The Internal Combustion Engine Division of ASME and the CIMAC World Congress has issued a call for papers for the 2004 CIMAC Congress on combustion en

The simple and cheap technique of nasal cytology was used to assess possible adverse effects of chronic exposure to diesel engine emission (DEE) on respiratory mucous membranes. Brush cytology probes were taken from the noses of 194 male, nonsmoking customs officers twice a year (January and July) over a period of 5 years. The study group of 136 officers was solely occupied with clearing of diesel trucks (8.4 hr/day, 42 hr/week). Measured DEE concentrations varied between 31 and 60 [micro]/[m.sup.3] and of benzo[a]pyrene concentrations were between 10 and 15 ng/[m.sup.3]. The control group of 58 officers worked only in the office. Over the 5-year period, similar results were obtained in summer and winter. In contrast to those not exposed to DEE, those who were had clear goblet cell hyperplasia with increased metaplastic and dysplastic epithelia and an increase in leukocytes. We found no evidence of progression of the cytopathologic changes. The findings may be described as a chronic inflammation of the nasal mucous membrane in the presence of chronic DEE exposure (chemical-induced rhinitis). Additionally, the findings of metaplastic and dysplastic nasal epithelia in the exposed subjects may indicate a genotoxic effect of chronic DEE exposure in humans. Key words: chemical-induced rhinitis, diesel engine emission, genotoxic air pollution, nasal cytopathology.
Since 1972, the north--south transit traffic through Switzerland of diesel heavy-goods vehicles has increased by a factor of almost five (1). Diesel engine emissions (DEEs) have increasingly aroused major concern about their potential health effects as air pollutants. DEE contains diverse, potentially toxic materials in the form of mucous membrane-irritating gases such as sulfur dioxide (S[O.sub.2]), acroleine, and formaldehyde, as well as in metals, chemicals, and particulate matter. Many of these complex products of complete and incomplete combustion are biologically genotoxic, cytotoxic, fibrogenic, and carcinogenic (2-6). Diesel engines produce many more particulate emissions than gasoline engines. These very fine solid particulates have a high deposition rate in the respiratory tract and consist of insoluble carbon-containing particles covered with solvent-extractible organic compounds (polycyclic aromatic hydrocarbons, nitrosamines, quinones) (7,8). DEE particles are mutagenic in the Ames assay and can induce unscheduled DNA synthesis and damage (9); however, the epidemiologic evidence is insufficient to establish DEE as a human lung carcinogen (10). DEE has been classified as a Group 2A carcinogen by the International Agency for Research on Cancer (6). Its role in urinary bladder carcinogenesis is rather suggestive (11).
Because the detectable health hazards of DEE in humans may have a long latency, the use of biomarkers for the early detection of relevant exposures has become increasingly important, particularly in epidemiologic investigations.
The nose is important for cleansing inhaled air and for modifying respiration and is an accessible source for investigation of exposure to airborne contaminants. The mucus layer is important in conditioning the inhaled air and provides a sticky surface for the entrapment of inhaled particles and gases. Because humans are nose breathers, the nasal cavity is the initial site of injury induced by inhaled irritants (12-14), a common site for particle deposition (15-20), and a site for the absorption of potentially noxious gases and vapors (21-23).
As site of first contact with inhaled toxins within the nasal cavity, it is the epithelium that deserves particular attention concerning the possible effects of air pollutants. An easy in vivo approach studying possible changes of the nasal epithelium is the brush biopsy (24-28), which aids data collection for the assessment of human risks from air pollutants. With this cytologic technique, we have found a significantly higher frequency of squamous cell metaplasia and dysplasia of the nasal epithelia in cigarette-smoking office workers compared with their nonsmoking colleagues (28). To evaluate whether the nasal mucosa responds similarly to DEE, we employed the same method among customs officers occupied with the customs clearance of heavy-duty vehicles. The results of this group were compared with those of their colleagues working only in the office.
Materials and Methods
Subjects and health assessment. Brush cytology nasal probes were taken from 194 male, nonsmoking customs officers twice a year (January and July) over a period of 5 years. The study group of 136 officers (age, 42.5 [+ or -] 8.10 years, mean [+ or -] SD) was occupied solely with the clearance of heavy-goods vehicles with diesel engines (8.4 hr/day; 42 hr/week).
The control group of 58 officers (age, 5006 [+ or -] 7.36 years) worked in offices without air conditioning in a 100-year-old building located off the main roads at the Lake of Lugano.
All customs officers underwent an internal medical examination every 2 years. There were no abnormal findings of clinical examination among the customs officers we examined cytologically. An abnormal finding was a reason for exclusion. Immediately before the cytologic swab was taken, the temperature of each subject was taken using a Thermoscan probe (Braun GmbH, Kronberg, Germany) in the auditory canal. All volunteers were afebrile during the cytologic examination. Because we examined the customs officers in the workplace, we assumed that they felt well enough to work (were not ill) on the day of examination and were in correspondingly good general physical condition.