Vehicular Exhaust and Air Pollution


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


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Dose Response

A common measurement for considering health effects from a contaminant is the dose response. A dose response is the amount of pollutant, in our case ozone and particulate matter, absorbed in the respiratory tract and its tissue and the health effects from this interaction.


Most studies performed to investigate biological responses to ozone concentration are with animals. However, some studies involving humans have shown that short-term exposure to ozone has caused inflammatory responses in the upper respiratory tract. A major study was performed in Mexico City that observed multiple responses in the nasal cavity, the first line of defense against contaminants but also the first warning sign of possible responses. The study chose Mexico City because the ozone concentration of 0.08 ppm per hour (maximum exposure) was exceeded. This study looked at the results of three different groups of male participants with similar histories. The control group consisted of males living in an area low in ozone concentration and two groups living in the highest area of ozone concentration. The two groups living in the higher ozone concentration were further divided into a group that worked inside and a group that worked outside. Both groups living in the higher ozone concentration area developed responses, such as increase nasal mucous production, nasal crusting and chest pain and coughing but the occurrence among the participants increased when exposure to the outdoors increased. There was also an increase in nasal lesions and the shortening of cilia.

Particulate Matter

Epidemiological studies performed in the early 1990’s showed an association between particulate matter concentration and the incidence of cardiac and respiratory-related emergency room visits and hospital admissions. Although somewhat difficult to quantify, the most serious effects were observed in patients with chronic heart disease, chronic obstructive pulmonary disease, or pneumonia, strongly suggesting that preexisting cardiopulmonary disease might be a substantial risk factor in PM toxicity (Watkinson et al., 1998). Only a few studies, though, have been performed on animals to assess the effects of particulate matter on a biological entity. To assess the effects of particulate matter, different studies used rats as the responsive media. Most of the studies used healthy rats and rats treated with monocrotaline (MCT). MCT was used because it induces vascular inflammation and hypertension, which are common symptoms of cardiopulmonary disease. Both healthy and treated rats were exposed to various levels of a residual oil fly ash. A study performed by Killingsworth et al. (1997), used a dose concentration of 580 ug/m3 and exposed the rats by inhalation for 6 hrs/day for three days. At this level, arrhythmic events occurred in both rat groups however, death occurred in only the MCT-treated rats. Watkinson et al. (1998) used doses of 250, 1000 and 2500 ug by intratracheal instillation. Arrhythmic events occurred in both rats. The severity of the events increased within the MCT-treated rats. Half of the rats treated with MCT died after instillation of the particulate matter. Kodavanti et al. (1999) dosed MCT-treated rats with 3.33 mg/kg by instillation and 15 mg/m3 by inhalation for 6 hrs/day for three days. In this study, deaths occurred to the MCT-treated rats instilled with the particulate matter but the rats exposed by inhalation all survived. This shows that the upper respiratory tract aids in the removal but doesn’t totally eliminate of the harmful effects of the particulate matter.


Calderon-Garciduenas, L.; Rodriguez-Alcaraz, A.; Villarreal-Calderon, A.; Lyght, O.; Janszen, D.; Morgan, K.T. (1998) Nasal epithelium as a sentinel for airborne environmental pollution. Toxicological Sciences. 46: 35-364.

Killingsworth, C.R.; Alessandrini, F.; Krishna Murthy, G.G.; Catalano, P.J.; Paulauskis, J.D.; Godleski, J.J. (1997) Inflammation, chemokine expression, and death in monocrotaline-treated rats following fuel oil fly ash inhalation. Inhalation Toxicology. 9: 541-565.

Kodavanti, U.P.; Jackson, M.C.; Ledbetter, A.D.; Richards, J.R.; Gardner, S.Y.; Watkinson, W.P.; Campen, M.J.; Costa, D.L. (1999) Lung injury from intratracheal and inhalation exposures to residual oil fly ash in a rat model of monocrotaline-induced pulmonary hypertension. Journal of Toxicological Environmental Health. 57: 101-121.

Watkinson, W.P.; Campen, M.J.; Costa, D.L. (1998) Cardiac arrhythmia induction after exposure to residual oil fly ash particles in a rodent model of pulmonary hypertension. Toxicological Sciences. 41: 209-216