Much has been made about Dr. Fowler’s testimony regarding the possibility of car exhaust having an effect. An open letter written by Roger Mitchell, former DC Chief Medical Examiner accused Dr. Fowler of an ethical breach and demanded an investigation by the Maryland Attorney General with an eye towards rescinding his medical license. Dr. Fowler, it is claimed, had no basis for considering car exhaust as a possible contributor, justifying the politics of personal destruction on the part of those advocating for the prosecution.
Of course, we all know that car exhaust can kill, by a number of mechanisms, in a closed environment. The mechanisms are carbon monoxide poisoning, exclusion of breathable air in the absence of carbon monoxide, and causing a cardiac arrhythmia by the effects of other products of combustion.
Carbon monoxide poisoning in open air
But, can car exhaust kill in the open air?
Why yes. Yes it can.
First, there are a number of examples of this happening in the literature. In 1987, DiMaio and Dana provided three cases of young men who died while laying near a car. In the first case, the head was between 1 and 2 feet from the exhaust pipe. In the other two cases, the heads of the victims were under the car(1).
In 1998, Jumbelic noted two cases. She writes(2): In the first case, a young man was four wheeling in a swampy area when his jeep became stuck in the mud as he continued to floor the accelerator. Carbon monoxide fumes entered the vehicle through the rusted floorboards, killing the driver. In the second case, two teens were skinny dipping behind a motor boat when they became affected by the boat exhaust. One of the youths was overcome and submerged into the lake.
In 2000, Easley presented a case of a young girl who became unconscious while swimming with friends behind a boat. She was resuscitated and lived, but was noted to have a carboxyhemoglobin saturation of 22%(3).
In 2003, the Centers for Disease Control and Prevention published an issue of Morbidity and Mortality Weekly Report reported (4):
“August 2002, two fatal and six nonfatal cases of carbon monoxide (CO) poisoning occurred in vacationers who were wading in or boating near the Bridgewater Channel of Lake Havasu (Lake Havasu City [LHC], Arizona) . They continue The surveys described in this report document excessive CO exposures in employees and excessive and fatal CO exposures in vacationers amid large numbers of boats. The surveys also document substantial CO exposures in the late afternoon during crowded boating conditions, mirrored by elevations in expired CO concentrations among employees and vacationers. The majority of LHC employees had estimated %COHb levels indicating the potential for adverse health effects. Vacationers tested had higher %COHb levels than employees. These results indicate that elevated %COHb levels can occur among persons in open, outdoor settings. Previously described outdoor boat-related poisonings involved dangers to occupants of individual boats (e.g., houseboats and ski-boats) … Persons in communities with lakes and rivers where boats congregate in large numbers should be aware of the dangers of open air, boat-related CO poisoning and the need to evaluate CO exposures during high-traffic periods.
It is thus completely appropriate to raise the issue of car exhaust in a person being detained on the ground next to an exhaust pipe. Much of the attack on Dr. Fowler centers on the fact that the carbon monoxide level in Mr. Floyd was not, in fact elevated. However, there are two issues with this when it comes to the lynch mob organized by Dr. Mitchell. The first is that the carbon monoxide level was not revealed to the defense until after Dr Fowler’s testimony — rather than during discovery. Only the decedent’s PO2 was revealed, without full description of the technology, to my knowledge. This is important because oximetry cannot distinguish between oxygenated hemoglobin and carboxyhemoglobin because both are red. As one article notes (5):
Acute carbon monoxide (CO) poisoning is usually suspected on the basis of a suggestive history, while the diagnosis of chronic CO intoxication is notoriously difficult [1,33] (table 1). Standard pulse oximetry (SpO2) CANNOT screen for CO exposure, as it does not differentiate carboxyhemoglobin from oxyhemoglobin (figure 4) [41,42]. Eight-wavelength pulse oximeters capable of measuring carboxyhemoglobin and methemoglobin are being developed, but need further study and should not be used for diagnosis… Blood PO2 measurements tend to be normal because PO2 reflects O2 dissolved in blood, and this process is not affected by CO. In contrast, hemoglobin-bound O2 (which normally comprises 98 percent of arterial O2 content) is profoundly reduced in the presence of COHb.
Thus, in the absence of other information, a “normal” PO2 by oximetry is not as diagnostic as those who want to lynch Dr. Fowler might think.
Cardiac effects of low level CO exposure
When talking about carbon monoxide intoxication, most people think of fatal carbon monoxide poisoning that is associated with high levels of CO. In fact, carbon monoxide can cause sudden death even at lower saturations if they rise acutely. For instance, in one study of environmental exposure, scientists took people with chronic heart disease with angina on exertion (chest pain) and had them exercise after being exposed to low concentrations of CO. In this study, subjects with a 2% saturation of CO suffered a 5.1% decrease in the time to signs of ischemia, and at 4% suffered a 12.1% decrease. Electrocardiographic changes were noted to be 11% more severe at 2% CO saturation and 17% more severe at 4% CO saturation.
The authors note (6):
The results of this study provide objective evidence that increasing the mean carboxyhemoglobin level from 0.6 percent to 2.0 percent worsens the ischemic response to mild graded exercise. Both the earlier development of myocardial ischemia and the increase in the maximal amplitude to the ST-segment change indicate that a blood level of 2 percent carboxyhemoglobin affect exercise capacity in subjects with symptomatic coronary artery disease. … Even a small increase in the carboxyhemoglobin level, representing a seemingly minor reduction in the oxygen-carrying capacity of hemoblbin was associated with statistically significant effects…
Thus, car exhaust can contribute to sudden cardiac death in a vulnerable individual even at low levels.
Similarly, in another study, researchers found(7):
This study demonstrates that low-level exposure to CO can significantly reduce exercise tolerance in subjects with stable angina, at an average carboxyhemoglobin level of 2.9% of saturation. These findings agree with those previously reported by Aronow and Isbell’ and Anderson et a1. In addition, we have confirmed the reduction in time to angina with concurrent reductions in measures of submaximal exercise.
Similar results were obtained by Adams, et al (8).
On the other hand, while this acute low-level intoxication is associated with increased ischemia, one study found that in patients without an underlying tendency towards ectopic beats, a small increase in CO saturation is not associated with arrhythmia (9). In contrast, Sheps et al also found little effect (10), but in a later study did find a mild increase in ectopic beats at 6% but not at 4% saturation (11) and there was no effect in a similar study by Dahms et al (12).
So, while low-level CO exposure increases the risk of ischemic effects in people with cardiac vulnerability, it does not seem to increase ectopic beats in people with healthy hearts.
Effects not related to CO
But wait, there’s more. You don’t actually need CO. It turns out the particulate matter is also dangerous. Exposure to exhaust is associated with acute myocardial infarction and sudden death not due to carbon monoxide poisoning. More studies have been done on diesel engines, but particulates exist in gas engine exhaust as well. Environmental particulate exposure, such as that from internal combustion engines, can have significant acute effects on the cardiovascular system. Exposure can cause inflammatory and thrombotic changes in blood vessels and acute autonomic dysfunction. The effect is more pronounced in people with pre-existing disease(13).
The authors write:
The study results suggest that urban particulate and gaseous pollutants may jointly impact cardiovascular health in subjects with CVD risk factors through multi-biological pathways. Our findings indicate that both particulate chemical components and gaseous pollutants, including OC, EC, SO2, NO2, and CO, may trigger prolonged inflammatory and thrombotic responses for 3 days in vulnerable subjects, while fine particulates immediately disturb the autonomic balance for 1 day. The estimates of response to air pollution observed in vulnerable subjects are stronger than that reported by Chuang et al. (2007) which focused on young healthy college students.
That “autonomic imbalance” thing is important if you remember the autonomic trigger issue in sudden death in vulnerable people.
Another group found that short term exposure to diesel exhaust particles was associated with inflammation and myocardial damage. In the following excerpt, DEP stands for “diesel exhaust particles” (14):
The study demonstrated the significant acute cardiac effects of short-term DEP exposure. After 24 h of DEP stimulation, not only left ventricular systolic function but also diastolic function, became deteriorated. The sympathetic tone increased and heart rate variability decreased after short-term DEP exposure. These changes could contribute to the acute cardiac dysfunction after short-term DEP exposure. In addition to the functional changes in cardiovascular system, the circulating pro-inflammatory cytokine proteins, including IL-1 and IL-6, increased. Moreover, the IL-1 expression in the cardiac compartment also increased after short-term DEP exposure. More cardiac injury with higher plasma cardiac troponin I level was noted after DEP exposure. It implies that myocardial dysfunction after short-term DEP exposure is not only caused by the increased sympathetic tones, but also by the myocardial injury.
Another study suggests that the pathway for this involves disruption of vascular tone (15). Another study notes:
At levels encountered in an urban environment, inhalation of dilute diesel exhaust impairs 2 important and complementary aspects of vascular function in humans: the regulation of vascular tone and endogenous fibrinolysis. These important findings provide a potential mechanism that links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction.
They conclude:
Exposure to increased levels of combustion-derived air pollution for as little as 1 hour can impair vasomotor function and endogenous fibrinolysis in humans. We provide evidence that this may be the result of reduced NO bioavailability in the vasculature and postulate that this effect is mediated by oxidative stress induced by the nanoparticulate fraction of diesel exhaust. These data provide a plausible mechanistic link to explain the association between air pollution and acute myocardial infarction.
Other studies confirm the vasoconstrictive effect of exhaust particles. For instance, Brook et al found (16):
Short-term inhalation of fine particulate air pollution and ozone at concentrations that occur in the urban environment causes acute conduit artery vasoconstriction.
Another study notes that this is a bigger problem in people with underlying cardiac disease, such as Mr. Floyd. They note(17):
Short-term particulate exposures contributed to acute coronary events, especially among patients with underlying coronary artery disease. Individuals with stable presentation and those with angiographically demonstrated clean coronaries are not as susceptible to short-term particulate exposure.
At least with diesel engines, merely walking by a running engine may be enough to cause a response. One study found (18):
“Diesel particulate matter concentrations during drive-by incidents easily reach or exceed the low concentrations that can cause acute health effects for brief periods of time. For the case of a particularly well-tuned late-model year vehicle, the mass of particulate matter inhaled during a drive-by incident is small compared to the mass inhaled daily at ambient conditions. On a per breath basis, however, the mass of particulate matter inhaled is large compared to the mass inhaled at ambient conditions. Finally, it was determined that children, infants, or people breathing at heights similar to that of a passing vehicle’s tailpipe may be exposed to higher concentrations of particulate matter than those breathing at higher locations, such as adults standing up.
Similarly, another study found that transient exposure increased the risk of sudden death by almost 300% within one hour of exposure (19).
Thus, even in the absence of carbon monoxide intoxication, automobile exhaust can contribute to sudden cardiac death in the context of a vulnerable heart and other factors contributing to autonomic dysfunction. In contrast to the assertions of the lynch mob wanting to destroy the life of Dr. Fowler for his politically incorrect testimony, it is perfectly appropriate to note it as another stressor in the perfect storm of events that cost Mr. Floyd his life.
Next: Putting it all together.
- DiMaio, V. J. M. and Dana, S. E., “Deaths Caused by Carbon Monoxide Poisoning in an Open Environment (Outdoors},” JournalofForensic Sciences, JFSCA, Vol. 32, No.6, Nov. 1987, pp. 1794-1795.
- Jumbelic M. Open Air Carbon Monoxide Poisoning J Forensic Sci 1998;43(1):228–230.
- Easley RB. Open air carbon monoxide poisoning of a child swimming behind a boat. Southern Med J 2000 93(4):430-432.
- MMWR weekly, Carbon Monoxide Poisonings Resulting from Open Air Exposures to Operating Motorboats —Lake Havasu City, Arizona, 2003 https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5315a3.htm
- Clardy PF, Manaker S, Perry H. Carbon monoxide poisoning UpToDate 2019 (text) 2021 https://www.uptodate.com/contents/carbon-monoxide-poisoning
- Allred, E. N., Bleecker, E. R., Chaitman, B. R., Dahms, T. E., Gottlieb, S. O., Hackney, J. D., … Warren, J. (1989). Short-Term Effects of Carbon Monoxide Exposure on the Exercise Performance of Subjects with Coronary Artery Disease. New England Journal of Medicine, 321(21), 1426–1432. doi:10.1056/nejm198911233212102
- Kleinman, M. T., Davidson, D. M., Vandagriff, R. B., Caiozzo, V. J., & Whittenberger, J. L. (1989). Effects of Short-Term Exposure to Carbon Monoxide in Subjects with Coronary Artery Disease. Archives of Environmental Health: An International Journal, 44(6), 361–369. doi:10.1080/00039896.1989.9935908
- Adams, K. F., Koch, G., Chatterjee, B., Goldstein, G. M., O’Neil, J. J., Bromberg, P. A., & Sheps, D. S. (1988). Acute elevation of blood carboxyhemoglobin to 6% impairs exercise performance and aggravates symptoms in patients with ischemic heart disease. Journal of the American College of Cardiology, 12(4), 900–909. doi:10.1016/0735-1097(88)90452-4
- Hinderliter, A. L., Adams, K. F., Price, C. J., Herbst, M. C., Koch, G., & Sheps, D. S. (1989). Effects of Low-Level Carbon Monoxide Exposure on Resting and Exercise-Induced Ventricular Arrhythmias in Patients with Coronary Artery Disease and No Baseline Ectopy. Archives of Environmental Health: An International Journal, 44(2), 89–93. doi:10.1080/00039896.1989.9934381
- Sheps, D. S., Adams, K. F., Bromberg, P. A., Goldstein, G. M., O’Neil, J. J., Horstman, D., & Koch, G. (1987). Lack of Effect of Low Levels of Carboxyhemoglobin on Cardiovascular Function in Patients with Ischemic Heart Disease. Archives of Environmental Health: An International Journal, 42(2), 108–116. doi:10.1080/00039896.1987.9935805
- Sheps DS, Herbst MC, Hinderliter AL, Adams KF, Ekelund LG, O’Neil JJ, Goldstein GM, Bromberg PA, Ballenger M, Davis SM, et al. Effects of 4 percent and 6 percent carboxyhemoglobin on arrhythmia production in patients with coronary artery disease. Res Rep Health Eff Inst 1991;41:1–46; discussion 47–58.
- Dahms, TE, Younis, LT, Wiens, RD, Zarnegar, S, Byers, SL, Chaitman, BR. Effects of carbon monoxide exposure in patients with documented cardiac arrhythmias. J Am Coll Cardiol 1993; 21: 442–450.
- Chen, S.-Y., et al., Particulate and gaseous pollutants on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease, Environmental Pollution (2017), http://dx.doi.org/10.1016/j.envpol.2017.01.037
- Huang CH, Lin LY, Tsai MS, et al. Acute cardiac dysfunction after short-term diesel exhaust particles exposure Toxicology Letters 192 (2010) 349–355
- Mills NL, Tornqvist H, Robinson SD, et al Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis Circulation. 2005;112:3930-3936.
- Brook RD, Brook JR, Urch B, et al. Inhalation of Fine Particulate Air Pollution and Ozone
Causes Acute Arterial Vasoconstriction in Healthy Adults Circulation. 2002;105:1534-1536 - Pope CA, Muhlstein JB, May HT, et al. Ischemic Heart Disease Events Triggered by Short-Term Exposure to Fine Particulate Air Pollution Circulation. 2006;114:2443-2448.
- Bruzzard NA, Clark NN, Guffey SE. Investigation into pedestrian exposure to near-vehicle exhaust
emissions Environmental Health 2009, 8:13 doi:10.1186/1476-069X-8-13 - Peters A, von Klot A, Heier M, et al. Exposure to Traffic and the Onset of Myocardial Infarction N Engl J Med 2004;351:1721-30.