Preface

This is a good time to step back and review our understanding of the health effects of exposure to ambient particulate matter (PM) and the implications for occupational exposures to PM. That is the goal of this issue of the Clinics in Occupational and Environmental Medicine. Why is it a good time? There are at least four reasons.

First, it has become clear from research conducted over the past 15 years that PM exposure is a major public health issue. Worldwide, outdoor PM pollution is estimated to cause 500,000 excess deaths annually. In the United States, recent epidemiological studies suggest that chronic PM exposure increases cancer risk similar to living with a smoker, and shortens life on the order of 1 or 2 years [1].

Second, remarkable progress has been made in the science of PM health effects and their mechanisms. Many of the scientific questions about PM health effects that were originally posed in a report of the National Academy of Sciences [2] have begun to be addressed. Major research funding initiatives in the United States and elsewhere, via the National Institutes of Health, the US Environmental Protection Agency (EPA), the Health Effects Institute, and other organizations, are bearing fruit. We now know that PM exposure at levels experienced outdoors in urban environments has effects on the blood and the heart, and increases risk for pulmonary and cardiovascular events in susceptible people. These findings have revolutionized our understanding of interactions between the lungs and the heart, and of the ability of inhaled particles to deposit in the respiratory system and gain access to the circulation and even the brain.

Third, the advancing science is informing and inspiring regulatory efforts aimed at reducing health risks, a process that will have widespread impact. Of course, the regulatory process is complex, and involves costs as well as benefits. In the United States, the EPA has recently readdressed the National Ambient Air Quality Standards for PM, a process required every five years under the Clean Air Act, amended in 1990. The issues are more controversial than ever: the EPA staff, and the EPA's own Clean Air Scientific Advisory Committee (CASAC) recommended tightening of air quality standards for fine PM and the introduction of a new standard for coarse PM, based on an extensive review of the scientific evidence [1]. However, the EPA administrator has promulgated less stringent standards for fine PM than those recommended by the CASAC, and did not recommend a coarse PM standard. Scientists knowledgeable about the issues have expressed surprise and concern at the failure of the US EPA to take its own advice [3].

Fourth, risks to workers from occupational exposures to PM are beginning to get long-overdue attention, and these risks are reviewed in this issue. Workers in “dusty” occupations are often exposed to PM concentrations that far exceed ambient urban levels, without obvious acute health consequences; this has occasionally been cited as evidence against PM-related health effects. However, recent evidence suggests that workplace PM exposure does carry long-term pulmonary and cardiovascular risks.

And what do we see in our crystal ball for the future? As in the past decade, the next should see formidable improvements in our understanding, and perhaps even control, of both individual and societal risks. The likelihood of an adverse response to an inhaled pollutant depends on the degree of exposure to the pollutant and on individual characteristics that determine the susceptibility of the exposed person. Although we have made significant progress in characterizing components of exposure, the challenges to identify factors responsible for individual susceptibility remain. Extensive use has been made of inbred mouse strains with varying susceptibility to air pollutant–induced lung injury and inflammation, particularly with ozone and PM [4]. In humans, one of the candidate genes most implicated in air pollution responses is GSTM1, an important enzyme in the glutathione pathway for protection against oxidant injury [5]. GSTM1 has a null allele with no protein expression, which confers reduction in antioxidant protection. This allele is present in 40% of the population of the United States. Children with the GSTM1 null allele have reduced lung function growth [6]. Children in Mexico City who carry the GSTM1 null appear to be more susceptible to the effects of ambient ozone exposure [7]. GSTM1 and GSTP1 polymorphisms may also play a role in enhancing the nasal IgE response to diesel exhaust particle exposure [8]. Other important susceptibility genes will surface. Furthermore, with the rapid advances in proteomics and genomics and their incorporation into the emerging discipline of molecular epidemiology, the potential for unraveling susceptibility at the population level appears as a realistic goal.

In addition, efforts to identify and link specific components of the PM mix with various PM-associated health effects are intensifying. As we better understand these relationships, the tool of source apportionment becomes increasingly important for controlling exposures. And perhaps most importantly, major sources of pollutants may be disappearing; for example, the promise of “clean” diesel lies in the immediate future. Nevertheless, the global burden of disease as a consequence of air pollution remains a growing threat [9]. Time-series epidemiological studies have shown increased risk for air pollution mortality and morbidity in groups with lower socioeconomic status. This has implications for growing urban populations, in both developed and underdeveloped countries. But as this volume of the Clinics in Occupational and Environmental Medicine of North America indicates, much progress has been made, and our understanding of the relationship between increased individual and population susceptibility, genes, and environment promises important benefits to society.