Related Air Pollution Exposure Research Articles

Climate change as a threat multiplier to environmental reproductive justice

Legacies of racial capitalism and colonialism drive present day racial disparities in perinatal health outcomes. Climate change amplifies existing social inequalities associated with environmental exposures and reproductive health, of which BIPOC (Black, Indigenous, and people of color) communities bear a disproportionate burden. Through case studies, this article summarizes three examples of climate justice issues with reproductive healthcare outcomes: traffic related air pollution exposure, chemical exposures in personal care products and plastics, and natural disaster frequency. We advocate for incorporation of climate justice and environmental health impact into medical school curriculum, increased prenatal screening for environmental toxins, and physician engagement with local environmental issues.

Prenatal depression increases susceptibility to periconceptional ambient air pollution exposure in relation to risk of gestational hypertension

Prenatal depression increases susceptibility to periconceptional ambient air pollution exposure in relation to risk of gestational hypertension

Adverse childhood experiences intensify retinal microvascular and inflammatory responses to semi-controlled acute traffic related air pollution exposure

Background: Potential synergy between childhood exposure to psychosocial stressors and traffic-related air pollution exposure, two factors that commonly overlap in socially disadvantaged groups, could increase the risk of cardiovascular disease and lead to greater health disparity than what is currently attributed to these factors independently. Aim: To test whether adverse childhood experiences (ACEs) potentiate the response of retinal microvasculature caliber and circulatory pro-inflammatory cytokines following a two-hour semi-controlled exposure to traffic related air pollution. Method: In a crossover experiment, 57 participants were exposed to near-traffic ambient air and filtered ambient air, in separate occasions for two hours each time. Central retinal arteriolar/venular equivalent (CRAE/CRVE), blood pressure, pulse, and circulating interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) were measured pre-exposure and, again, 1 hour and 24 hours post-exposure. ACEs were documented using the ACE questionnaire. Based on ACE scores, participants were grouped into high (ACE ≥ 4) and low (ACE ≤ 1) ACE groups. Microvascular and inflammatory response to the exposure were analyzed across groups. Results: ACE scores significantly predicted CRAE, IL-6, IL-8, and pulse reactivity. Left eye CRAE narrowing was greater in the high- vs. low-ACE group at 1-hour and 24-hours post-exposure. 24-hours post-exposure, IL-8 and pulse were significantly higher in the high- vs. low-ACE group. IL-6 was significantly lower in the high- vs. low-ACE group at 1-hour post-exposure. Conclusion: Our results support the hypothesis that ACEs may induce susceptibility to air pollution across the lifespan. These findings may thus help explain how health disparities develop and persist across the lifespan in persons who are most vulnerable to experiencing ACEs and poor air quality, leading to continued social disadvantage.

Association between traffic related air pollution exposure and direct health care costs in Northern California

BackgroundTraffic related air pollution (TRAP) is associated with a complex and diverse array of health effects. It is unknown whether these effects may be reflected by higher health care costs. ObjectivesEvaluate the association between TRAP exposure and direct health care costs in an elderly population. MethodsThis multi-ethnic population-based cohort of 25,684 elderly subjects, served by Kaiser Permanente Northern California (KPNC), were followed between 2013 and 2017. Hyperlocal long-term pollutant concentrations for nitrogen dioxide [NO2], nitric oxide [NO], and black carbon [BC] were measured at a resolution of 30 m using repeated street-level mobile measurements and linked to residential addresses. Health care utilization and costs were derived from KPNC databases and were used to calculate individual annual total health care, inpatient, outpatient, and emergency room (ER) and pharmacy costs. The associations between TRAP exposures and health care costs were evaluated using generalized estimating equation models adjusted for age, sex, race, BMI, smoking, SES and comorbidities. Subgroup analyses and interaction models were used to assess differences among specific susceptible population subgroups. ResultsAn IQR difference (10.1 ppb vs 4.2 ppb) in NO2 concentration was associated with a 3% (95% CI: -1%, 6%), 22% (95% CI:11%, 35%), and 5% (95% CI:1%, 8%) increase in annual total health care, ER and outpatient costs in the baseline model. Associations with black carbon showed similar patterns but were smaller in magnitude. Among those with cardiovascular diseases, an IQR increase in NO2 was associated with a 7% (95% CI: 1%, 13%) increase in total annual health care cost and 23% (95% CI: 17%, 29%) increase in ER costs. DiscussionHigher long-term TRAP exposure was associated with higher direct annual health care cost in this elderly cohort. Those with existing cardiovascular disease had particularly strong associations between TRAP exposure and direct annual health care costs.

Assessment of air pollution exposure in relation with smoking status in COPD patients from Iasi, Romania

Assessment of air pollution exposure in relation with smoking status in COPD patients from Iasi, Romania

Air pollution exposure in relation to guard duty at Tidworth Camp: A cross-sectional study

BackgroundAir pollution is the largest environmental health risk in the United Kingdom, and an issue of concern amongst outdoor workers. Road transport is a major source producing the largest amount of nitrogen dioxide (NO2) and ozone (O3) (as a secondary pollutant). Hundreds of vehicles enter and exit the Tidworth Camp’s main gate daily, potentially producing these pollutants. However, the air pollution exposure experienced by personnel on guard duty is unknown. This study aimed to determine and compare background NO2 and O3 levels experienced by personnel on guard duty.MethodsCross-sectional data was collected using a static sampling technic on randomly selected days of the week. Data analysis was done using IBM-SPSS-26 and a p-value of <0.05 was considered statistically significant.ResultsThe background concentration of NO2 and O3 pollutants were within recommended limits. There was no significant difference between mean morning and afternoon exposure levels for both pollutants. However, NO2 and O3 levels were significantly higher during weekdays compared to weekends (M = -0.022, SD = 0.007, t(6) = -8.672, p <0.0001 and M = -0.016, SD = 0.008, t(6) = -5.040, p = 0.002 respectively). Both pollutants showed no significant differences in exposure levels when only weekdays were compared. NO2 levels showed a weak positive correlation during weekdays (r = 0.04) and a strong positive correlation during weekends (r = 0.96). O3 levels had a positive correlation on both weekdays and weekends; however, levels on Monday showed a negative correlation (r = -0.55). Linear regression analysis showed that outside temperature was a significant predictor of O3 levels (p = 0.026).ConclusionPersonnel on guard duty experienced higher pollution levels during weekdays compared to weekends; however, air pollution levels for both pollutants were within recommended limits. Further studies are recommended over hotter months using a personal sampling technic to measure personal air pollution exposure levels in order to minimise any health and safety risks.

Traffic Related Air Pollution Exposure Effect on Circulating White Blood Cell Counts in Healthy Individuals

During this short term study a total of 110 samples were collected from the selected individuals of study area. This study was aimed to count the White blood cells in the blood samples of individuals, who were mostly exposed to exhaust fumes (air pollution), like traffic constables, cooks and shopkeepers. For this purpose blood samples were taken into an evacuee container having anticoagulant Ethylene diamine tetra-acetic acid (EDTA) so to prevent coagulation of blood, for the count of WBCs, heamocyto-meter was used. During the study the body mass index and blood pressure was also measured by digital blood pressure measuring apparatus. Samples were observed under the microscope. It was found that 15% (13,133±2544.081) sampled individuals had increased WBCs and 85% (7821±1482.76) normal WBCs. In female samples 50% (11900±2151.27) were observed with above range of WBCs and other 50% (8540±844.39) with normal range of WBCs count, non-had WBCs count lower than the normal WBCs. Mostly had normal and few had above the range. One way ANOVA has been used to analyze connection of exposure to air pollution with counts of circulating white blood cells.

Life Course Air Pollution Exposure and Cognitive Decline: Modelled Historical Air Pollution Data and the Lothian Birth Cohort 1936.

Background:Air pollution has been consistently linked with dementia and cognitive decline. However, it is unclear whether risk is accumulated through long-term exposure or whether there are sensitive/critical periods. A key barrier to clarifying this relationship is the dearth of historical air pollution data.Objective:To demonstrate the feasibility of modelling historical air pollution data and using them in epidemiologicalmodels.Methods:Using the EMEP4UK atmospheric chemistry transport model, we modelled historical fine particulate matter (PM2.5) concentrations for the years 1935, 1950, 1970, 1980, and 1990 and combined these with contemporary modelled data from 2001 to estimate life course exposure in 572 participants in the Lothian Birth Cohort 1936 with lifetime residential history recorded. Linear regression and latent growth models were constructed using cognitive ability (IQ) measured by the Moray House Test at the ages of 11, 70, 76, and 79 years to explore the effects of historical air pollution exposure. Covariates included sex, IQ at age 11 years, social class, and smoking.Results:Higher air pollution modelled for 1935 (when participants would have been in utero) was associated with worse change in IQ from age 11–70 years (β = –0.006, SE = 0.002, p = 0.03) but not cognitive trajectories from age 70–79 years (p > 0.05). There was no support for other critical/sensitive periods of exposure or an accumulation of risk (all p > 0.05).Conclusion:The life course paradigm is essential in understanding cognitive decline and this is the first study to examine life course air pollution exposure in relation to cognitive health.

Air Pollution Exposure in Relation to the Periconception Serum Metabolome in Women

Background/Aim: Periconception air pollution exposure has been linked with diminished fertility, adverse birth outcomes, and neurodevelopmental disorders. Identifying the metabolic changes induced by air pollution exposure among reproductive-aged women could enhance our understanding of the biological pathways underlying air pollution’s reprotoxicity. Thus, our objective was to identify metabolic alterations associated with periconception air pollution exposure in women using a metabolome-wide association study. Methods: Our study included 200 women undergoing in vitro fertilization (IVF) at a fertility center in Boston, Massachusetts (2005-2015). Women provided blood samples during controlled ovarian stimulation and untargeted metabolic profiling was conducted on the serum samples using liquid chromatography with ultra-high-resolution mass spectrometry. Spatiotemporal models estimated residence-based daily nitrogen dioxide (NO2), ozone (O3), and fine particulate (PM2.5) concentrations in the 3 months prior to starting IVF. We evaluated associations between each air pollutant and each metabolic feature using linear regression adjusted for age, BMI, education level, smoking status, and average temperature. Pathway analyses were employed to identify biological pathways related to air pollution exposure. Results: From the negative and positive ionization modes, 10,803 and 12,968 metabolic features were extracted, respectively. Higher exposure to NO2, O3, and PM2.5 was associated with 80, 35, and 246 features, respectively, after controlling for false discovery rate. Across all three pollutants, no common feature was significantly altered; however, higher exposure to NO2, O3, and PM2.5 resulted in perturbations in the glycine, serine, alanine and threonine and linoleate pathways and to a lesser extent in the leukotriene, urea cycle/amino group vitamin E, and prostaglandin formation from arachidonate pathways. Conclusions: In this cross-sectional study, periconception air pollution exposures were correlated with a variety of metabolic pathways such as amino acid metabolism, inflammation, and oxidative stress. Future studies should determine whether these pathways mediate associations between air pollution and couple fertility.

Association BetweenPM2.5Exposure and Preeclampsia

Background: Previous studies have suggested that traffic-related air pollution can increase risk of pregnancy complications. The purpose of this research is to investigate if PM2.5 exposure one year prior to conception is associated with preeclampsia. Methods: We obtained all live and still births from the Massachusetts state birth registry with an estimated conception date between January 2002 through December 2008. We randomly selected 2,000 infants conceived each year to serve as the study population. Of those 14,000 births, all mothers diagnosed with the main symptoms of preeclampsia, high blood pressure or proteinuria, were identified as cases. Cumulative PM2.5 exposure was assessed using 4-km spatial satellite remote sensing, meteorological and land use spatiotemporal models at geocoded birth addresses for the year prior to conception. We calculated crude and adjusted preeclampsia odds ratios (ORs) and 95% confidence intervals (CI) per 10 µg/m3 increase of PM2.5 exposure. Analyses of complete data were adjusted for demographic, socioeconomic, and reproductive characteristics of the mother. Births missing over 70% of PM2.5 data were excluded. Results: Our final analyses included 576 cases and 11,679 controls. Cumulative PM2.5 exposure during the year prior to conception was not associated with preeclampsia in the unadjusted analyses (OR: 1.02; 95%CI: 0.97,1.07). After adjusting for maternal age, race, education, language, insurance status, parity, smoking, drinking, adequacy of care, and year of birth, PM2.5 exposure remained not significantly associated with preeclampsia (OR: 1.04; 95%CI: 0.98,1.10). As confirmed by prior literature, Non-Hispanic Black mothers had almost double the risk of being a case compared to the referent group (Non-Hispanic White) (OR: 1.89; 95%CI: 1.44,2.48). Discussion: We did not find evidence to support the relationship between maternal traffic related air pollution exposure and preeclampsia. Future work will assess whether other areas with a higher threshold of air pollution exposure would be associated with preeclampsia.

Effects of low exposure to traffic related air pollution on childhood asthma onset by age 10 years

Although NO2, a major traffic related air pollutant, has been associated with onset of childhood asthma, young children may be more susceptible to traffic related air pollution exposure compared to other individuals. We linked data from National Longitudinal Survey of Children and Youths Cycle 1–5 (1994–2003) and the National Air Pollution Surveillance Program to determine the association between NO2 exposure and either early or late onset childhood asthma phenotypes. Children diagnosed with asthma from age 0–3 were defined as having early onset asthma. Children diagnosed with asthma from age 4–9 were defined as having late onset asthma. Mean NO2 exposure for each quartile was 6.31 ppb, 9.45 ppb, 11.83 ppb, and 17.9 ppb. Higher levels of NO2 exposure were more strongly associated with early childhood asthma (Quartile 3 OR: 2.11, 95% CI: 1.29, 3.44, Quartile 4 OR: 2.16, 95% CI: 1.27, 3.68) compared to the lowest level of NO2 exposure (Quartile 1). No such association was observed with risk of late childhood asthma onset. Asthma susceptibility to NO2 exposure may vary with the childhood developmental stage, and young children may be susceptible to NO2 exposure at levels well below national and international guidelines. Our study emphasizes the importance of considering the timing of childhood asthma onset in future studies and confirms the increased risk of early onset of childhood asthma associated even with relatively low NO2 exposure levels.

Reduced gray matter volume and cortical thickness associated with traffic-related air pollution in a longitudinally studied pediatric cohort.

Early life exposure to air pollution poses a significant risk to brain development from direct exposure to toxicants or via indirect mechanisms involving the circulatory, pulmonary or gastrointestinal systems. In children, exposure to traffic related air pollution has been associated with adverse effects on cognitive, behavioral and psychomotor development. We aimed to determine whether childhood exposure to traffic related air pollution is associated with regional differences in brain volume and cortical thickness among children enrolled in a longitudinal cohort study of traffic related air pollution and child health. We used magnetic resonance imaging to obtain anatomical brain images from a nested subset of 12 year old participants characterized with either high or low levels of traffic related air pollution exposure during their first year of life. We employed voxel-based morphometry to examine group differences in regional brain volume, and with separate analyses, changes in cortical thickness. Smaller regional gray matter volumes were determined in the left pre- and post-central gyri, the cerebellum, and inferior parietal lobe of participants in the high traffic related air pollution exposure group relative to participants with low exposure. Reduced cortical thickness was observed in participants with high exposure relative to those with low exposure, primarily in sensorimotor regions of the brain including the pre- and post-central gyri and the paracentral lobule, but also within the frontal and limbic regions. These results suggest that significant childhood exposure to traffic related air pollution is associated with structural alterations in brain.

Spatial variability in air pollution exposure in relation to socioeconomic indicators in nine European metropolitan areas: A study on environmental inequality

A limited number of studies have addressed environmental inequality, using various study designs and methodologies and often reaching contradictory results. Following a standardized multi-city data collection process within the European project EURO-HEALTHY, we conducted an ecological study to investigate the spatial association between nitrogen dioxide (NO2), as a surrogate for traffic related air pollution, and ten socioeconomic indicators at local administrative unit level in nine European Metropolitan Areas. We applied mixed models for the associations under investigation with random intercepts per Metropolitan Area, also accounting for the spatial correlation. The stronger associations were observed between NO2 levels and population density, population born outside the European Union (EU28), total crimes per 100,000 inhabitants and unemployment rate that displayed a highly statistically significant trend of increasing concentrations with increasing levels of the indicators. Specifically, the highest vs the lowest quartile of each indicator above was associated with 48.7% (95% confidence interval (CI): 42.9%, 54.8%), 30.9% (95%CI: 22.1%, 40.2%), 19.8% (95%CI: 13.4%, 26.6%) and 15.8% (95%CI: 9.9%, 22.1%) increase in NO2 respectively.The association with population density most probably reflects the higher volume in vehicular traffic, which is the main source of NO2 in urban areas. Higher pollution levels in areas with higher percentages of people born outside EU28, crime or unemployment rates indicate that worse air quality is typically encountered in deprived European urban areas. Policy makers should consider spatial environmental inequalities to better inform actions aiming to lower urban air pollution levels that will subsequently lead to improved quality of life, public health and health equity across the population.

Childhood fish oil supplementation modifies associations between traffic related air pollution and allergic sensitisation

BackgroundStudies of potential adverse effects of traffic related air pollution (TRAP) on allergic disease have had mixed findings. Nutritional studies to examine whether fish oil supplementation may protect against development of allergic disease through their anti-inflammatory actions have also had mixed findings. Extremely few studies to date have considered whether air pollution and dietary factors such as fish oil intake may interact, which was the rationale for this study.MethodsWe conducted a secondary analysis of the Childhood Asthma Prevention Study (CAPS) birth cohort, where children were randomised to fish oil supplementation or placebo from early life to age 5 years. We examined interactions between supplementation and TRAP (using weighted road density at place of residence as our measure of traffic related air pollution exposure) with allergic disease and lung function outcomes at age 5 and 8 years.ResultsOutcome information was available on approximately 400 children (~ 70% of the original birth cohort). Statistically significant interactions between fish oil supplementation and TRAP were seen for house dust mite (HDM), inhalant and all-allergen skin prick tests (SPTs) and for HDM-specific interleukin-5 response at age 5. Adjusting for relevant confounders, relative risks (RRs) for positive HDM SPT were RR 1.74 (95% CI 1.22–2.48) per 100 m local road or 33.3 m of motorway within 50 m of the home for those randomised to the control group and 1.03 (0.76–1.41) for those randomised to receive the fish oil supplement. The risk differential was highest in an analysis restricted to those who did not change address between ages 5 and 8 years. In this sub-group, supplementation also protected against the effect of traffic exposure on pre-bronchodilator FEV1/FVC ratio.ConclusionsResults suggest that fish oil supplementation may protect against pro-allergic sensitisation effects of TRAP exposure. Strengths of this analysis are that supplementation was randomised and independent of TRAP exposure, however, findings need to be confirmed in a larger experimental study with the interaction investigated as a primary hypothesis, potentially also exploring epigenetic mechanisms. More generally, studies of adverse health effects of air pollution may benefit from considering potential effect modification by diet and other factors.Trial registrationAustralia New Zealand Clinical Trial Registry. www.anzctr.org.au Registration: ACTRN12605000042640, Date: 26th July 2005. Retrospectively registered, trial commenced prior to registry availability.

Survival analysis with functions of mismeasured covariate histories: the case of chronic air pollution exposure in relation to mortality in the nurses' health study.

Environmental epidemiologists are often interested in estimating the effect of functions of time-varying exposure histories, such as the 12-month moving average, in relation to chronic disease incidence or mortality. The individual exposure measurements that comprise such an exposure history are usually mis-measured, at least moderately, and, often, more substantially. To obtain unbiased estimates of Cox model hazard ratios for these complex mis-measured exposure functions, an extended risk set regression calibration method for Cox models is developed and applied to a study of long-term exposure to the fine particulate matter (PM2.5) component of air pollution in relation to all-cause mortality in the Nurses' Health Study. Simulation studies under several realistic assumptions about the measurement error model and about the correlation structure of the repeated exposure measurements were conducted to assess the finite sample properties of this new method, and found that the method has good performance in terms of finite sample bias reduction and nominal confidence interval coverage.

Traffic Related Air Pollution and Transplant Failure

Background There is limited evidence that exposure to traffic related air pollution is associated with the development of chronic lung allograft dysfunction and graft failure among lung transplant recipients. The aim of the study is to explore associations between traffic related air pollution and transplant failure among lung and other solid organ transplant recipients in Great Britain. Methods All lung, heart, liver, and kidney transplants between 2000 and 2008 were included. The last follow up date was 2 nd March 2015. Using residential postcode at time of transplant, we calculated distance to nearest road and distance to nearest major road. In addition, annual average air pollution exposures were modelled for each transplant recipient, including nitrogen dioxide, nitrogen oxides and particulate matter (PM 10 , PM 2.5 ). Cox regression models were fitted to assess associations between each air pollutant and transplant failure after adjustment for age, sex, transplant year and donor age/smoking status. Results 780 lung, 1213 heart, 3650 liver and 11966 graft kidney transplant patients were included in the analysis. The estimated median follow up time (years) was 9.1, 10.0, 9.1 and 8.8 for lung, heart, liver and kidney respectively. We did not find any consistent association between first lung, liver and kidney transplant failure and any of the analysed air pollutants. Conclusions Our analysis does not confirm associations between traffic related air pollution exposure and the risk of transplant failure as reported by previous studies.

Air pollution exposure in relation to the commute to school: a Bradford UK case study

Air pollution exposure in relation to the commute to school: a Bradford UK case study

Air Pollution Exposure in Relation to the Commute to School: A Bradford UK Case Study

Walking School Buses (WSBs) provide a safe alternative to being driven to school. Children benefit from the contribution the exercise provides towards their daily exercise target, it gives children practical experience with respect to road safety and it helps to relieve traffic congestion around the entrance to their school. Walking routes are designed largely based in road safety considerations, catchment need and the availability of parent support. However, little attention is given to the air pollution exposure experienced by children during their journey to school, despite the commuting microenvironment being an important contributor to a child’s daily air pollution exposure. This study aims to quantify the air pollution exposure experienced by children walking to school and those being driven by car. A school was chosen in Bradford, UK. Three adult participants carried out the journey to and from school, each carrying a P-Trak ultrafine particle (UFP) count monitor. One participant travelled the journey to school by car while the other two walked, each on opposite sides of the road for the majority of the journey. Data collection was carried out over a period of two weeks, for a total of five journeys to school in the morning and five on the way home at the end of the school day. Results of the study suggest that car commuters experience lower levels of air pollution dose due to lower exposure and reduced commute times. The largest reductions in exposure for pedestrians can be achieved by avoiding close proximity to traffic queuing up at intersections, and, where possible, walking on the side of the road opposite the traffic, especially during the morning commuting period. Major intersections should also be avoided as they were associated with peak exposures. Steps to ensure that the phasing of lights is optimised to minimise pedestrian waiting time would also help reduce exposure. If possible, busy roads should be avoided altogether. By the careful design of WSB routes, taking into account air pollution, children will be able to experience the benefits that walking to school brings while minimizing their air pollution exposure during their commute to and from school.

Traffic-related air pollution and transplant failure in the UK

There is limited evidence that exposure to traffic-related air pollution is associated with the development of chronic lung allograft dysfunction and graft failure among lung transplant recipients. In this study we explore associations between traffic related air pollution and transplant failure among solid organ transplant recipients in Great Britain. We included all first lung, heart, liver and kidney transplants in Great Britain between 2000 and 2008. For each transplant recipient we used ESCAPE methods to model annual average air pollution exposure including nitrogen dioxide, nitrogen oxides and particulate matter (PM10, PM2.5, PMcoarse) for residential postcodes at time of transplant. We also included distance from residential postcode to nearest road and to nearest major road as well as traffic intensity on nearest major road. We fitted Cox regression models to assess associations between each air pollutant and transplant failure after adjustment for age, sex, socioeconomic and donor age/smoking status. We did not find any consistent association between first lung, liver, kidney or heart transplant failure and any of the analysed air pollutants or road metrics. The hazard ratio for distance to nearest road was 1.02 (95% CI 0.94-1.11), 1.01 (95% CI 0.91-1.11), 1.03 (95% CI 0.97-1.08) and 1.02 (95% CI 0.98-1.06) for lung, heart, liver and kidney failure, respectively. No consistent associations were seen in sensitivity analyses stratified by age-group (&gt;60 years vs &lt;60) and year of transplant. Our analysis did not find consistent associations between traffic related air pollution exposure and the risk of transplant failure. These findings contradict the limited current evidence on this topic and suggest that further work is need before any policies are developed.