Association between exposure to ambient air pollution and occurrence of inflammatory acne in the adult population.
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ABSTRACT: Background
Acne vulgaris is one of the most prevalent skin diseases responsible for dermatological consultations. Several internal and external factors can affect acne occurrence and severity. Outdoor air pollution is an external factor discussed to trigger inflammation of the skin. The objective of this study was to find a link between the exposure to ambient air pollution and inflammatory acne occurrence in the Lebanese adult population.Methods
A cross-sectional study was conducted, using an online questionnaire to collect the required data from different Lebanese regions. The survey covered pollution exposure questions as well as queries on several factors known to have a role on acne occurrence.Results
A total of 372 participants were included in the study, aged 18 to 55 years old. The results of a logistic regression taking the presence/absence of acne as the dependent variable, showed that female gender (aOR = 4.39), younger age (aOR = 1.05), using hydrating cream (aOR = 4.30), working near a power plant vs not (aOR = 3.07), having a severe NO2 exposure compared to none (aOR = 8.24), a higher number of family members with acne or history of acne (aOR = 1.48) were significantly associated with higher odds of having acne, whereas having a dry skin compared to normal (aOR = 0.20) was significantly associated with lower odds of having acne.Conclusion
The occurrence of inflammatory acne in Lebanese adults was found to be associated with ambient exposure to high levels of NO2 and employment near a power plant known to emit CO2, CO, SO2, NO2 and PM. Therefore, our findings can serve as a first step towards implementing awareness on a skin care routine suitable for highly polluted areas.
SUBMITTER: El Haddad C
PROVIDER: S-EPMC8439009 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectivesThe inflammatory bowel diseases (IBDs) emerged after industrialization. We studied whether ambient air pollution levels were associated with the incidence of IBD.MethodsThe health improvement network (THIN) database in the United Kingdom was used to identify incident cases of Crohn's disease (n=367) or ulcerative colitis (n=591), and age- and sex-matched controls. Conditional logistic regression analyses assessed whether IBD patients were more likely to live in areas of higher ambient concentrations of nitrogen dioxide (NO(2)), sulfur dioxide (SO(2)), and particulate matter <10 ?m (PM(10)), as determined by using quintiles of concentrations, after adjusting for smoking, socioeconomic status, non-steroidal anti-inflammatory drugs (NSAIDs), and appendectomy. Stratified analyses investigated effects by age.ResultsOverall, NO(2), SO(2), and PM(10) were not associated with the risk of IBD. However, individuals ?23 years were more likely to be diagnosed with Crohn's disease if they lived in regions with NO(2) concentrations within the upper three quintiles (odds ratio (OR)=2.31; 95% confidence interval (CI)=1.25-4.28), after adjusting for confounders. Among these Crohn's disease patients, the adjusted OR increased linearly across quintile levels for NO(2) (P=0.02). Crohn's disease patients aged 44-57 years were less likely to live in regions of higher NO(2) (OR=0.56; 95% CI=0.33-0.95) and PM(10) (OR=0.48; 95% CI=0.29-0.80). Ulcerative colitis patients ?25 years (OR=2.00; 95% CI=1.08-3.72) were more likely to live in regions of higher SO(2); however, a dose-response effect was not observed.ConclusionsOn the whole, air pollution exposure was not associated with the incidence of IBD. However, residential exposures to SO(2) and NO(2) may increase the risk of early-onset ulcerative colitis and Crohn's disease, respectively. Future studies are needed to explore the age-specific effects of air pollution exposure on IBD risk.
| S-EPMC3180712 | biostudies-literature
Project description:Importance:Air pollutants interact with estrogen nuclear receptors, but their effect on thyroid signaling is less clear. Thyroid function is of particular importance for pregnant women because of the thyroid's role in fetal brain development. Objective:To determine the short-term association of exposure to air pollution in the first trimester with thyroid function throughout pregnancy. Design, Setting, and Participants:In this cohort study, 9931 pregnant women from 4 European cohorts (the Amsterdam Born Children and Their Development Study, the Generation R Study, Infancia y Medio Ambiente, and Rhea) and 1 US cohort (Project Viva) with data on air pollution exposure and thyroid function during pregnancy were included. The recruitment period for the Amsterdam Born Children and Their Development Study was January 2003 to March 2004; for Generation R, April 2002 to January 2006; for Infancia y Medio Ambiente, November 2003 to January 2008; for Rhea, February 2007 to February 2008; and for Project Viva, April 1999 to November 2002. Statistical analyses were conducted from January 2018 to April 2019. Main Outcomes and Measures:Residential air pollution concentrations (ie, nitrogen oxide and particulate matter [PM]) during the first trimester of pregnancy were estimated using land-use regression and satellite-derived aerosol optical depth models. Free thyroxine, thyrotropin, and thyroid peroxidase antibody levels were measured across gestation. Hypothyroxinemia was defined as free thyroxine below the fifth percentile of the cohort distribution with normal thyrotropin levels, following the American Thyroid Association guidelines. Results:Among 9931 participants, the mean (SD) age was 31.2 (4.8) years, 4853 (48.9%) had more than secondary educational levels, 5616 (56.6%) were nulliparous, 404 (4.2%) had hypothyroxinemia, and 506 (6.7%) tested positive for thyroid peroxidase antibodies. Concentrations of nitrogen dioxide and PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) were lower and had less variation in women in the US cohort than those in European cohorts. No associations of nitrogen oxide with thyroid function were found. Higher exposures to PM2.5 were associated with higher odds of hypothyroxinemia in pregnant women (odds ratio per 5-?g/m3 change, 1.21; 95% CI, 1.00-1.47). Although exposure to PM with an aerodynamic diameter of 10 ?m or less was not significantly associated with hypothyroxinemia, the coefficient was similar to that for the association of PM2.5 with hypothyroxinemia (odds ratio per 10-?g/m3 change, 1.18; 95% CI, 0.93-1.48). Absorbances of PM2.5 and PM with aerodynamic diameter from 2.5 to 10 ?g and were not associated with hypothyroxinemia. There was substantial heterogeneity among cohorts with respect to thyroid peroxidase antibodies (P for heterogeneity, <.001), showing associations of nitrogen oxide and PM with thyroid autoimmunity only in the women in the Generation R Study. Conclusions and Relevance:The findings of this study suggest that first-trimester exposures to PM2.5 were associated with mild thyroid dysfunction throughout pregnancy. The association of PM2.5 exposure with thyroid function during pregnancy is of global health importance because air pollution exposure is widespread and hypothyroxinemia may adversely influence the brain development of offspring.
| S-EPMC6806433 | biostudies-literature
Project description:Environmental factors may play roles in the development of rheumatoid arthritis (RA), and some studies have shown that air pollution was associated with the development of autoimmune disease. This study was designed to investigate the effect of air pollutants on the development of adult RA. A nested case-control cohort study was performed using the National Health Insurance Service-National Sample Cohort during 2002⁻2014 in Korea. Air pollution data were collected from the National Ambient Air Monitoring System (NAMIS), and exposure levels were extrapolated using geographic information systems. The group with RA (n = 444) was compared with a propensity score-matched control group (n = 1776), and one-year average concentrations of air pollution were predicted at each patient's residence. The adjusted binary logistic regression analysis showed a positive association between O₃ exposure and the incidence risk of RA for the third (odds ratios (OR) = 1.45, 95% confidence intervals (CI): 1.08⁻1.96) and fourth (OR = 1.35, 95% CI: 1.00⁻1.83) quartiles in adults over 20 years of age. The third quartile CO exposure was also associated with an increased risk of RA (OR = 1.57, 95% CI: 1.16⁻2.12). The results of this nationwide population-based study showed that a one-year exposure to CO and O₃ in adults was associated with an increased risk of RA.
| S-EPMC6480037 | biostudies-literature
Project description:BackgroundEnvironmental factors may contribute to the development of Kawasaki disease in children, but prenatal environmental exposures are understudied.ObjectiveWe used a population-based cohort to investigate whether prenatal exposure to outdoor air pollution is associated with the incidence of Kawasaki disease in childhood.MethodsWe performed a longitudinal cohort study of all children born in Quebec, Canada, between 2006 and 2012. Children were followed for Kawasaki disease from birth until 31 March 2018. We assigned prenatal air pollutant exposure according to the residential postal code at birth. The main exposure was annual average concentration of ambient fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5) and nitrogen dioxide (NO2) from satellite-based estimates and land-use regression models. As secondary exposures, we considered industrial PM2.5, NO2, and sulfur dioxide (SO2) emissions estimated from dispersion models. We estimated hazard ratios (HRs) using Cox proportional hazards models, adjusted for maternal age, parity, sex, multiple birth, maternal smoking during pregnancy, socioeconomic status, birth year, and rural residence. We considered single and multipollutant models. We performed several sensitivity analyses, including assessing modifying effects of maternal comorbidities (e.g., diabetes, preeclampsia).ResultsThe cohort comprised 505,336 children, including 539 with Kawasaki disease. HRs for each interquartile range increase in ambient air pollution were 1.16 (95% CI: 0.96, 1.39) for PM2.5 and 1.12 (95% CI: 0.96, 1.31) for NO2. For industrial air pollution, HRs were 1.07 (95% CI: 1.01, 1.13) for SO2, 1.09 (95% CI: 0.99, 1.20) for NO2, and 1.01 (95% CI: 0.97, 1.05) for PM2.5. In multipollutant models, associations for ambient PM2.5 and NO2 (i.e., from all sources) were robust to adjustment for industrial pollution, and vice versa.DiscussionIn this population-based cohort study, both prenatal exposure to ambient and industrial air pollution were associated with the incidence of Kawasaki disease in childhood. Further studies are needed to consolidate the observed associations. https://doi.org/10.1289/EHP6920.
| S-EPMC7571626 | biostudies-literature
Project description:This study aimed to investigate the association between ambient air pollutants and cataracts in the general population aged 50 years or older using data from the Korean National Insurance Service-National Sample Cohort. Cataract patients were defined as those diagnosed by a physician and having undergone cataract surgery. After matching the average concentrations of PM2.5, PM10, NO2, CO, SO2, and O3 in residential areas, the association between quartile level of air pollutants and incidence of cataract was analyzed using a multivariate Cox-proportional hazard risk model. Among the 115,728 participants, 16,814 (14.5%) were newly diagnosed with cataract and underwent related surgery between 1 January 2004, and 31 December 2015. Exposure to PM10, NO2, and SO2 was positively associated with cataract incidence, while O3 was negatively associated. The adjusted hazard ratio (HR) with 95% confidence interval was 1.069 (1.025-1.115) in PM10 and 1.080 (1.030-1.133) in NO2. However, the association between cataract and the quartile of PM2.5 measured during one year in 2015 was not clear. The HR of female participants aged 65 or older was significantly increased according to quartile of air pollutants. We identified exposure to PM10, NO2, SO2, and O3 associated with cataract development in Korean adults aged ≥ 50 years. This information may be helpful for policymaking to control air pollution as a risk factor for eye health.
| S-EPMC7763970 | biostudies-literature
Project description:Rationale: House endotoxin and ambient air pollution are risk factors for asthma; however, the effects of their coexposure on asthma are not well characterized.Objectives: To examine potential synergistic associations of coexposure to house dust endotoxin and ambient air pollutants with asthma outcomes.Methods: We analyzed data of 6,488 participants in the National Health and Nutrition Examination Survey 2005-2006. Dust from bedding and bedroom floor was analyzed for endotoxin content. The Community Multiscale Air Quality Modeling System (CMAQ) and Downscaler Model data were used to determine annual average particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) exposures at participants' residential locations. The associations of the coexposures with asthma outcomes were assessed and tested for synergistic interaction.Measurements and Main Results: In adjusted analysis, PM2.5 (CMAQ) (odds ratio [OR], 1.12; 95% confidence interval [CI], 1.07-1.18), O3 (Downscaler Model) (OR, 1.07; 95% CI, 1.02-1.13), and log10 NO2 (CMAQ) (OR, 3.15; 95% CI, 1.33-7.45) were positively associated with emergency room visits for asthma in the past 12 months. Coexposure to elevated concentrations of house dust endotoxin and PM2.5 (CMAQ) was synergistically associated with the outcome, increasing the odds by fivefold (OR, 5.01; 95% CI, 2.54-9.87). A synergistic association was also found for coexposure to higher concentrations of endotoxin and NO2 in children (OR, 3.45; 95% CI, 1.65-7.18).Conclusions: Coexposure to elevated concentrations of residential endotoxin and ambient PM2.5 in all participants and NO2 in children is synergistically associated with increased emergency room visits for asthma. Therefore, decreasing exposure to both endotoxin and air pollution may help reduce asthma morbidity.
| S-EPMC6775869 | biostudies-literature
Project description:Ambient air pollution was known to cause central nervous system diseases and depressive symptoms. In this study, we examined the associations between air pollution exposure and the prevalence of insomnia in Taipei City of Taiwan. We applied the health information system of electrical medical records of Taipei City Hospital to collect a total of 5108 study subjects (insomniacs N = 912 and non-insomniacs N = 4196) over 18 years old from the family medicine and internal medicine outpatients of six branches of Taipei City Hospital. These patients were grouped into insomniacs and non-insomniacs following the primary insomnia diagnosis (ICD9:780.52, 780.54, 307.41, 307.42, ICD10: G47.00, G47.01, G47.09, F51.01, F51.09) and the prescription times of anxiolytics and hypnotics. We estimated one-year average concentrations of PM2.5, ozone, and NOx before the first date of insomnia diagnosis and the last date of outpatient visit for insomniacs and non-insomniacs, respectively, by using the data of nearest air quality monitoring stations relative to study subjects' residential addresses. Logistic regression analysis was employed to examine the independent effects of air pollution concentrations on the risk of insomnia. One-year average PM2.5, ozone, and NOx levels for insomniacs was significantly higher than those of non-insomniacs. After adjusting for confounding factors, increase each 1(μg/m3) in one-year average PM2.5 showed a statistically significant association with insomnia (the odds ratio 1.610, 95% CI [1.562,1.660]). As to multi pollutants, one-year average PM2.5 (1.624, [1.570, 1.681] and ozone (1.198, [1.094, 1.311]) exposure showed a significant association with insomnia. Subgroup analysis revealed that the influence of PM2.5 and ozone on insomnia have significant risks in people with major chronic disease. This study demonstrated a positive association between PM2.5 and ozone exposure and the prevalence of hypnotic-treated insomnia. Especially, the people with major chronic diseases were with obvious effect of PM2.5 and ozone on risk of insomnia.
| S-EPMC9646727 | biostudies-literature
Project description:Exposure to higher levels of ambient air pollution is a known risk factor for cardiovascular disease but long-term effects of pollution exposure on the pulmonary vessels are unknown.MethodsAmong 2428 Framingham Heart Study participants who underwent chest computed tomography (CT) between 2008 and 2011, pulmonary vascular volumes were calculated by image analysis, including the total vascular volume and small vessel volume (cross-sectional area <5 mm2; BV5 defined as small vessel volume). Using spatiotemporal models and participant home address, we assigned 1-year (2008) and 5-year (2004-2008) average concentrations of fine particulate matter (PM2.5), elemental carbon (EC), and ground-level ozone (O3), and distance to major roadway. We examined associations of 1- and 5-year exposures, and distance to road, with CT vascular volumes using multivariable linear regression models.ResultsThere was a consistent negative association of higher O3 with lower small vessel volumes, which persisted after adjustment for distance to road. Per interquartile range (IQR) of 2008 O3, BV5 was 0.34 mL lower (95% confidence intervals [CI], -0.61 to -0.06; P = 0.02), with similar results for 5-year exposure. One-year EC exposure and closer proximity to road were weakly associated with small vessel volumes; BV5 was 0.18 mL higher per IQR of 2008 EC (95% CI, -0.05 to 0.42; P = 0.13) and 0.40 mL higher per IQR closer proximity to road (95% CI: -0.10 to 0.89; P = 0.12). PM2.5 was not associated with small vascular volumes; BV5 was 0.26 mL lower per IQR of 2008 PM2.5 (95% CI: -0.68 to 0.16; P = 0.22).ConclusionsAmong community-dwelling adults living in the northeastern United States, higher exposure to O3 was associated with lower small pulmonary vessel volumes on CT.
| S-EPMC8043731 | biostudies-literature
Project description:ImportanceAir pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated.ObjectiveTo evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada.Design, setting, and participantsPopulation-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022.ExposuresWeekly average concentrations of ambient fine particulate matter with a diameter 2.5 μm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data.Main outcome and measuresCP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years.ResultsThe present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 μg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk.Conclusions and relevanceIn this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.
| S-EPMC11234239 | biostudies-literature
Project description:BackgroundFew population-based epidemiological studies of adults have examined the relationship between air pollution and leukaemias.MethodsUsing Danish National Cancer Registry data and Danish DEHM-UBM-AirGIS system-modelled air pollution exposures, we examined whether particulate matter (PM2.5), black carbon (BC), nitrogen dioxide (NO2) and ozone (O3) averaged over 1, 5 or 10 years were associated with adult leukaemia in general or by subtype. In all, 14,986 adult cases diagnosed 1989-2014 and 51,624 age, sex and time-matched controls were included. Separate conditional logistic regression models, adjusted for socio-demographic factors, assessed exposure to each pollutant with leukaemias.ResultsFully adjusted models showed a higher risk of leukaemia with higher 1-, 5- and 10-year-average exposures to PM2.5 prior to diagnosis (e.g. OR per 10 µg/m3 for 10-year average: 1.17, 95% CI: 1.03, 1.32), and a positive relationship with 1-year average BC. Results were driven by participants 70 years and older (OR per 10 µg/m3 for 10-year average: 1.35, 95% CI: 1.15-1.58). Null findings for younger participants. Higher 1-year average PM2.5 exposures were associated with higher risks for acute myeloid and chronic lymphoblastic leukaemia.ConclusionAmong older adults, higher risk for leukaemia was associated with higher residential PM2.5 concentrations averaged over 1, 5 and 10 years prior to diagnosis.
| S-EPMC7722932 | biostudies-literature