Effects of onboard insecticide use on airline flight attendants

Effects of onboard insecticide use on airline flight attendants

Kaye H. Kilburn

LIFTING OFF from Capetown, South Africa, on a 747 bound for Heathrow Airport in London in September 2004, I glanced across the cabin to see flight attendants spraying a mist against the ceiling. Surprise turned to horror. As visions flashed of 33 flight attendants from United Airlines poisoned by pyrethroid insecticides in 1997, I rang my call button. When the British Airways flight attendant answered my call light, I described to her that the danger of spraying insecticides indoors was most severe in the closed space of an airliner cabin. I protested; this action was a dangerous and inhumane experiment that violated my right to avoid danger. Furthermore, no review board for research on human subjects would consent to this experiment.

The flight attendants who conducted the spraying returned aft, and my wife, who was seated forward, said that no spray came from canisters when they reached her. That was fortunate, inasmuch as it could have triggered her asthma. I accepted my only option–that of filling out a complaint to British Airways–for I was told that the airliner could not take off unless passengers were sprayed in the cabin at departure.

Two flight attendants later told me of repeatedly feeling ill, nauseated, and dizzy following the spraying of the “mist.” They said I could read the label on the canister, because they did not know what insecticide was used. This access was not provided; therefore, I am unaware of whether the spray was a carbamate (carbaryl) that acts like an organophosphate, or synthetic pyrethroids, or both.

The spraying procedure to which I reacted so strongly was recommended by the World Health Organization approximately 40 yr ago to prevent the intercontinental transfer of insect vectors (e.g., malaria); it was broadened to include agricultural pest insects. In 1992, I was furious that I had to submit to spraying before landing at Auckland, New Zealand–a concern that was sharpened after my research revealed brain impairment among flight attendants exposed to pesticides. In 1994 the U.S. Department of Transportation called on 20 foreign governments to discontinue spraying insecticides in passenger planes. Clearly, South Africa and British Airways did not stop this procedure. Therefore, dangers to both airline personnel and passengers remain. The evidence of those dangers is presented herein.

Synthetic Pyrethroid Insecticides are sold for the purpose of killing ants, roaches, and mosquitoes. These agents are more toxic to insects and persist longer than the chrysanthemum (flower)-derived pyrethrins. Pyrethrins may be allergenic to some but have little human neurotoxicity. In contrast, pyrethroids resist detoxification; human poisonings (1) and deaths have been reported. (2)

In 1994, following complaints from passengers and flight attendants (FAs), the U.S. Department of Transportation called on more than 20 foreign governments to discontinue regulations that mandated the spraying of aircraft cabins with pesticides. Chemical pesticides were routinely sprayed in passenger cabins on flights to the Caribbean, Latin America, and the South Pacific.

The opportunity to assess the effects of pyrethroids was presented by 33 FAs. Three of the FAs developed mucous membrane irritation, memory loss, and dizziness following many international flights. These individuals were evaluated after they were unable to continue working and were found to have slight-to-severe neurobehavioral impairments. I discussed their findings with 60 FAs based in Los Angeles, California, and evaluated 33 of them in March 1997. Five FAs had recently retired for disability, and 28 remained at their jobs.

The FAs were exposed to pyrethroids by spraying the inside of airliner cabins prior to landing in Auckland, New Zealand, and Sidney, Australia. This practice, termed disinsection, was, as described earlier, devised approximately 40 yr ago to reduce intercontinental transfer of insects. (3,4) Canister bug bombs and aerosols were used in flight. In addition, airliners were “saturation sprayed” at 8-wk intervals by ground crews to create residual levels. Often 4 100-g cans of pyrethroids, such as permethrin (Perigen 500), were used on the ground prior to departure, and 4 additional cans were sprayed in cabins prior to descent. Occasionally, methyl carbamate (Baygon) in 1,1,1-tricholoroethane was added. Whereas various pesticides were used on airplanes, the FAs affirmed that pyrethroids were the most common pesticide used on their flights to Australia and New Zealand. These synthetic chemicals mimic the action of natural pyrethrins derived from chrysanthemum flowers.

The objective of this study was to determine whether impaired function accompanied the complaints of memory loss and dizziness presented by the 33 FAs. This objective was achieved by comparing the test results from the FAs with those of 202 unexposed control subjects.


All exposed and control subjects were non-Hispanic, English-speaking white individuals. The 33 exposed FAs were assessed with function tests used previously in insecticide- or chemically exposed patients, (5-8) The tests emphasize objective measurements such as blink reflex and balance, both of which require minimal cooperation, through tests of reaction time and vision, to more subjective psychological tests. Testing was achieved by trained personnel in accordance with established protocol for both exposed and unexposed subjects. Fixed-format questionnaires contained questions about demographics; educational background; exposures to chemicals; and medical, pulmonary, cardiovascular, neurologic, and psychiatric histories. The frequency of 35 symptoms was appraised on a 10-point scale from never to always, (5,6) and a standardized 65-factor Profile of Mood States (POMS) was completed and scored. (9) The 202 control subjects were volunteers recruited from voter registration rolls of an Arizona town without chemical exposures. These individuals were screened via questionnaire for personal chemical exposures and were found to be free of medical and neurological diseases. All had been evaluated by neurobehavioral and pulmonary function tests measured in 1993 and 1998, (10) and their data were used to compute the regression equations to compute predicted values for each neurobehavioral test. (10)

The 26 neurobehavioral tests included a range from simple and 2-choice visual reaction times that were measured from appearance to cancellation of block letters on a computer screen, (11) Body balance was measured by having the subject stand erect with feet together and then tracking a sound-emitting headband with 2 microphones. This information was processed in a computer and expressed as speed-of-sway in centimeters per second. (12) Blink reflex latency was elicited by supraorbital tap and measured for each eye by electromyography. (13) The color confusion index for each eye was tested with the Lanthony (14) desaturated hue test and scored by Bowman’s method. (15) A computerized automated perimeter bowl (Med Lab Technologies [Line Lexington, Pennsylvania]) mapped a 30[degrees] visual field. Hearing in each ear was measured by programmed audiometry.

Culture Fair tests nonverbal, nonarithmetical intelligence on the basis of the selection of designs for similarity, difference, completion, and pattern recognition, and transfer. (16,17) A 46-word vocabulary test from the multidimensional aptitude battery was also used. (18) Digit symbol substitution from the Wechsler Adult Intelligence Scale-revised (19) (WAIS-R) was used to test attention and integrative capacity. Similarities, information, and picture completion from the WAIS-R tested embedded memory.

Attention and perceptual motor speed were tested by timing the placement of 25 slotted pegs in a board; trail making A required connecting 25 numbered circles in order, and trail making B required connecting alternate numbers and letters and the number of errors in fingertip number writing. (20) Verbal recall of stories was also tested . (21)

The subjects answered 11 questions from the American Rheumatism Association’s criteria for lupus erythematosus. (22) The POMS score was obtained from 65 words or phrases that described feeling (rated from) not at all as 1 to extremely as 5. (9)

Vital capacity, forced expired volume in 1 sec, and pulmonary flows were obtained with standard procedures, (23) digitized, and compared as percentage predicted values, adjusted for height, age, sex, and years of cigarette smoking. (24)

Each subject’s individual scores were compared with their predicted values computed from equations on the basis of 264 control individuals who were well distributed for age, sex, and educational level from communities in 3 states. (10) Following graphic analysis to exclude values with undo influence, measurements were transformed to logarithm, reciprocal, square, or square root if this improved the symmetry of the distribution, regression modeling produced predictive equations for each test. Subjects’ observed values were divided by their predicted values, and percentage predicted was then calculated. The exposed group means were compared with those of 202 unexposed Arizona residents as percentage predicted, using analysis of variance (ANOVA).

Statistical analysis. All scores and computed data for all tests were transferred to a computer for additional analysis. Descriptive and analytical computations, including ANOVA, were completed after the author adjusted the data for age, education, sex, and height or weight, when applicable, using prediction equations on the basis of stepwise linear-regression modeling. (10) The author used Stata Statistical Software (Stata Corporation [College Station, Texas]). Other factors considered included family income, hours of general anesthesia, weight, and POMS score; however these factors demonstrated no statistical significance, as defined by p < 0.05.

The abnormality score for each subject was the sum of tests outside the 95% confidence interval, which was 1.5 times the standard deviation. Visual performance and balance were weighed as 1; bilateral functions such as hearing, blink reflex latency, and grip strength were weighed as 0.5 per side; and all other functions had a weight of 1.


The mean age of FAs (47.7 yr [range 32-60 yr]) was similar to the 45.0 yr of the control group, but FAs had significantly more years of education (14.2 yr versus 12.9 yr, respectively). These differences were adjusted when each individual’s predicted values were calculated. Incomes of FAs significantly exceeded those of controls, and fewer FAs smoked cigarettes (i.e., 6% current and 50% exsmokers in FA group). The FA group had significantly faster sway speed with eyes closed, lesser grip strength in the left arm, and inferior color discrimination in both eyes than controls (Table 1). Their blink reflex latencies were of less duration than the controls, and the differences were statistically significant. Other tests were in the expected ranges and included scores for long-term memory tests that were consistent with 14+ yr of education. Fifteen FAs had more than 2 abnormalities and 6 FAs had 6 or more abnormalities. The mean total number of abnormalities for the exposed group was significantly higher that for the control group (2.8 and 1.2, respectively [Table 2]).

The pulmonary function tests overall were normal, and mean flow values exceeded predicted values, thus indicating an absence of airway obstruction (Table 3). However, pulmonary symptoms were increased, compared with controls and included productive cough, wheezing, and shortness of breath.

Thirty-three of 35 symptoms had an average frequency of 5.0 in the FA group, which was nearly twice the 2.6 frequency in the comparison group (Table 2). Symptoms listed in order of frequency were extreme fatigue, loss of memory and concentration, loss of libido, dry mouth, somnolence, swollen stomach, and decreased alcohol tolerance. Infrequent symptoms that were not more frequent than in the comparison group were loss of consciousness, loss of appetite, coughing blood, and unusual exhilaration. Symptom frequencies were unrelated to numbers of abnormalities (regression analysis [p < 0.825, [r.sup.2] = .002, and standard error {SE} = 3.730]). POMS average score of 52 in the FA group was statistically significantly higher than the score of 21 in the unexposed subjects and included increased depression, tension, fatigue, confusion, and decreased vigor. Only the FAs' anger scores did not exceed that of control subjects. POMS scores were not correlated with numbers of abnormalities (p < 0.273, [r.sup.2] = .04, and SE = 3.648). However, symptom frequencies and POMS scores were correlated (p < 0.001, [r.sup.2] = .29, and SE = 1.179). Depression was diagnosed in 27% of the FAs, and 45% of them used tranquilizers–both of which occurred in significantly higher proportions than in the unexposed group.

Six FAs had 5 or more lupus erythematosus (LE) symptoms, and an additional 8 had 4 LE symptoms (i.e., using the American Rheumatism Association criteria). Numb fingers occurred in 18 FAs, 16 had anemia, 13 had sun-induced rash, and 12 had excessive hair loss, but antinuclear antibodies (ANA) were not significantly elevated.

The FAs’ histories of exposure to other chemicals were minimal and were not different from controls, except FAs experienced greater exposures to pesticides in airliner cabins.


FAs had impaired balance (with the eyes closed), strength of grip, and color discrimination, which, to date, are the most sensitive neurobehavioral tests we have used to evaluate effects of chemical exposures. The average impairment from pyrethroids was less than for persons exposed to organophosphate insecticides (7) or to organochlorine pesticides, (5,8) which is in keeping with ranking of these classes of agents. (1) Although it is possible that 2.8 abnormalities occurred by chance, this is unlikely. Nearly 50% of the FAs had 3-15 abnormalities, clearly more than the 1-2 that occur in referent groups by chance. (10) Comparison by total abnormalities was 2.8 versus 1.2 (p < 0.0001), and the test differences supported the biological significance of the comparison; i.e., the pattern of abnormalities was compatible with adverse effects from pyrethroids. The variation from 15 to 0 abnormalities was attributed to individual differences in susceptibility and in intensity and number of exposures. Balance, color discrimination, and blink were different from controls as were total abnormalities.

Strengths and weaknesses. This is the first report of objective evidence of neurobehavioral impairment in flight attendants. Balance, color discrimination, and blink reflex latency were significantly different from controls, and there were substantial differences in the number of total abnormalities. Although the exposure data was crude and fragmentary, such variability has characterized individuals exposed to other chemicals studied by these same methods. (2,6-8) Malingering or the manipulation of scores by FAs seemed unlikely inasmuch as this group’s objective scores for blink reflex latency and pulmonary flows exceeded those predicted. The effects appear to be lasting, not transitory.

The FAs were studied 48 h or more after their last shifts on airliners. Thus, none were sleep-deprived when studied, none had ethanol in alveolar air, and they had not smoked. Most FAs had 28 h of exposure per week from residual levels on the planes, with peak doses during spraying on board prior to landing, compared with 1 or 2 14-hr periods for passengers. Onset of symptoms was gradual in all but 1 FA. Many factors, including frequency of flights, flight duration, and manner of spraying, were examined for effect on number of abnormalities. Only 1 effect was found. One FA who was overcome with loss consciousness developed 15 abnormalities and was disabled. She had entered the crew quarters on a Boeing 747 immediately after it was sprayed with pyrethroids by the ground crew.

The FAs were self-selected, which may have elevated their symptom frequencies, but would not have affected their measured abnormalities. Neither elevated frequency of symptoms nor abnormal Mood States scores predict the numbers of abnormalities. FA ages did not predict elevated abnormal scores, elevated POMS scores, or frequency of symptoms. The 5 FAs who had retired for disability had 15, 4, 5, 2, and 1 abnormalities, higher than predicted symptom frequencies (7.7, 7.6, 5.9, 5.6, and 5.3, respectively), and elevated POMS scores (128, 103, 92, 92, and 62). The 2 FAs with the least abnormalities became symptomatic after exposures to common chemicals such as perfume, gasoline, and cigarette smoke; these individuals could not continue as FAs. Secondary gain seemed an unlikely motivation, as disability retirement compensation was less than that for ordinary retirement.

Different areas of the brain are responsible for impairments, symptoms, and moods. All are facets of central nervous system dysfunction. The frequency of LE symptoms seemed nonspecific because ANA titers were not elevated. The FAs’ complaints of depression absent other psychiatric disorders and their frequent use of tranquilizers may be responses to pyrethroids, but such an interpretation awaits comparison with an FA group that not been exposed to pesticides.

The study’s major limitation in attributing these effects to pyrethroids is the absence of a comparison group of international FAs who have not been exposed to pyrethroids. Such a study with unexposed FAs would help separate the effects of flying, changes in barometric pressure, time zones, and circadian rhythms. However, these experienced FAs had already been self-selected for health, tenacity, and adjustment to these factors, which reduces the possibility of such factors explaining the findings of this study.

The possibility that the effects observed were the result of methyl carbamate (Baygon) was considered. Carbamates act on the brain in a manner similar to organophosphates. (7) However, carbamates were applied only occasionally on planes, and have short durations of action and are less persistent. The organophosphate chlorpyrifos (Dursban) was used rarely by a few FAs, and they were not those with the most abnormalities. Therefore, the focus returns to pyrethroids. A comparison with pesticide applicators for pyrethroid effects was considered, but is not appropriate because pesticide applicators most always experience combined exposures to organophosphates, carbamates, and other pesticides.

The FAs occupy a unique exposure niche with repeated exposures to pyrethroids within a closed space. However, 4 non-FA subjects exposed at home and 1 who cleaned (i.e., swept) spilled pyrethroids were tested. These 5 individuals were similar to the FAs with respect to age and education. Four had abnormalities elevated above 2, POMS scores were more abnormal than FAs (i.e., averaging 77), and symptom frequencies were slightly below those observed for FAs (i.e., 4.3).

Pyrethroids were synthesized to decrease degradation, improve persistence, and decrease cost; the net result would be they could replace pyrethrins and other pesticides. (1) Pyrethroids act on mammalian nerves by keeping the Na+ channel in the open state for several seconds, causing repetitive nerve impulses. (25) Only a small fraction (< 1%) of open sodium channels produce poisoning. (26) In short, pyrethroids produce nervous system hyperactivity. They also inhibit the [gamma]-aminobutyric acid (GABA) receptor, thus causing excitability and convulsions at relatively high doses. Tremors, poor coordination, hyperactivity, and paralysis also occur.

By 1990, animal, cell, and nerve preparations showed dose-dependant toxicity of pyrethroids (e.g., in mouse bone marrow cells and sperm). (27) Pyrethroids slow the closing of sodium channels in nerve cells (28) and prolong elevation of the level of phosphorylation in key synaptic proteins in the optic lobe of the squid. (29) Other experiments in partially kindled rats evidenced reduction in seizure threshold and induced seizures by type I–but not type II–pyrethroids. (30) Both types reduced the amplitude of cholinergic contractions in preparations of guinea pig ileum. (31) Neonatal mice given pyrethroids at 1.2 mg/kg body weight developed choreoathetosis and tremors. (32) The synthetic pyrethroids, cypermethrin and fenvalerate, inhibit acetylcholinic esterase in cattle and buffalo. (33) They react competitively with human androgen receptors and a binding protein. (34) Finally, in long-term feeding experiments, deltamethrin increased lymphomas in mice and thyroid tumors in rats. (35)

More than 500 human pyrethroid poisonings–half occupational and half accidental or intentional, resulting in seven deaths–were studied in Beijing, China. (2) Patients had tingling paresthesia of the mouth and face, dizziness, headache, weakness, and fatigue. Unfortunately, no brain functions were measured. Earlier studies of 199 pyrethroid packaging workers showed that 70% had abnormal facial sensations, 32% experienced sneezing and increased nasal secretions, 14% had dizziness, 9% were fatigued, and 10% had nausea. (36) Fenvalerate was more potent than permethrin. Both pyrethroids caused cutaneous dysesthesia that was inhibited by topical vitamin E acetate. (37)

In Germany in 1993, 64 patients with chronic pyrethroid intoxication were reported to the federal health office, and 23 had neurologic examinations. Of these patients, 9 had various neurologic or psychiatric abnormalities, 8 were diagnosed with multiple chemical sensitivity, and 6 had normal clinical neurological examinations. Unfortunately, no neurobehavioral testing was done. (38)

In 1 study the persistence of pyrethroids in treated carpets, which appears comparable to that of airliner interiors, was investigated. The carpets retained concentrations of 115-150 mg/kg of dust for up to 10 yr indoors. (39) Similar levels were found in soil (40) and trees. (41,42) These results suggest that pyrethroids sprayed in aircraft persist by adsorption to fibers of carpets, seats, and other surfaces and provide a reservoir of exposure for flight attendants and passengers. If both passengers and airline personnel are to be protected, alternative methods of insect control should be used on airplanes.

The cooperation of international FAs of United Airlines based in Los Angeles is gratefully acknowledged. They paid for their examinations.

The cost of the first several evaluations billed to group health insurance were paid in full or in part. Bills for subsequent FAs were refused.

Submitted for publication January 10, 2005; accepted for publication May 4, 2005.

Requests for reprints should be sent to Kaye H. Kilburn, M.D., University of Southern California, Keck School of Medicine, Laboratory for Environmental Sciences, Bldg A7 #7401, 1000 S. Fremont Ave/Unit 2, Alhambra, CA 91803.

E-mail: Kilburn@usc.edu


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University of Southern California

Keck School of Medicine

Laboratory for Environmental Sciences

Alhambra, California

Table 1.–Flight Attendants (n = 33), Compared with Unexposed Persons

(n = 202), Adjusted for Age, Education Level, and Other Factors,

by Percentage Predicted of Analysis of Variance (ANOVA)

Exposed Unexposed

Characteristic Mean SD Mean SD p

Age (yr) 47.7 6.9 45.0 21.1 0.76

Educational level (yr) 14.3 1.9 12.9 2.3 0.0001 *

Physiological tests

Simple reaction time (ms) 100.3 4.1 99.9 3.7 0.545

Choice reaction time (ms) 100.5 3.2 100.0 2.5 0.249

Balance sway speed (cm/s)

Eyes open 102.2 3.6 99.8 22.0 0.380

Eyes closed 101.6 4.1 100.0 2.5 0.003 *

Blink reflex latency R-1 (ms) ([dagger])

Right 86.5 11.4 96.2 13.2 0.003R

Left 82.8 10.8 95.0 13.6 0.0003R

Hearing loss

Right 97.4 26.4 101.5 33.6 0.509

Left 91.1 25.0 99.3 21.8 0.149

Color discrimination errors

Right 82.7 47.0 102.6 51.1 0.038 *

Left 70.9 36.6 102.6 51.1 0.0008 *

Visual field performance

Right 102.7 17.1 100.0 22.8 0.640

Left 100.3 17.2 101.1 21.7 0.854

Grip strength

Right 94.3 22.2 99.3 17.5 0.149

Left 91.4 20.7 99.1 17.5 0.023

Psychological tests

Culture Fair 97.6 17.4 101.2 20.0 0.331

Digit symbol 100.8 10.2 101.5 9.2 0.678

Vocabulary 98.0 24.4 99.2 30.8 0.837

Verbal recall

Immediate 96.5 33.1 99.8 31.1 0.576

Delayed 99.8 46.2 99.9 41.3 0.980

Pegboard 99.9 14.5 101.8 25.7 0.690

Trails A 98.6 7.6 100.3 38.3 0.268

Trails B 99.6 7.9 100.4 7.5 0.596

Finger writing errors

Right 96.9 8.6 100.0 7.5 0.059

Left 98.0 9.0 100.0 7.8 0.234

Information 99.0 27.4 101.5 39.4 0.771

Picture completion 99.8 33.3 99.3 31.2 0.937

Similarities 95.5 31.7 98.1 41.2 0.707

Total abnormalities 2.8 3.5 1.2 1.6 0.0001

Profile of Mood States score 52.1 0.7 21.0 31.6 0.0001 *

Symptom frequency 5.0 1.4 2.6 1.2 0.0001 *

Note: SD = standard deviation.

* Percentage predicted is based on transformed values and, therefore,

may not reflect observed over predicted x 100.

([dagger]) R value for exposed lower (i.e., better) than unexposed.

Table 2.–Comparison of Frequencies of Symptoms in Exposed Flight

Attendants and Unexposed Subjects

Exposed Unexposed

Symptom Mean SD Mean SD P

Skin irritation 5.8 2.9 3.1 2.7 0.0001

Deformed finger nails 3.2 3.0 1.9 2.2 0.003

Chest tightness 3.0 2.9 2.2 1.8 0.0001

Palpitations 3.8 2.8 2.1 1.8 0.0001

Burning/tightness of chest 3.2 2.9 2.0 1.7 0.004

Shortness of breath 4.3 2.7 2.5 2.0 0.0001

Dry cough 4.5 2.7 2.6 1.8 0.0001

Cough with mucus 4.1 2.4 3.0 2.2 0.010

Cough with blood 1.6 1.4 1.2 0.7 0.017 *

Dry mouth 7.0 3.4 3.2 2.5 0.0003

Throat tight 5.7 3.0 2.8 2.0 0.0001

Eye irritation 6.3 3.0 2.8 2.3 0.0001

Decreased sense of smell 3.5 2.9 2.1 1.9 0.0003

Headache 6.8 2.8 4.1 2.7 0.0001

Nausea 4.2 2.7 2.4 1.9 0.0001

Dizziness 5.0 3.0 2.1 1.7 0.0001

Lightheadedness 5.5 3.0 2.5 1.9 0.0001

Exhilaration (unusual) 1.3 0.7 1.7 1.6 0.202 *

Loss of balance 4.2 2.9 2.3 1.9 0.0001

Loss of consciousness 1.5 1.2 1.3 1.0 0.208 *

Extreme fatigue 8.1 3.0 3.2 2.6 0.0001

Somnolence 6.9 3.4 2.5 2.1 0.0001

Insomnia 4.9 3.1 3.0 2.5 0.002

Wake frequently 5.4 3.5 2.8 2.3 0.0004

Sleep few hours 5.8 3.6 2.9 2.6 0.0001

Irritability 6.0 3.2 3.5 2.3 0.0001

Loss of concentration 7.4 3.4 3.5 2.7 0.0001

Loss of recent memory 7.6 3.1 3.5 2.7 0.0001

Long-term memory loss 6.1 0.4 2.5 2.2 0.0001

Unstable moods 4.5 3.2 2.6 2.4 0.0001

Loss of libido 7.1 3.4 3.2 2.7 0.0001

Decreased alcohol tolerance 6.4 3.5 2.5 2.8 0.0001

Indigestion 4.7 3.3 3.2 2.3 0.025

Loss of appetite 3.4 2.5 2.6 2.1 0.117 *

Swollen stomach 6.7 3.4 2.7 2.3 0.0001

Symptom frequency mean 5.0 1.4 2.6 1.2 0.0001

Notes: Comparison is rated on a scale of 1 to 11 by percentage

predicted of analysis of variance. SD = standard deviation.

* Not statistically significant.

Table 3.–Pulmonary Function Test Results of Exposed

Subjects, Compared with Unexposed Subjects, by

Percentage Predicted (Analysis of Variance)

Exposed Unexposed

Test Mean SD Mean SD p *

FVC 105.9 8.8 101.6 15.1 .118

[FEV.sub.1.0] 101.1 9.0 93.6 15.8 .009R

[FEF.sub.25-75] 94.6 9.0 88.1 35.0 .305

[FEF.sub.75-85] 74.7 22.8 78.1 22.8 .715

[FEV.sub.1.0]/FVC 77.0 4.6 72.8 9.5 .013R

Notes: Test = pulmonary function test, FVC = forced vital

capacity, [FEV.sub.1.0] = forced expiratory volume in 1 s, FEF =

forced expiratory flow, and SD = standard deviation.

* R = better than unexposed.

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COPYRIGHT 2005 Gale Group