Diesel exhaust modulates ozone-induced lung function decrements in healthy human volunteers

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.

Inflammatory Cytokines and White Blood Cell Counts Response to Environmental Levels of Diesel Exhaust and Ozone Inhalation Exposures

“…The protocol and consent form were approved by the University of North Carolina School of Medicine Committee on the Protection of the Rights of Human Subjects and the US EPA [ClinicalTrials.gov # NCT01874834]. Further description of the protocol can be seen in Madden et al 2014 (IRB Study #: 09–1344) [ 48 ].…”

Interactions of GST Polymorphisms in Air Pollution Exposure and Respiratory Diseases and Allergies

“…Neither of these studies found significant interactions for polymorphisms of GSTM1. Interestingly, another recent study in healthy individuals found no association between controlled exposure to diesel exhaust and ozone (O 3 ) and subsequent FEV 1 in those with GSTM1 null genotype [35]. A 2004 study by Gilliland and colleagues showed that co-exposure to diesel exhaust and ragweed allergen in ragweed-sensitized individuals resulted in enhanced IgE and histamine level in those with GSTP1 ile/ile or GSTM1 null genotype, but not in GSTT1 null carriers [7].…”

Reactive oxygen species (ROS) generation, impacts on tissue oxidation and dietary management of non-communicable diseases: A review

“…However, it has been shown to cause damage to mucosa and respiratory tissues in animals and plant tissues even at low concentrations from 100ppb (Loscalzo, 2004). The exposure to ozone alone or as combination with other atmospheric pollutants like diesel exhausts has been observed to induce decrements in lung function (Madden et al, 2014). The exposure is elevated by physical activities like exercising which increases frequency and depth of breathing, hence exposing sensitive lung tissue to the pollutants.…”