Latex allergen in respirable particulate 

air pollution 

P. Brock Williams, PhD, Martin P. Buhr, PhD, Richard W. Weber, MD, 

Micheal A. Volz, MD, Jerald W. Koepke, MD, and John C. Selner, MD 

Denver, Colo. 

Objective." Urban air samples contain numerous irregular respirable black particles, which may 

be airborne tire fragments. A major component of tires is natural latex. Proteins of natural 

latex can act as adjuvants and as antigens capable of eliciting immediate hypersensitivity, 

making their presence in particulate air pollution an important clinical issue. 

Methods: Particulate air pollutants were collected by volumetric sampling devices and 

characterized by optical microscopy, chemical solubility tests, and mass" spectrometry. Extracts 

of rubber tire fragments were tested for elutable latex antigens by antibody inhibition assays. 

Results: Identification of latex in air samples and milled material from automobile tires was 

supported by mass spectrometry results and was further confirmed by physical appearance and 

chemical solubility studies. Competitive immunoassay confirmed the presence of extractable 

latex antigens from rubber tire fragments. 

Conclusions: Latex antigens are extractable from rubber tire fragments, which are abundant in 

urban air samples. Given the adjuvant and sensitizing effects of latex, these airborne particles 

could contribute, through direct and indirect mechanisms, to the increase in both latex 

sensitization and asthma. The impact of these particles should be considered in the issue of 

morbidity and mortality rates associated with respiratory diseases and air pollution. 

(J ALLERGY CLIN IMMUNOL 1995;95.'88-95.) 

Key words: Latex, rubber tires; air pollution, asthma 

Natural latex is used in a wide variety of products that have become part of our everyday environment. The main source of natural latex is the 

sap of the tropical rubber tree, Hevea brasiliensis, 

and over 7 million metric tons are produced annually? Native latex coagulates by forming polymers 

of cis-l,4 isoprene several thousand units in 

length. 2 Proteins comprise about 2% of the total 

solids of uncoagulated latex? Two of these proteins involved in the polymerization of isoprene 

units have been implicated in hypersensitivity reactions to latex products. 4, 5 

Sensitivity to latex had not been considered a 

major clinical problem until recent years. The 

From the Allergy Respiratory Institute of Colorado and University of Colorado Health Sciences Center, Department of 

Immunology, Denver. 

Received for publication Mar. 4, 1994; revised June 16, 1994; 

accepted for publication June 23, 1994. 

Reprint requests: P. Brock Williams, PhD, Allergy Respiratory 

Institute of Colorado, 5800 East Evans Ave., Suite 100, 

Denver, CO 80222. 

Copyright © 1995 by Mosby-Year Book, Inc. 

0091-6749/95 $3.00 + 0 1/1/58674 

88 

marked increase in the use of latex products, 

particularly in the health care industry, has likely 

contributed to the increase in latex sensitization. 6 

Clinical reactions vary from skin rashes and mild 

rhinitis to more severe bronchial asthma and lifethreatening anaphylactic reactions. 7, 8 Risk factors 

identified include frequency of exposure and atopy.9 Recent studies indicate that up to 14% of 

health care workers are affected, as well as 64% of 

patients with spina bifida who undergo repeated 

surgery and catherization. 1°, 11 Latex sensitization 

of nearly 10% has been reported in atopic individuals undergoing routine aeroallergen skin testing. 9 

Relatively low concentrations of respirable particulate matter have been significantly associated 

with increases in daily mortality rates, acute bronchitis, and hospital visits for treatment of lower 

respiratory tract symptoms. 12-~5 Both morbidity 

and mortality rates for respiratory asthma have 

increased dramatically, particularly in urban areas 

throughout the world, a6-22 Children seem to be at 

particular risk, and particulate air pollution of 2 to 

10 ~m has been implicated. 2329 

A significant portion of particulate air pollution 
J ALLERGY CLIN IMMUNOL Williams et al. 89 

VOLUME 95, NUMBER 1, PART I 

in urban areas may consist of small irregularly 

shaped black particles. The most likely source of 

these particles is the abrasion of rubber tires on 

road surfaces. Tires are made of various mixtures 

of natural and synthetic rubber along with sulfur, 

carbon black, and zinc oxide. This results in a 

flexible yet sturdy material that can withstand heat 

and friction well. 3° However, tire wear releases 

particles of varying size, which may add to atmospheric pollution burden. 

In this study we confirmed that a large number 

of respirable tire fragments are found in urban air. 

We investigated the hypothesis that these fragments contain latex proteins. These particles could 

be partially responsible for the increase in latex 

sensitization, as well as the respiratory problems 

associated with air pollution. 

METHODS 

Physical and chemical characterization of 

particles 

Particulate samples were collected by three different 

procedures: rotary impaction sampling (Rotorod; Sampling Technologies Inc., Los Angeles, Calif.); highvolume air sampling with a PM~o sampler equipped with 

an inlet that discriminated against particles larger than 

10 Ixm (Sierra Instruments, Monterey, Calif.); and passive gravimetric air sampling with glass plates (20 × 

20 cm) coated with silicone grease. The impaction 

sampler was stationed 7.4 m above ground level, 48 m 

from a four-lane, moderately travelled road. The PMlo 

samplers were located at two different Colorado Department of Health sampling stations in the Denver metropolitan area. Rotorod samples were stained with Calberla's solution to facilitate pollen and particulate 

counting. 31 The glass plates were exposed at ground 

level 30 m from roadside air for 6 hours, and samples 

were harvested by scraping with a flat surgical blade. 

The size of the particles was determined with an 

optical microscope and a 45× achromatic lens. The 

eyepiece (10x) of the microscope was fitted with a 

graduated reticle to permit measurement of particle 

sizes. The reticle was calibrated with a 22 mm glass slide 

cover. Particle sizes were reported as their orthogonal 

mean diameters. Particle counts were performed by 

counting 1000 consecutive particles on five separate 

samples (n = 5000). 

Chemical identification of the particles was attempted 

by both qualitative solubility tests and semiquantitative 

gas chromatography/mass spectrometric analysis. The 

solvents used for the solubility tests included 5N HCL, 

5N NaOH, 20% sodium lauryl sulfate, 1,3-dichlorobenzene, 1,2-dichlorobenzene, chloroform, and 95% ethanol. Extracts in 1,3-dichlorobenzene of an authentic latex 

sample derived from latex gloves, a tire dust sample, and a 

PMao air sample were analyzed with a Hewlett Packard 

5890/5882 gas chromatography/mass spectrometry system 

(Hewlett-Packard Co., Palo Alto, Calif.). Extraction of 

samples was performed with a heated (50 ° C) ultrasonic 

bath. The chromatographic analysis was performed with an 

HP-1 capillary column operated in a temperature-controlled oven, programmed from 120 ° to 280°C at 10 

degrees per minute. The mass spectrometry detector was 

operated in electron impact mode and maintained at 

250 ° C. The mass range recorded was from mass to charge 

ratio = 30 to 500. 

Protein extraction and antigen studies 

A rubber tire (Turanza-QL10, steel-belted radial; 

Bridgestone Tires, Warren County, Tenn.) with moderate wear was milled with a fine-tooth electric handsaw. 

Fragments were collected on filter paper (Whatman Qualitative; Whatman PLC, Maidstone, Kent, England). A 100 

gm sample was extracted for 30 seconds with 200 ml of 

distilled water in a high-speed blender (Vitamix, Cleveland, 

Ohio). The preparation was filtered (Whatman Qualitative), dialyzed in cellulose dialysis tubing against distilled 

water (Spectropor with a nominal molecular weight cutoff 

of 1000 kd; Spectrum, Houston, Texas), concentrated 

fore'fold by evaporation at room temperature and lyophilized. The rubber glove extract was prepared according to 

the method of Kurup et ald 2 with powderless latex medical 

gloves (Aladan Co., Dothan, Ala.). Competitive inhibition 

assays were performed in duplicate with the Pharmacia 

CAP system (Kabi Pharmacia, Uppsala, Sweden). Equal 

volumes of serum and either lyophilized tire extract dissolved in saline solution, latex rubber glove extract dissolved in saline solution, or saline solution alone were 

incubated overnight at 4 ° C. Fifty-microliter aliquots of 

these samples were assayed in duplicate with native latex 

(Hevea brasiliensis) protein extract as the solid-phase allergen source (Pharmacia CAP system). Individual serum 

samples containing latex-specific IgE from patients with 

clinical histories of latex reactivity were used. Identical 

inhibitions were performed with a serum sample containing 5.3 kUa/L Altemaria-specific IgE for specificity controls. Inhibition was calculated with the formula: 

Percent inhibition 

= 100 x (1 - [response sample/response saline]) 

RESULTS 

The particles observed in the ambient air samples were black, rarely spherical, and typically 

coarse with ragged edges (Fig. 1). The airborne 

quantity ranged from 3800 to 6900 particles per 

cubic meter. Their size varied greatly, but over 

90% were between 2.2 and 35.2 Ixm in mean 

orthogonal diameter with a mode of 6.6 p~m (Fig. 

2). A birch pollen grain, which is consistently 

around 35 p~m (in Calberla's solution), was included in the photograph for reference. 31 A high 

percentage (58.5%) of the particles were in the 
90 Williams et al. J ALLERGY CLIN IMMUNOL 

JANUARY 1995 

FIG. 1. Photomicrograph of ambient air sample collected on impact sampler. A birch pollen 

grain (35 txm in diameter) was included for reference. (x450.) 

AIRBORNE TIRE DEBRIS SIZE DISTRIBUTION 

AMBIENT VOLUMETRIC SAMPLER COLLECTION 

Percentage of Total Particles (n=5000) 

20% 

10% 

15% 

5% 

0% 

2.2 6.6 11 15.4 19.8 24.2 28.6 33 

FIG. 2. Distribution of tire debris size from impact sampler (n = 5000). Particle sizes were determined with a 

calibrated reticule with light microscopy. (x450.) 

respirable range of less than 10 ~m. 33 There was a 

sharp drop in the number of particles below 4 p~m. 

Attempts to tease this material apart under the 

microscope indicated that it was pliable and resilient, regaining its original shape after stretching. In 

chloroform and the dichlorobenzenes the fragments underwent swelling, as is characteristic of 

cross-linked hydrophobic polymers. The smaller 

particles, in the range of 2 txm, seemed more 

rounded in shape and resembled oil droplets. 

However, these did not dissolve in any of the 

solvents, indicating that they were not simple bydrocarbons. The fragments produced in the laboratory exhibited similar characteristics and behaved similarly in the solvent tests. 

The total ion chromatograms for each of the 

three samples analyzed with gas chromatography/ 

mass spectrometry are shown in Fig. 3. The broad 

peak located between 16.5 and 18.5 minutes' retention time in each of the chromatograms is 

characteristic of a polymeric substance and produced similar mass spectra in each of the three 

samples. The most abundant ions in the mass 

spectra were at mass to charge ratio = 75, 149, and 

265, which is consistent with spectra observed for 

latex and cross-linked rubber. 34 

The results of the inhibition experiments are 

presented in Table I. All but one of the sera 

containing latex-specific IgE were inhibited by the 

rubber tire extract, with varying degrees of inhibition. For each serum sample, the inhibition was 

generally equivalent to that achieved with a latex 

glove extract (1 mg of protein per milliliter) but 

occasionally higher with the rubber tire fragment 

extract. The specificity of this cross-reactivity was 

confirmed by demonstrating no inhibition of Alternaria-specific IgE by the rubber tire extract. 

DISCUSSION 

This study supports the hypothesis that latex 

allergens are present in particulate air pollutants in 
J ALLERGY CLIN IMMUNOL Williams et al. 91 

VOLUME 95, NUMBER 1, PART 1 

8000 Latex rubber glove sample 

6o00 

e~ 

< 4000 4 

s 

2ooo~ i 

~ tD 0 1~5 " 20 

5000- 

4000.: 

3000 

2000 

1000 

0 

i Milled tire sample 

10 15 20 

5000 

4000 

3O0O 

200O 

1000 

Iiil i Ambient air sample 

lli! 

lo 15 2-b 

Retention time (minutes) 

FIG. 3. Total ion chromatograms for each of the three samples extracted in dichlorobenzene. 

The broad peak observed in each of the samples at 16 to 18 minutes of retention time is 

indicative of a polymeric structure. The mass spectra obtained for the species in these peaks 

were similar in each of the samples and were consistent with mass spectra observed for 

authentic latex samples. 

urban areas. The abundance of these black particles at a station 7.4 m above the surface ranged 

from 3800 to 6900 per cubic meter. The most 

prevalent size in our samples was 6 to 7 Ixm mean 

orthogonal diameter, and over 58.5% were of a 

size that is fully respirable. 33 Our hypothesis is that 

these particles represent abraded tire fragments, 

and it is supported by mass spectroscopic, physical, 

and chemical data. The mass spectroscopy indicated a similar spectrum for rubber tire fragments, 

latex gloves, and material collected from ambient 

air with a PMlo sampler. Physically, the particles 

were resilient, regaining their original shape after 

they were teased apart; and the inability of a 

variety of solvents to dissolve these fragments 

suggests that they are composed of highly structured polymeric material. 

The use of natural latex as a constituent of most 

tires presents the possibility that tire fragments 

could be immunologically active. This possibility 

was verified by demonstrating elutable latex antigen activity by the inhibition assays. Collectively, 

these data strongly indicate that respirable tire 

fragments, containing readily elutable latex antigens, are present in large quantities in urban air. 

Earlier studies on tire wear characterization 

failed to detect tire particles in the respirable 

rangeY 37 In a series of studies in 1974, Pierson 
92 Williams et al. J ALLERGY CLIN IMMUNOL 

JANUARY 1995 

TABLE I. Inhibition of latex-specific IgE with glove and tire fragment extracts 

Response to Response to % Inhibition Response % Inhibition 

Sample saline GE glove TE tire 

1 4,378 177 95.96 277 93.67 

2 4,762 815 82.88 594 87.53 

3 4,853 1,028 78.81 640 86.81 

4 6,665 1,345 79.82 1,742 73.86 

5 10,180 6,725 33.94 4,899 51.87 

6 11,848 10,071 14.99 7,955 32.86 

7 14,414 12,058 16.34 14,311 0.71 

GE, Glove extract; TE, tire extract. 

and Brachaczek 3s concluded that although tire 

wear was a significant pollutant (600,000 metric 

tons per year in the United States), most of this 

was in the form of nonsuspendable particles deposited adjacent to roadways. The majority of 

these data were derived from samples collected at 

ground level. They concluded that the average 

airborne amount (50,000 tons/yr) is equivalent to 

20% of airborne particulate matter from gasoline 

engine exhaust, which is a substantial amount of 

airborne material. Consumption of natural rubber 

for tires and associated products worldwide has 

increased since this time and measures approximately 3.9 million metric tons yearly. 39 In 1981, 

an Environmental Protection Agency laboratory 

study characterized tire wear particulates with the 

use of a stainless steel wearing surface. 4° This study 

failed to demonstrate rubber particles in the 1 to 

10 ~m range but suggested that the lack of small 

particles may have resulted from their experimental design. It is possible that freshly worn rubber 

particles without additional abrasive material 

would form aggregates, excluding small particles 

on cascade-type collectors. When cornstarch was 

added to their system as an abrasive, smaller 

particles were in fact observed. More recent studies indicate that tire dust of respirable size is a 

significant contribution to the carbonaceous aerosol of less than 3.5 txm in Los Angeles. 41 

Rubber tires are manufactured with varying 

concentrations of natural latex (cis 1,4-polyisoprene) and synthetic rubber (1,4-styrene polybutadiene). 3° Truck tires have highe r amounts of natural latex. 4° The natural latex is desirable because 

it causes less friction and can withstand higher 

temperatures but has the propensity to release 

smaller particles on abrasive wear. Wear of radial, 

as opposed to bias ply, constructed tires also 

results in smaller particles, g° The increased prevalence of radial tire use over the past 2 decades 

could account for the smaller particle sizes seen in 

our study. 

The fact that we were able to extract functionally 

intact latex antigens from abraded tire fragments 

was somewhat surprising, considering the high 

temperatures of vulcanization (130 ° C) and extensive cross-linking. 5 This extends other findings that 

latex allergens are thermally stable. 8 The serum 

samples used for these experiments were from 

patients clinically sensitive to products containing 

natural latex. All contained high amounts of IgE 

specific to latex-derived antigens. Our experiments 

demonstrate essentially equivalent results at maximal inhibition with latex glove antigens and the 

rubber tire extract in all the serum samples tested. 

This indicates that a close relationship exists between the specificities of the antibodies being 

inhibited. Further studies are in progress to define 

the quantitative relationships on a protein basis. 

Chronic exposure to respirable fragments of 

rubber that contain carbon black, latex antigens, 

and sulfur would be expected to have a number of 

health consequences. Respirable particles can act 

as irritants, inducing nonspecific inflammation. 

Small particles suspended in polluted air have 

been significantly linked to hospital admissions for 

treatment of asthma, particularly in young children. 42 Furthermore, several studies have linked 

fine particulate air pollution to increased mortality 

rates in infants, as well as in the general population 

in a number of U.S. cities. 23-25 It has been demonstrated that respiratory irritants stimulate IgE responses to environmental allergens. 43, 44 Thus the 

rubber particles by themselves or in conjunction 

with other particulates could contribute to allergic 

responses in respiratory tissues by acting as nonspecific adjuvants. 

Latex allergens may also act as specific adjuvants 

for IgE responses. Kurup et al. demonstrated high 

levels of IgE and blood eosinophilia in mice ex- 
J ALLERGY CLIN IMMUNOL Williams et ai. 93 

VOLUME 95, NUMBER 1, PART 1 

posed to latex proteins by intranasal and intraperitoneal routes. 45 The latex antigen exposed mice 

developed high levels of interleukins 4 and 5, 

consistent with the stimulation of CD4 ÷ T.e lymphocytes. Preferential stimulation of CD4 + T~etype lymphocytes results in enhanced production 

and secretion of IgE (interleukin-4 effect) and 

eosinophil differentiation (interleukin-5 effect). 46 

Thus latex allergens, by acting as an adjuvant for 

IgE responses, might contribute to allergic responses to unrelated allergens. 

Japanese studies have suggested an adjuvant 

effect of diesel fuel particulates. 47 These authors 

demonstrated that enhanced IgE responses occur 

in animals exposed to diesel fuel exhaust particulates. Experiments with suspended particulate matter from urban districts of Japan have also been 

shown to have potent adjuvant effects on IgE 

responses. 4s A dose of 0.25 txg given intranasally at 

3-week intervals was sufficient to obtain an appreciable IgE effect. The air along busy roads had 

concentrations of 200 to 480 txg/m 3 of this material. 48 Although not addressed by the authors, these 

samples of ambient polluted air were likely to 

contain rubber tire fragments, which could have 

contributed to the adjuvant effects observed. 

The interaction of airborne particulate matter 

with pollen grains has been studied, indicating a 

direct interaction between pollen surfaces and 

airborne particulates causing preactivation and 

altered antigenicity. 49, 5o Such effects were prominent in industrialized regions and near roads with 

heavy traffic. 51 These interactions, coupled to the 

adjuvant effects predicted for rubber tire fragments, might explain the elevated incidence of 

pollinosis in urban areas, as seen in a study that 

compared the incidence of Japanese red cedar 

(Cryptomeria japonica) pollinosis in urban and 

rural areas, s2 Pollen counts were similar in both 

areas, but an incidence of 13.2% among residents 

located near intercity roads was seen, whereas the 

incidence of cedar pollinosis among forest residents (exposed to little or no motorized traffic) was 

5.1%. These results support the concept that pollinosis is augmented by air pollution and automobile by-products. 

An additional consequence of exposure to latexcontaining airborne particles could be direct sensitization to latex antigens. The prevalence of latex 

sensitization has been increasing at an alarming 

rate. Recent reports indicate that up to 14% of 

health care workers and nearly 10% of atopic 

individuals are sensitized to latex; and the rate of 

sensitization in atopie individuals who are frequently exposed to latex has reached 36%. 9 Although increased use of latex gloves and other 

products has been suggested, an additional risk 

factor may be breathing urban air polluted with 

respirable tire fragments containing latex antigens. 

These fragments could be acting both specifically 

and nonspecifically as an adjuvant for enhancing 

IgE responses. For example, a nonspecific irritant 

effect could enhance sensitization to inhaled antigens, which could include latex itself. 

A variety of inhaled particulates have been 

linked to adverse health effects including declining lung function, shortness of breath, wheezing, 

asthma attacks, chronic obstructive pulmonary disease, increased rates of hospitalization, and increased mortality rates. 12-29 These may be due to 

inert physical properties, direct toxic effects, carcinogens, or stimulation of inflammatol~y reactions. 

We suggest that respirable rubber tire fragments, 

not mentioned in these prior studies, may represent a potent stimulus for both specific and nonspecific inflammatory responses, which are not 

mutually exclusive possibilities. In light of the 

potential adjuvant and antigenic properties of 

these fragments, serious consideration must be 

given to the possible role of these particles in the 

initiation and perpetuation of respiratory tract 

diseases such as asthma, allergic rhinitis, and allergic conjunctivitis. The role of these particles in the 

sensitization to latex revealed by subsequent acute 

systemic reactions to latex exposure in a medical 

context must also be considered. These observations permit the organization of systematic epidemiologic and immunologic studies to clarify the 

role of latex-bearing particulate air pollutants in 

pulmonary diseases and clinical latex allergy. 

We thank Timothy Sullivan, MD, (Emory University 

School of Medicine) for his advice and review of the 

manuscript; Don Steadman, PhD, (University of Denver); Robert Barkley, PhD, and Robert Sievers PhD, 

(University of Colorado) for their assistance and advice. 

We also thank Kabi Pharmacia for providing reagent 

support; Steven Arnold of the Colorado Department of 

Health for providing Denver ambient air filters; and 

Henry Van Engelen (Wolverine, Mich.) for his help in 

preparing the tire fragments. 

REFERENCES 

1. Greek BF, Rubber demand is expected to grow after 1991. 

Chem Engin News 1991;69:37-54. 

2. Light DR, Dennis MS. Purification of a phenyltransferase 

that elongates cis-polyisoprene rubber from the latex of 

Hevea brasiliensis. J Biol Chem 1989;264:18589-97. 
94 Williams et al. J ALLERGY CLIN IMMUNOL 

JANUARY 1995 

3. Semegen ST. Natural rubber. In: Morton M, ed. Rubber 

technology. New York: Von Nostrand Reinhold, 1973:152- 

77. 

4. Jaeger D, Kleinhans D, Czuppon AB, Xaver B. Latex 

specific proteins causing immediate-type cutaneous, nasal, 

bronchial, and systemic reactions. J ALLERGY CLIN 1MMUROE 1992;89:759-68. 

5. Czuppon AB, Chen Z, Rennert S, et al. The rubber elongation factor of rubber trees (Hevea brasiliensis) is the major 

allergen in latex. J ALLERGY CLIN IMMUNOL 1993;92:690-7. 

6. Iacobelli AM, McCuIlough JA, Ownby DR. The prevalence 

of latex allergy in high risk medical personnel [Abstract]. J 

ALLERGY CLIN IMMUNOL 1993;91:216. 

7. Eghrari-Sabet JS, Slater JE. Latex allergy: a potentially 

serious respiratory disorder. J Respir Dis 1993;14:473-82. 

8. Hamann CP. Natural rubber latex protein sensitivity in 

review. Am J Contact Dermatitis 1993;4:4-21. 

9. Moneret-Vautrin D-A, Beaudouin E, Widmer S, et al. 

Prospective study of risk factors in natural rubber latex 

hypersensitivity. J ALLERGY CLIN IMMUNOL 1993;92:668-77. 

i0. Yassin MS, Sanyurah S, Lieri MB, et al. Evaluation of latex 

allergy in patients with meningomyelocele. Ann Allergy 

1992;69:207-11. 

11. Turjanmaa K. Incidence of immediate allergy to latex gloves 

in hospital personnel. Contact Dermatitis 1987;17:270-5. 

12. Dockery DW, Pope CA, Xu X, et al. An association 

between air pollution and mortality in six U.S. Cities. N 

Engl J Med 1993;329:1753-9. 

13. Pope CA III, Dockery DW. Acute health effects of PM-10 

pollution on symptomatic and asymptomatic children. Am 

Rev Respir Dis 1992;145:1123-8. 

14. Chestnut LG, Schwartz J, Savitz DA, Burchfiel CM. Pulmonary function and ambient particulate matter: epidemiological evidence from NHANES I. Arch Environ Health 

1991;46:135-44. 

15. Xu XP, Dockery DW, Wang LH. Effects of air pollution on 

adult pulmonary function. Arch Environ Health 1991;46: 

198-206. 

16. Weiss KB, Wagener DK. Changing patterns of asthma 

mortality. JAMA 1990;294:1683-7. 

17. National Center for Health Statistics. Economic costs of 

respiratory diseases. Washington DC, U.S. Government 

Printing Office, 1986. 

18. Centers for Disease Control. Asthma-United States, 1980- 

1987. MMWR 1990;39:493-7. 

19. Gergen P J, Mullally DI, Evans R. National survey of 

prevalence of asthma among children in the United States, 

1976-1980. Pediatrics 1988;81:1-7. 

20. Williams MH. Increasing severity of asthma from 1960- 

1987. N Engl J Med 1989;320:1015-6. 

21. Fleming DM, Crombie DL. Prevalence of asthma and hay 

fever in England and Wales. Br Med J 1987;294:279-83. 

22. Kagamimori S, Katoh T, Naruse Y, et al. The changing 

prevalence of respiratory symptoms in atopic children in 

response to air pollution. Clin Allergy 1986;16:299-308. 

23. Rennick G J, Jarman FC. Are children with asthma affected 

by smog? Med J Aust 1992;156:837-41. 

24. Braun-Fahrlander C, Ackermann-Liebrich U, Schwartz J, 

Gnehm HP, Rutishauser M, Wanner HU. Air pollution and 

respiratory symptoms in preschool children. Am Rev Respir Dis 1992;145:42-7. 

25. Dockery DW, Ware JH, Ferris BG Jr, Speizer FE, Cook 

NR, Herman SM. Change in pulmonary function in children associated with air pollution episodes. J Air Pollut 

Control Assoc 1982;32:937-42. 

26. Schwartz J. Particulate air pollution and daily mortality in 

Detroit. Environ Res 1991;56:204-13. 

27. Fairley D. The relationship of daily mortality to suspended 

particulates in Santa Clara County, 1980-1986. Environ 

Health Perspect 1990;89:159-68. 

28. Schwartz J, Dockery DW. Particulate air pollution and 

daily mortality in Steubenville, Ohio. Am J Epidemiol 

1992;135:12-9. 

29. Pope CA III, Schwartz J, Ransom MR. Daily mortality and 

PM-10 pollution in Utah Valley. Arch Environ Health 

1992;47:211-7. 

30. Stephens HL. The compounding and vulcanization of rubber. In: Norton M, ed. Rubber technology. New York: Von 

Nostrand Reinhold, 1973:19-50. 

31. Smith EG. Sampling and identifying allergenic pollens and 

molds. San Antonio: Blewstone Press, 1984:22. 

32. Kurup VP, Kelly KJ, Resnick A, Bansal NK. Characterization of latex antigen and demonstration of latex-specific 

antibodies by enzyme-linked immunosorbent assay in patients with latex hypersensitivity. Allergy Proc 1992;13:329- 

34. 

33. Martini R. Fundamentals of anatomy and physiology. 2nd 

ed. Englewood Cliffs, New Jersey: Prentice-Hall, 1992;758- 

69. 

34. Akhtar S, Micheal RS, Ooij WJ. Static SIMS of some 

aliphatic hydrocarbon polymers. Polym Mater Sci Eng 

1988;59:1135-8. 

35. Dannis ML Rubber dust from normal wear of tires. 

Rubber Chem Tech 1974;47:1011-37. 

36. Cadle SH, Williams RE Gas and particle emissions from 

automobile tires in laboratory and field studies. GM Research Publication GMR-2542R, May 1978. 

37. Evans JV, Hites RD. Emission of pollutants from tire wear 

phase I preliminary report M71-166 EPA Project 6132, Oct 

1971. Ann Arbor: Calspan Corporation, 1971. 

38. Pierson WR, Brachaczek WW. Airborne particulate debris 

from rubber tires. Rubber Chem Technol 1974;47:1275-99. 

39. Reisch MS. Rubber, slow growth ahead. Chem Engineer 

News 1993;71:24-33. 

40. Bogdan L, Albrechinski TM. Characterization of tire wear 

particles. US Dept of Commerce EPA PB82-153586, 1981. 

41. Hildemann LM, Markowski GR, Cass GR. Chemical composition of emissions from urban sources of fine organic 

aerosol. Environ Sci Tech 1991;25:744-59. 

42. Tseng RY, Li CK, Spinks JA. Particulate air pollution and 

hospitalization for asthma. Ann Allergy 1993;68:425-32. 

43. Zetterstrom O, Osterman K, Machado L, Johansson SG. 

Another smoking hazard: raised serum IgE concentration 

and increased risk of occupational allergy. Br Med J 

198l;283:1215-7. 

44. Takafuji S, Suzuki S, Koizumi K, et al. Enhancing effect of 

suspended particulate matter on the IgE antibody production in mice. Int Arch Allergy Immnnol 1989;90:1-7. 

45. Kurup VP, Kumar A, Choi H, et al. Latex antigens induce 

IgE and eosinophils in mice. Int Arch Allergy Immunol 

1994;103:370-7. 

46. Mario R. T cells, cytokines, IgE and allergic inflammation. 

Int Arch Allergy Appl Immunol 1992;99:165-71. 

47. Muranaka M, Suzuki S, Koizumi K, et al. Adjuvant activity 

of diesel exhause particulates for the production of IgE 

antibody in mice. J ALLERGY CLrN IMMUNOL 1986;77:616- 

23. 

48. Takafuji S, Suzuki S, Ko/zumi K, et al. Diesel-exhaust 

particulates innoculated by the intranasal route have an 
J ALLERGY CLIN IMMUNOL Williams et aL 95 

VOLUME 95, NUMBER 1, PART 1 

adjuvant activity for IgE production in mice. J ALLERGY 

CLIN IMMUNOL 1987;79:639-45. 

49. Behrendt H, Becket WM, Friedrichs KH, Darsow U, 

Tomingas R. Interaction between aeroallergens and airborne particulate matter. Int Arch Allergy Appl Immunol 

1992;99:425-8. 

50. Wolters JHB, Matens MJM. Effects of air pollutants on 

pollen. Botany Rev 1987;53:372-414. 

51. Kainka-Stanicke E, Behrendt H, Fredrichs KH, Tomingas 

R. Morphological alterations of pollen and spores induced 

by airborne pollutants: observations from two differently 

polluted areas in West Germany. Allergy 1988;43:57. 

52. Ishizaka T, Koizumi K, Ilkemori R, Ishiyama Y, Kushibiki 

E. Studies of prevalence of Japanese cedar pollinosis 

among residents in a densely cultivated area. Ann A!lerg7 

1987;58:265-70. 

Bound volumes available to subscribers 

Bound volumes of THE JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY are available to 

subscribers (only) for the 1995 issues from the Publisher, at a cost of $73.00 for domestic, $99.51 

for Canadian, and $93.00 for international subscribers for Vol. 95 (January-June) and Vol. 96 

(July-December). Shipping charges are included. Each bound volume contains a subject and author 

index, and all advertising is removed. Copies are shipped within 30 days after publication of the last 

issue in the volume. The binding is durable buckram with the journal name, volume number, and 

year stamped in gold on the spine. Payment must accompany all orders. Contact Mosby-Year Book, 

Inc., Subscription Services, 11830 Westline Inductrial Dr., St. Louis, MO 63146-3318; phone 

1 (800) 453-4351 or (314) 453-4351. 

Subscriptions must be in force to qualify. Bound volumes are not available in place of a regular 

journal subscription.