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Exhausted by Diesel
Published by the Natural Resources Defense Council
Exhausted by Diesel
How America's Dependence on Diesel Engines Threatens Our Health


Chapter 1
DIESEL: HEAVY USE AND HIGH EXPOSURES

Nationally, trucks are moving an increasingly large portion of freight, and most heavy trucks are fueled by diesel. From 1950 to 1985 the miles driven by trucks in the United States increased by 235 percent and tons carried by trucks increased by 169 percent.(22) Trucks are now carrying a heavier load while traveling farther, increasing their overall emissions. In 1995, over half a million diesel trucks and over 20,000 diesel buses were sold in the United States, representing a doubling of annual sales since 1980.(23) A total of around six million heavy trucks, tractor-trailers, and buses were registered for use in the United States in 1995.(24) That same year, diesel vehicles nationwide consumed 37 billion gallons of diesel fuel.(25) California's 1995 diesel fuel consumption was roughly 2.1 billion gallons.(26) California and other western states have experienced higher than average growth in motor vehicle travel and have also experienced increased total vehicle emissions.(27)

Diesel exhaust is a major contributor to various types of air pollution, including smog-forming oxides of nitrogen (NOx) and fine particles (PM2.5). In 1996, diesel exhaust accounted for over one quarter of the 23,393,000 tons per year of NOx pollution produced nationally.28 In California, an estimated 26 percent of particles (PM10) from fuel combustion sources in outdoor air come from diesel engines.(11) Exhaust from heavy-duty diesel engines contains between 100 to 200 times more small particles than gasoline engine exhaust.(29)


Figure 1: 1996 Diesel Exhaust Contribution to National NOx Emissions




Source: Office of Air Quality Planning Standards. National Air Pollutant Emission Trends, 1900-1996.
United States Environmental Protection Agency. Appendix A. December 1997.



The California Air Resources Board estimates, based on a 1995 emissions inventory, that approximately 27,000 tons of diesel exhaust particles are emitted into California's air annually.(30) As Figure 2 illustrates, on-road mobile sources (heavy-duty trucks and buses, together with far smaller numbers of light-duty cars and trucks) are the major contributors, emitting 58 percent (approximately 15,680 tons per year) of total diesel exhaust particle emissions in California. Other mobile sources (mobile equipment, ships, trains, and off-road vehicles) contribute about 9,820 tons per year (37 percent). Stationary sources such as diesel generators, drilling equipment, and pumps contribute the remaining 1,400 tons per year (5 percent).



Figure 2: Sources of Diesel Particle Emissions in California, 1995



Source: California Air Resources Board, Emission Inventory 1995, Technical Support Division, October 1997.



Further, a study published by the Health Effects Institute reports that more than 98 percent of the total number of particles in diesel exhaust are less than 1 micron in size.(31) Small particles, such as those in diesel exhaust, are particularly hazardous because they penetrate deeper into the recesses of the lungs, and tend to remain in the lungs and surrounding lymph nodes rather than being cleared efficiently from the body(32) (see Focus #1 below).

The California Air Resources Board in its 1998 draft report on diesel estimated that the average diesel exhaust particle concentration in California outdoor air in 1995 was 2.2 micrograms/cubic meter (µg/m3).(33) This estimate averages levels in urban areas and rural areas, giving extra weight to the urban areas to account for the denser population. For example, average outdoor concentrations of diesel exhaust ranged from a low of 0.2 µg/m3 in the Great Basin valleys, to a high of 3.6 µg/m3 in the South Coast Air Basin.(34) Obviously people are exposed to the actual levels in their particular local environment, rather than the statewide or regional average.

The limited data available on actual measurements (rather than estimates) of diesel exposure show that in cities like Stockton, Fresno and Bakersfield -- cities with typically lower truck and bus traffic than more urban areas -- sampling from actual sites frequently measured particulate levels from motor vehicles near or above 10 µg/m3 (three times the level suggested as a statewide average).(35) A majority of the sites where the Air Resources Board measured particulate levels -- and from which it estimated the statewide average diesel exhaust levels -- were sites remote from heavy diesel traffic and from businesses that rely on diesel transport.(36)

Other data support a conclusion that the CARB exposure models underestimate actual exposures to diesel exhaust. In a study conducted in Los Angeles in the 1980s, diesel exhaust accounted for approximately 7 percent of the fine particles emitted into the air. Average ambient levels of diesel exhaust particles ranged from 1 to 3 µg/m3 in areas with low levels of air pollution. The highest average levels of diesel particles were approximately 10 µg/m3 during winter months. Other areas may have it even worse. For example, an estimated 52.8 percent of the airborne particles found in Manhattan's streets come from diesel tailpipes.(37) With total measured particles averaging roughly 50 µg/m3 on an annualized basis, that means the diesel exhaust concentration may be as high as 26.4 µg/m3 -- far higher than most American cities.

Short-term or peak exposures to diesel particulate matter, especially in urban settings such as street canyons, are usually higher than monthly or annual average concentrations.(38) For example, researchers have shown that "street canyons" between high buildings in cities can concentrate diesel exhaust levels to as high as 8.8 µg/m3 from light-duty diesel vehicles alone.(39) Because the Air Resources Board estimates that 96 percent of California's on-road diesel exhaust particles are emitted by heavy-duty vehicles,11 we can expect very high concentrations of diesel particles in urban streets where truck and bus traffic is high. In 1998, monitoring conducted by NRDC and the Coalition in such areas confirmed concentrations of diesel exhaust above 50 µg/m3 for a significant portion of the monitoring period.(40)

According to the Air Resources Board, most people spend more than 22 hours each day indoors.41 Indoor air contains diesel exhaust at levels which are affected both by outdoor concentrations and by the method of building ventilation. Modern buildings with heating, ventilation and air conditioning (HVAC) systems sometimes have particle filtration systems which can reduce diesel exhaust levels. Buildings with older or less expensive ventilation systems usually lack particle filtration. Where building inhabitants open windows and doors to ventilate the building, indoor diesel exhaust concentrations have been found to be just as high as outdoor levels.(42) If loading docks or garages where diesel trucks may idle are located near an air intake for the building, exposures may be greater than expected indoors, even in a tightly sealed building.






Focus#1: Particles -- Smaller is Worse(43)


The air we breathe contains not only gases, such as oxygen and carbon dioxide, but also numerous small particles, mostly invisible to the naked eye. These particles come from dust, fabrics, plant materials, and numerous sources of anthropogenic (human-made) pollution, such as industrial facilities and motor vehicles. All particles are not created equal. Larger particles, including the majority of naturally occurring particles, don't remain in the air for very long, and rapidly settle to the ground. Finer particles remain suspended in air for far longer, sometimes for weeks, and they can travel in winds hundreds of miles from their sources.

The larger particles don't actually get inhaled deep into the lungs. Instead they are captured by fine hairs and mucus in the nose, throat, and large airways (trachea and bronchi). These particles are then quickly cleared from the body by sneezing, coughing, or swallowing. Clearance occurs in 2-24 hours in healthy people. Small particles, less than about 10 microns in diameter (less than 1/7 the width of a human hair) are more likely to make their way past the upper airways and penetrate into the deeper portions of the lungs. Ultra-tiny particles, such as those in diesel exhaust, are even more likely to find their way into the deepest tissues of the lungs.* There the particles need to be cleared by cells of the immune system, a process which takes months or years. Some of the tiny particles are never cleared from the body, but instead accumulate in the lungs and the lymph nodes.44 Autopsy studies of people living in urban areas show significant blackening of the lungs due to accumulation of fine particles.45

The small particles which come from diesel exhaust are particularly dangerous because they are coated with a mixture of chemicals such as polycyclic aromatic hydrocarbons, nitroaromatics, benzene, dioxins, and other toxicants. The particles act like a special delivery system which places these toxic chemicals deep within our bodies. Some asthma medications use the principle of delivering a beneficial drug in a fine inhaled aerosol. Diesel exhaust is like a perversion of a drug delivery system which delivers hazardous toxicants into our lungs. The particles are retained in the body along with the toxic chemical hitchhikers which would otherwise be quickly eliminated. Thus the particles lengthen our exposures to the toxicants in diesel exhaust.





Notes:

*By far the largest deposition in the deepest airways occurs for particles between .005 and 2 micron (µ) in size. Calculation by Dale Hattis, Ph.D. based on International Commission on Radiological Protection, Human Respiratory Tract Model for Radiological Protection, ICRP Publication 66, Elsevier Science Inc., Tarrytown, NY

11. ARB, Draft Diesel Exposure Assessment, February 1998, p. A-24; American Automobile Manufacturers Association. 1997. Motor Vehicles Facts & Figures 1997. Detroit, Michigan. p. 78.
22. Gross, Marilyn, and Richard N. Feldman. National Transportation Statistics 1997. Bureau of Transportation Statistics: US Department of Transportation. December, 1996.
23. American Automobile Manufacturers Association. 1997. Motor Vehicles Facts & Figures 1997. Detroit, Michigan. p. 8.
24. Ibid. p. 35-36.
25. Davis, Stacy C. 1997. Transportation Energy Databook: Edition 17. Center for Transportation Analysis, Oakridge National Laboratory. P. 2-12.
26. California Energy Commission. 1997. California - End Use Energy by Fuel Type (Trillion BTU). www.energy.ca.gov/database/multisector/endfuel.html September 12.
27. American Automobile Manufacturers Association. 1997. Motor Vehicles Facts & Figures 1997. Detroit, Michigan. p. 40.
28. U.S. EPA Office of Air Quality Planning and Research, National Air Pollutant Emission Trends, 1900-1996, December 1997, Appendix A.
29. McClellan, R.O. Health Effects of Diesel Exhaust: A Case Study in Risk Assessment. Am Ind Hyg Assoc J., 47(1): 1-13, 1986.
30. Davis, Stacy C. 1997. Transportation Energy Databook: Edition 17. Center for Transportation Analysis, Oakridge National Laboratory. p. 2-12.
31. Bagley, Susan T., et al. 1996. Characterization of Fuel and Aftertreatment Device Effects of Diesel Emissions. Research Report Number 76. Health Effects Institute, Topsfield, Massachussetts. September.
32. Lippmann M, Environmental Toxicants: Human Exposures and Their Health Effects, Van Nostrand Reinhold, New York, 1992. P. 16-17.
33. ARB, 1998 Draft Diesel Exposure Assessment, February 1998, p. A-46.
34. ARB, 1998 Draft Diesel Exposure Assessment, February 1998, p. A-47.
35. ARB, 1994 Draft Diesel Exposure Assessment, June 1994, pp. 6-25, 6-27, and 6-30.
36. ARB, 1998 Draft Diesel Exposure Assessment, February 1998, Appendix A and B.
37. NYS DEC, State Implementation Plan for Inhalable Particulate (PM10), September 1995, p.9 and Appendix A-3.
38. GR Cass, HA Gray. 1995. Regional emissions and atmospheric concentrations of diesel engine particulate matter: Los Angeles as a case study. In: Health Effects Institute. 1995. Diesel Exhaust: A Critical Analysis of Emissions, Exposure, and Health Effects (A Special Report of the Institute's Diesel Working Group). Health Effects Institute, Cambridge, MA.
39. Volkswagen, Unregulated Motor Vehicle Exhaust Gas Components, Volkswagen AG, Research and Development, Project Coordinator: Dr. K. H Lies, 3180 Wolfsburg 1, Germany, 1989, cited in ARB, Draft Diesel Exposure Assessment, February 1998, p. A-43.
40. NRDC unpublished report, Diesel Particulate Monitoring at Vons Distribution Center, Santa Fe Springs, CA, January 1998.
41. ARB, Draft Diesel Exposure Assessment, February 1998, p. A-52.
42. Nazaroff, W. et al, Concentration and Fate of Airborne Particles in Museums, Environ. Sci. Technol., 24(1): 66-76, 1990; Ligocki, M.P. et al., Characteristics of Airborne Particles Inside Southern California Museums, Atmospheric Environment, 27A(5): 697-711, 1993.
43. This discussion is based on Lippman M, Environmental Toxicants: Human Exposures and Their Health Effects, Von Nostrand Reinhold, New York, 1992, p. 12-17.
44. 96% of the particles found in the lung parenchyma at autopsy in never-smoking adults are PM2.5. Churg A, Brauer M, Human Lung Parenchyma Retains PM2.5. Am J Respir Crit Care Med; 155(6): 2109-2111, 1997.
45. Pratt PC, Kilburn KH, Extent of pigmentation in autopsied human lungs as an indicator of particulate environmental air pollution.


Chapter 2
HUMAN HEALTH IMPACTS

The scientific evidence is clear: diesel exhaust is a complex mixture comprised of hazardous particles and vapors, some of which are known carcinogens and others probable carcinogens. Diesel exposure poses a significant and avoidable increase in human health risks. Compelling evidence from dozens of well-designed studies supports the conclusion that diesel exhaust causes cancer. In addition, fine particles from diesel exhaust aggravate respiratory illnesses such as bronchitis, emphysema and asthma and are associated with premature deaths from cardio-pulmonary disorders.9 The evidence of health effects is derived from extensive studies of human workers as well as some studies in animals, and observations of various kinds of mutagenic activity in culture systems. Based on extensive evidence, 41 constituents of diesel exhaust have been listed by the State of California as Toxic Air Contaminants, as shown in Table 1. The only reasonable conclusion one can draw from the massive scientific evidence is that exposure to diesel exhaust significantly increases human health risks.


Table 1: Substances in Diesel Exhaust Listed by Cal EPA as Toxic Air Contaminants





acetaldehyde, inorganic lead, acrolein, manganese compounds, aniline, mercury compounds, antimony compounds, methanol, arsenic, methyl ethyl ketone, benzene, naphthalene, beryllium compounds, nickel, biphenyl, 4-nitrobiphenyl, bis[2-ethylhexyl]phthalate, phenol, 1,3-butadiene, phosphorus, cadmium, chlorine, chlorobenzene, polycyclic organic matter, including polycyclic aromatic hydrocarbons (PAHs) and their derivatives, chromium compounds, propionaldehyde, cobalt compounds, selenium compounds, creosol isomers, styrene, cyanide compounds, toluene, dibutylphthalate, xylene isomers and mixtures, dioxins and dibenzofurans, o-xylenes, ethyl benzene, m-xylenes, formaldehyde, p-xylenes

Note: California Health and Safety Code section 39655 defines a "toxic air contaminant" as "an air pollutant which may cause or contribute to an increase in mortality or in serious illness, or which may pose a present or potential hazard to human health."


Diesel Exhaust and Cancer: Beyond a Reasonable Doubt

Many studies have shown that diesel exhaust causes mutations in chromosomes and damage to DNA, processes which are believed to be important in the causation of cancer.(10) There is also overwhelming evidence from studies of workers occupationally exposed to diesel exhaust revealing an increased cancer risk. Most of the over two dozen well-designed worker studies found lung cancer increases in those exposed to diesel exhaust for over a decade.(46) Similar increases in risk are found in studies that controlled for cigarette smoking, as in those where information about smoking was unavailable. A recent analysis shows that consistent findings of an approximately 30 percent increase in risk of lung cancer among diesel exposed workers is highly unlikely to be due to chance, confounders (such as smoking), or bias.(47) Unfortunately, many of these studies are limited by imprecise estimates of exposure levels, particularly for occupational exposures that occurred in the past.* The task of studying exposure to diesel exhaust is further complicated by the fact that there is no standard methodology for measurement of exposure, and there is uncertainty about which component or components of diesel exhaust may be most significant in inducing disease.

Despite these difficulties, the occupational studies consistently demonstrate that exposure to diesel exhaust for ten years or more does significantly increase the human incidence of lung cancer, and possibly of bladder cancers. U.S. EPA, Cal EPA, the National Institute of Occupational Safety and Health, and the International Agency for Research on Cancer have all consistently agreed on the relationship between diesel exhaust exposure and lung cancer.(48) Numerous independent analyses of the data by top scientists have come to the same conclusions.(49)

Many animal studies also indicate that inhalation of diesel exhaust causes cancer.(50) The studies primarily found tumors of the lung, but some also noted increased tumors at other sites.(51) However, the relevance of these studies has been questioned since the animals were exposed to very high diesel exhaust levels and the resulting inflammation and cell proliferation does not appear to occur at occupational or ambient diesel exposure levels.


Quantifying the Cancer Risk from Diesel Exhaust
Despite the extensive scientific data available, there is still uncertainty concerning exactly how potent a carcinogen diesel exhaust really is. Dale Hattis, Ph.D., a nationally recognized expert on diesel exhaust from Clark University, performed an independent calculation, based on the Cal EPA draft analysis, that sought to characterize the current uncertainty and estimate the diesel cancer risk.52 Among a million people exposed chronically to 1 microgram per cubic meter (µg/m³) of diesel exhaust, Dr. Hattis's estimated 90 percent confidence range indicates that 34 to 650 people might be expected to develop lung cancer. The average estimate is 230 per million so exposed.(53)

Unfortunately, most people are exposed to more than 1 µg/m³ of diesel exhaust every day. In fact, the California Air Resources Board estimates that the average total exposure for Californians who spend most of their time indoors is 1.54 µg/m³ of diesel exhaust, while the average outdoor air concentration of diesel exhaust in California in 1995 is 2.2 µg/m³. These estimates were arrived at by averaging levels in both rural and urban areas.54 Estimates of diesel exhaust exposure levels in urban areas range as high as 23 µg/m³. Chronic exposure at these levels would potentially result in many more lung cancer cases. We expect exposure levels in rural and urban areas throughout the country to be similar to those found in California.

The U.S. EPA suggests that a cancer risk may be "negligible" if a substance induces one excess cancer out of a million people exposed over a lifetime. Using the mean value in Dr. Hattis's uncertainty distribution for diesel exhaust potency, the expectation is that exposure to the average levels of diesel exhaust found in California-of 1.54 µ/m³ of diesel exhaust-is likely to result in an excess risk over a person's lifetime of about 350 cancers per million exposed.(55) This risk is far above U.S. EPA's "negligible risk" level. Applying these risk estimates, over a lifetime, exposure to diesel exhaust may cause 12,000 or more additional cancer cases in California alone.(56) The potential health risks nationally are staggering.

Moreover, these risk estimates are for the "average" person who breathes less than the statewide outdoor average concentration levels of diesel exhaust. People who are exposed to higher than average levels of diesel exhaust, such as urban residents, people living near major roads, distribution centers and other diesel "hot spots," and occupationally exposed individuals, would have higher risks of lung cancer from diesel. These estimates indicate the magnitude of the task before us in reducing the diesel risk and only hint at the enormous human tragedy due to diesel exposure. Lung cancer has a poor prognosis; the five-year survival rate is less than 14 percent.(57) Thus if 350 excess lung cancers are projected per million people exposed, 300 of these victims would likely die within five years.


Beyond Cancer: Other Health Impacts from Diesel Exhaust
Airborne particulate matter smaller than 10 microns in size, also called PM10, are respirable particles, meaning that they can make their way deep into our lungs. Even smaller particles, smaller than 2.5 microns in size (PM2.5), are even more likely to lodge and linger in the deepest air sacs of the lung. More than 98 percent of the total number of particles in diesel exhaust are PM2.5.31 PM10 has been regulated by the Air Resources Board since 1982 and by U.S. EPA since 1987. However, efforts to control PM10 alone will not suffice to reduce diesel exhaust concentrations to safe levels. Because measures of PM10 are mass-based, control strategies emphasize reductions of larger, heavier particles, such as those occurring from earth-moving in construction and agriculture, and are unlikely to focus on reducing the PM2.5 from diesel combustion. Recognizing the significant risks posed by tiny particles, U.S. EPA adopted new National Ambient Air Quality Standards for particles under 2.5 microns in size, which went into effect on September 16, 1997.(58)


Lung Damage
Great advances have been made in the 1990s in understanding the health effects of fine particles. Since 1987, more than two dozen community health studies have linked respirable particle concentrations below the level of the current air quality standards to reductions in lung function, and increased hospital and emergency room admissions. Long-term exposure has been related to decreases in lung function in both children(59) and adults.(60) Recurrent respiratory illnesses in children are associated with increased particulate exposures, and such a pattern of childhood illness may be a risk factor for later susceptibility to lung damage.(61)

Particulate matter exposure causes changes in lung function and inflammation of the small airways.(62) Furthermore, exposure to acidic particles may cause constriction of the bronchi and impair clearance processes which normally remove particles and infectious organisms from the airways.(63) The consequences may include aggravation of existing respiratory problems, more frequent or severe damage to tissues, or greater loss of lung function.


Infections and Asthma
Particulate exposure may increase susceptibility to bacterial or viral respiratory infections, and may increase the incidence of respiratory disease in vulnerable members of the population, including the elderly, people with chronic pulmonary diseases, and people with immune system dysfunction.64 In the presence of pre-existing heart or lung disease, respiratory exacerbations induced by air pollutants may lead to death.

Recent research indicates that diesel exhaust may increase the frequency and severity of asthma exacerbations and may lead to inflammation of the airways that can cause or worsen asthma.(65) This information is quite new and extremely important in light of the fact that the incidence of asthma is on the rise, increasing nearly 40 percent among U.S. children between 1981 and 1988.(66) There are an estimated 10.3 million people in the United States with asthma.(67) The death rate from asthma has increased by 118 percent from 1980 to 1993.68 Asthma occurs far more frequently in African-American and Latino children;(69) indeed, African-American children are four times more likely to die from asthma than white children.(70) Children of Latino mothers have a rate of asthma two-and-a-half times higher than whites and more than one-and-a-half times higher than African-Americans.


Premature Death
In December 1993, Harvard researchers published the results of a sixteen-year-long community health study that tracked the health of 8,000 adults in six U.S. cities with differing levels of air pollution. After adjusting for age and smoking, researchers found that residents of the most polluted city had a 26 percent higher mortality rate than those living in the least polluted city.(71) This translated into a one- to two-year shorter lifespan for residents of the most polluted cities.(72) Another major study corroborated these findings. The study correlated American Cancer Society data on the health of 1.2 million adults with air pollution data in 151 U.S. metropolitan areas. The study found that people living in the most polluted area had a 17 percent greater risk of mortality than people living in the least polluted city.(73)

A number of prestigious international panels, including a British Committee on the Medical Effects of Air Pollutants and a Committee of the Health Council of the Netherlands, have concluded that there is a cause-and-effect relationship between particulate pollution and premature death.(74) Such a conclusion is warranted based on the consistency of the association in different studies and situations, the dose-response relationship, and the biological plausibility.

In 1996, U.S. EPA published a risk assessment focusing on Southeast Los Angeles County. The U.S. EPA estimates over 3,000 excess deaths occur annually due to levels of particle pollution above the current federal standards in this particular area of Los Angeles alone.(75) The federal agency estimated more than 52,000 episodes of respiratory symptoms each year-including about 1,000 hospital admissions-from the particle levels observed in 1995 in Southeast Los Angeles. U.S. EPA estimates more than 40,000 particle-related health effects (including 300 to 700 deaths) would occur in Los Angeles even if the area brought pollution down to the current federal particle standards.

NRDC performed a study entitled Breath Taking: Premature Mortality Due to Particulate Air Pollution in 239 American Cities, which was based on the risk relationships identified in the American Cancer Society and Harvard studies. In this study, released in May, 1996, NRDC applied the known risk relationships to a variety of urban areas where particle levels had been adequately monitored. We found that nationally over 50,000 premature deaths per year may be attributable to the existing levels of particles in the air.


Other Non-Cancer Impacts
Many of the individual constituents of diesel exhaust are known to produce harmful effects. Benzene, for example, is known to cause disorders of the blood and the blood-forming tissues.(76) Formaldehyde and acetaldehyde can cause irritation of the eyes, nose, and throat.(77) Toluene, lead, cadmium, and mercury are known to cause birth defects and other reproductive problems.(78) Dioxins are toxic to the immune system, interfere with hormone function, and are toxic to reproduction.79 These non-cancer effects of diesel exhaust components can also be serious and damaging. The extent to which these effects may occur from current exposure levels is unclear.






Focus #2: The "Great" Diesel Invention


In 1892, Rudolf Diesel invented the diesel "compression ignition" engine. A diesel engine operates by introducing air and fuel into the cylinder and compressing it to a point where the temperature is high enough to ignite the fuel without the necessity of a spark plug. This type of compression ignition system produces a significant amount of power and is fuel-efficient and durable.

The use of diesel engines spread throughout the United States and Europe after 1900, ultimately replacing steam-powered engines. Diesel engines operate on fairly inexpensive fuel oils and can withstand heavy loads at relatively low speeds.80 Conventional gasoline engines were unable to perform as well under heavy load conditions and required more expensive fuel. Due to the heavy weight of the early engines, diesel was used almost exclusively for heavy-duty power generation in marine transportation and to a limited extent in industrial establishments.

The market for diesels broadened due to technological advances in the late 1930s that raised the operating speeds and decreased the engine weight, allowing the use of diesel engines for on-road applications. General Motors developed a two-cycle diesel engine that was suitable for railroad use, and was later adapted to drive trucks and buses. This was the beginning of a dependence on diesel for movement of freight and passengers, which has lasted through this century.





Notes:

*This limitation often means that the studies may underestimate human risk, as when studies designate all workers with any diesel exposure at all to a category of "exposed" workers, despite the fact that many had exposures little if any greater than the average person whose workplace involves no exposure to diesel.

9. Shprentz D, "Breathtaking: Premature Mortality Due to Particulate Air Pollution in 239 American Cities", NRDC, New York, May 1996, pp. 13-32.
10. Mauderly JL. Diesel Exhaust in Lippman M. (ed.) Environmental Toxicants: human exposures and their health effects. Van Nostrand Reinhold, New York, 1992
31. Bagley, Susan T., et al. 1996. Characterization of Fuel and Aftertreatment Device Effects of Diesel Emissions. Research Report Number 76. Health Effects Institute, Topsfield, Massachussetts. September.
46. See eg. Garshick et al. A Case-Control Study of Lung Cancer and Diesel Exhaust Exposure in Railroad Workers. Am Rev Resp Dis 135:1242-1248, 1987; Garshick et al. A Retrospective Cohort Study of Lung Cancer and Diesel Exhaust Exposure in Railroad Workers, Am Rev Resp Dis 137:820-825, 1988; Swanson GM et al. Diversity in the Association Between Occupation and Lung Cancer Among Black and White Men. Canc Epi Biomark Prev 2:313-320, 1993; Steenland K et al. Exposure to Diesel Exhaust in the Trucking Industry and Possible Relationships with Lung Cancer. Am J Ind Med 21:887-890, 1992
47. Bhatia R, Lopipero P, Smith AH, Diesel Exhaust Exposure and Lung Cancer. Epidemiology, 9:84-91, 1998.
48. Dawson, et. al., Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant, Part B: Health Risk Assessment for Diesel Exhaust. Public and Scientific Review Panel Review Draft [hereinafter referred to as OEHHA, 1998 Diesel Health Risk Assessment, February 1998, pp. 1-8 - 1-9.
49. Steenland K, Lung Cancer and Diesel Exhaust: a Review. Am J Ind Med, 10:177-189, 1986; Bhatia R, Lopipero P, Smith AH, Diesel Exhaust Exposure and Lung Cancer. Epidemiology, 9:84-91, 1998; Pepelko and Peirano, 1983, Health Effects of Exposure to Diesel Engine Emissions, J. Amer. Coll. Toxicol. 2: 253-306.
50. The National Institute for Occupational Safety and Health (NIOSH) states, "Exposure to diesel exhaust has been shown to produce benign and malignant tumors in rats and mice. Therefore, NIOSH recommends that whole diesel exhaust be regarded as a potential occupational carcinogen in conformance with the OSHA Cancer Policy (29 CFR 1990)." NIOSH Current Intelligence Bulletin 50, "Carcinogenic Effects of Exposure to Diesel Exhaust," U.S. Department of Health and Human Services, August 1988, p. 26.
51. Brightwell et al., 1986, Neoplastic and Functional Changes in Rodents After Chronic Inhalation of Engine Exhaust Emissions, in Ishinishi et al., eds., Carcinogenic and Mutagenic Effects of Diesel Engine Exhaust, Elsevier: Amsterdam, pp. 471-485; Brightwell et al, 1989, Tumors of the Respiratory Tract in Rats and Hamsters Following Chronic Inhalations of Engine Exhaust Emissions, J. Appl. Toxicol. 9: 23-31; Ishinishi et al., 1986, Long-term Inhalation Studies on Effects of Exhaust from Heavy and Light Duty Diesel Engines on F344 Rats, in Ishinishi et al., eds., Carcinogenicity and Mutagencity of Diesel Engine Exhaust, Elsevier: Amsterdam, pp. 329-348.
52. Cal EPA calculated a draft risk range in their report. According to their calculation, the unit risk range is from 1.3 cancers per 10,000 to 1.5 per 1000 (with exposure at 1 mg/m3). This means that if a million people are exposed chronically to 1 microgram of diesel particulate per cubic meter (mg/m3), between 130 and 1500 individuals may get lung cancer from that exposure. OEHHA, 1998 Diesel Health Risk Assessment, February 1998, p. 1-17.
53. Hattis D, A Probability-Tree Interpretation of the California EPA's Analysis of the Cancer Risk from Diesel Particulates. Submitted to the ARB on March 19, 1998.
54. This number is a third lower than the estimated 1990 average ambient diesel exposure level of 3.2 micrograms per cubic meter. Average ambient level in California are anticipated by ARB to decline to 1.8 microgram per cubic meter in the year 2000. Cal EPA and ARB, Draft Diesel Executive Summary, February 1998, p. ES-12.
55. This excess risk estimate is obtained by multiplying the 1.54 micrograms per cubic meter exposure estimate by the 230 in a million risk estimate derived by Dr. Hattis.
56. The 12,000 cancer case estimate is derived by multiplying the excess cancer risk estimate of 350 cancers per million people exposed by California's population of 34 million people. Using Cal EPA's draft risk range, the calculation would generate an estimate of 4,420 - 51,000 lung cancers in California. Calculated using OEHHA, 1998 Diesel Health Risk Assessment, February 1998, p. 1-17 Ries LAG, et al. (ed.) SEER Cancer Statistics Review, 1973-1994, National Cancer Institute, NIH Publication Number 97-2789, Bethesda, MD, 1997. p. 288.
57. Ries LAG, et al. (ed.) SEER Cancer Statistics Review, 1973-1994, National Cancer Institute, NIH Publication Number 97-2789, Bethesda, MD, 1997. p. 288.
58. U.S. EPA, National Ambient Air Quality Standards for Particulate Matter; Final Rule, Federal Register: July 18, 1997 (Volume 62, Number 138) p. 38651-38701.
59. Brunekreef B, Air pollution from truck traffic and lung function in children living near motorways., Epidemiology; 8(3):298-303, 1997.
60. Ackermann-Liebrich U, Lung function and long term exposure to air pollutants in Switzerland: Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) Team., Am J Respir Crit Care Med;155(1):122-129, 1997
61. Glezen WP, Antecedents of chronic and recurrent lung disease. Childhood respiratory trouble. Am Rev Respir Dis; 140(4):873-874, 1989; Gold DR, Acute lower respiratory illness in childhood as a predictor of lung function and chronic respiratory symptoms. Am Rev Respir Dis;140(4):877-884, 1989.
62. Li XY, Gilmour PS, et al. In vivo and in vitro proinflammatory effects of particulate air pollution (PM10). Environ Health Perspect 1997 Sep;105 Suppl 5:1279-1283. Bascom R, et al. Health Effects of Outdoor Air Pollution. Am J Respir Crit Care Med, 153:3-50, 1996. p. 33-36.
63. Bascom R, et al. Health Effects of Outdoor Air Pollution. Am J Respir Crit Care Med, 153:3-50, 1996. p. 33-36.
64. Delfino RJ, Murphy-Moulton AM. Effects of air pollution on emergency room visits for respiratory illnesses in Montreal, Quebec. Am J Respir Crit Care Med 1997 Feb;155(2):568-576; Schwartz J. Air pollution and hospital admissions for the elderly in Detroit, Michigan. Am J Respir Crit Care Med 1994 Sep;150(3):648-655; Schwartz J. What are people dying of on high air pollution days? Environ Res 1994 Jan;64(1):26-35.
65. See Miyamoto T., Epidemiology of pollution-induced airway disease in Japan, Allergy; 52(38 Suppl):30-34, 1997; Albright, JF and RA Goldstein, Airborne pollutants and the immune system, Otolaryngol Head Neck Surg; 114(2):232-8, 1996; Sagai M, A Furuyama and T Ichinose, Biological effects of diesel exhaust particles (DEP). III. Pathogenesis of asthma like symptoms in mice, Free Radic Biol Med;21(2):199-209, 1996.
66. Weitzman Met al., Recent Trends in the Prevalence and Severity of Childhood Asthma, JAMA; 268:2673-2677, 1992.
67. Morbidity and Mortality Weekly Report, 41(39), Oct 2, 1992, pp. 733-735.
68. Morbidity and Mortality Weekly Report, 45(17), May 3, 1996, pp. 350-1.
69. Weitzman M et al., Racial, Social and Environmental Risks for Childhood Asthma, AJDC, 144: 1189-94, November 1990; Schwartz J et al., Predictions of Asthma and Persistent Wheeze in a National Sample of Children in the United States, Am. Rev. Respir. Dis., 142:555-562, 1990; Cunningham J et al., Race, Asthma and Persistent Wheeze in Philadelphia School Children, Am. J. of Pub. Health, 86:1406-1409, October 1996.
70. Weitzman M et al., Racial, Social and Environmental Risks for Childhood Asthma, AJDC, 144: 1189-94, November 1990; Schwartz J et al., Predictions of Asthma and Persistent Wheeze in a National Sample of Children in the United States, Am. Rev. Respir. Dis., 142:555-562, 1990; Cunningham J et al., Race, Asthma and Persistent Wheeze in Philadelphia School Children, Am. J. of Pub. Health, 86:1406-1409, October 1996.
71. Dockery, DW, et. al., An Association Between Air Pollution and Mortality in Six U.S. Cities, New Eng J Med; 329(24): 1753-9, 1993.
72. Harvard School of Public Health Press Release, "Fine Particle Air Standards Not Sufficient to Protect Public Health," December 6, 1993.
73. Pope, CA, et. al., Particulate Pollution as a Predictor of Mortality in a Prospective Study of U.S. Adults, Am J Resp Crit Care Med; 151:669-74, 1995.
74. Particulate Air Pollution Including Assessment of an Integrated Criteria Document. Report of a Committee of the Health Council of the Netherlands to the Minister for Health, Welfare, and Sports, Vol 14, The Hague, October 1995; U.K. Department of the Environment, Expert Panel on Air Quality Standards: Particles, London: HMSO, 1995.
75. U.S. EPA, Office of Air Quality Planning and Standards, "Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment of Scientific and Technical Information," April 1996, table VI-6, page VI-13a.
76. Rosenstock L, and Cullen M (eds.), Textbook of Clinical Occupational and Environmental Medicine, WB Saunders Co., Philadelphia, 1994. p. 778.
77. Ibid, p. 109.
78. Paul M (ed.), Occupational and Environmental Reproductive Hazards: A Guide for Clinicians, Williams and Wilkins, Philadelphia, 1993. pp. 234-248, 273-4.
79. Birnbaum L, Developmental Effects of Dioxins and Related Endocrine Disrupting Chemicals, Toxicol Lett, 82/83: 743-750, 1995.
80. Williamson, HF and RL Andreano. The American Petroleum Industry: The Age of Energy 1899-1959. Northwestern University Press. Evanston, Il. 1963.


Chapter 3
WHO IS MOST AT RISK?
Most of the human studies on the health risks of diesel exhaust looked exclusively at healthy, adult men. To extrapolate from male worker studies to the general population may not adequately protect women, children, and the elderly. Furthermore, worker studies provide little information about health effects in people with chronic illnesses or depressed immune systems. We do know something about the susceptibility of some of these groups from research on the health effects of fine particle pollution.


Children
Children represent the largest subgroup of the population susceptible to the effects of air pollution.(81) Compared with adults, children spend more time outdoors, particularly at midday and during the afternoons when air quality is poorest, and engage in more vigorous physical activity.(82) As a result, children average a higher breathing rate, and receive greater relative doses of any pollutants in the air. At rest, an infant's metabolic rate and air intake is about twice that of an adult.(83) A forty-five pound child inhales over 9,000 liters of air per day.(84)

Children also have narrower airways and their lungs are still developing. Irritation caused by air pollutants that would produce only a slight response in an adult can result in potentially significant obstruction in the airways of a young child.(85) Furthermore, children have more frequent respiratory and other illnesses, perhaps due to incompletely developed immune protection.

Elevated levels of particulate pollution have been linked with an increased incidence of respiratory symptoms in children.(86) In an ongoing study comparing air pollution in six U.S. cities and the respiratory health of individuals living in those cities, the frequencies of coughs, bronchitis, and lower respiratory illnesses in preadolescent children were significantly associated with increased levels of acidic fine particles.(87) Illness and symptom rates were twice as high in the community with the highest air pollution concentrations compared with the community with the lowest concentrations. Rates of chronic cough, bronchitis, and chest illness during one school year were positively associated with particulate pollution.(88) One study suggested that though all children are at risk for increased respiratory symptoms due to particulate pollution, children with preexisting respiratory conditions (wheezing, asthma) are at greater risk.(89) In a diary study of 625 Swiss children between birth and five years of age, respiratory symptoms were associated with particulate concentrations, while the duration of symptoms was associated with levels of nitrogen oxide. Symptoms included coughing, upper respiratory episodes, and breathing difficulty.(90)

Hospital admission for respiratory illness is strongly associated with particulate air pollution and the association is stronger for children than adults. During months with peak particulate pollution levels, average hospital admissions for respiratory illness in children nearly tripled, whereas for adults comparable hospital admissions increased by 44 percent.(91) Several studies have demonstrated that children living near major roadways have poorer lung function than children living in cleaner areas.(92) The same studies showed that girls were more affected than boys. Lung function in both sexes was correlated with estimated levels of diesel exhaust measured in the schools.(93)


The Elderly
Substantial scientific evidence suggests that the elderly and those with pre-existing heart and lung disease are at greatest risk of premature mortality due to particulate air pollution. Several important studies have shown that those over 65 years of age are at greater risk of requiring emergency room services on days with higher particulate pollution.94 In addition, the relationship between particle exposure and death was about three times greater in the elderly.95 Because cardio-pulmonary disease is more common in older people, and cardiovascular and pulmonary function declines with age, the elderly are likely to have heightened sensitivity to particle exposure. To the extent that the elderly and chronically ill are slower to remove particles from deep lung tissues, they are likely to have greater risk from diesel exhaust exposure, because the time needed to clear small particles from the lungs appears to increase the risk of tumor development.96


Exposures Add Up Over a Lifetime
Cancers induced by diesel exhaust involve a latency period of a number of years between damaging exposure and development of cancer: risk increases with increasing duration of exposure.97 Exposure to diesel exhaust for nearly every human begins at birth and lasts throughout our lifetime. Neither animal, nor worker studies on diesel exhaust adequately capture this feature of the general public's exposure. Most of the animal studies involving diesel exhaust inhalation begin exposure with "adolescent" rats.98 For these reasons, direct extrapolation from traditional animal exposure studies as well as extrapolation from worker studies are likely to underestimate the risk to the public, whose exposure to ambient diesel exhaust begins in early childhood and lasts for many decades.






Focus #3: "Clean" Diesel is Still Dirty


Some industry advocates argue that 1996 model year and later diesel engines using new diesel fuel are "clean" diesel and are not a health threat. However, diesel engines-new and old-continue to pose cancer threats. In fact, recent studies suggest that, despite a substantial reduction in the total weight of particulate matter, the total number of particles in emissions from the more advanced 1991-model diesel engine is 15 to 35 times greater than the number of particles from the 1988 engine when both engines were operated without emission control devices. Thus, newer diesel may be emitting smaller particles but not fewer particles.99 Furthermore, these smaller particles are more likely to penetrate deeper in the lungs and to be trapped and retained. "Clean" diesel may not decrease risk from diesel exhaust exposure.

In addition, even the "cleaner," post-1996 diesel engines emit more smog forming nitrogen oxides and particulates than comparable alternative fueled engines. Diesel engines certified in 1998 emitted 60 percent more smog forming nitrogen oxides and 50 percent more particulates than similarly sized natural gas engines.100

A recent study comparing emissions from a new diesel engine running on older diesel fuel, and on a reformulated diesel fuel (required in California since 1993), revealed that the newer fuel only slightly reduces emissions of nitrogen oxides and particulates, and that more than 95 percent of the particle emissions are very fine (less than 1 micron in size). Dioxins were detected in diesel emissions, both with the older and newer fuel. Finally, levels of toxics such as benzene, toluene, 1,3-butadiene, and polycyclic aromatic hydrocarbons (PAHs) were essentially unchanged by use of the newer diesel fuel.101







Notes:

81. Centers for Disease Control, Populations at Risk from Air Pollution - United States, 1991, Morbidity and Mortality Weekly Report, vol. 42, no. 16, April 30, 1993.
82. California Air Resources Board, Study of Children's Activity Patterns: Final Report, September 1991, pp. 66a-67.
83. International Programme on Chemical Safety, Principles for Evaluating Health Risks From Chemicals During Infancy and Early Childhood: The Need for a Special Approach, Environmental Health Criteria 59,World Health Organization, 1986.
84. Cal EPA, Technical Support Document for Exposure Assessment and Stochastic Analysis - Public Review Draft, December 12, 1996.
85. Lipsett, "The Hazards of Air Pollution to Children." Environmental Medicine, S. Brooks et al., eds., St. Louis: Mosby, 1995.
86. Timonen KL, Pekkanen J. Air pollution and respiratory health among children with asthmatic or cough symptoms.Am J Respir Crit Care Med 1997 Aug;156(2 Pt 1):546-552.
87. Ware, J. H. et al., "Effects of Ambient Sulfur Oxides and Suspended Particles on Respiratory Health of Preadolescent Children," Am. Rev. Resp. Dis., vol. 133, 1986, pp. 834-842.
88. Dockery, D. et al., "Effects of Inhalable Particles on Respiratory Health of Children," Am. Rev. Respir. Dis., vol. 139, 1989, pp. 587-594; Schwartz, J. et al., "Acute Effects of Summer Air Pollution on Respiratory Symptom Reporting in Children," Am. J. Respir. Crit. Care Med., vol. 150, 1994, pp. 1234-42.
89. Pope and Dockery, "Acute Health Effects of PM10 Pollution on Symptomatic and Asymptomatic Children. Am. Rev. Respir Dis., vol.145, 1992, pp. 1123-1128.
90. Braun-Fahrlander, C. et al., "Air Pollution and Respiratory Symptoms in Preschool Children," Am Rev. Respir. Dis., vol. 145, 1992, pp. 42-47.
91. Pope, A., "Respiratory Disease Associated with Community Air Pollution and a Steel Mill, Utah Valley," Am. J. of Pub. Health, vol. 79, May 1989, pp. 623-628.
92. Pekkanen J, et al. Effects of ultrafine and fine particles in urban air on peak expiratory flow among children with asthmatic symptoms. Environ Res 1997;74(1):24-33.
93. Brunekreef B, et al. Air pollution from truck traffic and lung function in children living near motorways., Epidemiology; 8(3):298-303, 1997; Oosterlee A, et al. Chronic respiratory symptoms in children and adults living along streets with high traffic density. Occup Environ Med 1996 Apr;53(4):241-247.
94. Schwartz J. Air pollution and hospital admissions for the elderly in Detroit, Michigan. Am J Respir Crit Care Med 1994 Sep;150(3):648-655; Schwartz J, Short term fluctuations in air pollution and hospital admissions of the elderly for respiratory disease. Thorax 1995 May;50(5):531-538.
95. Schwartz J, Dockery DW, Increased mortality in Philadelphia associated with daily air pollution concentrations. Am Rev Respir Dis;145(3):600-604, 1992.
96. Bovornkitti S, Limlomwongse L, Environment and the aging lung. Respirology 1997 Sep;2(3):169-172.
97. Steenland, et al., Case-control study of lung cancer and truck driving in the Teamster Union, Am J Pub Hlth; 80: 670-674, 1990; Bhatia R, et al. Diesel Exhaust Exposure and Lung Cancer. Epidem 9:84-91, 1998.
98. In most of the studies summarized, the age of the rodents at the beginning of exposure ranged from 8 to 17 weeks. Because two years (104 weeks) is the average lifespan of a rat, a 17-week old rat is essentially comparable in age to a human adolescent.
99. Bagley, Susan T., Kirby J. Baumgard, Linda D. Gratz, John H. Johnson, and David G. Leddy. Characterization of Fuel and Aftertreatment Device Effects on Diesel Emissions; Health Effects Institute; Research Report Number 76; September 1996; p. i.
100. California Air Resources Board. 1998 Model Year Heavy-Duty On-Road Engine Certification Listing Update. April 9, 1998. El Monte, California. Pp. 1-2.
101. Arey, J, et. al., Evaluation of Factors That Affect Diesel Exhaust Toxicity (Draft Final Report). Submitted to the California Air Resources Board, January 2, 1998.








































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