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Chapter 2


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 polycyclic organic matter, including
chlorine polycyclic aromatic hydrocarbons (PAHs)
chlorobenzene 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 children59 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.


* 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.

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