Particulate matter in ambient air and mortality: toxicologic perspectives
Introduction
Many scientists, policy analysts, and governmental agencies in the United States and Europe believe that current concentrations of pollution-derived particulate matter (PM) in ambient (outdoor) air are deadly—causing thousands of premature deaths annually (Colburn and Johnson, 2003; Dockery et al., 1993; Dominici et al., 2003; Kjellstrom et al., 2002; Netherlands Aerosol Programme, 2002; Pope et al., 2002; Samet et al., 2000; Schwartz, 1991; U.S. EPA, 1997). Such premature deaths are thought to be due to both long-term and short-term exposure to ambient PM2.5 of any and all forms1, total concentrations of which average 10–20 μg/m3 in outdoor air in the U.S. Moreover, regulations intended to reduce these airborne concentrations by small percentages are justified largely on the basis of substantial numbers of lives “saved.” Thus, U.S. EPA (1997) predicted that compliance with the National Ambient Air Quality Standard (NAAQS) for PM2.52 will result in at least “3700 to 16,600 incidences of premature mortality avoided (corresponding to short-term and long-term mortality, respectively)” each year. Justifying the recently proposed Clear Skies Act (U.S. EPA, 2002a)—which would reduce airborne concentrations of sulfate salts and nitrate salts (forms of PM created by the atmospheric oxidation of airborne sulfur dioxide and nitrogen oxides)—EPA predicts “12,000 fewer premature deaths” each year. Similarly, EPA predicts that its recently proposed rule to reduce the sulfur content of diesel fuel and to modify non-road diesel engines (U.S. EPA, 2003a) would, by the year 2030, avert 9600 premature deaths each year due to PM2.5 of three types: diesel exhaust particulate matter (DPM), sulfate-PM, and nitrate-PM. The population-weighted reduction in ambient concentration of total PM2.5 estimated by EPA to result from this non-road engine rule, in 2030, is only 0.46 μg/m3. What are the bases for the belief that current airborne concentrations of PM, and minuscule increments thereto, are lethal?3
The primary answer is shown in Fig. 1, Fig. 2. In 1995, Pope colleagues associated two measures of ambient air pollution data (sulfate-based PM and total PM2.5) from metropolitan areas in the U.S. with mortality rates in those areas, and concluded that “increased mortality is associated with sulfate and fine particulate [PM2.5] air pollution at levels commonly found in U.S. cities.” These basic results were “replicated and validated” in an extensive re-analysis by Krewski et al. (2000) (Figs. 3A and B), and have been updated by Pope et al. (2002) with additional years of follow-up. The mainstream interpretation of these data is that long-term exposure to ambient PM2.5 shortens lives, and that no level of exposure is safe.
Numerous observational epidemiologic studies also report that daily fluctuations in the concentrations of ambient PM (in a given metropolitan area) correlate, weakly, with daily fluctuations in rates of death (in the same metropolitan area). The results of these “time-series” studies (Dominici et al., 2003; Samet et al., 2000; Schwartz, 1991; Schwartz et al., 1996; Stieb et al., 2002) are typically interpreted to mean that small increases in ambient PM (whether PM10 or PM2.5) are acutely lethal, again with no threshold in this incremental exposure–response relationship.4 Fig. 4 summarizes the relevant results of the National Morbidity, Mortality, and Air Pollution Study (NMMAPS). This study examined daily mortality as a function of daily changes in PM10 and other criteria pollutants in the 90 largest cities of the U.S., using data collected from 1987 to 1994. The result, when averaged nationally, indicates a very weak but statistically significant positive association between PM10 and mortality. Thus, the “national average lethal effect” for PM10 for 88 cities (excluding Honolulu and Anchorage) can be estimated as a 0.2% increase in total mortality at one day after a 10 μg/m3 increase in ambient PM10. However, only two cities, New York, NY and Oakland, CA, had individually positive associations that were statistically significant at a 95% confidence interval. Moreover, for 32 of the 88 cities, the effect of PM10 on mortality was either zero or negative – meaning that increases in ambient PM10 correlated with decreases in mortality (Dominici et al., 2002a, Dominici et al., 2002b). The weak and heterogeneous results overall have led analysts to raise a “concern that the associations are not reflecting the effects of the measured pollutants, but rather some factor or combination of factors, such as, for example, unmeasured air pollutants or uncontrolled features of meteorology that are correlated with the measured pollutants” (Vedal et al., 2003).
Fundamentally, if ambient PM or DPM kills people, concentrated exposures to these materials should also sicken and kill laboratory animals. In the sections following, we consider whether it does. Our focus is on recent studies testing ambient PM2.5 as a concentrated mixture, and on other studies that test airborne exposures to DPM and the associated gases in diesel engine exhaust. The toxicology of sulfates and nitrates is also discussed.
Section snippets
Acute toxicology of concentrated ambient PM2.5
To study ambient PM2.5 experimentally, investigators use devices that concentrate ambient particles in the size range 0.1–2 μm by drawing outdoor air through a series of three virtual impactors (Sioutas et al., 1995). These devices create “concentrated ambient particles” (CAP), which allow exposures that are some 30 to 50 times more concentrated than outdoor air with respect to PM2.5. Airborne gases are not concentrated by these devices.
As detailed below, toxicologic studies of CAP in laboratory
Toxicology of diesel engine exhaust particulate matter (DPM)
The toxic effects of diesel engine exhaust—both DPM and the gases and vapors that comprise the bulk of the exhaust—have been evaluated in numerous acute and chronic studies. Laboratory animals are believed to be good models for humans with regard to their responses to DPM (ILSI, 2000; U.S. EPA, 2002b), and some 17 chronic studies, involving laboratory rats, mice, hamsters, guinea pigs, cats, and monkeys, have evaluated the respiratory and systemic effects of exposure to DPM (IRIS, 2003; U.S.
Toxicology of airborne sulfates and nitrates
Airborne sulfates and nitrates have very limited toxicity (Schlesinger and Cassee, 2003). Acute exposures to airborne sulfate and nitrate salts have never succeeded in shortening the lives of any laboratory animals or other subjects: even exposures of 1,000,000–2,000,000 μg ammonium sulfate/m3 are not lethal to laboratory rats (Pepelko et al., 1980), and exposures of human subjects to less than 1000 μg/m3 of nitrate-based PM cause no symptomatic, functional, cellular, or biochemical responses (
Discussion
Observational epidemiology is an important source of information about disease and death. Like all forms of study, however, it has its strengths and weaknesses, and can rarely stand alone as a demonstration of cause and effect. The hypothesis that current ambient levels of pollution-derived PM actually increase “all-cause, cardiopulmonary, and lung cancer mortality” (Pope et al., 2002) could be correct, but has not been rigorously tested, even epidemiologically, and certainly finds no support
Acknowledgments
We benefitted from the helpful suggestions of anonymous peer reviewers, and from discussions and/or e-mail exchanges about these topics with many colleagues, including Michael Ames, Flemming Cassee, Edmund Crouch, John Godleski, Thomas Grahame, Roger McClellan, Suresh Moolgavkar, Robert Phalen, Adel Sarofim, Peter Valberg, George Wolff, and Steve Zemba. The Center for Energy and Economic Development (www.CEEDnet.org) provided a grant for partial support of the manuscript, and had no involvement
References (52)
- et al.
Pulmonary and cardiovascular effects of acute exposure to concentrated ambient particulate matter in rats
Toxicol. Lett.
(1998) - et al.
What’s wrong with the National Ambient Air Quality Standard (NAAQS) for fine particulate matter (PM 2.5)?
Regulat. Toxicol. Pharmacol.
(2002) - et al.
Diesel exhaust is not a pulmonary carcinogen in CD-1 mice exposed under conditions carcinogenic to F344 rats
Fundam. Appl. Toxicol.
(1996) Setting ambient air quality standards for particulate matter
Toxicology
(2002)- et al.
Comparative pulmonary toxicities and carcinogenicities of chronically inhaled diesel exhaust and carbon black in F344 rats
Fundam. Appl. Toxicol.
(1995) Particulate air pollution and daily mortality in Detroit
Environ. Res.
(1991)- Canadian Working Group (Canadian Environmental Protection Act/Federal/Provincial Working Group on Air Quality...
- CDC, 2002. Cigarette smoking among adults—United States, 2000. MMWR 51,...
- et al.
Urban air particulate inhalation alters pulmonary function and induces pulmonary inflammation in a rodent model of chronic bronchitis
Inhal. Toxicol.
(1999) - et al.
Age-related responses in rats to concentrated urban air particles (CAPs)
Inhal. Toxicol.
(2000)
Public health: air pollution concerns not changed by S-PLUS flaw
Science
An association between air pollution and mortality in six U.S. cities
N. Engl. J. Med.
On the use of generalized additive models in time-series studies of air pollution and health
Am. J. Epidemiol.
Airborne particulate matter and mortality: timescale effects in four US cities
Am. J. Epidemiol.
Effects of environmental aerosols on airway hyperresponsiveness in a murine model of asthma
Inhal. Toxicol.
Chronic inhalation exposure of Wistar rats and two different strains of mice to diesel engine exhaust, carbon black, and titanium dioxide
Inhal. Toxicol.
Chronic effects on the respiratory tract of hamsters, mice, and rats after long-term inhalation of high concentrations of filtered and unfiltered diesel engine emissions
J. Appl. Toxicol.
The Framingham Study: historical insight on the impact of cardiovascular risk factors in men versus women
J. Gend. Specif. Med.
Air pollution and its health impacts: the changing panorama
Med. J. Aust.
Variable pulmonary responses from exposure to concentrated ambient air particles in a rat model of bronchitis
Toxicol. Sci.
Cited by (33)
Coupling non-isothermal trickle-bed reactor with catalyst pellet models to understand the reaction and diffusion in gas oil hydrodesulfurization
2020, Chinese Journal of Chemical EngineeringCitation Excerpt :Refining of gas oil, one of the distillates of heavy crude oil, is of crucial importance to produce transportation fuels like gasoline and diesel fuel [1,2]. Due to the increasingly severe regulations for air quality over the world, the impurities in the gas oil especially for the sulfur compounds need to be removed before the refining operations to reduce SO2 emission [1,3–6]. Currently, hydrodesulfurization (HDS) is a widely used and efficient technology for the deep desulfurization [3,7].
GIS-based multielement source analysis of dustfall in Beijing: A study of 40 major and trace elements
2016, ChemosphereCitation Excerpt :In particular, its chemical components, such as major and trace elements, adversely affect human health (Zencak et al., 2007; Jeong et al., 2013). For example, some elements can increase the rates of carcinogenic and respiratory diseases, cause deterioration of lung function, and raise the need for emergency treatment (Green and Armstrong, 2003; Qian et al., 2007). Therefore, identifying the sources of airborne dust-carried elements is of vital importance to human daily life.
Spectroscopic investigation of PM<inf>2.5</inf> collected at industrial, residential and traffic sites in Taif, Saudi Arabia
2015, Journal of Aerosol ScienceA five-year study of particulate matter (PM2.5) and cerebrovascular diseases
2013, Environmental PollutionCitation Excerpt :The negative health effects caused by particle concentrations in the air depend on the pollutant (i.e., its physical-chemical composition) and its concentration (the level and time of exposure) (Upadhyay et al., 2011; Sicard et al., 2011; Schafer et al., 2011). Many epidemiologic studies have shown that airborne pollution causes significant damage to human health (Moolgavkar, 2000; Ding et al., 2011; Nicolescu et al., 2010; Green and Armstrong, 2003). The mechanism by which fine particles cause death and disease is unknown.
Determination of rare earth elements in dust deposited on tree leaves from Greater Cairo using inductively coupled plasma mass spectrometry
2013, Environmental PollutionCitation Excerpt :An extensive research on atmospheric particles in urban environments is available (Jaradat et al., 2004; Al-Rajhi et al., 1996; Rodríguez-Navarro and Sebastián, 1996; El Shazly, 1990). Quantitative elemental analysis of dust deposited on street tree leaves can generate highly specific source information of great environmental importance because some of the elements are related to the development of respiratory and carcinogenic diseases (Green and Armstrong, 2003). However, there is a lack of rare earth elements (REEs) information in the airborne dust deposited on urban tree leaves, which could provide important information on environmental pollution in urban areas.