David Q. Rich, ScD, assistant professor, Department of Epidemiology, UMDNJ-School of Public Health; Leena Kamat, MBBS, MPH, research assistant
Does air pollution trigger cardiovascular disease or adverse birth outcomes?
Numerous studies have reported associations between increases in ambient air pollution and risk of cardiorespiratory mortality and morbidity, but the mechanisms underlying these associations are still not clear. My current research is investigating potential mechanisms of these short term (within a few days) associations between heart disease and air pollution, specifically studying health effects of traffic pollution. I am also exploring the relationship between birth outcomes such as low birth weight and delivering too early and air pollution concentrations at different times during the pregnancy (1st trimester or 3rd trimester). These studies will provide valuable information on which to base future research studies.
Starting with air pollution episodes like the London Fog of 1952, where a temperature inversion trapped industrial pollution in the air shed of London, resulting in substantial increases in cardiorespiratory mortality, some research has focused on evaluating whether there is increased mortality and morbidity associated with air pollution at levels commonly observed in the U.S., Europe, and elsewhere. Although it was widely believed that air pollution caused these increases in mortality and morbidity, little was known about the pathophysiologic mechanisms and/or the specific pollutants and pollutant sources underlying these associations. Further, if air pollution does in fact lead to an increased incidence of cardiorespiratory disease, could it impact perinatal health, resulting in preterm births, low birth weight, or intrauterine growth retardation? If so, how?
Our research group has begun work on a number of studies to answer these questions, first evaluating several mechanistic pathways by which air pollution might trigger CVD.
In a previous study, I reported a significant doubling of risk of atrial fibrillation episodes (AF) associated with increases in ambient ozone concentration in the previous hour, and hypothesized that this may be a result of air pollution’s effect on autonomic tone. Therefore, I conducted a study to determine the feasibility of using automated mode-switching algorithms in dual chamber pacemakers (a mechanism in these devices that detects and changes the pacing mode in response to AF) to identify these AF episodes in order to study the association between acute increases (<24 hours before arrhythmia) in air pollution and triggering of these AF episodes. I reviewed medical charts and used case-crossover methods (an epidemiologic study design particularly suited to acute triggering studies) to assess the association between ambient air pollution and AF episodes detected by automatic mode switching (MSAF). We found a statistically significant 41% increase in risk of MSAF episodes associated with each 0.58 µg/m3 increase in 24-hour moving average black carbon concentration, and non-significantly increased risk associated with ozone and carbon monoxide (CO) concentrations, respectively, during the same time period. Black carbon, a type of particulate air pollution, and CO, a gaseous pollutant, are generally thought to be markers of motor vehicles. Although we found no evidence of effects within an hour of MSAF episodes, these findings were consistent with the previous study in that we found an air pollution/AF association. However, the timing of that response was different (mean 24 hour pollutant concentration vs. mean pollutant concentration in the 1 hour before AF), which may suggest alternative pathophysiologic mechanisms.
We are also currently conducting a panel study examining potential susceptibility to the health effects of traffic-generated particulate air pollution in Type II diabetics. Increased incidence of acute myocardial infarction (MI) has been observed following exposure to as little as 2 hours to several days of elevated particulate air pollution, as well as “time spent in traffic” in several U.S. and European cities. Although relative risks associated with pollution are small compared to those of known clinical risk factors, traffic pollution or proxies for traffic pollution, have been repeatedly implicated as risk factors for acute cardiorespiratory disease. My previous work—and that of others—has shown other CVD outcomes including ventricular arrhythmias, atrial fibrillation, stroke, and heart failure, as well as sub-clinical markers of cardiovascular damage such as decreased heart rate variability, endothelial dysfunction, etc, to have similar patterns of timing/risk. Since diabetes is characterized by abnormalities in many of these biomarkers, and previous studies have reported air pollution/CVD associations in diabetics, we are studying this potentially susceptible patient group. We are interested to learn if a simple 2- hour drive up and down the New Jersey Turnpike may adversely affect several markers of cardiovascular damage previously associated with MI and other CVD.
Changes in each biomarker from pre-car ride to immediately after the 2-hour car ride, as well as changes 24 hours later, will be related to changes in particulate and gaseous air pollutants measured in the vehicle during the car ride. This work is ongoing and is being done in collaboration with investigators from the Environmental and Occupational Health Sciences Institute (a collaboration between UMDNJ and Rutgers), the Department of Environmental Health at UMDNJ-School of Public Health (SPH), and the Department of Medicine at UMDNJ-Robert Wood Johnson Medical School (RWJMS). Traffic pollution is an emerging public health concern, particularly in urban environments. This pilot work will provide an evaluation of the health effects associated with real-world traffic pollution to which many are exposed each day.
In another series of analyses, we are exploring whether increased exposure to air pollution may result in increased incidence of adverse birth outcomes. We are particularly interested in examining whether air pollution exposure at different times during pregnancy (e.g. last week before birth or in the 1st trimester) is associated with preterm birth, low birth weight, and/or specific pregnancy complications. Using birth certificate data (maintained by the New Jersey Department of Health and Senior Services) for all births to mothers who are residents of New Jersey, and air pollution data from the New Jersey Department of Environmental Protection, we can examine these associations across the entire state for multiple years.
Numerous epidemiologic studies have reported associations between ambient air pollution and these adverse birth outcomes. However, some reported associations with concentrations in the first trimester/month and others reported associations with concentrations in the last trimester before birth. If there is a causal relationship between air pollution and adverse birth outcomes, does air pollution cause one or more pregnancy complications that then result in preterm birth and/or low birth weight? Or does air pollution cause preterm birth and/or low birth weight through some other yet unknown mechanism? This ongoing work is being done in collaborations with several colleagues from UMDNJ’s School of Public Health and Robert Wood Johnson Medical School, and will provide valuable data on which to base future large scale prospective cohort/panel studies that will study potential mechanisms of this and other environmental causes of adverse birth outcomes.
David Q. Rich received his BS from Rutgers University in 1994, his MPH from UMDNJ-School of Public Health in 1999, and his Doctor of Science from the Harvard School of Public Health (HSPH) in epidemiology and environmental health in 2004. After post-doctoral fellowships at HSPH and Brigham and Women’s Hospital, he returned to SPH as an assistant professor in the Department of Epidemiology in 2005.