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Background: Established risk factors for breast cancer include genetic disposition, reproductive factors, hormone therapy, and lifestyle-related factors such as alcohol consumption, physical inactivity, smoking, and obesity. More recently a role of environmental exposures, including air pollution, has also been suggested. The aim of this study, was to investigate the relationship between long-term air pollution exposure and breast cancer incidence. Methods: We conducted a pooled analysis among six European cohorts (n = 199,719) on the association between long-term residential levels of ambient nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone in the warm season (O3) and breast cancer incidence in women. The selected cohorts represented the lower range of air pollutant concentrations in Europe. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. Results: During 3,592,885 person-years of follow-up, we observed a total of 9,659 incident breast cancer cases. The results of the fully adjusted linear analyses showed a HR (95% confidence interval) of 1.03 (1.00-1.06) per 10 µg/m³ NO2, 1.06 (1.01-1.11) per 5 µg/m³ PM2.5, 1.03 (0.99-1.06) per 0.5 10-5 m-1 BC, and 0.98 (0.94-1.01) per 10 µg/m³ O3. The effect estimates were most pronounced in the group of middle-aged women (50-54 years) and among never smokers. Conclusions: The results were in support of an association between especially PM2.5 and breast cancer. Impact: The findings of this study suggest a role of exposure to NO2, PM2.5, and BC in development of breast cancer. [ABSTRACT FROM AUTHOR]

Most studies investigating the health effects of long-term exposure to air pollution used traditional regression models, although causal inference approaches have been proposed as alternative. However, few studies have applied causal models and comparisons with traditional methods are sparse. We therefore compared the associations between natural-cause mortality and exposure to fine particulate matter (PM 2.5) and nitrogen dioxide (NO 2) using traditional Cox and causal models in a large multicenter cohort setting. We analysed data from eight well-characterized cohorts (pooled cohort) and seven administrative cohorts from eleven European countries. Annual mean PM 2.5 and NO 2 from Europe-wide models were assigned to baseline residential addresses and dichotomized at selected cut-off values (PM 2.5 : 10, 12, 15 μg/m³; NO 2 : 20, 40 μg/m³). For each pollutant, we estimated the propensity score as the conditional likelihood of exposure given available covariates, and derived corresponding inverse-probability weights (IPW). We applied Cox proportional hazards models i) adjusting for all covariates ("traditional Cox") and ii) weighting by IPW ("causal model"). Of 325,367 and 28,063,809 participants in the pooled and administrative cohorts, 47,131 and 3,580,264 died from natural causes, respectively. For PM 2.5 above vs. below 12 μg/m³, the hazard ratios (HRs) of natural-cause mortality were 1.17 (95% CI 1.13–1.21) and 1.15 (1.11–1.19) for the traditional and causal models in the pooled cohort, and 1.03 (1.01–1.06) and 1.02 (0.97–1.09) in the administrative cohorts. For NO 2 above vs below 20 μg/m³, the HRs were 1.12 (1.09–1.14) and 1.07 (1.05–1.09) for the pooled and 1.06 (95% CI 1.03–1.08) and 1.05 (1.02–1.07) for the administrative cohorts. In conclusion, we observed mostly consistent associations between long-term air pollution exposure and natural-cause mortality with both approaches, though estimates partly differed in individual cohorts with no systematic pattern. The application of multiple modelling methods might help to improve causal inference. 299 of 300 words. [Display omitted] • We assessed associations between long-term PM 2.5 and NO 2 and natural-cause mortality. • We compared traditional Cox and causal inference models across large European cohorts. • We observed mostly consistent associations with both approaches. • Estimates partly differed in individual cohorts with no systematic pattern. • Application of multiple modelling methods is favorable to improve causal inference. [ABSTRACT FROM AUTHOR]

An increasing number of epidemiological studies have examined the association between ultrafine particles (UFP) and imbalanced autonomic control of the heart, a potential mechanism linking particulate matter air pollution to cardiovascular disease. This study systematically reviews and meta-analyzes studies on short-term effects of UFP on autonomic function, as assessed by heart rate variability (HRV). We searched PubMed and Web of Science for articles published until June 30, 2022. We extracted quantitative measures of UFP effects on HRV with a maximum lag of 15 days from single-pollutant models. We assessed the risk of bias in the included studies regarding confounding, selection bias, exposure assessment, outcome measurement, missing data, and selective reporting. Random-effects models were applied to synthesize effect estimates on HRV of various time courses. Twelve studies with altogether 1,337 subjects were included in the meta-analysis. For an increase of 10,000 particles/cm3 in UFP assessed by central outdoor measurements, our meta-analysis showed immediate decreases in the standard deviation of the normal-to-normal intervals (SDNN) by 4.0% [95% confidence interval (CI): 7.1%, −0.9%] and root mean square of successive R-R interval differences (RMSSD) by 4.7% (95% CI: 9.1%, 0.0%) within 6 h after exposure. The immediate decreases in SDNN and RMSSD associated with UFP assessed by personal measurements were smaller and borderline significant. Elevated UFP were also associated with decreases in SDNN, low-frequency power, and the ratio of low-frequency to high-frequency power when pooling estimates of lags across hours to days. We did not find associations between HRV and concurrent-day UFP exposure (daily average of at least 18 h) or exposure at lags ≥ one day. Our study indicates that short-term exposure to ambient UFP is associated with decreased HRV, predominantly as an immediate response within hours. This finding highlights that UFP may contribute to the onset of cardiovascular events through autonomic dysregulation. [Display omitted] • Twelve studies with 1,337 subjects were synthesized in the meta-analysis. • Short-term ultrafine particles (UFP) exposure was associated with decreased HRV. • The UFP effects on HRV were most prominent within 6 h after exposure. • Stronger UFP effects were reported in populations without coronary artery diseases. • UFP may contribute to cardiovascular events through autonomic dysregulation. [ABSTRACT FROM AUTHOR]

The aim of this study is to estimate the mortality burden attributable to low temperature in Athens, Lisbon and London from 2002 to 2011 and to discuss related inequalities in socioeconomic conditions. We address a lack of quantitative estimates of cold-related mortality, particularly for the cities of Lisbon and Athens. To estimate the mortality burden attributable to low temperature, time-series regression analyses were carried out on daily mortality with respect to daily mean temperature for the three metropolitan areas to estimate the relative risk associated with a decrease in temperature. The number of cold-related deaths was estimated using the population Attributable Fraction. Lisbon presents higher relative risk (RR) than London and Athens; the RR for Athens is lower than for London. The coldrelated death rate is higher in Lisbon (53.2 deaths per 100,000 inhabitants) than in Athens (32.6) and London (37.6). The spatial heterogeneity between the three metropolitan areas in the risk estimates and cold-related mortality may result from the significant disparities in the built environment. Adequate public health planning and preventive measures in the built environment may help reduce cold-related deaths and decrease vulnerability to cold in European cities. • Cold has significant impacts on human health. • Cold-related death rate is higher in Lisbon than in Athens and London. • Spatial heterogeneity to cold may result from the built environment characteristics. • Preventive measures may help to reduce cold-related deaths and vulnerability. [ABSTRACT FROM AUTHOR]