We investigated the association between total and cause-specific mortality and individual measures of long-term air pollution exposure in a cohort of Norwegian men followed from 1972-1973 through 1998. Data from a follow-up study on cardiovascular risk factors among 16,209 men 40-49 years of age living in Oslo, Norway, in 1972-1973 were linked with data from the Norwegian Death Register and with estimates of average yearly air pollution levels at the participants' home addresses from 1974 to 1998. Cox proportional-hazards regression was used to estimate associations between exposure and total and cause-specific mortality. During the follow-up time 4,227 men died from a disease corresponding to an ICD-9 (International Classification of Diseases, Revision 9) code < 800. Controlling for a number of potential confounders, the adjusted risk ratio for dying was 1.08 [95% confidence interval (CI), 1.06-1.11] for a 10- microg/m3 increase in average exposure to nitrogen oxides (NOx) at the home address from 1974 through 1978. Corresponding adjusted risk ratios for dying from a respiratory disease other than lung cancer were 1.16 (95% CI, 1.06-1.26); from lung cancer, 1.11 (95% CI, 1.03-1.19); from ischemic heart diseases, 1.08 (95% CI, 1.03-1.12); and from cerebrovascular diseases, 1.04 (95% CI, 0.94-1.15). The findings indicate that urban air pollution may increase the risk of dying. The effect seemed to be strongest for deaths from respiratory diseases other than lung cancer.

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In Oslo, traffic has been one of the dominating sources of air pollution in the last decade. In one part of the city where most traffic collects, two tunnels were built. A series of before and after studies was carried out in connection with the tunnels in use. Dispersion models were used as a basis for estimating exposure to nitrogen dioxide and particulate matter in two fractions. Exposure estimates were based on the results of the dispersion model providing estimates of outdoor pollutant concentrations on an hourly basis. The estimates represent concentrations in receptor points and in a square kilometre grid. The estimates were used to assess development of air pollution load in the area, compliance with air quality guidelines, and to provide a basis for quantifying exposure-effect relationships in epidemiological studies. After both tunnels were taken in use, the pollution levels in the study area were lower than when the traffic was on the surface (a drop from 50 to 40 micrograms m-3). Compliance with air quality guidelines and other prescribed values has improved, even if high exposures still exist. The most important residential areas are now much less exposed, while areas around tunnel openings can be in periods exposed to high pollutant concentrations. The daily pattern of exposure shows smaller differences between peak and minimum concentrations than prior to the traffic changes. Exposures at home (in the investigation area) were reduced most, while exposures in other locations than at home showed only a small decrease. Highest hourly exposures are encountered in traffic.

Annual concentration fields of SO2 and NOx for the period 1974-1998 are calculated for a 22 x 18 km2-grid in Oslo. In a study of lung cancer and air pollution in Oslo, 16209 men living in Oslo have been followed from 1972/73 to 1998. This paper presents a method for estimating their annual residential air pollution exposure for SO2 and NOx. In the exposure assessment the National Population Register provided information on home addresses. Each participant was given an annual average air pollutant concentration outdoors of the address he lived the largest part of that year. Persons living close to streets with high traffic were given an additional concentration, and persons who moved outside Oslo were given a region value for each year. Due to regulations of the sulfur content in fuel oil and a general change of local heating systems to electricity or distant heating, the SO2-concentrations in Central Oslo were reduced during the period from about 60 microg m(-3) in 1974-75 to about 4 microg m(-3) in 1997-98. Due to the increasing traffic the NOx-concentrations have increased slowly, from about 40 microg m(-3) in 1974-84 to about 60 microg m(-3) in 1989. After the introduction of catalyst cars the concentrations were reduced to about 45 microg m(-3) in 1997-98.