Personal Air Pollution Exposure Research Articles

User-Centred Design of a Final Results Report for Participants in Multi-Sensor Personal Air Pollution Exposure Monitoring Campaigns.

Using low-cost portable air quality (AQ) monitoring devices is a growing trend in personal exposure studies, enabling a higher spatio-temporal resolution and identifying acute exposure to high concentrations. Comprehension of the results by participants is not guaranteed in exposure studies. However, information on personal exposure is multiplex, which calls for participant involvement in information design to maximise communication output and comprehension. This study describes and proposes a model of a user-centred design (UCD) approach for preparing a final report for participants involved in a multi-sensor personal exposure monitoring study performed in seven cities within the EU Horizon 2020 ICARUS project. Using a combination of human-centred design (HCD), human–information interaction (HII) and design thinking approaches, we iteratively included participants in the framing and design of the final report. User needs were mapped using a survey (n = 82), and feedback on the draft report was obtained from a focus group (n = 5). User requirements were assessed and validated using a post-campaign survey (n = 31). The UCD research was conducted amongst participants in Ljubljana, Slovenia, and the results report was distributed among the participating cities across Europe. The feedback made it clear that the final report was well-received and helped participants better understand the influence of individual behaviours on personal exposure to air pollution.

Predicting the least air polluted path using the neural network approach

Air pollution exposure during daily transportation is becoming a critical issue worldwide due to its adverse effect on human health. Predicting the least air polluted healthier path is the best alternative way to mitigate personal air pollution exposure risk. Computing the least polluted path for th

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.

Feasibility and acceptability of monitoring personal air pollution exposure with sensors for asthma self-management

BackgroundExposure to fine particulate matter (PM2.5) increases the risk of asthma exacerbations, and thus, monitoring personal exposure to PM2.5 may aid in disease self-management. Low-cost, portable air pollution sensors offer a convenient way to measure personal pollution exposure directly and may improve personalized monitoring compared with traditional methods that rely on stationary monitoring stations. We aimed to understand whether adults with asthma would be willing to use personal sensors to monitor their exposure to air pollution and to assess the feasibility of using sensors to measure real-time PM2.5 exposure.MethodsWe conducted semi-structured interviews with 15 adults with asthma to understand their willingness to use a personal pollution sensor and their privacy preferences with regard to sensor data. Student research assistants used HabitatMap AirBeam devices to take PM2.5 measurements at 1-s intervals while walking in Philadelphia neighborhoods in May–August 2018. AirBeam PM2.5 measurements were compared to concurrent measurements taken by three nearby regulatory monitors.ResultsAll interview participants stated that they would use a personal air pollution sensor, though the consensus was that devices should be small (watch- or palm-sized) and light. Patients were generally unconcerned about privacy or sharing their GPS location, with only two stating they would not share their GPS location under any circumstances. PM2.5 measurements were taken using AirBeam sensors on 34 walks that extended through five Philadelphia neighborhoods. The range of sensor PM2.5 measurements was 0.6–97.6 μg/mL (mean 6.8 μg/mL), compared to 0–22.6 μg/mL (mean 9.0 μg/mL) measured by nearby regulatory monitors. Compared to stationary measurements, which were only available as 1-h integrated averages at discrete monitoring sites, sensor measurements permitted characterization of fine-scale fluctuations in PM2.5 levels over time and space.ConclusionsPatients were generally interested in using sensors to monitor their personal exposure to PM2.5 and willing to share personal sensor data with health care providers and researchers. Compared to traditional methods of personal exposure assessment, sensors captured personalized air quality information at higher spatiotemporal resolution. Improvements to currently available sensors, including more reliable Bluetooth connectivity, increased portability, and longer battery life would facilitate their use in a general patient population.

Long-term personal air pollution exposure and risk for acute exacerbation of idiopathic pulmonary fibrosis

BackgroundUrban air pollution is involved in the progress of idiopathic pulmonary fibrosis (IPF). Its potential role on the devastating event of Acute Exacerbation of IPF (AE-IPF) needs to be clarified. This study examined the association between long-term personal air pollution exposure and AE- IPF risk taking into consideration inflammatory mediators and telomere length (TL).MethodsAll consecutive IPF-patients referred to our Hospital from October 2013-June 2019 were included. AE-IPF events were recorded and inflammatory mediators and TL measured. Long-term personal air pollution exposures were assigned to each patient retrospectively, for O3, NO2, PM2.5 [and PM10, based on geo-coded residential addresses. Logistic regression models assessed the association of air pollutants’ levels with AE-IPF and inflammatory mediators adjusting for potential confounders.Results118 IPF patients (mean age 72 ± 8.3 years) were analyzed. We detected positive significant associations between AE-IPF and a 10 μg/m3 increase in previous-year mean level of NO2 (OR = 1.52, 95%CI:1.15–2.0, p = 0.003), PM2.5 (OR = 2.21, 95%CI:1.16–4.20, p = 0.016) and PM10 (OR = 2.18, 95%CI:1.15–4.15, p = 0.017) independent of age, gender, smoking, lung function and antifibrotic treatment. Introduction of TL in all models of a subgroup of 36 patients did not change the direction of the observed associations. Finally, O3 was positively associated with %change of IL-4 (p = 0.014) whilst PM2.5, PM10 and NO2 were inversely associated with %changes of IL-4 (p = 0.003, p = 0.003, p = 0.032) and osteopontin (p = 0.013, p = 0.013, p = 0.085) respectively.ConclusionsLong-term personal exposure to increased concentrations of air pollutants is an independent risk factor of AE-IPF. Inflammatory mediators implicated in lung repair mechanisms are involved.

Integrating monitor wearing to estimate household air pollution exposure parameters in the Ghana Randomized Air Pollution and Health Study (GRAPHS)

BACKGROUND AND AIM: Personal monitoring can enhance exposure-response studies. Prior studies employ a wearing compliance minimum threshold to reduce exposure misclassification. Leveraging the full range of device wearing data illuminates important exposure outcomes in the context of a large household air pollution cookstove intervention study with three arms (control, liquified petroleum gas (LPG), and improved biomass). METHODS: Evaluating the association between accelerometer-derived device wearing and mean 48-hr personal exposures in generalized estimating equations yields three parameters: (1) the y-intercept (0% device wearing) estimates community air pollution per study arm; (2) the difference between estimated concentrations per study arm at maximum device wearing is the effect of the cooking interventions on overall personal exposure; (3) estimated concentrations at maximum device wearing minus the y-intercept concentration estimates the average direct contribution of cooking events to personal exposure. RESULTS:Median device wearing during waking hours was 7- 8 hrs/day across study arms (range 0 - 15.9 hrs). Estimated community-level PM₂.₅ concentrations were similar across study arms (37-48 μg/m³). On average, the overall exposure was estimated at 108 ± 14 μg/m³ for the control arm and 53 ± 23 μg/m³ for LPG, suggesting a 50% reduction from this intervention. We estimate the direct contribution of individual cooking activities to exposure to be 60 ± 14 μg/m³ in the control arm and 6.2 ± 22.6 μg/m³ in the LPG arm (90% less). The improved biomass stove had negligible impact on reducing personal air pollution exposure. Using only data from cooking hours provided relatively similar % reductions for the LPG intervention (45% for overall; 85% for direct cooking impact). CONCLUSIONS:The association between device wearing and personal exposure allows quantification of important household air pollution exposure assessment outcomes, two of which previously could not be obtained without additional monitoring. KEYWORDS: Air pollution, Particulate matter, Modeling, Exposures

Prenatal and Postnatal Household Air Pollution Exposures and Pneumonia Risk: Evidence From the Ghana Randomized Air Pollution and Health Study

Nearly 40%of the world's population is exposed daily to household air pollution. The relative impact of prenatal and postnatal household air pollution exposure on early childhood pneumonia, a leading cause of mortality, is unknown. Are prenatal or postnatal household air pollution, or both, associated with pneumonia risk in the first year of life? The Ghana Randomized Air Pollution and Health Study enrolled 1,414 nonsmoking, pregnant women before 24weeks' gestation with prospective follow-up to the child's age of 1 year. We measured 72-h personal household air pollution exposures, indexed by carbon monoxide (CO), four times prenatally and three times postnatally. Weekly fieldworker surveillance identified ill-appearing children for physician pneumonia assessment. We used quasi-Poisson models to examine associations between prenatal and postnatal CO and physician-diagnosed pneumonia and severe pneumonia. Sex-specific effects were examined. Of the 1,306 live births, 1,141 infants were followed up with 55,605 child-weeks of fieldworker surveillance. The estimated risk for pneumonia and severe pneumonia in the first year of life increased by 10%(relative risk [RR], 1.10; 95%CI, 1.04-1.16) and 15%(RR, 1.15; 95%CI, 1.03-1.28), respectively, per 1-part per million (ppm) increase in average prenatal CO exposure and by 6%(RR, 1.06; 95%CI, 0.99-1.13) per 1-ppm increase in average postnatal CO exposure. Sex-stratified analyses suggest that in girls, higher prenatal CO exposure was associated with pneumonia risk, while no association was seen in boys. Prenatal household air pollution exposure increased risk of pneumonia and severe pneumonia in the first year of life. Clean-burning interventions may be most effective when begun prenatally. ClinicalTrials.gov; No.: NCT01335490; URL: www.clinicaltrials.gov.

Associations between time-weighted personal air pollution exposure and amino acid metabolism in healthy adults.

The molecular mechanisms underlying the associations between air pollution exposure and adverse cardiopulmonary effects remain to be better understood. Altered amino acid metabolism may plays an important role in the development of cardiopulmonary diseases and may be perturbed by air pollution exposure. To test this hypothesized molecular mechanism, we conducted an association analysis from an existing intervention study to examine the relations of air pollution exposures with amino acids in 43 Chinese healthy adults. Plasma levels of amino acids were measured using a UPLC-QqQ-MS system. Time-weighted personal exposure to O3, PM2.5, NO2, and SO2 over four time windows, i.e., 12h, 24h, 1week, and 2weeks, were calculated using the measured indoor and outdoor concentrations coupled with the time-activity data for each participant. Linear mixed-effects models were used to estimate the associations between air pollutants at each exposure window and amino acids by controlling for potential confounders. We observed significant associations between exposures and plasma concentrations of amino acids, with the direction of associations varying by amino acid and air pollutant. While there is little evidence of associations for NO2 and SO2, the associations with amino acids were fairly pronounced for exposure to PM2.5 and O3. In particular, independent O3 (12- and 24-hour) associations were observed with changes in the amino acids that were related to the urea cycle, including aspartate, asparagine, glutamate, arginine, citrulline, and ornithine. Our findings indicated that air pollution may cause acute perturbation of amino acid metabolism, and that O3 and PM2.5 may affect the metabolism of amino acids in different pathways. Main finding: Acute air pollution exposure might affect the perturbation of amino acid metabolism, and in particular, was associated with amino acids in relation to the urea cycle.

Environmental Determinants of Coronavirus Disease 2019 (COVID-19).

Purpose for ReviewSince the coronavirus SARS-CoV-2 outbreak in China in late 2019 turned into a global pandemic, numerous studies have reported associations between environmental factors, such as weather conditions and a range of air pollutants (particulate matter, nitrogen dioxide, ozone, etc.) and the first wave of COVID-19 cases. This review aims to offer a critical assessment of the role of environmental exposure risk factors on SARS-CoV-2 infections and COVID-19 disease severity.Recent FindingsIn this review, we provide a critical assessment of COVID-19 risk factors, identify gaps in our knowledge (e.g., indoor air pollution), and discuss methodological challenges of association and causation and the impact lockdowns had on air quality. In addition, we will draw attention to ethnic and socioeconomic factors driving viral transmission related to COVID-19. The complex role angiotensin-converting enzyme 2 (ACE2) plays in COVID-19 and future promising avenues of research are discussed.SummaryTo demonstrate causality, we stress the need for future epidemiologic studies integrating personal air pollution exposures, detailed clinical COVID-19 data, and a range of socioeconomic factors, as well as in vitro and in vivo mechanistic studies.

Effects of personal air pollution exposure on inflammatory responses: potential mediation by endogenous melatonin

Background/Aim: Melatonin is a free radical scavenger and an anti-inflammatory molecule. Air pollution exposure has been associated with increased inflammatory responses. We hypothesize that endogenous melatonin plays a role in inflammatory responses to air pollution exposure. Methods: We tested this hypothesis in a cohort of 53 healthy adults (22-52 years old, 16 women), none of whom were on melatonin supplementation. Early morning urine and blood were collected from each participant for up to three times. We analyzed urinary 6-sulfatoxymelatonin (aMT6s), as a surrogate of circulating melatonin, and pro- and anti-inflammatory cytokines in plasma. Indoor and outdoor air pollutants were measured and combined with participants' time-activity pattern to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week prior to biospecimen collection, respectively. Linear mixed effects models were used to examine the relationships of urinary aMT6s with personal pollution exposure and plasma cytokines controlling for covariates including temperature, humidity, sex, age, and respiratory infection &amp; smoking status. Mediation analysis was conducted to test whether aMT6s is a mediator for the relationships between pollution exposure and inflammatory cytokines. Results: A one interquartile range (4.2 ppb) increase in 2-week O3 exposure was associated with a -29.4% (95% CI: -50.0%, -0.50%) decrease in aMT6s, while the relationships of aMT6s with other pollutant exposures were nonsignificant. Within the range of endogenous aMT6s concentration (0.5-53.0 ng/ng creatinine), increasing aMT6s level was associated with decreasing levels of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8, IL-17A, IFN-γ, and TNF-α. The mediation analysis showed that 5.2%, 7.7%, 8.2%, 10.5%, 16.1%, and 8.3% of the total effects of 2-week O3 exposure on IL-1β, IL-6, IL-8, IL-17A, IFN-γ, and TNF-α were mediated by urinary aMT6s, respectively. Conclusions: Our findings suggest that air pollution exposure may decrease endogenous melatonin, which may further contribute to enhanced pro-inflammatory responses.

Household and personal air pollution exposure measurements from 120 communities in eight countries: results from the PURE-AIR study

SummaryBackgroundApproximately 2·8 billion people are exposed to household air pollution from cooking with polluting fuels. Few monitoring studies have systematically measured health-damaging air pollutant (ie, fine particulate matter [PM2·5] and black carbon) concentrations from a wide range of cooking fuels across diverse populations. This multinational study aimed to assess the magnitude of kitchen concentrations and personal exposures to PM2·5 and black carbon in rural communities with a wide range of cooking environments.MethodsAs part of the Prospective Urban and Rural Epidemiological (PURE) cohort, the PURE-AIR study was done in 120 rural communities in eight countries (Bangladesh, Chile, China, Colombia, India, Pakistan, Tanzania, and Zimbabwe). Data were collected from 2541 households and from 998 individuals (442 men and 556 women). Gravimetric (or filter-based) 48 h kitchen and personal PM2·5 measurements were collected. Light absorbance (10−5m−1) of the PM2·5 filters, a proxy for black carbon concentrations, was calculated via an image-based reflectance method. Surveys of household characteristics and cooking patterns were collected before and after the 48 h monitoring period.FindingsMonitoring of household air pollution for the PURE-AIR study was done from June, 2017, to September, 2019. A mean PM2·5 kitchen concentration gradient emerged across primary cooking fuels: gas (45 μg/m3 [95% CI 43–48]), electricity (53 μg/m3 [47–60]), coal (68 μg/m3 [61–77]), charcoal (92 μg/m3 [58–146]), agricultural or crop waste (106 μg/m3 [91–125]), wood (109 μg/m3 [102–118]), animal dung (224 μg/m3 [197–254]), and shrubs or grass (276 μg/m3 [223–342]). Among households cooking primarily with wood, average PM2·5 concentrations varied ten-fold (range: 40–380 μg/m3). Fuel stacking was prevalent (981 [39%] of 2541 households); using wood as a primary cooking fuel with clean secondary cooking fuels (eg, gas) was associated with 50% lower PM2·5 and black carbon concentrations than using only wood as a primary cooking fuel. Similar average PM2·5 personal exposures between women (67 μg/m3 [95% CI 62–72]) and men (62 [58–67]) were observed. Nearly equivalent average personal exposure to kitchen exposure ratios were observed for PM2·5 (0·79 [95% 0·71–0·88] for men and 0·82 [0·74–0·91] for women) and black carbon (0·64 [0·45–0·92] for men and 0·68 [0·46–1·02] for women).InterpretationUsing clean primary fuels substantially lowers kitchen PM2·5 concentrations. Importantly, average kitchen and personal PM2·5 measurements for all primary fuel types exceeded WHO’s Interim Target-1 (35 μg/m3 annual average), highlighting the need for comprehensive pollution mitigation strategies.

Characterization of outdoor air pollution from solid fuel combustion in Xuanwei and Fuyuan, a rural region of China

Outdoor air pollution is a growing public health concern, particularly in urban settings. However, there are limited epidemiological data on outdoor air pollution in rural areas with substantial levels of air pollution attributed to solid fuel burning for household cooking and heating. Xuanwei and Fuyuan are rural counties in China where the domestic combustion of locally sourced bituminous (“smoky”) coal has been associated with the highest lung cancer rates in China. We previously assessed indoor and personal air pollution exposures in this area; however, the influence of indoor coal combustion and household ventilation on outdoor air pollution has not been assessed. Therefore, we measured outdoor fine particulate matter (PM2.5), species of polycyclic aromatic hydrocarbons (PAHs) including naphthalene (NAP) and the known carcinogen benzo(a)pyrene (BaP), sulfur dioxide (SO2), and nitrogen dioxide (NO2) over two consecutive 24-h sampling periods in 29 villages. Just over half of the villages were revisited two to nine months after the initial sampling period to repeat all measurements. The overall geometric mean (GM) of outdoor PM2.5, BaP, NAP, and NO2 were 45.3 µg/m3, 9.7 ng/m3, 707.7 ng/m3, and 91.5 µg/m3, respectively. Using linear mixed effects models, we found that burning smoky coal was associated with higher outdoor BaP concentrations [GM ratio (GMR) = 2.79] and lower outdoor SO2 detection rates (GMR = 0.43), compared to areas burning smokeless coal. Areas with predominantly ventilated stoves (> 50% of stoves) had higher outdoor BaP (GMR = 1.49) compared to areas with fewer ventilated stoves. These results show that outdoor air pollution in a rural region of China was associated with the type of coal used for cooking and heating indoors and the presence of stove ventilation. Our findings suggest that efforts of household stove improvement to reduce indoor air pollution have resulted in higher outdoor air pollution levels. Further reducing adverse health effects in rural villages from household coal combustion will require the use of cleaner fuel types.

ASSESSMENT OF MICRONUCLEUS FREQUENCY AND RESPIRATORY HEALTH SYMPTOMS AMONG TRAFFIC POLICEMEN EXPOSED TO BTEX AND PM2.5 IN KLANG VALLEY, MALAYSIA

Volatile organic compounds such as benzene, toluene, ethylbenzene, xylene (BTEX), and particulate matter (PM) with a diameter of less than 2.5 microns (PM2.5) are often associated with traffic-related air pollution (TRAP) and harm the health of the community. This study aimed to evaluate the personal air pollutant exposure, micronucleus (MN) frequency, and respiratory health symptoms among 160 traffic policemen and 149 office workers in Klang Valley. Personal exposure concentrations for BTEX and PM2.5 among traffic police were 390.12 μg/m3 and 140.00 μg/m3 respectively, whereas 97.64 μg/m3 (BTEX) and 23.00 µg/m3 (PM2.5) among office workers. Statistical analysis for MN frequency between traffic policemen (6.2±2.6) and office workers (3.0±2.0) shows a significant difference (p &lt; 0.001). The Chi-Square test for respiratory health symptoms indicates that only cough shows the significant differences between traffic policemen and office workers (χ2 = 5.645, p = 0.018, PR = 1.800). In short, this study showed that TRAP exposure would increase the chromosomal damage that can cause high MN frequency among traffic policemen and would increase the prevalence of respiratory health symptoms among urban workers.

Long-standing LPG subsidies, cooking fuel stacking, and personal exposure to air pollution in rural and peri-urban Ecuador

Ecuador presents a unique case study for evaluating personal air pollution exposure in a middle-income country where a clean cooking fuel has been available at low cost for several decades. We measured personal PM2.5 exposure, stove use, and participant location during a 48-h monitoring period for 157 rural and peri-urban households in coastal and Andean Ecuador. While nearly all households owned a liquefied petroleum gas (LPG) stove and used it as their primary cooking fuel, one-quarter of households utilized firewood as a secondary fuel and 10% used induction stoves secondary to LPG. Stove use monitoring demonstrated clear within- and across-meal fuel stacking patterns. Firewood-owning participants had higher distributions of 48-h and 10-min PM2.5 exposure as compared with primary LPG and induction stove users, and this effect became more pronounced with firewood use during monitoring.Accounting for within-subject clustering, contemporaneous firewood stove use was associated with 101 μg/m3 higher 10-min PM2.5 exposure (95% CI: 94–108 μg/m3). LPG and induction cooking events were largely not associated with contemporaneous PM2.5 exposure. Our results suggest that firewood use is associated with average and short-term personal air pollution exposure above the WHO interim-I guideline, even when LPG is the primary cooking fuel.

Biomedical REAl-Time Health Evaluation (BREATHE): toward an mHealth informatics platform.

ObjectiveTo describe a configurable mobile health (mHealth) framework for integration of physiologic and environmental sensors to be used in studies focusing on the domain of pediatric asthma.Materials and MethodsThe Biomedical REAl-Time Health Evaluation (BREATHE) platform connects different sensors and data streams, contextualizing an individual’s symptoms and daily activities over time to understand pediatric asthma’s presentation and its management. A smartwatch/smartphone combination serves as a hub for personal/wearable sensing devices collecting data on health (eg, heart rate, spirometry, medications), motion, and personal exposures (eg, particulate matter, ozone); securely transmitting information to BREATHE’s servers; and interacting with the user (eg, ecological momentary assessments). Server-side integration of electronic health record data and spatiotemporally correlated information (eg, weather, traffic) elaborates on these observations. An initial panel study involving pediatric asthma patients was conducted to assess BREATHE.ResultsTwenty subjects were enrolled, during which BREATHE accrued seven consecutive days of continuous data per individual. The data were used to confirm knowledge about asthma (use of controller inhalers, time-activity behaviors, personal air pollution exposure), and additional analyses provided insights into within-day associations of environmental triggers and asthma exacerbations. Exit surveys focusing on mHealth usability, while positive, noted several translational challenges.DiscussionBased on these promising results, a longitudinal panel study to evaluate individual microenvironments and exposures is ongoing. Lessons learned thus far reflect the need to address various usability aspects, including convenience and ongoing engagement.ConclusionBREATHE enables multi-sensor mHealth studies, capturing new types of information alongside an evolving understanding of personal exposomes.

Personal exposure to particulate air pollution and vascular damage in peri-urban South India

ObjectiveAir pollution is a leading preventable risk factor for cardiovascular diseases. Previous studies mostly relied on concentrations at residence, which might not represent personal exposure. Personal air pollution exposure has a greater variability compared with levels of ambient air pollution, facilitating evaluation of exposure-response functions and vascular pathophysiology. We aimed to evaluate the association between predicted annual personal exposure to PM2.5 and black carbon (BC) and three vascular damage markers in peri-urban South India. MethodsWe analyzed the third wave of the APCAPS cohort (2010–2012), which recruited participants from 28 villages. We used predicted personal exposure to PM2.5 and BC derived from 610 participant-days of 24 h average gravimetric PM2.5 and BC measurements and predictors related to usual time-activity. Outcomes included carotid intima-media thickness (CIMT), carotid-femoral pulse wave velocity (cf-PWV) and augmentation index (AIx). We fit linear mixed models, adjusting for potential confounders and accounting for the clustered data structure. We evaluated nonlinear associations using generalized additive mixed models. ResultsOf the 3017 participants (mean age 38 years), 1453 (48%) were women. The average PM2.5 exposure was 51 µg/m3 (range 13–85) for men, and 61 µg/m3 (range 40–120) for women, while the average BC was 4 µg/m3 (range 3–7) for men and 8 µg/m3 (range 3–22) for women. A 10 μg/m3 increase of PM2.5 was positively associated with CIMT (0.026 mm, 95% CI 0.014, 0.037), cf-PWV (0.069 m/s, 95% CI 0.008, 0.131) and AIx (0.8%, 95% CI 0.3, 1.3) among men. The exposure-response function for PM2.5 and AIx among men showed non-linearity, particularly within the exposure range dominated by tobacco smoking and occupational exposures. Both PM2.5 and BC were positively associated with AIx among women (0.6%, 95% CI 0.2, 1.0, per 10 μg/m3 PM2.5; 0.5%, 95% CI 0.1, 0.8, per 2 μg/m3 BC). ConclusionsPersonal exposure to particulate matter was associated with vascular damage in a peri-urban population in South India. Personal exposure to particulate matter appears to have gender-specific effects on the type of vascular damage, potentially reflecting differences in sources of personal exposure by gender.

Inflammatory and oxidative stress responses of healthy adults to changes in personal air pollutant exposure

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22–52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O3, PM2.5, NO2, and SO2 exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O3 exposures and significantly but positively associated with 2-week O3 exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO2 exposures, respectively. However, we did not find clear associations of PM2.5 and SO2 exposure with proinflammatory cytokines and with MDA. The removal of an O3-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O3 for different time durations may affect systemic inflammatory responses in different ways.

Microenvironmental modelling of personal fine particulate matter exposure in Accra, Ghana

The health burden from exposure to fine particulate matter (PM2.5) is disproportionately concentrated in low- and middle-income countries. To evaluate strategies to reduce PM2.5 exposure, the contribution of different sources, both indoor and outdoor, to overall personal PM2.5 exposure needs to be identified. Despite this, exposure to PM2.5 from indoor and outdoor origin are most often considered separately. This work presents the first application of a microenvironmental modelling approach in a sub-Saharan African city (Accra, Ghana) to estimate personal PM2.5 exposures to population groups disaggregated by gender and age and identify the key factors determining these exposures. Time-activity profiles for each population group were combined with PM2.5 concentrations estimated for three home microenvironments using a dynamic microenvironmental model, INDAIR, and for work, school and transport microenvironments using a steady-state model to estimate personal PM2.5 exposures. In Accra, cooking using charcoal, compared to liquified petroleum gas (LPG), was estimated to result in substantially higher home PM2.5 concentrations, and higher personal PM2.5 exposure for the female adult and child population groups, compared with the male population groups. In households cooking using charcoal, more than 60% of total personal PM2.5 exposure was estimated to be due to residential cooking for the child and female population groups, which reduces to less than 10% when LPG was used for cooking, with the remaining contribution from PM2.5 of outdoor origin. The key parameters to which personal PM2.5 exposure estimates are sensitive are the air exchange rate between indoor and outdoors, the kitchen volume, and charcoal emission rates. This study therefore informs on the additional data collection and measurements that could substantially enhance the parameterisation of micro-environmental models for application in low- and middle-income countries where a limited number of studies have been conducted, and improve their utility in assessing strategies to reduce personal air pollution exposure of different population groups.

Dynamic classification of personal microenvironments using a suite of wearable, low-cost sensors.

Human exposure to air pollution is associated with increased risk of morbidity and mortality. However, personal air pollution exposures can vary substantially depending on an individual’s daily activity patterns and air quality within their residence and workplace. To develop and validate an adaptive buffer size (ABS) algorithm capable of dynamically classifying an individual’s time spent in predefined microenvironments using data from global positioning systems (GPS), motion sensors, temperature sensors, and light sensors. Twenty-two participants in Fort Collins, CO were recruited to carry a personal air sampler for a 48-hour period. The personal sampler was retrofitted with a GPS and a pushbutton to complement the existing sensor measurements (temperature, motion, light). The pushbutton was used in conjunction with a traditional time-activity diary to note when the participant was located at “home”, “work”, or within an “other” microenvironment. The ABS algorithm predicted the amount of time spent in each microenvironment with a median accuracy of 99.1%, 98.9%, and 97.5% for the “home”, “work”, and “other” microenvironments. The ability to classify microenvironments dynamically in real-time can enable the development of new sampling and measurement technologies that classify personal exposure by microenvironment.

Innovative Methods of Air Pollution Exposure Assessment for Environmental Safety

Abstract Indignation from air pollution is an early signal to instinctive health issues in human. Assessment of human exposure to pollutants for the epidemiological studies will be one of the subsidiary objectives of data analytics for precision medicine forecast for the individuals in the industrially polluted region. The objective of the research determines whether to estimate personal air pollution exposure or population exposure. The exposure can be long term and short term. It includes indoor and outdoor. Direct methods like personal monitoring by using smart phones, air pollution sensors are accurate but quite expensive for huge populations. Indirect methods incorporate information gained from questionnaires accompanied by measured pollutants from the monitoring sites. Lean on the nature of analysis, the assessment pattern may vary. This paper discusses most popular air pollution assessment methods applied in the epidemiological studies related to air pollution. Recent trends in epidemiological studies led to the development of air pollution exposure assessment models that rely on satellite measurement of pollutants. Usage of geographic information system for exposure assessment demands spatial analysis. Mobile applications and sensor technology equipment for personal exposure assessment are promising methods in this study. The articles discussed in this study also observes the method of measurement of each pollutant exposure to individuals by geocoding the addresses with the average pollutant concentration measured at fixed site stations.