Internal combustion and health.

The association between intense industrial air pollution and lung disease has been acknowledged since the 1930s, but surprisingly little is known about the effects of long term inhalation of urban concentrations of vehicle exhaust fumes. These contain several potentially harmful substances, including nitrogen oxides, hydrocarbons, carbon monoxide, lead, and, to a lesser extent, sulphur dioxide. In Great Britain the number of cars is predicted to double from 23 million to 42-56 million by 2025 so we need to know whether these substances are in fact doing us harm. The estimated 4000 deaths a year caused by atmospheric pollution in the first part of this century led to the Clean Air Act 1957, the establishment of the Clean Air Council, and the Medical Research Council's air pollution unit, measures to control emissions, and the setting up of an extensive network to monitor smoke and sulphur dioxide concentrations. The success of these measures, however, led to the dismantling of some of the mechanisms that made them possible: the Clean Air Council was abolished in 1979 and the Medical Research Council's air pollution unit a year later, and the monitoring network was disbanded. Monitoring is now done to comply with European Community directives on air quality, but Britain has few monitoring stations. The nitrogen oxide monitoring network, for example, consists of just six sites, only four ofwhich monitor areas affected by vehicle emissions (Japan has 1800 and The Netherlands 89). Yet comprehensive monitoring, along with epidemiological, clinical, and laboratory research, is badly needed to assess the extent to which Britain's citizens are vulnerable to vehicle emissions. Since the closure of the Medical Research Council's air pollution unit in 1980 there have been virtually no research publications on this subject from British sources. This is disappointing given the quality of research that followed the 1952 London smog' and contrasts sharply with the intense activity in the United States. One recent study of 944 bridge and tunnel workers in New York City showed that tunnel workers had significantly lower forced expiratory volumes at one second and forced vital capacities, more respiratory symptoms, and higher plasma carboxyhaemoglobin concentrations than the bridge workers. ' Pulmonary function and symptoms were significantly worse in all workers who had been employed for over 10 years. The relevance of such epidemiological work to individual risk and the clinical effect of long term minor changes in pulmonary function and oxygen carrying capacity are difficult to assess, but it is possible to identify groups ofpeople who may be vulnerable to such changes, such as those with asthma, chronic obstructive airways disease, and arterial disorders. Clinical studies in normal people showed that lung function is disturbed at concentrations of nitrogen dioxide above two parts per million, but below this the data are conflicting. In some people with asthma exposure to concentrations as low as 0-1 part per million causes moderate bronchoconstriction and greatly increases bronchial hyperreactivity. The European Community directive is that 98% of hourly average nitrogen dioxide concentrations should not exceed 0-1 part per million. This is achieved most of the time at urban sites in Britain that are not at the roadside, but hourly maximums of 0-2-0-4 parts per million are recorded in London's Cromwell Road, one of the government's monitoring sites.4