., 1974. Some interrelationship between Vitamin C (L-ascorbic acid) and mercury in the guinea pig. Food Cosmet. Toxicol. 12:511-516.
Blumenthal, D. S. & M. Greene. 1985. Air Pollution. Introduction to Environmental Health. D. S. Blumenthal, ed. Springer Publishing Co.; New York, N.Y. pp. 117-144.
Bokkenhause, V., J. Winter, & W. Kelly. Metabolism of biliary steroids by human fecal flora. Am. J. Clin. Nutr. 1978. 31(Suppl.):221-226.
Boulet LP et al., Comparative degree and type of sensitization to common indoor and outdoor allergens in subjects with allergic rhinitis and/or asthma. Clin Exp Allergy, 1997 Jan, 27:1, 52-9.
Calabrese, E.J. 1980. Nutrition and Environmental Health. The influence of nutritional status on pollutant toxicity and carcinogenicity. VOL. 2: Minerals and Macronutrients. John Wiley & Sons; New York. 468 pp.
Cerlewski, F., & R. M. Forbes. 1976. Influence of dietary zinc on lead toxicity in the rat. J. Nutr. 106:689-696.
Cheryan, M. l980. Phytic acid interactions in food systems. CRC Crit. Rev. Food. Sci. Nut. 13:297-333.
Coffin, D. L. & D. E. Gardner. 1972. Interaction of biological agents and chemical air pollutants. Ann. Occup. Hyg. 15:219-234
Conrad, M. E. & J. C. Barton. 1978. Factors affecting the absorption and excretion of lead in the rat. Gastroenterology. 74:731-740.
Cousins, R. J. l979. Metallothionein synthesis and degradation: relationship to cadmium metabolism. Environ. Hlth. Persp. 28:131-136.
Davis, A. Let's Get Well. Harcourt, Brace and World Co., New York. 1965.
DeFerreya, E. C. et al., 1974. Prevention and treatment of carbon tetrachloride hepatotoxicity by cysteine: studies about its mechanism. Toxicol. Appl. Pharmacol. 27:558-68.
Ellis, K. J., D. Vartsky, I. Zanzi, & S. H. Cohn. l979. Cadmium in vivo measurement in smokers and non-smokers. Science. 205:323-325.
Erlich, R. Changes in susceptibility to respiratory infection caused by exposure to photochemical oxidant pollutants. The biomedical effects of ozone and related photochemical oxidants. Lee, S.D., M.G. Mustafa, & M. A. Melman, eds. Princeton Scientific Publishers; Princeton, NJ. p. 273-285.
Ferris, B. G., I. T. T. Higgins, M. W. Higgins, & J. M. Peters. l973. Sulfur oxides and suspended particulates: possible effects of chronic exposure. Arch. Envir. Health. 27:179.
Fishbein, L. l981. Sources, transport, and alterations of metal compounds: an overview. I. Arsenic, beryllium, cadmium, chromium and nickel. Environ. Hlth. Persp. 40:43-64.
Fowler, B., et al., 1975. The morphologic effects of chronic cadmium administration on the renal vasculature of rats given low & normal calcium diets. Toxicol. Appl. Pharmacol. 34:233-252.
Fowler, B. A. l979. International conference on environmental cadmium: an overview. Environ. Hlth. Persp. 28:297-300.
Frisbey, A., et. al. Quarterly Bulletin of the Michigan Agriculture Experimental Station, 36, 477, 1954.
Gardner, D. E. et al., 1971. Loss of protective factor for alveolar macrophages when exposed to ozone. Arch. Intern. Med. 127:1078-1084.
Glovsky MM et al., Particulate air pollution: possible relevance in asthma. Allergy Asthma Proc, 1997 May-Jun, 18:3, 163-6.
Hegsted, D. M., J. J. Vitale, & H. McGrath. 1956. The effect of low temperatures and dietary calcium upon magnesium requirements. J. Nutr. 58:175.
Hutton, M. l983. Sources of cadmium in the environment. Ecotoxic. Environ. safety. 7:9-24.
Iritani, N. & J. Nogi. Effect of spinach and wakame on cholesterol turnover in the rat. Atherosclerosis. 1972. 15:87-92.
Jolles, B., M. Remington & P. S. Andrews. Effects of sulphated degraded laminarian on experimental tumor growth. BJC 1963.17:109-115.
Kowal, N. E.et al., 1979. Normal levels of cadmium in diet, urine, blood and tissues of inhabitants of the United States. J. Toxic. Environ. Health. 5:995-1014.
Leuchtenberger, C. & R. Leuchtenberger. 1977. Protection of hamster lung cultures by L-cysteine or Vitamin C against carcinogenic effects of fresh smoke from tobacco or marihuana cigarettes. Brit. J. Exper. Pathol. 58:625-634.
Livshits, O. D. Prophylactic role of pectin-containing foods during lead poisonings. Voprosy Pitanyia. l969. 28:76-77.
Lunn, J. E., J. Knowelden, & A. Handyside. 1967. Patterns of respiratory illness in Sheffiled infant school children. Brit. J. Prev. Soc. Med. 21:7.
Mahaffey, K. R. l983. Sources of lead in the urban environment. Am J. Publ. Hlth. 73:1357-1358.
Molfino, N.A. et al: The Effect of Air Pollution on Allergic Bronchial Responsiveness. Clinical and Experimental Allergy, 1992;22:667-672.
Mowrey, Daniel B. Ph.D. l986. The Scientific Validation of Herbal Medicine. Cormorant Books. 316 pp.
Mulinos, M. G. & G. B. J. Glass. The treatment of constipation with a new hydrosorbent material derived from kelp.Gastro. 1953.
Mushett, C. W.et al., l952. Antidotal efficacy of Vitamin B-12 (hydroxycobalamin) in experimental cyanide poisoning. Proc. Soc. Exp. Biol. Med. 81:539-543.
National Academy of Sciences. l981. Indoor Pollutants. National Academy Press; Washington, D.C.
Needleman, H. L., ed. l980. Low level lead exposure: the clinical implications of current research. Raven Press; New York.
Nordberg, G. F., and O. Andersen. 1981. Metal interactions in carcinogenesis: Enhancement, Inhibition. Environ. Hlth. Persp. 40:65-81.
Ostergaard, K. 1977. The concentration of cadmium in renal tissue from smokers and non-smokers. Acta Med. Scand. 202:193-5.
Petering, H. G., H. Choudhury, and K. L. Stemmer. 1979. Some effects of oral ingestion of cadmium on zinc, copper, and iron metabolism. Environ. Hlth. Persp. 28:97-106.
Piomelli, S et al., 1982. Threshold for lead damage to heme synthesis in urban children. Proc. Nat. Acad. Sci. USA. 79:3335-3339.
Piscator, M. l981. Role of cadmium in carcinogenesis with special reference to cancer of the prostate. Environ. Hlth. Persp. 40:107-120.
Pope, Andrew M: Indoor Allergens - Assessing and Controlling Adverse Health Effects. JAMA, June 2, 1993;269(21):2721.
Richards, W., S. P. Azen, J. Weiss, S. Stocking, J. Church. Los Angeles air pollution and asthma in children. Ann. Allergy. l981 47:348-354.
Roels, H. A. et al., l980. Exposure to lead by the oral and the pulmonary routes of children living in the vicinity of a primary lead smelter. Environ. Res. 22:81-94.
Rosen, F. L. What the physician should know about air pollution. Ann. Allergy. 1981. 47:345-347.
Salyers, A. A., J. K. Palmer, and T. D. Wilkins. Degradation of poly-saccharides by intestinal bacterial enzymes. Am. J. Clin. Nutr. l978. 31(Suppl.):128-130.
Sandiford CP et al., Measurement of airborne proteins involved in Bakers' asthma [see comments]. Clin Exp Allergy, 1994 May, 24:5, 450-6.
Scherer, G., and H. Barkemeyer. l983. Cadmium concentrations in tobacco and tobacco smoke. Ecotoxic. Environ. Safety. 7:71-78.
Shukla, G. S. and S. V. Chandra. l982. Effect of manganese on carbohydrate metabolism and mitochondrial enzymes in rats. Acta Pharmacol. Toxicol. 51:209-216.
Shukla, G. S. & R. L. Singhal. 1983. The present status of biological effects of toxic metals in the environment: lead, cadmium, and manganese. Can. J. Physiol. Pharm. 62:1015-31.
Skjei, E., and M. D. Whorton. l983. Of Mice and Molecules. Technology and Human Survival. The Dial Press; New York, N. Y. 347
Smith-Barbaro, P. D. Hanson, and B. S. Reddy. Carcinogenic binding to various types of dietary fiber. J. Nat. Ca. Instit. 1981. 67:495-497.
Stowe, H. D., R. A. Goyer, P. Medley, and M. Cates. 1974. Influence of pyridoxine on cadmium toxicity in rats. Arch. Environ. Health. 28:209-216.
Sutphen, E. I. l985. Soviet prophylactic nutrition for workers in toxic chemical occupational environments. Am J Clin Nutr 42:746-748.
Trevino RJ: Air pollution and its effect on the upper respiratory tract and on allergic rhinosinusitis. Otolaryngol Head Neck Surg, 1996 Feb, 114:2, 239-41.
Truelove, J. F., S. G. Gilbert, and D. C. Rice. 1985. Effect of diet on blood level concentration in the Cynomolgus monkey. Fund. Appl. Toxic. 5:588-596.
Tseng, Robert, Ying, Mei, M.D. et al: Particulate Air Pollution and Hospitalization for Asthma. Annals of Allergy, May 1992;68:425-432.
Tyihak, E., and B. Szende. Basic plant proteins with antitumor activity. Hungarian Patent 798. 1970.
Valanis BG: Epidemiology of lung cancer: a worldwide epidemic. Semin Oncol Nurs, 1996 Nov, 12:4, 251-9.
von Nieding, G. l978. Possible mutagenic properties and carcinogenic action of the irritant gaseous pollutants nitrou oxide, ozone, and sulfur dioxide. Environ. Hlth Persp. 22:91-92.
Waalkes, M. P. l986. Effect of dietary zinc deficiency on the accumulation of cadmium and metallothionein in selected tissues of the rat. J. Toxic. Environ. Hlth. 18:301-313.
Watsky KL: Airborne allergic contact dermatitis from pine dust. Am J Contact Dermat, 1997 Jun, 8:2, 118-20.
Wattenburg, L. Effects of dietary constituents on the metabolism of chemical carcinogens. Ca. Res. 1975. 35:3326-3331.
Wolnik, K. A. et al., 1983. Elements in major raw agricultural crops in the United States. I. Cadmium and lead in lettuce, peanuts, potatoes, soybeans, sweet corn and wheat. J. Agric. Food Chem.
Yamamoto, I. et al., Antitumor effects of seaweeds. 1. Anitumor effects of extracts from Sargassum and Laminaria. Jap. J. Exp. Med. l974. 44:543-546.
- Product Categories
- Detox & Immunity
- Digestive Health
- Joint Health
- Weight Loss
- Popular Products
- CellRenew Collagen Hyaluronic Acid
- Foundation Blue-Green Algae
- Reference Materials
- Product Testimonials
- Health Journal Archive
- Health Briefs
- Health Basics
- Frequent Product Q&A's
- Med-Scope (health database)
- Health Conditions
- Natural Solutions
- Alternative Therapies
- Toxicity Sources
- Foods Advice
- Anatomy & Fitness
We test only on humans