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Background: Short-term exposure to air pollution has been associated with changes in blood pressure (BP) and emergency department visits for hypertension, but little is known about the effects of long-term exposure to traffic-related air pollution on BP and hypertension., Objectives: We studied whether long-term exposure to air pollution is associated with BP and hypertension., Methods: In 1993-1997, 57,053 participants 50-64 years of age were enrolled in a population-based cohort study. Systolic and diastolic BP (SBP and DBP, respectively) were measured at enrollment. Self-reported incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. We used a validated dispersion model to estimate residential long-term nitrogen oxides (NO(x)), a marker of traffic-related air pollution, for the 1- and 5-year periods prior to enrollment and before a diagnosis of hypertension. We conducted a cross-sectional analysis of associations between air pollution and BP at enrollment with linear regression, adjusting for traffic noise, measured short-term NO(x), temperature, relative humidity, and potential lifestyle confounders (n = 44,436). We analyzed incident hypertension with Cox regression, adjusting for traffic noise and potential confounders., Results: A doubling of NO(x) exposure during 1- and 5-year periods preceding enrollment was associated with 0.53-mmHg decreases [95% confidence interval (CI): -0.88, -0.19 mmHg] and 0.50-mmHg decreases (95% CI: -0.84, -0.16 mmHg) in SBP, respectively. Long-term exposure also was associated with a lower prevalence of baseline self-reported hypertension (per doubling of 5-year mean NO(x): odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NO(x) exposure was not associated with incident self-reported hypertension during follow-up., Conclusions: Long-term exposure to traffic-related air pollution was associated with a slightly lower prevalence of BP at baseline, but was not associated with incident hypertension.

Background: Exposure to air pollution in early life contributes to the burden of childhood asthma, but it is not clear whether long-term exposure to air pollution can lead to asthma onset or progression in adulthood., Objectives: The authors studied the effect of exposure to traffic-related air pollution over 35 years on the risk for asthma hospitalisation in older people., Methods: 57 053 participants in the Danish Diet, Cancer and Health cohort, aged 50-65 years at baseline (1993-1997), were followed up for first hospital admission for asthma until 2006, and the annual nitrogen dioxide (NO(2)) levels were estimated as a proxy of the exposure to traffic-related air pollution at the residential addresses of the participants since 1971. The association between NO(2) and hospitalisation for asthma was modelled using Cox regression, for the full cohort and in people with and without previous hospitalisations for asthma, and the effect modification by comorbid conditions was assessed., Results: During 10.2 years' median follow-up, 977 (1.9%) of 53 695 eligible people were admitted to hospital for asthma: 821 were first-ever admissions and 176 were readmissions. NO(2) levels were associated with risk for asthma hospitalisation in the full cohort (HR and 95% CI per IQR, 5.8 μg/m(3): 1.12; 1.04-1.22), and for first-ever admissions (1.10; 1.01-1.20), with the highest risk in people with a history of asthma (1.41; 1.15-2.07) or chronic obstructive pulmonary disease (COPD) (1.30; 1.07-1.52) hospitalisation., Conclusions: Long-term exposure to traffic-related air pollution increases the risk for asthma hospitalisation in older people. People with previous asthma or COPD hospitalisations are most susceptible.

Background: Vehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer., Methods: We followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NO(x)) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders., Results: NO(x) at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 μg/m(3) NO(x)) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 μg/m(3) NO(x))., Conclusions: This hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.

Background: Previous studies have shown associations between air pollution and risk for lung cancer., Objective: We investigated whether traffic and the concentration of nitrogen oxides (NOx) at the residence are associated with risk for lung cancer., Methods: We identified 592 lung cancer cases in the Danish Cancer Registry among 52,970 members of the Diet, Cancer and Health cohort and traced residential addresses from 1 January 1971 in the Central Population Registry. We calculated the NOx concentration at each address by dispersion models and calculated the time-weighted average concentration for all addresses for each person. We used Cox models to estimate incidence rate ratios (IRRs) after adjustment for smoking (status, duration, and intensity), environmental tobacco smoke, length of school attendance, occupation, and dietary intake of fruit., Results: For the highest compared with the lowest quartile of NOx concentration at the residence, we found an IRR for lung cancer of 1.30 [95% confidence interval (CI), 1.05-1.61], and the IRR for lung cancer in association with living within 50 m of a major road (>10,000 vehicles/day) was 1.21 (95% CI, 0.95-1.55). The results showed tendencies of stronger associations among nonsmokers, among those with a relatively low fruit intake, and among those with a longer school attendance; only length of school attendance modified the effect significantly., Conclusions: This study supports that risk for lung cancer is associated with different markers of air pollution from traffic near the residence.

Rationale: Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood., Objectives: We assessed the effect of exposure to traffic-related air pollution over 35 years on the incidence of COPD in a prospective cohort study., Methods: We followed 57,053 participants in the Danish Diet, Cancer, and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO₂) and nitrogen oxides (NO(x)) at all residential addresses of the cohort participants since 1971 to an event or 2006 and used indicators of traffic near the residential address at recruitment. We assessed the association between exposure to air pollution and COPD incidence by Cox regression analyses for the full cohort, and for participants with and without comorbid conditions, including asthma, diabetes, or cardiovascular disease., Measurements and Main Results: A first hospital admission for COPD was recorded for 1,786 (3.4%) of 52,799 eligible subjects between recruitment (1993-1997) and 2006. COPD incidence was associated with the 35-year mean NO₂ level (hazard ratio, 1.08; 95% confidence interval, 1.02-1.14, per interquartile range of 5.8 μg/m³), with stronger associations in subjects with diabetes (1.29; 1.05-1.50) and asthma (1.19; 1.03-1.38)., Conclusions: Long-term exposure to traffic-related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma.

Exposure to traffic-related air pollution in urban environment is common and has been associated with adverse human health effects. In utero exposures that result in DNA damage may affect health later in life. Early effects of maternal and in utero exposures to traffic-related air pollution were assessed through the use of validated biomarkers in blood cells from mother-newborn pairs. A cross-sectional biomonitoring study with healthy pregnant women living in the Greater Copenhagen area, Denmark, was conducted. Bulky DNA adducts and micronuclei (MN) were measured in blood from 75 women and 69 umbilical cords, concurrently collected at the time of planned Caesarean section. Modeled residential traffic density, a proxy measure of traffic-related air pollution exposures, was validated by indoor levels of nitrogen dioxide and polycyclic aromatic hydrocarbons in 42 non-smoking homes. DNA adduct levels were similar and positively correlated in maternal and cord blood (1.40 vs. 1.37 n/10(8) nucleotides; r=0.99; p<0.01). Maternal MN frequencies were significantly associated with age (p<0.01), and higher than those of the newborns (7.0 vs. 3.2 MN per 1000 binucleated cells). Adduct levels were highest among mother-newborn pairs who lived near medium-traffic-density (>400-2500 vehicle km/24h; p<0.01) places. MN frequencies among newborns from women who lived at high-traffic-density homes (>2500 vehicle km/24h) were significantly increased (p=0.02). This trend remained after adjusting for potential confounders and effect modifiers. For the first time increased bulky DNA adducts and MN in cord blood after maternal exposures to traffic-related air pollution are found, demonstrating that these transplacental environmental exposures induce DNA damage in newborns. Given that increased DNA damage early in life indicate an increased risk for adverse health effects later in life, these findings justify intervention of pregnant women.