Environmental pollutants can have a large impact on the health of those with cardiovascular disease (CVD). Carbon monoxide (CO), a gas that is a product of incomplete combustion, is one such pollutant. One well-demonstrated way that CO impacts health is through its bonds with blood cells. Carbon monoxide binds to hemoglobin at approximately 250 times the affinity of oxygen (O2), blocking the ability of hemoglobin to bond to O2. This reduces the ability of blood cells to carry O2 throughout the body, stressing the cardiovascular system. However, CO likely affects the cardiovascular system in multiple other ways, including also interfering with binding of O2 to myoglobin and increasing oxidative stress.1
As shown in the Infographic, CO can come from multiple places. Common sources include smoking (cigarettes or other combusted products such as cigars or marijuana) including secondhand smoke, car exhaust, industrial emissions and power generation, and heating systems that use wood or gas (including campfires/other outdoor burning of materials).
Acute CO exposure has been shown to have considerable effects on the cardiovascular system. Even in those without established CVD, CO exposure decreases peak O2 uptake and exercise duration.2,3 However, those with established CVD are much more sensitive to the effects of CO than their healthier counterparts,1 and effects of CO exposure within this population are more serious. Exposure to CO in those with CVD decreases time to both angina and ST-elevation changes, reduces both the intensity and duration of exercise, and limits peak O2 uptake achieved during exercise.4,5 These outcomes are particularly troubling within secondary prevention, where cardiorespiratory fitness, and improving cardiorespiratory fitness, is so strongly tied to future morbidity and mortality.6
Effects of long-term exposure to CO are harder to quantify, as it is difficult to test experimentally. However, ambient CO level is associated with the rate of myocardial infarctions at the community level,7 working in occupations with regular CO exposure (eg, working with automobiles) is associated with higher rates of CVD-related morbidity and mortality,8 CO levels predict future CVD-related events in those with established disease,9 and preclinical work has shown chronic CO exposure accelerates heart failure in rats with ischemic heart disease.10
Screening for CO exposure can be done quickly and noninvasively. There are handheld monitors that measure the amount of CO in expired breath. A patient is instructed to breath slowly into the device, which reports CO as a measurement in parts per million or as an estimate of percent carboxyhemoglobin. A reading of >=4 parts per million should trigger a conversation about potential sources of CO exposure.11
In addition to the direct effects of CO, CO exposure often occurs with exposure to other harmful substances, such as particulate matter. This is especially true in the case of cigarette smoking. Whenever a patient is shown to have elevated CO levels, the source of CO exposure for that patient should be identified and addressed, whether that entails help with treatment of smoking, encouraging patients to have "no smoking" rules in place for their homes, checking that heating systems are properly vented, being mindful of workplace exposure, or reminding patients to limit time outdoors on days with a poor air quality index.
ACKNOWLEDGMENT
This Infographic was made using Biorender. Work on this product was supported by NIH awards U54DA036114, P20GM103644, and R33HL143305.
REFERENCES