A new study soon to appear in the Journal of Public Health suggests that air pollution and living in apartment buildings may be associated with an increased risk for dangerous conditions like heart disease, stroke, and type 2 diabetes.
Cardiovascular diseases are a leading cause of death in developing countries.
Hypertension and metabolic syndrome are important causes of cardiovascular diseases.
Metabolic syndrome is further associated with abdominal obesity, elevated blood pressure, and higher blood glucose levels.
These conditions are associated with a higher risk for various health problems.
The causes of these disorders are complex and are related to genetic factors, lifestyle, diet, and environmental factors including traffic air pollution, traffic noise, residential housing, and neighborhood quality.
Researchers here investigated the associations between a long-term exposure to ambient air pollution and residential distance to green spaces and major roads with the development of hypertension and some components of metabolic syndrome.
These associations were assessed among people living in private houses or multi-story houses in Kaunas City, a city of 280,000 and the second largest city of Lithuania.
In the present study, researchers investigated the association between a long-term exposure to ambient air pollution and the residential distance to green spaces and major roads with the development of hypertension and some components of metabolic syndrome.
These components included: a high triglyceride level, reduced high-density lipoprotein cholesterol, higher blood glucose, and obesity.
The associations were assessed among people who lived in either private or multifamily houses.
The results indicate that air pollution levels above the median are associated with a higher risk of reduced high density lipoprotein.
Traffic-related exposure was associated with the incidence of hypertension, higher triglyceride level and reduced high-density lipoprotein cholesterol.
However, the negative impact of traffic air pollutants was observed only in the participants who lived in multifamily buildings.
Since there is more traffic near the multifamily apartment buildings, this may be associated with the incidence of hypertension as well.
In addition, a built-up environment, high residential density, street traffic and its configurations are further factors associated with social interactions and supportive relationships, which could also impact cardiovascular health.
The greenness, size, and type (activity) of the available open public spaces were observed to be inversely related to the risk factors assessed.
Investigators have additionally found positive effects of the natural environment, and have emphasized the positive impact of such spaces on cardiovascular health.
“Our research results enable us to say that we should regulate as much as possible the living space for one person in multifamily houses, improve the noise insulation of apartments, and promote the development of green spaces in multifamily houses” said the study’s lead author, Agn Brazien.
Ambient air pollution is a growing global health problem estimated to contribute to as many as 3.1 million all-cause deaths per year (1–3).
Exposure to air pollution is the largest environmental health risk and ranks ninth among modifiable disease risk factors, above other common factors such as low physical activity, high cholesterol, and drug use (2). Most of the excess deaths attributable to air pollution exposure are due to acute ischemic/thrombotic cardiovascular events.
In addition to excess mortality, air pollution is associated with significant reductions in healthy life years and worker productivity (2, 4).
Air pollution may also be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus (5).
While the developing world is most burdened by air pollution-associated health effects, the association between air pollution and mortality is still evident in developed countries where pollution levels are well below target standards (6, 7).
The purpose of this article is (1) to introduce the reader to the major studies that have established the link between particulate matter (PM) air pollution and human cardiovascular and metabolic disease and (2) to discuss the mechanisms by which PM mediates its biologic effects.
For systematic review of the connection between air pollution and human disease, we refer the reader to several recent systematic reviews and meta-analyses (8–14).
Air pollution
Air pollution is a complex mixture of gaseous and particulate components, each of which has detrimental effects on cardiovascular and respiratory systems.
The composition of air pollution varies greatly, depending on the source, emission rate, and sunlight and wind conditions. Gaseous components of air pollution include nitrogen dioxide (NO2), nitric oxide (NO), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO) (2, 15, 16).
Particulate matter (PM) components of air pollution consist of carbonaceous particles with associated adsorbed organic chemicals and reactive metals. Common components of PM include nitrates, sulfates, polycyclic aromatic hydrocarbons, endotoxin, and metals such as iron, copper, nickel, zinc, and vanadium (2, 15, 17).
PM is subclassified according to particle size into (a) coarse (PM10, diameter <10μm), (b) fine (PM2.5, diameter <2.5μm), and (c) ultrafine (PM0.1, diameter <0.1μm). Coarse particles derive from numerous natural and industrial sources and generally do not penetrate beyond the upper bronchus. Fine and ultrafine particles are produced through the combustion of fossil fuels and represent a greater threat to health than coarse particles as they penetrate into the small airways and alveoli (16–19).
While the organic and metal components of particles vary with location, levels of PM2.5 have consistently correlated with negative cardiovascular outcomes regardless of location (15).
Epidemiological studies linking Pm exposure to morbidity and mortality in humans
The association between high levels of PM air pollution and adverse health outcomes has been known since the first half of the twentieth century.
Smog incidents in Meuse Valley, Belgium (1930), Donora, Pennsylvania (1948), and London, UK (1952) acutely caused increased hospitalizations and deaths, particularly in the elderly and those with preexisting cardiac and respiratory diseases.
An estimated 4,000 people died as a direct result of the London smog with 100,000 more suffering adverse health effects (20, 21).
These incidents resulted in policy changes including the implementation of Clean Air Act in 1970 (22).
The reduction in PM levels have led to gradual reduction in PM-associated morbidity and mortality; however, recent epidemiologic studies still consistently show a link between PM exposure and cardiopulmonary mortality.
Short-term exposure studies
The increased deaths due to the smog in Meuse Valley, Donora, and London clearly suggested that acute exposure to air pollution is associated with adverse health outcomes. These classic cases of air pollution-induced mortality represent extreme examples, with the London smog reaching air PM concentrations of 4.5 mg/m3 (World Health Organization current safety guideline is 25 μg/m3) (21).
A large number of short-term exposure studies have evaluated the associations between less extreme levels of air pollution and daily changes in mortality (15, 18).
A recent meta-analysis of 110 peer-reviewed studies revealed that every 10 μg/cm3 increase in PM2.5 concentration was associated with a 1.04% (95% CI 0.52%-1.56%) increase in all-cause mortality (10).
Hospitalizations and mortality due to cardiovascular and respiratory illnesses were positively correlated with increases in PM2.5 concentrations.
Several large, multi-city studies have been conducted in both North America and Europe, the largest being the NMMAPS (National Morbidity, Mortality, and Air Pollution Study) (23–25) and APHEA (Air Pollution and Health: A European Approach) (26, 27) studies.
Findings from these studies were remarkably consistent and demonstrated that PM levels are significantly associated with daily all-cause, cardiovascular, and pulmonary mortality. Seasonal and regional variations existed in both studies possibly attributable to different sources of pollutants, meteorological conditions, and population differences.
For example, the APHEA study found a stronger effect of PM on daily mortality in cities with a larger contribution of traffic emissions to total PM.
This is in agreement with a recent study on triggers of myocardial infarction (MI) in which traffic exposure was found to be as significant of a trigger of MI as physical exertion and alcohol use (28).
The NMMAPS study also found that the relationship between PM exposure and mortality was independent of gaseous co-pollutants, including NO2, CO, and SO2.
Studies carried out in Asia and the developing world have generally shown smaller effects on daily mortality due to PM than studies from the United States and Europe. A recent meta-analysis of 85 studies from 12 low- and middle-income countries showed a 0.47% (95% CI 0.34-0.61) increase for cardiovascular mortality and 0.57% (95% CI 0.28-0.86) increase for respiratory mortality for every 10 μg/cm3 increase in PM2.5 concentration (14).
The cities covered by this analysis have mean PM2.5 levels ranging from 56 to 179 μg/cm3, which is significantly higher than the mean the PM2.5 levels in cities in the US and Europe.
The reduced concentration-response relationship between PM2.5 levels and mortality in these countries is likely due to the higher baseline PM level seen in these countries. Indeed, current evidence suggests that the concentration-response relationship between PM2.5 levels and mortality is biphasic (29–33).
A steep concentration-response function is observed at lower PM concentrations, while the curve flattens at higher concentrations.
A recent study from Beijing, China found that while the slope of the concentration-response curve flattened at higher PM concentrations, there was no saturation for increased risk of ischemic heart disease mortality, even at PM concentrations as high as 500 μg/cm3 (33).
The biphasic relationship between PM concentration and adverse health outcomes means that the major health benefits from reducing PM levels will occur in countries with already cleaner air and that improvements in cardiovascular health will be more difficult to achieve in countries with higher levels of air pollution unless they can achieve a drastic improvement in PM concentrations.
The results of the NMMAPS and APHEA studies suggest that there is no “safe” threshold under which increases in PM are not associated with increased deaths.
Long-term exposure studies
In addition to studies on the acute effects of PM exposure, studies on the effect of chronic exposure to PM have revealed negative effects on long-term health outcomes.
The first of these was the Harvard Six Cities study, which prospectively measured the effect of air pollution on mortality in a cohort of 8,111 adults while controlling for individual risk factors, including smoking, body mass index, occupational exposures, hypertension, and diabetes (34).
The adjusted mortality rate ratio for the most polluted cities compared with the least polluted cities was 1.26 (95% CI 1.08-1.47). Air pollution, particularly PM2.5 and sulfates was positively associated with death from lung cancer and cardiopulmonary diseases.
A larger study, the ACS Cancer Prevention II study linked risk factor data for 552,138 adults with air pollution data and mortality statistics (35, 36).
Both PM2.5 and SO2 were positively correlated with all-cause, lung cancer, and cardiopulmonary mortality and every 10 μg/cm3increase in PM2.5 was associated with a 4, 6 and 8% increased risk of all-cause, cardiopulmonary, and lung cancer mortality, respectively. Coarse particles and gaseous co-pollutants other than SO2 were not significantly related to mortality.
A study on 22 European cohorts within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE) found an increased hazard ratio for all-cause mortality of 1.07 (95% CI 1.02-1.13) per 5 μg/cm3 PM2.5 (37).
Significant associations persisted even among participants exposed to PM2.5 levels below the European annual mean limit value of 25 μg/cm3.
Overall, the evidence from both short-term and long-term exposure studies demonstrates a consistent association between increased air pollution exposure and mortality. While the magnitude of this effect is small, the ubiquity of air pollution exposure makes it a significant source of early mortality.
A global assessment of mortality attributable to several risk factors, including air pollution was carried out in the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) (38).
This study estimated that PM2.5 is the fifth-ranking mortality risk factor, leading to 4.2 million deaths and 103.1 million disability-adjusted life-years in 2015. The largest number of deaths attributable to air pollution occurred in China with an estimated 1.11 million deaths.
These numbers are similar to the findings of a recent study from China that attributed 40.3% of deaths due to stroke, 26.8% of deaths due to ischemic heart disease, 23.9% of deaths due to lung cancer, and 18.7% of deaths due to chronic obstructive pulmonary disease (COPD) to PM2.5 exposure (39).
According to the GBD 2015 study, these represent the 1st, 2nd, 4th, and 5th leading causes of death in China, respectively (12).
Susceptibility to PM-induced morbidity and mortality
Enhanced risk of cardiovascular death from PM exposure has been linked to old age, low socioeconomic status, preexisting heart and lung disease, and smoking.
The APHENA (Air Pollution and Health: A Combined European and North American Approach) study, which analyzed data from the NMMAPS and APHEA studies found that the elderly and unemployed are at higher risk for the deleterious health effects associated with short-term exposure to PM (40).
The ACS study found that mortality from ischemic heart disease was positively correlated with chronic PM2.5 exposure among never smokers, former smokers, and current smokers (41). However, the risk for death due to arrhythmia, hearth failure, and cardiac arrest was not elevated by PM2.5 for never smokers, but significantly elevated for former and current smokers.
Studies have not shown a clear association between race and susceptibility to PM-induced health effects (42–44). However, air pollution in non-white neighborhoods tends to be higher than in majority-white areas, resulting in exposure disparities (45).
Indeed, inter-city gradients of PM (i.e., gradients among communities within a city) are associated with larger negative health effects than the average PM measurements within a city (46, 47).
Finally, it has been suggested that women may be more susceptible than men to the PM-induced health effects. Particularly, robust risk estimates have been reported for studies that include only women.
The Women’s Health Initiative Observational Study found that every 10 μg/cm3 increase in PM2.5 was associated with a 76% increase in fatal cardiovascular events while the Nurses’ Health Study found that every 10 μg/cm3 increase in PM10 was associated with a 43% increase fatal coronary heart disease (48, 49).
More recent large studies have given conflicting results (42, 43). On a global scale, exposure disparities may play a role in increased risk for women as use of biomass fuels for cooking in sub-Saharan Africa and south Asia expose women to disproportionately high levels of indoor air pollution (50).
More information: “Association between the living environment and the risk of arterial hypertension and other components of metabolic syndrome”Journal of Public Health (2019).
Journal information: Journal of Public Health
Provided by Oxford University Press
