Nitrogen Oxides Exposure Research Articles

Association between air pollution and bone mineral density: a Mendelian randomization study.

The association of air pollution with bone mineral density (BMD) has attracted increasing attention. However, establishing a causal relationship remains uncertain. We conducted a Mendelian randomization (MR) study employing PM2.5, PM2.5-10, PM10, nitrogen dioxide, and nitrogen oxides as exposures and BMD as the outcome to explore the causality between air pollution and the occurrence of decreased BMD. By employing the IVW method, we identified a negative causality between air pollution (PM2.5, PM10, and nitrogen oxides) and BMD. Our findings demonstrate that PM2.5, PM10 and nitrogen oxides exposure may contribute to decreased BMD.

Causal association between air pollution and autoimmune diseases: a two-sample Mendelian randomization study.

In recent years, an increasing number of observational studies have reported the impact of air pollution on autoimmune diseases (ADs). However, no Mendelian randomization (MR) studies have been conducted to investigate the causal relationships. To enhance our understanding of causality, we examined the causal relationships between particulate matter (PM) and nitrogen oxides (NOx) and ADs. We utilized genome-wide association study (GWAS) data on PM and NOx from the UK Biobank in European and East Asian populations. We also extracted integrated GWAS data from the Finnish consortium and the Japanese Biobank for two-sample MR analysis. We employed inverse variance weighted (IVW) analysis to assess the causal relationship between PM and NOx exposure and ADs. Additionally, we conducted supplementary analyses using four methods, including IVW (fixed effects), weighted median, weighted mode, and simple mode, to further investigate this relationship. In the European population, the results of MR analysis suggested a statistically significant association between PM2.5 and psoriasis only (OR = 3.86; 95% CI: 1.89-7.88; PIVW < 0.00625), while a potential association exists between PM2.5-10 and vitiligo (OR = 7.42; 95% CI: 1.02-53.94; PIVW < 0.05), as well as between PM2.5 and systemic lupus erythematosus (OR = 68.17; 95% CI: 2.17-2.1e+03; PIVW < 0.05). In East Asian populations, no causal relationship was found between air pollutants and the risk of systemic lupus erythematosus and rheumatoid arthritis (PIVW > 0.025). There was no pleiotropy in the results. Our results suggest a causal association between PM2.5 and psoriasis in European populations. With the help of air pollution prevention and control, the harmful progression of psoriasis may be slowed.

Post-stroke dysphagia and ambient air pollution are associated with dementia.

This cohort study aimed to explore the potential association between ambient air pollution and dementia incidence in adults who have experienced a stroke. Additionally, the study aimed to determine dysphagia as a predictive factor for the subsequent development of dementia in patients with stroke. This retrospective nested case-control study used data from the Kaohsiung Medical University Hospital Database in Taiwan. Data collected include average ambient air pollution concentrations within 3 months and 1 year after the index dysphagia date. The primary outcome includes incident dementia in patients with or without dysphagia. Logistic regression analysis was performed to examine the association between significant air pollution exposure and the risk of dementia while controlling for baseline demographic characteristics (age and sex), and comorbidities. The univariable regression models revealed a higher likelihood of dementia diagnosis in patients with dysphagia (odds ratio = 1.493, 95% confidence interval = 1.000-2.228). The raw odds ratios indicated a potential link between air pollution exposure and elevated dementia risks in the overall study population and patients with stroke without dysphagia, except for O3. Particulate matter (PM)2.5 and nitrogen oxides (NOx) exhibited significant effects on the risk of dementia in the stepwise logistic regression models. The presence of dysphagia following a stroke may pose a risk of developing dementia. Additionally, PM2.5 and NOx exposure appears to elevate the risk of dementia in patients with stroke.

42 Elucidating an Association Between Air Pollution and Mental Health

Abstract Air pollution (AP) is a significant environmental risk to human health. Historically, the impact of AP exposure has focused upon the physical health effects, yet the implications of AP on mental health have received limited attention. Despite this, recent research has highlighted emerging evidence supporting a possible aetiological link. The purpose of this study, therefore, was to investigate the potential consequences of AP upon mental health and well-being. In a PRISMA based systematic review multiple databases were searched from January 2012 to 2022 for peer-reviewed, English-language, human based primary research. Of the 2,224 studies identified in the literature search, 94 met the inclusion criteria. The mental health and wellbeing issues explored were psychosis, anxiety, suicide, mania, overall diagnosed conditions, and self-reported wellbeing symptoms. Depression was omitted due to the volume of attention the condition has received in the literature. Key air pollutants, particulate matter (PM10 and PM2.5), sulphur oxides (SOx), carbon monoxide (CO) and nitrogen oxides (NOx) were investigated. Data revealed a positive association between psychotic disorders and NOx exposure in ten studies with only one contradictory finding. Whereas the other conditions received multiple contradictory findings. To compare these results to real-life situations, currently a pilot study is exploring associations between psychotic disorder diagnoses and AP, specifically NOx, in Wales using the Secure Anonymised Information Linkage (SAIL) database. There is a large body of evidence showing associations between mental health and AP. However, due to research complexities and some contradictory findings more high-quality research is required to elucidate these relationships.

Air pollution and decreased bone mineral density among Women's Health Initiative participants.

Osteoporosis heavily affects postmenopausal women and is influenced by environmental exposures. Determining the impact of criteria air pollutants and their mixtures on bone mineral density (BMD) in postmenopausal women is an urgent priority. We conducted a prospective observational study using data from the ethnically diverse Women's Health Initiative Study (WHI) (enrollment, September 1994-December 1998; data analysis, January 2020 to August 2022). We used log-normal, ordinary kriging to estimate daily mean concentrations of PM10, NO, NO2, and SO2 at participants' geocoded addresses (1-, 3-, and 5-year averages before BMD assessments). We measured whole-body, total hip, femoral neck, and lumbar spine BMD at enrollment and follow-up (Y1, Y3, Y6) via dual-energy X-ray absorptiometry. We estimated associations using multivariable linear and linear mixed-effects models and mixture effects using Bayesian kernel machine regression (BKMR) models. In cross-sectional and longitudinal analyses, mean PM10, NO, NO2, and SO2 averaged over 1, 3, and 5 years before the visit were negatively associated with whole-body, total hip, femoral neck, and lumbar spine BMD. For example, lumbar spine BMD decreased 0.026 (95% CI: 0.016, 0.036) g/cm2/year per a 10% increase in 3-year mean NO2 concentration. BKMR suggested that nitrogen oxides exposure was inversely associated with whole-body and lumbar spine BMD. In this cohort study, higher levels of air pollutants were associated with bone damage, particularly on lumbar spine, among postmenopausal women. These findings highlight nitrogen oxides exposure as a leading contributor to bone loss in postmenopausal women, expanding previous findings of air pollution-related bone damage. US National Institutes of Health.

Associations between Gestational Exposure to Air Pollution and Maternal Vitamin D Levels

BACKGROUND and AIM Individuals living in areas with higher air pollution have lower levels of vitamin D than residents of areas with lower pollution. Evidence suggests non-optimal gestational vitamin D as an important determinant of pregnancy and child health outcomes. We investigated the association between gestational exposure to air pollution and maternal vitamin D levels. METHODS Participants were 16,553 pregnant women from birth cohorts in the UK (BiB), US (Project Viva), Netherlands (ABCD and Generation R), Poland (REPRO_PL), and Spain (INMA). Averaged concentrations of air pollutants from conception until vitamin D measurement were estimated at participants’ residential addresses using land-use regression or other spatiotemporal models. Cohorts measured 25-hydroxy vitamin D [25(OH)D] and/or 25(OH)D3 in serum or plasma at early or mid-pregnancy. We performed linear regression models in each cohort to estimate the association between air pollution exposure and vitamin D levels and pooled cohort-specific results in a random-effect meta-analysis. Models were adjusted for sociodemographic characteristics, smoking and alcohol use, parity, body mass index, and month of conception. RESULTS Concentrations of nitrogen dioxide and fine PM (PM2.5) were lower and had less variation in Project Viva and BiB than other cohorts. In REPRO_PL, 95% of women had vitamin D&amp;#x3c;20 ng/ml; this rate was 85% in BiB, 52% in Generation R, and &amp;#x3c;50% in other cohorts. We found an inverse association between PM2.5 and vitamin D levels (-1.4 ng/mL, 95%CI:-2.6,-0.2, per 5 &amp;#x3bc;g/m3 increase in PM2.5). Heterogeneity was high among cohorts, with associations driven by ABCD, BiB, and INMA. There was no association between nitrogen oxide exposure and vitamin D levels. CONCLUSIONS PM2.5 exposure might contribute to non-optimal levels of vitamin D in pregnancy. Future studies should focus on underlying mechanisms, including biological pathways, e.g., inducing metabolism of vitamin D, or other factors, e.g., reduced outdoor activity. KEYWORDS: 25(OH)D; PM2.5; pregnancy; women

Air pollution, genetic factors and the risk of depression

Both genetics and ambient air pollutants contribute to depression, but the degree to which genetic susceptibility modifies the effect of air pollution on depression remains unknown. We aimed to investigate the effect of the modification of genetic susceptibility on depression. Notably, 490,780 participants who were free of depression at baseline in the UK Biobank study were recruited from 2006 to 2010. A land use regression (LUR) model was performed to estimate the concentrations of particulate matter with diameters ranging from ≤2.5–≤10 μm (PM2.5, PM2.5–10 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx). The International Classification of Diseases 10th Revision (ICD-10) code was used to identify depression cases. Cox proportional hazard models adjusted for covariates were used to investigate the association between ambient air pollutants and depression. Moreover, the polygenic risk score (PRS) was calculated to evaluate cumulative genetic effects, and additive interaction models were established to explore whether genetic susceptibility modified the effects of air pollutants on depression. PM2.5, PM10, NO2 and NOx exposure were significantly positively associated with the risk of depression, and the hazard ratios and 95 % confidence intervals for a 10-μg/m3 increase in PM2.5, PM10, NO2 and NOx concentrations were 2.12 (1.82, 2.47), 1.12 (1.03, 1.23), 1.07 (1.05, 1.10) and 1.04 (1.03, 1.05), respectively. Air pollutants and genetic variants exerted significant additive effects on the risk of depression (relative excess risk due to the interaction [RERI]: 0.15 for PM2.5, 0.12 for PM10, 0.10 for NO2, and 0.12 for NOx; attributable proportion due to the interaction [AP]: 0.12 for PM2.5, 0.10 for PM10, 0.08 for NO2, and 0.09 for NOx). Air pollution exposure was significantly associated with the risk of depression, and participants with a higher genetic risk were more likely to develop depression when exposed to high levels of air pollution.

An Evaluation of Risk Ratios on Physical and Mental Health Correlations due to Increases in Ambient Nitrogen Oxide (NOx) Concentrations

Nitrogen oxides (NOx) are gaseous pollutants contributing to pollution in their primary form and are also involved in reactions forming ground-level ozone and fine particulate matter. Thus, NOx is of great interest for targeted pollution reduction because of this cascade effect. Primary emissions originate from fossil fuel combustion making NOx a common outdoor and indoor air pollutant. Numerous studies documenting the observed physical health impacts of NOx were reviewed and, where available, were summarized using risk ratios. More recently, the literature has shifted to focus on the mental health implications of NOx exposure, and a review of the current literature found five main categories of mental health-related conditions with respect to NOx exposure: common mental health disorders, sleep, anxiety, depression, and suicide. All the physical and mental health effects with available risk ratios were organized in order of increasing risk. Mental health concerns emerged as those most influenced by NOx exposure, with physical health impacts, such as asthma, only beginning to surface as the fourth highest risk. Mental health conditions occupied seven of the top ten highest risk health ailments. The results summarized in this narrative review show that there are clear positive correlations between NOx and negative physical and mental health manifestations, thus strengthening the argument in support of the reduction in ambient NOx levels.

Successful treatment of pulmonary injury due to nitrogen oxide exposure with extracorporeal membrane oxygenation: a report of two cases and literature review

Background: Severe nitrogen oxide poisoning can lead to life-threatening pulmonary injury. Methods: we report two cases of severe nitrogen-oxide-induced hypoxia treated with veno-venous extracorporeal membrane oxygenation (ECMO). After exposure, the conditions of both patients continued to deteriorate despite maximal mechanical ventilation with a fraction of inspired oxygen of 100%; therefore, we started veno-venous ECMO. The times from presentation to the initiation of ECMO in the two patients were 1 and 2 days. The hypoxemia and respiratory failure improved quickly after ECMO support. Results: The patients were discharged without complications. The durations of ECMO for the two patients were 5 and 6 days. Conclusion: This report describes how early ECMO support was used to treat potentially fatal pulmonary injury after exposure to nitrogen oxide. The duration of the ECMO run is a critical determinant of patient survival.

Associations of genetic risk factors and air pollution with incident hypertension among participants in the UK Biobank study

The purposes of this study were to quantify the association of the combination of air pollution and genetic risk factors with hypertension and explore the interactions between air pollution and genetic risk. This study included 391,366 participants of European ancestry initially free from pre-existing hypertension in the UK Biobank. Exposure to ambient air pollutants, including particulate matter (PM2.5 PM2.5-10, and PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOX), was estimated through land use regression modelling, and the associations between air pollutants and the incidence of hypertension were investigated using a Cox proportional hazards model adjusted for covariates. Furthermore, we established a polygenic risk score for hypertension and assessed the combined effect of genetic susceptibility and air pollution on incident hypertension. The results showed significant associations between the risk of hypertension and exposure to PM2.5 (hazard ratio [HR]: 1.41, 95% confidence interval [CI]: 1.29–1.53; per 10 μg/m3), PM10 (1.05, 1.00–1.09; per 10 μg/m3), and NOX (1.01, 1.01–1.02 per 10 μg/m3). Additive effects of PM2.5 and NOX exposure and genetic risk were observed. Compared to individuals with a low genetic risk and low air pollution exposure, participants with high air pollution exposure and a high genetic risk had a significantly increased risk of hypertension (PM2.5: 71% (66%–76%), PM10: 59% (55%–64%), NOX: 65% (60%–70%)). Our results indicate that long-term exposure to air pollution is associated with an increased risk of hypertension, especially in individuals with a high genetic risk.

Prenatal and early life exposure to air pollution and the incidence of Kawasaki disease

Kawasaki disease (KD) is the most common form of acquired pediatric cardiac disease in the developed world. However, its etiology is still unclear. Epidemiological studies have shown that air pollution is a plausible risk factor in stimulating oxidative stress, inducing inflammation and causing autoimmune diseases. This study aims to assess the connections between prenatal and early life air pollution exposure to the incidence of KD. The main data source of this nationwide longitudinal study was the National Health Insurance Research Database (NHIRD) of Taiwan. NHIRD was linked with Taiwan Maternal and Child Health Database to establish the link between mothers and children. In total, 4192 KD cases involving children under 6 years of age were identified between January 2004 and December 2010. Children in the control group were randomly selected at a 1:4 ratio and matched using their age and index year. Integrated data for the air pollutants were obtained from 71 Environmental Protection Agency monitoring stations across Taiwan. Patients who had main admission diagnosis of KD and subsequently received intravenous immunoglobulin treatment were defined as incidence cases. Ambient exposure, including pollutant standards index (PSI), carbon monoxide (CO), nitric oxide (NO), nitric dioxide (NO2), and nitrogen oxide (NOx) during pregnancy were all positively associated with KD incidence. Conversely, ozone (O3) exposure had a negative correlation. Exposure to CO, NO, NO2, and NOx after childbirth remained consistent with regards to having a positive association with KD incidence. Exposure to PSI and O3 after delivery displayed no significant association with KD. Both prenatal and postnatal cumulative CO, NO, NO2, and NOx exposure had a dose dependent effect towards increasing KD incidence. Certain prenatal and early life air pollutant exposure may increase the incidence of KD.

Dynamic succession patterns and interactions of phyllospheric microorganisms during NOx exposure

The phyllosphere plays a role in alleviating air pollution, potentially leveraging the native microorganisms for further enhancement. It remains unclear how phyllospheric microorganisms respond to nitrogen oxide (NOx) pollution and participate in abatement. Here, we exposed Schefflera octophylla to NOx to reveal microbial succession patterns and interactions in the phyllosphere. During exposure, phyllospheric ammonium (NH4+-N) significantly increased, with different alpha diversity changes between bacteria and fungi. Community successions enclosed core taxa with relatively excellent tolerance, represented by bacterial genera (Norcardiodes, Aeromicrobium) and fungal genera (Talaromyces, Acremonium). The exposure eliminated specific pathogens (e.g., Zymoseptoria) and benefitted plant growth-promoting populations (e.g., Talaromyces, Exiguobacterium), which might favor plant disease control, improve plant health and thus buffer NOx pollution. Cooccurrence networks revealed more negative correlations among bacteria and closer linkages among fungi during exposure. Our results also showed a functional shift from the predominance of pathotrophs to saprotrophs. Our study identified microbial successions and interactions during NOx pollution and thus enlightened prospective taxa and potential roles of phyllospheric microorganisms in NOx remediation.

Early Pregnancy Exposure to Ambient Air Pollution among Late-Onset Preeclamptic Cases Is Associated with Placental DNA Hypomethylation of Specific Genes and Slower Placental Maturation.

Exposure to ambient air pollution during pregnancy has been associated with an increased risk of preeclampsia (PE). Some suggested mechanisms behind this association are changes in placental DNA methylation and gene expression. The objective of this study was to identify how early pregnancy exposure to ambient nitrogen oxides (NOx) among PE cases and normotensive controls influence DNA methylation (EPIC array) and gene expression (RNA-seq). The study included placentas from 111 women (29 PE cases/82 controls) in Scania, Sweden. First-trimester NOx exposure was assessed at the participants’ residence using a dispersion model and categorized via median split into high or low NOx. Placental gestational epigenetic age was derived from the DNA methylation data. We identified six differentially methylated positions (DMPs, q < 0.05) comparing controls with low NOx vs. cases with high NOx and 14 DMPs comparing cases and controls with high NOx. Placentas with female fetuses showed more DMPs (N = 309) than male-derived placentas (N = 1). Placentas from PE cases with high NOx demonstrated gestational age deceleration compared to controls with low NOx (p = 0.034). No differentially expressed genes (DEGs, q < 0.05) were found. In conclusion, early pregnancy exposure to NOx affected placental DNA methylation in PE, resulting in placental immaturity and showing sexual dimorphism.

The built environment as determinant of childhood obesity: A systematic literature review.

We evaluated the epidemiological evidence on the built environment and its link to childhood obesity, focusing on environmental factors such as traffic noise and air pollution, as well as physical factors potentially driving obesity-related behaviors, such as neighborhood walkability and availability and accessibility of parks and playgrounds. Eligible studies were (i) conducted on human children below the age of 18 years, (ii) focused on body size measurements in childhood, (iii) examined at least one built environment characteristic, (iv) reported effect sizes and associated confidence intervals, and (v) were published in English language. A z test, as alternative to the meta-analysis, was used to quantify associations due to heterogeneity in exposure and outcome definition. We found strong evidence for an association of traffic-related air pollution (nitrogen dioxide and nitrogen oxides exposure, p < 0.001) and built environment characteristics supportive of walking (street intersection density, p < 0.01 and access to parks, p < 0.001) with childhood obesity. We identified a lack of studies that account for interactions between different built environment exposures or verify the role and mechanism of important effect modifiers such as age.

Prenatal Air Pollution Exposure and Longitudinal Infant Weight Gain Trajectories

BACKGROUND AND AIM: The prenatal period may play a critical role in childhood obesity development. We examined the association between prenatal nitrogen oxides (NOx) and nitrogen dioxide (NO2) exposure and weight trajectories from birth to 2-years-of-age among infants in the Maternal and Development Risks from Environmental and Social Stressors (MADRES) pregnancy cohort. METHODS: Participants were enrolled during pregnancy and their children were followed up to 2 years. Anthropometric measurements were collected using a combination of medical record abstractions and study-staff measurements (n=471 participants; n=4,287 observations). Residential exposure to NOx and NO2 were estimated as: 1) spatial interpolation from air quality monitoring stations (daily NO2, ambient background), 2) CALINE4 line source dispersion modeled contribution from nearby roadways (daily NOx, traffic-related), and predictions from a machine-learning based spatiotemporal model (weekly NO2 and NOx, R2=0.87, RMSE=2.80 ppb). Exposures were averaged across pregnancy accounting for variable gestation lengths. Sex-stratified quadratic growth curve models were used to assess the association between prenatal NO2/NOx exposure and infant weight trajectories. RESULTS:Prenatal spatiotemporal model predicted NO2 exposure was associated with infant growth trajectories for both sexes. Infants experienced the most rapid growth early on with an average deceleration in weight gain of 0.02 grams/day over the two-year period. Among females (n=243), a 1-SD increase (3.3 ppb) in NO2 exposure was significantly associated with growth acceleration of 0.001 grams/day (p=0.02) such that at 2-years-of-age, children exposed to higher prenatal NO2 weighed significantly more than lower-exposed individuals. Among males (n=228), the linear and quadratic parameters of growth were both statistically significant. However, by 2 years the trajectories converged and no significant differences in weight were observed. We found similar trends when examining NOx and ambient NO2 exposures. CONCLUSIONS:Our findings show prenatal NO2/ NOx exposure may play a role in childhood obesity, with more pronounced effects on weight gain in females. KEYWORDS: Air pollution, oxides of nitrogen, birth outcomes, children's environmental health

Early life air pollution exposure elevates general psychopathology risk at the transition to adulthood

BACKGROUND AND AIM: Air pollution exposure has been shown to damage the brain but its associations with the development of psychopathology are not fully characterized. This study tested whether early life air pollution exposure is associated with greater psychopathology at the transition to adulthood. METHODS: Air pollution exposure and young adult psychopathology were investigated in the Environmental-Risk (E-Risk) Longitudinal Twin Study, a population-representative UK-based cohort of 2,232 children born in 1994-1995 and followed to age 18 years. High-resolution annualized estimates of outdoor nitrogen oxides (NOx) and fine particulate matter (PM2.5) linked to age-10 and age-18 home addresses were combined with data on mental-health disorder symptoms assessed through structured interview at age 18. Symptom counts were transformed through confirmatory factor analysis into continuous measures of General Psychopathology and Internalizing, Externalizing, and Thought Disorder symptoms, all standardized to mean(SD)=100(15). Adjustments were made for high-resolution measures of disadvantageous neighborhood characteristics, including socioeconomic deprivation, physical dilapidation, social disconnection, and dangerousness. RESULTS:After adjustment for family and individual factors, each interquartile range increment increase in NOx exposure was associated with a 1.40-point increase (95%CI=0.41-2.38, P=.005) in General Psychopathology. Associations between continuously measured PM2.5 and General Psychopathology were non-significant; however, those in the highest quartile of PM2.5 exposure scored 2.04-points higher (95%CI=0.36-3.72, P=.017) than those in the bottom three quartiles. Co-pollutant models including both NOx and PM2.5 implicated NOx as the significant factor. NOx exposure was associated with all secondary outcomes, although associations were weakest for Internalizing, medium for Externalizing, and strongest for Thought Disorder symptoms. Despite NOx concentrations being highest in neighborhoods with worse physical, social, and economic conditions, adjusting estimates for neighborhood characteristics did not change the results. CONCLUSIONS:Youths exposed to higher levels of NOx outdoor-air pollution experienced greater psychopathology at the transition to adulthood. Air pollution may be a non-specific risk factor for the development of mental illness. KEYWORDS: Air pollution, Oxides of nitrogen, Mental health outcomes, Children's environmental health

Associations Between Prenatal Exposure to Air Pollution and Congenital Hypothyroidism.

Adequate thyroid hormone availability is required for normal brain development. Studies have found associations between prenatal exposure to air pollutants and thyroid hormones in pregnant women and newborns. We aimed to examine associations of trimester-specific residential exposure to common air pollutants with congenital hypothyroidism (CHT). All term infants born in Israel during 2009-2015 were eligible for inclusion. We used data on CHT from the national neonatal screening lab of Israel, and exposure data from spatiotemporal air pollution models. We used multivariable logistic regression models to estimate associations of exposures with CHT, adjusting for ethnicity, socioeconomic status, geographical area, conception season, conception year, gestational age, birth weight, and child sex. To assess residual confounding, we used postnatal exposures to the same pollutants as negative controls. The study population included 696,461 neonates. We found a positive association between third-trimester nitrogen oxide exposure and CHT (per interquartile-range change, odds ratio = 1.23, 95% confidence interval: 1.08, 1.41) and a similar association for nitrogen dioxide. There was no evidence of residual confounding or bias by correlation among exposure periods for these associations.

Early postnatal exposure to traffic-related air pollution and asthma in adolescents: vulnerability factors in the PARIS birth cohort

BackgroundAssociations between early traffic-related air pollution (TRAP) exposure and respiratory and allergic morbidity in adolescents are inconsistent. However, sub-groups might be more vulnerable to the health effects of this exposure. ObjectivesWe investigated associations between early exposure to TRAP and respiratory and allergic morbidity at age 13 years in the PARIS birth cohort, and potential modifying effects of sex, parental allergy, stressful family event and lower respiratory tract infections (LRTI). MethodsThis study deals with data from 732 children of the PARIS birth cohort followed up using repeated questionnaires until 13 years of age. Prenatal TRAP exposure was assessed by measuring daily concentrations of nitrogen dioxide at the nearest station to mother's home. Early postnatal TRAP exposure was calculated for each child during the first year of life by a nitrogen oxides (NOx) air dispersion model taking into account both residence and daycare. Associations between TRAP exposures and asthma, rhinitis and related symptoms were assessed using multivariable logistic regression models adjusted for potential confounding factors. Effect modification was explored by testing multiplicative interactions. ResultsAn increase in interquartile range (17.0 μg/m3) of early postnatal NOx exposure was positively related to current asthma (adjusted odds ratio aOR = 1.21; 95% confidence interval CI: 1.02, 1.43), severe wheeze (aOR = 1.23; 95% CI: 1.02, 1.47) and persistent asthma at 13 years old (aOR = 1.26; 95% CI: 1.03, 1.55) and tended to be associated with asthma ever. Parental history of allergy, asthma, early stressful family event and LRTI modified these associations with TRAP exposure. No relationship with rhinitis was found. Prenatal TRAP exposure did not show any association with respiratory and allergic morbidity. DiscussionThis study is one of the first to show several modifiers of the association between early postnatal TRAP exposure and asthma at adolescence. Not all adolescents seem equally affected by early postnatal TRAP exposure: those presenting parental history of allergy, especially asthma, those with early stressful family event or LRTI appear to be more vulnerable.

The impact of second-hand smoke on nitrogen oxides concentrations in a small interior

Nitrogen oxides (NOx), especially nitrogen dioxide (NO2), are among the most hazardous forms of air pollution. Tobacco smoke is a main indoor source of NOx, but little information is available about their concentrations in second-hand smoke (SHS), particularly in small indoors. This study presents data of NOx and its main components nitric oxide (NO) and NO2 in SHS emitted by ten different cigarette brands measured in a closed test chamber with a volume of 2.88 m3, similar to the volume of vehicle cabins. The results show substantial increases in NOx concentrations when smoking only one cigarette. The NO2 mean concentrations ranged between 105 and 293 µg/m3, the NO2 peak concentrations between 126 and 357 µg/m3. That means the one-hour mean guideline of 200 µg/m3 for NO2 of the World Health Organization was exceeded up to 47%, respectively 79%. The measured NO2 values show positive correlations with the values for tar, nicotine, and carbon monoxide stated by the cigarette manufacturers. This study provides NO2 concentrations in SHS at health hazard levels. These data give rise to the necessity of health authorities’ measures to inform about and caution against NOx exposure by smoking in indoor rooms.

Association of Air Pollution Exposure in Childhood and Adolescence With Psychopathology at the Transition to Adulthood

Air pollution exposure damages the brain, but its associations with the development of psychopathology are not fully characterized. To assess whether air pollution exposure in childhood and adolescence is associated with greater psychopathology at 18 years of age. The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born from January 1, 1994, to December 4, 1995, across England and Wales and followed up to 18 years of age. Pollution data generation was completed on April 22, 2020; data were analyzed from April 27 to July 31, 2020. High-resolution annualized estimates of outdoor nitrogen oxides (NOx) and particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) linked to home addresses at the ages of 10 and 18 years and then averaged. Mental health disorder symptoms assessed through structured interview at 18 years of age and transformed through confirmatory factor analysis into continuous measures of general psychopathology (primary outcome) and internalizing, externalizing, and thought disorder symptoms (secondary outcomes) standardized to a mean (SD) of 100 (15). Hypotheses were formulated after data collection, and analyses were preregistered. A total of 2039 participants (1070 [52.5%] female) had full data available. After adjustment for family and individual factors, each interquartile range increment increase in NOx exposure was associated with a 1.40-point increase (95% CI, 0.41-2.38; P = .005) in general psychopathology. There was no association between continuously measured PM2.5 and general psychopathology (b = 0.45; 95% CI, -0.26 to 1.11; P = .22); however, those in the highest quartile of PM2.5 exposure scored 2.04 points higher (95% CI, 0.36-3.72; P = .02) than those in the bottom 3 quartiles. Copollutant models, including both NOx and PM2.5, implicated NOx alone in these significant findings. NOx exposure was associated with all secondary outcomes, although associations were weakest for internalizing (adjusted b = 1.07; 95% CI, 0.10-2.04; P = .03), medium for externalizing (adjusted b = 1.42; 95% CI, 0.53-2.31; P = .002), and strongest for thought disorder symptoms (adjusted b = 1.54; 95% CI, 0.50-2.57; P = .004). Despite NOx concentrations being highest in neighborhoods with worse physical, social, and economic conditions, adjusting estimates for neighborhood characteristics did not change the results. Youths exposed to higher levels of outdoor NOx experienced greater psychopathology at the transition to adulthood. Air pollution may be a nonspecific risk factor for the development of psychopathology.