Pollution: The nose and sinuses DONALDA. LEOPOLD, MD. Baltimore, Maryland

The nose and sinuses are constantly exposed to the huge quantities of gases needed to maintain life. Not only Is the human nose well-equipped to warm and humidify this Inhaled air, but It Is also uniquely able to clean much of It. Any material other than physiologic amounts of oxygen, nitrogen, carbon dioxide, and water that accompanies the airstream can be considered a pOllutant, and this pollutant could potentially Inlure the Individual. The following discussion will review the defense mechanisms that allow the nose and sinuses to protect the lower airways. The effects of pollutants on the respiratory mucosa will then be described, Including some recent trends In those effects. These trends Include specific population consequences of Indoor and outdoor air pollution, and changes In risk for Individuals In several occupations. Throughout these discussions, specific areas that would benefit from further research will be mentioned. (OTOlARYNGOL HEAD NECK SURGERY 1992;106:713.)

NATURAL DEFENSE MECHANISMS OF NASAL AND SINUS MUCOSA

Airflow Patterns and Anatomic Factors As air enters the nasal cavity, it is immediately forced into a narrow space between the anterior septum and the lateral nasal wall. This nasal valve region causes the velocity of the airstream to increase. There is also an angulation of the airflow path as the air impacts against the anterior septum and speeds toward the middle meatus. These two factors, narrowed airspaces and angulation of the airstream, force inhaled pollutants against the moist, sticky surfaces of the nose and are the initial mechanisms for cleaning pollutants from the inhaled air. Once inside the nasal cavity, the airstream is squeezed into the 2 mm wide air channels from the palate to the cribriform region (Fig. 1).1 These narrow air passageways not only facilitate heat and moisture transfer, but they also optimize any pollutant contact with the mucosal walls. As the airstream approaches the nasopharynx, another sharp bend is made downward past the tonsils, adenoids, base of tongue, and toward the larynx. These lymphatic structures, as noted later, help in the immunologic defense of the airways.

From the Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University Medical School, Francis Scott Key Medical Center. Received for publication Jan. 28, 1992; accepted Feb. 3, 1992. Reprint requests: Donald A. Leopold, MD, Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University Medical School, Francis Scott Key Medical Center, 4940 Eastern Ave., A5W, Suite 595A, Baltimore, MD 21224. 23/1/36884

Renexe. The nasal cavity is lined with trigeminal and (at the top) olfactory sensors that are constantly assessing the incoming airstream. If that airstream were to become suddenly acrid or cold, breathing would momentarily cease, thus protecting the lungs from a potentially dangerous situation. Similar stimuli may also cause changes in heart beat, laryngeal aperture, or blood pressure. Although the mucosa covering the turbinates routinely swells and decongests throughout the day, sudden changes in the conditions of the airstream can cause alterations in the nasal airways. One of the most effective mechanisms for cleaning the nasal cavity is the sneeze. When the trigeminal nerve senses material (e.g., particles, mucus) in the nose-especially in the region of the anterior middle turbinate or nasal valve region-the deep inhalation and explosive exhalation through the nose is usually effective in clearing the airway. Muoocillary Clearance The nose and sinuses are lined with a respiratory epithelium that projects fine cilia into the nasal and sinus cavities. Overlying this ciliated surface is a double layer of nasal mucus, that is, at least in part, secreted by the submucosal seromucinous glands. The layer that surrounds the cilia is of low viscosity and allows free movement of the cilia, whereas the layer adjacent to the airstream touches just the tips of the cilia, is of higher viscosity, and is more mucinous. This arrangement allows the cilia to move the overlying mucinous layer with their outstretched tips during the "power" phase of the stroke, and to swing like a whip in the 713

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714 LEo'POLD

Streamline Patterns tor Resting Inspiratory Fluw Through Nasal Models

Fig. 1. Streamline patterns for resting nasal airflow through a large scale model (20 times normal size) of a healthy human nasal cavity, Lines show paths taken by small dust particles entering at the external nares,

periciliary fluid during the recovery phase." The rate of clearance of mucus. and the particles that become entrapped in it. has been shown (within limits) to be relatively independent of the size. density. and nature of the transported particles.' Changes in mucociliary clearance rates. rather. seem to be more dependent on variations in mucus secretions. systemic dehydration. and air pollutants. Large intcrindividual and intraindividual variations in nasal mucociliary clearance rates must he considered when these studies are evaluated. however.' The direction of mucus !low in the nose and sinuses seems to be constant.' In the anterior I or 2 ern of the nasal cavity. the flow is outward toward the nostrils. Otherwise. the flow is directed inferiorly and posteriorly toward the pharynx. where the mucus can he swallowed. Messcrklinger' has described some recirculation of mucus back into some sinuses. and Proctor' has suggested that this may be a way of continually renewing the nasal mucus surface. Particles and droplets that come into the nose along with the airstream impact on the mucus surface as a function of their aerodynamic equivalent diameter (AED). Approximately HO% of these particles and droplets that have an AED of 9 urn or greater stick to the nasal walls. whereas about half of particles 2 to 9 urn AED arc removed from the airstream. and only 4WIf· of particles less than 2 urn AED stick to the nasal walls. h In addition. as particles and droplets move through the nose. the hygroscopic particles will accumulate mois-

ture , becoming bigger and heavier. This also enhances the chance of impaction onto the sticky nasal walls. with resultant removal of the particle or droplet from the airstream. 7

Xenoblotlc Metabolism Xcnobiotics (foreign chemicals) in the nose have been received increased attention recently. with concerns over indoor air pollution and exposure to formaldehyde. Inhaled gas pollutants will be removed from the nasal airstream for many of the same reasons as particles and droplets. In addition. most polluting gases arc water soluble. such as sulfur dioxide or formaldehyde. and are solubilized on the wet surfaces of the nose. x This results in very little of these gases getting to the lungs. In the nasal mucus. and perhaps in the epithelial cells. these chemicals can have considerable effect in destroying the natural defenses of the nose. Many of the dusts that cause nasal irritation may accomplish this by chemically damaging the delicate balance of respiratory mucus and ciliated epithelium. Nasal carcinogenesis probably occurs with some toxic exposures as a result of the changes that occur in the epithelial genetic elements.

Immune Defenses A pollutant that is removed from the airstream onto the nasal mucosa is also subject to immune defenses that can remove or inactivate the pollutant. Humoral

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Pollution: The nose and sinuses 715

immune mechanisms, represented mostly by the IgA immunoglobulin, have a virus-neutralizing effect. Along with IgE, these antibodies can be specific for respiratory allergens." IgA also appears to prevent bacteria from colonizing mucosal surfaces and inhibits their growth. 10 Cellular immune mechanisms in the nose can act against infection from organisms like gram-negative bacteria, staphlococcal bacteria, fungi, or some enveloped viruses to protect the individual. Other immunoactive materials in the nasal secretions include (1) interferon. which is active against viruses, (2) lactoferrin, which has a broad spectrum of antibacterial activity, and (3) lysozymes, which lyse bacteria. All of these mechanisms are useful in fighting pollution, because the harmful part of many pollutants, like cotton dust, is actually biological. More study is needed to further define the extent of these mechanisms. whether they are effective against nonbiological pollutants, and how they may be better used.

EFFECTS OF POLLUTANTS ON THE RESPIRATORY MUCOSA Table I lists some of the pollutants that have been shown to have some effect on the nose and sinuses. Many of these pollutants also have pulmonary and systemic effects that are not listed here. In this next section, the specific effects that pollutants have on the nose and sinuses will be discussed in greater detail. Irrltaflon of the Mucu. Membrane. Most of the pollutants listed in Table I are either particulates or irritant aerosols. Because the nose is well innervated by the trigeminal nerve, responses of "irritation" by the subjects to a wide range of pollutants is not surprising. Indeed, Anderson and Proctor" noted that during their controlled climate chamber studies, the subjects "reported the same complaints, nasal irritation, and dryness of the nose irrespective of the substance studied." Many pollutants, like spice dust, newspaper dust, coffee dust, borax dust, and fiberglass dust, are simple irritants and have not been shown to have any other effects, such as being allergic, ciliotoxic, or neoplastic. Most of the other pollutants, however, are not only irritating, but also have some of these other effects. Cigarette smoke, for instance, which can provoke congestion, rhinorrhea, and sneezing (especially in sensitive individuals), does not stimulate an allergic response, but can decrease mucociliary function. Change. In Na.al Alrftow Re.lstance Rhinomanometry can be used to document the general patency of the nasal cavities to airflow. Isolated

narrowings of parts of the nose, however, may not change the total nasal pressure or airflow, but can be quite symptomatic for patients. As yet, there is no reliable way to document changes in the pattern of airflow inside the nose. If this information were available, a much better correlation could be made between nasal symptoms and airflow patterns. 12 In general, nasal airflow resistance can be increased with exposure to cold air and decreased with exercise. Anderson and Proctor" have demonstrated that neither the relative humidity nor elevated temperatures have an effect on nasal airflow resistance. Small concentrations of inert dust also have no effect, but a similarly small concentration of sulfur dioxide will increase nasal resistance. Anderson and Proctor" have also reported that community air pollution causes "nasal stuffiness," and this may be related to the sulfur dioxide that is often present in air pollution. Cigarette smoke is associated with a statistically significant increase in nasal airway resistance (p < 0.(01) in individuals known to be sensitive to it. 13 This response, however, was not seen in the nonsensitive group. In the absence of an allergic cause, this difference may be related to a chemical reaction at the level of the mucosa, and needs further research.

Impairment of Mucoclilary Clearance Table I illustrates that many of the pollutants are associated with a decrease in mucociliary clearance. As discussed earlier, the clearance of mucus from the nose and sinuses is related to both the status of the mucus and the function of the cilia. Any study of this area must take into consideration the general nutritional, hydrational, and pharmacologic status of the subjects, because these factors can all affect mucus flow. Specific changes in nasal or respiratory mucus are difficult to document; however, ozone and cigarette smoke are thought to alter the secretions. lW Further study will be needed to determine (a) if mucolytic drugs will be effective in the nose against such changes and (b) whether these drugs would disrupt pulmonary function." Nasal cilia activity can be disrupted by several types of pollutants. Carson et al. 16 have suggested that cigarette smoke, with several components, accomplishes this by first breaking down the protective mucus barrier over the cilia and then affecting the cilia themselves. 16 Systemic dehydration and sulfur dioxide (an outdoor pollutant) seem to slow mucociliary clearance by preventing the separation of the mucus from its glandular ducts. I? In addition, nasal epithelia from human beings exposed to sulfur dioxide show a trend toward compounding of the cilia, when two or more ciliary axo-

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716 LEOPOlD

Tabl.1. Pollutant effects on the nose and sinuses Probable mechanism of e"ect Exposure of occupatIon Grain dust Cigarette smoke

Acrylic-fingernail sculptors Spray painters Spice grinders Tobacco factory

Referencelsl

Nasal/sinus symptoms

Hurst & Dosrnan" Manfreda et al.29 Bascom et al. 13 Weber'9 Stanley et at.50 Hiipakka & Samimi 51

Stuffy nose Catarrhal rhinitis Congestion Rhinorrhea Sneezing Irritation

Hellquist et al.38 Chan et al.52

"Nonspecific" Sneezing Rhinorrhea Congestion

Newspaper dust

Kjaergaard & Pedersen 28 Theander& Bende~

Wool textile workers

Love et al.54

Green coffee bean processing Chili grinders Indoor air pollution

Uragoda55 Uragoda 25 Koenig 56

Irritation

SIR

DMF

XM

X

X

X

?

X

0

X

?

?

?

?

?

X

?

BHC

?

? ?

? ?

X

X

X

X

?

?

?

Sneezing Rhinorrhea Obstruction Rhinitis Nosebleeds Sneezing Rhinorrhea Irritation Irritation

X

?

?

?

X

?

?

?

Irritation

?

Nosebleeds Dryness Dryness Nosebleeds Irritation Rhinorrhea Irritation

X

X X X

MHC

? X ?

? ?

?

X

?

?

X

X

X

Anderson" Diesel exhaust particles Boric oxide Boric acid dust Borax dust Cotton dust Hair spray Sulfur dioxide Fiberglass dust Ozone Cadmium Nickel workers

Yu & Xu58 Barth & Blacker39 Garabrant et al.59 Garabrant et al.60 Haglind & Rylander 26 Borum et at 22 Friedman et al." Carson et al. 16 Anderson et al.31

Gross" Grose et al.62 Adalis et at.19 Doll et al.2O

Torjussen"

Freon Ionizing radiation Wood dust

Leather dust Formaldehyde

Borum et al.22 Friedman et al.6 1 Baldetorp et al.21 Haglind & Rylander 26 Black et al.65 Wilhelmsson et al.66 Holness et al.67 Wilhelmsson & DrettnerM Merler et al." Holmstrom et al.36 Hays et al."

Rhinorrhea Irritation Itching Irritation Rhinorrhea Rhinitis Polyps Carcinoma Congestion None

?

X

?

?

?

?

X

X

?

?

X

?

X

?

X

X

?

X

?

?

0

0

X

?

?

?

X

? ? ?

X

X

0

?

?

? X

X

X

X

X

X

X

0

? ? X

X

?

?

None Rhinorrhea Rhinitis Obstruction

? X

Irritation Rhinorrhea Irritation Rhinorrhea

X

?

?

X

X

X

?

?

X

?

X

SIR, SpecifiC immune reaction; DMF, decreased mucociliary function; XM, xenobiotic metabolism; BHC, benign histopathologic changes; MHC, malignant histopathologic changes; X, probable association; 0, proved nonassociation: ?, possible association,

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Pollution: The nose and sinuses 717

nemes become included in a common membrane. \8 This obviously will impede ciliary function. The permanence of these changes, as well as the long-term effects on other parts of the respiratory system, are unknown. Other pollutants that can affect ciliary activity include various heavy metals, like cadinium and nickel. 19,20 It is thought that they bind with ATPase and reduce the amount of ATP required for cilia beating. In other studies, Baldetorp et al." have demonstrated a short-lasting increase in tracheal cilia beat frequency after 5 seconds of ionizing irradiation. This effect may be a result of an outpouring of ATP from the mitochondria into the cell. With increased irradiation, the ciliary activity diminishes. A reversible reduction in nasal mucociliary flow for more than I hour has been noted after hairspray has been sprayed near a subject's hair." This effect is not a result of the freon propellant, and is likely caused by the ethyl alcohol, perfume, or acetates in the spray. Wood dust, on the other hand, appears to cause an irreversible decline in mucociliary flow." The result of this stagnant flow may be an increased contact time between carcinogenic wood dust and the nasal mucosa.

Impairment of Immune Defenses The dusts associated with many organic products contain biologically active materials like bacteria, bacterial endotoxins, and fungi":" (See Table 1). The humoral and cellular systems of immune protection, as well as the other mechanisms described earlier, help the body deal with these potentially dangerous pollutants. Often a systemic response of fever follows exposure to these pollutants. Grain dust has even been shown to be an allergen, eliciting a specific IgE response in sensitive individuals." Certainly there are many other natural allergens, like ragweed pollen. in inhaled air. To what extent many industrial or manmade pollutants are allergens is unknown. Cigarette smoke and fiberglass dust have been shown to be nonantigenic. 13,30 The interaction between viruses and the nasal mucosa can be influenced by chemicals in the nose. Although it is difficult to prove, when the protective functions of the nose. like mucociliary transport and immune mechanisms, are destroyed, viruses could more easily enter cells. In one study. subjects who received sulfur dioxide administered in conjunction with a nasal rhinovirus inoculation had a 50% decrease in nasal mucus flow rate compared with control subjects who did not receive the sulfur dioxide." The sulfur dioxide group. however. had fewer nasal symptoms than the control group. even though their antibody response was the same. It has also been suggested that zinc sulfate irrigations of the nasal cavity can be protective against polio virus. 32

Clearly more research needs to be done on both the hazardous and the beneficial effects of topically applied chemicals in the nose.

Damage to Cells When a pollutant overwhelms all of the nasal and sinus mucosal defenses. permanent damage to the delicate respiratory mucosa can occur. Septal perforations are seen in individuals who sniff cocaine and in workers exposed to arsenic and acids in the air. Carcinomas inside the nose and sinuses have been definitely linked to employment in the wood, leather, and nickel industries2o ,33. 3s (see also Table 1). Although exposure to formaldehyde has caused nasal tumors in animals. the definite associations to human beings have yet to be made.i":" In addition, premalignant cellular damage has been noted after exposure to spray paint" and diesel exhaust particles. 39

Sinusitis The end result of many nasal infections is sinusitis, either acute or chronic. Very few population studies have been performed to study the incidence of sinusitis. or whether that incidence is affected by pollution. One study of school children in Singapore compared the levels of air pollutants to respiratory symptoms." In this study. there seemed to be an association between sinusitis in children from an industrial region and elevated levels of atmospheric sulfur dioxide. In another study of hospital admissions for acute frontal sinusitis, Svonpaa and Antila" noted more than a threefold increase in the second of two consecutive 5-year periods for a town in Finland. They suggested that increasing air pollution in that town may have been responsible for the increase. Certainly more population studies like this are needed.

Trends In the Effecll of Pollution on the Nose and Slnu.e. There have been many studies of the association between nasal and sinus carcinoma and employment in the wood processing industry. Three recent studies suggest that as a result of an understanding of this risk. the incidence of tumors is decreasing. Hayes et al. 42 have observed that no cases of nasal adenocarcinoma have appeared in workers whose exposure to wood dust began after 1941. Finkelstein? and Irnbus'" did not demonstrate "a statistically significant excess of nasal cancer" in North American woodworkers. Finally, a 1989 German study found no nasal or sinus cancer in a wood dust-exposed population." Perhaps with a better understanding of how pollutants interact with human beings. further successes can be achieved in other areas. 46,47

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7••

~IVIW'rll"VIVV"-

LEOPOLD

Head and Neck Surgery

.In summary, the nose and sinuses are well equipped to filter and clean inhaled air. Many types of pollution, however, can overwhelm that protection and allow damage to occur to the nose, sinuses, lungs, and ultimately the whole individual. Blood pressure and respiration can be affected by nasally inhaled pollutants. The degree of these reactions, and other effects such as stress and pain syndromes (headache), need to be better understood. Certainly more study is needed to determine what the safe levels of exposure are, and what are the hazards of exposure to low levels of pollutants over long time periods. Occupationally, it is important for workers such as fire fighters, farm workers, and traffic control officers to know their risks. With advancing technology in materials, pesticides, and energy production, workers such as these are increasingly at risk. 48 REFERENCES I. Scherer PW, Hahn II, Mozell MM. The biophysics of nasal airflow. Otolaryngol Clin North Am 1989;22:265. 2. Sleigh MA, Blake JR, Liron N. The propulsion of mucus by cilia. Am Rev Respir Dis 1988;137:726-74. 3. Proctor OF. The mucociliary system. In: Proctor OF, Anderson I. eds. The nose. Amsterdam: Elsevier, 1982:245-78. 4. Liote H. Zahm J-M, Pierrot 0, Puchelle E. Role of mucus and cilia in nasal mucociliary clearance in health subjects. Am Rev Respir Dis 1989;140:132-6. 5. Messerklinger W. On the drainage of the normal frontal sinus of man. Acta Otolaryngol 1967;63:176-81. 6. Anderson I, Lundqvist OR, Proctor OF, Swift DL. Human response to controlled levels of inert dust. Am Rev Respir Dis 1979;119:619-27. 7. Vincent JH. The fate of inhaled aerosol: a review of observed trends and some generalizations. Ann Occup Hygiene 1990; 34:623-37. 8. Brain JD. The uptake of inhaled gases by the nose. Ann Otol Rhinol Laryngol 1970;79:529-39. 9. Plans-Mills TAB, von Maur RK. Ishizaka K, Norman PS, Lichtenstein LM. IgA and IgO anti-ragweed antibodies in nasal secretions. J Clin Invest 1976;57:1041-50. 10. Brandtzaer P, Fjellanger I, Gjeruldsen ST. Adsorption of immunoglobulin A onto oral bacteria in vivo. J Bacteriol 1968; 96:242-9. II. Anderson I, Proctor OF. The fate and effect of inhaled materials. In: Proctor DF, Anderson 1, eds. The nose. Amsterdam: Elsevier, 1982:423-55. 12. Leopold DA. The relationship between nasal anatomy and human olfaction. Laryngoscope 1988;98: 1232. 13. Bascom R, Kulle T, Kagey-Sobotka A. Proud A. Upper respiratory tract environmental tobacco smoke sensitivity. Am Rev Respir Dis 1991;143:1304-11. 14. Last JA, Jennings MD, Schwartz LW, Cross CEo Glycoprotein secretion by tracheal explants cultured from rats exposed to ozone. Am Rev Respir Dis 1977;116:695-704. IS. Dalharnn T, Pira U. Isoelectric analysis of respiratory mucus from normal rats and exposed to tobacco smoke. Am Rev Respir Dis 1979;119:779-84. 16. Carson S, Goldhamer R, Carpenter R. Responses of ciliated epithelium to irritants: mucus transport in the respiratory tract. Am Rev Respir Dis 1966;93:86-92.

17. Bang BO (quoted). In: Proctor DF, Anderson I, eds. The nose. Amsterdam: Elsevier, 1982:430. 18. Carson JL, Collier AM, Shih-Chin H. Smith CA, Stewart P. The appearance of compound cilia in the nasal mucosa of normal human subjects following acute, in vivo exposure to sulfur dioxide. Environ Res 1987;42:155-67. 19. Adalis D, Gardner DE, Miller FJ, Coffin DL. Toxic effects of cadmium on ciliary activity using a tracheal ring model system. Environ Res 1977;13:111-20. 20. Doll R, Morgan LG, Speizer FE. Cancers of the lung and nasal sinuses in nickel workers. Br J Cancer 1970;24:623-32. 21. Baldetorp L, Huberman D, Hakausson CH, Yoremalin NO. Effects of ionizing radiation on the activity of the ciliated epithelium of the trachea. Acta Radiol Ther Bioi 1976;15:225-32. 22. Borum P, Holten A, Loekkegaard N. Depression of nasal mucociliary transport by an aerosol hair-spray. Scand J Respir Dis 1979;60:253-9. 23. Black A, Evans JC, Hadfield EH, Macbeth RO, Morgan A, Walsh M. Impairment of nasal mucociliary clearance in woodworkers in the furniture industry. Br J Indust Med 1974;31: 10-7. 24. Hurst TS, Dosman JA. Characterization of health effects of grain dust exposures. Am J Indust Med 1990;17:27-32. 25. Uragoda CO. Symptoms among chili grinders. Br J Indust Med 1967;24:162. 26. Haglind P, Rylander R. Exposure to cotton dust in an experimental cardroom. Br J Indust Med 1984;41:340-5. 27. Enarson DA, Chan- Yeung M. Characterization of health effects of wood dust exposures. Am J Indust Med 1990;17:33-8. 28. Kjaergaard SK, Pedersen OF. Dust exposure, eye redness, eye cytology, and mucous membrane irritation in a tobacco industry. Int Arch Occup Environ Health 1989;61:519-25. 29. Manfreda J, Holford-Strevens V, Cheang M, Warren CPW. Acute symptoms following exposure to grain dust in farming. Environ Health Perspect 1986;66:73-80. 30. Gross P. The biologic categorization of inhaled fiber glass dust. Arch Environ Health 1976;31:101-7. 31. Anderson I, Jensen PL, Reed SE, Craig JW, Proctor DF, Adams OK. Induced rhinovirus infection under controlled exposure to sulfur dioxide. Arch Environ Health 1977;32:120-5. 32. Schultz EW, Gebhardt LP. Studies on chemical prophylaxis of experimental poliomyelitis. J Infect Dis 1942;70:7-50. 33. Brinton LA, Blot WJ, Becker JA, et al. A case-control study of cancers of the nasal cavity and paranasal sinuses. Am J Epidemiol 1984;119:896-906. 34. Shimizu H, Hozawa J, Saito H. et al. Chronic sinusitis and woodworking as risk factors for cancer of the maxillary sinus in northeast Japan. Laryngoscope 1989;99:58-61. 35. Merler E, Baldasseroni A, Laria R, et al, On the causal association between exposure to leather dust and nasal cancer: further evidence from a case-control study. Br J Indust Med 1986;43: 91-5. 36. Holmstrom M, Wilhelmsson B, Hellquist H, Rosen G. Histological changes in the nasal mucosa in persons occupationally exposed to formaldehyde alone in combination with wood dust. Acta Otolaryngol (Stockh) 1989;107:120-9. 37. Hays RB. Raatgever JW, DeBruyn A, Gerin M. Cancer of the nasal cavity and paranasal sinuses and formaldehyde exposure. Int J Cancer 1986;37:487-92. 38. Hellquist H, lrander R, Edling C, Odkvist LM. Nasal symptoms and histopathology in a group of spray-painters. Acta Otolaryngol (Stockh) 1983;96:495-500. 39. Barth DS, Blacker SM. The EPA program to assess the public

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40.

41. 42.

43. 44. 45.

46.

47. 48. 49. 50.

51.

52. 53. 54.

Pollution: The nose and sinuses 719

health significanceof deisel emissions. J Air Pollution Control Assoc 1978;28:768-71. Goh KT, Lun KC, Chong YM, Ong TC, Tan JL, Chay SO. Prevalence of respiratory illnesses of school children in the industrial, urban, and rural areas of Singapore. Trop Geogr Med 1986;38:344-50. Suonpaa J, Antila J. Increase of acute frontal sinusitis in southwestern Finland. Scand J Infec Dis 1990;33;562-8. Hayes RB, Gerin M, RaatgeverJW, DeBruyn A. Wood-related occupations. wood dust exposure, and sinonasal cancer. Am J Epidemiol 1986;124:569-77. Finkelstein MM. Nasal cancer among North American woodworkers: another look. J Occup Med 1989;32:899-901. Imbus HR. Nasal cancer in woodworkers(letter). J Occup Med 1990;32:422-3. Barthel E, Dietrich M. Retrospective cohort study of cancer morbidity in furniture makers exposed to wood dust. Z Gesamte Hyg 1989;35:279-81. Jones PA, Smith LC. Personal exposures to wood dust of woodworkers in the furniture industry in the High Wycombe area: a statistical comparison of 1983 and 1976/77 survey results. Ann Occup Hyg 1986;30:171-84. Landrigan PJ. Baker DB. The recognitionand control of occupational disease. JAMA 1991;266:676-80. Sidor R. Peters JM. Fire fighting and pulmonary function. Am Rev Respir Dis 1975;209:249-54. Weber A. Annoyance and irritation by passive smoking. Prev Med 1984;13:618-25. Stanley PJ, Wilson R. Greenstone MA. MacWilliamL. Cole P. Effect of cigarette smoking on nasal mucociliary clearance and ciliary beat frequency. Thorax 1986;41:519-23. Hiipakka D. Samimi B. Exposure of acrylic fingernail sculptors to organic vapors and methacrylatedusts. Am Induct Hyg Assoc J 1987;48:230-7. Chan OY, Lee CS. Tan KT. Thirumoorthy T. Health problems among spice grinders. Occup Moo 1990;40:111-5. Theander C. Bende M. Nasal hyperreactivity to newspapers. Clin Exp Allergy 1989;19:57-8. Love RG, Smith TA. Gurr D. SoutarCA. ScarisbrickOA.Seaton A. Respiratory and allergic symptoms in wool textile workers. Br J Indust Moo 1988;45:727-41.

55. Uragoda CG. Acute symptoms in coffee workers. J Trop Med Hyg 1988;91:169-72. 56. Koenig JQ. Indoor and outdoor pollutants and the upper respiratory tract. J Allergy Clin Immunol 1988;81:1055-9. 57. Anderson1. Scandinavianexperiences with indoor air pollution. Tokai J Exp Clin Med 1985;10:309-14. 58. Yu CPo Xu GB. Investigators' report-predictive models for desposition of inhaled diesel exhaust particles in humans and laboratory species. Res Rep Health Eff Inst 1987;10:3-22. 59. Garabrant DH. Bernstein L, Peters JM. Smith TJ. Respiratory and eye irritationfrom boron oxide and boric acid dusts. J Occup Med 1984;26:584-6. 60. Garabrant DH. Bernstein L. Peters JM. Smith TJ. Wright WE. Respiratory effects of borax dust. Br J Indust Moo 1985;42: 831-7. 61. FriedmanM, DoughertyR. Nelson SR, White RP, Sackner MA. Wanner A. Acute effects of an aerosol hair spray on tracheal mucociliary transport. Am Rev Respir Dis 1977;116;281-6. 62. Grose EC. Gardner DE, Miller FJ. Response of ciliated epithelium to ozone and sulfuric acid. Environ Res 1980;22:377-85. 63. Torjussen W. Rhinoscopical findings in nickel workers, with specialemphasison the influenceof nickelexposureand smoking habits. Acta Otolaryngol (Stockh) 1979;88:279-88. 64. Baldetorp L. v Mecklenburg C. HAkansson CH. Ultrastructural alterations in ciliary cells exposed to ionizing radiation. Cell Tissue Res 1977;180:421-31. 65. Black A. Evans JC, Esme HH. Macbeth RG, Morgan A. Walsh M. Impairment of nasal mucociliary clearance in woodworkers in the furniture industry. Br J Indust Moo 1974;31:10-7. 66. Wilhelmsson B. Hellquist H. Olofsson J, Klintenberg C. Nasal cuboidal metaplasia with dysplasia. Acta Otolaryngol (Stockh) 1985;99:641-8. 67. Holness DL. Sass-Kortsak AM. Pilger CWo NethercottJR. Respiratory function and exposure-effect relationships in wood dust-exposed and control workers. J Occup Med 1985;27: 501-6. 68. Wilhelmsson B, Drettner B. Nasal problems in wood furniture workers. Acta Otolaryngol (Stockh) 1984;98:548-55.

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Pollution: the nose and sinuses.

The nose and sinuses are constantly exposed to the huge quantities of gases needed to maintain life. Not only is the human nose well-equipped to warm ...
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