Is diesel exhaust a cause for increasing allergies?

Health effects due to air pollution arising from motor vehicles have recently become a major public and political concern worldwide. Rapidly growing urban populations and increasing levels of industrialization have inevitably led to greater energy demand and an increased requirement for transportation, with resultant large increases in vehicular emissions. The United Nations estimates indicate, that by the year 2000, 47% of the global population will be living in urban areas, when about 300–400 million city dwellers will be exposed to unhealthy and dangerous levels of motor vehicle generated air pollutants [1]. This rapid increase in motor vehicular traffic and its emissions have paralleled a worldwide increase in the incidence of allergic diseases such as asthma and rhinitis. Although genetic factors are important in the development of allergy, this rapid increase over the last two decades can only be explained by changes occurring in the environment. There is one school of thought to suggest that part of the rising trends can be explained by increasing levels of air pollutants emitted from motor vehicles [2]. Ultrafine particles generated by the heat combustion processes from vehicular exhausts, in particular, have become a cause of concern, especially since more than 60 studies conducted in different geographical locations have demonstrated a significant and consistent association between ambient levels of particles with several health outcomes, such as mortality and the incidence and exacerbation of allergies, asthma, chronic bronchitis, respiratory tract infections and ischaemic heart diseases [3–5]. Interestingly, these adverse events have been observed over a range of concentrations of particles in the ambient air, even at levels considered to be safe according to WHO guidelines [6]. On a worldwide scale, the United Nations Environment Programme has reported particulate matter pollution to be the most serious air pollution problem faced by many cities and towns [7]. Diesel exhaust is one of the major contributors to particulate matter pollution in urban areas, accounting for up to 90% of the ultrafine particulate mass in the ambient air of many major cities of the world [7,8]. The sales of diesel vehicles have increased rapidly over recent years, mainly because diesel engines are highly efficient and economical, need less maintenance and have been promoted by the motor vehicle industry as more ‘environmentally friendly’ than petrol engines, since they generate up to 25% less CO 2, a greenhouse gas implicated in global warming [9]. However, these advantages appear to be greatly compromised by the amount of particles and oxides of nitrogen (NOx) generated from diesel engines, since they emit up to 100– 150 times more particles and up to 2–20 times more NOx than do petrol engines fitted with catalytic convertors [9,10]. Ultrastructural studies of diesel exhaust particles (DEPs) suggest that over 80% of the DEPs are between 0.1 and 0.2 mm in diameter [11], hence remain buoyant in the air for long periods of time and are readily deposited in the lung. DEPs consist of a central carbon core nucleus onto which an estimated 18 000 combustion products are adsorbed, including toxic compounds such as polyaromatic hydrocarbons and transition metals [12]. Estimating the risk of DEP on human health has become a major worldwide health issue. Earlier epidemiological studies suggested a role for diesel exhaust in enhancing allergic respiratory diseases, when it was demonstrated that people living close to main roads with heavy diesel traffic suffered more respiratory symptoms and allergies than those living further away [13]. Several studies have reported decrements in lung function measurements and increased incidence of respiratory symptoms in people exposed to high levels of diesel exhaust at work [14,15]. However, most evidence implicating adverse health effects of diesel exhaust have come indirectly from a large number of epidemiological studies which have revealed a significant and consistent link between particulate matter in the ambient air (to which diesel exhaust is a major contributor) and various health outcome indices. The consistency and coherency of these observations argue for a causal relationship. However, statistical methods used to analyse such data cannot establish proof of a causal relationship but can only define an association with a certain probability. Causality is a matter of judgement that goes beyond any statement of statistical probability. The validity of any relationship identified by epidemiological studies can only be established by the xistence of plausible, underlying biological mechanisms. In this issue of the journal, Terada et al. [16] have demonstrated that DEPs up-regulate the expression of histamine-1 (H1) receptor mRNA in human airway epithelial and endothelial cells and enhance histamineinduced increase in IL-8 and GM-CSF production i vitro. This study is important because it offers a plausible underlying mechanism for DEPs in enhancing allergic responses and further supports a causal role for the relationship observed b tween ambient levels of particles and the increased expression of allergic respiratory diseases. The effect of diesel exhaust on the cell responses of the human airways was highlighted in the early 1990s by the finding that, when exposed to DE for one hour, healthy human volunteers demonstrated an increase in the number of alveolar macrophages, neutrophils and T lymphocytes in the bronchoalveolar lavage (BAL) fluid [17]. Since then,