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Copyright of Actualités Pharmaceutiques is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Actualités Pharmaceutiques is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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 [micro]m ([PM.sub.2.5]), particulate matter with aerodynamic diameter less than or equal to 10 [micro]m ([PM.sub.10]), and N[O.sub.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.sub.2.5], [PM.sub.10], and N[O.sub.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. N[O.sub.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 N[O.sub.2], we estimated that 1,677 (95% CI: 374, 2,914) new breast cancer cases were attributable to N[O.sub.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 [euro] (low, high: 570, 1,080) per year. Conclusion: These findings suggest that decreasing long-term N[O.sub.2] exposure or correlated air pollutant exposures could lower breast cancer risk. https://doi.org/10.1289/EHP8419, Introduction With more than 2 million incident cases worldwide in 2018 (corresponding to an age-standardized incidence rate of 46 per 100,000 person-years), breast cancer is the second most frequent cancer [...]

Ultrafine particles (UFP, particulate matter PM < 100 nm), through their small size, high number and surface area, and their chemical composition,[1] can induce serious health effects.[2] UFP are able to reach lung alveoli[3] and are toxic through mechanisms of oxidative stress, cell signaling and activation, and release of mediators initiating inflammatory processes in the respiratory tract and in the cardiovascular system.[[3]] Moreover, asthmatic/allergic children are likely to be more susceptible to UFP exposure than healthy children.[2] However, epidemiological data on the short-term respiratory health effects of UFP exposure, especially on the fraction of exhaled nitric oxide (FeNO) as a marker of eosinophilic airway inflammation[5] in children, remain limited.[2] Only one study used personal measurements of UFP exposure on a daily basis, taking into account all the microenvironments attended by children.[6] Children with persistent respiratory symptoms were participants with asthma-like symptoms reported by parents as persistent wheezing and/or asthma attacks at two or more time points from 4 years of age, or with doctor-diagnosed asthma until the age of 6 years. About 80% and 9% of children with persistent respiratory symptoms were diagnosed with asthma and allergic rhinitis (AR), respectively, until 9 years. The increase in 24-hour IQR personal UFP exposure (PNC 7069 pt/cm SP 3 sp or LDSA 15 m SP 2 sp /cm SP 3 sp ) was related to higher FeNO in all children, particularly in those with persistent respiratory symptoms, and most specifically in children with asthma/AR diagnosis (Figure). [Extracted from the article]

Background: Natural course and co‐occurrence of asthma, eczema, and allergic rhinitis through childhood are still not fully documented. We aim to identify and characterize profiles based on the time course, severity, and apparent triggers of respiratory/allergy symptoms in school‐aged children. Methods: Data on occurrence, severity, and triggers of asthma, rhinitis, and dermatitis symptoms were collected annually during the follow‐up of the PARIS birth cohort. Children with similar symptom trajectories until 8‐9 years were grouped into profiles using multidimensional (all symptoms considered simultaneously) cluster analysis. Associations between profiles and different health outcomes were analyzed using logistic or linear regression models. Results: Six distinct symptomatic profiles were identified. A profile was defined by persistent dermatitis symptoms, associated with sensitization to food and aeroallergens. Two profiles were characterized by wheezing: one with early transient wheezing and the other with persistent wheezing related to doctor‐diagnosed asthma, airway obstruction, and perennial aeroallergen sensitization. Three profiles were characterized by rhinitis symptoms: one non‐allergic and two allergic, either with persistent rhinitis symptoms related to allergic multimorbidity and sensitization to perennial aeroallergens, or with late‐onset symptoms, related to both pollen and perennial aeroallergens sensitization as well as low lung function. Conclusion: This study brings further insights into the developmental profiles of respiratory/allergic outcomes from birth to school age. The identified profiles clearly differed regarding objective features such as diagnosed morbidity, sensitization, or lung function measurements, thus highlighting their biologic and clinical relevance. Allergic rhinitis profiles deserve particular attention, since they were likely to be involved in multimorbidity patterns. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background Profiles of allergic sensitization are poorly documented in infancy. Relations between early sensitization and allergic morbidity need to be clarified. Methods This study dealt with children involved in the Pollution and Asthma Risk: an Infant Study ( PARIS), a population-based prospective birth cohort. Allergic sensitization to twelve food and four inhalant allergens was assessed at 18 months and defined by a specific immunoglobulin E (IgE) level ≥0.35 kUA/l. Health data were collected by standardized questionnaires at 2 and 6 years. Early allergic profiles were identified by an unsupervised cluster analysis based on health data at 2 years and IgE measurements. Profiles were compared with regard to allergic morbidity and multimorbidity at 6 years. Results Sensitization to any allergen concerned 13.6% of infants. By cluster analysis, 1525 infants were grouped into three profiles: 89.2% not or rarely sensitized (only 3.7% of sensitized), 9.2% mainly sensitized to one or few allergens (45.2% of monosensitized and 45.9% of paucisensitized) and 1.6% all polysensitized. The prevalence of doctor-diagnosed asthma, rhinitis, eczema, food allergy and multimorbidity at 2 years increased from profile one to profile three ( p-trend <0.001). At 6 years, symptoms of current asthma, rhinitis, eczema and multimorbidity were significantly more frequent in the last two profiles. Conclusions This study highlights, as early as 18 months of age, three profiles of increasing severity with regard to allergic sensitization and diseases. These profiles also differ in terms of allergic morbidity at 6 years. Early sensitization can predict allergic multimorbidity in childhood, and in the case of early polysensitization, multimorbidity is more frequent as soon as infancy. [ABSTRACT FROM AUTHOR]