Notes: Air Toxics
1) "The reaction of ozone with polyunsaturated fatty acids from the surfactant factor and pulmonary epithelial cells produces different reaction products which can cross the alveolar-capillary barrier and reach distant structures. Although only a few papers claim extrapulmonary changes in animals exposed to this gas, some neurological deficits, such as complaints of fatigue, lethargy, headache in humans, as well as significant disarrangements in the sleep pattern related to biochemical changes in the brain." -- Carlos DePaz, "Some Consequences of Ozone Exposure on Health", Archives of Medical Research, Vol 28, No. 2 (1997), p163-170.
2) "Ozone is the strongest oxidizing gas in air pollution... Brain tissue is highly susceptible to oxidative stress which has been attributed to the high content of polyunsaturated fatty acids, the high consumption of oxygen by neurons and the low levels of glutathione and anti-oxidant enzymes . ...the ozone exposed rats had the lowest means spine density in primary dendrites 4.4±0.13/20um and in secondary dendrites 8.42±0.16/20um (n 500) of granule cells (P<0.0001)... there was evident vacuolation of neuronal cytoplasm, swelling of Golgi apparatus... and mitochondrion and dilation of cisterns of the rough endoplasmic reticulum of the granule cells in the rats exposed to ozone. We also found that dendrites and spines were vacuolated. Those changes were only found in the ozone exposed animals. -- Colin-Barenque L, et al., "Morphologic Alteration Of The Olfactory Bulb After Acute Ozone Exposure In Rats", Neuroscience Letters, Vol 274 (1999), p1-4. Note: Bronx Zoo birds descriptions included streaking of the heart and brain hemorrhages. Ward Stone of the NYSDEC described lung damage as generally common in autopsied birds.
3) "Encephalopathy and polyneuropathy are the most common diseases related to neurology following the exposure to low levels of environmental substances. [...] The importance of... organic solvents and ozone is explained in their relation to neurology and clinical ecology. Mentioned is also the difficult concept of 'multiple chemical sensitivity'. Referring to the environmental consultation an open and evaluating attitude is recommended to avoid damage as a result of environmental poisoning equally to exaggerated medical activities." -- Hausotter W., "Neurological problems in environmental medicine", Wien Med Wochenschr 1998;148(3):46-51 PMID: 9592928, UI: 98255286
4) "Ozone is a reactive environmental oxidant molecule whose deleterious effects are enhanced by interaction with other photochemical oxidants. While the pulmonary system is the primary target for ozone toxicity, at a morphological and biochemical level, extrapulmonary toxic effects are well documented. The consequences of exposure to ozone depend on its concentration and are influenced by genetic and host factors." -- Mehlman MA, Borek C, "Toxicity and biochemical mechanisms of ozone.", Environ Res 1987 Feb;42(1):36-53; PMID: 3803343, UI: 87105450
5) "This study sought to determine if ozone at levels known to induce bronchial hyperreactivity in guinea pigs would inhibit tissue cholinesterase activity. Male, Hartley guinea pigs were exposed to filtered air, 0.1 ppm ozone, or 0.8 ppm ozone for 1 hr. Two hours after exposure, brain, lung, and diaphragm tissue samples were frozen for assay of cholinesterase activity. Brain cholinesterase activity was only minimally inhibited in either ozone exposure group. Both levels of ozone significantly inhibited lung cholinesterase activity compared to control animals' activity: a 17% decrease in activity in the 0.1 ppm ozone group (P less than .05) and a 16% decrease in the 0.8 ppm ozone group (P less than .05). Ozone at 0.8 ppm also inhibited activity in the diaphragm by 14% (P less than .02). To determine the degree of involvement of cholinesterase inhibition in bronchial hyperreactivity, parathion pretreated animals were challenged with histamine and the pulmonary function changes monitored. Parathion-treated animals had a peak resistance increase of 330 +/- 104% (mean +/- SE), while the control vehicle animals' increase was 165 +/- 48%. The differences were not statistically significant..." -- Gordon T, Taylor BF, Amdur MO, "Ozone inhibition of tissue cholinesterase in guinea pigs.", Arch Environ Health 1981 Nov-Dec;36(6):284-8; PMID: 7316565, UI: 82090050
6) "Some aspects of the mechanism of action of atmospheric pollutants (acetone, benzene, ammonia, formaldehyde, and ozone) on the central nervous system were studied by using methods of functional electroencephalography (analysis of the readjustment reaction to a rhythmic light stimulus, evoked potentials of the cerebral cortex, and determination of the photometrazol thresholds). Effects of the compounds were determined for the various structures of the cerebral cortex of experimental animals. The most sensitive structures were those which were first to associate in the reaction to toxic agents (the corticomedial nucleus of the amygdaloid complex and the olfactory bulb). EEG indices were observed which were indicative of an adverse effect (epileptoid activity in the most sensitive formations of the brain and a stable generalized stress rhythm in the neocortex and in the limbic ascending reticular system). During long-term action of toxic materials at low concentrations, changes were observed in the parameters of the primary and secondary responses of the visual evoked potential which were indicative of a disturbance of the cortical inhibition processes. This can be considered one effect of atmospheric pollutants at low concentrations." -- Bokina AI, Eksler ND, Semenenko AD, Merkur'yeva RV , "Investigation of the mechanism of action of atmospheric pollutants on the central nervous system and comparative evaluation of methods of study.", Environ Health Perspect, 1976 Feb;13:37-42, PMID: 1269506, UI: 76187298
|tx02||The EPA describes ozone health risk only in
terms of respiratory disease:
"OZONE: Ozone (O3) is a photochemical oxidant and the major component of smog. While O3 in the upper atmosphere is beneficial to life by shielding the earth from harmful ultraviolet radiation from the sun, high concentrations of O3 at ground level are a major health and environmental concern. O3 is not emitted directly into the air but is formed through complex chemical reactions between precursor emissions of volatile organic compounds (VOC) and oxides of nitrogen (NOx) in the presence of sunlight. These reactions are stimulated by sunlight and temperature so that peak O3 levels occur typically during the warmer times of the year. Both VOCs and NOx are emitted by transportation and industrial sources. VOCs are emitted from sources as diverse as autos, chemical manufacturing, dry cleaners, paint shops and other sources using solvents."
"The reactivity of O3 causes health problems because it damages lung tissue, reduces lung function and sensitizes the lungs to other irritants. Scientific evidence indicates that ambient levels of O3 not only affect people with impaired respiratory systems, such as asthmatics, but healthy adults and children as well. Exposure to O3 for several hours at relatively low concentrations has been found to significantly reduce lung function and induce respiratory inflammation in normal, healthy people during exercise. This decrease in lung function generally is accompanied by symptoms including chest pain, coughing, sneezing and pulmonary congestion." -- "Criteria" (http://www.epa.gov/oar/oaqps/greenbk/ page=o3co.htm)
"Acute health effects of ozone are defined as those effects induced by short-term and prolonged exposures to ozone... Acute health effects have been observed following prolonged exposures during moderate exertion at concentrations of ozone as low as 0.08ppm... Furthermore it is recognized that some individuals are unusually responsive to ozone and may experience much greater functional and symptomatic effects..." -- EPA's "Final Report: Evaluation of Air Pollutant Emissions from Subsonic Commercial Jet Aircraft", April 1999.
|Annual maximum ozone levels (1-hour average) can range from .175 to 0.249pmm in the tri-state area. See http://www.state.nj.us/dep Cholinesterase inhibition was noted in animals at 1 hour of exposure and at a dosage of 0.1ppm ozone. See above, 5). Yet NYSDEC interprets cholinesterase inhibition as pesticide poisoning even when pesticides cannot be found.|
1) "Nitrobenzene... Vapors from this compound are toxic... Symptoms of exposure may include irritation of the eyes, skin and mucous membranes, headache, signs of anoxia, including cyanosis of lips, nose, and ear lobes; eye irritation; dermatitis; anemia, nausea, vomiting, cramps, and CNS effects (tremors, twitching). Death may result from the intake of 2 ml of nitrobenzene. Other symptoms may include shock, stupor, coma; initial excitation followed by depression; unsteady gait and vertigo; dyspnea (difficult breathing); respiratory failure; myocardial depression, lowered blood pressure; altered pulse, varied skin temperature and circulatory failure; red blood cell damage, anemia and fatigue; jaundice; dark or brown red urine; black tongue; disturbed vision. Chronic exposure may result in hemolytic anemia, general body fatigue; bladder distress, peripheral neuritis and weight loss." -- Lawrence H. Keith and Mary M. Walker, Handbook of Air Toxics (1995), p484
2) "4-Nitrophenol may be toxic by... inhalation... Symptoms following exposure may include irritation of the skin, eyes, nose and throat, headache, loss of consciousness, drowsiness, nausea, cyanosis, liver and kidney damage, methemoglobinemia, central nervous system depression, dyspnea, sweating, dry throat, fever, muscular weakness, fatigue, irritability, abdominal cramps, dermatitis, corneal damage and hypothermia." -- Lawrence H. Keith and Mary M. Walker, Handbook of Air Toxics (1995), p487
4) Methyl nitrite: See MTBE, Item 3.
|tx04||The EPA describes nitrogen dioxide health
risk only in terms of respiratory disease:
NITROGEN DIOXIDE: Nitrogen dioxide (NO2) is a brownish, highly reactive gas that is present in all urban atmospheres. NO2 can irritate the lungs, cause bronchitis and pneumonia, and lower resistance to respiratory infections. Nitrogen oxides are an important precursor both to ozone (O3) and acid rain, and may affect both terrestrial and aquatic ecosystems. The major mechanism for the formation of NO2 in the atmosphere is the oxidation of the primary air pollutant nitric oxide (NO). NOx plays a major role, together with VOCs, in the atmospheric reactions that produce O3. NOx forms when fuel is burned at high temperatures. The two major emissions sources are transportation and stationary fuel combustion sources such as electric utility and industrial boilers." -- "Criteria" (http://www.epa.gov/oar/oaqps/greenbk/ page=o3co.htm)
1) Toxic effects of MTBE: www.oxybusters.org/toxic_f.htm with links to further sources. MTBE is made from methyl alcohol and ether. Incomplete combustion creates formaldehyde.
2) Regarding MTBE: "...the three symptoms documented here do not relate to any reaction with respiratory epithelium, but rather with the nervous system. This is not unexpected for MeONO, since there are analogous compounds, namely isobutyl and amyl nitrite, which are drugs of abuse due to neurological effects.(37,38) There is considerable evidence that the nervous system plays an important role in asthma; indeed, asthma could be defined as a dysfunction of the autonomic nervous system. Furthermore, there is an established effect called "neurogenic inflammation", in which certain nerve cells can incite an inflammatory reaction due to neurological stimulation. [...] "Data were presented showing large increases in visits to Philadelphia clinics for insomnia, cardiac dysrhythmia, and malaise since March 1993. These increases may be related to previously reported increases in various respiratory and inflammatory symptoms such as asthma, sinusitis, allergy, etc. It is argued from the timing, as well as from extensive anecdotal reports, that the problems are caused by an unrecognized combustion product of MTBE. Further evidence for this theory comes from experiments in Utah which demonstrated a doubling of SO4/SO2 ratio during the winter oxygenated fuel season of 1995-96. The hypothesis is proposed that MTBE combustion will produce methoxy radicals, and that these will combine with NO to produce methyl nitrite. [para] Methyl nitrite is an attractive hypothesis because it is very toxic and is known to produce some of the observed symptoms. Since analogous organic nitrites are drugs of abuse due to neurological effects, it is plausible that the nitrites act via the nervous system rather than as classical respiratory irritants. The fact that methyl nitrite is photolyzed by sunlight..." -- Peter M. Joseph, Professor, Dept. Radiology, University of Pennsylvania, Philadelphia, PA, 19104, "New Hypotheses for MTBE Combustion Products" (1999)
3) "I present new data on increases in purely neurological conditions in Philadelphia, as well as argue that the unknown MDT may be the indirect result of the production of methoxy radicals from MTBE pyrolysis. I especially emphasize the possible importance of methyl nitrite (CH3ONO) and hydro-peroxy radicals (HO2). [...] Working in a laboratory test reactor at a fixed temperature, they found a major difference between the pure MTBE and the MTBE-RFG situations. From pure MTBE combustion, they identified methanol as in reaction (3). However, when MTBE was mixed with RFG, they found no methanol but instead a roughly equimolar production of formaldehyde. [...] ...methyl nitrite is an attractive hypothesis to explain the persistent citizen complaints of symptoms from MTBE. It is known to be an extremely toxic compound. The LC50 for an acute exposure of four hours to rats is only 170 ppm; this is approximately 100 times smaller than the corresponding LC50 for benzene, for example. [...] If the ideas in this paper regarding MTBE are correct, then an obvious conclusion would be that any ether-based fuel would produce similar organic nitrites." -- Peter M. Joseph, Professor, Dept. Radiology, University of Pennsylvania, Philadelphia, PA, 19104, "New Hypotheses for MTBE Combustion Products" (1999)
4) "The Lone Star (Texas) Chapter of the Sierra Club strongly opposes all use of reformulated gasoline with MTBE, primarily for health reasons. The untold toxic story about the petroleum-based oxygenate suggests that MTBE may be more harmful than ozone." -- John C. Holmes, Dirty Air, Dirty Water: The Politics Of CarTest and Oxygenated Gasoline (1998)
5) "The preponderance of evidence argues against MTBE's ability to reduce ozone; because MTBE can increase NOx, MTBE may actually be raising the level of ozone." -- John C. Holmes, Dirty Air, Dirty Water: The Politics Of CarTest and Oxygenated Gasoline (1998)
6) The Collegium Ramazzini has found: "A major regulatory failure is that MTBE was not adequately tested for either acute or chronic toxic effects before it was added in significant quantities to gasoline. Many consumers and workers, when exposed to gasoline containing MTBE, complain of extreme headaches, vomiting, diarrhea, fever, cough, muscle aches, sleepiness, disorientation, dizziness, and skin and eye irritation. MTBE is known to cause central nervous system (CNS) depression, tremors, ataxia, labored breathing, chronic inflammation of nasal mucosa, eye irritation, and skin rashes." -- John C. Holmes, Dirty Air, Dirty Water: The Politics Of CarTest and Oxygenated Gasoline, 1998. http://members.mint.net/troberts/julian/message.html
7) The National Research Council: "The enleanment effect of oxygenated fuels presents the potential for increased NOx emissions from motor vehicles. Furthermore, much of the available data suggests that such an increase does occur. Any increase in NOx emissions could be detrimental in ozone non-attainment areas where exceedances have occurred during the period of the oxygenated fuels program" -- John C. Holmes, Dirty Air, Dirty Water: The Politics Of CarTest and Oxygenated Gasoline (1998)
8) "FTP [Federal Test Procedure] studies at 75 degrees F indicate a 26% increase in emissions of formaldehyde (Gorse et al., 1991), and 5% and 8% decreases in benzene and 1,3-butadiene emissions with the addition of 15% MTBE to the gasoline". -- John C. Holmes, Dirty Air, Dirty Water: The Politics Of CarTest and Oxygenated Gasoline (1998).
Note: Formaldehyde is a powerful CNS toxin.
9) A compilation of critical literature regarding unleaded fuel programs may be found on http://www.nexusmagazine.com//ulp1.html Catherine Simons, B.Sc., editor, "The Lies Of Unleaded Petrol"