Vehicular Exhaust and Air Pollution

Introduction

Individual tailpipe emissions

Transport and fate in the environment

Measuring exposures

Prevention and control of exposure

Exposure Pathway

Risk assessment

Adverse effects


Harmful Effects

Dose Response

Absorption, Metabolism and Molecular Mechanisms of Action

Organ Sites of Toxicity

Biomarkers

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Biomarkers for Exposure

Particulate Matter and Ozone

Measuring biomarkers for exposure to compounds from vehicular exhaust is a difficult task because the exposure is usually a chronic type scenario with low to moderate exposure levels over a long time period. Biomarkers for this type of exposure are visible microscopic alterations to the lung epithelial. However, there are few reliable biomarkers for exposure to air pollutants such as particulate matter and ozone. Recent studies have shown biomarkers are present for personal exposure as well as ambient exposure to some compounds. Personal exposure refers to concentrations of compounds that are higher than would be encountered in a day to day scenario.

Journal 1

This study looked at exposure to PM 2.5 and markers of oxidative stress in blood. They found that exposure to PM 2.5 even in moderate concentration can induce oxidative stress and increase RBCs in peripheral blood. The researchers also stressed that personal exposure was more closely related to this biomarker than was ambient background concentrations.

Sorensen M, Daneshvar B, Hansen M, Dragsted LO, Hertel O, Knudsen L, Loft S. Personal PM2.5 exposure and markers of oxidative stress in blood. Environ Health Perspect. 2003 Feb;111(2):161-6

Journal 2

This study looked at personal exposure to PM 2.5 and biomarkers of DNA damage. They looked for DNA damage in lymphocytes, strand breaks, endonuclease sensitive sites, and PAH adducts after 48 hours of personal exposure. They observed a positive association only between DNA damage in lymphocytes and personal exposure to PM 2.5. They concluded that moderate exposure to concentrations of particulate matter can induce oxidative DNA damage.

Sorensen M, Autrup H, Hertel O, Wallin H, Knudsen LE, Loft S. Personal Exposure to PM(2.5) and Biomarkers of DNA Damage, Cancer Epidemiol Biomarkers Prev. 2003 Mar;12(3):191-6.

Journal 3

In another study involving the lower airways, size fractionated particles were divided by size into three categories: ultrafine (<0.1um), fine (PM0.1-2.5), and coarse (PM2.5-10) particulate matter (PM). Particles were collected from two urban sites in the Netherlands, and were compared for effects on human alveolar macrophages (AM). They used inflammatory cytokine production, phagocytosis, and expression of phagocyte receptor CD11b as biomarkers for exposure. What they found was that the coarse particles (between PM 2.5 and 10) elicited a greater immune response than the ultrafine and fine particles. Based on this they concluded that the results suggest that PM recognition by human alveolar macrophages involves receptors evolved to recognize microbial cell structures, and that microbial products are preferentially found in the coarse particles. They may also be involved in inflammatory events and decreased pulmonary defenses associated with exposure to pollution particles.

Becker S, Soukup JM, Sioutas C, Cassee FR. Response of human alveolar macrophages to ultrafine, fine, and coarse urban air pollution particles. Exp Lung Res. 2003 Jan-Feb;29(1):29-44.

Journal 4

This study was conducted to determine possible biomarkers from ozone exposure in humans. The chemical reactivity of ozone toward biological targets and particularly its genotoxicity supports a possible link between exposure and cancer risk. The study showed that ozone is indeed a potent mutagen and they characterized the mutation spectrum it produced in human cells. Almost all mutations were base substitutions, essentially located at G:Cs (75%), typical of reactive oxygen species (ROS), but occurring in a specific pattern, i.e. a similar extent of GC:TA (28%), GC:CG (23%) and GC:AT (23%). The targeted distribution of mutations and identification of hotspot sequences define the first molecular fingerprint of mutations induced by ozone in human cells. They claim the results should help determine even further quantifiable biomarkers of ozone exposure in humans.

Jorge SA, Menck CF, Sies H, Osborne MR, Phillips DH, Sarasin A, Stary A. Mutagenic fingerprint of ozone in human cells. DNA Repair (Amst). 2002 May 30;1(5):369-78.