Jet Pollution The True Effects on Humans and Sedona


 

Typical Flights mid-day

Dumping Lead, Jet Exhaust and dispersing raw Jet Fuel one mile from the Sedona runway to lighten jet aircraft take off weights.sedona airport jet pollution

Sign Our Petition - Close Sedona AirportAIRPORTS, AIR POLLUTION, AND CONTEMPORANEOUS HEALTH
Wolfram Schlenker- NATIONAL BUREAU OF ECONOMIC RESEARCH
W. Reed Walker
Working Paper 17684
http://www.nber.org/papers/w17684 

December, 2011 -  (PDF – 2.32 MB)

Jet fuel is a complex chemical mixture and only 200 of its 2000+  chemicals have been formally identified.  All jet aircraft use Halon, a deadly, ozone-depleting chemical in their engines.  JP-8′s high flash point means it  evaporates more slowly and remains on the skin for a longer period of time.  Its performance-enhancing additives have also been found in published Air  Force studies to enhance the ability of fuel hydrocarbon chemicals to cross through skin and enter the bloodstream. Due to the fuel and combustion process air craft porduce PAH’s (polycyclic aromatic hydrocarbons).  These PAH’s are known to be extremely carinogenic even in minute quantities.   Sedona homeowners living near Red Rock Crossing under the jet flight path have high levels of carcinogenic, jet fuel petro chemicals in their blood. The highest number of jet events recorded in Sedona was during one weekend in May, 2007; one hundred and fifty jets landed in Sedona and took off in one weekend. 

Nitrogen dioxide (NO2) is a brownish gas that is produced primarily as a byproduct of high-temperature combustion. Sedona has some of the highest levels of atmospheric NO2 in the country despite being a rural area. On a scale of 1-10 with 10 being the best, Sedona rates 1.4 for NO2.

The primary locus of NO2 toxicity is the lung. Exposure to NO2 induces pulmonary injury in a number of ways. NO2 is converted to NO, HNO3 (nitric acid), and HNO2 (nitrous acid) in the distal airways, where it exerts direct toxic effects on type I pneumocytes and ciliated airway cells. NO2 initiates free radical generation in the terminal bronchioles, resulting in protein oxidation, lipid peroxidation, and subsequent cell membrane damage. NO2 also alters macrophage and immune function, causing impaired resistance to infection.

Methemoglobinemia may also be induced with the inhalation of NO2 because NO is absorbed through the lungs and binds to hemoglobin, forming nitrosyl hemoglobin. NO has an affinity for hemoglobin that is several thousand times greater than that of carbon monoxide. This complex is readily oxidized to methemoglobin. Methemoglobinemia serves to compound the preexisting hypoxemia by causing a leftward shift of the oxygen-hemoglobin dissociation curve and further impairing tissue oxygenation. NO is synthesized endogenously from L -arginine by numerous cell types and has multiple physiologic roles.

Benzene has hematological and immunological/lymphoreticular effects and is classified in EPA Group A (human carcinogen).

Aromatic EC5-9 Fraction: Indicator Compounds. This fraction consists of benzene, toluene, ethylbenzene and the xylenes (the BTEXs).

Health effects that are common to the BTEXs are neurological effects.

For the aliphatic EC>8-EC16 fraction, the database includes a number of studies of petroleum products whose major constituents fall within the EC range of this fraction. These included dearomatized petroleum streams and fuels (JP-5, JP-7, JP-8, kerosene). Studies of the dearomatized petroleum streams are largely unpublished, include oral studies in animals, and have been reviewed by the TPHCWG (1997c). The critical effects were judged to be hepatic. MRLs were available for intermediate and chronic inhalation exposure to JP-7 and JP-5 and JP-8; these are based on hepatic effects.

Children and fetuses may be at increased risk to benzene toxicity because their hematopoietic cell populations are expanding and dividing cells are at a greater risk than quiescent cells.

Based on studies of benzo(a)pyrene in animals, women may be at increased risk of reproductive dysfunction following exposure to high levels of PAHs.

Individuals with impaired pulmonary function may be more susceptible to the respiratory irritant effects of the volatile petroleum hydrocarbons (primarily the aromatic EC5-EC9 and aliphatic EC5-EC9 fractions).

Acute inhalation or aspiration of ingested aliphatic or aromatic petroleum hydrocarbons of low viscosity can lead to pulmonary irritation and hydrocarbon pneumonia, an acute hemorrhagic necrotizing disease. To counteract secondary bacterial infections and pulmonary edema, antibiotics and oxygen therapy are often applied when indicated by symptoms in particular patients (Klaassen 1996; Snodgrass 1997).

Specific aliphatic and aromatic hydrocarbons found in petroleum products are known to be-metabolized via cytochrome P-450 pathways to reactive metabolic intermediates that are thought to cause non-cancer and cancer effects from chronic exposure (e.g., peripheral neuropathy from 2,5-hexadione, a metabolite of hexane, and cancer effects from various intermediary metabolites of benzene and carcinogenic PAHs). There are no known clinical methods to interfere with these mechanisms of action.

Jet exhaust interacts with sunlight forming high levels of pollution

 

On a hot, sunny day in Sedona, Arizona, we suffer under dozens of jets taking off and landing inside our town.  As the jets power out off the mesa above my home I can smell the jet exhaust.  Thirty minutes later my blood pressure is rising, my heart is racing, I have muscles spasms and my liver starts to ache, sometimes it feels like a sharp stabbing pain. After living in this location for three years my health has declined drastically, I no longer go for walks or bike rides, there really is not point living here because the airport has destroyed my life.  I am luckier than some of my neighbors who have already died from liver cancer at age 21 and pancreatic cancer. 

Jet engine exhaust, through a chemical reaction catalyzed by sunlight, is transformed into ultrafine particle pollution at a rate much higher than previously thought, according to a new study. “It sort of blew our minds,” said Allen Robinson, lead researcher of the Carnegie Mellon University team that published the research in the journal “Atmospheric Chemistry and Physics.” The researchers determined that jet engine exhaust, in the presence of sunlight, is transformed into dangerous ultrafine pollution particles at a rate 35 times greater than the engine originally emitted and 10 times greater than computer models.  “Models that do not account for this processing will likely under predict the contribution of aircraft emissions to local and regional pollution,” the research team concluded.  Living in a small, tight valley with a dozen jets per day taking off over the airspace creates a deadly brew for local citizens to breath.   Imagine a hot, no wind day, as the jet exhaust falls to the ground in our basin area with no where to evacuate to?  I expect this study will generate increased attention to the role of airports as a significant source of local air pollution, especially within a few kilometers of the airport.  Previous research has measured jet emissions but never took into account the action of sunlight on the emissions. 

The entire study is available here as a pdf download. JETFUELTOXICITY11-4135-2011

 The Sedona Airport’s General Manager, Mac McCall, who formerly ran snow removal at Chicago O’Hare International Airport claimed in an article to the Red Rock News recently, “that jet fuel is not classified as hazardous by the EPA.” The Material Safety Data Sheet on jet fuel is available here as a pdf download: msdsjetfuel   I smell the jet exhaust in my yard and home, I live with the windows closed and can’t enjoy my property. I thought living in Sedona was supposed to be heaven?   That is why I paid a lot of money to live here, no one told me I would be breathing jet exhaust, raw jet fuel dumped over my home, lead and listening to an unending barrage of noise inside my home.  

Just how toxic is jet exhaust if you can actually smell it? odorstudyThresholdsversusdangerlevels  This jet exhaust falls down to the bottom of the valley and collects in the washes and canyons where people and animals breathe it.  The other night I heard coyotes crying after many jets had flown over us and they sounded sick, it was not a normal cry.

In anticipation of the impending outcry over jets taking off and landing inside in Sedona, this article was posted to the Sedona Airport website titled:

The Truth about Jets, Aircraft Noise & Air Pollution, Sedona Airport
and the Future of Sedona as a Tourist Destinaton  http://web.archive.org/web/20080908082217/http://sedonaairport.org/index15.html

 Somehow this article fails to address the impact of jets and the pollution levels in Sedona and instead talks about how the airport will get quieter.  There is no truth in this article and it has been subsequently removed from the airport’s website.

Jet Fuel is a toxic, chemical soup, all deadly on their own, more deadly when combined and exposed to sunlight.

A list of some of the chemicals found in the air around airports:

Freon 11, Freon 12, Methyl Bromide, Dichloromethane, cis-l,2-Dichloroethylene, 1,1,1-Trichloroethane, Carbon Tetrachloride, Benzene, Trichloroethylene, Toluene, Tetrachloroethene, Ethylbenzene, m,p-Xylene, o-Xylene, Styrene, 1,3,5-Trimethylbenzene, 1,2,4-Trimethylbenzene, o-Dichlorobenzene, Formaldehyde, Acetaldehyde, Acrolein, Acetone, Propinaldehyde, Crotonaldehyde, Isobutylaldehyde, Methyl Ethyl Ketone, Benzaldehyde, Veraldehyde, Hexanaldehyde, Ethyl Alcohol, Acetone, Isopropyl Alcohol, Methyl Ethyl Ketone, Butane, Isopentane, Pentane, Hexane, Butyl Alcohol, Methyl Isobutyl Ketone, n,n-Dimethyl Acetamide, Dimethyl Disulfide, m-Cresol, 4-Ethyl Toulene, n-Heptaldehyde, Octanal, 1,4-Dioxane, Methyl Phenyl Ketone, Vinyl Acetate, Heptane, Phenol, Octane , Anthracene, Dimethylnapthalene(isomers), Flouranthene, 1-methylnaphthalene, 2-methylnaphthalene, Naphthalene, Phenanthrene, Pyrene , Benzo(a)pyrene, 1-nitropyrene, 1,8-dinitropyrene , 1,3-Butadiene , sulfites, nitrites, nitrogen oxide, nitrogen monoxide, nitrogen dioxide, nitrogen trioxide, nitric acid, sulfur oxides, sulfur dioxide, sulfuric acid, urea, ammonia, carbon monoxide, ozone, particulate matter (PM10, PM2.5) and finally this compound; 3-nitrobenzanthrone.*

“According to chemist Hitomi Suzuki of Kyoto University, the last compound, 3-nitrobenzanthrone, may be the most hazardous compound ever to be tested for carcinogenicity, scoring substantially higher in the well-known Ames test than its nearest rival, 1,8-dinitropyrene listed above. (New Scientist, 25 October 1997.) Many of the other compounds indicated above are also considered to be carcinogens. Adding to the direct effect of any single chemical listed above, the probabilities of synergistic effects must be considered. The toxic brew of compounds is also subject to reactions caused by atmospheric and solar effects, resulting in new, consequent compounds.” (Source: Areco)

The EPA found in a study performed in 1993 that 99% of the cancer cases near Midway Airport were caused by aircraft emissions.

The following health effects occur with prolonged exposure to these chemicals:

 

ASPHYXIATION 
ASTHMA
BRAIN CANCER
CANCER
CONJUNCTIVE IRRITATION
COUGHING
DELAYED HYPERSENSITIVITY
DISTORTED PERCEPTIONS
DROWSINESS
DYSPNEA HEADACHE
EEG CHANGES
EMPHYSEMA
FLUSHING
HALLUCINATIONS
HEART DISEASE                                                                                                                                                                            HIGH BLOOD PRESSURE
HODGKIN’S DISEASE
KIDNEY DAMAGE
LACRIMATION
LIVER DAMAGE

LUNG DISEASE
LUNG STRUCTURE DAMAGE
LUNG TIGHTNESS
LYMPHOMA
MENTAL DEPRESSION
MULTIPLE ORGAN INVOLVEMENT
MUSCLE WEAKNESS
MUTATIONS
MYELOID LEUKEMIA
NASAL EFFECTS
NAUSEA, VOMITING
PULSE RATE DECREASE OR INCREASE
PULMONARY IRRITATION
RESPIRATORY SYSTEM DAMAGE
SKIN AND EYE IRRITATION
SYSTEMIC IRRITATION
TUMORS
WHEEZING


Benzene

Chronic exposure to benzene, a constituent of jet fuel is a known carcinogen, can lead to bone marrow damage, leukemia and depression of the immune system (e.g. Rinsky et al., 1987). A good understanding of source distributions and atmospheric transformations of BTEX compounds is therefore needed to investigate their impact on urban and regional atmospheric chemistry and human health. (BTEX–Benzene/Toluene/Ethylbenzene/m, p, o-Xylenes)

Toxicological profiles for constituents of jet fuel:

Benzene http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=40&tid=14

Toluene  http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=161&tid=29

Hexane  http://www.atsdr.cdc.gov/toxfaqs/tf.asp?id=392&tid=68

Naphthalene, 1-Methylnapthalene, 2-Methylnapthalen http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=240&tid=43

Affected Organ Systems: Hematological (Blood Forming), Hepatic (Liver), Neurological (Nervous System), Ocular (Eyes), Respiratory (From the Nose to the Lungs)
Cancer Effects: Reasonably Anticipated to be Human Carcinogens

Toxicological Profile for Jet Fuels JP-4 and JP-7 http://www.atsdr.cdc.gov/ToxProfiles/tp76.pdf 

http://www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=768&tid=149

 

Ozone

 Ozone (O3) plays a key role in atmospheric oxidation processes and photochemical air pollution. Although there is no general consensus about the critical levels for human health, environment agencies concur that 8-hourly levels in excess
of 50–60 ppbv and a 1-hourly average of 80 ppbv constitute health hazards (Ayres et al., 2006). Whereas high peak values are of particular importance for human health, permanent exposure to lower levels is also problematical (Bell et al., 2006). Furthermore, ambient mixing ratios of about 40 ppbv for extended periods of several months cause crop loss and damage to natural ecosystems (Emberson et al., 2003). Ozone is a secondary pollutant, formed during the oxidation of reactive carbon compounds and catalyzed by nitrogen oxides (NOx=NO+NO2), driven by ultraviolet sunlight.

 Deicing Chemicals at the airport

The chemicals used to deice aircraft are ethylene glycol and propylene glycol, both deadly substances in small quantities. Ethylene glycol causes central nervous depression and kidney and liver damage; propylene glycol, when used by the airports with anti-corrosion chemicals, is just as toxic.  The lethal dose in adults is 1.4 ml or 3.3 fl. No studies have been done on its effects on humans.  Each winter large amounts of fish and wildlife are poisoned to death by aircraft deicing chemicals.  Additional pollutants, including fuels and other toxic substances, are also washed off the planes during deicing procedures.  In Sedona these de-icing agents can be washed off the mesa into Carol Canyon which connects to Oak Creek.

Airports do virtually no reporting of the large volumes of de-icing agents (which are comprised of several toxic chemicals), fuel spills, oils, greases and other pollutants which regularly flow from airports and are shed from flying planes into nearby streams, lakes and aquifers. In addition to chemicals formed in exhaust, de-icing fluids are significant pollutants in surprisingly large amounts, not only during winter weather, but also in unexpected times such as summer, when some aircraft types are sprayed to prevent formation of ice on upper wing surfaces in cold, high-altitude operation.  De-icing fluids represent hazards to water tables, streams and the wildlife who depend on those water sources. As they are shed from planes, the fluids are corrosive to paint. How much of this hazardous chemical load is finding its way into your drinking water sources?  The Sedona Airport has a flight path over the riparian area of Oak Creek and Red Rock Crossing, Oak Creek flows into the federally protected Wild and Scenic Verde River.  Pollution is shed over an enormous area surrounding a busy airport, diminishing, of course, in a radius of at least 24 miles and from an elevation of about 3500 feet to the ground.  Of foremost concern to those living and working even as far as many miles from an airport or under aircraft flight paths are the hazardous and toxic air emissions.

The ultimate goal of any clean air policy is to develop strategies to reduce the risk of adverse effects on human health and the environment as a whole caused by ambient air pollution. With the existence of very susceptible populations and the ability to detect effects even if they are infrequent, we may be confronted with situations when the concept of thresholds is no longer useful in setting standards to protect public health. The principle of eliminating adverse effects with an adequate margin of safety even for the most susceptible groups may not be realistic but what we can do is remove the source of this pollution out of the middle of our community.

 

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