Long-term exposure to outdoor air pollution and the incidence of chronic obstructive pulmonary disease in a national English cohort.

OBJECTIVES: The role of outdoor air pollution in the incidence of chronic obstructive pulmonary disease (COPD) remains unclear. We investigated this question using a large, nationally representative cohort based on primary care records linked to hospital admissions. METHODS: A cohort of 812 063 patients aged 40-89 years registered with 205 English general practices in 2002 without a COPD diagnosis was followed from 2003 to 2007. First COPD diagnoses recorded either by a general practitioner (GP) or on admission to hospital were identified. Annual average concentrations in 2002 for particulate matter with an aerodynamic diameter <10 µm (PM10) and <2.5 µm (PM2.5), nitrogen dioxide (NO2), ozone and sulfur dioxide (SO2) at 1 km(2) resolution were estimated from emission-based dispersion models. Hazard ratios (HRs) per interquartile range change were estimated from Cox models adjusting for age, sex, smoking, body mass index and area-level deprivation. RESULTS: 16 034 participants (1.92%) received a COPD diagnosis from their GP and 2910 participants (0.35%) were admitted to hospital for COPD. After adjustment, HRs for GP recorded COPD and PM10, PM2.5 and NO2 were close to unity, positive for SO2 (HR=1.07 (95% CI 1.03 to 1.11) per 2.2 µg/m(3)) and negative for ozone (HR=0.94 (0.89 to 1.00) per 3 µg/m(3)). For admissions HRs for PM2.5 and NO2 remained positive (HRs=1.05 (0.98 to 1.13) and 1.06 (0.98 to 1.15) per 1.9 µg/m(3) and 10.7 µg/m(3), respectively). CONCLUSIONS: This large population-based cohort study found limited, inconclusive evidence for associations between air pollution and COPD incidence. Further work, utilising improved estimates of air pollution over time and enhanced socioeconomic indicators, is required to clarify the association between air pollution and COPD incidence

Estimating the health benefits associated with a speed limit reduction to thirty kilometres per hour: a health impact assessment of noise and road traffic crashes for the Swiss city of Lausanne

Reductions of speed limits for road traffic are effective in reducing casualties, and are also increasingly promoted as an effective way to reduce noise exposure. The aim of this study was to estimate the health benefits of the implementation of 30 km/h speed limits in the city of Lausanne (136'077 inhabitants) under different scenarios addressing exposure to noise and road crashes. The study followed a standard methodology for quantitative health impact assessments to derive the number of attributable cases in relation to relevant outcomes. We compared a reference scenario (without any 30 km/h speed limits) to the current situation with partial speed limits and additional scenarios with further implementation of 30 km/h speed limits, including a whole city scenario. Compared to the reference scenario, noise reduction due to the current speed limit situation was estimated to annually prevent 1 cardiovascular death, 72 hospital admissions from cardiovascular disease, 17 incident diabetes cases, 1'127 individuals being highly annoyed and 918 individuals reporting sleep disturbances from noise. Health benefits from a reduction in road traffic crashes were less pronounced (1 severe injury and 4 minor injuries). The whole city speed reduction scenario more than doubled the annual benefits, and was the only scenario that contributed to a reduction in mortality from road traffic crashes (one death per two years). Implementing 30 km/h speed limits in a city yields health benefits due to reduction in road traffic crashes and noise exposure. We found that the benefit from noise reduction was more relevant than safety benefits

Does night-time aircraft noise trigger mortality? A case-crossover study on 24 886 cardiovascular deaths

AIMS; : It is unclear whether night-time noise events, including from aeroplanes, could trigger a cardiovascular death. In this study, we investigate the potential acute effects of aircraft noise on mortality and the specific role of different night-time exposure windows by means of a case-crossover study design.; METHODS AND RESULTS; : We selected 24 886 cases of death from cardiovascular disease (CVD) from the Swiss National Cohort around Zurich Airport between 2000 and 2015. For night-time deaths, exposure levels 2 h preceding death were significantly associated with mortality for all causes of CVD [OR = 1.44 (1.03-2.04) for the highest exposure group (LAeq > 50 dB vs. <20 dB)]. Most consistent associations were observed for ischaemic heart diseases, myocardial infarction, heart failure, and arrhythmia. Association were more pronounced for females (P = 0.02) and for people living in areas with low road and railway background noise (P = 0.01) and in buildings constructed before 1970 (P = 0.36). We calculated a population attributable fraction of 3% in our study population.; CONCLUSION; : Our findings suggest that night-time aircraft noise can trigger acute cardiovascular mortality. The association was similar to that previously observed for long-term aircraft noise exposure

The association of road traffic noise with cognition in adolescents: a cohort study in Switzerland

Environmental noise exposure has been shown to affect children's cognition, but the concept of cognition is multifaceted, and studies on associations with noise are still inconclusive and fragmented. We studied cognitive change within one year in 882 adolescents aged 10-17 years in response to road traffic noise exposure. Participants filled in a comprehensive questionnaire and underwent cognitive testing twice at an interval of one year. Figural and verbal memory was measured with the Intelligenz-Struktur-Test (IST), and concentration accuracy and constancy were measured with FAKT-II and d2 test. Exposure to noise and other environmental stressors were modelled for school and home location at baseline. Missing data was addressed with multiple imputation. Cross-sectional multilevel analyses and longitudinal change score analyses were performed. In cross-sectional analyses, figural memory was significantly reduced by -0.27 (95%CI -0.49,-0.04) units per 10 dB road traffic noise increase at home (L(den)). Longitudinal analyses showed a significant reduction of concentration constancy Z-scores between baseline and follow-up by -0.13 (95%CI -0.25, 0.00) per 10 dB road traffic noise at home (L(den)). Our study indicates that road traffic noise at home reduces cognitive performance in adolescents. Larger cohorts with longer follow-up time are needed to confirm these results

Mortality attributable to ambient fine particulate matter and nitrogen dioxide in Switzerland in 2019: use of two-pollutant effect estimates

INTRODUCTION: Air pollution health risk assessments have traditionally used single-pollutant effect estimates for one proxy ambient air pollutant such as PM(2.5). Two-pollutant effect estimates, i.e. adjusted for another correlated pollutant, theoretically enable the aggregation of pollutant-specific health effects minimizing double-counting. Our study aimed at estimating the adult mortality in Switzerland in 2019 attributable to PM(2.5) from a single-pollutant effect estimate and to the sum of PM(2.5) and NO(2) from two-pollutant estimates; comparing the results with those from alternative global, European and Swiss effect estimates. METHODS: For the single-pollutant approach, we used a PM(2.5) summary estimate of European cohorts from the project ELAPSE, recommended by the European Respiratory Society and International Society for Environmental Epidemiology (ERS-ISEE). To derive the two-pollutant effect estimates, we applied ELAPSE-based conversion factors to ERS-ISEE PM(2.5) and NO(2) single-pollutant effect estimates. Additionally, we used World Health Organization 2021 Air Quality Guidelines as counterfactual scenario, exposure model data from 2019 and Swiss lifetables. RESULTS: The single-pollutant effect estimate for PM(2.5) (1.118 [1.060; 1.179] per 10 mug/m(3)) resulted in 2240 deaths (21,593 years of life lost). Using our derived two-pollutant effect estimates (1.023 [1.012; 1.035] per 10 mug/m(3) PM(2.5) adjusted for NO(2) and 1.040 [1.023; 1.058] per 10 mug/m(3) NO(2) adjusted for PM(2.5)), we found 1977 deaths (19,071 years of life lost) attributable to PM(2.5) and NO(2) together (23% from PM(2.5)). Deaths using alternative effect estimates ranged from 1042 to 5059. DISCUSSION: Estimated premature mortality attributable to PM(2.5) alone was higher than to both PM(2.5) and NO(2) combined. Furthermore, the proportion of deaths from PM(2.5) was lower than from NO(2) in the two-pollutant approach. These seemingly paradoxical results, also found in some alternative estimates, are due to statistical imprecisions of underlying correction methods. Therefore, using two-pollutant effect estimates can lead to interpretation challenges in terms of causality

Methods matter: a comparative review of health risk assessments for ambient air pollution in Switzerland

Objectives: Air pollution health risk assessments (AP-HRAs) provide a method to quantify health effects for entire populations. In Switzerland, AP-HRAs are included in Swiss assessments for Transport Externalities (STEs), ordered by public authorities since the 1990s. This study aimed to describe the differences among national and international AP-HRAs for Switzerland. Methods: We compared input data, approaches and results across AP-HRAs over time. Results and input data for each AP-HRA were expressed as a ratio compared to the most recent STE (in most cases STE-2010). Results: Substantial variation across AP-HRAs was found. For all-cause adult mortality attributed to particulate matter (the most frequent outcome-pollutant pair), the ratio in HRAs oscillated from 0.40 to 2.09 (times the STE-2010 value). Regarding input data, the ratio ranged from 0.69 to 1.26 for population exposure, from 0 to 1.81 for counterfactual scenario, from 0.96 to 1.13 for concentration-response function and from 1.03 to 1.13 for baseline health data. Conclusion: This study demonstrates that methods matter for AP-HRAs. Transparent and possibly standardized reporting of key input data and assumptions should be promoted to facilitate comparison of AP-HRAs

Association of transportation noise with sleep during the first year of life: a longitudinal study

STUDY OBJECTIVES: During infancy, adequate sleep is crucial for physical and neurocognitive development. In adults and children, night-time noise exposure is associated with sleep disturbances. However, whether and to what extent infants' sleep is affected, is unknown. Thus, this study investigated the relationship between nocturnal transportation noise and actimetry-derived habitual sleep behavior across the first year of life. METHODS: In 144 healthy infants (63 girls), nocturnal (23:00-7:00) transportation noise (i.e., road, railway, and aircraft) was modelled at the infants' individual places of residence. Using actimetry, we recorded movement patterns for 11 days in a longitudinal design at 3, 6, and 12 months of age and derived the recently proposed core sleep composites of night-time sleep duration, activity, and variability. Using linear mixed-effects models, we determined associations between noise exposure and sleep composites. Sex, gestational age, parents' highest educational level, infants' age, and the existence of siblings served as control variables. RESULTS: In models without interactions, night-time transportation noise was unrelated to sleep composites across the first year of life (p > .16). Exploratory analyses of an interaction between noise and the existence of siblings yielded an association between night-time transportation noise and sleep duration in infants without siblings only (p = .004). CONCLUSION: In our study, sleep in infants during the first year of life was relatively robust against external perturbation by night-time transportation noise. However, particularly in children without siblings increasing night-time transportation noise reduced sleep duration. This suggests that the habitual noise environment may modulate individual susceptibility to adverse effects of noise on sleep