Environmental Health Perspectives • VOLUME 116 | NUMBER 8 | August 2008 1023

Research

Acute exposure to ozone causes transient

respiratory symptoms, reversible decrements

in pulmonary function, and an inflammatory

response that may persist for at least 18–24 hr

after exposure. A thorough review of recent

epidemiologic and controlled human exposure studies is available elsewhere [U.S.

Environmental Protection Agency (EPA)

2006]. Controlled exposures of healthy young

adults show that the magnitude of these respiratory effects is a function of O3 concentration, minute ventilation (VE), and exposure

duration. The primary focus of this article is

the effect of short-term controlled O3 exposures on forced expiratory volume in 1 sec

(FEV1) as a measure of lung function in

healthy young adults. Because small changes

in spirometry in healthy young adults may

result from exercise, diurnal, or other effects in

addition to the effects of O3 during the course

of an exposure, we use the term “O3-induced”

here to designate effects that we have corrected for such extraneous responses as measured during filtered air (FA) exposures.

After prolonged, 6.6-hr exposures to O3 at

concentrations of ≥ 0.08 ppm, young healthy

adults develop significant reversible decrements

in FEV1 at a moderate level of exercise (VE =

40 L/min). Exposures to 0.04-ppm O3 result in

small, statistically nonsignificant O3-induced

responses (Adams 2002). Volunteers exposed

to 0.08 ppm O3 experience group mean O3-

induced FEV1 decrements that range from 6%

to 8% (Adams 2003, 2006; Horstman et al.

1990; McDonnell et al. 1991); those exposed

to 0.10 ppm have group mean decrements of

8–14% (Horstman et al. 1990; McDonnell

et al. 1991); and those exposed to 0.12 ppm

have group mean decrements of 13–16%

(Adams 2002; Folinsbee et al. 1988; Horstman

et al. 1990). The distribution of individual

responses becomes skewed with increasing

exposure concentration and magnitude of the

group mean FEV1 response (McDonnell

1996). Taken together, these data indicate that

FEV1 responses are clearly affected by 6.6-hr

exposures to O3 concentrations ≥ 0.08 ppm.

These data also suggest that smaller, but measurable, responses are likely to occur with 6.6-

hr exposure to concentrations somewhat below

0.08 ppm. We are particularly interested in

estimating the magnitude of FEV1 responses to

concentrations < 0.08 ppm, with the ultimate

goals of better characterizing the concentration–response (C–R) relationship and reducing

uncertainty in the assessment of risk at low O3

concentrations.

Until recently, published data have not

been available for 6.6-hr exposures to O3

concentrations between 0.04 and 0.08 ppm.

Adams (2006) provided results for healthy

young individuals (15 males, 15 females) randomly exposed for 6.6 hr on six separate

occasions to FA, to constant or square-wave

(S-W) 0.06 ppm and 0.08 ppm O3, and to

three variable concentration patterns having

mean overall exposure O3 concentrations of

0.04, 0.06, and 0.08 ppm. The subjects

(mean age ~ 23 years) were recruited from the

University of California, Davis, and the surrounding community. Measures of FEV1

were conducted before exposure and after

approximately 1, 2, 3, 4.6, 5.6, and 6.6 hr of

exposure. Each 6.6-hr exposure was conducted in an exposure chamber and included

six 1-hr periods in which participants alternated 50 min of exercise with 10 min of rest.

An additional 35-min rest/lunch period in

the chamber followed the third hour of exposure. Exercise was calibrated to generate a VE

of approximately 20 L/min/m2 body surface

area (BSA) for each volunteer. There was a

minimum of 4 days between exposures.

Additional details related to volunteer characteristics, study design, facilities, measurement

methods, exposure characterization, and

results are available from Adams (2006). 

The stated purpose of the Adams (2006)

study was to compare the responses to the

0.08-ppm S-W exposure with the responses

to the other five exposure conditions.

Comparisons of responses among the other

five exposure conditions (e.g., the 0.06-ppm

S-W exposure with the FA exposure) at various time points were also presented. After the

detection of statistically significant effects

within the data using a two-way analysis of

variance technique, the Scheffé multiple comparison test was used to identify which specific comparisons were significantly different.

Address correspondence to J.S. Brown, U.S.

Environmental Protection Agency, Office of Research

and Development, National Center for Environmental

Assessment, B243-01, Research Triangle Park, NC

27711 USA. Telephone: (919) 541-0765. Fax: (919)

541-1818. E-mail: Brown.James@epa.gov

W.F.M. was funded by U.S. EPA contract

EP07H001352. 

This document has been reviewed in accordance

with U.S. Environmental Protection Agency (EPA)

policy and approved for publication. Mention of trade

names or commercial products does not constitute

endorsement or recommendation for use. The views

expressed in this article are those of the authors and

do not necessarily reflect the views or policies of the

U.S. EPA. 

Unrelated to the production of this article, W.F.M.

received funding from the American Petroleum

Institute to evaluate new ozone health effects data

and to conduct research related to a human ozone

exposure–response model. The other authors declare

they have no competing financial interests.

Received 20 February 2008; accepted 21 April 2008.

Effects of Exposure to 0.06 ppm Ozone on FEV1 in Humans: 

A Secondary Analysis of Existing Data

James S. Brown,1 Thomas F. Bateson,2 and William F. McDonnell3

1National Center for Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA; 2National Center for Environmental Assessment, U.S. Environmental Protection Agency, Washington, DC, USA; 3William F. McDonnell

Consulting, Chapel Hill, North Carolina, USA

BACKGROUND: Ozone is a potent photochemical oxidant that produces transient, reversible decrements in the lung function of acutely exposed individuals. A recent study provided previously

unavailable clinical data for 30 healthy young adults exposed to O3 at 0.06 ppm. That study

showed significant effects of 0.08 ppm on lung function, confirming the findings of others.

However, exposure to 0.06 ppm O3 was not reported to significantly affect lung function.

OBJECTIVES: We conducted this analysis to reevaluate the existing lung function data of the volunteers previously exposed to 0.06 ppm O3.

METHODS: We obtained pre- and postexposure data on forced expiratory volume in 1 sec (FEV1)

for all subjects who were previously exposed for 6.6 hr to filtered air or to 0.06 ppm or 0.08 ppm

O3. We used standard statistical methods appropriate for paired comparisons to reanalyze FEV1

responses after exposure to 0.06 ppm O3 relative to filtered air.

RESULTS: Controlling for filtered air responses, 24 of the 30 subjects experienced an O3-induced

decrement in FEV1. On average, 0.06 ppm O3 exposure caused a 2.85% reduction in FEV1 (p <

0.002), which was consistent with the predicted FEV1 response from existing models. Although the

average response was small, two subjects had > 10% FEV1 decrements.

CONCLUSIONS: Exposure to 0.06 ppm O3 causes a biologically small but highly statistically significant decrease in mean FEV1 responses of young healthy adults.

KEY WORDS: air pollutants, photochemical oxidants, spirometry. Environ Health Perspect

116:1023–1026 (2008). doi:10.1289/ehp.11396 available via http://dx.doi.org/ [Online 21 April 2008]
None of the differences between the FEV1

responses of exposure to 0.06 ppm O3 and

FA were identified as statistically different

from zero. However, Figure 1, which we

adapted from Adams (2006), shows that

the response to 0.06-ppm O3 exposure

diverges over time from the response to FA.

Additionally, the lack of overlap of the SE

bars at the 6.6-hr time point suggests that the

postexposure differences between FA and

0.06 ppm O3 are not likely to be attributed to

chance alone.

Although the Scheffé method for detecting

specific differences in the context of correcting

for all possible contrasts in the data avoids type

1 statistical errors (false positives) at the level of

the overall study, it is characterized as having

relatively low power for detecting small differences for any single comparison of interest and

is recognized as being a conservative test

(Schwertman and Carter 1995). In the absence

of calculations of statistical power or the probability of making a type 2 statistical error for the

comparison between the postexposure

responses of the FA and 0.06-ppm O3 exposures, we interpret the reported results of the

Adams analysis as being inconclusive regarding

the existence of an effect of 0.06-ppm O3

exposure on FEV1 response. That is, the inability to reject the null hypothesis of no difference

between two conditions is not sufficient to

conclude that no such difference exists.

Because of the potential regulatory implications of the presence or absence of effects at

concentrations below the level of the current

National Ambient Air Quality Standard

(NAAQS) for O3 (currently 0.075 ppm)

(NAAQS 2008), we elected to further examine the responses to 0.06 ppm O3 documented in the Adams (2006) study. Because

the U.S. EPA risk assessment for lung function effects and the current NAAQS for O3

are generally based on the postexposure

responses of a group of published 6.6-hr S-W

studies, we conducted a targeted, secondary

analysis of the Adams data to focus on the

specific question of whether exposure to

0.06 ppm O3 for 6.6 hr results in FEV1

decrements relative to the FA exposure.

Materials and Methods

The data presented here were originally

collected for a recent study of humans exposed

to low levels of O3 (Adams 2006). The exposures of interest for the purpose of the analysis

presented here are the constant-concentration

or S-W exposures to 0.06 ppm O3 and to FA.

For purposes of comparison with other studies,

we also present some results from the 0.08-ppm

S-W O3 exposures from the Adams (2006)

study. Although only group statistics were presented in the Adams (2006) publication, each

subject’s FEV1 measurement before and after

the 6.6-hr exposures was made available by the

author to the U.S. EPA for inclusion in its Air

Quality Criteria Document for O3 and Related

Photochemical Oxidants (U.S. EPA 2006) and

its health risk assessment (U.S. EPA 2007). We

analyzed these individual pre- and postexposure

FEV1 data.

The question of interest here is whether a

6.6-hr exposure to 0.06 ppm O3 under the

conditions of the Adams (2006) study results

in postexposure FEV1 decrements greater than

those after a control exposure to FA. We calculated the FEV1 percent decrement for FA and

for 0.06-ppm O3 exposures for each of the 30

participants as 100% × (preexposure FEV1 –

postexposure FEV1)/preexposure FEV1. We

then calculated the FEV1 response due to O3

(i.e., O3-induced) by subtracting the percent

decrement after FA from the percent decrement after 0.06 ppm O3 for each volunteer.

The distribution of O3-induced responses in

these data did not appear to deviate markedly

from a Gaussian distribution. However, it is

well known that higher-dose O3 exposures that

produce larger group mean FEV1 responses

result in frequency distributions of response

that are quite skewed, thereby potentially challenging some of the assumptions of many parametric statistical tests (Kulle et al. 1985;

McDonnell 1996; Weinmann et al. 1995).

The nonparametric sign test, which assumes

only that the responses of each subject are

independent and makes no assumptions about

the distribution of the response data, is appropriate to test the null hypothesis that observed

values have the same probability of being positive or negative (Fisher and Belle 1993). We

therefore selected the sign test as our primary

test of the null hypothesis that the FEV1

responses for the FA and 0.06-ppm exposures

are not different.

Because the individual O3-induced decrements in this study were generally symmetrical

and because other studies have demonstrated

that exposures that produce mean responses of

the magnitude observed in this study result in

roughly symmetric response distributions

(Kulle et al. 1985; McDonnell et al. 1983), we

also compared the FA and 0.06-ppm O3

responses using other methods. We used the

Wilcoxon signed rank test, which makes the

assumption that the individual O3-induced

responses are symmetrically distributed, and

the paired t-test, which makes the further

assumption that the responses are normally

distributed (Fisher and Belle 1993).

We calculated two-sided statistical tests

using SYSTAT 5.0 (Systat, Inc., Evanston, IL),

and we examined Tukey box plots to assess

potential outlier data using Graph Pad Prism 5

(Graph Pad Software, Inc., San Diego, CA).

Results

Table 1 lists the individual percentage

decrements in FEV1 from baseline after the

FA and 0.06-ppm O3 exposures and the O3-

induced decrements. For the full data set (n =

30), the O3-induced FEV1 responses appear

to be symmetrically distributed around the

median of 2.91% and mean of 2.85%.

Twenty-four of the 30 individuals experienced an O3-induced decrement greater than

zero (range, 0.23–14.52%), whereas six experienced an improvement in FEV1 (range,

–0.43% to –7.42%) after the exposure. The

Brown et al.

1024 VOLUME 116 | NUMBER 8 | August 2008 • Environmental Health Perspectives

Table 1. Percent decrement in FEV1 for 6.6 hr of

exposure to FA and 0.06 ppm O3 for individuals in

the Adams (2006) study. 

Subject ΔFA ΔO3 ΔO3 – ΔFA

1 –1.46 –0.87 0.59

2 0.20 3.01 2.81

3 –0.29 5.93 6.23

4 –5.33 –3.52 1.81

5 –8.62 –3.75 4.87

6 –2.94 –3.89 –0.95

7 –0.21 0.21 0.42

8 –0.28 3.43 3.71

9 –3.12 3.91 7.03

10 –6.32 6.43 12.76a

11 –0.53 0.53 1.07

12 4.76 –2.66 –7.42a

13 –1.71 –2.87 –1.16

14 –0.42 2.87 3.29

15 –1.16 –0.57 0.58

16 –5.54 –1.74 3.80

17 –0.62 –1.05 –0.43

18 –4.35 1.88 6.23

19 –3.17 1.98 5.15

20 2.02 5.03 3.00

21 –2.19 3.66 5.85

22 –2.19 –5.13 –2.93

23 0.21 14.73 14.52a

24 –0.58 0.59 1.17

25 –0.27 0.54 0.81

26 –4.14 1.10 5.24

27 1.79 2.02 0.23

28 0.19 –0.40 –0.60

29 0.87 4.21 3.34

30 5.02 9.62 4.60

Mean –1.35 1.51 2.85

SD 2.98 4.24 4.28

ΔO3 – ΔFA represents the decrements due to 0.06 ppm O3

corrected for any FA effects. Data are FEV1 percent decrements from preexposure; a negative number indicates an

increase or improvement in FEV1. aPotential outlier according to the Tukey criteria.

Figure 1. Mean FEV1 decrements as function of

exposure duration and O3 concentration. Data are

for constant, S-W O3 protocols in the Adams (2006)

study. Error bars are the SE of responses at 6.6 hr.

Adapted from Adams (2006).

7

6

5

4

3

2

1

0

–1

–2

–3

FEV1 decrement (%)

Time (hr)

0 2 1 34 567

0.08 ppm

0.06 ppm

0 ppm
null hypothesis that there is no difference

between the median responses of the FA and

the 0.06-ppm exposures (or that the median

O3-induced decrement equals zero) is rejected

using the two-tailed sign test (p = 0.0019).

We also conducted alternative analyses of the

data using the Wilcoxon signed rank test and

the paired t-test. The null hypothesis of no

difference between responses for the FA and

0.06-ppm O3 exposures was rejected by both

tests (Table 2). Although the data had no

extreme outliers, we flagged three responses as

potential outliers according to the Tukey criteria. The characteristics of the data change

little with exclusion of the single most

extreme value (subject 23 in Table 1) or all

three potential outliers (subjects 10, 12, and

23 in Table 1) removed (Table 2).

Discussion

We have demonstrated that the FEV1 decrements that occur after a 6.6-hr exposure to

0.06 ppm O3 are statistically different from

those that occur after FA exposure (p < 0.01).

We arrive at the same finding regardless of the

statistical test we employ or the approach to

treating potential outliers in the data. That

the effect of 0.06 ppm O3 on FEV1 occurred

not by chance alone is further supported by

two additional observations. First, the FA and

0.06-ppm responses in FEV1 generally track

each other for the first 4.6 hr of exposure,

with no evidence of wide swings in the data.

The responses clearly diverge for both the

5.6- and 6.6-hr data points, indicating that

the response at 6.6 hr is not a single anomalous data point (Figure 1). The group mean

O3-induced decrement at 5.6 hr (~ 2.4%) is

only marginally smaller than that at 6.6 hr

(2.85%). This temporal pattern of response is

generally consistent with patterns of response

after 0.08 ppm, 0.10 ppm, and 0.12 ppm in

numerous studies in which the O3 response

begins to diverge from the FA response at earlier time points during exposure to higher

concentrations of O3 (Adams 2000, 2002,

2003; Folinsbee et al. 1988; Horstman et al.

1990). Second, the magnitude of the group

mean O3-induced response of this sample

after exposure to 0.08 ppm O3 is 6.07%,

which is quite consistent with observed

responses to 0.08-ppm exposure from other

studies (Figure 2), indicating that this sample

of volunteers is not unusually sensitive to O3.

We thus have no reason to suspect that the

observed average response at 0.06 ppm is

inflated because of attributes of the target

population or sampling error.

The existence of a small group mean

FEV1 decrement after a 6.6-hr exposure of

young exercising adults to 0.06 ppm should

not come as a surprise. Figure 2 presents

response data from studies that used an exposure protocol nearly identical to that used by

Adams (2006). These studies all used young,

healthy adults as volunteers; exposure duration was for 6.6 hr, and exercise pattern and

VE (~20 L/min/m2 BSA) were similar. The

group mean FEV1 response to the 0.08-ppm

exposure for the Adams (2006) study is consistent with other studies. Furthermore, the

observed FEV1 responses at 0.04 ppm O3

(Adams 2002) and 0.06 ppm O3 (Adams

2006) are almost identical to the response

predicted by a model based on data from 15

studies conducted at the U.S. EPA Human

Studies Facility in Chapel Hill, North

Carolina (McDonnell et al. 2007). The

smooth C–R curve illustrated in Figure 2 is

consistent with C–R curves for shorterduration (2 hr) exposures, which have typically

been observed to be smooth without obvious

discontinuities over a wide range of concentrations, including those where effects were near

zero (Avol et al. 1984; Hazucha 1987; Kulle

et al. 1985; McDonnell et al. 1983).

The stark difference between our conclusions and those of Adams (2006) with regard

to whether a 6.6-hr exposure to 0.06 ppm O3

induces statistically significant FEV1 decrements requires further explanation. We have

identified three factors that we believe contribute to the difference in conclusions. First,

no p-value is given in the original manuscript

for the comparison of the 6.6-hr FA and 0.06-

ppm responses. The group mean difference of

2.85% is simply reported as not being statistically significantly different from zero at α =

0.05 using the Scheffé test to correct for the

multiple comparisons. However, in Table 3 of

the original manuscript, the difference

between the 0.08-ppm and 0.06-ppm exposures after 6.6 hr (3.21%) is reported as being

statistically different from zero. Because the

analysis of variance and the Scheffé method

used by Adams assume equal variances for all

means, it is reasonable to assume that the difference of 2.85% between 0.06 ppm and FA

approached statistical significance—even with

this most conservative methodology.

A second factor causing differences in conclusions reached herein compared with those

of Adams (2006) results from differences in the

purpose of our reanalysis compared with the

purpose of the original study, the statistical

approaches used, and the approach to controlling for multiple statistical tests. The stated

purpose of the Adams (2006) study implies a

large number of comparisons among six exposure protocols and seven time points (0, 1, 2,

3, 4.6, 5.6, and 6.6 hr). The Scheffé method

allows all pairwise comparisons as well as an

infinite number of linear contrasts among the

cell means to be made while limiting the probability of making a single type 1 statistical error

among all the potential contrasts to 0.05.

Although there is nothing inherently wrong

with making a large number of contrasts and

strictly maintaining a studywide alpha level

using the Scheffé method, this approach comes

at the cost of reduced statistical power for

assessing differences for specific comparisons.

Setting aside all the theoretically possible linear

contrasts, there are 15 possible direct comparisons between the six protocols used by

Adams (2006) at the 6.6-hr time point. The

Bonferroni procedure would be the preferred

multiple comparison correction for this

Effect of 0.06 ppm ozone on lung function

Environmental Health Perspectives • VOLUME 116 | NUMBER 8 | August 2008 1025

Table 2. Descriptive and inferential statistics for O3-induced decrementsa in FEV1 for the full data set

(n = 30) and for two data sets with potential outliers removed.

Data set

n = 30 n = 29 n = 27

Mediana 2.91% 2.81% 2.81%

Meana 2.85% 2.45% 2.44%

SEa 0.78% 0.69% 0.51%

95% confidence intervala 1.26–4.45% 1.03–3.87% 1.38–3.49%

Sign test p-valueb 0.0019 0.0030 0.0021

Wilcoxon p-valueb,c 0.0008 0.0014 0.0004

Paired t-test p-valueb 0.0010 0.0014 <0.0001

aO3-induced decrements are the difference between percent decrements in FEV1 from the preexposure for the 0.06 ppm

O3 and FA exposures. bp-Values are two sided. cWilcoxon signed rank test. 

Figure 2. Cross-study comparison of mean

O3-induced FEV1 decrements due to 6.6 hr of constant, S-W exposure to varied O3 concentrations. All

exposures were conducted in a chamber, except for

a face-mask exposure to 0.04 ppm O3 in the Adams

(2002) study. All studies used a 6.6-hr exposure protocol in which volunteers alternated between 50 min

of exercise (VE ≈ 20 L/min/m2 BSA) and 10 min of rest

with an additional 35 min of rest after the third hour.

For this exposure protocol, the McDonnell et al.

(2007) curve illustrates the predicted FEV1 decrement at 6.6 hr as a function of O3 concentration for a

23-year-old. Error bars (where available) are the SE

of responses. The data at 0.08 and 0.12 ppm have

been offset for illustrative purposes.

20

15

10

5

O

0 3-induced FEV1 decrement (%)

O3 (ppm)

0.02 0.04 0.06 0.08 0.1 0.12 0.14

×

×

Adams (2006)

Adams (2003)

Adams (2002)

Folinsbee et al. (1988)

Horstman et al. (1990)

McDonnell et al. (1991)

McDonnell et al. (2007)

×
relatively small number of comparisons

(Schwertman and Carter 1995). A critical

alpha for the possible comparisons between the

six protocols at the 6.6-hr time point would be

0.05 ÷ 15, or 0.0033. We compared only the

FEV1 responses at 6.6 hr between FA and

0.06-ppm O3 S-W exposure. Even with a correction for the additional comparisons, which

we did not consider, all of the tests presented

in Table 2 remain statistically significant.

The third factor potentially contributing

to the disparity in our conclusions compared

with those of Adams (2006) involves errors

caused by data not meeting the criteria for the

statistical tests applied. The two-factor analysis

of variance and Scheffé method cited by

Adams (2006) assume that data are normally

distributed and that variances are equal within

cells. From previous studies of higher O3

exposures, we know that FEV1 responses

become skewed and that variance increases

(McDonnell 1996). This increase in variance

is clearly apparent in the Adams (2006) data,

with the standard deviation of FEV1 responses

increasing from 2.98% for FA to 4.24% for

0.06 ppm O3 to 8.65% at 0.08 ppm. It is possible that the wide range in variances among

the cells resulted in wider confidence levels

and inaccuracies of the reported p-values for a

subset of the comparisons.

Assuming for the moment that the O3-

induced decrement at 0.06 ppm is not zero and

that the best point estimate of the magnitude of

the mean decrement is 2.85% (95% confidence

interval, 1.26–4.45%), what can we say about

the possible clinical significance of reversible

effects of such magnitude? It is unlikely that

individuals experiencing a 3% reduction in

FEV1 would be aware of such an effect, and

effects of this magnitude are at the outer range

of expected day-to-day variability of the measurement. We know, however, that individuals

vary reproducibly in their responses to O3

exposure, and it is those most responsive individuals who are likely to experience clinically

significant effects. Although the average

response was small, two subjects in the Adams

(2006) study had > 10% FEV1 decrements

(12.8% and 14.5%). The U.S. EPA has considered any individual changes in FEV1 of

10–20% to be a moderate effect clearly outside

the range of normal within-day variability (U.S.

EPA 2006, 2007). In the Adams (2006) study,

2 of 30 individuals (i.e., 7%) experienced such

effects. This observed proportion of individuals

having a > 10% decrement in FEV1 at 0.06

ppm is consistent with a smooth C–R curve

that includes observed proportions from previous studies of 26% at 0.08 ppm, 41% at 0.10,

and 57% at 0.12 ppm [proportions calculated

for S-W exposures in U.S. EPA (2007),

Table 5-3]. If one converts the SD values to SE

values in Adams (2006, Table 4), the SEs for

the symptoms resulting from the 0.06-ppm

S-W exposure do not overlap those for the FA

exposure. This is suggestive of an effect of 0.06

ppm on respiratory symptoms as well as FEV1.

A reversible loss of lung function in combination with the presence of symptoms is considered adverse (American Thoracic Society 2000).

It thus appears that a small fraction of individuals exposed to 0.06 ppm O3 for 6.6 hr during

moderate exercise may approach a degree of

response that is considered to be adverse.

To meet the objectives of his study, Adams

(2006) required that a large number of comparisons be made and that comparisons not be

identified as statistically significant by chance

alone. Appropriately, the Scheffé test was

employed to meet these needs. Although

Adams (2006) did not find the FEV1 responses

of the 0.06 ppm O3 and FA exposures to be

statistically different, no measure of the probability of a type 2 statistical error was provided,

which would be required before drawing a

conclusion that a true difference does not exist.

The objective of the present study was to

reevaluate the lung function data of subjects

exposed for 6.6 hr to 0.06 ppm O3. Regardless

of the statistical test used, we found the postexposure FEV1 decrements for the FA and

0.06-ppm O3 exposures to be strongly significantly different. Complete resolution of this

question must necessarily await further studies

designed to address this specific question with

adequate statistical power. However, comparison with the results of other studies support

the interpretation that our finding is not due to

chance alone and, indeed, is consistent with a

smooth C–R curve.

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1026 VOLUME 116 | NUMBER 8 | August 2008 • Environmental Health Perspectives