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Background: Long-term exposure to air pollution has been associated with mortality in urban cohort studies. Few studies have investigated this association in large-scale population registries, including non-urban populations., Objectives: The aim of the study was to evaluate the associations between long-term exposure to air pollution and nonaccidental and cause-specific mortality in the Netherlands based on existing national databases., Methods: We used existing Dutch national databases on mortality, individual characteristics, residence history, neighborhood characteristics, and national air pollution maps based on land use regression (LUR) techniques for particulates with an aerodynamic diameter ≤ 10 μm (PM10) and nitrogen dioxide (NO2). Using these databases, we established a cohort of 7.1 million individuals ≥ 30 years of age. We followed the cohort for 7 years (2004-2011). We applied Cox proportional hazard models adjusting for potential individual and area-specific confounders., Results: After adjustment for individual and area-specific confounders, for each 10-μg/m3 increase, PM10 and NO2 were associated with nonaccidental mortality [hazard ratio (HR) = 1.08; 95% CI: 1.07, 1.09 and HR = 1.03; 95% CI: 1.02, 1.03, respectively], respiratory mortality (HR = 1.13; 95% CI: 1.10, 1.17 and HR = 1.02; 95% CI: 1.01, 1.03, respectively), and lung cancer mortality (HR = 1.26; 95% CI: 1.21, 1.30 and HR = 1.10 95% CI: 1.09, 1.11, respectively). Furthermore, PM10 was associated with circulatory disease mortality (HR = 1.06; 95% CI: 1.04, 1.08), but NO2 was not (HR = 1.00; 95% CI: 0.99, 1.01). PM10 associations were robust to adjustment for NO2; NO2 associations remained for nonaccidental mortality and lung cancer mortality after adjustment for PM10., Conclusions: Long-term exposure to PM10 and NO2 was associated with nonaccidental and cause-specific mortality in the Dutch population of ≥ 30 years of age.

We studied the spatial distribution of cancer incidence rates around a large steel plant and its association with historical exposure. The study population was close to 600,000. The incidence data was collected for 1995-2006. From historical emission data the air pollution concentrations for polycyclic aromatic hydrocarbons (PAH) and metals were modelled. Data were analyzed using Bayesian hierarchical Poisson regression models. The standardized incidence ratio (SIR) for lung cancer was up to 40% higher than average in postcodes located in two municipalities adjacent to the industrial area. Increased incidence rates could partly be explained by differences in socioeconomic status (SES). In the highest exposure category (approximately 45,000 inhabitants) a statistically significant increased relative risk (RR) of 1.21 (1.01-1.43) was found after adjustment for SES. The elevated RRs were similar for men and women. Additional analyses in a subsample of the population with personal smoking data from a recent survey suggested that the observed association between lung cancer and plant emission, after adjustment for SES, could still be caused by residual confounding. Therefore, we cannot indisputably conclude that past emissions from the steel plant have contributed to the increased risk of lung cancer.

A group of male amateur cyclists was studied in the summer of 1991 in the east of the Netherlands. Lung function was measured before and after training sessions or competitive races on a number of occasions. Continuous heart rate monitors were employed to document exercise levels. Heart rate averaged 161 beats/min during training, and 176 beats/min during races. Exercise duration averaged 75 min. Ozone concentrations during exercise were obtained from the nearest stations of the National Monitoring Network. The difference between pre- and postexercise lung function values was related to these ozone concentrations. Ozone concentrations were low on most occasions with an average of 87 micrograms/m3 and a maximum of 195 micrograms/m3. The difference between pre- and postexercise lung function was found to be negatively related to the ozone concentration during exercise. When all observations obtained at ozone concentrations higher than 120 micrograms/m3 were removed from the analysis, the relationship with ozone was still significant. The data also suggested that effects of ozone on lung function were stronger in midsummer than in the late summer. The difference between pre- and postexercise acute symptoms was positively related to ozone, for shortness of breath, chest tightness, and wheeze. Cough and eye irritation were not related to ozone. These results indicate that in healthy young men vigorously exercising outdoors, ozone is related to lung function changes and acute respiratory symptom changes at low levels of exposure.