Air Pollution Linked to Higher Heart Attack Risk

BETHESDA, Maryland, March 23, 2009 (ENS) – Scientific evidence is mounting that connects an increase in particulate air pollution with an increase in heart attacks and deaths. Research from the relatively new field of environmental cardiology includes a 16-year-long Harvard University study of six U.S. cities that found fine particulate pollution, even at levels below the federal health standard, can shorten lifespans by two years. A majority of these earlier deaths were due to heart disease.

A study in Salt Lake City found that when a steel mill shut down for a period of months, there was a four to six percent drop in mortality in neighboring areas. The mortality rose to previous levels when the steel mill reopened.

A study of 250 metropolitan areas around the world found that a spike in air pollution is followed by a spike in heart attacks.

The people who seem to be most susceptible to environmental pollutants are those who are already vulnerable, including the elderly and people with coronary artery disease. There is some evidence that diabetics, women and people who are obese may be at greater risk.

Cardiovascular disease is the leading cause of death in the industrialized world. In the United States, it kills approximately one million people per year, accounting for over 40 percent of all deaths.

To examine this emerging research in greater detail, Aruni Bhatnagar of the University of Louisville and Robert Brook of the University of Michigan have organized a symposium called Environmental Factors in Heart Disease, to take place April 21 at an Experimental Biology conference in New Orleans. The 120-year-old American Physiological Society is one of the sponsors of the annual conference.

Dr. Bhatnagar, from the Division of Cardiology, Department of Medicine, University of Louisville, will speak on environmental aldehydes exposure and cardiovascular disease. His research shows that the risk of having a heart attack increases in parallel with time spent in traffic the previous day.

Joggers in San Francisco traffic inhale fine particles into their lungs. (Photo by Sharad Gupta)

In animal experiments, Dr. Bhatnagar has found that aldehydes – a toxic class of chemicals found in most forms of smoke, including cigarette smoke and car exhaust – increase blood cholesterol levels and activate enzymes that cause plaque in the blood vessels to rupture. When plaques rupture, it can cause a blood clot, which may block an artery and lead to a heart attack.

Aldehydes are present in high concentrations in smog and are generated during combustion of any kind of organic material coal, wood, paper, or cotton. “Direct exposure to high concentrations of unsaturated aldehydes is cardiotoxic,” writes Dr. Bhatnagar in a 2004 editorial in the “American Journal of Physiology.”

The evidence strongly supports the view that “exposure to environmental toxins significantly increases CVD [cardiovascular disease] risk, which contributes to the overall health burden of air pollution,” he writes.

Dr. Brook, an associate professor in the Department of Internal Medicine at the University of Michigan will speak on environmental pollution and hypertension. He has found that fine particles and ultra-fine particles entering the lungs can make their way into the blood vessels. Within 15 minutes of inhaling pollutants, there is a very rapid increase in blood pressure, he says.

Blood vessels react to the pollutants by producing an inflammatory response to attack the foreign particles. However, the inflammatory response itself can set off a complex physiological reaction that is harmful to the blood vessels, Dr. Brook says.

If you live in an area where pollution levels may be high, you can take steps to reduce the risk of air pollution, Dr. Brook advises. “During times when air quality is unhealthy, exercise indoors, because indoor air is filtered. If you exercise outdoors, particularly if you’re at risk for heart disease, do it when pollutants are at lower levels. Avoid peak traffic times,” he says.

Other speakers at the symposium include Araujo Jesus of the University of California, Los Angeles, who will describe the the effects of ultrafine air pollution of blood vessels, and Murray Mittleman of the Harvard School of Public Health will speak on the connection between air pollution and strokes.

Copyright Environment News Service (ENS) 2009. All rights reserved.

Sierra magazine | Idling cars are an economic and an environmental disaster

Harming the environment is no idle threat | Idling cars are an economic and an environmental disaster

Sierra magazine, March/April 2009 issue, p. 14

How many times have you sat in line for several minutes at a bank or fast-food drive-through and wondered how much gas you were wasting? Perhaps you even thought of the possible environmental damage the idling cars was causing?

Idling is costly, in several ways: “Every hour you idle, you waste up to 0.7 gallons of gas (depending on your engine type) going nowhere. So it pays to turn your engine off if you’re going to be still for more than 30 seconds.

“In a given year, U.S. cars burn some 1.4 billion gallons of fuel just idling. Not to mention idling trucks, which waste another 1.5 billion gallons. Collectively, we emit about 58 million tons of carbon dioxide while we’re essentially doing nothing.”

Whether one goes to McDonald’s or Wendy’s or Burger King or another fast-food outlet, it takes on average close to 2 1/2 minutes to get your order and be on your way. McDonald’s consumers alone account for burning more than 7.25 million gallons of gas waiting in line!

The entire fast-food industry? We waste about 50 million gallons of gas!

All of that is bad enough. But we’re spreading our lazy, wastrel habits to the rest of the world which bodes nothing but ill for the future. “…McDonald’s plans to open 25 drive-throughs in China, following KFC’s lead. KFC installed its first drive-through there in 2002 and is working on 100 more. If China and India, which is also jumping aboard the drive-through bandwagon, get up to speed, they can idle away a truly staggering figure: 30 billion gallons of gas. Every year.”

Every breath you take — air quality in Europe

Every breath you take — air quality in Europe
Courtesy of European Environment Agency (EEA)
Originally published Mar. 2009

The characters in this story are fictional. However the data are real. The story is set on 27 July 2008 when an air quality warning was issued in Brussels. Anna is 37 years old and lives in the centre of Brussels. She and her young son Johan are planning a trip outside the busy city. Anna suffers from asthma and her doctor has warned of the dangers of air pollution, especially on hot summer days.

Anna has heard about the London fogs of the 1950s that killed 2 000 people in one week. She has childhood memories of evening news bulletins showing dead fish and dying trees as ‘ acid rain’ first came to popular attention in the 1970s.

Motherhood and a recent asthma attack have quite rightly brought air pollution back to mind. The fact is that emissions of many air pollutants have fallen substantially across Europe since Anna’s childhood. The air she and Johan breathe is much improved compared to the past, and air policy is one of the great success stories of the EU’s environmental efforts. In particular, EU policy has dramatically cut emissions of sulphur, the main component of ‘acid rain’.

In contrast, nitrogen — also a major component of ‘acid rain’ — has not been dealt with to the same extent and so continues to cause major problems. A significant proportion of Europe’s urban population still live in cities where EU air quality limits, protecting human health, are regularly exceeded. Each year, many more people die prematurely from air pollution in Europe than die in traffic accidents.

The European goal of achieving levels of air quality that do not damage people’s health or the environment has still not been reached. EEA analysis suggests that 15 of the 27 EU Member States will miss one or more of their legally binding 2010 targets to reduce harmful air pollutants.

Particulate matter and ozone
Two pollutants, fine particulate matter and ground-level ozone, are now generally recognised as the most significant in terms of health impacts. Long-term and peak exposure can lead to a variety of health effects, ranging from minor irritation of the respiratory system to premature death.

Particulate matter, a term used to describe a variety of tiny particles from sources such as vehicle exhausts and domestic stoves, affect the lungs. Exposure can harm people of all ages, but people with existing heart and respiratory problems are particularly at risk.

According to the latest EEA data, since 1997 up to 50 % of Europe’s urban population may have been exposed to concentrations of particulate matter above the EU limit set to protect human health. As much as 61 % of the urban population may have been exposed to levels of ozone that exceed the EU target. It has been estimated that PM2.5 (fine particulate matter) in air has reduced statistical life expectancy in the EU by more than eight months.

The EEA has noted that while emissions of these two key air pollutants have dropped since 1997, measured concentrations in the air we breathe have remained largely the same. As yet, we don’t know why there has not been a drop in ambient concentrations but it could be a combination of several factors: increased temperatures caused by climate change could be affecting air quality; perhaps we are on the receiving end of pollution from other continents or natural emissions of ozone forming substances released from trees, for example.

A day in the country
Anna is planning a day in the country with Johan. Before leaving her apartment she logs onto IRCEL, a government web service providing a host of regular information on air quality around Belgium. Using maps, Anna can scan readings and forecasts for particulate matter, ozone, nitrogen dioxide, sulphur dioxide among many others. The data are relayed to the web from monitoring stations around the country.

Improvements in monitoring and availability of information on air pollution are another of the success stories of recent years. For instance, local data on ozone levels are now passed onto the EEA ‘Ozone web’ (1) service that provides an overview of the situation across Europe.

Anna scrolls across a map of Belgium, zooming in on a monitoring station in the centre of Brussels, less than two kilometres from her home.

The reading, taken minutes earlier, shows high levels of ozone in Brussels. Indeed the website forecasts that levels will exceed EU target values later that day and again the following day ( Figure 1).

Anna leaves her apartment building and makes for the nearest Metro station, a 10 minute walk away. Out on the street, the full impact of the city’s traffic problems are easy to see — and smell.

Exhaust emissions from cars in the centre of Brussels, and all major cities, irritate the respiratory tract and eyes and lungs. Anna and Johan turn into their local train station and head for the countryside.

Soon, Anna and Johan are entering a national park just outside Brussels. A sign tells them that they are visiting a Natura 2000 site — one part of a European-wide ecological network, set up to secure natural habitats and to maintain the range of plant and animal life.

Figure 1: The location and levels of ozone at air quality monitoring stations in Brussels on Sunday 27 July 2008

But what’s that smell? A tractor is spraying liquid manure onto a field not far away. This is irritating, Anna thinks, but it’s also part of real country life which is shown in a rather more romantic way in Johan’s picture books.

The pungent smell is caused by as many as 40 different chemical substances emitted from the manure. Ammonia (NH3), a volatile nitrogen compound, is one of them. In very high concentrations NH3 is caustic and can damage the respiratory tract. However, the levels here are not dangerous for human health. Anna can breathe a sigh of relief, albeit a stinky one.
Nitrogen is an essential nutrient in nature. Reactive nitrogen forms are actually used by our bodies to produce proteins. However, excess nitrogen can lead to severe environmental and health problems.

‘Acid rain’ forms when high levels of sulphur and nitrogen oxides are present in the air. One of the great success stories of air pollution policy over the last decades has been the massive reduction in emissions of sulphur dioxide. The 32 EEA member countries reduced sulphur emissions by 70 % between 1990 and 2006. Nitrogen, on the other hand, has not been dealt with as successfully.

With sulphur emissions declining, nitrogen is now the principal acidifying component in our air. Agriculture and transport are the main sources of nitrogen pollution. Agriculture is responsible for more than 90 % of ammonia (NH3) emissions alone.

Suddenly Johan, who has been walking unsteadily loses his balance and falls into a clump of stinging nettles. Having picked him up and brushed him off, Anna notices nettles everywhere. She has vivid memories of them as a child in a neighbour’s garden. Then the nettles grew around a compost heap that was also used as a dump for poultry dung. That was no coincidence — the stinging plant is an indicator of high nitrogen concentrations in soils.

‘Eutrophication’ is the most likely cause of this explosion of stinging nettles surrounding Johan. It occurs when too many chemical nutrients (such as N) are available to an ecosystem either on land or in water. In water, excessive plant growth and subsequent decay occur, which in turn leads to further effects including oxygen depletion. Fish and other animals and plants ultimately suffocate as the oxygen supply is used up.

The abundance of the nettles here suggests that despite being a protected habitat, the Natura 2000 site is not immune from airborne nitrogen deposits. The fence protecting the area offers no defence — in fact building a greenhouse around the area would be the only way to protect it totally from airborne substances.

Looking ahead
Because air pollution pays no regard to national boundaries the problem needs to be tackled internationally. The United Nations Convention on Long-range Transboundary Air Pollution (LRTAP Convention) agreed in 1979, has been signed by 51 countries and forms the basis of the international fight to tackle air pollution.

In parallel, the EU has developed polices limiting the total emissions of each Member State, setting legally binding limits. The ‘ National Emissions Ceiling Directive’ (NECD) is a key EU policy. It sets ‘ceilings’ or limits for four pollutants: sulphur dioxide (SO2), nitrogen oxides (NOx), non-methane volatile organic compounds (NMVOCs), and ammonia (NH3). Member States should meet these ceilings by 2010.

The EEA considers that further emission cuts are still needed in order to properly protect environment and health. An EEA analysis of the most recent NECD data (2) indicates that 15 Member States expect to miss at least one of their four ceilings; with 13 anticipating missing ceilings for the 2 nitrogen-containing pollutants NOX and NH3 (3).

In 2009 the European Commission plans to publish a proposal to revise the current NECD, including stricter ceilings for the year 2020. National limits are likely to be proposed for fine particulate matter (PM2.5) for the first time.

The NECD is mirrored by air quality directives setting limit and target values for major air pollutants. A new one called the Cleaner Air For Europe (CAFE) Directive was adopted in April 2008. For the first time it sets legally binding limit values for PM2.5 concentrations (fine particulate matter), to be attained in 2015. The European Commission is also taking countries to task for having missed earlier limits and, where sufficient measures have not been outlined to improve performance, has begun infringement proceedings.

Later that evening Anna, while watching the evening news, sees that an air quality warning has been issued by the government in response to high ozone levels beyond the EU threshold. The warning advises people with breathing problems to take precautions such as avoiding strenuous exercise while the ozone levels remain high.

Climate change mitigation efforts will improve air quality

In January 2008, the European Commission proposed a Climate and Energy package to:

  • reduce greenhouse gas emissions by 20 % by 2020;
  • increase the share of renewable energy by 20 % by 2020;
  • improve energy efficiency by 20 % by 2020.

The efforts required to meet these targets will also cut air pollution in Europe. For example, improvements in energy efficiency and increased use of renewable energy will both lead to reduced amounts of fossil fuel combustion — a key source of air pollution. These positive side effects are referred to as the ‘co-benefits’ of climate change policy.

It has been estimated that the above package will cut the cost of meeting EU air pollution targets by EUR 8.5 billion per year. The savings to the European health services could be as much as six times that figure.

Long-Term Ozone Exposure and Mortality | The New England Journal of Medicine | Study

Long-Term Ozone Exposure and Mortality

Michael Jerrett, Ph.D., Richard T. Burnett, Ph.D., C. Arden Pope, III, Ph.D., Kazuhiko Ito, Ph.D., George Thurston, Sc.D., Daniel Krewski, Ph.D., Yuanli Shi, M.D., Eugenia Calle, Ph.D., and Michael Thun, M.D.

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Long-Term Ozone Exposure and Mortality

–><!– Michael Jerrett, Ph.D., Richard T. Burnett, Ph.D., C. Arden Pope, III, Ph.D., Kazuhiko Ito, Ph.D., George Thurston, Sc.D., Daniel Krewski, Ph.D., Yuanli Shi, M.D., Eugenia Calle, Ph.D., and Michael Thun, M.D. –>ABSTRACT

Background Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution–related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.

Methods Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are ≤2.5 µm in aerodynamic diameter [PM2.5]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.

Results In single-pollutant models, increased concentrations of either PM2.5 or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM2.5 was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.

Conclusions In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM2.5 was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

Studies conducted over the past 15 years have provided substantial evidence that long-term exposure to air pollution is a risk factor for cardiopulmonary disease and death.1,2,3,4,5 Recent reviews of this literature suggest that fine particulate matter (particles that are ≤2.5 µm in aerodynamic diameter [PM2.5]) has a primary role in these adverse health effects.6,7 The particulate-matter component of air pollution includes complex mixtures of metals, black carbon, sulfates, nitrates, and other direct and indirect byproducts of incomplete combustion and high-temperature industrial processes.

Ozone is a single, well-defined pollutant, yet the effect of exposure to ozone on air pollution–related mortality remains inconclusive. Several studies have evaluated this issue, but they have been short-term studies,8,9,10 have failed to show a statistically significant effect,1,3 or have been based on limited mortality data.11 Recent reviews by the Environmental Protection Agency (EPA)12 and the National Research Council13 have questioned the overall consistency of the available data correlating exposure to ozone and mortality. Similar conclusions about the evidence base for the long-term effects of ozone on mortality were drawn by a panel of experts in the United Kingdom.14

Nonetheless, previous studies have suggested that a measurable effect of ozone may exist, particularly with respect to the risk of death from cardiopulmonary causes. In one of the larger studies, ozone was significantly associated with death from cardiopulmonary causes15 but not with death from ischemic heart disease. However, the estimated effect of ozone on the risk of death from cardiopulmonary causes in this study was attenuated when PM2.5 was added to the analysis in copollutant models. On the basis of suggested effects of ozone on the risk of death from cardiopulmonary causes (which includes death from respiratory causes) but an absence of evidence for effects of ozone on the risk of death from ischemic heart disease, we hypothesized that ozone might have a primary effect on the risk of death from respiratory causes.


Health, Mortality, and Confounding Data

Our study used data from the American Cancer Society Cancer Prevention Study II (CPS II) cohort.16 The CPS II cohort consists of more than 1.2 million participants who were enrolled by American Cancer Society volunteers between September 1982 and February 1983 in all 50 states, the District of Columbia, and Puerto Rico. Enrollment was restricted to persons who were at least 30 years of age living in households with at least one person 45 years of age or older. After providing written informed consent, the participants completed a confidential questionnaire that included questions on demographic characteristics, smoking history, alcohol use, diet, and education.17 Deaths were ascertained until August 1988 by personal inquiries of family members by the volunteers and thereafter by linkage with the National Death Index. Through 1995, death certificates were obtained and coded for cause of death. Beginning in 1996, codes for cause of death were provided by the National Death Index.18

The study population for our analysis included only those participants in CPS II who resided in U.S. metropolitan statistical areas within the 48 contiguous states or the District of Columbia (according to their address at the time of enrollment) and for whom data were available from at least one pollution monitor within their metropolitan area. The study was approved by the Ottawa Hospital Research Ethics Board, Canada.

Data on “ecologic” risk factors at the level of the metropolitan area representing social variables (educational level, percentage of homes with air conditioning, percentage of the population who were nonwhite), economic variables (household income, unemployment, income disparity), access to medical care (number of physicians and hospital beds per capita), and meteorologic variables were obtained from the 1980 U.S. Census and other secondary sources (see the Supplementary Appendix, available with the full text of this article at These ecologic risk factors, as well as the individual risk factors collected in the CPS II questionnaire, were assessed as potential confounders of the effects of ozone.3,5,19,20

Estimates of Exposure to Air Pollution

Ozone data were obtained from 1977 (5 years before the identification of the CPS II cohort) through 2000 for all air-pollution monitors in the study metropolitan areas from the EPA’s Aerometric Information Retrieval System. Ozone data at each monitoring site were collected on an hourly basis, and the daily maximum value for the site was determined. All available daily maximum values for the monitoring site were averaged over each quarter year. The quarterly average values were reported for each monitor only when at least 75% of daily observations for that quarter were available.

The averages of the second (April through June) and third (July through September) quarters were calculated for each monitor if both quarterly averages were available. The period from April through September was selected because ozone concentrations tend to be elevated during the warmer seasons and because fewer data were available for the cooler seasons.

The average of the second and third quarterly averages for each year was then computed for all the monitors within each metropolitan area to form a single annual time series of air-pollution measurements for each metropolitan area for the period from 1977 to 2000. In addition, a summary measure of long-term exposure to ambient warm-season ozone was defined as the average of annual time-series measurements during the entire period from 1977 to 2000. Individual measures of exposure to ozone were then defined by assigning the average for the metropolitan area to each cohort member residing in that area.

Data on exposure to PM2.5 were also obtained from the Aerometric Information Retrieval System database for the 2-year period from 1999 to 2000 (data on PM2.5 were not available before 1999 for most metropolitan areas).5 The average concentrations of PM2.5 were included in our analyses to distinguish the effect of particulates from that of ozone on outcomes.

Statistical Analysis

Standard and multilevel random-effects Cox proportional-hazard models were used to assess the risk of death in relation to exposures to pollution. The subjects were matched according to age (in years), sex, and race. A total of 20 variables with 44 terms were used to control for individual characteristics that might confound or modify the association between air pollution and death. These variables, which were considered to be of potential importance on the basis of previous studies, included individual risk factors for which data had been collected in the CPS II questionnaire. Seven ecologic covariates obtained from the 1980 U.S. Census (median household income, the proportion of persons living in households with an income below 125% of the poverty line, the percentage of persons over the age of 16 years who were unemployed, the percentage of adults with less than a high-school [12th-grade] education, the percentage of homes with air conditioning, the Gini coefficient of income inequality [ranging from 0 to 1, with 0 indicating an equal distribution of income and 1 indicating that one person has all the income and everyone else has no income20], and the percentage of persons who were white) were also included. These variables were included at two levels: as the average for the metropolitan statistical area and as the difference between the average for the ZIP Code of residence and the average for the metropolitan statistical area. Additional sensitivity analyses were undertaken for ecologic variables that were available for only a subgroup of the 96 metropolitan statistical areas (see the Supplementary Appendix). Models were estimated for either ozone or PM2.5. In addition, models with both PM2.5 and ozone were estimated.

In additional analyses, our basic Cox models were modified by incorporating an adjustment for community-level random effects, which allowed us to take into account residual variation in mortality among communities.21 The baseline hazard function was modulated by a community-specific random variable representing the residual risk of death for subjects in that community after individual and ecologic risk factors had been controlled for (see the Supplementary Appendix).

A formal analysis was conducted to assess whether a threshold existed for the association between exposure to ozone and the risk of death (see the Supplementary Appendix). A standard threshold model was postulated in which there was no association between exposure to ozone and the risk of death below a specified threshold concentration and a linear association (on the logarithmic scale of the proportional-hazards model) above the threshold.

The question of whether specific time windows were associated with the health effects was investigated by subdividing the follow-up interval into four periods (1982 to 1988, 1989 to 1992, 1993 to 1996, and 1997 to 2000). Exposures were matched for each of these periods and also tested for a 10-year average on the basis of the 5-year follow-up period and the 5 years before the follow-up period (see the Supplementary Appendix).


The analytic cohort included 448,850 subjects residing in 96 metropolitan statistical areas (Figure 1). In 1980, the populations of these 96 areas ranged from 94,436 to 8,295,900. Data were available on the concentration of ambient ozone from all 96 areas and on the concentration of PM2.5 from 86 areas. The average number of air-pollution monitors per metropolitan area was 11 (range, 1 to 57), and more than 80% of the areas had 6 or more monitors.

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Figure 1. Ozone Concentrations in the 96 Metropolitan Statistical Areas in Which Members of the American Cancer Society Cohort Resided in 1982.

The average exposures were estimated from 1 to 57 monitoring sites within each metropolitan area from April 1 to September 30 for the years 1977 through 2000.

The average ozone concentration for each metropolitan area during the interval from 1977 to 2000 ranged from 33.3 ppb to 104.0 ppb (Figure 1). The highest regional concentrations were in Southern California and the lowest in the Pacific Northwest and parts of the Great Plains. Moderately elevated concentrations were present in many areas of the East, Midwest, South, and Southwest.

The baseline characteristics of the study population, overall and as a function of exposure to ozone, are presented in Table 1. The mean age of the cohort was 56.6 years, 43.4% were men, 93.7% were white, 22.4% were current smokers, and 30.5% were former smokers. On the basis of estimates from 1980 Census data, 62.3% of homes had air conditioning at the time of initial data collection.

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Table 1. Baseline Characteristics of the Study Population in the Entire Cohort and According to Exposure to Ozone.

During the 18-year follow-up period (from initial CPS II data collection in 1982 through the end of follow-up in 2000), there were 118,777 deaths in the study cohort (Table 2). Of these, 58,775 were from cardiopulmonary causes, including 48,884 from cardiovascular causes (of which 27,642 were due to ischemic heart disease) and 9891 from respiratory causes.

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Table 2. Number of Deaths in the Entire Cohort and According to Exposure to Ozone.

In the single-pollutant models, exposure to ozone was not associated with the overall risk of death (relative risk, 1.001; 95% confidence interval [CI], 0.996 to 1.007) (Table 3). However, it was significantly correlated with an increase in the risk of death from cardiopulmonary causes. A 10-ppb increment in exposure to ozone elevated the relative risk of death from the following causes: cardiopulmonary causes (relative risk, 1.014; 95% CI, 1.007 to 1.022), cardiovascular causes (relative risk, 1.011; 95% CI, 1.003 to 1.023), ischemic heart disease (relative risk, 1.015; 95% CI, 1.003 to 1.026), and respiratory causes (relative risk, 1.029; 95% CI, 1.010 to 1.048).

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Table 3. Relative Risk of Death Attributable to a 10-ppb Change in the Ambient Ozone Concentration.

Inclusion of the concentration of PM2.5 measured in 1999 and 2000 as a copollutant (Table 3) attenuated the association with exposure to ozone for all the end points except death from respiratory causes, for which a significant correlation persisted (relative risk, 1.040; 95% CI, 1.013 to 1.067). The concentrations of ozone and PM2.5 were positively correlated (r=0.64 at the subject level and r=0.56 at the metropolitan-area level), resulting in unstable risk estimates for both pollutants. The concentration of PM2.5 remained significantly associated with death from cardiopulmonary causes, cardiovascular causes, and ischemic heart disease when ozone was included in the model. The association of ozone concentrations with death from respiratory causes remained significant after adjustment for PM2.5.

Risk estimates for ozone-related death from respiratory causes were insensitive to the use of a random-effects survival model allowing for spatial clustering within the metropolitan area and state of residence (Table 1S in the Supplementary Appendix). The association between increased ozone concentrations and increased risk of death from respiratory causes was also insensitive to adjustment for several ecologic variables considered individually (Table 2S in the Supplementary Appendix).

Subgroup analyses showed that environmental temperature and region of the country, but not sex, age at enrollment, body-mass index, education, or concentration of PM2.5, significantly modified the effects of ozone on the risk of death from respiratory causes (Table 4).

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Table 4. Relative Risk of Death from Respiratory Causes Attributable to a 10-ppb Change in the Ambient Ozone Concentration, Stratified According to Selected Risk Factors.

Figure 2 illustrates the shape of the relation between exposure to ozone and death from respiratory causes. There was limited evidence that a threshold model specification improved model fit as compared with a nonthreshold linear model (P=0.06) (Table 3S in the Supplementary Appendix).

Figure 2
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Figure 2. Exposure–Response Curve for the Relation between Exposure to Ozone and the Risk of Death from Respiratory Causes.

The curve is based on a natural spline with 2 df estimated from the residual relative risk of death within a metropolitan statistical area (MSA) according to a random-effects survival model. The dashed lines indicate the 95% confidence interval of fit, and the hash marks indicate the ozone levels of each of the 96 MSAs.

Because air-pollution data from 1977 to 2000 were averaged, exposure values for persons who died during this period are based partly on data that were obtained after death had occurred. Further investigation by dividing this interval into specific time windows of exposure revealed no significant difference between the effects of earlier and later time windows within the period of follow-up. Allowing for a 10-year period of exposure to ozone (5 years of follow-up and 5 years before the follow-up period) did not appreciably alter the risk estimates (Table 4S in the Supplementary Appendix). Thus, when exposure values were matched more closely to the follow-up period and when exposure values were based on data obtained before the deaths, there was little change in the results.


Our principal finding is that ozone and PM2.5 contributed independently to increased annual mortality rates in this large, U.S. cohort study in analyses that controlled for many individual and ecologic risk factors. In two-pollutant models that included ozone and PM2.5, ozone was significantly associated only with death from respiratory causes.

For every 10-ppb increase in exposure to ozone, we observed an increase in the risk of death from respiratory causes of about 2.9% in single-pollutant models and 4% in two-pollutant models. Although this increase may appear moderate, the risk of dying from a respiratory cause is more than three times as great in the metropolitan areas with the highest ozone concentrations as in those with the lowest ozone concentrations. The effects of ozone on the risk of death from respiratory causes were insensitive to adjustment for individual, neighborhood, and metropolitan-area confounders or to differences in multilevel-model specifications.

There is biologic plausibility for a respiratory effect of ozone. In laboratory studies, ozone can increase airway inflammation24 and can worsen pulmonary function and gas exchange.25 In addition, exposure to elevated concentrations of tropospheric ozone has been associated with numerous adverse health effects, including the induction26 and exacerbation27,28 of asthma, pulmonary dysfunction,29,30 and hospitalization for respiratory causes.31

Despite these observations, previous studies linking long-term exposure to ozone with death have been inconclusive. One cohort study conducted in the Midwest and eastern United States reported an inverse but nonsignificant association between ozone concentrations and mortality.1 Subsequent reanalyses of this study replicated these findings but also suggested a positive association with exposure to ozone during warm seasons.3 A study of approximately 6000 nonsmoking Seventh-Day Adventists living in Southern California showed elevated risks among men after long-term exposure to ozone,11 but this finding was based on limited mortality data.

Previous studies using the CPS II cohort have also produced mixed results for ozone. An earlier examination based on a large sample of more than 500,000 people from 117 metropolitan areas and 8 years of follow-up indicated nonsignificant results for the relation between ozone and death from any cause and a significant inverse association between ozone and death from lung cancer. A positive association between death from cardiopulmonary causes and summertime exposure to ozone was observed in single-pollutant models, but the association with ozone was nonsignificant in two-pollutant models.3 Further analyses based on 16 years of follow-up in 134 cities produced similarly elevated but nonsignificant associations that were suggestive of effects of summertime (July to September) exposure to ozone on death from cardiopulmonary causes.5

The increase in deaths from respiratory causes with increasing exposure to ozone may represent a combination of short-term effects of ozone on susceptible subjects who have influenza or pneumonia and long-term effects on the respiratory system caused by airway inflammation,24 with subsequent loss of lung function in childhood,32 young adulthood,33,34 and possibly later life.35 If exposure to ozone accelerates the natural loss of adult lung function with age, those exposed to higher concentrations of ozone would be at greater risk of dying from a respiratory-related syndrome.

In our two-pollutant models, the adjusted estimates of relative risk for the effect of ozone on the risk of death from cardiovascular causes were significantly less than 1.0, seemingly suggesting a protective effect. Such a beneficial influence of ozone, however, is unlikely from a biologic standpoint. The association of ozone with cardiovascular end points was sensitive to adjustment for exposure to PM2.5, making it difficult to determine precisely the independent contributions of these copollutants to the risk of death. There was notable collinearity between the concentrations of ozone and PM2.5.

Furthermore, measurement at central monitors probably represents population exposure to PM2.5 more accurately than it represents exposure to ozone. Ozone concentration tends to vary spatially within cities more than does PM2.5 concentration, because of scavenging of ozone by nitrogen oxide near roadways.36 In the presence of a high density of local traffic, the measurement error is probably higher for exposure to ozone than for exposure to PM2.5. The effects of ozone could therefore be confounded by the presence of PM2.5 because of collinearity between the measurements of the two pollutants and the higher precision of measurements of PM2.5.37

Measurements of PM2.5 were available only for the end of the study follow-up period (1999 and 2000). Widespread collection of these data began only after the EPA adopted regulatory limits on such particulates in 1997. Since particulate air pollution has probably decreased in most metropolitan areas during the follow-up interval of our study, it is likely that we have underestimated the effect of PM2.5 in our analysis.

A limitation of our study is that we were not able to account for the geographic mobility of the population during the follow-up period. We had information on home addresses for the CPS II cohort only at the time of initial enrollment in 1982 and 1983. Census data indicate that during the interval between 1982 and 2000, approximately 2 to 3% of the population moved from one state to another annually (with the highest rates in an age group younger than that of our study population).38 However, any bias due to a failure to account for geographic mobility is likely to have attenuated, rather than exaggerated, the effects of ozone on mortality.

In summary, we investigated the effect of tropospheric ozone on the risk of death from any cause and cause-specific death in a large cohort, using data from 96 metropolitan statistical areas across the United States and controlling for the effect of particulate air pollutants. We were unable to detect a significant effect of exposure to ozone on the risk of death from cardiovascular causes when particulates were taken into account, but we did demonstrate a significant effect of exposure to ozone on the risk of death from respiratory causes.

Supported by the Health Effects Institute.

Dr. Krewski reports receiving grant support from the Natural Sciences and Engineering Research Council of Canada as holder of the Industrial Research Chair in Risk Science. This chair is funded by a peer-reviewed university–industry partnership program. No other potential conflict of interest relevant to this article was reported.

We thank the National Institute of Environmental Health Sciences for providing grant support (ES00260) to the New York University School of Medicine.

This article is dedicated to the memory of our coauthor and friend, Dr. Jeanne Calle, who died unexpectedly on February 17, 2009.

Source Information

From the University of California, Berkeley (M.J.); Health Canada, Ottawa (R.T.B.); Brigham Young University, Provo, UT (C.A.P.); New York University School of Medicine, New York (K.I., G.T.); the University of Ottawa, Ottawa (D.K., Y.S.); and the American Cancer Society, Atlanta (E.C., M.T.).

Address reprint requests to Dr. Jerrett at the Division of Environmental Health Sciences, School of Public Health, University of California, 710 University Hall, Berkeley, CA 94720, or at
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Comox councillor unhappy with ‘drive-thru’ approval

By Elaine Mitropoulos, Comox Valley Echo March 10, 2009

If Comox councillor Russ Arnott had his way, he wouldn’t let businesses pave paradise to put up a drive-thru.

Arnott, who sits on the community’s Business in Action committee, said businesses should be attracted to Comox for its “beauty.” Any corporations that demanded drive-thru accessibility, he said, could ultimately set up shop elsewhere.

“Is that really the business that we want?” he said during a March 4 council meeting. “I would just as soon say go on to the next town.”

Arnott’s comments come in the wake of the council approving a development that will see coffee giant Starbucks and the Toronto-Dominion Bank (TD Bank) housed next to the Shopper’s Drug Mart on the corner of Guthrie and Anderton roads.

Developer Moe Sihota of ACI Comox Ltd. told councillors that securing the corporate tenancies was contingent on installing drive-thrus that would allow for quick coffee breaks and convenient banking.

But Coun. Marcia Turner pointed to the environmental consequences of encouraging idling traffic, especially since the town was striving to meet its 2010 carbon-neutrality targets.

Turner motioned for the town’s planning department to prepare a report so that councillors could decide whether or not to ban drive-thrus from any future developments in Comox.

However, Sihota cautioned the council, saying that drive-thrus were an “economic reality” that drew in business in tough times.

A letter written to the town’s mayor from the Canadian Restaurant and Foodservices Association vice-president of Western Canada echoed Sihota’s concern.

“Not only would a ban on (drive-thrus) have a serious impact on jobs and investment in Comox, it would falsely blame (drive-thrus) as a leading contributor to poor air quality,” wrote Mark von Schellwitz.

The planning department’s report is slated for review by the town’s committee of the whole in about one month’s time.

What is the global-warming impact of the omnipresent drive-through?

February 25, 2009

Advice about recreational eating

Hey Mr. Green,
What is the global-warming impact of the omnipresent drive-through? Surely this has to be one of our biggest wastes of energy. –Robert in Biglerville, Pennsylvania

In drive-throughs or anyplace, idling is, to summon the old saying, the devil’s workshop. Every hour you idle, you waste up to 0.7 gallons of gas (depending on your engine type) going nowhere. So it pays to turn your engine off if you’re going to be still for more than 30 seconds.

In a given year, U.S. cars burn some 1.4 billion gallons of fuel just idling. Not to mention idling trucks, which waste another 1.5 billion gallons. Collectively, we emit about 58 million tons of carbon dioxide while we’re essentially doing nothing.

Taking the fast-food industry as an example, and taking into account that the average McDonald’s drive-through wait is 159 seconds, we can calculate that the company’s consumers burn some 7.25 million gallons of gas each year. The figure for the entire U.S. fast-food industry? Roughly 50 million gallons.

Though Wendy’s boasts that it zips you through in a mere 131 seconds, that’s about the amount of time it would take to slap together your own sandwich, or dump some leftovers in Tupperware, and bypass the lines (and perhaps a bypass) entirely.

The spread of American idle may be an exciting prospect for companies seeking to expand this lazy food-getting method to the rest of the world–but it’s a devastating one for the environment. Consider that McDonald’s plans to open 25 drive-throughs in China, following KFC’s lead. KFC installed its first drive-through there in 2002 and is working on 100 more. If China and India, which is also jumping aboard the drive-through bandwagon, get up to speed, they can idle away a truly staggering figure: 30 billion gallons of gas. Every year.