Abstract
The potential effects of combinations of dilute whole diesel exhaust (DE) and ozone (O3), each a common component of ambient airborne pollutant mixtures, on lung function were examined. Healthy young human volunteers were exposed for 2 hr to pollutants while exercising (~50 L/min) intermittently on two consecutive days. Day 1 exposures were either to filtered air, DE (300 μg/m3), O3 (0.300 ppm), or the combination of both pollutants. On Day 2 all exposures were to O3 (0.300 ppm), and Day 3 served as a followup observation day. Lung function was assessed by spirometry just prior to, immediately after, and up to 4 hr post-exposure on each exposure day. Functional pulmonary responses to the pollutants were also characterized based on stratification by glutathione S-transferase mu 1 (GSTM1) genotype. On Day 1, exposure to air or DE did not change FEV1 or FVC in the subject population (n = 15). The co-exposure to O3 and DE decreased FEV1 (17.6%) to a greater extent than O3 alone (9.9%). To test for synergistic exposure effects, i.e., in a greater than additive fashion, FEV1 changes post individual O3 and DE exposures were summed together and compared to the combined DE and O3 exposure; the p value was 0.057. On Day 2, subjects who received DE exposure on Day 1 had a larger FEV1 decrement (14.7%) immediately after the O3 exposure than the individuals’ matched response following a Day 1 air exposure (10.9%). GSTM1 genotype did not affect the magnitude of lung function changes in a significant fashion. These data suggest that altered respiratory responses to the combination of O3 and DE exposure can be observed showing a greater than additive manner. In addition, O3-induced lung function decrements are greater with a prior exposure to DE compared to a prior exposure to filtered air. Based on the joint occurrence of these pollutants in the ambient environment, the potential exists for interactions in more than an additive fashion affecting lung physiological processes.
Highlights
Numerous epidemiological studies have demonstrated an association between short-term exposure to ambient airborne particulate matter (PM) and adverse cardiopulmonary effects including premature mortality, increased hospitalizations for lung problems including infections, exacerbation of asthma symptoms, chronic bronchitis, and hospitalization for clinical cardiac events including arrhythmias, myocardial infarctions, and congestive heartOzone is one of the best studied gas phase pollutants in terms of lung biological effects
Individuals exercising on a bike outdoors for 2 hr with ambient O3 levels > 0.08 ppm had greater lung function decrements as a group when they possessed a glutathione-S-transferase mu 1 (GSTM1) null genotype coupled with wild type NQO1 compared to other combinations of those 2 gene polymorphisms [10]
This study primarily examined whether combinations of exposures to O3 and diesel exhaust (DE) can induce additive or synergistic effects related to lung function changes in healthy, normal adults, whether exposure to DE alters the response to a subsequent exposure to O3 approximately 20 hrs later, and whether GSTM1 genotype status has an effect on the lung function responses
Summary
Numerous epidemiological studies have demonstrated an association between short-term exposure to ambient airborne particulate matter (PM) and adverse cardiopulmonary effects including premature mortality, increased hospitalizations for lung problems including infections, exacerbation of asthma symptoms, chronic bronchitis, and hospitalization for clinical cardiac events including arrhythmias, myocardial infarctions, and congestive heartOzone is one of the best studied gas phase pollutants in terms of lung biological effects. Numerous epidemiological studies have demonstrated an association between short-term exposure to ambient airborne particulate matter (PM) and adverse cardiopulmonary effects including premature mortality, increased hospitalizations for lung problems including infections, exacerbation of asthma symptoms, chronic bronchitis, and hospitalization for clinical cardiac events including arrhythmias, myocardial infarctions, and congestive heart. With dozens of controlled human exposures, biological responses have been well documented for induction of decrements of lung function and inflammation typically expressed as decreased FEV1 and FVC [5] and lung neutrophilia [6,7]. Individuals exercising on a bike outdoors for 2 hr with ambient O3 levels > 0.08 ppm had greater lung function decrements as a group when they possessed a glutathione-S-transferase mu 1 (GSTM1) null genotype coupled with wild type NQO1 compared to other combinations of those 2 gene polymorphisms [10]. BMI has been proportionally associated with O3-induced lung function decrements [11]
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