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Purpose of Review: Stroke is the second leading cause of death worldwide, and exposure to particulate air pollution is now recognized as one of the major modifiable risk factors. However, air pollution can vary in terms of physicochemical composition and exposition specificities. Therefore, its relationships with stroke outcomes remain under intense investigation., Recent Findings: This review highlights, alongside particles, that short-term and long-term exposure to nitrogen dioxide (NO 2 ) and ozone is likely to be also linked to stroke-related morbidity and mortality. Moreover, air pollution may increase the risk of transitioning from a healthy status to incident stroke and morbimortality after stroke. Additionally, relationships may vary depending on the air pollution mixture (e.g., particle-related components, pollutant interactions), pollutant sources (e.g., traffic-related or not), stroke etiology (ischemic or hemorrhagic), or exposed individual's characteristics (e.g., age, sex, genetic predisposition, weight status). Nonlinear dose-response functions and short-term effect lags have been reported, but these features need further refinement., Summary: The relationship between stroke and air pollution is now well established. Nonetheless, future research should further consider the physicochemical properties of air pollutants, multiple exposures, and individual vulnerabilities. Moreover, advanced statistical methods should be more commonly used to better describe the relationship shapes., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Context: Policies aiming at decreasing air pollutants (e.g., fine particulate matter, PM 2.5 ) are often designed without targeting an explicit health benefit nor carrying out cost-benefit analyses., Methods: We developed a transdisciplinary backward and forward approach at the conurbation level: from health objectives set by local decision-makers, we estimated which reductions in PM 2.5 exposures and emissions would allow to reach them, and identified urban policies leading to these reductions (backward approach). We finally conducted health impact and cost-benefit analyses of these policies (forward approach). The policies were related to the most emitting sectors in the considered area (Grenoble, France), wood heating and transport sectors. The forward approach also considered the health impact and co-benefits of these policies related to changes in physical activity and CO 2 emissions., Findings: Decision-makers set three health targets, corresponding to decreases by 33% to 67% in PM 2.5 -attributable mortality in 2030, compared to 2016. A decrease by 42% in PM 2.5 exposure (from 13.9 µg/m 3 ) was required to reach the decrease by 67% in PM 2.5 -attributable mortality. For each Euro invested, the total benefit was about 30€ for policies focusing on wood heating, and 1 to 68€ for traffic policies. Acting on a single sector was not enough to attain a 67% decrease in PM 2.5 -attributable mortality. This target could be achieved by replacing all inefficient wood heating equipment by low-emission pellet stoves and reducing by 36% the traffic of private motorized vehicles. This would require to increase the share of active modes (walking, biking…), inducing increases in physical activity and additional health benefits beyond the initial target. Annual net benefits were between €484 and €629 per capita for policies with report on active modes, compared to between €162 and €270 without., Conclusions: Urban policies strongly reducing air pollution-attributable mortality can be identified by our approach. Such policies can be cost-efficient., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: There is only scant evidence that air pollution increases the risk of breast cancer., Objectives: We investigated this relationship for three air pollutants: nitrogen dioxide (NO 2 ) and particulate matter with an aerodynamical diameter below 10 µm (PM 10 ) and 2.5 µm (PM 2.5 )., Methods: We conducted a population-based case-control study on breast cancer in two French départements, including 1,229 women diagnosed with breast cancer in 2005-2007 and 1,316 control women frequency-matched on age. Concentrations of NO 2 , PM 10 and PM 2.5 at participants' addresses occupied during the last 10 years were assessed using a chemistry transport model. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using multivariable logistic regression models where each woman was assigned a weight depending on her probability of selection into the study., Results: The OR for breast cancer per 10-µg/m 3 increase in NO 2 was 1.11 (95% CI, 0.98, 1.26), and 1.41 (95% CI 1.07, 1.86) in the highest exposure quintile (Q5), compared to the first. The ORs per 10-µg/m 3 NO 2 did not markedly differ between pre- (OR 1.09, 95% CI 0.89, 1.35)) and post-menopausal women (OR 1.14, 95% CI 0.97, 1.33)), but the OR was substantially higher for hormone-receptor positive (ER+/PR+) breast tumor subtypes (OR 1.15, 95% CI 1.00, 1.31) than for ER-/PR- tumors (OR 0.95, 95% CI 0.72, 1.26). Breast cancer risk was not associated with either PM 10 (OR per 1 µg/m 3 1.01, 95% CI, 0.96, 1.06) or PM 2.5 (OR per 1 µg/m 3 1.02, 95% CI 0.95, 1.08), regardless of the menopausal status or of the breast tumor subtype., Discussion: Our study provides evidence that NO 2 exposure, a marker of traffic-related air pollutants, may be associated with an increased risk of breast cancer, particularly ER+/PR+ tumors., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: The epidemiological literature of associations between atmospheric pollutant exposure and breast cancer incidence has recently strongly evolved., Objectives: We aimed to perform a ) a meta-analysis of studies considering this relationship, correcting for publication bias and taking menopausal status and cancer hormone responsiveness into account; and b ) for the pollutants most likely to affect breast cancer, an assessment of the corresponding number of attributable cases in France and of the related economic costs., Methods: We conducted a literature review and random-effects meta-analyses of epidemiological studies examining the association of fine particulate matter with aerodynamic diameter less than or equal to 2.5 μ m ( PM 2.5 ), particulate matter with aerodynamic diameter less than or equal to 10 μm ( PM 10 ), and NO 2 long-term exposure with breast cancer incidence; additional analyses were stratified on menopausal status and on tumor hormone responsiveness status. The resulting dose-response functions were combined with modeled atmospheric pollutant exposures in 2013 for France, cancer treatments costs, lost productivity, and years of life lost, to estimate the number of breast cancers attributable to atmospheric pollution and related economic costs in France., Results: The review identified 32, 27, and 36 effect estimates for PM 2.5 , PM 10 , and NO 2 , respectively. The meta-analytical relative risk estimates of breast cancer corrected for publication bias were 1.006 [95% confidence interval (CI): 0.941, 1.076], 1.047 (95% CI: 0.984, 1.113), and 1.023 (95% CI: 1.005, 1.041), respectively. NO 2 estimated effects appeared higher in premenopausal than in postmenopausal women and higher for hormone responsive positive ( ER + / PR + ) than negative ( ER - / PR - ) breast cancers. Assuming a causal effect of NO 2 , we estimated that 1,677 (95% CI: 374, 2,914) new breast cancer cases were attributable to NO 2 annually in France, or 3.15% (95% CI: 0.70, 5.48) of the incident cases. The corresponding tangible and intangible costs were estimated to be € 825  million (low, high: 570, 1,080) per year., Conclusion: These findings suggest that decreasing long-term NO 2 exposure or correlated air pollutant exposures could lower breast cancer risk. https://doi.org/10.1289/EHP8419.

Background: Fine particulate matter (PM 2.5 ) exposure entails large health effects in many urban areas. Public measures aiming at decreasing air pollution are often designed without targeting an explicit health benefit. Our objective was to investigate the health and economic benefits and the social inequalities in exposure resulting from several scenarios of reduction of PM 2.5 exposure, in order to support decisions about urban policies., Material and Methods: In the French conurbations of Grenoble and Lyon (0.4 and 1.4 million inhabitants, respectively), PM 2.5 yearly average exposure was estimated on a 10-m grid by coupling a PM 2.5 dispersion model to population density. Changes in death cases, life expectancy, lung cancer and term low birth weight incident cases as well as associated health economic costs were estimated for ten PM 2.5 reduction scenarios differing in terms of amplitude of reduction and spatial extent. Changes in social differences in PM 2.5 exposure were also assessed., Results: During the 2015-2017 period, PM 2.5 average exposure was 13.9 μg/m 3 in Grenoble and 15.3 μg/m 3 in Lyon conurbations. Exposure to PM 2.5 led to an estimated 145 (95% Confidence Interval, CI, 90-199) and 531 (95% CI, 330-729) premature deaths, 16 (95% CI, 8-24) and 65 (95% CI, 30-96) incident lung cancers, and 49 (95% CI, 19-76) and 193 (95% CI, 76-295) term low birth weight cases each year in Grenoble and Lyon conurbations, respectively, compared to a situation without PM 2.5 anthropogenic sources, i.e. a PM 2.5 concentration of 4.9 μg/m 3 . The associated costs amounted to 495 (Grenoble) and 1767 (Lyon) M€/year for the intangible costs related to all-cause non-accidental mortality and 27 and 105 M€ for the tangible and intangible costs induced by lung cancer. A PM 2.5 exposure reduction down to the WHO air quality guideline (10 μg/m 3 ) would reduce anthropogenic PM 2.5 -attributable mortality by half while decreases by 2.9 μg/m 3 (Grenoble) and 3.3 μg/m 3 (Lyon) were required to reduce it by a third. Scenarios focusing only on the most exposed areas had little overall impact. Scenarios seeking to reach a homogeneous exposure in the whole study area were the most efficient in alleviating social inequalities in exposure., Conclusions: Reduction scenarios targeting only air pollution hotspots had little expected impact on population health. We provided estimates of the PM 2.5 change required to reduce PM 2.5 -attributable mortality by one third or more. Our approach can help targeting air pollution reduction scenarios expected to entail significant benefits, and it could easily be transposed to other urban areas., (Copyright © 2019. Published by Elsevier Ltd.)

Rationale: Although the effects of traffic-related air pollution on respiratory exacerbations have been well documented, its impact on lung function in childhood remains unclear., Objectives: Our aim was to investigate the associations of prenatal, early, and lifetime traffic-related air pollution exposure with lung function at 8-9 years studying possible effect modification by sex, sensitization at 8-9 years, and early lower respiratory tract infections., Methods: We conducted this study among 788 children from the PARIS (Pollution and Asthma Risk: an Infant Study) birth cohort. Lung function tests were performed during the medical examination at 8-9 years. Traffic-related air pollution exposure during each trimester of pregnancy was estimated using nitrogen oxides background measurements. Postnatal traffic-related air pollution exposure was assessed by a nitrogen oxides air dispersion model at both residential and daycare/school addresses. Associations between lung function and traffic-related air pollution exposure were analyzed by multiple linear regression models., Results: Higher prenatal nitrogen oxides levels, especially during the second trimester of pregnancy, were associated with a lower forced expiratory flow at 25-75% of the forced vital capacity, but there were no significant associations between prenatal nitrogen oxide levels and forced vital capacity, forced expiratory volume during 1 second, or the forced expiratory volume during 1 second/forced vital capacity ratio overall. Postnatal traffic-related air pollution exposure was associated with lower lung function among children with early lower respiratory tract infections or sensitization at 8-9 years, but not in the full cohort. In children with early repeated lower respiratory tract infections, an interquartile increase in lifetime nitrogen oxides exposure was associated with both a lower forced expiratory volume during 1 second (-62.6 ml; 95% confidence interval = -107.0 to -18.1) and forced vital capacity (-55.7 ml; 95% confidence interval = -109.5 to -1.8), but was not associated with the forced expiratory volume during 1 second/forced vital capacity ratio. There was an association between greater early postnatal nitrogen oxide exposure and a lower forced expiratory volume during 1 second/forced vital capacity ratio among sensitized children (-0.65%; 95% confidence interval = -1.25 to -0.05)., Conclusions: This study sheds new light, suggesting associations between postnatal traffic-related air pollution exposure and reduced lung function may be enhanced by early, repeated lower respiratory tract infections or allergic sensitization.