What to know:

1. Carbon monoxide is a molecule composed of one carbon and one oxygen. The American Congress of Governmental Industrial Hygienists lists a threshold limit value of no more than 25 parts per million over an eight-hour Time Weighted Average.

2. Depending on the configuration of the diesel cab, the ambient air pressure inside the cab and the condition of the cab ventilation system and the engine exhaust, there are conditions when carbon monoxide can seep from the engine through openings in the back wall and into the locomotive cab. This can occur during conditions when the cab is tightly sealed, i.e. in very cold or very hot weather when an air condition is being used in conjunction with a poorly-maintained engine exhaust system.

3. In September, 1961 a FELA case was brought to the Court of Civil Appeals in Waco, Texas.1 The plaintiff alleged that from September 1954 through January, 1957, while working in Houston’s Settegast railyard, he had been exposed to carbon monoxide as a component of diesel fumes. The Chief Justice wrote:

“The defendant contends very vigorously that Diesel engines do not give off carbon monoxide in quantities which will do injury to a human. While we think the proof shows to the contrary, we do not think that plaintiff’s case is limited and restricted to injury as the result of the inhalation of carbon monoxide, since the record reflects that there are other elements in Diesel fumes capable of causing injury to man, and we think that the record before us sustained the findings of the jury that plaintiff suffered injury as a result of inhalation of the fumes from the Diesel engines.

“We think the record reflects that the plaintiff was subjected to an unnecessary hazard which could have easily been eliminated, and amply supports the findings of the jury. Moreover, we think that the record as a whole sustains such findings, and that they are not against the great weight and preponderance of the evidence under the rule of law in re King’s Estate, 150 Tex. 662, 224 SW 2nd 660.” ¹

3. While some researchers have suggested exposure to carbon monoxide can induce hypotension (low blood pressure)² Multiple reports have linked carbon monoxide intoxication to risk for stroke. One group of researchers, Hyuk-Hoon Kim et al stated that “CO poisoning is a high-risk factor for the development of stroke, evidenced by high incidences of stroke after CO poisoning.”

• Atif Bayramoglu, Abdullah Osman Kocak, Esra Kadioglu. “Ischemic stroke due carbon monoxide intoxication: Two case reports.” World J. Emerg. Med. Vol. 9. No. 1, 2018.

• Cong Lui, Peng Yin et al. “Ambient carbon monoxide and cardiovascular mortality: a nationwide time-series analysis in 272 cities in China.” The Lancet. Vol. 2 Jan 2018.

• Hyuk-Hoon Kim, Sangchun Choi, Yoon Seok Jung, Young-Gi Min, Dukyong Yoon, Sung Eun Lee, “Stroke incidence in survivors of carbon monoxide poisoning in South Korea: A population-based longitudinal study.” Med Sci Monit. 2020: 26 e926116.

• Cho Y, Kang H, Oh J et al. “Risk of venous thromboembolism after carbon monoxide poisoning: A nationwide population-based study.” Ann. Emerg. Med. 2020, 75(5): 587-96.

Carbon Monoxide: The Basics

Carbon monoxide (CO) is a gas that is produced by burning of carbon material when there is insufficient oxygen to provide complete combustion. Carbon monoxide poisoning can occur when gas heaters malfunction and under poor ventilation conditions when exhaust gases are mixed with the ambient air inside homes or vehicles. Carbon monoxide can be produced in factories where propane-powered industrial trucks are used and there is insufficient outside air introduced into the work environment. Carbon monoxide can also be introduced into the indoor environment by holes in the heat exchanger of a fossil-fuel-burning space heater or furnace. Carbon monoxide is colorless, odorless and tasteless.

According to the Centers for Disease Control, each year an estimated 400-1,200 Americans die from carbon monoxide poisoning. Additionally, more than 50,000-100,000 visits to the emergency room and more than 14,000 are hospitalized due to carbon monoxide exposure.
Carbon monoxide has an affinity for hemoglobin about 200 times that of oxygen. As a result, carbon monoxide binds preferentially to hemoglobin molecules, forming a compound called carboxyhemoglobin. Carboxyhemoglobin (COHb) cannot be used by the cells in the body, thus reducing the availability of oxygen to the cells. Carboxyhemoglobin levels are measured using blood gas analysis. Carbonxyhemoglobin levels greater than 50 percent are lethal, however, with individuals who have cardiomyopathy, the lethal level of carboxyhemoglobin can be as low as 10 percent.

Carbon monoxide, through the preferential binding of hemoglobin to form carboxyhemoglobin, can damage the nervous system and the heart. Carbon monoxide can cause loss of consciousness, likely due to decreased cardiac output or cerebral ischemia, is a strong predictor of severe toxicity.³
Carbon monoxide poisoning can result in persistent or delayed brain damage that appears days or weeks after exposure. The neurologic complications reported include:
• Vision loss
• Loss of coordination
• Cognitive impairment
• Changes in personality and/or mood
• Short-term memory loss
• Dementia
• Psychosis
• Incontinence
• Parkinsonism

History of the Railroad’s response to Carbon Monoxide

During the 1940s and early 1950s, as the steam era of railroads faded into the past, the American Association of Railroads began to focus on the “atmospheres” in the cabs of the diesel locomotives. Air samples were taken in locomotive cabs, tunnels and shops and analyzed for the presence of carbon monoxide. Most analyses concluded like the one published in June, 1952, i.e. there was nothing to worry about. The researchers pointed out that the carbon monoxide concentrations found in the locomotive cabs were not at a level that would cause “any noticeable physiological effects;” the levels found in diesel cabs were actually less than would be found in the cabs of steam locomotives–and also less than what would be encountered by someone who inhaled tobacco
smoke.⁴

Additionally, the researchers reported that the blood “throws off” carbon monoxide when exposed to “uncontaminated air;” and, the presence of aldehydes serves as a clear warning that other toxic gases may be present–and serves as a signal to turn off the diesel engine if the locomotive has to remain in a tunnel for “extended periods.”⁵
The researchers also pointed out that the American Standards Association in 1941 had concluded that being exposed to 0.01 percent (100 ppm) of carbon monoxide was “unharmful to persons exposed continuously for eight hours to air containing this percentage of the gas.”⁶

In fact, the value of 0.01 percent carbon monoxide was accepted by the American Standards Association in 1941 as being unharmful to persons exposed continuously for eight hours to air containing this percentage of the gas. ⁶ The authors of this 1952 study helpfully noted that a prior study had reported the air in New York City as 290 parts per million.
The AAR researchers included Table IV: “the Effect of carbon monoxide on Man.” The table showed that breathing 400 parts per million concentration of carbon monoxide for 1 hour resulted in no effect. Breathing a concentration of 600 parts per million concentration for 1 hour resulted in a “headache.” Breathing 1000 ppm carbon monoxide for 10-15 minutes resulted in no effect. However, breathing a 4,000 parts per million concentration of carbon monoxide for 1 hour was fatal.

Since locomotives occasionally have to travel through tunnels, the AAR researchers also discussed reduction of oxygen levels:

“Actual danger from a deficiency of oxygen in railroad tunnel atmospheres is very unlikely, as man can work in atmospheres containing only 12 per cent oxygen. Carbon monoxide would overcome men long before the oxygen deficiency would reach 12
per cent.”

In retrospect, the AAR’s June 1952 analysis of carbon monoxide was:• inconsistent (CO levels necessary to produce “headache” were listed as both 150 ppm and 400 ppm); Also, these levels in Table IV do not appear to be consistent with Figure A found on page r6800-6 of the same document.

• terms like “small percentages” were never defined;

• statements such as the “blood throwing off carbon monoxide” or, “the range of oxygen content is which a man can work is from 12 per cent to 20.9 per cent.”⁷ were made without supporting references.

Since the 1950s and 1960s the toxicological effects of carbon monoxide have become better understood. In the present day, the deleterious effects of carbon monoxide exposure are known to include cardiac damage, myocardial effects, cardiac arrhythmias, stroke, cerebral edema, neurological damage and even damage to the retina. While it is always important in cases of suspected CO exposure to determine carboxyhemoglobin levels, the cherry-red skin discoloration once thought to be typical of CO poisoning, may not be particularly common.⁸

NOTES

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