Matches in SemOpenAlex for { <https://semopenalex.org/work/W3186349744> ?p ?o ?g. }
Showing items 1 to 78 of
78
with 100 items per page.
- W3186349744 endingPage "718" @default.
- W3186349744 startingPage "716" @default.
- W3186349744 abstract "Early life is critical window for development of asthma associated with environmental factors. Maternal smoking, secondhand smoke exposure, and ambient air pollution exposure during pregnancy have been frequently reported to be linked to development of asthma and allergic disease.1Burbank A.J. Sood A.K. Kesic M.J. Peden D.B. Hernandez M.L. Environmental determinants of allergy and asthma in early life.J Allergy Clin Immunol. 2017; 140: 1-12Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar Perinatal exposure to ambient air pollutants, including NO2, O3, and particulate matter less than 2.5 μm in diameter (PM2.5) or less than 10 μm in diameter (PM10), has also been reported to increase the incidence of asthma and allergic disease.1Burbank A.J. Sood A.K. Kesic M.J. Peden D.B. Hernandez M.L. Environmental determinants of allergy and asthma in early life.J Allergy Clin Immunol. 2017; 140: 1-12Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar In this issue of the Journal of Allergy and Clinical Immunology, Zhang et al report that in a cohort of 5733 children in Wuhan, China, prenatal and early-life exposure to particulate matter less than 1 μm in diameter (PM1), PM2.5, and PM10 was associated with increased risk of development of asthma by age 3 years.2Zhang Y. Wei J. Shi Y. Quan C. Ho H.C. Song Y. et al.Early-life exposure to submicron particulate air pollution in relation to asthma development in Chinese preschool children.J Allergy Clin Immunol. 2021; 148: 771-782Abstract Full Text Full Text PDF Scopus (13) Google Scholar All size fractions of PM had this effect, but it was especially notable for PM1, a size fraction between that which defines ultrafine particles (PM0.1) and PM2.5, the smallest size fraction for which there is a US National Ambient Air Quality Standard. The effect of prenatal exposure to PM1 was more pronounced in males. Zhang et al2Zhang Y. Wei J. Shi Y. Quan C. Ho H.C. Song Y. et al.Early-life exposure to submicron particulate air pollution in relation to asthma development in Chinese preschool children.J Allergy Clin Immunol. 2021; 148: 771-782Abstract Full Text Full Text PDF Scopus (13) Google Scholar also report than postnatal exposure to PM10 increased the risk of asthma development. It is noteworthy that the mean level of exposure to PM2.5 was 64.9 (range 41.4-109.3) mg/m3, which is notably higher than the US National Ambient Air Quality Standard PM2.5 annual standard of 12.0 μg/m3 or the 24-hour standard of 35.0 μg/m3. This suggests a relatively high PM exposure burden in this population. There are a number of other study design factors to consider in this study. The authors used a cross-sectional study design, and outcomes were self-reported rather than noted in medical records or determined by physician diagnosis. Nonetheless, these observations again highlight key concerns about the impact of perinatal exposure to PM pollution on long-term health outcomes. Among these concerns is the growing appreciation of the effect of perinatal exposure to PM size fractions smaller than PM2.5 on asthma development. Consistent with the findings from Zhang et al2Zhang Y. Wei J. Shi Y. Quan C. Ho H.C. Song Y. et al.Early-life exposure to submicron particulate air pollution in relation to asthma development in Chinese preschool children.J Allergy Clin Immunol. 2021; 148: 771-782Abstract Full Text Full Text PDF Scopus (13) Google Scholar are those by Lavigne et al,3Lavigne E. Donelle J. Hatzopoulou M. Van Ryswyk K. van Donkelaar A. Martin R.V. et al.Spatiotemporal variations in ambient ultrafine particles and the incidence of childhood asthma.Am J Respir Crit Care Med. 2019; 199: 1487-1495Crossref PubMed Scopus (46) Google Scholar who examined the relationship between exposure to ultrafine particles (UFPs), PM2.5, and NO2 and asthma development in a birth cohort of 160,641 singleton live birth infants in Toronto, Canada, from 2006 to 2012, with 27,062 of the cohort members developing asthma by the age of 6 years. Lavigne et al3Lavigne E. Donelle J. Hatzopoulou M. Van Ryswyk K. van Donkelaar A. Martin R.V. et al.Spatiotemporal variations in ambient ultrafine particles and the incidence of childhood asthma.Am J Respir Crit Care Med. 2019; 199: 1487-1495Crossref PubMed Scopus (46) Google Scholar found that exposure to UFPs during the second trimester of pregnancy was associated with increased risk of asthma development (hazard ratio 1.09), which was independent of the other assessed pollutant exposures. Hsu et al4Hsu H.H. Chiu Y.H. Coull B.A. Kloog I. Schwartz J. Lee A. et al.Prenatal particulate air pollution and asthma onset in urban children. Identifying sensitive windows and sex differences.Am J Respir Crit Care Med. 2015; 192: 1052-1059Crossref PubMed Scopus (185) Google Scholar examined the impact of PM2.5 exposure on asthma development in a cohort of 995 singleton birth infants who were born in Boston between 2002 and 2006 and had a physician diagnosis of asthma by the age of 6 years. They found that PM2.5 exposure during the second trimester of pregnancy was associated with increased risk of asthma, but only in male children. Small PM, including UFPs, derive from a variety of sources, with a substantial fraction produced by mobile sources. Other sources include biomass combustion, stationary sources, and UFPs produced from domestic sources. A relatively unique aspect of the toxicology of UFPs and nanoparticles is that they can be taken up into the blood from the respiratory tract and migrate to a number of end organs. Additionally, although PM2.5 is less likely to be taken up in distal tissues, it has been shown to have both airway and systemic effects.1Burbank A.J. Sood A.K. Kesic M.J. Peden D.B. Hernandez M.L. Environmental determinants of allergy and asthma in early life.J Allergy Clin Immunol. 2017; 140: 1-12Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar Thus, it is very plausible that prenatal exposure to small particles (UFPs and PM2.5) may have disproportionate effects on postnatal health. A number of studies have reported that epigenetic changes due to DNA methylation occur following prenatal roadway exposure to pollutants,1Burbank A.J. Sood A.K. Kesic M.J. Peden D.B. Hernandez M.L. Environmental determinants of allergy and asthma in early life.J Allergy Clin Immunol. 2017; 140: 1-12Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar as well as following discrete exposure to NO2, PM2.5, and PM10.5Rider C.F. Carlsten C. Air pollution and DNA methylation: effects of exposure in humans.Clin Epigenetics. 2019; 11: 131Crossref PubMed Scopus (87) Google Scholar A 2019 metanalysis of data from 9 European and US studies examined DNA methylation in 1949 children who experienced prenatal PM10 exposure and 1551 children with prenatal PM2.5 exposure.6Gruzieva O. Xu C.J. Yousefi P. Relton C. Merid S.K. Breton C.V. et al.Prenatal particulate air pollution and DNA methylation in newborns: an epigenome-wide meta-analysis.Environ Health Perspect. 2019; 127: 57012Crossref PubMed Scopus (64) Google Scholar The authors of this study observed that 6 CpG sites were associated with prenatal exposure to PM10 and 14 CpG sites were associated with prenatal exposure to PM2.5. Two of the PM10-associated CpGs mapped to FAM13A and NOTCH4, which are linked with lung growth and asthma. The same authors also found several differentially methylated regions associated with both PM10 and PM2.5. In addition to epigenetic changes, prenatal PM2.5 exposure has been associated with shortened telomeres, with the effect being significant in males born to women with decreased maternal antioxidant nutrition.7Lee A.G. Cowell W. Kannan S. Ganguri H.B. Nentin F. Wilson A. et al.Prenatal particulate air pollution and newborn telomere length: effect modification by maternal antioxidant intakes and infant sex.Environ Res. 2020; 187109707Crossref PubMed Scopus (16) Google Scholar These observations demonstrate potential mechanisms by which prenatal pollutant exposures affect asthma development. Many studies also note increased susceptibility to the adverse effects of prenatal exposure to PM in male children, highlighting the need to assess sex as a biologic variable in these studies.7Lee A.G. Cowell W. Kannan S. Ganguri H.B. Nentin F. Wilson A. et al.Prenatal particulate air pollution and newborn telomere length: effect modification by maternal antioxidant intakes and infant sex.Environ Res. 2020; 187109707Crossref PubMed Scopus (16) Google Scholar The risk posed by prenatal pollutant exposure for postterm effects on asthma and other diseases is real and has the potential to have a major impact on disease outcomes and health care costs. There is urgency to develop interventions that may mitigate the effect of PM exposure on health outcomes. As ambient air PM2.5 and UFPs can influence indoor airsheds, 1 approach that is being explored is use of filtration systems to remove PM from indoor spaces. There are compelling data suggesting that air filtration devices effectively decrease indoor PM2.5 levels, as reviewed by Allen and Barn.8Allen R.W. Barn P. Individual- and household-level interventions to reduce air pollution exposures and health risks: a review of the recent literature.Curr Environ Health Rep. 2020; 7: 424-440Crossref PubMed Scopus (13) Google Scholar Indoor deployment of high-efficiency particulate air filtration has been shown to reduce blood pressure, improve endothelial cell function, and reduce systemic inflammation. Although more studies of this type are needed, these results highlight the potential for residential high-efficiency particulate air filtration to reduce the impact of PM on health outcomes and to possibly become part of prenatal care during pregnancy. In theory, masks could be a useful adjunct for reducing PM2.5 exposure. There are data in studies using N95 face masks that show improvements in PM-impacted subclinical cardiovascular outcomes (blood pressure and heart rate variability). However, the effectiveness of face masks depends on proper mask fit and use, as well as on PM levels indoors, where individuals will likely not wear masks. Overall, a combination of masks and building air filtration may be effective adjuncts to reduced PM-induced adverse health effects. However, most of the available data on masks focus on filtering capability and not on health outcomes. Future studies of personal protective interventions will be needed both to confirm the plausibility of these approaches and to assess effective implementation by exposed populations.8Allen R.W. Barn P. Individual- and household-level interventions to reduce air pollution exposures and health risks: a review of the recent literature.Curr Environ Health Rep. 2020; 7: 424-440Crossref PubMed Scopus (13) Google Scholar Although personal measures to mitigate the impact of PM on health outcome remain unproved, environmental health–related public policy has been clearly shown to improve health outcomes associated with air pollution. It has recently been reported that improvement in air quality in California thanks to pollution control policies has resulted in improved lung growth, reduced acute exacerbations of disease, and (most importantly) reduced incidence of new asthma in childhood.9Garcia E. Berhane K.T. Islam T. McConnell R. Urman R. Chen Z. et al.Association of changes in air quality with incident asthma in children in California, 1993-2014.JAMA. 2019; 321: 1906-1915Crossref PubMed Scopus (70) Google Scholar Reduction of fossil fuel use by adoption of electrified vehicles represents an important opportunity for policy intervention. Supporting this idea are observations from Wuhan, China, in which restriction in transportation during the period of quarantine due to COVID-19 was associated with decreased air pollution and decreased numbers of deaths due to cardiovascular disease and chronic obstructive pulmonary disease.10Chen K. Wang M. Huang C. Kinney P.L. Anastas P.T. Air pollution reduction and mortality benefit during the COVID-19 outbreak in China.Lancet Planet Health. 2020; 4: e210-e212Abstract Full Text Full Text PDF PubMed Scopus (228) Google Scholar As depicted in Fig 1, sound public health policy approaches that focus on reduction of fossil fuel use are the most promising approach to reducing levels of ambient air UFPs, PM2,5, and PM10, as well as the perinatal morbidity associated with these pollutants. Early-life exposure to submicron particulate air pollution in relation to asthma development in Chinese preschool childrenJournal of Allergy and Clinical ImmunologyVol. 148Issue 3PreviewEmerging research suggested an association of early-life particulate air pollution exposure with development of asthma in childhood. However, the potentially differential effects of submicron particulate matter (PM; PM with aerodynamic diameter ≤1 μm [PM1]) remain largely unknown. Full-Text PDF" @default.
- W3186349744 created "2021-08-02" @default.
- W3186349744 creator A5010809550 @default.
- W3186349744 date "2021-09-01" @default.
- W3186349744 modified "2023-10-16" @default.
- W3186349744 title "Prenatal exposure to particulate matter air pollution: A preventable risk for childhood asthma" @default.
- W3186349744 cites W1904997767 @default.
- W3186349744 cites W2733928499 @default.
- W3186349744 cites W2917538622 @default.
- W3186349744 cites W2945953084 @default.
- W3186349744 cites W2947990506 @default.
- W3186349744 cites W2971578437 @default.
- W3186349744 cites W3025947294 @default.
- W3186349744 cites W3026936027 @default.
- W3186349744 cites W3110141071 @default.
- W3186349744 cites W3134270460 @default.
- W3186349744 doi "https://doi.org/10.1016/j.jaci.2021.07.007" @default.
- W3186349744 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34310929" @default.
- W3186349744 hasPublicationYear "2021" @default.
- W3186349744 type Work @default.
- W3186349744 sameAs 3186349744 @default.
- W3186349744 citedByCount "5" @default.
- W3186349744 countsByYear W31863497442022 @default.
- W3186349744 countsByYear W31863497442023 @default.
- W3186349744 crossrefType "journal-article" @default.
- W3186349744 hasAuthorship W3186349744A5010809550 @default.
- W3186349744 hasBestOaLocation W31863497441 @default.
- W3186349744 hasConcept C178790620 @default.
- W3186349744 hasConcept C185592680 @default.
- W3186349744 hasConcept C203014093 @default.
- W3186349744 hasConcept C24245907 @default.
- W3186349744 hasConcept C2776042228 @default.
- W3186349744 hasConcept C2779234561 @default.
- W3186349744 hasConcept C3018923374 @default.
- W3186349744 hasConcept C39432304 @default.
- W3186349744 hasConcept C46973012 @default.
- W3186349744 hasConcept C54355233 @default.
- W3186349744 hasConcept C559116025 @default.
- W3186349744 hasConcept C71924100 @default.
- W3186349744 hasConcept C86803240 @default.
- W3186349744 hasConcept C99454951 @default.
- W3186349744 hasConceptScore W3186349744C178790620 @default.
- W3186349744 hasConceptScore W3186349744C185592680 @default.
- W3186349744 hasConceptScore W3186349744C203014093 @default.
- W3186349744 hasConceptScore W3186349744C24245907 @default.
- W3186349744 hasConceptScore W3186349744C2776042228 @default.
- W3186349744 hasConceptScore W3186349744C2779234561 @default.
- W3186349744 hasConceptScore W3186349744C3018923374 @default.
- W3186349744 hasConceptScore W3186349744C39432304 @default.
- W3186349744 hasConceptScore W3186349744C46973012 @default.
- W3186349744 hasConceptScore W3186349744C54355233 @default.
- W3186349744 hasConceptScore W3186349744C559116025 @default.
- W3186349744 hasConceptScore W3186349744C71924100 @default.
- W3186349744 hasConceptScore W3186349744C86803240 @default.
- W3186349744 hasConceptScore W3186349744C99454951 @default.
- W3186349744 hasFunder F4320306107 @default.
- W3186349744 hasIssue "3" @default.
- W3186349744 hasLocation W31863497441 @default.
- W3186349744 hasLocation W31863497442 @default.
- W3186349744 hasOpenAccess W3186349744 @default.
- W3186349744 hasPrimaryLocation W31863497441 @default.
- W3186349744 hasRelatedWork W1564487381 @default.
- W3186349744 hasRelatedWork W1980969051 @default.
- W3186349744 hasRelatedWork W2004318300 @default.
- W3186349744 hasRelatedWork W2022735073 @default.
- W3186349744 hasRelatedWork W2089479653 @default.
- W3186349744 hasRelatedWork W2180424560 @default.
- W3186349744 hasRelatedWork W2381763096 @default.
- W3186349744 hasRelatedWork W2565454344 @default.
- W3186349744 hasRelatedWork W2611628767 @default.
- W3186349744 hasRelatedWork W4320723326 @default.
- W3186349744 hasVolume "148" @default.
- W3186349744 isParatext "false" @default.
- W3186349744 isRetracted "false" @default.
- W3186349744 magId "3186349744" @default.
- W3186349744 workType "article" @default.