Why Can't You Smoke Before A Ct Scan - T-Tees - Your Answers Await, Life's Questions Unraveled

Discussion

To study the potential effects of smoking on CT findings, CT scans were investigated and information on smoking habits obtained in an interview from 587 asbestos-exposed workers. The identification of such effects is important for differential diagnostics of CT findings and may be useful for the early detection of smoking-induced lung injury and consequently for the secondary prevention of such diseases.

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The study population consisted of construction workers with an asbestos-related occupational disease. Therefore, the results cannot be extrapolated directly to the general population, but this occupational group is of special interest for two reasons: 1) this group of people may be at an increased risk of smoking-induced diseases, since persons exposed to asbestos are more likely to be susceptible to the adverse effects of smoking, as has been shown in the case of lung cancer 6; and 2) workers exposed to asbestos (especially those with pleural plaques) are screened radiologically in many countries 7-9 and smoking-related CT findings may thus be a major differential diagnostic problem.

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The study had a large sample of subjects with CT scans. The scoring was based on a subjective scale following the guidelines, described in the image analysis section, rather than on exact measurements, which were not technically possible. However, the assessment was similar to that which takes place in clinical practice. All three radiologists had several years of experience in analysing CT scans (Professor of radiology at the Helsinki University Hospital, former head radiologist at the Finnish Institute of Occupational Health (FIOH) and the current head of radiology at FIOH). Intraobserver assessment was reliable in the present study and interobserver assessment was also good for most of the signs. Averaging the score given by several observers increased the accuracy of the assessment 10. Scoring all findings with a similar scale (e.g. all from 0-5) might have been preferable to keep the regression coefficients comparable.

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The basic protocol included four HRCT slices and allowed for more in unclear cases to keep the radiation burden to the study subjects as low as possible. Early on in the study, when it was realised that extra slices were useful, seven slices were routinely imaged. During the study ∼70% of the study population were imaged with seven slices. No standardised reference images are available for grading asbestos exposure- or smoking-related HRCT findings. The current manuscript is part of a project aimed at developing guidelines for such grading and is participating in an international effort to standardise such HRCT analysis. There seems to be relatively few studies and no consensus on the optimal window parameters in HRCT. The window setting used in this study (window level -700 HU and window width 1,000 HU) is recommended for general diagnostics of lung diseases 11, while a wide window might improve the visualisation of pleuroparenchymal abnormalities (adhesions, pleuroparenchymal lines and visceral pleural fibrosis). All patients were imaged in a similar way irrespective of their smoking (or asbestos exposure) status, so the selection of the window settings or any other technical parameter did not introduce any systematic error in the comparisons presented. In addition, the graders were unaware of the exposure status of the subjects, eliminating observer bias due to awareness of exposure.

The interviewer inquiring about smoking history was unaware of the CT findings of the subjects at the time of the interview. Although there were only 18 never-smokers in the present study population, there was wide variability in pack-yrs, extending up to 87.5 pack-yrs. The multivariate analyses adjusted for the subjects’ main occupation, age and length of their asbestos exposure to minimise their confounding effect. Respiratory symptoms or coexisting diseases were not adjusted for. Smoking is known to be a risk factor for a variety of respiratory symptoms and diseases, therefore removing such persons from the material would have biased the study and most likely diluted the smoking effect. As table 1⇓ shows, current smokers were found to have more symptoms related to chronic bronchitis which was consistent with the radiological findings. The mean C‐reactive protein value did not differ between the exposure groups indicating that the results were not biased by respiratory infections.

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There are only a few previous studies on the effects of smoking on HRCT findings. Remy-Jardin et al. 3 found several positive associations between the smoking status and HRCT findings (amount of parenchymal micronodules, ground-glass opacities, emphysema and dependent attenuation) in a population of asymptomatic smokers. Emphysema, ground-glass opacities, parenchymal micronodules, and bronchial wall thickening characterised current smokers in a study by Mastora et al. 12. In the present study, smoking was associated with increased occurrence of all types and manifestations of emphysema, which is consistent with the fact that smoking is an established cause of emphysema. Since loss of lung tissue, which characterises emphysema, represents a balance between injury and repair, it has been hypothesised that cigarette smoke contributes to the development of emphysema by inhibiting fibroblast action 13. Fibrosis is produced by excessive production of collagen fibres by fibroblasts, and their conversion into tropocollagen 14. Cigarette smoke extract has been shown to hinder the viability of human lung fibroblast-derived cells by inducing apoptosis in lower concentrations (10-25%) and necrosis in higher concentrations (50-100%) 15. Cigarette smoke extract is also known to inhibit lung fibroblast proliferation and chemotaxis 13 and to inhibit fibroblast-mediated collagen gel contraction 16.

Increased bronchial wall thickness may be an early sign of chronic bronchitis and this was also positively associated with smoking in the studied population. Increased peribronchial fibrosis has been observed post mortem in chronic bronchitis and bronchial asthma 17.

Subpleural curvilinear lines are a nonspecific radiological sign. These may be seen in a variety of lung diseases, especially in asbestosis and scleroderma, but may also occur in normal patients 11. In the present study, smoking was inversely related to the occurrence of curvilinear lines. Emphysema caused by tobacco smoke might hamper the detection of curvilinear lines, since emphysematous lungs may replace the fibrotic lung tissue. However, after adjustment with emphysema the findings from the study remained.

A significant inverse relation was observed between smoking and septal lines (interlobular septal thickenings). These are suggested to be associated with pneumoconioses, fibrosis and other aetiologies 11. The inverse association of CT findings with smoking in the subgroup with exposure to ≤10 pack-yrs also remained fairly constant after adjustment for emphysema. The deleterious effects of tobacco smoke on fibroblast function could theoretically explain the findings from this study on decreased fibrosis. However, Baumgartner et al. 18 associated smoking with an increased risk of developing idiopathic pulmonary fibrosis. A slight positive association was detected between smoked pack-yrs and ground-glass opacities, a sign that could indicate respiratory bronchiolitis 19.

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Researchers have tried to estimate the exposure to ETS by converting it to “cigarette equivalents” but the estimates have been variable depending on the biomarker used 20. Based on cotinine measurements, nonsmokers are exposed to slightly more than one “cigarette equivalent” per day at the workplace, but this may apply only to the nicotine exposure. Simultaneously, nonsmokers passively exposed to tobacco smoke are receiving as much benzene as smokers would smoking six cigarettes, as much 4‐aminobiphenyl as if smoking 17 cigarettes, and as much N‐nitrosodimethylamine as a person who has smoked 75 cigarettes 20. Models using data restricted to smokers with a low smoking rate have been used to estimate lung cancer risk related to exposure to ETS 21. As the interviews undertaken did not include the history of ETS exposure, this study used a similar approach for the evaluation of pulmonary CT changes. The associations between relatively minor cumulative smoking and paraseptal emphysema, bronchial wall thickening and bronchiectasis indicate that even limited smoke exposure is a health risk. This finding may have relevance when the potential respiratory effects of ETS exposure are considered.

In conclusion smoking was related to several abnormal radiological signs in computed tomography and high-resolution computed tomography. These relations were found even among those with a relatively minor exposure of up to 10 pack-yrs, indicating that computed tomography can detect changes due to smoking at an early stage. Tobacco smoking promotes all forms of emphysema and bronchial wall thickening, while it seems to be associated with reduced computed tomography signs of fibrosis. Interpreters of chest computed tomography should be familiar with the findings related to smoking.

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