Public health and components of particulate matter: the changing assessment of black carbon.

UNLABELLED: In 2012, the WHO classified diesel emissions as carcinogenic, and its European branch suggested creating a public health standard for airborne black carbon (BC). In 2011, EU researchers found that life expectancy could be extended four to nine times by reducing a unit of BC, vs reducing a unit of PM2.5. Only recently could such determinations be made. Steady improvements in research methodologies now enable such judgments. In this Critical Review, we survey epidemiological and toxicological literature regarding carbonaceous combustion emissions, as research methodologies improved over time. Initially, we focus on studies of BC, diesel, and traffic emissions in the Western countries (where daily urban BC emissions are mainly from diesels). We examine effects of other carbonaceous emissions, e.g., residential burning of biomass and coal without controls, mainly in developing countries. Throughout the 1990s, air pollution epidemiology studies rarely included species not routinely monitored. As additional PM2.5. chemical species, including carbonaceous species, became more widely available after 1999, they were gradually included in epidemiological studies. Pollutant species concentrations which more accurately reflected subject exposure also improved models. Natural "interventions"--reductions in emissions concurrent with fuel changes or increased combustion efficiency; introduction of ventilation in highway tunnels; implementation of electronic toll payment systems--demonstrated health benefits of reducing specific carbon emissions. Toxicology studies provided plausible biological mechanisms by which different PM species, e.g, carbonaceous species, may cause harm, aiding interpretation of epidemiological studies. Our review finds that BC from various sources appears to be causally involved in all-cause, lung cancer and cardiovascular mortality, morbidity, and perhaps adverse birth and nervous system effects. We recommend that the US. EPA rubric for judging possible causality of PM25. mass concentrations, be used to assess which PM2.5. species are most harmful to public health. IMPLICATIONS: Black carbon (BC) and correlated co-emissions appear causally related with all-cause, cardiovascular, and lung cancer mortality, and perhaps with adverse birth outcomes and central nervous system effects. Such findings are recent, since widespread monitoring for BC is also recent. Helpful epidemiological advances (using many health relevant PM2.5 species in models; using better measurements of subject exposure) have also occurred. "Natural intervention" studies also demonstrate harm from partly combusted carbonaceous emissions. Toxicology studies consistently find biological mechanisms explaining how such emissions can cause these adverse outcomes. A consistent mechanism for judging causality for different PM2.5 species is suggested.

Oxidative stress-induced telomeric erosion as a mechanism underlying airborne particulate matter-related cardiovascular disease.

Particulate matter (PM) pollution is responsible for hundreds of thousands of deaths worldwide, the majority due to cardiovascular disease (CVD). While many potential pathophysiological mechanisms have been proposed, there is not yet a consensus as to which are most important in causing pollution-related morbidity/mortality. Nor is there consensus regarding which specific types of PM are most likely to affect public health in this regard. One toxicological mechanism linking exposure to airborne PM with CVD outcomes is oxidative stress, a contributor to the development of CVD risk factors including atherosclerosis. Recent work suggests that accelerated shortening of telomeres and, thus, early senescence of cells may be an important pathway by which oxidative stress may accelerate biological aging and the resultant development of age-related morbidity. This pathway may explain a significant proportion of PM-related adverse health outcomes, since shortened telomeres accelerate the progression of many diseases. There is limited but consistent evidence that vehicular emissions produce oxidative stress in humans. Given that oxidative stress is associated with accelerated erosion of telomeres, and that shortened telomeres are linked with acceleration of biological ageing and greater incidence of various age-related pathology, including CVD, it is hypothesized that associations noted between certain pollution types and sources and oxidative stress may reflect a mechanism by which these pollutants result in CVD-related morbidity and mortality, namely accelerated aging via enhanced erosion of telomeres. This paper reviews the literature providing links among oxidative stress, accelerated erosion of telomeres, CVD, and specific sources and types of air pollutants. If certain PM species/sources might be responsible for adverse health outcomes via the proposed mechanism, perhaps the pathway to reducing mortality/morbidity from PM would become clearer. Not only would pollution reduction imperatives be more focused, but interventions which could reduce oxidative stress would become all the more important.

Cardiovascular health and particulate vehicular emissions: a critical evaluation of the evidence.

A major public health goal is to determine linkages between specific pollution sources and adverse health outcomes. This paper provides an integrative evaluation of the database examining effects of vehicular emissions, such as black carbon (BC), carbonaceous gasses, and ultrafine PM, on cardiovascular (CV) morbidity and mortality. Less than a decade ago, few epidemiological studies had examined effects of traffic emissions specifically on these health endpoints. In 2002, the first of many studies emerged finding significantly higher risks of CV morbidity and mortality for people living in close proximity to major roadways, vs. those living further away. Abundant epidemiological studies now link exposure to vehicular emissions, characterized in many different ways, with CV health endpoints such as cardiopulmonary and ischemic heart disease and circulatory-disease-associated mortality; incidence of coronary artery disease; acute myocardial infarction; survival after heart failure; emergency CV hospital admissions; and markers of atherosclerosis. We identify numerous in vitro, in vivo, and human panel studies elucidating mechanisms which could explain many of these cardiovascular morbidity and mortality associations. These include: oxidative stress, inflammation, lipoperoxidation and atherosclerosis, change in heart rate variability (HRV), arrhythmias, ST-segment depression, and changes in vascular function (such as brachial arterial caliber and blood pressure). Panel studies with accurate exposure information, examining effects of ambient components of vehicular emissions on susceptible human subjects, appear to confirm these mechanisms. Together, this body of evidence supports biological mechanisms which can explain the various CV epidemiological findings. Based upon these studies, the research base suggests that vehicular emissions are a major environmental cause of cardiovascular mortality and morbidity in the United States. As a means to reduce the public health consequences of such emissions, it may be desirable to promulgate a black carbon (BC) PM(2.5) standard under the National Ambient Air Quality Standards, which would apply to both on and off-road diesels. Two specific critical research needs are identified. One is to continue research on health effects of vehicular emissions, gaseous as well as particulate. The second is to utilize identical or nearly identical research designs in studies using accurate exposure metrics to determine whether other major PM pollutant sources and types may also underlie the specific health effects found in this evaluation for vehicular emissions.

Does improved exposure information for PM2.5 constituents explain differing results among epidemiological studies?

Contrary findings are often found among epidemiological studies examining associations of different types of airborne particulates against the same health endpoints. Some studies of heart rate variability (HRV) in humans find associations with either regional particulate material 2.5 microns or smaller (PM2.5) and/or with "sulfate" while some do not; some find associations with more local emissions such as black carbon (BC), while others do not. We explore if there might there be a consistent methodological explanation for inconsistent findings among HRV studies. To do this, we identify studies of HRV changes in humans examining associations with ambient PM2.5 and sulfate, ambient PM2.5 and BC, or all three; we briefly review findings and methodologies, including exposure issues; then we explore why studies may come to different conclusions. We tentatively conclude that differences in accuracy of subject exposure information for health-relevant emissions such as BC, which vary spatially over short distances in urban areas, may explain conflicting study results. HRV studies with accurate exposure information for BC or urban/industrial PM2.5 generally find large, significant associations with BC or urban/industrial PM2.5, but rarely with secondary sulfate or regional emissions generally. However, absent accurate exposure information for BC, studies appear more likely to find associations with less spatially variable secondary sulfate or PM2.5, and less likely to find strong associations with BC. However, research on this subject is limited, as are the number of studies evaluated here. Added research is necessary to confirm these findings (or otherwise), and to explore whether exposure misclassification might cause other health effects results to consistently vary.

Pinnacles and pitfalls for source apportionment of potential health effects from airborne particle exposure.

Since its origins in the 1970s, source apportionment using receptor modeling has improved to a point where both the chemical mass balance and various methods of factor analysis have been applied to many urban and regional data sets to infer major sources or source classes influencing airborne particle concentrations. Recently the factors from the latter analyses have been combined with regression techniques using human health endpoints to infer source influence on health effects. This approach is attractive for air quality management when the composition of particles is known, since it provides, in principle, a means of quantifying major source influence on health consequences. The factor-based analyses have been used for both epidemiological and toxicological studies with some success. While the method is useful in many ways, it also has important limitations that include failing to identify specific sources, misidentification from comingled source factors, and inconsistency or unreasonableness of results from the same locations using different factor techniques. Examples of ambiguities evolving from these limitations are cited in this article. Ambiguity found in the literature is fostered by loosely worded terminology that does not distinguish statistically based factors from actual sources, and from health impacts inferred by single centrally located air monitors, which are assumed to represent actual exposure or dosage to airborne particles.

Health effects of airborne particulate matter: do we know enough to consider regulating specific particle types or sources?

Researchers and regulators have often considered preferentially regulating the types of ambient airborne particulate matter (PM) most relevant to human health effects. While few would argue the inherent merits of such a policy, many believe there may not yet be enough information to differentially regulate PM species. New evidence, using increasingly sophisticated methodologies, has become available in the last several years, allowing more accurate assessment of exposure and resultant associations with specific types of PM, or PM derived from different sources. Such new studies may also allow differentiation of effects from different chemical components in the same study against the same health endpoints. This article considers whether this new evidence might be adequate to allow us to "speciate" PM types or sources by severity of health effects. We address this issue with respect to two widespread sources of PM, emissions from motor vehicles and coal-fired power plants. Emissions from less widespread sources, residual oil and steel/coking facilities, are also discussed in order to illustrate how health effects associated with such emissions might instead be associated with more widespread sources when accurate exposure information is unavailable. Based upon evaluation of studies and methodologies which appear to contain the most accurate information on exposure and response to important emissions, including variable local emissions, it is concluded that public health will likely be better protected by reduction of various vehicular emissions than by continued regulation of the total mass of fine PM (PM <2.5 microm, or PM2.5) as if all PM in this mode is equitoxic. However, the knowledge base is incomplete. Important remaining research questions are identified.

Evaluating the health risk from secondary sulfates in eastern North American regional ambient air particulate matter.

Epidemiological studies of particulate matter (PM) using central area monitors have associated total PM mass, as well as certain individual components of PM, including sulfate, with adverse human health effects. However, some recent studies that used concentrated ambient particles (CAPs) or analyzed the effects of air pollution from different sources or geographic areas suggest that while some particles may be harmful, other particulate species including secondary sulfates may have negligible health effects. Toxicology studies to date also suggest that secondary sulfates pose little health risk. While studies using central-area monitors implicitly assume that all residents of the area are exposed to the same levels of pollution, newer studies find substantial health effects for those in close proximity to major roads. These latter studies recognize that although population exposure to widespread pollutants, such as total PM mass and sulfates, may be relatively uniform over a wide area, exposure to pollutants from local sources is not. While there is an emerging literature associating several adverse health effects with proximity to local pollution sources, the current database provides limited information that allows identification of specific particulate species that may cause little to no harm. In this article, we suggest that ambient secondary sulfates, and eastern North American regional air masses generally, appear to have little adverse impact on public health. This suggestion is based on evidence gleaned from eight avenues of investigation: (1) recent non-central-area monitor studies, including exposure gradient or proximity studies; (2) CAPs studies; (3) studies that examine effects related to different geographic areas or sources; (4) toxicology studies; (5) the limited number of studies that analyze existing central-area monitor data to explicitly examine the health impacts of sulfate and acidity versus PM mass; (6) "modern" area monitor studies with additional capabilities to distinguish among sources of pollution; (7) partial reinterpretation of two pivotal cohort studies; and (8) studies separating effects of secondary sulfates from those of primary metal sulfates. However, uncertainties remain regarding the role that secondary sulfates may play in ambient PM chemistry pathways leading to potentially harmful products, such as the possible effects of secondary organic aerosols that may be the product of acid catalysis of sulfur dioxide. Thus, more targeted study is needed, and some research suggestions are made in this regard.

Using factor analysis to attribute health impacts to particulate pollution sources.

Laden et al. (2000) recently reported results of applying factor analysis to data taken in six cities from 1979 to 1988, identifying airborne particle sources potentially affecting daily mortality. These authors sought relationships between source groups and risk measures using source tracer elements, Se (coal combustion), Pb (light-duty motor vehicle sources), and Si (crustal--soil dispersion). Combined data analyses of this kind may overlook the complexity of source contributions, which have common tracer elements. In one of the cities, Boston, for example, the authors found coal combustion was an important source of mortality risk. For the city of Boston, the authors attribute coal combustion largely to distant upwind regional sources. The emphasis on coal combustion is confounded by the presence of major local sources of residual oil combustion, which contribute V, Se, and S (sulfur as sulfate) to the source apportionment. Evaluation of the source identification using single-element tracer analysis indicates that the detailed chemical composition or profile of major local sources needs to be taken into account in these investigations to minimize misclassification of airborne particle sources with potential adverse health effects.